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Mweetwal-Pharmacologist
 ROLE OF PHARMACISTS IN COMBATING DRUG RESISTANCE BY ENHANCING
EVIDENCE BASED PRACTICE
 BY MWEETWA L-PHARMACOLOGIST
Mweetwal-Pharmacologist
 What is antimicrobial resistance
 Why antibacterial resistance is a concern To
Pharmacists
 How antibacterials work
 Mechanisms of resistance to antibacterials
 Strategies to contain resistance
Mweetwal-Pharmacologist
Mweetwal-Pharmacologist
Microbiologist
Physician
Pharmacologist
Advise the
proper and
adequate
antibiotics with
balancing the
economy of
hospital
 Throughout history there has been a
continual battle between human beings and
multitude of micro-organisms that cause
infection and disease.
 The pharmacist's role in combating and
preventing infectious diseases is essential as
antibiotic and vaccine regimens become
more complex due to the continuously
evolving epidemiology of infections.
Mweetwal-Pharmacologist
 The decrease in drug development makes the
preservation of currently available
antibiotics paramount.
 Pharmacists as Custodian and experts in
Medicines Must Play a Pivotal Role In
combating Drug Resistance and Must
understand How drug resistance happens at
molecular level.
Mweetwal-Pharmacologist
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”
History
Nobel Lecture, December 11, 1945
Sir Alexander Fleming
The Nobel Prize in Physiology or Medicine
1945
Mweetwal-Pharmacologist
Mweetwal-Pharmacologist
Environmental
Factors
Drug
Related
Factors
Patient
Related
Factors
Prescriber
Related
Factors
Antibiotic
Resistance
 Huge populations and overcrowding
 Poor sanitation
 Ineffective infection control programs
 Widespread use of antibiotics in animal husbandry and
agriculture and as medicated cleansing products
Mweetwal-Pharmacologist
Mweetwal-Pharmacologist
 Over the counter availability of antimicrobials
 Counterfeit and substandard drug causing sub-
optimal blood concentration
 Irrational fixed dose combination of
antimicrobials
 Soaring use of antibiotics
Mweetwal-Pharmacologist
Policy
Decision at
Higher
level
 Poor adherence of dosage Regimens
 Poverty
 Lack of sanitation concept
 Lack of education
 Self-medication
 Misconception
Mweetwal-Pharmacologist
 Inappropriate use of available drugs
 Increased empiric poly-antimicrobial use
 Poor clinical practice
 Over prescribing is an antibiotic warranted for a given patient?
 Empirical antimicrobial selection,Is there clinical evidence,(Evidence-
based medicine
 Inadequate dosing
 Lack of current knowledge and training
Mweetwal-Pharmacologist
14
 Resistant organisms lead to treatment failure
 Increased mortality
 Resistant bacteria may spread in Community
 Add burden on healthcare costs
 Threat to return to pre-antibiotic era
 Selection pressure
Mweetwal-Pharmacologist
• 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.
•Principles Of Chemotherapy Must be
applied when selecting Which antibiotic to
use
Antibiotic Resistance
Mweetwal-Pharmacologist
Mweetwal-Pharmacologist
Mweetwal-Pharmacologist
Mweetwal-Pharmacologist
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.
Mweetwal-Pharmacologist
Mweetwal-Pharmacologist
Understanding Mechanism of Antibiotic
Resistance at Molecular Level
Intrinsic (Natural) Acquired
Genetic Methods
Chromosomal Methods
Mutations
Extra chromosomal Methods
Plasmids
Mweetwal-Pharmacologist
 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
Mweetwal-Pharmacologist
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,Mycobact
erium lepra , MRSA.
• Often mutants have reduced
susceptibility
Mweetwal-Pharmacologist
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
Mweetwal-Pharmacologist
Plasmids
• Extra chromosomal genetic elements can
replicate independently and freely in
cytoplasm.
• Plasmids carry resistant genes ( r-genes) or
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
Mweetwal-Pharmacologist
Mechanism of Resistance by
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
Mweetwal-Pharmacologist
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.
