Acute Haemophilus parainfluenzae endocarditis: a case report

<p>Abstract</p> <p>Introduction</p> <p>Numerous pathogens can cause infective endocarditis, including <it>Haemophilus parainfluenzae</it>. <it>H. parainfluenzae</it> is part of the <it>H. aphrophilus, Actinobacillus actinomycetemcomitans</it>,<it> Cardiobacterium hominis</it>,<it> Eikenella corrodens</it>, and <it>Kingella kingae</it> group that may cause about 3% of the total endocarditis cases, and is characterized by a subacute course and large vegetations.</p> <p>Case presentation</p> <p>Acute <it>H. parainfluenzae</it> endocarditis developed in a 54-year-old woman, with no underlying predisposing factors. The patient presented with fever of 3 days duration and a severe headache. Magnetic resonance imaging of the brain revealed multiple cerebral emboli with hemorrhagic foci. Upon suspicion of endocarditis, cardiac transesophageal ultrasonography was performed and revealed massive vegetations. The patient underwent emergency mitral valve replacement, and was further treated with ceftriaxone. Blood cultures grew <it>H. parainfluenzae</it> only after valve replacement, and a 6-week course of ceftriaxone was prescribed.</p> <p>Conclusion</p> <p>We underline the typical presentation of large vegetations in <it>H. parainfluenzae</it> endocarditis, which are associated with embolic phenomena and resulting severity. Although the majority of the few cases reported in the literature are subacute in progress, our case further underlines the possibility that <it>H. parainfluenzae</it> endocarditis may develop rapidly. Thus, awareness of the imaging characteristics of the pathogen may enhance early appropriate diagnosis and therapeutic response.</p

Impact of safety-related dose reductions or discontinuations on sustained virologic response in HCV-infected patients: Results from the GUARD-C Cohort

BACKGROUND: Despite the introduction of direct-acting antiviral agents for chronic hepatitis C virus (HCV) infection, peginterferon alfa/ribavirin remains relevant in many resource-constrained settings. The non-randomized GUARD-C cohort investigated baseline predictors of safety-related dose reductions or discontinuations (sr-RD) and their impact on sustained virologic response (SVR) in patients receiving peginterferon alfa/ribavirin in routine practice. METHODS: A total of 3181 HCV-mono-infected treatment-naive patients were assigned to 24 or 48 weeks of peginterferon alfa/ribavirin by their physician. Patients were categorized by time-to-first sr-RD (Week 4/12). Detailed analyses of the impact of sr-RD on SVR24 (HCV RNA <50 IU/mL) were conducted in 951 Caucasian, noncirrhotic genotype (G)1 patients assigned to peginterferon alfa-2a/ribavirin for 48 weeks. The probability of SVR24 was identified by a baseline scoring system (range: 0-9 points) on which scores of 5 to 9 and <5 represent high and low probability of SVR24, respectively. RESULTS: SVR24 rates were 46.1% (754/1634), 77.1% (279/362), 68.0% (514/756), and 51.3% (203/396), respectively, in G1, 2, 3, and 4 patients. Overall, 16.9% and 21.8% patients experienced 651 sr-RD for peginterferon alfa and ribavirin, respectively. Among Caucasian noncirrhotic G1 patients: female sex, lower body mass index, pre-existing cardiovascular/pulmonary disease, and low hematological indices were prognostic factors of sr-RD; SVR24 was lower in patients with 651 vs. no sr-RD by Week 4 (37.9% vs. 54.4%; P = 0.0046) and Week 12 (41.7% vs. 55.3%; P = 0.0016); sr-RD by Week 4/12 significantly reduced SVR24 in patients with scores <5 but not 655. CONCLUSIONS: In conclusion, sr-RD to peginterferon alfa-2a/ribavirin significantly impacts on SVR24 rates in treatment-naive G1 noncirrhotic Caucasian patients. Baseline characteristics can help select patients with a high probability of SVR24 and a low probability of sr-RD with peginterferon alfa-2a/ribavirin

Do we really understand what the immunological disturbances in inflammatory bowel disease mean?

The gastrointestinal tract uses a system of tolerance and controlled inflammation to limit the response to dietary or bacteria-derived antigens in the gut. When this complex system breaks down, either by a chemical or pathogenic insult in a genetically predisposed individual the resulting immune response may lead to inflammatory bowel disease. Although the aetiopathogenesis of inflammatory bowel disease remains unsolved current evidence indicates that defective T-cell apoptosis and impairment of intestinal epithelial barrier function play important roles. In inflammatory bowel disease, it has been reported that activation of macrophages seems to be as important as increased production of the macrophage-derived cytokines such as TNF-α, IL-1 and IL-6. The triggering factor for this cascade is still to be elucidated as to whether it represents an auto-antigen or a hetero-antigen. It has been also demonstrated that a serologic anti-microbial response exists. This response includes antibodies against saccharomyces cerevisiae (ASCA), E. coli outer membrane porin C (Omp-C), flagelin (cBir1) and pseudomonas aeroginosa (I2). Host response to microbial pathogens includes self-defense mechanisms including defensins, pattern recognition receptors and Toll-like receptors. Neuroimmunomodulation in inflammatory bowel disease (IBD) is another interesting approach with implications on the influence of brain-gut axis on intestinal inflammation and its perpetuation. It is probable that inflammatory bowel disease represents a heterogenic group of diseases that share similar mechanisms of tissue damage but have different initiating events and immunoregulatory abnormalities. A better understanding of all these events will hopefully provide new insights into the mechanisms of epithelial responses to microorganisms and ideas for therapies