Q fever

March

• Case definition – reformatted to include new subsections and align with the new structure.
• Laboratory testing guidelines section – new section.

For an overview of all updates made to the Communicable Disease Control Manual, refer to Updates to the Communicable Disease Control Manual – Health New Zealand | Te Whatu Ora .

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 New Zealand institute for Public Health and Forensic Science Limited (PHF Science) surveillance website (external link).

2–3 weeks.

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.

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.

Confirmed: A person who has a clinically compatible illness and has laboratory definitive evidence.

Probable: A person who has a clinically compatible illness and has laboratory suggestive evidence.

Under investigation: A person who has been notified to the medical officer of health, but information is not yet available to classify them further.

Not a case: A person that has been investigated and subsequently found not to meet the case definition. 

An illness characterised by a range of clinical syndromes caused by Coxiella burnetii. While asymptomatic infection may occur, onset of infection is usually acute and characterised by fever, rigors, sweats, severe headache, weakness and myalgia. Pneumonia may be present, and abnormal liver function tests are common. Chronic Q fever can manifest as non-specific febrile illness, pneumonia, subacute endocarditis, hepatitis and, less commonly, granulomatous lesions in bone, soft tissues or internal organs. A post-Q fever fatigue syndrome has been described.

There are no epidemiological criteria for Q fever.

Laboratory definitive evidence

Phase II immunoglobulin G (IgG) seroconversion with a titre of greater than 1:128.

OR

A 4-fold or greater increase in titre to phase II antigens as compared with phase I antigens in the absence of recent Q fever vaccination.

OR

Detection of C. burnetii nucleic acid by a molecular method such as polymerase chain reaction (PCR), 16S ribosomal RNA sequencing or metagenomic next-generation sequencing with negative phase I serology results confirms acute Q fever, however, serial serological testing is required to monitor for chronic infection.

Laboratory suggestive evidence

A single raised (1:256 or greater) convalescent IgG antibody to phase II antigen in the absence of phase I antigen is considered presumptive evidence of recent or active Q fever (C. burnetii) infection.

A follow-up sample should be taken 2 to 4 weeks’ post infection to check for development of antibody to phase I antigens.

It is important to know the date 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 on the laboratory request form.

Refer to Appendix 4: Direct laboratory notification of communicable diseases flowcharts for the direct laboratory notification process for Q fever.

Testing may be carried out for the following reasons.

• To confirm or exclude a diagnosis of Q fever in a suspected case.
• To track transmission pathways during a Q fever outbreak.
• To support public health services in their response to a Q fever case or outbreak.

If Q fever is suspected, the following information should be obtained and included on the laboratory request form.

• Symptoms including onset date.
• Vaccination details (pre-vaccination samples need to be clearly labelled on the request form).
• Travel history.
• Any known links to another case or outbreak.

Serology is the primary diagnostic tool for acute Q fever.

Refer to Laboratory criteria and case classifications for case classifications for confirmed and probably case interpretations.

Serology

Serological testing is the primary method for diagnosing acute Q fever. Diagnosis is based on detecting immunoglobulin G (IgG) phase II antibodies in the absence of phase I antibodies, and/or evidence of seroconversion or a significant rise in IgG titre. IgM and then IgG antibodies to phase II antigens typically develop 10 to 14 days after symptom onset. A solitary immunoglobulin M (IgM) phase II result has a low positive predictive value for acute Q fever because IgM phase II antibodies can persist for a long time. A rise in IgG phase II titre is clinically relevant during the acute phase and typically remains positive for years, sometimes lifelong. Recent vaccination information must be provided to the laboratory, as vaccination can cause a significant increase in anti C. burnetii antibodies.

Molecular

Polymerase chain reaction (PCR) testing or other molecular testing are performed on infected tissue (e.g. heart valve, bone marrow), blood or serum to diagnose acute infection caused by C. burnetii.

A positive result indicates the presence of C. burnetii deoxyribonucleic acid (DNA). A negative result indicates no detectable C. burnetii DNA but does not rule out the presence of the organism. After 2 weeks from symptom onset, C. burnetii DNA levels decline. Even then, PCR may be performed but serology should be added for sensitivity for the diagnosis of acute fever.

Detection of C. burnetii nucleic acid by molecular testing with negative phase I antigen serology results confirms acute Q fever; however, serial serological testing is required to monitor for chronic infection.

Attending health practitioners or laboratories must immediately notify the local medical officer or health of suspected cases. Notification should not await confirmation.

See Appendix 5: Escalation pathways for more information

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.

Nil.

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.

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.

Nil.

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 (external link). 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 national protection clinical team (use Appendix 5: Escalation pathways for pathways for notification for awareness, or for escalation). 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 (external link). 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 (external link) (accessed 1 September 2020).
• Heymann DL (ed). 2014. Control of Communicable Diseases Manual (20th edition). Washington: American Public Health Association.