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Toxoplasma gondii

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T. gondii tachyzoites
T. gondii tachyzoites
Scientific classification
Domain: Eukaryota
Kingdom: Chromalveolata
Superphylum: Alveolata
Phylum: Apicomplexa
Class: Conoidasida
Subclass: Coccidiasina
Order: Eucoccidiorida
Family: Sarcocystidae
Genus: Toxoplasma
Species: T. gondii
Binomial name
Toxoplasma gondii
(Nicolle & Manceaux, 1908)

Toxoplasma gondii is a species of parasitic protozoa in the genus Toxoplasma.[1] The definitive host of T. gondii is the cat, but the parasite can be carried by many warm-blooded animals (birds[2] or mammals). Toxoplasmosis, the disease of which T. gondii is the causative agent, is usually minor and self-limiting but can have serious or even fatal effects on a fetus whose mother first contracts the disease during pregnancy or on an immunocompromised human or cat.

Life cycle Edit

The life cycle of T. gondii has two phases. The sexual part of the life cycle (coccidia like) takes place only in members of the Felidae family (domestic and wild cats), which makes these animals the parasite's primary host. The asexual part of the life cycle can take place in any warm-blooded animal, like other mammals (including felines) and birds.

File:Toxoplasma gondii.jpg

In the intermediate hosts (as well the definitive host, felines), the parasite invades cells, forming intracellular so-called parasitophorous vacuoles containing bradyzoites, the slowly replicating form of the parasite.[3] Vacuoles form tissue cysts mainly within the muscles and brain. Since they are within cells, the host's immune system does not detect these cysts. Resistance to antibiotics varies, but the cysts are very difficult to eradicate entirely. Within these vacuoles T. gondii propagates by endodyogeny until the infected cell eventually bursts and tachyzoites are released. Tachyzoites are the motile, asexually reproducing form of the parasite. Unlike the bradyzoites, the free tachyzoites are usually efficiently cleared by the host's immune response, although some manage to infect cells and form bradyzoites, thus maintaining the infection.

Tissue cysts are ingested by a cat (e.g., by feeding on an infected mouse). The cysts survive passage through the stomach of the cat and the parasites infect epithelial cells of the small intestine where they undergo sexual reproduction and oocyst formation. Oocysts are shed with the feces. Animals and humans that ingest oocysts (e.g., by eating unwashed vegetables etc.) or tissue cysts in improperly cooked meat become infected. The parasite enters macrophages in the intestinal lining and is distributed via the blood stream throughout the body.

Acute stage Toxoplasma infections can be asymptomatic, but often give flu-like symptoms in the early acute stages, and like flu can become, in very rare cases, fatal. The acute stage fades in a few days to months, leading to the latent stage. Latent infection is normally asymptomatic; however, in the case of immunocompromised patients (such as those infected with HIV or transplant recipients on immunosuppressive therapy), toxoplasmosis can develop. The most notable manifestation of toxoplasmosis in immunocompromised patients is toxoplasmic encephalitis, which can be deadly. If infection with T. gondii occurs for the first time during pregnancy, the parasite can cross the placenta, possibly leading to hydrocephalus or microcephaly, intracranial calcification, and chorioretinitis, with the possibility of spontaneous abortion (miscarriage) or intrauterine death.

Toxoplasmosis Edit

Main article: Toxoplasmosis
File:Toxplasma.png

T. gondii infections have the ability to change the behavior of rats and mice, making them drawn to rather than fearful of the scent of cats. This effect is advantageous to the parasite, which will be able to sexually reproduce if its host is eaten by a cat.[4] The infection is almost surgical in its precision, as it does not affect a rat's other fears such as the fear of open spaces or of unfamiliar smelling food.

Studies have also shown behavioral changes in humans, including slower reaction times and a sixfold increased risk of traffic accidents among infected males.[5]

The prevalence of human infection by Toxoplasma varies greatly between countries. Factors that influence infection rates include diet (prevalence is possibly higher where there is a preference for less-cooked meat) and proximity to cats. It has been suggested that climate change will also influence Toxoplasma gondii prevalence in some regions of the world.[6]

History Edit

The organism was first described in 1908 in Tunis by Nicolle and Manceaux within the tissues of the gundi (Ctenodactylus gundi). In the same year it was also described in Brazil by Splendore in rabbits .

References Edit

  1. Ryan KJ, Ray CG (eds) (2004). Sherris Medical Microbiology, 4th, 722–7, McGraw Hill.
  2. Dubey JP, Webb DM, Sundar N, Velmurugan GV, Bandini LA, Kwok OC, Su C. (2007 Sep 30), "Endemic avian toxoplasmosis on a farm in Illinois: clinical disease, diagnosis, biologic and genetic characteristics of Toxoplasma gondii isolates from chickens (Gallus domesticus), and a goose (Anser anser)", Vet Parasitol. 148 (3-4): 207-12, PMID 17656021 
  3. Dubey JP, Lindsay DS, Speer CA (Apr 1998). Structures of Toxoplasma gondii tachyzoites, bradyzoites, and sporozoites and biology and development of tissue cysts. Clin. Microbiol. Rev. 11 (2): 267–99.
  4. Berdoy M, Webster JP, Macdonald DW (August 2000). Fatal attraction in rats infected with Toxoplasma gondii. Proc. Biol. Sci. 267 (1452): 1591–4.
  5. Flegr J, Klose J, Novotná M, Berenreitterová M, Havlíček J (2009). Increased incidence of traffic accidents in Toxoplasma-infected military drivers and protective effect RhD molecule revealed by a large-scale prospective cohort study. BMC Infectious Diseases 9 (72).
  6. Meerburg BG, Kijlstra A (2009). Changing climate—changing pathogens: Toxoplasma gondii in North-Western Europe. Parasitology Research 105 (1).

External links Edit

Template:Alveolata Template:Chromalveolate diseases

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