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Hypomagnesemic Tetany of Ruminants
Metabolic Diseases of Ruminant Livestock
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Hypomagnesemic Tetany of Ruminants Robert A. Smith, MS, DVM, * and William C. Edwards, DVMt
Hypomagnesemic tetany of ruminants is a noninfectious metabolic disorder that occurs in a wide range of nutritional and management conditions. Morbidity is usually low, but can exceed 25 per cent under some conditions. Low serum magnesium (Mg) concentrations are characteristic of the disease, and frequently serum calcium (Ca) concentrations are concurrently decreased. Lactating beef cows are most commonly affected in the United States; however, the condition also occurs in stocker calves, bulls, and nonlactating cows. The incidence is high in lactating dairy cows in areas of the world where milk production is based predominantly on grass feeding. Less commonly, it may occur in lactating ewes and goats. Hypomagnesemic tetany is also known as grass tetany, grass staggers, wheat pasture poisoning, barley poisoning, oat poisoning, hypomagnesemia, lactation tetany, and milk tetany.
ETIOLOGY AND PATHOGENESIS Although a similar clinical picture is presented in most cases of hypomagnesemic tetany (HT) , the precise pathogenesis may differ somewhat, based upon nutritional, environmental, and animal factors. For these reasons, synonyms have been given to various clinical manifestations of HT (for example, winter tetany, wheat pasture poisoning, and lactation tetany). These terms have resulted from the clinical and etiologic situation presented in various regions of the world. A marked decrease in serum magnesium concentration seems to be
*Diplomate, American Board of Veterinary Practitioners; Associate Professor and Field Services Clinician, Department of Medicine and Surgery, Oklahoma State University College of Veterinary Medicine, Stillwater, Oklahoma tDiplomate, American Board of Veterinary Toxicology; Professor and Toxicologist, Oklahoma Animal Disease Diagnostic Laboratory, Oklahoma State University College of Veterinary Medicine, Stillwater, Oklahoma
Veterinary Clinics of North America: Food Animal Practice-Vol. 4, No.2, July 1988
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the primary predisposing factor for HT. 21 This decrease often correlates with low Mg concentrations in the ration or a reduction in animal absorption and utilization. Older, lactating animals are most susceptible. Hypomagnesemic tetany has been classified into three main types, based on diet and season. 35 The spring type affects lactating cows a few days after they are put out on grass. The winter type affects cattle fed winter rations in confinement. The out-winter type occurs in late winter and affects cattle that have been maintained throughout the winter on sparse pasture plus supplemental hay. Cattle grazing on rapidly growing, cool season grasses and winter cereal grain pastures are particularly prone to tetany. The incidence of HT in ruminants grazing these forages correlates with a lowered plant dry matter content. The problem is practically nonexistent where cattle graze on native, unimproved pastures. The development of HT results from a complex interaction among climate, soil and plant minerals, nitrogen levels, organic acids, animal mineral metabolism, and the age and lactation status of the animal. The relationship of potassium (K), Ca, and Mg in forage is an important factor in the development of HT. Heavy K fertilization can cause HT even when Ca and Mg levels are within the normal range. Many forages are deficient in Ca and Mg when K levels rise,15,24 increasing the propensity for HT in animals grazing those pastures. Plant K levels increase when plant growth is rapid, which usually corresponds with increased temperature and adequate moisture. Hypomagnesemic tetany generally increases markedly when the ratio of K to Ca and Mg exceeds 2.2.19 High dietary levels of K apparently interfere with Mg absorption. l l Heavy nitrogen (N) fertilization of pastures has been associated with lowered serum Mg in grazing ruminants. Plant N levels increase during warmer spring weather when growth is rapid. The lowered serum Mg levels of livestock grazing forage high in N is not attributable to a decrease in Mg absorption, but rather to increases in urinary excretion. l l Heavy fertilization of pastures with poultry litter will increase the concentration of K and N in grasses and make them more prone to produce tetany. 39,40 When plant N is high, there is a corresponding increase in plant lipid content. 6,28 Decreased plasma Mg levels are found in cattle grazing forage with high crude protein and lipid contents. This is likely the result of the formation of insoluble soaps41 of Mg and Ca, which are excreted in the feces, rather than lowered levels of Ca and Mg in the forage per se. 6,24 Organic acids in rapidly growing forages contribute to the development of HT. Cereal forages, such as wheat and rye pasture, may have high levels of aconitic, malic, and citric acids. 6,24 Cattle grazing forages with organic acid levels exceeding 1 per cent should be considered to be prone to tetany. 36 Organic acid levels increase with increased levels of K fertilization and during rapid plant growth. In addition to plant conditions, animal factors play an equally important role in the development of HT. Older cows are more likely
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to develop HT than are their younger counterparts in the herd. The incidence is rather low in 2- to 3-year-old cows, but can be quite high in cows older than 6 years of age. 17 The labile reserve of body Mg, which is found primarily in bone, is decreased in older animals. A relationship between breed and the incidence of HT exists. Of beef breeds, Angus cows have the highest incidence l2 ,17 of HT, whereas Brahman cattle are least susceptible. 13 Brahman and Brahman crossbred cows seem to have the greatest capability for Mg absorption and retention. Some crossbred cattle have demonstrated a 10.7 per cent greater digestibility of Mg than purebred cattle, a fact that may be attributable to heterosis. 13 Among the dairy breeds, a greater incidence of HT is seen in Shorthorns than in Jersey or Holstein breeds. 17 The mortality rate follows a similar pattern. Holstein cows have been shown to consume more Mg than Jersey cows and to excrete more Mg in the feces; however, absorption is similar in the two breeds. 13 The difference in the consumption of Mg may be the result of differences in total feed intake. Body condition scores also correlate with the incidence of HT in adult cows. In cows that have moderate body condition, the incidence of HT is less than that in cows that are thin or overconditioned. 17 The increased incidence in thin cows may be attributable to energy deficiency, increased susceptibility to weather stress, or an increased predisposition to chronic hypomagnesemia. 22 Fat cows may be more susceptible to HT owing to increased lipolysis associated with increased lactation energy demands following calving. 14,32 Lactating ruminants are more likely to develop HT than their nonlactating counterparts. Lactating cows may lose up to 3.0 gm ofMg per day through the milk, resulting in a change from a positive to a negative Mg balance. 26 Although not as common as in cattle, deaths of lactating ewes can occur, usually 2 to 3 weeks after lambing. 38 Ewes nursing twins have higher morbidity rates than do ewes with single lambs. Cows are most likely to develop clinical HT just prior to calving and up to 30 days following calving. Cows grazing wheat pasture frequently develop hypocalcemia concurrently 'with hypomagnesemia. 4 In an Oklahoma study, 74 per cent of downer cows were hypocalcemic (less than 5 mg of Ca per dl), and 25 per cent were hypomagnesemic (less than 1.0 mg of Mg per dl).23 Cows with HT that graze wheat pasture demonstrate large increases in parathyroid hormone (PfH) levels and in 1,25-dihydroxyvitamin D 3, which further supports the role of hypocalcemia in inducing tetany. 4 Apparently, low levels of Mg reduce the mobilization rate of Ca33 ; however the mechanisms of this interrelationship are not well understood. Similar Ca and Mg patterns have been reported among cows in Tennessee grazing fescue and orchard grass in the spring. 16 Animals that develop HT while grazing other types of grasses do not necessarily have lowered blood calcium levels accompanying the hypomagnesemia. 9 Hypomagnesemic tetany occurs sporadically in cows not grazing rapidly growing grasses, particularly during the winter months. This
