Gram negative and gram negative bacteria have different functional characteristics along with different morphological structure. The essay particularly looks into the pathogenecity characteristics of Clostridium difficile and Acinetibacter and compares and contrasts their virulence characteristics. Clostridium is a pathogen associated with gut related disease whereas the Acinetobacter is involved wide range of nosocomial infection. Both of them have been found to have developed microbial resistance characteristics and the essay discussed the implementation of antimicrobial stewardship can help to counteract the ill effect of microbial resistance in these two strains of bacteria. Finally, an analysis is provided regarding the impact of outbreak of this bacterium in New Zealand residential care setting.
Clostridium difficile is a gram-positive, spore-forming, toxin producing anaerobic bacteria causing antibiotic-associated pseudomembranous colitis. Patients receiving antibiotic therapy develop this disease and the bacterium contributes to public health issues. It is a rod-shaped motile bacteria and the production of the S layer (polysaccharide capsule) contributes to its pathogenecity (Surawicz et al., 2013). The release of the large quantities of Toxin A (enterotoxins) and Toxin B (cytotoxin) are the two major virulence factors of C. difficile (Kuehne et al., 2014). Toxin A is referred as enterotoxin due to the accumulation in intestinal loop models and Toxin B is called the cytotoxin as it has cytopathic effect on tissue culture monolayers. These two toxin are endocytosed by the cell, has affect on the actin cytoskeleton and consequently lead to cell death. Inflammatory response and pseudomembrane formation takes place as cell death induces the production of tumor necrosis factor and pro-inflammatory interleukins. Toxin A causes necrosis and increase in intestinal permeability, whereas the toxin B has lethal effect in in-vitro cells (Abt et al., 2016).
Acinetobacter is a gram-negative bacteria from the class of Gammaproteobacteria that contributes to the mineralization of aromatic compounds. Acenitobacter baumannii species is specifically involved in nosocomial infection in seriously ill hospitalized patients. It has a coccobacillary morphology with twitching motility. Microorganism of this genus is responsible for different varieties of infectious diseases (Antunes, Visca, & Towner, 2014). The exact mechanism of the pathogenecity of this bacteria is not clearly established by research studies and the occurrence of community-acquired Acenitobacter pneumonia reflect its high pathogenecity. McConnell et al., (2013) has mentioned that iron-deficient condition is associated with release of receptors and iron-regulated catechol siderophores which creates the condition for expression of virulence factors. The lipopolysaccharide produced by the bacteria has been found to cause lethal toxicity in mice and its resistance to complement in the human sera facilitates bactericidal activity.
As anti-microbial resistance is increasing, antimicrobial stewardship has emerged as a solution to reduce microbial resistance and improve clinical outcome of patients. It prevents the spread of infection by promoting the appropriate use of antimicrobials. The main goal of anti-microbial stewardship is to help patients receive appropriate dose of antimicrobials, prevent misuse of antimicrobial and minimize the development of resistance (Brink et al., 2016).Certain C. difficile strain have emerged that are resistant to many anti-microbial agents and this complicates the treatment and prevention program for patients. C. difficile causes many diseases such as mild diarrhoea and chronic complications like psuedomembranous colitis (Tenover, Tickler, & Persing, 2012). Hence, in relation to the emergence of anti-microbial resistant strains of C. difficile, antimicrobial stewardship programs has positive implication for curtailing this effect and preventing adverse health outcome in patients (Slimings & Riley, 2014).
