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==Introduction==

==Introduction==

[[Image:Toxoplasmosis Life Cycle.jpg|thumb|right|300px| Life cycle of ''Toxoplasma gondii''. Source: Wikimedia Commons; Author: LadyofHats (2010)]]

[[Image:Toxoplasmosis Life Cycle.jpg|thumb|right|300px| Life cycle of ''Toxoplasma gondii''. Source: Wikimedia Commons; Author: LadyofHats (2010)]]

Toxoplasmosis is caused by ''[[Toxoplasma gondii]]'' infection. Its life cycle is described in the pathogen page, ''[[Toxoplasma gondii]]''.

Toxoplasmosis is caused by ''[[Toxoplasma gondii]]'' infection. Its life cycle is described in the pathogen page, ''[[Toxoplasma gondii]]''.

The outcome of primary infection depends on the immune status of the host, as well as the location of and degree of injury caused by tissue cysts. Primary infection normally results in chronic disease, where tissue cysts form but clinical signs are not normally apparent. In immunodeficient animals, or in animals with concurrent illness, chronic infections may become symptomatic as the organism is allowed to proliferate. Acute primary infection in these animals can, rarely, prove fatal.  

The outcome of primary infection depends on the immune status of the host, as well as the location of and degree of injury caused by tissue cysts. Primary infection normally results in chronic disease, where tissue cysts form but clinical signs are not normally apparent. In immunodeficient animals, or in animals with concurrent illness, chronic infections may become symptomatic as the organism is allowed to proliferate. Acute primary infection in these animals can, rarely, prove fatal.  

Demonstration of ''Toxoplasma gondii'' in the tissues with associated inflammation is required for the definitive diagnosis of clinical toxoplasmosis. For example, tachyzoites may be seen in blood, cerebrospinal fluid, peritoneal and pleural effusions, aqueous humour or transtracheal washes from clinically ill animals. ''Toxoplasma gondii'' may also be detected in these samples using PCR, tissue culture or animal inoculation techniques¹. These methods may be employed on tissue biopsies too, as well as examination under haematoxylin and eosin or immunohistochemical staining. Immunohistochemistry is preferred to H&E because it is specific for ''T. gondii''. Demonstration of the organism is often most easily achieved post-mortem, as the size of the sample is not restrictive to the likelihood of seeing ''T.gondii''. In the absence of demonstration of ''Toxoplasma gondii'' in the tissues or fluids ante-mortem, there is no one specific test to diagnose toxoplamosis. However, a combination of various diagnostic procedures can be used to build a presumptive diagnosis.   

Demonstration of ''Toxoplasma gondii'' in the tissues with associated inflammation is required for the definitive diagnosis of clinical toxoplasmosis. For example, tachyzoites may be seen in blood, cerebrospinal fluid, peritoneal and pleural effusions, aqueous humour or transtracheal washes from clinically ill animals. ''Toxoplasma gondii'' may also be detected in these samples using PCR, tissue culture or animal inoculation techniques¹. These methods may be employed on tissue biopsies too, as well as examination under haematoxylin and eosin or immunohistochemical staining. Immunohistochemistry is preferred to H&E because it is specific for ''T. gondii''. Demonstration of the organism is often most easily achieved post-mortem, as the size of the sample is not restrictive to the likelihood of seeing ''T.gondii''. In the absence of demonstration of ''Toxoplasma gondii'' in the tissues or fluids ante-mortem, there is no one specific test to diagnose toxoplamosis. However, a combination of various diagnostic procedures can be used to build a presumptive diagnosis.   

Firstly, clinical signs should be suggestive of toxoplasmosis, despite variation in the presentation of disease between individuals. Although no pathognomic changes for toxoplasmosis are seen on routine haematology, biochemistry and urinalysis, certain results are often seen in ''T. gondii'' infection. For example, most cats show a mild non-regenerative anaemia, and 50% of patients are initially leukopenic due to [[lymphopenia]]. [[Neutropenia]] may occur in conjunction with lymphopenia, and leukocytosis may occur during recovery⁴. Most patients also show and increase in creatine kinase, ALT, SAP, and hypoalbuminaemia is also common^{1, 4}. 25% of cats show hyperbilirubinemia and [[icterus]], and [[Pancreatitis - Dog and Cat|pancreatitis]] may cause low to low normal serum calcium. A mild proteinuria and bilirubinuria are often revealed by urinalysis.

Firstly, clinical signs should be suggestive of toxoplasmosis, despite variation in the presentation of disease between individuals. Although no pathognomic changes for toxoplasmosis are seen on routine haematology, biochemistry and urinalysis, certain results are often seen in ''T. gondii'' infection. For example, most cats show a mild non-regenerative anaemia, and 50% of patients are initially leukopenic due to [[lymphopenia]]. [[Neutropenia]] may occur in conjunction with lymphopenia, and leukocytosis may occur during recovery⁴. Most patients also show and increase in creatine kinase, ALT, SAP, and hypoalbuminaemia is also common^{1, 4}. 25% of cats show hyperbilirubinemia and [[icterus]], and [[Pancreatitis|pancreatitis]] may cause low to low normal serum calcium. A mild proteinuria and bilirubinuria are often revealed by urinalysis.

