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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.  

The mechanism of clinical disease in chronic toxoplasmosis is not fully understood, but may be related to low-level tachyzoite replication, or intermittent antigenaemia and parasitemia^{2 – SA page}. The pathogenesis of disease could also be associated with immunological reactions against the organism through formation and deposition of immune complexes, and delayed hypersensitivity reactions^{3 – SA page}.

The mechanism of clinical disease in chronic toxoplasmosis is not fully understood, but may be related to low-level tachyzoite replication, or intermittent antigenaemia and parasitemia². The pathogenesis of disease could also be associated with immunological reactions against the organism through formation and deposition of immune complexes, and delayed hypersensitivity reactions³.

==Signalment==

==Signalment==

Cats more commonly show clinical disease than dogs. Male cats are predisposed, and the average age of the feline toxoplasmosis patient is 4 years (range: 2 weeks to 16 years)⁴.  There are no breed predilections.

Cats more commonly show clinical disease than dogs. Male cats are predisposed, and the average age of the feline toxoplasmosis patient is 4 years (range: 2 weeks to 16 years)⁴.  There are no breed predilections.

==Diagnosis==

==Clinical Signs==

===Clinical Signs===

Clinical signs are determined by the site and extent of organ damage by tachyzoites, and may be acute or chronic. Acute signs manifest at the time of initial infection, whereas chronic signs are associated with reactivation of encysted infection during times of immunocompromise.

Clinical signs are determined by the site and extent of organ damage by tachyzoites, and may be acute or chronic. Acute signs manifest at the time of initial infection, whereas chronic signs are associated with reactivation of encysted infection during times of immunocompromise.  

In '''cats''', disease is most severe in transplacentally infected kittens, which may be stillborn or die before weaning. Those that survive are anorexic and lethargic, with a pyrexia that does not respond to antibiotics. The lungs, liver or CNS may be necrosed, leading to signs such as dyspnoea, respiratory noise, icterus, ascites and neurological signs. Kittens infected neonatally commonly show interstitial pneumonia, necrotising hepatitis, myocardidits, non-suppurative encephalits and uveitis on post-mortem examination<Sup>1</sup>.  

In cats, disease is most severe in transplacentally infected kittens, which may be stillborn or die before weaning. Those that survive are anorexic and lethargic, with a pyrexia that does not respond to antibiotics. The lungs, liver or CNS may be necrosed, leading to signs such as dyspnoea, respiratory noise, icterus, ascites and neurological signs. Cats infected post-natally most commonly display gastrointestinal and/or respiratory signs. Again, animals may be anorexic and lethargic, with an antibiotic non-responsive fever. Vomiting, diarrhoea, icterus or abdominal effusion may be apparent, and the cat may lose weight. Ocular signs such as uveitis, iritis and detachment of the retina are also common. Neurologic signs are seen in less than 10% of patients ⁴ and may present as circling, torticollis, anisocoria, seizures, blindness or inco-ordination. Signs progress rapidly in patients suffering acute disease, in whom respiratory and/or CNS involvement is common. Chronic infections tend to follow a slower course.

Cats infected post-natally most commonly display gastrointestinal and/or respiratory signs. Again, animals may be anorexic and lethargic, with an antibiotic non-responsive fever. Vomiting, diarrhoea, icterus or abdominal effusion may be apparent, and the cat may lose weight. Ocular signs such as uveitis, iritis and detachment of the retina are also common. Neurologic signs are seen in less than 10% of patients ⁴ and may present as circling, torticollis, anisocoria, seizures, blindness or inco-ordination. Signs progress rapidly in patients suffering acute disease, in whom respiratory and/or CNS involvement is common. Chronic infections tend to follow a slower course.

In young dogs, ''Toxoplasma gondii'' infection is usually generalised, causing fever, weight loss and anorexia. Dyspnoea, diarrhoea and vomiting may also be seen. Older animals more commonly experience localised infections which are primarily associated with the neural and muscular systems. When neurological signs are seen, they usually reflect diffuse inflammation of the CNS. For example, dogs might suffer seizures, ataxia, paresis or muscle weakness. Although cardiac involvement occurs, this is not normally clinically significant. Ocular changes are rare, but are similar to those described in cats.

In young '''dogs''', ''Toxoplasma gondii'' infection is usually generalised, causing fever, weight loss and anorexia. Dyspnoea, diarrhoea and vomiting may also be seen. Older animals more commonly experience localised infections which are primarily associated with the neural and muscular systems. When neurological signs are seen, they usually reflect diffuse inflammation of the CNS. For example, dogs might suffer seizures, ataxia, paresis or muscle weakness. Although cardiac involvement occurs, this is not normally clinically significant. Ocular changes are rare, but are similar to those described in cats.

===Laboratory Tests===

===Laboratory Tests===

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.   

[[Category:Tissue_Cyst_Forming_Coccidia]][[Category:Cat]]

[[Category:Tissue_Cyst_Forming_Coccidia]][[Category:Cat]]

[[Category:To_Do_-_Lizzie]] [[Category:To_Do_-_Review]]

[[Category:To_Do_-_Review]]