Recovery usually occurs when the animal is removed from the contaminated pasture. The chief danger to stock at this stage is caused by their lack of coordination, which may result in accidental death by falling in awkward places such as ditches and ponds.

The disease is particularly prevalent in New Zealand. It may be prevented by avoiding grazing pastures containing perennial ryegrass, or seeding pastures with resistant strains of ryegrass. Horses are particularly prone to this disease because of their habit of biting close to the ground, and sparse pastures may encourage heavier grazing with greater intake of infected material. Supplementary feeding may help, but hay from infected pasture should not be used because it may contain further toxins.

Herbicide applications aimed to reduce ryegrass population have been successful in reducing the risk of ARGT but have undesirable effects such as rapid reduction in pasture productivity and increase in ryegrass herbicide resistance.

A recently released biological control agent, the twist fungus, has been demonstrated to be effective in reducing the risk ARGT without the need of controlling ryegrass. The first use of the twist fungus inoculum was in 1997.

ARGT was first recorded in vicinity of Black Springs, South Australia, in the 1950s and then near Gnowangerup, Western Australia, in the 1960s. The disease has spread rapidly and approximately 40,000 to 60,000 square kilometres of farmland in Western Australia, and similar areas in South Australia are now infested by the ARGT-causing organisms. Most ARGT-related livestock losses occur during October to January, but losses have been recorded as late as April.

Thousand cankers disease can be spread by moving infected black walnut wood. Trees intended for shipment should be inspected for dieback and cankers and galleries after harvest. G. morbidia or the walnut twig beetle ("Pityophthorus juglandis") are not currently known to be moved with walnut seed . There is currently no chemical therapy or prevention available for the disease making it difficult to control the spread of the disease from the west to the eastern united states. Wood from infected trees can still be used for commercial value, but safety measures such as removing the bark, phloem, and cambium to reduce the risk of spreading the disease with shipment. Quarantines have been put in place in some states to reduce the potential movement of fungus or beetle from that region. On May 17th, 2010, the Director of the Michigan Department of Agriculture issued a quarantine from affected states to protect Michigan’s black walnut ecology and production. Contacting the appropriate entities about possible infections is important to stopping or slowing the spread of thousand cankers disease.

Red thread disease is a fungal infection found on lawns and other turfed areas. It is caused by the corticioid fungus "Laetisaria fuciformis" and has two separate stages. The stage that gives the infection its name is characterised by very thin, red, needle-like strands extending from the grass blade. These are stromata, which can remain viable in soil for two years. After germinating, the stromata infect grass leaf blades through their stomata. The other stage is visible as small, pink, cotton wool-like mycelium, found where the blades meet. It is common when both warmth and humidity are high.

Environment

"Laetisaria fuciformis", the fungus that causes red thread disease develops more often in cool (59-77°F) and wet conditions. These conditions are more present in the spring and fall when rainfall is higher and temperatures are slightly lower. Turf grass that is poor in nutrition and are slow growing are areas that are more susceptible to red thread disease. The fungus grows from the thread like red webbing structures called sclerotia. The sclerotia can survive in leaf blades, thatch, and soil for months to years. These areas that have been infected spread the disease by water, wind, and contaminated equipment. Since this fungus can survive for long periods of time it is essential to cure the infected area so further spreading of the disease does not occur.

Management

Managing red thread disease first starts by providing conditions that are not favorable for the fungal disease to develop. Having a balanced and adequate nitrogen fertilization program helps suppress the disease. This includes applying mild to substantial amounts of phosphorus and potassium to the turf. Other than properly fertilizing the turf, it is very important to maintain a soil pH between 6.5 and 7. Having a more basic pH creates less favorable conditions for a fungus to form. Reducing shade on turf areas also reduces chances of the fungal disease to form because shaded areas create a higher humidity near the turfs surface. Another technique to suppressing red thread disease is top dressing with compost. Suppression of the disease increases with the increase of compost used on the turf. Fungicides are not recommended to control red thread because the cost of chemical control is expensive and turf grasses usually recover from the disease quickly. If the use of fungicides is necessary, products containing strobilurins can be applied and can be very effective if applied before symptoms occur.

