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Communications to the Editor |

Chagas’ Disease FREE TO VIEW

Alfred Lemle, MD, FCCP
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Professor Titular De Tisiopneumologia Universidade Federal Do Rio De Janeiro Rio De Janeiro, Brazil



Chest. 1999;115(3):906. doi:10.1378/chest.115.3.906
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To the Editor:

In reference to the very interesting report by Spira and colleagues,1which appeared recently in CHEST, I would like to add another illness to Dr. Spira’s list: Chagas’ disease. This is an infection, endemic in Central and South America, mostly in the central heartlands of Brazil, caused by a protozoan, Trypanosoma cruzi. In its chronic stage, it causes a well-known myocardiopathy, as well as often very prominent esophageal and colonic lesions, the “megas.” Its bronchopulmonary manifestations have been recently and extensively reviewed.2T cruzi infects wild animals, such as armadillos, racoons, and rodents, as well as humans. Transmission is by the blood sucking beetles of the Triatominae subfamily, which live in the cracks of mud-walled housing; by night, they bite their victims, usually in uncovered areas, mostly the face, originating their vulgar name of “barbeiros” (barbers). In the United States, the disease may be seen in immigrants3 or be acquired by congenital or blood transfusion transmission.

Chagas’ disease may course with an acute phase, seen mostly in children, with fever and inflammation at the inoculation site. Occasionally, there is severe homolateral palpebral inflammation (Romaña’s sign). The chronic stage is usually marked by the myocardial lesions, as well as the esophageal and colonic dilatations. These produce severe symptoms (dysphagia, constipation) and typical radiologic and endoscopic findings. The myocardiopathy is characterized by arrhythmias and bundle-branch blocks, usually with severe and intractable heart failure at the late stages. The anatomic basis for all of these lesions is fundamentally similar. There is a gradual destruction of nerve cells in the digestive tube walls and of myocardial myofibrils by T cruzi Leishmania forms. The lungs may be affected secondarily to heart disease (congestion, thromboembolism, and amiodarone fibrosis) or to esophageal disease (aspiration pneumonia). More specific, rare and even more rarely significant, is the bronchopathy, which is the reason why Chagas’ disease should be included in Dr. Spira’s list. It is a veritable, if macabre, experiment in neurophysiopathology, perpetrated by nature. Essentially, it appears that the destruction of Leishmania bodies and the rupture of microcysts may denervate the bronchial walls. Lima Pereira, as noted in the study by Bethlem and colleagues,2 showed bronchial wall ganglia with a decrease in the number of neurons and with residual nodules, as well as ganglionitis, periganglionitis, and extensive denervation.

The ensuing bronchomotor functional disturbances have been extensively studied. In summary, a decrease in maximum expiratory flow rate has been observed by some, though inconsistently,4 but not by others.2,,5 Pharmacologic challenges have been inconclusive6; nifedipine may cause a fall in the maximum expiratory flow at very low lung volumes.2

Aside from the very challenging neurophysiopathologic model, the clinical impact of these bronchial lesions is certainly small. In 250 autopsies, Koeberle7 found 13 cases of bronchiectasis, as opposed to 69 cases of megacolon and 61 of megaesophagus. The dilatation may extend to the trachea, which does not happen in other diseases that course with bronchiectasis. CT and high-resolution CT studies should help to better evaluate these interesting lesions.

Correspondence to: Alfred Lemle, MD, FCCP, Rua Nascimento Silva 178, Apartment 501, Rio De Janeiro 22421-020, Brazil

Spira, A, Grossman, R, Balter, M (1998) Large airway disease associated with inflammatory bowel disease.Chest113,1723-1726. [PubMed] [CrossRef]
 
Bethlem, NM, Lemle, A, Saad, EA Pulmonary manifestations in Chagas’ disease. Sharma, OP eds.Lung disease in the tropics1991,251-277 Marcel Dekker. New York:
 
Kirchoff, LV, Neva, FA Chagas’ disease in Latin American immigrants.JAMA1985;254,3058-3060. [PubMed]
 
Manço, JC, Gallo, L, Jr, Amorim, DS Alterações funcionais pulmonares na Moléstia de Chagas: estudo espirográfico. Arq Bras Cardiol. 1976;;29 (suppl) ,.:132
 
Vargas FS. Mecânica respiratória em pacientes chagásicos sem insuficiência cardíaca. Dissertation. Faculdade de Medicina, Universidade de sâo Paulo, 1979.
 
Manço, JC, Godoy, RA, Gallo, L, Jr, et al Resposta ventilatória a metacolina na forma crônica da doença de Chagas: resultados preliminares de estudo espirográfico.Arq Bras Cardiol1967;20,175-178. [PubMed]
 
Koeberle, F Chagas: bronchiektasie.Tropenmed Parasitol1959;10,304-308
 

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Tables

References

Spira, A, Grossman, R, Balter, M (1998) Large airway disease associated with inflammatory bowel disease.Chest113,1723-1726. [PubMed] [CrossRef]
 
Bethlem, NM, Lemle, A, Saad, EA Pulmonary manifestations in Chagas’ disease. Sharma, OP eds.Lung disease in the tropics1991,251-277 Marcel Dekker. New York:
 
Kirchoff, LV, Neva, FA Chagas’ disease in Latin American immigrants.JAMA1985;254,3058-3060. [PubMed]
 
Manço, JC, Gallo, L, Jr, Amorim, DS Alterações funcionais pulmonares na Moléstia de Chagas: estudo espirográfico. Arq Bras Cardiol. 1976;;29 (suppl) ,.:132
 
Vargas FS. Mecânica respiratória em pacientes chagásicos sem insuficiência cardíaca. Dissertation. Faculdade de Medicina, Universidade de sâo Paulo, 1979.
 
Manço, JC, Godoy, RA, Gallo, L, Jr, et al Resposta ventilatória a metacolina na forma crônica da doença de Chagas: resultados preliminares de estudo espirográfico.Arq Bras Cardiol1967;20,175-178. [PubMed]
 
Koeberle, F Chagas: bronchiektasie.Tropenmed Parasitol1959;10,304-308
 
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