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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)
Funded by The Federal Ministry for Economic Affairs and Energy; Grant: 01MD19013D, Smart-MD Project, Digital Technologies
While the general prognosis is favorable, current studies indicate that West Nile Fever can often be more severe than previously recognized, with studies of various recent outbreaks indicating that it may take as long as 60–90 days to recover. People with milder WNF are just as likely as those with more severe manifestations of neuroinvasive disease to experience multiple long term (>1+ years) somatic complaints such as tremor, and dysfunction in motor skills and executive functions. People with milder illness are just as likely as people with more severe illness to experience adverse outcomes. Recovery is marked by a long convalescence with fatigue. One study found that neuroinvasive WNV infection was associated with an increased risk for subsequent kidney disease.
Risk factors independently associated with developing a clinical infection with WNV include a suppressed immune system and a patient history of organ transplantation. For neuroinvasive disease the additional risk factors include older age (>50+), male sex, hypertension, and diabetes mellitus.
A genetic factor also appears to increase susceptibility to West Nile disease. A mutation of the gene "CCR5" gives some protection against HIV but leads to more serious complications of WNV infection. Carriers of two mutated copies of "CCR5" made up 4.0 to 4.5% of a sample of West Nile disease sufferers, while the incidence of the gene in the general population is only 1.0%.
Treatment is similar to hepatitis B, but due to its high lethality, more aggressive therapeutic approaches are recommended in the acute phase. In absence of a specific vaccine against delta virus, the vaccine against HBV must be given soon after birth in risk groups.
Infection with Japanese encephalitis confers lifelong immunity. There are currently three vaccines available: SA14-14-2, IC51 (marketed in Australia and New Zealand as JESPECT and elsewhere as IXIARO) and ChimeriVax-JE (marketed as IMOJEV). All current vaccines are based on the genotype III virus.
A formalin-inactivated mouse-brain derived vaccine was first produced in Japan in the 1930s and was validated for use in Taiwan in the 1960s and in Thailand in the 1980s. The widespread use of vaccine and urbanization has led to control of the disease in Japan, Korea, Taiwan, and Singapore. The high cost of this vaccine, which is grown in live mice, means that poorer countries have not been able to afford to give it as part of a routine immunization program.
The most common adverse effects are redness and pain at the injection site. Uncommonly, an urticarial reaction can develop about four days after injection. Vaccines produced from mouse brain have a risk of autoimmune neurological complications of around 1 per million vaccinations. However where the vaccine is not produced in mouse brains but in vitro using cell culture there is little adverse effects compared to placebo, the main side effects are headache and myalgia.
The neutralizing antibody persists in the circulation for at least two to three years, and perhaps longer. The total duration of protection is unknown, but because there is no firm evidence for protection beyond three years, boosters are recommended every three years for people who remain at risk. Furthermore, there is also no data available regarding the interchangeability of other JE vaccines and IXIARO.
In September 2012 the Indian firm Biological E. Limited has launched an inactivated cell culture derived vaccine based on SA 14-14-2 strain which was developed in a technology transfer agreement with Intercell and is a thiomersal-free vaccine.
Many viral infections of the central nervous system occur in seasonal peaks or as epidemics, whereas others, such as herpes simplex encephalitis, are sporadic. In endemic areas it is mostly a disease of children, but as the disease spreads to new regions, or nonimmune travelers visit endemic regions, nonimmune adults are also affected.
Preventing Omsk Hemorrhagic Fever consists primarily in avoiding being exposed to tick. Persons engaged in camping, farming, forestry, hunting (especially the Siberian muskrat) are at greater risk and should wear protective clothing or use insect repellent for protection. The same is generally recommended for persons at sheltered locations.
Omsk hemorrhagic fever is caused by the Omsk hemorrhagic fever virus (OHFV), a member of the Flavivirus family. The virus was discovered by Mikhail Chumakov and his colleagues between 1945 and 1947 in Omsk, Russia. The infection is found in western Siberia, in places including Omsk, Novosibirsk, Kurgan, and Tyumen. The virus survives in water and is transferred to humans via contaminated water or an infected tick.
Hand, foot and mouth disease most commonly occurs in children under the age of 10. It tends to occur in outbreaks during the spring, summer, and autumn seasons. This is believed to be due to heat and humidity improving spread. HFMD is more common in rural areas than urban areas, however, socioeconomic status and hygiene levels need to considered. Poor hygiene is a risk factor for HFMD.
