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Problem of Antibiotic Resistance
  & Rational use of antibiotics




             Dr. Naser Tadvi
     Associate Prof., Pharmacology
Objectives
•   What is antimicrobial resistance
•   Why antibacterial resistance is a concern
•   How antibacterials work
•   Mechanisms of resistance to antibacterials
•   Indian scenario
•   NDM-1
•   Strategies to contain resistance
•   Treatment of some resistant bacterial infections
•   Summary
Introduction
• Throughout history there has been a continual
  battle between human beings and multitude
  of micro-organisms that cause infection and
  disease
History
                 Nobel Lecture, December 11, 1945

                                                    Sir Alexander Fleming
                                                    The Nobel Prize in Physiology or Medicine 1945


In his 1945 Nobel Prize lecture, Fleming himself warned of
the danger of resistance –
“It is not difficult to make microbes resistant to
penicillin in the laboratory by exposing them to
concentrations not sufficient to kill them, and the
same thing has occasionally happened in the body…
…and by exposing his microbes to non-lethal
quantities of the drug make them resistant.”
Timeline of Antibiotic Resistance
Why resistance is a concern
•   Resistant organisms lead to treatment failure
•   Increased mortality
•   Resistant bacteria may spread in Community
•   Low level resistance can go undetected
•   Added burden on healthcare costs
•   Threatens to return to pre-antibiotic era
•   Selection pressure
Drug Resistance

Drug resistance occurs in :

   BACTERIA—ANTIBIOTIC RESISTANCE
   Endoparasites
   Viruses—Resistance to antiviral drugs
   Fungi
   Cancer cells
Antibiotic Resistance
• The concentration of drug at the site of
infection must inhibit the organism and also
remain below the level that is toxic to human
cells.




 GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006)
Antibiotic Resistance

Defined as micro-organisms that are not
inhibited by usually achievable systemic
concentration of an antimicrobial agent with
normal dosage schedule and / or fall in the
minimum inhibitory concentration (MIC)
range.
             Antibiotic Resistance (DR)
           = MIC / MCC > Toxic Plasma Concentration
Antibiotic resistance
Myths of Antibiotic Resistance
1. Drugs (antibiotics) cause organisms
   antibiotic resistant.

2. Antibiotic resistant organisms are
   more virulent
Truth
• Antibiotics select out the resistant strain
• Faulty use of antibiotics or widespread use of
  antibiotics increases the probability of such
  selection.
• Antibiotic resistant strains appear to be more
  virulent because we cannot kill them or stop
  their growth.
Mechanisms of action of antibiotics
Mechanism Antibiotic Resistance



Intrinsic (Natural)    Acquired

                      Genetic Methods



Chromosomal Methods    Extra chromosomal Methods
     Mutations                   Plasmids
Antibiotic Resistance

Some microorganisms may ‘born’ resistant,

some ‘achieve’ resistance by mutation or some

have resistance ‘thrust upon them’ by plasmids

Some are born great, some achieve greatness
or some have greatness thrust upon them
Intrinsic Resistance

It occurs naturally.
1. Lack target :
   • No cell wall; innately resistant to penicillin
2. Innate efflux pumps:
   • Drug blocked from entering cell or ↑ export
      of drug (does not achieve adequate internal
      concentration). Eg. E. coli, P. aeruginosa
3. Drug inactivation:
   • Cephalosporinase in Klebsiella
Acquired resistance

Mutations
• It refers to the change in DNA structure of the
  gene.
• Occurs at a frequency of one per ten million cells.
• Eg.Mycobacterium.tuberculosis,Mycobacterium
  lepra , MRSA.
• Often mutants have reduced susceptibility
Plasmids
• Extra chromosomal genetic elements can replicate
  independently and freely in cytoplasm.
• Plasmids which carry genes resistant ( r-genes) are called R-
  plasmids.
• These r-genes can be readily transferred from one R-plasmid to
  another plasmid or to chromosome.
• Much of the drug resistance encountered in clinical practice is
  plasmid mediated
Mechanisms of Resistance Gene Transfer

• Transfer of r-genes from one bacterium to
  another
    Conjugation
    Transduction
    Transformation
• Transfer of r-genes between plasmids within
  the bacterium
    By transposons
    By Integrons
Transfer of r-genes from one bacterium to another

 Conjugation : Main mechanism for spread of resistance
   The conjugative plasmids make a connecting tube
  between the 2 bacteria through which plasmid itself
  can pass.
 Transduction : Less common method
  The plasmid DNA enclosed in a bacteriophage is
  transferred to another bacterium of same species.
  Seen in Staphylococci , Streptococci
 Transformation : least clinical problem.
  Free DNA is picked up from the environment (i.e..
  From a cell belonging to closely related or same strain.
Mechanisms of Resistance Gene Transfer
                  Transposons
Transposons are sequences of DNA
that can move around different
positions within the genome of single
cell.

 The donor plasmid containing the
Transposons, co-integrate with acceptor
plasmid. They can replicate during
cointegration

Both plasmids then separate and each
contains the r-gene carrying the
transposon.
                                    Eg ; Staphylococci,Enterococci
Antibiotic resistance
Mechanisms of Resistance Gene Transfer
                     Integrons
Integron is a large mobile DNA
can spread Multidrug resistance

Each Integron is packed with
multiple gene casettes, each
consisting of a resistance gene
attached to a small recognition site.

These genes encode several
bacterial    functions    including
resistance and virulence.

They cannot promote self transfer
Biochemical mechanisms of antibiotic
              resistance
• Prevention of drug accumulation in the bacterium

• Modification/protection of the target site

• Use of alternative pathways for metabolic / growth
requirements

• By producing an enzyme that inactivates the
antibiotic

• Quorum sensing
Decreased permeability: Porin Loss

        Antibiotics normally enter bacterial cells via porin channels
                               in the cell wall


Antibiotic
                                                                Porin channel
                                                                into organism


Cell wall




                                                           Interior of organism
Decreased permeability: Porin Loss
            New porin channels in the bacterial cell wall do not allow
                         antibiotics to enter the cells


Antibiotic                                                     New porin channel
                                                               into organism




Cell wall




                                                              Interior of organism
Efflux pumps
• Cytoplasmic membrane transport proteins.

