Dyspnea and Dysentery: A Case Report of Pleuropulmonary Amebiasis

Merica Shrestha, MD; Anita Shah, DO; Christopher Lettieri, MD


South Med J. 2010;103(2):165-168. 

In This Article


Only 10% of Entamoeba histolytica infections are symptomatic with intestinal manifestations such as abdominal pain and profuse, bloody diarrhea occurring 94–100% of the time. The most common site of extraintestinal infection is the liver. The trophozoites commonly seed the portal circulation, causing hepatic abscesses. This is manifested by fevers, hepatomegaly and right upper quadrant pain. Jaundice may occur if hepatic function is compromised.

The lungs are the second most common site of extraintestinal infection, though pleural invasion is a rare manifestation occurring in 2–3% of patients with invasive disease.[2,3] The incidence is higher in those with a hepatic abscess and can occur in 20% of cases. The mortality rate of amebic pleural empyemas is as high as 16%, which can increase to 42% if due to the rupture of a hepatic abscess into the pleural space.[3] There are four potential mechanisms for pleural transmission. Primary infection can occur via direct inhalation of the cysts or trophozoites. The infection can subsequently extend to the pleura. Additional routes for infection include hematogenous spread from the intestinal tract, lymphatic spread via hepatic channels, or direct rupture of a liver abscess through the diaphragm into the pleura, parenchyma or airway.[4] Pleuropulmonary disease usually manifests with an abrupt onset of pleuritic chest pain, dyspnea and cough. This most often occurs secondary to direct rupture of right liver lobe abscesses through the diaphragm. Sputum is classically described as having an anchovy-paste appearance. Hepatobronchial fistula and bronchial necrosis can also result in a productive cough. Peritoneal extension can occur in 5–10% of amebic liver abscess cases and pericardial involvement is more rare (<2%) and may also occur with rupture of left liver lobe abscesses.[3]

Although intestinal amebiasis can cause symptoms rapidly, pleuropulmonary disease often presents with a delay of symptoms and variation in presentation making diagnosis difficult. Symptoms may not always reveal the extent of infection, so suspicion must be high and radiological imaging should be performed early to prevent unforeseen complications. A chest radiograph often reveals an elevated hemidiaphragm, obliteration of the diaphragmatic border and opacification of lung fields secondary to a pleural effusion.[3–5] Parenchymal disease may present as a consolidated mass or alveolar infiltrate. CT scans can better characterize pleural fluid loculations which can guide thoracentesis and thoracoscopy.[3]

Basic laboratory tests reveal leukocytosis without eosinophilia, normocytic, normochromic anemia and generally normal liver-associated enzymes. Pleural empyema aspiration reveals dark, purulent fluid with a low pH, high WBC count, high LDH and low glucose count. Isolation of fecal trophozoites occurs in only 15% to 33% of extraintestinal cases.[3] Microscopy of a saline wet mount of feces is an insensitive method of diagnosis (<10%) and fecal or aspirate culture can also provide false negative results. Serum antibody testing has been reported as 100% sensitive in patients with amebic liver abscesses.[6] Elevation of serum IgM antibody indicates acute infection; however, levels decline after six months of infection. Serum IgG antibody elevation denotes prior infection, but can also be seen in asymptomatic carriers where E. histolytica is endemic. Newer modes of testing include enzyme-linked immunosorbent assay (ELISA) fecal antigen testing and the detection of amebic DNA via polymerase chain reaction (PCR). These tests can differentiate between E. histolytica and noninvasive strains, such as E. dispar and E. moshkovskii.[7] This differentiation is important in order to avoid unnecessary treatment, particularly in patients from endemic regions exposed to nonpathologic strains. However, if the suspicion for invasive amebiasis is high, treatment should not be withheld pending laboratory diagnosis.

The differential diagnosis of pleuropulmonary amebiasis is complex and its symptoms and radiographic images often mimic other disease processes. In endemic areas, malaria and schistosomiasis are the most common causes of parasitic deaths and can also present with unremitting fevers and hepatic injury.[5] Parasites that can cause pleural effusions include the tapeworm Echinococcus granulosis and the Paragonimus species of lung flukes. Inflammatory reactions of the diaphragm, subphrenic space, pleura and lungs can result in atelectasis, pleuritis and pulmonary consolidation which can commonly be confused with tuberculosis, pulmonary carcinoma or bacterial empyema.[8]

Metronidazole, a tissue agent, works by blocking amebic DNA replication and is given at a dose of 500–750 mg three times daily for 7–10 days. Its rapid intestinal absorption and widespread bioavailability make it effective against trophozoites, with cure rates greater than 90%. Defervescence of fevers and improvement in pain typically occurs within 48–72 hours.[3,5,8] Intraluminal agents such as paramomycin 25–30 mg/kg divided into three daily doses for 7 days or iodoquinol 650 mg three times daily for 20 days are given to eliminate intestinal cysts.[3,5,9] Liver abscesses are generally eradicated with oral therapy, but pleural effusions should be evacuated for symptomatic relief. Empyemas require chest tube thoracostomy and decortication to prevent recurrence and chronic infection.[3,8,10]

The constellation of symptoms in this patient living in an endemic region suggested amebic dysentery. The pulmonary symptoms and abnormal radiographs also raised the suspicion for pleuropulmonary invasion. The positive serum antibody and pleural antigen confirmed the diagnosis of invasive amebiasis. As in this case, empiric therapy should be initiated pending confirmation of the infection. Resolution of symptoms occurred within one week of therapy with metronidazole and paramomycin. Recurrence of disease after clinical resolution rarely occurs beyond 6–9 months and there is no role for continued treatment.[11] Due to clinical improvement, our patient was permitted to return to active duty in Liberia after proper education on improved sanitation methods and the necessity to boil local water and cook local foods thoroughly.


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