METABOLIC AND PATHOGENETIC ASPECTS OF LAMINITIS DEVELOPMENT IN HIGH-YIELDING COWS DURING TRANSITION PERIOD

УДК 619:617.3:616-002:636.2.034

Abstract

The traditional view of laminitis pathogenesis links its clinical manifestation exclusively with peak lactation and a high-concentrate diet in the postpartum period. This study revises these factors, proving the origin of destructive processes well before calving. The article presents the results of a study on the pathogenesis of laminitis induced by subclinical acidosis in dairy cows during the transition period. It was established that exposure to high levels of readily fermentable carbohydrates (starch at 12.78% of dry matter) and a high dietary cation-anion balance (+15.6 mEq/100g) during the early dry period provoke profound metabolic shifts. The animals’ blood biochemical profile revealed marked hypomagnesemia (magnesium levels dropping to 0.15±0.03 mmol/L), hypochloremia (chloride levels dropping to 66.50±1.50 mmol/L), enzymatic liver damage (AST levels rising to 166.70±10.80 U/L, GGT levels rising to 62.80±5.40 U/L), and a disruption of keratinization resulting from secondary zinc deficiency (a critical drop in zinc levels to 2.53±0.95 µmol/L) caused by an excess of calcium and phosphorus in the dry cow diet. This metabolic disorder led to delayed involuntary culling of cows, occurring primarily during the subsequent technological stages of early lactation and the initial phase of increasing milk yield (groups D0–D1), within 75-135 days of the pathology’s onset. The root cause was the concurrent development of hepatic dystrophy and destructive hoof lesions originating in the prenatal period, which conclusively proves the pre-calving origin of the laminitis.