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 clinical signs of milk fever can be divided into three distinct stages:

Stage 1: Cows are mobile but show signs of hypersensitivity and excitability such as restlessness, tremors, ear twitching, head bobbing and mild ataxia. If not treated, symptoms usually progress to stage 2.

Stage 2: Cows can no longer stand and present in sternal recumbency. Tachycardia, weakened heart contraction and peripheral pulses. Cows appear dull, have dry muzzles, cold extremities and a lower than normal body temperature. Smooth muscle paralysis can cause bloat, and the inability to urinate or defecate. Cows often tuck their heads into their flanks.

Stage 3: Lateral recumbency, muscle flaccidity, unresponsiveness to stimuli, and loss of consciousness progressing to coma. Heart rate can approach 120 bpm, with peripheral pulses becoming undetectable. If untreated, progression will continue to death.

Lathyrism or neurolathyrism is a neurological disease of humans and domestic animals, caused by eating certain legumes of the genus "Lathyrus". This problem is mainly associated with "Lathyrus sativus" (also known as "Grass pea", "Kesari Dal", "Khesari Dal" or "Almorta") and to a lesser degree with "Lathyrus cicera", "Lathyrus ochrus" and "Lathyrus clymenum" containing the toxin ODAP.

The lathyrism resulting from the ingestion of "Lathyrus odoratus" seeds ("sweet peas") is often referred to as odoratism or osteolathyrism, which is caused by a different toxin (beta-aminopropionitrile) that affects the linking of collagen, a protein of connective tissues.

Lathyrism is mainly due to consumption of Lathyrus sativus ( common name : Khesari ) containing Cyanoalanine(neurotoxin) and mainly causes muscle cramps and excessive consumption may even lead to paralysis

The consumption of large quantities of "Lathyrus" grain containing high concentrations of the glutamate analogue neurotoxin β-oxalyl-L-α,β-diaminopropionic acid (ODAP, also known as β-"N"-oxalyl-amino-L-alanine, or BOAA) causes paralysis, characterized by lack of strength in or inability to move the lower limbs, and may involve pyramidal tracts producing signs of upper motor neuron damage. The toxin may also cause aortic aneurysm. A unique symptom of lathyrism is the atrophy of gluteal muscles (buttocks). ODAP is a poison of mitochondria, leading to excess cell death, especially in motor neurons. Children can additionally develop bone deformity and reduced brain development.

Milk fever, postparturient hypocalcemia, or parturient paresis is a disease, primarily in dairy cattle, but also seen in beef cattle, characterized by reduced blood calcium levels (see: Hypocalcemia). It occurs following parturition, at onset of lactation, when demand for calcium for colostrum production exceeds the body's ability to mobilize calcium. "Fever" is a misnomer, as body temperature during the disease is generally not elevated. Milk fever is more commonly seen in older animals (which have reduced ability to mobilize calcium from bone) and in certain breeds (such as Channel Island breeds).

All plants require sufficient supplies of macronutrients for healthy growth, and nitrogen (N) is a nutrient that is commonly in limited supply. Nitrogen deficiency in plants can occur when organic matter with high carbon content, such as sawdust, is added to soil. Soil organisms use any nitrogen to break down carbon sources, making N unavailable to plants. This is known as "robbing" the soil of nitrogen. All vegetables apart from nitrogen fixing legumes are prone to this disorder.

Nitrogen deficiency can be prevented in the short term by using grass mowings as a mulch, or foliar feeding with manure, and in the longer term by building up levels of organic matter in the soil. Sowing green manure crops such as grazing rye to cover soil over the winter will help to prevent nitrogen leaching, while leguminous green manures such as winter tares will fix additional nitrogen from the atmosphere.

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.

