ANTIBIOTIC RESITANCE: A SIMPLE REVIEW
- Camila dos Santos Ferro
During the 20th century medicine evolved and improved, discovering new drugs as an example the antibiotic class. The antibiotic provided a technological development of medicine in combating infectious diseases and helped reduce the amount of deaths for that time. However, during the last century, these diseases started to increase again and the old drugs started to become obsolete, because no longer had the same effects on the microbes. This is the effect of resistance that can be defined as the capability of the bacteria to resist to the prejudicial effect of the antibiotics. Some authors believe that is related to the existing interaction between the antibiotic and the resistance to the transmission while others believe that the misuse of antibiotics due to wrong prescriptions and dispensation led to this effect. In the present review, I discuss some basic aspects of antibiotic resistance, introducing the antibiotics mechanism and choose for pathogens, the mechanisms of resistance and causes. In addition, I discuss some issues about antibiotic resistance.
During the 20th century medicine began to evolve and improve with the discovery of new drugs. An example of these new discoveries was the antibiotic class, which began with the discovery of penicillin. This new class of drugs provided a technological development of medicine in combating infectious diseases by reducing the amount of deaths that they caused previously (Laxminarayan et al., 2010; Aziz, 2013). Thereby making the class of drugs which more improved human health (Martinez and Baquero, 2014). However, during the last century, these diseases started to increase again and the old drugs started to become obsolete, because no longer had the same effects on the species of existing microbes (Moellering, Jr., 2011). While Guillemot (1999) suggests that this is related to the existing interaction between the antibiotic and the resistance in the transmission, some more recent article of Rodríguez-Rojas et al. (2013) and Darwish (2014) take the view that the misuse of antibiotics due to wrong prescriptions and dispensation, and lack of awareness caused resistance genes in microbial flora on people, animals and the environment. This has become a major worldwide health problem with the large growth in the difficulty of treating diseases caused by antimicrobial thereby increasing the need for new treatments (Darwish, 2014; Aziz, 2013)
ANTIBIOTICS: MECHANISM AND CHOOSE FOR PATHOGENS
Aziz (2013) asserts that antibiotics can work in different ways, and there are many ways that bacteria can be inhibited to grow or live, as examples:
- The prevention of the formation of the appropriate bacterial cell wall. The bacterial cell membrane is semipermeable (controls the amount of water in salt solutions). If the bacteria do not have an appropriate membrane water can pass through the cell membrane filling it with water and the ruptures it, thus killing the bacteria.
- By the prevention of the protein synthesis. For the living bacterial cell is necessary that new proteins are continually made, because old proteins can be damaged quickly when they lose their functions. Producing new proteins is also important for cell division that will start the new cells.
- Disrupting the synthesis of DNA, which needs to be continuous as cell division takes place. If replication of chromosomes is interrupted, the cells do not increase in number and also die by one of their main processes was impaired.
- Water and gases freely pass through the membrane, but other nutrients require specific transport proteins, which also affected the system of energy production. Therefore, any rupture in the membrane will kill the bacteria.
Aziz (2013) also comments about the appropriate types of antibiotics for each type of bacteria. The most part of classified bacteria are Gram-negative or Gram-positive, according to the positive or negative results of the Gram’s staining method, using a complex purple dye and iodine. The Gram-positive will present a blue / purple coloration due to the thick cell wall of peptidoglycan that will retain the primary stain, usually occurring in the skin, respiratory system and bone, and can cause infections such as cellulitis, pneumonia or wound infection. Instead, the Gram-negative will present a pink/red coloration due to the thin cell wall of peptidoglycan that will not retain the primary stain, usually occurring in the gastrointestinal tract, respiratory system and genitourinary system and can cause infections such as peritonitis, pancreatitis and urinary tract infection. There is also the classification as atypical that usually occurs in the chest or genitourinary system, and can cause infections such as pneumonia and urethritis and anaerobe that usually occurs in the mouth, throat, teeth and lower bowel, and can cause infections such as dental infection, peritonitis, appendicitis and abscesses. They are in the manly classes treated with antibiotics because the common infections. Initially, it is necessary to discover what organism is causing the infection and then make the antibiotic choice.