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form of HT may best be described as winter tetany. When nutrition is inadequate during winter months, cows that do not receive proper supplementation become susceptible to HT. Severe weather may precipitate the condition in cattle whose Mg intake is marginal. Stressors, such as hauling, handling, and predators, can cause cattle with subclinical Mg deficiencies to exhibit clinical signs. Weather and other stressors can affect feeding patterns and cause inconsistent intake of Mg supplements. Calves will develop HT if fed whole milk or milk replacer as the sole food source for extended periods of time. This condition is commonly called milk tetany. Signs of HT will generally occur within the first 3 months oflife. 2 Very young calves absorb Mg quite well, but the ability to absorb Mg declines very rapidly with age. 26 Feeding hay that is of good quality and a starter ration to calves raised in confinement should provide adequate Mg to avoid HT. Milk tetany is rarely seen in calves raised outdoors on pasture. Many cows being fed diets that are prone to produce tetany are hypomagnesemic but do not exhibit clinical signs of HT. In many cases, a decline in serum Ca is the event that triggers HT. The primary factor influencing the onset of clinical HT is the Mg level of the cerebrospinal fluid (CSF). The body is able to maintain adequate levels of Mg in the CSF for a period of time even when serum Mg levels are subnormal. l Clinical signs of HT are seen when concentrations of Mg in the CSF fall below critical levels (usually less than 1.25 to 1.45 mg per dl). A more detailed discussion of the physiologic aspects of the regulation of magnesium metabolism is discussed in the article by Reinhardt, Horst, and Goff entitled "Calcium, Phosphorus, and Magnesium Homeostasis in Ruminants" elsewhere in this issue. CLINICAL SIGNS Typically, clinical HT is not observed, and the only history is that a cow was found dead. The loss of one animal is often ignored by the owner, and it may not be until more animals are lost that veterinary assistance will be sought. Clinical signs vary considerably, depending upon serum Mg and Ca levels and the normal temperament of the animal. Clinical signs of HT can be classified as acute, subacute, and chronic. A key clinical feature in most recognizable cases of HT is a change in normal behavior. In acute cases, the onset of signs is rapid, although under range conditions, cattle and sheep may not be observed closely and some early signs may go undetected. Anorexia, decreased milk production, and separation from the herd are very early signs. These signs progress to an unusual alertness or vicious state. The cow may walk with a stiffened gait and may stagger or wobble. Tremors of the muscles and ears become apparent, and the membrane nictitans may protrude, as in tetanus, when the animal is excited. Nystagmus is often present. There is often excessive salivation and grinding of the teeth. As
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the condition progresses, the cow is often so ataxic that she falls on her side and experiences tetanic muscle spasms, thrashing, opisthotonus, and continued nystagmus and protrusion of the membrane nictitans. Following such a seizure-like episode, the cow will lie quietly for awhile, but noises or attempts to handle her during treatment will frequently precipitate another attack. During the acute attack, the body temperature will often rise to 104 OF or more owing to the violent muscular activity. Pulse and respiration rates increase dramatically, and the intensity of the heart sounds is sometimes so great that they can be heard without a stethoscope. 3 ,26 Death usually occurs within 1 hour if proper medical treatment is not administered. The onset of clinical signs in the subacute form of HT may take several days. Many of the signs are similar to those of the acute form but are not as dramatic. Affected animals are often aggressive and show signs of increased nervousness, such as frequent urination and defecation and an increased alertness. The cow may hold the head high, flinch, and have muscle tremors. These signs are followed by staggering, especially if the animal is continually provoked. Some cows recover spontaneously with time, whereas others may progress and develop signs of acute HT, although the signs are not usually as severe. One of the authors (RAS) has observed beef cows brought to the auction market that have progressed from the subacute to the acute form in less than an hour when exposed to anew, stressful environment. The history often reveals that the cow was stressed during round-up and hauling. When placed on concrete, tested for brucellosis, and penned near areas with human traffic, these cows progressively become more aggressive and eventually collapse and die. The clinical signs of the chronic form of HT are more vague. Usually, affected animals have a reduced appetite and exhibit weight loss. Temperament changes are variable. Since the signs are vague, chronic HT is easily confused with parasitism or other chronic, debilitating diseases. Clinical signs of milk tetany in calves are similar to those in adult cows. Hypomagnesemic tetany in sheep and goats presents a similar picture. 26
CLINICAL PATHOLOGY AND LESIONS There may be marked variations in blood chemistry values and hemograms associated with HT. These variations are, in part, the result of the complex pathophysiology and soil, plant, and animal relationship of the syndrome, as well as the interaction of nutrition, stress, management, and infection factors. In general, normal blood chemistry values should be determined by blood profiling to establish normal values in representative animals. The blood profile of a high-producing dairy herd may be quite different from the blood profile of range cows maintained on native pasture. Laboratory blood profiling and interpretations are an important part of the diagnostic process 20 and are dis-
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cussed in greater detail in the article by Ingraham and Kappel entitled "Metabolic Profile Testing" elsewhere in this issue. Healthy, normal cattle generally have serum Mg levels in the range of 1.8 to 3.0 mg per dl, or approximately 0.74 to 1.23 mmol per L. However, a review of the literature would, perhaps, show a wider normal range, as well as seasonal changes and geographic differences in serum Mg levels. Postmortem serum samples are generally of little value, as a considerable amount of Mg may be absorbed from the tissues. Likewise, high serum K levels may be related to the postmortem release of K from tissues or to hemolysis when clots are not removed from serum samples. Antemortem samples that are of value in assessing the Mg status of an animal are serum with the clot removed, CSF, and urine. Samples of diagnostic importance that may be collected from dead animals or moribund animals following euthanasia include intact eyeballs for analysis of aqueous and vitreous humors, CSF, and urine. Serum Mg levels that are considered to be deficient in the bovine species are generally less than 1.0 mg per d1. 30 * Blood samples collected from 12 cows affected by HT at the time of first clinical signs have been reported to be as low as 0.38 mg per dl at the time of tetany and 0.99 mg per dl 3 to 5 days later.16 These levels are consistent with those reported in studies on wheat pasture poisoning in Oklahoma and the Texas Panhandle. s Determination of Mg levels in CSF is perhaps a more reliable indicator of HT than are serum Mg levels. Once Mg levels in the CSF fall below 1.45 mg per dl, tetany may be expected to occur. 26 CSF without blood contamination is more difficult to collect from downer cattle than are serum and urine. Postmortem CSF samples should be collected from animals within 12 hours of death. Urine is an important and reliable specimen that is frequently overlooked as a useful diagnostic sample. 8 Antemortem urine Mg levels are good indicators of an animal's Mg status when there is a close relationship between Mg utilization, excretion, dietary intake, and absorption. Normal bovine urinary Mg levels are in the range of 1.0 to 20.0 mg per dl. Clinical signs of HT are associated with levels of less than 1.0 mg per dl and, frequently, levels of less than 0.1 mg per dl. When urine levels exceed 5 mg per dl, a diagnosis of HT would be questionable. The urine Mg level could, perhaps, be used as a predictor of impending HT or as a method of evaluating management and prevention programs, as a decrease in urinary Mg concentrations generally precedes decreases in serum Mg. * Postmortem urine samples are of greatest value when they are collected within 24 hours of the animal's death. Animal disease diagnostic laboratories have utilized chemical analyses of aqueous and vitreous humors as a diagnostic aid for several
*Haliburton
Je: Personal communication, 1988.
