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Q Fever

Q fever is a widespread zoonotic infection caused by the pathogen Coxiella burnetii. C. burnetii is a short, pleomorphic rod that is a strict intracellular bacterium. C. burnetii is highly infectious, persists in the environment, and can travel for miles once windborne . A single bacterium is sufficient to infect a human. Transmission can occur via inhalation of contaminated aerosols or dust. Cattle, sheep, and goats are the primary Q fever reservoirs. However, pets, including cats, rabbits, pigeons, and dogs may serve as sources of urban outbreaks. Transmission by tick bites and ingestion of unpasteurized dairy products has also been reported. Human to human transmission of infection has occurred by sexual contact and blood transfusion or bone marrow transplantation from infected human donors. Although infections occur throughout the year, the peak incidence occurs in the spring when livestock birthing and manure spreading are most common. When isolated from animals or humans, Q Fever is a nationally reportable disease in the United States.

Q fever is endemic throughout the United States with a national seroprevalence of 3%. The incubation period for acute infection is approximately 20 days (range 14 to 39). Acute Q fever usually causes a self-limited febrile illness. Less often it results in pneumonia or hepatitis. Most cases of pneumonia are mild with a non-productive cough and fever, but some patients develop acute respiratory distress and pleural effusion. Q fever hepatitis typically has a granulomatous pathology.

Chronic Q fever is defined as infection lasting for more than six months. It occurs in 1 to 5 percent of patients infected with C. burnetii and may develop insidiously over a long duration. During this time, C. burnetii multiplies in macrophages and produces a prolonged rickettsemia. The immune system responds by producing high concentrations of antibodies and immune complexes, which damage tissues and organs. The organ most commonly affected in chronic disease is the heart, followed by the arteries, bones, and liver. Pregnant women, immuno-suppressed persons, and patients with a preexisting heart-valve defect are at greatest risk for chronic Q fever. Clinical manifestations include endocarditis involving defective or prosthetic valves, infection of vascular grafts, hepatitis, osteoarthritis and osteomyelitis.

Laboratory findings during acute Q fever are nonspecific. Leukocyte count is usually normal but may be elevated in 25 percent of cases. Thrombocytopenia is noted in 25 percent of cases. Liver enzymes are elevated in as many as 85 percent of cases. Immune activation causes cross reactivity with many serological tests including antimitochondrial antibodies, anti-smooth muscle antibodies anticardiolipin antibodies, antineutrophil cytoplasmic antibodies HIV antibody, brucellosis and rapid plasma reagin.

Definitive diagnosis of Q fever is made by serologic testing and PCR. Seroconversion is usually detected 7 to 15 days after the onset of clinical symptoms. Approximately 90 percent of patients have detectable antibodies by the third week. An immunofluorescence assay (IFA) is the current reference method for the serodiagnosis of Q fever. IFA titers usually reach their maximum levels four to eight weeks after the onset of acute Q fever and then decrease gradually over the following 12 months.

An important characteristic of C. burnetii is its antigenic variation, called phase variation. When initially isolated from animals or humans, C. burnetii express phase I antigen. Phase 1 is the virulent highly infectious form. After subculturing in embyronated eggs or cell cultures, the lipopolysacchride capsule of C. burnetii undergoes modification resulting in an antigenic shift to the phase II avirulent form This antigenic shift can be measured and forms the basis for differentiating acute from chronic Q fever. Active Q fever infections are characterized by a fourfold increase in serum IgG titers between acute and convalescent samples and/or the presence of IgM antibodies directed against phase 2 organisms. In chronic Q fever the IgG and/or IgM response is most often directed against phase1 organisms, resulting in phase 1 titers that are greater than phase 2 titers. Reference values for IgG and IgM antibodies against phase 1 and 2 antigens is <1:16. Three percent of healthy adults in the U.S. have detectable antibodies to C. burnetii. Therefore, a single serum sample is less useful for the diagnosis of acute Q fever than paired acute and convalescent serum samples collected 3–6 weeks apart.

PCR assays targeting different genes have been developed for Q fever. To diagnose acute infection, PCR should be ordered within the first 2 weeks of symptom onset and within 24–48 hours after antibiotic administration. PCR results are positive in almost all patients with early acute Q fever before the antibody response develops. Either whole blood or serum can be tested.

PCR is also recommended for patients with suspected chronic Q fever because they can experience a recurrent bacteremia similar to early acute infection. PCR positivity rates have ranged from 33 to 64% of patients with Q fever endocarditis.

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