Ebola virus

Causes periodic outbreaks of severe hemorrhagic fever.

Illness includes multiple organ failure, possible death in previously healthy persons.

Sepsis is induced through cytokine storm and hemorrhagic complications occur via thrombocytopenia, hepatic necrosis, DIC and endothelial damage.

Thought to have originated in fruit bats, first detected near the Ebola river in Zaire.

One of 3 members of the Filoviridae family.

Comprises 5 distinct species.

Filoviruses are zoonotic pathogens maintainEd in reservoir species, perhaps bats, with occasional spill over into humans and other mammals, which may serve as an end, intermediate, or amplifying hosts.
Filoviruses appear occur on  regions close the African equator with most outbreaks in central and western African countries.

A single-stranded RNA virus.

Mortality rate can be as high as 90%.

Estimating case fatality rate about 70%.

Highest case fatality with Zaire ebolavirus of up to 90%.

Outbreaks typically originate with the introduction of the virus from a wild animal reservoir.

A zoonotic disease.

Most virus outbreaks have originated in sub Saharan Africa and travel to other countries via shipment of non-human primates, via travel of infected persons, or through accidental contamination in testing facilities.

Ebola virus disease (EVD) or Ebola hemorrhagic fever (EHF) is the human disease caused by the ebola virus.

Caused by four of five viruses classified in the genus Ebolavirus, family Filoviridae, order Mononegavirales.

Symptoms typically start two days to three weeks after contracting the virus.

Patients present with a fever, sore throat, muscle pains, and headaches.

Manifests with nausea, vomiting, diarrhea, impaired liver and renal function, followed by bleeding problems.

Acquired when a person comes into contact with the blood or bodily fluids of an infected animal.

Human to human transmission typically occurs through direct contact with infectious blood or bodily fluids.

For sustained transmission requires there to be as direct contact with blood or bloody

fluids from an infected person while he or she is ill.

Due to standard infection control practices in health care facilities, along with 

Sanitation procedures and public health care facilities, it is unlikely widespread community transmission of Ebola virus can occur in United States.

Infected animals include monkeys.

Sexual transmission is rare.

The initial introduction of Ebola virus into human population is likely due to contact with infected animal, such as a bat or monkey.

Subsequent human infections are results of direct contact of mucous membranes, or broken skin, with blood or body fluids of an infected patient.

Patients are contagious only when they are, and do not transmit the infection during the incubation period.

Infected patient’s blood, sweat, feces, and vomit are highly infectious.

Viral replication leads to the formation of intracellular inclusion bodies followed by cell necrosis.
Islands of necrosis occur in the liver with elevation of liver function tests.
Patients experience myositis along with increased creatinine kinase and aspartate aminotransferase levels.
Renal tubular cells in glomerular epithelium are altered and contribute to renal dysfunction.
Infection causes responses such as production of pro inflammatory cytokines and chemokines by infected dendritic cells, macrophages, and monocytes.
Infected macrophages produce tissue factor with fibrin deposition in the spleen, lymphoid tissues, glomeruli, and renal proximal tubules.
Clotting factor consumption from disseminated microthrombi, endothelial dysfunction and inhibition of platelet function contribute to the coagulopathy.
Macrovascular abnormalities, hypovolemia, fluid loss via vomiting and diarrhea can lead to tissue hypoperfusion and multiorgan system failure.
T-cells are activated and are rendered ineffective in severe cases because of T-cell exhaustion and apoptosis.

Pro inflammatory mediators cause dysfunction of the endothelium, followed by vascular permeability and fluid extravasation.

An infected human can spread the disease from one person to another.

May be able to be transmitted via semen.

Diagnosis can be made by identifying antibodies to the virus, the viral RNA, or the virus itself.

The most widely used technique for diagnosis is quantitative real time polymerase chain reaction assay.

Prevention includes decreasing the spread of the disease from infected monkeys and pigs to humans.

There is no specific treatment for the virus.

Management includes giving them either oral rehydration therapy or intravenous fluids.

Correcting electrolyte abnormalities and hypoglycemia and meeting nutritional needs are important.

Parenteral nutrition or renal replacement therapy may be necessary.

Mortality rate between 50% and 90%.

Typically occurs in outbreaks in tropical regions of Sub-Saharan Africa.

Between 1976 and 2014, fewer than 1,000 people a year have been infected.

