Ebola Virus Explained Essay

Ebola Virus Explained EssayIntroductionEbola computer virus is one of the most virulent and lethal pathogens known to human. Ebola virus epidemics have emerged from age to time since it was first discovered in 1976 from the Democratic Republic of Congo, formerly known as Zaire, save the largest known Ebola virus outbreak up to visit is ongoing at the time of writing this article, in West Africa. Approximately 550 000 cases are estimated to be reported from Sierra Leone and Liberia by the 20th of January 2015. The transmission of the contagious complaint to a number of countries including Guinea, Liberia, Sierra Leone, Nigeria and occasional cases being reported from USA, Canada, Netherland and India reveal the potential of the infection to get disseminate worldwide. Despite this illness being extremely contagious, career-threatening, and no specific treatment being found, it can be prevented with the use of proper infection legal community and control measures. The study of the Ebola virus disease is primary(prenominal) as that knowledge will pave the way for the reduction of victims, the invention of an effective drug and will also be useful in the heed of a sympathetic epidemic.VirologyEbola virus is a member of the family Filoviridae. As the name implies the virus is filamentous in shape. Marburg virus and Ebolavirus are the two main genera of the viral family which are medic ally important. Viruses of these two genera are studied and breaked together due to their m all similarities in the life cycle, the primary reservoirs, ways of transmission, clinical presentation, treatment and prevention measures. The alone noned difference is that the Marburgvirus is spread by bat species adequate to open forests such as savannah whereas Ebolavirus is spread by bat species adapted to deep rain forests(1).Five subtypes of Ebolavirus namely, Ebolavirus zaire, Ebolavirus sudan, Ebolavirus reston, Ebolavirus cote d Ivore, and Ebolavirus bundibugyo have been identified and named after the area in which they were first discovered(1). Of these E. Zaire was the first to be unaffectionate and studied(1) and it is answerable for the most number of outbreaks(1) including the latest outbreak in 2014 before which E. sudan accounted for of all Ebolavirus deaths(1). Except for the slight lower fatality rate, E. sudan is more or less similar to E. zaire. The case fatality rate of E. sudan is reported as 40-60% and that of E. zaire as 60-90% (3).TransmissionEbola is initially transmitted to human as a zoonosis. Various species of result bats found throughout central and sub Saharan Africa as hosts (2),( 4). Contact with bats through bites and scratches or exposure to their secretions and excretions through broken skin or mucous membranes can cause the infection in humans (2), (4). The infection can also be transmitted through other block up hosts. Those recorded from Africa are forest antelopes, porcupines, chimpanzees, gorillas, monkey s and other non-human primates. Attacks during hunting these animals or handling infected animal carcasses have resulted in the introduction of the virus to the human community from the wild (1).The outbreak of the epidemic begins with the subsequent transmission of the infection from the index case to secondary individuals. An outbreak often begins from a single introduction to a human from the wild, which involves virus variants of little genetic diversity. Records reveal that outbreaks stemmed from multiple introductions lead to distinct chains of human to human transmission with a greater diversity in the virus variants(5).EVD is highly contagious. The infection may spread in the community and in the hospital environment through direct speck with infected body unruffleds such as line of business, secretions and excretions or tissue of an acute patient or through direct contact with contaminated materials same(p) apparel and bed linen(1). One major reason for the rapid spre ad of the epidemic is the traditional funeral rituals, which include cleansing of the cadaver, removal of hair finger nails, toe nails and clothing. populate taking do of infected people including health care staff also have a high risk of contracting the disease. Moreover seminal fluid of male survivors is said to remain infectious for up to 82 twenty-four hour periods after the on found of the symptoms. As presbyopic as the virus remains in the body fluids the person remains infectious. Airborne transmission of Ebola virus is strongly suspected that is not yet experimentally proven.Clinical PresentationEVD caused by different strains of Ebola virus bring about different clinical features. Incubation period of Ebola virus is generally considered as 2 21 days. (1, 3) Ebola virus disease shows various acutely developing constitutional prodromal symptoms which lead to a wide range of differential diagnosis including not only other viral haemorrhagic fevers, but also malaria (3) , typhoid (3), cholera (1), other bacterial rickettsial and even non-infectious causes of haemorrhage.The evolution of the disease resembles that of a strong haemorrhagic fever. Patients present with high fever, temperatures being as high as 39-400C (3, 6), body aches and fatigue (3).Subsequently gastrointestinal symptoms such as epigastric pain nausea, vomits and /or diarrhoea without blood appear if fever persists until day 3 5 (6).After 4 5 days of illness (4) a macular rash may appear but it may not be clearly noticeable on dark skin (1). After this stage haemorrhage from different sites begin. Bleeding from both fastness and lower digestive tract, respiratory tract, urinary tract, vagina in females can be observed (1, 3). Further petechiae on the buccal mucosa, skin and conjunctivae develop. Recurrent episodes of vomiting which prevents any oral intake of fluids and large amounts of watery diarrhoea (5 or more liters per day) (6) contributes to a massive fluid loss leading to dehydration. If fluid re situatement is inadequate, prostration, severe lethargy and ultimately hypovolaemic shock follows.Hypovolaemic