Mweetwal-Pharmacologist
Transfer of r-genes from one
Bacterium to Another
 Transduction : Less common method
The plasmid DNA enclosed in a
bacteriophage is transferred to another
bacterium of same species. Seen in
Staphylococci , Streptococci
Mweetwal-Pharmacologist
Transfer of r-genes from one
Bacterium to Another
 Transformation : least clinical problem.
Free DNA is picked up from the
environment (i.e.. From a cell belonging
to closely related or same strain.
Mweetwal-Pharmacologist
 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.
Mweetwal-Pharmacologist
Mweetwal-Pharmacologist
 Integron is a large mobile DNA that 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.
Mweetwal-Pharmacologist
• 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 Mechanism-RGEFPD.
Mweetwal-Pharmacologist
Decreased permeability: Porin Loss
Interior of organism
Cell wall
Porin channel
into organism
Antibiotic
Antibiotics normally enter bacterial cells via porin channels
in the cell wall
Mweetwal-Pharmacologist
Decreased permeability: Porin Loss
Interior of organism
Cell wall
New porin channel
into organism
Antibiotic
New porin channels in the bacterial cell wall do not allow
antibiotics to enter the cells
Mweetwal-Pharmacologist
Mweetwal-Pharmacologist
Interior of organism
Cell wall
Modified target site
Antibiotic
Changed site: blocked binding
Antibiotics are no longer able to bind to modified binding proteins
on the bacterial cell surface
• Bacterias are capable of flushing out
antibiotics before they reach their target
site.
Mweetwal-Pharmacologist
Mweetwal-Pharmacologist
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
proteins (Strepto.pneumonia)
Penicillins
Mutation in DNA dependant
RNA polymerase
(M.tuberculosis)
Rifampicin
Mweetwal-Pharmacologist
Drug Mechanism of resistance
Pencillins &
Cephalosporiins
B Lactamase cleavage of the Blactam ring
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
Sulfonamides
Active export out of the cell & reduced
affinity of enzymes
Mweetwal-Pharmacologist
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
Mweetwal-Pharmacologist
 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
Mweetwal-Pharmacologist
 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
Mweetwal-Pharmacologist
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.Mweetwal-Pharmacologist
Mweetwal-Pharmacologist
 Develop new antibiotics
 Pharmacist-directed antibiotic
stewardship programs (ASPs)
 Judicious use of the existing antibiotics
Mweetwal-Pharmacologist
 Community Pharmacists as Gateway
Practitioners-Prevent Antibiotic Misuse.
 Vaccination-by preventing primary infection and
indirectly by preventing bacterial superinfection
Mweetwal-Pharmacologist
 Education:-
-Patient and clinician education
 infection-control practices such as
general hygiene, hand hygiene, cough
etiquette, immunizations, and staying
home when sick
Mweetwal-Pharmacologist
 Prudent antimicrobial prescribing
 UK hospitals have appointed microbiologists or
infectious diseases physicians with antibiotic
management , Pharmacists as Drug Experts Must
undertake such roles as Lead Antibiotics
Pharmacists
 Establishment of Hospital Antibiotic Policy
Mweetwal-Pharmacologist
 A dedicated antibiotic pharmacist has the time
and skills to monitor antibiotic prescribing and
manage it appropriately
 Key roles for antibiotic pharmacists include:-
 education of medical, pharmaceutical and
nursing staff,
 audit of local practices, monitoring of antibiotic
consumption, participation in infection control,
formulary development and appraisal of new
antimicrobials
Mweetwal-Pharmacologist
 Many physicians, medical microbiologists and
infectious diseases physicians might feel
threatened by such proposals but
Pharmacists are inseparable to drugs
 TB & Leprosy Corners?
Mweetwal-Pharmacologist
 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).
Mweetwal-Pharmacologist
Phage therapy
• Bacteriophages are viruses that invade bacterial
cells and disrupt bacterial metabolism and cause the
bacterium to lyse.
