The Nurses Role in Patient Advocacy

Caring originates in the relationships of shared human experience. The nurses primary roles of promoting health, preventing illness, restoring health and alleviating suffering places the nurse in a position to always remain an advocate for their patient. A scenario has been created in which a terminally ill patient has asked the doctor about alternative healthcare treatment options. The doctor in this case dismisses them as â€Å"quack† practices.What role does the nurse play in this situation? â€Å"When the patient’s wishes are in conflict with others, the nurse seeks to help resolve the conflict. Where conflict persists, the nurse’s commitment remains to the identified patient† (Code of ethics for nurses with interpretive statements, 2001). Moral courage is something that helps the nurse to address ethical issues and take action when doing the right thing is not always easy.When a patient and doctor relationship is strained the nurse can sometimes help mediate a situation while always remembering her legal and ethical obligations. Physicians and nurses have different roles and duties in the hospital.Although nurses do not have the power to make certain types of care decisions, they do have the responsibility to follow the chain of command according to facility policy, until satisfied that good decisions are being made for their patients. Nurses spend more one on one time with their patients than doctors.The closeness of this relationship may make it easier for some patients to disclose their complaints to the nurse rather than the doctor (Ofri, 2013). Nurse’s responsibilities are to provide the best care to the patients and to insure that all of their rights and interests are met.â€Å"Once healthcare interventions have been adapted to meet the special needs of the patient, the nurse’s role is to articulate the patient’s request for care within the multidisciplinary team, creating patient-centered patterns of health care† (Hewitt, 2002).As a patient advocate, ordering a consultation with those who can help further in the decision making process is paramount. Patient advocacy is described as â€Å"nursing activities aimed at securing patient’s legal and ethical rights and satisfying their existential needs, both on the level of the patient-nurse relationship and in the healthcare team or organization† (Vaartio-Rajalin & Leino-Kilpi, 2011).The nurse should stand for the patient’s rights, dignity and health when others will not, thus becoming the communicator between the physician and patient. This ascertains that the patient receives optimal treatment. The Patient Bill of Rights states: â€Å"A patient has the right to obtain information about the specific nature of proposed treatment or procedure, a disclosure of the risks involved, and information about medical alternatives† (Patient’s rights, 2013).Since the physician from our scenario has refus ed to discuss alternative health care options with the patient, it is the duty of the nurse to become a patient advocate. After first discussing this situation with the doctor, if the nurse is granted the doctor’s permission to provide information to the patient, there are some government agencies and resources like National Center for Complementary and Alternative Medicine (NCCAM), The National Cancer Institute, U. S. Food and Drug Administration (FDA) and CAM on PubMed.These organizations assist patients and their families in learning about Complementary and Alternative Medicine therapies (Complementary and Alternative Medicine in cancer treatment, 2013). If the doctor refuses to give permission, it should lead the nurse to share his or her opinions with the medical staff involved in the patient care, following the appropriate chain of command.Based on a survey held by The New England Journal of Medicine â€Å"most of the physicians reported that when a patient requests a legal medical intervention to which the physician objects for religious or moral reasons, it is ethically permissible for the physician to describe the reason for the objection but that the physician must also disclose information about the intervention and refer the patient to someone who will provide it† (Curlin, Lawrence, Chin, & Lantos, 2007). In order to provide the best care and safe environment to a patient, nurses need to band together and work as a team.Gloria Ohmart, EdD, MN, APRN, offers a few strategies to protect patient’s rights and nursing profession. Some of them are: 1. â€Å"Keep an accurate record of issues that may be dangerous, illegal or unethical; 2. Check with other coworkers to see if they feel the same way about the situation, compare notes and discuss what the problem is and present a united front; 3. Talk to a charge nurse, head nurse, or supervisor to bring the problem to someone else’s attention; 4. Go up the chain.If a superior doe s not act on the complaints, then nurses may need to go to the next level of administration and so on until they get to the top; 5. Pursue an advanced degree. Higher education empowers through knowledge and enables nurses to develop strong communication and conflict resolution skills, the ability to negotiate and provides a deeper understanding of professional ethics† ( Finn, 2013). â€Å"Nurses must examine the conflicts arising between their own personal and professional values, the values and interests of others who are also responsible for patient care and health decisions, as well as those of patients.Nurses strive to resolve such conflicts in ways that ensure patient safety, guard the patient’s best interests and pressure the professional integrity of the nurses† (Code of ethics for nurses with interpretive statements, 2001).The Code of Ethics for Nurses was developed as a guide for carrying out nursing responsibilities in a manner consistent with quality i n nursing care and the ethical obligations of the profession. When a hot topic arises in the industry, the American Nursing Association (ANA) will create an explanation, justification, or recommendation for a course of action otherwise known as a position statement.The Code for Nurses published by the ANA is the standard by which ethical conduct is guided and evaluated by the profession. It provides a framework within which nurses can make ethical decisions and discharge their professional responsibilities to the public, to other members of the health team, and to the profession.According to number eight of the position statement nurses must attend to and be aware of the conflicts of dual loyalty to patients, health care institutions, employers and agencies that provide payment for services (Code of ethics for nurses with interpretive statements, 2001).Care and compassion are two traits that most nurses excel in. However these two qualities alone cannot facilitate being a voice for a patient. Education and moral courage are also essential needs when standing for the rights of a patient. It is imperative that a nurse understand their legal and ethical obligations to society and be able to carry forward their role as a patient advocate.Nurses should always endeavor to become as skilled and qualified in their chosen field as possible by consistently trying to advance their education and training, as well as entering into a partnership with physicians and health professionals.Policymaking and workforce planning should be done effectively to collect data and provide for a better information infrastructure. Educating ourselves as nurses will be essential to teaching our patients and allowing us to be a strong patient advocate, while standing united and taking comfort in knowing we are not alone.

Eastern State Penitentiary Reflection Paper Essay

Eastern State Penitentiary is believed to be one of the very first prisons established, not only in the United States, but in the world. Eastern State was functional for 141 years until 1970 when the prison closed down. Located in Philadelphia, Pennsylvania the prison is now a stabilized ruin open to the public for tours. After personally touring the facility I was able to understand the main purpose of the prison, the living conditions and the daily routines of an Eastern State Penitentiary inmate, and attempted escapes which is why prisons like Eastern State should not be used in our modern Criminal Justice System. It was designed for strict solitary confinement and had little to no rehabilitation programs. The prison was and still is not temperature controlled. The inmates suffered extreme summers and harsh winters while staying at Eastern State. Their rooms were quite small and only had a bed, some sort of dresser, and a toilet. The condition of the cells, with the exception of Al-Capone’s cell which was much larger and more comfortable than the rest of the cells, suggest that the designers of the prison wanted the inmates stay at Eastern State to be unpleasant. This prison was built for the sole purpose of punishment. For example, Elmo Smith was the 350th person to be executed by the electric chair in the United States on April 2, 1962. He was also the last person to be killed using the electric chair in Pennsylvania. Although the inmates were required to work within the prison walls they did not receive help with the problems that landed them in Eastern State in the first place, such as alcohol and drug abuse. Therefore the type of punishment that was seen at Eastern State did not maximize the welfare of individuals because inmates were not rehabilitated. As stated earlier, the inmates worked in the kitchen, infirmary, workshops, and barbershops. In the twentieth century you could see an inmate barbershop in almost every cell block. The barbershops became a place of socialization by the inmates and often the guards would go in for a free cut. When I learned this I was shocked that the guards allowed the inmates to have sharp tools that had the potential of being used as weapons. In fact, one story we  heard on our audio tour was of a guard who said an inmate pressed his tool to the guard’s neck and threatened to take his life. The inmate was joking and the officer was left unharmed but inmates were known to create weapons that were used for protection and a way of threating other inmates. These weapons were called shanks or shivs and prison guards discovered a majority of them before any harm could occur. Unfortunately there were stories of inmates killing each other such as Joseph Havel who stabbed his fellow cellmate to death in the middle of the night. Another important component in the life of Eastern State Penitentiary inmates was the opportunity to practice in religious activities. Upon entry, every inmate was given a Bible in hopes of one day they would receive salvation. Also, in the beginning of the prison’s life there were weekly religious services in every cellblock that the inmates had the chance to listen to from their cells. In later years, Christians had the opportunity to worship in the chapel during Sundays while Jews had the opportunity to worship in the synagogue. Religious freedom was the only freedom that the inmates received. They were strictly monitored and had to wake, eat, work, and sleep when the guards told them too. Although the guar ds did their best to keep an eye on every inmate, the system employed at Eastern State was flawed. Eastern State Penitentiary was designed for strict solitary confinement but that system failed and the population of inmates increased dramatically leaving the guards outnumbered. They tried to maintain surveillance and control of the institution. One way they monitored the inmates was using forming the cellblocks into a pentagon and having a watch tower in the middle. This design was flawed because it was impossible for the guard in the watch tower to see every cell and every part of the cells. Prison guards at Eastern State hated working in the watch tower, a position left for new recruits, because they felt more restricted than the inmates. They could not listen to music or read, had little human contact, and had to call their commanding officer every fifteen minutes to check in. Prison officials liked to believe that these methods of surveillance worked but there were numerous riots and attempted escapes by the inmates. The largest riot was on January 8, 1961 in cellblock nine when two inmates over powered an office and then they proceeded to opening other cells. They tried to set their criminal  records on fire. Another example was William Francis Sutton who attempted to escape five times. Lastly, there was the great escape from cellblock seven, cell 68. Clarence Klinedinst had a reputation as a good worker which he used to be transfer to cellblock seven where he started using the tools from work to build a tunnel. Riots and escapes such as these lead to the closing of Eastern State Penitentiary in 1970. Prisons such as Eastern state should not be used today because, according to the utilitarian theory of justice, the ends do not justify the means. A lot of money is put into them when all they do is hold inmates for a number of years and then they are rel eased into the community. With no form of rehabilitation the released inmates revert back to crime and are reincarcerated. The cycle is never ending and prisons become overpopulated and prone to riots as was Eastern State Penitentiary.