Hosts and symptoms

The hosts of the red thread disease only include turf grass. Turf grass is primarily present on home lawns and athletic fields. Some of these turf grass species include annual bluegrass, creeping bentgrass, Kentucky bluegrass, pereninial ryegrass, fine fescue, and bermudagrass. These species of grass are not the only types of turf that can be diagnosed with red thread disease but are the most common hosts. Noticeable symptoms of red thread disease are irregular yellow patches on the turf that are 2 to 24 inches in diameter. Affected areas are diagnosed with faintly pinkish web like sclerotia on the leaf blades. This sclerotia is the fungus growing on the leaf blades. This sclerotia has a reddish to pink spider web look to it.

The genus Geosmithia (Ascomycota: Hypocreales) are generally saprophytic fungi affecting hardwoods. As of its identification in 2010, the species G. morbida is the first documented as a plant pathogen. The walnut twig beetle ("Pityophthorus juglandis") carries the mycelium and conidia of the fungus as it burrows into the tree. The beetle is currently only found in warmer climates, allowing for transmission of the fungus throughout the year. Generations of the beetle move to and from black walnut trees carrying the fungus as they create galleries, the adults typically moving horizontally, and the larvae moving vertically with the grain. As they move through the wood, the beetles deposit the fungus, which is then introduced into the phloem; cankers then develop around the galleries, quickly girdling the tree. The fungus has not been found to provide any value to the beetle. A study done by Montecchio and Faccoli in Italy in 2014 found that no fungal fruiting bodies were found around or on the cankers but in the galleries. Mycelium, and sometimes conidiophores and conidia were observed in the galleries as well. No sexual stage of the fungus has currently been found.

Feeding the lawn with a nitrogen based fertilizer will help the grass recover and help prevent future attacks.

Red Thread can be treated using a fungicide that contains benomyl or carbendazim. The infection will rarely kill the grass, usually only affecting the blades and not the roots, and the lawn should recover in time.

References

1) Ryzin, Benjamin Van. “Red Thread.” "Wisconsin Horticulture", 23 June 2013, hort.uwex.edu/articles/red-thread/

2) Harmon, Philip, and Richard Latin. “Red Thread.” "Purdue Extension", Dec. 2009, www.extension.purdue.edu/extmedia/bp/bp-104-w.pdf.

3) “Red Thread.” "Plant Protection", NuTurf, nuturf.com.au/wp-content/uploads/sites/2/2015/09/Red-Thread-Info.pdf.

4) “Suppression of Soil-Borne Plant Diseases with Composts: A Review.” "Taylor & Francis", www.tandfonline.com/doi/abs/10.1080/09583150400015904

5) “Red Thread — Laetisaria Fuciformis.” "Red Thread (Laetisaria Fuciformis) - MSU Turf Diseases.net - Disease Identification and Information. A Resource Guide from the Dept. of Plant Pathology at Michigan State University", www.msuturfdiseases.net/details/_/red_thread_14/.

6) “Lawn and Turf-Red Thread.” "Pacific Northwest Pest Management Handbooks", OSU Extension Service - Extension and Experiment Station Communications, 4 Apr. 2017, pnwhandbooks.org/plantdisease/host-disease/lawn-turf-red-thread.

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.

Bacterial leaf streak (BLS), also known as black chaff, is a common bacterial disease of wheat. The disease is caused by the bacterial species "Xanthomonas translucens" pv. undulosa. The pathogen is found globally, but is a primary problem in the US in the lower mid-south and can reduce yields by up to 40 percent. BLS is primarily seed-borne (the disease is transmitted by seed) and survives in and on the seed, but may also survive in crop residue in the soil in the off-season. During the growing season, the bacteria may transfer from plant to plant by contact, but it is primarily spread by rain, wind and insect contact. The bacteria thrives in moist environments, and produces a cream to yellow bacterial ooze, which, when dry, appears light colored and scale-like, resulting in a streak on the leaves. The invasion of the head of wheat causes bands of necrotic tissue on the awns, which is called Black Chaff.

The disease is not easily managed, as there are no pesticides on the market for treatment of the infection. There are some resistant cultivars available, but no seed treatment exists. Some integrated pest management (IPM) techniques may be used to assist with preventing infection although, none will completely prevent the disease.

