Drug delivery strategies for combating multiple drug resistance

DRUG DELIVERY
STRATEGIES FOR
COMBAT MULTIPLE
DRUG RESISTANCE
By Tanya Mittal
M-Pharmacy
Pharmaceutics
2nd
year
1

CONTENTS
 Darwin’s Theory
 Historical background of resistance
 Types of drug resistance
 Method of resistance
 Multiple drug resistance
 Mechanism of drug resistance
 Super bug
 Antibiotics and Antibiotic resistance
 Combating MDR by nanotechnology
 Conclusion
2
OVERVIEW

SURVIVAL OF THE FITTEST.
DARWIN’S THEORY RULES THE
MICROBES
Various microorganisms have survived for
thousands of years by their being able to
adapt to antimicrobial agents. They do
so via spontaneous mutation or by DNA
transfer. These microorganisms employ
several mechanisms in attaining
Multidrug resistance(MDR)
3

HISTORICAL BACKGROUND OF
DRUG RESISTANCE
 WHO report released April 2014 stated, "Multiple drug
resistance is a serious threat.
 At least 2 million people become infected with bacteria that
are resistant to antibiotics and at least 23,000 people die each
year
 Albert Alexander was the first who died due to infection. The
wound became infected by bacteria, Staphylococcus aureus
and wound turned septic and he lost his life. 4

DEFINITION
oDrug:
Any substance or therapeutic agents other than food used in the
prevention, diagnosis, alleviation, treatment, or cure of disease.
Drug resistance is the ability of microbes, such as bacteria,
viruses, parasites, or fungi, to grow in the presence of a drug that
would normally kill it or limit its growth.
 It is the reduction in effective-ness of a drug in curing a
disease or condition.
5

DEVELOPMENT OF RESISTANCE
 Bacterial cells that have developed
resistance are not killed off.
They continue to divide
Resulting in a completely
resistant population.
 Mutation and evolutionary pressure
cause a rapid increase in resistance
to antibiotics.

PRIMARY/NATURAL/NON
GENETIC ORIGIN OF
RESISTANCE
Bacteria possess an innate property to resist drug.
 EXAMPLE:
 The bacteria may infect host at sites
where drugs are inaccessible or not
active seen in Salmonellae.
 The cell wall may be covered with an outer membrane that
establishes a permeability barrier against the antibiotic as
seen in Gram negative bacteria.
10

 Bacteria may remain in dormant
resting state without multiplying and
become phenotypically resistant to
drugs as seen in M. tuberculosis.
 Micro-organisms may lose the specific
target structure for a drug for several
generations and become resistant.
An acid fast stain (Ziehl-
Neelsen) shows numerous
mycobacterium bacilli.
11

ACQUIRED/GENETIC ORIGIN OF
DRUG RESISTANCE
Bacteria acquire/develop resistance
to antibiotics either through the
modification of existing genetic
material (mutation) or the
acquisition of new genetic material
from another source (plasmid/gene
transfer).
Further classified into: 12

1. CHROMOSOME
MEDIATED RESISTANCE:
Resistance acquired due to spontaneous
mutation of gene that controls the
susceptibility to a given antimicrobial
drug.
 Structurally alters the target of the
drug or the transport system that
controls the uptake of the drug.
 2 types:
 Stepwise mutation: Penicillin

13

2. TRANSFERABLE DRUG
RESISTANCE
A. PLASMID MEDIATED RESISTANCE:
 Resistance acquired through the transfer of
extrachromosomal resistance plasmids( R factors)
 R factor = RTF (Resistance Transfer
Factor) + r determinant
 Main features:
 Frequency of resistance transfer is high.
 Resistance transfer can occur to cells of
different species.
15

 Plasmids can mediate resistance to multiple drugs.
 R factors provide resistance to metal ions and bacterial
viruses/bacteriophages.
 R factors code for enzymes causing inactivation of drug.
b) TRANSPOSON MEDIATED RESISTANCE:
 Transposons are genes/segments of DNA that are transferred
within themselves or between chromosomes and
extrachromosomal plasmids.
16

