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Ebola: Emerging or Re-Emerging Communicable Disease - Literature review Example

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The paper "Ebola: Emerging or Re-Emerging Communicable Disease" highlights that with respect to the environment, studies have also indicated that oral, guano, or respirator spread of the Ebolavirus may happen in confined spaces that provide environments that are conducive for bats to roost…
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Ebola: Emerging or Re-Emerging Communicable Disease Name Institution Introduction An emerging disease, as defined by Hatfill et al. (2014), refers to an infectious disease that has recently come about in a population, or is swiftly escalating in geographic or incidence scope. During the past three decades, animal hosts have transmitted close to 41 emerging infectious strains to the human population. According to Hatfill et al. (2014), some 1.407 disease-causing microbes have been identified, where some 58 percent of those identified were found to be animal diseases. Currently, some 177 pathogens have been found to be fundamental causes of newly emerging or re-emerging diseases. An example includes Ebolavirus (EBOV) that caused significant outbreak of Ebola in Sierra Leone and Liberia between 2012 and 2014. Ebolavirus refers to a fatal viral hemorrhagic fever that affects humans and other primates. In 2015, the disease had a high fatality rate of close to 50 percent in developed nations and, or up to 90 percent in many underdeveloped countries (Cenciarelli et al., 2015). Historically, Ebola infections were initially reported in the Democratic Republic of Congo (DRC) at Yambuku near the Ebola River and Nzara in Sudan (World Health Organisation, 2014). The Ebola outbreaks are known to become apparent sporadically, particularly in the tropical regions sub-Saharan Africa. Statics by the World Health Organisation (WHO) shows that an estimated 24 Ebola outbreaks involving approximately 1,736 cases were recorded between 1976 and 2013. However, a major outbreak was the West African epidemic of Dec 2013 to Jan 2016, where some 28,640 cases and nearly 11,320 deaths happened in Sierra Leone, Liberia, and certain areas in Nigeria (WHO, 2016a; 2016b; Cenciarelli et al., 2015). This paper analyses Ebola and its spread based on the Epidemiologic Triangle, which suggests three factors of analysis: agent, host, environmental factors. Epidemiologic Triangle The Centers for Disease Control and Prevention (2016) considered the triangular model as specifically designed for analysis of infectious disease. In their view, the triad suggests that the spread of infectious diseases calls for a susceptible host in addition to infective agent within an environment that brings the host and the agent together. The epidemiological triad features three vertices: the agent, host, and environment. Figure 1: Epidemiological triad of causal factors (Med Ottawa, 2016). The Agent The agent refers, as the Centers for Disease Control and Prevention (2016) defines it, is the cause of the disease. The disease-causing microbe for Ebola is a virus. In his synthesis of current and past literature on the virus’ epidemiology and pathogenesis, Michalek et al. (2015) concluded that causative agent for Ebola should be classified under the genus Ebolavirus of the Filoviridae family. Filoviruses, which are viruses covered by filamentous, contain non-segmented, negative-sense genomic RNA made up of around 19 kilobases. The single-stranded RNA virus has similar appearance to that of rhabdoviruses such as rabies and other features like mechanism for replication and genome organization and filamentous structure (Michalek et al., 2015). A recent review by Hatfill et al. (2014) explained that the Filoviruse encodes seven key structural proteins: polymerase cofactor (VP35), polymerase cofactor (VP35), RNA polymerase, transcription activator and nucleoprotein. The Filoviridae consists of the original Ebola virus, which contributes to lethal hemorrhagic fevers in nonhuman primates and humans. The virus is classified by the World Health Organization (WHO) as risk group 4 pathogen, which requires biosafety level 4 (BSL-4) restraint. According to Hatfill et al. (2014), the first documented outbreaks of hemorrhagic fever caused by a filovirus occurred more than three decades ago, but the amount of virus genetic diversity in the strains