• Major mechanism for resistance in Tetracyclines.

• Some gram -ve bacteria inhibit the plasmid
mediated synthesis of porin channels ,which
obstructs the influx of hydrophilic Penicillins
eg.ampicillin


                         ATP Binding Cassette
                         Major facilitator superfamily
                         Multidrug and toxic compound exporter
                         Small multidrug resistance transporters
                         Resistance-nodulation-division
Structurally modified antibiotic target site
            Antibiotics normally bind to specific binding proteins on the
                                bacterial cell surface


Antibiotic

                              Binding                                 Target site



Cell wall




                                                        Interior of organism
Structurally modified antibiotic target site

    Antibiotics are no longer able to bind to modified binding proteins
                        on the bacterial cell surface


Antibiotic
                                                           Modified target site



Cell wall




             Changed site: blocked binding                Interior of organism
Modification/Protection of the Target site


Resistance resulting from altered target sites :
        Target sites                 Resistant Antibiotics
  Ribosomal point mutation         Tetracyclines,Macrolides
                                         , Clindamycin
     Altered DNA gyrase                Fluoroquinolones
 Modified penicillin binding               Penicillins
proteins (Strepto.pneumonia)
 Mutation in DNA dependant                 Rifampicin
      RNA polymerase
       (M.tuberculosis)
Antibiotic inactivation
             Inactivating enzymes target antibiotics



Antibiotic

Enzyme
                      Binding                                   Target site



 Cell wall




                                                       Interior of organism
Antibiotic inactivation
             Enzymes bind to antibiotic molecules



Antibiotic                        Enzyme
                                  binding


Enzyme              Binding                                Target site



 Cell wall




                                                    Interior of organism
Antibiotic inactivation
             Enzymes destroy antibiotics or prevent binding to target sites

                               Antibiotic            Antibiotic altered,
                               destroyed             binding prevented

Antibiotic



Enzyme                                                                     Target site



 Cell wall




                                                                 Interior of organism
By producing enzymes that inactivates antibiotic

a)Inactivation of b-lactam antibiotics
   •S. aureus, N. gonorrohoea, H.influenza, Produce b-
   lactamase which cleaves -lactam ring

b)Inactivation of Chloramphenicol
   • Inactivated by chloramphenicol acetyltransferase .
   • Gram-ve (enzyme present constitutively hence higher
   resistance) gram +ve bacteria (enzyme is inducible )

c)Inactivation of Aminoglycosides
    • Inactivated by acetyl, phospho & adenylyl transferases
    Present in gram +ve and gram –ve .
Use of alternative pathways for metabolic / growth
                   requirements

• Resistance can also occur by alternate
  pathway that bypasses the reaction inhibited
  by the antibiotic.
• Sulfonamide resistance can occur from
  overproduction of PABA
Drug            Mechanism of resistance
Pencillins &      B Lactamase cleavage of the Blactam ring
Cephalosporiins

Aminoglycosides   Modification by phosphorylating, adenylating
                  and acetylating enzymes

Chloramphenicol   Modification by acetylytion

Erythromycin      Change in receptor by methylation of r RNA

Tetracycline      Reduced uptake / increased export

                  Active export out of the cell & reduced affinity
Sulfonamides      of enzymes
Quorum sensing
• Microbes communicate with each other and
  exchange signaling chemicals (Autoinducers)
• These autoinducers allow bacterial population
  to coordinate gene expression for virulence,
  conjugation, apoptosis, mobility and
  resistance
Why named quorum sensing
• Single autoinducer from single microbe is
  incapable of inducing any such change
• But when its colony reaches a critical density
  (quorum), threshold of autoinduction is
  reached and gene expression starts
• QS signal molecules AHL, AIP, AI-2 & AI-3 have
  been identified in Gm-ve bacteria
• AI-2 QS –system is shared by GM+ve bacteria
  also
WHY INHIBIT QUORUM SENSING
 Proved to be very potent method for bacterial virulence
  inhibition.

 Several QS inhibitors molecules has been synthesized which
  include AHL, AIP, and AI-2 analogues

 QS inhibitors have been synthesized and have been isolated
  from several natural extracts such as garlic extract.

 QS inhibitors have shown to be potent virulence inhibitor
  both in in-vitro and in-vivo,using infection animal models.
Indian scenario
Indian scenario
• Lack of community awareness
• Availability over the counter
• Absence of central monitoring agency
• In infants LRTI has taken over IMR due to
  diarrhoeal diseases due to use of ORT
• S. Pneumoniae fully resistant to cotrimoxazole
• Still sensitive to penicillins, macrolides and
  fluoroquinolones
Enteric pathogens
• Vibrio cholerae :
  – resistance to furazolidine, cotrimoxazole, nalidixic
    acid
  – Tetracycline remains effective
• Coliforms
  – ESBLs , extensive resistance to Beta lactum
    antibiotics
• Enteric fever
STD
• Penicillin and fluoroquinolone resistance is
  widespread to gonorhhoea
• Alternate drugs like Azithromycin and
  cephalosporins should be used
• Syphilis still susceptible to Penicillins
Gram positive Cocci
• Streptococci other than S. Pneumoniae
  – Resistant to tetracycline and macrolides (40%)
  – Still sensitive to penicillins
• Staph Aureus
  – Methicillin resistance 50%-100%
  – Vancomycin resistance also increasing
Mycobacteria
• Multidrug resistance
  – Combined resistance to rifampicin and isoniazid
• Extensively drug resistant TB
  – Additional acquisition of resistance to a
    fluroquinolone and one of the three injectable
    second line drugs (capreomycin, kanamycin and
    amikacin)
• Steady rise in these patients
What is NDM-1?
• NDM-1 stands for New Delhi metallo-beta-
  lactamase, an enzyme produced by certain
  strains of bacteria that have recently acquired
  the genetic ability to make this compound.
• The enzyme is active against other compounds
  that beta-lactam ring like penicillins,
  cephalosporins, and the carbapenems.
• bacteria that produce NDM-1 are resistant to
  all commonly used beta-lactam antibiotics,
  including carbapenems.
New Delhi metallo-beta-lactamase Why
      everyone concerned ?
• There are currently no
  new drugs in the research
  pipelines that aim to stop
  NDM-1.To date, some
  strains of E.coli and
  Klebseilla pneumoniae
  are known carriers of the
  gene, but the gene can be
  transmitted from one
  strain of bacteria to
  another through
  horizontal gene
  transfer.
Naming the strain as New Delhi creates
                  controversy
• The gene was named after New Delhi, the capital city
  of India, as it was first described by Yong et al. in 2009
  in a Swedish national who fell ill with an antibiotic-
  resistant bacterial infection that he acquired in India .
  The infection was unsuccessfully treated in a New Delhi
  hospital and after the patient's repatriation to Sweden,
  a carbapenem-resistant Klebsiella pneumoniae strain
  bearing the novel gene was identified. The authors
  concluded that the new resistance mechanism "clearly
  arose in India, but there are few data arising from India
  to suggest how widespread it is."
Treatment
• Many NDM-1 strains are resistant to all antibiotics
  except for colistin.
• Colistin is an older antibiotic that has not been
  used much in recent decades, because it is
  somewhat more toxic than other antibiotics.
• A few NDM-1 strains have been sensitive to
  tigecycline (Tygacil), but this agent should be used
  cautiously in serious infections because it does not
  achieve high levels in the bloodstream.
• A few strains have also been sensitive to
  aztreonam
The spread of NDM-1 can be
            contained with
                        ..
• The spread of NDM-1 within health-care
  facilities can be curbed through strict
  infection-control measures, including patient
  isolation and hand washing.
Strategy to Contain Resistance
• Develop new antibiotics
  – Bypass the drug resistance



