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==Description==

 

==Introduction==

Human exposure to toxoplasmosis is common: it is estimated that aroung 60% of healthy adults worldwide are seropositive to ''[[Toxoplasma gondii]]''. The most common route of human infection is ingestion of oocysts in water or food contaminated by cat faeces, although consumption of undercooked meat containing tissue cysts also occurs. Contact with abortion products from infected ewes is a risk for pregnant women. An immune response occurs in response to infection, and tissue cysts form in several organs. These cysts may later reactivate in immunocompromised patients, for example those suffering from AIDS. If initial infection occurs during pregnancy, or if cysts reactivate at this time, ''Toxoplasma'' may infect the foetus transplacentally. As most mothers are exposed to ''Toxoplasma gondii'' early in life, and are immunocompetent, transplacental infection is seen infrequently. Transmission via blood transfusions or organ transplantation can also occur in man.

 

 

 

Human exposure to toxoplasmosis is common: it is estimated that aroung 60% of healthy adults worldwide are seropositive to ''Toxoplasma gondii''. The most common route of human infection is ingestion of oocysts in water or food contaminated by cat faeces, although consumption of undercooked meat containing tissue cysts also occurs. Contact with abortion products from infected ewes is a risk for pregnant women. An immune response occurs in response to infection, and tissue cysts form in several organs. These cysts may later reactivate in immunocompromised patients, for example those suffering AIDs. If initial infection occurs during pregnancy, or if cysts reactivate at this time, ''Toxoplasma'' may infect the foetus transplacentally. As most mothers are exposed to ''Toxoplasma gondii'' early in life, and are immunocompetent, transplacental infection is seen infrequently. Transmission via blood transfusions or organ transplantation can also occur in man.

==Signalment==

==Signalment==

Despite the various methods of transmission to man, and the high seroprevalence to ''Toxoplasma gondii'', the risk of developing clinical disease is low and is generally restricted to foetuses infected ''in utero'', and immunosuppressed patients such as those infected with Human Immunodeficiency Virus.

Despite the various methods of transmission to man, and the high seroprevalence to ''Toxoplasma gondii'', the risk of developing clinical disease is low and is generally restricted to foetuses infected ''in utero'', and immunosuppressed patients such as those infected with Human Immunodeficiency Virus.

==Clinical Signs==

===Clinical Signs===

 

There are several manifestations of toxoplasmosis in man. Acute infection in healthy individuals is normally asymptomatic, but up to 20% of patients develop lymphadenopathy. This is sometimes accompanied by flu-like signs which may include pyrexia, pharyngitis and myalgia and last for several weeks before a full recovery is made.

There are several manifestations of toxoplasmosis in man. Acute infection in healthy individuals is normally asymptomatic, but up to 20% of patients develop lymphadenopathy. This is sometimes accompanied by flu-like signs which may include pyrexia, pharyngitis and myalgia and last for several weeks before a full recovery is made.

   

   

CNS signs are the most common presentation in immunocompromised patients suffering ''Toxoplasma'' infection or re-activation. Signs are due to intracranial mass lesions or encephalitis, and can include headaches, seizures, pyrexia, coma and focal neurological deficits. Ocular involvement is also possible and usually results from re-activation of a congenital infection. Inflammation of the choroid causes pain and visual disturbances. Occasionally, in severely immunocompromised patients, disease can be seen outwith the CNS and the eye. In these incidences, affected tissues and therefore clinical signs can be variable. For example, patients may suffer pneumonitis, myocarditis, high fevers or polymyositis, which may prove fatal without treatment.

CNS signs are the most common presentation in immunocompromised patients suffering ''Toxoplasma'' infection or re-activation. Signs are due to intracranial mass lesions or encephalitis, and can include headaches, seizures, pyrexia, coma and focal neurological deficits. Ocular involvement is also possible and usually results from re-activation of a congenital infection. Inflammation of the choroid causes pain and visual disturbances. Occasionally, in severely immunocompromised patients, disease can be seen outwith the CNS and the eye. In these incidences, affected tissues and therefore clinical signs can be variable. For example, patients may suffer pneumonitis, myocarditis, high fevers or polymyositis, which may prove fatal without treatment.

When infection is acquired for the first time during pregnancy, congenital toxoplasmosis can arise. This may also occur if a mother infected before conception becomes immunosuppressed during pregnancy. Foetuses infected congenitally may be aborted, stillborn, or born with toxoplasmosis. Infections later in gestation are more likely to give rise to a live but infected neonate. When neonates are born with toxoplasmosis disease can be severe, particularly if transplacental infection occured early in pregnancy. Signs can include rashes, icterus and hepatosplenomegaly as well as retinochoroiditis, cerebral calcifications, hydrocephalus/microcephaly, and psychomotor retardation. These last four signs together are characteristic of congenital toxoplasmosis. Infants infected during the third trimester are less severely affected and tend to appear normal at birth. However, signs may develop months to years later, and can include seizures, retinochoroiditis and intellectual disability.

