The First Report of mcr-1-Carrying Escherichia coli Originating from Animals in Serbia

The aim of this study was continuous monitoring of the presence of mcr-1 to mcr-5 genes in Enterobacterales isolated from cattle, pigs, and domestic poultry at intensive breeding facilities in Northern Vojvodina, Serbia, from 1 January 1 to 1 October 2020. Out of 2167 examined samples, mcr-1 was observed in five E. coli isolates originating from healthy turkeys. Four isolates belonged to the phylogenetic group B1, and one isolate to the phylogenetic group A. Detected E. coli serogenotypes (somatic O and flagellar H antigens) were O8:H25 and O29:H25. Core-genome multi-locus sequence typing (cgMLST) revealed three ST58 isolates clustering together in Clonal Complex (CC) 155 and two singletons of ST641-CC86 and ST410-CC23, respectively. Clonotyping revealed CH4-32 (n = 3), CH6-53 (n = 1) and CH4-24 (n = 1). In all isolates, the mcr-1 gene was located on a large IncX4 replicon type plasmid. Eight virulence-associated genes (VAGs) typical of avian pathogenic E. coli (APEC) (fyuA, fimH, hlyF, iss, ompT, sitA, traT, iroN) were detected in four isolates. These isolates were investigated for susceptibility to four biocides and revealed MIC values of 0.125% for glutardialdehyde, of 0.00003–0.00006% for chlorohexidine, of 4–6% for isopropanol and of 0.001–0.002% for benzalkonium chloride. All obtained MIC values of the tested biocides were comparable to the reference strain, with no indication of possible resistance. This is the first report of mcr-1.1-carrying E. coli from Serbia. Although only samples from turkeys were mcr-positive in this study, continuous monitoring of livestock samples is advised to prevent a spill-over from animals to humans.

Plasmid-Mediated Resistance to Extended-Spectrum Cephalosporins and Resistance to Fluoroquinolones in Escherichia Coli Isolates from Black-headed Gulls (Larus Ridibundus)

Although resistance to fluoroquinolones is common in E. coli isolates from farm and game animals in Serbia, currently no data are accessible on the occurrence of antibacterial resistances in E. coli isolates from gulls. Therefore, 45 cloacal swabs and 50 fecal samples from black-headed gulls were investigated for the presence of Escherichia coli isolates resistant to antibiotics. Multidrug resistance was detected in 22 E. coli isolates. High level resistance to fluoroquinolones was found in ten isolates with MIC values of ciprofloxacin ranging from 4 to 32 mg/L. Genotyping revealed single or double mutations in the quinolone resistance determining region (QRDR) of the gyrA or gyrA, parC and parE genes, respectively. Ten isolates showed resistance to extended-spectrum cephalosporin antibiotics. These ten isolates belonged to phylogenetic group B2 (five isolates), group D (four isolates) and group B1 (one isolate). An extended-spectrum β-lactamase resistance phenotype was detected in one isolate which carried the blaCTX-M-1 gene on a plasmid of the I2/FIB replicon type. Nine isolates carried blaCMY-2 genes, which were detected on conjugative plasmids in seven isolates. One transconjugant also carried hly, iroN, iss, ompT and cvaC virulence genes on the plasmid. Five different sequence types (ST38, ST2307, ST224, ST162 and ST34) were detected in E. coli isolates with ESBL or AmpC phenotype and genotype.

The ZIKA Virus Delays Cell Death Through the Anti-Apoptotic Bcl-2 Family Proteins

Zika virus (ZIKV) is an emerging human mosquito-transmitted pathogen of global concern, known to be associated with complications such as congenital defects and neurological disorders in adults. ZIKV infection is associated with induction of cell death. However, previous studies suggest that the virally induced apoptosis occurs at a slower rate compared to the course of viral production. In this present study, we investigated the capacity of ZIKV to delay host cell apoptosis. We provide evidence that ZIKV has the ability to interfere with apoptosis whether it is intrinsically or extrinsically induced. In cells expressing viral replicon-type constructions, we show that this control is achieved through replication. Finally, our work highlights an important role for anti-apoptotic Bcl-2 family protein in the ability of ZIKV to control apoptotic pathways, avoiding premature cell death and thereby promoting virus replication in the host-cell.

The ZIKA Virus Delays Cell Death through the Anti-Apoptotic Bcl-2 Family Proteins

Zika virus (ZIKV) is an emerging human mosquito-transmitted pathogen of global concern, known to be associated with complications such as congenital defects and neurological disorders in adults. ZIKV infection is associated with induction of cell death. However, previous studies suggest that the virally-induced apoptosis occurs at a slower rate compared to the course of viral production. In this present study, we investigated the capacity of ZIKV to delay host cell apoptosis. We provide evidence that ZIKV has the ability to interfere with apoptosis whether it is intrinsically or extrinsically induced. In cells expressing viral replicon-type constructions, we show that this control is achieved through replication. Finally, our work highlights an important role for anti-apoptotic Bcl-2 family protein in the ability of ZIKV to control apoptotic pathways, avoiding premature cell death and thereby promoting virus replication in the host-cell.

The ZIKA Virus Controls Cell Death through the Anti-Apoptotic Bcl-2 Family Proteins

Zika virus (ZIKV) is an emerging human mosquito-transmitted pathogen of global concern, known to cause severe complications such as congenital defects and neurological disorders in adults. ZIKV infection is associated with cell death. However, previous studies suggest that the virally-induced apoptosis occurs at a slower rate compared to the course of viral production. In this present study, we investigated the capacity of ZIKV to delay host cell apoptosis. We provide evidence that ZIKV has the ability to control programmed cell death whether it is intrinsically or extrinsically induced. In cells expressing viral replicon-type constructions, we show that this control is achieved through replication. Finally, our work highlights an important role for anti-apoptotic Bcl-2 family protein in the ability of ZIKV to control apoptotic pathways, avoiding premature cell death and thereby promoting virus replication in the host-cell.

Population structure and pangenome analysis of Enterobacter bugandensis uncover the presence of blaCTX-M-55, blaNDM-5 and blaIMI-1, along with sophisticated iron acquisition strategies

ABSTRACTEnterobacter bugandensis is a recently described species that has been largely associated with nosocomial infections. Here, we report the genome of a non-clinical E. bugandensis strain. We used this and other several publicly available E. bugandensis genomes to obtain the species pangenome, investigate the conservation of important genes, and elucidate general population structure features of the species. Core- and whole-genome multilocus sequence typing (cgMLST and wgMLST, respectively) allowed the detection of five E. bugandensis phylogroups (PG-A to E). We found important antimicrobial resistance and virulence determinants associated with specific PGs, notably PG-A and PG-E. IncFII was the most prevalent plasmid replicon type in this species. We uncovered several extended-spectrum β-lactamases, including blaCTX-M-55 and blaNDM-5, present in an IncX replicon type plasmid, described here for the first time in E. bugandensis. Genetic context analysis of blaNDM-5 revealed the resemblance of this plasmid with other IncX plasmids isolated from other bacteria from the same country. Further, three distinctive siderophore producing operons were found in the E. bugandensis pangenome: enterobactin (ent), aerobactin (iuc/iut), and salmochelin (iro). The latter operon is conserved in all PG-E isolates. Collectively, our findings provide novel insights on the lifestyle, physiology, antimicrobial, and virulence profiles of E. bugandensis.