Babesia

  • Current Advice on Parasite Control:

    Vector-Borne Diseases - Babesia

    Last reviewed and edited Mar 2013

  • Species

    Canine

    Babesia canis vogeli
    Babesia gibsoni
    Babesia conradae

    Babesia infections in domestic dogs include larger piroplasms collectively described as B. canis and smaller piroplasma that are often described as B. gibsoni. Three B. canis subspecies, B. canis canis, B. canis vogeli and B. canis rossi, are differentiated based on pathology, antigenic properties, tick vectors and genetic characterization, and these parasites are increasingly recognized as distinct species in current literature. Babesia canis vogeli (or B. vogeli) is enzootic to the United States.

    Feline

    Babesia spp. infection has not been reported in domestic cats in the United States.

  • Overview of Life Cycle

    • Dogs become infected with Babesia spp. when they are inoculated with sporozoites in tick saliva. After inoculation, Babesia sporozoites invade erythrocytes where they multiply asexually by binary fission. The resultant merozoites rupture the red blood cell and go on to invade additional erythrocytes. The genus Babesia is distinguished from other hemosporidian genera by the absence of an exoerythrocytic stage in the vertebrate host.
    • Following ingestion by the tick, Babesia undergoes sexual reproduction (gamogony) followed by asexual reproduction (often schizogony and always sporogony), resulting in numerous sporozoites (in the tick salivary glands) that are infective to vertebrate hosts.
    • Babesia canis is thought to cycle primarily between domestic dogs and Rhipicephalus sanguineus, the brown dog tick. However, Dermacentor variabilis, the American dog tick, is also a competent vector.
    • Babesia gibsoni is also transmitted by R. sanguineus; although this life cycle has not yet been confirmed for strains of B. gibsoni in the United States.
    • Iatrogenic transmission is also possible through blood transfusion or blood-contaminated fomites.
    • Fighting between dogs is a likely mode of mechanical transmission of B. gibsoni that may account, in part, for the relatively high prevalence of infection reported among American Staffordshire and American pit bull terriers.
  • Stages

    • Piroplasms of Babesia spp. can be found within erythrocytesBabesia_Canis_1.png on stained blood smears.
    • Babesia spp. in dogs may be differentiated to some degree by their size and general morphology. Babesia canis vogeli piroplasms (trophozoites) are larger and often found in pairs, whereas those of B. gibsoni and B. conradae and several emerging Babesia spp. are small, pleomorphic, ring-shaped organisms.
  • Disease

    • Dogs with babesiosis often present with moderate to severe hemolytic anemia and clinical illness characterized by fever, anorexia, depression, pallor, splenomegaly, and a bounding pulse. However, disease is considered uncommon in healthy, spleen-intact adult dogs in the United States.
    • In general, disease is less severe with B. canis vogeli infection than with B. gibsoni infection.
    • Coinfection with Babesia spp. and other tick-borne pathogens has been documented and when present, may complicate interpretation of the clinical presentation and diagnostic assays.
  • Incidence and Prevalence

    • Canine infection with Babesia spp.is common throughout the world. Infection is more common in areas where tick infestation pressure is high and when routine acaricide use is not practiced. Although B. canis (vogeli) is perhaps the most well known, infection with B. gibsoni occurs more commonly in some areas and in some canine breeds in the United States.
    • Babesia spp. are reported from throughout the United States, a distribution that follows that of the vector tick R. sanguineus. However, infections are more commonly seen in southern states.
    • Infection with B. gibsoni occurs more commonly in certain breeds, such as American Staffordshire and American pit bull terriers, a phenomenon that is thought to be attributable to direct dog-to-dog mechanical transmission via bite wounds.
  • Host Associations and Transmission Between Hosts

    • Babesia spp. are transmitted to dogs via tick feeding. Ticks are not able to transmit infection immediately upon first attachment to a host; they require a period of approximately 24 to 48 hours of initial feeding before organisms are able to pass across the salivary glands and into the vertebrate host. However, tick removal should not be delayed regardless of the average time to transmission of these parasites.
    • Rhipicephalus sanguineus and D. variabilis are the most common known arthropod vectors of etiologic agents of canine babesiosis in the United States.
    • Direct transmission of Babesia spp. from an infected to a naïve animal can also occur following blood transfusion or iatrogenic inoculation with contaminated needles or surgical instruments. Direct dog-to-dog transmission via dog bites is thought to be an important means of transmission for B. gibsoni and may account for the apparently high prevalence of this organism in American Staffordshire and American pit bull terriers.
  • Prepatent Period and Environmental Factors

    • Sporozoites enter the blood during tick feeding. Merozoites become evident within erythrocytes on blood smears in approximately 1 to 3 weeks.
    • Although clinical disease may resolve, Babesia infections are often persistent in dogs. Even after appropriate therapy, infection can persist for the life of the dog. Splenectomy of persistently infected dogs could result in recrudescence of latent infections and relapse of the clinical disease. The use of Babesia-positive dogs as blood donors is discouraged.
    • Infection with additional strains and/or species of Babesia also may occur when tick exposure or bite wound transmission continues.
  • Site of Infection and Pathogenesis