When infection is acquired for the first time during pregnancy, congenital toxoplasmosis can arise. This may also occur if a mother infected before conception becomes immunosuppressed during pregnancy. Foetuses infected congenitally may be aborted, stillborn, or born with toxoplasmosis. Infections later in gestation are more likely to give rise to a live but infected neonate. When neonates are born with toxoplasmosis disease can be severe, particularly if transplacental infection occurred early in pregnancy. Signs can include rashes, icterus and hepatosplenomegaly as well as retinochoroiditis, cerebral calcifications, hydrocephalus/microcephaly, and psychomotor retardation. These last four signs together are characteristic of congenital toxoplasmosis. Infants infected during the third trimester are less severely affected and tend to appear normal at birth. However, signs may develop months to years later, and can include seizures, retinochoroiditis and intellectual disability.

 

Changes in routine haematology and biochemistry may be seen in acute toxoplasmosis. These can include a mild anaemia and leukopenia, as well as increases in liver enzymes.

Changes in routine haematology and biochemistry may be seen in acute toxoplasmosis. These can include a mild anaemia and leukopenia, as well as increases in liver enzymes.

Indirect fluorescent antibody tests or an ELISA can be used to detect ''T. gondii''-specific IgG and IgM antibodies. The production of these antibodies follow different time courses: IgM appears in the first two weeks of infection, peaks at 4-8 weeks and declines over the following months, whereas IgG is produced more slowly and remains for months to years. Therefore, elevations in IgM alone indicates recent ''Toxoplasma gondii'' exposure, and an increased IgG with low IgM shows previous infection. In neonates, detection of specific IgM is consistent with congenital infection. This is because IgG crosses the placenta and could therefore come from an infected mother, but IgM does not and must therefore be produced by the foetus itself.

Indirect fluorescent antibody tests or an ELISA can be used to detect ''T. gondii''-specific IgG and IgM antibodies. The production of these antibodies follows different time courses: IgM appears in the first two weeks of infection, peaks at 4-8 weeks and declines over the following months, whereas IgG is produced more slowly and remains for months to years. Therefore, elevations in IgM alone indicates recent ''Toxoplasma gondii'' exposure, and an increased IgG with low IgM shows previous infection. In neonates, detection of specific IgM is consistent with congenital infection. This is because IgG crosses the placenta and could therefore come from an infected mother, but IgM does not and must therefore be produced by the foetus itself.

 

If toxoplasmosis involving the CNS is suspected, CT and/or MRI may be used. One or more dense, rounded lesions may be seen.

If toxoplasmosis involving the CNS is suspected, CT and/or MRI may be used. One or more dense, rounded lesions may be seen.

===Cytology===

==Cytology==

 

In the event of CNS toxoplasmosis, a CSF sample may show increased levels of protein and a lymphocytic pleocytosis.

In the event of CNS toxoplasmosis, a CSF sample may show increased levels of protein and a lymphocytic pleocytosis.

==Treatment==

==Treatment==

Asymptomatic infections in immunocompetent patients do not require treatment. However, immunocompromised people, neonates and pregnant women are usually treated with sulfadiazine and pyrimethamine. Clindamycin can also be used.

Asymptomatic infections in immunocompetent patients do not require treatment. However, immunocompromised people, neonates and pregnant women are usually treated with sulfadiazine and pyrimethamine. Clindamycin can also be used.

==Links==

==Links==

*[http://www.cdc.gov/toxoplasmosis/ Center for Disease Control and Prevention: Toxoplasmosis]

*[http://www.cdc.gov/toxoplasmosis/ Center for Disease Control and Prevention: Toxoplasmosis Factsheets]

*[http://www.hpa.org.uk/webw/HPAweb&HPAwebStandard/HPAweb_C/1195733799638 Health Protection Agency: Toxoplasmosis]

*[http://www.hpa.org.uk/webw/HPAweb&HPAwebStandard/HPAweb_C/1195733799638 Health Protection Agency: Toxoplasmosis]

==References==

==References==

#Beers, M H (2006) '''The Merck Manual of Diagnosis and Therapy (Eighteenth Edition)''', ''Merck''.

#Beers, M H (2006) '''The Merck Manual of Diagnosis and Therapy (Eighteenth Edition)''', ''Merck''.

[[Category:Tissue_Cyst_Forming_Coccidia]][[Category:Zoonoses]]

[[Category:Zoonoses]]

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