If early acute Q fever infection is suspected, collect a second specimen 2 to 3 weeks later and retest. Phase II antibody titers greater than or equal to phase I antibody titers are consistent with acute/active infection.Ī negative result argues against Coxiella burnetii infection. Phase I antibody titers greater than or equal to phase II antibody titers are consistent with chronic infection or convalescent phase Q fever. Titers seen in Q fever endocarditis are similar in magnitude, although the phase I titers are quite often higher than the phase II titers. 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. 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 chronic Q fever, the reverse situation is generally seen. Although a rise in phase I as well as phase II titers may occur in later specimens, the phase II titer remains higher. In acute Q fever, the phase II antibody is usually higher than the phase I titer, often by 4-fold, even in early specimens. Differences in the host antibody response between phase I and phase II antigens can help classify infections as either acute or chronic: Respiratory manifestations usually predominate endocarditis and hepatitis can be complications.ĭuring the course of the infection, the outer membrane of the organism undergoes changes in its lipopolysaccharide structure, called phase variation. The clinical spectrum of disease ranges from unapparent to fatal. The resistance of C burnetii to heat, chemical agents, and desiccation allows the agent to survive for extended periods outside the host.Ĭ 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. 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.
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