Blue Book

Guidelines for the Control of Infectious Diseases

THE BLUE BOOK

Acknowledgements Editorial Committee Dr John Carnie Dr Kath Taylor Dr Rosemary Lester Dr Sally Ng Ms Sheila Beaton Ms Pam Norris Sr Anne Murphy Dr Graham Rouch The editorial committee is grateful to: • the staff of the Microbiological Diagnostic Unit, especially: Dr G. Hogg, Director Dr J. Forsyth Dr D. Lightfoot Dr M. Veitch • other contributors: Dr Andrew Fuller, Alfred Hospital, Melbourne Dr Graeme Brown, Royal Melbourne Hospital Dr Noel Bennett, Department of Human Services Standing Committee on Infection Control Dr John Harrison, Department of Human Services Ms Gabrielle Keeshan. Department of Human Services. for their assistance to the preparation of these guidelines. This manual has been prepared to provide guidelines for Human Services and local government staff, general practitioners and infection control officers involved in preventing and controlling infectious diseases. Published by the Infectious Diseases Unit, Public Health Division, Victorian Government of Human Services. Design and production by Human Services Promotions Unit. This publication is available at Internet address: http://hna.ffh.vic.gov.au/phb/ (040AP96) ii

Disclaimer

These guidelines have been prepared following consultation with experts in the field of infectious diseases and are based on information available at the time of their preparation. Practitioners should have regard to any information on these matters which may become available subsequent to the preparation of these guidelines. Neither the Department of Human Services, Victoria, nor any person associated with the preparation of these guidelines accept any contractual, tortious or other liability whatsoever in respect of their contents or any consequences arising from their use. While all advice and recommendations are made in good faith, neither the Department of Human Services, Victoria, nor any other person associated with the preparation of these guidelines accepts legal liability or responsibility for such advice or recommendations.

iii

Contents

Introduction

1

Food - or Water-Borne Illness

53

Abbreviations Used

5

Giardiasis

59

7

Haemophilus influenzae Infections

61

Acquired Immunodeficiency Syndrome

Information Sheets

Acute Bacterial Conjunctivitis

64

11 Hand, Foot and Mouth Disease

67

Amoebiasis

13

Information Sheet

69

Anthrax

15

Hepatitis A

71

Arbovirus Infections

17

Hepatitis B

75

Hepatitis C

81

Ross River Virus Disease

17

Australian Arboencephalitis (AE)

19

Dengue

21

Kunjin

22

Hepatitis D

85

Botulism

23

Hepatitis E

87

Brucellosis

27

Herpes Simplex

89

Campylobacter Infection

29

Hydatid Disease

91

Chicken Pox/Herpes Zoster

31

Impetigo

93

Cholera

35

Influenza

95

Cryptococcal Infection

39

Infectious Mononucleosis

97

Cryptosporidiosis

41

Legionellosis

99

Cytomegalovirus (CMV) Infection 43

Leprosy

103

Diphtheria

45

Leptospirosis

105

Erythema Infectiosum

49

Listeriosis

109

Information Sheet

51

v

Malaria Information Sheet

Measles Meningococcal Infections Information Sheet

113

Rubella

173

Salmonellosis

177

Scabies

181

117

119 123

Information Sheets

127

Shigellosis Meningoencephalitis

129

Mumps

131

Mycobacterial Infections

133

Tuberculosis

133

Atypical (Non-Tuberculosis)

139

Pediculosis/Headlice Information Sheet

183

141

185

Streptococcal Disease Caused by Group A Beta-Haemolytic Streptococcus 187 Ta e n i a s i s

189

Te t a n u s

191

NH&MRC Recommendations

192

143

Pertussis

145

Plague

149

To x o p l a s m o s i s

193

Typhoid/Paratyphoid

195

Ty p h u s

199

Pneumonia due to Chlamydia pneumoniae

153

Verotoxin Producing E. coli

201

Poliomyelitis

155

Psittacosis

157

Viral Gastroenteritis Caused by Agents Other than Rotavirus

203

Q Fever

159

Viral Haemorrhagic Fevers

205

Yellow Fever

209

Vaccination Outlets

211

Information Sheet

162

Rabies

163

R ingw o rm/Tin ea

167

Information Sheet

Rotaviral Gastroenteritis vi

170

171

Ye r s i n i o s i s

215

Appendix 1: Telephone Numbers 217 Appendix 2: Glossary

219

Appendix 3: Outbreak Investigation

221

Appendix 4: Standard Precautions 223 Appendix 5: Procedure for Dealing with Spills of Blood and Body Fluids 225 Appendix 6: Management of Needlestick Injury and Exposure to Blood or Body Fluids 227 Appendix 7: Specimen Collection and Transport Guidelines 231 Appendix 8: Infections in Children’s Services Centres

237

Appendix 9: School Exclusion Table

239

vii

Introduction

Infectious diseases still occur frequently throughout the

A case of any of these diseases should be notified to

world and constant vigilance is required to prevent the

Human Services, Victoria, by telephone or facsimile upon

reappearance of diseases thought to have been con-

initial diagnosis (presumptive or confirmed) and written

quered. Changes in lifestyle have also led to the emer-

notification should follow within seven days. Notification

gence of new threats to public health from infections.

forms are available from the Department: Telephone (03) 9616 7777.

Health authorities depend on medical practitioners for information on the incidence of infectious diseases and

The telephone numbers for notification of diseases are:

notification is vital in efforts to prevent or control the

Infectious Diseases Unit (03) 9616 7777 or 1800 034 280.

spread of infection.

Fax: (03) 9616 8329 (Attention: Chief Health Officer). After hours, contact the duty medical officer.

The Health (Infectious Diseases) Regulations 1990 replaced the outdated legislative provisions relating to

Telephone the paging service on (03) 9625 5000 and give pager number 46870.

such diseases.

Group B Diseases Notifiable infectious diseases are to be found in schedule 2 of the Regulations and are divided into four groups on the basis of the method of notification and the information required.

Amoebiasis. Arbovirus infections (except for Australian Arboencephalitis and Yellow Fever). Brucellosis. Campylobacter infection.

Group A Diseases

Giardiasis.

Australian Arboencephalitis.

Hepatitis A.

Anthrax.

Hepatitis B.

Botulism.

Hepatitis C.

Cholera. Diphtheria. Food-borne and water-borne illness (two or more related cases). Legionellosis. Measles. Meningitis or epiglottitis due to Haemophilus influenzae. Meningococcal infection. Plague. Poliomyelitis. Primary amoebic meningo-encephalitis. Rabies. Typhoid and Paratyphoid fevers. Typhus. Viral haemorrhagic fevers. Yellow Fever.

Hepatitis non-A non-B. Hepatitis (viral, unspecified). Hydatid disease. Leprosy. Leptospirosis. Listeriosis. Malaria. Mumps. Pertussis. Psittacosis (Ornithosis). Q Fever. Rubella (including congenital Rubella). Salmonellosis. Shigellosis. Taeniasis (tape worm infections). Tetanus. Tuberculosis. Yersiniosis. 1

Note

For these, written notification only is sufficient, within seven days of confirmation of diagnosis.

Laboratory Notification Around Australia and overseas, it has been recognised that laboratory notification of infectious diseases should be an integral part of any disease surveillance system.

Group C Diseases Chancroid.

The Health (Infectious Diseases) Regulations 1990

Donovanosis.

require notification from laboratories under the

Gonorrhoea (all forms).

circumstanceslisted below.

Lymphogranuloma venereum. Other Chlamydial infections. Syphilis (all forms). Note

These sexually transmissible diseases should be notified using the same notification form but, to preclude identification of the patient, only the first two letters of the given

A. Food and Water Supplies Isolate the following pathogens from food for human consumption or from water supplies: • Campylobacter jejuni. • Listeria monocytogenes. • Salmonella species.

name and surname of the patient are required. Isolate the following pathogens from water supplies:

Not all chlamydial diseases are STDs.

• Campylobacter coli. • Campylobacter lari.

Group D Diseases Acquired lmmunodeficiency Syndrome.

• Vibrio cholerae. • Giardia cysts. • Cryptosporidium oocysts.

HIV was made notifiable in September 1996. Detection of any of the above organisms should be Note

notified in writing to Human Services within seven days,

Written notification is required within seven days of

stating the pathogen isolated, the source, the date of

confirmation of diagnosis.

isolation, and any batch identification (if appropriate).

A separate form is used for this purpose due to the need

B. Material of Human Origin

to have national uniformity in collection of data.

A laboratory test that indicates the probable presence of

To preclude identification of the patient, only the first two

a human pathogenic organism associated with an

letters of the given name and surname of the patient are

infectious disease listed in Groups A, B or C should be

required.

notified to Human Services.

Send all notifications to:

If the disease is in Group A, the notification should be

Freepost 547

made by telephone or other rapid transmission.

Infectious Diseases Unit Public Health Branch

If the disease is in Groups B or C, Human Services

GPO Box 4057

should be notified in writing within seven days.

Melbourne 3001 and mark them Confidential. 2

The notification from the laboratory should state the laboratory finding, the family name and given name of the patient (except for Group C diseases); the age, sex and postcode of the patient; and the name, address and telephone number of the doctor requesting the test. This manual has been published by the Infectious Diseases Unit, Public Health Division, Victorian Government Department of Human Services, Victoria, to assist all public health practitioners in the control and prevention of infectious diseases. Any comments and suggestions regarding the format of the manual, as well as on the information provided, are welcome and should be directed to: Dr John Carnie Manager Infectious Diseases Unit Public Health Branch Department of Human Services PO Box 4057 Melbourne 3001

3

Abbreviations Used

ADT

adult diphtheria tetanus vaccine

ALT

alanine aminotransferase

anti-HBc

hepatitis B core antibody

anti HBs

hepatitis B surface antibody

AST

aspartate aminotransferase

CDT

combined diphtheria tetanus vaccine

CF/CFT

complement fixation test

CNS

central nervous system

CSF

cerebro-spinal fluid

CT Scan

computerised tomography

DFA

direct fluorescent antibody

DTP

diphtheria tetanus pertussis vaccine

EBV

Epstein-Barr virus

EIA

enzyme immunoassay

ELISA

enzyme-linked immunosorbent assay

EM

electron microscopy

FA

direct fluorescent or immunofluorescent

HAI

haemagglutination inhibition test

HAV

hepatitis A virus

HBIG

hepatitis B immune globulin

HbsAg

hepatitis B surface antigen

HbeAg

hepatitis B e antigen

HBV

hepatitis B virus

HCV

hepatitis C virus

HDV

hepatitis D virus

Hib

Haemophilus influenzae type b

HIV

human immunodeficiency virus

IFA

indirect immunofluorescent antibody test

antibody test

IG

immune globulin

IHA

indirect haemagglutination

IM

intramuscular

IV

intravenous

MDU

Microbiological Diagnostic Unit

MIF

micro immunofluorescent test

MMR

measles-mumps-rubella vaccine

NH&MRC National Health and Medical Research Council PCR

polymerase chain reaction

VIDRL

Victorian Infectious Diseases Reference Laboratory

WHO

World Health Organisation 5

Acquired Immunodeficiency Syndrome

Victorian Statutory Re quirem en t

Public Health Significance and O c c u r re n c e

AIDS Group D notification.

Occurrence is worldwide.

HIV infection was made notifiable in September 1996. According to the World Health Organisation (WHO)

Infectious Agent

estimation, close to 6.8 million cases of AIDS and 22 million cases of HIV occurred by 1994.

Human Immunodeficiency virus (HIV), types 1 and 2 (retrovirus).

Of HIV infected persons, approximately 15–20 per cent will develop AIDS within five years, and about 50 per

Clinical Features AIDS is a severe, life-threatening disease that represents the late clinical stage of infection with HIV. Within several weeks after infection with HIV, many people will develop a self-limited mononucleosis-like

cent within 10 years. With modern antiviral therapy, these incubation periods have lengthened. By 1995, there were 1,234 cases of AIDS diagnosed in Victoria, and 926 notified deaths.

illness lasting for a week or two. In 1994, 217 new diagnoses of HIV were made, bringing Infected persons may then be free of clinical signs or

the total HIV infections in Victoria to 3372.

symptoms for months or years, before developing specific opportunistic infections and cancers and a range of other indicative diseases.

Method of Diagnosis Careful history and physical examination looking for risk

Major diseases that may be indicative of AIDS include:

factors and clinical manifestations of immunodeficiency.

• Pneumocystis carinii pneumonia. • Candidiasis.

Laboratory confirmation of diagnosis by:

• Kaposi sarcoma.

• Detecting HIV antibodies with ELISA test (confirmed by

• Herpes simplex infection. • Cryptococcosis. • Cryptosporidiosis.

Western blot analysis). • Diagnosing opportunistic infection or secondary cancer.

• Toxoplasmosis. • Cytomegalovirus infection. • Mycobacteriosis.

Reservoir

• Lymphoma.

Human.

• HIV encephalopathy. • HIV wasting disease.

7

Mode of Transmission HIV can be transmitted by: • Unprotected sexual intercourse with an infected

Presence of other sexually transmitted diseases, especially those causing genital ulceration, increases susceptibility for sexual transmission.

person. • Inoculation with infected blood, blood products and through transplantation of infected organs, bone graft,

Control of Case Standard fluid precautions apply to all patients.

tissue or semen. • From infected woman to the foetus during pregnancy or breastfeeding. Approximately 15 to 30 per cent of

Additional precautions apply for specific infections that occur in AIDS patients.

infants from HIV positive mothers are infected, but treatment during pregnancy can result in a marked reduction in infections.

Concurrent disinfection of equipment, contaminated with blood or body fluids.

• Needle-stick injuries or other exposure to blood and body fluids by health care or emergency workers. The rate of seroconversion following a needle stick injury involving HIV infected blood is said to be less than 0.5 per cent.

Patients and their sexual partners should not donate: • Blood. • Plasma. • Organs for transplantation. • Tissues.

Note

Social contact with HIV infected person carries no risk of transmission.

Incubation Period From infection to primary illness, three weeks to three

• Cells. • Semen for artificial insemination. • Breast milk for human breast banks. All HIV positive persons should be evaluated for the presence of tuberculosis.

months.

Tre a t m e n t The time from HIV infection to the diagnosis of AIDS ranges from about two months to 20 years or longer, with a median of 10 years.

Zidovudine (AZT), dideoxycytidine (DDC) and dideoxyinosine (DDI) are the current anti-retroviral drugs available in Australia specifically indicated for HIV infection.

Treatment lengthens the incubation period. Other treatment includes specific treatment or prophy-

Period of Communicability All antibody positive persons carry HIV.

laxis for the opportunistic infectious diseases that result from HIV infection.

Infectivity must be presumed to be lifelong. For further information, see Antibiotic Guidelines published by the Victorian Medical Postgraduate Foundation

Susceptibility and Resistance Susceptibility seems to be general.

8

Inc.

Control of Contacts

Epidemic Measures

If a person is diagnosed as having HIV infection, the

HIV infection is usually pandemic.

diagnosing practitioner has a responsibility to ensure that sexual and needle-sharing contacts are followed up. Assistance with partner notification may be provided by

International Measures

Human Services through its partner notification officers:

A global prevention and control program coordinated by

telephone (03) 9482 5700.

WHO was initiated in 1987.

Pre- and post-test counselling should be provided for all

Currently all countries have developed AIDS prevention

contacts who seek HIV testing.

and control programs.

Preventive Measures Personal: • Public education on the use of condoms and safer sex practices. • Public education should stress that having unprotected sex with multiple sexual partners and sharing needles (drug users) increases the risk of infection with HIV. • Sexual intercourse with persons with known or suspected HIV should be avoided. • HIV-infected persons should be offered confidential counselling. • Care sould be taken when handling, using and disposing of needles or other sharp instruments. • Use of needle exchange programs by injecting drug users.

Institutional: • Use of appropriate infection control measures by all health care and emergency workers. • Use of appropriate infection control measures in all premises where skin penetration is carried out; for example, by tattooists or beauty therapists carrying out electrolysis. • Blood and blood products for transfusion and tissues for donation should be tested for HIV infection. • Needle-stick/sharps injuries and parenteral exposure to laboratory specimens containing high titre of virus should be dealt with according to the Australian National Council on AIDS guidelines.

9

Acute Bacterial Conjunctivitis

Victorian Statutory Re quirem en t

It can be transmitted by ontact with:

Statutory notification not required except for gonococcal

• Discharge from the conjunctivae or upper respiratory

disease (ophthalmia neonatorum).

Mode of Transmission tract of infected persons. • Contaminated fingers or fomites (contaminated ob-

School and child care exclusion.

jects). • Infected mothers during vaginal delivery.

Infectious Agent Haemophilus influenzae, Streptococcus pneumoniae.

Incubation Period Usually 24–72 hours.

Other organisms include: • Staphylococcus aureus, Pseudomonas aeruginosa. • Neisseria gonorrhoeae in neonates.

Clinical Features Excessive tears, irritation and redness of eyes, followed by oedema of lids, photophobia and mucopurulent discharge which usually lasts from two days to two to three weeks.

Period of Communicability It is infectious while there is discharge.

Susceptibility and Resistance Children under five years are most often affected. Incidence decreases with age. Immunity after attack is low-grade.

Viral conjunctivitis can cause a similar clinical picture. A

Control of Case

blocked tear duct predisposes to recurrent infection.

Children should not attend school and child care settings until discharge from eyes has ceased. Soiled articles

Public Health Significance and Oc c u r re n c e

should be disinfected.

A common communicable disease, frequently epidemic,

Tre a t m e n t

affecting children under five years of age.

Local application of antibiotic ointment or drops.

Occurrence is worldwide.

Control of Contacts

Method of Diagnosis

Investigation of contacts and source of infection not practicable.

Microscopic examination of a smear or bacteriologic culture of the discharge.

Reservoir Human.

Preventive Measures Personal hygiene and proper treatment of infected eyes.

Epidemic Measures Not applicable.

11

Amoebiasis

Victorian Statutory Re quirem ent

Method of Diagnosis Microscopic examination for trophozoites or cysts in:

Group B notification.

• Fresh or suitably preserved faecal specimens. • Smears of aspirates or scrapings obtained by

Infectious Agent

proctoscopy. • Aspirates of abscesses or sections of tissue.

Entamoeba histolytica. As cysts are shed intermittently in asymptomatic and

Clinical Features

mild infections, repeated stool specimens may be needed to establish a diagnosis.

An infection with a protozoan parasite that exists in two forms: an infective cyst and a potentially pathogenic

The presence of trophozoites containing red blood cells

trophozoite. Further, the difficulty of distinguishing

is indicative of invasive amoebiasis.

infection with the non-pathogenic Entamoeba dispar must be noted.

Serology, raised titre of specific antibodies is valuable in diagnosis of amoebiasis.

Clinically, it may present as intestinal or extra-intestinal disease. Most infections are asymptomatic. Intestinal

X-ray, ultrasound and CT scan are used in diagnosis and

disease includes diarrhoea which may be bloody, fever

location of an amoebic liver abscess.

and abdominal discomfort. Intestinal amoebiasis may be complicated by:

Reservoir

• Granuloma of the large intestine.

Human.

• Colonic perforation and haemorrhage. • Perianal ulceration. • Extra-intestinal amoebiasis with abscess formation that

Mode of Transmission

occurs as a result of bloodstream spread to the liver,

Amoebiasis can be transmitted by:

brain or lungs.

• Ingestion of faecally contaminated water containing amoebic cysts.

Public Health Significance and Oc c u r re n c e

• Hand-to-mouth transfer of faecal contamination. • Contaminated raw vegetables. • Sexually, by unprotected oral-anal contact.

Occurrence is worldwide. High-risk groups include: • Patients in institutions for the intellectually disabled.

Incubation Period Average incubation period is two to four weeks.

• Male homosexuals. • People living in areas with poor sanitation.

Patients may present months after the initial infection.

• Travellers returning from developing countries. This active disease occurs mostly in young adults and is rare below the age of five years. 13

Period of Communicability Cases are infectious as long as cysts are present in the faeces.

• Educate the public about the possibility of transmitting the disease via sexual contact. • Protect public water supplies from faecal contamination.

In some instances, cyst excretion may persist for years.

Epidemic Measures Susceptibility and Resistance Recurrent infections can occur.

• Ensure proper laboratory confirmation of diagnosis. • Undertake epidemiological investigation to determine source of infection and to look for a common vehicle such as food or water.

Control of Case Amoebiasis can be controlled by: • Standard Precautions. • Exclusion of infected person from food handling until asymptomatic. • Sanitary disposal of faeces.

Tre a t m e n t For acute amoebic dysentery, use metronidazole. After initial treatment of invasive amoebiasis with metronidazole, cyst eradication with furamide may be indicated. For extra-intestinal amoebiasis, use metronidazole. Surgical aspiration of abscesses may be necessary.

Control of Contacts Routine investigation of contacts is not indicated. However, in residential institutions or in the case of fellow travellers, microscopic examination of faeces is advisable.

Preventive Measures • Educate the public in personal hygiene. • Provide information to intending travellers about the risk involved in eating uncooked vegetables and fruits and drinking contaminated water.

14

Anthrax

Victorian Statutory Re quirem ent Group A notification.

Intestinal Anthrax It is rare in developed countries, but may occur in explosive outbreaks. Gastro-intestinal symptoms may be followed by fever,

Infectious Agent

septicaemia and death (mortality rate is 25–75 per cent).

Bacillus anthracis, a Gram-positive, encapsulated sporeforming, non-motile aerobic rod.

Clinical Features

Public Health Significance and O c c u r re n c e Anthrax is primarily an occupational hazard for handlers

Anthrax is an acute bacterial disease usually affecting

of:

the skin.

• Processed hides. • Goat hair.

It may rarely involve the intestinal tract.

• Bone and bone products.

Cutaneous Anthrax Lesions are usually painless.

• Wool. • Infected wildlife. It can also be contracted by contact with infected meat; for example, knackery workers.

Itchiness is common followed by a skin lesion that progresses from a papule to a vesicle (which may be

New areas of infection in livestock may develop through

haemorrhagic), and in two to six days develops into a

introducing animal feed containing bone meal.

depressed black eschar (malignant pustule). Untreated lesions can progress to involve the regional

Cutaneous outbreaks sometimes occur in knackery workers and those handling pet meat.

lymph nodes. In severe cases, an overwhelming septicaemia can occur.

Known infectious land can remain contaminated for years.

Untreated cutaneous anthrax has a case fatality rate of between 5–20 per cent.

Pulmonary Anthrax

Method of Diagnosis Demonstrate the presence of Gram-positive Bacillus

anthracis in blood, lesions or discharges by:

This is very rare and often presents with mild and non-

• Direct staining of smears using Gram or special stains.

specific symptoms resembling common URTI.

• Isolation or animal inoculation in the laboratory.

This is followed three to five days later by acute respiratory distress and changes on X-ray.

Reservoir Dried or otherwise processed skins and hides of infected

Untreated, the mortality rate is 70–80 per cent.

animals may harbour spores for years. Spores remain viable in contaminated soil for many years. 15

Mode of Transmission Usually two to seven days. Most cases occur within 48 hours of exposure.

• Sterilise imported bone meal before use as animal feed. • Sterilise wool, hair, hides and other infected products by ethylene oxide gas or ionising (gamma) radiation.

Period of Communicability

Note

There is no evidence of direct spread from person to

Soiled articles require pressure steam sterilisation or

person.

incineration.

Articles and soil contaminated with spores may remain

Preventive Measures

infective for years.

• Educate employees who are handlers of potentially infected articles in the proper care of skin abrasions.

Susceptibility and Resistance Recovery is usually followed by prolonged immunity.

• Ensure proper ventilation in hazardous industries and use of protective clothing. • Sterilise hair, wool or hides, bone meal or other feed of

Control of Case To control anthrax, it is important to: • Seek laboratory confirmation. • Find out the occupation of patient. • Seek the source of infection.

animal origin prior to processing. • Use vaporised formaldehyde for terminal disinfection of textile mills contaminated with B. anthracis. • Collect a jugular blood sample from the animal for culture if anthrax is suspected in an animal. • Deeply bury carcasses with quicklime at site of death if

• Arrange isolation of patient in hospital. Soiled articles

possible. Do not necropsy or burn on open field.

require pressure steam sterilisation or incineration.

• Decontaminate soil or discharges with quicklime, or

• Use penicillin as the drug of choice. Tetracyclines, erythromycin, chloramphenicol or ciprofloxacin could be used if penicillin is contraindicated.

preferably bury deeply with carcass. • Promptly vaccinate all animals at risk and revaccinate annually. • Control effluent and trade wastes from factories that

Control of Contacts History of exposure to infected animals/products should be examined.

manufacture products from hair, wool or hides likely to be contaminated. • Decontaminate soil on infected farms with 5 per cent formalin.

Control of Environment

Treatment of Animals

To control the environment:

Symptomatic animals can be treated with penicillin or

• Seize suspected animal products.

tetracyclines.

• Incinerate infected animal products. • Use formaldehyde for disinfection of contaminated premises. • Inform the Department of Natural Resources and Energy of the case.

16

Epidemic Measures Trace the source of infection.

Arbovirus Infections

Victorian Statutory Re q u i re m e n t s Group A for Australian arboencephalitis. Group B for other arbovirus infections. Prevention of mosquito breeding (section 29 of the Health (Infectious Diseases) Regulations 1990).

Infectious Agents

The rash resolves within seven to 10 days, followed by a fine desquamation. Cervical lymphadenopathy occurs frequently, and parasthesiae and tenderness of palms and soles are present in a small percentage of cases. Fever is commonly absent.

Public Health Significance and O c c u r re n c e

Flaviviruses: Murray Valley Encephalitis (the cause of

Major outbreaks have occurred in Australia in the Murray

Australian arboencephalitis), Kunjin, Dengue.

Valley, Gippsland, coastal New South Wales, Northern Territory, Queensland and Western Australia, chiefly from

Alphaviruses: Ross River virus, Barmah Forest virus,

January to May.

Sindbis. Sporadic cases occur in other coastal regions of Aus-

Ross River Virus Disease (Epidemic Polyarthritis)

tralia and Papua New Guinea. In 1979, a major outbreak occurred in Fiji and spread to

Infectious Agent

other Pacific islands, including Tonga and the Cook

Ross River virus (alphavirus).

Islands. There were 15,000 cases in American Samoa in 1979–80.

Sindbis and particularly Barmah Forest viruses (both alphaviruses) can cause similar illnesses.

Morbidity: 30 per cent of the population will develop symptoms of the disease if infected.

Clinical Features A self-limited disease characterised by arthritis or arthralgia lasting from days to months and primarily

Infection is rare in prepubertal children and increases with age.

affecting the wrist, knee, ankle and small joints of the extremities. Prolonged symptoms are common.

In those affected, the disease can cause incapacity to work for two to three months and sometimes longer.

In some cases, there may be remissions and exacerbations of decreasing intensity for years.

Method of Diagnosis Serology can show a rise in antibody titre to Ross River

In many patients, the onset of arthritis is followed in one

virus. The virus may be isolated from the blood of acutely

to 10 days by a maculopapular rash (usually non-pruritic)

ill patients.

mainly affecting the trunk and limbs. Tests are usually necessary to distinguish it from other Buccal and palatal enanthema may occur.

causes of arthritis. However, in the event of a local outbreak clinical diagnosis may be sufficient. 17

Reservoir Probably macropods (for example, kangaroos); possibly

All family members should be questioned about symptoms and evaluate serologically if appropriate.

other marsupials and wild rodents.

Preventive Measures Transovarian transmission in the mosquito Aedes vigilax

Ross River virus can be prevented by:

has been demonstrated in the laboratory, making an

• Mosquito control measures (see local municipality).

insect reservoir a possibility.

• Personal protection measures (long sleeves and mosquito repellents).

Mode of Transmission It is transmitted by mosquitoes Culex annulirostris, Ae.

camptorhynchus. Ae. vigilax, Ae. polynesiensis and other Aedes spp. of mosquitoes.

• Avoidance of mosquito-prone areas. Vectors usually bite at dusk and dawn.

Epidemic Measures • Conduct a community survey to determine species of

Incubation Period Usually three to 11 days.

vector mosquitoes. Identify their breeding places and promote their elimination. • Use mosquito repellents for persons exposed because

Period of Communicability There is no evidence of transmission from person to person.

Susceptibility and Resistance

of occupation or otherwise to mosquito bites. • Identify the infection among animal reservoirs; for example, kangaroos, small marsupials, farm and domestic animals. Note

Recovery is universal and is followed by lasting immu-

See the Victorian Arbovirus Task Force Contingency Plan

nity. Second attacks are unknown.

for Outbreaks of Ross River Virus Disease.

Inapparent infections are common, especially in children,

International Measures

among whom the clinical disease is rare.

Airport vector control in Australia and Papua New Guinea.

Arthritis occurs more frequently among adult females and in persons with a particular HLA DR7 phenotype.

These measures may be necessary to prevent the spread from endemic areas in Australia and Papua New

Control of Case

Guinea to avert epidemics in countries where local

Not applicable.

vectors (for example, Ae polynesiensis) carry the dis-

Symptomatic treatment.

ease.

Control of Contacts Unreported or undiagnosed cases should be searched for in the region where the patient had been during the incubation period of their illness.

18

Australian Arboencephalitis (AE)

During the 1974 epidemic, of those affected, one-third

Infectious Agent

died, one-third were left with residual brain damage, and one-third recovered completely.

Murray Valley Encephalitis (MVE) virus. Kunjin virus may also cause an encephalitic illness indistinguishable from AE.

