Victoire de Lastours1, Françoise Chau2, Carine Roy3, Beatrice Larroque3, Bruno Fantin4. 1. Assistance Publique-Hôpitaux de Paris, Hôpital Beaujon, Service de Médecine Interne, F-92110 Clichy, France INSERM, IAME, UMR 1137, F-75018 Paris, France Univ Paris Diderot, IAME, UMR 1137, Sorbonne Paris Cité, F-75018 Paris, France. 2. INSERM, IAME, UMR 1137, F-75018 Paris, France Univ Paris Diderot, IAME, UMR 1137, Sorbonne Paris Cité, F-75018 Paris, France. 3. Assistance Publique-Hôpitaux de Paris, Hôpital Beaujon, Unité d'Epidémiologie et de Recherche Clinique Paris Nord, F-92110 Clichy, France. 4. Assistance Publique-Hôpitaux de Paris, Hôpital Beaujon, Service de Médecine Interne, F-92110 Clichy, France INSERM, IAME, UMR 1137, F-75018 Paris, France Univ Paris Diderot, IAME, UMR 1137, Sorbonne Paris Cité, F-75018 Paris, France bruno.fantin@bjn.aphp.fr.
Abstract
BACKGROUND: Quinolone resistance is a major global clinical problem. It primarily emerges in microbiota under selective pressure. Studies evaluating the incidence and risk factors for carrying quinolone-resistant bacteria in hospitalized patients treated with fluoroquinolones (FQs) are lacking. METHODS: We prospectively included hospitalized patients treated with FQs. Nasal, throat and rectal swabs were performed before FQ treatment, at the end of FQ treatment and 30 days later. A 'reference group' of patients not receiving FQs was also included to determine the rates of quinolone resistance acquisition not linked to FQ treatment. Prevalence and incidence of quinolone-resistant strains of nasal coagulase-negative staphylococci (CoNS) and Staphylococcus aureus, pharyngeal α-haemolytic streptococci and faecal Escherichia coli, and risk factors for emergence of quinolone resistance in FQ-treated patients were assessed. RESULTS: Four-hundred and fifty-one FQ-treated patients were included, as well as 119 subjects in the 'reference group'. Emergence of quinolone resistance occurred in 110/213 (51.6%), 50/336 (14.9%), 53/290 (18.3%) and 46/336 (13.7%) of FQ-treated patients for CoNS, S. aureus, α-haemolytic streptococci and E. coli, respectively, significantly more than for reference patients for CoNS (23/65; P < 0.05), S. aureus (5/91; P < 0.02) and E. coli (4/84; P < 0.05), but not for α-haemolytic streptococci (15/70; P = 0.55). Emergence of resistance was not associated with the type of FQ received, the duration of therapy or the duration of hospital stay, but was associated with host factors such as immunosuppression and altered performance status. CONCLUSIONS: FQs received during hospitalization account for high rates of emergence of resistance to FQs in clinically relevant bacteria from human microbiota, reflecting the important ecological impact of FQs. Host factors outweighed treatment or hospitalization characteristics as risk factors for carrying quinolone-resistant strains.
BACKGROUND:Quinolone resistance is a major global clinical problem. It primarily emerges in microbiota under selective pressure. Studies evaluating the incidence and risk factors for carrying quinolone-resistant bacteria in hospitalized patients treated with fluoroquinolones (FQs) are lacking. METHODS: We prospectively included hospitalized patients treated with FQs. Nasal, throat and rectal swabs were performed before FQ treatment, at the end of FQ treatment and 30 days later. A 'reference group' of patients not receiving FQs was also included to determine the rates of quinolone resistance acquisition not linked to FQ treatment. Prevalence and incidence of quinolone-resistant strains of nasal coagulase-negative staphylococci (CoNS) and Staphylococcus aureus, pharyngeal α-haemolytic streptococci and faecal Escherichia coli, and risk factors for emergence of quinolone resistance in FQ-treated patients were assessed. RESULTS: Four-hundred and fifty-one FQ-treated patients were included, as well as 119 subjects in the 'reference group'. Emergence of quinolone resistance occurred in 110/213 (51.6%), 50/336 (14.9%), 53/290 (18.3%) and 46/336 (13.7%) of FQ-treated patients for CoNS, S. aureus, α-haemolytic streptococci and E. coli, respectively, significantly more than for reference patients for CoNS (23/65; P < 0.05), S. aureus (5/91; P < 0.02) and E. coli (4/84; P < 0.05), but not for α-haemolytic streptococci (15/70; P = 0.55). Emergence of resistance was not associated with the type of FQ received, the duration of therapy or the duration of hospital stay, but was associated with host factors such as immunosuppression and altered performance status. CONCLUSIONS:FQs received during hospitalization account for high rates of emergence of resistance to FQs in clinically relevant bacteria from human microbiota, reflecting the important ecological impact of FQs. Host factors outweighed treatment or hospitalization characteristics as risk factors for carrying quinolone-resistant strains.
Authors: Douglas J Biedenbach; Michael D Huband; Meredith Hackel; Boudewijn L M de Jonge; Daniel F Sahm; Patricia A Bradford Journal: Antimicrob Agents Chemother Date: 2015-07-20 Impact factor: 5.191
Authors: Seung Yeon Song; Joo Hee Shin; Su Yeong Hyeon; Donguk Kim; Won Ku Kang; Soo-Han Choi; Yae-Jean Kim; Eun Young Kim Journal: PLoS One Date: 2017-05-17 Impact factor: 3.240