Symptoms are neurological and may develop one to two weeks after exposure to infected pasture. Symptoms may include head shaking and irregular eye movements, changes in gait, stiffness, staggering and falling. Recumbent animals may display tetanic spasms and may die through misadventure, dehydration, starvation, loss of rumen function or predation. In the case of horses, the animal may quiver or tremble, be easily startled and be awkward to handle. More severely affected animals may repeatedly nod their head, show a tendency to splay their legs, and stumble and fall. The hind-quarters, moreover, may become paralysed.

ARGT is a neurological condition and affects the brain. Sheep may at first appear perfectly normal, but if driven for a hundred metres or so, the slight stress will cause mildly affected animals to lag behind the rest of the flock and exhibit a high-stepping gait. More seriously affected animals may lose co-ordination and stumble, but will usually recover and join the rest of the flock if left quietly alone. The most-severely affected sheep will fall repeatedly and may be unable to get up. These sheep are likely to die, with death sometimes occurring within a few hours of the first symptoms appearing.

Perennial ryegrass staggers is poisoning by peramine, lolitrem B, and other toxins that are contained in perennial ryegrass ("Lolium perenne"), and produced by the endophyte fungus "Neotyphodium lolii" which can be present in all parts of the grass plant, but tends to be concentrated in the lower part of the leaf sheaths, the flower stalks and seeds. This condition can affect horses, cattle, sheep, farmed deer and llamas. It regularly occurs in New Zealand and is known spasmodically from Australia, North and South America, and Europe.

Annual ryegrass toxicity (ARGT) is the poisoning of livestock from toxin contained in bacterially infected annual ryegrass ("Lolium rigidum"). The toxin is produced by the bacterium "Rathayibacter toxicus" (formerly "Clavibacter toxicus"), which is carried into the ryegrass by the nematode "Anguina funesta".

Adult walnut twig beetles carry spores of the "Geosmithia morbida" fungus, which grows profusely around the pupal chamber of the beetles. Following emergence from trees the beetles subsequently tunnel into branches and trunks of walnut for production of egg galleries or overwintering shelters. The fungus is introduced into the tree during this wounding where it subsequently germinates and grows.

The fungal mycelium initially colonize tissue immediately surrounding the beetle galleries. However, in less than a month black, oval-shaped, inky cankers extend considerably beyond the galleries and may reach more than 3 cm in length in susceptible hosts (e.g., black walnut). In the beginning these cankers develop in phloem and tissues formed by the cork cambium. The affected area is very shallow and never show the ‘open-faced’, perennial, target-shape typical of many canker diseases of trees (e.g., Nectria canker). Instead in TCD the bark remains firmly attached to the canker face making the necrotic areas very difficult to observe. Branch cankers usually are not visible until the outer bark is shaved to expose the beetle tunnels, although during late stages of the disease a dark amber stain may form on the bark surface in association with the cankers.

Each time a beetle tunnels into a tree a canker is initiated. Cankers also may continue to expand and penetrate into the cambium of the tree. Each such injury destroys the phloem and robs the tree of its ability to store and move nutrients. As TCD progresses cankers coalesce to further girdle branches greatly restricting nutrient movement. As the tree declines, more bark beetles are attracted and more cankers are formed.

Eventually the enormous number of beetle attacks and subsequent canker formation overwhelms and kills the tree. Thousand cankers is a progressive disease and its effects result from the culmination of a large number of relatively small cankers over a period of time. Just as a thousand cuts was once used as a form of human execution in Imperial China, black walnuts are subjected to death by thousands of branch and trunk cankers produced by infection from the "Geosmithia" fungus.

In end stages of the disease external symptoms become visible. Leaf yellowing on the exterior of the crown is often the first symptom and may originally be restricted to a single branch. However, as the cumulative effects of the girdling progress increasingly large areas of the tree are affected. Sudden leaf wilting, ultimately involving large limbs, characterizes end stage thousand cankers disease. In susceptible hosts, trees are almost always killed within 2–3 years after external symptoms of leaf yellowing are first observed.

