antibiotics are crucial, without which mortality rates are high. Other contributors to poor outcome

include: multiple abscesses, non-Klebs pathogens, mixed bacterial and fungal abscesses, presence of

respiratory symptoms, presence of malignancy, and large size (>5 cm).8,9

AMEBIC LIVER ABSCESS

Amebic liver abscesses are caused by Entamoeba histolytica, a protozoan. Systemic infection, or

amebiasis, is most commonly asymptomatic, clinical manifestations include amebic dysentery and

extraintestinal manifestations. Amebic liver abscess is the most common extraintestinal manifestation

and is due to ascending portal infection. Amebiasis is most prevalent in tropical and subtropical regions

with poor sanitation, as fecal–oral transmission is the most common route of infection. It is estimated

that 40 to 50 million are infected each year worldwide, and in the United States the highest rates are

seen in immigrants from endemic areas. Again, most infections are asymptomatic, but amebic

dysentery, and pulmonary, cardiac, and brain involvement can occur, along with hepatic abscess.

Hepatic abscess occurs in only around 5% of cases of amebiasis. Men are affected 10 times more

commonly than women, peak incidence is in the third, fourth, or fifth decade of life, and corticosteroid

usage is a risk factor.2,10 Ingested cysts pass through the stomach and reach the intestine. There the cyst

wall is degraded and trophozoites are released. These infective particles multiply in the colonic lumen

and then may enter mesenteric veins and eventually the liver. Amebic trophozoites there cause

obstruction of venules, thrombosis and infarction of hepatic parenchyma, with resultant abscess

formation (Fig. 58-2).

Figure 58-1. Computed tomogram of a pyogenic hepatic abscess in a liver transplant recipient with occlusion of the hepatic artery.

Amebic liver abscesses range in size from several millimeters to massive (Fig. 58-3). Clinical

presentation is typically 8 to 20 weeks following return from endemic area and usually manifests as

right upper quadrant pain and fever. Cough, sweating, malaise, weight loss, and hiccough may be

present. Amebic abscesses are more common in the right lobe and tend to be singular. Lesions may

show an enhancing rim and when drained contained a dark, hemorrhagic, proteinaceous fluid often

referred to as “anchovy paste” (Fig. 58-4). Abscesses have been described in the past as acute or

chronic, and as benign or aggressive. Bacterial superinfection of amebic abscesses can occur and amebic

abscesses can rupture into surrounding tissues or spaces, most frequently into the chest.1,2,10–14 E.

histolytica is not found in stool specimens of infected patients but diagnostic antibodies are present in the

serum 7 to 10 days after the onset of symptoms in almost all patients.15 Chest x-ray is frequently

abnormal but CT scan is the diagnostic test of choice, often displaying the enhancing wall and a

surrounding edema. MRI will likewise be diagnostic.2,10,12

Treatment is based on amebicidal drugs to eliminate liver organisms and a luminal agent to eliminate

intraluminal cysts even if not seen in the stool given the low sensitivity of microscopy to identify

organisms. Preferred tissue agents include metronidazole 500 to 750 mg three times a day for 7 to 10

days. Tinidazole 2 g orally for 5 days is an alternative treatment that is better tolerated. To eradicate

intraluminal cysts, the following regimens can be used: paromomycin (25 to 30 mg/kg/day orally three

times a day for 7 days), diiodohydroxyquin (650 mg orally three times a day for 20 days), or diloxanide

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furoate (500 mg orally three times daily for 10 days for adults). Metronidazole treats both intestinal

and extraintestinal sites. Amebic abscesses can almost always be treated with medical therapy alone.

Percutaneous drainage is considered in cases with poor response, when superinfection is suspected, or if

there is risk of rupture. Open surgical drainage is almost never required and would be considered only

in severe complicated cases.2,10,13

Figure 58-2. Amebic abscess of the liver. A photomicrograph of the margin of an amebic abscess shows fibroblastic proliferation

surrounding the cavity and amebic trophozoites in the lumen. (Reproduced with permission from Rubin E, Farber JL. Pathology.

