DOCSLIB.ORG

Colistin Heteroresistance in Carbapenem-Resistant Klebsiella Pneumoniae

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Colistin Heteroresistance in Carbapenem-Resistant Klebsiella Pneumoniae Colistin heteroresistance in carbapenem-resistant Klebsiella pneumoniae Jean-Marc Rolain Aix Marseille University, IRD, APHM, MEPHI, IHU-Méditerranée Infection – Marseille – France Email: [email protected] ESCMIDSaturday, 13 April 019, Amsterdam,eLibrary Netherlands © by author ESCMIDNo conflict of eLibraryinterest © by author Outline of the lecture – History of emergence of resistance to colistin – Mechanism of action and resistance • General mechanisms • Definition of heteroresistance – What is known in K. pneumoniae and related bacteria : a review of the literature – Heteroresistance: does it matter? – Conclusion ESCMID eLibrary3 © by author Consequences of 3GC resistance: increase use of carbapenems and increase of carbapenem resistance in Gram-negative bacteria [ESBL or carbapenemase] and K. pneumoniae keywords 150 [PubMed, 1990-2011] 100 Klebsiella pneumoniae 50 0 NB ofNB publications Year Nb of publications (ESBL) Nb of publications (carbapenemase) Kempf et al, Int J Antimicrob Agents 2012 Increasing use of colistin ESCMIDIncrease UseeLibrary of colistin And …… © by author Colistin therapy for 3 – 6 months for MDR P. aeruginosa orthopedic infections A. ESCMID eLibrary © by author Colistin : mechanism of action and resistance Polymyxins: Polymyxin B and colistin (polymyxin E) discovered in 1947 in Paenibacillus polymyxa (formerly Bacillus polymyxa var. colistinus) available since 1959 for treatment of Gram negative bacterial infections cyclic polypeptide antibiotics secondary metabolite from nonribosomal peptide synthase (NRPS) mode of action : on bacterial cell membrane, binds to LPS and phospholipids in the outer cell membrane and displaces divalent cations (Ca and Mg) Cationic antimicrobial polypeptides Bactericidal activity against most Gram-negative bacteria Spectrum of activity: Two major categories of Gram-negative bacteria i. Naturally susceptible bacteria (Escherichia coli, Klebsiella pneumoniae, Salmonella, Acinetobacter baumannii, Pseudomonas aeruginosa) Active ii. Intrinsically resistant bacteria (Proteus, Providencia, Morganella, ESCMIDSerratia, Burkholderia) Not active eLibrary © by author General Mechanism of Colistin Resistance through Lipid A Modifications Review In Gram-negative Bacteria + 4-amino-4-deoxy-L-arabinose - arnT-pmrE operon -Phosphoethanolamine + + pmrA-pmrB mutation pmrC pmrD Lipid A + phoP-phoQ mutation pmrA-pmrB mutation mgrB mutation (negative regulator of phoPQ) ESCMIDOlaitan AO et al, FronteLibrary Microbiol 2014; Baron S et al, Int J Antimicrob Agents 2016 © by author Background Overall colistin resistance mechanism 1st description of a transferable gene confering colistin resistance - mcr-1 Liu YY, et al TheLancet Infectious Disease 2015 Molecular mechanisms of polymyxin resistance: knowns and unknowns. Baron S, Hadjadj L, Rolain JM, Olaitan AO. Int J AntimicrobESCMID Agents. 2016 Dec;48(6):583-591. eLibrary © by author Heteroresistance • Heteroresistance : phenomenon wherein a subpopulation of bacteria in an otherwise homogenous population display antibiotic resistance Difficulty to detect colistin heteroresistance with routine laboratory tests (broth microdilution or agar) A. Brauner, etESCMID al. Nat. Rev. Microbiol., 2016 eLibrary © by author Constant Colistin Heteroresistance • Disk diffusion method or E-test : first inhibition zone followed by regrowth in high colistin concentrations • Broth microdilution method : resistant or ‘skipped’ wells • Described in Gram negative bacteria for: – Serratia marcescens -> Intrinsic resistance Role of efflux? – Enterobacter spp.-> Acquired resistance Telke A, J. of Antimicrob Chemother., 2017 ESCMIDBaron SA, J. of Antimicrob Chemother., 2018 eLibrary © by author PAPs : Population Analysis Profiles Colistin mg/L Control 0,125 0,25 0,5 1 2 MIC True Colistin susceptibility? 