ABSTRACT
The present article documents a case of Fusobacterium sepsis with a transient anticardiolipin antibody increase in an otherwise healthy 24-year-old patient. He was presented to the emergency room with headache and fever. His temperature was 39.5°C, laboratory results revealed a white blood count of 15.2×10(3)/µl and C reactive protein 22.6 mg/dl. The patient was admitted. Chest X-ray showed the infiltrate in bilateral lower lung area. He received 400 mg of clarithromycin per day. His all symptoms did not change. On the 8(th) day in the hospital, the patient's antibiotics were switched to pazufloxacin. Chest and abdominal CT scan showed some irregular patchy nodules of around 1 cm in diameter in the bilateral lower lung fields and a round low density lesion 3 cm in diameter in the right upper segment (S8) in the liver. Blood culture revealed Fusobacterium necrophorum. On the 10(th) day, the antibacterial agent was changed from pazufloxacin to ampicillin sulbactam. On the 17(th) day, we added clindamycin. As a result his temperature gradually returned to normal. It is reported that the titer of anticardiolipin antibody increases in the sepsis patients caused by Fusobacterium necrophorum. As his symptoms disappeared, his titer of anticardiolipin antibody also decreased. So we considered he had a transient anticardiolipin titer increase.
Subject(s)
Fusobacterium necrophorum/isolation & purification , Lemierre Syndrome/complications , Lemierre Syndrome/microbiology , Liver Abscess/etiology , Pulmonary Embolism/etiology , Anti-Bacterial Agents/administration & dosage , Antibodies, Anticardiolipin/blood , Biomarkers/blood , Drug Substitution , Humans , Lemierre Syndrome/diagnosis , Lemierre Syndrome/drug therapy , Liver Abscess/diagnosis , Liver Abscess/drug therapy , Liver Abscess/microbiology , Male , Pulmonary Embolism/diagnosis , Pulmonary Embolism/drug therapy , Pulmonary Embolism/microbiology , Tomography, X-Ray Computed , Young AdultABSTRACT
A 69-year-old-woman presented with acute epigastric pain, nausea, vomiting and heartburn. Endoscopy disclosed acute gastric mucosal lesions including mucosal edema, erosions, and ulcers with blood crusts in the antrum. Touch cytology and histological assessment obtained from the affected mucosa revealed acute neutrophilic gastritis and single longer and more coiled organisms than Helicobacter pylori, suggesting Helicobacter heilmannii. Electron micropragh confirmed the characteristic morphology. Despite a positive rapid urease test, H. pylori was not isolated by culture or detected by histology and Gram smears. Based on these findings, a diagnosis of acute gastric mucosal lesions associated with H. heilmannii infection was established. This was successfully treated with a 2-week triple therapy consisting of lansoprazole, clarithromycin and metronidazole with persistent endoscopic and histological remission. This is a rare case of H. heilmannii-associated acute gastric mucosal lesions, diagnosed by morphology using touch cytology and histology. The patient might benefit from antimicrobial treatment employing the regimen effective for H. pylori.
