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Deep Learning Technology: Sebastian Arnold, Betty van Aken, Paul Grundmann, Felix A. Gers and Alexander Löser. Learning Contextualized Document Representations for Healthcare Answer Retrieval. The Web Conference 2020 (WWW'20)
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The most detailed study on the frequency, onset, and duration of MVD clinical signs and symptoms was performed during the 1998–2000 mixed MARV/RAVV disease outbreak. A maculopapular rash, petechiae, purpura, ecchymoses, and hematomas (especially around needle injection sites) are typical hemorrhagic manifestations. However, contrary to popular belief, hemorrhage does not lead to hypovolemia and is not the cause of death (total blood loss is minimal except during labor). Instead, death occurs due to multiple organ dysfunction syndrome (MODS) due to fluid redistribution, hypotension, disseminated intravascular coagulation, and focal tissue necroses.
Clinical phases of Marburg Hemorrhagic Fever's presentation are described below. Note that phases overlap due to variability between cases.
1. Incubation: 2–21 days, averaging 5–9 days.
2. Generalization Phase: Day 1 up to Day 5 from onset of clinical symptoms. MHF presents with a high fever (~40˚C) and a sudden, severe headache, with accompanying chills, fatigue, nausea, vomiting, diarrhea, pharyngitis, maculopapular rash, abdominal pain, conjunctivitis, & malaise.
3. Early Organ Phase: Day 5 up to Day 13. Symptoms include prostration, dyspnea, edema, conjunctival injection, viral exanthema, and CNS symptoms, including encephalitis, confusion, delirium, apathy, and aggression. Hemorrhagic symptoms typically occur late and herald the end of the early organ phase, leading either to eventual recovery or worsening & death. Symptoms include bloody stools, ecchymoses, blood leakage from venipuncture sites, mucosal & visceral hemorrhaging, and possibly hematemesis.
4. Late Organ Phase: Day 13 up to Day 21+. Symptoms bifurcate into two constellations for survivors & fatal cases. Survivors will enter a convalescence phase, experiencing myalgia, fibromyalgia, hepatitis, asthenia, ocular symptoms, & psychosis. Fatal cases continue to deteriorate, experiencing continued fever, obtundation, coma, convulsions, diffuse coagulopathy, metabolic disturbances, shock and death, with death typically occurring between Days 8 and 16.
The signs shown depend on the horse's age, the strain of the infecting virus, the condition of the horse and the route by which it was infected. Most horses with EVA infection don't show any signs; if a horse does show symptoms, these can vary greatly in severity. Following infection, the first sign is fever, peaking at , followed by various signs such as depression, nasal discharge, "pink eye" (conjunctivitis), swelling over the eye (supraorbital edema), urticaria, and swelling of the limbs and under the belly (the ventral abdomen) which may extend to the udder in mares or the scrotum of male horses. More unusual signs include abortion in pregnant mares, and, most likely in foals, severe respiratory distress and death.
Pathogenesis occurs in the same manner in hamsters as in mice. Symptoms in hamsters are highly variable, and typically indicate that the pet has been infected and shedding the virus for several months. Early signs may include inactivity, loss of appetite, and a rough coat. As the disease progresses, the animal may experience weight loss, hunched posture, inflammation around the eyes, and eventually death. Alternatively, some infected hamsters may be asymptomatic.
Marburg virus is a hemorrhagic fever virus of the "Filoviridae" family of viruses and a member of the species "Marburg marburgvirus", genus "Marburgvirus". Marburg virus (MARV) causes Marburg virus disease in humans and nonhuman primates, a form of viral hemorrhagic fever. Considered to be extremely dangerous, the WHO rates it as a Risk Group 4 Pathogen (requiring biosafety level 4-equivalent containment). In the United States, the NIH/National Institute of Allergy and Infectious Diseases ranks it as a Category A Priority Pathogen and the Centers for Disease Control and Prevention lists it as a Category A Bioterrorism Agent. It is also listed as a biological agent for export control by the Australia Group.
The virus can be transmitted by exposure to one species of fruit bats or it can be transmitted between people via body fluids through unprotected copulation and broken skin. The disease can cause bleeding (haemorrhage), fever and other symptoms much like Ebola. Funeral rituals are a particular risk. Actual treatment of the virus after infection is not possible but early, professional treatment of symptoms like dehydration considerably increase survival chances.
