Selenium deficiency in two Kunekune sows

Emily Rätsep, Adriana Prystay

Animal Health Laboratory, University of Guelph, Kemptville, ON (Rätsep), Almonte Veterinary Services, Almonte, ON (Prystay)

AHL Newsletter 2022;26(3):16.

Early in April 2022, two sows were presented for necropsy with a history of weakness progressing to an inability to stand or walk.  Both sows were housed in the same pen with a feeding history of brewer mix and kitchen scraps.  A mineral mix had recently been introduced.  At postmortem examination, sows had a small volume of serous fluid present in the pericardial sac or abdomen.  Trichuris spp. nematodes were observed in the intestinal lumens of both pigs.  The underlying cause of the weakness was grossly inapparent.

In histopathology sections, there was marked diffuse polyphasic myodegeneration and necrosis in both the skeletal muscles (epaxial and postural muscles) (Figs. 1A, 1B) and heart (Figs. 2A, 2B).  Mixed cellular infiltrates (predominantly histiocytic) were occasionally present in these areas, and were interpreted as cellular debridement and ‘clean-up’ of the necrotic myocytes.  Other changes observed included focal areas of mild cellular necrosis in the kidney and liver of one pig which were interpreted as a response to terminal hypoxia or cellular apoptosis following stress.

Liver was submitted for vitamin E and selenium testing.  In both sows, selenium was low to low normal (0.27 and 0.42 ug/g; normal reference interval of 0.4-1.2 ug/g); however, vitamin E was high normal in both (both 45 ug/g; normal reference interval of 15-50 ug/g).  No other significant viral or bacterial pathogens were detected.

Inadequate selenium or vitamin E in the diet can result in the reduced capacity of cells to detoxify endogenously-produced peroxides (i.e., secondary to sudden environmental stress factors), leading to membrane damage due to free radical exposure.  As part of this cellular damage, the resultant increased calcium influx overwhelms mitochondria, and causes hypercontraction, coagulation and degeneration of muscle fibres.  These changes can be observed in the heart (“Mulberry heart disease”) and/or skeletal muscle.

The presence of similar findings in two sows with the same housing and feeding history indicated the low selenium level as the most likely cause of the observed muscle findings, in the absence of any other potential underlying cause.  The comparable lesions in each of these cases raises a question of whether or not there may be a susceptibility particular to this breed.  However, there is no published literature addressing this possibility.  In result, selenium deficiency should be considered a differential diagnosis for muscle weakness in pigs, and perhaps in Kunekune pigs in particular.  The author would appreciate follow up with any reports of similar findings in this breed, if observed in the future.   AHL

Figure 1. Polyphasic epaxial and postural muscle degeneration and necrosis in two Kunekune sows.   A, B.  Hypereosinophilia and fragmentation of myofibres (*), infiltration of macrophages (m), and early regeneration (r). 20x. H&E stain.

 

Figure 1. Polyphasic epaxial and postural muscle degeneration and necrosis in two Kunekune sows.  

A, B.  Hypereosinophilia and fragmentation of myofibres (*), infiltration of macrophages (m), and early regeneration (r). 20x. H&E stain.

Figure 2. Myonecrosis in the hearts of two Kunekune sows. A-20x, B-60x. H&E stain.

Figure 2. Myonecrosis in the hearts of two Kunekune sows. A-20x, B-60x. H&E stain.

 

References

1. Oropeza-Moe M, et al. Selenium deficiency associated porcine and human cardiomyopathyies. J of Trace Elements in Medicine and Biology. 2015;31:148-156.

 2. Cooper BJ, Valentine BA. Muscle and Tendon, In: Jubb, Kennedy and Palmer’s Pathology of Domestic Animals, 6th edition. Maxie, MG, ed. Elsevier, 2016; vol 1:164-249.