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The Phenomenon Of Antibiotic Resistance Health Essay

The antibiotic resistance phenomenon in bacteria is reported regularly in the popular press and is a well recognized problem.In the past 20 years, there has been a new discovery on the impact in the usage of antibiotic against the microbes, which they develop into an antibiotic resistant form. This is believed to occur because of the natural selection theory, which they evolve to counter the effect of antibiotic, and become resistance to them, in order to survive in the presence of the antibiotics. In the evolution theory, the species which are the fittest will survive to a certain environment. Bacteria too, are a type of organisms. Some bacteria have undergone a billion years’ worth of mutations, and because they are a simple organisms, their evolution and mutation rate are a lot higher and faster in any high level organisms. These factors are the major contribution in the increase of antibiotic resistant strain of bacteria in the past 20 years. Introduction and widely usage of antibiotics drugs in order to eradicate some bacteria in turn causes them to adapt to the new environment, via mutation and evolution.

The Phenomenon of Antibiotic Resistance

Antibiotic resistance is a natural phenomenon and has been around as long as bacteria. The bacteria is isolated from a glacier formed long before the discovery and the uses of antibiotics that have been found to be resistant to some modern antibiotics. There is a certain level that the inherit bacterial resistance to antibiotics can be identified. However, surviving bacteria are those that are of low sensitivity or of a resistant stage. Often, the resistance results from either a change in a protein structure of the bacterium, an inactivation of the antibiotic drug, the prevention of antibiotic accumulation, or the block of its entry into a cell (Walsh C., 2003). The result of the used of antibiotics cause the development of “anti-antibiotic” strategies in bacterial cells to increase. This is because the use of antibiotics produces a strong selective pressure that favours those bacteria to acquire such mechanisms of resistance. In a population of bacteria that are sensitive or resistant to an antibiotic, it will prevent those bacteria from leaving descendant or daughter cells. However, there will be occasional random mutations in the protein sequence of the various enzymes within any particular cell in any population of bacteria. If one of these mutations gives rise to a protein that is unaffected to the action of the antibiotic, that cell will survive and produce daughter cells that are also resistant to the activity of the antibiotic. In fact, the biology of bacteria provides ideal opportunities for these chances of resistance to occur. Under an ideal condition, E. coli bacterium can divide every two hours and the chances that it might take making a beneficial mistake is high enough for such resistances to occur and flourish due to the antibiotic selection. Random mutation is not the only way that a bacterial cell can develop resistance to antibiotics. Bacteria can also take up foreign DNA from other bacteria and also from their environment. Thus, if it is found that a bacterium of one species is resistant to an antibiotic it is possible that the DNA encoding the resistant protein may be transferred to bacteria of another (formerly sensitive) species.

The acquisition of resistance in bacteria indeed a serious problem (Walsh C., 2000). The bacterial resistance to the antibiotic has spread worldwide, causing some antibiotics are no longer useful for treating infectious. Antibiotic resistant can develop and spread very quickly, rendering an antibiotic ineffective within only a few years. The development of new antibiotics is expensive and time-consuming. In some cases, bacteria are developing resistance to antibiotics faster than scientists can develop them. Therefore, it is hoped that we will continue to understand how important is the work of antibiotics and to keep these useful drugs available.

Genetic Mechanism of Resistance

Bacteria do not become resistant to antibiotics just by experiencing genetic mutations. In fact, there are at least three genetic mechanisms in which resistance may be occurred.

BIOLOGICAL (GERM) WARFARE: During conjugation, one bacterial cell (A) may transfer any gene from a plasmid to another cell (B). This process can even occur between cells of different species. The transfer provides bacterium B a resistance to a drug that formerly was not present in its own DNA. In this example, the plasmid contains a gene (shown in red) to manufacture the enzyme that destroys the drug’s ability to interfere with bacterial cell division (as in the case of penicillin)First, there are occurrence where mutation antibiotic-resistant strains of microorganisms. Second, there is the process of conjugation, in which two bacterial cells join and an exchange of genetic material occurs. In many bacterial strains, a circular DNA molecule that replicate independently which known as plasmid, codes for enzymes necessary for the bacteria’s survival. There are certain of these enzymes, coincidentally, assist in the breakdown of antibiotics, thus making the bacteria resistant to antibiotics. During the process of conjugation, plasmids in one organism that contain antibiotic resistant may be transferred to an organism that previously did not possess such resistance.

Third, there are two types of DNA transportation that bacteria can incorporate into their own genetic machinery foreign pieces of DNA. In transformation, DNA from the environment (perhaps from the death of another bacterium) is absorbed into the bacterial cell while, in transduction, a piece of DNA is transported into the cell by a virus. An organism can become resistant to antibiotics in the result of incorporating new genetic material. Walter J. ReMine wrote:

Transformation and transduction occur extremely infrequently, but this rarity can be offset somewhat by the enormous population sizes that bacteria can achieve, especially under laboratory conditions. By those three methods bacteria can acquire DNA that alters their survival. For example, DNA transposition can result in reduced permeability of the cell wall to certain substances, sometimes providing an increased resistance to antibiotics (1993, p. 404).

