Citizen Journalism Essay - 1411 Words

Citizen journalism is the concept of average citizens playing an active role in the media. Blogging, social networks and participatory news sites have helped to contribute to the growth of citizen journalism. The idea of reporting instantly from any place at any time has grown to become a key tool in journalism today. A blog is a regular informal entry by an individual commenting on news stories or describing an event. They can range in any topic from fashion to politics. A blogger can remove or add an entry at any time with the use of the internet. Also bloggers do not have any editing or boundaries when it comes to their pieces. Many newspapers have embraced the idea and use it as a tool to gain perspective and gather information. In†¦show more content†¦Blogs cover more than the traditional news stories of crime and politics they go as far to cover fashion, sports, hobbies and home and gardening. This is another reason why they are so popular. Bloggers tend to reach out to a specific audience and make it easier to grasp the attention. They want to relate to people specifically because a traditional press focuses on a broader audience. Discovered by the Technorati State of the Blogosphere 2010 there has been a significant growth in mobile blogging. Twenty five percent of bloggers are already engaged in mobile blogging and 40 percent of bloggers who use smart phones said that it changed the way they blog because it encourages them to post shorter, more spontaneous posts. Mom and women bloggers are another increasing trend in blogging today. Most of them blog about brands and gender related issues. Most people see the mom blog as a way to get advice on every day things such as family and cooking. It also is convenient because moms can stay at home and blog. Women bloggers focus on their audience by publicizing major gender related issues and advocating for equality. Igniting the interest of politicians, companies and the media to harness the buying and voting power, women and mom bloggers are more popular than ever. The changes of blogging are creating a positive medium not only for readers but for journalism as a whole. It gives a different perspective on issues and also gives all issues aShow MoreRelatedCitizen Journalism2824 Words   |  12 PagesI.3.1 The definition of Citizen Journalism Citizen journalism, can be defined as a community news and informationshared online and/or in print. The content is generated by users and readers. It can betext / blogs, digital storytelling, images, audio file, podcasting or video. Feedback anddiscussion on issues raised is received in the same way.2 Citizen journalism is a form of citizen media - where individuals write and orcomment on issues they feel are left out of the mainstream media. Many issuesaddressedRead More Citizen Journalism1587 Words   |  7 PagesJoan Cornell notes that the Internet democratizes the journalism which was in the hand of the few people (2003). The Internet makes the public access to information; at the same time, it creates the public to be journalists, opening blogs to put something new around on the Internet. Many news websites like The Guardian, the Washington Post, CNN and MSNBC allows some personification. The journalism nowadays is facing challenges not only from media and technology convergence, but also from audienceRead MoreThe Role Of Conventional Journalism And Citizen Journalism850 Words   |  4 PagesBefore the further discussion about the role of conventional journalism and citizen journalism, an introduction of the case is of central importance as it is such a complex story that c annot be reduced to several words. Two waves of blasts happened in a warehouse storing toxic chemicals in Ruihai International Logistics at the Binhai Industrial Park in the Chinese port city of Tianjin. It have killed more than a hundred people including firefighters, left hundreds more injured or homeless, and causedRead MoreThe View Of Citizen Journalism2163 Words   |  9 PagesDiscuss the view that citizen journalism represents a challenge to commercially-driven, conglomerate-owned journalism that is important both to the news industry and wider society. (2136/2000 words) Prediction 52: In the future, everyone will be a news reporter. (Addams, 1997) Coinciding with the growth of the internet, citizen journalism has generated popularity over the years and is no longer considered niche. Modernly armed with smartphones and social media outlets, the general public areRead MoreThe Trend Of Citizen Journalism920 Words   |  4 PagesThe Trend of Citizen Journalism – a Critical Development in Journalism With the advent of low cost consumer photography equipment, including camera phones, citizen journalism has become more widespread. During newsworthy incidents many people may be present with the capability to snap a picture. This capability of photography at the scene of a newsworthy event may produce information that can be helpful – and vital depending on the nature of the newsworthy event. While safety of the photographerRead MoreWhy Citizen Journalism Is Important1031 Words   |  5 Pagesnews or the newspaper. Professionals are also not the only people that can give us news. Citizen journalism is public amateur people collecting and reporting news and information (Wall, 2015). There are many risks and opportunities that comes with citizen journalism. This essay will describe these risks and opportunities in detail and will also discuss what compels a citizen journalist, why citizen journalism is important and how it is on a rise and continue to grow. There are risks such as goingRead MoreEssay on What ´s Citizen Journalism or Public Journalism?681 Words   |  3 PagesThe term citizen journalism or public journalism has spread widely around world as it has been connected to publishing the news and information. It can be defined simply as an alternative source of news which is produced and published by the general public. The concept of citizen journalism is not a new phenomenon and it has started long time ago. What has changed is the importance and the prevalence of the citizen journalists as an alternative source of information and news worldwide. There is anRead MoreWhy Citizen Journalism Is Affecting The World1100 Words   |  5 PagesCitizen journalism is defined as any news content, such as articles, videos etc. created by amateurs. Traditional and citizen journalism are often contrasted to each other, however it is important to note the similarities alongside the differences. Because of the growing popularity of citizen journalism du e to new technologies such as social media websites, it is essential to weigh the risks and opportunities to truly see how citizen journalism is affecting the world. It is vital to assess citizenRead MoreThe And Skeptics : Evaluating The Credibility Of Mainstream And Citizen Journalism1151 Words   |  5 PagesThe concept of journalism has always been regarded with skepticism. People are not sure which newspapers or news stations to trust. Naturally, the audience gravitates towards mainstream news providers like CNN or The New York Times. These sources, along with many others, have been accepted for their credibility. Recently, however, another source has been capturing the audience’s attention. This source is known as citizen journalism, and its contributions to society have had a huge impact. WhetherRead MoreDon’t Quit Your Day Job: Citizen Journalism816 Words   |  3 Pagesuniversity’s campus resulting in thirty-three deaths along with more than a dozen in juries and a permanent wound to the community. Journalist and writer, Lilly Yulianti, posted an article one day after the tragedy identifying a newer form of journalism identified as active citizen reporters. Yuliantis article, Praise for Student’s Footage of Virginia Tech Mass Killing, received a voice in an online news outlet where writings of new forms are welcomed. Time and incident met and a young man, by the name of Jamal

Clostridium Genus Humans

Sample details Pages: 22 Words: 6690 Downloads: 6 Date added: 2017/06/26 Category Science Essay Type Argumentative essay Did you like this example? Chapter 1 General Introduction: Members of the genus Clostridium are anaerobic, motile, Gram-positive, spore-forming rod present in nature especially in the soil. Microscopically, they have a long drumstick like appearance with a bulge situated at their terminal ends. Gram-staining is one of the easiest methods employed to identify them as the cell simply incorporates the dye while the spore does not take up the stain. Clostridium shows ideal growth when they are grown on blood agar at human body temperatures. Under unfavorable conditions for growth, however, the bacterium produces spores to tolerate the stressed environment where in, the active bacteria would not have survived. Clostridial species in their active forms secrete exotoxins responsible for specific and serious conditions such as tetanus, botulism and gas gangrene. The four clinically important species of Clostridium are C. botulinum, C. tetani, C. perfringens and C. difficile. Don’t waste time! Our writers will create an original "Clostridium Genus Humans | Sciences Dissertations" essay for you Create order 1.2 Types of Clostridium species important in humans 1.2.1 C. tetani Clostridium tetani is the bacterium which causes tetanus (lockjaw) in human beings. The spores of C. tetani can be acquired from all kinds of skin trauma and they outgrow in deep, necrotic wounds. In the anaerobic environment, the spores germinate and lead to the formation of active C. tetani cells. If these cells are present at the tissue level, then they release an exotoxin named tetanospasmin which affects the nervous system specifically by transmission via the neurons, eventually to the brain. One of the major effects of the toxin involves constant contraction of the skeletal muscles which occurs as a result of blockage of inhibitory interneurons which controls the contraction of muscles. Prolonged contraction of the muscles eventually leads to respiratory failure which has a high mortality rate if not treated early. One of the best ways to avert infections caused by C. tetani is to immunize oneself. 