Dr. Jekyll and Mr. Hide: How Enterococcus faecalis Subverts the Host Immune Response to Cause Infection

Kao, Patrick Hsien Neng; Kline, Kimberly

doi:10.1016/j.jmb.2019.05.030

Cited by 91 publications

(56 citation statements)

References 144 publications

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“…In addition, using a chlorine dosage that is lethal to E. coli but sub-lethal to E. faecalis led to the possibility of producing injured E. faecalis, which can uptake antibiotic-resistant plasmids released by dead ARB, resulting in the dissemination of antibiotics resistance across the bacterial genus. Due to Enterococci causing biofilmassociated opportunistic infections [30], such as wounds and infective endocarditis, promoting the natural transformation of released plasmids into chlorine-injured E. faecalis by the chlorination process may pose a potential risk to public health. Furthermore, the above results indicated that it was not ideal to use E. coli to determine the sanitary quality of drinking water, particularly for judging faecal contamination or predicting the possible presence of waterborne pathogens [13,43], considering that it would result in insufficient bacterial inactivation and the production of culturable chlorine-injured bacteria that show more resistance to chlorination than E. coli.…”

Section: Discussionmentioning

confidence: 99%

“…Herein, after the exposure of sodium hypochlorite (NaClO) to Escherichia coli, Salmonella aberdeen, P. aeruginosa and Enterococcus faecalis with plasmid RP4, the transferability of RP4 released from killed ARB (donor) and their genetic transformability to chlorine-injured bacteria (recipient) were observed. Then, the effects of physicochemical parameters, including pH, temperature, chemical oxygen demand (COD Mn ), ammonium nitrogen (NH 4 + -N) and metal ions (Ca 2+ and K + ) on the natural transformation frequency of released plasmid RP4 from killed bacteria into chlorine-injured E. faecalis, which are frequent causes of biofilm-associated opportunistic infections [29,30], were further explored. For the first time, we showed that cultivated chlorine-tolerant injured non-ARB, which was a kind of competent cell with cell membrane permeabilisation and a strong oxidative stress-response, could uptake released RP4 from sensitive donors and then shift into ARB persistently with a higher frequency.…”

Section: Introductionmentioning

confidence: 99%

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Chlorine disinfection promotes the exchange of antibiotic resistance genes across bacterial genera by natural transformation

Jin¹,

Liu²,

Da-ning³

et al. 2020

The ISME Journal

274

102

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Chlorine disinfection to drinking water plays an important role in preventing and controlling waterborne disease outbreaks globally. Nevertheless, little is known about why it enriches the antibiotic resistance genes (ARGs) in bacteria after chlorination. Here, ARGs released from killed antibiotic-resistant bacteria (ARB), and culturable chlorine-injured bacteria produced in the chlorination process as the recipient, were investigated to determine their contribution to the horizontal transfer of ARGs during disinfection treatment. We discovered Escherichia coli, Salmonella aberdeen, Pseudomonas aeruginosa and Enterococcus faecalis showed diverse resistance to sodium hypochlorite, and transferable RP4 could be released from killed sensitive donor consistently. Meanwhile, the survival of chlorine-tolerant injured bacteria with enhanced cell membrane permeabilisation and a strong oxidative stress-response demonstrated that a physiologically competent cell could be transferred by RP4 with an improved transformation frequency of up to 550 times compared with the corresponding untreated bacteria. Furthermore, the water quality factors involving chemical oxygen demand (COD Mn), ammonium nitrogen and metal ions (Ca 2+ and K +) could significantly promote above transformation frequency of released RP4 into injured E. faecalis. Our findings demonstrated that the chlorination process promoted the horizontal transfer of plasmids by natural transformation, which resulted in the exchange of ARGs across bacterial genera and the emergence of new ARB, as well as the transfer of chlorine-injured opportunistic pathogen from non-ARB to ARB. Considering that the transfer elements were quite resistant to degradation through disinfection, this situation poses a potential risk to public health.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Chlorine disinfection promotes the exchange of antibiotic resistance genes across bacterial genera by natural transformation

Jin¹,

Liu²,

Da-ning³

et al. 2020

The ISME Journal

274

102

View full text Add to dashboard Cite

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“…Enterococci species are part of the healthy human gut microbiota (12) and sometimes can also colonize in the urinary tract, causing different clinical settings from asymptomatic bacteriuria (AB) to…”

Section: Discussionmentioning

confidence: 99%

Urinary tract infection caused by enterococcus spp: risk factors and mortality.

