Kangaroo gait in lactating ewes is an unusual neurological disease of low flock prevalence that typically affects multiple bearing ewes of larger breeds 3-6 weeks after lambing. It is a polyneuropathy with preferential involvement of the radial nerves. Affected ewes have weak forelimbs, bearing most weight on their hind legs so when pressed, move with a characteristic hopping gait. Most ewes recover after lactation. This is a report of three cases of kangaroo gait in lactating ewes.
CASE 1. Keith, South Australia
In June 2012, one of 80 (1.25%) second-cross ewes presented with an abnormal gait. The four-year-old ewe had 3-4 weeks old lambs at foot. The mob was grazing lucerne and grass pasture and was supplemented with barley until six weeks prior to lambing. Another ewe was similarly affected in the previous year. This ewe recovered to some degree, but seven months later, she still had a shortened forelimb stride, hunched back and lameness in one hind limb.
CASE 2. Vittoria, (between Bathurst and Orange) NSW
In late September of 2012, 12 ewes (2.4%) in a mob of 500, two-year-old, Coopworth/Composite ewes were observed 2-3 weeks post-partum to have developed neurological signs consistent with kangaroo gait. The owner commented that while this mob had an exceptionally high prevalence, across 5,000 ewes in 30 mobs, 0.5 to 1.0% of 3-6 year old ewes were affected. This producer routinely joins ewes first as lambs. No cases were seen in these. A smaller number of similarly affected ewes had been seen in each of the previous three years.
This mob grazed pasture containing phalaris (Phalaris aquatica), cocksfoot (Dactylis glomerata) and some subterranean clover (Trifolium subterraneum). The property had received rain in March 2012, resulting in good winter pasture, preparing the ewes well for lambing. Four weeks prior to lambing, the ewes were crutched and two weeks later were given a controlled release combination anthelmintic capsule fortified with selenium and cobalt (BIONIC, Ancare Australia); in both instances all ewes appeared normal.
When first observed with the disorder, the ewes were between 3-4 fat score (as was the remainder of the mob), but as it progressed, these ewes lost condition, became difficult to drove and their lambs (usually multiples) appeared grow more slowly than their cohorts. One ewe, run separately, recovered after 4-6 weeks. It was understood that majority of the affected ewes recovered similarly. The ewes were not treated.
One lactating ewe, rearing two lambs, walked with a hunched posture, bearing most weight on her hind legs. She seemed reluctant to bear weight on her forelimbs tending to hypermetria, knuckling and stumbling. Neurological examination was otherwise normal and no foot lesions or cranial nerve deficits were found. Her fat score was 2/5, temperature 40.6°C and she was tachypnoeic with pink mucous membranes. Serum calcium and magnesium levels were normal (Ca 2.26, normal 2.12-2.87 mmol/L and Mg 0.94, normal 0.74-1.44 mmol/L).
CASE 3. Bathurst, NSW
On February 4 2013, a three year old, Black-faced Dorper ewe, with twin lambs at foot, in a mob of 48 (2.1%), presented with possible phalaris staggers. The lambs had been marked in the last week of December and the ewe was then apparently normal. The mob was run on a paddock containing 10-20% of phalaris. One week previously, the ewe was noticed to have an abnormal gait and the mob was moved to a sparser paddock with less phalaris. On examination, the ewe appeared reluctant to bear weight on the fore limbs and displayed a shortened, uncoordinated forelimb gait with knuckling of the fore-fetlocks and an arched back. She bore most weight on her hind limbs and hopped when forced to travel (figure 2). Clinical examination revealed no foot abnormalities, a normal range of movement in all fore and hind limb joints and no evidence of a cranial nerve deficit. Serum calcium and magnesium levels were normal (Ca 2.41, normal 2.12-2.87 mmol/L and Mg 1.27, normal 0.74-1.44 mmol/L).
Kangaroo gait in lactating ewes was first reported in New Zealand in 1978 (Moffat 1978). Ewes developed the condition 3-6 weeks post-lambing, were generally feeding multiple lambs and often recovered after the lambs were weaned. It has subsequently been reported in the United Kingdom and Australia (Duffell, Wells and Winkler 1986, Barlow and Greig 1986, O'Toole et al 1989, Clements et al 2003 and Bourke 2009). Clinical signs include incoordination, a high-stepping forelimb gait, bounding hind limb gait, arched back and poor distal limb control leading to knuckling and dropping of the fore and hind fetlocks. During locomotion the forelimbs and hind limbs are positioned centrally under the body, which can result in a kangaroo-like gait (Bourke 2009). A questionnaire of veterinarians and flock owners/managers in the United Kingdom found that the annual incidence was commonly <0.2% in affected flocks. Cases began in early and late lactation more often than during gestation and most cases occurred in commercial crossbred ewes run on lowland or upland farms rather than in hill flocks of Scottish Blackface and Cheviot ewes (Clements et al 2003). Ewes in Australia remained affected for 8-12 weeks and in some cases only approximately 50% recovered completely (Gabe Morrice pers. comm. and cited by Bourke 2009).
O’Toole et al (1989) summarised the pathology of kangaroo gait as an ‘acute-onset, lactation-associated neuropathy of the radial nerve which involves all fascicles equally and is usually bilateral; spontaneous improvement due to regeneration is common; the full size distribution of myelinated fibres is involved; unmyelinated fibres are spared.’
In the two cases reported here in which blood was collected, there was no evidence of metabolic disease. This is consistent with the findings of others (Barlow and Greig 1986, Duffell et al 1986) although perhaps not surprisingly for twin bearing ewes with difficulty moving freely, Moffat (1978) reported ketonaemia in four of nine cases. O’Toole et al (1986) suggested that ‘this neuropathy is due to severe local entrapment or compression in early lactation,’ but mentioned that this ‘attractive hypothesis’ is yet to be tested. They added that this disease was unlikely to have a toxic, metabolic or hereditary aetiology. It has been suggested that kangaroo gait in lactating ewes may be caused by or exacerbated by a deficiency of thiamine or nicotinic acid (Barlow and Greig 1986) but the authors are not aware of clinical trials or other evidence to support this.
Clements et al (2003) observed that veterinarians may underestimate the frequency of diseases such as kangaroo gait in lactating ewes, ‘particularly in an economically marginal species such as sheep and with a condition of low flock incidence from which affected animals recover.’ This may also be the case in Australia.
We would like to acknowledge the interested co-operation of the owners of the affected sheep.