 They are also known as jumping genes
and this mode of genetic transfer as
transposition.
 Transposons attach themselves to
chromosomal, plasmid or phage DNA
molecule and confer resistance to drugs
under suitable environmental conditions.
 Transposons are not self replicating.
 R determinant segments of R Factors are
said to be collections of Transposons.
17

METHODS OF TRANSFER OF
RESISTANCE
 Horizontal gene transfer is a
process whereby genetic material
contained in small packets of DNA
can be transferred between
individual bacteria of the same
species or even between different
species. a). Conjugation
b). Transformation
c). Transduction
19

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. Seen in E.coli
 Transduction: Less common method. The plasmid DNA
enclosed in a bacteriophage is transferred to another bacterium
of same species. Seen in Staphylococci , Streptococci
 Transformation: Free DNA is picked up from the environment
(i.e.. From a cell belonging to closely related or same strain. 20

MULTIPLE DRUG RESISTANCE
Multidrug resistance is a condition enabling a
disease-causing organism to resist
distinct drugs or chemicals of a
wide variety of structure and
function targeted at eradicating the
organism. Organisms that display
multidrug resistance can be pathologic
cells, including bacterial and neoplastic (tumor) cells
23

MULTIDRUG-RESISTANT
ORGANISMS MDRO:
DEFINITION
Multidrug-Resistant Organisms (MDROs) are defined as
microorganisms that are resistant to one or more classes of
antimicrobial agents.
Three most common MDROs are:
1. Methicillin-Resistant Staph aureus (MRSA)
2. Vancomycin Resistant Enterococci. (VRE)
3.Extended Spectrum Beta-Lactamase producing
Enterobacteriaceae. (ESBLs)
24

ANTI-MCROBIAL AGENTS WITH
MECHANISM OF ACTION AND
MECHANISM OF RESISTANCE
Antimicrobial agents MOA MOR
Sulfonamides Structural analogs of PABA – inhibit folate
synthetase -FA not formed
Increased production of PABA
Low affinity folate synthetase enzyme
Alternate folate metabolism pathway
Co-trimoxazole Inhibits dihydrofolate reductase (DHFRase) Low affinity DHFRase
Fluoroquinolones Inhibits bacterial enzyme DNA gyrase or
topoisomerase IV
Low affinity DNA gyrase or topoisomerase
IV
↓ permeability
↑ efflux
Beta lactams Inhibit transpeptidases (PBPs)– crosslinking
of peptidoglycan residues does not occur
β- lactamases
Altered PBPs
Active efflux
Tetracyclines Bind to 30S ribosomes – inhibit protein
synthesis
↓ influx
Active efflux
Inactivating enzymes
Chloramphenicol Bind to 50S ribosomes– inhibit protein
synthesis
Acetyl transferase – inactivates CPC
↓ influx
Low affinity ribosomes
26

MECHANISMS INVOLVED IN
MDR
 Enzymatic degradation
 Mutation at binding site
 Down regulation of outer membrane proteins
 Efflux pumps
27

MECHANISMS OF DRUG
RESISTANCE
1. Production of enzymes that destroy/modify the active drug.
2. Synthesis of an altered target site against which the drug has no
effect.
3. Reducing drug accumulation through:
a) Decreasing the permeability of cell membrane.
b) Actively exporting drugs through Multi Drug Resistant pump
(‘MDR’ OR EFFLUX pump).
28

STRUCTURALLY MODIFIED ANTIBIOTIC
TARGET SITE
Interior of organism
Cell wall
Target siteBinding
Antibiotic
Antibiotics normally bind to specific binding proteins on the
bacterial cell surface

STRUCTURALLY MODIFIED ANTIBIOTIC
TARGET SITE
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

Decreased permeability: Porin Loss
Cell wall
Porin channel
into organism
Antibiotic
Antibiotics normally enter bacterial cells via porin channels
in the cell wall

Decreased permeability: Porin Loss
Cell wall
New porin channel
into organism
Antibiotic
New porin channels in the bacterial cell wall do not allow
antibiotics to enter the cells

