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Antibiotic resistance
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Antibiotic resistance is the ability of a microorganism to withstand the effects of

antibiotics. It is a specific type of drug resistance. Antibiotic resistance evolves via
natural selection acting upon random mutation, but it can also be engineered by applying
an evolutionary stress on a population. Once such a gene is generated, bacteria can then
transfer the genetic information in a horizontal fashion (between individuals) by plasmid
exchange. If a bacterium carries several resistance genes, it is called multiresistant or,
informally, a superbug. The term antimicrobial resistance is sometimes used to
explicitly encompass organisms other than bacteria.

Antibiotic resistance can also be introduced artificially into a microorganism through

transformation protocols. This can aid in implanting artificial genes into the
microorganism. If the resistance gene is linked with the gene to be implanted, the
antibiotic can be used to kill off organisms that lack the new gene.

Contents
[hide]

• 1 Causes and risk factors

• 2 Mechanisms
• 3 Resistant pathogens
o 3.1 Staphylococcus aureus
o 3.2 Streptococcus and Enterococcus
o 3.3 Pseudomonas aeruginosa
o 3.4 Clostridium difficile
o 3.5 Salmonella and E. coli
o 3.6 Acinetobacter baumannii
• 4 Role of animals
• 5 Alternatives
o 5.1 Prevention
o 5.2 Phage therapy
• 6 Development of new drugs
• 7 Applications
• 8 See also
 • 9 References
• 10 Footnotes

• 11 External links

[edit] Causes and risk factors

Schematic representation of how antibiotic resistance evolves via natural selection. The
top section represents a population of bacteria before exposure to an antibiotic. The
middle section shows the population directly after exposure, the phase in which selection
took place. The last section shows the distribution of resistance in a new generation of
bacteria. The legend indicates the resistance levels of individuals.

Antibiotic resistance can be a result of horizontal gene transfer[1], and also of unlinked
point mutations in the pathogen genome and a rate of about 1 in 108 per chromosomal
replication. The antibiotic action against the pathogen can be seen as an environmental
pressure; those bacteria which have a mutation allowing them to survive will live on to
reproduce. They will then pass this trait to their offspring, which will result in a fully
resistant colony.

Several studies have demonstrated that patterns of antibiotic usage greatly affect the
number of resistant organisms which develop[citation needed]. Overuse of broad-spectrum
antibiotics, such as second- and third-generation cephalosporins, greatly hastens the
development of methicillin resistance. Other factors contributing towards resistance
include incorrect diagnosis, unnecessary prescriptions, improper use of antibiotics by
patients, the impregnation of household items and children's toys with low levels of
antibiotics, and the administration of antibiotics by mouth in livestock for growth
promotion.

Researchers have recently demonstrated the bacterial protein LexA may play a key role
in the acquisition of bacterial mutations.[2]

[edit] Mechanisms
The four main mechanisms by which microorganisms exhibit resistance to antimicrobials
are:

1. Drug inactivation or modification: e.g. enzymatic deactivation of Penicillin G in

some penicillin-resistant bacteria through the production of β-lactamases.
2. Alteration of target site: e.g. alteration of PBP—the binding target site of
penicillins—in MRSA and other penicillin-resistant bacteria.
3. Alteration of metabolic pathway: e.g. some sulfonamide-resistant bacteria do not
require para-aminobenzoic 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.[3]
5. 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.[4]

[edit] Resistant pathogens

[edit] Staphylococcus aureus

Staphylococcus aureus (colloquially known as "Staph aureus" or a Staph infection) is one

of the major resistant pathogens. Found on the mucous membranes and the skin of around
a third of the population, it is extremely adaptable to antibiotic pressure. It was the first
bacterium in which penicillin resistance was found—in 1947, just four years after the
drug started being mass-produced. Methicillin was then the antibiotic of choice, but has
since been replaced by oxacillin due to significant kidney toxicity. MRSA (methicillin-
resistant Staphylococcus aureus) was first detected in Britain in 1961 and is now "quite
common" in hospitals. MRSA was responsible for 37% of fatal cases of blood poisoning
in the UK in 1999, up from 4% in 1991. Half of all S. aureus infections in the US are
resistant to penicillin, methicillin, tetracycline and erythromycin.

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.

