Page content: Victorian statutory requirement | Infectious agent | Identification | Incubation period | Public health significance & occurrence | Reservoir | Mode of transmission | Period of communicability | Susceptibility & resistance | Control measures | Outbreak measures
Q fever infection (Group B disease) must be notified in writing within five days of diagnosis.
School exclusion is not applicable.
The rickettsia-like bacterium Coxiella burnetii is the causative agent.
Clinical features
The onset of Q fever infection 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. Orchitis occurs rarely. Abnormal liver function tests are common.
Chronic complications include granulomatous hepatitis and endocarditis. The latter is the most serious concern as it usually involves the aortic valve and occurs months to years after the acute illness. A relapsing fatigue syndrome may occur in 20–40% of cases.
Method of diagnosis
Acute and some chronic manifestations of Q fever can be diagnosed by serology.
Acute Q fever can be diagnosed by a fourfold rise in specific complement fixation (CF}) antibodies or by direct immunofluorescence (IF) antibody testing between acute and convalescent sera collected at least 14 days apart.
The diagnosis is supported by the detection of phase II IgM by ELISA testing but this may not appear until 10 days after the onset of symptoms. Q fever IgM may persist for many months after infection; hence its presence does not necessarily confirm the diagnosis.
If Q fever antibodies are present within three to four days of the onset of symptoms it is more likely to indicate past exposure rather than recent infection.
Chronic Q fever is suggested by a high CF antibody titre (?320) to phase I and II antigens and low or absent IgM antibody.
IgA class antibody to phase I antigen is highly suggestive of Q fever endocarditis.
The incubation period is typically 19–21 days although the range is from two weeks to two months.
It is an acute febrile rickettsial disease of low mortality but significant morbidity. It is most commonly found in abattoir workers who have recently handled contaminated stock such as feral goats or sheep from interstate endemic areas. It is an occupational hazard for tannery and knackery workers, shearers, meat inspectors, dairy workers, animal-farm workers, animal transporters, wool sorters and veterinary personnel. It also occurs in others handling fomites such as those laundering contaminated clothing.
Outbreaks are usually of short duration.
There is no known endemic reservoir in Victoria. The organism is commonly introduced in stock from interstate from animals including goats, cattle, sheep, other farm and domestic animals and some wild animals (including kangaroos and bandicoots).
Q fever is contracted through the respiratory route after inhalation of Coxiellae-contaminated dust or aerosols. This most commonly occurs as a result of:
Although Q fever is occasionally transmitted sexually, there is no evidence of person to person transmission through other routes. Direct transmission through blood and bone marrow transfusion has also been reported.
Drinking non-pasteurised milk from an infected animal has been suggested as a possible route but this has not been proven.
Person to person spread occurs very rarely by the sexual route. Contaminated clothing may also be a source.
All non immune people are susceptible to infection. Most cases are in male adults but this is probably due to their higher frequency of exposure to high risk environments, rather than differential susceptibility.
Infection usually confers lifelong immunity.
Preventive measures
Immunisation of those in high risk occupational groups is the primary preventive measure against Q fever. There is a risk of severe local reactions to the vaccine in those people previously exposed to Q fever or the vaccine. To assess prior exposure to Q fever or the vaccine, pre-vaccination screening is necessary and involves:
Any positive result on screening precludes vaccination. Vaccination induces lifelong immunity in most vaccinees. Training is recommended for medical practitioners intending to conduct Q fever screening and vaccination.
Access to high risk environments such as abattoirs and meat-processing plants should be restricted to immunised persons. This includes visitors, contractors and delivery drivers. Workers in these environments should also be educated about the nature of the disease.
Control of case
Acute cases of Q fever generally require treatment with doxycycline or chloramphenicol. Consult the current version of Therapeutic guidelines: antibiotic (Therapeutic Guidelines Limited).
In chronic disease or endocarditis, prolonged combination therapy together with cardiac surgery may be required. Consultation with an infectious diseases physician should be sought.
Isolation is not necessary. Articles contaminated with blood, sputum and excreta should be disinfected using standard precautions.
Control of contacts
No specific measures are required for household contacts.
Vaccination during the incubation period does not prevent the disease. Post-exposure prophylaxis is not recommended.
Control of environment
If a clear source is identified, disinfection can be performed using 0.05% hypochlorite (500 ppm available chlorine) or 5% peroxide.
All notified cases are investigated to ascertain the most likely source of exposure and to identify any other linked cases. If two or more cases are linked in time and place to a workplace, other staff should be assessed for immune status (if not already known) with antibody levels and skin testing.
Non-immune staff should be excluded from the worksite until vaccinated.
Last updated: 15 January, 2008
This web site is managed and authorised by Communicable Disease Control,
Public Health Branch,
Rural & Regional Health & Aged Care Services Division of the
Victorian State Government, Department of Human Services, Australia