4. Altering the metabolic
pathway so that the reaction
inhibited by the drug can be
bypassed.
5. Developing an altered enzyme
that is less inhibited by the
drug but can still perform its
metabolic function. 33

ENZYMATIC DEGRADATION
 Enzymatic deactivation of penicillin G in some penicillin-
resistant bacteria through the production of β-lactamases
 Protective enzymes produced by the bacterial cell wall add
an acetyl or phosphate group to a specific site on the
antibiotic, which will reduce its ability to bind to the
bacterial ribosomes and disrupt protein synthesis.
35

Enzymatic degradation
Mechanisms of b-lactamase
N
O
N
O
OH
S CH3
CH3
O
R
H
β-lactamase
CH2
OH
β-lactamase
CH2
OH
N
O
N
O
OH
S CH3
CH3
O
R
H
β-lactamase
CH2
O
H H2O
N
O
N
O
OH
S CH3
CH3
O
R
H
H
OH
β-lactamase
CH2
OH
+
Hydrolysis of Oxyimino group
Penicillin drug
Inactivated drug
36

ANTIBIOTIC INACTIVATION
Cell wall
Antibiotic
Target siteBinding
Enzyme
Inactivating enzymes target antibiotics

Cell wall
Antibiotic
Target siteBindingEnzyme
Enzyme
binding
Enzymes bind to antibiotic molecules

Cell wall
Antibiotic
Target siteEnzyme
Antibiotic
destroyed
Antibiotic altered,
binding prevented
Enzymes destroy antibiotics or prevent binding to target sites

MUTATION AT BINDING SITE
 In this binding of p53 to MDR is blocked at site (i.e. p53
DNA-binding site) and this mutation results in
enhancement of metastasis and mediate MDR
40

DOWN REGULATION OF THE
OUTER MEMBRANE PROTEINS
The outer membrane permeability is regulated by porin
proteins. Alteration in Outer membrane permeability
particularly due to the decreased expression of porin
proteins results in decreased influx of various drugs.
41

EFFLUX PUMPS
 Bacteria use ATP-powered membrane proteins to pump any
lipophilic molecule out of the cell common in antibiotic-
producing bacteria, to get drugs out of their cells without
poisoning themselves
 Powerful method of resistance, because many different drugs
will be equally affected by these efflux pumps
 Some gram -ve bacteria inhibit the plasmid mediated synthesis
of porin channels ,which obstructs the influx of hydrophilic
Penicillins eg.ampicillin
42

MECHANISMS OF
RESISTANCE: EFFLUX
 Active, energy dependent pumps cause efflux of drugs
Bacterial Cytosol
PG layer
Outer membrane
drug
Efflux pump
Dr.T.
V.Ra
o
MD
43

SUPERBUGS
Bacteria which have acquired
increased resistance towards
the antibiotic class used for their
treatment.
Multi-drug resistance acquired
by bacteria through various
mutations which enhance its
morbidity and mortality levels
44

CURRENTLY SPREAD OF
ANTIBIOTIC RSISTANCE
46

NDM-1 (NEW DELHI METALLO BETA
LACTAMASE
47

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
48

TUBERCULOSIS
Tuberculosis is an ancient disease & it remains the leading
cause of death of human being. It is mainly caused by
Mycobacterium tuberculosis
 Nine million people suffer from tuberculosis and Two million
people die each year.
 MDR-TB caused by strains of Mycobacterium Tuberculosis
resistant both Rifampicin and Isoniazid with or without
resistance to other drugs.
 Multidrug-resistant TB (MDR TB) is TB that is resistant to at
51

TUBERCULOSIS CONTD…..
least two of the best anti-TB drugs, isoniazid and rifampicin.
These drugs are considered first-line drugs and are used to
treat all persons with TB disease
 Extensively drug resistant TB (XDR TB) is a type of MDR
TB. XDR TB is defined as TB which is resistant to isoniazid
and rifampin, plus resistant to any fluoroquinolone and at least
one of three injectable second-line drugs (i.e., amikacin,
kanamycin, or capreomycin). 52

