Australia's Poisonous Plants, Fungi and Cyanobacteria: A Guide to Species of Medical and Veterinary Importance 0643092676, 9780643092679

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Australia’s Poisonous Plants, Fungi and Cyanobacteria A Guide to Species of Medical and Veterinary Importance Ross McKenzie

Australia’s Poisonous Plants, Fungi and Cyanobacteria A Guide to Species of Medical and Veterinary Importance

What is there that is not a poison? All things are poison and nothing [is] without poison. Solely the dose determines that a thing is not a poison. … While a thing may be a poison, it may not cause poisoning. (Often paraphrased as: The dose makes the poison.). Paracelsus [Philippus Aureolus Theophrastus Bombastus von Hohenheim] (1492–1541)

The animal species, the dose and the circumstances make the poison. (McKenzie’s Maxim) Ross McKenzie (1949– )

Australia’s Poisonous Plants, Fungi and Cyanobacteria A Guide to Species of Medical and Veterinary Importance

Ross McKenzie

© Ross Andrew McKenzie 2012 This digital edition published with corrections 2020 All rights reserved. Except under the conditions described in the Australian Copyright Act 1968 and subsequent amendments, no part of this publication may be reproduced, stored in a retrieval system or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, duplicating or otherwise, without the prior permission of the copyright owner. Contact CSIRO Publishing for all permission requests. The author asserts their moral rights, including the right to be identified as the author. A catalogue record for this book is available from the National Library of Australia. ISBN: 9780643092679 (hbk) ISBN: 9781486313877 (epdf) ISBN: 9781486313884 (epub) Published by CSIRO Publishing Locked Bag 10 Clayton South VIC 3169 Australia Telephone: +61 3 9545 8400 Email: [email protected] Web site: www.publish.csiro.au Front cover: Castanospermum australe (black bean or Moreton Bay chestnut) flowers photographed in the author’s home garden. Raw seeds of this tree are poisonous to humans and livestock, but are processed and used as food by Aboriginal people (see p. 590). Lorikeets and honeyeaters feed safely on the flower nectar. Back cover (left to right): Macrozamia lucida (zamia) female cone (p. 130); Isotropis cuneifolia (lamb poison) flower (p. 331); Solanum sturtianum (Sturt’s nightshade) flower (p. 556). Set in 10/12 Goudy Old Style Std and Optima Edited by Peter Storer Editorial Services Cover design by Andrew Weatherill Text design by James Kelly Typeset by Desktop Concepts Pty Ltd, Melbourne Printed in China by 1010 Printing International Ltd CSIRO Publishing publishes and distributes scientific, technical and health science books, magazines and journals from Australia to a worldwide audience and conducts these activities autonomously from the research activities of the Commonwealth Scientific and Industrial Research Organisation (CSIRO). The views expressed in this publication are those of the author(s) and do not necessarily represent those of, and should not be attributed to, the publisher or CSIRO. The copyright owner shall not be liable for technical or other errors or omissions contained herein. The reader/user accepts all risks and responsibility for losses, damages, costs and other consequences resulting directly or indirectly from using this information. The paper this book is printed on is in accordance with the standards of the Forest Stewardship Council® and other controlled material. The FSC® promotes environmentally responsible, socially beneficial and economically viable management of the world’s forests.

v

Dedication

To my wife Glenyth, with love and gratitude, And in memory of two good friends who shared my passion for the Australian bush Jon Geeves (1954–1994) and Colin Cornford (1931–2007) and of Bella (1997–2010), our much loved dog. Ball-in-mouth Bella, Springing high and happily – Light as summer breeze.

vi

About the author

Dr Ross McKenzie PSM DVSc is a retired veterinary pathologist, toxicologist and research scientist from the Queensland Department of Primary Industries where he diagnosed and researched diseases of livestock for 36 years (1973–2009). Known as ‘the whistling pathologist’, he carried his fair share of the veterinary workload of the central diagnostic laboratory at Yeerongpilly in Brisbane, such as personally handling 10,000 case accessions from livestock disease investigations throughout Queensland during 1990–2002. He is also a retired conjoint senior lecturer from the University of Queensland where he taught toxicology to veterinary students for 14 years (1994–2008). His students called him ‘Toxic Ross’ and his 2007 class gave him a ‘Joie de Vivre’ award for making the study of toxicology enjoyable. They had thought it would be deadly! He earned a Bachelor of Veterinary Science degree (with Honours) from the University of Queensland at the start of his career, then the degrees of Master of Veterinary Science and Doctor of Veterinary Science some 20 years later, recognising his research achievements. He won the Australian Veterinary Association Excellence in Teaching Award for 2002, the Queensland Natural History Award for 2004 and, in 2009, was honoured with the Public Service Medal within the Order of Australia for his research in veterinary pathology and

Ross McKenzie with Solanum quadriloculatum, June 2010. Photograph by Glenyth McKenzie.

toxicology. He has authored over 100 scientific publications and has contributed to several international veterinary text and reference books. He is now an Honorary Research Associate of Queensland Herbarium and of Biosecurity Queensland. He is also a (very) amateur botanist and photographer. His family roots are in the earth of the Maranoa district of rural Queensland. He lives in Brisbane with his wife Glenyth and a garden containing many poisonous plants.

vii

Contents

About the author

vi

Preface: why this book?

ix

Acknowledgements xi Warnings xiii Using this book

xvi

1

Understanding plants and plant poisoning

2

How to confirm tentative identifications

19

3

Common poisoning profiles

25

Part 1 Poisonous cyanobacteria (blue-green algae) 4

Poisonous cyanobacteria (blue-green algae)

Part 2 Poisonous fungi 5

Poisonous fungi

Part 3 Poisonous vascular plants

1

71 73

79 81

107

6

Poisonous ferns

109

7

Poisonous cycads

117

8

Poisonous grasses, sedges and mat-rushes

139

9

Poisonous grass-trees

185

10 Poisonous grass-like herbs (iris and lily families)

191

11 Poisonous forbs (non-grass-like herbs)

211

12 Poisonous vines (climbing plants and creepers)

415

13 Poisonous shrubs

453

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Australia’s Poisonous Plants, Fungi and Cyanobacteria

14 Poisonous trees

573

15 Digest of poisonous cyanobacteria, algae, slime moulds, macrofungi and plants in Australia

645

APPENDIX 1: Aids to identifying flowering plants

849

APPENDIX 2: The top killers

861

APPENDIX 3: Poisoning hot-spots

863

APPENDIX 4: Animals and the major species that poison them

864

APPENDIX 5: Body systems affected by the major poisonous species

873

APPENDIX 6: Australian states with major poisonous species

881

Glossary 891 References and further reading

903

Index 907

ix

Preface: why this book?

Aims of the book Better to light a candle than to curse the darkness. Chinese proverb

This book is a tool to help people prevent or manage poisonings of themselves, their children and their domestic animals by plants, fungi and cyanobacteria in Australia. It is based on evidence from past poisonings and scientific research to understand how poisonings happen and how to deal with them. However, I earnestly urge readers to consult medical, paramedical, veterinary or botanical professionals to help them deal with actual or potential plant poisonings and to confirm plant identifications. I have spent much of my working life studying plant poisoning and poisonous plants and advising animal owners and their professional advisors on diagnosing, managing and preventing plant poisoning in domestic animals. From 1994 to 2008, I was privileged to lecture the veterinary students of the University of Queensland on toxicology. Inevitably, plant poisoning was a major theme. The lack of a suitable reference book on poisonous plant identification, covering the whole of Australia and written primarily for non-professionals as well as the ongoing demand for information in this area, prompted me to write it. Nam et ipsa scientia potestas est [Knowledge itself is power]. Francis Bacon (1561–1626). Religious Meditations. Of Heresies.

In this book I offer you knowledge, and within it the power to prevent the pain and suffering of plant poisoning, and sometimes to cure it. I have written it to help householders, gardeners, parents of young children, child-care workers, school teachers, bushwalkers, pet and livestock owners, landholders, land custodians, medical and paramedical professionals, veterinarians, veterinary nurses, agricultural advisors, horticulturalists, park rangers and students throughout Australia.

It aims to help you do two main things: •• to recognise the main poisonous plants, fungi and cyanobacteria that occur here and that may threaten the health of yourselves, your children, persons for whom you are responsible or your animals •• to understand the circumstances leading to poisoning so that you may have the best chance of preventing poisoning by informed decision making. It also aims to give you information about: •• poisonous plants and plant poisoning in general so that you can place these plants into the context of the natural world that we belong to •• the toxins in the plants so that you can understand what happens when they poison animals. •• methods to manage poisonings when they happen, in partnership with your professional advisers •• plants that poison particular animal species, such as humans, horses and dogs •• plants that affect particular parts of the body, such as the heart, lungs or eyes •• the distribution of major poisonous species.

What is included? How were they chosen? The poisonous living organisms covered in this book include what most people usually call plants, algae, ergots and mushrooms (or toadstools), and known by professional biologists as vascular plants, cyanobacteria (also known as blue-green algae and cyanophytes or cyanoprokaryotes), ergot fungi and macrofungi, respectively. One poisonous gall-forming fungus is also included. Plants affecting humans, their companion animals, their performance animals and their livestock are included and listed in Appendix 4. Plants affecting native Australian animals are also included. Plants, fungi and cyanobacteria illustrated and described in detail were chosen because of their:

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Australia’s Poisonous Plants, Fungi and Cyanobacteria

•• capacity to cause serious illness in humans or other animals – threatening life, damaging important organs, such as eyes, or seriously distressing the patient •• relative abundance, wide distribution or both as native or naturalised plants in Australia, •• extensive cultivation as crops or pastures, or in gardens. These choices were evidence-based; that is, made using information from actual poisoning cases and from chemical and experimental studies published in the scientific literature.

What is not included? No book of this kind is perfect, so if you find errors or omissions, please tell me (through the publisher) so that future editions can be improved. This book does not include detailed illustrated entries for all the known poisonous species in Australia. Chapter 15 (the ‘Digest’) lists all poisonous plants, fungi, algae and cyanobacteria in Australia that were known to, or suspected by, me at the time of publication. This list aims to put the major species into perspective and to provide a resource not readily available elsewhere. Further information on many species of lesser importance may be found in the publications in the ‘References and further reading’ list. Poisonous mould fungi that grow in poorly stored or harvested foods and produce what are usually called mycotoxins are not included because they are often not apparent to the naked eye and require laboratory facilities for identification. This makes them unsuitable subjects for a field guide. For reviews of these, see Fungi of Australia Volume 1B, Introduction – Fungi in the Environment (Mallett and Grgurinovic 1996). Plants causing contact dermatitis or allergy in humans are not included because reactions to those causing allergy are not consistent across all humans for a given degree of plant exposure; that is, the effect produced is not dose-related. Allergy in particular is a very large subject in itself and, by its nature, affects or does not affect individuals in a manner that is difficult to predict just from a knowledge of the chemicals in plants. Only a very few that cause contact dermatitis

through urushiol poisoning or photosensitisation through furanocoumarin poisoning have been included. Information on these subjects is available in a variety of sources including Botanical Dermatology. Plants and Plant Products Injurious to the Skin (Mitchell and Rook 1979) which is now available on the internet at http://www.botanical-dermatology-database.info. Woods that cause irritation of the eyes, nose and throat are not covered because identification of wood is a difficult specialist skill. Timber workers, carpenters and wood turners should refer to the booklet Timber and Health (Bolza 1976). Plants causing taints (unpleasant flavours) in eggs, milk or meat are not included because these are minor effects. Some information on this topic has been gathered in Medical and Veterinary Aspects of Plant Poisons in New South Wales (McBarron 1977). Fish-poisoning plants containing rotenone, saponins and other toxins discovered and used by Australian Aboriginal peoples to harvest stunned fish from small water bodies are not included because this is also a minor effect with limited impact. Some information on this topic has been gathered in Guide to the Medicinal and Poisonous Plants of Queensland (Webb 1948) and in Aboriginal People and Their Plants (Clarke 2007).

‘Side shoots’ Scattered through the book are short essays expanding on certain interesting and unusual aspects of some poisonous plants. In order of their placement in the book, these are •• Box 6.1. ‘Nardoo and the deaths of Burke and Wills in 1861’ (see p. 116). •• Box 7.1. ‘Human brain and nerve disease, cycads and flying foxes in the Pacific’ (see p. 119). •• Box 13.1. ‘Poisonous honey stops an army’ (see p. 476). •• Box 13.2. ‘Death by umbrella’ (see p. 487). •• Box 13.3. ‘Discovering the poisonous nature of Gastrolobium plants in Western Australia’ (see p. 501). •• Box 14.1. ‘Pituri – the Australian Aboriginal narcotic’ (see p. 628).

xi

Acknowledgements

I am indebted above all others to my wife, Glenyth, for her love, forbearance, unstinting support and encouragement during the construction of this book and for her sharp eyes during plant-hunting journeys. Without her, this book would not have happened. I am very grateful to the directors and staff of the Queensland Herbarium, past and present, for their support of my professional activities over several decades. In particular, Megan Thomas, a long-standing and valued friend, has repeatedly gone out of her way to help with questions botanical. I thank the directors and staff of the state herbariums in Sydney, Melbourne, Hobart, Adelaide, Perth and Alice Springs who provided access to their collections and help with locating plants for photography. The Council of Heads of Australian Herbariums generously granted permission to use information in Australia’s Virtual Herbarium for distribution maps. The information used to compile this book has come partly from my own experience and learning, but mostly from the published, and sometimes unpublished, work of many botanical, mycological, chemical, medical and veterinary scientists, and the experiences of many other people as well. Some may recognise their own unique observations when they read them in the text. Sadly, I cannot acknowledge all these people by name due to lack of space and the ‘popular’ nature of a book written without formal references; nevertheless, I am truly grateful for their contributions. My memberships of the Society for Growing Australian Plants and the Queensland Naturalists’ Club have inspired and helped me to learn about native plants and to put the poisonous species into perspective within the whole flora. Journeys undertaken with SGAP and QNC members have been a wonderful source of knowledge and photographic subjects. In particular, I am indebted to Verna and the late Colin Cornford, Megan Thomas and the late Jon Geeves, Beth McRobert, Christina McDonald, and Noel and the late Jill Chopping for their friendship, knowledge and enthusiasm.

For this book, Jeremy Allen, my professional counterpart in Western Australia, provided unfailing enthusiastic support over many years. Fiona and Rob Richardson gave generously of their time, expertise and image collection. Jenny Milson very kindly photographed plants and provided images and timely local support. David Forshaw and ‘Bill’ Sandiford energetically collected and supplied plants and images. Nigel Fechner, Tom May and David Ratkowsky provided valuable comments on particular fungi. Peter Bostock, Paul Forster and Ailsa Holland helped find obscure etymologies. Ailsa Holland and John Thompson provided advice on field recognition of particular plants. Lindsay Bell, John Finnie, Margaret Hastie, Tristan Jubb, Chris Materne, Kerry Moore and Gordon Reyer helped me to locate particular plants or specimens. Ian Hall and Roger Shivas kindly helped me locate particular fungal images. Molly Anderson, with permission from her mum and dad, Therese and Michael, generously posed with a yellow oleander. Jeremy Allen, Christine Freudigmann, Ailsa Holland, Roger Kelly, Bronwyn Lingard, Glenyth McKenzie, Tamara Smith, Trisha and John Stadtmiller and Hal Young read all or parts of the draft text and provided valuable feedback for which I cannot thank them enough. Any remaining errors of fact or judgement are mine alone. Ted Hamilton, my publisher at CSIRO Publishing, was professional, extremely patient and unfailingly encouraging. I thank him for his support and for maintaining faith in the ultimate goal. Peter Storer (copy editor), Tracey Millen (editorial manager), Pilar Aguilera (production manager), Perry Karipidis (typesetter) and Lachlan Garland (proofreader) all willingly contributed their professional expertise and good humour to reaching that goal. I am very grateful to them all.

Photographic credits All the photographic images used in this book are mine, with the exception of those acknowledged below.

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Australia’s Poisonous Plants, Fungi and Cyanobacteria

I am very grateful to the following people and organisations for allowing the use of their images. Copyright of these images is the property of these individuals or organisations, as indicated: Anonymous (Queensland Herbarium): Brachyachne convergens clump Will Andrew: Mixed Tychonema bornetti and Phormidium sp. cyanobacterial bloom François and Marie-France Bahuaud: Helleborus viridis Lindsay Bell (CSIRO): Vicia benghalensis Todd Berkinshaw (Greening Australia): Xanthorrhoea semiplana blickwinkel/Alamy: Cannabis sativa male flowers (close-up) Joseph James Brock: Corchorus olitorius whole flowering plant Nigel Cattlin/Alamy: Claviceps purpurea in Phleum sp. seed-head Noel Chopping: Aseröe rubra with intact spore mass; Gastrolobium parvifolium in habitat; Phallus rubicundus; Phallus multicolor colony; Zieria arborescens flowering branches (Tasmania) Travis Columbus: Brachyachne convergens single plant and flower-head John Crellin (www.floralimages.co.uk): Aconitum napellus in habitat; Allium schoenoprasum flower-head; Allium vineale bulbils; Atropa belladonna fruit; flowering branch; Helleborus foetidus plant and flower; Iris foetidissima flowers Geoff Cunningham: Ranunculus undosus FloralImages/Alamy: Aconitum napellus inflorescence; Allium vineale inflorescence; Atropa belladonna flower; Iris unguicularis flower Ian Davis: Lachnagrostis filiformis seed-head with galls Ralph Dowling: Bowenia serrulata female cone Murray Fagg: Argentipallium blandowskianum in habitat and flower-heads Florapix/Alamy: Aconitum napellus garden plants Genevieve Gates: Cortinarius eartoxicus Ian Hall: Amanita phalloides (NZ) Steffen Hauser/botanikfoto/Alamy: Cannabis sativa leaves; Convallaria majalis whole flowering plants; Daphne mezereum fruiting plant Josef Hlasek (http://www.hlasek.com/floranahledy1an.html): Atropa belladonna in habitat; Cannabis sativa female plant tops; Convallaria majalis fruit and leaves; Daphne mezereum fruit and fruiting branch; Panaeolina foenisecii (three caps); Psilocybe semilanceata (among thistle leaves); Taxus baccata male cones and seeds ± arils Ailsa Holland: Rubinoboletus species undescribed imagebroker/Alamy: Convallaria majalis fruit

The late Emily Johnson, courtesy of Steve Stephenson: Panaeolina foenisecii (10 caps) David Jones: Gelsemium sempervirens JTB Photo Communications, Inc./Alamy: Helleborus niger flowering plant Tristan Jubb: Field images of Corallocytostroma ornicopreoides galls on Mitchell grass; Cucumis melo subsp. agrestis fruit with dry vines Glenn Leiper: Triunia robusta fruit Tony Lyon: Psilocybe semilanceata (among grass) Chris Materne: Acacia georginae pods (scanned) Tom May: Amanita phalloides (Melbourne) Alistair McTaggart: Claviceps purpurea in Hordeum vulgare Jenny Milson: Acacia georginae and Acacia cambagei pods; Sarcostemma brevipedicellatum flowers Sheldon Navie: Allium schoenoprasum flowering plant (mauve flowers); Amsinckia intermedia flowering stem; Aristolochia ringens flower; Lilium lancifolium flowering plant; Gomphocarpus fruticosus seeds; Robinia pseudoacacia seed pods Hugh Nicolson: Alstonia constricta fruit; Dendrocnide excelsa flowers; Dendrocnide moroides fruiting plant, flowers and fruit; Dendrocnide photinophylla buds, flowers and fruit; Triunia erythrocarpa flowers and fruit; Triunia montana flowers; Triunia youngiana ripe fruit John Noble: Dysphania glomulifera in habitat Michael Palmer: Gastrolobium cuneatum flowering plant Rimantas Pankevičius: Daphne mezereum flowering twig Rob and Fiona Richardson: Amsinckia lycopsoides flowering stems; Arctotheca calendula seed-head; Cannabis sativa male flowering plant top; Lachnagrostis filiformis; Lythrum hyssopifolia; Pennisetum clandestinum flowers; Polypogon monspeliensis flower-head; Prunus dulcis trees and fruiting branch; Prunus laurocerasus; Rumex conglomeratus; Taxus baccata female tree branches Malcolm Ryley: Claviceps africana sclerotia, sphacelia and Cerebella-infected sclerotia ‘Bill’ (Elizabeth) Sandiford: Schoenus asperocarpus in habitat, single flowering stem Science Photo Library/Alamy: Cannabis sativa plants and female flower with leaf Ros Shepherd: Daphne odora flowering shrub; Lilium lancifolium flower; Polypogon monspeliensis in habitat Lee Taylor: Aphanizomenon bloom Frank Taeker: Psilocybe subaeruginosa Lui Weber: Dendrocnide excelsa fruiting branch; Dendrocnide moroides young leaves

xiii

Warnings

Protect yourself Handling some of the plants, fungi or cyanobacteria listed in this book could cause you harm or illness. Do not expose your skin, eyes or other sensitive parts to cyanobacterial (blue-green algal) blooms, leaves of stinging trees (Dendrocnide species) or irritant plant saps (see Appendices 1 and 5). Wash your hands thoroughly with soap and water after handling any fungi or suspected poisonous plants and before handling food. Observe the rules for picking and eating mushrooms (Chapter 5).

Natural does not mean harmless Nature is neither benign nor malignant: ‘she’ is indifferent. All the poisons (toxicants) contained in the plants, fungi and cyanobacteria described in this book are natural. That is, they are produced within living organisms in nature, not by human industrial manufacture. It is mainly the animal species eating it and the amount (dose) eaten that determines if a plant or other organism will cause poisoning. So-called ‘organic’ foods may be certified as free from industrial chemicals, but they can contain natural poisons. For example, apple seeds and cassava tubers can generate cyanide naturally. See ‘What is a poisonous plant?’ (Chapter 1) for further discussion.

Have important identifications confirmed by professionals Identifications made using this book should be regarded as tentative. In circumstances where action is to be taken based on the identification, I strongly recommend that you confirm your tentative identification by sending a suitable specimen to a state herbarium. See the guidelines for ‘Collecting and handling specimens for identification’ (Chapter 2) for the contact details of your closest state herbarium. These services were free to the public at the time of writing for small numbers of plant specimens, particularly for suspected

poisonous plants in emergencies. Ask your nearest state herbarium about its own policy on charging for such services. Most will limit the number of specimens that they will identify for free for any one client at any one time.

Potentially harmful treatments should be given by professionals Most therapies (treatments) described in this book are best given by a veterinarian for domestic animals or by a medical practitioner or paramedic for humans. These professionals are all trained for this work. Untrained lay persons applying techniques such as injections or dosing materials into the stomach (drenching) are at serious risk of causing unintended damage to the patient. For example, accidental dosing of drenches into the lungs is often fatal.

Herbicide use Obtain up-to-date information Information on herbicides is continually changing. Types available, their formulations and trade names, and their application methods and rates all change. If you are considering plant control using herbicides, consult the expert authorities in government departments in your state for up-to-date information. Ask weed control authorities in departments of primary industries or agriculture as a first step. See the section on ‘Where to get advice on herbicides and other weed control methods’ (Chapter 1).

Recognise potentially increased poisoning risks Some poisonous plants become more attractive to animals, and so more dangerous, after being treated with a herbicide. Some toxicants, such as nitrate, may actually increase in concentration after herbicides are

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Australia’s Poisonous Plants, Fungi and Cyanobacteria

applied to plants. Animals should be kept away from herbicide-treated plants until the plants have died and their leaves have fallen.

Your legal responsibilities – Ignorance of the law is no defence State and Commonwealth government laws and regulations can apply in five areas of concern regarding poisonous plants and fungi (see below). These laws and regulations can change over time, so no attempt is made in this book to set out the details. For accurate information, you should consult the acts and regulations for the Commonwealth and your state or territory directly. The following websites allow public access to current documents. For accurate interpretation of these documents as they apply to your circumstances, consult a lawyer. Australian Commonwealth Legislation – http://australia.gov.au/publications/commonwealth-legislation Queensland, Office of the Parliamentary Counsel – http://www.legislation.qld.gov.au/ New South Wales Parliamentary Counsel’s Office – http://www.legislation.nsw.gov.au/ Victorian Legislation and Parliamentary Documents – http://www.legislation.vic.gov.au/ Tasmanian Legislation Online – http://www. thelaw.tas.gov.au South Australian Legislation – http://www.legislation.sa.gov.au Western Australia State Law Publisher – http:// www.slp.wa.gov.au Northern Territory Current Legislation Database – http://www.nt.gov.au/dcm/legislation/current.html Australian Capital Territory Legislation Register – http://www.legislation.act.gov.au/

Child protection laws Under state government legislation, operators of childcare centres are required to ensure that children are not exposed to poisonous, irritant or harmful trees, plants and shrubs. For example, in Queensland these laws are set out in the Child Care Act 2002 and Child Care Regulations 2003 - Section 43 (1) (j).

Animal welfare laws Under state government legislation, persons in charge of animals have a duty of care to protect their welfare. Theoretically, this extends to the prevention of poisoning. For example, off-loading hungry sheep into

stockyards full of plants such as Portulaca oleracea (pigweed) that are well known to accumulate the potentially lethal toxins nitrate and soluble oxalates could be held in law to be a breach of that duty of care. For example, in Queensland, these laws are set out in the Animal Care and Protection Act 2001 and Animal Care and Protection Regulations 2002.

Threatened species protection laws Certain species of poisonous plants, in particular species of cycads and Gastrolobium, are listed under state government environmental legislation as threatened (previously called rare and endangered). Restrictions apply to control measures aimed at protecting domestic animals from poisoning by these plants. For example, in Queensland, cycads are protected by laws set out in the Nature Conservation Act 1992 and the associated schedules in the Nature Conservation (Wildlife) Regulation 2006. Further, clearing on state land (leasehold land) requires a tree-clearing permit under the Vegetation Management Act 1999 and Vegetation Management Regulation 2000. The Convention on International Trade in Endangered Species of Wild Fauna and Flora (CITES) controls the import and export of the endangered species listed (http://www. cites.org). This includes Australian species of cycads. The Australian management authority for CITES is the Commonwealth Minister for the Environment who currently acts on the advice of the Australian Government Department of Sustainability, Environment, Water, Population and Communities.

Weed control laws – declared plants (noxious weeds) Occupiers of private land are required by legislation in all Australian states and territories to control declared plants on that land. Almost all legislation on declared plants, noxious weeds or proclaimed plants is enacted at the state or territory level of government, but monitored and enforced at local government level. Local governments may have subsidiary legislation that applies only within their particular jurisdictions. Plants included in this book that are declared in state or territory legislation are indicated in the text. Enquiries should be directed to state and local weed control authorities. See the section on ‘Where to get advice on herbicides and other weed control methods’ (Chapter 1).

Drugs of abuse Possession of certain hallucinogenic plants and fungi, in particular Cannabis sativa and Psilocybe species, may

Warnings

be an offence under Commonwealth and state government legislation.

Attention: Medical and Veterinary professionals Botanical expertise It is vital to accept that our core professional training in itself does not fit us to identify accurately all plants that we encounter in our professional lives. Accurate identification can be critical to positive case outcomes. In the interests of our patients and clients, we must view any identifications of plants or fungi that we make as only tentative. When appropriate to the case being managed, we should refer suitable specimens to the botanists and mycologists in state herbariums for a definitive identification (see Chapter 2).

Furthering evidence-based practice As professionals trained in science, we owe it to our colleagues present and future, to our patients and

xv

clients, and to the community in general to add to the knowledge base that we all draw on for the effective management of poisoning cases. High standard evidence-based practice is impossible without it. Case reports published in peer-reviewed journals are a cornerstone of this knowledge base. Unpublished data are data lost. Please publish! Consequently, when you encounter a plant, fungal or cyanobacterial poisoning case that your research of the literature indicates as novel or worthy of recording, remember that the identity of the organism must be established in perpetuity by placing a voucher specimen in an appropriate institution for future reference. See the discussion of ‘Herbariums and voucher specimens’ (Chapter 1). The acquisition numbers of vouchers must be cited in any description of the case that you write in the peerreviewed literature. Without this, your data may lose value if changes in taxonomy, nomenclature or both touch the name of the organism concerned.

xvi

Using this book

References to other information sources Where other publications are mentioned in the text, their author and year of publication are given in brackets after their title. All these are listed alphabetically by surname of first author in the ‘References and further reading’ list.

Information provided on each fungus and plant, and why The entries for the individual species of fungi and plants included are arranged in the 21 sections shown below. In some species profiles, some of these sections have been merged. Where appropriate, some entries deal with more than one species from the same genus.

Scientific name (‘preferred’ common name) See ‘Name that plant!’ (Chapter 1) for a discussion of scientific and common names. If a plant has several common names, I have chosen one of the most frequently used or one of the most distinctive as the ‘preferred’ common name to simplify the listings in this book. This is my personal choice and does not imply that everyone should use this name. Plants and fungi originating inside Australia are termed native. Those originating outside Australia are termed exotic. Exotic plants or fungi may be cultivated in gardens or as crops. If such plants or fungi have established themselves as self-sustaining populations in the environment independent of cultivation, they are termed naturalised. Many naturalised exotic species are regarded as weeds. The symbols used with botanical names are as follows: * : indicates a naturalised exotic plant or fungus, not originally native to Australia. These plants may

also be cultivated in agriculture or gardens (horticulture), be weeds or be both. This is a symbol commonly used by convention to indicate such plants. † : indicates a cultivated exotic plant or fungus, grown in agriculture or gardens (horticulture), and not known to be naturalised. This symbol is not conventionally used to indicate such plants, and its use for this purpose is confined to this book. ‡ : (in Chapter 15 only) indicates a rare species of Gastrolobium that is in danger of extinction. This symbol is not conventionally used to indicate such plants, and its use for this purpose is confined to this book.

Full scientific name and synonyms Names given in this section include authorities (see ‘Authorities’ in Chapter 1). When appropriate, a list of subspecies or varieties is included. Synonyms (previous or alternative scientific names) have been included so that information sources that use one of these other names can be used with confidence, knowing that the same plant or fungal species is being dealt with. For a discussion of plant names and their use in this book, see the section ‘Name that plant!’ (Chapter 1). Plant names and authorities used in this book have been checked for accuracy against the listings in the Australian Plant Names Index (APNI) at http://www.cpbr. gov.au/apni (native and naturalised species) and the International Plant Names Index at http://www.ipni. org (cultivated species).

Scientific name meaning Technically, the explanation of a scientific name’s meaning is called its etymology. Understanding what a scientific name means in plain English can help identification by focusing attention on important features of the plant or fungus. For example, the species name trichostachya in Pimelea trichostachya means ‘hairy spike’ in reference to the appearance of the flowers,

Using this book

xvii

thus separating this species from others in the genus Pimelea. Some plants and fungi can be named after prominent scientists or patrons of science. For example Swainsona plants are named after the physician Isaac Swainson (1746–1812) who designed and built a private botanical garden near London. These names are not helpful for identification.

Management options in decreasing order of likely successful outcomes:

Family

NN  Effective therapy is doubtful: general therapy

Recognising the family to which a plant or fungus belongs is often the first step to its accurate identification. Names of plant families used in this book are those used in the Flora of Australia series (Orchard 1999) with synonyms in parentheses. An exception to this is lily-like plants. Family names used in Flowering Plant Families of the World (Heywood et al. 2007) have been followed for these. A reassignment of many genera to families existing and new has recently been proposed by these authors. This re-arrangement has not been fully adopted by Australian herbariums and reflected in APNI at the time of writing, so I have decided to retain the previous arrangement for this edition of this book. Plant family names end with ‘-aceae’. Older family names given here as synonyms may end with ‘-ae’ or ‘-eae’.

Common names Where there is more than one common name for a species, they are listed in this section. The ‘preferred’ common name is always listed first. Common names used for plants vary from place to place within Australia and the world. These lists are not exhaustive.

Effects, toxins and poisoning management summary To help readers grasp the essentials of a poisoning as rapidly as possible, these symbols and short statements summarise important information. These are given for each common poisoning profile (Chapter 3) and for each fungus and plant profile in later chapters. Onset and duration of poisoning effects:

~  Acute effects M  Delayed onset or chronic effects Toxins:

þ  Toxins that cause the syndrome include: specific

toxin names are listed.

´  Toxin that causes poisoning is unidentified.

N  Specific

preventive measures available: brief details are listed.

∅  Effective therapy: brief details are listed.

N  No

specific therapy: general therapy can be applied, but no ‘antidotes’ are available. can be applied, but the severity of the poisoning may be too great for a successful outcome in most cases.

NNN No effective therapy. Description Professional scientific descriptions of plants and fungi use many technical terms for brevity and clarity (see the Glossary) and are impossible for non-professionals to understand without significant effort. I have drawn on many such descriptions and tried to ‘translate’ the technical terms into plain language for easy understanding.

Flowering and fruiting seasons Flowers and fruits are critical for identifying plants because they are the basis of the classification system used by botanists. Sometimes fruits are particularly critical (such as for species of Solanum). The non-flowering plants included in the book – ferns, cycads, cypress pines and yews (Chapters 6, 7 and 14) – have no flowering season, of course. Ferns bear spores, but the others are cone-bearing plants (gymnosperms) that can produce cones at particular times of year. These ‘coning’ seasons are listed within this section.

Main distinguishing features What sets this plant or fungus apart from all the others in its vicinity?

Confusing species Which other plants or fungi can cause you to make mistakes when identifying this species?

Distribution and habitat: includes a map of native and naturalised species When trying to identify a plant, both the description and the known distribution of the plant should be used in the process. The maps are included to help with this. These are based on information from

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Australia’s Poisonous Plants, Fungi and Cyanobacteria

Australia’s Virtual Herbarium (used with permission) – http://www.chah.gov.au/avh/. The maps were generated during 26–29 January and 15–18 February 2010. No maps are included for cyanobacteria because these are considered capable of blooming anywhere in Australia with suitable water conditions. The points on the maps are the locations at which the material was collected for the actual pressed and dried plant and fungal specimens in the permanent holdings of the state and Commonwealth herbariums in Australia: Sydney, Melbourne, Brisbane, Adelaide, Hobart, Darwin, Perth and Canberra. All identifications have been made professionally and are able to be verified by examining the specimens at the herbariums. Over time, any name changes are taken into account in the data used for the maps. Therefore, the maps broadly indicate the natural distribution of native and naturalised plants. They are less useful for cultivated plants and fungi and tend to under-estimate their distributions because the specimens of fungi and cultivated plants in herbariums are few compared with those of native and naturalised plant species. For this reason, maps of cultivated plants have usually been omitted. Important: The density of datum points on the maps should not be interpreted as an accurate measure of the density of plant populations in the field; the density of points on the maps reflects only the intensity of botanical collection of the plants; that is, the number of times that the plants have been actually collected and lodged in an official herbarium.

Weight of evidence for toxicity (toxicity confidence rank) See the explanation of these ranks below.

Degree of danger (danger rank) See the explanation of these ranks below.

Toxin(s) Known toxins have known predictable effects on animal bodies. Knowing the toxin helps with diagnosis and management of poisonings. Identifying and measuring the concentrations of toxins in plants is a specialist skill of analytical chemists.

Toxic parts of the plant Plants may protect all of themselves with toxins or only their critical parts, such as seeds – their guarantee of

passing their genes to the next generation. Different animal species may eat different parts of a living plant. These choices influence which animals may be poisoned. Cattle, sheep and horses commonly eat leaves from shrubs and trees or all parts above ground from grasses and forbs. In doing this, they may eat flowers and fruits as well as leaves. Pigs may eat roots as well as other parts. Humans and birds may eat just fruits or seeds.

Animals affected ‘The animal species makes the poison’. See ‘What is a poisonous plant?’ (Chapter 1).

Conditions of poisoning ‘The circumstances make the poison’. See ‘What is a poisonous plant?’ (Chapter 1).

Toxic dose ‘The dose makes the poison’. See ‘What is a poisonous plant?’ (Chapter 1).

Clinical signs (and symptoms for humans) See the definitions of the terms ‘clinical sign’ and ‘symptom’ in the Glossary. The individual effects of a particular poisoning taken together (the poisoning ‘syndrome’) can be significant for recognising (diagnosing) it. Recognising and assessing these effects in a living animal are specialist skills of medical and veterinary clinicians.

Post-mortem changes Changes seen in the body of an animal that has died of poisoning, or in tissue samples taken from the body and examined in a laboratory, can be critical to recognising (diagnosing) a specific poisoning. Recognising and assessing abnormal changes and interpreting laboratory test results are specialist skills of medical and veterinary pathologists.

Management (therapy, prevention and control) ‘Prevention is better than cure’ is never more important than when dealing with plant poisonings. Often there is no cure.

Using this book

Unfamiliar words and technical terms, symbols and abbreviations If you find unfamiliar technical terms or words, please see the Glossary for explanations of their meanings. Most common abbreviations and symbols are explained in the Glossary. For an explanation of the abbreviations used with plant names in this book, see the section ‘Name that plant!’ (Chapter 1), and of the symbols used, see ‘Scientific name (‘preferred’ common name)’ earlier in this chapter.

Identifying a plant or fungus Identifications made using this book should be regarded as tentative (see ‘Warnings’). The life forms – plants, fungi and cyanobacteria (blue-green algae) – included in this book are grouped together firstly by life form, then (for plants with flowers) by flower shape and finally by dominant colour of flowers and mature fruit. See ‘Features that may confuse easy identification’ (later in this chapter). You may simply leaf through the book, looking for illustrations that match the plant you are trying to identify, but the book is arranged to help you use a more methodical approach. Firstly, choose the life form that the organism of concern best fits. Life forms used here are: •• cyanobacteria or blue-green algae – form scums on water or discolour water •• fungi –– macrofungi – mushrooms or toadstools –– ergots – fungal fruiting bodies in seeds of grasses including grain crops –– gall-forming fungi •• plants –– ferns –– cycads –– grasses, sedges and mat-rushes –– grass-trees –– grass-like herbs (irises and lilies) –– forbs (non-grass-like herbs) –– vines (climbing plants and creepers) –– shrubs –– trees Then compare your plant or fungus with the descriptions and images to obtain the best fit. Important: If you need to rely on the identification for making important decisions, always have your tentative identification confirmed by a professional botanist or mycologist (see Chapter 2).

xix

For flowering plants, pay attention to (in descending order of importance) •• flower shape and colour, and fruit (including seedhead, seed pod and seed capsule) shape and colour •• leaf shape, colour and arrangement on stems See Appendix 1 for an understanding of a range of distinctive flower and flower-head shapes. Precise, accurate identification of many plants requires microscopic examination of specimens. A hand lens that magnifies ×10 is an essential tool if you need to use small structures to tell the difference between two similar plants. I have tried to focus as far as possible on the structures and properties of plants that are apparent to the naked eye.

Keys I have not tried to produce inclusive keys to the plants, fungi and cyanobacteria in this book for a number of reasons. People need lots of technical knowledge to use accurate and detailed keys easily and rapidly, and this is expertise that few people have mastered. One of the main reasons for this is that many technical terms need to be used to keep the keys to a manageable size. Also, features of plants that need a hand lens or a microscope to be seen are often essential for accurate keys. To be realistic, any key or keys would need to include a large number of non-poisonous species that could be confused with the poisonous species, making them too large to be useful. Keys that contained only the species in the book would be confused in many cases by similar non-poisonous species, and so made useless.

Features that may confuse easy identification Flower colour Flower colour is not a completely consistent feature of plants, so caution is needed. Plants often have a common flower colour, but with variations. For example, flowers of the poisonous species of Swainsona (Darling peas) are usually pink, but white and orange forms also occur. Flowers of Nerium oleander (common oleander) are most likely to be pink, but red, salmon and white forms are also grown. The most common natural variation in flower colour is its complete loss, thus producing white flowers. Cultivated ornamental garden plants are more likely to have variations in flower colour than uncultivated plants. See Appendix 1.

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Australia’s Poisonous Plants, Fungi and Cyanobacteria

Flower shape Flower shape (structure) is the most consistent feature used for identification, but cultivated ornamental garden plants may have ‘double’-flowered forms. These have flowers that contain more than the ‘normal’ number of petals, producing a fuller, often ‘frilly’ flower shape. Among poisonous garden plants, double-flowered forms of Nerium oleander (common oleander) and Rhododendron species (rhododendrons, azaleas) are grown. See Appendix 1.

Which plants can poison my child, pet or livestock? See Appendix 4 for major risks listed by animal species. Minor risks are included in the ‘Digest’ (Chapter 15).

Which plants can poison the brain (or other organ of the body)? See Appendix 5 for major risks listed by body system. Minor risks are included in the ‘Digest’ (Chapter 15). I have not listed plants or fungi by the clinical signs (or symptoms for humans) that they can induce in poisoned animals because such lists are very unwieldy

and common signs and symptoms are often quite non-specific and unhelpful. Instead, I have focused on organs and body systems to try to condense and clarify the great variety of effects caused by plant and fungal poisonings.

Is this plant poisonous? If you know the name of the plant (fungus or cyanobacterium), check the Index to see if your plant is included in the book. If you can’t find ‘your’ scientific name listed, it may be an out-dated synonym. To check this and to get the current name, consult the Australian Plant Names Index at http://www.cpbr.gov.au/apni (for native and naturalised species) and the International Plant Names Index at http://www.ipni.org (for cultivated species). If you do not know its name, use this book to help obtain a name or see Chapter 2 to begin naming your plant. Important: Common names can be misleading. See Chapter 1 for a discussion of this point.

How confident are we that this plant is poisonous? In answer to the question ‘Is this plant poisonous?’, there are a number of ways in which plants can be

Table A. Toxicity confidence rankings.

Field evidence of toxicity

Experimental feeding of plant produces poisoning

Toxin isolated

Toxin isolated experimentally reproduces field syndrome

««««

Consistent for several incidents

Yes

Yes

Yes

«««

Consistent for several incidents

Not attempted

Yes (known toxin)

Yes

««

Consistent for several incidents

Yes

Yes

No or not attempted

«

Consistent for several incidents

Yes

No

­–

Weight of evidence for toxicity (toxicity confidence rank) 1 – Definite toxicity

2 – Some evidence of toxicity ¶¶

Consistent for several incidents or a well-documented single case

No or not attempted

No

–

¶

No reports

Yes

No

–

Not attempted

Yes

Yes

Not attempted

No

-

Yes/No

Yes/No

Yes/No

3 – Known toxin isolated, but no field cases known r

No reports

4 – Suspected of toxicity ?

Poor or inconsistent

Qualifying term (placed around the rank symbol) []

Reports from outside Australia only; no known cases in Australia

Using this book

xxi

Table B. Assessing danger rankings Degree of danger (danger rank)

Score

Palatability

Dose/concentration

Rapidity of action

Severity

Effectiveness of therapy

«««

10

2

2

2

2

2

««

7

1

2

1

2

1

«

5

1

1

1

1

1

known to be poisonous (see Chapter 1). The various types of evidence each carry a certain weight. The more evidence we have, the more confident we can be that a plant or fungus is poisonous. The weight of evidence for and against poisonous properties has been considered and a toxicity confidence ranking has been given to each plant or fungus in the book. The ranks used (1st to 4th) with the modifying terms applied to them are listed in Table A in order of decreasing confidence.

How dangerous is this plant? A simplified degree of danger rating (danger rank) has been given to each plant, fungus or cyanobacterium by scoring the responses to the questions: •• How likely is it that the plant will be eaten? – The palatability of the plant. Scores: 2 = high, 1 = low •• How much needs to be eaten to produce poisoning? – The size of dose needed to produce illness (when known); the concentration of the toxin in the plant. Scores: 2 = a little, 1 = a lot •• How quickly does poisoning happen? – The rapidity of action of the toxin. Scores: 2 = acute, 1 = chronic •• How life-threatening is it? – The type and severity of effect the toxin has on the body. Scores: 2 = deadly, 1 = not deadly •• Can poisoned animals be cured? – The effectiveness of therapy for the poisoning. Scores: 2 = no, 1 = yes Ranks were given to each plant in descending order of dangerousness (1 to 3), with the most dangerous («««) with scores 9–10, moderate danger (««) with scores 7–8, and low danger («) with scores 5–6 (Table B). It is very important to understand that these ranks are only a rough guide and in practice would vary with animal species, toxins in the plant and circumstances of exposure or access to the plant. They apply only to the target animal species indicated in the text.

Is this known poisonous plant or fungus present in Australia? If the plant or fungus you are interested in is not included in either the body of the book or the ‘Digest’ (look up the Index), it is unlikely to be known in Australia. It is possible to obtain up-to-date information of this kind on plants growing naturally, using the plant’s scientific name, by consulting Australia’s Virtual Herbarium at the internet site http://www.chah.gov.au/ avh, and on fungi, using the fungus’s scientific name, by consulting Interactive Catalogue of Australian Fungi at the internet site http://www.rbg.vic.gov.au/ dbpages/cat/index.php/fungicatalogue. Cultivated and garden plants can be difficult to research in this way. For them, consult your state herbarium directly or use the five-volume Horticultural Flora of South-eastern Australia (Spencer 1995–2005) and The Aussie Plant Finder (Hibbert 2004).

