Toxoplasma gondii: Difference between revisions
From IDWiki
Toxoplasma gondii
m (Text replacement - "([Ss])olid-organ" to "$1olid organ") |
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| β | * |
+ | *Protozoan parasite associated with cats and raw beef mostly known for causing opportunistic infections and congenital infections |
| β | == |
+ | ==Background== |
| β | === |
+ | ===Microbiology=== |
| β | * Protozoan parasite |
||
| β | * Organized into twelve haplotypes |
||
| + | *Protozoan parasite |
||
| β | === Epidemiology === |
||
| + | *Organized into twelve haplotypes |
||
| β | * Zoonotic disease with worldwide distribution |
||
| β | * Modes of transmission |
||
| β | ** Ingesting tissue cysts in meat, or oocytes in food or water |
||
| β | ** Solid organ transplantation, especially heart |
||
| β | ** Vertical or transplacental transmission |
||
| β | ** Case reports of lab-acquired needlestick transmission |
||
| β | ** Theoretical risk with blood transfusion |
||
| β | * Seroprevalence around 10-18% in Canada [[CiteRef::shuhaiber2003se]][[CiteRef::ford-jones1996se]] |
||
| β | ** As high as 60% in Nunavut, however [[CiteRef::messier2009se]] |
||
| β | * There are large parts of South and Central America, as well as Pacific Islands, that have very high seroprevalence [[CiteRef::pappas2009to]] |
||
| β | === |
+ | ===Epidemiology=== |
| β | * The only definitive hosts are in the Felidae family, essentially housecats and their relatives |
||
| β | * Intermediate hosts are many, and include birds and rodents |
||
| β | * An infected cat sheds oocytes into the environment (for 1 to 3 weeks), where they spend 1 to 5 days sporulating |
||
| β | ** Each sporulated oocyst contains two sporocysts, and each sporocyst contains four sporozoites |
||
| β | * Intermediate hosts ingest the sporozoites, where they mature into tachyzoites |
||
| β | * Tachyzoites migrate to brain and muscle, where they encyst and become bradyzoites |
||
| β | * Bradyzoites are ingested by a cat, completing the life cycle |
||
| + | *Zoonotic disease with worldwide distribution |
||
| β | === Pathophysiology === |
||
| + | *Modes of transmission |
||
| β | * Following ingestion, bradyzoites and sporozoites invade the small intestinal mucosa and develop into tachyzoites within the gut epithelium |
||
| + | **Ingesting tissue cysts in meat, or oocytes in food or water |
||
| β | * There, they insert themselves into monocytes and other nucleated cells |
||
| + | **Solid organ transplantation, especially heart |
||
| β | * Infected cells travel throughout the body, carrying the tachyzoite with them |
||
| + | **Vertical or transplacental transmission |
||
| β | * Infection triggers a Th-1 response |
||
| + | **Case reports of lab-acquired needlestick transmission |
||
| + | **Theoretical risk with blood transfusion |
||
| + | *Seroprevalence around 10-18% in Canada [[CiteRef::shuhaiber2003se]][[CiteRef::ford-jones1996se]] |
||
| + | **As high as 60% in Nunavut, however [[CiteRef::messier2009se]] |
||
| + | *There are large parts of South and Central America, as well as Pacific Islands, that have very high seroprevalence [[CiteRef::pappas2009to]] |
||
| + | ===Life Cycle=== |
||
| β | == Clinical Manifestations == |
||
| β | === Immunocompetent === |
||
| β | * Asymptomatic in 80% of primary infections |
||
| β | * Symptoms, when they occur, can involve fever, cervical lymphadenopathy (painless and rubbery), myalgias, and weakness/fatigue |
||
| β | ** May mimic [[infectious mononucleosis]] |
||
| β | * Can also cause [[chorioretinitis]] |
||
| β | * Severity of illness depends in part on genotype, with strain II in North America and Europe being less severe |
||
| β | ** Rarely, unusual strains may cause pneumonitis, myocarditis, meningoencephalitis, or polymyositis, and can lead to death |
||
| + | *The only definitive hosts are in the Felidae family, essentially housecats and their relatives |
||
| β | === Immunocompromised === |
||
| + | *Intermediate hosts are many, and include birds and rodents |
||
| β | * May be from primary infection or, more commonly, reactivation |
||