1.2.2 C. botulinum Clostridium botulinum is identified to generate one of the most powerful toxins till date and is the causative agent of the c food poisoning. Due to the fact that Clostridium spores are ubiquitous, they sometimes find their way into foods placed in anaerobic storages such as cans and bottles. Once the cans are completely sealed, the spores begin to germinate and the bacteria then secretes their toxin which has an effect on the peripheral nerve cells (McLauchlin et al, 2006; McLauchlin, Grant et al.,2006). Patients suffer from muscular flaccid paralysis apart from blurred vision. Immediate administration of an anti-toxin to the patient is necessary to raise the probability of survival. Infantile botulism is also caused in a very similar way but is far milder than its adult counterpart. The most frequent source for the spores which germinate in the infants intestinal tract is however honey. 1.2.3 C. perfringens This is a non-motile bacterium which is an invasive pathogen that can be contracted from dirt via large cuts or wounds. After spore germination takes place, C. perfringens cells proliferate and release their exotoxin which causes necrosis of the surrounding tissue (Clostridial myonecrosis destroys muscular tissues). The bacteria themselves produce gas that leads to a bubbly deformation of the infected tissues (Smedley et al.,2004) (Smedley, Fisher et al.,2004). In the United Kingdom and United States they are the third most common cause of food-borne illness, with poorly prepared meat and poultry being the main culprits in harboring the bacterium (Lin and Labbe 2003). The clostridial enterotoxin mediating the disease is often heat-resistant and can be detected in contaminated food and feces. The bacteria are killed at cooking temperatures, but the heat-resistant spores they produce are able to survive and may actually be stimulated to germinate by the heat. If the food is not eaten at once but is allowed to cool slowly, the bacteria produced when the spores germinate multiply rapidly. Unless the food is reheated so that it is piping hot (at least to 60oC and preferably to 75oC), the bacteria will survive. After ingestion, if there are sufficient numbers present, the bacteria will produce toxins and the toxins will cause symptoms. Infection with Clostridium perfringens normally causes diarrhoea and severe abdominal pain. It may occasionally cause nausea but it rarely causes vomiting or fever. 1.2.4 C. difficile First described in the 1950s, pseudomembranous enterocolitis was thought to be due to either Staphylococcus aureus, an organism that had become prevalent in hospital in-house patients who had received antibiotics (Keidan and Sutherland 1954) or to Candida albicans. In 1974, a prospective study of 200 patients who were treated with clindamycin were detected with diarrhoea in 21% and pseudomembranous colitis in 10%. A toxin produced by a Clostridium species was proposed as the cause of clindamycin-induced ileocaecitis in hamsters in 1977 (Bartlett, Onderdonk et al.,1977); later this toxin was isolated from the samples of patients stool, with evidence and counter-evidence presented for C difficile and Clostridium sordellii as causative organisms. However, by 1978, C difficile had been clearly identified as the causal agent of antibiotic-associated colitis (Chang, Bartlett et al.,1978). 1.3 Microbiology of C. difficile C. difficile is a Gram-positive, motile bacterium, spore-forming rod, toxin-producing, obligate anaerobe that is present in nature. Colonies are relatively large (2à ¢Ã¢â€š ¬Ã¢â‚¬Å"17 ÃŽÂ ¼m in length) rough, grey and fast growing; CCFA medium (consisting of cycloserine, cefoxitin, and fructose agar in an egg-yolk agar base) is highly selective for its growth (Aslam, Hamill et al.,2005). Clostridium also shows optimum growth when plated on blood agar at human body temperatures [Figure 1]. Over the past decade, it has become a very prominent nosocomial infection worldwide. It is notable that C. difficile infection caused ward closures in 5% of UK hospitals in 1993, and by 1996, this figure had risen to 16% (Popoola, Swann et al.,2000). In 1935, Hall and OToole first isolated this organism, designated it to be Bacillus difficilis, from the meconium and faeces of newborn infants (Tabaqchali and Jumaa 1995). The difficult clostridium was resistant to early attempts at isolation and grew very slowly in culture. The organism was shown to produce a lethal toxin in experimental animals, but since it was commonly found in the stools of healthy neonates it was classified as commensal and subsequently attracted little attention until 1974, when a comprehensive study showed that C. difficile was widespread in nature and could be isolated from the stools of several animal species and from patients faeces and genitourinary tracts (Hafiz and Oakley 1976; Bartlett 2007). Clostridium difficile is now the most frequent bacterial enteric pathogen in the developed world. This organism has been the recognized agent of 20% to 25% of cases of antibiotic-associated diarrhea and around 90% of serious pseudomemraneous colitis cases since its discovery in 1978. Disease symptoms are due to the production of tow toxins (A and B). During the past 3 to 4 years there has been the recognition of a new strain designated the NAP-1/ ribotype 027 strain which has been associated with some unique features including epidemics in geographically defined areas, more serious forms of disease and relative refractoriness to standard therapy. This 027 strain is linked to several deadly hospital outbreaks of C. difficile-associated diarrhea (CDI) which are now found rather frequently in Canada, the United States, and in greater parts of Europe (Cloud and Kelly 2007). This strain was found to produce greater than 10 times as much of toxin A and toxin B, as historic isolates (Larson, Parry et al.,1977; Cloud and Kelly 2007). The link between clindamycin associated colitis and C. difficile was not made until 1977. Stool filtrate from a patient with pseudomembranous colitis showed a cytotoxic effect on tissue culture cells, which suggested the presence of a toxin of unknown source (Larson, Parry et al.,1977). At the same time investigators in the United States showed that clindamycin and other antibiotics induced a fatal caecitis in hamsters; the caecal contents contained a filterable toxin that was cytopathic in a cell culture assay and would reproduce the typical lesions when injected intracaecally (Bartlett, Onderdonk et al.,1977). An organism identified as C. difficile was isolated from the animals and was shown to be the source of the toxin. Soon after, C. difficile and its toxins were detected in the stools of patients with pseudomembranous colitis (Hopkin 1978; Larson, Price et al.,1978), and oral vancomycin was shown to be an effective treatment in animal models and in patients (Bartlett 1984). C difficile has since become established as a major cause of nosocomial diarrhoeal infection. Figure 2: Coloured transmission electron micrograph of Clostridium difficle forming an endospore (red). Dr Kari Lounatmaa/Science Photo Library 1.4 Genome of C. difficile The genome of C. difficile strain 630 which was known as a virulent and multidrug-resistant strain was completely sequenced by Sebaihia in 2006 (Sebaihia, Wren et al.,2006). A large proportion of the genome (11%) consists of mobile genetic elements, mainly in the form of transposons. These mobile elements are supposed to be responsible for the acquisition of an extensive numbers of genes which are involved in antimicrobial resistance, virulence, and host interaction. The metabolic abilities encoded in the genome show multiple adaptations which enable the bacteria to survive and grow within the gut in low acidic environment. The genome consists of a circular chromosome of 4,290,252 bp with a G+C content of 29.06%, an additional circular plasmid of 7,881 bp with a G+C content of 27.9%, and 3971 genes. There are two separate genes, tcdA and tcdB encoded for enterotoxin A (308kDa) and cytotoxin B (270kDa) (Barroso, Wang et al.,1990; Dove, Wang et al.,1990; Hundsberger, Braun et al.,1997). Both toxins A and B, share 63% of amino acid sequence homology; enzymatic domain, a hydrophobic region believed to be involved in translocation through endocytic vesicles into the cytosol, and a carboxy-terminal domain which contain the so-called clostridial repetitive oligopeptides (CROPs); the latter mediate. TcdA and TcdB are among the largest bacterial toxins reported to date and are joined by Clostridium sordellii lethal toxin (TcsL) and hemorrhagic toxin (TcsH) and Clostridium novyi alpha toxin (TcnÃŽÂ ±) to form the group of large clostridial toxins (Table 1). TcdA and TcdB, located in a 19.6-kb pathogenicity locus (PaLoc), which is a short chromosomal segment carried by pathogenic strains of C. difficile which also encompasses three other small open reading frames [Figure. 