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CASE NOTES

GRASS TETANY (HYPOMAGNESAEMIA) IN BEEF CATTLE—A SELECTIVE REVIEW

Bill Johnson, District Veterinarian, Goulburn

Posted Flock & Herd March 2012

Introduction

Grass tetany (hypomagnesaemia) kills more adult beef cows than any other disease in south-eastern Australia (Champness 2007). Sackett et al. (2006) considered grass tetany the fourth most significant disease affecting southern beef production, after bloat, internal parasites and pinkeye. They estimated the annual cost to be about $16M, with two thirds of that due to increased expenses.

While grass tetany deaths also occur in dairy cattle, Parkinson et al. (2010) associate subclinical hypomagnesaemia in dairy cows with reduced milk production and increased susceptibility to milk fever. They also note that chronic hypomagnesaemia in dairy cows is associated with wasting, anaemia, poor performance and chronic udder oedema (‘leather bag’).

Hypomagnesaemic tetany is also recognised in calves when fed almost exclusively on milk for veal production, at between two to four months of age.

Despite the accumulation of knowledge since first reports of the disease more than eighty years ago, grass tetany of grazing beef cattle continues to challenge both livestock producers and veterinarians. This paper highlights some of those on-going challenges, in the areas of diagnosis, prediction and prevention. Those seeking a more complete description of the disease are referred to the recommended reading list at the end of this paper.

THE DISEASE

Grass tetany in beef cattle occurs when the magnesium concentration in cerebrospinal fluid (CSF) falls below a critical level, preceded by a drop in serum magnesium concentration.

Pathogenesis

Serum magnesium concentration in the short term is the simple balance between uptake and loss. There is no specific homeostatic mechanism for regulation of magnesium (Mg), and the efficiency of both the absorption of magnesium from the gut and retrieval of magnesium from bone stores diminish with age.

In effect, regular dietary intake of magnesium is required to maintain serum and hence CSF magnesium concentration. Temporary interruption of magnesium uptake in the presence of marginal serum magnesium concentration may precipitate signs of grass tetany. Deaths of cows from grass tetany may be associated with inclement weather or yarding for management procedures such as calf marking, which prevent cows from grazing.

Dietary magnesium is absorbed mainly from the rumen and reticulum, with an efficiency of less than 30 percent in adult cows. Gut absorption is further reduced by high dietary potassium, high dietary nitrogen, high pH, low sodium, low phosphorus, and rapid transit time (eg high water content) (Parkinson et al., 2010).

Magnesium is lost in faeces, saliva (not all able to be reabsorbed) and milk, and any excess absorbed is excreted in urine. Milk contains about 0.13g/L magnesium, and the daily magnesium requirement for a cow in early lactation has been estimated at between 8 and 28 grams per day (Parkinson et al., 2010).

PREDICTING THE LIKELIHOOD OF HYPOMAGNESAEMIA

ASSESSING RISK FACTORS. Beef cows dying from grass tetany are likely to be high-producing middle-aged usually angus breed cows with two-week to two-month old calves at foot, calving in winter-early spring on green grass-dominant improved pastures or cereal crops. But as this describes most herds in southern and central NSW, attempts have been made to determine why the majority of herds suffer no grass tetany deaths (Sackett et al., 2006) while some herds lose significant numbers of cows (Anon, 2008).

SAMPLING THE LIVE ANIMAL. Samples from live cows are poor predictors of clinical hypomagnesaemia. Serum magnesium usually lies in the range 0.74-1.44mmol/L (normal magnesium reference range Regional Laboratory Services Benalla) although Parkinson et al. (2010) regards the normal range as between 0.6 and 1.1mmol/L. Not all cows with serum Mg below 0.74mmol/L show clinical signs. Radostits et al. (2008) note some cows with serum magnesium as low as 0.16mmol/L fail to show clinical signs, but signs of tetany usually occur when serum Mg falls below 0.5mmol/L (Radostits et al., 2008) or 0.4mmol/L (Caple et al., 1992; Parkinson et al. , 2010). The latter suggest supplementation of cows with a mean serum Mg concentration below 0.63mmol/L will usually prevent clinical grass tetany in the herd.

Concentration of magnesium in urine is related to surplus dietary magnesium, with cows on magnesium-deficient diets having very low to undetectable urine magnesium. However, Parkinson et al. (2010) warn that faecal contamination of urine samples during collection and the variation in urinary Mg concentration with changes in urine output both render the assessment unreliable. Sutherland et al. (1986) concluded urine magnesium adjusted for urinary creatinine concentration would be more reliable, and proposed a benchmark ratio for use as a herd test.

Mustering and handling of cattle for collection of blood or urine samples may precipitate grass tetany in susceptible cows, and may be impractical when many cows in the mob have young calves at foot.