Method of Diagnosis Serology: Two blood specimens are required seven to10

Clinical Features

days apart. Sera for diagnosis should be sent to the

Fever, headache and sometimes nausea and vomiting,

contact via the Royal Melbourne Hospital on (03) 9342

followed by the features of encephalitis.

7000.

A diagnosis of AE should be considered in any patient

Reservoir

who presents with encephalitis and who has been in the Murray Valley area within the incubation period of the disease, especially in the period between November and March.

Director of Virology, VIDRL, preceded by telephone

The primary hosts of AE during years of high virus activity are waterbirds. Ardeiformes (herons), particularly the Rufous Night-heron and the Pelicaniformes (cormorants/darters) show the strongest evidence of infection.

The disease may also be acquired at any time in the northern parts of Australia.

Modes of Transmission The primary mosquito vector during epidemics is Culex

Public Health Significance and O c c u r re n c e AE is endemic in Northern Australia and Papua New Guinea. Outbreaks of the disease occur approximately once

annulirostris. Other mosquitoes such as Culex australicus and some Aedes species may be involved in other aspects of MVE virus ecology.

Incubation Period Usually seven to 28 days.

every 20 years in South Eastern Australia when weather patterns promote large increases in water bird and

Period of Communicability

vector mosquito populations.

There is no evidence of person-to-person transmission.

This results in amplification of arboviruses in the mosqui-

Susceptibility and Resistance

toes that infect the non-immune human populations in the Murray-Darling catchment. Morbidity during an epidemic year is related to exposure. Cases of AE seem to occur in people who receive large numbers of mosquito bites during a single exposure.

One in every 800 people infected is said to show signs of the disease.

Control of Case Patients can be managed at any hospital, but facilities for providing artificial respiration must be available.

Serological studies show that only one person in every 800 who has seroconversion develops the disease.

19

Investigate the source of infection. Search for unreported or undiagnosed cases of encephalitis from the Murray-Darling drainage basin.

Control of Contacts Not applicable.

Preventive Measures • Apply mosquito control measures (local municipalities). • Use personal protection measures (long sleeves, long trousers, mosquito repellents and so on). • Avoid mosquito-prone areas; vectors usually bite at dusk and dawn.

Epidemic Measures See the Victorian Arbovirus Task Force Contingency Plan for outbreaks of AE for details.

20

Dengue

Method of Diagnosis

Infectious Agent

Serology: Rising titre to Dengue virus antibodies.

Dengue virus 1, 2, 3 and 4 (flavivirus).

Reservoir Clinical Features

Humans and monkeys (in most cases monkeys play no

Dengue Fever (Break Bone Fever)

role).

Classically, dengue fever presents as an acute febrile illness of sudden onset.

Mode of Transmission It is transmitted by the bite of an infected mosquito

It is characterised by fever (three to five days), myalgia,

usually Ae. aegypti and Ae. albopictus. (Other Aedes

arthralgia, retro-orbital pain, anorexia, gastrointestinal

species are involved in the enzootic monkey complex).

disturbance, rash and increased vascular permeability (see below).

Dengue Haemorrhagic Fever (Dengue Shock Syndrome) In contrast to classic dengue, myalgia and bone pains

Incubation Period Usually three to 14 days; commonly seven to 10 days.

Susceptibility and Resistance

are unusual in dengue haemorrhagic fever which is a

There is universal susceptibility but children usually have

disease of abrupt onset characterised by fever, palpable

a milder primary disease than adults.

lymph nodes and liver, scattered petechiae and rapid deterioration.

Recovery from infection with one serotype provides homologous immunity, but does not provide protection

Other haemorrhagic phenomena such as melaena,

against another serotype.

haematemesis and shock are poor prognostic signs. Death usually occurs on the fourth or fifth day.

A previous infection may exacerbate a second infection. Dengue antibodies from earlier infections appear to

Public Health Significance and O c c u r re n c e

promote infection by other serotypes.

Outbreaks of this disease have occurred throughout the

Control of Case

tropics and over the past 40 years.

• Isolate patient and prevent mosquito access until fever

A complication, dengue shock syndrome, is believed to

• Investigate source of infection.

subsides. be caused by immune enhancement of infection, in which dengue antibodies from prior infections appear to promote the infection of other serotypes.

Preventive Measures • Search for and eliminate breeding sites of Aedes aegypti. • Use mosquito repellents, mosquito nets and other

Outbreaks of dengue have occurred in Northern Australia but have been limited by the distribution of Aedes aegypti. The detection of larvae of Aedes albopictus (a potential vector overseas) on one occasion in South Australia in

methods of personal protection. • Control Aedes aegypti near airports. • Prevent importation of new vectors; for example, Aedes

albopictus.

imported car tyres is cause for concern. 21

Kunjin

Incubation Period

Infectious Agent

Uncertain, probably weeks.

Kunjin virus (flavivirus).

Period of Communicability Clinical Features

There is no evidence of person-to-person transmission.

Most infections are subclinical.

Susceptibility When symptoms occur, the syndrome varies from a mild

The ratio of subclinical to clinical infections appears to

febrile illness with nausea, lethargy, lymphadenopathy

be large but the precise ratio is unknown.

and a rash to encephalitis. Cross-reaction between MVE virus and Kunjin virus has

Public Health Significance and O c c u r re n c e Kunjin virus has been found in Australia and Sarawak. Unlike the Murray Valley Encephalitis virus (MVE), Kunjin

complicated the assessment of the prevalence of Kunjin infection in the general population.

Control of Case No specific treatment is required.

virus has been detected in Victoria on several occasions since the last outbreak of AE in 1974.

Investigate the source of infection and search for unreported or undiagnosed cases from the Murray-Darling

Further study is needed to define the morbidity rate of

drainage basin.

infections with Kunjin virus.

Control of Contacts Method of Diagnosis

Not applicable.

Serology: Two specimens, seven to 10 days apart. Sera should be sent to VIDRL.

Preventive Measures Intensify mosquito surveillance and control in areas

Reservoir

where cases are identified.

Kunjin virus can infect a wide range of mammals including cattle, sheep, horses and so on.

Epidemic Measures See the Victorian Arbovirus Task Force Contingency Plan

Birds, particularly waterbirds, are thought to be the major vertebral hosts during epidemics of AE caused by MVE virus. Their role in the transmission of Kunjin is unknown.

Mode of Transmission Culex annulirostris is the major vector of the Kunjin virus.

22

on AE.

Botulism

Victorian Statutory Re quirem ent

Outbreaks of type E are usually related to consumption

Group A notification.

toxin is destroyed by boiling.

Infectious Agent

Method of Diagnosis

Most human outbreaks are due to types A, B and E. of fish, seafood and meat from marine mammals. The

Clostridium botulinum, a spore-forming obligate anaero-

Botulism can be diagnosed by demonstration of specific

bic bacillus. Different types are recognised, for example,

toxin in serum, faeces and incriminated food, or by

types A, B, E, F and G.

culture of C. botulinum from stool in a clinical case.

Clinical Features

Wound botulism is diagnosed by serum toxin or positive wound culture.

There are three forms of botulism: the classical form, infant botulism and wound botulism.

Electro-myography may be useful in corroborating the clinical diagnosis in infant botulism.

Classical botulism is a severe and often fatal intoxication resulting from ingestion of toxin in contaminated food. Symptoms include double vision, dysphagia and dry

Reservoir

mouth. This may be followed by descending flaccid

Spores are ubiquitous in soil and are frequently recov-

paralysis in an alert person. Fever is absent unless a

ered from agricultural products. They are also found in

complicating infection occurs.

marine sediments and the intestinal tract of animals, including fish.

Infant botulism is the most common form, and usually affects infants under one year of age, but can affect adults who have altered gastrointestinal anatomy and

Mode of Transmission

microflora. The illness typically begins with constipation,

Classical botulism is acquired by ingestion of food in

followedby lethargy, listlessness, poor feeding, ptosis,

which toxin has been formed without subsequent ad-

difficulty in swallowing, and generalised muscle weak-

equate cooking. Suitable conditions for the formation of

ness (floppy baby).

toxin in foods have included inadequate heating during canning (especially home canning of alkaline foods) and

Wound botulism is rare, but has been seen after contami-

contamination of cans post-processing.

nation of wounds in which anaerobic conditions developed.

Most cases of wound botulism are secondary to contamination of the wounds by ground-in soil or gravel. Several cases have been reported among chronic drug abusers.

Public Health Significance and Oc c u r re n c e Rare but serious intoxication can occur from improperly

Infant botulism arises from ingestion of spores rather than preformed toxin. Sources of spores include foods

cooked, canned or preserved food. Infant and wound

(for example, honey) and dust. Honey has been de-

botulism are due to colonisation by the causative organ-

scribed in the US literature as a source of infection but

ism.

never implicated in Australia, nor have surveys of Australian honey shown C. botulinum. 23

Incubation Period Within 12–36 hours (sometimes several days) after eating contaminated food. In general, the shorter the incubation period, the more severe the disease and the higher the case fatality rate.

Investigation of contacts and source of toxin and search for other cases of botulism to rule out food-borne botulism.

Specific Treatment Intravenous and intramuscular administration as soon as possible of trivalent botulinum antitoxin (types A,B,E).

Period of Communicability There are no instances of secondary person-to-person transmission have been documented.

This is available from Centers for Disease Control, Atlanta. Limited supply is available from Commonwealth Serum Laboratories for use in hospitalised patients. Blood should be collected and antitoxin administered.

Control of Case

This should occur in an intensive care facility.

Suspected botulism is a medical emergency. Suspected cases should immediately be referred for specialist care.

For wound botulism, in addition to antitoxin, the wound should be debrided and/or drained, and appropriate

Isolation or quarantine is not needed, but hand washing

antibiotics (for example, penicillin) administered.

is indicated after handling soiled nappies. Usual sanitary disposal of faeces from infant cases is acceptable.

In infant botulism, meticulous supportive care is essential, and assisted respiration may be required. Antitoxin is

Any implicated food should be retained for collection and

not used because of sensitisation and anaphylaxis.

investigation by public health authorities.

Antibiotics have not been shown to affect the course of the disease.

Contaminated utensils should be cleaned by boiling or by using household bleach.

Preventive Measures • Ensure effective control of processing and preparation

Control of Contacts Those who have eaten incriminated food should be

of commercially canned and preserved foods. • Educate people undertaking home canning and other

purged, for example, cathartics, gastric lavage, high

food preservation techniques about cooking time,

enemas.

pressure, temperature, adequate refrigeration, storage and so on.

Administration of polyvalent antitoxin to asymptomatic

• Be aware that C. botulinum may or may not cause

individuals should be considered carefully; that is,

container lids to bulge and the contents to have

potential protection versus risk of sensitisation and

unpleasant odours.

reactions to horse serum.

24

• Recall any implicated food product immediately.

Epidemic Measures • Investigate home-preserved foods as prime source of single case or suspect group outbreak (for example, family). • Recall any food implicated by epidemiologic or laboratory findings immediately. • Submit food for laboratory examination. • Take sera and faeces from cases (and exposed but not ill persons) for reference laboratory examination, before administration of antitoxin. • Undertake international efforts, if necessary, to recover and test implicated foods. • This should be coordinated through the: Australia New Zealand Food Authority PO Box 7186 Canberra MC ACT 2610 Tel: (06) 271 2222

25

B r u c ello sis

Victorian Statutory Re quirem ent Group B notification.

Infectious Agents B. abortus, B. melitensis, B. suis and B. canis.

Brucellosis occurs worldwide. The sources of infection and responsible organism vary according to geographic area. Regions of concern are West Africa, Iran and India and Central America. Brucellosis used to be an occupational hazard in Australia for: • Farm workers. • Veterinarians.

Clinical Features

• Abattoir workers.

This is a systemic bacterial disease with acute or insidious onset.

Currently, the major risk factor for brucellosis is exposure to B. suis infection in feral pigs.

Localised suppurative infections may occur. Subclinical and unrecognised infections are frequent.

Method of Diagnosis Laboratory diagnosis is made by either isolating the

Fever is the most common symptom and may be associated with a variety of other complaints.

infectious agent from blood, bone marrow or other tissues or discharges of the patient, or by a specific antibody response.

Osteoarticular complications are common. The interpretation of serological results can be difficult. Less common are orchitis, epididymitis, osteomyelitis and endocarditis.

Reservoir Infection in humans can be transmitted from cattle,

Public Health Significance and Oc c u r re n c e

swine, goats, sheep and dogs.

Since the success of the national eradication campaign

Incubation Period

for B. abortus in cattle herds in 1989, only an occasional

Variable and difficult to ascertain.

case of brucellosis is now seen which is usually acquired overseas. In 1992, 29 cases were reported in Australia.

Usually five to 60 days; can be several months.

The majority of these (25) were due to B. suis, contracted in Queensland, often by people hunting or butchering feral pigs.

Mode of Transmission Brucellosis can be transmitted by contact with infected

In Victoria in 1991, two cases of B. abortus were re-

tissues, blood, urine, vaginal discharges, aborted animal

ported, and both were believed to be long-standing

foetuses and especially placentae; also by ingestion of

infections. One case notified in 1992 was an imported

raw milk and dairy products from infected animals.

case due to B. melitensis.

27

Epidemics are generally attributed to inhalation of aerosols. A small number of cases used to occur from accidental self-inoculation of strain 19 Brucella vaccine.

Period of Communicability There is no evidence of communicability from person to person.

Susceptibility and Resistance Severity and duration of clinical illness are subject to wide variation. Duration of acquired immunity is uncertain.

Control of Case • Treat with rifampicin and doxycycline for at least six weeks. • Inform the Department of Agriculture.

Control of Infected Source Enquire into source of infection and trace infection to common source. Recall incriminated products. Stop distribution of milk and milk products unless pasteurisation is instituted.

Preventive Measures • Educate the public against drinking untreated/unpasteurised milk or eating dairy products produced from such milk. Boiling milk is effective when pasteurisation is not available. • Educate farmers and handlers of potentially infected animals (for example, feral pigs) to reduce exposure and exercise care in handling placentae, discharges and foetuses. • Search for and investigate livestock at risk of infection. 28

Epidemic Measures Trace source of infection.

Campylobacter Infection

Victorian Statutory Re quirem ent

All age groups are affected, most commonly children less than five years of age and young adults. In developed countries, asymptomatic carriage is probably rare.

Group B notification. Note

Method of Diagnosis

Also notifiable if isolation of C. jejuni, C. coli or C. lari

Isolation of common types requires selective media and

from water supplies or C. jejuni from food.

microaerophilic conditions at 42˚C.

Infectious Agents

Other types may require more specialised techniques.

C. jejuni (commonest), C. coli, C. lari, C. upsaliensis and, rarely, other Campylobacter spp.

Clinical Features Gastrointestinal infection due to Campylobacter spp varies in severity from asymptomatic to severe. Typical cases of C. jejuni infection experience diarrhoea (which may be mucopurulent and/or bloody), abdominal pain

Subspeciation methods are available in specialist centres to assist in epidemiologic investigation.

Reservoir Many animals, including cattle, sheep, birds and poultry may be chronic carriers of Campylobacter spp. Household pets, including puppies and kittens, are another possible source of infection.

and fever. Symptoms usually last two to five days. Campylobacter

Mode of Transmission

infection has been associated with rare sequelae includ-

It is transmitted when organisms are ingested via con-

ing reactive arthritis and Guillain-Barre syndrome.

taminated food (particularly undercooked chicken) or water, or by contact with infected pets or infants.

Human infection with C. fetus is rare, but may cause localised abscesses or generalised sepsis, particularly in

The organism does not multiply in food or water, but the

immunosuppressed persons.

infectious dose required to cause illness is very low.

Public Health Significance Campylobacter infections are now the most commonly

Person-to-person transmission is a particular risk from infected infants to nappy changers (where there is poor personal hygiene).

notified cause of bacterial diarrhoea in Victoria. They occur worldwide and are common in the developing world.

Incubation Period Usually three to five days, with a range of one to 10

Most cases in Australia appear sporadic, but food- and

days.

water-borne outbreaks may occur.

29

Period of Communicability

Control of Contacts

Cases are infectious throughout their illness.

The diagnosis should be considered in symptomatic contacts.

Excretion of organisms may continue for some weeks after symptoms resolve.

Susceptibility and Resistance Most persons in the developed world are susceptible.

Preventive Measures • Ensure scrupulous hand washing and hygiene, especially in food handlers. • Thoroughly cook all meat and, particularly, poultry and avoid recontamination after cooking.

Immunity to serologically related strains may follow infection.

• Thoroughly wash utensils used to prepare raw meats and poultry before using them to prepare non-cooked food such as salads.

Control of Case • Report case to Department of Human Services. • Immediately report clusters of cases by telephone or fax. • Investigate related cases or outbreaks to identify a common source. • Use Standard Precautions for hospitalised patients. • Exclude infected children from child care centres until diarrhoea has ceased. • Exclude symptomatic persons from food handling, care of patients in hospitals, or care of infants in child care centres. • Exclude asymptomatic convalescent stool-positive individuals if strict attention to personal hygiene cannot be assured. • Stress hand washing/personal hygiene education. • Do not share towels, washers or personal items such as toys that may be contaminated.

Tre a t m e n t Antibiotics (for example, erythromycin) are indicated for severe illness or where prompt termination of faecal excretion of organisms is desired. Treatment given early in the illness may reduce the severity and duration of symptoms.

30

• Pasteurise milk and chlorinate water. • Recognise pets as sources of infection and encourage hand washing after handling animals. • Minimise contact with poultry and their faeces.

Chicken Pox/Herpes Zoster

Victorian Statutory Re quirem ent

V-Z Virus in Pregnancy

Statutory notification not required.

can cause spontaneous abortion but, overall, the risk is

Varicella infection during the first trimester of pregnancy not significantly increased.

School exclusion. In the third trimester, maternal varicella may precipitate

Infectious Agent

the onset of premature labour.

Human (alpha) herpesvirus 3 (Varicella-zoster or V-Z virus).

Severe maternal varicella and pneumonia at any stage of pregnancy can cause foetal death.

Clinical Features

Perinatal varicella is associated with a high mortality rate

Chicken pox presents with a low-grade fever, malaise

when maternal disease develops within five days prior to

and a rash that is maculopapular then vesicular for three

delivery and up to 48 hours postpartum. The neonatal

to four days, becoming crusted. Lesions appear in crops

fatality rate is reported as being up to 30 per cent.

on the trunk, face, scalp and mucous membranes of the mouth.

A foetal varicella zoster syndrome has been reported in a small number of cases.

Herpes zoster or shingles is characterised by a unilateral vesicular eruption within a dermatome, often associated

Clinical manifestations include growth retardation,

with severe pain that may precede lesions by 48–72

cutaneous scarring, limb hypoplasia and cortical atro-

hours. The rash lasts up to several weeks depending on

phy.

severity. A common complication in children with chicken pox is bacterial superinfection of the skin. Other complications

Public Health Significance and O c c u r re n c e

include aseptic meningitis, encephalitis and Reye’s

Chicken pox is a highly contagious but generally mild

syndrome. Varicella pneumonia may be a complication in

disease and is endemic in the population. It becomes

adults. Those at risk of a more severe form of infection

epidemic among susceptible individuals mainly during

are children who have acute leukaemia and those in

winter and early spring. More than 90 per cent of cases

remission following chemotherapy.

are children aged one to 14 years.

Herpes zoster in the immunosuppressed host is more

Herpes zoster, a sporadic disease, is the consequence

severe and prolonged than in the normal individual; for

of reactivation of a latent virus from the dorsal root

example, those who have received a bone marrow

ganglia. It is most commonly seen in the elderly.

transplant, those with Hodgkins disease, non-Hodgkins lymphoma or HIV infection.

Method of Diagnosis

A most debilitating complication of herpes zoster in all

Clinical: Isolation of the virus in cell cultures or visualisa-

patients is pain associated with acute neuritis and post-

tion by electron microscopy (EM) is not routinely re-

herpetic neuralgia and hyperaesthesia; the latter persists

quired.

for months after resolution of the disease. 31

Serological: • Complement fixation tests showing detectable IgM antibody. • Immunofluorescence on lesion swab/fluid. • ELISA (kit) now more commonly used.

Reservoir Humans.

Susceptibility Universal among those not previously infected but the disease is more severe in adults. Infection remains latent and may occur years later as shingles in some older adults. Neonates whose mothers are not immune and leukaemia patients may suffer severe, prolonged or fatal chickenpox.

Mode of Transmission

Adults with cancer, especially of lymphoid tissue,

It can be transmitted from person to person by direct

immunodeficient patients and those on immunosuppres-

contact, or by droplet or airborne spread of secretions

sive therapy may have increased frequency of severe

from the respiratory tract of chicken pox cases, or of the

zoster.

vesicle fluid of patients with herpes zoster. Indirect contact occurs through articles freshly soiled by discharges from vesicles of infected persons. Scabs are not infective.

Control of Case Chicken Pox: • Exclude from school until fully recovered, or at least

Chicken pox is highly contagious, and zoster has a much lower rate of transmission (the non-immune contact develops chicken pox).

one week after eruption first appears. • Avoid contact with immunosuppressed persons. • Exclude adults from work for the same time.

Herpes Zoster: Acyclovir is effective for treatment of

Incubation Period

varicella zoster infections in patients with a rash less than

From two to three weeks; usually 13–17 days.

72 hours old. It gives some pain relief, but is of no benefit on the incidence of post-herpetic neuralgia.

May be prolonged in the immunosuppressed, or following immune globulin.

Control of Contacts Contacts are not excluded from school.

Period of Communicability It is usually communicable for one to two days (up to five

The risk of spread to immunosuppressed patients means

days) before onset of rash, and for five days after the

that if a susceptible child with known exposure is in

appearance of the first crop of vesicles, but prolonged in

hospital, quarantine of these patients should be consid-

patients with altered immunity.

ered for days 10–21 after exposure (up to 28 days if immune globulin given).

Those with zoster may be infectious for a week after lesions appear.

32

Preventive Measures Immunosuppressed individuals should be protected from exposure. If exposure has occurred in these persons, varicella zoster immune globulin (VZIG) (prepared from the plasma of blood donors with high antibody titre to the V-Z virus) is effective in modifying or preventing the disease if given within 96 hours of exposure. VZIG is available from Australian Red Cross. VZIG may be given within 96 hours of exposure to newborns of mothers who develop chickenpox within five days prior to, or within 48 hours after, delivery. A live attenuated varicella virus vaccine protects children with leukaemia exposed to siblings with chickenpox (not yet available in Australia).

Epidemic Measures Not applicable aside from protection of immunosuppressed.

33

Cholera

Victorian Statutory Re quirem ent Group A notification.

Infectious Agent Vibrio cholerae serogroup O1 or O139. V. cholerae occurs in two major biovars: the classical and the El Tor type. These two differ in biological and

pain, occasional vomiting, rapid dehydration, acidosis and circulatory collapse. In untreated cases, death may occur in a few hours and the case fatality rate may exceed 50 per cent.

Public Health Significance and O c c u r re n c e Cholera can occur in epidemics or pandemics and, in any single epidemic, one particular biovar (that is, classical or El Tor) tends to predominate.

biochemical characteristics and both include organisms of the Inaba and Ogawa serotypes. Both biotypes can

Endemic cholera occurs in parts of Africa, Central

also be classified into various phage types.

Europe and Asia.

Note

Non-O1 vibrios, formerly known as non-agglutinable

The seventh cholera (EI Tor) pandemic that began in Asia in 1961 spread to Africa in 1970 and to South

vibrios (NAG) or non-cholera vibrios (NCV) are now

America in 1990–91.

included in the species Vibrio cholerae, but the reporting of Non-O1 infections as ‘cholera’ is inaccurate.

Over 300,000 cholera cases around the world were reported to WHO in 1994.

Most Non-O1 strains do not secrete enterotoxin but these strains can cause sporadic cases, and outbreaks of diarrhoeal illness due to them have occurred in Venice

In Victoria, only sporadic imported cases in returned travellers occur.

(1981 and 1984) and in Lima, Peru (1984). V. cholerae O1 is established in the riverine environment Large-scale epidemics of cholera caused by V.cholerae

in some parts of Queensland and NSW.

O139 have been seen in India and Bangladesh.

Method of Diagnosis Another confusing term (sometimes used but better avoided) is non-vibrio cholera (NVC) which refers to cases of cholera-like illness caused by organisms other than vibrios.

Culture of V. cholerae serogroup O1 or O139 from faeces. Faecal samples to be stored at 4˚C or added to transport media, and forwarded to MDU.

Clinical Features Asymptomatic illness is much more frequent than clinical

Visualisation by dark field or phase microscopy of

illness, and mild cases with diarrhoea are common,

characteristic motility, specifically inhibited by preserva-

especially among children.

tive-free serotype-specific antiserum.

In the severe case, however, there is sudden onset of symptoms with profuse watery stools not associated with

35

Reservoir Water and humans.

Infection results in a rise in agglutinating, vibriocidal and antitoxic antibodies with increased resistance to reinfection.

Marine waters where they may be associated with copepods or other zooplankton.

Control of Case Severely ill patients should be isolated in hospital, with

Mode of Transmission

Standard Precautions.

Cholera can be transmitted by: • Contaminated water.

Less severe cases can be managed at home.

• Ingestion of food contaminated by dirty water, soiled hands or flies; for example, vegetables fertilised with sewage or night soil or washed in contaminated water.

Concurrent disinfection is required of linen and articles used by the patient.

• Fish or shellfish obtained from contaminated waters. The organism can survive for long periods in water and ice.

Faeces and vomitus can be disposed of into the toilet without preliminary disinfection, except in areas without an adequate sewage disposal system.

Incubation Period

Terminal cleaning of the room and articles used by the

From a few hours to five days; usually two to three days.

patient is required.

Period of Communicability

Specific Treatment

Cholera is communicable during the acute stage and for

Prompt fluid therapy with adequate volumes of electro-

a few days after recovery.

lyte solution (Gastrolyte) should be undertaken.

By the end of the first week, 70 per cent of patients are

Patients with severe dehydration require urgent intrave-

non-infectious, and by the end of the third week 98 per

nous fluid therapy with Hartmann’s solution or WHO

cent are non-infectious.

solution (NaCl 4.0 g/l, KCl 1.0 g/l, Sod acetate 6.5 g/l and glucose 8.0 g/l), or other similar fluid.

Occasionally the carrier state may persist for months, and exceptionally chronic biliary infection with intermit-

Antimicrobial agents (to which the strain is sensitive)

tent shedding of organisms may last for years.

shorten the duration of diarrhoea and the duration of vibrio excretion:

Susceptibility and Resistance Even in severe epidemics, attack rates of overt disease rarely exceed 2 per cent. Gastric achlorhydria increases risk of disease. Breastfed infants are protected.

36

• Adults: Tetracycline drugs (if strain sensitive). • Children: Co-trimoxazole (if strain sensitive).

Control of Contacts

Epidemic Measures

Contacts should be observed for five days from the date

• Immediately notify Communicable Diseases Network,

of last exposure.

Australia and New Zealand (CDN-ANZ) and WHO. • Initiate thorough investigation to determine the vehicle

This may include, for example, all air travellers on a flight

and circumstances of transmission and plan control

from overseas.

measures accordingly. • Educate the population at risk about the need to seek

Stool culture of any contacts with symptoms of diarrhoea and stool culture of all household contacts, even if asymptomatic, should be underaken.

appropriate treatment without delay. • Adopt emergency measures to assure a safe water supply. • Assure careful supervision of food and drink prepara-

Cases should also be looked for among those possibly

tion.

exposed to a common source. Note Immunisation of contacts is not indicated.

Immunisation of contacts is not indicated, even in the epidemic situation.

Investigate Possible Sources of Infection For example, in a non-traveller, look for sources of contaminated food or water.

Preventive Measures Cholera vaccine is a heat-killed suspension of the Inaba and Ogawa serotypes of the classical biotype of V.

cholerae O1. It provides partial protection (approximately 50 per cent) for three to six months. It is not routinely recommended and advice to overseas travellers should emphasise careful selection of food and water rather than immunisation. Officially, cholera vaccination certificates are no longer required by any country or territory. Unofficially, some countries may still require such a certificate, in which case a single dose of cholera vaccine would satisfy this requirement.

37

Cryptococcal Infection

Victorian Statutory Re quirem ent Notification not required.

CSF and serum should be tested for cryptococcal antigen. Pulmonary cryptococcosis in non-HIV infected persons usually manifests as a nodule, which must be distin-

Infectious Agent

guished from a malignancy (which may coexist).

Cryptococcus neoformans, an encapsulated yeast-like fungus.

C. neoformans var. neoformans (serotypes A & D). C. neoformans var. gattii (serotypes B & C).

Reservoir C. neoformans var. neoformans occurs worldwide, frequently in association with pigeon or other bird droppings.

C. neoformans var. gattii occurs in endemic foci in the

Clinical Features

tropical and sub-tropical world where certain eucalypts

Cryptococcal infection usually presents as a sub-acute

provide an ecological niche.

or chronic meningo-encephalitis with headache and altered mental state. Lung involvement may cause symptoms of lower respira-

Mode of Transmission It is transmitted by inhalation.

tory tract infection or may be asymptomatic.

Communicability The skin, bone and other organs are less frequently

Cryptococcal infection is not spread from person-to-

infected.

person or animal-to-person.

Public Health Significance and Oc c u r re n c e

Susceptibility

Sporadic cryptococcal infections occur worldwide.

therapy, lymphoma and sarcoidosis are at increased risk

Persons with impaired immunity due to corticosteroid of crytococcal infection.

