Toxoplasma gondii: Difference between revisions
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Toxoplasma gondii
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=== Congenital === |
=== Congenital === |
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* Can be acquired during maternal parasitemia associated with primary infection |
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** Risk of transplacental infection of fetus is lowest in first trimester and highest in third |
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** Symptom severity increases is highest in first trimester and lowest in third |
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* Others: thrombocytopenia, hepatitis, hepatosplenomegaly |
* Others: thrombocytopenia, hepatitis, hepatosplenomegaly |
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Revision as of 00:24, 19 September 2019
- Protozoan parasite associated with cats and raw beef mostly known for causing opportunistic infections and congenital infections
Microbiology
- Protozoan parasite
- Organized into twelve haplotypes
Epidemiology
- Zoonotic disease with worldwide distribution
- Modes of transmission
- Ingesting tissue cysts in meat, or oocytes in food or water
- Solid-organ transplantation, especially heart
- Vertical or transplacental transmission
- Case reports of lab-acquired needlestick transmission
- Theoretical risk with blood transfusion
- Seroprevalence around 10-18% in Canada 12
- As high as 60% in Nunavut, however 3
- There are large parts of South and Central America, as well as Pacific Islands, that have very high seroprevalence 4
Life Cycle
- The only definitive hosts are in the Felidae family, essentially housecats and their relatives
- Intermediate hosts are many, and include birds and rodents
- An infected cat sheds oocytes into the environment (for 1 to 3 weeks), where they spend 1 to 5 days sporulating
- Each sporulated oocyst contains two sporocysts, and each sporocyst contains four sporozoites
- Intermediate hosts ingest the sporozoites, where they mature into tachyzoites
- Tachyzoites migrate to brain and muscle, where they encyst and become bradyzoites
- Bradyzoites are ingested by a cat, completing the life cycle
Pathophysiology
- Following ingestion, bradyzoites and sporozoites invade the small intestinal mucosa and develop into tachyzoites within the gut epithelium
- There, they insert themselves into monocytes and other nucleated cells
- Infected cells travel throughout the body, carrying the tachyzoite with them
- Infection triggers a Th-1 response
Clinical Presentation
Immunocompetent
- Asymptomatic in 80% of primary infections
- Symptoms, when they occur, can involve fever, cervical lymphadenopathy, myalgias, and weakness/fatigue
- May mimic infectious mononucleosis
- Can also cause chorioretinitis
- Severity of illness depends in part on genotype, with strain II in North America and Europe being less severe
- Rarely, unusual strains may cause pneumonitis, myocarditis, meningoencephalitis, or polymyositis, and can lead to death
Immunocompromised
- May be from primary infection or, more commonly, reactivation
- Unlike in immunocompetent people, it is always a serious infection in the immunocompromised
- Major risk factor is cellular immunodeficiency, as in HIV and some immunosuppressive medications
- In HIV, beware with CD4 < 100
- Typically presents with CNS involvement as encephalitis
- Symptoms include fever, headache, lethargy, incoordination, ataxia, hemiparesis, loss of memory, dementia, or seizures
- Can also present with pneumonitis, chorioretinitis, or myocarditis, and rarely involves essentially any other organ
Pregnancy
Congenital
- Can be acquired during maternal parasitemia associated with primary infection
- Risk of transplacental infection of fetus is lowest in first trimester and highest in third
- 85% of infected babies are asymptomatic at birth; 15% symptomatic
- Symptom severity increases is highest in first trimester and lowest in third
- Classic triad of chorioretinitis (most common), intraparenchymal cerebral calcifications, and hydrocephalus
- Others: thrombocytopenia, hepatitis, hepatosplenomegaly
Diagnosis
Management
Further Reading
- Epidemiology of and Diagnostic Strategies for Toxoplasmosis. Clin Microbiol Rev. 2012;25(2):264. doi: [10.1128/CMR.05013-11]
References
- ^ Samar Shuhaiber, Gideon Koren, Rada Boskovic, Thomas R Einarson, Offie Porat Soldin, Adrienne Einarson. Seroprevalence of Toxoplasma gondiiinfection among veterinary staff in Ontario, Canada (2002): Implications for teratogenic risk. BMC Infectious Diseases. 2003;3(1). doi:10.1186/1471-2334-3-8.
- ^ EL Ford-Jones, I Kitai, M Corey, R Notenboom, N Hollander, E Kelly, H Akoury, G Ryan, I Kyle, R Gold. Seroprevalence of Toxoplasma Antibody in a Toronto Population. Canadian Journal of Infectious Diseases. 1996;7(5):326-328. doi:10.1155/1996/172651.
- ^ V. Messier, B. Lévesque, J.-F. Proulx, L. Rochette, M. D. Libman, B. J. Ward, B. Serhir, M. Couillard, N. H. Ogden, É. Dewailly, B. Hubert, S. Déry, C. Barthe, D. Murphy, B. Dixon. Seroprevalence of Toxoplasma gondii Among Nunavik Inuit (Canada). Zoonoses and Public Health. 2009;56(4):188-197. doi:10.1111/j.1863-2378.2008.01177.x.
- ^ Georgios Pappas, Nikos Roussos, Matthew E. Falagas. Toxoplasmosis snapshots: Global status of Toxoplasma gondii seroprevalence and implications for pregnancy and congenital toxoplasmosis. International Journal for Parasitology. 2009;39(12):1385-1394. doi:10.1016/j.ijpara.2009.04.003.
