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Guidelines for the Control of

Infectious Diseases





A c k n o w l e d g e m e n t s

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 guide-lines.

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.



These guidelines have been prepared following consul-tation 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.



Food - or Water-Borne Illness




Haemophilus influenzae



Information Sheets 64

Hand, Foot and Mouth Disease


Information Sheet 69

Hepatitis A


Hepatitis B


Hepatitis C


Hepatitis D


Hepatitis E


Herpes Simplex


Hydatid Disease






Infectious Mononucleosis




L e p r o s y








Abbreviations Used


Acquired Immunodeficiency

S y n d r o m e


Acute Bacterial Conjunctivitis


A m o e b i a s i s


A n t h r a x


Arbovirus Infections


Ross River Virus Disease 17

Australian Arboencephalitis (AE) 19

Dengue 21

Kunjin 22





Campylobacter Infection


Chicken Pox/Herpes Zoster




Cryptococcal Infection




Cytomegalovirus (CMV) Infection 43



Erythema Infectiosum


Information Sheet 51




Information Sheet 117



Meningococcal Infections


Information Sheet 127



M u m p s


Mycobacterial Infections


Tuberculosis 133 Atypical (Non-Tuberculosis) 139



Information Sheet 143





Pneumonia due to Chlamydia

p n e u m o n i a e






Q Fever


Information Sheet 162









Information Sheets 183



Streptococcal Disease Caused by

Group A Beta-Haemolytic

St re ptococcus


Ta e n i a s i s


Te t a n u s


NH&MRC Recommendations 192

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




Ty p h u s


Verotoxin Producing E. coli


Viral Gastroenteritis Caused

by Agents Other than Rotavirus


Viral Haemorrhagic Fevers


Yellow Fever


Vaccination Outlets 211


Appendix 3: Outbreak



Appendix 4: Standard Precautions 223

Appendix 5: Procedure for

Dealing with Spills of Blood and

Body Fluids


Appendix 6: Management of

Needlestick Injury and Exposure

to Blood or Body Fluids


Appendix 7: Specimen Collection

and Transport Guidelines


Appendix 8: Infections in

Children’s Services Centres


Appendix 9: School Exclusion



Infectious diseases still occur frequently throughout the world and constant vigilance is required to prevent the reappearance of diseases thought to have been con-quered. Changes in lifestyle have also led to the emer-gence of new threats to public health from infections.

Health authorities depend on medical practitioners for information on the incidence of infectious diseases and notification is vital in efforts to prevent or control the spread of infection.

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

Group A Diseases

Australian Arboencephalitis. Anthrax. Botulism. 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.

A case of any of these diseases should be notified to Human Services, Victoria, by telephone or facsimile upon initial diagnosis (presumptive or confirmed) and written notification should follow within seven days. Notification forms are available from the Department:

Telephone (03) 9616 7777.

The telephone numbers for notification of diseases are: Infectious Diseases Unit (03) 9616 7777 or 1800 034 280. Fax: (03) 9616 8329 (Attention: Chief Health Officer). After hours, contact the duty medical officer.

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

Group B Diseases


Arbovirus infections (except for Australian Arboencephalitis and Yellow Fever). Brucellosis. Campylobacter infection. Giardiasis. Hepatitis A. Hepatitis B. Hepatitis C.

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.


Taeniasis (tape worm infections). Tetanus.

Tuberculosis. Yersiniosis.



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

Group C Diseases



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


These sexually transmissible diseases should be notified using the same notification form but, to preclude identifi-cation of the patient, only the first two letters of the given name and surname of the patient are required.

Not all chlamydial diseases are STDs.

Group D Diseases

Acquired lmmunodeficiency Syndrome. HIV was made notifiable in September 1996.


Written notification is required within seven days of confirmation of diagnosis.

A separate form is used for this purpose due to the need to have national uniformity in collection of data.

To preclude identification of the patient, only the first two letters of the given name and surname of the patient are required.

Send all notifications to: Freepost 547

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.

The Health (Infectious Diseases) Regulations 1990 require notification from laboratories under the circumstanceslisted below.

A. Food and Water Supplies

Isolate the following pathogens from food for human consumption or from water supplies:

• Campylobacter jejuni.

• Listeria monocytogenes.

• Salmonella species.

Isolate the following pathogens from water supplies: • Campylobacter coli.

• Campylobacter lari.

• Vibrio cholerae.

• Giardia cysts.

