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Expository Essay on Ebola Virus

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Introduction

The Ebola virus is one of the most dangerous and deadly viruses known to humans. The Ebola epidemic since its discovery in 1976 came from the Democratic Republic of Congo, formerly known as Zaire, but the largest Ebola outbreak known to date is still ongoing at the time of writing, in the West Africa. An estimated 550 000 reported incidents from Sierra Leone and Liberia took place on January 20, 2015.

The virus is prevalent in many countries including Guinea, Liberia, Sierra Leone, Nigeria as well as occasional reported cases in the USA, Canada. The Netherlands and India show the potential for infection to spread globally. Despite the fact that the disease is highly contagious, life-threatening, and no specific treatment is available, it can be prevented through the use of appropriate measures to prevent and control infection. The study of the Ebola virus is important as such knowledge will pave the way for the reduction of victims, the development of an effective drug and will be useful in controlling the same epidemic.

The Ebola virus is a member of the Philoviridae family. As the name implies the virus has a filamentous shape. Marburg virus and Ebolavirus are two major generations of the virus family that are important in medicine. Bacteria of these two species are studied and presented together due to their many similarities in the life cycle, water storage areas, transmission methods, clinical presentation, treatment and prevention measures. The only difference is that Marburgvirus is still distributed by forest-dwelling bats such as the savannah while Ebolavirus is distributed by bats species accustomed to deep rain forests.

Five subspecies of Ebolavirus, namely, Ebolavirus Zaire, Ebolavirus Sudan, Ebolavirus reston, Ebolavirus cote d’Ivore, and Ebolavirus bugs, have been identified and named after the place where they were first discovered. Of these E. Zaire was the first to be isolated and studied and is responsible for a large number of outbreaks  including recent outbreaks in 2014 before that E. Sudan accounted for ¼ of all Ebolavirus deaths. With the exception of a slightly lower mortality rate, E. Sudan is almost identical to E. Zaire. E death rate of E case. Sudan is reported as 40-60% and E. Zaire as 60-90%.

Ebola was originally transmitted to humans as a zoonosis. Different species of bats are found throughout sub-Saharan Africa such as. Contact with bats by biting and scratching or exposure to their discharges and discharges through broken skin or mucous membranes can cause infection in humans. The infection can also be spread to other end users. Those recorded in Africa are deer, wildebeests, chimpanzees, chimpanzees, gorillas, monkeys, and other non-humans. Attacks during the hunting of these animals or handling carcasses of infected animals have led to the introduction of the virus to humans from the wild. Outbreaks appear to be exacerbated during pregnancy and in childbirth. Records show that outbreaks appear to be exacerbated by the presence of multiple pathogens.

EVD is highly contagious. Infection can be spread in the community and in a hospital setting by direct contact with infected body fluids such as blood, fluid and discharge or the patient’s tissues or by direct contact with contaminants such as clothing and bed linen. One of the main reasons for the rapid spread of the epidemic is traditional funeral rites, which include cadaver cleaning, removal of fingernails, toenails and clothing. Caregivers, including health workers, are also at greater risk of contracting the disease. In addition the sperm of the surviving male is said to remain infected for up to 82 days after the onset of symptoms. As long as the virus stays in the body fluids a person stays infected. The spread of the Ebola virus is highly suspected but has not been proven by experiments.

Clinical Introduction

EVD caused by different types of Ebola virus brings different clinical features. The incubation period of Ebola virus is generally considered to be 2 – 21 days. Ebola virus disease shows a variety of symptoms that develop deep in the prodromal constitution leading to various diagnoses including not only other viral hemorrhagic diseases, but also malaria, typhoid, cholera, and others. bacterial rickettsia and non-infectious causes of bleeding.

The onset of the disease is similar to that of severe hemorrhagic fever. Patients have high fever, fever reaching 39-400C, body aches and fatigue. Subsequent abdominal symptoms such as epigastric pain, vomiting and / or bloodless diarrhea appear if the fever persists throughout the day. 3-5.

After 4 – 5 days of illness macular degeneration may be visible but may not be clearly visible on dark skin. After this stage the bleeding from different areas begins. Bleeding in both the upper and lower digestive tract, the respiratory tract, the urinary tract, the vagina in women can be detected. Continuous petechial in the buccal mucosa, skin and conjunctivae grow. Repeated cleansing bumps that prevent any oral fluid intake and a large amount of wet diarrhea (five liters or more per day) contribute to the loss of excess fluid leading to dehydration. If fluid changes are not enough, bending, extreme fatigue and hypovolemic shock eventually.

Hypovolemic shock was reported in 60% of cases. Despite high body temperature, patients experience cold edges due to peripheral vasoconstriction. Rapid and cord pulses, tachypnea, oliguria or anuria can be detected. At the same time features such as asthma and abdominal pain, muscle and joint pain and headache increase. Although in some cases coughing and dyspnoea occur as a result of pulmonary haemorrhage, other respiratory symptoms are uncommon. Conjunctival injection is a common clinical feature. The most common neurologic symptoms are hypoactive and hyperactive delirium characterized by decreased mental function, confusion, dizziness and unusual tremors. As the disease changes the internal bleeding may also begin but more often by this time the patients are already in a coma.

It is reported that only 5% of patients have bleeding from the gastrointestinal tract before death. Most of the reported deaths occurred as a result of shock during the 7th to 12th day of illness. Symptoms of 40% of patients have improved by day 10 although symptoms such as mouth sores and thrush have already appeared. Most patients who survived until day 13 showed a high chance of finally recovering. Some patients who showed early improvement in symptoms have had stiff necks and reduced cognitive levels associated with late death.

Post-mortem examinations and post-mortem biopsies are very useful in the study of the pathology of the Ebola virus disease. Because of the biosafety risk in autopsy staff when handling models, pathological explanations of only a limited number of available conditions.

The most common findings of Haematoxylin and eosine-stained tissue components are oval-shaped or filamentous eosinophilic intracellular inclusions formed by a combination of viral nucleobases. These implants can be found in macrophages, hepatocytes, endothelial cells, fibroblasts of connective tissue etc. Immunohistochemically stains express viral antigens to various infected tissue cells including macrophages, dendritic cells, epithelial cells and sweat glands, intermediate cells and kidney tubes. , seminiferous tubes, endothelial cells and endocardial cells. In addition necrotic cells and cellular waste contain antigens in abundance. Electron microscopy shows an abundance of free viral particles in the alveolar glands, liver sinusoids, and connective tissue cells of the testis and dermal collagen. Karyorrhexis and apoptosis are found in portal triads cells, macrophages of the red spleen pulp and epithelial cells of the tubular kidneys.

Liver tissue exhibits histopathological symptoms including concentrated or widespread necrosis of hepatocytes and central steatosis. Although inflammation is usually mild, hyperplasia of kupfer cells and infiltration of mononuclear inflammatory cells is observed. The infected lung shows congestion, bleeding and intra-alveolar edoema but inflammation is not significant. Concentrated infiltration of mononuclear inflammatory cells is known to occur in the lamina propria of the small intestine and colon. Skin biopsies reveal dermal edoema, concentrated bleeding, petechiae, ecchymosis, and macular rashes. Spleen and lymph nodes show widespread lymphoid depletion due to apoptosis and necrosis. Inflammation of the kidneys is undetectable although acute tubular necrosis is more common. Even if the heart endocardium contains viral antigens, the myocardium does not show significant damage. Brain histology shows panencephalitis and perivascular infiltration of lymphocytes.

The World Health Organization (WHO) has recommended a set of measures to prevent and control infection in health workers, including safety measures to be taken in the various stages of EVD patient management.

1. General precautionary measures

Regardless of the disease, it is recommended that health professionals take precautionary measures when treating all patients, as it is difficult to diagnose EVD patients at the onset of the disease. These are,

2. Doing hand hygiene

Use disposable gloves before handling items that may be infected w ear eye protection and a coat before engaging in procedures that body fluids may predict.

3. Hand hygiene

Hand hygiene should be done using soap and water or an alcohol-based hand sanitizer solution, in accordance with WHO guidelines, before wearing gloves and protective equipment (PPE) after exposure to a patient’s body fluids after contact with a dirty area or equipment after extracting PPE. if the hands appear dirty.

4. Personal Protective Equipment (PPE)

PPE should be worn before entering EVD patient care facilities in accordance with the WHO-recommended order and removed before leaving the care facility. Contact with used PPE on any part of the face or fragile skin should be avoided. PPE covers,

  • Non-sterile gloves are the right size
  • Non-slip and long-sleeved dress
  • Face shield
  • Locked shoes that prevent piercing and intrusion

5. Patient placement and management

Suspected or certified EVD patients should be kept in isolation and if possible kept in a single room. Otherwise they must be placed in beds with a gap of at least 1m in between. Visitors should have no restrictions other than those necessary for the patient’s well-being as a parent.

Management of used equipment and other items

It is recommended that equipment such as stethoscopes be refined and disinfected before reuse, if different equipment is not available. Parental equipment, surgical blades, syringes and needles should not be reused. They should be discarded in barrels that are resistant to piercing. All solid non-solid waste should be disposed of in non-leaky bags or bins.

Used linen should be collected from non-perishable bags stored during use. They should be washed with water and detergent, rinsed, soaked in 0.05% chlorine for 30 minutes and then dried.

All barrels must remain upright and must be closed when ¾ is full. Before being removed from the wards the outer surfaces of these containers should be disinfected using 0.5% chlorine.

1. Clean the environment

Cleaners should wear heavy rubber gloves, and non-slip, non-slip rubber boots over PPE. Water and cleaning should be used to clean work areas and the floor of the hospital. This should be done at least once a day. Some dirty areas and contaminants should be cleaned and disinfected using 0.5% chlorine.

2. Biological management

Performing autopsies, post-mortem biopsies and other laboratory tests of certified EVD tissue samples or suspected patients should be minimized and should only be performed by qualified personnel. Full PPE should be worn during template handling. All specimens should be submitted with clearly marked, non-leaky, non-breakable containers, with an antiseptic exterior.

Carcasses should never be washed or embalmed. They should be sealed in two bags, disinfected with 0.5% chlorine and buried immediately. Some cultural and religious practices can be changed if necessary, but body care should be kept to a minimum and full PPE should be worn at all times.

3. In the case of exposure to infected body fluids

All current operations should be safe and dry immediately and PPE should be safely removed. Affected skin should be washed with soap and water and any affected pores such as conjunctiva should be washed with plenty of running water. The person should be tested for fever and other symptoms for 21 days.

4. Pathogenesis

The pathogenesis of the Ebola virus shows similarity to that of most other filo viruses that include immunosuppression, increased vascular permeability and coagulopathy. The Ebola virus enters the scrotum even through skin scratches, either through mucous membranes or by accidental injection. The virus enters monocytes, macrophages and dendritic cells and is carried by lymphatics to circulation. It then spreads to the liver and spleen to infect tissue macrophages and fibroblastic reticular cell. The main cellular targets of this virus are macrophages, dendritic cells and kupfer cells. The Ebola virus shows an interaction between a variety of cellular proteins which is why the infection is characterized by broad tissue and organ tropism.

5. Immunopathology

In many cases of the virus, the immune system plays a key role in controlling the spread of the virus. However the tissues and organs of the fatal EVD cases show less inflammation, which raises the damage to the immune response.

It has been found that the proteins of the structure of filo viruses e.g. VP24 (Virion protein) and VP35 inhibit interferon reactions and thus avoid the host’s natural defences. As previously mentioned, apoptosis of natural killer cells and T lymphocytes was revealed in histopathology describing the suppression of dynamic immune responses.

As with most complex phones, the Ebola virus infection also causes significant release of pro-inflammatory and vasoactive substances. Even if pro-inflammatory mediators promote inflammation and inflammation, the spread of the infection system is not effectively controlled. This is due to vasodilation connected by active ingredients.

6. Endothelial dysfunction and coagulopathy

The virus attacks endothelial cells and endocardial cells and causes injury (18). This causes internal bleeding, fluid and electrolyte imbalance and cardiovascular failure. Endothelial damage leads to platelet aggregation and use. The increased level of inflammatory factors and increased production of surface tissue factor protein in infected monocytes and macrophages promotes coagulation decay. As a result of hepatocellular damage the production of coagulation factors, fibrinogen, protein C and S also decreases. Other social and economic problems associated with the Ebola virus epidemic

In view of the current outbreak, in addition to the large number of lives that have been claimed by the disease, it has created many other serious problems not only in Ebola-affected countries, but also in other African countries.

Agriculture contributes significantly to the African economy. As more and more farmers die of the disease and many leave their farms for fear of contracting the disease, there is a severe shortage of workers in these countries and a decline in food production. The emergence of food shortages in the near future is predicted by experts.

Chocolate companies and many other industries are particularly affected by the shortage of workers. Nigeria and Ivory Coast are the largest cork producing countries but most of the workers are from Liberia and Guinea. International companies such as Nestle and Mars have introduced education and fundraising programs to prevent the spread of the virus to cork workers.

Many schools have been closed because of a deadly epidemic that has swept across the country. Apart from the impact on education, the child support system in government has stalled as a result.

Tourism is another area affected by the epidemic. Although Africa is a larger continent than Europe, the USA and China combined; visitors often see it as a single country since the Ebola epidemic broke out. For example, Tanzania, a popular wildlife sanctuary, is an East African country, located more than 6,000 miles from the Ebola-affected area. Tanzanian hotels reportedly lost 50% of bookings in 2015.

Many African countries refused to host international events and conferences because of the risk of the Ebola outbreak. For example, Morocco, the host of the Africa Cup of Nations, scheduled for January 2015, is calling for a postponement. The government says, “There is no way we can be serious about the health and safety of Moroccan citizens.”

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  • v.8(7); 2019 Jul

Ebola virus: A global public health menace: A narrative review

Shamimul hasan.

1 Department of Oral Medicine and Radiology, Faculty of Dentistry, Jamia Millia Islamia, New Delhi, India

Syed Ansar Ahmad

2 Department of Oral Surgery, Faculty of Dentistry, Jamia Millia Islamia, New Delhi, India

Rahnuma Masood

3 Department of Conservative Dentistry, Faculty of Dentistry, Jamia Millia Islamia, New Delhi, India

Shazina Saeed

4 Department of Amity Institute of Public Health, Amity University, Noida, Uttar Pradesh, India

Ebola virus disease (EVD), a fatal viral hemorrhagic illness, is due to infection with the Ebola virus of the Filoviridae family. The disease has evolved as a global public health menace due to a large immigrant population. Initially, the patients present with nonspecific influenza-like symptoms and eventually terminate into shock and multiorgan failure. There exists no specific treatment protocol for EVD and only supportive and symptomatic therapy is the line of treatment. This review article provides a detailed overview of the Ebola virus; it's clinical and oral manifestations, diagnostic aids, differential diagnosis, preventive aspects, and management protocol.

Introduction

Ebola, earlier termed as Ebola hemorrhagic fever (EHF), is a critically lethal ailment which primarily affects the humans and nonhuman primates. Ebola virus disease (EVD) occurs due to a virus infection which belongs to the family Filoviridae and genus Ebolavirus .[ 1 ] EVDs has posed diagnostic challenges and has been a universal public health threat since its discovery. While investigating an alleged yellow fever case, Dr. Peter Piot in the year 1976 first detected the disease in Zaire, Africa (presently the Democratic Republic of Congo).[ 2 ] The name “Ebola” was termed as the disease was noticed near the Ebola river in Congo.[ 3 ]

Fruit bats of Pteropodidae family, such as Hypsignathus monstrous, Epomops franqueti , and Myonycteris torquata serve as the natural hosts of the EBOV in Africa. Nonhuman primates may develop the infection by eating the partly eaten fruits and may also transmit the infection to humans.[ 4 ] Indian population is an impending threat to EVD, as India falls in the home range of Pteropodidae family of fruit bats.[ 5 ]

Ebola virus transmission primarily takes place through close bodily contact with the infected patient or their fluids, contaminated tissue surfaces, and clothing from alive, infected or deceased individuals. Unsafe traditional burial practices also play a pivotal role in the disease transmission.[ 6 ] There is documented evidence regarding the sexual mode of disease transmission, although transmission through the air is unlikely.[ 7 ]

EVD present with bizarre and atypical manifestations mimicking other viral diseases, especially in the initial disease phase. Constitutional symptoms, such as fever, myalgia, headache, vomiting, and diarrhea are the early presenting features. Hemorrhagic rash, internal and external bleeding are usually the warning manifestations in the late stages.[ 8 ] Bleeding from the body apertures is a distinguishing EVD manifestation.[ 9 ] Gum bleeding, odynophagia, and atypical oral manifestations constitute the oral features of EVD.[ 10 ]

Till date, there is no precise antiviral management or vaccination for EVD. The management protocol mainly relies on supportive and symptomatic therapy, along with monitoring coagulopathies and multiorgan dysfunction.[ 2 ]

The World Health Organization (WHO) affirmed the EVD outbreak as a “Public Health Emergency of International Concern” on August 8 th , 2014.[ 5 ]

With the enormous immigrant population, India is estimating the likelihood of a probable EVD outbreak. The Ministry of Health and Family Welfare, Government of India, in collaboration with other agencies has appraised the situation and recommended travel instructions by air, land, and sea and health care professionals.[ 11 ]

The virus belongs to the Ebola virus genus, Filoviridae family, and Mononegavirales order.[ 12 ] The genus Ebolavirus includes the following species- Zaire ebolavirus (EBOV), Reston ebolavirus (RESTV), Bundibugyo ebolavirus (BDBV), Taï Forest ebolavirus (TAFV), Sudan ebolavirus (SUDV), and the newly identified Bombali ebolavirus (BOMV).[ 13 ] Except for exclusive identification of RESTV in the Philippines, all the other species causes endemic West African EVD.[ 14 ]

EBOV responsible for the EHF causes the highest human mortality (57%–90%), followed by SUDV (41%–65%) and Bundibugyo virus (40%). TAFV has caused only two nonlethal human infections to date, whereas RESTV causes asymptomatic human infections.[ 15 ]

Figure 1 shows the taxonomy of Ebola virus.

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Object name is JFMPC-8-2189-g001.jpg

Taxonomy of Ebola virus

Transmission

Based on the Centers for Disease Control and Prevention (CDC) classification, Ebola virus is considered as a biosafety level 4 and category A bioterrorism pathogen with an immense likelihood for massive nationwide transmission.[ 16 ]

Source of Infection

Intimate physical contact with the patients in the acute disease stages and contact with the blood/fluids from the dead individuals constitutes the most important modes of transmission.[ 17 ]

The long-established funeral ceremonies in the African countries entail direct handling of the dead bodies, thus significantly contributing to the disease dissemination. Unsafe conventional burial procedures accounted for 68% infected cases in 2014 EVD outburst of Guinea.[ 18 ]

EBOV RNA may be identified for up to a month in rectal, conjunctival, and vaginal discharges and semen specimens may demonstrate the virus presence up to 3 months, thus signifying the presence of EBOV in recuperating patients.[ 14 ] The sexually transmitted case of EVD has been reported between a convalescent patient and close family member. Another study demonstrated a case in a recuperating male patient. The patient's semen specimen tested positive with Ebola viral antigen almost 3 months after the disease onset.[ 19 ]

Asymptomatic EBOV carriers are not infectious and do not have a major role play in the EVD outburst, and the field practice in Western Africa supported this assumption.[ 20 ] However, this presumption was refuted after the documentation of a pioneer asymptomatic carrier case in North Gabon epidemic (1996).[ 21 ]

EBOV has been detected from blood, saliva, semen, and breast milk, while RNA has been isolated from sweat, tears, stool, and on the skin, vaginal, and rectal swabs, thus highlighting that exposure to infected blood and bodily secretions constitute the major means of dissemination.[ 22 ]

Eating uncooked infected animal meat such as bats or chimpanzees account significantly to oral EVD transmission, especially in the African countries.[ 23 ] The demonstration of the Ebola virus in the Filipino pigs in 2008 triggered the likelihood of an extensive range of possible animal hosts.[ 24 ]

EVD dissemination has also been reported with hospital-acquired infections, particularly in areas with poor hygiene conditions. The infected needles usage was responsible for the 1976 EVD outbreak in Sudan and Zaire.[ 25 , 26 ] Improper hygiene and sterilization were the crucial factors for the 1967 Yambuku EVD outburst.[ 27 ]

EVD dissemination may also occur through the inanimate materials with infected body secretions (fomites).[ 19 ] However, disease transmission through the airborne and droplet infection is ambiguous.[ 10 ]

Figure 2 shows the primary and secondary transmission of disease.