Demonstration of antibodies in serum is indicative of exposure to ''T. gondii'', but does not necessarily show active infection. This could be overcome by testing for ''T. gondii'' antigen or immune complexes, but these methods are currently only available to researchers. Several techniques are commercially available for detection of antibody, including [[ELISA testing|ELISA]], [[Immunofluorescence|immunofluorescent antibody testing]], Sabin-Feldmann dye test, and [[Agglutination|agglutination tests]]. Although these tests are theoretically able to detect all classes of immunoglobulin against ''Toxoplasma gondii'' in many species, it seems that feline serum positive for IgM only often reads as a false negative^{5, 6}. Therefore, careful interpretation is necessary, particularly since the IgM antibody class appears to correlate more closely to clinical disease than IgG⁷. IgG antibody persists at high levels for at least six years after infection, and so a single IgG measurement is not particularly useful for clinical diagnosis. A rising IgG titre may be more suggestive of active toxoplasmosis: however, IgG is not produced until 2-3 weeks post-infection which may be too late to be useful in acute cases, and many animals with chronic toxoplasmosis will not be assayed until IgG is already at its maximal titre. A more practically useful form of serology is examination of IgM in aqueous humour or cerebrospinal fluid. IgM, in contrast to IgG and IgA, has only been detected in the aqueous humour and CSF of cats with clinical disease ^{5, 6}. Therefore, an IgM titre of above 1:64 is highly suggestive of recent or active ''T. gondii'' infection.

Demonstration of antibodies in serum is indicative of exposure to ''T. gondii'', but does not necessarily show active infection. This could be overcome by testing for ''T. gondii'' antigen or immune complexes, but these methods are currently only available to researchers. Several techniques are commercially available for detection of antibody, including [[ELISA testing|ELISA]], [[Immunofluorescence|immunofluorescent antibody testing]], Sabin-Feldmann dye test, and [[Agglutination|agglutination tests]]. Although these tests are theoretically able to detect all classes of immunoglobulin against ''Toxoplasma gondii'' in many species, it seems that feline serum positive for IgM only often reads as a false negative^{5, 6}. Therefore, careful interpretation is necessary, particularly since the IgM antibody class appears to correlate more closely to clinical disease than IgG⁷. IgG antibody persists at high levels for at least six years after infection, and so a single IgG measurement is not particularly useful for clinical diagnosis. A rising IgG titre may be more suggestive of active toxoplasmosis: however, IgG is not produced until 2-3 weeks post-infection which may be too late to be useful in acute cases, and many animals with chronic toxoplasmosis will not be assayed until IgG is already at its maximal titre. A more practically useful form of serology is examination of IgM in aqueous humour or cerebrospinal fluid. IgM, in contrast to IgG and IgA, has only been detected in the aqueous humour and CSF of cats with clinical disease ^{5, 6}. Therefore, an IgM titre of above 1:64 is highly suggestive of recent or active ''T. gondii'' infection.

Within 2-3 days of clindamycin or trimethoprim-sulphonamide administration, most clinical signs should begin to resolve and the prognosis is good. However, anti-''Toxoplasma'' drugs are unlikely to completely eradicate the organism from the host, and so recurrences are common. Ocular and CNS toxoplasmosis respond more slowly to therapy and carry a worse prognosis. Some neuromuscular signs may be persistent due to permanent nervous damage. Animals with hepatic or pulmonary disease have a poor prognosis.

Within 2-3 days of clindamycin or trimethoprim-sulphonamide administration, most clinical signs should begin to resolve and the prognosis is good. However, anti-''Toxoplasma'' drugs are unlikely to completely eradicate the organism from the host, and so recurrences are common. Ocular and CNS toxoplasmosis respond more slowly to therapy and carry a worse prognosis. Some neuromuscular signs may be persistent due to permanent nervous damage. Animals with hepatic or pulmonary disease have a poor prognosis.

==Literature Search==

[[File:CABI logo.jpg|left|90px]]

|literature search = [http://www.cabdirect.org/search.html?q=%28title%3A%28%22toxoplasma+gondii%22%29+OR+title%3A%28toxoplasmosis%29%29+AND+od%3A%28cats%29+ Toxoplasmosis in cats publications]

'''[[Toxoplasmosis - Human|Human Toxoplasmosis]]'''</big>

[http://www.cabdirect.org/search.html?q=%28title%3A%28%22toxoplasma+gondii%22%29+OR+title%3A%28toxoplasmosis%29%29+AND+od%3A%28cats%29+ Toxoplasmosis in cats publications]

 

*[http://www.vet.cornell.edu/fhc/brochures/toxo.html Cornell College of Veterinary Medicine Toxoplasmosis Factsheet]

*[http://www.vet.cornell.edu/fhc/brochures/toxo.html Cornell College of Veterinary Medicine Toxoplasmosis Factsheet]

#Quinn, P J and McCraw, B M (1972) Current status of toxoplamsa and toxoplasmosis: A review. '' The Canadian Veterinary Journal'', '''13(11)''', 247-262.

#Quinn, P J and McCraw, B M (1972) Current status of toxoplamsa and toxoplasmosis: A review. '' The Canadian Veterinary Journal'', '''13(11)''', 247-262.

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