The virulence factors of staphylococcus aureus

The virulence factors of staphylococcus aureus Staphylococcus aureus is faculatively anaerobic, catalase-positive, coagulase-positive, gram-positive cocci. It is non sporulating, non motile and non capsulated bacteria. 30% of Staphylococcus aureus can be found in skin, mucous of membrane and nasal passages in a healthy person as normal flora. However, Staphylococcus aureus infections are capable of leading to meningitis, pneumonia, osteomyetilis, spectic arthritis and septicemia. It is also difficult to treat Staphylococcus aureus infections if it is a methicillin resistant strain as the only antibiotic, vancomycin, is able to inhibit methicillin resistant Staphylococcus aureus(MRSA). Virulence Factors Virulence factors from Staphylococcus aureus can be structural or secreted products that lead to pathogenesis. They are classified into catogeries such as surface proteins, secreting toxins and superantigen toxin. Surface proteins in Staphylococcus aureus provide attachments to host tissues which will colonize and lead to infections. Such proteins are protein A/B which binds to immunoglobulin G, clumping factor A and B to help adherence to bacterial cells. [Plata, Rosato et al. 2009] Alpha-heamolysin, beta-heamolysin, gamma-heamolysin and Panton Valentine Leucocidine (PVL) are examples of secreting toxins which form pores in the host membrane and lyses the cells while staphylococcus enterotoxins weaken the host immune system and toxic shock syndrome toxin 1 causes toxic shock by food poisoning. These virulence factors that are produced [Plata, Rosato et al. 2009] by Staphylococcus aureus and often cause life-threatening diseases. These factors overcome and disguise themselves from th e body immune system so that Staphylococcus aureus can colonize and bind to connective tissues which lead to infections. They are also responsible for the symptoms of the disease. The main diagnostic features can be detected by having coagulase agglutination tests and test for the production of thermostable nuclease which break down DNA. [Greenwood, Slack et al. 2007] Exotoxins (TSST1-toxic shock syndrome toxin 1) TSST1 are one of the virulence factors that cause a variety of diseases in humans. TSST1 has short N-terminal ÃŽ ± helix which lead to ÃŽ ² barrel structure also known as B domain or oligosaccharide binding. It is then connected to C-terminal wall of the ÃŽ ² strands (Domain A). This structure cause cysteine loop which result in emetic activity. If there is no loop, TSST1 will be superantigenic [Orwin, Fitzgerald et al. May 2003]. As Staphylococcus aureus invade the body, TSST1 is produced in the bacteria and release to host. It then inhibits host immune responses. It crosses mucosal surfaces and reactivates bacterial cell wall induced arthritis. [Diages, Orwin et al. Jan 2000] TSST1 also stimulate proliferation of T cells. These T cells will not only increase its concentration in the body, but they are also unable to recognize specific antigen in the bacterial cells. Subsequently, T cells cannot eradicate Staphylococcus aureus. Therefore, TSST1 is also known as superantigenicity, py rogenicity and boost the lethality of the toxins. Acquired heart disease in children is often associated with TSST1. Also, TSST1 is linked to women who use tampons regularly as it increases the exposure to Staphylococcus aureus infections. TSST1 helps to release massive amount of cytokines which results in fever, rash, low blood pressure, tissue damage and shock. [Dermnet.org] Exotoxins (Panton Valentine Leucocidin-PVL) Panton Valentine Leucidin (PVL) is usually found in community-acquired Staphylococcus aureus (CA-MRSA). Tristan (2007) stated that it is categorized as bicomponent synergohymenotropic toxin which lyses host cell membrance and it targets on human polymorphonuclear neutrophils (PMN), monocytes and macrophages. Plasma membrane of myeloid cells form octamer pores and target leukocytes by Panton Valentine Leucidin [Kobayashi and Deleo 2009]. Inflammatory mediators such as leukotriene B4, IL-8 and histamine are released to the cell surrounding as PVL activates Ca2+ channels to open leading to calcium influx in PMN, monocytes and macrophages. As long as Ca2+ channels are opened and inflammatory mediators concentration is greatly rising, it is a fatal outcome. Thus, neutrophils, monocytes and macrophages lyses as pores form in their cell membranes and this usually results in toxic shock or refractory hypoxemia. Panton Valentine Leucidin plays a major role in severe necrotizing fasciitis, pne umonia, leukocyte destruction and tissue necrosis. [Libert, Batjom et al. Jan 2009] Staphylococcus enterotoxins-SE Staphylococcus enterotoxins are the common cause