2]. Nontoxigenic and nonpathogenic strains of C. difficile contain a 127-bp sequence (Hammond and Johnson 1995). The sequence similarity and its position suggests that the tcdA and tcdB genes are the result of gene duplication (von Eichel-Streiber, Laufenberg-Feldmann et al.,1992). The lack of toxin activity for nontoxigenic strains can be explained by the absence of at least part of the toxin A gene. The expression of these two genes is regulated by tcdC gene. The expression of the tcdC gene and weak transcription of the genes encoding toxin A (tcdA), toxin B (tcdB), a positive regulator (tcdD), and a holin-like protein (tcdE) (Hundsberger, Braun et al.,1997). The inverse is seen during the stationary phase, suggesting that tcdC negatively regulates toxin expression (Hundsberger, Braun et al.,1997) (232 amino acid residues). This gene is believed to result in over expression of tcdA and tcdB and increased production of toxins A and B, which may be responsible for the apparent higher pathogenicity in certain ribotypes (i.e., PCR type 027). Some strains also have cdtA and cdtB which are encoded for binary toxin (Sebaihia, Wren et al.,2006). 1.5 Pathophysiology The pathogenesis of CDI is complex and not fully understood but what is known is that important pathophysiological features of C. difficile include heat-resistance of the spore and toxin production. Also the precipitating event for C. difficile colitis is disruption of the normal colonic microflora which is usually caused by broad-spectrum antibiotics most commonly implicated (Figure 4), (Kyne, Hamel et al.,2002; Wilcox 2003) such as clindamycin, broad-spectrum penicillins, and cephalosporins. There are a number of antibiotics with a reduced propensity to induce infection such as aminoglycosides, metronidazole, antipseudomonals, and vancomycin. The risk of developing antibiotic-associated diarrhea is twice more when antibiotic therapy is received for longer than three days (Wistrom, Norrby et al.,2001). After disruption of the colonic microflora, colonization of C. difficile generally occurs by ingestion of the heat-resistant spores, which in turn switch over to their vegetative forms in the colon. Depending on the immunological status and the host factors, an asymptomatic carrier state or clinical manifestations of C. difficile colitis develop. Manifestation of the disease ranges from mild diarrhea to life-threatening- C. difficile colitis. C. difficile-associated diarrhea can occur up to eight weeks after the discontinuation of antibiotics. In most cases, C. difficile infection occurs on days 4 through 9 of antibiotic therapy (Cloud and Kelly 2007). As the leading cause of hospital-acquired diarrhoea, C. difficile colonizes the large bowel of patients receiving antibiotic therapy and produces two toxins, which are responsible for the disease pathologies. Toxin B is around 1000 times more cytotoxic than toxin A (Kabins and Spira 1975). Toxin A is also an enterotoxin in that it loosens the tight junctions between the epithelial cells that line the colon, which in turn helps toxin B to enter into the epithelial cells. These two toxins, TcdA and TcdB, are encoded on a pathogenicity locus with both negative and positive regulators of their expression. Following expression and release from the bacterium, TcdA and TcdB translocate to the cytosol of target cells and inactivate small GTP-binding proteins, which include Rho, Rac, and Cdc42. Inactivation of these substrates occurs through monoglucosylation of a single reactive threonine, which lies within the effector-binding loop and coordinates a divalent cation critical to binding GTP. By glucosylating small GTPases, TcdA and TcdB cause actin condensation and cell rounding, which is followed by death of the cell. TcdA elicit effects primarily within the intestinal epithelium, while TcdB has a broader cell tropism (Farrell and LaMont 2000; Voth and Ballard 2005). 1.6 Host factors The major host factors predisposing patients to the development of symptomatic C. difficile-associated Infections (CDI) include antibiotic therapy. A cohort study of Sherbrooke inpatients recorded that fluoroquinolone use (especially ciprofloxacin) has emerged as the major risk factor for CDI in the context of ongoing epidemic (Pepin, Saheb et al.,2005). Other risk factors include advanced age, especially people over 65 years; number and severity of underlying diseases and abnormal immune response to C. difficile toxins (Hundsberger, Braun et al.,1997). Patients who recently received immunosuppressive therapy or recently underwent surgical procedures are at the highest risk for fulminant disease, and those with a previous history of CDI. The increased risk may be due partly to the debilitated patients inability to mount an IgG antibody immune response against C. difficile toxin A. The ability to mount an immune response is not protective against C. difficile colonization, but is associated with decreased morbidity, mortality, and recurrence of CDI (Kyne, Hamel et al.,2002; Sebaihia, Wren et al.,2006). 1.7 Clinical presentation The presentation of the infection can range from asymptomatic colonization or self-limiting diarrhea to severe diarrhea, pseudomembranous colitis [Figur7], megacolon, colonic perforation, and death (Larson, Price et al.,1978). The incidence of diarrhea in hospitalized patients who receive antibiotics ranges from 3% to 29%. C difficile has been found as the causative agent in 10à ¢Ã¢â€š ¬Ã¢â‚¬Å"25% of patients with antibiotic-associated diarrhea, 50à ¢Ã¢â€š ¬Ã¢â‚¬Å"75% of those with antibiotic-associated colitis, and 90à ¢Ã¢â€š ¬Ã¢â‚¬Å"100% of those with antibiotic-associated pseudomembranous colitis (Bartlett 1990). Mortality of CDI ranges from 6% to 30% when pseudomembranous colitis is shown to be present (Olson, Shanholtzer et al.,1994; Moshkowitz, Ben et al.,2004; Pepin, Valiquette et al.,2004), and is substantial even in the absence of colitis. Most patients present with passing of large amounts of watery stool which is well known by healthcare workers who can often recognize it from its unique characteristic foul smell (Brazier 1998; Wilcox 1998). It was found in prospective case-controlled study that patients also present with paralytic ileus (21%), abdominal pain (22%), fever (28%) and a raised white cell count (50%) (Gerding, Johnson et al.,1995). Dehydration and electrolyte imbalance are often found due to passing large amount of diarrhea and, when disease is prolonged, significant malnutrition can develop (Brazier 1998). The incubation period for disease after exposure or acquisition is probably 1 week. Infection with C. difficile can be diagnosed up to 4 weeks after discontinuing an implicated antibiotic. It can also be triggered by other drugs such as cytotoxic drugs, antacids, stool softeners and laxatives which may trigger CDI (Hundsberger, Braun et al.,1997). Certain procedures such as nasogastric intubation, enemas and other intensive care procedures may also predispose to the infection (Cunney, Magee et al.,1998). 1.8 Treatment The initial treatment for CDI was oral vancomycin. In the early 1980s, metronidazole was also shown to be effective, perhaps equally so, and a strong preference to avoid the use of vancomycin in hospital inpatients, reinforced by several sets of therapeutic recommendations (Gerding, Johnson et al.,1995), has led to increasing reliance on metronidazole. In 1997, the American Gastroenterology Association published recommendations for treating CDI which include discontinuation of antibiotics to avoid tissue damage, supportive non-specific therapy, and addition of metronidazole for those who failed to respond within 2à ¢Ã¢â€š ¬Ã¢â‚¬Å"3 days (Fekety 1997). However, oral vancomycin was recommended for the following categories of patients: those who were critically ill, unable to tolerate metronidazole, pregnant women, or those under the age of 10 years, those who failed initial therapy with metronidazole, or those whose infecting organism proved to be metronidazole resistant. The past few years have witnessed an increase in the failure rate of antimicrobial therapy (Pepin, Valiquette et al.,2004). Some patients simply fail to respond to conventional therapy, and others relapse after discontinuation of treatment. The Cochrane database reports only nine well-designed randomized trials that have assessed treatments for CDI. Importantly, antimicrobial susceptibility testing of contemporary and historic isolates of NAP1/027 indicates a substantial increase in resistance to all fluoroquinolones (McDonald, Killgore et al.,2005). Fluoroquinolones are now the most widely prescribed antibiotics in many developed countries, (Linder, Huang et al.,2005) and the acquisition of fluoroquinolone resistance has been thought to promote the emergence of NAP1 (McDonald, Killgore et al.,2005). A substantial increase in the proportion of patients who fail to respond to metronidazole and a doubling of the frequency of postmetronidazole relapses have been noted, which could also promote the dissemination of this strain. 1.9Recommendations for treatment Treatment with the offending antibiotic has to be stopped, if possible. Fluids and electrolytes are given to compensate fluid loss during diarrhea. Antimotility agents should not be given. If specific treatment is required, metronidazole 500 mg is given orally every 6à ¢Ã¢â€š ¬Ã¢â‚¬Å"8 hours for 7à ¢Ã¢â€š ¬Ã¢â‚¬Å"10 days. Vancomycin at a dose of 125 mg orally every 6 hours is a second-line alternate agent. If the patient cannot tolerate the drug orally, intravenous metronidazole is used, but this should be switched to oral therapy once the patient is able to tolerate it. In the case of ileus or toxic megacolon, intravenous metronidazole is used, perhaps adding vancomycin retention enemas in a dose of 500 mg mixed in 100 mL normal saline. Vancomycin is avoided unless metronidazole seems to be ineffective, the patient is pregnant or allergic to metronidazole, or true resistance is shown. In case of recurrence, the agent that had been used to treat the initial episode of CDI is re-used, usually metronidazole. In case of multiple recurrences or refractory disease, the use of probiotics, immunoglobulin, or steroid is considered. In all cases, strict contact isolation of the patient is essential in controlling the spread of the disease to other patients. Symptom-free carriers not to be treated. Emergency colectomy reduces mortality in patients with fulminant CDI. Like patient who aged 65 years or more, in those immunocompetent, those with a leukocytosis or=20 x 10(9)/L or lactate between 2.2 and 4.9 mmol/L (Lamontagne, Labbe et al.,2007). 