Gold SST - spin
Red - spin and separate
Serum separator (SST) tube or LabCorp 12mL plastic transport tube
Refrigerated (preferred) - 30 days
Frozen - 30 days
Ambient - 48 hours
Contaminated, highly lipemic, grossly hemolyzed, or specimens outside the listed stability.
Immunofluorescence Assay (IFA)
<1:16 No antibody detected, Phase I and II
Positive results will reflex to a Q Fever IgG Phase I Ab Titer (LC 806608)
Coxiella burnetii, the causative agent of Q fever, is an obligate intracellular parasite from the family Rickettsiae, with worldwide distribution. The infection is spread by the inhalation of infected material, mainly from sheep and goats. Infection in these animals is enzootic and nearly always unapparent. 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.