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MRSA strains carry an extra gene (mecA) that encodes a penicillin binding protein (called PBP2a) that replaces the wildtype penicillin binding proteins when any drug related to penicillin is present. SCCmec type IV, containing ccr allotype 2 and mec class A, is the type of SCCmec  that has become a genetic marker for community-associated MRSA in a variety of ancestral lineages around the globe.  In contrast to the healthcare associated SCCmec types, mecIV does not usually contain any other antibiotic resistance genes besides mecA. The designation of USA300 refers to the SmaI restriction fragment pattern of the strain resolved by pulsed field gel electrophoresis.  The significance of USA300 is that it is currently highly prevalent as a cause of skin and soft tissue infection, necrotizing pneumonia, and sepsis in individuals with little or no risk factors for healthcare- associated MRSA infection. Why is Panton Valentine Leukocidin (PVL) important for the virulence of community–associated MRSA? As a result of consumer concern about food safety, the association between animal and human health has become a prominent issue.
While most of the curing agents and procedures used to date have demonstrated certain levels of success in curing antibiotic resistant bacteria, there is still much work to be done. DNA through an electrical field, the gel will be stained with methylene blue, a dye which binds to DNA. Information about Drugs Antibiotic ResistanceAntibiotic ResistanceAntibiotic Resistance is the adaptation of bacterial strains to certain of the ANTIBIOTIC MEDICATIONS doctors prescribe to treat infections the BACTERIA cause, rendering the antibiotic ineffective. Bacteria are single-cell microorganisms that exist in broad families with numerous strains, or variations, within the same family. Antibiotics kill bacteria, either by direct toxicity to the bacteria or by preventing the bacteria from reproducing. Spontaneous MUTATION is when changes occur within the DNA alter the bacteria’s adaptive ability across the bacterial strain. Transformation is when the DNA from resistant bacteria enter another bacteria that are not yet resistant.
Plasmid transfer is when plasmids (molecules that contain incomplete fragments of genetic material) move among different kinds of bacteria. Resistance resulting from spontaneous, or evolutionary, mutation is the most common adaptation process and accounts for most of the resistant strains of GONORRHEA and Staphylococcus aureus infections.
Antibiotic use itself is the precipitating factor for the adaptive changes that occur in bacteria to result in antibiotic resistance, as these changes represent natural survival efforts. Inappropriate prescribing of antibiotics for infections that are viral or of uncertain cause.
Failing to complete the full course of antibiotic therapy, which allows some bacteria to escape eradication.
Prophylactic antibiotics given to food animals such as cattle, pigs, and chickens to prevent them from getting infections that slow their growth. The most effective measure for reducing antibiotic resistance is to decrease the use of antibiotics. Wash hands frequently with soap and warm water to prevent the spread of infection-causing bacteria and other pathogens. Health experts also are reexamining the practice of ANTIBIOTIC PROPHYLAXIS (administering antibiotics to prevent infection in people who are IMMUNOCOMPROMISED or exposed to risk for NOSOCOMIAL INFECTIONS). Conjugation:Transfer of genetic material (usually plasmids) from one bacterium to another through the mediation of sex pili.
A variation in the phenotype of a microorganism, where the genetic constitution remains unchanged is a non-heritable variation.
S-R variation in Salmonella typhi that is characterized by loss of O antigen and change in colony morphology to rough type. Complex genetic arrays (staphylococcal chromosomal cassette mec elements or the vanA operon) have been acquired by S.
In 1952 an experiment conducted by Joshua and Esther Lederberg showed that penicillin-resistant bacteria existed before penicillin treatment. In 1962, the presence of penicillinase was detected in dormant Bacillus licheniformis endospores, revived from dried soil on the roots of plants, preserved since 1689 in the British Museum. Six strains of Clostridium, found in the bowels of William Braine and John Hartnell (members of Franklin Expedition) showed resistance to cefoxitin and clindamycin.
Nonetheless there is an evidence that heavy metals and some pollutants may select for antibiotic-resistant bacteria, generating a constant source of them in small numbers. Since then, many more antibiotics isolated from fungi (molds) and bacteria have been used to treat a wide range of human and animal infections. One group of bacteria, the Streptomyces, produces most of the medically important antibiotics.Streptomyces release antibiotics into the soil in a sort of "biochemical warfare" scenario to eliminate competing organisms from their environment. Other antibiotics, such as penicillin, block the assembly of the bacterial cell wall causing it to weaken and burst.
