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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
Currently, antibiotic drugs such as penicillin or tetracycline are the only effective methods for disease treatment. Within wild populations, disease control consists of reducing the amount of bacterial spores present in the environment. This can be done by removing contaminated carcasses and scat.
In laboratory animals, prevention includes a low-stress environment, an adequate amount of nutritional feed, and appropriate sanitation measurements. Because animals likely ingest bacterial spores from contaminated bedding and feed, regular cleaning is a helpful method of prevention. No prevention methods are currently available for wild animal populations.
As of 2017, there was no cure for BSE; some of the symptoms like twitching can be managed but otherwise treatment is palliative care.
However, simple husbandry changes and practical midge control measures may help break the livestock infection cycle. Housing livestock during times of maximum midge activity (from dusk to dawn) may lead to significantly reduced biting rates. Similarly, protecting livestock shelters with fine mesh netting or coarser material impregnated with insecticide will reduce contact with the midges. The "Culicoides" midges that carry the virus usually breed on animal dung and moist soils, either bare or covered in short grass. Identifying breeding grounds and breaking the breeding cycle will significantly reduce the local midge population. Turning off taps, mending leaks and filling in or draining damp areas will also help dry up breeding sites. Control by trapping midges and removing their breeding grounds may reduce vector numbers. Dung heaps or slurry pits should be covered or removed, and their perimeters (where most larvae are found) regularly scraped.
The use of antifungals and heat-induced therapy has been suggested as a treatment of "B. dendrobatidis." " "However, some of these antifungals may cause adverse skin effects on certain species of frogs. And although we do use them to treat species that are infected by chytridiomycosis, the infection never fully eradicates. A study done by Rollins-Smith and colleagues suggests that itraconazole is the antifungal of choice when it comes to treatment of "Bd." This is favored in comparison to amphotericin B and chloramphenicol because of their toxicity, specifically chloramphenicol as it is correlated with leukemia in toads. This becomes a difficult situation because without treatment, frogs will suffer from limb deformities and even death, but may also suffer skin abnormalities with treatment. Treatment of chytridiomycosis isn’t always successful, and some frogs are not able to handle the treatment process. It is important to consult with a veterinarian before treating frogs that suffer from chytridiomycosis"."
Individuals infected with "B. dendrobatidis" are bathed in intraconazole solutions, and within a few weeks, previously infected individuals test negative for "B. dendrobatidis" using PCR assays. Heat therapy is also used to neutralize "B. dendrobatidis" in infected individuals. Temperature-controlled laboratory experiments are used to increase the temperature of an individual past the optimal temperature range of "B. dendrobatidis". Experiments, where the temperature is increased beyond the upper bound of the "B. dendrobatidis" optimal range of 25 to 30 °C, show its presence will dissipate within a few weeks and individuals infected return to normal. Formalin/malachite green has also been used to successfully treat individuals infected with chytridiomycosis. An Archey's frog was successfully cured of chytridiomycosis by applying chloramphenicol topically. However, the potential risks of using antifungal drugs on individuals are high.
In unvaccinated humans, rabies is almost always fatal after neurological symptoms have developed.
Vaccination after exposure, PEP, is highly successful in preventing the disease if administered promptly, in general within 6 days of infection. Begun with little or no delay, PEP is 100% effective against rabies. In the case of significant delay in administering PEP, the treatment still has a chance of success.
Five of the first 43 patients (12%) treated with the Milwaukee protocol survived, and those receiving treatment survived longer than those not receiving the treatment.
As the infection is usually transmitted into humans through animal bites, antibiotics usually treat the infection, but medical attention should be sought if the wound is severely swelling. Pasteurellosis is usually treated with high-dose penicillin if severe. Either tetracycline or chloramphenicol provides an alternative in beta-lactam-intolerant patients. However, it is most important to treat the wound.
Infected fish should be moved into high quality water, where they may recover if their clinical signs are mild.
If disease occurs eradication is required. Once the disease is eradicated good husbandry, surveillance and biosecurity measures are necessary to prevent recurrence. In countries free of epizootic ulcerative syndrome, quarantine and health certificates are necessary for the movement of all live fish to prevent the introduction of the disease.
Treatment after exposure can prevent the disease if administered promptly, generally within 10 days of infection. Thoroughly washing the wound as soon as possible with soap and water for approximately five minutes is effective in reducing the number of viral particles. Povidone-iodine or alcohol is then recommended to reduce the virus further.
