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Biology Class Xii Cbse Investigatory Project On Antibiotics PDF
Biology Class Xii Cbse Investigatory Project On Antibiotics PDF
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Acknowledge
ment
I feel proud to present my investigatory
project in
Biology on the antibiotics-good or bad for us?
This project would not have been feasible
without the proper rigorous guidance of
biology teacher Mrs.Neena Dhawan. Who
guided me throughout this project in every
possible way? An investigatory project
involves various difficult lab experiments,
which have to obtain the observations and
conclude the reports on a meaningful note.
Thereby, I would like to thanks Mrs.Neena
Dhawan for guiding me on a systematic basis
and ensuring that in completed all my
research with ease. Rigorous hard work has
put in this project to ensure that it proves to
be the best. I hope that it proves to be the
best. I hope that this project will prove to be a
breeding ground for the next generation of
students and will guide them in every possible
way.
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Introduction
In common usage, an antibiotic (from the Ancient Greek: anti , "against",
and bios , "life") is a substance or compound that kills bacteria or inhibits
their growth.[1] Antibacterial is an alternative name. Antibiotics belong to the
broader group of antimicrobial compounds, used to treat infections caused by
microorganisms, including fungi and protozoa.
The term "antibiotic" was coined by Selman Waksman in 1942 to describe any
substance produced by a microorganism that is antagonistic to the growth of other
microorganisms in high dilution.[2] This original definition excluded naturally
occurring substances that kill bacteria but are not produced by microorganisms
(such as gastric juice and hydrogen peroxide) and also excluded synthetic
antibacterial compounds such as the sulfonamides . Many antibiotics are relatively
small molecules with a molecular weight less than 2000 atomic mass units.
The primary cause of antibiotic resistance is antibiotic use both within medicine
and veterinary medicine. The greater the duration of exposure the greater the risk
of the development of resistance irrespective of the severity of the need for
antibiotics.
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First we have to study antibiotics-
Antibiotic
n common usage, an antibiotic (from the Ancient Greek: anti, "against", and
bios, "life") is a substance or compound that kills bacteria or inhibits their growth.
Antibacterial is an alternative name. Antibiotics belong to the broader group of
antimicrobial compounds, used to treat infections caused by microorganisms, including
fungi and protozoa.
The term "antibiotic" was coined by Selman Waksman in 1942 to describe any substance
produced by a microorganism that is antagonistic to the growth of other microorganisms
in high dilution. This original definition excluded naturally occurring substances that kill
bacteria but are not produced by microorganisms (such as gastric juice and hydrogen
peroxide) and also excluded synthetic antibacterial compounds such as the sulfonamides.
Many antibiotics are relatively small molecules with a molecular weight less than 2000
atomic mass units.
With advances in medicinal chemistry, most antibiotics are now semi synthetic
modified chemically from original compounds found in nature, as is the case with beta-
lactase (which include the penicillins, produced by fungi in the genus Penicillium, the
cephalosporins, and the carbapenems). Some antibiotics are still produced and isolated
from living organisms, such as the amino glycosides, and others have been created
through purely synthetic means: the sulfonamides, the quinolones, and the
oxazolidinones. In addition to this origin-based classification into natural, semi synthetic,
and synthetic, antibiotics may be divided into two broad groups according to their effect
on microorganisms: Those that kill bacteria are bactericidal agents, whereas those that
only impair bacterial growth are known as bacteriostatic agents.
