Secondary Biology. Student book. Form Four 9781941940419

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SECONI'ARY

BIOTOGY FORM FOUR STUDENT BOOK Biology Writers L. Hassan Ahmed Jama (Hassan Biology) 2. Mukhtar Awmuse Hassan (Cawl) 3. Mahdi Hassan Suldaan 4. Sagal Ali Aden Designing and Cover pages

t.

Hamud Khaireh Yusuf

2. Liibaan Cali H. Raabi 3. Mohamud Abdilahi Khalif Editors 1. Aiderus Hamud Ahmed

2. Hassan Ahmed Jama (Hassan Biology)

Biology Textbook @ Ministry

of Education and Higher Studies

Republic of Somaliland

Curriculum Development Institute of the Somaliland Ministry of Education and Higher Studies is responsible for the curriculum development and textbook production.

Design and layout O HEMA Books 20L6

First Edition 2016

All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, without prior permission in writing of Ministry of Education and Higher Studies of the Republic of Somaliland, or are expressly permitted by law.

rsBN:

978-1-941940-41-9

Printed by HEMA Books Hargeisa, Somaliland

ii

ACKT{OWLEDGEMENT

The development and writing of national textbooks based on the Somaliland new outcome-based curriculum and syllabus is a national responsibility.For a long period, the National Institute of Curriculum Development of the Somaliland tX4inistry of Education and Higher Studies have been putting a lot of effortto develop and ptrblish textbooks for primary and secondary schools. All prajse is due to Allah; thanks to the Almighty Allah for blessing us to finish this rewarding task. We indulge deep gratitude to the governrnent of Somaliland led by His Excellence President Ahmed Mohamed Moharnoud (siilaanyo) for their encouragernent and contribution to realization and development ofprimary and secondary tenbooks locally since 1997. My specialthanks goes to the Curriculum Development Institute led by Mr. AbdillahiYasin Derie and his team for planning and coondlnating the primary and secondary textbooks development process. We appreciate every atternpt they have to identify appropriate curriculum advisors, textbooks writers and quallty tenbooks reviewers with the help of the Ministry of Education who have successfully produced

for the primary and secondary schools'

ln addition to that, we are thankful to national curriculum

advisors, textbooks writers (subject specialists), editors{reviewers} and designers who helped us in recommending effective approach in writing and reviewing the teltbookswhile serving as catalysts for the idea to write and publish textbooks

for Somaliland chlldren. Their creatjve, functional approaches in writing and team work have enabled the currfcr"llum development institute to produce quality primary and secondary textbooks' My sincere appreciation goes tc the State Minister Mohamed H. Aden Elmi, Deputy-Minister Yusuf Osman Garas, Director General Abib Ahmed Ali and chairman of the examination board Da'ud Ahmed Farah for their remarkable contribution in the development of the national cunriculum and the production of quatity textbooks for Somaliland schools. My acknowledgernent is also due to the technical advisors of the ministry and technical review team for their advisory role in reviewing the textbooks. express my sincere gratitude to the fsrmer Ministers of Education and Higher Studies Honorable Madam Zamzam Abdi Aden and Mr. Farah Elmi Geedoole for their tremendous effort of establishing strong foundation for the national curriculurn and textbooks production. Also,l would like

to

Ministry of Education and Higher Studies is grateful to HEMA Books for their contribution towards the development and writing of the Somaliland primary and secondary school textbooks' We're grateful to great HEMA's significant contribution to the process of writing textbooks, graphic designing and their effort in printing and distributingquality and affordableprimary and secondary textbook. Finally, the MoE&HS is grateful to any other individual or organizations, who are not listed here, for their

contribution to the process of curriculum

development" ,/

Honorable Abdillahi lbrahim Habane Minlster of Education and tligher Studies, Repuhlic of

ilt

r/

V '

Somaliland

:'

PREFACE

up-toBiology (Form One to Four) First Edition aims to provide an date and comprehensive coverage of the Core and Extended curriculum in Biology, specified in the current standardized outcome based Somaliland syllabus.

chapters in the This first edition has been completely structured to align the and book with the syllabus. Each chapter starts with the syllabus objectives

overview diagrams

to be covered in that chapter, and ends with a

review questions, summarizing the important points covered' to test your The questions included at the end of each chapter are intended answer the understanding of the text you have just learnt' lf you cannot question in question straightaway, read that section of text again with the mind.

To help draw attention to the more important words, scientific terms glossary is added at the end of the text book.

t 7.4. Water and Inorganic

ions...........

.,..................144

membrane Chapter 8: Nutrition and Respiration.............. 8.1 Autotrophic Nutrition...... 8.2 Heterotrophic Nutrition.. 8.3 Respiration and Gaseous Exchange..... 7.6. Plasma

vtl

.....................160 ......167 .......170 ........ t77

.......185

Microorganisms and humans

.i\:

a

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+

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By the end of each topic, the learner should be able

. . o

to

explain what is meant by the terms health and disease name the different categories of disease and to give one example of each explain the terms pandemic, epidemic and endemic

o state that

infectious diseases are caused by viruses, bacteria, fungi or protozoa

. state the ways that

diseases can be transmitted (through air, contamination of food and water, by vectors, contagion) and controlled

describe the causes of cholera, malaria, AIDS and TB and explain how these diseases are tra nsmitted discuss the roles of social, economic and biological factors in the prevention and control of cholera, malaria, AIDS and TB

be aware of the world-wide importance of infectious diseases

outline the role of antibiotics in the treatment of infectious disease

Somaliland

iql;::; 1t:.

1.1 Diseases Health

Health is defined the physical, mental and social state of a person. Health is more than being free from disease. Health may be good or poor. The table below shows different traits for each good health and poor health Traits of good

health

r Physically fit . Optimistic o Respect norms, values and traditions of the society (well-adjusted in society) o Without too much difficult can

o o o o

Traits of poor health Physically unfit Pessimistic

Violates norms, values and traditions of the society (well-adjusted in society) Can't undertake mental and physical tasks necessary for daily life

undertake mental and physical tasks necessary for daily life Disease Disease or illness is disorder or bad functioning (malfunction of mind or body which leads to

departure of good health. Malfunction can affect tissue, organ, organ system or whole organism. Disease can be: o Uni-factorial this type is caused single factor such as malaria o Multi-factorial this is caused by many factors such as heart disease Diseases are characterized by signs and symptoms. Diseases can be differentiated into: a. Acute which have sudden onset with rapid changes and lasts for a short period of time such as lnfluenza b. Chronic which develops gradually and continue for months or years such as Tuberculosis

1.2 Categories of disease Disease can possible be categorized into mental and physical or between infectious and noninfectious. Nine broad categories are recognized and are

Physical diseases

This type is of diseases involve damage to part of body and are associated with permanent ortemporary. Such as Leprosy, broken leg.

lnfectious diseases

Infectious diseases are those caused by pathogen such as viruses, bacteria, fungi, protoctista, worms and insects. They are called also communicable diseases because the pathogens are transmitted from one person to another or from animal to person. such as malaria

of Somaliland

non-infectious

Every disease that are not caused by pathogen. This includes all the following categories. such as stroke

diseases

deficiency disease(nutritional diseases)

lnherited diseases (genetic disease or genetic disorder)

r

This is caused by inadequate or unbalanced diet. Deficiency diseases result from missing or short supply of essential nutrients. This can be classified into Vitamin deficiency disease Mineral deficiency disease Protein deficiency disease This type of disease is caused by genes or faulty gene and therefore can be passed from parent to children such as sickle cell anemia, Huntington's disease and cystic fibrosis

Cystic fibrosis is an inherited disease. The disease is because of fault in a gene coding for a channel protein that is meant to allow chloride ions to flow out of cells, and since chloride ions take water with them this presents a problem. lf neither move out, the alveoli is hindered by a thick sticky mucus, making breathing difficult and forming a breeding ground for bacteria, resulting in infections. Regular physiotherapy can help to loosen and remove the mucus.

