Ebola Symptoms And Signs Pdf

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Ebola: What you need to know

Thank you for visiting nature. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer.

In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. EVD outbreaks typically start from a single case of probable zoonotic transmission, followed by human-to-human transmission via direct contact or contact with infected bodily fluids or contaminated fomites.

EVD has a high case—fatality rate; it is characterized by fever, gastrointestinal signs and multiple organ dysfunction syndrome. Diagnosis requires a combination of case definition and laboratory tests, typically real-time reverse transcription PCR to detect viral RNA or rapid diagnostic tests based on immunoassays to detect EBOV antigens.

Recent advances in medical countermeasure research resulted in the recent approval of an EBOV-targeted vaccine by European and US regulatory agencies. The results of a randomized clinical trial of investigational therapeutics for EVD demonstrated survival benefits from two monoclonal antibody products targeting the EBOV membrane glycoprotein.

New observations emerging from the unprecedented — Western African EVD outbreak the largest in history and the ongoing EVD outbreak in the Democratic Republic of the Congo have substantially improved the understanding of EVD and viral persistence in survivors of EVD, resulting in new strategies toward prevention of infection and optimization of clinical management, acute illness outcomes and attendance to the clinical care needs of patients.

To date, 12 distinct filoviruses have been described 1. This subcategorization of FVD is largely based on the increasing evidence of molecular differences between ebolaviruses and marburgviruses, differences that may influence virus—host reservoir tropism, pathogenesis and disease phenotype in accidental primate hosts 2. Thus far, five ebolaviruses have been associated with human infections, and four of them have been identified as pathogens. However, it is tempting to speculate that Ebola virus disease EVD is a zoonosis that is, an infectious disease caused by an agent transmitted between animals and humans because retrospective epidemiological investigations have often been able to track down the probable index cases of EVD outbreaks.

These individuals had been in contact with wild animals or had handled the carcass of a possible accidental EBOV host 7 , Parts c and d courtesy of J. Wada and J. Since the discovery of filoviruses in ref. The epidemiological definition of outbreak is one or more cases above the known endemic prevalence.

The overall limited numbers of FVD cases — 2, cases including 1, deaths 4 , the typical remote and rural locations of outbreaks and the often delayed announcement of new outbreaks to the international community 7 have prevented the systematic study of clinical FVD in humans.

Thus, the commonly used description of FVD was derived either from observation of small groups of patients in care settings that were not well-equipped for diagnosis, treatment and disease characterization, or from observations of even smaller samples, such as individuals who were transferred from Equatorial Africa to Europe and the USA or who fell sick in Europe or the USA after contracting the virus elsewhere.

Pathological characterization of FVD via autopsies has been rare 7 , 8. In the absence of extensive human clinical data, FVD could only be defined further via the use of experimental animal infections 9 , From late to early , EBOV caused the largest outbreak to date, which spread from Guinea to other countries in Western Africa, leading to 28, human infections and 11, deaths The location and scale of the — outbreak was entirely unexpected Consequently, local, national and international organizations were caught unprepared for an outbreak caused by what, until then, was considered an exotic pathogen of largely negligible consequence for global public health 13 , 14 , Ultimately, the outbreak was contained, but it devastated individuals, families, communities, health-care systems and economies In most affected countries, the response included the establishment of Ebola virus disease Treatment Units ETUs 17 , 18 , 19 , in which medical professionals and biomedical scientists managed large cohorts of patients with suspected or confirmed EVD in controlled settings.

From this experience, scientists were able to better understand a virus previously best known as a potential bioweapons agent 20 , In addition to the Western African outbreak, an ongoing outbreak in the Ituri, Nord-Kivu and Sud-Kivu Provinces of the Democratic Republic of the Congo is the second largest outbreak in terms of the number of cases and deaths, with 3, infections and deaths as of 28 January 22 Table 1 , Fig. The map shows the location and years of all reported Ebola virus disease EVD outbreaks.