URINARY TRACT INFECTION
 UTI imply invasion of urinary tract by pathogens, which may
involve the upper or lower tract depending on the infection
in the kidney, ureters or bladder and urethra.
 Most UTI are caused by E.Coli, derived from periurethral fecal
flora.
 Bacterial adhesion by pili bind to cell surface by recognizing a
glycosphingolipid recepter. Which is critical in the genesis of
pyelonephritis.
 Leads to activation of cytokines which produces adhesion
molecules and chemotaxix of leukocytes.
54

55
E.coli, Proteus, klebsiella, staphylococcus epidermidis and
streptococcus faecalis Proteus and pseudomonas Fungi i.e
candida albicans are the main causative agents and required
prolonged antibiotic therapy.
VIRULENCE FACTORS-
O antigen of E.Coli induces inflammation and fever and
capsular
K antigen for resistance to phagocytosis and the bactericidal
effect of serum.
Bacteria produce hemolysin and damages the uroepithelium
and aerobactin for scavenging iron from urine needed in
metabolism.

CDC IN 2013, CDC PUBLISHED A
REPORT OUTLINING THE TOP DRUG-
RESISTANT THREATS
Bacteria Disease Infection/y
ear
Deaths Publication
date
Clostridim
difficile
Diarrhoea 25,000 14,000 July 3,2014
Cartapenem –
resistant
enterobacter-
iaceae
Blood
stream
infection
9,000 6,000 August 14, 1998
Neisseria
gonorrhea
STD 820,000 - Sep 2, 1999
Acinobacter Pneumonia 12,000 500 Nov 25,1988
Campylobacter Diarrhea 31,000 120 May 20, 1994
Flucanazole
resistant candida
Candiasis 46,000 220 Feb 12, 2000
Streptococcus
pneumonia
Ear and
Sinus
Infection
1,200,000 7000 Feb 16,1996
57

ANTIBIOTICS
 Antibiotics are antimicrobial drug used in the treatment and
prevention of bacterial infections.
 Antibiotics are not effective against viruses and their
inappropriate use allows the emergence of resistant organisms.
 In 1928, Alexander Fleming identified penicillin, the first
chemical compound . Fleming was working on a culture of
disease-causing bacteria when he noticed the spores of a little
green mold (Penicillium chrysogenum). 58

ANTIBIOTICS CONTD…..
 Combination therapy (i.e., the concurrent application of two or
more antibiotics) has been used to delay or prevent the emergence
of resistance.
 Combined effect of two antibiotics is better than their individual
effect.
 For ex: Methicillin-resistant Staphylococcus aureus infections
may be treated with a combination therapy of fusidic acid and
rifampin. 59

HISTORY OF ANTIBIOTIC
RESISTANCE
 APPEARANCE
DRUG INTRODUCTION OF RESISTANCE
Penicillin 1943 1946
Streptomycin 1945 1959
Tetracycline 1948 1953
Erythromycin 1952 1988
Vancomycin 1956 1988
Methicillin 1960 1961
Ampicillin 1961 1973
Cephalosporins 1964 late 1960’s
60

RECENTLY USED ANTIBIOTICS
1962- Quinolone antibiotics first
discovered
1970s- Linezolid discovered but not
pursued
1980s- Fluorinated Quinolones
introduced, making then clinically useful
2000- Linezolid introduced into clinical
practice
61

HOW ANTIBIOTIC RESISTANCE
SPREAD
62

THE CRISIS IN THE ANTIBIOTICS
Superbugs are on the rise Antibiotic development is dwindling
Antibiotic resistance is ancient Pharmaceutical firm abandon antibiotics
Long term persistence of antibiotics development: economic and regulatory
resistance barriers.
63

ANTIBIOTICS KILL BACTERIA,
NOT VIRUSES
If a virus is making you
sick, taking antibiotics may
do more harm than good.
most respiratory tract
infections are caused by
viruses, so antibiotics
won’t have any effect.