3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 1999.)

Figure 58-3. Sonogram (A) and computed tomogram (B) in a patient with multiple amebic abscesses (arrows).

ECHINOCOCCUS (HYDATID DISEASE)

Echinococcal infection, also called hydatid disease, is a parasitic disease due to echinococcal tapeworms

including Echinococcus granulosus or E. multilocularis in humans. Echinococcus is endemic in the

Mediterranean or other parts of the world in sheep rearing economies but is uncommon in the United

States. The liver is most commonly affected by E. granulosus. Dogs are the definitive host and the life

cycle of the organism is such that when the canine host ingests infected viscera (from sheep or cattle)

scoleces released in the intestine develop into adult worms. Humans, an intermediate host, acquire

echinococcal eggs by ingestion of contaminated foods or with infected animals. The echinococcal egg is

digested in the duodenum and yields an embryo (oncospheres). Embryos invade the intestinal wall and

reach the liver via the portal circulation. Surviving embryos lodge in the hepatic capillaries and develop

into hydatid cysts. Though the liver is the most common location of hydatid cysts (50% to 75% of cases)

the lungs can also be affected (25% of cases). E. granulosus and E. vogeli cause liver cysts while E.

multilocularis is associated with alveolar disease.12,16,17,18

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Figure 58-4. Amebic abscesses of the liver. The cut surface of the liver shows multiple abscesses containing “anchovy paste”

material. (Reproduced with permission from Rubin E, Farber JL. Pathology. 3rd ed. Philadelphia, PA: Lippincott Williams &

Wilkins; 1999.)

Liver involvement with echinococcal cyst can lead to venous obstruction, portal hypertension, sepsis,

and cholangitis. Hydatid cysts are fluid filled, round, and contain three layers of host tissue: an outer 2-

to 4-mm-thick fibrous pericyst composed of compressed and fibrotic liver tissue, a 2-mm-thick middle

anuclear hyaline layer or ectocyst, and an internal germinal layer or endocyst derived from the

parasites. As the cyst matures, invagination of the germinal layer leads to development of daughter

cysts in the periphery (Fig. 58-5). Calcifications are frequently observed radiographically in both viable

and nonviable cysts.12,17,18

Cysts may grow at an annual rate of around 1 to 3 cm/year. Enlarging cysts can cause symptoms of

abdominal pain, biliary obstruction, and jaundice, or less commonly portal hypertension. Masses may be

palpable clinically on examination. Involvement of the biliary tree is variable. Biliary findings result due

to communication between the pericyst and the bile ducts or due to rupture of the cyst into the biliary

tree. Fistulous communication between the cyst and the biliary tract may result in superinfection of the

cyst, cholangitis, and biliary obstruction. This bacterial contamination occurs in around 25% of cases.

Occasionally, cysts may rupture into the peritoneal cavity causing abdominal pain and anaphylaxis.

Multiple intra-abdominal cysts may develop due to intraperitoneal leakage. Hepatic hydatid cysts may

perforate the diaphragm and lead to empyema, biliary-bronchial fistula, or pericardial collection.19

Laboratory tests may be normal or reveal biliary obstruction, and eosinophilia is frequently present.

Serologic ELISA-based screening tests are associated with high false-positive and negative rates.

Confirmatory electrophoresis when available has a higher accuracy rate. Hydatid cysts have a

stereotypic appearance on radiographic studies. US imaging may show daughter cysts, a calcified rim,

and the so-called water lily sign of the curved bands of the delaminated endocyst. CT scan shows a

hypoattenuating lesion with daughter cysts (75%) and a calcified rim (50%). MRI often well displays

daughter cysts, pericyst, and the “hydatid sand” of free scoleces. ERCP may be helpful in cases

involving the biliary tree.12,16

Figure 58-5. A partly opened hepatic hydatid cyst. Brood capsule and daughter cysts are visible in the cavity. (Reproduced with

permission from Kean BH, Sun T, Ellsworth RM. Color Atlas/Text of Ophthalmic Parasitology. New York: Igaku-Shoin; 1991:188.)

