Rocky Mountain spotted fever (RMSF) is a disease of humans and dogs that is caused by Rickettsia rickettsii. R rickettsii and closely related members of the spotted fever group of rickettsiae are considered endemic throughout much of North, South, and Central America. These pathogens are transmitted primarily through the bites of infected ticks. The ability of genetically similar rickettsial organisms, such as R parkerii, to cause clinically similar disease in dogs is unknown. Because of their susceptibility to R rickettsii and relatively higher rates of tick exposure, dogs may serve as excellent sentinels of risk for R rickettsii infection in humans. Clusters of disease are frequently reported in defined geographic areas, and temporally associated infections may be seen in both dogs and their owners.
In the USA, Dermacentor variabilis (the American dog tick) and D andersoni (the Rocky Mountain wood tick) are considered the primary vectors for R rickettsii. The organism has also been isolated from Rhipicephalus sanguineus ticks, which appears to be the primary vector in some focal areas of Arizona and may also play an as-yet unappreciated role in outbreaks elsewhere in the USA. R sanguineus ticks are associated with transmission of R rickettsii in Central America. The pathogen is acquired by larval and nymph stages of ticks while feeding on infected vertebrate hosts, and is also passed from female ticks to progeny through transovarial transmission. An estimated 1–3% of Dermacentor spp of ticks carry R rickettsii, even in areas considered highly endemic.
Seroprevalence in dogs from endemic areas ranges from 4.3–77%, but these values do not accurately reflect infection rates due to the detection of cross-reacting antibodies to other genetically similar rickettsiae. RMSF transmission through blood transfusion has been documented in a single human case, and should be considered when selecting canine blood donors. Direct transmission from dogs to humans has not been reported, although human infection may occur following contact of abraded skin or conjunctiva with tick hemolymph or excreta during removal of engorged ticks from pets.
Dogs are highly susceptible to clinical infection with R rickettsii; in contrast, RMSF infection is rarely diagnosed in cats. Early signs in dogs may include fever (up to 105°F [40.5°C]), anorexia, lymphadenopathy, polyarthritis, coughing or dyspnea, abdominal pain, vomiting and diarrhea, and edema of the face or extremities. Petechial hemorrhages of the conjunctiva and oral mucosa may be observed in severe cases. Focal retinal hemorrhage may be observed during the early course of disease. Neurologic manifestations such as altered mental states, vestibular dysfunction, and paraspinal hyperesthesia may occur.
Thrombocytopenia is common. Leukopenia develops during the early stages of infection and, in untreated cases, is followed by progressive leukocytosis. Serum biochemical abnormalities may include hypoproteinemia, hypoalbuminemia, azotemia, hyponatremia, hypocalcemia, and increased liver enzyme activities. Case fatality rates of ∼1–10% are expected.
Vascular endothelial damage is due to direct cytopathic effects of the rickettsiae. Severity of the necrotizing vasculitis can be directly correlated to the infective dose. Vascular endothelial damage and thrombocytopenia contribute to development of petechiae and ecchymoses. Necrosis of the extremities (acryl gangrene) or disseminated intravascular coagulation can develop in severely affected dogs.
Indirect fluorescent antibody titer is preferred for serologic testing. However, because of the high incidence of cross-reacting antibodies to a variety of nonpathogenic spotted fever group rickettsiae, as well as longterm persistence of antibodies following acute RMSF infection, demonstration of a 4-fold rise in titer should be documented in conjunction with a compatible clinical syndrome. Differential diagnoses include other causes of fever of unknown origin. The therapeutic response is usually dramatic, as it is in other canine rickettsial diseases. Animals with neurologic dysfunction may have residual deficits. Immunity appears to be lifelong after natural infection; therefore, recurrent episodes should not be attributed to RMSF.
Antibiotic treatment should be administered based on clinical suspicion without waiting for results of serologic tests, because delayed administration of antibiotics may result in higher rates of severe or fatal outcome. Doxycycline should be administered at a dosage of 5–10 mg/kg, PO or IV, sid for 10–21 days. Tetracycline at 22 mg/kg, PO, tid for 2 wk is also effective. Supportive care for dehydration and hemorrhagic diathesis may be necessary. Due to alterations in vascular integrity, conservative rates of fluid administration are advised. Precautions should be taken for the safe removal and control of ticks.
Last full review/revision March 2012 by Jennifer H. McQuiston, DVM, MS