1.10 Epidemiology CDI is increasingly recognised as one of the most important healthcare associated infections. A number of aspects classify CDI as a severe potential threat associated with receiving healthcare. The number of cases reported on a weekly basis has steadily increased in Scotland over the last 10 years. Increasing numbers of outbreaks in hospitals and other healthcare institutions have been observed in Scotland as well as the rest of the UK. Some of these outbreaks have included cases of severe disease and deaths. Mortality rates for all deaths mentioning CDI as underlying or direct cause of disease have more than doubled from 1999-2004 in England and Wales. Reports indicate that patients complicated with CDI spend 1-3 weeks longer in hospitals than control group patients. Frequent relapses of the disease are contributing to difficulties with the treatment and may cause adverse health effects. The increasing numbers of elderly is furthermore expected to increase the risk of epidemics in t he future (Health Protection Scotland) Toxin-producing strains of C. difficile are carried in the normal colonic microflora of only about 5% of healthy adults (Kelly, Pothoulakis et al.,1994). However, 15% to 70% of neonates are carriers of C. difficile (Riley 1998). This percentage varies as a result of the degree of hospital exposure, birth in an environment where C. difficile is abundant, or if the neonate obtained maternal antibodies through breast milk. Although neonates are more frequent carriers of C. difficile, they do not often develop pseudomembranous colitis unless gastrointestinal motility disorders or other conditions (eg, severe neutropenia with leukemia) are present to increase the risk. Neonatal resistance to C. difficile colitis is believed to be due to the inability of the toxins to attach to the mucosa of newborns, because of immature membrane toxin receptors, or the protection from the toxins by maternally-acquired antibodies. After the first year of life, the carrier rate gradually decreases, reachin g adult levels by three years of age (Reinke and Messick 1994; Matsuki, Ozaki et al.,2005; Tonooka, Sakata et al.,2005; Trejo, Minnaard et al.,2006). Clostridium difficile-associated diarrhea (CDI) has become an increasing clinical problem as a nosocomial disease affecting mainly the elderly, patients with serious underlying diseases, and surgical patients (Bignardi 1998; Brazier 1998; Karlstrom, Fryklund et al.,1998). C. difficile probably represents the most common current cause of bacterial diarrhea in developed countries and, besides caliciviruses, the most common nosocomial diarrheal pathogen (Samore, DeGirolami et al.,1994; Karlstrom, Fryklund et al.,1998). Based on laboratory reports, at least 5,000 cases of CDI occur every year in Sweden, corresponding to 60 cases per 100,000 inhabitants per year, and more than 70% of the cases are associated with a hospital stay (Karlstrom, Fryklund et al.,1998). Currently over 6,000 cases were reported in Scotland from October 2006 until September 2007 (Health Protection Scotland). Clusters of nosocomial cases of CDI have been attributed to transmission of C. difficile between patients but also indirectly through the hands of health care workers or via contaminated surfaces or vomit (McFarland, Mulligan et al.,1989; Clabots, Johnson et al.,1992). Furthermore, some strains may be more transmissible and also more virulent than others and thus be associated with higher attack rates and a high local incidence of CDI (Johnson, Samore et al.,1999). A study performed over 10 years ago reported a low frequency of CDI in the community (7.7 cases/100 000 person-years of observation) (Hirschhorn, Trnka et al.,1994). A more recent report from the Centers for Disease Control and Prevention estimated that the minimum annual incidence of community-acquired CDI in the Philadelphia area between July 2004 and June 2005 was 7.6 cases/100 000 population (2005). Nine percent of patients in the present study had no previous exposure to the healthcare system, and were considered to be genuine cases of community-acquired CDI (Price, Dao-Tran et al.,2007). It was difficult to ascertain genuine cases of community-acquired CDI admitted to this tertiary care hospital. C. difficile is now the first organism suspected by health care personnel when a hospitalized patient develops diarrhea. C. difficile infection is a nosocomial disease that spread primarily by the medical staff, and hospital epidemics are relatively common. Usually, patients acquire the organism from the hospital and not from their own flora. C. difficile-associated disease (CDI) is increasingly being reported in many regions throughout the world. Moreover, severe disease has been reported in non-traditional hosts (e.g. younger age, seemingly healthy, non-institutionalized individuals residing in the community, and some without apparent antimicrobial exposure). In addition to the sudden increase in frequency of CDI, an increased rate of relapse/recurrence, disease severity and resistance to traditional treatment have also been noted. Much of this change was due to the emerg ence of one toxigenic strain, classified according to PCR as ribotype 027/toxinotype III and pulsed-field gel electrophoresis (PFGE) as NAP1 (Warny, Pepin et al.,2005) (Figure 8). This epidemic strain represented 2à ¢Ã¢â€š ¬Ã¢â‚¬Å"3% of hospital isolates of C difficile (Rupnik, Avesani et al.,1998; Rupnik, Brazier et al.,2001; Geric, Rupnik et al.,2004). By using restriction endonuclease analysis, the same genotype as NAP1/027 (also known as type BI) was found in only 14 of more than 6000 US historic isolates obtained before 2001 (McDonald, Killgore et al.,2005). NAP1/027 was not reported to cause either severe disease or outbreaks until recently, when it was identified as the cause of several outbreaks in the USA (McDonald, Killgore et al.,2005). In Sherbrooke, between 2003 and 2004, it was found that as many as a sixth of inpatients with health-care-associated C difficile as a direct or indirect consequence of this infection (Pepin, Valiquette et al.,2005). On June 4, 2004 tow outbreaks of NAP1 were reported in Montreal, Quebec and Calgary, Alberta, in Canada (Eggertson 2004). Sources put the death count as low as 36 and high as 89, with approximately 1,400 cases in 2003 and within the first few months of 2004.C .difficile infection continues to be a problem in the Quebec health care system in the 2004. As of March 2005, it has spread into the Toronto, Ontario area, hospitalizing 10 people. One has died while the others have been discharged. A dominant strain that was pulsed-field gel electrophoresis (PFGE) type NAP1, toxinotype III, and contained a tcdC deletion and ctdB was also discovered in samples from a Stoke Mandeville Hospital in the United Kingdom between 2003 and 2005 and from other outbreaks which were associated with increased morbidity, frequent need for colectomy, and mortality in the USA (McEllistrem, Carman et al.,2005). This strain has also been implicated in an epidemic at two Dutch hospitals (Harderwijk and Amersfoort, both 2005). Moreover, retrospectively the strain has been identified in isolates from sporadic US cases obtained in the early 1980s (McDonald, Killgore et al.,2005). The finding of an association between NAP1/027 (or BI) and high toxin production in the context of an epidemic associated with a high case-fatality ratio confirms the suspicion that the epidemic in Quebec and UK is caused by a more virulent strain (Pepin, Valiquette et al.,2005). In the UK, where the number of reported cases of CDI doubled over 3 years, NAP1/027 is the cause of ongoing outbreaks in at least three hospitals with a high case-fatality ratio (health protection agency). The appearance of this virulent strain, in association with certain environmental and antimicrobial exposure factors, may be combining to create the perfect storm (Owens 2007). In 2005 C. difficile spores was isolated from 12 (20%) of 60 retail ground meat samples purchased over a 10-months in Canada. Eleven isolates were toxigenic, and 8 (67%) were classified as toxinotype III. which suggests that C. difficile also could be responsible for food poisoning or at least be foodborne. Previously, a study investigating the role of psychrotrophic clostridia on blown pack spoilage of commercial packages of chilled vacuum-packed meats and dog rolls reported 2 incidental isolates of C. difficile (Moorhead and Bell 1999). In Bacteriological evaluation of commercial canine and feline raw diets C. difficile was isolated on direct culture from 1 turkey-based food (Weese, Rousseau et al.,2005). In terms of cost and productivity, C. difficile is a major burden to our health care system. There are estimated to be 250,000 to 300,000 cases of C. difficile a year in U.S. hospitals, which cost hundreds of millions of dollars for hospital care. Hospital costs for this condition in the USA (Kyne, Hamel et al.,2002) and UK (Wilcox, Cunniffe et al.,1996) exceed US$4000 per case. A typical case results in 1 to 2 extra weeks of patient care costing roughly $10,000. This price assumes that the patient responds to treatment and does not relapse or develops complications (Wilkins and Lyerly 2003). The incidence of CDI has increased in the past decade, with a 10-fold increase reported in Quebec (Pepin, Valiquette et al.,2004), as has the proportion of patients who have severe, refractory, or recurrent disease (Musher, Aslam et al.,2005). The successful control of C. difficile will require healthcare systems (including administrators, and leadership within several departments such as environmental services, infection control, infectious diseases, gastroenterology, surgery, microbiology and nursing), clinicians, long-term care and rehabilitation facilities, and patients themselves to be proactive in a collaborative effort (Owens 2007). 