Ebola

Jul 3, 2017 | 0 comments

Jul 3, 2017 | Miscellaneous | 0 comments

Ebola Virus: Human Immunity

  1. Describe how the Ebola virus infects a human

The Ebola virus is very infectious. According to Quammen (2014), if one Ebola particle enters the bloodstream of a person it may be fatal. The most common entry route is believed to be the inner surface wet membrane of the eyelid, which a person with a contaminated fingertip may touch. However, the Ebola virus, in particular, is believed to be transmitted through contact with blood and sweat, which contain high Ebola particles concentration (Quammen 2014).

Once the particles of Ebola enters the bloodstream of a person, it drifts and sticks to a cell of the host. The particle gets pulled inside the cell taking control of the machinery of the cell and causing the cell to begin making copies of the virus. Hart (2004) pointed out that many cold viruses replicate in the throat and the sinuses. Ebola virus attacks many body tissues at once, except the bones and the skeletal muscles. It has an affinity that is special to the cells that line the psychological effects. For example, blood vessels, especially in the liver. Hart (2004) stated that after eighteen hours, the cells that are infected release thousands of new particles of Ebola, which sprout in threads from the cell until the cell appears like a tangled yarn ball. The Ebola particles detach and are transported in the bloodstream, and start attaching everywhere in the body to more cells. The cells that are infected begin spewing out a large number of Ebola particles, hence infecting more cells until the virus reaches amplification crescendo. The infected cells die leading to tissue destruction throughout the body. Many organs fail, and the patient goes into a steep, sudden decline ending in death.

Similarly, once inside the body, the Ebola virus attacks monocytes and macrophages, and relies on host antibodies and complementing component 1 to infect efficiently(Takada et al 2003).In response, the white management of the patients who are hospitalized. The infections linked to the intravenous therapy may affect the blood cells release proinflammatory cytokines in large amounts that increase vascular endothelium permeability, hence facilitating the easier entry of the Ebola virus to the endothelial cells, the secondary targets(Takada et al 2003). Moreover, the cytokines also released recruit more macrophages to the area, and this maximizes the cell number that Ebola uses in spreading in the body entirely(Geisbert et al 2003).

2. Complete the test on the lymphatic system and tissue tolerance


(a) The test on the lymphatic system

In testing the lymphatic system, the doctor will perform the following tests: MRI or CT scan, lymphoscintigraphy, and Lymphangiography (Wordinger et al 2012).
MRI scan– this uses radio waves and magnetic field and produces 3-D images of high resolution
Computed tomography (CT) scan– this is an x-ray technique that produces cross-sectional detailed images of the structures of the body. CT scan can show the lymphatic system blockages
Doppler Ultrasound-this conventional ultrasound variation looks at pressure and blood flow by bouncing sound waves (ultrasound) of the high frequency of the red blood cells. Doppler ultrasound helps find obstructions.
Lymphoscintigraphy– during the process of testing, the patient is injected with radioactive dye and scanned by a machine. The images will show the moving dye through the lymph vessels, and highlight the blockages (Wordinger et al 2012).
Lymphangiography– the Lymphangiogram is a special lymph node and lymph vessels x-ray. Lymph nodes produce lymphocytes that help in fighting infections, and filter and trap the cells of cancer. Wordinger et al (2012) indicated that lymph vessels and nodes cannot be seen on a normal x-ray. Therefore a radioisotope or dye is injected into the patient’s body to highlight areas under study.

(b) The test of tissue tolerance

Tissue tolerance is the skin and supporting structure able to withstand the unrelieved pressure effects (Leading Age n.d). Before the start of the test on tissue tolerance, observe and record any area or breakdown or redness

Phase I

The resident is positioned in bed or chair (note position on back or side) for an interval of one hour.

  • After an interval of 1-hour, the resident is repositioned off the exposed area to pressure and observe and document any redness areas
  • After 30-45 minutes, the area is rechecked
  • Is there persistent redness or did the redness resolve?
  • The test is STOPPED if the redness has persisted. This area is considered to be stage The resident repositions at an interval that is shorter than one hour
  • Continue to phase II if there is no persistent redness (Leading Age n.d).

Phase II

The resident is positioned in bed or chair for an interval of 1 ½ hour on the same location used in Phase I

  • After an interval of 1 ½ hour, the resident is repositioned off the exposed area to pressure, and any areas of redness are then observed and documented
  • The steps are repeated as outlined above
  • The test is STOPPED if the redness persists, and the area is considered to be stage The resident need to be repositioned at an interval of less than every one hour
  • Continue to phase II if there is no persistent redness (Leading Age n.d).