Two cases of laboratory-acquired EVD occurred in Russia not shown. Typically, EVD begins with a nonspecific febrile illness followed by severe gastrointestinal symptoms and signs. In highly viraemic patients who often also have dysregulated immune responses, EVD progresses to a complex multiple organ dysfunction syndrome that can be fatal.

A subset of patients, usually with lower viraemia, have less-severe disease progression and organ dysfunction 27 , Ultimately, these patients develop robust immune responses leading to clearance of viraemia and a resolution phase. In this Primer, we outline the current improved understanding of EVD based on the most recently published human clinical data. Most outbreaks can be traced back to a single spillover introduction of EBOV into the human population from an unknown reservoir by unknown means.

Subsequently, the virus is transmitted by direct, typically non-aerosol, human-to-human contact or contact with infected tissues, bodily fluids or contaminated fomites Fig. The potential for infection of an index case and subsequent spread — locally and globally — has been estimated by considering reservoir species distribution, along with governance, communications, isolation, infrastructure, health care and international connectivity These predictions are crucial to identify regions that require increased surveillance and investments.

Tracking EBOV within the human population after a zoonotic transmission event can be challenging, especially as the single natural reservoir has not been identified.

A strong risk factor linked to human-to-human EBOV propagation is contact with infected bodily fluids 33 , 34 , Indeed, infectious EBOV has been recovered from breast milk, saliva, urine, semen, cerebrospinal fluid, and aqueous humor, in addition to blood and blood derivatives, and detected in amniotic fluid, tears, skin swabs and stool by reverse transcription RT -PCR 36 , 37 , 38 , 39 , Fortunately, the risk of widespread outbreaks in middle-income and high-income countries remains relatively low, partially owing to our ability to keep the reproductive number R 0 , the average number of individuals to whom an infected person will transmit the pathological agent over the course of the infectious period of EBOV below 1 with simple infection prevention control and contact tracing measures By current albeit incomplete understanding, sex differences in susceptibility have not been identified, but women as care-givers may be at higher risk of being exposed to EBOV, and the incidence of EVD increases almost linearly with age to a peak at 35—44 years.

Although children typically constitute a disproportionately small number of EVD cases, they have shorter incubation periods, and a more rapid disease course. Possible explanations for the low incidence of EVD in children include behavioural factors, such as deliberate prevention of exposure to infected individuals 46 , and differences in susceptibility across age groups Occasionally, spikes in incidence of EVD in children have been recorded in correspondence to malaria outbreaks and were probably related to nosocomial infections Infected pregnant women are at high risk of miscarriage or stillbirths, and newborn babies of infected mothers rarely survive Indeed, EBOV can be transmitted transplacentally 52 and also lead to fetal death related to placental insufficiency.

Transmission of EBOV from infected pregnant women to their embryos or fetuses or from infected mothers to their children occurs frequently and is associated with elevated in utero and neonatal lethality The risk of fetal loss in survivors of EVD who become pregnant after recovery remains unclear; some data suggest an increased risk over baseline, especially early after recovery 53 , although healthy pregnancy outcomes are possible EBOV RNA has been detected at high concentrations in amniotic fluid, placenta, fetal tissue and breast milk 39 , 55 , 56 , 57 , Although unpublished observations of varying disease clinical signs or levels of severity depending on the specific outbreak have been described, these findings are not necessarily reflected in the published literature.

On the basis of comparative statistics on CFRs, a fundamental difference in virulence between ebolaviruses that cause lethal human disease is not observed; the oft-repeated notion that EBOV is the most virulent ebolavirus let alone filovirus is not supported by available data 4. The mean CFRs for each ebolavirus are Accordingly, whether one ebolavirus is more dangerous than another is statistically unclear.

The reasons for fluctuating CFR data are not truly understood. Possible reasons include differences in health status nutrition, immunity and co-infection status , genetics ethnicity-dependent haplotypes or random polymorphisms , health-seeking behaviour, case recognition and reporting capacities and the development and accessibility of health-care facilities providing supportive care in the affected African countries. Revised IDSR guidelines from include guidance for developing case definitions for routine and community-based surveillance of such diseases.

