Abstract

Purpose: A 37 year-old Portuguese male, with genotype 4 hepatitis C cirrhosis (Child-Pugh class B), was submitted to antiviral treatment with Peg-interferon α-2a and ribavirin in 2006, with no response. At that time he had no complications of portal hypertension. In December 2010, he was admitted in our Gastroenterology Ward due to fever, abdominal pain and watery profuse diarrhea starting 72 hours prior to admission. Laboratory workup revealed hypokalemia (2.8 mEq/L) and an elevated C-reactive protein (165 mg/L). He received fluids reposition and antibiotherapy (third-generation cephalosporin and metronidazol). Abdominal X-ray was normal; Human Immunodeficiency Virus 1 and 2, Hepatitis B, Cytomegalovirus, Herpes 1 and 2 serologies were negative. Salmonella, Shigella, Campylobacter, parasitology exam, virology exam, micobacterology exam and toxin Clostridium difficile in stool samples were negative. Blood culture yielded curved gram-negative bacillus (fig. 1), identified as Vibrio cholerae and confirmed by molecular methods. Vibrio cholerae serogroups non O1 and non O139 were excluded by serology. He was discharged, asymptomatic, without ascites or encephalopathy. He lived in an urban area and there were no similar complaints in his family members or recent travels. He was not exposed to seawater, but he had consumed cooked shrimps, 72 hours prior to admission. V. cholerae strains not agglutinating with O1 or O139 antisera are referred to as non-O1 and non-O139. Only O1 and O139 serogroups of V. cholerae are responsible for the epidemic or pandemic cholera by secreting a non-invasive enterotoxin, bacteraemia is rare. V. cholerae non-O1 and non-139 may cause sporadic cases of diarrhea but may also lead to invasive extraintestinal illness and bacteraemia. This is a rare condition and is potentially fatal. The majority of reported cases occurred in patients with cirrhosis or haematological maligancies associated with seafood consumption, as in this case.Figure: No Caption available.

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