| + | *An infected cat sheds oocytes into the environment (for 1 to 3 weeks), where they spend 1 to 5 days sporulating |
||
| β | * Unlike in immunocompetent people, it is always a serious infection in the immunocompromised |
||
| + | **Each sporulated oocyst contains two sporocysts, and each sporocyst contains four sporozoites |
||
| β | * Major risk factor is cellular immunodeficiency, as in HIV and some immunosuppressive medications |
||
| + | *Intermediate hosts ingest the sporozoites, where they mature into tachyzoites |
||
| β | ** In HIV, beware with CD4 < 100 |
||
| + | *Tachyzoites migrate to brain and muscle, where they encyst and become bradyzoites |
||
| β | * Typically presents with CNS involvement as '''encephalitis''' |
||
| + | *Bradyzoites are ingested by a cat, completing the life cycle |
||
| β | ** Symptoms include fever, headache, lethargy, incoordination, ataxia, hemiparesis, loss of memory, dementia, or seizures |
||
| β | * Can also present with pneumonitis (especially with bone marrow transplant), chorioretinitis, or myocarditis, and rarely involves essentially any other organ |
||
| β | === |
+ | ===Pathophysiology=== |
| β | * As with other immunocompetent people, it is largely asymptomatic |
||
| β | * Only half of women can identify a significant risk factor [[CiteRef::boyer2011un]] |
||
| β | * 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 |
||
| + | *Following ingestion, bradyzoites and sporozoites invade the small intestinal mucosa and develop into tachyzoites within the gut epithelium |
||
| β | === Congenital === |
||
| + | *There, they insert themselves into monocytes and other nucleated cells |
||
| β | * Refer to [[Congenital toxoplasmosis]] |
||
| + | *Infected cells travel throughout the body, carrying the tachyzoite with them |
||
| + | *Infection triggers a Th-1 response |
||
| + | ==Clinical Manifestations== |
||
| β | == Diagnosis == |
||
| + | ===Immunocompetent=== |
||
| β | * Immunocompetent or pregnant women with primary infection: IgG/IgM serology, possibly with avidity testing for pregnant women |
||
| β | * Fetus, to rule out congenital infection following maternal primary infection: PCR of amniotic fluid |
||
| β | * Newborn, to rule out congenital infection: PCR of placenta or cord, or serology |
||
| β | * Immunocompromised patient, to diagnose cerebral or disseminated disease: PCR of blood, CSF, BAL, or tissue |
||
| β | * Patient with chorioretinitis: Parallel serologies from aqueous humour and serum, or PCR of aqueous humour |
||
| + | *Asymptomatic in 80% of primary infections |
||
| β | === Serology === |
||
| + | *Symptoms, when they occur, can involve fever, cervical lymphadenopathy (painless and rubbery), myalgias, and weakness/fatigue |
||
| β | * ELISA IgG for prior exposure; ELISA IgM for acute infection |
||
| + | **May mimic [[infectious mononucleosis]] |
||
| β | * IgM titres plateau within 1 month, and IgG within 2-3 months |
||
| + | *Can also cause [[chorioretinitis]] |
||
| β | * IgM is still detectable for months or years after infection |
||
| + | *Severity of illness depends in part on genotype, with strain II in North America and Europe being less severe |
||
| β | * IgM avidity testing can help to assess how recently the infection was acquired |
||
| + | **Rarely, unusual strains may cause pneumonitis, myocarditis, meningoencephalitis, or polymyositis, and can lead to death |
||
| β | ** Provides a measure of how tightly the antibodies bind, which is highest in early infection |
||
| β | ** A high avidity ratio (weak binding) suggests that the infection was acquired at least 4 months prior |
||
| β | === |
+ | ===Immunocompromised=== |
| β | * Not routinely done |
||
| β | * May be helpful from CSF or vitreous humour |
||
| β | * Not helpful on brain biopsy tissue |
||
| + | *May be from primary infection or, more commonly, reactivation |
||
| β | == Management == |
||
| + | *Unlike in immunocompetent people, it is always a serious infection in the immunocompromised |
||
| β | * In general, in the setting of known HIV and one or more suspicious lesions, treat empirically for CNS toxoplasmosis and reassess with repeat imaging at around 10 days, at which time there should be some response |