Konzo can be prevented by use of the “wetting method,” which is used to remove residual cyanogens from cassava flour, as an additional processing method. Cassava flour is placed in a bowl and the level marked on the inside of the bowl. Water is added with mixing until the height of the wet flour comes up to the mark. The wet flour is placed in a thin layer on a mat for 2 hours in the sun or 5 hours in the shade to allow the escape of hydrogen cyanide produced by the breakdown of linamarin by the enzyme linamarase. The damp flour is then cooked in boiling water in the traditional way to produce a thick porridge called “fufu” or “ugali”, which is flavoured by some means such as a sauce. The wetting method is accepted by rural women because it requires little extra work or equipment and produces fufu which is not bitter, because the bitter tasting linamarin has gone.

In 2010 the wetting method was taught to the women in Kay Kalenge village, Popokabaka Health Zone, Bandundu Province, DRC, where there were 34 konzo cases. The women used the method and during the intervention there were no new konzo cases and the urinary thiocyanate content of the school children fell to safe levels. Konzo had been prevented for the first time ever in the same health zone in which it had first been discovered by Dr Trolli in 1938. Fourteen months after the intervention ceased the village was visited again. It was found that there were no new cases of konzo, the school children had low urinary thiocyanate levels, the wetting method was still being used and it had spread by word of mouth to three nearby villages. It is important to teach the women that konzo is due to a poison present in their food, to get them to regularly use the wetting method and posters are available in 13 different languages as a teaching aid as an additional method to remove residual cyanogens.

The wetting method has now been used in 13 villages in DRC with nearly 10000 people. The time of the intervention has been reduced from 18 months in the first intervention, to 12 months in the second intervention, to 9 months in the third and fourth interventions. This has reduced the cost per person of the intervention to prevent konzo by removing cyanogens from cassava flour, to $16 per person. This targeted method to reduce cyanide intake is much cheaper and more effective in preventing konzo than broad based interventions.

Konzo has been reported in outbreaks mainly among women and children in remote rural populations in DR Congo, Mozambique (where it is known as mantakassa), Tanzania, Central African Republic, Cameroon and Angola.

The first reported outbreak occurred in Bandundu Province in present-day DR Congo in 1936-1937 and the second in Nampula Province of Northern Mozambique in 1981. Each of these outbreaks numbered more than 1000 cases. Familial clustering is common. Outbreaks typically occur in the dry season in households living in absolute poverty that have sustained themselves for weeks or months on insufficiently processed bitter cassava. Both smaller outbreaks and sporadic cases have been reported from all the countries above.

In Northern Europe, the disease occurs after winter housing. But in Australia and New Zealand, where the cows are not housed, the disease occurs in similar conditions, when the animal enters lush, grass-dominant pastures. In North America, grass tetany occurs most commonly when range stock are moved onto lush early pasture or when housed stock are turned out onto such pasture in the spring. A second high-risk period may occur in the fall. Although cereal grasses (e.g. winter wheat) and crested wheatgrass may be especially conducive to grass tetany, the problem can also occur with several other grass species. "Winter tetany" may occur with some silages, low-magnesium grass hays, or corn stover.

Zamia staggers is a fatal nervous disease affecting cattle where they browse on the leaves or fruit of cycads—in particular, those of the genus Zamia (thus the name). It is characterised by irreversible paralysis of the hind legs because of the degeneration of the spinal cord. It is caused by the toxins cycasin and macrozamin, β-glycosides (the sugars of which are glucose and primeverose, respectively) of methylazoxymethanol (MAM), and which are found in all cycad genera.

Following ingestion the sugar is removed by bacterial glycosidase in the gut, with the MAM being absorbed. The metabolized toxin produces tumours of the liver, kidney, intestine and brain after a latent period which may be a year or longer. The disease has been known in Australia since the 1860s and was the subject of a Queensland Government investigation during the 1890s.

Progressive symptoms may include grazing away from the herd, irritability, muscle twitching, staring, incoordination, staggering, collapse, thrashing, head thrown back, and coma, followed by death. However, clinical signs are not always evident before the animal is found dead.