The Nice Guy

Case Analysis: The Nice Guy Introduction This case study begins with Paul Kennedy on a slow morning commute in Cleveland. During his drive, he’s worried about his wife and family, his boss, his associate, a stranger in a nearby vehicle, and even about the state of the Cleveland Browns. He is also excited about his plans to expand Daner Associates into the European market and his impending promotion to CEO. But when Paul meets with his boss, Larry, that afternoon, he discovers that he has been misreading signals. Larry is actually considering Paul for the number two role in the company and considering promoting another Daner executive, George, into the CEO position. Background Paul has been with Daner Associates for ten years. He believes that he is being groomed for to take over the CEO position when Larry retires. Thus, Paul is understandably shocked when he discovers that Larry thinks of him as the number two guy, and is considering promoting George to CEO instead. Paul thinks that George lacks the polish and experience to be effective in the CEO position. Problem Statement Paul needs to demonstrate to Larry that he has what it takes to be the next CEO: A strong leader with effective communication, people relationship and management skills. Analysis and Issues Paul does not have to become a complete jerk, like George, to get the CEO position. He does, however, need to do a thorough self-assessment to identify his strengths and weaknesses, chose a path that is in his own best interest, then clearly and consistently state his personal and managerial views. Paul has clear advantages over his rival, George, in terms of experience and length of time with the company. His employees like him and trust him to lead them. He possesses most of the elements of an effective CEO, but Larry thinks that Paul is too nice to be effective as CEO. Paul needs to exploit the advantages he has and stop letting his niceness get in the way of his own business success. If Paul wants the top job, he needs to prove that he can be effective in managing his relationships with others, including his relationship with Larry, where he has allowed communications to break down to where he and Larry were on completely different wavelengths on his promotion to CEO. In his interactions with Larry, it seems that Paul has been hearing only what he wants to hear. Paul has apparently misread Larry’s intentions, resulting in misaligned expectations. Paul and Larry have very different leadership styles and attitudes on people management. This disparity in their styles is a core part of their communications issues. Paul’s self-referent criteria have prevented him from effectively listening to what Larry has been telling him about his leadership skills and potential to be promoted to CEO. It seems that George has an advantage over Paul in being able to relate easily to Larry. Larry and George have a similar philosophy on people management, which gives George an advantage on effective communications with Larry. Larry immediately empathizes with George’s perspective, because it is similar to his own. This puts the onus on Paul to get outside of his own frame of reference to examine himself from Larry’s perspective. The nice-guy disorder is having a negative effect on Paul’s ability to make choices. His decision-making ability is impaired when he gives away his power to others, including George and Larry, denying his own goals and desires. When he feels strongly about an issue, as he does in the case of breaking into the biotech industry, he needs to build his case, avoid the analysis paralysis that comes with over-analyzing the data, and present his case with confidence and the good judgment that has come with ten years of experience. It is that type of conviction in his ideas and opinions that will earn respect from both Larry and George. Paul prefers to hold back his opinions rather than speaking his mind in many situations to avoid confrontations. Overly nice guys, like Paul, tend to avoid situations where they disagree with someone or need to confront someone about poor job performance. Paul chooses to remain silent on issues in order to avoid judgment or spare the feelings of others. Paul allows his concern for others to lead him to prioritize their needs over his own work responsibilities and career. He also has a tendency to look the other way when managerial issues arise, as they have with his associate, Lisa. Because he wants to be a nice guy, and he feels bad about Lisa’s personal situation, Paul has been excessively lenient with her and continues to avoid confronting her about the decline in her work performance. Speaking his mind consistently and effectively will be one of the most challenging skills Paul will have to master. Recommendations In order to be an effective leader and CEO, Paul needs to become much more self-aware. Like many â€Å"nice guys,† Paul does not have a high level of self-awareness, which thwarts his ability to reach higher levels of effectiveness. He must become aware of how his choices are holding him back. He needs to develop an honest self-awareness that will enable him to deal constructively with his weaknesses and fully benefit from his strengths. Since Larry has been Paul’s boss for ten years, he probably knows Paul’s strengths and weaknesses better than Paul knows himself. Paul needs to muster up the confidence to ask Larry for his constructive criticism. In this way, Paul will tap into Larry’s insight to help identify and minimize his weaknesses and identify and employ his strengths in order to maximize his effectiveness as a leader. Paul needs to drop his defensive attitude in order to hear and really listen to Larry’s advice, understand it as he never has before, and then take immediate action on that on that advice. Paul needs to start thinking of confrontation as an effective communication tool that will enable him to solve problems as quickly as possible. He must realize that his leniency with Lisa has reached a point where it compromises his ability to deliver on his business commitments. His reticence to speak frankly with her to resolve the work issues is ultimately harming both of them. Paul needs to address the issues in an honest and open conversation with Lisa; otherwise her work may continue to suffer, leaving him with only unpleasant options for dealing with it. Conclusion/Summary Paul has become overly focused on trying to be helpful and nice to others, resulting in an imbalance that has diminished his effectiveness as a leader. When Larry told him that he was not the first choice for CEO, presenting Paul with the evidence that things were not going as he thought, Paul continued to look externally to blame George for the misunderstanding. Paul needs to take a good, hard look inward to grasp an understanding of the connection between his nice-guy behavior and its negative consequences, and then accept that he must alter those behaviors in order to achieve his business success targets. As he becomes aware of his shortcomings, he will be able to find ways to eliminate them through training, mentoring, and by surrounding himself with people who have complementary skills. While identifying and minimizing his weaknesses through self discovery, Paul also needs to identify and emphasize his strengths. He cannot allow his nice-guy, self-sacrificing tendencies to lead him down the path to a job that is not in alignment with his talents and goals. Essentially, Paul needs to find a balance between his natural tendency toward niceness and an appropriate level of assertiveness. References Edelman, R. C. , Hiltabiddle, T. R. , & Manz, C. C. (2008). Nice Guys Can Get the Corner Office: Eight Strategies for Winning in Business Without Being a JERK. New York, NY: Penguin Group (USA) Inc.

The Roots and Backwash of Exxon Valdez Oil Spill Research Paper

The Roots and Backwash of Exxon Valdez Oil Spill - Research Paper Example The Exxon Valdez supertanker was traveling outside normal shipping lanes as it was avoiding ice and after 6 hours of grounding, the ship damaged 8 of its 11 tankers and spilled a portion of its Prudhoe Bay oil cargo (Cutler, 2008).   Massive cleanup efforts by Exxon and the US Coast Guard were immediately started.   Thousands of Alaskan residents helped in the cleanup efforts and eventually after about three years, the US Coast Guard declared the clean-up complete (Exxon Mobil, n.d).   The cleanup started in April 1989 until September of 1989 for the first year and went on in 1990 and 1991 during the summer months and some shoreline monitoring in the winter months (Cutler, 2008).   Based on the assessment of the National Transportation Safety Board, there were 5 possible causes of the grounding: 1). The third mate failed to properly maneuver the vessel possibly because of fatigue and excess workload; 2). The master failed to give proper navigation watch probably because of al cohol intoxication; 3). Exxon Shipping Company did not supervise the master and provide rest for their crew; 4). The US Coast Guard did not provide an effective vessel traffic system, and 5). There were no sufficient pilot and escort services (Cutler, 2008).  Ã‚   The environmental and economic consequences of the disaster amount to more than just three years of cleanup; they amount to profits lost, damage to coasts, and other sea and bird life.   These consequences shall now be discussed in detail.   These economic consequences shall cover the ecological cost of the oil spill itself, the economic costs as shouldered by Exxon Company during the cleanup, and the penalties charged against the company for the disaster.  Ã‚  Ã‚   About 3700 to 5800 mammals from 9 different species were affected by the oil spill.   Three hundred direct mortalities were reported for seals while 2,800 mortalities were reported for otters and these deaths were mostly due to the breathing and ingestion of the toxic oil.

Provide relevant detailed analysis of sony in its global context Essay

Provide relevant detailed analysis of sony in its global context - Essay Example Today, the Sony brand exemplifies a unique combination of popularity, strong identity, recognition, and excellent communication of the brand values and mission to the consumers. In the meantime, the company should be more attentive to the cultural aspects of its brand development in the global contexts. That Sony is one of the strongest and most popular global brands cannot be denied. Throughout the years of successful performance, Sony was able to move its brand onto the new level of consumer recognition and turn the Sony brand into an indispensable component of its organizational and marketing culture. The importance of the Sony brand to the future of the company is difficult to underestimate. Every year, in April, new employees join Sony to become its members and contribute to the development of the future successful trends. â€Å"And what I always say to them is that we have many marvelous assets here. The most valuable asset are the four letters, S, O, N, Y† (Sony). The company does everything possible not only to raise brand recognition among consumers but to ensure that employees in all company divisions worldwide have a clear understanding of the company’s brand messages and values. Some executives feel a strong need to communicate and re-articulate the interr elationship between the brand and the culture, in which it works (Sony). Others are confident that it is high time Sony leveraged its brand beyond products and created a customer-centered brand identity, which would serve an effective driver of consumer recognition and satisfaction with Sony products. Today, however, it is important to reconsider the relevance and efficiency of the Sony brand through the prism of the principal theoretical concepts. The significance of the global brand organization, the construction of brand equity, brand measurement, and the importance of culture for the development of global brand identity will create on objective

Comparing two university websites in terms of e-HRM Research Paper

Comparing two university websites in terms of e-HRM - Research Paper Example This is a research project proposal that will use the different views and theories on electronic Human Resource Management and human resource at large. They will be used to compare the employed systems in two universities. The two universities for comparison are Zayed and Texas. The project will review current empirical work on electronic Human Resource Management (e-HRM) and explain some consequences for future research work. With reference to definitions and previous framework, the project will analyze the incorporated theories, the empirical methodologies, the chosen analytical levels, the discussed topics and findings. The project will show a previous entity of work from different studies, majorly non-theoretical work, employing a variety of empirical methodologies, and having reference from many analytical levels and will diversify the core topics of e-HRM. The project will discuss some previous theoretical, methodological, and topical consequences in order to enhance future research on electronic Human Resource Management (Strohmeier, 19-37). With appropriate reference upon various literatures, an e-HRM research model is developed and, with the model’s guide, the two universities to be compared that are already practicing e-HRM for a significant period. The project will take 14 weeks. The first 9 weeks will be for the preparation of the proposal and collection of all the relevant resources for the project. From the 10th week, there will be an oral presentation and a written paper on the same. Human resource (HR) can guarantee an upper hand in organizational competition because of its valuation, rareness, imperfectly imitable with no substitutes. Organizations in competition can copy competitive advantage gained through better technology, strategies and services, but it is a challenge to copy competitive advantage gained through improved management of the labor force (Balgobind, 2012). The project will try to prove that the goals of e-HRM are to

Vulnerabilities Research Paper Example | Topics and Well Written Essays - 500 words

Vulnerabilities - Research Paper Example Certificate Authority (CA) and is considered to be the most efficient control in terms of email security (Ellison & Schneier, 2000). In case of secure email, one has to make sure about the sender possessing the key is the one who is the authentic sender. Likewise, when signed email is verified, one of the checks includes the source of the email i.e. the sender. However, if encryption is applied to the public key infrastructure, there is a requirement of identifying people possessing the relevant key to decrypt the message (Ellison & Schneier, 2000). This is the point where email certificates starts to operate, as the certificate ID is a digitally signed message from the CA that is transmitted to the user linked with the public key. However, the (PKI) possess many risks that may lead to vulnerabilities and in the end threats. One of the risks incorporates a breach of keys associated with the signer via unauthorized access or by any other means (Ellison & Schneier, 2000). However, efficient Certificate Authorities can mitigate risks by en effective physical security, personnel security and secure network. Pretty Go od Privacy ‘PGP’ counters these issues as well by incorporating ‘Web of Trust’ including self-governing signatures linked with the single certificate (Ellison & Schneier, 2000). Moreover, for addressing internal security, monitoring of employee emails is a regulatory requirement. However, there are many procedures, tasks and functions associated with it. The requirements can be met by utilizing tools from outlook express that are capable of retrieving certain keywords used in the email. For example, the keyword ‘account’ can retrieve all emails including this specific word. (Bhatnagar, 2012). However, these outlook tools only work individually on each workstation and can be solved by incorporating Microsoft Exchange server. As the server will retrieve all emails of all employees containing the specific

World poverty Article Example | Topics and Well Written Essays - 1500 words

World poverty - Article Example The annual income required to a family to survive according to federal governments is the most general definition of poverty, which is established through the statistical evaluation. Michael Darby (1997:4) states that the actual definition of poverty is political, whose purpose is to level the growth related to programs. According to US census, keeping in view the inflation the poverty line regarding family of four in 2000 was $17,050 income. However, this definition of poverty has many issues according to several scholars of poverty such as; treatment of taxes, special work associated expenditures, regional dissimilarities in the price of living, cash income (Blank 1997; Quigley, 2003). Poverty annihilation due to political, ethical and economic urgency is necessary. The statement was given, in Copenhagen, fifteen years ago at the World Summit for Social Development by the global leaders. For growth, since then poverty annihilation has become the prime target, and it is being considered a common destructive element for the whole of humanity. To overcome poverty has become a global goal and it must be achieved until 2015. The goal, which was set fifteen years ago, could not obtain still. Still, poverty lingering everywhere except East Asia and China and at some level India, which have achieved incredulous success. According to the Social Summit 1995, the definition of poverty comprised of lack of participation, deprivation, and social exclusion and today the definition has extended in several other dimensions, and the goal is still very far. In sub-Saharan Africa, the rate of poverty is inflexibly and ineptly high. Moreover, in South Asia, poverty reduction is very low despite a sustainable development. To minimize and eradicate poverty economic growth seems a very significant factor; however, the growth at the same time in other directions is also mandatory such as; education,

Research Methods in Management Assignment Example | Topics and Well Written Essays - 2000 words

