Autolysis control hypotheses for tolerance to wall antibiotics
Antibiotics are divided into two classes: bacteriostatic and bactericidal. The reasons for their classification are usually self-evident, although seldom proven. For example, chloram-phenicol stops protein synthesis and is bacteriostatic, probably because when it is removed growth can recommence. Pe...
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Veröffentlicht in: | Antimicrobial agents and chemotherapy 2001-10, Vol.45 (10), p.2671-2675 |
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description | Antibiotics are divided into two classes: bacteriostatic and bactericidal. The reasons for their classification are usually self-evident, although seldom proven. For example, chloram-phenicol stops protein synthesis and is bacteriostatic, probably because when it is removed growth can recommence. Penicillin and congeners are bactericidal, probably because continued cytoplasmic synthesis should lead to increased cellular pressure and eventually to the rupture of the wall and to cell death. Lethality is not always the outcome, and certain strains may neither grow nor lyse in the presence of lactams they are called "tolerant.". |
doi_str_mv | 10.1128/AAC.45.10.2671-2675.2001 |
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Lethality is not always the outcome, and certain strains may neither grow nor lyse in the presence of lactams they are called "tolerant.".</description><subject>Anti-Bacterial Agents</subject><subject>Anti-Bacterial Agents - pharmacology</subject><subject>Autolysis - metabolism</subject><subject>Cell Wall</subject><subject>Cell Wall - chemistry</subject><subject>Cell Wall - drug effects</subject><subject>Cell Wall - metabolism</subject><subject>Drug Tolerance</subject><subject>Drug Tolerance - physiology</subject><subject>Guest</subject><subject>Guest Commentary</subject><subject>N-Acetylmuramoyl-L-alanine Amidase</subject><subject>N-Acetylmuramoyl-L-alanine Amidase - metabolism</subject><subject>Staphylococcus aureus - drug effects</subject><subject>Staphylococcus aureus - metabolism</subject><subject>Streptococcus mutans - drug effects</subject><subject>Streptococcus mutans - metabolism</subject><subject>Streptococcus pneumoniae - drug effects</subject><subject>Streptococcus pneumoniae - metabolism</subject><issn>0066-4804</issn><issn>1098-6596</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNUU1LxDAQDaK46-pfkJ68tSZpvgoilMUvELzoOaRp6nZJmzVplf33puzix0kvM_OYeTOPeQAkCGYIYXFZlsuM0CxCzDhKY6AZhhAdgDmChUgZLdghmEPIWEoEJDNwEsIaRkwLeAxmCFHKCc3n4LocB2e3oQ2Jdv3gnU1W240bViaYkDTOJ7FtvOq1iVXyoaxNVD-0VeuGVodTcNQoG8zZPi_Ay-3N8_I-fXy6e1iWj6kikKG0aBrRNDBeVFhgQnSlOEd1XeS6YBznwjAlhFBUE8p43lCI60rnnGBcc1yYfAGudns3Y9WZWpsoVVm58W2n_FY61crfnb5dyVf3LgvIEY30iz3du7fRhEF2bdDGWtUbNwbJEWKcCf7nIBIIQxIVL4DYDWrvQvCm-dKCoJw8ktEjSegEJ4-mQOXkUaTSHVWFDsu1G30fX_cf3vnPH3wf3JuZfwLFGJ3M</recordid><startdate>20011001</startdate><enddate>20011001</enddate><creator>Koch, A L</creator><general>American Society for Microbiology</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20011001</creationdate><title>Autolysis control hypotheses for tolerance to wall antibiotics</title><author>Koch, A L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-a4061-9ff8ff0453a28244cba771dd93c967238e6a888a5c45673f502dbc37422d729e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Anti-Bacterial Agents</topic><topic>Anti-Bacterial Agents - pharmacology</topic><topic>Autolysis - metabolism</topic><topic>Cell Wall</topic><topic>Cell Wall - chemistry</topic><topic>Cell Wall - drug effects</topic><topic>Cell Wall - metabolism</topic><topic>Drug Tolerance</topic><topic>Drug Tolerance - physiology</topic><topic>Guest</topic><topic>Guest Commentary</topic><topic>N-Acetylmuramoyl-L-alanine Amidase</topic><topic>N-Acetylmuramoyl-L-alanine Amidase - metabolism</topic><topic>Staphylococcus aureus - drug effects</topic><topic>Staphylococcus aureus - metabolism</topic><topic>Streptococcus mutans - drug effects</topic><topic>Streptococcus mutans - metabolism</topic><topic>Streptococcus pneumoniae - drug effects</topic><topic>Streptococcus pneumoniae - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Koch, A L</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Antimicrobial agents and chemotherapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Koch, A L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Autolysis control hypotheses for tolerance to wall antibiotics</atitle><jtitle>Antimicrobial agents and chemotherapy</jtitle><stitle>Antimicrob. Agents Chemother</stitle><addtitle>Antimicrob Agents Chemother</addtitle><date>2001-10-01</date><risdate>2001</risdate><volume>45</volume><issue>10</issue><spage>2671</spage><epage>2675</epage><pages>2671-2675</pages><issn>0066-4804</issn><eissn>1098-6596</eissn><abstract>Antibiotics are divided into two classes: bacteriostatic and bactericidal. The reasons for their classification are usually self-evident, although seldom proven. For example, chloram-phenicol stops protein synthesis and is bacteriostatic, probably because when it is removed growth can recommence. Penicillin and congeners are bactericidal, probably because continued cytoplasmic synthesis should lead to increased cellular pressure and eventually to the rupture of the wall and to cell death. 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subjects | Anti-Bacterial Agents Anti-Bacterial Agents - pharmacology Autolysis - metabolism Cell Wall Cell Wall - chemistry Cell Wall - drug effects Cell Wall - metabolism Drug Tolerance Drug Tolerance - physiology Guest Guest Commentary N-Acetylmuramoyl-L-alanine Amidase N-Acetylmuramoyl-L-alanine Amidase - metabolism Staphylococcus aureus - drug effects Staphylococcus aureus - metabolism Streptococcus mutans - drug effects Streptococcus mutans - metabolism Streptococcus pneumoniae - drug effects Streptococcus pneumoniae - metabolism |
title | Autolysis control hypotheses for tolerance to wall antibiotics |
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