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Microbiological diagnosis: The human endometrial microbiome—Endometritis
Published in Carlos Simón, Linda C. Giudice, The Endometrial Factor, 2017
Inmaculada Moreno, Carlos Simón
It is critical that the isolation of pathogens in the endometrium or endometrial fluid be the standard for CE diagnosis. Common bacteria like Corynebacterium, Enterococcus faecalis, E. coli, G. vaginalis, Klebsiella pneumoniae, Proteus mirabilis, Proteus morganii, Pseudomonas aeruginosa, Staphylococcus epidermidis, Staphylococcus haemolitycus, Staphylococcus hominis, Staphylococcus simulans, Streptococcus agalactiae, Streptococcus bovis, Streptococcus mitis, Streptococcus α-haemolyticus, Streptococcus milleri, Streptococcus pyogenes, and Streptococcus viridans; pathogenic bacteria such as N. gonorrhoeae, C. trachomatis, and U. urealyticum; and yeasts like Saccharomyces cerevisiae, Candida albicans, Candida glabrata, Candida ciferrii, and Candida tropicalis are all likely to be found in endometrial samples (83,84). The most prevalent infectious agents responsible for CE are Gram-negative bacteria from the intestinal flora (E. coli and E. faecalis) (accounting for 31.1% of the identified bacteria), Streptococcus and Staphylococcus spp. (38.1%), Mycoplasma spp. and U. urealyticum (11%), C. trachomatis (3%), G. vaginalis, and N. gonorrhoeae (depending on the population analyzed). Nonetheless, the mere presence of infectious agents in the uterine cavity does not necessarily lead to CE, and it will be useful to determine the identity or pathogenicity and minimum amount of each pathogen that may establish an endometrial infection.
Linezolid
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Linezolid resistance in CoNS is also recognized. The first reports were of scattered mutations of the 23s rRNA. The G2576T mutation, as well as other mutations in the 23S rRNA gene, has been detected in linezolid-resistant isolates of S. epidermidis, S. capitis, S. cohnii, Staphylococcus haemolyticus, Staphylococcus pettenkoferi, Staphylococcus hominis, and Staphylococcussimulans (Zhu et al., 2007; Liakopoulos et al., 2009; Petinaki et al., 2009; Bongiorno et al., 2010; Mendes et al., 2010; Sorlozano et al., 2010; Mazzariol et al., 2012; Mihaila et al., 2012; de Almeida et al., 2013; Takaya et al., 2015; Zhou et al., 2015). Later, reports of alterations to ribosomal proteins L3 and L4 began to emerge (Bonilla et al., 2010; Kosowska-Shick et al., 2010; de Almeida et al., 2013; LaMarre et al., 2013; Tewhey et al., 2014), as well as acquisition of cfr, the latter increasingly associated with outbreaks and endemic linezolid resistance (Campanile et al., 2013; Yang et al., 2013; Tewhey et al., 2014; Zhou et al., 2015; Decousser et al., 2015). Multiple different mechanisms also seem to coexist in the same isolate more frequently in CoNS than in the other Gram-positive pathogens (Sorlozano et al., 2010; Kosowska-Shick et al., 2010; LaMarre et al., 2013; Tewhey et al., 2014; O’Connor et al., 2015; Takaya et al., 2015), and can be additive regarding effect on MIC. It has also been suggested that combined resistance factors may help offset fitness cost, particularly of mutations of multiple 23s rRNA alleles (Mendes et al., 2012). Multiple reports have now been published of clonal dissemination of linezolid-resistant CoNS (Potoski et al., 2006; Kelly et al., 2008; Treviño et al., 2009; Bonilla et al., 2010; de Almeida et al., 2012; Mendes et al., 2012; Mihaila et al., 2012; O’Connor et al., 2015). MICs as high as > 256 have been reported, and increasing linezolid use in the relevant institutions is suggested as a risk factor (Kelly et al., 2008; Treviño et al., 2009; Mulanovich et al., 2010). Additional cases have been reported (Kelly et al., 2006; Cieloszyk et al., 2007). Two analyses of linezolid-resistant S. aureus and S. epidermidis demonstrated that resistant strains had emerged independently in multiple clones of these organisms (Wong et al., 2010, Quiles-Melero et al., 2013). A widely disseminated linezolid-resistant clone of S. epidermidis in Greece is unusual in that most tested isolates demonstrate linezolid dependence (Kokkori et al., 2014; Karavasilis et al., 2015). This group of organisms is likely to become more important, both as agents of resistant infection in their own right given increasing device use, but also as a reservoir for cfr, which may be transmitted to S. aureus.
The impact of medicinal brines on microbial biofilm formation on inhalation equipment surfaces
Published in Biofouling, 2018
Natalia Jarząb, Maciej Walczak, Dariusz Smoliński, Alina Sionkowska
The hydrolytic activity of the biofilm formed in pure saline (control conditions) on PVC, expressed as the amount of released fluorescein, ranged from 0.123 to 1.940 µg ml−1 (Figure 6). The maximum biofilm activity (1.940 µg ml−1) was recorded for the biofilm formed by B. faecium after incubation for five days. The smallest activity of biofilm (0.123 µg ml−1) was recorded for the Staphylococcus simulans biofilm formed after incubation for 48 h.
Intestinal phages interact with bacteria and are involved in human diseases
Published in Gut Microbes, 2022
Phages infect their target bacteria with receptor-binding proteins (RBPs) on the surface of the bacteria. RBPs belong to different biochemical families, mainly represented by surface proteins, polysaccharides and lipopolysaccharides (LPSs). Bacteria prevent phages from binding to receptors by regulating receptor expression, mutating receptors and hiding receptors. For example, V. cholerae reduces O1 antigen expression by regulating the expression of manA and wbeL, two variable genes required for O1 antigen biosynthesis, which helps it avoid phage adsorption.40 The E. coli F strain can produce the outer membrane protein (OMP) TraT and prevents phage adsorption by masking or modifying the OmpA conformation.41 The capsule of the Staphylococcus simulans strain inhibits phage U16 from binding to its receptor, thus inhibiting phage U16 adsorption. Phages bind to Pseudomonas by polysaccharides.42 To prevent infection, Pseudomonas selects for mutations at many common sites associated with mucoid transformation, including mucA and algU, and inhibiting mucoidy.43 However, phages are also not static and can change their structure to bind to new receptors. The RBP of λ phage is encoded by the J gene and can bind to the host surface receptor LamB. When the expression of the LamB gene is suppressed, phages complete subsequent infection by changing the terminal structure of protein J and binding to the new receptor protein OmpF.44 Small modifications can also disguise receptors from phages. The E. coli K1 capsule can block phage T7 infection,45 and Pseudomonas aeruginosa O antigen modification and type IV pilus glycosylation can block phage infection.46,47 However, when E. coli produces a capsule to mask its LPS receptor, phage H4489A often encodes an extracellular hyaluronic acid lyase to degrade the capsule, thereby aiding adsorption.48 In addition, bacteria can also prevent phage adsorption by producing an extracellular matrix and through competitive inhibition. E. coli and V. cholerae reduce phage infection by providing phage-sensitive receptors on outer membrane vesicles (OMVs).49,50E. coli FhuA is an iron transporter and an entry port for T5 phage. The antimicrobial molecule Microcin J25 uses FhuA as its receptor and competes with phage T5 for binding sites,51 resulting in a reduced chance of infection success.