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Object name is JFMPC-8-2189-g002.jpg

Primary and secondary transmission

Table 1 depicts the possible routes of transmission.

Possible routes of transmission

Epidemiology

The vast majority of EVD cases and outbursts have been endemic to African continent ever since the disease detection in 1976,[ 28 ] and 36 such outbreaks have occurred in six African countries.[ 29 ]

Table 2 shows Ebola epidemiological outbreaks between 1976 and 2014.

Ebola outbreaks between 1976 and 2014 (Adapted from WHO 2014)

UVRI: Uganda Virus Research Institute; CDC: Centers for Disease Control and Prevention

The 2014–2016 EVD started in South East Guinea rural surroundings and eventually became a global public health menace by rapidly disseminating to urban localities and other countries.[ 28 ]

Figure 3 depicts the geographical distribution of Ebola virus disease.

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Geographic distribution of Ebola virus disease outbreaks

The conducive environmental surroundings of the African continent facilitate EVD endemicity. However, intermittent imported Ebola cases have also been noticed in United States, United Kingdom, Canada, Spain, and Thailand.[ 30 , 31 ]

Figure 4 depicts the distribution of Ebola virus disease in West African Countries.

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Distribution of Ebola virus disease in West African Countries

Out of the unparalleled globally reported 28,616 cases and 11,310 casualties, Liberia accounted for almost 11,000 cases and over 4,800 deaths.[ 32 ]

Table 3 shows the statistics of the 2014–16 West African outbreak.

Statistics of 2014-16 West African outbreak

Pathogenesis

Ebola viruses penetrate the human body through mucous membranes, skin lacerations/tear, close contact with infected patients/corpse, or by direct parental dissemination.[ 33 ] EBOV has a predilection to infect various cells of immune system (dendritic cells, monocytes, and macrophages), endothelial and epithelial cells, hepatocytes, and fibroblasts where it actively replicates by gene modulation and apoptosis and demonstrate significantly high viremia.[ 34 ] The virus reaches the regional lymph nodes causing lymphadenopathy and hematogenous spread to the liver and spleen promote an active inflammatory response.[ 35 ] Release of chemical mediators of inflammation (cytokines and chemokines) causes a dysregulated immune response by disrupting the vasculature system harmony, eventually causing disseminated intravascular coagulation and multiple organ dysfunction.[ 36 ]

Figure 5 demonstrates the pathogenesis of Ebola virus disease.

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Pathogenesis of Ebola virus disease

Clinical Features

Due to the bizarre and atypical manifestations in the initial phase, mimicking dengue fever, typhoid fever, malaria, meningococcemia, and other bacterial infections, EVD poses diagnostic dilemmas.[ 37 ]

The incubation period ranges from 2 to 21 days. However, symptoms usually develop 8–11 days following infection.[ 38 , 39 ]

The initial disease phase is represented by constitutional symptoms.[ 40 ] High-grade fever of >38 o C is the most frequently reported symptom (85–95%), followed by other vague symptoms such as general malaise (85–95%), headaches (52–74%), dysphagia, sore throat (56–58%), and dry cough.[ 41 , 42 ] The progressively advanced disease is accompanied by abdominal pain (62–68%), myalgia (50–79%), nausea, vomiting, and diarrhea (84–86%).[ 41 ]

Variety of hemorrhagic manifestations forms an integral component of the late disease phase.[ 38 ] Gastrointestinal tract bleeding manifests as petechiae, hematuria, melena, conjunctival bleeding, contusion, or intraperitoneal bleeding. Mucous membrane and venipuncture site bleeding, along with excess clot formation may also occur. As the features advances with time, the patients experience dehydration, confusion, stupor, hypotension, and multiorgan dysfunction, resulting in fulminant shock and ultimately death.[ 43 , 44 ]

Maculopapular exanthema constitutes a characteristic manifestation of all Filovirus infection, including EVD.[ 45 ] The rash usually appears during the 5 th to 7 th day of disease and occur in 25–52% of patients in the past EVD outbreaks.[ 46 ]

Table 4 shows the clinical manifestations of Ebola virus disease.

Clinical manifestations of Ebola virus disease

Although EVD has a number of similar features with other viral hemorrhagic fevers (e.g. dengue), there are differences that set them apart.

Table 5 depicts the differentiating features of the Ebola virus and dengue virus infection.

Differentiating features of Ebola and dengue virus infection

Orofacial features

Gum bleeding, atypical mucosal lesions, and odynophagia comprise the distinctive oral manifestations. Epistaxis (nasal bleed), bleeding from venipuncture sites, conjunctivitis, and cutaneous exanthema are the other manifestations.[ 9 ] Bleeding tendencies and gum bleeding is not seen in asymptomatic or initial EBOV patients reporting to the dental hospital.

EVD dissemination in the field of oral and dental health may appear nonsignificant; although, probable situations which may pose a risk to dental health professional have been appraised by Samaranayake et al. [ 21 ] and Galvin et al. [ 10 ]

Table 6 depicts the various orofacial manifestations of Ebola virus disease

Orofacial manifestations of Ebola virus disease

EVD patients usually demonstrate altered laboratory parameters based on the stage of the disease.

Table 7 shows the laboratory findings in Ebola virus disease.

Laboratory findings in Ebola virus disease

The WHO (2014) recommended the sample collection of whole blood or oral swab at suitable centres called Ebola treatment centers.[ 47 ] Reverse transcriptase polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) are the most frequently utilized tests for laboratory affirmation of the EVD.[ 43 ] RT-PCR is capable of detecting viral RNA in the blood samples of infected patients immediately after the commencement of signs and symptoms,[ 42 , 48 ] has a high sensitivity (up to 100%), and gives results within 1–2 days in cases of epidemics. ELISA detects the immunoglobulins G and M in samples of infected patients, has a low sensitivity (91%) and is not suitable for initial affirmation during an outbreak.[ 42 , 49 ]

The most imperative strategy in EVD is to avert the vulnerable population from getting infected and limit the transmission. These preventive strategies entail intensive and rigorous endeavors from the Government, public health amenities, medical units, and personals.[ 50 ]

The most essential aspect to curb EVD transmission is to avert direct bodily contact with infected individuals and their body fluids.[ 51 ]

Health caregivers are extremely vulnerable and experience an augmented professional threat for EVD.[ 52 ] Thus, scrupulous adherence to the universal infection control measures is fundamental in all the hospitals, laboratories, and other health care services.[ 53 ] The U.S. CDC has advocated the appropriate use of various personal protective equipment as a mandate for health care professionals.[ 50 ]

The risk of rapid importation of Ebola virus into human beings can be prevented by averting the direct bush meat and bats contact.[ 54 ]

Unsafe traditional burial procedures, especially in the African continent significantly contributed to the EVD transmission. Hence, it is essential to practice safe and guarded funeral rituals to prevent the disease spread.[ 55 ]

WHO recommends the implementation of safe sex practices to combat the sexual transmission of EVD. Strict abstinence or proper and regular condom use in male EVD survivors at least for a period of 12 months of the symptom onset or until their semen has twice tested negative should be followed.[ 56 ]

Dental health care personals are extremely susceptible to EVD as they are in regular contact with blood and saliva during the routine diagnostic procedures. There is no documented case of EVD through saliva till date. A study on the identification of EBOV in oral fluids affirmed that patients presenting with demonstrable serum levels of EBOV RNA also exhibit identifiable salivary levels.[ 57 ] The incubation period for all body fluids including saliva is 21 days; hence, oral health personals are vulnerable to develop the disease if universal infection control protocol is not followed.[ 58 ]

Table 8 demonstrates the various infection control measures to prevent the Ebola virus spread.

Infection control measures to prevent Ebola virus spread

Box 1 shows the travel guidelines to EBOV affected regions.

Shows the UK Travel guidelines to EBV infested regions.

Till date, there is no precise antiviral management or vaccination for EVD.[ 51 ] The management protocol mainly relies on supportive and symptomatic therapy. Public health strategies emphasizing on epidemiological surveillance, contact tracing, and quarantine of the patient have been recommended to combat the dissemination of EVD.[ 59 ]

Rehydration, adequate nourishment, analgesics, and blood transfusion form a keystone supportive treatment of EVD patient.[ 60 ] Intravenous fluids and oral rehydration solution endow with proper electrolytes substitute and maintain the intravascular volume. Unrelenting vomiting and diarrhea are taken care of by the use of antiemetics and antidiarrheal drugs.[ 35 , 60 , 61 ] Suspected cases of secondary bacterial infections and septicemia are best managed by the use of prophylactic antibiotic regimen (third generation I.V. cephalosporins).[ 62 ] Concurrent parasitic coinfections may also be seen and require prompt investigations and management.[ 63 ]

A number of investigative clinical trials emphasizing on the development of vaccine, antibody therapies, and antiviral drugs have been conducted for EVD.[ 64 ]

Table 9 shows experimental treatment for Ebola virus disease.

Experimental treatment for Ebola virus disease

Various clinical trials in Africa, Europe, and the United States suggest that Ebola vaccines are in various development stages (Phase I–III). A number of candidate vaccines employ diverse platforms, including recombinant viral vectors (most evolved vaccine candidate), DNA vaccines, inactivated viral particles, subunit proteins, recombinant proteins, and virus-like particles. Example of viral vectors expressing ebolavirus glycoproteins include recombinant simian adenovirus (cAd3), recombinant vaccinia virus, recombinant human adenovirus (Ad26), and a live vesicular stomatitis virus used alone or in prime-booster regimens.[ 65 ]

However, Ebola virus having the glycosylated surface proteins and preferentially infecting the immune cells impedes the development of an effective vaccine.[ 66 ]

Dental Management

Dental health care professionals in Europe have not encountered a case of EVD so far. However, health care personals (including dental surgeons) are more prone to EVD while treating patients in West or sub-Saharan Africa. Dental professionals are more likely to encounter asymptomatic EVD patients or those with early-stage vague symptoms.[ 27 ]

Individuals with a travel history to Ebola endemic regions, but with no direct intimate contact with the disease fall in the low-risk category and may undergo any medical/dental health care procedures without restrictions. However, all the nonessential procedures should be postponed for 21 days in individuals with direct exposure to the virus. The regional Health Service Executive Department of Public Health needs to be notified when the exposed patient's treatment cannot be deferred or controlled with pharmacotherapy.[ 10 ]

EVD has emerged as a significant global public health menace due to multiple disease outbreaks in the last 25 years. Recent advancements are being carried out in the form of effective Ebola virus vaccine and anti-Ebola virus drugs. However, rapid geographic dissemination, nonspecific clinical presentation, lack of vaccine, and specific diagnostic test are the possible challenges to combat this dreaded public health menace.

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Conflicts of interest.

There are no conflicts of interest.

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Ebola was first discovered 1976 in Africa, on the banks of the Ebola river, after which the virus has been named. Back then, there were two major outbreaks of the virus, and this is how people learned about it. There exist several strains of the Ebola virus, some of them are deadly to people, and some are not.

The main symptoms of Ebola can appear in a period between the second and the 21st days of contamination, but usually it happens on the eighth through 10th day (CDC). Among the symptoms that appear in the first turn, one should mention fever and chills, strong headaches, pain in joints and muscles, and general weakness. These symptoms are not too different from those that people usually experience when catching a severe cold, or flu, so victims may even ignore these symptoms, or try to treat them as a common sickness. However, as the virus keeps progressing, a patient develops nausea with vomiting, diarrhea, chest and stomach pains, red eyes and rashes over the body, severe weight loss, and bleeding from almost all bodily orifices (Mayo Clinic).

The virus is usually transmitted either through blood or through waste. Contagion through blood usually takes place if a person consumes infested meat, or even touches it (for example, butchering can also lead to contamination). Also, there were cases when people got infected after stepping in feces of infected mammals, mostly bats (Mayo Clinic). The other ways of getting infected is through skin by receiving bodily fluids through pores.

Even though there is no specific cure from Ebola, doctors still try to treat it. In order to diagnose Ebola, doctors usually take tests on such diseases as cholera or malaria, because it is difficult to diagnose Ebola based solely on symptoms. After the diagnosis has been made, doctors start treating the symptoms, which includes eliminating infected cells, electrolytes, blood pressure medication, blood transfusions, oxygen therapy, and so on (WebMD).

Though Ebola is a highly dangerous disease, it is not likely that it will spread globally. It is most deadly in anti-sanitary conditions, which many African countries are notorious for. As for first world countries, even though there is still no universal cure, they are at much lesser risk than African countries. Though the symptoms of Ebola are severe and getting infected is not difficult, with the correct handling of an outbreak, the virus should not be able to spread.

“Signs and Symptoms.” Centers for Disease Control and Prevention. Centers for Disease Control and Prevention, 03 Oct. 2014. Web. 05 Oct. 2014. .

“Ebola Virus and Marburg Virus.” Causes. N.p., n.d. Web. 06 Oct. 2014. .

“Ebola Virus: Symptoms, Treatment, and Prevention.” WebMD. WebMD, n.d. Web. 05 Oct. 2014. .

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Home > Books > Emerging Challenges in Filovirus Infections

Essay on the Elusive Natural History of Ebola Viruses

Submitted: 15 April 2019 Reviewed: 29 July 2019 Published: 01 October 2019

DOI: 10.5772/intechopen.88879

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Emerging Challenges in Filovirus Infections

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This chapter presents a review of what is known about the natural history of the Ebolaviruses in Central and West Africa as well as in the Philippines. All the previous hypotheses on the natural cycle of Ebolavirus are revisited. Also, the main factors driving the virus natural cycle are summarized for the different ecosystems where the Ebolavirus is known to have emerged, including the virus species, the date of emergence, the seasonality, the environmental features, as well as the potential risk and associated factors of emergence. The proposed hypothesis of the Ebolavirus natural cycle prevails an inter-species spillover involving several vertebrate hosts, as well as biotic and abiotic changing environmental factors among other original features of a complex natural cycle. It is also compared with other virus having such type of cycle involving chiropteran as potential reservoir and vector and presenting such original inter-outbreak epidemiological silences. Ultimately, these observations and hypotheses on Ebolavirus natural cycles give some insight into the potential drivers of virus emergence, host co-evolution, and a spatiotemporal dimension of risk leading to identify high risk areas for preventing emerging events and be prepared for an early response.

  • natural cycle

Author Information

Jean-paul gonzalez *.

  • Division of Biomedical Graduate Research Organization, Department of Microbiology and Immunology, School of Medicine, Georgetown University, USA
  • Centaurus Biotech LLC, USA

Marc Souris

  • Institute of Research for Development (IRD), France

Massamba Sylla

  • Ministry of Health, Senegal

Francisco Veas

  • Faculty of Pharmacy, Montpellier University, France

Tom Vincent

  • CRDF Global, USA

*Address all correspondence to: [email protected]

1. Introduction

It has been several decades since an unknown fever dramatically emerged, close to the Ebola river, a small tributary of the great Ubangi river in the heart of the Congolese tropical forest of Africa. Since that time, even though the virus responsible for this new hemorrhagic fever has been identified and characterized, the natural history of the eponymic Ebolavirus remains largely unknown. The cradle of the virus remains enigmatic and the emergence of the Ebola fever unsolved. Indeed, the arcane of Ebolavirus natural history is still hypothesized, thanks to an elusive virus that always risen where it was not expected, violent and devastating, and surprising local populations and health systems, as well as the international scientific community. This Ebolavirus eco-epidemiology remains complex while the Ebola fever (alias Ebolavirus Disease) can be considered as an exemplary disease that can be eventually comprehended only with a transdisciplinary approach that has recently been promoted as a One Health concept. Indeed, it is only when we take into account all disease and virus drivers, including biotic and abiotic factors of the natural and human environments, that some mechanisms of the Ebolavirus disease emergence, such as spread and circulation, can be ultimately unveiled. For that, we have collected all information available, often estimated, from the time and place of the virus emergence long before the emerging event was identified as it and the epidemic phase was brought to public attention. Moreover, when available we also collect all data on potential natural and accidental hosts, weather and environment chorology, among other multiple factors potentially involved.

Historically, Ebolavirus emerged in Central Africa in the late 1970s, and has re-emerged most recently with the active epidemic (April 2019) in the eastern Democratic Republic of Congo (DRC), by encompassing more than 24 epidemic events from Central to West Africa, to imported infected monkey from Asia to Virginia, and the emerging new Ebola species of the Philippines archipelago [ 1 ].

Among the negative sense RNA viruses of the Filoviridae family five genera are known, including Cuevavirus, Ebolavirus, Marburgvirus , Thamnovirus . Among the Ebolavirus genus, five Ebolavirus (EBOV) species have been identified [ 2 ].

Ebolavirus’ (EBOV) first emergence occurred in 1976, as two different EBOV species in two different places in sub Saharan Africa. The Zaire Ebolavirus (ZEBOV) species and the Sudan Ebolavirus (SUDV) were detected concomitantly, a few weeks apart, respectively in the Northeastern Equator province of the Democratic Republic of Congo, DRC (alias Zaire), and in the Bahr el Ghazal province of South Sudan. On the 26th of August 1976 ZEBOV was isolated from missionaries and local villagers of the Yambuku, in the rain forest close to the Ebola river. However, earlier in June 1976, the SUDV had broken out among cotton factory workers in Nzara, Sudan (now in South Sudan) [ 3 ].

Then, in 1989, the Reston Ebolavirus species surprisingly (RESTV) emerged in the US (!) and was identified during an outbreak of simian hemorrhagic fever virus in crab-eating macaques from Hazleton Laboratories (now Covance) of Reston county, Virginia. Such primate specimens were found to be recently imported from the Philippines. Then, in 1994 a fourth new species of Ebolavirus was isolated from chimpanzee leaving in the Tai Forest of Côte d’Ivoire and named Côte d’Ivoire ebolavirus (CIEBOV). Finally, in November 2007, a fifth Ebolavirus species, was detected from infected patients in Uganda in the Bundibugyo District and was subsequently identified by the eponymic name of Bundibugyo Ebolavirus [ 4 ].

Briefly and extraordinarily among the world of the viruses, the filovirus virion presents a bacilliform (filamentous) shape, like a Rhabdovirus, but presents unique pleomorphic figures with branches and other tortuous shapes. Ebolaviruses have also an unusual and variable long length - up to 805 nanometers (only some plant virus can compete to this filamentous extensive length). However, the internal structure is more classical with a ribonucleoprotein nucleocapsid, a lipid envelope and seven nanometers size spikes. The genome is non-segmented, single stranded RNA of negative polarity with lengths of about 18.9 kb that code for seven proteins, each one having a specific function [ 5 ].