PRACTICE CONTRIBUTING TO
MISUSE OF ANTIBIOTICS
 Inappropriate specimen selection and
collection
 Inappropriate clinical tests
 Failure to use stains/smears
 Failure to use cultures and susceptibility tests
 Use of antibiotics with no clinical
indication ( for viral infections)
 Use of broad spectrum antibiotics when not indicated
65

PRACTICE CONTRIBUTING TO
MISUSE OF ANTIBIOTICS
CONTD….
 Inappropriate choice of empiric antibiotics
 Lack of quality control in manufacture or outdated
antimicrobial
 Inadequate surveillance or defective susceptibility assays
 Use of antibiotics in foods
 Inappropriate dose and route - ineffective concentration of
antibiotics at site of infection
 Inappropriate duration
66

DRUG DELIVERY STRATEGIES TO
COMBAT MDR
 Different antimicrobial delivery systems involving nano-
technology which refers to the design, production and
application of nano-sized materials (1-100 nm).
67

DRUG DELIVERY STRATEGIES TO
COMBAT MDR CONTD….
 Their unique physical and chemical properties (small size,
high surface-to-volume ratio and amenable for surface
modification) may be exploited as vehicles to carry various
therapeutic or diagnostic agents.
 High surface-to-volume ratio allows nano-materials for
increased potential to interact with pathogens and
membranes. Thus, they can be potentially used for medical
applications including targeted drug delivery, and gene
therapy
68

BACTERIOPHAGE THERAPY
 Bacteriophages, or simply 'phages', are viruses
that infect and in some cases destroy bacterial
cells. Phages are devour.
 Phages are a natural part of the microbial
ecosystem.
 Phage species are specific to particular
bacterial species.
 Phage ‘cocktail’
69

CHITOSAN
 Chitosan is a natural polysaccharide derived from chitin.
 Chitosan is able to enter the nuclei of bacteria and fungi and
inhibit mRNA and protein synthesis by binding to microbial
DNA
 Nano-scaled chitosan that has a higher surface-to-volume ratio,
resulting in higher surface charge density, leads to increased
affinity to bacteria and fungi and greater antimicrobial activity.
 For antibiotic encapsulation and efficient delivery using this
nano-material
71

LIPOSOMES
 Liposomes are spherical vesicles consisting of one or more
phospholipid bilayers surrounding a water space.
 The diameter of the liposome varies from 0.02 to 10 μm.
 Encapsulation of the antibiotics in lipid vesicles is a good
solution for designing the required p’kinetic and p’dynamic
properties.
 This process may improve pharmacokinetics and
biodistribution, decreased toxicity, enhanced activity 72

LIPOSOMES CONTD…..
against intracellular pathogens, target selectivity, enhanced
activity of antibiotics against extracellular pathogens, in
particular to overcome antibiotic resistance.
73

INORGANIC NANO-MATERIALS
 Inorganic nano-materials are used as antimicrobials.
 Noble metals (like silver, gold, platinum, and palladium),
carbon-based materials (carbon nano-fibers and different kinds
of carbon nano-tubes), semiconducting materials (CdSe, CdS,
ZnS, TiO2, PbS, InP, Si/SiO2), magnetic materials (Fe3O4,
Co, CoFe2O4, FePt, CoPt and their composites) and
lanthanide materials (Gd2O3, Eu2O3) are some of the
important inorganic nanomaterials used as antimicrobials as
well as antibiotic delivery system
74

SILVER
 Silver used for the treatment of burns and wounds to prevent
infection.
 Due to the smaller size of silver and silver ions (< 10 nm), they
are able to penetrate bacterial cell walls and membranes via
interaction with sulfur-containing proteins or thiol groups.
 Once inside the cell, Ag/Ag+ targets and damages bacterial DNA
and respiratory enzymes, leading to loss of the cell’s replicating
abilities and ultimately cell death AgNPs have also been
found to augment the efficacy of other antibiotics,
75

SILVER CONTD……
like the activity of penicillin G, amoxicillin,
erythromycin, clindamycin and vancomycin increased
against S. aureus and E. coli when mixed with AgNPs.
76