The condition results from hypomagnesemia (low magnesium concentration in blood) which may reflect low magnesium intake, low magnesium absorption, unusually low retention of magnesium, or a combination of these. Commonly, apparent symptoms develop only when hypomagnesemia is accompanied by hypocalcemia (blood Ca below 8 mg/dL).

Low magnesium intake by grazing ruminants may occur especially with some grass species early in the growing season, due to seasonally low magnesium concentrations in forage dry matter. Some conserved forages are also low in magnesium and may be conducive to hypomagnesemia.

High potassium intake relative to calcium and magnesium intake may induce hypomagnesemia. A K/(Ca+Mg) charge ratio exceeding 2.2 in forages has been commonly considered a risk factor for grass tetany. Potassium fertilizer application to increase forage production may contribute to an increased K/(Ca+Mg) ratio in forage plants, not only by adding potassium to soil, but also by displacing soil-adsorbed calcium and magnesium by ion exchange, contributing to increased susceptibility of calcium and magnesium to leaching loss from the root zone during rainy seasons. In ruminants, high potassium intake results in decreased absorption of magnesium from the digestive tract.

Trans-aconitate, which accumulates in some grasses, can be a risk factor for hypomagnesemia in grazing ruminants. (Tetany has been induced in cattle by administration of trans-aconitate and KCl, where the amount of KCl used was, by itself, insufficient to induce tetany.) Relatively high levels of trans-aconitate have been found in several forage species on rangeland sites conducive to hypomagnesemia. Although at least one rumen organism converts trans-aconitate to acetate, other rumen organisms convert trans-aconitate to tricarballylate, which complexes with magnesium. Using rats as an animal model, oral administration of tricarballylate has been shown to reduce an animal's magnesium retention. Potassium fertilizer application results in increased concentration of aconitic acid in some grass species.

Atopy is a hereditary and chronic (lifelong) allergic skin disease. Signs usually begin between 6 months and 3 years of age, with some breeds of dog, such as the Golden Retriever showing signs at an earlier age. Dogs with atopic dermatitis are itchy, especially around the eyes, muzzle, ears and feet. In severe cases the irritation is generalised. If the allergens are seasonal, the signs of irritation are similarly seasonal. Many dogs with house dust mite allergy have perennial disease. Some of the allergens associated with atopy in dogs include pollens of trees, grasses and weeds, as well as molds and House dust mite. Ear and skin infections with the bacteria "Staphylococcus pseudintermedius" and the yeast "Malassezia pachydermatis" are common secondary to atopic dermatitis.

Food allergy can be associated with identical signs and some authorities consider food allergy to be a type of atopic dermatitis.

Diagnosis of atopic dermatitis is by elimination of other causes of irritation including fleas, scabies and other parasites such as Cheyletiella and lice. Food allergy can be identified through the use of elimination diet trials in which a novel or hydrolysed protein diet is used for a minimum of 6 weeks and allergies to aeroallergens can be identified using intradermal allergy testing and/or blood testing (allergen-specific IgE ELISA).

Treatment includes avoidance of the offending allergens if possible, but for most dogs this is not practical or effective. Other treatments modulate the adverse immune response to allergens and include antihistamines, steroids, ciclosporin and immunotherapy (a process in which allergens are injected to try to induce tolerance). In many cases shampoos, medicated wipes and ear cleaners are needed to try to prevent the return of infections.

New research into T-cell receptor peptides and their effects on dogs with severe, advanced atopic dermatitis are being investigated.

Skin disease may result from deficiency or overactivity of immune responses. In cases where there is insufficient immune responses the disease is usually described by the secondary disease that results. Examples include increased susceptibility to demodectic mange and recurrent skin infections, such as Malassezia infection or bacterial infections. Increased, but harmful immune responses, can be divided into hypersensitivity disorders such as atopic dermatitis, and autoimmune disorders (autoimmunity), such as pemphigus and discoid lupus erythematosus.

