Tuberculosis in sickle cell disease patients.

OBJECTIVE: Tuberculosis (TB) disease has rarely been reported in patients with sickle cell disease, but it is associated with an increased risk of bacterial infections. In France, sickle cell disease is frequent in populations with the highest prevalence of TB disease. We aimed to highlight clinical aspects of TB disease in patients with sickle cell disease. PATIENTS AND METHODS: Over a 10-year period, we retrospectively included all adults with sickle cell disease who had a positive culture for Mycobacterium tuberculosis managed in the adult sickle cell center of Henri-Mondor hospital. Sickle cell patients with TB disease were matched for comparison to adults without hemoglobinopathy and with documented TB disease in a 1:2 ratio. Logistic regression mixed models were performed. RESULTS: Twelve patients with sickle cell disease and documented TB disease (median age: 29years; IQR [25-34]) were compared to 24 non-sickle cell patients (median age: 33years; IQR [27.5-38.5]). Baseline characteristics were similar between groups except for sickle cell disease. Ten of the 12 patients with sickle cell disease had pulmonary TB. TB disease characteristics were similar between sickle cell and non-sickle cell patients although sickle cell patients had fewer positive sputum smears for acid-fast bacilli (P=0.003) and fewer lung cavitations (P=0.03). CONCLUSIONS: TB disease in sickle cell patients was globally similar to non-sickle cell patients, even though less infectious. Regular follow-up in specialized centers might allow for earlier TB disease diagnosis in sickle cell patients.

Coagulase-negative staphylococci are associated to the mild inflammatory pattern of healthcare-associated meningitis: a retrospective study.

The epidemiology of healthcare-associated meningitis (HAM) is dominated by commensal bacteria from the skin, as coagulase-negative staphylococci (CoNS). We hypothesized that the pauci-symptomatic and mild inflammatory patterns of HAM are related to the low pathogenic state of CoNS. Our aim was to describe clinical and biological features of CoNS HAM, compared to other HAM. All consecutive patients with HAM admitted in our hospital were retrospectively included from 2007 to 2014. HAM due to CoNS were compared to HAM caused by other bacteria (controls) for clinical and laboratory patterns. Seventy-one cases of HAM were included, comprising 18 CoNS and 53 controls. Patients were not different in terms of baseline characteristics. CoNS HAM occurred later after the last surgery than controls (17 vs. 12 days, p = 0.029) and had higher Glasgow Coma Scale (GCS) score (14 vs. 13, p = 0.038). Cerebrospinal fluid (CSF) analysis revealed a lower pleocytosis (25 vs. 1340/mm3, p < 0.001), a higher glucose level (3.75 vs. 0.8 mmol/L, p < 0.001), and a lower protein level (744 vs. 1751 mg/L, p < 0.001) in the CoNS group than in the control group, respectively. HAM due to CoNS was significantly less symptomatic and less inflammatory than HAM due to other bacteria.

First nosocomial outbreak of vanA-type vancomycin-resistant Enterococcus raffinosus in France.

BACKGROUND: Vancomycin-resistant Enterococcus raffinosus has rarely been associated with nosocomial infection and outbreaks. AIM: To report the successful control of a nosocomial outbreak of vanA-type vancomycin-resistant E. raffinosus in a surgical intensive care unit. METHODS: The investigation of the outbreak is reported with control measures taken. Molecular typing of vancomycin-resistant E. raffinosus isolates was performed by repetitive sequence-based polymerase chain reaction (PCR). FINDINGS: Between September and October 2014, vancomycin-resistant E. raffinosus isolates were isolated from four patients. The index patient had been hospitalized previously in Portugal, and was not found to be colonized by vancomycin-resistant enterococci on screening cultures obtained at admission. However, vancomycin-resistant E. raffinosus was isolated from a bile sample 19 days after hospital admission. All four isolates were resistant to both vancomycin and teicoplanin due to the presence of the vanA gene, while remaining susceptible to daptomycin and linezolid. Repetitive sequence-based PCR confirmed the spread of a single vanA-positive E. raffinosus clone. Infection control measures including direct PCR screening on rectal specimens, contact precautions, and cohorting of patients and personnel led to successful control of the outbreak. CONCLUSION: This is the first reported outbreak of vanA-type vancomycin-resistant E. raffinosus in France in both clinical and screening specimens among hospitalized patients. The inability of routine selective screening media to detect the vancomycin-resistant E. raffinosus in the index case likely contributed to the outbreak.

Prevalence and pathogenicity of binary toxin-positive Clostridium difficile strains that do not produce toxins A and B.

Clostridium difficile causes antibiotic-associated diarrhoea and pseudomembranous colitis. The main virulence factors of C. difficile are the toxins A (TcdA) and B (TcdB). A third toxin, called binary toxin (CDT), can be detected in 17% to 23% of strains, but its role in human disease has not been clearly defined. We report six independent cases of patients with diarrhoea suspected of having C. difficile infection due to strains from toxinotype XI/PCR ribotype 033 or 033-like, an unusual toxinotype/PCR ribotype positive for CDT but negative for TcdA and TcdB. Four patients were considered truly infected by clinicians and were specifically treated with oral metronidazole. One of the cases was identified during a prevalence study of A(-)B(-)CDT(+) strains. In this study, we screened a French collection of 220 nontoxigenic strains and found only one (0.5%) toxinotype XI/PCR ribotype 033 or 033-like strain. The description of such strains raises the question of the role of binary toxin as a virulence factor and could have implications for laboratory diagnostics that currently rarely include testing for binary toxin.

[Optimal vancomycin serum level in Staphylococcus aureus infections?]. / Comment optimiser le taux sérique de vancomycine dans le traitement des infections à Staphylococcus aureus?

Vancomycin is the cornerstone of therapy against methicillin-resistant Staphylococus aureus in both community and nosocomial-acquired infections. Because vancomycin is a concentration-independent or time-dependant antibiotic, most clinicians have abandoned the routine practice of determining peak serum concentrations to rely solely on monitoring serum concentrations. The so-called therapeutic range most often quoted for vancomycin was assessed for through serum concentrations of 5-10 mg/l. But prolonged exposure to serum concentration close to the MIC is associated with the emergence of resistance. More recent guidelines recommended vancomycin in concentrations of 15-20 mg/l for the treatment of severe Staphylococcus infections or in situations where vancomycin penetration is poor. However, because of the great variability of vancomycin MIC(S) (0,12-4 mg/l) of susceptible Staphylococcus strains, guidelines should recommend through serum concentrations of 5-10 times the MIC.