15
(especially poultry) and soil/animal manure, while limited personnel protection
equipments are provided to them. At these sites, intensive rearing of animals is
done, biosecurity, hygiene, food security and bio-containment facilities are rarely
monitored or available, and thus, the emergence of antibiotic resistant microbes is
further accelerated. One study reported that both humans and poultry harbored the
same Salmonella typhimurium strains shown by phage typing (phage DT56 based
similarity) and also resistance against same antibiotics (Kagambèga et al. 2013).
Humans can get affected by antibiotic resistant microbes through three main mechanisms. First, humans may accidentally consume food or water contaminated with
antibiotic resistant microbes, and it is not transmitted to other humans. Millions of
cases of infection by Salmonella spp. and Camplylobacter spp. are reported every
year in US itself and such hazards to humans are amenable to mathematical modelling for risk assessment (McEwen 2012). Such risks assessment predictions and its
strong correlation with the actual disease incidences, led regulatory authorities to
ban the usage of fluoroquinolones in poultry in US.
Second, infected human can transmit it to other humans either directly or indirectly, and this also constitutes breaking of the ‘species barrier’ for the pathogens.
Many such transmission of pathogenic infections between humans have been
reported in Europe and Netherlands (Armand-Lefevre et al. 2005; Spoor et al.
2013). In case of vancomycin resistant enterococci, it has been proposed that the
widespread usage of avoparcin (a glycopeptide) led to emergence of many resistant
strains in animals and their transfer through mechanism 1 must have provided the
initial seed in humans. These microbes normally colonize human gut and they further acquired resistance to multiple antibiotics over repeated exposures during their
residence in the human gut (Bonten et al. 2001). However, more information is
needed in this regard to identify the source of resistant bacteria and its transfer
between humans. Third, antibiotic resistance genes get transferred to human pathogens through horizontal gene transfer and these pathogens infect the humans
(Lipsitch et al. 2002). Many examples exist for transfer of antibiotic resistance gene
from a harmless commensal of one animal species into microbes pathogenic to
humans (Dowson et al. 1993; Bowler et al. 1994). A recent examples is of vanA and
vanB, which provide resistance against an advanced antibiotic – vancomycin. It has
been found to easily transmit between Enterococcus spp., due to high recombination frequencies in this group of microbes and amenability of this resistance gene
for horizontal gene transfer (Willems et al. 2011). This clearly suggests to another
scary impendence that antibiotic resistance genes originating in harmless microbes
due to different agricultural/livestock activities might be getting transferred to the
human pathogens.
Quite correctly, it is reasoned that the level of resistance in microbes associated
with humans is dependent upon the amount of antibiotic being consumed. This dosage is further dependent upon community response towards antibiotics, biogeographical conditions, population density, socio-economic conditions, drug
prescription pattern of health professionals and market dynamics of incentives
between the vendors and prescribers of the antibiotics (Sahoo et al. 2012).
Unarguably, antibiotic resistance in humans is adverse, but even general infection
1 Antimicrobial Resistance Paradigm and One-Health Approach
(especially poultry) and soil/animal manure, while limited personnel protection
equipments are provided to them. At these sites, intensive rearing of animals is
done, biosecurity, hygiene, food security and bio-containment facilities are rarely
monitored or available, and thus, the emergence of antibiotic resistant microbes is
further accelerated. One study reported that both humans and poultry harbored the
same Salmonella typhimurium strains shown by phage typing (phage DT56 based
similarity) and also resistance against same antibiotics (Kagambèga et al. 2013).
Humans can get affected by antibiotic resistant microbes through three main mechanisms. First, humans may accidentally consume food or water contaminated with
antibiotic resistant microbes, and it is not transmitted to other humans. Millions of
cases of infection by Salmonella spp. and Camplylobacter spp. are reported every
year in US itself and such hazards to humans are amenable to mathematical modelling for risk assessment (McEwen 2012). Such risks assessment predictions and its
strong correlation with the actual disease incidences, led regulatory authorities to
ban the usage of fluoroquinolones in poultry in US.
Second, infected human can transmit it to other humans either directly or indirectly, and this also constitutes breaking of the ‘species barrier’ for the pathogens.
Many such transmission of pathogenic infections between humans have been
reported in Europe and Netherlands (Armand-Lefevre et al. 2005; Spoor et al.
2013). In case of vancomycin resistant enterococci, it has been proposed that the
widespread usage of avoparcin (a glycopeptide) led to emergence of many resistant
strains in animals and their transfer through mechanism 1 must have provided the
initial seed in humans. These microbes normally colonize human gut and they further acquired resistance to multiple antibiotics over repeated exposures during their
residence in the human gut (Bonten et al. 2001). However, more information is
needed in this regard to identify the source of resistant bacteria and its transfer
between humans. Third, antibiotic resistance genes get transferred to human pathogens through horizontal gene transfer and these pathogens infect the humans
(Lipsitch et al. 2002). Many examples exist for transfer of antibiotic resistance gene
from a harmless commensal of one animal species into microbes pathogenic to
humans (Dowson et al. 1993; Bowler et al. 1994). A recent examples is of vanA and
vanB, which provide resistance against an advanced antibiotic – vancomycin. It has
been found to easily transmit between Enterococcus spp., due to high recombination frequencies in this group of microbes and amenability of this resistance gene
for horizontal gene transfer (Willems et al. 2011). This clearly suggests to another
scary impendence that antibiotic resistance genes originating in harmless microbes
due to different agricultural/livestock activities might be getting transferred to the
human pathogens.
Quite correctly, it is reasoned that the level of resistance in microbes associated
with humans is dependent upon the amount of antibiotic being consumed. This dosage is further dependent upon community response towards antibiotics, biogeographical conditions, population density, socio-economic conditions, drug
prescription pattern of health professionals and market dynamics of incentives
between the vendors and prescribers of the antibiotics (Sahoo et al. 2012).
Unarguably, antibiotic resistance in humans is adverse, but even general infection
1 Antimicrobial Resistance Paradigm and One-Health Approach