Case 231. 
Trypanosoma cruzi myocarditis (Chagas disease) (62 y-o M)
         
    Autopsied arrhythmic heart (720 g) in a Nisei farmer who stayed in Brasil for 40 years    
         
   
Key words : 
Trypanosoma cruzi, Chagas disease, chronic chagastic cardiopathy, megacolon    
     
 
     
A few cardiomyocytes contain granulated inclusions in the cytoplasm. Inflammatory reaction is scarcely seen in this case (HE, lower power).   High powered view discloses accumulation of round granules (amastigote-type protozoa) in the cytoplasm of the cardiomyocyte, confirming the diagnosis of chronic chagastic cardiopathy (HE).
     
 
     
Reference case 231A
Another autopsy case of a Bolivian adult suffering from Chagas disease (HE). In this case, lymphocytic infiltration is diffusely noted in the edematous interstitium of the heart muscle. An infected heart muscle cell is seen in the center.
  Experimental T. cruzi myocarditis in a nude mouse
Intracellular proliferation of the protozoa becomes pronounced when the cellular immunity is severely suppressed (HE). Brain lesions showing marked protozoan infection in glial cells may be formed when the patient with Chagas disease contracts AIDS.
     
 
     
T. cruzi infection in the mouse liver.
Kuffper cells contain amastigote-type protozoa, and the histologic features are similar to visceral leishmaniasis (HE, oil immersion). In case of trypanosomiasis, an eosinophilic rod (kinetoplast) is distinct, adjacent to the basophilic nucleus.
  Reference case 231B
Surgical specimen of megacolon seen in Chagas disease in Bolivia (gross findings). Infection of T. cruzi in the myenteric plexus caused the loss of ganglion cells in the dilated portion. The megacolon is rare in Chagas disease in central America.
     
 
     
Reference case 231B
Cut surfaces of the megacolon in Chagas disease in Bolivia. Megavisceral phenomenon may also be seen in the digestive tract, bronchus, ureter and uterus.
  Reference case 231C
Cardiac toxoplasmosis in adult T-cell leukemia (50 y-o F), the same patient as case 96. The cardiac lesion is histologically indistinguishable from Chagas disease. At autopsy, T. gondii was systemically disseminated to the heart, lungs, bone marrow, liver, spleen, lymph nodes, adrenals, striated muscles, thyroid and spinal cord.
     
   
     
Reference case 231C
Immunostaining for T. gondii antigens show positive reaction in the infected pathogens. Positivity of T. gondii antigens should be differentiated from the fine lipofuschin granules in the cytoplasm of the heart muscle cells.