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.

Summary Six, clinically healthy horses, of mixed age and sex, were infused via a jugular venous catheter with 100 ml of pyrogen‐free sterile saline (PFSS; 0.9% NaCl). Animals were infused with Escherichia coli O55:B5 endotoxin (total dose = 50 ng/kg bwt), 24 (LPS‐1) and 48 h (LPS‐2) after PFSS infusion. Blood was collected before, and every 15 min after, each infusion for the first 8 h and then every 2 h for the following 14 h. Clinical responses (rectal temperature, heart rate, respiration rate and blood pressure) were determined before and every 4 h after each infusion for 20 h. Geometric mean anti‐endotoxin antibody titres in serum samples, harvested just before each infusion, were unchanged over the course of the experiment. Serum tumour necrosis factor‐alpha (TNFα) activity was estimated using a cytotoxic bioassay and WEHI 164 clone 13 murine fibrosarcoma cells as targets. Mean clinical parameter values and geometric mean serum TNFα activity at given time points were compared across the 3 infusions. Both LPS‐1 and LPS‐2 resulted in elevated mean rectal temperature at 4 h after infusion. However, duration of mean rectal temperature elevation was greater (P<0.05) after LPS‐1 (through 12 h) than after LPS‐2 (through 8 h). More substantial increases in systolic and diastolic blood pressure were observed after LPS‐1 than LPS‐2 and mean systolic blood pressure after LPS‐1 was elevated at 4 h when compared to PFSS (P<0.05). Decreased systolic and diastolic blood pressures were observed at 16 h after both LPS infusions, when compared to PFSS infusion. Heart rate was increased, compared to PFSS, after both LPS‐1 (8–12 h) and LPS‐2 (4–12 h) (P<0.05). No significant elevations in mean respiratory rate were observed after either LPS‐1 or LPS‐2 when compared to PFSS. However, at 4 h post infusion, mean respiratory rate after LPS‐2 was greater (P<0.05) than that after LPS‐1. Serum TNFα activity was not detected after infusion of PFSS, but was detected after both LPS‐1 and LPS‐2. Serum TNFα activity was elevated earlier, was present in higher concentrations and persisted longer after LPS‐1 than after LPS‐2 (P<0.05). The decreased duration of fever and attenuated serum TNFα response subsequent to successive sublethal LPS challenge observed in this study support the conclusion that these horses developed early‐phase endotoxin tolerance (EPET) and, therefore, contributes to the understanding of the role of endotoxaemia in a number of clinical conditions in horses.

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