RESISTANCE: MECHANISM AND CAUSES
According to Aziz (2013) the resistance can be defined as the capability of the bacteria to resist to the prejudicial effect of the antibiotics. Theuretzbacher (2013) observes that bacteria are the main responsible for infections related to multidrug resistance. Multidrug resistance is a term defined by a diversity of ways. In the European Centre for Disease Prevention and Control (ECDC) and the US Centers for Disease Control and Prevention (CDC) this terminology helps to grade and report comparable data about several profiles of antimicrobial resistance. Using this nomenclature, multidrug resistant (MDR) is determined as a microbe that is not susceptible to at least 1 in 3 or more classes of antimicrobials. Extensively drug-resistant (XDR) is determined as a microbe that is not susceptible to at least 1 in each and 2 or fewer classes of antimicrobial. Finally pandrug-resistant (PDR) is determined as a microbe that is not susceptible to all classes of antimicrobials. According to Rodríguez-Rojas et al. (2013) bacteria can acquire resistance by several different mechanisms, such as modifications in the cell membrane, mutations and genetic changes. The interaction between the suppression of microbial development and the antibiotic is successfully achieved in one case the antibiotics recognize their prey and the drug concentration is adequate for the desired inhibition. For that interaction to be successful, antibiotics should go a long way interacting with different bacterial envelopes or be triggered by enzymes as it works in isoniazid. The existing mechanisms of resistance are summarized in this modification or reduction in the concentration of free antibiotic used to get access to the target. Genetic mutations occur in proteins that can activate the pre-antibiotic, targets, or transporters. However, this kind of mechanism did not touch on the antibiotic itself and thus can be called ‘Passive resistance mechanisms’. Transfers by the horizontal gene transfer (HGT), normally do not confer resistance (but can occur in topoisomerases’ mutation in Streptococcus pneumoniae), and it shows that the main way of transmission is the clonal expansion for the mutation-acquired antibiotic resistance. Besides these mechanisms, the diminution of the active quantity can result in antibiotic resistance is caused by efflux through multidrug efflux pumps or antibiotic-inactivating enzymes. These are named ‘active mechanisms of resistance’ and may make resistance, and they can spread by HGT or clonal expansion. Modifications or protections on the target that difficult the action of the antibiotics can also be called ‘active mechanisms of resistance’ and can spread by HGT. Moreover, a recent study has shown in this class of antibiotic resistance that elements from basic metabolism of bacteria can collaborate for the vulnerability of antimicrobials (Martinez and Baquero, 2014). . Theuretzbacher (2013) and Gould (2008) connect some of the main MDR pathogens with their resistant antibiotic. As examples the Staphylococcus aureus that resist to β- lactam antibiotics (except new anti- meticillin-resistant Staphylococcus aureus [MRSA] cephalosporins), aminoglycosides, macrolides and fluoroquinolones. The Enterococcus spp. (particularly E. faecium) that resist to ampicillin, glycopeptides and aminoglycosides (high-level). The Enterobacteriaceae (e.g. Escherichia coli, Klebsiella pneumoniae) that resist to cephalosporins (extended-spectrum β -lactamases [ESBLs]-producers), aminoglycosides, fluoroquinolones and carbapenems. The Pseudomonas aeruginosa that resist to ceftazidime piperacillin/tazobactam, aminoglycosides, carbapenems and ciprofloxacin. The Acinetobacter that resists to ceftazidime, carbapenems, fluoroquinolones and aminoglycosides.
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Guillemot (1999) suggests about the risk of spread of antibiotic resistance in the future having consideration the evolution of resistance by mathematical models calculate in populations. These models found two different directions. In the first one, models of within-host dynamics offer expressions part of the bacteria that has antibiotic resistance, but these models ignore the movement of bacteria between the individuals and taking into account reservoir just as the environment. In the second one, he individual hosts are analyzed in a population that interacts with each other and differentiate themselves as disease and its mode of exposure to antibiotic. Both approaches include the way the consumption of antimicrobial drugs acts in the prevalence of spread of bacteria and evaluate the standards for determining the evolution of resistance and prevent it. In addition, they allow the evaluation of the local impact of infection control measures, and are an important educational tool for staff in small communities, like hospitals. These models can be used to analyze antibiotic use and resistance in animal and humans. However, the numbers of pathogens that are resistant to antimicrobials according to Mainous III and Pomeroy (2010) still increasing. Some examples of the risks to public health are methicillin-resistant Staphylococcus aureus, multidrug-resistant tuberculosis vancomycin-resistant Enterococcus, and amantadine/rimantadine-resistant and oseltamivir-resistant influenza virus. The frequency and implications of these pathogens result in deaths and morbidity and ultimately establish the impact on public health. One of the topics analyzed by Theuretzbacher (2013) is the surveillance needed. Arguing about the fact that the knowledge of the size of the problem in many regions of the world is imprecise and not reliable becoming limited. Many regions with the highest resistance rates as example Asia, Africa and Latin America use their own systems and calculations to measure as a method of analysis. These regions are those that have more chances to do not have a comprehensive and standardized surveillance system while in Europe have good examples of reliable reports. Despite surveillance systems are being improved, these limitations cause confusion in the published data and leave only part of the problem in sight. This article also comments about the resistance hotspot categories. Resistance can vary locally, depending on the type of site to be analyzed (e.g. Hospitals) and with the characteristics of the patient. However, international statistics intend to show trends in large-scale, global policies to guide antibiotic distribution and provide references without the need to consider the complex evolution and artificial influence system. The article of Golkar et al. (2013) gives some examples of economic factors in the United States such as the medical costs per patient that suffer from an antibiotic-resistant infection that can vary from $18,588 to $29,069 USD, and annual value can achieve the value of $20 billion in health care system costs per year. Patients who are suffering from antibiotic-resistant had their period in hospital extended to 6.4-12.7 day losing wages because they are unable to work. For the country these costs can reach the total of $35 billion annually. Per year around two million American develop hospital-acquired infections (HAIs) leading in 99,000 fatalities, and the major part of these are due to antibacterial-resistant pathogens. Alone sepsis and pneumonia (HAIs) killed around 50,000 people in 2006 and cost the US health care system more than $8 billion in that year, and these are just a few examples.
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