Skip to main content Accessibility help
×
Hostname: page-component-7c8c6479df-8mjnm Total loading time: 0 Render date: 2024-03-28T19:36:59.768Z Has data issue: false hasContentIssue false

197 - Toxoplasma

from Part XXIV - Specific Organisms – Parasites

Published online by Cambridge University Press:  05 March 2013

Roderick Go
Affiliation:
SUNY School of Medicine at Stony Brook
Benjamin J. Luft
Affiliation:
SUNY School of Medicine at Stony Brook
David Schlossberg
Affiliation:
Temple University School of Medicine, Philadelphia
Get access

Summary

Toxoplasmosis, caused by the obligate intracellular parasite Toxoplasma gondii, is responsible for significant morbidity and mortality throughout the world. Although it has long been recognized as a serious congenital disease, it is only with the advent of acquired immunodeficiency syndrome (AIDS) and the increased use of immunosuppressive therapy that toxoplasmosis has reached epidemic proportions.

Humans are incidental hosts in the life cycle of T. gondii. Acute infection occurs via ingestion of meats or beverages contaminated with tissue cysts or tachyzoites or by handling cats, the definitive host. Once the human host develops an adequate immune response, tissue cysts are formed and a chronic or latent infection ensues. Antibodies against T. gondii will be present in serum for life. When a chronically infected person becomes immunocompromised, particularly with defects in cell-mediated immunity, devastating reactivation of the latent infection may occur.

CLINICAL MANIFESTATIONS AND DIAGNOSIS

Toxoplasmosis in the AIDS patient is most commonly manifested by toxoplasmic encephalitis (TE), usually alone but sometimes as part of a multiorgan infection. Isolated organ involvement without central nervous system (CNS) disease is uncommon. In most cases, TE develops when the CD4 lymphocyte count falls below 100 mm3, although the risk of developing overt infection begins when CD4 counts fall below 200 mm3. The clinical manifestations of TE are protean, including signs and symptoms of focal or generalized neurologic dysfunction or more commonly both, depending on the number, size, and location of the lesions.

Type
Chapter
Information
Publisher: Cambridge University Press
Print publication year: 2008

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

Save book to Kindle

To save this book to your Kindle, first ensure coreplatform@cambridge.org is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about saving to your Kindle.

Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

Find out more about the Kindle Personal Document Service.

Available formats
×

Save book to Dropbox

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Dropbox.

Available formats
×

Save book to Google Drive

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.

Available formats
×