ISSN 2398-2969      



Dan Ohad

Gad Baneth

Synonym(s): Chagas' disease


  • Cause: hemoflagellated trypanozoon protozoa:
    • Trypanosoma cruzi in South, Central and rarely, in North America.
    • Trypanosoma brucei brucei or Trypanosoma congolense in Africa.
  • Incidence: very low in North America (8% reported seropositive in Texas; 5% in Louisiana).
  • Signs: weakness, lethargy, ascites, cardiac arrhythmia, ataxia, collapse and sudden death.
  • Diagnosis: trypomastigote ("blood form") parasites identified in wet, thick peripheral and buffy coat blood films during acute disease; serological tests; cultures; xenodiagnosis.
  • Treatment:
    • For T cruzi: nifurtimox when organisms found in blood. Allopurinol and benznidazole for chronic stages.
    • For T brucei brucei and T congolense: isometamidium chloride, cymelarsan, difluoromethylornithinie (DMFO) with diminazene.
  • Prognosis: guarded for acute phase, poor for chronic phase as outcome usually fatal.



  • Flagellate protozoan hemoparasites.
    • Class: Zoomastigophoera.
    • Family: Trypanosomatidae.
    • Subgenus: Trypanozoon.
  • Feline trypanosomiasis:
    • Cats may be susceptible to specific S American isolates of T cruzi.
    • Domestic feline trypanosomiasis not reported in N America.
  • Specific canine trypanozoon spp:
    • Trypanosoma cruzi in South, Central and southern parts of N America.
  • Caninetrypanozoon spp of the subgenus Nannomonas in Africa (T brucei brucei and T congolense).
  • Insect vectors:
    • Africa: tsetse flies of the genus, Glossina.
    • Americas:
      • Family: Reduviid.
      • Subfamily: Triatomae Trypanosomiasis: triatoma gerstaeckeri (kissing bug or assassin bug).

Reservoir mammal hosts

  • South America:
    • Opossums.
    • Raccoons.
    • Armadillos.
    • Dogs.
    • Cats.
    • Guinea pigs.
    • Capybaras.
    • Human beings.
  • Foci in southern parts of eastern and central N American states:
    • Opossums.
    • Raccoons.
  • Foci in southern parts of western N American states:
    • Mice.
    • Squirrels.
    • Rats.
  • Africa:
    • Many different wildlife spp.
    • Domestic mammals.
    • Livestock.

Life cycle and infection

  • Three morphologic forms exist:
    • Blood form: trypomastigote Trypanosomiasis: tryptomastigote.
    • Intracellular form: amastigote.
    • Vector form: epimastigote (transformed from trypomastigote form in hind gut of American triatomae vector and in salivary glands of African tsetse vector).
  • Routes of African canine trypanosomiasis infection:
    • Epimastigotes are inoculated by the tsetse fly, from salivary glands to mammalian host, during blood meals. Transform into trypomastigotes in mammalian host circulation.
  • Routes of American canine trypanosomiasis infection:
    • Most common route: trypomastigotes deposited in vector's feces when taking a blood meal, contaminating fresh bite wound.
    • Less common routes of infection:
      • Oral ingestion of infected vectors in opossums and possibly, in dogs.
      • Blood transfusions (potentially more important zoonotic risk in N America than others routes).
      • Transmammary or transplacental.
      • Ingestion of:
        • Meat contaminated with vector-feces.
        • Meat from infected animals.
        • Milk from infected lactating animals.
  • Hematogenous (T cruzi) and hemolymphatic (T brucei brucei, T congolense) dissemination followed by trypomastigote entry into macrophages and locally or systemically into reticuloendothelial (and in some cases, neurological) system organs, skeletal and commonly, cardiac myocytes.
  • Intracellular transformation into amastigotes.
  • Loss of flagellae.
  • Rapid intracellular multiplication of amastigotes by binary fission.
  • Intracellular transformation of amastigotes back into trypomastigotes.
  • Rupture of infected cells results in both massive local cell destruction and in massive release of trypomastigotes into circulation, resulting in acute parasitemia before effective immunity develops.
  • Trypomastigotes reinfect other cells as well as enter macrophages and organs of reticuloendothelial system.
  • Insect vectors become infected by ingesting circulating trypomastigotes when taking blood meal from mammalian hosts.
  • Trypomastigotes transform into epimastigotes (T cruzi in vector's midgut; T brucei brucei orT congolense in salivary glands), which then multiply by binary fission.
  • Epimastigotes differentiate back into infective metacyclic trypomastigotes in vector's GI system (salivary glands in Glossinae spp or hind gut in Triatomae spp).


