Tuesday, May 5, 2020

A Review of Ebora Viral Disease Samples †MyAssignmenthelp.com

Question: Discuss about the Review of Ebora Viral Disease. Answer: Ebola Viral Disease EBOV is the agent responsible for the transmission of Ebola disease. This disease has spawned several epidemics the past four decades. For instance, in 2014, Ebola became an epidemic after spreading from Africa to other continents. The fact that the there was no effective treatment confused the whole world. This virus has a relatively unique structure. It is lethal, and it has a high infectivity rate which even makes it hard to control. This paper will provide a review of the acknowledged facts of Ebola virus disease (EVD), its etiological facts, epidemiology, and information regarding its management. Epidemiology The world label Ebola virus as an emerging and re-emerging pathogen. Ebola hemorrhagic fever (EHF) or EVD was first reported in Democratic Republic of Congo (DRC) in the 1976 outbreak (Rosello et al., 2015). Since then, there have been numerous additional EVD outbreaks. The dangerous one occurred in 2000-2001 in Gulu District, Uganda. The outbreak caused 425 cases which lead to 53% fatality rate (Shears O'Dempsey, 2015). The Ebola strain in West Africa exhibits is homologically 97% similar to the DRC sample (Shoman, Karafillakis Rawaf, 2017). This strain has a record of causing the highest mortality of 90%. The recent case of EVD epidemic happened in Guinea in December 2013. By August 17, 2014, the disease had spread forcing WHO to declare it as an epidemic (Chan, 2014). By mid-September 2014, Ebola's fatality rate had stretched to 70.8% which also remained constant within Guinea, Sierra Leon and Liberia (Rosello et al., 2015). Nigeria showed a lower fatality of 45.5%. In Nigeria, the fatality rate remained lower at 45.5%. However, studies base their current assessments on just 11 latest cases. The in-patient fatality rate recorded 64.3 percent (Shears O'Dempsey, 2015). This valuation was lower when compared with all patients with clear outcomes. This rate was also consistent with rates from other countries. A health worker died in Liberia. Also, the number of new cases increased every week despite having multisectoral and multinational participation in countering the disease. At the same time, some of the humanitarian aid practitioners had to go back to their countries for medical care after contracting Ebola (Kaner Schaack, 2016). These workers had contacted the disease despite wearing the personal protection equipment (PPE). One of them led the case of Ebola in Spain. In October 2014, Liberia citizen traveled to Dallas, Texas. He was hospitalized and died of Ebola. This patient led to the infection of other individuals some of them being two healthcare workers who also had their PPE (Mbonye et al., 2014). The WHO Ebola Response Team predicted an increase of deaths by November 2014 urging the global community to respond to more efficient methods of managing the diseases (Mbonye et al., 2014). Agents of EVD EBOV belong to the species Zaire ebolavirus, the genus Ebolavirus, and the family Filoviridae (Weston, Burgess Roberts, 2016). The genus Ebolavirus has five different viruses. These include the Sudan virus (SUDV), Bundibugyo virus, EBOV, Reston virus, and Tai Forest virus (Lukashevich Shirwan, 2014). Among these, EBOV causes EHF and it has the highest fatality rate between 57 and 90 percent in humans (Weston, Burgess Roberts, 2016). SUDV follows with a rate between 41 and 65 percent. Bundibugyo virus has a fatality rate of percent (Weston, Burgess Roberts, 2016). The work of (Sanford, West Jacob, 2017) states that Tai Forest virus has only caused two human infections which are nonfatal. Reston virus is the causing agent for asymptomatic condition in humans. The Structure Filoviridae Both the MARV and EBOV genomes encode seven protein structures. The study of (Kaner Schaack, 2016) states that EBOV encoding two nonstructural soluble glycoproteins (GP). These are the small soluble GP product and the soluble GP (Hoenen et al., 2015). MARV strains have only one species known as the Lake Victoria marburgvirus. eBOV strains have four distinct species (Lukashevich Shirwan, 2014). These are the Sudan ebolavirus (SEBOV), Zaire ebolavirus (ZEBOV), Reston ebolavirus (REBOV) and Cte dIvoire ebolavirus (CIEBOV). However, there is a newly discovered species proposed to be the fifth one called the Bundibugyo ebolavirus (BEBOV) (Ealy, 2016). These species exhibit a variance in their pathogenic effects on humans. The most pathogenic are ZEBOV which has a fatality rate of up to 90 percent (Rezza Ippolito, 2017). SEBOV follows with a fatality rate of 50%. BEBOV follows third with a fatality rate of 40%. Records link REBOV and CIEBOV with lethal infections in other primates apart from human beings. The EBOV and MARV's systematic viral replication causes the increased levels of