The production of antibiotics by these organisms provides them with a competitive advantage over non-resistant bacteria in their environment. Interestingly, all three types of antibiotic-resistant genes that produce efflux pumps, ribosomal protection proteins, and modifying enzymes are found in Streptomyces species, the producers of many antibiotics. A unique bacterial characteristic that has not been demonstrated in plant and animal cells is the ability to transfer genes from one bacterium to another, a process called lateral gene transfer. This allows a species of bacteria to possess enough genetic variability to adapt to a changing environment and to compete with its neighbors.
While this directly contradicts the claims made by many proponents of evolution, the molecular data for antibiotic resistance are very clear. This cost of a€?relative fitnessa€? appears to vary considerably depending on both the organism and the antibiotic. A recent study published by Ramchandani and coworkers (2005) found that many of the Escherichia coli strains responsible for urinary tract infections in women can be traced back to E. The development of functional foods (German et al., 1999) and the desire to decrease antibiotic use in animal feeds, have led researchers to evaluate potential alternatives to highly toxic curing compounds.
Effect of a yeast cell wall extract on prevalence of ampicillin-resistant Salmonella over time.Figure 4.
Such adaptation is an evolutionary mechanism that allows the strain of bacteria to survive.
Under supportive circumstances each individual strain can cause unique and specific infections.
Antibiotics are effective for treating only bacterial infections; they cannot treat viral infections. Resistance due to spontaneous mutation, also called evolutionary mutation, develops over multiple generations of the bacterial strain. Also called DNA uptake, transformation expedites the mutation process to allow bacterial strains to become more rapidly resistant than they would through spontaneous mutation. Plasmids impart limited genetic encoding related primarily to the survivability of a bacterial strain and can result in rapid adaptation to produce antibiotic resistance. Transformation, or DNA uptake, is a more sophisticated, biologically intentional process than spontaneous mutation. The US Centers for Disease Control and Prevention (CDC) believes about half of the 100 million antibiotic prescriptions US doctors write each year are unnecessary because the conditions they are treating are not bacterial.
It is important to take a therapeutic antibiotic long enough to kill all the bacter ia, extending through their complete life cycle, that are causing infection. The constant exposure to the same antibiotics fosters adaptive mutation in bacteria that may then become infective agents in people. The US Food and Drug Administration (FDA), which oversees drug approval and prescribing practices in the United States, issued new regulations in 2003 that establish stringent criteria for doctors to follow in prescribing antibiotics and is spearheading public education efforts to improve public awareness of antibiotic resistance.
Genotypic variation can occur as a result of changes in the genes by way of mutation, loss or acquisition of new genetic elements. Phenotypic variations are seen temporarily when bacteria are grown under certain environmental conditions. Any property that is coded on a transmissible plasmid can be transferred to a recipient bacterium.
Only those strains of Corynebacterium diphtheriae that are infected by a beta phage are toxigenic. Such variations are seen due to a change in environmental conditions and such variations are neither permanent nor heritable. While experimenting at the University of Wisconsin-Madison, Joshua Lederberg and his graduate student Norton Zinder also demonstrated preexistent bacterial resistance to streptomycin. It was suggested that penicillinase may have emerged as a defense mechanism for the bacteria in their habitats, as in the case of penicillinase-rich Staphylococcus aureus, living with penicillin-producing Trichophyton. By the 1940s, penicillin was available for medical use and was successfully used to to treat a wide range of infections. These antibiotics are small molecules that attack different parts of an organism's cellular machinery.
Penicillin is an effective antibiotic for human diseases because it interferes with a biological component in bacteria (cell wall) not found in human cells. Just as large organisms such as plants and animals must compete for living space, food, and water, these microbes use antibiotics to eliminate competition with other microbes for these same resources. Many possess genes that encode proteins to neutralize the affects of antibiotics and prevent attacks on their cell machinery.Efflux pumps, located in the cell membrane, are one method of protection that many bacteria use against the influx of antibiotics.
It appears this is the method Streptomyces uses to protect itself from its own antibiotics.
Mutations in rdxA can prevent synthesis of a functional NADPH nitroreductase activity, which prevents metronidazole from becoming activated.
However, a mutation that causes loss of regulatory control (in this case the repressor protein, MarR) does not offer a genetic mechanism that can account for the origin of this regulatory control.
