Principal Infectious Diseases of Childhood, 2nd Edition 9781487574536

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PRINCIPAL INFECTIOUS DISEASES OF CHILDHOOD

Principal Infectious Diseases of Childhood SECOND EDITION

N. SILVERTHORNE M.B.

Active Consulting Physician, Hospital for Sick Children, Toronto

C. S.ANGLIN M.D. Associate Physician, Hospital for Sick Children, Toronto Associate in Paediatrics, University of Toronto

M. SHUSTERMAN M.D., F.R.C.S.(C), D.A.8.0. Clinical Fellow in Ophthalmology, University of Toronto Assistant Surgeon, Hospital for Sick Children, Toronto

UNIVERSITY OF TORONTO PRESS

Copyright, Canada, 1958 by University of Toronto Press SECOND EDITION

@ UNIVERSITY OF TORONTO PRESS, 1966

Reprinted in 2018 ISBN 978-1-4875-8577-8 (paper)

Published and distributed in the U.S.A. by Charles C Thomas · Publisher Bannerstone House 310-327 East Lawrence Avenue, Springfield, Illinois, U.S.A. Natchez Plantation House 735 North Atlantic Boulevard, Fort Lauderdale, Florida, U .S.A.

Printed in Canada

Preface

THE PURPOSE of this book is to describe in a clear, concise manner the important features of the common infectious diseases encountered in this geographic area, and thereby serve as a guide to medical students and physicians in general paediatric practice. In many parts of this book the sections are prepared as a general guide or classification of infectious diseases and are not meant to serve as a complete reference text or give all the clinical and laboratory details of the various patterns of the specific diseases discussed. Important features such as epidemiology, unusual or bizarre complications, and the historical background of infectious diseases are not dealt with to any great extent. Rather an attempt has been made to consider the usual clinical picture, the management and preventive or control measures widely accepted in these infections. Emphasis is placed on differential diagnosis comparing the common infectious diseases, particularly those with a specific rash, to other diseases with similar features. This ability to differentiate diseases with similar presenting symptoms appears one of the major problems of medical students and practising physicians. While this ability comes mainly

vi Preface

with vast experience, it is hoped this book may help clarify some of the essential differential diagnostic points in these common infectious diseases. N.S. C. S. A. M.S.

Contents

Preface

V

1

Infections in the New-Born

3

2

Ocular Infections in Children

16

3

Infectious or Communicable Diseases

41

4

Infections of the Nervous System

79

5

Virus Diseases

98

6

Respiratory Infections (Non-Virus)

125

PRINCIPAL INFECTIOUS DISEASES OF CIDLDHOOD

t I Infections in the New-Born

in the new-born may be divided into two categories according to whether their effects are local or general. INFECTIONS

LOCAL INFECTIONS

Local infections are: omphalitis, mastitis, pustular dermatitis, impetigo, furunculosis, paronychia, conjunctivitis, vaginitis, and cutaneous myiasis. Most of these conditions can be prevented if proper aseptic techniques are used in connection with all activities of persons caring for the new-born. Omphalitis Omphalitis is an infection occurring at and around the umbilicus. A smear and culture of this area should be taken in order to determine the cause, which may be any of the common bacterial types, for example, staphylococcus, streptococcus or B. coli; diphtheria also has caused this infection in past years. With the improvement of obstetrical technique and more careful aseptic supervision of the new-born, however, infections of all types in this area are now rare. TREATMENT. Local treatment should consist of the application of warm compresses followed by an ointment

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Principal Infectious Diseases of Childhood

containing one of the sulphonamides or antibiotics. These should be applied every three or four hours until the lesion has healed. To prevent a generalized infection of the blood stream, penicillin or another appropriate antibiotic may be administered every four hours or twice daily especially if the local area is extending over a wider area. Mastitis

Most babies' breasts are congested in the early days and weeks of life, and a secretion of fluid from them can often be noticed. On occasions, however, an area to one side of the nipple becomes red and swollen. This is the beginning of a breast abscess which may suppurate, fluctuate and ultimately discharge; it may, however, have to be incised. TREATMENT. Breasts congested with fluid should be left completely alone. If there is any inflammation, sulphonamides, penicillin, or a broad spectrum antibiotic should be given in appropriate doses by mouth or injected intramuscularly. Most often these breast abscesses become suppurated and fluctuate, and should be incised, drained and dressed with moist dressings until they heal, using an appropriate antibiotic ointment. Pustular Dermatitis

Pustular dermatitis usually develops from some skin irritation and a low-grade pustular infection. It may appear on any area which is irritated and subject to constant contact with moisture. Particularly vulnerable is the skin of the lower abdomen and that covered by the diaper. The lesions consist of a red, inflamed base with myriads of small pinpoint pustules superimposed on the erythematous surface. TREATMENT. The lesions often respond well to bathing with alcohol followed by a dusting powder, such as 1 per

Infections in the New-Born

5

cent calomel in starch. If the rash does not respond quickly to this treatment, then an ointment containing sulphonamides or antibiotics is recommended. In most cases, exposure, for several periods during the day, of the infected parts to dry heat from an electric light cradle, placed well away from the baby, is indicated. Impetigo Impetigo is one of the most common skin conditions found in the new-born. Although the disease is seen in epidemics in nurseries, babies born at home also develop it. Usually it is caused by the staphylococcus. The lesions, which are quite typical irregular sacs or blisters of skin filled with fluid, occur initially as a red spot ½6 to ¼ or ½ inches in diameter with irregular borders. The fluid inside the blister rapidly becomes purulent, breaks down and spreads to other areas. The actual reason for the occurrence of these lesions has never been discovered. They occur more frequently in warm weather, crowded nurseries and in areas of the skin where moisture and irritation are liable to occur: the diaper area, lower abdomen, under the arms, and around the neck and shoulders. Often they are very persistent and resist treatment, with new lesions occurring daily. TREATMENT. The blisters should be carefully broken down and the discharge from them taken up by absorbent cotton. Crusted lesions should be soaked off with soap and lukewarm sterile water. After the lesions have been cleansed in this way, ointments of sulphathiazole or those containing antibiotics should be applied directly to them every four hours. If the lesions are generally distributed, penicillin or a broad spectrum antibiotic should be injected intramuscularly twice daily. All treatment should be continued until the lesions have healed and no more appear. In this disease,

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Principal Infectious Diseases of Childhood

as with pustular dermatitis, a light cradle or the heat from a goose-neck lamp helps greatly in keeping the exposed parts dry. Care should be taken that there is no danger to the baby from contact with the lamp or a bum from the heat. Phisohex may be used in nurseries or at home; bathing the baby in an appropriate solution will help to prevent further lesions. Epidermolysis bullosa, an extremely uncommon, inherited disease, is mentioned here because of its slight resemblance to impetigo. The lesions consist of large bullous blebs with clear serum in them, huge irregular blisters with sterile fluid constantly recurring, leaving red inflamed areas which rarely heal completely. Scarring, deformity, and invalidism result. There is no satisfactory treatment. Furunculosis

Furunculosis manifests itself as a small subcutaneous abscess. It usually affects new-born children who have not been very well cared for and who belong to the lower socio-economic level. These lesions look like miniature boils, with a somewhat more reddened indurated conical base than is seen in impetigo, and a raised pointed top extruding pus. They are usually caused by the staphylococcus. TREATMENT. Treatment consists of the application of warm or alcohol compresses, local applications of sulphonamide or antibiotic ointments, injections of one of the antibiotics, and exposure to a heat cradle. If the lesions persist or recur, a course of injections of staphylococcus toxoid should be administered. Paronychia

These lesions also occur in the early days of the infant's life and are most annoying and at times difficult to treat.

Infections in the New-Born

1

The lesion is usually due to the staphylococcus and appears as a red inflamed area along the side of the nail bed which may become purulent and discharge. It is usually seen beside the nails of the thumbs or fingers, but may also be present along the toe nails. TREATMENT. The same treatment may be employed for this condition as has been outlined for the other skin infections. In addition, it is wise to prevent the patient from using his hands to scratch his face or other parts of his body. Vaginitis Vaginitis in the new-born is not uncommon. At birth a white mucous discharge is always present between the labia minora. This discharge is quite normal. Occasionally, however, a non-specific vaginitis is present and some infants may suffer from a gonococcal vaginitis from which there is a profuse purulent discharge. TREATMENT. Vaginitis in the new-born should be treated by gentle irrigations or wiping the discharge away with a sterile cotton wool soaked in sterile water, and by the injection of penicillin or a broad spectrum antibiotic every four hours until the discharge has cleared up and cultures of the discharge repeatedly show no growth of the offending bacterial species. Cutaneous Myiasis This disease is extremely rare, occurring, in this climate, in the month of June and is caused by a gravid female insect (Wolfarhtia vigil Walker) which deposits larvae directly into the normal tissues of the new-born. The larvae crawl between the creases of skin or skin folds, such as those over the eyelids, between the orbit and the eyelid, at the

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Principal Infectious Diseases of Childhood

neck, under the arms or at the groin. The parasite then burrows deep into the superficial layers of the skin causing a small furuncle-like lesion. TREATMENT. Each larva should be extracted with forceps from the lesions. They are quite easy to pick out. Thereafter, the lesions heal quickly. GENERAL INFECTIONS

General infections are: upper respiratory disease, lower respiratory disease, sepsis of the new-born. Upper Respiratory Disease This disease is not common in the new-born if all methods known to prevent cross infection are followed in the nursery and home. It is not unusual to find infants suffering from upper respiratory disease where there is overcrowdingfor example, in nurseries where there are many physicians, students, nurses, and visiting relatives, and the babies are thus exposed to adults with respiratory infections. This state of affairs should not exist with our present-day knowledge of measures to prevent disease in the new-born. When the new-born infant has been in contact with a carrier or an individual suffering from a nasopharyngitis, he easily contracts an infection. Usually it is not serious and manifests itself in a slight rise in fever, discharging nose, irritability and often a refusal to nurse or feed. The infant's nose is often plugged with mucus and he has difficulty in breathing while feeding, cries and draws his head away from the nipple. He may also have an associated otitis media which manifests itself in red swollen inflamed ear drums . . PREVENTION. The nursery in the hospital should be so

Infections in the New-Born

9

constructed that the babies are, except when examination and nursing are necessary, isolated from all visitors except the regular nursery attendant. When it is necessary for the physician to make his examination, he should put on a sterile gown and mask, wash his hands and use the instruments provided by the nursery. The baby should be brought to him by the nursery nurse in a special room and returned to the nursery after examination. It is also important that the nursery attendant take the baby out to the mother for nursing and return him to the nursery. The mother should wash her hands before wiping off her nipples with sterile water in preparation for nursing her baby. If these measures are followed, there is much less opportunity for the baby to develop a respiratory infection. In the home, the newborn should be isolated most of the time from other members of the family, and the physician, nurse and mother should observe the precautions already mentioned for hospital care. TREATMENT. The treatment of an upper respiratory infection in the new-born should be similar to that for the older child; namely, the freeing of the nares of annoying discharges, the use of aqueous ephedrine nose drops when needed, and the administration of sulphonamides or antibiotics in appropriate doses-for example, 1 grain per pound per day of some sulphonamide preparation or 50,000 units of penicillin taken orally every four hours or penicillin injected twice daily or a broad spectrum antibiotic. Lower Respiratory Disease This disease may be caused by: ( 1) aspiration of mucus or feeding, (2) upper respiratory disease due to the usual common bacterial species with a pneumonic extension, ( 3) virus infections.

10

Principal Infectious Diseases of Childhood

A pneumonia may develop in the new-born as a result of one of the above infections. The baby sudenly becomes ill with fever, may have a blue spell (from aspiration), becomes distressed in breathing with the usual signs of pneumonia-flaring nares, expiratory grunt, marked lower costal indrawing, cough, and spells of choking and blueness due to excessive amounts of mucus in the small passages. Diminished air entry in both sides, degrees of atelectasis and fine crackling rales are often found. PREVENTION. Preventing an infant from aspirating the feeding or mucus is of paramount importance. Proper administration of the food to prevent it from being taken too quickly, with subsequent choking and aspiration, is very important in the prevention of an aspiration pneumonia. The other methods of prevention have been referred to under "Upper Respiratory Disease." TREATMENT. The baby who has aspirated his feeding should be treated immediately by gentle suction through a laryngoscope, or, if the condition is more severe, with bronchoscopic suction. The baby should be placed in 40-60 per cent exygen and cared for, preferably, by special nurses. Gentle electric suction with a small rubber catheter removes the mucus which has collected in the throat and nares. Antibiotics and sulphonamides should be given in the doses already indicated under "Upper Respiratory Disease." Feedings should be administered with great care by the nursing mother or the attending nurse, with special care that the administration of the feeding proceeds in small amounts and not too quickly, with frequent pauses in order to allow the baby to swallow and breathe properly. Nurseries where outbreaks of upper and lower respiratory disease have developed should be closed to further admissions and isolated from all others.

Infections in the New-Born

11

Sepsis of the New-Bom In its broadest sense, the term "sepsis" would include any infection of the new-born of a general nature and possibly metastasizing to various organs. It is difficult to understand the nature of this syndrome exactly. If the causative agent or agents were always known it would be best classified under some bacterial cause. Various aetiological agents have been found to be responsible for sepsis of the new-born. Some authors include septicaemia, peritonitis, meningitis, pneumonia, septic arthritis and gastro-intestinal infections under this general heading. It is possible that most cases of general sepsis commence with a focus of infection: for example, skin infections, umbilical infections and respiratory infections which disseminate by way of the blood stream and metastasize to the peritoneal cavity, bones and joints, the subarachnoid space and other tissues. In most of these infections, there is usually a common group of symptoms and signs which may vary with the type of infecting agent, and also with the system finally involved. AETIOLOGY. The most common causative agents are: haemolytic staphylococcus, haemolytic streptococcus, pneumococcus and B. coli. More rarely, infections of the new-born have been caused by: gonococcus, meningococcus, Bacillus pyocyaneus, Bacterium lactis aerogenes, Friedlander's bacillus and tetanus bacillus. There have been new-born patients suffering from an infection due to Bacillus anitratum, which may cause meningeal or gastro-intestinal infections. PORTAL OF ENTRY. Usually entry is by way of the umbilicus; at times this may appear quite clear while at other times there is an omphalitis. Certain skin infections may lead to general sepsis, especially impetigo when it is not adequately treated. In other infections, the portal of

12

Principal Infectious Diseases of Childhood

entry may be the respiratory passages, and in epidemic diarrhoea of the new-born the portal of entry is the gastrointestinal tract, usually as the result of infected food. PATHOLOGY. The pathological findings usually depend on the portal of entry and the metastases. If the infection travels by way of the umbilicus, there may be a positive culture of some specific infecting species or an actual suppurative thrombophlebitis of the umbilical veins leading to the liver. There are often pyogenic abscesses in the various organs with haemorrhagic manifestations-for example, purulent material in joints, peritoneal cavity, meninges, pleural cavity or multiple abscesses of soft tissues. There may be cloudy swelling of organs and enlargement of liver and spleen. SIGNS AND SYMPTOMS. Babies with sepsis usually appear ill and drowsy, may refuse their feedings, vomit, lose weight, have diarrhoea, become irritable, appear dehydrated and also develop intoxication. Most babies have a fever, often of an irregular septic type, at the onset of sepsis; there are some in whom the onset is very insidious and they may have no rise in temperature which at times may actually be subnormal. There is often enlargement of the liver and spleen and jaundice may accompany the sepsis. DIAGNOSIS. Sepsis must be differentiated from such conditions as inanition fever and local upper respiratory infections causing fever. The baby with sepsis is much more ill in appearance than the baby with other febrile conditions or local infections. If the baby has a septic fever, is restless, drowsy at times, vomiting, has diarrhoea, feels hot, is dehydrated and has an enlarged or palpable spleen with or without jaundice, he may be considered to have sepsis of the new-born. An elevated white count may also aid

Infections in the New-Born

13

in the diagnosis and a positive blood culture is confirmatory evidence. LABORATORY FINDINGS. Often a blood culture will reveal some causative agent and cultures of some specific aetiological agent may be obtained from various metastatic foci-for example, peritoneal cavity, cerebrospinal fluid, pleural fluid, abscess cavities and sometimes the gastrointestinal tract. There is usually an elevated white blood count with a preponderance of polymorphonuclear leukocytes, although on occasion a leukopenia may exist. INCIDENCE. Years ago many infants died of sepsis but its incidence has been materially lessened by the improved obstetrical care of the mother and improved conditions in nurseries for the new-born. At present, the disease is rare in centres where asepsis is practised both in the obstetrical hospital and in the new-born nursery, and the early management of the suspected case by sulphonamide and antibiotic therapy has also reduced the incidence of this condition. PROGNOSIS. The prognosis has very materially improved, mainly as the result of better facilities for treatment and more energetic treatment at the onset with specific chemoand antibiotic therapy. The prognosis of the more severe types, such as peritonitis and meningitis, must still be guarded especially during the first few days of life. TREATMENT. Prevention, of course, is the key-note to proper treatment. This is best done by aseptic procedures in the obstetrical department and by care of the skin and umbilicus of the baby. The usual nursery technique of masking, gowning, washing of hands of attending personnel and isolation for each baby does much to prevent sepsis and its spread from one baby to another. Keeping all persons, especially those with any infection, out of the

14

Principal, Infectious Diseases of Childhood

nursery, except the regular nursery attendant, is paramount. Where any attempt at resuscitation has involved the possibility of a lung infection, some antibiotic should be administered for two or three days. This is best given at regular intervals or in an adequate dose twice daily by intramuscular injection. The infant who develops sepsis is usually quite ill and often has an infection of the blood stream. Treatment should always follow certain definite procedures. ( 1 ) Fluids, lactose water, glucose solution or diluted milk formulae should be given at more frequent intervals than usual. (2) Continuous intravenous injections of appropriate glucose saline mixtures should be administered. ( 3) Interstitials should be given two or three times daily if there is no pyogenic skin involvement and if intravenous therapy is not considered necessary. ( 4) Blood transfusions may be given and repeated depending on the severity of the individual cases. ( 5) Sulphonamides and antibiotics in adequate doses should be given intravenously, intramuscularly and/or by mouth if there is no extensive vomiting or diarrhoea. Usually the antibiotic or chemotherapeutic agent especially effective against the causative agent should be used as soon as this cause is known. If the causative agent has not been isolated or ascertained, sulphadiazine or some other intravenous sulphonamide in doses of 1 to 2 grains per lb. per day should be used along with some antibiotic effective against a wide range of bacteria. Penicillin, staphcillin, erythromycin or chloromycetin may also be used for the gram positive group of bacteria. Undoubtedly in the future there will be many other antibiotics equally or more effective which may be given intravenously or intramuscularly. DISCUSSION. Sepsis includes other well-known infections of the new-born such as peritoneal, genito-urinary infec-

Infections in the New-Born

15

tions, meningeal infections and more rare infections such as tetanus. Some of these will be dealt with in other chapters describing diseases in the child, but it is important to emphasize that most of these conditions are merely metastatic manifestations of septicaemia (sepsis) of the new-born and as such should be treated in much the same manner. If sepsis is treated early with adequate doses of chemotherapeutics and antibiotics, many of these metastatic foci will not develop. INANITION FEVER

A sudden rise in temperature to 102° F.-105° F. is sometimes noted on the second, third, or fourth day after birth. In the absence of any other findings related to some infection, local or general, this rise may be considered to be due to dehydration, which is likely the cause of inanition fever. The baby may also reveal certain physical symptoms -for example, sudden loss in weight, dry lips and tongue, glassy eyes, wrinkled face, and evidences of skin dehydration. The equally sudden return to a normal temperature after the administration of fluids by mouth, interstitially or intravenously, usually confirms the diagnosis. TREATMENT. The treatment consists of the administration of fluid, either by mouth, interstitially or, in severe cases, intravenously-usually 10 cc. per lb. of 5 per cent glucose in normal saline is adequate.

21 Ocular Infections in Children

of infections may involve the eye and its adnexa in infants and children but only those commonly encountered in this area will be mentioned. Most of the microorganisms affecting other parts of the body may also afflict the ocular tissues. The commonly involved ocular tissues will be considered in turn.

A LARGE NUMBER

THE CONJUNCTIVA

Infection of the conjunctiva, conjunctivitis, is a very common clinical condition of multiple etiology but characterised in all cases by superficial conjunctiva! hyperemia or congestion. The appearance is that of a "red eye," the redness being most marked in the fomix and decreasing toward the limbus. The other symptoms and signs of inflammation are also present: pain, chemosis (edema of the conjunctiva), exudation of cells and fluid, and the reaction of the tissue cells. The conjunctival epithelium may show a simple thickening or become hyperplastic and form reddish papillae. When small and numerous, the latter non-specific structures will impart a velvety appearance to the palpebral and fomix conjunctiva. Another reaction of the tissue cells which may occur, but only in older children, is the forma-

Ocular Infections in Children

11

tion of lymph follicles from the normal lymphoid tissue of the stroma ( which is absent at birth and slowly develops after the third month of life). The follicles are usually seen in the fornix conjunctiva near the proximal border of the tarsus and appear grossly as greyish, round or oval elevations, resembling frog's eggs. TREATMENT. Precautions should be taken to prevent the spread of the infection. If severe, or if the patient is living in close proximity to others, isolation techniques are indicated. Active treatment consists of removing the exudate or secretions by simple wiping of the lids with a cotton ball or swab stick. On rare occasions, gentle irrigation of the conjunctiva! sac with warm water or saline is necessary to remove sticky or adherent secretions. This is followed by frequent instillations of an appropriate anti-microbial agent. In infants, ointments are usually applied every three or four hours. In older, more cooperative children, drops are instilled every two or three hours. Eye drops have the advantage of not blurring the patient's vision but they require more frequent usage. Ointments keep the suspended drug in longer contact with the tissues but the greasy film tends to blur the vision and spill over the lid margins onto the delicate eyelid skin, thereby being more likely to produce contact allergy. If the infection is severe or there is difficulty opening the eyelids to instil the medication, systemic therapy may also be used. It is not necessary to wait for a laboratory report before starting treatment. After the feasible laboratory tests have been initiated, a topical antimicrobial agent of broad activity may be initiated. We favour, at the present time, the frequent instillation of a sulfonamide ( usually Sulfacetamide 10 per cent to 30 per cent or Gantrisin 4 per cent). The antimicrobal agent should be changed in two or three days

18

Principal Infectious Diseases of Childhood

if indicated by the laboratory sensitivity tests or if the clinical reponse is poor. Several forms of infectious conjunctivitis are recognized clinically and these will now be noted. Hyperacute (Purulent) Conjunctivitis

This is a severe acute conjunctivitis with marked chemosis, eyelid edema, profuse purulent discharge and a tendency to corneal involvement. The common etiological agent is the gonococcus (Neisseria gonorrhoeae), occasionally the meningococcus (Neisseria meningitidis), and very rarely micrococcus catarrhalis (Neisseria catarrhalis). The Mimeae, a recently recognized tribe of bacteria, may also produce purulent conjunctivitis. As their name indicates, they mimic the gonococcus clinically and appear as gram negative diplococci on smear but their cultural characteristics and antigenic structure differentiate them from gonococci and other bacteria. Finally, mixed infections, especially secondary bacterial invasion of a primary viral conjunctivitis ( as often occurs in patients with inclusion conjunctivitis), will also produce a hyperacute conjunctiva! inflammation. (a) GONOCOCCAL CONJUNCTIVITIS IN OLDER CHILDREN. This disease, acquired by contact with the highly contagious gonorrheal pus, has an incubation period of one to three days. A tentative diagnosis can be made by the history of exposure, short incubation period and the severe ocular reaction. A definite diagnosis is made by the usual smear and cultural methods, remembering to inoculate the proper culture medium--chocolate agar incubated in 10 per cent carbon dioxide atmosphere-and the sugars glucose and maltose. Another diagnostic aid is the gentle scraping of the palpebral conjunctiva with a blunt spatula or dull blade,

Ocular Infections in Children

19

spreading the epithelial cells onto a glass slide, then staining with Wright or Giemsa stain and finally searching for the characteristic gram negative diplococci. Treatment. The measures previously outlined for the treatment of infectious conjunctivitis in general should be rigidly followed. Penicillin is still the specific treatment of choice. Topical eye drops, 2,000 to 10,000 units per c.c., should be instilled every hour for the first thirty-six hours. As the signs diminish, the frequency of eye drop instillation is decreased. Concurrent systemic penicillin therapy is usually administered. In the patient allergic to penicillin or with penicillin-resistant gonococci, the tetracyclines, sulfonamides or chloramphenicol are employed. (b) GONOCOCCAL CONJUNCTIVITIS IN THE NEWBORN.

