in Polymicrobial Skinand Soft Tissue Infections: Impact of Inter-Species Interactionsin Disease Outcome.

Polymicrobial biofilms provide a complex environment where co-infecting microorganisms can behave antagonistically, additively, or synergistically to alter the disease outcome compared to monomicrobial infections. skin and soft tissue infections (Sa-SSTIs) are frequently reported in healthcare and community settings, and they can also involve other bacterial and fungal microorganisms. This polymicrobial aetiology is usually found in chronic wounds, such as diabetic foot ulcers, pressure ulcers, and burn wounds, where the establishment of multi-species biofilms in chronic wounds has been extensively described.

Interspecies interactions in mixed-species biofilms formed by and gram-negative bacteria isolated from polymicrobial diabetic foot ulcers.

Diabetic foot ulcers (DFU) are exacerbated by bacterial colonisation. Here, a high prevalence of was observed in DFU patients from an Argentinean hospital. was frequently co-isolated with , , and .

Exposure of multidrug-resistant biofilms to 1,8-cineole leads to bacterial cell death and biomass disruption.

is a common cause of health-care associated infections. The rise of antibiotic resistance and the ability to form biofilm among strains are two key factors associated with antibiotic treatment failure. The present study investigates the antibiofilm activity of 1,8-cineole against preformed biofilms of multidrug-resistant extended-spectrum β-lactamase-producing clinical isolates.

Cell death and biomass reduction in biofilms of multidrug resistant extended spectrum β-lactamase-producing uropathogenic Escherichia coli isolates by 1,8-cineole.

Escherichia coli is the most frequent agent of urinary tract infections in humans. The emergence of uropathogenic multidrug-resistant (MDR) E. coli strains that produce extended spectrum β-lactamases (ESBL) has created additional problems in providing adequate treatment of urinary tract infections.

outcompetes in artificial urine medium through secretion of ammonia and other volatile compounds.

and form mixed biofilms in catheter-associated urinary tract infections. However, co-inoculation of with in artificial urine medium (AUM) resulted in a drastic reduction of cells in both biofilm and planktonic growth. Here, the mechanism behind this competitive interaction was studied.

Role of nutrient limitation in the competition between uropathogenic strains of Klebsiella pneumoniae and Escherichia coli in mixed biofilms.

Klebsiella pneumoniae and Escherichia coli form mixed species biofilms in catheter-associated urinary tract infections. Recently, a detrimental effect of K. pneumoniae over E.

Xanthomonas citri ssp. citri requires the outer membrane porin OprB for maximal virulence and biofilm formation.

Xanthomonas citri ssp. citri (Xcc) causes canker disease in citrus, and biofilm formation is critical for the disease cycle. OprB (Outer membrane protein B) has been shown previously to be more abundant in Xcc biofilms compared with the planktonic state.

Adhesive properties of YapV and paralogous autotransporter proteins of Yersinia pestis.

Yersinia pestis is the causative agent of plague. This bacterium evolved from an ancestral enteroinvasive Yersinia pseudotuberculosis strain by gene loss and acquisition of new genes, allowing it to use fleas as transmission vectors. Infection frequently leads to a rapidly lethal outcome in humans, a variety of rodents, and cats.

Xanthan chain length is modulated by increasing the availability of the polysaccharide copolymerase protein GumC and the outer membrane polysaccharide export protein GumB.

Xanthan is a polysaccharide secreted by Xanthomonas campestris that contains pentameric repeat units. The biosynthesis of xanthan involves an operon composed of 12 genes (gumB to gumM). In this study, we analyzed the proteins encoded by gumB and gumC.

Tn5AraOut mutagenesis for the identification of Yersinia pestis genes involved in resistance towards cationic antimicrobial peptides.

Bacterial pathogens display a variety of protection mechanisms against the inhibitory and lethal effects of host cationic antimicrobial peptides (CAMPs). To identify Yersinia pestis genes involved in CAMP resistance, libraries of DSY101 (KIM6 caf1 pla psa) minitransposon Tn5AraOut mutants were selected at 37°C for resistance to the model CAMPs polymyxin B or protamine. This approach targeted genes that needed to be repressed (null mutations) or induced (upstream P(BAD) insertions) for the detection of CAMP resistance, and predictably for improved pathogen fitness in mammalian hosts.

Biosafety level 2 model of pneumonic plague and protection studies with F1 and Psa.

Attenuated Yersinia pestis pgm strains, such as KIM5, lack the siderophore yersiniabactin. Strain KIM5 does not induce significant pneumonia when delivered intranasally. In this study, mice were found to develop pneumonia after intranasal challenge with strain KIM5 when they were injected intraperitoneally with iron dextran, though not with iron sulfate.

Capsular antigen fraction 1 and Pla modulate the susceptibility of Yersinia pestis to pulmonary antimicrobial peptides such as cathelicidin.

Inhaled Yersinia pestis produces a severe primary pneumonia known as pneumonic plague, which is contagious and highly lethal to humans and animals. In this study, we first determined the susceptibility of Y. pestis KIM6 to antimicrobial molecules of the airways.

The Psa fimbriae of Yersinia pestis interact with phosphatidylcholine on alveolar epithelial cells and pulmonary surfactant.

The pH 6 antigen (Psa) of Yersinia pestis consists of fimbriae with adhesive properties of potential importance for the pathogenesis of plague, including pneumonic plague. The Psa fimbriae mediate bacterial binding to human alveolar epithelial cells. The Psa fimbriae bound mostly to one component present in the total lipid extract from type II alveolar epithelial cells of the cell line A549 separated by thin-layer chromatography (TLC).

Effects of Psa and F1 on the adhesive and invasive interactions of Yersinia pestis with human respiratory tract epithelial cells.

Yersinia pestis, the causative agent of plague, expresses the Psa fimbriae (pH 6 antigen) in vitro and in vivo. To evaluate the potential virulence properties of Psa for pneumonic plague, an Escherichia coli strain expressing Psa was engineered and shown to adhere to three types of human respiratory tract epithelial cells. Psa binding specificity was confirmed with Psa-coated polystyrene beads and by inhibition assays.

Functional interaction of Escherichia coli heat-labile enterotoxin with blood group A-active glycoconjugates from differentiated HT29 cells.

Human colon adenocarcinoma cells (HT29-ATCC) and the clone HT29-5F7 were cultured under conditions that differentiate cells to a polarized intestinal phenotype. Differentiated cells showed the presence of junctional complexes and intercellular lumina bordered by microvilli. Intestinal brush border hydrolase activities (sucrase, aminopeptidase N, lactase and maltase) were detected mainly in differentiated HT29-ATCC cells compared with the differentiated clone, HT29-5F7.

Ability of blood group A-active glycosphingolipids to act as Escherichia coli heat-labile enterotoxin receptors in HT-29 cells.

We examined the ability of blood group A-active glycoconjugates to act as receptors for Escherichia coli heat-labile type I enterotoxin (LT-I) in HT-29 cells. These cells contained ~4 times more specific binding sites for LT-I than for cholera toxin (CT). Binding of LT-I could not be blocked by the B subunit of CT (CT-B), indicating the existence of LT-I receptors in addition to the glycosphingolipid GM1.