Trypanosoma cruzi: Difference between revisions
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Trypanosoma cruzi
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== Background == |
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* Causes '''Chagas disease''' (South American trypanosomiasis) |
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*Causes '''Chagas disease''' (South American trypanosomiasis) |
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== Microbiology == |
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===Microbiology=== |
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* Protozoan parasite |
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*Protozoan parasite |
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== Life Cycle == |
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===Epidemiology=== |
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[[File:Chagas_LifeCycle_19.jpg|T. cruzi Lifecycle]] |
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*Endemic '''throughout the Americas''' from the southern half of the United States to Argentina |
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== Epidemiology == |
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**Particularly in rural, impoverished areas |
|||
**A small number of autochthonous cases of Chagas disease in the US |
|||
*Reservoirs include '''armadillos''', opossums, raccoons, woodrats, some other rodents, and domestic dogs |
|||
*'''Triatomine''' vector species for trypanosomiasis belong to the genera ''Triatoma'', ''Rhodnius'', and ''Panstrongylus'' |
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**Bugs live in substandard dwellings (especially wood, mud, or stone houses) |
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**Vector is present from southern US to southern Argentina |
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**Transmission is via feces, either in direct contact with mucous membranes (especially conjunctivae), breaks in the skin, or contaminating the bite of the insect |
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*Can also be transmitted via '''blood transfusion''' or '''vertically''' from mother to child or via '''ingestion''' of contaminated food and drink |
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===Pathophysiology=== |
|||
* Endemic '''throughout the Americas''' from the southern half of the United States to Argentina |
|||
** Particularly in rural, impoverished areas |
|||
** A small number of autochthonous cases of Chagas disease in the US |
|||
* Reservoirs include '''armadillos''', opossums, raccoons, woodrats, some other rodents, and domestic dogs |
|||
* '''Triatomine''' vector species for trypanosomiasis belong to the genera ''Triatoma'', ''Rhodnius'', and ''Panstrongylus'' |
|||
** Bugs live in substandard dwellings (especially wood, mud, or stone houses) |
|||
** Vector is present from southern US to southern Argentina |
|||
** Transmission is via feces, either in direct contact with mucous membranes (especially conjunctivae), breaks in the skin, or contaminating the bite of the insect |
|||
* Can also be transmitted via '''blood transfusion''' or '''vertically''' from mother to child or via '''ingestion''' of contaminated food and drink |
|||
*Infective metacyclic trypomastigotes from feces enter the skin or mucosa |
|||
== Pathophysiology == |
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*Multiply in host cells as amastigotes, developing into trypomastigotes intracellularly and rupturing the cell, releasing more trypomastigotes |
|||
**Chagoma develops at site of inoculation |
|||
**Intracellular amastigotes visible as characteristic pseudocysts on histopathology |
|||
*Hematogenous spread to distant sites, especially muscles, with the cycle repeating |
|||
**Especially tropic for myocardium, where it causes biventricular enlargement, thinning of ventricular walls, apical aneurysms, and mural thrombi |
|||
*Parasitemia maintained for years |
|||
==Clinical Manifestations== |
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* Infective metacyclic trypomastigotes from feces enter the skin or mucosa |
|||
* Multiply in host cells as amastigotes, developing into trypomastigotes intracellularly and rupturing the cell, releasing more trypomastigotes |
|||
** Chagoma develops at site of inoculation |
|||
** Intracellular amastigotes visible as characteristic pseudocysts on histopathology |
|||
* Hematogenous spread to distant sites, especially muscles, with the cycle repeating |
|||
** Especially tropic for myocardium, where it causes biventricular enlargement, thinning of ventricular walls, apical aneurysms, and mural thrombi |
|||
* Parasitemia maintained for years |
|||
===Acute Disease=== |
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== Clinical Manifestations == |
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*Often asymptomatic |
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=== Acute disease === |
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*Incubation period of about [[Usual incubation period::1 week]] |
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*Usually mild febrile illness, sometimes with hepatosplenomegaly, rash, edema, local inflammation |
