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Infections in Humans
Infections in Animals
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Q fever results from infection by Coxiella burnetii. This organism is an obligate intracellular pathogen and has been traditionally placed in the family Rickettsiaceae; however, recent phylogenetic studies have demonstrated that C. burnetii is more closely related to Legionella, Francisella and Rickettsiella in the gamma subdivision of Proteobacteria.

C. burnetii forms unusual spore-like structures that are highly resistant to environmental conditions. The organism also has two distinct antigenic phases. Phase I is pathogenic and is found in infected animals or in nature; phase II is less pathogenic and is recovered after bacteria are passaged repeatedly in cell cultures or eggs.

Geographic Distribution

Q fever has been found worldwide, except in New Zealand.


C. burnetii can be transmitted by aerosols or direct contact; it is also spread by ingestion of an infected placenta, other reproductive discharges or milk. Organisms localize in the mammary glands, supramammary lymph nodes, uterus and placenta in domestic ruminants and other susceptible species; bacteria can be shed in milk, the placenta and reproductive discharges during subsequent pregnancies and lactations. C. burnetii can also be found in the feces and urine. Ticks seem to spread infections among ruminants and sometimes people. Transmission has occurred in blood transfusions and by sexual contact in humans. Organisms have also been found in the semen of bulls. Vertical transmission is possible but rare.

C. burnetii is highly resistant to environmental conditions and is easily spread by aerosols; infectious airborne particles can travel a half-mile or more. Viable organisms can be found for up to 30 days in dried sputum, 120 days in dust, 49 days in dried urine from infected guinea pigs, and for at least 19 months in tick feces. At 4-6°C, organisms can survive for 42 months in milk and 12 to 16 months in wool.


C. burnetii is highly resistant to physical and chemical agents. Variable susceptibility has been reported for hypochlorite, formalin and phenolic disinfectants; a 0.05% hypochlorite, 5% peroxide or 1:100 solution of Lysol® may be effective. C. burnetii is also susceptible to glutaraldehyde, ethanol, gaseous formaldehyde, gamma irradiation or temperatures of 130°C for 60 min. High temperature pasteurization destroys the organism.

Infections in Humans

Incubation Period

In humans, the incubation period varies from 2 to 40 days; the typical incubation period is approximately 2 to 5 weeks.

Clinical Signs

The symptoms of Q fever appear acutely and can include fever, chills, a severe headache, fatigue, malaise, myalgia and chest pains. The illness generally lasts from a week to more than 3 weeks. A nonproductive cough, with pneumonitis on X-ray, sometimes develops during the second week. In severe cases, lobar consolidation and pneumonia may occur; severe infections are particularly common in elderly or debilitated patients. Hepatitis is seen in approximately one third of patients with prolonged disease; the clinical signs may include fever, malaise, right upper abdominal pain, hepatomegaly and sometimes jaundice. In pregnant women, infections can result in premature delivery, abortion and placentitis.

Complications are not common but may include chronic hepatitis, aseptic meningitis, encephalitis, osteomyelitis, vasculitis and endocarditis. Endocarditis usually occurs in people who have pre-existing damage to the heart valves. The symptoms are similar to subacute bacterial endocarditis.


Person to person spread is very rare but has been seen in people with pneumonia.

Diagnostic Tests

In humans, Q fever is usually diagnosed by serology. Serologic tests can be done as early as the second week of illness; they may include immunofluorescence, ELISA, agglutination or complement fixation. Antibodies to the protein antigens found in phase II organisms appear in acute Q fever; antibodies to the lipopolysaccharide of phase I organisms indicate chronic Q fever. Organisms are occasionally found in stained tissue samples but this test is not routinely used in humans.

Isolation of C. burnetii is dangerous to laboratory personnel and is rarely done. Organisms can be recovered from blood samples; bacteria are isolated in cell cultures, embryonated chicken eggs or laboratory animals including mice, hamsters and guinea pigs. Blood cultures from patients with endocarditis are usually negative.

Treatment and Vaccination

Antibiotics can shorten the course of acute illness and reduce the risk of complications. Treatment of chronic cases is more difficult and may require long-term antibiotic therapy. Surgical replacement is sometimes necessary for damaged valves.