Ebolaviruses are known for their high case-fatality rate (CFR) with always less than 2/3 of survivors among the identified cases. ZEBOV, the most frequently isolated Ebolavirus species during the outbreaks, has the highest CFR, up to 90% in some instances, with an average of 83% for the past 37 years. The Uganda BDBV outbreak had a mortality rate of 34%. RESTV imported to the US did not cause disease in exposed human laboratory workers. The scientist performing the necropsies on CIEBOV infected chimpanzees got infected and developed a Dengue-like fever, fully recovered 6 weeks after the infection while treated in Switzerland.

2. When Ebolavirus raised his head in the heart of darkness

Dates and time make History. Indeed, the various reports on the emergence of Ebolavirus in Africa show discrepancies and lack accuracy, for multiple reasons (remote event, reports by different person or team, at different time…) but the only way to forge the history is to label the events with date, time and the environmental factors observed. On July 27, 1976, the first (known) victim to contract Ebolavirus was a cotton factory worker from Nzara, Sudan. Then, in Zaire (DRC) on September 1, 1976, the first Ebolavirus (Zaire ebolavirus, ZEBOV) victim was a teacher who had just returned from a family visit to northern Zaire (6 Jennifer Rosenberg Internet). These two events were the very beginning of the boundless journey of a deadly Ebolavirus outbreaks.

2.1 The Ebolavirus species emerging events

When the virus becomes epidemic in a human population, it does so weeks or months after the emergent event of the virus switching from its silent transmission in a natural cycle to a zoonotic/epidemic manifestation, revealed to the local health system. Let us see in more detail such emerging events of Ebolavirus species (ICTV, 2018) as there were reported or sometime interpreted, in time and place.

Sudan ebolavirus (SEBOV) occurred when the first recorded SUDV broke out among cotton factory workers in Nzara, South Sudan in June 271,976. This was indeed, the first case of Ebolavirus infection recorded and confirmed and also reported as potentially exposed to chiropteran. Indeed, at the Nzara Cotton Manufacturing Factory this first patient was a cloth room worker where bats (mostly Tadarida - mops - trevori ) have a large population in the roof space of their premises. He died in the Nzara hospital on July 6, 1976. Local animals and insects were tested for Ebolavirus without success [ 6 , 7 ].

Zaire ebolavirus (ZEBOV) was reported in the Mongala district of the Democratic Republic of Congo (DRC; alias Zaire) in August 1976, when a 44-year-old schoolteacher of the Yambuku village, became the first recorded case of Ebolavirus infection in DRC. Also, the schoolteacher travel earlier in August 1976 near the Central African Republic border and along the Ebola River, estimated 90 km NW from the village [ 6 ].

Reston ebolavirus (REBOV) had its first emerging event as an imported infected cynomolgus monkey ( Macaca fascicularis ) in October 1989 imported from a facility in the Philippines (Mindanao Island) to Reston, Virginia, USA, where the primate got sick and the virus isolated [ 8 ]. In the Philippines, in several instances, the virus was found to infect pigs, in June and September 2008 ill pigs were confirmed to be infested by REBOV (Ecija and Bulacan, Manila island), as well during 2008–2009 epizootics in the island of Luzon (Philippines) [ 9 ].

Cote d’Ivoire ebolavirus (CIEBOV) was isolated for the first time, and as an only known appearance, in November 1994, from wild chimpanzees presenting severe internal bleeding of the Taï Forest in Côte d’Ivoire, Africa. A researcher became infected when practicing a necropsy on one of these primates, he developed a dengue syndrome and survived. At that time, many dead chimpanzees were discovered and tested positive for Ebolavirus. However, the source of the virus was believed to be of infected western red colobus monkeys ( Piliocolobus badius ) upon which the chimpanzees preyed [ 10 ].

Bundibugyo ebolavirus (BDBV) was then discovered during an outbreak of Ebolavirus in the Bundibugyo District (Bundibugyo and Kikyo townships), on August 1st, 2007, in Western Uganda (Towner et al. [ 11 ]). BDBV second emerging event was observed in the DRC in August 17, 2012 in Isiro, Pawa and Dungu, districts of the Province Orientale [ 11 ].

With the exception of REBOV in Philippines and CIEBOV in West Africa, all other EBOVs species emerged in the Central African region. Also, all EBOVs are known to emerged in the tropical rain forest during the inter-season between dry and rainy seasons. Also, REBOV appears to actively circulate in the tropical rain or moist deciduous forest of the Philippines [ 12 ].

2.2 From Central Africa to West Africa

2.2.1 concurrent emergences of ebolaviruses.

On several occasions, concurrent emerging events of Ebolavirus have been observed. Indeed, such events occurred in places geographically distant, independent, and unconnected. The Ebolavirus was isolated and the strains different, even they belonged to the same species of Ebolavirus, altogether in favor of a different origin from an elusive natural reservoir, thus eliminating the notion of leaping from one site to the other. In that matter, the following observations are a paradigm: From its inceptive emergence the Ebolavirus was identified in Sudan at the cotton factory and a few days later at Yambuku, Zaire. The Ebola Sudan and Ebola Zaire viruses emerged concurrently in 1976 in the Congo basin of Central Africa; More than 20 years later the virus emerged and reemergence from 1994 to 1996 in a different places in Gabon, in a successive and timely overlapping events but in unconnected areas from where different strains of the same EBOVZ were isolated [ 13 ]; More recently, during the 2014–2016 dramatic Ebolavirus disease (EVD) emergence of in West Africa where the virus emerged in late December 2013 of a 18-month-old boy from the small village of Meliandou (Guéckédou district, South-Eastern Guinea) believed to have been infected by bats [ 14 ], concurrently, in August 2013, the Ebolavirus reemerged in the Equator province of DRC - different places and different strain of ZEBOV [ 15 ].

It is remarkable that most of these emerging events occurred during or close to the end of the rainy season which generally stretches from August to October in the domain of the Congo basin tropical rain forest.

Altogether, these observations are in favor of environmental factors of emergence favoring, when they occur synchronously in the same place, the spillover of the virus from its hidden natural cycle to an accidental and susceptible host. Therefore, these plural and concomitant emerging events play against the theory of Ebola virus diffusing in oil spot in Central Africa [ 16 ]. This original pattern of concurrent emergences could explain also the relative stability of the virus strains which remain for years in the same environment, and the interepidemic silences which require several fundamentals (i.e. concurrent risk factors) to be broken.

2.2.2 An unexpected broader domain of Ebolavirus circulation

The first evidence that showed that Ebola virus had previously circulated in areas without any known cases of disease came in 1977, near the Ebola outbreak in Tandala, DRC, just 200 miles west of the first known cases in 1976 [ 17 ]. Blood samples obtained from individuals in areas with no previous symptoms of Ebola were found to contain antibodies for Ebolavirus, indicating a previous or ongoing infection with that virus. Because subclinical illness is always a possibility with viral infections, the presence of these Ebolavirus-specific antibodies could only be explained by exposure to the virus, which is somewhat reasonable in an area that is endemic to the disease. But how do we know the true endemic zone of a virus such as Ebolavirus?

Endemic zones are primarily based on where disease can most likely be expected, and are determined by historical accounts of disease, as well as supplemental information such as where animals or insects that might transmit the disease are located. With respect to the Ebola virus, outbreaks that occur in Central Africa, in or near the Congo River Basin, are expected; outbreaks that take place elsewhere are unexpected and can be problematic, as was the case for the 2014–2016 West African outbreak. And yet, scientists have highlighted the presence of Ebola antibodies well outside the endemic zone for disease for decades.

In the early 1980’s, research based at the Pasteur Institute in Bangui, Central African Republic, demonstrated for the first time that the population of central Africa presented natural antibodies against the Ebolavirus strains of Zaire and Sudan [ 3 , 4 ]. Research also showed for the first time that several mammal species had Ebolavirus-reacting antibodies, including rodents, dogs, and others. Initially, the scientific community was skeptical of the findings, due to the type of antibody tests used, and because the prevalence of these antibodies was unbelievably dispersed and at a high level of prevalence. However, a 1989 follow-up study confirmed methodology and preliminary observations, and expanded the results to include similar observations in Cameroon, Chad, Gabon, and Republic of Congo (the latter two of these countries would have their first Ebola outbreaks in 1994 and 2001, respectively) [ 5 ]. Moreover, such Ebolavirus antibody prevalence was found in West Africa (e.g. Senegal, Chad, Sierra Leone), preceding the catastrophic 2014–2016 Ebolavirus outbreak [ 18 ]. Subsequent studies have determined that 20–25% of persons living in or near the Congolese rain forest are seropositive for Ebola, despite never exhibiting symptoms [ 19 ].

Today, Ebola antibody prevalence is widely distributed across the African continent in the absence of severe clinical presentation and/or outbreak manifestation. A 1989 study even found Ebola Zaire antibodies among people living in Madagascar, an island country that has never had a single known case of Ebola, and which has been geographically separated from continental Africa for 100 million years [ 20 ].

Risk mapping, including ecological and geographical distribution <10-13 cm/s first hour, and extended, highly sensitive and specific environmental and biogeographical models based on EBOVs susceptible mammalian biogeography in Africa, show a robust and precise potential distribution of EBOVs in Africa that clearly overlap the African tropical rain forest biome of the Guinea-Congo forests (including the Congo basin rain forest, and the Occidental relic of the Congolese rain forest spreading from Guinea to Ghana) and the southern band of the Sudan-Guinea Savanna [ 21 ].

Also, as a result of potential Ebolavirus (or Ebolavirus antigen) exposure, serological markers have been found in vertebrates outside of Africa. With the exception of Philippines, where REBOV is known to circulate in monkeys and pigs, thus showing its ability to infect multiple animal species, in several instances serological evidence of Ebolavirus exposure has been detected in many vertebrates, particularly chiropterans [ 9 ]. Definitely, bat populations in Bangladesh and China present antibodies against ZEBOV and REBOV proteins [ 22 , 23 ]. Ultimately, it appears that EBOVs are widely distributed throughout Africa, West and Central, and Asia. Moreover, risk mapping of filovirus ecologic niches suggests potential areas of EBOVs distribution in Southeast Asia [ 24 ].

The unexpected detection of REBOV first in Virginia, for the reason we know, and then the astonishing discovery of its circulation and natural cycle in the Philippines gave a rethinking of the entire family of Ebola viruses previously known mainly on the African continent [ 25 ].

From these observation and facts, the potential circulation of EBOVs in its natural cycle appears much wider than expected, while the emerging events we can witness appears to be only a tip of the iceberg in the wide Congolese tropical rain forest.

2.3 From the index case to the epidemic chain, outbreak, and pandemic

The fundamentals of emergence are changing in the heart of the rainforest and elsewhere: changing times, when the means of transmission switch from foot to motorbike, when knowledge conveyance has switched from paper reporting to the internet.

Let us examine the risk of expansion for Ebolavirus. Indeed, the factors of transmission of the virus to man and man to man are essential to take into account in this context. Moreover, it is extremely important to note that these factors are subject to permanent changes in societies whose trade and means of communication are drastically changing as a result of health systems, responses and preparedness for epidemics at national and international levels, policies, and the economy.

So, with the experience gained for more than 40 years, the strategies of struggle are clearly defined, but the societal changes that are taking place make their application difficult and sometimes impossible (e.g., the 2019 outbreak in the DRC, where political institutions have prevented an adapted response). Situation and the epidemic are perpetuated.

There is also a growing means of communication, both smartphones and motorized transport, to travel more quickly as ever, between the epidemic zone of EVD and the family [ 26 ].

Thus, during the emergence of the Ebola virus in West Africa, all of this means of communication played a fundamental role in the regional spread of the epidemic, until it became a pandemic risk when the virus was exported to other countries of the African continent and, outside Africa in Europe and North America [ 27 ].

3. A strange iteration of epidemic events with unexplained virus disappearance

It is known for several other transmitted viruses that during the inter-epidemic silences several factors can be responsible. In general mass herd immunity (natural of due to acquired immunization i.e. vaccine) of the permissive hosts force the virus in its natural cycle without apparent clinical manifestation in the hosts (e.g. Most by the arbovirus classically yellow fever, Dengue, Japanese encephalitis, West Nile, Zika etc.).

The Paramyxoviridae and Rhabdoviridae are the two other viral families in the order Mononegavirales, genetically closely related to the Filoviridae and having chiropteran as reservoir and/or vector [ 28 ]. Indeed, it is interesting to note that megachiropteran fruit bats are reservoirs of Hendra and Nipah viruses of the Paramyxoviridae family [ 29 ]. When, Microchiroptera bats are the probable ancestors of all rabies virus variants of the Lyssavirus genus in the family Rhabdoviridae and infecting presently terrestrial mammals [ 30 ]. Both also present this cryptic interepidemic silences that has not been yet clearly understood. The Nipah emerged one time in Malaysia (1999), thought to have its original cycle in PNG, and ultimately reemerged more than 3500 km away in Bangladesh in 2001. From its inception, again the Marburgvirus (the closest to EBOVs in the family of Filovirus), emerging events from an expected natural foci occurred within the path of time including 4 to 11 years of inter-epidemic silences occurring mostly in distant sites of Eastern and South Africa (Uganda, Zimbabwe, Angola, Kenya).

If one were to describe the history of Ebola outbreaks, one could simply construct a timeline, with a point on the line for each outbreak. You could create this timeline with a varying number of points, depending on your methodology, but regardless of how you built your timeline, there would be spaces between these points. This is due to the nature of Ebola; it appears, it disappears, and it appears again. To the Ebola virus, these gaps are periods of convalescence. To us, they are periods of absence and mystery, and one of these gaps stands out as the most mysterious ( Figure 1 ).

an expository essay on ebola virus

Timeline of Ebolavirus emergence. Emerging events (bars) red = EBOV; blue = SEBOV; green = BDBV; horizontal axis = years 1972–2018; vertical axis = no value. Numbers above brackets = years of silent inter-emerging event.

The CDC lists five Ebola outbreaks in the late 1970’s. The “first” Ebola outbreak took place in 1976, though we now recognize the event as two simultaneous and separate outbreaks. Between June and November 1976, 284 cases (151 deaths) of Ebola Sudan occurred near what is now Nzara, South Sudan; between September and October 1976, 318 cases (280 deaths) of Ebola Zaire occurred near what is now Yambuku, Democratic Republic of Congo (DRC). In November 1976, a researcher in England that was working with samples from the Nzara outbreak accidentally infected himself; CDC lists this accident as the third Ebola outbreak (the individual recovered). In June 1977, a child became sick and died from Ebola Zaire in Tandala, DRC though there was only one confirmed case, subsequent epidemiological investigations of the area uncovered several other historical, probable cases. Finally, between July and October 1979, 34 cases (22 deaths) of Ebola Sudan occurred, unbelievably, in Nzara, Sudan – the same community where the first cases of Ebola emerged just 3 years prior. In the span of just 39 months, the terror of Ebola had introduced itself to the world five times (638 cases, 454 deaths) and then… silence.

Ebola would not reappear for 10 whole years, and even then, the subtype was Ebola Reston, which we now know does not affect humans. Though CDC lists four Ebola Reston outbreaks between 1989 and 1992, the world would not see another case of Ebola virus disease in humans until late-1994, in Gabon. Even then, the outbreak (52 cases, 31 deaths) was mischaracterized as yellow fever for several months. Perhaps the virus’s long absence from the spotlight had removed it from the collective consciousness in 1994, certainly in the presence of those pathogens that had been circulating and consuming our attention in the meantime.

This fifteen-year disappearance of Ebola, particularly in light of its frequent and severe outbreaks in the late 1970’s, has perplexed researchers for decades. The mystery lay, to some extent, within the lack of complete knowledge of the virus reservoir, though scientists are now having their long-held suspicions in bats confirmed. It’s hard to detect disease when you cannot pinpoint the source. Surveillance and reporting have been another confounding element. How many times in that fifteen-year period was an illness misdiagnosed as yellow fever, dengue hemorrhagic fever, or some other similar illness, because of lack of knowledge or diagnostic capabilities, or simply because there was no health care around? We will probably never be able to answer this question. Finally, our perceived zone of endemicity at the time was limited to northern DRC and southern Sudan. Was the virus appearing elsewhere, unbeknownst to us? We certainly were not expecting it to emerge in Gabon in 1994, and Uganda in 2000, and West Africa in 2014 [ 31 ].

Scientists today continue to be perplexed by the emergence of the virus. What brings Ebola out from its hiding place? Is its emergence/re-emergence tied to climate change? globalization? the changing interface between humans and wildlife? If it has to do with any of these increasingly significant factors, how do they explain the fifteen-year disappearance?

These days, the virus comes and goes with some predictability—since 2000, outbreaks have approached a near-annual incidence, sometimes skipping a year, sometimes lasting more than a year. The periods between outbreaks are growing shorter. Is this because our capability to detect Ebola outbreaks is improving, or is the virus able to infect humans more frequently? One thing is for sure: the world knows that when one outbreak ends, another will eventually follow, and we need not wait 15 years.

4. Toward the discovery of the natural cycle of the Ebolaviruses

4.1 the discovery of a putative natural reservoir of ebolavirus.

Since the ZEBOV and SEBOV emergence, extended field studies have been conducted to discover the reservoir of EBOVs [ 32 ] including the 1976 first recorded DRC outbreaks and Sudan, the 1979 outbreak in DRC in 1979 and 1995 following the Kikwit outbreak, the same year in the Tai Forest and in 1999 in the Central African Republic [ 33 , 34 , 35 , 36 , 37 , 38 ] . A total of more than 7000 vertebrates and 30,000 invertebrates were sampled and tested for the presence of EBOVs. Limited finding was inconclusive for an potential EBOVs reservoir status among all these animals. Moreover, while several animal species (Bats, birds, reptiles, mollusks, arthropods, and plants) were experimentally infected with ZEBOV, only two fruit bat species ( Epomophorus spp. and Tadarida spp.) developed a subclinical transient viremia [ 39 ]. If these results were not confirmed in the natural settings, they indicated the potential for chiropteran to be natural for EBOVs [ 40 ].

Also, historically, the first documented case of EVD in Sudan in 1976, the index case was located (by the World Health Organization) in a cotton factory far from the forest block, where the only wild significantly abundant species was an insectivorous bat species [ 21 ].

Since the discovery of EBOV in 1976, more than half of the epidemic outbreaks caused by EBOVs have broken down between Gabon and the DRC. Following the successive EBOV outbreaks in Gabon from 1995 to 2001 affecting several animal species non-human primates, and wild ungulates and responsible of the dramatic decline of great apes (gorilla and chimpanzee) populations in the region (Leroy et al. [ 16 ]), researchers engaged several missions of captures of wild animals in the forest areas affected by the recent past epidemics. Also, 1030 animals were captured and analyzed, only three species of fruit bats were found infected with the ZEBOV by PCR including: Hypsignathus monstrosus ; Epomops franqueti; and Myonycteris torquata . Moreover, antibody reacting anti-Ebola were detected in these species as well as for the genus Myonycteris spp. leading ultimately to design Chiropteran as a potential reservoir of EBOVs [ 41 ].