CA-MRSA (Community-acquired MRSA) has now emerged as an epidemic that is

responsible for rapidly progressive, fatal diseases including necrotizing pneumonia,
severe sepsis and necrotizing fasciitis.[5] Methicillin-resistant Staphylococcus aureus
(MRSA) is the most frequently identified antimicrobial drug-resistant pathogen in US
hospitals. The epidemiology of infections caused by MRSA is rapidly changing. In the
past 10 years, infections caused by this organism have emerged in the community. The 2
MRSA clones in the United States most closely associated with community outbreaks,
USA400 (MW2 strain, ST1 lineage) and USA300, often contain Panton-Valentine
leukocidin (PVL) genes and, more frequently, have been associated with skin and soft
tissue infections. Outbreaks of community-associated (CA)-MRSA infections have been
reported in correctional facilities, among athletic teams, among military recruits, in
newborn nurseries, and among active homosexual men. CA-MRSA infections now
appear to be endemic in many urban regions and cause most CA-S. aureus infections.[6]

[edit] Streptococcus and Enterococcus

Streptococcus pyogenes (Group A Streptococcus: GAS) infections can usually be treated

with many different antibiotics. Early treatment may reduce the risk of death from
invasive group A streptococcal disease. However, even the best medical care does not
prevent death in every case. For those with very severe illness, supportive care in an
intensive care unit may be needed. For persons with necrotizing fasciitis, surgery often is
needed to remove damaged tissue.[7] Strains of S. pyogenes resistant to macrolide
antibiotics have emerged, however all strains remain uniformly sensitive to penicillin.[8]

Resistance of Streptococcus pneumoniae to penicillin and other beta-lactams is increasing

worldwide. The major mechanism of resistance involves the introduction of mutations in
genes encoding penicillin-binding proteins. Selective pressure is thought to play an
important role, and use of beta-lactam antibiotics has been implicated as a risk factor for
infection and colonization. Streptococcus pneumoniae is responsible for pneumonia,
bacteremia, otitis media, meningitis, sinusitis, peritonitis and arthritis.[8]

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.

Enterococcus faecium is another superbug found in hospitals. Penicillin-Resistant

Enterococcus was seen in 1983, vancomycin-resistant enterococcus (VRE) in 1987, and
Linezolid-Resistant Enterococcus (LRE) in the late 1990s.

[edit] Pseudomonas aeruginosa

Pseudomonas aeruginosa is a highly prelevant opportunistic pathogen. One of the most

worrisome characteristics of P. aeruginosa consists in its low antibiotic susceptibility.
This low susceptibility is attributable to a concerted action of multidrug efflux pumps
with chromosomally-encoded antibiotic resistance genes (e.g. mexAB-oprM, mexXY etc)
and the low permeability of the bacterial cellular envelopes. Besides intrinsic resistance,
P. aeruginosa easily develop acquired resistance either by mutation in chromosomally-
encoded genes, or by the horizontal gene transfer of antibiotic resistance determinants.
Development of multidrug resistance by P. aeruginosa isolates requires several different
genetic events that include acquisition of different mutations and/or horizontal transfer of
antibiotic resistance genes. Hypermutation favours the selection of mutation-driven
antibiotic resistance in P. aeruginosa strains producing chronic infections, whereas the
clustering of several different antibiotic resistance genes in integrons favours the
concerted acquisition of antibiotic resistance determinants. Some recent studies have
shown that phenotypic resistance associated to biofilm formation or to the emergence of
small-colony-variants may be important in the response of P. aeruginosa populations to
antibiotics treatment.[9]

[edit] Clostridium difficile

Clostridium difficile is a nosocomial pathogen that causes diarrheal disease in hospitals

world wide.[10][11] Clindamycin-resistant C. difficile was reported as the causative agent of
large outbreaks of diarrheal disease in hospitals in New York, Arizona, Florida and
Massachusetts between 1989 and 1992.[12] Geographically dispersed outbreaks of C.
difficile strains resistant to fluoroquinolone antibiotics, such as Cipro (ciprofloxacin) and
Levaquin (levofloxacin), were also reported in North America in 2005.[13]

[edit] Salmonella and E. coli

E. 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.
[edit] Acinetobacter baumannii

On the 5th November 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.[14][15]

[edit] Role of animals

Methicillin Resistant Staphylococcus Aureus (MRSA) is acknowledged to be a human
commensal and pathogen. MRSA has been found in cats, dogs and horses, where it can
cause the same problems as it does in humans. Owners can transfer the organism to their
pets and vice-versa, and MRSA in animals is generally believed to be derived from
humans.

This article may be inaccurate in or unbalanced towards certain viewpoints.

Please improve the article by adding information on neglected viewpoints, or
discuss the issue on the talk page.