inflammatory cytokines, abnormalities in the coagulation and problems in the fluid distribution (Greenwood Barer, 2012). These processes cause vascular leakage and hemorrhage which eventually causes organ failure and shock. The 1979 discoveries were the first to confirm ZEBOV as the fatal species (Greenwood Barer, 2012). These species held a fatality rating going up to a level of 90% in humans and 100% lethality. Reservoir Recent evidence has confirmed that bats play a potential role as the most likely reservoir species of filoviruses. Medical experts believe that EHF persists in reservoir species located within endemic regions. Mammalian species like man and Ape seem to be more susceptive to Ebola virus infections as last hosts of Ebola rather than being the reservoir (Rezza Ippolito, 2017). Despite various studies trying to establish a potential host, there has been no host linked to Ebola. However, the study of (Kaner Schaack, 2016) states that rodents and bats could be possible reservoir species. Other reviews on arthropods have always been negative, including bedbugs that can bite different persons. Environment Factors and the Spread of EVD Viruses are acellular, an obligate organism that needs a host to remain active. Hosts provide an environment where virus's viral receptor attaches to the host's plasma membrane (Greenwood Barer, 2012). Eventually, the virus genome gets integrated into the hosts DNA. As the host's cell undergo subdivisions, the viral genome also rapidly undergoes subdivision. The result of the viral genome subdivision supports rapid mutation which increases its pathogenicity (Rezza Ippolito, 2017). The presence of glycoproteins in the host allows the enveloped virus to infect the host. These glycoproteins play a significant role in communication between the infected cells and other cells (Singh Ruzek, 2013). They also sustain the virus when it comes to an outside environment. Most of the enveloped viruses exist in the animal wastes such as feces and urine and feces. This kind of environment facilitates the persistence of the enveloped virus once outside the hosts body. In this regard, it is critical that people should maintain a clean environment as a means for controlling the emergence of Ebola disease. For instance, many African countries have poor sanitation which presents a high risk to entire public health. Poor sanitation in African can be one of the reasons behind high cases of EVD mortality rate (Rezza Ippolito, 2017). Another environmental factor is contaminated water since Ebola transmission mainly works through contact with fluids. Another environmental contribution is the scarcity of food. In Africa, the people's interaction while they search for food and their contact with infected animals can lead to the transmission of Ebola (Vidal, 2017). Poverty is also a contributing factor to the occurrence of EVD. People in developing countries lack basic needs, and government resources are scarce which leads to population displacement as people search for resources (Shoman, Karafillakis Rawaf, 2017). This factor becomes a significant contribution especially where one person is a carrier. These are some of the environmental factors that facilitate the reemerging cases of Ebola. Transmission Most of EVD cases result from body contact with an infected animal or person. Nevertheless, all cases of transmission between people occur through coming into contact with contaminated body fluid. These fluids can be breast milk, blood, vomitus, saliva, sweat, urine, stool, tears, or respiratory secretions from an infected patient (Ealy, 2016). Another main cause is body contact with infected objects. This form of transmission occurs when an uninfected person uses contaminated objects in their mouths or eyes (Rezza Ippolito, 2017). This mode of transmission keeps home caregivers at the highest risk of exposure since they do not have PPE. Some studies state that of EBOV and MARV can spread via aerosol particles but this method has rarely happened either in the case of a hospital or a home setting infection (Vidal, 2017). Sexual contact has also proved to be a possible mode of transmission. EVD virus has been traced in semen and remains until after seven weeks of recovery. People are advised to use condoms during sexual intercourse. Mothers should also stop breastfeeding their children for at least three months after recovery as a preventive measure. Diagnosis Ebola virus takes 2 to 21 day as the incubation period. The shorter incubation periods correlate with exposure to a more massive load of virus (Nelson, 2014). Viremia corresponds to the abrupt start of signs and symptoms of the EVD. The WHO and the Centers for Disease Control and Prevention (CDC) have confirmed the effective criteria for the diagnosis of EVD. One of these is a sudden emergence of high fever. Also, a patient may develop a headache, diarrhea, lethargy, reduced