Since then, many studies have converged in favor of the role of chiropters in maintaining EBOV in the wild (Caron et al. [ 42 ], Leendertz). In addition, a recent study of bats in Sierra Leone showed the association of an EBOV like with several species of bats ( Mops condylurus and Chaerephon pumilus ) from the Molossus family [ 43 ]. Moreover, a potential direct exposure to Ebola infected fruit bats was also reported as a putative index case of large epidemics [ 44 , 45 ]. Moreover, further studies reported on direct infection of natural hosts (primates) by EBOV infected bats as highly plausible, given that bats, especially fruit bats, are frequently hunted and consumed as bushmeat by human when Cercopithecus species hunt roosting bats for consumption [ 46 ] also preying on bats has been reported in Cercopithecus ascanius and C. mitis (East Africa) as well as bonobos (DRC) [ 47 ]. It is also possible that different modes of exposure to Ebola virus could lead to different antibody profiles, that is, contaminated fruit vs. contact with infected bats during hunting [ 44 , 47 , 48 ].

Altogether, several fruit bats ( Epomophorus wahlbergi ) and insectivorous bats ( Chaerephon pumilus, Mops condylurus ) experimentally survive to EBOV infections [ 39 ], EBOV RNA and/or anti EBOV reacting antibodies were detected also in several other fruit bat species ( Epomops franqueti, Hypsignathus monstrosus, Myonycteris torquata , Eidolon helvum, Epomophorus gambianus, Micropteropus pusillus, Mops condylurus, Rousettus aegyptiacus, Rousettus leschenaultia ) giving more insight of the potential for chiropteran to be a potential host or reservoir host of EBOVs [ 22 , 49 , 50 ].

Interestingly, REBOV was also found associated with the bats in its natural habitat of the Philippines [ 51 ]. Also, again in this same Filoviridae family, Marburg viruses in Africa are clearly associated with bats [ 32 , 52 ] as well as the Cueva virus in Europe [ 53 ]. While REBOV has been find associated with fruit bats, Roussetus spp. (Pteropodid family), each filovirus genus is associated with a specific chiropteran group including: Marburgvirus with a specific fruit bat, Roussetus aegyptiacus (Pteropodid family); and Cuevavirus with insectivorous bat, Miniopterus schreibersii (Miniopterid family); except for Thamnovirus isolated form fresh water fish.

Moreover, several virus groups are known to hold bat-borne viruses including the coronaviruses, hantaviruses, lyssaviruses, lassa virus, Henipavirus, filovirus which are among the most severe of the emerging viruses [ 54 , 55 ].

Conclusively, this was the first evidence of chiropteran as a potential reservoir and/or vector of EBOV, while several wild animals, in particular great apes were find highly sensitive to EBOV infection. Also, if several species of chiropteran have been identified as a potential virus reservoir,

4.2 The most complete figure of a putative Ebolavirus natural cycle in the central African raining forest

From all above observations, records and historical events of EBOVs emerging events, several fundamentals of emergence have been identified as well putative time and space of such events where, that is when the virus jump from the cryptic natural cycle of the reservoir-vector to manifest itself clearly as an open index case of infection in a susceptible host and the potential opening epizootic or epidemic chain.

4.2.1 The actors

Again, from the literature numerous vertebrates appears to be permissive to infection by EBOVs, however, due to their ethology, including environmental habits, societal structure, density and their ability of intra and interspecies to mingle. Altogether primates appear highly susceptible to EBOVs infection including non-human primate apes, gorilla and chimpanzee, but also cercopithecids (e.g. colobus) but also small wild ungulates (e.g. forest duikers) and eventually domestic animals (e.g. dogs) [ 32 , 56 , 57 , 58 ].

One can summarize that EBOVs natural hosts belongs to chiropteran as a potential host reservoir represented mostly by Pteropodidae in Africa (REBOV and Roussetus; Bombali virus and Molossidae), and as secondary natural or accidental wild and domestic hosts including several other mammals: primates (Colobus, Cercopithecus), non-human primates (Gorilla, chimpanzee), wild ungulates (duikers) and, human primates. Also this needs to be taken into account with respect to other permissive species to EBOVs, indeed, as an example, if Roussetus spp. was shown to carry EBOVs reacting antibodies more recently R. aegyptiacus bats were demonstrated to unlikely able to maintain and perpetuate EBOV in nature while the natural transmission of filovirus in R. aegyptiacus , resulting viral replication and shedding are unknown [ 59 ].

4.2.2 The stages

The African Rain forest of the Congolese basin appears to be the epicenter of EBOVs emerging events. More than 80% of the emerging events of EBOVs occurred in the Tropical zone under the influence of the (Intertropical converging zone, ITCZ) from five degree North to 5 degrees south and oscillating as much as 40 to 45° of latitude north or south of the equator based on the pattern of land and ocean beneath it [ 28 ] ( Figure 2 ).

an expository essay on ebola virus

Emerging events of Ebolavirus and climate since the Ebola fever inception in Africa. Left = annual rainfall; right = annual temperature. To illustrate the association temperature/rainfall and emergence, the month of May was chosen because it is at this time of the year that we observe the most emergent events of the Ebola virus. Temperature and rainfall are expressed as an annual average for the period under consideration. The precise location of 32 Ebola emergent events are here integrated into the global climatic map of Africa. Only 30-year average values per month of rainfall are available for the study period (ref.: WorldClim world databases) as well for the average monthly temperature.

Temperature and precipitation data for Africa (average data computed from 1960 to 1990, 300 m resolution [HIJ 05]) were integrated with the distribution map of the emergent events of the Ebola virus and the values ​​calculated for each of the emergence points [ 60 ].

On all emergence points, the temperature at the time of emergence is not significantly different from the average annual temperature over 30 years. The difference in temperature between the moment of emergence and the average temperature (of 30 years monthly average) of the hottest month does not show any difference either. Emergence would not be directly related to temperature.

When we compare Ebolavirus emerging events time and the rainfall, there is strict quantitative correlation between rainfall and emergence: Most of the emergent events (93.8%) occurred during the rainy season ( Figure 2 ). For precipitation values, there is a slightly statistically significant (p = 0.02) positive difference between the average precipitation of the month of emergence and the average of the monthly average precipitation (over 30 years), indicating that precipitations are higher when emergences occur. There is an even more statistically significant (p = 0.003) positive difference when considering precipitation of the month preceding the emergence. Emergence is therefore likely to be associated with rainfall intensity and the rainy season. 10/32 emergences occur at the beginning of the rainy season, 9/32 in the middle, and 11/32 at the end. Only 2/32 emergences occurred in the dry season.

When referring to land use ( Figure 3 ) the temperature at the 6 emergence points in “Cropland” is highly significantly less (p = 0.005) than 15% (21.6°C) at temperature (24.4°C) to the 9 points in “Tree cover, broadleaved, evergreen, closed to open”, however the average temperature of the Cropland (21.6°) is to a degree less, significantly lower (p = 0.01) than that of the “Tree cover” (24.5°C).

an expository essay on ebola virus

Environmental factors surrounding Ebolavirus emerging event: Land use and places of Ebola virus emergence in Africa from 1976 to 2014. Land use from ESA 2015, 300 m resolution; red circle = putative place of the Ebola virus emergence (index case). Estimated Ebola emergence places are superimposed on the land use layer. The identification of the land use types were 32 points (red circle) representing the putative places of Ebolavirus emergence are superimposed and are distributed as follows: (1) cropland: 6, (2) herbaceous cover: 5, (3) cropland mosaic: 5 (> 50% natural vegetation vs. <50% tree, shrub, herbaceous cover), (4) tree cover with: (a) 15% of broadleaved, evergreen, closed to open: 9, (b) 15–40% of broadleaved, deciduous, open: 2, (5) flooded, fresh or brackish water: 1, (6) urban areas: 3, and (7) water bodies: 1. The limitations of this interpretation are linked to the accuracy of the location of Ebolavirus emergence sites (from literature and reports) and, to the evolution of vegetation cover over the past decades since the first emergence of the Ebolavirus occurred in Africa.

Ultimately, taking into account these environmental factors, when we look for an association between the emergent events of the Ebola virus and the characteristics of the places of these emergences (i.e. land use, temperature, rainfall) it turns out that the emergences are always in the zone of heavy rainfall, but nevertheless do not follow the moving of the rainy season. Moreover, these emergences remain always and remarkably close enough to the Equator, therefore in the equatorial forest area with a high hygrometry, and a moderate annual temperature. However, the temperature at the time of emergence is not significantly different from the average annual temperature (at the points of emergence) which does not allow to distinguish seasonal effect in the emergence-temperature relationship. Conclusively, we did not identify a seasonality associated with the time of emergence, however the emerging events occur in specific geographic zone characterized by several environmental factors. Finally, the emergence zones are in areas of Land Use with specific temperatures not related to seasonality. Ultimately, it is also remarkable that all these emerging events occurred in an area with a highly potential presence of apes, virus-sensitive hosts.

4.2.3 Fundamentals and domains of emergence: a theory for a natural cycle of EBOVs in Africa

Also, the EBOVs species are closely genetically related, their seems to occur by foci in nature. The host appears to be the same, natural or accidental, and the transmission done by direct contact with infected hosts or its biological products [ 50 , 61 ]. Altogether, in the early 2000s, before the identification of chiropteran as a potential host-reservoir of the EBOVs, a hypothetic natural cycle was described empirically based on seasonal environmental climatic factors [ 55 ]. Then, taking into account bats as a potential reservoir-host, the question of virus transmission was central to consider while environmental factors appears to play a major role to the host and their natural cycle (Chiropteran physiology) (climate/fructification, chorology, bats physiology). Several factors of emergence were then listed including: Chronic infection, infected organs, virus shedding, close encounters between reservoir and susceptible hosts, food and water resource, seasonality, chorology (i.e. causal effect between geographical phenomena – season) in the tropical rain forest and the spatial distribution of chiropteran (i.e. index site of Ebola emerging events).

Epidemiological field surveys indicate that mass mortalities of apes and monkey species due to Ebola virus often appear at the end of the dry season, a period when food resources are scarce. Restricted access to a limited number of fruit-bearing trees can lead to spatiotemporal clustering of diverse species of frugivorous animals, such as bats, nonhuman primates, and other terrestrial species foraging on fallen partially eaten (by bats) fruits. These aggregates of wild animal species favor the contact between infected and susceptible individuals and promote virus transmission. The dry season aggregation of reservoir host species involved in natural maintenance cycles, augmented by incidentally infected secondary hosts serving as sources for intra- and interspecific transmission chains independent of repeated spillover from the reservoir host, provides an ecological setting for amplifying enzootic transmission of Ebola virus when a vertebrate hosts are concentrated around a scarce number of water sources [ 62 ].

In addition to this dietary impoverishment, there are behavioral and physiological events occurring among bats during the tropical dry favor the contact frequency and intimacy between bats, which can promote transmission of Ebola virus to others and increase R0. As an example, megachiropteran fruit bats breeding activities and intraspecific competitions between males and grouped kidding of females favor the contact between individuals. Moreover, pregnancy can involve physiological changes among female bats that alter immune functions and eventually favor virus shedding. Parturition among the African megachiropteran bats occurs throughout the year, although seasonal peaks provide birthing fluids, blood, and placental tissues, potentially Ebolavirus infected, falling on the ground as a medium highly attractive and readily available to scavenging terrestrial mammals [ 50 , 56 , 63 ] ( Figure 4A and B ).

an expository essay on ebola virus

(A) Understanding Ebolavirus enzootic and epidemics. Red arrows = cycles of transmission; dashed square = a putative natural cycle of Ebolavirus in Central Africa (see B). Fruit bats are considered to be a putative reservoir of Ebola virus in Central Africa after 2004; In 2009, several non-human primate epizootic are reported; 1976 was the first emerging events and subsequent epidemic chains in remote area of the rain forest and close by; 2012 showed a dramatic spread of the virus associated with motorized transportation and ground network; In 2014 urban epidemics are reported as well as a pandemic risk and become an international public health emergency. (B) Putative natural cycle of Ebolavirus in Central Africa. Red arrow indicates Ebolavirus transmission. Numbered red circle of transmission: (1) sylvatic inter- and intra-species transmission; (2) chiropteran migration; (3) chiropter to primate (close contact of dejection); (4) primate inter species (Cercopithecus/chimpanzee); (5) primate to primate (non-human primates); (6) non-human primate epizootic (gorillas); (7) chiropter to duikers; and (8) consumption of chiropteran infected food by shrew or wild pig.

5. If we had to conclude

Based on historical data and observations, the presented hypothesis of the natural cycle of Ebolavirus emergence prevail an inter-species spillover as the complex natural cycle involving several hosts (reservoir, vector, amplifier), as well as biotic and abiotic factors in a changing environment among other original features.

Although the natural cycle of EBOVs remains in the darkness of the rain forest, strong findings and comparative analysis of close parents of the filovirus throw some light to a potential natural cycle of EBOVs in Africa. EBOVs clearly appear linked to chiropteran and dependent for merging events in the environmental factors. Indeed, it appears that filoviridae are often associated with chiropteran while the emergence of the virus strains occurs as a sparse focus with a silent period of cryptic virus circulation. When virus transmission, i.e. spillover, from a hidden natural cycle, to accidental hosts occurs, it happened in a specific time-frame often linked to the season.

One can retain is that the EBOVs complex natural cycle is yet not on entirely elucidated and certainly dependent on environmental factors – associated with a specific environment of the chiropteran species incriminated (i.e. Different territories, different cycle) - leading to multiple, sometime concurrent, temporally and timely emergence in focus.

Although, other hypothesis has been suggested elsewhere including the Ebola virus Disease as an arthropod borne disease among others [ 42 ], there is important fundamental matters to consider as well before providing more.

However, beyond these hypotheses, fundamental questions subsist in order to go further learn. We can cite in particular the mystery of kin between the Reston virus of Asia and the Ebola viruses of Africa, would there not be a missing link in a geographic area yet to discover. Do the filovirus exist in the Americas hidden in the darkness of the tropical forest? Also, the Ebolavirus seems genetically stable, related to particular species of chiropter, was it to think about a co-evolution of the host and the virus in this closed environment of the forest of the tropical? Today, with the endless epidemic unfolding in the DRC, should we revisit our tools and strategy of struggle in an ever-changing world? [ 64 ].

Acknowledgments

We sincerely thank for their supports, brings to all the authors of this deep and never-ending research and scientific thought around an outstanding and fascinating subject: Georgetown University, Centaurus Biotech LLC., The DHS Emeritus Center for Emerging Zoonotic and Animal Diseases at Kansas State University.

Conflict of interest

All authors do not have any conflict of interest whatsoever with this published manuscript.

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  • 62. Shaman J, Day JF, Stieglitz M. Drought-induced amplification of Saint Louis encephalitis virus Florida. Emerging Infectious Diseases. 2002; 8 :575-580
  • 63. Pourrut X, Kumulungui B, Wittmann T, Moussavou G, Delicat A, Yaba P, et al. The natural history of Ebola virus in Africa. Microbes and Infection. 2005; 7 (7-8):1005-1014
  • 64. Gonzalez JP, Souris M, Valdivia-Granda W. Global spread of hemorrhagic fever viruses: Predicting pandemics. Methods in Molecular Biology. 2018; 1604 :3-31. DOI: 10.1007/978-1-4939-6981-4_1

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Essays About Ebola Virus

Ebola virus essay topics and outline examples, essay title 1: unmasking ebola: origins, transmission, and global response.

Thesis Statement: This essay provides an in-depth analysis of the Ebola virus, including its origins, modes of transmission, symptoms, and the global efforts in containing and managing Ebola outbreaks.

  • Introduction
  • Understanding Ebola: History, Types, and the Zaire Ebola Virus
  • Transmission and Symptoms: How Ebola Spreads and Its Impact on the Human Body
  • Outbreaks and Epidemics: Notable Ebola Outbreaks and Their Consequences
  • Global Response: International Organizations, Research, and Medical Interventions
  • Lessons Learned: Preparing for Future Ebola Outbreaks and Emerging Diseases
  • Conclusion: The Ongoing Battle Against Ebola and Infectious Disease Preparedness

Essay Title 2: Ebola's Socioeconomic Impact: Health Systems, Communities, and Resilience

Thesis Statement: This essay explores the broader socioeconomic implications of Ebola outbreaks, examining their impact on healthcare systems, affected communities, and the resilience strategies employed in response to the crisis.

  • Healthcare Infrastructure: Vulnerabilities and Challenges During Ebola Outbreaks
  • Community Resilience: Coping Strategies and Local Responses to Ebola
  • Economic Consequences: Impact on Livelihoods, Trade, and Economic Stability
  • Psychosocial Effects: Stigma, Trauma, and Mental Health Considerations
  • Global Aid and Assistance: International Support for Affected Regions
  • Recovery and Rebuilding: Post-Ebola Rehabilitation and Strengthening Systems
  • Conclusion: Beyond the Epidemic - Long-term Recovery and Strengthening Resilience

Essay Title 3: Ebola Vaccines and Therapeutics: Advances, Challenges, and Future Prospects

Thesis Statement: This essay delves into the development of Ebola vaccines and therapeutics, discussing recent advancements, challenges in deployment, and the potential for future innovations in combating Ebola.

  • The Race for a Vaccine: Historical Context and the Quest for Immunization
  • Therapeutics and Treatment: Experimental Drugs, Blood Plasma, and Supportive Care
  • Vaccine Development: Progress in Vaccine Trials and Their Efficacy
  • Challenges in Deployment: Ethical Considerations, Access, and Distribution
  • Future Prospects: Potential Innovations in Ebola Prevention and Treatment
  • Global Health Security: Ebola Preparedness and Pandemic Response
  • Conclusion: Advancing Science and Preparedness in the Fight Against Ebola

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  • Introduction

The Ebola virus is one of the most dangerous and deadly viruses known to humans. The Ebola epidemic since its discovery in 1976 came from the Democratic Republic of Congo, formerly known as Zaire, but the largest Ebola outbreak known to date is still ongoing at the time of writing, in the West Africa. An estimated 550 000 reported incidents from Sierra Leone and Liberia took place on January 20, 2015.

The virus is prevalent in many countries including Guinea, Liberia, Sierra Leone, Nigeria as well as occasional reported cases in the USA, Canada. The Netherlands and India show the potential for infection to spread globally. Despite the fact that the disease is highly contagious, life-threatening, and no specific treatment is available, it can be prevented through the use of appropriate measures to prevent and control infection. The study of the Ebola virus is important as such knowledge will pave the way for the reduction of victims, the development of an effective drug and will be useful in controlling the same epidemic.

The Ebola virus is a member of the Philoviridae family. As the name implies the virus has a filamentous shape. Marburg virus and Ebolavirus are two major generations of the virus family that are important in medicine. Bacteria of these two species are studied and presented together due to their many similarities in the life cycle, water storage areas, transmission methods, clinical presentation, treatment and prevention measures. The only difference is that Marburgvirus is still distributed by forest-dwelling bats such as the savannah while Ebolavirus is distributed by bats species accustomed to deep rain forests.

Five subspecies of Ebolavirus, namely, Ebolavirus Zaire, Ebolavirus Sudan, Ebolavirus reston, Ebolavirus cote d’Ivore, and Ebolavirus bugs, have been identified and named after the place where they were first discovered. Of these E. Zaire was the first to be isolated and studied and is responsible for a large number of outbreaks  including recent outbreaks in 2014 before that E. Sudan accounted for ¼ of all Ebolavirus deaths. With the exception of a slightly lower mortality rate, E. Sudan is almost identical to E. Zaire. E death rate of E case. Sudan is reported as 40-60% and E. Zaire as 60-90%.