0,5 McF suspension Colistin susceptible Colistin Hetero- resistant Control 0,125 0,25 0,5 1 2 4 8 16 32 Colistin mg/L ESCMID eLibraryPersistance of colonies = Heteroresistance © by author Time Kill Assays of colistin against colistin-heteroresistant K. pneumoniae isolates HR isolate HR isolate • Regrowth observed after 4h in all the heteroresistant (HR) isolates • Concentrations needed to kill HR isolates unachievable in vivo HR isolate Susceptible isolate ESCMID eLibrary © by author Development of Diagnostic tools : the problematic of colistin resistance • Colistin Resistance defined as MIC > 2µg/ml –isolates with borderline MICs • Disk diffusion method is not reproducible for detection broth microdilution Carba R (MIC > 2mg/L) n = 209 n = 256 72,6 % 89 % ESCMID eLibrary © by author Colistin heteroresistance in carbapenem-resistant K. pneumoniae – Review of the literature 20 carbapenem resistant K. pneumoniae 16 colistin-susceptible isolates by BMD 12 isolates colistin-heteroresistant ESCMID(PAPs) eLibrary © by author Heteroresistance in K. pneumoniae 2015 Emergence of a colistin-resistant subclone dueESCMID to mutation Asp191Tyr in protein PhoP eLibrary © by author ESCMID eLibrary © by author Mechanisms of Heteroresistance in K. pneumoniae Mutations found in mgrB, phoQ, yciM, lpxM yciM contributes to cell wall integrity by regulating LPS biosynthesis LpxM is responsible for the addition of one of the secondary acyl chains to lipid A in Enterobacteriaceae HalabyESCMIDT, Antimicrob, Agents and Chemother, 2016 eLibrary © by author 2017 Emergence of a colistin-resistant subclone due to mutations in mgrB KP_LB1 CMI > 48 µg/mL KP_LB2 CMI = 0.125 µg/mL ESCMID eLibrary © by author Typing subpopulation 1) LB1 LB2 3) 4) AMX-6 AMC-14 FEP-34 TPZ-25 AMX-6 AMC-14 FEP-34 TPZ-25 ATM-32 CRO-31 ETP-30 IPM-30 ATM-32 CRO-31 ETP-30 IPM-30 RIF-10 NF-15 FF-20 CN-22 RIF-10 NF-15 FF-20 CN-22 CIP-30 SXT-6 Colistin-10 NA-22 CIP-30 SXT-6 Colistin-15 NA-22 1) Same AST 2) MLST : ST86 3) Same PFGE (XbaI) 4) Same MALDI-TOF Gel View BardetESCMIDet al, Antimicrob Agents Chemother., 2017 eLibrary © by author Other example in Enterobacter Efflux pump overexpression due to a complex mechanism!! Efflux pump inhibitor E. cloacae NH52 E. asburiae E. cloacae NH52 E. asburiae Temoin PAβN ESCMIDTelke A et al , J Antimicrob Chemother, 2017; Dandachi I et al submitted eLibrary © by author Carbonyl Cyanide m- 2,4-dinitrophenol (DNP) X X Chlorophenylhydrazine (CCCP) ME: membrane externe Efflux pump inhibitor -> Objectif: Evaluate the effect of CCCP on a collection of colistin-resistant strains ESCMIDof Gram negative eLibrary bacteria. © by author Role of efflux in Gram negative bacteria [CCCP]= 10 mg/L Strains tested: -90 Enterobacteriaceae including: -32 K. pneumoniae -24 E. coli -7 Enterobacter sp. -2 Salmonella sp. -13 S. marcescens -3 Morganella morganii -4 Providencia spp. -3 Pseudomonas aeruginosa CCCP rescue also colistin heteroresistance ESCMIDBaron S and Rolain JM , J Antimicrob Chemother, 2018 eLibrary © by author Heteroresistance and antibiotic failure Does it matter? E-test Nat. microbiol, 2016 • Suggested in Enterobacter cloacae • Not detected with E-test method • Responsible for treatment failure in mice Survival % in infection model on mice caused by a susceptible strain (left) and the resistant subpopulation (right) PAP ESCMID eLibrary © by author Heteroresistance: does it matter? ESCMID eLibrary © by author One hyperviscoumucous KPC-3 isolate (out of 265 isolates) Colistin Heteteroresistant (CDC98) ESCMID eLibrary © by author Perspectives • Not new but probably under-diagnosed • Need to improve the detection of heteroresistance in routine laboratory • Understanding the real impact of this heteroresistance : – Risk of therapeutic failure ? – Alternatives? • Management of the use of colistin to treat carbapenem-resistant K. pneumoniae • Limit its use ? • Only in combination ? ESCMID eLibrary © by author ESCMID eLibrary © by author Staff and students from my team Thank you for your attention ESCMIDhttp://www.mediterranee eLibrary-infection.com © by author.