Some examples of antibiotic resistant bacteria

There are few examples of antibiotic resistant bacteria, which although comparatively rare of concern, include:

MRSA - methicillin/oxacillin-resistant (Staphylococcus aureus) 

EMRSA - a strain of MRSA

VRE - vancomycin-resistant enterococci

ESBLs - extended-spectrum beta-lactamases (which are resistant to monobactams and cephalosporins)

PRSP - penicillin-resistant (Streptococcus pneumonia)

Mycobacterium tuberculosis

Figure 1. Mycobacterium tuberculosis

(http://embryology.med.unsw.edu.au/Defect/images/Mycobacterium-tuberculosis.jpg)

Mycobacterium tuberculosis is a pathogenic bacterial species in the genus Mycobacterium that causes tuberculosis in many cases. (Ryan & Ray, 2004). Mycobacterium tuberculosis has an unusual, waxy coating on the cell surface (primarily mycolic acid), which makes the cells unaffected to Gram staining; therefore acid-fast detection techniques are used instead. They are classified as acid-fast Gram-positive bacteria because of their lack of an outer cell membrane (Ryan & Ray, 2004). One of the ability for M. tuberculosis is their adaptation to different environments in the infected host, and it is very essential in their pathogenicity. (Manganelli et.al., 1999). The bacteria is also oxygen-dependent; they require oxygen for living. They also can withstand weak disinfectants and in a dry state for weeks. Its unusual cell wall, rich in lipids (e.g., mycolic acid), is responsible for this resistance and is a key virulence factor (Murray et.al., 2005).

The antibiotics drugs that were developed to eradicate the M. tuberculosis was targeted on 3 main component which support the bacteria’s life, which are protein synthesis, nucleic acid synthesis and cell wall synthesis. M. tuberculosis has shown resistant on the 3 types of drugs developed; they has shown resistant on Streptomycin, which inhibits the synthesis of protein mechanisms, Rifampicin and Fluoroquinolones, which inhibits the synthesis of nucleic acid mechanisms, Isoniazid , Ethionamide, and Elhambutol, which inhibits the synthesis of cell wall. (Blanchard, 1996). M. tuberculosis has a doubling time of <24 hr (Hiriyanna & Ramakrishnan, 1986), compared to other bacteria such as E.Coli, and this slow-growing nature making them more complicated to eradicate via chemoteraphy (Blanchard, 1996). Mitchison (1985) has suggested that pathogenic mycobacterial populations be divided into four components: actively metabolizing and rapidly growing, semidormant in an acidic intracellular environment, semidormant in a nonacidic intracellular environment, and dormant. Therefore, it is harder for a drugs to react on dormant bacteria.

According to Bonomo R. A. & Tolmasky M.E (2007), in February 1994 dozens of students at La Quinta High School in southern California were exposed to the pathogenic (disease-causing) agent, Mycobacterium tuberculosis, and eleven were diagnosed with active tuberculosis. Many strains of this bacterium are multi-drug resistant (MDR). Despite the antibiotic resistant properties of the M. tuberculosis, there are still hopes on founding new and more effective drugs against them. For example, Blanchard (1996) suggested that the p-lactam inhibitors of peptidoglycan biosynthesis is used against them. Mycobacteria are naturally insensitive to P-lactams, because of their extremely hydrophobic cell wall (Jarlier et.al, 1991) and the presence of both periplasmic penicillin-binding proteins (Basu et. al, 1992) and an active P-lactamase (Fattorini, 1992, Jarlier et. al.,1991). However, the combined administration of P-lactams and P-lactamase inhibitors has recently been shown to be effective in inhibiting the growth of mycobacteria (Prabhakan et. al, 1993, Zhang, 1992).

Methicillin-resistant Staphylococcus aureus (MRSA) 

Figure 2. Methicillin-resistant Staphylococcus aureus (MRSA)

(http://www.2n2u.com/wp-content/uploads/2011/01/MRSA.jpg)

Staphylococcus aureus is a species of bacterium that is commonly found in the noses of healthy people or on the skin. Even though it is usually harmless at the certain sites, it may occasionally get into the body. For examples, it can usually breaks through people’s skin because it will affects them, such as cuts, wounds, abrasions, the indwelling catharses, surgical incisions and also cause infections. According to the certain disease, these infections may be mild (pimples or boils) or serious (infection of the bloodstream, bones or joints. Mostly, it caused painful skin and soft tissue conditions such as boils, scalded-skin syndrome, and impetigo. When it is more discovered by the scientist, it becomes more serious forms of S. aureus infection can progress to bacterial pneumonia and bacteria in the bloodstream which are both of which can be fatal. 