indicate that the Filoviridae are much older. Michalek et al. (2015) agree with this conception, in their view, the first Ebola filovirus was documented in 1982, before several changes were made in 2011. Still, the large number of virus genetic diversity in the strain show that the Filoviridae could be older than currently estimated. Figure 2: Florivirus Ebola Zaire (Hatfill et al., 2014) Michalek et al. (2015) and Hatfill et al. (2014) further agree that key 5 species found in the Ebolavirus genus include Sudan ebolavirus (SEBOV), Zaire ebolavirus (ZEBOV), Taï Forest ebolavirus (TEBOV), Reston ebolavirus (REBOV) and Bundibugyo ebolavirus (BEBOV). While their particularly genomes may vary by up to 40%. While occurrence of the other Ebolavirus genus are yet to be identified or discovered except for REBOV, which was initially isolated in Philippines between1989 and 1990. In 2008, pigs from pig farms close to Manilla (Philippines) also tested positive for REBOV. The family Filoviridae is made up of two genera: Marburg viruses and Ebola and. The two are also considered the most virulent pathogens to the human population (Hatfill et al., 2014). The Ebola virus of Zaire species was discovered to the causative agent of one of the most severe Ebola breakout that happened between 2014 and 2015 in parts of West Africa. In the incident, fatality rate has been reported to be as high as 70%, although in earlier cases, the fatality rates were as 90% (Michalek et al., 2015; Hatfill et al., 2014) The Host The hosts consist of organisms, often an animal, or a human being, that become exposed to and harbour a disease. The Centers for Disease Control and Prevention (2016) defines a host as an organism that becomes infected or carries the disease, and may get or not get sick as a result. In an attempt to describe the hosts for Ebola, there is a consensus among current scholars that two main disease spread modes into human population exist. These include through direct contact with animals that have contracted Ebola from a reservoir, or directly through contact with a reservoir (Agnandji et al., 2015; Cenciarelli et al., 2015). In two past major outbreaks in 1996 and 1994 in Gabon and Coˆte d’Ivoire respectively, epidemiologic research established that chimpanzees were the host of the disease (Hatfill et al., 2014). Burd (2015) explains that the spread of Ebolavirus into the human population also occurs through a direct contact with contaminated blood. Direct contact with contaminated bodily fluid like sweat, milk, semen or saliva, as well as bodily tissues of infected or dead people also causes the spread of the disease. However, a number of epidemiological surveys and field studies conducted in West Africa by the World Organisation for Animal Health (OIE) (2015) have showed extensive antibody occurrence of Ebolaviruses in fruit bats. This provides vital evidence that fruit bats may be natural hosts for the virus. A past survey also provided the possibility of insectivorous bats being hosts, although the study was largely inconclusive and requires the hypothesis to be scientifically tested. When bats and other vertebrate species were inoculated during an experiment, fruit bats were infected, which also shed virus in faeces despite not indicating any apparent clinical signs (Lyons-Weiler, 2015). However, in a rare review of filovirus ecology to determine the infectivity of Ebolavirus, Hatfill et al. (2014) examined studies that investigated the potential hosts in samples of different classes of vertebrates and invertebrates. They concluded that EBOV was replicated and recovered from infected insectivorous bats (Tadarida spp.), despite the fact that there were no observable histopathologic lesions, or even evidence of extensive tissue infection. On the other hand, the World Organisation for Animal Health (2015) argued that monkeys (Macaca fascicularis) could not be classed under the category of natural hosts due to their tendency to be highly sensitive to the Ebolavirus and their high mortality rate when infected. On the other hand, the role of pigs in transmission of ebolavirus remains unclear. In some cases, disease spread through inanimate objects that have come into contact with infected bodily fluids has been observed. There is a general agreement among researchers reviewed that the main mode of spread in human epidemics is human-to-human spread through direct contact with a dead person or symptomatic person, as