Trypanosoma cruzi

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Trypanosoma cruzi /
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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
  • 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, weightloss, 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
  • 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