The potential for effective curing of antibiotic resistant bacteria with non-toxic natural alternatives would revolutionize both animal and human health care regimes. Though in most situations the strain of bacteria remains sensitive to other antibiotics even as it develops resistance to a particular antibiotic, antibiotic resistance is a very serious concern in modern health care because the more common strains of bacteria are developing broad bases of resistance to multiple antibiotics.
Most bacteria that cause INFECTION in people are normally present in the body and the environment.
Chronic conditions such as BRONCHITIS and OTITIS media (middle EAR infection) are often viral, yet are among the top ailments for which doctors prescribe antibiotics. These adaptations include increased resistance to the antibiotics that people take to fight the infections the strain causes. Because antibiotic resistance has become a key purpose of plasmid transfer, researchers designate such plasmids as R plasmids. Among the three mutation processes plasmid transfer is the most efficient and creates the greatest concern in regard to antibiotic resistance.

Bacteria that are exposed to the antibiotic but do not die have the opportunity to undergo adaptive mutation, which results in antibiotic resistance.
Humans become vulnerable to infection from resistant bacteria through eating meat from treated animals that is not thoroughly cooked, which allows the bacteria to enter the body.
Most of these mutants die, but a when a mutant can adapt itself to the environment more readily; it may emerge as a new variant.
Change from R form of Streptococcus pneumoniae to S form as demonstrated by Griffith is due to transformation. Properties such drug resistance mediated by beta-lactamases, bacteriocin production etc can be transferred by conjugation. These genes may be transferred from non-disease-causing bacteria to those that do cause disease, leading to clinically significant antibiotic resistance. Streptomyces-produced quinolone and coumarin antibiotics, such as novobiocin, interfere with a protein called gyrase that assists in the normal separation of double-stranded DNA during replication of DNA or transcription of messenger RNA. The offensive antibiotic is pumped out of a cell that possesses these pumps before the antibiotic can cause harm to the cellular machinery.
Aminoglycoside antibiotic-inactivation enzymes in actinomycetes similar to those present in clinical isolates of antibiotic-resistant bacteria. Tetracycline antibiotics: mode of action, applications, molecular biology, and epidemiology of bacterial resistance.
Even more significantly many of these organisms were found to be resistant to a variety of antibiotics, which often results in increased treatment cost and rehabilitation time. These natural alternatives may act to cure the bacteria of their potentially hazardous plasmids or inhibit the organism’s ability to share the plasmid with neighboring bacteria in the environment. A few strains have mutated to resist all available antibiotics, presenting a worrisome challenge for fighting the infections they cause. Ordinarily these bacteria are harmless or even beneficial to body functions, such as the bacteria in the gastrointestinal tract that aid in digestion. It is not possible to determine the cause of an infection by evaluating the symptoms, though certain characteristics make it more likely that an infection is bacterial.
Plasmids can transfer among different strains of bacteria within a bacterial family, sharing adaptive mutations for multiple resistance.
Search for a penicillinase ancestor has focused on the class of proteins that must be a priori capable of specific combination with penicillin.
Failure of DNA to properly separate during these processes results in a bacterium not being able to divide normally or produce functional proteins. Although many efflux pumps may be specific for the substrate they pump out of the cell, they are not uncommon.
Proceedings of the National Academy of Sciences USA 172:3628-3632) The efflux pumps that Streptomyces use to pump out antibiotics to eliminate their competitors are likely the same pumps that other species of bacteria are now using to pump out the offensive antibiotic delivered from Streptomyces! Until recently, researchers were only interested in the development of antibiotic resistance one antibiotic at a time.
The effect of antibiotic usage in food animals on the development of antimicrobial resistance of importance for human in Campylobacter and Escherichia coli. Only a laboratory culture of cells from the infection, in which cells of a bacterial strain may or may not grow in the lab, can identify the cause of an infection as bacterial. Plasmid transfer accounts for resistance to entire classifications of drugs such as the quinolones, a family of antibiotics that attack enzymes that facilitate DNA cleavage (the division of DNA in preparation for cell reproduction) in bacteria.