shock has been reported in 60% of the cases (6). Despite the high body temperatures, patients acquire cold extremities due to peripheral vasoconstriction. Rapid and thready pulses, tachypnea, oliguria or anuria can be observed (6). Simultaneously features such as asthenia chest and abdominal pains, pains in muscles and joints and headaches develop. Although in some cases cough and dyspnea occur due to pulmonary haemorrhages, other respiratory symptoms except for hiccups are uncommon (6). Conjunctival injection is a common clinical feature. Neurologic symptoms that are usually seen are hypoactive and hyperactive delirium characterized by slowed cognitive functions, confusion, agitation and rarely seizures (6). As the disease evolves internal bleeding can also start but generally by this time patients are already in a state of un understanding (1) .It is reported that only 5% of the patients present with haemorrhage from gastro intestinal tract before death. Most of the reported deaths have occurred due to shock during the 7th to twelfth day of illness. Symptoms of 40% of the patients have improved around the 10th day though symptoms worry oral ulcers and thrush have developed. Most of the patients who survived up to the 13th day have shown a higher chance of ultimately getting recovered. Some patients who showed initial improvement of symptoms have developed neck rigidity and lowered levels of consciousness which are associated with late mortality.PathologyExamination of autopsies and post-mortem biopsies is extremely useful in the study of the pathology of the ebola virus disease. Due to the biosafety risk to the autopsy personnel when handling specimens, pathological descriptions of only a limited number of cases are available (7).A common finding of Haematoxilin and eosine stained tissue sections is oval shaped or filame ntous eosinophilic intra boothular inclusions which are formed by the aggregation of nucleocapsids of the virus. These inclusions can be detected in macrophages, hepatocytes, endothelial cells, connective tissue fibroblasts etc. Immunohistochemical stains reveal viral antigens in cells of various infected tissues including macrophages, dendritic cells, epithelial cells of sweat and sebaceous glands, interstitial and tubular cells of the kidney, seminiferous tubules, endothelial cells and endocardial cells. In addition necrotic cells and cell debris contain antigens in large quantities. Electron microscopy exhibits abundant free virus particles in alveolar spaces, liver sinusoids, and interstitial cells of the testis and in epidermic collagen. Karyorrhexis and apoptosis are seen in the cells of the portal triads, macrophages of the red pulp of the spleen and in the tubular epithelial cells of the kidney (7).Liver tissue shows the most symptomatic histopathological features including central or widespread necrosis of hepatocytes and mild steatosis. Although usually inflammation is minimal, hyperplasia of kupfer cells and infiltration of mononuclear inflammatory cells is seen. Infected lung shows congestion, haemorrhage and intra-alveolar oedema but inflammation is not significant. Mild central infiltrates of mononuclear inflammatory cells are known to occur in the lamina propria of the stomach small intestine and the colon. Skin biopsies reveal dermal oedema, focal haemorrhages, petechiae, ecchymoses, and macular rashes. The spleen and lymph nodes exhibit widespread lymphoid depletion due to apoptosis and necrosis. Inflammation of the kidney is not evident although acute tubular necrosis is a usual finding. even though the endocardium of the heart contains viral antigens, the myocardium does not show any significant damage. Brain histology shows panencephalitis and perivascular infiltration of lymphocytes (7).PreventionWorld Health organization (WHO) has reco mmended a set of infection prevention and control measures for health-care workers that include precautions that should be taken at different stages of managing EVD patientsStandard precautionsRegardless of the diagnosis it is recommended for health-care workers to take standard precautions when handling all patients, as it is difficult to identify EVD patients during early stages of the disease. These are,Performing hand hygienicsUsing disposable gloves before touching materials probable of being contaminated with virusWearing eye protection and gown before involving in procedures which have a possibility of body fluids being projected.Hand hygieneHand hygiene must be performed using soap and water or alcohol-based hand rub solution, following WHO recommended technique,before wearing gloves and personal protective equipment (PPE)after an exposure to a patients body fluidsafter a contact with a contaminated surface or equipmentafter removing PPE.if hands are visibly soiledPersonal P rotective Equipment (PPE)PPE should be worn before entering EVD patients care areas according to the recommended order by WHO and removed before leaving the care area. Contact of a used PPE with any part of the face or non-intact skin should be avoided. The PPE includes,Non-sterile gloves of the correct sizeImpermeable and disposable gown with long sleevesFace shieldPuncture skanky and impermeable closed shoesPatient placement and managementSuspected or affirm EVD patients should be isolated and if possible kept in single rooms. If not they must be placed in beds with at least(prenominal) 1m gap in between. Visitors must be restricted except for those who are needed for the well-being of the patient such as a childs parent.Management of used equipment and other materialsIt is recommended that equipment like stethoscopes should be decontaminated and sterilized before reuse, if separate equipment is not available. Parenteral medication equipment, surgical blades, syringes and needl es should never be reused. They should be disposed in puncture resistant bins. All non-sharp solid waste should be disposed in to leak-proof bags or bins.Used linen should be collected in leak-proof bags kept at the place of use. They should be washed with water