Simultaneous Amoebic Liver Abscess and Hepatitis A Infection Eli Schwavtz and Nancy Piper-Jenks

Hepatitis A virus (HAV) infection and amoebic liver abscess have an identical mode of transmission (fecal-oral route) and similar epidemiology. Either of these diseases might be considered in patients present- ing with clinical signs and symptoms of liver disease in areas of the world where hepatitis and Entarnaeha /zi.dyticu are endemic. The following two cases describe patients with simultaneous infection of HAV and amoebic liver abscess.This report emphasizes the role of dual infection in patients from endemic areas. It also challenges the assumption that jaundice in patients with amoebic liver abscess is due to amoebic hepatitis, rather than co- infection with viral hepatitis.

Case No. 1

A 28-year-old Israeli male, who had been traveling for 3 months in India and 1 month in Nepal, presented to CIWEC clinic (a western medical facility in Kath- mandu serving expatriates and travelers) after 3 days of fever, anorexia and fatigue, followed by production of dark colored urine.

O n examination he looked moderately ill and jaun- diced, with significant liver tenderness. His temperature was normal and he had no hepatosplenomegaly nor lymphadenopathy. Urine analysis was strongly positive for direct bilirubin, and a clinical diagnosis of HAV was made. (The patient had not received serum immune globulin nor hepatitis A vaccine before travel.) Liver transaminase, a test not readily available m Nepal, was not measured at this time. A serum sample was sent as part of a survey of hepatitis patients from Nepal to the Armed Forces Research Institute of Medical Sciences in Bangkok, Thailand.' Serology showed IgM hepatitis A antibody positive, confirming the diagnosis of acute hepatitis A infection.

fii Schwartz, MD, DTMHThe Medical Center for theTraveller, Misgav Ladach General Hospital, Jerusalem, Israel; Nancy Piper-Jenks, MS, FNP: Research Fellow, Center of the Evaluation of Vaccination, Department of Epidemiology and Community Medicine, University of Antwerp, Antwerp, Belgium.

Reprint requests: Eli Schwartz, MD, The Medical Center for theTraveller, Misgav Ladach General Hospital, P0.B. 90, Jerusalem, Israel 91000.

JTravel Med 1998; 5:95-96.

Over the next several days his general condition improved. Ten days later, however, the patient returned to the clinic complaining of new onset of febrile episodes, headache, and a recurrence of a right upper quadrant (RUQ) pain. A complete blood count revealed a white blood cell (WBC) count of 17,000/mm3 with 61% neu- trophils, 2% bands, 21% lymphocytes and 11% monocytes. Liver enzymes were elevated (normal ranges are shown in parentheses): bilirubin 4.5 mg/dL (0.3-1 .O), serum glu- tamic oxalacetic transaminase (SGOT) 530 IU/L (G35), alkaline phosphatase 1260 IU/L (25-140). Blood and stool cultures were negative. Widal test was negative. Broad-spectrum antibiotics of chloramphenicol and co- trimoxazole were administered, with no change in the course of the disease.

An abdominal ultrasound revealed a cystic lesion in the right liver lobe, measuring 60 X 55 mm.With a pre- sumptive diagnosis of E. histolyticu as the causative agent of the liver abscess, oral tinidazole 2g/day was initiated. After 24 hours the patient's fever and pain subsided and his overall condition dramatically improved. Following a 5-day course of tinidazole, a 10-day course of dilox- anide furoate 500 mg three times/day was given. The patient had a complete and uneventful recovery. Over the next 2 months, repeated ultrasonography demonstrated complete resolution of the hepatic abscess.

Case No. 2

A 30-year-old Israeli woman, who had been trav- eling for 5 months in India and 4 months in ruralTibet, complained of bloody diarrhea accompanied by abdom- inal pain, nausea and vomiting. Several days later she noticed that she was jaundiced. Her general condition deteriorated and she was eventually evacuated to Kath- mandu, Nepal. In a local hospital, severe amoebic coli- tis with perforation was diagnosed and a right hemicolectomy was performed.

Due to an unremitting fever, ultrasonography was performed 7 days later which revealed four hepatic abscesses, three in the right liver lobe and one in the left. Laboratory results showed a white blood cell (WBC) count of 21,000/mm3 and a hematocrit of 16%. Liver enzymes were elevated: bilirubin 3.6 mg/dL (0.3-1 .O), serum glutamic oxalacetic transaminase (SGOT) 61 IU/L (0-35), alkaline phosphatase 430 IU/L (25-140). The pathologic specimen of the colon and stool examination showed numerous amoebic trophozoites. Amoebic

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serology was positive, with a titer of 1 :2048. Anti-HAV IgM was positive.

She was treated following surgery with metronida- zole 500 mg three times/day for 4 weeks with gradual clinical improvement and slow resolution of the abscesses. The complete resolution as shown by ultrasonography took 6 months.

Discussion

These two cases clearly demonstrate the coexis- tence ofamoebic liver abscess and hepatitisA virus infec- tion which are both transmitted through a fecal-oral route. In each case the development ofjaundice can be explained by the HAV. In patients with amoebic liver abscess, liver enzymes may be mildly to moderately ele- vated, but jaundice is rarely reported and its etiology is unclear.Anecdota1 cases ofjaundice with liver abscess have been reported when the abscess is compressing the bile duct, causing obstructive jaundice,2 however, in most cases jaundice in relation to liver abscess is not under- sto0d.A report of 11 patients from India with amoebic liver abscess andjaundice failed to show on post mortem any hepatic inflamrnati~n.~

In the cases presented here, the unusual pattern of the illnesses suggested a dual infection. Co-infection with viral hepatitis was the cause ofjaunhce in these cases.The patients were both travelers, and the viral hepatitis was due to HAV infection, whch is the most common viral hepati- tis of a nonimmune population. Adults in endemic areas are immune to HAV, and among them hepatitis E (enter- ically transmitted non-A non-B) is the most conmon eti- 010gy.~ Hepatitis E has been a diagnosis of exclusion, but

the recent availability of hepatitis E markers has made it possible to positively identify it.

Simultaneous occurrence of enterically transmitted diseases must not be overlooked in countries where these diseases are endemic. Concomitant typhoid fever and HAV has been reported5 and one case of HAV and amoebic liver abscess.'With the possibility of dual infec- tion, one must he cautious in attributing jaundice in patients with amoebic liver abscess solely to the disease process (amoebic abscess) unless there is obstruction by the abscess. One should rather look to possible co- infection with viral hepatitis, especially hepatitis A or hepatitis E.

References

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Schwartz E, lnnes BL, Shlim D R , Snitbhum K.Vira1 hepati- tis in expatriate residents and travellers in Nepal. J Wilder- ness Med 1991; 2:88-93. Ramachandran S, Pakianathan V, Aiyathurai JEJ. Severe obstructive jaundice due to amoebic liver abscess. Med J Aust 1976; 1:925. Datta DV, Saha S, Singh SA. The clinical pattern and prog- nosis of patients with amoebic liver abscesses and jaundice. Am J Dig Dis 1973; 18:887-898. Bradley DW. Enterically transmitted non-A, non-B hepati- tis. Br Med Bull 1990; 46:442-461. Schwartz E, Piper-Jenks N, Shlim DR.'Typhoid hepatitis' or typhoid fever and acute viral hepatitis.Trans K SocTrop Med

Orenstein WA,Wu E,Wilkins J. et al. Simultaneous amoebic liver abscess and hepatitis A. Am J Gastroenterol 1981; 75:52-54.

Hyg 1994; 88:437-438.