Load more

Recommended publications
  • General Items
    Essential Medicines List (EML) 2019 Application for the inclusion of imipenem/cilastatin, meropenem and amoxicillin/clavulanic acid in the WHO Model List of Essential Medicines, as reserve second-line drugs for the treatment of multidrug-resistant tuberculosis (complementary lists of anti-tuberculosis drugs for use in adults and children) General items 1. Summary statement of the proposal for inclusion, change or deletion This application concerns the updating of the forthcoming WHO Model List of Essential Medicines (EML) and WHO Model List of Essential Medicines for Children (EMLc) to include the following medicines: 1) Imipenem/cilastatin (Imp-Cln) to the main list but NOT the children’s list (it is already mentioned on both lists as an option in section 6.2.1 Beta Lactam medicines) 2) Meropenem (Mpm) to both the main and the children’s lists (it is already on the list as treatment for meningitis in section 6.2.1 Beta Lactam medicines) 3) Clavulanic acid to both the main and the children’s lists (it is already listed as amoxicillin/clavulanic acid (Amx-Clv), the only commercially available preparation of clavulanic acid, in section 6.2.1 Beta Lactam medicines) This application makes reference to amendments recommended in particular to section 6.2.4 Antituberculosis medicines in the latest editions of both the main EML (20th list) and the EMLc (6th list) released in 2017 (1),(2). On the basis of the most recent Guideline Development Group advising WHO on the revision of its guidelines for the treatment of multidrug- or rifampicin-resistant (MDR/RR-TB)(3), the applicant considers that the three agents concerned be viewed as essential medicines for these forms of TB in countries.
    [Show full text]
  • New Β-Lactamase Inhibitor Combinations: Options for Treatment; Challenges for Testing
    MEDICAL/SCIENTIFIC AffAIRS BULLETIN New β-lactamase Inhibitor Combinations: Options for Treatment; Challenges for Testing Background The β-lactam class of antimicrobial agents has played a crucial role in the treatment of infectious diseases since the discovery of penicillin, but β–lactamases (enzymes produced by the bacteria that can hydrolyze the β-lactam core of the antibiotic) have provided an ever expanding threat to their successful use. Over a thousand β-lactamases have been described. They can be divided into classes based on their molecular structure (Classes A, B, C and D) or their function (e.g., penicillinase, oxacillinase, extended-spectrum activity, or carbapenemase activity).1 While the first approach to addressing the problem ofβ -lactamases was to develop β-lactamase stable β-lactam antibiotics, such as extended-spectrum cephalosporins, another strategy that has emerged is to combine existing β-lactam antibiotics with β-lactamase inhibitors. Key β-lactam/β-lactamase inhibitor combinations that have been used widely for over a decade include amoxicillin/clavulanic acid, ampicillin/sulbactam, and pipercillin/tazobactam. The continued use of β-lactams has been threatened by the emergence and spread of extended-spectrum β-lactamases (ESBLs) and more recently by carbapenemases. The global spread of carbapenemase-producing organisms (CPOs) including Enterobacteriaceae, Pseudomonas aeruginosa, and Acinetobacter baumannii, limits the use of all β-lactam agents, including extended-spectrum cephalosporins (e.g., cefotaxime, ceftriaxone, and ceftazidime) and the carbapenems (doripenem, ertapenem, imipenem, and meropenem). This has led to international concern and calls to action, including encouraging the development of new antimicrobial agents, enhancing infection prevention, and strengthening surveillance systems.
