Experimental Reproduction of Turkey Syndrome ’65 with Mycoplasma meleagridis

Wise, D.R.; Fuller, M.K.; Thornton, G.A.

doi:10.1016/s0034-5288(18)33689-0

Cited by 22 publications

(3 citation statements)

References 4 publications

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“…Bone deformities and swollen joints have also resulted from experimental infection of poultry with M. iozvae. Infected turkeys developed chondrodystrophy (Bradbury et al, 1988) and the condition was indistinguishable from TS-65 which was associated with M. meleagridis infection acquired in ovo or at a very early age (Wise et al, 1974). In the field, Trampel & Goll (1994) reported isolation of M. iowae from several tissues, including hock joints, of a flock of 17-day-old commercial poults with leg weakness and deformities including chondrodystrophy.…”

Section: Discussionmentioning

confidence: 99%

“…Chondrodystrophy, a failure of growth plate cartilage proliferation resulting in shortening of the long bones (Jordan & Pattison, 1996), has been reported in turkeys as a consequence of mycoplasma infections. Investigations of turkey syndrome-65 (TS-65) identified Mycoplasma meleagridis as the causative organism (Wise, et al, 1913;Peterson, 1968); subsequent experimental studies have shown that infection of young birds with Mycoplasma gallisepticum (MG) (Wise et al, 1974;Wannop et al, 1971) or with Mycoplasma iowae (Bradbury et al, 1988) can also lead to chondrodystrophy.…”

Section: Introductionmentioning

confidence: 99%

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The development of lameness and bone deformity in the broiler following experimental infection withMycoplasma gallisepticumorMycoplasma synoviae

et al. 1997

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Groups of eight 7-day-old Mycoplasma-free broiler chicks were inoculated with one of two strains of M. gallisepticum (MG/S6, MG/B31/85) or one of two strains of M. synoviae (MS/B31/88 and MS/B94/91) into the left hock joint. Controls were similarly inoculated with sterile mycoplasma broth. The birds were assessed at 2, 3, 4 and 5 weeks of age (1, 2, 3 and 4 weeks post-injection) for lameness and joint and limb lesions. At 5 weeks of age they were killed and examined for gross skeletal abnormalities and microscopic lesions of both hock joints. The in-contact controls showed no joint swelling or lameness. The mycoplasma did not apparently spread to cause gross pathology in the joints of in-contact control birds, or to other joints in a bird injected with mycoplasma. Each mycoplasma strain caused specific pathologies manifest as varying degrees of lameness, left hock joint swelling, bone deformity and differences in the severity of articular cartilage and chondrodystrophic growth plate pathology. Shortening and bowing of the right tibiotarsus in the birds injected with mycoplasma indicated unilateral increased limb loading contributing to bone deformity. Chondrodystrophy seen with three mycoplasmal strains may have contributed to bone deformity in these birds. Lameness appeared to be a consequence of either joint swelling and/or bone deformity resulting in mechanical dysfunction. The role of joint pain in the lameness was not determined.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The development of lameness and bone deformity in the broiler following experimental infection withMycoplasma gallisepticumorMycoplasma synoviae

et al. 1997

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“…Most of the leg abnormalities seen in the industry today are not due to a simple nutrient deficiency (Ferguson et al, 1978;Ogura, 1977) nor does any one particular environment continually produce similar symptoms (Pierson et al, 1981). That the problem must be complex in nature or the result of induced nutrient deficiencies has been suggested by a number of workers (Riddell, 1976;Summers, 1980;Wise et al, 1974).…”

Section: Introductionmentioning

confidence: 99%

Influence of Vitamin Deficiency and Level of Dietary Protein on the Incidence of Leg Problems in Broiler Chicks

et al. 1984

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Diets containing either 22 or 30% protein were supplemented with a vitamin mix where one of 11 added vitamins were singly eliminated from the mix. Male, day-old broilers were fed these diets to 3 weeks of age, and weight gains, feed utilization, and leg problems were recorded. In general, the higher protein diet did not result in a greater incidence of leg problems; however, it did alter performance of several of the vitamin-deficient diets as compared to the lower protein diet. Of the 11 vitamins studied only nonsupplementation of riboflavin markedly reduced weight gain and feed utilization during the 3-week feeding period. However, deletions of vitamin D3 and niacin also resulted in reduced performance. Riboflavin deficiency resulted in paralysis in a high percentage of the birds while the niacin-deficient diet gave a high percentage of birds with deformed legs and problems of mobility. The results demonstrate that a high incidence of leg problems may be present in a flock with little or no signs of reduced gain or feed utilization. The data suggest that under practical conditions the elimination of a particular vitamin from a diet for a short period of time would probably have a negligible effect on performance.

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