This type of hyperacute conjunctivitis presents a clinical picture similar to gonococcal conjunctivitis in older children and adults but both eyes are usually involved. The incubation period may vary from twelve hours to four days, most cases showing the initial discharge one or two days after birth. The infection is acquired by contact of the infant's conjunctiva and lid margin with the mother's infected cervix. The Crede method of prophylaxis---cleansing the eyelids immediately after birth and instilling a drop of 1 per cent silver nitrate into the conjunctiva! sac of each eye-usually destroys any gonococci present. In some hospitals, the silver nitrate has been replaced by an antimicrobial agent with similar good results. Treatment. The active treatment is the same as that outlined for gonorrheal conjunctivitis in the older child. (c) OPHTHALMIA NEONATORUM. This term is applied to any case of severe or hyperacute conjunctivitis in the newborn infant. With this broad definition, the etiological agent

20

Principal Infectious Diseases of Childhood

is classified as infectious (usually bacterial or viral) or noninfectious ( usually a chemical irritant) . In the latter group, the silver nitrate of the Crede prophylaxis is at fault. In these cases, the ocular discharge appears within twelve to twentyfour hours after birth and usually disappears spontaneously in three or four days. In the infectious group, the gonococcus and other Neisseriae as well as the Mimeae have already been noted in earlier paragraphs of this section. In addition, any of the common pathogenic bacteria may be isolated. Pathogenic staphylococci ( those which can ferment mannitol, liquefy gelatin or produce coagulase or accomplish all three tests), pneumococci, streptococci, pseudomonas (pyocyaneous), coliform and influenza! microorganisms may occur. In most of these, the ocular discharge develops after the fifth day of life. The only viral agent which may occur in ophthalmia neonatorum is that of Inclusion Blennorrhea (Inclusion Conjunctivitis). The incubation period is relatively long, varying from five to ten days. The purulent conjunctivitis produced may become very severe if secondary infection occurs. In all cases, the etiological agent should be determined by secretion smears, gentle conjunctiva! scrapings and cultures; appropriate therapy is instituted as outlined in previous sections. Acute Catarrhal Conjunctivitis

This is also known as acute mucopurulent or acute simple conjunctivitis. It is recognized clinically by a moderate amount of superficial conjunctiva! hyperemia and accompanied by a mucoid or mucopurulent discharge. The latter is contagious and the disease easily spreads among children in the same household or institution, hence this condition has also been called Epidemic Pink eye. The condition will

Ocular Infections in Children

21

usually heal spontaneously in one or two weeks but sometimes a subacute or chronic catarrhal conjunctivitis persists ( often because a blepharitis, almost always staphylococcal, has also developed). In occasional cases, the condition causes small, greyish, round areas to form in the periphery of the cornea. These are called marginal corneal infiltrates; if they stain with fluorescein solution they are termed marginal catarrhal ulcers. In this area, the commonest cause of acute catarrhal conjunctivitis in infants and children is the pathogenic staphylococcus, followed in frequency by hemophilus influenzae and diplococcus pneumoniae (pneumococci). Other pathogenic organisms such as streptococci, Neisseria catarrhalis, Escherichia coli and Proteus vulgaris are occasionally found. The Koch-Weeks bacillus (hemophilus egyptius, hemophilus conjunctivitidis), a common cause in southern climates, is very rare in the Toronto area. Treatment. This was outlined in the general section on conjunctivitis. Chronic Catarrhal ConjonctMtis This is also known as subacute catarrhal or chronic simple conjunctivitis. It is a chronic inflammation of the conjunctiva of both eyes with symptoms and signs similar to those found in the acute form but milder in degree. The most frequent complication is blepharitis and this may result in trichiasis, loss of cilia, eczema of the lids and eversion of the lower punctum. Corneal complications which may occur are marginal infiltrates and ulcers, minute epithelial erosions and superficial punctate keratitis. Recurrence of a chronic conjunctivitis is common, especially if the etiological factors are not completely eliminated or recur. As in the acute form, the commonest cause in this area is

22

Principal Infectious Diseases of Childhood

the pathogenic staphylococcus. Cultures and smears may occasionally reveal other pathogenic bacteria such as Streptococcus viridans, Neisseria catarrhalis, Escherichia coli and Moraxella lacunata (Morax-Axenfeld diplobacillus). As yet, no virus, per se, has been found to cause chronic catarrhal conjunctivitis. The condition may follow acute conjunctivitis or may be due to improper hygiene, such as insufficient sleep, uncorrected refractive errors, and prolonged exposure to such irritants as wind, dust, smoke or volatile chemicals. In some cases, allergic factors are paramount, in others seborrheic blepharitis is the underlying element. Treatment. As outlined previously, the cause or causes must be found and eliminated. Unilateral chronic conjunctivitis suggests the presence of either a foreign body in one fornix, especially in the less accessible upper one, or an inflammation of the lacrimal drainage system, or a wart somewhere along the lid margin discharging desquamated products into the conjunctiva! sac. Any associated blepharitis is treated by the methods outlined in the section on eyelids. ANGULAR CONJUNCTMTIS. This is a descriptive term used to identify a type of bilateral chronic catarrhal conjunctivitis with associated excoriation of the skin of the eyelids at the angles, especially the lateral. The usual cause in this northern locality is the pathogenic staphylococcus and it responds to the topical use of sulfonamides or antibiotics. In other areas, the diplobacillus of Morax-Axenfeld (Moraxella lacunata) is described as the common cause and responds to frequent instillations of zinc sulphate 0.25 per cent or sulfonamides. However, in the Toronto area, this bacillus is rarely found. LACRIMAL CONJUNCTIVITIS. This term identifies a type

Ocular Infections in Children

23

of unilateral chronic conjunctivitis which accompanies dacrocystitis and is caused by the infectious discharge from the diseased lacrimal sac. As outlined in the section on chronic dacrocystitis, the underlying etiology is obstruction of the nasolacrimal duct, either congenital or acquired. Some cases are due to concretions which partially or completely block the lacrimal canaliculi. Smears of the concretions show Gram positive filaments, unbranched, and accompanied by numerous conidia or spores. This organism is a fungus, Streptothrix foesteri, an actinomyces of low pathogenicity. Treatment consists of dilating the puncta and canaliculi, inserting tiny curettes and removing all the concretions. This is followed by irrigation of the lacrimal passages to remove all traces of the micro-organism. Acute Follicular Conjunctivitis

This is an acute inflammation of the conjunctiva, usually caused by a virus, and characterised by hyperplasia of the subconjunctival lymphoid tissue with the production of surface follicles (previously described in the introductory general section of Conjunctivitis). In this acute disease the inciting organism is sufficiently toxic to induce enlargement of the regional lymph nodes. The common types of acute follicular conjunctivitis in this geographic locale will be briefly noted. (a) INCLUSION CONJUNCTIVITIS (Inclusion Blennorrhea). This bilateral condition, caused by a virus which can be isolated, affects the conjunctiva of infants and older children, the urethra of the adult male and the cervix of the adult female. The newborn infant acquires the disease during the birth process from the infected cervix. After an incubation period of five to ten days, the newborn develops an acute purulent conjunctivitis without adenopathy or

24

Principal Infectious Diseases of Childhood

follicles ( the infant's conjunctiva being initially incapable of developing follicular hypertrophy). If untreated, the acute phase subsides into a chronic follicular conjunctivitis with spontaneous healing in three to twelve months. The cornea is never affected. In the older child or adult, the disease is usually acquired by swimming in contaminated pools ("swimming pool conjunctivitis") but occasionally is caused by accidental contamination with the contagious discharge. The disease is similar to that of the infant except it is follicular from the beginning and most cases show some preauricular lymphadenopathy. The diagnosis is made on the basis of the clinical picture and the finding of cytoplasmic basophilic inclusion bodies in the conjunctiva! epithelial cells which have been gently scraped off, placed on a glass slide and stained by Giemsa's method. The scraping will also reveal that the exudate is predominantly neutrophilic, in contrast to the mononuclear cell exudate found in most ocular viral infections. Treatment. In the infant, the frequent instillation of a topical sulfonamide or tetracycline will be efficacious. In the older child or adult, some cases may require systemic as well as local administration of one of these drugs in order to halt a chronic course of the disease. (b) ADENOVIRUS CONJUNCTIVITIS. The adenoviruses cause two types of follicular conjunctivitis, Pharyngoconjunctival Fever (part of a symptom complex) and Epidemic Keratoconjunctivitis ( a specific type of keratoconjunctivitis). In both types, conjunctiva! scrapings and secretion smears show a preponderance of mononuclear cells and no inclusion bodies or bacteria. PHARYNGOCONJUNCTIVAL FEVER (PCF). This form of acute follicular conjunctivitis occurs sporadically and ap-

Ocular Infections in Children

25

pears as an acute hyperemia with follicles predominantly in the lower fornix and inferior tarsal conjunctiva. The preauricular nodes are palpably enlarged. Examination with a slit-lamp microscope may reveal an epithelial keratitis, sometimes with minimal subepithelial infiltrates. The disease is usually bilateral and shows systemic signs of fever and sore throat. It is self-limited and heals with no sequelae in two or three weeks. Of the many types of adenoviruses, types 2, 3 and 6 have been recovered in these sporadic cases, type 3 being most frequent. The disease also occurs epidemically, usually during the warm summer months, with swimming pools being the usual source of infection. A recent epidemic in this area revealed type 7 adenovirus. In the epidemic form, the disease is readily recognized by the characteristic triad of symptoms-pharyngitis, conjunctivitis and fever-with children being more severely affected than adults. EPIDEMIC KERATOCONJUNCTIVITIS (EKC) . This condition is less common than pharyngoconjunctival fever but is a more severe ocular infection. It may be endemic or epidemic and is caused by type 8 adenovirus. It appears as a severe acute pseudomembranous or follicular conjunctivitis with prominent regional lymphadenopathy. A characteristic keratitis appears seven to ten days after onset-small, round, discrete, greyish infiltrates in the pupillary zone. Except in rare infantile cases, this condition is not associated with fever or pharyngitis. Treatment. Since all adenoviruses are unaffected by the presently available antibacterial drugs, treatment is symptomatic. Cold or warm compresses may be applied to the eyelids. Virus vaccination or injection of gamma globulin may be useful to prevent spread during epidemics. (c) ACUTE PRIMARY HERPETIC KERATOCONJUNCTMTIS.

26

Principal Infectious Diseases of Childhood

The primary attack of herpes simplex in infants and young children may be a subclinical infection or an acute keratoconjunctivitis of one or both eyes, occurring alone or with systemic manifestations of fever, malaise, enlargement of lymph nodes and vesicular lesions of the skin of the eyelids and mouth. Vesicular eruptions may also occur in the palpebral conjunctiva. The usual conjunctiva! appearance is follicular but occasionally a pseudomembrane is present on the surface. The typical corneal changes consist of one or more superficial branching or dendritic-shaped lesions which quickly develop into an ulcer. As in adenoviral infections, conjunctiva! scrapings reveal a mononuclear cell exudate and no inclusion bodies or bacteria but, in addition, giant multinucleated epithelial cells typical of herpes simplex virus infection. As in adenoviral infections, the laboratory diagnosis is definitively based on the isolation of the virus and the demonstration of a rising titer of neutralizing antibody during the illness and convalescence. Treatment. This consists of the very frequent instillation of 0.1 per cent solution of IDU (5-iodo-2 deoxyuridine, idoxuridine). Corticosteroids are contraindicated. In some resistant cases, the corneal lesions must be cauterised with tincture of iodine, 2 ½ to 3 ½ per cent, care being taken to remove all the affected and adjacent epithelium. Chronic Follicular Conjunctivitis This is a group of diseases caused by a variety of chronic conjunctiva! irritants and manifested by prolonged follicular hypertrophy of the conjunctiva. Apart from Parinaud's oculoglandular conjunctivitis, the various types of chronic follicular conjunctivitis do not show regional lymphadenopathy.

Ocular Infections in Children 21

(a) TOXIC OR REACTIVE CHRONIC FOLLICULAR CON-

This consists of a group of conditions in which the conjunctiva! follicles result from a secondary toxic stimulus rather than from a primary disease of the conjunctiva. The two conditions commonly seen in children are both viral warts of the skin, molluscum contagiosum and verruca vulgaris ( the common wart). The former is characterised by the production of firm, flat-topped or umbilicated papillae on any part of the skin, especially the chest and face. When located on the margin of an eyelid, the desquamated material from the nodule falls into the conjunctival sac and produces a chronic follicular conjunctivitis with scanty exudate. If unrecognized, the condition continues indefinitely and may develop a keratitis with pannus ( often of the upper third of the cornea regardless of the position of the molluscum nodule) and conjunctiva} thickening resembling trachoma. In contrast, verruca vulgaris on the lid margin usually produces a subacute or chronic catarrhal conjunctivitis with mild papillary formation but also with scanty secretion. If unrecognized, it too can continue and produce a keratitis (but this is usually confined to the epithelium and may resemble recurrent corneal erosions). In both these virus infections, conjunctiva! scrapings and smears reveal a mononuclear reaction and no inclusions in the conjunctiva! epithelial cells. The diagnosis of either condition can definitively be made by histopathological examination of the excised lid margin lesion since each produces its own characteristic picture. Treatment. In both conditions, the treatment is the removal of the lid margin lesion by surgery, chemicals or electrocoagulation. (b) PARINAUD'S OCULOGLANDULAR CONJUNCTMTIS. This name is applied to any unilateral chronic conjunctivitis, JUNCTIVITIS.

28

Principal Infectious Diseases of Childhood

usually follicular and with regional lymphadenopathy, caused primarily by one or more granulomas, vegetations, or ulcers involving the conjunctiva and adjacent tissues. The original reported cases were due to infection with the fungus leptothrix but it is now recognized that all the granulomatous diseases including syphilis, tuberculosis, sarcoidosis, tularemia and sporotrichosis can produce this syndrome. Cat-scratch disease and certain viral infections, such as lymphogranuloma venereum and conjunctiva! vaccinia, may also produce this picture. The diagnosis in most cases is made by biopsy of the nodule or ulcer. Treatment. Once the diagnosis is revealed by excisional biopsy, appropriate measures are instituted. In those cases due to a fungus, excision of the nodules and necrotic areas will hasten the patient's recovery. Membranous and Pseudomembranous Conjunctivitis Under this clinical heading are the relatively uncommon cases of conjunctivitis in which the inflammatory exudate forms a membrane on the surface of the conjunctiva. A pseudomembrane is one which can be stripped off easily, without bleeding and leaving the underlying epithelium intact. It has a greyish, translucent, porcelain-like appearance and covers the tarsal and never the bulbar conjunctiva. The less common true membrane is one which cannot be easily stripped off and, if removed, the underlying conjunctiva! epithelium comes with it leaving a raw bleeding surface. The fibrin content of the inflammatory exudate in membranous conjunctivitis is higher than in pseudo-membranous and coagulation occurs within the epithelium as well as on its surface. Thus a true membrane is indicative of a more severe form of conjunctivitis.

Ocular Infections in Children

29

Almost any infectious conjunctivitis, if severe enough, can develop a membrane in occasional instances. The commonest causes are the Corynebacterium diphtheriae ( the Klebs-Loeffler bacillus) and the beta hemolytic streptococcus. Each may produce a membranous or pseudomembranous conjunctivitis, the clinical type which occurs depending upon the severity of the process. The causative micro-organism will be indentified by the bacteriological examination. The treatment will be along the lines outlined in the general section on Conjunctivitis with the appropriate antibiotic being administered topically and systemically. Conjunctivitis Associated with Systemic Infectious Diseases MEASLES. This viral infection, considered in detail in another chapter, commonly involves the eye to produce an acute catarrhal conjunctivitis and a diffuse epithelial keratitis. In debilitated children, a severe membranous or pseudomembranous conjunctivitis may occur. Typical Koplik's spots may be found on the conjunctiva, semilunar fold and caruncle. It is noteworthy that this bilateral conjunctivitis may be one of the earliest signs of the prodromal period; the typical Koplik's spots may occur on the conjunctiva before appearing on the other mucous membranes. Treatment of the conjunctivitis is symptomatic, as outlined in the general section on Conjunctivitis. If photophobia is present, the room lighting may be diminished and the patient kept away from direct bright lights. In cases of secondary bacterial infection, heralded by the presence of a profuse purulent discharge, topical anti-microbial therapy is instituted. OTHER INFECTIOUS DISEASES. Chicken pox (Varicella) may occasionally cause a mild catarrhal conjunctivitis,

30

Principal Infectious Diseases of Childhood

usually associated with eruptions on or near the eyelid margins. Mumps may also, on occasions, cause a mild conjunctivitis, usually without any secretion. THE CORNEA

Infections of the cornea in children are not as common as infections of the conjunctiva but they are always serious owing to the possibility of visual impairment from the scarring which may occur. The cornea reacts to infection in a different manner than the conjunctiva. Initially, there is a small greyish area of infiltration. It may soon suppurate, casting off the superficial layers and forming an ulcer. This loss of substance may extend into the depths of the corneal stroma. It will be accompanied by circumcomeal ( ciliary) injection of the conjunctiva! blood vessels. The limbic blood vessels may invade the cornea. If the corneal ulceration is severe, neighbouring ocular structures become inflamedconjunctivitis, iritis and cyclitis. At times, there is exudation into the anterior chamber ( hypopion) . The symptoms are photophobia, lacrimation, pain, blepharospasm and impaired vision. They will vary according to the severity of the infecting organism and the corneal area involved. The presence and extent of ulceration may be diagnosed by instilling a drop of fluorescein 2 per cent solution or touching the globe and fornices with a filter paper soaked in this solution. Any excess dye is removed by instilling a few drops of water or saline solution. All ulcerated areas in the cornea will be stained a greenish colour. Central Corneal Ulcers

Ulcers involving the central or pupillary portion of the

Ocular Infections in Children

31

cornea are due to micro-organisms which invade the corneal stroma, commonly after the corneal epithelium has been broken by trauma or tissue resistance lowered by such conditions as malnutrition, xerosis, edema or neuroparalytic conditions. (a) BACTERIAL CAUSES. The most frequent bacteria causing central ulcers are Diplocococcus pneumoniae (pneumococcus), beta hemolytic Streptococcus, Pseudomonas aeruginosa (Bacillus pyocyaneus), Moraxella liquefaciens (Diplobacillus of Petit) and Klebsiella pneumoniae (Friedlander's bacillus). Less commonly, Proteus vulgaris, Escherichia coli and other bacteria have been found. An etiological diagnosis can usually be made immediately by taking a scraping of the ulcer, spreading it on a glass slide and performing a Gram stain. A culture of the ulcer and its discharge will grow the micro-organism. Clinically, a bacterial central ulcer often develops a hypopion and may be then called a hypopion ulcer. Of all the bacterial causes, Pseudomonas is the most severe and fulminating. Abscess of the cornea in the form of a ring abscess may occur, often accompanied by a severe panophthalmitis. Treatment. Any constitutional conditions are corrected. Pre-existing local abnormalities, such as ·embedded foreign material, conjunctivitis, blepharitis and dacrocystitis, must be diagnosed and treated. A specific antimicrobial agent, as indicated by the antibiotic sensitivity tests, is vigorously given. Cauterization of the advancing ulcer borders may be necessary to stop the spread of the pathologic process. Secondary iritis and cyclitis are controlled by topical mydriatics. ( b) VIRAL CAUSES. The commonest and most important cause of central corneal ulcers at the present time is the virus of herpes simplex. The lesion produced is very characteristic and is termed dendritic keratitis or ulcer since it is

32 Principal Infectious Diseases of Childhood

branching or dendritic-shaped with the lateral branches ending in knob-like extremities. The sensitivity of the cornea becomes diminished. The conjunctiva usually shows follicular hypertrophy but occasionally a pseudomembrane develops on the surface. Preauricular lymphadenopathy occurs. The dendritic ulcer may remain confined to the corneal epithelium and may heal spontaneously. In other cases, especially if a corticosteroid hormonal preparation has been used topically, the ulcer enlarges, deepens and involves the corneal stroma. The ulcer shape will change to an ameboid or geographic map configuration. A hypopion may occur. The diagnosis can be made on the typical clinical picture. The laboratory diagnosis and the treatment were outlined in the section on herpetic keratoconjunctivitis. If the ulcer is large and resistant to medical therapy, surgery in the form of a therapeutic lamellar corneal graft is indicated. Occasionally, vaccinia (cowpox) corneal ulceration occurs. It is seen mostly in infants and young children as a result of autoinoculation from a primary vaccination. The vaccinia pustule of the cornea leads to ulceration and scarring. If the latter is large and centrally placed, visual loss will occur. The mumps virus occasionally affects the cornea and produces a transient unilateral interstitial keratitis. In some instances a nodular or disciform keratitis occurs and results in central scarring. In measles, a widely scattered superficial punctate keratitis may occur. The small epithelial erosions are more prominent in the pupillary area. There is no specific topical therapy and the keratitis heals spontaneously as the systemic infection subsides. ( c) FUNGAL CAUSES. Fungal or mycotic ulcers, once

Ocular Infections in Children

33

very rare, are now being seen in an increasing incidence. This parallels the increased use of topical antibiotics and steroids which potentiate the growth of fungi in the external ocular tissues. In most patients there is a history of some form of corneal trauma. In others, the keratomycotic ulcer occurs as a superinfection from overtreatment of a herpetic or bacterial ulcer. In others, the keratomycoses has resulted from the use of contaminated eye drops. The corneal lesion usually develops rather slowly and may vary in severity from patient to patient. The lesion appears as a superficial nodular raised plaque or, more commonly, as an ulcer with a dull, dry surface. The floor of the ulcer is usually opaque. At times, fine lateral and deep extensions are noted giving the appearance of satellite formation. A hypopion is usually present. The common fungi causing corneal ulceration are Aspergillus, Candida albicans, Fusarium oxysporum, Cephalosporium and Nocardia. The laboratory diagnosis is established by fresh preparations of corneal scrapings, stained smears, and cultures on suitable media ( notably Sabouraud's Agar). Treatment. Sulfacetamide 30 per cent solution, topically administered frequently, has some fungistatic properties. It is more effective if given by iontophoresis. If this therapy is combined with thimerosal (Merthiolate) 1 : 1000 ointment, applied topically between iontophoresis treatments, cures can be obtained within five or ten days. Copper sulphate 0.8 per cent solution is also effective topically. Amphotericin B (Fungizone) administered intravenously or topically is of value in many mycotic infections. Marginal Corneal Ulcers lTicers involving the marginal or peripheral portions of the cornea occur more often than central ulcers. Most are

