Mechanisms of antimicrobial resistance - Revision history

Bosmana fem at 07:38, 14 April 2023

2023-04-14T07:38:18Z

Bosmana fem: /* FEM PAGE CONTRIBUTORS */

2023-04-10T21:39:46Z

FEM PAGE CONTRIBUTORS

← Older revision		Revision as of 21:39, 10 April 2023
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	References: not provided yet.		References: not provided yet.

	==FEM PAGE CONTRIBUTORS==		<div style="display: inline-block; width: 25%; vertical-align: top; border: 1px solid #000; background-color: #d7effc; padding: 10px; margin: 5px;">
	* Vladimir Prikazsky		'''FEM PAGE CONTRIBUTORS 2007'''
	* luca		:Vladimir Prikazsky
			:luca
			</div>
	- ECDC		- ECDC

	[[Category:Main pathogens and resistance]]		[[Category:Main pathogens and resistance]]

Bosmana fem at 14:30, 23 March 2023

2023-03-23T14:30:21Z

Bosmana fem at 14:24, 23 March 2023

2023-03-23T14:24:06Z

← Older revision		Revision as of 14:24, 23 March 2023
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			Genetic mechanisms of acquired antimicrobial resistance (the title of the page was rephrased as the content is about the mechanisms of resistance rather than about genetic mechanisms)

			=1. Prevention of the antimicrobial from reaching its target by reducing its ability to penetrate into the cell=
			Antimicrobial compounds almost always require access into the bacterial cell to reach their target site where they can interfere with the normal function of the bacterial organism. Porin channels are the passageways by which these antibiotics would normally cross the bacterial outer membrane. Some bacteria protect themselves by prohibiting these antimicrobial compounds from entering past their cell walls. For example, a variety of Gram-negative bacteria reduce the uptake of certain antibiotics, such as aminoglycosides and beta lactams, by modifying the cell membrane porin channel frequency, size, and selectivity. Prohibiting entry in this manner will prevent these antimicrobials from reaching their intended targets that, for aminoglycosides and beta lactams, are the ribosomes and the penicillin-binding proteins (PBPs), respectively.

			This strategy have been observed in:
			* Pseudomonas aeruginosa e.g. against imipenem (a beta-lactam antibiotic);
			* Enterobacter aerogenes and Klebsiella spp. against imipenem;
			* glycopeptide intermediate-resistant S. aureus so-called “GISA” strains with thickened cell wall trapping vancomycin/teicoplanin;
			* many Gram-negative bacteria against aminoglycosides;
			* many Gram-negative bacteria against quinolones.

			=2. Inactivation of antimicrobial agents via modification or degradation=

			Another means by which bacteria preserve themselves is by destroying the active component of the antimicrobial agent. A classic example is the hydrolytic deactivation of the beta-lactam ring in penicillins and cephalosporins by the bacterial enzyme called beta lactamase. The inactivated penicilloic acid will then be ineffective in binding to PBPs (penicillin binding proteins), thereby protecting the process of cell wall synthesis. This strategy has also been observed in:

			Enterobacteriaceae against chloramphenicol (acetylation)
			Gram negative and Gram positive bacteria against aminoglycosides (phosphorylation, adenylation, and acetylation).

			=3. Expulsion of the antimicrobial agents from the cell via general or specific efflux pumps=

			To be effective, antimicrobial agents must also be present at a sufficiently high concentration within the bacterial cell. Some bacteria possess membrane proteins that act as an export or efflux pump for certain antimicrobials, extruding the antibiotic out of the cell as fast as it can enter. This results in low intracellular concentrations that are insufficient to elicit an effect. Some efflux pumps selectively extrude specific antibiotics such as macrolides, lincosamides, streptogramins and tetracyclines, whereas others (referred to as multiple drug resistance pumps) expel a variety of structurally diverse anti-infectives with different modes of action e.g. the qac genes which pump out chlorhexidine, propamidine and quaternary ammonium agents. This strategy has also been observed in:
			* E. coli and other Enterobacteriaceae against tetracyclines;
			* Various members of the Enterobacteriaceae against chloramphenicol;
			* Staphylococci against macrolides and streptogramins;
			* Staphylococcus aureus and Streptococcus pneumoniae against fluoroquinolones.

