Abstract

Rickettsia typhi, the agent of murine (endemic) typhus, is a small obligately intracellular gram-negative coccobacillus. The disease is endemic in tropical and subtropical seaboard regions throughout the world. Rats serve as the primary reservoir, and the rat flea (Xenopsylla cheopis) is the principal vector. In the United States, most cases are reported in southern California and Texas, where an alternate cycle of transmission involves opossums as the presumed reservoir and the cat flea (Ctenocephalides felis) as the vector. Human infection occurs when R. typhi–infected flea feces are inoculated into a flea bite wound or onto mucous membranes. Frequent symptoms include fever, headache, malaise, myalgias, nausea, and vomiting. Rash occurs in about half of patients, is usually macular, and typically occurs on the trunk but may also occur on the extremities. Frequent laboratory abnormalities include elevations in serum hepatic transaminases, thrombocytopenia, hypoproteinemia, hypoalbuminemia, and hyponatremia. Although patients are often ill enough to be hospitalized, the clinical course is usually uncomplicated. Occasionally, central nervous system abnormalities, renal insufficiency, respiratory failure, and death occur. Early diagnosis is based on clinical suspicion and epidemiology. Serology is the mainstay of diagnosis, with the indirect immunofluorescence assay being the test of choice. Antirickettsial antibodies are seldom present during early illness. Therefore a serologic diagnosis is generally retrospective and relies on seroconversion or a fourfold increase in antibody titer between acute- and convalescent-phase sera. Doxycycline, 100 mg twice daily for 7 days, is the treatment of choice. Chloramphenicol, where available, and fluoroquinolones are alternatives.

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