34 Principal Infectious Diseases of Childhood

simple catarrhal ulcers and secondary to an acute or chronic catarrhal conjunctivitis. The latter condition and its etiology were discussed earlier in this chapter. Since scrapings and direct cultures of marginal catarrhal ulcers rarely show bacteria, they are considered to be toxic or allergic in origin. Occasionally, in systemic allergic conditions, a catarrhal ulcer unaccompanied by conjunctivitis is seen. Clinically, one or more small greyish areas are seen in the periphery of the cornea. They stain with fluorescein solution. The diagnosis is made by recognizing the underlying conjunctivitis and isolating the causative organism. As the conjunctivitis treatment (previously outlined) is carried out, the marginal ulcer will also respond. Small doses of topical corticosteroid drops, judiciously used, will aid in clearing the larger ulcers. Any co-existing blepharitis must be treated to prevent recurrence of the ulceration. Some cases of recurrent staphylococcal corneal ulcers become resistant to drug medication but will respond to autogenous vaccine or staphylococcus toxoid immunization. THE EYELIDS

Jpflammation of the Lid Margin: Blepharitis

This is a common chronic inflammation of the eyelids affecting primarily the structures of the lid margins and, in severe cases, the adjacent skin, conjunctiva and cornea. Two clinical forms are recognized: ( 1 ) Squamous or Seborrheic -yellowish white, often oily or greasy, scales encrust the eyelashes and lid margins; (2) Ulcerative or Staphylococcal -yellow, hard, tenacious crusts adhere to the eyelashes and reddened lid margins, which, in severe cases, show cracks, excoriations and ulcers. Either type may show loss

Ocular Infections in Children

35

of cilia, lid margin redness and thickening, associated styes, conjunctivitis, marginal corneal infiltrates and ulcers but these complications occur more frequently with ulcerative blepharitis. The underlying etiology of squamous blepharitis is a hypersecretion of the sebaceous and meibomian glands in the eyelids associated with a general seborrheic state and dandruff. Other contributing factors are lack of sleep, ocular fatigue and uncorrected refractive errors, dietary deficiencies, exposure to irritants, general debility, systemic diseases, and a familial tendency. The yeastlike fungus, Pityrosporum ovale, is found in increasing numbers on the lid margins as the severity of the disease increases. Secondary bacterial infection, usually pathogenic staphylococci, is common and aggravates the condition. The ulcerative form is due to a chronic infection of the glands and margins of the lids by pathogenic staphylococci. The anterior nares may also show staphylococcic infection. The general factors noted above may play a role in some patients. Treatment. Any systematic factors mentioned above should be controlled. In the squamous type, the seborrheic dermatitis and dandruff should be treated. The scales should be removed mechanically from the lid margins and cilia. This is followed by twice daily applications of ammoniated mercury 3 % ointment. Expression of secretion from the meibomian glands may be necessary. Secondary bacterial infection should be cultured and appropriate topical antibiotics applied. In the ulcerative form, the crusts also require removal followed by the application of a suitable antimicrobial agent to the lid margins. In addition, the meibomian glands may require expression every few days in order to eliminate bacteria within them. If periodic exacerbations occur despite adequate local therapy, immunization

36 Principal Infectious Diseases of Childhood

with autogenous vaccine or staphylococcus toxoid is indicated. Stye (Hordeolum Extemum)

This is an acute inflammation of the outer edge of the lid margin, caused by staphylococcal infection of the Moll (sweat) and Zeiss (sebaceous) glands located in this area. The condition is very common in children and young adults and is often associated with blepharitis or lowered general health. Clinically, a small reddish lump, accompanied by pain, tenderness and edema, appears among the eyelashes at the outer edge of the lid margin. In a day or two the lump will develop a small yellowish peak indicating suppuration. When the pus discharges, the lump and surrounding edema, which may be considerable, will begin to subside. Treatment. This consists of warm moist compresses, applied frequently, to hasten suppuration. When the yellow head appears, it may be allowed to open spontaneously but the process can be accelerated by careful incision to evacuate the obvious pus formation. In this self-limiting condition, systemic antibiotics are usually unnecessary. To prevent recurrences, any associated blepharitis should be treated. Systemic factors should be controlled. A proper diet, keeping the fingers from the eyelids and the use of a soap containing hexachlorophene are helpful. Occasional recurrent cases may require immunization with autogenous vaccine or staphylococcal toxoid. Chalazion (Hordeolum Intemum)

This is a chronic granulomatous inflammation of one of the meibomian (sebaceous) glands of the eyelid. It is postulated that an obstruction occurs in the gland or its duct, the

Ocular Infections in Children

37

secretion is retained and a chronic inflammatory granuloma results. It is believed that in many cases staphylococcal infection plays an important role in causing obstruction of the meibomian gland or its duct. The condition occurs less commonly in children than in adults and is often confused with a stye. Clinically, a lump or swelling occurs in the eyelid, usually about the middle of the tarsal plate, not at the outer lid margin. In some cases there are few, if any, symptoms whereas others are accompanied by pain, tenderness and considerable edema. The latter group usually develops secondary infection, chiefly caused by staphylococci, and the whole lid may become swollen. A marginal chalazion is one that forms in the duct or at the mouth of a meibomian gland and projects from the lid border. Treatment. If the chalazion is small, it may be left alone since many of them regress spontaneously in a few months' time. A larger chalazion, which may press on the eyeball and alter the refraction of the eye or cause irritative symptoms, should be removed by surgery. When secondary infection is present, frequent warm moist compresses are applied and pus evacuated if suppuration occurs. A marginal chalazion will respond to surgery or electrocoagulation. To prevent recurrences, any associated blepharitis or meibomitis should be treated. Systemic factors which lower the state of health should be controlled. THE LACRIMAL SAC Acute Dacrocystitis This is an acute inflammation of the lacrimal (tear) sac manifested by swelling and redness, of the medial portion of

38

Principal Infectious Diseases of Childhood

the lower lid ( the tear sac area). The edema may spread into the upper eyelid. This is usually accompanied by epiphora or a purulent conjunctiva! exudate. Abscess formation may occur or the inflammation subsides into a chronic phase with persisting epiphora or purulent discharge. The condition is caused by obstruction of the nasolacrimal duct, the channel which normally drains the tear fluid from the lacrimal sac into the nasal cavity. As a result of the naso-lacrimal duct obstruction, the tears stagnate in the lacrimal sac and infection follows. Cultures may show the presence of one or more pathogenic bacteria; those commonly found are the pneumococci, streptococci, influenza bacilli and staphylococci. The nasolacrimal duct obstruction may be congenital or acquired. The congenital obstructions are seen in the newborn infant and occur either as a result of atresia, the common site of obstruction being at the lower end of the duct, or from debris being retained in the duct. Rare cases are due to bony obstruction caused by malformation of the face or nose. Treatment of the newborn in the acute stage consists of cold compresses to reduce the swelling and appropriate systemic anti-microbial agents. If abscess formation occurs, the tear sac should be incised and pus evacuated. After the inflammation has subsided, the tear sac is massaged and failing this, the lacrimal passages should be probed in order to remove any obstructions present. If simple probing fails or bony obstruction is present, a new drainage channel into the nose ( dacrocystorhinostomy) is made, the operation usually being delayed until the child is about ten or eleven months of age. The acquired obstructions of the nasolacrimal duct are seen in older children and are commonly caused by nasal or sinus infections but occasionally by trauma, granuloma-

Ocular Infections in Children

39

tous infections of the sac and nasal tumours. Treatment in the acute phase is again conservative since many cases, especially those due to adjacent nasal or sinus disease, may resolve completely. The underlying cause of the obstruction should be determined by careful investigation and removed. Some cases will require one or two probings and if unsuccessful, a dacrocystorhinostomy. Chronic Dacrocystitis

This is a chronic inflammation of the lacrimal sac resulting from the same obstructive etiology as acute dacrocystitis. The patient has constant epiphora and this is increased by exposure to wind, cold and irritants. The stagnant tear fluid in the lacrimal sac tends to slowly distend the sac walls resulting in the formation of a mucocele. A smooth swelling or fullness will then be noted in the lacrimal sac area. Pressing on such a sac will cause watery or, if infected, mucopurulent fluid to escape from the puncta. As previously noted in the section on conjunctivitis, these patients may show a chronic conjunctivitis with the medial portion of the conjunctiva most affected (lacrimal conjunctivitis). At any time during the long chronic course of this condition, acute dacrocystitis may occur. It is noteworthy that this condition may be present at birth due to the same congenital obstructions previously noted with the acute form. Since many infants do not secrete an appreciable amount of tears until the tenth or twelfth day of life, the constant epiphora may not be noted until after this time. Treatment. As with the acute form, the initial therapy is conservative. In the newborn infant, massage of the sac is performed several times of the day in an effort to empty the sac and possibly force open the nasolacrimal duct. If

40

Principal Infectious Diseases of Childhood

unsuccessful, a probing is then performed. As with the acute form, if two probings fail or bony obstruction is present, dacrocystorhinostomy is carried out. A similar regime is performed in the older child after a careful investigation has been done to discover and eliminate any acquired obstructive factors.

3 I Infectious or Communicable Diseases or communicable diseases can be divided into those caused by bacteria and those caused by viruses. Bacterial infections are: scarlet fever, diphtheria, whoopingcough, tetanus, typhoid-paratyphoid fever and dysentery or gastro-enteritis. Virus infections are: measles, mumps, chicken-pox, rubella, roseola infantum and smallpox. Isolation and quarantine regulations for these diseases vary considerably from place to place and are constantly being revised. The reader is referred to the quarantine regulations of his local municipality for information. INFECTIOUS

BACTERIAL INFECTIONS

Scarlet Fever

Scarlet fever is a general toxic manifestation of a streptococcal infection. AETIOLOGY. Haemolytic streptococcus is the aetiological agent, but most of the general and exanthematous manifestations are due to the dissemination of its toxin. The child who develops the fever has most likely been exposed to a person with scarlet fever or streptococcal throat infection or to a healthy carrier. CLINICAL ASPECTS. The incubation period is stated to be

42

Principal Infectious Diseases of Childhood

between two and seven days, but 48 hours is the most common time. Three clinical types have been seen: simple, toxic, and septic. These types probably depend on the virulence of the invading micro-organisms and the susceptibility of the host in the individual patient. Simple scarlet fever is most commonly seen where the signs and symptoms are relatively mild. Toxic scarlet fever is seen during epidemics and is characterized by an increase in signs and symptoms due to the toxins of the disease: high fever, very sore throat, severe headache, intense rash and cervical adenitis. Septic scarlet fever is very rarely seen, but has all the characteristics of local and general sepsis: purulent discharge from nose and throat, enlargement of cervical glands, otitis media, a very septic appearance and a positive blood culture caused by the invading streptococcus. SYMPTOMS. Sudden onset, headache, fever, nausea and vomiting, sore throat and rash. SIGNS. Exanthem : (a) Flushed face; (b) circumoral pallor; ( c) erythema of skin with superimposed small pinpoint papules which spreads from the upper part of the neck and chest downward; (d) petechiae in the axillaries region; ( e) flexor colouration at the bend of the elbow. The rash is seen over the surface of the body being most marked on chest and abdomen, back and flexor surfaces of the arms and thighs. Occasionally, a morbilliform type is seen on the extensor surfaces of the forearms. Enanthem: The mouth and throat show a number of characteristic findings. (a) Tongue: first day--desquamation of sides and tips, white-coated surface with red papillae showing through the coat; second and third day--desquamation approximately one-half to three-quarters of surface of the tongue, with red base and large swollen red papillae;

Infectious or Communicable Diseases

43

fourth day--complete desquamation of the tongue with red base and red papillae, the so-called "red strawberry" tongue. The final stage is atrophy of the surface of tongue and papillae which leaves a shiny surface. ( b) Throat: this is a fiery red colour with a fine erythematous rash on the soft palate and there is a swollen uvula with petechiae on it. The tonsils are red and swollen and a purulent discharge is often seen in the crypts. These signs and symptoms last from one to four days depending on the severity of the case and the rash begins to fade on the third or fourth day. Desquamation may start on the face early in the first week and later on the body where a scaly or pin-point desquamation occurs over the upper part and spreads downward. Later, in the third week of the disease, there is the so-called "glove-type" desquamation, in which large flakes of skin peel off the extremities. DIAGNOSIS. For fully developed scarlet fever in which all signs and symptoms are present, diagnosis is not difficult, although such diseases as German measles, roseola, serum disease and drug rashes may at times be confusing. Anyone familiar with all aspects of these conditions will encounter very little difficulty in differentiating them from scarlet fever. COMPLICATIONS. These are mostly associated with upper respiratory conditions such as cervical adenitis, otitis media, sinusitis, mastoiditis, laryngitis, retropharyngeal and peritonsillar adenitis and abscess; occasionally, septic tracheitis, myocarditis, nephritis, arthritis and septicaemia in varying severity are seen. At present, complications are uncommon owing to the use of antibiotics in the acute phase of the disease. PROGNOSIS. With modem treatment recovery is very quick

44

Principal Infectious Diseases of Childhood

in the average case of scarlet fever, without the complications and sequelae seen some years ago. TREATMENT. (1 ) The patient should be kept in bed for at least two or three weeks from the onset of the disease. ( 2) Fluids should be given in the acute phases of the disease, followed by a soft diet and later a full diet. ( 3) The complications are treated in the usual way-for example, local treatment for otitis media and antibiotics. ( 4) The use of sulphonamides and/or penicillin at the onset of the disease is definitely indicated in scarlet fever. Intramuscular or oral doses of penicillin should be given daily for seven to ten days. (5) As symptoms occur, they are treated accordingly. (6) Antitoxin in severe cases may be a valuable adjunct to therapy. Diphtheria

Diphtheria is an acute infectious disease characterized by a local inflammation with pseudo-membrane formation in the upper respiratory passages and a generalized systemic toxaemia. In severe cases, myocardial and neurological complications occur and, on occasions, death ensues. ETIOLOGY. The disease is caused by toxins produced from various strains of corynebacterium diphtheria, also known as the Klebs-Loeffler bacillus. CLINICAL FEATURES. The disease has an insidious onset and its symptoms are a low-grade fever, headache, general debility, generalized aches and pains and a sore throat. The constitutional symptoms are often out of proportion to the local symptoms, the patient often complaining of aches and pains and generally feeling unwell and yet may not refer to the soreness of the throat. There are four clinical types: ( 1) Nasal diphtheria may be acute or chronic, although more often the patient has a chronic foul sanguinous dis-

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45

charge which produces the characteristic pungent odour of diphtheria. If this is of long standing and is not treated there may be an extensive absorption of toxins resulting in myocardial and paralytic phenomena. The membrane in this type often lines the nasopharynx and may at times be seen at the entrance to the nostrils. Nasal infection may be associated with pharyngeal and faucial diphtheria or may be merely a nasal condition in an apparently healthy child. (2) Faucial diphtheria is the most common type. The pharynx and fauces are congested with a grayish exudate (removable in the first 24 hours of the disease) which later becomes impregnated into the body of the underlying tissues, forming the characteristic pseudo-membrane which bleeds when removal is attempted. Oedema also is often present over the surrounding tissues. There is usually some degree of toxic cervical adenitis which becomes more prominent with the severity of the disease until in very severe forms one sees great swelling of the cervical lymph glands with oedema, which "pits" on pressure, under the chin and around the neck. The membrane in the most severe cases is extremely tough and thick and has been seen to extend over the surface of the whole palate. There is also a characteristic pungent odour to the breath which by itself is almost diagnostic to experienced clinicians. ( 3) Laryngeal diphtheria and tracheo-bronchial diphtheria. Laryngeal diphtheria may be either primary or secondary. Usually it is secondary to faucial and pharyngeal diphtheria and manifests itself by hoarseness of voice, a croupy cough, increasing stridor with spasms of acute respiratory distress, extreme general restlessness, cyanosis, pallor and finally asphyxia. Tracheo-bronchial diphtheria may occur in severely ill patients whose disease has been untreated for some days. On occasions, the whole cast of the trachea and

46

Principal Infectious Diseases of Childhood

lung composed of the pseudo-membrane has been removed. This may be done by direct laryngoscopy or at the post mortem and usually after diphtheria antitoxin has "loosened" the membrane. The victims are severely ill, manifesting an associated faucial, pharyngeal or laryngeal type of the disease whose signs, however, are more closely those of tracheal obstruction. In these patients the stridor is often both inspiratory and expiratory with extreme restlessness, marked upper and lower respiratory obstruction, manifesting itself by lower costal margin indrawing of the chest wall. With any form of treatment the outlook in this type and at this stage is extremely grave. Fortunately, at present, cases are extremely rare in this country. ( 4) Cutaneous diphtheria is occasionally seen with pseudo-membrous lesions in areas on the skin surface when it is directly infected, e.g., the umbilicus in infants and other skin areas which may be infected on occasion in older children. The course of diphtheria is rapid and progressive unless checked with adequate, appropriate measures. The exudate in the throat quickly becomes the pseudo-membrane which extends over the whole upper respiratory and lower respiratory system. From this membrane, which includes mainly cellular debris and bacteria, the toxins of the diphtheria bacillus spread by way of the blood stream and ultimately cause a generalized systemic toxaemia with complete circulatory collapse and death. If death does not occur in the early stages, the membrane may clear away or partially clear away and the toxins which have been generally distributed in the acute phase of the illness produce cardiac and neurological lesions, cardiac failure, partial or complete heart block, local and general peripheral paralyses and death three to five weeks later. Early in the disease there may be a slight palatal and

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pharyngeal paralysis as a result of the direct action of toxin on the muscles underlying the membrane. Later complications may be local and general. For example, local: palatal and pharyngeal paralysis, facial paralysis, and ocular palsies with the usual signs found as a result of these areas being involved; general: peripheral paralysis of arms and legs. Some patients have been completely paralysed, with diaphragmatic and inter-costal paresis; this type of complication is highly fatal. Myocardial involvement manifests itself by a frightened, apprehensive look on the part of the patient, extreme pallor, cyanosis around the nares and mouth, poor heart sounds, rapid or slow rate, extra systoles and occasionally systolic murmurs. There may be partial or complete heart block at times resulting in death. Unfortunately, there is little or no treatment other than complete bed rest in an absolutely prone position for a period of weeks or months, depending upon the severity of the disease. PROGNOSIS. With diphtheria, the prognosis depends largely on early diagnosis and treatment. In simple cases, early diagnosis and the use of adequate doses of antitoxin result in complete recovery. It is difficult to give any prognosis after the severe types of complications have occurred. However, if the patient does survive, there are no sequelae and a patient who has had severe cardiac and neurological complications may make a complete recovery. p ATHOLOGY AND p ATHOGENESIS. Corynebacterium diphtheria sets up a local inflammation in the upper respiratory passages, and in the early stage of the disease, a whitish exudate is formed which comes away quite readily. After 24-48 hours however the inflammation continues and the exotoxin of the diphtheria bacillus causes poisoning and death of local tissue. A more extensive exudate develops

48

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with necrotic cells, debris and bacteria found enmeshed in a pseudo-membrane which is quite resistant to disintegration and is firmly adherent by fibrinous attachments to the underlying throat tissues. As the disease progresses ( usually as the result of not being treated) the membrane extends from a small area in the fauces ultimately to involve the larynx and trachea and may form an extensive pseudo-membrane involving trachea and lungs. If however the patient receives adequate treatment the membrane ceases to spread, tends to dry up, curl at the edges and finally disintegrates leaving a red inflamed healing base. EPIDEMIOLOGY. Diphtheria is uncommon in areas or communities where diphtheria toxoid has been employed and where fortifying doses have been given over years. In the past, however, Diphtheria was known to be spread by persistent carriers. People were known to carry the bacillus for years and it was almost impossible to eradicate these sources of spread by any known method. Often these carriers were older children and were confined to institutions for many months. Other sources of infection were chronically infected umbilical discharges in the newborn, or chronically infected wounds. The disease in many communities is still sporadic and on occasion becomes endemic. Sometimes epidemics occur in localized areas. The disease is usually spread either by carriers or by acute cases with subclinical infection. DIAGNOSIS : CLINICAL-LABORATORY. (1) Clinical. It is important to diagnose diphtheria as early as possible since there is specific treatment for this disease. Usually the characteristic odour, membrane formation and severe toxaemia distinguish it from other conditions such as scarlet fever (before the rash) septic sore throat and Vincent's

Infectious or Communicable Diseases 49

angina. (2) Laboratory. The final and confirming diagnosis must be made by demonstration of Gram positive tubshaped rods with metachomatic granules in a direct smear stained by the Gram technique and especially by isolation of Corynebacterium diphtheria organisms by inoculation of tellurite blood agar plates and Loeffles slopes. TREATMENT. Prophylactic: the general use of diphtheria toxoid in children prevents its occurrence. Therapeutic: ( 1) rest in bed is of paramount importance. The patient must be kept absolutely flat in bed without a pillow for at least three or four weeks even in the mildest type of the disease and in more severe types for several months, depending on the patient and the extent of the complications. Later in the course of the disease, depending on the individual patient, the head may be elevated with pillows for certain periods of time during the day. It is best to err on the side of long bed rest and slow return to normal movement than to get the patient up too early. ( 2) Diphtheria antitoxin should be given intramuscularly as soon as possible after diagnosis: mildly ill types20-50,000 units ( this may be repeated if thought necessary on clinical evidence); moderately ill types-50,000200,000 units intramuscularly each day for two to three days or longer; severely ill types-200,000 units of diphtheria antitoxin daily for several days. ( 3) Antibiotics and sulphonamides are adjuncts to treatment, for mixed or secondary infections, but in no way replace the use of antitoxin. The dosage of these drugs used in other infections may be adhered to. ( 4) In addition to rest in bed, good nursing and constant attention to the patient's wants are very important. Sedative and stimulative drugs are contra-indicated because of possible myocardial and neurological complications. Feeding

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with fluids in the early stages requires skilled nursing and the treatment of the laryngeal types of the disease necessitates constant watching of the patient and dealing with the mechanical situation as it arises; here the nose and throat surgeon is involved. If intubation and/or tracheotomy is to be done, it must be before the patient's life is endangered by an acute respiratory obstruction. Skill in looking after the tracheotomy tube to ensure a good air passage is a very important post-operative nursing technique. After the onset of respiratory paresis or paralysis the patient may need a respirator. Whooping-Cough

The incubation period of this disease ranges from ten to fourteen days. AETIOLOGY. Bordet first observed the causative agent of whooping-cough in the oral mucus of his fivemonth-old infant daughter during the time she was afflicted with whooping-cough in the year 1900. In 1906, Bordet and Gengou first cultured the bacillus on the medium which is still used although modifications of their original medium. In 1937, Eldering and Kendrick, Bradford and Slavins isolated from patients with a "whooping-cough like" disease a haemophilic bacillus morphologically the same as H. pertussis but culturally and serologically different. This micro-organism was named H. parapertussis by Eldering and Kendrick. This latter disease has been said to be of a milder type than that caused by H. pertussis but, in view of the extreme variation in cases of whooping cough caused by H. pertussis, the disease caused by H. parapertussis may not be very different clinically. The literature reveals repeatedly and convincingly that phase one H. pertussis is the causative agent of this disease.