			=4. Modification of the antimicrobial target within the bacteria=
			Some resistant bacteria evade antimicrobials by reprogramming or camouflaging critical target sites to avoid recognition. Therefore, in spite of the presence of an intact and active antimicrobial compound, no subsequent binding or inhibition will take place. This strategy has been observed in:

			Staphylococci against methicillin and other beta-lactams (Changes or acquisition of different PBPs that do not sufficiently bind beta-lactams to inhibit cell wall synthesis);
			Gram-positive cocci: erythromycin-resistant methylase is encoded by erm genes and causes structural changes to rRNA which prevent macrolide binding and allow synthesis of bacterial proteins to continue;
			* Enterococci against vancomycin (alteration in cell wall precursor components to decrease binding of vancomycin);
			* Mycobacterium spp. against streptomycin (modification of ribosomal proteins or of 16s rRNA);
			* Various microbes which develop mutations in RNA polymerase resulting in resistance to the rifamycins e.g.Staphylococcus spp;
			* members of Enterobacteriaceae with mutations in DNA gyrase resulting in resistance to quinolones


			Link to European IC/HH Core Competencies: Area 4. Infection control activities

			References: not provided yet.

			==FEM PAGE CONTRIBUTORS==
			* Vladimir Prikazsky
			* luca

	[[Category:Main pathogens and resistance]]		[[Category:Main pathogens and resistance]]

Bosmana fem: Created page with " Category:Main pathogens and resistance"

2023-03-23T12:23:57Z

Created page with " Category:Main pathogens and resistance"

New page

[[Category:Main pathogens and resistance]]

← Older revision		Revision as of 07:38, 14 April 2023
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	~~Genetic mechanisms of acquired antimicrobial resistance (the title of the page was rephrased as the content is about the mechanisms of resistance rather than about genetic mechanisms)~~

	=1. Prevention of the antimicrobial from reaching its target by reducing its ability to penetrate into the cell=		=1. Prevention of the antimicrobial from reaching its target by reducing its ability to penetrate into the cell=
	Antimicrobial compounds almost always require access into the bacterial cell to reach their target site, where they can interfere with the normal function of the bacterial organism. Porin channels are the passageways by which these antibiotics would normally cross the bacterial outer membrane. Some bacteria protect themselves by prohibiting these antimicrobial compounds from entering past their cell walls. For example, various Gram-negative bacteria reduce the uptake of certain antibiotics, such as aminoglycosides and beta-lactams, by modifying the cell membrane porin channel frequency, size, and selectivity. Prohibiting entry in this manner will prevent these antimicrobials from reaching their intended targets, which are the ribosomes and the penicillin-binding proteins (PBPs) for aminoglycosides and beta-lactams, respectively.		Antimicrobial compounds almost always require access into the bacterial cell to reach their target site, where they can interfere with the normal function of the bacterial organism. Porin channels are the passageways by which these antibiotics would normally cross the bacterial outer membrane. Some bacteria protect themselves by prohibiting these antimicrobial compounds from entering past their cell walls. For example, various Gram-negative bacteria reduce the uptake of certain antibiotics, such as aminoglycosides and beta-lactams, by modifying the cell membrane porin channel frequency, size, and selectivity. Prohibiting entry in this manner will prevent these antimicrobials from reaching their intended targets, which are the ribosomes and the penicillin-binding proteins (PBPs) for aminoglycosides and beta-lactams, respectively.

	This strategy ~~have~~ been observed in:		This strategy has been observed in:
	* Pseudomonas aeruginosa e.g. against imipenem (a beta-lactam antibiotic);		* Pseudomonas aeruginosa e.g. against imipenem (a beta-lactam antibiotic);
	* Enterobacter aerogenes and Klebsiella spp. against imipenem;		* Enterobacter aerogenes and Klebsiella spp. against imipenem;
Line 13:		Line 12:
	=2. Inactivation of antimicrobial agents via modification or degradation=		=2. Inactivation of antimicrobial agents via modification or degradation=

	Another ~~means by which~~ bacteria preserve themselves is by destroying the active component of the antimicrobial agent. A classic example is the hydrolytic deactivation of the beta-lactam ring in penicillins and cephalosporins by the bacterial enzyme called beta lactamase. The inactivated penicilloic acid will then be ineffective in binding to PBPs (penicillin binding proteins), thereby protecting the process of cell wall synthesis. This strategy has also been observed in:		Another way bacteria preserve themselves is by destroying the active component of the antimicrobial agent. A classic example is the hydrolytic deactivation of the beta-lactam ring in penicillins and cephalosporins by the bacterial enzyme called beta-lactamase. The inactivated penicilloic acid will then be ineffective in binding to PBPs (penicillin-binding proteins), thereby protecting the process of cell wall synthesis. This strategy has also been observed in:

	Enterobacteriaceae against chloramphenicol (acetylation)		Enterobacteriaceae against chloramphenicol (acetylation)
	Gram negative and Gram positive bacteria against aminoglycosides (phosphorylation, adenylation, and acetylation).		Gram-negative and Gram-positive bacteria against aminoglycosides (phosphorylation, adenylation, and acetylation).

