Clinical outcomes of type III Pseudomonas aeruginosa bacteremia*

Abstract

Background Pseudomonas aeruginosa bacteremia is a serious and life-threatening infection associated with high mortality. Among the multitude of virulence determinants possessed by P. aeruginosa, the type III secretion system (TTSS) has been implicated with more acute and invasive infection in respiratory diseases. However, the relationship between TTSS and clinical outcomes in P. aeruginosa bacteremia has not been investigated. Objectives To determine the association between the TTSS virulence factor in P. aeruginosa blood stream infection and 30-day mortality. Design Retrospective analysis of 85 cases of P. aeruginosa bacteremia. Setting Tertiary care hospital. Interventions Bacterial isolates were assayed in vitro for secretion of type III exotoxins (ExoU, ExoT, and ExoS). Strain-relatedness was analyzed using randomly amplified polymorphic DNA PCR genotyping. Antimicrobial susceptibilities were determined by means of the Kirby-Bauer disk-diffusion test. Measurements and Main results At least one of the TTSS proteins was detected in 37 out of the 85 isolates (44%). Septic shock was identified in 43% of bacteremic patients with TTSS+ isolates compared to 23% of patients with TTSS− isolates (p=0.12). A high frequency of resistance in the TTSS+ isolates was observed to ciprofloxacin (59%), cefipime (35%), and gentamycin (38%). There was a significant difference in the 30-day cumulative probability of death after bacteremia between secretors and nonsecretors (p=0.02). None of the TTSS+ patients who survived the first 30 days had a P. aeruginosa isolate which exhibited ExoU phenotype. Conclusions The expression of TTSS exotoxins in bacteremic isolates of P. aeruginosa confers poor clinical outcomes independent of antibiotic susceptibility profile.

Molecular epidemiological survey of the quinolone- and carbapenem-resistant genotype and its association with the type III secretion system in Pseudomonas aeruginosa

“…Although this relationship was not assessed in our study, the exoS gene was found in all clinical isolates whilst the presence of the exoT and exoY genes varied, and unlike other studies (El-Solh et al, 2012;Wareham & Curtis, 2007), the presence of the exoU gene occurred at low frequency in our study (9.4 %).…”

“…Indirect evidence from epidemiological studies suggests that fluoroquinolone resistance and expression of TTSS virulence are independently associated with poor outcomes resulting from MDR P. aeruginosa infections (Bleves et al, 2010;El-Solh et al, 2012;Roy-Burman et al, 2001;WongBeringer et al, 2008). Although this relationship was not assessed in our study, the exoS gene was found in all clinical isolates whilst the presence of the exoT and exoY genes varied, and unlike other studies (El-Solh et al, 2012;Wareham & Curtis, 2007), the presence of the exoU gene occurred at low frequency in our study (9.4 %).…”

Molecular Detection of the VirulentExoUGenotype ofPseudomonas aeruginosaIsolated from Infected Surgical Incisions

“…One of the virulence mechanisms possessed by P. aeruginosa is known as TTSS, which is a syringe-like structure that allows the introduction of toxins (e.g., ExoS and ExoU) into target cell cytoplasm [26]. A substantial association between TTSS-associated virulence and poor clinical outcome for P. aeruginosa-infected patients has been reported [27], with higher incidence of massive tissue destruction and spread of blood infection and increased mortality, which was found to be higher with genotypes expressing various exotoxins rather than those with no toxin-expression [28,29]. For that reason, it was important to evaluate the association of the TTSS genotype related to surgical site infection.…”

Pseudomonas aeruginosa flagellum is critical for invasion, cutaneous persistence and induction of inflammatory response of skin epidermis

“…T3SS also enhances infection severity in several animal models: acute pneumonia [19,21,52], keratitis [52], bacteremia [22], peritonitis [53], burn infections [20] and gut-derived sepsis in neutropenia [54]. Moreover, T3SS in vitro detection was correlated with increased morbi-mortality and relapse in human P. aeruginosa ventilator-associated pneumonia and blood stream infections [55,56]. Previously, T2SS has been shown to be strongly involved in P. aeruginosa chronic infection [57].…”