||
| + | *Major risk factor is cellular immunodeficiency, as in HIV and some immunosuppressive medications |
||
| β | * First-line is a combination of [[Is treated by::pyrimethamine]] and [[Is treated by::sulfadiazine]] |
||
| + | **In HIV, beware with CD4 < 100 |
||
| β | ** [[Is treated by::Pyrimethamine]] (with folinic acid) is the backbone |
||
| + | *Typically presents with CNS involvement as '''encephalitis''' |
||
| β | ** The second agent is typically [[Is treated by::sulfadiazine]], which can be replaced with [[Is treated by::clindamycin]] if needed |
||
| + | **Symptoms include fever, headache, lethargy, incoordination, ataxia, hemiparesis, loss of memory, dementia, or seizures |
||
| β | ** Encephalitis: pyrimethamine 200 mg load followed by 50-75 mg/day |
||
| + | *Can also present with pneumonitis (especially with bone marrow transplant), chorioretinitis, or myocarditis, and rarely involves essentially any other organ |
||
| β | ** Infection during pregnancy: pyrimethamine 100 mg daily for 2 days followed by 25 to 50 mg/day |
||
| β | * Alternatives |
||
| β | ** [[Is treated by::TMP-SMX]] |
||
| β | ** [[Is treated by::Atovaquone]] |
||
| β | === |
+ | ===Pregnancy=== |
| β | * [[Is treated by::Pyrimethamine]] 200 mg PO once, followed by dose based on body weight: |
||
| β | ** Body weight β€60 kg: [[Is treated by::pyrimethamine]] 50 mg PO daily + [[Is treated by::sulfadiazine]] 1000 mg PO q6h + leucovorin 10β25 mg PO daily (can increase to 50 mg daily or BID) |
||
| β | ** Body weight >60 kg: [[Is treated by::pyrimethamine]] 75 mg PO daily + [[Is treated by::sulfadiazine]] 1500 mg PO q6h + leucovorin 10β25 mg PO daily (can increase to 50 mg daily or BID) |
||
| β | * Alternatives |
||
| β | ** [[Is treated by::Pyrimethamine]] (with leucovorin) plus [[Is treated by::clindamycin]] 600 mg IV or PO q6h |
||
| β | ** [[Is treated by::TMP-SMX]] (TMP 5 mg/kg and SMX 25 mg/kg) (IV or PO) BID |
||
| β | ** [[Is treated by::Atovaquone]] 1500 mg PO BID + [[Is treated by::pyrimethamine]] (leucovorin) |
||
| β | ** [[Is treated by::Atovaquone]] 1500 mg PO BID + [[Is treated by::sulfadiazine]] |
||
| β | ** [[Is treated by::Atovaquone]] 1500 mg PO BID |
||
| + | *As with other immunocompetent people, it is largely asymptomatic |
||
| β | === Pregnancy === |
||
| + | *Only half of women can identify a significant risk factor [[CiteRef::boyer2011un]] |
||
| β | * [[Is treated by::Pyrimethamine]] is relatively contraindicated in pregnancy as it is toxic to the young fetus |
||
| + | *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 |
||
| β | * If life-threatening, should likely need treatment and consider abortion (if early in pregnancy) |
||
| β | * [[Is treated by::Spiromycin]] is safe, and decreases transmission to fetus, but is not enough to treat CNS disease |
||
| β | == |
+ | ===Congenital=== |
| β | * Cats: hand hygiene after handling cat, use gloves and wash hands when handling litter, wash litter tray with hot >60ΒΊC water, keep litter out of kitchen |
||
| β | * Soil: use gloves for gardening, wash hands after soil contact |
||
| β | * Water: avoid tap water in highly endemic countries, avoid ingestion of lake and river water |
||
| β | * Food: avoid raw oysters/clams/mussels, wash all vegetables/fruits/herbs, cook meat well down |
||
| + | *Refer to [[Congenital toxoplasmosis]] |
||
| β | == Further Reading == |
||
| + | |||
| β | * Epidemiology of and Diagnostic Strategies for Toxoplasmosis. ''Clin Microbiol Rev''. 2012;25(2):264. doi: [[https://doi.org/10.1128/CMR.05013-11 10.1128/CMR.05013-11]] |
||
| + | ==Diagnosis== |
||
| + | |||
| + | *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 |
||
| + | |||
| + | ===Serology=== |
||
| + | |||
| + | *ELISA IgG for prior exposure; ELISA IgM for acute infection |
||
| + | *IgM titres plateau within 1 month, and IgG within 2-3 months |
||
| + | *IgM is still detectable for months or years after infection |
||
| + | *IgM avidity testing can help to assess how recently the infection was acquired |
||