Ebola was originally transmitted to humans as a zoonosis. Different species of bats are found throughout sub-Saharan Africa such as. Contact with bats by biting and scratching or exposure to their discharges and discharges through broken skin or mucous membranes can cause infection in humans. The infection can also be spread to other end users. Those recorded in Africa are deer, wildebeests, chimpanzees, chimpanzees, gorillas, monkeys, and other non-humans. Attacks during the hunting of these animals or handling carcasses of infected animals have led to the introduction of the virus to humans from the wild. Outbreaks appear to be exacerbated during pregnancy and in childbirth. Records show that outbreaks appear to be exacerbated by the presence of multiple pathogens.

EVD is highly contagious. Infection can be spread in the community and in a hospital setting by direct contact with infected body fluids such as blood, fluid and discharge or the patient’s tissues or by direct contact with contaminants such as clothing and bed linen. One of the main reasons for the rapid spread of the epidemic is traditional funeral rites, which include cadaver cleaning, removal of fingernails, toenails and clothing. Caregivers, including health workers, are also at greater risk of contracting the disease. In addition the sperm of the surviving male is said to remain infected for up to 82 days after the onset of symptoms. As long as the virus stays in the body fluids a person stays infected. The spread of the Ebola virus is highly suspected but has not been proven by experiments.

Clinical Introduction

EVD caused by different types of Ebola virus brings different clinical features. The incubation period of Ebola virus is generally considered to be 2 – 21 days. Ebola virus disease shows a variety of symptoms that develop deep in the prodromal constitution leading to various diagnoses including not only other viral hemorrhagic diseases, but also malaria, typhoid, cholera, and others. bacterial rickettsia and non-infectious causes of bleeding.

The onset of the disease is similar to that of severe hemorrhagic fever. Patients have high fever, fever reaching 39-400C, body aches and fatigue. Subsequent abdominal symptoms such as epigastric pain, vomiting and / or bloodless diarrhea appear if the fever persists throughout the day. 3-5.

After 4 – 5 days of illness macular degeneration may be visible but may not be clearly visible on dark skin. After this stage the bleeding from different areas begins. Bleeding in both the upper and lower digestive tract, the respiratory tract, the urinary tract, the vagina in women can be detected. Continuous petechial in the buccal mucosa, skin and conjunctivae grow. Repeated cleansing bumps that prevent any oral fluid intake and a large amount of wet diarrhea (five liters or more per day) contribute to the loss of excess fluid leading to dehydration. If fluid changes are not enough, bending, extreme fatigue and hypovolemic shock eventually.

Hypovolemic shock was reported in 60% of cases. Despite high body temperature, patients experience cold edges due to peripheral vasoconstriction. Rapid and cord pulses, tachypnea, oliguria or anuria can be detected. At the same time features such as asthma and abdominal pain, muscle and joint pain and headache increase. Although in some cases coughing and dyspnoea occur as a result of pulmonary haemorrhage, other respiratory symptoms are uncommon. Conjunctival injection is a common clinical feature. The most common neurologic symptoms are hypoactive and hyperactive delirium characterized by decreased mental function, confusion, dizziness and unusual tremors. As the disease changes the internal bleeding may also begin but more often by this time the patients are already in a coma.

It is reported that only 5% of patients have bleeding from the gastrointestinal tract before death. Most of the reported deaths occurred as a result of shock during the 7th to 12th day of illness. Symptoms of 40% of patients have improved by day 10 although symptoms such as mouth sores and thrush have already appeared. Most patients who survived until day 13 showed a high chance of finally recovering. Some patients who showed early improvement in symptoms have had stiff necks and reduced cognitive levels associated with late death.

Post-mortem examinations and post-mortem biopsies are very useful in the study of the pathology of the Ebola virus disease. Because of the biosafety risk in autopsy staff when handling models, pathological explanations of only a limited number of available conditions.

The most common findings of Haematoxylin and eosine-stained tissue components are oval-shaped or filamentous eosinophilic intracellular inclusions formed by a combination of viral nucleobases. These implants can be found in macrophages, hepatocytes, endothelial cells, fibroblasts of connective tissue etc. Immunohistochemically stains express viral antigens to various infected tissue cells including macrophages, dendritic cells, epithelial cells and sweat glands, intermediate cells and kidney tubes. , seminiferous tubes, endothelial cells and endocardial cells. In addition necrotic cells and cellular waste contain antigens in abundance. Electron microscopy shows an abundance of free viral particles in the alveolar glands, liver sinusoids, and connective tissue cells of the testis and dermal collagen. Karyorrhexis and apoptosis are found in portal triads cells, macrophages of the red spleen pulp and epithelial cells of the tubular kidneys.

Liver tissue exhibits histopathological symptoms including concentrated or widespread necrosis of hepatocytes and central steatosis. Although inflammation is usually mild, hyperplasia of kupfer cells and infiltration of mononuclear inflammatory cells is observed. The infected lung shows congestion, bleeding and intra-alveolar edoema but inflammation is not significant. Concentrated infiltration of mononuclear inflammatory cells is known to occur in the lamina propria of the small intestine and colon. Skin biopsies reveal dermal edoema, concentrated bleeding, petechiae, ecchymosis, and macular rashes. Spleen and lymph nodes show widespread lymphoid depletion due to apoptosis and necrosis. Inflammation of the kidneys is undetectable although acute tubular necrosis is more common. Even if the heart endocardium contains viral antigens, the myocardium does not show significant damage. Brain histology shows panencephalitis and perivascular infiltration of lymphocytes.

The World Health Organization (WHO) has recommended a set of measures to prevent and control infection in health workers, including safety measures to be taken in the various stages of EVD patient management.

1. General precautionary measures

Regardless of the disease, it is recommended that health professionals take precautionary measures when treating all patients, as it is difficult to diagnose EVD patients at the onset of the disease. These are,

2. Doing hand hygiene

Use disposable gloves before handling items that may be infected w ear eye protection and a coat before engaging in procedures that body fluids may predict.

3. Hand hygiene

Hand hygiene should be done using soap and water or an alcohol-based hand sanitizer solution, in accordance with WHO guidelines, before wearing gloves and protective equipment (PPE) after exposure to a patient’s body fluids after contact with a dirty area or equipment after extracting PPE. if the hands appear dirty.

4. Personal Protective Equipment (PPE)

PPE should be worn before entering EVD patient care facilities in accordance with the WHO-recommended order and removed before leaving the care facility. Contact with used PPE on any part of the face or fragile skin should be avoided. PPE covers,

  • Non-sterile gloves are the right size
  • Non-slip and long-sleeved dress
  • Face shield
  • Locked shoes that prevent piercing and intrusion

5. Patient placement and management

Suspected or certified EVD patients should be kept in isolation and if possible kept in a single room. Otherwise they must be placed in beds with a gap of at least 1m in between. Visitors should have no restrictions other than those necessary for the patient’s well-being as a parent.

Management of used equipment and other items

It is recommended that equipment such as stethoscopes be refined and disinfected before reuse, if different equipment is not available. Parental equipment, surgical blades, syringes and needles should not be reused. They should be discarded in barrels that are resistant to piercing. All solid non-solid waste should be disposed of in non-leaky bags or bins.

Used linen should be collected from non-perishable bags stored during use. They should be washed with water and detergent, rinsed, soaked in 0.05% chlorine for 30 minutes and then dried.

All barrels must remain upright and must be closed when ¾ is full. Before being removed from the wards the outer surfaces of these containers should be disinfected using 0.5% chlorine.

1. Clean the environment

Cleaners should wear heavy rubber gloves, and non-slip, non-slip rubber boots over PPE. Water and cleaning should be used to clean work areas and the floor of the hospital. This should be done at least once a day. Some dirty areas and contaminants should be cleaned and disinfected using 0.5% chlorine.

2. Biological management

Performing autopsies, post-mortem biopsies and other laboratory tests of certified EVD tissue samples or suspected patients should be minimized and should only be performed by qualified personnel. Full PPE should be worn during template handling. All specimens should be submitted with clearly marked, non-leaky, non-breakable containers, with an antiseptic exterior.

Carcasses should never be washed or embalmed. They should be sealed in two bags, disinfected with 0.5% chlorine and buried immediately. Some cultural and religious practices can be changed if necessary, but body care should be kept to a minimum and full PPE should be worn at all times.

3. In the case of exposure to infected body fluids

All current operations should be safe and dry immediately and PPE should be safely removed. Affected skin should be washed with soap and water and any affected pores such as conjunctiva should be washed with plenty of running water. The person should be tested for fever and other symptoms for 21 days.

4. Pathogenesis

The pathogenesis of the Ebola virus shows similarity to that of most other filo viruses that include immunosuppression, increased vascular permeability and coagulopathy. The Ebola virus enters the scrotum even through skin scratches, either through mucous membranes or by accidental injection. The virus enters monocytes, macrophages and dendritic cells and is carried by lymphatics to circulation. It then spreads to the liver and spleen to infect tissue macrophages and fibroblastic reticular cell. The main cellular targets of this virus are macrophages, dendritic cells and kupfer cells. The Ebola virus shows an interaction between a variety of cellular proteins which is why the infection is characterized by broad tissue and organ tropism.

5. Immunopathology

In many cases of the virus, the immune system plays a key role in controlling the spread of the virus. However the tissues and organs of the fatal EVD cases show less inflammation, which raises the damage to the immune response.

It has been found that the proteins of the structure of filo viruses e.g. VP24 (Virion protein) and VP35 inhibit interferon reactions and thus avoid the host’s natural defences. As previously mentioned, apoptosis of natural killer cells and T lymphocytes was revealed in histopathology describing the suppression of dynamic immune responses.

As with most complex phones, the Ebola virus infection also causes significant release of pro-inflammatory and vasoactive substances. Even if pro-inflammatory mediators promote inflammation and inflammation, the spread of the infection system is not effectively controlled. This is due to vasodilation connected by active ingredients.

6. Endothelial dysfunction and coagulopathy

The virus attacks endothelial cells and endocardial cells and causes injury (18). This causes internal bleeding, fluid and electrolyte imbalance and cardiovascular failure. Endothelial damage leads to platelet aggregation and use. The increased level of inflammatory factors and increased production of surface tissue factor protein in infected monocytes and macrophages promotes coagulation decay. As a result of hepatocellular damage the production of coagulation factors, fibrinogen, protein C and S also decreases. Other social and economic problems associated with the Ebola virus epidemic

In view of the current outbreak, in addition to the large number of lives that have been claimed by the disease, it has created many other serious problems not only in Ebola-affected countries, but also in other African countries.

Agriculture contributes significantly to the African economy. As more and more farmers die of the disease and many leave their farms for fear of contracting the disease, there is a severe shortage of workers in these countries and a decline in food production. The emergence of food shortages in the near future is predicted by experts.

Chocolate companies and many other industries are particularly affected by the shortage of workers. Nigeria and Ivory Coast are the largest cork producing countries but most of the workers are from Liberia and Guinea. International companies such as Nestle and Mars have introduced education and fundraising programs to prevent the spread of the virus to cork workers.

Many schools have been closed because of a deadly epidemic that has swept across the country. Apart from the impact on education, the child support system in government has stalled as a result.

Tourism is another area affected by the epidemic. Although Africa is a larger continent than Europe, the USA and China combined; visitors often see it as a single country since the Ebola epidemic broke out. For example, Tanzania, a popular wildlife sanctuary, is an East African country, located more than 6,000 miles from the Ebola-affected area. Tanzanian hotels reportedly lost 50% of bookings in 2015.

Many African countries refused to host international events and conferences because of the risk of the Ebola outbreak. For example, Morocco, the host of the Africa Cup of Nations, scheduled for January 2015, is calling for a postponement. The government says, “There is no way we can be serious about the health and safety of Moroccan citizens.”

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Ebola was first discovered 1976 in Africa, on the banks of the Ebola river, after which the virus has been named. Back then, there were two major outbreaks of the virus, and this is how people learned about it. There exist several strains of the Ebola virus, some of them are deadly to people, and some are not.

The main symptoms of Ebola can appear in a period between the second and the 21st days of contamination, but usually it happens on the eighth through 10th day (CDC). Among the symptoms that appear in the first turn, one should mention fever and chills, strong headaches, pain in joints and muscles, and general weakness. These symptoms are not too different from those that people usually experience when catching a severe cold, or flu, so victims may even ignore these symptoms, or try to treat them as a common sickness. However, as the virus keeps progressing, a patient develops nausea with vomiting, diarrhea, chest and stomach pains, red eyes and rashes over the body, severe weight loss, and bleeding from almost all bodily orifices (Mayo Clinic).

The virus is usually transmitted either through blood or through waste. Contagion through blood usually takes place if a person consumes infested meat, or even touches it (for example, butchering can also lead to contamination). Also, there were cases when people got infected after stepping in feces of infected mammals, mostly bats (Mayo Clinic). The other ways of getting infected is through skin by receiving bodily fluids through pores.

Even though there is no specific cure from Ebola, doctors still try to treat it. In order to diagnose Ebola, doctors usually take tests on such diseases as cholera or malaria, because it is difficult to diagnose Ebola based solely on symptoms. After the diagnosis has been made, doctors start treating the symptoms, which includes eliminating infected cells, electrolytes, blood pressure medication, blood transfusions, oxygen therapy, and so on (WebMD).

Though Ebola is a highly dangerous disease, it is not likely that it will spread globally. It is most deadly in anti-sanitary conditions, which many African countries are notorious for. As for first world countries, even though there is still no universal cure, they are at much lesser risk than African countries. Though the symptoms of Ebola are severe and getting infected is not difficult, with the correct handling of an outbreak, the virus should not be able to spread.

“Signs and Symptoms.” Centers for Disease Control and Prevention. Centers for Disease Control and Prevention, 03 Oct. 2014. Web. 05 Oct. 2014. .

“Ebola Virus and Marburg Virus.” Causes. N.p., n.d. Web. 06 Oct. 2014. .

“Ebola Virus: Symptoms, Treatment, and Prevention.” WebMD. WebMD, n.d. Web. 05 Oct. 2014. .

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Home > Books > Emerging Challenges in Filovirus Infections

Essay on the Elusive Natural History of Ebola Viruses

Submitted: 15 April 2019 Reviewed: 29 July 2019 Published: 01 October 2019

DOI: 10.5772/intechopen.88879

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Emerging Challenges in Filovirus Infections

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This chapter presents a review of what is known about the natural history of the Ebolaviruses in Central and West Africa as well as in the Philippines. All the previous hypotheses on the natural cycle of Ebolavirus are revisited. Also, the main factors driving the virus natural cycle are summarized for the different ecosystems where the Ebolavirus is known to have emerged, including the virus species, the date of emergence, the seasonality, the environmental features, as well as the potential risk and associated factors of emergence. The proposed hypothesis of the Ebolavirus natural cycle prevails an inter-species spillover involving several vertebrate hosts, as well as biotic and abiotic changing environmental factors among other original features of a complex natural cycle. It is also compared with other virus having such type of cycle involving chiropteran as potential reservoir and vector and presenting such original inter-outbreak epidemiological silences. Ultimately, these observations and hypotheses on Ebolavirus natural cycles give some insight into the potential drivers of virus emergence, host co-evolution, and a spatiotemporal dimension of risk leading to identify high risk areas for preventing emerging events and be prepared for an early response.

  • natural cycle

Author Information

Jean-paul gonzalez *.

  • Division of Biomedical Graduate Research Organization, Department of Microbiology and Immunology, School of Medicine, Georgetown University, USA
  • Centaurus Biotech LLC, USA

Marc Souris

  • Institute of Research for Development (IRD), France

Massamba Sylla

  • Ministry of Health, Senegal

Francisco Veas

  • Faculty of Pharmacy, Montpellier University, France

Tom Vincent

  • CRDF Global, USA

*Address all correspondence to: [email protected]

1. Introduction

It has been several decades since an unknown fever dramatically emerged, close to the Ebola river, a small tributary of the great Ubangi river in the heart of the Congolese tropical forest of Africa. Since that time, even though the virus responsible for this new hemorrhagic fever has been identified and characterized, the natural history of the eponymic Ebolavirus remains largely unknown. The cradle of the virus remains enigmatic and the emergence of the Ebola fever unsolved. Indeed, the arcane of Ebolavirus natural history is still hypothesized, thanks to an elusive virus that always risen where it was not expected, violent and devastating, and surprising local populations and health systems, as well as the international scientific community. This Ebolavirus eco-epidemiology remains complex while the Ebola fever (alias Ebolavirus Disease) can be considered as an exemplary disease that can be eventually comprehended only with a transdisciplinary approach that has recently been promoted as a One Health concept. Indeed, it is only when we take into account all disease and virus drivers, including biotic and abiotic factors of the natural and human environments, that some mechanisms of the Ebolavirus disease emergence, such as spread and circulation, can be ultimately unveiled. For that, we have collected all information available, often estimated, from the time and place of the virus emergence long before the emerging event was identified as it and the epidemic phase was brought to public attention. Moreover, when available we also collect all data on potential natural and accidental hosts, weather and environment chorology, among other multiple factors potentially involved.

Historically, Ebolavirus emerged in Central Africa in the late 1970s, and has re-emerged most recently with the active epidemic (April 2019) in the eastern Democratic Republic of Congo (DRC), by encompassing more than 24 epidemic events from Central to West Africa, to imported infected monkey from Asia to Virginia, and the emerging new Ebola species of the Philippines archipelago [ 1 ].

Among the negative sense RNA viruses of the Filoviridae family five genera are known, including Cuevavirus, Ebolavirus, Marburgvirus , Thamnovirus . Among the Ebolavirus genus, five Ebolavirus (EBOV) species have been identified [ 2 ].

Ebolavirus’ (EBOV) first emergence occurred in 1976, as two different EBOV species in two different places in sub Saharan Africa. The Zaire Ebolavirus (ZEBOV) species and the Sudan Ebolavirus (SUDV) were detected concomitantly, a few weeks apart, respectively in the Northeastern Equator province of the Democratic Republic of Congo, DRC (alias Zaire), and in the Bahr el Ghazal province of South Sudan. On the 26th of August 1976 ZEBOV was isolated from missionaries and local villagers of the Yambuku, in the rain forest close to the Ebola river. However, earlier in June 1976, the SUDV had broken out among cotton factory workers in Nzara, Sudan (now in South Sudan) [ 3 ].

Then, in 1989, the Reston Ebolavirus species surprisingly (RESTV) emerged in the US (!) and was identified during an outbreak of simian hemorrhagic fever virus in crab-eating macaques from Hazleton Laboratories (now Covance) of Reston county, Virginia. Such primate specimens were found to be recently imported from the Philippines. Then, in 1994 a fourth new species of Ebolavirus was isolated from chimpanzee leaving in the Tai Forest of Côte d’Ivoire and named Côte d’Ivoire ebolavirus (CIEBOV). Finally, in November 2007, a fifth Ebolavirus species, was detected from infected patients in Uganda in the Bundibugyo District and was subsequently identified by the eponymic name of Bundibugyo Ebolavirus [ 4 ].

Briefly and extraordinarily among the world of the viruses, the filovirus virion presents a bacilliform (filamentous) shape, like a Rhabdovirus, but presents unique pleomorphic figures with branches and other tortuous shapes. Ebolaviruses have also an unusual and variable long length - up to 805 nanometers (only some plant virus can compete to this filamentous extensive length). However, the internal structure is more classical with a ribonucleoprotein nucleocapsid, a lipid envelope and seven nanometers size spikes. The genome is non-segmented, single stranded RNA of negative polarity with lengths of about 18.9 kb that code for seven proteins, each one having a specific function [ 5 ].

