Mariana Dos Santos flag Denunciar. Manipulating dietary anions and cations for prepartum dairy cows to reduce the incidence of milk fever. Dairy Sci. The response to the balance of mayor minerals by the dairy cow, In: Carnsworthy, P.
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Ricardo A. Costa 3. An outbreak of hypomagnesemia is reported in Holstein dairy cattle grazing lush oat Avena sativa pasture in Uruguay. Nine of 3. These nine cows were from 2 to 9-years-old 1st-6th lactation , with 22 to days of lactation and Two cows with acute sialorrhea, muscle spasms, lateral recumbency, weakness, opisthotonos, and coma, were euthanized and necropsied. No significant macroscopic or histological lesions were found.
One untreated clinically-affected cow and eight out of 14 clinically healthy cows of the same group under similar management and production conditions had low serum levels of Mg lower than 0. Secondarily, both clinically affected cows and six out of 14 healthy cows had low serum Ca levels. The difference between the contribution-requirement of minerals in the diet was established and a daily deficiency of Mg The diet was reformulated to correct the deficiencies and the disease was controlled by the daily administration of 80g of magnesium oxide, 80g of calcium carbonate and 30g sodium chloride per cow.
It is concluded that hypomagnesemia is a cause of mortality in dairy cattle in Uruguay, and that the condition can be prevented by appropriate diet formulation. Hypomagnesemia is a disorder of ruminants biochemically characterized by low serum magnesium Mg Grunes et al.
It most commonly affects grazing cattle, which may be asymptomatic or develop clinical signs, or die abruptly sometimes leading to high mortality rates Grunes et al. Blood levels of Mg depend on the balance between absorption and excretion rates Martens et al. In cattle, Mg is excreted in milk 4. Additionally, in pregnant cattle, Mg requirements in developing fetuses during late gestation are 0.
Normal values of Mg in plasma for dairy cattle range between 0. In the cerebrospinal fluid of cows, the Mg ranges from 0. The concentration of Mg in vitreous humor is 0. Mg concentration in vitreous humor is stable for up to approximately 48h postmortem, which can be used in the postmortem diagnosis of hypomagnesemia McCoy In the presence of mineral disorders, it is important to evaluate not only Mg but also Ca levels, because in general both minerals are low in blood Reinhardt et al.
In cases of Mg deficiency, low Ca values are attributed to hypomagnesemia Van Mosel et al. Hypomagnesemia affects cattle, sheep and goats, but cattle are more susceptible Grunes et al. The annual morbidity and mortality registered in dairy cattle farms in southwestern Victoria, Australia, was 2. In England and Wales, a 7. In Uruguay, outbreaks of hypomagnesemia have been recorded in beef cattle under stress caused by weaning, transportation and prolonged confinement without access to food or water Dutra , Primary hypomagnesemia occurs when Mg deficit in the diet is less than 1.
The rumen is the primary absorption site for Mg Martens et al. The solubility and absorption of Mg decrease when the ruminal pH is less than 6.
Therefore, high content of K in the diet affect the absorption of Mg in ruminants. In contrast, fatty acids, such as linolenic, linoleic and palmitic, form insoluble salts with Mg decreasing its absorption in the rumen Goff Transaconitate is a forage metabolite that chelates Mg and can contribute to its deficiency Cook et al.
Hypomagnesemia is more frequent in adult multiparous cows Reinhardt et al. Calves can be affected when consume only milk or milk replacers deficient in Mg Naik et al. Hypomagnesemia is also influenced by body condition. Cows with body condition greater than 3.
Hypomagnesemia is favored by environmental factors Larvor In general, the annual winter grasses oat, wheat and ryegrass are rich in K and deficient in Mg, therefore they pose a greater risk for grass tetany Metson et al.
Therefore, hypomagnesemia commonly occurs in cattle grazing perennial forages of autumn-winter growth Metson et al. The shortage of non-structural carbohydrates of these forages Bohman et al.
Annual winter growing grasses also have high water content that increases the transit speed of the forage in the gastrointestinal tract and thus reduces the absorption of Mg in the rumen Grunes et al.
Pasture management practices may affect the availability of Mg. For example, fumigation against broadleaf weeds reduces legumes with higher levels of Mg, such as clover and alfalfa Jones In addition, the increase in animal density together with the excessive use of fertilizers containing N and K Macdonald et al. The disease is exacerbated by stress conditions such as heat, overcrowding, transportation, changes in diet or starvation Larvor , Rayssiguier Hypomagnesemia can be subclinical, with plasma Mg between 0.