The United States Food and Drug Administration has responsibility for determining the
safety of food as well as drugs. Drugs are frequently used for animals the same way they
are used in people – to treat illness and improve the health of the animals. 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.
Therefore, FDA has the responsibility to review drugs intended for use in food animals,
and to be sure that the use of the drugs does not result in harmful residues in food or
create resistant pathogens that can harm human health. For example, farm animals,
particularly pigs, are believed to be able to infect people with MRSA.[16] In 1951, the
FDA approved the use of antibiotics in animal feed without a veterinary medical
prescription; Concerns about resistance have been revisited several times since then, and
most antimicrobials have not been shown to be a hazard. Europe quickly followed suit.
As the spread of drug-resistant bacteria became a concern, countries began questioning
the practice. In 1969, Britain issued the Swann Report[17], which recommended that
human therapeutic antibiotics be banned from being used as growth promoters in
agriculture. The report was largely ignored. It's pointed out by industry, that most of the
routine feed drugs are either not used in human medicine, or are older compounds that
have long been superseded by later-generation drugs.

Nearly 30 years later, the World Health Organization concluded that antibiotics as growth
promoters in animal feeds should be prohibited (in the absence of risk assessments). And
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.[18] With good animal husbandry and hygiene,
there shouldn't be adverse effects, health-wise or production-wise, from not using
antibiotics in animal feed. In Scandinavia, there's evidence that the ban has led to a lower
prevalence of antimicrobial resistance in (non-hazardous) animal bacterial populations.[19]
Meanwhile, in the poultry industry, the ban hasn't had a deleterious effect. Economic
performance in poultry production wasn't adversely affected either. Whether banning feed
drugs has had any actual benefit to public health has been the topic of several reviews.
Foodborne incidence and resistance patterns in humans, have not declined in countries
featuring animal bans, in fact some have increased. Meanwhile, there were higher
mortality in swine populations following bans. the "success" of Scandinavain and EU
bans is therefore highly questionable as a useful policy, according to several published
reviews. In the United States, antibiotic use in animal feeds remains controversial, due to
a well-financed anti-agricultural campaign.[citation needed] The FDA first called for restrictions
in 1997[20], which generated many studies and reports on the issue. In 1980, the Institute
of Medicine reviewed the subject and recommended that more studies be conducted.[21] In
1999, the General Accounting Office (GAO) also concluded that the evidence was
inconclusive. A follow-up 2004 GAO study[22] found that evidence existed of antibiotic-
resistant bacteria being transferred from animals to humans. But since federal agencies
don't collect data on antibiotic use in animals, conclusions on the potential impact on
human health couldn't be made. Therefore, antibiotics are still used in U.S. animal feed—
along with evidence of other worrisome ingredients.[23][24]

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.[25] Within FDA, the animal drug review duties have
been assigned to one of the Agency’s operating units, the Center for Veterinary Medicine.
Their guidance is used to evaluate all types and uses of antimicrobials, including what
some refer to as subtherapeutic use. Although that term has not been defined by
regulation, it describes the use of a product to boost an animal’s ability to grow and
produce more food, instead of treating or preventing an infectious disease. It could also
be used to evaluate antimicrobials if they are used for growth promotion, and for
antimicrobials that are products of genetic engineering. Antimicrobials are used with
animals that we use to produce food for human consumption, including cows (for beef
and milk production), pigs, chickens, turkeys, fish, and sheep, to increase production.
Antimicrobials are used in feeds for some species, and the animals fed the antimicrobial
feeds often grow faster while consuming less feed than animals not given antimicrobials
in feed. In addition to determining whether the use of a drug would result in residues left
in the meat, milk, or eggs, FDA must ensure that the use of antimicrobials in food-
producing animals does not lead to the development of resistant bacteria that can become
a public health concern. This document[clarification needed] is one way that drug sponsors can
submit information that address the issue of the microbial safety of antimicrobial new
animal drugs. A sponsor is free to use other scientifically valid approaches to demonstrate
the safety of their proposed product. CVM first said in December 1999 that it would
consider the question of the fostering of antimicrobial resistance when reviewing
antimicrobials for use in animals. That announcement was followed a year later with
what was called FDA’s “Framework Document,” which first described the FDA’s plan to
use risk assessments of the development of antimicrobial resistance in determining the
safety of antimicrobials for food-producing animals. The guidance document was first
published as a draft in September 2002, to allow the scientific community to comment on
the concept and on the science FDA used to develop the guidance document. The FDA
allows the use of antimicrobials because they are a valuable tool that veterinarians can
use to treat sick animals, and so livestock producers can use antimicrobials to produce
meat, milk, and eggs more efficiently.