    [Show full text]
  • Penicillin Allergy Guidance Document
    Penicillin Allergy Guidance Document Key Points Background Careful evaluation of antibiotic allergy and prior tolerance history is essential to providing optimal treatment The true incidence of penicillin hypersensitivity amongst patients in the United States is less than 1% Alterations in antibiotic prescribing due to reported penicillin allergy has been shown to result in higher costs, increased risk of antibiotic resistance, and worse patient outcomes Cross-reactivity between truly penicillin allergic patients and later generation cephalosporins and/or carbapenems is rare Evaluation of Penicillin Allergy Obtain a detailed history of allergic reaction Classify the type and severity of the reaction paying particular attention to any IgE-mediated reactions (e.g., anaphylaxis, hives, angioedema, etc.) (Table 1) Evaluate prior tolerance of beta-lactam antibiotics utilizing patient interview or the electronic medical record Recommendations for Challenging Penicillin Allergic Patients See Figure 1 Follow-Up Document tolerance or intolerance in the patient’s allergy history Consider referring to allergy clinic for skin testing Created July 2017 by Macey Wolfe, PharmD; John Schoen, PharmD, BCPS; Scott Bergman, PharmD, BCPS; Sara May, MD; and Trevor Van Schooneveld, MD, FACP Disclaimer: This resource is intended for non-commercial educational and quality improvement purposes. Outside entities may utilize for these purposes, but must acknowledge the source. The guidance is intended to assist practitioners in managing a clinical situation but is not mandatory. The interprofessional group of authors have made considerable efforts to ensure the information upon which they are based is accurate and up to date. Any treatments have some inherent risk. Recommendations are meant to improve quality of patient care yet should not replace clinical judgment.
    [Show full text]
  • Carbapenem-Resistant Acinetobacter Threat Level Urgent
    CARBAPENEM-RESISTANT ACINETOBACTER THREAT LEVEL URGENT 8,500 700 $281M Estimated cases Estimated Estimated attributable in hospitalized deaths in 2017 healthcare costs in 2017 patients in 2017 Acinetobacter bacteria can survive a long time on surfaces. Nearly all carbapenem-resistant Acinetobacter infections happen in patients who recently received care in a healthcare facility. WHAT YOU NEED TO KNOW CASES OVER TIME ■ Carbapenem-resistant Acinetobacter cause pneumonia Continued infection control and appropriate antibiotic use and wound, bloodstream, and urinary tract infections. are important to maintain decreases in carbapenem-resistant These infections tend to occur in patients in intensive Acinetobacter infections. care units. ■ Carbapenem-resistant Acinetobacter can carry mobile genetic elements that are easily shared between bacteria. Some can make a carbapenemase enzyme, which makes carbapenem antibiotics ineffective and rapidly spreads resistance that destroys these important drugs. ■ Some Acinetobacter are resistant to nearly all antibiotics and few new drugs are in development. CARBAPENEM-RESISTANT ACINETOBACTER A THREAT IN HEALTHCARE TREATMENT OVER TIME Acinetobacter is a challenging threat to hospitalized Treatment options for infections caused by carbapenem- patients because it frequently contaminates healthcare resistant Acinetobacter baumannii are extremely limited. facility surfaces and shared medical equipment. If not There are few new drugs in development. addressed through infection control measures, including rigorous
    [Show full text]
  • Management of Penicillin and Beta-Lactam Allergy
