Metabolic diseases have been identified as a cause of sheep deaths in NE Victoria since the 1960s. Metabolic diseases cause mortalities in Hume Livestock Health and Pest Authority sheep flocks each year. Stock at risk include lactating and pregnant ewes and occasionally growing lambs, particularly in autumn and winter when grazing lush green pasture and crop.
Investigations of sudden deaths in sheep flocks In Hume LHPA may include several metabolic disorders in the differential diagnosis and laboratory results often confirm more than one metabolic abnormality.
Hypomagnesaemia may be suspected on the basis of clinical signs of tetany and excitement or nervous behaviour, but metabolic disease cases that are sampled often show more than one imbalance, commonly combinations of hypomagnesaemia, hypocalcaemia and ketosis.
This article will attempt to relate what we see in local cases to some of the published work on hypomagnesaemia in sheep, and present some clinical data on cases that have been sampled from the Hume LHPA case files.
The difficulties of sample interpretation will also be considered.
The clinical syndrome of grass tetany is well recognised in sheep as being characterised by nervous system signs of excitability and recumbancy with tetanic spasms or fits. It is accepted that it is a deficiency in available magnesium in the sheep. Risk factors that affect the absorption and metabolism of magnesium make the clinical syndrome quite complex.
Recognised risk factors include grazing on grass dominant pasture or crop, being in a production phase with high energy and high mineral demands (such as lactation, late pregnancy and growth) being exposed to an interruption in access to feed(yarding off feed, transport - such as in transit tetany), sudden cold weather change, low sodium and high ruminal potassium.
In our experience, when there is an opportunity to sample animals thought to be presenting as typical of grass tetany, other mineral imbalances and metabolic conditions may be identified as occurring concurrently.
Research to quantify and better understand the clinical syndrome of grass tetany has been underway for over 50 years.
Grass Tetany in ewes has been recognised in Australia since the 1960s1 and the association of grass tetany with hypocalcaemia and hypomagnesaemia was confirmed in 1962. 1
Grass tetany outbreaks in 1963 and 1965 were associated with a higher than usual incidence of pregnancy toxaemia in some flocks1.
Some of the work in the 1960s suggested that tetany did not occur with hypomagnesaemia unless accompanied by hypocalcaemia; however outbreaks were halted by supplementation of magnesium oxide alone.2
Extreme hypomagnesaemia can be encountered in clinically normal sheep with no signs of tetany.3, 4 Individual ovine plasma magnesium levels and responses to magnesium supplementation are reported to be extremely variable 3.
Hypomagnesaemia can be produced by feeding magnesium deficient diets, and clinical tetany can be produced under these experimental conditions4.
The potential for protein or ammonia and potassium to interfere with magnesium absorption in the rumen has been identified5, 6. As low dietary sodium has the potential to affect the sodium: potassium balance in sheep and increase potassium in the saliva and ruminal contents, low sodium is also considered a risk factor for hypomagnesaemia, as well as high potassium7,8,9,.
Trigger factors that may be associated with outbreaks of grass tetany include yarding for management procedures that interrupt feed intake1. Work in 1965 examined the effect of fasting on serum calcium and magnesium levels in lactating cows and ewes10 and showed that serum magnesium dropped significantly at the end of the fasting periods but also continued to fall to its lowest level for 24 hours after returning to normal grazing. Calcium levels returned to normal more quickly. Tetany could be produced by fasting11.
Magnesium and calcium plasma levels dropped in sheep with exposure to cold12. Cold stress was reproduced experimentally in climate chambers by creating a sudden drop in temperature from +8Co or +30Co to -20Co with 4mph winds, in 2 acute exposures, after shearing. Equal numbers were kept on high and low planes of nutrition12.
Cattle and sheep appear to have a different degree of sensitivity to high dietary or ruminal potassium levels affecting magnesium absorption,13 sheep being less sensitive.
Calcium and magnesium levels in blood, vitreous humour and aqueous humour are subject to change over time when exposed to metabolising cells. Some contradictory data may be explained by the delays post mortem in sampling and processing samples collected in the field14, 15, 16, 17. Plasma magnesium may rise before death due to convulsions14.
Regional Laboratory Services at Benalla have conducted validation work on aqueous humour and will currently test eye fluid for several metabolites. It is their preferred sample as it is considered more stable than cerebrospinal fluid or blood.17
From examination of a selection of pathology case reports from Hume Livestock Health and Pest Authority records, it becomes clear that there are cases that have 'typical' risk factors and clinical signs, enough to give a presumptive diagnosis of grass tetany, that may not be not supported by a pathology result of low magnesium levels.
In 18 cases sampled with either a clinically suspect diagnosis of hypomagnesaemia, or clinical signs of tetany being observed; only 4 cases had animals with low magnesium alone without concurrent low calcium. One of these was a pregnancy toxaemia case. The calcium levels were all at the low end of the normal range in the other 3 cases.
Results could be quite variable between individuals within the same case. Some animals had low calcium and normal magnesium, and others low calcium and low magnesium .There could be animals with results in the normal range for calcium and magnesium but at the low end of the range. One animal had high magnesium and low calcium while its cohort had low calcium and low magnesium.
Some sample results return with low levels of calcium and magnesium as part of what seems to be a more complicated clinical picture. Two cases involving weaners being yarded or trucked and held off feed had concurrent elevated muscle enzymes in some samples. Another case occurred with concurrent suspect water /salt intoxication when lambs were returned to water after being trucked and held off feed and water for 2-3 days.
