Hepatic abscess. Hepatic abscess is the most common extraintestinal lesion produced by E. histolytica, resulting from the embolization of pathogenic trophozoites into the portal venous system via the mesenteric-splanchnic circulation. The time lapse between the colonic mucosal-vascular penetration and damage to the liver parenchyma is unknown; however, experimental animal studies have demonstrated early hepatic alterations three hours after embolization of the trophozoites. The process begins with minimal dilatation of the sinusoids containing amebae, surrounded by varying amounts of polymorphonuclear leukocytes, some of which undergo lysis. Twenty-four to 48 hours later, the leukocytic lysis increases with proportional cellular necrosis of the adjacent liver tissue. By the fifth to seventh day, extensive necrosis with little inflammatory reaction can be observed. These experimental studies can be extrapolated to humans. Neutrophiles tend to be sparse in amebic lesions generally, but especially so in amebic abscesses of the liver. The two essential features of any abscess are destruction of tissue and the accumulation of neutrophils and fibrin. The amebic "abscess" of liver therefore is considered somewhat of a misnomer because, although the "abscess" is characterized by necrosis, it contains few if any neutrophiles after several days' development.

Macroscopically, the hepatic amebic abscess is identified as a well-delineated area where the liver parenchyma has been replaced by necrotic tissue of yellowish color and creamy consistency,resembling anchovy paste. A rind of congested hepatic tissue surrounds the abscess. The necrotic center can be solid, soft or semi-liquid, sometimes containing mucus. The size of a hepatic abscess is variable, ranging from miliary spread to huge lesions that can replace 90% of the normal organ. At autopsy (Figs. 1.8 and 1.9), the average size is 5 to 15 cm in diameter. Most abscesses occur in the right lobe and are more often single than multiple. A hepatic abscess may rupture into the peritoneal cavity followed rapidly by an acute peritonitis. Rupture can also occur into the abdominal viscera, such as the stomach, duodenum, and colon, or into the biliary ducts, portal vein, or inferior vena cava, or toward the retroperitoneal space and, most frequently, the thoracic cavity (Fig. 1.9). Cerebral amebiasis. Spread of E. histolytica to the brain is thought to be hematogenous from the colon via hepatic, pulmonary, or vertebral veins. Lombardo et al, however, found intestinal symptomatology in little more than 50% of the cases of cerebral amebiasis which they reviewed. The reported incidence of amebic brain abscesses (Fig. 1.10). in patients with confirmed amebic liver abscesses varies from 0.6% to 8.1%; central nervous system infection without hepatic involvement is rare.