    Management of Penicillin and Beta-Lactam Allergy (NB Provincial Health Authorities Anti-Infective Stewardship Committee, September 2017) Key Points • Beta-lactams are generally safe; allergic and adverse drug reactions are over diagnosed and over reported • Nonpruritic, nonurticarial rashes occur in up to 10% of patients receiving penicillins. These rashes are usually not allergic and are not a contraindication to the use of a different beta-lactam • The frequently cited risk of 8 to 10% cross-reactivity between penicillins and cephalosporins is an overestimate based on studies from the 1970’s that are now considered flawed • Expect new intolerances (i.e. any allergy or adverse reaction reported in a drug allergy field) to be reported after 0.5 to 4% of all antimicrobial courses depending on the gender and specific antimicrobial. Expect a higher incidence of new intolerances in patients with three or more prior medication intolerances1 • For type-1 immediate hypersensitivity reactions (IgE-mediated), cross-reactivity among penicillins (table 1) is expected due to similar core structure and/or major/minor antigenic determinants, use not recommended without desensitization • For type-1 immediate hypersensitivity reactions, cross-reactivity between penicillins (table 1) and cephalosporins is due to similarities in the side chains; risk of cross-reactivity will only be significant between penicillins and cephalosporins with similar side chains • Only type-1 immediate hypersensitivity to a penicillin manifesting as anaphylaxis, bronchospasm,
    [Show full text]
  • Β-Lactam/Β-Lactamase Inhibitors for the Treatment of Infections Caused by Extended-Spectrum Β-Lactamase (ESBL)-Producing Enterobacteriaceae
    β-lactam/β-lactamase Inhibitors for the Treatment of Infections Caused by Extended-Spectrum β-Lactamase (ESBL)-producing Enterobacteriaceae Alireza FakhriRavari, Pharm.D. PGY-2 Pharmacotherapy Resident Controversies in Clinical Therapeutics University of the Incarnate Word Feik School of Pharmacy San Antonio, Texas November 13, 2015 Learning Objectives At the completion of this activity, the participant will be able to: 1. Describe different classes of β-lactamases produced by gram-negative bacteria. 2. Identify β-lactamase inhibitors and their spectrum of inhibition of β-lactamases. 3. Evaluate the evidence for use of β-lactam/β-lactamase inhibitors compared to carbapenems for treatment of ESBL infections. β-lactam/β-lactamase inhibitors for the treatment of infections caused by ESBL-producing Enterobacteriaceae 1 1. A Brief History of the Universe A. Timeline: 1940s a. β-lactams and β-lactamases i. Sir Alexander Fleming discovered penicillin from Penicillium notatum (now Penicillium chrysogenum) in 1928.1,2 ii. Chain, Florey, et al isolated penicillin in 1940, leading to its commercial production.3 iii. First β-lactamase was described as a penicillinase in Escherichia coli in 1940.4 iv. Giuseppe Brotzu discovered cephalosporin C from the mold Cephalosporin acremonium (now Acremonium chrysogenum) in 1945, but cephalosporins were not clinically used for another 2 decades.2,5 b. What are β-lactamases? i. β-lactamases are enzymes that hydrolyze the amide bond of the β-lactam ring, thereby inactivating them.6 Figure 1: Mechanism of action of β-lactamases ii. β-lactamase production is the principal mechanism by which gram-negative bacteria resist β-lactam antibiotics.6 iii.
    [Show full text]
  • Non-Penicillin Beta-Lactam Drugs: a CGMP Framework for Preventing Cross- Contamination
    Guidance for Industry Non-Penicillin Beta-Lactam Drugs: A CGMP Framework for Preventing Cross- Contamination U.S. Department of Health and Human Services Food and Drug Administration Center for Drug Evaluation and Research (CDER) April 2013 Current Good Manufacturing Practices (CGMPs) Guidance for Industry Non-Penicillin Beta-Lactam Drugs: A CGMP Framework for Preventing Cross- Contamination Additional copies are available from: Office of Communications Division of Drug Information, WO51, Room 2201 Center for Drug Evaluation and Research Food and Drug Administration 10903 New Hampshire Ave. Silver Spring, MD 20993-0002 Phone: 301-796-3400; Fax: 301-847-8714 [email protected] http://www.fda.gov/Drugs/GuidanceComplianceRegulatoryInformation/Guidances/default.htm U.S. Department of Health and Human Services Food and Drug Administration Center for Drug Evaluation and Research (CDER) April 2013 Current Good Manufacturing Practices (CGMP) Contains Nonbinding Recommendations TABLE OF CONTENTS I. INTRODUCTION....................................................................................................................1 II. BACKGROUND ......................................................................................................................2 III. RECOMMENDATIONS.........................................................................................................7 i Contains Nonbinding Recommendations Guidance for Industry1 Non-Penicillin Beta-Lactam Drugs: A CGMP Framework for Preventing Cross-Contamination This guidance
