Appropriate antibiotics, commenced soon after the onset of the illness, is the usual therapy.


As stated earlier, the major life-threatening complication of acute Q fever is chronic endocarditis which may develop shortly after the acute attack but more often, does not become apparent until 2 to 4 years or even longer following the acute attack. The complication is rare; estimates vary, but a rate of around 1% of acute cases is probably realistic.

Other complications in which the Q fever organism can readily be demonstrated by special techniques include chronic granulomatous hepatitis, in the absence of endocarditis, and infections of the bone (osteitis).

Women infected clinically or subclinically with C.burnetii, either before conception, or in early pregnancy, may experience a reactivation of infection at parturition and excrete the organism in the products of conception. Fortunately, the infection reactivation is usually without effec on mother or child, although foetal damage has been reported.

In recent years it has become apparent that there is another different, chronic, disabling sequel to acute Q fever which takes the form of a prolonged debility and fatigue syndrome. This sequel has features in common with the chronic fatigue syndrome thought to follow proven virus infections (eg., Ross River fever, glandular fever) or virus-like episodes in which a viral cause is not established by laboratory tests.

Depending on the stringency of diagnostic criteria, the post Q fever fatigue syndrome (QFS) follows about 20% of acute Q fever cases. As it may last for 5-10 or more years the cost to the industry, occupational health insurers and Health Services is considerable.

Patients suffer from an incapacitating fatigue on minor exertion, muscle and joint pains, headaches, profuse sweats, particularly at night, interrupted sleep patterns, altered mental concentration, volatile moods and depression, among other symptoms. Unfortunately, at present, the diagnosis depends almost entirely on the patients’ account of symptoms and there are no readily available laboratory tests, such as antibody tests, to confirm the diagnosis. However, several surveys of QFS patients and controls in Australia and the United Kingdom have confirmed the existence of the syndrome as a sequel to acute Q fever.

It should be noted that the symptoms described are common in the first six months after acute Q fever in patients who will eventually make an uncomplicated recovery; in contrast, QFS patients are still symptomatic 3-5 years after the acute illness. Although standard clinical, physical examination and clinical pathology tests are frustratingly negative, recent research work has revealed that QFS patients have evidence of chronic dysregulation of the cellular immune system possibly resulting from a low level persistence of the Q fever organism or its antigens after the original acute attack. The results of this research have still to be translated into a readily available routine laboratory test to confirm the clinical diagnosis.

Given the disabling nature of QFS, its duration, the conflicts over diagnosis, and its costs, the advantages of vaccination to prevent the condition and the other chronic sequels are self-evident.