Research Methods in Management - Assignment Example Next, methods of analysis of data will be highlighted. Finally a conclusion will synthesize the main points to demonstrate the importance of knowledge of research methods in management. In experimental research there is the explicit assumption that the universe functions according to causal laws (Creswell, 2003). The purpose of an experimental design is to establish the cause-effect relationship between sets of variables, by way of isolating assumed casual factors, and controlling suspected confounding or extraneous variables. It is hypothesized that an independent variable causes changes in a dependent variable, and that alternate hypotheses can be provided by other factors that are able to influence the results. The design uses random selection procedures to recruit a sample and randomly allocates participants to two or more groups (i.e., treatment group/s and a control group) (Neely, Gregory & Plats, 2005). Due to these random procedures, experimental methods allow for high external validity (generalization of results to a wider population), as the sample is more likely to be representative of that population. Alternatively, a quasi-experimental research design does not use random allocation of participants to groups, instead they are self-selecting (e.g., they have cancer or they do not have cancer) (Bryman, 2002). The quasi-experimental design is used in studies that are unable to control the independent variable, or when it is considered unethical or unfeasible to attempt to control the IV. The two main types of quasi-experimental designs are: 1) the non-equivalent control group; and 2) the pre-post design. Non-equivalent control group designs have both a treatment and a control group, whereas the pre-post design has no comparison group, as each participants serves as their own control in regards to their pre-test data. Due to the lack of random allocation the results of quasi-experiments cannot be generalized to a wider population with as much confidence as with an experimental design.There is also the non-experimental design in which no treatments (i.e., independent variable/s) are g iven to participants (Bryman, 2002). There is no random selection or random allocation of participants, and so the results of the study are unable to be generalized at all, as no causal relationships can be predicted. These designs tend to be used to investigate naturally occurring phenomenon in which the independent and dependent variables vary without researcher intervention.The advantages of experimental research methods are that the use of quantitative levels measurement (i.e., numerical data), random selection and allocation procedures, and a controlled environment, allow for higher confidence in the results, as well as greater generalizability of the results (Creswell, 2003). The results are more

Quality management and competition in the parcel delivery industry Essay

Quality management and competition in the parcel delivery industry - Essay Example Conveyor belts and packet sorting machines were pressed into service in big cities by parcel management companies by the time of World War II. Now parcel delivery management too grown from a one based on simple modal operations to a series of complex computer aided and monitored systems. Parcel Management has undergone a lot of experimentation and evolution in more than century of its existence. There was a time when parcel delivery management was based on two simple linear functions of fast delivery at as low a price as possible. Jim Casey, the founder of UPS used the slogan: "Best Service and Lowest Rates." (www.ups.com) .Now the parcel delivery companies offer a choice of multiple speeds of delivery that vary in direct proportion to the cost of delivery. The higher the speed of delivery, higher is the transportation cost. Parcel companies advertise in advance about the exact timings at which time bound parcels can be picked up so that they go into the sorting and delivery mechanis m of the company at the earliest possible. A parcel company has multiple parcel management, collection and distribution hubs that are equipped with high speed conveyors and mechanised sorting machines. In areas, where volumes of parcel are low, manual sorting and distribution is practised. The delivery and collection channels emanating from a hub are called the spokes. A large parcel delivery company has multiple hubs and spokes. To integrate land and air operations parcel management companies have established ‘air hubs’ that serve as the air ‘spokes’ of the companies. This integration of air and land in a parcel delivery operation is also called a multi-mode activity. The hub and spoke system serves to cut down on needless road and air journeys and optimisation of operations thus saving a lot of overheads for companies. Due to pressing costs

Sustainable development Essay Example | Topics and Well Written Essays - 2000 words

Sustainable development - Essay Example he concept of sustainable development is created to represent the goal of making sure that future generations will have an intact environment that will ensure their subsistence. However, even though the real meaning of the concept of sustainable development is unambiguous and certain, the literal definition and explanation of sustainable development have roused intense debates. Problems associated with the definition of sustainable development reveal that the concept is complicated, which merges intergenerational justice, equality, and efficiency derived from environmental, social, and economic factors. This essay presents a critical evaluation of the concept of sustainable development. It is worth mentioning that various disciplines have different definitions of sustainable development. Ecologists define the concept as a process that protects biodiversity; sociologists view it as a process that strengthens and sustains communities; and economists define it as a process that ensures that the quality of subsistence of future generations is better than or the same as that of the current generation (Ciegis, Ramanauskiene, & Martinkus, 2009). The concept of sustainability was introduced by the International Union for Conservation of Nature and Natural Resources (IUCN) in 1980. Several years later, the Brundtland Report released its official definition of sustainable development: â€Å"development that meets the needs of the present without compromising the ability of future generations to meet their own needs† (Lee, McNeill, & Holland, 2000, p. 42). In exploring the most serious environmental issues today and the ideal solutions to these problems, the Brundtland Report created the foundation within which the clashing principles of economic development and environmental protection could be reconciled. Much of the global community, by the end of 1992, had espoused the UNFCCC to â€Å"stabiliz[e]†¦ greenhouse gas concentrations in the atmosphere at a level that would

16 Questions to be Graded Essay Example for Free

16 Questions to be Graded Essay 1. The researchers analyzed the data they collected as though it were at what level of measurement? a. Nominal b. Ordinal c. Interval/ratio d. Experimental 2. What was the mean posttest empowerment score for the control group? 97.12 3. Compare the mean baseline and posttest depression scores of the experimental group. Was this an expected finding? Provide a rationale for your answer. The mean baseline for depression 14.00 and the post-test for depression was 13.36. The post-test score is 0.64 lower than the baseline score which is what the study hypothesized. The study results state â€Å"This study found that there were significant differences in improvement of empowerment, self-care self-efficacy, and depression in patients who were in the intervention group using empowerment strategies than with the control group patients† (Grove, 2007). 4. Compare the mean baseline and posttest depression scores of the control group. Do these scores strengthen or weaken the validity of the research results? Provide a rationale for your answer. The mean baseline and post-test depression score was 10.40. These scores strengthen the validity of the research results because it shows that depression did not improve for the patients within the control group but the scores did change for the patients in the experimental group. 5. Which groups test scores had the least amount of variability or dispersion? Provide a rationale for your answer. The control group had the least amount of variability with the depression  score which stayed with a SD of 10.4. 6. Did the empowerment variable or self-care self-efficacy variable demonstrate the greatest amount of dispersion? Provide a rationale for your answer. The empowerment variable demonstrated the greatest amount of dispersion because the mean not only went up by 6.64 the SD also went down by 1.91 suggesting the scores are also closer to accurate. 7. The mean () is a measure of __central__ __tendency__ of a distribution while the SD is a measure of __dispersion_____ of its scores. Both and SD are ____descriptive_____ statistics. 8. What was the mean severity for renal disease for the research subjects? What was the dispersion or variability of the renal disease severity scores? Did the severity scores vary significantly between the control and the experimental groups? Is this important? Provide a rationale for your answer. The mean severity for renal disease for the research subjects was moderately severe with a mean of 6.74, SD of 2.97, from a range of 0-10. The severity scores did not vary significantly and it is important to have the same severity of disease across the board so the outcomes can be true. 9. Which variable was least affected by the empowerment program? Provide a rationale for your answer. The mean for the control group was least affected by the empowerment program only rising 0.4. 10. Was it important for the researchers to include the total means and SDs for the study variables in Table 2 to promote the readers’ understanding of the study results? Provide a rationale for your answer. Yes it was important to include the totals so at a glance anyone can see that even when the experimental and control groups are combined the results still show an improvement in all three categories. References Grove, S. K. (2007). Statistics for Health Care Research: A Practical Workbook. [VitalSource Bookshelf version]. Retrieved from http://pageburstls.elsevier.com/books/978-1-4160-0226-0/outline/16The citation provided is a guideline, please check each citation for accuracy before use.

Tax Compliance And Smes Economics Essay

Tax Compliance And Smes Economics Essay According to Marti (2010) tax compliance is a complex term to define. Simply put, tax compliance refers to fulfilling all tax obligations as specified by the law freely and completely. It has been found that regulatory burdens fall disproportionately on small and medium enterprises internationally (Pope Abdul-Jabbar, 2008). Their size and nature makes the issue of tax compliance one of particular importance especially since most SMEs have access to limited resources and inadequate expertise to comply with diverse and complicated regulation. He also believes that high compliance costs can result in tax avoidance, tax fraud, and inhibit investment by way of diminishing competitiveness of the country in terms of taxation attractiveness. Tax non-compliance may be in one of many forms; it could either be failure to submit a tax return within the stipulated period or non submission, understatement of income, overstatement of deductions, failure to pay assessed taxes by due date. (Kasipillai Abdul Jabbar, 2006) and in some cases non-compliance may mean an outright failure to pay levied taxes. Studies have shown that the problem of tax evasion is a widespread one (Kasipillai Abdul Jabbar, 2006). Furthermore, Fagbemi, Uadile Noah (2010) found that it is prevalent in developing countries and it hinders development thereby leading to economic stagnation and other socio-economic problems. Chipeta (2002) identified tax rates as one of the causes of tax evasion. He pointed out that a higher tax rate increases taxpayers burden and reduces their disposable income therefore, the probability of evading tax is higher. 2.5 Tax Policy and Level of Voluntary Compliance among SMEs Small taxpayers under the regular system of taxation are discriminated against, since the compliance requirements, cost of compliance and tax rate are the same for both small and large enterprises. Reducing the compliance costs and tax rate increases the small enterprises profit margin. It also increases the Governments tax revenue, since the simplified provisions for small and medium enterprises reduce the size of the informal economy and the number of non-complying registered taxpayers (Vasak, 2008). Furthermore, SMEs usually have to operate in an overbearing regulatory environment with the plethora of regulatory agencies, multiple taxes, cumbersome importation procedure and high port charges that constantly exert serious burden on their operations. An overly complex regulatory system and tax regime or one opaque in its administration and enforcement makes tax compliance unduly burdensome and often have a distortionary effect on the development of SMEs as they are tempted to morph into forms that offer a lower tax burden or no tax burden at all (Masato, 2009), and this results in a tax system that imposes high expenses on the society. A poorly executed tax system also leads to low efficiency, high collection charges, waste of time for taxpayers and the staff, and the low amounts of received taxes and the deviation of optimum allocation of resources (Farzbod, 2000). Existing empirical evidence clearly indicates that small and medium sized businesses are affected disproportionately by these costs: when scaled by sales or assets, the compliance costs of SMEs are higher than for large businesses www.ccsenet.org/ijbm International Journal of Business and Management Vol. 7, No. 12; June 2012 Published by Canadian Center of Science and Education 91 (Weichenrieder, 2007). 2.6 Tax Policy that will Encourage Voluntary Compliance by SMEs SMEs constitute untapped revenue potential and an uneven playing field in many countries (International Tax Dialogue, 2007) as such they need to be captured by the tax net. However, though legislations are necessary regulator for protection of the business environment and security of the economic agents, for establishment of the necessary social security regulations, they may also hamper compliance and the growth of business through additional expenditures and administrative obstacles. Thus Shahroodi, (2010) stated that for a tax system to be efficient, the tax policy needs to be designed such that the tax rates are appropriate and rational, the exemptions are lower in amount, the tax collection organization are more efficient, the tax burden of the indigent people should be lighter and the fight against corruption and tax evasion should be much more intense. Tax policies can be designed in such a way that they do not only directly affect SMEs but also indirectly push for voluntary compliance and their growth. Yaobin (2007), emphasized declared that special tax regimes for SMEs may be appropriate policy instruments for minimizing the cost of collection. Because awareness of the dangers of inadequate taxation of SMEs has grown because of the potential of uneven tax enforcement to cause distortions of competition, voluntary compliance by larger enterprises and by wage earners, (International Tax Dialogue, 2007), government intervention should help maintain balance while ensuring that countries exploit the social benefits from greater competition and entrepreneurship. Pro-business (and Pro-SME) Tax regimes and enforcement should be simple, consistent and predictable should to lower compliance and administrative costs, and hence reduce uncertainty faced by taxpayers as well as improve the levels of voluntary compliance (Kasipillai, 2005). 2.7 Theories of Tax Compliance Various opinions exist about the best ways to improve tax compliance. Given the chance, a lot of businesses will not pay taxes unless there is a motivation to do so. Some believe that the best way is to increase incentives (Feld Frey, 2007) others believe the best way is to increase penalties. Tax compliance theories can be broadly classified into two. They are; economics based theories and psychology based theories. 2.7.1 Economic Based Theories They are also known as deterrence theory and they place emphasis on incentives. The theory suggests that taxpayers are amoral utility maximizers- they are influenced by economic motives such as profit maximization and probability of detection. As such they analyze alternative compliance paths for instance whether or not to evade tax, the likelihood of being detected and the resulting repercussions and then select the alternative that maximises their expected after tax returns after adjusting for risk. This process is referred to as playing the audit lottery by Trivedi and Shehata (2005). Therefore according to the theory, in order to improve compliance, audits and penalties for non-compliance should be increased. 2.7.2 Psychology Theories Psychology theories on the other hand posit that taxpayers are influenced to comply with their tax obligations by psychological factors. They focus on the taxpayers morals and ethics. The theories suggest that a taxpayer may comply even when the probability of detection is low. As opposed to the economic theories that emphasize increased audits and penalties as solutions