appetite, vomiting, hiccupping, painful joints and muscles, stomach pains, dyspnea, or dysphagia (Rezza Ippolito, 2017). With the occurrence of the named signs, a position confirmation requires a positive serology test for Ebola virus. There are multiple serologic tests for the confirmation and diagnosis of EVD. One of these is the antibody-capture enzyme-linked immunosorbent assay (Vidal, 2017). Another test is reverse-transcriptase polymerase chain reaction assay and electron microscopy (Park, Lee, Lee, Jee Choi, 2016). These technological methods are widely available, but their associated biohazards hiders many world laboratories from safely utilizing them. The only place for performing these tests is in a level-4 biosafety facility (Burd, 2014). These viruses are highly virulent and have higher chances of transmission via an aerosol. This state also gives them a higher mortality rate. Apart from that, the equipment for the mentioned tests are not movable, and the tests results take longer (Burd, 2014). The WHO has requested for proposals for coming up with a portable device. The conditions for these devices are that they should not need a biosafety level-4 facility and would provide Ebola results in less than three hours (Zhang et al., 2017). The devices should also have a high level of specificity and selectivity. Such a device is essential for identifying individuals requiring isolation more quickly. It will also help in the identifications of those individuals having similar symptoms but suspected to have been exposed to the virus. Treatment and prevention There have been major developments in the studies of EBOV and MARV on several animal models. However, no study has presented a licensed vaccine or an approved treatment (Martnez, Salim, Hurtado Kilgore, 2015). This means that any person working within the containment facilities, or people living within the areas marked with infection are a higher risk of possible infection. Studies have confirmed the effectiveness of passive transfer of serum obtained from a patient who survived Junin virus or Lassa virus (Dye et al., 2012). However, the efficacy of this therapies requires treatment to start immediately after infection. On the other hand, this method does not work in treating filovirus infections. During the 1995 EBOV outbreak in DRC, specialists transferred whole blood from convalescent EBOV to eight patients who had EBOV (Gebre, Gebre Peters, 2014). Out of these, only one patient who did not survive. This case brought a lethality rate of 12.5% which was significantly lower than the overall 80% fatality cases of EBOV epidemic(Gebre, Gebre Peters, 2014). However, the concept does not explain the role of antibodies since the patient received whole blood instead just antibodies. The 1995 epidemic led to the production of equine IgG product from WHO (Lukashevich Shirwan, 2014). The equine IgG came from horses hyper vaccinated with EBOV. Though equine IgG had some success in hamadryas baboons, it could only delay the death of cynomolgus macaques instead of protecting them. Recently, there has been great attention towards unlicensed treatments and vaccines. One of this was a cocktail drug (ZMapp), humanized-mouse antibodies (Ledgerwood et al., 2017). This one forms a part of the several therapeutics showing promising results with primates which are nonhuman. ZMapp demonstrated clinical improvements on two US citizens who were evacuated from Liberia (Vidal, 2017). Another therapeutics trials are RNA polymerase inhibitors and small interfering RNA nanoparticles. There has been a success when small interfering RNAs was used in treating primate and guinea pigs, the non-humans who had Ebola diseases (Lukashevich Shirwan, 2014). The results imply that RNA interference could work efficiently as vaccination treatment strategies for patients with EVD or other VHF causative agents (Nelson, 2014). Unfortunately, there is a challenge in the production cost issues which can frustrate this approach. Another therapy is a preclinical evaluation. This one has also been initiated for different proposed vaccines. One of these is chimpanzee adenovirus vector vaccine (Ledgerwood et al., 2017). Another proposed vaccine includes vesicular stomatitis virus pseudotypes. Scientists have been trying to develop different vaccines and treatment against filoviruses for the past decades. Though no vaccine or treatment platforms have proven to be highly effective, most of them have been successful in EBOV and MARV infections (Gebre, Gebre Peters, 2014). Some of these include Recombinant Vesicular Stomatitis Virus (rVSV), Venezuelan Equine Encephalitis Virus Replicon Particle Vaccine, virus-like particles, Replication-defective adenovirus serotype 5 vectors, and replication competent recombinant human parainfluenza virus 3 (Wu et al., 2015). All these vaccines have proven to be successful in nonhuman primates models. The