Osteolathyrism is a collagen cross-linking deficiency brought on by dietary over-reliance on the seeds of "Lathyrus sativus" or grass pea, a legume often grown as a famine crop in Asia and East Africa. Other members of the genus are also known to cause the disease, including "L. sylvestris", "L. cicera", and "L. clymenum". "L. sativus" grows well under famine conditions, often severe drought, where it is cultivated. The condition results in damage to bone and mesenchymal connective tissues. It is seen in people in combination with neurolathyrism and angiolathyrism in areas where famine demands reliance on a crop with known detrimental effects. It occurs in cattle and horses with diets overreliant upon the grass pea. Osteolathyrism is caused by a variety of osteolathyrogenic compounds, specifically excitatory amino-compounds. The most widely-studied of these compounds is beta-aminopropionitrile (BAPN), which exerts its deleterious effect by an unknown yet potently irreversible mechanism. Other instigators are ureides, semicarbazides and thiosemicarbazides, which are believed to chelate the prosthetic Cu(II)-bipyridine cofactor complex in the enzyme lysyl oxidase.

Diagnosis of clinical poisoning is generally made by documenting exposure, identifying the neurologic signs, and analyzing serum for alpha-mannosidase activity and swainsonine.

In mule deer, clinical signs of locoism are similar to chronic wasting disease. Histological signs of vacuolation provide a differential diagnosis.

Sub-clinical intoxication has been investigated in cattle grazing on "Astragalus mollissimus". As the estimated intake of swainsonine increased, blood serum alpha-mannosidase activity and albumin decreased, and alkaline phosphatase and thyroid hormone increased.

The neuromuscular symptoms of hypocalcemia are caused by a positive bathmotropic effect due to the decreased interaction of calcium with sodium channels. Since calcium blocks sodium channels and inhibits depolarization of nerve and muscle fibers,reduced calcium lowers the threshold for depolarization. The symptoms can be recalled by the mnemonic "CATs go numb" - convulsions, arrhythmias, tetany, and numbness in the hands and feet and around the mouth.

Plants look thin, pale and the condition is called "general starvation".

Hypocalcaemia, also spelled hypocalcemia, is low calcium levels in the blood serum. The normal range is 2.1–2.6 mmol/L (8.8–10.7 mg/dL, 4.3–5.2 mEq/L) with levels less than 2.1 mmol/L defined as hypocalcemia. Mildly low levels that develop slowly often have no symptoms. Otherwise symptoms may include numbness, muscle spasms, seizures, confusion, or cardiac arrest.

Common causes include hypoparathyroidism and vitamin D deficiency. Others causes include kidney failure, pancreatitis, calcium channel blocker overdose, rhabdomyolysis, tumor lysis syndrome, and medications such as bisphosphonates. Diagnosis should generally be confirmed with a corrected calcium or ionized calcium level. Specific changes may be seen on an electrocardiogram (ECG).

Initial treatment for severe disease is with intravenous calcium chloride and possibly magnesium sulfate. Other treatments may include vitamin D, magnesium, and calcium supplements. If due to hypoparathyroidism, hydrochlorothiazide, phosphate binders, and a low salt diet may also be recommended. About 18% of people who are in hospital have hypocalcemia.

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.

Locoweed (also crazyweed and loco) is a common name in North America for any plant that produces swainsonine, a phytotoxin harmful to livestock. Worldwide, swainsonine is produced by a small number of species, most in three genera of the flowering plant family Fabaceae: "Oxytropis" and "Astragalus" in North America, and "Swainsona" in Australia. The term locoweed usually refers only to the North American species of "Oxytropis" and "Astragalus", but this article includes the other species as well. Some references may list "Datura stramonium" as locoweed.

Locoweed is relatively palatable to livestock, and some individual animals will seek it out. Livestock poisoned by chronic ingestion of large amounts of swainsonine develop a medical condition known as locoism (also swainsonine disease, swainsonine toxicosis, locoweed disease, and loco disease; North America) and pea struck (Australia). Locoism is reported most often in cattle, sheep, and horses, but has been reported also in elk and deer. It is the most widespread poisonous plant problem in the western United States. Agricultural Research Service and New Mexico State University scientists have been collaborating since 1990 to help solve the problem that locoweed presents to livestock farmers. The research involved identifying the fungal species that produces the locoweed toxins, pinpointing levels of toxicity in animals once they have ingested locoweed, observing the effects of locoweed toxins on livestock’s reproduction and grazing preferences, etc. Together, the scientists assembled a grazing management scheme to help farmers avoid the poisonous locoweed.

