Amebic Pericarditis
Amebiasis, transmitted by the protozoan Entamoeba histolytica, is considered initially and predominantly an intestinal disease, but it involves the liver in a substantial proportion of patients. The infective encysted form of the parasite, communicated person to person without an intermediate host and usually by water or food contaminated by human fecal material, enters the intestinal tract by the mouth, passes through the stomach, and loses its cystic wall in the small intestine. There the cyst, 5 to 20 ยต in diameter, having matured during its passage, releases from one to four trophozoites (vegetative form), which in contrast to the cyst, are mobile but do not survive outside the host’s body. The amebas, which have attached themselves to the colonic wall, migrate into the crypts and penetrate the epithelium and muscularis. From the submucosa, the amebas move along to other organs, particularly the liver, creating there the chronic nonsuppurative form of amebic hepatitis or producing abscesses. Other trophozoites are excreted in the encysted form, thus maintaining the life cycle.
These events may proceed with only
mild symptoms (not necessarily associated with the bowels) and thus may account
for the carrier stage. On careful examination of the feces, however, this
stage may be detected in up to 10% of the population in endemic U.S. areas. Some
disturbances of the host-parasite relationship result in the activation of the dormant
form of the ameba, causing the clinical picture of colitis, dysentery, or liver
abscess.
Another manifestation of amebiasis is
amebic pericarditis. Until 1964, only 65 cases of this rare condition had been recorded
in the world’s medical literature. More recently, another 25 cases have been reported
in South Africa. Pericardial involvement in amebiasis occurs by direct extension
from an amebic abscess of the left lobe of the liver, only occasionally resulting
from a lung abscess or an abscess in the right lobe of the liver (see Plate 6-148). The salient features of amebic pericarditis
are epigastric pain, a palpable mass in the epigastrium or left hypochondrium, tenderness
over the liver area, dyspnea, pericardial friction rub, and high temperature. Radiography
usually shows an elevated left diaphragm and enlargement of the heart shadow. Mild
anemia and polymorphonuclear leukocytosis are usually present. The ECG shows the
usual signs of pericarditis (e.g., generalized ST-segment elevation, inverted T
waves, low voltage). Emetine and chloroquine administration is the treatment of
choice; however, pericardial aspiration, often repeated, is usually necessary.
Amebic pericarditis is a fatal disease
in more than 50% of patients. Even the patient who survives has a high risk of developing constrictive pericarditis,
necessitating pericardiectomy. Another diagnostic link between amebiasis and the
heart is penetrating precordial pain or discomfort often seen in chronic amebiasis
and likely caused by heart disease. Radiographs show a characteristic configuration
of the liver consisting of a tonguelike descending enlargement of the right lobe,
with or without elevation of the right dome or bulging near the cardiac shadow.
This bulging is probably responsible for the complaints derived from the heart.
In fact, these symptoms are caused by
the elevation of the diaphragm resulting from hepatomegaly, which is extremely common
in amebiasis. Another association between the heart and amebic infection is from
the toxic effect of emetine on the heart. Treatment with emetine often causes ECG
abnormalities, mainly flattening and inversion of the P and T waves, which are reversible
and should cause no concern. Emetine is contraindicated only in the presence of
serious cardiac disease.
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