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CLINICAL FEATURES. Whooping-cough is an acute communicable disease beginning as a simple cough which becomes much worse as days and weeks pass. Commencing usually as a night cough, the coughing develops into spasms of several coughs ending with an inspiratory whoop, coughing and vomiting up large amounts of "stringy mucus." Uncomplicated, the disease is associated primarily with the upper and lower respiratory tract. Starting insidiously in an otherwise healthy child, it ends, in severe cases, in prolonged spells of coughing, whooping and vomiting which only time remedies. The duration of the disease is one of the most variable of any childhood infection, ranging from a five-day cough with recovery (proven by positive coughplate culture), to spasms of coughing, whooping and vomiting lasting from six to nine months. In most accounts of the disease, references are made to three stages, the catarrhal, spasmodic and convalescent. Our experience with cases in the early days or the first week of the disease in which cough-plates have been taken have not shown too many of these patients with the early upper respiratory infection so commonly mentioned. In the early phase, the infant or child is comparatively healthy with only a night cough. After about a week to ten days of this cough, the spells become more intense and spasmodic with several expulsive coughs occurring before inspiration takes place. In the second and third week, after the severe spasmodic expiratory coughs is heard the inspiratory "whoop" so typical of this disease. These spasms of coughing with subsequent whooping are followed by severe vomiting of mucus and food. Other than these, there are very few symptoms. In these spasms of expiratory coughing, the child often protrudes the tongue, his face becomes red and ultimately blue

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Principal Infectious Diseases of Childhood

from the lack of the inspiratory act. In cases of long standing, haemorrhages from extreme coughing may occur in the nose, the subconjunctival membranes and the brain. The coughing spells tend to produce spasms ending in a stage of asphyxia with deep cyanosis, the child becoming paler after the asphyxia! stage, finally returning to a normal colour. Signs and symptoms of pneumonia develop only after an infection with the usual secondary invading microorganisms which cause pneumonia. Recurrent attacks of whooping-cough are unlikely. A child who has had whooping cough may, with other subsequent infections, develop all the mechanical signs of his original infection with H. pertussis, having attacks of coughing, whooping and vomiting. COMPLICATIONS. Local. Haemorrhages from the nose, in the subconjunctiva, and brain have been seen. Frenal ulceration under the tongue, from constant friction of its passage across the lower central incisor teeth in coughing spasms, has been seen in severe cases. General. Bronchopneumonia is still the worst common complication and is usually due to secondary invading bacterial micro-organism. It results in a very serious condition following the already severe damage of the respiratory tract. This complication often results in the death of young infants and must be treated in the same way as any acute bronchopneumonia. Convulsions are the next common complication, usually occurring in the latter part of the second, third or fourth week of the disease and commencing after a severe bout of coughing with cyanosis. They have been said to be due to oedema of the brain, small petechial haemorrhages or a temporary state of cerebral anoxia. The treatment is the same as for convulsions produced by other causes.

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Diarrhoea and vomiting are also complications which occur in certain patients. SEQUELAE. The usual case of whooping cough has no aftermath, although in cases of severe and prolonged bronchopneumonia, bronchiectasis may develop. DIAGNOSIS. The clinical diagnosis becomes definite only after the typical spasmodic coughing and whooping attacks occur. Thus the child is a source of infection to other children before a clinical diagnosis can be made. The first week of the disease is highly contagious as revealed by cough plate cultures. At this stage, the white blood count of 20,000 or more leucocytes per cubic mm with a predominance of the lymphocytic type of cell may be helpful in the diagnosis. In very young infants, other conditions, especially with an attendant persistent coughing spasm, asphyxia and choking on mucus may simulate infection with H. pertussis. Therefore, the only definite and early evidence of whooping cough is the isolation by nasal culture or cough plate culture of the aetioligic agent, H. pertussis. The culture of the cough may be best obtained by giving the infant or child a drink of water, placing the finger just above the suprastemal notch and gently pressing on the trachea. Pressure in this area usually excites in most children enough coughing episode to take two cough plate cultures. The cough plates are held three to six inches from the mouth. Sputum or vomitus on the plates must be avoided. Occasionally, myriads of colonies of H. pertussis will be seen in the culture from the droplets of a few coughs in the first week of the disease. Usually the colonies have to be carefully searched for. PROGNOSIS. Whooping-cough with its attendant pneumonia or convulsions is still responsible for deaths in infants and young children. In older children, bronchiectasis may

54 Principal Infectious Diseases of Childhood

prevent complete recovery until the condition is adequately treated. The ordinary case of whooping cough rarely has any serious complication. TREATMENT. Prevention of whooping-cough is available and protects approximately 80 per cent of children from the disease or at least from a severe attack of the disease. It is recommended that all children be immunized with phase I H. pertussis vaccine and given in repeated fortifying doses over the years. Every child with whooping-cough should be isolated from other members of the family because of the serious nature of the disease in infants and young children. Treatment will vary according to the intensity of the symptoms. ( 1 ) The child who is incapacitated with severe bouts of coughing spasms, or with bronchopneumonia, must be confined to bed. Usually rest is best for any child since exertion aggravates and increases the number of spasms. (2) Chloromycetin or the tetracyclines have been recommended in the treatment of the disease. ( 3) In severe cases, especially in young infants having severe spasms with cyanosis, 10 ccs. of hyperimmune human antipertussis serum or B~ ccs. of Cutters, hypertussis human serum is injected intramuscularly for two to five days depending on the severity of the individual patient. ( 4) In infants and children with cyanosis, asphyxia! attacks and bronchopneumonia, 40 per cent to 60 per cent oxygen should be administered continuously. ( 5) A seriously ill infant or young child should have continuous nursing supervision as it is difficult to be sure when the patient will go into a respiratory spasm, cease breathing and need resuscitation. ( 6) Suction of as much mucus as possible from the mouth

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of the infant should be undertaken before commencing artificial resuscitation. ( 7) Small amounts of fluid of high caloric value warmed to body temperature should be given frequently when spasms of whooping produce much vomiting. After the vomiting, the fluid meal should be repeated. From a nutritional standpoint, it may take months for the patient with severe whooping-cough to make a complete recovery. As the child improves, a soft diet may be given with lukewarm foods which will not irritate the throat and produce severe coughing spasms. ( 8) Sulphonamides, pencillin or chloromycetin should be given if pneumonia is present. Most drugs given orally may irritate the throat causing coughing followed by vomiting. Sedative cough mixtures at times may relieve severe bouts of coughing and rectal sedatives may help to control the cough by giving the child some sleep. Prophylactic penicillin should be given to all cases of pertussis in an effort to prevent secondary bronchopneumonia. ( 9) The use of the croupette with cool moist air seems to benefit many cases of young children with severe pertussis. Chest X-rays should be taken prior to patient's discharge to ascertain if atelectasis or pneumonia is present. Tetanus

Tetanus or "lock-jaw" is a disease caused by an infection of superficial or deep tissues as a result of some penetrating injury. The exotoxin of the infecting agent produces an effect on the motor cells of the central nervous system resulting in marked spasms of voluntary groups of muscles. AETIOLOGY. The disease is caused by a gram positive anaerobic spore bearing bacillus named clostridium tetani,

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Principal Infectious Diseases of Childhood

widely distributed in the soil. In addition to other poisons, the bacillus produces a neuro-exotoxin which circulates and produces general spasticity of the voluntary muscles of the body. As in diphtheria, however, an attack of tetanus does not produce elevated antitoxin in the blood of the recovered person; nevertheless, tetanus toxoid will raise the antitoxic level in the blood to protective levels. Punctured wounds are not always the site of entrance for the tetanus bacilli and, hence, it is difficult to discover the source of the infection with the tetanus bacillus in some children. In certain patients, there is no history of injury. CLINICAL ASPECTS. Although there are cases every month of the year, the disease is more common in July, August, and September, as more injuries to children outdoors at play occur in this period. It is also more common in boys, probably because they are exposed to injury more than girls. There is an extreme variability in the clinical course of the disease in each patient. The majority of cases are quite severe. Most patients come to the hospital with only the slightest symptoms and signs. The child's mouth may be quite normal, apart from the difficulty in opening it. During the next 24 hours, there is more stiffness of the jaw, more marked general rigidity, more opisthotonos is noted, spasms commence, and the whole musculature including the abdominal muscles becomes rigid. Earlier or later on the day of admission the patient may begin having tetanospasms. In these seizures, the jaw locks very powerfully and so quickly that often the tongue is bitten. The face goes into the set state of "risus sardonicus." Trismus is noted, the head goes back in marked opisthotonos and the limbs go into a spasm in the extended position with clenched hands and feet. There is intense sweating, the patients suffer extreme pain (like a cramp of all the body

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muscles), the spine is arched and, finally, the larynx goes into a spasm which causes asphyxia with cyanosis. Death or a relaxation on return to consciousness follows. These episodes of spasms may become more frequent and, finally, death ensues. In other patients, after several days, the spasms become less frequent and less severe until, after the seventh day, the outlook is much better. The muscles remain in a very spastic condition, even the masseter muscles being in spasm from several weeks to two months after the original attack. Some patients have very mild cases, revealing only masseter spasm and slight chronic generalized spasm. Some attacks begin with spasms of abdominal pain and the characteristic rigid abdomen of tetanus. A few of the patients seem to improve for a while, but may go into an unconscious state which occasionally develops early in the disease, and die in the second or third week. The cerebro-spinal fluid reveals normal findings in respect of culture and cell count. COMPLICATIONS. Death is often caused by asphyxia from laryngeal spasm or a spasm of the respiratory muscles. Except for pneumonia which may add to the inherent dangers, there are few complications which are not an actual part of the whole disease. In addition, fractures of the spinal vertebrae from the intense spasms of the spinal muscles have been found. PROGNOSIS. After a patient is well on the road to recovery he is perfectly normal in every way. But to give a prognosis during the course of the illness, especially in the first week or ten days, is to reveal immaturity in experience with this treacherous clinical entity. Frequently, patients who have been admitted with few signs and symptoms and appeared well, have died in a few days. Hence, one hesitates to give any prognosis until the patient has ceased having severe

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Principal Infectious Diseases of Childhood

spasms which asphyxiate him. Usually the prognosis is worse the shorter the incubation period. The rapidity of the invasion period is, however, a better prognostic index than the duration of the incubation period. If severe spasms, becoming increasingly difficult to control, occur at shorter intervals soon after admission to the hospital, then the outlook is extremely grave. TREATMENT. The balance between giving enough sedation, antitoxin and intravenous fluid to control the spasms, neutralize the toxin and feed the patient, and preventing death from pulmonary oedema or pneumonia, due to too much sedation, reaction from serum disease, and too much intravenous fluid is extremely fine. The patient with tetanus should ( 1 ) be kept in a quiet darkened room with as little external stimulation as possible; (2) have nurses in constant attendance; (3) receive Seconal gr. 1 ½ to gr. 4 rectally or sodium amytal intravenously; ( 4) receive 50,000 to 100,000 units of tetanus antitoxin, administered intramuscularly, daily for five days or more; (5) receive a continuous intravenous injection of % 5 per cent glucose and ½ normal saline; ( 6) be fed only by mouth until spasm or stiffness makes it necessary to use intravenous treatment; ( 7) have tracheotomy performed before spasms become so severe that they asphyxiate the patient; ( 8) receive all injectable therapy that may disturb at the same time each day; (9) receive 500,000 units of penicillin daily; (10) have the wound excised early if it is in an accessible position and ( 11) receive 5 to 20,000 units of tetanus antitoxin around the local focus. The whole treatment of tetanus is much more difficult than the above itemized outline indicates. The value of excising the wound is doubtful in certain cases; some patients have developed repeated spasms occurring in rapid

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succession and have died after excision of the focus; others have improved. Every wound should be thoroughly examined and any deep wound thoroughly excised, explored and cleansed days before any sign of tetanus occurs. In our experience, curare and curare-like derivatives have never altered the course of the disease in the few patients to whom they have been given. It has been said that a certain amount of tetanus antitoxin will raise the blood levels to adequate heights to prevent more circulating toxin from fixing itself to nervous tissue, but we have had patients who had received what we considered adequate amounts of antitoxin relapse and commence to have more spasms. The daily intramuscular injection of 50,000 to 100,000 units of antitoxin has then been recommended and the spasms have decreased in number and severity and the patients have recovered completely. Typhoid and Paratyphoid Fever

These diseases are not seen very commonly in children, largely because there have been for some time better public health measures controlling milk and water supplies. The disease is an acute infection of the blood stream and gastrointestinal tract-the result of ingestion of food or fluid contaminated with the causative agent of the disease. It occurs at times in epidemic form, but in this country it is largely endemic or sporadic. AETIOLOGY. These diseases are caused by two of the Salmonella species known as S. typhi and S. paratyphi A and B. They are motile gram negative rod-type bacilli and have flagella. The bacteria enter the body orally, going through the mucosa of the gastro-intestinal tract, lodging in the mesenteric glands and proceeding thence to the blood stream. These micro-organisms then filter out into the liver

60 Principal Infectious Diseases of Childhood

and spleen where a secondary incubation period takes place and the bacteria re-enter the blood stream proceeding to the lymphoid tissue of the bowel and the Peyer patches. Usually the bacteria are transmitted to the human through the medium of infected food, carried there by flies or, in certain cases, by a typhoid carrier. CLINICAL ASPECTS. Since this disease starts as an infection of the blood stream followed by gastro-enteritis, there are general symptoms of fever, headache, generalized aches and pains, nausea and vomiting, abdominal pain or discomfort and sometimes epistaxis. The face appears toxic and flushed, with a dull expression. The fever is moderate to high, with temperatures of 102°F. to 104°F. There may be constipation although diarrhoea occurs in many cases. Frequently, there is relatively little to find except a fever, headache, a palpable spleen and, on occasions, a few of the so-called "rose spots," small¼ inch to ½6 inch red macules, which at times may be slightly papular and blanch on pressure; there is some diarrhoea, but the typical "pea soup" stools so often mentioned are not always found. Unless the disease is suspected, the diagnosis may be doubtful. However, there is practically always a leukopenia, the blood culture may be positive early in the disease and a positive agglutination reaction is present. In severe cases there may be extreme delirium and the fever remains high during the first seven to ten days, later falling by lysis in the third week of the disease. The rose spots are usually seen sparsely distributed over the abdomen. COMPLICATIONS. In children these are few and usually the child makes a complete recovery. On occasions, however, haemorrhage or perforation occurs, with abdominal pain, vomiting and signs of peritoneal soiling. These complications require urgent surgical measures. Jaundice, res-

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piratory infections, bronchopneumonia and such neurological manifestations as stupor and delirium are seen. Typhoid meningitis has been reported. DIAGNOSIS. The diagnosis in the usual mild case in childhood can be made only if the disease is suspected, especially during the summer and autumn seasons of the year. The presence of fever with few other findings than rose spots, enlarged spleen and a leukopenia leads one to suspect these infections. Confirmation is made by examination of the blood for culture and for agglutinins. PROGNOSIS. The disease in childhood is rarely serious and the patient usually makes a complete recovery with or without specific therapy ( chloromycetin). Occasionally a severe form of the disease occurs and complications of haemorrhage and/or perforation may result in death. PROPHYLAXIS. In addition to vaccination as a prophylactic, public health measures should be taken immediately to search for the contaminated source of the infection and instigate control by regulations for milk, water, and food supplies. TREATMENT. ( 1 ) The patient should be isolated and all discharges and excreta properly disposed of by techniques which sterilize the material containing the aetiological agent. (2) Good nursing technique and bed rest for three to four weeks is indicated. ( 3) High caloric fluid diets are necessary. ( 4) For the young infant who may be extremely ill with an intoxication, intravenous fluids may be indicated and a blood transfusion may be needed. Later a soft diet should be given. ( 5) Chloromycetin is the drug of choice and may be given orally in doses of 150 to 250 mg. every four hours for several days or longer. The blood of these patients should be examined periodically during and after treatment.

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Dysentery or Gastro-Enteritis Dysentery is an acute infectious disease involving the gastro-intestinal tract and resulting from an ingestion of contaminated fluid or food. This disease is now seen in children in endemic and sporadic outbreaks, but has occurred in world-wide epidemics, with serious results and, on occasion, death. AETIOLOGY. The disease is caused by the Shigella group of bacteria, of which there are several types: for example, Flexner and Sonne. These two bacilli have been the cause of dysentery in this part of the country; the majority of bacilli isolated from patients were of the Sonne type. Many infants were admitted to our Hospital with all the symptoms and signs of intestinal intoxication; from their stools Johnston and collaborators at the Hospital were able to isolate the Shigella group, but most common was the Sonne bacillus. The disease is directly due to various foods and fluids being contaminated, probably by flies carrying infected material from contaminated sources to food stuffs. Human carriers are important factors in the spread of this disease. In recent years there have been other bacterial causes of gastro-enteritis ( for example, staphylococcus). CLINICAL ASPECTS. Although so-called intestinal intoxication may be due to several causative agents, some patients suffering from it are infected with the Shigella group of bacteria. The incubation period is not definitely known, but is probably relatively short (likely one to four days). In the infant this disease is clinically indistinguishable from intestinal intoxication. The disease commences with diarrhoea, green watery stools, mucus and blood accompanied by vomiting. There may be pain from abdominal distension or from excessive gas and increased peristalsis. The vomiting, diarrhoea and refusal of food continue and the baby has

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alternate periods of irritability and drowsiness. As the symptoms progress, the eyes become sunken, the colour is pale and often ashen and the infant becomes dehydrated, the skin refusing to return to its usual position when picked up between the fingers (loss of elasticity). There is usually fever with a temperature of 102 ° F .-104 ° F. at the onset, and older children may at this time have convulsions with generalized toxaemia. Usually the disease is confined to the gastro-intestinal tract although there are always varying degrees of general toxaemia. Very rarely is there septicaemia, but in some patients the Shigella group of bacteria have been isolated from the blood stream. In the older child there is often abdominal tenderness which is general, indefinite and not localized in the appendiceal area. This disease varies from the very mildest type in an infant with a few days of diarrhoea and vomiting, to the type with fever and more prolonged symptoms, to the severe form resembling intestinal intoxication. In the acute phase there are six to twenty loose green stools per day. Other stools reveal considerable quantities of blood. Occasionally diarrhoea may continue in young infants for weeks and months; this type, I believe, may be the forerunner of the early stage of the coeliac syndrome. Many cases of this chronic type are erroneously considered to be the result of allergies. In recent years, many other bacterial species have caused gastro-enteritis. DIAGNOSIS. In the majority of infants and children the diagnosis of dysentery or gastro-enteritis is extremely simple. There are, however, other common conditions to think of. The most common cause of vomiting and diarrhoea in infants is a parenteral infection. Infections due to the Salmonella group must also be considered. In the younger infant acute intestinal intussusception must always be

64 Principal Infectious Diseases of Childhood

considered as a possibility and in the older child acute appendicitis. With either of these diseases frank diarrhoea, like that which occurs with gastro-enteritis or dysentery, is rare. If stools are examined quickly after rectal swabs are taken or the fresh stool is passed, cultures of the material properly incubated and examined occasionally reveal the causative agent. With many infants whose trouble does not clear up quickly, there are difficult feeding problems. COMPLICATIONS. These are mainly associated with the upper and lower respiratory systems. Often the child contracts a nasopharyngitis, otitis media, bronchitis or bronchopneumonia. PROGNOSIS. The prognosis with the usual case, with diarrhoea and vomiting resulting from dysentery, is good. Most patients make an uninterrupted recovery. Some fifteen to twenty years ago the case fatality rate in infants was quite high but, in recent years, with earlier diagnosis and more adequate drug and fluid therapy a child rarely dies with this disease or its complications. When death in infants occurs it is usually the result of a complete circulatory collapse from the overwhelming toxaemia or a complication such as bronchopneumonia. PROPHYLAXIS. There is no known prophylactic inoculation against dysentery or gastro-enteritis, probably because there are too many causes of these conditions to make a satisfactory specific immunizing agent. A great deal may be done by searching for the causes of infection of food, and by taking proper hygienic measures to control flies, milk, water, food supplies and human carriers of the disease. Dysentery does not occur where milk, water and food supplies are kept from contamination by flies and human excreta. TREATMENT. (1 ) Infants and children with diarrhoea

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and vomiting or proven dysentery should be completely isolated from other members of the family, and kept in bed. Aseptic nursing techniques should be practised. All food, fluid, bedding, excreta, etc., coming from the patient, should be kept from flies and all materials sterilized or disposed of to destroy any possibility of contamination. (2) Fluids of the clear type, sugar solutions and fruit juices should frequently be given orally in small amounts. With more dehydrated infants and children interstitials and/or intravenous injections of fluids should be given. If the acid base equilibrium in the patient is unknown, the safest solution to use is a mixture of % 5 per cent glucose in ¼ normal saline. ( 3) Sulphonamides may be given by mouth in doses of 1 grain per pound per day. Tetracyline and neomycin have been used and streptomycin may be given intramuscularly. Paregoric mixtures are very satisfactory and should be given orally to control the diarrhoea. VIRUS INFECTIONS Measles

Measles is an acute, highly communicable disease occurring in sporadic, endemic and epidemic outbreaks. AETIOLOGY. Measles is caused by a filtrable virus which has a predilection for the respiratory passages and skin. The incubation period is ten to fourteen days; the invasion period two to five days; the fastigium two to five days ; the revovery period two to four days. The convalescent period may be protracted depending on the severity of the disease. CLINICAL ASPECTS. The disease usually commences as an insignificant head cold with a slight febrile reaction of 99° F.-100° F. There are several types of febrile onset,

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but the most common is a "step ladder" type, the temperature rising to higher levels each day of the invasion period until at the height of the disease the fever also is usually at its height. There are daily remissions during the invasion period. The head cold, instead of improving rapidly, becomes worse, with red eyes, swollen lids, inflammed conjunctiva, running nose, an uncontrollable and persistent irritating cough and, finally, the rash. The patient rapidly becomes very ill with a rising fever and appears most miserable. SIGNS AND SYMPTOMS. Running nose, rising fever, red swollen eyes with photophobia, exanthemata and enanthemata. Enanthem. In the early stages the throat may reveal only an intense redness along the anterior pillars, the uvula, and the lower part of the soft palate and tonsils. In addition to this redness, small pin-point, bright red spots almost petechial in type, are seen. In our experience these lesions appear early, before the typical pearly white Koplik spots which may be seen on a bright red spotty background over any part of the oral mucous membranes but usually over the buccal mucous membranes and deep in the furrow of mucous membrane leading to the line of the teeth. The whole inside of the mouth becomes a dull red. Exanthem. There may be two stages of the exanthem in certain patients. During the invasion period before the true rash appears, one may observe a small, very sparsely distributed macular rash: the prodromal rash which is usually over the face and the trunk. This rash either fades or is followed quickly by the true morbilliform rash of measles. The true rash starts as a blotchy macular rash over the face and often begins earlier behind the ears. The rash spreads from above downward as a maculo-papular red rash and

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later many of the lesions become confluent. In some instances, it becomes so intense that the child appears to have a red swollen face and parts of the rash on the body have a swollen appearance also. At the height of the disease the patient is very ill, with a high fever and often a temperature of 104°F.-105°F., a severe hacking cough, sore eyes and toxaemia with rapid respirations due to the virus involving all parts of the upper and lower respiratory system. This state lasts from two to four days, depending on the patient, and then as the temperature begins to fall in the early recovery period, the rash starts to fade, leaving a faint brownish mottled staining to the skin and later a fine type of desquamation. Convalescence may be very rapid or extremely slow. Some patients become normal and all symptoms and signs disappear quickly, while others tend to show continuing respiratory involvement, with a loose type of cough and running nose for one week to one month. ATYPICAL TYPES OF ONSET. ( 1) Epistaxis. Patients have been seen with severe nose bleeds in the very early invasion phase of the disease. (2) Acute laryngitis. Measles may occasionally be ushered in with acute laryngitis with an intense croupy cough and on occasions a rather serious obstruction to inspiration. Usually this condition improves as the disease becomes more manifest. (3) Convulsions. Rarely, the disease begins with a severe convulsion or repeated convulsions. This is not to be mistaken for encephalitis which occurs later as a complication and which also may begin with a series of convulsions. ( 4) Acute appendicular colic. Many clinicians and authors have recognized this mode of onset. The child has all the symptoms of an acute appendix, but the abdominal pain usually subsides as the disease progresses. Occasionally, however, there is a definite suppurative appendicitis which must be treated surgically.

