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Toxoplasma gondii

Microbiology > Parasitology > Protozoa
Structure:    Kingdom Protozoa, Phylum Sporozoa, an intracellular parasite

• Worldwide distribution; seroprevalence studies performed in the United States indicate that approximately 9% to 11% of individuals between the ages of 6 and 49 have antibodies to T. gondii.
• Toxoplasmosis is acquired by humans through ingestion of food or water contaminated with cat feces or through eating undercooked meat containing tissue cysts from animals serving as intermediate hosts.
• Transmission can also occur transplacentally, through blood transfusions and organ transplantation.  
• Following primary infection, T gondii can remain latent for the life of the host; the risk for reactivation is highest among immunosuppressed individuals.

• The only known definitive host is the common house cat and other felines.  Infections are generally established when infected rodents or birds are consumed.
• The parasite infects the cat intestinal epithelial cells, reproduces and oocysts are excreted in feces. The oocyst matures into an infective form within 1-5 days, which may then be ingested by an intermediate host.
• In the intermediate host, the ingested oocysts develop into tachyzoites which localize in the neural and muscle tissue and develop into tissue cyst bradyzoites.

Laboratory diagnosis:
• Serologic testing of IgM and IgG (although false positive IgM’s may occur using commercial tests).   May be unreliable or difficult to interpret in immunocompromised patients and suspected intrauterine infection.
• Demonstration of organisms in stained tissues and body fluids.
• Detection of Toxoplasma DNA by PCR in blood, CSF, amniotic fluid, tissue or ocular fluid.

Disease manifestation:
• Most infected, immunocompetent individuals are asymptomatic.
• Symptoms may occur as the organism moves from the blood to tissues where it becomes an intracellular parasite.  In the human host it is commonly found in the lung, heart, lymphatic organs, eye and CNS.
• Acute disease: chills, fever, headache, myalgia’s, lymphadenopathy and fatigue (mono-like illness).
• Chronic disease: lymphadenopathy, hepatitis, encephalomyelitis and myocarditis; occasionally chorioretinitis.
• Congenital infection: First trimester: spontaneous abortion, stillbirth or severe disease.  Second-third trimester: multiple severe neurologic problems.
• Immunocompromised or older patients: reactivation of latent infection, usually manifesting as neurologic symptoms.  A major cause of encephalitis in AIDs patients, with multifocal brain lesions.

Differential diagnosis:
• Severe encephalitis, especially in HIV or other immune-compromised patients.
• Observe ring enhancing lesions on CT/MRI or brain biopsy to differentiate from CNS lymphoma.
• Infectious mononucleosis

• Acute T. gondii is susceptible to pyrimethamine plus sulfadiazine or clindamycin.
• Pregnant patients: clindamycin or spiramycin
• Trimethoprim-sulfamethoxazole for disseminated or CNS toxoplasma and also as prophalaxis to  prevent toxoplasma reactivation in immunocompromised patients.
• Corticosteroids therapy if cerebral edema and/or severe ocular infection.

Prevention and control:
• Avoiding raw or undercooked meat and exposure to cat feces (litter boxes, contaminated soil or water), especially for pregnant women and immunocompromised hosts.
• Good hand hygiene and food sanitation practices.
• Serologic screening of patients prior to organ transplantation and early in the course of HIV infection.

Key words:
Sporozoa, Toxoplasma, Toxoplasmosis, Toxoplasma gondii, T. gondii

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Life Cycle:

The only known definitive hosts for Toxoplasma gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat’s feces  . Although oocysts are usually only shed for 1-2 weeks, large numbers may be shed. Oocysts take 1-5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water or plant material contaminated with oocysts  . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites  . Cats become infected after consuming intermediate hosts harboring tissue cysts  . Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment  . Humans can become infected by any of several routes:  eating undercooked meat of animals harboring tissue cysts  , consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat)  , blood transfusion or organ transplantation  , transplacentally from mother to fetus  .  In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens  . Diagnosis of congenital infections can be achieved by detecting T. gondii DNA in amniotic fluid using molecular methods such as PCR  .

source: CDC DPDH

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