1.2.2 Mechanism of antibiotic resistance
Bacteria may become resistant to various antimicrobial agents through several mechanisms. Major mechanisms of antibiotic resistance in bacteria includes : (1) modification in target site so the antibiotic cannot recognise the target; (2) enzyme production that will inactivate or modify the drug before its effect; (3) expelling or extruding the antibiotic outside the cell by one or more efflux pumps so the drug is unable to reach the target site to exert its antibacterial action; and (4) alterations in the cell membrane permeability that inhibits the access of drug into the cell (Périchon & Courvalin, 2009; Verraes et al., 2013).
Antimicrobial resistance could be intrinsic or acquired. Intrinsic resistance is an inherent capacity of organisms making them insensitive to all antibiotics, whereas acquired resistance is a result of chromosomal mutation in bacterial genome or acquisition of resistance conferring genetic material from a different source (Périchon & Courvalin, 2009; Sefton, 2002; Tenover, 2006). Some bacteria are intrinsically or naturally resistant to many antimicrobials. This type of antimicrobial resistance in bacteria is often due to the absence of target site for the action of antibiotic or in ability of the drug to pass through the cell wall or bacterial membrane for its action. Bacteria, which are sensitive to antimicrobials, may become resistant by mutation in genetic material or acquire new genetic material from resistant bacteria by horizontal gene transfer (HGT) (Verraes et al., 2013). There are three mechanism of HGT among bacteria: conjugation, transformation, and transduction (Davies, 1994; McManus, 1997; Verraes et al., 2013). 1.2.3 Mechanism of antimicrobial resistance in Salmonella to selected classes of antimicrobials The development of antimicrobial resistance in Salmonella is determined by one of multiple mechanisms such as: enzyme production to deactivate antimicrobial agent through degradation or structural modification, decrease in cell permeability to antimicrobial agents, efflux pumps activation by antibiotics and modifications of the cellular target site of drug action (Sefton, 2002). Resistance to cephalosporins and penicillin by Salmonella is related to production of β-lactamase enzymes produced by different Salmonella serovars. The chemical structures of limited antimicrobial agents are degraded by β-lactamase enzymes, whereas a wide array of antimicrobial agents are degraded by broad spectrum β- lactamases (Finch et al., 2003). The most common and important mechanism for β-lactam antibiotic resistance is attributable to β-lactamases production by Salmonella spp (Finch et al., 2003; Revathi et al., 1998). AmpC enzyme is one of the β-lactamase enzymes, which are encoded by blaCMY and has been shown to mediate resistance to most β-lactam antibiotics including ampicillin, ceftiofur and ceftriaxone (Aarestrup et al., 2004). In Salmonella, resistance to tetracycline is encoded by the tet genes. Most of the tet genes code for efflux pumps and several others code for ribosomal protection proteins. The majority of tet genes in bacteria are present on the mobile genetic elements such as plasmids, transposons, conjugative trasnposons and integrons (Chopra & Roberts, 2001). Antimicrobial resistance in Salmonella to chloramphenicol is encoded by flor or cml (Butaye et al., 2003; Chopra & Roberts, 2001). Resistance to tetracycline and chloramphenicol is accomplished by reduction in intracellular levels of antimicrobial agent …show more content…
Poultry products are a major source of Salmonella infection in humans. In Australia, currently there are no published studies describing antimicrobial resistance pattern in Salmonella isolated from commercial egg farm or eggs. However, results from the Australian Reference Centre have shown differences in resistance pattern in Salmonella isolates recovered from egg and meat producing chickens (Australian Salmonella Reference Centre, 2009). Of the 1475 meat chicken isolates, 31, 10, 7 and 6 % were resistant to streptomycin, tetracycline, sulphonamides and ampicillin respectively. Whereas, of the 265 isolates from egg farms, 2, 4, 2 and 5% were resistant to streptomycin, tetracycline, sulphonamides and ampicillin respectively (Australian Salmonella Reference Centre, 2009). Resistance to fluoroquinolones and ceftiofur was not detected in any of the isolates tested. Multidrug resistance (resistance to 4 or more antibiotics) was observed in 3% and 0.4% of chicken meat and egg farm isolates respectively (Australian Salmonella Reference Centre, 2009; Ndi & Barton, 2011). In Australia, antimicrobial resistance in Salmonella spp isolated from poultry is low compared to other parts of the world due to the restricted use of antibiotics however, the contamination of egg and egg products remains a significant concern for the
Bacteria may become resistant to various antimicrobial agents through several mechanisms. Major mechanisms of antibiotic resistance in bacteria includes : (1) modification in target site so the antibiotic cannot recognise the target; (2) enzyme production that will inactivate or modify the drug before its effect; (3) expelling or extruding the antibiotic outside the cell by one or more efflux pumps so the drug is unable to reach the target site to exert its antibacterial action; and (4) alterations in the cell membrane permeability that inhibits the access of drug into the cell (Périchon & Courvalin, 2009; Verraes et al., 2013).