of food poisoning. As individual digests a large amount of Staphylococcus aureusthrough contaminated water or food, enterotoxins are produced. It has a major cross linking with major histocompability complex (MHC) class II antigen and T cell receptor (TCR) [Fraser and Proft 2008]. T cell receptor will recruit neutrophils and release a wide variety of inflammation mediators to the stomach and small intestine. Accumulation of inflammation mediators results in hyperemic mucosa and crypt extension develops in jejunum. The disruption of the lining of the small intestine influences the rate of absorption of substances. Thus, gastroenteritis forms and will bring about the systemic symptoms such as fever and hypotension.[ Diages, Orwin et al. Jan 2000]. Vomiting and diarrhea is also a common symptom in SE food poisoning. Food poisoning by Staphylococcus aureusis less severe than other infections by the same species. It is often self limiting a s well. [Diages, Orwin et al. Jan 2000] Protein A Protein A is characterized as a cell wall associated monomeric protein. [Gomez, Lee et al. 2004]. It has role in causing pneumonia by targeting polymorphonuclear (PMN) cell migration in the airway passages. Protein A binds to the Fc region of immunoglobulin G (IgG) and causes opsonization. [Greenwood, Slack et al. 2007]. It also phosphorylates mitogen activated protein kinases (MAPKs) as pro-inflammatory signaling. IL-8 is made and secreted out from epithelial cells. In addition, protein A also mimics TNF-ÃŽ ± (tumour necrosis factor ÃŽ ±) that will bind to TNFR1, which is distributed at airways (tumour necrosis factor receptor 1). This will recruit TRADD (TNFR1 associated death domain protein) and TRAF2 (TNF receptor associated factor 2). Both will be activated, protein A and TRAF2 with RIP1 will coimmunoprecipitate in the airways [Gomez, Lee et al. 2004]. Furthermore, protein A inhibits phagocytic engulfment. In the same paper, Gomez also stated that if Staphylococcus aureusis lacking in protein A or TNFR1, bacterial virulence will be lower and accumulation of PMN in the lung will be decrease as well. It is harmless to activate PMN as it is to protect the lung, however, when there is an increase in protein A binding to PMN, PMN is activated and enhancing the inflammatory mediators to be released in the airways. Therefore, an increase in protein A will generate a greater inflammatory response and subsequently pneumonia develops. Staphylokinase (SAK) Staphylokinase is an enzyme that produces by Staphylococcus aureus. When staphylokinase is released from Staphylococcus aureus and targeted to neutrophils, ÃŽ ±-defensins is produced and followed by neutralization of short peptides by Staphylococcus aureus. This results in inhibition of bactericidal effects of defensins by the activation of plasminogen and staphylokinase increases bacterial infection process. [Bergmann and Hammerschmidt 2007] Plasminogen is tightly regulated and it is a part of fibrinolysis mechanism which coagulates fibrin when a blood vessel is injured. Staphylococcus aureus changes plasminogen to fibrin with the help of fibrin as co-factor. Staphylokinase is encoded by the Sak gene and regulated by the agr gene. Its structure has a central ÃŽ ±-helix and 5 ÃŽ ² sheet strands. [Bokarewa, Jin et al. 2006]. Once neutophils is bound to the central ÃŽ ±-helix, it induces conformational changes. Consequently, plasminogen is converted to plasmin. Fibrin clots is then bro ken down by plasmin and kept the infection localized. Staphylokinase-plasminogen complexes also help Staphylococcus aureus to enter the host tissues. Furthermore, Maria stated that if 2 staphylokinase form a dimer due to the central ÃŽ ±-helical, it will reduce antigenicity. Several binding sites to neutrophils can be found in staphylokinase. This will induced in releasing of ÃŽ ±-defensins and affect the bactericidal properties as peptides are being neutralized. Staphylococcus aureusis then resistant to phagocytosis by neutrophils. [Bokarewa, Jin et al. 2006]. Staphylokinase infections are usually found in sepsis, immunocompromised and elderly patients as they are more prone to Staphylococcus aureus. Antibiotics are the usual therapy of these infections. Virulence Factors in Staphylococcus aureusare the main components that causing life threatening diseases. It is mostly the mediators released by the immune system gives the symptoms for the diseases. If there are any mutations in these virulence factors, it will be less virulent to the bacteria and the symptoms of disease will lessen as these virulence factors will not target neutrophils, macrophages and other immune system components. Therefore, inflammation mediators are not released in a great amount at once.