Degenerative diseases Mentaldiseases

Socialdiseases

Self inflicted diseases

There are two versions of every gene in each of the bodies cells, called alleles. There are two types of alleles - dominant and recessive, and cystic fibrosis is caused by a recessive allele. Let's say that A is the healthy allele, and a is the cystic fibrosis allele, and is recessive. Someone with AA is healthy, someone with Aa is a carrier but is healthy (because the healthy A is dominant over the unhealthy a). Two people with Aa and Aa are both healthy, but if they produce a child there is a L/4 chance that this child will have the genotype aa, which means they will suffer from cystic fibrosis. Gradual decline in function. Repair mechanisms failing, immune system begins to attack itself. Alzheimers, strokes, cancers. Changes to the mind, possibly with a physical cause. Any disease that affects a person's mind. Sometimes a visible degeneration of brain tissue is present, as in CJD. CJD, Alzheimer's, dementia, schizophrenia Social environment or behavior. How a persons life affects their health, exposing or protecting them

from certain diseases. Hypothermia, CHD Cause by him or her Self deliberately. Willful damage to own person's body by themselves. Attempted suicide

of Somaliland

Epidemic endemic and pandemic Endemic Disease can become endemic,oif the infectious disease is always present in population. Epidemic This occurs when a disease suddenly spreads rapidly to affect many people, such as that spread across the country. E.g. influence Pandemic This is when a disease spreads over large area, such as a continent or even worldwide. E.g Aids and TB

1.3 Infectious diseases Infectious diseases are those caused by pathogen such as viruses, bacteria, fungi, protozoa, worms and insects. They are called also communicable diseases because the pathogens are transmitted from one person to another or from animal to person'

Bacterial disease

Tetanus (lock jaw) Agent

Transmission

Site of

symptoms

prevention

The bacteria make a toxin,which is absorbed by body

Injection of tetanus toxoid

action

Clostridium tetani 1R

spore-forming

anaerobe

bacterium is the cause)

The spores may be found in environment.eg. in the

Body muscles

soil & feces of animals lf you step on rusty nail

muscles, stiff muscles, & causing spasm that make it difficult to breath

or iron by getting cut or laceration and animal bite like dog, clostridium tetani may infect people.

Cholera Pathogen Method of transmission Incubation period Sit of infection

Clinical features Method of diagnosis Control

Vibriocholorea Food borne, water borne 1-5 davs Wall of small intestine Severe diarrhea, loss of salt and water, dehydration and weakness' Microscopial analvsis of faeces. Drinking water should be chlorinated or boiled, the hygiene should be kept, hands must be washed after visiting toilets, infected people should be treated and vaccination should be carried out.

of Somaliland

Tuberculosis Pathogen

Methods of transmission Incubation period Site of action of

pathogen Clinical features

Methods of diagnosis Control

Mycobactelium tuberculosis and mycobacterium bovis Airborne; via un-pasteurized milk from cattle. Few weeks or months or a year.

Primary infection in lungs; secondary infection in lymph nodes, bones and gut. Racking cough, coughing blood, chest pain, shortness of breath, fever, sweating, weight loss Microscopial examination of sputum for bacteria, Chest X- ray.

Avoid close contact with infected people, milk must be pasteurized, TB in cattle must be eradicated and patients must be treated.

Diphtheria Pathogen

Coryne bacterium diphtheria

Method of transmission Site of action

Through inhalation of cough droplets from an infected person.

Symptoms

Sore throat, nose and throat get blocked.

Control

Treatment and vaccination against diphtheria.

Nose, throat and larynx.

Syphilis Agent Treponema

pallidum

Transmission STD

Site of action

Symptoms

Reproductive

Primary lesion or "chancre" develops at the site of inoculation

organs

prevention Early medication

Chancre:

and

o

prevention

Progresses from macule

papule to ulcer

of Somaliland

to

.

Typically painless, indurated, and has a clean base o Highly infectious o Heals spontaneously within L to 5 weeks. Secondary lesions occur 3 to 5 weeks after the primary chancre appears; may persist for weeks to

months. Mucocutaneous lesions most common manifestations: o Many rashes o Lymphadenopathy o Mucous patches o lnvasion of the CNS can occur and cause madness

Gonorrhea

Agent

Transmission

Site of

Symptoms

prevention

action Diplococcus ( Neisseria orrhoeae)

STD

Can affect

the cervix of female and

urethra of male

Female o Increased vaginal discharge o Painful urination o Lower abdominal pain o Bleeding after sex and between periods

Can be

treated with antibiotics

o

Pain during sex Male o Thick, yellowish-green discharge from penis. Painful urination o Testicular pain or swelling o Rectal pain, discharge or itching A bacterial infection that progresses in stages o Primary: (3 days - 3 months) starts as a small, painless sore called a chancre; goes away on its own

of Somaliland

7

o Secondaryt B

Q-

24 weeks) rash on

the body, palms of hands & soles of feet, hair loss, feeling sick o Latent: lesions or rashes can recur

Whooping cough Pathogen Transmission Symptoms

Control

Bordetella pertusis Through inhalation of cough droplets from an infected child. Mild sneezing, running nose and fever. Later there is hard and dry cough, whooping, wheezing and vomiting. Secondary bacterial infection leads to pneumonia. Treatment and vaccination against whooping cough.

Protozoa diseases Malaria Pathogen

Plasmodium falciparum, P. vivax, P.ovule, P.malaria

Transmission

By

Site of action

Liver, red blood cells, brain

of pathogen Symptoms

Method of diasnosis Control

the bites of infected mosquitoes of the genus anopheles (insect vector)

Fever, anaemia, nausea, headache, muscle and enlarged spleen.

joint pain, backache, shivering,

Microscopial examination of blood

To use treated nets or to eliminate breading grounds by spraying stagnant water, ponds, lakes by using oil and insecticides which suffocate or poison the larvae or to use prophylactic drug.

of Somaliland

Amoeba Pathogen

Entamoebna histolytica.

Method of transmission

Water borne and food borne

Site of action

Lining of intestine

Symptoms

Diarrhoea and vomiting, dehydration and faeces with blood.

Control

To boil or chlorinate the water. Medication and keep the hygiene

Pothoqen

Methods of transmission

Site of action of pathogen incubation period Site of action of pathogen Clinical features

Humon immunodeficiencv virus (HlV) In semen and vaginal fluids during sexual intercourse, transfusion of infected blood, sharing contaminated needles and hypothermic syringes, mother to fetus across placenta, mother to infant in breast milk. T helper lymphocytes, macrophages, brain cells A few weeks, but up to ten years or more before symptoms of AIDS may develop. T helper lymphocytes, macrophages, brain cells

Flu-like symptoms, AIDS-opportunistic infections including pneumonia, TB and cancers. Weight loss, diarrhea, fever, sweating, and dementia.

Method of diasnosis

Blood test for antibodies

to

HlV.

of Somaliland

Fungal parasites

t

Fungal infections of the skin are very common and include and

athlete's foot, jock itch, ringworm,

yeast infections.

Athlete's Foot Athlete's foot, also called tinea pedis, is a fungal infection of the foot. lt causes peeling, redness, burning, and sometimes

blisters

itching,

and sores.

Jock Itch Jock itch, also called tinea cruris, is a common skin infection that is caused by a type of fungus called

tinea. The fungus thrives in warm, moist areas of the body and as a result, infection can affect the genitals, inner thighs, and buttocks. Infections occur more frequently in the summer or in warm, wet climates. Jock itch appears as a red, itchy rash that is often ring-shaped. Jock itch is only mildly contagious. The condition can be spread from person to person through direct contact or indirectly from objects carrying the fungus.

Ringworm Ringworm, also called tinea corporis, is a fungal infection of the skin. lt can appear anywhere on the body and it looks like a circular, red, flat sore. lt is often accompanied by scaly skin. The outer part of the sore can be raised while the skin in the middle appears normal. Ringworm can spread by direct contact with infected people. lt also may be spread on clothing or furniture, Heat and humidity may help to spread the infection.

