Magnesium supplements are used to prevent the disease when ruminants, for obvious economic reasons, must have access to dangerous pastures.

The affected animal should be left in the pasture, and not forced to come back to stall because excitation can darken the prognosis, even after adequate treatment.

Intravenous mixed calcium and magnesium injection are used. Subcutaneous injection of magnesium sulfate (200 ml of 50% solution) is also recommended.

Fertilisers like ammonium phosphate, calcium ammonium nitrate, urea can be supplied. Foliar spray of urea can be a quick method.

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 visual symptoms of nitrogen deficiency mean that it can be relatively easy to detect in some plant species. Symptoms include poor plant growth, and leaves that are pale green or yellow because they are unable to make sufficient chlorophyll. Leaves in this state are said to be chlorotic. Lower leaves (older leaves) show symptoms first, since the plant will move nitrogen from older tissues to more important younger ones. Nevertheless, plants are reported to show nitrogen deficiency symptoms at different parts. For example, Nitrogen deficiency of tea is identified by retarded shoot growth and yellowing of younger leaves.

However, these physical symptoms can also be caused by numerous other stresses, such as deficiencies in other nutrients, toxicity, herbicide injury, disease, insect damage or environmental conditions. Therefore, nitrogen deficiency is most reliably detected by conducting quantitative tests in addition to assessing the plants visual symptoms. These tests include soil tests and plant tissue test.

Plant tissue tests destructively sample the plant of interest. However, nitrogen deficiency can also be detected non-destructively by measuring chlorophyll content.

Chlorophyll content tests work because leaf nitrogen content and chlorophyll concentration are closely linked, which would be expected since the majority of leaf nitrogen is contained in chlorophyll molecules. Chlorophyll content can be detected with a Chlorophyll content meter; a portable instrument that measures the greenness of leaves to estimate their relative chlorophyll concentration.

Chlorophyll content can also be assessed with a chlorophyll fluorometer, which measures a chlorophyll fluorescence ratio to identify phenolic compounds that are produced in higher quantities when nitrogen is limited. These instruments can therefore be used to non-destructively test for nitrogen deficiency.

Proper dietary management will prevent most cases of milk fever. This generally involves close attention to mineral and fiber levels in the diet prior to calving, as well as improving cow comfort to eliminate other problems that may interfere with appetite and so trigger hypocalcemia.

Oral administration of a dose of a calcium salt in a gel has been advised by some veterinarians.

An orally administered bolus containing a much higher concentration of calcium than the injectable solutions can also be given so long as the cow is standing or sitting up. If the cow is lying 'flat out' then immediate intravenous therapy is required to avoid death.

The prognosis is generally good, even in advanced cases. However, some cows can relapse the following day, and even a third time the day after.

Recent research suggests that sulfur amino acids have a protective effect against the toxicity of ODAP.

Eating the chickling pea with grain having high concentrations of sulphur-based amino acids reduces the risk of lathyrism if grain is available. Food preparation is also an important factor. Toxic amino acids are readily soluble in water and can be leached. Bacterial (lactic acid) and fungal (tempeh) fermentation is useful to reduce ODAP content. Moist heat (boiling, steaming) denatures protease inhibitors which otherwise add to the toxic effect of raw grasspea through depletion of protective sulfur amino acids. During times of drought and famine, water for steeping and fuel for boiling is frequently also in short supply. Poor people sometimes know how to reduce the chance of developing lathyrism but face a choice between risking lathyrism or starvation.

The underlying cause for excessive consumption of grasspea is a lack of alternative food sources. This is a consequence of poverty and political conflict. The prevention of lathyrism is therefore a socio-economic challenge.

Because a significant portion of calcium is bound to albumin, any alteration in the level of albumin will affect the measured level of calcium. A corrected calcium level based on the albumin level is: Corrected calcium (mg/dL) = measured total Ca (mg/dL) + 0.8 * (4.0 - serum albumin [g/dL]).