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conditions, such as HT, nitrate poisoning, forensic drug analysis, and estimations of the postmortem interval. Vitreous humor is readily available as a postmortem sample and is more stable than other body fluids. Postmortem enucleated eyeballs can conveniently be bagged, packed in ice, and shipped to a laboratory where the vitreous or aqueous humor can be analyzed quickly. Vitreous humor analysis, in particular, should be considered a useful indicator of serum chemical values if variables such as time and temperature after death are taken into account. 25 Vitreous humor Mg levels of less than 2.0 mg per dl would indicate a Mg deficiency (subclinical syndrome), and levels of less than 1.5 mg per dl would support a diagnosis of HT. When the eyeball is properly handled, Mg levels should be stable for 48 hours postmortem. Hypocalcemia is often associated with HT. However, HT can also occur when Ca levels are within the normal range. Hyperkalemia and hypocupremia have also been reported in some HT syndromes. 34 Following some tetanic episodes, there may be a transient rise in serum aspartate aminotransferase (AST) and creatine phosphokinase (CPK) levels. Gross pathologic lesions may include petechial and ecchymotic hemorrhages on the serosal surfaces. Such lesions are of limited diagnostic value and may only reflect violent tetanic antemortem activity. Likewise, histopathologic lesions are not always apparent, but may include degenerative changes of the vascular walls in muscle tissue and deposition of Ca salts in soft tissues, such as the splenic trabeculae, arterial walls, and muscle fibers. 29 These lesions have minimal diagnostic value. DIAGNOSIS Although acute tetanic signs are easy to recognize clinically, prodromal signs and downer cow syndrome present more challenging diagnostic problems. HT should be considered in the differential diagnosis whenever there are clinical signs of hyperesthesia and tetany. It should also -be considered when dead or downer cattle are observed under conditions that would make such a diagnosis probable. These conditions would include factors such as time of year, stage of lactation, type of feed and pasture, weather, and stress level. Recovery following Mg therapy would provide additional support for a field diagnosis of HT. Specimens to be submitted for laboratory confirmation should include serum samples with clot removed, urine, and CSF from representative downer animals. Postmortem samples should include heart blood, CSF, urine, enucleated intact eyeballs, and assorted tissues, both fresh and formalin fixed, for histopathologic,microbiologic, and other evaluations, if necessary. On a herd basis, serum and urine from several randomly selected animals would be an important diagnostic aid. The differential diagnosis, pending confirmation, should include
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rabies, tetanus, lead poisoning, polioencephalomalacia, nitrate poisoning, water deprivation, urea poisoning, nervous ketosis, lightning strike, poisonous plants, meningitis, hypocalcemia, paspalum staggers, bermuda grass staggers, anaplasmosis, and, less commonly, strychnine poisoning. Clostridial diseases should be considered as a differential diagnosis when younger animals die suddenly.
CLINICAL MANAGEMENT Prompt treatment of HT is essential for a favorable response rate. Delays by the owner in seeking veterinary assistance decrease the effectiveness of treatment. Mortality ranges from 20 to 100 per cent. Animals to be treated should be handled as quietly as possible to minimize their aggressive behavior and their exposure to stress. Range conditions often result in the severely affected animal dying during capture and restraint. Once the animal is restrained, the use of a blindfold will generally reduce excitement and aggressiveness. The use of a sedative or tranquilizer to calm the animal during treatment and the lag time before response will reduce the likelihood of self-inflicted trauma. The deficiencies to be corrected during treatment involve Mg and, in many cases, Ca. Although Mg deficiency is the classic etiology ofHT, Ca is deficient in a significant percentage of cases. Therefore, therapy should be directed toward restoring proper levels of both ions. Commercial Ca-Mg preparations are readily available. Solutions selected for treating affected animals should approximate a 20 to 25 per cent (weight per volume) Ca borogluconate and a 4 to 5 per cent (weight per volume) Mg hypophosphite concentration. * The usual dosage for the adult beef cow is approximately 500 ml, administered by slow intravenous infusion, whereas ewes require about 50 ml for treatment. The dosage for calves is generally a percentage of that for adult cows; the adjustment is based on estimated body weight. Serum Mg levels are restored to normal very quickly following intravenous therapy. From 30 minutes to 1 hour 27 is the time required for the Mg levels in the CSF to return to normal following intravenous treatment; this explains the short delay between treatment and response seen in some animals. Serum Mg levels may fall to pretreatment levels within 3 to 6 hours3 of intravenous therapy, which may be responsible for relapse. To reduce the incidence of relapses of HT, a subcutaneous injection of 125 to 150 ml of 50 per cent Mg sulfate can be given at the time of initial treatment. This appears to sustain body levels of Mg for an additional 48 hourst and may result, in a more favorable response, as this allows the animal more time to respond to oral supplementation.
*Cal-Phos No.2 (sterile), Tech America, Kansas City, Missouri; Cal-Dextro No.2 (sterile solution), Ft. Dodge Laboratories, Ft. Dodge, Iowa. tBarron S}: Personal communication, 1988.
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When treating ruminants with intravenous Ca-Mg solutions, the heart should be monitored and the rate of administration adjusted so that the solution does not cause cardiac embarrassment. Concentrated Mg solutions, when administered intravenously, may cause medullary depression, respiratory embarrassment, and death. If Mg solutions alone are to be administered intravenously, pretreatment with a Ca solution enhances the safety of this mode of treatment. Oral Mg supplementation is necessary to maintain body Mg levels. Administering 60 gm of MgO orally in gelatin capsules to adult beef cows at the time of intravenous and subcutaneous treatment will stimulate rumen function and provide additional Mg supplementation. This oral treatment regimen should be continued for 5 to 6 days or until the animal is consuming adequate mineral supplements or feed containing Mg. Offering legume hay, such as alfalfa, is also a means of increasing Mg and Ca levels.
PREVENTION AND CONTROL Ruminants are apparently unable to store Mg in a readily mobilizable form; therefore, no functional reserves exist. Most of the Mg present in the feed consumed is lost from the serum within 20 to 30 hours of consumption. 3o It is essential, therefore, that Mg be consumed by animals on a daily basis. Long-term Mg supplementation of cows prior to grazing tetanigenic pastures is of no benefit. 31 Cows grazing forages likely to cause HT should be supplemented at least 2 weeks prior to calving to stabilize the daily intake of Mg. Effective control of HT during the critical tetany period is best accomplished by daily feeding of Mg salts. Lactating beef cows require about 21 to 22 gm of Mg per day. The Mg requirement of cows in most grazing programs is 0.20 per cent Mg on a dry-matter basis. Most rapidly growing spring grasses are usually low in Mg, containing about 0.10 to 0.12 per cent. 7 Pastures vary considerably in their Mg and Ca contents. Pastures with a grass and legume mix have much higher levels of Mg than those without legumes. Daily Mg supplementation is accomplished most often by offering mineral mixes containing MgO. Salt-mineral mixes should contain at least 10 per cent Mg to prevent tetany. 10 Lactating beef cows ideally should consume 60 gm of MgO daily, which would provide about 30 gm of Mg. The intake of a salt-mineral mix is often lower than desired when attempting to achieve consumption of MgO at a rate of 60 gm per day. It may be more realistic to provide actual Mg supplementation of 20 gm per cow daily, rather than the 28- to 30-gm level. The dosage for lactating ewes is 7 gm of MgO per day. 14 Mineral mixes containing MgO are not very palatable and often require mixing with cottonseed meal or molasses to ensure adequate intake. Palatability, uniform ingredients, and proper mixing are the advantages of using commercial preparations rather than those mixed by the livestock owner. An example of a commercial salt-mineral mix suitable for lactating beef cows
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and containing both Ca and Mg is shown in Table 1. The mixing of Mg with supplemental grain when the forage is prone to producing tetany is not always practical because many animals prefer to eat the new, green pastures; in these cases, Mg intake will be inadequate. Daily feeding by hand is also labor intensive. Salt-mineral feeders should be placed conveniently around the pastures to ensure that animals have daily access to them. Of course, minerals must be kept in them at all times. Average daily intake should be calculated periodically to determine whether consumption is sufficient. If consumption is inadequate, the ratio of salt-mineral to molasses or other ingredients added for palatability should be adjusted. Another method of supplementation is to dust pastures with Mg at a rate of 25lb per acre. This can be done with a fertilizer spreader. One application is usually effective for 2 weeks, even with rainy weather. When pastures are short, the Mg is consumed more quickly. Dusting of alternate strips of pasture is apparently effective. I8 Addition of Mg to water supplies has several disadvantages. Mg compounds are often unpalatable, thereby resulting in a reduced water intake. If ponds and streams are present, livestock will prefer to drink from them rather than from tanks containing Mg compounds. Moreover, many Mg products are insoluble in water and will settle to the bottom of the water tanks. Magnesium solutions have been injected into bales of hay to provide a source of supplemental Mg. The quantity to be used is a function of concentration of Mg in the slurry and the estimated hay intake of the animals. This system is labor intensive and, if not done daily, the slurry dries and creates a lot of dust in the hay. Mg can be mixed with molasses, diluted with water, and sprayed onto hay in windrows 3 as the hay is baled. The molasses increases palatability and helps the Mg adhere to the hay. For animals that are susceptible to HT, the provision of shelter during severe weather is an essential management factor. Many cows grazing pastures prone to producing tetany will have marginal serum and CSF Mg levels, and weather stress, and perhaps irregular feeding during inclement weather, will cause many to develop clinical HT. Delaying the calving season until later in the spring should also reduce the incidence of HT in lactating cows during the peripartum period, as forages have increased dry matter and Mg contents in late spring. This practice does, however, have disadvantages. Calves born
Table 1. Mineral Supplement Containing Magnesium * Calcium Phosphorus Salt Magnesium
14% 6% 22% 10%
*Average analysis of macrominerals. See product label for guaranteed analysis and micromineral content. (Co-op Green Pasture Mineral, Farmland Industries, Inc, Kansas City, Missouri 64116.)