Which poisonous plants and fungi grow in my region of Australia? See Appendix 6. Within the states, the distribution maps in the book show broadly where particular native or naturalised plants grow.

What is the most poisonous plant in Australia? See Appendix 2 for my attempt to define the top killers.

When and where is plant poisoning most likely? See Chapter 1 for a discussion of factors and Appendix 3 for a short list of the poisoning hot spots.

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1

1  Understanding plants and plant poisoning

Does plant poisoning really touch me? It is easy to understand how important plant poisoning is when it strikes our children or our pets – those with whom we are emotionally engaged. These impacts are painful, immediate, deep and personal. Less easy to realise is the importance to our own lives of plant poisoning of livestock such as cattle, sheep, pigs and poultry. Generally, we, the general public, are not emotionally engaged with the animals that we eat or that provide fibre for our clothes. Modern life separates us from them while they live. We encounter them only as food on our plates, as cuts of meat or plastic-wrapped chicken carcases in supermarkets or butcher shops or as woollen, mohair or alpaca jumpers in department or clothing stores. When poisoned, these animals suffer as much as, or even more than, any child or pet that chews on a garden plant. Farmers and graziers are emotionally engaged with them, of course, and suffer the emotional cost involved. But, as consumers, we are affected as well. As well as our community responsibility for the welfare of animals used for the community’s wellbeing, the cost of livestock production is increased when deaths or stunted growth follows encounters with poisonous plants. This leads inevitably to higher prices for meat and for the fibre used to produce our clothing. We are all touched by the impact of plant poisoning. But there is a positive side to plant toxins. Certain poisons in some of the plant foods that we eat actually benefit our health. The plant’s way to protect itself from insects (see ‘Why are plants poisonous?’) can help us to ward off harmful chemicals. This is discussed in more detail in the section on ‘Plant and fungal toxins in human food and beverages’.

Name that plant! Knowing the name of a plant accurately is the essential first step to knowing its properties. Get the name

wrong and any further research that you do on its properties will be astray. The name that really counts is the scientific or botanical name (see below). For detailed instructions on establishing a plant’s name, see ‘Using this book’ and Chapter 2.

Advantages and disadvantages of common names and scientific names Scientific (botanical) names are often unfamiliar and hard to pronounce and remember. Not only that, but these technical names for particular plants that you know may seem to be changing all the time, frustrating and confusing you! For example, ‘yellow oleander’ was named Thevetia peruviana until recently, but is now named Cascabela thevetia. However, obtaining the correct and current scientific name for a plant or fungus is vital because it allows your professional advisers (veterinary and medical practitioners, chemists and botanists) to search the scientific literature for accurate information. They can then use this to assess the plant’s toxic properties and to help manage any toxic risk it poses. Scientific names have the overwhelming advantages that they always refer to one, and only one, plant, fungal or cyanobacterial species throughout the world and can be traced to one or a group of scientists (botanists, mycologists or phycologists) who originated and published them. That is why they are given prominence in this book. Common or vernacular names are usually easy to pronounce and remember and are often well known, but can be confusing for different reasons. They can be created by anyone. They are often of only local significance. Different, and often several, common names frequently apply to the same plant or fungus in different districts of the same country, and this is even more likely in different countries. One common name can refer to more than one plant, each with very different toxins. For example, in Australia ‘potato weed’ can mean Heliotropium europaeum containing pyrrolizidine

2

Australia’s Poisonous Plants, Fungi and Cyanobacteria

alkaloids or one of a number of species of Solanum containing steroidal glycosides. Similarly ‘castor oil plant’ can mean Ricinus communis containing the toxalbumin ricin or Datura stramonium containing the tropane alkaloids scopolamine and hyoscine. A common name can give a misleading idea of the toxic properties of a plant. For example, in some places, the common weed Solanum nigrum (in the broad sense of this name), a mildly poisonous plant, is called ‘deadly nightshade’ – a name more properly applied to the much more toxic Atropa belladonna, which is rare in Australia. Again, Solanum mauritianum may be called ‘tree tobacco’ or ‘wild tobacco’, but is not a type of Nicotiana (the true tobaccos) and does not contain nicotine or other tropane alkaloids, but steroidal glycosides.

Scientific names and name changes Names explained In this book, both scientific and common names are given for the plants and fungi included. Scientific names are always given, but some plants and fungi do not have common names. The scientific name of a species of organism is in two parts, each based on Latin or Ancient Greek words or Latinised proper names such as that of the person first discovering it. This system of naming plants, fungi, bacteria and animals was established by the Swedish naturalist Linnaeus (Carl von Linné 1707–1778). The two parts are firstly the genus and then the species, for example Eremophila maculata – the genus name being Eremophila (combined from the Greek roots eremo- and -phila together meaning ‘desert-loving’) and the species name being maculata (from the Latin word macula meaning a spot, hence maculata means spotted). In interpreting the name of a species of plant (or other organism), the genus can be thought of as a sort of ‘family’ name and the species as a ‘given’ or individual name to distinguish one ‘family’ member from another. So, if we imagine that I am a species classified using this system, my name might be ‘Mckenzie ross’. In fact many Asian people use this system with the family (‘genus’) name coming first, for example Sun Yat-Sen from the Sun family. For brevity, when talking about a number of species together or the same species repeatedly, the genus name is often shortened to the first letter of the word. For example, Arctotheca calendula (cape weed) will be shortened to A. calendula. This is the same process that gives us the commonly used name E. coli for the full bacterial name Escherichia coli. Related genera (the plural of genus) are grouped into a plant family, whose modern scientific name ends in the suffix -aceae, e.g. daisies are in the family Asteraceae

(also called Compositae) and grasses in the family Poaceae (also called Gramineae). Confusingly, you will see that the old names for families ended in the suffix -ae or -eae. In biology, a species is defined as a group of like individuals (a population) who interbreed to produce fertile offspring. Breeding between individuals of different species may produce hybrid offspring, but these are infertile. The scientific name for a hybrid is a combination of the parent species’ scientific names, e.g. hybrid mother-of-millions is called Bryophyllum daigremontianum × B. delagoense or Bryophyllum × houghtonii. Fine distinctions of form may be seen within a species. Botanists indicate such different forms by using additional names, usually either subspecies (abbreviated as subsp.) or variety (abbreviated as var.); e.g. Pimelea simplex subsp. continua and Crotalaria medicaginea var. neglecta. A variety produced by artificial breeding for horticulture is called a cultivated variety, or a cultivar (indicated by the cultivar name given in single quotation marks); e.g. Duranta erecta ‘Sheena’s Gold’. The abbreviation ‘cv.’ was previously used for this term, but this is no longer accepted practice.

Authorities In writing with precision about plants, their scientific names are given as genus and species, followed by their authorities (authors), which are the name or names of the scientist (or scientists) who first validly published a formal description of the plant. Usually authorities are abbreviated using a list of standardised abbreviations, e.g. L. stands for Linnaeus and R.Br. stands for Robert Brown, the botanist on Matthew Flinders’ ship HMS Investigator during 1801–03. In some cases author’s names are given in full. The use of authorities with scientific names is a check on the accuracy of use of the name, helps to define the plant referred to more precisely, and helps with the understanding of the history of classification of the plant.

Name changes You may have seen the scientific name of a plant that you know changed to a new and unfamiliar name. This can certainly be frustrating (even for non-botanist professionals), but must be accepted if we are to understand the natural relationships between plants correctly. The science of naming living organisms is called taxonomy or systematics. The basic aims of taxonomy are to recognise and define all the different kinds of plants, fungi, cyanobacteria and other organisms living on Earth and to place them within a framework that allows us to understand the genetic relationships between species, accepting the evolution of species through natural selection first explained satis-

1 – Understanding plants and plant poisoning

factorily by Charles Darwin, and later independently by Alfred Russel Wallace. Botanists researching plants will change their scientific names from time to time for a number of reasons. These changes are strictly in line with two sets of international rules agreed among botanists – the International Code of Botanical Nomenclature and the International Code of Nomenclature for Cultivated Plants. For more details, see Plant Names. A Guide to Botanical Nomenclature (Spencer et al. 2007). The name changes stem from new understanding of relationships between species. This new understanding is based on new information from discoveries of previously unknown plants, from re-examinations of plant collections in herbariums and increasingly from explorations of plant DNA, the chemical basis of inheritance. Out-dated or alternative scientific names are called synonyms. These may be given in brackets after the current name, preceded by the abbreviation ‘syn.’. Current information on the scientific names of native and naturalised plants in Australia is available from the Australian Plant Names Index (APNI) (http://www.cpbr.gov.au/apni). Information on scientific names of cultivated plants is available from the International Plant Name Index (IPNI) (http://www.ipni.org).

Herbariums and voucher specimens Herbariums are scientific research institutions that employ professional botanists. They are the authorities on scientific knowledge about plants. They house large permanent collections of pressed and dried plants that are used as raw material for research into the names, relationships, distribution and properties of plants. In Australia, the state governments each support a herbarium in their capital city and there is a national herbarium in Canberra. University botany departments also have herbariums. Herbarium plant collections are vigorously defended against mould fungi and insects, such as booklice, that can rapidly destroy dried plants. Some of the actual plant specimens collected by Sir Joseph Banks and Daniel Solander on James Cook’s 1770 voyage in HMS Endeavour up the eastern coast of Australia are housed in Australian herbariums. These are still in useful condition, demonstrating that herbarium collections potentially have a very long life. They are a uniquely irreplaceable source of information for the future and deserve community support. Pressed and dried specimens of many of the individual plants illustrated in this book have been placed in the permanent collections of state herbariums in Australia. These are called voucher specimens. They are a permanent physical record of the actual plant photographed. Their existence allows the correct

3

current scientific name of the photographed plant to be re-determined whenever botanical research leads to name changes in the family, genus or species of the specimen. Where available, the Queensland Herbarium acquisition numbers (AQ numbers) of vouchers are given in the picture captions of this book. Voucher specimens are even more valuable when linked to published scientific papers describing natural or experimental plant poisonings and chemical investigations of plants for toxins. They ensure that the ongoing usefulness of the information in the publication is not diminished or lost through future name changes obscuring the accurate identity of the plants concerned. For further details, see ‘Name that plant scientifically, please!’ (McKenzie 2008).

What is a poisonous plant? Broadly, a poisonous plant is one containing chemical substances in amounts that can harm or kill animals (including humans) eating it. However, the idea that there are two distinct types of plants – poisonous and safe – is false. It is the amount and type of chemicals they contain, the type of animal eating them, the amount eaten in relation to body weight (the dose), the time taken to eat that amount and the state of chemical processes in the animal’s body that together determine if poisoning is likely to happen or not. To say that a plant is poisonous, we need to say also which animals it can poison and under what conditions. A plant that poisons one animal species does not necessarily poison another species. There are sometimes quite striking differences in toxicity of the same plant or plant toxin between multi-stomached animals (ruminants), such as cattle, and simple-stomached animals (monogastrics), such as horses or humans. For instance, the native Australian grass Dactyloctenium radulans (button grass) will poison sheep or cattle, but not horses. But this happens only if it grows in stockyards and only if it is eaten in large amounts and rapidly. Outside stockyards it is wholesome feed for all types of grazing animals. Other examples of different degrees of hazard for different animal species are the poisoning of parrots by small amounts of avocado flesh that humans eat avidly and safely and the poisoning of dogs by onions, Macadamia kernels or grapes in amounts that do not cause illness in humans. To update the saying ‘The dose makes the poison’ derived from the great renaissance alchemist and medical practitioner known as Paracelsus who first recognised that this principle applied to human poisonings, ‘The animal species, the dose and the circumstances make the poison’. I call this McKenzie’s Maxim.

4

Australia’s Poisonous Plants, Fungi and Cyanobacteria

Why are plants poisonous? Plants, being unable to escape by movement from the animals that feed on them, have developed defence methods to prevent or minimise the damage done to them by being eaten. These defence methods are both physical defence methods, such as thorns and sticky outpourings from wounds, and chemical defence methods. We now look on many of the products of this chemical defence effort as poisons or toxins. These chemical defences have evolved against invertebrate animals (animals lacking backbones), such as insects, slugs and snails, and against vertebrate animals (those with backbones), such as mammals and birds. Planteaters (herbivores), both invertebrate and vertebrate, and the plants with which they evolved over millions of years of geological time have largely reached a state of active balance (called a dynamic equilibrium) between the plants’ chemical make-up and the animals’ capacity to eat them unscathed. Plants have also developed similar chemical defences against infection by microbes (bacteria, fungi and viruses). Herbivores’ resistance to plant toxins is through modified behaviour and through chemical-based defences. Certain insects have developed to a point where plant toxins form part of their own defence, thus turning a former hazard into an asset. The classic example of this is the bond between milkweeds (Asclepias and Gomphocarpus species) and monarch butterflies whose larvae store the bitter and toxic cardiac glycosides from the plant. These deter birds from feeding on the caterpillars. Generally, insects eat only one, or a limited range of, plant species and have developed specific chemical means of dealing with the toxins in those plants. In contrast, plant-eating mammals generally use a wider range of plants and depend on taste, smell and learning to avoid poisonous species. To back up this first line of defence, they have more broadly based chemical detoxification systems in the chemical processes of their livers and other organs and in the microbes in their stomachs and intestines. The balance of plant chemical defence against herbivore resistance is upset when herbivores are moved by humans from their natural habitat to encounter a new set of plant foods. This has been the experience of Europeans migrating to the Americas, Africa, Australia and New Zealand and bringing their domesticated livestock with them. Deaths and illnesses among introduced flocks and herds from the effects of toxic chemicals in the local plants were common and widespread in each of these places, and continue to this day. In a similar way, animals native to Australia have been poisoned by plants introduced as livestock food from Europe and elsewhere (see ‘Are Australian native

animals poisoned by plants?’ below). This balance is also upset when humans restrict the freedom of herbivores by enclosing land and confining their choices to a few food plants or a single food plant, such as by grazing cattle on a crop. Plants develop hazardous amounts of toxic chemicals for various known reasons including: •• defence against attack by herbivores such as insects, slugs and snails (molluscs) in the first place, but also mammals. For example, cyanogenic glycosides are effective against insects and molluscs, and pyrrolizidine alkaloids are effective against insects. There is a biological ‘arms race’ between a plant species’ capacity to produce these defence chemicals and the capacity of its herbivores to detoxify these chemicals, which is ‘refereed’ by natural selection. So, the poisoning of mammals by certain plants can be thought of as ‘collateral damage’: that is, an outcome beyond the stimulus–response cycle between insects and plants that promoted the development of the toxins. On the other hand, certain alkaloids in flowering plants have been suggested as defence against being eaten by mammals through their effects on mammalian neurotransmitters (the chemical messengers between brain cells), such as nicotine mimicking acetylcholine and atropine blocking the effect of acetylcholine. •• defence against microbial infections by fungi and bacteria through producing small (low-molecular weight) anti-microbial chemicals called phytoalexins in response to such infections, such as the furanocoumarins produced by celery responding to attack by mould fungi that produce photosensitisation in animals as a side effect. •• competitive advantage through slowing or stopping the growth of competing nearby plants by so-called allelopathic chemicals, such as chemicals of the atractyloside group produced by such plants as Xanthium strumarium (Noogoora burr). These spread out in the soil surrounding the roots and stop or slow the growth of other types of plants in the vicinity. The poisoning of animals by these toxins is another example of ‘collateral damage’. •• disturbance of normal plant physiology by environmental conditions; for example, nitrate accumulates in plant stems during cloudy weather when the sunlight-driven photosynthesis needed to produce energy for converting nitrate into protein is not sufficient. Of course, there are many plant toxins for the production of which we have no satisfactory specific explanation so far. For example, we do not really understand why certain plants accumulate soluble oxa-

1 – Understanding plants and plant poisoning

lates: one of the more serious toxins that poison animals such as sheep. Oxalates seem to be involved in the regulation of the amount of calcium and other essential components in plant cells. This being the case, poisoning by them probably has little or nothing to do with plant defence against herbivores or other plants. But, to step back and take a broad view, we can see that the production of toxins is likely to be of survival value to the plants that make them, simply because their production must use energy and chemical resources. In the struggle for survival, waste of energy and resources on toxins that could otherwise have been used on vital structures and functions would lead to failure and extinction in the long run.

Why do different plants share the same toxins? When plants in the same or closely related families share the same complex organic toxins, this is evidence that they evolved from a common ancestor and that the capacity to produce the toxins were retained during the evolution of new species through natural selection. The presence of the same toxin in plants in widely different families, such as galegine in Galega officinalis (dicots of the family Fabaceae), Verbesina encelioides (dicots of the family Asteraceae) and Schoenus asperocarpus and Schoenus rigens (monocots of the family Cyperaceae), may be evidence of common ancestry or of parallel evolution; that is, a shared solution to a common life challenge, developed independently in each species in the same way that wings evolved independently in insects, birds and bats.

Do poisonous properties run in plant families? This may be broadly true for some toxins and plant families or genera, such as the common occurrence of pyrrolizidine alkaloids in plants in the family Boraginaceae and in many species of Crotalaria (family Fabaceae) and Senecio (family Asteraceae). Similarly, cardiac glycosides commonly occur in plants in the families Apocynaceae, Iridaceae and Crassulaceae. However, there can be stark differences in the toxins produced by plants in the same family or even in the same genus. It is important not to assume that all plants in the same plant family will have the same toxin and be poisonous if one member of the family is known to have it. For example, in the family Myoporaceae, only Eremophila maculata generates dangerous amounts of cyanogenic glycosides, and Eremophila deserti and some species of Myoporum generate completely different deadly poisons in the furanosesquiter-

5

pene group. All of the many other species of Eremophila and Myoporum appear to be harmless.

How do we know that a plant is poisonous? We know that a plant (or a fungus or a cyanobacterium) is poisonous by gathering and weighing evidence from poisonings that occur naturally, from experiments with animals and from chemical analysis of the plant or other organism. Our confidence in labelling an organism as poisonous is founded on one or a combination of the following types of evidence: •• A consistent field syndrome: being linked closely with several cases of poisoning that all have the same features. Gathering reliable evidence of this type may take a long time if poisoning cases are rare or if they are not carefully observed or recorded. •• Experimental confirmation: yielding positive results from feeding experiments in the animal species affected by natural cases. That is, the effects seen in the experiment match those seen in natural cases. This method has been very important in the past, but is now strictly limited by respect for animal welfare to special circumstances and is rarely used. It is the most powerful and swiftest method of confirming the poisonous nature of a plant or toxin. •• Known toxin present: having known toxins found in hazardous amounts in the plant, fungus or cyanobacterium when chemically analysed. To establish that certain chemicals in plants are toxins originally required experiments that produced the effects seen in natural poisoning cases when the suspected toxins were given to animals. The more evidence of these types that we have, the more confident we can be that we are dealing with a poisonous plant, fungus or cyanobacterium. I have tried to convey this by using toxicity confidence ranks to express the weight of evidence for toxicity. Each plant, fungus or cyanobacterium included in this book has such a rank assigned to it. See ’How confident are we that this plant is poisonous?’ in ‘Using this book’ for an explanation of toxicity confidence ranks.

How do we get trustworthy evidence of poisonous properties? Trustworthy evidence of the poisonous nature of plants, fungi or cyanobacteria is obtained through careful observation and research by botanists, mycologists, microbiologists, natural products chemists, and

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Australia’s Poisonous Plants, Fungi and Cyanobacteria

medical and veterinary practitioners and pathologists. The observations of non-scientists, such as human victims of poisoning who survive and owners or managers of poisoned animals, can be equally as valid and useful. The skills of people in the various scientific disciplines of taxonomy, chemistry and the health sciences complement each other, because they generate different kinds of evidence that together form a whole picture of the organism and its poisonous properties. Botanists and mycologists accurately identify and classify the plants and fungi. Natural products chemists extract (isolate) and identify (characterise) the chemical structure of toxins from them. This can be a difficult process needing complicated and expensive equipment. Medical and veterinary practitioners observe and treat natural poisoning cases. Medical and veterinary pathologists carry out post-mortem examinations on fatally poisoned patients and then examine tissues microscopically to observe any damage caused by toxins. Natural products chemists may analyse tissues from dead animals to identify and measure the amounts of the toxins or their break-down products that are present. To complete the process, all of these scientists record their findings in scientific journals where their articles (called scientific papers) are anonymously scrutinised for accuracy by eminent scientists in the same field before being accepted for publication. This is the peer-review process that attests to the scientific rigour of their work. The end result of this process is scientific knowledge that is reliable and that can be built on by others or used with confidence.

How can I prevent plant poisoning? Adopting a two-fold approach It is far better to prevent plant poisoning than to try to cure it. To be able to do this yourself, you need to: •• recognise the presence of potentially poisonous plants where you, your children or your animals are •• understand the circumstances under which poisoning by these plants can occur. Achieving these two aims will allow you to avoid exposing susceptible humans and domestic animals to poisonous plants under conditions likely to lead to poisoning. So …

that exude milky sap when injured are always poisonous. Some certainly are poisonous, but there are others such as lettuce (Lactuca sativa) and the rubber tree (Hevea brasiliensis) that are not. It is said that poisonous plants (or fungi) have an unpleasant taste. This will be true of plants with a significant alkaloid content or cyanide potential – both being generally bitter – but is not a useful rule to judge all plants by. Plants that contain deadly amounts of nitrate or fluoroacetate have no distinctive taste and are quite acceptable to grazing animals, making such plants very dangerous. The kernels of Triunia (spice bush) fruits taste very like macadamia nuts, but certainly poison people badly. Deadly Amanita phalloides (death cap) mushrooms taste no different to ordinary mushrooms, to the intense regret of those few who survive the mistake of eating them. Simple rules claiming to tell poisonous from non-poisonous do not work. See ‘What is a poisonous plant?’ earlier in this chapter. So, we need to learn to recognise the known toxic species one by one. This book will help with the task, but does not cover in detail all known toxic plants in Australia, only the ones judged to be important (see the criteria listed in the Preface). Others are listed briefly in Chapter 15. Features of plants to focus on when trying to identify them include growth habit (type of plant), leaf shape and, if they carry flowers, the flower shape and colour, and fruit shape and colour. Final accurate identification requires botanical expertise; that is, examination by a professional botanist. For this, fertile specimens are required. These are specimens with attached reproductive structures (flowers, fruit, cones or spores, depending on the type of plant). For further details, see the section ‘Name that plant!’ (earlier in this chapter), Chapter 2 and the section on toxicity confidence ranks in ‘Using this book’.

What circumstances lead to poisonings of domestic animals? It can be very difficult to explain why a particular poisoning case has happened, but we can identify some factors that tend to influence animals to eat poisonous plants and others that tend to make plants more poisonous (see Appendix 3 for a list of ‘poisoning hot-spots’).

How can I recognise a poisonous plant?

Plant factors

No simple features of shape, colour, taste or other physical features distinguish poisonous from nonpoisonous plants or fungi. It is often said that plants

Palatability (how tasty a plant is), and thus attractiveness to animals, varies significantly among known poisonous plants. Many fluoroacetate-containing plants

Palatability

1 – Understanding plants and plant poisoning

are consistently palatable, making them particularly dangerous to browsing animals. Applying herbicides may temporarily increase the palatability of poisonous weeds, boosting the hazard. This is known to occur with variegated thistle (Silybum marianum). Plants containing alkaloids are generally bitter and non-palatable. Cardiac glycoside-containing plants are usually unpalatable. These plants are likely to be eaten only when other feed is scarce or lacking, they are mixed with more palatable feedstuffs or animals are very hungry.

Stage of plant growth This can affect the concentration and distribution of toxins in plants. Toxin concentrations may vary in different plant parts or at different stages of plant maturity. Nitrate concentrates in stems. Cyanogenic glycosides and soluble oxalates concentrate in young leaves. Defence chemicals are concentrated in the plant’s most vulnerable parts, particularly in its seeds, cotyledons (seed leaves) and young shoots. Not all parts of all poisonous plants are toxic. In some plants, only the seeds may be poisonous (e.g. Leiocarpa brevicompta and Castanospermum australe). In others, only the young leaves may be poisonous (e.g. Sorghum plants). Root suckers may be the most hazardous part of toxic trees, such as in Erythrophleum chlorostachys, because the leaves on the suckers are within easy reach of browsing animals when the leaves on the tree itself are too high to reach.

Physical condition and plant disease Wilting, herbicide damage, insect damage, and bacterial, fungal or virus infections all influence concentrations of toxins. These all increase concentrations of nitrates. Wilting boosts steroidal saponin concentrations of some grasses to hazardous amounts.

Animal factors Animal species The details of the chemical processes within body cells and tissues (metabolism) differ between ruminant mammals, monogastric mammals and birds. This can cause differences in the susceptibility of these groups to particular toxins through differences in the efficiency of processes that destroy or make toxins harmless through chemical reactions (detoxification mechanisms). These differences can be very wide, so that one toxin can be fatal to one group but harmless to another. Another very important distinction between animal species is the ruminal microflora; that is, the bacteria and single-celled animals (protista or protozoa) living in the paunch (rumen or forestomach) of animals, such

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as cattle, sheep and goats, that help them to digest plants. These are very important to their host’s chances of surviving plant toxins in their food. They can either protect the ruminant by destroying these chemicals (detoxify them) or betray the ruminant by changing them into more poisonous forms (potentiate them) before they are absorbed from the intestines into the animal’s bloodstream. This double-edged-sword effect of the ruminal microflora underlies some of the major differences in susceptibility to poisoning between ruminants and other mammals. For example, oxalates are largely destroyed in the rumen, but the rumen microbes convert the relatively harmless nitrate into the potentially deadly nitrite.

Age Young animals are generally more susceptible to poisoning than adults because they have less effective detoxification mechanisms established in their body organs. They may also be more curious than adults and more likely to eat unfamiliar foods. The adult females of some herd animal species, such as cattle, seem to teach their young by their example which foods are safe to eat in environments to which they have become accustomed. Young animals denied this experience will be more likely to eat potentially dangerous plants.

Degree of hunger Animals are hungrier after transport or yarding and this may result in more rapid eating of a large amount of toxic material and less discrimination in the choice of the plants eaten. Hungry animals are thus more likely to be poisoned.

Rank within a group of animals The power structure within groups of animals is called the dominance hierarchy. Leading or dominant animals in a group are more likely to eat larger amounts of food more rapidly than their fellows and this may lead to poisoning where more moderate behaviour would not. Leaders will demand and obtain first access to limited food supplies. In these circumstances, such as when hay containing potentially poisonous nitrate concentrations is fed to hungry travelling cattle, dominant animals may be the only ones to die. In the paddock, dominant animals may take more of certain normally choice plant foods, such as the high protein seed pods of legumes, and thus be more likely to be poisoned when these have the highest concentration of toxins, such as the fluoroacetate in Acacia georginae.

State of nutrition Poorly fed animals, such as those during a drought, are generally more susceptible to poisoning than well-fed

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Australia’s Poisonous Plants, Fungi and Cyanobacteria

animals because they tend to have smaller reserves of the chemicals obtained from food that are needed by the body to deal with toxins through detoxification mechanisms. If they run out of these essential chemicals, poisoning can result as the body fails to counteract the absorbed toxins.

Type of food on offer Hand-fed animals are open to poisoning when their food is contaminated with hazardous material and they are unable to choose not to eat the toxic component. This happens when toxic weed seeds contaminate feed grains, such as Heliotropium europaeum seeds containing pyrrolizidine alkaloids in feed wheat or when toxic weeds themselves contaminate hay, such as one-leaf cape tulip (Moraea flaccida) containing cardiac glycosides or mintweed (Salvia reflexa) containing nitrate. Grazing animals may lack dietary choice because they may be fenced into small enclosures and forced to eat what is available. In some circumstances, this can be a monoculture such as a crop or sown pasture. A widespread example in northern Australia is horses forced to graze pure swards of tropical pasture grasses such as buffel grass (Pennisetum ciliare) from which they cannot extract calcium because it is bound to oxalates. They develop big head (nutritional secondary hyperparathyroidism) because of this.

Access to drinking water Some toxins may not be released from eaten plants and absorbed from the animal’s digestive tract until after the animal has drunk water, such as in Solanum sturtianum poisoning of ruminants. In extensive pastoral areas, the few water supply points effectively limit livestock to grazing the pasture within a day’s walking distance of the water supply. This, in fact, increases the grazing pressure near water and can reduce the animals’ ability to select from all the feed growing in large paddocks, influencing their intake of potentially poisonous plants.

Familiarity with surroundings Newcomers in unfamiliar environments may eat plants that they would ignore in their home paddocks. That is, they tend to make less discriminating food choices. This is made worse by the increased degree of hunger experienced by animals after being transported. The ultimate example of this factor came into play when livestock of European and Asian origin were transported here and had to eat Australian plants. Most survived, but over the centuries many have died because their genetic heritage was not shaped for ‘peaceful co-existence’ with local poisonous plants by eons of natural selection through exposure to the toxins they contained.

Length and intensity of exposure – tolerance Chronic toxicities naturally take time to emerge; for example, pyrrolizidine alkaloids accumulate in the liver over time, but illness does not result until damage exceeds a certain threshold and this can take months to years. Tolerance may develop to otherwise lethal doses of certain toxins if the body is exposed to lesser doses over a period of time and detoxification processes, either of the rumen microflora or of the liver, have time to develop greater efficiency. For example, ruminants exposed to small non-toxic amounts of oxalates over a period of time are often able to withstand a larger dose that would kill animals lacking that exposure. This process is tolerance, not immunity. Immunity is the process through which the immune system of the body generates antibodies and immune cells to resist foreign organisms such as viruses and bacteria. At the chemical level, immunity is triggered by large foreign protein molecules. The size of toxin molecules is generally far too small to trigger this kind of response in the body.

Environmental factors Season of the year This dictates the presence or absence of particular annual plants that only grow for part of the year in the habitat. It also dictates the stage of growth and the physiological state of plants, and consequently the presence or absence of flowers, fruit, seeds or young leaves, only some of which may be poisonous in a particular plant species. For example, Bryophyllum poisoning usually occurs during winter when the plants flower.

Rainfall or snowfall history Dry conditions produce wilting, which may increase the concentrations of some toxins such as steroidal saponins, making the plants containing them more likely to produce poisoning. Droughts decrease the food choices for grazing animals by decreasing the variety and amount of food plants available. Animals without enough nutritious grasses may turn to eating shrubs and trees, which may be toxic. Floods decrease food choice to grazing animals by decreasing the area of land available for foraging. Heavy snow can prevent access to pasture, forcing animals to browse on potentially poisonous trees such as oaks (Quercus species).

Daily weather conditions Air temperatures influence the water balance of plants, with high temperatures leading to wilting and higher concentrations of certain toxins in plant tissues.

1 – Understanding plants and plant poisoning

Cold temperatures reduce the rate of conversion of nitrate into proteins, thus increasing the concentration of toxic nitrates in some plants. Plants containing cyanogenic glycosides appear to be more dangerous during conditions of light rainfall or drizzle. Fog is reputed to boost the toxicity of Phalaris aquatica. Cloud cover, if heavy and prolonged, decreases photosynthesis and in consequence the energy production by the plant. This slows or stops the conversion of nitrates to proteins, boosting the concentration of potentially toxic nitrates in plants.

Soil Local soil mineral content can influence poisoning hazards; for example, selenium-accumulating plants will be most toxic when growing on soils rich in selenium. Total amounts of plant nutrients can influence the amount of certain toxins that plants generate; for example, soils high in nitrogen predispose plants to develop large concentrations of nitrates and oxalates. Stockyard soils heavily fertilised by manure and urine provide large amounts of nitrogen and thus promote dangerous concentrations of nitrate and oxalate in plants growing in them. The same species of plants growing a short distance from the stockyards commonly contain harmless amounts of these toxins. The balance of plant nutrients can be important; for example, nitrogen and other minerals, particularly phosphorus, sulphur and molybdenum, can influence plant nitrate content. If soil is rich in nitrogen but poor in one of the other elements, nitrate ions are taken up by plants such as Salvia reflexa and Silybum marianum, but are not readily converted to ammonium ions and thus to proteins, leaving the plants with large toxic nitrate concentrations.

Herbivores or plant pathogens Insect damage may increase the concentration of defence chemicals, such as the boost to cyanogenic glycosides in Sorghum spp. produced by grasshopper attack. Bacterial, fungal or viral damage may increase the concentration of defence chemicals such as the phytoalexins, including furanocoumarins, or interfere with normal physiological processes and increase the concentration of certain toxins such as nitrate as an incidental by-product.

What circumstances lead to poisonings of humans? There are similarities between the factors leading to plant poisonings of domestic animals and of humans and they can be considered under the following headings:

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Susceptible types of people Plant poisoning of people is very rare. People who are at points in their lives where exploration of their surroundings, experimentation with novel substances or both occur, are more likely to suffer adverse effects of plant or fungus eating than other types of people. Curiosity then combines with lack of knowledge of the possible consequences of behaviour, or a relative disregard for them. Young children (‘toddlers’) naturally exploring their environment for the first time and older children and young adults experimenting with ‘mind-altering’ chemicals fall into these categories. Young children may eat garden or house plants, some of which are potentially poisonous; older children and adults may experiment with plants and fungi that contain (or that they hope contain) hallucinogenic chemicals and suffer the effects of overdosing. Another group of humans who are more likely than the bulk of us to be poisoned by plants are non-Aboriginal bush tucker or wild food enthusiasts who misidentify the plants they are sampling or who try out leaves, seeds or fruit of plants they encounter in the bush or countryside without carefully identifying and researching them first. Armed services members on survival exercises have fallen victim to this mistake, in part prompting the work of Major Les Hiddins, the ‘Bush Tucker Man’ – see his Bush Tucker Field Guide (Hiddins 2001). Immigrants to Australia from cultures where the harvesting of wild foods is normal should not assume that seemingly familiar plants or fungi in Australia are the same species as those in their lands of origin. Natural does not mean harmless! (See the section on ‘Australian Aboriginal bush tucker and poisons’ later in this chapter.) Young children are more susceptible to poisonings than adults for the same reasons noted for domestic animals above. In many cases, young children sample potentially poisonous plants rather than avidly eat large amounts of them, so the doses of toxins entering their bodies are commonly small and not life-threatening. (See the section on ‘How often are children poisoned by garden and house plants?’ later in this chapter.)

Mushroom gatherers Fungal harvesters are something of a special case because a number of fungal species are collected from their natural habitat for human food and confusing edible with poisonous species is the main reason for poisonings. These poisonings can affect children and adults of any age. Australians with a mainland European heritage, rather than a British or Irish one, are more likely to collect ‘wild mushrooms’ for food and be

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Australia’s Poisonous Plants, Fungi and Cyanobacteria

the victims of poisoning. Assuming that fungal species here are the same as those collected and eaten over thousands of years in Europe can be dangerous. There is a saying that ‘There are plenty of old mushroom hunters and plenty of bold mushroom hunters, but there are no old, bold mushroom hunters.’ Accurate fungal identification is the key to continued good health. See Box 5.1 ‘Rules for picking and eating mushrooms’ (Chapter 5).

Professional plant-handlers Florists, nursery workers (horticulturists) and workers handling large amounts of vegetable produce (greengrocers) are at risk of developing skin complaints from certain plants that they come into contact with regularly. Species of Grevillea are well known in floristry for causing dermatitis. The species of Grevillea featured in this book are the extreme end of this problem and cause immediate severe skin damage through the urushiol in their sap. Florists and horticulturists are more likely to develop minor skin irritation after handling common species and cultivars of Grevillea and perhaps other plants in the family Proteaceae that contain urushiol in lesser amounts. Vegetables containing furanocoumarins, either in their healthy state or after being damaged by microbe infections (rots), cause skin damage in people handling them in quantity. This is a form of primary photosensitisation and will show up after contact with the vegetables then followed by sunlight shining on the skin that has been affected. Handling a lot of parsnips, parsley, celery or, more rarely, other vegetables closely related to these in the family Apiaceae [syn. Umbelliferae] such as dill and lovage, can produce this effect. Handling lemons, limes (species of Citrus) and other members of the family Rutaceae such as rue (Ruta graveolens) can also induce it. This syndrome in humans goes by a large number of alternative names including celery-handler’s disease, percutaneous photosensitisation, dermatitis bullosa pratensis (or bullosa pratensis striata or bullosa striata pratensis), meadow dermatitis, phytogenic photodermatitis, phytophotodermatitis, phytophotosensitisation and vesicular dermatitis.

Sensitive individuals subject to allergies Allergic reactions are not poisonings. Both of the effects described in the previous section are true poisonings where the chemicals in the plants directly damage tissues in proportion to their dose. That is, the bigger the amount of toxin, the greater the effect. There is another outcome of plant handling that is less direct and less predictable. This is the allergic reaction causing skin damage (allergic dermatitis) that some individual people may develop after contact with some

plants. It happens when those people’s immune system is triggered to react by certain chemicals in plants. It is not a poisoning because the reaction of the body is not related to the dose of chemical to which the sensitised individual is exposed. A tiny dose may produce a very intense reaction. Some people are badly affected by this. Others exposed to the same degree are not affected at all. ‘Hay fever’ – an allergy to air-borne plant pollens – falls into this category of ailments. This is a condition that is not dealt with further in this book because of its less predictable and non-toxic nature. Serious or persistent skin reactions to plant contact (contact dermatitis) should be investigated by consulting your medical practitioner who may need to refer you to a specialist dermatologist equipped to investigate allergies.

Access and actions of humans Circumstances leading to poisonings include: •• poisonous species of common ornamental garden plants accessible to young children, (e.g. oleanders). •• certain normal food sources incorrectly handled, such as potatoes being allowed to turn green through exposure to excess light, or the insufficient preparation of taro or cassava tubers to remove cyanide •• certain normal foods given to individuals with greater-than-normal susceptibility, such as carambolas eaten by people with poor kidney function •• certain herbal remedies used inappropriately or in excessive doses, such as comfrey •• contamination or substitution of herbal remedies with or by poisonous species, such as Aristolochia species •• field-collected poisonous fungi eaten mistakenly as edible species •• cyanobacterial-contaminated drinking water or recreational water bodies •• native poisonous plant species in the natural environment eaten out of curiosity or during bushwalking emergencies or survival exercises, such as the seeds of black bean trees. It is not safe to assume that fruits seen to be eaten by birds are safe for humans to eat. Birds are much less susceptible than mammals (including humans) to some poisons, such as cardiac glycosides. Cassowaries feed on the fleshy red fruits of the rosy apple (Phaleria clerodendron) in northern Queensland, but humans are likely to be poisoned by irritant diterpenoids in these same fruits.

1 – Understanding plants and plant poisoning

Plant and fungal toxins in human foods and beverages Many people eat plants that contain some toxins of which they are unaware, but they do not get ill because the dose is not great enough to cause problems. If circumstances change and the dose becomes large enough, illness results.

Toxins that are a normal part of the plants we eat Careful storage and preparation of plant foods normally protect us from poisoning by some toxins that plants produce naturally. There are many examples. Potato tubers need protection from light to prevent the generation of poisonous steroidal glycoalkaloids by the green tissue under their skins. Cassava and taro need to be processed to remove their potential for generating cyanide before they can be safely eaten. Celery, parsley and parsnips can generate large amounts of furanocoumarins if damaged by bacteria or fungi during storage. Red kidney beans (Phaseolus vulgaris) need cooking to destroy lectins that can cause abdominal pain, diarrhoea and vomiting. Bitter lupin seeds (Lupinus species) need processing to remove their poisonous alkaloids. Lupins intended for human and livestock food have been bred to reduce their alkaloid content to harmless concentrations. See the section on ‘Lupin (quinolizidine alkaloid) poisoning’ (Chapter 3).

Normally safe foods and beverages contaminated by toxins Cereal grains such as wheat and barley can be contaminated by the seeds of weeds and by ergots of rye. Some weed seeds such as Heliotropium europeum and Echium plantagineum contain pyrrolizidine alkaloids. Others such as the thornapples (Datura species) contain tropane alkaloids. These weed seeds and ergots must be removed from grain before it is used. There are legal standards in Australia aimed at preventing any such contaminated grain reaching human food. These standards are routinely upheld by grain marketing authorities. One unresolved problem is that dust from weed seeds may remain on grain that has been cleaned of the actual seeds. This dust may contain substantial amounts of the toxins. This means that weed control in grain crops is even more important for preventing the contamination in the first place. See ‘Plant-associated toxins in the human food supply’ (Colegate et al. 1998). Plant foods may also be contaminated by the toxins (called mycotoxins) produced by microscopic fungi

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and food-poisoning bacteria. These organisms are not subjects covered by this book. For detailed information on mycotoxins in human food, see Fungi and Food Spoilage (Pitt and Hocking 1997) and ‘Current mycotoxin issues in Australia and Southeast Asia’ (Pitt and Hocking 2004). Briefly, the major mycotoxin problem for humans in Australia is aflatoxin in peanuts (groundnuts, Arachis hypogea) resulting from infection by the mould Aspergillus flavus. Aflatoxin contamination is effectively controlled by good farm and product management practices. A second problem is the potential presence of ochratoxin A in grapes and grape products, resulting from infection by the mould Aspergillus carbonarius. Good quality control before and during winemaking prevents harmful concentrations occurring in wine, but amounts of ochratoxin A may be greater in dried vine fruit. Toxins generated by Fusarium fungi sometimes occur in cereals in Australia, but probably to a lesser extent than in grains from any other world region. Drinking water may be contaminated at its source by toxins from blooms of cyanobacteria growing in water storage reservoirs. The normal filtration and chlorination of reticulated drinking water usually removes these toxins effectively before they reach consumers.

Plant toxins in edible animal tissues and products A rare type of poisoning is called secondary poisoning because the poisonous plant is not eaten directly by the victim, but its toxin is obtained from the dead body of a victim of primary poisoning; that is, an animal that did eat the plant and died of it. Sometimes the original eater of the poisonous plant does not have to be ill or die from the poisoning to pass on a toxic dose to another animal that eats meat or offal from its carcase. Very rarely, scavenging dogs may eat enough stomach contents from a poisoned animal to be poisoned directly by the plant that killed the original victim.

Meat and offal Dogs (or cats) may be poisoned if they eat parts of herbivores that have recently died from certain plant poisonings. This is rare. Toxins that can lead to this include fluoroacetate, cyanide, indolizidine alkaloids of Alstonia constricta (bitter bark) and the unidentified muscle-damaging toxin in Senna plants. In southwestern Western Australia, the local wildlife is used to eating the local fluoroacetate-containing plants. These animals are very resistant to this toxin and can have significant amounts in their bodies with no ill effects. Sometimes dogs or cats that kill and eat such

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Australia’s Poisonous Plants, Fungi and Cyanobacteria

wildlife as pigeons may be fatally poisoned. In South Africa only, certain bufadienolide-type cardiac glycosides in carcase tissues of poisoned sheep or goats can damage dogs’ or humans’ nervous systems. Dogs fed meat from horses or camels that have grazed on Indigofera linnaei in inland Australia can develop fatal liver failure from the indospicine (an amino acid) that the grazing animal has picked up from the plant. The horses and camels it comes from may be healthy, but the dogs can still be poisoned. When plants that contain pyrrolizidine alkaloids are eaten, the alkaloids are absorbed and changed in the liver to very chemically reactive forms called pyrrolic metabolites. These pyrrolic metabolites attach firmly to the large molecules in liver cells, such as proteins and DNA, as forms called adducts, remaining there for the life of the cell. We do not know if these adducts can be released from their bonds to do further damage to the tissues of animals (including humans) that may eat such livers, but this is very unlikely.

Milk Milk from animals that have eaten some poisonous plants may contain their toxins. These include ptaquiloside, dihydroxycoumarins and swainsonine. Offspring may be poisoned through milk without eating the plants themselves. This is most commonly known from dihydroxycoumarins in calves, but this is very rare in Australia. Pyrrolizidine alkaloids in the N-oxide form that is common in plants can be absorbed from eaten plants and then excreted into milk. The N-oxides are not poisonous themselves, but can be converted to the toxic alkaloid form by bacteria in the intestines of offspring and then cause liver damage. This is rare. The danger to humans from drinking cow’s or goat’s milk containing such toxins is removed by the large dilution (‘watering down’) that occurs through the mixing of many batches from widely different milking herds in commercial milk products. Those who drink contaminated raw milk at the source are at some risk. Products of Cannabis sativa toxins enter the milk of ruminants that eat that plant.

Honey Honey may be contaminated by toxins such as pyrrolizidine alkaloids or grayanotoxins if bees forage on plants containing these substances. The toxins can be in nectar, pollen or both. It has been known from ancient times that humans can be poisoned by eating honey from bees that forage on Rhododendron and related plants – so-called ‘mad honey’ that contains

grayanotoxins. No cases of poisoning from pyrrolizidine alkaloids in honey are known, but there is a risk. A plant called tutu (Coriaria arborea) that grows only in New Zealand is the source of honey that has poisoned people in that country now and again, causing convulsions, vomiting and memory loss. When their usual nectar sources are scarce, bees pick up this toxin (tutin) from the honey-dew excreted onto the plant’s leaves by passion vine hoppers (Scolypoda australis) feeding on the plant’s sap.

