Q fever



Last Review Date: December 4, 2020


What is it?

This illness was named “Q (for query) fever” in 1937 when the first cases of the disease were reported but very little was known about it. Since then, the cause and routes of the disease have been discovered but the name has been retained.

Q fever is caused by an intracellular bacterium called Coxiella burnetii. The name is derived from the Australian and American researchers who discovered the microorganism. Macfarlane Burnet and Edward Derrick isolated it from patients in Queensland and Herald Cox recovered bacteria from ticks collected in Montana.

Q fever can have acute or chronic stages and there is increasing recognition of a post Q Fever Fatigue Syndrome (QFS).

Acute Q fever has an incubation period of 15 to 25 days. Acute infection may be asymptomatic however commonly presents as an influenza-like illness with fever, severe headache often worst behind the eyes, rigors, drenching sweats, muscle pain and acute weight loss. There is usually some evidence of liver disease. In addition, acute infection can include pneumonia with a cough and chest pain. The acute illness lasts 2 to 6 weeks. About 20 per cent of acutely ill people may develop QFS lasting more than 6 months after resolution of the acute disease.

A small number of people who suffer acute Q fever will go on to develop chronic Q fever. This can occur months or years after acute illness. Most commonly chronic Q fever is a result of the organism infecting the heart valves (endocarditis) however other sites of infection such as bone (osteomyelitis) or the liver (hepatitis) are recognised. People with pre-existing heart disease or underlying immunosuppression are at greatest risk of developing chronic Q fever after an acute episode.

Disease is endemic to much of the world including all states and territories of Australia. Diagnosis of Q fever is not easy, as signs and symptoms are non-specific. A history of exposure to cattle, sheep or goats may be a useful pointer to the diagnosis, but there are many other routes of transmission.


Tests

Two types of tests can assist the diagnosis:

  1. Immunological antibody response can be assessed using serology assays. Different laboratories may use immunofluorescence (IF) assays, enzyme immunoassay (EIA) or complement fixation (CF) based tests or combinations of these to detect different classes of antibodies to phases II and I of Q fever bacteria. IF and CF tests may be reported as titres proportional to the amount of antibody in a patient’s blood. Significant titres may take 3-4 weeks to appear so blood samples should be taken initially during acute illness and then at least four weeks after the onset of the disease.
    Paradoxically, antibodies to the phase II organism are high in acute disease, and antibodies to the phase I organism are raised in chronic disease. In acute Q fever phase II IgM and IgG antibodies are detected. For chronic Q-fever development of a phase I IgG IF titre >800 and possibly exceeding the phase I IgG IF titre is suggestive of chronic Q-fever. However, elevated phase I IgG titres may persist for a several months after acute infection without the disease progressing to chronic disease.
    Q fever serology results are often complex and should be interpreted by a clinical microbiologist or infectious disease specialist.
  2. The actual pathogen can be detected by molecular testing using the polymerase chain reaction (PCR). It holds the promise of timely diagnosis, since it should be positive before antibodies are detectable. However, the average sensitivity of PCR performed on blood has been low (~20%). PCR is much more sensitive on tissue samples such as heart valves, which accumulate much higher concentrations of bacteria than serum.
    Laboratory cultures of Q fever bacteria are very complex and dangerous and are not used for diagnostic purposes.

Prevention and treatment

Most Q fever infections result from inhalation of infectious aerosol particles from ruminants that have just given birth or have been slaughtered. Environmental contamination related to these events lasts for months and possibly years in soil, so the inhalation of dust is also important. Cattle, sheep and goats are the main sources of human infections. In Australia the association with abattoirs has been emphasised. Non-immune new employees or visitors to animal-related industries are at highest-risk. Occupational exposure to animal products, particularly hides and wool, is also a risk. The microorganism is highly resistant to heat, drying and sunlight.

A whole cell vaccine (Q-Vax-CSL) has been licensed in Australia since 1989. Pre-vaccination screening is essential, and includes skin test and serology. The vaccine is only given if there is no history of Q fever disease or vaccination, and the blood test and skin test are both negative to avoid adverse reactions in those found to be Q fever positive.

Acute Q fever is often treated with antibiotics.


Common Questions

  1. What are the symptoms of Q fever?

    Acute Q fever may be asymptomatic however usually presents as an influenza-like illness with fever, severe headache often worst behind the eyes, rigors, drenching sweats, muscle pain and acute weight loss. In addition, acute infection can include pneumonia.

  2. Can I pass Q fever to other people?

    Not usually as this disease is acquired through contact with aerosols from infected animal products rather than human-to-human contact. However, human-to-human transmission has been described in labour attendants of mothers suffering Q fever, especially in those who have contact with the placenta.

  3. Is there a vaccine for Q fever?

    A whole cell vaccine (Q-Vax CSL) has been licensed in Australia since 1989. Pre-vaccination screening is essential, and includes skin tests and serology. The vaccine is only given if there is no history of Q fever disease or vaccination, and the blood test and skin test are both negative to avoid adverse reactions in those found to be seropositive due to previous exposure. It is only recommended for abattoir workers and veterinarians.

  4. Can children be affected by Q fever?

    Q fever is usually a disease of adult farmers and abattoir workers. It might be included in the differential diagnosis of febrile illness in children as it has been recorded in children as young as three years of age in Queensland. It should be noted that vaccination is currently not recommended for kids under the age of 15 in Australia.

  5. What kind of animals can be infected by Q fever bacterium?

    A wide variety of animals can be infected with Coxiella burnetii, including domesticated animals such as cows, goats, sheep, dogs, and cats; non-human primates; wild rodents and small mammals including kangaroos; big game wildlife; and non-mammalian animals, including reptiles, amphibians, birds, fish, and many ticks. Although swine become infected they rarely infect humans. Of these animals, cattle sheep and goat are the most significant source of human infection. Animals shed bacteria in milk, faeces, urine, and especially in birth by-products. The organism is quite persistent in the environment and maybe spread by the dissemination of wind-blown contaminated soil.


Related pages

Elsewhere on the web
Queensland Health: Q fever
Better Health Channel: Q fever


Article sources

NOTE: This article is based on research that utilises the sources cited here as well as the collective experience of the Lab Tests Online AU editorial review board. This article is periodically reviewed by the editorial board and may be updated as a result of the review. Any new sources cited will be added to the list and distinguished from the original sources used.
 

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Marrie TJ (Ed). Q fever. Vol.1. The disease. CRC Press, 1990.

Cutler SJ, Bouzid M, Cutler RR. Q fever. J Infect 2007;54:313-318.

Cuhna BA. The atypical pneumonias: clinical diagnosis and importance. Clin Microbiol Infect 2006;12 (suppl.3):12-24.

Marmion BP. Q fever, Your questions answered. 1999 CSL publication

Fournier PE, Marrie TJ, Raoult D. Diagnosis of Q fever. J Clin. Microbiol 1998;36:1823-1834.

(2016) https://www.cdc.gov/mmwr/preview/mmwrhtml/rr6203a1.htm