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Genomic insights into a Proteus mirabilis strain inducing avian cellulitis. | LitMetric

AI Article Synopsis

  • * A pan-genomic approach was used to investigate if unique genes in a specific P. mirabilis strain (LBUEL-A33) contribute to avian cellulitis, revealing multiple unique genes but inconclusive links to their function in the disease.
  • * The study suggests that multiple factors are needed for P. mirabilis to cause avian cellulitis and emphasizes the need for more research to comprehend the mechanisms involved for effective control and prevention strategies.

Article Abstract

Proteus mirabilis, a microorganism distributed in soil, water, and animals, is clinically known for causing urinary tract infections in humans. However, recent studies have linked it to skin infections in broiler chickens, termed avian cellulitis, which poses a threat to animal welfare. While Avian Pathogenic Escherichia coli (APEC) is the primary cause of avian cellulitis, few cases of P. mirabilis involvement are reported, raising questions about the factors facilitating such occurrences. This study employed a pan-genomic approach to investigate whether unique genes exist in P. mirabilis strains causing avian cellulitis. The genome of LBUEL-A33, a P. mirabilis strain known to cause this infection, was assembled, and compared with other P. mirabilis strains isolated from poultry and other sources. Additionally, in silico serogroup analysis was conducted. Results revealed numerous genes unique to the LBUEL-A33 strain. No function in cellulitis was identified for these genes, and in silico investigation of the virulence potential of LBUEL-A33's exclusive proteins proved inconclusive. These findings support that multiple factors are necessary for P. mirabilis to cause avian cellulitis. Furthermore, this species likely employs its own unique arsenal of virulence factors, as many identified mechanisms are analogous to those of E. coli. While antigenic gene clusters responsible for serogroups were identified, no clear trend was observed, and the gene cluster of LBUEL-A33 did not show homology with any sequenced Proteus serogroups. These results reinforce the understanding that this disease is multifactorial, necessitating further research to unravel the mechanisms and underpin the development of control and prevention strategies.

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http://dx.doi.org/10.1007/s42770-024-01508-6DOI Listing

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