Q fever is caused by Coxiella burnetii, an obligate intracellular bacterium.1 The organism is inactivated at pasteurisation temperatures. It survives well in air, soil, water and dust, and may also be disseminated on fomites such as wool, hides, clothing, straw and packing materials.2,3 C. burnetii has been weaponised and is considered a Category B biothreat agent.
4.15.2 Clinical features
Q fever can be acute or chronic, and there is increasing recognition of long-term sequelae. Infection is asymptomatic in at least half of cases.
Acute Q fever usually has an incubation period of 2 to 3½ weeks, depending on the inoculum size and other variables7 (range from 4 days up to 6 weeks). Clinical symptoms vary by country, but, in Australia, the most common presentation is rapid onset of high fever, rigors, profuse sweats, extreme fatigue, muscle and joint pain, severe headache and photophobia.5,6 As the attack progresses, there is usually evidence of hepatitis, occasionally with frank jaundice; a proportion of patients may have pneumonia, which is usually mild but can require mechanical ventilation. If untreated, the acute illness lasts 1 to 3 weeks and may be accompanied by substantial weight loss in more severe cases. Infection often results in time off work, lasting a few days to several weeks.
C. burnetii may cause chronic manifestations, the most commonly reported being subacute endocarditis. Less common presentations include granulomatous lesions in bone, joints, liver, lung, testis and soft tissues. Infection in early pregnancy, or even before conception, may recrudesce at term and cause fetal damage.
Studies have also identified a late sequela to infection, post Q fever fatigue syndrome (QFS), which occurs in about 10 to 15% of patients who have previously had acute Q fever. Research suggests that non-infective antigenic complexes of C. burnetii persist for many years after acute Q fever, and the maintenance of immune responses to these antigens might be the biological basis by which QFS occur