Phase III

The resident is positioned in bed or chair for an interval of 2 hours on the same location used in phase I and II

  • After an interval of 2 hours, the resident is repositioned off the exposed area to pressure, and any areas of redness are then observed and documented
  • The steps are repeated as outlined above
  • The test is STOPPED if the redness persists, and the area is considered to be stage The resident needs to be repositioned at an interval of less than every 1 1/2 hour.
  • If there exists no persistent redness, the resident needs repositioning at an interval of 2
  • Test over (Leading Age n.d).
  1. Explain the sequence of events that leads to acquired immunity from infection.

Acquired immunity is an obtained immunity either from the antibody’s development in response to antigen exposure, as from an attack of an infectious disease or vaccination, or antibodies transmission, as from the mother to the unborn fetus through place or antiserum injection. According to Parham (2005), there are two mechanisms of getting acquired immunity; passive and active. Inactive immunity, protection is produced by the immune system of a person and is usually permanent. On the other hand, in passive immunity, protection is gotten by produced products by humans or animals, and transferred to another person, by injection. It provides protection that is effective and wanes with time. Parham (2005) stated that passive immunity is antibody transfer from one human to another, for example from the mother to an infant through the placenta. However, Stewart (2004) elaborated that active immunity is an immune system stimulation to produce an antigen humoral that is specific or an antibody. One of the ways of acquiring active immunity is by having natural diseases. In summary, when an individual recover from an infectious disease, for the rest of their lives, they will be immune to the disease.

Parham (2005) pointed out that another way of producing active immunity to the human body is by vaccination. Vaccines administered into the body interact with the human immune system producing a similar immune response to that produced by natural infection. However, it does not subject the recipient of the vaccine to the disease and the potential complications.

4. Produce a report on three commonly used vaccines

ACTIVE IMMUNITY

(1) Gardasil (Vaccine)

Safety of the vaccine

  • The vaccine has no live virus hence cannot cause HPV infection or any related disease
  • Not recommended for children aged below 9years
  • Not usable to people who are allergic to any of its ingredients
  • Should not be administered to pregnant women

The feverish illness affects the effectiveness of the vaccine

Herd community

Several studies have shown HPV infection reductions and related diseases in populations that are unvaccinated (Tabrizi et al 2012; Ali et al 2013; Kahn et al 2012). this implies that preventing infections of HPV in individuals that are vaccinated the likelihood of exposing the unvaccinated individuals. For instance, in Australia, the HPV vaccination program primarily focused on females. The results indicated a decline in genital warts incidence more than 80% among the heterosexual men between 2007-2011 aged under 21 years but did not change among the gay men (Ali et al 2013).

Evaluation of vaccine efficacy

Gardasil vaccine is effective because it protects humans against four HPV strains (HPV11, HPV6, HPV18, and HPV16).this implies that it protects humans also from genital warts and cervical cancer. In 2011 in the UK, the health department switched to the Gardasil vaccine since it was a safer option than condoms. In the UK, there are about 100,000 new genital warts cases per year.

The safety of the vaccine is also seen in the United States, studies show that in 2013, over 56 million HPV American medicine led to the discovery that a healthy person can also carry the disease. Besides, it led to the discovery of antibiotics and vaccines had been administered (CDC 2013).
(2) Rotavirus vaccine
Safety of the vaccine (Rotarix® (RV1) and RotaTeq® (RV5))

Evidence shows that its safe since Rotarix has been used extensively in many countries like Canada, Austria, Finland, Belgium, and all African countries, and no safety concerns have been reported (NHS n.d).moreover, before its approval, it was tested on more than 70,000 children and it proved to be safe
There are no available factors that affect the effectiveness of the vaccine
Herd community

Before its introduction, the most common cause of diarrhea in young children and infants was rotavirus with over 400,000 deaths and 100 million cases globally every year. However, after the introduction of the Rotarix, the epidemiology us changing rapidly since the 2000s (Seybolt & Bégué 2012).

Factors affecting vaccine effectiveness

  • Allergic children to the earlier dose of the vaccine
  • Severe or moderate illness at the time of vaccination (WebMD n.d).

Evaluation of vaccine efficacy

The vaccine is very effective giving good immunity to the babies against rotavirus infection. Since its introduction in 2013, the virus incidences have reduced by 69%. WebMD. (n.d) also indicated that the rotavirus vaccine can prevent about 74% of infections of rotavirus. More significant is that it can prevent about 96% of hospitalizations and 98% of severe infections
PASSIVE IMMUNITY
(3)Antitetanus vaccine (DTaP, Tdap, DT, and Td)
Safety of the vaccine

Just like any other vaccine, there can be a slight reaction with the tetanus vaccine which includes redness during the injection, pain, fatigue, headache, and slight discomfort.

