This is the first experimental evidence of intra- and inter-species transfer of a plasmid harbouring a bla NDM-1 gene in A. baumannii via OMVs with high transformation frequency.
Accumulation of mutations within the genome is the primary driving force in viral evolution within an endemic setting. This inherent feature often leads to altered virulence, infectivity and transmissibility, and antigenic shifts to escape host immunity, which might compromise the efficacy of vaccines and antiviral drugs. Therefore, we carried out a genome-wide analysis of circulating SARS-CoV-2 strains to detect the emergence of novel co-existing mutations and trace their geographical distribution within India. Comprehensive analysis of whole genome sequences of 837 Indian SARS-CoV-2 strains revealed the occurrence of 33 different mutations, 18 of which were unique to India. Novel mutations were observed in the S glycoprotein (6/33), NSP3 (5/33), RdRp/NSP12 (4/33), NSP2 (2/33), and N (1/33). Non-synonymous mutations were found to be 3.07 times more prevalent than synonymous mutations. We classified the Indian isolates into 22 groups based on their co-existing mutations. Phylogenetic analysis revealed that the representative strains of each group were divided into various sub-clades within their respective clades, based on the presence of unique co-existing mutations. The A2a clade was found to be dominant in India (71.34%), followed by A3 (23.29%) and B (5.36%), but a heterogeneous distribution was observed among various geographical regions. The A2a clade was highly predominant in East India, Western India, and Central India, whereas the A2a and A3 clades were nearly equal in prevalence in South and North India. This study highlights the divergent evolution of SARS-CoV-2 strains and co-circulation of multiple clades in India. Monitoring of the emerging mutations will pave the way for vaccine formulation and the design of antiviral drugs.
The convergence of a vulnerable population and a notorious pathogen is devastating, as seen in the case of sepsis occurring during the first 28 days of life (neonatal period). Sepsis leads to mortality, particularly in low-income countries (LICs) and lower-middle-income countries (LMICs). Klebsiella pneumoniae, an opportunistic pathogen is a leading cause of neonatal sepsis. The success of K. pneumoniae as a pathogen can be attributed to its multidrug-resistance and hypervirulent-pathotype. Though the WHO still recommends ampicillin and gentamicin for the treatment of neonatal sepsis, K. pneumoniae is rapidly becoming untreatable in this susceptible population. With escalating rates of cephalosporin use in health-care settings, the increasing dependency on carbapenems, a “last resort antibiotic,” has led to the emergence of carbapenem-resistant K. pneumoniae (CRKP). CRKP is reported from around the world causing outbreaks of neonatal infections. Carbapenem resistance in CRKP is largely mediated by highly transmissible plasmid-encoded carbapenemase enzymes, including KPC, NDM, and OXA-48-like enzymes. Further, the emergence of a more invasive and highly pathogenic hypervirulent K. pneumoniae (hvKP) pathotype in the clinical context poses an additional challenge to the clinicians. The deadly package of resistance and virulence has already limited therapeutic options in neonates with a compromised defense system. Although there are reports of CRKP infections, a review on neonatal sepsis due to CRKP/ hvKP is scarce. Here, we discuss the current understanding of neonatal sepsis with a focus on the global impact of the CRKP, provide a perspective regarding the possible acquisition and transmission of the CRKP and/or hvKP in neonates, and present strategies to effectively identify and combat these organisms.
To investigate the mobilizable elements associated with bla in Enterobacteriaceae isolated from septicaemic neonates at a NICU in India, during December, 2008-2011. An attempt was also made to understand whether there was a pattern in the temporal acquisition of bla within the unit. Transferability of carbapenem resistance was tested by conjugation and transformation. Plasmid types and addiction systems were analysed. The genetic background of bla and association with class 1 integron were evaluated by PCR mapping. RFLP was carried out to discriminate plasmids of same incompatibility group. Transfer of carbapenem resistance was successful in 13/15 cases. bla was associated with different plasmid scaffolds (IncFII, IncL/M, IncN, IncR, IncHIB-M/FIB-M), IncF type being the prevalent one. Addiction systems ccdAB and hok/sok were associated with transferable plasmids. Genetic structures surrounding bla showed its association with at least a remnant of ISAba125 at its 5'-end. The spread of NDM-1 was not related to class 1 integron which possessed resistance determinants against trimethoprim (dfrA12, dfrA1, dfrA5), streptomycin (aadA2, aacA4), and rifampicin (arr-3). RFLP showed that three isolates possessed the same FII/FIIs plasmid; two of these three isolates were from a single neonate, implying interspecies transfer of bla The predominance of FII plasmids and ISAba125 along with bla was noted, but no specific pattern in the temporal acquisition of mobile genetic elements could be identified. To the best of our knowledge, this report is the first to inform the in-vivo interspecies plasmid transfer event of bla in a neonate.
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