Search bioRxiv⌕ Search

bioRxiv · 10.1101/2021.07.23.453547

Virulence and antimicrobial resistance profile of non-typhoidal Salmonella enterica serovars recovered from poultry processing environments at wet markets in Dhaka, Bangladesh

Abstract

The rapid emergence of virulent and multidrug-resistant (MDR) non-typhoidal Salmonella (NTS) enterica serovars are a growing public health concern globally. The present study focused on the assessment of the pathogenicity and antimicrobial resistance (AMR) profiling of NTS enterica serovars isolated from chicken processing environments at wet markets in Dhaka, Bangladesh. A total number of 870 samples consisting of carcass dressing water (CDW), chopping board swabs (CBS), and knife swabs (KS) were collected from 29 wet markets. The prevalence of Salmonella was found to be 20% in CDW, 19.31% in CBS and 17.58% in KS, respectively. Meanwhile, the MDR Salmonella was found to be 72.41%, 73.21% and 68.62% in CDW, CBS, and KS, respectively. All isolates were screened by polymerase chain reaction (PCR) for eight virulence genes, namely invA, agfA, IpfA, hilA, sivH, sefA, sopE, and spvC. The S. Enteritidis and untyped Salmonella isolate harbored all virulence genes while S. Typhimurium isolates carried six virulence genes except sefA and spvC. Phenotypic resistance revealed decreased susceptibility to ciprofloxacin, streptomycin, ampicillin, tetracycline, gentamycin, sulfamethoxazole-trimethoprim, amoxicillin-clavulanic acid and azithromycin. Genotypic resistance showed higher prevalence of plasmid mediated blaTEM followed by tetA, sul1, sul2, sul3, and strA/B genes. Harmonic and symmetrical trend was observed among the phenotypic and genotypic resistance patterns of the isolates. The research findings anticipate that MDR and virulent NTS enterica serovars are prevailing in the wet market environments which can easily enter into the human food chain. There was a resilient and significant correlation existent among the phenotypic and genotypic resistance patterns and virulence genes of Salmonella isolate recovered from carcass dressing water, chopping board swabs, and knife swabs (p < 0.05), respectively.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Siddiky, N. A., Sarker, M. S., Khan, M. S. R., Rahman, M. T., Kafi, M. A., Samad, M. A.. 2021-07-23. Virulence and antimicrobial resistance profile of non-typhoidal Salmonella enterica serovars recovered from poultry processing environments at wet markets in Dhaka, Bangladesh. https://doi.org/10.1101/2021.07.23.453547

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Prevalent Integration of both Xenotropic and Ecotropic Murine Leukemia Virus in the Human Genome of Xenografts

Humanized mouse models are widely used in medical research to represent human conditions (1, 2), but their fidelity could be compromised by mouse-originated infections. However, their susceptibility to mouse pathogens are rarely questioned (3). Here we screened 1,619 publicly available genomic sequencing runs from patient-derived xenograft (PDX) models for the integration of murine leukemia virus (MLV), a rodent retrovirus exists in the mouse genome as an endogenous retrovirus (4), within the human genome. We discovered substantial enrichment of human-MLV chimeric DNA in approximately 25% of them. Analyzing the human-MLV junctions, we found about 90% of them bearing the unmistakable hallmarks of retroviral integration, including the canonical MLV boundaries and the distinctive 4-bp target site duplications (5, 6). It was also assumed that mouse strains without the highly infectious Bxv1 provirus are safe from MLV contamination in xenografts (7, 8). However, we found many PDX models derived from Bxv1- strains, including the widely used NSG strain, are also contaminated by the supposedly rodent-specific ecotropic MLV (E-MLV). We further confirmed a complete E-MLV integrated into the human genome by both HiFi and sanger sequencing. Our discovery raises concerns that mouse-to-human retroviral transmission and integration is more common and less restrictive than previously appreciated. They support examination of MLV integration as a feature of humanized mouse models with implications on the fidelity of these models in recapitulating human cells and tissues. Our discovery also has underscored the importance of comprehensively inactivation of porcine endogenous retroviruses for the clinical application of xenotransplatation (9, 10).

microbiology↗

Necroptosis is a targetable driver of severe coronavirus pathogenesis

Human-pathogenic coronaviruses differ dramatically in pathogenicity but the underlying mechanisms are incompletely understood. Here, we demonstrate that highly pathogenic coronaviruses trigger necroptosis in the infected cells and lung tissues, whereas necroptosis is not detected in cells infected by seasonal coronavirus. Mechanistically, highly pathogenic coronaviruses produce Z-RNA, activate ZBP1 and initiates necroptotic cell death signaling, triggering necroinflammation and lung injury. In contrast, seasonal coronaviruses produce little to no Z-RNA, and do not activate necroptosis. Importantly, small-molecule inhibition of necroptosis attenuates inflammatory cytokine expression and markedly ameliorates lung damage in mice infected with all three highly pathogenic coronaviruses, independent of virus clearance. Overall, our study identifies necroptosis as a dominant mediator of coronavirus pathogenesis, and positions necroptosis blockade as a new therapeutic target against severe coronavirus diseases.

microbiology↗

POM121 regulates lentiviral nuclear import in a capsid-host factor-dependent manner

Lentiviruses such as human immunodeficiency virus 1 (HIV-1) access the nuclear lumen through the nuclear pore complex (NPC), a process coordinated by the interactions between the viral capsid and nucleoporins (NUPs). Here, using unbiased proteomic screens, we identified several capsid-associated NUPs, including POM121. Depletion of POM121 impaired HIV-1 infection in multiple cell lines and in primary CD4+ T cells, whereas equine infectious anaemia virus (EIAV) infection was enhanced, indicating that POM121 effect is virus-specific. A cytoplasmic carboxy-terminal fragment of POM121, containing its FG-rich region inhibited HIV-1 and a broader range of lentiviruses. Analysis of HIV-1 capsid mutants showed that physical interaction with POM121 does not predict functional dependence, as capsids retaining POM121 binding remained insensitive to its depletion. Strikingly, loss of cyclophilin A (CypA) completely abolished HIV-1 dependence on POM121, whereas depletion of CPSF6 produced only partial rescue, demonstrating that POM121 sensitivity is dictated by the broader network of capsid-host interactions. Finally, POM121 depletion impaired HIV-1 nuclear accumulation and selectively disrupted the nuclear import of other viral and cellular cargo. Together, these findings identify POM121 as a selective regulator of lentiviral nuclear entry whose functional contribution is determined by capsid and host-factor context.

microbiology↗