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during a later calving season will not be mature enough to utilize forages during the time that forage quality is highest. Cows will reach their peak in lactation later in the grazing season, and the lowered forage quality may decrease forage intake and milk production. Average weaning weights of calves born in the late spring will be reduced. Providing ruminants with hay containing higher Mg levels also reduces the incidence of HT. Alfalfa, clover, and other legume hays are good sources of Mg. Absorption of Mg is generally greater from hay than from spring grass, as hay is harvested when grasses are mature and forage levels of Mg are increased. 1o Overseeding pastures that are prone to producing tetany with legumes provides a daily source of Mg as the animals are grazing. Attempts have been made to prevent HT by using slow-release Mg alloy ruminal boluses. The release rate is approximately 1 gm per day, which is much less than the daily supplemental Mg requirements. This slow-release rate may prevent HT in borderline cases of lowered Mg levels; however, it is unlikely to prevent HT when Mg availability is low, demands are high, and absorption is impaired as a result of dietary factors.37 This management concept, however, if perfected, may offer a valuable means of providing supplemental Mg on a daily basis. Farmers should have soil samples checked regularly to determine the need for K-containing fertilizers. Sometimes fertilizers are used unnecessarily owing to tradition. Application of proper levels of K, Mg, and N fertilizer ensures that these compounds are balanced and will not make pastures unnecessarily prone to producing tetany. Attention to soil analysis and proper fertilization techniques also produces maximum dry matter per acre, and hence greater animal production. Prevention of HT in calves (milk tetany) is easily achieved by offering legume hay of good quality and a balanced, palatable starter ration. Economics on most dairies raising calves in confinement dictate this method of management. Calves that are provided with grain and legume hay are generally weaned from milk by 6 weeks of age. With this system, the incidence of HT is low. Beef calves raised on pasture are usually not affected by HT.
REFERENCES 1. Allsop TF, Pauli JV: Magnesium concentrations in the ventricular and lumbar cerebrospinal fluid of hypomagnesemic cows. Res Vet Sci 38:61-64, 1985 2. Blaxter KL, Sharman GAM: Hypomagnesemic tetany in beef cattle. Vet Rec 67:108-115, 1955 3. Blood DC, Radostits OM, Henderson JA: Veterinary Medicine. Edition 6. Philadelphia, Lea & Febiger, 1983, pp 989-994 4. Bohman YR, Horn FP, Littledike ET, et al: Mechanisms of tetany in cows grazed on wheat pasture. In Horn GW (ed): National Wheat Pasture Symposium. Oklahoma Agricultural Experimental Station Miscellaneous Publication No. 115, June 1984, pp 131-144 5. Bohman YR, Horn FP, Littledike ET, et al: Wheat pasture poisoning. ll. Tissue composition of cattle grazing cereal forages and related to tetany. J Anim Sci 57:1364-1373,1983
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6. Bohman VR, Horn FP, Stewart BA, et al: Wheat pasture poisoning. I. An evaluation of cereal pastures as related to tetany in beef cows. J Anim Sci 57:1352-1363, 1983 7. Boling JA: Grass tetany in beef cattle. Anim Nutr Health 37(7):20-24. November/ December 1982 8. Collins JD: A screening test for monitoring the magnesium status of dairy cows. Vet Rec 106:367 -368, 1980 9. Cseh SB, Fay JP, Casaro A: Changes in blood composition of pregnant cows during the onset of hypomagnesemia. Vet Rec 115:567-570,1984 10. Fontenot JP: Magnesium. Anim Nutr Health 35(6):38-40, August/September 1980 11. Fontenot JP, Wise MB, Webb KE: Interrelationships of potassium, nitrogen, and magnesium in ruminants. Proceedings of the 13th Annual Ruminant Nutrition Conference. Fed Proc 32:1925-1928, 1973 12. Greene LW, Baker JF, Byers FM, et al: Incidence of grass tetany in a cow herd of a five-breed diallel during four consecutive years. J Anim Sci 61(suppl1):60, 1985 13. Greene LW, Solis JC, Byers FM, et al: Apparent and true digestibility of magnesium in mature cows of five breeds and their crosses. J Anim Sci 63:189-196, 1986 14. Grunes DL: Grass tetany of cattle and sheep. In Matches AG (ed): Antiquality Components of Forages. Madison, Wisconsin, Crop Science SOciety of America, 1973, pp 113-140 15. Grunes DL, Hutcheson DP, Horn, FP: Mineral composition of wheat forage as related to metabolic disorders of ruminants. In Horn GW (ed): National Wheat Pasture Symposium. Oklahoma Agricultural Experimental Station Miscellaneous Publication No. 115, June 1984, pp 99-113 16. Hall RF, Reynolds RA: Concentrations of magnesium and calcium in plasma of Hereford cows during and after hypomagnesemic tetany. Am J Vet Res 33: 1 7111713,1972 17. Harris DJ, Lambell RG, Oliver CJ: Factors predisposing dairy and beef cows to grass tetany. Aust Vet J 60:230-234, 1983 18. Herrick JB: Grass Tetany. Vet Med Small Anim Clin. 1974, P 317 19. Kemp A, 't Hart ML: Grass tetany in grazing milking cows. Neth J Agric Res 5:4-17, 1957 20. Kradel DC, Adams RS, Jung GA, et al: Blood profiling in cattle-the Pennsylvania experience. Proceedings of the 18th Annual Meeting of the American Association of Veterinary Laboratory Diagnosticians, 1975, pp 327 -351 21. Littledike ET, Young JW, Beitz DC: Common metabolic disorders of cattle: Ketosis, milk fever, grass tetany, and downer cow complex. J Dairy Sci 64: 1465 -1482, 1981 22. Martens H, Rayssiguier Y: Proceedings of the 5th International Symposium on Ruminal Physiology. Clermont-Ferrand, MTP Press Ltd, 1979, pp 447 -466 23. Mayer GP: As cited in Horn GW: Wheat pasture poisoning. Stillwater, Oklahoma State University, 1980 24. Mayland HF, Grunes DL, Lazar VA: Grass tetany hazard of cereal forages based upon chemical composition. Agron J 68:665, 1976 25. McLaughlin PS, McLaughlin BG: Chemical analysis of bovine and porcine vitreous humors: Correlation of normal values with serum chemical values and changes with time and temperature. Am J Vet Res 48:467 -473, 1987 26. Merrall M, West DM: Ruminant hypomagnesemic tetanies. In Howard JL (ed): Current Veterinary Therapy 2-Food Animal Practice. Edition 2. Philadelphia, WB Saunders, 1986, pp 328 - 332 27. Meyer H, Busse FW: Zentralbl Veterinarmed 22:780-784, 1975. As cited in Allsop TF, Pauli JV: Magnesium concentrations in the ventricular and lumbar cerebrospinal fluid of hypomagnesemic cows. Res Vet Sci 38:61-64, 1985 28. Molloy LF, Metson AJ, Collie TW: Grass tetany. IV. Relationship between higher fatty acids and nitrogen in some New Zealand herbages. NZ J Agric Res 16:457, 1973 29. Ohshima K, Miura S, Numakunai S, et al: Pathological studies on grass tetany (hypomagnesemia) in cattle occurring in Japan. Jpn J Vet Sci 35:231-238, 1973 30. Pfander WH, Wheaton HN, Moseley BL: Grass Tetany. Science and Technology
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Guide. Columbia, University of Missouri-Columbia Extension Publication, 1974, pp 2101-2104 Ritter RJ, Boling JA, Gay N: Labile magnesium reserves in beef cows subjected to different prepasture supplementation regimens. J Anim Sci 59:197 -201, 1984 Roberts CJ, Reid 1M, Rowlands GJ, et al: A fat mobilization syndrome in dairy cows in early lactation. Vet Rec 108:7 -9, 1981 Sansom BF, Manston R, Vagg MJ: Magnesium and milk fever. Vet Rec 112:447, 1983 Singer RH, Grainger RB, Baker FH: Investigations on a complicated grass tetany syndrome in ruminants in Kentucky. I. Preliminary observations. University of Kentucky, Kentucky Agricultural Experimental Station Bulletin, 658, 1958, p 12 Stewart J: Hypomagnesemia and tetany of cattle and sheep. Scott Agric 34:68, 1954. As cited in Littledike ET, Young JW, Beitz DC: Common metabolic disorders of cattle: Ketosis, milk fever, grass tetany, and downer cow complex. J Dairy Sci 64:1465-1482, 1981 Stout PR, Brownell J, Burau RG: Occurrences of trans-aconitate in range forage species. Agron J 59:21, 1967 Stuedemann JA, Wilkinson SR, Lowrey RS: Efficacy of a large magnesium alloy rumen bolus in the prevention of hypomagnesemic tetany in cows. Am J Vet