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T. gondii is a parasite of warm blooded animals which is present throughout the world. It is the causative agent of the diseases known as Toxoplasmosis.
The organism exhibits a definitive protozoan lifestyle.The life cycle begins with an oocyst in the intestines of cats, the definitive host of T. gondii. The oocyst contains bradyzoites or sporozoites. Oocysts enter prospective hosts through ingestion of cat fecal matter. Once inside a host, bradyzoites, after being released from the oocyst, infect the intestinal mucosa. Within the host cell, tachyzoites rapidly divide, eventually rupturing the cell. The released tachyzoites spread throughout the host, repeating the lysis process or forming zoitocysts (which are, like oocysts, filled with bradyzoites) in host tissue. Three weeks after infection, there are no longer tachyzoites present in the tissues. The cysts reenter the cycle when ingested by another host, unless the host is a cat. In this case, oocysts will be formed in the cat's intestine and will be shed.
Life Cycle Illustration
T. gondii is a protozoan (eukaryote) which exists in several distinct stages.
|The tachyzoite stage:||Tachyzoites rupturing host cell:
|Bradyzoites in a Zoitocyst:
Most people who are infected with Toxoplasma gondii are asymptomatic.
In some cases, the parasite may cause inflammation of the lymphatic system,
resulting in flulike symptoms including fever and muscle aches. These symptoms
can last for a month.
In fewer cases, the infection results in more severe disease. T. gondii can infect the eyes and brain, often resulting in blindness and severe neurological disease. Neurological damage (encephalitis) occurs in children who contract the infection congenitally and in immunocompromised individuals. In immunocompromised individuals, encephalitis caused by toxoplasmosis progresses gradually. Patients may begin to experience headaches and dizziness, then memory loss, degradation of motor skills, and sometimes coma and death.
Congenital infections may result in spontaneous abortion or birth defects including ocular damage and severe mental retardation.
Toxoplasma gondii is common throughout the world. A CDC study
from 2003 showed that in the United States in 1999-2000, 16% of the population
aged 12 to 49 years carried IgG antibodies against the parasite. The prevalence
is higher in foreign-born U.S. residents.One in one thousand infants born
in the U.S. expresses antibodies against T. gondii. However, there
are only about 300 clinical cases of congenital toxoplasmosis per year.Toxoplasmosis
is more common in warm, moist climates because these environments favor
the survival of oocysts outside the host.
T. gondii causes disease through cell necrosis. This necrosis occurs due to reproduction. Tachyzoites reproduce to large numbers within a cell, eventually bursting from it. The interaction between T. gondii and the host immune system is a widely studied field due to the prevalence of the organism. The organism is able to cause disease by modulating the host immune response. One virulence factor which contributes to modulation is a parasitic heat shock protein, TgHSP70. The protein induces maturation in host dendritic cells. When dendritic cells mature, their phagocytic activity decreases. T. gondii HSP70 is a possible target for vaccine development.
The parasite induces an IL-12-linked immune response which serves to control the abundance of active tachyzoites in the host. This contributes to the host's survival, which provides greater opportunity for spreading of the pathogen.
Alberti et al. 2004 "Turning it on and off: regulation of dendritic cell function in toxoplasma gondii infection" Immunol. Rev. 201(1)
Dobbin, Smith, and Johnson 2002. "Heat Shock protein 70 is a potential virulence factor in murine toxoplasma infection via immunomodulation of host NF-kappaB and nitric oxide" J.Immunol. 169 p958-965
Kang et al 2004 "toxoplasma gondii-derived heat shock protein 70 stimulates the maturation of human monocyte-derived dendritic cells" Biochemical and biophysical research communications 322