• Cryptosporidium oocysts.

Detection of any of the above organisms should be notified in writing to Human Services within seven days, stating the pathogen isolated, the source, the date of isolation, and any batch identification (if appropriate).

B. Material of Human Origin

A laboratory test that indicates the probable presence of a human pathogenic organism associated with an infectious disease listed in Groups A, B or C should be notified to Human Services.

If the disease is in Group A, the notification should be made by telephone or other rapid transmission.


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 Govern-ment DepartGovern-ment of Human Services, Victoria, to assist all public health practitioners in the control and preven-tion 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


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 antibody test

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 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


PCR polymerase chain reaction

VIDRL Victorian Infectious Diseases Reference Laboratory


Acquired Immunodeficiency Syndrome

Victorian Statutory

Re q u i re m e n t

AIDS Group D notification.

HIV infection was made notifiable in September 1996.

Infectious Agent

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

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 illness lasting for a week or two.

Infected persons may then be free of clinical signs or symptoms for months or years, before developing specific opportunistic infections and cancers and a range of other indicative diseases.

Major diseases that may be indicative of AIDS include: • Pneumocystis carinii pneumonia.

• Candidiasis. • Kaposi sarcoma.

• Herpes simplex infection. • Cryptococcosis. • Cryptosporidiosis. • Toxoplasmosis. • Cytomegalovirus infection. • Mycobacteriosis. • Lymphoma. • HIV encephalopathy. • HIV wasting disease.

Public Health Significance and

O c c u r re n c e

Occurrence is worldwide.

According to the World Health Organisation (WHO) estimation, close to 6.8 million cases of AIDS and 22 million cases of HIV occurred by 1994.

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

In 1994, 217 new diagnoses of HIV were made, bringing the total HIV infections in Victoria to 3372.

Method of Diagnosis

Careful history and physical examination looking for risk factors and clinical manifestations of immunodeficiency.

Laboratory confirmation of diagnosis by:

• Detecting HIV antibodies with ELISA test (confirmed by Western blot analysis).

• Diagnosing opportunistic infection or secondary cancer.

Re s e r voi r



Mode of Transmission

HIV can be transmitted by:

• Unprotected sexual intercourse with an infected person.

• Inoculation with infected blood, blood products and through transplantation of infected organs, bone graft, tissue or semen.

• From infected woman to the foetus during pregnancy or breastfeeding. Approximately 15 to 30 per cent of infants from HIV positive mothers are infected, but treatment during pregnancy can result in a marked reduction in infections.

• 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.


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

Incubation Period

From infection to primary illness, three weeks to three months.

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.

Treatment lengthens the incubation period.

Period of Communicability

All antibody positive persons carry HIV.

Infectivity must be presumed to be lifelong.

Presence of other sexually transmitted diseases, espe-cially those causing genital ulceration, increases suscep-tibility for sexual transmission.

Control of Case

Standard fluid precautions apply to all patients.

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

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

Patients and their sexual partners should not donate: • Blood.

• Plasma.

• Organs for transplantation. • Tissues.

• Cells.

• Semen for artificial insemination. • Breast milk for human breast banks.

All HIV positive persons should be evaluated for the presence of tuberculosis.

Tre a t m e n t

Zidovudine (AZT), dideoxycytidine (DDC) and

dideoxyinosine (DDI) are the current anti-retroviral drugs available in Australia specifically indicated for HIV infection.

Other treatment includes specific treatment or prophy-laxis for the opportunistic infectious diseases that result from HIV infection.


pub-Control of Contacts

If a person is diagnosed as having HIV infection, the diagnosing practitioner has a responsibility to ensure that sexual and needle-sharing contacts are followed up. Assistance with partner notification may be provided by Human Services through its partner notification officers: telephone (03) 9482 5700.

Pre- and post-test counselling should be provided for all contacts who seek HIV testing.

Preventive Measures


• 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

sus-pected HIV should be avoided.

• HIV-infected persons should be offered confidential counselling.

• Care sould be taken when handling, using and dispos-ing of needles or other sharp instruments.

• Use of needle exchange programs by injecting drug users.


• 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.

Epidemic Measures

HIV infection is usually pandemic.

International Measures

A global prevention and control program coordinated by WHO was initiated in 1987.

Currently all countries have developed AIDS prevention and control programs.


Acute Bacterial Conjunctivitis

Victorian Statutory

Re q u i re m e n t

Statutory notification not required except for gonococcal disease (ophthalmia neonatorum).