Res 45:698-702,1984 West DM, Bruere AN: Hypomagnesemia in sheep. NZ Vet J 29:85-87,1981 Wilkinson SR, Williams DJ, Jones JB Jr: Recycling broiler house litter on tall fescue pastures at disposal rates and evidence of beef cow health problems. In Livestock Waste Management and Pollution Abatement. Proceedings of the International Symposium on Livestock Wastes, Columbus, Ohio. American Society of Agricultural Engineers, St. Joseph, Michigan. As cited in Grunes DL: Grass tetany of cattle and sheep. In Matches AG (ed): Antiquality Components of Forages. Madison, Wisconsin, Crop Science Society of America, 1973, pp 113-140 Williams DJ, Stuedemann JA, Wilkinson SR: Management practices to prevent animal health problems on fescue pastures heavily fertilized with poultry litter. Georgia Cooperative Extension Service Miscellaneous Unnumbered Publication, 1972. As cited in Grunes DL: Grass tetany of cattle and sheep. In Matches AG (ed): Antiquality Components of Forages. Madison, WI, Crop Science Society of America 1973, pp 113-140 Wilson CF, Reid CSW, Molloy LF, et al: Grass tetany. I. InHuence of starch and peanut oil supplements on plasma magnesium, calcium and phosphorus levels in grazing dairy cows. NZ Agric Res 12:467 -488, 1969
Department of Medicine and Surgery College of Veterinary Medicine Oklahoma State University Stillwater, OK 74078
0749-0720/88 $0.00
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Hypomagnesemic Tetany of Ruminants Robert A. Smith, MS, DVM, * and William C. Edwards, DVMt
Hypomagnesemic tetany of ruminants is a noninfectious metabolic disorder that occurs in a wide range of nutritional and management conditions. Morbidity is usually low, but can exceed 25 per cent under some conditions. Low serum magnesium (Mg) concentrations are characteristic of the disease, and frequently serum calcium (Ca) concentrations are concurrently decreased. Lactating beef cows are most commonly affected in the United States; however, the condition also occurs in stocker calves, bulls, and nonlactating cows. The incidence is high in lactating dairy cows in areas of the world where milk production is based predominantly on grass feeding. Less commonly, it may occur in lactating ewes and goats. Hypomagnesemic tetany is also known as grass tetany, grass staggers, wheat pasture poisoning, barley poisoning, oat poisoning, hypomagnesemia, lactation tetany, and milk tetany.
ETIOLOGY AND PATHOGENESIS Although a similar clinical picture is presented in most cases of hypomagnesemic tetany (HT) , the precise pathogenesis may differ somewhat, based upon nutritional, environmental, and animal factors. For these reasons, synonyms have been given to various clinical manifestations of HT (for example, winter tetany, wheat pasture poisoning, and lactation tetany). These terms have resulted from the clinical and etiologic situation presented in various regions of the world. A marked decrease in serum magnesium concentration seems to be
*Diplomate, American Board of Veterinary Practitioners; Associate Professor and Field Services Clinician, Department of Medicine and Surgery, Oklahoma State University College of Veterinary Medicine, Stillwater, Oklahoma tDiplomate, American Board of Veterinary Toxicology; Professor and Toxicologist, Oklahoma Animal Disease Diagnostic Laboratory, Oklahoma State University College of Veterinary Medicine, Stillwater, Oklahoma
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the primary predisposing factor for HT. 21 This decrease often correlates with low Mg concentrations in the ration or a reduction in animal absorption and utilization. Older, lactating animals are most susceptible. Hypomagnesemic tetany has been classified into three main types, based on diet and season. 35 The spring type affects lactating cows a few days after they are put out on grass. The winter type affects cattle fed winter rations in confinement. The out-winter type occurs in late winter and affects cattle that have been maintained throughout the winter on sparse pasture plus supplemental hay. Cattle grazing on rapidly growing, cool season grasses and winter cereal grain pastures are particularly prone to tetany. The incidence of HT in ruminants grazing these forages correlates with a lowered plant dry matter content. The problem is practically nonexistent where cattle graze on native, unimproved pastures. The development of HT results from a complex interaction among climate, soil and plant minerals, nitrogen levels, organic acids, animal mineral metabolism, and the age and lactation status of the animal. The relationship of potassium (K), Ca, and Mg in forage is an important factor in the development of HT. Heavy K fertilization can cause HT even when Ca and Mg levels are within the normal range. Many forages are deficient in Ca and Mg when K levels rise,15,24 increasing the propensity for HT in animals grazing those pastures. Plant K levels increase when plant growth is rapid, which usually corresponds with increased temperature and adequate moisture. Hypomagnesemic tetany generally increases markedly when the ratio of K to Ca and Mg exceeds 2.2.19 High dietary levels of K apparently interfere with Mg absorption. l l Heavy nitrogen (N) fertilization of pastures has been associated with lowered serum Mg in grazing ruminants. Plant N levels increase during warmer spring weather when growth is rapid. The lowered serum Mg levels of livestock grazing forage high in N is not attributable to a decrease in Mg absorption, but rather to increases in urinary excretion. l l Heavy fertilization of pastures with poultry litter will increase the concentration of K and N in grasses and make them more prone to produce tetany. 39,40 When plant N is high, there is a corresponding increase in plant lipid content. 6,28 Decreased plasma Mg levels are found in cattle grazing forage with high crude protein and lipid contents. This is likely the result of the formation of insoluble soaps41 of Mg and Ca, which are excreted in the feces, rather than lowered levels of Ca and Mg in the forage per se. 6,24 Organic acids in rapidly growing forages contribute to the development of HT. Cereal forages, such as wheat and rye pasture, may have high levels of aconitic, malic, and citric acids. 6,24 Cattle grazing forages with organic acid levels exceeding 1 per cent should be considered to be prone to tetany. 36 Organic acid levels increase with increased levels of K fertilization and during rapid plant growth. In addition to plant conditions, animal factors play an equally important role in the development of HT. Older cows are more likely
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to develop HT than are their younger counterparts in the herd. The incidence is rather low in 2- to 3-year-old cows, but can be quite high in cows older than 6 years of age. 17 The labile reserve of body Mg, which is found primarily in bone, is decreased in older animals. A relationship between breed and the incidence of HT exists. Of beef breeds, Angus cows have the highest incidence l2 ,17 of HT, whereas Brahman cattle are least susceptible. 13 Brahman and Brahman crossbred cows seem to have the greatest capability for Mg absorption and retention. Some crossbred cattle have demonstrated a 10.7 per cent greater digestibility of Mg than purebred cattle, a fact that may be attributable to heterosis. 13 Among the dairy breeds, a greater incidence of HT is seen in Shorthorns than in Jersey or Holstein breeds. 17 The mortality rate follows a similar pattern. Holstein cows have been shown to consume more Mg than Jersey cows and to excrete more Mg in the feces; however, absorption is similar in the two breeds. 13 The difference in the consumption of Mg may be the result of differences in total feed intake. Body condition scores also correlate with the incidence of HT in adult cows. In cows that have moderate body condition, the incidence of HT is less than that in cows that are thin or overconditioned. 17 The increased incidence in thin cows may be attributable to energy deficiency, increased susceptibility to weather stress, or an increased predisposition to chronic hypomagnesemia. 