Ebolaviruses are known for their high case-fatality rate (CFR) with always less than 2/3 of survivors among the identified cases. ZEBOV, the most frequently isolated Ebolavirus species during the outbreaks, has the highest CFR, up to 90% in some instances, with an average of 83% for the past 37 years. The Uganda BDBV outbreak had a mortality rate of 34%. RESTV imported to the US did not cause disease in exposed human laboratory workers. The scientist performing the necropsies on CIEBOV infected chimpanzees got infected and developed a Dengue-like fever, fully recovered 6 weeks after the infection while treated in Switzerland.

2. When Ebolavirus raised his head in the heart of darkness

Dates and time make History. Indeed, the various reports on the emergence of Ebolavirus in Africa show discrepancies and lack accuracy, for multiple reasons (remote event, reports by different person or team, at different time…) but the only way to forge the history is to label the events with date, time and the environmental factors observed. On July 27, 1976, the first (known) victim to contract Ebolavirus was a cotton factory worker from Nzara, Sudan. Then, in Zaire (DRC) on September 1, 1976, the first Ebolavirus (Zaire ebolavirus, ZEBOV) victim was a teacher who had just returned from a family visit to northern Zaire (6 Jennifer Rosenberg Internet). These two events were the very beginning of the boundless journey of a deadly Ebolavirus outbreaks.

2.1 The Ebolavirus species emerging events

When the virus becomes epidemic in a human population, it does so weeks or months after the emergent event of the virus switching from its silent transmission in a natural cycle to a zoonotic/epidemic manifestation, revealed to the local health system. Let us see in more detail such emerging events of Ebolavirus species (ICTV, 2018) as there were reported or sometime interpreted, in time and place.

Sudan ebolavirus (SEBOV) occurred when the first recorded SUDV broke out among cotton factory workers in Nzara, South Sudan in June 271,976. This was indeed, the first case of Ebolavirus infection recorded and confirmed and also reported as potentially exposed to chiropteran. Indeed, at the Nzara Cotton Manufacturing Factory this first patient was a cloth room worker where bats (mostly Tadarida - mops - trevori ) have a large population in the roof space of their premises. He died in the Nzara hospital on July 6, 1976. Local animals and insects were tested for Ebolavirus without success [ 6 , 7 ].

Zaire ebolavirus (ZEBOV) was reported in the Mongala district of the Democratic Republic of Congo (DRC; alias Zaire) in August 1976, when a 44-year-old schoolteacher of the Yambuku village, became the first recorded case of Ebolavirus infection in DRC. Also, the schoolteacher travel earlier in August 1976 near the Central African Republic border and along the Ebola River, estimated 90 km NW from the village [ 6 ].

Reston ebolavirus (REBOV) had its first emerging event as an imported infected cynomolgus monkey ( Macaca fascicularis ) in October 1989 imported from a facility in the Philippines (Mindanao Island) to Reston, Virginia, USA, where the primate got sick and the virus isolated [ 8 ]. In the Philippines, in several instances, the virus was found to infect pigs, in June and September 2008 ill pigs were confirmed to be infested by REBOV (Ecija and Bulacan, Manila island), as well during 2008–2009 epizootics in the island of Luzon (Philippines) [ 9 ].

Cote d’Ivoire ebolavirus (CIEBOV) was isolated for the first time, and as an only known appearance, in November 1994, from wild chimpanzees presenting severe internal bleeding of the Taï Forest in Côte d’Ivoire, Africa. A researcher became infected when practicing a necropsy on one of these primates, he developed a dengue syndrome and survived. At that time, many dead chimpanzees were discovered and tested positive for Ebolavirus. However, the source of the virus was believed to be of infected western red colobus monkeys ( Piliocolobus badius ) upon which the chimpanzees preyed [ 10 ].

Bundibugyo ebolavirus (BDBV) was then discovered during an outbreak of Ebolavirus in the Bundibugyo District (Bundibugyo and Kikyo townships), on August 1st, 2007, in Western Uganda (Towner et al. [ 11 ]). BDBV second emerging event was observed in the DRC in August 17, 2012 in Isiro, Pawa and Dungu, districts of the Province Orientale [ 11 ].

With the exception of REBOV in Philippines and CIEBOV in West Africa, all other EBOVs species emerged in the Central African region. Also, all EBOVs are known to emerged in the tropical rain forest during the inter-season between dry and rainy seasons. Also, REBOV appears to actively circulate in the tropical rain or moist deciduous forest of the Philippines [ 12 ].

2.2 From Central Africa to West Africa

2.2.1 concurrent emergences of ebolaviruses.

On several occasions, concurrent emerging events of Ebolavirus have been observed. Indeed, such events occurred in places geographically distant, independent, and unconnected. The Ebolavirus was isolated and the strains different, even they belonged to the same species of Ebolavirus, altogether in favor of a different origin from an elusive natural reservoir, thus eliminating the notion of leaping from one site to the other. In that matter, the following observations are a paradigm: From its inceptive emergence the Ebolavirus was identified in Sudan at the cotton factory and a few days later at Yambuku, Zaire. The Ebola Sudan and Ebola Zaire viruses emerged concurrently in 1976 in the Congo basin of Central Africa; More than 20 years later the virus emerged and reemergence from 1994 to 1996 in a different places in Gabon, in a successive and timely overlapping events but in unconnected areas from where different strains of the same EBOVZ were isolated [ 13 ]; More recently, during the 2014–2016 dramatic Ebolavirus disease (EVD) emergence of in West Africa where the virus emerged in late December 2013 of a 18-month-old boy from the small village of Meliandou (Guéckédou district, South-Eastern Guinea) believed to have been infected by bats [ 14 ], concurrently, in August 2013, the Ebolavirus reemerged in the Equator province of DRC - different places and different strain of ZEBOV [ 15 ].

It is remarkable that most of these emerging events occurred during or close to the end of the rainy season which generally stretches from August to October in the domain of the Congo basin tropical rain forest.

Altogether, these observations are in favor of environmental factors of emergence favoring, when they occur synchronously in the same place, the spillover of the virus from its hidden natural cycle to an accidental and susceptible host. Therefore, these plural and concomitant emerging events play against the theory of Ebola virus diffusing in oil spot in Central Africa [ 16 ]. This original pattern of concurrent emergences could explain also the relative stability of the virus strains which remain for years in the same environment, and the interepidemic silences which require several fundamentals (i.e. concurrent risk factors) to be broken.

2.2.2 An unexpected broader domain of Ebolavirus circulation

The first evidence that showed that Ebola virus had previously circulated in areas without any known cases of disease came in 1977, near the Ebola outbreak in Tandala, DRC, just 200 miles west of the first known cases in 1976 [ 17 ]. Blood samples obtained from individuals in areas with no previous symptoms of Ebola were found to contain antibodies for Ebolavirus, indicating a previous or ongoing infection with that virus. Because subclinical illness is always a possibility with viral infections, the presence of these Ebolavirus-specific antibodies could only be explained by exposure to the virus, which is somewhat reasonable in an area that is endemic to the disease. But how do we know the true endemic zone of a virus such as Ebolavirus?

Endemic zones are primarily based on where disease can most likely be expected, and are determined by historical accounts of disease, as well as supplemental information such as where animals or insects that might transmit the disease are located. With respect to the Ebola virus, outbreaks that occur in Central Africa, in or near the Congo River Basin, are expected; outbreaks that take place elsewhere are unexpected and can be problematic, as was the case for the 2014–2016 West African outbreak. And yet, scientists have highlighted the presence of Ebola antibodies well outside the endemic zone for disease for decades.

In the early 1980’s, research based at the Pasteur Institute in Bangui, Central African Republic, demonstrated for the first time that the population of central Africa presented natural antibodies against the Ebolavirus strains of Zaire and Sudan [ 3 , 4 ]. Research also showed for the first time that several mammal species had Ebolavirus-reacting antibodies, including rodents, dogs, and others. Initially, the scientific community was skeptical of the findings, due to the type of antibody tests used, and because the prevalence of these antibodies was unbelievably dispersed and at a high level of prevalence. However, a 1989 follow-up study confirmed methodology and preliminary observations, and expanded the results to include similar observations in Cameroon, Chad, Gabon, and Republic of Congo (the latter two of these countries would have their first Ebola outbreaks in 1994 and 2001, respectively) [ 5 ]. Moreover, such Ebolavirus antibody prevalence was found in West Africa (e.g. Senegal, Chad, Sierra Leone), preceding the catastrophic 2014–2016 Ebolavirus outbreak [ 18 ]. Subsequent studies have determined that 20–25% of persons living in or near the Congolese rain forest are seropositive for Ebola, despite never exhibiting symptoms [ 19 ].

Today, Ebola antibody prevalence is widely distributed across the African continent in the absence of severe clinical presentation and/or outbreak manifestation. A 1989 study even found Ebola Zaire antibodies among people living in Madagascar, an island country that has never had a single known case of Ebola, and which has been geographically separated from continental Africa for 100 million years [ 20 ].

Risk mapping, including ecological and geographical distribution <10-13 cm/s first hour, and extended, highly sensitive and specific environmental and biogeographical models based on EBOVs susceptible mammalian biogeography in Africa, show a robust and precise potential distribution of EBOVs in Africa that clearly overlap the African tropical rain forest biome of the Guinea-Congo forests (including the Congo basin rain forest, and the Occidental relic of the Congolese rain forest spreading from Guinea to Ghana) and the southern band of the Sudan-Guinea Savanna [ 21 ].

Also, as a result of potential Ebolavirus (or Ebolavirus antigen) exposure, serological markers have been found in vertebrates outside of Africa. With the exception of Philippines, where REBOV is known to circulate in monkeys and pigs, thus showing its ability to infect multiple animal species, in several instances serological evidence of Ebolavirus exposure has been detected in many vertebrates, particularly chiropterans [ 9 ]. Definitely, bat populations in Bangladesh and China present antibodies against ZEBOV and REBOV proteins [ 22 , 23 ]. Ultimately, it appears that EBOVs are widely distributed throughout Africa, West and Central, and Asia. Moreover, risk mapping of filovirus ecologic niches suggests potential areas of EBOVs distribution in Southeast Asia [ 24 ].

The unexpected detection of REBOV first in Virginia, for the reason we know, and then the astonishing discovery of its circulation and natural cycle in the Philippines gave a rethinking of the entire family of Ebola viruses previously known mainly on the African continent [ 25 ].

From these observation and facts, the potential circulation of EBOVs in its natural cycle appears much wider than expected, while the emerging events we can witness appears to be only a tip of the iceberg in the wide Congolese tropical rain forest.

2.3 From the index case to the epidemic chain, outbreak, and pandemic

The fundamentals of emergence are changing in the heart of the rainforest and elsewhere: changing times, when the means of transmission switch from foot to motorbike, when knowledge conveyance has switched from paper reporting to the internet.

Let us examine the risk of expansion for Ebolavirus. Indeed, the factors of transmission of the virus to man and man to man are essential to take into account in this context. Moreover, it is extremely important to note that these factors are subject to permanent changes in societies whose trade and means of communication are drastically changing as a result of health systems, responses and preparedness for epidemics at national and international levels, policies, and the economy.

So, with the experience gained for more than 40 years, the strategies of struggle are clearly defined, but the societal changes that are taking place make their application difficult and sometimes impossible (e.g., the 2019 outbreak in the DRC, where political institutions have prevented an adapted response). Situation and the epidemic are perpetuated.

There is also a growing means of communication, both smartphones and motorized transport, to travel more quickly as ever, between the epidemic zone of EVD and the family [ 26 ].

Thus, during the emergence of the Ebola virus in West Africa, all of this means of communication played a fundamental role in the regional spread of the epidemic, until it became a pandemic risk when the virus was exported to other countries of the African continent and, outside Africa in Europe and North America [ 27 ].

3. A strange iteration of epidemic events with unexplained virus disappearance

It is known for several other transmitted viruses that during the inter-epidemic silences several factors can be responsible. In general mass herd immunity (natural of due to acquired immunization i.e. vaccine) of the permissive hosts force the virus in its natural cycle without apparent clinical manifestation in the hosts (e.g. Most by the arbovirus classically yellow fever, Dengue, Japanese encephalitis, West Nile, Zika etc.).

The Paramyxoviridae and Rhabdoviridae are the two other viral families in the order Mononegavirales, genetically closely related to the Filoviridae and having chiropteran as reservoir and/or vector [ 28 ]. Indeed, it is interesting to note that megachiropteran fruit bats are reservoirs of Hendra and Nipah viruses of the Paramyxoviridae family [ 29 ]. When, Microchiroptera bats are the probable ancestors of all rabies virus variants of the Lyssavirus genus in the family Rhabdoviridae and infecting presently terrestrial mammals [ 30 ]. Both also present this cryptic interepidemic silences that has not been yet clearly understood. The Nipah emerged one time in Malaysia (1999), thought to have its original cycle in PNG, and ultimately reemerged more than 3500 km away in Bangladesh in 2001. From its inception, again the Marburgvirus (the closest to EBOVs in the family of Filovirus), emerging events from an expected natural foci occurred within the path of time including 4 to 11 years of inter-epidemic silences occurring mostly in distant sites of Eastern and South Africa (Uganda, Zimbabwe, Angola, Kenya).

If one were to describe the history of Ebola outbreaks, one could simply construct a timeline, with a point on the line for each outbreak. You could create this timeline with a varying number of points, depending on your methodology, but regardless of how you built your timeline, there would be spaces between these points. This is due to the nature of Ebola; it appears, it disappears, and it appears again. To the Ebola virus, these gaps are periods of convalescence. To us, they are periods of absence and mystery, and one of these gaps stands out as the most mysterious ( Figure 1 ).

an expository essay on ebola virus

Timeline of Ebolavirus emergence. Emerging events (bars) red = EBOV; blue = SEBOV; green = BDBV; horizontal axis = years 1972–2018; vertical axis = no value. Numbers above brackets = years of silent inter-emerging event.

The CDC lists five Ebola outbreaks in the late 1970’s. The “first” Ebola outbreak took place in 1976, though we now recognize the event as two simultaneous and separate outbreaks. Between June and November 1976, 284 cases (151 deaths) of Ebola Sudan occurred near what is now Nzara, South Sudan; between September and October 1976, 318 cases (280 deaths) of Ebola Zaire occurred near what is now Yambuku, Democratic Republic of Congo (DRC). In November 1976, a researcher in England that was working with samples from the Nzara outbreak accidentally infected himself; CDC lists this accident as the third Ebola outbreak (the individual recovered). In June 1977, a child became sick and died from Ebola Zaire in Tandala, DRC though there was only one confirmed case, subsequent epidemiological investigations of the area uncovered several other historical, probable cases. Finally, between July and October 1979, 34 cases (22 deaths) of Ebola Sudan occurred, unbelievably, in Nzara, Sudan – the same community where the first cases of Ebola emerged just 3 years prior. In the span of just 39 months, the terror of Ebola had introduced itself to the world five times (638 cases, 454 deaths) and then… silence.

Ebola would not reappear for 10 whole years, and even then, the subtype was Ebola Reston, which we now know does not affect humans. Though CDC lists four Ebola Reston outbreaks between 1989 and 1992, the world would not see another case of Ebola virus disease in humans until late-1994, in Gabon. Even then, the outbreak (52 cases, 31 deaths) was mischaracterized as yellow fever for several months. Perhaps the virus’s long absence from the spotlight had removed it from the collective consciousness in 1994, certainly in the presence of those pathogens that had been circulating and consuming our attention in the meantime.

This fifteen-year disappearance of Ebola, particularly in light of its frequent and severe outbreaks in the late 1970’s, has perplexed researchers for decades. The mystery lay, to some extent, within the lack of complete knowledge of the virus reservoir, though scientists are now having their long-held suspicions in bats confirmed. It’s hard to detect disease when you cannot pinpoint the source. Surveillance and reporting have been another confounding element. How many times in that fifteen-year period was an illness misdiagnosed as yellow fever, dengue hemorrhagic fever, or some other similar illness, because of lack of knowledge or diagnostic capabilities, or simply because there was no health care around? We will probably never be able to answer this question. Finally, our perceived zone of endemicity at the time was limited to northern DRC and southern Sudan. Was the virus appearing elsewhere, unbeknownst to us? We certainly were not expecting it to emerge in Gabon in 1994, and Uganda in 2000, and West Africa in 2014 [ 31 ].

Scientists today continue to be perplexed by the emergence of the virus. What brings Ebola out from its hiding place? Is its emergence/re-emergence tied to climate change? globalization? the changing interface between humans and wildlife? If it has to do with any of these increasingly significant factors, how do they explain the fifteen-year disappearance?

These days, the virus comes and goes with some predictability—since 2000, outbreaks have approached a near-annual incidence, sometimes skipping a year, sometimes lasting more than a year. The periods between outbreaks are growing shorter. Is this because our capability to detect Ebola outbreaks is improving, or is the virus able to infect humans more frequently? One thing is for sure: the world knows that when one outbreak ends, another will eventually follow, and we need not wait 15 years.

4. Toward the discovery of the natural cycle of the Ebolaviruses

4.1 the discovery of a putative natural reservoir of ebolavirus.

Since the ZEBOV and SEBOV emergence, extended field studies have been conducted to discover the reservoir of EBOVs [ 32 ] including the 1976 first recorded DRC outbreaks and Sudan, the 1979 outbreak in DRC in 1979 and 1995 following the Kikwit outbreak, the same year in the Tai Forest and in 1999 in the Central African Republic [ 33 , 34 , 35 , 36 , 37 , 38 ] . A total of more than 7000 vertebrates and 30,000 invertebrates were sampled and tested for the presence of EBOVs. Limited finding was inconclusive for an potential EBOVs reservoir status among all these animals. Moreover, while several animal species (Bats, birds, reptiles, mollusks, arthropods, and plants) were experimentally infected with ZEBOV, only two fruit bat species ( Epomophorus spp. and Tadarida spp.) developed a subclinical transient viremia [ 39 ]. If these results were not confirmed in the natural settings, they indicated the potential for chiropteran to be natural for EBOVs [ 40 ].

Also, historically, the first documented case of EVD in Sudan in 1976, the index case was located (by the World Health Organization) in a cotton factory far from the forest block, where the only wild significantly abundant species was an insectivorous bat species [ 21 ].

Since the discovery of EBOV in 1976, more than half of the epidemic outbreaks caused by EBOVs have broken down between Gabon and the DRC. Following the successive EBOV outbreaks in Gabon from 1995 to 2001 affecting several animal species non-human primates, and wild ungulates and responsible of the dramatic decline of great apes (gorilla and chimpanzee) populations in the region (Leroy et al. [ 16 ]), researchers engaged several missions of captures of wild animals in the forest areas affected by the recent past epidemics. Also, 1030 animals were captured and analyzed, only three species of fruit bats were found infected with the ZEBOV by PCR including: Hypsignathus monstrosus ; Epomops franqueti; and Myonycteris torquata . Moreover, antibody reacting anti-Ebola were detected in these species as well as for the genus Myonycteris spp. leading ultimately to design Chiropteran as a potential reservoir of EBOVs [ 41 ].

