Interbacterial mechanisms of colonization resistance and the strategies pathogens use to overcome them

Sorbara, Matthew T.; Pamer, Eric G.

doi:10.1038/s41385-018-0053-0

Cited by 223 publications

(192 citation statements)

References 169 publications

(195 reference statements)

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“…Experimental studies have shown beneficial effects of a bacteriocin produced by probiotic strains of C. butyricum in preventing infection in other Clostridia, including Clostridium difficile [55] and Clostridium pasteurianum [56], yet its effect on C. botulinum remains to be investigated. Additional mechanisms for competitive microbial resistance may include nutrient limitation, enhancing the intestinal mucosal barrier, and activation of host immunity [57].…”

Section: The Possible Role Of the Gut Microbiome In Colonizationmentioning

confidence: 99%

Adult Intestinal Toxemia Botulism

Harris

Anniballi

Austin

2020

Toxins

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Intoxication with botulinum neurotoxin can occur through various routes. Foodborne botulism results after consumption of food in which botulinum neurotoxin-producing clostridia (i.e., Clostridium botulinum or strains of Clostridium butyricum type E or Clostridium baratii type F) have replicated and produced botulinum neurotoxin. Infection of a wound with C. botulinum and in situ production of botulinum neurotoxin leads to wound botulism. Colonization of the intestine by neurotoxigenic clostridia, with consequent production of botulinum toxin in the intestine, leads to intestinal toxemia botulism. When this occurs in an infant, it is referred to as infant botulism, whereas in adults or children over 1 year of age, it is intestinal colonization botulism. Predisposing factors for intestinal colonization in children or adults include previous bowel or gastric surgery, anatomical bowel abnormalities, Crohn's disease, inflammatory bowel disease, antimicrobial therapy, or foodborne botulism. Intestinal colonization botulism is confirmed by detection of botulinum toxin in serum and/or stool, or isolation of neurotoxigenic clostridia from the stool, without finding a toxic food. Shedding of neurotoxigenic clostridia in the stool may occur for a period of several weeks. Adult intestinal botulism occurs as isolated cases, and may go undiagnosed, contributing to the low reported incidence of this rare disease.

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Section: The Possible Role Of the Gut Microbiome In Colonizationmentioning

confidence: 99%

Adult Intestinal Toxemia Botulism

Harris

Anniballi

Austin

2020

Toxins

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“…Colonisation resistance occurs through an array of direct or indirect bacterial and host interactions including competition for nutrients, host metabolites and physical space 10 . An example of nutrient competition is the commensal Bacteroides thetaiotaomicron which consumes carbohydrates essential to murine pathogen Citrobacter rodentium causing it to be excluded 11 .…”

Section: Introductionmentioning

confidence: 99%

Dissecting individual pathogen-commensal interactions within a complex gut microbiota community