This disease is prevalent in some areas of Bangladesh, Ethiopia, India and Nepal, and affects more men than women. Men between 25 and 40 are particularly vulnerable.

Because "O. sericea" is both frequently encountered and relatively palatable to livestock, it is an important cause of economic losses in livestock production. Keeping livestock away from locoweed infested pasture in spring and fall when grass and other forbs are not actively growing is recommended. Another suggested remedy is to provide palatable supplemental nutrients if animals are to be kept in infested pasture. These remedies take into account livestock preference for locoweed during seasons when grass is dry and not very nutritious. Conditioned food aversion has been used experimentally to discourage livestock from eating it. In horses, a small study has shown promising results using lithium chloride as the aversive agent.

Management of this condition includes|:

- Intravenous calcium gluconate 10% can be administered, or if the hypocalcaemia is severe, calcium chloride is given instead. This is only appropriate if the hypocalcemia is acute and has occurred over a relatively short time frame. But if the hypocalcemia has been severe and chronic, then this regimen can be fatal, because there is a degree of acclimatization that occurs. The neuromuscular excitability, cardiac electrical instability, and associated symptoms are then not cured or relieved by prompt administration of corrective doses of calcium, but rather exacerbated. Such rapid administration of calcium would result in effective over correction – symptoms of hypercalcemia would follow.

- However, in either circumstance, maintenance doses of both calcium and vitamin-D (often as 1,25-(OH)-D, i.e. calcitriol) are often necessary to prevent further decline

Day to day requirements of vitamin d are set around 800-1000IU to maintain healthy levels which in most cases can be provided by sun exposure. Increased amounts are required for individuals who are previously diagnosed as deficient. For those of moderate deficiencies,oral supplementation can be implemented into the diet at levels of 3000-5000 IU per day for a 6- to 12-week period continued by an ongoing reduced dose of 1000- 2000 IU per day to maintain stores in the body.

Severe deficiency is treated through megadose therapy where patients are given doses around 100 000 IU to assist in raising stores faster to ensure physical health in restored to prevent further illness or disease.

There are no tests required to diagnose widow spider bites, or latrodectism symptoms. The diagnosis is clinical and based on historic evidence of widow spider bites. Pathognomonic symptoms such as localized sweating and piloerection provide evidence of envenomation. Unlike the brown recluse, the widow species are easily identified by most people.

Diagnosis is obvious in most people reporting contact with a "Latrodectus" spider. However, without a spider, either through inability to communicate or unawareness, the diagnosis may be missed as symptoms overlap with a variety of other serious clinical syndromes such as tetanus or acute abdomen. Blood values are typically unimportant but may be needed to show myocarditis or dehydration from vomiting.

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.

Respiratory alkalosis is very rarely life-threatening, though pH level should not be 7.5 or greater. The aim in treatment is to detect the underlying cause. When PaCO2 is adjusted rapidly in individuals with chronic respiratory alkalosis, metabolic acidosis may occur. If the individual is on a mechanical ventilator then preventing hyperventilation is done via monitoring ABG levels.

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.

Treatment of HSH involves administration of high doses of magnesium salts. These salts may be taken orally or otherwise (e.g. subcutaneously). This treatment works by increasing magnesium absorption through the non-TRPM6 mediated paracellular uptake pathways. This treatment must be continued throughout life.

HSH was originally believed to be an X-linked disorder due to the preponderance of affected males. With the finding that mutations in TRPM6 (on chromosome 9) are causative for the disorder this is no longer the case. Of recent interest, however, is the characterization of a patient with symptoms similar to HSH who has a translocation of the chromosomes 9 and X.

http://www.lawnandmower.com/red-thread-disease.aspx

http://www.grassclippings.co.uk/RedThread.pdf

Chvostek's sign is not a very specific sign of tetany as it may be seen in 10% to 25% of healthy adults. It is therefore not a reliable clinical sign for diagnosing latent tetany. The sensitivity is lower than that in the corresponding Trousseau sign as it is negative in 30% of patients with hypocalcemia. Due to the combination of poor sensitivity and specificity the clinical utility of this sign is reduced.