History of antibiotics
Many treatments for infections prior to the beginning of the twentieth century were based
on medicinal folklore. Treatments for infection in many ancient cultures using
concoctions with antimicrobial properties were described over 2000 years ago. Many
ancient cultures, including the ancient Egyptians and ancient Greeks used molds and
plants to treat infections. The discovery of the natural antibiotics produced by
microorganisms stemmed from earlier work on the observation of antibiosis between
micro-organisms. Louis Pasteur observed that, "if we could intervene in the antagonism
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observe d between some bacteria, it would off er perhap s the grea test hopes for therapeu
tics". Synthetic antib iotic chemotherapy a s a science and the st ory of antib iotic
development began in Germa ny with Pa ul Ehrlich, a German medical scientist in th e late
what
1880s. Scientific endeavour s to under stand the science behind caused these
of
diseases, the development of synthetic antibiotic chemotherapy, the isolation the
natural a
ntibiotics marked milestones in antibiotic development.
as antibiosis, antibiotics were dr ugs which acted against bacteria.
Originally known The
term an tibiosis, wh ich means "against life," was introduced b y the French bacteriologist
Vuillemin as a des criptive na me of the phenomeno n exhibited by these drugs.(Antib
iosis was first described in 1877 in bacteria when Louis Pasteur a nd Robert Koch obse
rved that an airborne b acillus could inhibit the growth of Bacillus anthracis.). These d
rugs were later renamed antibiotics by Sel man Waks man, an American microbiologist
in 1942.
Bacterial antagonism of Penicillium spp. were first described i n England by John Tyndall in
1875.The significance to antibiotic discovery was not realize d until the work of Eh rlich on
synth etic antibi otic chemotherapy, wh ich marked the birth of the antibiotic revolu tion.
Ehrlich noted that certain dye s would bin d to and c olor human, animal, or bacterial cells,
while others did no t. He then extended the idea that it might b e possible to make ce rtain
dyes or chemicals that would act as a m agic bullet or selectiv e drug that would bi nd to and
kill bacteria while not harming the human host. Aft er much experimenta tion, screening
hundreds of dyes against vario us organism s, he disco vered a me dicinally useful drug, t he
man-made antibi otic, Salva rsan. In 1928 Flem ing made an impo rtant observa tion
concerning the antibiosis by penicillin. Fleming postulated th at the effect was mediated by a
yet-unidentified antibiotic-like compound that could be explo ited. Although he initially
characterized some of its antib iotic prope rties, he did not purs ue its development. In th e
meantim e, another synthetic antibacteri al antibioti c Prontosil was developed and man
ufactured for comme rcial use by Domagk i n 1932. Prontosil, the first commercially
available antibacterial antibiotic, was developed by a research team le d by Gerhard Domagk
(who received the 193 9 Nobel Pri ze for Med icine for his efforts) a t the Bayer Laboratories
of the IG Farben conglomerate in Germany . Prontosil had a relatively broad e ffect again st
Gram-po sitive cocc i but not a gainst ent erobacteria. The disco very and development o f
this first sulfonamide drug op ened the era of antibiotics. In 1 939, discover y by Rene Dubos
of the first n aturally der ived antibi otic-like s ubstance n amed gramici din from B. brevis. It
was one of the first c ommercially manufactured antibiotics in use d uring Wo rld War II to
prove highly effective in tr eating wounds and ulcers.
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Florey and Chain succeeded in purifying penicillin. The purified antibiotic displayed
antibacterial activity against a wide range of bacteria. It also had low toxicity and could
be taken without causing adverse effects. Furthermore, its activity was not inhibited by
biological constituents such as pus, unlike the synthetic antibiotic class available at the
time, the sulfonamides. The discovery of such a powerful antibiotic was unprecedented.
The development of penicillin led to renewed interest in the search for antibiotic
compounds with similar capabilities.Because of their discovery of penicillin Ernst Chain,
Howard Florey and Alexander Fleming shared the 1945 Nobel Prize in Medicine. Florey
credited Dubos with pioneering the approach of deliberately, systematically searching for
antibacterial compounds. Such a methodology had led to the discovery of gramicidin,
which revived Florey's research in penicillin.