Hassall

Unnikrishnan

2020

Preprint

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14Interactions of commensal bacteria within the gut microbiota and with invading pathogens 15 are critical in determining the outcome of an infection. While murine studies have been 16 valuable, we lack in vitro tools to monitor community responses to pathogens at a single-17 species level. We have developed a multi-species community of nine representative gut 18 species cultured together as a mixed biofilm and tracked numbers of individual species over 19 time using a qPCR-based approach. Introduction of the major nosocomial gut pathogen, 20Clostridiodes difficile, to this community resulted in increased adhesion of commensals and 21 inhibition of C. difficile multiplication. Interestingly, we observed an increase in individual 22Bacteroides species accompanying the inhibition of C. difficile. Furthermore, Bacteroides 23 dorei reduced C. difficile growth within biofilms, suggesting a role for Bacteroides spp in 24 prevention of C. difficile colonisation. We report here an in vitro tool with excellent 25 applications for investigating bacterial interactions within a complex community. 26 27 28 Disturbed microbiota and the loss of colonisation resistance are associated with several 49 pathogen infections including Clostridioides difficile 8 , Enterohemorrhagic E. coli 15 , and 50 Campylobacter jejuni 16 . 51 In the case of C. difficile, a leading cause of healthcare-associated diarrhoea worldwide, 52 colonisation occurs only when the microbiota is altered, usually due to treatment with 53 antibiotics such as fluoroquinolones 17 . The increased susceptibility of C. difficile infection (CDI) 54 after antibiotic-induced dysbiosis of the gut microbiota is well documented 18,19 . While most 55 4 studies demonstrating the link between CDI and antibiotic therapy are based on changes in 56 microbial populations by microbiota sequencing, recent studies have reported mechanisms by 57 which the microbiota can prevent C. difficile infections 20 . The microbiota in a healthy state 58 consumes or converts primary bile acid into secondary bile acids, reducing the ability of C. 59 difficile to germinate 21 . Secondary bile acids such as deoxycholic acid (DCA) and lithocholic 60 acid (LCA), are toxic to vegetative C. difficile 22,23 . Additionally, gut bacteria like Clostridium 61 scindens which encode secondary bile acid synthesis enzymes have been associated to 62 resistance to C. difficile infection 24 . The microbiota not only competes for resources but 63 actively inhibits C. difficile through production of bacteriocins such as the thuricin CD, 64 produced by Bacteroides thuringiensis 25 . 65While the microbiota is clearly important in preventing infections, current knowledge is mainly 66 based on microbiota profiles from faeces. The gut microbiota is composed of bacteria within 67 the lumen, which are usually detected in faeces and bacteria associated with the gut mucosa. 68Few studies have profiled the adherent microbiota population of healthy human guts as they 69 require invasive biopsies 26 . While not much is known abou...

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“…56 Establishment of these key pathogens in murine guts has been linked to antibiotic-induced decrease in anaerobic flora. 14,[21][22][23][50][51][52][53]57 ESBL K. pneumoniae colonization has been associated with piperacillin-tazobactam, ceftriaxone, and ceftazidime when administered in large doses. 29 We know that the invading E. coli and K. pneumoniae strains used in our study do not persist in healthy murine guts without antibiotic pressure (controls here and 34 ), indicating that their persistence was a direct consequence of dysbiosis.…”

Section: Discussionmentioning

confidence: 99%

Differential effects of antibiotic treatment with piperacillin/tazobactam or ceftriaxone on the murine gut microbiota

Venturini

Bowring

Fajardo-Lubián

et al. 2020

Preprint

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Effective antimicrobial stewardship requires a better understanding of the impact of different antibiotics on the gut microflora. Studies in humans are confounded by large inter-individual variability and difficulty in identifying control cohorts. However, controlled murine models can provide valuable information. We examined the impact of a penicillin-like antibiotic (piperacillin/tazobactam, TZP) or a third-generation cephalosporin (ceftriaxone, CRO) on the murine gut microbiota. We analyzed gut microbiome composition by 16S-rRNA amplicon sequencing and effects on the Enterobacteriaceae by qPCR and standard microbiology.Colonization resistance to multidrug resistant Escherichia coli ST131 and Klebsiella pneumoniae ST258 was also tested. Changes in microbiome composition and a significant (p<0.001) decrease in diversity occurred in all treated mice, but were more marked and longer lasting after CRO exposure with a persistent rise in Proteobacteria levels. Increases in the Enterobacteriaceae occurred in all antibiotic treated mice, but were transient and associated with direct antibiotic pressure. Co-habitation of treated and untreated mice attenuated the detrimental effect of antibiotics on treated animals, but also caused disturbance in untreated co-habitants. At the height of dysbiosis after antibiotic termination, the murine gut was highly susceptible to colonization with both multidrug resistant pathogens. The administration of a third-generation cephalosporin caused a significantly prolonged dysbiosis in the murine gut microflora, when compared to a penicillin/β-lactam inhibitor combination with comparable activity against medically important virulent bacteria. At the height of dysbiosis, both antibiotic treatments equally led to microbial imbalance associated with loss of resistance to gut colonization by antibiotic-resistant pathogens.

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Interbacterial mechanisms of colonization resistance and the strategies pathogens use to overcome them

Cited by 223 publications

References 169 publications

Adult Intestinal Toxemia Botulism

Adult Intestinal Toxemia Botulism

Dissecting individual pathogen-commensal interactions within a complex gut microbiota community

Differential effects of antibiotic treatment with piperacillin/tazobactam or ceftriaxone on the murine gut microbiota

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