Summary
Before the onset of bovine paresis a stage of hyperactivity and hypersensitivity was observed in clinical as well as in immunologically provoked cases. By gas chromatographic analysis of choline (Ch) in plasma and serum from four immunologically provoked cows this stage was verified to be an initial immunocholinergic hyperactivation. In the first hour after antigen challenge with 0.5 mg nematode AChE there was a very sharp rise in Ch mainly from agonist‐stimulated and phospholipase mediated phosphatidylcholine (PC) breakdown. A secondary massive influx of Ca into cells was mirrored in a 1 mmol/l depression of serum‐Ca values during the first hours. The hyperagonism mediated Ca‐translocation brought water into cells, resulting in reduced plasma volume. The generally supposed mechanism of secondary, Ca‐mediated cell damage and cell death was initiated and sometimes resulted in “Downers” with persisting paralysis. All acetylcholine (ACh)‐stimulated parts from CNS to the periphery are irregularily involved explaining the very varied clinical appearence of bovine paresis, and the influence on for instance the autonomous nerve system, adrenals and pancreas.
In the experimental group, ACh in plasma showed a sharp fall within the first hour, while there were fairly constant values of serum‐ACh in the first four hours, possibly indicating some antibody protection. When paresis was established between 15–28 hours after challenge the general anergetic state was characterised by low ACh‐levels.
Also in a larger field group ACh‐levels were significantly depressed in paretic compared to healthy cows. The unexpected finding in this group was considerably higher levels of ACh and especially Ch in serum compared to plasma. The origin of ACh and Ch had to be blood cells. Preliminary gaschromatographic analysis has confirmed ACh‐synthesis by leucocytes and an integrated immuno‐cholinergic system of great importance can be anticipated.
The general feature of bovine paresis is updated by immune‐etiological, pathophysiological, blood chemical, clinical‐experimental and nomenclature considerations.
The exact mechanism of pathogenesis is not revealed in this investigation, though many circumstances favour an anti‐Id mediated hyperagonism. Other types of investigations and above all more basic knowledge of distribution and functional character of cholinergic components on immune cells are required.