In five experiments, each consisting of four or six groups with seven or 14 brown laying hens per group, birds were inoculated with an Escherichia coli strain, isolated from a layer with the E. coli peritonitis syndrome (EPS) by different routes between 23 and 33 weeks of age. Aerosol-exposed hens inhaled 10 5.1 to 10 6.2 colony-forming units per hen; hens inoculated by other routes received 10 7.6 to 10 9.1 colony-forming units per hen. In one experiment, one-half of the birds of each group were injected intraperitoneally with sterile egg yolk simultaneously with E. coli. Dead and surviving birds were necropsied and bacteriological examination of the bone marrow was performed. The percentage of birds with EPS that died was 89 (159/179). Nearly all dead birds showed septicaemia (155/159 097%), while most had septicaemia and peritonitis (126/159 079%). Surviving hens with EPS (20/179 011%) showed chronic peritonitis and inactive ovaries. Taking all experiments together, exposure of hens by the intravenous, intratracheal and intraperitoneal routes induced EPS in 84% (41/49), 80% (55/69) and 76% (16/21), respectively, while aerosol and intravaginal exposure resulted in EPS percentages of 57% (32/56) and 49% (28/57), respectively. Except for orally inoculated groups (7/56 013% EPS), in all other groups the EPS rates differed significantly (P B0.01) from those of the placebo-exposed groups (0/42). Neither the age of hens nor the presence of free yolk in the abdomen influenced the EPS rate. The results of the present study are suggestive of the respiratory and vaginal origin of EPS in the field.

The effect of sodium lactate and sodium lactate combined with sodium chloride (NaCl) on toxin production by proteolytic strains of Clostridium botulinum was determined in peptone-yeast extract medium, pH 6.1. Both inhibitors were also tested for their effect on thermal destruction of spores. Additionally, the effect of sodium lactate on germination of spores was assessed. The inhibitory effect of sodium lactate was dependent on the applied incubation temperature. The best inhibition was obtained at low temperatures. Toxin production was delayed at 15 and 20°C by sodium lactate concentrations of 2 and 2.5%, respectively. Complete inhibition of toxin production at 15, 20 and 30°C occurred at concentrations of 3, 4 and >4%, respectively. Further, sodium lactate inhibited germination of the C. botulinum spores, which may partially explain the inhibitory effect of sodium lactate on growth and toxin formation. The inhibitory effect of NaCl at concentrations resulting in an identical water activity value as obtained by sodium lactate was negligible, indicating that the inhibitory effect of sodium lactate was not caused by decreasing water activity. No clear synergistic effect of sodium lactate (1.5 or 2.5%) and NaCl (2.1%) was observed.

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