Artero

Campo

García

et al. 2019

Preprint

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Purpose: Complicated urinary tract infections (UTIs) are frequently caused by Enterococcus spp. We aim to define the risk factors involved in UTIs caused by Enterococcus. Determine the overall mortality and predictive risk factors.Methods: A retrospective study was conducted. We compared the results with those of a random sample of patients with complicated UTIs infection caused by Escherichia coli.Results: We found 106 in-patients with UTIs caused by Enterococcus spp., 56 of whom had positive blood cultures. Distribution by species: 83% E. faecalis and 17% E. faecium, with a Charlson comorbidity index of 5.9±2.9. Only male sex with an OR of 2.8 (95%CI 1.2-6.4), nosocomial infection with an OR of 2.8 (95%CI 1.1-7), urinary catheter with an OR of 4.5 (95%CI 1.8-11.3), urinary cancer with an OR of 6.4 (2.1-19.4), and previous antimicrobial treatment with an OR of 4.3 (1.8-10.2) were independent predictors of Enterococcus infection. Overall, in-patient mortality was 16.5%, which was associated with a higher Sequential Organ Failure Assessment (SOFA) score (>4), severe comorbidity such as immunosuppression, malignant hemopathy and nephrostomy, or Enterococcus faecium species and its pattern or resistance to ampicillin or vancomycin (p<0.05). Appropriate empiric antibiotic therapy was not associated with a better prognosis (p >0.05).Conclusions: Enterococcus spp. is a frequent cause of complicated UTI by a profile of risk factors. High mortality secondary to a severe clinical setting and high comorbidity may be sufficient reasons for implementing empiric treatment of patients at risk, although we did not show a higher survival rate in patients with this treatment strategy.

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“…On the other hand, E. faecalis employs a multitude of strategies to subvert the host immune responses. For a thorough appreciation of those strategies, we refer the reader to a recent review that highlights the mechanisms used by E. faecalis to suppress, evade, or inactivate host immune responses (22). Most of the factors that lead to enterococcal virulence in animal models are associated with tissue colonization, such as enterococcal surface protein (Esp) (23), endocarditis-and biofilm-associated pili (Ebp) (24), and the collagen adhesins of E. faecalis (Ace) (25)(26)(27) and E. faecium (Acm) (27,28), with the exception of the acute cytotoxicity conferred by cytolysin (29).…”

Section: Introductionmentioning

confidence: 99%

Adaptation to Adversity: the Intermingling of Stress Tolerance and Pathogenesis in Enterococci

Gaca

Lemos

2019

Microbiol Mol Biol Rev

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SUMMARY Enterococcus is a diverse and rugged genus colonizing the gastrointestinal tract of humans and numerous hosts across the animal kingdom. Enterococci are also a leading cause of multidrug-resistant hospital-acquired infections. In each of these settings, enterococci must contend with changing biophysical landscapes and innate immune responses in order to successfully colonize and transit between hosts. Therefore, it appears that the intrinsic durability that evolved to make enterococci optimally competitive in the host gastrointestinal tract also ideally positioned them to persist in hospitals, despite disinfection protocols, and acquire new antibiotic resistances from other microbes. Here, we discuss the molecular mechanisms and regulation employed by enterococci to tolerate diverse stressors and highlight the role of stress tolerance in the biology of this medically relevant genus.

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Dr. Jekyll and Mr. Hide: How Enterococcus faecalis Subverts the Host Immune Response to Cause Infection

Cited by 91 publications

References 144 publications

Chlorine disinfection promotes the exchange of antibiotic resistance genes across bacterial genera by natural transformation

Chlorine disinfection promotes the exchange of antibiotic resistance genes across bacterial genera by natural transformation

Urinary tract infection caused by enterococcus spp: risk factors and mortality.

Adaptation to Adversity: the Intermingling of Stress Tolerance and Pathogenesis in Enterococci

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