School and child care exclusion.

Infectious Agent

Haemophilus influenzae, Streptococcus pneumoniae.

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.

Viral conjunctivitis can cause a similar clinical picture. A blocked tear duct predisposes to recurrent infection.

Public Health Significance and

Oc c u r re n c e

A common communicable disease, frequently epidemic, affecting children under five years of age.

Occurrence is worldwide.

Method of Diagnosis

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

R e s er v o i r


Mode of Transmission

It can be transmitted by ontact with:

• Discharge from the conjunctivae or upper respiratory tract of infected persons.

• Contaminated fingers or fomites (contaminated ob-jects).

• Infected mothers during vaginal delivery.

Incubation Period

Usually 24–72 hours.

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.

Control of Case

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

Tre a t m e n t

Local application of antibiotic ointment or drops.

Control of Contacts

Investigation of contacts and source of infection not practicable.

Preventive Measures

Personal hygiene and proper treatment of infected eyes.

Epidemic Measures

Not applicable.


A m o e b i a s i s

Victorian Statutory

Re q u i re m e n t

Group B notification.

Infectious Agent

Entamoeba histolytica.

Clinical Features

An infection with a protozoan parasite that exists in two forms: an infective cyst and a potentially pathogenic trophozoite. Further, the difficulty of distinguishing infection with the non-pathogenic Entamoeba dispar

must be noted.

Clinically, it may present as intestinal or extra-intestinal disease. Most infections are asymptomatic. Intestinal disease includes diarrhoea which may be bloody, fever and abdominal discomfort.

Intestinal amoebiasis may be complicated by: • Granuloma of the large intestine.

• Colonic perforation and haemorrhage. • Perianal ulceration.

• Extra-intestinal amoebiasis with abscess formation that occurs as a result of bloodstream spread to the liver, brain or lungs.

Public Health Significance and

Oc c u r re n c e

Occurrence is worldwide.

High-risk groups include:

• Patients in institutions for the intellectually disabled. • Male homosexuals.

• People living in areas with poor sanitation. • Travellers returning from developing countries.

This active disease occurs mostly in young adults and is rare below the age of five years.

Method of Diagnosis

Microscopic examination for trophozoites or cysts in: • Fresh or suitably preserved faecal specimens. • Smears of aspirates or scrapings obtained by


• Aspirates of abscesses or sections of tissue.

As cysts are shed intermittently in asymptomatic and mild infections, repeated stool specimens may be needed to establish a diagnosis.

The presence of trophozoites containing red blood cells is indicative of invasive amoebiasis.

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

X-ray, ultrasound and CT scan are used in diagnosis and location of an amoebic liver abscess.

Re s e r voi r


Mode of Transmission

Amoebiasis can be transmitted by:

• Ingestion of faecally contaminated water containing amoebic cysts.

• Hand-to-mouth transfer of faecal contamination. • Contaminated raw vegetables.

• Sexually, by unprotected oral-anal contact.

Incubation Period

Average incubation period is two to four weeks.


Period of Communicability

Cases are infectious as long as cysts are present in the faeces.

In some instances, cyst excretion may persist for years.

Susceptibility and Resistance

Recurrent infections can occur.

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 metronida-zole, 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. How-ever, in residential institutions or in the case of fellow travellers, microscopic examination of faeces is advis-able.

Preventive Measures

• Educate the public in personal hygiene.

• Provide information to intending travellers about the

• Educate the public about the possibility of transmitting the disease via sexual contact.

• Protect public water supplies from faecal contamina-tion.

Epidemic Measures

• 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.


A n t h r a x

Victorian Statutory

Re q u i re m e n t

Group A notification.

Infectious Agent

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

Clinical Features

Anthrax is an acute bacterial disease usually affecting the skin.

It may rarely involve the intestinal tract.

Cutaneous Anthrax

Lesions are usually painless.

Itchiness is common followed by a skin lesion that progresses from a papule to a vesicle (which may be haemorrhagic), and in two to six days develops into a depressed black eschar (malignant pustule).

Untreated lesions can progress to involve the regional lymph nodes. In severe cases, an overwhelming septi-caemia can occur.

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

Pulmonary Anthrax

This is very rare and often presents with mild and non-specific symptoms resembling common URTI.

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

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

Intestinal Anthrax

It is rare in developed countries, but may occur in explosive outbreaks.