| + | **Provides a measure of how tightly the antibodies bind, which is highest in early infection |
||
| + | **A high avidity ratio (weak binding) suggests that the infection was acquired at least 4 months prior |
||
| + | |||
| + | ===PCR=== |
||
| + | |||
| + | *Not routinely done |
||
| + | *May be helpful from CSF or vitreous humour |
||
| + | *Not helpful on brain biopsy tissue |
||
| + | |||
| + | ==Management== |
||
| + | |||
| + | *In general, in the setting of known HIV and one or more suspicious lesions, treat empirically for CNS toxoplasmosis and reassess with repeat imaging at around 10 days, at which time there should be some response |
||
| + | *First-line is a combination of [[Is treated by::pyrimethamine]] and [[Is treated by::sulfadiazine]] |
||
| + | **[[Is treated by::Pyrimethamine]] (with folinic acid) is the backbone |
||
| + | ***[[Pyrimethamine]] 200 mg PO once followed by 50 mg PO daily if β€60 kg or 75 mg PO daily if >60 kg |
||
| + | ***[[Leucovorin]] 10-25 mg PO daily |
||
| + | **The second agent is typically [[Is treated by::sulfadiazine]], which can be replaced with [[Is treated by::clindamycin]] if needed |
||
| + | ***[[Sulfadiazine]] 1000 mg PO q6h if β€60 kg or 1500 mg PO q6h if >60 kg |
||
| + | ***[[Clindamycin]] 600 mg PO/IV qid |
||
| + | *Alternatives |
||
| + | **[[Is treated by::TMP-SMX]] |
||
| + | **[[Is treated by::Atovaquone]] 1500 mg PO bid + [[pyrimethamine]] |
||
| + | **[[Atovaquone]] 1500 mg PO bid Β± [[sulfadiazine]] |
||
| + | **[[Azithromycin]] 900-1200 mg PO daily + [[pyrimethamine]] |
||
| + | |||
| + | ===HIV=== |
||
| + | |||
| + | *[[Is treated by::Pyrimethamine]] 200 mg PO once, followed by dose based on body weight: |
||
| + | **Body weight β€60 kg: [[Is treated by::pyrimethamine]] 50 mg PO daily + [[Is treated by::sulfadiazine]] 1000 mg PO q6h + leucovorin 10β25 mg PO daily (can increase to 50 mg daily or BID) |
||
| + | **Body weight >60 kg: [[Is treated by::pyrimethamine]] 75 mg PO daily + [[Is treated by::sulfadiazine]] 1500 mg PO q6h + leucovorin 10β25 mg PO daily (can increase to 50 mg daily or BID) |
||
| + | *Alternatives |
||
| + | **[[Is treated by::Pyrimethamine]] (with leucovorin) plus [[Is treated by::clindamycin]] 600 mg IV or PO q6h |
||
| + | **[[Is treated by::TMP-SMX]] (TMP 5 mg/kg and SMX 25 mg/kg) (IV or PO) BID |
||
| + | **[[Is treated by::Atovaquone]] 1500 mg PO BID + [[Is treated by::pyrimethamine]] (leucovorin) |
||
| + | **[[Is treated by::Atovaquone]] 1500 mg PO BID + [[Is treated by::sulfadiazine]] |
||
| + | **[[Is treated by::Atovaquone]] 1500 mg PO BID |
||
| + | |||
| + | ===Pregnancy=== |
||
| + | |||
| + | *To treat active disease in mother: |
||
| + | **[[Is treated by::Pyrimethamine]] is relatively contraindicated in pregnancy as it is toxic before 14 weeks gestation |
||
| + | **If life-threatening, should likely need treatment and consider abortion (if early in pregnancy) |
||
| + | *To prevent congenital toxoplasmosis: |
||
| + | **[[Is treated by::Spiromycin]] 1 g q8h is safe throughout pregnancy, and decreases transmission to fetus, but is not enough to treat CNS disease |
||
| + | **After fetal infection is confirmed around 18 weeks, [[pyrimethamine]] 50 mg bid for 2 days then 50 mg daily, plus [[sulfadiazine]] 75 mg/kg/d split bid for 2 days then 50 mg/kg bid, plus [[leucovorin]] 10-20 mg daily |
||
| + | |||
| + | ==Prevention== |
||
| + | |||
| + | *Cats: hand hygiene after handling cat, use gloves and wash hands when handling litter, wash litter tray with hot >60ΒΊC water, keep litter out of kitchen |
||
| + | *Soil: use gloves for gardening, wash hands after soil contact |
||
| + | *Water: avoid tap water in highly endemic countries, avoid ingestion of lake and river water |
||
| + | *Food: avoid raw oysters/clams/mussels, wash all vegetables/fruits/herbs, cook meat well down |
||
| + | |||
| + | ==Further Reading== |
||
| + | |||
| + | *Epidemiology of and Diagnostic Strategies for Toxoplasmosis. ''Clin Microbiol Rev''. 2012;25(2):264. doi: [[https://doi.org/10.1128/CMR.05013-11 10.1128/CMR.05013-11]] |
||
{{DISPLAYTITLE:''Toxoplasma gondii''}} |
{{DISPLAYTITLE:''Toxoplasma gondii''}} |
||
