Q fever, also termed query fever, is a zoonotic infectious disease caused by Coxiella burnetii, an obligate intracellular Gram-negative bacterium that proliferates in acidified phagolysosome-like vacuoles and exhibits antigenic phase variation [2][4]. The disease was first recognized in Australia in 1937 and occurs globally with variable geographic distribution [2][3][4].
Disease overview
Bacterial Evidence-backed information EN 5/7 applicable sections · ZH 5/7 applicable sections Updated Oct 23, 2026
Q fever is a worldwide zoonotic disease caused by the intracellular bacterium Coxiella burnetii, first described in Australia in 1937, with substantial economic impact on livestock industries [1][2]. Human infection arises predominantly from animal contact, particularly through inhalation of contaminated aerosols, and affects rural populations and occupational groups most heavily [1][3][4]. Although most cases are self-limited, a small proportion progress to severe chronic forms such as endocarditis [1][5].
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Acute infection is typically asymptomatic or presents as a febrile flu-like illness, pneumonia, hepatitis, or self-limiting febrile disease [1][5][4]. Chronic Q fever develops in approximately 1–5% of primary infections and commonly manifests as life-threatening endocarditis, while rare fatalities occur in acute disease [1][5][4]. Clinical expression depends on both bacterial virulence and patient-specific risk factors [2][5].
Q fever is found worldwide with epidemiological patterns ranging from endemic to hyperendemic and including large epidemic outbreaks that vary by geographic area [2][4]. Domesticated ruminants such as cattle, sheep, and goats are the principal reservoirs, and outbreaks have been linked to occupational exposure and medical research with pregnant sheep, as well as metropolitan cat-associated transmission [1][3][4]. The condition predominantly affects rural inhabitants and those in contact with animals [4].
Humans usually acquire infection by inhaling aerosols contaminated with C. burnetii, especially those generated from infected livestock and placental derivatives [1][3][4]. Exposure occurs through contact with domestic animals, wild animals, and ticks as reservoirs, with recent urban outbreaks implicating cats as carriers to humans [3][4].
Prevention and control should focus on groups with occupational or high-risk exposure and the surrounding environment, with vaccination representing the most effective prophylactic measure [1][3]. An effective whole-cell vaccine is licensed in Australia, and other live or acellular candidates have been studied but not licensed; vaccination is also advised for those at higher risk of chronic disease such as cardiac valve defects, vascular aneurysms, and immunocompromised persons, though clinical data are limited [1][5]. Minimizing exposure among animal workers and handlers of birth products is recommended [4].
- 1 Škultéty L et al. Q fever and prevention. Epidemiol Mikrobiol Imunol. 2020 Spring. PMID: 32819108. PubMed: https://pubmed.ncbi.nlm.nih.gov/32819108/
- 2 Eldin C et al. From Q Fever to Coxiella burnetii Infection: a Paradigm Change. Clin Microbiol Rev. 2017 Jan. PMID: 27856520. doi: 10.1128/CMR.00045-16. PubMed: https://pubmed.ncbi.nlm.nih.gov/27856520/
- 3 Reimer LG et al. Q fever. Clin Microbiol Rev. 1993 Jul. PMID: 8358703. doi: 10.1128/CMR.6.3.193. PubMed: https://pubmed.ncbi.nlm.nih.gov/8358703/
- 4 España PP et al. Q Fever (Coxiella Burnetii). Semin Respir Crit Care Med. 2020 Aug. PMID: 32629489. doi: 10.1055/s-0040-1710594. PubMed: https://pubmed.ncbi.nlm.nih.gov/32629489/
- 5 Parker NR et al. Q fever. Lancet. 2006 Feb 25. PMID: 16503466. doi: 10.1016/S0140-6736(06)68266-4. PubMed: https://pubmed.ncbi.nlm.nih.gov/16503466/
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