ISSN 2398-2969      

Toxoplasma gondii


Synonym(s): T. gondii




  • Toxoplasma gondii is an obligate intracellular coccidian parasite within the family Sarcocystidae.
  • There are more than 100 strains and at least 3 clonal lineages of T. gondii, varying in pathogenicity for different species.


  • First recognized in 1908 in the gondi (Ctenodactylus gundi), a small North African rodent.

Active Forms

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Clinical Effects



  • Definitive hosts are all members of the Felidae family.
  • Intermediate hosts include any mammal or bird.
  • Oocysts are found in the environment, after being shed in cat feces.


  • Cats (definitive hosts) usually become infected by T. gondii following ingestion of encysted organisms present in the tissues of a chronically infected intermediate host.
  • The cyst wall is digested by the cat, releasing infectious organisms into the intestinal lumen. The organisms penetrate through the intestinal wall and replicate throughout the body as rapidly dividing tachyzoites (extra-intestinal cycle). 
  • Simultaneously, the organisms invade and replicate within the intestinal epithelial cells (entero-epithelial cycle). 
  • This entero-epithelial cycle culminates in sexual reproduction and the formation of oocysts, which are excreted in the feces within 3-10 days. Shedding continues for approximately 10-14 days, during which time the environment is contaminated with many millions of oocysts.
  • As the cat develops an immune response, oocyst shedding is halted, and the development of tachyzoites is also arrested with the resultant formation of bradyzoites (slowly replicating forms of the organism) contained within tissue cysts.
  • Tissue cysts are present in a variety of sites throughout the body of chronically infected animals, each cyst containing large numbers of bradyzoites.
  • Intermediate hosts, such as the rabbit, become infected following ingestion of sporulated oocysts from the environment.
  • As in the cat, an extra-intestinal cycle of infection occurs, tachyzoites spread by the hematogenous route and multiply asexually in cells.
  • The subsequent immune response results in the development of encysted bradyzoites. The tissue cysts probably remain viable (contain infectious organisms) for the life of the animal.
  • Unlike infection in the cat, an enteroepithelial cycle (with oocyst production) does not occur in intermediate hosts.


  • By ingestion of bradyzoites, tachyzoites or oocysts; generally by ingestion of sporulated oocysts.
  • Transplacental transmission of tachyzoites.
  • Tachyzoites have been shown to be present in the milk of infected animals.
  • Rabbits and other herbivore animals are infected when drinking water or eating vegetable matter (grass, hay) contaminated with fecal oocysts. In addition, they can also get infected by fomites or from animal handlers.

Pathological effects

  • Sporozoites are released from the ingested oocysts, penetrate the intestinal epithelium, and invade macrophages and other types of cells.
  • The parasite lies within a parasitophorous vacuole, where it undergoes binary fission by a unique process called endodyogeny. Endodyogeny is a specialized type of division in which the two daughter cells form within the mother cell. These trophic forms are called tachyzoites.
  • The host cell will rupture and release the tachyzoites which will invade new host cells and repeat the replicative cycle. Infected macrophages will disseminate the tachyzoites throughout the host during this acute infection.
  • Clinical disease in most infections is caused by organ necrosis from tachyzoite multiplication.
  • Immunosuppression is likely to predispose to infection. It has been proposed that the high susceptibility of hares to toxoplasmosis may be due to a negative impact of stress on the hare's immune system.
  • The fatal outcome of T. gondii infection in the hares is probably due, at least in part, to the lack of cellular response.
  • Persistence of bradyzoites in cysts occurs in chronic infections. They have been found in pigeons, rats and mice up to 3 years after infection.
  • Some strains are more virulent than others.
  • Prenatally acquired toxoplasmosis is more commonly seen in man and sheep and is usually more severe than postnatally acquired toxoplasmosis.

Other Host Effects

  • In hares toxoplasmosis is an acute and fatal disease, whereas in rabbits only subclinical manifestations are usually seen and the infection passes easily to the latent stage.
  • Most infections with T. gondii are probably asymptomatic.


Control via animal

  • Some laboratory rabbit lines are supplied free of T. gondii.