Method of Diagnosis HIV-infected persons may have cryptococcal meningitis,

Persons with AIDS are particularly prone and now constitute a majority of cryptococcal infection cases.

even in the absence of inflammatory cells in the cerebrospinal fluid (CSF). CSF should be stained with an India ink stain. CSF, blood, sputum and urine should be cultured for cryptococci.

39

Control of Case The diagnosis should be established. The possibility of underlying HIV infection should be considered. Referral to a specialist centre should occur. Therapy for cryptococcal meningitis usually involves at least six weeks of antifungal medications: Amphotericin B in combination with 5-flucytosine. Persons with AIDS then require lifelong suppressive therapy, usually with an imidazole antifungal agent. Discrete lung lesions may need diagnosis by biopsy and the need for antifungal therapy depends upon the underlying health of the host. Immunosuppressed persons are usually treated to prevent dissemination.

Control of Contacts Contacts of cases need no specific follow-up.

Preventive Measures Remove large accumulations of bird droppings.

Epidemic Measures Clusters have not been reported.

40

Cryptosporidiosis

Victorian Statutory Re quirem ent Statutory notification is not required.

Oocysts may be identified by microscopy of faecal smears treated with a modified acid fast stain. A monoclonal antibody test is useful for detecting oocysts in faecal and environmental samples. Oocyst excretion is most intense during the first days of illness. Oocysts are

Note

rarely recovered from solid faeces.

Notification if Cryptosporidium spp are isolated from water supplies, or are associated with a food or waterborne illness outbreak.

Infectious Agents Cryptosporidium spp. (coccidian protozoa).

Clinical Features Cryptosporidiosis is a parasitic protozoan infection that affects the gastrointestinal tract.

ELISA assays have been developed for the detection of antibodies, but these are not in routine use.

Reservoir Humans, domestic and wild animals.

Modes of Transmission Cryptosporidium spp. are spread by the faecal-oral route directly from person-to-person and animal-to-person, and via contaminated food and water.

The major symptoms are watery diarrhoea associated with cramping abdominal pain.

Incubation Period The disease may sometimes be mild, but in persons with

From one to 12 days, with an average of about seven

impaired immunity, particularly those with AIDS, it may

days.

be a life-threatening illness.

Period of Communicability

Public Health Significance and Oc c u r re n c e

excreted in the stool: from the onset of symptoms until

Cryptosporidiosis occurs worldwide. Young children, the

several weeks after symptoms resolve.

Cases may be infectious for as long as oocysts are

families of infected persons, homosexual men, travellers, health care workers and people in close contact with

Under suitable conditions, oocysts may survive in soil

animals comprise most reported cases.

and be infective for up to six months.

Small outbreaks may occur related to child care centres.

Susceptibility and Resistance

Substantial water-borne outbreaks have been reported in the United States in 1993.

People with normal immune systems usually have asymptomatic or self-limited symptomatic disease.

Method of Diagnosis

People with impaired immunity may experience pro-

The laboratory should be informed of clinical suspicion of

longed illness, depending on the course of their altered

cryptosporidiosis.

immune function.

41

Control of Case • Exclude symptomatic persons from food handling and direct care of hospitalised and institutionalised patients until asymptomatic. • Stress the importance of hand washing. • Disinfect soiled articles. • Exclude symptomatic persons from direct care of children in child care centres. • Exclude children with diarrhoea from child care centres until their diarrhoea has ceased.

Tre a t m e n t Symptomatic. Supportive care with fluid and electrolyte replacement and anti-diarrhoeal agents may be needed by severely affected cases, particularly those with underlying immune deficiency.

Control of Contacts The diagnosis should be considered in symptomatic contacts.

Preventive Measures • Educate the public in personal hygiene. • Dispose of faeces in a sanitary manner. • Insist on careful hand washing by persons in contact with animals. • Filter or boil contaminated drinking water (chemical disinfectants such as chlorine are not effective against oocysts at the concentrations used in water treatment).

Epidemic Measures Investigate clustered cases. Look for sources of infection such as water or raw milk supplies.

42

Cytomegalovirus (CMV) Infection

Victorian Statutory Re quirem ent

Public Health Significance and O c c u r re n c e

Notification is not required.

Serosurveys of adult populations have shown widespread evidence of previous CMV infection, particularly

Infectious Agent Cytomegalovirus, a human herpesvirus.

in developing countries where crowding and poor hygiene facilitate the spread of infection. In Australia, approximately 50 per cent of young adults have been infected.

Clinical Features Primary CMV infection of children and adults may cause a mononucleosis syndrome very similar to that caused by the Epstein-Barr virus (‘glandular fever’). Features include fever, lymphadenopathy, mild hepatitis

CMV is not readily spread by casual contact but requires prolonged, intimate exposure for transmission. This can occur in settings such as child care centres where toddlers shed the virus in saliva and urine and thereby spread the infection among themselves.

and, more rarely, anaemia, thrombocytopenia, pneumonitis, meningoencephalitis and Guillain-Barre syndrome.

Method of Diagnosis CMV may be detected in urine, saliva and other body

Many cases, particularly young children, have few symptoms. Congenital infection occurs when a non-immune pregnant woman experiences primary or reactivated CMV infection.

fluids (including breast milk, semen and cervical secretions) during primary and reactivated infection. Isolation of CMV from urine and saliva does not necessarily imply acute infection, as CMV may be excreted for months to years following infection. The clinician should consider diagnostic tests for CMV in conjunction with the

Congenital infection may cause severe generalised

clinical presentation.

sepsis of the foetus, with death in utero or in the neonatal period.

CMV causes typical ‘cytomegalic’ cells in tissue culture and characteristic histologic features in affected tissues.

Sequelae in survivors include deafness, mental retardation, psychomotor disability and neurological problems.

Rapid diagnostic tests using monoclonal antibodies to early CMV antigens are available in specialist centres.

Immunosuppressed persons (for example, with advanced HIV/AIDS or organ transplants), are at risk of serious illness due to CMV infection. In such persons, disease is usually due to reactivation of previous infec-

False-positive and false-negative serological tests may occur, but a fourfold or greater rise in serum antibody titres to CMV suggests acute infection.

tion. Manifestations include sight-threatening retinitis, pneu-

Reservoir

monitis, gastrointestinal ulceration and inflammation, and

Humans.

neurological disease, particularly affecting the brain and spinal cord. 43

Modes of Transmission

Control of Case

CMV may be transmitted by:

• Use standard precautions for hospitalised and acute

• Transplacental infection of the foetus of a mother with primary or reactivated infection. • Perinatal infection of neonates via infective maternal cervical secretions or breast milk or infective secre-

cases. • Do not need exclude cases from school or child care. • Seek specialist advice if CMV infection is suspected during pregnancy.

tions of attendants or siblings. • Blood transfusion or organ transplantation. • Close personal contact with infective secretions of

Tre a t m e n t

infected persons:

There is no specific treatment for primary CMV infection

– Children: peers and siblings.

of normal hosts.

– Adults: peers, sexual partners and young children. Immunosuppressed persons with severe CMV infection

Incubation Period

are treated in specialist centres with ganciclovir and/or foscarnet.

The incubation period of cases of sporadic cases of CMV usually cannot be determined.

Preventive Measures

Perinatal infection develops three to 12 weeks after

• Wash hands after handling nappies or exposure to the

delivery. In adults, illness usually occurs three to eight weeks after blood transfusion, and between four weeks and four months after organ transplantation.

secretions of young children. • Educate persons working in hospitals, child care centres and centres for the disabled to adhere to infection control precautions and to regard all body

Period of Communicability CMV is excreted in urine and saliva for months to years after primary infection.

fluids as potentially infectious. • Advise women of childbearing age of the risk which CMV infection may pose. • Avoid transfusing neonates with CMV seropositive blood or transplanting organs from CMV seropositive

Neonatal infection in particular is associated with prolonged excretion. The period of excretion seems to be shorter in adults.

Susceptibility and Resistance Immunosuppressed persons are at increased risk of severe disease due to CMV infection.

44

donors to seronegative recipients.

Diphtheria

Victorian Statutory Re quirem ent

Method of Diagnosis Culture of C. diphtheriae from the infected site.

Group A notification. School exclusion.

Presumptive Diagnosis Whitish membrane on tonsils, especially if extending to uvula and soft palate with cervical lymphadenopathy or a

Infectious Agent

serosanguinous nasal discharge. If strong suspicion of

Corynebacterium diphtheriae.

diphtheria, give antitoxin immediately and commence antibiotic treatment after bacteriological specimens are

Clinical Features Acute bacterial disease of tonsils, pharynx, larynx, nose and occasionally other mucous membranes, skin,

taken without waiting for results.

Bacteriological Investigations

conjunctivae and genitalia. The throat is sore in faucial or

• Verify diagnosis.

pharyngotonsillar diphtheria with cervical lymph nodes

• Determine toxigenicity of C. diphtheriae. Non-toxigenic

enlarged and tender. In severe cases, there is marked

strains can sometimes be associated with disease: skin

swelling and oedema of the neck.

lesions, pharyngitis, bacteraemia, arthritis and endocarditis.

Cutaneous diphtheria also occurs, generally without systemic symptoms. Laryngeal disease is serious in infants and young children. Case fatality rate is 5–10 per cent for non-cutaneous diphtheria.

Collection of Specimens For cases: • Nasopharyngeal cultures should be obtained with a flexible alginate swab that reaches deep into the posterior nares. • Throat cultures should be taken with a cotton swab that is firmly applied to any area with a membrane or inflammation.

Public Health Significance

• Any chronic crusting lesion should also be swabbed.

Cases are now rare since widespread immunisation.

Before cultures of wounds are taken, lesions should be

They occur mainly in winter, generally in unimmunised

cleansed with sterile normal saline and crusted mate-

children under 15 years, but also in unimmunised adults.

rial removed. A cotton-tipped applicator is then firmly applied to the base of the wound.

Case fatality rate is high, especially if there is delay in diagnosis and treatment with antitoxin.

For contacts: • Ideally the nasopharynx, the tonsillar fossae, posterior

Outbreaks have occurred in Europe among non-immu-

pharynx and retrouvular areas should be sampled as

nised populations.

well as any crusting lesion. • Where large-scale screening is to be carried out, nose and throat swabs should suffice.

45

For transport: • If no extended delays in culture setup are anticipated, ordinary semi-solid transport medium, such as Amies or Stuarts, is adequate. • When longer transit times (greater than 24 hours) are unavoidable, swabs should be shipped in silica gel.

Control of Case • Isolate until two cultures taken more than 24–48 hours apart are clear (the first to be taken more than 24 hours after the cessation of antibiotics). • Isolate for l4 days, if no culture available. Disinfect contact articles.

Reservoir Humans only.

Specific Treatment If strong suspicion of diphtheria:

Mode of Transmission

• Make bacteriological diagnosis, take cultures. • Give Antitoxin without delay:

Transmission occurs by droplet spread through contact

– First test for hypersensitivity.

with a patient or carrier, or articles soiled with discharges

– Dose (Equine) Antitoxin (20,000–100,000 units) IM.

from infected lesions.

Dose depends on assessed clinical severity. – May need IV antitoxin in addition if very severe

Incubation Period Usually two to five days.

infection (diluted and given as IV infusion). Administration of antitoxin is the most important facet of treatment and must not be delayed until bacteriological

Period of Communicability It is variable, until virulent bacilli disappear from discharges (usually more than two weeks; seldom more than four weeks).

confirmation. Antibiotics are commonly used. These are used to eradicate C. diphtheriae from disease sites: • Oral erythromycin (preferred to penicillins). • IM procaine penicillin.

Rarely chronic carriage.

Susceptibility and Resistance Infants born of immune mothers are relatively immune. Passive immunity is usually lost by six months. Clinical attack does not always lead to lasting immunity. Immunity may be acquired through inapparent infection.

• Benzathine penicillin (single dose).

Control of Contacts Swabs should be taken for culture from throat and nose. Contacts should be kept under surveillance for seven days (regardless of immunisation status). lf cultures are positive, carriers should be treated with erythromycin. Those who handle food or work with school children should be excluded from work or school

Prolonged active immunity is induced by immunisation with diphtheria toxoid. Antitoxic immunity protects against systemic disease but not against local infection in the nasopharynx. 46

until cultures are negative.

Household contacts should be excluded from schools and children’s services centres until investigated by the Medical Officer of Health or a health officer of Human Services and shown to be clear of infection. Previously immunised contacts should be given a booster dose of a diphtheria vaccine according to age as diphtheria toxoid, CDT (under eight years of age), or diphtheria toxoid diluted for adult use, ADT (more than eight years of age). For previously unimmunised or incompletely immunised contacts: • Start primary immunisation. • Give oral erythromycin for seven days. • Keep under daily medical surveillance.

Preventive Measures Diphtheria toxoid is recommended for all persons at two, four, six, 18 months and five years (given as DTP (Triple Antigen)) and at 15 years and every 10 years thereafter (given as ADT). Health workers and those at high risk of patient exposure should be fully immunised and receive 10-year boosters.

Epidemic Measures • Define population groups at special risk. • Immunise the largest possible proportion of the population group involved, especially infants and preschoolers. • Repeat immunisation efforts one month later to provide at least two doses to recipients.

47

Erythema Infectiosum (also known as ‘Slapped Cheek Disease’ and ‘Fifth Disease’) Victorian Statutory Re quirem ent

Public Health Significance and O c c u r re n c e

Notification is not required.

Human parvovirus infection occurs worldwide and is a common childhood disease. Outbreaks occur during

School exclusion is not required.

winter and spring. Up to 50 per cent of susceptible household contacts and 10–60 per cent of child care or

Infectious Agent Human parvovirus B19.

school contacts may be infected during outbreaks.

Method of Diagnosis

Clinical Features

The diagnosis can usually be made on clinical grounds.

Human parvovirus B19 infection causes a mild illness,

Serological tests for IgG and IgM antibodies can be

with little or no fever but a striking redness of the cheeks

performed on serum and amniotic fluid.

(hence ‘slapped cheek disease’). This is followed one to four days later by a lacy pink rash on the trunk and limbs

PCR can be used for confirmation of the above.

that fades but may recur over several weeks on exposure to heat. The illness may also cause headache, itch and

Electron microscopy can also be performed on foetal

upper respiratory tract symptoms.

tissue.

In adults, the rash is often atypical or absent but pain,

Other diagnostic techniques may be available in some

inflammation and swelling of joints may occur and, rarely,

specialised centres.

persist for months. Asymptomatic infection is common.

Reservoir Humans.

Several groups of people are at particular risk from the effects of parvovirus infection on developing red blood cells. Persons with chronic haemolytic diseases (for example, sickle cell disease) may develop transient aplastic crises after parvovirus infection, and immunosuppressed persons may develop severe chronic anaemia. Adverse effects from parvovirus infection during pregnancy are uncommon, but infection of the foetus may cause foetal anaemia, hydrops foetalis and foetal death (in fewer than 10 per cent of cases of maternal infection). Parvovirus infection has been associated with spontaneous abortion, but does not appear to cause congenital abnormalities.

49

Mode of Transmission

Pregnant Women

The infection is transmitted by contact with infected

A pregnant woman who believes she has been in

respiratory secretions. It may be spread vertically from

contact with a case of parvovirus infection should

mother to foetus and, rarely, by transfusion of blood or

consult the doctor supervising her pregnancy.

blood products. Antibody testing is available at VIDRL and this may

Incubation Period

assist doctors advising women who are pregnant or

Usually one to two weeks.

parvovirus infection poses.

Period of Communicability Children with erythema infectiosum are most infectious

contemplating pregnancy of the risk, if any, which

There is no risk to women who have antibodies due to previous infection.

before the onset of the rash, and are probably not infectious after the rash appears. Persons with aplastic crises are infectious for a week after the onset of symptoms. Immunosuppressed persons with chronic infection and anaemia may excrete virus for years.

Preventive and Outbreak Me a s u re s Non-immune persons who are immunosuppressed (due to illness and/or treatment), have chronic haemolytic disorders, or who are pregnant are at risk of potentially serious outcomes from parvovirus infection. All ‘at risk’ persons in close contact with children in

Susceptibility and Resistance Generally 5–10 per cent of preschool children and more than 50 per cent of adults have serological evidence of infection. Infection confers immunity.

settings where parvovirus infection may occur (schools, child care centres, health care facilities and so on) should be advised of the risk that parvovirus infection may pose, and warned of school and child care centre outbreaks.

Control of Case Persons with parvovirus infection need not be excluded from child care or schools. There is no specific treatment for erythema infectiosum. Specialist advice should be sought if a person with immunodeficiency or a blood disorder suffers parvovirus infection. The risk of transmission to staff should be considered when immunosuppressed persons are hospitalised with anaemia associated with parvovirus infection.

50

Information Sheet Erythema Infectiosum (also known as ‘Slapped Cheek Disease’ and ‘Fifth Disease’)

Erythema infectiosum, also known as ‘slapped cheek disease’ or ‘fifth disease’ is a common childhood viral infection caused by human parvovirus B19.

Control Measures • Non-immune persons who are immunosuppressed (due to illness and/or treatment), have chronic haemolytic disorders, or are pregnant are at risk of potentially

Clinical Features Human parvovirus B19 infection generally causes a mild illness with little or no fever but a striking redness of the

serious outcomes from parvovirus infection. • Such ‘at risk’ persons should, if possible, avoid contact with infectious cases of parvovirus infection.

cheeks (hence ‘slapped cheek disease’). This is followed

• A pregnant woman who believes she has been in

one to four days later by a lace-like rash on the trunk and

contact with a case of parvovirus infection should

limbs that fades but may recur over several weeks on

consult the doctor supervising her pregnancy.

exposure to heat. There is no specific treatment for the

• School/child care exclusion is not required.

infection. Adults often have little rash, but may experience joint pains and swelling that are sometimes pro-

If you require further information, telephone the

longed. Many cases experience no symptoms at all.

Infectious Diseases Unit, Human Services, Victoria on (03) 9616 7777.

The diagnosis can usually be made on clinical grounds, but blood tests to confirm current or past infection are

For specific advice relating to infection and pregnancy,

available.

consult the Genetic Clinic, Royal Women’s Hospital or the Foetal Diagnostic Unit, Monash Medical Centre.

Several groups of people are at particular risk from the effects of parvovirus infection on developing red blood cells. People with impaired immunity and/or chronic blood disorders may develop severe anaemia after parvovirus infection. Infection during pregnancy can rarely cause a fatal form of anaemia in the unborn child. Parvovirus infection does not cause congenital abnormalities.

Spread of Infection Parvovirus infection is spread by contact with infected respiratory secretions and can spread rapidly in child care centres and schools. Spread from mother to foetus occurs by blood. The incubation period of the infection is one to two weeks and cases are most infectious before the onset of the rash but are probably not infectious after the rash appears. Persons with impaired immunity may be infectious for much longer. 51

Food- or Water-Borne Illness

Victorian Statutory Re quirem ent Group A notification.

Viruses: • Hepatitis A virus. • Norwalk and Norwalk-like viruses (small round structured viruses—SRSV). • Rotavirus.

Food handling exclusion.

Parasites: School exclusion.

• Cryptosporidium spp. • Entamoeba histolytica.

Infectious Agent

• Giardia lamblia.

The more common infectious agents of food- or waterborne illnesses are bacteria, viruses and certain parasites. The illness may also be caused by:

Note

Refer to specific sections for more details.

• Heavy metals that can produce acute gastrointestinal symptoms. Some of these are antimony, cadmium, copper, lead, tin and zinc. • Fish toxicants that may be present in shellfish or fish from Queensland resulting in conditions such as

Clinical Symptoms Symptoms vary with the infectious agent and range from slight abdominal pain and nausea to retching, vomiting, abdominal cramps and diarrhoea—all of varying severity.

paralytic shellfish poisoning or ciguatera. • Plant toxicants naturally occurring in some foods such as toxic fungi and potatoes. • Toxic cyanobacteria (blue green algae) in water. Some of the infectious agents are bacteria and their enterotoxins, viruses and parasites.

Bacteria and their enterotoxins: • Toxin in food: – Staphylococcus aureus. – Clostridium botulinum. – Bacillus cereus. • Toxin in gut: – Clostridium perfringens. – Campylobacter spp, E. coli. – Listeria monocytogenes. – Salmonella serovars. – Shigella spp.

Vomiting, with or without diarrhoea, abdominal cramps and fever are common symptoms of viral disease or staphylococcal intoxication. Symptoms may be severe enough to result in hospitalisation. The gastrointestinal symptoms may be accompanied by fever, chills, malaise and muscular pains. The duration of illness varies: short-lived (lasting 24–48 hours in viral and staphylococcal infections), to days, even weeks, in salmonellosis and campylobacteriosis. Certain food-borne illnesses can present with meningitis or septicaemia (listeriosis) or with neurological symptoms (paralytic shellfish poisoning, botulism).

– S. Typhi/Paratyphi. – Vibro cholerae/V. parahaemolyticus. – Yersinia enterocolitica.

53

Public Health Significance and Oc c u r re n c e Occurrence is worldwide with sporadic cases and common source outbreaks reported. Incidence varies from country to country.

Water is rendered unsafe by human or animal faecal contamination. Food may be contaminated by contact with raw materials, including animal products, environmental pathogens or carrier humans or animals.

In Victoria, outbreaks where food and water have been implicated have occurred in association with hospitals,

Incubation Period

school camps, nursing homes and restaurants.

Typically short for toxin-producing bacteria and longer for the others (see chart).

In recent years, there has been an increasing number of documented outbreaks of viral origin, especially SRSV.

Method of Diagnosis

Period of Communicability Viruses: Generally during the acute phase and up to two days after recovery.

Bacteria: • Isolation from faeces or implicated food.

Bacteria: Generally during the acute diarrhoeal stage.

• Detection of toxin.

Parasites: Refer to relevant sections. Parasites: Microscopy of fresh or appropriately preserved faeces.

Viruses:

Susceptibility With most infections, susceptibility is general.

• Electron microscopy (EM) of stools. • Immune EM.

Rotavirus and E. coli occurs typically in infants and

• Paired sera from patients to detect seroconversion.

young children.

• Seek advice from VIDRL or from MDU regarding other specific tests.

SRSV is found in older children and adults.

Reservoir

Investigation Procedures

Soil, dust, cereals.

• Verify diagnosis. • Obtain case histories to determine if outbreak has

Fish, birds, reptiles, wild and domestic animals for most bacteria and parasites.

occurred. • Estimate incubation period, duration of illness (if possible) to indicate likely infectious agent (see chart).

Humans for viruses.

• Obtain food history for the 72 hours before onset of illness (from other exposed, but asymptomatic, per-

Mode of Transmission The mode of transmission is mainly faecal-oral, but sometimes person to person or airborne. 54

sons as well). • Inform MDU and Virology Laboratory of impending samples.

• Obtain clinical specimens of:

Avoidance of contamination of food. This can be

– Faeces. Forward to MDU.

achieved by:

– Blood (if collected). Forward to VIDRL.

• Providing raw materials of better microbiological

– Suspected food/water. Forward to MDU. • Investigate place where foods are produced or prepared. • Trace source of contamination.

quality. • Educating food handlers about proper food processing, preparation, storage and in personal hygiene. • Adopting the following ‘Ten Golden Rules for Safe Food Preparation’ developed by WHO:

Control of Case

– Choose food processed for safety.

As appropriate, ranging from supportive treatment and

– Eat cooked food immediately.

rehydration, to hospitalisation.

– Store cooked food carefully.

– Cook food thoroughly.

– Reheat cooked food thoroughly. Exclusion from food handling and schools and children’s services centres.

– Avoid contact between raw foods and cooked foods. – Wash hands repeatedly.

Exclusion from nursing duties if employed in an area with

– Keep all kitchen surfaces meticulously clean.

high-risk patients such as special care nurseries or

– Protect food from insects, rodents, and other

nursing homes.

animals. – Use pure water.

Note

Cases are excluded until diarrhoea has ceased.

Incorporation of HACCP (Hazard Analysis Critical Control Point) system into good manufacturing practices for food

Control of Contacts/ En v i ro n m e n t

industries.

Contacts who are food handlers may require surveil-

Epidemic Measures

lance.

• Withdraw implicated food from sale. • Close implicated source of water or issue boiling order

Implicated food (if in retail outlets) to be withdrawn from sale.

on water supplies. • Issue closing order on food establishments if necessary.

Investigation of place of manufacture/preparation of

• Issue public warning if necessary.

incriminated food and institute corrective action.

Preventive Measures Prevention of the contamination of potable water. Contaminated water should be treated by adequate filtration and disinfection, or by boiling.

55

Common Food- or Water-Borne Pathogens Causative Agent

Incubation Period

Duration of Illness

Predominant Symptoms

Foods Commonly Implicated

2–5 days occ.

Sudden onset of

Raw or undercooked

>10 days

diarrhoea, abdominal

poultry, raw milk,

pain, nausea, vomit-

meat, untreated

ing.

water.

Bacteria Campylobacter jejuni

E. coli enteropatho-

3–5 days

Severe colic, watery

Many raw foods,

genic, enterotoxigenic, (enterotoxigenic)

12–72 hrs

3–14 days

to profuse diarrhoea,

unpasteurised milk,

enteroinvasive,

sometimes bloody.

contaminated water,

See also Haemolytic

minced beef.

longer in others

enterohaemorrhagic

Uraemic Syndrome. Salmonella serovars

6–72 hrs

3–5 days

Abdominal pain,

Meat, chicken, eggs

diarrhoea, chills,

and egg products.

fever, malaise. S. Typhi/Paratyphi

Typhoid 1–3 weeks

Days–weeks (chronic

Sustained fever,

Raw shellfish, salads,

Paratyphoid 1–10

carriers occur)

headache, constipa-

contaminated water,

tion rather than

foods from unsafe

diarrhoea—systemic

sources.

days

illness.

Shigella spp.

12–96 hrs

4–7 days

Malaise, fever,

Any contaminated

vomiting, diarrhoea

food or water.

(blood and mucus).

Yersinia enterocolitica 3–7 days

V. cholerae

Few hours to 5 days

1–21 days

3–4 days

Acute diarrhoea

Raw meat and

sometimes bloody,

poultry, milk and milk

fever, vomiting.

products.

Asymptomatic to

Raw seafood, con-

profuse dehydrating

taminated water.

diarrhoea.

V. parahaemolyticus

L. monocytogenes

12–24 hrs

1–90 days

1–7 days

Days

Abdominal pain

Raw and cooked fish,

diarrhoea/vomiting of

shellfish, other

moderate severity.

seafoods.

Gastrointestinal

Unpasteurised milk,

symptoms rare; flu-

soft cheese, pate,

like symptoms to

coleslaw.

meningitis/septicaemia; infection in pregnancy can result in abortions, neonatal infection.

56

Common Food- or Water-Borne Pathogens (continued) Causative Agent

Incubation Period

Duration of Illness

Predominant Symptoms

Foods Commonly Implicated

Severe vomiting,

Oysters, clams, other

diarrhoea.

food contaminated by

Viruses Norwalk and other

24–48 hrs

12–48 hrs

SRSV

human excreta. Rotaviruses

24–72 hrs

3–7 days

Malaise, headache,

Contaminated water.

fever, vomiting, diarrhoea. Hepatitis A

15–50 days

Contaminated water,

Usually 1–2

Fever, nausea,

weeks

abdominal discomfort, shellfish, salads. possibly jaundice.

Parasites Cryptosporidium

G. lamblia

1–12 days

1–3 weeks

4–21 days

1–2 weeks to months

Profuse watery

Contaminated water

diarrhoea.

and food.

Loose pale greasy

Contaminated water,

stools, abdominal

food contaminated by

pain.

infected food handlers.

E. histolytica

2–4 weeks

Weeks-months

Colic, mucous or

Contaminated water

bloody diarrhoea.

and food.

Nausea, vomiting,

Cereals, rice, meat

diarrhoea, cramps.

products, soups,

Toxin Producing Bacteria B. cereus

1–6 hours

< 24 hours

(toxin in food)

vegetables.

C. botulinum

12–36 hours

Variable

(Neurotoxin) hence

Canned food, often

blurred or double

home canned food

vision, difficulty

(low acid).

swallowing, respiratory paralysis.

C. perfringens

8–20 hours

24 hours

(toxin in gut)

Sudden onset colic,

Meats poultry, stews,

diarrhoea.

gravies, (often reheated).

Staphylococcus aureus (toxin in food)

30 mins–8 hours

24 hours

Acute vomiting,

Cold foods (much

purging, may lead to

handled during

collapse.

preparation) milk products, salted meats.

57

Giardiasis

Victorian Statutory Re quirem ent

Reservoir Humans.

Group B notification. The possible contribution of domestic (dogs, cats) and School exclusion.

wild animals is unknown.

Infectious Agent

Modes of Transmission

Giardia lamblia.

Person-to-person by hand to mouth transfer of cysts from infected faeces or faecally contaminated surfaces.

Clinical Features

Water-borne outbreaks due to faecal contamination of

A protozoan infection that is usually asymptomatic but

public water supplies.

may present as an acute or chronic diarrhoea, malnutrition, fatigue and abdominal cramps.

Direct transmission of infection from animals to people, and vice versa.

Fat malabsorption may lead to steatorrhoea.

Public Health Significance and Oc c u r re n c e

Incubation Period Usually one to three weeks or longer; on average seven to 10 days.

Giardiasis is a common infection that affects children more frequently than adults. It spreads very easily in institutions such as day care

Period of Communicability It is communicable for the entire period of cyst excretion.

centres among children who are not toilet trained.