As increasing numbers of patients with possible EVD present to health facilities at the beginning of an outbreak, case definitions are refined from standard public health case definitions to reflect clinical and epidemiological features associated with a particular outbreak context. A robust case definition and accurate confirmatory testing are key to ensuring that individuals with suspected EBOV infection are efficiently identified and, upon admission to an ETU, isolated for confirmation of diagnosis and treatment.

Importantly, patient screening time should be minimized to limit exposure of uninfected individuals, including ETU staff, to potentially infected individuals.

Particularly in a setting with a low community incidence of EVD, the sensitivity of the case definition should be maximized. Given these considerations, currently no EVD case definition is globally applied. Indeed, the EVD case definition can be reiterated during the course of an outbreak; such variations in case definition were used during the — Western African outbreak for example, in Sierra Leone 61 as the outbreak evolved from a high incidence to a low incidence.

The — Western African EVD outbreak was the first to be largely characterized by molecular epidemiological evidence. These samples included single genomes from single patients, multiple different genomes from the same patient and the same genome from different patients.

Subsequent phylogenetic analyses traced EBOV movement through the human populations of all affected countries and pinpointed multiple back-and-forth border crossings 63 Fig. Such molecular epidemiological investigations are now becoming routine. From there, person-to-person transmission enabled EBOV to spread coloured lines throughout the country, to cross borders and ultimately to affect a total of 15 countries see also Fig.

The direction of EBOV spread is represented by the lines and goes from the thick end to the thin end. White borders delineate the provinces Guinea , districts Sierra Leone and counties Liberia.

Adapted from ref. Molecular approaches have also enabled progress in understanding of within-outbreak and within-host viral evolution During the two most recent EVD outbreaks in the Democratic Republic of the Congo, deep sequencing revealed single spillover EBOV transmission events into the human populations with subsequent person-to-person transmission 25 , Molecular approaches revealed that sexual transmission of EBOV may rarely occur from apparently healthy survivors of EVD in whom EBOV may persist in the semen for extended periods of time, with the latest documented transmission event days after EVD onset 41 , 66 , 67 , The importance of molecular epidemiology is not limited to an individual outbreak but provides valuable information to scientists and decision makers regarding the long-term evolution of EBOV.

Current medical countermeasures MCMs , such as vaccines and therapeutics, have often been designed to specifically match a known EBOV isolate, or designed as a consensus of multiple ones to account for genomic variation. Molecular epidemiology enables assessment of the potential efficacy of available MCMs based on the sequence of a newly circulating EBOV isolate. The analysis of 65 EBOV GP sequences from isolates collected from to demonstrated that the temporal evolution of EBOV is mostly due to neutral genetic drift, suggesting that the emergence of completely novel isolates that would not respond to current MCMs is unlikely Many outstanding questions still surround the pathophysiology of EVD.

Findings from animal studies, in vitro work and clinical data from humans are beginning to decipher the normal course of EVD in humans and to link disease progression to the molecular bases of EBOV pathogenesis. With these data, researchers may be able to identify the crucial pathways involved in effective immune responses to EBOV infection and the various candidate MCMs that may be developed to augment any host response shortcomings.

Exposure of immunocompetent laboratory mice, Syrian hamsters Mesocricetus auratus and domesticated guinea pigs Cavia porcellus to EBOV does not yield severe or any disease, and EBOV must be adapted via serial passages in rodents before lethal infection is achieved 71 , Even when adapted viruses are used, these rodent models do not fully mimic human disease.

Indeed, much of the information on viral pathogenesis has been derived from studies with wild-type EBOV predominantly in crab-eating macaques Macaca fascicularis and rhesus monkeys M. On the basis of experimental animal data, two factors that may influence development and severity of human EVD may be the EBOV exposure route and dose. Direct contact with infected biological materials or contaminated non-biological materials via cuts or scratches or via contact with mucosal membranes oral or, theoretically, nasopharyngeal or conjunctival mucosa is considered the most frequent mode of human-to-human EBOV transmission However, these transmission pathways are difficult to simulate in experimental settings.