S. aureus acquired from improperly prepared or stored food can also cause a form of food poisoning. In the late 1940s and throughout the 1950s, S. aureus developed resistance to penicillin. Methicillin, a form of penicillin, was introduced to counter the increasing problem of penicillin-resistant S. aureus and is one of most common types of antibiotics used to treat S. aureus infections; but, in 1961, British scientists identified the first strains of S. aureus bacteria that resisted methicillin. This was the so-called birth of MRSA. The first reported human case of MRSA in the United States came in 1968. Subsequently, new strains of bacteria have developed that can now resist previously effective drugs, such as methicillin and most related antibiotics. MRSA is actually resistant to an entire class of penicillin-like antibiotics called beta-lactams. This class of antibiotics includes penicillin, amoxicillin, oxacillin, methicillin, and others.S. aureus is evolving even more and has begun to show resistance to additional antibiotics. In 2002, physicians in the United States documented the first S. aureus strains resistant to the antibiotic, vancomycin, which had been one of a handful of antibiotics of last resort for use against S. aureus. Though it is feared that this could quickly become a major issue in antibiotic resistance, thus far, vancomycin-resistant strains are still rare at this time.

According to a study published October 2007 in the Journal of the American Medical Association (JAMA), there were close to 100,000 cases of invasive methicillin-resistant Staphylococcus aureus (MRSA) infections in the United States in 2005, which lead to more than 18,600 deaths. To put that number into perspective, HIV/AIDS killed 17,000 people that year.

Extended-spectrum beta-lactamases (ESBLs)

Figure 4. Extended-spectrum beta-lactamases (ESBLs)

(http://www.hotbizpro.com/articles/Antibiotic_Resistant_Disease_Killing_Humans_and_Swine.htm)

Extended-spectrum beta-lactamases are enzymes that can be produced by bacteria making them resistant to cephalosporins and monobacteria such as cefuroxime, cefotaxime and ceftazidime. ESBLs were first described in the mid-1980s and during the 1990s were mostly found in Klebsiella species. A new class of ESBL which called CTX-M enzymes has emerged and these have been widely detected among E. coli bacteria. These ESBL produced E.coli is able to resist penicillins and cephalosporins and found most often in urinary tract infection though not simple cystitis. Multiple of antimicrobial resistance is often a characteristic of ESBL producing gram-negative bacteria. ESBLs are producing organisms cause a wide spectrum of clinical disease ranging from colonization to serious infection and the common types of infections include urinary tract infections, peritonitis, cholangitis and intraabdominal abscess. They are a common cause of nosocomial pneumonia and central venous linerelated bacteremia. ESBL can be present in patients in the hospital and residents in personel care homes. This bacterium can be spread by not washing their hands, especially after using the bathroom and it can spread these bacteria. The spread of ESBL in a hospital can occur most commonly through contact with another person that has ESBL or on the hands of health care workers. Recent studies reveled that patients with infection such as septicemia with ESBLs producing organisms had significantly higher fatality rate than those with non-ESBL isolates. (Mehrgan et al., 2008).

In addition, the majority of these organisms were resistant to other common antibiotics used for treatment of urinary tract infections (UTI). A majority of the extended-spectrum β-lactamases of β-lactamase genes and are generally located on plasmids. These enzymes differ in only a few amino acids. ESBLs producing isolates are generally resistant to extended-spectrum cephalosporins and aztreonam as well as to many older β-lactam antibiotics. (Ma Nurul Atifah et al., 2005).

VRE—Vancomycin-Resistant Enterococci

Figure 4. VRE—Vancomycin-Resistant Enterococci

(http://www.health-res.com/EX/08-05-02/DrugResistance.gif)

Vancomycin-resistant enterococcus (VRE) is the name given to a group of bacterial species of the genus Enterococcus that is resistant to the antibiotic vancomycin. (John Stouffer,2009). VRE species have ability to pass resistant genes to other bacterial. They also can be found in the mouth, throat and vagina. These bacteria rarely cause illness in healthy people. However, when VRE gets into open wounds and skin sores, they can cause infections in the wounds. VRE can also cause more serious infections of the blood or other body tissues. Vancomycin is an antibiotic used to treat serious infections. Enterococcus is a facultative anaerobic gram positive coccus which normally colonises our gastrointestinal tract. This antibiotic also used to treat enterococco because these bacteria are resistant to many other drugs. Resistant means that an antibiotic is not effective in treating the bacteria. Sometimes, bacteria such as enterococci become resistant to Vancomycin and the drug no longer works. It becomes more difficult to treat the enterococcal infection. By virtue of the fact that the organism that are frequently resistant to commonly used antibiotics, the emergence of vancomycin resistant enterococi that occurred nearly 30 years after vancomycin was introduced is bound to occur. (A W Zuba idah et al, 2006). Two of the most common of the microorganisms are E. faecalis and E. faecium. High risk patients include those in intensive care units, those with chronic renal failure or cancer, organ transplant recipients and those with a history of vancomycin usage and the first case of hospital acquired VRE in Malaysia was first described in 1996 from University Malaya Medical Centre. (A W Zuba idah et al, 2006.)