The progress of thousand cankers will vary due to several factors, notably the susceptibility of the host. There appears to be a considerable range of TCD susceptibility among various "Juglans" species with "Juglans nigra" (black walnut) being particularly susceptible. Conversely, Arizona walnut ("Juglans major") appears to be quite resistant to the disease, with bark beetle attacks largely limited to small diameter branches, the fungus growing to a very limited extent, and effects of the disease rarely, if ever, progressing to involve large areas of the tree. Similarly southern California walnut ("Juglans californica") and little walnut ("Juglans microcarpa") may show fairly high resistance. Northern California walnut ("Juglans hindsii") and the commercial nut-producing Persian (English) walnut ("Juglans regia") apparently show various degrees of intermediate TCD susceptibility.

The first signs of infection are small irregular patches of brown/yellowing grass. Upon closer inspection, either the tiny red needles or the pink fluffy mycelium will be visible. As the infection spreads, the small patches will join to form large brown areas.

Thousand cankers disease is a recently recognized disease of certain walnuts ("Juglans" spp.). The disease results from the combined activity of the walnut twig beetle ("Pityophthorus juglandis") and a canker producing fungus, "Geosmithia morbida". Until July 2010 the disease was only known to the western United States where over the past decade it has been involved in several large scale die-offs of walnut, particularly black walnut, "Juglans nigra". However, in late July 2010 a well-established outbreak of the disease was found in the Knoxville, Tennessee area. This new finding is the first locating it within the native range of its susceptible host, black walnut.

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.

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.

The onset of paralysis (spastic paraparesis) is sudden and symmetrical and affects the legs more than the arms. The resulting disability is permanent but does not progress. Typically, a patient is standing and walking on the balls of the feet with rigid legs and often with ankle clonus.

Initially, most patients experience generalized weakness during the first days and are bedridden for some days or weeks before trying to walk. Occasional blurred vision and/or speech difficulties typically clear during the first month, except in severely affected patients. Spasticity is present from the first day, without any initial phase of flaccidity. After the initial weeks of functional improvement, the spastic paraparesis remains stable for the rest of life. Some patients may suffer an abrupt aggravating episode, e.g. a sudden and permanent worsening of the spastic paraparesis. Such episodes are identical to the initial onset and can therefore be interpreted as a "second onset".

The severity of konzo varies; cases range from only hyperreflexia in the lower limbs to a severely disabled, bedridden patient with spastic paraparesis, associated weakness of the trunk and arms, impaired eye movements, speech and possibly visual impairment. Although the severity varies from patient to patient, the longest upper motor neurons are invariably more affected than the shorter ones. Thus, a konzo patient with speech impairment always shows severe symptoms in the legs and arms.

Recently, neuropsychological effects of konzo have been described from DR Congo.

The WHO has recommended three criteria for the diagnosis of konzo:

- a visible symmetric spastic abnormality of gait while walking or running;

- a history of onset of less than one week followed by a non-progressive course in a formerly healthy person;

- bilaterally exaggerated knee or ankle jerk reflexes without signs of disease of the spine.

Depending on its severity, konzo is divided into three categories: mild when individuals are able to walk without support, moderate when individuals need one or two sticks to walk, and severe when the affected person is unable to walk unsupported.

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.

Bacterial leaf streak is a pathogen known to infect and damage wheat varieties. The pathogen has also been known to infect other small grain all cereal crops such as rice, barley and triticale. The strains of the pathogen are named differently according to the species they infect. It is one of the most destructive diseases in rice.

Resistant wheat cultivars offer the best protection against yield loss, but little is known about the inheritance of resistance. The disease is most common on wheat and can be found on winter and summer wheat varieties.

Symptoms of this pathogen can be seen on the stem, leaves, and glumes. Stem symptoms are not always present, but can be seen as a dark brown to purple discoloration on the stem below the head and above the flag leaf. In the early stages of the disease, translucent water soaked streaks can be seen on the leaves often accompanied by a shiny glaze or clumps of dried bacteria on the leaf surface. These markings turn to brown lesions after just a few days, and may be surrounded by a lime green halo. Lesions can stretch the entire leaf blade.

BLS exhibits similar symptoms to those of "Septoria nodorum", a common fungal infection. A common sign that will distinguish this pathogen from "Septoria nodorum" is the lack of spores on the leaves, which appears as tiny black spots on the leaf surface with a "Septoria" infection. A cream to yellow colored bacterial ooze produced by BLS infected plant parts is also a distinguishing sign of the pathogen.

