, 2004) could have contributed to a permissive environment allowing the rapid spread of the K-12 core-containing strains, such as the members of ST131 clone, in the gut and in extraintestinal niches. As most of the epidemiological studies revealing the frequency of various core types and core-specific antibodies were conducted
prior the emergence of the ST131 clone (Gibb et al., 1992; Appelmelk et al., 1994; Amor et al., 2000; Gibbs et al., 2004), it remains to be seen whether its ZVADFMK recent spread has had any effect on the prevalence of antibodies with the respective specificities. As our clinical isolates were preselected according to ESBL production, these data do not allow drawing a direct conclusion regarding the current frequency of strains with a K-12 core type in UTI. However, as the incidence of third-generation cephalosporin resistance among local E. coli isolates during the period of strain collection was 23.7% (Al-Kaabi et al., 2011) and because 44.6% of the ESBL-producing isolates were positive with the K-12 core PCR, a considerable increase in K-12-type E. coli compared to the figures found earlier, that is, 2.2–5.6% (Gibb et al., 1992; Appelmelk et al., 1994; Amor et al., 2000), can be anticipated. The rapid spread ATM/ATR inhibitor clinical trial of the ST131 clone and the fact that it still keeps evolving by acquiring genes as blaKPC-2 or blaNDM-1 (Morris et al., 2011; Peirano et al., 2011) further extending
its antibiotic resistance emphasize the need to identify the factors
responsible for its fitness and virulence. Revealing the genetic background for its LPS core OS synthesis may contribute to finding some of the answers and may even lead to the development of preventive and curative interventions. This work was supported by grants FMHS NP-10/07, UAEU1636-08-01-10 and 1439-08-02-01. V.S.Z., G.N. and E.N. are employees of a Arsanis, a biotechnology company. The authors declare no potential conflict of interest. “
“Trypanosoma cruzi, the aetiological agent of Chagas’ find more disease, is exposed to extremely different environment conditions during its life cycle, and transporters are key molecules for its adaptive regulation. Amino acids, and particularly arginine, are essential components in T. cruzi metabolism. In this work, a novel T. cruzi arginine permease was identified by screening different members of the AAAP family (amino acid/auxin permeases) in yeast complementation assays using a toxic arginine analogue. One gene candidate, TcAAAP411, was characterized as a very specific, high-affinity, l-arginine permease. This work is the first identification of the molecular components involved specifically in amino acid transport in T. cruzi and provides new insights for further validation of the TcAAAP family as functional permeases. Chagas’ disease is a zoonosis caused by the parasite Trypanosoma cruzi, a haematic protozoan transmitted by insects of the Reduviidae family.