The authors report a disease in large number occurring for long period in two large scale pig holdings (mark "V" and "K") - for two years in one of the herds - based on the damage of peripheral nerves. In both herds diseases started in one-two weeks of age and did not recover. Course of the clinical signs and disease was similar in the two herds. Abnormal position of one or both hind limbs, step on the dorsal surface of flexed hoof (Figure 1) or "rabbit-like" standing because of firm flexion of tarsal joints (Figure 2) were characteristic. Later In the hind limbs of these animals purulent-suppurating inflamation developed as a result of skin lesions and secondary bacterial infection and sometimes the animal lost its limb because of the severe lesion. Pathological and histopathological lesions, however, were different in the two herds. In the herd "V" in the ischiadic nerve primary damage of nerve fibres, comparing to the control (Figure 3 and 4), vacuolar degeneration of the myelin sheath and demyelinisation (Figure 5, G and 7) and necrosis of the axon (Figure 8 and 3) developed. In the herd "K" sere-sanguineous infiltration of the peri- and epineurium (Figure 10 and 11) and perineuritis (Figure 12) were in the background of clinical signs following intramuscular treatment. In herd "V" etiology was not cleared up and in herd "K" following the change of site of day-old intramuscular treatment no new case occurred.

Over a period of almost 2 years, a progressive motor disturbance was found to occur in 20-50% of the litters of both primiparous and multiparous sows in a large pig herd of 1000 sows. The motor disturbance sometimes affected the entire litter; however, in most cases only a few piglets per litter were affected. The clinical signs appeared at 3-5 days of age and consisted of difficult movement followed by anteflexion or retroflexion of the tarsal joints or 'rabbit-like posture'. Subsequently, primarily after weaning, inflammatory and necrotic lesions developed on the paralysed limbs as a result of secondary infections of injuries. The tibial nerve and the common fibular nerve of recently affected (5- to 6-day-old) piglets showed degeneration, demyelination and necrosis of some of the nerve fibres, accompanied by restorative changes in more chronic cases. The central nervous system, bones, skeletal muscles, tendons and joints showed no lesions that could have accounted for the symptoms of motor disturbance. Aetiological investigations excluded the possibility of lead, copper and cadmium toxicity. Vitamin B2 administered orally at 1 day old proved to be ineffective. The disease did not develop in piglets of sows kept at another farm under the same management and fed a diet prepared according to an identical formula from the same ingredients as those used on the affected farm, but with no milk whey added. This raised the suspicion of triaryl phosphate (TAP) poisoning, but this was found not to be the cause of the disease. New boars had not been brought to the farm in the year preceding the onset of disease, and the disease could not be linked to a specific boar or boar line. The aetiology of the disease has remained unclear.

Clinical symptoms, patho-morphological changes and diagnostic observations have been reported in case of a poisoning caused by feeding redroot pigweed (Amaranthus retroflexus L.) in a swine stock. The mortality was 36%. A stock of 50, three months old gilts kept under closed circumstances before were moved onto a run where the fauna consisted of significant amounts of redroot pigweed, as well as smaller amounts of jimson weed (Datura stramonium) and lamb's weed (Chenopodium album). Clinical symptoms (straggering movement, flaccid paralysis of the hind legs, sternal recumbency,lying on their sides, coma) appeared first on the day 6 after driving out and the majority of pigs died within a short period. Further deaths were observed after housing again, i. e. 18 pigs died. The pathological changes were characterized by a pale discolourization of kidneys, retroperitoneal perirenal oedema, straw-yellow serous effusion in the thoracic and abdominal cavities. The histological examination revealed degeneration of tubular epithelium, necrosis and desquamation of the epithelial cells of renal tubules (Pig. 2) and precipitation of double refracting, possibly oxalate crystals in the cytoplasm by polarization microscopic examination (Pig. 3). In an experiment for diagnostic purpose, clinical symptoms could not be observed when feeding pigs of similar age only with redroot pigweed for two weeks. However severe hydronephrosis (Fig. 4) and fibrosis, as well as precipitation of oxalate crystals could be observed in the kidneys of pigs exsanguinated 10 days later.

