An investigation of moose calves from females with Moose Wasting Syndrome (Alces alces L.)

Abstract: Moose Wasting Syndrome in moose (Alces alces) was first discovered in Sweden in the 1980’s. It was characterised by atrophied lymphoid organs, ulcers and erosions of the mucus membranes of the digestive tract, e.g. glossitis, gingivitis, esophagitis, rumenitis and abomasitis. Clinical signs seen in affected moose were diarrhoea, dehydration, alopecia, weakness, anorexia, impaired vision, emaciation and central nervous system disturbances. The etiology of the wasting syndrome is still unknown. There are many hypothesis as to the cause of the disease; however, none have been definitively proven. In this project, an experimental study of seven moose calves born by mothers suspected of being affected with MWS is compiled and reviewed. The calves were born between May 15 and June 15, 1992. They were captured in the south of Sweden where MWS was known to occur. The calves were stabled in a specific-pathogen-free surrounding as laboratory animals between 7 to 11 months and any diseases contracted by the calves were treated. They were given controlled deer milk formula and feed with known ingredients. Extra minerals and vitamins were given at a regular basis and they had constant access to saltstones and water. The calves were observed daily to detect any abnormalities. Investigations for blood biochemistry, hematology, gross pathology and histopahology were done. Results show that the calves developed some clinical, gross pathological and histopathological findings similar to those found in MWS affected moose. Some of the clinical signs shown by the calves were diarrhoea, alopecia, inappetence and lesions in the mouth. No pronounced neurological disturbances were shown by the calves. Gross pathology showed enlarged and congested liver and spleen, hemorrhages in the adrenal cortex, lung consolidation, hyperemic trachea, discolouration of the renal cortex and medulla and lesions in the mouth, myocardium, lungs and cerebral meninges. In the intestinal tract congestion, discolourations, bleedings, flaccidity of the intestinal walls and thin Peyer’s patches were seen. Histopathology revealed hyperplasia of lymph nodes, alveolar emphysema, mononuclear cell infiltration in the myocardium and mucosa of some areas of the intestinal tract among other findings. The brain did not display any histopathological lesions indicating classical spongiform encephalopathy. Hematology and biochemistry showed increases and decreases in total leukocyte, lymhocyte, neutrophil and eosinophil count but no uniform changes were seen. In conclusion, there were indications that MWS was contracted by the calves via their mother’s directly or transplacentally, suggesting an infectious cause of MWS. It is possible that other, more severe MWS characteristic clinical and gross pathological lesions would have appeared if the calves had been stabled for a longer time and been investigated when the disease had progressed further. No evidence of classic prion disease (BSE) was shown in this study, however, with the long incubation period for prion diseases like CWD, as Benestad & Telling (2018) declare, it is possible that more pronounced lesions would have developed in the moose calves, given more time. Future studies are needed, using up to date technology and methods to determine if prions is the cause of MWS.