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**Incurs in 20% of infections |
|||
**More common in children |
|||
*Nodular lesions ("chagomas") may develop at site of inoculation |
|||
**Romaña sign if periorbital, often with ipsilateral lymphadenopathy |
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**Often 1-2 weeks after exposure |
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*Acute myocarditis, pericardial effusion, and meningoencephalitis in 1-5% |
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===Indeterminate Phase=== |
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* Often asymptomatic |
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* Incubation period of about 1 week |
|||
* Usually mild febrile illness, sometimes with hepatosplenomegaly, rash, edema, local inflammation |
|||
** Incurs in 20% of infections |
|||
** More common in children |
|||
* Nodular lesions ("chagomas") may develop at site of inoculation |
|||
** Romaña sign if periorbital, often with ipsilateral lymphadenopathy |
|||
** Often 1-2 weeks after exposure |
|||
* Acute myocarditis, pericardial effusion, and meningoencephalitis in 1-5% |
|||
*Following acute infection, may enter a latent phase |
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=== Indeterminate phase === |
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===Chronic Disease=== |
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* Following acute infection, may enter a latent phase |
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*Following acute infection can remain asymptomatic (indeterminate form) |
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=== Chronic disease === |
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*Cardiac complications in 25-30% (1.5-5% per year) |
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**Non-ischemic dilated biventricular (right more than left) cardiomyopathy with heart failure |
|||
**Apical aneurysms and mural thrombi |
|||
**Conduction defects, with heart blocks, bundle branch blocks, sinus node dysfunction, bradycardia, and ventricular arrhythmias |
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**Can cause sudden cardiac death |
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*GI involvement in 10-15% |
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**Megaesophagus, with dysphagia, odynophagia, chest pain, cough, and regurgitation |
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***May result in aspiration and recurrent pneumonias |
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**Megacolon, with constipation and abdominal pain |
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*Meningoencephalitis |
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*Other: polyneuropathy, stroke syndrome |
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===Immunocompromised Patients=== |
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* Following acute infection can remain asymptomatic (indeterminate form) |
|||
* Cardiac complications in 25-30% (1.5-5% per year) |
|||
** Non-ischemic dilated biventricular (right more than left) cardiomyopathy with heart failure |
|||
** Apical aneurysms and mural thrombi |
|||
** Conduction defects, with heart blocks, bundle branch blocks, sinus node dysfunction, bradycardia, and ventricular arrhythmias |
|||
** Can cause sudden cardiac death |
|||
* GI involvement in 10-15% |
|||
** Megaesophagus, with dysphagia, odynophagia, chest pain, cough, and regurgitation |
|||
*** May result in aspiration and recurrent pneumonias |
|||
** Megacolon, with constipation and abdominal pain |
|||
* Meningoencephalitis |
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* Other: polyneuropathy, stroke syndrome |
|||
*May have reactivation following immune suppression or HIV |
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=== Immunocompromised patients === |
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*Severe acute infection; may have skin lesions and cerebral masses/abscesses |
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*Meningoencephalitis |
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==Diagnosis== |
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* May have reactivation following immune suppression or HIV |
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* Severe acute infection; may have skin lesions and cerebral masses/abscesses |
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* Meningoencephalitis |
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== |
===Acute Disease=== |
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*'''Direct microscopy''' blood film or tissue biopsy (e.g. lymph node, bone marrow, pericardial fluid, CSF) |
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=== Acute disease === |
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**In immunocompromised, these other samples are even more important |
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*Hemoculture is only 50% sensitive and takes several weeks |
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*Serology for IgM is useless |