2 Open surgical resection is the treatment of choice for symptomatic or complicated hydatid cysts

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(Fig. 58-6). Surgical extirpation aims to remove the cyst intact without spillage of cyst contents.

Alternatively, some have described aspiration of cyst contents prior to resection to minimize the result

of any cyst spillage. After aspiration injection with ethyl alcohol or 20% sterile saline is undertaken to

kill remaining scoleces. In cases where the aspirate is bilious and a communication with the biliary tree

is thus suspected the cyst should be resected without alcohol injection to prevent the occurrence of

sclerosing cholangitis. Laparoscopic resection and percutaneous aspiration techniques have been

reported, especially in conjunction with albendazole. Albendazole should be started 1 week prior to

surgery and generally continued for at least 4 weeks postoperatively. It is poorly absorbed and should

be given with a high-fat meal to increase bioavailability (15 mg/kg/day up to maximum of 400 mg

twice daily). Mebendazole may be used as an alternative therapy but is less well absorbed.

Postoperative morbidity and mortality are low following resection but not zero and recurrence after

surgery is reported from 2% to 25%, and is associated with residual cysts or intraoperative spillage of

cyst contents.16–23

Figure 58-6. The external surface of the liver of a patient with echinococcosis before operation. (Reproduced with permission from

Sun T. Parasitic Disorders: Pathology, Diagnosis, and Management. 2nd ed. Baltimore, MD: Lippincott Williams & Wilkins; 1999.)

SCHISTOSOMA

Schistosoma mansoni, S. japonicum, S. haematobium, and S. mekongi are species of trematode fluke that

infect humans in endemic areas or visitors to these sites. Liver disease is especially severe with S.

mansoni, S. japonicum, and S. mekongi. The life cycle of Schistosoma species alternates between sexual

reproduction in humans and asexual multiplication in water snails. Cercariae enter the human host by

penetrating the skin. An irritating maculopapular rash that lasts for several days is an early

manifestation of infection. Schistosomes live in the intestinal lumen and eggs reach the liver via the

portal circulation where they cause an inflammatory reaction.17,18,24

Infection in the liver is characterized by the presence of inflammatory granuloma surrounding

schistosomal eggs. Acute schistosomiasis is seen typically in nonimmune visitors to endemic areas and

presents as hepatomegaly and severe splenomegaly, often in children and adolescents. Severe cases with

high egg infestation can lead to widespread hepatic necrosis and death. In contrast, chronic

schistosomiasis is seen in young and middle-aged adults. It is usually asymptomatic until manifestations

of portal hypertension declare themselves, such as variceal hemorrhage. Patients will typically present

with hepatosplenomegaly, no ascites, and preserved synthetic function due to the presinusoidal nature

of the condition. Hepatocellular carcinoma (HCC), colon cancer, and follicular lymphoma of the spleen

have been reported in association with hepatic schistosomiasis.12,17,18,25,26

Diagnosis is typically made via the presence of schistosomal eggs in the stool (Kato–Katz smears),

epidemiologic data, and biochemical or serologic findings. Typical laboratory features include

eosinophilia and elevated alkaline phosphatase. Serum transaminases are typically normal. ELISA serum

antibody tests are highly sensitive. Biopsy will show prominent granuloma formation and severe portal

fibrosis (Fig. 58-7). Imaging studies are not typically useful in diagnosis of acute infection. In chronic

cases US may show portal vein wall thickening. Hypertrophy of the left lobe, splenomegaly, and

engorged venous collaterals may all be observed as well. CT may show fibrosis around portal vein

branches as well presenting as low attenuation rings through the liver parenchyma.