ISSN 2398-2985      

Toxoplasmosis

4ferrets

Synonym(s): Toxoplasma gondii infection


Introduction

  • Cause: Toxoplasma gondii.
  • Signs: chronic disease most common and can be subclinical. Anorexia, lethargy, pyrexia in acute disease. Central nervous system signs (altered mentation, ataxia, seizures) often associated with chronic disease.
  • Diagnosis: serological testing, PCR on cerebrospinal fluid (CSF), post-mortem and histopathological examination.
  • Treatment: only of value in acute disease. Sulfadiazine with pyrimethamine, or clindamycin.
  • Prognosis: fair in chronic disease, acute disease can carry a guarded to poor prognosis.

Pathogenesis

Etiology

  • Toxoplasma gondii.
  • Protozoan parasite, from the Phylum Apicomplexa, Family Sarcocystiidae.
  • Asexual lifestage occurs in the intermediate host, which can be any mammalian or avian species.
  • Sexual lifestage occurs in the definitive host, the domestic cat and other felids

Predisposing factors

General

  • Ingestion of food or water contaminated with cat feces, or ingestion of infected prey animals.
  • Clinical disease most common in immunocompromised or young animals with immature immune systems.
  • Vertical transplacental infection to the fetus has been reported in minks. Although this was reported not to occur in black-footed ferrets.

Specific

  • Animals born to a dam with active infection during the gestation period.

Pathophysiology

  • The domestic cat and other felids are the final hosts where gametology (sexual reproduction) of the organism occurs.
  • Unsporulated oocysts are released into the external environment via feline feces.
  • Under suitable environmental conditions, the oocysts become sporulated.
  • The intermediate host can become infected by one of two modalities:
    • Ingestion of contaminated food or water containing sporulated oocysts:
      • Sporozoites within the oocyst are liberated within the intestinal tract and rapidly penetrates intestinal epithelial cells.
      • Tachyzoites define the stage of rapid asexual multiplication within infected host cells followed by host cell rupture and invasion to other tissues via the lymphatic and hematogenous route.
      • The intermediate host typically survives this acute phase of toxoplasmosis and produce antibodies that limit the invasiveness of the tachyzoites.
      • Tissue cysts are formed as a result; typically in muscle, but can also occur in the lungs, visceral organs, and the central nervous system.
      • Cysts contain thousands of bradyzoites, where multiplication of the organism is slowed due to the acquired immunity of the intermediate host.
      • Tissue cysts can rupture if the immunity of the intermediate host wanes.
      • Bradyzoites are released and resume the invasive characteristics of tachyzoites.
    • Ingestion of undercooked meat or prey carcasses containing Toxoplasma cysts. Digestion of the cyst wall in the intestinal tract releases bradyzoites, which resume the invasive characteristics of tachyzoites.
  • Clinical signs in the intermediate host are associated with the extra-intestinal phase of development.

Timecourse

  • Sporulation of toxoplasma oocysts occurs in 1-5 days after passage in feces of affected felids.
  • Clinical signs associated with acute disease typically develop around one week after infection:
    • Signs were reported to last between 2-16 days in black-footed ferrets.
    • Sudden death in young or immunocompromised animals may be seen without other clinical signs. Death in black-footed ferret kits occurred 10-26 days after initial exposure.
  • Clinical signs associated with chronic disease in black-footed ferrets developed 6-69 months after infection. Signs lasted 1-29 months and resulted either in death or euthanasia Euthanasia.

Epidemiology

  • Acute disease most common in young animals with immature immune systems and immunocompromised individuals.
  • Reactivation of chronic toxoplasmosis in healthy animals can occur with immunosuppression later in life.
  • Naïve populations or species-specific immune response deficiencies may increase vulnerability to clinical disease.
  • Seroprevalence reported to be high in wild carnivores, including the European polecat (Mustela putorius), although clinical disease was less common.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Dubey J P, Murata F H A, Cerqueira-Cézar C K & Kwok O C H (2021) Recent epidemiologic and clinical Toxoplasma gondii infections in wild canids and other carnivores: 2009-2020. Vet Parasitol 290, 109337.
  • Śmielewska-Łoś & Turniak W (2004) Toxoplasma gondii infection in Polish farmed mink. Vet Parasitol 122, 201-206 PubMed.
  • Burns R, Williams E S, O'Toole D & Dubey J P (2003) Toxoplasma gondii infections in captive black-footed ferrets (Mustela nigripes), 1992-1998: clinical signs, serology, pathology, and prevention. J Wildl Dis 39, 787-797 PubMed.
  • Frank R K (2001) An outbreak of toxoplasmosis in farmed mink (Mustela vison S.).  J Vet Diagn Invest 13, 245-249 PubMed.

Other sources of information

  • Huynh M & Piazza S (2020) Musculoskeletal and Neurologic Diseases. In: Ferrets, Rabbits and Rodents - E-Book : Clinical Medicine and Surgery. 4th edn. Eds: Quesenberry K, Mans C, Orcutt C & Carpenter J W. Elsevier - Health Sciences Division, USA.
  • Taylor M A, Coop R L & Wall R L (2015) Veterinary Protozoology. In: Veterinary Parasitology. Eds: Taylor M A, Coop R L & Wall R L. 

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