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As of November 2013, no identifiable cause for the disease had been found. Pathogenic bacteria did not seem to be present, and though the plague might be caused by a viral or fungal pathogen, no causal agent had been found. Each episode of plague might have a different cause.
Other possible causes of the condition that have been suggested include high sea temperatures, oxygen depletion and low salinity due to freshwater runoff. Research suggests that high water temperatures are indeed linked to the disease, increasing its incidence and virulence. The disease also seems more prevalent in sheltered waters than in open seas with much wave movement. One result of global warming is higher sea temperatures. There is a wave of unusually warm water along the west coast of the United States, which is where all of the sea stars are dying off. These may impact both on starfish and on echinoderm populations in general, and a ciliate protozoan parasite ("Orchitophrya stellarum") of starfish, which eats sperm and effectively emasculates male starfish, thrives at higher temperatures.
Research in 2014 showed that the cause of the disease is transmissible from one starfish to another and that the disease-causing agent is a microorganism in the virus-size range. The most likely candidate causal agent was found to be the sea star-associated densovirus (SSaDV), which was found to be in greater abundance in diseased starfish than in healthy ones.
Necrotic ring spot can be managed through chemical and cultural controls. Cultural control includes the use of ammonium sulfate or other acidifying fertilizers to suppress the pathogen by lowering the pH of the soil to between 6.0 and 6.2. The more acidic soil discourages the activity of "O. korrae" (9) When reducing pH to these levels, additional manganese applications should be undertaken to compensate for lower pH. As of now, there are only two resistant cultivars of bluegrass, which are ‘Riviera’, and ‘Patriot’ (9). One component of their resistance could be that they are tolerant to low temperature, because the grass is more susceptible to the pathogen under colder temperatures(8). In addition, reducing watering inputs and growing turf on well drained soils can lessen disease symptoms.
Many different fungicides are used to control the pathogen, Fenarimol, Propiconazole, Myclobutanil, and Azoxystrobin (8). Historically, Fenarimol and Myclobutanil were predominantly used (14). In a study where diluted pesticides were sprayed throughout infested test plots, Fenarimol was found to be the most effective with a 94.6% reduction of the disease. Myclobutanil also decreased the amount of disease, but only by 37.7% (8). Myclobutanil is generally recognized as a very weakly acting demethylation inhibitor (DMI) fungicide and fenarimol is no longer registered for turf so a number of other DMI fungicides have been employed successfully, including Propiconazole, Tebuconazole, Metconazole and others. Pyraclostrobin and Fluoxastrobin have also been used to control the pathogen.
In 2014, Point Defiance Zoo and Aquarium lost more than half of its 369 sea stars, and by September 2015 they numbered fewer than 100. The aquarium treated its affected sea stars with antibiotics in 2014, which proved effective. Although a mechanism is still unknown, evidence suggests that a single mutation in the elongation factor 1-alpha locus in "Pisaster ochraceus" may be associated with reduced mortality.
Currently, the most effective treatment is transferring the affected fish to a freshwater bath for a period of 2 to 3 hours. This is achieved by towing the sea cages into fresh water, or pumping the fish from the sea cage to a tarp filled with fresh water. Mortality rates have been lowered by adding Levamisole to the water until the saturation is above 10ppm. Due to the difficulty and expense of treatment, the productivity of salmon aquaculture is limited by access to a source of fresh water. Chloramine and chlorine dioxide have also been used. Other potential in-feed treatments such as immunosupportive-based feeds, mucolytic compounds such as L-cysteine ethyl ester and the parasticide bithionol have been tested with some success although not developed for commercial use.
Chemically speaking, bletting brings about an increase in sugars and a decrease in the acids and tannins that cause the unripe fruit to be astringent.
