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 105.1 to 106.2 colony-forming units per hen; hens inoculated by other routes received 107.6 to 109.1 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 = 97%), while
most had septicaemia and peritonitis (126/159 = 79%). Surviving hens with EPS (20/179 = 11%) 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 = 13% EPS), in all other groups the EPS rates differed significantly (P <0.01) 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.
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Document Type: Research Article
GD - Animal Health Service, Arnsbergstraat 77418,EZ,Deventer, the Netherlands
Department of Farm Animal Health, Faculty of Veterinary Medicine,Utrecht University, Yalelaan 73584,CL,Utrecht, the Netherlands
Publication date: April 1, 2013
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