• Judicious use of the existing
  antibiotics:
  – Containment of drug resistance
New Antibiotic Development
• Only 15 antibiotics of 167 under development
  had a new mechanism of action with the
  potential to combat of multidrug resistance.

• Lack of incentive for
  companies to develop
  antibiotics.
Antibiotic resistance
Hope is not exhausted….yet
• Phage therapy
• Use of the lytic enzymes found in mucus and
  saliva
• Agents that target type IIA topoisomerases
• Antimicrobial peptides (AMPs), lipopeptides
  (AMLPs)      target bacterial membranes,
  making it nearly impossible to develop
  resistance (bacteria would have to totally
  change their membrane composition).
Alternate Approaches
Phage therapy
• Phage Therapy is the therapeutic use of lytic bacteriophages to
   treat pathogenic bacteria infections
• Bacteriophages are viruses that invade bacterial cells and
   disrupt bacterial metabolism and cause the bacterium to lyse.
• Bacteriophage therapy is an important alternative to antibiotics
• The success rate was 80–95% with few gastrointestinal or
   allergic side effects. British studies also demonstrated significant
   efficacy of phages against Escherichia coli, Acinetobacter spp.,
   Pseudomonas spp and Staphylococcus aureus.
Efflux Pump Inhibitors:
Some newer antibiotics
• Linezolid: targets 50S ribosome
• Tigecycline: targets 30S ribosome
• Daptomycin: depolarization of bacterial cell
  membrane
• Dalbavacin: inhibits cell wall synthesis
• Telavacin: inhibition of cell wall synthesis and
  disruption of membrane barrier function
• Ceftibirole/ ceftaroline: cephalosporins
• Iclaprim: inhibits Dihydrofolate reductase
Judicious Use of Antibiotics
• Can only contain antibiotic resistance
• Cannot eliminate the possibility of
  antibiotic development as resistance is
  an evolutionary process
Containment of Resistance
• Containment of antibiotic resistance is a
  multi-pronged program
• Involves all stake holders
  – Physicans
  – Patients
  – Pharmaceuticals
Factors of Antibiotic Resistance
Drug Related                   Environmental
  Factors                         Factors


                  Antibiotic
                  Resistance

                                 Prescriber
Patient Related
                               Related Factors
    Factors
1. Environmental Factors
• Huge populations and overcrowding
• Rapid spread by better transport facility
• Poor sanitation
• Increases community acquired resistance
• Ineffective infection control program
• Widespread use of antibiotics in animal husbandry
  and agriculture and as medicated cleansing products
2. Drug Related
• Over the counter availability of antimicrobials

• Counterfeit and substandard drug causing sub-
  optimal blood concentration

• Irrational fixed dose combination of
  antimicrobials
                                            Policy
• Soaring use of antibiotics             Decision at
                                         Higher level
3. Patient Related

• Poor adherence of dosage Regimens
• Poverty
• Lack of sanitation concept
• Lack of education
                                 Patient
• Self-medication
                               Counseling,
• Misconception                Awareness
                                Program
Prescriber Related

• Inappropriate use of available drugs

• Increased empiric poly-antimicrobial use

• Overuse of antimicrobials

• Inadequate dosing

• Lack of current knowledge and training
Strategy of Containment
                 Antibiotic Resistance

      Evolutionary                      Faulty Use of
        Process                          Antibiotics


 Hospital Acquired           Hospital              Environmental
Antibiotic Resistance                             Community Acquired
                                                  Antibiotic Resistance

       Empirical Use                     Definitive Use
Use of antimicrobials before
pathogen responsible for a particular
illness or the susceptibility to a
particular antimicrobial is known
Poor Clinical Practice

• Poor clinical practice that fail to incorporate

  the pharmacological properties of

  antimicrobials amplify the speed of

  development of drug resistance.
Faulty Antibiotic Use
• Antimicrobials are over prescribed
• Available without prescription
Over Prescribed Antibiotics
• Clinician should first determine whether
  antimicrobial therapy is warranted for a given
  patient
Empirical Microbial Selection
• Is antimicrobial agents indicated on the
  basis of clinical findings?



                         Or is it prudent to wait
                                until such clinical
                                 findings become
                                        apparent?
Empirical Microbial Selection
• Can some simple bed side test done to
  confirm your suspicion?
  – Microscopy
  – Gram staining
Empirical Microbial Selection
• Have appropriate clinical
  specimens been obtained to
  establish a microbial diagnosis?
Empirical Microbial Selection
• What are the likely etiologic agents
  for the patient’s illness?
Empirical Microbial Selection
• What measures should be taken to protect
  individuals exposed to the index case to
  prevent secondary cases (1), and what
  measures should be implemented to prevent
  further exposure (2)?




