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Toxoplasmosis - Cat and Dog (view source)
Revision as of 20:31, 12 August 2010
, 20:31, 12 August 2010→Pathogenesis
===Pathogenesis===
===Pathogenesis===
Fatal toxoplasmosis can either result from overwhelming
primary infection or bradyzoites in tissue cysts may be
induced to replicate rapidly and disseminate again as
tachyzoites. Primary infection resulting in death generally
occurs in immunodeficient individuals, such as
transplacentally infected fetuses. Conversely, primary
infection in immunocompetent individuals usually produces
clinical signs which are mild or remain undetected.
Activation of bradyzoites occurs during severe
immunodeficiency. For example, disseminated fatal
toxoplasmosis can be induced in healthy, experimentally
T gondii oocyst shedding by experimentally inoculated cats
with and without feline immunodeficiency virus (FIV)
infection. The cats were inoculated with FIV 14 months prior
to T gondii ('TX')
infected cats by administration of extremely high doses
of glucocorticoids (Dubey and Beattie 1998). People
with chronic toxoplasmosis and the acquired immune
deficiency syndrome (AIDS) commonly develop activated
cerebral toxoplasmosis as CD4+ lymphocyte counts
diminish.
The mechanism of disease in chronic, sublethal toxoplasmosis
is unknown. Disease may be related in part to
low level tachyzoite replication. Intermittent antigenaemia
and parasitaemia have been detected in experimentally
inoculated cats (Burney and others 1999).
T gondii-specific antigens and DNA are detected in aqueous
humour in more cats with uveitis than without
uveitis, suggesting that organism replication in ocular tissues
is occurring (Lappin and others 1992b, 1996). The
organism is rarely documented in ocular tissues of cats
without fatal disease, yet not all cats with T gondii in
aqueous humour are diseased. Most cats with uveitis have
lymphocytes and plasma cells in the ciliary body (Peiffer
and Wilcock 1991). The pathogenesis of disease may
relate to immunological reactions against the organism;
immune complex formation and deposition in tissues and
delayed hypersensitivity reactions may be involved.
Interleukin 6 is a probable mediator of inflammation in
ocular toxoplasmosis (Lappin and others 1997).
==Signalment==
==Signalment==