Candidiasis Candidiasis is a disease caused by yeast-like fungi called candida. They occur when yeast on the skin grows

infections are not contagious. Yeast infections may affect nearly any skin surface on the body, but are most likely to occur in warm, moist, creased areas including the armpits and the groin. Candida infection is especially common among people more actively and causes a red, scaling, itchy rash on the skin. Yeast

who are obese. Candida can cause

diaper rash

candida infection that

is

Oralthrush is a form of vaginal yeast infections.

in infants and can cause infections of the nail.

found in the mouth. Candida also causes

I

ffiMXffiPWER 2 Livestock health and diseases

5

%

By

the end of each topic, the learner should be able to;

a

Define livestock health and disease give lmportance of keeping livestock healthy state pre-disposing factors of livestock diseases

a a o a a

a a a a a

o

describe Signs of ill-health in livestock Explain Dangers posed to human beings State cause and vector(where applicable), livestock diseases that attacked and signs and symptoms Able to classify livestock diseases according to the pathogen and vector that causes Name causal agents, symptoms,transition and control measures of bacterial diseases Name causal agents, symptoms,transition and control measures of Viral diseases Name causal agents, symptoms,transition and control measures of Protozoan diseases Name causal agents, symptoms ,transition and control measures of nutritional diseases Name and describe the general methods of disease control such as Vaccination, Quarantine/lsolation, Housing, Hygiene, Controlled breeding Able to mention control and management practice such as Hoof trimming, Dehorning, Castration, Culling

Republic of Sonirhland

4^

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Y &

I

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-1

2.1 Health and disease lntroduction Poor livestock health account for a considered reduction in yield of livestock-related products. Affected animals should be appropriately treated because it is only when they are in a state of optimal hedth that losses can be minimized. lt is important for the farmer to observe whatever precautions necessary to minimize the occurrence of disease on the animals. Animals should be also being handled well because proper animal management help to avert disorders and outbreaks of disease. Poor animal health may also lead to death among animals. Diseases animals are also expensive to keep because of the cost of their farmer. Health: health is a state of the body whereby all organs and systems function normally. Disease: disease is the deviation from the normal functioning of the body organs and systems of an animal. lmportance of keeping livestock healthy I Healthy animals produce high quantity and quality products. t Healthy animals live longer hence long production period. t Healthy animals produce healthy offspring which manure faster. o Healthy animals have low production costs. I Health animals attract better prices in the market compared to sick animals. t Healthy animals work for long period. Pre-disposing factors of livestock disease t Age of animal. Certain livestock diseases attack only young animals. t Sex of the animal. Some diseases are gender-specific, examples they affect only a particular sex of animal. Mastitis, for example, is disease of female animals. r Skin cooler. The colour of an animal can (in same cases) influence the extent to which the suns heat may affect it by sunburn. t Species of animal. The species of animal effect disease. Thus, for example, swine fever only affects pigs. t Climate change. Same animals become sick when the weather is cold. o Poor and inadequate feeding and watering. o lmproper handling of animals. Some signs (symptoms)of ill-health in livestock 0 Reduce appetite. t Reduced production (for example, milk). t The condition of animal coat: the condition of an animal coat may be an indicated of diseases. I Restlessness may be a symptom of pain or distress. I The stool: excessively loose dung (diarrhea). t Excessive (abnormal) salivation may be a symptom. r Swelling- any abnormal swelling (such as, for example, of the lymph nodes) is likely to be a symptom. t A sudden or gradual loss of weight shows that an animal's healthy is not normal. (An emaciated animal is ill.)

Republic of Somaliland

13

I t i t

Abnormal coloration of the urine- This may be caused by factors such as the presence of blood in the urine, or the presence of other substances. Frequency of urination can also be an important symptom. Mucous- the presence of an excess of mucous ( in the eye for example) Temperature- A high body temperature may indicate presence of fever. Pu lse rate - the heart may be observed to be beating in an abnormal manner (either too fast or too slow rate).

2.2 Causes of livestock disease livestock diseases are caused by the follow factors l. living organisms which can be two groups; ) Micro-orgonisms, such as bacteria, protozoa, viruses and fungi. I Porositic orgonisms. Are including insects such as flies and ticks ll. Chemical poisoning: the animal may become ill after swallowing a poisons or a poisonous substance (same plants, for example are poisonous to the animal) lll. Poor feeding or nutrition: a diet that is not properly balanced to suit the animal's needs, as well as over-feeding or under-feeding may make an animal ill. lV. Physical iniuries. Once an organism such as a virus, bacteria, fungi or protozoa has infected or enters into the animals system.

Review questions Circle the correct letter in front of the following 1) The disease that can affect only a particular sex of animal is

a.

2l 3)

4l

Mastitis c. Diarrhea b. Swine fever which one of the following diseases affect only particular species a. Mastitis c. Diarrhea b. Swine fever Which one of the following is a symptom of ill health in livestock? a. Mucous in eyes c. Swelling of lymph nodes b. Abnormal coloration d. allof them of the urine Which one of the following is not microorganisms which cause livestock disease a. protozoa c. ticks b. Fungi. d. viruses

Structured questaons A. Mention four factors that cause livestock disease? t.

il.

ilt. tv.

14

B.

ldentify some factors influehce livestock diseases?

2.3 Classification of livestock diseases

Disease and livestock

2.3.1 .Bacterial diseases Symptoms

Causal agent

attacked

Anthrax It attacks cattle, sheep and goats

Bacillus anthracis

o o

Control measures Proper disposal of carcasses Quarantine Vaccination

Sudden death Watery blood oozes through all

body openings

o Mastitis It attacks all lactating female animals

Streptococcus Straphylococcus

Fowltyphoid It attacks poultry

Salmonella bacteria

Foot rot It attacks cattle, goats and sheep

Brucellosis It attacks cattle, sheep and pigs

High

temperature Presence of blood in milk Swollen udder or teats

o o

Sudden death Comb and wattle pale

o o

feeding Greenish yellow diarrhea

Brucella abortus

o o o o

o o

Treating with

antibiotics High hygiene Practising complete milking Quarantine Proper feeding High hygiene

Less

Lameness Swollen and

Fusiformis spp

o

painful hoof Hoof contains pus and smells rotten Abortion Brownish vaginal discharge Retention of placenta lnflamation of

Republic of Somaliiand

o o

Practising hoof

trimming Providing a foot

bath of copper (ii) sulphate

o o

Vaccination

o

bulls Proper

o

sanitation Use of artificial

Use of healthy

insemination

testis Black quarter

It attacks cattle, sheep and goats Scours

Clostridium

thauvoei

Escherichia coli

It attacks calves, piglets, lambs and kids

Disease and livestock

attacked Foot and mouth disease

o o o o

o o o

a

Vaccination

Shivering

a

High fever

a

Quarantine Proper disposal

Foot and mouth disease virus

of carcasses High hygiene Proper feeding Treating and isolating sick animals

Lack of appetite

Dehydration Blood and mucus stains in faeces

White or yellowish diarrhea with pungent smell

2.3.2. Viraldiseases Causal agent Symptoms

Control measures Mass slaughter

Lameness

It attacks cattle, sheep,goats and pigs

Newcastle It attacks poultry

Lameness

Loss appetite

Quarantine

High fever

Vaccination

Blisters in the

Newcastle disease virus

o o o o

Fowl pox It attacks poultry

Fowl pox virus

Rinderpest It attacks cattle, sheep, goats and pigs

Rinderpest virus

o o o o

mouth, teats and udder Nasal discharge Watery greenish diarrhea Breathing difficulties Coughing and sneezing Lesions on skin, comb, leg and vent Breathing difficulties Poor growth Poor egg production

Vaccination

Quarantine Killing infected birds Practicing hygiene Vaccination Killing infected birds

Nasal discharge

a

Lacrimation

a

Fever

a

Animals grinding

their teeth

of Somaliiand

Quarantine Vaccination Mass slaughter

Gumboro It attacks young

Gumboro virus

a

poultry African swine fever It attacks pigs

Watery diarrhea Pecking of vent due to irritation Breathing d ifficu lties Diarrhea Pigs appear blue

a

n

African swine fever vt

o

rus

o o

Vaccination Practicing hygiene Vaccination

a

o

a a

Quarantine Mass slaughter

o

2.3.3. Protozoan diseases Disease and livestock

Causal agent

Control measures

Symptoms

attacked East coast fever

Theileria parva

Controlling ticks Treating using appropriate

Swollen lymph

It attacks cattle

nodes

Breathing ifficu lties High body

drugs

d

o o

Anaplasmosis It attacks cattle, sheep and goats

Anaplasma mariginale

Coccidiosis It attacks calves, poultry, lambs and

Coccidia of Elmeria spp

temperature Constipation

a

Rise in

a

temperature Diarrhea, which may be whitish or blood stained Ruffled feathers Drooping wings

young rabbits

o .