2                  1
Empirical Microbial Selection
• Is there clinical evidence (e.g. from clinical
  trials) that antimicrobial therapy will confer
  clinical benefit for the patient?
             (Evidence-based medicine)
Definitive Treatment
1. Can a narrower spectrum agent be
   substituted for initial empiric drug?
Definitive Treatment (2)
1. Is one agent or combination of agents
   necessary?
Examples
• -lactam + Aminoglycosides
• Extended spectum Penicillins + -lactamase
  Inhibitors
• Anti-tubercular regimen
• Anti-leprotic regimen
• Co-trimoxazole
• Sulphadoxin + pyrimethamine
• Artemisinin based Combination Therapy (ACT) in
  Malaria
Definitive Treatment
What are the
 – optimum dose,
 – route of administration and
 – duration of therapy?
Definitive treatment

What specific test to identify patients
who will not respond to treatment?
Definitive Treatment

What adjunctive measures can be
undertaken to eradicate infection?
–   Vaccination
–   Steroid
–   Drainage of pus
–   Amputation
–   Removal of catheter
Who’s Work?



Microbiologist
Bacterial
sensitivity test
and find out
the possible
causes of                              Physician
development
                                 Treat Infection
Who’s Work?



 Microbiologist

Advise the proper
   and adequate
  antibiotics with
                                    Physician
    balancing the
      economy of
          hospital Pharmacologist
Hospital Acquired Drug Resistance
• Hospital Antibacterial Policy
• Hospital Antibiogram
  Hospital specific antibacterial Resistance
  Pattern
• Identification of potential pathogen most
  likely to cause infection
• Previous antibacterial therapy
• Prescription auditing
Hospital Antibiotic Policy
• To curb the common misuse and overuse of
  antibiotics
• Restricts the occurrence of antibacterial
  resistance among the hospital strains
• Controls the spread of such infections to
  susceptible and critically ill patients in the
  hospital and the subsequent infection into the
  community.
• Saves money for the patient and increases
  patient satisfaction with decreased side effect.
Hospital Antibiogram
• A periodic summary of antimicrobial
  susceptibilities of local bacterial isolates
  submitted to the hospital's clinical
  microbiology laboratory.
• Used by clinicians to assess local susceptibility
  rates, as an aid in selecting empiric antibiotic
  therapy, and in monitoring resistance trends
  over time within an institution
Treatment options for selected highly
             resistant bacteria
Sr. Organism          Resistance     Antibiotic used
No
1 E. Faecalis         Penicillin      Vancomycin, Ampicillin -SLB
2 MRSA                Methicillin etc Linezolid , quinpristine,
                      Vancomycin      dalfopristine , daptomycin,
                                      telavacin
3    S. Epidermidis   Methicillin     Vancomycin + Rifampicin+
                                      Gentamicin
4    S. Pneumoniae Penicillin G      Ceftriaxone, cefotaxime,
                                     Telithromycin
                      MIC>4          Vancomycin + Rifampicin
5    C. Jejuni        FQ             Macrolides, doxycycline,
                                     clindamycin
Treatment options for selected highly
             resistant bacteria
Sr. Organism      Resistance         Antibiotic used
No
6 E. Coli         Cotrimoxazole,     Fosfomycin, Nitrofurantoin,
                  oral               Ertapenum
                  cephalosporins ,
                  FQ
7    K            III Gen            Imipenum, Meropenum,
     Pneumoniae   Cephalosporins     Colistin
                  & Ceftazidime
8    P. aeruginosa Imipenum,         Antipseudomal
                   meropenum         Aminoglycosides , Colistin,
                                     Ceftazidime
In our hospital antibiotics
Gm +ve bacteria recommended
  First line            Second line
  • Penicillin          • Vancomycin
  • Oxacillin           • Ofloxacin
  • Amoxy –Clav         • Clindamycin
  • Cephalothin         • Clarithromycin
  • Erythromycin        • Linezolid
  • Cotrimoxazole
  • Ciprofloxacin
  • Gentamicin
In our hospital antibiotics
Gm -ve bacteria  recommended
  First line             Second line
  • Amoxy-clav           • Cefta Clav
  • Gentamicin           • Cefipime
  • Ciprofloxacin        • Imipenum
  • Ceftazidime          • Netilimycin
  • Cefuroxime           • Tobramycin
  • Cefazoline
  • Amikacin
In our hospital antibiotics
      MRSA     recommended

•   Topical Fusidic acid
•   Vancomycin
•   Teicoplanin
•   Linezolid
•   Minocycline
•   Sparfloxacin
•   Rifampicin
In our hospital antibiotics
P. Aeruginosa recommended
•   Piperacillin
•   Cefaperazone
•   Amikacin
•   Ciprofloxacin
•   Gatifloxacin
•   Tobramycin
•   Netilimycin
•   Cefipime
•    piperacillin –Tazobactum
•   Ceftazidime
Take Home Message
• Target definitive therapy to known pathogen
• Treat infection, not contamination
• Treat infection, not colonization
• Know when to say “no” to Vancomycin,
  Carbepenems and Cephalosporin IV Generation
• Isolate Pathogen
• Break the chain of contagion – Keep your hands
  clean.
• Start simple bed side test: Gram stain,
  microscopy
Antibiotic resistance