SAMPLING PASTURE OR SOIL. Because other factors determine the amount of magnesium in the diet that is available to the animal, pasture magnesium concentration alone is not a good guide to adequacy of intake. The recommended pasture magnesium concentration for lactating cows is at least 2g/kg DM (0.2% dry matter) (Radostits et al., 2008). Parkinson et al. (2010) suggest a level of Mg about 0.35% DM is required where pasture potassium concentration is also high.

Recognising the influence of potassium (K) on absorption of magnesium, several researchers have developed guidelines based on the ratio K/(Mg+Ca) for both pastures and soils. Using values for each element expressed in mEq, pastures are deemed at risk of producing grass tetany when the ratio is more than 2.2 (Radostits et al. 2008). Elliott (2008), in outlining factors responsible for the uptake of anions by plants, notes that their relative concentrations can change markedly over a few days, and are influenced by temperature. This limits the predictive usefulness of this ratio in plants.

Soil analysis could be of greater benefit in predicting likelihood of grass tetany. Cattle producers often recognise that losses from grass tetany only occur in certain paddocks, and district records indicate that losses occur more commonly on certain soil types. Lewis and Sparrow (1991), in research in South Australia, concluded that cattle were at risk from grass tetany when the ratio of K/(Mg+Ca) in soils exceeded 0.07-0.08. Elliott (2008) recommended these same values for southern New South Wales without reference to the possible mitigating effect of pasture composition, in particular clover content, discussed by Lewis and Sparrow.

Mark Conyers, Principal Research Scientist with NSW DPI, discussed the predictability of grass tetany at a gathering of beef cattle producers at Bathurst in June 2011, and further cautioned against using the soil ratio in isolation. He explained that the soil K/(Mg+Ca) ratio needed to be ‘calibrated ’ for NSW soils, and more importantly, the benchmark ratio of >0.07 was subject to modification based on pasture composition. He demonstrated no history of grass tetany in some paddocks where soils had a ratio in excess of 0.15. Clover made up a significant proportion, estimated at least 25%, of the pastures in these paddocks. On other properties, grass tetany deaths occurred on paddocks which the soil ratio predicted to be ‘safe’, at 0.05. Pastures in these paddocks were assessed as grass-dominant with little to no legume component.

DIAGNOSING HYPOMAGNESAEMIA IN THE DEAD ANIMAL

There are no gross post-mortem lesions specific for grass tetany. Age, lactation status, history including weather conditions and pasture availability may all suggest grass tetany as the cause of sudden death. There may be signs consistent with terminal struggling. Gross post-mortem lesions are restricted to agonal haemorrhages in organs and tissues, especially the heart.

Laboratory analysis of post-mortem samples may assist with the diagnosis. Serum collected immediately after death may show low magnesium (<0.7mmol/L), but quickly becomes unreliable with onset of intravascular haemolysis and leakage of magnesium from surrounding tissues (McCoy 2004). Several authors cited by McCoy (2004) also warn that serum magnesium often increases at point of death, associated with increased muscle activity.

Urine magnesium concentration reflects both recent dietary intake and serum magnesium level, making interpretation difficult post-mortem.

Magnesium concentration in aqueous humour closely reflects serum magnesium, with levels below 0.25mmol/L associated with experimentally induced hypomagnesaemic tetany (McCoy 2004). Anon (2011) suggests the substantially higher figure of <0.6mmol/L as indicative of magnesium deficiency. However, McCoy (2004) found aqueous to be unstable post-mortem, and concluded that vitreous humour was more reliable even up to 48 hours after death, depending on ambient temperature. Cows in McCoy's trials showed severe hypomagnesaemia and tetany when vitreous magnesium concentration fell below 0.55mmol/L. Both authors discuss the importance of obtaining clear eye fluid samples free from contamination with blood and cells. McCoy recommends using a 16gx25mm needle and 10ml syringe with only gentle pressure for collection of vitreous humour, to avoid aspirating fragments of retina.

The concentration of magnesium in ventricular cerebrospinal fluid determines the onset of hypomagnesaemic tetany. Clinical signs were seen in cows with CSF Mg of 0.51mmol/L (Radostits et al. 2008) or less than 0.45mmol/L (Pauli and Allsop, 1974). There is disagreement about the usefulness of CSF for diagnosis. McCoy (2004) states that CSF Mg increases quickly after death due to tissue leakage, while Radostits et al. (2008) suggests CSF samples were diagnostic up to 12 hours after death; Parkinson et al. (2010) indicate CSF samples are suitable up to 48 hours post-mortem. McCoy (2004) also advises of the difficulty obtaining a suitable CSF sample uncontaminated with blood.

PREVENTION

Techniques aimed at preventing grass tetany deaths have changed little in the last couple of decades. Provision of hay laced with magnesium oxide is still regarded as the most reliable (Elliott, 2009), with the provision of 60g per head per day of Causmag recommended. The supplement should be fed daily or at most every second day (120grams). This latter rate, however, may destroy rumen flora required for magnesium absorption and feed digestion (Parkinson et al., 2010). It may be expensive in terms of labour and hay cost, as well as difficult especially when paddocks become boggy, to feed hay and Causmag. Some large-scale operations have greatly improved efficiency through purchase of an automated powder dispenser which is attached to the discharge chute of a hay feed-out trailer.