1.11 Reservoirs, sources, and transmission of C. difficile The major reservoirs for C. difficile in the hospital and community infection are patients with CDI or asymptomatic carriers of C. difficile. Patients with symptomatic disease heavily contaminate their immediate hospital environment and the spores can persist for several months on surfaces. Shedding of C. difficile into the environment depends on the patients status. In one study, they compared the rate of environmental contamination in rooms of patients with C. difficile-associated diarrhea to that of contamination in rooms of C. difficile asymptomatic carriers. They showed that contamination was significantly higher in rooms of patients with diarrhea compared to asymptomatic carriers. They also analyzed contamination in rooms without C. difficile-positive patients and found a contamination rate of 8%, showing that spores of C. difficile can persist, despite routine cleaning of rooms (McFarland, Surawicz et al.,1990). C. difficile diarrhea was reported as a community acquired infection in Ireland in 1998 (Kyne, Merry et al.,1998). CDI has also been reported in the community as an emerging pathogen in animals. Early typing comparisons did not identify animals as an important source for human Infection. In 1983 C. difficile was isolated in household pets such as dogs and cats in the UK (Borriello, Honour et al.,1983). In 2001 in Canada C. difficile was also associated with diarrhea in dogs and cats (Weese, Staempfli et al.,2001) but recent report in 2006 from Canada have shown a marked overlap between isolates from calves and humans, including two of the predominant outbreak types, 027 and 017 which suggested that C. difficile may be associated with calf diarrhea, and cattle may be reservoirs of C. difficile for humans (Rodriguez-Palacios, Stampfli et al.,2006). C. difficile has also been found in retail meat samples, suggesting that food could be involved in the transmission of C. difficile from animals to humans (Rupnik 2007). Over the past 5 years, C. difficile has emerged as a major cause of neonatal enteritis in pigs. Piglets 1à ¢Ã¢â€š ¬Ã¢â‚¬Å"7 days of age are affected (Songer and Anderson 2006; Yaeger, Kinyon et al.,2007), with gross lesions frequently including mesocolonic edema. Colonic contents may be pasty-to-watery and yellow, although some piglets are constipated or obstipated. In 2007 a study was carried out to assess the correlation between the presence of C. difficile toxins (TCd) in the colon contents of neonatal pigs and a number of parameters, including gross evidence of diarrhea mesocoloninc edema, typhlitis, and colitis. They found C. difficile may represent an important subclinical issue in neonatal swine (Yaeger, Funk et al.,2002). In 2006 study from Zimbabwe was to determine the prevalence of C. difficile in faeces of domestic animals (chickens, rabbits ,cattle, and goat), soil and drinking water in a rural community. The results of the study have shown that 95% of the samples were positive for C. difficile and chickens are a major reservoir of C. difficile in rural communities in Zimbabwe, where it was isolated in 17.4% of chicken feces samples. Detection of C. difficile in well water and household-stored water demonstrates the potential of water as a source of infection. Some of the water contamination may have been through faecal material of some domestic animals such as chickens, cattle and goats, which are kept as free-range animals in the community studied. Also it was found that C. difficile was not-uncommon cause of enteric disease in mature horses, mostly when they are treated with antimicrobials and hospitalized (Baverud, Gustafsson et al.,2003; Baverud 2004). In 2006 a first report of C. difficile as the main cause of fatal enterocolitis in elephant came from Denmakr when they retorted two cases of fatal enteritis caused by C. difficile in captive Asian elephants are reported from an outbreak affecting five females in the same zoo. It is speculated that the feeding of large quantities of broccoli, a rich source of sulforaphane, which has been shown to inhibit the growth of many intestinal microorganisms may have triggered a subsequent overgrowth by C. difficile (Bojesen, Olsen et al.,2006). Transmission of C. difficile is thought to occur via the oroà ¢Ã¢â€š ¬Ã¢â‚¬Å"fecal route. Outbreaks in hospitals and typing of strains suggested that transmission is probably via staff hands. A study documented positive hand cultures in 59% of hospital personnel caring for patients with positive culture (Samore, Venkataraman et al.,1996). Transmission can also occur by direct contact with contaminated surfaces. Some reports also suggested a transmission by direct inoculation into the bowel via contaminated materials such as thermometers (Jernigan, Siegman-Igra et al.,1998). Factors that may explain the ease of transmission include resistance of the spores to the most commonly used disinfectants and antiseptics, the antibiotic pressure in hospitalised patients and the promiscuity of patients. Unrecognized patients with C. difficile, or re-admissions of patients with C. difficile, can contribute to the reintroduction and spread of C. difficile to other patients or the environment. By using restriction endonuclease as a typing method, showed that 84% of cases of nosocomial acquisition of C. difficile strains were preceded by a documented introduction of the strain to the ward by another asymptomatic admission (Clabots, Peterson et al.,1988). 1.12 C. difficile typing methods 1.12.1 Phenotyping method: C. difficile has been typed by using different methods based on phenotypic properties; one of these methods was antibiograms, which was one of the early methods. Isolates resistant to three different antibiotics were found in one of the first documented outbreak investigations (Burdon 1982). Those isolates were found in the surgical ward and were distinct from isolates in the rest of the hospital. However, this method is at best only preliminary, and more detailed approach was tried by WÃÆ' ¼st and co-workers who combined soluble protein polyacrylamide gel electrophoresis (PAGE), plasmid analysis, immunoelectrophoresis of extracellular antigens and antibiograms to a number of isolates from related cases of C. difficile infection (Wust, Sullivan et al.,1982). By using these methods, they showed that 12 of the 16 strains were similar, showing strong evidence, that cross-infection had taken place. A combination of bacteriophage typing and bacteriocin methods has been used which showed a high percentage of non-typeable strains (Sell, Schaberg et al.,1983). In 1981 the immuno-chemical fingerprinting of EDTA-treated cell extracts of C. difficile was evaluated (Poxton and Byrne 1981). Nakamura and co-workers were the first investigators to use serum agglutination as a typing method by raising three antisera against C. difficile (Nakamura, Mikawa et al.,1981). This method could differentiate four marked serovars among 79 isolates from healthy carriers. In 1985 DelmÃÆ' ©es group improved this method and developed a serotyping scheme that could recognise 19 distinct sero-groups (Delmee, Homel et al.,1985). This method is repeatedly used as the standard by which other typing methods are compared. These early typing methods were developed to understand the epidemiology of C. difficile infection at a local level, which were adequate for local use; there was a need for typing schemes that could be implemented to further understanding of the epidemiology of C. difficile disease on a wider scale. To facilitate this, comparisons between typing schemes were performed, and in 1988 Mulligan and co-workers found good correlation between the types recognised by serotyping, PAGE, plasmid profiling of cell surface antigens and immunoblotting (Mulligan, Peterson et al.,1988). Sodium dodecyl sulfate (SDS)-PAGE of whole-cell proteins was applied to 79 isolates in an outbreak investigation, which yielded a maximum of approximately 40 bands ranging in size from 18 to 100 kilo-daltons (kDa). This investigation showed 60 of the 79 isolates was similar. Serogrouping was compared to SDS-PAGE of EDTA-extracted cell surface antigens and 61 isolates were analyzed (Ogunsola, Ryley et al.,1995). This method showed bands of sizes between 30 and 67 kDa and distributed their 79 isolates into 17 groups, which were similar to the results of serogrouping. A method of whole-cell fingerprinting by pyrolysis mass spectrometry (PMS) has been successfully used in investigating C. difficile outbreaks which had the advantage that it could cope with a large number of strains and had a high degree of differentiation (Magee, Brazier et al.,1993). However, the disadvantages of this method were the high cost of the equipment and its inability to assign a permanent type to a strain. 