Chagas disease in photos

Symptoms and syndromes in photos

Main » Infectious diseases » Arthropod-borne Infection » Chagas disease

Distribution Chagas' disease

Distribution Chagas' disease exists in localised endemic zones in Central and South America from the Andes to the Atlantic coast as far south as the latitude of the River Plate.

Trypanosoma cruzi in human bljjd film.

Photo 1. Trypanosoma cruzi in human blood film. The causative agent is T. cruzi. It occurs characteristically in blood films as short 'C' or 'S' shaped trypomastigotes with a prominent kinetoplast. It is otherwise monomorphic. (x 900)

Trypanosoma cruzi in human bljjd film too.

Photo 2. Trypanosoma cruzi in human blood film too.

Typical vector biting.

Photo 3. Typical vector biting. Typical vector biting Reduviid bugs (also known as 'assassin' or 'kissing' bugs), particularly in the genera Triatoma, Rhodnius and Panstrongylus, transmit T. cruzi while feeding, not by inoculation but by faecal contamination. (x 1.5)

life cycle in vector.

Photo 4. life cycle in vector. Trypomastigotes picked up in the blood meal transform to epimastigotes in the midgut of the bug. They reproduce as epimastigotes, then pass to the hindgut where they transform again to the infective stages (metacyclic trypomastigotes). The figures show epimastigote stages in the vector. (x 900) 

life cycle in vector too.

Photo 5. life cycle in vector(2).

Metacyclie stage in faeces.

Photo 6. Metacyclie stage in faeces. Infection is through contamination by parasites in bug faeces produced on the skin. These may invade the site of the bite or adjacent mucosa (eg the conjunctiva), (x 900)

Ecology of vectors.

Photo 7. Ecology of vectors. The favourite habitats of the reduviid bugs are cracks in the walls of mud huts in poor rural areas. Here the insects shelter and breed. Transmission occurs predominantly at night.

Armadilio, reservoir host.

Photo 8. Armadilio, reservoir host. It has an extensive mammalian reservoir both in wild hosts (especially armadillos and opossums), as well as domestic animals.

Romana's sign.

Photo 9. Romana's sign. The infection often begins with a local lesion, the chagoma. It causes marked local oedema which, should it occur in the region of the eye or within the conjunctival sac, is accompanied by swelling of the lids and chemosis. These unilateral periorbital changes constitute Romaha's sign.

Amastigotes in heart muscle.

Photo 10. Amastigotes in heart muscle.

 After a stage of initial parasitaemia associated with fever (often unrecognised), trypomastigotes pass to the cardiac muscle and smooth muscle lining the intestinal tract. Here they transform to the amastigote stage (Leishman-Donovan bodies) in which they multiply to form pseudocysts. In the heart this is associated with severe myocarditis especially in the early stages of the infection. (x350)

T. cruzi dividing amastigotes in tissue culture.

Photo 11. T. cruzi dividing amastigotes in tissue culture. The basic structure of the amastigote is similar to that of the trypomastigote (145 & 146) but the flagellum is very short and the mitochondrion is poorly developed. (x 1250)

ECG showing heart block.

Photo 12. ECG showing heart block. Dysrhythmias of various types and degrees are a characteristic feature of Chagas' disease. Complete heart block with Stokes- Adams attacks can occur and may result in sudden death.

Cardiomegaly.

Photo 13. Cardiomegaly. The heart shows gross enlargement and dilatation. The dilatation of the right atrium and both ventricles is marked in this specimen. The pathogenesis seems to be associated with a loss of autonomic control due to destruction of the ganglionic plexuses.

Apical aneurysm of heart.

Photo 14. Apical aneurysm of heart. Mural thrombi may be present at the apex of the left ventricle, with marked thinning of both ventricular walls. Apical aneurysmal formation is commonly seen.

X-ray of megacolon.

Photo 15. X-ray of megacolon. Muscular degeneration and denervation of segments of the alimentary tract through destruction of the cells of Auerbach's plexus cause megaoesophagus, megastomach and megacolon, etc, which can be detected radiologically.

Post-mortem megacolon.

Photo 16. Post-mortem megacolon. Gross megacolon is shown here in a woman who died of chronic Chagas' disease.

Parasites in oesophageal muscle.

Photo 17. Parasites in oesophageal muscle. Pseudocysts containing amastigotes of T. cruzi can rarely be demonstrated in ganglion cells of the intestinal tract, although the smooth muscle is often invaded. (x350)

Xenodiagnosis.

Photo 18. Xenodiagnosis. Absolute confirmation of active infection is obtained by demonstrating that the patient can infect the vector (xenodiagnosis). Laboratory- bred clean reduviid bugs are fed on patients suspected of having trypanosomiasis. Two weeks later the hindgut is dissected out and is examined for metacyclic trypanosomes.

Machado-Guerreiro reaction.

Photo 19. Machado-Guerreiro reaction.

 A complement fixation test employing antigen from epimastigotes of T. cruzi cultivated in vitro is widely used, and is one of the most sensitive means of diagnosis. It does not necessarily imply the presence of active infection. (Top row - negative control; second row - positive control titre 1 /256; third row - patient's serum titre 1/512; fourth row - complement control.)

Immunofluorescence of T. cruzi.

Photo 20. Immunofluorescence of T. cruzi. Fluorescent antibody tests may also be employed using whole cultured epimastigotes as the antigen. (x600) (Right: negative control)

Trypanozoma rangeli.

Photo 21. Trypanozoma rangeli. T. rangeli is a long slender trypanosome also trans­mitted by reduviid bugs from wild animals to man. It is readily distinguished by its shape from T. cruzi in blood films and appears to be non-pathogenic to man. (X 600)

Cycle in man and triatomid bugs.

Photo 22. Cycle in man and triatomid bugs.

 Metacyclic trypanosomes (4) of Trypano- somi cruzi passed in the faeces of infected triatomid bugs (A) penetrate the skin or mucous membranes to reach the blood (5). They enter various muscular tissues, eg cardiac muscle (B), smooth muscle of the gut (C) or skeletal muscle (D). Here they transform to amastigotes which divide, producing pseudocysts. Subsequently, the daughter amastigotes transform back to trypomastigotes (6, 7). These enter the blood from which they may reinvade muscular tissues, or be picked up by another triatomid bug when it feeds. In the bug the parasites transform to epimastigotes (1, 2, 3) which divide in the gut. Finally some epimastigotes pass to the hindgut where they transform back to infective, metacyclic trypomastigotes (4) which are passed in the faeces as the bug next feeds. {See also 145-150, 154, 155, 161.)

 

 


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