EBV disease begins with a sudden onset of an influenza-like stage characterized by general malaise, fever with chills, sore throat, severe headache, weakness, joint pain, muscle pain, and chest pain.

Respiratory symptoms include pharyngitis, cough, dyspnea, and hiccups.

Central nervous system involvement includes headaches, agitation, confusion, fatigue, seizures, and sometimes coma.

Cutaneous abnormalities include: maculopapular rash, petechiae, purpura, ecchymoses, and hematomas.

Hemorrhagic symptoms is indicative of a negative prognosis, but is not the cause of death.

Death occurs due to multiple organ dysfunction syndrome (MODS).

Death due to fluid redistribution, hypotension, disseminated intravascular coagulation, and focal tissue necroses.

Average time between contracting the infection and the onset of symptoms is 13 days, but can be as long as 25 days.

All infected patients show some level of coagulopathy, and circulatory system symptomology.

Mucous membranes and puncture sites bleeding is reported in 40–50% of cases.

Hemorrhagic manifestations include hematemesis, hemoptysis, melena, mucous membranes of the gastrointestinal tract, nose, vagina and gingiva.

Major hemorrhage is rare.

Infection occurs after an ebola virus is transmitted to a human index case via contact with an infected animal’s bodily fluids.

Human-to-human transmission occurs via direct contact with blood or bodily fluids from an infected person.

Transmission can occur by the embalming of an infected dead person, or by contact with contaminated medical equipment, particularly needles and syringes.

Aerosol transmission has not been observed during EVD outbreaks.

The potential for widespread epidemics is low due to the high case-fatality rate, rapidity of demise of patients, and the often remote areas where infections occur.

Bushmeat has been linked to the transmission of diseases to people, including Ebola.

Bats are suspected to be reservoir hosts.

Transmission between natural reservoirs and humans are rare, and outbreaks are usually traceable to a single index case where an individual has handled the carcass of gorilla, or chimpanzee.

Fruit bats are smoked, grilled or made into a spicy soup, and can spread the virus person-to-person within families, hospitals, and during some mortuary rituals.

The virus is transmitted through body fluids,

Transmission through oral exposure and through conjunctiva exposure is likely.

Filoviruses are not naturally transmitted by aerosol, but are highly infectious as breathable 0.8–1.2 micrometre droplets in laboratory conditions.

Such viruses have been classified as Category A biological weapons.

All epidemics occur in sub-optimal hospital conditions, where practices of basic hygiene and sanitation are limited.

In isolated settings such as a quarantined hospital or a remote village, most victims are infected shortly after the first case of infection is present.

The quick onset of symptoms from the time the disease becomes contagious in an individual makes it easy to identify sick individuals and limits an individual’s ability to spread the disease by traveling.

Bodies of the deceased are infectious and must be properly disposed of.

Ebolavirions are filamentous particles that may appear in the shape of a U or a 6, and they may be coiled, or branched.

Ebolavirions are 80 nm in width generally, but can vary in length.

The median particle length of ebolaviruses ranges from 974 to 1,086 nm, but particles as long as 14,000 nm have been detected in tissue culture.

Ebolavirions consist of seven structural proteins.

At the center of the Ebolavirus is the helical ribonucleocapsid, which consists of the genomic RNA wrapped around a polymer of nucleoproteins.

Associated with the ribonucleoprotein is the RNA-dependent RNA polymerase, the polymerase cofactor (VP35) and a transcription activator (VP30).

The ribonucleoprotein is embedded in a matrix, formed by the major (VP40) and minor (VP24) matrix proteins.

Niemann–Pick C1 (NPC1) appears to be essential for Ebola infection.

Ebola virus cell entry and replication requires the cholesterol transporter protein (NPC1) Niemann-Pick C1.

The ebolavirus life cycle begins with virion attachment to specific cell-surface receptors.

Following vision attachment to cell surface receptors a fusion of the virion envelope with cellular membranes and release of the virus nucleocapsid into the cytosol occurs.

Endothelial cells, mononuclear phagocytes, and hepatocytes are the main targets of the Ebola infection.

Ebola infection results in the secretion of glycoprotein (sGP) known as the Ebola virus glycoprotein.

Ebola virus replication overwhelms protein synthesis of infected cells and host immune defenses.

The GP binds the virus to the endothelial cells lining the interior surface of blood vessels.