Effective vaccines may be available for people who are occupationally exposed. A licensed vaccine is available in Australia. In the United States, an investigational vaccine can be obtained from special laboratories such as the U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID).

Morbidity and Mortality

Most cases of Q fever occur in people occupationally exposed to farm animals or their products: farmers, abattoir workers, researchers, laboratory personnel, dairy workers and woolsorters have an increased risk of infection. Approximately 60% of cases are thought to be asymptomatic. An additional 38% of infected people experience mild illness, while 2% develop severe disease and require hospitalization.

Q fever is usually a self-limiting illness; most cases resolve spontaneously within 2 days to 2 weeks. The mortality rate is 1% in untreated cases and lower in those who are treated. A biological attack with aerosolized organisms is expected to be similar to a natural outbreak.

Infections in Animals

Species Affected

Sheep, goats and cattle are the most common domestic animal reservoirs. Dogs, cats, rabbits, horses, pigs, camels, buffalo, rodents, pigeons, geese and other fowl may carry C. burnetii. Antibodies to C. burnetii have been found in badgers, coyotes, raccoons, opossums, badgers, jackrabbits, feral pigs, black bears and musk ox. Ticks and wild birds can also harbor this organism.

Incubation Period

The incubation period is variable; reproductive failure is usually the only symptom in animals. Abortions generally occur late in pregnancy.

Clinical Signs

Abortion, stillbirth, retained placenta, endometritis, infertility and small or weak offspring can be seen in ruminants, cats, dogs, rabbits and other species. Most abortions occur near term. Several abortions may be followed by uncomplicated recovery, particularly in small ruminants; in other cases, the disease may recur yearly.

With the exception of reproductive disease, animals are usually asymptomatic. Goats sometimes have a poor appetite and are depressed for 1 to 2 days before an abortion. Clinical signs including fever, anorexia, mild coughing, rhinitis and increased respiratory rates occur in experimentally infected sheep but have not been reported in natural infections. Experimentally infected cats develop fever and lethargy.


Yes. Large numbers of organisms are found in the placenta, fetal fluids, aborted fetus, milk, urine and feces. Serologically negative animals may shed organisms.

Diagnostic Tests

C. burnetii can be detected in vaginal discharges, the placenta, placental fluids and aborted fetuses, as well as milk, urine and feces. Organisms are not shed continuously in milk and colostrum. In the placenta, organisms can be identified in exudates or areas of inflammation with a modified Ziehl-Neelsen or Gimenez stain; C. burnetii is an acid-fast, pleomorphic, small coccoid or filamentous organism. This organism is not usually detected by Gram stains. Bacterial identity can be confirmed by immunohistochemistry. Polymerase chain reaction techniques are also available in some laboratories. Fresh, frozen or paraffin-embedded samples of serum, buffy coat, milk, feces, vaginal exudates, cerebrospinal fluid, bone marrow, placenta, liver, cardiac valve, fetal tissue and other tissues can be tested by PCR.

A number of serologic tests are available; the most commonly used tests include indirect immunofluorescence, enzyme-linked immunosorbent assay (ELISA) and complement fixation. Cross-reactions have been seen between some strains of C. burnetii and Chlamydia in ELISA and immunoblot assays.

C. burnetii can be isolated in cell cultures, embryonated chicken eggs or laboratory animals including mice, hamsters and guinea pigs; however, isolation is dangerous to laboratory personnel and is rarely used for diagnosis.

Treatment and Vaccination

Little is known about the efficacy of antibiotic treatment in ruminants or other domestic animals. Treatment is sometimes recommended to reduce the risk of abortion. Antibiotics may in some cases suppress rather than eliminate infections. Isolating infected pregnant animals and burning or burying the reproductive membranes and placenta can decrease transmission.

Vaccines are not available for domestic ruminants in the United States but are used in other countries. Vaccines may prevent infections in calves, decrease shedding of organisms and improve fertility in infected animals. They do not eliminate shedding of the organism.