Gastro-intestinal symptoms may be followed by fever, septicaemia and death (mortality rate is 25–75 per cent).

Public Health Significance and

O c c u r re n c e

Anthrax is primarily an occupational hazard for handlers of:

• Processed hides. • Goat hair.

• Bone and bone products. • Wool.

• Infected wildlife.

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

New areas of infection in livestock may develop through introducing animal feed containing bone meal.

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

Known infectious land can remain contaminated for years.

Method of Diagnosis

Demonstrate the presence of Gram-positive Bacillus anthracis in blood, lesions or discharges by:

• Direct staining of smears using Gram or special stains. • Isolation or animal inoculation in the laboratory.

R e se rvo i r

Dried or otherwise processed skins and hides of infected animals may harbour spores for years.

Spores remain viable in contaminated soil for many years.


Mode of Transmission

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

Period of Communicability

There is no evidence of direct spread from person to person.

Articles and soil contaminated with spores may remain infective for years.

Susceptibility and Resistance

Recovery is usually followed by prolonged immunity.

Control of Case

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

• Arrange isolation of patient in hospital. Soiled articles require pressure steam sterilisation or incineration. • Use penicillin as the drug of choice. Tetracyclines,

erythromycin, chloramphenicol or ciprofloxacin could be used if penicillin is contraindicated.

Control of Contacts

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

Control of Environment

To control the environment:

• Seize suspected animal products. • Incinerate infected animal products.

• 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.


Soiled articles require pressure steam sterilisation or incineration.

Preventive Measures

• Educate employees who are handlers of potentially infected articles in the proper care of skin abrasions. • Ensure proper ventilation in hazardous industries and

use of protective clothing.

• Sterilise hair, wool or hides, bone meal or other feed of 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 possible. Do not necropsy or burn on open field. • Decontaminate soil or discharges with quicklime, or

preferably bury deeply with carcass.

• Promptly vaccinate all animals at risk and revaccinate annually.

• Control effluent and trade wastes from factories that manufacture products from hair, wool or hides likely to be contaminated.

• Decontaminate soil on infected farms with 5 per cent formalin.

Treatment of Animals

Symptomatic animals can be treated with penicillin or tetracyclines.


Arbovirus Infections

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

Major outbreaks have occurred in Australia in the Murray Valley, Gippsland, coastal New South Wales, Northern Territory, Queensland and Western Australia, chiefly from January to May.

Sporadic cases occur in other coastal regions of Aus-tralia and Papua New Guinea.

In 1979, a major outbreak occurred in Fiji and spread to other Pacific islands, including Tonga and the Cook Islands. There were 15,000 cases in American Samoa in 1979–80.

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

Infection is rare in prepubertal children and increases with age.

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

Method of Diagnosis

Serology can show a rise in antibody titre to Ross River virus. The virus may be isolated from the blood of acutely ill patients.

Tests are usually necessary to distinguish it from other causes of arthritis. However, in the event of a local outbreak clinical diagnosis may be sufficient.

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

Flaviviruses: Murray Valley Encephalitis (the cause of Australian arboencephalitis), Kunjin, Dengue.

Alphaviruses: Ross River virus, Barmah Forest virus, Sindbis.

Ross River Virus Disease

(Epidemic Polyarthritis)

Infectious Agent

Ross River virus (alphavirus).

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

Clinical Features

A self-limited disease characterised by arthritis or arthralgia lasting from days to months and primarily affecting the wrist, knee, ankle and small joints of the extremities. Prolonged symptoms are common.

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

In many patients, the onset of arthritis is followed in one to 10 days by a maculopapular rash (usually non-pruritic) mainly affecting the trunk and limbs.


R e s e r v o i r

Probably macropods (for example, kangaroos); possibly other marsupials and wild rodents.

Transovarian transmission in the mosquito Aedes vigilax

has been demonstrated in the laboratory, making an insect reservoir a possibility.

Mode of Transmission

It is transmitted by mosquitoes Culex annulirostris, Ae. camptorhynchus. Ae. vigilax, Ae. polynesiensis and other

Aedes spp. of mosquitoes.

Incubation Period

Usually three to 11 days.

Period of Communicability

There is no evidence of transmission from person to person.

Susceptibility and Resistance

Recovery is universal and is followed by lasting immu-nity. Second attacks are unknown.

Inapparent infections are common, especially in children, among whom the clinical disease is rare.

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

Control of Case

Not applicable.