The sGP forms a dimeric protein that interferes with the signaling of neutrophils.

Viral particles and cell damage release of cytokines TNF-α, IL-6, IL-8 associated with fever and inflammation.

Infection in the endothelial cells results in a loss of vascular integrity causing damage to the liver and leads to coagulopathy.

Differential diagnosis: Marburg virus disease, falciparum malaria, typhoid fever, shigellosis, rickettsial diseases, gram-negative septicemia, borreliosis. leptospirosis, scrub typhus, plague, Q fever, candidiasis, histoplasmosis, trypanosomiasis, visceral leishmaniasis, hemorrhagic smallpox, measles, and fulminant viral hepatitis. acute promyelocytic leukemia, hemolytic uremic syndrome, snake envenomation, clotting factor deficiencies/platelet disorders, thrombotic thrombocytopenic purpura, hereditary hemorrhagic telangiectasia, Kawasaki disease, and even warfarin intoxication.

Diagnosis requires medical history, especially of travel and occupation, and history of person’s exposure to wildlife.

Diagnosis can be confirmed by isolating the virus or by detection of ebolavirus antigen or genomic or subgenomic RNA in patient blood samples during the acute phase of the infection.

Ebola virus isolation is performed by inoculation of grivet kidney epithelial Vero E6 or MA-104 cell cultures or by inoculation of human adrenal carcinoma SW-13 cells.

Filovirions can be visualized and identified in cell culture by electron microscopy due to their filamentous shapes.

Immunofluorescence assays are used to identify ebola virus in cell cultures.

During an outbreak, virus isolation and electron microscopy are not feasible, and most common diagnostic methods are RT-PCR in conjunction with antigen-capture ELISA.

Genetic change are 100 times slower than influenza A, but on the same magnitude as those of hepatitis B.

The five characterised Ebola species.

Zaire virus has the highest case-fatality rate of the ebolaviruses, up to 90% in some epidemics, with an average case fatality rate of approximately 83% over 27 years.

Zaire ebolavirus associated with outbreaks more than of any other species.

Ebola viruses are highly infectious as well as contagious.

Bodily fluids from diarrhea, vomiting, and bleeding represent a hazard.

Epidemics occur mostly in poor, isolated areas without modern hospitals or well-educated medical staff.

Ebolaviruses are not transmitted by aerosol during natural EVD outbreaks.

The natural maintenance hosts of ebolaviruses are unidentified, therefore to avoid Ebola risk factors such as contact with bats, nonhuman primates, and bush meat should be avoided.

Prevention during EVD outbreaks is achieved by not touching patients, their excretions, body fluids, or possibly contaminated materials and utensils.

Patients should be isolated.

Medical staff should be trained and apply strict barrier techniques such as disposable face mask, gloves, goggles, and a gown at all times.

Individuals such as healthcare workers and household care providers who come in contact with patients with Ebola disease without proper personal protective equipment are at highest risk for secondary infection.

Burial rituals requiring embalming of bodies, should be discouraged or modified.

In the laboratory the wearing of proper personal protective required.

No specific ebola virus treatment exists.

Treatment is primarily supportive in nature and includes balancing fluids and electrolytes, administration of anticoagulants early in infection to prevent or control disseminated intravascular coagulation, administration of procoagulants late in infection to control hemorrhaging, maintaining oxygen levels, pain management, and administration of antibiotics or antimycotics to treat secondary infections, replenishing fluids, maintaining proper blood pressure, replacing lost blood, and treating related infections.

Has a high mortality rate: often between 50 percent and 90 percent.

Recovery may be quick, complete, or prolonged with long term problems, such as inflammation of the testicles, joint pains, muscle pains, skin peeling, or hair loss.

Eye symptoms include light sensitivity, excess tearing, iritis, iridocyclitis, choroiditis and blindness.

EBOV may be able to persist in the semen of some survivors, which could give rise to infections and disease via sexual intercourse.

Outbreaks of EVD have occurred mainly in Africa.

The virus had a very low pathogenicity to humans.

Filovirus infections usually begin with viral particles being deposited a mucous membranes and perhaps skin, but occasionally can occur percutaneously.
After uptake of the viral particles by dendritic cells and macrophages, the virus replication potentially shirts down early innate immune responses by blocking interference production and signaling.
Viral dissemination probably occurs through the migration of dendritic cells  to lymphoid tissues and release the virus into the circulation, leading to infection of fixed macrophages in the liver, spleen, and other tissues.