Morbidity and Mortality

Information on the prevalence of infection is limited. In an endemic region in California, 18 to 55% of sheep had antibodies to C. burnetii; the number of seropositive sheep varied seasonally and was highest soon after lambing. In other surveys, 82% of cows in some California dairies were seropositive, as well as 78% of coyotes, 55% of foxes, 53% of brush rabbits and 22% of deer in Northern California. In Ontario, Canada, infections were found in 33 to 82% of cattle herds and 0 to 35% of sheep flocks. Close contact with sheep appears to increase the risk of infection in dogs.

Significant morbidity can be seen in some species. In sheep, abortions can affect 5 to 50% of the flock. In one California study, Q fever may have been responsible for 9% of all abortions in goats. Deaths are rare in natural infections.

Post-Mortem Lesions

Placentitis is the most characteristic sign in ruminants. The placenta is typically leathery and thickened and may contain large quantities of white-yellow, creamy exudate at the edges of the cotyledons and in the intercotyledonary areas. In some cases, the exudate may be reddish- brown and fluid. Severe vasculitis is uncommon, but thrombi and some degree of vascular inflammation may be noted. Fetal pneumonia has been seen in goats and cattle and may occur in sheep; however, the lesions in aborted fetuses are usually non-specific.

Internet Resources

black arrow graphic Animal Health Australia. The National Animal Health Information System (NAHIS)
black arrow graphic Material Safety Data Sheets –Canadian Laboratory Center for Disease Control
black arrow graphic Medical Microbiology
black arrow graphic The Merck Manual
black arrow graphic The Merck Veterinary Manual
black arrow graphic Office International des Epizooties (OIE)
Manual of Standards for Diagnostic Tests and Vaccines
black arrow graphic Q Fever: An Overview
United States Animal Health Association


“Control of Communicable Diseases.” Edited by J. Chin. American Public Health Association, 2000, pp.407-411.

De la Concha-Bermejillo, A., E.M. Kasari, K.E. Russell, L.E. Cron, E.J. Browder, R. Callicott and R.W. Ermel1. “Q Fever: An Overview. United States Animal Health Association. 4 Dec 2002

Marrie, T.J. “Q Fever.” Edited by S.R. Palmer, E.J.L. Soulsby and D.I.H Simpson. New York: Oxford University Press, 1998, pp. 171-185.

Martin J. and P. Innes. “Q Fever.” Ontario Ministry of Agriculture and Food, Sept 2002. 4 Dec 2002 <>.

“Material Safety Data Sheet –Coxiella burnetii.” Canadian Laboratory Centre for Disease Control, January 2001. 2 Dec 2002

“Q Fever.” In Manual of Standards for Diagnostic Tests and Vaccines. Paris: Office International des Epizooties, 2000, pp. 822-831.

“Q Fever.” In Medical Management of Biological Casualties Handbook, 4 th ed. Edited by M. Kortepeter, G. Christopher, T. Cieslak, R. Culpepper, R. Darling J. Pavlin, J. Rowe, K. McKee, Jr., E. Eitzen, Jr. Department of Defense, 2001. 2 Dec 2002 <>.

“Q Fever.” In The Merck Manual, 17 th ed. Edited by M.H. Beers and R. Berkow. Whitehouse Station, NJ: Merck and Co., 1999. 7 Oct 2002

“Q Fever.” In The Merck Veterinary Manual, 8 th ed. Edited by S.E. Aiello and A. Mays. Whitehouse Station, NJ: Merck and Co., 1998, pp. 486-7.

Van der Lugt, J, B. van der Lugt and E. Lane. “An approach to the diagnosis of bovine abortion.” Paper presented at the mini-congress of the Mpumalanga branch of the SAVA, 11 March 2000. Pathology for the practicing veterinarian, Large Animal Section, no. 1 (April 2000). 2 December 2002 <>.

Walker, D.H. “Rickettsiae.” In Medical Microbiology. 4 th ed. Edited by Samuel Baron. New York; Churchill Livingstone, 1996. 3 December 2002 <>.

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Center for Food Security and Public Health
Iowa State University College of Veterinary Medicine
Ames Iowa USA 50011
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