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. 2025 Apr 14;26(8):3711.
doi: 10.3390/ijms26083711.

Identification of Novel Staphylococcus aureus Core and Accessory Virulence Patterns in Chronic Rhinosinusitis

Simon P Goldie  1   2 , Laurie C Lau  1 , Huw A S Jones  2 , Philip G Harries  2 , Andrew F Walls  1 , Rami J Salib  1   2
Affiliations

Identification of Novel Staphylococcus aureus Core and Accessory Virulence Patterns in Chronic Rhinosinusitis

Simon P Goldie et al. Int J Mol Sci. .

Abstract

Staphylococcus aureus (S. aureus) colonizes the nasal cavities of both healthy individuals and patients with chronic rhinosinusitis (CRS) with (CRSwNP) and without (CRSsNP) nasal polyps. Treatment-resistant S. aureus biofilms and intracellular persistence are common in CRS patients, requiring the expression of specific virulence factor genes to transition into these forms. We hypothesized that S. aureus isolates from non-diseased controls, CRSsNP patients, and CRSwNP patients would exhibit distinct virulence factor patterns contributing to persistence and intracellular survival in CRS patients. Nasal swabs from seventy-seven individuals yielded S. aureus cultures in eight non-diseased controls, eight CRSsNP patients, and five CRSwNP patients. Whole-genome sequencing analyzed stress, antimicrobial resistance, and virulence genes, including plasmids and prophages. Four virulence factor gene patterns emerged: a core set (hlgA, icaC, hlgB, hlgC, hld, and aur) present in all isolates, and accessory sets, including the enterotoxin gene cluster (seo, sem, seu, sei, and sen) and a partial/complete invasive virulence factor set (splE, splA, splB, lukE, and lukD) (p = 0.001). CRSwNP isolates exhibited incomplete carriage of the core set, with frequent loss of scn, icaC, and hlgA (p < 0.05). These findings suggest that S. aureus has clusters of virulence factors that may act in concert to support the survival and persistence of the bacteria, resulting in enhanced pathogenicity. This may manifest clinically with resistant disease and refractoriness to antibiotics.

Keywords: Staphylococcus aureus; biofilms; chronic rhinosinusitis; quorum sensing; virulence factors.

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Conflict of interest statement

The authors declare no conflicts of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

Figures

Figure 1
Figure 1
Stress and antimicrobial resistance gene carriage in control, CRSsNP, and CRSwNP S. aureus isolates. Each heatmap demonstrates the presence (blue) or absence (white) of (a) stress and (b) antimicrobial resistance genes from each isolate.
Figure 2
Figure 2
Virulence gene carriage in control, CRSsNP, and CRSwNP S. aureus isolates. The heatmap demonstrates the presence (blue) or absence (white) of virulence genes in each isolate.
Figure 3
Figure 3
T-distributed stochastic neighbor embedding of virulence factor presence and absence matrix demonstrating the clustering of virulence factor patterns. Isolates are labelled using their titles. The blue bubble represents the core virulence factors alone, and the pink bubble represents the core and enterotoxin gene cluster. The yellow bubble represents a partial invasive virulence gene cluster, and the purple bubble represents the core and invasive virulence gene clusters.
Figure 4
Figure 4
Plasmid identification and genes. (a) Heatmap of Blast high-scoring pairs from MOB-suite. The presence of HSP is indicated by the blue rectangle and its absence is indicated by the white rectangle. (b) Heatmap of sequenced genes from each identified plasmid listed by group (blue = present and white = absent).
Figure 5
Figure 5
Heatmap of PhiSpy with the identified phage genes listed by group (blue = present and white = absent).
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