Since then, many studies have converged in favor of the role of chiropters in maintaining EBOV in the wild (Caron et al. [ 42 ], Leendertz). In addition, a recent study of bats in Sierra Leone showed the association of an EBOV like with several species of bats ( Mops condylurus and Chaerephon pumilus ) from the Molossus family [ 43 ]. Moreover, a potential direct exposure to Ebola infected fruit bats was also reported as a putative index case of large epidemics [ 44 , 45 ]. Moreover, further studies reported on direct infection of natural hosts (primates) by EBOV infected bats as highly plausible, given that bats, especially fruit bats, are frequently hunted and consumed as bushmeat by human when Cercopithecus species hunt roosting bats for consumption [ 46 ] also preying on bats has been reported in Cercopithecus ascanius and C. mitis (East Africa) as well as bonobos (DRC) [ 47 ]. It is also possible that different modes of exposure to Ebola virus could lead to different antibody profiles, that is, contaminated fruit vs. contact with infected bats during hunting [ 44 , 47 , 48 ].

Altogether, several fruit bats ( Epomophorus wahlbergi ) and insectivorous bats ( Chaerephon pumilus, Mops condylurus ) experimentally survive to EBOV infections [ 39 ], EBOV RNA and/or anti EBOV reacting antibodies were detected also in several other fruit bat species ( Epomops franqueti, Hypsignathus monstrosus, Myonycteris torquata , Eidolon helvum, Epomophorus gambianus, Micropteropus pusillus, Mops condylurus, Rousettus aegyptiacus, Rousettus leschenaultia ) giving more insight of the potential for chiropteran to be a potential host or reservoir host of EBOVs [ 22 , 49 , 50 ].

Interestingly, REBOV was also found associated with the bats in its natural habitat of the Philippines [ 51 ]. Also, again in this same Filoviridae family, Marburg viruses in Africa are clearly associated with bats [ 32 , 52 ] as well as the Cueva virus in Europe [ 53 ]. While REBOV has been find associated with fruit bats, Roussetus spp. (Pteropodid family), each filovirus genus is associated with a specific chiropteran group including: Marburgvirus with a specific fruit bat, Roussetus aegyptiacus (Pteropodid family); and Cuevavirus with insectivorous bat, Miniopterus schreibersii (Miniopterid family); except for Thamnovirus isolated form fresh water fish.

Moreover, several virus groups are known to hold bat-borne viruses including the coronaviruses, hantaviruses, lyssaviruses, lassa virus, Henipavirus, filovirus which are among the most severe of the emerging viruses [ 54 , 55 ].

Conclusively, this was the first evidence of chiropteran as a potential reservoir and/or vector of EBOV, while several wild animals, in particular great apes were find highly sensitive to EBOV infection. Also, if several species of chiropteran have been identified as a potential virus reservoir,

4.2 The most complete figure of a putative Ebolavirus natural cycle in the central African raining forest

From all above observations, records and historical events of EBOVs emerging events, several fundamentals of emergence have been identified as well putative time and space of such events where, that is when the virus jump from the cryptic natural cycle of the reservoir-vector to manifest itself clearly as an open index case of infection in a susceptible host and the potential opening epizootic or epidemic chain.

4.2.1 The actors

Again, from the literature numerous vertebrates appears to be permissive to infection by EBOVs, however, due to their ethology, including environmental habits, societal structure, density and their ability of intra and interspecies to mingle. Altogether primates appear highly susceptible to EBOVs infection including non-human primate apes, gorilla and chimpanzee, but also cercopithecids (e.g. colobus) but also small wild ungulates (e.g. forest duikers) and eventually domestic animals (e.g. dogs) [ 32 , 56 , 57 , 58 ].

One can summarize that EBOVs natural hosts belongs to chiropteran as a potential host reservoir represented mostly by Pteropodidae in Africa (REBOV and Roussetus; Bombali virus and Molossidae), and as secondary natural or accidental wild and domestic hosts including several other mammals: primates (Colobus, Cercopithecus), non-human primates (Gorilla, chimpanzee), wild ungulates (duikers) and, human primates. Also this needs to be taken into account with respect to other permissive species to EBOVs, indeed, as an example, if Roussetus spp. was shown to carry EBOVs reacting antibodies more recently R. aegyptiacus bats were demonstrated to unlikely able to maintain and perpetuate EBOV in nature while the natural transmission of filovirus in R. aegyptiacus , resulting viral replication and shedding are unknown [ 59 ].

4.2.2 The stages

The African Rain forest of the Congolese basin appears to be the epicenter of EBOVs emerging events. More than 80% of the emerging events of EBOVs occurred in the Tropical zone under the influence of the (Intertropical converging zone, ITCZ) from five degree North to 5 degrees south and oscillating as much as 40 to 45° of latitude north or south of the equator based on the pattern of land and ocean beneath it [ 28 ] ( Figure 2 ).

an expository essay on ebola virus

Emerging events of Ebolavirus and climate since the Ebola fever inception in Africa. Left = annual rainfall; right = annual temperature. To illustrate the association temperature/rainfall and emergence, the month of May was chosen because it is at this time of the year that we observe the most emergent events of the Ebola virus. Temperature and rainfall are expressed as an annual average for the period under consideration. The precise location of 32 Ebola emergent events are here integrated into the global climatic map of Africa. Only 30-year average values per month of rainfall are available for the study period (ref.: WorldClim world databases) as well for the average monthly temperature.

Temperature and precipitation data for Africa (average data computed from 1960 to 1990, 300 m resolution [HIJ 05]) were integrated with the distribution map of the emergent events of the Ebola virus and the values ​​calculated for each of the emergence points [ 60 ].

On all emergence points, the temperature at the time of emergence is not significantly different from the average annual temperature over 30 years. The difference in temperature between the moment of emergence and the average temperature (of 30 years monthly average) of the hottest month does not show any difference either. Emergence would not be directly related to temperature.

When we compare Ebolavirus emerging events time and the rainfall, there is strict quantitative correlation between rainfall and emergence: Most of the emergent events (93.8%) occurred during the rainy season ( Figure 2 ). For precipitation values, there is a slightly statistically significant (p = 0.02) positive difference between the average precipitation of the month of emergence and the average of the monthly average precipitation (over 30 years), indicating that precipitations are higher when emergences occur. There is an even more statistically significant (p = 0.003) positive difference when considering precipitation of the month preceding the emergence. Emergence is therefore likely to be associated with rainfall intensity and the rainy season. 10/32 emergences occur at the beginning of the rainy season, 9/32 in the middle, and 11/32 at the end. Only 2/32 emergences occurred in the dry season.

When referring to land use ( Figure 3 ) the temperature at the 6 emergence points in “Cropland” is highly significantly less (p = 0.005) than 15% (21.6°C) at temperature (24.4°C) to the 9 points in “Tree cover, broadleaved, evergreen, closed to open”, however the average temperature of the Cropland (21.6°) is to a degree less, significantly lower (p = 0.01) than that of the “Tree cover” (24.5°C).

an expository essay on ebola virus

Environmental factors surrounding Ebolavirus emerging event: Land use and places of Ebola virus emergence in Africa from 1976 to 2014. Land use from ESA 2015, 300 m resolution; red circle = putative place of the Ebola virus emergence (index case). Estimated Ebola emergence places are superimposed on the land use layer. The identification of the land use types were 32 points (red circle) representing the putative places of Ebolavirus emergence are superimposed and are distributed as follows: (1) cropland: 6, (2) herbaceous cover: 5, (3) cropland mosaic: 5 (> 50% natural vegetation vs. <50% tree, shrub, herbaceous cover), (4) tree cover with: (a) 15% of broadleaved, evergreen, closed to open: 9, (b) 15–40% of broadleaved, deciduous, open: 2, (5) flooded, fresh or brackish water: 1, (6) urban areas: 3, and (7) water bodies: 1. The limitations of this interpretation are linked to the accuracy of the location of Ebolavirus emergence sites (from literature and reports) and, to the evolution of vegetation cover over the past decades since the first emergence of the Ebolavirus occurred in Africa.

Ultimately, taking into account these environmental factors, when we look for an association between the emergent events of the Ebola virus and the characteristics of the places of these emergences (i.e. land use, temperature, rainfall) it turns out that the emergences are always in the zone of heavy rainfall, but nevertheless do not follow the moving of the rainy season. Moreover, these emergences remain always and remarkably close enough to the Equator, therefore in the equatorial forest area with a high hygrometry, and a moderate annual temperature. However, the temperature at the time of emergence is not significantly different from the average annual temperature (at the points of emergence) which does not allow to distinguish seasonal effect in the emergence-temperature relationship. Conclusively, we did not identify a seasonality associated with the time of emergence, however the emerging events occur in specific geographic zone characterized by several environmental factors. Finally, the emergence zones are in areas of Land Use with specific temperatures not related to seasonality. Ultimately, it is also remarkable that all these emerging events occurred in an area with a highly potential presence of apes, virus-sensitive hosts.

4.2.3 Fundamentals and domains of emergence: a theory for a natural cycle of EBOVs in Africa

Also, the EBOVs species are closely genetically related, their seems to occur by foci in nature. The host appears to be the same, natural or accidental, and the transmission done by direct contact with infected hosts or its biological products [ 50 , 61 ]. Altogether, in the early 2000s, before the identification of chiropteran as a potential host-reservoir of the EBOVs, a hypothetic natural cycle was described empirically based on seasonal environmental climatic factors [ 55 ]. Then, taking into account bats as a potential reservoir-host, the question of virus transmission was central to consider while environmental factors appears to play a major role to the host and their natural cycle (Chiropteran physiology) (climate/fructification, chorology, bats physiology). Several factors of emergence were then listed including: Chronic infection, infected organs, virus shedding, close encounters between reservoir and susceptible hosts, food and water resource, seasonality, chorology (i.e. causal effect between geographical phenomena – season) in the tropical rain forest and the spatial distribution of chiropteran (i.e. index site of Ebola emerging events).

Epidemiological field surveys indicate that mass mortalities of apes and monkey species due to Ebola virus often appear at the end of the dry season, a period when food resources are scarce. Restricted access to a limited number of fruit-bearing trees can lead to spatiotemporal clustering of diverse species of frugivorous animals, such as bats, nonhuman primates, and other terrestrial species foraging on fallen partially eaten (by bats) fruits. These aggregates of wild animal species favor the contact between infected and susceptible individuals and promote virus transmission. The dry season aggregation of reservoir host species involved in natural maintenance cycles, augmented by incidentally infected secondary hosts serving as sources for intra- and interspecific transmission chains independent of repeated spillover from the reservoir host, provides an ecological setting for amplifying enzootic transmission of Ebola virus when a vertebrate hosts are concentrated around a scarce number of water sources [ 62 ].

In addition to this dietary impoverishment, there are behavioral and physiological events occurring among bats during the tropical dry favor the contact frequency and intimacy between bats, which can promote transmission of Ebola virus to others and increase R0. As an example, megachiropteran fruit bats breeding activities and intraspecific competitions between males and grouped kidding of females favor the contact between individuals. Moreover, pregnancy can involve physiological changes among female bats that alter immune functions and eventually favor virus shedding. Parturition among the African megachiropteran bats occurs throughout the year, although seasonal peaks provide birthing fluids, blood, and placental tissues, potentially Ebolavirus infected, falling on the ground as a medium highly attractive and readily available to scavenging terrestrial mammals [ 50 , 56 , 63 ] ( Figure 4A and B ).

an expository essay on ebola virus

(A) Understanding Ebolavirus enzootic and epidemics. Red arrows = cycles of transmission; dashed square = a putative natural cycle of Ebolavirus in Central Africa (see B). Fruit bats are considered to be a putative reservoir of Ebola virus in Central Africa after 2004; In 2009, several non-human primate epizootic are reported; 1976 was the first emerging events and subsequent epidemic chains in remote area of the rain forest and close by; 2012 showed a dramatic spread of the virus associated with motorized transportation and ground network; In 2014 urban epidemics are reported as well as a pandemic risk and become an international public health emergency. (B) Putative natural cycle of Ebolavirus in Central Africa. Red arrow indicates Ebolavirus transmission. Numbered red circle of transmission: (1) sylvatic inter- and intra-species transmission; (2) chiropteran migration; (3) chiropter to primate (close contact of dejection); (4) primate inter species (Cercopithecus/chimpanzee); (5) primate to primate (non-human primates); (6) non-human primate epizootic (gorillas); (7) chiropter to duikers; and (8) consumption of chiropteran infected food by shrew or wild pig.

5. If we had to conclude

Based on historical data and observations, the presented hypothesis of the natural cycle of Ebolavirus emergence prevail an inter-species spillover as the complex natural cycle involving several hosts (reservoir, vector, amplifier), as well as biotic and abiotic factors in a changing environment among other original features.

Although the natural cycle of EBOVs remains in the darkness of the rain forest, strong findings and comparative analysis of close parents of the filovirus throw some light to a potential natural cycle of EBOVs in Africa. EBOVs clearly appear linked to chiropteran and dependent for merging events in the environmental factors. Indeed, it appears that filoviridae are often associated with chiropteran while the emergence of the virus strains occurs as a sparse focus with a silent period of cryptic virus circulation. When virus transmission, i.e. spillover, from a hidden natural cycle, to accidental hosts occurs, it happened in a specific time-frame often linked to the season.

One can retain is that the EBOVs complex natural cycle is yet not on entirely elucidated and certainly dependent on environmental factors – associated with a specific environment of the chiropteran species incriminated (i.e. Different territories, different cycle) - leading to multiple, sometime concurrent, temporally and timely emergence in focus.

Although, other hypothesis has been suggested elsewhere including the Ebola virus Disease as an arthropod borne disease among others [ 42 ], there is important fundamental matters to consider as well before providing more.

However, beyond these hypotheses, fundamental questions subsist in order to go further learn. We can cite in particular the mystery of kin between the Reston virus of Asia and the Ebola viruses of Africa, would there not be a missing link in a geographic area yet to discover. Do the filovirus exist in the Americas hidden in the darkness of the tropical forest? Also, the Ebolavirus seems genetically stable, related to particular species of chiropter, was it to think about a co-evolution of the host and the virus in this closed environment of the forest of the tropical? Today, with the endless epidemic unfolding in the DRC, should we revisit our tools and strategy of struggle in an ever-changing world? [ 64 ].

Acknowledgments

We sincerely thank for their supports, brings to all the authors of this deep and never-ending research and scientific thought around an outstanding and fascinating subject: Georgetown University, Centaurus Biotech LLC., The DHS Emeritus Center for Emerging Zoonotic and Animal Diseases at Kansas State University.

Conflict of interest

All authors do not have any conflict of interest whatsoever with this published manuscript.

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  • v.8(7); 2019 Jul

Ebola virus: A global public health menace: A narrative review

Shamimul hasan.

1 Department of Oral Medicine and Radiology, Faculty of Dentistry, Jamia Millia Islamia, New Delhi, India

Syed Ansar Ahmad

2 Department of Oral Surgery, Faculty of Dentistry, Jamia Millia Islamia, New Delhi, India

Rahnuma Masood

3 Department of Conservative Dentistry, Faculty of Dentistry, Jamia Millia Islamia, New Delhi, India

Shazina Saeed

4 Department of Amity Institute of Public Health, Amity University, Noida, Uttar Pradesh, India

Ebola virus disease (EVD), a fatal viral hemorrhagic illness, is due to infection with the Ebola virus of the Filoviridae family. The disease has evolved as a global public health menace due to a large immigrant population. Initially, the patients present with nonspecific influenza-like symptoms and eventually terminate into shock and multiorgan failure. There exists no specific treatment protocol for EVD and only supportive and symptomatic therapy is the line of treatment. This review article provides a detailed overview of the Ebola virus; it's clinical and oral manifestations, diagnostic aids, differential diagnosis, preventive aspects, and management protocol.

Ebola, earlier termed as Ebola hemorrhagic fever (EHF), is a critically lethal ailment which primarily affects the humans and nonhuman primates. Ebola virus disease (EVD) occurs due to a virus infection which belongs to the family Filoviridae and genus Ebolavirus .[ 1 ] EVDs has posed diagnostic challenges and has been a universal public health threat since its discovery. While investigating an alleged yellow fever case, Dr. Peter Piot in the year 1976 first detected the disease in Zaire, Africa (presently the Democratic Republic of Congo).[ 2 ] The name “Ebola” was termed as the disease was noticed near the Ebola river in Congo.[ 3 ]

Fruit bats of Pteropodidae family, such as Hypsignathus monstrous, Epomops franqueti , and Myonycteris torquata serve as the natural hosts of the EBOV in Africa. Nonhuman primates may develop the infection by eating the partly eaten fruits and may also transmit the infection to humans.[ 4 ] Indian population is an impending threat to EVD, as India falls in the home range of Pteropodidae family of fruit bats.[ 5 ]

Ebola virus transmission primarily takes place through close bodily contact with the infected patient or their fluids, contaminated tissue surfaces, and clothing from alive, infected or deceased individuals. Unsafe traditional burial practices also play a pivotal role in the disease transmission.[ 6 ] There is documented evidence regarding the sexual mode of disease transmission, although transmission through the air is unlikely.[ 7 ]

EVD present with bizarre and atypical manifestations mimicking other viral diseases, especially in the initial disease phase. Constitutional symptoms, such as fever, myalgia, headache, vomiting, and diarrhea are the early presenting features. Hemorrhagic rash, internal and external bleeding are usually the warning manifestations in the late stages.[ 8 ] Bleeding from the body apertures is a distinguishing EVD manifestation.[ 9 ] Gum bleeding, odynophagia, and atypical oral manifestations constitute the oral features of EVD.[ 10 ]

Till date, there is no precise antiviral management or vaccination for EVD. The management protocol mainly relies on supportive and symptomatic therapy, along with monitoring coagulopathies and multiorgan dysfunction.[ 2 ]

The World Health Organization (WHO) affirmed the EVD outbreak as a “Public Health Emergency of International Concern” on August 8 th , 2014.[ 5 ]

With the enormous immigrant population, India is estimating the likelihood of a probable EVD outbreak. The Ministry of Health and Family Welfare, Government of India, in collaboration with other agencies has appraised the situation and recommended travel instructions by air, land, and sea and health care professionals.[ 11 ]

The virus belongs to the Ebola virus genus, Filoviridae family, and Mononegavirales order.[ 12 ] The genus Ebolavirus includes the following species- Zaire ebolavirus (EBOV), Reston ebolavirus (RESTV), Bundibugyo ebolavirus (BDBV), Taï Forest ebolavirus (TAFV), Sudan ebolavirus (SUDV), and the newly identified Bombali ebolavirus (BOMV).[ 13 ] Except for exclusive identification of RESTV in the Philippines, all the other species causes endemic West African EVD.[ 14 ]

EBOV responsible for the EHF causes the highest human mortality (57%–90%), followed by SUDV (41%–65%) and Bundibugyo virus (40%). TAFV has caused only two nonlethal human infections to date, whereas RESTV causes asymptomatic human infections.[ 15 ]

Figure 1 shows the taxonomy of Ebola virus.