Trypanosoma spp

o e o o

o

Rough coat

o

Enlarged lymph nodes

o

Loss of condition Loss

of hair

Using coccid iostats

o rrypanosomrasrs It attacks cattle, sheep, goats, pigs, dogs and horses

Controlling ticks Treating using appropriate drues Observing hygiene

Avoiding overcrowding Treating with appropriate drugs Conrolling tstse f

lies

Treating with

appropriate drugs

Republic of Somaliland

17

r-

2.3.4. Nutritional diseases Symptoms

Disease and livestock

attacked Milk fever It attacks cattle, goats and sheep

Bloat It attacks cattle, sheep and goats

Causal agent

-

-.;.::

Control measures

D

o

Low level of calcium in the blood

o o

Excessive feeding of animals on green Succulent pastures Blockage of oespnagus

o o o

o

twitching

Feeding animals on diet rich in

Staggering

calcium

Muscular

Animal lies with neck twisted backwards

o

lntravenous injection with calcium

o

Exercising the sick animal

o

Feeding the

Paralysis Coma

Left side of the

abdomen is excessively

animals on dry forage before allowing them to graze on lush

distended

o o

Difficulty in breathing Profuse salivation

pastu res

.

Using trocar and

cannula to remove gas

from the stomach

2.4 General methods of diseases control

t

Sanitation: this involves the provision of an appropriate clean environment that is free from disease-causing organisms.

t

Proper feeding: this involves the providing animals with a balanced diet.

t

Quarantine: sick animals are deliberately isolated from healthy animals.

a

The regular vaccination of animal: vaccination enables the animal's body to produce those antibodies that will help to make it immune to the disease concerned.

t

The control of parasite:this may do through dipping and spraying.

o

Culling: this involves the removal of sick and unproductive animals from the herd.

Republic of Somaliland

Quarantine: sick animals are deliberately isolated from healthy animals. This prevents cross -infection. t The proper housing of animals: housing should match the animals known needs. Mammals for example, do not thrive in overcrowded or wet and damp conditions.

Appropriate methods of handling livestock

l.

Hoof trimming:

This is cutting back of overgrown hooves on animal. Over-growing of hooves is common in sheep's, goats and cattle

{ Side

h,j

Boflou of hml

Frut rrflT

--.-.-.-_r-'--

,r/ A) Shows over grown

hooves before

Bl shows holding and twisting a sheep to restrain it in sifting position

C) Shows proper

hoofappearance

aftertrimmed

trimming

Fig.2.1. Above shows before trimming, sheep adjusting for trimming and appearance after trimming

Hoof trlmming procedure

Fi9.2.2. Hoof trimming

for hoof trimming To facilitate easy movement. To control foot rot disease. To prevent the ram from injuries the ewe during mating

Reasons

0 0 0

Republic of Somaliland

"19

,.n

{.

Dehorning or disbudding:

Dehorning is the practices of removing, stopping or discouraging the growth of horns in

cattle,

b

Dehorning of cattle

Fig.2.3. Dehorning Reasons

for dehorning

t t o o

Animals are easy to handle. lt prevents the injuries.

Transportation and feeding Reduce farm destruction.

is

ma easy.

N. Castration: Castration is the practices of making the testicles of male none functional.

Fig.2.4. Castration

Castration procedure

Republic of Somaliland

20

_-d-+*l--i

Reasons for castration 0 To control breeding and inbreeding. 0 To encourage faBt growth rate. 0 To control breeding disease i. Culling: this is the practice of removing unproductive animals for the breeding herd or flock. Culling is done on the following basis. I Poor health. r Old age. t Poor production. a Heredity defects. t Incapability to produce young ones. t To avoid inbreeding. t Poor mothering ability. * Docking i Docking is the removal of tail in sheep. lt is carried out within the first two weeks after birth. lt is also referred to as tailing. t Docking can be carried out using an elastrator and rubber ring, a burdizzo, a knife or a hot iron.

Fig.2.5. Tail docking of sheep

Tail docking of sheep

Reasons for docking sheep:-

o o o o

To enable even fat distribution in the body To make mating easy For cleanliness To avoid occurrence of blowfly attack

Republic of Somaliland

N.

Caponization Copanization is the process of removing tests from male birds or cock.

--l

JE

al

JE

1e)

,)

-'r

f.g

6

--1 Jd

JdL

el

El

-f JEe,J

--1

El

Fig.2.6. Caponization of chicken Reasons of caponization

o o o

To remove docile. To improve meat quality. To reduce breeding.

Methods of caponization

i ii

Surgical operations: this involves opening scrotal removed from tests. Stil bestrol: this is ahormone that is taken from females 6y injection

Review question Aswer the following questions T. Name the causes of the following diseases.

i Fowltyphoid ii East coast fever iii Foot rot iv Coccidiosis,

v

2. 3

4.

Newcastle disease Name two diseases caused lameness in

cattle? Whis is the notifiable diseases in livestock? Name four notifiable diseases in livestock?

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5. 5.

7.

Explain the term of quarantine in

animals?.... How does livestock disEases affect farm income? State an appropriate way of handling of cattle during treatmet?

8. State general methods

9. State predisposing

of disease control?

factors of livestock?

10. What are the effects of parasite?

'J.1.. Define the following terms. A. Vaccine

B.

lsolation

C.

Poor feeding

D. Quarantine

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t

Livestock Parasites

h By

the end ofthis chapter, the student should be able to:

r o o o o o o . o o r r o . o o o o r o o

define the term parasite identify parasites illustrate how to select parasites identify signs of parasite infestation describe signs of parasite infestation explain losses caused by parasites discuss Iosses caused by parasites name dangers posed to human beings and how to avoid them discuss dangers posed to human beings and how to avoid them draw life cycles of parasites describe life cycles of parasites

identify ticks (1-,2,3 host) describe tsetse fly name types of tape warms identify tape warms describe diseases caused by tape warms identify liver flukes identify diseases caused by liver flukes describe methods of parasite control in livestocx describe hygiene in field, housing and water, handling describe drainage

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&:

3.1. Introduction Definition: a parasite is organisms which obtain its livelihood from another organism (host) which suffers darnage. Host: a host is an organism that supports another living organism (parasite) for food and shelter. Parasitism: Parasitism is a relationship between two different organisms where the parasite

harms the host. Effects of parasite 0 They cause anemia. 0 Sucking blood. 0 Damaged the organs of the host 0 Cause irritation on the skin of the host. 0 Destruction oh hides and skins. 0 Transmission of diseases. 3.2. Identify signs of parasite infestation General symptoms of parasite infestation Emaciation.

0 0 0 0 0 0

Potbelliedcondition. Swelling in the jaw or other areas. Anemia. Diarrhea. Presence of worm segment and blood.

3.3. Classification of

parasite

Parasite can be classified into two types: External parasites (ectoparasites). Internal parasite (endoparasite)

I t

a) External parasite (ectoparasites). External parasites live outside the body of the host, although they depend on the animal for their survival. Examples of external parasite include

0 0 0 0 0 0

ticks, fleas, lice,

mites, Keds and

tsetse fly.

rr.*,

Fleas Fleas are blood suckin4insects that are wingless and can leap over wide lengths of distance. They help lay their eggi on the host animal in the ground. Their eggs hatch in to the larva which normally feed on organic matter. The larva the changes in to pupa and finally adult

Livestock attack:

0 0 0 0

Cattle.' Sheep Goats.