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*'''PCR''' is sensitive and specific |
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*Xenodiagnosis |
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===Indeterminate and Chronic Disease=== |
|||
* '''Direct microscopy''' blood film or tissue biopsy (e.g. lymph node, bone marrow, pericardial fluid, CSF) |
|||
** In immunocompromised, these other samples are even more important |
|||
* Hemoculture is only 50% sensitive and takes several weeks |
|||
* Serology for IgM is useless |
|||
* '''PCR''' is sensitive and specific |
|||
* Xenodiagnosis |
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*No gold standard |
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=== Indeterminate and chronic disease === |
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*Serology for IgG is most useful |
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**Detectable after 6 to 9 months following infection |
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**Many assays (ELISA, indirect hemagglutination, chemiluminescence, and IFA) |
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*PCR (of blood) less sensitive |
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==Management== |
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* No gold standard |
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* Serology for IgG is most useful |
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** Detectable after 6 to 9 months following infection |
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** Many assays (ELISA, indirect hemagglutination, chemiluminescence, and IFA) |
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* PCR (of blood) less sensitive |
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== |
===Acute=== |
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*Treatment is most useful in acute disease, congenital Chagas, and children with chronic infection up to 18 years |
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=== Acute === |
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**It can decrease illness severity and mortality |
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**Start ASAP before infection can become established |
|||
**However, treatment may not result in parasitologic cure |
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*Treatment options |
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**Nifurtimox: 90-120 day treatment course; AEs include anorexia, weight loss, neurologic symptoms |
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**Benznidazole: 60 day treatment course; AEs include hypersensitivity, GI upset, rare polyneuropathy and agranulocytosis |
|||
*Adverse events are common during treatment |
|||
===Chronic=== |
|||
* Treatment is most useful in acute disease, congenital Chagas, and children with chronic infection up to 18 years |
|||
** It can decrease illness severity and mortality |
|||
** Start ASAP before infection can become established |
|||
** However, treatment may not result in parasitologic cure |
|||
* Treatment options |
|||
** Nifurtimox: 90-120 day treatment course; AEs include anorexia, weightloss, neurologic symptoms |
|||
** Benznidazole: 60 day treatment course; AEs include hypersensitivity, GI upset, rare polyneuropathy and agranulocytosis |
|||
* Adverse events are common during treatment |
|||
*Less clear benefit to antiparasitic treatment |
|||
=== Chronic === |
|||
*Cardiac disease |
|||
**May benefit from pacemaker in patients with conduction disease |
|||
***Monitor with ECG q6mo |
|||
**May need heart transplantation, though this can become complicated by ongoing chronic infection or recrudescence |
|||
*Megaesophagus: balloon dilatation or surgical management |
|||
*Megacolon may need surgical management |
|||
==Prevention== |
|||
* Less clear benefit to antiparasitic treatment |
|||
* Cardiac disease |
|||
** May benefit from pacemaker in patients with conduction disease |
|||
*** Monitor with ECG q6mo |
|||
** May need heart transplantation, though this can become complicated by ongoing chronic infection or recrudescence |
|||
* Megaesophagus: balloon dilatation or surgical management |
|||
* Megacolon may need surgical management |
|||
*Screening immigrants and then following up with regular cardiac screening, if positive |
|||
== Prevention == |
|||
*Avoid sleeping in dilapidated dwellings in endemic countries, use insect repellent and bed nets |
|||
*Improve housing in endemic areas |
|||
===Canadian Blood Services=== |
|||
* Screening immigrants and then following up with regular cardiac screening, if positive |
|||
* Avoid sleeping in dilapidated dwellings in endemic countries, use insect repellent and bed nets |
|||
* Improve housing in endemic areas |
|||
*Samples are only tested for antibodies when increased risk is present, determined by the donor screening questions |
|||
=== Canadian Blood Services === |
|||
*No reported cases since screening began in 2010 |
|||
* Samples are only tested for antibodies when increased risk is present, determined by the donor screening questions |
|||
* No reported cases since screening began in 2010 |
|||
