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Chagas’ Disease 151

disease is a major human health problem in induced by T. cruzi include myocardial • ECG: expect ventricular premature
South America, Mexico, and Central America. necrosis/fibrosis, local coronary spasm, and complexes/ventricular tachycardia or second-/
VetBooks.ir Clinical Presentation • Myocardial lesions lead to systolic dysfunc- • Thoracic radiographs: cardiomegaly with or Diseases and Disorders
third-degree AV block
possible autoimmune progression.
DISEASE FORMS/SUBTYPES
without evidence of CHF (e.g., pulmonary
tion (dilated cardiomyopathy) and/or CHF,
The disease occurs in three phases:
edema) can occur
• Acute phase: 0-4 weeks after inoculation; peak severe bradyarrhythmias (advanced second- • Holter monitoring (24-hour ambulatory
degree or third-degree atrioventricular [AV]
at 2 weeks. In younger dogs, usually lethargy, block), and ventricular tachyarrhythmias. ECG [p. 1120]) if severe arrhythmias on
fever, and generalized lymphadenopathy. Less • Protective immunity does not develop. ECG and syncope
commonly, acute myocarditis with severe • Echocardiography (p. 1094): to identify
bradyarrhythmia/tachyarrhythmia and risk DIAGNOSIS chamber dilation and poor systolic function,
of sudden death. Absence of clinical signs if present
common in older dogs. T. cruzi present in Diagnostic Overview • Serum cardiac troponin I concentration: high
peripheral blood. The disease is suspected when hunting dogs (acute phase only); not specific for chagasic
• Indeterminate (latent) phase: lasts months that are kept outside develop myocardial failure myocarditis
to years. Absence of clinical signs and and/or complex cardiac arrhythmias (brady-/
electrocardiographic (ECG) abnormalities tachyarrhythmias) when living in or traveling Advanced or Confirmatory Testing
• Chronic phase: late complications in some to endemic areas. Higher suspicion is justified if • Cytologic identification of trypomastigotes
infected dogs, with myocardial failure and the breed is not predisposed to primary cardiac during acute phase
recurrence of arrhythmias, resulting in diseases. Markedly increased cardiac troponin I • Chagas’ titer in dogs suspected of chagasic
congestive heart failure (CHF) and risk of blood level confirms myocarditis with ongoing myocarditis. Titer is typically positive by 3
sudden death cardiomyocyte death. Trypomastigotes may be weeks after infection and persists throughout
detected in blood samples during the acute the life of the animal. Cross-reactivity with
HISTORY, CHIEF COMPLAINT phase. Confirmation requires a Chagas’ titer. antibodies to Leishmania
History of travel to/residence in southernmost • Serologic testing
United States, Mexico, or Central or South Differential Diagnosis ○ Indirect fluorescent antibody test (offered
America. Detection of arrhythmias, lethargy, • Dilated cardiomyopathy (idiopathic) (p. by Texas A&M Veterinary Medical Lab
syncope, and/or CHF 263) [http://tvmdl.tamu.edu/] and IDEXX
• Other causes of myocarditis (p. 675) [www.idexx.com])
PHYSICAL EXAM FINDINGS • Other causes of right heart failure (p. 409) ○ ELISA
• Acute phase: may be normal in adult dog; • Other causes of AV block (p. 101) ○ Radioimmunoprecipitation
irregular cardiac rhythm and pulse deficits; • Other causes of ventricular tachycardia (p. • Polymerase chain reaction (PCR): high
peripheral lymphadenopathy; occasionally 1033) specificity but low sensitivity in chronic cases
fever • Histopathologic identification of amastigotes
• Indeterminate phase: normal physical Initial Database in myocardium at necropsy
examination • Serum biochemistry profile: liver enzymes
• Chronic phase: bradyarrhythmia or tachyar- may show mild to moderate elevation TREATMENT
rhythmia with/without pulse deficits, weak • CBC: lymphocytosis is common
pulses, soft systolic heart murmur, dyspnea • Blood smear or buffy coat (better) stained Treatment Overview
and tachypnea, abdominal distention from with Giemsa or Wright stain (acute phase Supportive treatment for arrhythmias and CHF
ascites/hepatomegaly, jugular distention only): definitive diagnosis if organism is seen is recommended. There is no effective treat-
(trypomastigotes, flagellate organisms are 2-3 ment to eliminate the organism. Therapeutic
Etiology and Pathophysiology times as long as the diameter of erythrocytes). goals:
• Trypomastigotes (circulating flagellated form) Can also examine lymph node aspirates, • Palliation of clinical signs caused by CHF
are deposited in the vector’s feces at the ascitic or pleural fluid. and/or arrhythmias
insect’s bite site and enter the bloodstream
through the infected bite. Alternatively, direct
ingestion of infected triatomine bug or of
an infected reservoir host (e.g., armadillo,
opossum, raccoon, mouse, squirrel, rat).
Blood transfusion–mediated and transpla-
cental and transmammary transmission also
occur.
• Trypomastigotes enter monocytes and
macrophages in cardiac and skeletal tissue
(possibly nervous tissue) and transform into
amastigotes (nonflagellated form) and then
multiply rapidly, leading to cell rupture and
causing clinical signs.
• The amastigotes transform back to trypomas-
tigotes before cell rupture. Rising parasitemia
occurs, peaking at 2-3 weeks after inoculation
and decreasing by 4 weeks after inoculation.
Signs of acute myocarditis are possible during
this period.
• Latent stage starts 4 weeks after inoculation.
• Late complications (months to years after CHAGAS’ DISEASE Protozoal pseudocyst containing many amastigotes within a cardiomyocyte (arrow) from
infection) from inflammatory reaction a 5-month-old dog who died of Chagas’ disease (40× magnification, hematoxylin-eosin stain).

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