In 2009, expanded clinical trials of an Ebola and Marburg vaccine began in Kampala, Uganda.
LCMV causes callitrichid hepatitis in New World primates. The onset of the infection is nonspecific and may include fever, anorexia, dyspnea, weakness and lethargy. Jaundice is characteristic and petechial hemorrhages may develop. Prostration and death usually follow.
Necropsy lesions in primates with callitrichid hepatitis show signs of jaundice, hepatomegaly, splenomegaly, and subcutaneous and intramuscular hemorrhages. Pleural and pericardial effusion, sometimes sanguineous, has also been reported. On histology, multifocal necrosis with acidophilic bodies and mild inflammatory infiltrates are typically found in the liver.
Marburg virus disease (MVD) is the official name listed in the World Health Organization's International Statistical Classification of Diseases and Related Health Problems 10 (ICD-10) for the human disease caused by any of the two marburgviruses Marburg virus (MARV) and Ravn virus (RAVV). In the scientific literature, Marburg hemorrhagic fever (MHF) is often used as an unofficial alternative name for the same disease. Both disease names are derived from the German city Marburg, where MARV was first discovered.
In dogs, signs of distemper vary widely from no signs, to mild respiratory signs indistinguishable from kennel cough, to severe pneumonia with vomiting, bloody diarrhea and death.
Commonly observed signs are a runny nose, vomiting and diarrhea, dehydration, excessive salivation, coughing and/or labored breathing, loss of appetite, and weight loss. If neurological signs develop, incontinence may ensue. Central nervous system signs include a localized involuntary twitching of muscles or groups of muscles, seizures with salivation and jaw movements commonly described as "chewing gum fits", or more appropriately as "distemper myoclonus". As the condition progresses, the seizures worsen and advance to grand mal convulsions followed by death of the animal. The animal may also show signs of sensitivity to light, incoordination, circling, increased sensitivity to sensory stimuli such as pain or touch, and deterioration of motor capabilities. Less commonly, they may lead to blindness and paralysis. The length of the systemic disease may be as short as 10 days, or the start of neurological signs may not come until several weeks or months later. Those few that survive usually have a small tic or twitch of varying levels of severity. With time, this tic will usually diminish somewhat in its severity.
Equine viral arteritis (EVA) is a disease of horses caused by equine arteritis virus, an RNA virus of the genus "Arterivirus". The virus which causes EVA was first isolated in 1953, but the disease has afflicted equine animals worldwide for centuries. It has been more common in some breeds of horses in the United States, but there is no breed "immunity". In the UK, it is a notifiable disease. There is no known human hazard.
A dog that survives distemper will continue to have both nonlife-threatening and life-threatening signs throughout its lifespan. The most prevalent nonlife-threatening symptom is hard pad disease. This occurs when a dog experiences the thickening of the skin on the pads of its paws as well as on the end of its nose. Another lasting symptom commonly is enamel hypoplasia. Puppies, especially, will have damage to the enamel of teeth that are not completely formed or those that have not yet grown through the gums. This is a result of the virus's killing the cells responsible for manufacturing the tooth enamel. These affected teeth tend to erode quickly.
Life-threatening signs usually include those due to the degeneration of the nervous system. Dogs that have been infected with distemper tend to suffer a progressive deterioration of mental abilities and motor skills. With time, the dog can acquire more severe seizures, paralysis, reduction in sight and incoordination. These dogs are usually humanely euthanized because of the immense pain and suffering they face.
Bovine viral diarrhea (BVD) or bovine viral diarrhoea (UK English), and previously referred to as bovine virus diarrhoea (BVD), is a significant economic disease of cattle that is endemic in the majority of countries throughout the world. The causative agent, bovine viral diarrhea virus (BVDV), is a member of the "Pestivirus" genus of the family Flaviviridae.
BVD infection results in a wide variety of clinical signs, due to its immunosuppressive effects, as well as having a direct effect on respiratory disease and fertility. In addition, BVD infection of a susceptible dam during a certain period of gestation can result in the production of a persistently infected (PI) fetus.