Most of the 2000 species of "Astragalus", including many that are commonly known as locoweeds, do not produce swainsonine. Some species, including a few that produce swainsonine, accumulate selenium. This has led to confusion between swainsonine poisoning and selenium poisoning due to this genus.

Diagnosis typically occurs during the first 6 months of life due to characteristic neurological symptoms. These symptoms include muscle spasms, tetany, and seizures. Laboratory testing indicates hypomagnesemia (decreased serum magnesium levels), hypocalcemia (decreased serum calcium levels), and little to no measurable parathyroid hormone levels. Diagnosis is confirmed with these symptoms and can be further solidified with genetic sequencing of the TRPM6 gene.

Wheat yellow rust ("Puccinia striiformis" f.sp. "tritici"), also known as stripe rust, is one of the three wheat rust diseases principally found in wheat grown in cooler environments. Such locations are generally associated with northern latitudes or cooler seasons.

Alkalosis is the result of a process reducing hydrogen ion concentration of arterial blood plasma (alkalemia). In contrast to acidemia (serum pH 7.35 or lower), alkalemia occurs when the serum pH is higher than normal (7.45 or higher). Alkalosis is usually divided into the categories of respiratory alkalosis and metabolic alkalosis or a combined respiratory/metabolic alkalosis.

The smuts are multicellular fungi characterized by their large numbers of teliospores. The smuts get their name from a Germanic word for dirt because of their dark, thick-walled, and dust-like teliospores. They are mostly Ustilaginomycetes (of the class Teliomycetae, subphylum Basidiomycota) and can cause plant disease. The smuts are grouped with the other basidiomycetes because of their commonalities concerning sexual reproduction.

Smuts are cereal and crop pathogens that most notably affect members of the grass family ("Poaceae"). Economically important hosts include maize, barley, wheat, oats, sugarcane, and forage grasses. They eventually hijack the plants' reproductive systems, forming galls which darken and burst, releasing fungal teliospores which infect other plants nearby. Before infection can occur, the smuts need to undergo a successful mating to form dikaryotic hyphae (two haploid cells fuse to form a dikaryon).

Metabolic alkalosis is usually accompanied by low blood potassium concentration, causing, e.g., muscular weakness, muscle pain, and muscle cramps (from disturbed function of the skeletal muscles), and muscle spasms (from disturbed function of smooth muscles).

It may also cause low blood calcium concentration. As the blood pH increases, blood transport proteins, such as albumin, become more ionized into anions. This causes the free calcium present in blood to bind more strongly with albumin. If severe, it may cause tetany.

Signs and symptoms of respiratory alkalosis are as follows:

- Palpitation

- Tetany

- Convulsion

- Sweating

As R.P. Singh, J. Huerta-Espino, and A.P. Roelfs say in their (undated) comprehensive review of literature on the wheat rusts for UN FAO:

"Although Gadd first described stripe rust of wheat in 1777, it was not until 1896 that Eriksson and Henning (1896) showed that stripe rust resulted from a separate pathogen, which they named P. glumarum. In 1953, Hylander et al. (1953) revived the name P. striiformis."

Respiratory alkalosis is a medical condition in which increased respiration elevates the blood pH beyond the normal range (7.35–7.45) with a concurrent reduction in arterial levels of carbon dioxide. This condition is one of the four basic categories of disruption of acid–base homeostasis.

Hypomagnesemia with secondary hypocalcemia (HSH) is an autosomal recessive genetic disorder affecting intestinal magnesium absorption. Decreased intestinal magnesium reabsorption and the resulting decrease in serum magnesium levels is believed to cause lowered parathyroid hormone (PTH) output by the parathyroid gland. This results in decreased PTH and decreased serum calcium levels (hypocalcemia). This manifests in convulsions and spasms in early infancy which, if left untreated, can lead to mental retardation or death. HSH is caused by mutations in the TRPM6 gene.

Human’s clinical signs consisted of swelling and eye infections. There were nodules underneath the skin, abscesses or cysts, and lesions running throughout the body. There were papules, plaques and granulomatous damages on the body. In extreme cases there were deep infections within the eyes, bones, heart and central nervous system.