In the US, the Centers for Disease Control and Prevention recommends people receive one dose of human rabies immunoglobulin (HRIG) and four doses of rabies vaccine over a 14-day period. The immunoglobulin dose should not exceed 20 units per kilogram body weight. HRIG is expensive and constitutes most of the cost of post exposure treatment, ranging as high as several thousand dollars. As much as possible of this dose should be injected around the bites, with the remainder being given by deep intramuscular injection at a site distant from the vaccination site.
The first dose of rabies vaccine is given as soon as possible after exposure, with additional doses on days 3, 7 and 14 after the first. Patients who have previously received pre-exposure vaccination do not receive the immunoglobulin, only the postexposure vaccinations on days 0 and 3.
The pain and side effects of modern cell-based vaccines are similar to flu shots. The old nerve-tissue-based vaccinations that require multiple painful injections into the abdomen with a large needle are inexpensive, but are being phased out and replaced by affordable World Health Organization intradermal-vaccination regimens.
Intramuscular vaccination should be given into the deltoid, not the gluteal area, which has been associated with vaccination failure due to injection into fat rather than muscle. In infants, the lateral thigh is recommended.
Awakening to find a bat in the room, or finding a bat in the room of a previously unattended child or mentally disabled or intoxicated person, is an indication for post-exposure prophylaxis (PEP). The recommendation for the precautionary use of PEP in bat encounters where no contact is recognized has been questioned in the medical literature, based on a cost–benefit analysis. However, a 2002 study has supported the protocol of precautionary administering of PEP where a child or mentally compromised individual has been alone with a bat, especially in sleep areas, where a bite or exposure may occur without the victim being aware. Begun with little or no delay, PEP is 100% effective against rabies. In the case in which there has been a significant delay in administering PEP, the treatment should be administered regardless, as it may still be effective. Every year, more than 15 million people get vaccination after potential exposure. While this works well, the cost is significant.
A ban on feeding meat and bone meal to cattle has resulted in a strong reduction in cases in countries where the disease was present. In disease-free countries, control relies on import control, feeding regulations, and surveillance measures.
In UK and US slaughterhouses, the brain, spinal cord, trigeminal ganglia, intestines, eyes, and tonsils from cattle are classified as specified risk materials, and must be disposed of appropriately.
An enhanced BSE-related feed ban is in effect in both the United States and Canada to help improve prevention and elimination of BSE.
Outbreaks in southern Europe have been caused by serotypes 2 and 4, and vaccines are available against these serotypes (ATCvet codes: for sheep, for cattle). However, the disease found in northern Europe (including the UK) in 2006 and 2007 has been caused by serotype 8. Vaccine companies Fort Dodge Animal Health (Wyeth), Merial and Intervet were developing vaccines against serotype 8 (Fort Dodge Animal Health has serotype 4 for sheep, serotype 1 for sheep and cattle and serotype 8 for sheep and cattle) and the associated production facilities. A vaccine for this is now available in the UK, produced by Intervet. Fort Dodge Animal Health has their vaccines available for multiple European Countries (vaccination will start in 2008 in Germany, Belgium, Switzerland, Spain and Italy). However, immunization with any of the available vaccines preclude later serological monitoring of affected cattle populations, a problem which could be resolved using next-generation subunit vaccines currently in development.
In January 2015, Indian researchers launched its vaccine. Named 'Raksha Blu', it will protect the animals against five strains of the ‘bluetongue’ virus prevalent in the country.
Foot-and-mouth disease or hoof-and-mouth disease (Aphthae epizooticae) is an infectious and sometimes fatal viral disease that affects cloven-hoofed animals, including domestic and wild bovids. The virus causes a high fever for approximately two to six days, followed by blisters inside the mouth and on the feet that may rupture and cause lameness.
Foot-and-mouth disease (FMD) has very severe implications for animal farming, since it is highly infectious and can be spread by infected animals comparatively easily through contact with contaminated farming equipment, vehicles, clothing, feed and by domestic and wild predators. Its containment demands considerable efforts in vaccination, strict monitoring, trade restrictions, quarantines and occasionally the culling of animals.
Susceptible animals include cattle, water buffalo, sheep, goats, pigs, antelope, deer, and bison. It has also been known to infect hedgehogs and elephants; llamas and alpacas may develop mild symptoms, but are resistant to the disease and do not pass it on to others of the same species. In laboratory experiments, mice, rats, and chickens have been successfully infected by artificial means, but they are not believed to contract the disease under natural conditions. Humans are very rarely infected.