22 Fat cows may be more susceptible to HT owing to increased lipolysis associated with increased lactation energy demands following calving. 14,32 Lactating ruminants are more likely to develop HT than their nonlactating counterparts. Lactating cows may lose up to 3.0 gm ofMg per day through the milk, resulting in a change from a positive to a negative Mg balance. 26 Although not as common as in cattle, deaths of lactating ewes can occur, usually 2 to 3 weeks after lambing. 38 Ewes nursing twins have higher morbidity rates than do ewes with single lambs. Cows are most likely to develop clinical HT just prior to calving and up to 30 days following calving. Cows grazing wheat pasture frequently develop hypocalcemia concurrently 'with hypomagnesemia. 4 In an Oklahoma study, 74 per cent of downer cows were hypocalcemic (less than 5 mg of Ca per dl), and 25 per cent were hypomagnesemic (less than 1.0 mg of Mg per dl).23 Cows with HT that graze wheat pasture demonstrate large increases in parathyroid hormone (PfH) levels and in 1,25-dihydroxyvitamin D 3, which further supports the role of hypocalcemia in inducing tetany. 4 Apparently, low levels of Mg reduce the mobilization rate of Ca33 ; however the mechanisms of this interrelationship are not well understood. Similar Ca and Mg patterns have been reported among cows in Tennessee grazing fescue and orchard grass in the spring. 16 Animals that develop HT while grazing other types of grasses do not necessarily have lowered blood calcium levels accompanying the hypomagnesemia. 9 Hypomagnesemic tetany occurs sporadically in cows not grazing rapidly growing grasses, particularly during the winter months. This
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form of HT may best be described as winter tetany. When nutrition is inadequate during winter months, cows that do not receive proper supplementation become susceptible to HT. Severe weather may precipitate the condition in cattle whose Mg intake is marginal. Stressors, such as hauling, handling, and predators, can cause cattle with subclinical Mg deficiencies to exhibit clinical signs. Weather and other stressors can affect feeding patterns and cause inconsistent intake of Mg supplements. Calves will develop HT if fed whole milk or milk replacer as the sole food source for extended periods of time. This condition is commonly called milk tetany. Signs of HT will generally occur within the first 3 months oflife. 2 Very young calves absorb Mg quite well, but the ability to absorb Mg declines very rapidly with age. 26 Feeding hay that is of good quality and a starter ration to calves raised in confinement should provide adequate Mg to avoid HT. Milk tetany is rarely seen in calves raised outdoors on pasture. Many cows being fed diets that are prone to produce tetany are hypomagnesemic but do not exhibit clinical signs of HT. In many cases, a decline in serum Ca is the event that triggers HT. The primary factor influencing the onset of clinical HT is the Mg level of the cerebrospinal fluid (CSF). The body is able to maintain adequate levels of Mg in the CSF for a period of time even when serum Mg levels are subnormal. l Clinical signs of HT are seen when concentrations of Mg in the CSF fall below critical levels (usually less than 1.25 to 1.45 mg per dl). A more detailed discussion of the physiologic aspects of the regulation of magnesium metabolism is discussed in the article by Reinhardt, Horst, and Goff entitled "Calcium, Phosphorus, and Magnesium Homeostasis in Ruminants" elsewhere in this issue. CLINICAL SIGNS Typically, clinical HT is not observed, and the only history is that a cow was found dead. The loss of one animal is often ignored by the owner, and it may not be until more animals are lost that veterinary assistance will be sought. Clinical signs vary considerably, depending upon serum Mg and Ca levels and the normal temperament of the animal. Clinical signs of HT can be classified as acute, subacute, and chronic. A key clinical feature in most recognizable cases of HT is a change in normal behavior. In acute cases, the onset of signs is rapid, although under range conditions, cattle and sheep may not be observed closely and some early signs may go undetected. Anorexia, decreased milk production, and separation from the herd are very early signs. These signs progress to an unusual alertness or vicious state. The cow may walk with a stiffened gait and may stagger or wobble. Tremors of the muscles and ears become apparent, and the membrane nictitans may protrude, as in tetanus, when the animal is excited. Nystagmus is often present. There is often excessive salivation and grinding of the teeth. As
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the condition progresses, the cow is often so ataxic that she falls on her side and experiences tetanic muscle spasms, thrashing, opisthotonus, and continued nystagmus and protrusion of the membrane nictitans. Following such a seizure-like episode, the cow will lie quietly for awhile, but noises or attempts to handle her during treatment will frequently precipitate another attack. During the acute attack, the body temperature will often rise to 104 OF or more owing to the violent muscular activity. Pulse and respiration rates increase dramatically, and the intensity of the heart sounds is sometimes so great that they can be heard without a stethoscope. 3 ,26 Death usually occurs within 1 hour if proper medical treatment is not administered. The onset of clinical signs in the subacute form of HT may take several days. Many of the signs are similar to those of the acute form but are not as dramatic. Affected animals are often aggressive and show signs of increased nervousness, such as frequent urination and defecation and an increased alertness. The cow may hold the head high, flinch, and have muscle tremors. These signs are followed by staggering, especially if the animal is continually provoked. Some cows recover spontaneously with time, whereas others may progress and develop signs of acute HT, although the signs are not usually as severe. One of the authors (RAS) has observed beef cows brought to the auction market that have progressed from the subacute to the acute form in less than an hour when exposed to anew, stressful environment. The history often reveals that the cow was stressed during round-up and hauling. When placed on concrete, tested for brucellosis, and penned near areas with human traffic, these cows progressively become more aggressive and eventually collapse and die. The clinical signs of the chronic form of HT are more vague. Usually, affected animals have a reduced appetite and exhibit weight loss. Temperament changes are variable. Since the signs are vague, chronic HT is easily confused with parasitism or other chronic, debilitating diseases. Clinical signs of milk tetany in calves are similar to those in adult cows. Hypomagnesemic tetany in sheep and goats presents a similar picture. 26
CLINICAL PATHOLOGY AND LESIONS There may be marked variations in blood chemistry values and hemograms associated with HT. These variations are, in part, the result of the complex pathophysiology and soil, plant, and animal relationship of the syndrome, as well as the interaction of nutrition, stress, management, and infection factors. In general, normal blood chemistry values should be determined by blood profiling to establish normal values in representative animals. The blood profile of a high-producing dairy herd may be quite different from the blood profile of range cows maintained on native pasture. Laboratory blood profiling and interpretations are an important part of the diagnostic process 20 and are dis-
