This study was aimed at monitoring the effect of melatonin implants on selected hematological and biochemical indices as well as on morphology changes of lungs, liver, spleen, kidneys and brain in minks. Experiments were carried out on 300 minks aged 2 years, bred under conditions of a large-herd farm and fed identical feedstuff. Melatonin implants were inserted subcutaneously to the minks in the form of granules containing 6 mg of melatonin. The control group consisted of minks from the basic herd. A better appetite and higher body weights characterized the experimental minks. Skins obtained were larger, thinner and covered with springy hair with a good sheen, yet were stragglier than in the control group. The hematological indices analyzed did not differ between the groups and were within referential values. Biochemical indices of liver and kidneys profiles were better in the experimental group. In the experimental minks, histopathological examinations demonstrated lesser intensity of disorders in brain and liver circulation, lesser intensity of degenerative lesions in liver tissues and kidneys as well as smaller infiltration of lymphocytic and plasmatic cells in lungs and liver.

The study was conducted at the "scanbrown" mink breeding farm. After weaning, the animals were divided into two groups, 50 units each (I treatment, II control). Both groups were fed a diet having an identical composition and energy level, but group I received a dietary preservative and antioxidant additives. Sodium pyrosulphite was added at a dose of 0.2-0.3% ready feed mass and Hadox antioxidant at a dose of 0.15-0.20 g per 1 kg ready feed until November. The slaughtered animals (10 units from each group) were subjected to postmortem and pathomorphological examinations. Histopathological examinations were carried out on sample specimens of the internal organs essential to the digestive and absorption processes and metabolism (stomach and duodenum, small intestine, large intestine, liver, kidneys). The feed preserved with sodium pyrosulphite and Hadox antioxidant did not show microbiological contamination at a level which would be hazardous to animal health. Supplementing the feed with a preservative and antioxidant resulted in a variation within the histopathological changes in the liver of both groups of animals. The kidneys were reported to show slight epithelium steatosis of the I order and convoluted tubules. No pathological changes were recorded in the images of the mink's alimentary tract.

This article presents the cause of hepatic encephalopathy in minks on a farm consisting of 18 000 basic pack animals and 95 000 young minks. Minks were given a meat-based diet containing 40% raw fish (cod - 10%, sprat - 30%), 40% poultry offal, 9% extruded bruised grain, 2% sugar beet pulp, 1% petals from maize, 1% soya bean oil, 5% meal from blood and feathers and turkey. The meat and fish feed were preserved with sodium pyrosulphate (2 kg/t) and with Rendox antioxidant (300 g/t) and stored at -30degreesC temperature for several weeks. Several hundred animals fell ill quite suddenly. The affected minks manifested symptoms like lack of appetite and thirst, epileptical attacks, paralysis of the back limbs, turning round along cephalocaudal axis, lacrimation, photophobia, conjunctivitis and polyuria. In a 2-5 day period lethal results followed. From among 95 000 young animals over 4000 minks died over the course of several days. Laboratory investigations like bacteriological, virusological examinations and biological test eliminated infectious diseases and alimentary intoxication. The histopathological examinations revealed the following changes: considerable histologic lesions and degeneration of brain, liver, kidneys and intestinal villuses. Those damages produced the impairment of detoxicating reactions in liver cells, limited the elimination of kidney waste products and the facilitation of absorption of toxins from the gastrointestinal tract. This caused a disease symptom complex typical for hepatic encephalopathy relating to nutrition developed after feeding raw fish rich in an enzyme called thiaminase, which is a factor inactivating vitamin B1 in feedstuff. Fresh diet supplemented with high level of vitamin B1 caused the return to health of minks within 3-5 days.