Disease Caused by Parasite of Genus Trypanosoma

Disease Caused by Parasite of Genus Trypanosoma Human trypanosomiasis caused by Trypanosoma evansi and Trypanosoma lewisi in India : A matter of concern Introduction Disease produced by the parasite of genus Trypanosoma called as trypanosomiasis. It is one of the most important hemoprotozoan diseases, widely distributed in animals and human beings. It is endemic in Africa and America, are deadly pathogens that threaten millions of people in at least 36 countries in Africa. It is estimated that approximately 60 million people are at risk and 3, 00,000 new cases found every year in Africa (WHO Report 1998). Both African and American trypanosomes rank within the top 10 in terms of global impact. Despite the impact of these parasites, how they cause disease is relatively less is understood. In Africa, the disease is commonly known as human African trypanosomiasis (HAT) or sleeping sickness whereas the American trypanosomiasis recognized as Chagas disease. They not only infect vertebrates groups (amphibians, reptiles, birds, fish, and mammals) but also many invertebrates (Crithidia, Leptomonas). Human African trypanosomiasis belongs to genus Trypanoso ma, subgenus trypanozoon. Classification phylum sacromastigophora, order kinetoplastida and the family trypanosomatidae. Genus Trypanosoma includes subgenus which is divided into major group, salivaria and stercoraria that infect vertebrates (Hoare C. A.1964). Trypanozoon (T. brucei ssp, T. evansi, T. equiperdum), Duttonella (T. vivax,T. uniforme), Nannomonas (T. congolense, T. simiae), Pycnomonas (T. suis), Tejeraia (T. rangeli) belongs to salivaria group. Under stercoraria group Herpetosoma (T. lewisi, T. musculi,T. microti), Megatrypanum (T. theileri, T. melophagium), Schizotryponum (T. cruzi, T. dionisii) come. T. brucei. brucei, T. brucei. gambiense and T. brucei. rhodesiense are the subspecies of the Trypanozoon. Sleeping sickness is caused by T. brucei. gambiense, a chronic form of HAT in West and Central Africa lasting from months to years or T. brucei. rhodesiense, an acute form of HAT in East and Southern African with a duration of weeks to months. Whereas, closely relate d parasite T. brucei. brucei is non pathogenic to humans. The American trypanosomiasis is caused by T. cruzi. rhodesiense. These forms of the disease is deadly and develop within weeks to months, the gambiense form takes year. Trypanosomes cause animal trypanosomiasis has a wide geographic distribution. Surra is caused by T. evansi and infects mainly camels, cattle, buffalos, horses, deer and other wild animals. T. b. Brucei causes nagana in tropical Africa and affects only cattle; T. vivax and T. congolense infect domestic and small animals while T.lewisi is a commensally of rats. T. equiperdum causes dourine disease in horse and donkey of India, Europe, America and North Africa. African trypanosomes are transmitted by tsetse flies, a species of Glossina, and South American trypanosomes by reduvid bugs. Normally human are resistant to animal species of Trypanosoma due to the trypanolytic factor of human serum. However, there are several cases of human infection with animal trypanosomes such as Trypanosoma evansi; Trypanosoma lewisi and Trypanosoma congolense have been discussed later in this article. This proves not just a rare cases but the beginning of new era in the history of human trypanosomes, put in dilemma whether they develop potential of new diseases of humans or just a biological accidently transmission. In Asia, first documented evidence found in 1933, human trypanosomiasis in Malaysia, a four month old infant infected with T. lewisi (Johnson P. D, 1933). Later in 1974 K. Shrivastava and colleague reported T. lewisi-like Herpetosoma infection, diagnosed in two adult patients in India during malaria eradication program. All three human Herpetosoma infected patients were recovered without treatment. More recently the cases of a two-month-old infant in the Gambia (Howie, S. et al., 2006) and India (Kaur, R. et al., 2007) infected with T. lewisi-like trypanosome is reported but Gambian case has invasion of central nervous system. One more case in Thailand is reported; Trypanosoma lewisi-like infected 45-day-old male infant was recovered with the treatment of antibiotic gentamicin (Sarataphan, N. et al., 2007). Suspected case, 40 aged female in State of west Bengal of India, infected with trypanosomiasis in January 2005 however T. evansi was concluded by considering only the fact, specie s isolated from these area is T. evansi in cattle, buffaloes, and goats (see Ref. Meeting of the Ad Hoc Group of the World Organization for Animal Health (OIE), Paris 2006). Animal trypanosomiasis Trypanosoma evansi caused to human in India, state of Maharashtra. The patient was 45 year old man and veterinary quack from Seoni village in Taluka Shindevahi of District Chandrapur from Maharashtra State. He was admitted to rural hospital; initially symptoms observed were headache, intermittent fever, disoriented, sensory scarcity, saliva dribble from mouth and violent behaviour. Blood thick smear, stained by Fields stain, examination was done by local microbiologist Mrs. Bharti U Sable; she suspects trypanosome along with plasmodium falciparum (figure 01). He was treated with antimalarial drug along with oral hematenics. She marked as the founder of Indian trypanosome, T. evansi. Later patient was transferred to the Government Medical College and Hospital (GMC) in Nagpur, India. Stained blood smear shows numerous flagellated trypanosomes parasite only, was confirmed morphologically, position of nucleus and small kinetoplast at central and posterior respectively indicate that the contributory mediator was T. evansi (Joshi, PP. et al., 2005). Anoth er unique character of T. evansi has homogenous DNA minicircles (Borst et al., 1987; Songa et al., 1990; Masiga and Gibson, 1990; Lun et al., 1992) and absence of DNA maxicircles in the kinetoplast unlike T. brucei (Borst et al., 1987; Songa et al., 1990). Several methods has been evolvedmicroscopy, card agglutination test (C. Gutierrez et. al., 2000), microhematocrit centrifugation technique (Woo, PTK 1970), enzyme-linked immunosorbent assay (Indrakamhang, P et al.1996), DNA hybridization (Viseshakul, N., Panyim, S., 1990) and polymerase chain reaction (Wuyts, N.et.al. 1994; Wuyts, N.et al.1995; Omawa, S et al 1999) for detection of T. evansi infection. To confirm morphological identification of parasite, additional test of blood, serum and cerebrospinal fluid (CSF) was done in the Department of Microbiology, Government Medical College and Hospital, Nagpur and at the Institut de Recherche pour le Dà ©veloppement in Montpellier, France. Parasitological and serological tests conducted at GMC, Nagpur, are as followed (Joshi, PP. et al., 2005): Biochemical quantitative analysis of serum was performed with less tiny significance on lipid levels, indication of Tangier disease. Tangier disease is a rare autosomal recessive genetic disorder, high density lipoprotein deficiencies associated with this disease include dramatically lowered level of APO A1 (Von Eckardstein, A., et al., 1998), was found to be non trypanolytic (Rifkin, M R. 1978a), however controversial data, fresh sera of a patient with Tangier disease is trypanolytic exhibiting bothTLF-1 and TLF-2 activity, reported (Tomlinson et al., 1995). The demonstration of specific antibodies has been employed by using card agglutination test for trypanosomiasis (CATT) for T. evansi using whole blood and serum was conducted. CATT test initially developed for T. brucei. gambiense (Diall et al., 1994). Sensitivity of CATT for T. evansi in Kenya was 65.5% (Z.K. Njiru et al.2004) and 68.6% (Ngaira et al.2003).False positive result of CATT was reported (Stijn Deborggraeve et al.2008). Mini-anion centrifugation technique is used for purification and concentration of trypanosomes using heparinised blood before and after treatment of suramin A direct latex IgM agglutination test was conducted with CSF to reveal functionless of parasite in the blood brain barrier. Sediment of CSF after centrifugation was examined by bright field microscopy for the presence of trypanosomes. Thomas chamber is used to count lymphocytes in the CSF, presence demonstrate the incursion of parasite. Molecular technique and serological tests conducted at the Institut de Recherche pour le Dà ©veloppement in Montpellier, France, are as followed (Joshi, PP. et al., 2005). Three independent PCR assay were performed using DNA of trypanosome Related to the subgenus Trypanozoon using a seminested PCR method, primer used ITS1/2 based on internal transcribed spacer (ITS) of ribosomal DNA. Related to T.brucei group using a single PCR of the 177- basepair. Amplification of T. evansi was conducted using a 994- basepair mitochondrial kinetoplast minicircle template with the primer TEV 1/2. Reference strains used are T. b.gambiense Bat 6118 and T. evansi CIRDES. PCR provided high specificity and sensitivity molecular biology technique among others for diagnosis of infectious diseases and also permits identification of micro organisms such as mycobacterium (Garcia-Quintanilla, A et al., 2002) , detection and differentiation of Entamoeba histolytica and Entamoeba dispar (Gonin, P et. al.,2003), simultaneous detection of tick-borne hemoprotozoan parasites Babesia caballi and Babesia equi in horse blood (Alhassan, A. et. al., 2005) and detection of influenza A Virus (Nicole L. Z et. al, 2006). In spite of these, PCR are not usual in some countries (Holland et al., 2001). It has been reported about reproducibility problems, for diagnosis of both human and animal trypanosomes, of PCR results (Solano et al., 2002; Malele et al., 2003). Recently a new DNA amplification method, loop-mediated isothermal amplification developed for diagnosis of species and sub-species specific trypanosomes (Thekisoe OM et al., 2007). Disease developed due to absence of trypanolytic factor in normal human serum hence immune status of patient was checked to resolve possible infection with human immunodeficiency virus (HIV). Three tests were conducted to corroborate the results of Enzyme-linked immunosorbent assay (ELISA) in India. HIV 1/2 assay Specific enzyme-linked immunosorbent assay (ELISA) NNO-LIA HIV 1/2 Score test Investigation of parasite Unusual transmission of animal trypanosomiasis, T. evansi to human requires rationalization, for this P. Truc and collaborator, 2007 studied genetic characterization of T. evansi. Generally, genetic variability of T. evansi has been detected by using isoenzyme (Gibson et al., 1983; Stevens et al., 1989), restriction fragment length polymorphism (RFLP) (Songa et al., 1990), microsatellite (Biteau et al., 2000) and random amplified polymorphic DNA (RAPD) analysis (Lun et al., 2004; Ventura et al., 2002); all these above technique found isolated T. evansi were genetically homogenous. Micro heterogeneity reported (Gibson et al., 1983; Stevens et al., 1989), may due to low-resolution techniques and no genetic exchange of T. evansi in vector like others T. brucei ssp, that leads to absence of recombination which play role for micro heterogeneity (Jenni et al.1986). Nevertheless, some genetic variability of isolated T. evansi from Kenya reported through PCR (Ngaira et al.2004, 2005; Njiru e t al.2006) and amplified fragment length polymorphism (AFLP) along with RAPD. Among later, AFLP admittance more polymorphisms, was able to differentiate and separate the Type A T. evansi into two clades (Masiga et al., 2006). Direct comparison of high-resolution molecular techniques microsatellites or simple sequence repeats (SSR) and Inter-simple sequence repeats (ISSR) PCR revealed that latter technique demonstrate greater genetic variability of T evansi isolates from different geographical area (Z.K. Njiru et al 2007). Recently molecular analysis of T. b. brucei by PCR and microsatellite PCR of reported blood slides was successfully conducted (Stijn Deborggraeve et al.2008). Isolated T. evansi has been termed into type A and type B (Masiga and Gibson, 1990). Unlike to type B detected only from Kenya, isolates type A are most copious (Borst et al., 1987). It has been shown however, that most of T. evansi from South America are dyskinetoplastic- lacking both maxicircles and minicir cles (Masiga and Gibson, 1990; Ventura et al., 2000; Schnaufer et al., 2002). Normally T. evansi diagnosed through variant surface glycoprotein (VSG) Rode Trypanozoon antigen type (RoTat) 1.2, a diagnostic antigen. Songa and Hamers, 1988 developed CATT for veterinary use, which based on RoTat 1.2 gene (Songa and Hamers, 1988). Both PCR test and serological-CATT test are highly sensitive and specific in divergent geographical region (Verloo et al., 2000), former test can be trustworthy for detection of isolates of both dyskinetoplastic and DNA minicircles in kinetoplast of T. evansi (Claes et al., 2004) also it based on RoTat 1.2 gene (Urakawa et al., 2001). On the other hand, most of T. evansi from Kenya were not detected by test, which based on VSG of T. evansi RoTat 1.2 gene because few isolates lack both RoTat 1.2 gene and their linked protein-VSG while other isolates having only RoTat 1.2 gene (Ngaira et al. 2004). Characterization of non-RoTat 1.2 T. evansi, specific PCR test developed in these 273 base pair was present in disparity to RoTat 1.2 T. evans i (J.M. Ngaira et al., 2005). Microscopic examination of dissected organs of tsetse flies was done for identification of trypanosome infections (Lloyd and Johnson, 1924). Parasites are, generally indentified in the mouthparts, salivary glands and mid-guts. Trypanosome species from vector is isolated and employed in isoenzyme electrophoresis technique for identifications (Gashumba et al., 1986). Another approach as recombinant DNA probes have been used for the identification both mature and immature trypanosomes in tsetse fly (Gibson et al., 1988; Majiwa et al., 1993).Dot-ELISA is another technique used for detecting trypanosomes in tsetse flies (Bosompem et al., 1996; Ouma, J. O et al., 2000) How T. evansi differs from other Trypanozoon The subgenus Trypanozoon includes three species, namely Trypanosoma brucei, T. evansi and T. equiperdum. T. evansi is judge against, concerning their morphological, mode of transmission, biochemical and molecular characteristics, rest of species. Bloodstream stages of these three parasites are often morphologically indistinguishable (Brun R et al., 1998; Gibson, 2003). T. evansi is mechanically transmitted of infected blood through insects of the genera Tabanus, Stomoxys, Atylotus and Lyperosia. Horseflies (Tabanus spp), Stableflies (Stomoxys spp) are the most capable vectors for the transmission of T. evansi in Indonesia and China (Luckins, 1988; Lun et al., 1993). In Africa, south and Central America, tsetse fly (Glossina spp) and vampire bats Desmodus rotundus an extra host-vector-reservoir of the T. evansi, respectively can mechanically transmitted this parasite. Direct transmissions through milk or during coitus involved T. evansi (Wang, 1988). Besides mechanical and direct tran smission of T. evansi, T. equiperdum transmitted directly during coitus and with rare possibility through bloodsucking insects (see ref. Brun, R et al.,1998). Trypanosoma brucei gambiense, sleeping sickness parasites have been able to spread through tsetse flies of palpalis group (Glossina palpalis, Glossina tachinoides) while T. b. rhodesiense was generally transmitted by tsetse of the morsitans group (Glossina morsitans, Glossina pallidipes). All 31 species of tsetse flies are able to transmit trypanosomes (Aksoy S, et al., 2003). Other major parasites T. congolense, T. vivax and T. simiae that are pathogens of domesticated animals, transmitted by tsetse fly. Both parasites, T. evansi and T. equiperdum are closely related to T. brucei, most likely developed from Trypanosoma brucei by independently deletion of kinetoplast DNA and should be regarded as two subspecies Trypanosoma brucei evansi and Trypanosoma brucei equiperdum respectively (Lai et al., 2008). Absence of maxicircles in kinetoplast DNA explained inexistence of procyclic or insect stage in these parasites and can propagate only as the mammal-infective bloodstream form (Borst et al., 1987).This facilitate to explain wide range of mechanical transmission of T. evansi outside of Africa (Lun and Desser, 1995). Procyclic form (PCF) T.brucei strain cannot survival with a partial or complete loss of kinetoplast DNA as with some Blood stream form (BSF) strains. This kinetoplast DNA deficient T.brucei strains appear naturally or induced by drugs (Schnaufer A et al.2002). Drug inducers are acriflavine, ethidium bromide, methoxy-9-ellipticine, hydroxystilbamidine, berenil, pentamidine, an trycide, and para-rosaniline, grouped as DNA intercalators and non intercalating drugs (Hajduk, 1978). Nevertheless, the existence of T. equiperdum has been complexity; Claes et al. suggested that, in fact, some strains of Trypanosoma equiperdum are actually Trypanosoma brucei and all other remaining misidentified strains such as Swiss Tropical Institute Basel (STIB) 818 are Trypanosoma evansi. However, based on PCR amplification of the fragment of DNA maxicircles in the kinetoplast, T. equiperdum Onderstepoort Veterinary Institute (OVI) and Bordeaux Trypanosoma antigen type (BoTat) 1.1 strains are T. brucei and other STIB 818, STIB 841 and STIB 842 T. equiperdum strains are not cluster together with T. evansi as it maintains maxicircles and allied genes. (Li et al., 2006). Both parasites have homogeneous minicircles. Although in all T. evansi strains maxicircles are totally lost but T. equiperdum shows more assortment, some strains seems to bear complete maxicircles with no active essential gene; others are missing one of the genes; and a few devoid the entire maxicircles (Lai et al., 2008). Unlike other DNA, T. brucei mitochondrial DNA termed kinetoplast DNA include a network of interlocked DNA rings (Liu, B. et al. 2005). This network of T. brucei ssp. comprised of several thousands of heterogeneous minicircles and several dozen of homogeneous maxicircles (Borst and Hoeijmakers, 1979). T. evansi has largely homogenous and limited heterogeneous minicircles in kinetoplast DNA (Borst et al., 1987). Results (Joshi, PP. et al., 2005; P. Truc et al., 2007) A careful examination of morphological characteristic demonstrates the presence of T. evansi. Patient had normal level of APO A-1 indicate no sign of Tangier disease. The result of CATT for T. evansi was positive suspect stalwartly presence of RoTat 1.2 gene. Latex IgM test, a diagnostic for trypanosome invasion in CSF, and lymphocytes count in the CSF indicated no invasion of parasite. An attempt to isolate and propagate trypanosome in wistar rat was failed. For molecular diagnosis of T. evansi PCR conducted, test was positive. Results of ELISAs for HIV, conducted in France and India were negative. Genetic characterization, Indian patient has homogenous DNA minicircles in kinetoplast of T. evansi of type A and devoid of SRA gene. Treatment Treatment was started 109 days after initial admission to hospital using suramin. Suramin is manufactured by Bayer and donated to WHO as Germanin, used against sleeping sickness in 1922 (Voogd et al., 1993). Suramin was used as a first stage of treatment for HAT caused by Trypanosoma brucei gambiense (chronic form) or T. b. rhodesiense (acute form). Efficacy of suramin against T. evansi infection was studied in cattle by Gill BS, Malhotra MN, 1963. It was requested and provided by Department of Public Health, Government of Maharashtra State, India and World Health Organisation respectively. As patient falls under first stage of infection, drugs have to be used pentamidine or suramin sodium. Pentamidine has more adverse effect than suramin, according to author; hence suramin was used in this patient. Drug suramin acts by interfering with enzyme of glycolytic pathway (Wierenga RK, et.al., 1987) in trypanosomes and produce hot spot, function as a signal for import into glycosome. It is preferred to give slow intravenous injection as suramin is poorly absorbed from intestine and causes intense local irritation when given intramuscularly (Voogd TE, et.al., 1993). Suramin does not cross the blood-brain barrier to kill trypanosome in the CSF however able to cure model of stage 2 diseases at a high dose greater than 80 mg per kg (Jennings FW, et.al., 1995). Follow-up study was commenced after the end of treatment and at 3rd and 6th months, all previous tests-CATT for T. evansi, latex IgM agglutination test, Mini anion-exchange centrifugation technique and examination of CSF by bright field microscopy are repeated at GMC Nagpur excepts biochemical analysis of serum for Tangier disease (P. P. Joshi et al. 2006). Tests result indicates first patient of human trypanosomiasis infected with T. evansi was recovered, Joshi and collaborators concluded that same schedule would follow in treatment if more cases observed. Suramin Suramin is less active against procyclic form of trypanosomes than bloodstream form, former normally reside in the tsetse flies (Scott AG, et.al., 1996). Suramin inhibit number of glycolytic enzyme which is essential to bloodstream form rather than procyclic form (Fairlamb AH, et.al., 1977, Fairlamb AH, et.al., 1980). Hanau and colleagues proposed other likely target of drug, competitive inhibitor of an enzyme 6-phosphogluconate dehydrogenase of pentose phosphate pathway (Hanau S, et.al., 1996). Suramin is an effective microfilaricide for Onchocerca spp. and Brugia pahangi worms (Hawking, et al., 1981; Howells, et al., 1983). It is a known ATP/UTP purine receptor (P2 receptor) antagonist (V. Ralevic and G. Burnstock, 1998). Nevertheless suramin inhibit ample varieties of enzymes like reverse transcriptase, dihydrofolate reductase, furamse, glycerol-3-phosphate dehydrogenase, hexokinase, L-a-glycerophosphate oxidase, receptor mediated uptake of low density lipoprotein, RNA polymerase and kinases, thymidine kinase, trypsin (P ´epin and Milord, 1994; Wang, 1995). Besides its trypanocidal activity, suramin is also useful in hormone-refractory prostate cancer, however survival rate was not affected (Small et al., 2000; Ahles et al., 2004). Suramins antitumor activity has been attributed to its inhibition of various growth factors which include platelet-derived growth factor, fibroblast growth factor, transforming growth factors alpha and beta, insulin- like growth factors 1(Stein CA,1993). Osteosarcoma is the malignant tumor of the bone; suramin exerts an inhibitory effect on osteosarcoma cell growth of established cell lines (Benini et al., 1999), newly established osteosarcoma cell lines and stimulation of osteosarcoma cells by physiological compounds, such as 1, 25-dihydroxy-Vitamin D3 (K. Trieb, H. Blahovec, 2002). Furthermore, results in an inhibiting capacity of suramin on various cell functions include production of alkaline-phosphatase or telomerase activi ty (K. Trieb, H. Blahovec, 2002). Suramin blocked CD154 (Emilio Margolles-Clark et al., 2009) from interacting with its receptor CD40 (U. Schà ¶nbeck and P. Libby, 2001; I.S. Grewal and R.A. Flavell, 1998), costimulatory interactions are therapeutically important to modulate immune responses (C.P. Larsen et al., 2006; F. Vincenti and M. Luggen, 2007). Suramin inhibited the binding of TNF-a to its receptor TNF-R1 (F. Mancini et al., 1999) and its ability to inhibit CD40-CD154 interaction was 30 fold more active compared to it (Emilio Margolles-Clark et al., 2009). Suramin has also been shown to suppress T cell activity (C. Schiller et al., 1994), antiproliferative effects on lymphoid cells (Z. Spigelman et al., 1987). Suramin can causes toxicities which include adrenal and renal insufficiency, coagulation factor abnormalities and poly-neuropathy (T.E. Voogd et al., 1993; D.J. Cole et al., 1994), at relatively high concentration inhibited the binding of IL2 to its cell surface recept or (G.B. Mills et al.,1990), greater than therapeutic use (S.A. Grossman et al., 2001; S.T. Eichhorst et al., 2004). It concentration-dependently inhibited proteolytic and phospholipase A2 (PLA2) activities of Bothrops jararacussu venom- potential to be used as antivenom, suramin also antagonise the cardiotoxic effect of Bothrops jararacussu venom in rats heart (Daniel N. Sifuentes et al., 2008). Uptake of suramin by bloodstream form of trypanosome is through receptor mediated endocytosis which is most likely route of entry (Fairlamb AH, et al., 1980). Suramin intensively bound to plasma proteins such as low density lipoproteins, albumins, globulins, fibrinogen, etc. According to Bastin et al. 1996, Coppens and Courtoy 2000 and Green et.al 2003 suggested that suramin might enter while bound to low density lipoprotein (LDL), it has high affinity to bind many serum proteins including LDL (Vansterkenburg ELM, et al., 1993). The high rate of fluid-phase endocytosis occurs in the trypanosomes of bloodstream form (Engstler, et al., 2004). This mechanism could be involved in the uptake of suramin into T. brucei that does not require specialized receptors. Trypanosomes cannot synthesise their own fatty acid and cholesterol de novo hence LDL uptake is essential for propagation (Coppens I, et al., 2000). It does not make any worse however in procyclic form, uptake of suramin is through receptor mediated endocytosis and not coupled with LDL uptake (Pal A, et al., 2002). Suramin involves inhibition of various