• Efflux Pump Inhibitors:?
Alternate Approaches
Mweetwal-Pharmacologist
 Dedicated Hospital Pharmacist Antibiogram
Experts
 Whose task is to perform a periodic summary of
antimicrobial susceptibilities of local bacterial
isolates submitted to the hospital's clinical
microbiology laboratory.
 And assess local susceptibility rates, as an aid in
selecting empiric antibiotic therapy, and in
monitoring resistance trends over time within an
institution

Mweetwal-Pharmacologist
 Provides current appropriate data on use of
antimicrobial therapy with improved patient
outcomes
 Slow the development of antimicrobial resistance
 Acts as Liaison Officer with other clinical staffs to
Develop evidence- based Treatment guidelines
 Educate providers and staff regarding antibiotic
guidelines
 Track resistance patterns and report back to medical
and hospital staff
Mweetwal-Pharmacologist
 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
 Ceftibiprole/ ceftaroline: cephalosporins
 Iclaprim: inhibits Dihydrofolate reductase
Mweetwal-Pharmacologist
 Target definitive therapy to known pathogen
 Treat infection, not contamination
 Treat infection, not colonization
 Isolate Pathogen, utilise your microbiology lab
 Break the chain of contagion – Keep your hands clean.
 Start simple bed side test: Gram stain, microscopy
Mweetwal-Pharmacologist
 The information contained in this presentation is
for information purposes only, and may not apply
to your situation.The author provides no
warranty about the content or accuracy of
content enclosed. Information provided is
subjective. Keep this in mind when reviewing this
guide.
 Neither the Publisher nor Author shall be liable
for any loss of profit or any other commercial
damages resulting from use of this guide. All links
are for information purposes only and are not
warranted for content, accuracy, or any other
implied or explicit purpose, all rights, images,Mweetwal-Pharmacologist
 Thank You, Twalumba, Zikomo !!!!!!!!!!!!
Mweetwal-Pharmacologist

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Role of pharmacists in combating drug resistatnce

  • 1. Mweetwal-Pharmacologist  ROLE OF PHARMACISTS IN COMBATING DRUG RESISTANCE BY ENHANCING EVIDENCE BASED PRACTICE  BY MWEETWA L-PHARMACOLOGIST
  • 3.  What is antimicrobial resistance  Why antibacterial resistance is a concern To Pharmacists  How antibacterials work  Mechanisms of resistance to antibacterials  Strategies to contain resistance Mweetwal-Pharmacologist
  • 5.  Throughout history there has been a continual battle between human beings and multitude of micro-organisms that cause infection and disease.  The pharmacist's role in combating and preventing infectious diseases is essential as antibiotic and vaccine regimens become more complex due to the continuously evolving epidemiology of infections. Mweetwal-Pharmacologist
  • 6.  The decrease in drug development makes the preservation of currently available antibiotics paramount.  Pharmacists as Custodian and experts in Medicines Must Play a Pivotal Role In combating Drug Resistance and Must understand How drug resistance happens at molecular level. Mweetwal-Pharmacologist
  • 7. 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” History Nobel Lecture, December 11, 1945 Sir Alexander Fleming The Nobel Prize in Physiology or Medicine 1945 Mweetwal-Pharmacologist
  • 9.  Huge populations and overcrowding  Poor sanitation  Ineffective infection control programs  Widespread use of antibiotics in animal husbandry and agriculture and as medicated cleansing products Mweetwal-Pharmacologist
  • 11.  Over the counter availability of antimicrobials  Counterfeit and substandard drug causing sub- optimal blood concentration  Irrational fixed dose combination of antimicrobials  Soaring use of antibiotics Mweetwal-Pharmacologist Policy Decision at Higher level
  • 12.  Poor adherence of dosage Regimens  Poverty  Lack of sanitation concept  Lack of education  Self-medication  Misconception Mweetwal-Pharmacologist
  • 13.  Inappropriate use of available drugs  Increased empiric poly-antimicrobial use  Poor clinical practice  Over prescribing is an antibiotic warranted for a given patient?  Empirical antimicrobial selection,Is there clinical evidence,(Evidence- based medicine  Inadequate dosing  Lack of current knowledge and training Mweetwal-Pharmacologist
