Antibiotics rank as the most powerful weapons against bacterial infection, but their use is often limited by antibiotic-associated diarrhoea (AAD). Here, we reported that glutamine deficiency might act as a new link between clindamycin-induced dysbiosis and intestinal barrier dysfunction during AAD progression. Using a mouse model, we demonstrated that glutamine became a conditionally essential amino acid upon persistent therapeutic-dose clindamycin exposure, evidenced by a dramatic decrease in intestinal glutamine level and glutaminase expression. Mechanistically, clindamycin substantially confounded the abundance of butyrate-producing strains, leading to the deficiency of faecal butyrate which is normally a fundamental fuel for enterocytes, and in turn increased the compensatory use of glutamine. In addition to its pivotal roles in colonic epithelial cell turnover, glutamine was required for nitric oxide production in classic macrophage-driven host defence facilitating pathogen removal. Importantly, oral administration of glutamine effectively attenuated clindamycin-induced dysbiosis and restored intestinal barrier dysfunction in mice. Collectively, the present study highlighted the importance of gut microbiota in host energy homoeostasis and provided a rationale for introducing glutamine supplementation to patients receiving long-term antibiotic treatment.

Between January 2006 and May 2008, 2624 pregnant S. Korean women between 35–37 weeks gestation were screened for group B streptococcus (GBS). Resistance to antimicrobials was tested by disk diffusion and serotype determined using co-agglutination assays and microarray methods. Overall, 8% of pregnant women were colonized. Serotype III was the predominant serotype (43·8%), followed by serotypes V (20·3%), Ia (12·1%), and Ib (9·5%). GBS was frequently resistant to clindamycin (54·0%) and erythromycin (25·6%); 3·7% were resistant to cefazolin. More than three-quarters of serotype V were resistant to clindamycin or erythromycin or both, and 71% of serotype III were resistant to clindamycin but only 12% were resistant to erythromycin. GBS prevalence exceeded earlier reports by one-third. This is the first report of cefazolin resistance in Korea. These results underscore the need to establish screening measures and chemoprophylaxis guidelines regarding GBS infections in Korea.

This study retrospectively investigated the microbiology and management of 40 children who suffered from chronic sinusitis.

The sinuses infected were the maxillary (15 cases), ethmoid (13), and frontal (seven). Pansinusitis was present in five patients. All aspirates were cultured for aerobic and anaerobic bacteria. A total of 121 isolates (97 anaerobic and 24 aerobic) were recovered. Anaerobes were recovered from all 37 culture- positive specimens, and in 14 cases (38 per cent) they were mixed with aerobes. Twenty-three 3- lactamase-producing bacteria were isolated from 16 (43 per cent) patients. The 15 patients who received clindamycin had the most rapid response to therapy and a change of therapy and surgical drainage was required in one case. Of the 16 patients who received amoxycillin or ampicillin, 16 responded to therapy, six needed a change of therapy, including four who also had surgical drainage. Of the six who were treated with erythromycin, three needed antibiotic change, two with surgical drainage. Of the three that received cefaclor, two were cured, and one had an antibiotic change. Resistant organisms were recovered in all the cases that required therapeutic change.

These findings support the important role of anaerobic bacteria in the polymicrobial cause of chronic sinusitis in children, and the superiority of therapy effective against these organisms.