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COMPLICATIONS. These are usually connected with the upper and lower respiratory system and the brain. They are: stomitis, otitis media, mastoiditis, sinusitis, bronchopneumonia with or without empyema, eye conditions such as conjunctivitis and corneal ulcers. Encephalitis may occur approximately two to six days after the true rash has become obvious. It usually begins with repeated convulsions, drowsiness or a change in behaviour, with the other signs of involvement of the central nervous system. SEQUELAE. The patient should be watched most carefully for bronchiectasis and any changes in behaviour following encephalitis. PROGNOSIS. The prognosis is usually good. Children rarely die in an attack of measles or become mentally defective after an attack of encephalitis. DIAGNOSIS. The diagnosis of measles may be difficult in the early invasion phase of the disease; a history of contact helps immensely because otherwise one can only say that the patient is suffering from a nasopharyngitis and an infected throat. As the signs and symptoms develop, the diagnosis becomes obvious. Usually one must differentiate between measles and German measles, drug rashes, serum disease, roseola infantum, rashes of sepsis and a host of conditions giving a skin rash which to some extent may simulate measles. TREATMENT. Prophylactic. It is hoped in the near future that measles like so many other of our acute infectious diseases will be materially reduced. At present, there are very effective attenuated live measles virus vaccines which may be given alone or with an additional injection of gamma globulin. These vaccines produce active immunity to measles and likely need no additional doses when live attenuated strains are injected. Gamma globula or convalescent measles

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serum may be given to contacts to prevent or modify the disease. Therapeutic. ( 1) Bed for one week after the peak of the true rash. It is not necessary to keep the room in darkness unless the patient does not wish the irritation of the light; the old idea that light "hurts the eyes" is not true. (2) Treating symptoms is all that any one can do for this virus disease for which there is no specific therapy. Nose drops may be administered for congestion of the membranes and a sedative cough mixture for relief of the cough, although it is often impossible to relieve the latter with any form of treatment. Apply calamine lotion to the itchy skin and give aspirin for fever. ( 3) Some physicians use antibiotics in an attempt to prevent secondary infections with the common bacteria. Mumps Mumps is an acute communicable disease and, in the majority of cases, its onset is characterized by fever and parotid swelling with very slight general constitutional symptoms. Other glands and the nervous system may be involved in certain patients. The incubation period varies from fourteen to twenty-one days. The invasion period is usually two to three days and the fastigium is variable but usually two to three days although intense swelling of the parotids has occurred in an otherwise well child for as long a period as three weeks. After the fever and swelling subside, the recovery and convalescent periods are very rapid and it is usually difficult to control the activities of the child. AETIOLOGY. The virus which causes mumps has been filtered from the salivary secretions of infected individuals and the disease has been produced in susceptible monkeys by injection into Stenson's duct.

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Principal Infectious Diseases of Childhood

CLINICAL ASPECTS. In children the disease usually occurs in epidemics or endemically, although many children in an epidemic show relatively few symptoms and signs. It is not quite as contagious as measles and chicken-pox; children under seemingly constant exposure sometimes do not develop the disease on that occasion, but develop it later from a less likely source of contact. Mild type. Usually the child may have a slight fever with temperatures of 101 °F.-102°F.-103°F. and some headache and show a slight enlargement at the angle of the jaw with some swelling over the cheek just anterior to the ear. There may be tenderness at the angle of the jaw just under the lobe of the ear. This mild type is most common and at times diagnosis is very questionable. In other cases, however, there is very definite swelling and tenderness of one or both parotid glands and there may be some redness and swelling at the openings of Stensen's duct. Occasionally, only submaxillary glands are involved making diagnosis difficult, and on rare occasions the sublingual glands are involved. Severe type. In these cases there may be severe constitutional and local signs and symptoms, high fever, severe headache, intense swelling and tenderness of the parotids with the oedematous swelling extending down the sides and around the front of the neck and actual oedema over the sternum. The swelling of the parotids in this type lasts for days or weeks. Atypical type. Mumps may occur, we believe, with the only symptom being a general constitutional upset and fever for a period of twenty-four to forty-eight hours. In our experience, two children in a family had a definite mumps contact 17 days previously; one developed typical mumps with parotitis while the other had only a constitutional upset

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with fever. Mumps may develop as does poliomyelitis or any other type of meningeal reaction. Meningo-encephalitis with headache, fever, vomiting and nuchal rigidity may develop before or after the glandular swelling during the course of the disease. COMPLICATIONS. Meningo-encephalitis is likely to be not only a part of the disease, but may occur many times in house practice and not be diagnosed if no lumbar puncture is done and the cerebrospinal fluid is not examined. At other times, this complication is diagnosed by an examination of the spinal fluid, which will yield approximately 500 or more lymphocytes per cubic mm., a higher count than is found in the average case of poliomyelitis. Orchitis ( epididymo-orchitis) is a very rare complication in childhood being more common in adrilts as is ovaritis in the female. Signs and symptoms of orchitis are pain and swelling. Acute pancreatitis occurs in rare instances and causes acute upper abdominal pain, intense vomiting and tenderness in the region of the pancreas. DIAGNOSIS. During an epidemic the diagnosis of mumps is usually quite simple; the child runs a fever, with parotid swelling. There are, however, a number of very mild cases with only a febrile reaction and little or no swelling. Occasionally, other swellings of the parotid are seen. In rare cases, the patient has recurrent attacks of parotid swelling which clear and recur after months or years. There is also the occasional case of an acute suppurative parotitis. Often sero-purulent material may issue from Stensen's duct. PROPHYLAXIS. The effectiveness of mumps convalescent serum or gamma globulin to prevent mumps after contact has not been conclusively proven, but either may be given when it is important for certain reasons to prevent the

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disease. In some isolated instances in our experience it has seemed to protect the individual from developing mumps, although this would be at present hard to prove since we know that many children escape the disease even with constant, direct contact. TREATMENT. There is no specific treatment for mumps. ( 1) The patient should be kept in bed until all fever and/or swelling of the gland or any clinical evidence of complication has subsided. ( 2) Local applications do not alter the course of the glandular swelling; some children may prefer heat or cold, while others may not. ( 3) In the acute stages if there is pain and restlessness, fluids by mouth, aspirin and codeine may make the patient more comfortable. Chicken-Pox (Varicella) AETIOLOGY. Chicken-pox is caused by a specific virus, which is related to the virus of herpes zoster in biological properties. They are similar as regards elementary bodies, inclusion bodies and pathogenicity to animals and, although serologic observations are not in complete agreement, cross reactions have been demonstrated between the two viruses. CLINICAL ASPECTS. The incubation period is approximately thirteen to twenty-one days. The illness usually begins with a very mild fever and possibly some slight general toxaemia for twenty-four hours. This is followed by red macules, then papules which in a matter of hours develop into the vesicles. The fully developed lesion appears like a "water blister" on an elevated red papule. All do not appear at the same time, but develop in crops distributed over the face and trunk and possibly on the arms, legs, mucous membranes of the mouth, throat and occasionally the larynx and lungs. The genital mucosa, conjunctiva and cornea reveal lesions in rare instances. In a few days the lesions form a scab which ultimately dries and falls off.

Infectious or Communicable Diseases

13

COMPLICATIONS. Local. Skin complications result from a superimposed skin infection; a bacterial agent (such as the staphylococcus) is carried to the skin by some contaminated object (usually by scratching). Complications are: (a) impetigo, ( b) erysipelas and ( c) cellulitis. These infections may occasionally spread to the blood stream and septicaemia develops. General. (a) In a very serious type of chicken-pox in a child who has no immunity, the lesions quickly become haemorrhagic and necrotic, and coma with death follows rapidly. ( b) A typical encephalitis may develop approximately four to ten days after the onset of the disease. DIAGNOSIS. The diagnosis is usually quite simple, but chicken-pox must be differentiated from (a) unknown maculo-papular rashes, ( b) sensitivity rashes, ( c) impetigo, ( d) smallpox and ( e) Kaposi's varicelliform eruption. In smallpox, all macules appear, then all papules, then vesicles, and then pustules. In chicken-pox, macules, papules and vesicles are all seen at one time when the patient is examined. PROGNOSIS. With proper care of the lesions the outlook is good. Scarring may occur but only to a limited extent and in patients with a great number of lesions. The pits are small and as the child grows they become less noticeable. TREATMENT. ( 1 ) The child is best kept in bed during the acute febrile stage and kept indoors until the scabs come off. (2) Prevent scratching by keeping the child in light non-irritating clothing. (3) Treat the lesions with calamine lotion or Caladryl.

German Measles (Rubella) Usually seen in epidemics, German measles is a mild, very communicable disease with transient constitutional symptoms, faint rash, lymphadenopathy and quick recovery.

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AETIOLOGY. It is caused by a filtrable virus. In 1942, Hold reported successful culture of the virus on the chorioallantoic membrane of the developing chick embryo. He was able to infect monkeys after several passages on the chorioallantoic membrane. CLINICAL ASPECTS. The incubation period is usually fourteen to twenty-one days. The onset of the illness is so mild that prodromal symptoms are minimal or absent. There may be a slight indisposition with a very low-grade fever, 99°F.-100°F., a sensation of soreness in the throat, slightly injected conjunctiva and possibly a slight headache. In twelve to twenty-four hours a faint pink macular rash with spots the size of a pin-head to ¼ inch in diameter develops. These spots are discrete and appear on the face within twelve hours, spreading over the body. In addition to the rash there is often enlargement and tenderness of the posterior auricular, occipital and cervical group of lymph glands. Sometimes the fine maculo papules resemble the rash in a mild case of simple measles. The rash fades quickly ( within twenty-four hours) and the patient is quite well. COMPLICATIONS. These are few although, on extremely rare occasions, encephalitis has occurred in children. It usually has the clincal aspects of the same complication in simple measles. DIAGNOSIS. In an epidemic the diagnosis of German measles is not difficult, but when a few cases only occur, a diagnosis of German measles is uncertain. There are a whole host of as yet unknown macular rashes, as well as a group of skin reactions to drugs, allergins, antibiotics and sulphonamides which are extremely confusing. The main conditions which should be taken into account in making the diagnosis are mild scarlet fever, the early stage of a mild type of simple measles, roseola infantum, infec-

Infectious or Communicable Diseases 15

tious mononucleosis and pityriasis rosea, the differential points of which are all discussed under these diseases. Our experience has led us to believe that one must be sure of a definite epidemic and more than one child in the same family developing the symptoms before diagnosing German measles. PROGNOSIS. The prognosis in children is good, almost without exception. PROPHYLAXIS. There is no proven means of prevention. Where it is imperative, as with women in the first three months of pregnancy, gamma globulin may be used. It has been noted by Gregg of Australia that women who contracted German measles early in their pregnancy bore a significantly large number of infants with congenital anomalies, namely, eye defects (cataracts), deaf-mutism, mental retardation and congenital cardiac defects. Women who are in the first three or four months of pregnancy have to be instructed to be extremely careful about contact with anyone suspected of having German measles. Babies having the rubella syndrome may excrete live rubella virus for up to six months and therefore should be isolated, and certainly pregnant women should avoid contact with such cases. TREATMENT. There is little treatment. ( 1) If the child is upset, he may be kept in bed for twenty-four to fortyeight hours. (2) Use calamine lotion on the skin rash and bathe the eyes with cool sterile water. Roseola Infantom Roseola infantum is an acute febrile illness which occurs in infants and young children between the ages of six months and three years. The disease is usually endemic. It may be a worry to physician and parent for it is often the infant's first illness with high fever. AETIOLOGY. The cause of the disease is not definitely

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Principal Infectious Diseases of Childhood

known, but it is most likely of virus origin. No bacterial species has been proven to be a cause. CLINICAL ASPECTS. The incubation period is, as far as is known, from ten to fifteen days although longer incubation periods are possible. Usually the baby manifests a high fever of 103°F.-104°F. without other local or constitutional findings. He otherwise appears happy and in good health. Daily examination often reveals nothing but a slight infection of the throat which does not seem severe enough to be the cause of the high fever. After two or three days of high fever, a fine macular rash appears as the fever recedes. In the majority of patients this is the whole illness. DIAGNOSIS. Before the rash appears, the age of the patient and the absence of findings with the presence of a high fever, should suggest a diagnosis of roseola infantum. Once all the manifestations of the disease have occurred there is little difficulty in differentiating it from the other acute exanthemata or macular eruptions. TREATMENT. Aspirin for the fever and calamine lotion for the rash are all that is required since there is no treatment which will alter the course of the disease. Smallpox

Smallpox is an acute communicable disease characterized by a severe general constitutional upset with a macular, papular, vesicular and pustular rash followed by desquamation with the possibility of permanent scarring. Strictly speaking, there are two types of smallpox: variola minor and variola major. AETIOLOGY. These two varieties of smallpox are caused by viruses which can be recognized by biological means, and, according to Rhodes and van Rooyen, they "are members of the pack-producing group which includes also the

Infectious or Communicable Diseases

17

causal agents of cowpox, rabbit pox and vaccinia." (A. J. Rhodes and C. E. van Rooyen, Textbook of Virology, Toronto: Nelson, 1949, p. 113). CLINICAL ASPECTS. Clinically there is little difference between the two forms of smallpox except in severity. The incubation period varies from ten to fourteen days with a usual incubation period of twelve days. The onset of the disease is characterized by extreme constitutional symptoms; headache, fever, aching of back and limbs and extreme rashes are seen in this early period. These rashes may be petechial or erythematous. A number of authors and clinicians have described a bright erythematous type of rash whose colour is similar to that of a boiled lobster. This phase of the illness is characterized by a high fever, often of 105°F. or over. On the third or fourth day the true eruption appears. In contrast to chicken-pox, the different types of lesions all appear and develop through their different stages simultaneously. First, macules are seen, followed by hard palpable shot-like papules, then vesicles with umbilication, then pustules, later desquamation, red-bluish discolouration of the pitted scars, and finally, permanent scarring with small circular pits in the skin. Scarring occurs only with patients suffering from a severe type with extensive and confluent skin lesions. In milder cases the lesions are less in number and discrete. There is a characteristic distribution of the lesions over the body. In contrast to chickenpox in which the lesions tend to be centripetal, in smallpox they tend to be centrifugal; they are most numerous on exposed and pressure surfaces, namely, the face, shoulders and external surfaces of the anus, wrists, legs and feet. In severe cases, however, they may also appear on the abdomen. The febrile reaction has two phases. At the onset the patient has a sharp fever, which tends to fall as the macules begin to appear and rises later in the pustular stage.

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The pustules often contain secondary infecting microorganisms. COMPLICATIONS. Local infections of the skin from secondary invaders have been reported as well as corneal ulcers and pustules of the eyelids. General infections such as septicaemia, pneumonia and encephalitis have been seen. Pneumonia and septicaemia are probably due to secondary invaders. PROGNOSIS. Years ago, there was a severe form of the disease, haemorrhagic smallpox, which was accompanied by a high death rate. The few patients that we have seen had a mild type, and in recent years the mortality bas been much lower. DIAGNOSIS. There is usually no difficulty in diagnosis if the main characteristics of the disease, and the differences between smallpox, chicken-pox, vaccinia and Kaposi's varicelliform eruption, are kept in mind. There is little, if any, smallpox in countries where vaccination against it has been constantly practised. If there is any doubt, some of the material from the vesicle may be placed on the scarified cornea of a rabbit's eye and vesicles will appear in fortyeight ours. TREATMENT is largely general. ( 1 ) The patient should be kept in bed and measures taken to keep down the tendency to secondary infections both locally and generally. The patient should be completely isolated for two weeks or longer if the skin lesions have not healed or the disease remains active. Terminal disinfection is necessary for all bed-clothes and other articles surrounding the child. (2) If the child is severely ill, dehydrated and extremely toxic, fluids by mouth are not adequate and intravenous fluids must be given. (3) The sulphonamide drugs and/or antibiotics may be used in treating secondary infections of the skin.

41 Infections of the Nervous System

MENINGITIS is an inflammatory reaction of the meninges ( subarachnoid spaces) which is usually the result of an invasion of some specific micro-organism or virus. Meningitis, or meningeal inflammations of any kind, are still considered to be serious in infants and children despite improved methods of treatment and they call for the earliest, most rigorous forms of treatment. It is still a matter of academic interest as well as of therapeutic importance to ascertain as early as possible the underlying cause of the meningeal reaction so that treatment may be administered accordingly. The history in the acute forms, as reported by the parent, is usually that of an upper respiratory infection initially, which may have been treated inadequately or, in some instances, with apparent success. Usually however, with an infection of the upper respiratory passages which spreads by way of the blood stream to the meninges, the child becomes more drowsy, fever continues, he becomes irritable with a piercing cry, often vomits, refuses food; the older child will complain of headache. Mothers often state that the neck is sore or that the baby cries on being handled. In some, there is actually a bulging of the "soft spot." In chronic forms, the history is of longer duration with attacks MENINGITIS

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of vomiting, headache, drowsiness and irritability. In some instances, anorexia and a marked change in disposition with no desire to play occur. In the acute forms, convulsions may occur either in the invasion period or after the meningitis is well established. In chronic forms, if convulsions occur, it is usually late in the disease. Physical findings are much the same in most children with definite meningeal inflammation. ( Signs of specific types will be outlined later.) At an early stage, the child is irritable and often more drowsy that he should be with an ordinary infection. There may be a peculiar "staring" expression in the eyes of the young infant or child and he may pay little attention to his surroundings. When the doctor approaches the bed, the child will often be seen to lie on his side with the head slightly retracted and the knees drawn up in the flexed position. When attempts are made to turn a drowsy child on his back, he usually becomes irritable, cries out and assumes the original position. Examination of the nervous system usually reveals a definite nuchal rigidity, a positive Brudzinski's sign and a positive Kernig's sign. In infants, the anterior fontanelle is usually tense or bulging, and there is a generalized stiffness to the whole spine. These findings are similar for any of the purulent meningitides and other meningeal infections. In the lymphocytic forms the signs may not be quite as striking. Various clinical and laboratory differences in the different types will now be discussed. Acute Bacterial

(a) MENINGOCOCCAL INFECTIONS. This disease is so termed because all forms of it do not progress to meningitis, but may remain as a meningococcaemia. This disease was first reported by Vieusseux in 1805, and its pathology was

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described by Mathey in 1806 long before Weichselbaum defined the meningococcus as the causative agent "diplococcus intracellularis meningitidis" in 1887. Space does not permit discussion of the many interesting historical accounts which have been written. In both England and France, types of meningococci were identified by Gordon and Neter, and by Debre. The four Gordon types are now differentiated into Group I with types I and III, which have very similar serological characteristics, and types II and 11A (Branham), the latter being encapsulated. This disease occurs in epidemics (usually in army personnel) and sporadically in children. The latter form is of more concern to us. AETIOLOGY. The disease is caused by a gram negative diplococcus. This micro-organism, the meningococcus, belongs to a group of gram negative diplococci commonly known as the Neisseria. (The flat sides of this gram negative diplococcus are opposed; in contrast, in the gram positive diplococcus, the pneumococcus, the ends are opposed.) The bacteria are usually found in small numbers in the spinal fluid; some are intracellular, others extracellular. Carriers of the meningococcus are usually adults or, occasionally, children in the immediate family contact. These individuals usually suffer from a mild upper respiratory infection with the same strain of meningococcus. Although there are healthy carriers, as well, the individuals who actually suffer from an upper respiratory infection due to the menincococcus are likely as much responsible for its spread as healthy carriers. PATHOGENESIS. The meningococcus, which causes an initial upper respiratory infection in the patient, is believed to spread through the blood stream, entering the cerebrospinal fluid by way of the choroid plexus.

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CLINICAL TYPES. As has already been indicated, the meningococcus does not always cause meningitis and different clinical types of the disease are observed. Acute meningococcaemia. Bacteriaemia or septicaemia due to the meningococcus may reveal itself clinically and appear like any other septicaemia without meningeal involvement. There is usually a petechial or purpuric rash, diffusely distributed, occurring over any part of the body. The blood culture reveals the meningococcus, and blood smears of the purpuric lesions stained by Gram's method reveal a gram negative diplococcus. Acute meningeal type. This is the most common. In addition to the usual signs of meningitis and a purulent spinal fluid containing the meningococcus, it manifests skin rashes of various types: haemorrhagic, herpetiform or morbilliform. Acute fulminating type. The child is critically ill with a high fever, flushed, irrational, semi-comatose, and shocked, with poor pulse and low blood pressure. Circulatory changes reveal wide areas of bluish discoloured skin, and there are haemorrhagic tendencies with or without meningeal involvement. The patient dies within twelve to forty-eight hours with or without haemorrhages into the adrenal gland. Chronic basilar type. When the usual type of meningitis is treated too late or inadequately, opisthotonos with nuchal and spinal rigidity persist. In this type there is a purulent inflammation around the base of the brain and involving the area of the optic chiasma. In addition to hydrocephalus there may be ocular palsies. CLINICAL ASPECTS. Signs and symptoms. Almost always the patient has a history of one to three days of fever, upper respiratory infection, headache, vomiting and sore-

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ness of the neck. On examination, he is drowsy and irritable when disturbed. In most patients there is nuchal rigidity, generalized rigidity, a positive Brudzinski's sign, in some a positive Kernig's sign, and, occasionally, rashes of different types: morbilliform, herpetiform or haemorrhagic, although a petechial or purpuric rash is the most common. There is usually bulging of the fontanelle in infants. DIAGNOSIS. The clinical diagnosis of all forms of meningeal inflammation can usually be made by examination. An infant or child who alternates irritability with periods of drowsiness out of proportion to the febrile state, who has nuchal rigidity, a bulging fontanelle and a Brudzinski's sign should certainly be considered as having some type of meningeal inflammation. A lumbar puncture should be performed, followed by an examination of the spinal fluid, since the diagnosis of meningococcal infection or other forms of purulent meningitis can only be made with accuracy by this method. The fluid is examined microscopically and culturally for the presence of the infecting organism. Careful search of a smear stained by Gram's method usually reveals the gram negative diplococcus intra- or extracellular, generally in small numbers. Culturally the growth reveals meningococcus after twenty-four to forty-eight hours of incubation. COMPLICATIONS. Since the advent of chemo- and antibiotic therapy fewer complications are seen. In the meningococcal variety hydrocephalus was one of the most common complications while otitis media and deafness have been observed. Various eye complications such as corneal ulceration, purulent choroiditis and panophthalmitis have been seen in the past; arthritis, endocarditis and pneumonia also occurred before improved methods of treatment were developed.