Porter’s five forces Essay

Michael E Porter developed the Porter’s five forces analysis in 1979 which serves as a framework for industry analysis and business strategy development. Its five forces determine the competitive intensity and therefore attractiveness of a market. Attractiveness in this context refers to the overall industry profitability. Three of Porter’s five forces refer to competition from external sources. The remainder are internal threats. It is useful to use Porter’s five forces in conjunction with SWOT analysis (Strengths, Weaknesses, Opportunities, and Threats). Porter referred to these forces as the micro environment. They consist of those forces close to a company that affect its ability to serve its customers and make a profit. The stronger the forces, the less profit they will make and vice-versa. A change in any of the forces normally, requires a business unit to re-assess the marketplace given the overall change in industry information. The overall industry attractiveness does not imply that every firm in the industry will return the same profitability. Porter’s five forces include – three forces from ‘horizontal’ competition: threat of substitute products, the threat of established rivals, and the threat of new entrants; and two forces from ‘vertical’ competition: the bargaining power of suppliers and the bargaining power of customers. The threat of the entry of new competitors The treat of new entrants depend on the ease with which they can enter the market. Markets with high profits will attracts new firms. The major barriers are: * Need for economies of scale * High entry costs * Lack of distribution channels * Government policies such as selective subsidies * Cost advantages of existing firms such as access to raw materials, know how * Strong product- loyal customers The intensity of competitive rivalry Strong rivalry will reduce profits. This occurs when: * Many firms, none dominant * Slow market growth * Fixed costs are high * High exit costs * Similar products In high competitive markets, threat of new entrants is high.

