Ebola Hemorrhagic Fever - Research Paper Example

Ebola Hemorrhagic Fever Ebola Hemorrhagic Fever Ebola virus belongs to the family of enveloped viruses, Filoviridae. Filoviridae family contains single genus Filovirus. Filovirus is divided into two more serotypes which are named as Marburg and the other one is Ebola. Ebola virus is further divided into four types which are Ivory Coast, Zaire, Sudan and Reston (Georgiev 2009). Ebola virus is the causative agent of the Ebola hemorrhagic fever which has been established as a very severe and sometimes deadly disease not only in humans but also in monkeys and chimpanzees. It is named after a river in Congo, Africa where this virus was first discovered as a causative agent for this infectious disease. Excluding the Reston subtype of Ebola virus, all other types cause infection in the humans (Reddy 2002). The virus was identified initially in the year 1967 in Marburg, Germany after the presence of this virus was seen in workers of a laboratory. This was owing to their continuous contact with monkeys in the laboratory (Carruthers et al 2005). Ebola viruses are structurally classified as complete viral particles which show pleomorphism in their shapes. It can be long, filamentous or in circular forms. The dimensions of the virus are length of 14,000 nm and diameter of 80nm, encompassed in a membrane composed of lipid molecules. Ebola is a single-stranded RNA virus and it multiplies through the process of asexual reproduction, budding. Ebola virus consists of seven structural and one non-structural protein. Nucleoprotein is the major structural protein and others include virion structural protein (VP) 30, VP 35 and large protein (L) (Georgiev 2009). Ebola virus’s natural habitat is still not completely known by the microbiologists but it has, however, been established that Ebola virus is an animal-borne or zoonotic virus. Therefore, it maintains its natural reservoirs in animal hosts (Reddy 2002). Ebola life cycle initiates with the entry of the virus into different types of cells through the viral surface glycoprotein which regulate the entry of the virus. Figure 1 provides an overview of the entry of the virus into the host cell. Certain receptors on the cell surfaces promote the entry of the virus and render them vulnerable to the attack of the virus. These receptors include folate receptor-a, proteins of C-type lectin family and L-SIGN receptors expressed on Jurkat cells, macrophages and endothelial cells respectively. Once, binding and fusion of the virus in the cells is complete, the viral genome is uncoated. However, little is known about this process. The RNA of the virus encodes eight different types of proteins out of which seven are structural and one is non-structural. After viral transcription and replication is completed, nucleocaspids are formed in the cytoplasm, which are then sent to the cell membrane. At the cell membrane assembly of the viral proteins occurs, there is an initiation of the process of budding (Halfmann 2008). The glycoprotein is considered as the primary pathogenic factor of the Ebola virus which promotes its infectivity and results in decrease in circulating T-cells and decreased immunity of the host (Georgiev 2009). Fig 1: A diagrammatic representation of the viral entry of the Ebola virus from entry into host cell to binding and fusion to the host receptors. At the end budding and multiplication of the virus has been shown. (Science Daily 2011). Transmission of the Ebola virus infection in humans is incidental as humans are not the natural reservoirs of this virus. The spread in humans is caused due to first contact with an infected animal. The first person to be infected in an outbreak is termed as an index case, which can spread the infection to other humans through several different ways. It can spread through direct contact with body secretions and blood of a person with Ebola virus. It can also be spread through contact with unsterilized equipment which has been previously contaminated with Ebola virus. Because of its transmission through body fluids, its spread is rapid among families and friends. Nosocomial transmission is another method of spread and is common in health-care centers (Reddy 2002). Spread through air-borne particles like cough droplets has not yet been established for the Ebola virus (Georgiev 2009). With invasion of the Ebola virus, the infection is basically caused by the immunosuppression and the rapid release of cytokines in the blood. The main types of cells involved in the pathogenesis of the hemorrhagic fever caused by Ebola virus, include the endothelial cells and the macrophages. These cells produce mediators like hydrogen peroxide and tumor necrosis factor which cause vascular dysfunction causing increased permeability. Endothelial damage is caused by the viral replication and the coagulation pathways are also interrupted by the pro-inflammatory cytokines resulting in massive bleeding. Visceral organs are also affected and undergo necrosis which is mainly caused by the damage to the parenchymal cells caused by the destructive viral replication. Liver, renal system, blood vessels and the coagulation pathways are remarkably affected by the Ebola virus leading to the clinical manifestations in the host (Georgiev 2009). The clinical manifestations of hemorrhagic fever caused by Ebola virus differ in various people. Within a few days of infection from Ebola virus, the onset of disease is sudden with high-grade fever, abdominal cramps, myalgias, fatigue, diarrhea and headache. In few patients symptoms of hiccups, sore throat, itchy eyes, blood in vomit and bloody diarrhea have also been reported (Reddy 2002). The patient appears dehydrated and lethargic. Moreover, there is a characteristic non-pruritic, maculopapular rash that is centripetal in its origin and fades off after a week of the infection has passed. Bleeding signs and symptoms are characteristic and define the prognosis of the disease. Gastrointestinal bleeding, petechia in mucous membranes and puncture wounds are also common (Georgiev 2009). The incubation period of the disease is from 2 to 21 days approximately (Carruthers et al 2005). Long term symptoms