Pathogenesis and Immunity, Clinical Syndrome - Coxiella burnetii

Pathogenesis and Immunity

C. burnetii causes infection by penetrating through abraded skin,mucosa, lung, or intestinal tract. They typically grow and multiply in acidic environment of fused phagosome and lysosome. Phase 1 form of C. burnetii is protected from the action of antibodies.

Coxiella affects lungs and heart valves and has also beenfound in macrophages in the lungs and in vegetations of heart valves. The bacteria also cause granulomatous changes in retic-uloendothelial organs, such as liver, spleen, etc. Host-mediated pathogenic mechanisms are believed to play an important role in the pathogenesis of Q fever.

Clinical Syndrome

C. burnetii causes Q fever, which can occur in acute or chronicforms.

◗ Q fever

Incubation period is 20 days. The acute stage of Q fever mani-fests as sudden onset of severe headache, high fever, chills, and myalgia. The bacteria produce a respiratory infection mimicking the atypical pneumonia. They also cause hepatosplenomegaly, which is found in approximately half of the patients.

The chronic form of Q fever has a long incubation period varying from months to years. Onset of the disease is usually insidious. Subacute endocarditis on a previously damaged heart valve or a prosthetic heart valve is the most common manifestation of the condition. Hepatitis and meningoenceph-alitis are the other manifestations of the disease.

Uncomplicated acute disease is a self-limiting disease, which lasts for 1–2 years. Complications in chronic diseases may increase mortality rate to as high as 30–60%.