One case in ewes revealed ketosis and uraemia concurrent with low-normal magnesium and low calcium. In another case in a ewe, hypoproteinaemia was seen as well as hypocalcaemia and hypomagnesaemia. This animal showed tetanic clinical signs and was recently lambed on grass dominant pasture.
We think of grass tetany in sheep as being associated with primarily a hypomagnesaemia, but our experience in the Hume district suggests that even many 'textbook cases' are a more complex metabolic disorder.
Sample interpretation can be complex. We can see variable magnesium levels in normal sheep and in a flock sample involving several clinical animals there may be variations in calcium and magnesium levels in those sampled.
In cases of more complicated syndromes involving other biochemical disorders, it may be that the low magnesium is secondary to the condition.
Our confirmation of the diagnosis may be being disrupted by delays post mortem in collecting and transporting samples for processing.
In cases in which the history, clinical signs and response to treatment supported a diagnosis of hypomagnesaemia/hypocalcaemia, and results fall in the low end of the normal range, we may still consider the diagnosis of hypocalcaemia/hypomagnesaemia to be valid.
In our experience, low normal readings may be considered to be of significance when interpreting laboratory results of tests for calcium and magnesium levels. Delays of more than 24 hours, and up to 72 hours between sampling and testing are not uncommon in our district. Most of our samples are sent directly or indirectly to Regional Laboratory Services, Benalla.
If clinical signs are associated with a fall in magnesium levels in the cerebrospinal fluid, perhaps one difficulty is being able to confirm this by testing CSF in a timely manner in the field.
Grass tetany is a well recognised clinical syndrome in sheep in south eastern NSW and north eastern Victoria. Extensive research has given us a model for the disease in sheep that explores and explains risk factors as they impact on magnesium metabolism in the sheep. Case results from our records show that many cases also show hypocalcaemia. Very few cases associate hypomagnesaemia alone with the clinical tetany syndrome in sheep, within the limits of the testing available to us in the field.
Eighteen cases were sourced from Hume Livestock Health and Pest Authority files. Nine examples are summarised below to demonstrate the range of clinical signs and history in cases selected for having a differential diagnosis of hypocalcaemia/hypomagnesaemia and signs of tetany.
1. Suspect hypocalcaemia
300 merino ewes with lambs at foot. Sudden collapse was observed in ewes after access to crop. 9 were dead. One was observed twitching and unstable and showed a response to Ca/Mg injection. Clinical signs included sudden collapse, struggling, convulsions when handled, and dying within the hour. At autopsy increased vascularity was noted in the small intestine and venous congestion of liver and kidney observed.
Of 2 animals sampled one Aqueous Humour had low Mg and low /normal Ca, the other low Ca and low /normal Mg.
2. Suspect metabolic
In mob of 200 4yo ewes with lambs at foot grazing short green pasture, 8 had died suddenly over the previous week. One presented in lateral recumbency with opisthotonis and some excitability. Autopsy showed some pneumonia/pleurisy and congestion lungs and small intestine.
Aqueous humour -Low Ca, low normal Mg. Negative for nitrate.
3. Suspect metabolic
Twenty reported sick/200 drought reared BL lambs. The lambs were yarded overnight and deaths and recumbency occurred when they returned to paddock. Symptoms were typical of hypocalcaemia in some, and hypomagnesaemia in others, and some showed severe frothing at the mouth. Some responded to Calcium-Magnesium injection.
2 were sampled- 2/2 had low Ca, one also had low Mg (blood)
4. Suspect water intoxication
In 865 weaner sheep, 200 were sick and 113 dead. The weaners were trucked from WA to Hume LHPA over 3 days, with no feed or water on the trip. They walked off truck to water at a creek and problems were observed within an hour. Clinical signs were staggering, weakness, frothing at the mouth and convulsions. Calcium- Magnesium therapy was given with mixed results and some relapses, repeat treatments and samples taken the following day.
Mg low in one/3 and low Ca in 3/3 (blood)
5. Neurological signs
Ten lactating ewes out of 137 grazing triticale died suddenly and 10 more were affected with clinical signs.
Deaths were preceded by neurological signs (fits). At autopsy-congested lungs, a small fibrin clot in pericardial, agonal epicardial haemorrhage, mucosal congestion in the abomasums and liver was observed.
Aqueous Humour taken from 2 ewes-2/2 low Mg, 2/2 Ca low normal
6. Suspect transit tetany
Weaners were yarded for sale, transported, given silage, off feed at least 2 days. Now some noticed with a stiff and hunched gait. Some were down, with fever, panting and progressing to death.
High serum CK, Ca low in 2/2 sampled, Mg low in one and low normal in the other.
5 yo Merino ewe, recently lambed, presented recumbent with neurological signs, head back, opisthotonis, grazing oats/phalaris.
Ca and Mg low in one the animal sampled .Hypoproteinaemic.
8. Suspect hypocalcaemia / hypomagnesaemia
6/300 XB weaners were affected. Weaners were yarded over the weekend then 6 went down, showing clinical signs of mild tetany. They responded to intravenous calcium-magnesium. Some continued to show knuckling and one was sampled.
It showed biochemical evidence of muscle damage (High AST & CK) and low normal magnesium Mg and low normal Ca from a blood sample.
9. Suspect hypomagnesaemia / hypocalcaemia / ketosis
3/220 6yo lactating ewes with large lambs at foot died suddenly after grazing oat stubble for the previous 3 weeks. 1 ewe died in the paddock at the time of the veterinary visit and was sampled.
The autopsy was unremarkable, although a fatty liver was noted. Mild uraemia and azotaemia was diagnosed from high BHB and urea. Blood and aqueous humour Mg levels low, Ca low normal.