Ripe medlars, for example, are taken from the tree, placed somewhere cool, and allowed to ripen for several weeks. In "Trees and Shrubs", horticulturist F. A. Bush wrote about medlars that "if the fruit is wanted it should be left on the tree until late October and stored until it appears in the first stages of decay; then it is ready for eating. More often the fruit is used for making jelly." Ideally, the fruit should be harvested from the tree immediately following a hard frost, which starts the bletting process by breaking down cell walls and speeding softening.
Once the process is complete, the medlar flesh will have broken down enough that it can be spooned out of the skin. The taste of the sticky, mushy substance has been compared to sweet dates and dry applesauce, with a hint of cinnamon. In "Notes on a Cellar-Book", the great English oenophile George Saintsbury called bletted medlars the "ideal fruit to accompany wine."
Skeletal eroding band (SEB) is a disease of corals that appears as a black or dark gray band that slowly advances over corals, leaving a spotted region of dead coral in its wake. It is the most common disease of corals in the Indian and Pacific Oceans, and is also found in the Red Sea.
So far one agent has been clearly identified, the ciliate "Halofolliculina corallasia". This makes SEB the first coral disease known to be caused by a protozoan. When "H. corallasia" divides, the daughter cells move to the leading edge of the dark band and produce a protective shell called a lorica. To do this, they drill into the coral's limestone skeleton, killing coral polyps in the process.
A disease with very similar symptoms has been found in the Caribbean Sea, but has been given a different name as it is caused by a different species in the genus "Halofolliculina" and occurs in a different type of environment.
A survey in the Caribbean Sea conducted in 2004 and published in 2006 reported a disease with very similar symptoms, affecting 25 species of coral within 6 families. Although the authors initially suspected "H.corallasia", more detailed examination showed that the culprit was another species that was previously unknown and has not yet been formally named, although it is clearly a member of the same genus, "Halofolliculina". A follow-up analysis noted that the Caribbean infestations were commonest in oceanic waters, while those in the Indian and Pacific Oceans were more prevalent in coastal waters. Because of these two differences, the authors gave this new manifestation the name "Caribbean ciliate infection". Coral diseases are a relatively new topic of research, and the use of standardized terminology has not yet been fixed.
This pathogen is important because it affects homeowners lawns and also golf courses. It also affects parks and recreational areas. It is important because it can impede people and their ability to enjoy their landscapes. The dead patches are also unsightly, so it is important to control the disease, and keep it from spreading.
Corals growing in the Caribbean Sea are particularly affected by disease, perhaps because of the limited water circulation and the density of the human population on the surrounding land masses. Disease is also present in the tropical Indo-Pacific, but it is not so widespread, perhaps because of the more dispersed locations of the reefs.
Coral diseases, comprising the diseases that affect corals, injure the living tissues and often result in the death of part or the whole of the colony. These diseases have been occurring more frequently in the twenty-first century as conditions become more stressful for many shallow-water corals. The pathogens causing the diseases include bacteria, fungi and protozoa, but it is not always possible to identify the pathogen involved.
Cases have been found in Bermuda in 2011, 2014 and 2015 with Paradise Lakes proving particularly bad. In 2015 many felt the effects after swimming in Mangrove Bay and Harrington Sound.
At certain times of the year this can be a problem in some areas of the Bahamas particularly around New Providence.
Bald sea urchin disease is a bacterial disease known to affect several species of sea urchins on Mediterranean Sea, North Atlantic and California coastlines. Research suggests two pathogens are responsible for the disease, "Listonella anguillarum" and "Aeromonas salmonicida".
Infection generally occurs at the site of an existing physical injury. The affected area turns green and spines and other appendages are lost. If the lesion remains shallow and covers less than 30% of the animal's surface area, the animal tends to survive and eventually regenerates any lost tissue. However if the damage is more extensive or so deep that the hard inner test is perforated, the disease is fatal.