Antibiotic resistance
The underlying molecular mechanisms leading to antibiotic resistance can vary. Intrinsic
resistance may naturally occur as a result of the bacteria's genetic makeup. The bacterial
chromosome may fail to encode a protein that the antibiotic targets. Acquired resistance
results from a mutation in the bacterial chromosome or the acquisition of extra-
chromosomal DNA. Antibiotic-producing bacteria have evolved resistance mechanisms
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that have been shown to be similar to, and may have been transferred to, antibiotic-
resistant strains. The spread of antibiotic resistance mechanisms occurs through vertical
transmission of inherited mutations from previous generations and genetic recombination
of DNA by horizontal genetic exchange. Antibiotic resistance is exchanged between
different bacteria by plasmids that carry genes that encode antibiotic resistance that may
result in co-resistance to multiple antibiotics. These plasmids can carry different genes
with diverse resistance mechanisms to unrelated antibiotics but because they are located
on the same plasmid multiple antibiotic resistances to more than one antibiotic is
transferred. On the other hand, cross-resistance to other antibiotics within the bacteria
results when the same resistance mechanism is responsible for resistance to more than
one antibiotic is selected for.
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Causes
The widespread use of antibiotics both inside and outside of medicine is playing a
significant role in the emergence of resistant bacteria. Antibiotics are often used in
rearing animals for food and this use among others leads to the creation of resistant
strains of bacteria. In some countries antibiotics are sold over the counter without a
prescription which also leads to the creation of resistant strains. In supposedly well-
regulated human medicine the major problem of the emergence of resistant bacteria is
due to misuse and overuse of antibiotics by doctors as well as patients. Other practices
contributing towards resistance include the addition of antibiotics to the feed of livestock.
Household use of antibacterials in soaps and other products, although not clearly
contributing to resistance, is also discouraged (as not being effective at infection control).
Also unsound practices in the pharmaceutical manufacturing industry can contribute
towards the likelihood of creating antibiotic resistant strains.
Certain antibiotic classes are highly associated with colonisation with superbugs
compared to other antibiotic classes. The risk for colonisation increases if there is a lack
of sensitivity (resistance) of the superbugs to the antibiotic used and high tissue
penetration as well as broad spectrum activity against "good bacteria". In the case of
MRSA, increased rates of MRSA infections are seen with glycopeptides, cephalosporins
and especially quinolones. In the case of colonisation with C difficile the high risk
antibiotics include cephalosporins and in particular quinolones and clindamycin.
In medicine
The volume of antibiotic prescribed is the major factor in increasing rates of bacterial
resistance rather than compliance with antibiotics. A single dose of antibiotics leads to a
greater risk of resistant organisms to that antibiotic in the person for up to a year.
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Poor hand hygiene by hospital staff has been associated with the spread of resistant
organismsand an increase in hand washing compliance results in decreased rates of these
organisms.
Drugs are used in animals that are used as human food, such as cows, pigs, chickens, fish,
etc., and these drugs can affect the safety of the meat, milk, and eggs produced from
those animals and can be the source of superbugs. For example, farm animals,
particularly pigs, are believed to be able to infect people with MRSA. The resistant
bacteria in animals due to antibiotic exposure can be transmitted to humans via three
pathways, those being through the consumption of meat, from close or direct contact with
animals, or through the environment.
The World Health Organization concluded that antibiotics as growth promoters in animal
feeds should be prohibited (in the absence of risk assessments). In 1998, European Union
health ministers voted to ban four antibiotics widely used to promote animal growth
(despite their scientific panel's recommendations). Regulation banning the use of
antibiotics in European feed, with the exception of two antibiotics in poultry feeds,
became effective in 2006. In Scandinavia, there is evidence that the ban has led to a lower
prevalence of antimicrobial resistance in (non-hazardous) animal bacterial populations. In
the USA federal agencies do not collect data on antibiotic use in animals but animal to
human spread of drug resistant organisms has been demonstrated in research studies.
Antibiotics are still used in U.S. animal feedalong with other ingredients which have
safety concerns.
Growing U.S. consumer concern about using antibiotics in animal feed has led to a niche
market of "antibiotic-free" animal products, but this small market is unlikely to change
entrenched industry-wide practices.