Revision as of 18:18, 28 August 2020
- Protozoan parasite associated with cats and raw beef mostly known for causing opportunistic infections and congenital infections
Background
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 Manifestations
Immunocompetent
- Asymptomatic in 80% of primary infections
- Symptoms, when they occur, can involve fever, cervical lymphadenopathy (painless and rubbery), 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 (especially with bone marrow transplant), 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
- 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
- Refer to Congenital toxoplasmosis
Diagnosis
- 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
Serology
- ELISA IgG for prior exposure; ELISA IgM for acute infection
- IgM titres plateau within 1 month, and IgG within 2-3 months
- IgM is still detectable for months or years after infection
- IgM avidity testing can help to assess how recently the infection was acquired
- Provides a measure of how tightly the antibodies bind, which is highest in early infection
- A high avidity ratio (weak binding) suggests that the infection was acquired at least 4 months prior
PCR
- Not routinely done
- May be helpful from CSF or vitreous humour
- Not helpful on brain biopsy tissue
Management
- In general, in the setting of known HIV and one or more suspicious lesions, treat empirically for CNS toxoplasmosis and reassess with repeat imaging at around 10 days, at which time there should be some response
- First-line is a combination of pyrimethamine and sulfadiazine
- Pyrimethamine (with folinic acid) is the backbone
- Pyrimethamine 200 mg PO once followed by 50 mg PO daily if β€60 kg or 75 mg PO daily if >60 kg
- Leucovorin 10-25 mg PO daily
- The second agent is typically sulfadiazine, which can be replaced with clindamycin if needed
- Sulfadiazine 1000 mg PO q6h if β€60 kg or 1500 mg PO q6h if >60 kg
- Clindamycin 600 mg PO/IV qid
- Pyrimethamine (with folinic acid) is the backbone
- Alternatives
- TMP-SMX
- Atovaquone 1500 mg PO bid + pyrimethamine
- Atovaquone 1500 mg PO bid Β± sulfadiazine
- Azithromycin 900-1200 mg PO daily + pyrimethamine
HIV
- Pyrimethamine 200 mg PO once, followed by dose based on body weight:
- Body weight β€60 kg: pyrimethamine 50 mg PO daily + sulfadiazine 1000 mg PO q6h + leucovorin 10β25 mg PO daily (can increase to 50 mg daily or BID)
- Body weight >60 kg: pyrimethamine 75 mg PO daily + sulfadiazine 1500 mg PO q6h + leucovorin 10β25 mg PO daily (can increase to 50 mg daily or BID)
- Alternatives
- Pyrimethamine (with leucovorin) plus clindamycin 600 mg IV or PO q6h
- TMP-SMX (TMP 5 mg/kg and SMX 25 mg/kg) (IV or PO) BID
- Atovaquone 1500 mg PO BID + pyrimethamine (leucovorin)
- Atovaquone 1500 mg PO BID + sulfadiazine
- Atovaquone 1500 mg PO BID
Pregnancy
- To treat active disease in mother:
- Pyrimethamine is relatively contraindicated in pregnancy as it is toxic before 14 weeks gestation
- If life-threatening, should likely need treatment and consider abortion (if early in pregnancy)
- To prevent congenital toxoplasmosis:
- Spiromycin 1 g q8h is safe throughout pregnancy, and decreases transmission to fetus, but is not enough to treat CNS disease
- After fetal infection is confirmed around 18 weeks, pyrimethamine 50 mg bid for 2 days then 50 mg daily, plus sulfadiazine 75 mg/kg/d split bid for 2 days then 50 mg/kg bid, plus leucovorin 10-20 mg daily
Prevention
- Cats: hand hygiene after handling cat, use gloves and wash hands when handling litter, wash litter tray with hot >60ΒΊC water, keep litter out of kitchen
- Soil: use gloves for gardening, wash hands after soil contact
- Water: avoid tap water in highly endemic countries, avoid ingestion of lake and river water
- Food: avoid raw oysters/clams/mussels, wash all vegetables/fruits/herbs, cook meat well down
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. LΓ©vesque, J.-F. Proulx, L. Rochette, M. D. Libman, B. J. Ward, B. Serhir, M. Couillard, N. H. Ogden, Γ. Dewailly, B. Hubert, S. DΓ©ry, 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.
- ^ 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.