well as contact with contaminated materials like clothing or bedding or surfaces (Agnandji et al., 2015; Cenciarelli et al., 2015; Hatfill et al., 2014; Burd, 2014). However, Hatfill et al. (2014) further indicated that the transmission risks tend to be low during the prodromal phase, or initial phase of the disease in humans, although viral loads in bodily fluids and blood tend to augment in the course of the disease, where the utmost intensity of virus shedding becomes observable during the late phases of the course of the disease of patients who are severely ill. It has also been observed by CDC (2016b) that handling of infected dead bodies also plays a crucial role in transmitting Ebola, an idea that is consistent with Burd’s (2014) findings. High cases of Amplified transmission have also been observed to happen in hospitals. According to the World Organisation for Animal Health (2015), nearly 50 percent of cases of transmission among health care practitioners happen in hospitals while handling Ebola patients. Following a study of the spread of Ebola Virus Disease Outbreak in West Africa in 2013-2014 Cenciarelli et al. (2015), concluded that Ebola virus’ natural reservoirs or host are yet to be identified, as studies that observed the manner in which Ebola virus materialised in humans during the initial stages of infection or at the outset of an outbreak are not necessarily comprehensive. However, an earlier review by the World Health Organisation (2012) appears to disagree with Cenciarelli’s et al. (2015) view that Ebola virus’ natural reservoirs or host are yet to be identified. According to the WHO, however, fruit bats are essentially the reservoirs for Ebola. Similar findings were made by Nidom et al. (2012) in their attempt to discover serological evidence of Ebolavirus infection in apes in Indonesia. Following their study, Nidom et al. (2012) were convinced that bats were possible reservoir for Ebolavirus in Bangladesh. They discovered antibodies against Zaire ebolaviruses that circulated in 3.5 percent of the 276 bats they studied. Further discover of antibodies to Ebola virus infection in orangotans indicated an existence of varioues filoviruses. However, there are concerns over the origin and methodology the researchers used in collecting samples used in the study, as the information of Nidom et al. (2012) is contradictory and insufficient. Conversely, there is a consensus among current studies that the first Ebola patient becomes infected once he or she comes into direct contact with an infected animal, particularly non-human primate like monkey and apes, or other mammals like a fruit bat (Roussettus aegyptiacus). Such kinds of transmissions from the hosts, according to the Centers for Disease Control and Prevention (CDC) (2015b), are called a ‘spillover event.’ Subsequently, person-to-person transmission occurs, which is observed to be a major contributory factor to extensive infection of the human population. In a number of documented incidents of the outbreak or the virus, some primates were observed to have become infected with the Ebola virus, contributing to a number of spill-over events, which occur when they ate or came into direct contact with infected non-human primates (CDC, 2015b). A recent study by the CDC (2015a) also observed an occurrence of Ebola virus in the semen of men who have been infected with the virus, as well as men who have just recovered from Ebola. The CDC study showed that the Ebolavirus potential becomes transmitted when humans come into contact with semen, particularly during sex. Still, the study was not able to ascertain the length of time the virus is carried in human semen. Similar studies by the European Food Safety Authority (2015) concluded that it appears the virus count could shrink with time and even eventually leave the semen. The European Food Safety Authority (2015) also elaborated that tears and saliva also carry the risks of infection to other humans. Consumption of bush meat has also been linked to Ebola epidemiology. In August 2014, for instance, the Ebolavirus was detected in the Democratic Republic of Congo (DRC), specifically in the Northwestern parts of the country. The case was linked to bush meat preparation. The causative virus was discovered to be ZEBOV, although strongly linked to Zaire Ebolavirus (ZEBOV), such as the 1995 DRC outbreak, although it was not epidemiologically linked to the West African outbreak in the same year (Agnandji et al., 2015). Non-human primates and other mammalians may also be infected by Ebola virus and considered as host, although the Ebola virus’ reservoir was for a long time unknown. As a result, concentrated efforts were made to discover the natural reservoir (Lyons-Weiler, 2015). In the past, some studies had indicated that bats and rodents could serve vital roles as reservoir animals of Ebola virus. Indeed, the first report on the virus highlighted how bats had been infected with Ebola virus, after the virus was confirmed through an exposure of antibodies and viral RNA in three species of the mammal. This was proof that bats played crucial roles in the spread or transmission of the virus (Hoenen et al., 2012). Some studies have also indicated that transmission of Ebola virus to human populations in sub-Saharan Africa happened via contact with living or dead infected mammals, such as antelopes and non-human primates (Agnandji et al., 2015; Cenciarelli et al., 2015; Hatfill et al., 2014; Burd, 2014). Indeed, Hatfill et al. (2014) traced the disease back to butchering the animals or skinning the carcasses. In their review of literature, Hatfill et al. (2014) observed that butchering of antelopes by humans did lead to human infections. Fruit bats and chimpanzees have as well been found in some previous outbreaks in Sierra Leone and Liberia to be potential hosts of the virus. In a past study by Leroy et al. (2002), it was discovered that an outbreak among humans was made up of a variety of simultaneous epidemics that happened as a result of varied viral strains, where each epidemic came about as a result of handling chimpanzee, duiker or gorilla carcass. What this shows is that a survey of wildlife health, as well as their mortality may assist in predicting and preventing the outbreak of Ebola. The Environment The environment refers to the surroundings and physical conditions outside the host that provide conducive setting that potentially facilitates transmission of disease (CDC, 2016). Studies have indicated that oral, guano or respirator spread of the Ebolavirus may happen in confined spaces that provide environments that are conducive for bats to roost. Hatfill et al. (2014) reviews filovirus ecology to determine the virus’ infectivity. In one of the experiments, Ebolavirus was observed in endothelial cells of lung tissues of bats sacrificed on the eighth day of post inoculation. Additionally, recovery of Ebolavirus was observed in the faeces of fruit bats on the twenty-first day post inoculation. The significance of this to the occurrence of Ebolvirus indicates that oral, guano or respirator spread of the virus may happen in confined spaces that provide favourable environment for bats to roost. Hatfill’s et al. (2014) comprehensive review of article to discover what happened when the virus was isolated from bat faeces suggested existence of mechanisms for transmitting Ebolavirus to other animals. Some researchers like Piercy et al. (2010) have also conducted laboratory studies to determine the survival rate of filoviruses in certain liquids and solutions, on solid substrates, as well as in aerosol. Piercy’s et al. (2010) objective was to determine the environmental conditions conducive for transmission and persistence of Ebolavirus. They established that the virus titered or concentrated on solid surfaces that are contaminated, and may reduce radically at room temperature although the viability may persist for a number of days when the room temperature was maintained at 4°C. Piercy et al. (2010) also established that no ebolavirus was recoverable from metallic surfaces at any moment, and that although it could be slightly recovered in organic debris, it was prone to drying up. In a related study, Burd (2015) mentioned in his review of literature that theoretically, the half-life for Ebolavirus is nearly 15 minutes, while the time for nearly 99 percent of the initial ebolavirus concentration is approximately 104 minutes. The survivability rate for Ebolavirus in tissue culture media and guinea pig sera is generally high. In a comprehensive study to determine the survivability rate of the virus, Piercy et al. (2010) did a laboratory test of the virus in guinea pig sera and tissue culture media, and observed that the virus could survive for up to 46 days in these solutions, although there was a radical decreased viability once the solutions were stored at room temperature. Some environments