In 2001, the Union of Concerned Scientists estimated that greater than 70% of the
antibiotics used in the US are given to food animals (e.g. chickens, pigs and cattle) in the
absence of disease. In 2000 the US Food and Drug Administration (FDA) announced
their intention to revoke approval of fluoroquinolone use in poultry production because of
substantial evidence linking it to the emergence of fluoroquinolone resistant
campylobacter infections in humans. The final decision to ban fluoroquinolones from use
in poultry production was not made until five years later because of challenges from the
food animal and pharmaceutical industries. Today, there are two federal bills (S. 549 and
H.R. 962) aimed at phasing out "non-therapeutic" antibiotics in US food animal producti
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Mechanis ms
Antibiotic resistanc e can be a result of ho rizontal gene transfer, and also of unlinked
point m utations in the pathoge n genome and a rate o f about 1 i n 108 per ch
romosomal replication. The an tibiotic action against the pathoge n can be se en as an
en vironment al pressure; those bacteria which have a mutation allow ing them to
survive w ill live on to reprodu ce. They w ill then pas s this trait to their offspring,
which will result in a fully resistant colony.
The fou r main mechanisms by which mic roorganism s exhibit resistance to antimicro
bials are:
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1. Drug inactivation or modification: e.g. enzymatic deactivation
of Penicillin G in some penicillinresistant bacteria through
the production of lactamases.
2. Alteration of target site: e.g. alteration of PBPthe
binding target site of penicillinsin MRSA and other
penicillinresistant bacteria.
3. Alteration of metabolic pathway: e.g. some sulfonamide
resistant bacteria do not require paraaminobenzoic acid
(PABA), an important precursor for the synthesis of folic acid and
nucleic acids in bacteria inhibited by sulfonamides. Instead, like
mammalian cells, they turn to utilizing preformed folic acid.
4. Reduced drug accumulation: by decreasing drug permeability
and/or increasing active efflux (pumping out) of the drugs
across the cell surface.
There are three known mechanisms of fluoroquinolone resistance. Some types of efflux
pumps can act to decrease intracellular quinolone concentration. In gram-negative
bacteria, plasmid-mediated resistance genes produce proteins that can bind to DNA
gyrase, protecting it from the action of quinolones. Finally, mutations at key sites in DNA
gyrase or Topoisomerase IV can decrease their binding affinity to quinolones, decreasing
the drug's effectiveness. Research has shown that the bacterial protein LexA may play a
key role in the acquisition of bacterial mutations giving resistance to quinolones and
rifampicin.
Resistant pathogens
1. Staphylococcus aureus
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This left vancomycin as the only effective agent available at the time. However, strains
with intermediate (4-8 ug/ml) levels of resistance, termed GISA (glycopeptide
intermediate Staphylococcus aureus) or VISA (vancomycin intermediate Staphylococcus
aureus), began appearing in the late 1990s. The first identified case was in Japan in 1996,
and strains have since been found in hospitals in England, France and the US. The first
documented strain with complete (>16 ug/ml) resistance to vancomycin, termed VRSA
(Vancomycin-resistant Staphylococcus aureus) appeared in the United States in 2002.
A new class of antibiotics, oxazolidinones, became available in the 1990s, and the first
commercially available oxazolidinone, linezolid, is comparable to vancomycin in
effectiveness against MRSA. Linezolid-resistance in Staphylococcus aureus was reported
in 2003.
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Penicillin-resistant pneumonia caused by Streptococcus pneumoniae (commonly known
as pneumococcus), was first detected in 1967, as was penicillin-resistant gonorrhea.
Resistance to penicillin substitutes is also known as beyond S. aureus. By 1993
Escherichia coli was resistant to five fluoroquinolone variants. Mycobacterium
tuberculosis is commonly resistant to isoniazid and rifampin and sometimes universally
resistant to the common treatments. Other pathogens showing some resistance include
Salmonella, Campylobacter, and Streptococci.