glycolytic enzymes, effects rates of respiration as aerobic glycolysis is closely related with it in bloodstream forms (Fairlamb AH, et al., 1980, Opperdoes, F.R. et al., 1989). Diminished growth rate of trypanosome in vivo is a consequence of decrease in respiration (Fairlamb AH, et al., 1980). Suramin is also used as veterinary trypanocide; report on resistance in T. evansi that infects animals is reported (El Rayah et al., 1999, Zhou, J.L. et al., 2004). Some cases have been described of drug resistance when suramin is used against Trypanosoma brucei rhodesiense in humans (W ´ery, M., 1994). Suramin reduced sensitivity towards T. b. rhodesiense (Bacchi et al., 1990) and failure of treatment up to 25-30% observed (P ´epin and Milord, 1994, Burri, C et al., 2004). Failures of treatment are common due to misdiagnosed late stage infection (Burri et al., 2004). De Koning argued one of the reasons of suramin resistance is associated with reduction in drug uptake; molecule is large and highly charged which plasma membrane transporter takes up. Role of apolipoprotein L-1 and haptoglobin-related protein T. evansi affects mainly domesticated animals such as camels, cattle and water buffalo, spread by mechanical transmission of infected blood through insect such as tabanid flies. Due to these, it spread apart from sub-Saharan Africa to South America, North America and Asia. Normally humans are resistant to animal trypanosomes, immunity against T.brucei brucei is due to trypanolytic activity of an apolipoprotein L-1 (APOL-1) bound to high density lipoprotein (HDL) (Vanhamme L. et al., 2003). Previously it was concluded that trypanolytic activity in normal human serum was due to immunoglobin M (Aaronovitch, S. Terry, R. J. 1972). Later in 1973, Hawking and colleagues resolute there were two trypanolyic factors. These two factors differ in their activity (in vivo and vitro), molecular mass, quantity in serum and sensitivity to antagonists (Hawking et al., 1973b). HDL was identified as trypanolyic factor by Rifkin in 1978, she also characterised the two trypanolyic factors determined by Hawking (Rifkin, M. R. 1978b). Trypanolyic factors in human serum shows inhomogeneous properties (Tomlinson et al., 1995; Raper et al., 1996b). Both TLF are a subset of HDLs commonly referred to as HDL3 (Lorenz et al., 1995), contain haptoglobin-related protein (Hpr) (Smith et al., 1995) and APOL-1 (Vanhamme, L. et al., 2003).TLF-1 is a 500 kDa lipid rich while TLF-2,1000 kDa protein complex containing IgM, lipid poor HDL particle (Raper, J. et al., 1999; Lugli, E.B. et al., 2004). Apolipop rotein A-1 (APOA-1) is a component of TLF-1(Smith et al., 1995) and, although previously reported that APOA-1 could not detected in TLF-2(Tomlinson, S. et al., 1995), is a component of TLF-2 (Raper, J. et al., 1999). Previously unknown proteins, human cathelicidin antimicrobial peptide (hCAP18), glycosylphosphatidylinositol-specific phospholipase D (GPI-PLD) and paraoxonase are associated with TLF-1(Smith AB et al., 1995; Lugil E et al., 2004). APOA-1 suggests a role in trypanolysis later controversial report supporting a lytic role (Gillett, M. Owen, J. 1992a) or not favor lytic role (Rifkin, 1991; Seed et al., 1993). Later it was confirmed that APOA-1 was not toxic (Tytler, 1995) but may indirectly play role of trypanolytic (Owen et al., 1996). For trypanosomes, HDLs contain 16,000-65,000 binding site per cell having moderate affinity (Gillett, M. Owen, J. 1992b). However, binding of lytic factor, TLF-1 appeared to involve two binding site, low affinity have 65,000 and high affinity 350 binding sites (Drain et al., 2001). Host macromolecules, interact with bloodstream trypanosomes, transferrin (Borst, P.1991) and low-density lipoprotein (LDL) (Coppens, I et al., 1987) through receptor-mediated endocytosis occur at the flagellar pocket of trypanosome (Gull, K., 2003). APOL-1 is a bacterial colicins and Bcl-2 family members like protein containing pore forming domain as well as a region for the membrane insertion of it (Pà ©rez -Morga D et al., 2005, Pays E et al., 2006). APOL-1 is taken up in the parasite by endocytosis, able to kill by the parasite by forming anion selective pores in the lysosomal membrane of parasite, this pore allows the influx of chloride ions into the lysosome, subsequent cell death as a consequence of entry of water and induces uncontrolled osmotic swelling of vacuole ((Pà ©rez-Morga D et al., 2005; Pays E et al., 2006; B. Vanhollebeke et al., 2007a). APOL-1 could not be involved in apoptosis but in programmed cell death (B. Vanhollebeke et al., 2006a). Resistance of T.brucei rhodesiense and T.brucei gambiense to APOL-1 is developed which allows these parasites to infect and cause HAT. Single protein termed serum resistance-associated protein (SRA) is main reason of resistance of T.brucei rhodesiense to APOL-1.SRAP interacts strongly with APOL-1 and provide specific resistance to T.brucei rhodesiense (Xong HV et al., 1998; Gibson WC, 2005). T brucei gambiense is also resistant to APOL-1; mechanism is not understood (Pays E et al., 2006). Indian case with T. evansi infection, human serum devoid of APOL-1, reason for the absence was due to independent frameshift mutation in both APOL-1 alleles (B. Vanhollebeke et al., 2006b). Another HDL component, plays a toxic role for full trypanolytic activity of normal human serum, haptoglobin-related protein (Hpr).Indian case has normal concentration of Hpr bound HDL but short of trypanolytic activity. Hpr is a haemoglobin (Hb) binding protein induces, within acidic lysosome of T.b.brucei, Fenton like reaction between H202 and iron that lead to formation of free hydroxyl radicals, which would prompt the reaction of lipid peroxidation of lysosomal membrane (Smith AB et al., 1995; Hager KM et al., 1994; Bishop JR et al., 2001; Justin Widener et al., 2007). Nevertheless action of trypanolysis of Hpr and APOL-1, biological function is not clear. Optimal trypanolytic activity requires presence of both APOL-1 and Hpr on same subset of HDL particle (B. Vanhollebeke et al., 2007b). Vanhollebeke et al. (2007b) reported trypanosome survival assay in normal as well as mutant human sera. Survival of trypanosomes occurs in human serum devoid of APOL-1 and fetal calf serum (FCS). FCS is nonlytic and contains neither APOL-1 nor Hpr. Human serum deficient of Hpr and haptoglobin (Hp) but with normal HDL b Disease Caused by Parasite of Genus Trypanosoma Disease Caused by Parasite of Genus Trypanosoma Human trypanosomiasis caused by Trypanosoma evansi and Trypanosoma lewisi in India : A matter of concern Introduction Disease produced by the parasite of genus Trypanosoma called as trypanosomiasis. It is one of the most important hemoprotozoan diseases, widely distributed in animals and human beings. It is endemic in Africa and America, are deadly pathogens that threaten millions of people in at least 36 countries in Africa. It is estimated that approximately 60 million people are at risk and 3, 00,000 new cases found every year in Africa (WHO Report 1998). Both African and American trypanosomes rank within the top 10 in terms of global impact. Despite the impact of these parasites, how they cause disease is relatively less is understood. In Africa, the disease is commonly known as human African trypanosomiasis (HAT) or sleeping sickness whereas the American trypanosomiasis recognized as Chagas disease. They not only infect vertebrates groups (amphibians, reptiles, birds, fish, and mammals) but also many invertebrates (Crithidia, Leptomonas). Human African trypanosomiasis belongs to genus Trypanoso ma, subgenus trypanozoon. Classification phylum sacromastigophora, order kinetoplastida and the family trypanosomatidae. Genus Trypanosoma includes subgenus which is divided into major group, salivaria and stercoraria that infect vertebrates (Hoare C. A.1964). Trypanozoon (T. brucei ssp, T. evansi, T. equiperdum), Duttonella (T. vivax,T. uniforme), Nannomonas (T. congolense, T. simiae), Pycnomonas (T. suis), Tejeraia (T. rangeli) belongs to salivaria group. Under stercoraria group Herpetosoma (T. lewisi, T. musculi,T. microti), Megatrypanum (T. theileri, T. melophagium), Schizotryponum (T. cruzi, T. dionisii) come. T. brucei. brucei, T. brucei. gambiense and T. brucei. rhodesiense are the subspecies of the Trypanozoon. Sleeping sickness is caused by T. brucei. gambiense, a chronic form of HAT in West and Central Africa lasting from months to years or T. brucei. rhodesiense, an acute form of HAT in East and Southern African with a duration of weeks to months. Whereas, closely relate d parasite T. brucei. brucei is non pathogenic to humans. The American trypanosomiasis is caused by T. cruzi. rhodesiense. These forms of the disease is deadly and develop within weeks to months, the gambiense form takes year. Trypanosomes cause animal trypanosomiasis has a wide geographic distribution. Surra is caused by T. evansi and infects mainly camels, cattle, buffalos, horses, deer and other wild animals. T. b. Brucei causes nagana in tropical Africa and affects only cattle; T. vivax and T. congolense infect domestic and small animals while T.lewisi is a commensally of rats. T. equiperdum causes dourine disease in horse and donkey of India, Europe, America and North Africa. African trypanosomes are transmitted by tsetse flies, a species of Glossina, and South American trypanosomes by reduvid bugs. Normally human are resistant to animal species of Trypanosoma due to the trypanolytic factor of human serum. However, there are several cases of human infection with animal trypanosomes such as Trypanosoma evansi; Trypanosoma lewisi and Trypanosoma congolense have been discussed later in this article. This proves not just a rare cases but the beginning of new era in the history of human trypanosomes, put in dilemma whether they develop potential of new diseases of humans or just a biological accidently transmission. In Asia, first documented evidence found in 1933, human trypanosomiasis in Malaysia, a four month old infant infected with T. lewisi (Johnson P. D, 1933). Later in 1974 K. Shrivastava and colleague reported T. lewisi-like Herpetosoma infection, diagnosed in two adult patients in India during malaria eradication program. All three human Herpetosoma infected patients were recovered without treatment. More recently the cases of a two-month-old infant in the Gambia (Howie, S. et al., 2006) and India (Kaur, R. et al., 2007) infected with T. lewisi-like trypanosome is reported but Gambian case has invasion of central nervous system. One more case in Thailand is reported; Trypanosoma lewisi-like infected 45-day-old male infant was recovered with the treatment of antibiotic gentamicin (Sarataphan, N. et al., 2007). Suspected case, 40 aged female in State of west Bengal of India, infected with trypanosomiasis in January 2005 however T. evansi was concluded by considering only the fact, specie s isolated from these area is T. evansi in cattle, buffaloes, and goats (see Ref. Meeting of the Ad Hoc Group of the World Organization for Animal Health (OIE), Paris 2006). Animal trypanosomiasis Trypanosoma evansi caused to human in India, state of Maharashtra. The patient was 45 year old man and veterinary quack from Seoni village in Taluka Shindevahi of District Chandrapur from Maharashtra State. He was admitted to rural hospital; initially symptoms observed were headache, intermittent fever, disoriented, sensory scarcity, saliva dribble from mouth and violent behaviour. Blood thick smear, stained by Fields stain, examination was done by local microbiologist Mrs. Bharti U Sable; she suspects trypanosome along with plasmodium falciparum (figure 01). He was treated with antimalarial drug along with oral hematenics. She marked as the founder of Indian trypanosome, T. evansi. Later patient was transferred to the Government Medical College and Hospital (GMC) in Nagpur, India. Stained blood smear shows numerous flagellated trypanosomes parasite only, was confirmed morphologically, position of nucleus and small kinetoplast at central and posterior respectively indicate that the contributory mediator was T. evansi (Joshi, PP. et al., 2005). Anoth er unique character of T. evansi has homogenous DNA minicircles (Borst et al., 1987; Songa et al., 1990; Masiga and Gibson, 1990; Lun et al., 1992) and absence of DNA maxicircles in the kinetoplast unlike T. brucei (Borst et al., 1987; Songa et al., 1990). Several methods has been evolvedmicroscopy, card agglutination test (C. Gutierrez et. al., 2000), microhematocrit centrifugation technique (Woo, PTK 1970), enzyme-linked immunosorbent assay (Indrakamhang, P et al.1996), DNA hybridization (Viseshakul, N., Panyim, S., 1990) and polymerase chain reaction (Wuyts, N.et.al. 1994; Wuyts, N.et al.1995; Omawa, S