1.12.2 Molecular typing methods: In terms of the stability of marker expression and providing greater levels of typeability, molecular typing methods are generally regarded as superior to phenotypic methods and a number of molecular methods have been used in C. difficile. Due to the sparse distribution of the extra-chromosomal genetic elements within the species, plasmid profiling proved largely unsuccessful. However, in 1987 Kuijpers group analyzed the chromosomal DNA of C. difficile by using whole cell DNA restriction endonuclease analysis (REA) in which HindIII was used in the investigation which showed cross-infection between two patients in the same room (Kuijper, Oudbier et al.,1987). REA is a highly reproducible and discriminatory method; however, the disadvantages are it is very labor-intensive and a technically demanding procedure, especially for large numbers of isolates. An alternative genotypic method (Saiki, Scharf et al.,1985) called the restriction fragment length polymorphism (RFLP) which involves initial REA digestion followed by gel electrophoresis and Southern blotting was used to detect specific restriction site heterogeneity. RFLP, however, is also a very labor-intensive method and REA/RFLP methods have generally been replaced by methods based on the polymerase chain reaction (PCR). Another genotypic method is called arbitrarily primed PCR (AP-PCR) which permits the detection of polymorphisms within the target genome without prior knowledge of the target nucleotide sequence. A closely related method is called random amplified polymorphic DNA (RAPD). This method commonly uses two oligonucleotide primers which are arbitrary sequences and short in length (c.10 bp). In 1994, a method was evaluated by Barbut and co-workers using two 10-bp primers in an investigation of antiobiotic-associated diarrhea (AAD) in AIDS patients (Barbut, Mario et al.,1994). The discriminating ability of t this method was virtually unlimited as it was always possible to use other random primers. It is also simpler and more rapid than the other molecular methods which came later on such as restriction enzyme analysis or pulsed field gel electrophoresis. PCR ribotyping was first applied to C. difficile by using specific primers complementary to sites within the RNA operon this was carried out by Gurtler who targeted the amplification of the spacer region between the 16S and 23S rRNA regions (Gurtler 1993). C. difficile was shown to possess many copies of the rRNA genes, which differ in number and size between strains and also within the same genome. This approach was modified by Cartwright and co-workers who tested it in 102 isolates obtained from 73 symptomatic patients (Cartwright, Stock et al.,1995). The primers used in this study were the same primers used by Gurtler, and instead of using denaturing PAGE gels, their PCR fragments were separated by straightforward agarose gel electrophoresis. Furthermore, they showed that the quantity of DNA used in the reaction does not affect the banding patterns which was a problem associated with AP-PCR and RAPD methods. This approach was modified for the routine use by ONeill and co-workers who improved and simplified the DNA extraction method by using modified primers to the 16Sà ¢Ã‹â€ Ã¢â‚¬â„¢23S spacer region. This method was able to produce fragments ranging from 250 to 600 bp separated by agarose gel electrophoresis (Cartwright, Stock et al.,1995). Since 1995, this method has been used routinely by the UK Anaerobe Reference Unit in Cardiff, which provides a C. difficile typing service for the UK. A library consisting of 116 distinct ribotypes from over 3000 strains from all sources examined, has been constructed (Stubbs, Brazier et al.,1999). Contrary to the other methods, the whole genome is analyzed by pulsed field gel electrophoresis (PFGE) after digestion with rare cutting restriction endonucleases, such as SmaI, KspI, SacII or NruI, which result in 10 fragment length polymorphisms per strain. PFGE has been applied successfully to investigate 30 epidemiologically unrelated isolates and 22 isolates of C. difficile from an outbreak in an elderly care centre (Talon, Bailly et al.,1995). PCR ribotyping was considered more distinctive than AP-PCR and PFGE methods in a study (Collier, Stock et al.,1996). The disadvantages of PFGE include the initial cost of the equipment, the slowness of the procedure and its complexity. Bidet and co-workers compared all three methods and concluded that PCR ribotyping, is the best technique for C. difficile ribotyping (Bidet, Lalande et al.,2000). It was noted that some strains are untypeable by PFGE due to degradation of the extracted DNA and those strains belong to serogroup G, which corresponds to PCR ribotype 1 in the Stubbs group library (Stubbs, Brazier et al.,1999). Rupnik has developed the toxinotyping method by describing 11 toxinotypes and has been compared to PCR ribotyping (Rupnik, Brazier et al.,2001). Good correlation has been noted between the two methods, whilst applying toxinotyping to each type in the PCR ribotype library, five novel toxinotypes were discovered (Brazier 2001).

The Evident Existence of Races Free Essays

string(25) " areas of the community\." Many sociologists believe that ‘races† do not exist therefore have to find alternative groupings to study racism or patterns of racial disadvantage in the United Kingdom. There exist many differing theories but no finite method of determining the true cause of racism. This dissertation will outline the different theories used by sociologists and attempt to show the patterns of ethnic disadvantage present in Britain. We will write a custom essay sample on The Evident Existence of Races or any similar topic only for you Order Now Racism is thought by many to be the notion that some ethnic groups are naturally superior to others. The Oxford Dictionary†s definition of the word ‘race† is ‘ A group of persons of common stock† ‘Human abilities are determined by â€Å"race†Ã¢â‚¬ . Although ‘Race† and Racism are defined in the oxford dictionary sociologists claim that ‘races† do not exist. They have considered the work of human biologists who in turn have studied the genes of many individuals that are said to be associated with different ‘races†. The results of these studies show that there is no distinctive gene that defines which ‘race† a person belongs to. Blood groups have been examined and results show that while some ‘races† have higher tendencies to certain blood types, no one ‘race† has been found to have one particular blood type unique to their origin. Due to there being no conclusive biological evidence biologists refer to different ‘races† as different populations. Any cultural differences are said to be ethnic differences, not differences in race. There is a belief that if ‘race† does not exist then sociologists can†t rightfully use the term in their study of different populations. It is due to this belief that they must find alternative ways of analysing population differences. The history of ‘race† is important to examine in the attempt to show why ordinary people, known as actors, still think that ‘race† exists. Racism is thought to have always existed. The Romans considered slaves as being inferior to themselves, but there has been no scientific evidence to support claims of superiority. In the early 18th century until early in the 19th century there was a progressive belief that there was basic similarity between all men, that social differences were due to the environment. This view was overridden by the rise of scientific racism where all social differences found previously were labelled and explained as ‘natural†. But again ‘race† has never been a scientific concept. It was due to this that in the 20th century political/moral reasons forced scientific racism into decline and was eventually replaced by cultural racism, which shares the same beliefs. Racism is thought to be a set of beliefs and racial discrimination the set of practices that are synonymous with these beliefs. There are several contrasting views of racism and racial discrimination. The functionalist model looks upon it via the perspective of ‘race† relations, that racism exists due to the creation of bad relations between ‘races†. Due to ‘race† not existing, functionalists study situations that are apparent in society. They look at events which actors define as racial, and by this expedient they examine the processes of racialism. John Rex a radical weberian believes in the conflictional view that competition over scarce resources in different markets is the cause of conflict between Afro-Caribbean†s, Asians and whites in relation to employment and housing (Bulmer et al, 1999:335). He say†s that it is not due to the lower wages which ethnic minorities receive. The Marxist perspective focuses on labour relations. An ideology masking contradiction of capital between capitals† need for free labour and nationalism. Robert Miles, a hard line Marxist believes that class is the determining factor and all inequalities derive from class inequalities. Miles is very much alone in his claim but gives the example of the white working class fearing immigrants due to a rise in unemployment levels and a decline in standard of living. However, Miles states that the immigrants were not the cause of this. He claims that capitalism was. He states many find this hard to see because: ‘We are offered definitions and theories of racism which are so specific to the history of overseas colonisation (that is specific to the domination of ‘white† over ‘black† as so many writers express it) that they are of little value in explaining any other non-colonial) context† (Miles, R (Bulmer et al, 1999:344)) Another Marxist theory focuses on wider relations. ‘Race† has no reality but can be used in analysis, this theory is concerned with racial politics and how they may be independent of class. Marxists