    [Show full text]
  • Journal Club: “Effect of Piperacillin-Tazobactam Vs
    Infectious Disease Update 02/25/19 Steven T. Park Division of Infectious Diseases Objectives • Zosyn versus Meropenem for ESBL bacteremia • 7 versus 14 days for gram negative bacteremia • Oral versus IV for osteomyelitis “Effect of Piperacillin-Tazobactam vs Meropenem on 30-Day Mortality for Patients With E coli or Klebsiella pneumoniae Bloodstream Infection and Ceftriaxone Resistance” (MERINO trial) Harris PNA et al. JAMA 2018. Sep 11; 320:984. Introduction • Treatment of choice for ESBL organisms are thought to be carbapenems • Reports of failure of non-carbapenems in the past even when microbiologic data showed susceptibility • Most reported before CLSI lowered the breakpoints for Enterobacteriaceae • Recent reviews looking at retrospective data conclude that you can use non-carbapenems (Zosyn, Cefepime) for urine infections • However no randomized controlled trial testing this hypothesis • First randomized controlled trial testing whether Zosyn is equivalent to meropenem for ESBL bacteremia Design, Setting, Participants • Non-inferiority, parallel group, randomized clinical trial • Hospitalized patients enrolled from 26 sites in 9 countries (mostly from Singapore, Australia, Italy, Saudi Arabia, and Turkey) from February 2014 to July 2017 • Patients over the age of 21 was eligible if he/she had at least 1 positive blood culture with E coli or Klebsiella spp that was non-susceptible to ceftriaxone but susceptible to pip-tazo and meropenem • Of 1646 patients screened, 391 were included in the study. • Meropenem 1g IV q8h (n = 191) or piperacillin/tazobactam 4.5g IV q6h (not extended infusion, n = 188) was given for a minimum of 4 days and up to 14 days. The duration of therapy was determined by the treating clinician.
    [Show full text]
  • Carbapenem-Resistant Enterobacteriaceae a Microbiological Overview of (CRE) Carbapenem-Resistant Enterobacteriaceae
    PREVENTION IN ACTION MY bugaboo Carbapenem-resistant Enterobacteriaceae A microbiological overview of (CRE) carbapenem-resistant Enterobacteriaceae. by Irena KennelEy, PhD, aPRN-BC, CIC This agar culture plate grew colonies of Enterobacter cloacae that were both characteristically rough and smooth in appearance. PHOTO COURTESY of CDC. GREETINGS, FELLOW INFECTION PREVENTIONISTS! THE SCIENCE OF infectious diseases involves hundreds of bac- (the “bug parade”). Too much information makes it difficult to teria, viruses, fungi, and protozoa. The amount of information tease out what is important and directly applicable to practice. available about microbial organisms poses a special problem This quarter’s My Bugaboo column will feature details on the CRE to infection preventionists. Obviously, the impact of microbial family of bacteria. The intention is to convey succinct information disease cannot be overstated. Traditionally the teaching of to busy infection preventionists for common etiologic agents of microbiology has been based mostly on memorization of facts healthcare-associated infections. 30 | SUMMER 2013 | Prevention MULTIDRUG-resistant GRAM-NEGative ROD ALert: After initial outbreaks in the northeastern U.S., CRE bacteria have THE CDC SAYS WE MUST ACT NOW! emerged in multiple species of Gram-negative rods worldwide. They Carbapenem-resistant Enterobacteriaceae (CRE) infections come have created significant clinical challenges for clinicians because they from bacteria normally found in a healthy person’s digestive tract. are not consistently identified by routine screening methods and are CRE bacteria have been associated with the use of medical devices highly drug-resistant, resulting in delays in effective treatment and a such as: intravenous catheters, ventilators, urinary catheters, and high rate of clinical failures.
