Q Fever in Cows (Bovis) | Vetlexicon
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Q Fever

ISSN 2398-2993

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Synonym(s): Coxiella burnetii, Q fever, Abortion, Coxiellosis


  • Cause: domestic ruminants are considered to be the major source of Coxiella burnetii, the causal agent of Q fever. Q fever is the name applied to infection caused by the Gram negative obligate intracellular organism, C. burnetii. Primarily important as a cause of abortion in ruminant livestock and as a zoonotic pathogen. C. burnetii is resistant to disinfection, remains infectious at low doses, and can be easily spread by aerosolization. These factors make it a potential agent of bioterrorism.
  • Signs: in cattle, C. burnetii infection typically presents as a subclinical disease and as such, may be under reported. C. burnetii can be reactivated due to the stress associated with pregnancy or parturition. Disease may be associated with abortions, premature births, infertility, still births, weak calf syndrome, metritis and mastitis.
  • Diagnosis: laboratory submission of products of abortion/parturition, vaginal mucus, milk or feces for PCR or immunohistochemistry. Herd status may be defined through bulk milk ELISA tests.
  • Treatment: supportive therapy and treatment of metritis and mastitis.
  • Prognosis: good.

Presenting signs

  • In cattle, disease is often subclinical in nature.

Acute presentation

  • If clinical disease is present reduced fertility performance, abortions, infertility, premature births, weak calf syndrome, metritis, still births and mastitis may be seen.

Geographic incidence

  • World-wide distribution, with the exception of New Zealand.

Age predisposition

  • Although infection can occur at any age, increasing age has been associated as an epidemiological risk factor for disease.

Public health considerations

  • Q fever is a zoonotic pathogen capable of causing a variety of disease manifestations in humans:
    • Many infected people (up to 60%) seroconvert but remain healthy.
    • The most common manifestation of illness is an acute, flu-like febrile illness.
    • Atypical pneumonia may be associated with fever, headache, and myalgia.
    • Chronic disease manifestations occur in only a small percentage of infected people.
    • Recurrent abortion occurs in infected women just as it does in infected animals.
    • Chronic fatigue syndrome has been associated with Q fever in humans.
    • Q fever is responsible for as many as 2-10% of endocarditis cases in humans.
    • A variety of other manifestations are reported in humans, including meningoencephalitis, headache, pericarditis, and pancreatitis.
    • Disease manifestations of chronic infection may occur months or even years after exposure to the organism.
  • Human exposure is related primarily to inhalation of aerosols. Because the organisms are extremely resistant in the environment, dust contaminated with body fluids (including amniotic fluid) or desiccated placenta from infected ruminants is a primary means of exposure.
  • Humans can also be infected through consumption of infected milk or direct contact with infected tissues.
  • Groups most at risk are farm workers, abattoir workers and veterinarians.
Aborted material should be bagged, sealed, and disposed of as biohazardous material.
  • Potentially contagious organisms may also be found in urine, feces, milk, or blood of infected animals.
  • Organisms in the environment are resistant to temperature, desiccation, ultraviolet light, and even many chemical disinfectants.
  • A 30-minute exposure to 70% alcohol or 5% chloroform will destroy environmental sporulates.
  • Inactivated when held at 63°C/145.4°F for 30 min or 72°C/161.6°F for 15 sec. Current milk pasteurization standards are based on the temperature and hold time required to inactivate the endospore-like forms of C. burnetii.

Cost considerations

  • Financial losses my occur from abortions, still births, premature births, metritis, mastitis or infertility.



  • Q fever is caused by infection with C. burnetii Coxiella burnetii, a gram-negative obligate intracellular pathogen historically considered as Rickettsia.
  • The organism is shed in milk, urine, feces and the products of abortion/parturition.
  • Shedding is often more pronounced around the time of abortion or parturition when recrudescence of latent infection can occur.
  • Q fever is an airborne disease and inhalation of infected aerosols and dust is the main route of infection of domestic ruminants. Cattle may also become infected through the ingestion of contaminated pasture or feed sources.
  • It is likely that C. burnetii contaminated manure plays a role on the maintenance of infection in animal populations.
  • Biting arthropods such as ticks are also a potential transmission pathway for C. burnetii.

Predisposing factors



  • Increasing age has been associated as an epidemiological risk factor for disease, which is more pronounced in dairy than beef herds.


