Rickettsiae are small pleomorphic gram-negative bacilli that are obligate intracellular parasites. They can in general survive only briefly outside the host; the exception, Coxiella burnetii, which causes Q fever, is a hearty organism that resists desiccation, heat, and sunlight and is transmitted mainly by airborne spread.¹ Rickettsial organisms have been broadly divided into spotted fever and typhus groups based on antigenic similarities and intracellular growth characteristics.¹ An overview of common rickettsial diseases and organisms is given in Table 1.

Rickettsial organisms are maintained in nature through a cycle involving reservoirs in mammals and vectors in insects. Humans are incidental hosts, and in general, humans are not useful in propagating the organism in nature.¹ Rampant outbreaks of potentially fatal disease, such as typhus or trench fever in humans, have occurred when people are crowded together in conditions of poor hygiene. Most rickettsial disease in the United States today occurs when humans have incidental contact with insect vectors in the organism life cycle.

Rickettsial organisms exist in a classical commensal fashion with their insect vectors. One exception is Rickettsia prowazekii, which causes murine typhus; this organism causes the death of its vector, the human body louse, in 1 to 3 weeks. The mammalian reservoirs rickettsiae are many and varied but are generally composed of small animals and livestock.

Rickettsial diseases endemic in the United States today are RMSF (tick), Q fever (tick), and murine typhus (flea).² Sporadically occurring in the United States still are rickettsialpox (mite) and epidemic typhus (body louse). Brill-Zinsser disease (recrudescent louseborne typhus) in immigrants who lived in Europe during World War II (Table 1) was endemic for a time but has effectively been eliminated.

The findings of fever, headache, fatigue, lymphandenopahty, and rash in the appropriate season (usually spring and summer) should alert the physician to consider rickettsial etiology. A careful clinical history with attention to possible vector exposure (e.g., camping, hiking, tick or flea exposure) can identify patients who may be at risk. The pathogenesis of rickettsial disease is vasculitis that manifests as a cutaneous rash caused by the proliferation of organisms on the endothelial lining of small arteries, veins, and capillaries; Q fever, however, produces no rash.¹ Rickettsial organisms can be found in the cytoplasm of vascular endothelial cells in histopathologic biopsy specimens in most cases; one exception is that RMSF organisms can be found in the nuclei of infected cells. Intracellular organisms transmitted by tick bites can also be identified by immunofluorescence, which aids in diagnosis by using skin biopsy specimens during the skin rash stage. The most common confirmatory test is measurement of serum antibody titers (see section on Laboratory Diagnosis).