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Bruce Watt, Tablelands Livestock Health and Pest Authority, Bathurst

Posted Flock & Herd October 2013


Mature late pregnant ewes are susceptible to hypocalcaemia and ketosis, especially if held off feed and subject to handling and other stressful procedures (Blumer et al 1939, Simmons 1975, Sansom et al 1982, Larsen et al 1986, West et al 2009).

In this outbreak, 21 of 250 mature merino ewes suffered from clinical hypocalcaemia after they were held off feed for 26 hours, as they were mustered, crutched and drenched. Sixteen of 21 ewes recovered with treatment. Five of 21 ewes either died or were euthanased when they did not respond adequately.


A mob of 250 3-4 yo Merino ewes, joined to lamb commencing on the 7 April 2013, were mustered 3.00pm on 25 March 2013. Although fat score 3+, the ewes had, for the last few weeks, been run in a paddock with limited feed. The pasture was not examined but was described by the owner as a mix of native and improved pasture species without weeds likely to cause oxalate poisoning. On the 26 March the ewes were crutched and drenched with a triple combination anthelmintic (Triguard, Merial) then taken about 2 km back to paddock at 5:00 pm. Five ewes were found to be weak that afternoon and on the morning of the 27 March, 14 were down and one was dead.


Five recumbent ewes were examined. All were in fat score 3 or more and appeared to be in advanced pregnancy. One ewe was dull and unresponsive but the others were bright and alert but were in sternal recumbency and unable to stand (Figure 1). All ewes had pink mucous membranes and had no evidence of mastitis.

Image of recumbent ewes in paddock
Figure 1. Three recumbent ewes

Clotted blood samples were collected from the 5 ewes examined (cases 1-5) while the aqueous humor sample was collected from case 6.


Table of laboratory findings
Note BHB is an abbreviation for beta-hydroxy butyrate

A worm egg count on faecal samples collected from the mob at random revealed an average of 4100 epg, consisting of 98% Haemonchus.


One ewe was necropsied. This ewe (Case 6) was in fat condition and was bearing twin, near term foetuses. The liver was dark red. On gross examination, no Haemonchus were seen in the abomasum.


Within 24 hrs of the start of the outbreak, 21 ewes (8.4% of the mob) were affected. The owner treated all affected ewes once with 70 ml of a proprietary product containing calcium borogluconate plus glucose (FloPak Plus 4:1, Bomac. containing calcium borogluconate 330g, glucose 182g, magnesium hypophospite 4.7g, and phosphorus hypophosphite 12.2g per litre) subcutaneously and 70 mls of a concentrated electrolyte and glucose mix (Vytrate Liquid Concentrate, Jurox) orally. The ewes were commenced on grain oats and were supplemented with equal parts of lime and salt in a loose mix in drums. The ewes were then drifted onto a paddock of good feed for lambing. The owner later reported that one ewe (Case 6) died prior to treatment and another four of the 21 treated ewes failed to respond to treatment and were euthanased after being down 2-3 days. Most ewes responded to treatment within 1-2 hrs. No further cases occurred.


In the experience of the author, primary hypocalcaemia and pregnancy toxaemia can both occur together in an outbreak. However, as ewes with both pregnancy toxaemia and hypocalcaemia become anorectic it is possible that either condition can occur as a secondary consequence of the other. However, the management of these conditions is different and can be more targeted if the primary disease is identified.

Primary hypocalcaemia was considered to be the major problem in this outbreak because blood or aqueous calcium levels were profoundly low, magnesium levels were normal, the ewes were mostly bright and alert but recumbent (clinically consistent with hypocalcaemia rather than pregnancy toxaemia), the necropsy findings were consistent with hypocalcaemia and most ewes responded to treatment. However, the ewes had previously been run in a paddock with limited feed, some ewes had elevated beta-hydroxy butyrate levels and some ewes did not respond to treatment suggesting either a concurrent or secondary ketosis in some cases. As it was considered that primary hypocalcaemia was the main condition in this case, the flock was managed accordingly although some supplementary feeding was advised as would be appropriate for managing pregnancy toxaemia.

While none of the ewes examined were clinically anaemic, the WEC of 4100 epg, comprising almost entirely of Haemonchus, suggests that haemonchosis cannot be ruled out as a contributing factor in this outbreak.


  1. Blumer CC, Madden FJ and Walker DJ (1939). Hypocalcaemia, grass tetany or grass staggers in sheep. Aust Vet J 15, pp 24-27
  2. Larsen JWA, Constable PD and Napthine DV (1986). Hypocalcaemia in ewes after a drought. Aust Vet J. 63:25
  3. Sansom, BF. Bunch, KJ and Drew SM. (1982) Changes in plasma calcium, magnesium, phosphorus and hydroxyproline concentrations in ewes from twelve weeks before until three weeks after lambing. Br vet J 138, 393-401
  4. Simmons RE (1975). Transport tetany (hypocalcemia) in a band of western ewes. J Am Vet Med Assoc. 166 (6) 582-3
  5. West DM, Bruere AN and Ridler AL (2009). The Sheep: Health, Disease and Production, Third Edition, pp 225-227


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