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Background: Carbapenem-Resistant Enterobacterales (CRE) has been categorized as pathogens of critical priority by World Health organization (WHO) as they pose significant threat to global public health. Carbapenemase production considered as the principal resistance mechanism against carbapenems and with the recent surge and expansion of carbapenemases and its variants among clinically significant bacteria in India, the present study reports expansion blaOXA−78 and blaOXA−58 of in CRE of clinical origin. Methods: Bacterial isolates were collected from a tertiary referral hospital and identified through VITEK® 2 Compact automated System (Biomerieux, France). Rapidec® Carba NP (Biomerieux, France) was used to investigate carbapenemase production followed by antibiotic susceptibility testing through Kirby-Bauer Disc Diffusion method and agar dilution method. Class D carbapenemase genes were targeted through PCR assay followed by investigation of horizontal transmission of blaOXA−58 and blaOXA−78. Whole genome sequencing was carried out using Illumina platform to investigate the genetic context of blaOXA−58 and blaOXA−78 genes and further characterization of the CRE isolates. Results: The carbapenem-resistant Escherichia coli (BJD_EC456) and Serratia marcescens (BJD_SM81) received during the study from the tertiary referral hospital were isolated from sputum and blood samples respectively. PCR assay followed by whole genome sequencing revealed that the isolates co-harbor blaOXA−58 and blaOXA−78, a variant of blaOXA−51. Horizontal transfer of blaOXA−58 and blaOXA−78 genes were unsuccessful as these genes were located on the chromosome of the study isolates. Transposon Tn6080 was linked to blaOXA−78 in the upstream region while the insertion sequences ISAba26 and ISCfr1 were identified in the upstream and downstream region of blaOXA−58 gene respectively. In addition, both the isolates were co-harboring multiple antibiotic resistance genes conferring clinical resistance towards beta-lactams, aminoglycosides, fluroquinolones, sulphonamides, tetracyclines. BJD_EC180 belonged to ST2437 while BJD_SM81 was of an unknown sequence type. The nucleotide sequences of blaOXA−78 (OQ533021) and blaOXA−58 (OQ533022) have been deposited in GenBank. Conclusions: The study provides a local epidemiological information regarding carbapenem resistance aided by transposon and insertion sequences associated blaOXA−78 and blaOXA−58 genes associated and warrants continuous monitoring to prevent their further dissemination into carbapenem non-susceptible strains thereby contributing to carbapenem resistance burden which is currently a global concern. [ABSTRACT FROM AUTHOR]

Background: Foodborne illness is a global concern and identification of pathogens that cause foodborne disease is a public health priority. Serratia marcescens is an opportunistic pathogen responsible for food poisoning due to its ability to colonize the gastrointestinal surfaces. Serratia marcescens is also responsible for causing a wide range of extraintestinal infections such as pneumonia, urinary tract infection, and keratitis. Aim: The current study investigated the presence of antibiotic-resistant virulent S. marcescens from street food samples. Methods: Two pigmented S. marcescens were recovered from panipuri samples which were then identified using VITEK® GN cards. The virulence genes and the antibiotic resistance genes harbored by the S. marcescens isolates were investigated and further transformation assay was conducted to check the horizontal transferability of the plasmid carrying the antimicrobial resistance genes. Incompatibility typing of the transformants was also assessed and enterobacterial repetitive intergenic consensus polymerase chain reaction was performed to check the heterogeneity of the S. marcescens isolates. Results: Two S. marcescens isolates harboring virulence genes as well as antibiotic resistance genes were detected in this study and it was observed that Inc FIB type plasmid was carrying the resistance genes. Conclusion: The co-existence of both the virulence and antibiotic resistance genes in the two S. marcescens isolates warrants proper surveillance in order to prevent the spread of such pathogenic strains in the environment as well as the community through food samples. [ABSTRACT FROM AUTHOR]

The present study investigated the distribution, sources, bioavailable fractions, and ecological risks of nine metals (Al, Cd, Co, Cr, Cu, Fe, Mn, Pb, and Zn) in water, sediment, and vegetation samples collected from a shallow lake within the industrial town of Ranipet, India. The lake water samples exceeded the concentrations of Al, Cd, Cr, Cu, Fe, Mn, and Pb beyond BIS (Bureau of Indian Standards) limits for drinking water with Cr to be highest as 6.73 mg/L. The Geo-accumulation index for lake bed sediment samples were in the order of Cr>Cu>Co>Mn>Zn>Pb. The bioavailability of the metals in sediment samples determined through Sequential Extraction Procedure (SEP) showed Cr>Co>Zn>Cu>Pb>Mn>Fe>Al. The sediment samples collected from the root zone of different plant species (Cynodon dactylon, Sida acuta, and Eclipta prostrata) exhibited varied bioavailable fractions than lake bed sediments, which indicated the influence of plants in mobilising and fixing the metals. The plant samples had metals concentration in the order of Root>Stem>Leaves and showed the possibility of phytoremediation. Principle Component Analysis (PCA) and Pearson Correlation Matrix (PCM) in the lake bed sediment samples identified the clustering of Al and Fe which indicated probable lithological origin. The lone clustering of Cr from Co, Mn, and Cu indicated separate anthropogenic sources. Further Al, Fe, and Mn showed strong correlations with TOC (Total Organic Carbon) substantiate their distribution under influence of TOC. The study indicated elevated metals pollution is water, sediment, and plants samples from lake area which require immediate attention from all the stakeholders. The assessment of pollution in small and shallow lakes amidst industrial belts need to be prioritised as they often become victims of industrial encroachment and cease to exist in long run. [ABSTRACT FROM AUTHOR]

Ethanol exposure in neonatal mice induces acute neurodegeneration followed by long-lasting glial activation and GABAergic cell deficits along with behavioral abnormalities, providing a third trimester model of fetal alcohol spectrum disorders (FASD). Retinoic acid (RA), the active form of vitamin A, regulates transcription of RA-responsive genes and plays essential roles in the development of embryos and their CNS. Ethanol has been shown to disturb RA metabolism and signaling in the developing brain, which may be a cause of ethanol toxicity leading to FASD. Using an agonist and an antagonist specific to RA receptor α (RARα), we studied how RA/RARα signaling affects acute and long-lasting neurodegeneration and activation of phagocytic cells and astrocytes caused by ethanol administered to neonatal mice. We found that an RARα antagonist (BT382) administered 30 min before ethanol injection into postnatal day 7 (P7) mice partially blocked acute neurodegeneration as well as elevation of CD68- positive phagocytic cells in the same brain area. While an RARα agonist (BT75) did not affect acute neurodegeneration, BT75 given either before or after ethanol administration ameliorated long-lasting astrocyte activation and GABAergic cell deficits in certain brain regions. Our studies using Nkx2.1-Cre;Ai9 mice, in which major GABAergic neurons and their progenitors in the cortex and the hippocampus are labeled with constitutively expressed tdTomato fluorescent protein, indicate that the long-lasting GABAergic cell deficits are mainly caused by P7 ethanol-induced initial neurodegeneration. However, the partial reduction of prolonged GABAergic cell deficits and glial activation by post-ethanol BT75 treatment suggests that, in addition to the initial cell death, there may be delayed cell death or disturbed development of GABAergic cells, which is partially rescued by BT75. Since RARα agonists including BT75 have been shown to exert anti-inflammatory effects, BT75 may rescue GABAergic cell deficits by reducing glial activation/neuroinflammation. [ABSTRACT FROM AUTHOR]