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Quaternary ammonium compounds can be added to the water of infected adult fish and fry. Alternatively, the antibiotic oxytetracycline can be given to adults, fry and broodstock. To prevent the disease, it is necessary to ensure water is pathogen-free and that water hardening is completed effectively for eggs.
Stress often serves as the final precursor to BRD. The diseases that make up BRD can persist in a cattle herd for a long period of time before becoming symptomatic, but immune systems weakened by stress can stop controlling the disease. Major sources of stress come from the shipping process
and from the co-mingling of cattle.
Weather may be another possible factor. Cases are more common in the fall (although this is the traditional time to sell cattle), and while the relationship between weather and BRD is poorly understood, it is often suggested to avoid transporting cattle during extreme weather.
Bacterial cold water disease (BCWD) is a bacterial disease of salmonid fish. It is caused by "Flavobacterium psychrophilum" (previously classified in the genus "Cytophaga"), a gram-negative rod-shaped bacterium of the family Flavobacteriaceae. The disease typically occurs at temperatures below 13⁰C, and it can be seen in any area with water temperatures consistently below 15⁰C. Salmon are the most commonly affected species. This disease is not zoonotic.
Asymptomatic carrier fish and contaminated water provide reservoirs for disease. Transmission is mainly horizontal, but vertical transmission can also occur.
BCWD may be referred to by a number of other names including cold water disease, peduncle disease, fit rot, tail rot and rainbow trout fry mortality syndrome.
In the absence of vaccination (often because calves are bought unvaccinated), antibiotics can help to stop the bacterial factors of the disease. The Virginia Cooperative Extension recommends Micotil, Nuflor, and Baytril 100 as newer antibiotics that do not need daily dosing, but also notes that Naxcel, Excenel, and Adspec are effective as well.
Some fish species serve as vectors for the disease and have subsequently spread the pathogen to other parts of the world. An example is the fathead minnow ("Pimephales promelas") which is responsible for the spread of redmouth disease to trout in Europe. Other vectors include the goldfish ("Carassius auratus"), Atlantic and Pacific salmon ("Salmo salar"), the emerald shiner ("Notropis atherinoides"), and farmed whitefish ("Coregonus" spp.). Infections have also occurred in farmed turbot ("Scophthalmus maximus"), seabass ("Dicentrarchus labrax"), and seabream ("Sparus auratus"). It can now be found in North and South America, Africa, Asia, and Australia, as well as Europe.
Several antibiotics are available for the treatment of redmouth disease in fish. Vaccines can also be used in the treatment and prevention of disease. Management factors such as maintaining water quality and a low stocking density are essential for disease prevention.
Disease cures are almost always more expensive and less effective than simple prevention measures. Often precautions involve maintaining a stable aquarium that is adjusted for the specific species of fish that are kept and not over-crowding a tank or over-feeding the fish. Common preventive strategies include avoiding the introduction of infected fish, invertebrates or plants by quarantining new additions before adding them to an established tank, and discarding water from external sources rather than mixing it with clean water. Similarly, foods for herbivorous fish such as lettuce or cucumbers should be washed before being placed in the tank. Containers that do not have water filters or pumps to circulate water can also increase stress to fish. Other stresses on fish and tanks can include certain chemicals, soaps and detergents, and impacts to tank walls causing shock waves that can damage fish.
Staphylococcal enteritis may be avoided by using proper hygiene and sanitation with food preparation. This includes thoroughly cooking all meats. If food is to be stored longer than two hours, keep hot foods hot (over 140 °F) and cold foods cold (40 °F or under). Ensure to refrigerate leftovers promptly and store cooked food in a wide, shallow container and refrigerate as soon as possible. Sanitation is very important. Keep kitchens and food-serving areas clean and sanitized. Finally, as most staphylococcal food poisoning are the result of food handling, hand washing is critical. Food handlers should use hand sanitizers with alcohol or thorough hand washing with soap and water.
Tips for hand washing:
1. Wash hands with warm, soapy water before and after handling raw foods.
2. Always wash your hands after using the bathroom, after changing a baby's diaper, after touching pets or other animals, and after sneezing or coughing
3. Properly dress or glove.
Mud fever is caused by an infection of the skin by bacteria, including "Dermatophilus congolensis", and often "Staphylococcus spp." Dermatophytes (fungal organisms such as "Malassezia" or "Trichophyton") can also contribute, as can chorioptic mange mites. Photosensitivity or irritant contact may contribute in certain cases. Rarely, vasculitis can cause continued inflammation.