Examples include methicillin resistance in Staphylococcus aureus, Multi-drug resistance in Mycobacterium tuberculosis. The resistance to cefoxitin and clindamycin in turn was speculatively attributed to Braine's and Hartnell's contact with microorganisms that naturally produce them or to random mutation in the chromosomes of Clostridium strains. Ribosomes, the structures where protein synthesis is catalyzed, are the targets of many other Streptomyces antibiotics such as spectinomycin, tetracycline, and streptomycin. Ribosomal protection proteins (RPP) are another source of resistance bacteria use to protect themselves from antibiotics.
The antibiotic-resistant bacteria likely have acquired the genes for these efflux pumps through lateral gene transfer. Today we know that it is much more common for antibiotic resistant bacteria to be resistant to two or more compounds.
Bacteria have adopted many survival mechanisms that neutralize the beneficial effects of antibiotics.Unfortunately, bacteria are also very accustomed to sharing this survival mechanism within the wider bacterial population. Spectinomycin and tetracycline prevent proteins from being assembled by the cell and streptomycin induces the assembly of the wrong amino acids into the translated protein.
Unfortunately, neither banning antibiotics, surveys, changes in production practices or hospital drug utilization, nor curing of plasmids (when implemented alone) will dramatically reduce the problem of antibiotic resistance. The change in the ribosome shape prevents an antibiotic from binding and interfering with protein synthesis. Simply one solution alone will not eliminate the ability of bacteria to resist the effects of antibiotics. The slight differences between human ribosomes which are not bound by these antibiotics and bacterial ribosomes make this type of antibiotic ideal for treating many illnesses. The RPP-bound ribosomes are able to function normally during protein synthesis, an important feature of this method of antibiotic resistance.
The solution to this complex issue is an aggressive multi-level approach that will include all of these strategies. Some bacteria produce enzymes that neutralize antibiotics by adding acetyl (COCH3) or phosphate (PO32-) groups to a specific site on the antibiotic.This modification reduces the ability of the antibiotic to bind to ribosomes, rendering it harmless to the cell. The challenge is to identify the most beneficial combinations in order to maintain the effectiveness of our current antibiotics for the protection of human and animal health.
The incidence of resistance varies depending on the environment (Levy, 1997; McEwen and Fedorka-Cray, 2002). The most frequently proposed hypothesis is that genes involved in antibiotic resistance originated in antibiotic-producing organisms and acted to prevent self-destruction in these organisms (Davies, 1992). Table 1 illustrates the mode of action of the antibiotic against the bacterial cell and the potential response of a resistant organism.Streptomyces species produce aminoglycoside antibiotics. In 1973, a study demonstrated that Streptomyces species contain aminoglycoside-modified enzymes that allow this species to overcome the effects of the antibiotic (Benveniste and Davies, 1973).
During the process of purification from these antibiotic-producing organisms, remnants of the DNA containing antibiotic-resistant genes are also co-extracted and can be recovered in the antibiotic preparation. Elimination of R factors among Escherichia coli strains with special reference to norfloxacin. To overcome this situation, the antibiotic methicillin was used to replace penicillin and a S.
However, the abundance of antibiotic-resistant bacteria in the natural environment where the bacteria have not been exposed to antibiotics may suggest that antibiotic-resistant genes can be kept stable in the absence of antibiotic pressure (Salyers and Amabile-Cuevas, 1997).A zoonosis is an infectious disease transmissible from vertebrate animals to man (Acha and Szyfres, 1994).
In industrialized countries, the zoonoses that are most frequently seen are food-borne infections caused by species of Campylobacter, enterohemorragic E.
Kinetics of conjugative transfer: a study of the plasmid pXO16 from Bacillus thuringiensis subsp. Many food-borne infections result from fecal contamination during slaughter or cross-contamination with fecal material during further processing (Aarestrup and Wegener, 1999).Development of antibiotic resistance in zoonotic bacteria constitutes a public health risk due to the possibility of treatment failures and the propagation of antimicrobial resistance in humans (Aarestrup and Wegener, 1999). The potential human-health consequences have been demonstrated by outbreaks of quinolone-resistant S.
A comparison of kinetics of plasmid transfer in the conjugation systems encoded by the F plasmid from Escherichia coli and plasmid pCF10 from Enterococcus faecalis. Nourseothricin resistance was detected in the pigs, farm employees and their relatives, as well as in residents from the surrounding communities (Hummel et al., 1986). Effect of Plumbago zeylanica extract and certain curing agents on multidrug resistant bacteria of clinical origin. Martel and Coudert (1993) suggested that the emergence of antibiotic resistant organisms was greater in young calves compared with older cattle, reasoning that drug use is greater with young calves because of greater susceptibility to bacterial diseases. Calves that received milk from cows treated with antibiotics for mastitis developed bacteria that were resistant to streptomycin whereas calves in the group fed milk replacer without antibiotics did not shed antibiotic resistant organisms into the environment.