Bletting is a process of softening that certain fleshy fruits undergo, beyond ripening. There are some fruits that are either sweeter after some bletting, such as sea buckthorn, or for which most varieties can be eaten raw only after bletting, such as medlars, persimmons, quince, service tree fruit, and wild service tree fruit ("chequers"). The rowan or mountain ash fruit must be bletted and cooked to be edible, to break down the toxic parasorbic acid (hexenollactone) into sorbic acid.
Amoebic gill disease (AGD) is a potentially fatal disease of some marine fish. It is caused by "Neoparamoeba perurans", the most important amoeba in cultured fish. It primarily affects farm raised fish of the Salmonidae family, most notably affecting the Tasmanian Atlantic Salmon (Salmo salar) industry, costing the A$20 million a year in treatments and lost productivity. Turbot, bass, bream, sea urchins and crabs have also been infected.
The disease has also been reported affecting the commercial salmon fisheries of the United States, Australia, New Zealand, France, Spain, Ireland and Chile. It was first diagnosed in the summer of 1984/1985 in populations of Atlantic Salmon off the east coast of Tasmania and was found to be caused by the "Neoparamoeba perurans" n.sp.
Ulcerative dermal necrosis (UDN) is a chronic dermatological disease of cold water salmonid fish that had a severe impact on north Atlantic Salmon and sea trout stocks in the late 1960s, the 1970s and 1980.
Affected fish developed severe skin lesions over large parts of their body which penetrated into skeletal muscle. The onset of symptoms only occurred after migration into freshwater. Lesions became quickly infected with overgrowths of "Saprolegnia" fungus giving the affected fish an appearance of being covered in slimy white pustules. The most severely affected fish frequently die before spawning.
Although the worst effects of the disease were seen in the 1970s and 1980, even now large numbers of salmon will succumb to the disease after spawning. This is thought be due in part to their weak post-spawning condition, and lack of food for several months whilst in the river.
Those fish that do make it back to the sea are thought to make a good recovery.
As first described by Dunstan in 1977, white plague type 1 produces lesions on any part of the colony. These increase gradually in size, advancing at the rate of a few millimetres per day. The advancing edge exhibits a sharp boundary between the apparently healthy tissue and the bare skeleton. Type II, first appearing in 1995 is similar, but it usually starts at the base of the colony, and the edge advances at a faster rate, up to per day. White plague type III advances at a rate in excess of two centimetres per day.
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.
no approved human vaccine exist against "Dermatophytosis". For horses, dogs and cats there is available an approved inactivated vaccine called "Insol Dermatophyton" (Boehringer Ingelheim) which provides time-limited protection against several trichophyton and microsporum fungal strains.
Advice often given includes:
- Avoid sharing clothing, sports equipment, towels, or sheets.
- Wash clothes in hot water with fungicidal soap after suspected exposure to ringworm.
- Avoid walking barefoot; instead wear appropriate protective shoes in locker rooms and sandals at the beach.
- Avoid touching pets with bald spots, as they are often carriers of the fungus.
The cat should be taken to a veterinarian. The most suspected cause of skin problems in cats will be fleas. Other causes of over-grooming are not as easily ascertained. As household antiseptics are known to be toxic to cats, veterinary antiseptics for cats can be used to treat open sores, if they do occur. Sores can also be treated with cream, oral or injected anti-inflammatories, however if the problem continues to recur it may be more cost effective to subject the cat to laboratory testing early on. It may be difficult to keep a clean dressing on a cat's belly, and an anti-lick collar is adequate to let the wound heal. If an anti lick collar is used, a soft anti-lick collar is less cumbersome, although they are less durable. If the cat wears a plastic anti-lick collar, it may use the edge of the collar to grind against existing wounds, making them worse. A soft anti lick collar will become less effective as it is kicked out of the shape by the cat's hind leg, and will need prompt replacement. The cat can sanitize the wound if the collar is removed for daily short periods of time, also giving the cat an opportunity for an overall grooming. Scratches and wounds can heal completely using this method. When the cat stops wearing the collar, thinned hair, redness of skin or cracked nipples on the cat are early indicators that the cat has started to over-groom again.