Susceptibility and Resistance The rate of asymptomatic carriage may be high.

Susceptibility is general. Asymptomatic carrier rate is high.

Occurrence is worldwide. Infection is frequently self-limited.

Method of Diagnosis The identification of cysts or trophozoites in: • Faeces. • Duodenal secretion. • Mucosa obtained by small intestinal biopsy (rarely indicated). • Repeated examination of stool may be necessary. However, in the presence of strong clinical suspicion, examination of duodenal aspirate would be indicated.

59

Control of Case • Dispose of faeces in a sanitary manner. • Disinfect Soiled clothing and other articles concurrently.

Tre a t m e n t Metronidazole for seven days or tinidazole. Relapses may occur.

Control of Contacts Microscopic examination of faeces of household members and other suspected contacts only if they are symptomatic. There is rarely an indication for case finding or treatment of asymptomatic carriers.

Preventive Measures • Educate families, and adult personnel of day care centres in personal hygiene such as the need for hand washing before meals, after toilet use and changing nappies. • Protect public water supplies against faecal contamination. • Exclude a child from attending school or a day care centre until diarrhoea has ceased.

Epidemic Measures Epidemic investigation of outbreaks of disease, especially in day care centres and institutions, must be based upon documented microbiological diagnosis and consideration of the phenomenon of asymptomatic carriage.

60

Haemophilus influenzae Infections

Victorian Statutory Re quirem ent

Since the introduction of Hib vaccines, there has been a dramatic fall in the number of invasive cases in children under five years.

Group A notification for meningitis or epiglottitis. Epiglottitis also occurs in adults and this diagnosis

Infectious Agent H. influenzae is a Gram-negative cocco-bacillus. Inva-

should be considered when an adult presents with fever and signs of upper respiratory obstruction.

sive infections are commonly caused by serotype b. Immune-suppressed individuals of any age are also at

Clinical Features Meningitis: The onset can be subacute or sudden with fever, vomiting, lethargy and meningeal irritation with a bulging fontanelle in infants and stiff neck and back in older children.

risk of Hib infection.

Method of Diagnosis Presumptive diagnosis based on Gram strain of CSF: • CSF culture (meningitis). • Blood culture (meningitis or epiglottitis).

Epiglottitis: The patient, usually a child, presents with signs of upper respiratory obstruction and a characteristic expiratory snore, difficulty in swallowing with drooling of saliva, irritability, restlessness and fever. Complete respiratory obstruction may occur. Note

H. influenzae type b (Hib) may cause other conditions, such as pneumonia, septic arthritis, cellulitis, osteomyelitis and so on. These are not notifiable, but the Department of Human Services would appreciate information

• Throat or epiglottis swabs (epiglottitis). Epiglottal swabbing should not be attempted unless facilities for ensuring a clear airway are immediately available. • Detection of Hib antigen in CSF and/or urine (meningitis or epiglottitis).

Reservoir Humans. It is estimated that approximately 5 per cent of children under six years are colonised with Hib. It is generally carried in the nasopharynx without causing symptoms for a period of months before it disappears.

on cases to increase its knowledge of the epidemiology of these infections.

Carriage rates decline with age, though they are higher in household and other contacts of children with estab-

Public Health Significance

lished Hib infections.

Prior to the introduction of vaccine, Hib infections were the most common serious invasive bacterial infections in children.

Mode of Transmission It is transmitted by droplet infection and discharges from nose and throat during the infectious period.

The mean age in patients with epiglottitis tended to be older than that of patients with meningitis.

The portal of entry is most commonly nasopharyngeal.

Aboriginal children are at a five to six times greater risk of developing Hib disease, and they acquire it at a much

Incubation Period

younger age than do other children.

Unknown. Probably short: two to four days. 61

Period of Communicability

Control of Contacts

It is communicable for as long as the organisms are

All contacts under the age of six years should be placed

present in the nasopharynx.

under surveillance for the earliest signs of illness so that prompt medical attention can be sought.

It is non-communicable within 24–48 hours after starting effective antibiotic therapy.

A surveillance letter should be provided as soon as possible to the parents of contacts in a kindergarten or

Susceptibility and Resistance Prior to the introduction of vaccine, the risk of secondary

day care centre.

cases in household contacts within 30 days of the index

Antibiotic Prophylaxis

case has been estimated to be 3.3 per cent for children

Rifampicin is the drug of choice. It is given in a dose of

under two years, 1.4 per cent for children two to three

20 mg/kg/day once daily for four days (up to a maximum

years, 0.06 per cent for children four to five years, and nil

of 600 mg daily). Note that the dose used is different

over the age of six years.

from that used in meningococcal infections. (For adverse effects and contraindications to rifampicin, see section

Most secondary cases among close contacts occur

on meningococcal infections.) For infants less than one

within the first week after exposure, though late second-

month old, reduce the dose to 10 mg/kg once daily for

ary cases are reported.

four days.

Control of Case

All household members, irrespective of age, should be offered prophylaxis where there are children in the

Cefotaxime, ceftriaxone, or chloramphenicol are used for

household under four years of age (apart from the index

treatment.

case), even if immunised.

The patient should be given a course of rifampicin prior

Chemoprophylaxis for household contacts is useful up to

to discharge from hospital to ensure elimination of the

one month after the index case has been diagnosed,

organism from the nasopharynx (for dosage see below).

though ideally it should be commenced as soon as possible after diagnosis.

If the treated patient is less than two years of age and has not been immunised, a course of Hib vaccine should

In day care centres, kindergartens and so on, all room

be given after discharge from hospital.

contacts, teachers and children should be offered prophylaxis if two or more cases of Hib disease have

Respiratory isolation is recommended for 24 hours after

occurred within a period of 120 days.

the start of treatment. Concurrent or terminal disinfection is not required.

Note

Chemoprophylaxis does not eliminate the need for surveillance, and parents of contacts should be advised of the risk of late secondary cases despite prophylaxis.

62

Investigative Procedures In households with siblings under four years of age, determine if household contacts have been offered chemoprophylaxis and ensure that this is done by treating doctor. Any missed immunisations should be brought up to date. If the child attends a kindergarten, day care centre, baby sitter and so on, determine the last date of attendance, and ensure that surveillance letters are distributed to parents. If more than two cases have occurred in the same day care centre, arrange for chemoprophylaxis for all contacts. Determine if the patient has been immunised against Hib disease. Note

Nose and throat swabs are not routinely recommended.

Preventive Measures All children should receive Hib immunisation, usually at two, four and six months of age, and a booster dose at 18 months. Children at high risk of early disease such as Aboriginal/ Torres Strait Islander (ATSI) children should receive a vaccine that has been demonstrated to give early protection, such as PedvaxHIB. Note

Vaccination may be recommended for older persons who are immune suppressed.

Epidemic Measures Increased surveillance and chemoprophylaxis for all household and day care centre contacts as detailed above. Throat swabs may be indicated in the epidemic situation to assess carriage rates.

63

Information Sheet Haemophilus influenzae type b Infection (Epiglottitis) A case of epiglottitis (swelling of the throat causing difficulty in breathing) has occurred in a child, at this school/creche/child minding centre/kindergarten. This disease is spread through droplets, which may be produced when coughing and sneezing, and may spread to intimate and household contacts. The indications of this illness to look for are fever, sore throat and noisy and difficult breathing. Another serious type of infection by the same bacteria is meningitis, indications of which include intense headache, nausea and often vomiting. Serious signs include drowsiness, neck stiffness, delirium, coma and sudden collapse. Even the earliest sign (that is, fever) in such contacts warrants immediate attention from your local doctor or nearest hospital. Please take this letter with you. If you need any further information, please telephone: Public Health Nurse or Medical Officer, Infectious Disease Unit: (03) 9616 7777.

64

Information Sheet Haemophilus influenzae type b Infection (Meningitis) A case of haemophilus meningitis has occurred in a child, at this school/creche/child minding centre/kindergarten. This disease is spread through droplets, which may be produced when coughing and sneezing, and may spread

to intimate and household contacts. The indications of this illness to look for are fever, intense headache, nausea and often vomiting. Serious signs include drowsiness, neck stiffness, delirium, coma and sudden collapse. Even the earliest sign (that is, fever) in close contacts warrants immediate medical attention from your local doctor or the nearest hospital. Please take this letter with you. If you need any further information, please telephone: Public Health Nurse or Medical Officer, Infectious Disease Unit: (03) 9616 7777.

65

Information Sheet Rifadin (Rifampicin)

Warning • Should not be taken in cases of impaired liver function. • Should not be taken in pregnancy. • Can interrupt the effectiveness of oral contraception. • May produce a reddish colour of the urine, sputum and tears and so discolour contact lenses. • May increase the requirement for anticoagulant drugs. • This medication will usually eliminate the bacterium from the nose/throat.

However, if in spite of taking this medication you or your child develop any of the symptoms of fever, nausea, vomiting, headache, lethargy or neck stiffness, we recommend that you seek immediate medical attention from your local doctor or the nearest hospital. Please take this letter with you. If you need any further information, please telephone: Public Health Nurse or Medical Officer, Infectious Disease Unit: (03) 9616 7777.

66

Hand, Foot and Mouth Disease (Enteroviral Vesicular Stomatitis with Exanthem) Victorian Statutory Re quirem ent

Reservoir Humans.

Statutory notification not required. Note School exclusion not required.

This disease is not related to foot and mouth disease of animals.

Infectious Agent Coxsackievirus group A, mainly type 16.

Mode of Transmission It is transmitted by:

Clinical Features This viral infection occurs mainly in children under 10 years of age and in young adults. It lasts seven to 10

• Direct contact with fluid from the vesicular lesions. • Direct contact with nose and throat discharges and faeces of an infected person. • Aerosol droplet spread.

days. The clinical picture consists of sore throat, fever and vesicular lesions on the buccal surfaces of the cheeks,

Incubation Period Usually three to seven days.

gums and sides of the tongue.

Period of Communicability Papulovesicular lesions of the palms, fingers and soles commonly occur; occasionally maculopapular lesions appear on the buttocks.

It is communicable during the acute stage of disease from nose and throat secretions, and as long as there is fluid in the lesions. Viruses persist in the stools for several weeks.

Public Health Significance and Oc c u r re n c e

Susceptibility and Resistance

Hand, foot and mouth disease occurs worldwide sporadi-

Immunity to the specific virus may be acquired due to

cally and in epidemics; the greatest incidence is in

previous infection.

summer and early autumn. Second attacks may occur with group A coxsackievirus Outbreaks occur frequently among groups of children in

of a different serotype.

child care centres and schools.

Control of Case Method of Diagnosis Usually clinical (viral isolation from nasopharyngeal or stool specimens is rarely indicated).

• Do not exclude children with hand, foot and mouth disease as the virus is present in the faeces for many weeks. • Cover lesions on hands and feet if possible and allow to dry naturally. • Avoid piercing lesions. • Take care with hand washing and disposing of soiled articles. 67

Tre a t m e n t Usually none required. Paracetamol may be used for fever and discomfort.

Control of Contacts Of no practical value.

Preventive Measures Use of hand washing and other hygienic measures at home and at child care centres.

Epidemic Measures General practitioners should be informed about periods of increased incidence of the disease.

68

Information Sheet Hand, Foot and Mouth Disease

This is a viral disease that usually lasts seven to 10 days.

• Exclusion from school and child care centres is not usually recommended because the virus may be

The incubation period is between three to seven days.

present in the faeces for many weeks.

This disease is spread by direct contact with fluid from

Note

the blisters, nose and throat discharges, droplets (sneez-

This disease is not to be confused with foot and mouth

ing, coughing) and faeces (stools).

disease in cattle.

Symptoms • Fever. • Sore throat. • Small, blister-like lesions that may occur on the inside of the mouth, sides of the tongue, palms of the hands, fingers and soles of the feet and nappy area.

To Avoid the Spread of This Disease • Wash hands carefully after handling nose and throat discharges. • Wash hands carefully after handling faeces (nappy changing). • Wash hands carefully after contact with the blister-like lesions. • Allow blisters to dry naturally. • Do not pierce blisters as the fluid within is infectious. • Use separate eating and drinking utensils for each child.

Infectious Period • As long as there is fluid in the blisters. • The faeces can remain infectious for several weeks.

Tre a t m e n t • Usually none is required. • Use paracetamol for fever and any discomfort. Do not use aspirin where there is fever. • The disease itself is not serious. If the child complains of severe headache and fever persists, consult your local doctor immediately. 69

Hepatitis A

Victorian Statutory Re quirem ent

Method of Diagnosis

Group B notification.

recent infection. These antibodies are present for two to

A blood test showing IgM anti-HAV antibodies confirms four months after infection. IgG antibodies alone are

School and child care exclusion (see below).

Infectious Agent Hepatitis A virus (HAV) (RNA picornavirus).

evidence of past infection. Blood biochemical testing shows elevated transaminase levels during the acute phase of hepatitis. Later in the illness, the pattern of liver function tests may be nonspecific.

Clinical Features Illness due to hepatitis A typically causes acute fever, malaise, anorexia, nausea and abdominal discomfort, followed a few days later by dark urine and jaundice. Symptoms usually last several weeks, although convalescence may sometimes be prolonged.

Adults usually experience a distinct illness with acute onset of symptoms and jaundice, but a high index of suspicion is needed to diagnose young children with few symptoms. Related adult cases are a clue.

Reservoir Humans.

Severe illness may rarely occur when hepatitis A complicates pre-existing liver disease.

Mode of Transmission

Infants and young children infected with hepatitis A may

The highly infectious hepatitis A virus is spread by the

have few or no recognised symptoms, and are often

faecal-oral route from person to person directly or via

anicteric (without jaundice).

fomites (contaminated objects). It may also be spread via food or water.

Public Health Significance

Non-cooked foods, such as salads, may be contami-

Hepatitis A occurs worldwide.

nated by infectious food handlers, and filter-feeding shellfish raised in contaminated waters may harbour the

In developing countries, most people are infected during

virus.

childhood. In the developed world, with good sanitation and hygiene, most people now reach adulthood without

The precise timing and mode of transmission are often

experiencing infection. They are, therefore, at risk of

difficult to define.

infection from sporadic low-level transmission that occurs in the community. A large outbreak affecting homosexual men occurred in Australia and overseas during the early

Incubation Period

1990s.

Usually 15 to 50 days; the average 28 to 30 days.

Common source outbreaks due to contaminated food are rare.

71

Period of Communicability Cases are most infectious from the latter half of the incubation period until a few days after the onset of jaundice (corresponding to a peak in transaminase levels in anicteric cases). Most cases are not infectious after the first week of jaundice.

IG is rarely given to persons exposed to a potential common source of hepatitis A (such as food or water) because cases related to such a source are usually recognised too long after the exposure for IG to be effective for the co-exposed persons. Timely administration of IG will prevent or modify clinical illness for approximately six weeks after the dose. However, people exposed and infected before the

Long-term carriage or excretion does not occur.

administration of IG may still experience a mild infection, and may have the potential to infect others if their personal hygiene is not exemplary.

Susceptibility and Resistance Most persons born in Australia after 1945 are suscepti-

Surveillance of contacts in a household or workplace

ble. Immunity after infection is probably lifelong.

should be maintained.

Control of Case

should not be administered for three months after a dose

• Determine the occupation of the case.

of IG, and may also be ineffective if given in the 14 days

• Exclude the case from child care, school or work for

prior to IG. Reschedule such routine vaccinations.

Live vaccines (for example, Mumps-Measles-Rubella)

one week after the onset of illness or jaundice. • Educate the case and family on the need for strict hygiene practices. • Do not prepare family meals while infectious, nor share eating utensils, toothbrushes, towels and face washers. • Dispose of or thoughly wash nappies of infants with hepatitis A.

When the case is a food handler: • Consider serological testing of co-workers to determine whether they have been infected or are susceptible. • Place uninfected susceptible co-workers under surveillance and give them immunoglobulin prophylaxis. These persons remain at a risk of developing mild illness (modified by immunoglobulin) but can generally

Control of Contacts Normal immunoglobulin (IG), 0.02 ml/kg body weight, intramuscularly, is recommended for: • Household and sexual contacts of the case. • Staff and children in close contact with a case in a child care centre. IG is not recommended for usual office, school or factory contacts.

continue to work provided their personal hygiene and

food handling practices are exemplary. • Undertake surveillance for hepatitis A in patrons by seeking a history of exposure to the food premises from cases notified over the next two to three months. • Carefully consider the role of the infected food handler. If transmission to patrons appears likely, consider urgent follow-up of exposed patrons to offer them immunoglobulin prophylaxis. Note that when the index

case is a patron, it is usually too late to offer immunoglobulin prophylaxis to other diners, although

IG must be given within seven to 10 days of exposure to be effective.

personal contacts of the patron case/s should be offered immunoglobulin according to the usual protocol.

72

Control of Environment A source of infection should always be sought. For apparently sporadic cases, consider contact with another known case and recent travel to an area where the disease is endemic. If these do not provide an answer,

The dose is one ml (720 ELISA units) administered intramuscularly into the deltoid. A second dose must be given two to four weeks after the first dose, and a third dose should be given six to 12 months after the first dose.

acquisition from young children, particularly those in child care, should be considered.

Protective immunity is acquired approximately two weeks after the second dose, and long-term immunity (up to 10

A number of cases occurring at the one time should

years) is expected to follow the third dose.

prompt a search for a common source, particularly food or water.

Alternatively, if ‘Havrix 1440’ is used (one ml contains 1440 ELISA units), then a single dose followed by a

Special attention should be given to toilet hygiene in schools and child care centres. Ensure soap and water

booster dose at six to 12 months provides long-term immunity.

are available and are used. Travellers to countries where hepatitis A is common (for Clusters of cases, possibly related to a single source, may require epidemiologic investigation, including case finding and surveillance, and public health measures to prevent further cases.

example, Asia, Africa, Central and South America), have previously been offered short-term protection with immunoglobulin, but should now be offered active vaccination with inactivated hepatitis A vaccine, particularly if their stay is long or ‘rough’.

Preventive Measures

Further indications for vaccine are being considered by

Good hygiene is very important, particularly hand

the NH&MRC. These may include such persons at

washing before eating or handling food and after using

increased risk of hepatitis A infection as staff in child

the toilet.

care centres, residents and staff in institutions for intellectually disabled persons, some health care workers

Inadequate sanitation and housing may contribute to

exposed to the faeces of potentially infected persons,

endemic illness.

homosexual men, injecting drug users and others.

Use IG for contacts.

The role of active immunisation in managing outbreaks has not yet been determined.

Active Immunisation Inactivated hepatitis A vaccine (‘Havrix’, SmithKline Beecham) is licensed for use for persons aged more than five years.

73

Passive Immunisation

When cases occur in three or more staff, attendees or

In most instances where prophylactic immunisation is

families with members at the centre, or new cases occur more than three weeks after the onset of the first case,

undertaken, vaccine should be used.

consider giving IG to all family contacts of all children However, when immunoglobulin is used to provide passive protection, the following dosages are recommended:

aged two years or less at the centre, and all attendees, staff and family contacts of cases.

Food- and Water-Borne Outbreaks The source of such outbreaks is usually recognised too

Dosage of Immunoglobulin

late for IG to be usefully given to persons exposed to the Dosage Person’s Weight (Kg) Under 25 25 to 50 Over 50

Short-Term

source. Long-Term

Prophylaxis

Prophylaxis

(six weeks) (ml)

(5 months) (ml)

0.5 1.0 2.0

1.0 2.5 5.0

Epidemic Measures Outbreaks Associated with Child Care Centres Clusters of cases of hepatitis A associated with child care centres are not uncommon. When centre staff and/ or family of attendees develop hepatitis A, it usually reflects an outbreak of hepatitis among young children at the centre. When one nappy-wearing attendee of a child care centre has hepatitis A diagnosed, IG should be administered to family contacts of the case, to all centre attendees, and to all staff at the centre. When the index case is an older, toilet-trained child, the use of IG within the centre may be restricted to staff in contact with the case, and attendees in the same room as the case. Where several cases of hepatitis A occur in association with a child care centre, it may be necessary to administer IG to a wider circle of contacts of potential cases.

74

Contacts of acutely ill cases should be given IG according to the usual guidelines.

Hepatitis B

Victorian Statutory Re quirem ent Group B notification. School exclusion of acute cases.

Public Health Significance Hepatitis B is carried by an estimated 300 million people worldwide. HBV is a major cause of chronic hepatitis, cirrhosis and hepatocellular carcinoma.

Infectious Agent Hepatitis B virus (HBV) ( a DNA hepadnavirus).

The prevalence of the carrier state varies widely between populations with parts of Africa, Oceania and Asia having carrier rates of approximately 10 per cent.

Clinical Features The onset is usually insidious with anorexia, abdominal discomfort, nausea, vomiting, dark urine and jaundice.

Method of Diagnosis The diagnosis is established by a blood test and clinical features. (See Case Definition.)

Rarely, arthralgia, rashes and renal disease may occur. The severity ranges from inapparent cases to fatal cases of acute hepatic necrosis.

Case Definitions for Hepatitis B The screening definition for hepatitis B infection is the presence of HBV surface antigen (HBsAg) in serum.

Reservoir Humans.

Mode of Transmission Although HBsAg has been found in virtually all body secretions and excretions, only blood, semen and vaginal fluids have been shown to be infectious.

For acute hepatitis B: • IgM core antibody (anti-HBc IgM) detected in serum usually indicates recent infection. • Clinical illness consistent with acute viral hepatitis (jaundice, elevated serum transaminase levels).

Transmission occurs by three main routes: • Percutaneous exposure (when infected body fluids gain entry via inoculation, breaks in skin or by contact with mucous membrane). • Sexual.

For chronic carriers and chronic hepatitis B:

• Perinatal.

• Negative anti-HBc IgM. • Positive anti-HBc IgG or positive anti-HBc total. • No clinical illness consistent with acute viral hepatitis.

Note

• Presence of HBe antigen (HBeAg) indicates high

childhood but not perinatally.

Most cases in Africa and many in Asia are acquired in

infectivity of blood and body fluids. Note

The presence of HBV surface antibody (anti-HBs)

Incubation Period Usually 60 to 90 days. The range is 45 to 180 days.

indicates immunity to HBV.

75

Period of Communicability Blood from infected persons is infective many weeks before the onset of symptoms and remains infective through the acute clinical course of the disease and during the chronic carrier state, which may persist for life. The proportion of infected individuals who become carriers is inversely related to the age at infection. Persons who are HBeAg positive are highly infectious.

Susceptibility and Resistance Usually, the disease is milder and often anicteric in children; in infants it is usually asymptomatic. Protective immunity follows infection if anti-HBs develops and HBsAg is absent. More data are needed on the duration of immunity after immunisation.

76

Serology of Hepatitis B Infection Acute Hepatits

Resolution

Titre Anti-HBs

Anti-HBcIgM

HBsAg HBeAg

INFECTION

Anti-HBcIgG Anti-HBe

6 months

12 months

10 years

Source: Australian Gastroenterology Institue

Chronic Hepatitis B and Failure to Clear Virus Chronic Hepatits

Acute Hepatits

Hepatocellular Carcinoma

Cirrhosis

Titre Anti-HBcIgM HBsAg

Anti-HBclgG HBeAg

6 months 12 months INFECTION

Anti-HBe

10 years

20 years

INTEGRATION

Source: Australian Gastroenterology Institue Hepatitis B: An information Booklet for Health Care Providers

77

Recommendations for Hepatitis B Prophylaxis Following Percutaneous or Permucosal Exposure Treatment When Source Found To Be: Source not Tested HBsAg-positive

HBsAg-negative

or Unknown

HBIG x 1* and initiate HB

Initiate HB vaccine.

If known high-risk source,

Exposed Person Unvaccinated

may treat as if source

vaccine.

were HBsAg-positive. Previously Vaccinated Known sero-conversion

Test exposed for anti-HBs

No treatment.

No treatment.

No treatment.

If known high-risk source,

1. If adequate**, no treatment. 2. If inadequate, HB vaccine booster dose. Known non

HBIG x 2 or HBIG x 1 plus

sero-conversion

1 dose HB vaccine.

may treat as if source were HBsAg-positive.

Unknown sero-conversion

Test exposed for anti-HBs.

No treatment.

Test exposed for anti-HBs.

1. IG inadequate,

1. If inadequate, HB

HBIG x1 plus HB vaccine

vaccine booster dose

booster dose.

plus HBIG x1.

2. If adequate, no

2. If adequate, no

treatment.

treatment.

* Hepatitis B Immunoglobulin (HBIG). Adult dose 400 Units. ** An adequate antibody level is greater than 10 milli International Units per ml, approximately equivalent to 10 sample ratio units (SRU) by radioimmune-assay (RIA) or positive by enzyme-immuno-assay (EIA).

78

Control of Case Exclusion from school and work until the diagnosis is confirmed. Blood and body fluid precautions should be observed until the disappearance of HBsAg and the appearance of anti-HBs.

Paediatric hepatitis B vaccine is given for: • Infants of HBsAg positive mothers (as discussed above). • Infants in ethnic groups of high HBsAg endemicity, whether the mother is a carrier or not. • Children up to 10 years of age in both of the above groups.

Control of Contacts Household contacts should be tested for anti-HBc and

WHO recommends that hepatitis B vaccine should be

HBsAg and offered vaccination if susceptible.

included in all childhood immunisation protocols.

Sexual contacts should: • Be offered HBIG (400 IU IM) within 14 days of sexual contact. • Commence active immunisation at the same time. Infants born to HBsAg positive mothers should: • Be given HBIG (100 IU IM) within 12 hours of birth. • Commence active immunisation within seven days. This can be given at the same time as HBIG but at a separate site.

Preventive Measures Pre-exposure vaccination is recommended for: • Health care workers. Individual risk depends on HBsAg carrier rate in the population served, degree of blood (not patient) exposure, and thoroughness of hygiene measures in dealing with blood. • Haemodialysis patients and recipients of blood products such as factors VIII and IX. • Residents and staff in institutions for the intellectually disabled. • Those with multiple sexual contacts. • Injecting drug users. • Household and sexual contacts of hepatitis B virus carriers. • Inmates of long-term correctional facilities.

79

Hepatitis C

Victorian Statutory Re quirem ent Group B notification.

Infectious Agent Hepatitis C virus (HCV), a small RNA virus, is closely related to the flaviviruses and animal pestiviruses.

Approximately 20 to 30 per cent of chronic carriers may progress to liver cirrhosis within a period of about 20 years, and a proportion of those with cirrhosis will develop primary liver cancer within a further five to 10 years. There are at least six major genotypes of HCV and it is thought that some are more pathogenic than others. It is also believed that repeat infection of a HCV carrier with a different strain may exacerbate underlying liver disease.

Clinical Features

At present, the main genotypes found in the Australian

Most patients with HCV are asymptomatic.

population are 1 (52 per cent), 3 (41 per cent) and 2 (7 per cent).

In the acute stage, patients develop elevated serum alanine aminotransferase (ALT) levels. Up to 25 per cent of patients may develop jaundice.

Method of Diagnosis Laboratory diagnosis is based on detection of antibodies directed against the products of expressed clones or

Symptoms and signs, when they occur, are similar to other forms of hepatitis, but are usually milder than those

peptides of the hepatitis C virus and/or demonstration of HCV RNA by polymerase chain reaction (PCR).

seen in hepatitis B. First generation enzyme immunoassay (EIA) became The majority of patients progress to the chronic carrier state that is also, in most cases, asymptomatic. Symptoms, when they occur, may be non-specific and include

available in Australia in 1990 and since then the second and third generation EIAs have improved sensitivity and specificity.

fatigue, headaches and nausea. Supplemental tests are also available in the form of recombinant immunoblot assays (RIBA). Equivocal

Public Health Significance and O c c u r re n c e

reactivity by EIA tests and indeterminate reactivity by RIBA testing remains problematic in low-risk groups.

Hepatitis C occurs worldwide. A positive PCR test is a marker for viraemia and infectivThe estimated prevalence in the Australian community based on blood donor screening is 0.14 to 0.45 per cent,

ity, but a negative PCR does not rule out infection as viraemia may be intermittent.

but the percentage of HCV positive individuals is higher in certain groups, such as injecting drug users. In injecting drug users, seropositivity approaches 100 percent in those injecting for more than eight years. Infection with HCV results in the chronic carrier state in over 70 per cent of cases.

Current EIA tests cannot distinguish between patients who are currently infectious and those who have recovered from infection and developed immunity.

Reservoir Humans. 81

Mode of Transmission

Incubation Period

It is primarily transmitted by blood-to-blood contact.

Ranges from two weeks to six months—most commonly six to nine weeks after which serum ALT levels rise.

In Australia and other Western countries, sharing inject-

Current HCV antibody tests become positive two to three

ing equipment by drug users is the most common mode

months after exposure.

of transmission. Tattooing, earpiercing and body piercing using unsterile equipment are other potential sources.

Period of Communicability Communicability occurs during the acute clinical stage and indefinitely in the chronic carrier stage.

Health care and laboratory staff handling blood and blood products are at increased risk. The risk of con-

All HCV positive individuals need to be considered

tracting hepatitis C from a needle-stick injury from a

potentially infectious.

seropositive source has been estimated at 3 per cent, compared to 0.3 per cent for HIV infection and 30 per cent for hepatitis B infection. Sexual transmission rates of HCV are very low, but the

Susceptibility and Resistance Susceptibility is general. The degree of immunity following infection is unknown.

risk is increased if the HCV positive partner is immunocompromised as the virus titre may be increased.

