The physiological response in the mammary gland to Escherichia coli infection reflects a conflict between glucose need for milk production and immune response
Upon entry into the mammary gland, mammary pathogenic strains of Escherichia coli rapidly grow using milk as a nutrient source, in a manner highly dependent on the expression of the ferric-dicitrate system by these bacteria. Intra-mammary challenge with distinct mammary pathogenic E. coli (MPEC) strains result in development of clinical acute mastitis, with peak bacterial counts in milk at 16-24 h post-challenged and profound immune changes found in the milk. The main biochemical changes measured in milk were partially in accord with lipopolysaccharide-induced mastitis, with increased glucose-6-phosphate and lactate dehydrogenase activity or prolonged lactate dehydrogenase, and Glu6P/Glu alterations. Changes also reflect physiological responses to inflammation in the mammary gland, as in the balance between aerobic and anaerobic metabolism (citrate to lactate ratios). Some alterations measured in milk resolved with days after challenge but other remained for above one month, regardless of bacterial clearance. The results suggest that E. coli mastitits can be divided into two stages: an acute, clinical phase, as an immediate response to bacterial infection in the mammary gland and a chronic phase, independent of bacteria clearance, and in response to the tissue damage caused in the first phase.