Under normal circumstances the skin acts as a protective barrier, preventing microorganisms from entering the horse's system and doing any damage. However, the integrity of the epidermis can become compromised through the abrasion of soil grit, sand or stable bedding on cold, wet skin. The continual wetting of the skin causes a breakdown of the protective barrier of the epidermis, allowing the bacterium to enter and cause infection.
Shared boots, wraps, grooming supplies, and horse-handler's hands can all serve as fomites, carrying the causative organism(s) from one individual to another. For this reason, mud fever should be considered a contagious disease, and general hygiene steps should be taken to limit cross-contamination.
Horses and ponies standing for hours in muddy, wet paddocks and at gates are a common sight during the winter months and early spring. It is in these conditions that mud fever thrives. Generally, those horses and ponies with white socks are more prone to the condition, although Mud Fever will affect horses of all breeds, ages and colours.
As with any bacterial infection, mud fever can become a very serious condition very quickly. The legs can become swollen and sore and open sores can become quickly infected. Often, such is the level of damage to the skin that these open sores can become very difficult to heal and can result in proud flesh, permanent hair loss and in severe cases the need for skin grafts.
In draft horses, particularly Clydesdales, Shires, and Belgians, a similar-appearing, but more serious condition occurs called chronic progressive lymphedema. This condition appears to be genetically-linked, starting early in life and progressing, causing thickening, fibrosis, and predisposing to secondary infections. This disease can progress enough to require euthanasia.
Ornamental fish kept in aquariums are susceptible to numerous diseases. Due to their generally small size and the low cost of replacing diseased or dead fish, the cost of testing and treating diseases is often seen as more trouble than the value of the fish.
Due to the artificially limited volume of water and high concentration of fish in most aquarium tanks, communicable diseases often affect most or all fish in a tank. An improper nitrogen cycle, inappropriate aquarium plants and potentially harmful freshwater invertebrates can directly harm or add to the stresses on ornamental fish in a tank. Despite this, many diseases in captive fish can be avoided or prevented through proper water conditions and a well-adjusted ecosystem within the tank.
The horse should be kept in a clean, dry indoor barn stall with wood shavings for bedding to prevent a moist environment around the legs.
"S. aureus" is an enterotoxin producer. Enterotoxins are chromosomally encoded exotoxins that are produced and secreted from several bacterial organisms. It is a heat stable toxin and is resistant to digestive protease. It is the ingestion of the toxin that causes the inflammation and swelling of the intestine.
The World Health Organization concluded that inappropriate use of antibiotics in animal husbandry is an underlying contributor to the emergence and spread of antibiotic-resistant germs, and that the use of antibiotics as growth promoters in animal feeds should be restricted. The World Organisation for Animal Health has added to the Terrestrial Animal Health Code a series of guidelines with recommendations to its members for the creation and harmonization of national antimicrobial resistance surveillance and monitoring programs, monitoring of the quantities of antibiotics used in animal husbandry, and recommendations to ensure the proper and prudent use of antibiotic substances. Another guideline is to implement methodologies that help to establish associated risk factors and assess the risk of antibiotic resistance.
Infectious diarrhea acquired in the wilderness is caused by various bacteria, viruses, and parasites (protozoa). The most commonly reported are the protozoa "Giardia" and "Cryptosporidium". Other infectious agents may play a larger role than generally believed and include "Campylobacter", hepatitis A virus, hepatitis E virus, enterotoxogenic "E. coli", "E. coli" O157:H7, "Shigella", and various other viruses. More rarely, "Yersinia enterocolitica", "Aeromonas hydrophila", and "Cyanobacterium" may also cause disease.
"Giardia lamblia" cysts usually do not tolerate freezing although some cysts can survive a single freeze-thaw cycle. Cysts can remain viable for nearly three months in river water when the temperature is 10 °C and about one month at 15–20 °C in lake water. "Cryptosporidium" may survive in cold waters (4 °C) for up to 18 months, and can even withstand freezing, although its viability is thereby greatly reduced. Many other varieties of diarrhea-causing organisms, including "Shigella" and "Salmonella typhi", and hepatitis A virus, can survive freezing for weeks to months. Virologists believe all surface water in the United States and Canada has the potential to contain human viruses, which cause a wide range of illnesses including diarrhea, polio and meningitis.