  • 14. 14
  • 15.  Resistant organisms lead to treatment failure  Increased mortality  Resistant bacteria may spread in Community  Add burden on healthcare costs  Threat to return to pre-antibiotic era  Selection pressure Mweetwal-Pharmacologist
  • 16. • 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. •Principles Of Chemotherapy Must be applied when selecting Which antibiotic to use Antibiotic Resistance Mweetwal-Pharmacologist
  • 20. 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. Mweetwal-Pharmacologist
  • 22. Understanding Mechanism of Antibiotic Resistance at Molecular Level Intrinsic (Natural) Acquired Genetic Methods Chromosomal Methods Mutations Extra chromosomal Methods Plasmids Mweetwal-Pharmacologist
  • 23.  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 Mweetwal-Pharmacologist
  • 24. 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,Mycobact erium lepra , MRSA. • Often mutants have reduced susceptibility Mweetwal-Pharmacologist
  • 25. 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 Mweetwal-Pharmacologist
  • 26. Plasmids • Extra chromosomal genetic elements can replicate independently and freely in cytoplasm. • Plasmids carry resistant genes ( r-genes) or 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 Mweetwal-Pharmacologist
  • 27. Mechanism of Resistance by 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 Mweetwal-Pharmacologist
  • 28. 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. Mweetwal-Pharmacologist
  • 29. Transfer of r-genes from one Bacterium to Another  Transduction : Less common method The plasmid DNA enclosed in a bacteriophage is transferred to another bacterium of same species. Seen in Staphylococci , Streptococci Mweetwal-Pharmacologist
  • 30. Transfer of r-genes from one Bacterium to Another  Transformation : least clinical problem. Free DNA is picked up from the environment (i.e.. From a cell belonging to closely related or same strain. Mweetwal-Pharmacologist
  • 31.  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. Mweetwal-Pharmacologist
  • 33.  Integron is a large mobile DNA that 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. Mweetwal-Pharmacologist
  • 34. • 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 Mechanism-RGEFPD. Mweetwal-Pharmacologist
  • 35. Decreased permeability: Porin Loss Interior of organism Cell wall Porin channel into organism Antibiotic Antibiotics normally enter bacterial cells via porin channels in the cell wall Mweetwal-Pharmacologist
  • 36. Decreased permeability: Porin Loss Interior of organism Cell wall New porin channel into organism Antibiotic New porin channels in the bacterial cell wall do not allow antibiotics to enter the cells Mweetwal-Pharmacologist
  • 37. Mweetwal-Pharmacologist Interior of organism Cell wall Modified target site Antibiotic Changed site: blocked binding Antibiotics are no longer able to bind to modified binding proteins on the bacterial cell surface
  • 38. • Bacterias are capable of flushing out antibiotics before they reach their target site. Mweetwal-Pharmacologist
  • 40. 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 proteins (Strepto.pneumonia) Penicillins Mutation in DNA dependant RNA polymerase (M.tuberculosis) Rifampicin Mweetwal-Pharmacologist
  • 41. Drug Mechanism of resistance Pencillins & Cephalosporiins B Lactamase cleavage of the Blactam ring 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 Sulfonamides Active export out of the cell & reduced affinity of enzymes Mweetwal-Pharmacologist
  • 42. 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 Mweetwal-Pharmacologist
  • 43.  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 Mweetwal-Pharmacologist
  • 44.  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 Mweetwal-Pharmacologist
  • 45. 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.Mweetwal-Pharmacologist
  • 47.  Develop new antibiotics  Pharmacist-directed antibiotic stewardship programs (ASPs)  Judicious use of the existing antibiotics Mweetwal-Pharmacologist
  • 48.  Community Pharmacists as Gateway Practitioners-Prevent Antibiotic Misuse.  Vaccination-by preventing primary infection and indirectly by preventing bacterial superinfection Mweetwal-Pharmacologist