Antidepressants for cats may be suggested by a vet.
PSP has been implicated as a possible cause of sea otter mortality and morbidity in Alaska, as one of its primary prey items, the butter clam "(Saxidonus giganteus)" bioaccumulates saxitoxin as a chemical defense mechanism. In addition, ingestion of saxitoxin-containing mackerel has been implicated in the death of humpback whales
Additional cases where PSP was suspected as the cause of death in Mediterranean monk seals ("Monachus monachus") in the Mediterranean Sea have been questioned due to lack of additional testing to rule out other causes of mortality.
The first step in treatment following a bee sting is removal of the stinger itself. The stinger should be removed as quickly as possible without regard to method: studies have shown the amount of venom delivered does not differ whether the sting is pinched or scraped off and even a delay of a few seconds leads to more venom being injected. Once the stinger is removed, pain and swelling should be reduced with a cold compress. A topical anesthetic containing benzocaine will kill pain quickly and menthol is an effective anti-itch treatment. Itching can also be relieved by antihistamine or by a steroid cream.
Many traditional remedies have been suggested for bee stings including damp pastes of tobacco, salt, baking soda, papain, toothpaste, clay, garlic, urine, onions, aspirin or even application of copper coins. As with jellyfish stings, ammonia and ammonia-containing liquids, such as window cleaner, are often suggested as a way to immediately cleanse the skin and remove excess venom, and sweat itself (which also contains small amounts of ammonia) may provide some small relief.
Bee venom is acidic, and these interventions are often recommended to neutralize the venom; however, neutralizing a sting is unlikely to be effective as the venom is injected under the skin and deep into the tissues, where a topically applied alkali is unable to reach, so neutralization is unlikely to occur. In any case, the amount of venom injected is typically very small (between 5 and 50 micrograms of fluid) and placing large amounts of alkali near the sting site is unlikely to produce a perfectly neutral pH to stop the pain. Many people do claim benefit from these home remedies but it is doubtful they have any real physical effect on how much a sting hurts or continues hurting. The effect is probably related to rubbing the area or the mind perceiving benefit. Furthermore, none of these interventions have been proven to be effective in scientific studies and a randomized trial of aspirin paste and topical ice packs showed that aspirin was not effective in reducing the duration of swelling or pain in bee and wasp stings, and significantly increased the duration of redness. The study concluded that ice alone is better treatment for bee and wasp stings than aspirin.
The sting may be painful for a few hours. Swelling and itching may persist for a week. The area should not be scratched as it will only increase the itching and swelling. If swelling persists for over a week or covers an area greater than , medical attention should be sought. Doctors often recommend a tetanus immunization. For about 2 percent of people, a hypersensitivity can develop after being stung, creating a more severe reaction when stung again later. This sensitisation may happen after a single sting, or after a series of stings where they reacted normally. A highly allergic person may suffer anaphylactic shock from certain proteins in the venom, which can be life-threatening and requires emergency treatment. People known to be highly allergic may carry around epinephrine (adrenaline) in the form of a self-injectable EpiPen for the treatment of an anaphylactic shock.
For patients who experience severe or life-threatening reactions to insect stings, allergy injections composed of increasing concentrations of naturally occurring venom may provide protections against future insect stings.
Psychogenic alopecia, also called "over-grooming" or "psychological baldness," is a compulsive behavior that affects domestic cats. Generally, psychogenic alopecia does not lead to serious health consequences or a decreased lifespan.
Thoroughly cleaning boats, trailers, nets and other equipment when traveling between different lakes and streams also
helps. The only EPA-approved disinfectant proven effective against VHS is Virkon AQUATIC (made by Dupont). Chlorine bleach kills the VHS virus, but in concentrations that are much too caustic for ordinary use. Disinfecting stations can be found at various inland lake boat launches in the Great Lakes region.