A feeding trial with naturally deoxynivalenol (DON)-contaminated oats included in feed mixtures at graded levels was conducted in growing pigs. The DON concentrations were 0, 0.7, 1.7, and 3.5 mg/kg of complete feed mixture given ad libitum to different groups. The data recorded were feed consumption, body weight gain, slaughter weight, biochemical and haematological data including serum immunoglobulin A, clinical condition and post-mortem pathology including histopathology. Significantly decreasing body weight gain throughout the experimental period, decreased slaughter weight and reduced feed utilization efficiency were observed for the group fed a diet containing 3.5 mg/kg of DON. At the same DON concentration, there were increased liver weights and decreased concentrations of serum protein and albumin, and a temporary fall in packed blood cell volume, serum calcium and serum phosphorus. For the groups fed diets containing 1.7 and 3.5 mg/kg of DON, a statistically significant, dose-related decrease in daily feed consumption was observed. No other effects on haematological, biochemical or immunological parameters were recorded. The carcass quality was not affected in any group. It was concluded that significant effects in growing pigs may be observed at a dietary DON concentration of 1.7 mg/kg, originating from naturally contaminated oats included in a diet that was otherwise adequate and contained only minor traces of other mycotoxins.

However, the results of the coagulation assay showed some overlap between groups II and III. In addition, the immunoassay appeared to be much less laborious than the coagulation assay. Therefore, the former assay is recommended in any search for similar families.The results of our family investigation confirm the findings of Egeberg (1965) that inherited antithrombin-III deficiency, giving rise to plasma levels between 50 and 600% of normal, causes thrombophilia and that the pattern of inheritance is autosomal dominant.

Hypocomplementaemic hereditary membranoproliferative glomerulonephritis (MPGN) type II is a common cause of the early loss of piglets in the Norwegian Yorkshire breed. The disease is associated with extensive complement activation due to a deficiency of factor H, a plasma protein which regulates complement. To investigate its mode of inheritance, 33 litters were bred from healthy animals associated with the disease, and a total of 385 recorded offspring were produced. The examination of renal tissue from the hypocomplementaemic piglets consistently revealed diagnostic signs of MPGN type II, including thickening of the glomerular capillary wall and proliferation of mesangial cells, dense intramembranous deposits, and massive glomerular deposits of complement component C3 and the terminal complement complex. No such glomerular lesions were detected in 20 normocomplementaemic littermates. The 88 affected piglets were present in 27 litters containing a total of 317 piglets, and there were approximately equal numbers of each sex. Retrospective immunoblot analysis and enzyme immunoassay of plasma samples from the MPGN-affected piglets and their healthy littermates revealed that the affected piglets were deficient in factor H, whereas the healthy piglets were not. It is concluded that porcine factor H deficiency is inherited as a simple autosomal recessive trait with complete penetrance, and consistently results in hypocomplementaemia and lethal membranoproliferative glomerulonephritis type II.

Some B-cell neoplasms, including hairy cell leukemia (HCL), lack expression of the adhesion molecule leukocyte function antigen-1 (LFA- 1/CD11a). Additionally, HCL cells express relatively low amounts of intercellular adhesion molecule-1 (ICAM-1/CD54) and may therefore be an inappropriate target for recognition by T cells or lymphokine-activated killer (LAK) cells. We tested whether these molecules were inducible on HCL cells and if induction would lead to enhanced susceptibility to lysis by LAK cells or cytolytic T cells. CD11a expression was induced by incubation with interferon-alpha (IFN-alpha) or interleukin-4. CD54 was induced by culturing the cells irrespectively of the addition of cytokines. Expression of CD11a and CD54 did not enhance susceptibility to either autologous or allogeneous LAK cells. However, induction of these adhesion molecules was accompanied by enhanced susceptibility to lysis by cytotoxic T lymphocyte clones. This lysis could be reversed by the addition of anti-CD11a and anti-CD54 antibodies. Finally, we monitored the expression of CD11a and CD54 on HCL cells from patients during IFN-alpha therapy. In one of four patients monitored, we observed rapid in vivo induction of CD11a and CD54 on the leukemic cells during IFN-alpha therapy. These studies provide a model for studying immunosurveillance in HCL.

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