Infectious stunting syndrome of chickens in Great Britain: Field and experimental studies

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Abstract
Field cases of infectious stunting syndrome, and experimental cases produced by inoculating 1‐day‐old chicks with intestinal homogenates obtained from field cases, were studied. In the intestines of stunted 4‐ to 6‐day‐old chickens there was degeneration and necrosis of enterocytes in the crypts of Lieberkühn and an infiltration of macrophages and lymphocytes into the lamina propria. Some crypts were distended with necrotic and degenerating cells, including heterophils, and there was hypertrophy of enterocytes in the crypts and zones of maturation. The proximal jejunum was more severely affected than other sections of the small intestine, and up to 25% of the crypts were involved. Cold stress increased the severity and extent of these intestinal lesions at 5 days of age. In chickens more than 8 days of age there were a few cystic crypts lined by cuboidal to squamous epithelium, and an apparent loss of crypts. Necrosis and degeneration of epithelial cells lining pancreatric ducts and ductules were observed in 9% of field cases aged 4 to 6 days and 2% of experimentally infected chickens at 5 days of age. Pancreatic degeneration was noted in 35% of field cases aged more than 13 days of age, but in only 0.75% of experimentally infected cases at 14 days of age. Five‐day‐old experimentally infected broiler chickens had a greater intestinal length per unit live‐weight than controls, and they also had a greater intestinal weight per unit length. In field cases, the greatest intestinal length per unit live‐weight was in severely stunted chickens with pancreatic degeneration. Osteodystrophy was a frequent, but not consistent, feature in poorly grown birds in many broiler flocks over 2 weeks of age which had infectious stunting syndrome, but it was not prominent in experimental cases.