Antibiotic resistance dr sachin
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Antibiotic resistance dr sachin

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Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in ...

Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.

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  • By 1946, 6% of S. aureus strains were resistant to penicillin By 1960 up to 60% of S. aureus strains were resistant to penicillin

Antibiotic resistance dr sachin Antibiotic resistance dr sachin Presentation Transcript

  • ANTIBIOTIC RESISTANCE Dr. Sachin Verma MD, FICM, FCCS, ICFC Fellowship in Intensive Care Medicine Infection Control Fellows Course Consultant Internal Medicine and Critical CareWeb:- http://www.medicinedoctorinchandigarh.com Mob:- +91-7508677495
  • Lecture overview Definition of multidrug resistance History of antibiotics How does resistance develop? Why is it important? Multidrug resistance organisms (MDROs) Control
  • Multidrug-Resistant Organisms( MDROs)  Microorganisms that are resistant to one or more classes of antimicrobial agents. MDRSP refers to isolates resistant to 2 or more of the following antibiotics: penicillin, second- generation cephalosporins, macrolides, tetracycline, and trimethoprim/sulfamethoxazoleCDC: Management of Multidrug-Resistant Organisms in Healthcare Settings, Healthcare Infection Control Advisory Committee, Jane D. Siegel et. al. pg 7-12 View slide
  • History of antibiotics 1928: Penicillin first discovered by Alexander Fleming Chain and Florey, helped develop penicillin into a widely available medical product View slide
  • History of antibiotics 1943- Drug companies begin mass production of penicillin 1944 – U.S. Military takes Penicillin to the battlefield
  • History of antibiotics 1945, Fleming, Chain and Florey awarded the Nobel Prize in Physiology and Medicine After 2nd World War many more antibiotics were developed Today about 150 types
  • History of antibiotics Many experts were confident the tide had turned in the war against bacterial infections 1969, the then US Surgeon General, William Stewart, boldly told the US Congress it was time to "…close the books on infectious diseases."
  • March 1942A 33 year-old lady lay dying of streptococcalsepsis in Connecticut, USABest efforts of doctors fail to clear thebloodstream infectionDoctors manage to obtain small amount ofnewly discovered penicillin which wheninjected cautiously, clears the streptococci fromthe bloodThe patient miraculously survives. And lives upto 90 years
  • November 2011A 16 year-old girl is being treated for pneumonia causedby Klebsiella pneumonia in Ivy Hospital MohaliDespite best medical care – ALL antibiotics available forklebsiella , treating physicians unable to clear thepatient’s bloodThe patient dies, still with bloodstream infection
  • We have come almostfull circle and arrived at apoint as frightening asthe pre-antibiotic era
  • Dr.T.V.Rao MD 12
  • How does resistance develop?
  • A variety of mutations can lead to antibiotic resistanceMechanisms of antibiotic resistance 1. Enzymatic destruction of drug 2. Prevention of penetration of drug 3. Alteration of drugs target site 4. Rapid ejection of the drugResistance genes are often on plasmids or transposons that canbe transferred between bacteria
  • BACTERIA MUTATE TO PROTECTTHEMSELVES FROM ANTIBIOTIC
  • THE MUTATED BACTERIA EVENTUALLY THERE ARE MORESURVIVE AFTER THE ANTIBIOTIC-RESISTANTANTIBIOTICS ARE GONE BACTERIA THAN NON- RESISTANT
  • Why is Resistance a Concern?Resistant organisms are becoming commonplaceBacterial resistance often results in treatment failure andincreased mortality and costThe problem is no longer confined to the hospital settingBacterial resistance will continue to worsen if notaddressedThere are no antibiotics on the immediate horizon withactivity against these multi-drug resistant pathogens
  • Number of New Molecular Entity (NME) Systemic Antibiotics Approved by the US FDA Per Five-year Period, Through 3/11. Clin Infect Dis. 2011;52:S397-S428
  • Risk factors for acquisition of MDROs ICU stay Previous exposure to antimicrobial agents Underlying diseases Dialysis Invasive devices Recurrent admissions to hospital Nursing home Previous colonization of a multidrug-resistant organism Advanced age