Organizational Strategies for Quality Assessment and Improvement Essay

Ambiguous medical notations are one of the most common and preventable causes of medication errors (Grissinger & Kelly, 2005). Drug names, dosage units, and directions for use should be written clearly to minimize confusion. The Institute for Safe Medication Practices (ISMP) and the Food and Drug Administration recommend that error-prone abbreviations are considered whenever medical information is communicated (Institute for Medical Safety, 2012). Medication errors result in thousand of adverse drug events, deaths, and preventable reactions every year (Grissinger & Kelly, 2005). Healthcare personnel, IMSP, the pharmaceutical industry, and The Food and Drug Administration (FDA) are some of the groups responsible for determining how these medication errors occur and designing strategies to reduce these errors (Institute for Medical Safety, 2012). ISMP is a nonprofit organization made up of nurses, pharmacist, and physicians. IMSP was founded in 1944 and are dedicated in educating and increasing awareness of medication error prevention and safety measures (About ISMP, 2012). They base their non-punitive initiatives on five key areas: analysis, communication, cooperation, education, and knowledge (About ISMP, 2012). The IMSP get their data by healthcare professionals reporting so that they can assist in learning and understanding the causes of the error and everything is confidential (About ISMP, 2012) IMSP Objectives The objective of the ISMP is to help the healthcare providers clarify any order that is not clearly legible or obvious especially with error-prone abbreviations, dose designations, and making sure that orders with abbreviations are clarified and written out completely, and verbal orders are read back, repeated if misunderstood, and spelled out (About ISMP, 2012). Also to hold webinar educational programs and medication safety issues. They offer tool kits for healthcare facilities to get the word out like posters, videos, patient brochures, books, and other drug safety tools. IMSP will conduct risk assessments on-site risk of medication safety in healthcare facilities and respond to sentinel events (About ISMP, 2012). IMSP Propose Strategies or Recommendations Suggest for the Acute Care Setting Here are some strategies that healthcare facilities can employ to  help eliminate the use of dangerous abbreviations. One is encouraging all healthcare professionals to avoid using medication error-prone abbreviations in all electronic and written communication (National Patient Safety Agency (NPSA), 2010). Another is identifying and promoting Physician Champions who will not only support accreditation-related activities but also advocate for full compliance. Healthcare facilities can assist in providing educational seminars and webinars to update all healthcare professionals and staff at the beginning of their employment period. Another way is for healthcare management and safety personnel to use advertised posters, create laminated cards with error-prone medication abbreviations, and dosage classifications throughout the acute care facility. The healthcare professionals should have these items at their disposal and distributed out at the beginning of employment (National Patient Safety Agency (NPSA), 2010). Lastly, making sure that the healthcare personnel avoids the use of medication abbreviations on CPOEs, labels generated from the system and bins, drug storage, and shelves. All the while making sure that the facility and personnel are adhering to guidelines, charts, and protocols (National Patient Safety Agency (NPSA), 2010). Reference â€Å"About ISMP.† (2012). Institute for Safe Medication Practices. Retrieved from http://www.ismp.org/about/default.asp Grissinger, M., & Kelly, K. (2005). Reducing the risk of medication errors in women. Journal Of Women’s Health (15409996), 14(1), 61-67. doi:10.1089/jwh.2005.14.61 Institute for Medical Safety. (2012). Acute Care. â€Å"Medical Safety Alert!†. Retrieved from www.imsp.com National Patient Safety Agency (NPSA). (2010) Rapid response report NPSA/2010/RRR009: reducing harm from omitted and delayed medicines in hospital. Retrieved from www.nrls.npsa.nhs.uk/resources/type/alerts/?entryid45=66720

Analysis Of Mahatma Gandhi A Lesson In Servant Leadership

Jesus Vera Analyzing Leadership Roles Instructor: Christine Hayda May 31, 2017 Mahatma Gandhi: A Lesson in Servant-Leadership Born Mohandas Karamchand Gandhi, Mr. Gandhi was and is one of the greatest examples of a servant leader. Being a servant leader does not mean a leader becomes a servant. A servant leader thinks of the needs of others when they are leading. So loved was Mr. Gandhi that he became known as Mahatma Ghandi. According to Google, Mahatma is defined as â€Å"a person regarded with reverence or loving respect; a holy person or a sage† (Unknown, Definition of Mahatma). Mahatma Gandhi tried to unify his native India strictly by using non-violent methods. His birthday, October 2nd, is a national holiday in India and,†¦show more content†¦He was roughed up by a white stagecoach driver for refusing to give his seat up for a European passenger. Ordered by a magistrate, a judge, to remove his turban in a courtroom, Gandhi refused and had to leave the courtroom. Later during his residence in South Africa, Mr. Gandhi exercised his method of non-violence, non-compliance for the first time. There was a law passed in which every person from India had to register with the South African government. Mr. Gandhi asked everyone not to register, no matter the consequences. Thousands were arrested in the following years because they listened to Mr. Gandhi’s plea. The South African government agreed to concessions due to the pressure felt from the movement. Mr. Gandhi returned to his native India after spending 21 years in South Africa. During a tour of India, Gandhi visited a representative of the farmers of a village named Champaran. The farmers were forced by the British to grow indigo, which was a crop that was not very profitable, in three out of twenty parts of their land. (Pai) The farmers were forced to grow indigo year-round, which caused problems since no other crops could be grown. In fact, the situation caused a famine-like situation. 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