Aminoglycosides: antibiotic-inactivating enzymes in actinomycetes similar to those present in clinical isolates and antibiotic-resistant bacteria. AntibioticSelection for antibiotic resistanceThe widespread development of resistance to several different antibiotics is generally a result of lateral or horizontal gene transfer. Three mechanisms of horizontal gene transfer have been identified: transduction, transformation and conjugation. Nosocomial outbreak caused by antibiotic-resistant strain of Salmonella typhimurium acquired from dairy cattle.
Transduction involves the ability of bacteriophage to transfer DNA between two closely related bacteria (e.g. This process is dependent on the close association of the bacteria with the free DNA and their ability to first take the DNA into the cell and then incorporate the genetic information in their own DNA.The final and arguably most important mechanism for horizontal gene transfer is conjugation. Conjugation is known to be the major mechanism by which Gram(-) bacteria exchange DNA (Woo et al., 2003). Conjugation requires cell-to-cell contact for transfer of mobilizable elements from donor to recipient cell (Droge et al., 1998). Conjugation between Gram(+) and Gram(-) bacteria has been described, for example the intergeneric conjugation from E. The primary mobile elements are plasmids and conjugative transposons, which are broad-host range conjugal elements. Plasmids are extrachromosomal DNA elements that replicate independently of the chromosome of the bacterial cell. Purification, characterization and antimicrobial spectrum of a bacteriocin produced by Pediococcus acidilacti. Plasmids are generally small, circular, double stranded molecules that can be identified in a variety of bacterial types. The genes contained on plasmids are considered to be non-essential but often offer some competitive advantage to the bacterium.
Resistance plasmids or ‘R plasmids’ code for enzymes that can inactivate antibiotics, prevent the uptake of an antibiotic or pump out the particular antibiotic (Madigan et al., 2003).
Antibiotic resistanceconferring plasmids have been described in virtually all bacteria and are widely dispersed in nature. In Gram (-) bacteria, this resistance frequently occurs with multiple antibiotics (Neu, 1989).

Conjugation of plasmid transfer is common among Enterobacteriaceae, Pseudomonas and many anaerobic bacteria (Neu, 1992).Gram(-) bacilli causing nosocomial infections are usually multiple-antibiotic resistant, resulting in significant problems for treatment. The antibiotics most commonly associated with resistance are penicillins, first to third generation cephalosporins and aminoglycosides, particularly gentamicin.
Recently a new class of mobile genetic elements called intregons has been described in many Gram(-) bacteria throughout the world. These intregons are horizontal gene transfer systems usually linked to transposons or conjugative plasmids, which allow them to be spread easily in the presence of antibiotic use.Hugues and Datta (1983) determined that most of the plasmids studied today are similar to those found prior to the beginning of the antibiotic era, except these plasmids carried no resistance genes at that point.
The F plasmids exist frequently as a single-copy plasmid in Enterobacteriaceae, which proliferate in the animal digestive tract (Waters, 1999).
Conjugation occurs at significantly higher frequency and efficiency than transformation, and several resistant genes can be obtained simultaneously at a rate of 10-1 per organism (Waters, 1999).
For the process, basic elements must be present: the donor bacteria containing the F factor (pili) and the recipient bacteria that will obtain the genetic material (R plasmid). Electron micrograph of two bacteria in the process of conjugation.Among the earliest events in the conjugation process, contact between donor and recipient is an essential step. Some adhesins are assembled into hair-like appendages called pili or fimbriae that extend from the bacterial surface (Figure 2). Based on their assembly and system pathway, adhesins can occur in a variety of ways (Soto and Hultgren, 1999).
A prominent example of an adhesin associated with antibiotic resistance-carrying plasmids is called a Type I pili. These appendages are prototypic class I fimbriae and are important virulence determinants in E. Type I pili mediate binding to the mannose-containing oligosaccharide receptors of the host cell (Sokurenko et al., 1992).