  • 49.  Education:- -Patient and clinician education  infection-control practices such as general hygiene, hand hygiene, cough etiquette, immunizations, and staying home when sick Mweetwal-Pharmacologist
  • 50.  Prudent antimicrobial prescribing  UK hospitals have appointed microbiologists or infectious diseases physicians with antibiotic management , Pharmacists as Drug Experts Must undertake such roles as Lead Antibiotics Pharmacists  Establishment of Hospital Antibiotic Policy Mweetwal-Pharmacologist
  • 51.  A dedicated antibiotic pharmacist has the time and skills to monitor antibiotic prescribing and manage it appropriately  Key roles for antibiotic pharmacists include:-  education of medical, pharmaceutical and nursing staff,  audit of local practices, monitoring of antibiotic consumption, participation in infection control, formulary development and appraisal of new antimicrobials Mweetwal-Pharmacologist
  • 52.  Many physicians, medical microbiologists and infectious diseases physicians might feel threatened by such proposals but Pharmacists are inseparable to drugs  TB & Leprosy Corners? Mweetwal-Pharmacologist
  • 53.  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). Mweetwal-Pharmacologist
  • 54. Phage therapy • Bacteriophages are viruses that invade bacterial cells and disrupt bacterial metabolism and cause the bacterium to lyse. • Efflux Pump Inhibitors:? Alternate Approaches Mweetwal-Pharmacologist
  • 55.  Dedicated Hospital Pharmacist Antibiogram Experts  Whose task is to perform a periodic summary of antimicrobial susceptibilities of local bacterial isolates submitted to the hospital's clinical microbiology laboratory.  And assess local susceptibility rates, as an aid in selecting empiric antibiotic therapy, and in monitoring resistance trends over time within an institution  Mweetwal-Pharmacologist
  • 56.  Provides current appropriate data on use of antimicrobial therapy with improved patient outcomes  Slow the development of antimicrobial resistance  Acts as Liaison Officer with other clinical staffs to Develop evidence- based Treatment guidelines  Educate providers and staff regarding antibiotic guidelines  Track resistance patterns and report back to medical and hospital staff Mweetwal-Pharmacologist
  • 57.  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  Ceftibiprole/ ceftaroline: cephalosporins  Iclaprim: inhibits Dihydrofolate reductase Mweetwal-Pharmacologist
  • 58.  Target definitive therapy to known pathogen  Treat infection, not contamination  Treat infection, not colonization  Isolate Pathogen, utilise your microbiology lab  Break the chain of contagion – Keep your hands clean.  Start simple bed side test: Gram stain, microscopy Mweetwal-Pharmacologist
  • 59.  The information contained in this presentation is for information purposes only, and may not apply to your situation.The author provides no warranty about the content or accuracy of content enclosed. Information provided is subjective. Keep this in mind when reviewing this guide.  Neither the Publisher nor Author shall be liable for any loss of profit or any other commercial damages resulting from use of this guide. All links are for information purposes only and are not warranted for content, accuracy, or any other implied or explicit purpose, all rights, images,Mweetwal-Pharmacologist
  • 60.  Thank You, Twalumba, Zikomo !!!!!!!!!!!! Mweetwal-Pharmacologist

Editor's Notes

  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 bacteria Antibiotic use promotes Darwinian selection of resistant bacterial species Bacteria have efficient mechanisms of genetic transfer – this spreads resistance Bacteria double every 20 minutes, humans every 30 years Development 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 dosages Resistant MIC is higher than normally attainable levels in body fluids Intermediate (moderately sensitive, moderately resistant) MIC is between sensitive and resistant levels, may be able to treat with increased dosage
  4. ACYl HOMOSERINE LACTONE,
  5. COLONIZATION means that the organism is present in or on the body but is not causing illness. Adopt WHO Strategies and Policies Vaccination 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.