Control of Case The patient needs to be considered for possible Inter-

Mother-to-baby transmission is also very low but may be

feron therapy that is available, for selected patients,

increased if the mother is also infected with HIV or has a

under the Highly Specialised Drugs Program of the

high titre of HCV in the blood. The risk of transmission

Commonwealth at certain liver clinics in Melbourne.

through breast milk is considered minimal. Assessment would include examination for signs of liver Community or household transmission of HCV is consid-

disease, monitoring of the ALT levels and a PCR test.

ered rare.

Advice should be sought from a liver clinic when necessary.

A proportion of HCV individuals do not fall into any known subgroup. It is thought that some may have had

About 50 per cent of patients treated with Interferon

exposure to injecting drugs many years ago that they

respond initially, but about 50 per cent of these relapse

have forgotten or are unwilling to discuss.

after treatment ceases.

Poorly cleaned needles used by medical practitioners in some countries, and cultural practices that involve skin piercing, are other potential sources of infection.

82

Counselling of the patient is a very important part of the management. This counselling should include: • Likely source of the infection. • Current knowledge of the natural history. • Possible symptoms. • Advice on prevention of further transmission of infec-

Preventive Measures • Use standard precautions by all health care providers with potential contact with blood or body fluids. • Use disposable equipment for all skin penetration procedures, or use adequate sterilisation methods when reusable needles are used for any procedure.

tion. • Lifestyle issues, such as immunisation against hepatitis B, minimisation of alcohol intake, cessation of smoking, healthy diet. The patient should be advised not to: • Donate blood or body organs. • Share injecting equipment. • Share personal items such as toothbrushes or razors. They should also be advised to: • Advise any health care providers of their HCV status when undergoing any dental or medical procedure. • Wipe up any blood spills with household bleach and disposable paper towels. • Cover any cuts or wounds with a dressing. • Place blood-stained paper tissues, sanitary towels or dressings in a plastic bag before disposal. • Use ‘safer sex’ practices. People in long-term stable relationships will need to discuss condom use with their health care provider.

Control of Contacts There is no vaccine available for hepatitis C. The role of prophylactic immunoglobulin for contacts has not been established.

83

Hepatitis D

Victorian Statutory Re quirem ent

Incubation Period Not firmly established.

Group B notification (as hepatitis non-A, non-B, or associated with hepatitis B).

Period of Communicability Blood is potentially infectious during all stages of active

Infectious Agent

HDV infection.

Hepatitis D virus (HDV) is a virus-like particle consisting of a coat of HBsAg and a unique internal antigen (delta antigen). (Replication can only occur in the presence of hepatitis B virus.)

Clinical Features Two types of infection with hepatitis D occur:

Control of Case As for hepatitis B.

Control of Contacts As for hepatitis B.

• Co-infection: simultaneous acute infection with HBV and HDV. This usually causes a self-limited hepatitis. • Superinfection: HDV infection in a HBV carrier. This often causes a fulminant acute hepatitis that

Susceptibility and Resistance All persons who are susceptible to hepatitis B or who are HBV carriers can be infected with HDV.

progresses to chronic active hepatitis. Among HBV carriers, avoiding exposure to any potential

Public Health Significance and Oc c u r re n c e

source of HDV is the only effective measure.

Two general epidemiological patterns are recognised: • Endemic infection occurs in Italy, the Middle East, some areas of Africa and South America, although the ratio of the two infections varies widely with location. Transmission occurs primarily within the household setting. • Non-endemic infection occurs in Australia, North America and Western Europe, where HDV occurs sporadically in the HBsAg population and is largely confined to the risk group of injecting drug users.

Method of Diagnosis Identification of HDV antigen or anti-HDV in the serum.

Mode of Transmission The mode of transmission is similar to hepatitis B (see

Public Health Significance). 85

Hepatitis E

Victorian Statutory Re quirem ent

Incubation Period

Group B notification (as hepatitis non-A non-B).

to 42 days in different epidemics.

Infectious Agent

Period of Communicability

Hepatitis E virus (RNA virus).

Unknown.

Clinical Features

Susceptibility and Resistance

Clinical course is similar to that of hepatitis A.

Susceptibility unknown.

A high mortality rate (up to 40 per cent) has been de-

Control of Case

scribed in pregnant women affected in their third trimester of pregnancy.

Two weeks to two months; the mean has varied from 26

• Determine occupation of the patient. • Exclude the patient from food handling until at least one week after the onset of jaundice.

Public Health Significance and O c c u r re n c e Sporadic and epidemic cases have occurred in India,

• Educate the patient on the need for strict hygiene practices such as hand washing after toilet and before eating.

areas of the former Soviet Union, some African countries, Mexico and parts of Asia.

Control of Contacts No specific measures.

Imported cases have been identified in Australians, and one case in the Northern Territory in a patient who had not been overseas.

The efficacy of immunoglobulin has not been established.

Method of Diagnosis Immune electron microscopy of faeces. Serological tests, including fluorescent antibody assay and EIR, are available through VIDRL.

Reservoir Humans, transmissible to some other primates.

Mode of Transmission Hepatitis D can be transmitted: • From contaminated water. • Person-to-person by the faecal-oral route. 87

Herpes Simplex

Victorian Statutory Re quirem ent

Public Health Significance and O c c u r re n c e

Statutory notification not required.

Asymptomatic infections with HSV type 1 virus are common. Seventy to 90 per cent of adults have circulat-

Infectious Agent

ing antibodies to HSV type 1 virus, indicating previous infection.

Human herpes virus 1 and 2 (HSV). HSV type 1 is a common cause of meningoencephalitis.

Clinical Features This viral infection is characterised by a localised primary lesion, latency and a tendency to local recurrence. The two causal agents, HSV types 1 and 2, generally produce distinct clinical syndromes, depending on the

Vaginal delivery in pregnant women with active genital infection carries a high risk to the newborn. It can cause disseminated visceral infection, encephalitis and death. HSV type 2 has been associated with aseptic meningitis.

portal of entry.

Method of Diagnosis HSV type 1:

Cytologic changes in tissue scrapings or biopsy.

• The primary infection may be mild and generally occurs in early childhood before the fifth year of life. • About 10 per cent of primary infections cause a more

Confirmation by direct FA tests or isolation of the virus from oral or genital lesions.

severe form of disease manifested by fever and malaise. • This may last a week or more, and is associated with

Techniques are available differentiate type 1 from type 2 antibody.

vesicular lesions in the mouth, eye infection or a generalised skin eruption complicating chronic eczema. • Reactivation of latent infection results in cold sores

Reservoir Humans.

appearing as clear vesicles on an erythematous base, usually on the face and lips, which crust and heal in a few days. • This reactivation may be precipitated by trauma, fever or intercurrent disease.

Mode of Transmission Contact with type 1 in the saliva of carriers is the most important mode of spread.

HSV type 2:

Infection on the hands of health care personnel from

• This virus is the usual cause of genital herpes, al-

patients shedding HSV results in an infection of the tip of

though this can also be caused by type 1 virus.

the finger. It begins with intense itching and pain, and is

• Genital herpes occurs mainly in adults and is sexually transmitted.

followed by deep vesicle formation and tissue destruction.

• Primary and recurrent infections occur, with or without symptoms.

89

Transmission of HSV type 2 to non-immune adults is usually by sexual contact.

Preventive Measures • Emphasise personal hygiene to minimise the transfer of infectious material.

Incubation Period Usually two to 12 days.

• Avoid contamination of the skin of patients with eczema. • Wear gloves when in direct contact with infectious lesions and wash hands with soap and water after-

Period of Communicability Secretion of virus in the saliva may occur up to seven weeks after recovery from stomatitis.

ward. • Advise cesarean section before membranes rupture when primary or recurrent genital infections occur in late pregnancy because of the risk of neonatal infec-

Patients with primary genital lesions are infective for

tion.

seven to 10 days. Those with recurrent disease are infective for four to seven days.

Epidemic Measures Not applicable.

Susceptibility and Resistance Severe extensive disease may occur in immunosuppressed individuals.

Control of Case The patient should be kept away from newborns, children with burns or eczema, and immunosuppressed patients.

Tre a t m e n t Treatment includes: • Idoxuridine (Stoxil) for cutaneous lesions. • Povidone-iodine ointment and paint (Betadine). • Acyclovir (Zovirax tablets) for initial and recurrent genital herpes. • Acyclovir intravenous infusion for H. simplex encephalitis and immunosuppressed patients.

Control of Contacts Contact isolation is necessary only for neonatal or severe primary lesions. No immunisation is available.

90

Hydatid Disease

Victorian Statutory Re quirem ent

As result of the success of the Tasmanian hydatid control campaign, no new cases of human hydatid disease has been reported from Tasmania for the past decade.

Group B notification. Cases notified in Victoria are usually those who have a

Infectious Agent Echinococcus granulosus (dog tapeworm).

long standing history of infection that was acquired from areas such as Greece, Cyprus or the former Yugoslavia, or from areas in rural Victoria. A few cases of recently acquired hydatid infection occur in visitors to rural areas

Clinical Features

where there are infected sheep or dingoes. The mode of

Hydatid disease is produced by cysts that are the larval

transmission is the urban dog that accompanies the

stages of the tapeworm Echinococcus.

traveller. People who trap wild dogs are similarly at risk.

Symptoms depend on the location of the cyst, and

Method of Diagnosis

develop as a result of pressure, leakage or rupture.

Dignosis can occur by plain X-ray, ultrasound or CT. The most common site for the cysts is the liver; less commonly brain, lungs, kidneys, and uncommonly the heart, thyroid and bone.

If a cyst ruptures, examine for protoscolices, brood capsules and cyst wall in sputum, vomitus, faeces and urine.

Cysts remain viable or die and calcify. They may be detected on routine X-ray.

Serological Tests Screening, ELISA and IHA.

Prognosis is generally good and depends on the site and potential for rupture and spread.

Diagnosis, Immune electrophoresis (IEP), IHA and ELISA.

Sudden rupture of the brood capsules and liberation of the daughter cysts may cause fatal anaphylaxis.

IEP is used as a follow-up after surgery or chemotherapy (negative within two years of surgical cure).

Persons who have a calcified cyst detected on X-ray may have active infection.

Public Health Significance and Oc c u r re n c e

There is no longer a place for the Casoni skin test.

Reservoir Dogs, foxes and dingoes.

Occurrence is worldwide. Sheep are the major intermediate hosts. Pigs, goats and It is mainly associated with sheep farming.

some species of wallaby and kangaroo can act as intermediate hosts.

In Australia, most human cases are notified from New South Wales, followed by Western Australia, the Australian Capital Territory, Victoria and Queensland. 91

Mode of Transmission

Tre a t m e n t

Infection occurs by hand-to-mouth transfer of tapeworm

Surgery is the treatment of choice.

eggs from dog faeces. The larvae penetrate the intestinal mucosa, enter the portal system and are carried to

Mebendazole (Vermox) is used when surgery is contrain-

various organs where they produce cysts in which

dicated.

infectious protoscolices develop. Albendazole (special access scheme) has been used The important life cycle is dog-sheep-dog. A

successfully.

dingo-wallaby-dingo (or wild dog) sylvatic cycle also occurs. A dog-wild pig-dog cycle has recently been recognised with risks for hunters from urban areas.

Control of Contacts Household contacts should be examined for evidence of

Incubation Period Variable: from months to years.

infection. Dogs in contact with the patient should be investigated (obtain advice from the Department of Natural Resources

Period of Communicability It is not communicable through person-to-person transmission.

and Energy).

Preventive Measures • Educate the public on the danger of close association

Dogs pass eggs approximately seven weeks after

with dogs and on the need to wash hands after contact

infection.

with dogs. • Treat infected dogs and destroy unwanted dogs.

In the absence of reinfection, this ends in about one year.

• Control the slaughter of animals, particularly sheep. The area should be enclosed to prevent access by dogs and have adequate drainage, an incinerator and/

Susceptibility and Resistance Children are more often infected than adults.

or disposal pit. • Do not allow children to play with strange dogs, especially in rural areas. • Dispose of animal carcasses as soon as possible.

Control of Case No need for isolation, or concurrent disinfection. No vaccine is available.

• Report all stray dogs to the local council. • Destroy wild and stray dogs in highly endemic areas. • Control dogs on farms at all times and do not allow them to have access to vegetable gardens. • Treat all dogs for E. granulosus regularly (every six weeks) in rural or endemic areas with praziquantel (Droncit). • Do not feed offal to dogs.

92

Impetigo

Victorian Statutory Re quirem ent

Mode of Transmission

Statutory notification not required.

with patients or asymptomatic carriers.

School exclusion.

It is rarely transmitted through indirect contact with

Impetigo can be transmitted by direct or intimate contact

objects or hands.

Infectious Agent Streptococcus pyogenes (Group A streptococci).

Period of Communicability It is communicable while active lesions persist.

Staphylococcus aureus.

Susceptibility and Resistance Clinical Features

Susceptibility to streptococcal and staphylococcal skin

It is a superficial vesiculo-pustular skin infection seen

infection is general.

mainly in children. It begins as a papule that vesiculates and then breaks leaving a denuded area covered by a honey-coloured crust. Local lymph nodes may be enlarged and the affected child may be acutely ill.

Control of Case Local treatment-crusts should be bathed with cetrimide 0.1 per cent lotion or saline or water. General bathing with antibacterial soap such as Sapoderm or Gamophen should occur. The lesions should be covered with a watertight dress-

Public Health Significance and Oc c u r re n c e Occurrence is worldwide. Impetigo is a rapidly spreading, highly infectious skin rash that frequently occurs in children’s settings such as

ing. Treatment should continue until lesions have healed. In outbreak situations, lesions should be swabbed and systemic antibiotic given for severe cases.

day care centres, kindergartens and schools. Flucloxacillin is usually used for staphylococal impetigo.

Method of Diagnosis

The child should be excluded from child care settings

Culture taken from active skin lesions.

until sores have fully healed. The child may be allowed to return earlier provided that

Reservoir

appropriate treatment has begun and sores on exposed

Humans.

surfaces such as scalp, face, hands or legs are properly covered with moisture-proof dressings.

93

Preventive Measures Personal hygiene. Public education in modes of transmission and possible complications. The necessity for completing a full course of antibiotic therapy when prescribed should be reinforced within the community.

Epidemic Measures • Investigate if a cluster of two or more concurrent cases occur in a hospital nursery or maternity ward. • Take swabs from all patients, care personnel and search for active lesions. • Investigate if a a large number of cases occur in schools and community settings. • See attached sheet of investigative procedures for protocol.

Epidemic Investigative Procedures for Impetigo Case: • Obtain swab of discharging lesion. • Obtain nasal swab. • Instruct patient to cover active lesion with dressings. • Dispose of soiled dressings appropriately. • Educate regarding personal hygiene. Emphasise hand washing, especially after changing dressings, and the importance of avoiding sharing toilet articles, towels or clothing. • Instruct on the use of anti-bacterial soap for bathing for two to three weeks (Gamophen soap). Contacts: • Obtain nasal swabs. • Educate about modes of transmission. Environment: • Trace source of infection. • Swab communal laundry facilities if applicable. • Educate public in modes of infection and personal hygiene. 94

I n fl u en z a

Victorian Statutory Re quirem ent

Method of Diagnosis

Statutory notification not required.

from nasopharyngeal aspirate or throat washing by the

Inluenza can be diagnosed by isolation of influenza virus FA test (send specimens to VIDRL).

Infectious Agent

It can be confirmed by virus culture.

Influenza virus (A, B, C). Influenza A virus subtypes are classified by the antigenic uniqueness of the surface glycoproteins haemagglutinin (H) and neuraminidase (N).

Serology In outbreak situations, special arrangements can be made with the WHO Collaborating Centre for Influenza References and Research and the Commonwealth

Clinical Features It is an acute respiratory tract illness characterised by

Serum Laboratories for the isolation of influenza virus. (Contact Mr Alan Hampson, Deputy Director.)

fever, headache, myalgia, prostration, coryza, sore throat and cough. Recovery is usual in two to seven days; however, cough may be longer lasting.

Reservoir Humans. Animal reservoirs are suspected as sources of new human subtypes (perhaps by reassortment with human strains) and may occur particularly when people and livestock (for example, pigs, ducks) live closely

Public Health Significance and Oc c u r re n c e

together.

Influenza occurs as pandemics, epidemics and as

Mode of Transmission

sporadic cases.

It is predominately transmitted by airborne spread. Transmission also occurs by direct contact through

Type A viruses cause most epidemics. Mixed A and B

droplet spread.

epidemics also occur. Direct contact may be important as the virus will survive The emergence of completely new subtypes of A virus

some hours in dried mucus.

(antigenic shift) occurs at irregular intervals and is responsible for pandemics. Minor antigenic changes (antigenic drift) are responsible

Incubation Period Usually one to five days.

for annual epidemics and regional outbreaks. During major epidemics, severe disease and complica-

Period of Communicability

tions (especially viral and bacterial pneumonia) occur

It is probably communicable for three to five days from

primarily among the elderly and those debilitated by a

clinical onset in adults; up to seven days in young

chronic disease.

children.

In temperate zones, outbreaks tend to occur in winter. 95

Susceptibility and Resistance When a new subtype appears, all are susceptible except those who have lived through earlier epidemics caused by a related subtype.

• Aboriginal and Torres Strait Islander adults over 50 years of age, partly because of the greatly increased risk of premature death from respiratory disease. • Children with cyanotic congenital heart disease. • Staff caring for immunosuppressed patients.

Infection produces immunity to the specific infecting virus, but the duration and breadth of immunity depends on the degree of antigenic drift and the number of previous infections.

Control of Case Symptomatic treatment only.

• Staff and residents of nursing homes and other chronic care facilities. • Adults and children receiving immuosuppressive therapy.

Epidemic Measures Surveillance of the extent and progress of the epidemic and reporting of findings to the community are important.

Amantadine given early in the course of influenza A is said to reduce symptoms and virus titre in respiratory secretions but is not routinely used.

Control of Contacts No routine measures. Chemoprophylaxis with amantadine may be considered, in special circumstances, against influenza A strains.

Preventive Measures Inactivated influenza vaccine is formulated annually so that changes in composition can be made to counter antigenic shifts and antigenic drift. The vaccine confers about 70 per cent protection against infection for approximately 12 months. Annual immunisation is recommended for individuals in the following categories: • Persons over 65 years of age. • Adults and children with chronic debilitating disease, especially those with chronic cardiac, pulmonary, renal and metabolic disorders.

96

Infectious Mononucleosis (Glandular Fever)

Victorian Statutory Re quirem ent

Method of Diagnosis

Statutory notification not required.

lymphocytes of 50 per cent or more, including 10 per

A full blood examination shows mononucleosis and cent or more atypical cells.

Infectious Agent

Paul Bunnell Test.

Epstein-Barr virus (EBV). Liver Function Tests (AST, ALT) abnormal.

Clinical Features It is an acute viral infection affecting mainly young adults.

Serological ELISA IgG and IgM for viral capsid antigen.

Clinical features include fever, sore throat (usually with exudative pharyngotonsillitis) and lymphadenopathy.

ELISA IgG for nuclear antigen, takes two to three months to become positive.

Splenomegaly occurs in 50 per cent of cases; jaundice in 4 per cent.

Reservoir Humans.

In young children the disease is mild or asymptomatic. Duration is from one to several weeks. The disease is rarely fatal.

Mode of Transmission It is transmitted by person-to-person spread by the oropharyngeal route via saliva.

A chronic form is suggested as one of the causes of Chronic Fatigue Syndrome.

Young children may be infected by saliva on the hands of attendants or on toys.

A syndrome resembling infectious mononucleosis clinically and haematologically may be caused by herpesvirus 6, cytomegalovirus or toxoplasmosis.

Incubation Period From four to six weeks.

Public Health Significance and Oc c u r re n c e

Period of Communicability

Glandular fever is most commonly seen in high school

The period of communicability is prolonged.

and university students. Pharyngeal excretion may persist for a year or more after About 50 per cent of those infected will develop the

infection.

disease that is spread by close, personal contact. Healthy adults may be long-term oropharyngeal carriers. Occurrence is worldwide and widespread in early childhood in developing countries.

97

Susceptibility and Resistance Infection confers a high degree of resistance. Reactivation of EBV may occur in immunosuppressed individuals.

Control of Case Isolation is not necessary.

Tre a t m e n t None. Steroids may be of some value in severe, toxic cases.

Control of Contacts Investigation of contacts is not necessary. No immunisation is available.

Preventive Measures • Use hygienic measures including hand washing to help prevent spread. • Disinfect articles soiled with nose and throat discharges.

Epidemic Measures None.

98

Legionellosis

Victorian Statutory Re quirem ent Group A notification, Prevention of Legionellosis Health (Infectious Diseases) Regulations 1990, Division 3.

• There is usually multi-system involvement with diarrhoea, vomiting, mental confusion, delirium and renal failure. • In epidemics, it has an attack rate of up to 5 per cent and a case fatality rate of around 15 per cent. • Legionnaires’ disease was made notifiable in Victoria in

Infectious Agent

1979.

The infectious agent is Gram negative bacilli belonging to the genus Legionella.

Pontiac fever: • The non-pneumonic form, presents mainly as a flu-like

There are currently more than 30 species, but L.

pneumophila (with 14 recognised serogroups) is responsible for at least 75 per cent of cases in Australia and overseas.

illness with spontaneous recovery and no reported deaths. • It has a high attack rate (95 per cent) and outbreaks have been reported overseas. • Pontiac fever has not been reported in Australia.

Variations in the species/serogroups implicated have

• It was made notifiable in Victoria in May 1990.

been noted in a number of countries at different times. In 1988, L. micdadei accounted for the majority of cases reported in Victoria. In 1993, 20 of the 37 reports of Legionellosis in Victoria were caused by L. longbeachae.

Public Health Significance and O c c u r re n c e Sporadic and epidemic forms of Legionnaires’ disease

Another species, L. bozemanii, has been implicated in Victorian cases.

have occurred overseas and in Australia. Major outbreaks have been reported in South Australia and New South Wales, but not in Victoria.

Though commonly found in aquatic habitats, Legionella spp. are fastidious organisms requiring specific conditions for culture in the laboratory. The bacteria will not grow on conventional culture media.

Most of the overseas outbreaks have been associated with cooling towers and warm water systems. Some outbreaks have occurred in hospitals where the case fatality rate has been high (for example, in 1985 at Stafford District Hospital in the UK, the case fatality rate

Clinical Features

was 28 per cent).

Legionellosis (infection by any Legionella species) is an acute bacterial infection with two recognised presenta-

The largest outbreak in Australia occurred at

tions:

Wollongong, NSW, in 1987 where there were at least 44

Legionnaires’ disease:

cases and 10 deaths. The implicated cooling tower was

• This is the pneumonic form of the illness where the

situated 50 m to 70 m from the Gateway Shopping

patient typically presents with severe pneumonia that

Centre that was visited by most of the cases.

frequently culminates in respiratory failure. • Early symptoms are anorexia, malaise, myalgia and fever (flu-like).

99

In 1988–1989, an outbreak, where L. longbeachae SG1

Reservoir

was implicated, occurred in South Australia. Epidemio-

The bacterium is water-associated and ubiquitous.

logical investigations found an association with the use of potting mix. Further work by the Institute of Medical and

It is often isolated from natural habitats (rivers, creeks,

Veterinary Science, Adelaide (IMVS) found L.

hot springs) and from artificial equipment such as

longbeachae to be present in approximately 70 per cent

cooling towers associated with airconditioning and

of samples of commercial potting mix tested.

industrial processes, and in warm water systems where the temperature is maintained around 43˚C favouring

Case fatality in the Victorian cases is around 20 per cent. Since the disease was made notifiable in 1979, the

proliferation of the bacteria.

L. longbeachae has been found in potting mixes.

number of cases has been slowly increasing over the years, possibly due to increased awareness on the part of the clinician.

Mode of Transmission Legionellosis is transmitted through inhalation of con-

Case Definition and Method of Diagnosis

taminated aerosols. Aerosols of less than five microns are particularly effective in reaching the lower depths of the lungs.

It is diagnosed by a clinically compatible illness (pneumonia) and at least one of the following:

The mode of transmission with potting mix is less clear

• Isolation of Legionella species from lung tissues,

and is under further study.

respiratory secretions, pleural fluid, blood, or other tissues. or • A fourfold or greater rise in (IFA) titre against

Legionella species, to at least 128, between acute and

Incubation Period Legionnaires’ disease: usually five to six days but can range from two to 10 days.

convalescent phase sera (four to six weeks apart). or

Pontiac fever: four to 66 hours.

• A stable high Legionella titre (at least 512) in convalescent phase serum.

Susceptibility

or

Legionnaires’ disease has a low attack rate and males

• Demonstration of Legionella species antigens in urine,

are more frequently affected than females.

lung tissue, respiratory secretions or pleural fluid. In Victoria, the mean age of patients affected is now in Note

the low 60s.

Most cases are diagnosed by serological tests; hence, the diagnosis is usually a retrospective one.

Though the disease can affect any age group, it is rarely reported in children.

Antigen to L. longbeachae was included in the Indirect Fluorescent Antibody (IFA) tests in 1992. This has led to an increase in the number of cases reported due to L. longbeachae. Cultures can take up to 10 days. 100

Other groups at risk include the immunosuppressed, diabetics, those perhaps who smoke and/or consume alcohol excessively, and those with chronic respiratory disease.

Period of Communicability There have been no reports of person-to-person transmission.

The possibility of undetected, associated case/s (mainly through the personnel manager, sickness records and work doctor/nurse, hospital medical records) should be investigated.

Control of Case

Where necessary, meetings should take place with staff,

Specific antibiotic treatment includes erythromycin and

occupational health and safety representatives, union

rifampicin.

representatives to: • Discuss the presentation of disease.

Supportive treatment is needed if there is respiratory

• Allay fears.

failure. To help identify a common source, serology should be Dialysis may be required if there is renal failure.

considered for work colleagues. Tests are generally offered to those who have been away four or more

Investigation

consecutive days with a respiratory illness.

After estimating the onset of illness, the patient’s move-

These tests are, however, of limited value as 13 to 35 per

ments during the incubation period should be estab-

cent of the normal population (WA) and 30 per cent (SA)

lished.

have been found to have antibodies to L. pneumophila serogroup 1.

Inspection should be underatken of places where the following aerosol generating equipment may be present:

Clotted blood, 10 ml should be sent to Legionella Refer-

• Cooling towers.

ence Laboratory, VIDRL. Ample warning should be given

• Fountains or sprinklers.

of expected numbers of specimens.

• Spas. • Humidifiers.

Potential sources should be sampled, and the tempera-

• Showers, especially associated with warm water

ture of water recorded.

systems (temperature especially ranging from 35˚C to 43˚C). • Oxygen nebulizers.

Water sample (100 ml) should be collected in containers (available from MDU) and sent to MDU.

• Others (be suspicious). Places inspected may include workplaces, hospitals,

En v i ro n m e n t

homes and others.

As indicated from inspection and/or results of samples.

Immediate recommendations may include dosing the The temperature of water should be checked.

cooling tower with a chlorine-releasing compound, followed by:

Maintenance records, where appropriate, should be checked to ensure compliance with the Health (Infectious Diseases) Regulations 1990 (Division 3).

• Decontaminating cooling towers as per Guidelines*. (See 5.14 of these guidelines.) • Decontaminating the reticulated water system as per

Guidelines*. (See 6.9 of these guidelines.) Shutting down the system (there should not be any need for evacuation). 101

Long-term measures may include advice on: • The maintenance procedures of cooling towers. • Elevation of temperature of hot and warm water sys-

Epidemic Measures An outbreak is defined as more than one case associated in time and place.

tems. • Engineering modifications. • Relocation of cooling towers. • Relocation of air intakes.

When an epidemic occurs, activate Displan which allows for investigation for common source of infection and resultant action as indicated.

• Replacement of cooling towers by air-cooled systems. * Guidelines refers to Guidelines for the Control of

Pre ve n t i o n As eradication of Legionella spp. in artificial systems is impractical, preventing or controlling Legionellosis is based on appropriately maintaining aerosol-generating equipment. The folowing recommended measures aim to minimise the proliferation of the bacteria: • Ensure compliance with Health (Infectious Diseases) Regulations 1990. • Improve future design of aerosol-generating equipment to facilitate maintenance and to reduce aerosols. • Ensure appropriate siting of cooling towers; that is, away from air intakes, areas of public access, and so on. • Promote ongoing education of building owners and managers regarding preventive measures as outlined in the Guidelines*.

Potting Mix To minimise the risk of infection, gardeners should: • Open the bag with care to avoid inhalation of airborne potting mix. • Moisten the contents to avoid creating dust. • Wear gloves to avoid transferring the potting mix from hand to mouth. • Wash hands after handling potting mix, even if gloves have been worn. • Adopt the same measures when handling other gardening material such as compost.

102

Legionnaires’ Disease, 1989.

Leprosy (Hansen’s Disease)

Victorian Statutory Re quirem ent

Public Health Significance and O c c u r re n c e

Group B notification.

It is occasionally seen on routine refugee screening.

Infectious Agent

The world prevalence is estimated to be between 10 to 12 million cases.

Mycobacterium leprae. The disease is endemic in tropical and subtropical Asia,

Clinical Features It is a chronic bacterial infection involving the cooler body tissues, skin, superficial nerves, nose, pharynx,

Africa, Central and South America, Pacific regions and the USA (Hawaii, Texas, California, Louisiana, Puerto Rico).

larynx, eyes and testicles.

