Abstract

One of the major challenges of modern medicine includes the failure of conventional protocols to characterize the pathogenicity of emerging pathogens. This is particularly apparent in the case of Plesiomonas shigelloides. Although a number of infections have been linked to this microorganism, experimental evidence of its virulence factors (VFs), obtained by traditional approaches, is somewhat inconclusive. Hence, it remains unclear whether P. shigelloides is a true or opportunistic one. In the current study, four publicly available whole-genome sequences of P. shigelloides (GN7, NCTC10360, 302-73, and LS1) were profiled using bioinformatics platforms to determine the putative candidate VFs to characterize the bacterial pathogenicity. Overall, 134 unique open reading frames (ORFs) were identified that were homologous or orthologous to virulence genes identified in other pathogens. Of these, 52.24% (70/134) were jointly shared by the strains. The numbers of strain-specific virulence traits were 4 in LS1; 7 in NCTC10360; 10 in 302-73; and 15 in GN7. The pathogenicity islands (PAIs) common to all the strains accounted for 24.07% ORFs. The numbers of PAIs exclusive to each strain were 8 in 302-73; 11 in NCTC10360; 14 in GN7; and 18 in LS1. A PAI encoding Vibrio cholerae ToxR-activated gene d protein was specific to 302-73, GN7, and NCTC10360 strains. Out of 33 antibiotic multi-resistance genes identified, 16 (48.48%) genes were intrinsic to all strains. Further, 17 (22.08%) of 77 antibiotic resistance islands were found in all the strains. Out of 23 identified distinct insertion sequences, 13 were only harbored by strain LS1. The number of intact prophages identified in the strains was 1 in GN7; 2 in 302-73; and 2 in NCTC10360. Further, 1 CRISPR element was identified in LS1; 2 in NCTC10360; and 8 in 302-73. Fifteen (78.95%) of 19 secretion systems and secretion effector variants were identified in all the strains. In conclusion, certain P. shigelloides strains might possess VFs associated with gastroenteritis and extraintestinal infections. However, the role of host factors in the onset of infections should not be undermined.

Highlights

  • Plesiomonas shigelloides possesses various virulence factor (VF) that result in its emerging pathogen status

  • Pathogenomics support the findings of Sanyal et al (1980), provided exhaustive genetic accessories that enable the bacterium with diarrheagenic potential

  • Homology shown by various Plesiomonas open reading frame (ORF) to genes linked to the invasiveness of other pathogens suggests its inherent propensity for invasive virulence

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Summary

Introduction

Plesiomonas shigelloides (hereafter Plesiomonas) possesses various VFs that result in its emerging pathogen status. E.g., the pathophysiology of Plesiomonas in certain infections has been attributed to possible endotoxin production by this bacterium (Okawa et al, 2004; Kaszowska et al, 2016). Endotoxins have been proposed to be central to septic shock and sepsis associated with plesiomonad infections (Alexander and Rietschel, 2001), and to biofilm formation, attachment, invasion of eukaryotic host cells, complement-resistance in the serum, or blood (Aquilini et al, 2013). Plesiomonas have been credited with causing many infections over the years These include gastroenteritis and various forms of diarrhea (Tsukamoto et al, 1978; Wong et al, 2000; Chakour et al, 2002; Klontz et al, 2012; Pfeiffer et al, 2012; Novoa-Farías et al, 2016). While the majority of traditional approaches yielded inconclusive data with respect to the bacterium’s pathogenicity, others concluded that the virulence potential of the microorganism is low (Olsvik et al, 1990; Abbott et al, 1991)

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