Amebiasis and Echinococcal Diseases of the Lung

William L. Ring

AMEBIASIS

Amebiasis is caused by the protozoan Entamoeba histolytica and is most common in tropical and subtropical regions. E. histolytica is morphologically identical to the nonpathogenic species E. dispar and E. moshkovskii. In the United States, infection is observed most commonly in (1) travelers and immigrants exposed in endemic areas, (2) patients in mental health institutions, and (3) HIV-positive patients. The organism is usually confined to the colon, producing either no symptoms or amebic dysentery. The disease is usually contracted by ingestion of food or water contaminated by feces or by fecal–oral contact.

Rarely, mature organisms (trophozoites) penetrate the bowel wall and migrate to the liver by the hepatic veins, where an abscess may form. This invasive form of amebiasis is 3 to 10 times more common in men, is associated with alcohol abuse, and is more common in individuals who are malnourished or immunosuppressed. Most patients with invasive disease present with several weeks of right upper quadrant abdominal pain and fevers. By the time a hepatic abscess forms, no dysenteric symptoms are present in up to two-thirds of patients, and most patients do not have parasites detectable in their stool.

Thoracic involvement occurs in 13% to 35% of patients with hepatic amebiasis. The usual route of pleuropulmonary infection is by extension from a hepatic or subdiaphragmatic abscess. Less commonly, direct parasitic migration occurs into the thorax. In addition, hematogenous spread to the lung rarely occurs by hemorrhoidal veins or lymphatics. All modes of spread can result in empyema or lung abscess. Pleuropulmonary disease can also occur without actual parasitic invasion in the form of lower-lobe infiltrates and exudative effusions; the mechanism for this is not clear, but it is presumably a response to subdiaphragmatic infection.

Amebic pleuropulmonary disease is 10 to 15 times more common in men than in women, with a peak incidence between ages 20 and 40. Patients usually have a history of amebic dysentery and may complain of right upper quadrant pain, weight loss, and cough. Rarely, the cough is productive of thick, dark chocolate sauce or anchovy paste sputum or even bile (biliptysis), indicating hepatobronchial and bronchobiliary fistulas, respectively. Fever and signs of empyema or consolidation may also be present. Chest roentgenogram typically reveals a right-sided effusion or right lower-lobe lung abscess. In addition, areas of consolidation may be seen in the right lower lobe, middle lobe, or both. The right hemidiaphragm may be elevated and have decreased motility. In cases involving the left lobe of the liver, changes can occur in the left lung. Computerized tomography will show the liver abscess. Magnetic resonance imaging can directly visualize the secondary diaphragmatic rupture. Thoracentesis usually reveals a sterile exudate; however, organisms are rarely present.

Routine laboratory examination may show a mild leukocytosis and eosinophilia. Cysts are rarely found in the sputum or the pleural fluid; however, when present, they confirm the diagnosis. A serum hemagglutination test for antibodies to amebae is positive in up to 95% of invasive infections, and will remain positive for years after the infection. Fecal antigen detection tests for amebae are rapid, highly specific, and widely available.

It is reasonable to initiate therapy in the presence of an appropriate clinical presentation. The generally recommended medications for extraintestinal amebiasis are metronidazole (750 mg tid) orally for 10 days followed by a luminal agent such as iodoquinol (650 mg tid for 20 days), paromomycin (25–35 mg/kg/day in three divided doses for 7 days), or diloxanide furoate (500 mg tid for 10 days). Failure to respond to treatment should call into question the diagnosis or suggest the possibility of a secondary bacterial infection. The rare patient with invasive amebiasis who does not respond to this regimen should be treated with chloroquine and percutaneous drainage of the liver abscess and any pleural fluid. Surgery is rarely indicated.

ECHINOCOCCAL DISEASE

Echinococcosis or hydatid disease is caused by the postlarval metacestode stage of the tapeworm Echinococcus. Humans are an intermediate host for this parasite. After ingestion of contaminated food, water, or soil, the oncosphere penetrates the intestine and migrates into the systemic circulation, whereby it is ultimately deposited within an organ, especially the liver or lungs. Once in an organ, cellular differentiation occurs, resulting in the development of a hydatid cyst. The mature cyst consists of an inner germinal layer, the endocyst; an outer chitinous layer, the exocyst; and a peripheral fibrous layer caused by host reaction, the pericyst.

Four species of Echinococcus cause human disease. E. granulosus is the most common because of its wide distribution and its high prevalence in sheep; it involves the lung 60% of the times and often has a protracted and relatively benign course. E. granulosus causes cystic echinococcosis, the classic hydatid disease, with often large, unilocular cysts. E. multilocularis is less common. It is primarily a liver disease with occasional involvement of the lung and typically has an aggressive, malignant course. E. multilocularis causes alveolar echinococcosis, with somewhat smaller, multilocular cysts, which at pathology appear to have an alveolar appearance. E. vogeli and E. oligarthus are restricted to parts of Central and South America and only rarely cause human disease. They cause polycystic echinococcosis.

E. granulosus

Only gold members can continue reading. Log In or Register to continue