et al 1999) for detection of T. evansi infection. To confirm morphological identification of parasite, additional test of blood, serum and cerebrospinal fluid (CSF) was done in the Department of Microbiology, Government Medical College and Hospital, Nagpur and at the Institut de Recherche pour le Dà ©veloppement in Montpellier, France. Parasitological and serological tests conducted at GMC, Nagpur, are as followed (Joshi, PP. et al., 2005): Biochemical quantitative analysis of serum was performed with less tiny significance on lipid levels, indication of Tangier disease. Tangier disease is a rare autosomal recessive genetic disorder, high density lipoprotein deficiencies associated with this disease include dramatically lowered level of APO A1 (Von Eckardstein, A., et al., 1998), was found to be non trypanolytic (Rifkin, M R. 1978a), however controversial data, fresh sera of a patient with Tangier disease is trypanolytic exhibiting bothTLF-1 and TLF-2 activity, reported (Tomlinson et al., 1995). The demonstration of specific antibodies has been employed by using card agglutination test for trypanosomiasis (CATT) for T. evansi using whole blood and serum was conducted. CATT test initially developed for T. brucei. gambiense (Diall et al., 1994). Sensitivity of CATT for T. evansi in Kenya was 65.5% (Z.K. Njiru et al.2004) and 68.6% (Ngaira et al.2003).False positive result of CATT was reported (Stijn Deborggraeve et al.2008). Mini-anion centrifugation technique is used for purification and concentration of trypanosomes using heparinised blood before and after treatment of suramin A direct latex IgM agglutination test was conducted with CSF to reveal functionless of parasite in the blood brain barrier. Sediment of CSF after centrifugation was examined by bright field microscopy for the presence of trypanosomes. Thomas chamber is used to count lymphocytes in the CSF, presence demonstrate the incursion of parasite. Molecular technique and serological tests conducted at the Institut de Recherche pour le Dà ©veloppement in Montpellier, France, are as followed (Joshi, PP. et al., 2005). Three independent PCR assay were performed using DNA of trypanosome Related to the subgenus Trypanozoon using a seminested PCR method, primer used ITS1/2 based on internal transcribed spacer (ITS) of ribosomal DNA. Related to T.brucei group using a single PCR of the 177- basepair. Amplification of T. evansi was conducted using a 994- basepair mitochondrial kinetoplast minicircle template with the primer TEV 1/2. Reference strains used are T. b.gambiense Bat 6118 and T. evansi CIRDES. PCR provided high specificity and sensitivity molecular biology technique among others for diagnosis of infectious diseases and also permits identification of micro organisms such as mycobacterium (Garcia-Quintanilla, A et al., 2002) , detection and differentiation of Entamoeba histolytica and Entamoeba dispar (Gonin, P et. al.,2003), simultaneous detection of tick-borne hemoprotozoan parasites Babesia caballi and Babesia equi in horse blood (Alhassan, A. et. al., 2005) and detection of influenza A Virus (Nicole L. Z et. al, 2006). In spite of these, PCR are not usual in some countries (Holland et al., 2001). It has been reported about reproducibility problems, for diagnosis of both human and animal trypanosomes, of PCR results (Solano et al., 2002; Malele et al., 2003). Recently a new DNA amplification method, loop-mediated isothermal amplification developed for diagnosis of species and sub-species specific trypanosomes (Thekisoe OM et al., 2007). Disease developed due to absence of trypanolytic factor in normal human serum hence immune status of patient was checked to resolve possible infection with human immunodeficiency virus (HIV). Three tests were conducted to corroborate the results of Enzyme-linked immunosorbent assay (ELISA) in India. HIV 1/2 assay Specific enzyme-linked immunosorbent assay (ELISA) NNO-LIA HIV 1/2 Score test Investigation of parasite Unusual transmission of animal trypanosomiasis, T. evansi to human requires rationalization, for this P. Truc and collaborator, 2007 studied genetic characterization of T. evansi. Generally, genetic variability of T. evansi has been detected by using isoenzyme (Gibson et al., 1983; Stevens et al., 1989), restriction fragment length polymorphism (RFLP) (Songa et al., 1990), microsatellite (Biteau et al., 2000) and random amplified polymorphic DNA (RAPD) analysis (Lun et al., 2004; Ventura et al., 2002); all these above technique found isolated T. evansi were genetically homogenous. Micro heterogeneity reported (Gibson et al., 1983; Stevens et al., 1989), may due to low-resolution techniques and no genetic exchange of T. evansi in vector like others T. brucei ssp, that leads to absence of recombination which play role for micro heterogeneity (Jenni et al.1986). Nevertheless, some genetic variability of isolated T. evansi from Kenya reported through PCR (Ngaira et al.2004, 2005; Njiru e t al.2006) and amplified fragment length polymorphism (AFLP) along with RAPD. Among later, AFLP admittance more polymorphisms, was able to differentiate and separate the Type A T. evansi into two clades (Masiga et al., 2006). Direct comparison of high-resolution molecular techniques microsatellites or simple sequence repeats (SSR) and Inter-simple sequence repeats (ISSR) PCR revealed that latter technique demonstrate greater genetic variability of T evansi isolates from different geographical area (Z.K. Njiru et al 2007). Recently molecular analysis of T. b. brucei by PCR and microsatellite PCR of reported blood slides was successfully conducted (Stijn Deborggraeve et al.2008). Isolated T. evansi has been termed into type A and type B (Masiga and Gibson, 1990). Unlike to type B detected only from Kenya, isolates type A are most copious (Borst et al., 1987). It has been shown however, that most of T. evansi from South America are dyskinetoplastic- lacking both maxicircles and minicir cles (Masiga and Gibson, 1990; Ventura et al., 2000; Schnaufer et al., 2002). Normally T. evansi diagnosed through variant surface glycoprotein (VSG) Rode Trypanozoon antigen type (RoTat) 1.2, a diagnostic antigen. Songa and Hamers, 1988 developed CATT for veterinary use, which based on RoTat 1.2 gene (Songa and Hamers, 1988). Both PCR test and serological-CATT test are highly sensitive and specific in divergent geographical region (Verloo et al., 2000), former test can be trustworthy for detection of isolates of both dyskinetoplastic and DNA minicircles in kinetoplast of T. evansi (Claes et al., 2004) also it based on RoTat 1.2 gene (Urakawa et al., 2001). On the other hand, most of T. evansi from Kenya were not detected by test, which based on VSG of T. evansi RoTat 1.2 gene because few isolates lack both RoTat 1.2 gene and their linked protein-VSG while other isolates having only RoTat 1.2 gene (Ngaira et al. 2004). Characterization of non-RoTat 1.2 T. evansi, specific PCR test developed in these 273 base pair was present in disparity to RoTat 1.2 T. evans i (J.M. Ngaira et al., 2005). Microscopic examination of dissected organs of tsetse flies was done for identification of trypanosome infections (Lloyd and Johnson, 1924). Parasites are, generally indentified in the mouthparts, salivary glands and mid-guts. Trypanosome species from vector is isolated and employed in isoenzyme electrophoresis technique for identifications (Gashumba et al., 1986). Another approach as recombinant DNA probes have been used for the identification both mature and immature trypanosomes in tsetse fly (Gibson et al., 1988; Majiwa et al., 1993).Dot-ELISA is another technique used for detecting trypanosomes in tsetse flies (Bosompem et al., 1996; Ouma, J. O et al., 2000) How T. evansi differs from other Trypanozoon The subgenus Trypanozoon includes three species, namely Trypanosoma brucei, T. evansi and T. equiperdum. T. evansi is judge against, concerning their morphological, mode of transmission, biochemical and molecular characteristics, rest of species. Bloodstream stages of these three parasites are often morphologically indistinguishable (Brun R et al., 1998; Gibson, 2003). T. evansi is mechanically transmitted of infected blood through insects of the genera Tabanus, Stomoxys, Atylotus and Lyperosia. Horseflies (Tabanus spp), Stableflies (Stomoxys spp) are the most capable vectors for the transmission of T. evansi in Indonesia and China (Luckins, 1988; Lun et al., 1993). In Africa, south and Central America, tsetse fly (Glossina spp) and vampire bats Desmodus rotundus an extra host-vector-reservoir of the T. evansi, respectively can mechanically transmitted this parasite. Direct transmissions through milk or during coitus involved T. evansi (Wang, 1988). Besides mechanical and direct tran smission of T. evansi, T. equiperdum transmitted directly during coitus and with rare possibility through bloodsucking insects (see ref. Brun, R et al.,1998). Trypanosoma brucei gambiense, sleeping sickness parasites have been able to spread through tsetse flies of palpalis group (Glossina palpalis, Glossina tachinoides) while T. b. rhodesiense was generally transmitted by tsetse of the morsitans group (Glossina morsitans, Glossina pallidipes). All 31 species of tsetse flies are able to transmit trypanosomes (Aksoy S, et al., 2003). Other major parasites T. congolense, T. vivax and T. simiae that are pathogens of domesticated animals, transmitted by tsetse fly. Both parasites, T. evansi and T. equiperdum are closely related to T. brucei, most likely developed from Trypanosoma brucei by independently deletion of kinetoplast DNA and should be regarded as two subspecies Trypanosoma brucei evansi and Trypanosoma brucei equiperdum respectively (Lai et al., 2008). Absence of maxicircles in kinetoplast DNA explained inexistence of procyclic or insect stage in these parasites and can propagate only as the mammal-infective bloodstream form (Borst et al., 1987).This facilitate to explain wide range of mechanical transmission of T. evansi outside of Africa (Lun and Desser, 1995). Procyclic form (PCF) T.brucei strain cannot survival with a partial or complete loss of kinetoplast DNA as with some Blood stream form (BSF) strains. This kinetoplast DNA deficient T.brucei strains appear naturally or induced by drugs (Schnaufer A et al.2002). Drug inducers are acriflavine, ethidium bromide, methoxy-9-ellipticine, hydroxystilbamidine, berenil, pentamidine, an trycide, and para-rosaniline, grouped as DNA intercalators and non intercalating drugs (Hajduk, 1978). Nevertheless, the existence of T. equiperdum has been complexity; Claes et al. suggested that, in fact, some strains of Trypanosoma equiperdum are actually Trypanosoma brucei and all other remaining misidentified strains such as Swiss Tropical Institute Basel (STIB) 818 are Trypanosoma evansi. However, based on PCR amplification of the fragment of DNA maxicircles in the kinetoplast, T. equiperdum Onderstepoort Veterinary Institute (OVI) and Bordeaux Trypanosoma antigen type (BoTat) 1.1 strains are T. brucei and other STIB 818, STIB 841 and STIB 842 T. equiperdum strains are not cluster together with T. evansi as it maintains maxicircles and allied genes. (Li et al., 2006). Both parasites have homogeneous minicircles. Although in all T. evansi strains maxicircles are totally lost but T. equiperdum shows more assortment, some strains seems to bear complete maxicircles with no active essential gene; others are missing one of the genes; and a few devoid the entire maxicircles (Lai et al., 2008). Unlike other DNA, T. brucei mitochondrial DNA termed kinetoplast DNA include a network of interlocked DNA rings (Liu, B. et al. 2005). This network of T. brucei ssp. comprised of several thousands of heterogeneous minicircles and several dozen of homogeneous maxicircles (Borst and Hoeijmakers, 1979). T. evansi has largely homogenous and limited heterogeneous minicircles in kinetoplast DNA (Borst et al., 1987). Results (Joshi, PP. et al., 2005; P. Truc et al., 2007) A careful examination of morphological characteristic demonstrates the presence of T. evansi. Patient had normal level of APO A-1 indicate no sign of Tangier disease. The result of CATT for T. evansi was positive suspect stalwartly presence of RoTat 1.2 gene. Latex IgM test, a diagnostic for trypanosome invasion in CSF, and lymphocytes count in the CSF indicated no invasion of parasite. An attempt to isolate and propagate trypanosome in wistar rat was failed. For molecular diagnosis of T. evansi PCR conducted, test was positive. Results of ELISAs for HIV, conducted in France and India were negative. Genetic characterization, Indian patient has homogenous DNA minicircles in kinetoplast of T. evansi of type A and devoid of SRA gene. Treatment Treatment was started 109 days after