have also been identified to be less favourable to the existence of Ebolavirus. In a study by the Public Health Agency of Canada, it was established that ebolaviruses are vulnerable to alcohol-based dilutions and products, acetic acid, household bleach, such as sodium hypochlorite, as well as bleach powder (calcium hypochlorite) (Burd 2015). These solutions, as Burd (2015) explains in her review, can be crucial for cleaning up surfaces and materials to prevent spread of the disease. In an attempt to determine less favourable environments for Ebolavirus, the World Health Organization (WHO) verified these solutions as suitable for cleaning up infected blood or body fluids spills. Burd (2015) and Piercy et al. (2010) agree that no evidence of airborne transmission of ebolavirus may ever exist in natural settings. Conclusion The causative agent for Ebola is classified under the genus Ebolavirus of the Filoviridae family. The Filoviridae consists of the original Ebola virus, which contributes to lethal hemorrhagic fevers in nonhuman primates and humans. Regarding the hosts or reservoirs, it is established that fruit bats are essentially the reservoirs for Ebola. Conversely, there is a consensus among current studies that the first Ebola patient becomes infected once he or she comes into direct contact with an infected animal, particularly non-human primate like monkey and apes or other mammals like a fruit bat. In respect to the environment, studies have also indicated that oral, guano or respirator spread of the Ebolavirus mayhappen in confined spaces that provide environments that are conducive for bats to roost. The survivability rate for Ebolavirus in tissue culture media and guinea pig sera is generally high. Additionally, the virus on solid surfaces that are contaminated may reduce radically at room temperature, although the viability may persist for a number of days. However, no ebolavirus was recoverable from metallic surfaces at any moment, and that although it could be slightly recovered in organic debris; it was prone to drying up. References Agnandji, S., Huttner, A., Zinser, M. et al. (2015). Phase 1 trials of rVSV Ebola vaccine in Africa and Europe — Preliminary report. The New England Journal of Medicine, 1(1), DOI: 10.1056/NEJMoa1502924 Burd, E. (2015). Ebola virus: A clear and present danger. Journal of Clinical Microbiology, 53(1), 4-8 Cenciarelli, O., Pietropaoli, S., Malizia, A. et al. (2015). Ebola Virus Disease 2013-2014 Outbreak in West Africa: An Analysis of the Epidemic Spread and Response. International Journal of Microbiology, 1-12 Centers for Disease Control and Prevention (CDC). (2016). Lesson 1 understanding the epidemiologic triangle through infectious disease. Retrieved: Hatfill, S., Nordin, T. & Shapiro, G. (2014). Ebola virus disease. Journal of American Physicians and Surgeons, 19(4), 101-107 Hoenen, T., Groseth, A. & Feldmann, H. (2012). Current ebola vaccines. Expert Opin Biol Ther, 12(7), 859–872 Leroy EM, Rouquet P, Formenty P, et al. (2002). Multiple Ebola virus transmission events and rapid decline of Central African wildlife. Science, 303, 387- 390 Lyons-Weiler, J. (2015). Ebola: An evolving story. New York: World Scientific, Med Ottawa. (2016). Agent, host and environment model of causation. Retrieved: Michalek, P., Krejcova, L., Adam, V. & Kizek, R. (2015). Epidemiology and pathogenesis of Ebola viruses. Journal of Metallomics and Nanotechnologies, 1, 48—52 Nidom CA1, Nakayama E, Nidom RV, Alamudi MY, Daulay S, Dharmayanti IN, Dachlan YP, Amin M, Igarashi M, Miyamoto H, Yoshida R, Takada A. (2012). Serological evidence of Ebola virus infection in Indonesian orangutans. PLoS One, 7(7), 1 Piercy, T., Smither, S., Steward, J., Eastaugh, L., Lever, M. (2010). The survival of filoviruses in liquids, on solid substrates and in a dynamic aerosol. Journal of Applied Microbiolology, 109, 1531–1539 World Health Organisation. (2012). Ebola virus disease – an introduction. Retrieved: < http://www.searo.who.int/entity/emerging_diseases/ebola/ebola_virus_disease_intro.pdf> World Health Organisation. (2016a). Ebola outbreak in East Africa - Case counts. Retrieved from WHO website: World Health Organisation. (2016b). New Ebola case in Sierra Leone. WHO continues to stress risk of more flare-ups. Retrieved from WHO website: World Organisation for Animal Health (OIE). (2015). Ebola Virus Disease. Retrieved: Read More
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