The Impact of Non-Pathogenic Bacteria on the Spread of Virulence and Resistance Genes

Detalhes bibliográficos
Autor(a) principal: Dionisio, Francisco
Data de Publicação: 2023
Outros Autores: Domingues, Célia P. F., Rebelo, João S., Monteiro, Francisca, Nogueira, Teresa
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
Texto Completo: http://hdl.handle.net/10451/58767
Resumo: This review discusses the fate of antimicrobial resistance and virulence genes frequently present among microbiomes. A central concept in epidemiology is the mean number of hosts colonized by one infected host in a population of susceptible hosts: R0. It characterizes the disease’s epidemic potential because the pathogen continues its propagation through susceptible hosts if it is above one. R0 is proportional to the average duration of infections, but non-pathogenic microorganisms do not cause host death, and hosts do not need to be rid of them. Therefore, commensal bacteria may colonize hosts for prolonged periods, including those harboring drug resistance or even a few virulence genes. Thus, their R0 is likely to be (much) greater than one, with peculiar consequences for the spread of virulence and resistance genes. For example, computer models that simulate the spread of these genes have shown that their diversities should correlate positively throughout microbiomes. Bioinformatics analysis with real data corroborates this expectation. Those simulations also anticipate that, contrary to the common wisdom, human’s microbiomes with a higher diversity of both gene types are the ones that took antibiotics longer ago rather than recently. Here, we discuss the mechanisms and robustness behind these predictions and other public health consequences.
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spelling The Impact of Non-Pathogenic Bacteria on the Spread of Virulence and Resistance GenesThis review discusses the fate of antimicrobial resistance and virulence genes frequently present among microbiomes. A central concept in epidemiology is the mean number of hosts colonized by one infected host in a population of susceptible hosts: R0. It characterizes the disease’s epidemic potential because the pathogen continues its propagation through susceptible hosts if it is above one. R0 is proportional to the average duration of infections, but non-pathogenic microorganisms do not cause host death, and hosts do not need to be rid of them. Therefore, commensal bacteria may colonize hosts for prolonged periods, including those harboring drug resistance or even a few virulence genes. Thus, their R0 is likely to be (much) greater than one, with peculiar consequences for the spread of virulence and resistance genes. For example, computer models that simulate the spread of these genes have shown that their diversities should correlate positively throughout microbiomes. Bioinformatics analysis with real data corroborates this expectation. Those simulations also anticipate that, contrary to the common wisdom, human’s microbiomes with a higher diversity of both gene types are the ones that took antibiotics longer ago rather than recently. Here, we discuss the mechanisms and robustness behind these predictions and other public health consequences.MDPIRepositório da Universidade de LisboaDionisio, FranciscoDomingues, Célia P. F.Rebelo, João S.Monteiro, FranciscaNogueira, Teresa2023-07-26T17:42:21Z2023-01-162023-01-16T00:00:00Zinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleapplication/pdfhttp://hdl.handle.net/10451/58767eng10.3390/ijms24031967info:eu-repo/semantics/openAccessreponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãoinstacron:RCAAP2023-11-08T17:07:29Zoai:repositorio.ul.pt:10451/58767Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireopendoar:71602024-03-19T22:08:47.978670Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãofalse
dc.title.none.fl_str_mv The Impact of Non-Pathogenic Bacteria on the Spread of Virulence and Resistance Genes
title The Impact of Non-Pathogenic Bacteria on the Spread of Virulence and Resistance Genes
spellingShingle The Impact of Non-Pathogenic Bacteria on the Spread of Virulence and Resistance Genes
Dionisio, Francisco
title_short The Impact of Non-Pathogenic Bacteria on the Spread of Virulence and Resistance Genes
title_full The Impact of Non-Pathogenic Bacteria on the Spread of Virulence and Resistance Genes
title_fullStr The Impact of Non-Pathogenic Bacteria on the Spread of Virulence and Resistance Genes
title_full_unstemmed The Impact of Non-Pathogenic Bacteria on the Spread of Virulence and Resistance Genes
title_sort The Impact of Non-Pathogenic Bacteria on the Spread of Virulence and Resistance Genes
author Dionisio, Francisco
author_facet Dionisio, Francisco
Domingues, Célia P. F.
Rebelo, João S.
Monteiro, Francisca
Nogueira, Teresa
author_role author
author2 Domingues, Célia P. F.
Rebelo, João S.
Monteiro, Francisca
Nogueira, Teresa
author2_role author
author
author
author
dc.contributor.none.fl_str_mv Repositório da Universidade de Lisboa
dc.contributor.author.fl_str_mv Dionisio, Francisco
Domingues, Célia P. F.
Rebelo, João S.
Monteiro, Francisca
Nogueira, Teresa
description This review discusses the fate of antimicrobial resistance and virulence genes frequently present among microbiomes. A central concept in epidemiology is the mean number of hosts colonized by one infected host in a population of susceptible hosts: R0. It characterizes the disease’s epidemic potential because the pathogen continues its propagation through susceptible hosts if it is above one. R0 is proportional to the average duration of infections, but non-pathogenic microorganisms do not cause host death, and hosts do not need to be rid of them. Therefore, commensal bacteria may colonize hosts for prolonged periods, including those harboring drug resistance or even a few virulence genes. Thus, their R0 is likely to be (much) greater than one, with peculiar consequences for the spread of virulence and resistance genes. For example, computer models that simulate the spread of these genes have shown that their diversities should correlate positively throughout microbiomes. Bioinformatics analysis with real data corroborates this expectation. Those simulations also anticipate that, contrary to the common wisdom, human’s microbiomes with a higher diversity of both gene types are the ones that took antibiotics longer ago rather than recently. Here, we discuss the mechanisms and robustness behind these predictions and other public health consequences.
publishDate 2023
dc.date.none.fl_str_mv 2023-07-26T17:42:21Z
2023-01-16
2023-01-16T00:00:00Z
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dc.relation.none.fl_str_mv 10.3390/ijms24031967
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