Multi-Drug Resistant Pseudomonas Aeruginosa Essay Examples & Outline
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Multi-Drug Resistant Pseudomonas Aeruginosa
Multi-drug resistant pseudomonas aeruginosa is one of the major problems facing most countries in fighting pneumonia. These drug resistant pathogen has proved challenging for many drug manufacturers because of its mechanisms of action.
The thesis of this essay is to analyze the mechanisms of action of pseudomonas aeruginosa. Further, my essay entails the appropriate drug therapy options for countering the pathogen. This includes the primary choice and secondary choice of drug therapy.
Pseudomonas aeruginosa is the most common cause of nosocomial infections. In order to evaluate the effectiveness of various drug therapies, a research was conducted on critically ill patients. The research comprised of various drug testing on the patents and their results. These drugs included b-lactams, flouroquinolones, aminoglycosides and carbapenems. According to the research observations, it was more effective using combination therapy to treat the infection rather than single therapy. The combination of flouroquinolone or aminoglycoside with b-lactam was more effective than a combination of flouroquinolone and aminoglycoside (Deutschman & Neligan, 2012).
The success of the combination therapy is a key breakthrough in the fight against multi-drug resistant infections. Even though the resistance ability of the pathogen is linked to cystic fibrosis and isolated outbreaks that allow the pathogens to develop, medical practitioners point out that lack of adequate novel agents is the greatest challenge.
In the treatment of multi-drug resistant pseudomonas aeruginosa antimicrobial therapy is very crucial. Antimicrobial therapy determines the success of the diagnosis. In most mortality cases, lack of appropriate primary and secondary microbial therapy is the cause of loss of lives. Nevertheless, the therapeutic options for critically ill patients have proved to be very redundant.
In order to determine what therapeutic option to undertake as a medical practitioner, it is essential to assess the mechanisms of resistance of the pathogen. The most common mechanism of resistance for these pathogen is the ability to produce B-lactamase. B-lactamase enables the pathogen to counter B-lactam antibiotics. B-lactamase enzymes have extended their spectrum of action through point gene mutations. Moreover, the secretion of carbapenemases by the pathogens adds more resilience to the pathogens. This is mostly because most antimicrobial therapy drugs were previously made of carbapenems. Thus, pathogens were previously subjected to high levels of selected pressure by carbapenems. However, the ability of the pathogens to trigger a point mutation secretion of carbapenemases led to the resilience of these pathogens (Mayers, 2013).
Pseudomonas aeruginosa has numerous drug resilience adaptations. For instance, it was later discovered that pseudomonas aeruginosa pathogens were able to resist drugs through production of beta-lactamases, outer membrane modifications and efflux pump.
In therapeutic treatment, there are various options for drug therapy determining on the development of the infection. The choices for drug therapy range between primary choice and secondary choice drug therapy.
Primary choice drug therapy entails the use of first line anti-microbial options such as carbapenems, tigecycline, B-lactamase inhibitor combinations, cephalosporins, aminoglycosides, trimethoprim-sulfamethoxazole and fluoroquinolones.
Carbapenems are used in treating ESBL producing pathogens. The diagnoses range between half grams of the drug every six hours to one gram in every eight hours in case of serious infections. The use of carbapenems showed low rates of mortality among patients compared to other antibiotic agents (Deutschman & Neligan, 2012).
Furthermore, tigecycline is preferred in treating most complex skin infections and in some cases community-acquired pneumonia. On the other hand, B-lactamase inhibitor combinations such as clavulanate, sulbactam and tazobactam all have varying levels of inhibitory activity against most ESBL enzymes. Cephalosporins are used in patients who are not in critical condition. This is because they have lower vitro susceptibility than other antimicrobial drugs. Thus, they should not be used on patients with microbial infections, which have ESBL-producing organisms.
Flouroquinolones, trimethoprim-sulfamethoxazole and aminoglycosides are also poor inhibitors of ESBL-enzymes. Thus, they should be used in mild cases with close monitoring (Deutschman & Neligan, 2012).
Secondary choice drug therapy consists of more effective drugs, most which are used in critical conditions. Their mode of action towards ESBL producing organisms is more effective than in primary choice drug therapy. These drugs include colistin, fosfomycin and rifampin. Although colistin resistance has been noticed among some resistant pathogens, combination therapy still appears successful in most cases. Colistin can be used together with fosfomycin to reduce the susceptibility of the drugs to the pathogens. Moreover, rifampin is mostly used against carbapenemase-producing pathogens (Mayers, 2013).
The use of combination therapy can lead to various side effects. For instance, the use of combination therapy can lead to nephrotoxicity, photosensitivity and anaphylactoid reactions. Consequently, combination therapy can lead to ototoxocity. Chemical agents in these drugs can also alter the mitochondrion. This is because when some of these antimicrobial agents are used together they work more adversely within the host’s body to alter the development of the parasite. This process may occur within the body cells (Aronson, 2014).
The success of combination therapy is still debatable. This is because the side effects of combination therapy may lead to a greater harm on the patient. However, researches are still undergoing to evaluate the effectiveness of the procedure and the harm posed to the patient.
Aronson, J. K. (2011). Side effects of drugs annual 29: A worldwide yearly survey of new data and trends in adverse drug reactions. Amsterdam: Elsevier.
Mayers, D. (2009). Antimicrobial drug resistance handbook: Volume 2. Totowa, N.J: Humana.
Deutschman, C. S., & Neligan, P. J. (2010). Evidence-based practice of critical care. Philadelphia, PA: Saunders/Elsevier.