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

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