EBOLA VIRUS 5
Description of the Microorganism:
The Ebola virus, similar to the Marburg virus, belongs to theFiloviridae family. The virus is linear, non-segmented and negative –sense-stranded RNA akin to rhabdoviruses such as rabies. Its genomereplication and organization mechanisms resemble that ofparamyxoviruses existent in mumps and measles. Under a microscope,the virus appears as a long stretched thread and has a filamentousstructure. The filaments assume a curvy appearance similar to number6. Ebola virus is classified into five species that include Taiforest Ebola virus (TAFV), Bundibugyo Ebola virus (BDBV), RestonEbola virus (RESTV), Sudan Ebola virus (SUDV), and E-BOV (Goeijenbieret al., 2014). For observation under a microscope, the virus isstained by using Methylamine tungstate negative staining method(Golding et al., 2016).
The development of Ebola after infection entails a complex interplaybetween the virus, the environment, and the host. The EBOV contagionis the most fatal and has a casual fatality rate of 50- 80%. Itlowers the body’s immunity by affecting various cells such as themonocytes, dendritic cells, and macrophages. It also influences theendothelial and epithelial cells, hepatocytes, fibroblasts, adrenal,and gland tissues. The virus replicates in the concerned cells andresults in high peak viremia. It leads to the death of cells ornecrosis of the affected lymphocytes as well as reduces theproduction of the clotting factor associated with lymphocytes. Italso contributes to the formulation of symptoms such as failure ofthe immune system to respond to the illness and hemorrhage.
Although Ebola is an immunosuppressive disease, the human bodyresponds to the virus by activating both T and B cells. Variousstudies have indicated a higher concentration of plasma blastfrequencies of B cells within a range of 10 -50% compared to lessthan 1% associated with healthier individuals. The human bodyproduces positive IgG plasma blasts in response to Ebola viruses. Thesecond immunity emanates from the production of CD4 T cells, whichhave been found to have a concentration of 5-30% in patients comparedto 1-2 % in healthy individuals. Besides, the human body alsoproduces CD8 T cells as an immune response to the Ebola virus thatcontinues after the elimination of the virus from the blood plasma(McElroy et al., 2015).
Infectious Disease Information:
Severe attacks of the Ebola virus causes a hemorrhagic fever due tothe damage of the blood vessels. Consequently, it results inextensive internal and external bleeding. It also results inheadaches, weaknesses, muscle pain, diarrhea and vomiting (McElroy etal., 2015).
Mr. Morissey arrived at the hospital’s emergency waiting roomcomplaining of dizziness, abdominal pain, headache, and nausea. Thetriage nurse recorded a temperature of 100.1-Fahrenheit on thepatient. After admission, the patient’s illness progressed toexhibit deeply sunken eyes, dryness, and soreness of the throat. Onthe fifth day, the patient began bleeding from the mouth and gums andthe nose. The patient travel history indicated that he had traveledto the United States to get married to his fiancée. He was fromAfrica where he made contact with the virus. Additional specificindicators of the disease include neck stiffness, confusion, loss ofskin turgor oral fissuring and dry mucous membranes (Dunning et al.,2016).
Currently, there is no licensed vaccine for the disease. However,efforts to generate a cure by scientists have led to the developmentof adenovirus type 26 vector vaccine encoding Ebola glycoprotein(Ad26.ZEBOV). Besides, scientists have developed the modifiedvaccinia Ankara vector vaccine encoding glycol proteins(MVA-BN-Filo). The two developments indicate the ability to boosthumans’ immune response against the Sudan, Marburg and Tai forestsvirus (Milligan et al., 2016).
There is no specific treatment for the Ebola virus. However, effortsto create a cure have led to the development of a small RNAinterfering non-particle lipid (TM130803) to treat the Ebola virus.The safety and efficacy of the lipid remain uncertain on humans(Dunning et al., 2016).
The real prevalence of Multidrug resistance of Ebola virus remainsmysterious. However, scientists believe that the virus is associatedwith fecal colonization by multi-drug resistant enterobacteriacease(Plachoura et al., 2015).
Dunning, J. et al., (2016). Experimental treatment of Disease with TKM-130803: A Single-Arm Phase 2 Clinical Trial. Journalof PLOS Medicine, 1(1) 1-19. Retrieved fromhttp://journals.plos.org/plosmedicine/article/asset?id=10.1371%2Fjournal.pmed.1001997.PDF
Goeijenbier, M., Kampen, J., Reusken, C., Koopmans, M. & Gorp V.(2014). Ebola virus disease: A review on epidemiology, symptoms,treatment and pathogenesis. The Netherlands Journal of Medicine,72(9) 442-448. Retrieved fromhttp://ead.sjteducacaomedica.com.br/pluginfile.php/894/mod_resource/content/2/Ebola%20virus-%20Review.pdf
Golding, C., Lamboo, L., Beniac, D. & Booth, T. (2016). Thescanning electron microscope in microbiology and diagnosis ofinfectious disease. Scientific Reports. Retrieved on 04September 2016 from http://www.nature.com/articles/srep26516
McElroy, A., Akondy, R., Davis, C., Ellebedy, A.,Mehtae, A.,Kraft, C., Lyon, M., Ribner, B., Varkey, Jay, Sidney, J., Sette, A.,Campbell, S., Ströher, U., Damon, I., Nicho, S., Spiropoulou, C. &Ahmed, R. (2015). Human Ebola virus infection results in substantialimmune activation. PNAS, 112(15) 4719–4724. Retrieved fromhttp://www.pnas.org/content/112/15/4719.full.pdf
Milligan et al., (2016). Safety and immunogenicity of noveladenovirus type 26– and modified vaccinia Ankara–Vectored Ebolavaccines. The Journal of American Medical Association, 315(15), 1610-1623. doi:10.1001/jama.2016.4218.
Plachoura, D., Monnet, D., & Catchpol, M. (2015). Severe Ebolavirus infection complicated by gram-negative septicemia. The NewEngland Journal Of Medicine, 372, 1376-1377. Retrieved fromhttp://www.nejm.org/doi/full/10.1056/NEJMc1500455#t=article