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cussed in greater detail in the article by Ingraham and Kappel entitled "Metabolic Profile Testing" elsewhere in this issue. Healthy, normal cattle generally have serum Mg levels in the range of 1.8 to 3.0 mg per dl, or approximately 0.74 to 1.23 mmol per L. However, a review of the literature would, perhaps, show a wider normal range, as well as seasonal changes and geographic differences in serum Mg levels. Postmortem serum samples are generally of little value, as a considerable amount of Mg may be absorbed from the tissues. Likewise, high serum K levels may be related to the postmortem release of K from tissues or to hemolysis when clots are not removed from serum samples. Antemortem samples that are of value in assessing the Mg status of an animal are serum with the clot removed, CSF, and urine. Samples of diagnostic importance that may be collected from dead animals or moribund animals following euthanasia include intact eyeballs for analysis of aqueous and vitreous humors, CSF, and urine. Serum Mg levels that are considered to be deficient in the bovine species are generally less than 1.0 mg per d1. 30 * Blood samples collected from 12 cows affected by HT at the time of first clinical signs have been reported to be as low as 0.38 mg per dl at the time of tetany and 0.99 mg per dl 3 to 5 days later.16 These levels are consistent with those reported in studies on wheat pasture poisoning in Oklahoma and the Texas Panhandle. s Determination of Mg levels in CSF is perhaps a more reliable indicator of HT than are serum Mg levels. Once Mg levels in the CSF fall below 1.45 mg per dl, tetany may be expected to occur. 26 CSF without blood contamination is more difficult to collect from downer cattle than are serum and urine. Postmortem CSF samples should be collected from animals within 12 hours of death. Urine is an important and reliable specimen that is frequently overlooked as a useful diagnostic sample. 8 Antemortem urine Mg levels are good indicators of an animal's Mg status when there is a close relationship between Mg utilization, excretion, dietary intake, and absorption. Normal bovine urinary Mg levels are in the range of 1.0 to 20.0 mg per dl. Clinical signs of HT are associated with levels of less than 1.0 mg per dl and, frequently, levels of less than 0.1 mg per dl. When urine levels exceed 5 mg per dl, a diagnosis of HT would be questionable. The urine Mg level could, perhaps, be used as a predictor of impending HT or as a method of evaluating management and prevention programs, as a decrease in urinary Mg concentrations generally precedes decreases in serum Mg. * Postmortem urine samples are of greatest value when they are collected within 24 hours of the animal's death. Animal disease diagnostic laboratories have utilized chemical analyses of aqueous and vitreous humors as a diagnostic aid for several
*Haliburton
Je: Personal communication, 1988.
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conditions, such as HT, nitrate poisoning, forensic drug analysis, and estimations of the postmortem interval. Vitreous humor is readily available as a postmortem sample and is more stable than other body fluids. Postmortem enucleated eyeballs can conveniently be bagged, packed in ice, and shipped to a laboratory where the vitreous or aqueous humor can be analyzed quickly. Vitreous humor analysis, in particular, should be considered a useful indicator of serum chemical values if variables such as time and temperature after death are taken into account. 25 Vitreous humor Mg levels of less than 2.0 mg per dl would indicate a Mg deficiency (subclinical syndrome), and levels of less than 1.5 mg per dl would support a diagnosis of HT. When the eyeball is properly handled, Mg levels should be stable for 48 hours postmortem. Hypocalcemia is often associated with HT. However, HT can also occur when Ca levels are within the normal range. Hyperkalemia and hypocupremia have also been reported in some HT syndromes. 34 Following some tetanic episodes, there may be a transient rise in serum aspartate aminotransferase (AST) and creatine phosphokinase (CPK) levels. Gross pathologic lesions may include petechial and ecchymotic hemorrhages on the serosal surfaces. Such lesions are of limited diagnostic value and may only reflect violent tetanic antemortem activity. Likewise, histopathologic lesions are not always apparent, but may include degenerative changes of the vascular walls in muscle tissue and deposition of Ca salts in soft tissues, such as the splenic trabeculae, arterial walls, and muscle fibers. 29 These lesions have minimal diagnostic value. DIAGNOSIS Although acute tetanic signs are easy to recognize clinically, prodromal signs and downer cow syndrome present more challenging diagnostic problems. HT should be considered in the differential diagnosis whenever there are clinical signs of hyperesthesia and tetany. It should also -be considered when dead or downer cattle are observed under conditions that would make such a diagnosis probable. These conditions would include factors such as time of year, stage of lactation, type of feed and pasture, weather, and stress level. Recovery following Mg therapy would provide additional support for a field diagnosis of HT. Specimens to be submitted for laboratory confirmation should include serum samples with clot removed, urine, and CSF from representative downer animals. Postmortem samples should include heart blood, CSF, urine, enucleated intact eyeballs, and assorted tissues, both fresh and formalin fixed, for histopathologic,microbiologic, and other evaluations, if necessary. On a herd basis, serum and urine from several randomly selected animals would be an important diagnostic aid. The differential diagnosis, pending confirmation, should include
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rabies, tetanus, lead poisoning, polioencephalomalacia, nitrate poisoning, water deprivation, urea poisoning, nervous ketosis, lightning strike, poisonous plants, meningitis, hypocalcemia, paspalum staggers, bermuda grass staggers, anaplasmosis, and, less commonly, strychnine poisoning. Clostridial diseases should be considered as a differential diagnosis when younger animals die suddenly.
CLINICAL MANAGEMENT Prompt treatment of HT is essential for a favorable response rate. Delays by the owner in seeking veterinary assistance decrease the effectiveness of treatment. Mortality ranges from 20 to 100 per cent. Animals to be treated should be handled as quietly as possible to minimize their aggressive behavior and their exposure to stress. Range conditions often result in the severely affected animal dying during capture and restraint. Once the animal is restrained, the use of a blindfold will generally reduce excitement and aggressiveness. The use of a sedative or tranquilizer to calm the animal during treatment and the lag time before response will reduce the likelihood of self-inflicted trauma. The deficiencies to be corrected during treatment involve Mg and, in many cases, Ca. Although Mg deficiency is the classic etiology ofHT, Ca is deficient in a significant percentage of cases. Therefore, therapy should be directed toward restoring proper levels of both ions. Commercial Ca-Mg preparations are readily available. Solutions selected for treating affected animals should approximate a 20 to 25 per cent (weight per volume) Ca borogluconate and a 4 to 5 per cent (weight per volume) Mg hypophosphite concentration. * The usual dosage for the adult beef cow is approximately 500 ml, administered by slow intravenous infusion, whereas ewes require about 50 ml for treatment. The dosage for calves is generally a percentage of that for adult cows; the adjustment is based on estimated body weight. Serum Mg levels are restored to normal very quickly following intravenous therapy. From 30 minutes to 1 hour 27 is the time required for the Mg levels in the CSF to return to normal following intravenous treatment; this explains the short delay between treatment and response seen in some animals. Serum Mg levels may fall to pretreatment levels within 3 to 6 hours3 of intravenous therapy, which may be responsible for relapse. To reduce the incidence of relapses of HT, a subcutaneous injection of 125 to 150 ml of 50 per cent Mg sulfate can be given at the time of initial treatment. This appears to sustain body levels of Mg for an additional 48 hourst and may result, in a more favorable response, as this allows the animal more time to respond to oral supplementation.
*Cal-Phos No.2 (sterile), Tech America, Kansas City, Missouri; Cal-Dextro No.2 (sterile solution), Ft. Dodge Laboratories, Ft. Dodge, Iowa. tBarron S}: Personal communication, 1988.
