Coxiellosis / Q fever

edited October 20, 2015


The Coxiellosis / Q fever in cats guidelines that the present article is updating were published in J Feline Med Surg 2013; 15: 573-575; this update has been compiled by Herman Egberink.



Q fever is a zoonotic disease caused by Coxiella (C.) burnetii. Farm animals and pets are main reservoir hosts of the bacterium, and exposure of cats is relatively common: in the UK, a seroprevalence as high as 61.5 % was demonstrated (Meredith et al., 2014). The disease in cats is usually subclinical; abortion may occur. After experimental infection, cats develop fever, anorexia and lethargy.

Coxiella burnetti causes Q fever in man. Cats have been implicated as a source of infection for humans, in particular through contact with bacteria excreted during abortion. A Q fever outbreak amongst veterinary hospital personnel was linked to a caesarean section on a parturient queen. The breeding queen was seropositive, and antibodies were demonstrated in 26 % of the cats living in the same cattery (Kopecny et al., 2013).



Bacterial properties


Coxiella burnetii is a Gram-negative, obligate intracellular, small, pleomorphic bacterium belonging to the order Legionellales. This organism has a complicated life cycle with different morphological stadia. It may occur as a small-cell and a large-cell variant. The small-cell variant is the resistant spore-like form that can survive for long periods in the environment, being resistant to various means of chemical and physical inactivation (Angelakis and Raoult, 2010).



Epidemiology and pathogenesis


Many species of mammals, birds and ticks can be infected with C. burnetii. However, the most common reservoirs are cattle, sheep and goats. Since the bacterium has a tropism for the uterus and mammary gland, the placenta and foetal membranes may be heavily contaminated. Aerosols from foetal membranes, urine, faeces, or milk of infected animals are considered the main source of infection for humans. Especially during parturition, large amounts of bacteria are excreted and contaminate the environment.


Cats can also become infected and have been implicated as a source of infection for humans (Langley at al., 1988; Kosatsky, 1984; Marrie et al., 1988a, b). Cats most commonly become infected via tick bites, ingestion of contaminated carcasses or after aerosol exposure. Exposure of cats is relatively common as serological studies have shown (Matthewman et al., 1997; Higgins and Marrie, 1990; Htwe et al., 1992; Komiya et al., 2003); results range from 2% to 19% seropositive cats. In one study, a much higher rate was found in stray cats (41.7%) as compared to pet cats (14.2%; Komiya et al., 2003). In a study on the prevalence of bacterial DNA in vaginal and uterine samples from healthy shelter or client-owned cats, 4 out of 47 uterine biopsies were found positive by PCR (Cairns et al., 2007). Like in farm animals, C. burnetii colonizes the placenta of infected cats during pregnancy, and the agent could be cultured from uterine samples for 10 weeks after parturition (Higgins and Marrie, 1990). After experimental infection, C. burnetii was cultured for 2 months from the urine (Green, 2012).
Q fever pneumonia in humans has been recorded after exposure to placenta and amniotic fluid of aborting, but also of apparently healthy cats (Langley at al., 1988; Kosatsky, 1984; Marrie et al., 1988a; Pinsky et al., 1991). In a case-control study from Maritime Canada, the risk for developing Q fever was strongest associated with exposure to stillborn kittens and parturient cats (Marrie et al., 1988b).


In a study of US veterinarians, contact with cats was not associated with C. burnetii seropositivity (Whitney et al., 2009). Risk factors rather included age, routine contact with ponds, and veterinary treatment of cattle, swine and wildlife. In another study, no connection was found between cat and dog ownership and increased seropositivity (Skerget et al., 2003).
In conclusion, peri-parturient cats should be considered a potential risk – but farm animals are by far the most important source of infection for humans.