Symptomatic treatment.

Control of Contacts

All family members should be questioned about symp-toms and evaluate serologically if appropriate.

Preventive Measures

Ross River virus can be prevented by:

• Mosquito control measures (see local municipality). • Personal protection measures (long sleeves and

mosquito repellents).

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

Epidemic Measures

• Conduct a community survey to determine species of vector mosquitoes. Identify their breeding places and promote their elimination.

• Use mosquito repellents for persons exposed because of occupation or otherwise to mosquito bites.

• Identify the infection among animal reservoirs; for example, kangaroos, small marsupials, farm and domestic animals.


See the Victorian Arbovirus Task Force Contingency Plan for Outbreaks of Ross River Virus Disease.

International Measures

Airport vector control in Australia and Papua New Guinea.

These measures may be necessary to prevent the spread from endemic areas in Australia and Papua New Guinea to avert epidemics in countries where local vectors (for example, Ae polynesiensis) carry the dis-ease.


Australian Arboencephalitis (AE)

Infectious Agent

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

Clinical Features

Fever, headache and sometimes nausea and vomiting, followed by the features of encephalitis.

A diagnosis of AE should be considered in any patient 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.

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

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

This results in amplification of arboviruses in the mosqui-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.

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

During the 1974 epidemic, of those affected, one-third died, one-third were left with residual brain damage, and one-third recovered completely.

Method of Diagnosis

Serology: Two blood specimens are required seven to10 days apart. Sera for diagnosis should be sent to the Director of Virology, VIDRL, preceded by telephone contact via the Royal Melbourne Hospital on (03) 9342 7000.

R e s e r v o i r

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

Modes of Transmission

The primary mosquito vector during epidemics is Culex 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.

Period of Communicability

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

Susceptibility and Resistance

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.


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.



Infectious Agent

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

Clinical Features

Dengue Fever (Break Bone Fever)

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

It is characterised by fever (three to five days), myalgia, arthralgia, retro-orbital pain, anorexia, gastrointestinal disturbance, rash and increased vascular permeability (see below).

Dengue Haemorrhagic Fever (Dengue

Shock Syndrome)

In contrast to classic dengue, myalgia and bone pains are unusual in dengue haemorrhagic fever which is a disease of abrupt onset characterised by fever, palpable lymph nodes and liver, scattered petechiae and rapid deterioration.

Other haemorrhagic phenomena such as melaena, haematemesis and shock are poor prognostic signs. Death usually occurs on the fourth or fifth day.

Public Health Significance and

O c c u r re n c e

Outbreaks of this disease have occurred throughout the tropics and over the past 40 years.

A complication, dengue shock syndrome, is believed to be caused by immune enhancement of infection, in which dengue antibodies from prior infections appear to promote the infection of other serotypes.

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 imported car tyres is cause for concern.

Method of Diagnosis

Serology: Rising titre to Dengue virus antibodies.

R e s e r v o i r

Humans and monkeys (in most cases monkeys play no role).

Mode of Transmission

It is transmitted by the bite of an infected mosquito usually Ae. aegypti and Ae. albopictus. (Other Aedes

species are involved in the enzootic monkey complex).

Incubation Period

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

Susceptibility and Resistance

There is universal susceptibility but children usually have a milder primary disease than adults.

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

A previous infection may exacerbate a second infection. Dengue antibodies from earlier infections appear to promote infection by other serotypes.

Control of Case

• Isolate patient and prevent mosquito access until fever subsides.

• Investigate source of infection.

Preventive Measures

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

methods of personal protection. • Control Aedes aegypti near airports.

• Prevent importation of new vectors; for example, Aedes albopictus.



Infectious Agent

Kunjin virus (flavivirus).

Clinical Features

Most infections are subclinical.

When symptoms occur, the syndrome varies from a mild febrile illness with nausea, lethargy, lymphadenopathy and a rash to encephalitis.

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

Further study is needed to define the morbidity rate of infections with Kunjin virus.

Method of Diagnosis

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

R e s e r v o i r

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

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

Incubation Period

Uncertain, probably weeks.

Period of Communicability

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


The ratio of subclinical to clinical infections appears to be large but the precise ratio is unknown.

Cross-reaction between MVE virus and Kunjin virus has complicated the assessment of the prevalence of Kunjin infection in the general population.

Control of Case

No specific treatment is required.

Investigate the source of infection and search for unre-ported or undiagnosed cases from the Murray-Darling drainage basin.