There is also rise in the emergence of Acinetobacter species that are resistant to majority of antimicrobial agents. This is a great area of concern for health care as it exposes patients to different risk of infection (Kwon et al., 2007). This form of resistance develops in Acinetobacter baumannii due to mechanism of anti-microbial inactivating enzymes, little access to bacterial target because of loss of outer membrane permeability and mutation in penicillin binding protein. Acinetobacter has many beta-lactamases enzyme that provide resistance to antibiotics like penicillin and cephalosporins (Shaikh et al., 2015). Secondly, carbapenem resistance to leads to the loss of protein in the bacterium as porin channels cannot gain access to bacterial targets. Certain point mutation also affects the function of the bacteria resulting in decreased affinity of the antimicrobial agent (Manchanda, Sanchaita, & Singh, 2010). Hence, this mechanism of the resistance of Acinetobacter shows that A. baumannii infection is a critical challenge to health care systems. It can acquire resistance at a much faster rate than other gram negative bacteria thus leading to nosocomial outbreaks and other infections. Therefore, in order to reduce the manner in which resistance characteristics is spreading in Acinetobacter species, implementation of antibiotic stewardship program is necessary. It will help to promote rational use of antimicrobials to control the spread of infection (Moradi, Hashemi, & Bahador, 2015).
The above explanation about the pathogenecity of both Acinetobacter and C.difficile reveals that both have difference structural and functional characteristics imparting virulence properties to the gram negative and gram positive bacteria respectively. In case of C. difficile, toxin A and toxin B is the major virulence factor, whereas in Acinetobacter, iron deficient condition and production of polysaccharide imparts virulence to the bacterium. Other known virulence factor of C. difficile includes production of the capsule, association with gut cell, production of hydrolytic enzymes and other toxins and the involvement of fimbariea (Janoir, 2016).The Acinetobacter is an opportunistic pathogen known to cause range of threatening nosocomial infection (Erac et al., 2014). On the other hand, C. difficile mainly causes gut related diseases such as pseudomembranous colitis.
As mentioned earlier, there is a rise in the emergence of multi-drug resistant Acinetobacter baumannii strains and the virulence characteristics in this cell is seen due to motility, biofilm formation, serum resistance and efflux pumps. All these mechanism support the bacterium to survive in adverse environmental condition and cause infection to vulnerable people. A study regarding virulence characteristics in the strain showed that biofilm production is found in almost all clones, whereas serum resistance develops only in some dominant clones. These mechanism plays a major role in the pathogenesis of this strains and better understanding of this mechanism will help to identify certain control measures to prevent infections and disease (Erac et al., 2014). Another study reveals colistin resistance mechanism influences the virulence of Acinetobacter baumannii. Polymixins act against the gram-negative bacteria by targeting the lipopolysaccharide (LPS). Two different colistin resistance mechanism were seen in the strain is loss of LPS and the inactivation of the lipid synthesis pathway. The impact of these mechanisms of the cell was analyzed in vitro and the final inference was that colistin resistance is most likely to be seen in patients who are treated with colistin (Beceiro et al., 2014). Hence, unlike the role of toxin A and toxin B in C. difficile’s virulence, several functional charecteristics impact virulence to Acinetobacter.
Difficile is known for its role in gut associated disease like mild diarrhea to life threatening pseudomembranous colitis (Janoir, 2016). Infection occurs after contamination with the resistant spores which disrupts the gut microbiota. After the colonization process, production of glucosylating toxins A and B is needed for the clinical manifestation of infection. They bind to unknown surface protein and leads to endocytosis of the cell. Acidification of endosomal lumen exposes the hydrophobic region and toxin molecules enter the enterocyte. Finally inside the cell, the glycosylation of the Rho and the Ras proteins causes the disruption of the cytoskeleton. This results in opening of the tight junction of the cell and the release of fluid (diarrhea) (McFarland, 2009). Persistence of the spore can lead to relapse of symptoms in patients (Janoir, 2016).
De Almeida et al., (2013) reported high incidence of severe Clostridium difficile infection in New Zealand and PCR-ribotype 244 was regarded as the strain involved in this infection. Though, this strain is very uncommon in New Zealand, however still certain cases were reported in New Zealand. Infection with this strain was associated with severe community outbreak of disease. As there are many other strain also available, so the severity of clinical outbreak of infection due to RT 244 was compared with other strains of the bacterium. The antibmicrobial susceptibility testing of the strains revealed that severe disease was seen mostly from RT 244 strain compared to other associated strain of the bacteria. Hence, considering the severity of this strain in causing harm to community dwelling people in New Zealand, urgent level action was proposed. This was related to creating awareness of this strain and engaging in early testing of patients who have certain risk factors of Clostridium difficile infection. It was also proposes to identify the main reservoir of the strain and prevent the transmission of the strain in health care setting.