Clinical signs


In humans

In humans, C. burnetii infection is often asymptomatic (60%), but acute and chronic forms of the disease may develop (Angelakis And Raoulr, 2010). The acute disease is often mild, with fever, headache, myalgia and with a spontaneous recovery (Caron et al., 1998). However, pneumonia, hepatitis, abortion and more serious, fatal complications like meningo-encephalitis, sepsis and myocarditis may occur. Chronic disease many months to years after infection has been reported, which is mainly endocarditis and occurs almost exclusively in patients with predisposing conditions (Fenollar et al., 2001).


In cats

In animals the disease is usually subclinical, but abortion may occur. In experimentally infected cats, fever, anorexia and lethargy has been noted. Clinical signs started 2 days after inoculation and lasted for 3 days (Greene, 2012).





In humans, the definite diagnosis of Q fever is based on serology and isolation of the organism. A fourfold increase in paired serum samples is considered diagnostic. The organism shows a phase variation during the course of the infection: antibodies against phase I and II antigens can be determined to establish the stage of infection. During acute infection, titres against phase II antigens are much higher than those against phase I antigens. PCR and immunohistochemistry have been used on tissue samples from patients; similar techniques might be used in cats, but laboratory diagnosis is not routinely performed.





If a diagnosis has been established in a cat with clinical signs, tetracyclines and chloramphenicol can be used.





Cats infected with C. burnetii through contact with farm animals or ticks may excrete bacteria during parturition. To minimize the zoonotis risk, gloves and goggles should be worn when attending parturient or aborting cats. Predation and ectoparasite exposure put the cat at risk of infection and tick prevention is recommended (see ESCCAP guideline 03, june 2012; Control of ectoparasites in dogs and cats). Vaccines are not available for cats.







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Cairns K, Brewer M, Lappin MR (2007). Prevalence of Coxiella burnetii DNA in vaginal and uterine samples from healthy cats of north-central Colorado. J Feline Med Surg 9:196-201.


Caron F, Meurice JC, Ingrand P, Bourgoin A, Masson P, Roblot P, et al (1998). Acute Q fever pneumonia: a review of 80 hospitalized patients. Chest 114(3):808-813.


Egberink H, Addie D, Bélak S, Boucraut-Baralon C, Frymus T, Gruffydd-Jones T, et al. Coxiellosis/Q fever in cats. ABCD guidelines on prevention and management. J Feline Med Surg 2013; 15: 573-575.


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Kopecny L, Bosward KL, Shapiro A, Norris JM (2013). Investigating Coxiella burnetii infection in a breeding cattery at the centre of a Q fever outbreak. J Feline Med Surg 15:1037-1045.


Kosatsky T (1984). Household outbreak of Q-fever pneumonia related to a parturientcat. Lancet 2(8417-8418):1447-1449.


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Marrie TJ, Langille D, Papukna V, Yates L (1989). Truckin’ pneumonia – an outbreak of Q fever in a truck repair plant probably due to aerosols from clothing contaminated by contact with newborn kittens. Epidemiol Infect 102(1):119-127.


Marrie TJ, MacDonald A, Durant H, Yates L, McCormick L (1988a). An outbreak of Q      fever probably due to contact with a parturient cat. Chest 93(1):98-103.


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Meredith AL, Cleaveland SC, Denwood MJ, Brown JK, Shaw DJ (2014). Coxiella burnetii (Q-Fever) Seroprevalence in Prey and Predators in the United Kingdom: Evaluation of Infection in Wild Rodents, Foxes and Domestic CatsUsing a Modified ELISA. Transboundary and emerging diseases DOI: 10.1111/tbed.12211


Pinsky RL, Fishbein DB, Greene CR, Gensheimer KF (1991). An outbreak of cat-associated Q fever in the United States. J Infect Dis 164(1):202-204.


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Whitney EA, Massung RF, Candee AJ, Ailes EC, Myers LM, Patterson NE, et al. (2009). Seroepidemiologic and occupational risk survey for Coxiella burnetiiantibodies among US veterinarians. Clin Infect Dis 48(5):550-557.


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