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Antibiotic resistance

  • 1. Problem of Antibiotic Resistance & Rational use of antibiotics Dr. Naser Tadvi Associate Prof., Pharmacology
  • 2. Objectives • What is antimicrobial resistance • Why antibacterial resistance is a concern • How antibacterials work • Mechanisms of resistance to antibacterials • Indian scenario • NDM-1 • Strategies to contain resistance • Treatment of some resistant bacterial infections • Summary
  • 3. Introduction • Throughout history there has been a continual battle between human beings and multitude of micro-organisms that cause infection and disease
  • 4. History Nobel Lecture, December 11, 1945 Sir Alexander Fleming The Nobel Prize in Physiology or Medicine 1945 In his 1945 Nobel Prize lecture, Fleming himself warned of the danger of resistance – “It is not difficult to make microbes resistant to penicillin in the laboratory by exposing them to concentrations not sufficient to kill them, and the same thing has occasionally happened in the body… …and by exposing his microbes to non-lethal quantities of the drug make them resistant.”
  • 6. Why resistance is a concern • Resistant organisms lead to treatment failure • Increased mortality • Resistant bacteria may spread in Community • Low level resistance can go undetected • Added burden on healthcare costs • Threatens to return to pre-antibiotic era • Selection pressure
  • 7. Drug Resistance Drug resistance occurs in :  BACTERIA—ANTIBIOTIC RESISTANCE  Endoparasites  Viruses—Resistance to antiviral drugs  Fungi  Cancer cells
  • 8. Antibiotic Resistance • The concentration of drug at the site of infection must inhibit the organism and also remain below the level that is toxic to human cells. GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006)
  • 9. Antibiotic Resistance Defined as micro-organisms that are not inhibited by usually achievable systemic concentration of an antimicrobial agent with normal dosage schedule and / or fall in the minimum inhibitory concentration (MIC) range. Antibiotic Resistance (DR) = MIC / MCC > Toxic Plasma Concentration
  • 11. Myths of Antibiotic Resistance 1. Drugs (antibiotics) cause organisms antibiotic resistant. 2. Antibiotic resistant organisms are more virulent
  • 12. Truth • Antibiotics select out the resistant strain • Faulty use of antibiotics or widespread use of antibiotics increases the probability of such selection. • Antibiotic resistant strains appear to be more virulent because we cannot kill them or stop their growth.
  • 13. Mechanisms of action of antibiotics
  • 14. Mechanism Antibiotic Resistance Intrinsic (Natural) Acquired Genetic Methods Chromosomal Methods Extra chromosomal Methods Mutations Plasmids
  • 15. Antibiotic Resistance Some microorganisms may ‘born’ resistant, some ‘achieve’ resistance by mutation or some have resistance ‘thrust upon them’ by plasmids Some are born great, some achieve greatness or some have greatness thrust upon them
  • 16. Intrinsic Resistance It occurs naturally. 1. Lack target : • No cell wall; innately resistant to penicillin 2. Innate efflux pumps: • Drug blocked from entering cell or ↑ export of drug (does not achieve adequate internal concentration). Eg. E. coli, P. aeruginosa 3. Drug inactivation: • Cephalosporinase in Klebsiella
  • 17. Acquired resistance Mutations • It refers to the change in DNA structure of the gene. • Occurs at a frequency of one per ten million cells. • Eg.Mycobacterium.tuberculosis,Mycobacterium lepra , MRSA. • Often mutants have reduced susceptibility
  • 18. Plasmids • Extra chromosomal genetic elements can replicate independently and freely in cytoplasm. • Plasmids which carry genes resistant ( r-genes) are called R- plasmids. • These r-genes can be readily transferred from one R-plasmid to another plasmid or to chromosome. • Much of the drug resistance encountered in clinical practice is plasmid mediated
  • 19. Mechanisms of Resistance Gene Transfer • Transfer of r-genes from one bacterium to another  Conjugation  Transduction  Transformation • Transfer of r-genes between plasmids within the bacterium  By transposons  By Integrons
  • 20. Transfer of r-genes from one bacterium to another  Conjugation : Main mechanism for spread of resistance The conjugative plasmids make a connecting tube between the 2 bacteria through which plasmid itself can pass.  Transduction : Less common method The plasmid DNA enclosed in a bacteriophage is transferred to another bacterium of same species. Seen in Staphylococci , Streptococci  Transformation : least clinical problem. Free DNA is picked up from the environment (i.e.. From a cell belonging to closely related or same strain.
  • 21. Mechanisms of Resistance Gene Transfer Transposons Transposons are sequences of DNA that can move around different positions within the genome of single cell.  The donor plasmid containing the Transposons, co-integrate with acceptor plasmid. They can replicate during cointegration Both plasmids then separate and each contains the r-gene carrying the transposon. Eg ; Staphylococci,Enterococci
  • 23. Mechanisms of Resistance Gene Transfer Integrons Integron is a large mobile DNA can spread Multidrug resistance Each Integron is packed with multiple gene casettes, each consisting of a resistance gene attached to a small recognition site. These genes encode several bacterial functions including resistance and virulence. They cannot promote self transfer
  • 24. Biochemical mechanisms of antibiotic resistance • Prevention of drug accumulation in the bacterium • Modification/protection of the target site • Use of alternative pathways for metabolic / growth requirements • By producing an enzyme that inactivates the antibiotic • Quorum sensing
  • 25. Decreased permeability: Porin Loss Antibiotics normally enter bacterial cells via porin channels in the cell wall Antibiotic Porin channel into organism Cell wall Interior of organism
  • 26. Decreased permeability: Porin Loss New porin channels in the bacterial cell wall do not allow antibiotics to enter the cells Antibiotic New porin channel into organism Cell wall Interior of organism
  • 27. Efflux pumps • Cytoplasmic membrane transport proteins. • Major mechanism for resistance in Tetracyclines. • Some gram -ve bacteria inhibit the plasmid mediated synthesis of porin channels ,which obstructs the influx of hydrophilic Penicillins eg.ampicillin ATP Binding Cassette Major facilitator superfamily Multidrug and toxic compound exporter Small multidrug resistance transporters Resistance-nodulation-division
  • 28. Structurally modified antibiotic target site Antibiotics normally bind to specific binding proteins on the bacterial cell surface Antibiotic Binding Target site Cell wall Interior of organism
  • 29. Structurally modified antibiotic target site Antibiotics are no longer able to bind to modified binding proteins on the bacterial cell surface Antibiotic Modified target site Cell wall Changed site: blocked binding Interior of organism
  • 30. Modification/Protection of the Target site Resistance resulting from altered target sites : Target sites Resistant Antibiotics Ribosomal point mutation Tetracyclines,Macrolides , Clindamycin Altered DNA gyrase Fluoroquinolones Modified penicillin binding Penicillins proteins (Strepto.pneumonia) Mutation in DNA dependant Rifampicin RNA polymerase (M.tuberculosis)
  • 31. Antibiotic inactivation Inactivating enzymes target antibiotics Antibiotic Enzyme Binding Target site Cell wall Interior of organism
