DILLA UNIVERSITY

COLLEGE OF MEDICINE AND HEALTH SCIENCE

DEPARTEMENT OF MEDICAL LABORATOR

BY : Name ID
NO
1. Alem Abiti............................ ........... 6233/19
2. Mubarak Berka................................. 7422/19
3. Getachew Wale ................................ 1188/19
Discuss about update on Antimicrobial resistance
microgansimis?
 Objective
At the end this presentation they will be understand
 Diffention of Antimicrobial resistance
 Factors for the emergence and spreadof antimicrobial
resistance
 Different mechanism of resistance microgansimis for drug
 Drug resistance in some bacteria , virus fungus parasite
 Treatment and prevention of Antimicrobial resistance
microgansimis
 Introduction
• WHO has declared that AMR is one of the top 10 global
public health threats facing humanity.
• Antimicrobial is a medication used to treat microbes.
• Antimicrobials – including antibiotics, antivirals, antifungals
and antiparasitics – are medicines used to prevent and
treat infections in humans, animals and plants.
• Misuse and overuse of antimicrobials are the main drivers
in the development of drug-resistant pathogens.
• Antimicrobial Resistance (AMR) occurs when bacteria,viruses,
fungi and parasites change over time and no longer respond
to medicines making infections harder to treat and increasing
the risk of disease spread, severe illness and death.

• This means previously effective antimicrobial drugs (e.g.

antibiotics) used to treat or prevent infections may no longer
work.
 Factors emergence and spread
of antimicrobial resistance?
• misuse and overuse of antimicrobials;
• lack of access to clean water, sanitation and hygiene (WASH) for
bothhumans and animals;
• poor infection and disease prevention and control in health-
care facilities and farms;
• poor accessto quality, affordable medicines, vaccines and
diagnostics;
• lack of awareness and knowledge; and lack of enforcement of
legislation.
Mechanism of Resistance
 Enzymatic inhibition
 Alteration of bacterial membranes
 Efflux /influx mechanism
 Modification of target sites
 1.Enzymatic inhibition
Beta lactamase

1. Those that hydrolyze oxacillin and related penicillins

2. Carbenicillinases
3. Those that break extended spectrum beta lactams like
aztreonam
4. Those that break down oxyimino B lactams
5. Carbapenemases-found in pseudomonas.Most
cephalosporinases are inhibited by clavulanate,sulbactam
or tazobactam. Carbapenamases are metallo enzymes
inhibited by EDTA but not clavulanate or sulbactam

Production of enzymes modifying antibiotics

. Aminoglycosides, chloramphenicol-coded by plasmids or
chromosomal genes
Alteration of bacterial membranes
Outer membrane permeability—outer membrane of gram neg
acts as a barrier to antibiotics esp hydrophobic ones.
Inner membrane permeability- rate of entry of aminoglyco-
sides into bacterial cells is a function of them binding to a non
saturable anionic transporter,where they retain their positive
charge and are pulled across the cytoplasmic membrane by
the internal charge of the cell.This is an energy dependent
process. The energy generation or proton motive force may be
altered through mutation
2.Efflux /influx mechanism
Bacterial cells have an intrinsic capacity to restrict the entry of
small molecules especially gram neg-outer membrane is prote
ctive,gram pos no outer membrane hence more antibiotic
sensitive
Restriction of influx is a physiological way to reduce toxcixity
to bacterial cell.
The most wellstudied efflux system in E. coli is the AcrAB/TolC
system this system comprises of an inner membrane
proteinAcr B, and an outer membrane protein, Tol C, linked by
a periplasmic protein, Acr A
When activated, the linker protein is believed to fold on itself,
bringing the AcrB and Tol C proteins in close contact, thus pro-
viding an exit path from the inside to the outside of the cell.
Antibiotics are pumped out through this channel.
3. Modification of target sites
Alteration of ribosomal target sites-hence failure to inhibit
protein synthesis and cell growth.
Affected antibiotics are aminoglycosides ,tetracyline,
macrolides,lincosamides.
 Antibiotics resistance in bacteria
• Antibiotics treat infections caused by bacteria.
• Modern medicine, especially surgery and cancer treatments,
depends on effective antibiotics to minimise the risk of
infection.
• Overuse of unnecessarily broad spectrum antibiotics can drive
antimicrobial resistance.
• It is preferable to narrow spectrum antibiotics wherever
possible.
• For example, the rate of resistance to ciprofloxacin, an
antibiotic commonly used to treat urinary tract infections,
varied from 8.4% to 92.9% for Escherichia coli and from 4.1% to
79.4% for Klebsiella pneumoniae in countries reporting to the
Global.
• Over 20% of E.coli isolates the most common pathogen in
urinary tract infections were resistant to both first-line drugs
(ampicillin and co-trimoxazole) and second-line treatments
(fluoroquinolones).
• Colistin is the only last resort treatment for life-threatening
infections caused by carbapenem resistant Enterobacteriaceae
(i.e. E.coli, Klebsiella , etc).
• Bacteria resistant to colistin have also been detected in several
countries and regions, causing infections for which there is no
effective antibiotic treatment at present
• the frequency of bloodstream infections due to two specific
drug resistant pathogens: methicillin- resistant Staphylococcus
aureus (MRSA); and E. coli resistant to third generation
cephalosporins (3GC).
• N.gonorrhoeae Resistance has rapidly emerged to
sulphonamides, penicillins, tetracyclines,
macrolides,fluoroquinolones, and early generation
cephalosporins.
• Over 60% of Neisseria gonorrhoea isolates, a common
sexually transmitted disease, have shown resistance to one of
the most used oral antibacterials, ciprofloxacin.
• Currently, in most countries, the injectable extended-
spectrum cephalosporin (ESC) ceftriaxone is the only
remaining empiric monotherapy for gonorrhoea.