Poultry

Fleas have the following undesirable effects on the host: They cause irritation. They suck the blood whereby causing anemia.

0 0 0 0 0

They cause wounds on the host's skin. Reduction of body weight. Birds may be blinded especially by fleas on the eyelids. Fleas can be controlled by Dusting the animal with insecticides.

0 0 0 0

fig:3.1- fleas

Cleaning the houses.

Dipping the animals using dip wash (insecticides). Keeping the host's sleeping place clean.

Lice These are flat wingless insects which divided into two groups

0 0

Sucking

Biting. Livestock attack:

0 0 0 0

Cattle.' Sheep Goats

fig:3.2 lice Poultry Note: cattle are attacked by both biting and sucking while sheep goats are attacked by biting lice.

lice have the following undesirable effects on the host: 0 lrritation.

0 0 0 0

Reduced feeding.

of body condition. Reduced production especially in birds. Loss

Cause anaemia.

Lice can be controlled by:

0 0

Dipping infested animals in an insecticide. Spaying using appropriate insecticides.

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, .

,). ::,,

Mites

I

These are small rounded'or an overall organism belongs to class arachinda. They have eight legs which are very short.

Livestock attack: Cattle.

0 0 0 0 0

Sheep Goats

Poultry. Horses.

Fig:3.3 mites

Mites have the following undesirable effects on the host: 0 Loss of hair. 0 Weight loss. 0 Anaemia ( especially young animals) 0 Decreases wool production.

0

Skin disease.

Mites can be controlled by: 0 Spraying the animals using miticides. 0 Dipping the animals in acaricides/miticides. 0 Dusting poultry. 0 Rubbing oil engine oil on perches Keds These are brown or reddish wingless insects found in most part of the word their bodies are

small measuring about half centimeter. The body is covered with bristly hairs. Livestock attack:

0

0

Sheep

Dusting animals with insecticides.

Fig:3.4 keds

29

Harm

Harmful effect of ke&s. 0 There is irritation which cause the sheep to rub themselves against object 0 Reduced growth. 0 Loss of body condition. 0 They cause anaemia esPeciallY 0 Damage wool due to continuous rubbing against object' Keds be controlled bY: 0 Shearing sheep and then spraying with insecticides.

0 0 0

'

Routine dipping. Rotational grazing.

fencing Tsetse fly The tsetse fly sucks blood of both domestic animals and wild game. lt normally bites during day time, they can be found under certain type's tree shade. lt is a true insect, and undergoes complete life cycle, starting from egg to adult larva and pupa. Livestock attack: 0 Cattle.

0 0 0

Camels. Sheep. Horse.

Harm harmful effect of tsetse flY: Dry coat.

0 0 0 0

Loss of appetite.

Fig: 3.5 tsetse flY

lrregular fever. Anaemia,

Control measures of tsetse flY 0 Catching /trapPing using nets. 0 Bush clearing. 0 Controlled burning. 0 Using insecticides, hand spraying, or aerial spraying. Ticks Ticks are not insects. They belong to the Arachnida class of small animal that are characterized by having eight pairs of legs. Life cycle of ticks Eggs are laid in the cracks on the ground. They hatch in 4-6 weeks into two larvae which climb on the grass waiting for passing animal. a) One-Host tick This requires one host to complete its life cycle. 0 Eggs on the ground hatch into larvae.

30

The larvae climb onto the first host. They feed by sucking blood from the host and become engorged. The larvae moult into nfmphs while still on the host. The emerging nymphs feed on the same host and become engorged. The nymphs moult into adults.

0 0 0 0 0

& ffi,ffi (!+($..*@ Larvao rerNtairl on thR ho6t and become adults after Eggs hatch tnlo six-l€gg€d larvae.

t\4'o moltg.

O Femolog drop off the host to lay eggs.

/iL,=

Diagnostic

stage

O GrevtoJ fumates lay eggg in the env,ironmenL

Fig: 3. 6 one host

b)

tick

Two-Host tick

This requires two different host to complete its life cycle. The eggs are laid on the ground where by hatch. The larvae attaches themselves on the first host. In the first host they develop into a nymph. The nymph falls to the ground and moults into adult. The adults then attach themselves to the second host and feed on blood. The adults mate and the females fall off the host to lay eggs and the cycle continues.

0 0 0 0 0 0

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ArtuHt attcftl to th€

Bqwr'd hoHl l6t b€dhlg and nmtirg

Fir:t Year

A

AO Sp*irru

A - Infeqtrw sta$e A= Diag"octrc $tage

Fig:3.7 two host tick

c)

Three-Host tick This reguires three host to complete its life cycle. 0 The eggs are laid on the ground. 0 They hatch into larva which attacks on the fist animal(host). 0 on the fist hot, they feed on blood and then fail off to moult into nymphs. 0 The nymph look for second ( host) animal ,feed on blood om blood ,fall off and mount into adult. 0 The adults climb on to the third host,suck blood and mate . 0 The females then fall to the ground to lay eggs and the cycle continues.

io lhF rhild hrdt in fts BsrirE Adu$13 FHEch

tss

fegdlq grd matrnd

A A

Thwd Vesr

Seccrd Yeer

tf!!o {HYSO

o

ffas ft|

A H;'ffi;ff'.n hos!

LuvF€ mg6 into nlnlplts Bllsr l6*vrrt g

fitrst

ftx5:l ho$l en.d

A"tnrnt**$tas* A. " D{a+rrost c Stnge

o'fffl{Htler

Fig: 3.8 three host tick

Tick control I Dipping /sprying/hand dressing with a caricides. o Rotational grazing . I Hand picking and killing. t Fencing of the grazing fields to keep off other animals.

b) Internal parasit e(endo-p flrasite) These are the organisms that inhabit internal organs of livestock. These are three main classes:-

o t t

Liver flukes, Round worms.

Tape worms. Liver flukes There are two species of flukes: Fasciola gigantica

0 0

Fasciola hepatica.

Fig:3.9 liver flukes

33

ltr '

r';. ,,, :, 1:1;1.

,;,, ,, :

I

The latter is command. lt is commonly found in the liver and bile ducts of cattle, sheep's and goars.

Life cycle of liver fluke

cattle eat cysts with grass,

fiukes hatch out inside ----ttF animal and move to liver laruae climb grass and form cysts eggs hatch and larvae enter water

secondary larvae

fig: 3.10 Liver fluke Effect of liver flukes

0 0 0 0

Presence of proglottide in animal faeces. Loss of weight.

Rough coat. Blockage of the intestine.

Tape worms Tape worms belong to a group of flat worms which infect both human and domestic

animals. Life cycle of tape worms 0 The lifecycle of taena spp starts with the realse of eggs by mature segments. Tne seggents cut off from the main type worm and drop off in faeces. each segments contain several eggs.

0 0

The embryonated eggs develop if eaten by suitable host such as cattle. When the embryo reaches the elimentary canal (small intestine ) it penetrates the intestines and gets into the blood stream where it is taken to heart and finally to the active muscle.

0 0

lt forms into a cyst called baldder worms which remain in the mucles for severar years. lf the infested animal is slaughtered and eaten by man and the meat is partially cooked or eaten raw, the bladder worms get into the small instetines where they develop into

full tapeworm( adult stage),

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*

One mature the segments cut off and are adropped with faeces and life cycle starts again.

1-r

ti

tl

it

*\

*-.# Fig: 3.11tape worm

Roundworms (Ascaris) The round worm is a serious internal parasite in pigs although it also affects other farm animals such as cattle, sheep, goats and poultry.

Effect of liver round worm The animal may diarrhoea. Blood may be found in faces. Increaed appetite. Fig:3.12 round worm Coughing. Losses of body weight. The animal may become anemia.