The virus responsible for the disease is a picornavirus, the prototypic member of the genus "Aphthovirus". Infection occurs when the virus particle is taken into a cell of the host. The cell is then forced to manufacture thousands of copies of the virus, and eventually bursts, releasing the new particles in the blood. The virus is genetically highly variable, which limits the effectiveness of vaccination.
The incubation period for foot-and-mouth disease virus has a range between one and 12 days. The disease is characterized by high fever that declines rapidly after two or three days, blisters inside the mouth that lead to excessive secretion of stringy or foamy saliva and to drooling, and blisters on the feet that may rupture and cause lameness. Adult animals may suffer weight loss from which they do not recover for several months, as well as swelling in the testicles of mature males, and in cows, milk production can decline significantly. Though most animals eventually recover from FMD, the disease can lead to myocarditis (inflammation of the heart muscle) and death, especially in newborn animals. Some infected ruminants remain asymptomatic carriers, but they nonetheless carry FMDV and may be able to transmit it to others. Pigs cannot serve as asymptomatic carriers.
In epizoology, an epizootic (from Greek: "epi-" upon + "zoon" animal) is a disease event in a nonhuman animal population, analogous to an epidemic in humans. An epizootic may be: restricted to a specific locale (an "outbreak"), general (an "epizootic") or widespread ("panzootic"). High population density is a major contributing factor to epizootics. Aquaculture is an industry sometimes plagued by disease because of the large number of fish confined to a small area.
Defining an epizootic can be subjective; it is based upon the number of new cases in a given animal population, during a given period, and must be judged to be a rate that substantially exceeds what is expected based on recent experience ("i.e." a sharp elevation in the incidence rate). Because it is based on what is "expected" or thought normal, a few cases of a very rare disease (like a TSE outbreak in a cervid population) might be classified as an "epizootic", while many cases of a common disease (like lymphocystis in esocids) would not.
Common diseases that occur at a constant but relatively high rate in the population are said to be "enzootic" ("cf." the epidemiological meaning of "endemic" for human diseases). An example of an enzootic disease would be the influenza virus in some bird populations or, at a lower incidence, the Type IVb strain of VHS in certain Atlantic fish populations.
An example of an epizootic would be the 1990 outbreak of Newcastle disease virus in double-crested cormorant colonies on the Great Lakes that resulted in the death of some 10,000 birds.
Prophylaxis by vaccination, as well as preventive measures like protective clothing, tick control, and mosquito control are advised. The vaccine for KFDV consists of formalin-inactivated KFDV. The vaccine has a 62.4% effectiveness rate for individuals who receive two doses. For individuals who receive an additional dose, the effectiveness increases to 82.9%. Specific treatments are not available.
Sylvatic plague is an infectious bacterial disease caused by the bacterium "Yersinia pestis" that primarily affects rodents such as prairie dogs. It is the same bacterium that causes bubonic and pneumonic plague in humans. Sylvatic, or sylvan, means 'occurring in wildlife,' and refers specifically to the form of plague in rural wildlife. Urban plague refers to the form in urban wildlife.
It is primarily transmitted among wildlife through flea bites and contact with infected tissue or fluids. Sylvatic plague is most commonly found in prairie dog colonies and some mustelids like the black-footed ferret.
A vaccine has been conditionally approved for use in animals in the US. It has been shown that knockout of the NSs and NSm nonstructural proteins of this virus produces an effective vaccine in sheep as well.
As for other flavivirus infections, no cure is known for yellow fever. Hospitalization is advisable and intensive care may be necessary because of rapid deterioration in some cases. Different methods for acute treatment of the disease have been shown not to be very successful; passive immunisation after emergence of symptoms is probably without effect. Ribavirin and other antiviral drugs, as well as treatment with interferons, do not have a positive effect in patients.
A symptomatic treatment includes rehydration and pain relief with drugs such as paracetamol (acetaminophen in the United States). Acetylsalicylic acid (aspirin) should not be given because of its anticoagulant effect, which can be devastating in the case of internal bleeding that can occur with yellow fever.
White plague is a suite of coral diseases of which three types have been identified, initially in the Florida Keys. They are infectious diseases but it has proved difficult to identify the pathogens involved. White plague type II may be caused by the gram negative bacterium "Aurantimonas coralicida" in the order Rhizobiales but other bacteria have also been associated with diseased corals and viruses may also be implicated.
Rinderpest (also cattle plague or steppe murrain) was an infectious viral disease of cattle, domestic buffalo, and many other species of even-toed ungulates, including buffaloes, large antelope and deer, giraffes, wildebeests, and warthogs. The disease was characterized by fever, oral erosions, diarrhea, lymphoid necrosis, and high mortality. Death rates during outbreaks were usually extremely high, approaching 100% in immunologically naïve populations. Rinderpest was mainly transmitted by direct contact and by drinking contaminated water, although it could also be transmitted by air. After a global eradication campaign, the last confirmed case of rinderpest was diagnosed in 2011.