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Taxonomy of Ebola virus

Transmission

Based on the Centers for Disease Control and Prevention (CDC) classification, Ebola virus is considered as a biosafety level 4 and category A bioterrorism pathogen with an immense likelihood for massive nationwide transmission.[ 16 ]

Source of Infection

Intimate physical contact with the patients in the acute disease stages and contact with the blood/fluids from the dead individuals constitutes the most important modes of transmission.[ 17 ]

The long-established funeral ceremonies in the African countries entail direct handling of the dead bodies, thus significantly contributing to the disease dissemination. Unsafe conventional burial procedures accounted for 68% infected cases in 2014 EVD outburst of Guinea.[ 18 ]

EBOV RNA may be identified for up to a month in rectal, conjunctival, and vaginal discharges and semen specimens may demonstrate the virus presence up to 3 months, thus signifying the presence of EBOV in recuperating patients.[ 14 ] The sexually transmitted case of EVD has been reported between a convalescent patient and close family member. Another study demonstrated a case in a recuperating male patient. The patient's semen specimen tested positive with Ebola viral antigen almost 3 months after the disease onset.[ 19 ]

Asymptomatic EBOV carriers are not infectious and do not have a major role play in the EVD outburst, and the field practice in Western Africa supported this assumption.[ 20 ] However, this presumption was refuted after the documentation of a pioneer asymptomatic carrier case in North Gabon epidemic (1996).[ 21 ]

EBOV has been detected from blood, saliva, semen, and breast milk, while RNA has been isolated from sweat, tears, stool, and on the skin, vaginal, and rectal swabs, thus highlighting that exposure to infected blood and bodily secretions constitute the major means of dissemination.[ 22 ]

Eating uncooked infected animal meat such as bats or chimpanzees account significantly to oral EVD transmission, especially in the African countries.[ 23 ] The demonstration of the Ebola virus in the Filipino pigs in 2008 triggered the likelihood of an extensive range of possible animal hosts.[ 24 ]

EVD dissemination has also been reported with hospital-acquired infections, particularly in areas with poor hygiene conditions. The infected needles usage was responsible for the 1976 EVD outbreak in Sudan and Zaire.[ 25 , 26 ] Improper hygiene and sterilization were the crucial factors for the 1967 Yambuku EVD outburst.[ 27 ]

EVD dissemination may also occur through the inanimate materials with infected body secretions (fomites).[ 19 ] However, disease transmission through the airborne and droplet infection is ambiguous.[ 10 ]

Figure 2 shows the primary and secondary transmission of disease.

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Primary and secondary transmission

Table 1 depicts the possible routes of transmission.

Possible routes of transmission

Epidemiology

The vast majority of EVD cases and outbursts have been endemic to African continent ever since the disease detection in 1976,[ 28 ] and 36 such outbreaks have occurred in six African countries.[ 29 ]

Table 2 shows Ebola epidemiological outbreaks between 1976 and 2014.

Ebola outbreaks between 1976 and 2014 (Adapted from WHO 2014)

UVRI: Uganda Virus Research Institute; CDC: Centers for Disease Control and Prevention

The 2014–2016 EVD started in South East Guinea rural surroundings and eventually became a global public health menace by rapidly disseminating to urban localities and other countries.[ 28 ]

Figure 3 depicts the geographical distribution of Ebola virus disease.

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Geographic distribution of Ebola virus disease outbreaks

The conducive environmental surroundings of the African continent facilitate EVD endemicity. However, intermittent imported Ebola cases have also been noticed in United States, United Kingdom, Canada, Spain, and Thailand.[ 30 , 31 ]

Figure 4 depicts the distribution of Ebola virus disease in West African Countries.

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Distribution of Ebola virus disease in West African Countries

Out of the unparalleled globally reported 28,616 cases and 11,310 casualties, Liberia accounted for almost 11,000 cases and over 4,800 deaths.[ 32 ]

Table 3 shows the statistics of the 2014–16 West African outbreak.

Statistics of 2014-16 West African outbreak

Pathogenesis

Ebola viruses penetrate the human body through mucous membranes, skin lacerations/tear, close contact with infected patients/corpse, or by direct parental dissemination.[ 33 ] EBOV has a predilection to infect various cells of immune system (dendritic cells, monocytes, and macrophages), endothelial and epithelial cells, hepatocytes, and fibroblasts where it actively replicates by gene modulation and apoptosis and demonstrate significantly high viremia.[ 34 ] The virus reaches the regional lymph nodes causing lymphadenopathy and hematogenous spread to the liver and spleen promote an active inflammatory response.[ 35 ] Release of chemical mediators of inflammation (cytokines and chemokines) causes a dysregulated immune response by disrupting the vasculature system harmony, eventually causing disseminated intravascular coagulation and multiple organ dysfunction.[ 36 ]

Figure 5 demonstrates the pathogenesis of Ebola virus disease.

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Pathogenesis of Ebola virus disease

Clinical Features

Due to the bizarre and atypical manifestations in the initial phase, mimicking dengue fever, typhoid fever, malaria, meningococcemia, and other bacterial infections, EVD poses diagnostic dilemmas.[ 37 ]

The incubation period ranges from 2 to 21 days. However, symptoms usually develop 8–11 days following infection.[ 38 , 39 ]

The initial disease phase is represented by constitutional symptoms.[ 40 ] High-grade fever of >38 o C is the most frequently reported symptom (85–95%), followed by other vague symptoms such as general malaise (85–95%), headaches (52–74%), dysphagia, sore throat (56–58%), and dry cough.[ 41 , 42 ] The progressively advanced disease is accompanied by abdominal pain (62–68%), myalgia (50–79%), nausea, vomiting, and diarrhea (84–86%).[ 41 ]

Variety of hemorrhagic manifestations forms an integral component of the late disease phase.[ 38 ] Gastrointestinal tract bleeding manifests as petechiae, hematuria, melena, conjunctival bleeding, contusion, or intraperitoneal bleeding. Mucous membrane and venipuncture site bleeding, along with excess clot formation may also occur. As the features advances with time, the patients experience dehydration, confusion, stupor, hypotension, and multiorgan dysfunction, resulting in fulminant shock and ultimately death.[ 43 , 44 ]

Maculopapular exanthema constitutes a characteristic manifestation of all Filovirus infection, including EVD.[ 45 ] The rash usually appears during the 5 th to 7 th day of disease and occur in 25–52% of patients in the past EVD outbreaks.[ 46 ]

Table 4 shows the clinical manifestations of Ebola virus disease.

Clinical manifestations of Ebola virus disease

Although EVD has a number of similar features with other viral hemorrhagic fevers (e.g. dengue), there are differences that set them apart.

Table 5 depicts the differentiating features of the Ebola virus and dengue virus infection.

Differentiating features of Ebola and dengue virus infection

Orofacial features

Gum bleeding, atypical mucosal lesions, and odynophagia comprise the distinctive oral manifestations. Epistaxis (nasal bleed), bleeding from venipuncture sites, conjunctivitis, and cutaneous exanthema are the other manifestations.[ 9 ] Bleeding tendencies and gum bleeding is not seen in asymptomatic or initial EBOV patients reporting to the dental hospital.

EVD dissemination in the field of oral and dental health may appear nonsignificant; although, probable situations which may pose a risk to dental health professional have been appraised by Samaranayake et al. [ 21 ] and Galvin et al. [ 10 ]

Table 6 depicts the various orofacial manifestations of Ebola virus disease

Orofacial manifestations of Ebola virus disease

EVD patients usually demonstrate altered laboratory parameters based on the stage of the disease.

Table 7 shows the laboratory findings in Ebola virus disease.

Laboratory findings in Ebola virus disease

The WHO (2014) recommended the sample collection of whole blood or oral swab at suitable centres called Ebola treatment centers.[ 47 ] Reverse transcriptase polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) are the most frequently utilized tests for laboratory affirmation of the EVD.[ 43 ] RT-PCR is capable of detecting viral RNA in the blood samples of infected patients immediately after the commencement of signs and symptoms,[ 42 , 48 ] has a high sensitivity (up to 100%), and gives results within 1–2 days in cases of epidemics. ELISA detects the immunoglobulins G and M in samples of infected patients, has a low sensitivity (91%) and is not suitable for initial affirmation during an outbreak.[ 42 , 49 ]

The most imperative strategy in EVD is to avert the vulnerable population from getting infected and limit the transmission. These preventive strategies entail intensive and rigorous endeavors from the Government, public health amenities, medical units, and personals.[ 50 ]

The most essential aspect to curb EVD transmission is to avert direct bodily contact with infected individuals and their body fluids.[ 51 ]

Health caregivers are extremely vulnerable and experience an augmented professional threat for EVD.[ 52 ] Thus, scrupulous adherence to the universal infection control measures is fundamental in all the hospitals, laboratories, and other health care services.[ 53 ] The U.S. CDC has advocated the appropriate use of various personal protective equipment as a mandate for health care professionals.[ 50 ]

The risk of rapid importation of Ebola virus into human beings can be prevented by averting the direct bush meat and bats contact.[ 54 ]

Unsafe traditional burial procedures, especially in the African continent significantly contributed to the EVD transmission. Hence, it is essential to practice safe and guarded funeral rituals to prevent the disease spread.[ 55 ]

WHO recommends the implementation of safe sex practices to combat the sexual transmission of EVD. Strict abstinence or proper and regular condom use in male EVD survivors at least for a period of 12 months of the symptom onset or until their semen has twice tested negative should be followed.[ 56 ]

Dental health care personals are extremely susceptible to EVD as they are in regular contact with blood and saliva during the routine diagnostic procedures. There is no documented case of EVD through saliva till date. A study on the identification of EBOV in oral fluids affirmed that patients presenting with demonstrable serum levels of EBOV RNA also exhibit identifiable salivary levels.[ 57 ] The incubation period for all body fluids including saliva is 21 days; hence, oral health personals are vulnerable to develop the disease if universal infection control protocol is not followed.[ 58 ]

Table 8 demonstrates the various infection control measures to prevent the Ebola virus spread.

Infection control measures to prevent Ebola virus spread

Box 1 shows the travel guidelines to EBOV affected regions.

Shows the UK Travel guidelines to EBV infested regions.

Till date, there is no precise antiviral management or vaccination for EVD.[ 51 ] The management protocol mainly relies on supportive and symptomatic therapy. Public health strategies emphasizing on epidemiological surveillance, contact tracing, and quarantine of the patient have been recommended to combat the dissemination of EVD.[ 59 ]

Rehydration, adequate nourishment, analgesics, and blood transfusion form a keystone supportive treatment of EVD patient.[ 60 ] Intravenous fluids and oral rehydration solution endow with proper electrolytes substitute and maintain the intravascular volume. Unrelenting vomiting and diarrhea are taken care of by the use of antiemetics and antidiarrheal drugs.[ 35 , 60 , 61 ] Suspected cases of secondary bacterial infections and septicemia are best managed by the use of prophylactic antibiotic regimen (third generation I.V. cephalosporins).[ 62 ] Concurrent parasitic coinfections may also be seen and require prompt investigations and management.[ 63 ]

A number of investigative clinical trials emphasizing on the development of vaccine, antibody therapies, and antiviral drugs have been conducted for EVD.[ 64 ]

Table 9 shows experimental treatment for Ebola virus disease.

Experimental treatment for Ebola virus disease

Various clinical trials in Africa, Europe, and the United States suggest that Ebola vaccines are in various development stages (Phase I–III). A number of candidate vaccines employ diverse platforms, including recombinant viral vectors (most evolved vaccine candidate), DNA vaccines, inactivated viral particles, subunit proteins, recombinant proteins, and virus-like particles. Example of viral vectors expressing ebolavirus glycoproteins include recombinant simian adenovirus (cAd3), recombinant vaccinia virus, recombinant human adenovirus (Ad26), and a live vesicular stomatitis virus used alone or in prime-booster regimens.[ 65 ]

However, Ebola virus having the glycosylated surface proteins and preferentially infecting the immune cells impedes the development of an effective vaccine.[ 66 ]

Dental Management

Dental health care professionals in Europe have not encountered a case of EVD so far. However, health care personals (including dental surgeons) are more prone to EVD while treating patients in West or sub-Saharan Africa. Dental professionals are more likely to encounter asymptomatic EVD patients or those with early-stage vague symptoms.[ 27 ]

Individuals with a travel history to Ebola endemic regions, but with no direct intimate contact with the disease fall in the low-risk category and may undergo any medical/dental health care procedures without restrictions. However, all the nonessential procedures should be postponed for 21 days in individuals with direct exposure to the virus. The regional Health Service Executive Department of Public Health needs to be notified when the exposed patient's treatment cannot be deferred or controlled with pharmacotherapy.[ 10 ]

EVD has emerged as a significant global public health menace due to multiple disease outbreaks in the last 25 years. Recent advancements are being carried out in the form of effective Ebola virus vaccine and anti-Ebola virus drugs. However, rapid geographic dissemination, nonspecific clinical presentation, lack of vaccine, and specific diagnostic test are the possible challenges to combat this dreaded public health menace.

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Essays About Ebola Virus

Ebola virus essay topics and outline examples, essay title 1: unmasking ebola: origins, transmission, and global response.

Thesis Statement: This essay provides an in-depth analysis of the Ebola virus, including its origins, modes of transmission, symptoms, and the global efforts in containing and managing Ebola outbreaks.

  • Understanding Ebola: History, Types, and the Zaire Ebola Virus
  • Transmission and Symptoms: How Ebola Spreads and Its Impact on the Human Body
  • Outbreaks and Epidemics: Notable Ebola Outbreaks and Their Consequences
  • Global Response: International Organizations, Research, and Medical Interventions
  • Lessons Learned: Preparing for Future Ebola Outbreaks and Emerging Diseases
  • Conclusion: The Ongoing Battle Against Ebola and Infectious Disease Preparedness

Essay Title 2: Ebola's Socioeconomic Impact: Health Systems, Communities, and Resilience

Thesis Statement: This essay explores the broader socioeconomic implications of Ebola outbreaks, examining their impact on healthcare systems, affected communities, and the resilience strategies employed in response to the crisis.

  • Healthcare Infrastructure: Vulnerabilities and Challenges During Ebola Outbreaks
  • Community Resilience: Coping Strategies and Local Responses to Ebola
  • Economic Consequences: Impact on Livelihoods, Trade, and Economic Stability
  • Psychosocial Effects: Stigma, Trauma, and Mental Health Considerations
  • Global Aid and Assistance: International Support for Affected Regions
  • Recovery and Rebuilding: Post-Ebola Rehabilitation and Strengthening Systems
  • Conclusion: Beyond the Epidemic - Long-term Recovery and Strengthening Resilience

Essay Title 3: Ebola Vaccines and Therapeutics: Advances, Challenges, and Future Prospects

Thesis Statement: This essay delves into the development of Ebola vaccines and therapeutics, discussing recent advancements, challenges in deployment, and the potential for future innovations in combating Ebola.

  • The Race for a Vaccine: Historical Context and the Quest for Immunization
  • Therapeutics and Treatment: Experimental Drugs, Blood Plasma, and Supportive Care
  • Vaccine Development: Progress in Vaccine Trials and Their Efficacy
  • Challenges in Deployment: Ethical Considerations, Access, and Distribution
  • Future Prospects: Potential Innovations in Ebola Prevention and Treatment
  • Global Health Security: Ebola Preparedness and Pandemic Response
  • Conclusion: Advancing Science and Preparedness in the Fight Against Ebola

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an expository essay on ebola virus

Here you have an Expository Essay on Ebola Virus, Lets start with the introduction. Introduction. The Ebola virus is one of the most dangerous and deadly viruses known to humans. The Ebola epidemic since its discovery in 1976 came from the Democratic Republic of Congo, formerly known as Zaire, but the largest Ebola outbreak known to date is still ongoing at the time of writing, in the West Africa.

Free example of expository essay about Ebola virus: Ebola was first discovered 1976 in Africa, on the banks of the Ebola river, after which the virus has been named... AI Tools; Writing; Text editing; Coding; ... More from Expository Essay Examples and Samples. Nov 23 2023. Why Is Of Mice And Men Banned. 5 min read. Nov 07 2023. Pride and ...

This chapter presents a review of what is known about the natural history of the Ebolaviruses in Central and West Africa as well as in the Philippines. All the previous hypotheses on the natural cycle of Ebolavirus are revisited. Also, the main factors driving the virus natural cycle are summarized for the different ecosystems where the Ebolavirus is known to have emerged, including the virus ...

In 2014, Ebola hemorrhagic fever caused an outbreak in West Africa that officially ended in 2016. The Centers for Disease Control and Prevention (CDC) says, "Ebola is a rare and deadly disease caused by infection with one of the Ebola virus species" ("Ebola (Ebola Virus Disease)").

1. Introduction. The Ebola virus (EBOV) belongs to the family Filoviridae, which is a group of single-stranded RNA viruses that can lead to severe hemorrhagic fever in humans and other primates. This virus is an extremely infectious virus with a high rate of fatalities (up to 90%) which makes it one of the deadliest viral diseases (Ebola virus ...

Introduction. Ebola, earlier termed as Ebola hemorrhagic fever (EHF), is a critically lethal ailment which primarily affects the humans and nonhuman primates. Ebola virus disease (EVD) occurs due to a virus infection which belongs to the family Filoviridae and genus Ebolavirus . [ 1] EVDs has posed diagnostic challenges and has been a universal ...

Fruit bats are considered to be a putative reservoir of Ebola virus in Central Africa after 2004; In 2009, several non-human primate epizootic are reported; 1976 was the first emerging events and ...

Ebola Virus Is A Serious Virus Disease. Ebola Virus is a serious transmitted disease by both humans and animals. The disease first appeared in 1976 in 2 simultaneous outbreaks, one in Nzara, Sudan, and the other in Yambuku, Democratic Republic of Congo. The latter occurred in a village near the Ebola River, from which the virus received its name.

Ebola Virus Essay Topics and Outline Examples Essay Title 1: Unmasking Ebola: Origins, Transmission, and Global Response. Thesis Statement: This essay provides an in-depth analysis of the Ebola virus, including its origins, modes of transmission, symptoms, and the global efforts in containing and managing Ebola outbreaks.

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  1. ⇉The Ebola Virus: What is It? Essay Example

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  2. Ebola and International Business

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  3. Discovery of the Ebola Virus Essay Example

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  4. Expository Essay on Ebola Virus

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  5. ≫ Ebola Virus Disease What Factors Caused the Spread of the Disease

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  6. How to Write an Expository Essay: Examples and 25 Topic Ideas

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  1. Expository Essay on Ebola Virus

    Here you have an Expository Essay on Ebola Virus, Lets start with the introduction. Introduction. The Ebola virus is one of the most dangerous and deadly viruses known to humans. The Ebola epidemic since its discovery in 1976 came from the Democratic Republic of Congo, formerly known as Zaire, but the largest Ebola outbreak known to date is still ongoing at the time of writing, in the West Africa.

  2. Ebola virus: A global public health menace: A narrative review

    Introduction. Ebola, earlier termed as Ebola hemorrhagic fever (EHF), is a critically lethal ailment which primarily affects the humans and nonhuman primates. Ebola virus disease (EVD) occurs due to a virus infection which belongs to the family Filoviridae and genus Ebolavirus . [ 1] EVDs has posed diagnostic challenges and has been a universal ...

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  5. Ebola virus disease: A narrative review

    1. Introduction. The Ebola virus (EBOV) belongs to the family Filoviridae, which is a group of single-stranded RNA viruses that can lead to severe hemorrhagic fever in humans and other primates. This virus is an extremely infectious virus with a high rate of fatalities (up to 90%) which makes it one of the deadliest viral diseases (Ebola virus ...

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    In 2014, Ebola hemorrhagic fever caused an outbreak in West Africa that officially ended in 2016. The Centers for Disease Control and Prevention (CDC) says, "Ebola is a rare and deadly disease caused by infection with one of the Ebola virus species" ("Ebola (Ebola Virus Disease)").

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