Many animals such as horses, pigs and various species of wildlife suffer from exertional rhabdomyolysis or capture myopathy, but it is not normally encountered in sheep. However, it has been reported in sheep that are chased excessively by dogs (Radostits et al 2010). This is a case report in which 10 of 600 ewes died from exertional rhabdomyolysis after being harassed by dogs.
The Young office of the Lachlan LHPA was contacted to discuss the cause of young ewes dying. The mob of 600, two-year-old Merino ewes were just joined. Over the previous few weeks, the producer found the occasional ewe that was unable to stand but otherwise appeared bright and alert with no signs of trauma. The ewes had not responded to a proprietary mix of calcium borogluconate, magnesium, phosphorus and glucose or rest with hand feeding. After a few days, they either died or were euthanized.
On 22/4/13, the producer presented a ewe in lateral recumbency. She had increased respirations and was reluctant to move her limbs. She had a rectal temperature of 40.2, a heart rate of 120 bpm and was in body condition score 4.0. On presentation, the producer advised that a dog had been seen in the paddock chasing the mob the day before. An inspection of the legs revealed a small puncture wound on the left hock. Both hind legs had firm swelling just proximal to the hock joint and generalized swelling below the hock.
On post-mortem, there was severe generalized hemorrhage of the distal hind legs and both gastrocnemius muscles appeared to be ruptured. The muscles were pale and firm on cut surface.
Histopathology of these muscles confirmed extensive areas of necrosis and haemorrhages infiltrated by macrophages and neutrophils. The finding of severe, subacute myonecrosis was consistent with exertional rhabdomyolysis. The biochemical profile also confirmed severe muscle damage.
|AST||0 - 130 U/L||2433|
|Bilirubin||0.0 - 6.8 umol/L||20.3|
|CK||0 - 300 U/L||8502|
|Urea||2.9 - 7.1 umol/L||7.8|
The brain was submitted for TSE surveillance and found to be negative.
Capture Myopathy has four distinct clinical syndromes (Fowler 1993).
1. Capture shock - usually results in death within 1-6 hours of capture and includes signs of depression, shallow rapid breathing, tachycardia, and fever followed by death. Post mortem lesions include congestion and oedema of the lungs and severe congestion of the small intestine and liver.
2. Ataxic myoglobinuric - is generally the most common of the syndromes and appears within a few hours to several days post-exertion. Clinically these animals show ataxia and myoglobinuria. If signs are mild, the animal may recover but more severely affected animals die. Muscle enzymes and BUN are elevated. The lesions are found in the kidneys (swollen and dark) and the skeletal muscles (pale dry areas in lumbar muscles and in flexor and extensor muscles of the limbs).
3. Ruptured muscles - Clinical signs tend to appear after 24-48 hours and are manifested by a marked drop in the hindquarters or an inability to stand. Muscle enzymes are markedly elevated while BUN tends to be normal or only slightly elevated. Grossly there is massive subcutaneous haemorrhage of the hind limbs. Multiple small to large ruptures can be found mostly in the gastrocnemius, subscapularis, middle and deep gluteal, semitendinosis and semimembranosis muscles. The lesions are bilateral but not symmetrical.
4. Delayed - peracute - this form is rare and occurs after 24 hours post-exertion. Animals die from ventricular fibrillation after trying to move suddenly when disturbed or stressed.
One ewe (Figure 3) showed the ruptured muscle syndrome from the dog chasing the mob for a lengthy period. Though the dog did not appear to attack the sheep and produce typical "dog attack" wounds, the damage was still substantial with a total of 10 ewes lost out of 600.