Ebola Hemorrhagic Fever
Disease Details
Family Health Simplified
- Description
- Ebola Hemorrhagic Fever is a severe, often fatal illness in humans caused by the Ebola virus, characterized by sudden onset of fever, severe weakness, muscle pain, and bleeding.
- Type
- Ebola hemorrhagic fever is caused by the Ebola virus, a member of the Filoviridae family. The disease is not transmitted genetically; it is primarily spread through direct contact with bodily fluids of infected individuals, tissues of infected animals, or contaminated surfaces and materials.
- Signs And Symptoms
-
Ebola hemorrhagic fever, also known simply as Ebola, is a severe and often fatal illness in humans. The signs and symptoms typically appear 2 to 21 days after exposure to the virus. Initial symptoms are nonspecific and can include:
- Sudden onset of fever
- Severe headache
- Muscle pain
- Fatigue
- Weakness
As the disease progresses, more severe symptoms may develop:
- Vomiting
- Diarrhea (which can be severe and watery)
- Abdominal pain
- Unexplained bleeding or bruising (hemorrhagic symptoms)
- Red eyes
- Rash
- Chest pain and cough
In advanced stages, patients may experience multi-organ failure and shock. The disease has a high fatality rate, which can range from 25% to 90% in past outbreaks. Early supportive care with rehydration and symptomatic treatment improves survival. - Prognosis
-
EVD has a risk of death in those infected of between 25% and 90%. As of September 2014, the average risk of death among those infected is 50%. The highest risk of death was 90% in the 2002–2003 Republic of the Congo outbreak.
Early admission significantly increases survival rates Death, if it occurs, follows typically six to sixteen days after symptoms appear and is often due to low blood pressure from fluid loss. Early supportive care to prevent dehydration may reduce the risk of death. - Onset
- The onset of Ebola hemorrhagic fever typically includes sudden symptoms such as fever, severe headache, muscle pain, weakness, fatigue, and sore throat. These initial symptoms can appear 2 to 21 days after exposure to the virus, with an average of about 8-10 days.
- Prevalence
- The prevalence of Ebola hemorrhagic fever, caused by the Ebola virus, varies depending on the region and the timing of outbreaks. Sporadic and localized outbreaks have occurred primarily in Africa, with significant outbreaks in countries like Guinea, Sierra Leone, Liberia, and the Democratic Republic of the Congo. Due to the nature of the disease, global prevalence remains low, but the impact can be severe during outbreaks.
- Epidemiology
- The disease typically occurs in outbreaks in tropical regions of Sub-Saharan Africa. From 1976 (when it was first identified) through 2013, the WHO reported 2,387 confirmed cases with 1,590 overall fatalities. The largest outbreak to date was the Ebola virus epidemic in West Africa, which caused a large number of deaths in Guinea, Sierra Leone, and Liberia.
- Intractability
- Ebola hemorrhagic fever, caused by the Ebola virus, is considered a serious and often fatal illness. Historically, managing and containing Ebola outbreaks has been challenging due to several factors such as its high mortality rate, the need for specialized care, and the requirement for stringent infection control measures. While there is no specific cure, supportive care like rehydration and treatment of specific symptoms can improve survival rates. There are also vaccines and experimental treatments that have shown promise in controlling outbreaks. However, the disease can be considered intractable in resource-limited settings where access to medical care and containment resources is inadequate.
- Disease Severity
- Ebola hemorrhagic fever, now more commonly referred to simply as Ebola virus disease (EVD), is a severe, often fatal illness in humans. The disease severity is high, with case fatality rates averaging around 50%, but varying from 25% to 90% in past outbreaks.