Method of Diagnosis Skin lesions may occur as pale, anaesthetic macular

Clinical examination.

lesions or erythematous infiltrated nodules. Laboratory tests which show: Neurologic disturbances are manifested by nerve infiltration and thickening with anaesthesia, neuritis, paraesthesia and trophic ulcers.

• The demonstration of acid-fast bacilli in scrapings from skin or the nasal septum. • A typical histologic picture in a biopsy of skin or of a thickened involved nerve.

The disease is divided clinically and by laboratory tests into two overlapping types: lepromatous and tuberculoid. The lepromatous type is progressive with nodular skin

Reservoir Humans.

lesions, slow symmetric nerve involvement, numerous acid-fast bacilli in the skin lesions and a negative lepromin skin test.

Mode of Transmission The mode of transmission is not clearly established. The

The tuberculoid type is benign and non-progressive with

disease is probably transmitted by aerosol with a high

localised skin lesions, asymmetric nerve involvement,

subclinical rate of infection.

few bacilli present in the lesions and a positive lepromin skin test.

Household and prolonged close contact seem to be important.

Leprosy should always be suspected in any patient with an undiagnosed peripheral neuropathy or chronic skin

In cases of children under one year of age, transmission

lesions.

is probably transplacental.

103

Incubation Period The incubation period is difficult to determine.

For tuberculoid leprosy, the recommended regimen is rifampicin and dapsone for a period of six months (for detailed treatment see Control of Communicable Dis-

It probably ranges from nine months to 20 years; on

eases in Man by Benenson).

average four years, for tuberculoid leprosy and eight years for lepromatous leprosy.

Control of Contacts Investigation of contacts and source of infection.

Period of Communicability Leprosy is not infectious after three months of continuous

Early detection and treatment of new cases.

treatment with dapsone or clofazimine, or after two to three weeks of treatment with rifampicin.

Prophylactic BCG has resulted in a considerable reduction in the incidence of tuberculoid leprosy among contacts in some trials.

Susceptibility and Resistance Infection among close contacts of leprosy patients is frequent, but clinical disease occurs only in a small proportion.

Control of Case No isolation is required for cases of tuberculoid leprosy; contact isolation is required for cases of lepromatous leprosy. Nasal discharges of infectious patients should be concurrently disinfected.

Tre a t m e n t The minimal regimen recommended by WHO for lepromatous leprosy is rifampicin, dapsone and clofazimine and, recently, ofloxacin. The treatment should be continued until skin smears become negative for at least two years.

104

Epidemic Measures Not applicable.

Leptospirosis

Victorian Statutory Re quirem ent

Method of Diagnosis See checklist at the end of this section.

Group B notification. Laboratory diagnosis:

Infectious Agent Leptospira species (many serovars). In Victoria, the most common serovar is Leptospira borgpetersenii var hardjo.

• Rising titres on repeated serology. • Take blood during acute illness and two to three weeks later. • Isolate leptospires: – Blood (days 0 to 7).

Clinical Features

– CSF (days 4 to 10) lumbar puncture. – Urine (after 10 days).

Clinical features include fever, headache, chills, myalgia and red eyes.

Repeated blood cultures, into specific media during the first week of disease are usually successful.

Other manifestations are diphasic fever, rash, meningitis, haemolytic anaemia, haemorrhage into skin and mucous

Preferably take blood cultures before antibiotic therapy is

membranes, hepato-renal failure, jaundice, mental

commenced.

confusion/depression, pulmonary involvement and haemoptysis.

Reservoir

Clinical illness lasts a few days to three weeks or more.

Many animal hosts. In Victoria, cows, rats and pigs.

Recovery, if untreated, may take months.

Mode of Transmission

Public Health Significance and Oc c u r re n c e It is a zoonotic disease that needs exposure to water

It can be transmitted by: • Contact of skin, especially if abraded, or of mucous membranes with water, moist soil or vegetation contaminated with urine of infected animals.

contaminated by animal urine, or contact with tissues or

• Direct contact with urine or tissues of infected animals.

urine of infected animals.

• Ingestion of foods contaminated with urine of infected rats.

It is an occupational hazard for farmers, sewer workers,

• Inhalation of droplet-aerosols of contaminated fluids.

miners, dairy and abattoir workers and fish workers, and a recreational hazard to bathers, campers and sportsmen.

Incubation Period Usually 10 to 12 days (the range is four to 19 days).

Many cases have arisen in herringbone-style milking sheds.

Period of Communicability Leptospires may be excreted in the urine of animals for one month usually (but up to 11 months has been reported).

105

Susceptibility and Resistance Immunity to the specific serovar follows infection, but may not protect against infection with a different serovar.

• Consult the Department of Natural Resources and Energy on herd immunisation. • Prevent the contamination of accommodation, working and recreational areas.

Control of Case • Isolate the case with blood/body fluid precautions. • Disinfect articles soiled with urine. • Use antibiotic treatment: penicillin, doxycycline or amoxycillin.

Investigation • Ascertain occupational exposure. • Seek the source of the infection; for example, contact with contaminated water, farm or domestic animals, rodent infestations. • Inform the Department of Natural Resources and Energy.

Control of Contacts No human vaccine is available. Search for exposure to infected animals and potentially contaminated waters.

Control of Environment Recognise potentially contaminated waters and soil, and drain such waters when possible.

Preventive Measures • Educate the public on modes of transmission to avoid swimming or wading in potentially contaminated waters, and to use proper protection when work requires such exposure. • Protect workers in hazardous occupations with boots and gloves. • Control rodents. • Segregate infected domestic animals.

106

Epidemic Measures • Seek source of infections and eliminate contamination or prohibit use of infected waters. • Search for industrial and occupational source.

Diagnosis of Leptospirosis in Humans This checklist is designed for those who deal directly with the patient. To use the list, note the main clinical features listed, mark Yes or No, and write the appropriate score in the right-hand column. A presumptive diagnosis of leptospirosis may be made if: • Part A, or Parts A and B score: 26 or more. • Parts A, B and C total: 25 or more. A score between 20 and 25 suggests leptospirosis as a possible, but unconfirmed, diagnosis. Question

Answer

Score

A. Has the patient: • Headache of sudden onset?

Yes = 2

No = 0

____

• Fever?

Yes = 2

No = 0

____

• If yes, is the temperature 39˚C or more?

Yes = 2

No = 0

____

• Red eyes (bilateral)?

Yes = 4

No = 0

____

• Meningism?

Yes = 4

No = 0

____

• Muscle pains (especially calf muscles)?

Yes = 4

No = 0

____

Yes = 10

No = 0

____

• Jaundice?

Yes = 1

No = 0

____

• Albuminuria or nitrogen retention?

Yes = 2

No = 0

____

• Are all three features (red eyes, muscle pains and meningism) present together?

Total Score for Part A

_____

Yes = 10

No = 0

____

B. Epidemiological factors: • Has there been contact with animals at home, work, leisure, or in travel, or contact with known (or possibly) contaminated water?

C. Bacteriological laboratory findings: • Isolation of leptospires in culture—diagnosis certain. • Positive serology—leptospirosis endemic: Single positive, low titre (that is, < 200).

Yes = 2

No = 0

____

Single positive, high titre (that is, > 400).

Yes = 10

No = 0

____

Paired sera, rising titre ( ≥ 4 fold).

Yes = 25

No = 0

____

Single positive, low titre (that is, < 200).

Yes = 5

No = 0

____

Single positive, high titre (tha is, > 400).

Yes = 15

No = 0

____

Paired sera, rising titre ( ≥ 4 fold).

Yes = 25

No = 0

____

• Positive serology—leptospirosis not endemic:

Total ______________

Source: Courtesy of Dr Ben Adler, Microbiology Dept, Monash University 107

L i s t e rio sis

Victorian Statutory Re quirem en t Group B notification. Note

Also isolation of L. monocytogenes from food is notifiable under the Health (Infectious Diseases) Regulations 1990.

Infectious Agent L. monocytogenes is a Gram positive bacterium belong-

• The immunosuppressed, alcoholics, diabetics, debilitated and the elderly. Infection of healthy adults is usually transient with mild to moderate flu-like symptoms, but in pregnant women, foetal infection through the placenta can result in abortion, stillbirth or premature birth of severely affected babies (early-onset neonatal listeriosis). Late-onset neonatal listeriosis generally affects full-term babies who are usually healthy at birth.

ing to the genus Listeria. The onset of symptoms in these babies occurs several Of the seven recognised species, it is currently the only one implicated in human cases. Serotypes 1/2a, 1/2b and 4b account for the majority of human isolates serotyped in the USA.

L. monocytogenes grows over a wide range of temperatures, from 1˚C to 45˚C; hence, it has the unusual ability to multiply and survive for long periods in refrigerated

days to weeks after birth (a mean of 14 days has been reported), possibly as a result of infection acquired from the mother’s genital tract during delivery or postnatally through cross-infection. In non-pregnant cases, listeriosis can also be subacute or sudden in onset. Fever, severe headache, nausea and vomiting can lead to prostration and shock.

foods. The reported case fatality rate has been around 30 per It has been found in a variety of foods, particularly raw

cent in both groups.

meat, dairy products (especially soft cheese), and smallgoods. The bacterium is relatively heat resistant, but will not survive pasteurisation in milk at 72˚C for 15 seconds.

Public Health Significance and O c c u r re n c e Listeriosis is an uncommon disease in humans. An incidence of around four cases per million population has been quoted in the UK, and a study by the Centers for

Clinical Features

Disease Control in 1986 estimated an overall annual

Although focal infections (such as pneumonia, endocar-

incidence in the USA of 7.1 cases per million population.

ditis, infected prosthetic joints and hepatitis) have been described, listeriosis presents usually as an acute

Although most human cases appear to be sporadic,

meningoencephalitis and/or septicaemia.

three large outbreaks documented in the past decade have clearly established L. monocytogenes to be a food-

The infection predominantly affects two main groups of

borne pathogen.

people: • Pregnant women, resulting in severe infection of their foetuses or newborn babies.

109

These three outbreaks in the Maritime Provinces (1981), Massachusetts (1983) and Los Angeles County (1985)

Incubation Period Unknown and may be up to 90 days.

involved a total of 232 cases. The overall case fatality rate was 36 per cent.

In pregnancy, the foetus is infected within a few days of the mother’s illness.

The implicated foods were coleslaw, pasteurised milk and Mexican-style soft cheese.

Period of Communicability Method of Diagnosis Culture of the organism from blood, CSF, placenta,

Mothers of infected newborns may shed the infectious agent in vaginal discharges and urine for seven to 10 days.

meconium and other sites of infection.

Reservoir L. monocytogenes is widespread in the environment and is commonly isolated from sewage, silage, sludge, birds, wild and domestic animals.

Susceptibility Although healthy people can be infected, the disease generally affects vulnerable groups in the community, such as: • Neonates. • Elderly, diabetics, alcoholics.

It has caused infection in many animals and resulted in abortion in sheep and cattle. The bacteria are commonly

• The immunosuppressed. • Pregnant women, with their foetuses most affected.

isolated from poultry. Thus, it is a common contaminant of raw food.

Control of Case

In humans, asymptomatic vaginal carriage occurs, and

tion with aminoglycosides.

Specific treatment with penicillin or ampicillin in combinafaecal carriage of up to 5 per cent in the general population has been reported.

In penicillin-sensitive patients, co-trimoxazole, tetracycline and chloramphenicol may be effective.

The significance of these carriers in the epidemiology of listeriosis is unknown.

Investigation Procedures

Mode of Transmission

• Obtain medical history from attending doctor (physi-

The main route of transmission is oral, through ingestion

• Obtain food history from patient.

of contaminated food.

• Test suspect food (especially inspect refrigerator) for

Other routes include mother to foetus via the placenta or

• Arrange for faecal examination of all members of the

cian, obstetrician, paediatrician).

isolation of Listeria (send samples to MDU). at birth.

family (including case). • Assess the possibility of common source outbreaks if

The infectious dose is unknown.

110

there is a cluster of cases.

Control of Contacts/ En v i ro n m e n t The significance of vaginal and faecal carriers is unknown.

• Utilising a multidisciplinary approach to the investigation of cases. New regulations for the control of Listeria approved by the National Food Standards Council became effective from September 1994. These regulations require that

When implicated, food is to be withdrawn from sale.

pâté, soft cheese, smoked fish and smoked seafood have zero Listeria at the point of wholesale distribution.

Preventive Measures A surveillance program should be estblished to monitor: • The epidemiological aspects of the disease. • The presence of Listeria in food and its public health importance.

Epidemic Measures • Epidemiological investigation of cases should be used to detect outbreaks and to determine source. • Molecular subtyping should be used to determine the association between isolates from cases and food

This is achieved through notification and surveys of atrisk foods.

samples. • If a common source is detected, implicated food should be withdrawn from sale.

Dairy products should be withheld from sale should

Listeria be isolated. The Australian Manual for Control of Listeria in the Dairy Industry issued by the Chief Dairy Officers Committee, sets out procedures designed to: • Prevent Listeria contamination in the processing plant, hence in milk and milk products. • Facilitate clearance of product for sale should Listeria be found in either the dairy product or in the environment of the plant. The presence of L. monocytogenes in other food is currently being monitored. Other procedures of importance are: • Developing a code of hygienic practice to prevent, limit and (where possible) eliminate the presence of the bacteria in processed food. • Educating pregnant women and the immunosuppressed about the foods likely to be contaminated, and the importance of reheating food to a core temperature of at least 70˚C. Reheating in a microwave oven may be inadequate for this purpose.

111

Malaria

Victorian Statutory Re quirem ent

anti-malarial chemoprophylaxis may show an atypical

Group B notification.

clinical picture with wide variations in incubation period.

Individuals who are partially immune or have been taking

Most antibiotics also can modify the course of malaria.

Infectious Agent The malarial parasite, Plasmodium spp.

Malaria due to species other than P. falciparum is generally not life threatening except in the very young, very old, and those with immunodeficiency or other

Four species can infect humans: P. vivax, P. ovale, P.

concurrent disease.

malariae and P. falciparum. Infection is most commonly caused by P. vivax and/or P.

falciparum.

Public Health Significance and O c c u r re n c e The malaria situation worldwide is deteriorating. There

Mixed infections may occur in endemic areas.

are increasing levels of transmission, and it has returned to areas where it had been previously eradicated. Drug

Clinical Features

resistance has increased and there has been a spread of

The features include indefinite malaise and slowly rising

resistance of the vector to insecticides.

fever of several days duration. This is followed by shaking chills and rapidly rising temperature, that ends with

There are said to be over 220 million new infections a

profuse sweating.

year worldwide, and the disease is endemic in areas of Asia, Africa and Central and South America.

The fever is usually accompanied by headache and nausea.

Australia was certified by WHO as being free of endemic malaria in 1981, but several hundred imported cases are

While, classically, fever due to malaria may occur every

recorded each year. However, the region lying north of a

second or third day, in practice, the fever may have no

line joining Townsville on the east coast and Port

specific pattern.

Hedland on the west remains receptive and vulnerable to the re-establishment of the disease due to the presence

Falciparum malaria (malignant tertian) may present a

of known or suspected vectors, suitable environmental

varied clinical picture with an atypical onset including

conditions, and the continual arrival of malaria-infected

diarrhoea.

travellers.

The above features may progress to jaundice, coagula-

Many cases occur among migrants returning to their

tion defects, shock, renal and hepatic failure, acute

native country for holidays after many years, when they

encephalopathy, pulmonary and cerebral oedema, coma

may have lost their immunity.

and death. A large percentage of Australian cases originate in Every year, Australians die of falciparum malaria when

Papua New Guinea.

diagnosis or treatment has been delayed. Any person returning from an endemic area who develops a fever should be promptly investigated. 113

Method of Diagnosis Malaria can be diagnosed by demonstration of malaria parasites in blood films. Blood samples should be sent to

reach the lumen of these glands that communicates with the salivary ducts and are then passed into a skin wound in the salivary fluid when the insect next bites a human.

a laboratory with experience in the diagnosis of malaria by the use of thick and thin films. Repeated examination may be necessary due to variations in density of para-

The cycle in the mosquito takes eight to 35 days, depending on the species and the temperature.

sites. In the human host, the period between the infective bite Confirmation of the species should be sought from a reference laboratory.

and the appearance of parasites in the blood is called the pre-patent period. This period varies from six to nine days for P. falciparum, P. vivax and P. ovale, and 12 to 16 days for P. malariae.

Reservoir Humans are the only important reservoir of human

Malaria can also be transmitted by transfusion of blood

malaria, although other Plasmodium species may natu-

of infected persons, or by using contaminated needles or

rally infect non-human primates.

syringes.

Mode of Transmission Malaria is transmitted by the bite of an infective female anopheles mosquito, most species of which feed at dusk or in the early night hours.

Congenital transmission occurs rarely.

Incubation Period The time between the infective bite and the appearance of symptoms is approximately 12 days for P. falciparum,

On introduction into the body, the young parasites

14 days for P. vivax and P. ovale and 30 days for P.

(sporozoites) circulate in the blood for less than one hour

malariae.

and then invade liver cells where they multiply. Occasionally there can be a protracted incubation After this liver stage, the parasites again enter the

period, especially with strains from temperate regions.

bloodstream where they invade red cells and multiply by asexual reproduction to produce merozoites that rupture the cell and invade further red cells.

Period of Communicability For infection of mosquitoes, it is communicable for as

Some merozoites do not multiply in the red cell but

long as infective gametocytes remain in the blood.

become the male and female gametocytes that multiply by sexual reproduction when taken up by the insect vector.

Gametocytes usually appear within three days of parasitaemia with P. vivax and P. ovale, and after 12 to 14 days with P. falciparum.

In the mosquito, the male and female gametes fuse to form an oocyst within which sporozoites develop. These are set free in the insect’s haemocoele, then carried to all parts of its body including the salivary glands. They

Untreated or inadequately treated patients may be a source of mosquito infection for more than three years with P. malariae, one to two years with P. vivax, and generally not more than one year with P. falciparum.

114

Infected mosquitoes remain infective for life.

Control of Contacts The diagnosis of malaria in travelling companions should

Transmission by transfusion may occur as long as

be considered.

asexual forms remain in the circulating blood; with P.

malariae, this can continue for over 40 years.

In transfusion-induced malaria, all donors must be located and their blood tested for malaria parasites and

Stored blood can remain infective for 16 days.

Susceptibility and Resistance With P. vivax and P. ovale infections, parasites can remain dormant in liver cells and mature months later to

anti-malarial antibodies. If a history of needle sharing is obtained from a malaria patient, all persons who shared the equipment should be investigated and treated.

produce true relapses, and this can occur for up to two and five years respectively.

Preventive Measures Advice to travellers intending to visit malarial areas of the

With P. malariae infections, low levels of erythrocytic forms can persist for many years to multiply at some

world should include both self-protection measures against mosquito bites and the use of chemoprophylaxis.

future time and produce disease. Over-reliance on either measure, particularly chemopro-

Control of Case Prompt and adequate treatment is required for the prevention of complications and relapses. The drugs used in treatment include chloroquine, primaquine, quinine, doxycycline, Fansidar and mefloquine.

phylactic drugs, is ill-advised (drug resistance by the malaria parasite continues to change and travellers may not always take the recommended drug/s as directed). There is no drug that is completely safe and completely effective for prophylaxis against malaria. The decision to recommend chemoprophylaxis and the choice of drug/s

For complete details, please see the annual publication

International Travel and Health from WHO, available from Hunter Publications, or Antibiotic Guidelines published by the Victorian Postgraduate Medical Foundation.

must involve an analysis of the risks and benefits based on the following considerations: • Prevalence and type of resistance to the available drugs. • Level of malaria transmission.

Isolation of the patient is not required, but blood precautions should be taken. Concurrent or terminal disinfection is not required.

• Duration and place of stay, particularly in rural areas. • Intensity of vector mosquito contact. • Availability of adequate health care. • Age. • Traveller’s current health and medical history. • Risk of traveller not complying with recommendations. Travellers should be advised of the symptoms of malaria and warned to seek medical attention as soon as possible if they occur.

115

Malaria poses a serious threat to pregnant women as it can compromise foetal development, possibly resulting in premature labour or miscarriage.

International Measures Aircraft, ships and other vehicles should be sprayed with insecticides on arrival if there is reason to suspect importation of malaria vectors.

Pregnant women should be advised to avoid travel to malarious areas if possible.

Anti-mosquito sanitation should take place within the mosquito flight range of all ports and airports.

Similarly, malaria presents considerable risks for children, particularly the very young, and the choice of suitable drugs is limited. Mosquito avoidance measures should be emphasised. Self-protection measures include: • Avoiding outdoor exposure between dusk and dawn. • Wearing long, loose clothing after dusk, preferably in light colours. • Avoiding perfumes and colognes. • Using effective insect repellents; for example, products containing up to 20 per cent DEET. • Using knock-down sprays, mosquito coils, or plug-in vaporising devices indoors. • Using mosquito nets.

Chemoprophylaxis Drugs used for this purpose include chloroquine, mefloquine and doxycycline. See table provided and obtain further details from the publication Health Information for International Travel issued by the Commonwealth Department of Health and Family Services. Patients should be warned that if they develop any signs of fever or other illness while travelling or after their return to Australia in spite of having had chemoprophylaxis, they should seek prompt medical attention.

116

WHO should be notified by national health administrations of details of cases twice yearly for the WHO Malarial Surveillance Program.

Information Sheet Malaria

Malaria Prophylaxis • Travellers should be advised of the appropriate type of prophylaxis for the area which they wish to visit. • Many areas are now chloroquine resistant. • The only drugs recommended are chloroquine (when appropriate), doxycycline and mefloquine. Chloroquine

Multi-Drug Resistant Areas (includes resistance to m e fl o q u i n e ) Forests and rural areas in Cambodia, Myanmar (Burma), Thailand, Vietnam, Laos.

should be started two weeks before, mefloquine one week before, and doxycycline two days before entering

Short stay (less than 8 weeks):

the malarious area. All must be continued for up to four

– Doxycycline (100 mg/day).

weeks after leaving the area. • Special precautions should be taken for pregnant women and children. (see publications listed). • Whatever drugs are prescribed, personal protection measures against mosquitoes should also be advised. • Travellers should be advised of the symptoms of

Long stay (more than 8 weeks): – Chloroquine (300 mg/week) and doxycycline (50 mg/day). or – Chloroquine (300 mg/week) with mefloquine carried for presumptive self-treatment.

malaria and warned that they should seek medical attention as soon as possible if they occur.

Chloroquine-Resistant Areas

Chloroquine-Sensitive Areas Short and long stay: – Chloroquine (300 mg/week).

• A major part of Africa and the Kruger National Park. • Papua New Guinea, Solomon Islands, Vanuatu. • India, parts of Indonesia, Malaysia, Nepal, Pakistan, Philippines and parts of Sri Lanka. • Iran and parts of Saudi Arabia. • Central and South America including Bolivia, Brazil (Amazon Basin).

Malaria Prophylaxis

Proguanil is now available in Australia, although not yet recommended by the NH&MRC. It is effective against

Pl.falciparum, can be given to children and has been used by pregnant women. Combined with chloroquine, the dose for adults is: – Chloroquine 300 mg/week (2 tablets). – Proguanil 200 mg/day (2 tablets).

Short stay (less than 8 weeks): – Doxycycline (100 mg/day). or

For children, the dose of proguanil is 3.5 mg/kg body weight daily.

– Mefloquine (250 mg/week). Long stay (more than 8 weeks): – Chloroquine (300 mg/week) and Doxycycline (50 mg/day). or – Chloroquine (300 mg/week) with Mefloquine carried

Chloroquine for children: – 1 to 4 years1/2 tablet per week. – 4 to 8 years1 tablet per week. – > 8 years adult dose.

for presumptive self-treatment.

117

Further Information • For up-to-date recorded advice, telephone the International Travel Health Info Line on (06) 269 7815. • The following publications: – Health Information for International Travel, 1995, fourth edition, Australian Government Publishing Service, Canberra. – International Travel and Health, Vaccination Require-

ments and Health Advice, World Health Organisation, Geneva. (published annually). • Any travel health clinic. The address of the nearest clinic may be obtained by ringing Infectious Diseases Unit (03) 9616 7777.

118

Measles

Victorian Statutory Re quirem ent Group A notification.

• A fourfold or greater change in measles antibody titre between acute and convalescent-phase sera, obtained at least two weeks apart, with the tests preferably conducted at the same laboratory. or

School exclusion.

• Isolation of measles virus from a clinical specimen. or

lnfectious Agent Measles virus (morbillivirus).

• A clinically compatible case epidemiologically related to another case.

Clinical features include prodromal fever, conjunctivitis,

Public Health Significance and O c c u r re n c e

coryza, cough and Koplik’s spots on the buccal mucosa.

It was once a common, acute highly communicable

Clinical Features

disease with potentially serious sequelae. It is much rarer The characteristic red, blotchy rash appears on the third

since the introduction of widespread immunisation, but

to seventh day. It begins on the face before becoming

epidemics are still occurring, especially in school-aged

generalised. It generally lasts four to seven days.

children.

Complications can include otitis media, pneumonia and

Death is rare but does occur.

encephalitis. Subacute sclerosing panencephalitis (SSPE) develops very rarely as a late sequel. Persons who have been previously immunised may present with non-classical features.

Case Definition It is defined as an illness characterised by all the following features: • A generalised maculopapular rash lasting three or

Method of Diagnosis See Case Definition.

Reservoir Humans.

Mode of Transmission Its transmission is airborne by droplet spread, or it is transmitted by direct contact with infected nasal or throat secretions.

more days. • A fever (at least 38˚C if measured). • Cough or coryza or conjunctivitis or Koplik’s spots. or • Demonstration of measles-specific IgM antibody. or

Incubation Period Incubation period is approximately 10 days, but varies from seven to 10 days from exposure to the onset of fever. It is usually 14 days until the rash appears.

119

Period of Communicability From slightly before the beginning of the prodromal period to four days after the appearance of the rash.

Classroom contacts without a valid school entry immunisation certificate must be excluded for 13 days from the first appearance of rash in the last occurring case, unless they are immunised within 72 hours of first contact.

Susceptibility and Resistance Vaccination at 12 months produces antibody in approximately 95 per cent of recipients. It is not yet clear whether vaccine-induced immunity is lost over time, but the majority of evidence suggests that this is uncommon.

Preventive Measures Live attenuated measles vaccine is recommended for all persons born after 1970 unless specific contraindications to live vaccines exist.

Control of Case

It is recommended to be given as measles-mumps-

School exclusion for at least five days from the appear-

rubella (MMR) vaccine at 12 months and at 10–16 years

ance of the rash, or until receipt of a medical certificate

(or Year 6 in Victoria).

of recovery from infection.

Epidemic Measures Control of Contacts

A measles outbreak exists whenever one case of mea-

Household and other general contacts should be

sles is confirmed.

checked for documentation of measles immunisation. If non-immune, immunisation should be given within 72

The diagnosis should establish that the disease is

hours of contact.

actually measles (see clinical or laboratory case definition).

Persons born before 1970 are generally regarded as immune as they would have contracted measles in

Nasopharyngeal aspirates may be collected and rapidly

childhood.

transported to Royal Childrens Hospital or VIDRL for immunofluorescent identification of measles antigen. This

Children aged between six to 12 months should be given

is a rapid method of virus identification. The specimen is

a measles-containing vaccine, but should be

then cultured for virus.

revaccinated at 12 months or three months after the last dose, whichever is later. It is also acceptable to give

Alternatively, a blood sample (10 ml in a plain tube)

normal immunoglobulin to children in this age group in a

should be collected immediately after the child presents

dose of 0.2 ml/kg then to vaccinate them at 12 months

with the rash, and sent to VIDRL to look for measles-

(or three months after the administration of immuno-

specific IgM.

globulin). A second specimen 10 days later is useful if the IgM In school, immunisation status of close contacts should be checked. This refers to classroom contacts of the child, not the whole school.

120

result is equivocal.

For school-based outbreaks: class levels involved should be revaccinated, for all children who do not have documented evidence of two doses of measles-containing vaccine.

For outbreaks involving preschool-aged children: • Children aged six to 12 months: These children can be offered MMR vaccine, which may prevent measles occurring if given within 72 hours of contact. If these children are immunised, they should be given another dose of MMR at 12 months of age or three months after the first dose, whichever is later. These children do not need to be excluded from the centre if the parents do not wish them to be immunised yet. • Children aged from birth to six months: These children can be offered immunoglobulin (an injection of antibodies from blood donors), which may prevent measles if given within six days of contact. These children do not need to be excluded if the parents do not wish them to have immunoglobulin.

121

Meningococcal Infections

Victorian Statutory Re quirem ent

Public Health Significance and O c c u r re n c e

Group A notification.

In the absence of prompt diagnosis and appropriate treatment, acute meningococcal infections have a high

School exclusion of household contacts.

case fatality rate, especially in children.

Infectious Agent

They occur in all areas of the world with a high incidence

Neisseria meningitidis (the meningococcus) is a Gram

in certain endemic regions such as the sub-Saharan region of mid-Africa (predominantly Group A organisms).

negative diplococcus. Epidemics of Groups A, B or C disease have occurred in Several serogroups have been recognised: Groups A, B,

different countries and, in Australia, Group A outbreaks

C, 29E, H, I, K, L, W135, X, Y and Z.

have occurred among Aboriginal communities in central Australia.

Within these groups, certain serotypes have been identified; for example, Group B serotypes 2b and 15.

Most cases occur in winter and spring, and the infection is more common in children under five years. In young

In Victoria at present, Groups B and C organisms are the

adults outbreaks typically occur in crowded living

most common.

conditions, such as in military barracks and institutions.

