ArticleBrazilian journal of microbiology : [publication of the Brazilian Society for Microbiology]2024
Genomic insights into a Proteus mirabilis strain inducing avian cellulitis.
Article in Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology], 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
10 authors.
Funding
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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