0 0 0 0 0 0

Life cycle of round worm Adult of round worm mate intestine. Female lay large number of eggs which are released together with faeces. The eggs develop larvae which is infective. The larvae are ingested by livestock together where feed and the capsule is digested away. The larvae emerge and penetrate through the intestine to the blood stream and migrate to the liver. They then migrate to the lungs after few days and stay in the lungs for a week'

0

0 0

0

0

35

After a week they get out of the lungs and move to the trachea causing irritation and 0 0 0

coughing. When coughing, they are brought to the mouth. They are than swallowed when they get to the back of the mouth from the trachea. They finally develop into mature worms in a small intestine .the males and females mate. The whole life cycle takes about 8 weeks after infestation. Ingested Lafvae Matur€

in lntestlnal T.act

3rd Stage larvae, Only Infectiw $tagp

Stage Larvae 1st

2nd Stage Larvae

Fig: 3.13 round worms

Control measures of round worm 0 Drenching using recommended drugs. 0 Proper disposal of feacal matter. 0 Rotational grazing. 0 Ploughing in pasture. 0 Inspection of offal's and advice on control.

Revision exercise

Answer the following questions L. Define the following terms a. Parasitism:

b. Parasite:

c. Host:

2.

List

four effects of parasite?

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D

ffiffiffiwwffiffi

ffi

Immune syste m/ rmrnunolo gy

By

the end of each topic, the learner should be able to

o e o o o o r e o o

explain the meaning of the term immune response explain the difference between the terms antibody and antigen explain the origin and maturation of leucocytes explain and differentiate nonspecific sand specific immune system describe the role of phagocytes and lymphocytes in defense against pathogens explain the cells of immune response distinguish between B lymphocytes and T lymphocytes in fighting infection distinguish between active, passive, natural and artificial immunity describe the function of antibodies explain how vaccination can control drsease

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lntroduction lmmunology is the study of thephysiological defenses by which the body (the "host") destroys or neutralizes foreign matter, both living and nonliving things.

lmmune defenses perform

a) b)

c)

Protect against infection by microbes-viruses, bacteria, fungi, and parasites; lsolate or remove non-microbial foreign substances; and Destroy cancer cells that arise in the body, a function known as immune surveillance.

lmmune defenses, or immunity, can be classified into two categories, which interact with each other. Nonspecific immune defenses lalso colled innote immunityl o Protect against foreign substances or cells without having to recognize their specific identities. o The mechanisms of protection used by these defenses are not unique to the particular foreign substance or cell. Specific immune defenses (also called ocquired immunity\ Depend upon specific recognition, by lymphocytes, of the substance or cellto be attacked and the launching of an attack against it that is unique for that substance or

o

cell.

Recognition of pathogen by immune defenses These defenses must, of course, recognize some generol property marking the invader as

foreign. What mark invaders as a foreign can be; o The most common are particular classes of carbohydrates or lipids that are frequent constituents of microbial cell walls. o Plasma-membrane receptors on certain immune cells as well as variety of circulating proteins (particularly a family called complement) are able to bind to these carbohydrates and lipids which then identify as a foreign substance.

4.1. Nonspecific defenses of the body Human body is defended from infection in three successive ways; 1. Walls and moats. The outermost layer of the vertebrate body, the skin, is the first barrier to penetration by microbes. Mucous membranes in the respiratory and digestive tracts are also important barriers that protect the body from invasion 2. Roaming patrols. lf the first line of defense is penetrated, the response of the body is to mount a cellular counterattack, using immune cells specially phagocytes and

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chemicals that kill microbes. These defenses act very rapidly after the onset of

infection.

r

A-Skin and other external barriers: The First Line of defense The Skin as a Barrier The skin is the largest organ of the vertebrate body, accounting for t5% of an adult human's total weight. o The skin not only defends the body by providing a nearly impenetrable barrier, o but also reinforces this defense with chemical weapons on the surface. o Oil and sweat glands give the skin's surface a pH of 3 to 5, acidic enough to inhibit the growth of many microorganisms. o Sweat also contains the enzyme lysozyme, which digests bacterial cell walls and defending the body against invasion by viruses and microorganisms, o the skin prevents excessive loss of water to the air through evaporation.

Other External In addition to the skin, two other potential routes of entry by viruses and microorganisms must be guarded:

The digestive tract. Microbes are present in food, but many are killed by saliva (which also contains lysozyme), by the very acidic environment with low PH of the stomach, and by digestive enzymes in the i ntesti ne.

The respiratory tract Microorganisms are also present in inhaled air. The cells lining the smaller bronchi and bronchioles secrete a layer of sticky mucus that traps most microorganisms before they can reach the warm, moist lungs, which would provide ideal breeding grounds for them. Other cells lining these passages have cilia that continually sweep the mucus toward the glottis. This use also defense mechanisms such as, coughing, and sneezing to expel the pathogens

Blood clotting Blood clotting helps to seal wounds rapidly, until a more permanent repair is produced by mitosis of the cells surrounding the wound

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B- Cellular Counterattack: The Second Line of Defense The surface defenses occas[onally breached, allowing invaders to enter the body. The body uses non- specific cellular and chemical devices to defend itself at this point. We refer to this as the second line of defense. These devices all have one property in common: they respond to ony microbial infection without pausing to determine the invader's identity. Although these cells and chemicals of the nonspecific immune response roam

through the body, there is a central location for the collection and distribution of the cells of the immune system; it is called the lymphatic system (fig 4.1). The lymphatic system consists of a network of lymphatic capillaries, ducts, nodes and lymphatic organs, and although it has other functions involved with circulation, it also stores cells and other agents used in the immune response. These cells are distributed throughout the body to fight infections, and also stored in the lymph nodes where foreign invaders can be eliminated as body fluids pass through to the outside.

rcune 4,1 ThG lyrnphalic systsn The lymphatrac qrB{Em consids of lyrtrph.tic vessEls,lyrrph nodes, ard lymphatic f

ortrffrs, lncludiftil tfte sBlee|| tnd lhvmus glOnd

Cells That Kill Invading Antigen

to how leukocytes (white blood cells) originate and develop. Also their appearance under microscope

The following figure show as

\r

Myeloid stern

cell

Lymphoid stern cell

wigrcnurecyre

fmonocvtel / \ Granulocytes / l\

-) cellg

'a

1Sil .* Platelets

Fig 4.2 Origin and

ocyte

Neut

I

T lYmPhocYte killer csll t_

White blood ceils

development of white blood cells

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perhaps the most important of the vertebrate body's non- specific defenses are white blood

invading microbes within cells called leukocytes that circulate through the body and attack microorganisms tissues. There are three basic fiinds of these cells, and each kills invading differently.

c. origin, maturation and mode of action

of phagocytes

stem cells' Phagocytes are produced throughout life in the bone marrow by Neutrophils form about 60% of WBC s in blood' They are stored in bone marrow untilthey are becoming mature. to tissue' They travel throughout the body by squeezing the capillary walls During infection they are released in large numbers from their stores ln addition' neutrophils Like macrophages, ingest and kill bacteria by phagocytosis' that kill other release chemicals (some of which are identical to household bleach)

o o o o

bacteria in the neighborhood as well as neutrophils themselves. Monocytes are formed in the bone marrow by stem cells' o Monocytes leave the bone marrow before being fully functional and attain maturity in the blood stream. . Monocytes settle in the tissue and increases in size slightly, and become macrophages' MacroPhages ("big eaters") . Macrophages are larger than neutrophils o They are found and settle in organs, such as lungs, liver, spleen, kidney lymph nodes and

o o

thYmus. Macrophages are long-lived cells' They play role in initiating immune response

D)

Vechanism of action of phagocytes (Phagocyto sis lkilling by enguffingl

)

The mechanism is described below." This is caused Chemotaxis, i.e., the process by which cells are attracted to the bacteria. is a type of antibody that by the materials released by the bacteria and opsonin which renders bacteria in order that phagocytes destroy or by agglutination' 2. Attachment , the phagocyte and bacteria attach together' 3. Endocytosis, the formation of false feet [pseudopodia] or a simple invagination of the ce||membranethatresu|tsintheforeignbodybeingengu|fed. 4. Vacuole formation, upon engulfment a phagocytic vacuole (phagosome) forms around the bacteria/foreign bodY. 5. Killing/tysis, this can be done byHydrogen Peroxideor other lysins' Remember or other engulfed hydrogen peroxide production requires O z so the lysis of bacteria of certain components is a very much aerobic process. And also the contraction orientation of the contractile proteins, microfilaments is responsible for the changes in energy' requires process also cell membrane associated with vacuole formation so this

1.