  • How do patients acquire MDRO’s? Select out the resistant strains due to repeated courses of antibiotics Spread from person to person  environment  hands of HCW  patient equipment  contact with patient
  • Resistance is accelerated throughinappropriate use of antimicrobials –Standard treatment guidelines not provided –Provided but not adhered to 50 % prescriptions are inappropriate –Drugs not accessible 50% populations in developing countries do not have access –Accessible but poor quality or expensive –Inadequate monitoring 50% of patients do not adhere to recommended regimen –Irrational self-administration or prescription –Extensive use for therapeutic and growth promotion in animals 50% of national antibiotic consumption is for non-therapeutic purposes in animals
  • Multi-drug resistant organisms Gram positive organisms  MRSA  VRE Gram negative organisms  ESBLs  CRE
  • MRSA NNIS (2004) – 60% of S. aureus are methicillin resistant Nosocomial  mecA gene encodes low affinity for PBP resulting in resistance to all beta-lactams  Usually multi-drug resistant Community-acquired  More virulent – Panton-Valentine leukocidin  Skin and soft tissue infections in children and young adults  Usually susceptible to non beta-lactam drugs
  • VRE Non-existent as recently as 1989 NNIS report (2004) – 30% of all enterococcal isolates are resistant Mediated by vanA and vanB genes resulting in alteration of target site Clonal spread via poor infection control
  • Resistance in Gram negatives Acinetobacter  Uncommon in most U.S. medical centers  Incidence as high as 10% in some geographic locations  Carbapenems are drug of choice Pseudomonas aeruginosa  Multi-drug resistance increasing nationwide  Fluoroquinolones: 29% resistance (NNIS 2004)  Beta-lactams: metallo-beta-lactamase producing strains have been reported
  • ESBLs a growing concern Resistant to all penicillins, cephalosporins, and aztreonam Carbapenems are the drug of choiceFluoroquinolone resistance NNIS 2004 report: 8% E.coli resistant Chromosomal and plasmid mediated alterations in target site or decreased access to targetCarbapenem resistance Klebsiella pneumoniae carbapenemase Metallo-beta-lactamases ampC beta-lactamase + loss of outer membrane channels
  • IVY HOSPITAL ANTIBIOGRAM(DEC 2010 - MAR 2011)LACTOSE FERMENTING GNB (E. coli,Klebsiella spp., Citrobacter spp., Enterobacter spp., etc.)TOTAL= 112 isolates
  • Percentage break up OF LFGNB( n= 112)
  • NON LACTOSE FERMENTING GNB(Acinetobacter spp, Pseudomonas spp. etc)TOTAL = 55 ISOLATES
  • Staphylococcus aureus(Total 21 isolates)
  • Prevention of antimicrobial resistance Prevent Infection  Vaccinate  Remove catheters Diagnose and Treat Infection Effectively  Isolate the pathogen  Target the pathogen  Access the experts
  • Prevention of antimicrobial resistance Appropriate prescribing of antibiotics  Only prescribe antibiotics when necessary  Use local data  Treat infection, not contamination  Treat infection, not colonisation  Stop treatment when infection is cured or unlikely
  • Prevention of antimicrobial resistance Surveillance:  Moniters trends in resistance patterns, incidence of MDROs, emerging MDROs  Locally, regionally, nationally, internationally  Moniters effectiveness of interventions
  • Prevention of transmission to other patients Spread from person to person  Environment, hands of HCW, patient equipment, contact with patient Hand hygiene Environmental cleaning
  • Antibiotic Stewardship Program Optimal selection, dosage, and duration of antimicrobial treatment that  Results in the best clinical outcome for the treatment or prevention of infection  With minimal toxicity to the patient and  With minimal impact on subsequent resistance
  • Antibiotic Stewardship Program Involves  Prescribing antimicrobial therapy only when it is beneficial to the patient  Targeting therapy to the desired pathogens  Using the appropriate drug, dose, and duration
  • Antibiotic Policy : To Minimise Antibiotic Resistance Appropriate Use of Antibiotics and specific guidelines e.g. Therapy Recommendations In serious infections; start with ultra-broad antibiotic then de- escalate to narrow spectrum depending on culture report Limit use of Broad Spectrum Antibiotics where possible Antibiotic cycling/rotation