The role of dietary copper in enhancing resistance to Escherichia coli mastitis was investigated in first-lactation heifers. Twenty-three primigravid Holstein heifers were maintained on a basal (6.5 ppm copper; -Cu) diet or a diet supplemented (20 ppm) with copper sulfate (+Cu) beginning 60 d prepartum through 42 d of lactation. Liver biopsies and blood samples were taken for liver and blood minerals and plasma ceruloplasmin. Milk samples were taken weekly postpartum for bacteriology. The overall mean liver Cu concentration was about threefold higher, and the overall mean plasma Cu concentration was greater in the +Cu group than the -Cu group. At 34 d of lactation, one pathogen-free quarter per animal was infused with 22 cfu of Escherichia coli strain 727. Plasma Cu was greater at -24, 0, 18, 24, 36, 96, 192, and 240 h relative to infusion for +Cu animals. Plasma Zn concentration was higher at 24 h for the +Cu group. Milk bacterial count (log10 cfu/ml) was lower at 12, 18, and 48 h for the +Cu group. Somatic cell count (log10/ml) was lower at 18 h in +Cu animals. Clinical score at 24 h was lower for +Cu cows, while at 144 h, clinical score was lower for -Cu cows. Rectal temperature was lower at 18 h for the +Cu group. Plasma ceruloplasmin and Fe, dry matter intake and milk production did not differ. Copper supplementation reduced the clinical response during experimental E. coli mastitis, but duration was unchanged.
The susceptibility of uninfected or Staphylococcus chromogenes-infected quarters to challenge with Staphylococcus aureus was measured. Seventeen S. chromogenes-infected quarters were challenged by infusion of S. aureus into the teat sinus; 47% (8 of 17) became infected and all 18 uninfected quarters challenged similarly with S. aureus became infected. No differences in daily milk yield were seen between uninfected quarters and S. chromogenes-infected quarters prior to S. aureus infusion. Postinfusion, milk yield for S. aureus-infected, S. chromogenes-infected, and S. chromogenes- and S. aureus-infected quarters differed. Somatic cell counts were elevated in S. chromogenes-infected quarters compared with uninfected quarters prior to S. aureus infusion. Somatic cell counts were not different between S. aureus- and S. chromogenes- and S. aureus-infected quarters postinfusion, but were different for S. chromogenes-infected quarters. Chloride concentrations in S. chromogenes- and S. aureus-infected quarters were different from either S. aureus-infected or S. chromogenes-infected quarters. Staphylococcus aureus colony forming units in quarters with preexisting S. chromogenes infections were lower than S. aureus colony-forming units in previously uninfected quarters. Possible protective mechanisms induced by S. chromogenes against superinfection by S. aureus are discussed.
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