Eggs Eggs may be contaminated by pyrrolizidine alkaloids if free-range fowls eat plants containing them or if feed grains fed to fowls are contaminated by weed seeds containing these toxins. No cases of poisoning from pyrrolizidine alkaloids in eggs are known, but there is a risk.

Australian Aboriginal bush tucker and poisons Over 50 000 years of experience with Australian plants and fungi have given Aboriginal people extensive knowledge of their poisonous and edible properties. As one author expressed it, this experience began as a process of ‘eat, die and learn’ and grew into a large body of useful knowledge. Ultimately, this was used to remove poisons from plants that were then used for food, to avoid other plants that could not be made safe to eat, and to catch game animals and to fish by poisoning waterholes. Plant toxins were also used to cure ailments, to murder enemies and to produce alterations of mind. In all these ways, the first Australians behaved just the same as all other indigenous people the world over. Aboriginal Australians and Australians of European descent have compiled lists of many plants used by the first Australians in various ways, but it is very likely that much knowledge has been lost since 1788. Despite this, Aboriginal communities still hold much valuable knowledge of plants in their regions. Plants known to be used by Aboriginal people and discussed in the main section of this book include species used for hunting (Duboisia hopwoodii and Gastrolobium grandiflorum), as fish poisons (Abrus precatorius and Duboisia myoporoides), for homicide (Castanospermum australe and Alstonia constricta), as narcotics (Duboisia hopwoodii and species of Nicotiana) and for food (cycad seeds, Castanospermum australe seeds, Pteridium esculentum rhizomes, Marsilea drummondii sporocarps and Alocasia brisbanensis roots). ‘Bush tucker’ gathered from these plants must be carefully prepared to remove the toxins before eating. Natural does not mean harmless! See the ‘Reference and

1 – Understanding plants and plant poisoning

further reading list’ for sources of more information on this topic.

Are Australian native animals poisoned by plants? As explained earlier in this chapter under ‘Why are plants poisonous?’, plant-eaters (herbivores including mammals and insects) have developed ways of avoiding being poisoned under their normal living conditions. A good example of the adaption of Australian mammals to a plant toxin is the interaction of some Western Australian animals with the many fluoroacetate-containing Gastrolobium species in the southwestern part of the state. Brush-tailed possums, bush rats and western grey kangaroos from this area have evolved an efficient fluoroacetate detoxification process in their livers. They are capable of safely eating these plants, which are rapidly fatal for Australian native mammals from eastern Australia if fed these plants experimentally and, of course, for livestock. Because plant-eaters are well adapted to their natural environments, poisoning occurs only when those environments are seriously disturbed and animals are forced to leave their accustomed ecological niches to feed on dangerous plants. These disturbances can be such things as drought, human interference or exotic weed invasion. Koalas are believed to have been poisoned by cyanide while feeding on fresh young regrowth of manna gums (Eucalyptus viminalis) after bushfires in Victoria. Kangaroos are susceptible to poisoning by a number of introduced pasture plants such as Phalaris aquatica, garden plants such as Duranta erecta and Taxus baccata, and weeds such as Lantana camara. There is concern that pyrrolizidine alkaloids may poison the threatened orange-bellied parrot (Neophema chrysogaster) through feeding on the seeds of the introduced weeds Heliotropium europaeum and Echium plantagineum while wintering in southern mainland Australia after migrating from their breeding grounds in Tasmania, but evidence of actual cases is unrecorded so far. Introduced Aristolochia elegans vines attract native birdwing butterflies to lay eggs on them in mistake for their normal food sources – the native Aristolochia species – and then poison the caterpillars that emerge.

Will climate change change plant poisoning in Australia? Changes in the long-term temperature and rainfall patterns in Australia brought on by human activity leading to climate change will influence the occurrence, distribution and density of native

13

and naturalised plants in both positive and negative directions for us, depending on where we are in Australia. An increasing frequency of droughts in southern Australia will probably also increase the frequency of plant poisonings and influence the toxicity of cultivated plants, as well as native and naturalised ones. Nitrate-nitrite poisoning of ruminants is likely to be strongly influenced by changes in rainfall. Increased droughts will increase the likelihood that plants, particularly crop plants, will take up more nitrogen from soils as the amount of leaching by rainfall declines. Herbivores are likely to be hungrier as rain-grown pasture declines in quantity and this will cause them to eat more of the plants, including poisonous ones, that they eat sparingly or ignore now. More rainfall in north-western Australia may allow poisonous plants such as pyrrolizidine alkaloid-containing Crotalaria ramosissima to be present for more of the year and to increase their density. It may also increase the frequency of poisonings by Corallocytostroma ornicopreoides, the Mitchell grass gall-forming fungus. Declining oil supplies pushing up the cost of livestock transport in large articulated motor vehicles (road trains and semi-trailers) may prompt a return to droving as a means of moving herds and flocks to markets. This will increase the risk of plant poisonings as more hungry animals encounter plants such as Nicotiana species (native tobaccos), Neobassia proceriflora (soda bush) and Eremophila deserti (Ellangowan poison bush, turkey bush) on stock routes, the impact of which has been lessened by motor transport in recent decades.

Does this animal have plant poisoning? Accurate diagnosis of the cause of illness is a process that needs knowledge and skill in the investigator, backed up by specialised laboratory analysis in many cases. The process must take into account all possible causes including infections, genetic defects and nutritional deficiencies, as well as poisonings. Medical and veterinary practitioners are trained and experienced in this work: they should be consulted in any case of serious illness in humans or domestic animals, respectively. The details of diagnostic methods for poisonings are beyond the scope of this book. For this information, veterinarians should consult my Toxicology for Australian Veterinarians (McKenzie 2002). Medical practitioners could consult Medical Toxicology (Dart 2004), the Toxicology Handbook (Murray et al. 2007) and the Handbook of Poisonous and Injurious Plants (Nelson et al. 2007). I strongly urge lay people to leave this to professionals because …

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Australia’s Poisonous Plants, Fungi and Cyanobacteria

A little learning is a dang’rous thing; Drink deep, or taste not the Pierian spring: There shallow draughts intoxicate the brain, And drinking largely sobers us again. Alexander Pope (1688–1744) An Essay on Criticism. 1711

Gathering sufficient evidence to diagnose plant poisoning with high probability requires meeting some or all the following conditions. Not all conditions need be met, or are even technically possible, in all cases. Assay methods for suspected toxins may be unavailable. Conditions that need to be met in most cases are: •• The suspected plant has been identified accurately, allowing meaningful searching of the published scientific literature. •• The circumstances of the case (its epidemiology), and its clinical signs, clinical pathology, necropsy and histopathology findings match those known to be produced by the suspected plant or its contained toxin. •• The patient or group had access to the suspected plant in amounts capable of producing poisoning of the observed severity or extent. •• There is evidence that the suspected plant has been eaten in amounts capable of producing poisoning of the observed severity or extent, either from examination of the remaining vegetation at the site of the incident, examination of stomach contents, or both. Additional useful conditions are: •• The suspected plant contains enough toxin measured by chemical assay to account for the observed syndrome. •• The suspected plant has been found in the alimentary tract (rumen or stomach) of poisoned animals. •• The plant toxin (or known derivatives of it) has been detected in alimentary tract or tissues of poisoned animals. Detection methods are limited to specific toxins and in many cases to particular laboratories. A final rarely needed condition is: •• A feeding trial with the suspected plant reproduces the syndrome under investigation. This step is hard to carry out to a satisfactory conclusion. Failure to reproduce the syndrome is not conclusive because it can be very hard to match in an experiment the natural circumstances leading to poisoning. Respect for animal welfare now precludes this option in virtually all cases.

How can I deal with plant poisoning threats? It is very true that in most cases preventing poisoning is much easier and more effective than treating it. Approaches to the control of poisoning include the following.

Learn the facts, teach the facts Promoting knowledge in parents of young children and owners or managers of animals of the potentially poisonous plants in their region and the circumstances that could lead to poisoning is the best method of prevention available at present. This book tries to provide a sound basis of knowledge to achieve this. However, it is often a case of ‘You can lead a horse to water, but you can’t make it drink’. Knowledge transfer from reliable sources such as the scientific literature to the intended audience (parents or animal managers) is patchy at best, and strongly influenced by their personal priorities: ‘When you are up to your armpits in alligators, it’s hard to remember that you intended to drain the swamp!’

Stop access to known poisoning ­hazards by susceptible individuals Logically, preventing access to potentially poisonous plants under circumstances likely to lead to poisoning is a rational risk management strategy flowing from knowledge of those factors. Plant control is one method to achieve this (see ‘How can I control poisonous plants?’ later in this chapter). Specific management strategies have been worked out successfully for some plants that poison domestic animals. These are currently available for Darling peas (species of Swainsona), Leucaena leucocephala in ruminants and Indigofera linnaei in horses. Others may be devised in future from study of the features (epidemiology and pathophysiology) of poisonings such as those by species of Pimelea in cattle. Work in North America and South Africa has demonstrated that it is possible to prevent animals from eating particular poisonous plants that are common in their environments by causing an intense distaste for the plants through conditioned food aversion. This is achieved by training methods using the unpleasant-tasting chemical lithium chloride fed at the same time as the plants. This technique has apparently not been tried in Australia so far. It is unlikely to be useful except in specific circumstances with small groups of animals.

1 – Understanding plants and plant poisoning

Feed grain for livestock that is contaminated by poisonous weed seeds or ergots can be made safe by diluting the batch with clean uncontaminated grain until the concentration of the seeds or ergots is less than hazardous. Screening out the weed seeds or ergots if they differ significantly in size from the individual grains is an alternative method. Heat treatment through pelleting of feed may destroy the toxicity of some weed seeds, such as those of Ricinus communis (castor oil plant). Fodder crops with hazardous concentrations of cyanogenic glycosides can be made safe by ensiling. The resulting silage should be checked before feeding. Alkaloids will generally survive the ensiling process. Fodder or contaminated grain that is poisonous for one animal species may be able to be used safely if it is fed to a different species; for example, sheep and goats are less susceptible to pyrrolizidine alkaloids than cattle, but using this option is a last resort and only a short-term solution because sheep and goats will eventually be poisoned if fed such material for long enough.

Increase the individual’s resistance to plant toxins Immunisation (‘vaccination’) is possible with some plant toxins that affect livestock, but has not come into general use so far. Its potential practical use is restricted to a very small number of candidate toxins by a number of serious technical and economic hurdles in the research and development process. Candidate poisonings need to cause significant economic loss to make them attractive as commercial ventures for vaccine manufacturers. The market for the ‘vaccine’ needs to be as large as possible and demand needs to be steady to provide a reasonable return on investment. The candidate poisonings should be chronic and cause little damage to the victim’s organs to allow a reasonable chance of success for the antibodies generated by the ‘vaccine’. Technical problems with producing an effective product are a major hurdle. The small molecules of plant toxins need to be attached to larger molecules such as proteins to make them ‘visible’ to the immune system after injection. On their own, they are too small to generate antibodies or immunity. Then, even if antibodies are generated, they may not protect the animal effectively against the toxin. This was the fate of an experimental ‘vaccine’ against Pimelea poisoning of cattle in the 1990s. Manipulation of the rumen microflora to destroy plant toxins has been explored for a number of plant

15

poisonings of cattle and sheep. It has been very successful against mimosine in Leucaena leucocephala through introducing an existing natural bacterium capable of doing this into commercial cattle herds browsing leucaena in Australia. But this method cannot be used in horses or pigs because they do not have rumens for it to live in. Prevention of fluoroacetate poisoning has been achieved in ruminants in Australia by producing a genetically modified bacterium that destroys fluoroacetate. So far, this organism has not been released for commercial use because of concerns that it could be transferred from inoculated livestock to feral goats or rabbits and so prevent the effective use of 1080 baits for their control. Genetic modification of rumen bacteria may be applied successfully in the future to other plant poisonings such as those caused by the pyrrolizidine alkaloids. Livestock protected by these methods must be carefully managed to guard against land degradation caused by surrendering to the temptation to overstock sensitive environments that were previously protected by the presence of poisonous plants.

Use therapy in appropriate cases Therapy may be effective in some plant poisonings. In all cases, the earlier the treatment starts after poisoning is suspected, the better the outcome. Emergency treatment of poisoned patients is exacting and intensive work demanding professional medical or veterinary expertise for success. However, recovery from serious poisoning cannot be guaranteed, even with swift appropriate therapy. Organ damage can be too far advanced when the first signs of poisoning occur for recovery to be possible. Specific therapy (the use of ‘antidotes’) for poisoning victims is often unrewarding in practice. This is because delays between the first signs of poisoning occurring and the start of treatment are often too great for the treatment to reverse the effects of poisoning. Effective drugs can be helpful in some poisonings such as those caused by cyanide, nitrate-nitrite, thiaminase, oxalates, cardiac glycosides and Lantana camara. Non-specific therapy for poisonings is much more commonly applied than ‘antidotes’. The broad principles applied are first stabilising vital body functions, then removing or stopping absorption of toxins from the gastrointestinal tract, promoting the swift excretion of toxins that have already been absorbed into the body and lastly providing general supportive measures for the patient. Heroic measures such as organ transplants may be needed to save some human victims of certain poisonings, such as from death cap mushrooms (Amanita phalloides)

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Australia’s Poisonous Plants, Fungi and Cyanobacteria

and Cortinarius mushrooms. The small list of poisonings for which effective specific therapy is available emphasises yet again that prevention is by far the better option.

increase in concentration after herbicides are applied to plants. Animals should be kept away from herbicide-treated plants until they have died and their leaves have fallen.

How can I control poisonous plants?

Grazing with less-susceptible herbivores

Note the warnings in the section on ‘Your legal responsibilities’ (in ‘Warnings’) when considering control measures for certain poisonous plants.

Goats or sheep can be used in some circumstances, but must be at stocking rates heavy enough to make sure that the amounts eaten by individuals are less than a toxic dose of the plants. For further information on the use of goats, refer to The Palatability and Potential Toxicity of Australian Weeds to Goats (Simmonds et al. 2000).

Methods for weedy species

Biological control agents

Effective methods will vary with weed species, location, habitat, population density and other factors. No single method should be applied in isolation. Modern integrated weed management practice demands that, for effective long-term weed control, a combination of methods should be applied in a manner appropriate to the particular circumstances and must be combined with pasture development. For example, see Pasture Management for Weed Control. A Grazier’s Guide to Controlling Annual Weeds in Southern Australian Improved Pastures (Burton and Dowling 2004). Entry to internet resources on this issue may be made through Weeds Australia (http://www.weeds.org.au/index. html). Individual methods include: physical removal, fire, herbicides, grazing with less-susceptible herbivores and biological control.

Biological control using insects and microbial pathogens is applicable only to exotic, naturalised plant species, and then only to carefully selected weed species. Complex screening procedures are needed to make sure that introduced agents (usually fungi and insects) attack only the intended target. Unforseen damage to non-target plants are an increasing concern. This is a very expensive and complex method and, even when very successful, reduces the density of the target weeds, but does not eliminate them.

Physical removal Hand pulling or cutting, ploughing, and other such methods are as old as agriculture itself. But, to be effective, the weeds must be safely and thoroughly destroyed to prevent their further spread through seeds. Do not allow livestock access to plants removed in this way because they can remain poisonous for some time and may be more palatable when they dry off, increasing the risk of poisoning.

Fire Fire has been used successfully to control some poisonous weeds such as Bryophyllum species and Lantana species. Fuel loads need to be adequate for this to be effective. Local and state government regulations apply to ‘burning off’.

Herbicides See ‘Where to get advice on herbicides and other weed control methods’ later in this chapter. Some poisonous plants become more attractive to animals, and so more dangerous, after being treated with a herbicide. Some toxicants, such as nitrate, may actually

Where to get advice on herbicides and other weed control methods Recommendations for herbicide use are not given in this book. This is because they change regularly as new research results become available and any specific information would become out-dated within a relatively short time. Up-to-date information on herbicides and other methods is available from state government departments with responsibility for weed control.

Should we grow poisonous plants in our gardens, homes and public spaces? Why do we grow plants in our private gardens, as house plants or in our public parks and streets? Some of the more important reasons include the pleasure we get from the appearance or fragrance of plants, their use as food and their capacity to improve the physical conditions in our homes and public spaces by shading, boosting humidity, moderating wind and providing privacy. Unless the poisonous plants that we may grow are likely to be eaten in dangerous amounts by susceptible individuals (usually young children or domestic animals) in particular circumstances, no hazard exists and we can enjoy their benefits in the same way as for any other garden plant. As a general rule, it is wise to

1 – Understanding plants and plant poisoning

check the poisonous properties of all your garden plants so that you understand the degree of risk that they may pose. Prevention is certainly far more certain than cure for plant poisonings.

Labelling potentially harmful plants on sale In recent socially responsible action by the Nursery and Garden Industry Association of Australia, comprehensive guidelines for the voluntary labelling of potentially harmful plants offered for sale by nurseries and other ‘green life’ sellers have been published for the first time – the National Plant Labelling Guidelines available through the NGIA website at http://www.ngia.com.au/. The Guidelines will be reviewed and up-dated periodically. New labels will give consumers information on the known potentially harmful properties of plants so that they can make informed choices about what to grow in their gardens and homes.

How often are children poisoned by garden and house plants? Rarely. Only about 2% of calls to the Queensland Poisons Information Centre (http://www.health.qld. gov.au/PoisonsInformationCentre/) are about exposure of humans to plants, with most of these about children under 4 years old. Only about 180 hospital admissions in Queensland in the 2005–06 financial year were suspected plant poisonings. A 1998–99 survey of poisonings in children presented to hospital emergency departments in South Brisbane, Mackay and Mt. Isa, Queensland, revealed that there was an average of 56 suspected plant poisonings in children aged 0–4 years presented for each 100 000 people in these regions overall. To place this statistic in context, there was an average of 366 suspected poisonings by medications – 88 by paracetamol, 44 by essential oils (‘natural’ does not mean harmless!), 31 by sedatives, 175 by household chemicals and 90 by rodenticides

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and pesticides in children in this age group for each 100 000 people in these regions. The average number of suspected plant poisonings in children aged 5–9 years was 7 and in those aged 10–14 was 1 for each 100 000 people in these regions, respectively. The authors of the report stated that the overall rates of suspected poisoning presentations in children did not seem to have changed in the last 50 years, but the outcomes had improved significantly.

How often are pets poisoned by garden and house plants? Rarely. A recent survey of plant poisonings of pets in Queensland revealed that plant poisonings diagnosed in dogs were only 0.06% of all the cases seen during the 5 years 2002–06 by the 25 veterinary practices providing information; that is, 289 plant poisonings in 500 573 cases. For pet birds, the equivalent figure was 0.03% (seven in 23 807) and for cats 0.01% (19 in 174 651). The potentially fatal poisonings reported for dogs from garden plants in this survey were by Brunfelsia fruits (36 cases), cycad seeds (28 cases), Duranta erecta plants (12 cases) and cardiac-glycoside-containing plants (Nerium, Cascabela) (eight cases). The potentially fatal garden plant poisonings of cats were by lilies (Lilium species) (13 cases). Pets were much more likely to be poisoned by being deliberately or accidentally fed poisonous plants as human food or drugs – Macadamia kernels (83 cases in dogs), marijuana (Cannabis sativa) (62 cases in dogs, one cat), onions (34 cases in dogs) and avocado (Persea americana) (six cases in pet birds). The three grape, raisin or sultana (Vitis vinifera) poisoning cases reported in dogs may have been an underestimate of the real situation because this poisoning has been recognised only recently.

Your legal responsibilities We have certain legal responsibilities for our use (or abuse) of plants. Please see the section ‘Your legal responsibilities’ under ‘Warnings’.

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2  How to confirm tentative identifications

All identifications made using this book should be regarded as tentative until confirmed by persons with expertise in naming plants, fungi or cyanobacteria. These are usually professional botanists and mycologists employed in state herbariums or in other learned institutions such as universities.

Australian state herbariums (plant identification services) State herbariums in Australia offer plant identification services to the general public. These services were free to the public at the time of writing for small numbers of plant specimens, particularly for suspected poisonous plants in emergencies. Ask your nearest state herbarium about its own policy on charging for such services. Most will limit the number of specimens that they will identify for free for any one client at any one time. Their contact details at the time of writing are listed below. Updates to contact details may be found at the Resources of Australian Herbaria website (http:// www.anbg.gov.au/chah/resources/index.html). Australian Capital Territory: Plant Enquiry Service, Centre for Plant Biodiversity Research, Australian National Botanic Gardens, Clunies Ross Street, Black Mountain, (GPO Box 1777) Canberra, ACT 2601. Phone (02) 6250 9450. Fax (02) 6250 9599. E-mail: [email protected]. New South Wales: Botanical Enquiry Section, National Herbarium of New South Wales, Royal Botanic Gardens, Mrs Macquaries Road, Sydney, NSW 2000. Phone (02) 9231 8111. Fax (02) 9251 4403. E-mail: [email protected]. Northern Territory: Northern Territory Herbarium, Department of Natural Resources, Environment, The Arts and Sport, The Boulevard, Palmerston, Darwin NT 0831 (PO Box 496). Phone (08) 8999 4516. Fax (08) 8999 4527. E-mail: [email protected]. Queensland: Identification and Advisory Service, Queensland Herbarium (Department of Environment and Resource Management), Brisbane Botanic Gardens

Mt. Coot-tha, Mt. Coot-tha Rd, Toowong Qld 4066. Phone (07) 3896 9318 Fax (07) 3896 9624. E-mail: [email protected]. South Australia: State Herbarium of South Australia, Adelaide Botanic Garden, Hackney Road, Adelaide, SA 5000 (PO Box 2732, Kent Town, SA 5071). Phone (08) 8228 2311. Fax (08) 8223 1809. E-mail: [email protected]. Tasmania: The Curator, Tasmanian Herbarium, College Road, University of Tasmania, Sandy Bay, Hobart, (GPO Box 252c, Hobart, TAS 7001). Phone (03) 6226 2635. Fax (03) 6226 7865. E-mail: [email protected]. Victoria: National Herbarium of Victoria, Royal Botanic Gardens, Birdwood Avenue, South Yarra, Vic 3141 (Private Bag 2000, Birdwood Avenue, South Yarra). Phone (03) 9252 2300. Fax (03) 9252 2350. E-mail: no general address available. Plant Identification Service public access on weekdays 10 a.m. to 1 p.m. Western Australia: Western Australian Herbarium (Department of Environment and Conservation), cnr George Street and Hayman Road, Kensington, Perth (Locked Bag 104, Bentley Delivery Centre, WA 6983). Phone (08) 9334 0500. Fax (08) 9334 0515. E-mail: [email protected].

Collecting and handling specimens for identification Preamble Diagnostic investigations: If plant, fungal or cyanobacterial specimens are collected as part of an investigation of animal disease that involves sending specimens from animals to a veterinary diagnostic laboratory, include the plant, fungal or cyanobacterial specimens with these. The diagnostic laboratory will send them on to other centres of expertise for identification as needed, and the data will then be effectively integrated into the whole investigation.

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Australia’s Poisonous Plants, Fungi and Cyanobacteria

Legal requirements: Collection of plant specimens from private property requires the permission of the owner. Collection of plants from public land (road or rail reserves, state forests, national parks or other nature reserves) requires the prior written permission of the responsible authority. Collection of threatened plants from both private and public land requires the prior written permission of the responsible authority. In general, declared plants (weeds) are not to be transported unless for identification at a state herbarium; legislation on this varies between states.

Conventional technique for plants – pressed and dried fertile specimens What to collect Botanists require fertile specimens if they are to make a definitive identification of a plant. Fertile specimens are those carrying flowers, fruit or both for flowering plants and the reproductive structures for non-flowering plants such as ferns and cycads. However, in poisoning emergencies, any specimen is better than none. For flowering plants in general, a specimen should comprise a small branch or part of the stem about 20–30 cm long with leaves plus flowers, fruits or both, all still attached. It is difficult, and sometimes impossible, to identify plants from leaves alone. Cut the specimen from the plant neatly by using secateurs, rather than by breaking or tearing the specimen from the plant. Specimens from certain types of plants need to have particular material in them and information with them to allow accurate identification: •• From species of Eucalyptus and Corymbia (‘gum trees’), collect specimens bearing flower buds, seed capsules, adult leaves (and juvenile leaves if available). Information about the bark type at the base of the tree and its extent and the bark type on the upper branches is important. •• From species of Solanum (nightshades), collect specimens bearing fruits as well as flowers. •• From species of Xanthorrhoea (grass-trees), collect a whole leaf showing the shape of the leaf base and a portion of the flower spike including the base and attachment onto the stem (scape), measure the lengths of both the flowering spike and non-flowering scape (the ratio of scape to flowering spike length is an important identification character), measure the height of the trunk if present, describe the leaf colour (e.g. bluegreen, greyish, green). •• For small plants, grasses and sedges, collect the whole plant, including underground roots, runners, stems, bulbs or tubers. For grasses and sedges, the base of the plant and the flower- or

seed-head are essential for identification. Make sure that grass or sedge flowers (florets), seeds or nuts (in sedges) are still present and haven’t fallen from the plant. •• For ferns (other than tree ferns), collect the fertile (spore-bearing) fronds with a sample of the rhizome (underground stem or root-like structure) attached together. The scales or hairs at the base of tree-fern frond stalks are essential for identification. These can be collected by slicing off a sliver of the outer stem (with scales attached) with a knife. •• For plants with large leaves (e.g. palms or cycads) or flower-heads, collect the uppermost (apical) and lowermost (basal) portions of the leaves or heads, measure the overall dimensions and report this with the specimens. A photograph of cycad plants is helpful. Enough material should be collected to make at least two sets of specimens with the duplicates numbered identically and numbers attached to the specimens. Send one set to the veterinary laboratory or the herbarium (depending on the type of investigation being done) and keep one for your future reference so that you can match the name provided by the herbarium to the appropriate plant. Thoroughly dry the specimens that you keep and take precautions to prevent insect damage to them. Eventually, specimens unprotected from insect attack will be destroyed by such insects as booklice and tobacco beetles.

Recording specimen details The following information should be recorded at the time of collection and sent with the specimens: •• Collector’s name and address •• Date of collection •• Collection locality. The latitude and longitude determined by a global positioning system (GPS) receiver are the ultimate locality record, but acceptable alternatives are the distance and direction from the nearest township or road junction, such as ‘15 km west of Roma on the Warrego Highway’. The data should be detailed enough to allow another person to return to the same locality to find the plant. •• Features of the plant that are not visible from the specimen or that cannot be deduced reasonably from it. Photographs may be useful for some of these purposes, but are not always an adequate substitute for careful written descriptions. These details include the: –– type and growth habit of the plant (e.g. upright, drooping, spreading, multi-stemmed) –– height –– flower colour –– bark type

2 – How to confirm tentative identifications

–– situation (e.g. in pasture, on a stream bank or in open forest) –– surrounding vegetation –– soil type. State herbariums normally have forms to be completed and sent with specimens, available from the herbarium or their website, with space to record such information.

Fresh specimens Fresh specimens may be presented to a herbarium in person on the day of collection. If this time constraint cannot be met, they should be pressed and dried. Fresh specimens should not be mailed because they deteriorate and become mouldy during transport, making them unsuitable for identification. One exception is cacti, which may be mailed fresh if packed carefully in a box with a warning label fixed to the outside if they are spiny. Other succulent plants should be frozen before pressing and drying (see ‘Succulent plants’ later in this chapter).

Drying All specimens must be dried to preserve the plant tissues, help keep their colour and prevent them becoming mouldy. Mouldy specimens are unsuitable for identification. Drying can be done by placing the plant specimen between several sheets of newspaper and replacing the sheets daily for about a week until drying is completed. The specimens must be kept flat during drying so that they will not shrink and become distorted. A flat piece of plywood, chipboard or Masonite® can be placed over the paper and weighed down with a heavy object such as a large book or a brick. Plant presses Serious plant collectors use portable plant presses consisting of two light-weight rectangular wooden lattice frames between which are placed a number of sheets of corrugated cardboard cut to fit the frame, the whole being held together by quick-release straps, such as Velcro®. Plants to be pressed and dried are placed between paper sheets (as above) and these are placed between the cardboard spacers. Air flowing through the corrugated sections of the cardboard speeds drying. Securely attaching the plant press to the exterior of a motor vehicle (e.g. in a cargo rack) in full sunlight will rapidly dry plants during the progress of the vehicle. Use a ‘belt and braces’ approach to securing the press – several independent straps or ropes are recommended. Naturally, the press should not be placed outside the vehicle if there is a risk of rain, nor should the press be left on the vehicle overnight because condensation (dew) will wet the specimens. Important:

21

Declared plants (weeds) should not be dried on the exterior of a vehicle because of the risk of spreading seeds while driving. When collections are being made frequently and over a period of time (such as when doing a botanical survey of a paddock where animals have died from suspected plant poisoning), it may be more convenient to use a ‘day’ press consisting of two boards containing between them a number of corrugated cardboard spacers and the pressing paper ready for use, the whole held together by Velcro® strips to facilitate rapid opening and closing and with handles for easy carrying attached to the boards. Plants collected into this day press can then be transferred into the main plant press at the end of the day. Artificial heat sources to speed drying The speed of drying can be improved if the pressed plants are placed in a position that allows good air flow around and between them. Further improvement can be made by placing a hot air source, such as a fanheater or air-conditioner outflow, to blow heated air over the pressed plants. Using corrugated cardboard sheets between the plant specimens (as used in professional plant presses, above) will greatly improve this airflow, carrying away moisture very effectively. Placing pressed plants into a domestic oven to speed drying is not recommended because of the real risk of accidentally scorching or burning the specimens and the lack of airflow to carry away moisture. Microwave ovens are unsuitable for plant drying. Insect damage during drying Small insects, such as caterpillars, unnoticed on the specimen when it is put into the press may damage the specimen during drying if not removed. Inspect the pressed plants carefully within a few hours (at the end of the day), looking for the adult or larval insects themselves or evidence of their presence (frass or insect droppings). Remove or kill them immediately to prevent further damage. Loss or change of colour during drying Plants, particularly flowers, often change colour during drying. This is natural and cannot be prevented. Record the original colour of leaves, flowers and fruit and send this information to the herbarium with the specimens. Photographs of the plant taken before collection may be a useful record. Delicate plant parts Delicate plant parts, such as petals, may stick to the paper used for drying and accidentally become detached or torn when the drying paper is changed. To prevent this, it is acceptable to place such parts between sheets of facial tissue or waxed paper and

22

Australia’s Poisonous Plants, Fungi and Cyanobacteria

leave this material in place when transferring the specimen to fresh paper during drying. Detachment of plant parts while drying The plant parts of some species may fall off the main specimen while drying. This may happen if the time to achieve dryness is prolonged. Keep these parts in a paper envelope and send them with the main specimen, also clearly marked with the specimen’s number. Fleshy or bulky plant parts Fleshy specimens such as large fruits do not dry easily and are distorted if pressed flat. These should be preserved in alcohol such as methylated spirits or photographed in colour. Succulent plants Succulent plants are difficult to dry successfully and some, such as Bryophyllum species, will continue leaf and plantlet growth while in a plant press. Stopping this requires killing the tissues by freezing the specimen for 1–2 days. Succulent specimens that dry very slowly tend to disintegrate with leaves detaching from stems, resulting in an unsatisfactory result. Good results can be achieved if succulent specimens are frozen as soon as possible after collection. When removed from the freezer, these specimens should be pressed in the usual manner. Large volumes of water are released from these plant tissues as soon as they thaw, so specimens need to be inspected frequently and the paper changed more frequently than usual to remove this water and achieve successful and rapid drying before mould growth occurs. Consider applying an artificial heat source (see ‘Artificial heat sources to speed drying’ earlier in this chapter) to speed drying of succulent specimens. Cacti are an exception that should be sent fresh and whole (see ‘Fresh specimens’ earlier in this chapter).

Labelling Number the sets of specimens clearly, with the duplicate specimens from each plant carrying the same number. Small blank price tags (jewellers’ tags) attached to a thread that is tied to the specimen are useful for this task. Alternatively, tape the numbered tag to the base of the stem of the specimen. The number will be quoted in the report on the specimens from the herbarium.

Packing Do not send fresh plants to herbariums in plastic bags. They allow condensation and promote mould and bacterial growth on specimens, turning them rotten and unidentifiable. Dry the specimens, or (if urgent) pack the specimens well with newspaper before sending them (but this is not recommended for very moist specimens).

Pack dried specimens flat in newspaper between sheets of cardboard to prevent crushing and breakage during transport. Do not use adhesive (‘sticky’) tape to secure the specimens to the paper because you may cover and obscure some essential feature needed for identification. Weeds should always be packed carefully to stop the escape of seeds during transport. Do not send liquids in the mail. Include a completed herbarium specimen submission form or a cover note with your name and address, the information requested from the herbarium and the extra details recorded about the plants as described above.

Preventing insect damage in stored specimens Duplicate specimens kept for reference need to be protected from insect attack. There are various ways of doing this. One of the simplest is periodical freezing of the specimens to kill insects and their eggs. Place the dried pressed specimens in their paper sheets into a plastic bag, seal it and place the bag and contents into a freezer, leaving it there for several days or until required. After freezing, the bag and contents should be allowed to return to room temperature before opening to prevent condensation of water onto the specimens. Camphor and naphthalene as insecticides are no longer recommended as preservatives because of health and safety concerns. They are thought to be carcinogenic and a fire hazard.

Rapid technique for plants – digital photographs or scans Important: This method is not a substitute for a definitive identification based on a conventional pressed dried specimen submitted as above. If you use this method, follow through by then pressing and drying the specimen as above and submitting it for confirmation of the rapid identification.

Applications When a rapid identification is required in an emergency, an image of the plant in question can be generated and sent electronically to a herbarium for a rapid tentative identification. This approach uses either a digital camera or a flat-bed scanner and a computer with an e-mail connection. Mobile phone cameras that produce good resolution images would also be suitable. Using a photocopier and a facsimile machine is a much less satisfactory alternative. Important: The herbarium needs to be willing to provide an identification from this material and must be alerted that you are about to send them images. Check with your local herbarium before using this method.

2 – How to confirm tentative identifications

23

Specimen and information collection

Recording specimen details

Follow the protocol set out above.

See the protocol for plants above. A checklist of details useful to the mycologist for identification of ‘mushroom’-type fungi follows. It can be adapted for use with other types of fungi. •• Date of collection •• Location •• Habitat (under eucalypts, in pasture, in garden, etc.) •• Surrounding vegetation (common plants nearby) •• Substrate (wood, soil, leaf litter, etc.) •• Occurrence (single, in clusters or groups?) •• Shape of cap (conical, convex, etc.) •• Colour of cap •• Scales present on cap? •• Cap slimy? •• Does fungus change colour if cut? If so, what is the new colour? •• Colour of gills? •• Stem ring present? •• Cup present on the stem base? •• Stem slimy? •• Colour of stem •• Describe odour •• Any changes in colour following handling? •• Any other observations •• Sketch of fruiting body (including cross-section if possible). Photographs of the fungus are essential. Use the checklist above to prompt you to include the important structures in your images.

Method Photograph, scan or (as a last resort) photocopy the plant specimen carefully, ensuring that any reproductive structures are not obscured by leaves. Include a scale in the image. This can be a small ruler or a coin. Take close-up images of key plant structures such as flowers and fruit, as well as wider images. Save digital images from the camera or scanner as JPEG files, then transmit the image to the herbarium with the details collected on it, requesting identification (if possible). When using a flat-bed scanner, a blue background (a sheet of blue paper or card placed over the specimen after it has been positioned on the scanner glass) may give best results.

Fungi (macrofungi – ‘mushrooms’ and ‘toadstools’) Important: Not all herbariums provide an identification service for fungi. It is wise to contact your local herbarium for advice before submitting specimens or photographs of fungi so that a trained mycologist can be contacted. It is not always possible to identify wild fungi with precision.

What to collect Collect the whole fruiting body intact (do not cut the stalks) and place it in a paper bag or twist of paper to protect it. If specimens of differing ages of the same species are available, collect a range of them. Collection may involve digging the structure from the soil or cutting out a section of the wood or other substrate supporting it. If more than one species is collected at the same time, it is vital to keep them separately wrapped to prevent cross-contamination of spores. If the only specimen available has been partly eaten by the patient, collect that – it may retain sufficient structure for identification. Because dried specimens of fungi do not retain the shape or colour of the material at the time of collection, coloured photographs or sketches of the specimen can be a useful aid to identification. Ideally, these should show young, mature and old specimens, some in longitudinal section, and should contain a scale graduated in millimetres or a standard object (e.g. small coin) to indicate the size of the fungus. Some species of fungi disintegrate rapidly and do not dry well. For identification of these, photographs or sketches with notes on the colour or colours of the various parts of the specimen are essential. Important: Always wash your hands thoroughly after handling fungi.

Handling, spore-printing and drying Clean off excess soil and debris, being careful not to remove any delicate structures such as veils or any attached mycelium at the base. Avoid freezing, bruising, breaking or squashing specimens. Collect the specimens into paper bags. Do not use plastic bags or containers. Keep specimens cool, but do not refrigerate them if a spore print is to be made. If the specimen can be transported to a herbarium swiftly, do this. If there will, or could be, a delay in submitting the specimen to a herbarium, make a spore print (if applicable to the type of fungus collected) and dry the specimen before transporting it. Spore printing Make a spore print of all mushroom, bracket, coral and club fungi to determine the colour of spores and to provide a sample for microscopic examination. Place a mature cap, spore-bearing structures (gills, pores) down, onto white paper. Cover the preparation to prevent the cap from drying out and air movement from wrecking the direct fall of spores. Spore printing may take from 1 hour to overnight. Record the colour

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Australia’s Poisonous Plants, Fungi and Cyanobacteria

of the spore print as soon as possible as it may change on drying and after storage. Dry the paper carrying the spore print, then fold it in half with the spore deposit facing inwards. Store in an envelope (or zip-lock plastic bag, but only if thoroughly dry). Drying Before drying, cut one or two fruiting bodies of mushroom-like fungi in half longitudinally; cut all trufflelike fungi in half. Air-drying is preferable to freezedrying. Do not use liquid preservatives such as methylated spirits. Placing a specimen in good air circulation in the sun for about 2 days in warm, low-humidity weather or in the airflow from an electric hair dryer are two methods suggested by some mycologists. Heating overnight at 45–50°C in a drying cabinet or a food dryer is ideal. Drying can also be achieved by placing specimens on a wire mesh over a radiator or fan heater. Important: Always wash your hands thoroughly after handling fungi.

Labelling See the protocol for plants above. Label the specimen, photographs and spore print of each fungus with the same number.

Packing Dried fungi should be placed in crush-resistant containers to protect them from vibration and impact so that they will retain their shape while being transported to the herbarium. Include the spore print. Do not use plastic bags because they trap moisture and lead to the rapid decomposition of the specimens. Include a completed herbarium specimen submission form or a cover note with your name and address, the information requested from the herbarium and the extra details recorded about the fungus as described above. Fresh specimens should be delivered to the herbarium on the day of collection.

Cyanobacteria (blue-green algae, cyanophytes) Important: Avoid skin contact with bloom material. Always wear rubber gloves and adopt normal hygiene precautions such as washing off any splashes and washing the hands immediately after the procedure. Samples of cyanobacteria from suspected poisoning incidents should be submitted to laboratories equipped for toxicity testing. These are usually the regional laboratories maintained by, or on behalf of, state departments of agriculture/primary industries or health or laboratories within universities. Some herbariums

provide an identification service for these organisms, but none do toxicity testing. For identification and toxicity testing, collect two samples of the surface scum of the organisms, one for each purpose. For toxicity testing, fill a 1 L container with a representative sample of the most concentrated part of the bloom, leaving at least a 25 mm air gap on the top of the container. Submit the sample on ice (not frozen) in an insulated container to arrive at the testing laboratory within 24 hours of sampling. For identification of the organisms, preserve a separate 20 mL representative bloom sample by adding 1 mL of 10% formalin and submit that with the chilled sample. Important: Using alcohol (ethanol or methylated spirits) to preserve cyanobacterial bloom material may cause distortion of the cells making their identification difficult and is not recommended.

Safe transport of specimens Properly packaged specimens (see above) may be delivered to herbariums in person, or be sent by post or by courier services. You must consult Australia Post or the individual transport company for advice on regulations governing the transport of the specimens. As a rule, dried plants and dried fungi do not need special consideration. However, International Air Transport Authority (IATA) Dangerous Goods Regulations may apply in certain circumstances. In particular, these apply to specimens in preservative or to cyanobacterial specimens that may pose a health risk to persons handling them if breakage or spillage occurs during transport. You are responsible for the safe packaging of such material to prevent any adverse consequences from accidental damage to the package. Failure to comply may lead to litigation – you may find yourself charged with a criminal offense.

What happens to specimens? Do not expect herbariums to return specimens to you. They do not have the time or the funds for this. Most specimens sent to herbariums are discarded and destroyed a short time after they have been examined and a report provided to the sender. Only those specimens of special interest to the herbarium staff may be kept in the permanent herbarium collection. If you are undertaking research with the plants that may lead to scientific publication, it is essential that you request clearly that the specimen be retained in the herbarium as a voucher and the acquisition number be reported to you for citation in any published papers. See the section on ‘Herbariums and voucher specimens’ (Chapter 1).

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3  Common poisoning profiles

This chapter describes types of poisoning caused by more than one plant, fungus or cyanobacterium to avoid unnecessary duplication later in the text on individual species. These profiles are arranged alphabetically by the name of the toxin responsible. However, where the toxin is not identified (such as in oesophageal ulceration of horses), or where more than one toxin type is involved in a poisoning syndrome (such as in photosensitisation), the syndrome name is used instead. This accounts for the somewhat eccentric arrangement of the profiles at first glance. In the list below, syndromes for which the responsible toxin is unidentified are followed by the symbol ´; those for which there are several responsible toxins are followed by the symbol þ. Some syndromes fall into both of these categories. One of the main aims of toxicological research is to learn the identity of the toxin responsible for every poisoning syndrome. Knowing the toxin allows rational efforts to manage the poisoning to be directed against the toxin on a molecular level, hopefully giving a better chance of success. The profiles included are: •• acute liver necrosis þ ´ •• cardiac glycoside poisoning •• corynetoxin poisoning •• cucurbit triterpene poisoning •• cyanide poisoning •• dihydroxycoumarin poisoning •• ergot alkaloid poisoning •• fern norsesquiterpene glycoside poisonings •• fluoroacetate poisoning •• galegine poisoning •• glucosinolate poisoning •• grayanotoxins poisoning •• iforrestine poisoning •• irritant diterpenoid poisoning

•• lily poisoning of cats ´ •• lupin (quinolizidine alkaloid) poisoning •• macrofungal poisoning gastrointestinal syndrome ´ •• methylazoxymethanol (MAM) poisoning •• nicotine and other pyridine alkaloid poisoning •• nitrate-nitrite poisoning •• oesophageal ulceration of horses (Chillagoe horse disease) ´ •• oxalate poisoning: soluble forms •• oxalate: big head of horses from calcium oxalate crystals in grasses •• oxalate raphide crystals •• phomopsin poisoning or lupinosis •• photosensitisation þ ´ •• pregnane glycoside poisoning •• protoanemonin poisoning •• phyto-oestrogen poisoning (‘clover disease’) •• psilocybin poisoning •• pyrrolizidine alkaloidosis •• selenium poisoning •• Senna poisoning (muscle damage) ´ •• simplexin poisoning •• steroidal glycoalkaloid poisoning •• stypandrol poisoning •• sulphur poisoning •• sulphur-containing organic compound (SMCO and others) poisonings •• swainsonine and calystegine poisonings •• tannin poisoning •• thiaminase poisoning •• toxalbumin poisoning •• tremorgen poisonings •• tropane alkaloid poisoning •• urushiol poisoning •• wamps ´ •• zamia staggers ´

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Australia’s Poisonous Plants, Fungi and Cyanobacteria

Acute liver necrosis NN

  Effective therapy is doubtful, but general decontamination and supportive measures should be attempted as advised by a Poisons Information Centre, a medical practitioner or a veterinarian.