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PROGNOSIS. Before the advent of chemo- and antibiotic therapy and during the era of antimeningococcal serum therapy, the case fatality rate in our clinic was in the neighbourhood of 30 per cent. Since the use of sulphonamides and penicillin in the case diagnosed early ( eliminating the fulminating types), the case fatality rate has been about 2 per cent. One of us has reported three cases of meningococcaemia with recovery; the patients' blood revealed the development of bactericidal antibodies to the respective strains of meningococcus causing their infection. None of these patients received treatment. TREATMENT. The treatment of this and the other types of acute meningitis will be discussed after brief references to some of the differences in the other types. ( b) STREPTOCOCCAL MENINGITIS. This type may be seen either in the new-born or in older infants and children. The disease may be an extension from an upper respiratory infection due to the haemolytic streptococcus, or secondary to some existing focus of infection such as otitis media, sinusitis or mastoid disease. The history and physical findings are much the same as in all forms of acute meningitis and the diagnosis is made in the same way as for the meningococcal variety, namely, by an examination of the cerebrospinal fluid after clinical signs have suggested meaningeal inflammation. The finding of gram positive cocci and culturing of the haemolytic streptococcus are diagnostic. ( C) PNEUMOCOCCAL MENINGITIS. This is an acute infection of the meninges caused by any type of pneumococcus. Although all ages may be affected, the disease is more common in young infants than in older children. Pneumococcal meningitis may appear as the primary disease or, more usually, develop as a result of an upper respiratory infection or pneumonia producing bacteriaemia

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followed by meningitis. The child does not seem to improve as rapidly as he should from the usual respiratory infection, the fever continues and very soon the signs and symptoms of meningitis develop. In all respects these signs and symptoms are similar to those of other forms of purulent meningitis. In certain young infants, however, the onset may be very abrupt with high fever, rapid respirations, cyanosis, shock, coma and death before adequate therapy may be commenced. The diagnosis of this type of meningitis is best made by an examination of the spinal fluid and the finding of gram positive diplococci on direct smear of the fluid and by culturing the pneumococcus. ( d) INFLUENTIAL MENINGITIS. This is usually seen in children from six months to three years of age ( 80 per cent of the cases are in this age group). The disease has been much commoner since the advent of sulphonamides and antibiotics than forms of meningitis caused by streptococci and pneumococci. The latter have probably decreased in incidence because upper respiratory infections preceding the meningitis are caused by streptococci and pneumococci and these bacteria are very sensitive to the action of the chemo-therapeutic and antibiotic agents. These drugs likely prevent the bacteria causing the respiratory infections from progressing to the meningeal stage. Influenzal meningitis is caused by one of the types of haemophilus influenza. Pittman of the United States Public Health Service has described types A, B, C, D, E, and F but experience has revealed that 99 per cent of the strains isolated from patients with this form of meningitis are due to type B. ( Seventy out of seventy-one strains which have been typed were type B.) Clinically this disease is similar to the other purulent types and its history is usually that of an upper respiratory infection not subsiding in the infant. Following

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a nasopharyngitis the signs and symptoms of meningitis develop. In past years, a type of the disease in which the joints or tissues surrounding the joints were involved was seen. Most cases probably develop following septicaemia or bacteriaemia due to the influenza bacillus type B. The diagnosis is made by an examination of the spinal fluid. Examination of the direct smear of the centrifugalized fluid reveals a pleomorphic thin gram negative bacillus, which on culture medium suited to its growth reveals a culture of H. influenzae. This is further identified as type B by the phenomenon of capsular swelling, by a precipitation test or an agglutination reaction. ( e) STAPHYLOCOCCAL MENINGITIS. This type is extremely rare ( in twenty-five years at our Hospital there have only been about twenty-six cases). Clinically the disease is no different in signs and symptoms from the other purulent forms, but usually follows a primary focus of staphylococcal infection such as furunculosis or some area of osteomyelitis. It is caused by the haemolytic staphylococcus extending from the primary focus either locally or by way of the blood stream to the meninges. The diagnosis, suspected when meningeal signs develop in a child with a known staphylococcal infection, is confirmed by finding the gram positive coccus in the smear of the spinal fluid and culturing staphylococcus from medium planted with the infected spinal fluid. (f) MENINGITIS DUE TO E. COLI. This is almost exclusively found in new-born infants who are infected in nurseries having other infections caused by B. coli. The clinical signs and symptoms of meningitis are similar to those of the other forms , but the infant is often more toxic and drowsy and there may be very little accompanying febrile reaction. The diagnosis is only made on examination

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of the spinal fluid where a gram negative bacillus is seen and B. coli cultured. (g) RARER FORMS OF BACTERIAL MENINGITIS. Almost any type of bacterial pathogen may cause meningitis. Reports of isolated cases caused by these rarer bacterial agents are too numerous to mention, but it is only necessary to remember that there are other types of bacteria which cause meningitis and that the signs and symptoms are similar to the more common types. It is only by an examination of the spinal fluid to isolate the aetiological agent that these rarer types of meningitis are found. We shall now discuss the complications and prognosis of forms (b)-(g) . COMPLICATIONS. Before the chemo-therapeutic and antibiotic era, 98-100 per cent of patients with streptococcal, pneumococcal, influenza!, staphylococcal and E. coli meningitis died. Since the advent of specific forms of treatment, more patients recover, but there are complications, usually mechanical in nature, the result of inflammatory scarring in one part or another of the central nervous system. Hydrocephalus, deafness, focal areas of brain damage, convulsions and sometimes mental retardation are the sequelae which are seen. PROGNOSIS. The prognosis of meningitis depends on several factors: the duration of the disease before the diagnosis is made; the effectiveness of the treatment; the type and number of infecting micro-organisms; and the age of the child. The earlier the diagnosis and treatment, the better the prognosis, of course. So, too, the older the child, the better the prognosis; and, most likely, the fewer the infecting micro-organisms in the spinal fluid, the better the prognosis. Before the introduction of chemo-therapeutics and antibiotics, all victims of meningitis, with the exception

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of those with meningococcus infection, died (98-100 per cent) . There has been a gradual reduction in the case fatality rate with the development of sulphonamides and antibiotics and the treatment of the various purulent forms of meningitis with these drugs. At present, most of our patients with influenza!, streptococcal and pneumococcal meningitis recover without any serious complications or sequelae. B. coli meningitis has not responded as well to modern therapeutic methods and the prognosis in this form of the disease is still guarded owing to the extreme youth of the patient and the fact that B. coli does not seem to respond to the action of the newer drugs in the same spectacular way as do the other bacterial agents causing meningitis. In the course of the past fifty years there has thus been a remarkable reversal in the outcome of these types of meningitis. The common types no longer have a 90 to 100 per cent fatality rate, but, because of the development of agents such as sulphonamides and antibiotics have a 90 to 100 per cent recovery rate. PREVENTION. It is well known that most of the causative agents ( the meningococcus, pneumococcus, streptococcus and influenza bacillus type B) of bacterial meningitis are the primary cause of many of the upper and lower respiratory infections of children and that all of these microorganisms ( with the possible exception of H. influenzae) are killed or inhibited in their growth by therapeutic agents such as the sulphonamides and antibiotics. Meningitis, with its complications, sequelae and former death rate, is so serious a disease that one must recommend that most upper and lower respiratory infections be treated by sulphonamides and/or antibiotics. The use of these drugs in such infections, early and in adequate doses, will unquestionably

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prevent many cases of meningitis from developing. In other patients the early excision of the foci of infection should be undertaken. Children with frequently recurring upper respiratory infections, laryngitis, otitis media who are, as a result, only partially healthy, should have the offending foci removed. This is particularly true of tonsils and adenoids. ACUTE PURULENT MENINGITIS THERAPY. General: ( 1) isolation of the patient ( this is advisable, but need be enforced only in meningococcal infection); (2) bed rest; ( 3) maintenance of fluid and electrolyte balance--continuous intravenous of % 5 per cent glucose in ½ normal saline solution, 90-100 cc. lb. body weight, per 24 hours or same solution in subcutaneous infusion; if the patient is not vomiting and hydration is satisfactory, oral fluids 3 oz./ lb./day should be given; ( 4) blood transfusion, 10 cc./lb. body weight, of whole matched blood if shock or anaemia is present or the patient appears seriously ill; (5) drainage of foci of infection such as mastoids or sinuses; ( 6) continuous nursing, preferably. Specific: Great advances have been made in meningitis therapy as a result of improved antimicrobial agents reducing the fatality rate, sequelae and duration of the illness. Various combinations of antimicrobial agents are used in different centres and the following regimes have proven highly satisfactory at the Hospital for Sick Children in Toronto. (a) M eningococcal meningitis. ( 1 ) Sulfadiazine is the drug of choice and should be given intravenously or subcutaneously. The dosage is for infants 2-3 gr./lb. body weight per 24 hours every six hours and for older children one-half of this, to obtain a blood and cerebrospinal fluid level of 10-15 mg. per cent. After twenty-four to forty-eight hours sulfadiazine may be given orally if the patient is not vomiting. In addition to sulfadiazine, penicillin may be

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given intravenously every six hours in 800,000 to 1,000,000 units daily or daily intramuscular injections of procaine penicillin may be given. Antimicrobial therapy may be discontinued after five days if clinical and cerebrospinal fluid findings indicate that the patient is cured. (2) If the patient is shocked and extremely ill, 50-100 mg. of cortisone given intravenously followed by 50 mg. every twelve hours is indicated, plus 25-50 cc. adrenal cortical extract given intravenously every four to six hours for twenty-four hours. ( b) Streptococcal meningitis. (1) For infants sulfadiazine 2-3 gr./lb./24 hours every six hours should be given intravenously or subcutaneously; one-half this dosage is adequate for older children. After twenty-four to forty-eight hours sulfadiazine may be given orally if the patient is not vomiting. (2) Penicillin, intravenously: 200,000-l,000,000 units every four hours; crystalline aqueous penicillin for three days; then 1,000,000 units procaine penicillin given intramuscularly twice a day for four days. Antimicrobial therapy may be discontinued after seven days if clinical and cerebrospinal fluid findings indicate that the patient is cured. ( 3) If pneumococcal meningitis is associated with mastoid or sinus infections these foci should be drained early in the course of the disease. ( c) Pneumococcal meningitis: same as streptococcal. (d) H. influenzae (type B) meningitis. (1) Sulfadiazine should be given intravenously or subcutaneously 3 gr./lb. body weight per 24 hours four times daily for the first twenty-four to forty-eight hours. After this period 2-3 gr./lb. body weight per 24 hours oral sulfadiazine may be given every six hours if vomiting has stopped. The purpose

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of this is to maintain sulfadiazine blood or cerebrospinal fluid levels at 10-15 mg. per cent. (2) Chloramphenicol: 40-50 mg./lb. body weight per day given intramuscularly every twelve hours or 80 mg./lb. body weight per 24 hours given orally every six hours. In most cases antimicrobial therapy may be discontinued after seven days if clinical and cerebrospinal fluid findings indicate that the patient is cured. ( 3) It is now the consensus of opinion in most centres that streptomycin and intrathecal therapy are no longer indicated in this type of meningitis. ( e) Staphylococcal meningitis. This should be treated as are pneumococcal and streptococcal meningitis. The sensitivity of the organism should be determined as early as possible and if it is only moderate or the organism is resistant to penicillin, administer erythromycin 20 mg./lb./day every six hours and chloromycetin or bacitracin and staphcillin 300-600 u./lb./day intramuscularly three times daily. (f) Meningitis due to gram negative bacilli (Escherichia coli, Pseudomonas, paracolon, Proteus and Aerobacter aerogines) . Sensitivity should be determined promptly because of the variability in the strain resistance of these organisms. Coliform organisms generally are sensitive to chloramphenicol and neomycin. Proteus vulgaris and Pseudomonas are difficult to treat but the most effective therapy is with neomycin and polymyxin B respectively. In recurrent meningitis in the same patient the possibility of agammaglobulinaemia or dysgammaglobulinaemia should be investigated and the patient treated with prophylactic antibiotic. Infected dural sinus with communication between the meninges and the exterior should also be considered and, if present, removed surgically. In a patient with meningitis whose clinical course is not satisfactory after four or five days' therapy ( continued fever, persistent

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neurological signs, vomiting and convulsions), the possibility of subdural collection of fluid should be considered and subdural taps done. Serous Meningitis

When a focus of infection exists in tissues adjacent to the dura, e.g. mastoid, middle ear, paranasal sinuses, petrous temporal bone, irritation of the meninges may produce a polymorphonuclear cellular response in the spinal fluid and typical signs of meningitis in the patient. In this condition, however, no organism is present in the spinal fluid on examination by smear or culture. Treatment consists of general supportive measures and efforts directed to the elimination of the primary focus by antimicrobial agents and for surgical drainage. Meningismus

This term is used to describe a symptom complex seen not infrequently in children in whom signs of meningitis are present including fever, headache, nausea, vomiting and stiff neck. In this condition the spinal fluid is under increased pressure but does not have an abnormal cell count and is sterile with no organisms present on smear or culture. This symptom-complex may be associated with a number and variety of febrile illnesses in children but is most frequently seen in respiratory infections, cervical adenitis, gastro entiritis, and pyclonephritis. Symptomatic relief may be obtained by performing a lumbar puncture on the patient. This reduces the spinal fluid pressure and frequently causes the headache, stiff neck and nausea to subside rapidly. The underlying condition of course should receive appropriate treatment.

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Chronic Inflammatory There are two divisions here: chronic basilar and tuberculous. (a) CHRONIC BASILAR

AETIOLOGY. Chronic basilar should usually be considered as a type of meningococcal infection since the majority of patients with a persistent reaction at the base of the brain are probably those who have recovered only partially from a meningococcal infection. The bacteria are no longer present, but an inflammatory reaction at the base of the brain remains. The signs and symptoms of this condition are those of a chronic basilar lesion : nuchal rigidity, opisthotonos and a tendency to develop hydrocephalus. PREVENTION of this end-stage lesion is early diagnosis and prompt administration of sulphonamides and antibiotics. TREATMENT of this end-stage basilar meningitis is very unsatisfactory. ( b) TuBERCULOUS MENINGITIS. There is no better review of this disease than the classical description in Still's Diseases of Children (Still, G. F., Common Disorders and Diseases of Childhood, London: Milford, 1924) . It must be pointed out here, however, that in contrast to the acute purulent forms, tuberculous meningitis is a chronic basilar type with a more insidious onset, a prolonged course, a lymphocytic pleocytosis, a characteristic cerebrospinal fluid pellicle and the presence of tubercle bacilli in the cerebrospinal fluid and sometimes in the choroid coat of the eye with generalized or other tuberculous foci throughout the body. The onset of the disease has three stages. The first is indisposition in which the child manifests a changed disposition or personality, has attacks of vomiting, headache

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and a general feeling of malaise. The second stage is that of irritability where there are signs and symptoms such as those found with meningeal irritation: irritability, drowsiness, night or sleep screams, headache, vomiting, meningeal signs with Biot's breathing, positive tache cerebrale and changes in the circulatory system manifested by slowing of the pulse and heart rate. The third or final stage is paralysis manifested by lifelessness, sunken eyes, very slow shallow respirations occasionally of a sighing type, scaphoid abdomen, extreme drowsiness with paralyses often spastic in type and, occasionally, twitchings and convulsive movements with final coma and death. PREVENTION is by preventing all forms of tuberculous infection, both human and bovine. TREATMENT. Until streptomycin was used, no method of treatment offered much hope for these children. Now, by prolonged use of streptomycin and isonicotinic acid hydrazide, patients treated after an early diagnosis stand a good chance of recovery with normal mentality. They are treated as follows: ( 1 ) INH 10 mg. per kilo per day in two doses, one every 12 hours, for four months, then 5 mg. per kilo per day to the end of the year and 2½ mg. per kilo after one year. (2) Streptomycin, given intramuscularly, ½gm.per day for two to four weeks, then every second day, then every third day, discontinued after six months. ( 3) Lumbar puncture at one week to ten days to relieve pressure. VIRUS INFECTIONS

There are at least thirty-five antigenically distinct viruses which may cause infection of the central nervous system;

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some differ one from another in biological properties, but others are closely related. These viruses are classified by distinguishing the antigenic relationships of neurotropic viruses. Some of the methods used in studying them are complement fixation tests, virus neutralization tests and cross resistance tests in immunized laboratory animals. The most obvious clinical differentiation is between (a) viruses in which the involvement of the nervous system is secondary to a primary virus infection elsewhere in the body and ( b) infections due to neurotropic virus invasion of the central nervous system. The best example of a primary virus infection secondarily involving the nervous system is encephalitis following mumps, measles, chicken-pox, herpes simplex or influenza. Examples of a primary neurotropic invasion are such diseases as poliomyelitis, equine encephalitis and epidemic encephalitis. Certain materials may be collected in order to study the causative virus or to isolate it for identification of the particular disease. Any sample or specimen obtained for this purpose is best frozen at a temperature of 0°-60°C. The following materials should be kept for investigation: brain and cord tissue; cerebrospinal fluid; stools; oral pharyngeal washings; and at least two samples of sera, the first taken at the onset of the disease and a second taken some weeks, or, in certain virus infections, months later. Vims Meningitis (Aseptic Meningitis)

This term is a general one to describe various lymphocytic reactions in the cerebrospinal fluid ( other than the neurological manifestations, secondary to measles, or chickenpox) . When no other primary involvement is present, the primary invasions of the nervous system by a neurotropic

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virus may be by the viruses of poliomyelitis or, on occasion, by the viruses of mumps, herpes simplex or by the coxsackie virus. TREATMENT. There is no specific treatment. General measures for the treatment of this type of meningitis are recommended, namely, the confinement of the patient to bed and the use of drugs for his relief. Mumps-Meningo-Encephalitis This condition is probably due to an extension of the virus infection causing mumps. Clinically, the disease manifests all the signs and symptoms of meningeal irritation and five hundred or more lymphocytes are found in the spinal fluid. It occurs as a part of mumps or as a complication prior to, after or without glandular swelling ( see the description of mumps, above). The prognosis is good in all cases as complete recovery occurs in a matter of days after the meningeal signs and symptoms have been present. The treatment is bed-rest until the fever is normal and the symptoms have subsided. Lymphocytic Choriomeningitis This disease is very rare in children. The virus has been discovered in mice and reported by a number of investigators. Before virus studies were done, the disease was very likely to be considered a form of serous meningitis. CLINICAL ASPECTS. The incubation period is usually one to three weeks. The illness begins with upper respiratory manifestations such as a fever, chills, a cough, and a sore throat. Later there is meningeal involvement with signs and symptoms of headache, vomiting and nuchal rigidity. The disease is not unlike many other types of acute lymphocytic

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meningitides. It is of short duration usually ending in recovery. EPIDEMIOLOGY. The virus is carried in some way by laboratory mice and hence the disease usually occurs in laboratory personnel. DIAGNOSIS. This is made by injecting the spinal fluid intracerebrally into mice. Serologic tests are done by virus neutralization and complement fixation techniques, the convalescent serum being withdrawn three months after the onset of the disease. Herpetiform Meningitis

See the description of Herpes simplex in the next chapter.

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a number of virus mfections seen in children other than those affecting the central nervous system and other than the communicable diseases caused by viruses. THERE ARE

SKIN DISEASE

Molluscum Contagiosum

Occasionally seen in children, this is characterized by small wart-like elevations of the skin which are seen on the back, face and arms. A central dimple is noted and a lightcoloured secretion may be seen exuding from the dimple. The disease spreads usually by direct contact. The virus cannot be cultivated but can be transmitted by intradermal inoculation. There is no specific treatment. Warts

These are virus infections of the skin appearing most commonly on the hands although they may be found on other parts of the body. They are small round or oval plaque-like elevations of the skin. They spread by direct contact. The incubation period is several weeks. Usually warts disappear spontaneously in a matter of months, and this makes it difficult to evaluate various possible treatments. They may

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be removed surgically with caustic agents and by electrodesiccation. Herpes Zoster (Shingles)

This is occasionally seen in children, as a vesicular eruption occurring on one side of the body only. Eruptions may appear over the distribution of any nerves, but the most common sites are the forehead and the sides of the nose and face. In some instances they occur along the nerves on the flexor surface of the arm starting at the midline near the shoulder. Occasionally a lymphocytic meningitis may result from herpes infection. It is difficult to say how the virus enters the body, but in secondary zoster it may be lying latent in the respiratory tract. A relationship between this virus and that of chickenpox has been suggested. In some instances chicken-pox in one child has followed the incubation period of 17 to 21 days from contact with another child in a family suffering from herpes. The relationship is not entirely clear since there is no constant appearance of this type of cross-infection. At most, these two viruses share antigenic components and are members of the same group of viruses but are not identical. Calamine lotion is the best treatment; the lesions gradually clear up spontaneously. Herpes Febrilis (Simplex)

This is caused by a distinctly different virus from herpes zoster. Children may show a variety of manifestations of the herpes infection from separate vesicular eruptions to a fatal nervous disease. There is a type of stomatitis in children due to the herpes virus, and Vincent's fusiform bacilli and Spirochaeta are

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secondary invaders. Herpes febrilis is seen as separate lesions on the lips alone or accompanying such diseases as pneumonia, meningococcal infections, Kaposi's varicelliform eruption ( seen on the surface of eczema) and it is associated with a benign lymphocytic meningitis. The disease is usually spread by salivary secretions or by direct lip to lip contact. Diagnosis can be made by applying a few drops of vesicular fluid to the scarified eye of a rabbit and, if the virus is present, a keratitis develops in three or four days. RESPIRATORY DISEASES CAUSED BY VIRUSES

The common cold and minor respiratory illnesses are most likely caused by the group of bacteria found in upper and lower respiratory infections ( usually the pneumococcus and streptococcus). In fact, the common cold is probably nature's first defence against more serious disease produced by a multiplicity of micro-organisms entering the upper respiratory passages of man. In this sense, an upper respiratory disease is an immunity reaction. There are several wellknown viruses which affect the upper respiratory tract of children. These are: the virus of the common cold; the virus of undifferentiated respiratory disease; the virus of influenza and the virus of primary atypical pneumonia. The Common Cold The usual signs and symptoms of the common cold and their sequence are well known. The sense of burning and smarting, the sneezing, the serous discharge, the congested nares, the purulent discharge, the cough and the general feeling of

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wretchedness are the most common. The cold is spread by direct contact with another sufferer by droplet transmission or from fomites; carriers of the cold virus may also be a factor in its spread. The mechanism of its spread is not, however, entirely understood although it has been shown that filtrates of nose and throat secretions from persons with the common cold infect a certain percentage of volunteers. Different viruses are probably responsible for the common cold and the undifferentiated acute respiratory diseases. Influenza

Infants and children suffer from influenza in the fall, winter and spring seasons of the year; at this time it is seen in outbreaks. It is almost certain that if nasal washing could be inoculated into eggs and serologic tests made with the patient's serum, many respiratory conditions in the months when they are epidemic and showing a leukopenia would be found to be due to the virus of influenza. Usually, in the infant and young child, the signs and symptoms are those of a severe respiratory infection with marked distress in breathing and the appearance of an asthmatic type of bronchopneumonia. In the older child, symptoms of the adult type are present: sudden onset, aching of back and extremities, high fever and involvement of the respiratory tract. This clinical picture may also be seen in epidemic form as a result of other infections, since there are other types of undifferentiated virus and bacterial infections which may give the same clinical picture as epidemic influenza from which the virus of influenza is not isolated. The disease is seen in all parts of the world and is spread by direct contact through droplet infection from sufferers

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and likely from carriers. The virus is found in the upper respiratory passages at the onset of the disease and several types of virus have been found. Viruses A, B and C occur in epidemics; viruses B and C more commonly cause the sporadic type of the disease. DIAGNOSIS may usually be made clinically when the typical symptoms and signs appear and a high fever and a leukopenia are present. Confirmation is possible only by injecting ferrets and observing the development of the disease in these animals or by making serological tests from the serum of the patient such as haemagglutination inhibition and complement fixation in which the antibody titre in the early and late serum is compared. TREATMENT. The usual treatment for upper respiratory infections should be carried out: ( 1) fluids such as sweetened fruit juices; ( 2) antipyretics; ( 3) sulphonamides and penicillin or other antibiotics. These are given in the hope that the disease may be of bacterial origin. However, true influenza caused by viruses A, B and C does not respond to any of the sulphonamides or antibiotics. Primary Atypical Pneumonia

Most pneumonia in infants and children has been caused by the pneumococcus, streptococcus, staphylococcus, haemophilus influenzae and other well-known bacterial species. Some cases are probably the direct result of the virus of influenza and other undifferentiated respiratory viruses. However, when these causes have been ruled out and a pneumonia occurs which is persistent in its signs and symptoms in spite of treatment with sulphonamides and antibiotics, it is most likely due to the virus causing primary atypical pneumonia.

