Amebiasis of the Brain

This is a rare condition that occurs in less that 1% of patients with dysenteric amebiasis. However, it accounts for 4.2% to 8.5% of deaths from amebiasis.

Pathology. The arrival of amebae to the central nervous system is by a hematogenous route, either secondary to intravascular rupture or through the systemic circulation combined with a paradoxical event across a patent foramen ovale or a pulmonary arteriovenous fistula. The systemic flow to the brain represents 20% of the cardiac output. Thus, once in the systemic circulation, the parasite can easily reach the central nervous system.

The lesions can be single or multiple, and range from microscopic to 5 cm in diameter. Grossly, they appear as a conglomerate of petechiae with softening of the brain and congestion. The larger lesions are necrotic with well-defined margins containing a yellowish-green exudate. The meninges may show a localized or generalized inflammatory response that may be indistinguishable from other types of acute purulent meningitis.

Clinical manifestations. Symptomatology includes convulsive disorder, hemiplegia, monoplegia, cranial nerve involvement, meningitis, and signs of increased intracranial pressure. The clinical behavior is basically that of an acute space-occupying lesion with spontaneous hemorrhage. Tumor and other parasitic infestations, such as cysticercosis, paragonimiasis and hydatid disease, are part of the differential diagnosis. Unfortunately, most cases go undiagnosed since cerebral amebiasis is rarely included in the list of potential etiologies. When an early diagnosis is made, a dramatic positive response to specific treatment is observed.

Imaging features. Amebic brain abscesses are hypodense on CT and hypointense on T1-weighted MRI with peripheral ring enhancement after intravenous contrast media; surrounding edema is present (Fig. 1.102). These abscesses, whether solitary or multiple, commonly involve cortical and deep grey matter. The frontal lobes and basal ganglia are the commonest sites of involvement; the left side is more common than the right by a ratio of 2.3:1. The CT appearance cannot be differentiated from other causes of brain abscess. The differential diagnosis also includes tuberculosis, nocardiosis, and metastases. The MR images do not differ significantly from those seen with pyogenic abscesses. T1-weighted images show central hypointensity with a surrounding thin rim of isointensity, presumably representing a capsule of granulation tissue (DeVilliers and Durra; also Dietz et al). The T2-weighted images show central hyperintensity, presumably representing central necrosis and liquified brain. The presumed granulation tissue capsule is hypointense, and what is presumed to be surrounding edema is hyperintense, similar to that seen with pyogenic abscess.

These findings are nonspecific for cerebral amebic abscess and, unfortunately, the premortem or presurgical diagnosis is only accomplished in a few patients. Because the condition is potentially lethal, it should be considered in differential diagnosis, especially in endemic areas, and metronidazole or other appropriate antiamebic therapy should be instituted after the diagnosis is confirmed by serology or other laboratory tests. MRI is superior to CT in demonstrating small cerebral lesions, but neither modality is available in most endemic regions, and thus the true incidence of brain involvement in amebiasis is probably underestimated.

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Fig. 1.102A-D. MRI of multiple amebic brain abscesses in a 38-year-old South African man. (A) T1-weighted (SE 500/10) image shows multiple hypointense lesions in the right frontoparietal area. (B) On the T2-weighted (SE 260/90) image the lesions showed central hyperintensity of the abscess contents surrounded by low-intensity halos representing the abscess walls, which were in turn surrounded by hyperintense zones of edema. (C and D) Following intravenous gadolinium DTPA (0.1 mmol/kg), there was pronounced ring enhancement of all lesions, with demonstration of additional small lesions in the head of the left caudate nucleus and in the left occipital area (small arrows in C). (Courtesy of Drs. J.P. De Villiers and G. Durra and Clinical Radiology, 1998.) The patient, who was from a rural area, was admitted complaining of hemoptysis, dyspnea, and right upper quadrant pain. He appeared ill with a temperature of 38°C, a tender liver, and signs of a right basal pleural effusion. He had slightly depressed consciousness, but no focal neurological signs. He was somewhat anemic but his white cell count was normal and he was HIV-negative. There was no change in the nature of his stools. A chest radiograph revealed an elevated right hemidiaphragm with a moderate right pleural effusion. Ultrasound of the abdomen demonstrated a 6 cm round hypoechoic lesion in the right lobe of the liver. Aspiration of the liver lesion under ultrasound guidance revealed pink pus. Microscopy revealed the presence of amebae and indirect hemagglutination for E. histolytica was positive at 1:4096, confirming systemic amebiasis. Stool microscopy was unremarkable. Oral metronidazole was initiated. On the same day, the patient developed a left hemiplegia with neck stiffness and a left upper motor neuron facial nerve palsy. A CT scan of the head revealed multiple low-density lesions in the right frontoparietal region of the brain and a single lesion in the head of the left caudate nucleus. Marked mass effect was present. The contrast-enhanced scan demonstrated ring enhancement of all lesions, with additional vague increased density noted in the occipital region.