Entamoeba histolytica Infection

A 2½-year-old boy with no significant medical history presented to the emergency department with a 1-month history of generalized abdominal pain. No position made the pain better or worse, and it had no relationship to meals. He also had had intermittent fevers up to 39.4°C over the past 2 months. There was no associated diarrhea, gross blood in the stool, vomiting, or weight loss.

The boy had been seen by his primary pediatrician 3 weeks ago and had received a diagnosis of constipation. One week prior to presentation, he had been evaluated while in Mexico and had received a diagnosis of sinusitis and acute otitis media, for which he had been prescribed a 10-day course of amoxicillin/clavulanic acid. He had been feeling much better until the day of presentation, when the abdominal pain returned, and he refused to eat.

Physical examination revealed an afebrile, mildly ill-appearing boy in no apparent pain. His weight was below the 5th percentile and his height was in the 29th percentile. His abdomen was soft, nondistended, and mildly tender to palpation in the right upper quadrant and epigastrium. Bowel sounds were normal. The liver edge was palpable 1.5 cm below the right costal margin. He had no guarding, rebound tenderness, scleral icterus, or jaundice. The rest of the examination findings were noncontributory.

Laboratory tests revealed a white blood cell count of 27,000/µL, with 82.6% neutrophils, 9.5% lymphocytes, 7.7% monocytes, and 0.1% eosinophils; a hemoglobin level of 9.4 g/dL; mean corpuscular volume of 82 µm³; and a platelet count of 802,000/µL. A comprehensive metabolic panel disclosed normal serum electrolytes; aspartate aminotransferase, 41 U/L; alanine aminotransferase, 24 U/L; alkaline phosphatase, 360 U/L; and total bilirubin, 0.5 mg/dL. Results of a coagulation profile were normal. The erythrocyte sedimentation rate and C-reactive protein level were increased at 104 mm/h and 202 mg/L, respectively.

A computed tomography (CT) scan of the abdomen with oral and intravenous contrast was performed, revealing a 5.2 × 4.5 × 5.9-cm abscess occupying the entire left lateral segment of the liver (A). Giemsa stain of fluid aspirated from the liver lesion, viewed at ×40 magnification, showed multinucleated cysts consistent with Entamoeba histolytica (B).

The patient received a diagnosis of hepatic abscess and was admitted for intravenous piperacillin/tazobactam and metronidazole. On day 2, CT-guided percutaneous drainage under sedation yielded 60 mL of purulent fluid. A percutaneous pigtail catheter was secured and drained approximately 50 mL of fluid per day. Gram stain of the fluid revealed no organisms. Giemsa and Papanicolaou stains of smears, as well as hematoxylin-eosin stain and periodic acid-Schiff reaction testing of cell block sections showed amoebic trophozoites and/or cysts. The sample was sent to the Centers for Disease Control and Prevention, where real-time polymerase chain reaction (PCR) test results for E histolytica returned positive. On discharge, the boy’s medications were transitioned to oral metronidazole followed by a 20-day course of iodoquinol.

After discharge, the boy had good weight gain with no residual symptoms. Follow-up stool study results were normal 2 weeks after hospital discharge, and results of abdominal ultrasonography 6 weeks out confirmed the complete resolution of the hepatic abscess. The boy’s mother and father both had positive stool cultures for E histolytica, while his 6-month-old sibling’s stool culture results were negative.