Grass tetany deaths in fat, older cows, frequently those in body condition score 4 or more and six to eight years of age, is often associated with under feeding and weight loss after calving (Champness 2007). With no readily accessible magnesium store in the body, the normal physiological process of breakdown of body tissues to provide for increased milk output requires additional dietary magnesium. Hypomagnesaemia may be prevented by feeding sufficient hay to counteract that weight loss. Champness (2007) recommends feeding four kilograms of good quality hay per head daily.

Elliott (2009) also suggests magnesium supplements based on cereal grains. High rumen pH reduces magnesium absorption, and is often associated with digestion of green grass (Parkinson et al., 2010). Depending on the quantity fed, grain in these magnesium supplements may have two benefits, both reducing rumen pH and providing dietary energy to help counteract weight loss and aid magnesium absorption (Radostits et al., 2008).

Slow-release magnesium rumen capsules aid in the prevention of grass tetany, and are routinely used in some herds. However, they release about two grams of magnesium a day (based on initial weight and a projected 90-day payout), significantly less than the daily requirement of the highest-risk cows.

Many cows dying with grass tetany are found to be concurrently hypocalcaemic and hypomagnesaemic. This suggests a supplement containing both elements would be beneficial. Dolomite contains roughly equal parts of calcium carbonate and magnesium carbonate. However, National Research Council considers availability of magnesium from dolomite is negligible (Anon, 2001).

Several proprietary and home-mixed loose mineral supplements and blocks containing magnesium are available. Intake is variable (Elliott 2009) but is improved where cows are previously accustomed to licks (Champness 2007). One product requiring further investigation is DCS-Syrup, a by-product of commercial ethanol production. As a supplement for cattle, it appears highly palatable despite pH3.5, with ME 15MJ, 0.6% magnesium and 2.2% potassium on a dry matter basis. No controlled trials have been conducted, but farmer observations on its use in lactating beef cows are positive. The availability of the product is increasing along with mandated inclusion of ethanol in petrol.

RECOMMENDED READING

The veterinary texts by Radostits et al. (2008) and Parkinson et al. (2010) both discuss hypomagnesaemia in detail. The Agriculture Note by Champness (2007) is a concise yet thorough summary suitable for cattle owners.

References

  1. Anon. Nutrient requirements of dairy cattle. National Research Council. 2001, 130
  2. Anon. Grass tetany of cattle. In Animal Health Surveillance. NSW DPI. 2008; (3):5
  3. Anon. Hypomagnesaemia. Veterinary Laboratory Manual. NSW DPI. 9th edition, accessed on-line Dec 2011
  4. Caple IW, West DM. Ruminant hypomagnesaemic tetanies. Current Veterinary Therapy Food Animal Practice. Saunders. 1992, 318-321
  5. Champness D. Grass tetany (hypomagnesaemia) in beef cattle. Agriculture Notes. Victoria Department of Primary Industries; 2007. AG0579
  6. Elliott MG. Grass tetany in cattle - predicting its likelihood. Primefacts . NSW DPI, 2008, Primefact 785
  7. Elliott MG. Grass tetany in cattle - treatment and prevention. Primefacts. NSW DPI, 2009, Primefact 421
  8. Lewis DC, Sparrow LA. Implications of soil type, pasture composition and mineral content of pasture components for the incidence of grass tetany in the South East of Australia. Australian J Exp Agric. CSIRO ; 1991; 31(5): 609-615
  9. McCoy MA. Hypomagnesaemia and new data on vitreous humour magnesium concentration. Magnesium Research. 2004, 17(2): 137-45
  10. Parkinson TJ, Vermunt JJ, Malmo J. Disorders of magnesium metabolism. Diseases of cattle in Australasia. New Zealand Veterinary Association Foundation for Continuing Learning. 2010, 532-541
  11. Pauli JV, Allsop TF. Plasma and cerebrospinal fluid magnesium, calcium and potassium concentrations in dairy cows with hypomagnesaemic tetany. New Zealand Veterinary Journal 1974; 22:227-231
  12. Radostits OM, Gay CC, Hinchcliff KW, Constable PD. Veterinary Medicine 10th Edition, Saunders Elsevier 2008; 1652-1659
  13. Sutherland KJ. A comparative study of diagnostic tests for the assessment of herd magnesium status in cattle. New Zealand Veterinary Journal. 1986, 34:133-135
  14. Sackett D, Holmes P, Abbott K, Jephcott S and Barber M. Assessing the economic cost of endemic disease on the profitability of Australian beef cattle and sheep producers. Project code: AHW.087 ISBN: 1741910021. Meat & Livestock Australia Limited. April 2006

 

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