Canis ISSN: 2398-2942

Rickettsia rickettsii

Contributor(s): Gad Baneth, Leah Cohn

Introduction

Classification

Taxonomy

  • Order: Rickettsiales; Family: Rickettsiaceae; Tribe: Rickettsieae.
  • One of at least 18 members of the Spotted Fever Group organisms within the genus Rickettsia.

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Clinical Effects

Epidemiology

Habitat

  • Even in endemic areas, only 1-3% of susceptible ticks are infected with R rickettsii.
  • Infections often occur in limited geographic pockets within endemic areas.
  • Vector for transmission in the Eastern and Central USA is Dermacentor variabilis (American dog tick).
  • Vectors for transmission in the western USA include both D variabilis (American dog tick) Rocky Mountain Spotted Fever: American dog tick and D andersonii (American wood tick/Rocky Mountain wood tick) Rocky Mountain Spotted Fever: Rocky Mountain wood tick.

Lifecycle

  • Ticks can become infected during nymphal and larval stages while feeding on small mammals.
  • Venereal transmission between ticks can occur at time of mating.
  • Infection of ticks with R rickettsii is transtadial as well as transovarial. Infected ticks may remain infected during every stage of life.
  • Transovarial transmission from female tick to her offspring is very efficient.
  • Small mammals and ticks themselves serve as reservoirs of infection.
  • Dogs do not serve as reservoirs of infection because of short duration, low level rickettsemia in this species.

Transmission

  • R rickettsii can not be transmitted directly between dogs.
  • R rickettsii is transmitted to dogs via salivary secretions during feeding of infected ticks.
  • From 5 to 20 hours of feeding is required for reactivation of the organism prior to transmission.

Pathological effects

  • See serum protein electrophoresis Serum protein electrophoresis.
  • Serum IgM response becomes detectable at approximately 9 days post infection, peaks by day 20 and remains detectable for 2 to 3 months.
  • Serum IgG response becomes detectable at approximately 25 days post infection, peaks by day 42 and gradually declines over 6 to 9 months.
  • Immunological response to R rickettsii can result in elimination of infection.
  • Challenge inoculation following experimental exposure failed to induce disease even 3 years after disease recovery.
  • R rickettsii is inoculated through salivary secretions of an infected tick during feeding.
  • After attachment and entry into endothelial cells, organism proliferates within cell cytosol and nuclei.
  • Infection is spread centripetally from cell to cell in microcirculation of skin and organs.
  • Intracellular endothelial infection results in central feature of the disease Rocky Mountain Spotted Fever Rocky Mountain Spotted Fever (RMSF) ; lymphocytic vasculitis.
  • Disease pathology and complications result from vasculitis of microcirculation in a variety of tissues and organs.

Other Host Effects

  • Fever results from both endogenous (especially inflammatory cytokines) and exogenous (bacterial cell wall components) pyrogens.
  • Vasculitis leads to clinical manifestations including petechial hemorrhage, central nervous system signs, respiratory and gastrointestinal signs, peripheral edema and dermal necrosis.
  • Vasculitis leads to clinicopathologic manifestations including thrombocytopenia, hypoalbuminemia Hypoproteinemia , and hyponatremia.

Control

Control via animal

  • Prevention of tick attachment prevents disease transmission.
  • Antimicrobial therapy Therapeutics: antimicrobial drug effective when administered early in disease course.
  • Dogs not a significant reservoir of infection for other animals.

Control via chemotherapies

Control via environment

  • Control accomplished by preventing attachment and feeding of ticks.

Vaccination

  • No commercial vaccine available.

Diagnosis

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Further Reading

Publications

Refereed papers

  • Recent references from VetMedResource and PubMed.
  • Gasser A M, Birkenheuer A J & Breitschwerdt E B (2001) Canine Rocky Mountain spotted fever: a retrospective study of 30 casesJ Am Anim Hosp Assoc 37(1), 41-48.
  • Hackstadt T (1996) The biology of RickettsiaeInfect Agents & Dis 5(3), 127-143.
  • Sexton D J, Kanj S S, Wilson K et al (1994) The use of a polymerase chain reaction as a diagnostic test for Rocky Mountain spotted feverAm J Trop Med & Hygiene 50(1), 59-63.
  • Breitschwerdt E B, Levy M G, Davidson M G et al (1990) Kinetics of IgM and IgG responses to experimental and naturally acquired Rickettsia rickettsii infection in dogsAm J Vet Res 51(8), 1312-1316.
  • 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 Mountian spotted feverJ Infect Dis 135(6), 911-917.
  • Keenan K P, Buhles W C Jr, Huxsoll D L et al (1977) Studies on the pathogenesis of Rickettsia rickettsii in the dog: clinical and clinicopathologic changes of experimental infectionAm J Vet Res 38(6), 851-856.

Other sources of information

  • Centers for Disease Control, National Center for Infectious diseases, 1600 Clifton Road NE, MS G-13, Atlanta, Georgia 30333, USA. www.cdc.gov/ncidod/dvrd/rmsf

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