Submitted to: Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/21/1997
Publication Date: N/A
Interpretive Summary: One thousand turkeys from each of 2 commercial strains were tested for their ability to mount an immune response when injected into the toe-web with a plant substance known to stimulate immune cells. One strain had a much stronger response to this test. When the turkeys were later challenged with a bacteria that causes respiratory disease, more birds from mthe high response strain lost weight, developed respiratory disease, and died than did the birds with a lower response. Turkeys that died from respiratory disease had infections in the bone and muscle similar to those which characterize turkey osteomylelitis complex. This work supports the idea that respiratory infection may be a source for the bacteria which cause bone and muscle infection in turkeys. It also appears that a very strong immune response to the infection can result in a greater chance of damage to the respiratory system which allows bacteria to enter the blood and cause bone and muscle infection.
Technical Abstract: One thousand 5-week-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 hours after toe-web inoculation with 100 ug of phytohemagglutinin-P (PHA-P). The CBH response for Strain A was higher than Strain B (P =0.00001) and ranged from m0 to 1.95 mm, with a mean of 0.66, whereas the CBH response for Strain B ranged from 0 to 1.67 mm with a mean of 0.38. At 6 weeks of age 36 birds from each of the 6 response groups were inoculated into the left thoracic air sac with 1.5 * 10**7 CFU of an early log phase broth culture of Escherichia coli. Samples of 5 or 10 birds were necropsied from each of the six groups at 7, 14, 28, and 42 days post-infection (PI). Birds were scored for air-sacculitis/pericarditis )AS) and turkey osteomyelitis complex (TOC). Overall mortality of E. Coli inoculated birds was 31%. There were no mortalities in unchallenged controls. Strain A had significantly higher week 1 mortality, marginally higher overall mortality (P + 0.1) and higher AS scores than Strain B. There were no TOC lesions detected until 7 days PI, after which all mortalities had TOC lesions in multiple sites. The differences in CBH response within each strain were unable to predict E. Coli susceptibility. However, these data suggest that air sac inoculation of E. Coli can provide a useful model for the study of TOC. The greater incidence of disease in Strain A indicates that an enhanced inflammatory response may increase susceptibility to E. Coli septicemia.