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Rocky Mountain Spotted Fever (RMSF)(Spotted Fever; Tick Fever; Tick Typhus)

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Rocky Mountain spotted fever is caused by Rickettsia rickettsii and transmitted by ixodid ticks. Symptoms are high fever, severe headache, and rash.

Epidemiology

Rocky Mountain spotted fever (RMSF) is limited to the Western Hemisphere. Initially recognized in the Rocky Mountain states, it occurs in practically all of the US, especially the Atlantic states, and throughout Central and South America. In humans, infection occurs mainly from March to September, when adult ticks are active and people are most likely to be in tick-infested areas. In southern states, sporadic cases occur throughout the year. The incidence is highest in children < 15 yr and in people who frequent tick-infested areas for work or recreation.

Hard-shelled ticks (family Ixodidae) harbor R. rickettsii, and infected females transmit the agent to their progeny. These ticks are the natural reservoirs. Dermacentor andersoni (wood tick) is the principal vector in the western US. D. variabilis (dog tick) is the vector in the eastern and southern US. RMSF is probably not transmitted directly from person to person.

Pathophysiology

Small blood vessels are the sites of the characteristic pathologic lesions. Rickettsiae propagate within damaged endothelial cells, and vessels may become blocked by thrombi, producing vasculitis in the skin, subcutaneous tissues, CNS, lungs, heart, kidneys, liver, and spleen. Disseminated intravascular coagulation often occurs in severely ill patients (see Coagulation Disorders: Disseminated Intravascular Coagulation (DIC)).

Symptoms and Signs

The incubation period averages 7 days but varies from 3 to 12 days; the shorter the incubation period, the more severe the infection. Onset is abrupt, with severe headache, chills, prostration, and muscular pains. Fever reaches 39.5 to 40° C within several days and remains high (for 15 to 20 days in severe cases), although morning remissions may occur. Between the 1st and 6th day of fever, most patients develop a rash on the wrists, ankles, palms, soles, and forearms that rapidly extends to the neck, face, axillae, buttocks, and trunk. Initially macular and pink, it becomes maculopapular and darker. In about 4 days, the lesions become petechial and may coalesce to form large hemorrhagic areas that later ulcerate.

Neurologic symptoms include headache, restlessness, insomnia, delirium, and coma, all indicative of encephalitis. Hypotension develops in severe cases. Hepatomegaly may be present, but jaundice is infrequent. Nausea and vomiting are common. Localized pneumonitis may occur. Untreated patients may develop pneumonia, tissue necrosis, and circulatory failure, sometimes with brain and heart damage. Cardiac arrest with sudden death occasionally occurs in fulminant cases.

Diagnosis

Clinicians should suspect RMSF in any seriously ill patient who lives in or near a wooded area anywhere in the Western Hemisphere and has unexplained fever, headache, and prostration, with or without a history of tick contact. A history of tick bite is elicited in about 70% of patients. For specifics of diagnosis, see Rickettsiae and Related Organisms: Diagnosis.

Treatment

Starting antibiotics early significantly reduces mortality, from about 20 to 5%, and prevents most complications.If patients who have been in an endemic area have a tick bite but no clinical signs, antibiotics should not be given immediately.

If fever, headache, and malaise occur with or without a rash, antibiotics should be started promptly. Primary treatment is doxycycline Some Trade Names
PERIOSTAT
VIBRAMYCIN
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200 mg po once followed by 100 mg bid until the patient improves and has been afebrile for 24 to 48 h but continued for at least 7 days. Chloramphenicol Some Trade Names
CHLOROMYCETIN
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500 mg po or IV qid for 7 days is 2nd-line treatment.

No effective vaccine is available. Measures can be taken to prevent tick bites (see Sidebar 1: Rickettsiae and Related Organisms: Tick Bite PreventionSidebars).

Last full review/revision November 2007 by William A. Petri, Jr., MD, PhD

Content last modified November 2007

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