{{DISPLAYTITLE:''Trypanosoma cruzi''}} |
{{DISPLAYTITLE:''Trypanosoma cruzi''}} |
Latest revision as of 15:43, 6 March 2023
Background
- Causes Chagas disease (South American trypanosomiasis)
Microbiology
- Protozoan parasite
Epidemiology
- Endemic throughout the Americas from the southern half of the United States to Argentina
- Particularly in rural, impoverished areas
- A small number of autochthonous cases of Chagas disease in the US
- Reservoirs include armadillos, opossums, raccoons, woodrats, some other rodents, and domestic dogs
- Triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and Panstrongylus
- Bugs live in substandard dwellings (especially wood, mud, or stone houses)
- Vector is present from southern US to southern Argentina
- Transmission is via feces, either in direct contact with mucous membranes (especially conjunctivae), breaks in the skin, or contaminating the bite of the insect
- Can also be transmitted via blood transfusion or vertically from mother to child or via ingestion of contaminated food and drink
Pathophysiology
- Infective metacyclic trypomastigotes from feces enter the skin or mucosa
- Multiply in host cells as amastigotes, developing into trypomastigotes intracellularly and rupturing the cell, releasing more trypomastigotes
- Chagoma develops at site of inoculation
- Intracellular amastigotes visible as characteristic pseudocysts on histopathology
- Hematogenous spread to distant sites, especially muscles, with the cycle repeating
- Especially tropic for myocardium, where it causes biventricular enlargement, thinning of ventricular walls, apical aneurysms, and mural thrombi
- Parasitemia maintained for years
Clinical Manifestations
Acute Disease
- Often asymptomatic
- Incubation period of about 1 week
- Usually mild febrile illness, sometimes with hepatosplenomegaly, rash, edema, local inflammation
- Incurs in 20% of infections
- More common in children
- Nodular lesions ("chagomas") may develop at site of inoculation
- Romaña sign if periorbital, often with ipsilateral lymphadenopathy
- Often 1-2 weeks after exposure
- Acute myocarditis, pericardial effusion, and meningoencephalitis in 1-5%
Indeterminate Phase
- Following acute infection, may enter a latent phase
Chronic Disease
- Following acute infection can remain asymptomatic (indeterminate form)
- Cardiac complications in 25-30% (1.5-5% per year)
- Non-ischemic dilated biventricular (right more than left) cardiomyopathy with heart failure
- Apical aneurysms and mural thrombi
- Conduction defects, with heart blocks, bundle branch blocks, sinus node dysfunction, bradycardia, and ventricular arrhythmias
- Can cause sudden cardiac death
- GI involvement in 10-15%
- Megaesophagus, with dysphagia, odynophagia, chest pain, cough, and regurgitation
- May result in aspiration and recurrent pneumonias
- Megacolon, with constipation and abdominal pain
- Megaesophagus, with dysphagia, odynophagia, chest pain, cough, and regurgitation
- Meningoencephalitis
- Other: polyneuropathy, stroke syndrome
Immunocompromised Patients
- May have reactivation following immune suppression or HIV
- Severe acute infection; may have skin lesions and cerebral masses/abscesses
- Meningoencephalitis
Diagnosis
Acute Disease
- Direct microscopy blood film or tissue biopsy (e.g. lymph node, bone marrow, pericardial fluid, CSF)
- In immunocompromised, these other samples are even more important
- Hemoculture is only 50% sensitive and takes several weeks
- Serology for IgM is useless
- PCR is sensitive and specific
- Xenodiagnosis
Indeterminate and Chronic Disease
- No gold standard
- Serology for IgG is most useful
- Detectable after 6 to 9 months following infection
- Many assays (ELISA, indirect hemagglutination, chemiluminescence, and IFA)
- PCR (of blood) less sensitive
Management
Acute
- Treatment is most useful in acute disease, congenital Chagas, and children with chronic infection up to 18 years
- It can decrease illness severity and mortality
- Start ASAP before infection can become established
- However, treatment may not result in parasitologic cure
- Treatment options
- Nifurtimox: 90-120 day treatment course; AEs include anorexia, weight loss, neurologic symptoms
- Benznidazole: 60 day treatment course; AEs include hypersensitivity, GI upset, rare polyneuropathy and agranulocytosis
- Adverse events are common during treatment
Chronic
- Less clear benefit to antiparasitic treatment
- Cardiac disease
- May benefit from pacemaker in patients with conduction disease
- Monitor with ECG q6mo
- May need heart transplantation, though this can become complicated by ongoing chronic infection or recrudescence
- May benefit from pacemaker in patients with conduction disease
- Megaesophagus: balloon dilatation or surgical management
- Megacolon may need surgical management
Prevention
- Screening immigrants and then following up with regular cardiac screening, if positive
- Avoid sleeping in dilapidated dwellings in endemic countries, use insect repellent and bed nets
- Improve housing in endemic areas
Canadian Blood Services
- Samples are only tested for antibodies when increased risk is present, determined by the donor screening questions
- No reported cases since screening began in 2010