Modes of acquiring infection from these causes are limited to fecal-oral transmission, and contaminated water and food. The major factor governing pathogen content of surface water is human and animal activity in the watershed. The risk of WAD from untreated water may have been over-stated relative to the risk from insufficient hygiene.
Bacteria with resistance to antibiotics predate medical use of antibiotics by humans. However, widespread antibiotic use has made more bacteria resistant through the process of evolutionary pressure.
Reasons for the widespread use of antibiotics in human medicine include:
- increasing global availability over time since the 1950s
- uncontrolled sale in many low or middle income countries, where they can be obtained over the counter without a prescription, potentially resulting in antibiotics being used when not indicated. This may result in emergence of resistance in any remaining bacteria.
Other causes include:
- Antibiotic use in livestock feed at low doses for growth promotion is an accepted practice in many industrialized countries and is known to lead to increased levels of resistance.
- Releasing large quantities of antibiotics into the environment during pharmaceutical manufacturing through inadequate wastewater treatment increases the risk that antibiotic-resistant strains will develop and spread.
- It is uncertain whether antibacterials in soaps and other products contribute to antibiotic resistance, but antibacterial soaps are discouraged for other reasons.
Growth of the bacteria is possible between 32–90 °F, with the most ideal conditions between 70–80 °F. Post-harvest storage and transportation is difficult for tropical and other warm environments when the air is not properly ventilated during these processes. Higher temperatures and high humidity are ideal growing conditions for the bacteria making ventilation a big priority when trying to combat this disease.
Bacterial wilt of turfgrass is the only known bacterial disease of turf. The causal agent is the Gram negative bacterium Xanthomonas campestris pv. graminis. The first case of bacterial wilt of turf was reported in a cultivar of creeping bentgrass known as Toronto or C-15, which is found throughout the midwestern United States. Until the causal agent was identified in 1984, the disease was referred to simply as C-15 decline. This disease is almost exclusively found on putting greens at golf courses where extensive mowing creates wounds in the grass which the pathogen uses in order to enter the host and cause disease.
Bacterial soft rots are caused by several types of bacteria, but most commonly by species of gram-negative bacteria, "Erwinia", "Pectobacterium", and "Pseudomonas". It is a destructive disease of fruits, vegetables, and ornamentals found worldwide, and effects genera from nearly all the plant families. The bacteria mainly attack the fleshy storage organs of their hosts (tubers, corms, bulbs, and rhizomes), but they also affect succulent buds, stems, and petiole tissues. With the aid of special enzymes, the plant is turned into a liquidy mush in order for the bacteria to consume the plant cell's nutrients. Disease spread can be caused by simple physical interaction between infected and healthy tissues during storage or transit. The disease can also be spread by insects. Control of the disease is not always very effective, but sanitary practices in production, storing, and processing are something that can be done in order to slow the spread of the disease and protect yields.
One study suggests that on very long trips in the wilderness, taking multivitamins may reduce the incidence of diarrhea.
General biocides such as copper, Junction, or ZeroTol offer a potential solution to bacterial wilt of turf grass, however such chemical control ages must be applied after every mowing which may be economically impractical and ultimately phytotoxic. If bacterial wilt is present of the golf course, the best option may be to designate a mower for use on infected greens only in order to prevent the spread of the pathogen to other greens. Other viable methods include simply limiting the number of wounds the plant incurs, thereby limiting entry sites for the pathogen. A simple example would be less frequent mowing. It has also been proven that the disease is most devastating in grass cut to a length of between 1/8 and 3/16 of an inch, but less so in grass over 1/4 of an inch in length or longer, which presents an additional argument for limiting mowing. Another example is limiting sand topdressing as this is also a very abrasive technique which can create small wounds which allow entry of bacteria into the plant.
A major factor complicating the control of Xanthomonas campestris pv. graminis is weather. While it is not possible to control the weather per se, a study found great decreases in pathogen efficacy at temperatures below 20 °C, suggesting that cooling measures may be effective in combating this pathogen.
Ideally, resistant strains of the host plant should be used to control such a plant pathogen, however no resistant cultivars of turf grass have been identified to date. While no completely resistant cultivars exist, golf course owners can find solace in the fact that certain cultivars such as Penncross and Penneagle are more resistant to bacterial wilt and may thus reduce the need for frequent chemical applications and other cultural controls. Researchers are making gains towards the identification of resistant cultivars as evidenced by the finding that variation in genetic linkage groups 1, 4, and 6 accounted for over 43% of resistance among Italian rye grass.
