Line 17: |
Line 17: |
| ===Pathogenesis=== | | ===Pathogenesis=== |
| | | |
− | Fatal toxoplasmosis can either result from overwhelming
| + | The outcome of primary infection depends on the immune status of the host, as well as the location a''Toxoplasma gondii'' infection may prove fatal. Bradyzoites in tissues cysts may also become activated in immunodeficient states, producing disease. However, primary infection of immunocompetent animals most often causes mild or undetectable clinical signs. |
− | 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 | | The mechanism of disease in chronic, sublethal toxoplasmosis |
| is unknown. Disease may be related in part to | | is unknown. Disease may be related in part to |