Relaxases, or nicking enzymes, will cleave specific strands of the DNA at the origin of transfer (oriT), resulting in a single strand of relaxed DNA (Waters, 1999). Occurrence and diversity of tetracycline resistance genes in lagoons and groundwater underlying two swine production facilities. The relaxosome then moves towards the cytoplasmic side of the cell envelope to the transport pore (Gomis-Ruth et al., 2002).
The Mating Pair Bridge is then formed (at the donor cell) and is responsible for the transfer of DNA from the donor to the recipient.
The mating bridge is a multiprotein complex apparatus that spans the cytoplasmic membrane (Gram(+)) and outer membrane (Gram(-)), forming a pore or channel. Finally the transfer signal will open the bridge pore, which will allow the rapid transfer of a nicked and protein-bound single strand of DNA (Waters, 1999). The DNA transport apparatus, a type IV secretion system, enables conjugative plasmids to control and finally transfer DNA from a donor to a recipient cell, which then becomes a potential donor.
In order to quantitatively express the spread of plasmids, Andrup and coworkers (1998) used a mathematical model based on the similarity of bacterial conjugation to Michaelis and Menten enzyme kinetics. The process of conjugative transfer could be explained as a catalytic change of genetic information from recipients to transconjugants, mediated by the donors. In this case, donor and recipients are analogous to the enzyme and the substrate, respectively. The mating pair is comparable to the activated complex; and the transconjugant is equivalent to the product.
First, ‘Vmax’, which is related to the maximal conjugation rate or the number of transconjugants produced per donor per minute. The second constant will be ‘Km’, which relates to the recipient concentration where the conjugation rate is half its maximal value (Andrup and Andersen, 1999).
The conjugation process.Antibiotic resistance in the environmentMany studies have demonstrated that plasmid transfer between bacteria occurs in diverse environments.
It seems that there is no distinction between plasmids derived from bacteria of human, animal or fish origin (Kruse and Sorum, 1994).
Kruse and Sorum (1994) obtained frequencies of plasmid transfer for bacteria of different species and origins (human, bovine and marine) mimicking natural environments (untreated seawater, minced meat on a cutting board and feces from pigs) similar to frequencies measured under standard laboratory cultural conditions. The IncP plasmidencoded cell envelope-associated DNA transfer complex increases cell permeability. Pukall and coworkers (1996) demonstrated that in a soil microcosm there were high frequencies of plasmid transfer from sewage and manure origin (including broad- and narrow-host range), mainly IncP plasmid between E. The presence of antibiotic resistant bacteria in different environments represents a real threat, not only as a source of possible diseases, but also for the potential spread of R plasmids to other pathogenic or non-pathogenic microorganisms of diverse origins (Kruse and Sorum, 1994).‘CURING’ ANTIBIOTIC RESISTANCECuring is the process of removing plasmids from a bacterial cell.
Initially it was thought that this phenomenon would be an appropriate solution to control the development of antibiotic resistance in formerly antibiotic susceptible bacteria.
Simply remove the offending antibiotic from the bacterium’s environment and it would ultimately revert to its previously antibiotic receptive form. Unfortunately we now know that many plasmids are conserved even in the absence of the selective agent.
Many possible reasons for this conservation exist, including the presence of DNA cassettes that encode for stability (Zielenkiewicz and Ceglowsk, 2001). In the quest to find a solution to the problem of antibiotic resistance some researchers have searched for compounds that might retard the spread of these determinants or eliminate them from the bacteria. The objective would be to identify a safe substance that could be fed to livestock and poultry to eliminate resistance plasmids from intestinal bacterial or prevent the transfer of these plasmids among the bacteria. As a result, the prevalence or degree of resistance of the intestinal flora may be reduced.Antibiotics such as mitomycin, rifampin, and flavophospholipol and DNA intercalating dyes such as acridine orange and ethidium bromide have been shown to cure many plasmids. As a result of this plasmid loss the bacterium will no longer have the genetic advantages contained on the plasmid. This compound is found in the Indian medicinal plant Plumbago zeylanica, which has been associated with antimicrobial, antimutagenic, antitumor and radiomodifying properties (Krishnaswami and Purushothoman, 1980). In a study evaluating the effect of this plant extract on multi-antibiotic resistant bacteria of clinical origin, 14% of the plasmid containing bacteria exhibited curing. This percentage of curing is equivalent to the more widely accepted curing agents acridine orange and ethidium bromide (36%), but pefloxacin was the most efficient agent (88%) (Beg and Ahmad, 2000). Many phenolic compounds can interfere with DNA replication and consequently result in the elimination of plasmids (Lakshmi et al., 1989). Pefloxacin is an antibacterial compound with similar structure to norfloxacin and ofloxacin (Ahmad et al., 1993). Some may contain the genetic determinants for resistance to other environmental stressors such as heavy metals and toxins or the plasmids might provide other survival advantages to the bacterium such as virulence, toxin production or the formation of compounds like pediocin. Pediocin is a bacteriocin produced by pediococci that inhibits the growth of many Gram(+) pathogenic and food spoilage bacteria (Bhunia et al., 1988).
