Chikungunya virus (CHIKV) emerged in Indian Ocean islands in 2005 and is causing an ongoing outbreak that involves >260,000 patients, including travelers returning home from these islands. We investigated cases in 4 patients returning from Mayotte and Reunion Islands with CHIKV infection and a nurse infected in metropolitan France after direct contact with the blood of a traveler. Four patients had tenosynovitis and pain at wrist pressure, and 1 had life-threatening manifestations. Four CHIKV strains were isolated, including 1 from the patient with the autochthonous case. The complete genomic sequence identified a new CHIKV variant emerging from the East/ central African evolutionary lineage. Aedes albopictus, the implicated vector of CHIKV in Indian Ocean islands, has dispersed worldwide in recent decades. High viral loads in patients returning from Indian Ocean islands to countries where Ae. albopictus is prevalent may be a source

we prospectively evaluated the prevalence of resistance to penicillins, cephalosporins, carbapenem, quinolones, aminoglycosides, and trimethoprim-sulfamethoxazole (SXT) in 320 Escherichia coli isolates isolated from hospitalized patients with acute urinary tract infections (UTIs). We also studied for these strains risk factors for resistance to amoxicillin-clavulanic acid (AMC), fluoroquinolones (FQs), and SXT. Resistance rates were consistent with those from major recent studies reported in the literature. Multivariate analyses selected the following factors as being significantly associated with E. coli resistance: (i) for resistance to AMC, prior (1 year) UTI (odds ratio [OR] ‫؍‬ 2.71, P ‫؍‬ 0.006), prior (1 year) urinary catheter (OR ‫؍‬ 2.98, P ‫؍‬ 0.0025), and prior (6 months) antibiotic exposure (OR ‫؍‬ 2.68, P ‫؍‬ 0.005); (ii) for resistance to FQs male sex (OR ‫؍‬ 3.87, P ‫؍‬ 0.03), with a trend toward significance for age >65 years (OR ‫؍‬ 7.67, P ‫؍‬ 0.06) and prior (1 year) UTI (OR ‫؍‬ 2.98, P ‫؍‬ 0.07); and (iii) for resistance to SXT, male sex (OR ‫؍‬ 1.91, P ‫؍‬ 0.046), hospitalization in an intermediate-term-care unit (OR ‫؍‬ 2.18, P ‫؍‬ 0.008), and prior (1 year) UTI (OR ‫؍‬ 2.03, P ‫؍‬ 0.03). Ours results suggest that prior UTI is a common risk factor for resistance to the different antibiotics tested. Although few studies on risk factors for E. coli resistance to antibiotics have been published, careful interpretation of their findings, taking into consideration the population, infection site, and period studied, should contribute to the formulation of a better strategy that can be used to overcome antibiotic resistance.Escherichia coli, the most common member of the family Enterobacteriaceae implicated in human infectious diseases, has not been spared acquisition of antibiotic resistance, a complex therapeutic problem (7,15,38). The evolution of this microorganism's antibiotic resistance patterns identified from clinical isolates has been reported in many studies on amoxicillin (AMZ), amoxicillin-clavulanic acid (AMC), fluoroquinolones (FQs), and trimethoprim-sulfamethoxazole (SXT). Also, the intimate mechanisms of E. coli antibiotic resistance have been studied and explained in numerous publications (23,24,26,35,39). Unfortunately, few analyses of the demographic, epidemiological, and clinical data for patients with E. coli infection for determination of risk factors for resistance to antimicrobial agents have been reported (1,10,13,17,27,31).To evaluate the prevalence of resistance to a panel of antibiotics, including penicillins, cephalosporins, carbapenem, quinolones, aminoglycosides, and SXT, of E. coli strains isolated from hospitalized patients with acute urinary tract infections (UTIs) and to identify the risk factors for E. coli resistance to AMC, FQs, and SXT, which are routinely used to treat these infections, we conducted a prospective study in our hospital over a 3-month period. We discuss our observations, taking into consideration the most recent major studies on E. coli resist...

Most human immunodeficiency virus (HIV) drug susceptibility studies have involved subtype B strains. Little information on the impact of viral diversity on natural susceptibility to antiretroviral drugs has been reported. However, the prevalence of non-subtype-B (non-B) HIV type 1 (HIV-1) strains continues to increase in industrialized countries, and antiretroviral treatments have recently become available in certain developing countries where non-B subtypes predominate. We sequenced the protease and reverse transcriptase (RT) genes of 142 HIV-1 isolates from antiretroviral-naive patients: 4 belonged to group O and 138 belonged to group M (9 subtype A, 13 subtype B, 2 subtype C, 5 subtype D, 2 subtype F1, 9 subtype F2, 4 subtype G, 5 subtype J, 2 subtype K, 3 subtype CRF01-AE, 67 subtype CRF02-AG, and 17 unclassified isolates). No major mutations associated with resistance to nucleoside reverse transcriptase inhibitors (NRTIs) or protease inhibitors were detected. Major mutations linked to resistance to non-NRTI agents were detected in all group O isolates (A98G and Y181C) and in one subtype J virus (V108I). In contrast, many accessory mutations were found, especially in the protease gene. Only 5.6% of the 142 strains, all belonging to subtype B or D, had no mutations in the protease gene. Sixty percent had one mutation, 22.5% had two mutations, 9.8% had three mutations, and 2.1% (all group O strains) had four mutations. In order of decreasing frequency, the following mutations were identified in the protease gene: M36I (86.6%), L10I/V (26%), L63P (12.6%), K20M/R (11.2%), V77I (5.6%), A71V (2.8%), L33F (0.7%), and M46I (0.7%). R211K, an accessory mutation associated with NRTI resistance, was also observed in 43.6% of the samples. Phenotypic and clinical studies are now required to determine whether multidrug-resistant viruses emerge more rapidly during antiretroviral therapy when minor resistance-conferring mutations are present before treatment initiation.

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Doxorubicin was given by short i.v. infusion (dose range 25-72 mg/m2) to 18 patients who underwent three to seven successive courses of chemotherapy (total, 57 courses). Plasma levels of doxorubicin and its major metabolite doxorubicinol were determined by high-performance liquid chromatography over a 48-h period after the infusion. Pharmacokinetic parameters for the parent drug and its metabolite were calculated for each course of treatment. The results show considerable inter- and intraindividual variations for most parameters. The coefficients of variation (CV) ranged from 37% to 93% (inter-individual) and from 6% to 59% (intra-individual). Nevertheless, we observed a good stability over successive courses for terminal half-life in six patients (CV, 6%-25%) and for clearance and AUC in four subjects (CV, 10%-22%). The ratio of the AUCs for doxorubicinol: doxorubicin averaged 0.514. The pharmacokinetic pattern of doxorubicinol was biphasic in plasma of the majority of patients. We propose a model for curve-fitting of these metabolite plasma concentrations that is based on two successive releases of the compound in the plasma compartment, separated by a lag time.