and detergent, rinsed, soaked in 0.05% chlorine for 30 minutes and then dried.All bins must always remain upright and should be sealed when full moon. Before being taken out of the wards the outer surfaces of these containers must be disinfected using 0.5% chlorine.Environmental cleaningCleaners should wear heavy-duty golosh gloves, and impermeable, puncture proof boots in addition to the PPE. Water and detergent must be used to clean the work surfaces and floors of the hospital. This should be practiced at least once a day. other contaminated surfaces and objects must be cleaned and disinfected using 0.5% chlorine.Handling of biological materialPerforming autopsies, post-mortem biopsies and other laboratory tests of tis sue samples of EVD confirmed or suspected patients should be minimized and should only be performed by trained personnel. Full PPE must be worn during handling specimens. All specimens should be delivered in clearly labeled, leak-proof, non-breakable, containers with disinfected outer surfaces.Dead bodies must never be washed or embalmed. They should be sealed in double bags, disinfected with 0.5% chlorine and inhumed promptly. Some cultural and religious rituals can be adapted if needed, but handling of the body must be kept to a minimum and full PPE must be worn at all times.In case of exposure to infected body fluidsAll current tasks must be safely and immediately stopped and PPE must be removed safely. Affected skin should be washed with soap and water and any affected mucous membranes like conjunctiva should be washed off with a plenty of running water. The person should be checked for fever and other symptoms for 21 days.PathogenesisPathogenesis of Ebola virus shows a propor tion to that of most of the other filoviruses which involves immunosuppression, increased vascular permeability and coagulopathy (7, 18). Ebola virus enters the host though abrasions of the skin, though mucous membranes or though injection by accident. The virus enters monocytes, macrophages and dendritic cells and gets carried away via lymphatics to the circulation. It then spreads to the liver and spleen infecting tissue macrophages and fibroblastic reticular cells. The main cellular targets of the virus are macrophages, dendritic cells and kupfer cells. Ebola virus shows interaction between varieties of cellular proteins which is why the infection is characterized by broad tissue and organ tropism.ImmunopathologyIn most of the viral infections immune system plays a major graphic symbol in containing the infection from spreading. However the tissues and organs of fatal EVD cases show minimal inflammation, suggesting of impairment in the immune responses.It has been found that str uctural proteins of filoviruses e.g. VP24 (Virion protein) and VP35 inhibit interferon responses and thus outwit the host innate immunity. As previously mentioned, apoptosis of natural killer cells and T lymphocytes is revealed in histopathology which explains the suppression of the adaptive immune responses.As in many severe infections, Ebola virus infection also causes a massive release of pro-inflammatory mediators and vasoactive substances. Even though the pro-inflammatory mediators promote inflammation and coagulation, the systemic spread of the infection is not effectively controlled. This is probably due to the vasodilation mediated by the vasoactive substances.Endothelial dysfunction and coagulopathyThe virus invades endothelial cells and endocardial cells and causes injury (18). This results in internal haemorrhage, fluid and electrolyte imbalance and cardiovascular failure. Endothelial damage results in the platelet aggregation and consumption. The increased level of pro- inflammatory factors and the increased production of surface tissue factor protein in infected monocytes and macrophages promote the coagulation cascade. Due to the hepatocellular damage the production of coagulation factors, fibrinogen, protein C and S are also decreased .Collectively this results in disseminated intravascular coagulation.Other socio-economic problems related to Ebola virus epidemicsWhen considering the current outbreak, in addition to the huge number of lives that has been succumbed to the disease, it has created many other critical problems not only in Ebola hit countries, but in other African countries as well.Agriculture has the biggest contribution to the African economy. As many farmers have died of the epidemic and many have abandoned their farmlands in the fear of catching the disease, there is a huge labour shortage in these countries and a fall of food production. An emergence of a food scarceness in the near future is predicted by experts.Chocolate pro ducing companies and many other industries are greatly affected by labour shortage. Nigeria and Ivory Coast are major chocolate tree producing countries but most of the workers are migrants from Liberia and Guinea. International companies like Nestle and Mars have launched education and fundraising programmes to prevent the spread of the infection among cacao workers.Many schools have been closed owing to the deadly infection surging through the country. Besides the impact on education, the feeding programme carried on by the governments for children has come to a standstill as a consequence.Tourism is another sector hit by the epidemic. Even though Africa is a large clean bigger than Europe, USA and China combined tourists tend to see it as a single country since the Ebola epidemic has emerged. For instance, Tanzania, a famous wild life destination is an East African country, more than 6000 miles away from an Ebola hit land. It is reported that hotels of Tanzania have lost 50% of bookings for 2015 (21).Many African countries refuse to host internationalistic events and conferences due to the risk of the Ebola epidemic being introduced. For example, Morocco, the host of African Cup of Nations, which is scheduled to January 2015, requests a postponement. The government says, There is no way we can be lenient with the health and safety of the Moroccan citizens (24).