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Resumen:
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Streptococcus pneumoniae is primarily responsible for acute community pneumonia and causes other diseases such as otitis, sinusitis, meningitis and bacteraemia (Henriques-Normark and Tuomanen, 2013). It can form biofilms, which are essential when colonizing the nasopharynx and during infection (Bogaert et al., 2004; Simell et al., 2012). Biofilm can also decrease bacteria susceptibility to antimicrobials (Wolcott and Ehrlich, 2008).The pneumococcal vaccine is the main preventive measure against infection, but only protects against 14-25 % of serotypes, increasing the incidence of non-vaccine serotypes (Geno et al., 2015). The control of the disease is based on antibiotherapy, hindered by the emergence of ?-lactams- and macrolides resistance (Jacobs and Johnson, 2003) and also now by to fluoroquinolones (FQs) resistance (Domenech et al, 2014). They inhibit type II DNA topoisomerases (topoisomerase IV or gyrase) (Muñoz and de la Campa, 1996; Simoens et al., 2011), causing an inappropriate level of supercoiling on the chromosome that leads to cell death (Drlica and Zhao, 1997). Lethality of FQs such as levofloxacin (LVX) or moxifloxacin (MXF) is increased by the production of reactive oxygen species (ROS), mediated by increases in iron and hydrogen peroxide (Ferrándiz and de la Campa, 2014; Ferrándiz et al., 2016). In addition, both FQs can induce the lytic cycle by carried prophages in lysogenic strains of S. pneumoniae (López et al., 2014). In response to FQs resistance, seconeolitsin (SCN) has been synthesized, a new alkaloid that can prevent the growth of S. pneumoniae by inhibiting type I DNA topoisomerase (Topo I) of the bacteria (García et al., 2011)...
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