    [Show full text]
  • Antibiotics Currently in Clinical Development
    A data table from Sept 2014 Antibiotics Currently in Clinical Development As of September 2014, an estimated 38 new antibiotics1 with the potential to treat serious bacterial infections are in clinical development for the U.S. market. The success rate for drug development is low; at best, only 1 in 5 candidates that enter human testing will be approved for patients.* This snapshot of the antibiotic pipeline will be updated periodically as products advance or are known to drop out of development. Please contact Rachel Zetts at [email protected] or 202-540-6557 with additions or updates. Cited for potential Development Known QIDP4 Drug name Company Drug class activity against gram- Potential indication(s)?5 phase2 designation? negative pathogens?3 Approved (for acute Acute bacterial skin and skin structure bacterial skin and skin infections, hospital-acquired bacterial Tedizolid Cubist Pharmaceuticals Oxazolidinone Yes structure infections), pneumonia/ventilator-acquired bacterial June 20, 2014 pneumonia Approved, May 23, Acute bacterial skin and skin structure Dalbavancin Durata Therapeutics Lipoglycopeptide Yes 2014 infections Approved, August 6, Acute bacterial skin and skin structure Oritavancin The Medicines Company Glycopeptide Yes 2014 infections New Drug Application (NDA) submitted (for Complicated urinary tract infections, complicated urinary complicated intra-abdominal infections, Novel cephalosporin+beta- Ceftolozane+tazobactam8 tract infection and Cubist Pharmaceuticals Yes Yes acute pyelonephritis (kidney infection), lactamase
    [Show full text]
  • Trend Analysis of Antibiotics Consumption Using WHO Aware Classification in Tertiary Care Hospital
    International Journal of Basic & Clinical Pharmacology Bhardwaj A et al. Int J Basic Clin Pharmacol. 2020 Nov;9(11):1675-1680 http:// www.ijbcp.com pISSN 2319-2003 | eISSN 2279-0780 DOI: https://dx.doi.org/10.18203/2319-2003.ijbcp20204493 Original Research Article Trend analysis of antibiotics consumption using WHO AWaRe classification in tertiary care hospital Ankit Bhardwaj*, Kaveri Kapoor, Vivek Singh Saraswathi institute of Medical Sciences, Pilakhuwa, Hapur, Uttar Pradesh, India Received: 21 August 2020 Accepted: 21 September 2020 *Correspondence: Dr. Ankit Bhardwaj, Email: [email protected] Copyright: © the author(s), publisher and licensee Medip Academy. This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. ABSTRACT Background: Aim of the study was to assess trend in antibiotics consumption pattern from 2016 to 2019 using AWaRe classification, ATC and Defined daily dose methodology (DDD) in a tertiary care hospital. Antibiotics are crucial for treating infectious diseases and have significantly improved the prognosis of patients with infectious diseases, reducing morbidity and mortality. The aim of the study is to classify the antibiotic based on WHO AWaRe classification and compare their four-year consumption trends. The study was conducted at a tertiary care center, Pilakhuwa, Hapur. Antibiotic procurement data for a period of 4 years (2016-2019) was collected from the Central medical store. Methods: This is a retrospective time series analysis of systemic antibiotics with no intervention at patient level. Antibiotic procurement was taken as proxy for consumption assuming that same has been used.
    [Show full text]
  • Carbapenem-Resistant Enterobacteriaceae Investigative Guidelines December 2019
    PUBLIC HEALTH DIVISION Acute and Communicable Disease Prevention Carbapenem-Resistant Enterobacteriaceae Investigative Guidelines December 2019 1. DISEASE REPORTING 1.1 Purpose of Reporting and Surveillance 1. To prevent transmission of infections with carbapenem-resistant Enterobacteriaceae (CRE) between patients, within or among health care facilities, or between health care facilities and the community. 2. To prevent CRE from becoming endemic in Oregon, necessitating empiric use of even broader- spectrum antibiotics. 3. To identify outbreaks and potential sources or sites of ongoing transmission. 4. To better characterize the epidemiology of these infections. 1.2 Laboratory and Physician Reporting Requirements 1. Providers and laboratories must report cases to local public health authorities (LPHAs) within one working day. 2. Clinical and reference laboratories must forward isolates from any sterile or non-sterile site (e.g., urine, blood, sputum, endotracheal aspirate, BAL, wound) that meet the confirmed CRE case definition below along with the automated test system susceptibility printouts (Vitek or Microscan report) to the Oregon State Public Health Laboratory (OSPHL). 3. Isolates of Proteus, Providencia, or Morganella which show only imipenem non-susceptibility, in the absence of resistance to another carbapenem, do not need to be submitted. 1.3 Local Public Health Authority Reporting and Follow-Up Responsibilities 1. LPHAs will confirm that a case meets the case definition by reviewing the isolate's susceptibility information (antibiogram) as necessary, or in consultation with the ACDP epidemiologist. Both minimum inhibitory concentration (MIC) values and interpretations are needed to verify a case meets the definition. (See Confirmed Case §3.1.) 2. If a case meets the case definition, the LPHA will investigate.
    [Show full text]