Herd community

The reported mortality rate in the United States due to tetanus has constantly declined since the 1900s. Moreover, documented incidences of tetanus have declined in the  United States since the  1940s. From the  2009 national surveillance e system, a total of 2 deaths and 19 tetanus cases were reported. The factors that have contributed to the tetanus mortality and morbidity decline since the  1940s in the  United States include the widespread use of the tetanus toxoid-containing vaccine.

Factors affecting vaccine effectiveness
There are no available factors that affect the effectiveness of the vaccine

Evaluation of vaccine efficacy

Ant tetanus vaccine is effective 98% when administered in 2-3 doses to prevent neonatal tetanus deaths and neonatal tetanus in under-resourced settings (Demicheli et al 2005). Single doses of the vaccine are not adequate in preventing neonatal tetanus deaths. 

References

Ali H, Donovan B, Wand H, Read Tr, Regan Dg, Grulich Ae, Fairley Ck, & Guy Rj. (2013). Genital warts in young Australians five years into national human papillomavirus vaccination program: national surveillance data. BMJ (Clinical Research Ed.). 346. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/23599298

Centers For Disease Control And Prevention (Cdc). (2013). Human papillomavirus vaccination coverage among adolescent girls, 2007-2012, and postlic ensure vaccine safety monitoring, 2006-2013 – United States. MMWR. Morbidity and Mortality Weekly Report. 62, 591-5. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/23884346

Demicheli V, Barale A, & Rivetti A. (2005). Vaccines for women to prevent neonatal tetanus. The Cochrane Database of Systematic Reviews.

Geisbert, T. W., Hensley, L. E., Larsen, T., Young, H. A., & Reed, D. S. (2003). Pathogenesis of Ebola Hemorrhagic Fever in Cynomolgus Macaques. Ft. Belvoir, Defense Technical Information Center.

Hart, C. A. (2004). Microterrors: the complete guide to bacterial, viral, and fungal infections that threaten our health. Buffalo, N.Y., Firefly Books.

Kahn Ja, Brown Dr, Ding L, Widdice Le, Shew Ml, Glynn S, & Bernstein Di. (2012). Vaccine-type human papillomavirus and evidence of herd protection after vaccine introduction. Pediatrics. 130, 249-56. Retrieved from http://deainfo.nci.nih.gov/advisory/pcp/annualReports/HPV/Part1Sect3.htm#sthash.h3tspVmV.dpuf

Leading Age. (n.d). Resident-Specific Turning & Positioning Schedules An F314 Essential. (n.d.).

NHS (n.d).Rotavirus vaccine. Retrieved February 13, 2015, from http://www.nhs.uk/conditions/vaccinations/pages/rotavirus-vaccine.aspx

Parham, P. (2005). The immune system. New York: Garland Science.

Quammen, D., & Quammen, D. (2014). Ebola: The natural and human history of a deadly virus.

Seybolt LM, Bégué RE. (2012). Rotavirus vaccination and herd immunity: an affected by mental or physical health disability. However, research evidence-based review. Dove Press.

Stewart, G. J. (2004). The immune system. Philadelphia: Chelsea House Publishers.

Tabrizi, S. N., Brotherton, J. M., Kaldor, J. M., Skinner, S. R., Cummins, E., Liu, B., Bateson, D., … Garland, S. M. (January 01, 2012). Fall in human papillomavirus prevalence following a national vaccination program. The Journal of emergency department patients with pyelonephritis. Clinical Infectious Diseases, 206, 11, 1645-51. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/23087430

Takada, A., Feldmann, H., Ksiazek, T. & Kawaoka, Y. (2003). Antibody-Dependent Enhancement of Ebola Virus Infection. Journal of Virology, 77(13), 7539–7544.

WebMD. (n.d). Rotavirus Vaccine (RV): Schedule and fact that the young school children are medicated, absolute proof of the benefits is unavailable. Moreover, unintended Side Effects. Retrieved February 13, 2015, from http://www.webmd.com/children/vaccines/rotavirus-rv-vaccine

Wordings, R. J., Caffrey, M. H., Hendryx, J. T., Texas College of Osteopathic Medicine., & Texas College of Osteopathic Medicine. (2012). Immune system. Fort Worth, Tex: T.C.O.M.