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Diagnosing Q fever
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 Coxiella burnetii to heat, chemical agents, and desiccation allows the agent to survive for extended periods outside the host.
The infection is spread by the inhalation of infected material, mainly from sheep and goats. They shed the organism in feces, milk, nasal discharge, placental tissue, and amniotic fluid.
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 phase I and phase II antigen presentation can help determine if the infection is acute or chronic:
-In acute Q fever, the phase II antibody is usually 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 drawn 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.
Q FEVER PHASE I ANTIBODY, IgG
Q FEVER PHASE II ANTIBODY, IgG
Q FEVER PHASE I ANTIBODY, IgM
Q FEVER PHASE II ANTIBODY, IgM
Phase I antibody titers greater than or equal to phase II antibody titers are consistent with chronic infection or convalescent phase Q fever.
Phase II antibody titers greater than or equal to phase I antibody titers are consistent with acute/active infection.
A negative result argues against Coxiella burnetii infection. If early acute Q fever infection is suspected, draw a second specimen 2 to 3 weeks later and retest.
In Q fever sera, it is common to see IgG titers of 1:128 or greater to both phase I and phase II antibody titers. IgG class antibody titers appear very early in the disease, reaching maximum phase II titers by week 8 and persisting at elevated titers for longer than a year. Phase I titers follow the same pattern, although at much lower levels, and may not be initially detected until convalescence.
In Q fever sera, it is common to see IgM titers of > or =1:64.
IgM class antibody titers appear very early in the disease, reaching maximum phase II titers by week 3 and declining to very low levels by week 14. Phase I titers follow the same pattern, although at much lower levels, and may not be initially detected until convalescence.
Serologic responses are time-dependent. Specimens drawn too early in the disease may not have detectable antibody levels. A second specimen 2 to 4 weeks later may be necessary to detect antibody.
1. Levy PY, Carrieri P, Raoult D: Coxiella burnetii pericarditis: report of 15 cases and review. Clin Infect Dis 1999;29:393-397
2. Caron F, Meurice JC, Ingrand P, et al: Acute Q fever pneumonia: a review of 80 hospitalized patients. Chest 1998;114:808-813