Coxiellosis / Q fever in cats
updated November 2020, last review June 2022
The Coxiellosis / Q fever in cats guidelines were first published in J Feline Med Surg 2013; 15: 573-575; this update has been drafted by Herman Egberink.
Q fever is a zoonotic disease caused by Coxiella burnetii. Farm animals and pets are the main reservoirs of infection.
Infection of cats with Coxiella burnetii occurs frequently, as shown by seroprevalence studies.
Cats become infected by tick bites or contact with farm animals, by ingestion or inhalation of the bacteria.
The disease in cats is usually subclinical; abortion may occur. Coxiella burnetii has been isolated from the placenta of aborting cats, but also from cats that have had normal parturition.
After experimental infection, cats develop fever, anorexia and lethargy.
Infection with C. burnetii can be diagnosed by isolation of the agent or serology.
Coxiella burnetii 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 or parturition. Wearing gloves and a mask when attending parturient or aborting cats can minimize risk of infection. Tick prevention is recommended.
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 variant 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. Contaminated aerosols from foetal membranes, urine, faeces, or milk of infected animals are considered the main reservoir of infection for humans. Especially during parturition, high numbers of bacteria are excreted, thereby contaminating the environment.
Cats can also become infected via tick bites, ingestion of contaminated carcasses or after aerosol exposure and have been implicated as a source of infection for humans (Kosatsky, 1984; Langley et al., 1988; Marrie et al., 1988a; 1988b; 1989). C.burnetii DNA was also detected in raw meat from kangaroos intended for pet consumption (Shapiro et al., 2020).The potential role of certain raw meets in transmission to cats and humans needs further investigation. Exposure of cats is relatively common as serological studies have shown (Higgins and Marrie, 1990; Htwe et al., 1992; Matthewman et al., 1997; Komiya et al., 2003). In these studies, results range from 2 to 19% of cats being seropositive. In a study from the UK, a 61.5% seroprevalence was demonstrated (Meredith et al., 2014). In one study, a significantly higher antibody positive rate was demonstrated in stray cats (41.7%) as compared to pet cats (14.2%) (Komiya et al., 2003). The differences in seroprevalence found in these studies are possibly associated with differences in the populations studied, but lack of standardized serological techniques may play a role (Cicutin, 2017). Infection has also been demonstrated in free-living European wild cats (Candela et al., 2017).
In a study on the prevalence of C. burnetii DNA in vaginal and uterine samples from healthy shelter or client-owned cats, 4 out of 47 uterine biopsies were shown to be positive by PCR (Cairns et al., 2007). In another study 2 out of 26 uterine tissues from healthy cats and 1 out of 11 from cats with reproductive abnormalities were PCR positive (Fujishiro et al., 2015). As in farm animals, C. burnetii colonizes the placenta of infected cats during pregnancy in high numbers and it could be cultured from the uterus of cats for 10 weeks after parturition (Higgins and Marrie, 1990). After experimental infection, C. burnetii was cultured for 2 months from the urine of infected cats (Greene, 2012).
Studies have been published indicating an association between Q fever pneumonia in humans after exposure to placenta and amniotic fluid of aborting or apparently healthy cats (Kosatsky, 1984; Langley et al., 1988; Marrie et al., 1988a; Pinsky et al., 1991; Malo et al., 2018). In a case-control study from Maritime Canada, several risk factors for developing Q fever in human patients were identified. The strongest association was with exposure to stillborn kittens and parturient cats (Marrie et al., 1988b). Results from a large questionnaire among Australian cat breeders support the assumption that cat breeders are an at-risk group of acquiring Q fever (Shapiro et al., 2017). Husbandry practices that may increase the risk of infection have been identified: feeding and handling of raw meat, parturition at home in the living environment and assistance provided at the time of birth (such as mouth-to mouth resuscitation). In an outbreak at an animal refuge and veterinary clinic in southeast Queensland, a parturient cat was identified as the most likely source (Malo et al., 2018). A Q fever outbreak amongst Veterinary hospital personnel was linked to a Caesarean section on a parturient queen. The breeding queen showed strong seropositivity against C. burnetii and antibodies indicating recent or past infection were demonstrated in 26% of the cats living in the same cattery (Kopecny et al., 2013). In a serological investigation of four different sub-populations of cats, the seroprevalence was highest in cattery-confined breeding cats (Shapiro et al., 2015). In this population, 9.3% of the cats were seropositive compared to 1% of pet cats and 0% in both feral and shelter cats populations. In a sero-epidemiological study among US veterinarians, contact with cats was not shown to be associated with C. burnetii seropositivity (Whitney et al., 2009). In this study, risk factors associated with seropositivity included age >46 years, routine contact with ponds and treatment of cattle, swine and wildlife. In another study, no relation was found between cat and dog ownership and an increased incidence of seropositivity for C. burnetii (Skerget et al., 2003).
In conclusion, peri-parturient cats should be considered a potential source of infection. However, farm animals are by far the most important source of infection for humans.
Clinical signs in cats
In animals the disease is usually subclinical, but abortion might occur. In experimentally infected cats, fever, anorexia and lethargy have been noted. Clinical signs started 2 days after inoculation and lasted for 3 days (Greene, 2012).
In humans, a 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, antibody titres against phase II antigens are much higher than against phase I. 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 can be used such as oral doxycycline at 10 mg/kg q24h for 2 weeks (Greene, 2012).
Predation and ectoparasite exposure put the cat at risk of infection and tick prevention is recommended (see ESCCAP guideline 03, June 2018; Control of ectoparasites in dogs and cats; ESCCAP, 2018). Vaccines are not available for cats.
Cats infected with C. burnetii through contact with infected farm animals or recent tick infections may shed bacteria during parturition.
In humans, C. burnetii infection is often asymptomatic (60%), but acute and chronic forms of the disease may develop (Angelakis and Raoult, 2010). The acute disease is often a mild disease with fever, headache, myalgia and spontaneous recovery (Caron et al., 1998). However, signs of pneumonia, hepatitis and abortion and more serious complications especially meningo-encephalitis, sepsis and myocarditis followed by death of the patient may occur. Chronic disease many months to years after infection has been reported. The chronic form is mainly characterized by endocarditis and occurs almost exclusively in patients with predisposing conditions (Fenollar et al., 2001).
To minimize the zoonotic risk, gloves, goggles and sleeves should be worn when attending parturient or aborting cats. Parturition in designated birthing environments (and not near or within the living environment of people) will reduce the risk of transmission. In Australia, vaccination against Q-fever of susceptible individuals with occupational or regularly exposure to parturient cats has been proposed (Malo et al., 2018).
ABCD Europe gratefully acknowledges the support of Boehringer Ingelheim (the founding sponsor of the ABCD) and Virbac.
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