initial admission to hospital using suramin. Suramin is manufactured by Bayer and donated to WHO as Germanin, used against sleeping sickness in 1922 (Voogd et al., 1993). Suramin was used as a first stage of treatment for HAT caused by Trypanosoma brucei gambiense (chronic form) or T. b. rhodesiense (acute form). Efficacy of suramin against T. evansi infection was studied in cattle by Gill BS, Malhotra MN, 1963. It was requested and provided by Department of Public Health, Government of Maharashtra State, India and World Health Organisation respectively. As patient falls under first stage of infection, drugs have to be used pentamidine or suramin sodium. Pentamidine has more adverse effect than suramin, according to author; hence suramin was used in this patient. Drug suramin acts by interfering with enzyme of glycolytic pathway (Wierenga RK, et.al., 1987) in trypanosomes and produce hot spot, function as a signal for import into glycosome. It is preferred to give slow intravenous injection as suramin is poorly absorbed from intestine and causes intense local irritation when given intramuscularly (Voogd TE, et.al., 1993). Suramin does not cross the blood-brain barrier to kill trypanosome in the CSF however able to cure model of stage 2 diseases at a high dose greater than 80 mg per kg (Jennings FW, et.al., 1995). Follow-up study was commenced after the end of treatment and at 3rd and 6th months, all previous tests-CATT for T. evansi, latex IgM agglutination test, Mini anion-exchange centrifugation technique and examination of CSF by bright field microscopy are repeated at GMC Nagpur excepts biochemical analysis of serum for Tangier disease (P. P. Joshi et al. 2006). Tests result indicates first patient of human trypanosomiasis infected with T. evansi was recovered, Joshi and collaborators concluded that same schedule would follow in treatment if more cases observed. Suramin Suramin is less active against procyclic form of trypanosomes than bloodstream form, former normally reside in the tsetse flies (Scott AG, et.al., 1996). Suramin inhibit number of glycolytic enzyme which is essential to bloodstream form rather than procyclic form (Fairlamb AH, et.al., 1977, Fairlamb AH, et.al., 1980). Hanau and colleagues proposed other likely target of drug, competitive inhibitor of an enzyme 6-phosphogluconate dehydrogenase of pentose phosphate pathway (Hanau S, et.al., 1996). Suramin is an effective microfilaricide for Onchocerca spp. and Brugia pahangi worms (Hawking, et al., 1981; Howells, et al., 1983). It is a known ATP/UTP purine receptor (P2 receptor) antagonist (V. Ralevic and G. Burnstock, 1998). Nevertheless suramin inhibit ample varieties of enzymes like reverse transcriptase, dihydrofolate reductase, furamse, glycerol-3-phosphate dehydrogenase, hexokinase, L-a-glycerophosphate oxidase, receptor mediated uptake of low density lipoprotein, RNA polymerase and kinases, thymidine kinase, trypsin (P ´epin and Milord, 1994; Wang, 1995). Besides its trypanocidal activity, suramin is also useful in hormone-refractory prostate cancer, however survival rate was not affected (Small et al., 2000; Ahles et al., 2004). Suramins antitumor activity has been attributed to its inhibition of various growth factors which include platelet-derived growth factor, fibroblast growth factor, transforming growth factors alpha and beta, insulin- like growth factors 1(Stein CA,1993). Osteosarcoma is the malignant tumor of the bone; suramin exerts an inhibitory effect on osteosarcoma cell growth of established cell lines (Benini et al., 1999), newly established osteosarcoma cell lines and stimulation of osteosarcoma cells by physiological compounds, such as 1, 25-dihydroxy-Vitamin D3 (K. Trieb, H. Blahovec, 2002). Furthermore, results in an inhibiting capacity of suramin on various cell functions include production of alkaline-phosphatase or telomerase activi ty (K. Trieb, H. Blahovec, 2002). Suramin blocked CD154 (Emilio Margolles-Clark et al., 2009) from interacting with its receptor CD40 (U. Schà ¶nbeck and P. Libby, 2001; I.S. Grewal and R.A. Flavell, 1998), costimulatory interactions are therapeutically important to modulate immune responses (C.P. Larsen et al., 2006; F. Vincenti and M. Luggen, 2007). Suramin inhibited the binding of TNF-a to its receptor TNF-R1 (F. Mancini et al., 1999) and its ability to inhibit CD40-CD154 interaction was 30 fold more active compared to it (Emilio Margolles-Clark et al., 2009). Suramin has also been shown to suppress T cell activity (C. Schiller et al., 1994), antiproliferative effects on lymphoid cells (Z. Spigelman et al., 1987). Suramin can causes toxicities which include adrenal and renal insufficiency, coagulation factor abnormalities and poly-neuropathy (T.E. Voogd et al., 1993; D.J. Cole et al., 1994), at relatively high concentration inhibited the binding of IL2 to its cell surface recept or (G.B. Mills et al.,1990), greater than therapeutic use (S.A. Grossman et al., 2001; S.T. Eichhorst et al., 2004). It concentration-dependently inhibited proteolytic and phospholipase A2 (PLA2) activities of Bothrops jararacussu venom- potential to be used as antivenom, suramin also antagonise the cardiotoxic effect of Bothrops jararacussu venom in rats heart (Daniel N. Sifuentes et al., 2008). Uptake of suramin by bloodstream form of trypanosome is through receptor mediated endocytosis which is most likely route of entry (Fairlamb AH, et al., 1980). Suramin intensively bound to plasma proteins such as low density lipoproteins, albumins, globulins, fibrinogen, etc. According to Bastin et al. 1996, Coppens and Courtoy 2000 and Green et.al 2003 suggested that suramin might enter while bound to low density lipoprotein (LDL), it has high affinity to bind many serum proteins including LDL (Vansterkenburg ELM, et al., 1993). The high rate of fluid-phase endocytosis occurs in the trypanosomes of bloodstream form (Engstler, et al., 2004). This mechanism could be involved in the uptake of suramin into T. brucei that does not require specialized receptors. Trypanosomes cannot synthesise their own fatty acid and cholesterol de novo hence LDL uptake is essential for propagation (Coppens I, et al., 2000). It does not make any worse however in procyclic form, uptake of suramin is through receptor mediated endocytosis and not coupled with LDL uptake (Pal A, et al., 2002). Suramin involves inhibition of various glycolytic enzymes, effects rates of respiration as aerobic glycolysis is closely related with it in bloodstream forms (Fairlamb AH, et al., 1980, Opperdoes, F.R. et al., 1989). Diminished growth rate of trypanosome in vivo is a consequence of decrease in respiration (Fairlamb AH, et al., 1980). Suramin is also used as veterinary trypanocide; report on resistance in T. evansi that infects animals is reported (El Rayah et al., 1999, Zhou, J.L. et al., 2004). Some cases have been described of drug resistance when suramin is used against Trypanosoma brucei rhodesiense in humans (W ´ery, M., 1994). Suramin reduced sensitivity towards T. b. rhodesiense (Bacchi et al., 1990) and failure of treatment up to 25-30% observed (P ´epin and Milord, 1994, Burri, C et al., 2004). Failures of treatment are common due to misdiagnosed late stage infection (Burri et al., 2004). De Koning argued one of the reasons of suramin resistance is associated with reduction in drug uptake; molecule is large and highly charged which plasma membrane transporter takes up. Role of apolipoprotein L-1 and haptoglobin-related protein T. evansi affects mainly domesticated animals such as camels, cattle and water buffalo, spread by mechanical transmission of infected blood through insect such as tabanid flies. Due to these, it spread apart from sub-Saharan Africa to South America, North America and Asia. Normally humans are resistant to animal trypanosomes, immunity against T.brucei brucei is due to trypanolytic activity of an apolipoprotein L-1 (APOL-1) bound to high density lipoprotein (HDL) (Vanhamme L. et al., 2003). Previously it was concluded that trypanolytic activity in normal human serum was due to immunoglobin M (Aaronovitch, S. Terry, R. J. 1972). Later in 1973, Hawking and colleagues resolute there were two trypanolyic factors. These two factors differ in their activity (in vivo and vitro), molecular mass, quantity in serum and sensitivity to antagonists (Hawking et al., 1973b). HDL was identified as trypanolyic factor by Rifkin in 1978, she also characterised the two trypanolyic factors determined by Hawking (Rifkin, M. R. 1978b). Trypanolyic factors in human serum shows inhomogeneous properties (Tomlinson et al., 1995; Raper et al., 1996b). Both TLF are a subset of HDLs commonly referred to as HDL3 (Lorenz et al., 1995), contain haptoglobin-related protein (Hpr) (Smith et al., 1995) and APOL-1 (Vanhamme, L. et al., 2003).TLF-1 is a 500 kDa lipid rich while TLF-2,1000 kDa protein complex containing IgM, lipid poor HDL particle (Raper, J. et al., 1999; Lugli, E.B. et al., 2004). Apolipop rotein A-1 (APOA-1) is a component of TLF-1(Smith et al., 1995) and, although previously reported that APOA-1 could not detected in TLF-2(Tomlinson, S. et al., 1995), is a component of TLF-2 (Raper, J. et al., 1999). Previously unknown proteins, human cathelicidin antimicrobial peptide (hCAP18), glycosylphosphatidylinositol-specific phospholipase D (GPI-PLD) and paraoxonase are associated with TLF-1(Smith AB et al., 1995; Lugil E et al., 2004). APOA-1 suggests a role in trypanolysis later controversial report supporting a lytic role (Gillett, M. Owen, J. 1992a) or not favor lytic role (Rifkin, 1991; Seed et al., 1993). Later it was confirmed that APOA-1 was not toxic (Tytler, 1995) but may indirectly play role of trypanolytic (Owen et al., 1996). For trypanosomes, HDLs contain 16,000-65,000 binding site per cell having moderate affinity (Gillett, M. Owen, J. 1992b). However, binding of lytic factor, TLF-1 appeared to involve two binding site, low affinity have 65,000 and high affinity 350 binding sites (Drain et al., 2001). Host macromolecules, interact with bloodstream trypanosomes, transferrin (Borst, P.1991) and low-density lipoprotein (LDL) (Coppens, I et al., 1987) through receptor-mediated endocytosis occur at the flagellar pocket of trypanosome (Gull, K., 2003). APOL-1 is a bacterial colicins and Bcl-2 family members like protein containing pore forming domain as well as a region for the membrane insertion of it (Pà ©rez -Morga D et al., 2005, Pays E et al., 2006). APOL-1 is taken up in the parasite by endocytosis, able to kill by the parasite by forming anion selective pores in the lysosomal membrane of parasite, this pore allows the influx of chloride ions into the lysosome, subsequent cell death as a consequence of entry of water and induces uncontrolled osmotic swelling of vacuole ((Pà ©rez-Morga D et al., 2005; Pays E et al., 2006; B. Vanhollebeke et al., 2007a). APOL-1 could not be involved in apoptosis but in programmed cell death (B. Vanhollebeke et al., 2006a). Resistance of T.brucei rhodesiense and T.brucei gambiense to APOL-1 is developed which allows these parasites to infect and cause HAT. Single protein termed serum resistance-associated protein (SRA) is main reason of resistance of T.brucei rhodesiense to APOL-1.SRAP interacts strongly with APOL-1 and provide specific resistance to T.brucei rhodesiense (Xong HV et al., 1998; Gibson WC, 2005). T brucei gambiense is also resistant to APOL-1; mechanism is not understood (Pays E et al., 2006). Indian case with T. evansi infection, human serum devoid of APOL-1, reason for the absence was due to independent frameshift mutation in both APOL-1 alleles (B. Vanhollebeke et al., 2006b). Another HDL component, plays a toxic role for full trypanolytic activity of normal human serum, haptoglobin-related protein (Hpr).Indian case has normal concentration of Hpr bound HDL but short of trypanolytic activity. Hpr is a haemoglobin (Hb) binding protein induces, within acidic lysosome of T.b.brucei, Fenton like reaction between H202 and iron that lead to formation of free hydroxyl radicals, which would prompt the reaction of lipid peroxidation of lysosomal membrane (Smith AB et al., 1995; Hager KM et al., 1994; Bishop JR et al., 2001; Justin Widener et al., 2007). Nevertheless action of trypanolysis of Hpr and APOL-1, biological function is not clear. Optimal trypanolytic activity requires presence of both APOL-1 and Hpr on same subset of HDL particle (B. Vanhollebeke et al., 2007b). Vanhollebeke et al. (2007b) reported trypanosome survival assay in normal as well as mutant human sera. Survival of trypanosomes occurs in human serum devoid of APOL-1 and fetal calf serum (FCS). FCS is nonlytic and contains neither APOL-1 nor Hpr. Human serum deficient of Hpr and haptoglobin (Hp) but with normal HDL b