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From Petri (1996), with permission.

From Petri (1996), with permission.

et al., 1987; Adams and MacLeod, 1977a; Jammal et al., 1985). Colonic lesions can vary from only mucosal thickening to flask shaped ulcerations to necrosis of intestinal wall (Figure 9.5).

Fig. 9.5 Amebic colitis. (A) Multiple mucosal ulcers are visible in the resected section of colon (smallest division of scale is mm). (B) Mucosal ulceration of amebic colitis, with extension of the ulcer into the submucosa (hematoxylin and eosin). From the collection of the late Harrison Juniper

Atypical manifestations of amebic colitis do occur and include acute necrotizing colitis, ameboma (granulation tissue in colonic lumen mimicking colonic cancer in appearance), cutaneous amebiasis and recto-vaginal fistulas. Acute fulminant or necrotizing colitis is the most feared complication, occurs in about 0.5% of cases, usually requires surgical intervention and has a mortality >40% (Ellyson et al., 1986; Aristizabal et al., 1991). Abdominal pain, distension and rebound tenderness are present in most patients with fulminant colitis, although frank guarding is uncommon. Indications for surgery in fulminant disease include free extraperitoneal perforation, failure of a perforation with a localized abscess to respond to anti-amebic drugs, and persistence of abdominal distension and tenderness while on anti-amebic therapy. With localized colonic disease, partial colectomy with exteriorization of the ends is recommended over primary anastomosis, as anastomoses may fail due to the friable condition of the bowel wall. Better surgical results for extensive disease have been achieved with total colectomy with exterioriza-tion of the proximal and distal ends (Ellyson et al., 1986; Aristizabal et al., 1991).

Liver Abscess

Typically, signs of amebic liver abscess include right upper quadrant pain, fever of 38.5-39.5°C, leukocytosis, abnormal serum transaminases and alkaline phosphatase, an elevated right hemi-diaphragm and a defect on hepatic imaging study (Table 9.5; Figures 9.6 and 9.8) (Adams and MacLeod, 1976; Maltz and Knauer, 1991;

Table 9.5 Symptoms and signs of amebic liver abscess

Length of symptoms >4 weeks 21-51%

Fever 85-90%

Abdominal tenderness 84-90%

Hepatomegaly 30-50%

Jaundice 6-10%

Diarrhea 20-33%

Weight loss 33-50%

Cough 10-30%

Male:female 9:1

Resident, immigrant or traveler exposed in Most endemic area

From Petri (1996), with permission.

Fig. 9.6 Amebic liver abscess. Gross (A) and microscopic (B, C) pathology of amebic liver abscess. E. histolytica trophozoites are surrounded by amorphous eosinophilic debris (B. hematoxylin and eosin). Host inflammatory cells are present only at the periphery of the lesion, most likely a reflection of the parasite's ability to lyse macrophages. (C) Microscopic example of erythrophagocytosis by E. histolytica. (A) and (C) from the collection of the late Harrison Juniper; (B) courtesy of Dr Sharon Reed

Thompson and Glasser, 1986). A more chronic presentation of 2-12 weeks of weight loss, fever and abdominal pain has been reported in a subset of patients with single abscesses (Katzenstein et al, 1982). The majority (90%) of adult patients with liver abscess are made with equal sex distribution in children (Nazir and Moazam, 1993; Johnson et al., 1994). Amebic liver abscess is usually single and in the right lobe of the liver 80% of the time. The location is not helpful in distinguishing the etiology of an abscess, since the most common location for a pyogenic abscess is also in the right lobe (Mehta et al., 1986; Hai et al., 1991). Patients with pyogenic, as opposed to amebic, liver abscesses are more likely to be older (>50 years), have a palpable mass and present with jaundice, pruritis, sepsis or shock (Conter et al., 1986).

Although a history of dysentery within the last year can sometimes be obtained, most patients with liver abscess do not have concurrent colitis. Atypical presentations of liver abscess include an acute illness with fever, right upper abdominal tenderness and pain, or subacutely with prominent weight loss, fever and abdominal pain. Laboratory abnormalities include leukocytosis and an elevated alkaline phosphatase level. Elevation of the right hemidiaphragm in radiographic studies is evident in most patients (Chuah et al., 1992; Greaney et al., 1985; Ravdin and Guerrant, 1981). Early evaluation of the hepatobiliary system with ultrasound, CT or MRI is essential to demonstrate the abscess in the liver.

The differential diagnosis of a hepatic lesion includes pyogenic abscess (less likely if the gall bladder and intrahepatic ducts appear normal), hepatoma and echinococcal cyst (patients are usually asymptomatic and are unlikely to present acutely with fever and abdominal pain).

Severe amebic liver abscesses occur and were defined in one study as abscesses that rupture despite at least 3 days of anti-amebic treatment, or abscesses complicated by secondary bacterial infection. These are associated with dyspnea, elevated right hemidiaphragm and pleural effusion, jaundice, anemia and diabetes mellitus (Chuah et al., 1992; Greaney et al., 1985). Patients with findings listed above that are associated with more severe disease might benefit from early drainage. Intrathoracic and intra-

peritoneal rupture of an amebic liver abscess can be adequately treated with anti-amebic therapy without surgery if secondary bacterial infection is absent (Greaney et al., 1985). Unusual extraintestinal manifestations of amebiasis include direct extension of the liver abscess to pleura or pericardium, brain abscess and genitourinary amebiasis.

Cutaneous Amebiasis

This is a rare, albeit reported, complication of amebic infection. Cases of amebiasis involving the abdominal wall, face, vulva and vagina, and penis have been reported (Rimsza and Berg, 1983; Baez Mendoza and Ramirez Barba, 1986; Citronberg and Semel, 1995; Loschiavo et al., 1997). These conditions are thought to occur from fistulous tracts that arise from underlying enteric disease or hepatic abscesses. Significant tissue necrosis can occur in these cases and often requires significant surgical debridement in addition to antibiotic treatment.

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