Toxoplasma spp

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Toxoplasma gondii oocysts under light microscopy[1]
Toxoplasma gondii tachyzoites[2]
Toxoplasma gondii, organizing cerebral abscess in a human

Toxoplasmosis is a common ampicomplexan zoonotic protozoa which is ubiquitous in nature and infects most mammals, including dogs.

Toxoplasma, one of the world's most successful parasites, infects approximately 5-20% of urban dogs[3] and 20% of rural and wild dogs worldwide[4].

The life cycle is relatively simple, with ingestion of oocysts, followed by proteolytic activation of sporozoites. These enter and multiply in intestinal epithelium and associated lymph nodes to form rapidly multiplying tachyzoites which then disseminate and form bradyzoites in the brain, lover, striated muscle and remain viable for the life of the host. Bradyzoites are indistinguishable from sporozoites except using periodic acid-Schiff's reagent. Definitive hosts are infected by ingesting bradyzoites in tissue or oocysts passed in the feces[5].

Species which are pathogenic to dogs include:

  • Toxoplasma gondii

The oocysts of this species are physically identical to Neospora caninum and Hammondia hammondi parasites, and can only be distinguished via PCR assays[6].

Dogs are normally infected with T. gondii by ingestion of tissue cysts in meat, but spread via semen[7] and transplacental transmission also occur[8][9], with tachyzoites isolated from the brain of pups born from infected bitches[10].

In adult dogs, T. gondii is usually nonpathogenic, and recrudescence is the primary concern in coexisting disease such as distemper, or immunocompromised dogs with immune-mediated disease, or receiving cyclosporin, cyclophosphamide or prednisolone. Furthermore, another special feature of this evolutionarily successful parasite is the fact that it usually causes asymptomatic infections and in most cases does not kill immunocompetent hosts. However, without sufficient therapy, reactivation of T. gondii in immunocompromised individuals frequently results in death of the host.

Symptoms are more common in younger dogs, where disseminated toxoplasmosis may present as acute fever, hepatitis, pneumonia and ulcerative dermatitis. Neurological diseases such as acute protozoal polyradiculoneuritis (as is observed with N. caninum)[11], myositis, hindlimb paresis, chorioretinitis[12], seizures and death have been reported.

Diagnosis is based on presenting clinical signs, fecal examination for oocysts (usually unreliable), ELISA detection of T. gondii antibodies in tissue samples[13], light microscopy identification of tachyzoites in CSF or other tissues and PCR assays for species identification.

A differential diagnosis in deaths associated with neonatal acute pup deaths would include canine herpesvirus and canine distemper virus[14]. Other protozoan parasites and some bacteria can cause similar symptoms and must be excluded as a possible cause, including Neospora caninum[15], Leishmania spp[16], Giardia spp and Brucella spp[17].

The recommended drug of choice in treatment is clindamycin (10 - 50 mg/kg orally for 2 - 4 weeks), with aggressive supportive therapy in acutely ill pups.

Dogs of any age with neurological signs have a more guarded prognosis.

References

  1. CDC
  2. Brain Bank
  3. Duan G et al(2012) Seroprevalence of Toxoplasma gondii infection in pet dogs in Kunming, Southwest China. Parasit Vectors 5:118
  4. Nguyen TT et al (2012) Seroprevalence of Toxoplasma gondii and Neospora caninum in dogs from Korea. Acta Parasitol 57(1):7-12
  5. Bowman, DD (2003) Georgi’s Parasitology for Veterinarians. St. Louis, MO: Saunders. pp 100-102
  6. Hill,m DE et al (2001) Specific detection of Neospora caninum oocysts in fecal samples from experimentally-infected dogs using the polymerase-chain reaction. J Parasitol 87:395
  7. Arantes TP et al (2009) Toxoplasma gondii: Evidence for the transmission by semen in dogs. Exp Parasitol 123(2):190-194
  8. Montoya, JG & Remington, JS (2008) Management of Toxoplasma gondii infection during pregnancy. Clin Infect Dis 47:554-566
  9. Dubey JP, Lappin MR. (2006) Toxoplasmosis and Neosporosis. In: Greene C, ed. Infectious Diseases of the Dog and Cat, 3rd ed. St. Louis, MO: Elsevier, pp 754-768
  10. Al-Qassab S et al (2009) Isolation of Toxoplasma gondii from the brain of a dog in Australia and its biological and molecular characterization. Vet Parasitol 164(2-4):335-339
  11. Holt N et al (2011) Seroprevalence of various infectious agents in dogs with suspected acute canine polyradiculoneuritis. J Vet Intern Med 25(2):261-266
  12. Plugge NF et al (2011) Occurrence of antibodies against Neospora caninum and/or Toxoplasma gondii in dogs with neurological signs. Rev Bras Parasitol Vet 20(3):202-206
  13. Hosseininejad M et al (2010) Development of an indirect ELISA test using an affinity purified surface antigen (P38) for serodiagnosis of canine Neospora caninum infection. Vet Parasitol 171(3-4):337-342
  14. Nghiem PP & Schatzberg SJ (2010) Conventional and molecular diagnostic testing for the acute neurologic patient. J Vet Emerg Crit Care (San Antonio) 20(1):46-61
  15. Lopes MG et al (2011) Presence of antibodies against Toxoplasma gondii, Neospora caninum and Leishmania infantum in dogs from Piauí. Rev Bras Parasitol Vet 20(2):111-114
  16. Cabezón O et al (2010) Kennel dogs as sentinels of Leishmania infantum, Toxoplasma gondii, and Neospora caninum in Majorca Island, Spain. Parasitol Res 107(6):1505-1508
  17. Valadas S et al (2010) Occurrence of antibodies anti-Neospora caninum, anti-Toxoplasma gondii, and anti-Leishmania chagasi in serum of dogs from Pará State, Amazon, Brazil. Parasitol Res 107(2):453-457