Outbreaks have relatively recently in China, Japan, Hong Kong, the Republic of Korea, Malaysia, Singapore, Thailand, Taiwan and Vietnam. HFMD most commonly affects young children under the age of 10 and more often under the age of 5, but can also affect adults with varying symptoms.
Since 1997 there have been 71 large enterovirus outbreaks reported, mostly in East and South East Asia, primarily affecting children. From the years 2008 to 2014, more than 1 million HFMD cases have been reported in China each year.
The majority of MVEV infections are sub-clinical, i.e. do not produce disease symptoms, although some people may experience a mild form of the disease with symptoms such as fever, headaches, nausea and vomiting and only a very small number of these cases go on to develop MVE. In fact, serological surveys which measure the level of anti-MVEV antibodies within the population estimate that only 1 in 800-1000 of all infections result in clinical disease.
The incubation period following exposure to the virus is around 1 to 4 weeks. Following infection, a person will have lifelong immunity to the virus. When a patient appears to show MVE symptoms and has been in an MVE-endemic area during the wet season, when outbreaks usually occur, MVE infection must be confirmed by laboratory diagnosis, usually by detection of a significant rise of MVE-specific antibodies in the patient's serum.
Of those who contract MVE, one-quarter die from the disease.
The disease can be prevented in horses with the use of vaccinations. These vaccinations are usually given together with vaccinations for other diseases, most commonly WEE, VEE, and tetanus. Most vaccinations for EEE consist of the killed virus. For humans there is no vaccine for EEE so prevention involves reducing the risk of exposure. Using repellent, wearing protective clothing, and reducing the amount of standing water is the best means for prevention
The La Crosse encephalitis virus is a type of arbovirus called a bunyavirus. The Bunyavirales are mainly arboviruses.
Most cases of LAC encephalitis occur in children under 16 years of age. LAC virus is a zoonotic pathogen cycled between the daytime-biting treehole mosquito, "Aedes triseriatus", and vertebrate amplifier hosts (chipmunks, tree squirrels) in deciduous forest habitats. The virus is maintained over the winter by transovarial transmission in mosquito eggs. If the female mosquito is infected, she may lay eggs that carry the virus, and the adults coming from those eggs may be able to transmit the virus to chipmunks and to humans.
Anyone bitten by a mosquito in an area where the virus is circulating can get infected with LACV. The risk is highest for people who live, work or recreate in woodland habitats, because of greater exposure to potentially infected mosquitoes.
Meningitis is a very common in children. Newborns can develop herpes virus infections through contact with infected secretions in the birth canal. Other viral infections are acquired by breathing air contaminated with virus-containing droplets exhaled by an infected person. Arbovirus infections are acquired from bites by infected insects (called epidemic encephalitis). Viral central nervous system infections in newborns and infants usually begin with fever. The inability of infants to communicate directly makes it difficult to understand their symptoms. Newborns may have no other symptoms and may initially not otherwise appear ill. Infants older than a month or so typically become irritable and fussy and refuse to eat. Vomiting is common. Sometimes the soft spot on top of a newborn's head (fontanelle) bulges, indicating an increase in pressure on the brain. Because irritation of the meninges is worsened by movement, an infant with meningitis may cry more, rather than calm down, when picked up and rocked. Some infants develop a strange, high-pitched cry. Infants with encephalitis often have seizures or other abnormal movements. Infants with severe encephalitis may become lethargic and comatose and then die. To make the diagnosis of meningitis or the diagnosis of encephalitis, doctors do a spinal tap (lumbar puncture) to obtain cerebrospinal fluid (CSF) for laboratory analysis in children.
People reduce the chance of getting infected with LACV by preventing mosquito bites. There is no vaccine or preventive drug.
Prevention measures against LACV include reducing exposure to mosquito bites. Use repellent such as DEET and picaridin, while spending time outside, especially at during the daytime - from dawn until dusk. "Aedes triseriatus" mosquitoes that transmit (LACV) are most active during the day. Wear long sleeves, pants and socks while outdoors. Ensure all screens are in good condition to prevent mosquitoes from entering your home. "Aedes triseriatus" prefer treeholes to lay eggs in. Also, remove stagnant water such as old tires, birdbaths, flower pots, and barrels.
Lábrea fever is a coinfection or superinfection of hepatitis D or delta virus and hepatitis B (HBV). The infection by delta virus may occur in a patient who already has the HBV, or both viruses may infect at the same time a previously uninfected patient. Delta virus can only multiply in the presence of HBV, therefore vaccination against HBV prevents infection. Thus, American and Brazilian scientists have determined that the delta virusa, virus, which is a small circular RNA virus, is normally unable to cause illness by itself, due to a defect. When it is combined with HBV, Lábrea hepatitis may ensue. The main discovery of delta virus and HBV association was done by Dr. Gilberta Bensabath, a leading tropical virologist of the Instituto Evandro Chagas, of Belém, state of Pará, and her collaborators.