Control via chemotherapies

  • Where treatment is attempted, sulfa drugs, pyrimethamine, tetracyclines or pyrimethamine with triple sulfa may be used.

Clindamycin should not be used in rabbits.


  • Vaccines available for sheep and pigs.
  • Due to low impact of toxoplasmosis in rabbits, vaccine does not seem an effective way of controlling the infection.

Other countermeasures

  • Feed cats only dried, canned or cooked food.
  • Good husbandry and hygiene is essential.
  • Cats should not be allowed to contaminate the rabbit's environment.
  • Do not feed rabbits food which may have been contaminated with cat feces.
  • Limit the contact of animal handlers with cats.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Figueroa-Castillo J A, Duarte-Rosas V, Juárez-Acevedo M et al (2006) Prevalence of Toxoplasma gondii antibodies in rabbits (Oryctolagus cuniculus) from Mexico. J Parasitol 92 (2), 394-395 PubMed.
  • Garweg J G & Boehnke M (2006) The antibody response in experimental ocular toxoplasmosis. Graefes Arch Clin Exp Ophthal 244 (12), 1668-1679 PubMed.
  • Almería S, Calvete C, Pagés A et al (2004) Factors affecting the seroprevalence of Toxoplasma gondii infection in wild rabbits (Oryctolagus cuniculi) from Spain. Vet Parasitol 123 (3-4), 265-270 PubMed.
  • Sroka J, Zwolinski J, Dutkiewicz J et al (2003) Toxoplasmosis in rabbits confirmed by strain isolation: a potential risk of infection among agricultural workers. Ann Agric Environ Med 10 (1), 125-128 PubMed.
  • Hill D & Dubey J P (2002) Toxoplasma gondii: transmission, diagnosis and prevention. Clin Microbiol Infect 8 (10), 634-640 PubMed.
  • Sedlák K, Literák I, Faldyna M et al (2000) Fatal toxoplasmosis in brown hares (Lepus europaeus): possible reasons of their high susceptibility to the infection. Vet Parasitol 93 (1), 13-28 PubMed.
  • Garweg J G, Kuenzli H & Boehnke M (1998) Experimental ocular toxoplasmosis in naive and primed rabbits. Ophthalmologica 212 (2), 136-141 PubMed.
  • Gustafsson K, Uggla A & Järplid B (1997) Toxoplasma gondii infection in the mountain hare (Lepus timidus) and domestic rabbit (Oryctolagus cuniculi). I. Pathology. J Comp Pathol 117 (4), 351-360 PubMed.
  • Gustafsson K, Wattrang E, Fossum C et al (1997) Toxoplasma gondii infection in the mountain hare (Lepus timidus) and domestic rabbit (Oryctolagus cuniculi) II. Early immune reactions. J Comp Pathol 117 (4), 361-369 PubMed.
  • Dubey J P, Brown C A, Carpenter J L et al (1992) Fatal toxoplasmosis in domestic rabbits in the USA. Vet Parasitol 44 (3-4), 305-309 PubMed.
  • Leland M M, Hubbard G B & Dubey J P (1992) Clinical toxoplasmosis in domestic rabbits. Lab Anim Sci 42 (3), 318-319 PubMed.
  • Ishikawa T, Nishino H, Ohara M et al (1990) The identification of a rabbit-transmitted cervical toxoplasmosis mimicking malignant lymphoma. Am J Clin Path 94 (1), 107-110 PubMed.
  • Friedrich R & Müller W A (1989) [The effect of a subretinal injection of Toxoplasma gondii on the serum antibody titer in a rabbit model of ocular toxoplasmosis.] Angew Parasitol 30 (1), 15-17 PubMed.
  • Tassignon M J, Brihave M, De Meuter F et al (1989) [Efficacy of treatments in experimental toxoplasmosis.] Bull Soc Belge Ophthal 230, 59-72 PubMed.

Other sources of information

  • Pritt S, Cohen K, Sedlacek H (2012) Parasitic Disease. In: The Laboratory Rabbit, Guinea Pig, Hamster and other Rodents. Eds: Suckow M, Stevens K & Wilson R. Academic Press, USA. pp 415-446.

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