COPPER
 Copper is utilized for its antifungal and antibacterial activity
 But the mechanism remains unknown.
 The use of CuO nano-particles (CuO-NPs) as a novel
antimicrobial agent.
 When compared to AgNPs, CuO-NPs were shown to be less
effective against E. coli and methicillin-resistant S. aureus but
more effective against B. subtilis, which may be due to copper’s
greater interaction with amine and carboxyl groups on the cell
surface of this pathogen
77

CARBON NANO-TUBES
 Carbon nano-tubes (CNTs) are emerging as a new family of
nano-vectors for the delivery of different types of therapeutic
molecules given their capacity to interact with macromolecules
such as proteins, antibiotics and oligosaccharides.
 Covalent modification by the organic functionalization of end
groups and side walls of f-CNTs allows for a dramatic increase
of the solubility of functionalized carbon nano-tubes in a range
of solvents, including water. 78

CARBON NANO-TUBES CONTD….
 Water-soluble carbon nano-tubes interact with
mammalian cells, leading to their cytoplasmic
translocation
 Due to this f-CNTs it has been an effective vehicle for
oral administration of AmB
79

DENDRIMERS
 Dendrimers are hyperbranched polymers with precise
nanoarchitecture and low polydispersity, which are surrounded
by a core unit, resulting in a high level control of size,
branching points (drug conjugation capability), and surface
functionality.
 The highly branched nature of dendrimers provides enormous
surface area to size ratios that generate great reactivity to
microorganisms in vivo.
80

DENDRIMERS CONTD…..
 The highly dense surface of functional groups allows the
synthesis of dendrimers with specific and high binding
affinities to a wide variety of viral and bacterial
receptors.
 Polymeric nano-particles have been explored to deliver
various antimicrobial agents and greatly enhanced
therapeutic efficacy in treating many types of infectious
diseases. 81

TARGETED DRUG-CARRYING
PHAGES
 These are a new class of nanomedicines that combines biologic
and chemical components into a modular nano-metric drug
delivery system (bioconjugated delivery system).
 The core of the system is filamentous phage particles which are
produced in the bacterial host Escherichia coli.
 Target specificity is provided by a targeting moiety, usually an
antibody that is displayed on the tip of the phage particle.
82

PHAGES
CONTD…..
A large drug payload is chemically conjugated to the protein
coat of the phage via a chemically or genetically engineered
linker that provides for controlled release of the drug after the
particle homed to the target cell.
 Hepatitis B virus (HBV) vaccine is one of the best examples of
bio-conjugated nano-particles delivery system.
83

PHAGES CONTD….
Receptor and antibody specificity can be exploited for targeted delivery. Genetically engineered filamentous
phage loaded with drug molecules inside its protein coat and displaying antibody on its tip can burst to
release drug molecules when it binds with its complementary receptors. The released drug molecules attack
pathogenic bacteria and kill it specifically. Here ‘A’ stands for antibody; ‘B’ for bacteria; ‘P’ for protein coat;
‘D’ for drug/ antibiotic; ‘L’ for chemical linker and ‘R’ for receptor.
84

INFECTIONS COULD BE CURE FOR
SUPERBUGS
A one thousand year old
Anglo-Saxon remedy for
eye infections which
originates from a
manuscript in the British
Library has been found to
kill the modern-day
superbug MRSA in an
unusual research
collaboration at The
University of Nottingham.
85

GEL FILLED WITH NANOSPONGES
CLEANS UP MRSA INFECTIONS
86

STAPHEFEKT-THE FIRST ENDOLYSIN
AVAILABLE FOR HUMAN USE ON
INTACT SKIN
87
Specific lysis of MRSA and MSSA by Staphefekt

TEIXOBACTIN DEVELOPED IN
2015
88
Used to treat S.
aureus (MRSA),
and Streptococcus
pneumoniae.