3. Pseudomonas aeruginosa
4. Clostridium difficile
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5. Salmonella and E. coli
Escherichia coli and Salmonella come directly from contaminated food. Of the meat that
is contaminated with E. coli, eighty percent of the bacteria are resistant to one or more
drugs made; it causes bladder infections that are resistant to antibiotics (HSUS Fact
Sheet). Salmonella was first found in humans in the 1970s and in some cases is resistant
to as many as nine different antibiotics (HSUS Fact Sheet). When both bacterium are
spread, serious health conditions arise. Many people are hospitalized each year after
becoming infected, and some die as a result.
6. Acinetobacter baumannii
On November 5, 2004, the Centers for Disease Control and Prevention (CDC) reported
an increasing number of Acinetobacter baumannii bloodstream infections in patients at
military medical facilities in which service members injured in the Iraq/Kuwait region
during Operation Iraqi Freedom and in Afghanistan during Operation Enduring Freedom
were treated. Most of these showed multidrug resistance (MRAB), with a few isolates
resistant to all drugs tested.
Alternatives
Prevention
There is clinical evidence that topical dermatological preparations containing tea tree oil
and thyme oil may be effective in preventing transmittal of CA-MRSA.
Vaccines do not suffer the problem of resistance because a vaccine enhances the body's
natural defenses, while an antibiotic operates separately from the body's normal defenses.
Nevertheless, new strains may evolve that escape immunity induced by vaccines; for
example an update Influenza vaccine is needed each year.
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duration of effectiveness of the antibodies produced. Development and testing of more
effective vaccines is under way.
Phage therapy
Phage therapy, an approach that has been extensively researched and utilized as a
therapeutic agent for over 60 years, especially in the Soviet Union, is an alternative that
might help with the problem of resistance. Phage therapy was widely used in the United
States until the discovery of antibiotics, in the early 1940s. Bacteriophages or "phages"
are viruses that invade bacterial cells and, in the case of lytic phages, disrupt bacterial
metabolism and cause the bacterium to lyse. Phage therapy is the therapeutic use of
lytic bacteriophages to treat pathogenic bacterial infections.
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Research
New medications
Until recently, research and development (R&D) efforts have provided new drugs in time to treat
bacteria that became resistant to older antibiotics. That is no longer the case.[citation needed] The
potential crisis at hand is the result of a marked decrease in industry R&D, and the increasing
prevalence of resistant bacteria. Infectious disease physicians are alarmed by the prospect that
effective antibiotics may not be available to treat seriously ill patients in the near future.
The pipeline of new antibiotics is drying up. Major pharmaceutical companies are losing interest
in the antibiotics market because these drugs may not be as profitable as drugs that treat chronic
(long-term) conditions and lifestyle issues.
The resistance problem demands that a renewed effort be made to seek antibacterial agents
effective against pathogenic bacteria resistant to current antibiotics. One of the possible
strategies towards this objective is the rational localization of bioactive phytochemicals. Plants
have an almost limitless ability to synthesize aromatic substances, most of which are phenols or
their oxygen-substituted derivatives such as tannins. Most are secondary metabolites, of which at
least 12,000 have been isolated, a number estimated to be less than 10% of the total .In many
cases, these substances serve as plant defense mechanisms against predation by microorganisms,
insects, and herbivores. Many of the herbs and spices used by humans to season food yield useful
medicinal compounds including those having antibacterial activity.
Traditional healers have long used plants to prevent or cure infectious conditions. Many of these
plants have been investigated scientifically for antimicrobial activity and a large number of plant
products have been shown to inhibit growth of pathogenic bacteria.A number of these agents
appear to have structures and modes of action that are distinct from those of the antibiotics in
current use, suggesting that cross-resistance with agents already in use may be minimal. For
example the combination of 5'-methoxyhydnocarpine and berberine in herbs like Hydrastis
canadensis and Berberis vulgaris can block the MDR-pumps that cause multidrug resistance.