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CLINICAL ASPECTS. The onset of this infection is usually more gradual, with signs of an upper respiratory infection which does not improve. There is often a very prominent, persistent cough, resistant to treatment. In the infant a "wheezing" asthmatic type of bronchopneumonia is present with indefinite and inconstant areas of crackling fine rales and these may be scattered over various parts of the chest. There is a fever which lasts much longer than that of an ordinary bacterial pneumonia. The temperature ranges from 100°F.-103°F., for several days or even weeks. Changes found in the lungs of these patients are those of an interstitial pneumonia with bronchitis or bronchiolitis; peribronchial changes and the infiltration of alveoli and interstitial tissues with mononuclear cells and some polymorphonuclear leukocytes. The development of cold agglutinins in the convalescent stage and the consequent finding of agglutinins for the M.G. streptococcus are valuable in the diagnosis. AETIOLOGY. This is obscure, but it is believed that a specific respiratory virus will ultimately be discovered. The disease has been transmitted to human volunteers by spraying their throats with filtered and unfiltered throat washings and sputa. Smears made of the secretions in the lungs and sputum of infants with this disease have revealed intracellular nuclear inclusion bodies ( a usual finding in virus pneumonia). TREATMENT. The usual treatment of pneumonia is attempted in case the disease is bacterial and not viral in origin. The treatment should be as follows: (1 ) bed; ( 2) fluids by mouth, sweetened fruit juices; (3) fluids by hypodermoclysis or intravenous if necessary; ( 4) oxygen administration 40 per cent or over and (5) sulphonamides

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and antibiotics given in adequate doses do not affect the virus but may help in the treatment of secondary bacterial invaders. Infectious Hepatitis

This disease was known in past years as catarrhal jaundice. It occurs in children in a sporadic form and during wartime is seen in armies where lower standards of sanitation and hygiene exist. CLINICAL ASPECTS. The incubation period is usually thirty days and a generalized disturbance develops in the patient before jaundice appears. The usual symptoms are loss of appetite, weakness, fever, abdominal discomfort, headache and vomiting. Occasionally photophobia is seen. These signs and symptoms last from one to three weeks before jaundice develops. The sclera may first be tinged and then generalized jaundice appears. During this stage the symptoms may be accentuated. Certain patients become intensely jaundiced and the disease progresses to a fatal termination ( acute yellow atrophy). Clay-coloured stools are seen, as well as bilinuria, urobilinogenuria, albuminuria and glycosuria. Recovery is usually complete and relapses or complications are rare. The blood usually reveals a leukopenia with a lymphopenia and neutropenia in the early stages, followed by relative lymphocytosis with atypical lymphocytes resembling those found in infectious mononucleosis. The liver reveals necrosis of the hepatic cells associated with an infiltration of leukocytes and histiocytes. Changes are seen in the central part of the lobule. AETIOLOOY. The disease is due to a virus, but its mode of spread is not definitely known. The only information as to the nature of the infection has been obtained from the

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feeding of filtrates of the stools of patients with the disease to human volunteers who come down with the disease seventeen to thirty days later. There have been consistently negative results with attempts to infect laboratory animals. TREATMENT. Prevention of the disease is difficult since its mode of spread is not clearly known. It is wise, however, to carry out precautions against infection with each patient. Known contacts should be given gama globulin. The improvement of sanitation and personal hygiene, the disinfection of stools, bedpans, dishes and clothing of the patient will likely do much to limit the spread of the disease. The treatment consists of general measures since there is no specific treatment indicated. Rest in bed, and a high carbohydrate fat-free diet with lots of fruits and vegetables are usually recommended. In the acute febrile stages a fluid diet of fruit juice is all that is necessary. Homologous Serum Jaundice

There have been few cases of this disease in childhood; it may occur if groups of children receive human serum which harbours the virus causing the disease. The main difference from acute infectious hepatitis is that serum jaundice has a longer incubation period ( 40-160 days) . Infectious Mononucleosis CLINICAL ASPECTS. This disease, occasionally seen in children, is characterized by the development of an acute sore red throat with enlargement of the cervical glands, and in some cases there is general glandular enlargement with tenderness. It has a somewhat protracted course of from one to three weeks before recovery. AETIOLOGY. The disease is caused by a specific virus. SIGNS AND SYMPTOMS. The child develops a fever, a red

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throat, swollen, tender glands and is moderately ill. The throat is quite sore at times and appears quite inflamed in some patients. Usually an acute tonsillitis is suspected with enlargement of the cervical glands. DIAGNOSIS. Differentiating this disease from an acute upper respiratory infection with an inflamed throat and enlarged tender glands is difficult except by examination of the blood. The blood shows a positive heterophile agglutination test and the smear of the blood shows the characteristic large lymphocytes found in this disease. PROGNOSIS. After the disease has run its somewhat protracted course, the child with infectious mononucleosis makes a complete recovery. TREATMENT. There is no specific treatment. ( 1) The child should be kept in bed until all fever and glandular swelling has subsided. (2) Fluids should be given by mouth. ( 3) Drugs of the type that cause reduction in fever may be used and aspirin or other antipyretics may be given. ( 4) There is no good reason to give sulphonamides or antibiotics but these drugs have likely been given to many patients since the disease simulates the usual type of upper respiratory infection of bacterial origin. "NEW" VIRUS INFECTIONS

Enterovirus Infections in Children

As a result of the investigation of illnesses throughout the world in recent years, a number of "new" viruses have been isolated which have been firmly established as the causative agents in specific clinical syndromes. This statement is based on the reasonable assumption

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that the repeated association of a specific virus with a clinical syndrome (e.g. coxsackie virus with epidemic pleurodynia) is strong evidence in support of the etiological basis of the infection. For descriptive purposes, these viral agents may be divided into the following groups and sub-groups. Enteroviruses: (1) Poliomyelitis Virus Types I, Il, m. (2) Coxsackie Virus Type A-23 strains, Type B-6 strains; ( 3) Echo Virus-30 or more antigenic types. Each of these viruses and the diverse clinical syndromes which they may produce will be considered in this section. See the classification outline which follows. CLASSIFICATION OF ENTEROVIRUSES

( 1 ) Poliomyelitis Virus Infections Types I, IT, Non-paralytic and paralytic disease (2) Coxsackie Virus Infections Type A (a) Aseptic meningitis (b) Herpangina ( c) Respiratory illness ( d) Exanthemata Type B (a) Aseptic meningitis (b) Pleurodynia ( c) Myocarditis ( d) Exanthemata (3) Echo Virus Infections (a) Aseptic meningitis (b) Exanthemata ( c) Diarrheal disease ( d) Respiratory tract infection

m

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Identification of Viruses as Causative Agents in Specific Inspections Before proceeding to a discussion of the various viral agents and the clinical syndromes they may produce, it is important to outline briefly some of the more practical laboratory methods and techniques employed in virus identification. TISSUE CULTURE. Improved tissue culture techniques have led to the identification and typing of many viral agents. The chief stimulus to this work on newer viruses was the discovery by Enders, Weller and Robbins that polio virus causes degenerative changes in cultures of human embryonic tissue and that this change is prevented by specific immune serum. These so-called "cytopathogenic" changes can be observed under the low power of an ordinary microscope on unstained material. The main tissues used for culture of viral agents are monkey kidney, human amnion and Hela cells. By inoculating these tissue cultures with specially prepared specimens of stool, throat washings, CSF and blood, a viral agent may be identified by the cytopathogenic effect it produces. By the addition of specific antisera to the tissue culture, the viral agent may be more completely and definitively identified. ANIMAL INOCULATION. In addition to growing viruses on tissue culture, some viruses may be identified by the fact that certain laboratory animals such as suckling (newborn) mice, monkeys and the chick embryo have been found to support the growth or proliferation of specific viral agents, e.g. Coxsackie, polio, influenza viruses. SEROLOGIC TECHNIQUES. By comparing the acute and convalescent serum antibody titres in a patient with a suspected acute viral infection, the viral basis for the illness

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may be established if a significant rise in titre is demonstrated. Complement fixation (C.F.), neutralization tests (N.T.) and haemagglutination inhibition (H.I.) are the chief serological means of virus identification. Using the above virus laboratory techniques, the virologist may be of great assistance to the practicing physician in identifying the specific ·etiological agent in many clinical illnesses. Specimens of the material suspected of containing virus (CSF, throat washing, stool, vesicle fluid) should be carefully obtained from the patient, adequately preserved in special containers and sent for study and reporting to the hospital or government virus laboratory with a brief outline of the patient's illness. (1) Poliomyelitis Virus Infections

There are three recognized immunologic strains of poliomyelitis viruses, Types I, II, and m which, until the widespread use of Salk and Sabin vaccines, produced world-wide epidemic of serious and crippling disease. Type I is the strain most frequently implicated in paralytic cases; however, all three types may cause infection. Depending on a number of varying factors primarily related to immunity and the localization of the virus activity, poliomyelitis infection may produce various clinical entities: (a) healthy carrier; ( b) minor illness; ( c) non-paralytic disease (aseptic meningitis); (d) paralytic disease: (i) bulbar, ( ii) spinal-intercostal, diaphragm, upper and lower limbs; ( e) polioencephalitis including cerebellar involvement with ataxia. TRANSMISSION OF DISEASE. The polio virus is most frequently spread by oral droplet infection through close

110 Principal Infectious Diseases of Childhood

contact with an infected person, e.g. playmate or household contact. The virus is present in the oropharynx during the incubation period and approximately one week after the onset of illness. Spread by fecal contamination is also a strong possibility, especially among the younger age group ( diaper stage), as the virus may remain in the fecal excretions of infected children up to 2 ½ to 3 months. PATHOGENESIS. It is believed, with good experimental support, that the virus first gains access to the body through the oral route, multiplies in the oropharynx from whence it enters the blood stream which is the principal avenue by which virus reaches the central nervous system. Following the widespread use of poliomyelitis vaccine in the U.S. and Canada (Sabin and Salk types), the incidence of paralytic poliomyelitis, and in fact, recognizable poliomyelitis infection, has been dramatically reduced. In communities where immunization is carried out in a conscientious manner with booster injections maintained, clinical poliomyelitis is now a rare entity. It is therefore reasonable in this book to present only a brief outline of the various clinical manifestation of this disease which should now be mainly of only historical significance. CLINICAL FORMS OF POLIOMYELITIS INFECTION

(a) Healthy Carrier. Persons immunized by Salk vaccine while immune to paralytic disease may at times if exposed to wild virus temporarily harbour virus in the oropharynx and gastrio-intestinal tract thus acting as healthy carriers and a source of infection for non-immunized members of the community. (b) Minor Illness. During epidemics of poliomyelitis, many individuals have suffered from vague flu-like illnesses

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with headache, sore throat, abdominal pain, nausea and vomiting, and low-grade fever. The illness is self-limited and subsides in a few days. Some of these patients have been found to harbour polio virus in the oropharynx and GI tract. It is believed that this so-called "minor illness" syndrome may be caused by polio infection in a partially immunized individual in whom the virus fails to invade the central nervous system. ( c) Aseptic Meningitis Syndrome. In some cases, the minor illness picture is more severe and complicated by the presence of a stiff neck and back with muscular aches and pains. A lumbar puncture reveals clear to ground glass CSF with a pleocytosis of 20-500 cells, mostly monocytes. These patients do not progress to any degree of muscle paralysis or paresis and the disease subsides in seven to fourteen days with no sequelae. A number of investigations into the aetiology of aseptic meningitis have incriminated one of the immunologic types of polio virus in this form of illness. ( d) Paralytic Poliomyelitis. The manifestations of paralytic disease are superimposed on the clinical picture of onset as outlined under the heading above of non-paralytic disease, namely, fever, headache, nausea, vomiting, stiff neck, general malaise, and, in a certain percentage of cases, less frequently may be sore throat, abdominal pain, muscular aches, pains and spasm. The poliomyelitis virus may attack cells in any part of the central nervous system causing temporary or permanent impairment of all functions. Depending on the area of the nervous system involved, the clinical divisions of paralytic disease have been classified under the following headings of which there may be considerable overlapping in the individual patient. ( i) Bu/bar Polio. The most lethal form of poliomyelitis

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results when the virus infects the bulbar region of the central nervous system where the cardiac and respiratory centres and the cranial nerve nuclei are located. From this type of central nervous system involvement, disorders of respiration and cardiac function may be produced resulting in death early in the disease. With involvement of the upper cranial nerve nuclei I-VIII, weakness of the oculomotor and facial muscles can produce strabismis and asymmetry of the facial musculature. When the lower cranial nerve nuclei are involved IX-XII, weakness in the muscles of the tongue, soft palate, pharynx, larynx and oesophagus produce varying degrees of impairment in swallowing and phonating. Secretions accumulate in the oropharynx because of the inability to swallow and interfere with the breathing mechanism and may cause laryngeal spasm and aspiration pneumonia, serious complications of this form of poliomyelitis. (ii) Spinal Paralytic Polio. When the virus attacks the anterior horn cells of the spinal cord, varying degrees of paresis and paralysis of the musculature of the trunk and extremities may be produced. With the involvement of the cervival and thoracic region of the cord, weakness of the diaphragm and intercostal muscles results in respiratory embarrassment. Involvement of other regions of the spinal cord produce weakness in the various muscle groups of the trunk and extremities which may be temporary or permanent. (e) Polioencephalitis. A small percentage of patients with polio infection present with sudden onset of fever, vomiting, severe headache, ataxia and nystagmus and rapidly lapse into varying degrees of lethargy to coma. Sometimes this form of disease presents with a convulsion which is an unusual manifestation of poliomyelitis.

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This form of poliomyelitis is believed to be caused by invasion of the cerebral cortex by the polio virus although some investigations account for this clinical picture upon the basis of hypoxia resulting from involvement of the respiratory mechanism. li there is no other involvement apparent, these patients make a dramatic recovery in a few days with no sequelae. DIAGNOSIS. In non-paralytic forms of polio infection, the only conclusive means of accurate diagnosis is the isolation of the virus from the patient and the finding of an elevated antibody titre to the specific polio strain on examination of acute and convalescent sera. In paralytic polio, the diagnosis can be made with reasonable assurance on the clinical picture; however, other causes of paralytic or pseudoparalytic disease must be considered such as diphtheria, peripheral neuritis, Guillain-Barrie syndrome, scurvy, hysteria and lead encephalopathy. PREVENTION. Salk vaccine: two subcutaneous injections one month apart followed by a third injection six to seven months later ( now incorporated in quadruple vaccine given at three, four, five months with booster at twelve to sixteen months and every two years thereafter). Sabin oral vaccine: feeding of vaccine at three, four, five months with booster feeding at sixteen months, using trivalent live attenuated vaccine. Treatment and Management of Polio NON-PARALYTIC. These forms of infection treated by bed rest, fluids, aspiration until clinical recovery five to ten days. PARALYTIC FORM. Bed rest, fluids oral or intravenous aspiration, position of comfort. Hot packing and splinting may be helpful in relieving pain and preventing contractions.

114 Principal Infectious Diseases of Childhood SPECIAL SITUATIONS: (a) bulbar involvement; ( b) respiratory and cardiac centre involvement. Supportive therapy to maintain clear air way and improve cardiac and respiratory function. Tracheotomy with mechanical aids to respiration using positive pressure machine (Bennet Bird) or tank respirator may be life-saving measures. LOWER CRANIAL NERVE NUCLEI INVOLVEMENT. Bed rest in head low position with suction as necessary to remove secretions from oropharynx, maintaining clear air way. If this does not handle secretions adequately, tracheotomy should be done and in addition, mechanical aids for respiration may be required. To prevent atelectasis and pneumonia, it is imperative to maintain the tracheo-bronchial toilet in an adequate state. DIAPHRAGM AND INTERCOSTAL MUSCULAR WEAKNESS. If the patient is unable to adequately ventilate himself as evidenced by clinical appraisal, blood pH, CO2 and 02 determination, then mechanical aids to respiration should be employed in the form of Tank Respirator, Rocking Bed, chest cuirass or positive pressure respirator until such time as recovery of respiratory function has occurred. WEAKNESS OF THE MUSCLES OF THE TRUNK AND EXTREMITIES. The muscles should be provided with rest,

warmth, and comfortable positioning during the early stages of the disease while pain and spasm are prominent features. As the patient's temperature returns to normal and he is able to comfortably tolerate physiotherapy, passive then active movement of the joints and muscles should be commenced to avoid contractures and deformities. POLIOENCEPHALITIS. Bed rest, maintenance of pH, fluid and electrolyte balance by intravenous therapy and adequate ventilation are the main supportive measures necessary to

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11S

tide these patients through the acute stage of this form of polio infection. (2) Coxsackie Virus Infection While studying outbreaks of poliomyelitis-like illnesses in New York State in 1947, Dolldorf & Sickles first discovered a new field of human pathogenic viruses detectable by the inoculation of newborn mice with material collected from patients suffering from febrile illnesses. These were named the Coxsackie group of viruses of which over 30 strains have been recognized to date. They have been divided into 2 main groups, A and B, by histologic examination of the infected laboratory animal. TRANSMISSION. These viruses are probably spread by the oral droplet route from direct contact with infected persons or carriers or by indirect contact by the fecal-oral route. COXSACKIE GROUP A INFECTIONS (23 ANTIGENIC TYPES). These viruses are associated with four main forms of illness in man: (a) aseptic meningitis; (b) herpangina; (c) respiratory illness; (d) exanthemata. (a) Aseptic Meningitis due to Coxsackie A Virus. Many of the group A viruses, but mainly 7 and 9, are capable of producing the aseptic meningitis syndrome in man. Clinical Picture. There is a prodromal period of several days characterized by loss of appetite, malaise, nausea, abdominal pain or discomfort and fever. Then follows headache, vomiting with drowsiness, stiff neck and myalgic pains. The course may be bi-phasic. The fever persists three to ten days and the whole illness in most cases runs a benign course. On occasions, however, there may be some muscle paralysis, but recovery is usually complete although fatigue and irritability particularly in adults may persist for months. Coxsackie A 7 virus has been found associated with a severe

116 Principal Infectious Diseases of Childhood

clinical paralytic poliomyelitis-like illness reported in Russia and Europe. C.S.F. There is an increase in cells up to 500 monocytes with an elevation in protein and normal sugar. ( b) Herpangina. Characterized by abrupt onset of fever, sore throat and, occasionally, vomiting. Examination of the throat reveals discrete characteristic lesions which start as greyish white papules or vesicles 1-2 mm. in diameter surrounded by a red areola. The lesions rapidly expand and ulcerate leaving the tonsils and pharyngeal wall dotted with small greyish craters surrounded by a hyperemic areola. These lesions may also occur on the buccal mucous membrane and vagina. The disease has a brief duration of 2-4 days. The most serious complication is febrile convulsions in children. Coxsackie A 16 virus has been associated with a syndrome called hand, foot, mouth disease in which ulcers occur on the tongue and vesicles appear on the hands and feet. (c) Respiratory Illness. Coxsackie A21 (Coe Virus) has been associated with upper respiratory illness and influenzalike outbreaks. Coxsackie A9 has been reported as the aetiologic agent in fatal secondary interstitial pneumonia. ( d) Exanthemata. Coxsackie A9 infection is reported as one of the newer exanthemata. This illness is characterized by the appearance of papulovesicular lesions starting on the head and trunk and resembling the vesicles of chicken-pox. The lesions are centrally distributed, quite superficial, and do not crust or scar and resolve in a few days. Coxsackie A16 has been called vesicular stomatitis with exanthem or hand, foot and mouth disease. In this disease, the characteristic vesicular lesions first appear on the extremities and spread centrally. In addition, there are lesions

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similar to those found in herpangina on the buccal mucous membrane, palate and oropharynx.

COXSACKIE VIRUSES GROUP B ( 6 ANTIGENIC TYPES).

Produce four main types of illness in man: (a) aseptic meningitis; (b) pleurodynia (Bornholm Disease); (c) myocarditis; (d) exanthemata (BS) . (a) Aseptic Meningitis. All six types of Coxsackie B virus have been isolated from the C.S.F. of patients with aseptic meningitis. Clinically, the illness is indistinguishable from that produced by Coxsackie A virus, ECHO and non-paralytic polio aseptic meningitis. (b) Pleurodynia (Bornholm Disease). The symptoms of this condition come on abruptly after a few hours of indisposition. Characteristically, in association with fever, severe chest pain occurs unilaterally or substemally which is exaggerated by movement or deep breathing. It may continue from a few days up to two weeks. Abdominal pain is somewhat less frequent and may be misdiagnosed as acute appendicitis. Pain may be related to a shoulder or the upper extremities. A pleural rub may be heard and in some cases, a pleural effusion occurs. The disease is self-limited and gradually the symptoms completely disappear over a five- to ten-day period. The illness may be associated with an aseptic meningitis. (c) Myocarditis. The role of Coxsackie virus infection producing acute myocarditis was first discovered in newborn infants of infected mothers in Johannesburg, South Africa. This is assumed to be an intra-uterine or neonatal infection from the mother. Myocarditis produced by Coxsackie B infection has subsequently been observed in older children but the disease is most frequently encountered and is most lethal in newborns.

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Clinically, the infants present with a sudden onset of circulatory collapse, rapidly enlarging liver, cyanosis and a rapid, weak pulse. A high case fatality rate is present with this type of infection. An encephalitis in newborns may be associated with the myocarditis. Virus has been isolated from the heart and brain in fatal cases. ( d) Exanthemata. Coxsackie B5 virus has been associated with infections in children and adults resembling the Roseola syndrome or exanthem subitum. After a febrile period of a few days, the temperature subsides at which time a fine maculo papular eruption appears, centrally distributed. This illness is of short duration and occurs predominantly in children under one year of age. (3) Echo Virus Infections

A group of viruses have been isolated from the stools of patients which have produced cytopathogenic changes in tissue culture preparations but which are not neutralized by antisera to the three of polio viruses and are not pathogenic for suckling mice, consequently not qualifying for inclusion in the Coxsackie Group. These viruses of which there are now over thirty strains recognized have been placed in a group known as the Enteric Cytopathogenic Human Orphan viruses, hence the name ECHO. The ECHO virus infections are probably spread by direct contact with patients or carriers via the respiratory secretions or fecal-oral route. ECHO viruses are responsible for a wide variety of clinical syndromes with a great deal of overlapping but have been primarily associated with 4 main types of illness in man: (a) aseptic meningitis; (b) exanthemata, ECHO 9

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pandemic; (c) Diarrheal disease; (d) Respiratory tract infection. (a) Aseptic Meningitis. Many of the ECHO virus serotypes have been isolated from the C.S.F. and feces of patients with aseptic meningitis. Types 4, 6 and 9 have been most frequently reported. The peak incidence for outbreak of aseptic meningitis due to ECHO virus is in the late summer and fall in this country. The clinical picture is similar to that of aseptic meningitis produced by many other viral agents. The main presenting symptoms are fever, headache, nausea, vomiting, photophobia, stiffness of the neck with muscular pain and lassitude. The illness is self-limited, running a course of five to seven days followed by an uneventful recovery in practically all cases. The diagnosis is established by the presence of the typical history, physical findings and the presence of lymphocytic response in the C.S.F. and is confirmed by the isolation of the specific ECHO virus in the Virus Laboratory. DIFFERENTIAL DIAGNOOIS. It is only of academic interest to differentiate outbreaks of ECHO virus aseptic meningitis from other viral agents capable of producing a similar syndrome such as polio, Coxsackie and mumps viruses. It is of much more importance to differentiate early tuberculous meningitis which may simulate these viral meningitides in the initial stages. ( b) Exanthemata. ECHO viruses have been associated with outbreaks of febrile exanthematons illness in many parts of Europe, U.S.A. and Canada. It is of considerable importance to differentiate these "newer" exanthemata from measles, rubella, scarlet fever and meningococcal infection, which are the better known

120 Principal Infectious Diseases of Childhood

and heretofore more readily recognized febrile illnesses of children associated with a rash. Most of these exanthemata due to ECHO virus infection have a short incubation period of two to seven days. The duration of illness is short, three to seven days, while secondary cases in the family contacts are frequent. ECHO 9 infection. Cases first described in Europe but now pandemic. The rash is characteristically maculo-papular but may be petechial and resemble meningococcaemia. The rash is frequently found on the palms and soles. An exanthem of greyish spots on the buccal mucous membrane have been described in some cases. Frequently, there is an associated aseptic meningitis. ECHO 16 INFECTION. This illness was first reported in 1951 and described under the name of Boston Exanthem. Characteristically, a maculo-papular rash appears centrally distributed after two or three days of febrile illness. As in Roseola, the rash may appear as the fever subsides and is found on the face, neck, trunk, extremities and frequently the palms and soles. A vesicular exanthem occurred in the Boston series. The illness is of short duration, three to five days, and subsides with no sequelae. Many other ECHO virus probably produce rashes and only await further study and identification. ( c) Diarrheal Disease. In diarrheal disease of infants and children, there has been a high incidence of virus isolation from the stools in some centres. Polio, Coxsackie, ECHO and adenoviruses have been reported and have been suspect as the aetiological agent in outbreaks of gastroenteritis. The fact that some viruses have been isolated from the stool of healthy children in the community would indicate that some have become carriers or else the virus may not be the agent responsible for the symptomatology.

