Ascariasis‐induced eosinophilic cholecystitis – a unique case

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Sir, I would like to bring to the attention of your readers the following unique case of ascariasis-induced eosinophilic cholecystitis. The condition was first described in 1949 and is characterized by dense, transmural infiltration of the gall bladder wall with eosinophils 1. This rare condition has received attention from French workers 2 who consider it to be a discrete clinical and pathological entity due to a local allergic process within the gall bladder. On occasion, a large number of eosinophil leukocytes are seen in the wall of surgically removed gall bladders. It is recognized that eosinophils may appear in and often from a substantial component of the pleomorphic cellular infiltrate which is found in gall bladders removed 2–3 weeks after an episode of acute cholecystitis, but the significance of an almost pure eosinophilia of the gall bladder is usually not clear either to the histopathologist or the surgeon. Eosinophilic infiltration of the biliary tract may be idiopathic or may represent a variant of eosinophilic gastroenteritis or may be associated with parasitic infestation. Histopathologically there should be little problem in differentiating eosinophilic cholecystitis from the more usually encountered varieties, clinically there seems to be no difference. The presence of eosinophilia in certain parasitic infections, particularly those helminthic infections that invade tissue, has been recognized particularly from the time the eosinophil was discovered. Yet its role in parasitic disease is still disputed. Although eosinophils are capable of phagocytosing bacteria and other microorganisms, their efficacy in this regard is felt to be inferior to the neutrophil. A 40-year-old female presented to our hospital with signs and symptoms of acute cholecystitis. Abdominal ultrasonography revealed a distended thick-walled gall bladder with a long coiled tubular echogenic structure within it. A diagnosis of gall bladder ascariasis with acute cholecystitis was made. The patient was managed conservatively but did not show any improvement even after 1 week's treatment. Cholecystectomy was carried out and on histopathological examination of the specimen a pure transmural infiltration of numerous eosinophils in the gall bladder tissue was seen and a final diagnosis of eosinophilic cholecystitis was made. This is the first reported case of eosinophilic cholecystitis induced by gall bladder ascariasis. The parasite may have induced a hypersensitivity reaction with numerous eosinophils in the gall bladder wall. In a recent report of eosinophilic cholecystitis associated with hepatic hydatid cyst ruptured into biliary tract, the cause of eosinophilic cholecystitis was similarly attributed to the hypersensitivity reaction 3. We would agree with the French workers 2 who consider this to be a local allergic process that should be referred to as a discrete clinical and pathological entity.