6,502
edits
Changes
Jump to navigation
Jump to search
Toxoplasmosis - Cat and Dog (view source)
Revision as of 09:28, 13 August 2010
, 09:28, 13 August 2010→Laboratory Tests
===Laboratory Tests===
===Laboratory Tests===
DIAGNOSIS OF CLINICAL FELINE
TOXOPLASMOSIS
Definitive diagnosis of clinical feline toxoplasmosis
requires demonstration of the organism in the tissues in
association with inflammation. This is usually achieved
at necropsy in cats with overwhelming tachyzoite replication.
Occasionally, a definitive diagnosis of clinical
feline toxoplasmosis is made antemortem by demonstrating
bradyzoites or tachyzoites in tissues or effusions.
Since T gondii-specific antibodies can be detected in
the serum, CSF and aqueous humour of normal animals,
as well as those with clinical signs of disease, it is not
possible to make an antemortem diagnosis of clinical
toxoplasmosis based on these tests alone. However, a
presumptive antemortem diagnosis of clinical feline
toxoplasmosis may be based on the following combination
of findings:
* Demonstration of antibodies in serum, aqueous
humour or CSF (documents exposure to T gondii);
* Demonstration of an IgM titre of above 1:64 or a
fourfold or greater increase in IgG titre, or the documentation
of local antibody production or DNA in aqueous
humour or CSF (suggests recent or active infection);
* Clinical signs of disease referable to toxoplasmosis;
* Exclusion of other common aetiologies;
* Positive response to appropriate treatment (see
below).
Routine haematology, biochemistry and urinalysis show no changes specific for toxoplasmosis. However, during ''T. gondii'' infection, several features may be seen and could be suggestive. For haematology, these might include: non-regenerative anaemia, neutrophilic leucocytosis, lymphocytosis, monocytosis, neutropenia or eosinophilia. Biochemical profiles could show increased creatine kinase, ALT, SAP, bilirubin and total protein, and proteinuria and bilirubinuria may be revealed by urinalysis.<sup>1</sup>
Routine haematology, biochemistry and urinalysis show no changes specific for toxoplasmosis. However, during ''T. gondii'' infection, several features may be seen and could be suggestive. For haematology, these might include: non-regenerative anaemia, neutrophilic leucocytosis, lymphocytosis, monocytosis, neutropenia or eosinophilia. Biochemical profiles could show increased creatine kinase, ALT, SAP, bilirubin and total protein, and proteinuria and bilirubinuria may be revealed by urinalysis.<sup>1</sup>
in cats.
in cats.
Diagnosis is made by biologic, serologic, or histologic methods, or by some combination of the above. Clinical signs of toxoplasmosis are nonspecific and are not sufficiently characteristic for a definite diagnosis. Antemortem diagnosis may be accomplished by indirect hemagglutination assay, indirect fluorescent antibody assay, latex agglutination test, or ELISA. IgM antibodies appear sooner after infection than IgG antibodies but generally do not persist past 3 mo after infection. Increased IgM titers (>1:256) are consistent with recent infection. In contrast, IgG antibodies appear by the fourth week after infection and may remain increased for years during subclinical infection. To be useful, IgG titers must be measured in paired sera from the acute and convalescent stages (3-4 wk apart) and must show at least a 4-fold increase in titer. Additionally, CSF and aqueous humor may be analyzed for the presence of tachyzoites or anti- T gondii antibodies. Postmortem, tachyzoites may be seen in tissue impression smears. Additionally, microscopic examination of tissue sections may reveal the presence of tachyzoites or bradyzoites. T gondii is morphologically similar to other protozoan parasites and must be differentiated from Sarcocystis spp (in cattle), S neurona (in horses), and Neospora caninum (in dogs).
Diagnosis is made by biologic, serologic, or histologic methods, or by some combination of the above. Clinical signs of toxoplasmosis are nonspecific and are not sufficiently characteristic for a definite diagnosis. Antemortem diagnosis may be accomplished by indirect hemagglutination assay, indirect fluorescent antibody assay, latex agglutination test, or ELISA. IgM antibodies appear sooner after infection than IgG antibodies but generally do not persist past 3 mo after infection. Increased IgM titers (>1:256) are consistent with recent infection. In contrast, IgG antibodies appear by the fourth week after infection and may remain increased for years during subclinical infection. To be useful, IgG titers must be measured in paired sera from the acute and convalescent stages (3-4 wk apart) and must show at least a 4-fold increase in titer. Additionally, CSF and aqueous humor may be analyzed for the presence of tachyzoites or anti- T gondii antibodies. Postmortem, tachyzoites may be seen in tissue impression smears. Additionally, microscopic examination of tissue sections may reveal the presence of tachyzoites or bradyzoites. T gondii is morphologically similar to other protozoan parasites and must be differentiated from Sarcocystis spp (in cattle), S neurona (in horses), and Neospora caninum (in dogs).