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Acalculous cholecystitis by P. falciparum in a 3-year old child.

Acute cholecystitis involves inflammation of the gallbladder and can be seen with cholelithiasis (calculous) or in the absence of gallstones (acalculous). Acute acalculous cholecystitis (ACC) is rare, but important cause of cholecystitis in pediatrics (1). It is estimated that in children, 30-50% of cholecystitis cases are acalculous, compared with 2 to 17% of cases in adult patients (2). In children ACC mainly result from antecedent bacteremia and localization of bacteria in the gallbladder. So the majority cases have been managed by medical treatment alone. Gastrointestinal manifestations are common in malaria3, but the ACC is extremely a rare manifestation of malaria and a very few cases have been reported previously. Here we report a case of ACC attributed to severe Plasmodium falciparum malaria infection in a 3-year old child.

A 3-year old female child presented with history of intermittent fever since five days associated with rigors. History of abdominal pain and vomiting was present. Vomiting was non-projectile and non-bilious. On physical examination she was irritable, temperature 39[degrees]C, pulse rate 120/min, respiratory rate 28/min and blood pressure 96/60 mm Hg. She was severely pale. Icterus, cyanosis or lymphadenopathy was absent. On per abdomen examination revealed tenderness in right upper quadrant. Hepatosplenomegaly was present. Murphy's sign was positive. Other systemic examinations were normal.

On investigation, peripheral smear showed a ring stage of P. falciparum and the parasite density was 50,000/[micro]l. The rapid diagnostic test (antigen HRP2) for P. falciparum was positive. Complete blood cell count showed a hemoglobin 5.4 g%, WBC 14100 cu/ (85% polymorphs, 42% lymphocytes, 2% eosinophils and 1% monocytes), hematocrit 17.5, platelet count 56,000/mm (3). Liver function and renal function tests were within normal limit. Widal test was nonreactive. Blood and urine culture were sterile. Hemoglobin electrophoresis was AA type. USG abdomen revealed thickened gallbladder (wall thickness was 6 mm) and hepatosplenomegaly. No abnormality detected on X-ray abdomen and chest. Child was put on IV antibiotics and antimalarial (artesunate) drug. Packed-cell blood transfusion was given. On the basis of clinical and USG findings the diagnosis of acute cholecystitis was made. After five days of treatment, child condition was improved.

ACC has been reported with various infectious agents like Salmonella typhi, Escherichia coli, Mycoplasma pneumoniae, leptospirosis, brucellosis, rocky mountain spotted fever, group A streptococci, and Staphylococcus aureus sepsis. In immunocompromised hosts, acalculous cholecystitis has been reported in fungal infection with Candida or Aspergillus, Giardia and Cryptosporidium1. The diagnosis of ACC was made according to clinical features and sonographic findings. The clinical manifestations were fever, right upper quadrant tenderness, and a positive Murphy's sign. Sonographic findings were a thickened gallbladder wall (defined as wall thickness > 4 mm) in absence of ascitis and hypoalbuminemia, a positive sonographic Murphy's sign (defined as maximum tenderness of the sonographically localized gallbladder), pericholecystic fluid collection, and no stone(s) in the gallbladder (4). Patients had no recent history of burns, trauma, vasculitis, or recent surgery.

The exact pathogenesis of ACC is not clearly understood, but cholestasis and increased bile viscosity from prolonged fasting, spasm of the ampulla of vater, endotoxemia, microangiopathy and ischemicreperfusion injury, among the other causes have been suggested (5-7). Intense sequestration of parasite in vascular endothelium, visceral ischemia and increased vascular permeability (8), are well-known pathogeneses of falciparum malaria responsible for major gastrointestinal manifestations. Similarly, it appears to be responsible for the pathogenesis of acute cholecystitis in our case. The other possible reason for ACC in falciparum malaria could be Salmonella infection, as it is related to a transient immunosuppression induced by malaria (9), but in our case blood culture was negative. So in this case the former mechanism appear to be involved for the pathogenesis of ACC. Although the pathogenesis of ACC remains controversial, malaria should be included in the differential diagnosis of ACC, especially in endemic zones of malaria.

Key words Acalculous--cholecystitis--falciparum malaria

Received: 19 October 2007 Accepted: 29 November 2007


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(4.) Bilhart LE. Acalculous cholecystitis, adenomatosis, cholesterosis, and polyps of the gallbladder. In: Slieisenger MH, Fordtran JS, editors. Gastrointestinal and liver disease. VI edn. Philadelphia: Saunders 1999; p. 993-1005.

(5.) Shapiro MJ, Luchtefeld WB, Kurzurki JE. Acute acalculous cholecystitis in the critically ill. Am Surg 1994; 60: 335-9.

(6.) Hakala T, Nuutinen PJO, Roukonen ET, Alhava E. Microangiopathy in acute acalculous cholecystitis. Br J Surg 1997; 84: 1249-2.

(7.) Savoca PE, Lryo WE, Pastemark B, Gusberg RJ. Dose visceral ischemia plays a role in the pathogenesis of acalculous cholecystitis? J Clin Gastroenterol 1990; 12: 33-6.

(8.) White NJ. Malaria. In: Gordon C, Cook Z, Alimuddin, editors. Mamon's Tropical Diseases, XXI edn. London: Saunders 2003; p. 1223-5.

(9.) HOM, Webster HK.T-cell response in acute falciparum malaria. Immunol Lett 1990; 25: 135-8.

Corresponding author: Dr Arvind Kumar, Department of Pediatrics, Mahatma Gandhi Institute of Medical Sciences, Sevagram, Wardha- 442 102, India. E-mail:

Arvind Kumar, Amar M. Taksande & K.Y. Vilhekar

Department of Pediatrics, Mahatma Gandhi Institute of Medical Sciences, Wardha, India
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Title Annotation:Case Report
Author:Kumar, Arvind; Taksande, Amar M.; Vilhekar, K.Y.
Publication:Journal of Vector Borne Diseases
Date:Mar 1, 2008
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