  • 32. Antibiotic inactivation Enzymes bind to antibiotic molecules Antibiotic Enzyme binding Enzyme Binding Target site Cell wall Interior of organism
  • 33. Antibiotic inactivation Enzymes destroy antibiotics or prevent binding to target sites Antibiotic Antibiotic altered, destroyed binding prevented Antibiotic Enzyme Target site Cell wall Interior of organism
  • 34. By producing enzymes that inactivates antibiotic a)Inactivation of b-lactam antibiotics •S. aureus, N. gonorrohoea, H.influenza, Produce b- lactamase which cleaves -lactam ring b)Inactivation of Chloramphenicol • Inactivated by chloramphenicol acetyltransferase . • Gram-ve (enzyme present constitutively hence higher resistance) gram +ve bacteria (enzyme is inducible ) c)Inactivation of Aminoglycosides • Inactivated by acetyl, phospho & adenylyl transferases Present in gram +ve and gram –ve .
  • 35. Use of alternative pathways for metabolic / growth requirements • Resistance can also occur by alternate pathway that bypasses the reaction inhibited by the antibiotic. • Sulfonamide resistance can occur from overproduction of PABA
  • 36. Drug Mechanism of resistance Pencillins & B Lactamase cleavage of the Blactam ring Cephalosporiins Aminoglycosides Modification by phosphorylating, adenylating and acetylating enzymes Chloramphenicol Modification by acetylytion Erythromycin Change in receptor by methylation of r RNA Tetracycline Reduced uptake / increased export Active export out of the cell & reduced affinity Sulfonamides of enzymes
  • 37. Quorum sensing • Microbes communicate with each other and exchange signaling chemicals (Autoinducers) • These autoinducers allow bacterial population to coordinate gene expression for virulence, conjugation, apoptosis, mobility and resistance
  • 38. Why named quorum sensing • Single autoinducer from single microbe is incapable of inducing any such change • But when its colony reaches a critical density (quorum), threshold of autoinduction is reached and gene expression starts • QS signal molecules AHL, AIP, AI-2 & AI-3 have been identified in Gm-ve bacteria • AI-2 QS –system is shared by GM+ve bacteria also
  • 39. WHY INHIBIT QUORUM SENSING  Proved to be very potent method for bacterial virulence inhibition.  Several QS inhibitors molecules has been synthesized which include AHL, AIP, and AI-2 analogues  QS inhibitors have been synthesized and have been isolated from several natural extracts such as garlic extract.  QS inhibitors have shown to be potent virulence inhibitor both in in-vitro and in-vivo,using infection animal models.
  • 41. Indian scenario • Lack of community awareness • Availability over the counter • Absence of central monitoring agency • In infants LRTI has taken over IMR due to diarrhoeal diseases due to use of ORT • S. Pneumoniae fully resistant to cotrimoxazole • Still sensitive to penicillins, macrolides and fluoroquinolones
  • 42. Enteric pathogens • Vibrio cholerae : – resistance to furazolidine, cotrimoxazole, nalidixic acid – Tetracycline remains effective • Coliforms – ESBLs , extensive resistance to Beta lactum antibiotics • Enteric fever
  • 43. STD • Penicillin and fluoroquinolone resistance is widespread to gonorhhoea • Alternate drugs like Azithromycin and cephalosporins should be used • Syphilis still susceptible to Penicillins
  • 44. Gram positive Cocci • Streptococci other than S. Pneumoniae – Resistant to tetracycline and macrolides (40%) – Still sensitive to penicillins • Staph Aureus – Methicillin resistance 50%-100% – Vancomycin resistance also increasing
  • 45. Mycobacteria • Multidrug resistance – Combined resistance to rifampicin and isoniazid • Extensively drug resistant TB – Additional acquisition of resistance to a fluroquinolone and one of the three injectable second line drugs (capreomycin, kanamycin and amikacin) • Steady rise in these patients
  • 46. What is NDM-1? • NDM-1 stands for New Delhi metallo-beta- lactamase, an enzyme produced by certain strains of bacteria that have recently acquired the genetic ability to make this compound. • The enzyme is active against other compounds that beta-lactam ring like penicillins, cephalosporins, and the carbapenems. • bacteria that produce NDM-1 are resistant to all commonly used beta-lactam antibiotics, including carbapenems.
  • 47. New Delhi metallo-beta-lactamase Why everyone concerned ? • There are currently no new drugs in the research pipelines that aim to stop NDM-1.To date, some strains of E.coli and Klebseilla pneumoniae are known carriers of the gene, but the gene can be transmitted from one strain of bacteria to another through horizontal gene transfer.
  • 48. Naming the strain as New Delhi creates controversy • The gene was named after New Delhi, the capital city of India, as it was first described by Yong et al. in 2009 in a Swedish national who fell ill with an antibiotic- resistant bacterial infection that he acquired in India . The infection was unsuccessfully treated in a New Delhi hospital and after the patient's repatriation to Sweden, a carbapenem-resistant Klebsiella pneumoniae strain bearing the novel gene was identified. The authors concluded that the new resistance mechanism "clearly arose in India, but there are few data arising from India to suggest how widespread it is."
  • 49. Treatment • Many NDM-1 strains are resistant to all antibiotics except for colistin. • Colistin is an older antibiotic that has not been used much in recent decades, because it is somewhat more toxic than other antibiotics. • A few NDM-1 strains have been sensitive to tigecycline (Tygacil), but this agent should be used cautiously in serious infections because it does not achieve high levels in the bloodstream. • A few strains have also been sensitive to aztreonam
  • 50. The spread of NDM-1 can be contained with .. • The spread of NDM-1 within health-care facilities can be curbed through strict infection-control measures, including patient isolation and hand washing.
  • 51. Strategy to Contain Resistance • Develop new antibiotics – Bypass the drug resistance • Judicious use of the existing antibiotics: – Containment of drug resistance
  • 52. New Antibiotic Development • Only 15 antibiotics of 167 under development had a new mechanism of action with the potential to combat of multidrug resistance. • Lack of incentive for companies to develop antibiotics.
  • 54. Hope is not exhausted….yet • Phage therapy • Use of the lytic enzymes found in mucus and saliva • Agents that target type IIA topoisomerases • Antimicrobial peptides (AMPs), lipopeptides (AMLPs) target bacterial membranes, making it nearly impossible to develop resistance (bacteria would have to totally change their membrane composition).
  • 55. Alternate Approaches Phage therapy • Phage Therapy is the therapeutic use of lytic bacteriophages to treat pathogenic bacteria infections • Bacteriophages are viruses that invade bacterial cells and disrupt bacterial metabolism and cause the bacterium to lyse. • Bacteriophage therapy is an important alternative to antibiotics • The success rate was 80–95% with few gastrointestinal or allergic side effects. British studies also demonstrated significant efficacy of phages against Escherichia coli, Acinetobacter spp., Pseudomonas spp and Staphylococcus aureus. Efflux Pump Inhibitors:
  • 56. Some newer antibiotics • Linezolid: targets 50S ribosome • Tigecycline: targets 30S ribosome • Daptomycin: depolarization of bacterial cell membrane • Dalbavacin: inhibits cell wall synthesis • Telavacin: inhibition of cell wall synthesis and disruption of membrane barrier function • Ceftibirole/ ceftaroline: cephalosporins • Iclaprim: inhibits Dihydrofolate reductase