Control of Contacts

Not applicable.

Preventive Measures

Intensify mosquito surveillance and control in areas where cases are identified.

Epidemic Measures

See the Victorian Arbovirus Task Force Contingency Plan on AE.



Victorian Statutory

Re q u i re m e n t

Group A notification.

Infectious Agent

Clostridium botulinum, a spore-forming obligate anaero-bic bacillus. Different types are recognised, for example, types A, B, E, F and G.

Clinical Features

There are three forms of botulism: the classical form, infant botulism and wound 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 mouth. This may be followed by descending flaccid paralysis in an alert person. Fever is absent unless a complicating infection occurs.

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 microflora. The illness typically begins with constipation, followedby lethargy, listlessness, poor feeding, ptosis, difficulty in swallowing, and generalised muscle weak-ness (floppy baby).

Wound botulism is rare, but has been seen after contami-nation of wounds in which anaerobic conditions devel-oped.

Public Health Significance and

Oc c u r re n c e

Rare but serious intoxication can occur from improperly cooked, canned or preserved food. Infant and wound botulism are due to colonisation by the causative organ-ism.

Most human outbreaks are due to types A, B and E. Outbreaks of type E are usually related to consumption of fish, seafood and meat from marine mammals. The toxin is destroyed by boiling.

Method of Diagnosis

Botulism can be diagnosed by demonstration of specific toxin in serum, faeces and incriminated food, or by culture of C. botulinum from stool in a clinical case.

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

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

Re s e r voi r

Spores are ubiquitous in soil and are frequently recov-ered from agricultural products. They are also found in marine sediments and the intestinal tract of animals, including fish.

Mode of Transmission

Classical botulism is acquired by ingestion of food in which toxin has been formed without subsequent ad-equate cooking. Suitable conditions for the formation of toxin in foods have included inadequate heating during canning (especially home canning of alkaline foods) and contamination of cans post-processing.

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

Infant botulism arises from ingestion of spores rather than preformed toxin. Sources of spores include foods (for example, honey) and dust. Honey has been de-scribed in the US literature as a source of infection but never implicated in Australia, nor have surveys of Aus-tralian honey shown C. botulinum.


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.

Period of Communicability

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

Control of Case

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

Isolation or quarantine is not needed, but hand washing is indicated after handling soiled nappies. Usual sanitary disposal of faeces from infant cases is acceptable.

Any implicated food should be retained for collection and investigation by public health authorities.

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

Control of Contacts

Those who have eaten incriminated food should be purged, for example, cathartics, gastric lavage, high enemas.

Administration of polyvalent antitoxin to asymptomatic individuals should be considered carefully; that is, potential protection versus risk of sensitisation and reactions to horse serum.

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

Specific Treatment

Intravenous and intramuscular administration as soon as possible of trivalent botulinum antitoxin (types A,B,E). 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. This should occur in an intensive care facility.

For wound botulism, in addition to antitoxin, the wound should be debrided and/or drained, and appropriate antibiotics (for example, penicillin) administered.

In infant botulism, meticulous supportive care is essen-tial, and assisted respiration may be required. Antitoxin is not used because of sensitisation and anaphylaxis. Antibiotics have not been shown to affect the course of the disease.

Preventive Measures

• Ensure effective control of processing and preparation of commercially canned and preserved foods.

• Educate people undertaking home canning and other food preservation techniques about cooking time, pressure, temperature, adequate refrigeration, storage and so on.

• Be aware that C. botulinum may or may not cause container lids to bulge and the contents to have unpleasant odours.


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 labora-tory 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


B r u c e l l o s i s

Victorian Statutory

Re q u i re m e n t

Group B notification.

Infectious Agents

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

Clinical Features

This is a systemic bacterial disease with acute or insidi-ous onset.

Localised suppurative infections may occur.

Subclinical and unrecognised infections are frequent.

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

Osteoarticular complications are common.

Less common are orchitis, epididymitis, osteomyelitis and endocarditis.

Public Health Significance and

Oc c u r re n c e

Since the success of the national eradication campaign for B. abortus in cattle herds in 1989, only an occasional case of brucellosis is now seen which is usually acquired overseas. In 1992, 29 cases were reported in Australia. The majority of these (25) were due to B. suis, contracted in Queensland, often by people hunting or butchering feral pigs.

