Lipooligosaccharide locus class of Campylobacter jejuni: sialylation is not needed for invasive infection

Abstract

Campylobacter jejuni is a highly diverse enteropathogen that is commonly detected worldwide. It can sometimes cause bacteraemia, but the bacterial characteristics facilitating bloodstream infection are not known. A total of 73 C. jejuni isolates, consecutively collected from blood-borne infections during a 10-year period all over Finland and for which detailed clinical information of the patients were available, were included. We screened the isolates by PCR for the lipooligosaccharide (LOS) locus class and for the presence of the putative virulence genes ceuE, ciaB, fucP, and virB11. The isolates were also tested for γ-glutamyl transpeptidase production. The results were analysed with respect to the clinical characteristics of the patients, and the multilocus sequence types (MLSTs) and serum resistance of the isolates. LOS locus classes A, B, and C, which carry genes for sialylation of LOS, were detected in only 23% of the isolates. These isolates were not more resistant to human serum than those with the genes of non-sialylated LOS locus classes, but were significantly more prevalent among patients with underlying diseases (p 0.02). The fucose permease gene fucP was quite uncommon, but was associated with the isolates with the potential to sialylate LOS (p <0.0001). LOS locus classes and some of the putative virulence factors were associated with MLST clonal complexes. Although some of the bacterial characteristics studied here have been suggested to be important for the invasiveness of C. jejuni, they did not explain why the clinical isolates in the present study were able to cause bacteraemia.

Virulence Traits of Inpatient Campylobacter jejuni Isolates, and a Transcriptomic Approach to Identify Potential Genes Maintaining Intracellular Survival

“…Recent studies demonstrated the importance of sialylated LOS in invasion [97], an increased occurrence of bloody diarrhoea, and a longer duration of symptoms [98,99]. Our findings did not reveal any correlation between the presence of cstII and cgtB [28,100] and the invasive potential and clinical outcomes of the isolates as previously demonstrated [101]. However the high rate of expression of various synthases, transferases, and epimerases that take part in LOS synthesis ( Supplementary Table S2E) and Oand N-linked glycosylation ( Supplementary Table S2O,P) strongly suggest that these systems have supportive roles in maintaining intracellular C. jejuni survival.…”

Lipooligosaccharide locus classes and putative virulence genes among chicken and human Campylobacter jejuni isolates

“…Some studies have also proposed that C. jejuni strains with sialylated LOS might be involved in more severe symptoms of enteritis as well as invasive infection [5, 13, 14]. However in previous studies, we have not been able to find any associations between such strains and severe enteritis or with invasive infection in patients [7, 8]. The prevalence of C. jejuni strains with genes for sialylation of LOS among enteritis patients seems to vary between 50 and 60 % [5, 8, 15].…”

“…The mechanisms behind the pathogenicity of C. jejuni are poorly understood. The existence of virulence associated genes has been proposed in several studies but few have been correlated to disease severity in clinical materials [2, 4, 5, 7–10]. The structure of the lipooligosaccharide (LOS) layer of C. jejuni has been suggested to be an important determinant of the pathogenicity of certain postinfectious sequelae [4, 5, 10].…”

Knowledge gaps in control ofCampylobacterfor prevention of campylobacteriosis

“…Furthermore, it was proposed that C. jejuni strains with sialylated LOS might be more invasive and cause more severe symptoms of enteritis (Godschalk et al, 2007). The prevalence of strains with genes for sialylation of LOS among human enteritis patients seemed to vary from 50% to 60% (Ellstr€ om, Hansson, Nilsson, Rautelin, & Olsson Engvall, 2016;Ellstr€ om et al, 2014;Habib et al, 2009). Furthermore, host factors may have important roles in the pathogenesis of campylobacteriosis in humans (Dasti et al, 2010 (Oberhelman & Taylor, 2000;Skirrow, 1994).…”

“…The mechanisms behind pathogenicity of Campylobacter are poorly understood. Studies of virulence factors or virulence-associated genes in Campylobacter have so far not given conclusive evidence of genes correlated with the disease in humans (Ellstr€ om, Feodoroff, H€ anninen, & Rautelin, 2013;Ellstr€ om, Feodoroff, H€ anninen, Rautelin, & Allerberger, 2014). There is no simple animal model available that mimics human disease for studying and possibly discriminating between (for humans) pathogenic and non-pathogenic strains (Janssen et al, 2008).…”