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When treating ruminants with intravenous Ca-Mg solutions, the heart should be monitored and the rate of administration adjusted so that the solution does not cause cardiac embarrassment. Concentrated Mg solutions, when administered intravenously, may cause medullary depression, respiratory embarrassment, and death. If Mg solutions alone are to be administered intravenously, pretreatment with a Ca solution enhances the safety of this mode of treatment. Oral Mg supplementation is necessary to maintain body Mg levels. Administering 60 gm of MgO orally in gelatin capsules to adult beef cows at the time of intravenous and subcutaneous treatment will stimulate rumen function and provide additional Mg supplementation. This oral treatment regimen should be continued for 5 to 6 days or until the animal is consuming adequate mineral supplements or feed containing Mg. Offering legume hay, such as alfalfa, is also a means of increasing Mg and Ca levels.
PREVENTION AND CONTROL Ruminants are apparently unable to store Mg in a readily mobilizable form; therefore, no functional reserves exist. Most of the Mg present in the feed consumed is lost from the serum within 20 to 30 hours of consumption. 3o It is essential, therefore, that Mg be consumed by animals on a daily basis. Long-term Mg supplementation of cows prior to grazing tetanigenic pastures is of no benefit. 31 Cows grazing forages likely to cause HT should be supplemented at least 2 weeks prior to calving to stabilize the daily intake of Mg. Effective control of HT during the critical tetany period is best accomplished by daily feeding of Mg salts. Lactating beef cows require about 21 to 22 gm of Mg per day. The Mg requirement of cows in most grazing programs is 0.20 per cent Mg on a dry-matter basis. Most rapidly growing spring grasses are usually low in Mg, containing about 0.10 to 0.12 per cent. 7 Pastures vary considerably in their Mg and Ca contents. Pastures with a grass and legume mix have much higher levels of Mg than those without legumes. Daily Mg supplementation is accomplished most often by offering mineral mixes containing MgO. Salt-mineral mixes should contain at least 10 per cent Mg to prevent tetany. 10 Lactating beef cows ideally should consume 60 gm of MgO daily, which would provide about 30 gm of Mg. The intake of a salt-mineral mix is often lower than desired when attempting to achieve consumption of MgO at a rate of 60 gm per day. It may be more realistic to provide actual Mg supplementation of 20 gm per cow daily, rather than the 28- to 30-gm level. The dosage for lactating ewes is 7 gm of MgO per day. 14 Mineral mixes containing MgO are not very palatable and often require mixing with cottonseed meal or molasses to ensure adequate intake. Palatability, uniform ingredients, and proper mixing are the advantages of using commercial preparations rather than those mixed by the livestock owner. An example of a commercial salt-mineral mix suitable for lactating beef cows
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and containing both Ca and Mg is shown in Table 1. The mixing of Mg with supplemental grain when the forage is prone to producing tetany is not always practical because many animals prefer to eat the new, green pastures; in these cases, Mg intake will be inadequate. Daily feeding by hand is also labor intensive. Salt-mineral feeders should be placed conveniently around the pastures to ensure that animals have daily access to them. Of course, minerals must be kept in them at all times. Average daily intake should be calculated periodically to determine whether consumption is sufficient. If consumption is inadequate, the ratio of salt-mineral to molasses or other ingredients added for palatability should be adjusted. Another method of supplementation is to dust pastures with Mg at a rate of 25lb per acre. This can be done with a fertilizer spreader. One application is usually effective for 2 weeks, even with rainy weather. When pastures are short, the Mg is consumed more quickly. Dusting of alternate strips of pasture is apparently effective. I8 Addition of Mg to water supplies has several disadvantages. Mg compounds are often unpalatable, thereby resulting in a reduced water intake. If ponds and streams are present, livestock will prefer to drink from them rather than from tanks containing Mg compounds. Moreover, many Mg products are insoluble in water and will settle to the bottom of the water tanks. Magnesium solutions have been injected into bales of hay to provide a source of supplemental Mg. The quantity to be used is a function of concentration of Mg in the slurry and the estimated hay intake of the animals. This system is labor intensive and, if not done daily, the slurry dries and creates a lot of dust in the hay. Mg can be mixed with molasses, diluted with water, and sprayed onto hay in windrows 3 as the hay is baled. The molasses increases palatability and helps the Mg adhere to the hay. For animals that are susceptible to HT, the provision of shelter during severe weather is an essential management factor. Many cows grazing pastures prone to producing tetany will have marginal serum and CSF Mg levels, and weather stress, and perhaps irregular feeding during inclement weather, will cause many to develop clinical HT. Delaying the calving season until later in the spring should also reduce the incidence of HT in lactating cows during the peripartum period, as forages have increased dry matter and Mg contents in late spring. This practice does, however, have disadvantages. Calves born
Table 1. Mineral Supplement Containing Magnesium * Calcium Phosphorus Salt Magnesium
14% 6% 22% 10%
*Average analysis of macrominerals. See product label for guaranteed analysis and micromineral content. (Co-op Green Pasture Mineral, Farmland Industries, Inc, Kansas City, Missouri 64116.)
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during a later calving season will not be mature enough to utilize forages during the time that forage quality is highest. Cows will reach their peak in lactation later in the grazing season, and the lowered forage quality may decrease forage intake and milk production. Average weaning weights of calves born in the late spring will be reduced. Providing ruminants with hay containing higher Mg levels also reduces the incidence of HT. Alfalfa, clover, and other legume hays are good sources of Mg. Absorption of Mg is generally greater from hay than from spring grass, as hay is harvested when grasses are mature and forage levels of Mg are increased. 1o Overseeding pastures that are prone to producing tetany with legumes provides a daily source of Mg as the animals are grazing. Attempts have been made to prevent HT by using slow-release Mg alloy ruminal boluses. The release rate is approximately 1 gm per day, which is much less than the daily supplemental Mg requirements. This slow-release rate may prevent HT in borderline cases of lowered Mg levels; however, it is unlikely to prevent HT when Mg availability is low, demands are high, and absorption is impaired as a result of dietary factors.37 This management concept, however, if perfected, may offer a valuable means of providing supplemental Mg on a daily basis. Farmers should have soil samples checked regularly to determine the need for K-containing fertilizers. Sometimes fertilizers are used unnecessarily owing to tradition. Application of proper levels of K, Mg, and N fertilizer ensures that these compounds are balanced and will not make pastures unnecessarily prone to producing tetany. Attention to soil analysis and proper fertilization techniques also produces maximum dry matter per acre, and hence greater animal production. Prevention of HT in calves (milk tetany) is easily achieved by offering legume hay of good quality and a balanced, palatable starter ration. Economics on most dairies raising calves in confinement dictate this method of management. Calves that are provided with grain and legume hay are generally weaned from milk by 6 weeks of age. With this system, the incidence of HT is low. Beef calves raised on pasture are usually not affected by HT.
REFERENCES 1. Allsop TF, Pauli JV: Magnesium concentrations in the ventricular and lumbar cerebrospinal fluid of hypomagnesemic cows. Res Vet Sci 38:61-64, 1985 2. Blaxter KL, Sharman GAM: Hypomagnesemic tetany in beef cattle. Vet Rec 67:108-115, 1955 3. Blood DC, Radostits OM, Henderson JA: Veterinary Medicine. Edition 6. Philadelphia, Lea & Febiger, 1983, pp 989-994 4. Bohman YR, Horn FP, Littledike ET, et al: Mechanisms of tetany in cows grazed on wheat pasture. In Horn GW (ed): National Wheat Pasture Symposium. Oklahoma Agricultural Experimental Station Miscellaneous Publication No. 115, June 1984, pp 131-144 5. Bohman YR, Horn FP, Littledike ET, et al: Wheat pasture poisoning. ll. Tissue composition of cattle grazing cereal forages and related to tetany. J Anim Sci 57:1364-1373,1983
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Department of Medicine and Surgery College of Veterinary Medicine Oklahoma State University Stillwater, OK 74078