In Victoria in 1991, two cases of B. abortus were re-ported, and both were believed to be long-standing infections. One case notified in 1992 was an imported case due to B. melitensis.

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 Aus-tralia for:

• Farm workers. • Veterinarians. • Abattoir workers.

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

Method of Diagnosis

Laboratory diagnosis is made by either isolating the infectious agent from blood, bone marrow or other tissues or discharges of the patient, or by a specific antibody response.

The interpretation of serological results can be difficult.

R e se rvo i r

Infection in humans can be transmitted from cattle, swine, goats, sheep and dogs.

Incubation Period

Variable and difficult to ascertain.

Usually five to 60 days; can be several months.

Mode of Transmission

Brucellosis can be transmitted by contact with infected tissues, blood, urine, vaginal discharges, aborted animal foetuses and especially placentae; also by ingestion of raw milk and dairy products from infected animals.


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/unpas-teurised 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

Epidemic Measures

Trace source of infection.


Campylobacter Infection

Victorian Statutory

Re q u i re m e n t

Group B notification.


Also notifiable if isolation of C. jejuni, C. coli or C. lari from water supplies or C. jejuni from food.

Infectious Agents

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 and fever.

Symptoms usually last two to five days. Campylobacter infection has been associated with rare sequelae includ-ing reactive arthritis and Guillain-Barre syndrome.

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

Public Health Significance

Campylobacter infections are now the most commonly notified cause of bacterial diarrhoea in Victoria. They occur worldwide and are common in the developing world.

Most cases in Australia appear sporadic, but food- and water-borne outbreaks may occur.

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

Method of Diagnosis

Isolation of common types requires selective media and microaerophilic conditions at 42˚C.

Other types may require more specialised techniques.

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

Re s e r voi r

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

Mode of Transmission

It is transmitted when organisms are ingested via con-taminated food (particularly undercooked chicken) or water, or by contact with infected pets or infants.

The organism does not multiply in food or water, but the infectious dose required to cause illness is very low.

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

Incubation Period

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


Period of Communicability

Cases are infectious throughout their illness.

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

Susceptibility and Resistance

Most persons in the developed world are susceptible.

Immunity to serologically related strains may follow infection.

Control of Case

• Report case to Department of Human Services. • Immediately report clusters of cases by telephone or


• 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.

Control of Contacts

The diagnosis should be considered in symptomatic contacts.

Preventive Measures

• Ensure scrupulous hand washing and hygiene, espe-cially in food handlers.

• Thoroughly cook all meat and, particularly, poultry and avoid recontamination after cooking.

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

• Pasteurise milk and chlorinate water.

• Recognise pets as sources of infection and encourage hand washing after handling animals.


Chicken Pox/Herpes Zoster

Victorian Statutory

Re q u i re m e n t

Statutory notification not required.

School exclusion.

Infectious Agent

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

Clinical Features

Chicken pox presents with a low-grade fever, malaise and a rash that is maculopapular then vesicular for three to four days, becoming crusted. Lesions appear in crops on the trunk, face, scalp and mucous membranes of the mouth.

Herpes zoster or shingles is characterised by a unilateral vesicular eruption within a dermatome, often associated with severe pain that may precede lesions by 48–72 hours. The rash lasts up to several weeks depending on severity.

A common complication in children with chicken pox is bacterial superinfection of the skin. Other complications include aseptic meningitis, encephalitis and Reye’s syndrome. Varicella pneumonia may be a complication in adults. Those at risk of a more severe form of infection are children who have acute leukaemia and those in remission following chemotherapy.

Herpes zoster in the immunosuppressed host is more severe and prolonged than in the normal individual; for example, those who have received a bone marrow transplant, those with Hodgkins disease, non-Hodgkins lymphoma or HIV infection.

A most debilitating complication of herpes zoster in all patients is pain associated with acute neuritis and post-herpetic neuralgia and hyperaesthesia; the latter persists for months after resolution of the disease.

V-Z Virus in Pregnancy

Varicella infection during the first trimester of pregnancy can cause spontaneous abortion but, overall, the risk is not significantly increased.

In the third trimester, maternal varicella may precipitate the onset of premature labour.

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

Perinatal varicella is associated with a high mortality rate when maternal disease develops within five days prior to delivery and up to 48 hours postpartum. The neonatal fatality rate is reported as being up to 30 per cent.

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

Clinical manifestations include growth retardation, cutaneous scarring, limb hypoplasia and cortical atro-phy.

