Thiamine deficiency encephalopathy in foxes and mink.

Abstract

Thiamine deficiency encephalopathy in f o x e ~ ' . ~ . ~ and mink7.10 was originally described as Chastek paralysis (CP). We have experienced this disorder in Hokkaido, the first occurrence was in Japan. It occurred during a parturient period from April to July 1983 on a ranch where approximately 170 male and 850 female adult foxes, and 170 male and 1,000 female adult mink were raised. Initial clinical signs of anorexia, weakness, and diarrhea were followed by recumbency, tonic convulsions, spastic paralysis, and death after a period of 2 to 3 days. Approximately 500 dams and 1,000 cubs aged 3 to 14 days died in the fox group, and several hundred male and female adults as well as 2,500 kits aged 3 to 14 days died in the mink group. Both groups received the same feed from February consisting of 60% raw fish, 12% grain, 7% offal from slaughter houses, 6% boiled porcine blood, 6% chicken offal, 6% porcine or bovine liver, and 3% vegetables, supplemented with vitamins A, D, E, and B complex. Nineteen fox (1 3 dams and 6 d b s ) and seven mink (3 male and 3 female adults and 1 kit) were examined pathologically. Specimens from major organs, brain, and spinal cord were fixed in 10% formalin. The brain was cut coronally at 3 to 4 mm intervals. Paraffin sections were stained with hematoxylin and eosin (HE). Selected sections were stained by Kluver-Barrera (KB), phosphotungstic acid hematoxylin (PTAH), and Masson's trichrome methods. Thiamine content in the feed was determined by the thiochrome m e t h ~ d , ~ and the thiaminase activity was measured by the method described elsewhere6 in the frozen raw meat and organs of bullhead (Myoxocephalus stelleri Tilesius) and flounder (Lirnanda punctatissirna) used for feed. These measurements were done at Japan Food Research Laboratory, Tokyo, Japan. Gross lesions were particularly striking in fox dams and adult male mink. Bilaterally symmetrical hemorrhages were in the piriform, temporal, parietal, and occipital lobes of the cerebrum of fox dams (Case Nos. 1, 2, 4-8, 11, 12). Hemorrhagic necrosis was recognized as yellowish-brown lesions on the cut surface of transverse sections of the formalin-fixed brain (Fig. 1). The right cardiac ventricles of all the fox dams were dilated and flabby, and the myocardium was cloudy. The livers of all the adult animals were pale yellowish-brown. No gross lesions were detected in the brain and heart of fox cubs, and adult female and newborn mink. Microscopic lesions in the fox brains were located in the suprasylvian, ectosylvian, and suprasplenial cortex, brainstem nuclei, and cerebellar lingula and nodulus (Fig. 2). Acute changes such as ischemic changes of nerve cells, perineuronal edema, and perivascular hemorrhages were seen in the cerebral cortex, nuclei of inferior colliculi, and cerebellar lingula and nodulus. In addition, homogenizing cell changes were seen in the cerebral nerve cells and Purkinje cells. Cerebellar granule cells were hyperchromatic in the affected area of vermis. In subacute lesions, there was hypertrophy and hyperplasia of capillaries, astrocytes with swollen cytoplasm, and a few fat granule cells. Malacic foci were usually located in the brainstem nuclei, e.g., the nuclei of the inferior colliculi and vestibular nuclei (Fig. 3), and in the cerebellar lingula and nodulus. Demyelination and accumulation of numerous fat granule cells were conspicuous. Adventitial cells of small blood vessels were occasionally hypertrophic. Two adult male mink had mild early ischemic changes, demyelination, and perivascular hemorrhages in the nuclei