	=3. Expulsion of the antimicrobial agents from the cell via general or specific efflux pumps=		=3. Expulsion of the antimicrobial agents from the cell via general or specific efflux pumps=

	Antimicrobial agents must also be present at a sufficiently high concentration within the bacterial cell to be effective. Some bacteria possess membrane proteins that act as an export or efflux pump for certain antimicrobials, extruding the antibiotic ~~out of~~ the cell as fast as it can enter. This results in low intracellular concentrations that are insufficient to elicit an effect. Some efflux pumps selectively extrude specific antibiotics such as macrolides, lincosamides, streptogramins and tetracyclines, whereas others (referred to as multiple drug resistance pumps) expel a variety of structurally diverse anti-infectives with different modes of action e.g. the qac genes which pump out chlorhexidine, propamidine and quaternary ammonium agents. This strategy has also been observed in:		Antimicrobial agents must also be present at a sufficiently high concentration within the bacterial cell to be effective. Some bacteria possess membrane proteins that act as an export or efflux pump for certain antimicrobials, extruding the antibiotic from the cell as fast as it can enter. This results in low intracellular concentrations that are insufficient to elicit an effect. Some efflux pumps selectively extrude specific antibiotics such as macrolides, lincosamides, streptogramins and tetracyclines, whereas others (referred to as multiple drug resistance pumps) expel a variety of structurally diverse anti-infectives with different modes of action, e.g. the qac genes which pump out chlorhexidine, propamidine and quaternary ammonium agents. This strategy has also been observed in:
	* E. coli and other Enterobacteriaceae against tetracyclines;		* E. coli and other Enterobacteriaceae against tetracyclines;
	* Various members of the Enterobacteriaceae against chloramphenicol;		* Various members of the Enterobacteriaceae against chloramphenicol;
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	=4. Modification of the antimicrobial target within the bacteria=		=4. Modification of the antimicrobial target within the bacteria=
	Some resistant bacteria evade antimicrobials by reprogramming or camouflaging critical target sites to avoid recognition. Therefore, despite an intact and active antimicrobial compound~~, no subsequent binding or inhibition will occur~~. This strategy has been observed in:		Some resistant bacteria evade antimicrobials by reprogramming or camouflaging critical target sites to avoid recognition. Therefore, no subsequent binding or inhibition will occur despite an intact and active antimicrobial compound. This strategy has been observed in:

	Staphylococci against methicillin and other beta-lactams (Changes or acquisition of different PBPs that do not sufficiently bind beta-lactams to inhibit cell wall synthesis);		Staphylococci against methicillin and other beta-lactams (Changes or acquisition of different PBPs that do not sufficiently bind beta-lactams to inhibit cell wall synthesis);
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	* Enterococci against vancomycin (alteration in cell wall precursor components to decrease binding of vancomycin);		* Enterococci against vancomycin (alteration in cell wall precursor components to decrease binding of vancomycin);
	* Mycobacterium spp. against streptomycin (modification of ribosomal proteins or of 16s rRNA);		* Mycobacterium spp. against streptomycin (modification of ribosomal proteins or of 16s rRNA);
	* Various microbes which develop mutations in RNA polymerase resulting in resistance to the rifamycins e.g.Staphylococcus spp;		* Various microbes which develop mutations in RNA polymerase resulting in resistance to the rifamycins, e.g.Staphylococcus spp;
	* members of Enterobacteriaceae with mutations in DNA gyrase resulting in resistance to quinolones		* members of Enterobacteriaceae with mutations in DNA gyrase resulting in resistance to quinolones

← Older revision		Revision as of 14:30, 23 March 2023
Line 2:		Line 2:

	=1. Prevention of the antimicrobial from reaching its target by reducing its ability to penetrate into the cell=		=1. Prevention of the antimicrobial from reaching its target by reducing its ability to penetrate into the cell=
	Antimicrobial compounds almost always require access into the bacterial cell to reach their target site where they can interfere with the normal function of the bacterial organism. Porin channels are the passageways by which these antibiotics would normally cross the bacterial outer membrane. Some bacteria protect themselves by prohibiting these antimicrobial compounds from entering past their cell walls. For example, ~~a variety of~~ Gram-negative bacteria reduce the uptake of certain antibiotics, such as aminoglycosides and beta lactams, by modifying the cell membrane porin channel frequency, size, and selectivity. Prohibiting entry in this manner will prevent these antimicrobials from reaching their intended targets ~~that, for aminoglycosides and beta lactams~~, are the ribosomes and the penicillin-binding proteins (PBPs), respectively.		Antimicrobial compounds almost always require access into the bacterial cell to reach their target site, where they can interfere with the normal function of the bacterial organism. Porin channels are the passageways by which these antibiotics would normally cross the bacterial outer membrane. Some bacteria protect themselves by prohibiting these antimicrobial compounds from entering past their cell walls. For example, various Gram-negative bacteria reduce the uptake of certain antibiotics, such as aminoglycosides and beta-lactams, by modifying the cell membrane porin channel frequency, size, and selectivity. Prohibiting entry in this manner will prevent these antimicrobials from reaching their intended targets, which are the ribosomes and the penicillin-binding proteins (PBPs) for aminoglycosides and beta-lactams, respectively.

