Experimental reproduction of Turkey Syndrome '65 by infection with M. gallisepticum

SUMMARYIn turkey poults aged up to 28 days, a virulent S6 strain of Af. gallisepticum was recovered more frequently from more tissues for a longer time than were other strains. The virulent strain caused nervous signs and gross brain lesions in poults, and was often isolated from the brain, suggesting its neurotropism. All M. Gallisepticum strains were isolated from the synovial fluid of hocks, but swollen hocks and foot pads were seen only in poults infected with the A514 strain. It would seem, therefore, that although proclivity for joints was shown by all strains, only A514 produced grossly pathogenic effects in these young birds. All strains of Af. gallisepticum showed some proclivity for respiratory tissues. Signs, gross lesions and recoveries of mycoplasma frequently failed to correlate. Perosis was seen in only two poults; these were infected with M. gallinarum with which the condition may, or may not, be associated. Serological reactions to both the rapid serum agglutination and haemagglutination inhibition tests developed in the 3rd and 4th weeks of life in all poults infected with Af. gallisepticum strains although false positives and negatives were recorded.The main results of infection with the strains in turkey poults and in a similar study in chicks are summarised. INTRODUCTIONIn a previous paper, Power and Jordan (1976) used three strains of M. gallisepticum and one strain of M. gallinarum and showed they differed in virulence as assessed by mortality in chicks and turkey poults. This present paper describes a sequel experiment in which the same four strains of mycoplasma were used to infect turkey poults under similar conditions in order to examine effects other than mortality. Clinical signs, gross lesions and the distribution and persistence of mycoplasma in a wide variety of tissues, together with serological results, were recorded in turkey poults at specified intervals after infection.

Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 97%

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The response of turkey poults to experimental infection with strains ofM. gallisepticumof different virulence and withM. gallinarum

Varley

Jordan²

1978

“…It was subsequently ascribed to early infection with M. meleagridis (Peterson, 1968;Wise et al, 1974) and it was also reproduced experimentally withM. gallisepticum by Wannop et al (1971) and by Wise and Fuller (1975). It is interesting to note Wise and Fuller (1976) described a similar syndrome in turkeys and pheasants artificially infected with a mycoplasma designated "W8".…”

Section: Fig 11 Micrograph Of Kidney Of a Three-week-old Poult Infementioning

confidence: 92%

Mycoplasma iowaeinfection in young Turkeys

Bradbury

Ideris

1988

SUMMARYA comparison was made of the effect of five different strains of M. iowae after inoculation of one-day-old poults via the thoracic air sac and foot pad. Three strains appeared to be more virulent and more invasive than the other two, causing stunting, poor feathering and leg abnormalities including chondrodystrophy. One of these three strains was used in a second experiment in which three routes of infection were compared. Infection in ovo caused a severe generalised disease in hatched poults with high mortality. The only two birds which survived into the third week developed chondrodystrophy. One group was infected orally at one day of age and some birds developed bone and joint abnormalities but another group, infected via both the thoracic air sac and the foot pad, also at one day of age, developed a higher incidence of these, abnormalities, which included chondrodystrophy, rotated tibia, deviated toes and, in a few cases, erosion of the articular cartilage of the hock joint. Some of the control uninfected birds developed leg abnormalities but never chondrodystrophy, rotated tibia or cartilage erosion. M. iowae was most widely disseminated in tissues following in ovo infection and least after oral infection. Isolations became less frequent with age and no organisms were recovered in birds sampled at 12 weeks. In neither experiment could antibodies to M. iowae be detected by rapid agglutination.

“…Chondrodystrophy has been reported in turkeys as a consequence of mycoplasma infections; investigations of turkey syndrome 65 identified Mycoplasma meleagridis as the causative organism (Peterson, 1968;Wise et al, 1973); subsequent experimental studies have shown that infection of young birds with M. gallisepticum (Wannop et al, 1971;Wise & Fuller, 1975) or with M. iowàe (Bradbury et al, 1988) can also lead to chondrodystrophy. The skeletal changes reported in turkey syndrome 65 have been likened to a nutritional chondrodystrophy, and it is suggested that the mycoplasma is causing an impairment of the supply of nutrients to the growth plate cartilage (Wise et al, 1973).…”

Section: Chondrodystrophymentioning

confidence: 99%

Skeletal disorders in the fowl: A review

Thorp

1994

127

SUMMARYSelection pressure for production traits in modern lines of poultry has placed increasing demands on skeletal integrity. Disruption of the normal process of skeletal growth and homeostasis results in bone diseases that are manifest throughout the modern poultry industry. Bone conditions in poultry can be grouped under three headings based on the age and type of fowls affected, and are indicative of the genetic and production stresses applied to the skeleton. In broilers during growth it is primarily pathologies of the growth plate that lead to most skeletal disorders. In broiler and turkey breeding stock the progressive degeneration of the articular cartilage results in osteoarthrosis, lameness and a consequential loss of reproductive performance. In laying hens bone fragility is most frequently the result of osteoporosis. Before attempting to determine the aetiology of a skeletal disorder an accurate diagnosis must be made. Only then can short-and long-term strategies be developed for the prevention and control of skeletal disorders. Diagnosis requires gross and histological examination, and also dietary, environmental and management analyses. The pathology often reflects lesions initiated when the bird was considerably younger and analyses must extend to assessing the factors prevalent during the initiation of lesions. Current studies are furthering the understanding of the aetiopathogenesis of avian skeletal disorders. For example, structural bone loss at the onset of follicular activity before egg-laying is pivotal to the development of osteoporosis in layers and deficiencies in growth factor expression are integral to the development of tibial dyschondroplasia.