Immunological aspects

  • Rapid intracellular multiplication cycles (by binary fission) of amastigotes prior to intracellular transformation to trypomastigote form, ensure rapid rise in parasitemia once cells rupture and release large quantities of trypomastigotes, prior to development of effective immunity.
  • Trypomastigotes also escape immune response by being transported throughout body primarily within macrophages.
  • African trypanozoons further escape immune defense system by continually undergoing antigenic variation of outer glycoprotein coat.
  • Profound immunosuppression probably occurs in acutely infected dogs due to altered interleukin-2 activity and may be reason for development of distemper-like neurological signs Canine distemper disease secondary to meningoencephalitis Meningitis in puppies.
  • Spleen is an important organ for immune response against T brucei brucei and T congolense. Although splenectomy delays onset of anemia Anemia: immune mediated hemolytic , increased parasitemia and febrile response follow.
  • Immunological phenomena thought to play major role in pathogenesis of chronic myocardial disease Heart: myocarditis.


Trypanosoma cruzi (the Americas)

  • Acute disease signs are attributed to cell damage and destruction during trypomastigote rupture from host cells, especially cardiac myocytes and in some cases, from neurological tissue.
  • Chronic, progressive cardiomegaly occurs through an unknown pathogenetic process. Speculated mechanisms include:
    • Impact of cardiotoxic parasite products.
    • Autoimmunity against autonomic nervous system.
    • Microvascular coronary spasm leading to progressive myocardial ischemia and cell death, followed by replacement fibrosis.

Trypanosoma brucei brucei and Trypanosoma congolense (Africa)

  • Inflammation disseminating through hemolymphatic vessels to lymph nodes and spleen.
  • Perimyocarditis.
  • Anemia, thrombocytopenia, leukocytosis and possibly DIC Disseminated intravascular coagulation.
  • Central nervous system invasion with terminal, diffuse meningoencephalitis.


