Extended-Spectrum ß-Lactamases in Human Isolates of Multidrug-Resistant Non-typhoidal Salmonella enterica.

A total of 291 non-duplicate isolates of non-typhoidal Salmonella (NTS) were collected from the fecal samples of patients with salmonellosis in Armenia and Georgia during 1996-2016. The isolates were tested for resistance to antimicrobials, including extended-spectrum ß-lactamases (ESBL). The high prevalence of multidrug-resistance (MDR) and ESBL-producer phenotypes was detected among Salmonella enterica subsp. enterica serovar Typhimurium (S. Typhimurium) isolates collected from patients in Armenia between 1996 and 2016. A total of 36 MDR NTS isolates were subjected to whole genome sequencing (WGS) to determine the genetic background of antimicrobial resistance (AMR) and mobile genetic elements. All ESBL-producing S. Typhimurium isolates belonged to the same sequence type (ST328). The ESBL-producer phenotype was associated with plasmid-encoded CTX-M-5 production. A range of other plasmids was associated with resistance to other antimicrobials, including the MDR phenotype.

Systemic Concentrations of Short Chain Fatty Acids Are Elevated in Salmonellosis and Exacerbation of Familial Mediterranean Fever.

Gut microbiota-produced short chain fatty acids (SCFAs) play an important role in the normal human metabolism and physiology. Although the gradients of SCFAs from the large intestine, where they are largely produced, to the peripheral blood as well as the main routes of SCFA metabolism by different organs are known well for the healthy state, there is a paucity of information regarding how these are affected in disease. In particular, how the inflammation caused by infection or autoinflammatory disease affect the concentration of SCFAs in the peripheral venous blood. In this work, we revealed that diseases caused either by infectious agents (two Salmonella enterica serovars, S. Enteritidis, and S. Typhimurium) or by the exacerbation of an autoinflammatory disease, familial Mediterranean fever (FMF), both result in a significantly elevated systemic concentration of SCFAs. In the case of salmonellosis the concentration of SCFAs in peripheral blood was significantly and consistently higher, from 5- to 20-fold, compared to control. In the case of FMF, however, a significant increase of SCFAs in the peripheral venous blood was detected only in the acute phase of the disease, with a lesser impact in remission. It seems counterintuitive that the dysbiotic conditions, with a reduced number of gut microorganisms, produce such an effect. This phenomenon, however, must be appraised within the context of how the inflammatory diseases affect the normal physiology. We discuss a number of factors that may contribute to the "leak" and persistence of gut-produced SCFAs into the systemic circulation in infectious and autoinflammatory diseases.

Differential induction of total IgE by two Salmonella enterica serotypes.

The main goal of this study was to establish how the inflammation caused by infection with two different Salmonella enterica serotypes, S. Typhimurium and S. Enteritidis, may lead to the predisposition to allergy as measured by total IgE level in the blood. Infection by S. Typhimurium did not affect the systemic IgE concentration while in S. Enteritidis-infected patients there was a significant 3.5-fold increase. This effect was especially profound in patients >4 years old, with up to the 8-fold increase above the norm. The degree of dysbiosis in these two infections measured with the comparative counts of cultivated bacteria showed an inverse relationship with the IgE concentration. Earlier we reported the elevated level of IL-17 in patients infected by S. Enteritidis. In the current study a significant correlation was found between the concentrations of IL-17 and IgE suggesting a possible role played by this cytokine in triggering the production of IgE in response to S. Enteritidis infection.