  • Reservoir hosts include multiple domestic and wild animal species, birds, and arthropods. Biting ectoparasitic arthropods such as ticks Ticks: overview likely play a role in spread of the infection, especially in the sylvan setting.
  • The bacterium has two distinct life stages. Although it is an obligate intracellular organism inside the host, an endospore form (which is resistant to harsh environmental conditions) exists in the environment.
  • The large-cell variant is the metabolically active intracellular state associated with acute infection.
  • The small-cell variant is the metabolically inactive stage. This stage may be found in tissues of chronically infected animals during latent infection, and it is this stage which persists in the environment.
  • Acute infection may be cleared without clinical consequences.
  • Pathophysiology of infection in pet animals is not well documented. Chronic infection can result after the organism disseminates to multiple organs hematogenously (through the blood). The bacterium survives inside cell phagosomes.
  • In subclinically infected animals, the organism appears to remain latent until pregnancy and parturition.


  • In cattle we are currently uncertain of the time course for disease or the time for seroconversion.
  • During pregnancy, latent infections may become reactivated. New infection or reactivation of latent infection may result in abortion, stillbirths, or the birth of weakened neonates Weak calf syndrome.
  • Normal pregnancy and healthy offspring may result from infected animals.
  • Clinically infected animals have been demonstrated to shed C. burnetti in milk for up to 13 months.
  • In asymptomatic herds, shedding of C. burnetii in milk has been shown to occur for several months or even years.


  • In the UK disease is considered to be endemic, with seroepidemiological studies suggesting up to 70% of UK dairy herds have exposure to C. burnetii. However, regional variation in infection rates may be seen.


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Further Reading


Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Ryan E D, Wrigley K, Hallinan A, McGrath G & Clegg T A (2018) Antibodies to Coxiella burnetii in Irish bulk tank milk samples. Vet Rec 182 (19), 550 PubMed.
  • Pexara A, Solomakos N & Govaris A (2018 ) Q fever and seroprevalence of Coxiella burnetii in domestic ruminants. Vet Ital 54 (4), 265-279 PubMed.
  • Chisnall T L T (2017) Variance of Coxiella burnetii strains in bulk tank milk samples and associated Q fever exposure in veterinary undergraduates. Cattle Pract 25 (3),167-168 VetMedResource.
  • Garcia-Ispierto I, utusaus T & Lo´pez-Gatius F (2014) Does Coxiella burnetii affect reproduction in cattle? A clinical update. Reprod Domest Anim 49 (4), 529–535 PubMed.
  • Van Engelen E, Schotten N, Schimmer B et al (2014) Prevalence and risk factors for Coxiella burnetti (Q fever) in Dutch dairy cattle herds based on bulk milk testing. Preventative Vet Med 117 (1),102-109 PubMed.
  • Saegerman C, Speybroeck N, Dal Pozzo F & Czaplicki G (2012) Clinical indicators of exposure to Coxiella burnetii in dairy herds. Transbound Emerg Dis 62 (1), 46–54 PubMed.
  • Valergakis G E, Russell C, Grogono Thomas R et al (2012) Coxiella burnetii in bulk tank milk of dairy cattle in south-west England. Vet Rec 171 (6), 156 PubMed.
  • Alvarez A, Perez A, Mardones F O et al (2012) Epidemiological factors associated with the exposure of cattle to Coxiella burnetii in the Madrid region of Spain. Vet J 194 (1) 102-1-7 PubMed.
  • Cooper A, Hedlefs R, McGowan M, Ketheesana N & Govana B (2011) Serological evidence of Coxiella burnetii infection in beef cattle in Queensland. Aust Vet J 89 (7), 260-264 PubMed.
  • Guatteo R, Seegers H, Frieda Taural A, Joly A & Beaudeau F (2011) Prevalence of Coxiella burnetii infection in domestic ruminants: A critical review. Vet Microbiol 149 (1-2), 1-16 PubMed.
  • Pritchard G C, Smith R P, Errington J et al (2011) Prevalence of Coxiella burnetii in livestock abortion material using PCR. Vet Rec 169 (15), 391 PubMed.
  • Ryan E D, Kirby M, Collins D M et al (2011) Prevalence of Coxiella burnetii (Q fever) antibodies in bovine serum and bulk-milk samples. Epidemiol Infect 139 (9), 1413–1417 PubMed.

Other sources of information


  • European Food Standards Authority (2010) Scientific Opinion on Q fever1 EFSA Panel on Animal Health and Welfare (AHAW)2,3 EFSA Panel on Biological Hazards (BIOHAZ)2,3 (Chapter 4 on Food Safety). EFSA Journal 2010; 8 (5),1595.