Amebiasis is a parasitic infection caused by the protozoan E histolytica, which inhabits the large intestinal lumen of humans and primates.¹ Although 80% to 90% of cases are asymptomatic, amebiasis rarely can give rise to intestinal disease and extraintestinal manifestations, including liver abscess (most common) and pulmonary, cardiac, and cerebral dissemination.²

Amebiasis occurs in 1% to 5% of the world’s population, with prevalence rates highest in the tropics and in areas of crowding and poor sanitation.¹ In developed countries such as the United States, it is seen mainly in migrants from and travelers to endemic countries.² The infection route is fecal-oral, usually when cysts are ingested from contaminated water and food. After exposure, symptoms may develop in a few days to as late as 1 year, if at all, but 2 to 4 weeks is most common.³

Symptoms depend on the site and extent of involvement and may include fever, malaise, abdominal pain, and anorexia, which may progress to liquid stools with flecks of blood or mucus.¹ Extraintestinal involvement primarily is due to hematogenous spread, with the liver as the most common site and occurring in less than 5% of cases.¹ Invasive amebiasis is a serious life-threatening disease in children, and delay in diagnosis significantly increases morbidity and mortality.

Identifying cysts or trophozoites in the feces is diagnostic of intestinal amebiasis. A single stool specimen evaluation has a yield of 50% to 60%, with higher sensitivity of approximately 95% with successive evaluations daily over 3 days, since cyst excretion is intermittent.^1,2 Endoscopic scrapings also can be examined.¹ A newer PCR test can differentiate E histolytica from the morphologically identical Entamoeba dispar—an important distinction, because infection with the latter does not require treatment.³

Liver abscess aspirates rarely have the classic “anchovy paste” appearance⁴ and, when examined microscopically, seldom show trophozoites or leukocytes. If extraintestinal disease is suspected, serologic assays may be helpful in that they are more than 95% sensitive.¹ However, seropositivity also can indicate prior infection and may be delayed or absent in very young patients.³

The choice of amebicide is based on the location and severity of disease. Asymptomatic intestinal disease can be treated with paromomycin, iodoquinol, or diloxanide furoate. Therapy duration ranges from 7 to 20 days depending on the agent. The choice can be guided by expense, availability, and adherence factors. Extraintestinal disease is treated with 5 days of tinidazole or 7 to 10 days of metronidazole, followed by the same course as that of asymptomatic amebiasis.⁵ Some authors promote needle aspiration as an additional routine therapy for the treatment of uncomplicated liver abscess.⁶ Relapses are rare, but examination of feces should be repeated monthly for 4 to 6 months after therapy. Household contacts also should be examined for asymptomatic infection and treated if test results are positive.

Amebiasis is uncommon, especially outside endemic areas. Its presentation is extremely variable and unpredictable. Diagnosis requires a high degree of suspicion, especially in children.

Our case underlines the importance of keeping amebic liver abscess in the differential diagnosis in a child with prolonged abdominal pain with fever and elevated inflammatory markers. Our patient’s symptoms preceded his travel to an endemic area (Mexico); thus, we suspect he likely was infected via contamination from his parents, who were asymptomatic carriers.

References

1. Diaz R, Maqbool A. Parasitic infections. In: Liacouras C, Piccoli D, eds. Pediatric Gastroenterology: The Requisites in Pediatrics. Philadelphia, PA: Mosby Elsevier; 2008:170-186.

2. Salvana EMT, Salata RA. Amebiasis. In: Kliegman RM, Stanton BF, St. Geme JW III, Schor NF, Behrman RE, eds. Nelson Textbook of Pediatrics. 19th ed. Philadelphia PA: Elsevier Saunders; 2011:1178-1180.

3. Parasites - amebiasis (also known as Entamoeba histolytica infection). Centers for Disease Control and Prevention Web site. http://www.cdc.gov/parasites/amebiasis/. Updated November 2, 2010. Accessed August 20, 2015.

4. Merten DF, Kirks DR. Amebic liver abscess in children: the role of diagnostic imaging. AJR Am J Roentgenol. 1984;143(6):1325-1329.

5. Amebiasis. In: Pickering LK, ed. Red Book: 2012 Report of the Committee on Infectious Diseases. 29th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2012:228-231.

6. Khan R, Hamid S, Abid S, et al. Predictive factors for early aspiration in liver abscess. World J Gastroenterol. 2008;14(13):2089-2093.