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Appraisal of microbial evolution to commensalism and pathogenicity in humans.

Ghosh AR - Clin Med Insights Gastroenterol (2013)

Bottom Line: The human body is host to a number of microbes occurring in various forms of host-microbe associations, such as commensals, mutualists, pathogens and opportunistic symbionts.While this association with microbes in certain cases is beneficial to the host, in many other cases it seems to offer no evident benefit or motive.The present discussion examines this interaction while tracing the origins of this association, and attempts to hypothesize a possible framework of selective pressures that could have lead microbes to inhabit mammalian host systems.

View Article: PubMed Central - PubMed

Affiliation: Centre for Infectious Diseases and Control, Division of Medical Biotechnology, School of Biosciences and Technology, VIT University, India.

ABSTRACT
The human body is host to a number of microbes occurring in various forms of host-microbe associations, such as commensals, mutualists, pathogens and opportunistic symbionts. While this association with microbes in certain cases is beneficial to the host, in many other cases it seems to offer no evident benefit or motive. The emergence and re-emergence of newer varieties of infectious diseases with causative agents being strains that were once living in the human system makes it necessary to study the environment and the dynamics under which this host microbe relationship thrives. The present discussion examines this interaction while tracing the origins of this association, and attempts to hypothesize a possible framework of selective pressures that could have lead microbes to inhabit mammalian host systems.

No MeSH data available.


Related in: MedlinePlus

Possible mechanism of genetic exchange between the microflora of the human intestine. Gut is the best anatomical niche in humans where commensals, asymptomatic carriers and symptomatic pathogens sustain and survive well. It is assumed that either certain commensals gain virulence by horizontal gene transfer and turn into pathogens, or pathogenic counterparts lose the traits required to become commensals. Likely, an asymptomatic carrier evolved either from commensal or pathogens by different mechanisms to survive better in the host system, maybe by gene silencing or gene augmenting. It is assumed that the order of evolution occurred from commensals to asymptomatic pathogens to pathogens, or vice versa.
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f4-cgast-6-2013-001: Possible mechanism of genetic exchange between the microflora of the human intestine. Gut is the best anatomical niche in humans where commensals, asymptomatic carriers and symptomatic pathogens sustain and survive well. It is assumed that either certain commensals gain virulence by horizontal gene transfer and turn into pathogens, or pathogenic counterparts lose the traits required to become commensals. Likely, an asymptomatic carrier evolved either from commensal or pathogens by different mechanisms to survive better in the host system, maybe by gene silencing or gene augmenting. It is assumed that the order of evolution occurred from commensals to asymptomatic pathogens to pathogens, or vice versa.

Mentions: Now if a genetic exchange of transposable virulent genes and other factors are necessary for colonization and if it is so common in the host system, why do we have so few pathogens compared to the large numbers of commensal in the body? Why is pathogenicity so rare? The answer to this could again lie in the arrangement of genes required for pathogenicity.73 Bacterial populations are clonal in nature;68,74,75 thus, distinct bacterial clones are often the cause of diseases, as well as an increase in outbreaks and infection frequencies. The inheritance of PAI and other mobile elements responsible for virulence does not necessarily create a new pathogenic species. The analysis of pathogenic bacterial species indicates that a certain unique combination of the pathogenic genes may arise only once during the evolutionary process of the same species,21,68,75 but due to an inappropriate arrangement of virulent genes, they remain non pathogenic, and do not express their pathogenicity. In other words, they become non-virulent (or asymptomatic), yet they remain virulent gene-containing carriers. Moreover, very rarely, a pathogen horizontally transfers its entire set of virulent genes to another related or unrelated strain in the same dangerous arrangement, explaining the limited rise of newer pathogenic strains (Fig. 4). Could this be an evolutionarily ingrained control mechanism evolved by the host system to check the growing number of pathogens? A deeper understanding of this mechanism might hold the answer to the changing virulence patterns faced by people in recurring bouts of infectious diseases, where each new outbreak pops up a new causative strain of the same species.