~  Acute effects M  Delayed onset or chronic effects in some cases, such as *Amanita phalloides poisoning of humans

´

  Toxins that cause this syndrome are unidentified in some cases

þ

  Toxins that cause this syndrome include: methylazoxymethanol (MAM), cyanobacterial and macrofungal peptide toxins, furanosesquiterpenes, diterpenoid (kaurene) glycosides, trematoxin. Cyanobacterial, fungal and plant sources of acute liver damaging toxins included in this book: Cyanobacteria: Microcystis aeruginosa, Nodularia spumigena and species of Anabaena. Fungi: *Amanita phalloides (death cap). Cycads: species of Bowenia (Byfield ‘fern’, zamia ‘fern’), Cycas (zamia), Lepidozamia (zamia) and Macrozamia (zamia). Forbs: Argentipallium blandowskianum (woolly everlasting), *Salvia reflexa (mintweed), Wedelia asperrima (sunflower daisy) and *Xanthium strumarium (Noogoora burr). Shrubs: *Cestrum parqui (green cestrum), Eremophila deserti (Ellangowan poison bush, turkey bush) and Myoporum montanum (boobialla). Trees: Trema tomentosa (poison peach). A number of quite different toxins in plants, fungi and cyanobacteria can all produce this effect. Usually ruminants are affected, but humans, horses, pigs, camels, deer and dogs are susceptible and have been poisoned from time to time. The liver is the first organ through which blood flows after it collects the products of digestion from the stomach and intestines. This means that it is the first line of defence for the body against harmful chemicals absorbed from food. The liver is well equipped chemically to change toxic substances coming from the gut to harmless ones and to discard them from the body in bile or into the blood for elimination through the kidneys. But some are too toxic for the liver’s normal chemical defences to be effective. Others, ironically, are changed from relatively harmless compounds into

highly toxic ones by the very liver processes that usually safeguard the body from chemical attack. Many of the plants containing liver-destroying toxins are not very palatable for animals and are only eaten in dangerous amounts if animals are very hungry or if little or no alternative feed exists and the hazardous plants are available in large amounts. Toxic doses of these plants are given in the accounts of the individual plants. Poisoned animals stop eating and become lethargic and dull within a few hours of a toxic dose of these plants. The rumen in cattle, sheep and goats will stop contracting. Simple-stomached animals such as humans, pigs and dogs usually vomit. Horses and ruminants do not. Signs of abdominal pain are seen such as standing with limbs widely spaced (a ‘saw-horse’ stance), occasional kicking at the belly, groaning and grinding of teeth. Jaundice may be detected in the mucous membranes of the mouth or the whites of the eyes. If the dose was fatal, the sick animal will go down and will commonly die within 24 hours. The damage to the liver will have effects on brain function. This can show up in several ways. Muscles may twitch and tremor. The affected animal may appear blind and not respond to noise, touch or movement. It may suddenly become highly excited, spring to its feet and act in a deranged or very aggressive manner. Convulsions may set in before a final coma precedes death. The carcase after death is often jaundiced, but may not be so if death has been particularly rapid. The liver is swollen with rounded edges, often engorged with blood, and may have a distinct mottled pattern of pale and dark areas visible on its surface, particularly after being cut open. In those species with a gall bladder (horses and deer lack one), its wall and the tissues attaching the gall bladder to the liver may be swollen with fluid (oedematous). There may be haemorrhages in the intestines. Microscopically, large numbers of liver cells are dead (necrotic). Usually there are only a few surviving liver cells present. The pattern of damage to liver cells seen microscopically in preserved tissue sections can vary widely between cases. This pattern can be useful for suggesting possible causes of the poisoning. Most commonly, one zone of liver cells is killed and the rest remain alive, even if many are damaged to some degree. The most common patterns of damage are periacinar (or centrilobular) necrosis, then periportal necrosis. Rarely, all liver cells are killed (panacinar necrosis). Midzonal necrosis is even rarer. No specific treatment is available, but general decontamination measures should be attempted. Most affected animals will die, but the dose that they have received varies from case to case and aggressive treatment will be rewarding occasionally. Recognising the

3 – Common poisoning profiles

plants, fungi and cyanobacteria capable of causing these effects and preventing access to them provides the only practical defence against poisoning by them.

Cardiac glycoside poisoning ∅  Effective therapy: activated charcoal, antiarrhythmic drugs, rehydration; antibodies against cardenolides (expensive – human and companion animal therapy). Early intervention is essential for a positive outcome. Therapeutic measures are expensive in materials and time and thus usually economically feasible only in humans and valuable domestic animals.

~  Acute effects M  Delayed onset or chronic effects Plant sources of cardiac glycosides included in this book: Grass-like herbs: Diplarrena moraea (butterfly flag), *Moraea flaccida (one-leaf cape tulip), *Moraea miniata (two-leaf cape tulip) and *Moraea setifolia (thread iris). Forbs: *Adonis microcarpa (pheasant’s eye), *Asclepias curassavica (red cotton), *Bryophyllum × houghtonii (hybrid mother-of-millions), *Bryophyllum delagoense (mother-of-millions), *Bryophyllum pinnatum (live leaf), *Bryophyllum proliferum, *Corchorus olitorius (jute), †Convallaria majalis (lily-of-the-valley), *Digitalis purpurea (foxglove), *Gomphocarpus (balloon cotton) and †Helleborus (hellebores). Vines: *Araujia sericifera (white moth plant) and *Cryptostegia grandiflora (rubber vine). Shrubs: *Calotropis procera (calotrope). Trees: †Acokanthera oblongifolia (bushman’s poison), *Cascabela thevetia (yellow oleander) and †Nerium oleander (oleander). There are many known plant sources of hazardous amounts of cardiac glycosides in addition to the list above (see Chapter 15). Cardiac glycosides occur in plants as either cardenolides or bufadienolides: two slightly different chemical forms. Toxins similar to bufadienolides also occur in the skin glands of toads such as the cane toad (Bufo marinus). All animal species are susceptible to acute poisoning. Most cases occur in cattle and horses. Pigs and dogs have been poisoned. Humans are occasionally poisoned. Birds tend to be quite resistant, but poisoning is known. Plants containing cardiac glycosides are usually not palatable and are not eaten readily in their normal state. They may be eaten when other feed is very scarce. Toxic doses of these plants are given in the

27

accounts of the individual plants. Because their toxicity is retained when they dry out, garden waste or hay containing these plants are dangerous to livestock consuming them. The seeds of some species may contaminate feed grains and cause poisoning by that means. Young children may eat the flowers of oleanders. Insect larvae (caterpillars) that eat the leaves of cardenolide-containing plants may take up the cardenolides as a defence mechanism against birds. Birds that eat such caterpillars, or the butterflies that develop from them, vomit. This causes them to avoid such caterpillars or butterflies in future. The heart is the main organ affected, with the lungs, the gastrointestinal tract and the kidneys also involved either directly or as a result of damage to the heart. The most obvious sign of poisoning in mammals is diarrhoea, usually with blood in the faeces. Vomiting occurs in simple-stomached animals such as pigs, dogs and humans. Pigs may refuse to eat contaminated food. The rate and rhythm of the heart is affected. It may be faster or slower than normal. There may be dropped beats. Badly affected animals have difficulty breathing and die rapidly. Affected animals may die suddenly if exercised, so mustering or handling of such animals must be done very carefully. The rumen will stop working in cattle, sheep or goats. Horses often have signs of pain in the abdomen (colic). Humans can have constant nausea, headache and neurological effects, including sleepiness, apathy and mental confusion, agitation, difficulty with concentration and visual disturbances such as yellow halos or flashing lights. Post-mortem examination and subsequent microscopic examination of tissues typically reveals small scattered groups of dead and dying muscle fibres in the hearts of animals that have survived poisoning for 12 or more hours. These changes have not had time to develop in those dying sooner, despite heart failure being the underlying cause of death. Either collapsed portions (atelectasis) or fluid build-up (oedema) may be seen in the lungs of animals dying rapidly. In some cases, recognisable plant parts may be seen in the stomach or rumen, such as oleander leaves or motherof-millions flowers. Haemorrhage into the intestines is commonly seen. Ulceration of the lining of the third stomach (omasum) may be seen in those ruminants that survive for several days before death. The earlier that treatment is started, the better the chance of a successful outcome. The chances of successful treatment decrease progressively with the onset of dropped heart beats (heart block), a racing heart (tachycardia) and breathing difficulties (dyspnoea). Treatment of poisoned domestic animals should be by a veterinarian, because restricted drugs are involved and clinical judgement is needed for the effective use of

28

Australia’s Poisonous Plants, Fungi and Cyanobacteria

various components of the treatment. Veterinary treatment is directed at preventing further absorption of toxins by drenching with activated charcoal, at rehydrating by including electrolyte-replacement solution with the activated charcoal drench, and at supporting the heart by injections of atropine and other antiarrhythmic drugs if judged necessary by the veterinarian. Horses are first given drugs to relieve the pain of colic. Human cases can be treated with antibody fragments that bind to the toxins and prevent their effects on the body, but these are usually too expensive for use in domestic animals. Humans may also be treated with activated charcoal by mouth or by dialysis. Weed control methods useful for Bryophyllum plants are fire or herbicides followed by pasture ­rehabilitation. Bryophyllum plants should be burned along with the leaf litter that they commonly favour as a growth medium. Herbicide sprays for Bryophyllum plants must contain a suitable wetting agent to prevent the fluid running off their waxy coating. Neat diesel fuel has been used successfully as a ­herbicide. Weed control authorities should be consulted for the most recent recommendations. There are prospects for biological control of Bryophyllum species in Australia through selected insects imported from Madagascar. Biological control agents have been imported to Australia or are under active study for a number of the weedy species in this category such as rubber vine and mother-of-millions.

Corynetoxin poisoning ∅  Effective therapy: cyclodextrins (?). Early intervention is essential for a positive outcome.

  Specific preventive measures available M  Delayed onset or chronic effects Plant sources of corynetoxins included in this book: Grasses: *Lolium rigidum (annual ryegrass) linked with ARGT, Lachnagrostis filiformis (blow-away grass) linked with floodplain staggers, and *Polypogon monspeliensis (annual beard grass) linked with Stewart’s Range syndrome. Chemically, corynetoxins are tunicaminyluracils: glycolipids that are a subclass of nucleoside antibiotics, which also includes tunicamycins and streptovirudins. Poisoning by corynetoxins has occurred in grazing livestock in distinct locations and on different pastures in southern Australia, leading to three names for the disease:

•• ‘annual ryegrass toxicosis (ARGT)’ seen in southwestern Western Australia and southern South Australia •• ‘floodplain staggers’ seen in north-western New South Wales, and •• ‘Stewart’s Range syndrome’ seen in south-eastern South Australia. Sheep are most commonly the victims of this poisoning, but cattle and, less commonly, horses, are affected. Corynetoxins are generated by bacteria (Rathayibacter toxicus) infected with viruses (bacteriophages). The bacteria grow in plant galls produced in the seeds of grasses by the invasion of nematode worms (Anguina agrostis and A. paludicola), which carry the bacteria attached to their skin. The multiplying bacteria may produce a yellow slime on the seed-heads of infected pasture grasses, but this is readily washed off by rain. The nematode-induced galls may distort the seed-head of the grass, but they can be hard to distinguish from uninfected seed-heads without careful inspection. The toxins accumulate in the body and toxic doses are 3–5 mg/kg. The toxins interfere with the structure of small blood vessels by inhibiting the production of glycoproteins that make up cell membranes. This interferes with delivery of oxygen to tissues. The brain is the most affected organ. Most poisoning occurs when livestock graze infected mature seed-heads on standing pasture. Most cases on pasture occur from November to January, with some as late as April. Signs of poisoning commonly occur first at 4–6 days after grazing starts, but may take up to 12 weeks. Forced exercise and high environmental temperatures trigger signs or worsen them. Cobalt-deficient sheep are more susceptible to this poisoning. Hay contaminated with galled annual ryegrass retains its toxicity, probably for the life of the hay (several years). Feed grains, such as wheat, barley or canola, contaminated with infected annual ryegrass seed galls and the residue from cleaning such contaminated grain may be toxic. Typical poisoning causes several bouts of convulsions, which finally end in death in many affected animals. Those affected first have an unsteady highstepping gait or a ‘rocking-horse’ gait where fore and hind limbs move together. There is twitching of muscles and nodding or swaying of the head. Affected animals collapse with rolling of the eyes (nystagmus), severe stiffening spasms of the limbs and neck (opisthotonus, tetanic spasms) and violent paddling motions of the limbs. Affected animals left undisturbed often regain their feet and apparently return to normal. Deaths may occur within a few hours or up to 8 days after onset of signs (including after removal

3 – Common poisoning profiles

29

from the infected paddock). Doses of the toxin too small to cause outright poisoning can depress wool growth and fibre diameter. There are no characteristic findings at post-mortem examination, but microscopic changes may be detected in preserved sections of the brain where fluid leaks around small blood vessels, and in the liver where the cells appear foamy (hepatocyte vacuolation). Managing an affected group of animals involves gently removing them from the toxic pasture or removing the toxic feedstuff. The CSIRO has developed a promising antidote (cyclodextrins) that can be injected into the abdominal cavity (intraperitoneal injection), but at the time of writing these were not commercially available for animal treatment. Controlling poisoning involves several measures, including regular checking of pasture for the presence of the toxic bacterium in nematode galls, grazing management and pasture management. The CSIRO has also developed an immunisation method against the toxins (a vaccine), which may become the ultimate method of prevention, but is yet to be registered as a commercial product. Effective grazing management involves grazing infected pastures before they ‘hay off’ (mature), regularly and frequently inspecting flocks on potentially toxic pasture (twice-daily or daily) for clinical signs, and avoiding suddenly increased stocking rates that may force animals to eat infected seed-heads that they had previously avoided. Effective management of infected pasture involves mowing, burning or using herbicides to remove seed-heads or destroy toxic pasture, encouraging legume growth in the pasture and preventing spread to uninfected pastures through uncleaned seed, hay, uncleaned vehicles and machinery. It generally takes 10–15 years from the introduction of infected nematodes to the onset of stock poisoning. The increasing herbicide resistance of annual ryegrass in cropping areas is making it harder to manage this problem.

Cucurbitacins (bitter principles of cucurbits) are tetracyclic triterpenes. Stemodiosides are glycosides of cucurbitane triterpene steroids. They prevent or reduce eating of their plants by most insects, excluding the cucumber beetle, which is attracted by them. They are somewhat similar in structure to cardiac glycosides and can produce some similar effects in poisoned animals. Melons, cucumbers and courgettes or zucchinis with a bitter taste are revealing the presence of cucurbitacins to our human tastebuds. Bitterness (reflecting cucurbitacin content) is boosted by strong light, dry air, sudden rise in day temperature, low night temperature and a high plane of nutrition for the plants. Ripe fruits appear to be the most poisonous part of the plants for domestic animals, with cattle and sheep the usual victims. Poisoning occurs only after a large amount of fruit is eaten. Toxic doses of these plants are given in the accounts of the individual plants. Cucurbitacins directly irritate the lining of the gastrointestinal tract and damage the integrity of blood vessel walls within it. They can affect the function of heart muscle. Affected animals may die suddenly after a large toxic dose or have severe diarrhoea and dehydration. Some develop jaundice. Postmortem examination reveals congestion of blood vessels and haemorrhage in the stomach and intestines. The walls of forestomachs (rumen, reticulum and omasum) can be thickened by fluid leaking from damaged blood vessels. The remains of fruit and many seeds can often be found in the rumen. Microscopic examination of preserved rumen wall can reveal inflammation, including microscopic blisters (microvesicles) from chemical irritation similar to that seen in grain overload (ruminal acidosis) and small patches of heart muscle fibres can be damaged (necrotic). Treatment of poisoned animals has not been reported, but surgically emptying the rumen or dosing with activated charcoal or bentonite and rehydrating with oral or intravenous fluids are options. The chances of successful treatment are likely to be small.

Cucurbit triterpene poisoning

Cyanide poisoning

NN

  Effective therapy is doubtful. Apply general decontamination and supportive measures advised by a veterinarian.

~  Acute effects Plant sources of cucurbit triterpenes included in this book: Vines: *Citrullus colocynthis (colocynth), *Citrullus lanatus (wild melon), Cucumis melo subsp. agrestis (Ulcardo melon) and *Cucumis myriocarpus (prickly paddy melon).

∅  Effective therapy: sodium thiosulphate (‘hypo’) for acute poisoning only. Early intervention is essential for a positive outcome.

~  Acute effects M  Delayed onset or chronic effects Plant sources of cyanide included in this book: Grasses: Brachyachne convergens (native couch), *Glyceria maxima (reed sweet-grass), *Sorghum × almum (Columbus grass), *Sorghum bicolor (grain,

30

Australia’s Poisonous Plants, Fungi and Cyanobacteria

fodder or forage sorghums), *Sorghum halepense (Johnson grass) and *Zea mays (maize). Forbs: Chamaesyce dallachyana (caustic weed), Chamaesyce drummondii (caustic weed), *Colocasia esculenta (taro), Dysphania carinata (green crumbweed), Dysphania cristata (crested crumbweed), Dysphania glomulifera (red crumbweed), Dysphania littoralis (red crumbweed), Dysphania rhadinostachya (mouse-tail crumbweed), Leptopus decaisnei (andrachne), Lotus australis (native bird’s-foot trefoil) and *Trifolium repens (white clover). Shrubs: Eremophila maculata (fuchsia bush), Goodia lotifolia (golden tip), †Manihot esculenta (cassava) and †Osteospermum ecklonis and hybrid cultivars (South African daisy). Trees: Alectryon oleifolius (boonaree), Eucalyptus cladocalyx (sugar gum), †Prunus armeniaca (apricot), †Prunus dulcis (almond), *Prunus laurocerasus (cherry laurel) and †Prunus persica (peach and nectarine). There are many known plant sources of potentially hazardous amounts of cyanide in addition to those listed above (see Chapter 15). In plants, cyanide (one carbon and one nitrogen atom combined into the radicle indicated by the symbol CN) is bonded to sugars and other chemicals into compounds called cyanogenic glycosides. When eaten, these can be broken down in a two-step process to release the highly toxic hydrogen cyanide (HCN) also known as prussic acid. The breakdown process involves enzymes present in the plant tissue, in the bacteria of the rumen or in both. The most important enzyme is b-glucosidase. Potentially dangerous plants have been estimated to yield more than 200 mg HCN/kg wet weight (equivalent to 0.02% or 7.5  mmol HCN/g) or more than 500  mg HCN/kg air-dry weight (0.05%). Note that the cyanide yield from plants is often expressed as a percentage (%); to convert % to mg/kg, multiply by 10 000; for example, 0.05%  =  500  mg/kg. Of course, actual poisoning depends on variables including the rate of intake and rate of release of HCN from the plant, so these data are guidelines, not absolute rules. The minimum lethal dose of potassium cyanide (KCN) by mouth is about 2.0  mg/kg body weight in most domestic mammal species. Fowls are about 10 times less sensitive. Depending on the yield of cyanide, actual doses of fresh plants that have killed ruminants can be very small: about 100–200 g in some cases. All animal species can be poisoned by plant cyanide, but poisoning is much more likely in ruminants and South American camelids or lamoids (alpacas and llamas) than in monogastrics (including humans). This is because the intense stomach acidity of monogastrics slows down or stops the activity of

b-glucosidase, the main enzyme that releases cyanide from the glycosides. Also, this enzyme is present in bacteria in the rumen and the first stomach compartment of alpacas and llamas, and the activity of these bacteria releases cyanide rapidly and in large amounts. Many plants that contain cyanogenic glycosides also contain the enzyme b-glucosidase to release cyanide from them. This is part of the plant’s defence against being eaten. The glycoside and the enzyme are stored separately in the plant’s cells. When plant tissues are damaged, say by a caterpillar or grasshopper chewing on a leaf, the two components are brought together and cyanide is released to try to stop more damage. Some plants that contain cyanogenic glycosides do not contain b-glucosidase. These can only cause poisoning if the cyanide is released by another source of b-glucosidase, such as the bacteria in the rumen of cattle or other such animals. There are several factors that influence the occurrence of cyanide poisoning from plants. The capacity of plants to produce cyanogenic glycosides is genetically based (inherited), so that different plants, such as different cultivars of sorghum plants, will differ in the amount of cyanide they generate under the same conditions. The largest concentrations of cyanogenic glycosides occur in young leaves, so actively growing plants are more hazardous. Agents or circumstances that place stress on plants will increase their cyanogenic glycoside production. These include drought causing water stress, insect damage such as from grasshoppers on sorghum crops, and light frosts causing minor tissue damage. Plant nutrition influences cyanogenic glycoside production. Increased nitrogen boosts it and increased sulphur depresses it. Animals are most at risk if they are hungry when they gain access to a hazardous plant and therefore eat more in a shorter time than usual. Animals that have had a small non-toxic intake of cyanide in the recent past will have a greater capacity to detoxify poisonous quantities and may escape serious poisoning when they eat otherwise dangerous plants. The bodies of animals that die of cyanide poisoning can fatally poison dogs fed on them because the cyanide persists in dangerous amounts for several hours in the muscles and other tissues of the carcase. Acute cyanide poisoning causing sudden death is the most common and important outcome of eating plants containing cyanogenic glycosides. Cyanide that is absorbed from the gastrointestinal tract is partly converted by the liver to the less toxic chemical thiocyanate for removal through the kidneys. Some cyanide is breathed out through the lungs. If the amount of cyanide entering the body is more than can be handled by these protective processes, it enters the general circulation and causes poisoning. Lethal

3 – Common poisoning profiles

cyanide concentrations in blood can occur within 5  minutes of a poisonous dose of plant being eaten. Cyanide starves the body’s cells of oxygen by blocking its use by the fundamental energy-producing system of the cell: the mitochondria. Organs that use the most energy, and thus need the most oxygen –­ the brain, heart and liver – are worst affected and death follows through failure of the brain to maintain breathing. Acute cyanide poisoning produces death so rapidly that affected animals are often found dead without being seen to be ill – so-called sudden death. When affected animals are seen before death they breathe rapidly and deeply, have a weak irregular pulse and muscle weakness before collapsing into a coma, convulsing and dying rapidly. Typically, their blood is bright red because the oxygen in it cannot be used by the tissues. Their tissues do not consistently have the blue discoloration called cyanosis that indicates a lack of oxygen in the blood. Post-mortem examination soon after death reveals bright red blood, but no specific changes in body organs either during the examination or by histopathology. There may be death (necrosis) of individual liver cells in some cases. To treat an affected animal, sodium thiosulphate (also known as photographic ‘hypo’) must be given intravenously at 500  mg/kg or more (for individual cattle, 150 g hypo in 300 mL water; for a sheep, 30 g in 60  mL), plus doses of the same material by mouth or directly into the rumen (for individual cattle, 30 g; for a sheep, 5 g). Additional intravenous doses may be needed if cyanide continues to be released from the gastrointestinal tract and the patient has further signs of poisoning. Intravenous sodium thiosulphate in high dose (500 mg/kg or more) can be effective when given up to 30  minutes after a toxic dose of a cyanide-containing plant is eaten, but the earlier treatment is started, the more likely it is to be effective. ‘Normal’ animals in the same group as those affected should also be dosed by mouth or they may succumb later. Legislation enacted in all Australian states and territories to try to prevent the production of chemical residues of therapeutic drugs in the tissues of food-producing animals prohibits the treatment of more than one individual animal of a foodproducing species in a herd or flock with an unregistered drug at any one time. Sodium thiosulphate has not been so registered, but is specifically exempted from these regulations and may be used for treating herds of ruminants poisoned by cyanide. Apply a withholding period of 24 hours to milk from treated cows and for animals to be slaughtered for meat. For sorghum crops, avoid grazing when the crop is less than 75 cm tall or when regrowth is sprouting. The cyanide potential of sorghum plants declines when

31

flowering starts. Ensiling sorghum with a hazardous cyanide content will reduce the concentration, but the end product should be checked before feeding it to stock. Cyanide will persist in hazardous amounts in hay made from plants containing dangerous concentrations of cyanogenic glycosides. Sulphur is essential to the conversion of cyanide to harmless chemicals (detoxification) by the liver. Putting out sulphur-containing licks or blocks or molasses (which is naturally rich in sulphur) for animals exposed to cyanide-containing crops may improve their production and may help prevent poisoning. Sulphur should not be regarded as a complete means of prevention. Avoiding the circumstances likely to lead to poisoning is also necessary. Too much sulphur (more than 0.4% of the diet) can itself be poisonous, producing brain damage (polioencephalomalacia) in ruminants (see the section on ‘Sulphur poisoning’ later in this chapter). Chronic effects attributed to cyanide intake by ruminants and horses are rarely reported. These can be swaying of the hindquarters (posterior ataxia) and dribbling of urine (urinary incontinence), congenital deformities (goitre or arthrogryposis) and sulphurresponsive reduced production. Posterior ataxia and urinary incontinence has been seen in cattle, sheep and horses grazing regrowth of sorghum crops and drought-fed on Alectryon oleifolius (boonaree or rosewood). There is damage to the white matter of the spinal cord, leading to loss of full control of the hind limb muscles and a swaying uncoordinated gait. Paralysis of the bladder with continuous dribbling of urine is a major effect. Bacterial infection can occur in the urinary bladder (cystitis) in a proportion of these cases. Antibiotic treatment can be usefully given to these animals. Mildly affected animals can recover. A similar syndrome (tropical ataxic neuropathy or konzo) causing weakness and paralysis and optic nerve degeneration leading to permanent blindness is seen in humans in Africa, Jamaica and Malaysia who use Manihot esculenta (cassava) root tubers as a staple food and do not process them enough to remove all their cyanide potential before cooking. Goitre in newborn children may result from this practice as well. Congenital fixation of limb joints (arthrogryposis: skeletal muscle shrinkage [atrophy] resulting from loss of its nerve supply after white matter degeneration in the brain and spinal cord) has happened to foals and calves of dams grazing Sorghum plants. Difficulty giving birth (dystocia) is a common outcome. Certain virus infections of the foetus can also produce these effects. Congenital goitre has been seen in lambs of ewes grazing some Cynodon species grasses overseas. Reduced production is reported in sheep and cattle grazing sorghum; this has been

32

Australia’s Poisonous Plants, Fungi and Cyanobacteria

corrected by using lick blocks with a 5–10% sulphur content. More sulphur than this risks copper deficiency and brain damage (polioencephalomalacia).

Dihydroxycoumarin poisoning ∅  Effective therapy: vitamin K1. Early intervention is essential for a positive outcome.

M  Delayed onset or chronic effects Plant sources of dihydroxycoumarin included in this book: Grasses: *Anthoxanthum odoratum (perennial sweet vernal grass) Forbs: *Melilotus albus (white sweet clover). Shrubs: Wikstroemia indica (tie bush) appears to be able to poison without being mouldy. This is an uncommon poisoning in Australia, but common in North America where it is called white sweet clover poisoning. Plants containing significant amounts of coumarol are toxic when used as hay or silage to feed ruminants or horses, but only when the plants have mould fungi growing on them after harvest. The fungi convert the coumarol to dihydroxycoumarin, which interferes with the action of vitamin K in the body. Vitamin K is essential for blood clotting to occur, so poisoning by dihydroxycoumarin leads to widespread bleeding. Toxicity depends on the amount of dihydroxycoumarin generated in particular batches of mouldy fodder. For cattle, a dihydroxycoumarin concentration in hay of less than 20 mg/kg (ppm) is apparently safe, 20–30  mg/kg will cause poisoning if fed for a long period (130 days or more) and more than 50 mg/kg will cause poisoning in about 15 days. The bleeding into the tissues that occurs in this poisoning can affect various organs and be seen as a range of signs. Bleeding is most likely to occur where movement or trauma occurs. Lameness or stiff gait can result from bleeding into and around joints. The mucous membranes of the mouth, nose, eyes and vagina are pale and may contain small haemorrhages: pin-point or larger in size. Fresh blood or dark discoloration may be seen in the dung or there may be dysentery. Bleeding may occur from the nose or into the urine, turning it red. Pregnant animals may abort. Blood samples collected from affected animals take much longer than usual to clot and the needle puncture wound may bleed for a long time. Post-mortem examination reveals extensive bleeding in various body organs and tissues.

Therapy requires the injection of vitamin K1 using the smallest practical needle size and spreading the dose in several different sites. For cattle, 1–3  mg/kg should be given intramuscularly every 12  hours for 5 days or until clotting returns to normal. The best measure of blood clotting capacity in this poisoning is obtained by laboratory measurement of prothrombin time and activated partial thromboplastin time from blood samples. Both of these are related to the function of vitamin K in the clotting mechanism. Prevention of poisoning rests with ensuring that susceptible plants harvested for hay have a low moisture content before baling and that silage made from them is stored in a way that prevents widespread mould growth.

Ergot alkaloid poisoning N  No specific therapy (except for decreased

milk production). Apply general decontamination and supportive measures advised by a Poisons Information Centre, a medical practitioner or a veterinarian.

~  Acute effects M  Delayed onset or chronic effects Fungal and plant sources of ergot alkaloids included in this book: Fungi: *Claviceps purpurea (ergot of rye) and *Claviceps africana (sorghum ergot) Grasses: *Festuca arundinacea (tall fescue) infected by the endophytic fungus Neotyphodium coenophialum, *Lolium rigidum (annual ryegrass) infected by *Claviceps purpurea (ergot of rye) and *Lolium perenne (perennial ryegrass) infected by the endophytic fungus Neotyphodium lolii. Fungal endophytes can only be detected by microscopic examination or culture of the plant in a laboratory. Ergotism is the general term for poisoning by ergot alkaloids. Other names are used for particular occurrences of ergotism. Abnormally high body temperature (hyperthermia) in hot weather has been called bovine hyperthermia, summer slump, idiopathic hyperthermia and fescue summer toxicosis. Gangrene of the limbs and other extremities in cold weather has been called fescue foot (of cattle) and St Anthony’s fire (of humans). Additionally, nervous ergotism has been described in humans, but its existence in domestic animals is disputed. Human ergotism has a long history with infections of grain crops by Claviceps purpurea (ergot of rye) contaminating bread and causing

3 – Common poisoning profiles

poisonings including St Anthony’s fire. Some scholars believe this was behind many accusations of witchcraft in Europe and North America in the 16th to 18th centuries. Known mass human poisonings occurred in Europe in the 9th century and continued into the late 20th century. There are many different ergot alkaloids, but the main ones that cause poisoning are ergovaline from ergot of rye and the tall fescue endophyte and dihydroergosine from sorghum ergot. Only the ergot or resting stage of Claviceps fungi in cereals and grasses produces these toxins. The honey dew stage does not. Humans and cattle are the most common victims of poisoning, but pigs and horses are also affected. Poisoning of sheep is rare. Ergot alkaloids cause the blood vessels of the extremities of the body to constrict, reducing blood flow to the ends of limbs, tail and ears. In hot weather, this prevents effective cooling of the body through reducing the loss of heat at the body surface and forcing up the body temperature. In cold weather, this leads to inadequate blood supply to the ends of limbs, tail and ears and death of tissues (gangrene) in these structures. In pregnant horses, this interferes with blood flow through the placenta to the unborn foal. The alkaloids also interfere with prolactin secretion by the pituitary gland at the base of the brain. Prolactin is the hormone that stimulates milk production. By this means, ergot alkaloids stop milk production (cause agalactia) in nursing (lactating) females, thus potentially starving their offspring. Poisoning occurs if grain contaminated with ergots (or bread made from it) is eaten or animals graze annual ryegrass infected with ergots or endophyte-containing tall fescue pastures. Silage containing ergots is toxic. Sometimes silage made from perennial ryegrass is toxic. The risk of grain crops being infected by rye ergots (Claviceps purpurea) is greater in wet years. Sorghum crops planted late in the summer growing season are more likely to be infected by sorghum ergots (Claviceps africana). Infection of sorghum occurs when plants are flowering during cool, humid weather. Hyperthermia can happen to poisoned cattle in direct sunlight, even if the air temperature is below 30°C. Hyperthermia from ergotism affects all or many animals in a herd or flock and they may be ill for months. Feed intake drops, resulting in loss of body weight. Rectal temperatures of affected cattle are around 41–42°C (normal is less than 39.5°C). There is drooling of saliva, and an increased breathing rate up to, and including, panting and there may be difficulty breathing (dyspnoea) with the head and neck stretched forwards, the mouth open and the tongue

33

protruding. Affected animals may seek shade or stand in water bodies and be reluctant to move. Exercise rapidly makes the effects worse and affected cattle may die if moved when air temperatures exceed 30°C. In dairy cattle, seriously decreased milk production or drying up (agalactia) and an increased occurrence of mastitis are seen. The decreased or stopped milk production can cause death of offspring from starvation, particularly in piglets, but also in calves and lambs. Abortion from ergotism is rarely seen in domestic animals, except in mares grazing endophyte-infected tall fescue. Mares suffer a delay of 2 weeks or more past the normal birth date of their foal. This causes a difficult birth (dystocia) that may kill the mare and the foal. The placenta in these cases is very swollen with fluid (oedematous), may separate from the uterus early in the birth process and emerge before the foal. If the mare survives, the foal is either stillborn or born large but weak, sometimes with contracted legs. Affected mares have no udder development (agalactia) or poor milk production, further reducing the foal’s chance of survival. Gangrenous ergotism is rarely seen. It causes dry gangrene of the tissues of the lower limbs. Dry gangrene involves the death and subsequent shrinkage with drying and brown progressing to black discoloration of affected tissues by reduced or gradually blocked blood supply. Affected tissues are cold, lack a pulse and have a sharp line of demarcation from normal tissue. The end of the tail and the ear tips may be affected as well. The limb damage causes severe lameness and an inability to stand and walk and this can be the first sign noticed in grazing animals. Manage ergotism incidents by identifying and removing the alkaloid sources from the food supply. Do not handle or move affected animals if ambient temperatures exceed 30°C. Apply water sprays (if possible) to cool affected animals under these conditions. The dopamine-like effects that cause pituitary dysfunction affecting milk production may be treated with dopamine antagonists, such as domperidone and metoclopramide, but the other effects of the alkaloids are not directly treatable. Screen ergots from infected grain (a less than 0.02% inclusion rate is recommended). Control Lolium rigidum (annual ryegrass) as a weed of cereal crops, but this is becoming harder because of the grass’s increasing resistance to herbicides. The total concentration of ergot alkaloids in diets for animals should not exceed 0.5  mg/kg for cattle and sows, 5  mg/kg for grower pigs and 10 mg/kg for poultry. Endophyte-free tall fescue varieties are available, but these are more susceptible to insect attack. Do not graze mares on

34

Australia’s Poisonous Plants, Fungi and Cyanobacteria

endophyte-infected tall fescue pastures beyond day 300 of their pregnancies.

Fern norsesquiterpene glycoside poisonings NNN  No effective therapy M  Delayed onset or chronic effects Plant sources of fern glycosides included in this book: Ferns: Pteridium esculentum (austral bracken), Pteridium revolutum (hairy bracken), Cheilanthes sieberi (mulga fern) and Cheilanthes distans (woolly cloak fern). Norsesquiterpene glycosides are toxins found only in ferns. Ptaquiloside is the first and most prominent of this type. It has been shown experimentally to cause poisoning of cattle and sheep. Other chemicals in this group called ptesculentoside and caudatoside have also been found in similar amounts in bracken fern species in Australia. These other chemicals are probably as toxic as ptaquiloside. Fern glycosides affect cattle (and very rarely sheep) in Australia, producing two syndromes: extensive haemorrhage (osteomyelotoxic fern glycoside poisoning: the so-called ‘bracken poisoning’) and benign or malignant tumours of the urinary bladder (carcinogenic fern glycoside poisoning or bovine enzootic haematuria). Bovine enzootic haematuria is sometimes called ‘red water’, but should not be confused with tick fever infections by Babesia and Anaplasma blood parasites that are given this same disease name. Damage to the retina in the eyes of sheep (‘bright blindness’ or retinotoxic fern glycoside poisoning) from prolonged bracken fern intake has been seen, but so far only in Britain. Norsesquiterpene glycosides occur in the leaves of certain ferns and are most concentrated in young leaves. Concentrations of ptaquiloside in bracken in Australia tend to be greater in southern parts of the country. Poisoning requires cattle to eat these ferns in large amounts for 2–4 weeks before ‘bracken’ poisoning occurs. Calves are more likely to be affected by ‘bracken’ poisoning than adults. Bovine enzootic haematuria occurs only after small quantities of the ferns are eaten repeatedly over several years. These quantities are less than are required to cause ‘bracken’ poisoning. Mature animals are affected by bovine enzootic haematuria. The disease rarely occurs in animals less than 3 years old. ‘Bracken’ poisoning damages the bone marrow, destroying its capacity to produce platelets (small cell fragments that are essential for blood clotting) and

neutrophils (white blood cells that defend the body against bacterial infection). Affected cattle bleed freely into internal organs and from accidental wounds. Inspection of the gums and the whites of the eyes commonly reveals paleness and pin-point and larger haemorrhages beneath the surface. Blood may be seen in dung, urine or in mucus from the nose. Late in the course of the poisoning, bacterial infections may be superimposed on the bleeding and affected cattle will be fevered. Post-mortem examination reveals widespread haemorrhages in the body. Microscopic examination of bone marrow confirms the lack of plateletproducing cells (megakaryocytes). Bovine enzootic haematuria is seen first as bloodtinged urine. The affected animal continuously loses blood from the tumours in its bladder. Whole blood clots may be passed in some cases. Affected animals appear otherwise normal at first. Loss of blood leads to chronic anaemia, which is eventually seen as marked paleness of the gums. Affected animals waste away over months to years and will eventually die from the blood loss. There is no effective specific treatment for either condition. Antibiotics and blood transfusions are positive measures that can be used in ‘bracken’ poisoning, but are usually futile and most affected animals die. Prevention of poisoning is through reducing the density of ferns in pasture. This can be hard and requires measures to kill or weaken the ferns (regular slashing of bracken or using selected herbicides) combined with an active pasture improvement program.

Fluoroacetate poisoning NN

  Effective therapy is doubtful, but should be attempted as advised by a veterinarian, a Poisons Information Centre or a medical practitioner. Early intervention is essential for a positive outcome.

~  Acute effects Plant sources of fluoracetate included in this book: Shrubs: Gastrolobium bennettsianum (cluster poison), Gastrolobium bilobum (heart-leaf poison), Gastrolobium calycinum (York Road poison), Gastrolobium crassifolium (thick-leaf poison), Gastrolobium cuneatum (river poison), Gastrolobium floribundum (wodjil poison), Gastrolobium grandiflorum (wall-flower poison, heart-leaf or desert poison bush), Gastrolobium laytonii (kite-leaf poison), Gastrolobium microcarpum (sandplain poison), Gastrolobium oxyloboides (Champion Bay poison), Gastrolobium parviflorum (box poison), Gastrolobium parvifolium (berry poison), Gastrolobium polystachyum

3 – Common poisoning profiles

(horned poison), Gastrolobium racemosum (net-leaf poison), Gastrolobium reflexum, Gastrolobium spinosum (prickly poison), Gastrolobium tetragonophyllum (brotherbrother), Gastrolobium velutinum (Stirling Range poison) and Gastrolobium villosum (crinkle-leaf poison). Trees: Acacia georginae (Georgina gidyea). Sodium monofluoroacetate is the toxic constituent of compound 1080, the poison used for control of vertebrate pests such as dingos, wild dogs, foxes, feral pigs and rabbits. The same toxin is present in a number of native Australian plants (and in some plants in Africa and South America). Dogs are the most sensitive animals to this toxin, with a lethal dose of around 0.05–1.0  mg/kg; that is, 1–20 mg for a 20 kg (medium-sized) dog. Cattle, sheep, pigs and horses are all similarly sensitive, but about half to a quarter as susceptible as dogs. Birds are 10 to 30 times less sensitive than dogs. Native animals that live in habitats with numerous fluoroacetate-containing Gastrolobium plants in south-western Australia are quite tolerant of the toxin when compared with the same species of animals in other parts of Australia. Brush-tailed possums from south-western Australia are more than 120 times less sensitive to fluoroacetate than those in eastern Australia. Natural selection has resulted in populations of possums, native rats, wallabies and other native animal species surviving among plants that would kill such animals brought in from outside this habitat. The sheep and cattle of the early European settlers were such animals and many died of this poisoning before the dangerous nature of the plants was clearly understood (see Box 13.3). Leaves, flowers and seed pods of these plants are all toxic, with flowering plants often the most dangerous. Seedlings and root suckers can also be very toxic. These plants concentrate the largest amounts of toxin in those parts of the plant most critical for its future: the young leaves, flowers and seed pods. In animal bodies, fluoroacetate is taken into the very important chain of biochemical reactions that produce energy in animal cells, but, instead of fuelling this process, the products made from fluoroacetate block them, starve the cell of energy and kill it. Those parts of the body with the most demand for energy are the most seriously affected: the heart and the brain. In carnivores and pigs, the most affected organs are the brain and the digestive system. In herbivores, the heart is the most damaged organ. Plants containing fluoroacetate are quite palatable to herbivores, making them very dangerous because they are both highly toxic and readily eaten. The bodies of poisoned cattle, sheep or pigs are toxic to

35

dogs, dingos or other animals such as pigs that may feed on them. Such bodies can remain toxic for months after death. Poisoned dogs and pigs vomit, froth at the mouth and nostrils, urinate and defecate frequently and become hysterical, running wildly, barking and howling. Collapse in convulsions precedes death. These effects result from interference with brain function and the barking, howling and convulsions do not necessarily indicate that the victim is experiencing pain. Some herbivores may have such signs, but most collapse suddenly from heart failure and may die quietly or in convulsions. Usually no abnormalities are seen during a post-mortem examination, but fibrous scarring may be found microscopically in the hearts of herbivores that survived a previous bout of poisoning. Poisoned dogs require emergency veterinary treatment, including prolonged anaesthesia to suppress convulsions. Despite this, many dogs still die. Otherwise there are no proven useful simple and readily available treatments. No practical treatment is available for poisoned livestock. Dogs at risk of eating poisoned carcases (or 1080 baits in poisoning campaigns) should be muzzled. Livestock grazing pastures that contain fluoroacetatecontaining plants should be managed to avoid exposure to these plants at times of the year when they are most likely to cause poisoning. Most poisoning from Acacia georginae happens during July–November when pods are plentiful and pasture is sparse. Research in Australia has produced genetically engineered bacteria that can live in the rumen of cattle, sheep and goats, break down the fluoroacetate from plants that they eat and protect the animal from poisoning. These bacteria have not been made available to livestock owners to date because of concerns that they may be passed naturally to feral animals, such as goats and rabbits, and protect them as well. This would greatly diminish or even destroy the effectiveness of 1080 as a tool for control of these pests. The researchers are trying to adapt their bacteria to allay these concerns. A further concern about the use of fluoroacetatedestroying bacteria to protect livestock is that this creates the temptation to exploit land that was previously protected from use and potential overgrazing by the presence of highly dangerous plants. Wise husbandry of bacteria-protected livestock by graziers so that land degradation does not flow from their use is crucial for the continued health of the land that supports fluoroacetate-containing plants. Important: Be aware of the legal requirements for the conservation of threatened Gastrolobium species in Western Australia. It is vitally important to consult

36

Australia’s Poisonous Plants, Fungi and Cyanobacteria

state government nature conservation authorities to obtain the latest information on your legal position before taking any action to control these plants. Ignorance of the law is not a defence if you break laws or regulations when managing them. See ‘Warnings’ in the preliminary pages.

Galegine poisoning NNN  No effective therapy ~  Acute effects Plant sources of galegine included in this book: Sedges: Schoenus asperocarpus (poison sedge). Forbs: *Verbesina encelioides (crownbeard). This toxin also occurs in †Galega officinalis (goat’s rue) and Schoenus rigens (Chapter 15). Galegine is an amine (an isoprenoid guanidine derivative) found in toxic amounts in only four plant species worldwide. Three of those have caused poisonings in Australia. This is an uncommon type of poisoning of sheep and cattle, and sometimes goats and pigs, which occurs mostly in Western Australia, New South Wales and Queensland. A fatal dose of galegine for sheep is 30–40 mg/kg body weight given into the peritoneal cavity. Toxic doses of the plants are given in the accounts of the individual plants. Galegine damages the lining cells (endothelium) of the many blood vessels in the lungs. They then fail to hold the fluid component of the blood (plasma) within the blood vessels. This protein-rich fluid floods the lung tissue (pulmonary oedema), flows into the major airways (the bronchi and trachea) and leaks into the chest cavity (hydrothorax), virtually drowning the animal. Poisoning follows hungry livestock gaining access to large amounts of the galegine-containing plants. This most often occurs during droughts for the normally unpalatable Verbesina encelioides (crownbeard) when grazing animals eat mature plants wet by rain. For Schoenus asperocarpus (poison sedge), sheep are most commonly poisoned by new growth in autumn at the break of the season when other plants are scarce or after they sprout following fires. Poisoned animals are either found dead or struggling to breathe before collapsing and dying rapidly. Post-mortem examination reveals free clear yellow fluid in the chest cavity (thorax) and stable foam in the large airways (bronchi and trachea). The chest fluid clots on exposure to air. There is no effective treatment. Prevention involves denying access to the plants by hungry animals. Herbicides or physical destruction may be useful in control of the source plants.

Glucosinolate poisoning NNN

  No effective therapy. Apply supportive measures advised by a veterinarian.