who follow this belief say that groupings and conflicts intersect, and may not actually be connected with class. With the term ‘race† being seen as invalid by many people the question has arisen. Are we better to talk about ethnicity rather that ‘race†? Ethnicity is a sense of identity to a group that shares a common history. Ethnic groups are also held together by ties of language, culture and group spirit that are now referred to as nationalism. There are also territorial ties, although many ethnic groups had previously left their homeland they still share a common geographical link. The term ethnicity is often confused with ‘race†, again when talking about ethnicity there have never been boundaries whether cultural or geographical that clearly states the limits of ethnic groups, even though many believe ethnicity is naturally determined. The idea that ethnicity is ‘natural† is said to be ‘wrong†. Ethnic differences are cultural, we all have an identity, though we may not always be conscious of it. There has recently been a revival of ethnic differences followed by reactions to discrimination and racial disadvantage. An example of this is Afro-Caribbean†s beliefs of what Britain would be able to offer them, these beliefs have changed due to certain types of discrimination and disadvantage. Cultural and religious issues can now be seen as more significant than economic inequalities. There are however some problems with ethnicity. Emphasis is placed on difference and cultural issues of power and inequality, therefore, ethnic groups may be seen to be fixed racial groups with another identity. Racial disadvantage in the United Kingdom is visible in many different areas of the community. You read "The Evident Existence of Races" in category "Papers" Employment, education and crime are just a few examples. Throughout employment, horizontal segmentation can be seen to be apparent via clustering. Ethnic minorities are more likely to work for themselves, graduates from these backgrounds tend to do relatively badly, many Asians are self-employed and Afro-Caribbean†s are largely recruited to the private sector. This shows that ethnic or racial factors are involved in stratification in Britain. Within the generalisation that, ethnic minorities are treated less equally, individual successes and inter-group variations are present. This is shown by vertical segmentation, Afro-Caribbean†s being placed at lower levels of employment than Asians. When the ‘The Race Relations Act ‘ was amended in 1976 The Commission for Racial Equality was established to promote racial harmony. This was to try to counter the acts which had been enforced prior to the Race Relations Act of 1965. Such acts, for instance, as the British Nationality Act 1948 and the Commonwealth Act 1962 which where more concerned with restricting immigration than trying to promote good ‘race† relations. In the context of the recruitment of employees, the Race Relations Act 1976 stated that it is unlawful to discriminate: By a company giving racial instructions to a personnel officer or an employment agency. In relation to terms of pay. By rejecting an applicant or refusing to consider him for the post on the basis of race. These laws were enacted in order to try to increase equality in employment. As a mechanism to bring about change to employment rights the Commission for Racial Equality has made extensive recommendations to successive governments including a move to make ethnic monitoring compulsory for all employers with an excess workforce of 250. In the belief that ethnic monitoring is essential for progressing to racial equality. Racial disadvantage has also been found to be present in the theatre of education. Before 1973 it was known that white pupils topped the performance list with Asians and Afro Caribbean†s coming further down. The differences in levels of performance were considered to be related to the duration of the pupils† stay in the UK. Newcomers would have experienced problems adapting to a new way of living and may even have encounter communication problems. Moving on to early 1970†³s – 1980†³s the focus of discrimination in education moved to examine the effects of class and the school at which they enrolled. It was found that ethnic minorities are more likely to go to an underachieving school than their white counterparts due to their class framework, lower income and location. Curriculum was also thought to be a cause of the poor academic findings relating to ethnic minorities. The syllabus that the schools were offering was not relevant to children from ethnic backgrounds, a ‘white curriculum† concentrated on ‘white history† and the history of Britain. This was modified to give a wider education on the history of ethnic countries in an attempt to make studies more relative for ethnic minorities. With these problems tackled, education monitoring in the 1980†³s showed children from ethnic backgrounds to be improving at a faster rate than white children of the same age. Schools support the right of all children to receive quality education and fair treatment. The governing body of education aims to ensure that no one receives less favourable treatment on the grounds of race or any other social/cultural labels. It is believed that racism can be learned from an early age but to control this unwanted learning the children must be taught respect for other people in-order that they might learn ‘rights from wrongs† ‘If segregation of the sexes or races prevails, if authoritarianism and hierarchy dominate the system the child cannot help but learn that power and status are dominant factors in human relationships†¦.If the teacher and the children are each respected units, the lesson for respect for the person will easily register† The Race Relations Act of 1976 again places barriers on education by stating that; ‘By excluding a pupil from the establishment or by treating him unfavourably in any other way† is unlawful. Now in higher education a higher percentage of ethnic children stay on after 16 years old. This is encouraging but fewer now enrol at university, on academic courses and more drop out. This however can no longer be explained due to lack of adjustment since most were born here and therefore need no time to adjust to the a new community or learn a new language. Within the Criminal Justice System racial discrimination also exists. It is understood that black people are far worse off at every stage of law enforcement. They are more likely to be stopped by Police, charged with serious offence, prosecuted, convicted, and imprisoned. They are less likely to be given lenient treatment for example, fined, put on probation, or allowed bail. It has been declared that in 1997 the United Kingdom had one of the highest levels of racist orientated attacks in Europe, and that 1 in 3 British citizens classed themselves as racist (Thompson B., Roots of poison). Racial hatred and prejudice is an example of extremism, when cultural differences start being connected to ‘race† a persistent hatred can occur. Racism, it is argued, is a specific form of discrimination usually associated with skin colour and ethnicity. It involves the use of power of one group over another. When this power is unequal it enables those that share a particular culture to deny others access to opportunities, hence treat them in a racist way. As well as being more inclined to be the perpetrators of crimes, ethnic minorities are also prone to be the victims. These crimes are not however due to ethnic background but are due to the social background of their class. Despite this, people are sometimes ignorant to this fact and state that ethnic crimes are more apparent because they are of an inferior race. A Report by Sir William Macpherson that examined the Lawrence case (in which it was claimed that the police neglected their job because the victim was ‘black†), was published on 24th February 1999. In the report, which was presented to the Government and to the Home Office, McPherson revealed that the problems, which occurred during the case, were the result of Institutional Racism defined as; ‘The collective failure of an organization to provide an appropriate and professional service to people because of their colour, culture or ethnic origin† It was said that institutional racism can not be used in the labeling of individuals but must be a label that is associated with the organization as a whole. It is due to the finding of racial disadvantage, that the police have set up ‘Operation Athena† to tackle the problems outlined in the report. The operation aims to improve prevention, awareness, communication, response and the identification of needs in the context of ethnic minorities. The three examples of employment, education and crime are only a selection of the sectors of the community that show racial disadvantage. Although there is no finite definition of ‘race† there has been continual work to improve the social conditions for ethnic minorities. It is hoped that in the future there will be racial harmony between all populations and that ‘true† equality will be gained. How to cite The Evident Existence of Races, Papers

Proposition 187 Dont Mess With Texas Essay Example For Students

