Toxoplasma gondii: Difference between revisions

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Toxoplasma gondii
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== Diagnosis ==
 
== Diagnosis ==
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{| class="wikitable"
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! Patient population
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! Diagnostic testing
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|-
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| Immunocompetent or pregnant women with primary infection
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| IgG/IgM serology, possibly with avidity testing for pregnant women
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|-
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| Fetus, to rule out congenital infection following maternal primary infection
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| PCR of amniotic fluid
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|-
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| Newborn, to rule out congenital infection
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| PCR of placenta or cord, or serology
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|-
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| Immunocompromised patient, to diagnose cerebral or disseminated disease
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| PCR of blood, CSF, BAL, or tissue
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|-
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| Patient with chorioretinitis
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| Parallel serologies from aqueous humour and serum, or PCR of aqueous humour
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|}
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* IgM avidity testing can help to assess how recently the infection was acquired
   
 
== Management ==
 
== Management ==

Revision as of 20:43, 18 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
  • 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

  • As with other immunocompetent people, it is largely asymptomatic
  • Only half of women can identify a significant risk factor 5
  • Can cause fetal loss
  • Risk of transmission to fetus is with parasitemia associated with primary infection, so women who are seropositive are not at risk of having a child with congenital infection

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

Patient population Diagnostic testing
Immunocompetent or pregnant women with primary infection IgG/IgM serology, possibly with avidity testing for pregnant women
Fetus, to rule out congenital infection following maternal primary infection PCR of amniotic fluid
Newborn, to rule out congenital infection PCR of placenta or cord, or serology
Immunocompromised patient, to diagnose cerebral or disseminated disease PCR of blood, CSF, BAL, or tissue
Patient with chorioretinitis Parallel serologies from aqueous humour and serum, or PCR of aqueous humour
  • IgM avidity testing can help to assess how recently the infection was acquired

Management

Further Reading

  • Epidemiology of and Diagnostic Strategies for Toxoplasmosis. Clin Microbiol Rev. 2012;25(2):264. doi: [10.1128/CMR.05013-11]

References

  1. ^  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.
  2. ^  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.
  3. ^  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.
  4. ^  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.
  5. ^  K. Boyer, D. Hill, E. Mui, K. Wroblewski, T. Karrison, J. P. Dubey, M. Sautter, A. G. Noble, S. Withers, C. Swisher, P. Heydemann, T. Hosten, J. Babiarz, D. Lee, P. Meier, R. McLeod. Unrecognized Ingestion of Toxoplasma gondii Oocysts Leads to Congenital Toxoplasmosis and Causes Epidemics in North America. Clinical Infectious Diseases. 2011;53(11):1081-1089. doi:10.1093/cid/cir667.