Public Health Significance and

O c c u r re n c e

Chicken pox is a highly contagious but generally mild disease and is endemic in the population. It becomes epidemic among susceptible individuals mainly during winter and early spring. More than 90 per cent of cases are children aged one to 14 years.

Herpes zoster, a sporadic disease, is the consequence of reactivation of a latent virus from the dorsal root ganglia. It is most commonly seen in the elderly.

Method of Diagnosis

Clinical: Isolation of the virus in cell cultures or visualisa-tion by electron microscopy (EM) is not routinely re-quired.



• Complement fixation tests showing detectable IgM antibody.

• Immunofluorescence on lesion swab/fluid. • ELISA (kit) now more commonly used.

Rese rvoir


Mode of Transmission

It can be transmitted from person to person by direct contact, or by droplet or airborne spread of secretions from the respiratory tract of chicken pox cases, or of the vesicle fluid of patients with herpes zoster. Indirect contact occurs through articles freshly soiled by dis-charges from vesicles of infected persons. Scabs are not infective.

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

Incubation Period

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

May be prolonged in the immunosuppressed, or follow-ing immune globulin.

Period of Communicability

It is usually communicable for one to two days (up to five days) before onset of rash, and for five days after the appearance of the first crop of vesicles, but prolonged in patients with altered immunity.


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 chicken-pox.

Adults with cancer, especially of lymphoid tissue, immunodeficient patients and those on immunosuppres-sive therapy may have increased frequency of severe zoster.

Control of Case

Chicken Pox:

• Exclude from school until fully recovered, or at least 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 varicella zoster infections in patients with a rash less than 72 hours old. It gives some pain relief, but is of no benefit on the incidence of post-herpetic neuralgia.

Control of Contacts

Contacts are not excluded from school.

The risk of spread to immunosuppressed patients means that if a susceptible child with known exposure is in hospital, quarantine of these patients should be consid-ered for days 10–21 after exposure (up to 28 days if immune globulin given).


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.


C h o l e r a

Victorian Statutory

Re q u i re m e n t

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 biochemical characteristics and both include organisms of the Inaba and Ogawa serotypes. Both biotypes can also be classified into various phage types.


Non-O1 vibrios, formerly known as non-agglutinable vibrios (NAG) or non-cholera vibrios (NCV) are now included in the species Vibrio cholerae, but the reporting of Non-O1 infections as ‘cholera’ is inaccurate.

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 (1981 and 1984) and in Lima, Peru (1984).

Large-scale epidemics of cholera caused by V.cholerae O139 have been seen in India and Bangladesh.

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.

Clinical Features

Asymptomatic illness is much more frequent than clinical illness, and mild cases with diarrhoea are common, especially among children.

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

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.

Endemic cholera occurs in parts of Africa, Central Europe and Asia.

The seventh cholera (EI Tor) pandemic that began in Asia in 1961 spread to Africa in 1970 and to South America in 1990–91.

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

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

V. cholerae O1 is established in the riverine environment in some parts of Queensland and NSW.

Method of Diagnosis

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.

Visualisation by dark field or phase microscopy of characteristic motility, specifically inhibited by preserva-tive-free serotype-specific antiserum.


Rese rvoir

Water and humans.

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

Mode of Transmission

Cholera can be transmitted by:

• Contaminated water.

• 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. • Fish or shellfish obtained from contaminated waters.

The organism can survive for long periods in water and ice.

Incubation Period

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

Period of Communicability

Cholera is communicable during the acute stage and for a few days after recovery.

By the end of the first week, 70 per cent of patients are non-infectious, and by the end of the third week 98 per cent are non-infectious.

Occasionally the carrier state may persist for months, and exceptionally chronic biliary infection with intermit-tent shedding of organisms may last for years.

Susceptibility and Resistance

Even in severe epidemics, attack rates of overt disease rarely exceed 2 per cent.

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

Control of Case

Severely ill patients should be isolated in hospital, with Standard Precautions.

Less severe cases can be managed at home.

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

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

Terminal cleaning of the room and articles used by the patient is required.

Specific Treatment

Prompt fluid therapy with adequate volumes of electro-lyte solution (Gastroelectro-lyte) should be undertaken.

Patients with severe dehydration require urgent intrave-nous fluid therapy with Hartmann’s solution or WHO 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.

Antimicrobial agents (to which the strain is sensitive) shorten the duration of diarrhoea and the duration of vibrio excretion:

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




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