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[26]. This 2001 report, however, has been shown to over-estimate animal
usage rates. Antibiotic use in food animal production has been associated with the
emergence of antibiotic-resistant strains of bacteria including Salmonella,
Campylobacter, Escherichia coli and Enterococcus, among others. There is substantial
evidence from the US and European Union that these resistant bacteria cause antibiotic-
resistant infections in humans[citation needed]. The American Society for Microbiology
(ASM)[citation needed], the American Public Health Association (APHA) and the American
Medical Association (AMA) have called for substantial restrictions on antibiotic use in
food animal production including an end to all "non-therapeutic" uses. The food animal
and pharmaceutical industries have fought hard to prevent new regulations that would
limit the use of antibiotics in food animal production, pointing out that while concerns
exist, risk assessments and actual data have demonstrated little to no risk in this area. For
example, in 2000 the US Food and Drug Administration (FDA) announced their intention
to rescind approval for 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 5 years later because of challenges from the food animal
and pharmaceutical industries.[27] Today, there are two federal bills (S. 549[28] and H.R.
962[29]) aimed at phasing out "non-therapeutic" antibiotics in US food animal production.
These bills are nominally endorsed by many public health and medical organizations
including the American Nurses Association (ANA))[citation needed], the American Academy of
Pediatrics (AAP)[citation needed], and the American Public Health Association (APHA)[citation
needed]
. Other professional groups, notably animal science, food science, veterinary, and
industry groups do not support this legislation, however, pointing out that current uses are
not shown to be hazardous and have legitimate disease prevention roles.

[edit] Alternatives
[edit] Prevention

Rational use of antibiotics may reduce the chances of development of opportunistic

infection by antibiotic-resistant bacteria due to dysbacteriosis. In one study the use of
fluoroquinolones are clearly associated with Clostridium difficile infection, which is a
leading cause of nosocomial diarrhea in the United States,[30] and a major cause of death,
worldwide.[31]
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.

While theoretically promising, anti-staphylococcal vaccines have shown limited efficacy,

because of immunological variation between Staphylococcus species, and the limited
duration of effectiveness of the antibodies produced. Development and testing of more
effective vaccines is under way.

The Commonwealth Scientific and Industrial Research Organization (CSIRO), realizing

the need for the reduction of antibiotic use, has been working on two alternatives. One
alternative is to prevent diseases by adding Cytokines instead of antibiotics to animal
feed. These proteins are made in the body naturally after a disease, so they do not
contribute to making antibiotics resistant (“Alternatives to Antibiotics”). Furthermore,
studies on using Cytokines have shown that they also enhance the growth of animals like
antibiotics. Cytokines do not endanger human health because they are a natural protein.
Secondly, CSIRO is working on vaccines for diseases. If the animals were vaccinated for
the disease, then farms wouldn’t have to be worries about diseases spreading. Also, it
would save money for the farmers by protecting animals from dying (“Alternatives to
Antibiotics”). Both alternatives provide safe ways to prevent diseases without the use of
antibiotics.

[edit] 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.[32][33][34]

Bacteriophage therapy is an important alternative to antibiotics in the current era of

multidrug resistant pathogens. A review of studies that dealt with the therapeutic use of
phages from 1966–1996 and few latest ongoing phage therapy projects via internet
showed: phages were used topically, orally or systemically in Polish and Soviet studies.
The success rate found in these studies was 80–95% with few gastrointestinal or allergic
side effects. British studies also demonstrated significant efficacy of phages against
Escherichia coli, Acinetobacter spp., Pseudomonas spp and Staphylococcus aureus. US
studies dealt with improving the bioavailability of phage. Phage therapy may prove as an
important alternative to antibiotics for treating multidrug resistant pathogens.[35][36]

[edit] Development of new drugs

This article needs additional citations for verification.
Please help improve this article by adding reliable references. Unsourced material may be
 challenged and removed. (January 2008)

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. 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.[37]

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[citation needed]. 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.[38][39][40]

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.[41]

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.[42]

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 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.[43]

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.[3]

[edit] Applications
Antibiotic resistance is an important tool for genetic engineering. By constructing a
plasmid which contains an antibiotic resistance gene as well as the gene being engineered
or expressed, a researcher can ensure that when bacteria replicate, only the copies which
carry along the plasmid survive. This ensures that the gene being manipulated passes
along when the bacteria replicates.

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.