- Healthcare Professionals
- Disease Ontology ID - DOID:4325
- Pathophysiology
- Like other filoviruses, EBOV replicates very efficiently in many cells, producing large amounts of virus in monocytes, macrophages, dendritic cells and other cells including liver cells, fibroblasts, and adrenal gland cells. Viral replication triggers high levels of inflammatory chemical signals and leads to a septic state.EBOV is thought to infect humans through contact with mucous membranes or skin breaks. After infection, endothelial cells (cells lining the inside of blood vessels), liver cells, and several types of immune cells such as macrophages, monocytes, and dendritic cells are the main targets of attack. Following infection, immune cells carry the virus to nearby lymph nodes where further reproduction of the virus takes place. From there the virus can enter the bloodstream and lymphatic system and spread throughout the body. Macrophages are the first cells infected with the virus, and this infection results in programmed cell death. Other types of white blood cells, such as lymphocytes, also undergo programmed cell death leading to an abnormally low concentration of lymphocytes in the blood. This contributes to the weakened immune response seen in those infected with EBOV.Endothelial cells may be infected within three days after exposure to the virus. The breakdown of endothelial cells leading to blood vessel injury can be attributed to EBOV glycoproteins. This damage occurs due to the synthesis of Ebola virus glycoprotein (GP), which reduces the availability of specific integrins responsible for cell adhesion to the intercellular structure and causes liver damage, leading to improper clotting. The widespread bleeding that occurs in affected people causes swelling and shock due to loss of blood volume. The dysfunctional bleeding and clotting commonly seen in EVD has been attributed to increased activation of the extrinsic pathway of the coagulation cascade due to excessive tissue factor production by macrophages and monocytes.After infection, a secreted glycoprotein, small soluble glycoprotein (sGP or GP) is synthesised. EBOV replication overwhelms protein synthesis of infected cells and the host immune defences. The GP forms a trimeric complex, which tethers the virus to the endothelial cells. The sGP forms a dimeric protein that interferes with the signalling of neutrophils, another type of white blood cell. This enables the virus to evade the immune system by inhibiting early steps of neutrophil activation. Furthermore, the virus is capable of hijacking cellular metabolism. Studies have shown that Ebola virus-like particles can reprogram metabolism in both vascular and immune cells.
- Carrier Status
-
For Ebola Hemorrhagic Fever:
**Carrier Status:** Humans and nonhuman primates (such as monkeys, gorillas, and chimpanzees) can carry and transmit the Ebola virus. The virus can also be present in certain animal species like fruit bats, which are considered natural hosts and potential carriers. These carriers can transmit the virus to humans, leading to outbreaks.
**Nan:** No additional information specified under "nan." If this is a query for "none applicable" or a specific category abbreviation, please clarify for further details. - Mechanism
-
Ebola Hemorrhagic Fever is caused by the Ebola virus, which is a member of the Filoviridae family. The virus primarily targets endothelial cells, liver cells, and immune cells, leading to severe immune dysfunction and damage to blood vessels.
Mechanism:
1. **Infection and Entry**: The Ebola virus enters the host through mucous membranes, breaks in the skin, or parenterally. The virus uses glycoproteins to bind to host cell receptors and facilitate entry via macropinocytosis.
2. **Replication**: Once inside the cell, the viral RNA genome is transcribed and replicated in the cytoplasm. New viral particles are assembled and bud from the host cell, often destroying the cell in the process.
3. **Immune Evasion**: The virus produces several proteins, like VP35 and VP24, that interfere with the host's immune response. VP35 inhibits interferon production, while VP24 disrupts signaling pathways critical for immune activation.
4. **Spread and Pathogenesis**: The virus quickly spreads to various tissues, notably the liver, spleen, and lymph nodes, causing widespread damage. The destruction of endothelial cells leads to vascular instability and leakage, contributing to the characteristic hemorrhaging.
Molecular Mechanisms:
1. **Glycoprotein (GP)**: The envelope glycoprotein of Ebola virus plays a key role in the attachment and entry into host cells. It undergoes cleavage by host cell proteases, facilitating fusion with the host membrane.
2. **VP24 and VP35 Proteins**: VP24 inhibits the nuclear transport of STAT1, a transcription factor critical for the antiviral response. VP35 inhibits the RIG-I-like receptor (RLR) pathway, which is pivotal for the production of interferons.
3. **RNA-dependent RNA Polymerase (L Protein)**: This enzyme is essential for viral RNA synthesis. It copies the viral RNA genome and transcribes mRNA from it, enabling the production of viral proteins.
4. **sGP (secreted Glycoprotein)**: A soluble form of the glycoprotein, sGP is thought to act as a decoy for the immune system, soaking up neutralizing antibodies and allowing the virus to evade immune detection.
These mechanisms and molecular interactions collectively account for the high virulence and mortality associated with Ebola Hemorrhagic Fever. - Treatment
-
Treatment for Ebola hemorrhagic fever primarily focuses on supportive care, as no specific antiviral treatment has been universally approved, except for treatments like monoclonal antibodies (e.g., Inmazeb, Ebanga). Supportive care includes:
1. **Rehydration:** Replenishing fluids and electrolytes lost due to vomiting, diarrhea, and fever.
2. **Oxygen Therapy:** Administering oxygen to maintain oxygen status.
3. **Blood Pressure Management:** Using medications to maintain blood pressure.
4. **Management of Coagulation Factors:** Addressing bleeding and coagulation issues.
5. **Pain Relief:** Providing pain management solutions.
6. **Treating Secondary Infections:** Administering antibiotics or antifungals for any secondary infections.
7. **Nutritional Support:** Ensuring adequate nutrition to bolster the immune system.