Infected glumes, known as black chaff, are darkened and necrotic. Severe symptoms will result in kernels that are discolored due to black and purple streaks. Plants infected with bacterial leaf streak will exhibit an orange cast from leaf symptoms and suffer yield and quality loss.

Grass tetany or hypomagnesemic tetany, also known as grass staggers and winter tetany, is a metabolic disease involving magnesium deficiency, which can occur in such ruminant livestock as beef cattle, dairy cattle and sheep, usually after grazing on pastures of rapidly growing grass, especially in early spring.

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.

The symptoms of aquagenic urticaria or water allergy (being allergic to water) are similar to all the other types of physical hives that are caused by various things. This may include wheals or small raised hives, intense itching, skin flushing in the areas that are prone to water contact. The symptoms may appear within minutes after the body comes in contact with the water. Aquagenic urticaria is a rare condition in which itchy urticaria (hives) develop rapidly after the skin comes in contact with water, regardless of its temperature. The hives associated with aquagenic urticaria are typically small (approximately 1–3 mm), red- or skin-colored welts (called wheals) with clearly defined edges. The rash most commonly develops on the neck, upper trunk and arms, although it can occur anywhere on the body. Some people have itching too. Once the water source is removed, the rash generally fades within 30 to 60 minutes.

Skin disorders are among the most common health problems in dogs, and have many causes. The condition of a dog's skin and coat are also an important indicator of its general health. Skin disorders of dogs vary from acute, self-limiting problems to chronic or long-lasting problems requiring life-time treatment. Skin disorders may be primary or secondary (due to scratching, itch) in nature, making diagnosis complicated.

The exact underlying cause of aquagenic urticaria is poorly understood.

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.

Many allergens such as dust or pollen are airborne particles. In these cases, symptoms arise in areas in contact with air, such as eyes, nose, and lungs. For instance, allergic rhinitis, also known as hay fever, causes irritation of the nose, sneezing, itching, and redness of the eyes. Inhaled allergens can also lead to increased production of mucus in the lungs, shortness of breath, coughing, and wheezing.

Aside from these ambient allergens, allergic reactions can result from foods, insect stings, and reactions to medications like aspirin and antibiotics such as penicillin. Symptoms of food allergy include abdominal pain, bloating, vomiting, diarrhea, itchy skin, and swelling of the skin during hives. Food allergies rarely cause respiratory (asthmatic) reactions, or rhinitis. Insect stings, food, antibiotics, and certain medicines may produce a systemic allergic response that is also called anaphylaxis; multiple organ systems can be affected, including the digestive system, the respiratory system, and the circulatory system. Depending on the rate of severity, it can cause a skin reactions, bronchoconstriction, swelling, low blood pressure, coma, and death. This type of reaction can be triggered suddenly, or the onset can be delayed. The nature of anaphylaxis is such that the reaction can seem to be subsiding, but may recur throughout a period of time.

Allergies, also known as allergic diseases, are a number of conditions caused by hypersensitivity of the immune system to something in the environment that usually causes little or no problem in most people. These diseases include hay fever, food allergies, atopic dermatitis, allergic asthma, and anaphylaxis. Symptoms may include red eyes, an itchy rash, sneezing, a runny nose, shortness of breath, or swelling. Food intolerances and food poisoning are separate conditions.

Common allergens include pollen and certain food. Metals and other substances may also cause problems. Food, insect stings, and medications are common causes of severe reactions. Their development is due to both genetic and environmental factors. The underlying mechanism involves immunoglobulin E antibodies (IgE), part of the body's immune system, binding to an allergen and then to a receptor on mast cells or basophils where it triggers the release of inflammatory chemicals such as histamine. Diagnosis is typically based on a person's medical history. Further testing of the skin or blood may be useful in certain cases. Positive tests, however, may not mean there is a significant allergy to the substance in question.

Early exposure to potential allergens may be protective. Treatments for allergies include avoiding known allergens and the use of medications such as steroids and antihistamines. In severe reactions injectable adrenaline (epinephrine) is recommended. Allergen immunotherapy, which gradually exposes people to larger and larger amounts of allergen, is useful for some types of allergies such as hay fever and reactions to insect bites. Its use in food allergies is unclear.