Antimicrobial resistance could be intrinsic or acquired. Intrinsic resistance is an inherent capacity of organisms making them insensitive to all antibiotics, whereas acquired resistance is a result of chromosomal mutation in bacterial genome or acquisition of resistance conferring genetic material from a different source (Périchon & Courvalin, 2009; Sefton, 2002; Tenover, 2006). Some bacteria are intrinsically or naturally resistant to many antimicrobials. This type of antimicrobial resistance in bacteria is often due to the absence of target site for the action of antibiotic or in ability of the drug to pass through the cell wall or bacterial membrane for its action. Bacteria, which are sensitive to antimicrobials, may become resistant by mutation in genetic material or acquire new genetic material from resistant bacteria by horizontal gene transfer (HGT) (Verraes et al., 2013). There are three mechanism of HGT among bacteria: conjugation, transformation, and transduction (Davies, 1994; McManus, 1997; Verraes et al., 2013). 1.2.3 Mechanism of antimicrobial resistance in Salmonella to selected classes of antimicrobials The development of antimicrobial resistance in Salmonella is determined by one of multiple mechanisms such as: enzyme production to deactivate antimicrobial agent through degradation or structural modification, decrease in cell permeability to antimicrobial agents, efflux pumps activation by antibiotics and modifications of the cellular target site of drug action (Sefton, 2002). Resistance to cephalosporins and penicillin by Salmonella is related to production of β-lactamase enzymes produced by different Salmonella serovars. The chemical structures of limited antimicrobial agents are degraded by β-lactamase enzymes, whereas a wide array of antimicrobial agents are degraded by broad spectrum β- lactamases (Finch et al., 2003). The most common and important mechanism for β-lactam antibiotic resistance is attributable to β-lactamases production by Salmonella spp (Finch et al., 2003; Revathi et al., 1998). AmpC enzyme is one of the β-lactamase enzymes, which are encoded by blaCMY and has been shown to mediate resistance to most β-lactam antibiotics including ampicillin, ceftiofur and ceftriaxone (Aarestrup et al., 2004). In Salmonella, resistance to tetracycline is encoded by the tet genes. Most of the tet genes code for efflux pumps and several others code for ribosomal protection proteins. The majority of tet genes in bacteria are present on the mobile genetic elements such as plasmids, transposons, conjugative trasnposons and integrons (Chopra & Roberts, 2001). Antimicrobial resistance in Salmonella to chloramphenicol is encoded by flor or cml (Butaye et al., 2003; Chopra & Roberts, 2001). Resistance to tetracycline and chloramphenicol is accomplished by reduction in intracellular levels of antimicrobial agent …show more content…
Poultry products are a major source of Salmonella infection in humans. In Australia, currently there are no published studies describing antimicrobial resistance pattern in Salmonella isolated from commercial egg farm or eggs. However, results from the Australian Reference Centre have shown differences in resistance pattern in Salmonella isolates recovered from egg and meat producing chickens (Australian Salmonella Reference Centre, 2009). Of the 1475 meat chicken isolates, 31, 10, 7 and 6 % were resistant to streptomycin, tetracycline, sulphonamides and ampicillin respectively. Whereas, of the 265 isolates from egg farms, 2, 4, 2 and 5% were resistant to streptomycin, tetracycline, sulphonamides and ampicillin respectively (Australian Salmonella Reference Centre, 2009). Resistance to fluoroquinolones and ceftiofur was not detected in any of the isolates tested. Multidrug resistance (resistance to 4 or more antibiotics) was observed in 3% and 0.4% of chicken meat and egg farm isolates respectively (Australian Salmonella Reference Centre, 2009; Ndi & Barton, 2011). In Australia, antimicrobial resistance in Salmonella spp isolated from poultry is low compared to other parts of the world due to the restricted use of antibiotics however, the contamination of egg and egg products remains a significant concern for the