Thus, animal models of EVD have been established using injection and aerosol methods of EBOV exposure to model accidental needlestick injury and respiratory routes of exposure, respectively, despite the lack of evidence that these exposure routes have any relevant roles during natural EVD outbreaks Most studies in NHPs rely on either intramuscular injection or small-particle aerosol exposure of 1, plaque-forming units pfu of EBOV, a dose that ensures that all infected animals will develop a disease that is almost always lethal 74 ; thus, significant results can be achieved with overall low animal numbers.

The lethality associated with this low virus dose suggests that very few virions may be required to initiate a lethal disease course in humans, although insufficient data preclude robust median lethal dose calculation and speculations on the effects of different variants on human disease.

A mutation leading to an amino acid residue change, A82V, in EBOV glycoprotein GP 1,2 occurred in viral genomes isolated from samples collected early in the — Western African outbreak and remained present in genomes from all later samples 76 , 77 , In vitro, this mutation enhances EBOV GP 1,2 -mediated virus entry into human cells 78 , possibly by weakening the stability of the prefusion conformation of GP 1,2 and hence lowering the activation barrier required for fusion of EBOV particle membranes with host cell membranes However, in vivo experiments have yet to unambiguously ascribe a phenotype to A82V and similar mutations in the context of pathogenesis.

This lack of an effect may be due to the true lack of effect of these mutations on pathogenesis, limitations of the in vivo studies such as compensatory mutations for the A82V phenotype observed in vitro , or intrinsic differences among laboratory mice, NHPs and humans, such as infection cofactors or immune responses. Consequently, a convincing explanation for positive selection of certain mutations in EBOV genomes over the course of the outbreak is still lacking.

Clinical presentations and outcomes of patients with Ebola virus disease in Freetown, Sierra Leone

Ebola virus disease EVD is a serious illness that was first discovered in a remote part of Central Africa in Symptoms of Ebola include fever, tiredness, muscle aches, severe headache, red eyes, sore throat, vomiting and diarrhea that can be bloody. Fever is usually the first symptom of Ebola. Ebola can also cause kidney and liver problems. When the disease progresses, there may be a rash and bleeding from inside and outside the body. Ebola can cause death but early medical care increases the chances of survival.

Metrics details. The study admitted patients with confirmed EVD and followed them up till the endpoint recovery or death. Among the lab-confirmed EVD cases in Jui Government Hospital, recovered and died, with an overall survival rate of Most non-survivors More than half survivors

Ebola virus disease

Data collected during the Ebola virus disease EVD epidemic in the Democratic Republic of the Congo were analysed for clinical signs, symptoms and case fatality of EVD caused by Bundibugyo virus BDBV , establishment of differential diagnoses, description of medical treatment and evaluation of the quality of clinical documentation. In a quantitative observational prospective study, global epidemiological data from 52 patients 34 patients within the community, 18 patients treated in the Ebola Treatment Centre were entered anonymously into a database, subsequently matched and analysed. Relevant findings include an over-representation of females among community EVD cases All ETC patients had fever

Ebola virus disease EVD is a public health emergency of international concern. There is limited laboratory and clinical data available on patients with EVD. This is a meta-analysis to assess the utility of clinical signs, symptoms, and laboratory data in predicting mortality in EVD.

Ebola virus disease is a serious, often fatal condition in humans and nonhuman primates. Ebola is one of several viral hemorrhagic fevers, caused by infection with a virus of the Filoviridae family, genus Ebolavirus. The fatality rates of Ebola vary depending on the strain. For example, Ebola-Zaire can have a fatality rate of up to 90 percent while Ebola-Reston has never caused a fatality in humans. The infection is transmitted by direct contact with the blood, body fluids, and tissues of infected animals or people.


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