On 14 October 2010, the United Nations Food and Agriculture Organization (FAO) announced that field activities in the decades-long, worldwide campaign to eradicate the disease were ending, paving the way for a formal declaration in June 2011 of the global eradication of rinderpest. On 25 May 2011, the World Organisation for Animal Health announced the free status of the last eight countries not yet recognized (a total of 198 countries were now free of the disease), officially declaring the eradication of the disease. In June 2011, the United Nations FAO confirmed the disease was eradicated, making rinderpest only the second disease in history to be fully wiped out (outside laboratory stocks), following smallpox.
Rinderpest is believed to have originated in Asia, later spreading through the transport of cattle. The term "Rinderpest" is a German word meaning "cattle-plague". The rinderpest virus (RPV) was closely related to the measles and canine distemper viruses. The measles virus emerged from rinderpest as a zoonotic disease between 1000 and 1100 AD, a period that may have been preceded by limited outbreaks involving a virus not yet fully acclimated to humans.
The hypothesis that pesticide use has contributed to declining amphibian populations has been suggested several times in the literature. Interactions between pesticides and chytridiomycosis were examined in 2007, and sublethal exposure to the pesticide carbaryl (a cholinesterase inhibitor) was shown to increase susceptibility of foothill yellow-legged frogs ("Rana boylii") to chytridiomycosis. In particular, the skin peptide defenses were significantly reduced after exposure to carbaryl, suggesting pesticides may inhibit this innate immune defence, and increase susceptibility to disease.
Sylvatic plague is most commonly found in prairie dog colonies; the flea that feeds on prairie dogs (and other mammals) serves as the vector for transmission to the new host.
In 1977, a disease of scleractinian corals appeared on reefs off the Florida Keys in the United States and was termed white plague. It caused white lesions and was shown to be an infectious disease, being particularly prevalent in "Mycetophyllia ferox". This disease caused little mortality and occurred sporadically, but was still present in the area in 1984. It is now known as white plague type 1.
In 1995, a new coral disease was described as an epizootic disease in the same reefs in the Florida Keys. Many species of coral found in the area were affected and the mortality rate of these was up to 38%. The pathogen involved was found to be a previously unknown species of bacterium in the order Rhizobiales, which was placed in the newly created genus "Aurantimonas" and given the name "Aurantimonas coralicida", and the disease was described as white plague type 2. The pathogen was isolated from a diseased colony of "Dichocoenia stokesi" and cultured in the laboratory, subsequently being used to inoculate two healthy colonies which then developed the disease. In the next few months, it had spread over of reef and was killing seventeen species of coral. Over the next four years, it spread further, but interestingly, was most severe in different regions each year.
However, white plague is an enigmatic disease. Further research cast into doubt the role of "A. coralicida" as a causative agent by finding that bacterium on healthy parts of colonies of "Orbicella annularis" affected by white plague disease but absent from diseased parts. In these diseased colonies, an α-proteobacterium similar to one which causes a disease in juvenile oysters has been implicated, being found on the diseased parts of the coral but not on the sound tissues. These anomalous findings may be caused by the fact that there are two or more diseases with similar symptoms, both known as white plague.
In 1999, a third and still more virulent variant appeared in the northern Florida Keys. White plague type III mostly affected "Colpophyllia natans" and "Orbicella annularis".
A white-plague like disease reported from the Red Sea in 2005 has been shown to be caused by a different bacterial pathogen, "Thalassomonas loyana". Further research has shown that viruses may be involved in white plague infections, the coral small circular ssDNA viruses (SCSDVs) being present in association with diseased tissue. This group of viruses is known to cause disease in plants and animals.
Death rates during outbreaks were usually extremely high, approaching 100% in immunologically naïve populations. The disease was mainly spread by direct contact and by drinking contaminated water, although it could also be transmitted by air.
Initial symptoms include fever, loss of appetite, and nasal and eye discharges. Subsequently, irregular erosions appear in the mouth, the lining of the nose, and the genital tract. Acute diarrhea, preceded by constipation, is also a common feature. Most animals die six to twelve days after the onset of these clinical signs.
The virus is thought to have been introduced into Eritrea in 1887 by Indian cattle brought by the Italians for their campaign against Somalia. It spread throughout the Horn of Africa, and crossed the Zambezi in March of 1896.