rVSV platform has been a more reliable vaccine against filoviruses (Wu et al., 2015). There have been various evaluations of the effectiveness of rVSV in vaccines. The researchers have noted protective efficacy with rVSV against ZEBOV and MARV infections. However, there is no information regarding the use of rVSV on post-exposure (Nelson, 2014). Since rVSV is a vaccine that triggers the body to respond with extreme immune activity, it has worked in overcoming filovirus-driven suppression. It manages to inhibit the replication of hence preventing the spread of an infection. Studies have shown that rVSVs targets the same cells that filoviruses target, so their viral interference causes a block to MARK and EBOV replication (de La Vega, Wong, Kobinger Qiu, 2015). Currently, there are at least several promising vaccine schemes for full protection against MARV or EBOV infection in nonhuman primates (Nelson, 2014). All of them have shown efficacy in nonhuman primate on filoviral hemorrhagic fever. Out of them, the two best options are the one established on a replication-defective adenovirus serotype 5, and rVSV which has proven perfect protection when administered as a single injection to other primates except the humans (de La Vega, Wong, Kobinger Qiu, 2015). Currently, there are no licensed vaccines for EBOV or MARV for humans. Despite that EBOV and MARV hemorrhagic fevers rarely occur, having a vaccine in place could be an important preventive mechanism (Sanford, West Jacob, 2017). This move can be important in case an epidemic of such infection occurs. There is a hope that activated protein C, a recombinant inhibitor of factor VIIa/tissue factor and modipafant could be a forthcoming solution for cases of Ebola infections (de La Vega, Wong, Kobinger Qiu, 2015). Studies have given an insight that transgenic mice exhibiting extreme levels of human mannose-binding lectin (MBL) intensities could resist more to fatal Ebola infections when compared with wild-type mice (Wu et al., 2015). These results suggest that modulation of MBL activities can be one area for advanced clinical assessment. Key Preventive Interventions There are various primary prevention approaches. The first one is rigorous precaution actions within a healthcare setting. The leading risk of Ebola transmission happens in the situations where patients do not get detected or isolated immediately after exposure (Vidal, 2017). Therefore, those patients who have already been diagnosed are less risky. The second method of prevention focuses on education. The society needs education and support regarding infections (Nelson, 2014). It needs to understand the risk of getting in contact with bodies of people who have died of Ebola. For instance, some communities need to modify their traditional burial programs that take long preparations. Burials that take extended preparations increases chances of direct contacts with the fluids from the deceased. This issue of burials is culturally sensitive (Weston, Burgess Roberts, 2016). Those offering education programs need to exercise cultural awareness and use of appropriate educational program resources. The next preventive method is to evade all forms of direct contacts and products from wild animals (Weston, Burgess Roberts, 2016). Hunting communities should be encouraged to avoid meat from wild animals. People should also avoid direct contact with bats as they are the initial natural reservoir of Ebola virus. Avoiding bats can eradicate the risks of early exposure to Ebola infection. Precaution Practices Among Healthcare Workers Healthcare workers practices and knowledge involves reliable infection-prevention gears which include proper use of PPE to both the workers and the patients (Vidal, 2017). Different studies have shown that the major area of transmission is within a healthcare center whenever there is an outbreak. The process should start with the immediate isolation of any patient suspect to be exposed to the virus. Besides, strict precautions should be utmost while handling specimens to avoid chances of spread of the infection within care units (Nelson, 2014). Tools and other equipment should always be used such as eye protection, gowns, gloves, masks, and face protection. Moreover, the CDC policies suggest respiratory protection through N-95 respirators equipment (Nelson, 2014). Thorough disinfection and treatment of contaminated areas should be encouraged and decontaminating surfaces and care should be taken while handling objects used on patients. Conclusions Ebola disease is a saddening disease that reminds people that its outburst can emerge from anywhere and pose a risk the entire world. It is a disease that spreads rapidly whenever it gets out of control. The WHO endeavors to implement health operations in the high-risked countries to eradicate the possibility of the spread of EVD before it becomes an emergency situation. Although there have been significant improvements, a better surveillance remains a necessity. The primary transmission of Ebola virus occurs through contact with the infected person's body fluids. Therefore, healthcare workers can minimize the spread by tracing people who have been in contact with the patients since their exposure to the virus. References Rosello, A., Mossoko, M., Flasche, S., Van Hoek, A. J., Mbala, P., Camacho, A., Muyembe Tamfum, J.