aureus is able to import heme, when supplied as either hemin or h

aureus is able to import heme, when supplied as either hemin or hemoglobin, in the absence of isdE and htsA. Thus, the lipoprotein-encoding

genes isdE and htsA are dispensable for heme Idelalisib ic50 acquisition by S. aureus. This precludes the use of the ΔhemBΔisdEΔhtsA strain to definitively study the role of heme acquisition in heme-auxotrophic SCVs in an in vivo model. It also indicates that the reduced virulence of the ΔisdEΔhtsA in a murine systemic infection model cannot be explained by an inability to import heme (Mason & Skaar, 2009). These data lend further weight to the already strong body of evidence that HtsA is solely involved in transport of the siderophore staphyloferrin A (Beasley et al., 2009; Grigg et al., 2010). Furthermore, these experiments contradict the suggestion that IsdE may transfer heme to the HtsBC transporter, as heme import is still functional in the absence of both htsA and isdE (Hammer & Skaar, 2011). The proposed transport pathway from hemoglobin, bound by IsdB and IsdH, via IsdA and IsdC to IsdE (Muryoi et al., 2008; Zhu et al., 2008; Hammer & Skaar, 2011) also cannot be fully dependent on IsdE, given the continued function of heme import from hemoglobin in the ΔhemBΔisdEΔhtsA strain. This strongly suggests that additional components,

which have yet to be identified, are involved in the transport of heme into the S. aureus cytoplasm. To examine the role of heme import in heme-auxotrophic SCVs, identification of these heme transport components is required. This research was supported by Arthritis Research UK project

grant funding SGI-1776 nmr (grant number 18294). “
“Neisseria gonorrhoeae is a strict human pathogen that causes the sexually transmitted infection termed gonorrhea. Recent reports indicate that gonococci can form a biofilm in vivo and under Selleck Gefitinib laboratory conditions. It is unclear, however, if formation of such biofilms or their dispersal are influenced by host factors that would be encountered during infection. In this respect, physiological levels of polyamines have been reported to influence biofilm structures formed by other Gram-negative bacteria as well those formed by Gram-positive bacteria and can cause dispersal of a biofilm formed by Bacillus subtilis. Based on these reports, we examined the influence of polyamines on gonococcal biofilm formation and their dispersal. We now report that physiological levels of certain polyamines, notably spermine, can significantly decrease the capacity of gonococci to form a biofilm, but do not cause dispersal of a preformed biofilm. In the context of natural gonococcal infection, the presence of physiological levels of spermine may be antagonistic for gonococci to form a biofilm and this may be of importance in the spread of the pathogen from a localized region. “
“Although it is known that Escherichia coli O157 is capable of long-term soil survival, little is known about the mechanisms involved.

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