~  Acute effects M  Delayed onset or chronic effects Plant sources of glucosinolates included in this book: Forbs: †Brassica napus (rape), †Brassica oleracea (kale), †Brassica rapa (turnip) and *Rapistrum rugosum (turnip weed). Most glucosinolate-containing plants are in the families Brassicaceae, Capparaceae and Caricaceae, but they also occur in 13 other families. Glucosinolates occur in the plants themselves and also in the meals produced as by-products of oil production from seeds (‘oilseeds’) of Brassica napus (rape, oilseed rape, cole, coleseed or canola). Glucosinolates are sulphur-containing organic compounds linked to sugar molecules (glycosides of β-D-thioglucose–(Z)-N-hydroximinosulphate esters, with a sulphur-linked β-D-glucopyranose (sulphonated oxime) moiety and an amino acid-derived side chain). Crushing (including chewing) of fresh glucosinolatecontaining plant material releases the enzyme thioglucosidase (myrosinase), which splits glucosinolates into glucose, a hydrosulphuric acid ion and a sulphur-andnitrogen-containing aglycone. Further splitting of the aglycone yields a thiocyanate, an isothiocyanate or an organic nitrile. Intestinal bacteria also contain thioglucosidase and may contribute to glucosinolate breakdown. Each plant contains several different glucosinolates and thus may produce a variety of such products, the amount and type formed depend on the parts of the plants involved and how they are treated. Several derivatives of glucosinolates (goitrins, cheirolin, thiocyanates and isothiocyanates) are goitrogens, producing goitre (swelling of the thyroid glands) in piglets, chickens, calves, lambs and kids that is apparent at birth (congenital goitre). This can often be seen as a rounded swelling under the skin on either side of the windpipe (trachea) in the upper neck. This is caused by poorly functioning thyroid tissue that is trying to make up for its failure to produce enough thyroid hormones by producing yet more tissue. Affected animals have poor weight gain. Low dietary iodine predisposes to congenital goitre. Goitrins block iodine use by thyroid tissue and interfere with thyroid hormone secretion, actions that are not reversed by increased dietary iodine. Thiocyanates and isothiocyanates block iodine uptake by the thyroid glands, an effect that is worst when the iodine content of the diet

3 – Common poisoning profiles

is low and which can be reversed by increased dietary iodine. Nitriles from rapeseed meal may be partly converted to thiocyanate. Rape seed meal fed at 10–20% of the sow diet has triggered congenital goitre in piglets. Indole glucosinolates (glucobrassicin) broken down in the gut to form 3‑hydroxymethylindole can cause atypical interstitial pneumonia: an effect produced only in cattle. It has been seen in cattle grazing lush glucosinolate-containing crops or weeds or fed large amounts of cabbages. Signs of difficulty breathing (head and neck extended, open mouth, frothing at the mouth and grunting) called dyspnoea occur 7–10 days after first access to the plants. There may also be loss of rumen movement (ruminal atony), constipation, diarrhoea, jaundice and air bubbles under the skin (subcutaneous emphysema), which have escaped from the damaged lungs. If subcutaneous emphysema occurs, the chance of recovery is very slim. Post-mortem examination reveals fluid and dark red patches in the lungs, with air bubbles in the partitions between the lung sections (interstitial emphysema). There may be liver damage (periacinar necrosis) caused by lack of oxygen supply from the damaged lungs. Organic isothiocyanates are very irritant to tissues that they contact, injuring blood vessel walls and causing intense inflammation and pain in harmful doses. These are the compounds that give mustard its characteristic flavour. Cattle fed glucosinolate sources, such as large amounts of some kinds of Brassica seeds, can develop inflammation of the rumen wall (ruminitis) because of this, but this is rare. Abdominal pain, collapse and rapid death follow. Fluid swelling (oedema) of the rumen wall, and probably haemorrhages, are seen at post-mortem examination. Fatty haemorrhagic liver syndrome of poultry has been linked with feeding a diet containing rape to hens in lay that are in fat condition. Affected birds die very rapidly from haemorrhage from within the liver. At post-mortem examination, the liver is swollen, pale and fatty, carcase tissues are very pale and there may be blood in the body cavity. Poultry also may develop perosis (slipped hock tendons) and lowered egg production and pigs may develop enlarged livers when fed rapeseed meal.

Grayanotoxins poisoning N  No specific therapy. Apply general decon-

tamination and supportive measures advised by a Poisons Information Centre, a medical practitioner or a veterinarian.

~  Acute effects M  Delayed onset or chronic effects

37

Plant sources of grayanotoxins included in this book: Shrubs: Species of †Rhododendron (rhododendrons, azaleas and vireyas). These toxins also occur in species of Kalmia, Leucothoë and Pieris grown in Australian gardens (Chapter 15). Grayanotoxins (named after Leucothoë grayana) are water-soluble diterpenoid compounds. Andromedotoxin is grayanotoxin I, acetylandromedol or rhodotoxin. Over 30  grayanotoxin-related compounds are known. Grayanotoxins bind to, and modify, the sodium channels of cell membranes, increasing membrane permeability to sodium ions and producing prolonged depolarisation and excitation and an increase in calcium inflow. This leads to increased force of heart muscle contractions (a positive inotropic effect), similar to the effects of cardiac glycosides (see ‘Cardiac glycoside poisoning’ earlier in this chapter). Animals that have been poisoned by these compounds include sheep, goats, cattle, buffaloes, llamas, alpacas, horses, donkeys, kangaroos, dogs, cats, elephants, tortoises, birds, bees and humans. Andromedotoxin is a recognised insecticide, killing the insects by paralysing them. Rhododendron molle flowers have been used in this role. Poisoning commonly happens when ruminants (particularly goats) and other animals gain access to garden waste or to gardens or pastures where shrubs may be browsed. Humans are poisoned by eating honey – so-called ‘mad honey’ – made from nectar of the flowers of source plants. A lethal dose of leaves for herbivores can be as little as 0.1% of body weight (1 g/kg). For humans, about 2 tablespoons of a toxic honey (50 g or 75 mL) will produce poisoning. In fatal cases, death may occur within a few hours of the first signs of poisoning. There can be up to 4 days delay between access to plants and onset of signs in goats and sheep. Early signs of poisoning in ruminants are drooling of saliva and regurgitation of paunch contents (‘vomiting’), which is an unusual sign of disease in this type of animal. Repeated swallowing and retching with green foamy fluid flowing from the nostrils or the mouth occur. Some animals develop diarrhoea and signs of abdominal pain, such as teethgrinding. The heart is affected and either slows down (bradycardia) or speeds up (tachycardia) and may develop an irregular rhythm. Sudden death from heart failure can occur. Signs of lung involvement, such as laboured breathing, coughing, choking, panting, bluish gums (cyanosis) and fever, can follow entry of regurgitated rumen contents to the airways leading to pneumonia. Affected animals are often weak and staggering. Humans poisoned by contaminated honey develop low blood pressure and a slow heart rate. They may have vomiting, vertigo, a sensation of pressure on the chest. Some lose consciousness and have seizures.

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Australia’s Poisonous Plants, Fungi and Cyanobacteria

Post-mortem findings in fatally poisoned animals commonly include identifiable source plant material in the paunch contents and pneumonia caused by aspiration of rumen contents. Some laboratories may be able to assay rumen contents for grayanotoxins. Rhododendron pollen can be identified microscopically in poisonous honey. Surviving animals should be denied further access to the plants. Dosing with activated charcoal and fluids should be done by a veterinarian. It may be appropriate to empty the rumen or stomach surgically in some circumstances. Anti-arrhythmic drugs can be used to support heart function. If there has been aspiration of rumen contents, recovery may be difficult or impossible and will rely on prompt and effective antibiotic dosing. Poisoned humans usually recover with appropriate medical treatment. Heat has been used to detoxify honey, but is not always successful.

Iforrestine poisoning NNN

  No effective therapy. Apply supportive measures advised by a veterinarian.

~  Acute effects Plant sources of ifforestine included in this book: Forbs: Isotropis cuneifolia (lamb poison). Shrubs: Isotropis atropurpurea (poison sage). Iforrestine is a heterocyclic alkaloid isolated from (and named after) Isotropis forrestii that was collected from the site of sheep deaths at Meekatharra in Western Australia. The consistent kidney-damaging (nephrotoxic) effects of a number of species of Isotropis in ruminants strongly suggest that they all contain iforrestine. Sheep and cattle have been poisoned by this group of plants in Western Australia, the Northern Territory and New South Wales. The plants are very palatable and travelling livestock are most at risk. Poisoning follows exposure to fresh new growth or mature plants, most often in late winter or early spring. Poisoning may occur in summer after unseasonal rain. The toxicity of plants may vary between seasons and localities. Sheep that eat 500  g to 1  kg of plant die rapidly. A fatal dose of Isotropis forrestii for sheep was 300 g dried plant (9–11 g dry matter/kg body weight). Poisoned animals lose appetite and become lethargic. They develop diarrhoea that becomes persistent and faeces may contain blood and mucus. Their output of urine slows (oliguria) and then stops (anuria). They become weak and collapse, typically dying in 2–7 days. Large doses can kill within an hour. Such rapid deaths

may be due to effects on the heart. Blood samples collected before death have increased concentrations of urea and creatinine in plasma. Post-mortem examination reveals pale swollen kidneys surrounded by watery fluid (perirenal oedema) and haemorrhage and congestion of the lining of the abomasum and intestines, particularly of the large intestines. There is fluid swelling (oedema) of the wall of the abomasum and an excessive amount of straw-coloured fluid in the abdominal cavity. There may also be excess fluid in the chest. When tissue sections are examined by microscope, kidney damage (necrosis of proximal renal convoluted tubules) is consistently present. In some cases, there may be death of liver cells (scattered or periacinar coagulation necrosis) or heart muscle cells (focal myocardial necrosis) and fluid in the lungs (pulmonary oedema). There is no effective treatment for poisoned animals. Hungry animals should be stopped from gaining access to concentrations of these plants. In recent decades, the risk of livestock being poisoned in south-western Australia has been significantly reduced through widespread cultivation of areas where the plants grow, making poisoning rare. The plants still pose a significant risk in the uncultivated regions where they occur.

Irritant diterpenoid poisoning N  No specific therapy. Apply general decon-

tamination and supportive measures advised by a Poisons Information Centre, a medical practitioner or a veterinarian.

~  Acute effects Plant sources of irritant diterpenoids included in this book: Forbs: Spurges (Family Euphorbiaceae) – Euphorbia parvicaruncula (bottletree caustic), Euphorbia planiticola (bottletree caustic), Euphorbia stevenii (bottletree caustic) and Euphorbia tannensis subsp. eremophila (bottletree caustic). Riceflowers (Family Thymelaeaceae) – Pimelea decora (Flinders poppy), Pimelea elongata, Pimelea haematostachya (pimelea poppy), Pimelea simplex subsp. continua, Pimelea simplex subsp. simplex (desert rice-flower [NSW]) and Pimelea trichostachya (flax-weed). Shrubs: Spurges (Family Euphorbiaceae) – †Euphorbia tirucalli (naked lady), *Jatropha curcas (physic nut), *Jatropha gossypifolia (belly-ache bush), †Jatropha multifida (coral plant), †Jatropha podagrica (Guatamala rhubarb) and †Synadenium grantii (African milk bush). Riceflowers (Family Thymelaeaceae) – †Daphne odora

3 – Common poisoning profiles

(daphne), †Daphne mezereum (mezereon), Pimelea latifolia subsp. altior, Pimelea neo-anglica (poison pimelea) and Wikstroemia indica (tie bush). Trees: Phaleria clerodendron (rosy apple). Irritant diterpenoids are potent and have a direct irritant effect on the gastrointestinal tract in very small doses. Ruminants, horses and humans have been poisoned. Spurges and rice-flowers are unpalatable, so poisoning of livestock usually occurs only when animals are forced to eat them in the absence of more wholesome feed. Children (and human adults) have been poisoned by eating leaves or fruits. Colic (abdominal pain) and severe diarrhoea are the main effects of poisoning. There may be blood and mucus in the faeces. Some affected individuals have inflammation of the mouth and tongue (gingivitis or glossitis, respectively) or may be drowsy between bouts of diarrhoea. Dehydration sets in and death may follow within 24 hours in severe cases. At necropsy, damage (haemorrhage, necrosis and oedema) to the stomach and intestines is the main finding. Treatment is non-specific, in most cases, through oral dosing with replacement fluids and adsorbants such as activated charcoal or bentonite. Livestock should be provided with adequate wholesome feed if there is a risk that they will be exposed to these plants. The spurges (members of family Euphorbiaceae) can contain bitter milky sap (latex) that is irritant to skin and sensitive tissues such as eyes and mucous membranes such as the lips, mouth, tongue and genitals. Humans may be affected through contact of the latex with skin and sensitive tissues, particularly the eyes. Painful temporary blindness can result from damage to the cornea. Local anaesthetic drops have been reported to relieve the pain of eye irritation, but vision is not fully restored until the cornea heals. Humans with irritant skin reactions from the latex may possibly obtain relief by bathing the affected parts in a weak solution of bicarbonate of soda (baking soda). Soap and water may not remove latex from human skin, but washing or swabbing with alcohol can be effective.

Lily poisoning of cats N  No specific therapy. Apply general decon-

tamination and supportive measures advised by a veterinarian.

~  Acute effects M  Delayed onset or chronic effects ´  Toxin that causes poisoning is unidentified

39

Plant sources of this syndrome included in this book: Grass-like herbs: species of †Hemerocallis and †Lilium. The toxin responsible for this syndrome is unidentified, but is suspected to be 3-methoxy-2(5H)-furanone found in the European plant Narthecium ossifragum (bog asphodel) and in N. asiaticum, or a similar compound. This compound causes kidney damage in ruminants. Some cats will eat lilies if they encounter them in gardens, as pot plants or as cut flowers. The reasons why some cats eat plants are not clear. The toxic dose of lilies for cats is small: less than a single leaf or less than a single flower can be enough to cause severe poisoning. Signs of poisoning commonly start within 2 hours of eating lilies. Vomiting and excessive salivation start early and may persist for 4–6 hours (12 hours in some cases). Loss of appetite and depression continue and intensify during the 24–72 hours after onset. Tremors and seizures have been seen in about a third of cats that eat species of Hemerocallis. In many cases, excessive urination (polyuria) occurs 12–30  hours after onset and complete lack of urination (anuria) develops in untreated cats 24–48 hours after onset. Laboratory assays of blood reveal large increases in plasma creatinine, urea and phosphorus, starting in the 24–72 hours after onset. Laboratory assay of urine reveals glucose and microscopic examination reveals cells from the kidney (epithelial casts) within 18 hours. Untreated cases commonly die within 5 days. Postmortem examination followed by microscopic examination of tissues confirms severe damage to the kidneys (necrosis of renal tubular epithelial cells) and may reveal pancreatic damage (pancreatic acinar cell cytoplasmic vacuolation). Cat kidneys damaged by lilies can regenerate if therapy is prompt and aggressive. Postponing therapy for longer than 18 hours after the plant was eaten can lead to irreversible kidney failure and death. The chance of recovery is better if treated cats have only the gastrointestinal signs: vomiting and excessive salivation. Twenty-two cases studied in one series had follow-up information available for 11 (50%). Of seven cats with confirmed kidney failure, none survived. Of four cats with only gastrointestinal signs, and treated intensely within 24–36 hours of exposure, all recovered with no indications of kidney damage. Cats have a very low chance of recovery if they stop urinating. Recommended therapy consists of induced vomiting followed by dosing with activated charcoal and a cathartic to speed evacuation of the bowls. At the same time, forced fluid intake by intravenous catheter for at least 48 hours is needed to maintain an increased urine flow at double the normal output. In some cases,

40

Australia’s Poisonous Plants, Fungi and Cyanobacteria

kidney function has been restored using peritoneal dialysis. Prevention of poisoning is by stopping cats gaining access to lilies.

Lupin (quinolizidine alkaloid) poisoning NNN  No effective therapy ~  Acute effects M  Delayed onset or chronic effects Plant sources of quinolizidine alkaloids included in this book: Forbs: Lupinus species (cultivated and naturalised lupins). Lupin poisoning of livestock, also known as transient poisoning, alkaloidal poisoning, American lupinosis or lupin madness, is caused by a number of quinolizidine alkaloids and must not be confused with lupinosis (phomopsin poisoning) which is caused by fungal toxins. More than 70  quinolizidine alkaloids have been identified in lupins. In Australia, lupins originating in the Mediterranean region are mostly grown as pulse crops (for their seed) and sometimes as green manure in south-western Australia, but also in other states as far north as the Emerald and Callide Valley areas of Queensland. Lupin seed is fed to pigs and poultry and used as supplements for grazing livestock and in feedlots. Lupins of American origin are grown in gardens as ornamental plants. Lupin poisoning of livestock is much reduced because the concentration of quinolizidine alkaloids in the seeds of cultivated species of Lupinus grown as crops has been reduced by plant breeders to below toxic concentrations or eliminated completely. Plant breeding to reduce the alkaloid content of lupin seed apparently abolished poisoning in livestock grazing lupin crops in Western Australia by the 1970s. Modern cultivars of lupins grown in Australia normally contain less than 0.03% total alkaloids and are called ‘sweet’ (low-alkaloid) lupins, in contrast with ‘bitter’ (highalkaloid) lupins. The mean value of total alkaloid content of lupin seed handled by the marketing authority in Western Australia in 1982–85 was 0.015%. Seeds of naturalised *Lupinus cosentinii and of garden lupin varieties, such as the Russell lupins (†Lupinus × regalis) from North America, may still contain these toxins. Lupin poisoning still happens regularly in Western Australia when livestock eat the ripening pods of *Lupinus cosentinii in spring. Some other plants

in the pea family (Fabaceae) may have significant amounts of quinolizidine alkaloids in their seeds and be dangerous if eaten. Sheep were the usual victims of this syndrome, and were poisoned by eating large amounts of lupin seeds that contained the alkaloids. Horses, cattle, pigs and deer are also susceptible and have been poisoned. Clinical signs occur most often with exercise – after galloping, affected animals collapse onto their sides in convulsions (frothing at the mouth and grinding their teeth) and breathing with difficulty. If left undisturbed, they usually recover. Death may occur from respiratory failure if the dose was great enough. There are no significant post-mortem findings. Intake of quinolizidine alkaloids by pregnant animals in doses too small to directly poison them can result in malformations of the skeleton in their foetuses: the co-called ‘crooked calf disease’ of North America. This can include cleft palate, twisting of the spinal cord (scoliosis) and contracted fixed limbs (arthrogryposis). In Western Australia, lambs and calves born to mothers that ate *Lupinus cosentinii during pregnancy can have malformed limbs (hemimelia). Pigs have been poisoned by contamination of sweet lupin seed with seed from bitter varieties in growing pig diets. Pigs have rejected feed containing 0.33  g lupin alkaloids/kg, but accepted feed with 0.07 g/kg. As well as feed rejection or decreased feed intake, pigs have decreased growth rate. Rarely they may vomit and die. With unrestricted feeding, growing pigs can tolerate up to 0.20 g total lupin alkaloids/kg feed. For each increase of 0.1  g total alkaloids/kg, growth rate decreased by 47.1 g/day and feed intake by 0.12 kg/day. Very rarely, humans using lupin seed as food may be poisoned. ‘Sweet’ lupin seed is harmless, but ‘bitter’ lupin seed needs to be processed to leach out the alkaloids before cooking. If this process is not done properly, or if the water used to leach alkaloids from ‘bitter’ lupin seed is drunk, poisoning can result. Poisoning has also happened when pods or unripe seeds of garden lupins were eaten raw. In most cases, the dose is too small to cause symptoms. In toxic doses, poisoning upsets the nervous system and humans affected acutely can have nausea, vomiting, dizziness, headache, dilated pupils (mydriasis), blurred vision, a dry mouth, difficulty swallowing or talking, a racing or a slowed heart (tachycardia or bradycardia), low blood pressure (hypotension) and retention of urine. Longterm poisoning can produce difficulties with muscle control, and in one case, malformation of the skeleton in a newborn baby.

3 – Common poisoning profiles

Macrofungal poisoning gastrointestinal syndrome N  No specific therapy. Apply general decon-

tamination and supportive measures advised by a Poisons Information Centre, a medical practitioner or a veterinarian.

~  Acute effects ´  Toxin that causes poisoning is unidentified Fungal sources of this syndrome included in this book: Agaricus xanthodermus (yellow stainer), Chlorophyllum molybdites (green-gilled parasol) and Scleroderma (earth-balls). Many ‘mushrooms’ can cause poisoning when eaten raw by humans, but individual susceptibility can vary. Some people may be unaffected by species that have poisoned others. At the other extreme, deaths have occurred from this poisoning. Dogs have probably also been poisoned occasionally. Cooking often removes this toxicity. Toxic doses of these fungi are given in the accounts of the individual fungi. The nature of the toxin or toxins causing the effect in not known in most cases. Poisoning consists of nausea and vomiting with abdominal pain (colic) and diarrhoea. Australian cases of Chlorophyllum molybdites poisoning begin with drowsiness in some cases about half an hour after ingestion. After 1–2 hours, the main effects occur with nausea, violent vomiting, dehydration and severe stomach pain followed by diarrhoea with faeces containing mucus and blood. Cyanosis of the mouth, tongue and fingernails may occur. Adult victims recover rapidly and completely, usually within 2 days. Fatalities are known. Immediate urgent medical or veterinary attention including hospitalisation is essential to deal with severe effects, particularly the dehydration. All field-collected ‘mushrooms’ for human consumption should be thoroughly cooked.

Methylazoxymethanol (MAM) poisoning NN

  Effective therapy for acute effects is doubtful, but general decontamination and supportive measures should be attempted as advised by a Poisons Information Centre, a medical practitioner or a veterinarian.

41

NNN  No effective therapy for chronic effects ~  Acute effects M  Delayed onset or chronic effects Plant sources of methylazoxymethanol included in this book: Cycads: Australian native species of Bowenia, Cycas, Lepidozamia and Macrozamia and exotic cycads in gardens. Methylazoxymethanol (MAM) occurs in the tissues of cycads, mainly in the seeds, but also in leaves, combined with sugar molecules in chemical compounds called cycad glycosides. The main cycad glycosides are called cycasin and macrozamin. MAM is released from cycad glycosides by the action of the enzyme b-glucosidase in either the plant itself or in bacteria in the rumen of cattle, sheep or other ruminants. Humans, dogs, sheep and cattle have all been poisoned by MAM in Australia and elsewhere, usually by eating the seeds of cycads. Certain dog breeds including Labrador and Golden Retrievers and Staffordshire Bull Terriers, appear to be more prone to eating unusual foods including cycad seeds. All cycads, both Australian native species and exotic species cultivated in gardens such as the Japanese Cycas revoluta (sago ‘palm’), species of Encephalartos and Stangeria from Africa and species of Chigua, Ceratozamia, Dioon, Microcycas and Zamia from America, should be considered potentially poisonous. MAM is changed in the liver to a more chemically reactive compound that damages liver cells, blood vessels in the liver and then the intestinal lining after being excreted in the bile. If the dose of MAM is large enough, these effects are similar to those described in the section on acute liver necrosis and include bloody diarrhoea (dysentery). Lesser doses or large doses spread over longer time periods produce damage to the liver of lesser intensity, but this involves enlargement (megalocytosis) and loss of liver cells and a build-up of scar tissue (fibrosis) that can finally produce liver failure, if it is severe enough. These chronic changes look similar microscopically to those produced by pyrrolizidine alkaloids, and have similar effects including loss of body condition and behavioural changes. However, dogs are known to develop a life-threatening degree of liver and intestinal damage, with persistent bloody vomiting and diarrhoea that is usually fatal from just one cycad seed. MAM has produced neoplasia (‘cancer’) in laboratory animals and is regarded as a carcinogen (cancer causing chemical).

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Australia’s Poisonous Plants, Fungi and Cyanobacteria

No specific treatment is available for the acute effects, but general decontamination measures should be attempted. Many affected animals will die, but the dose that they have received varies from case to case and aggressive treatment will be rewarding occasionally. There is no effective treatment for the chronic effects of MAM on the liver. Aboriginal Australians used cycad kernels as a major food source before the European invasion of Australia. Their processing methods effectively removed the toxins. See the account of cycad neurotoxicosis (zamia staggers) for a discussion of measures aimed at preventing these poisonings in grazing livestock. Dogs should be prevented from eating the seeds of garden specimens of female cycads either by removing individual plants or removing the female cones before they mature. However, dogs have also been poisoned by eating cycad leaf material, so complete removal of cycads may be needed if particular dogs are prone to eating garden plants. Important: Be aware of the legal requirements for the conservation of native cycad species. It is vitally important to consult state government nature conservation authorities to obtain the latest information on your legal position before taking any action to control native cycads in their natural habitat.

Nicotine and other pyridine alkaloid poisonings N  No specific therapy. Apply general decon-

tamination and supportive measures advised by a Poisons Information Centre, a medical practitioner or a veterinarian.

~  Acute effects M  Delayed onset or chronic effects Plant sources of pyridine alkaloids included in this book: Forbs: Nicotiana megalosiphon (long-flowered native tobacco), Nicotiana suaveolens (scented native tobacco) and Nicotiana velutina (velvet native tobacco). Trees: Duboisia hopwoodii (pituri) and *Nicotiana glauca (tree tobacco). The pyridine alkaloids nicotine and nor-nicotine occur naturally in native and introduced species of Nicotiana (tobaccos) and in pituri (Duboisia hopwoodii). Other pyridine alkaloids in these plants are anabasine and anatabine, usually in smaller concentrations. Nicotine functions as an anti-insect defence chemical in plants and has been used as an insecticide and a worm drench (anthelmintic) in livestock. Poisoning is uncommon in

modern times. All animal species are susceptible, but poisonings usually have affected hungry travelling cattle and sheep that ate large amounts rapidly on encountering fresh green native tobacco plants after a period with no green feed. The smallest toxic dose of native Nicotiana established by experiment in cattle has been 4 g fresh plant/kg body weight. In individual sheep, Duboisia hopwoodii leaf was non-fatal at an oral dose of 28 g of fresh plant and fatal at 85 g or more. Dried plants are less toxic than fresh plants, but suckers of Duboisia hopwoodii harvested in hay have poisoned livestock. Horses and camels have been affected, as well as ruminants. Aboriginal people used branches of Duboisia hopwoodii to poison waterholes and so make emus easy to catch. Minimum lethal doses of nicotine itself are: for horses 0.2–0.3 g; for sheep 0.1–0.2 g; and for dogs and cats 0.02–0.10 g. The acute oral LD50 for rats is 50–60 mg nicotine/kg body weight. The human lethal oral dose of nicotine is 40–60 mg. Poisoning may cause sudden death with no observed signs if the dose is large, or a syndrome including unwillingness to move, incoordination, muscle tremor, weakness, pupil dilation, recumbency and continuous paddling movements of the limbs progressing to paralysis may be seen. Some animals may have diarrhoea and signs of abdominal pain (groaning and turning the head to the flank). Post-mortem findings can include congestion of the intestines in individuals that had diarrhoea. The plants responsible for poisoning may be recognisable in stomach or rumen contents. No specific treatment is recommended. Affected livestock left undisturbed often recover. Preventing hungry animals from eating native tobaccos or pituri can be hard, but it is the only effective control measure. Anabasine is a teratogenic pyridine alkaloid and can cause deformities of the newborn in the same way as lupin (quinolizidine) alkaloids.

Nitrate-nitrite poisoning ∅  Effective therapy: methylene blue. Early intervention is essential for a positive outcome.

~  Acute effects M  Delayed onset or chronic effects: abortion Plant sources of significant nitrate concentrations included in this book are: Grasses: *Avena sativa (oats), Dactyloctenium radulans (button grass), *Lolium perenne (perennial ryegrass), *Pennisetum clandestinum (Kikuyu grass), *Sorghum × almum (Columbus grass), *Sorghum bicolor (grain, fodder or forage sorghums), *Sorghum halepense (Johnson grass),

3 – Common poisoning profiles

*Urochloa panicoides (liverseed grass) and *Zea mays (maize). Forbs: *Amaranthus retroflexus (red-root amaranth), *Amaranthus spinosus (needle burr), †Apium graveolens (celery), *Arctotheca calendula (cape weed), Atriplex muelleri (annual saltbush), †Beta vulgaris (beet), †Brassica napus (rape), †Brassica oleracea (kale), †Brassica rapa (turnip), *Chenopodium album (fat hen), *Chenopodium murale (green fat hen), Dysphania glomulifera (red crumbweed), Dysphania littoralis (red crumbweed), Dysphania rhadinostachya (mouse-tail crumbweed), *Malva parviflora (small-flowered mallow), Portulaca oleracea (pigweed), Portulaca sp. aff. oleracea (munyeroo), *Raphanus raphanistrum (wild radish), Rumex brownii (swamp dock), *Silybum marianum (variegated thistle), *Sisymbrium irio (London rocket), *Salvia reflexa (mintweed), *Trianthema portulacastrum (black pigweed) and Trianthema triquetra (red spinach) Vines: †Ipomoea batatas (sweet potato) and Tribulus terrestris (caltrop). There are many known plant sources of hazardous amounts of nitrate in addition to those listed above (see Chapter 15). Nitrate-nitrite poisoning (commonly called ‘nitrate poisoning’) usually results from eating crops, pasture plants or weeds that have accumulated large amounts of nitrate (nitrate ions, NO3–) in their tissues. Ruminants (such as cattle, sheep and goats) and South American camelids or lamoids (alpacas and llamas) are the victims of this form of poisoning because their ruminal or stomach microbes convert the nitrate in plants into nitrite (NO2–). This nitrite is absorbed from the stomach into the bloodstream where it changes the haemoglobin in red blood cells from its normal red, oxygen-carrying state to a brown, non-oxygen-carrying state called methaemoglobin. If more than 75% of haemoglobin is converted to methaemoglobin, the blood cannot keep up the oxygen supply to tissues, and vital organs such as the brain, heart and liver become starved of oxygen, and the animal dies. Monogastric animals such as horses, pigs and birds are very rarely poisoned in this way, and only if the nitrite is formed in the food material by bacterial action on nitrate before the food is eaten. This can occur if plant feed high in nitrate, such as oaten hay, becomes wet for long enough (about 24 hours) to allow significant bacterial growth in it. Dogs and cats have suffered this type of poisoning from the excessive use of sodium nitrite as a preservative in pet meat. Humans (and other animals) are susceptible to this kind of poisoning by nitrite when it occurs in water supplies. Dogs and cats have never been recorded as poisoned directly by plants containing nitrate.

43

Table 3.1. Nitrate contents equivalent to 1.5% KNO3. A nitrate content greater than this is hazardous to ruminants.

Alternative expressions of nitrate content in plants

Equivalent to 1.5% KNO3. mg/kg = parts per million (ppm)

Nitrate-nitrogen (N)

2100 mg/kg

Nitrite-nitrogen (N)

2100 mg/kg

Nitrate (NO3)

9200 mg/kg

Nitrite (NO2)

9600 mg/kg

Sodium nitrate (NaNO3)

12 600 mg/kg

Nitrate in vegetables and in drinking water can pose minor health risks for humans after it is converted to nitrite and N-nitroso compounds in saliva or in the gastrointestinal tract. Nitrite can cause methaemoglobinaemia in young infants less than 3  months old: a so-called ‘blue baby syndrome’. In some circumstances, stomach cancer has been linked to N-nitroso compounds. Nitrate in large amounts can also interfere with iodine uptake by the thyroid glands and nitrate in drinking water has been linked with some cases of childhood-onset diabetes mellitus. However, the risk of cancer from N-nitroso compounds is usually more than compensated for by the positive antioxidant properties of vegetables, and nitrate intake may also boost the body’s defences against bacterial infection, so ‘eat your greens’ is still very sound advice. Plants are regarded as hazardous to ruminants if they contain 1.5% or more of nitrate measured as potassium nitrate (KNO3) equivalent in the dry matter. Different laboratories express assays for nitrate in different ways. Table 3.1 allows comparisons to be made. Nitrate is concentrated in the stems of plants, but also occurs in leaves. A very early name for nitratenitrite poisoning was corn stalk poisoning. Nitrate persists in toxic amounts if plants are dried, such as in hay. Ensiling may destroy nitrate, but is not guaranteed to make high-nitrate fodder safe. Circumstances leading to the build up of potentially toxic amounts of nitrate in plants are those that promote uptake of nitrogen from soil, but prevent its rapid conversion to protein. Large soil concentrations of nitrogen can occur from heavy application of nitrogenous fertilisers on crops or pastures, from large amounts of manure such as occur in and around stockyards, from uptake of nitrogen from air during long fallow periods and from the lack of leaching of nitrogen from soil during drought. Conversion of nitrogen to protein in plants requires energy produced by photosynthesis from the action of sunlight on chlorophyll, the green pigment in plants. Reduced

44

Australia’s Poisonous Plants, Fungi and Cyanobacteria

photosynthesis, and thus reduced energy supply in the plant, tends to cause a build-up of nitrate. Low light conditions from overcast skies and cold conditions boost nitrate concentrations in plants by reducing photosynthesis rates. Nitrate concentrations are also boosted by factors damaging plant tissues such as some herbicides, attack by insects, fungi or plant viruses. Certain herbicides that boost the nitrate content of sprayed weeds such as variegated thistle (Silybum marianum) can also boost their attractiveness to grazing ruminants and make them more dangerous. Less important factors that boost nitrate concentrations in plants include water stress and some soil mineral deficiencies (e.g. sulphur deficiency). Ruminants are most likely to be poisoned if they are hungry and eat large amounts of hazardous feed rapidly. Hay is more dangerous than fresh plants because a toxic dose of nitrate can be taken in more rapidly in hay than in fresh fodder. The rumen flora will become adapted to deal harmlessly with otherwise toxic amounts of nitrate in feed if grazing animals are gradually introduced to the feed or if they have continuous access to the feed and environmental conditions gradually boost its nitrate content to concentrations that would poison unadapted animals. For example, dairy cattle will adapt to graze ryegrass pastures containing 8% KNO3 in dry matter if gradually introduced to it. On the other hand, factors that interfere with the rumen flora’s capacity to deal with toxic amounts of nitrate can result in poisoning. Dosing cattle that are adapted to grazing high nitrate ryegrass with the anti-bloat or growth-promoting compound monensin can do this. An adequate supply of dietary carbohydrate, such as grain fed in the milking bails to dairy cattle, will help ensure that rumen bacteria are able to deal effectively with incoming nitrate. Many animals affected by this poisoning are likely to be found dead. If affected animals are seen alive, they will be suffering from lack of oxygen in vital organs, with signs including rapid deep breathing, an irregular weak pulse, muscle weakness and possible muscle spasms or tremors, followed by coma, possible terminal convulsion and rapid death. There may be a brown discoloration of the linings of the mouth and, in cows, the lining of the vulva. This change from pink to grey-brown can be used as early warning that dairy cattle are being fed too much nitrate. It is common for pregnant animals to abort 3–7 days after surviving a bout of this poisoning. Post-mortem examination reveals chocolate-coloured blood in many cases. This fades with time after death, disappearing in a few hours. A diagnostic test is available to detect nitrate in plants and in fluid from the front of the eye (aqueous humour) collected after death.

To treat an affected animal, a 2–4% solution of methylene blue must be given intravenously at a dose of 2 mg/kg. Relapse can occur if nitrite continues to be absorbed from the rumen, so further doses may be needed. Apply a withholding period of 4 days to milk from treated cows and 14 days for animals to be slaughtered for meat. Legislation enacted in all Australian states and territories to try to prevent the production of chemical residues of therapeutic drugs in the tissues of food-producing animals prohibits the treatment of more than one individual animal of a food-producing species in a herd or flock with an unregistered drug at any one time. Methylene blue has not been registered or exempted from these regulations to date. This has produced a conflict of interest with the duty of care that livestock owners and managers owe their animals and that has been enshrined in law in some states. This conflict of interest needs resolving to protect animal welfare. The risk to human health from residues of methylene blue in meat or milk of treated animals is almost zero. Methylene blue is used in human medicine. There is no practical alternative to methylene blue for treating methaemoglobinaemia in domestic ruminants. Not using it condemns them to suffer and die. The withholding periods given above are enough to prevent significant residues of methylene blue in products destined for human food. To prevent nitrate-nitrite poisoning, do not expose hungry ruminants to stockyards containing lush plants of known capacity to accumulate nitrate. Check the colour of the vulval lining in dairy cows grazing hazardous crops or pastures for a change to grey-brown as early warning of poisoning. Use a field spot test kit to check the nitrate content of crops suspected of having hazardous nitrate concentrations, such as under drought or cloudy conditions, before allowing ruminant stock access. Oats crops pose a high nitrate risk if they look very dark green, blue, stunted or frosted. If ruminants need to be given access to crops or other plants with known or suspected hazardous nitrate content, feed roughage (hay) immediately before access to reduce their rate of intake. If practical, feed grain or another carbohydrate source to animals before access to boost the capacity of rumen bacteria to deal with nitrate and nitrite. Ensiling potentially hazardous crops or pastures may reduce their nitrate content if the fermentation rate is slower than optimum; that is, reaching a stable pH after several days to weeks instead of a couple of days. Such slowly produced silage will have lesser nutrient quality. Urea, calcium carbonate or ammonia extend silage fermentation time. The nitrate content of corn silage has been reduced by 15% or 13% through adding urea or calcium carbonate, respectively. No reductions were achieved by adding ammonium hydroxide or a microbial inoculant. Ensil-

3 – Common poisoning profiles

ing corn (Zea mays) stalks can reduce their nitrate content by 50%. Check the nitrate content of any silage made from hazardous plants before feeding. Mixing hazardous feed with safe feed to dilute the total nitrate content below hazardous concentrations can be a useful option. As a final option, forage hazardous for ruminants may be used by feeding it to horses or pigs.

45

Oesophageal ulceration of horses (Chillagoe horse disease)

of gullet obstruction. Badly affected horses that are not treated die of starvation and dehydration. A few affected horses recover unassisted, but most need nursing. Treatment consists of trying to relieve the blockage, under anaesthesia if needed, and then passing a stomach tube through which food and water can be given until the ulcers heal. Giving easily swallowed food such as molasses may help. Preventing horses getting access to the responsible plants in large amounts is recommended. They may need to be fenced off or feed supplements given when pastures dry off.

N  No specific therapy. Apply supportive meas-

Oxalate poisoning: soluble forms

M  Delayed onset or chronic effects ´  Toxin that causes poisoning is unidentified

∅  Effective therapy: calcium salts. Warning: outcomes of treating acute oxalate poisoning are clouded by the common sequel of fatal kidney failure. Early intervention is essential for a positive outcome.

ures advised by a veterinarian.

Plant sources of Chillagoe horse disease included in this book: Shrubs: Crotalaria aridicola subsp. aridicola (Chillagoe horse poison) and Crotalaria medicaginea var. neglecta (trefoil rattlepod). Other subspecies and varieties of these species occur across northern Australia, but these have not been linked with poisoning of horses to date. Chillagoe horse disease, also known as coastal horse disease in the Capricornia region, is unique to Queensland, and affects only horses. The first cases were recognised in north Queensland in about 1910. The toxin or toxins that cause it are not known, but the disease occurs when horses eat large amounts of certain native species of Crotalaria under poor pasture conditions for periods of at least 2  weeks at a time, usually 4–5 weeks. Horses are said to develop a liking for these plants and to actively seek them in pasture. Horses may not start to have signs for up to 4 weeks after removal from hazardous paddocks. Poisoning occurs intermittently, with up to 20 years between cases on particular properties. Affected horses develop severe ulceration of the lining of the gullet (oesophagus) and of the first or oesophageal part of the stomach that is lined with tissue identical to that lining the gullet. This leads to partial or complete blockage of the gullet, interfering with swallowing of food and then water. Affected horses lick their lips, drool saliva, grind their teeth and drink water in small amounts. Appetite and thirst are increased as the disease worsens and food and water will be taken avidly. Severe cases with gullet obstruction make vigorous but vain swallowing attempts that end in regurgitation of food through the nostrils. This material may contain fresh blood. Coughing occurs during attempts at feeding and is frequent. The breath may be foulsmelling. There may be swelling of the neck above sites

~  Acute effects M  Delayed onset or chronic effects Plant sources of soluble oxalates included in this book are: Grasses: *Pennisetum ciliare (buffel grass) and *Setaria sphacelata (setaria). Forbs: *Acetosa vesicaria (ruby dock), *Acetosella vulgaris (sheep sorrel), *Amaranthus retroflexus (red-root amaranth), Atriplex muelleri (annual saltbush), †Beta vulgaris (beet), *Chenopodium album (fat hen), *Chenopodium murale (green fat hen), *Colocasia esculenta (taro), *Emex australis (spiny emex), *Mesembryanthemum crystallinum (common ice plant), *Mesembryanthemum nodiflorum (slender ice plant), *Oxalis pescaprae (soursob), Portulaca oleracea (pigweed), Portulaca sp. aff. oleracea (munyeroo), *Rheum × cultorum (garden rhubarb), Rumex brownii (swamp dock), *Rumex conglomeratus (clustered dock), *Rumex crispus (curled dock), *Salsola australis (soft roly-poly), *Trianthema portulacastrum (black pigweed) and Trianthema triquetra (red spinach) Shrubs: Enchylaena tomentosa (ruby saltbush), Neobassia proceriflora (soda bush ) and Sclerolaena calcarata (red burr). Trees: †Averrhoa carambola (carambola). There are many known plant sources of hazardous amounts of soluble oxalates in addition to those listed above (see Chapter 15). Acute oxalate poisoning results from eating plants containing large amounts of watersoluble forms of oxalates, typically those with greater than 2.0–2.5% soluble oxalate in the dry matter. Many plants of this type contain more than 10% soluble

46

Australia’s Poisonous Plants, Fungi and Cyanobacteria

oxalate. Oxalate ions bind avidly to calcium and this is the basis of the effects of poisoning. Ruminants (such as cattle, sheep and goats) are the victims of this type of poisoning. Poisoning of horses is extremely rare. Dogs and cats suffer a similar form of poisoning if they drink ethylene glycol used as anti-freeze for car radiators. Humans are sometimes poisoned. Calcium in blood is necessary for normal function of nerves and muscles. Poisoning removes most of this from the bloodstream (hypocalcaemia) because the absorbed oxalate binds the calcium. The resulting calcium oxalate occurs as crystals. The crystals may be formed in the wall of the rumen, but are usually formed in the kidney tubules, causing kidney failure sooner or later if the dose of oxalate was great enough. Soluble oxalate concentrations in plants are greatest in young actively growing leaves. Their concentrations are boosted by added nitrogen in soil through nitrogenous fertiliser application to crops and pastures or from manure in and around stockyards. Hungry animals that eat large amounts of hazardous plants quickly are the most likely to be poisoned. If ruminants have access to less-than-toxic amounts of soluble oxalates in plants, their rumen bacteria can adapt by increasing their capacity to use the oxalate as a nutrient source, thus preventing its absorption into the body. Such animals can safely eat plants that would poison unadapted animals. Poisoned animals are commonly found dead. Those seen affected have signs including difficulty with breathing, staggering or stiffness of the gait, collapse, coma and death without struggling. Some animals may have twitching of muscles and be overly sensitive to external stimulus such as touch or sound. Blood samples taken from affected animals will have only very small concentrations of calcium. Post-mortem examination reveals reddened and fluid-filled lungs, possibly reddening of the rumen lining and pale swollen kidneys. Diagnosis can be aided by measuring calcium, urea and creatinine in blood of live affected animals, by assay of soluble oxalates in plants being eaten and by microscopic examination of kidneys from dead animals for the presence of numerous calcium oxalate crystals in them. Animals affected by acute oxalate poisoning can be treated with intravenous or subcutaneous 25% calcium borogluconate solution: for sheep, give 50–­100 mL; for cattle, 300–500 mL. Additional fluids may help reduce the degree of kidney damage. All cases are at risk of dying from kidney failure days to weeks after the poisoning emergency despite successful treatment of the initial depressed blood calcium concentrations. Prevention of acute oxalate poisoning may

be helped by trying to establish and maintain adaption of the rumen flora to small oxalate intakes in feed. Human oxalate poisoning is rare, but can be serious when it happens. Cooking does not destroy toxicity. Effects of eating large amounts of rhubarb leaves by humans are abdominal pain (colic), diarrhoea and vomiting, persisting for several hours. There may be blood in the vomited stomach contents (haematemesis) and blood clotting may be impaired. The patient becomes very tired and produces only small volumes of urine (oligouria) that contains acetone and albumin. Jaundice has been seen in some cases. Reduced plasma concentrations of calcium (hypocalcaemia) and muscle twitching and convulsions can occur. In fatal cases, severe kidney damage (nephrosis) with deposits of calcium oxalate crystals is seen in tissue sections examined by microscope. These effects are essentially the same as those seen in poisoned domestic animals. The lethal dose of oxalic acid is thought to be about 10–15 g in adults and 5–10  g in children. Poisoned children have eaten 20–100 g of raw rhubarb leaves and stems. Excessive consumption of cooked rhubarb stalks by humans can lead to poisoning through interference with calcium absorption by the oxalates. Humans affected by rhubarb poisoning should immediately seek emergency medical attention. Livestock, particularly sheep, grazing certain oxalate-containing plants such as Oxalis pes-caprae (soursob) for months, may develop chronic oxalate poisoning, producing kidney failure seen as gradual loss of weight, excessive urine production (polyuria) and death in an emaciated condition. Annual death losses of up to 1% have been reported in sheep flocks grazing O. pes-caprae. Up to 25% of sheep in many of these flocks have been affected in south-western Australia during autumn and early winter, but only a few die. Protein in urine (proteinuria) may be the only sign in sheep early in the disease. Blood samples reveal evidence of kidney damage (azotaemia) and a low concentration of protein (hypoproteinaemia). Anaemia may be seen in 50% of affected sheep. Cobalt deficiency needs to be ruled out as an alternative diagnosis – loss of condition and anaemia occur in both syndromes. At post-mortem examination, kidneys are shrunken (‘half the normal size and weight’) and scarred (fibrotic – ‘pale and mottled’). Examination of sections of preserved kidney by microscope reveals chronic kidney damage with scar tissue (fibrosis), loss of tubules and blockage of tubules by many rosettes of birefringent calcium oxalate crystals. There is no treatment for chronic oxalate poisoning. Long-term grazing of plants with substantial soluble oxalate content, such as Oxalis pes-caprae, must be avoided.