Acute illness is characterized by violent movements of the limbs, usually there is foam at the mouth and nostrils; sudden death can occur and is often the sole manifestation of the disease.
Cows with subacute course show spasms in the face with continuous involuntary muscle movements. Some animals show nervousness, aggressiveness, teeth grinding, salivation or strong vocalization. Blindness, muscle spasms, excitability, rigid gait, dysmetria, and ataxia can be observed. Weight loss and decreased production are hallmarks of the chronic form of hypomagnesemia Reinhardt et al.
To prevent hypomagnesemia, it is necessary to supplement Mg in the diet by administering 0. Diets should be adjusted according to production requirements. Unnecessary management that imposes stress to the animals should be reduced, animals should not be transported in the last 6 weeks of gestation, and abrupt changes in diet should be avoided Elliott Cattle consuming lush fast-growing grasses should be supplemented with Mg.
It has been suggested that subclinical hypomagnesemia in the postpartum is a heritable trait Tsiamadis et al. Clinical cases of hypomagnesemia can be treated by administering Mg solutions intravenously or subcutaneously. The objective of this work is to describe an outbreak of hypomagnesemia in dairy cattle in Uruguay and make recommendations for the prophylaxis and control of the disease.
Nine lactating cows died acutely within 59 days May July 16, in a herd of Holstein cows. Two cows with acute clinical signs that were in permanent recumbency and moribund were subjected to clinical examination, followed by euthanasia and necropsy. Blood samples were collected from the two clinically affected cows and from 14 clinically healthy cows in the same herd under similar management and production conditions. Total blood P was determined by the ammonium molybdate method measured at nm wave-length, and Mg concentration was assessed by the xylidyl blue reaction Wiener lab?
Tissue samples from lung, kidney, liver and cerebrospinal fluid CSF were subjected to microbiological culture on blood, chocolate and McConkey agars. The CSF was cultured in selective medium for Listeria spp. Oat grass samples including 10 subsamples from each of two pastures A and B were obtained for mineral evaluation. Pasture A was being grazed by the ill animals, and pasture B had previously been grazed by the same herd.
Additionally, samples of the concentrate ration, corn silage and water were collected. The P available in the water was determined by the digestion technique with ascorbic acid and colorimetry at the same laboratory.
Intake of DM was estimated based on the data obtained in the farm on diet and milk production, according to the NRC To calculate the mineral contributions, the ingested quantities of oat grass, corn silage, ration, water and the mineral supplement were considered. The difference contribution-requirements of the diet was calculated, and a correction of the deficiencies was formulated.
The farm had lactating Holstein cows managed in a single herd. The animals were consuming lush oat pastures in two daily grazing shifts, as well as corn silage and a ration consisting of ground corn kernels, ground barley grain, soybean meal, mineral supplement and monensin.
Mortality in the study period was 3. The 9 dead cows were between 2 and 9-years of age 1st to 6th lactation , with 22 to days of lactation and Two cows were found moribund. Cow was in right lateral recumbency and had opisthotonos, muscular spasms, profuse salivation and ruminal atony. The rectal temperature was normal Cow was in sternal and later in lateral recumbency, with weakness, sialorrhea and comatose state. The daily concentrate ration per cow was composed of 2.
Table 1 shows the data and the results of the evaluation of P, Ca and Mg in the serum of two clinically-affected cows and 14 healthy cows within 42 to days of lactation and milk production between 17 and Cow with clinical signs, that had not received any medical treatment, had low serum levels of Mg and Ca. Cow with clinical signs, had been treated with a solution of Ca and Mg, and with methylene blue.
In this cow, the serum Mg values were within normal parameters, but the values of Ca and P were low.
The serum values of these minerals in the 14 clinically healthy untreated cows were distributed as follows: four cows had low values of Mg only, four cows had low values of Mg and Ca, two cows had low values of Ca and P, and four cows showed normal values of the three minerals.
Table 1. Epidemiological data and blood serum levels of Ca, P and Mg of lactating cows with clinical signs or clinically healthy cows. The dietary values of minerals are shown in Table 2. The tetanizing potential of the oat forages pastures A and B , corn silage and the ration were 5. The Ca:P ratio was 0.
Table 2. Table 3 shows the estimate of DM intake according to the components of the diet at the time of the visit to the farm. A daily consumption of Table 3. Dry matter intake considering all components of the diet. Daily deficiency was found in the contribution of Mg K Table 4.
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