Campylobacter fetus sepsis in an immunocompetent patient with haematological complication.
ABSTRACT Campylobacter fetus sepsis is rare, especially among young, immunocompetent patients. We present the case of a 43-year-old man with a history of ulcerative colitis who was diagnosed with C fetus bacteraemia with endovascular manifestation. The patient was found to have a low vitamin K level and a high international normalised ratio, and developed deep vein thrombosis. The patient was fully recovered with oral antibiotic treatment, anticoagulation and supportive therapy. Clinicians should be aware that this type of infection, although extremely rare, can occur even in younger, healthy adults and immediate diagnosis and treatment are required to avert life-threatening complications.
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ABSTRACT: Patients with inflammatory bowel disease who develop deep vein thrombosis or pulmonary embolism often have active disease at the time of thromboembolism. We therefore aimed to quantify the risk of venous thromboembolism prospectively during different activity phases of inflammatory bowel disease. From the General Practice Research Database, we matched patients with prospectively recorded inflammatory bowel disease from November, 1987, until July, 2001 with up to five controls by age, sex, and general practice. A flare was defined as the period 120 days after a new corticosteroid prescription. We used Cox regression analysis with time-varying covariates to accommodate changes in the state of inflammatory bowel disease, and whether patients were at high risk of venous thromboembolism after hospitalisation. 13 756 patients with inflammatory bowel disease and 71 672 matched controls were included in the analysis, and of these 139 patients and 165 controls developed venous thromboembolism. Overall, patients with inflammatory bowel disease had a higher risk of venous thromboembolism than did controls (hazard ratio 3.4, 95% CI 2.7-4.3; p<0.0001; absolute risk 2.6 per 1000 per person-years). At the time of a flare, however, this increase in risk was much more prominent (8.4, 5.5-12.8; p<0.0001; 9.0 per 1000 person-years). This relative risk at the time of a flare was higher during non-hospitalised periods (15.8, 9.8-25.5; p<0.0001; 6.4 per 1000 person-years) than during hospitalised periods (3.2, 1.7-6.3; p=0.0006; 37.5 per 1000 person-years). Trials of primary prophylaxis of venous thromboembolism are warranted to find out whether this important complication can be prevented. National Association for Colitis and Crohn's Disease.The Lancet 02/2010; 375(9715):657-63. DOI:10.1016/S0140-6736(09)61963-2 · 45.22 Impact Factor
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ABSTRACT: Campylobacter is a very rare cause of bloodstream infection, although it has been found relatively frequently in patients infected with human immunodeficiency virus (HIV). The impact of highly active antiretroviral therapy (HAART) and new forms of immunosuppression on the incidence of Campylobacter bacteremia has not been sufficiently assessed. In this study we analyzed the incidence and microbiologic and clinical characteristics of Campylobacter bacteremia over 23 years.We reviewed the clinical records of all patients who had Campylobacter bacteremia from 1985 to 2007. Available strains were reidentified using universal polymerase chain reaction (PCR).During the study period, there were 71 episodes of Campylobacter bacteremia in 63 patients (0.24% of all bloodstream infections), and the incidence remained stable (mean, 0.06/1000 admissions per year and 0.47/100,000 inhabitants per year). Median age was 52 years (interquartile range, 31.25-72.5 yr), and 82% of patients were male. The underlying conditions included liver disease (21/64, 32.8%), HIV infection (15/64, 23.4%), malignancy (7/64, 10.9%), solid organ transplantation (2/64, 3%), hypogammaglobulinemia (10/64, 15.6%), and other (18/64, 31.2%). Twelve patients shared more than 1 underlying condition. Campylobacter bacteremia was community acquired in 81% of the episodes. The origin of the bloodstream infection was abdominal (43.5%), primary (26%), or extraintestinal (31%: respiratory 15%, cellulitis 4.8%, urinary 8%, other 3%). C jejuni was recovered in 66% of cases, C fetus in 19%, and C coli in 12%.Universal PCR was performed on 14 available strains. Molecular and conventional identification matched in 8 isolates. In contrast, molecular methods classified as C fetus (n = 2) and C jejuni (n = 1) 3 strains formerly identified only to genus level as Campylobacter species. In another 3 isolates, molecular identification was not consistent with the phenotypic identification (C fetus identified as C jejuni).Complications appeared in 23.9% of patients. Quinolone resistance was observed in 50% of the isolates. Only 37.8% of patients received appropriate empirical therapy. Mortality was 16.4%, although it was higher in HIV-infected patients than uninfected patients (33% vs. 10%; p = 0.04), in cases of hospital-acquired Campylobacter bacteremia compared with community-acquired cases (38.5% vs. 9.4%; p = 0.02), and in the presence of complications compared with patients without complications (100% vs. 0%; p < 0.001). The incidence of recurrence was 5% (3 patients with humoral immunodeficiency). There was a higher proportion of HIV-infected patients among patients with Campylobacter bacteremia in the pre-HAART era (1985-1996) than in the HAART era (1997-2007)-27.5% (11/40) vs. 14.3% (4/28)-although the difference was not statistically significant. Debilitating diseases such as chronic obstructive pulmonary disease emerged as predisposing conditions in the HAART era (0% before HAART era vs. 14.3% in HAART era; p = 0.032).Campylobacter bacteremia is no longer a significant disease of HIV-positive patients on HAART, but often affects other immunocompromised patients as well. Campylobacter bacteremia has an extraintestinal origin in as many as 31% of cases, and humoral immunodeficiency must be sought in patients with recurrent episodes. Quinolones should not be considered for empirical therapy.Medicine 09/2010; 89(5):319-30. DOI:10.1097/MD.0b013e3181f2638d · 4.87 Impact Factor
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ABSTRACT: Thromboembolic complications may occur in inflammatory bowel disease. Recently, we had the opportunity to observe a case of a cerebral arterial thrombosis in a young patient with active ulcerative colitis. Investigation of blood coagulation revealed a temporary Protein C, Protein S and Factor II deficiency. To our knowledge, this is the first reported case of a temporary Protein C and S deficiency in a patient with thrombosis and inflammatory bowel disease.Blut 12/1990; 61(5):307-10. DOI:10.1007/BF01732883