ISSN 2398-2969      

Rocky Mountain Spotted Fever (RMSF)


Gad Baneth

Leah Cohn

Synonym(s): Rickettsia rickettsii infection


  • Cause: Rickettsia rickettsii, an intracellular bacterial pathogen.
  • Signs: acute, febrile vasculitis.
  • Diagnosis: presumptive diagnosis confirmed by serology, PCR or immunohistochemistry.
  • Treatment: doxycycline, chloramphenicol or enrofloxacin.
  • Prognosis: fair to good with rapid anti-microbial therapy, but can be fatal if treatment delayed.
  • Interpretation: RMSF is an acute, febrile vasculitis. Severity of disease varies from inapparent or mild illness to a rapidly fatal disease. This zoonotic disease requires a tick vector for transmission and responds rapidly to early anti-microbial intervention.



  • Rickettsia rickettsii, intracellular pathogen in Rickettsiacae family.
  • Transmission of R rickettsii is dependent on tick vector.
  • Common tick vectors in the USA include Dermacentor variabilis Dermacentor variabilis Rocky Mountain Spotted Fever: American dog tick and D andersoni Dermacentor andersoni Rocky Mountain Spotted Fever: Rocky Mountain wood tick.
  • R rickettsii is the most pathogenic of the large group of Spotted Fever Group rickettsial organisms. Canine infection with other Spotted Fever Group organisms can cause serologic cross reactivity with R rickettsii, but is unlikely to result in disease.

Predisposing factors


  • Primarily identified in dogs with a history of tick exposure.
  • Although a tick vector is required for transmission, absence of visible ticks should not be used to rule out a diagnosis of RMSF.
  • Because of greater exposure to tick vectors, dogs that spend more time outdoors are more likely to be infected than indoor dogs.
  • Infection is most likely in the spring and summer months while tick vectors are active.



  • R rickettsii is transmitted from the tick to dog after the tick has fed for several hours.
  • Organism is endotheliotropic and results in damage to vascular endothelium.
  • Vasculitis is the major pathologic lesion responsible for both clinical disease signs and clinicopathologic abnormalities.
  • Disease presentation is multi-systemic and severity of each manifestation depends on extent of vascular damage in a given tissue.
  • Severity of disease manifestations depends in large part on number of infecting organisms, but is also dependent on differences in virulence between strains and on host factors including breed and previous exposure to rickettsial organisms.


  • R rickettsii is injected with salivary secretions of infected tick and quickly gains entry to host circulation.
  • The organisms replicates inside host endothelial cells.
  • Endothelium of the pre-capillary arterioles and post-capillary venules are particularly susceptible.
  • Thrombosis, hemorrhage or a combination may occur as a result of vasculitis in any given tissue.
  • Vasculitis resulting from disruption of damaged endothelial cells is underlying cause of clinical and laboratory signs attributable to RMSF.
  • Immunity to infection can eliminate infection and provide long-lasting protection from re-infection.


  • R rickettsii is not competent for transmission until reactivated by feeding of vector tick. Reactivation requires from 5 to 20 hours of tick attachment.
  • Disease manifestations develop within 3 to 5 days of infection.
  • Rickettsemia and febrile illness may persist up to two weeks.
  • Animals may die during the course of rickettsemia.
  • Anti-microbial therapy Therapeutics: antimicrobial drug produces a rapid halt to rickettsemia.
  • Rickettsemia may be terminated by immunologic response to infection.
  • Chronic infections do not occur.
  • Recovery from infection depends on severity of disease. Complete recovery from mild to moderate disease is rapid. Parenchymal organ damage or dermal necrosis prolongs recovery.
  • Post-infection immunity is long lasting and can be permanent.


  • Infection not contagious between dogs; requires tick vector for transmission.
  • Dogs not a reservoir for infection due to short duration of rickettsemia and limited degree of rickettsemia in species.
  • In nature, R rickettsii cycles between ticks and small mammals, especially rodents.
  • Even in endemic areas, only a very small percentage of susceptible ticks are infected.
  • R rickettsii can be passed transtadially in the tick vector (egg, larvae, nymph, and adult). Every stage except for the egg must feed prior to the next stage of development.
  • Infected females pass infection on to their offspring. Transovarial transmission is more efficient than transtadial transmission.
  • Venereal transmission between ticks is also possible.
  • Infection can be passed on to mammals by larvae, nymphs or adult ticks during feeding.
  • Because small mammals do not travel widely and due to efficient transovarial transmission, infections tend to occur in small geographic pockets within endemic regions.
  • Multiple dogs within a neighborhood may be infected because they live in same small geographic pocket with infected ticks.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Gasser A M, Birkenheuer A J & Breitschwerdt E B (2001) Canine Rocky Mountain Spotted fever: a retrospective study of 30 cases. J Am Anim Hosp Assoc 37 (1), 41-48 PubMed.
  • Abramson J S & Givner L B (1999) Rocky mountain spotted fever. Pediat Infect Dis J 18 (6), 539-540 PubMed.
  • Breitschwerdt E B, Papich M G, Hegarty B C et al (1999) Efficacy of doxycycline, azithromycin, or trovafloxacin for treatment of experimental Rocky Mountain spotted fever in dogs. Antimicrob Agents & Chemoth 43 (4), 813-821 PubMed.
  • Drost W T, Berry C R, Breitschwerdt E B et al (1997) Thoracic radiographic findings in dogs infected with Rickettsia rickettsii. Vet Radiol & Ultrasound 38 (4), 260-266 PubMed.
  • Breitschwerdt E B, Davidson M G, Aucoin D P et al (1991) Efficacy of chloramphenicol, enrofloxacin, and tetracycline for treatment of experimental Rocky Mountain spotted fever in dogsAntimicrob Agents & Chemoth 35 (11), 2375-2381 PubMed.
  • Davidson M G, Breitschwerdt E B, Walker D H et al (1990) Vascular permeability and coagulation during Rickettsia rickettsii infection in dogs. Am J Vet Res 51 (1), 165-170 PubMed.
  • Davidson M G, Breitschwerdt E B, Nasisse M P et al (1989) Ocular manifestations of Rocky Mountain spotted fever in dogs. J Amer Vet Med Assoc 194 (6), 777-781 PubMed.
  • Davidson M G, Breitschwerdt E B, Walker D H et al (1989) Identification of rickettsiae in cutaneous biopsy specimens from dogs with experimental Rocky Mountain spotted fever. J Vet Int Med 3 (1), 8-11 PubMed.
  • Weiser I B & Greene C E (1989) Dermal necrosis associated with Rocky Mountain spotted fever in four dogs. J Amer Vet Med Assoc 195 (12), 1756-1758 PubMed.
  • Keenan K P, Buhles W C Jr, Huxsoll D L et al (1977) Pathogenesis of infection with Rickettsia rickettsii in the dog: a disease model for Rocky Mountain spotted fever. J Infect Dis 135 (6), 911-917 PubMed.

Other sources of information

  • Centers for Disease Control, National Center for Infectious diseases, 1600 Clifton Road NE, MS G-13, Atlanta, Georgia 30333, USA.

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