TREATMENT USED FOR
TUBERCULOSIS
89

DRUG USED FOR URINARY TRACT
INFECTION
90

RESISTANCE
 Indiscriminate use of antibiotics in
a) Agriculture and veterinary practice
which can accumulate in food and
water.
b) Genetically modified crops.
c) Hospital environment and infections.
d) Inappropriate selling of antibiotics
over the counter to the general
public .
92

PREVENTION OF DRUG
RESISTANCE
 Patients must stop taking antibiotics for self
limiting infections.
 Doctors have to stop giving unnecessary
antibiotic prescriptions.
 Patients must follow complete antibiotic
prescriptions.
 Stop the use of antibiotics as growth-
promoting substances in farm animals. 93

PREVENT INFECTION
 Patients can do:
Wash your hands frequentlyDon't share personal items Get vaccinated.

WHAT ELSE PATIENTS
CAN DO:
•Take antibiotics exactly as the
doctor prescribes.
•Only take antibiotics prescribed for you
•Do not save antibiotics for the next illness.
•Do not ask for antibiotics when your doctor
thinks you do not need them
Prevent antibiotic resistance

CHOOSE THE
APPROPRIATE ANTIBIOTIC
Think before
prescribing
Are we using
Right drug
for the Right
bug ?
Dr.T.V.RaoMD
96

WHAT PRECAUTIONS MIGHT BE IN
PLACE IF I WORK IN A HOSPITAL?
Universal precautions:
•Hand hygiene
•Safe collection and disposal of sharps
• Gloves for contact with body fluids,
non-intact skin and mucous
membranes
•Wearing a mask, eye
protection and a gown if
blood or other body fluids
might splash
Avoid Needle Stick Injuries

We need to preserve this
resource by working
together
Because
No action today,
no cure tomorrow
Antibiotics are
invaluable resources

CONTROL
Search for new antibiotics:
Biotechnology and pharmaceutical
companies must constantly research,
develop and test new antimicrobials in order
to maintain a pool of effective drugs in the
market against the rise of resistant bacteria.
The report estimates that, Unless urgent
action is taken, drug-resistant infections
will kill 10 million people a year by 2050
99

REFERENCES
1. A Textbook of Microbiology-P Chakravarthy.
2. Textbook Of Microbiology- Ananthnarayan and Paniker
3. Review of medical microbiology and Immunology-Warren levinson (McGraw
Hill publications.)
4. Jawetz, Melnick and Adelberg’s Medical Microbiology- Geo F Brooks, Janet S
Butel , Stephen A Mosse
5. Vyas S.P. and Dixit V.K. “Pharmaceutical Biotechnology” 1st
Edition 1998, Page
No. 341
6. Tripathy KD “Essentials of Medical Pharmacology” 6th
Edition, Page No. 37
100

REFERENCES CONTD…..
7. Nano-technology for targeted drug delivery to combat antibiotic
resistance
8. https://en.wikipedia.org/wiki/Antimicrobial_resistance
9. http://www.economist.com/news/briefing/21699115-evolution-pathogens-
making-many-medical-problems-worse-time-take-drug-resistance
10. http://www.slideshare.net/doctorrao/multi-drug-resistant-bacteria
11.https://www.google.co.in/webhp?sourceid=chrome-
instant&ion=1&espv=2&ie=UTF-8#q=define+medicine
12.http://www.medicalnewstoday.com/articles/283963.php
13.http://chealth.canoe.com/channel/Infection/Overview/Superbugs-What-
are-they-and-how-are-they-formed
14.http://www.nps.org.au/publications/health-professional/medicinewise-
news/2014/reducing-antibiotic-resistance 101

REFERENCES CONTD……
15.http://www.lung.org/lung-health-and-diseases/lung-disease
lookup/tuberculosis/drug-resistant-tb.html
16.http://www.who.int/features/qa/79/en/
17.From slides and www.wikipedia.com
18.http://www.cell.com/cell/fulltext/S0092-8674(07)00311-X
19. THE TRIBUNE NEWSPAPER.
20.http://www.cdc.gov/drugresistance/biggest_threats.html
21.http://textbookofbacteriology.net/resantimicrobial_3.html
22. Internet sources: ..too many!
 www.google.com
 www.wikipedia.com
 Slides share
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Drug delivery strategies for combating multiple drug resistance

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