Part of the Communicable Disease Control Manual
Chapter reviewed and updated in February 2021. A description of changes can be found at Updates to the Communicable Disease Control Manual.
- Epidemiology in New Zealand
- Case definition
- Spread of infection
- Notification procedure
- Management of case
- Management of contacts
- Other control measures
- References and further information
Q fever was once considered part of the genus Rickettsia. It is now classified in a separate genus and is a separate notifiable infectious disease.
Coxiella burnetii, the only member of an intracellular bacteria genus that is related to the Rickettsia genus, causes Q fever. C. burnetii is not endemic in New Zealand. C. burnetii has a reservoir in birds and mammals, especially cattle, sheep and goats, and is most often an occupational disease affecting farmers, veterinarians and abattoir workers.
More detailed epidemiological information is available on the ESR surveillance website.
Q fever causes a variety of clinical syndromes. Asymptomatic infection may occur, but the onset of infection is usually acute and characterised by fever, rigors, sweats, severe headache, weakness and myalgia. Pneumonia may be a feature, and abnormal liver function tests are common. Features of chronic infection include non-specific febrile illness, pneumonia, subacute endocarditis, hepatitis and, less commonly, granulomatous lesions in bone, soft tissues or body organs. A post-Q fever fatigue syndrome has been described.
Laboratory test for diagnosis
Consult ESR or LabPlus for appropriate testing and interpretation of results.
Laboratory definitive evidence for acute Q fever requires at least one of the following:
- detection of C. burnetii nucleic acid
- seroconversion or ≥4-fold increase in antibody level to phase II antigen in paired sera tested in parallel in the absence of recent Q fever vaccination.
Detection of C. burnetii nucleic acid by NAAT with negative serology results confirms acute Q fever; however, serial serological testing is required to monitor for chronic infection.
Laboratory suggestive evidence for acute Q fever requires at least one of the following:
- presence of IgM antibody to phase II antigen
- single raised convalescent IgG antibody to phase II antigen.
It is important to know the date on which the person became unwell. A serological response to Q fever vaccination is transient, but if the person has been vaccinated, the date of vaccination should be provided.
- Under investigation: A case that has been notified, but information is not yet available to classify it as probable or confirmed.
- Probable: A clinically compatible illness with a single raised antibody titre.
- Confirmed: A clinically compatible illness that is laboratory confirmed.
- Not a case: A case that has been investigated and subsequently found not to meet the case definition.
Mode of transmission
C. burnetii can be found in many different body fluids and excreta of infected animals but are particularly concentrated in placental tissues. Humans acquire C. burnetii by inhaling contaminated aerosols or dust generated by placental tissues, birth fluids or excreta of infected animals. Airborne particles containing organisms may travel for more than 1 km. Transmission may also occur from direct contact with infected animals or other contaminated matter such as wool, straw or fertiliser.
Period of communicability
Q fever rarely spreads from person to person, reported only from cases with pneumonia. C. burnetii is highly resistant to drying and to a variety of physical and chemical agents, so viable organisms may remain in contaminated soils for several months.
Attending health practitioners or laboratories must immediately notify the local medical officer or health of suspected cases. Notification should not await confirmation.
Obtain a history of travel and direct contact with animals, wool, straw or fertiliser. Ensure acute and convalescent serological diagnosis has been attempted.
When applying for laboratory testing, ensure that the travel history and likely incubation period are recorded on the laboratory form as these details inform the laboratory’s choice of test kit. For infections probably acquired overseas, it may be useful to discuss testing with the laboratory.
Consult an infectious diseases physician. Tetracyclines and chloramphenicol are the drugs of choice.
Advise the case and their caregivers of the nature of the infection and its mode of transmission.
For anyone exposed to the same potential animal or arthropod source, advise them of the incubation period and typical symptoms of the infection. Encourage them to seek medical attention if symptoms develop. Prophylactic doxycycline may prevent clinical Q fever illness when begun 8–12 days after exposure and continued for 5 days.
Identification of source
- If the infection may have been acquired in New Zealand, liaise with Ministry for Primary Industries staff to investigate potential animal or bird reservoirs of infection.
Disinfection and cleaning
In the event of a New Zealand-acquired Q-fever infection, consider direct communication with local parents, schools and health professionals to encourage prompt reporting of symptoms. In communications with doctors, include recommendations for diagnosis and treatment.
Ensure complete case information is entered into EpiSurv. The current disease option for Q fever in EpiSurv is caused by C. burnetii.
On receiving a notification, medical officers of health should immediately notify the Ministry of Health Communicable Diseases Team. The Ministry will then notify the appropriate staff in the Ministry for Primary Industries so that further investigation of the source can be undertaken.
- Communicable Disease Network Australia. 2018. Q Fever: CDNA National Guidelines for Public Health Units. Canberra: Department of Health.
- Cook GC, Zumla AI (eds). 2008. Manson’s Tropical Diseases (22nd edition). London: WB Saunders.
- Department of Health and Human Services, State Government of Victoria. Q fever (accessed 1 September 2020).
- Heymann DL (ed). 2014. Control of Communicable Diseases Manual (20th edition). Washington: American Public Health Association.