PI animals recognise intra-cellular BVD viral particles as ‘self’ and shed virus in large quantities throughout life; they represent the cornerstone of the success of BVD as a disease.
West Nile virus (WNV) is a single-stranded RNA virus that causes West Nile fever. It is a member of the family Flaviviridae, specifically from the genus Flavivirus which also contain the Zika virus, dengue virus, and the yellow fever virus. The West Nile virus is primarily transmitted through mosquitoes, mostly by the Culex species. However, ticks have been found to carry the virus. The primary hosts of WNV are birds, so that the virus remains within a "bird-mosquito-bird" transmission cycle.
BVDV infection has a wide manifestation of clinical signs including fertility issues, milk drop, pyrexia, diarrhoea and fetal infection. Occasionally, a severe acute form of BVD may occur. These outbreaks are characterized by thrombocytopenia with high morbidity and mortality. However, clinical signs are frequently mild and infection insidious, recognised only by BVDV’s immunosuppressive effects perpetuating other circulating infectious diseases (particularly scours and pneumonias).
The length of time between exposure to the virus and the development of symptoms (incubation period) is between 2 and 21 days, and usually between 4 and 10 days. However, recent estimates based on mathematical models predict that around 5% of cases may take greater than 21 days to develop.
Symptoms usually begin with a sudden influenza-like stage characterized by feeling tired, fever, weakness, decreased appetite, muscular pain, joint pain, headache, and sore throat. The fever is usually higher than . This is often followed by vomiting, diarrhea and abdominal pain. Next, shortness of breath and chest pain may occur, along with swelling, headaches and confusion. In about half of the cases, the skin may develop a maculopapular rash, a flat red area covered with small bumps, 5 to 7 days after symptoms begin.
Oropouche fever is characterized as a acute febrile illness, meaning that it begins with a sudden onset of a fever followed by severe clinical symptoms. It typically takes 4 to 8 days from the incubation period to first start noticing signs of infection, beginning from the bite of the infected mosquito or midge.
Fevers are the most common symptom with temperatures as high as 104F. Clinical symptoms include chills, headache, myalgia, arthralgia, dizziness, photophobia, vomiting, joint pains, epigastric pain, and rashes.
There also have been some cases where rashes resembles rubella and patients presented systematic symptoms including nausea, vomiting, diarrhea, conjunctive congestion, epigastric pain, and retro-orbitial pain.
The initial febrile episode typically passes after a few days, but it is very common to have a reoccurrence of these symptoms with a lesser intensity. Studies have shown this typically happens in about 60% of cases.
Mayaro virus disease is a mosquitoborne zoonotic pathogen endemic to certain humid forests of tropical South America. Infection with Mayaro virus causes an acute, self-limited dengue-like illness of 3–5 days' duration. The causative virus, abbreviated MAYV, is in the family Togaviridae, and genus Alphavirus. It is closely related to other alphaviruses that produce a dengue-like illness accompanied by long-lasting arthralgia. It is only known to circulate in tropical South America.
The disease has a fatality rate of 3-10%, and it affects 400-500 people annually.
Recovery may begin between 7 and 14 days after first symptoms. Death, if it occurs, follows typically 6 to 16 days from first symptoms and is often due to low blood pressure from fluid loss. In general, bleeding often indicates a worse outcome, and blood loss may result in death. People are often in a coma near the end of life.
Those who survive often have ongoing muscular and joint pain, liver inflammation, decreased hearing, and may have continued tiredness, continued weakness, decreased appetite, and difficulty returning to pre-illness weight. Problems with vision may develop.
Additionally, survivors develop antibodies against Ebola that last at least 10 years, but it is unclear if they are immune to repeated infections.
The symptoms of the disease include a high fever with frontal headaches, followed by haemorrhagic symptoms, such as bleeding from the nasal cavity, throat, and gums, as well as gastrointestinal bleeding. Other symptoms include vomiting, muscle stiffness, tremors, absent reflexes, and mental disturbances.
An affected person may recover in two weeks time, but the convalescent period is typically very long, lasting for several months. There will be muscle aches and weakness during this period and the affected person is unable to engage in physical activities.
