We screened 19 404 isolates (90% of cases) for ofloxacin resistance and measured

levofloxacin minimum inhibitory concentrations (MICs) for all isolates that were ofloxacin resistant. Non-susceptibility to levofloxacin was defined as an MIC of 4 mg/L or more. EPZ004777 cell line Nasopharyngeal pneumococcal carriage was assessed in 65 children in two tuberculosis hospitals where invasive pneumococcal disease caused by levofloxacin-non-susceptible S pneumoniae had been detected.

Findings 12 cases of invasive pneumococcal disease were identified as being non-susceptible to levofloxacin, an in children aged under 15 years. All isolates were rifampicin resistant. Outcome was known for 11 of these patients; five (45%) died. Invasive

disease caused by levofloxacin-non-susceptible S pneumoniae was associated with a history of tuberculosis treatment (eight [89%] of nine children with non-susceptible isolates had a history of treatment vs 396 [18%] of 2202 children with susceptible isolates; relative risk [RR] 35 . 78, 95% Cl 4.49-285.30) and nosocomial invasive pneumococcal disease (eight [80%] of ten children with non-susceptible AG-120 supplier isolates had acquired infection nosocomially vs 109 [4%] of 2709 with susceptible isolates; RR 88.96, 19.10-414.29). 31 (89%) of 35 pneumococcal carriers had bacteria that were non-susceptible to levofloxacin.

Interpretation Our data suggest that the use of fluoroquinolones to treat multidrug-resistant tuberculosis in children has led to the emergence of invasive pneumococcal disease caused by levofloxacin-non-susceptible S pneumoniae and its nosocomial spread.

Funding National Institute for Communicable Diseases

of the National Health Laboratory Service (South Africa), US Agency for International Development FRAX597 research buy Antimicrobial Resistance Initiative, US Centers for Disease Control and Prevention.”
“After recovery from acute muscle pain even minor subsequent muscle use can initiate recurrence of the same mechanical hyperalgesia months or years after the initial injury. We have recently developed a model of this chronic latent hyperalgesia in the rat. In this study, we have examined the possibility that interleukin-6 (IL-6), an inflammatory mediator produced during acute muscle inflammation, can mediate the production of this chronic latent hyperalgesic state in which subsequent exposure to inflammatory mediators produces a markedly prolonged mechanical hyperalgesia. We now report that i.m. injection of IL-6 produced mechanical hyperalgesia, lasting several hours, that was prevented by intrathecal injection of antisense to glycoprotein 130 (gp130), an IL-6 receptor subunit. Furthermore, following complete recovery from i.m. IL-6-induced hyperalgesia, i.m. prostaglandin E-2 produced a mechanical hyperalgesia that was remarkably prolonged compared with naive controls, indicating the presence of chronic latent hyperalgesia.