  • Incubation period is 2-4 weeks.
  • Parasitemia develops within days and peaks 2-3 weeks post infection, coinciding with acute clinical signs.
  • Earlier clinical signs may/may not coincide with earlier, smaller magnitude infective cycles where newly formed trypomastigotes burst out of cells to infect other tissues and transform back into intracellular amastigotes in new infection sites.
  • By 4 weeks post infection, parasitemia is no longer detectable, likely due to rising specific (humoral) immune response to parasite. Acute clinical signs resolve accordingly.
  • Dogs remain asymptomatic for ~8 months to ~3 years, during which there is:
    • Progressive myocardial damage.
    • Myocyte degeneration.
    • Possible replacement fibrosis leading eventually to bilateral cardiomegaly and both systolic and diastolic dysfunction.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Herwaldt B L, Grijalva M J, Newsome A L et al (2000) Use of polymerase chain reaction to diagnose the fifth reported US case of autochthonous transmission of Trypansoma cruzi, in Tennessee, 1998. J Infect Dis 181 (1), 395-399 PubMed.
  • Andrade Z A, Andrade S G, Sadigursky M et al (1997) The indeterminate phase of Chagas disease: ultrastructural characterization of cardiac changes in the canine model. Am J Trop Med Hyg 57 (3), 328-336 PubMed.
  • Kirchhoff L V, Votava J R, Ochs D E et al (1996) Comparison of PCR and microscopic methods for detecting Trypanosoma cruzi. J Clin Microbiol 34 (5), 1171-1175 PubMed.
  • Barr S C, van Beek O, Carlisle-Nowak M S et al (1995) Trypanosoma cruzi infection in Walker Hounds from Virginia. Am J Vet Res 56 (8), 1037-1044 PubMed.
  • Harrus S, Harmelin A, Presenty B & Bark H (1995) Trypanosoma congolense infection in two dogs. J Small Anim Pract 36 (2), 83-86 PubMed.
  • Andrade Z A, Andrade S G, Correa R et al (1994) Myocardial changes in acute Trypanosoma cruzi infection: ultrastructural evidence of immune damage and the role of microangiopathy. Am J Pathol 144 (6), 1403-1411 PubMed.
  • Egbe-Nwiyi T N & Anita R E (1993) The effect of trypanocidal drug treatment on the hematological changes in Trypanosoma brucei brucei infected splenectomised dogs. Vet Parasitol 50 (1-2), 23-33 PubMed.
  • Barr S C, Holmes R A & Klei T R (1992) Electrocardiographic and echocardiographic features of trypanosomiasis in dogs inoculated with North American Trypanosoma cruzi isolates. Am J Vet Res 53 (4), 521-527 PubMed.
  • Karsten V, Davis C & Kuhn R (1992) Trypanosoma cruzi in wild raccoons and opossums in North Carolina. J Parasitol 78 (3), 547-549 PubMed.
  • Tanowitz H B, Kirchhoff L V, Simon D et al (1992) Chagas' disease. Clin Microbiol Rev (4), 400-419 PubMed.
  • Barr S C (1991) Canine American trypanosomiasis. Comp Cont Educ Pract Vet 13, 745-755.
  • Barr S C, Brown C, Dennis V A et al (1991) The lesions and prevalence of Trypanosoma cruzi in opposums and armadillos from southern Louisiana. J Parasitol 77 (4), 624-627 PubMed.
  • Barr S C, Dennis V A & Klei T R (1991) Serologic and blood culture survey of Trypanosoma cruzi for infection in four canine populations of southern Louisiana. Am J Vet Res 52 (4), 570-573 PubMed.
  • Barr S C, Gossett K A & Klei T R (1991) Clinical, clinicopathologic, and parasitologic observations of trypanosomiasis in dogs infected with North American Trypanosoma cruzi isolates. Am J Vet Res 52 (6), 954-960 PubMed.
  • Barr S C, Schmidt S P, Brown C C et al (1991) Pathologic features of dogs inoculated with North American Trypanosoma cruzi isolates. Am J Vet Res 52 (12) , 2033-2039 PubMed.
  • Berger S L, Palmer R H, Hodges C C et al (1991) Neurologic manifestations of trypanosomiasis in a dog. J Am Vet Med Assoc 198 (1), 132-134 PubMed.
  • Chukwu C C, Anene B M, Onuekwusi K O et al (1990) Relapse infection after chemotherapy in dogs experimentally infected with Trypanosoma brucei brucei. J Small Anim Pract 31 (3), 141-144 PubMed.
  • Barr S C, Simpson R M, Schmidt S P et al (1989) Chronic dilative myocarditis caused by Trypanosoma cruzi in two dogs. J Am Vet Med Assoc 195 (9), 1237-1241 PubMed.
  • Morris S A, Weiss L M, Factor S et al (1989) Verapamil ameliorates clinical, pathologic and biochemical manifestations of experimental chagasic cardiomyopathy in mice. J Am Coll Cardiol 14 (3), 782-789 PubMed.
  • Hudson L (1981) Immunobiology of Trypanosoma cruzi infection and Chagas' disease. Trans R Soc Trop Med Hyg 75 (4), 493-498 PubMed.
  • Burkholder J E, Allison T C & Kelly V P (1980) Trypanosoma cruzi (Chagas) (protozoa: kinetoplastida) in invertebrate, reservoir and human hosts of the lower Rio Grande Valley of Texas. J Parasitol 66 (2), 305-311 PubMed.
  • Camargo M & Rebonato C (1969) Cross-reactivity in fluorescence tests for Trypanosoma and Leishmania antibodies. A simple inhibition procedure to ensure specific results. Am J Trop Med Hyg 18 (4), 500-505 PubMed.

Other sources of information

  • Carter G R (2003) Major Infectious diseases of Dogs and Cats, Part 1. In: A Concise Guide to Infectious and Parasitic diseases of Dogs and Cats. Ed G R Carter. International Veterinary Information Service, Ithaca NY (, B0405.0403.
  • Barr S C (1998) American Trypanosomiasis. In: Infectious diseases of the Dog and Cat, Second Edition. Ed C E Greene. W B Saunders, Philadelphia, PA. pp 445-448.
  • Greene C E (1998) African Trypanosomiasis. In: Infectious diseases of the Dog and Cat, Second Edition. Ed C E Greene. W B Saunders, Philadelphia, PA. pp. 449-450.
  • Kittleson M D (1998)Primary myocardial disease leading to chronic myocardial failure (dilated cardiomyopathy and related diseases). In: Small Animal Cardiovascular Medicine. Eds: M D Kittleson & R D Kienle. Mosby Inc, St Louis, MO. pp 319-346.
  • Meurs K M, Miller M W & Helman R G (1995) Canine Chagas' Myocarditis. In: Kirk's Current Veterinary Therapy, XII: Small Animal Practice. Ed. J D Bonagura. W B Saunders, Philadelphia, PA.
  • Barr S C (1990) American Trypanosomiasis. In: Infectious diseases of the Dog and Cat. Ed. C E Greene. W B Saunders, Philadelphia, PA. pp 763-768.
  • Kagan I G (1980) Serodiagnosis of parasitic diseases. In: Manual of Clinical Microbiology. 3rd ed. Eds E H Lennet, A Balows, W J Hausler, J P Truant. Washington: American Society for Microbiology. 724-750.
  • Training in Tropical diseases (TDR), World Health Organization; URL:
  • The Merk Veterinary Manual on-line, URL:

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