Investigational treatments and vaccines continue to be developed and tested. - Compassionate Use Treatment
-
Compassionate use treatment and experimental therapies for Ebola Hemorrhagic Fever primarily include:
1. **Monoclonal Antibodies**: ZMapp, REGN-EB3 (Inmazeb), and mAb114 (Ansuvimab, Ebanga) have shown effectiveness in various outbreaks.
2. **Antiviral Drugs**: Remdesivir has been used on an experimental basis, though its efficacy is still being evaluated.
3. **Vaccines**: The rVSV-ZEBOV (Ervebo) vaccine has been used during outbreaks to prevent infection, though it's primarily preventative rather than a treatment.
4. **Convalescent Plasma**: Plasma from recovered Ebola patients containing antibodies against the virus has been used experimentally.
5. **Favipiravir**: An antiviral drug initially developed for influenza, used off-label in some Ebola cases.
These treatments are typically administered under specific regulatory frameworks like compassionate use or emergency use authorizations, especially during outbreaks where approved options are limited. - Lifestyle Recommendations
-
For Ebola Hemorrhagic Fever, here are lifestyle recommendations to minimize the risk of infection:
1. **Avoid Contact with Infected Individuals**: Refrain from physical contact with those infected or their bodily fluids.
2. **Practice Good Hygiene**: Regularly wash hands with soap and water or an alcohol-based sanitizer.
3. **Avoid High-Risk Areas**: Refrain from traveling to regions experiencing an Ebola outbreak.
4. **Use Protective Gear**: If you must care for someone with Ebola, use appropriate personal protective equipment (PPE) like gloves, masks, and gowns.
5. **Safe Burial Practices**: Avoid direct contact with the bodies of those who have died from Ebola and leave burials to trained professionals.
6. **Cook Animal Products Thoroughly**: Ensure all meat and animal products are properly cooked to eliminate pathogens.
7. **Avoid Contact with Wild Animals**: Steer clear of handling or consuming bushmeat, and avoid areas where bats or other potential carriers are prevalent.
8. **Stay Informed**: Keep up-to-date on the latest guidance from health authorities regarding Ebola outbreaks and preventions. - Medication
- There is no specific antiviral medication approved for Ebola hemorrhagic fever. Treatment primarily involves supportive care, including intravenous fluids, maintaining oxygen status and blood pressure, and treating any complicating infections. In some cases, investigational treatments and monoclonal antibodies like Inmazeb (atoltivimab, maftivimab, and odesivimab-ebgn) or Ebanga (ansuvimab-zykl) may be used.
- Repurposable Drugs
-
As of current knowledge, several drugs have been investigated for potential repurposing to treat Ebola hemorrhagic fever. These include:
1. **Remdesivir**: Initially developed for treating hepatitis C and later tested for Ebola, it has shown antiviral activity against Ebola virus in preclinical studies.
2. **Favipiravir**: An antiviral drug approved for influenza in Japan, it has been studied for its efficacy against Ebola virus.
3. **Regeneron's REGN-EB3 and Mapp Biopharmaceutical's ZMapp**: Both are monoclonal antibody therapies initially developed specifically for Ebola, but they underscore the potential for monoclonal antibodies in treating viral hemorrhagic fevers.
These medications are under various stages of research and clinical testing. Always consult healthcare providers for treatment decisions. - Metabolites
- For Ebola hemorrhagic fever, specific metabolites of diagnostic significance are not well-established in clinical practice. However, metabolic disturbances often observed in patients include elevated liver enzymes (AST and ALT), electrolyte imbalances (like hyponatremia and hypokalemia), and signs of disseminated intravascular coagulation (e.g., elevated D-dimer).
- Nutraceuticals
-
Nutraceuticals are food-derived products that offer health benefits, including the prevention and treatment of disease. Currently, there is no specific nutraceutical proven to prevent or treat Ebola hemorrhagic fever effectively. The primary focus for Ebola is on antiviral treatments, supportive care, and vaccines. While nutraceuticals may support general health and immune function, they cannot replace standard medical treatments for Ebola.
Nanotechnology (nan) holds potential in improving diagnostics, drug delivery, and treatment for Ebola hemorrhagic fever. Nanoparticles can be engineered to target and neutralize the virus, enhance the effectiveness of antiviral drugs, or improve the delivery of vaccines. Research in this area is ongoing, and while promising, practical applications in clinical settings are still under investigation. - Peptides
- Ebola Hemorrhagic Fever, caused by the Ebola virus, does not typically relate directly to "peptides" in its primary medical context. However, research in therapeutics may involve peptides as antiviral agents. There is no widely recognized connection to the term "nan," which is likely a shorthand notation for something else not standardly associated with Ebola. If you need more specific information about Ebola Hemorrhagic Fever's treatment or prevention, please specify.