Proposition 187: Dont Mess With Texas Essay Proposition 187: Dont Mess With TexasIn November of 1994, Californians passed the most controversial piece ofstate legislation this decade. Proposition 187 was designed to stem the flow ofillegal aliens into California by withholding all non-emergency medical benefitsfrom non-naturalized citizens. Latinos turned out in record numbers to voicetheir disapproval, and for good reason too. The health care resolutions ofProposition 187 were products of poor reason and unsound economic judgment. Theresolutions did not get the state any closer to a balanced budget, and onlyserved to worsen the health care outlook for the future of California. It isclear that Proposition 187 was a mistake, and should not be encouraged to berepeated in Texas. The most popular reason for passage, that supporters of Proposition 187used, was the theory that a cut in illegal health services would save statetaxpayers several million dollars a year. This argument only applies to statesthat have a personal income tax, often used to help fund health care for thestate, and when the illegal immigrants avoid paying this tax. Texas does nothave such a tax, so health care is funded by the taxes that everyone in thestate pays. That means that illegal aliens are paying just as much as realAmericans are in sales taxes, gas taxes, liquor taxes, and cigarette taxes. Forexample, illegal aliens in San Diego, California accounted for 26.6 milliondollars in health care costs in 1994 (Serb 63). Not a single person would denythat this is a lot of money, and therefore would seem to be an excellent reasonto cut funding right this minute. However, the logical person has to realizehow important those same aliens are to filling the states excise tax cofferseach year. Excise taxes paid by illegals were accounting for up 60.5 millionin state tax alone (63). In retrospect, it hardly seems right to say thatillegal immigrants are not paying their fair tax share for their health needs. It also isnt fair that U.S. businesses need Mexican workers for low-payingjobs, but dont want them to have access to heath care while they are here(Hudson 37). Another economically based reason, that proponents of 187-likelegislation have made, is that Texans will save money by denying non-emergencycare to illegal aliens. Without close scrutiny, this seems to be a claim to makethe pocket book happy. After all, we would still allow the aliens the rightto life saving treatments, but we would also save a bundle by cutting the littlevisits to the doctor for fevers, colds, and sprained ankles. What Texans have toask, though, is how do we save money when we deny a forty-five dollar visit tothe doctor for strep throat, but allow a twenty thousand dollar visit tointensive care when that alien develops scarlet fever from the strep infection(Cowley 53). It would have been much more cost-effective to have provided directcare services up front, and California quickly found this to be true. Prematurebabies cost San Diego more than $500, 000 dollars. Complications frompregnancies added an additional $112,000 to the bill (Serb 63). According to theclaims made, these types of costs should have disappeared after #187 was passed. The illegal immigrants were supposed to return to Mexico for their pre-natalcare, but the evidence proves they didnt. Instead, the illegal mothers receivedno pre-natal care, and had emergencies that cost the state even more money. There are more problems with Proposition 187-like proposals than justeconomic problems. Texans must be aware of the moral and ethical problems wewould create if we supported a similar plan for Texas. For instance, CatholicBishop John Ricard points out that if Texans explicitly set out to identify allillegal aliens, and stop them from receiving care, we are likely to have adiscriminatory situation. Every American with tan skin and a name ending in zis likely to be perceived as potential illegal immigrants (Health 248). TheNational Christian Coalition also points out that to measure national healthcare decisions more by economic than moral or compassionate standards isappalling (248). But even more appalling is what we are asking our nationsdoctors to do. By requiring that physicians report every immigrant withoutdocumentation, and to refuse them treatment when ill, we are boldly demandingthat they violate their sacred Hippocratic oath. Care providers have based theirprofessions on hel ping any person in need since the time of the ancient Greeks. .u9766c260e0aa8c1134699156be078bc3 , .u9766c260e0aa8c1134699156be078bc3 .postImageUrl , .u9766c260e0aa8c1134699156be078bc3 .centered-text-area { min-height: 80px; position: relative; } .u9766c260e0aa8c1134699156be078bc3 , .u9766c260e0aa8c1134699156be078bc3:hover , .u9766c260e0aa8c1134699156be078bc3:visited , .u9766c260e0aa8c1134699156be078bc3:active { border:0!important; } .u9766c260e0aa8c1134699156be078bc3 .clearfix:after { content: ""; display: table; clear: both; } .u9766c260e0aa8c1134699156be078bc3 { display: block; transition: background-color 250ms; webkit-transition: background-color 250ms; width: 100%; opacity: 1; transition: opacity 250ms; webkit-transition: opacity 250ms; background-color: #95A5A6; } .u9766c260e0aa8c1134699156be078bc3:active , .u9766c260e0aa8c1134699156be078bc3:hover { opacity: 1; transition: opacity 250ms; webkit-transition: opacity 250ms; background-color: #2C3E50; } .u9766c260e0aa8c1134699156be078bc3 .centered-text-area { width: 100%; position: relative ; } .u9766c260e0aa8c1134699156be078bc3 .ctaText { border-bottom: 0 solid #fff; color: #2980B9; font-size: 16px; font-weight: bold; margin: 0; padding: 0; text-decoration: underline; } .u9766c260e0aa8c1134699156be078bc3 .postTitle { color: #FFFFFF; font-size: 16px; font-weight: 600; margin: 0; padding: 0; width: 100%; } .u9766c260e0aa8c1134699156be078bc3 .ctaButton { background-color: #7F8C8D!important; color: #2980B9; border: none; border-radius: 3px; box-shadow: none; font-size: 14px; font-weight: bold; line-height: 26px; moz-border-radius: 3px; text-align: center; text-decoration: none; text-shadow: none; width: 80px; min-height: 80px; background: url(https://artscolumbia.org/wp-content/plugins/intelly-related-posts/assets/images/simple-arrow.png)no-repeat; position: absolute; right: 0; top: 0; } .u9766c260e0aa8c1134699156be078bc3:hover .ctaButton { background-color: #34495E!important; } .u9766c260e0aa8c1134699156be078bc3 .centered-text { display: table; height: 80px; padding-left : 18px; top: 0; } .u9766c260e0aa8c1134699156be078bc3 .u9766c260e0aa8c1134699156be078bc3-content { display: table-cell; margin: 0; padding: 0; padding-right: 108px; position: relative; vertical-align: middle; width: 100%; } .u9766c260e0aa8c1134699156be078bc3:after { content: ""; display: block; clear: both; } READ: The Value Of A Jury System Essay SummaryIn true spirit doctors should know no boundaries between two lands. In fact, whyshould they refuse to give treatment because a person happens to be on this sideof the Rio Grande when they fall ill? After all, bacteria and virusesdistribute themselves without regard for national borders (Gaffney 228), anddiseases like tuberculosis do not check for immigration status (Health 248). Some citizens might believe that diseases like tuberculosis were a thing of thepast, but a Californian study found that seventy percent of all immigrantsarrive carrying the germs that cause tuberculosis (Cowley 53). Remember thatthese are immigrants that were able to save up enough money at home to make thevoyage to America, and not be broke when they got here. The percentage ofillegal aliens carrying diseases is probably a lot higher than 70%. They dontget sick because they have built-in immunities for the diseases found in theirhomelands, but we do not have many of the same immunities that illegals have. The result is that the diseases go undetected until an emergency arises and the alien can be seen by a doctor. By not allowing illegal aliens to receive non-emergency care, we are putting our little Texans at risk. As we prepare for the possibility that similar proposals might beadvocated in Texas, let us all remember the ideals of humanity that we like tosay that we all share. Every American likes to think that they have a kind andcaring attitude toward the less fortunate, but a short case study published inNewsweek shows exactly how kind and caring legislation like Prop. 187 would be. In the case study, the family of Julio Cano, a twelve-year-old, anguish overwhether or not to take their son to a doctor in California. Julio had developeda deep cough accompanied by severe shooting pains down his back. The familydecided not to risk a doctor visit because Proposition 187 had just ordered thatany illegal seeking care be reported. Instead the family waited until thecondition worsened enough to be able to call the paramedics, but by then it wastoo late. Little Julio died from leukemia on the way to the hospital. We must keep our pocket books out of the decision to reform health care,and instead keep the true story of Julio Cano in our hearts. Why should we turnour backs on aliens residing in this country just because a few citizens, mostwith little real knowledge of the true situation, think that this is the way toend illegal immigration. Illegal aliens are hired by many, many people to mowthe lawn, watch the kids, clean the house, or to cook for the family. A lot oftimes, you neighbors do not claim these workers as employees in order to skipout on taxes themselves, and thus avoid paying their fair share. With thebenefit of hindsight, Californians are now able to see just how poor theirreasoning was when they passed Proposition 187. There is no doubt that Texanswill meet that call to find other ways besides cutting health care to stem thetide of illegal immigrants. Maybe health care costs of aliens can become a partof the federal budget. Also, the federal government could try and improverela tions with Mexico and persistently show the economic burden that their lackof border control is having on states such as Texas. Whatever is done though,Texans will not jump hastily into action. Any resolution will be the product ofcareful reasoning and informed economic judgements.