Appraisal of microbial evolution to commensalism and pathogenicity in humans.

Ghosh AR - Clin Med Insights Gastroenterol (2013)

Possible mechanism of genetic exchange between the microflora of the human intestine. Gut is the best anatomical niche in humans where commensals, asymptomatic carriers and symptomatic pathogens sustain and survive well. It is assumed that either certain commensals gain virulence by horizontal gene transfer and turn into pathogens, or pathogenic counterparts lose the traits required to become commensals. Likely, an asymptomatic carrier evolved either from commensal or pathogens by different mechanisms to survive better in the host system, maybe by gene silencing or gene augmenting. It is assumed that the order of evolution occurred from commensals to asymptomatic pathogens to pathogens, or vice versa.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4020404&req=5

f4-cgast-6-2013-001: Possible mechanism of genetic exchange between the microflora of the human intestine. Gut is the best anatomical niche in humans where commensals, asymptomatic carriers and symptomatic pathogens sustain and survive well. It is assumed that either certain commensals gain virulence by horizontal gene transfer and turn into pathogens, or pathogenic counterparts lose the traits required to become commensals. Likely, an asymptomatic carrier evolved either from commensal or pathogens by different mechanisms to survive better in the host system, maybe by gene silencing or gene augmenting. It is assumed that the order of evolution occurred from commensals to asymptomatic pathogens to pathogens, or vice versa.
Mentions: Now if a genetic exchange of transposable virulent genes and other factors are necessary for colonization and if it is so common in the host system, why do we have so few pathogens compared to the large numbers of commensal in the body? Why is pathogenicity so rare? The answer to this could again lie in the arrangement of genes required for pathogenicity.73 Bacterial populations are clonal in nature;68,74,75 thus, distinct bacterial clones are often the cause of diseases, as well as an increase in outbreaks and infection frequencies. The inheritance of PAI and other mobile elements responsible for virulence does not necessarily create a new pathogenic species. The analysis of pathogenic bacterial species indicates that a certain unique combination of the pathogenic genes may arise only once during the evolutionary process of the same species,21,68,75 but due to an inappropriate arrangement of virulent genes, they remain non pathogenic, and do not express their pathogenicity. In other words, they become non-virulent (or asymptomatic), yet they remain virulent gene-containing carriers. Moreover, very rarely, a pathogen horizontally transfers its entire set of virulent genes to another related or unrelated strain in the same dangerous arrangement, explaining the limited rise of newer pathogenic strains (Fig. 4). Could this be an evolutionarily ingrained control mechanism evolved by the host system to check the growing number of pathogens? A deeper understanding of this mechanism might hold the answer to the changing virulence patterns faced by people in recurring bouts of infectious diseases, where each new outbreak pops up a new causative strain of the same species.

Bottom Line: The human body is host to a number of microbes occurring in various forms of host-microbe associations, such as commensals, mutualists, pathogens and opportunistic symbionts.While this association with microbes in certain cases is beneficial to the host, in many other cases it seems to offer no evident benefit or motive.The present discussion examines this interaction while tracing the origins of this association, and attempts to hypothesize a possible framework of selective pressures that could have lead microbes to inhabit mammalian host systems.

View Article: PubMed Central - PubMed

Affiliation: Centre for Infectious Diseases and Control, Division of Medical Biotechnology, School of Biosciences and Technology, VIT University, India.

ABSTRACT
The human body is host to a number of microbes occurring in various forms of host-microbe associations, such as commensals, mutualists, pathogens and opportunistic symbionts. While this association with microbes in certain cases is beneficial to the host, in many other cases it seems to offer no evident benefit or motive. The emergence and re-emergence of newer varieties of infectious diseases with causative agents being strains that were once living in the human system makes it necessary to study the environment and the dynamics under which this host microbe relationship thrives. The present discussion examines this interaction while tracing the origins of this association, and attempts to hypothesize a possible framework of selective pressures that could have lead microbes to inhabit mammalian host systems.

No MeSH data available.


Related in: MedlinePlus