Clinical Features

The worldwide incidence of meningococcal infections

Clinical features include an acute onset of meningitis and/or septicaemia, the typical features of which are

has been rising in recent years. In Victoria 63 cases were notified in 1993, 59 in 1994 and 75 in 1995.

fever, intense headache, nausea, vomiting and neck stiffness.

Method of Diagnosis Diagnosis is usually made on clinical grounds confirmed

There may be a petechial or purpuric rash on the trunk

by laboratory tests. These are:

and limbs that may sometimes cover large areas of the

• A presumptive diagnosis is made following Gram stain

body.

of cerebro-spinal fluid or of material obtained by needling an area of rash.

In fulminating cases, there is sudden prostration and

• Blood and CSF culture.

shock associated with the characteristic rash and this condition has a high fatality rate.

If treatment has been given before a blood or CSF sample is taken, a throat swab should be done.

Chronic meningococcal septicaemia can also occur with febrile episodes, skin rashes and fleeting joint pains.

Although serogrouping may be performed in some hospital laboratories, meningococcal isolates from all cases of invasive disease should be sent to MDU, The University of Melbourne, to ensure appropriate monitoring of serogroups and to perform susceptibility testing.

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Detection of meningococcal antigen in CSF and/or serum

Patients deficient in certain complement components in

can be obtained by techniques such as counter-current

the blood are prone to recurrent meningococcal infec-

immuno-electrophoresis (CIE). This is particularly useful

tions.

in partially treated cases where both smear and culture may be negative.

There is an increased and prolonged risk of secondary infections in close contacts. In one series, the incidence

Reservoir

of such infection was 0.5 per cent with a median interval of seven weeks between the index and secondary cases.

Humans. Asymptomatic naso-pharyngeal carriers of the organism can spread infection, but there is no consistent

Secondary cases have been reported up to five months

relationship between the carrier rate in a given commu-

later. The risk in household contacts is 500 to 800 times

nity and the incidence of disease.

higher than in the general population.

Carrier rates of up to 25 per cent or more may exist without cases of meningitis.

Mode of Transmission Transmission can occur through direct contact including airborne droplets from nose and throat of infected persons.

Control of Case and the En v i r o n m e n t Prompt treatment with parenteral penicillin in adequate doses should begin when a presumptive clinical diagnosis is made prior to laboratory confirmation. In cases with a very acute onset, such treatment should commence prior to transfer of the patient to hospital,

Transmission by fomites is insignificant.

even though there may be some interference with laboratory confirmation by culture. Suitable alternatives

Incubation Period It is commonly three to four days, but can vary from two

for patients who are allergic to penicillin include ceftriaxone, cefotaxime or chloramphenicol.

to 10 days. Respiratory isolation is recommended for 24 hours after

Period of Communicability

commencing treatment. There should be concurrent disinfection of discharges from nose or throat and

It is communicable until the organisms are no longer

articles soiled with such discharges. Articles used by the

present in discharges from the nose and mouth.

patient should be terminally cleaned. Since penicillin only temporarily suppresses but does not

Susceptibility and Resistance

eradicate the organisms in the nasopharynx, all patients

Susceptibility to clinical disease is low as evidenced by

should be treated with a drug such as rifampicin prior to

the usual high ratio of carriers to cases.

discharge from hospital (for dosage, see below).

Susceptibility decreases with age. However, a secondary

If ceftriaxone is used in treatment, rifampicin need not be

peak of meningococcal meningitis occurs in adolescents

given.

and young adults in the age group of 15 to 24 years.

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Contacts

When indicated, chemoprophylaxis should be instituted

All household and other contacts should be placed

as soon as possible, preferably within 24 to 48 hours of

under close surveillance for the earliest signs of infection

diagnosis of the index case.

(such as fever, headache, nausea/vomiting or rash), so that prompt treatment can be instituted. A surveillance

Note

letter should be provided as soon as possible to the

Antibiotic prophylaxis does not eliminate the need for

parents of all children in a class, school or day care

close surveillance of contacts.

centre where a case has occurred. Household contacts must be excluded from school or child care until they have received appropriate chemotherapy for at least 48 hours.

Selection of Antibiotic for Pr o p h y l a x i s Rifampicin is the drug of choice. It is given in a dose of: • An adult: 600 mg.

Antibiotic Prophylaxis

• A child over one month old: 10 mg/kg. • A child less tha one month old: 5.0 mg/kg.

All family and household contacts and other close contacts should be offered antibiotic prophylaxis. Close

This dose is given twice daily for two days in all cases.

contacts include those who have shared sleeping quarters or eating utensils, sexual contacts in older

Rifampicin may cause a red-orange colouration of urine,

patients, and those who have kissed the patient in the 10

faeces, saliva, sputum, sweat and tears, and may cause

days prior to onset of illness.

permanent staining of soft contact lenses.

In a school class, only the patient’s close friends would

Itching, rashes and gastro-intestinal reactions may

require antibiotic treatment. However in a day care

occur. It should be used with caution in patients with liver

centre, because of the high risk in young children,

damage, and is contraindicated in pregnant or lactating

everybody (including staff) should be offered antibiotic

women. Patients on oral contraceptives should be

treatment unless groups of children are kept quite

advised to use other contraceptive methods during

separate, in which case only children in the patient’s

treatment with this drug and for the remainder of the

group need treatment.

cycle.

Special circumstances may justify wider use of antibiotic

Patients receiving anticoagulants may need to increase

prophylaxis, such as attendance of the index case in the

their prescribed dose.

10 days before onset at a party where young children and teenagers were present.

Alternatives to rifampicin include: • Ceftriaxone. 5.0 mg/kg to a maximum of 250 mg IM as

Health care personnel do not usually require antibiotic treatment except where intimate contact (such as mouthto-mouth resuscitation) has occurred.

a single dose (safe in pregnancy), reduce to 125 mg in children under 15 years of age. • Ciprofloxacin. 500 mg orally as a single dose. It should not be prescribed to children under 12 years of age or 40 kg body weight, or to pregnant women.

125

Note

Antibiotic prophylaxis of family and household contacts is the responsibility of the treating hospital while the Department of Human Services will take responsibility for follow-up of other contacts. Rifampicin supplies are available through the Public Health nurses or through the

Preventive Measures A quadrivalent vaccine is available in Australia against Groups A, C, Y and W135. Group C vaccine does not induce a reliable antibody response under two years of age, but Group A vaccine can elicit a response in children as young as three months.

Department. Written consent should be obtained prior to administration of any antibiotic prophylaxis to children.

However, in children aged three months to two years, two doses are given three months apart instead of a

Throat or Nasopharyngeal Swabs Obtaining such swabs prior to chemoprophylaxis is

single dose as in older children and adults. The vaccine provides effective immunity one to two weeks after administration which lasts for more than one year (though the duration of protection is limited in young children).

unnecessary, of no value in control and therefore not routinely recommended. They may be of some value during epidemics to estimate the prevalence of carriage of the causative strain.

It is recommended for travellers to epidemic and highly endemic areas such as Brazil, Mongolia, Vietnam, India, Nepal and sub-Saharan Africa and is a requirement for visits to Mecca. There is, at present, no effective vaccine

Routine post-prophylaxis swabs are also not cost-

against Group B available.

effective as rifampicin is effective in eliminating carrier status in 90 to 95 per cent of patients.

Epidemic Measures Investigative Procedures

The major emphasis is on surveillance and early detection of cases.

• Determine if household and other close contacts have been offered chemoprophylaxis by the treating doctor. Ensure that this is done. • Determine if there is a school, kindergarten, child care centre, baby sitter and so on involved, and ensure that all close contacts in such situations are offered chemoprophylaxis. • Ensure that surveillance letters are distributed to all close contacts or their parents.

Individuals should be separated and living and sleeping quarters of those in crowded conditions ventilated. Rifampicin is not recommended for mass prophylaxis because of the danger of producing drug-resistant strains. If the epidemic is due to Groups A or C, vaccination of persons in a given area should be considered.

126

Information Sheet Meningococcal Septicaemia/Meningitis

A case of meningococcal infection has occurred in a child at this school/creche/child minding centre/kindergarten. This disease generally spreads to close intimate and household contacts and can progress very quickly. The indications of this illness to look for are fever, rash, intense headache, nausea and often vomiting. Serious signs include drowsiness, neck stiffness, delirium, coma and sudden collapse. Even the earliest sign (that is, fever), in such contacts warrants immediate medical attention from your local doctor or the nearest hospital. Please take this letter with you. The most important period in which to look for these signs is up to 10 days from the last date of contact with the patient. If you need any further information, please telephone: Public Health Nurse or Medical Officer, Infectious Disease Unit: (03) 9616 7777.

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Meningoencephalitis (Primary Amoebic)

Victorian Statutory Re quirem ent Group A notification.

Two cases notified in Victoria in 1992 and one in 1996 were caused by a free-living amoeba hitherto regarded as an innocuous soil organism incapable of infecting mammals. This is the Balamuthia mandrillaris. It is a rare cause of meningoencephalitis.

Infectious Agent Naegleria fowleri, Acanthamoeba culbertsoni and other species of Acanthamoeba, Balamuthia mandrillaris.

Method of Diagnosis It can be diagnosed by: • Microscopic examination of fresh CSF.

Clinical Features It is a serious disease of brain and meninges.

• Culture on non-nutrient agar plates spread with bacteria (for example, E. coli). • Culture on cell cultures of monkey kidney (Balamuthia

Naegleria spp enter the brain via the nasal mucosa and

spp).

olfactory nerve and causes a syndrome of fulminating pyogenic meningoencephalitis with sore throat, severe headache, neck stiffness and death within 10 days,

Reservoir The amoebae are free-living in water, soil and vegetation.

usually on the fifth or sixth day.

Acanthamoeba spp invade through skin lesions and

Mode of Transmission

spread to the brain and meninges causing insidious and

Naegleria fowleri: By diving, jumping into, or underwater

prolonged disease. Balamuthia spp appears to behave

swimming in warm, fresh water, stagnant ponds or lakes,

similarly and prolonged skin lesions may be present.

or inadequately maintained public heated swimming pools, when water is forced into the nose.

Public Health Significance and Oc c u r re n c e

from the site of primary colonisation (for example,

It is a rare disease with a high case fatality rate.

damaged skin mainly in chronically ill or

Acanthamoeba culbertsoni: Haematogenous spread

immunosuppressed patients) with unknown source of Infection with N. fowleri occurs mainly in young people

infection.

as opposed to infection with Acanthamoeba spp that attacks the chronically ill or immunosuppressed.

Incubation Period

Meningoencephalitis due to N. fowleri has been reported

Usually three to seven days for N. fowleri; longer for

from the USA, Europe, Australia, New Zealand. PNG,

Acanthamoeba spp.

Thailand, India, West Africa, Venezuela and Panama. Cases caused by Acanthamoeba spp have been reported from Africa, India, Korea, Japan, Peru, Venezuela,

Period of Communicability There is no person-to-person transmission.

Panama and the USA.

129

Control of Case No isolation, concurrent disinfection or quarantine is necessary.

Tre a t m e n t Amphotericin B, miconazole and rifampicin. Recovery from infection is rare.

Control of Contacts Investigation of contacts and source of infection should take place.

Preventive Measures • Educate the public on the danger of swimming in lakes and ponds where the infection has been acquired. • Maintain a residual chlorine of 1 to 2 ppm in swimming pools. • Chlorinate public water supplies that are naturally warm.

Epidemic Measures Any grouping of cases needs proper epidemiological investigation.

130

Mumps

Victorian Statutory Re quirem ent

Method of Diagnosis Mumps is usually diagnosed clinically.

Group B notification. School exclusion.

Serologic tests (CF, HAI, EIA) are useful in confirming the diagnosis.

Infectious Agent

The virus can be isolated in duck embryo or cell cultures

Mumps virus (paramyxovirus).

from saliva, blood, urine and CSF during the acute phase of the disease.

Clinical Features Mumps is an acute viral disease characterised by fever, swelling and tenderness of one or more salivary glands,

Reservoir Humans.

usually the parotid.

Mode of Transmission Orchitis occurs in 20–30 per cent of postpubertal males,

It is transmitted by droplet spread and by direct contact

and oophoritis in about 5 per cent of females. Involve-

with saliva of an infected person.

ment of the CNS results in meningitis, encephalitis or meningoencephalitis in up to 15 per cent of cases but permanent sequelae are rare.

Incubation Period Usually 12–25 days; commonly 18 days.

Nerve deafness is one of the most serious of the rare complications (one in 500 hospitalised cases). Pancreati-

Period of Communicability

tis, neuritis, arthritis, mastitis, nephritis, thyroiditis and

It is communicable from six days before to nine days

pericarditis may also occur.

after the onset of swelling of glands.

Public Health Significance and Oc c u r re n c e

illness.

Occurrence is worldwide. Serologic studies show 85 per

Inapparent infection can be communicable.

Maximum infectivity occurs 48 hours before onset of

cent or more people have had mumps infection by adult life.

Susceptibility and Resistance

Most infections in children less than two years of age are

Immunity is lifelong and develops after inapparent and

subclinical.

clinical infections.

Due to effective immunisation, the greatest risk of infec-

Control of Case

tion has shifted to older children, adolescents and young adults.

Exclusion from school, child care or workplace until nine days after the onset of swelling. No specific treatment.

131

Control of Contacts Isolation is unnecessary. Susceptible contacts should be offered immunisation.

Preventive Measures Live attenuated vaccine is available singly or combined with rubella and measles. It is recommended for all children at any age after 12 months, unless specific contraindications to live vaccines exist. Two doses of MMR vaccine are recommended: the first at 12 months and the second at 10–16 years (or Year 6 in Victoria).

Epidemic Measures Susceptible persons should be immunised, especially those at risk of exposure. Those who are not certain of their immunity can be vaccinated if no specific contraindications to live vaccines exist.

132

Mycobacterial Infections Tubercu l o si s

Victorian Statutory Re quirem en t Group B notification.

In the USA, large outbreaks of TB have occurred in institutions, particularly prisons and hospitals. These outbreaks have predominantly affected HIV-infected persons.

School exclusion. WHO estimated that a third of the world’s population is

Infectious Agent Mycobacterium tuberculosis (human tuberculosis). Mycobacterium bovis (cattle tuberculosis).

infected and, globally, tuberculosis accounts for three million deaths annually, with one-fifth of all deaths in adults in developing countries related to TB. Two-thirds of the world’s tuberculosis-infected people reside in Asia and this will have a significant impact on the control of

Clinical Features

TB in Australia as a result of increased immigration.

Tuberculosis (TB) is an acute or chronic infection caused by the tubercle bacillus, Mycobacterium tuberculosis

In Victoria, notified cases of TB have dropped dramati-

and, rarely, by Mycobacterium bovis.

cally, from 1,000 cases in 1954 to 336 in 1994. However, the incidence rate increased from 5.9 per 100,000 in

The initial infection usually goes unnoticed with lesions

1992 to 7.5 per 100,000 in 1994. The proportion of

healing and leaving no residual changes except pulmo-

notified cases in the overseas-born has also increased

nary or tracheo-bronchial lymph node calcifications.

from 37 per cent in 1970 to 75.8 per cent in 1994. The highest country-specific incidence rates are in the

The infection may, however, progress to pulmonary

Vietnamese, Cambodian, Filipino and Chinese-born

tuberculosis or, through blood or lymphatic spread,

populations. This reflects the pattern of disease in their

produce miliary, meningeal or other extrapulmonary

countries of birth.

involvement. Of the overseas-born patients, almost 50 per cent Common symptoms include:

presented within five years and 30 per cent within two

• A chronic cough, especially with haemoptysis.

years of their arrival in Australia.

• Fevers and night sweats. • Loss of weight. • Feeling generally unwell.

Method of Diagnosis TB can be diagnosed by: • Clinical presentation.

Public Health Significance and Oc c u r re n c e Tuberculosis occurs worldwide and had been decreasing steadily over past decades in developed countries. This pattern, however, has been reversed with the arrival

• Tuberculin skin test, using the Mantoux procedure. • Radiographic examination sometimes including CT scans. • Bacteriology, direct staining and culture of sputum or other specimens for the presence of M. tuberculosis.

of HIV and increased mobility of the world’s population. In the USA, TB is on the increase. A combination of factors is thought to be responsible for this increase, including the high rate of HIV infection, overcrowding, limited health care resources and falling living standards.

Definitive diagnosis of TB rests on isolation of M. tuber-

culosis (or M. bovis) from sputum, urine, biopsy material, CSF or other clinical specimens. A negative sputum, however, does not rule out a diagnosis of TB. 133

Recovery and identification of mycobacteria from speci-

In practice, the greatest risk of transmitting infection is in

mens has been made more rapid with test procedures

the period prior to diagnosis of an open case; a sputum

such as the Bactec Systems and DNA probes. Further

smear positive case is more infectious than a case only

information on these tests can be obtained from the

positive on culture.

Mycobacterium Reference Laboratory, VIDRL. The risk of transmitting the infection is significantly

Reservoir

reduced within days to two weeks after commencing appropriate chemotherapy.

Primarily humans; rarely diseased cattle.

Mode of Transmission

Susceptibility and Resistance Clinical suspicion of active disease should be high in

TB is transmitted mainly by inhalation of infectious

those who have a newly positive tuberculin reaction,

droplets produced by persons with pulmonary or laryn-

juveniles with positive tuberculin reactions, and those

geal tuberculosis during coughing, laughing, shouting or

with a history of inadequately treated active tuberculosis.

sneezing. Positive tuberculin reactors with inactive tuberculosis on Invasion may occur through mucous membranes or

chest X-ray without a previous diagnosis of active

damaged skin.

tuberculosis remain at some risk.

Extrapulmonary tuberculosis, other than laryngeal, is

The risk of developing the disease is highest in children

generally not communicable.

under three years of age, lowest in later childhood, but rises again for adolescents, young adults and the very

Urine is infectious in cases of renal tuberculosis.

old.

Bovine tuberculosis results mainly from ingestion of

Special groups at risk:

unpasteurised milk and dairy products.

• Recent immigrants and refugees from countries with a high incidence of tuberculosis. These countries include

Aerosol transmission has been reported among abattoir workers.

Vietnam, Cambodia, China and the Philippines. • Aboriginal people and Torres Strait Islanders. • Drug- and alcohol-dependent people.

Incubation Period From infection to the primary lesion or significant tuberculin reaction: about four to 12 weeks.

• The elderly. • Institutionalised persons including prisoners. • The socially disadvantaged. • Those with HIV infection and AIDS. • Immunosuppressed patients.

Period of Communicability In theory, the patient is infectious as long as viable bacilli are being discharged from the sputum.

• Health professionals. • Diabetics. • Those in close contact with a case of active TB. Of all these groups, the highest risk of active TB is in patients with AIDS.

134

Control of Case

There is, however, a potential risk of MDRTB in Victoria

Tre a t m e n t

as most of the patients notified each year are foreign-

Adequate anti-TB chemotherapy for an appropriate

resistance.

born and developing countries have high rates of drug

period of time will result in almost 100 per cent cure rate. Short treatment regimes have been in use for some

Control of Contacts

years. These involve the use initially of three or four

Contact tracing and surveillance is the responsibility of

drugs (isoniazid, rifampicin, pyrazinamide and ethambu-

the Department and is managed by the TB Program.

tol) for two months, and continuing with isoniazid and

Anyone identified by health care workers as a contact of

rifampicin for a further four months.

a case of TB should be referred to the TB Program on (03) 9616 7777.

Where there is evidence of drug resistance to INH or rifampicin or to both, short course anti-TB chemotherapy

Contact investigation consists of:

would be inappropriate.

• History taking. • Tuberculin testing.

With the introduction of potent anti-TB drugs, hospitalisa-

• Radiographic examination.

tion of tuberculous patients is no longer mandatory unless social conditions or coexisting medical conditions

The extent of investigation is governed by the character-

dictate otherwise.

istics of the source case.

The success of treatment relies heavily on patient

The scope of investigation is extended when the follow-

compliance and direct supervision should be the aim of

ing factors in the source case are present:

any treatment program.

• AFB in sputum smear. • Cavitation on chest X-ray.

Compliance is important to prevent the development of

• Laryngeal TB.

drug resistance.

• Cough. • High volume and reduced viscosity of respiratory

For drugs used in treatment of tuberculosis, see TB in

Australia and New Zealand into the 1990s, Australian Government Publishing Services, Canberra. Telephone:

secretions. • Where there is evidence of tuberculin conversion in any of the contacts.

(06) 289 7646, or fax (06) 289 6957. Note

Multi-Drug Resistant TB (MDRTB)

Tuberculosis testing should never be omitted for child

Resistance to at least isoniazid and rifampicin (whether

contacts.

or not it is also resistant to other drugs) is classified as multi-drug resistant. MDRTB is rare in Australia. It has remained at less than 2 per cent per year in the past 15 years.

135

Following tuberculin testing, contacts can be grouped

See Management, Control and Prevention of

as:

Tuberculosis,Guidelines for Health Care Providers

• Initial negative reactors:

published by Human Services and available from Infor-

– Tuberculin conversion takes a few weeks and may not have occurred yet in these contacts.

mation Services, Human Services, telephone: (03) 9616 7333.

– Testing should be repeated in eight to 12 weeks after a break of contact or in some cases, initial testing may be delayed for eight weeks.

Preventive Measures The public should be educated about the mode of

– Chest X-rays may be indicated.

spread and methods of control and the importance of early diagnosis.

Initial positive reactors: • Definition of a positive tuberculin reactor. Conditions

Dimension of Induration (greater than or equal to)

No BCG, adult Past BCG, adult HIV-infected individual No BCG, child BCG 5 years ago—child

10 mm 15 mm 5 mm 5 mm 15 mm 10 mm

Chemoprophylaxis should be given to persons with a positive tuberculin reaction without any clinical or radiological evidence of active tuberculosis including those who are HIV sero-positive. The only drug currently used for routine chemoprophylaxis is isoniazid given for six to 12 months as a single daily dose of 5.0 mg/kg bodyweight up to a maximum of

Initial positive reactors should be evaluated to exclude

300 mg.

active disease. The positive tuberculin test may signify recent tuberculin conversion.

People who should be considered for chemoprophylaxis are recent convertors, particularly children and teenag-

Contacts identified by the TB Program as requiring

ers, and contacts who react strongly to the tuberculin

further assessment are referred to chest physicians.

test.

When X-ray and physical examination are normal,

Chemoprophylaxis is not usually recommended for

contacts with positive reaction should be offered isoni-

people over 35 years of age because of the hepatotoxic-

azid chemoprophylaxis given once daily at a dosage of

ity of isoniazid.

5mg/kg body weight to a maximum of 300 mg daily. However, there is a group of people who, in spite of their Treatment should be for a minimum period of six months.

age (over 35), should be considered for chemoprophylaxis.

Contacts, with positive reactions, who refuse isoniazid should be kept under surveillance and followed up with

This group includes all tuberculin-positive persons

chest X-rays taken at six months and 12 months.

receiving corticosteroids, on immunosuppressive drugs, insulin-dependent diabetics, persons following gastrectomy and persons with silicosis.

136

Epidemic Measures • Recognise and treat new cases. • Search for the sources of infection.

International Measures Individuals from high-prevalence countries should be Xray screened upon immigration.

137

Mycobacterial Infections Atypical (Non-Tuberculosis)

Victorian Statutory Re quirem ent Group B notification (under tuberculosis).

Cases of M. kansasii lung infection have occurred in western Victoria in recent years. Infection with M. marinum is associated with contact with swimming pools, aquariums and other bodies of water.

Infectious Agents Mycobacteria other than Mycobacterium tuberculosis. These include M. avium-intracellulare complex (MAC), M.

kansasii, M. scrofulaceum, M. fortuitum, M. marinum, M.

M. ulcerans infection should be considered as a possible diagnosis of chronic skin lesions in persons exposed to the eastern Victorian coastal environment.

ulcerans, M. chelonae. Atypical mycobacteria may colonise and infect persons

Clinical Features MAC and M. kansasii are rare causes of lung disease in

without causing clinical disease. Skin tests to tuberculin and other mycobacterial derivatives may be positive in such persons.

humans, and mainly affect middle-aged and elderly persons with underlying chronic lung conditions. Disseminated MAC infection frequently occurs in advanced HIV infection, but is rare in immunocompetent hosts.

Method of Diagnosis Clinicians who suspect infection with atypical mycobacteria should liaise with a pathology laboratory to ensure that clinical specimens are appropriately collected and transported.

Cervical and submandibular lymphadenitis due to MAC,

M. scrofulaceum and M. kansasii may occur in otherwise healthy young children.

To establish a definite diagnosis of atypical mycobacterial infection, organisms must be cultured from a case with clinically compatible disease or identified by direct

M. fortuitum and M. chelonae cause skin and wound infections and abscesses. They are frequently associated with trauma or surgery.

M. marinum causes ‘swimming pool granuloma’, a nodular lesion that may ulcerate and is usually located on an extremity.

smear on at least two occasions. Histologic examination of biopsies of clinical lesions may also assist in the diagnosis.

Reservoir Mycobacteria are ubiquitous in the environment. Some pathogenic non-tuberculous mycobacteria have been cultured from various environmental sources (such as

M. ulcerans infection causes ‘Bairnsdale’ or ‘Buruli’ ulcer, a chronic ulcerative skin lesion, usually of an extremity.

ground waters, dust and soil), while the environmental niches of many others remain unknown.

Public Health Significance and Oc c u r re n c e Disease due to atypical mycobacterial infection is relatively rare.

139

Mode of Transmission The mode of transmission can rarely be determined for individual cases. Atypical mycobacteria are probably transmitted by aerosol from soil, dust or water, by

Disseminated and pulmonary infections are treated with combinations of antimycobacterial drugs. The clinical outcome is strongly influenced by the underlying health of the host.

ingestion, or by skin inoculation. No specific measures are needed for contacts of cases. Person-to-person spread of atypical mycobacteria is rare. M. avium causes disease in poultry and pigs but animal-to-human transmission is rare.

Incubation Period The incubation periods of atypical mycobacterial infections can rarely be determined, but are probably weeks to several months.

Period of Communicability Communicability of human cases is usually not a practical concern. Localised foci of disease due to atypical mycobacteria suggest that an established environmental focus of organisms may remain the source of infections for years.

Susceptibility and Resistance Persons with tissue damage (skin trauma, pulmonary disease) and immunodeficiency may be at increased risk of atypical mycobacterial infection.

Control of Case Cases of atypical mycobacterial infection usually require specialist management. Skin lesions and childhood lymphadenopathy are usually cured by surgery, sometimes with antimycobacterial drugs.

140

P e d ic ulo sis/ Headlice

Victorian Statutory Requirem en t

Method of Diagnosis

Statutory notification not required.

parted.

Lice may be seen on the scalp if the hair is rapidly

School exclusion. Eggs (nits) are detected on the hair shaft close to the

Infectious Agent

scalp, behind the ears and at the back of the neck. (Nits

Pediculus capitis:

dead.)

further than 10–15 mm from the scalp are hatched or

• Lice are tiny parasitic insects, about 2 mm to 3 mm long and coloured reddish brown to whitish brown. • The louse is wingless, has a flat body and six legs.

Discarded skins and black sandy excrement are seen on pillows and collars.

Headlice remain close to the scalp and move quickly when disturbed. • The adult louse is capable of laying eggs (nits) after 10

Itching of the scalp causing the person to scratch may prompt examination.

days. • Eggs are tiny specks that are firmly glued to the hair close to the scalp. • Eggs that are more than 12 mm from the base of the

Reservoir Humans, usually affecting most family members.

scalp are dead or are only empty egg casings that are pearly white and resemble dandruff. • The life cycle of the louse is about 28–30 days.

Mode of Transmission Spread of lice is mainly by head-to-head contact.

Clinical Features

Other modes of transmission are shared headgear and

Itching occurs, generally behind the ears and at the back

shared combs but these are less common.

of the neck. Head lice do not live in bedding, furniture or clothes.

Public Health Significance and O c c u r re n c e

Incubation Period

Headlice infestation is more of a social problem than a

The incubation period varies slightly according to the

public health problem as head lice do not transmit any

temperature needed for egg hatching.

disease. Eggs usually hatch in seven to 10 days. Outbreaks are common among children in schools and child care facilities.

Sexual maturity occurs eight to 10 days after hatching.

Lice may infest people of any socioeconomic position,

Period of Communicability

age or sex.

Communicability can occur as long as lice or eggs remain alive on the infested person.

141

Susceptibility and Resistance Lice are host-specific.

Note

Pregnant women, people with sensitive skin, and parents with children less than 12 months old should consult a

Those that live on animals will not infest humans, al-

doctor before using pediculicides.

though they may be present transiently.

Preventive Measures Repeated infestations often result in dermal hypersensitivity.

• Exclude infested children until treated. • Educate children, child care workers and parents about headlice and the importance of regular inspec-

Control of Case • Exclude confirmed or suspected case from school or child care facility. • Readmit the day after appropriate treatment has commenced. • Do not preclude readmission because of the presence of a few remaining nits. • Treat with an appropriate lotion that kills louse and egg. • Use products containing maldison or permethrin as the first line of treatment. • Apply again seven to 10 days after treatment if using a product that does not kill the egg, such as pyrethrins. • Take care to avoid contact with the eyes, nose and throat. • Wash clothes, linen and towels on a hot water cycle, and soak combs and brushes in hot water and detergent for 10 minutes. Note

To prevent unnecessary or repeated exposure to pediculicides, the person applying the chemical should wear protective gloves.

