Hypomagnesemia
It is also known as grass staggers or lactation or grass tetany and results in clonic and tonic muscular spasms and convulsions.
Etiology: Magnesium is primarily present inside the cells and its concentration in blood or extracellular fluid is determined by the balance between magnesium intake, loss in faeces and milk, and its homeostasis by kidney. Magnesium is continually required by the body as there is no specific depot for magnesium storage. There are several factors which can cause hypomagnesaemia. The diarrhoea reduces absorption of magnesium from intestine. Temporary starvation or stress caused due to bad weather, transportation or excess movement may also result in development of hypomagnesaemia. The diets low in sodium cause sodium deficiency in saliva. Low sodium and high potassium in saliva reduces the uptake of magnesium and the disease develops. The disease is commonly seen in the dairy animals of second or third lactation within 2 months of calving.
Pathogenesis: Deficiency of magnesium affects the impulse transmission at the neuromuscular junctions. The release of acetyl choline and sensitivity of motor end plate are affected resulting in muscular irritability. Hypomagnesemia also results in low magnesium concentration in cerebrospinal fluid and thereby altering functioning of the central nervous system.
Clinical signs: The time of onset of hypomagnesemia in lactating period is important in developing the symptom. The disease occurs in acute, subacute or chronic forms. In acute form, animals stop eating and ruminating and become alert and uncomfortable. Twitching of muscles and ears, hyperesthesia, staggering gait, clonic convulsions for short duration and tetany of limbs are seen. During stage of convulsions, opisthotonus, nystagmus, champing of jaw, retraction of eyelids and excess salivation are observed. Body temperature and pulse and respiration rates are increased and these animals die due to respiratory failure. In subacute form of disease, onset is gradual and symptoms are almost same but are of mild in nature. Appetite and milk yield of animal are reduced and they show spasmodic urination, frequent defecation, muscle tremors and mild tetany. Such animals recover after proper treatment. In chronic form of the disease, animals show dullness, reduced appetite, gradual reduction in milk yield and unthriftiness. Lactating animals may reveal paresis and it resembles to hypocalcaemia but these animals do not respond to calcium therapy.
Diagnosis: The cases in recently calved dairy animals can be tentatively diagnosed by clinical sign and can be confirmed by measuring magnesium level in serum, urine or cerebrospinal fluid. Estimation of its level in CSF is more appropriate in detecting the disease. Affected animals also reveal low calcium.
It should be differentiated from other diseases associated with calving, acute form of surra, tetanus, acute lead poisoning, mad cow syndrome, rabies and nervous form of ketosis. In lead poisoning, mania and blindness are seen while in rabies ascending paralysis occur and tetany is absent whereas in nervous form of ketosis, tetany is absent and ketonuria occurs. Similarly in surra or tetanus, ketonuria is absent. The course of mad cow syndrome is quite prolonged.
Treatment: Usually calcium magnesium borogluconate containing 25% calcium borogluconate and 5% magnesium hypophosphite is given @500 ml intravenously followed by 200 ml given subcutaneously after 12 h. The cases can also be treated by giving 200-300 ml of 20% magnesium sulphate solution intravenously followed by 200-300 ml of 5% solution subcutaneously. Magnesium gluconate is also quite effective in its treatment and 200-400 ml of 15% solution can be given intravenously followed by same dose of 5% solution subcutaneously. As the animals suffer from convulsions, sedatives may be given to relieve the convulsions. Diets may be supplemented with magnesium carbonate, magnesium oxide or magnesium sulphate for prevention of the disease.