In light of the increase of vitamin D deficiency throughout Australia the federal government introduced mandatory fortification of vitamins and minerals such as vitamin D in certain foods like edible oil spreads as indicated in the: Australian Standard 2.4.2. It is mandatory for all food manufacturing companies producing table spreads like butter and margarine to have no less than 55 mg/kg of vitamin D, as a response to a growing public health requirements.

In response to recent advances, public policies are being reconsidered to ensure vitamin D is evidently being measured. With the vitamin D deficiency resurfacing the nutrient reference value guidelines were established, in turn creating the dietary vitamin D recommendations.

The dietary vitamin D guidelines are assuming limited exposure to UVB sun light are:

Infants, Children and Adults <50 years: 5 µg/day

Adults >50 - <70 years: 10 µg/day

Adults >70 years: 15 µg/day

There are two types of respiratory alkalosis: chronic and acute as a result of the 3-5 day delay in kidney compensation of the abnormality.

- "Acute respiratory alkalosis" occurs rapidly, have a high pH because the response of the kidneys is slow.

- "Chronic respiratory alkalosis" is a more long-standing condition, here one finds the kidneys have time to decrease the bicarbonate level.

A diagnostic test for statin-associated auto-immune necrotizing myopathy will be available soon in order to differentiate between different types of myopathies during diagnosis. The presence of abnormal spontaneous electrical activity in the resting muscles indicates an irritable myopathy and is postulated to reflect the presence of an active necrotising myopathic process or unstable muscle membrane potential. However, this finding has poor sensitivity and specificity for predicting the presence of an inflammatory myopathy on biopsy. Further research into this spontaneous electrical activity will allow for a more accurate differential diagnosis between the different myopathies.

Currently a muscle biopsy remains a critical test, unless the diagnosis can be secured by genetic testing. Genetic testing is a less invasive test and if it can be improved upon that would be ideal. Molecular genetic testing is now available for many of the more common metabolic myopathies and muscular dystrophies. These tests are costly and are thus best used to confirm rather than screen for a diagnosis of a specific myopathy. Due to the cost of these tests, they are best used to confirm rather than screen for a diagnosis of a specific myopathy. It is the hope of researchers that as these testing methods improve in function, both costs and access will become more manageable

The increased study of muscle pathophysiology is of importance to researchers as it helps to better differentiate inflammatory versus non-inflammatory and to aim treatment as part of the differential diagnosis. Certainly classification schemes that better define the wide range of myopathies will help clinicians to gain a better understanding of how to think about these patients. Continued research efforts to help appreciate the pathophysiology will improve clinicians ability to administer the most appropriate therapy based on the particular variety of myopathy.

The mechanism for myopathy in individuals with low vitamin D is not completely understood. A decreased availability of 250HD leads to mishandling of cellular calcium transport to the sarcoplasmic reticulum and mitochondria, and is associated with reduced actomyosin content of myofibrils.

Diagnosis is by measurement of calcium, serum albumin (for correction) and PTH in blood.

If necessary, measuring cAMP (cyclic AMP) in the urine after an intravenous dose of PTH can help in the distinction between hypoparathyroidism and other causes.

Differential diagnoses are:

- Pseudohypoparathyroidism (normal PTH levels but tissue insensitivity to the hormone, associated with mental retardation and skeletal deformities) and pseudopseudohypoparathyroidism.

- Vitamin D deficiency or hereditary insensitivity to this vitamin (X-linked dominant).

- Malabsorption

- Kidney disease

- Medication: steroids, diuretics, some antiepileptics.

Other tests include ECG for abnormal heart rhythms, and measurement of blood magnesium levels.