Clinical Information

Q fever, a rickettsial infection caused by Coxiella burnetii, has been recognized as a widely distributed zoonosis with the potential for causing both sporadic and epidemic disease. The resistance of C burnetii to heat, chemical agents, and desiccation allows the agent to survive for extended periods outside the host.

C burnetii is spread by the inhalation of infected material, largely from dried sheep and goat reproductive material; the organism is also shed in feces, milk, nasal discharge, placental tissue, and amniotic fluid from ruminant animals.

The clinical spectrum of disease ranges from unapparent to fatal. Respiratory manifestations usually predominate; endocarditis and hepatitis can be complications.

During the course of the infection, the outer membrane of the organism undergoes changes in its lipopolysaccharide structure, called phase variation. Differences in the host antibody response between phase I and phase II antigens can help classify infections as either acute or chronic:

-In acute Q fever, the phase II antibody is generally higher than the phase I titer, often by 4-fold, even in early specimens. Although a rise in phase I as well as phase II titers may occur in later specimens, the phase II titer remains higher.

-In chronic Q fever, the reverse situation is generally seen. Serum specimens collected late in the illness from chronic Q fever patients demonstrate significantly higher phase I titers, sometimes much greater than 4-fold.

-In the case of chronic granulomatous hepatitis, IgG and IgM titers to phase I and phase II antigens are quite elevated, with phase II titers generally equal to or greater than phase I titers.

-Titers seen in Q fever endocarditis are similar in magnitude, although the phase I titers are quite often higher than the phase II titers.