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6.

Digestion, lysosomes attache to the phagocytic vacuole and release their contents inside them. Subsequent digestion reduces the bacteria to useful amino acids , respiratory sub*rates [glucose etc] which are taken up by cell for future use. lr

-----\* \\

ff

Ghomotaris snd adhoroncr ol micfobo lo phogocylo"

S

tngonion ot microbo by phlgocyro.

ffi

Formation ol a phrgoeom€

$

fusion of lho phagosomo

S

Digesrion ol ingotrod mlcrobe by GruyrneE.

ffi

rormrtion ot foerduel body

Pseudopod

wlth ! ly$osorlto lo torm s phegolysoromo

conlEining indlgosllb|€

mrl€riEl.

Phagocyte

ffi

oisctrarge of r/voatc mstotlel9.

[.3. Process of phagocytosis

Natural killer cells Natural killer cells

do not attack invading

Killer

microbes directly. Instead, they kill cells of the body that have been infected with viruses. They kill not by phagocytosis, but rather by creating a hole in the plasma membrane of the target cell

cell

Perforin

(figure 4.4.).Proteins, called perforins, are released from the natural killer cells and insert into the membrane of the target cell, forming a pore. This pore allows water to rush into the target cell, which then swells and bursts. Natural killer cells also attack cancer cells, often before the cancer cells have had a chance to develop into a detectable tumor. The vigilant surveillance by natural killer cells is one of the body's most potent defenses agai nst

ca

ncer.

,/

-/"-_--_=-r Nucleus

\

figure 4.4. How natural killer cells kill target cells.

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Proteins That Kill Invading Foreign Particle The cellular defenses of vertdbrates are enhanced by a very effective chemical defense

called the complement system. r This system consists of approximately 20 different proteins that circulate freely in the blood plasma. When they en- counter a bacterial or fungal cell wall, these proteins aggregate to inserts itself into the foreign cell's plasma membrane, forming a pore (figure 4.5). o Water enters the foreign cell through this pore, causing the cell to swell and b u rst. . Aggregation of the complement proteins is also triggered by the binding of antibodies to invading microbes.

lnterferon

Plasma rnembrane

Compl€menl prol0in$

Figure 4.5. Complement protein forming a pore in foreign cells plasma membrane

Another class of protein that plays a key role in body defense is an interferon. Interferon prevents viral replication and protein assembly in the body cells. Interferon is also a part of immunological defense against infection and cancer cells.

The Inflammatory Response The inflammatory response is a localized, nonspecific response to infection. a) Infected or injured cells release chemicalalarm signals, most notably histamine. b) These chemicals promote the dilation of local blood vessels, which increases the flow of blood to the site of infection or injury and causes the area to become red and

warm.

c) d)

e)

f)

They also increase the permeability of capillaries in the area, producing the edema (tissue swelling) so often associated with infection. The more permeable capillaries allow phagocytes (monocytes and neutrophils)to migrate from the blood to the extracellular fluid, where they can attack bacteria. Neutrophils arrive first, spilling out chemicals that kill the bacteria in the vicinity (as well as tissue cells and themselves); the pus associated with some infections is a mixture of dead or dying pathogens, tissue cells, and neutrophils, Monocytes follow, become macrophages and engulf pathogens and the remains of the dead cells (figure4.5).

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irr',:,:

-1,;,:,

,tF$r.,*r"1

y{/! i{rl

t

h

i

Figure 4.6 Events of local inflammation

The Temperature Macrophages that encounter invading microbes release a regulatory molecule called interleukin-l, which is transported by the blood to the brain. 1. Interleukin-l and other pyrogens (Greek pyr,"fire") such as bacterial endotoxins cause neurons in the hypothalamus to raise the body's temperature several degrees above the normal value of 37"C. 2. The elevated temperature results a fever 3. Fever contributes to the body's defense by stimulating phagocytosis and causing the liver and spleen to store iron, reducing blood levels of iron, which bacteria need in large amounts to grow. 4. How- ever, very high fevers are hazardous because excessive heat may inactivate critical enzymes. 5. In general, temperatures greater than 39.4'C are considered dangerous for humans, and those greater than 40.5"C (105"F) are often fatal.

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4.2. Specific Immune Response:The Third Line of Defense Over view of Summary of sfecific immune response

1 | vi."",

infect the cell. Viral proteins are displayed on the cell surface.

Antibodies bind to viral proteins, some displayed on the surface of inf-cted

uleu ""rn cells. ::lli""

qzY

a

|

1

r

:rsa

YY Y{v

r?

r+

V

1-Y

Viruses and viral proteins on infecled cells slimulate macropnages.

11 | Nl"r,opn"g".

destroy viruses and cells tagged wilh antibodies.

lnterleukin-2 activates B cells and cytotoxic T cells.

Some B cells become memory cells.

Fig.4.7 Summary of specific immune response

a;\ Helperrcelr (L-/ )€ \.a-t-__J lnterleukin-1 activates helper T cells, which release interleukin-2.

Interleukin-1

3

| srimutateo macrophages release interleukin-1.

The Immune Response: Chicken pox is an illness thtt many of us experience before we reach our teens. lt is a disease of childhood, because most of us catch it as children and never cqtch it ogoin. Once you have had the disease, you are usually immune to it. Who provides this? lt is Specific immune defense mechanisms provide this immunity.

Introduction about the lmmune Response that milkmaids who had caught a much milder form of "the pox" called cowpox (presumably from cows) rarely caught smallpox. A scientist set out to test the idea that cowpox conferred protection against smallpox. He infected people with cowpox and as he had predicted, many of them became immune to smallpox. We now know that smallpox and cowpox are caused by two different viruses with similar surface antigens. This procedure of injecting a harmless microbe in orderto Smallpox was a common and deadly disease in early days, however,

confer resistance to a dangerous one is called vaccination.

Key Concepts of Specific lmmunity

An antigen is a molecule that provokes a specific immune response. Antigens are large, complex molecules such as proteins; they are generally foreign to the body, usually present of the surface of pathogens. Particular lymphocytes have receptor proteins on their surfaces that recognize an antigen and direct a specific immune response against either the antigen or the cell that carries the antigen. Lymphocytes called B cells respond to antigens by producing proteins called antibodies. Antibody proteins are secreted into the blood and other body fluids and thus provide humoral immunity. (The term humor here is used in its ancient sense, relerring to a body fluid.) Other lymphocytes called T cells do not secrete antibodies but instead directly attack the cells that carry the specific antigens. These cells are thus described as producing cell-mediated immunity The specific immune responses protect the body in two ways. A. First, an individual can gain immunity by being exposed to a pothogen (disease-causing agent) and perhaps getting the disease. This is ocquired immunity, such as the resistance to the chicken pox that you acquire after having the disease in childhood. Another term for this process is active immunity. B. Second, an individual can gain immunity by obtaining the antibodies from another individual. This happened to you before you were born, with antibodies made by your mother being transferred to you across the placenta. lmmunity gained in this way is called passive immunity