Acinetobacter causes severe form of nosocomial infection and this is the reason for considerable antibiotic overuse by patients in secondary care hospitals in New Zealand. One severe nosocomial infection includes bacteriuria. It is a urinary tract infection causes in elderly which may be symptomatic or asymptomatic. High prevalence of the condition may lead to overdiagnosis and overuse of antibiotic which may cause certain complications in patients. To control the misuse of drugs, the management of the infection was assessed in care hospitals of New Zealand and it revealed that 30% of patients have bacteriuria post admission. This suggests that inappropriate urine screening was done in the hospitals and more than 50% of antibiotic treatment was initiated unnecessarily. Improvement in health care practices of New Zealand is needed to diagnose disease effectively and prevent overuse of antibiotics (Blakiston & Zaman, 2014).
New Zealand has implemented guidelines for the control of drug-resistant organisms in the community. This was considered important considering the increase in patient morbidity and mortality associated with multi-drug resistant organism their contribution in additional cost of treatment in health care setting. The guideline clearly defined different types of multi-drug resistant organism and showed how antibiotic stewardship programs like using antibiotics prudently can help to control the ill effect of these type of bacteria. Certain preventive measures include decreasing the mode of transmission and eliminating the risk factor for the transmission of these bacteria. This may play a role in reducing the incidence of nosomial infection in hospital setting (Toombs-Ruane et al. 2017).
Conclusion
The essay summarized the role of Acinetobacter and Clostridium difficile in causing certain nosocomial infection and gut related disease respectively. The explanation of the pathogenecity of both bacteria helped to identify virulence mechanism for both bacteria. As development of resistance in both bacteria was a reason for increased mortality and morbidity of disease, microbial stewardship was regarded as an effective step in controlling the drug resistant bacteria. The analysis of the outbreak of these two bacteria in New Zealand also indicates that several community level actions have been taken to prevent the transmission of these strains in the community.
References
Abt, M. C., McKenney, P. T., & Pamer, E. G. (2016). Clostridium difficile colitis: pathogenesis and host defence. Nature Reviews Microbiology.
Antunes, L. C., Visca, P., & Towner, K. J. (2014). Acinetobacter baumannii: evolution of a global pathogen. Pathogens and disease, 71(3), 292-301.
Beceiro, A., Moreno, A., Fernández, N., Vallejo, J. A., Aranda, J., Adler, B., … & Bou, G. (2014). Biological cost of different mechanisms of colistin resistance and their impact on virulence in Acinetobacter baumannii. Antimicrobial agents and chemotherapy, 58(1), 518-526.
Blakiston, M., & Zaman, S. (2014). Nosocomial bacteriuria in elderly inpatients may be leading to considerable antibiotic overuse: an audit of current management practice in a secondary level care hospital in New Zealand. Infection and drug resistance, 7, 301.
Brink, A. J., Messina, A. P., Feldman, C., Richards, G. A., Becker, P. J., Goff, D. A., … & Alliance, N. A. S. S. (2016). Antimicrobial stewardship across 47 South African hospitals: an implementation study. The Lancet Infectious Diseases, 16(9), 1017-1025.
Brink, A. J., Messina, A. P., Feldman, C., Richards, G. A., Becker, P. J., Goff, D. A., … & Alliance, N. A. S. S. (2016). Antimicrobial stewardship across 47 South African hospitals: an implementation study. The Lancet Infectious Diseases, 16(9), 1017-1025.
De Almeida, M. N., Heffernan, H., Dervan, A., Bakker, S., Freeman, J. T., Bhally, H., … & Roberts, S. A. (2013). Severe Clostridium difficile infection in New Zealand associated with an emerging strain, PCR-ribotype 244. New Zealand Medical Journal, 126(1380), 9-14.
Erac, B., Yilmaz, F. F., Hosgor Limoncu, M., Ozturk, I., & Aydemir, S. (2014). Investigation of the virulence factors of multidrug-resistant Acinetobacter baumannii isolates. Mikrobiyol Bul, 48(1), 70-81.