In humans, the virus can cause several syndromes. Usually, sufferers have either no symptoms or only a mild illness with fever, headache, muscle pains, and liver abnormalities. In a small percentage of cases (< 2%), the illness can progress to hemorrhagic fever syndrome, meningoencephalitis (inflammation of the brain and tissues lining the brain), or affect the eye. Patients who become ill usually experience fever, generalised weakness, back pain, dizziness, and weight loss at the onset of the illness. Typically, people recover within two to seven days after onset.
About 1% of people with the disease die of it. In livestock, the fatality level is significantly higher. Pregnant livestock infected with RVF abort virtually 100% of foetuses. An epizootic (animal disease epidemic) of RVF is usually first indicated by a wave of unexplained abortions.
Other signs in livestock include vomiting and diarrhoea, respiratory disease, fever, lethargy, anorexia and sudden death in young animals.
Human parainfluenza viruses (HPIVs) are the viruses that cause human parainfluenza. HPIVs are a group of four distinct single-stranded RNA viruses belonging to the Paramyxoviridae family. These viruses are closely associated with both human and veterinary disease. Virions are approximately 150–250 nm in size and contain negative sense RNA with a genome encompassing ~15,000 nucleotides.
The viruses can be detected via cell culture, immunofluorescent microscopy, and PCR. HPIVs remain the second main cause of hospitalisation in children under 5 years of age suffering from a respiratory illness (only respiratory syncytial virus causes more respiratory hospitalisations for this age group).
Signs and symptoms of VHFs include (by definition) fever and bleeding. Manifestations of VHF often also include flushing of the face and chest, small red or purple spots (petechiae), bleeding, swelling caused by edema, low blood pressure (hypotension), and shock. Malaise, muscle pain, headache, vomiting, and diarrhea occur frequently. The severity of symptoms varies with the type of virus. The “VHF syndrome” (capillary leak, bleeding diathesis, and circulatory compromise leading to shock) appears in a majority of people with filovirus hemorrhagic fevers (e.g., Ebola and Marburg virus), Crimean–Congo hemorrhagic fever (CCHF), and the South American hemorrhagic fevers caused by arenaviruses, but only in a small minority of patients with dengue, Rift Valley fever, and Lassa fever.
Viral entry is the earliest stage of infection in the viral life cycle, as the virus comes into contact with the host cell and introduces viral material into the cell. The major steps involved in viral entry are shown below. Despite the variation among viruses, there are several shared generalities concerning viral entry.
In 80% of cases, the disease is asymptomatic, but in the remaining 20%, it takes a complicated course. The virus is estimated to be responsible for about 5,000 deaths annually. The fever accounts for up to one-third of deaths in hospitals within the affected regions and 10 to 16% of total cases.
After an incubation period of six to 21 days, an acute illness with multiorgan involvement develops. Nonspecific symptoms include fever, facial swelling, and muscle fatigue, as well as conjunctivitis and mucosal bleeding. The other symptoms arising from the affected organs are:
- Gastrointestinal tract
- Nausea
- Vomiting (bloody)
- Diarrhea (bloody)
- Stomach ache
- Constipation
- Dysphagia (difficulty swallowing)
- Hepatitis
- Cardiovascular system
- Pericarditis
- Hypertension
- Hypotension
- Tachycardia (abnormally high heart rate)
- Respiratory tract
- Cough
- Chest pain
- Dyspnoea
- Pharyngitis
- Pleuritis
- Nervous system
- Encephalitis
- Meningitis
- Unilateral or bilateral hearing deficit
- Seizures
Clinically, Lassa fever infections are difficult to distinguish from other viral hemorrhagic fevers such as Ebola and Marburg, and from more common febrile illnesses such as malaria.
The virus is excreted in urine for 3–9 weeks and in semen for three months.
A viral disease (or viral infection) occurs when an organism's body is invaded by pathogenic viruses, and infectious virus particles (virions)
attach to and enter susceptible cells.
Viral disease is usually detected by clinical presentation, for instance severe muscle and joint pains preceding fever, or skin rash and swollen lymph glands.
Laboratory investigation is not directly effective in detecting viral infections, because they do not themselves increase the white blood cell count. Laboratory investigation may be useful in diagnosing associated bacterial infections, however.
Viral infections are commonly of limited duration, so treatment usually consists in reducing the symptoms; antipyretic and analgesic drugs are commonly prescribed.