Rocky Mountain Spotted Fever

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Rocky Mountain spotted fever is a rickettsial disease caused by Rickettsia rickettsi, a small intracellular parasite. Infection is acquired by a tick bite. The majority of infections are acquired in the south Atlantic coastal and the western and southern central states with the highest incidence in Virginia, North Carolina, South Carolina, Oklahoma, and Tennessee. The disease typically occurs during spring and summer. Fever, rash, and a history of exposure to ticks is the classic triad of Rocky Mountain spotted fever. The illness usually begins 5 to 7 days after the tick bite. The majority of patients have fever, severe frontal headache, malaise, myalgia, and vomiting. An altered level of consciousness and meningismus may develop during the course of the illness in addition to abdominal pain, hepatosplenomegaly, respiratory failure, renal dysfunction, and myocarditis.

The classic rash of Rocky Mountain spotted fever first appears as macules on the wrists and ankles and subsequently spreads to involve the trunk, face, palms, and soles. The rash appears 1 to 15 days after the onset of the illness. [w] The rash is initially a diffuse erythematous maculopapular rash that blanches with pressure. It progresses to a petechial rash, then to a purpuric rash, and if untreated, to skin necrosis or gangrene. The rash begins on the wrists and ankles and then spreads distally and proximally within a few hours. Ten percent of patients do not have a rash (spotless Rocky Mountain spotted fever). Neurological manifestations of Rocky Mountain spotted fever include severe bifrontal headache that is unresponsive to common analgesics, delirium, confusion, seizures, coma, hyperreflexia, spastic paraparesis or quadraparesis, facial diplegia, nystagmus, and/or ataxia. Stupor and coma occur in approximately 25 percent of patients and are associated with a poorer prognosis than those cases without signs of encephalitis. Laboratory abnormalities in patients with Rocky Mountain spotted fever include thrombocytopenia, hyponatremia, and elevated liver enzyme abnormalities. CSF abnormalities include a mild (rarely more than 100 cells/ mm 3 ) lymphocytic pleocytosis and an elevated protein concentration. In the acute stage, the diagnosis of Rocky Mountain spotted fever can be made by skin biopsy with




Duration of Therapy


25 to 50 mg/kg/d (oral dose) in 4 divided doses

7 to 10 days


500 mg (oral dose) 4 times daily

7 to 10 days


100 mg (oral dose) 2 times daily

7 to 10 days

Chloramphenicol (for children under 8 years of age)

50 mg/kg/d IV in 4 divided doses

7 to 10 days

*Not recommended for children under the age of 8 years to avoid staining of the teeth.

Reproduced with permission from Pourmand, Roos KL: Seasonal (spring-summer) encephalitides. In Roos KL (ed): Central Nervous System Infectious Diseases and Therapy. New York, Marcel Dekker, 1997, pp 193-211.

the demonstration of rickettsiae in the endothelial cells of blood vessels by immunofluorescence. Serological tests are useful for the confirmation of the diagnosis and include an indirect immunofluorescent antibody assay (IFA), an indirect hemagglutination assay (IHA), latex agglutination (LA), and complement fixation (CF). According to the Centers for Disease Control and Prevention, diagnostic titers for Rocky Mountain spotted fever include a titer of 1:64 for IFA, 1:16 for CF, and a four-fold increase between acute and convalescent sera for LA and IHA. The PCR is also under development for the diagnosis of this disease. The treatment of Rocky Mountain spotted fever is outlined in Table ...42-6 [109]

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