    • Ticks inoculate sporozoites of Babesia spp. directly into the bite wound. Organisms invade circulating erythrocytes and begin multiplying asexually.
    • Rupture of red blood cells during asexual replication leads to intravascular hemolysis and hemolytic anemia. Immune-mediated clearance of parasitized erythrocytes contributes to the anemia.
    • Thrombocytopenia, hypoalbuminemia, and hyperglobulinemia also occur.
    • Splenectomy can exacerbate both parasitemia and clinical disease from infection with Babesia spp.
    • Similarly, splenectomy and immunosuppression (e.g., via corticosteroids) can result in recrudescent parasitemia and relapse clinical disease from latent Babesia.
  • Diagnosis

    • Definitive diagnosis of Babesia spp. infection relies on identification of piroplasms in erythrocytes on stained blood smears. Although organisms may be numerous in blood smears from animals with acute babesiosis, parasitemias are often low, and organisms may rarely be found in samples collected from dogs with chronic babesiosis or asymptomatic carriers.
    • Serology may be helpful in identifying the presence of antibodies to B. canis, which cross-react with those to B. gibsoni, thereby allowing indirect detection of previous infection with either organism. Indirect fluorescent antibody (IFA) assays to determine IgM and IgG titers to B. canis are available through diagnostic laboratories.
    • Particularly during primary infections, dogs with acute babesiosis may be serologically negative, necessitating repeat testing using convalescent sera.
    • Molecular diagnosis of Babesia spp. infection in dogs and cats via polymerase chain reaction (PCR) of whole blood has become readily available. However, such results should be interpreted with caution because the techniques used in different diagnostic laboratories vary. Amplification of related organisms by nonspecific primers can result in false-positive reactions. Conversely, apparent false-negatives may occur if extraction procedures fail to remove PCR inhibitors present in a blood sample or if the level of circulating parasitemia falls below the level of assay detection due to a normal decrease in circulating organisms or temporary suppression of infection following treatment. To maximize the utility of molecular diagnostics, blood samples should be collected early in the course of clinical disease, preferably before the initiation of chemotherapy, and these samples should be submitted to experienced diagnostic laboratories with stringent quality control measures in place.
  • Treatment

    • Dogs infected with B. canis vogeli usually respond to treatment with imidocarb diproprionate at a dose of 6 mg/kg IM administered twice at 14-day intervals. A higher dose administered once is recommended occasionally but can result in neurotoxicity.
    • Babesia gibsoni is considered more difficult to treat than B. canis vogeli. Recommended treatment protocols for B. gibsoni and B. conradae involve combining atovaquone (13 mg/kg PO q8h for 10 days) with azithromycin (10 mg/kg PO q 24 h for 10 days); imidocarb diproprionate is not considered effective for treating B. gibsoni.
    • Babesia spp. infections can also be treated with pentamidine isethionate (16 mg/kg IM q24h for 2 doses).
    • Treatment for babesiosis reduces parasitemia and supports resolution of clinical signs, but it is important to remember that the infection itself may not be eliminated. Dogs diagnosed with Babesia spp. should be considered permanent carriers of the infection.
  • Control and Prevention

    • Stringent adherence to routine application of effective acaricides is essential for preventing infection with Babesia spp.
    • Vaccines are not available to prevent Babesia spp. infection of pets in North America.
    • Babesia spp. are primarily transmitted by R. sanguineus, a tick that can survive indoors and thus year-round as established long-term infestations in homes and kennels. Although more common in warmer months and milder climates, when/where outdoor survival of R. sanguineus is optimal, this tick can occur anywhere there are dogs. CAPC recommends that all pets be maintained on tick-control products year-round.
    • Attached ticks found on pets should be removed promptly to prevent transmission of any pathogens they may harbor. To avoid potential exposure to zoonotic pathogens and accidental inoculation of agents into the pet during the removal process, ticks should be retracted using forceps or a commercial tick-removal device, and care should be taken to avoid contact with tick contents, ideally by wearing gloves. Careful attention to handwashing following tick removal is also recommended.
    • Blood donors should be screened for infection with Babesia spp. by serology, PCR, and blood smear, and any dogs testing positive excluded.
    • Splenectomy or corticosteroid treatments of Babesia-positive dogs should be avoided as much as possible.
    • Discourage dog fighting to prevent direct dog-to-dog transmission of B. gibsoni.
  • Public Health Considerations

    • Babesia canis and B. gibsoni are not known to infect people.
    • People can become infected with Babesia microti and other related Babesia spp. that normally infect rodents. In North America, Ixodes spp. ticks are the only known vectors of human infections with zoonotic Babesia spp.; dogs are not implicated in the maintenance or transmission of these zoonotic infections.
  • Selected References

    • Uilenberg, 2006. Babesia--a historical overview. Vet Parasitol. 138(1-2):3-10. PubMed PMID: 16513280.
    • Irwin, 2010. Canine babesiosis. Vet Clin North Am Small Anim Pract. 40(6):1141-56. PubMed PMID: 20933141.
    • Sikorski et al., 2010. Babesiosis caused by a large Babesia species in 7 immunocompromised dogs. J Vet Intern Med. 24(1):127-31. PubMed PMID: 20002547.
    • Di Cicco et al., 2012. Re-emergence of Babesia conradae and effective treatment of infected dogs with atovaquone and azithromycin. Vet Parasitol. 8;187(1-2):23-7. PubMed PMID: 22305297.