The resulting food product is often unacceptable because proper fermentation is dependent on the growth of healthy starter cultures.
As a result, the food industry has investigated several ways to cure the pediocin encoded plasmids from these organisms.
The problem behind the increase in resistant populations are the ‘easy to get’ and ‘hard to lose’ resistance genes (Salyers and Amabile-Cuevas, 1997).
Some plasmids are very stable and can be maintained through consecutive generations (Trevors, 1986).
Quinolone resistance in campylobacter isolated from man and poultry following the introduction of fluoroquinolones in veterinary medicine. It has been reported that certain physical treatments and chemical compounds as well as growth conditions may increase the frequency of elimination of drug-resistant R plasmids, resulting in sensitive cells that were previously resistant to antibiotics (Lakshmi et al., 1989). Curing refers to the ability of bacteria to spontaneously lose their resistance plasmid under the effect of certain compounds, thus reverting to antibiotic sensitive bacteria (Trevors, 1986).
The most effectiveconcentrations of a particular curing agent depend upon the species being treated, efficiency of the curing agent and the mode of action of that particular compound (Carlton and Brown, 1981).
Transferable drug resistance associated with coliforms isolated from hospital and domestic sewage.
Using combinations like ethidium bromide and novobiocin or imipramine and methylene blue resulted in curing six plasmids from Salmonella of avian origin of the 17 strains evaluated (Poppe and Gyles, 1988). Contrary to these results, studies with Lactobacillus plantarum showed that intercalating agents, such as acriflavine and ethidium bromide, were not as effective as novobiocin in curing plasmids (Ruiz- Barba et al., 1991). In fact, intercalating dyes do not cure large plasmids (>250 mDa) (Stanisich, 1984).The mode of action of many of these curing agents is not fully understood. The concentrations at which curing occurs is just slightly lower than the concentration that might inhibit or kill the host organism.
Comermycin, novobiocin or rifampicin act as curing agents by inhibition of DNA gyrase or RNA polymerease. Acquisition of drug resistance plasmid converts Salmonella enteritidis phage type 4 to phage type 24. Their action inhibits DNA plasmid replication and consequently promotes the very effective degradation or elimination of antibiotic resistant plasmids (Danilevskaya, 1980; Trevors, 1986). Sodium dodecyl sulfate is an ionic detergent found in household products (shampoos) and is widely used as a protein-denaturing compound in electrophoresis systems. Epigallocatechin gallate (EGCg) is a tea catechin that is suggested to act by blocking or significantly reducing the transfer of conjugative R plasmids between E. Induction of topoisomerase II mediated DNA cleavage by the plant naphthoquinones plumbagin and shikonin. It was shown that this compound had a better curing effect in a multi-species community or in densely populated normal flora, such as GI tract, skin, etc (Molnar et al., 2003). A natural alternative to many of the potentially toxic curing compounds described in the literature might be extracted yeast cell wall. Studies recently performed at the University of Kentucky have shown that the prevalence in a growing population of streptomycin- and ampicillin-resistant strains of Salmonella is reduced in the presence of some yeast cell wall preparations (Figures 3 and 4).
Strategies using these types of materials for decreasing the prevalence of antibiotic resistant bacteria are attractive since the use materials that can be safely introduced into an animals diet without the concerns associated with most of the chemical curing agents.Even elevated temperatures (43–44°C) have been successfully used not only to cure tetracycline-resistant and penicillinase-positive strains of S.
A change in lipopolysaccharide composition and shorter O-specific side chains were seen in S.
Plasmid associated bacteriocin production and sucrose fermentation in Pediococcus acidilactici.

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