Although genetic factors govern susceptibility to atopic disease, increases in atopy have occurred within too short a time frame to be explained by a genetic change in the population, thus pointing to environmental or lifestyle changes. Several hypotheses have been identified to explain this increased rate; increased exposure to perennial allergens due to housing changes and increasing time spent indoors, and changes in cleanliness or hygiene that have resulted in the decreased activation of a common immune control mechanism, coupled with dietary changes, obesity and decline in physical exercise. The hygiene hypothesis maintains that high living standards and hygienic conditions exposes children to fewer infections. It is thought that reduced bacterial and viral infections early in life direct the maturing immune system away from T1 type responses, leading to unrestrained T2 responses that allow for an increase in allergy.

Changes in rates and types of infection alone however, have been unable to explain the observed increase in allergic disease, and recent evidence has focused attention on the importance of the gastrointestinal microbial environment. Evidence has shown that exposure to food and fecal-oral pathogens, such as hepatitis A, "Toxoplasma gondii", and "Helicobacter pylori" (which also tend to be more prevalent in developing countries), can reduce the overall risk of atopy by more than 60%, and an increased rate of parasitic infections has been associated with a decreased prevalence of asthma. It is speculated that these infections exert their effect by critically altering T1/T2 regulation. Important elements of newer hygiene hypotheses also include exposure to endotoxins, exposure to pets and growing up on a farm.

The more poignant part of this disorder is the lack of desensitization for water and aqua intile injection as allergen even on repeated exposure. Avoidance of allergen as a general principle in any allergic disorder necessitates the evasion of water exposure. Topical application of antihistamines like 1% diphenhydramine before water exposure is reported to reduce the hives. Oil in water emulsion creams, petrolatum as barrier agents for water can be used prior to shower or bath with good control of symptoms. Therapeutic effectiveness of various classes of drugs differs from case to case.

The allergic diseases—hay fever and asthma—have increased in the Western world over the past 2–3 decades. Increases in allergic asthma and other atopic disorders in industrialized nations, it is estimated, began in the 1960s and 1970s, with further increases occurring during the 1980s and 1990s, although some suggest that a steady rise in sensitization has been occurring since the 1920s. The number of new cases per year of atopy in developing countries has, in general, remained much lower.

Aquagenic urticaria, once known as a rare physical urticaria, is reclassified as separate subtype of urticaria. It was first reported by Walter B Shelley et al. in 1964. Pruritic hives on contact with water mostly presenting for the first time during puberty in females of reproductive age is seen in aquagenic urticaria. Males are less often affected. Even if majority cases are sporadic in nature, familial cases are also recorded. Water in all forms such as tap or sea water, swimming pool, sweat, tears, saliva can induce the lesions.

Allergic rhinitis is the type of allergy that affects the greatest number of people. In Western countries, between 10 and 30 percent of people are affected in a given year. It is most common between the ages of twenty and forty.

One way to prevent allergic rhinitis is to wear a respirator or mask when near potential allergens.

Growing up on a farm and having multiple brothers and or sisters decreases the risk.

Allergic conjunctivitis occurs more frequently among those with allergic conditions, with the symptoms having a seasonal correlation.

Allergic conjunctivitis is a frequent condition as it is estimated to affect 20 percent of the population on an annual basis and approximately one-half of these people have a personal or family history of atopy.

Giant papillary conjunctivitis accounts for 0.5–1.0% of eye disease in most countries.

The Allergic Alсоhоl from the original on 30 April 2012. Retrieved 2010-04-08.

Although the occurrence of DCS is not easily predictable, many predisposing factors are known. They may be considered as either environmental or individual.

Decompression sickness and arterial gas embolism in recreational diving are associated with certain demographic, environmental, and dive style factors. A statistical study published in 2005 tested potential risk factors: age, gender, body mass index, smoking, asthma, diabetes, cardiovascular disease, previous decompression illness, years since certification, dives in the last year, number of diving days, number of dives in a repetitive series, last dive depth, nitrox use, and drysuit use. No significant associations with risk of decompression sickness or arterial gas embolism were found for asthma, diabetes, cardiovascular disease, smoking, or body mass index. Increased depth, previous DCI, larger number of consecutive days diving, and being male were associated with higher risk for decompression sickness and arterial gas embolism. Nitrox and drysuit use, greater frequency of diving in the past year, increasing age, and years since certification were associated with lower risk, possibly as indicators of more extensive training and experience.