3 – Common poisoning profiles

Oxalate: big head of horses from calcium oxalate crystals in grasses ∅  Effective therapy: calcium and phosphorus supplementation

N  Specific preventive measures available M  Delayed onset or chronic effects Plant sources of non-raphide oxalate crystals included in this book: Grasses: *Brachiaria decumbens (signal grass), *Megathyrsus maximus (Guinea grass), *Megathyrsus maximus var. pubiglumis (green panic), *Panicum coloratum (coolah grass), *Pennisetum ciliare (buffel grass), *Pennisetum clandestinum (kikuyu grass) and *Setaria sphacelata (setaria). Grasses that have been linked with big head cases or that contain enough calcium oxalate to be a hazard to horses include: •• Brachiaria brizantha (palisade grass), B. decumbens (signal grass), B. humidicola (koroniva grass), B. mutica (para grass) •• Cenchrus setiger (Birdwood grass) •• Digitaria eriantha [syn. D. decumbens, D. pentzii] (pangola grass) •• Megathyrsus maximus [syn. Panicum maximum] (Guinea grass), M. maximus var. pubiglumis [syn. P. maximum var. trichoglume] (green panic) •• Melinis minutiflora (molasses grass) •• Panicum coloratum (coolah grass) •• Pennisetum americanum [syn. P. typhoides] (pearl or bullrush millet), P. ciliare [syn. Cenchrus ciliaris] (buffel grass), P. clandestinum (kikuyu), P. polystachyon (mission grass), P. purpureum (elephant or Napier grass) •• Setaria incrassata (purple pigeon grass), S. italica (foxtail millet), S. sphacelata (setaria) •• Urochloa mosambicensis (sabi grass). Nutritional secondary hyperparathyroidism of horses is also known as big head because of the jaw swelling that occurs in severe cases. The changes produced in the bones are called fibrous osteodystrophy (osteodystrophia fibrosa) and osteoporosis. Only horses are affected by this particular disease while grazing pastures. Hand-fed horses given too much grain or grain by-products such as bran can also develop this disease. However, these cases happen because grains have not enough calcium, too much phosphorus and phytate (a

47

form of phosphorus present in grains), which interferes with uptake of calcium. Grains contain virtually no oxalate. Strictly speaking, this disease is an anti-nutritive condition, not a poisoning. This is because the horses affected are suffering a deficiency of calcium, not from the effects of an absorbed toxin. However, it seems reasonable to include it in a book of this type. Calcium oxalate crystals present in the leaves of many tropical pasture grasses bind up virtually all the calcium in the plant’s tissues. These crystals are not of the needle-like raphide type seen in other plants and described later in this chapter. For horses to absorb calcium from their feed, the calcium needs to be in a form able to be dissolved (soluble) in water. Calcium oxalate is not soluble in water under the conditions in the upper small intestine where calcium absorption takes place in horses, so they cannot extract calcium from these tropical grasses. If they have no other feed source of calcium, they must draw on the calcium in their bones to keep the critical concentrations of calcium steady in muscle and nerve cells so that their body can continue to function properly. This reaction is controlled by secretion of extra hormone by the parathyroid glands, four small organs in the neck of the horse. Because the stimulation of the parathyroid glands in these horses is prolonged and intense, the glands increase in size and activity – a state called secondary hyperparathyroidism. The increased amount of parathyroid hormone in the body reduces the loss of calcium from the kidneys in urine and boosts the rate of calcium removal from bones. Phosphorus is also lost from the body because it is removed from the bones in parallel with the calcium. Because there are unavoidable and continuous losses of calcium from the body in urine, sweat and dung, the bone reserves of calcium and phosphorus are slowly run down, weakening the bones. In most bones, such as those of the limbs, this process of bone resorption widens the normal microscopic canals through the bone producing the pathological state called osteoporosis. Where the bones support the cartilage linings of joints, cavities appear in the bone beneath the cartilage and wedges of joint cartilage drop down into them. This creates a pockmarked appearance in the usually smooth joint surface and probably contributes to the vague lameness that is commonly the first sign of the disease. In the bones of the jaws, the process of resorption is extreme. Most of the bone is removed. To try to maintain the strength needed in the jaw bones, the body produces large amounts of fibrous scar tissue where the bone once was. Because the innate strength of this material is much less than that of missing bone, much more is needed and local swelling occurs.

48

Australia’s Poisonous Plants, Fungi and Cyanobacteria

Weaned foals and nursing mares are most at risk of developing the disease because they are the horses with the greatest need for calcium in their diet. Hazardous grasses are those with a ratio of calcium to total oxalate content of less than 0.5 and these grasses usually have over 0.5% total oxalate in their dry matter. The disease occurs if horses continuously graze pure or near-pure swards of hazardous grasses for a prolonged period, usually more than 2  months. This is most likely to happen in the subtropical to tropical parts of Australia. Clinical signs are usually first a shifting lameness that may be just a stiffness of gait initially and loss of weight followed by generalised swellings of the jaws. The upper and lower jaws may be affected together or only the upper or only the lower jaw may be affected in individual horses. Some horses have a small swelling across the middle of the face just below the eyes. If the disease is allowed to progress, the horse may go down. Fractures occur much more easily than normal. The chance of recovery is negligible in horses with fractures or persistent recumbency. Nursing mares may develop eclampsia (milk ‘fever’ or hypocalcaemia). Remove affected horses to non-hazardous pasture if available. To restore the calcium and phosphorus content of the bones, feed a mineral supplement with its calcium and phosphorus content in the ratio of 2:1 at the rate of 2 kg of supplement in 3 kg of molasses for each horse each week and keep this up for about 6 months. This may seem like a very large amount of mineral, but remember that the aim is to replace much of the horse’s skeleton. Other carriers may be substituted for molasses if intake can be maintained. Some alternative supplements include: •• 2 kg of rock phosphate (with a fluorine content less than 2.0%) •• 2 kg of a mixture of one part ground limestone (CaCO3) to two parts dicalcium phosphate (DCP) [0.6 kg CaCO3 + 1.4 kg DCP]. Kynaphos may be substituted for DCP. •• 1.4 kg of dolomite + 1.4 kg of DCP. Supplements in molasses will be consumed in a few days, but provide sufficient calcium and phosphorus for the week. Commercial products are available formulated to deliver calcium and phosphorus in the ratio of 2:1 in sufficient amounts to prevent or treat this condition and do not require the mixing that the above formulas do. The use of injections of vitamin D or of calcium preparations alone is not enough to correct the problem, even though they may help a little. Adding calcium to horses’ drinking water alone is insufficient to meet their calcium needs because calcium cannot be dissolved in sufficient quantity, but any calcium from water will (of course) make a positive contribution to intake. This treatment method should

return the horse to normal form and function. Lameness resolves well. Horses with severe jaw swelling may have some swelling left after therapy, but most cases eventually return to normal. To prevent the disease: •• Graze horses on hazardous pastures for no more than 1 month at a time. •• Maintain a significant legume component in the pasture if possible. Legumes are good calcium sources. Unfortunately, legumes tend not to persist with vigorous grasses such as buffel grass and setaria, so this can be a hard option to achieve, although it is the best long-term solution in many cases. In buffel grass pasture, seca stylo (Stylosanthes scabra ‘Seca’) and butterfly pea (Clitoria ternatea) may prove useful in this role. •• Graze non-hazardous pastures, which include: –– Rhodes grass (Chloris gayana) –– paspalums (Paspalum spp.) –– couch grasses (Cynodon spp.) –– creeping blue grass (Bothriochloa insculpta) –– floren blue grass or Angleton grass (Dichanthium aristatum) –– temperate pastures grasses (Lolium, Phalaris, Festuca, etc.) –– all native grass species. •• If non-hazardous pasture is unavailable, feed half the supplement dose given above weekly for each horse (1 kg in 1.5 kg molasses) for as long as they are grazing the hazardous pasture. Supplying an equivalent amount of calcium and phosphorus from good quality lucerne would need 20 kg of lucerne for each horse each week.

Oxalate raphide crystals N  No specific therapy. Apply general decon-

tamination and supportive measures advised by a Poisons Information Centre, a medical practitioner or a veterinarian.

~  Acute effects Plant sources of oxalate raphide crystals included in this book: Forbs: Alocasia brisbanensis (cunjevoi), †Anthurium species and cultivars (flamingo flowers), *Colocasia esculenta (taro), †Dieffenbachia seguine (dumb cane) and *Zantedeschia aethiopica (arum lily). Vines: †Philodendron species and cultivars (philodendron). Microscopic needle-shaped crystals of calcium oxalate called raphides can be packed in bundles under pres-

3 – Common poisoning profiles

sure in specialised explosive ejector cells called idioblasts in the leaves of plants, particularly those in the arum family (family Araceae). When an animal eats the leaves, the crystals burst from the idioblasts and are driven into the mucous membranes of the mouth causing intense local irritation. The reaction may be due to the physical penetration by the crystals alone or this may be increased by the injection of other irritant chemicals at the same time. Children, dogs and cats and, to a lesser extent, canaries, cattle, horses and other plant-eaters are known to be affected by these plants. Young children, puppies and kittens explore their surroundings. Part of this exploration involves chewing objects within their reach and injury by these plants can result. Herbivores may eat them if they occur as weeds in pasture, such as arum lilies (Zantedeschia aethiopica), or if they gain access to gardens where the plants are cultivated. In domestic animals, damage is usually confined to the mouth and tongue and does not last long. The affected individual reacts to the local pain and may clutch or claw at the mouth. A profuse flow of saliva occurs. The lining of the mouth and tongue can become reddened and swollen. In some extreme cases, the swelling may extend into the throat and impede breathing, calling for professional emergency intervention. Otherwise the damage is self-limiting. In the very rare event that impeded breathing leads to death, post-mortem findings would include cyanosis of mucous membranes, fluid swelling (oedema) of the throat and larynx obstructing the upper airway and fine spot haemorrhages (petechiation) of the lining of the trachea. In humans, usually children, who chew or eat these plants, there is a burning sensation in the mouth, an increased flow of saliva and swelling of the tongue. This swelling can produce a sensation of suffocation and prevent swallowing. Lips can have a tickling sensation and become swollen and ulcerated. The burning sensation in the mouth may extend to the oesophagus and stomach and the patient can become feverish. The face may swell at the same time as the tongue or after some delay. In uncomplicated cases, healing normally takes 3 to 5 days, with some patients having swallowing difficulties or pins-and-needles (paraesthesia) of the tongue for 7 days. Pain in the mouth can persist for 4 to 5 days in some cases. Fatal cases in children have been extremely rare, but are more often reported than in domestic animals. They followed children eating flowers, leaves or stems of these plants causing the expected irritation and swelling of the lips, tongue and throat, but with severe stomach irritation, nausea and vomiting. Breathing difficulties (dyspnoea) have occurred in some cases. In others, there has been severe diarrhoea followed by death from exhaustion and shock.

49

Injuries have followed humans getting sap from Dieffenbachia plants in their eyes. There is acute pain, intense sensitivity to light (photophobia), bleeding in the conjunctiva and a temporary loss of clear vision. Healing takes 4 to 7 days. These plants have also caused contact dermatitis in humans with itching, reddening (erythema) and blistering of the skin (vesicular eruption). Professional medical or veterinary treatment to relieve the signs and symptoms of poisoning are needed only in severe cases. Anti-inflammatory drugs may help ease the effects. In rare cases, where there is swelling of the throat that blocks breathing, an emergency surgical incision into the windpipe (tracheotomy) is required. Prevention of poisoning is by recognising and removing potentially hazardous plants from the reach of young children and pets. Denying access of livestock to gardens and controlling those species that infest pastures will prevent intoxication of those species.

Phomopsin poisoning or lupinosis NNN  No effective therapy N  Specific preventive measures available:

immunogen (‘vaccine’) under development

M  Delayed onset or chronic effects Plant sources of phomopsin included in this book: Forbs: Lupinus species (cultivated and naturalised lupins). Phomopsins cause a poisoning called lupinosis: a mycotoxicosis. Lupinosis-associated myopathy (LAM) is a variation on the poisoning affecting skeletal muscles. Phomopsins are produced by the fungus Diaporthe toxica (previously incorrectly known as Phomopsis leptostromiformis), a saprophyte growing in dead lupin stubble remaining in the paddock usually after the harvesting of seeds from lupin crops. More rarely, phomopsins can occur in lupin seed itself. Phomopsins are linear hexapeptides; that is, molecules made up of six amino acids joined in a chain. Lupinosis affects sheep, cattle and rarely horses that graze lupin stubbles. It is usually fatal in sheep. Phomopsins accumulate in the body from small doses until poisoning occurs. They interfere with the mechanism of cell division. Affected sheep are lethargic and lose their appetite leading to weight loss. They are jaundiced and may be anaemic. Some may have photosensitisation. Those with LAM also are reluctant to walk, have a stiff gait and stand with their backs arched and their feet placed

50

Australia’s Poisonous Plants, Fungi and Cyanobacteria

under the body. Affected cattle have similar signs or may have ketosis. Affected horses are lethargic, lacking appetite, jaundiced and with signs of abdominal pain. They may have red urine (haemoglobinuria) and become recumbent. Post-mortem examination reveals either jaundice and a swollen pale liver or no jaundice and a shrunken firm liver. Excessive fluid may occur in the abdominal cavity (ascites). In LAM, muscles are pale. Microscopically, liver cells are destroyed (necrotic), fatty or halted in the midst of cell division. There is a build-up of scar tissue in parts of the liver (periportal fibroplasia and biliary ductular hyperplasia). In LAM there is destruction of skeletal muscle fibres. Treating affected sheep with selenium and α-tocopherol (vitamin E) together may be useful in LAM, but there is no effective treatment for lupinosis. Diaporthe-resistant types of lupins have been developed and these have greatly reduced the prevalence of lupinosis. Supplementing sheep with subcutaneous injections of 2000 IU a-tocopherol acetate (vitamin E) plus 0.1  g selenium as selenomethionine/kg body weight is the most effective prevention for LAM but does not prevent lupinosis. Dissolve the required amount of selenomethionine into 10  mL of an emulsion of a-tocopherol acetate in an aqueous detergent solution (200 g a-tocopherol acetate/L).

Photosensitisation Depending on the cause: ∅  Effective therapy is available: *Lantana camara (lantana) or

N  No specific therapy. Apply general decon-

tamination and supportive measures advised by a veterinarian.

N

  Specific preventive measures available: Hypericum perforatum (St John’s wort)

~  Acute effects M  Delayed onset or chronic effects þ  Toxins that cause the syndrome include:

hypericin, furanocoumarins, steroidal saponins, lantadenes, sporidesmin, phomopsins and certain tannins

´

  Toxins that cause the syndrome are unidentified in some cases Photosensitisation is not sunburn. It is due to an increased sensitivity of skin to sunlight of all wavelengths, not only ultraviolet as with sunburn. It has an immediate effect on skin, not the delayed effect seen

with sunburn. Unlike sunburn, it is not blocked by glass. The increased skin sensitivity is caused by particular chemicals, called sensitiser molecules, lodging in the blood vessel walls of the lower skin layer (dermis). These sensitiser molecules are changed (activated) by sunlight penetrating into the skin, making them highly chemically reactive with surrounding structures. Their immediate reaction with blood vessel walls and other tissues then causes the skin inflammation (dermatitis) that we see as photosensitisation. Penetration of sunlight into the skin is blocked by pigment (melanin) in the upper skin layer (epidermis), indicated by coloured skin and hair, or by a long hair coat such as thick wool in sheep. Only unpigmented (white) skin is affected. In newly shorn white sheep, the protective wool layer is removed, the skin of the body comes within the range of incoming light and photosensitisation can occur along the backline. There are two types of plant-induced photosensitisation: primary and secondary. These two types are distinguished from one another by their different sensitiser molecules and by either affecting (secondary) or not affecting (primary) the liver. Sensitiser molecules in primary photosensitisation are fluorescent plant pigments that lodge unchanged in skin blood vessels after being absorbed either from the gastrointestinal tract or directly through the skin. Only furanocoumarins directly penetrate the skin. In contrast, in secondary photosensitisation, the more common form by far, the only sensitiser molecule is always phylloerythrin. Phylloerythrin is produced in the intestines by bacterial breakdown of chlorophyll, the green pigment of plants, and any absorbed into the body is rapidly and completely excreted by the liver by passing it into bile. The several known plant toxins that start secondary photosensitisation do so indirectly by damaging liver cells or small bile ducts enough to disrupt the liver’s capacity to rid the body of phylloerythrin. Secondary photosensitisation is also known as hepatogenous photosensitisation because it starts with liver damage. The damage caused to liver cells or bile ducts is usually not enough to rapidly kill them and the animal, as occurs in acute liver necrosis cases as described earlier in this chapter. These liver-damaging toxins that lead to photosensitisation are lantadenes (terpenes), steroidal or lithogenic saponins, sporidesmin and phomopsins (mycotoxins) and certain tannins. Plant and fungal sources included in this book: Primary photosensitisation Forbs: hypericin in *Hypericum perforatum (St. John’s wort); furanocoumarins in *Ammi majus (bishop’s weed), †Apium graveolens (celery), Cullen patens (spreading scurf-pea), Cullen cinereum (hoary scurf-

3 – Common poisoning profiles

pea), †Pastinaca sativa (parsnip) and †Petroselinum crispum (parsley). Secondary or hepatogenous photosensitisation Fungi: sporidesmin in the mould fungus Pithomyces chartarum growing on dead pasture litter often in *Lolium perenne (perennial ryegrass) pastures; phomopsins in the fungus Diaporthe toxica growing in stubble or seeds of *Lupinus (lupin) crops. Grasses: steroidal or lithogenic saponins in *Brachiaria decumbens (signal grass), *Panicum coloratum (coolah grass), Panicum decompositum (native millet), Panicum effusum (hairy panic), * Panicum gilvum (sweet grass) and * Panicum miliaceum (French millet). Vines: steroidal or lithogenic saponins in Tribulus terrestris (caltrop). Shrubs: lantadenes (terpenes) in *Lantana camara (lantana). Trees: tannins in Terminalia oblongata (yellow-wood). Some cases of photosensitisation are caused by plants for which the toxins and even the type of photosensitisation are unidentified. Some of these plants are common crops that are normally beneficial, or at least harmless, but rarely and sporadically become toxic for poorly understood reasons usually described as ‘stresses’ of various kinds. Such plants include cereals (fodder wheat and fodder oats), fodder grasses such as *Sorghum × drummondii (Sudan grass), Brassica species used as fodder (canola, rape, kale and turnips), Persicaria species (smartweeds), Verbena species, the pasture legumes Medicago (medic) and Trifolium (clover) species (causing so-called ‘trefoil dermatitis’ or ‘aphis disease’) and several other plants, including species of Chamaesyce (caustic weeds) and Cucumis melo subsp. agrestis (Ulcardo melon). Photosensitisation usually affects grazing or browsing livestock (ruminants and horses), but cases do occur in pigs and birds. Young animals are particularly susceptible to steroidal or lithogenic saponin poisoning. Humans who frequently handle vegetable foodstuffs such as celery, parsley or parsnips have been affected occasionally by furanocoumarins directly penetrating skin coming into contact with such plants. Particularly susceptible skin sites in different animal species include the ears, eyelids, face, lips and around the top of hooves (coronets) in sheep, the teats, udder, escutcheon, muzzle and beneath the tip of the tongue in cattle, the snout in pigs and the beak, comb, wattles, legs and feet of fowls, ducks and geese. Affected skin is reddened (erythema) and there is often marked fluid swelling under the skin (subcutaneous oedema), sometimes with seepage of clear or yellow fluid through the inflamed skin. The fluid build up can lead to swollen drooping ears, swollen

51

lips and swelling of the whole head (particularly in sheep), with a raw weeping muzzle. The jaundice and fluid swelling has lead to the name ‘yellow big head’ for this condition in sheep. Cattle habitually lick their noses, exposing the underside of their tongues to sunlight. This area can be affected and sores (ulcers) can form beneath the tip of the tongue – in cattle with no white hair or skin, this and weeping eyes can be the only external sign of photosensitisation. Photosensitisation of the skin around the top of hooves (coronitis) may cause lameness, particularly in sheep. The eyes may be affected, causing repeated blinking (blepharospasm), discharges (conjunctivitis) and, in cases due to furanocoumarins, milky or bluish discoloration of the eyes – so-called ‘blue-eye’ (corneal oedema, keratitis or both), leading to blindness. Furanocoumarins can also cause blistering (vesication) of the skin and this is most serious on the snouts of pigs where it may be mistaken for the effects of the highly contagious exotic virus diseases foot-and-mouth disease, vesicular exanthema, vesicular stomatitis and swine vesicular disease. Humans affected by contact with some vegetables may also have skin blisters at the sites of contact. The skin and eye irritation of photosensitisation in domestic animals leads to such abnormal behaviours as restlessness, head shaking, rubbing, scratching, kicking at affected parts and seeking shade (photophobia). Photosensitised sheep may display bizarre behaviour on contacting water, such as at creek crossings or in plunge dips, presumably due to the very sensitive nature of their skin lesions, and this may interfere with mustering or handling of sheep so affected. This behaviour is not convulsive in the strict sense, but may appear so. In time, affected skin may die (skin necrosis) causing ear tips to curl up and lips to become immobilised in sheep, and beaks to become deformed in ducks and geese. In secondary (hepatogenous) photosensitisation only, there may be jaundice appearing as a yellow discoloration of mucous membranes, best seen in the whites of the eyes (sclera), the gums or the vulval lining in females. Not all cases will have detectable jaundice and assay of blood samples for bilirubin and liver cell-associated enzymes is needed to confirm the diagnosis. Specific treatment measures are given in the sections dealing with individual plants, such as Lantana camara. Importantly, managing photosensitisation incidents requires general measures as well, including the need to: •• Reduce or prevent exposure to sunlight by housing affected animals in farm buildings as a first choice or moving them to shady paddocks where they can shelter during the day and feed at night. Applying human sunscreens or home-made

52

••

••

••

••

••

Australia’s Poisonous Plants, Fungi and Cyanobacteria

alternatives (zinc oxide in lanolin) to unpigmented skin such as teats and udders of cattle may be considered. Sump oil should not be used because of the potential for poisoning from lead and other constituents and the risk of creating carcase residues. Offer non-green feed (with a minimum of chlorophyll in it) to minimise the production of phylloerythrin in cases of secondary (hepatogenous) photosensitisation. Remove animals from green feed and offer limited amounts of grain and good quality non-green hay in a shaded area with access to clean water. Important: This will not be useful in primary photosensitisation. Apply anti-inflammatory therapy in early cases. Antihistamines and corticosteriods have been used with good effect, but side effects, such as abortions induced by corticosteroids in cattle, need to be considered and managed by your veterinarian. Treat secondary bacterial infections of skin and eye lesions with medications applied directly to the affected skin or eyes or systemic antibiotics. In secondary (hepatogenous) photosensitisation, antibiotics excreted by the kidney are preferred to those excreted through bile. Restore and maintain hydration with oral fluid therapy. Electrolyte replacement solutions are preferred to water alone. Adult cows require a minimum of 20 L or 10% of their body weight daily. More severely affected animals will benefit from intravenous fluids. Provide nutritional support. Feed a limited amount of grain and good quality hay (see the above comments on chlorophyll). High-producing dairy cows may need treatment for hypocalcaemia (milk fever) and benefit from propylene glycol for reduced feed intake.

Pregnane glycoside poisoning N  No specific therapy. Apply general decon-

tamination and supportive measures advised by a Poisons Information Centre, a medical practitioner or a veterinarian.

~  Acute effects Plant sources included in this book that are thought to contain pregnane glycosides are: Vines: Hoya australis subsp. australis (wax flower), Sarcostemma brevipedicellatum (pencil caustic) and Sarcostemma viminale subsp. australe (pencil caustic).

Pregnane glycosides are closely chemically related to steroidal saponins, but have a quite different action on the body. They act on the central nervous system and are apparently speedily eliminated from the body. Some pregnane glycosides inhibit acetylcholinesterase activity. The oral lethal dose in sheep of cynafosides, a pregnane glycoside isolated from Cynanchum africanum from southern Africa, is about 4–12 mg/kg body weight. Sheep, cattle, pigs and horses have been poisoned by plants containing (or probably containing) these toxins. Toxic doses of these plants are given in the accounts of the individual plants. Clinical signs in poisoned animals are restlessness, then staggering, muscle tremors, vomiting in pigs and collapse onto one side (lateral recumbency), then a series of ongoing seizures or convulsions set in with running movements (limb ‘paddling’ or clonic seizures), muscle spasms causing clenching of the jaws and forceful extension of the neck and legs (tetanic seizures or opisthotonus), or both. Frothing at the mouth and saliva drooling occur. Breathing and heart rate speed up and laboured breathing sets in. Pigs may vocalise intermittently. Ruminants have distension of the rumen. Affected animals are over-sensitive to external stimuli such as touch and sound and these may set off the seizures. Side-to-side involuntary movements of the eyeballs (nystagmus) occur and the pupils may be dilated with no response to light. Death may take up to 7 days after signs first occur. There are no characteristic post-mortem findings. No effective treatment for poisoning is known. Prevention is by denying susceptible animals access to significant amounts of the plant sources when other feed is scarce.

Protoanemonin poisoning N  No specific therapy. Apply general decon-

tamination and supportive measures advised by a Poisons Information Centre, a medical practitioner or a veterinarian.

~  Acute effects Plant sources of protoanemonin included in this book: Forbs: †Helleborus species (hellebores), Ranunculus inundatus (river buttercup), *Ranunculus sceleratus subsp. sceleratus (celery-leaved buttercup) and Ranunculus undosus (river buttercup). The volatile oily irritant protoanemonin, the lactone of g-hydroxyvinylacrylic acid and a ‘hemiterpenoid’ lactone, is the hydrolysis product of the glycoside ranunculin. It is unstable and readily links to itself

3 – Common poisoning profiles

(dimerises) to produce the non-toxic crystalline anemonin on drying. The protoanemonin content of plants increases as they grow, peaking at flowering. Drying destroys toxicity as the protoanemonin is converted to the non-toxic anemonin, so dried plants contaminating hay do not cause poisoning. Poisoning is rare because plants in this group are unpalatable; to humans, they have an acrid taste. Poisoning of livestock, usually cattle or sheep, follows ingestion of fresh (flowering) plants when other feed is scarce. Palatability can be increased by herbicide damage. Cases can follow eating of plants in garden refuse. Humans can develop blistering of the skin on contact with the protoanemonin in plant tissues. Signs of poisoning in livestock start with excessive salivation linked with irritation of the mouth and tongue (stomatitis and glossitis), sometimes causing blisters progressing to ulceration. There are signs of abdominal pain and laboured breathing (dyspnoea). Reddening of the mucous membranes of the nose and fluid swelling of the muzzle (oedema) occur, indicating direct irritation of these structures. Some animals develop diarrhoea, with dark faeces, blood and mucus being produced by violent straining. There may be dark or blood-stained urine and frequent urination. Unusual signs have been impaired vision or blindness, abortion or photosensitisation (hepatogenous) (see ‘Photosensitisation’ earlier in this chapter). Fatal cases are rare; convulsions may precede death. Post-mortem examination reveals irritation of the stomach and intestines with haemorrhages, sometimes with ulcerations. There is no specific treatment for the poisoning. Decontamination and supportive measures, such as activated charcoal given by stomach tube and fluid replacement, may help.

Phyto-oestrogen poisoning (clover disease) NNN  No effective therapy N  Specific preventive measures available M  Delayed onset or chronic effects Plant sources of phyto-oestrogens included in this book: Forbs: Trifolium subterraneum (subterranean clover) and Trifolium pratense (red clover). Clover disease or clover infertility caused by phytooestrogens can affect sheep, and rarely cattle, grazing certain introduced legume pastures in southern Australia for long periods.

53

There are two types of phyto-oestrogens of concern to ruminant livestock. Formononetin from clovers is converted in the animal to the more active equol. These are very weakly active and need to be eaten for long periods to have any noticeable effect. Phosphorus-deficient soils can boost the phyto-oestrogen content of clovers. Coumestrol occurs in medics, including lucerne, and some clovers. These are at greatest concentration in stressed or damaged plants, such as those infected by fungi, where they act to defend the plant from attack (as phytoalexins). Both types act by mimicking the female hormone oestrogen, producing the effects of oestrogen overdose in the organs of the reproductive system in both sexes. Ewes grazing certain clovers can become permanently sterile and defeminised in severe cases. In these sheep, the lining of the womb (uterus) has its normal structure permanently changed as its cells proliferate rapidly and it develops many cysts within it (cystic hyperplasia of the endometrium). In the early stages, there can be difficulty giving birth to lambs (dystocia) either through lack of contraction of the womb (uterine inertia) or through failure of the neck of the womb (cervix) to dilate. Prolapse of the womb or massive fluid build-up in the womb (hydrops uteri) may occur rarely. Wethers grazing certain clovers develop enlarged teats and internal changes in their urinary tracts that may lead to blockage, with bladder rupture as the final outcome. Cattle grazing fungus-infected lucerne have developed problems with fertility including cyst formation in their ovaries, but this is rare. Treatment of affected animals is futile. Plant breeders have reduced the phyto-oestrogen content of clovers significantly over the decades since the problem first occurred. Severe clover disease no longer occurs, but there remains a small risk of mildly reduced fertility in sheep flocks grazed on them. Preventing problems involves ensuring adequate fertilisation of pastures and strategic grazing. Prime young breeding stock should be grazed on the least oestrogenic pastures. Genetic selection for more resistant sheep is possible. Research into immunisation techniques for sheep has not prevented the disease. Haymaking may reduce the concentration of phyto-oestrogens, but ensiling does not.

Psilocybin poisoning N  No specific therapy. Apply general decon-

tamination and supportive measures advised by a Poisons Information Centre, a medical practitioner or a veterinarian.

~  Acute effects

54

Australia’s Poisonous Plants, Fungi and Cyanobacteria

Fungal sources of psilocybin included in this book: Gymnopilus junonius (spectacular rustgill), Panaeolina foenisecii (brown hay cap), Psilocybe cubensis (golden top), Psilocybe semilanceata (liberty caps) and Psilocybe subaeruginosa (blue meanies). Hallucinogenic fungi have been sought and deliberately eaten by humans for religious, ceremonial and recreational reasons in many parts of the world, with psilocybin-containing species, particularly species of Psilocybe, prominent among them. Domestic animals may have been poisoned accidentally during these activities, but evidence has not reached the scientific literature. Animals voluntarily eating psilocybin-containing fungi without direct human involvement are on record in Europe, but not in Australia to date. Poisoning by these fungi is called psilocybin syndrome, mycetismus cerebralis, psychotropic poisoning, psilocybin/psilocin poisoning and hallucinogenic mushroom poisoning. Psilocybin (4-phosphoryloxy-N, N-dimethyltryptamine) is a tryptamine derivative and indole alkaloid related to LSD (lysergic acid diethylamide). It is converted to psilocin, a more potent hallucinogen, by the body after eating. Psilocin also occurs with psilocybin in living fungal tissue. Baeocystin and nor-baeocystin are other tryptamine-derived hallucinogens from species of Psilocybe. Bruising of tissues of fungal species containing psilocybin or psilocin (Psilocybe, Conocybe and Stropharia) results in blue or bluegreen discoloration at the site of damage that develops in 2–3 hours through enzyme action. The intensity of colour is not consistently related to psilocybin content. Blue discoloration in bruised species of Boletus results from a different chemical process and does not indicate the presence of psilocybin. As a general rule, gilled macrofungi with purplish-brown to black spores whose flesh bruises bluish are very likely to contain psilocybin. Humans either deliberately poison themselves or mistake the poisonous species for edible ones. Psilocybin oral toxic doses in humans are 4 mg, causing mild intoxication, and 6–20 mg, causing marked psychotropic changes. Raw or cooked fungi, or the liquor in which fungi are cooked, are all poisonous. Toxins are largely excreted in urine within hours of ingestion. Domestic animals such as dogs and horses have been poisoned in Europe through access to large numbers of fruiting bodies in pastures. Desired effects of deliberate human self-intoxication (euphoria, visual and auditory hallucinations) are often accompanied by undesirable ones (confusion, agitation, tremors, paranoia, palpitations, visual disturbances and respiratory difficulties). Onset of the undesirable effects occurs in less than an hour after ingestion and these include rapid pulse, dilated pupils

(mydriasis), blurred vision, restlessness, nausea, vomiting, laboured breathing, headache, difficulty with standing and walking and making incoherent or foolish remarks (‘drunkenness’), delirium to varying degrees, sometimes with uncontrollable laughter, visual aberrations of speed, light and colour, and sometimes acute panic from frightening mental disorientation. Poisoned horses have apparent hallucinations resulting in aggression (attacking their handlers) and fear reactions or periods of excessive sensitivity to stimulation such as touch (hyperexcitability), followed by periods of immobility either standing or lying down, muscle tremors, slight but persistent straining to pass dung (tenesmus), teeth-grinding, a moderately increased body temperature, rapid pulse and dilated pupils (mydriasis). Cases are usually not fatal unless misadventure intervenes during hallucinations, so post-mortem findings are not reported. Highly sensitive assay methods are available to detect psilocybin and psilocin. Urine is the specimen of choice for laboratory testing, but blood samples may be used. Observation of the patient is needed to prevent or manage dangerous behaviour. Spontaneous recovery usually occurs within 6–18 hours in humans. Domestic animals may need to be confined to a darkened room or stall. Sedation may be needed in some cases.

Pyrrolizidine alkaloidosis NNN  No effective therapy M  Delayed onset or chronic effects Plant sources of pyrrolizidine alkaloids included in this book: Forbs: *Echium plantagineum (Patterson’s curse), Trichodesma zeylanicum (camel bush) and species of *Amsinckia (ironweeds), Crotalaria (rattlepods), *Heliotropium (heliotropes), Senecio (fireweeds and ragwort) and †Symphytum (comfreys). Shrubs: species of Crotalaria (rattlepods) and Senecio (fireweeds). All species in these genera should be regarded as potentially poisonous until proven otherwise. The plant sources of pyrrolizidine alkaloids hazardous to animals mostly occur in the plant families Fabaceae [syn. Papilionaceae, Leguminosae] (the pea plants), Boraginaceae (borage and its relatives) and Asteraceae [syn. Compositae] (the daisies). Pyrrolizidine alkaloids (PAs) are among the most important toxins affecting livestock in Australia and the world. Their properties can directly damage human and domestic animal health and consequently they

3 – Common poisoning profiles

can strongly affect national and international trade in grain and livestock products. The disease they cause, pyrrolizidine alkaloidosis, is known by regional names such as ‘Kimberley horse disease’, by names referring to the plants involved such as ‘seneciosis’ (after Senecio spp.) and by names descriptive of the effects on animals, such as ‘walkabout disease’. About half the known PAs, of which there are several hundred recognised in plants, can damage the liver. Of these, some are lung-damaging and some are kidney-damaging as well. Individual PAs occur in plants in two forms: the alkaloids themselves and N-oxides in which an extra oxygen atom is attached to the ring of the alkaloid molecule. N-oxides are not toxic and, when they are absorbed from the intestines into the blood, they are easily removed from the body into urine by the kidneys. N-oxides can be changed to the toxic alkaloid forms in the intestines by the action of the bacteria there and so they do contribute to the overall toxicity of plants that contain them. Pigs are the most susceptible domestic animals to poisoning by PAs – say they have a resistance rating of 1. They are followed in increasing order of resistance by poultry (with a resistance rating relative to pigs of 5), cattle and horses (each rated at 15) and finally sheep and goats (each rated at 150). Humans are susceptible, but poisoning is rare. PAs are dangerous toxins because they are cumulative, building up in the body over time until the damage that they cause is severe enough to show up as illness. Usually this illness is permanent and very often fatal. The build up of the toxins may occur over months to years, depending on the species of animal and the species and amount of plant eaten. For example, a horse may not become ill from grazing on Crotalaria crispata or Crotalaria ramosissima in the Kimberley region in the dry season until months later in the wet season; typically, ‘Kimberley horse disease’ occurs during January–April. Similarly, a sheep flock in southern New South Wales may graze a hazardous pasture containing Heliotropium europaeum in one season with few ill effects, but if grazed on it for a second season most of the flock may succumb to poisoning from the burden of 2 year’s toxin intake. In another complicating twist to the story, it can take months for a single toxic dose of PAs taken in over one or a few days to produce visible disease in animals. Experimentally, calves have taken 18  months to become ill after a single toxic dose of PAs. Because PAs are changed by the liver from the form in which they were absorbed from the gastrointestinal tract into highly chemically reactive forms (pyrrolic metabolites), the liver is where most of the dose stays in the body and is usually the organ most

55

damaged by their presence. In some cases, other organs may be damaged severely. Some plants contain PAs that damage the lungs. In pigs, the main damage occurs in the kidneys and the liver is mostly spared. Small amounts may enter the milk and rarely they may cross the placenta to damage the foetus. PAs are regarded as potential carcinogens. The pyrrolic metabolites of PAs kill some liver cells directly, stop surviving liver cells from dividing so that they continue to grow in size becoming enormous (the so-called megalocytes) and can damage blood vessels. These effects are slow in onset and result in a chronically damaged organ with much scar tissue and greatly diminished numbers of greatly enlarged cells. Plants containing hazardous quantities of PAs are not usually very palatable and so are not readily eaten by domestic animals. There are three main circumstances that promote consumption: a lack of alternative wholesome fodder, such as during droughts or the dry season in northern Australia, the contamination of hay or silage by PA-containing plants, and the contamination of feed grains such as wheat or sorghum by seeds of PA-containing plants harvested with them. Humans have been poisoned through weed seed contamination of grain and through consumption of herbal teas made from PA-containing plants such as comfrey (Symphytum spp.) and Crotalaria spp. (rattlepods). Poisoning takes weeks to months after the plants are eaten for signs to appear. This can make it very hard to identify the source of the poisoning, because the offending plants often die and disappear from the pasture before the animal becomes ill. The poisoning lasts for weeks. The dominant effects in horses are loss of body weight to the point of emaciation and death because the liver (kidneys in pigs) fails to work properly through loss of cells and scarring. Other common consequences of this can be persistent diarrhoea and straining to pass dung, dullness and persistent yawning (‘dummy syndrome’), constant compulsive walking or galloping (hence the name ‘walkabout disease’), blindness, leading to collisions with objects and skin wounds to the face, neck, chest and forelegs, or pressing of the head against solid obstacles, muscle tremors, irritability and, in some cases, jaundice. Importantly, affected horses can be very dangerous for persons trying to handle or restrain them because they can suddenly become highly excited and aggressive and lash out in a deranged manner. The changed behaviour of affected animals is due to effects on the brain from chemicals released to the general blood circulation by the damaged liver. A range of less common consequences of poisoning may occur in horses, including fluid build up under

56

Australia’s Poisonous Plants, Fungi and Cyanobacteria

the skin (subcutaneous oedema) of the chest, belly and legs, photosensitisation, rupture of red blood cells in the bloodstream (haemolysis) showing up as red urine (haemoglobinuria), paralysis of the larynx, the tongue or both, and impaction of the stomach. In a syndrome called ‘jaagsiekte’ (an Afrikaans word meaning ‘driving disease’ and referring to the increased severity when horses are exercised) in horses poisoned by some Crotalaria species, fever (intermittent and not present in all cases), cough, a sudden increase in the rate of breathing to 100–120 breaths/ minute, difficulty with breathing (dyspnoea), wheezing (rales), noisy breathing (stridor) and increased heart rate occur and sometimes air bubbles appear under the skin (subcutaneous emphysema). Cattle are less dramatically affected and usually suffer from weight loss and persistent diarrhoea with straining. Some may have behavioural change, including blindness, and some may have lung damage with difficulty breathing (dyspnoea). Sheep, once they become affected, besides the chronic effects of liver failure, have an increased tendency to accumulate copper in their livers. Once a large amount of copper is stored, stresses of various kinds can trigger its massive release into the bloodstream where it immediately ruptures red blood cells (causes haemolysis) and kills the sheep very quickly. This is called ‘toxaemic jaundice’: a dramatic effect of chronic copper poisoning. This is often linked to poisoning by Heliotropium europaeum (common heliotrope) or Echium plantagineum (Patterson’s curse). Sheep or goats that rapidly eat large amounts (about 10–15 g fresh plant/kg body weight) of certain species of Crotalaria can develop an ‘acute lung damage’ syndrome in which they collapse and die rapidly (in about 15 minutes) within 24 hours of eating the plant after having difficulty breathing (dyspnoea) and blueing of the lips and gums (cyanosis). Post-mortem examination reveals wet heavy lungs, with foam in the major airways (pulmonary oedema) and excessive volumes of fluid in the chest cavity (hydrothorax) and around the heart (hydropericardium) that may clot when exposed to air. Rarely, calves can develop this syndrome as well (doses of 25–80 g/kg). Rarely, acute liver necrosis (described earlier in this chapter) has followed a rapid intake of large amounts of seed from some species of Crotalaria. Humans poisoned by PAs also suffer liver failure, often resulting in build up of fluid in the abdominal cavity (ascites or dropsy) at the same time as emaciation occurs. Post-mortem examination in typical cases reveals a wasted carcase without fat reserves and usually a liver distorted by scar tissue. There may be an excessive

volume of fluid in the abdomen. Microscopically, the organisation of the liver is highly disrupted, with the number of liver cells greatly reduced and their size greatly increased – so-called megalocytosis. This is accompanied by much scar tissue, often around blood vessels in what is called ‘veno-occulusive disease’, and an over-growth of small bile ducts. In some cases, individual liver cells appear to escape the influence of the toxins and form growing groups of normal cells called regeneration nodules. In cases of ‘jaagsiekte’ in horses, the lungs fail to collapse when the chest is opened at the post-mortem examination and there are scattered thickened and reddened zones (atelectasis and congestion), and thickened fluid-filled partitions between lung segments (oedematous interlobular septa). There may be air bubbles in these partitions (interstitial emphysema) and fluid may have accumulated in the chest (hydrothorax) and in the sac enclosing the heart (hydropericardium). Microscopic examination of lung tissue reveals overgrowth of the lining cells of small airways (multifocal hyperplasia of bronchiolar epithelium), inflammation and scarring. Some ‘jaagsiekte’ cases may also have the liver and kidney abnormalities of the more common syndrome. There is no effective treatment for this disease. Some affected animals do recover, but they are likely to have significant scarring of their livers and tend to be always susceptible to relapse if stressed. Preventing consumption through weed control and pasture improvement are the major avenues of control. In the past, grazing hazardous pastures with sheep or goats to remove sources of PAs before allowing access to cattle or horses was a popular method of control, but, although more resistant than cattle and horses, sheep and goats will be poisoned if they eat enough PAs, so this method has lost favour for ethical and chemical residue reasons. Herbicide control of weed sources of PAs may be economical in some situations. For some of the major weeds containing PAs, insect and fungal biological control agents have been introduced and are reducing the impact of this poisoning in some parts of Australia. Screening toxic weed seeds from feed grains is often effective, but can be expensive. Legislated regulations intended to deter the sale of dangerously contaminated grain for human or livestock feed are not totally effective and in some seasons serious livestock poisoning can occur from this source; thousands of poultry and pigs have been killed this way in some seasons. Attempts to protect cattle from poisoning by transferring rumen microbes to them from sheep have been successful in experiments, but this approach probably has only limited application under natural conditions because sheep themselves

3 – Common poisoning profiles

are never totally protected. All other attempts to protect animals from poisoning through immunisation, manipulation of rumen flora or breeding for resistance have failed so far.

Selenium poisoning (chronic selenosis) N  No specific therapy. Apply general supportive measures.

