Date post: | 14-Apr-2017 |
Category: |
Science |
Upload: | tanimittal |
View: | 86 times |
Download: | 0 times |
DRUG DELIVERY STRATEGIES FOR
COMBAT MULTIPLE DRUG RESISTANCE
By Tanya MittalM-PharmacyPharmaceutics 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
Conclusion2
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
6
7
DEVELOPMENT OF RESISTANCE
Bacterial cells that have developed
resistance are not killed off.They continue to divideResulting in a completely
resistant population. Mutation and evolutionary pressure
cause a rapid increase in resistance
to antibiotics.
TYPES OF DRUG RESISTANCE
9
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
One step mutation: Streptomycin
13
14
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
Transposition
18
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
21
CONJUGATION
22
MULTIPLE DRUG RESISTANCEMultidrug 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) cells23
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
25
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
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
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
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
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
34
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
ON
O
OH
S CH3CH3O
RH
b-lactamase
CH2
OHb-lactamase
CH2
OH
N
ON
O
OH
S CH3CH3O
RH
b-lactamase
CH2
OH H2O
N
ON
O
OH
S CH3CH3O
RH
HOHb-lactamase
CH2
OH
+Hydrolysis of Oxyiminogroup
Penicillin drug
Inactivated drug36
ANTIBIOTIC INACTIVATION
Interior of organism
Cell wall
Antibiotic
Target siteBindingEnzyme
Inactivating enzymes target antibiotics
ANTIBIOTIC INACTIVATION
Interior of organism
Cell wall
Antibiotic
Target siteBindingEnzyme
Enzymebinding
Enzymes bind to antibiotic molecules
ANTIBIOTIC INACTIVATION
Interior of organism
Cell wall
Antibiotic
Target siteEnzyme
Antibioticdestroyed
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 levels44
ORIGIN OF SUPERBUG
45
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
49
50
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 at51
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
53
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 capsularK 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.
56
CDC IN 2013, CDC PUBLISHED A REPORT OUTLINING THE TOP DRUG-RESISTANT THREATS
Bacteria Disease Infection/year
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 25,1988Campylobacter Diarrhea 31,000 120 May 20, 1994Flucanazole resistant candida
Candiasis 46,000 220 Feb 12, 2000
Streptococcus pneumonia
Ear and Sinus Infection
1,200,000 7000 Feb 16,199657
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 1946Streptomycin 1945 1959Tetracycline 1948 1953Erythromycin 1952 1988Vancomycin 1956 1988Methicillin 1960 1961Ampicillin 1961 1973Cephalosporins 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
practice61
HOW ANTIBIOTIC RESISTANCE SPREAD
62
THE CRISIS IN THE ANTIBIOTICS
Superbugs are on the rise Antibiotic development is dwindlingAntibiotic resistance is ancient Pharmaceutical firm abandon antibioticsLong 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 indicated65
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 duration66
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
70
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 system74
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 pathogen77
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
TARGETED DRUG-CARRYING PHAGESCONTD…..
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
TARGETED DRUG-CARRYING 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
ANCIENT TREATMENT FOR EYE 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
87Specific 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
91
PROMOTERS OF DRUG 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
.Rao M
D
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 splashAvoid 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
REFERENCES1. 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” 1stEdition 1998,
Page No. 341
6. Tripathy KD “Essentials of Medical Pharmacology” 6th Edition, Page No. 37100
REFERENCES CONTD…..
7. Nano-technology for targeted drug delivery to combat antibiotic resistance8. https://en.wikipedia.org/wiki/Antimicrobial_resistance9. http://www.economist.com/news/briefing/21699115-evolution-pathogens-
making-many-medical-problems-worse-time-take-drug-resistance10. http://www.slideshare.net/doctorrao/multi-drug-resistant-bacteria11.https://www.google.co.in/webhp?sourceid=chrome-
instant&ion=1&espv=2&ie=UTF-8#q=define+medicine12.http://www.medicalnewstoday.com/articles/283963.php13.http://chealth.canoe.com/channel/Infection/Overview/Superbugs-What-are-
they-and-how-are-they-formed14.http://www.nps.org.au/publications/health-professional/medicinewise-
news/2014/reducing-antibiotic-resistance101
REFERENCES CONTD……15.http://www.lung.org/lung-health-and-diseases/lung-disease
lookup/tuberculosis/drug-resistant-tb.html16.http://www.who.int/features/qa/79/en/17.From slides and www.wikipedia.com18.http://www.cell.com/cell/fulltext/S0092-8674(07)00311-X19. THE TRIBUNE NEWSPAPER.20.http://www.cdc.gov/drugresistance/biggest_threats.html21.http://textbookofbacteriology.net/resantimicrobial_3.html
22. Internet sources: ..too many!
www.google.com
www.wikipedia.com
Slides share102
103