VARIATION IN TOE-WEB RESPONSE OF TURKEY POULTS TO PHYTOHEMAGGLUTININ-P AND THEIR RESISTANCE TO ESCHERICHIA-COLI CHALLENGE

Citation
Gr. Bayyari et al., VARIATION IN TOE-WEB RESPONSE OF TURKEY POULTS TO PHYTOHEMAGGLUTININ-P AND THEIR RESISTANCE TO ESCHERICHIA-COLI CHALLENGE, Poultry science, 76(6), 1997, pp. 791-797
Citations number
38
Categorie Soggetti
Agriculture Dairy & AnumalScience
Journal title
ISSN journal
00325791
Volume
76
Issue
6
Year of publication
1997
Pages
791 - 797
Database
ISI
SICI code
0032-5791(1997)76:6<791:VITROT>2.0.ZU;2-I
Abstract
One thousand 5-wk-old male turkeys from each of two commercial strains (A and B) were grouped into low, medium, and high responders based on the cutaneous basophil hypersensitivity (CBH) response obtained 24 h after toe-web inoculation with 100 mu g of phytohemagglutinin-P (PHA-P ). The CBH response for Strain A was higher than strain B (P = 0.00001 ) and ranged from 0 to 1.95 mm, with a mean of 0.66, whereas the CBH r esponse for Strain B ranged from 0 to 1.67 mm with a mean of 0.38. At 6 wk of age, 36 birds from each of the six response groups were inocul ated into the left thoracic air sac with 1.5 x 10(7) cfu of an early l og phase broth culture of Escherichia coli. Samples of 5 or 10 birds w ere necropsied from each of the six groups at 7, 14, 28, and 42 d post infection (PI). Birds were scored for air-sacculitis/pericarditis (AS) and turkey osteomyelitis complex (TOC). Overall mortality of birds in oculated with E. coli was 31%. There were no mortalities in unchalleng ed controls. Strain A had significantly higher Week 1 mortality, margi nally higher overall mortality (P = 0.1), and higher AS scores than St rain B. There were no TOC lesions detected until 7 d PI, after which a ll mortalities had TOC lesions in multiple sites. The differences in C BH response within each strain were not clearly correlated to E. coli susceptibility. However, these data suggest that air sac inoculation o f E. coli can provide a useful model for the study of TOC. The greater incidence of disease in Strain A indicates that an enhanced inflammat ory response may increase susceptibility to E. coli septicemia.