Summary Thirteen (65 per cent) of 20 horses subjected to carbohydrate overload developed Obel Grade 3 lameness within 56 h. Increases in plasma endotoxin from control levels of less than 0.1 ng/litre to values ranging from 2.4 to 81.53 ng/litre were measured in 11 (85 per cent) of 13 horses during the onset of Obel Grade 3 lameness. Obel Grade 3 lameness was associated with rises in plasma Gram‐negative endotoxin levels in 11 (92 per cent) of 12 horses. Two peak increases separated by 16 h were verified in five (45 per cent) of 11 horses that exhibited both endotoxaemia and Obel Grade 3 lameness. The first peak occurred, on average, at 32 h and (he second peak at 48 h post overload when only one peak was measured, this occurred in four horses at the average time of 24 h whereas in another three horses only a 48 h or 56 h peak was detected after carbohydrate overload.

Summary Fourteen mares and their foals were attended at parturition. After mare‐foal bonding, 8 colostrum‐deprived (CD) foals were removed from their dams, deprived of colostrum, and provided with an alternative milk source for the first 24 h of life. The mares were milked out every 2–4 h during this period to remove colostrum, after which the CD foals were returned to their mares and allowed to nurse. Six colostrum‐fed (CF) foals were allowed to suck colostrum in the normal manner. Foal serum IgG concentration was determined by single radial immunodiffusion (means, CD = 0 mg/dl; CF = 1,508 mg/dl). Accepted methods were used to minimise infections in the neonatal foals. Of the 8 CD foals, 7 demonstrated clinical signs of sepsis. Septicaemia was confirmed in 5 of the 7 septicaemic CD foals by ante‐mortem blood culture or by culture of tissue at necropsy. Organisms isolated included: Actinobacillus equuli, Escherichia coli, undifferentiated coliforms, Pseudomonas spp., and Actinomyces pyogenes. Clinically ill foals were treated with antimicrobial drugs, intravenous fluid therapy, flunixin meglumine, and anti‐endotoxin hyperimmune serum. Three septicaemic CD foals survived. Four of 7 septicaemic CD foals died or were destroyed. Post‐mortem lesions included bacterial embolic pneumonia, glomerulonephritis/nephritis, lymphoid depletion/atrophy, splenic and lymphoid necrosis, hepatitis, septic arthritis, and systemic bacterial embolism. None of the CF foals bècame septicaemic. One CF foal had foal heat diarrhoea and 1 CF foal had a serum IgG concentration of 160 mg/dl (i.e. failure of passive transfer), but both foals were otherwise normal. Despite the precautions taken to prevent infection in these foals, the severity, rapidity of disease onset, and extent of this outbreak of septicaemia in CD foals demonstrate the importance of colostral immunity in protecting neonatal foals from opportunistic and pathogenic bacterial infection.