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1) Cells of the Specific Immune System The immune defense mechanisfiis of the body involve the actions of white blood cells, or leukocytes. Leukocytes that include phagocytes are involved in the second line of defense, Lymphocytes (T cells and B cellsl, which are not phagocytic cells but are critical to the specific immune response, the third line of defense. o T cells direct the cell-mediated response, o B cells the humoral response. After their origin in the bone marrow, T cells migrate to the thymus (hence the designationn"T"), a gland just above the heart. During maturation process the genes that code for the specific shape of the cells are changed into a variety of ways in order that each one becomes specific to one type of antigen. There they develop the ability to identify microorganisms and viruses by the antigens exposed on their surfaces. Each specializing in the recognition of one particular antigen. There are four principal kinds of T cells:

o

inducer T cells oversee the developmen of T cells in the thymus; o helper T cells (often symbolized TH) initiate the immune response; . cytotoxic l"cell-poisoning"l T cells (often symbolized TC) lyse cells that have been infected by viruses; and . suppressor T cells terminate the immune response. B cells complete their maturation in the bone marrow. From the bone marrow, B cells are released to circulate in the blood and lymph. Individual B cells, like T cells, are specialized to

recognize particular foreign antigens. When a B cell encounters the antigen to which it is targeted, it begins to divide rapidly, and its progeny differentiate into plasma cells and memory cells. Each plasma cell is a miniature factory producing antibodies that stick like flags to that antigen wherever it occurs in the body, marking any cell bearing the antigen for destruction. The immunity that Pasteur observed resulted from such antibodies and from the continued presence of the B cells that prod (stimulate).

2)

Initiating the Immune Response

How the third line of defense works lmagine you have just come down with the flu. Influenza viruses enteryour body in small water droplets inhaled into your respiratory system. lf they avoid becoming ensnared in the mucus lining the respiratory membranes (first line of defense), and avoid consumption by macrophages (second line of defense), the viruses infect and kill mucous membrane cells.

50

At this point macrophages initiate the immune defense' Macrophages inspect the surfaces of all cells they encounter. The surfaces of most vdrtebrate cells possess glycoproteins produced by a group of genes called the maior histocompatibility complex (MHC). These glycoproteins are called MHC proteins or, specifically in humans, human

o o o

o o o o

leukocyte antigens (HtA). The genes encoding the MHC proteins are polymorphic (hove many forms); for example, the human MHC proteins are specified by genes that are the most polymorphic known. Only rarely will two individuals have the same combination of alleles, and the MHC proteins are thus different for each individual, much as fingerprints are. As a result, the MHC proteins on the tissue cells serve as self markers that enable the individual's immune system to distinguish its cells from foreign cells, an ability called self-versus-non-self recogn ition. T cells of the immune system will recognize a cell as self or nonself by the MHC proteins present on the cell surface.

3) T cells: The Cell-Mediated Immune Response (T cells organize attacks against invading microbes) The cell-mediated immune response, carried out by T cells, protects the body from virus infection and cancer, killing abnormal or virus-infected body cells. Once a helper T cell that initiates this response is presented with foreign antigen together with MHC proteins by a macrophage or other antigen-presenting cell, a complex series of steps is initiated. An integral part of this process is the secretion of autocrine regulatory molecules known generally as cytokines, or more specifically as lymphokines if they are secreted by lymphocytes. When a cytokine is first discovered, it is named according to its biological activity (such as B cell-stimulating factor). However, because each cytokine has many different actions, such names can be misleading. Scientists have thus agreed to use the name interleukin, followed by a number, to indicate a cytokine whose amino acid sequence has been determined. lnterleukinI, for example, is secreted by macrophages and can activate the T cell system. B cellstimulating factor, now called interleukin- , is secreted by T cells and is required for the proliferation and clone development of B cells. tnterleukin-2 ond 3 is released by helper T cells and, among its effects, is required for the activation of cytotoxic T lymphocytes.

Cell Interactions in the T cell Response When macrophages process the foreign antigens, they secrete interleukin-l, which stimulates cell division and proliferation of T cells (figure 4.8). Once the helper T cells have been activated by the antigens presented to them by the macrophages, they secrete the cytokines known as macrophage colony-stimulating factor and gamma interferon, which promote the activity of macrophages. In addition, the helper T cells secrete interleukin-2, which stimulates the

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proliferation of cytotoxic T cells that are specific for the antigen. (tnterleukin-2 also stimulotes B cells). Cytotoxic T cells can destroy infected cells only if those cells display the foreign antigen together with their MHC-l prcteins.

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Figure 4'8 The T cell immune defense. After a macrophage has processed an antigen, it releases interleukin-1, signaling helper T cells to bind to the antigen-MHC protein complex.

T Cells in Transplant Rejection

Cytotoxic T cells will also attack any foreign version of MHC-l as if it signaled a virus-infected cell. Therefore, even though vertebrates do not evolve the immune system as a defense against tissue transplants, their immune systems will attack transplanted tissue and cause graft rejection. Recallthat the MHC proteins are polymorphic, but because of their genetic basis, the closer that two individuals are related, the less variance in their MHC proteins and the more likely they will tolerate each other's tissues-this is why relatives are often sought for kidney transplants. The drug cyclosporin inhibits graft rejection by inactivating cytotoxic T cells. Helper T cells are only activated when a foreign antigen is presented together with MHC antigens by a macrophage or other antigen-presenting cells. The helper T cells are also stimulated by interleukin-l secreted by the macrophages, and, when activated, secrete a number of lymphokines. lnterleukin-2 and 3, secreted by helper T cells, activates both cytotoxic T cells and B cells. Cytotoxic T cells destroy infected cells, transplanted cells, and cancer cells by cell mediated attack.

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hat are specific for the antigen. ( 'oy infected cells only if those cells disp 5.

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helper T cells activated by interleukin- 1. Like cytotoxic T cells, B cells s on their surface, one type of receptor for each type of B cell. B cells crobes much as cytotoxic T cells recognize infected cells, but unlike do not go on the attack themselves. Rather, they mark the pathogen for nisms that have no "lD check" system of their own. response, the markers placed by B cells alert complement proteins to ing them. Later in the immune response, the markers placed by B cells and natural killer cells. Unlike the receptors on T cells, which bind only to complexes on antigen-presenting cells, B cell receptors can bind to free, . When a B cell encounters an antigen, antigen particles will enter the B get processed. re able to recognize the specific antigen will bind to the antigen-MHC B cell and release interleukin-2, which stimulates the B cellto divide' In sed antigens stick to antibodies on the B cell surface. This antigen n more B cell proliferation. B cells divide to produce long-lived memory B that serve as short-lived antibody factories (figure 4.9.) The antibodies are plasma and lymph which transport to all parts of the body to destroy

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4) B Celt: The Humoral Immune lB

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to helper T cells activated by interleukin- 1. Like cytotoxic T cells, B cells have receptor proteins on their surface, one type of receptor for each type of B cell. B cells recognize invading microbes much as cytotoxic T cells recognize infected cells, but unlike cytotoxic T cells, they do not go on the attack themselves. Rather, they mark the pathogen for destruction by mechanisms that have no "lD check" system of their own. Early in the immune response, the markers placed by B cells alert complement proteins to attack the cells carrying them. Later in the immune response, the markers placed by B cells activate macrophages and natural killer cells. Unlike the receptors on T cells, which bind only to antigen-MHC protein complexes on antigen-presenting cells, B cell receptors can bind to free, unprocessed antigens. When a B cell encounters an antigen, antigen particles will enter the B cell by endocytosis and get processed. Helper T cells that are able to recognize the specific antigen will bind to the antigen-MHC protein complex on the B cell and release interleukin-2, which stimulates the B cell to divide. In addition, free, unprocessed antigens stick to antibodies on the B cell surface. This antigen exposure triggers even more B cell proliferation. B cells divide to produce long-lived memory B cells and plasma cells that serve as short-lived antibody factories (figure 4.9.) The antibodies are released into the blood plasma and lymph which transport to all parts of the body to destroy pathogens. B cells also respond

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Figure4.9 TheBcell immunedefense. lnvadingparticlesareboundbyBcells,whichinteractwithhelperTcellsandare activated to divide. The multiplying B cells produce either memory B cells or plasma cells that secrete antibodies which bind to invadins microbes and tas them for destruction bv macrophaqes.

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Function of

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