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    by: muhammed rashid ak

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    1 : DRUG RESISTANCE By Muhammed rashid ak Medical college calicut
    2 : Unresponsiveness of a microorganism to an antimicrobial. Drug resistance is the reduction in effectiveness of a drug such as an antimicrobial or an antineoplastic in curing a disease or condition. When an organism is resistant to more than one drug, it is said to be multidrug-resistant.
    3 : It took less than 20 years for, bacteria to show signs of resistance. Staphylococcus aureus, which causes blood poisoning and pneumonia, started to show resistance in the 1950s. Today there are different strains of S. aureus resistant to every form of antibiotic in use.
    4 : Natural resistance- some microbes are always been resistant to certain AMA. They lack the metabolic process or the target site which is affected by the particular drug. Species or group charecteristics. Eg:gram negative bacilli are normally. unaffected by penicillin G,M.tuberculosis to tetracycline's. Does not pose clinical problem.
    5 :
    6 : Acquired Resistance Development of resistance by an organism which was sensitive before ,due to the use of an AMA over a peried of time. This can happen with any organism and is a majour clinical problem. Devolopment of resistance is dependent on the microorganism as well as the drug. Eg: Staphylococci,coliforms,tubercle bacilli-rapid acquisition of resistance.
    7 : Mechanisms of drug resistance Drug inactivation or modification: e.g., enzymatic deactivation of Penicillin G in some penicillin-resistant bacteria through the production of ß-lactamases. Alteration of target site: e.g., alteration of PBP— the binding target site of penicillins — in MRSA and other penicillin-resistant bacteria. Alteration of metabolic pathway: e.g., some sulfonamide-resistant bacteria do not require (PABA), an important precursor for the synthesis of folic acid and nucleic acids in bacteria inhibited by sulfonamides. Instead, like mammalian cells, they turn to utilizing preformed folic acid.
    8 : Reduced drug accumulation: By decreasing drug permeability and/or increasing active efflux (pumping out) of the drugs across the cell surface.
    9 : Antibiotics promote resistance If a patient does not complete course of antibiotic Or forgets to take the doses regularly, then resistant strains get a chance to build up. The antibiotics also kill innocent by standers bacteria which are non-pathogens. reduces the competition for the resistant pathogens. The use of antibiotics also promotes antibiotic resistance in non-pathogens too. These non-pathogens may later pass their resistance genes on to pathogens .
    10 : Resistance gets around When antibiotics are used on a person, the numbers of antibiotic resistant bacteria increase in other members of the family. In places where antibiotics are used extensively e.g. hospitals and farms antibiotic resistant strains increase in numbers
    11 : Resistant pathogens Staphylococcus aureus Major resistant pathogen. Found on the mucous membranes and the human skin of around a third of the population. extremely adaptable to antibiotic pressure. Community-acquired MRSA responsible for rapidly progressive, fatal diseases, including necrotizing pneumonia, severe sepsis and necrotizing fasciitis. , oxazolidinones, (oxazolidinone, linezolid),vancomycin are the antibiotics used.
    12 : Streptococcus and Enterococcus S. pneumonia is responsible for pneumonia, bacteremia, otitis media, meningitis, sinusitis, peritonitis and arthritis. Resistance of Streptococcus pneumoniae to penicillin and other beta-lactams is increasing worldwide.
    13 : Pseudomonas aeruginosa Clostridium difficile Salmonella and e.coli
    14 : Resistance To ß-lactam Antibiotics Act by inhibiting the carboxy or transpeptidase or penicillin binding protiens in peptidoglaycon synthesis. Resistance is caused by ß-lactamase(most common) Mutation in the PBPs –reduced affinity Reduced uptake and efflux.
    15 : ß-lactamases Catalyse the ring opening reaction of ß-lactam moity. Classified as classes A-D based on peptide sequence. Class A,C,D have a serine at the active site. Class B have four zinc atoms at their active site. So called-metallo ß-lactamase. Class A-active against benzyl pencillin. Class B-effective against penicillins and cephalosporins. .
    16 : Class C-Inducible,mutation lead to over expression. Class D-composed of OXA type enzymes which can hydrolyse oxacillin. ß-lactamase Inhibitors Clavunalic acid,sulbactam Altered PBP is responsible for resistance by Streptococcus pneumoniae(PBP1a,PBP2b,PBP2x). Haemophilus influenzae(PBP3A,PBP3b).
    17 : Resistance to Glycopeptide Antibiotic Vancomycine and teicoplanin. Bind the terminal D-alanine side chains of pepetidoglycan and prevent cross linking in gram positive bacteria. Resistance to vancomycin is via a sensor histidine kinase(vanS) and a response regulator (vanR). Van H encodes a D-lactate dehydrogenase\alpha-keto acid redutase and generates D-lactate ,which is the substrate for VanA(D-Ala-D-Lac ligase). Cell wall precurser terminate at D-Ala-D-Lac to which vancomycin bind with very low affinity. This change in affinity is mediated by one Hydrogen bond. Selective pressure.

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