A 1987 study found evidence of a possible biocontrol strategy for bacterial wilt of turf grass. The researchers found that antiserum to Pseudomonas fluorescens or Erwinia herbicola from hosts which have survived infections by the corresponding pathogens is capable of reducing wilt symptoms in turf grass caused by Xanthomonas campestris pv. graminis. The researchers did note, however, that while it is important to ensure the presence of a higher number of competing bacterial cells in order to reduce symptoms, one should take care to avoid over-infecting the host with a new bacterial pathogen.
Further gains towards host resistance were made in 2001 when researchers found that inoculation of meadow fescue during breeding with a single aggressive strain of the bacterial wilt pathogen greatly increased resistance in offspring, thereby demonstrating the potential of selective breeding to reduce bacterial wilt pathogenesis on turf and rye grasses.
The disease can tolerate warm or freezing temperature, but favorable conditions for the disease include wet and humid weather. Irrigated fields provide a favorable environment for the disease. The disease has become quite prevalent in semi-tropical regions, but can found all over the world where wheat is grown. Strong winds that blow soils help contribute to the spread of disease. When the spread is initiated by wind blown soil particles, symptoms will be found most readily towards the edges of the field.
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.
Bacteria are a common cause of foodborne illness. In the United Kingdom during 2000, the individual bacteria involved were the following: "Campylobacter jejuni" 77.3%, "Salmonella" 20.9%, 1.4%, and all others less than 0.56%. In the past, bacterial infections were thought to be more prevalent because few places had the capability to test for norovirus and no active surveillance was being done for this particular agent. Toxins from bacterial infections are delayed because the bacteria need time to multiply. As a result, symptoms associated with intoxication are usually not seen until 12–72 hours or more after eating contaminated food. However, in some cases, such as Staphylococcal food poisoning, the onset of illness can be as soon as 30 minutes after ingesting contaminated food.
Most common bacterial foodborne pathogens are:
- "Campylobacter jejuni" which can lead to secondary Guillain–Barré syndrome and periodontitis
- "Clostridium perfringens", the "cafeteria germ"
- "Salmonella" spp. – its "S. typhimurium" infection is caused by consumption of eggs or poultry that are not adequately cooked or by other interactive human-animal pathogens
- "" enterohemorrhagic (EHEC) which can cause hemolytic-uremic syndrome
Other common bacterial foodborne pathogens are:
- "Bacillus cereus"
- "Escherichia coli", other virulence properties, such as enteroinvasive (EIEC), enteropathogenic (EPEC), enterotoxigenic (ETEC), enteroaggregative (EAEC or EAgEC)
- "Listeria monocytogenes"
- "Shigella" spp.
- "Staphylococcus aureus"
- "Staphylococcal enteritis"
- "Streptococcus"
- "Vibrio cholerae", including O1 and non-O1
- "Vibrio parahaemolyticus"
- "Vibrio vulnificus"
- "Yersinia enterocolitica" and "Yersinia pseudotuberculosis"
Less common bacterial agents:
- "Brucella" spp.
- "Corynebacterium ulcerans"
- "Coxiella burnetii" or Q fever
- "Plesiomonas shigelloides"
The term alimentary mycotoxicoses refers to the effect of poisoning by Mycotoxins (The term 'mycotoxin' is usually reserved for the toxic chemical products produced by fungi that readily colonize crops) through food consumption. Mycotoxins sometimes have important effects on human and animal health. For example, an outbreak which occurred in the UK in 1960 caused the death of 100,000 turkeys which had consumed aflatoxin-contaminated peanut meal. In the USSR in World War II, 5,000 people died due to Alimentary Toxic Aleukia (ALA). The common foodborne Mycotoxins include:
- Aflatoxins – originated from Aspergillus parasiticus and Aspergillus flavus. They are frequently found in tree nuts, peanuts, maize, sorghum and other oilseeds, including corn and cottonseeds. The pronounced forms of Aflatoxins are those of B1, B2, G1, and G2, amongst which Aflatoxin B1 predominantly targets the liver, which will result in necrosis, cirrhosis, and carcinoma. In the US, the acceptable level of total aflatoxins in foods is less than 20 μg/kg, except for Aflatoxin M1 in milk, which should be less than 0.5 μg/kg. The official document can be found at FDA's website.