This has been shown for Staphylococcus aureus.
Archaeocins is the name given to a new class of potentially useful antibiotics that are derived
from the Archaea group of organisms. Eight archaeocins have been partially or fully
characterized, but hundreds of archaeocins are believed to exist, especially within the
haloarchaea. The prevalence of archaeocins is unknown simply because no one has looked for
them. The discovery of new archaeocins hinges on recovery and cultivation of archaeal
organisms from the environment. For example, samples from a novel hypersaline field site,
Wilson Hot Springs, recovered 350 halophilic organisms; preliminary analysis of 75 isolates
showed that 48 were archaeal and 27 were bacterial.
In research published on October 17, 2008 in Cell, a team of scientists pinpointed the place on
bacteria where the antibiotic myxopyronin launches its attack, and why that attack is successful.
The myxopyronin binds to and inhibits the crucial bacterial enzyme, RNA polymerase. The
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myxopyronin changes the structure of the switch-2 segment of the enzyme, inhibiting its function
of reading and transmitting DNA code. This prevents RNA polymerase from delivering genetic
information to the ribosomes, causing the bacteria to die.
One of the major causes of antibiotic resistance is the decrease of effective drug concentrations
at their target place, due to the increased action of ABC transporters. Since ABC transporter
blockers can be used in combination with current drugs to increase their effective intracellular
concentration, the possible impact of ABC transporter inhibitors is of great clinical interest. ABC
transporter blockers that may be useful to increase the efficacy of current drugs have entered
clinical trials and are available to be used in therapeutic regimes.
Applications
The most commonly used antibiotics in genetic engineering are generally "older" antibiotics
which have largely fallen out of use in clinical practice. These include:
ampicillin
kanamycin
tetracycline
chloramphenicol
Industrially the use of antibiotic resistance is disfavored since maintaining bacterial cultures
would require feeding them large quantities of antibiotics. Instead, the use of auxotrophic
bacterial strains (and function-replacement plasmids) is preferred.
If this emerging public health threat is ignored, sooner or later the medical community could
be confronted with carbapenem-resistant (bacteria) that cause common infections, resulting
in treatment failures with substantial increases in health-care costs
Walsh and his international team collected bacteria samples from hospital patients
in two places in India, Chennai and Haryana, and from patients referred to Britains
national reference laboratory between 2007 and 2009.They found 44 NDM1
positive bacteria in Chennai, 26 in Haryana, 37 in Britain, and 73 in other sites in
Bangladesh, India, and Pakistan.
Experts commenting on Walshs findings said it was important to be alert to the new bug and
start screening for it early. It seems to be more dangerous than Swine flu, since it is working on
Resistance of Human body.
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Articles on superbug in news papers
A new hospital-acquired superbug that cannot be treated using existing drugs is spreading from
India to the rest of the world, claim British scientists. Indian surgeons rubbish the claim saying
its just another attempt to stop thousands of pounds from leaving the floundering British
economy to
related stories
0 Linking India to superbug unfair and wrong, says India
0 Govt condemns naming of superbug, refutes its linkage
0 Some interpretations made without my knowledge: Superbug author
According to CII estimates, 1.1 million foreigners travel to India each year for cheaper
treatments and surgeries. A heart bypass surgery costs $6,500 (R 3,03,550) in a corporate
hospital in India, as compared to $30,000 (R 14,01,000)to $50,000 (R 23,35,000) in the US.
So convinced are British scientists about the superbug infection being fuelled by Indias Rs
1,200-crore medical tourism industry that they have chosen to provocatively name the
newly-identified gene that causes the drug resistance as the New Delhi metallo-beta-
lactamase (NDM-1).
A study published in The Lancet Infectious Diseases, British scientists report NDM-1 is
becoming more common in Bangladesh, India, and Pakistan and is being imported back
to Britain through patients returning after treatment.
