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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 results are often seen in ''T. gondii'' infection. For example, most cats show a mild non-regenerative anaemia, and 50% of pateients are initially leukopenic due to lymphopenia. Neutropenia may occur in conjunction with lymphopenia, and leukocytosis may occur during recovery<sup>4</sup>. Most patients also show and increase in creatine kinase, ALT, SAP, and hypoalbuminaemia is also common<sup>1, 4</sup>. 25% of cats show hyperbilirubinemia and icterus, and 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 results are often seen in ''T. gondii'' infection. For example, most cats show a mild non-regenerative anaemia, and 50% of pateients are initially leukopenic due to lymphopenia. Neutropenia may occur in conjunction with lymphopenia, and leukocytosis may occur during recovery<sup>4</sup>. Most patients also show and increase in creatine kinase, ALT, SAP, and hypoalbuminaemia is also common<sup>1, 4</sup>. 25% of cats show hyperbilirubinemia and icterus, and pancreatitis may cause low to low normal serum calcium. A mild proteinuria and bilirubinuria are often revealed by urinalysis.
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Demonstration of antibodies in serum, aqueous humour or CSF 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,
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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,
immunofluorescent antibody testing, western blot immunoassay, Sabin-Feldmann dye test, and 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<sup>5, 6</sup> and so careful interpretation is necessary, particularly since the IgM antibody class appears to correlate more closely to clinical disease than IgG<sup>7</sup>.
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immunofluorescent antibody testing, Sabin-Feldmann dye test, and 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<sup>5, 6</sup> and so careful interpretation is necessary, particularly since the IgM antibody class appears to correlate more closely to clinical disease than IgG<sup>7</sup>. 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.
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A more practically useful form of serology is examination IgM in aqueous humour or cerebrospinal fluid. Demonstration of an IgM titre of above 1:64 or a
T gondii-specific IgG can be detected by ELISA in
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serum in the majority of healthy, experimentally inoculated
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cats within three to four weeks of infection (Lappin
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1996, Dubey and Lappin 1998). IgG antibody titres can
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be detected for at least six years after infection (Dubey
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1995); since the organism probably persists for life, IgG
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antibodies probably do as well. Single, high IgG titres do
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not necessarily suggest recent or active infection -
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healthy cats commonly have titres of above 10,000 six
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years after experimental induction of toxoplasmosis. The
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demonstration of an increasing IgG titre can document
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recent or active disease but, in experimentally infected
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cats, the time span from the first detectable positive IgG
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titre to the maximal IgG titre is approximately two to
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three weeks. Many cats with sublethal clinical toxoplasmosis
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have chronic, mild clinical signs and may not be
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evaluated serologically until their IgG antibody titres
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have reached their maximal values. In humans and cats
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with reactivation of chronic toxoplasmosis, IgG titres
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rarely increase.
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Western blot immunoassay can be used to determine
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the T gondii antigens recognised by humoral immune
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responses. Transplacentally infected kittens could be distinguished
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from T gondii-naive kittens with antibodies in
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serum from colostrum ingestion by comparing antigen
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recognition patterns between the queen and kittens.
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* Demonstration of an IgM titre of above 1:64 or a
   
fourfold or greater increase in IgG titre, or the documentation
 
fourfold or greater increase in IgG titre, or the documentation
 
of local antibody production or DNA in aqueous
 
of local antibody production or DNA in aqueous
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