	This strategy have been observed in:		This strategy have been observed in:
Line 20:		Line 20:
	=3. Expulsion of the antimicrobial agents from the cell via general or specific efflux pumps=		=3. Expulsion of the antimicrobial agents from the cell via general or specific efflux pumps=

	~~To be effective, antimicrobial~~ agents must also be present at a sufficiently high concentration within the bacterial cell. Some bacteria possess membrane proteins that act as an export or efflux pump for certain antimicrobials, extruding the antibiotic out of the cell as fast as it can enter. This results in low intracellular concentrations that are insufficient to elicit an effect. Some efflux pumps selectively extrude specific antibiotics such as macrolides, lincosamides, streptogramins and tetracyclines, whereas others (referred to as multiple drug resistance pumps) expel a variety of structurally diverse anti-infectives with different modes of action e.g. the qac genes which pump out chlorhexidine, propamidine and quaternary ammonium agents. This strategy has also been observed in:		Antimicrobial agents must also be present at a sufficiently high concentration within the bacterial cell to be effective. Some bacteria possess membrane proteins that act as an export or efflux pump for certain antimicrobials, extruding the antibiotic out of the cell as fast as it can enter. This results in low intracellular concentrations that are insufficient to elicit an effect. Some efflux pumps selectively extrude specific antibiotics such as macrolides, lincosamides, streptogramins and tetracyclines, whereas others (referred to as multiple drug resistance pumps) expel a variety of structurally diverse anti-infectives with different modes of action e.g. the qac genes which pump out chlorhexidine, propamidine and quaternary ammonium agents. This strategy has also been observed in:
	* E. coli and other Enterobacteriaceae against tetracyclines;		* E. coli and other Enterobacteriaceae against tetracyclines;
	* Various members of the Enterobacteriaceae against chloramphenicol;		* Various members of the Enterobacteriaceae against chloramphenicol;
Line 27:		Line 27:

	=4. Modification of the antimicrobial target within the bacteria=		=4. Modification of the antimicrobial target within the bacteria=
	Some resistant bacteria evade antimicrobials by reprogramming or camouflaging critical target sites to avoid recognition. Therefore, ~~in spite of the presence of~~ an intact and active antimicrobial compound, no subsequent binding or inhibition will ~~take place~~. This strategy has been observed in:		Some resistant bacteria evade antimicrobials by reprogramming or camouflaging critical target sites to avoid recognition. Therefore, despite an intact and active antimicrobial compound, no subsequent binding or inhibition will occur. This strategy has been observed in:

	Staphylococci against methicillin and other beta-lactams (Changes or acquisition of different PBPs that do not sufficiently bind beta-lactams to inhibit cell wall synthesis);		Staphylococci against methicillin and other beta-lactams (Changes or acquisition of different PBPs that do not sufficiently bind beta-lactams to inhibit cell wall synthesis);
	Gram-positive cocci: erythromycin-resistant methylase is encoded by erm genes and causes structural changes to rRNA which prevent macrolide binding and allow synthesis of bacterial proteins to continue;		Gram-positive cocci: erythromycin-resistant methylase is encoded by erm genes and causes structural changes to rRNA, which prevent macrolide binding and allow synthesis of bacterial proteins to continue;
	* Enterococci against vancomycin (alteration in cell wall precursor components to decrease binding of vancomycin);		* Enterococci against vancomycin (alteration in cell wall precursor components to decrease binding of vancomycin);
	* Mycobacterium spp. against streptomycin (modification of ribosomal proteins or of 16s rRNA);		* Mycobacterium spp. against streptomycin (modification of ribosomal proteins or of 16s rRNA);
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	* members of Enterobacteriaceae with mutations in DNA gyrase resulting in resistance to quinolones		* members of Enterobacteriaceae with mutations in DNA gyrase resulting in resistance to quinolones


	Link to European IC/HH Core Competencies: Area 4. Infection control activities		Link to European IC/HH Core Competencies: Area 4. Infection control activities

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	* Vladimir Prikazsky		* Vladimir Prikazsky
	* luca		* luca

			- ECDC

	[[Category:Main pathogens and resistance]]		[[Category:Main pathogens and resistance]]