Ionophor antibiotic (monesin, narasin, salinomycin maduramycin) poisonings were diagnosed in 9 cases. In one each cases, poisoning was caused by overdose of Dizenzin (containing monensin) and Salocin (containing salinomycin) and drug-incompatibility due to the simultaneous application of salinomycin and tiamulin. In the other cases, the cause of poisoning was suspected due to the overdose of premixes, as well as feeding premixes or feeds by swine produced for chickens. In all the cases, the clinical symptoms were characterized by motor disturbances, first of all weakness of the posterior body half and laying in more severe cases. Besides these symptoms, signs of circulatory disturbances, dyspnoea, as well as discharge of red-brown urine were also observed. The gross-pathological investigation revealed - first of all - discolouration of mass extremity muscles, sometime of the heart muscle greyish-white paleness of certain muscle fibres, as well as lung oedema were observed. The histopathological examinations revealed Zenker-type necrosis of muscle fibres in the acute stage of poisoining (Figs 1a and 1b). In subacute and chronic stages, some of the necrotic muscle fibres showed calcification and signs of reparation and regeneration (Figs 2 and 3). Ionophor antibiotics - in high amounts in most cases - were demonstrated by chemical methods in the gastric content of swine died during the acute phase of the poisoning and also in the feed samples. In case of simultaneous application of salinomycin and tiamulin their total quantities were relatively small (approx. 7.2 mg/body-mass kg/day). It was also proposed that their toxic effect was increased by the T-2 toxin contamination of feeds and/or selenium vitamin E deficiency of pigs.

On a back-yard farm the following clinical symptoms were observed in the fattening pigs: anorexia, weakness, incoordinated movement due to the weakness of the posterior body half, frequent and increased drinking-water consumption, as well as diarrhoea in certain pigs and skin haemorrhages all over the body. Pathological examination of two died and 10 emergency slaughtered pigs revealed enlargement of kidneys, varicoloured and later on diffuse, pale, greyish-brown discolouration of the cortical substance (Fig. 1). Great number of small, greyish-white compact foci of size of pin-pricks to pinhead, cysts, filled with liquid, telangiectasis and petechias were observed in the compact cortical substance. Other organs showed no alterations. Occasionally pulmonary plethora, oedema and focal pneumonia were observed. The light and electron microscopic examinations revealed focal or diffuse renal fibrosis, accompanied with parenchymal atrophy (Figs 2 and -3). Exudate, rich in fibrin accumulated in the intact renal bodies, lumen of Bowman's capsules and glomerules (Fig. 4), cystiform dilatation of the lumen of certain renal bodies, as well as sections of tubules (Fig. 5), atrophy of tubular epithelium (Fig 7), and sporadically inflammatory cellular infiltration and crystallization were observed (Figs 6 and 8). During the toxicological investigations, ochratoxin-A was demonstrated in a quantity of 0.03 mg/kg and 0,05 mg/kg in the kidneys and blood sera of four emergency slaughtered pigs, respectively.

The authors describe the course, clinical symptoms, pathologic lesions and diagnostic experiences with monenzin intoxication in a herd of fattening bulls and one of dairy cows leading to numerous death cases. In the first case the intoxication developed as a result of unique feeding 300 mg/kg monenzin per kg industrial compound feed, but in the second one due to erroneously feeding 1.65% monenzin in the feed instead of the mineral premix. The symptoms started with anorexia, food redusal, profuse diarrhoea for several days, dyspnoe and movement disorders. In the cows sporadically myoglobinuria and blood in the faeces also occurred. Early death cases were preceded by dullness and constant lying, later affected cattle succumbed suddenly to the intoxication without showing any clinical symptoms. Most death cases occured within 10 days of monezin uptake (see Table), but some losses occurred even 3 months later (mainly after parturition or forced movement). Gross- and histopathological investigation of succumbed or emergency slaughtered intoxicated cattle showed (Figures 1-6) multiplex focal degeneration of the myocard, lesions pointing to heart insufficiency (lung hyperaemia and oedema, accumulation of serous exudate in the peritoneal and abdominal cavities), acute inflammation of the abomasum and enteritis as well as centrolobular hydropic or pathologic fatty liver distrophy. The electron microscopic investigation of the affected myocard sections (Figures 7 and 8) revealed swelling and decay of the tissue structure of myofibrils, swelling of mitochondria with vacuolization and lysis of their crists. In cattle succumbed to the intoxication several weeks later, multiplex focal cicatrization of the myocard (with accumulated reparative angiofibroblast tissue on the place of decayed and resorbed myofibrils) could be observed. In the rumen content as well as also in the liver of cattle succumbed 3 to 5 days after monenzin uptake, this substance along with metabolites of it could be demonstrated. On the basis of their experiences, the authors stress the need for exact dosage of monenzin for therapeutic or nutritive purposes as well as to the risk of errors in supplying compound feeds with premixes.