VRE is most commonly spread by direct hand contact with infected person. VRE also spread by touching surfaces such as railings, faucets or door handles that have been contaminated by other people which also had infected with the bacteria. ). Even infection of healthy individuals is uncommon; they could colonize with newly-resistant bacteria. As an infection control technique, it has been shown to be effective for identifying patients colonized with VRE and reducing VRE infections. Furthermore, risk factors for one antibiotic resistant bacteria are often common risk factor for other antibiotic resistant bacteria. Therefore, a strategy of active surveillance for VRE may also be an effective measure to prevent patient-to-patient transmission of other antibiotic resistant bacteria.

Conclusion

The effects of antibiotic resistance are reflected in the agriculture, food, medical, and pharmaceutical industries. Livestock are fed about half of the antibiotics manufactured in the United States as a preventative measure, rather than in the treatment of specific diseases. Such usage has resulted in hamburger meat that contains drug-resistant and difficult-to-treat Salmonella Newport, which has led to seventeen cases of gastroenteritis including one death. Some MDR-tuberculoid strains arise because patients are reluctant to follow the six-months or more of treatment needed to effectively cure tuberculosis. If the drug regimen is not followed, less sensitive bacteria have the chance to multiply and gradually emerge into resistant strains. In other cases the "shotgun" method of indiscriminately prescribing/taking several antibiotics runs the risk of creating "super MDR-germs." Moreover, millions of antibiotic prescriptions are written by physicians each year for viral infections, against which antibiotics are useless. The patient insists on a prescription, and many doctors willingly go along with the request.

Because global travel is common, the potential of creating pandemics is looming. In many Third World countries, diluted antibiotics are sold on the black market. The dosage taken is often too low to be effective, or the patient takes the drug for a very short time. All these behaviours contribute to the development of resistant strains of infectious organisms. If humans are to gain the upper hand against MDR bacteria, it is the responsibility of these industries and the public to educate themselves and to engage in careful practices and therapy. The suggestion that the development in bacteria of resistance to antibiotics as a result of genetic mutations or DNA transposition somehow “proves” organic evolution is flawed. Macroevolution requires change across phylogenetic boundaries. In the case of antibiotic-resistant bacteria, that has not occurred.

Appendix

Pandemics- an epidemic of infectious disease that is spreading through human populations across a large region; for instance multiple continent, or even worldwide.

Phylogenetic- study of evolutionary relatedness among groups of organism ( e.g. species, populations), which is discovered through molecular sequencing data and morphological data matrices.

Tuberculosis- is an infection with the bacterium Mycobacterium tuberculosis, which most commonly affects the lungs (pulmonary TB) but can also affect the central nervous system (meningitis),lymphatic system, circulatory system (miliary TB), genitourinary system, bones and joints.

Periplasmic- around the plasma membrane; between the plasma membrane and the cell wall of a bacterium

Mycolic acid- the component of mycobacterial cell walls that confirms their acid-fast characteristic.

Enterococco- A genus of gram-positive, coccoid bacteria consisting of organisms causing variable hemolysis that are normal flora of the intestinal tract. Previously thought to be a member of the genus Streptococcus, it is now recognized as a separate genus. Enterococcus is a genus of bacteria of the phylum Firmicutes. They are round gram-positive cells which occur in pairs and are difficult to distinguish from Streptococcus.

Peritonitis- Inflammation of the peritoneum (see abdominal cavity), with pus accumulating between the parietal and the visceral peritoneum, abdominal pain and distension, vomiting, and fever. It may be acute or chronic, local or generalized. Acute peritonitis usually results from inflammation elsewhere (e.g., by spread of bacterial infection). Primary peritonitis often comes from a perforated gastrointestinal tract, as with rupture in appendicitis. Control of the source problem may be followed by remission, adhesions, or abscesses (much rarer since the development of antibiotics).

Cholangitis- The term cholangitis means inflammation of the bile ducts. The term applies to inflammation of any portion of the bile ducts, which carry bile from the liver to the gallbladder and intestine. The inflammation is produced by bacterial infection or sometimes other causes.

Intraabdominal- Occurring or being within the cavity of the abdomen

Vancomycin- an antibiotic produced by Streptomyces orientalis, highly effective against gram-positive bacteria, especially against staphylococci; used as the hydrochloride salt.

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