Infection that spreads to adjacent hepatocytes, fibroblasts in other cells.

The virus has the potential agent for biological warfare.

Outbreaks among human populations result from handling infected wild animal carcasses.

Declines in animal populations precede outbreaks among human populations.

Can be transmitted to dogs and pigs.

The deadliest form of the virus could be transmitted by air between species.

Pigs might be one of the reservoir hosts for the virus.

The fruit bat has long been considered as the reservoir.

Fruit bats have been implicated in transmission and the virus can replicate in bats and have been cultured from bat guano.

Non human primates, such as monkeys, may serve as intermediate hosts.

Black market Bush meat trade has been Implicated in bringing this disease to human populations.

Outbreaks due to human-human transmission .

Outbreaks enhanced by nosocomial spread.

Incubation period 2-21 days, And typically 6-10 days.

Patients have abrupt onset of symptoms 8-10 days after exposure with the range of 2-21 days.

Symptoms initially maybe non specific with fever, chills, myalgias, malaise, and a possible maculopapular eruption.

Initial presentation is with nonspecific febrile illness characterized by malaise, fatigue, and myalgia, subsequently a few days later G.I. manifestations include anorexia, nausea, vomiting, and diarrhea.
Fluid losses up to 10 L per day can occur.
Other common signs and symptoms are: dysphasia, headache, conjunctival injection, abdominal pain, arthralgia, and maculopapular rash.
Bleeding abnormalities occur in less than half of patients, usually manifesting as bleeding from the gums, petechiae, oozng from venous sites, subconjunctival hemorrhage, and blood in vomit and stool.

Because it is spread mainly through contact with body fluids of symptomatic patients, transmission can be stopped by early diagnosis, contact tracing, patient isolation and care, infection control and safe burial.

Case incidence can be reduced within 2-3 weeks after introduction of control measures.

No post exposure prophylaxis or effective antiviral therapy presently exists.

Healthcare workers account for one quarter of cases in prior out outbreaks, making them at particular risk for acquiring Ebola infection.

There appears to be low infectivity early in the infection, when patients are in the community, but as the severity of the infection increases infectivity increases.

The virus is found in blood fluids that include blood, urine, vomitus, and stool.

The virus can be transmitted via the skin.

Gastrointestinal fluid losses can be up to 5-10 L/day with significant droplet virus dispersion.

Patients dying with Ebola infection may have viral loads that can reach 10 million copies per milliliter.

Indirect contact virus transmission with fomites has been documented, but is uncommon.

After five days patients develop abdominal pain, severe watery diarrhea, nausea, vomiting and hemorrhagic sequelae including, hematochezia, petechiae, ecchymoses, and mucosal hemorrhage.

Patients who develop fatal disease have severe clinical signs and symptoms earlier in their course and death typically occurs 6-16 days after the symptom onset.

Nonfatal cases typically have resolution of fever between day 6-11, followed by prolonged period of recovery with weakness fatigue, poor, and failure to gain weight that had previously been lost.

Post Ebola syndrome can occur with musculoskeletal pain, headache, encephalitis, and ocular problems in survivors.

Laboratory abnormalities associated with Ebola virus disease include thrombocytopenia hemoconcentration, initial lymphopenia followed by neutrophilia a with a left shift, often elevation in transaminase levels, fibrin degradation product elevation and prolongation of prothrombin time and partial thromboplastin time, providing evidence of DIC.

Diagnostic tests include polymerous chain reaction, viral culture, IGM and IgG enzyme linked immunoabsorbent assay test.

Treatment for ebola virus disease is largely supportive and include: blood product transfusion, electrolyte and fluid resuscitation and ventilatory support.

Goals of treatment: supportive care to maintain or restore normal physiology, treatment of discomfort, present this treatment of any undiagnosed infections that are concurrent.

Availability of sophisticated supportive care likely improves patient outcomes a substantial manner.

Hypoperfusion from volume deficits due to vascular leakage in G.I. losses as well as intravascular coagulation is the most serious derangement.

Volume replacement either orally or intravenously is the primary intervention.

Presently there are no licensed medications available for the treatment of Ebola virus disease and there are no current licensed vaccines available.

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