  • 57. Judicious Use of Antibiotics • Can only contain antibiotic resistance • Cannot eliminate the possibility of antibiotic development as resistance is an evolutionary process
  • 58. Containment of Resistance • Containment of antibiotic resistance is a multi-pronged program • Involves all stake holders – Physicans – Patients – Pharmaceuticals
  • 59. Factors of Antibiotic Resistance Drug Related Environmental Factors Factors Antibiotic Resistance Prescriber Patient Related Related Factors Factors
  • 60. 1. Environmental Factors • Huge populations and overcrowding • Rapid spread by better transport facility • Poor sanitation • Increases community acquired resistance • Ineffective infection control program • Widespread use of antibiotics in animal husbandry and agriculture and as medicated cleansing products
  • 61. 2. Drug Related • Over the counter availability of antimicrobials • Counterfeit and substandard drug causing sub- optimal blood concentration • Irrational fixed dose combination of antimicrobials Policy • Soaring use of antibiotics Decision at Higher level
  • 62. 3. Patient Related • Poor adherence of dosage Regimens • Poverty • Lack of sanitation concept • Lack of education Patient • Self-medication Counseling, • Misconception Awareness Program
  • 63. Prescriber Related • Inappropriate use of available drugs • Increased empiric poly-antimicrobial use • Overuse of antimicrobials • Inadequate dosing • Lack of current knowledge and training
  • 64. Strategy of Containment Antibiotic Resistance Evolutionary Faulty Use of Process Antibiotics Hospital Acquired Hospital Environmental Antibiotic Resistance Community Acquired Antibiotic Resistance Empirical Use Definitive Use Use of antimicrobials before pathogen responsible for a particular illness or the susceptibility to a particular antimicrobial is known
  • 65. Poor Clinical Practice • Poor clinical practice that fail to incorporate the pharmacological properties of antimicrobials amplify the speed of development of drug resistance.
  • 66. Faulty Antibiotic Use • Antimicrobials are over prescribed • Available without prescription
  • 67. Over Prescribed Antibiotics • Clinician should first determine whether antimicrobial therapy is warranted for a given patient
  • 68. Empirical Microbial Selection • Is antimicrobial agents indicated on the basis of clinical findings? Or is it prudent to wait until such clinical findings become apparent?
  • 69. Empirical Microbial Selection • Can some simple bed side test done to confirm your suspicion? – Microscopy – Gram staining
  • 70. Empirical Microbial Selection • Have appropriate clinical specimens been obtained to establish a microbial diagnosis?
  • 71. Empirical Microbial Selection • What are the likely etiologic agents for the patient’s illness?
  • 72. Empirical Microbial Selection • What measures should be taken to protect individuals exposed to the index case to prevent secondary cases (1), and what measures should be implemented to prevent further exposure (2)? 2 1
  • 73. Empirical Microbial Selection • Is there clinical evidence (e.g. from clinical trials) that antimicrobial therapy will confer clinical benefit for the patient? (Evidence-based medicine)
  • 74. Definitive Treatment 1. Can a narrower spectrum agent be substituted for initial empiric drug?
  • 75. Definitive Treatment (2) 1. Is one agent or combination of agents necessary?
  • 76. Examples • -lactam + Aminoglycosides • Extended spectum Penicillins + -lactamase Inhibitors • Anti-tubercular regimen • Anti-leprotic regimen • Co-trimoxazole • Sulphadoxin + pyrimethamine • Artemisinin based Combination Therapy (ACT) in Malaria
  • 77. Definitive Treatment What are the – optimum dose, – route of administration and – duration of therapy?
  • 78. Definitive treatment What specific test to identify patients who will not respond to treatment?
  • 79. Definitive Treatment What adjunctive measures can be undertaken to eradicate infection? – Vaccination – Steroid – Drainage of pus – Amputation – Removal of catheter
  • 80. Who’s Work? Microbiologist Bacterial sensitivity test and find out the possible causes of Physician development Treat Infection
  • 81. Who’s Work? Microbiologist Advise the proper and adequate antibiotics with Physician balancing the economy of hospital Pharmacologist
  • 82. Hospital Acquired Drug Resistance • Hospital Antibacterial Policy • Hospital Antibiogram Hospital specific antibacterial Resistance Pattern • Identification of potential pathogen most likely to cause infection • Previous antibacterial therapy • Prescription auditing
  • 83. Hospital Antibiotic Policy • To curb the common misuse and overuse of antibiotics • Restricts the occurrence of antibacterial resistance among the hospital strains • Controls the spread of such infections to susceptible and critically ill patients in the hospital and the subsequent infection into the community. • Saves money for the patient and increases patient satisfaction with decreased side effect.
  • 84. Hospital Antibiogram • A periodic summary of antimicrobial susceptibilities of local bacterial isolates submitted to the hospital's clinical microbiology laboratory. • Used by clinicians to assess local susceptibility rates, as an aid in selecting empiric antibiotic therapy, and in monitoring resistance trends over time within an institution
  • 85. Treatment options for selected highly resistant bacteria Sr. Organism Resistance Antibiotic used No 1 E. Faecalis Penicillin Vancomycin, Ampicillin -SLB 2 MRSA Methicillin etc Linezolid , quinpristine, Vancomycin dalfopristine , daptomycin, telavacin 3 S. Epidermidis Methicillin Vancomycin + Rifampicin+ Gentamicin 4 S. Pneumoniae Penicillin G Ceftriaxone, cefotaxime, Telithromycin MIC>4 Vancomycin + Rifampicin 5 C. Jejuni FQ Macrolides, doxycycline, clindamycin
  • 86. Treatment options for selected highly resistant bacteria Sr. Organism Resistance Antibiotic used No 6 E. Coli Cotrimoxazole, Fosfomycin, Nitrofurantoin, oral Ertapenum cephalosporins , FQ 7 K III Gen Imipenum, Meropenum, Pneumoniae Cephalosporins Colistin & Ceftazidime 8 P. aeruginosa Imipenum, Antipseudomal meropenum Aminoglycosides , Colistin, Ceftazidime
  • 87. In our hospital antibiotics Gm +ve bacteria recommended First line Second line • Penicillin • Vancomycin • Oxacillin • Ofloxacin • Amoxy –Clav • Clindamycin • Cephalothin • Clarithromycin • Erythromycin • Linezolid • Cotrimoxazole • Ciprofloxacin • Gentamicin
  • 88. In our hospital antibiotics Gm -ve bacteria recommended First line Second line • Amoxy-clav • Cefta Clav • Gentamicin • Cefipime • Ciprofloxacin • Imipenum • Ceftazidime • Netilimycin • Cefuroxime • Tobramycin • Cefazoline • Amikacin
  • 89. In our hospital antibiotics MRSA recommended • Topical Fusidic acid • Vancomycin • Teicoplanin • Linezolid • Minocycline • Sparfloxacin • Rifampicin
  • 90. In our hospital antibiotics P. Aeruginosa recommended • Piperacillin • Cefaperazone • Amikacin • Ciprofloxacin • Gatifloxacin • Tobramycin • Netilimycin • Cefipime • piperacillin –Tazobactum • Ceftazidime
  • 91. Take Home Message • Target definitive therapy to known pathogen • Treat infection, not contamination • Treat infection, not colonization • Know when to say “no” to Vancomycin, Carbepenems and Cephalosporin IV Generation • Isolate Pathogen • Break the chain of contagion – Keep your hands clean. • Start simple bed side test: Gram stain, microscopy