-J. (2015). Ebola virus disease in the Democratic Republic of the Congo, 1976-2014.eLife,4, e09015. https://doi.org/10.7554/eLife.09015 Shears, P., O'Dempsey, T. (2015). Ebola virus disease in Africa: epidemiology and nosocomial transmission.Journal Of Hospital Infection,90(1), 1-9. https://dx.doi.org/10.1016/j.jhin.2015.01.002 Kaner, J., Schaack, S. (2016). Understanding Ebola: the 2014 epidemic.Globalization And Health,12(1). https://dx.doi.org/10.1186/s12992-016-0194-4 Chan, M. (2014). Ebola Virus Disease in West Africa No Early End to the Outbreak.New England Journal Of Medicine,371(13), 1183-1185. https://dx.doi.org/10.1056/nejmp1409859 Mbonye, A., Wamala, J., Nanyunja, M., Opio, A., Makumbi, I., Aceng, J. (2014). Ebola Viral Hemorrhagic Disease Outbreak in West Africa- Lessons from Uganda.African Health Sciences,14(3), 495. https://dx.doi.org/10.4314/ahs.v14i3.1 Ledgerwood, J., DeZure, A., Stanley, D., Coates, E., Novik, L., Enama, M. et al. (2017). Chimpanzee Adenovirus Vector Ebola Vaccine.New England Journal Of Medicine,376(10), 928-938. https://dx.doi.org/10.1056/nejmoa1410863 Shoman, H., Karafillakis, E., Rawaf, S. (2017). The link between the West African Ebola outbreak and health systems in Guinea, Liberia and Sierra Leone: a systematic review.Globalization And Health,13(1). https://dx.doi.org/10.1186/s12992-016-0224-2 Hoenen, T., Marzi, A., Scott, D., Feldmann, F., Callison, J., Safronetz, D. et al. (2015). Soluble Glycoprotein Is Not Required for Ebola Virus Virulence in Guinea Pigs.Journal Of Infectious Diseases,212(suppl 2), S242-S246. https://dx.doi.org/10.1093/infdis/jiv111 Lukashevich, I., Shirwan, H. (2014).Novel Technologies for Vaccine Development(1st ed.). Vienna: Springer Vienna. Nelson, K. (2014).Infectious disease epidemiology(3rd ed.). Burlington, Mass: Jones Bartlett. Rezza, G., Ippolito, G. (2017).Emerging and re-emerging viral infections(6th ed.). Cham, Switzerland: Springer. Weston, D., Burgess, A., Roberts, S. (2016).Infection prevention and control at a glance (1st ed.). John Wiley Sons. Sanford, C., West, T., Jacob, S. (2017). Ebola Virus Disease and Hemorrhagic Fevers.The Travel And Tropical Medicine Manual, 391-400. https://dx.doi.org/10.1016/b978-0-323-37506-1.00028-3 Greenwood, D., Barer, M. (2012).Medical microbiology(18th ed.). Edinburgh: Churchill Livingstone. Singh, S., Ruzek, D. (2013).Viral Hemorrhagic Fevers(1st ed.). London: CRC Press. Ealy, G. (2016).Ebola(1st ed.). SUDBURY: JONES BARTLETT LEARNING. Vidal, Y. (2017).How to Prevent the Spread of Ebola: Effective Strategies to Reduce Hospital Acquired Infections(1st ed.). Lara Publications Inc. Park, S., Lee, Y., Lee, W., Jee, Y., Choi, W. (2016). One-Step Reverse Transcription-Polymerase Chain Reaction for Ebola and Marburg Viruses.Osong Public Health And Research Perspectives,7(3), 205-209. https://dx.doi.org/10.1016/j.phrp.2016.04.004 Burd, E. (2014). Ebola Virus: a Clear and Present Danger.Journal Of Clinical Microbiology,53(1), 4-8. https://dx.doi.org/10.1128/jcm.03115-14 Zhang, Y., Gong, Y., Wang, C., Liu, W., Wang, Z., Xia, Z. et al. (2017). Rapid deployment of a mobile biosafety level-3 laboratory in Sierra Leone during the 2014 Ebola virus epidemic.PLOS Neglected Tropical Diseases,11(5), e0005622. https://dx.doi.org/10.1371/journal.pntd.0005622 Martnez, M., Salim, A., Hurtado, J., Kilgore, P. (2015). Ebola Virus Infection: Overview and Update on Prevention and Treatment.Infectious Diseases And Therapy,4(4), 365-390. https://dx.doi.org/10.1007/s40121-015-0079-5 Dye, J., Herbert, A., Kuehne, A., Barth, J., Muhammad, M., Zak, S. et al. (2012). Postexposure antibody prophylaxis protects nonhuman primates from filovirus disease.Proceedings Of The National Academy Of Sciences,109(13), 5034-5039. https://dx.doi.org/10.1073/pnas.1200409109 Gebre, Y., Gebre, T., Peters, A. (2014). The Ebola virus: a review of progress and development in research.Asian Pacific Journal Of Tropical Biomedicine,4(12), 928-936. https://dx.doi.org/10.12980/apjtb.4.201414b419 Wu, X., Yao, H., Wu, N., Gao, H., Wu, H., Jin, C. et al. (2015). Ebolavirus Vaccines: Progress in the Fight Against Ebola Virus Disease.Cellular Physiology And Biochemistry,37(5), 1641-1658. https://dx.doi.org/10.1159/000438531 de La Vega, M., Wong, G., Kobinger, G., Qiu, X. (2015). The Multiple Roles of sGP in Ebola Pathogenesis.Viral Immunology,28(1), 3-9. https://dx.doi.org/10.1089/vim.2014.0068

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