M  Delayed onset or chronic effects Plant sources of selenium included in this book: Forbs: Neptunia amplexicaulis (selenium weed). Vines: Morinda reticulata (mapoon). Plants that accumulate hazardous amounts of selenium in Australia store it combined within the non-protein amino acid selenocystathionine. They can build up these stores from soils of normal selenium content. Morinda reticulata commonly contains over 200 mg of selenium per kg dry matter. Neptunia amplexicaulis can contain over 4000 mg/kg. Horses are most likely to be poisoned by plantbased selenium in Australia, but cattle and sheep are also susceptible. Poisoning occurs when seleniumaccumulating plants form a large part of the diet of grazing animals, such as when Morinda reticulata produces young palatable shoots first after fire has removed other pasture components or when Neptunia amplexicaulis grows densely after soil disturbance. Cattle, horses and sheep fed diets containing 5–40 mg Se/kg in dry matter for over 30 days develop signs of poisoning. Cattle fed diets containing 0.28 or 0.8 mg Se/kg in the form of selenomethionine or 0.8 mg Se/kg in the form of sodium selenite for 4 months develop mild to severe forms of poisoning. In poisonous amounts, selenium replaces sulphur in the chemical structure of sulphur-containing amino acids. Because sulphur-containing amino acids are important in the construction of keratin, the protein from which hair and hoof wall are formed, the substitution of selenium for sulphur disrupts the protein structure and interferes with the normal production of hair and hoof wall. Selenium-poisoned horses lose the hair from their mane and the tail and go lame because their hooves crack. In severe poisoning, hooves may be shed completely. Only these skin structures are affected. There is no internal damage in horses. Fleeces can spontaneously fall off some sheep in a flock that grazes a lot of N. amplexicaulis. Some poisoned sheep

57

can die rapidly, with no abnormalities found during post-mortem examinations. No specific treatment is available. Supplementary feeding should be provided during times when selenium-accumulating plants dominate a pasture.

Senna poisoning (muscle damage) NNN  No effective therapy ~  Acute effects ´  Toxin that causes the syndrome is

unidentified

Plant sources of Senna muscle damage included in this book: Shrubs: *Senna obtusifolia (sickle pod) and *Senna occidentalis (coffee senna). Senna poisoning damages muscle tissue, including heart muscle. Seeds are the poisonous part of these plants and animals eating large amounts of seed pods are most likely to be poisoned. The toxin responsible for this syndrome is unidentified. It is suspected that it may be dianthrone (an anthraquinone-derived compound), but this needs to be confirmed. It is thought that whatever the responsible toxin is, it causes damage to the energy-producing system of cells and that this particularly damages muscle cells because of their large demand for energy. Natural cases of poisoning are known mostly in cattle, but cases are also known in pigs, horses, sheep, goats and captive gemsbok (Oryx gazella). Experimental poisoning has been produced in cattle, sheep, goats, rabbits, rats and poultry. Poisoning of dogs has followed their scavenging of the carcase of a beast that died from the effects of Senna occidentalis. This is called a secondary poisoning. Signs of poisoning are muscle weakness, leading to a stiff, then a stumbling gait. The affected animal goes down and is unable to rise to its feet or to stand if helped to its feet. The urine is discoloured red because the muscle breakdown releases myoglobin, the red pigment from muscle cells. This enters the blood and is lost through the kidneys. Some affected animals die suddenly if their heart muscle is sufficiently affected. The anthraquinone glycosides in seed pod tissue causes diarrhoea in affected animals. Testing of blood samples reveals very large amounts of enzymes leaking from damaged muscle tissue (creatine phosphokinase and aspartate aminotransferase). Post-mortem examination reveals very pale muscles and a pale heart, and red

58

Australia’s Poisonous Plants, Fungi and Cyanobacteria

urine in the bladder. Microscopic examination of preserved sections of muscle tissue reveals death (necrosis) of muscle fibres in large numbers. There may also be microscopic evidence of pancreas necrosis and liver necrosis. Investigators should rule out other causes of red urine including babesiosis of cattle (‘red water’) and copper poisoning of sheep and goats. There is no effective therapy for this poisoning. Dosing with selenium and vitamin E may make it worse. Management relies on preventing animals eating large amounts of seed pods (or seeds) by denying them access. Herbicides are one option for removing plants from pastures. Biological control agents are being evaluated for Senna obtusifolia in Australia.

Simplexin poisoning NNN  No effective therapy M  Delayed onset or chronic effects Plant sources of simplexin included in this book: The forbs Pimelea elongata, Pimelea simplex subsp. continua, Pimelea simplex subsp. simplex (desert rice-flower) and Pimelea trichostachya (flax-weed) are the main causes of this syndrome. Other shrubby species of Pimelea have caused the disease occasionally. Those included here are Pimelea latifolia subsp. altior and Pimelea neo-anglica (poison pimelea). Simplexin poisoning or Pimelea poisoning is more commonly called St George disease (named after the town in southern Queensland) or Marree disease (named after the town in northern South Australia). It is also known in some areas as flax-weed poisoning and big head disease. The last name refers to the fluid swelling of the head and should not be confused with similarly named diseases such as photosensitisation of sheep or nutritional secondary hyperparathyroidism of horses. Simplexin, a highly irritant chemical (a diterpene ester related to phorbol esters), is the main toxin in the source plants, but they do contain smaller amounts of other such chemicals. Flowering plants contain the most toxin. Poisoning occurs in southern Queensland, north-western New South Wales, north-eastern South Australia and, rarely, in the southern Northern Territory. Pimelea plants are very unpalatable, only being eaten as a last resort and then causing severe diarrhoea. Overstocking of pastures, soil disturbance through cultivation or fire can promote the growth of Pimelea plants to dangerous densities. Pimelea density is usually greatest where pasture density is poorest, but they can persist in dense grass growth, such as in sown

Pennisetum ciliare (buffel grass) pastures. Pimelea plants are most likely to cause poisoning if they are growing intermingled with pasture grasses, stopping cattle from avoiding them. Most poisonings result from breathing in or swallowing fine plant particles, including plant hairs, during flowering and after the plants have died and disintegrated. Simplexin is very stable and persists in this dead plant material that contaminates the dust of infested paddocks and the surfaces of other pasture plants. Dead Pimelea stalks may also be eaten if mixed closely with other pasture plants. Most poisoning occurs during August to December in years when more winter rain than normal promoted the growth of Pimelea plants in large numbers and was followed by less spring–summer rain than normal or by drought. The reduced spring–summer rains fail to adequately wash the dry Pimelea particles from the pastures and to promote their breakdown by soil microbes. Some cases can occur at any time of year. Cattle bear the brunt of this poisoning. Usually more than 3 weeks (21 days) exposure is needed before signs of poisoning are seen. The shortest time recorded between introduction of cattle to a toxic pasture and onset of clinical signs is 12 days. The smallest oral dose known to cause poisoning experimentally in cattle is 15  mg of dry plant/kg body weight/day; for a 400  kg beast, that is 6  g of dry plant daily – a very small amount of plant. Many affected cattle develop a poorly working heart (circulatory dysfunction) causing distended pulsing jugular veins in the neck and massive fluid build-up in the chest (thorax), the brisket and the head. The swellings of the brisket and head can cause spectacular deformity in individual cattle. This aspect of the poisoning results from persistent constriction of the small veins in their lungs, increasing the blood pressure. This expands and weakens the right side of the heart and thereby distends the jugular veins in a flow-on effect. Simultaneously it causes leakage of fluid from the lung blood vessels into the chest. The chest fluid then flows out under the skin to the brisket and down the neck to the head. Persistent diarrhoea from direct irritation of the intestines by the toxins also afflicts many cattle and chronic anaemia, seen as pale gums, also develops in poisoned cattle. The way the anaemia develops is not fully understood. The volume of the fluid part of the blood (the plasma volume) increases, but the rate of production of red blood cells by the bone marrow does not increase in step with this. The reason for this lack of response of the bone marrow is not known. So, the red cells are diluted, causing anaemia (watery blood). The poorly working heart, seen most clearly as the fluid swellings, and the diarrhoea can be present in varying degrees in each affected beast. Some animals will have a poorly

3 – Common poisoning profiles

working heart without diarrhoea and others diarrhoea without serious heart problems. Cattle with diarrhoea rapidly lose weight to the point of emaciation and are more likely to die. Sudden death can occur in affected cattle, particularly if strenuously exercised. In the worst-affected cattle, death can occur within 10–14 days of their becoming ill. Very rarely, horses can develop the disease if exposed to large amounts of the plants. Grazing livestock other than cattle usually only develop diarrhoea, but horses have rarely been affected by the full syndrome. The irritant effects of these toxins have been reported to affect humans handling the plants. Finely chaffed or ground-up P. trichostachya is extremely irritant to the eyes and nose of people handling it. Post-mortem findings in cattle are dominated by large volumes of fluid in the chest cavity, a distended right ventricle of the heart and a swollen blue-black liver distended with blood. The liver change is called peliosis hepatis and is unique to livestock poisoned by Pimelea plants, except for some very rare unrelated disease conditions in humans. It is important to remember that the plants responsible for the poisoning may not be recognisable in the pasture at the time that animals are affected. There is no effective specific treatment (‘antidote’) for this poisoning. Treatment of the diarrhoea with anti-scour drenches and fluid therapy can be useful. Diuretics have been used to improve the condition, but should not be thought of as a cure, because they treat only some effects of the poisoning. Effective management of a poisoning incident is by gentle and prompt removal of the herd from the pasture on which they were poisoned as soon as diarrhoea, pulsing distended jugular veins or signs of fluid swelling are seen. Move them to pasture on a different soil type known to be free of Pimelea, to cultivated fodder crops free of Pimelea or to hand-feeding in yards. Most affected cattle will completely recover if separated from the source of the toxin. Cattle should not be returned to hazardous pastures until after enough summer rain has fallen to produce strong pasture growth. ‘Enough’ rain is generally accepted to be 25–50 mm. One attempt to produce an immunogen (‘vaccine’) to prevent this poisoning failed. Even a successful immunogen would be very unlikely to be commercially viable. Future research will probably concentrate on means to reduce the density of Pimelea plants in cattle pastures. The current estimate of the smallest average concentration of Pimelea plants likely to trigger poisoning in cattle is fewer than five plants/m2. Making an accurate estimate is difficult, complicated by the naturally uneven distribution of the plants, among other factors. Cattle have grazed pastures with more

59

than this amount of Pimelea without being poisoned. No matter what the Pimelea density, graziers need to avoid overstocking pastures in which Pimelea plants grow and to avoid soil disturbance (particularly ploughing) to prevent their density from increasing. There is no good evidence that fire reduces Pimelea density. Herbicides may be useful under certain conditions, such as in fallowed paddocks between crops, but their use in pastures is costly and needs further research before specific recommendations can be made. A detailed discussion of options available to manage this poisoning is in the booklet Understanding Pimelea Poisoning of Cattle (Fletcher et al. 2009).

Steroidal glycoalkaloid poisoning N  No specific therapy. Apply general decon-

tamination and supportive measures advised by a Poisons Information Centre, a medical practitioner or a veterinarian.

~  Acute effects Plant sources of steroidal glycoalkaloids included in this book: Forbs: †Solanum tuberosum (potato). Shrubs: Solanum quadriloculatum (wild tomato) and Solanum sturtianum (Sturt’s nightshade). All species of Solanum should be considered as potential sources of poisonous amounts of these compounds unless proven safe, but very few actually cause poisoning. Glycoalkaloids are part of plants’ defences against insects, snails, slugs and fungi, and may also give the Solanum plants an advantage by suppressing the germination and growth of competing plants. In Australia, poisoning by glycoalkaloids has probably been given more weight than is justified by the available evidence, with certain exceptions such as Solanum sturtianum and S. quadriloculatum. This may be because of the poisonous reputation of many members of the nightshade family (Solanaceae) in Europe, including Atropa belladonna (deadly nightshade), and the misidentification of local Solanum species with it. It should be remembered that certain species of Solanum are important human food plants – potato (S. tuberosum) and eggplant or aubergine (S. melongena). Australian Aboriginal people use the ripe fruits of species such as S. centrale as a major food source (‘bush tucker’) in the arid zone. Unripe fruits of Solanum plants are usually their most poisonous parts, but all green parts may be poisonous. Toxic doses of these plants are given in the

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Australia’s Poisonous Plants, Fungi and Cyanobacteria

accounts of the individual plants. Hungry travelling or grazing livestock are the usual victims of poisoning. Humans and livestock can also be poisoned by eating potato tubers that have sprouted or have been stored in light and become green. The time from ingestion to onset of signs is usually some hours (up to 24 hours). These toxins are not well absorbed from the digestive tract and normally cause only non-fatal colic and severe diarrhoea, with vomiting in those species capable of it. Faeces may contain mucus and blood. If large amounts of the plants are eaten, some of the dose of toxins may be absorbed, then red blood cells may be ruptured (haemolysis) leading to red discoloration of urine (haemoglobinuria, ‘red water’) and brain function may be depressed causing stupor, but these effects are rare. Even more rare effects seen can include slobbering or drooling of saliva, dilated pupils in the eyes, laboured breathing, heart irregularities, fluid build-up in body cavities, muscle twitching and seizures. Humans poisoned by potatoes mostly have colic, nausea, vomiting and diarrhoea, and then recover. The more severely affected may have various combinations of restlessness, delirium, visual disturbances, drowsiness, extreme lethargy, weakness and prostration, laboured breathing and coma. Deaths are very rare. Post-mortem findings may include inflammation of the digestive tract. Treatment for the usual type of poisoning (diarrhoea) should include replacement of lost fluids and may need adsorbants such as activated charcoal or bentonite. Glycoalkaloids are not fully destroyed by ensiling (or cooking, in the case of potatoes). Potato haulms (the green above-ground parts of the plants after tuber harvest) have been successfully ensiled and fed to ruminants. In one study, the total glycoalkaloid content of haulms from nine different potato cultivars varied from 630 to 2660 mg/kg dry matter. After ensiling, total glycoalkaloid content varied from 230 to 2730  mg/kg dry matter, so it is wise to be cautious if using this method.

Stypandrol poisoning NNN  No effective therapy M  Delayed onset or chronic effects Plant sources of stypandrol included in this book: Grass-like herbs: Stypandra glauca (blind grass) and rhizomes of species of †Hemerocallis (day lilies). Stypandrol is a bisnaphthalene tetrol. Stypandrol has affected sheep, goats, cattle, horses and poultry that

have eaten Stypandra glauca as a flowering plant or as young shoots after winter rains; 300 g of young shoots has been toxic to sheep. Humans have been poisoned after taking large doses of Chinese herbal medicines containing Hemerocallis (day lily) ‘roots’ (rhizomes). The toxin attacks the integrity of the insulating membranes surrounding the nerve fibres in the nerves of the eyes (optic nerves) and in the brain, producing fluid build-up within the fibres (intralamellar myelinic oedema) and interfering with nerve conduction. Large doses produce blindness, incoordination and death within 5 days. Survivors have permanent blindness with dilated pupils in the eyes. The optic nerves and the retinas are destroyed. There is no effective treatment known. Prevention of poisoning by S. glauca is through denying susceptible animals access to the plants when there is little wholesome pasture available.

Sulphur poisoning ∅  Effective therapy: thiamine (vitamin B1). Early intervention is essential for a positive outcome.

~  Acute effects M  Delayed onset or chronic effects Plant sources of significant concentrations of sulphur included in this book: Forbs: †Beta vulgaris (beet), †Brassica napus (rape), †Brassica oleracea (kale), †Brassica rapa (turnip), *Chenopodium album (fat hen), *Raphanus raphanistrum (wild radish), *Rapistrum rugosum (turnip weed) and *Sisymbrium irio (London rocket). Sulphur poisoning may be called ‘rape blindness’ and sulphur-associated polioencephalomalacia (PEM). Some authorities consider that ‘rape blindness’ is a separate syndrome caused by an unidentified toxin. An alternative term for PEM is cerebrocortical necrosis. PEM in ruminants can have other causes such as lead, salt or thiaminase poisoning (as described later in this chapter), or cobalt deficiency. Only ruminants are affected by this syndrome. Cattle are the usual victims, but sheep, goats and alpacas have been affected. Any of these animal species with more than 40% forage in their diet are at risk of developing this syndrome if their whole diet contains more than 0.5% sulphur. When assessing the sulphur content of diets, it is important to include both feed and water in the calculations (see Box 3.1 for a method of calculating the total sulphur content of a diet). In practice,

3 – Common poisoning profiles

Box 3.1. A method for calculating the contributions of water (%Sw) and feed (%SF) to the total sulphur intake of cattle (total S content in dry matter) To calculate the water S contribution (%Sw): •• water S content may be reported by analytical laboratories as either S or SO4 in ppm (= mg/L). Convert SO4 to S: mg SO4/L divided by 3 = mg S/L. •• daily water intake in litres (L) for beef cattle = 8%, 10% and 18% of body weight in kilograms (kg) for ambient temperatures of 5°C, 21°C and 32°C, respectively. •• daily water intake for lactating beef cattle = 10%, 15% and 15% of body weight (kg) for ambient temperatures of 5°C, 21°C and 32°C, respectively. •• water intake (L) × mg S/L = daily S intake (mg). Divide by 1000 = daily S intake in grams (g). •• daily dry matter (DM) intake = 2 to 3% of body weight in kilograms (kg). Daily total S intake (g) divided by kg dry matter intake divided by 10 = %Sw on a dry matter basis. To calculate the feed S contribution (%SF): •• S concentration in feed is usually reported by analytical laboratories as %S in dry matter (DM). •• for more than one feed component, multiply the %S in DM for each by the proportion of the diet that it represents. Then add these figures for all components to give %SF. Then the total S content in the diet on a dry matter basis = %Sw + %SF. if ruminants graze pastures heavily dominated by such plants continuously for more than a week, they are at risk of developing this syndrome. Not all exposed animals will be affected. Sulphur-associated PEM in grazing ruminants is not common. This syndrome is more likely to occur in cattle in feedlots within 3 weeks of introduction to diets dominated by grain, in which case more than 0.35% sulphur in the diet can be enough to trigger it. Molasses is a rich source of sulphur. The way that sulphur causes the brain damage of PEM is not fully understood, but probably involves hydrogen sulphide (H2S or rotten egg gas) generated by bacteria in the rumen. This gas is belched up and breathed in by the animal and then appears to

61

interfere with blood supply to the brain. There may also be destruction of thiamine (vitamin B1) by sulphur in the rumen: a similar effect to that of thiaminase poisoning (as described later in this chapter). Cattle may die suddenly without first appearing ill, or be found dead in the paddock. Others will stop feeding and be lethargic before collapsing. Difficulty with breathing (dyspnoea) and blueness (cyanosis) of gums may be seen in these acute cases. There may be a smell of rotten eggs on the breath. Cattle that do not die rapidly are depressed and commonly have ­episodes of excitement. They behave in a manner suggesting blindness by walking into obstacles and not responding to sudden movement or being approached quietly. They may stand with their head pressed against solid obstacles or try to walk through fences. They may walk aimlessly or in circles and finally collapse in convulsions before dying. Some affected animals may survive without treatment, but permanent blindness is likely. The effects on sheep are similar. The smell of rotten eggs may be noticed when the rumen is opened during post-mortem examination of a fresh carcase, but will disappear a few hours after death. No other reliable changes helpful to diagnosis are seen in the carcase. There may be changes to be seen in the brain during post-mortem examination, such as swelling and patchy discoloration of the cerebral hemispheres, but these can be subtle and should not be relied on for diagnosis. Microscopic examination of the whole brain, removed and preserved in formalin then sent to a diagnostic laboratory, is needed to find the characteristic changes of polioencephalomalacia. Prompt and early treatment of affected animals is vital for a good outcome and is best given by a veterinarian. If the animals are on their feet and eating and drinking, moving them to a low-sulphur diet can lead to partial to full recovery. Moderately to severely affected animals should be given 10–20 mg thiamine (vitamin B1)/kg into a vein twice or three times on the first day, followed by the same dose into a muscle twice a day for 2 to 3  more days. If animals do not respond to thiamine, euthanasia should be considered. Extra drugs to reduce brain swelling (cerebral oedema) and control seizures may be justified in valuable animals. Corticosteroids and diuretics may be helpful. Seizure control may be tried with other drugs (diazepam or barbiturates). Note that corticosteroids may cause abortion in pregnant cattle. Young animals that survive episodes of polioencephalomalacia with some evidence of brain damage may still be capable of productive life, including reproduction, if conditions are favourable.

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Australia’s Poisonous Plants, Fungi and Cyanobacteria

Sulphur-containing organic compound (SMCO and others) poisonings N  No specific therapy. Apply general decon-

tamination and supportive measures advised by a veterinarian.

M  Delayed onset or chronic effects Plant sources of sulphur-containing organic compounds included in this book: Grass-like herbs: †Allium ampeloprasum (leek), †Allium cepa (onion), †Allium sativa (garlic), †Allium schoenoprasum (chives), *Allium triquetrum (three-cornered garlic), †Allium tuberosum (garlic chives) and *Allium vineale (crow garlic) Forbs: †Brassica napus (rape), †Brassica oleracea (kale), †Brassica rapa (turnip), *Raphanus raphanistrum (wild radish), *Rapistrum rugosum (turnip weed) and *Sisymbrium irio (London rocket). This type of poisoning may be called kale anaemia or onion poisoning. The source chemicals in the plants leading to poisoning are either the amino acid S-methylcysteine sulphoxide (SMCO) or prop(en)yl disulphides (including N-propyl disulphide) and thiosulphates, depending on the plant involved. Both of these contain a large amount of sulphur. SMCO is changed by bacterial action in the forestomachs of ruminants to dimethyl disulphide, the actual toxin in poisoning by Brassica plants. Plants in the Brassica family can poison cattle, sheep and goats, with signs occurring after 1 to 3 weeks of continuous access. Dried plants remain toxic. Dogs, cats, horses and cattle may be poisoned by members of the onion family (Allium species). Cattle fed 7 kg of onions each daily have been poisoned. Dogs have been poisoned by single meals of 600 to 800 g of raw onion, by feeding raw onions at 11–15 g for each kg of body weight for several days and by diets containing 7% raw garlic. Cats have been poisoned by 112 g of raw onion each daily for 3 days. Horses have been poisoned by 0.4 g of garlic for each kg of body weight fed for 4 days. Sheep and goats can be highly resistant to onion poisoning. Cooking onions or their relatives does not destroy their capacity for poisoning and kitchen scraps and human meal residues (e.g. pizza, mince and Chinese recipes) containing onion-type vegetables are hazardous for dogs and cats. Effects can be seen within a day of consumption. The toxic compounds damage the haemoglobin molecules and other proteins in red blood cells and ultimately cause premature removal from the

circulation and rupture of damaged red blood cells (haemolysis). Affected animals have red urine (haemoglobinuria), lose their appetite, are weak and lethargic and have pale mucous membranes from blood loss. Some affected animals may also die suddenly or have jaundice, increased heart rate or diarrhoea. Pregnant females may abort. Damaged red blood cells contain so-called Heinz bodies. There may be evidence of liver and kidney damage in serum assays. Post-mortem examination reveals very dark red to black kidneys, dark red-brown urine and, in some cases, jaundice. Animals diagnosed early enough will survive, recovering over a period of weeks. Onions should not contribute more than 25% of cattle diets.

Swainsonine and calystegine poisonings NNN  No effective therapy N  Specific preventive measures available M  Delayed onset or chronic effects Plant sources of swainsonine and/or calystegine included in this book: Forbs: Swainsona brachycarpa (small-flowered Darling pea), Swainsona canescens (grey Swainson pea), Swainsona galegifolia (smooth Darling pea), Swainsona greyana (Darling pea), Swainsona luteola (dwarf Darling pea), Swainsona procumbens (Broughton pea) and Swainsona swainsonioides (downy Swainson pea). Vines: Ipomoea muelleri (poison morning glory) and Ipomoea polpha subsp. weirana (Weir vine). Poisoning by swainsonine can be called ‘pea-struck’, Darling pea poisoning or Weir vine poisoning, depending on the source of toxin. In North America, poisoning by the same toxin is called locoism, as in ‘loco’ from Mexican Spanish meaning crazy. Microscopic fungi (endophytes) growing harmlessly within the tissues of some locoweeds (Astragalus species) in North America have recently been recognised as producing swainsonine. Similar endophytes have been found in samples of S. canescens plants from Australia. It is possible that these fungi are the actual source of these toxins, but further research needs to be done to confirm this. Swainsonine and calystegines are polyhydroxylated alkaloids of the indolizidine and nortropane classes, respectively. Swainsonine blocks the processing of the sugar mannose by cells by inhibiting the action of the enzyme α-mannosidase, so that mannose builds up in

3 – Common poisoning profiles

numerous tiny spherical structures (lysosomes) in the body (cytoplasm) of the cells in most tissues and so interferes with cell function. The affected lysosomes swell to produce a foamy appearance in the cell cytoplasm. This has its greatest effect in the brain, but can be seen microscopically in white blood cells, the liver, heart and many other organs. Calystegines inhibit other sugar-handling enzymes, including β-glucosidase and α-galactosidase, producing a build-up of other sugars (such as glucose and galactose) in cells. Horses are about twice as susceptible to poisoning as sheep, goats or cattle. Plants containing these toxins are palatable and may form the bulk of edible material in a pasture under some conditions. Those containing 0.001% or more of swainsonine are capable of poisoning livestock if they are eaten over a prolonged period. Horses need to eat these plants continuously for at least 2 weeks to be affected and ruminants for 4 weeks. Species of Swainsona or Ipomoea are at their most dangerous in spring and early summer after winter rains have caused them to sprout, but follow-up rains have failed to produce adequate grass growth. Floods in autumn–winter and drought-breaking rains can also trigger hazardous growth. Animals will selectively graze Swainsona plants and seem to actively seek them among the available forage, behaviour tantamount to addiction. Affected animals lose weight (some sheep progress to emaciation and death without nervous signs), are sleepy until disturbed or have staring eyes and ‘stargaze’, with the nose pointed skywards, head shaking or tremor, and press their heads against obstacles. They are uncoordinated, with an arched back and a paddling or staggering gait with legs widely spread. If chased, affected animals’ hindquarters get progressively lower until they collapse. They have muscle tremor and are easily over-excited (hyperexcitable), displaying erratic manic behaviour when handled (particularly in horses). This can be dangerous to persons trying to handle affected horses. Difficulty with grasping and chewing feed and reduced fertility including abortion are also seen in some cases. Weir vine-poisoned animals may pass urine frequently. Calves, lambs and cats drinking milk from cows or ewes fed the locoweed Oxytropis sericea in North America – a plant that poisons through its content of swainsonine – have also been poisoned. Post-mortem examination reveals only emaciation. Microscopically, tissue cells are filled with numerous fine globules containing mannose and other sugars and giving the cell substance a foamy appearance. This is particularly evident in the large cells (neurones) of the brain and in white blood cells. Animals dying of Weir vine poisoning may have kidney damage (nephrosis).

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There is no effective treatment available. Affected animals can recover if removed from access to the plants and if the brain damage is not too far advanced. Non-pregnant cattle and sheep can be grazed on infested pasture for up to 4 weeks without serious poisoning and horses for 2 weeks. After this, spell all stock for 4 weeks before re-exposing them to the plants. Heavy stocking rates for short periods to reduce the swainsonine intakes of individual animals, while eating out the plants may be effective in some circumstances. Preventing poisoning under seasonal conditions where the plants in question are abundant requires hand feeding with alternative wholesome fodder or agistment of livestock until desirable pasture plants have again become dominant. Animals that develop ‘addiction’ to eating the plants need to be physically separated from them as soon as possible.

Tannin poisoning NNN

  No effective therapy. Apply supportive measures advised by a veterinarian.

~  Acute effects M  Delayed onset or chronic effects Plant sources of poisonous tannins included in this book: Trees: species of †Quercus (oaks) and Terminalia oblongata (yellow-wood). Forbs: Lythrum hyssopifolia (lesser loosestrife) poisoning is suspected to be caused by these toxins. Tannins are very common chemical compounds in plants. Most are condensed tannins and these are usually not poisonous. Hydrolysable tannins are usually poisonous, but much less common, occurring only in dangerous amounts in a few species of trees. Oak, oak bud or acorn poisoning and yellow-wood poisoning (Mackenzie River cattle disease) result from cattle, and sometimes sheep, goats or horses, eating large amounts of these plants that contain usually hydrolysable tannins. Large intakes of hydrolysable tannins are required before poisoning occurs. Toxic doses of these plants are given in the accounts of the individual plants. For oaks, the young green leaves and the acorns are the most poisonous parts. Seasons producing large crops of acorns are particularly hazardous. For yellow-wood, root suckers or fallen trees are the most dangerous. The common site of primary damage from hydrolysable tannins is the kidneys. Secondary effects are seen in the gastrointestinal tract as a result of the damage to kidneys. Yellow-wood poisoning in its

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Australia’s Poisonous Plants, Fungi and Cyanobacteria

early stages affects the liver as well, and this appears to be caused by a hydrolysable tannin, punicalagin, while the kidney damage from this plant is caused by a condensed tannin, terminalin (at least in part). Affected animals lose appetite, become dehydrated and progressively lose body weight. They pass large volumes of urine (polyuria) that contains protein and sometimes blood. Urine is commonly passed frequently. The hairs around the vulva or prepuce may be matted with chalky deposits from the urine. They may have diarrhoea with mucus, again sometimes containing blood or appearing very dark or black (melena). There may be fluid swelling of the tissues around the anus (perineal oedema), and fluid may accumulate in the abdomen (ascites, dropsy) and brisket. Death may take 1 to 4 weeks from the time of onset of the illness. Some animals recover completely. Animals suffering the early stages of yellow-wood poisoning may be jaundiced and have photosensitisation. Post-mortem examination reveals damaged kidneys that appear swollen and pale early in the disease or shrunken and distorted late in its course. They may be blue, slate grey or a grey-green colour. Erosions and ulcers occur at various places in the lining of the gastrointestinal tract. Numerous acorns may be found in the stomach contents of oak-poisoned animals. Brown pigment may be seen in ulcerations of the abomasum in yellow-woodpoisoned cattle. The urinary bladder wall and lining may be thickened and inflamed. The liver of yellowwood poisoned animals may be swollen, pale and jaundiced early in the disease. There is no specific treatment for poisoned animals. Circumstances that may allow animals to eat large amounts of these tannin sources in a short time should be avoided. Adequate alternative wholesome feed should be made available to animals at risk to reduce oak or acorn intake. Adding calcium hydroxide at 5–15% to a diet containing toxic amounts of tanninladen plants has prevented poisoning in calves and goats. Laboratory studies with tannins from T. oblongata indicated that calcium hydroxide was more effective at binding its tannins than activated charcoal, polyvinylpyrolidone (PVP) or the two proteins casein and pepsin. To date, this approach has not been tested in the field against yellow-wood poisoning. Polyethylene glycol (PEG) has been suggested as a detoxifying agent to be fed with oak leaves to ruminants at a dose of 10  g or more daily for each animal. Traditionally, clays were mixed with acorn meal before being eaten by the indigenous people of Sardinia and California and this reduced the tannin content by as much as 77%. A modern equivalent could be bentonite or other commercially available clay minerals.

Thiaminase poisoning ∅  Effective therapy: thiamine (vitamin B1). Early intervention is essential for a positive outcome.

M  Delayed onset or chronic effects Plant sources of thiaminase included in this book: Ferns: Marsilea drummondii (nardoo), Cheilanthes sieberi (mulga fern or rock fern), Cheilanthes distans (woolly cloak fern) and Pteridium esculentum (austral bracken). Thiaminase is an enzyme (a protein) in some ferns that destroys thiamine (vitamin B1) in the gastrointestinal tract of animals that eat them in quantity. The lack of this vitamin leads to damage to the brain, most often seen in horses and sheep, but sometimes in cattle. The outcome is called bracken staggers in horses. The technical name for the disease in sheep and cattle is polioencephalomalacia or cerebrocortical necrosis, a condition that can have other causes such as lead, salt or sulphur poisoning or cobalt deficiency in these species. Pigs can be poisoned by thiaminase, but this is rare. In contrast with other animals, pigs suffer from heart failure when poisoned. Lush young fern fronds have the greatest amounts of thiaminase present. Grazing animals are at risk if large amounts of ferns are available in pasture, such as on inland floodplains dominated by nardoo. Horses may eat dangerous amounts of bracken in pasture, if it contaminates hay or if it is used as bedding. Pigs have been affected by digging up and eating the underground stems (rhizomes) of bracken. Animals need to eat the ferns for several days to weeks, depending on the amount of thiaminase present. Nardoo is the richest source, followed by C. sieberi, with about one quarter as much, and bracken with 100 times less than nardoo. The final ill-health and death of the leaders of the Burke and Wills expedition in central Australia in 1861 has been blamed partly on thiaminase in nardoo flour. Thiamine deficiency in humans is commonly called beri-beri and has several forms affecting either the peripheral nerves (dry beri-beri), the heart (wet beri-beri), the brain (Wernicke-Korsakoff syndrome) or all three in sequence. Some of the clinical signs described by William Wills are consistent with dry beri-beri, but his condition was also the result of general starvation (see Box 6.1). Poisoned horses have severe incoordination of gait made worse by exercise. Typically, their hind legs are

3 – Common poisoning profiles

placed far apart. Other signs include lack of appetite, low carriage of the head, head nodding and ear twitching, yawning and a tendency to overexcitement. Heart beats are fast and irregular. Blindness and rapid sideto-side movements of the eyeballs (nystagmus) may occur. Finally, the horse collapses in convulsions and death occurs from 2 to 10 days after illness began. Poisoned sheep separate from the flock and wander aimlessly or stand motionless. They are apparently blind and may have nystagmus and ‘star-gaze’ or press their heads against obstacles. There may be teethgrinding with frothing of saliva. There may be muscle tremors. Occasionally, they will shake their heads and this becomes more vigorous after they go down. Collapse is followed by convulsions, particularly if handled. Death usually occurs in 2–4 days after illness begins. If forced to exercise, sheep develop breathing difficulties, collapse and die in 6–12 hours. Poisoned pigs lose their appetite and become listless. Their heart function is affected causing slowing (bradycardia) and abnormal rhythms (heart block). Difficulty with breathing (dyspnoea) may occur. Death may be sudden or take 2 –14 days after signs first appear. Post-mortem examination of horses can reveal signs of heart failure such as excessive fluid around the heart and in the chest. Microscopically, there may be damage to heart muscle fibres. Post-mortem examination of sheep is marked by degenerative changes (polioencephalomalacia) in the main brain lobes (cerebral cortex), which may be hard to recognise without using a microscope. Sometimes affected areas have a yellowish discoloration, but this should not be relied on for diagnosis and the brain needs to be preserved for laboratory examination. Post-mortem examination of pigs may reveal signs of heart failure including an enlarged mottled heart, and excessive amounts of blood (congestion) in the lungs and liver. Horses that have not gone down stand a good chance of recovery if treated promptly. Intravenous injections of thiamine (vitamin B1) are required for several days to reverse the effects. Affected sheep and pigs should also be given intravenous or subcutaneous injections of thiamine. Affected flocks present problems of logistics and cost for ideal multiple treatments, so, under practical conditions, if sheep do not respond favourably to two treatments, euthanasia is recommended. Significant numbers can be expected to respond to single subcutaneous thiamine injections if they have not been affected for more than 24 hours. See the account of sulphur-associated polioencephalomalacia earlier in this chapter for more details of treatment of valuable individual animals.

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Toxalbumin poisoning N  No specific therapy. Apply general decon-

tamination and supportive measures advised by a Poisons Information Centre, a medical practitioner or a veterinarian.

~  Acute effects Plant sources of toxalbumins included in this book: Vines: Abrus precatorius (gidee-gidee) contains abrin. Shrubs: *Ricinus communis (castor oil plant) contains ricin and *Jatropha curcas (physic nut) contains curcin. Trees: *Robinia pseudoacacia (black locust) contains robin. Toxalbumins are proteins. Their molecules are much larger than most other plant toxins and comprise two peptide chains often linked through two sulphur atoms (a disulphide bridge). Their method of poisoning is to interfere with the construction of proteins in animal cells, leading to the cell’s death. Seeds or bark are the main sources of these toxins. Poisoning is rare. Humans and all species of domestic mammals have been affected. Birds are relatively resistant. Unbroken Ricinus communis or Abrus precatorius seeds are said to pass through the gut without releasing toxin, but if toxin is released, the consequences can be severe (so do not risk it!). One Ricinus communis seed contains enough toxin to be potentially fatal for a dog or an adult human. The fatal dose of R. communis seed for horses is 0.1 g/kg body weight; one seed weighs about 0.25  g, meaning that 45  g or about 180 seeds are a lethal dose for a 450 kg horse. Half of one ripe Abrus precatorius seed is potentially fatal for an adult human. Sufficient heat (cooking) chemically denatures these toxins, making them harmless. Feed grains contaminated with Ricinus communis seeds have poisoned livestock. Livestock that chew the bark of Robinia pseudoacacia trees have been poisoned. Children (and adult humans) who chew and swallow seeds of these plants are at risk of poisoning. In poisoned animals, there is a delay of a few hours to a few days between eating the toxin source and onset of clinical signs of poisoning. The main effects are colic (severe abdominal pain) and severe diarrhoea with dysentery (blood in the faeces) in some cases. Nausea, repeated vomiting, weakness, inability to stand, shock, rupture of red blood cells (haemolytic anaemia), kidney failure and circulatory collapse are also described in poisoned humans, as are bleeding into the eye (retina) and from mucous membranes. At necropsy, the stomach and intestines are inflamed and

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Australia’s Poisonous Plants, Fungi and Cyanobacteria

there can be damage to the liver and kidneys (degeneration or necrosis) and haemorrhages throughout the body, and swelling of lymph nodes and spleen. Treatment is non-specific in most cases through oral dosing with replacement fluids and adsorbants such as activated charcoal or bentonite. It is possible to immunise animals against ricin and abrin, but this has no practical application in preventing poisoning. The best option is to prevent consumption of these plants.

Tremorgen poisonings N  No specific therapy. Apply general decon-

tamination and supportive measures advised by a veterinarian.

N

  Specific preventive measures available: for perennial ryegrass staggers

M  Delayed onset or chronic effects Plant and fungal sources of tremorgens included in this book: *Lolium perenne (perennial ryegrass) containing the endophyte Neotyphodium lolii and *Claviceps paspali (paspalum ergot) infecting seeds of species of Paspalum grasses. Tremorgens are toxins (lipid-soluble complex substituted indoles) produced by fungi (mycotoxins). These toxins generate muscle tremors in animals, hence the name ‘tremor-gen’. They include lolitrems and paspalitrems. Lolitrems are produced by strains of the endophytic fungus Neotyphodium lolii inhabiting Lolium perenne (perennial ryegrass) and cause perennial ryegrass staggers. The highest concentrations of fungus occur in leaf sheaths towards the base of the plants and in flowering stems, reaching maximum density in late summer. Fungal endophytes can only be detected by microscopic examination or culture of the plant in a laboratory. Paspalitrems are produced by paspalum ergot (Claviceps paspali) infecting the seeds of species of Paspalum pasture grasses and cause paspalum staggers. Ergot alkaloids are not responsible for this tremorgenic syndrome. Sheep, cattle, deer, alpacas and horses are known to be susceptible. Poisoning follows access to infected pastures. Perennial ryegrass staggers usually takes 1–2 weeks to occur after access and most cases are seen on well-cropped pastures, particularly under dry conditions in summer and autumn. Hay and seed screenings from toxic perennial ryegrass can cause poisoning. In one experiment, a toxic dose of paspalum ergots for cattle was 1.0–5.0 kg fed for 2–6 days. Clinical signs from both tremorgen sources in affected animals are markedly increased if the animals are disturbed by handling or forced exercise such as

mustering. Animals left undisturbed may appear normal. Signs include restlessness and an increased sensitivity to external stimuli, with muscle tremors, head weaving or nodding the earliest indications of poisoning. Exercise provokes incoordination of gait, staggering and high-stepping (hypermetria) progressing to collapse with struggling and limb spasms in usually unsuccessful attempts to regain their feet. These animals recover rapidly if left alone. There may be drooling of saliva. Post-mortem findings are not specific or helpful for diagnosis. There is no specific therapy for this syndrome, but tranquilisers may be useful in some circumstances. Gentle removal from the infected pasture is usually sufficient to bring about recovery in 2–10 days without the need for drug treatments. Very few animals should die of this syndrome. Toxic perennial ryegrass pastures should be managed so that animals are not forced to graze the lower parts of the pasture during summer and autumn. AR1 endophyte-infected perennial ryegrass does not produce lolitrems but retains the protection from insect attack provided by other chemicals produced by the endophyte. Establishing pastures with ‘non-toxic’ endophytes requires herbicide application and cultivation of toxic endophyte-infected pasture to kill plants and bury toxic ryegrass seed produced from natural re-seeding during the summer before sowing the replacement non-toxic strain. Paspalum pastures prone to ergot infection can be heavily grazed during their summer growth period to try to reduce the density of seed-heads available for infection. Slashing or mowing an ergotised Paspalum pasture will remove most of the infected seed-heads, but those remaining can still be toxic for months.

Tropane alkaloid poisoning ∅  Effective therapy: physostigmine. Early intervention is essential for a positive outcome. Apply general decontamination and supportive measures advised by a Poisons Information Centre, a medical practitioner or a veterinarian.

~  Acute effects Plant sources of tropane alkaloids included in this book: Forbs: †Atropa belladonna (deadly nightshade). Shrubs: †Brugmansia × candida (angel’s trumpet), †Brugmansia sanguinea (red angel’s trumpet), *Datura ferox (fierce thornapple) and *Datura stramonium (common thornapple). Trees: Duboisia leichhardtii (corkwood), Duboisia myoporoides (corkwood) and Duboisia leichhardtii × D. myoporoides (hybrid duboisia).

3 – Common poisoning profiles

These alkaloids all have a similar action in the body. They include atropine, scopolamine (= hyosine) and hyoscyamine. The toxins affect the brain and the autonomic nervous system (sympathetomimetic action) that regulates the normal functions of body organs. All animal species, including humans, are susceptible to poisoning. Green Datura plants are usually unattractive to animals and are rarely eaten. Duboisia plants have been browsed by cattle and horses. Seeds of Datura plants (thornapples) commonly contaminate grain intended for stock feed and this is the most likely way that domestic animals are exposed to poisoning. Dried Duboisia plants grown as a source of pharmaceuticals can poison humans and pet animals during processing, often through inhalation of dust. Tropane alkaloid-containing plants may be deliberately used as hallucinogens by humans. Some of these people die of this poisoning. Poisoning produces a depressed appetite in cattle that have eaten Datura seeds and this may prevent deaths by limiting the dose they receive to non-lethal amounts. The pupils become dilated (mydriasis) and vision is impaired. In humans exposed to Duboisia dust, this may be called ‘cork-eye’ after the common name of the plants – corkwood. The nose and mouth become dry. Bloating, colic, constipation and straining to defecate (tenesmus) may occur. The heart rate rises (tachycardia) and, in pigs and humans, the visible pale skin is flushed. There is significantly increased thirst and decreased urination. Respiration is depressed. Restlessness, tremors, extreme agitation, heightened aggression, visual disturbances, disorientation, delirium and hallucinations are reported by affected humans. In fatal cases, convulsions and paralysis precede coma and death. Post-mortem examination may not reveal significant abnormalities. In some cases, there may be haemorrhage in the stomach and intestines (haemorrhagic gastroenteritis). Rupture of the stomach has been seen in horses. Physostigmine is an ‘antidote’ for poisoning by tropane alkaloids and needs to be given under medical or veterinary supervision, combined with other treatment measures. Opiates are contraindicated when treating tropane alkaloid poisoning.

Urushiol poisoning N  No specific therapy. Apply supportive measures advised by a medical practitioner or a veterinarian.

~  Acute effects Plant sources of urushiols included in this book: Trees: Grevillea dimidiata, Grevillea mimosoides and Grevillea pyramidalis (caustic bushes).

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The word urushiol is derived from the Japanese word kiurushi meaning the lacquer from the Japanese lac tree (Toxicodendron vernicifulum), which is used as a finish on furniture and artefacts. The name was first applied to the mixture of irritant chemicals isolated from the lac tree. Later, similar urushiols were found in poison ivy, poison oaks and sumac (other species of Toxicodendron) in North America. Plants that contain urushiols often exude a resinous juice (sap) when damaged that turns black and hardens on exposure to air and is a potent source of the urushiols. Urushiols (alkyl and alkenyl phenols) are oily resinous substances that are chemically derived from catechols, resorcinols, phenols and salicylic acid. Their molecules are simple 6-carbon ring structures with one or two hydroxyl groups and a long unbranched side chain, commonly containing 15–17 carbon atoms. Victims of damage from these chemicals are usually humans. On rare occasions, birds, pigs, dogs, horses and cattle have been affected. Goats appear to be able to eat at least some of the plant sources of urushiols without suffering any damage. The first human cases of the toxic effects of urushiols in Australia were recorded by Ludwig Leichhardt during his 1844–45 expedition from Moreton Bay, Queensland, to Port Essington, Northern Territory. His party were affected by a Grevillea, probably G. mimosoides (caustic bush), and Semecarpus australiensis (native cashew). Susceptibility varies between individual humans. Humans can become sensitised to contact with urushiols and then suffer serious allergic reactions from very minor exposures. Many people may not be sensitive and suffer no ill effects. Problems in sensitive people result from direct skin or mucous membrane contact with the plants or their sap or sawdust. Indirect skin or mucous membrane contact with sap on objects that have come into contact with the source plants can cause damage. If leaves or fruits are eaten, there may be serious gastric upset, even death, but this is very rare. A toxic dose is not a concept easily applied to cases where contact dermatitis is the main effect of poisoning. Any contact with sap or exudate should be considered potentially harmful. Affected individuals suffer intense irritation, an itchy (pruritic) rash and swelling (oedema) at points of skin contact with plants or sap, followed by blistering (vesication, vesiculobullous eruption) and oozing (exudation) of serum that dries to scales and crusts. Ulcers may form at points of contact in severe cases. The skin of the arms, legs, face and torso are commonly affected, in descending order of frequency. Blindness may be caused by sap contacting the eye. Painful burning of the lips and tongue can follow tasting a plant source. Pigs that are affected by eating source plants have blisters of the snout and tongue that can be mistaken for the effects of the serious exotic virus diseases foot and

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Australia’s Poisonous Plants, Fungi and Cyanobacteria

mouth disease, vesicular exanthema, vesicular stomatitis and swine vesicular disease (see also ‘Photosensitisation’ earlier in this chapter). Haemorrhages have been described in the stomach lining and intestines of poisoned pigs. In human cases, immediate and thorough washing of affected skin with soap will remove the toxin and occasionally prevent subsequent dermatitis. Protective clothing should be used before handling known sources of urushiols.

