Q fever is a zoonosis due to the rickettsial-like organism Coxiella burnetii. This organism is smaller than true rickettsiae, more resistant to physical and chemical injury and has a negative Weil-Felix reaction, since it does not share common antigens with Proteus. Clinically, Q fever differs from rickettsial illnesses as the rash is not a major feature and transmission of the disease to humans is independent of an arthropod vector. Important modes of spread to humans are thought to be dust, aerosols and unpasteurized milk from infected cows. C. burnetii is widespread in domestic and farm animals. It is spread between them by ticks, which constitute an important arthropod reservoir of the disease.
Fever begins insidiously, together with other symptoms of an influenza-like illness, 1-2 weeks after exposure. The acute illness may resolve spontaneously without treatment, but with persisting infection, symptoms and signs of pneumonia may develop, followed by endocarditis. A petechial rash may be apparent at this stage. Occasionally epididymo-orchitis, uveitis and osteomyelitis may be present. Untreated chronic infection is usually fatal.
Serodiagnosis by complement fixation tests is important since C. burnetii is an obligate intracellular organism and does not grow on standard microbiological culture media. The organism possesses two classes of antigens, phase I and phase II. Antibodies to the phase I antigens appear later in the illness than antibodies to the phase II antigens; high tit res are diagnostic in endocarditis. Persistently high tit res of both antibodies confirm chronic infection.
etracycline is the treatment of choice for acute infection. For endocarditis a prolonged course of treatment is required, clindamycin often being given in association with tetracycline. Co-trimoxazole and rifampicin may also be useful.