Allergies are common. In the developed world, about 20% of people are affected by allergic rhinitis, about 6% of people have at least one food allergy, and about 20% have atopic dermatitis at some point in time. Depending on the country about 1–18% of people have asthma. Anaphylaxis occurs in between 0.05–2% of people. Rates of many allergic diseases appear to be increasing. The word "allergy" was first used by Clemens von Pirquet in 1906.

Allergic rhinitis may be seasonal or perennial. Seasonal allergic rhinitis occurs in particular during pollen seasons. It does not usually develop until after 6 years of age. Perennial allergic rhinitis occurs throughout the year. This type of allergic rhinitis is commonly seen in younger children.

Allergic rhinitis may also be classified as Mild-Intermittent, Moderate-Severe intermittent, Mild-Persistent, and Moderate-Severe Persistent. Intermittent is when the symptoms occur 4 days/week and >4 consecutive weeks. The symptoms are considered mild with normal sleep, no impairment of daily activities, no impairment of work or school, and if symptoms are not troublesome. Severe symptoms result in sleep disturbance, impairment of daily activities, and impairment of school or work.

The characteristic symptoms of allergic rhinitis are: rhinorrhea (excess nasal secretion), itching, sneezing fits, and nasal congestion and obstruction. Characteristic physical findings include conjunctival swelling and erythema, eyelid swelling, lower eyelid venous stasis (rings under the eyes known as "allergic shiners"), swollen nasal turbinates, and middle ear effusion.

There can also be behavioural signs; in order to relieve the irritation or flow of mucus, people may wipe or rub their nose with the palm of their hand in an upward motion: an action known as the "nasal salute" or the "allergic salute". This may result in a crease running across the nose (or above each nostril if only one side of the nose is wiped at a time), commonly referred to as the "transverse nasal crease", and can lead to permanent physical deformity if repeated enough.

People might also find that cross-reactivity occurs. For example, someone allergic to birch pollen may also find that he/she has an allergic reaction to the skin of apples or potatoes. A clear sign of this is the occurrence of an itchy throat after eating an apple or sneezing when peeling potatoes or apples. This occurs because of similarities in the proteins of the pollen and the food. There are many cross-reacting substances. Hay fever is not a true fever, meaning it does not cause a core body temperature in the fever over 37.5–38.3 °C (99.5–100.9 °F).

DCS is classified by symptoms. The earliest descriptions of DCS used the terms: "bends" for joint or skeletal pain; "chokes" for breathing problems; and "staggers" for neurological problems. In 1960, Golding "et al." introduced a simpler classification using the term "Type I ('simple')" for symptoms involving only the skin, musculoskeletal system, or lymphatic system, and "Type II ('serious')" for symptoms where other organs (such as the central nervous system) are involved. Type II DCS is considered more serious and usually has worse outcomes. This system, with minor modifications, may still be used today. Following changes to treatment methods, this classification is now much less useful in diagnosis, since neurological symptoms may develop after the initial presentation, and both Type I and Type II DCS have the same initial management.

Decompression sickness (DCS; also known as divers' disease, the bends or caisson disease) describes a condition arising from dissolved gases coming out of solution into bubbles inside the body on depressurisation. DCS most commonly refers to problems arising from underwater diving decompression (i.e., during ascent), but may be experienced in other depressurisation events such as emerging from a caisson, flying in an unpressurised aircraft at altitude, and extravehicular activity from spacecraft. DCS and arterial gas embolism are collectively referred to as decompression illness.

Since bubbles can form in or migrate to any part of the body, DCS can produce many symptoms, and its effects may vary from joint pain and rashes to paralysis and death. Individual susceptibility can vary from day to day, and different individuals under the same conditions may be affected differently or not at all. The classification of types of DCS by its symptoms has evolved since its original description over a hundred years ago.

Risk of DCS caused by diving can be managed through proper decompression procedures and contracting it is now uncommon. Its potential severity has driven much research to prevent it and divers almost universally use dive tables or dive computers to limit their exposure and to control their ascent speed. If DCS is suspected, it is treated by hyperbaric oxygen therapy in a recompression chamber. If treated early, there is a significantly higher chance of successful recovery.