Janoir, C. (2016). Virulence factors of Clostridium difficile and their role during infection. Anaerobe, 37, 13-24.
Kuehne, S. A., Collery, M. M., Kelly, M. L., Cartman, S. T., Cockayne, A., & Minton, N. P. (2014). Importance of toxin A, toxin B, and CDT in virulence of an epidemic Clostridium difficile strain. Journal of Infectious Diseases, 209(1), 83-86.
Kwon, K. T., Oh, W. S., Song, J. H., Chang, H. H., Jung, S. I., Kim, S. W., … & Shin, S. Y. (2007). Impact of imipenem resistance on mortality in patients with Acinetobacter bacteraemia. Journal of Antimicrobial Chemotherapy, 59(3), 525-530.
Manchanda, V., Sanchaita, S., & Singh, N. P. (2010). Multidrug resistant acinetobacter. Journal of global infectious diseases, 2(3), 291.
McConnell, M. J., Actis, L., & Pachón, J. (2013). Acinetobacter baumannii: human infections, factors contributing to pathogenesis and animal models. FEMS microbiology reviews, 37(2), 130-155.
McFarland, L. V. (2009). Renewed interest in a difficult disease: Clostridium difficile infections–epidemiology and current treatment strategies. Current opinion in gastroenterology, 25(1), 24-35.
Moradi, J., Hashemi, F. B., & Bahador, A. (2015). Antibiotic resistance of Acinetobacter baumannii in Iran: a systemic review of the published literature. Osong public health and research perspectives, 6(2), 79-86.
Shaikh, S., Fatima, J., Shakil, S., Rizvi, S. M. D., & Kamal, M. A. (2015). Antibiotic resistance and extended spectrum beta-lactamases: Types, epidemiology and treatment. Saudi journal of biological sciences, 22(1), 90-101.
Slimings, C., & Riley, T. V. (2014). Antibiotics and hospital-acquired Clostridium difficile infection: update of systematic review and meta-analysis. Journal of Antimicrobial Chemotherapy, 69(4), 881-891.
Surawicz, C. M., Brandt, L. J., Binion, D. G., Ananthakrishnan, A. N., Curry, S. R., Gilligan, P. H., … & Zuckerbraun, B. S. (2013). Guidelines for diagnosis, treatment, and prevention of Clostridium difficile infections. The American journal of gastroenterology, 108(4), 478-498.
Tenover, F. C., Tickler, I. A., & Persing, D. H. (2012). Antimicrobial-resistant strains of Clostridium difficile from North America. Antimicrobial agents and chemotherapy, 56(6), 2929-2932.
Toombs-Ruane, L. J., Benschop, J., Burgess, S., Priest, P., Murdoch, D. R., & French, N. P. (2017). Multidrug resistant Enterobacteriaceae in New Zealand: a current perspective. New Zealand veterinary journal, 65(2), 62-70.
Essay Writing Service Features
Our Experience
No matter how complex your assignment is, we can find the right professional for your specific task. Contact Essay is an essay writing company that hires only the smartest minds to help you with your projects. Our expertise allows us to provide students with high-quality academic writing, editing & proofreading services.
Free Features
Free revision policy
$10Free bibliography & reference
$8Free title page
$8Free formatting
$8How Our Essay Writing Service Works
First, you will need to complete an order form. It's not difficult but, in case there is anything you find not to be clear, you may always call us so that we can guide you through it. On the order form, you will need to include some basic information concerning your order: subject, topic, number of pages, etc. We also encourage our clients to upload any relevant information or sources that will help.
Complete the order form
Once we have all the information and instructions that we need, we select the most suitable writer for your assignment. While everything seems to be clear, the writer, who has complete knowledge of the subject, may need clarification from you. It is at that point that you would receive a call or email from us.
Writer’s assignment
As soon as the writer has finished, it will be delivered both to the website and to your email address so that you will not miss it. If your deadline is close at hand, we will place a call to you to make sure that you receive the paper on time.
Completing the order and download