Infected patients show extensive destruction of liver tissue, with steatosis of a particular type (microsteatosis, characterized by small fat droplets inside the cells), and infiltration of large numbers of inflammatory cells called "morula cells", comprised mainly by macrophages containing delta virus antigens.
In the 1987 Boca do Acre study, scientists did an epidemiological survey and reported delta virus infection in 24% of asymptomatic HBV carriers, 29% of acute nonfulminant hepatitis B cases, 74% of fulminant hepatitis B cases, and 100% of chronic hepatitis B cases. The delta virus seems to be endemic in the Amazon region.
There is no specific vaccine against or treatment for exanthema subitum, and most children with the disease are not seriously ill.
There is no specific treatment for Japanese encephalitis and treatment is supportive, with assistance given for feeding, breathing or seizure control as required. Raised intracranial pressure may be managed with mannitol. There is no transmission from person to person and therefore patients do not need to be isolated.
A breakthrough in the field of Japanese encephalitis therapeutics is the identification of macrophage receptor involvement in the disease severity. A recent report of an Indian group demonstrates the involvement of monocyte and macrophage receptor CLEC5A in severe inflammatory response in Japanese Encephalitis infection of the brain. This transcriptomic study provides a hypothesis of neuroinflammation and a new lead in development of appropriate therapeutic against Japanese encephalitis.
A vaccine known as the EV71 vaccine is available to prevent HFMD in China as of December 2015. No vaccine is currently available in the United States.
MVEV is a mosquito-borne virus that is maintained in a bird-mosquito-bird cycle. Water birds from the order Ciconiiformes, including herons and cormorants, provide the natural reservoir for MVEV. The major mosquito vector is "Culex annulirostris". Human infection occurs only through bites from infected mosquitoes; the virus cannot be transmitted from person to person.
There is currently no established treatment.
Half of all cases results in permanent neurological damage and 10-15% result in death.
Viral encephalitis is a type of encephalitis caused by a virus.
It is unclear if anticonvulsants used in people with viral encephalitis would prevent seizures.
There are no vaccines or any other treatments specifically for Saint Louis encephalitis virus, although one study showed that early use of interferon-alpha2b may decrease the severity of complications.
Rocio viral encephalitis is an epidemic flaviviral disease of humans first observed in São Paulo State, Brazil, in 1975. Low-level enzootic transmission is likely continuing in the epidemic zone, and with increased deforestation and population expansion, additional epidemics caused by Rocio virus are highly probable. If migratory species of birds are, or become involved in, the virus transmission cycle, the competency of a wide variety of mosquito species for transmitting Rocio virus experimentally suggest that the virus may become more widely distributed. The encephalitis outbreak in the western hemisphere caused by West Nile virus, a related flavivirus, highlights the potential for arboviruses to cause severe problems far from their source enzootic foci.
The causative Rocio virus belongs to the genus "Flavivirus" (the same genus as the Zika virus) in family Flaviviridae and is closely related serologically to Ilhéus, St. Louis encephalitis, Japanese encephalitis and Murray Valley encephalitis viruses.
TBE is caused by tick-borne encephalitis virus, a member of the genus "Flavivirus" in the family Flaviviridae. It was first isolated in 1937. Three virus sub-types are described: European or Western tick-borne encephalitis virus, Siberian tick-borne encephalitis virus, and Far-Eastern tick-borne encephalitis virus (formerly known as Russian spring summer encephalitis virus).
Russia and Europe report about 5,000–7,000 human cases annually.
The former Soviet Union conducted research on tick borne diseases, including the TBE viruses.
Roseola is caused by two human herpesviruses, "human herpesvirus 6" (HHV-6) and "human herpesvirus 7" (HHV-7), which are sometimes referred to collectively as Roseolovirus. There are two variants of HHV-6 (HHV-6a and HHV-6b) and studies in the US, Europe, Dubai and Japan have shown that exanthema subitum is caused by HHV-6b. This form of HHV-6 infects over 90% of infants by age 2.
There is no cure for EEE. Treatment consists of corticosteroids, anticonvulsants, and supportive measures (treating symptoms) such as intravenous fluids, tracheal intubation, and antipyretics. About four percent of humans known to be infected develop symptoms, with a total of about six cases per year in the US. A third of these cases die, and many survivors suffer permanent brain damage.