Control of Contacts All household contacts should be treated simultaneously. Close contacts should be inspected regularly for signs of infestation.

142

tion of heads, and discourage sharing of personal items such as combs and hats. • Promote grooming and general hygiene. • Educate the public.

Information Sheet H e a d lic e/ Pedic ulosis

What are Head Lice? Head lice are tiny insects that live on the human scalp and feed on blood. The adult louse is wingless, about 2 mm long, has a flat body, six legs and varies in colour from whitish-brown to

Transmission may occur indirectly by sharing personal items such as combs, brushes and hats but is far less common. Head lice are not spread by lack of cleanliness and may affect people of any social class.

reddish-brown. They do not spread disease. Head lice remain close to the scalp and move quickly when disturbed.

Lice that live on animals do not live on humans, and vice versa.

They cannot fly or jump; they only crawl.

What are the Signs of Head Lice? The life cycle of the louse is about 28–30 days.

Nits are usually noticed first and are easier to see behind the ears and at the back of the neck.

What are Nits? Head lice lay eggs called nits that are oval-shaped

An itchy scalp: lice bites result in generalised scratching.

specks that firmly attach to the hair very close to the scalp (within 6 mm).

Lice may be seen on the scalp if the hair is rapidly parted.

Young lice usually hatch from the eggs within seven to 10 days and leave a pearly white empty case behind still cemented to the hair. Nits found more than 12 mm out from the scalp are dead or are only empty casings since human hair grows

Finding a dry black powder, grey casts or skins on the pillows in the morning, suggests the presence of lice.

What is the Incubation Period? Nits usually hatch in seven to 10 days.

approximately 1 cm/month. Lice are capable of laying eggs eight to 10 days after Once hatched, the lice are capable of laying eggs within

hatching.

10 days. Large numbers of nits resemble dandruff, except that nits cannot be brushed out.

What is the Contagious Period? As long as lice or nits (eggs) remain alive on the infested person.

How do Head Lice Spread? Head lice outbreaks are common among children in

How To Control Spread

schools and child care facilities because children have

• Exclude confirmed or suspected cases from school or

close head contact with one another throughout the day

child care facility. Readmit the day after appropriate

in classroom and playgrounds. This enables easy

treatment has commenced. The presence of a few

transmission from person to person.

remaining nits does not preclude readmission. 143

• Treat with an appropriate lotion that kills louse and nits. • Use a fine metal comb or fingernails to remove nits. • Treat all household contacts simultaneously. • Wash clothes, bed linen and towels on a hot water cycle. • Wash combs and brushes in hot water and detergent. • Never share combs, brushes or hats. • Inspect close contacts regularly for signs of infestation.

How To Treat Head Lice • There are a number of effective products available for the treatment of head lice. These products can be

Note

The whole family should be treated if one member is found to have head lice. Compliance with product instructions eliminates the need for nit removal after treatment. For children less than 12 months of age, the recommended treatment is Lyban Foam or Pyrifoam. • Lyban Foam, Pyrifoam and Banlice Mousse are also recommended as safe preparations in pregnancy.

obtained from a chemist without prescription. • Resistant head lice can be eradicated by switching to a different product.

If Lice Are Found Following Tre a t m e n t

• The most effective products contain maldison or

The lotion may have been inadequately applied.

permethrins: 0.5 per cent Malathion or Maldison Lotion (Lice Rid or Cleensheen). • The lotion should be applied to dry hair and left for 12 hours. Care should be taken to protect the eyes. • The hair is then washed and combed with a fine-tooth comb. • Permethrins (Nix Creme Rinse, Quellada Creme Rinse, Quellada Head Lice Treatment, Pyrifoam Shampoo). These liquids are applied to clean, damp hair for 10 minutes, then rinsed out. An application of Nix may be repeated in two weeks if necessary. The other applications may be repeated after one week. • Pyrethrins (Lyban Foam, Banlice Mousse) should be applied according to directions.

The person may have been in contact with another infected person.

Prevention • Ordinary hair care is the best way to discourage head lice. • Daily brushing is likely to damage the lice. • To obtain effective control of head lice, the whole community should be involved. • Parents should be encouraged to screen themselves and their children regularly in the home, and to treat themselves only when necessary.

Listing of Currently Available Head Lice Preparations, August 1997 Product

Dose/Form

Active Ingredients

Concentration

Cleensheen Lice Rid Nix Creme Rinse Quellada Creme Rinse Quellada Head Lice Treatment Pyrifoam Lyban Foam

Liquid Liquid Liquid Liquid Liquid Shampoo(foam) Liquid (foam)

Banlice Mousse

Mousse

Maldison Maldison Permethrin Permethrin Permethrin Permethrin Pyrethrins Piperonyl butoxide Pyrethrins Piperonyl butoxide Quaternium-52

0.5 per cent 0.5 per cent 1.0 per cent 1.0 per cent 1.0 per cent 10 mg/ml 0.165 per cent 2.0 per cent 1.65 mg 16.5 mg 10 mg/g

144

Pertussis (Whooping Cough)

Victorian Statutory Re quirem ent Group B notification. School exclusion.

• An illness lasting two weeks or more with one of the following: – Paroxysms of coughing. or – Inspiratory ‘whoop’ without other apparent causes. or – Post-tussive vomiting.

Infectious Agent Bordetella pertussis.

Public Health Significance and O c c u r re n c e

Clinical Features

It is a distressing and often serious illness, particularly in

The catarrhal state may be indistinguishable from a viral

children under one year of age.

upper respiratory tract infection. The mortality rate is 0.5 per cent in infants under six The infection damages respiratory epithelium, producing respiratory obstruction and paroxysmal coughing, often

months.

with a characteristic whoop.

High immunisation levels reduce cases, and good nutrition and medical care reduce case fatality.

There is little fever. Many vaccinated adults may have asymptomatic infecApnoea, seizures and encephalopathy may occur.

tion and act as a source of infection for younger children.

Infants aged less than six months and adults often do not have the characteristic whoop.

Method of Diagnosis It can be diagnosed by:

Paroxysms frequently end with the expulsion of clear,

• Elevated B. pertussis-specific IgA in serum.

tenacious mucus, often followed by vomiting.

• DFA identification of B. pertussis in nasopharyngeal specimens.

Pneumonia is the most common cause of death. Fatal encephalopathy, probably hypoxic, and inanition from

• Culture:

repeated vomiting occasionally occur.

– The definitive diagnosis of B. pertussis infection relies on the culture of the organism from nasopharyngeal

Case Definition

– Unfortunately, the organism is fastidious and slow growing and its culture is usually complicated by

swabs.

The case can be defined by: • Isolation of Bordetella pertussis from a clinical specimen. or • Elevated Bordella pertussis-specific IgA in serum, or B.

pertussis antigen in a nasopharyngeal specimen using

contamination and overgrowth of other nasopharyngeal organisms. – Nasopharyngeal (not anterior nares) specimens should be taken with Dacron or calcium alginate swabs rather than cotton swabs. – Patient specimens should be directly plated on

immunofluorescence with a history of clinically compat-

selective transport media; for example, Charcoal

ible illness.

agar, Regan-Lowe, Modified Stainer-Scholte agar,

or

Fresh Bordet-Gengou medium. 145

– Isolation rates are highest in the first three to four weeks of illness. Prior antibiotic treatment will mark-

Thereafter, communicability decreases and becomes negligible in about three weeks.

edly decrease the detection rate. • Fluorescent antibody tests: – Direct fluorescent antibody identification of B. pertus-

sis in nasopharyngeal specimens is a useful tech-

When treated with erythromycin, the period of infectivity usually lasts five days or less after commencement of therapy.

nique. – This needs good reagents and experienced personnel.

Susceptibility and Resistance

– False negative and false positive results occur.

Young infants are at risk of disease as there is poor

– These tests are particularly useful in situations later in

placental transfer of immunity.

disease or during antimicrobial therapy when viable organisms are no longer present. • Other tests:

Severity is greatest in young infants; milder and atypical cases occur in all age groups.

– Polymerase Chain Reaction (PCR). – Serology, anti-B. pertussis IgA, IgG or IgM may be utilised in diagnosis. The role of these studies in

Incomplete immunisation or waning immunity results in cases occurring in older children and adults.

clinical practice remains to be clarified. There may not be lifelong immunity, even after clinical

Reservoir Humans only.

disease.

Control of Case The suspected case should be excluded from the

Mode of Transmission

presence of others outside the home (especially young

It is transmitted primarily by direct contact with dis-

children and infants) until the patient has received more

charges from respiratory mucous membranes of infected

than five days of a minimum 14-day course of antibiotics.

persons by the airborne route, probably droplet spread. Antibiotics: Erythromycin shortens the period of commuAdults and older siblings may be infected despite

nicability. Antibiotics do not reduce symptoms unless

adequate vaccination, and may transmit infection without

they are given during the incubation period or early in the

clinical disease.

catarrhal stage of the disease. (A 14-day course of cotrimoxazole should be given if erythromycin is contraindi-

Incubation Period

cated.)

It is commonly seven to 10 days; rarely more than 14

Antibiotics should be given if case has been coughing

days.

less than three weeks.

Period of Communicability It is highly communicable in the early catarrhal stage before the onset of paroxysmal cough.

146

Exclusion from school should take place until a medical certificate of recovery from infection has been received. This certificate is issued when the case has received at least five days of 14-day course of erythromycin.

Note

This is in accordance with NH&MRC guidelines for school exclusion. The Infectious Diseases Regulations in Victoria will be amended accordingly.

Preventive Measures • Educate the public to the dangers of whooping cough and the advantages of initiating immunisation at two months of age and adhering to the immunisation schedule (DTP at two, four, six and 18 months and five

Control of Contacts Vaccination: • Protection is not afforded by passive immunisation. • Close contacts under eight years of age who have not received five doses of DTP should be given a DTP dose as soon after exposure as possible.

years). • Delay immunisation only for significant intercurrent infection or evolving neurological disorder. Minor URTI is not a contraindication to immunisation.

Health Care Workers When there is an outbreak, consider protection of health

Antibiotics: A 14-day course of erythromycin for house-

workers at high risk of exposure by using a 14-day

hold or other close contacts, regardless of immunisation

course of erythromycin.

status, is recommended. Erythromycin should be given as soon as possible. It should be given no later than 14 days after the recipient’s first contact with the primary

Epidemic Measures

case during the infectious period (in high-risk household

• Search for unrecognised and unreported cases and

exposure settings, chemoprophylaxis may be considered

ensure their exclusion from schools and child care

for up to 21 days).

centres. Protect preschool children from exposure and assure adequate preventive measures for exposed

Exclusion: Inadequately immunised household contacts under eight years old should be excluded from school

children. • Consider accelerated immunisation with the first dose

and child care centres until cases and contacts have

at two weeks of age and the second and third doses at

received a minimum of five days of a 14-day course of

four-week intervals. Complete immunisation for those

erythromycin.

who have already commenced a course. • Initiate antibiotic therapy for all exposed individuals.

Investigation: A search for early, missed and atypical cases is indicated where a non-immune infant or young child is, or might be, at risk, in school. Check immunisation status of close contacts. Note

Close contacts may include all children in a child care centre, or all children in the same school classroom. Please contact the Department of Human Services for further advice.

147

Plague

Victorian Statutory Re quirem ent

Public Health Significance and O c c u r re n c e

Group A notification.

This is a highly infectious disease, which is endemic in Indonesia, Burma and especially in Vietnam.

Infectious Agent

Plague is not present in Australia.

Yersinia pestis, the plague bacillus. Wild rodent plague exists in parts of USA, South

Clinical Features It is an acute, severe infection appearing in a bubonic or pneumonic form.

America, Africa, Central and South East Asia. Human plague has occurred recently in several countries in Africa and in India.

Bubonic plague:

Method of Diagnosis

• This is the most common form.

It can be diagnosed by:

• Onset is abrupt and associated with chills.

• Visualisation of Gram-negative organisms on direct

• Enlarged lymph nodes (buboes) appear with, or shortly before, the fever. • The most commonly involved lymph nodes are femoral or inguinal followed by axillary and cervical. • The nodes are tender, firm and fixed, and may suppu-

microscopic examination of Gram-stained smear of clinical material. Examination by FA test is more specific and particularly useful in sporadic cases. • An antigen capture ELISA test (if available) may permit an early rapid diagnosis in acute cases.

rate in the second week. Diagnosis is confirmed by:

Primary pneumonic plague: • Onset is abrupt with high fever, tachycardia and headache. • Cough develops within 24 hours. Sputum is mucoid at first and then becomes bright red and foamy.

• Culture of the organism from blood, sputum, CSF or lymph node aspirate. • A fourfold rise or fall in titre in a serological test (the passive haemagglutination test (PHA) is most commonly used).

• Chest X-rays show a rapidly progressing pneumonia.

Secondary pneumonic plague:

Reservoir

• Occurrence as a complication of bubonic plague, due

Wild rodents.

to septicaemia with lung involvement. • This clinical form may be a source of primary pneumonic or pharyngeal plague due to aerosolised drop-

Rabbits, hares and domestic cats may also be a source of infection.

lets of sputum.

149

Mode of Transmission It is transmitted from rodent to human by the bite of an infected flea vector.

effective therapy. For patients with pneumonic plague, isolate the case to prevent airborne spread until the completion of three days of appropriate antibiotic therapy with clinical improvement.

Human-to-human transmission comes from inhalation of infected droplets spread by coughing patients with plague pneumonia or pharyngitis.

• Disinfect sputum, purulent discharges and soiled articles concurrently. • Clean terminally. • Handle bodies of plague victims with strict aseptic

It can also be transmitted by handling tissues of infected animals.

precautions. • Use streptomycin, tetracyclines, chloramphenicol early when they are highly effective.

Incubation Period Usually one to six days.

Control of Contacts Contacts and sources of infection should be investigated.

Period of Communicability It is communicable as long as fleas remain infective.

Close contacts of confirmed or suspected plague pneumonia cases should be offered chemoprophylaxis

Fleas may remain infective for months under suitable

with tetracycline or sulphonamides and placed under

conditions of temperature and humidity.

surveillance for seven days.

Bubonic plague is not usually transmitted from person to

Preventive Measures

person unless there is contact with pus from suppurating buboes.

• Reduce the likelihood of people being bitten by infected fleas, or being exposed to pneumonic plague

Pneumonic plague may be highly communicable under appropriate climatic conditions; overcrowding facilitates transmission.

patients. • Educate the public on the importance of appropriate storing food to reduce rodent problem, and avoiding flea bites by using insecticides and repellents. • Control rats on ships, docks and in warehouses.

Susceptibility and Resistance The disease does not always confer immunity.

• Immunise with a vaccine of killed bacteria that gives protection for at least several months (two to three primary doses plus booster). This vaccine is used for

Control of Case • Use a safe insecticide to rid the patient (including clothing and baggage) of fleas. • Hospitalise the case. For cases with bubonic plague, if there are no respiratory symptoms, secretion precautions are indicated for three days after the start of

150

people entering high-incidence areas, and laboratory or field workers handling plague bacilli or infected animals. The vaccine is available from CSL.

Epidemic Measures • Investigate all possible plague deaths by autopsy and laboratory examination. • Inform the public through the press and news media (but avoid panic). • Destroy all rodents within affected areas, after satisfactory flea control has been achieved. • Protect field workers against fleas by using insecticide powders and insect repellents.

International Measures Within 24 hours, government should notify WHO and adjacent countries of the first cases of plague in any area previously free of the disease according to the International Health Regulations. Measures applicable to ships, aircraft, land transport and international travellers arriving from plague areas are specified in International Health Regulations 1969, third annotated edition 1983, WHO, Geneva. Prior to departure from an area where there is an epidemic of pulmonary plague, those suspected of significant exposure should be placed in isolation for six days after their last exposure. On arrival of a suspected infected ship or aircraft, travellers should be disinfected and kept under surveillance for not more than six days from the date of arrival.

151

Pneumonia Due to Chlamydia pneumoniae

Victorian Statutory Re quirem ent

Method of Diagnosis

Nil.

positive for any chlamydial infection.

CFT is used but is only genus-specific and may be

Currently, the laboratory diagnosis of C. pneumoniae

Infectious Agent

infection is made by detecting a rise in antibody titre

Chlamydia pneumoniae strain TWAR. Chlamydia

using MIF.

pneumoniae (TWAR) was named in 1989 as a new member of the chlamydia family with C. trachomatis and

More recently, antigen detection in nasopharyngeal

C. psittaci.

aspirate, throat swabs or bronchial lavages by direct immunofluorescence has become available.

Clinical Features

Diagnosis by PCR methodology is under development.

These are similar to psittacosis with headache, fever, myalgia and the development of a dry cough on days three to five.

Reservoir Humans.

Sore throat and sinusitis are occasionally seen. A chest X-ray usually reveals lower zone changes.

Mode of Transmission The mode of transmission is not defined. Possibly, it

Most cases of the C. pneumoniae pneumonia are consid-

occurs through direct contact with secretions, via fo-

ered mild to moderate in severity.

mites, and airborne spread.

Patients who have died usually have had underlying

Incubation Period

disease or additional bacterial infections.

Public Health Significance and Oc c u r re n c e C. pneumoniae is a common respiratory pathogen

Usually five to 10 days.

Period of Communicability The period of communicability is not defined, but presumed to be prolonged. Outbreaks may last for months.

causing a recognisable clinical pattern. A carrier state is probably important in maintaining and

Susceptibility and Resistance

spreading infection in the community.

There is increased likelihood of clinical disease in the presence of pre-existing chronic disease.

In a Melbourne study, 10 per cent of cases of community-acquired pneumonia were due to this pathogen.

Immunity usually occurs after infection, but reinfection may occur.

153

Control of Case • Apply personal hygiene measures. • Cover mouth when coughing. • Dispose of discharges from mouth and nose in a sanitary manner and wash hands.

Tre a t m e n t Doxycycline for 14 days. Erythromycin for 14 days is an alternative, although relapses have occurred with short courses. Roxithromycin is also effective.

Preventive Measures • Avoid crowding in living and sleeping quarters. • Educate the public in hygiene measures.

Epidemic Measures Case finding and treatment.

154

Poliomyelitis

Victorian Statutory Re quirem en t

Method of Diagnosis

Group A notification.

culture systems with CSF, faecal specimens or oropha-

It is diagnosed by isolation of virus by inoculating cell ryngeal secretions.

School exclusion. The National Polio Reference Laboratory should be

Infectious Agents Poliovirus, types 1, 2 and 3 (enterovirus).

Clinical Features The clinical features range from inapparent infection,

contacted.

Reservoir Humans only. There are no long-term carriers.

through non-specific febrile illness, aseptic meningitis,

Mode of Transmission

paralytic disease and death.

Transmission is by direct contact through close association.

When symptoms occur they include fever, malaise, headache, nausea and vomiting, muscle pain, stiffness

Faecal-oral route is especially important where sanitation

of the neck and back with or without flaccid paralysis.

is poor.

Case Definition

Pharyngeal spread is more important where there is good sanitation and during epidemics.

The disease is defined as an acute onset of a flaccid paralysis of one or more limbs with decreased or absent tendon reflexes in the affected limbs without other

Incubation Period

apparent cause, and without sensory or cognitive loss.

Usually seven to 14 days; the range is three to 35 days for paralytic cases.

Public Health Significance Each case of indigenous poliomyelitis needs a complete

Period of Communicability

clinical, laboratory and epidemiological investigation and

The risk of transmission of infection is greatest for the

should be regarded as an outbreak since each case

seven to 10 days prior to and following the onset of

probably represents 100–200 infected persons (unless

symptoms.

the case is vaccine-associated). The virus persists in the pharynx for approximately one Outbreaks have occurred in developed countries among

week and in the faeces for up to six weeks, or longer in

pockets of unimmunised persons.

the immunosuppressed.

Polio is still endemic in many developing countries.

155

Control of Case

Epidemic Measures

• Obtain details of vaccine history, lot number, virus

After a single case of paralytic poliomyelitis from wild

type, severity and persistence of residual paralysis 60

poliovirus, a dose of OPV should be given to all persons

days after onset (if vaccine-associated).

in the immediate neighbourhood of the case, regardless

• Isolate patient with Standard Precautions in hospital.

of their previous immunisation history.

Exclude from schools and children’s settings until at least 14 days after onset of illness and until receipt of a

All suspected cases of polio must have appropriate

medical certificate of recovery from infection.

faecal specimens sent to the National Polio Reference

• Disinfect throat discharges, faeces and soiled articles.

Laboratory.

• Determine whether the patient’s disease represents an indigenous or imported case.

Control of Contacts

International Measures National health administrations are expected to promptly inform WHO of outbreaks.

Vaccination of families and other close contacts contributes little to immediate control because susceptible

The notification should be supplemented with details of

contacts are generally already infected by the time the

source, nature, extent of the epidemic and virus identity

first case is recognised.

type.

A thorough search for unrecognised cases, especially among children, ensures early detection and facilitates control.

Preventive Measures OPV (Sabin) is recommended at two, four and six months, five years and 15 years. IPV (Salk) should be substituted in those for whom the oral vaccine is contraindicated (that is, those who are immunosuppressed). Persons who have a household contact who is immunosuppressed should receive IPV. For unimmunised or incompletely immunised adults, a course of OPV should be commenced or completed if there is risk of exposure; for example, travel to an endemic area, or a person in the household being immunised with OPV.

156

Psittacosis

(Ornithosis)

Victorian Statutory Re quirem ent Group B notification.

Infectious Agent Chlamydia psittaci.

• For infants with pneumonia, swabs may be collected from the posterior nasopharynx or the throat, although aspirates collected by intubation appear to be superior.

Birds: • Special transport medium and culture techniques are required so it is necessary to contact the Avian Medicine Section at the Victorian Institute of Animal Sci-

Clinical Features

ence, Attwood (03) 9333 1200 to obtain further details

The onset is usually abrupt with fever, chills, malaise,

of specimen collection and transport requirements.

headache, myalgia and upper or lower respiratory tract symptoms.

Transport: • For transport of specimen, see appendix 7.

Cough is often a feature with little sputum. Chest X-rays often show focal consolidation.

Reservoir Birds of many different types, especially parakeets, parrots, pigeons, waterfowl, seabirds, budgerigars,

The illness, which usually lasts for seven to 10 days, is mild or moderate, but may be severe in older, untreated

turkeys and ducks. Healthy birds may be carriers. Wild birds may be a source of infection.

patients. Complications include encephalitis, endocarditis, myo-

Mode of Transmission

carditis and thrombophlebitis. Relapses may occur.

Infection is generally acquired by inhaling the agent from desiccated droppings and secretions (ocular and nasal)

Public Health Significance and Oc c u r re n c e

of infected birds in an enclosed space, or directly from

Outbreaks generally occur in individual households or

Laboratory infections and rare person-to-person trans-

are associated with pet shops or aviaries. They can

mission associated with paroxysmal coughing have

occur occupationally in poultry workers.

occurred.

Chlamydia psittaci is highly infectious, and immunity

Incubation Period

following infection is incomplete and transitory.

infected birds.

Usually four to 15 days; commonly 10 days.

Method of Diagnosis Humans: • Infection is also generally diagnosed by serology using paired acute and convalescent phase sera.

Period of Communicability Infected birds may shed the agent for a prolonged period.

• Culture of the organism from sputum, blood or biopsy material (spleen, liver) is generally not performed (because of danger to laboratory workers). 157

Susceptibility and Resistance Immunity following infection is incomplete and transitory. Older adults have a more severe illness.

Wearing gloves and dust masks are recommended when cleaning areas where bird nests are found.

Preventive Measures • Educate the public about the danger of household or

Control of Case Isolation is not necessary, but instruct patient to cough into disposable tissues.

occupational exposure to infected pet birds. • Prevent or eliminate infections of birds by quarantine and antibiotic treatment. • Implement appropriate surveillance of commercial

All discharges should be disinfected and terminal cleaning performed.

Tre a t m e n t Tetracyclines should be continued for 10–14 days after temperature returns to normal. If tetracyclines are contraindicated (pregnancy, children less than eight years) erythromycin should be used.

psittacine birds, pet shops and aviaries. • Destroy or treat infected birds and disinfect premises.

Epidemic Measures Cases should be investigated in order to recognise more extensive outbreaks. Outbreaks should be reported to Department of Human Services, Victoria and the Department of Natural Resources and Energy.

Control of Contacts The diagnosis in symptomatic contacts should be considered.

Control of Environment The origin of suspected birds should be traced. The Department of Natural Resources and Energy should be informed. Large doses of tetracycline will suppress, but not eliminate, infection in poultry flocks and may complicate investigations. Appropriate disinfectants for infected premises are iodophors (for cages), 5 per cent formalin (for surfaces) and phenol (for wastes). For routine daily or weekly disinfection of floors and cages respectively, iodophors or formalin are used.

158

Q Fever

Victorian Statutory Re quirem ent

It can be diagnosed by a demonstrated rise in specific

Group B notification.

antibodies by complement fixation (CF) test.

Scheduled WorkCover compensable disease for certain

Preferably, blood samples are collected 14 days apart.

Method of Diagnosis

occupations.

Acute Q Fever:

Infectious Agent Coxiella burnetii.

Clinical Features The onset is usually acute and characterised by fever, chills, sweats, severe headache (especially behind the eyes), weakness, anorexia, myalgia and cough. Transient mild rashes are an occasional feature.

• Fourfold rise in CFT antibodies to phase II antigen that can be confirmed with phase II IgM ELISA.

Chronic Q Fever: • High CFT antibody titre to phase I and II, and low or absent IgM antibody. • An alternative and improved serological test for diagnosis is based on direct immunofluorescence (IF) testing.

Abnormal liver function tests are common.

Reservoir

Chronic complications include granulomatous hepatitis

No endemic reservoir is known in Victoria (even though

and endocarditis. The latter is the most serious concern

Victorian sheep are sero-positive).

as it usually involves the aortic valve and occurs months to years after the acute illness.

The organism is commonly introduced in stock from interstate.

A relapsing fatigue syndrome may occur in 20–40 per cent of cases.

Animals include goats, cattle, sheep, other farm and domestic animals and some wild animals (including

Public Health Significance It is an acute febrile rickettsial disease of low mortality but significant morbidity.

kangaroos, bandicoots and feral pigs).

Mode of Transmission Q fever can be transmitted by:

It is most commonly found in abattoir workers who have

• Inhaling water droplets and dust that have been

recently handled contaminated stock (for example, feral

contaminated by placental tissues, birth fluids or

goats or sheep from interstate endemic areas). It is an occupational hazard for tannery and knackery workers,

• Having direct contact with contaminated materials

shearers, meat inspectors, dairy workers, farm workers, animal transporters, wool sorters and veterinary personnel. It also occurs in others handling fomites; for example, laundering contaminated clothing.

excreta of infected animals. such as straw, wool or hides, or during slaughtering of infected animals. • Drinking unpasteurised milk from an infected animal.

Incubation Period Usually two to four weeks, commonly 19–21 days, and

Outbreaks are usually of short duration.

occasionally up to 60 days. 159

Period of Communicability

Epidemic Measures

Person-to-person spread occurs rarely, if ever.

All notified cases should be investigated to ascertain if other associated cases are likely to have occurred.

Susceptibility and Resistance Infection usually confers lifelong immunity.

If two or more related cases are evident in the same workplace, staff should be assessed for immune status (if not already known) with CFT levels and skin testing.

Control of Case The notification details required are: • Occupation. • Possible source of infection (for example, batch of stock from endemic areas). • Any other known recent cases (for example, at

Non-immune staff should be offered vaccination. The Department of Natural Resources and Energy and the Occupational Health and Safety Organisation should be notified.

workplace). • Immunisation status for Q Fever.

Q Fever Guidelines Persons who wish to be vaccinated should first complete

Specific treatments are:

a questionnaire to elicit the type and duration of their

• Tetracycline for two to three weeks. When endocarditis

work (abattoir, shearer, farmer, veterinary surgeon),

occurs, treatment should be prolonged and rifampicin

previous Q Fever infection, previous Q Fever vaccination,

may be used in combination with tetracycline.

egg allergy and current medications such as cortisone.

• Isolation is not necessary. • Articles contaminated with blood, sputum and excreta should be disinfected. • Immunisation of household contacts is not necessary.

Skin Testing Vaccine dilution: • The required dilution of vaccine for a skin-testing solution can be achieved by diluting 0.1 ml of vaccine

Preventive Measures

in 30 ml normal saline.

• Eliminate source of infection if known. • Disinfect incriminated stock-holding facilities if practicable; for example, 0.05 per cent hypochlorite (500 ppm available chlorine) or 5 per cent peroxide. • Immunise high-risk occupational groups. Note

Prevaccination assessment with CFT levels and skin testing is essential to reduce risk of severe local reactions in those already immune. A certain degree of training is required to recognise positive skin tests.

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Skin-test procedure: • Prepare the skin with methylated spirits. • Dry well before injecting. • Inject 0.1 ml of the diluted vaccine solution intradermally into the volar surface of the left forearm. Choose a smooth, unblemished area of skin. • Cover with a bandaid if returning to work. • Instruct the patient to remove the bandaid when showering then leave uncovered.

Reading The skin test can be read between three to 10 days (optimum seven days). After 10 days, it is unreliable. A positive reaction is indicated by induration at the site of the injection.

Note

Where a history of Q Fever infection or previous vaccination is given, confirm results through the admitting hospital, laboratory or LMO. If the results are negative, vaccination is recommended. In immunosuppressed individuals and in pregnancy, the risk-benefit ratio should

Serology (CF):

be evaluated before use.

• Positive titre: 1:2.5 and above. • Negative titre: