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.