of the infection which manifest after a week of the virus infestation include chest pain, shock and can end in death of the patient. In fewer patients it can also cause blindness (Reddy 2002). Women who are pregnant at the time of infection are at an extremely increased risk of abortions and children born to infected mothers also show a comparatively greater death rate. The recovery period of this disease is quite long and it may take several weeks before the patients fully recover. The patients may develop uveitis, psychosis, hepatitis and myelitis during the convalescence period. Death from this disease is mostly caused by hemorrhagic and hypovolemic shock within a period of 6 to 16 days of prevailing circumstances. It has been indicated that the disease causes death in 30 percent of the infected individuals (Carruthers et al 2005; Georgiev 2009). Laboratory data gives helpful information in diagnosing this disease. Leucopenia, atypical lymphocytes, thrombocytopenia and raised levels of serum transaminase levels are the positive findings in hemorrhagic fever. Raised levels of protein in the blood as well as increased levels of protein in the urine are also significant (Georgiev 2009). ELISA tests, IgG ELISA and PCR are some of the tests which help in detecting Ebola and diagnosing the hemorrhagic fever. Virus isolation and immunohistochemistry are other two methods of diagnosing the disease in the laboratory. Microscopic evaluation is also used in the laboratories (Reddy 2002). Fig. 2 depicts the picture of the virus as seen through an electron microscope. Fig 2: A colored image of Ebola virus colony taken from electron micrograph showing its long filamentous colonial structure (Dell’Amore 2011). Any specific treatment against Ebola virus has not yet been established. However, supportive treatment should be provided to compensate the blood loss and electrolyte disturbances. Clinical manifestations like shock, renal failure, coagulation disturbances and cerebral edema should be managed immediately to protect the patient. The Ebola virus is resistant against the anti-viral drugs because of its ability to resist the interferon. Hence, anti-viral therapy is of not much value in the hemorrhagic fever. Heparin administration should be carried out when disseminated intravascular coagulation (DIC) has been confirmed in the patient (Georgiev 2009). Maintenance of oxygen support and blood pressure is also crucial (Reddy 2002). Thus the main aim of treatment is to provide symptomatic relief to the patient as no effective therapy against the virus has been established as yet. Prevention of the disease is crucial when an outbreak is evident or feared. Complete isolation of the patient is always recommended to avoid further spread of the infection. Quick diagnosis and detection of the disease is also necessary to avoid contamination and spread of the infection (Carruthers et al 2005). Certain hemorrhagic fever isolation precautions have to be employed in order to prevent this disease. These include wearing protective masks, gloves, goggles and gowns. The equipment should be clean and sterilized. Contaminated syringes should be disposed immediately to prevent the spread of Ebola virus. The body of a deceased person, who died of Ebola infection, should also be kept in isolation from others, as it can also transmit the infection (Reddy 2002). Hand washing is also strongly recommended for prevention of not only Ebola virus but for any kind of infection before eating any meal or drinks. Alcohol-based hand washes or soaps should be used for this purpose as these prevent contamination. With proper and regular hand washing and respiratory masks and protective clothing, contamination of surrounding materials and people can be effectively controlled (Carruthers et al 2005). Any licensed vaccine is not yet available for the prevention of the Ebola virus but several advancements have been made in the development of vaccines for hemorrhagic fever. Virus inactivated vaccines were experimented on guinea pigs but poor protection levels were observed. Other vaccines which are being researched are the DNA vaccines which showed a 78% protection result in mice; however, their safety levels are still controversial. Other vaccines include Virus-Like Particles (VLPs) and Live attenuated Ebola vaccines. Live-attenuated vaccines showed complete protection results after experiments and have a high potential as vaccines. However, their safety levels are quite low (Halfmann 2008). A vaccine strategy which has turned out to be quite effectual is the use of DNA vaccines along with adenoviral vectors. This preventive strategy was effectual as it produced viral proteins that enhanced the humoral immunity of the host (Georgiev 2009). Challenges faced by the health professionals and researchers in preventing this infection are owing to the lack of effective treatment modalities accompanied with the absence of proper vaccines to prevent the disease. Furthermore, the necessity of the application of proper precautionary measures to prevent the spread and transmission of this disease is another obstacle. With effectual researches and studies prevention and treatment advances can be made (Reddy 2002). References Top of Form Carruthers, K., Jackson, M., McKinnon, S., Gulli, B., Carruthers, K., & American Academy of Orthopaedic Surgeons. (2005). Preventing infectious diseases. Sudbury, Mass: Jones and Bartlett. Bottom of Form Dell’Amore, C. (August 22, 2011). “New Drug Cures Multiple Viruses in Human Cells”. National Geographic News.Retrieved from: http://news.nationalgeographic.com/news/2011/08/110822-drug-virus-common-cold-flu-science-health/ Top of Form Georgiev, V. S. (2009). National Institute of Allergy and Infectious Diseases, NIH: Volume 2. Totowa, N.J: Humana. Bottom of Form Halfmann.(2008). Novel Strategies to Combat Ebalovirus.The University of Wisconsin- Madison.ProQuest LLC. Reddy, L. R. (2002). Bio-terrorism. New Delhi: A.P.H. Pub. Corp. Science Daily. (2011, August 24). “Researchers find key used by Ebola virus to unlock cells and spread deadly infection”. ScienceDaily. Retrieved from: http://www.sciencedaily.com/releases/2011/08/110824131537.htm Read More