A case of Crimean-Congo haemorrhagic fever with acalculous cholecystitis and intra-abdominal abscess

Abstract number: P1405

Caylan R., Hasanoglu I., Yapar D., Tasyaran M.A.

Crimean Congo Haemorrhagic Fever (CCHF) is a fatal systemic viral infection and it is an important health problem in Turkey. Since it leads to diffuse endothelial damage, many complications can be seen during the course of the disease. We report here an atypical presentation of CCHF with acute acalculous cholecystitis (AAC) and intraabdominal abscess (IAA).

Case presentation: A 29-year old previously healthy female applied to a regional health-care facility with complaints of fever, headache, myalgia and fatigue. Despite no tick-bite history, her doctor recommended hospitalization based on elevated liver enzymes, leukopenia and thrombocytopenia with a prediagnosis of CCHF and referred to our hospital because of severe trombocytopenia.

Upon admission her body temperature was 39.7°C and had a platelet count of 12000 K/mcL, aspartate aminotransferase (AST) 160 U/L, alanine aminotransferase (ALT) 68 U/mL and lactate dehydrogenase (LDH) 596 U/L. Her CCHF diagnosis was confirmed by RT-PCR. She had severe epistaxis and was treated with fresh frozen plasma, platelet transfusions and nasal packing. Meanwhile, she developed somnolence and had right hypocondrial and epigastric pain. Her liver enzymes elevated suddenly (AST 4045 U/L, ALT 1223 U/mL). Ultrasonography showed that her gallbladder wall thickness was 16 mm and there was no gallstone, so she was diagnosed as having CCHF with AAC. Her oral intake was ceased immediately and ciprofloxacin was initiated. Twenty days after admission, the patient's fever was still high despite antibiotheraphy. The abdominal tomography (CT) showed multiple IAA. Her clinical status improved with antibiotheraphy and percutaneous drainage. A control CT showed considerable reduction in the dimensions of the abcesses.

Since endothelial damage is a main contributor in the pathogenesis of CCHF, it can be seen in many different clinical manifestations and complications. Although it is known as a rare complication of viral haemorrhagic fevers, AAC hasn't been reported in the course of CCHF. Our case was also complicated with IAA which hasn't been reported as a complication of CCHF as well. It is difficult to explain IAA in this case while many aspects of the CCHF pathogenesis remain unclear. This may have been caused by bacterial translocation during the development of multiple haemorrhage sites seen in cases with aggressive courses. In conclusion, CCHF is a systemic viral infection which can be seen with many complications such as AAC and IAA.

Session Details

Date: 10/04/2010
Time: 00:00-00:00
Session name: Abstracts 20th European Congress of Clinical Microbiology and Infectious Diseases
Location: Vienna, Austria, 10 - 13 April 2010
Presentation type:
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