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Toxoplasma gondii

obovis
Contributor(s):

Ash Phipps

Andrew Forbes


Introduction

Classification

T. gondii is rarely of clinical significance in cattle. It is primarily of concern in sheep.

Taxonomy

  • Phylum: Apicomplexa.
  • Class: Conoidasida.
  • Order: Eucoccidiorida.
  • Family: Sarcocystidae.
  • Genus: Toxoplasma.
  • Species: Toxoplasma gondii.

Active Forms

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Clinical Effects

Epidemiology

Habitat

  • Oocysts survive and remain infective in the environment in which they are defecated on (soil, water, plant material etc).

Lifecycle

  • Prepatent period = 3 - >14 days.
  • Members of Felidae are the definitive host for Toxoplasma gondii.
  • Cattle are occasional intermediate hosts; sheep are the most important from a veterinary perspective.
  • Toxoplasma undergoes the sexual component of the lifecycle in members of Felidae only and the asexual component of the lifecycle occurs in the intermediate host.
  • Members of Felidae, become infected by ingesting meat/animals containing infective bradyzoites or oocysts containing sporozoites.
  • In the small intestine cells of the Felidae, the parasite undergoes sexual development and reproduction -> merozoites (from bradyzoites) or  sporozoites to schizonts to gametes to produce thick walled (zyogote containing) oocyst.
  • The intestinal cells rupture releasing the unsporulated oocysts into the intestinal lumen.
  • The oocysts are passed into the environment via defecation.
  • Sporulation of the oocysts occurs in the environment (1 to 5 days after excretion).
  • Infection of the intermediate host via ingestion of the sporulated oocysts and proteolytic digestion of the cell wall results in the release of sporozoites.
  • Sporozoites then invade the intestinal cells and undergo differentiation into tachyzoites (capable of rapid replication).
  • The tachyzotes form tissue cysts within a specialized vacuole (parasitophorous vacuole) in the invaded host cells
  • Replication occurs in the specialized vacuole until the host cell dies and ruptures releasing the tachyzoites into the bloodstream to be disseminated throughout the body.
    • Note: transplacental transmission can occur.
  • As the host builds an immune response to tachyzoites in the tissues of the body, the tachyzoites undergo development into bradyzoites which form tissue cysts (commonly in the brain, eye, heart and muscles).
  • Chronic infection occurs and the bradyzoite cysts can remain in the intermediate host for life. However, the tissue cysts often rupture and re-encyst in the intermediate host.

Transmission

  • Members of Felidae become infected from ingestion of infected meat/animals with tissues cysts or oocysts containing sporozoites.
  • Members of Felidae pass the unsporolated oocyts in faeces that is ingested by the intermediate host.
  • Vertical transmission can occur in the intermediate host.

Pathological effects

  • Infection in cattle is rarely of any clinical significance and is not recognised as a cause of abortion.
  • The following signs have been reported:
  • Calves:
    • Pyrexia.
    • Diarrhea.
    • Weight loss.
    • Reduced feed intake.
    • Depression.
    • Lethargy.
    • Weakness.
    • Respiratory disease.
    • Nervous signs - seizures, tremors, altered gait and hyper-excitability or dullness. Bruxism is often observed.
    • Calves usually die within 2-6 days of the onset of clinical signs.
  • Adult non-pregnant cattle:
    • Asymptomatic infections (likely to be due to rapid elimination of the parasite).
  • Adult pregnant cattle:
    • Vertical transmission to calves may occur.
      • It is hypothesized that this may result in abortions, stillborn or weak non-viable calves, however there is very limited evidence to prove that this is the case.

Control

Control via chemotherapies

  • Seldom carried out in cattle.

Control via environment

  • Control domestic cat and wild cat populations to reduce the risk of exposure of Toxoplasma gondii to cattle.
  • Remove any cat feces from the environment; particularly from the feeding areas of cattle (feed bunks, calf sheds etc).
    • Note: the above measures may be difficult to achieve on some farms.

Vaccination

  • No current vaccine available to be used in cattle.

Diagnosis

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Further Reading

Publications

Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Dumètre A, Dubey J P, Ferguson D J, Bongrand P. Aza, N & Puech P H (2013) Mechanics of the Toxoplasma gondii oocyst wall. Proceedings of the National Academy of Sciences 110 (28), 11535-11540 PubMed.
  • Klun I, Djurković-Djaković O, Katić-Radivojević S & Nikolić A (2006) Cross-sectional survey on Toxoplasma gondii infection in cattle, sheep and pigs in Serbia: seroprevalence and risk factors. Vet Parasitol 135 (2), 121-131.
  • Esteban-Redondo I, Maley S W, Thomson K, Nicoll S, Wright S, Buxton D & Innes E A (1999) Detection of T. gondii in tissues of sheep and cattle following oral infection. Vet Parasitol 86 (3), 155-171 VetMedResource.
  • Dubey J P, Lindsay D S & Speer C A (1998) Structures of Toxoplasma gondiitachyzoites, bradyzoites, and sporozoites and biology and development of tissue cysts. Clinical microbiology reviews 11 (2), 267-299 PubMed.
  • Dubey J P (1992) Isolation of Toxoplasma gondii from a naturally infected beef cow. J Parasitol, 151-153 PubMed.
  • Dubey J P (1986) A review of toxoplasmosis in cattle. Vet Parasitol 22 (3-4), 177-202.
  • Dubey J P & Streitel R H (1976) Prevalence of Toxoplasma infection in cattle slaughtered at an Ohio abattoir. JAVMA 169 (11), 1197-1199 PubMed.

Other sources of information

  • Blood D C, Gay C C, Radostits O M & Hinchcliff K W (2000) Veterinary medicine: a textbook of the diseases of cattle, sheep, pigs, goats and horses. W B Saunders Company Limited.

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