Related Experiment Video
Updated: Jul 14, 2026

Milk Collection Methods for Mice and Reeves' Muntjac Deer
Published on: July 19, 2014
Hyperketonemia and the impairment of udder defense: a review
W Suriyasathaporn1, C Heuer, E N Noordhuizen-Stassen
1Division of Farm Animal Health, Utrecht University, The Netherlands. Suriyasathaporn@hotmail.com
Abstract:
The objective of this study was to review the possible relationships between hyperketonemia and the function of phagocytes with respect to the bovine udder defense mechanism. We hypothesize that an increased incidence of clinical mastitis in high-producing cows is caused by the impairment of the udder defense mechanism during hyperketonemia. First, we review the acute phase of udder defense mechanisms after intramammary infection. The physiological changes of cows in negative energy balance are subsequently discussed. Finally, possible relationships between udder defense and physiological changes during negative energy balance, especially hyperketonemia, are reviewed. The three stages of an acute phase of udder defense are: (1) immediately eliminating invading pathogens by phagocytes, (2) releasing inflammatory substances, especially chemoattractants, and (3) migration of polymorphonuclear leukocytes into the infected udder. Leukocytes from hyperketonemia subjects show a lower capacity of the phagocytic defense mechanism. In addition, the phagocytic and bactericidal capacities of neutrophils are reduced when these cells are acting in the presence of high concentrations of ketone bodies. Lower amounts of cytokine production after bacterial infection are observed in ketotic subjects. The chemotactic capacity of blood leukocytes is impaired in leukocytes obtained from ketotic cows. Lower numbers of blood leukocytes are observed in ketotic cows. In conclusion, the impairment of the udder defense mechanism in negative energy balance cows seems related to hyperketonemia.
Related Concept Videos
Overview of Protein Metabolism
Amino acids play various roles in the body once they are absorbed into cells. They are restructured...
Inborn Errors of Metabolism
Chronic Kidney Disease II: Clinical Manifestations
Complications of Diabetes Mellitus
Diabetic Ketoacidosis l: Introduction
Diabetic Ketoacidosis ll: Pathophysiology

