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Fatal Septic Shock with Multiple Organ Failure Due to Campylobacter jejuni
Author(s) -
Valérie Meyrieux,
Guillaume Monneret,
Alain Lepape,
M. Chomarat,
V. Banssillon
Publication year - 1996
Publication title -
clinical infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.44
H-Index - 336
eISSN - 1537-6591
pISSN - 1058-4838
DOI - 10.1093/clinids/22.1.183
Subject(s) - campylobacter jejuni , medicine , septic shock , campylobacter , shock (circulatory) , multiorgan failure , intensive care medicine , microbiology and biotechnology , sepsis , bacteria , immunology , surgery , biology , genetics
Campylobacter jejuni infections are among the most common causes ofgastroenteritis. However, severe extraintestinal infections have been occasionally described, mainly in immunodeficient patients and patients with neoplasia [1, 2]. To our knowledge, we describe the first case of fatal septic shock due to C. jejuni in a thalassemic patient who had undergone splenectomy. A 41-year-old man was admitted to the hospital with fever (temperature to 38°5), chills, low blood pressure (80170 mm Hg), tachycardia (pulse rate, 120), respiratory distress, and drowsiness. Two days before admission, he had had diarrhea, abdominal pain, and fever and had been treated with ampicillin. The patient had a complex medical history of thalassemia intermedia for which he had undergone splenectomy 15 years before. Recurrent venous thrombosis necessitated treatment with oral anticoagulants. He underwent frequent blood transfusions because of a recent diagnosis of hemochromatosis with cirrhosis, diabetes mellitus, and right ventricular failure. Owing to the deterioration ofhis clinical status, he was admitted to the intensive care unit. Laboratory studies showed hemolytic anemia (hemoglobin level, 9 g/dL; reticulocyte count, 479 X 10 hemoglobin F level, 39.6%; hemoglobin A2 level, 4.2%; indirect bilirubin level, 51 J,tmol/L; very low haptoglobin level), severe acidosis (lactate level, 8 mmol/L; pH, 7.26), acute renal failure (creatinine level, 216 J,tmol/L), coagulation disorders (prothrombin time, 55 seconds [22%]; activated partial thromboplastin time, 85 seconds [normal, 32 seconds]; normal factor V level), and leukocytosis (WBC count, 19,000/mm) . HIV serology was negative. A chest roentgenogram showed cardiac enlargement and adult respiratory distress syndrome. Abdominal and renal echography disclosed mesenteric lymph nodes and hepatomegaly. Despite aggressive fluid treatment, the patient's condition further deteriorated, and he had to be mechanically ventilated. A Swan-Ganz catheter was inserted to optimize administration of catecholamines and measurement of right-ventricle filling pressure. Empirical antibiotic treatment with piperacillin/tazobactam and amikacin was started. Four blood culture specimens obtained during admission yielded a motile gram-negative rod after 2 days of incubation. Subcultures on Campylosel medium (biolvlerieux, Marcy l'Etoile, France) at 42°C under microaerophilic conditions yielded excellent growth of a little gray colony. The microorganism was oxidase-positive, catalase-positive, hippurate-positive, and urease-negative. The isolate was susceptible to nalidixic acid and resistant to cephalothin, amoxicillin, amoxicillin/clavulanate, aminoglycosides, erythromycin, and pefloxacin; it was identified as C.jejuni. Bronchoalveolar lavage fluid, a protected brush specimen, urine, and a rectal swab culture remained negative. The treatment was changed to pefloxacin and amikacin. In spite of all the therapeutic efforts, the patient died 7 days after admission of multiple organ failure, including

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