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ECHO virus 18 has been described as the cause of an outbreak of gastroenteritis in a premature nursery and other members of the ECHO group may undoubtedly be responsible for symptoms of gastro-intestinal infections. ( d) Respiratory Tract Infection. A number of strains of ECHO viruses have been isolated from patients presenting with acute pharyngitis (ECHO 4, 6, 9, 16, 20) and have been incriminated as the causative agent for the clinical picture in these illnesses. Treatment. Primarily symptomatic as no anti-viral agent has been shown to be effective to date. Adenovirus Infections in Children

The adenoviruses cause catarrhal inflammation of the mucous membranes of the eye, gastro intestinal and respiratory tracts of man. There are now 31 distinct antigenic types identified which are responsible for about 5 per cent of all respiratory infections in children. Types 3, 4, 7, 8 are most frequently identified with respiratory and eye infections. The original members of the group were recovered from adenoid tissue and consequently were called "adenoid degenerating agent" or A.D. virus. Other writers gave names such as respiratory illness (R.I.) or acute respiratory disease virus (A.R.D.) . The name adenoidal-pharyngeal conjunctiva! virus (A.P.C.) was originally suggested to cover the entire group but this name has been replaced by the term adenovirus. These agents share a common complement fixing antigen but can be differentiated by virus neutralization tests on acute and convalescent sera. In the laboratory these viruses may be demonstrated by inoculation of tissue cultures of human epithelial cells, usually Hela cells. TRANSMISSION. Principally by the respiratory tract but

122 Principal Infectious Diseases of Childhood

fecal-oral route is also possible as virus is excreted in the stool in many cases. INCUBATION PERIOD is relatively short, three to seven days. Clinical Syndromes Caused by Adenovirus Infection Illnesses produced by these viruses in children may vary from a mild febrile illness to severe lower respiratory infections with a fatal pneumonia. Predominantly, however, the adenoviruses produce the following clinical states: (1) Acute Febrile Pharyngitis. Types 1, 2, 3, and 5 adenovirus are responsible for this entity with type 3 infection the most common. Children present with fever, headache and sore throat. Small patches of yellow-greyish exudate may be seen on the tonsils and pharynx. Respiratory symptoms of cough and nasal congestion may occur as well as conjunctivitis. The usual duration of the illness is three to five days. Spontaneous recovery occurs with symptomatic and supportive therapy alone. Outbreaks of this disease among children have been reported from a number of centres in the U.S. and Canada. In 1955 an outbreak occurred in Toronto in which conjunctivitis was a prominent feature. Spread of the illness was traced to contact through swimming pools. Bacterial infections of the nasopharynx should be differentiated from this entity as well as other viral diseases such as herpangina and infectious mononucleosis. The diagnosis may only be confirmed by specific virus laboratory tests. (2) Acute Respiratory Disease. Type 4 and 7 adenoviruses most frequently produce this syndrome characterized by nasal congestion, hoarseness, cough, chest pain and general constitutional signs of fever and malaise. This is

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a disease of overcrowding and occurs most frequently among military recruits. Severe atypical pneumonia in infants has been described in which adenovirus types 1, 3, and 7 have been isolated. These patients failed to develop cold agglutinins and Strep. MG agglutinins. There is a high fatality rate in infants with this disease. Adenoviruses however cause only a small proportion of the atypical pneumonias seen in children. ( 3) Conjunctivitis ( See section on Ocular Infections). A number of the adenoviruses have been found associated with conjunctivitis, including 3, 6, 7, 8, 9. Type 8 has been established as a major cause of epidemic conjunctivitis. Many cases of conjunctivitis are caused by other agents including viruses, bacteria, and chemicals. VIRUSES PRODUCING INFECTION OF 'IHE REsPIRATORY 'TRACT AND AssOCIATED SYNDROMES* VIRUS

NO.OF STRAINS

Myxoviruses Influenza A.B.C.

3

Para influenza

4

Respiratory Syncitial

1

SIGNIFICANCE

SYNDROMES PRODUCED

2½ % respiratory Nasopharyngitis tract illness 7-16% of total Types 1, 2, 3 account respiratory for 30 % croup infections in paediatric age group Single most 26--40 % Bronchiolitis (1-6 months age) important virus in infants with Pneumonia respiratory Croup infection Bronchitis 9.5 % of all U.R.I. pediatric resp. tract illness

*Chart after R. M. Chanock, R. H. Parrott.

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Principal Infectious Diseases of Childhood

VIRUS

NO. OF STRAINS

Adenoviruses

31

Picornaviruses Enterovirus Coxsackie A

23

Coxsackie B

6

Echo

29

Mycop/asma M Pneumonia (Eton) P.P.L.O.

Rhinoviruses (Common Cold Virus)

60+

SIGNIFICANCE

SYNDROMES PRODUCED

Pharyngitis 8-9 % of total respiratory Conjunctivitis illness in Atypical pneumonia children In military recruits up to 50%

Less than 1 % resp. tract infection in childhood

21 (COE) U.R.I. influenza-like illness 2-4-5-6-8-10 Herpangina, tonsillo pharyngitis. A 16-Hand, foot, mouth 1-6 Febrile respiratory disease, pleurodynia Pharyngitis

1-10% of lower resp. tract illness in children

Major cause atypical pneumonia (Susceptible to tetracycline)

4-5% of respiratory illness in children

U.R.I. Croup, bronchitis, bronchiopneumonia

Red Viruses (Formerly Echo 9) 40---50% respiratory illness due to viruses and mycoplasmas

61 Respiratory Infections

of the respiratory passages caused by viruses have been described above. There are, however, many upper and lower respiratory infections caused by bacterial species responsible for other infections in man, namely, the meningococcus, pneumococcus, streptococcus, staphylococcus and the influenza bacillus, both the respiratory group of influenza bacteria and influenzae type "B" of the meningeal strain. The streptococcus is most often the cause of many upper respiratory infections. These infections are: acute nasopharyngitis, acute otitis media and mastoiditis, acute sinusitis, peritonsillar adenitis and abscess, retropharyngeal adenitis and abscess, acute laryngitis, acute laryngo-tracheitis, acute bronchitis, and pneumonia. Diagnosis is based largely on the anatomical position rather than on the aetiological cause. Any of these respiratory infections may be a complication or a part of a number of well-known diseases (such as acute laryngitis in diphtheria, measles and scarlet fever) . One might say here that respiratory infections of one type or another comprise the largest part of the practice of medicine with children. DISEASES

Acute Nasopharyngitis and Tonsillitis As with acute laryngitis, these may be the initial conditions in a number of diseases and it is well known that, in

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addition to a virus aetiology for these conditions, there are many other agents which cause similar diseases. In our research, a virulent meningococcus has been isolated from a number of patients suffering from meningococcal meningitis with a nasopharyngitis. It would be a wide stretch of the imagination to suggest that the upper respiratory infection of such an individual was caused by a virus. Thus, many of the common bacterial species are probably responsible for respiratory infections both of the upper and of the lower respiratory tract. The signs and symptoms of acute nasopharyngitis are commonly known and are adequately described in the section on viruses. Treatment will be dealt with later under the general treatment of respiratory disease. Acute Otitis Media and Mastoiditis

Inflammation of the ear drum usually occurs secondary to some upper respiratory infection, or secondary to some general infection such as measles or scarlet fever. It is usually an extension of the nasopharyngeal of throat infection. CLINICAL ASPECTS. The physician's attention is usually drawn to this condition when there is a history of excessive crying and of pulling of the ear lobes by the infant. In the young child crying because of pain in the ear is a very common complaint. There may be fever and an accompanying inflammation of the nose and throat. On the other hand, infants and children may have very few symptoms and may not have a fever. Hence, with any upset in an infant or small child the physician should examine the ear drum. The normal ear drum shows the handle of the malleus and a pearly-grey, shiny drum membrane with a light reflex. The first stage of an inflamed drum is redness with the landmarks intact. The second stage is redness and oedema

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of the drum membrane and the beginning of loss of normal landmarks. The third stage is a bulging, swollen, reddened drum which often appears to fill the canal. The fourth stage is a swollen, bulging ear drum with inflammation and a yellowish-white area in one part of the drum similar to the "pointing of pus" in an abscess. TREATMENT. In the first three stages of an inflamed ear drum soothing ear-drops warmed to body temperature may be placed by the mother in the canal by pulling the lobe of the ear upwards and backwards ( usually two to three drops every four hours is sufficient). In the fourth stage the drum should be incised and the pus drained out. In the first three stages, a course of 100,000 units of penicillin given orally every four hours or 400,000 to 800,000 units given intramuscularly once or twice daily may be administered. If the ear drum does not improve in appearance and its normal landmarks do not begin to return, it is best to discontinue the use of an antibiotic. Penicillin or other antibiotics have been known to mask an infection which smoulders away and ultimately involves the mastoid and the lateral sinus. A five- to seven-day trial with these drugs is indicated; after this, they are likely to do more harm than good. Mastoiditis results from an ear condition which does not subside. There may be a swollen, boggy drum membrane with a chronic purulent discharge. Usually a profuse discharge from the ear for over three weeks is evidence that the mastoid is involved. There may or may not be tenderness and swelling over the mastoid bone. An X-ray of the mastoid area will aid in the diagnosis. TREATMENT of the condition is obvious. The mastoid must be explored and all purulent material and destroyed bone tissue removed.

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Acute Sinusitis This is an inflammation of the maxillary, sphenoid, ethmoid and frontal sinuses. In its X-ray appearance an allergic condition of the nose may often simulate sinusitis of an inflammatory origin. Usually, however, the sinuses are involved as the result of an upper respiratory infection. Almost always sinusitis accompanies a nasopharyngitis, clearing up when the coryza clears. Sometimes, however, a sinus infection persists after the upper respiratory infection has partially subsided. CLINICAL ASPECTS are a persistent nasal discharge, a cough which is worse in the morning and at night when the patient lies down, a low-grade type of fever, a headache and a general, but mild constitutional upset. Sometimes pain over the maxillary sinuses is prominent. An X-ray of the sinuses will help to decide whether they are involved and, if so, to what extent. TREATMENT. In addition to the general treatment of upper and lower respiratory infections, discussed at the end of this chapter, local treatment of the area is indicated. Usually ½ to 1 per cent of ephedrine in normal saline solution is dropped into the nostril with the head placed low and turned to one side. Three to four drops of this solution are instilled in the nostril on the lower side. After one or two minutes, the nose may be gently blown. This treatment is repeated three times daily for one week. Steam inhalations are useful as are warm compresses over the front of the face. These may be applied frequently during the day. To relieve the pain ¼ to ½ grain of codeine phosphate may be given orally. Peritonsillar and Refropharyngeal Adenitis and Abscess These conditions are usually complications of a severe

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upper respiratory infection and may follow a sharp attack of nasopharyngitis and tonsillitis. In addition to signs of an upper respiratory disease and a severe sore throat with difficulty in swallowing, the patient has difficulty in breathing, inhaling and exhaling through the mouth in a "gurgling fashion" due to extreme swelling in the throat. If the condition is a peritonsillar abscess or adenitis, one tonsil is red, swollen, enlarged, and bulging across the mid-line of the throat. The head of the patient, especially with infants, is retracted and there is always an associated tenderness and swelling of the neighbouring anterior cervical glands. The same signs and symptoms are present with retropharyngeal inflammation. Although the tonsil is not involved, the retropharyngeal glands are swollen and are seen passing from the back of the throat across the mid-line. Digital examination with a mouth gag in place confirms the presence of retropharyngeal adenitis or abscess. If there is a peritonsillar or retropharyngeal abscess, it should be opened, the patient turned face downwards immediately after the incision and the area thoroughly aspirated by means of suction. The patient is placed in bed with his head low and his face down. Acute Laryngitis, Laryngo-Tracheitis and Acute Epiglottitis In recent years, croup, laryngitis and acute laryngotracheitis have been very common conditions in paediatric practice and have caused more concern and needed more active and urgent treatment than have many of the other respiratory infections. Although these diseases often result from upper respiratory infection, they are often a symptom or complication of some other disease. These diseases may be caused by (a) bacterial infections such as streptococcus, pneumococcus, staphylococcus or influenza bacillus type B; ( b)

130 Principal Infectious Diseases of Childhood

general infections such as diphtheria, scarlet fever and measles; and ( c) infections which, it is claimed, may be of virus aetiology. In spite of some evidence regarding the virus nature of these conditions, no specific virus has been isolated as their cause. It is of some academic and possibly some therapeutic value to obtain material for culture from these infections, including, if this is possible without disturbing the patient too much, a laryngeal culture. On the other hand, the danger of asphyxiation is so great for young children that early diagnosis and active treatment should be commenced at the expense of determining the cause of the disease. CLINICAL ASPECTS. The child has usually developed an upper respiratory infection prior to the onset of laryngeal signs and symptoms. The infant and young child are most susceptible because of the small size of the larynx in these early age groups. The first sign is often a croupy cough with inspiratory distress when disturbed and crying. The child has some suprastemal and costal border indrawing on inspiration. The more the trachea and bronchi are involved, the more continuously is the patient distressed, progressing to constant inspiratory stridor, indrawing of the costal borders and duskiness of skin with ultimate cyanosis. These symptoms call for early, active treatment. TREATMENT. ( 1) If the child is suffering from mild croup or laryngitis, steam inhalation, adequate antibiotic therapy and bed-rest with sedatives result in a very rapid improvement and cure in the majority of instances. (2) If, however, the symptoms and signs persist and become more constant and more marked within a few hours, then the patient should be admitted to hospital and treated with moist inhalations, oxygen, and sedatives ( nembutal or seconal) ½ grain to

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1½ grains given rectally. Oxygen and cool moist inhalation are best given by means of a croupette. ( 3) If there is no improvement and the symptoms and signs become worse in the next half to one hour, a tracheotomy should be performed. Laryngoscopic and bronchoscopic suction should be done under general anaesthesia prior to tracheotomy. The child is returned to bed and the croupette is used, leaving the tracheotomy tube in situ. ( 4) It is best to give these children continuous nursing, especially during the immediate pre-operative and post-operative period. It is so necessary to suction the patient and keep the tracheotomy tube clear of mucus and inflammatory material that a nurse in attendance all the time, post-operatively, is imperative. ( 5) Large doses of streptomycin and penicillin or other antibiotics such as chloromycetin should be given every four hours in the acute stages of the disease and twice daily for several days after the acute phase. Later, as he improves, the child is allowed out of the croupette and the tube is finally removed, allowing the area to heal, while a little sterile protective dressing remains over the tracheotomy incision. Acute Bronchitis

This usually accompanies or occurs just after a severe nasopharyngitis. It is due to an inflammation of the bronchi and bronchioles from a number of bacterial species already mentioned. CLINICAL ASPECTS. The child with bronchitis is usually not as ill as the child with pneumonia. Bronchitis may be only the result of infection and this type is seen in most children at one time or another. On the other hand, in children with asthma or other allergic phenomena, bronchitis

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may be accompanied by "wheezing" and the typical expiratory and inspiratory rhonchi on auscultation. In such children the cough and bronchitis persist for a much longer period of time, usually weeks or months. The usual type of bronchitis shows some mild constitutional signs such as coryza, cough, general ill health, mucopurulent sputum and a low-grade fever, 99°F.-101 °F. In addition to these findings there are local signs. There may be an increase in the respiratory rate. There is little, if any, change from normal on palpation or percussion. On auscultation, rhonchi and coarse moist rales are heard posteriorly on both sides and especially at the base of the lungs. The patient with bronchitis usually responds to treatment in two weeks' time. If, however, the sinus is involved or bronchiectasis has begun, the cough and sputum will persist for weeks and months. If the cough and sputum continue, it is necessary to rule out sinusitis, asthma, an allergic condition or bronchiectasis. TREATMENT. See general treatment of respiratory infections under pneumonia. Pneumonia

This is an inflammation of all parts of the lung, but the aveoli are more involved than with bronchitis. Pneumonia is usually secondary to an infection farther up in the respiratory passages and, in this respect, is an extension of the infection. In the past, various types of pneumococci have caused pneumonia more frequently than any other microorganisms. Types I and II were the common types seen in older children and types XIV and XIX in infants, although the incidence of the various types of pneumococci likely varied considerably at different times and in different places. Next in importance was the streptococcus, staphylococcus and influenza bacillus. In addition, in many patients a

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mixture of bacterial species was found, so that it was difficult to be certain of the true cause of the pneumonia. Without serological evidence, the cause is not absolutely certain even if a definite type of bacterial species is found in the respiratory passages during the disease. Recently, the staphylococcus has been found in the respiratory passages of patients with pneumonia. A type of pneumonia of longer duration than usual, the so-called primary atypical pneumonia, is supposedly of virus origin ( see the chapter on virus infections) . Pneumonia may be primary as the result of causes already mentioned or secondary or generalized infections or some infectious diseases. In these secondary types of pneumonia, the cause is likely the same as the aetiological agents already mentioned and pneumonia in generalized infections is probably the result of the so-called secondary invading bacterial or virus species. CLINICAL ASPECTS. Pneumonia of the primary atypical variety and other types may be present in the infant and child with constitutional signs and a low-grade fever. This clinical type is unusual and more often the child is quite ill, flushed and feverish, with a temperature of 103°F.-104°F. and rapid respiration, degrees of cyanosis, a cough, and a disposition to stay in bed. The history reveals that the disease has started after an upper respiratory infection which did not clear up. On physical examination a cough, increased respiratory rate with flaring of the nares, expiratory grunt and a duskiness of colour around the nose and mouth are found. The costal margins of the chest may be moving rapidly with lower costal indrawing and there may be limitation of the normal lung excursion on one or both sides of the chest. There may be palpable rhonchi. On percussion there may be little

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change on the two sides. Wherever there is more of the pneumonic process than usual, there may be dullness on percussion and if fluid is present in the pleural cavity, there is a flat note on percussion with marked limitation in movement on that side of the chest. On auscultation, fine moist rales are heard posteriorly, especially at the bases, and sometimes may be heard generally throughout the chest. As a result of sulphonamide and antibiotic therapy the course of the disease is now much shorter. The fever lasts from two to five days and then gradually falls, the chest gradually clears of moisture and the patient becomes more active and less ill from a constitutional standpoint. Complications now are rare, but empyema and bronchiectasis are still seen when the infection fails to respond to treatment. Such complications should always be ruled out before it is assumed that the patient is cured. X-rays of the chest early in the disease and later, when complications are suspected, may be a valuable aid in diagnosis. TREATMENT OF RESPIRATORY INFECTIONS

In conclusion, treatment that is commonly used in all these respiratory infections will be outlined. In the sections in which each type of respiratory infection has been discussed will be found descriptions of special methods employed with certain types of respiratory disease. PREVENTION. Although there is no known specific prophylactic for the common cold or other respiratory diseases, it is believed that certain measures taken in the early stages of upper respiratory disease may prevent more serious types from developing. In an infant or child who is ill with an

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upper respiratory disease, the early administration of sulphonamides, penicillin or other antibiotics may help to prevent the more serious types of respiratory disease from occurring. TREATMENT. General treatment for respiratory infections consists of the following: ( 1) Rest. The child should be kept in bed with any of these respiratory diseases. (2) Diet. Fluids such as sugar solutions, clear fluids, fruit juices and broth should be given in the acute phase of the disease followed by a soft diet and later by a full diet as the child returns to normal. ( 3) Drugs. Sulphonamides such as sulphadiazine and sulphadine should be given for two to five days in the acute stage of the disease, 1 to 2 grains per lb. per day administered in divided doses every four hours. Penicillin in doses of 100,000 to 200,000 units may be given intramuscularly every four hours; ¼ to ½ gram of streptomycin every four to six hours may be used with penicillin or separately if penicillin has not been found beneficial, or if the aetiological agent resists its action. Newer antibiotics such as erythromycin, chloromycetin, and tetracycline 50 mg. to 250 mg. every four or six hours, may be used in certain patients with pneumonia. ( 4) Nursing. Children with pneumonia are best treated by a special nurse since the constant administration of fluids, clearing the respiratory passages of infectious material and the administration of drugs as well as other measures are very important in the acute part of the illness. (5) General measures. Mustard plasters for five-minute application ( 1 part mustard to 5 parts flour) may be used every four hours. Nose drops and cough medicines should

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be used only if necessary. Cough medicines are not indicated in infants, but a sedative cough medicine may be used in older children. Sedatives such as phenobarbital, nembutal, or seconal may be used for restlessness and lack of sleep. Immunization Schedules

The immunization schedule recommended for the protection of children against diphtheria, pertussis ( whooping cough), tetanus, poliomyelitis, smallpox and measles is shown in the accompanying tables. It should be remembered that, with new knowledge and the advent of new immunizing materials and chemotherapeutic agents, the recommendations for immunizing programmes are in a constant state of flux, changing literally every few months. Certain local and general reactions may occur in children receiving their immunizing agents, and it is wise to advise parents of the possibility of their child having pain, redness and swelling at the site of the injection and varying degree of febrile response. It is never advisable to give a routine immunizing injection to an infant or child who has a concurrent illness. Vaccination against smallpox is strongly contra indicated in any child with eczema or other acute skin disease, nor should a child with eczema be in contact with a recently vaccinated person because of the possibility of developing eczema vaccinatum.

Respiratory Infections (Non-Virus)

TABLE 1 IMMUNIZATION SCHEDULE. RE.COMMENDED PAEDIATRIC PRACTICE

FOR

Infants Age

(mo.)

Material

2-3

D.P.T.&P.• D.P.T.&P. D.P.T.&P. Vaccinia Live measles

3-4

4-S

6-12 9-10

vaccine with Gamma Globulin

or further attenuated live

Dose (cc.)

1.0 1.0 1.0

0.1

o.s

0.01/lb

measles vaccine ( Schwartz strain) without Gamma Globulin

Pre-School Age

(yr.)

Material

11

D .P.T. & P. D.P.T. & P. D.P.T. & P. Vaccinia

3

s s

Dose (cc.)

1.0 1.0 1.0 0.1

School Age Age (yr.) 8

11 11

14

Material

Dose (cc.)

D.T.P. (adult) t D.T.P. (adult) Vaccinia D.T.P. (adult)

1.0 1.0 0.1 1.0

*D.P.T. & P.: Diphtheria Toxoid, Pertussis vaccine, Tetanus Toxoid, Polio Vaccine tD.T.P.: Diphtheria Toxoid, Tetanus Toxoid, Polio Vaccine

137

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TABLE 2 RECOMMENDATIONS FOR USE OF LIVE ORAL POLIOMYELITIS VACCINE, 'fRivALENT SABIN ATTENUATED (WHEN AVAILABLE)

Age (months) 4 6 8

18

Vaccine Feeding first second third fourth