Wamps N  No specific therapy. Apply supportive measures advised by a veterinarian.

M  Delayed onset or chronic effects ´  Toxin that causes poisoning is unidentified Plant sources of this syndrome included in this book: Grass-trees: Xanthorrhoea fulva (swamp grass-tree), Xanthorrhoea johnsonii (northern forest grass-tree), Xanthorrhoea quadrangulata (yacca), Xanthorrhoea semiplana (yacca) and Xanthorrhoea australis (yacca). Mat-rushes: Lomandra longifolia (spiny-headed mat-rush). ‘Wamps’ (or ‘womps’), the name given to poisoning of cattle by Xanthorrhoea plants in Queensland, imitates the sound made by an affected animal hitting the ground after falling over. Poisoning occurs in Queensland, New South Wales, South Australia and Tasmania. It is also known as ‘cripples’, wallum or coastal disease and yacca poisoning. Xanthorrhoea are called yaccas in South Australia and Tasmania. They should not be confused with yucca plants (species of Yucca) from America that are grown in gardens in Australia. Wallum is the local name for coastal sandy heath land in Queensland, with its original vegetation containing Banksia aemula (wallum banksia). Neither of the names coastal disease nor wallum disease is quite accurate because cases do occur in inland areas as well. The toxin responsible for wamps is unidentified. Only cattle have been affected by Xanthorrhoea plants, but sheep can be affected by Lomandra plants as can cattle. Flower spikes are the most toxic part of Xanthorrhoea plants, but eating large amounts of leaves has caused cases. Xanthorrhoea leaves are palatable and readily eaten by sheep, cattle and other animals. It is not known if flowering Lomandra plants are more toxic than non-flowering ones, but their leaves appear to be eaten by cattle from time to time. One curious feature of poisoning in some cases is the delayed appearance of

clinical signs, which may be up to 12 weeks after the last time Xanthorrhoea were eaten. Wamps is usually reversible, in contrast with zamia staggers (later in this chapter) that produces a similar effect but is irreversible. Experimentally, the smallest dose to cause poisoning occurred in cattle fed the stalks of X. johnsonii flower spikes and was 1.45 kg daily for 32 days: a total intake of 46.3 kg at 7.6 g/kg/day. Wamps causes animals to lose weight and develop a consistent sideways lurching of the hindquarters to one particular side in any one affected animal (posterior ataxia). Affected animals fall easily and struggle to regain their feet. They hold their tails high and frequently or continuously dribble urine (urinary incontinence). Some cattle feeding on X. johnsonii have developed cataracts – opaque lenses in the eyes – that make them blind if it is severe enough. There are no significant changes useful for diagnosis to be seen at necropsy. Some animals have mild damage to the white matter of the spinal cord and parts of the brain that can only be seen microscopically (Wallerian degeneration). Affected animals should be nursed by providing adequate feed and water. Animals that are down need to be regularly moved and checked to prevent pressure sores (decubitus). Recovery occurs in 2–3  weeks in most cases.

Zamia staggers NNN  No effective therapy M  Delayed onset or chronic effects ´  Toxin that causes poisoning is unidentified Plant sources of this syndrome included in this book: Zamia staggers is caused by cycads in the genera Cycas, Macrozamia and Bowenia. Species of Lepidozamia probably have the potential to cause this syndrome, but no natural poisoning cases are known to date. Zamia staggers (cycad neurotoxicosis) affects cattle in those parts of Australia where natural populations of cycads occur. This disease has also been called ‘rickets’ in the past, but strictly speaking, this term should be reserved to describe vitamin D deficiency causing deformity of bones. The toxin that causes this poisoning is not known at this time. It is suspected to be derived from methylazoxymethanol (MAM) by the action of ruminal microbes. Poisoning occurs through cattle eating the young fronds or the ripe seeds of cycads in large amounts. Under experimental conditions, cattle have to be fed the plants daily for several months before signs of

3 – Common poisoning profiles

illness occur. Poisoning causes irreversible damage to the nerve fibres in the spinal cord. In central Queensland, where cattle have access to Macrozamia moorei plants, about 1% of a herd is usually affected each year, rising to 3–5% in particular years, with more cattle (up to 40–50%) affected in certain paddocks. Years causing most trouble seem to be those with good summer rains followed by no rain through autumn and winter. This reduces the pasture nutrients at the same time that the cycads produce a heavy seed crop. The fall of seeds from the female cones begins in autumn when pasture quality is rapidly falling. Cases then begin to occur in winter. Young green fronds are particularly dangerous after plants and their habitat are burnt and little or no other feed is available. About 50% of a cattle herd can be affected after exposure to cycad regrowth after a bushfire. Affected cattle have an irregular stiff goose-stepping gait in the hind limbs, knuckling of the hind fetlocks, wasting of the hindquarter muscles and, finally, paralysis of the hindquarters. The worst-affected animals cannot obtain sufficient feed or cannot reach water and die as a result. Post-mortem examination may reveal some scarring of the liver, but detection of the spinal cord damage requires microscopic examination of preserved tissue in a laboratory. There is no treatment for this poisoning. Effective and practical prevention and control measures can be hard to achieve under Australian conditions. Preventing access of livestock to cycad plants with fruit or

69

young fronds underlies all measures. Where other options are neither economical nor practical, trying to reduce the intake of cycads by providing cattle with supplementary feed is worth attempting, although this approach has not been scientifically assessed. Plants may be killed with herbicides or physically removed from pastures and cattle may be excluded from dense populations by strategic fencing. Chemical control of cycads is hard. Cycads will reshoot from the base if control techniques are not thorough. Local authorities should be consulted for the most effective herbicides available. In northern Australia, best results are achieved by integrating fire with chemical application. The area to be treated is burnt in August–September (which destroys existing fruit, interrupts cycad fertilisation and stimulates young leaf growth) then actively growing plants are sprayed overall with herbicide. Where cycad populations are widespread and dense, consider removing cycads from suitable small paddocks to be reserved for use in seasons when the plants are producing fresh leaves or fruit and other feed is scarce. Important: Be aware of the legal requirements for the conservation of native cycad species. It is vitally important to consult state government nature conservation authorities to obtain the latest information on your legal position before taking any action to control native cycads in their natural habitat. Ignorance of the law is not a defence if you break laws or regulations when managing cycads. See ‘Warnings’.

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PART 1 Poisonous cyanobacteria (blue-green algae) We’re Annie, Noddie, Mike and Cy! Drink us straight down, then wait to die. Your liver’s shot, your nerves are too. Bid life farewell, the grave’s for you! [Annie = Anabaena, Noddie = Nodularia, Mike = Microcystis and Cy = Cylindrospermopsis]

The cyanobacteria (also called blue-green algae, cyanophytes or cyanoprokaryotes) are single-celled to multi-celled microorganisms whose cells do not contain a nucleus (are prokaryotic) and which generate oxygen from photosynthesis using the green pigment chlorophyll a. They are among the most ancient life forms on Earth today and were the ancestors of all green plants. Those included here all live in water (are aquatic) and can multiply very rapidly to form dense masses (blooms or scums) on or in water under suitable conditions. Cyanobacteria listed as occurring in Australia number some 400 species. Of these, some 20 (about 5%) are known, or suspected, to be toxic (Chapter 4). The chlorophyll in their cells often gives their blooms a bright green appearance when alive. When dead and drying out, they develop a blue-green colour that gives them their alternative name.

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4  Poisonous cyanobacteria (blue-green algae)

For reviews of cyanobacterial poisoning internationally and in Australia, see Toxic Cyanobacteria in Water. A Guide to their Public Health Consequences, Monitoring and Management (Chorus and Bartram 1999) and Health Effects of Toxic Cyanobacteria (Blue-Green Algae) (Ressom et al. 1994), respectively.

Identifying bloom organisms Poisonous cyanobacterial blooms that form floating masses or scums on fresh or brackish water bodies, or that discolour the water without forming floating scums, cannot be distinguished easily from each other or from non-poisonous similar organisms, such as true algae, without examining samples with a microscope and testing them for toxins or toxicity. Consequently, this guide does not set out to distinguish each poisonous cyanobacterial species included in the text, but provides illustrations of blooms for general guidance only. Professional help is needed to identify accurately individual species and to find out if they are poisonous. To do this, water samples containing bloom material should be sent to laboratories specialising in this work. These can be found in local government bodies (shire or city councils), in state government departments of primary industries, agriculture, health, natural resources, water or environmental protection, in hospitals or in universities. For the recommended collection methods and samples to collect, see Chapter 2. Important: Do not expose your bare skin to such blooms because irritation can occur. Use rubber gloves when sampling them.

Confusing species From a distance, certain non-toxic floating plants, such as species of Lemna (duckweed) and species of Azolla (floating ferns), may be mistaken for cyanobacterial blooms. Closer inspection immediately allows these to be distinguished from potentially dangerous cyanobacterial blooms.

Distribution The various cyanobacteria included here can occur in fresh and brackish water throughout Australia. Micro-

cystis aeruginosa can occur in fresh water anywhere. Nodularia spumigena prefers brackish water and will grow in sea water of low salinity. Cylindrospermopsis raciborskii appears to prefer subtropical and tropical areas, but will also bloom in temperate waters. All these species are regarded as native to Australia as part of very widespread global distributions.

Conditions leading to hazardous bloom formation Blooms of cyanobacteria occur because of factors including: •• increased concentrations of plant nutrients, particularly nitrogen and phosphorus, in water bodies. These nutrients can come from runoff following rain that washes fertilisers or body waste from livestock or humans or soil into water storages. •• seasonally reduced flow rates in inland river systems in Australia, leading to strong layering of the water body, particularly in impoundments behind weirs. •• reduced salinity. Blooms of Nodularia spumigena in estuaries and coastal lagoons are thought to be triggered by the reduced salinity that may follow inflows of fresh water after rainfall or sewage discharges. •• a lack of oxygen in the bottom water layer of water bodies may cause mats of species of Oscillatoria to detach from the bottom and float as rafts on the water surface, thus bringing them into contact with animals drinking from or entering the water.

Circumstances leading to poisoning Animals are poisoned by drinking water containing bloom material. Wind may concentrate floating blooms in farm dams or streams used for livestock drinking water at the points of access for livestock, forcing them to drink the bloom material. Humans are also affected by swimming in, or otherwise coming into contact with, bloom material.

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Microcystis aeruginosa surface bloom on a farm dam

Floating rafts (brown) of a toxic mixed Tychonema bornetti and a Phormidium sp. bloom that has detached from the bottom of a dam. Dogs were poisoned by this bloom.

Microcystis aeruginosa surface bloom at the edge of a creek

Cylindrospermopsis raciborskii-type bloom dispersed in upper dam water layers (not floating)

Microcystis aeruginosa bloom edge with blue-green drying material

Toxic Aphanizomenon sp. bloom dispersed in upper dam water layers (not floating). Cattle were poisoned by this bloom.

Microcystis aeruginosa bloom edge breaking up into floccules

Confusing species (not cyanobacteria): Lemna disperma and Azolla sp. at a distance

4 – Poisonous cyanobacteria (blue-green algae)

Confusing species (not cyanobacteria): Lemna disperma (green leaves) and Azolla sp. (red-brown leaves) close-up

Diagnosing cyanobacterial poisoning Confirming a suspected fatal poisoning by cyanobacteria requires collecting bloom material preserved for identification of the organism and unpreserved (chilled) for toxicity testing either by dosing laboratory mice or chemical analysis (see Chapter 2 for details) and a post-mortem examination of dead animals, with sampling of tissues for toxin detection and preserved for microscopic examination (histopathology).

Treating poisoned animals Very early veterinary treatment with activated charcoal or bentonite as a drench by stomach tube at a dose rate of 5 g/kg body weight may be helpful in preventing further absorption of toxins from the gastrointestinal tract, but cannot guarantee survival.

Managing existing blooms Prevent direct human contact with cyanobacterial blooms by public notices at the water body and announcements in the media. Persons who must come into contact with the bloom material, such as during sampling for laboratory tests, must wear protective gloves and clothing. Animals should be stopped from drinking from the floating bloom material to prevent poisoning. To prevent intake of intact surface blooms: •• Draw water supplies from sites away from blooms. •• Use floating booms to separate blooms (top 10 cm of water) from outlet points. •• Draw water from aquifers beside contaminated streams, thus allowing the soil of the stream banks to filter out the cyanobacterial cells and toxins. This method is more useful for water supplies for small human communities than for livestock. Effective positioning of wells will vary depending

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on local conditions, with wells placed 20 m and 50 m from the River Murray at Paringa, South Australia, being suitable to remove microcystins, but salinity needed to be managed. Chlorination and activated charcoal filtration of water supplies for human communities should be used to prevent poisoning of consumers when blooms occur in reservoirs or streams supplying these communities. It is better to allow blooms to decay and disperse naturally, but if circumstances demand active removal, the methods used to destroy or disperse bloom material include: •• adding algicides to the water. Important: This will release the toxins into the water when the cyanobacterial cells die and rupture. Livestock should not be given access to this treated water for at least 5 days (and preferably longer) because it will remain poisonous. Copper sulphate solution has been used to destroy blooms, but is no longer recommended because of unwanted side-effects. Other algicides, such as quinones and organic herbicides, are available but their usefulness is not fully explored. •• alternatively, adding precipitants of cyanobacteria and of phosphorus to the water, causing the cyanobacterial cells to sink without rupturing, so that no toxins are released into the water and the phosphorus is removed, helping to prevent further blooms. Lime (calcium carbonate) at 100–250 mg/L, ferric alum at 100kg/ML and gypsum at 50 kg/ML have been used in this role. •• alternatively or additionally, adding barley straw bales to the water body. This has been very effective at clearing blooms in Europe and with certain varieties (Schooner, Parwon and Clipper) used at 100 g straw to 1000 L. Attempts to use this method often have been unsatisfactory in Australia. The mechanism is not understood.

Bloom prevention To prevent blooms from forming, the conditions that cause them must be prevented. The most important of these is the entry of excessive amounts of nutrients, particularly phosphorus, into the water body. To prevent this contamination, water catchment control measures are needed. These apply to small farm dams and small streams, as well as to large reservoirs, and include: •• minimising phosphate-containing fertiliser use in the catchment area •• fencing livestock out of water sources and pumping their drinking water to troughs. This stops urine and manure (containing nitrogen and phosphorus)

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directly entering the water and prevents soil erosion of the banks. Fenced water sources with pumps and troughs need regular inspection two to three times weekly to make sure that any problems are corrected before stock run out of water. Kangaroos or wallabies can become bogged and die in some fenced dams. •• minimising soil erosion. Soil particles washing into streams and dams carry nutrients with them. •• increasing and protecting the growth and density of trees, shrubs and groundcover vegetation as a buffer zone along the banks of streams. Plants slow water flows and trap nutrients for their own use, so reducing the amounts that enter water storages. They also prevent soil erosion. •• reintroducing or introducing wetland vegetation or reed beds as buffer zones at the inflow regions of reservoirs. This approach has been used successfully for farm dams by planting local native water plants at the margins of the dams after fencing stock out. The plants intercept and use incoming nutrients and clarify the water, breaking down the stratification caused by suspended clay particles. Blooms of cyanobacteria do not recur despite inflows of rainwater carrying cattle manure. Obtain the advice of your local environmental protection agency or equivalent authority on the most suitable plant species for your district and circumstances. •• removing feral fish (European carp) that stir up sediments, which may contain phosphorus, from the base of the water body •• minimising or preventing livestock manure and human sewage inflows. Site the supplementary feeding points for grazing livestock outside the water catchment areas of stock water supply dams. This will prevent the large amounts of manure that build up at such places being washed into the dams by heavy rain. Shifting the feeding points will also encourage stock to establish their camping areas there, and this will also reduce the build up of manure in dam catchment areas. Human sewage treatment can reduce or remove phosphates. Sewage treatment outflows can be used for irrigation instead of directly discharging into water bodies. Additional remedial action that can be taken in water bodies in which cyanobacterial blooms occur repeatedly include: •• precipitating phosphates out of the water column into the bottom sediment with alum and iron salts or lime or gypsum (applicable to small reservoirs) or Phoslock™: a CSIRO-developed phosphorus-absorbing clay slurry sprayed on the

water surface. In farm dams, powdered alum has been used at 500 g/5000 L in mid-winter, followed by blocks of ferric alum at 250 g/5000 L suspended in nets above the mud and replaced as they dissolved in October, December, February and April. •• aerating the bottom layer of water bodies mechanically by pumped air. This prevents stratification within the water body and thus mobilisation of phosphate from bottom sediment by anaerobic (oxygen-hating) bacteria. •• managing weirs on inland river systems to prevent water column stratification through controlling the rate and frequency of discharge and the level from which the discharge is tapped.

Variable bloom toxicity Not every cyanobacterial bloom is poisonous. Genetic variations within species mean that some blooms produce toxins while others do not. Each bloom should be considered potentially poisonous until laboratory testing has been completed and non-toxic results have been obtained.

Toxin groups There are three known major groups of cyanobacterial toxins, each produced by a number of different cyanobacterial species. In descending order of importance and occurrence, they are: firstly, the peptides microcystins and nodularin; secondly, the nervous systemdamaging alkaloid paralytic shellfish toxins and anatoxins; and, thirdly, the alkaloid cylindrospermopsin. Each group produces poisoning with different features. An additional minor group of toxins produced by many blooms, the lipopolysaccharides, cause skin and eye irritation in humans who come into contact with some bloom material.

Liver-damaging cyanobacterial toxins (peptides)

NNN  No effective therapy ~  Acute effects Weight of evidence for toxicity: «««« Degree of danger: ««« These are the most common causes of poisoning by cyanobacterial blooms. These liver-damaging (hepato-

4 – Poisonous cyanobacteria (blue-green algae)

toxic) cyanobacterial toxins are cyclopeptides (a number of amino acids linked into rings) and include the microcystins and nodularin. Common cyanobacteria that produce toxins of this type are Microcystis aeruginosa Kutz. and Nodularia spumigena Mertens. Other cyanobacterial producers of peptide toxins include other species of Microcystis and species of Anabaena, Oscillatoria, Nostoc, Anabaenopsis, and Planktothrix. Hepatotoxic peptide concentrations in the range 1000–5000  mg/g cyanobacterial dry weight are common in Australian blooms. Lethal doses of these toxins are in the range 0.05–0.07 mg/kg body weight. Guidelines for drinking water in Australia suggest an upper limit of 1  mg toxin/L water or 5000  cells/mL water. All animal species are susceptible to poisoning by these toxins. Most cases occur in grazing livestock drinking from contaminated farm dams or streams. Dogs and pigs have also been poisoned. The toxins destroy liver cells (acute hepatic necrosis), with fatal doses destroying a majority of the cells in the liver. Affected animals may be simply found dead or may develop signs and post-mortem lesions described under ‘Acute liver necrosis’ in Chapter 3. Blue or blue-green stains may be seen around the mouth and on the legs where animals have entered the water to drink. Humans drinking town water sourced from a contaminated reservoir in inland Australia have been mildly affected, with evidence of liver damage detected in laboratory tests on blood; no deaths have resulted. Diarrhoea, nausea, vomiting, muscle weakness, sore throat, respiratory difficulty or headache occurred in humans exposed to Anabaena circinalis blooms in the River Murray, South Australia, in the summer of 1991–1992.

Nervous system-damaging cyanobacterial toxins (alkaloid neurotoxins)

NNN  No effective therapy ~  Acute effects Weight of evidence for toxicity: «««« Degree of danger: ««« This form of poisoning by cyanobacteria is rare. It is caused by cyanobacterial alkaloid neurotoxins (nerve toxins) that include the paralytic shellfish poisoning toxins and the anatoxins. Common cyanobacteria that produce toxins of this type include species of Ana-

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baena. All animal species are susceptible to poisoning by these toxins. In Australia, sheep, cattle and dogs have been their victims. Dogs have been affected soon after swimming in lakes with floating bloom material. These toxins act very rapidly, causing paralysis. Affected animals are usually found dead. Those seen alive have difficulty breathing before collapsing and dying rapidly. Some dogs may vomit. No abnormalities are seen at post-mortem examination. Blue or bluegreen stains may be seen around the mouth and on the legs where animals have entered the water to drink. Experimentally, 4-aminopyridine is a promising antidote to paralytic shellfish toxin poisoning in humans.

Cylindrospermopsin

NNN  No effective therapy M  Delayed onset or chronic effects Weight of evidence for toxicity: «««« Degree of danger: ««« Cylindrospermopsin is an alkaloid. Common cyanobacteria that produce toxins of this type include Cylindrospermopsis raciborskii (Wolosz.) Seenaya et Subba Raju. Rarely, other cyanobacteria are known to produce cylindrospermopsin. C. raciborskii commonly forms blooms coloured green or red-brown and dispersed below the surface in the upper layers of the water body. These blooms do not float on the water surface. Red-brown blooms of this species are considered the more toxic. Toxin production peaks in winter in northern Australia. Cattle and humans have been affected in Australia. Affected cattle become weak, lie down and die after some days. Post-mortem examination may reveal a pale liver with a distended gall bladder and, in some cases, jaundice. Microscopic inspection of tissue sections from these cattle reveals damage to the liver (death and loss of scattered liver cells and swelling and degeneration of the remainder; proliferation of bile ductule cells and fibrous tissue), kidneys (swelling and loss of tubule cells in the cortex) and heart muscle (foci of dead muscle fibres). In humans, ‘Palm Island mystery disease’ and ‘Barcoo spews’ have both been attributed to cylindrospermopsin poisoning. ‘Palm Island mystery disease’ occurred in November 1979 and affected 138 children (2–16 years old) and 10 adults in successive waves over a 3-week period. This illness occurred in three phases

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– the hepatitis phase lasting 2 days, the lethargic phase (severe electrolyte imbalance) lasting 1–2 days, then the diarrhoeal phase usually lasting 5 days. Symptoms early in the disease were malaise, loss of appetite, vomiting and a tender swollen liver, with headache in 48% of patients and abdominal pain in 32%. All children were constipated when first examined; 21% had temperatures above 38°C. In the 24 to 48 hours after onset of the lethargic stage (‘shocked state’), profuse diarrhoea occurred in 39% of children with 94% of these having bright red blood in the stools. In some children, the bloody diarrhoea persisted for 3 weeks. Congested or bleeding mucous membranes occurred in 12%. Acute abdominal tenderness developed in 2%. Inflamed salivary glands (parotitis or parotiditis), usually with fever, occurred in 18% at some time during the illness. The overall course of illness in the children was between 4 and 26 days. ‘Barcoo spews’ affected travellers in inland Australia, mostly in the 19th and early 20th centuries, causing nausea and vomiting.

Lipopolysaccharides

N  No specific therapy. Apply general decon-

tamination and supportive measures advised by a Poisons Information Centre or a medical practitioner.

Weight of evidence for toxicity: «««« Degree of danger: « Lipopolysaccharides are chemicals composed of lipids (‘fats’) linked to polysaccharides (chains of sugar molecules). All cyanobacterial species produce toxins of this type. Humans are affected when skin and eyes come into contact with cyanobacterial blooms. Eye irritation and itchy skin rashes of varying severity are produced, including blistering in very severe cases. Allergic reactions may be induced as well.

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PART 2 Poisonous fungi

Fungi are not plants. They are an important group of living organisms with members presently placed in the three Kingdoms Protoctista, Chromista and Eumycota (the ‘true’ fungi – the organisms discussed in this book) and distinct from algae (including cyanobacteria), plants and animals. Fungal cells have nuclei, so they are eucaryotic, like plants and animals, but they do not contain chlorophyll, the green pigment in plant and cyanobacterial cells, and so do not photosynthesise. Their cell walls are composed mostly of glucans and chitin, not cellulose as in plants. Fungi usually form complex sedentary networks of thread-like structures called hyphae within or on substrates. A network of hyphae is called a mycelium. Fungi feed by secreting digestive enzymes into their surroundings and then absorbing the resulting products formed from the breakdown of organic matter in their vicinity. They reproduce by generating microscopically small spores in great numbers. Macrofungi are the readily visible spore-bearing structures of Ascomycetes and Basidiomycetes, commonly called mushrooms or toadstools, but also including puffballs, stinkhorns and truffles. The English word ‘mushroom’ may have originated from the French name mousseron for the edible Calocybe gambosa (St George’s mushroom). The terms ‘mushroom’ and ‘toadstool’ are not useful for differentiation of edible from toxic macrofungi. As is the case with vascular plants, there is no simple method for telling toxic from non-toxic fungi. The fungi of Australia are relatively poorly known, with an estimated 250 000 species occurring here, but only a very few of these have been actually named scientifically. Of Australian fungi, about 10 000 are macrofungi. Known or suspected poisonous species account for very few of these. Groups of poisonous fungi that are included in this book are: •• macrofungi (Chapter 5) •• ergot fungi (Chapter 5) •• gall-forming fungi (Chapter 5)

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5  Poisonous fungi

Macrofungi The macrofungi are those fungi with fruiting bodies – strictly speaking spore-producing bodies – large enough to be recognised with the naked eye and usually called mushrooms or toadstools. There are a number of distinct groups of macrofungi. Those included here are: •• gilled ‘mushrooms’ (agarics) – fungi with ‘gills’ or flat sheets arranged like spokes of a wheel under their caps •• pored ‘mushrooms’ (boletes) – fungi with sporetubes opening as tiny holes (pores) under their caps •• earth-balls – fungi without stems that split open to release their spores •• stinkhorn fungi (phallales) – fungi with exposed stinking slimy spore masses that attract flies Important: It is wise to treat all macrofungi growing wild in Australia as potentially harmful, unless they have been positively identified by an expert as definitely edible. Reliable scientific information on edible and poisonous fungi in Australia is scant and hard to find. Dr Alan Cribb has expressed the situation best: ‘It would be surprising if Australia, with such a diverse range of habitats and climates, did not support some indigenous species … which have not yet been recognised as toxic.’ Do not assume that fungi growing wild in Australia that resemble well-known edible species from other countries are edible here. Doing so has led to death. If you do intend to eat wild-harvested fungi, adopt the rules outlined in Box 5.1 below.

Gilled ‘mushrooms’ (Agarics) Fungi in this category included here are: •• Agaricus xanthodermus (yellow stainer) •• *Amanita muscaria (fly agaric) •• *Amanita phalloides (death cap) •• Chlorophyllum molybdites (green-gilled parasol) •• Cortinarius eartoxicus (a webcap fungus) •• Gymnopilus junonius (spectacular rustgill)

•• Panaeolina foenisecii (brown hay cap) •• Species of Psilocybe (blue meanies, golden top, liberty caps)

Agaricus xanthodermus (yellow stainer)

´  Toxin that causes poisoning is unidentified ~  Acute effects N  No specific therapy. Apply general decontamination and supportive measures advised by a Poisons Information Centre, a medical practitioner or a veterinarian.

Full scientific name: Agaricus xanthodermus Genev. Scientific name meaning: Agaricus comes from the name for the region of Agaria in Sarmatia (now Ukraine); xanthodermus comes from the Ancient Greek words xanthos (yellow) and derma (skin). Family (Order): Agaricaceae (Agaricales) Common names: yellow stainer, yellow-staining mushroom Description: A gregarious species forming clumps or ‘fairy rings’. Caps are white to brownish, 3–15  cm in diameter, with a flattened top and smooth or scaly with fragments of veil at the edges. Gills are free of the stem, becoming pink then brown. Stems are white or yellowish, hollow at the base and with a double ring (annulus) at the top. Cutting or bruising the flesh of cap or stem, particularly near the stem base, immediately produces an intense yellow colour in the damaged tissue. This later fades to brown. An unpleasant odour of phenol (carbolic acid) is commonly smelled. Confusing species: Edible agarics with pink gills when young and brown gills when mature: Agaricus bisporus (common mushroom), A. campestris (field mushroom) and A. arvensis (horse mushroom). A professional

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Box 5.1. Rules for picking and eating mushrooms These rules are based on Edible and Poisonous Mushrooms of the World (Hall et al. 2003). •• Do not eat any mushroom if you have any doubts about its identity or edibility. •• Carefully check every mushroom you are going to eat, first in the field and then at home. •• Be absolutely certain of the identity of any mushroom that has a ring or volva on the stalk, scales or warts on the surface of the cap, or white gills. •• Cut small ‘puffballs’ in two to check for any structures that may suggest Scleroderma or the button stages of Amanita. •• Pick only mushrooms that have no signs of decomposition: worms, insect larvae or evidence of their presence. •• No folklore, such as simple tests for edibility like peeling caps, holds true in all cases. •• Do not eat raw mushrooms picked from the wild. Some toxins are destroyed by cooking. •• Do not eat any small Lepiota, Agaricus that stains yellow, Lactarius that does not have red or orange milk, boletes that stain blue when bruised and/or are orange or red on the underside of the cap, brain-like mushrooms (Gyromitra), chanterellelike mushrooms (Gomphus and Hygrophoropsis mycologist should be consulted for accurate and reliable identification of these fungi. To achieve this, dried specimens with a spore print and coloured images of the fresh fungus should be sent to a state herbarium. Main distinguishing features: Yellow colour of the cut surface of the lower stem produced immediately after exposure to air. Important: There are probably a number of other species of Agaricus in Australia with this characteristic that are also poisonous, and some that are edible. At this stage of our knowledge of these fungi, it seems wise not to eat any ‘mushrooms’ that stain yellow when cut or bruised. Distribution and habitat: Native to Australia but occurring also in Europe and North America. Occurs during February–July in bare humus-rich soil or lawns in sheltered locations or in the open in Queensland, New South Wales, Victoria, Tasmania, South Australia and Western Australia. Weight of evidence for toxicity: ¶¶

aurantiaca), unidentified coral-like mushrooms (Ramaria), or little brown mushrooms. •• Eat a small amount of a mushroom the first time you try it and wait 48 hours before eating more of it or another species. Allergies may take 24 hours to show up. •• Save a couple of uncooked mushrooms in a refrigerator to confirm their identity in case of illness. •• Do not eat mushrooms from roadsides where lead concentrations may be high, or from soil that may be rich in cadmium, chromium, or mercury, or from locations sprayed with pesticides or herbicides. •• Never assume that a mushroom you have picked in another country is the same species as a similar one you have eaten safely at home. •• If you experience illness after eating mushrooms, consult a medical practitioner or a hospital emergency department immediately. Take the saved specimens with you. The National Poisons Information Centre network (Telephone 13 1126 from anywhere in Australia) can also help. •• A large proportion of Australian fungi remain unknown to or undescribed by science, let alone with information on edibility or toxicity being available to us. Degree of danger: «« Toxin: Unidentified. Phenol is present and may be involved in poisoning.

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Toxic parts: All parts are toxic. Animals affected: Humans. Some people can tolerate eating this species, but it is impossible to predict which individuals will be affected and which will not. Conditions of poisoning: Mistaken for edible species. Effects are most severe when raw fungus is eaten. Toxic dose: A single mushroom cap may be sufficient to cause symptoms. A yellow-staining Agaricus species in habitat [RAM07/1]. This particular fungus poisoned an adult human.

Clinical signs and symptoms and management: See the descriptions under ‘Macrofungal poisoning gastrointestinal syndrome’ in Chapter 3. Do not eat any ‘mushroom’ that stains yellow when cut or bruised.

*Amanita muscaria (fly agaric)

~  Acute effects N  No specific therapy. Apply general decon-

tamination and supportive measures advised by a Poisons Information Centre, a medical practitioner or a veterinarian.

Cut surface of the lower stem of a yellow-staining Agaricus species [RAM07/1]

Full scientific name: Amanita muscaria (L. : Fr.) Lam. Scientific name meaning: Amanita comes from the Ancient Greek for ‘affectionate’, meaning attractive and used in an ironic way for these fungi, many species of which are poisonous; muscaria translates as ‘of flies’ and refers to its use in milk to attract and kill house flies (Musca domestica). Family (Order): Amanitaceae (Agaricales)

Underside of caps and cut lower stem of a yellow-staining Agaricus species [RAM10/1]

Description: A thick bright red to orange cap, 8–25 cm in diameter, with concentric circles of scattered white to yellow warty fragments carried on a white cylindrical stem, to 22  cm tall by 3  cm in diameter. Stem is swollen at the base, originally arising from a basal cup (volva), the fragmentary remains of which occur as several scaly bands on the swollen stem base. Gills are free of the stem and white to cream. A white membranous ring (annulus) is fixed to the stem. Main distinguishing features: Red cap with white ‘warts’; remains of a basal cup on the stem base.

Bruised stem of a yellow-staining Agaricus species [RAM10/1]

Confusing species: Stropharia aurantiaca – has a red cap and red-tinted stems but no cup at the stem base (volva); the vermilion grisette (Amanita xanthocephala) – much smaller with no ring, growing close to Eucalyptus trees. A professional mycologist should be consulted for accurate and reliable identification of these fungi. To achieve this, dried specimens with a spore

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A group of Amanita muscaria – under a conifer, South Australia

Toxins: Isoxazoles (ibotenic acid and muscimol). Muscarine is present in only trace amounts and is not responsible for poisoning by this fungus. Toxic parts: All parts are toxic. Animals affected: Humans, dogs and flies

Amanita muscaria – Tasmania [AQ751383], mature cap

Conditions of poisoning: Deliberate ingestion (humans) and access to the fungi growing in parks and gardens (dogs). Flies are attracted by the 1,3-diolein in the caps. Toxic dose: A single mushroom cap may be sufficient to cause symptoms in humans. A fatal dose is suggested to be about 15 or more caps. Technically, the effects are induced in humans by 6 mg muscimol or by 30–60  mg ibotenic acid, but the concentrations of these toxins can vary widely between individual fungi.

Amanita muscaria – Tasmania [AQ751383], young cap

print and coloured images of the fresh fungus should be sent to a state herbarium. Distribution and habitat: Introduced from Europe. Naturalised in Victoria, South Australia, New South Wales, Tasmania and southern Queensland ­(Toowoomba) as solitary fruiting bodies or in groups in association with exotic tree species such as pine, oak, spruce, fir and birch. Occurs usually during March–May. Weight of evidence for toxicity: «««« Degree of danger: «««

Clinical signs (and symptoms for humans): In humans, poisoning is known as pantherina syndrome or ibotenic acid–muscimol poisoning. Onset of signs occurs 30  minutes to 2 hours after ingestion. Effects reported are dizziness, difficulties with balance and movement coordination, excitement with euphoria or depression and anxiety, auditory and visual hallucinations (heightened colour perception) and tiredness, progressing to sleep in some cases. Tiredness and excitement may alternate repeatedly. Other effects are increased body temperature, dry skin and mucous membranes, red face and dilated pupils. Nausea, vomiting and diarrhoea are frequent. Muscular weakness and gastric tenderness occur. Sweating and excess salivation may occur in some people. Lack of memory of the events of intoxication frequently happens. Severe poisoning can produce tremor, seizures (convulsions), loss of consciousness and life-threatening respiratory and circulatory malfunctions.

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In one dog poisoned in South Australia, the effects were muscle tremors, uncoordinated movements, head jerking, constricted unresponsive pupils, excessive salivation, apparent hallucinations (‘the dog appeared to be in extreme terror and/or pain, started screaming violently, dashed into the nearest corner, cowered and defecated.’), diarrhoea (foamy, green and foul-smelling), convulsions with ‘screaming’, and finally respiratory arrest. Management (therapy, prevention and control): Medical or veterinary intervention is essential. The poisoned dog recovered after treatment that included controlling convulsions and removing the remaining fungus from its stomach.

*Amanita phalloides (death cap)

~  Acute effects M  Delayed onset ∅  Effective therapy is possible. Starting very early in the course of poisoning is essential for positive outcomes. Full scientific name: Amanita phalloides (Vaill. ex Fr.) Link Scientific name meaning: Amanita comes from the Ancient Greek for ‘affectionate’, meaning attractive and used in an ironic way for these fungi, many species of which are poisonous; phalloides means like an erect penis (phallus). Family (Order): Amanitaceae (Agaricales) Common names: death cap, deadly amanita, deadly angel, death cup, destroying angel, angel-of-death Description: A gilled fungus with caps 5–15  cm in diameter, domed at first and becoming almost flattopped in large mature specimens. The cap colour varies from pale yellow-green to deep olive green to olive brown; typically olive green in the centre becoming yellowish-green towards the outer edges. A white variety is less common. The cap surface is usually smooth, but may have some white patches, which are remnants of the veil that covers the young growth stages. Gills are free of the stem and are white, sometimes yellowing with age. The spore print is white. Stems are white with faint greenish or brownish tints, 8–20 cm tall and cylindrical (1–2 cm in diameter). A membranous ring with a striped upper surface is fixed to the stem. At the base of the stem is a well-developed cup (volva) with free edges.

Main distinguishing features: Yellowish to greenish cap, white free gills, large cup at stem base. Confusing species: The smooth white parasol (Leucoagaricus leucothites) – has no green colour in the cap and no stem-base cup – and the common rosegill (Volvariella speciosa) – has no green colour in the cap, no ring and a pink-brown spore print. There are over 120 recognised and described species of Amanita in Australia, with many more undescribed. A professional mycologist should be consulted for accurate and reliable identification of these fungi. To achieve this, dried specimens with a spore print and coloured images of the fresh fungus should be sent to a state herbarium. Distribution and habitat: Introduced from Europe. A. phalloides is naturalised in association with oak trees (species of Quercus) in Victoria, the Australian Capital Territory and South Australia (Adelaide only). The presence of long-established oak trees in Tasmania makes its occurrence there very likely. Australia’s Virtual Herbarium records specimens also collected at Albany, Western Australia, and Sydney and the Hunter Valley, New South Wales, but those records need verification. It is possible that this fungus could grow as far north as the southern Darling Downs area where temperate zone tree species are grown as garden ornamentals. Weight of evidence for toxicity: «««« Degree of danger: ««« Toxins: Amatoxins – bicyclic octapeptides with an indole-(R)-sulphoxide bridge – are considered the main toxins, capable experimentally of reproducing all the effects of poisoning by their parent fungus. Amatoxins are heat stable and resist freezing or drying. Toxins of lesser importance are the phallotoxins, bicyclic

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Part 2 – Poisonous fungi

Amanita phalloides – under an oak tree, Melbourne

Amanita phalloides – showing the cup (volva) at the stem base, New Zealand

Amanita phalloides – upper cap surface, Melbourne

Amanita phalloides – underside of mature cap showing white gills and a recently emerged fruiting body with the veil still partly intact, New Zealand

heptapeptides with an indole/thio-ether bridge that include phalloidin, phalloin, phallisin, phallacin and phallacidin as the most toxic components. Other lesser toxins are the virotoxins – monocyclic heptapeptides – including viroidin, alloviroidin, desoxoviroidin, viroisin and desoxoviroisin.

humans, there is a long interval (latent period) between ingestion and onset of signs and symptoms – 6–24 h, usually 8–12 h – then a two-stage (biphasic) course dominated first by gastrointestinal signs including bloody diarrhoea and then by signs of liver and kidney failure.

Toxic parts: All parts are toxic.

Post-mortem changes: See the description under ‘Acute liver necrosis’ in Chapter 3. Severe liver and kidney necrosis is reported as the main finding in fatal cases in humans and dogs.

Animals affected: Humans and dogs Conditions of poisoning: Mistaken for edible species by human collectors. It has been responsible for a small number of human and two young dog deaths in Australia. The dogs encountered the fungi under oaks in private gardens in Melbourne, Victoria. Toxic dose: A human lethal dose of A. phalloides is less than 50 g of fresh fungus (5–7 mg of amatoxins), which is equivalent to one fruiting body (one ‘mushroom’). Clinical signs and symptoms: Poisoning of humans by this fungus is called amatoxin syndrome or phalloides syndrome (cyclopeptide poisoning). See the description under ‘Acute liver necrosis’ in Chapter 3. In

Management (therapy, prevention and control): Immediate emergency medical or veterinary assistance should be obtained. This is a life-threatening poisoning and a proportion of patients die despite treatment. Deaths in poisoned humans occur in about 10–15% of cases, reducing to 5–6% with aggressive intensive care. See the description under ‘Acute liver necrosis’ in Chapter 3. Additional measures can be applied. Repeated oral doses of activated charcoal to prevent reabsorption of toxins excreted into the intestines through the bile (interruption of the enterohepatic circulation) are useful and have been life saving. Intrave-

5 – Poisonous fungi

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nous infusions of penicillin G or silymarin or silibinin block the excretion of amatoxins into bile and thus also interrupt the enterohepatic circulation of toxins. Silybinin and silymarin are extracts of the thistle Silybum marianum (see Chapter 11 for this plant’s toxic properties) and have been used successfully in humans and dogs. Maintaining an adequate urinary output with good hydration is important to reduce reabsorption of toxins from kidney tubules. In dogs, 90% of an ingested dose of amatoxins was excreted by the end of 6 h. Liver transplantation is an option employed in very severe human cases ( cattle > sheep > goats, but recent research in New South Wales with local plants indicates that sheep are more susceptible than cattle (see data on toxic doses below). Humans taking St John’s wort as an anti-depressant medication may be affected if exposed to strong light sources. Conditions of poisoning: Access to large amounts of the plants. Most poisoning happens in summer during flowering, but can occur in any season. Signs of poisoning are seen after hypericin in unpigmented skin is exposed to sunlight for 3–5 hours on successive days. An adverse reaction to sunlight may then happen for up to 4 days after a single hypericin dose.

Clinical signs (and symptoms for humans): See the description under ‘Photosensitisation’ in Chapter 3. Additional information specific to H. perforatum poisoning is as follows. Rectal temperatures increased above 40oC (hyperthermia) indicate hypericin poisoning in sheep and cattle with access to the plant. Affected animals remain sensitive to light for over 7 days after plant intake stops. As well as photosensitisation, effects on nervous function have been seen in sheep: namely restlessness, confusion, reduced awareness of surroundings and response to sight and sound, increased respiratory and heart rates, and incoordination (ataxia). In these sheep, hind limb weakness causing dog-sitting, knuckling of hind fetlocks, going down on the chest in an upright posture (sternal recumbency) and adopting an unresponsive trancelike ‘frozen’ state (catalepsy) may all happen now and again. Other effects on sheep include abortion or a complete stop to, or reduced, milk production. Rarely, humans taking H. perforatum as an anti-depressant medication may develop significant altered feeling in hands and arms (polyneuropathy) and mild photosensitisation. Post-mortem changes: See the description of primary photosensitisation lesions under ‘Photosensitisation’ in Chapter 3. Management (therapy, prevention and control): For general treatment measures, see the description under ‘Photosensitisation’ in Chapter 3. For control of the plant, several approaches are possible: destruction of the plants by herbicides or by ploughing on arable land must be combined with active pasture improvement (e.g. by establishing phalaris and subterranean clover). Biological control – 37 insect species attack the plant in Europe, eight of these were liberated in Australia between 1929 and 1955 and four have established. Chrysolina [syn. Chrysomela] beetles (C. hyperici, C. quadrigemina) can be effective in open country but must be combined with pasture improvement measures as follow-up to prevent re-infestation by the plant. Agrilus hyperici is restricted to a small area around Mudgee, NSW. The gall midge Zeuxidiplosis giardi

11 – Poisonous forbs (non-grass-like herbs)

reduces seed production, but has little significant effect. Strategic grazing – using goats or sheep may be effective if plant hypericin concentrations are low enough for a significant period of the year (late autumn to early spring) and animals are sufficiently resistant to poisoning – some genetic variation in poisoning resistance between individual animals is known. This approach is useful on steep land inaccessible to machinery where boom-spraying with herbicides or cultivation are not practical. Flowering, growth and vigour of H. perforatum can be significantly reduced by applying heavy grazing pressure (greater than 50 dry sheep equivalents/ha) during dormant or slow-growth periods. Grazed areas must be frequently monitored so that stock can be removed before flower spikes reach 5–10 cm tall and hypericin content reaches toxic concentrations. Sheep suitable for this technique are adult Merinos from a fine wool (