- Altertoxins – are those of Alternariol (AOH), Alternariol methyl ether (AME), Altenuene (ALT), Altertoxin-1 (ATX-1), Tenuazonic acid (TeA) and Radicinin (RAD), originated from Alternaria spp. Some of the toxins can be present in sorghum, ragi, wheat and tomatoes. Some research has shown that the toxins can be easily cross-contaminated between grain commodities, suggesting that manufacturing and storage of grain commodities is a critical practice.
- Citrinin
- Citreoviridin
- Cyclopiazonic acid
- Cytochalasins
- Ergot alkaloids / Ergopeptine alkaloids – Ergotamine
- Fumonisins – Crop corn can be easily contaminated by the fungi Fusarium moniliforme, and its Fumonisin B1 will cause Leukoencephalomalacia (LEM) in horses, Pulmonary edema syndrome (PES) in pigs, liver cancer in rats and Esophageal cancer in humans. For human and animal health, both the FDA and the EC have regulated the content levels of toxins in food and animal feed.
- Fusaric acid
- Fusarochromanone
- Kojic acid
- Lolitrem alkaloids
- Moniliformin
- 3-Nitropropionic acid
- Nivalenol
- Ochratoxins – In Australia, The Limit of Reporting (LOR) level for Ochratoxin A (OTA) analyses in 20th Australian Total Diet Survey was 1 µg/kg, whereas the EC restricts the content of OTA to 5 µg/kg in cereal commodities, 3 µg/kg in processed products and 10 µg/kg in dried vine fruits.
- Oosporeine
- Patulin – Currently, this toxin has been advisably regulated on fruit products. The EC and the FDA have limited it to under 50 µg/kg for fruit juice and fruit nectar, while limits of 25 µg/kg for solid-contained fruit products and 10 µg/kg for baby foods were specified by the EC.
- Phomopsins
- Sporidesmin A
- Sterigmatocystin
- Tremorgenic mycotoxins – Five of them have been reported to be associated with molds found in fermented meats. These are Fumitremorgen B, Paxilline, Penitrem A, Verrucosidin, and Verruculogen.
- Trichothecenes – sourced from Cephalosporium, Fusarium, Myrothecium, Stachybotrys and Trichoderma. The toxins are usually found in molded maize, wheat, corn, peanuts and rice, or animal feed of hay and straw. Four trichothecenes, T-2 toxin, HT-2 toxin, diacetoxyscirpenol (DAS) and deoxynivalenol (DON) have been most commonly encountered by humans and animals. The consequences of oral intake of, or dermal exposure to, the toxins will result in Alimentary toxic aleukia, neutropenia, aplastic anemia, thrombocytopenia and/or skin irritation. In 1993, the FDA issued a document for the content limits of DON in food and animal feed at an advisory level. In 2003, US published a patent that is very promising for farmers to produce a trichothecene-resistant crop.
- Zearalenone
- Zearalenols
Bacterial leaf streak of wheat is not easily prevented, but can be controlled with clean seed and resistance. Some foliar products, such as pesticides and antibiotic compounds, have been tested for effectiveness, but have proven to have insignificant outcomes on the bacterial pathogen.
Using clean seed, with little infection, has yielded effective results for researchers and producers. The pathogen, being seed-borne, can be controlled with the elimination of contaminated seed, however, clean seed is not always a sure solution. Because the pathogen may still live in the soil, the use of clean seed is only effective if both the soil and seed are free of the pathogen. Currently, there are no successful seed treatments available for producers to apply to wheat seed for the pathogen.
Variety resistance is another option for control of the disease. Using cultivars such as Blade, Cromwell, Faller, Howard or Knudson, which are resistant to BLS may reduce the impact of the disease and potentially break the disease cycle. Avoiding susceptible cultivars such as Hat Trick, Kelby, and Samson may also reduce the presence of the disease and reduce the amount of bacterial residue in the soil. Using integrated pest management techniques such as tillage to turn over the soil and bury the infection as well as rotating crops may assist with disease management, but are not a definitive control methods. Depending on conditions, the bacteria may survive for up to 81 months. Because the bacteria is moisture driven, irrigation may also increase the risks of BLS infection.