Subacute nutritional muscular dystrophy (NMD) or white muscle disease is a myodegenerative disease caused by selenium deficiency. It affects both calves and lambs, targeting the limb muscles, while the acute form of the disease affects the myocardial and respiratory muscles. When the muscles of the limbs are affected, it causes the animal to adopt a stiff, stilted gait while cardiomyopathy can manifest as sudden death (Radostits et al., 2007; Parkinson et al., 2010). Although selenium deficiency as judged by low blood glutathione peroxide (GSHPx) levels is widespread on the central tablelands of NSW, clinical white muscle disease is rare.
On the 23rd September 2011, two 6 to 8 week old Angus calves (a steer and heifer) were examined on a beef cattle property near Tarana on the central tablelands of NSW. The owner reported that these calves appeared to be weak and lame. The owner reported that two weeks previously, two well-grown calves died suddenly in the paddock and that another calf had died a few days later. All were from the same July-August 2011 drop and had been in good body condition.
The affected calves were from a mob of 46 cows, of 160 breeding cows on the property. The farm has granite soils and the owner has applied superphosphate annually since acquiring it in 1991. The affected calves had been in a paddock with approximately 75% clover and 25% grasses; these grasses included phalaris, cocksfoot and ryegrass.
The steer calf appeared weak and reluctant to stand (Figures 1,2). When encouraged to walk, it had a stiff gait, would occasionally tremble and would lie down as soon as possible. The rectal temperature was 39.7C. The heifer calf also had a stiff gait but was able to walk reasonably well. The heifer's temperature was also elevated at 39.8C. No other abnormalities were detected.
Blood samples were collected from both affected calves and from five randomly selected clinically normal cows from the same mob (No. 1-5). Creatine kinase (CK) levels were measured in the samples from the two affected calves, while glutathione peroxidase (GSH Px) levels were determined for all 7 samples. Bulk vitamin B12 levels were also assessed using the samples from the 5 cows.
All calves including the clinically affected animals treated with a subcutaneous injection of barium selenate (Deposel, Novartis) on 26th September 2011. The remainder of the herd was treated on 30th September 2011. The owner reported that about a month later, the heifer responded to treatment and appeared almost normal. The steer also improved although its gait was still stiff. No further cases were reported after treatment.
A number of diseases, including polyarthritis, myositis induced by trauma or infectious agents, neurological diseases including tetanus, meningoencephalitis and myelitis and organo-phosphate poisoning may manifest as stiffness and recumbency in calves (Radostits et al., 2007, Divers and Peek, 2008). In this case, NMD was suspected based on a history of sudden death (which was presumed to be from the myocardial form of the disease) and when two calves with signs consistent with a skeletal myopathy were presented. The extremely elevated CK levels, markedly low GSHPx levels and a response to treatment support the diagnosis. However, CK levels can also become elevated secondarily in recumbent animals and not all cattle with low GSHPx levels present with clinical signs of selenium deficiency. The option to confirm the myopathy by histopathology did not present.
Clinical cases of selenium deficiency most commonly present with non-specific signs such as reduced growth rate, ill thrift and decreased fertility. Although not as common, other specific presentations such as white muscle disease, Heinz-body anaemia, and abortion, can also occur (Ellison, 2002; Radostits et al., 2008, and Parkinson et al., 2010).
Interestingly, although a survey has indicated that almost half the cattle in the eastern tablelands are likely to be deficient in selenium, as reflected by their low GSH-Px levels (Watt, 2007), clinical disease, such as NMD, remains an uncommon diagnosis (Parkinson et al 2010; Watt, 2011). This suggests that the likelihood of disease subsequent to selenium deficiency is influenced by other factors (Parkinson et al., 2010). These include the level of protection offered by other (non-selenium dependent) anti-oxidants, the presence of protective non-enzymes such as vitamin E and the degree of dietary oxidant challenge, particularly from polyunsaturated fatty acids (PUFA) (Suttle, 2004). Experimental studies have demonstrated that some calves can have low GSH-Px activity in the blood reflecting low selenium levels, as in this case in Tarana, but not develop clinical myopathy (Arthur, 1988). In this study, calves fed indoors did not develop myopathy, while those fed the same diet outdoors did. This suggests that exercise or other stresses are necessary to precipitate clinical disease (Arthur, 1988). An earlier study by Rice and McMurray (1982) found that a selenium-deficient diet that is also high in PUFA, such as lush, high-quality pasture, significantly increases the risk of calves developing NMD.
The symptoms of selenium deficiency in older cattle include ill-thrift and poor growth, suboptimal milk yield, suboptimal fertility and retained foetal membranes (Radostits et al., 2007; Parkinson et al., 2010). It is of interest that the mature cows in this herd, despite having barely detectable GSHPx levels (ranging from 0 to 1U/gHb) were in excellent condition with glossy coats and according to the owner, of normal fertility with no evidence of retained foetal membranes. The calves also appeared well grown. As mentioned, throughout the central tablelands, selenium deficiency in cattle is common and yet clinical disease is rare. Under these circumstances, we consider that ascribing a particular disease to selenium deficiency is risky without substantial supporting evidence. We however consider that in this case the evidence we have presented (that our clinical and laboratory findings are consistent with NMD, a well recognised syndrome and that the calves responded to treatment) is sufficient for us to make a diagnosis of NMD.
CK is released into the blood following myodegeneration or unaccustomed exercise. It is highly specific for heart and skeletal muscle and has a short half-life (2-4 hours) making it a valuable laboratory support in a diagnosis of myopathy (Radostits et al., 2007). In our experience, CK levels are often moderately elevated in sick, intermittently recumbent animals. The levels in this case are markedly elevated indicating the levels attained in a presumed severe primary myopathy.
Finally, it is of interest that this property was included in the 2006 serological and trace mineral survey of heifers (Watt, 2007) and at the time of collection on 18 May 2006, had normal GSHPx levels (averaging 55 U/gHb and ranging from 44-73). It is presumed that the regular application of superphosphate and the subsequent clover dominant pastures have now rendered this property selenium deficient. Seasonal and yearly fluctuations in GSHPx levels should also be borne in mind. Caple et al., (1980) in a survey of Victorian sheep found that GSHPx levels were on average 30% higher at their peak in the autumn and were lowest in spring. Fortunately, long acting injectible barium selenate provides a convenient and economical remedy.