Notas del editor

  1. Bubonic plague, TB , Malaria,hiv have affected significant number of hyman beings and caused mortality and morbidity Adult humans contains 1014 cells, only 10% are human – the rest are bacteriaAntibiotic use promotes Darwinian selection of resistant bacterial speciesBacteria have efficient mechanisms of genetic transfer – this spreads resistanceBacteria double every 20 minutes, humans every 30 yearsDevelopment of new antibiotics has slowed – resistant microorganisms are increasing
  2. Antimicrobial agents were viewed as miracle cure when introduced into clinical practice. However it became evident rather soon after the discovery of penicillin that resistance develops quickly terminating the miracle. This serious development is ever present with each new antimicrobial agents and threatens end of antimicrobial area. Today even major class of antibiotics are resistant
  3. If this can be achieved, the microorganism is considered susceptible to the antibiotic. If an inhibitory or bactericidal concentration exceeds that which can be achieved safely in vivo, then the microorganism is considered resistant to that drug. Antibiotic resistance refers to unresponsiveness of microorganism to antimicrobial agents.Susceptible MIC is at a concentration attainable in blood or other appropriate body fluid using usually recommended dosagesResistant MIC is higher than normally attainable levels in body fluidsIntermediate (moderately sensitive, moderately resistant) MIC is between sensitive and resistant levels, may be able to treat with increased dosage
  4. Presence of few mutants not sufficient to produce resistance Single step : E.coli & staph to RifampicinMultistep : erythromycin, tetracyclines, chloramphenicol
  5. The new DNA is then incorporated into the genome of the bacteria which becomes resistant.
  6. They have insertion sequence at end of gene.
  7. They are commonly associates with Transposons.
  8. Commonly operate in E.coli,P.aeruginosa,S.typhi,Staph.aureus,N.gonorroea.
  9. ACYl HOMOSERINE LACTONE,
  10. It remains to be seen if widespread use of antibiotics in syndromic control of LRTI chanfes pattern overtime
  11. Shigella
  12. superbugsgene transfer.
  13. Some antibiotics like aminoglycosides and fluoroquinolones do not contain beta-lactam rings. Unfortunately, the bacteria that have acquired NDM-1 have also acquired other resistance factors and most are already resistant to aminoglycosides and fluoroquinolones. The addition of NDM-1 production has the ability to turn these bacteria into true superbugs (bacteria resistant to usually two or more antibiotics) which are resistant to virtually all commonly used antibiotics.
  14. There are two different approaches to managing antibiotic resistance:1.Managing existing resistant pathogens 2.Avoiding future evolution of more resistanceThe first can be done by, in the case of MRSA, improving hygiene in hospitals, screening hospital visitors and isolating patients
  15. COLONIZATION means that the organism is present in or on the body but is not causing illness.Adopt WHO Strategies and PoliciesVaccination is the most logical and effective means to contain resistance by preventing infection in the first place. For ARIs, diarrhoeal diseases and malaria in children, WHO has developed the Integrated Management of Childhood Illness (IMCI). For the treatment of TB, WHO recommends use of the DOTS strategy. Antimicrobial resistance surveillance – another critical tool in the fight against antimicrobial resistance – identifies and tracks resistance trends in specific infections and geographical locations. INFECTION means that the organism is present and is causing illness.