Healthcare experts in India say the British are just worried because they are losing patients to
hospitals here. Its a false alarm, I track infection and have not seen a single case in my
hospital. Hospital-acquired infections are far more common in Britain and the West than
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in India, said Dr Yatin Mehta, chairman, institute of critical care and
anaesthesia, Medanta The Medicity.
We offer better surgical outcomes at one-fifth the cost, he added. Dr Ashok Seth,
chairman and chief interventionist, Escorts Heart Institute and Research Centre said,
Most hospitals in India, including Escorts, have national and international
accreditations... who send auditors to track quality including infections four times
a year. The audits show that corporate hospitals here are safer than the West. Theyre
definitely safer than Britains National Health Service.
For the study, author Timothy Walsh from Cardiff University and his team collected
bacteria samples from patients admitted in hospitals in Tamil Nadu and Haryana, and
from patients referred to Britains national reference laboratory between 2007 and 2009.
Several not all British NDM-1 positive patients had recently traveled to India or
Pakistan for hospital treatment, including cosmetic surgery.
The 'superbug' resistant to almost all known antibiotics has been found in
UK patients treated in Indian hospitals. Named after the Indian capital, it is
a gene carried by bacteria that causes gastric problems, enters the blood
stream and may cause multiple organ failure leading to death.
" India also provides cosmetic surgery for Europeans and Americans, and it
is likely the bacteria will spread worldwide," scientists reported in The
Lancet Infectious Diseases Journal on Wednesday. While the study has the
medical world turning its focus on infection control policies in Indian
hospitals, the Indian Council of Medical Research has alleged a bias in the
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report and said it is an attempt to hurt medical tourism in the country that
is taking away huge custom from hospitals in the West. "Such infections can
flow in from any part of the world. It's unfair to say it originated from India,"
said ICMR director Dr VM Katoch.
Katoch has reasons to fume, as the superbug NDM1 ( New Delhi metallo
betalactamase) is named after the national capital, where a Swedish
patient was reportedly infected after undergoing a surgery in 2008. Since
then there have been several cases reported in the UK and in 2009, the
health protection agency in the UK issued an alert on the 'gram negative'
bacterial infection that is resistant to even the most powerful and reserved
class antibiotics called carbapenems.
What makes the superbug more dangerous is its ability to jump across
different bacterial species. So far, it has been found in two commonly
seen bacteria, E coli and K pneumoniae. "We have found that the
superbug has the potential to get copied and transferred between
bacteria, allowing it to spread rapidly. If it spreads to an already hard
totreat bacterial infection, it can be turn more dangerous,"
Kumarasamy said.
For a long time, India has been seeing Extended Spectrum Beta
Lactamase (ESBL), which are enzymes that have developed a resistance to
antibiotics like penicillin. ESBL enzymes are most commonly produced by
two bacteria E coli and K pneumoniae, the two bacteria in which the new
superbug has been found. "These were treated by a reserved class of
antibiotics called carbapenems. We have seen at least 3% of people
infected with this do not react to these reserved drugs," he said.
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and India, as a medical hub, should be geared for the challenge. Katoch,
who is also the secretary, department of medical research, agrees. "At
present, we don't have any system in place. There are neither rules for
hospitals nor a registry to record hospitalacquired infections. We are now
in the process of forming a cell that will activate a registry and issue
guidelines for an integrated surveillance system," he said.
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Conclusion-
On the basis of above information we can say that
antibiotics has to be take in low amount otherwise
it effect is worst than its advantage. Therefore
antibiotics are good but within limited value.
Result-
09Antibiotics are good but within limited value.
09Its disadvantage dominates to is
advantage.
09Deaths of people increases with time due to
antibiotic resitance.
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Bibliography
-
www.wikipedia.com
www.google.com
www.newsnet.com
www.technopedia.com
-Hindustan times
-navbharat times
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