• Nontyphoidal Salmonella (NTS) and Shigella species:

resistance to fluoroquinolones.
• an estimated 3.4% of new TB cases and 18% of previously
treated cases had MDR-TB/ RR-TB
• theemergence of resistance to new ‘last resort’ TB drugs
to treat drug resistant TB poses a major threat.
 Drug resistance in virus
• Most antiviral agents target nucleic acid synthesis, in
many cases by acting as nucleoside analogues.
• These are molecules that are incorporated into viral DNA
instead of the normal deoxynucleosides.
• They prevent extension of the chain because DNA
polymerase is unable to act on them.

• Resistance has developed to most antivirals including

antiretroviral (ARV) drugs.
 All antiretroviral (ARV) drugs, including newer classes, are at
risk of becoming partly or fully inactive because of
theemergence of drug-resistant HIV (HIVDR).
 People receiving antiretroviral therapy can acquire HIVDR,
and people can also be infected with HIV that is already drug
resistant.
 In sub-Saharan Africa, over 50% of the infants newly
diagnosed with HIV carry a virus that is resistant to NNRTI.
 Drug resistance in malaria parasites

 The emergence of drug-resistant parasites poses one of the

greatest threats to malaria control and results in increased
malaria morbidity and mortality.
 Artemisinin-based combination therapies (ACTs) are the
recommended first-line treatment for uncomplicated P.
falciparum malaria and are used by most malaria endemic
countries.
 In Africa, evidence has recently been published showing
emergence of mutations linked to partial artemisinin
resistance in Rwanda
 further spread of resistance to artemisinin and ACT partner
drugs could pose a major public health challenge
 Drug resistance in fungi
 The prevalence of drug-resistant fungal infections is increasing
and exasperating the already difficult treatment situation.
 Drug-resistant Candida auris , one of the most common
invasive fungal infections, is already widespread with
increasing resistance reported to fluconazole, amphotericin B
and voriconazole as well as emerging caspofungin resistance.
 How is antimicrobial resistance
treated?
Anyone with an antimicrobial-resistant infection may need to:
• Use a different medication.
• Take a higher dose of an antimicrobial.
• Take the medication for a longer period.
• Try multiple medications in combination.
 How can antimicrobial resistance
be prevented?
 It’s not possible to eliminate antimicrobial resistance, as
microbes will always be able to modify themselves and adapt
to their environment. However, there are some ways you could
limit your exposure:
1. Only prescribing antibiotics that are needed.
2. Targeting the medicine as soon as possible
to the specific bacteria involved.
3. Prescribing medicines for only as long as
needed.
4. Follow the directions exactly for any prescription medication.
5. Never take another person’s prescription medication or share
yours with them.
6. Never save old prescription drugs for use at a later time.
7. Get vaccinations as recommended.
 Summary
 Antimicrobials – including antibiotics, antivirals, antifungals
and antiparasitics – are medicines used to prevent and treat
infections in humans, animals and plants.
 Antimicrobial Resistance (AMR) occurs when
bacteria,viruses, fungi and parasites change over time and
no longer respond to medicines
 It’s not possible to eliminate antimicrobial resistance, as
microbes will always be able to modify themselves and
adapt to their environment.
 Misuse and overuse of antimicrobials are the main drivers
in the development of drug-resistant pathogens.
 Reference
• Cleveland Clinic medical professional on 2021.
• Antimicrobial resistance world health organization report
November 17,2021
• Regional Infection Prevention and Control WebEx
SessionsWashington DC, 10 July 2018
Tha
nks
!!!