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Genetic solutions to health and welfare problems in poultry caused by painful skeletal disorders

Contract nr: FAIR-CT95-0075
Project nr: 75
Project type: SC
Starting date: 01/03/1996
Duration: 36 months
Total cost: 1,528,000 EUR
EC Contribution: 764,000 EUR
Scientific Officer: Lucia PENA ALBERDI
Research topic: Animal health
Acronym: Skeletal disorder genetics

Skeletal disorders are a major cause of suffering, poor welfare and bad health in poultry throughout the EU. Each year 65 million laying hens suffer bone fractures as a result of bone fragility caused by osteoporosis (OP) and 700 million broilers suffer moderate to severe disablement from leg abnormalities, a major cause of which is tibial dyschondroplasia (TD).

The main objective of this project is to develop genetic solutions to both osteoporosis in laying hens and tibial dyschondroplasia in broilers.

The physiological bases of osteoporosis and TD are entirely different, so the project is divided into two parts. As regards TD, the objective is to identify the gene(s) causing TD. Selection using radiography has resulted in broiler lines with both high and low incidence of TD, but this method cannot eliminate TD because the system is unable to detect small lesions. A more sensitive genetic marker is required. The results of this part of the work will identify genetic strategies for eliminating TD from commercial broilers and will also contribute to other projects to map the poultry genome. The objectives of the second part of the project will be to breed lines of hens that are resistant or susceptible to OP, to determine the inheritability of bone structural and strength characteristics, and to study the benefits of improved resistance to OP. The lines of susceptible and resistant hens will form a resource for future genome analysis studies.

Current situation/results:
The project has been completed.
TD is known to be heritable and current selection procedures involve the use of an X-ray fluoroscope (Lixiscope) to detect lesions in the proximal tibia of live birds. Experimental lines of broiler chicken were selected with high and low incidences of TD and these were used as the basis of further studies to obtain information on the inheritance of TD. The occurrence of TD was determined in F1 and F2 crosses and eight backcross lines obtained from the parent lines. It was established that there was a strong maternal component to the inheritance of TD. Procedures in commercial breeding programmes have tended to concentrate selection against TD on males and male lines. This new information suggests that greater emphasis should be placed on selection in females and female lines.
It is difficult to detect small TD lesions with the Lixiscope and therefore this procedure can never eliminate TD from broiler flocks. More effective marker-based strategies for preventing TD could be developed if more was known about the genes involved in the development of TD. Molecular studies were carried out to try to identify novel candidate genes for TD and to determine the association of these and other candidate genes with the condition. TD arises as a result of a failure in differentiation of growth plate chondrocytes. Agarose gel differential display was used to study the expression of genes in chondrocytes that had been cultured in the presence and absence of ascorbic acid, an agent that stimulates differentiation. Nine gene fragments exhibiting a response to ascorbic acid treatment were cloned and sequenced. Of these, five were shown to be differentially expressed in vivo within the growth plate and were thus designated as candidate genes for TD. The segregation with TD of these genes and a further 15 possible candidate genes was followed in the backcrosses from the breeding programme. Expression of the genes was determined in late proliferative and early prehypertrophic cell fractions separated by a specially-developed method of percoll gradient centrifugation from the growth plates of normal and TD-affected birds. The expression of one gene was found to differ in many but not all cases of TD. The involvement of this gene in TD requires further study to establish whether it could form the basis for a more effective, marker-based strategy for selection against TD.
The objectives of the second part of the project were to determine whether there was a genetic basis to osteoporosis and, if so, to establish methods of breeding for resistance to osteoporosis and to determine the correlated responses. Initial studies indicated that the heritabilities of some bone morphological characteristics used to assess osteoporosis were poor, but that other characteristics associated with bone strength were highly heritable. A Bone Index was established based on measurements of tibial (TSTR) and humeral (HSTR) strength and keel radiographic density (KRD) that had a high heritability (h2 = 0.4). Three generations of divergent selection were carried out using this Bone Index, with retrospective selection of offspring based on post- mortem measurements on parent hens at end of lay. The lines diverged progressively in the selection characteristics and after the three generations of selection differed by 13% for HSTR, 25% for TSTR and 19% for KRD. There was a six-fold difference between the lines in humeral fracture incidence under commercial breeding conditions. Although selection was based on measurements taken in hens, it was found to affect bone strength in males as well, with the differences between the lines being TSTR 10%, HSTR 13% and KRD 15%.
The welfare characteristics of the lines were compared in birds from the second generation of selection housed in battery cages or in an aviary system. Fracture incidences at the time of depopulation were higher in the caged birds but bones were stronger in the high Bone Index line and fracture incidence was lower. Tibial strength of birds in the aviary was higher, but the difference between the lines was the same as in caged birds. Egg production, egg weight and food intake did not differ between the lines but shell strength was lower and incidence of cracked eggs was higher in the high Bone Index line.
Studies on the morphological characteristics of osteoporosis suggested that structural bone formation largely ceased at the onset of sexual maturity and that new bone formation seemed to be confined to medullary bone. Osteoclastic resorption of all bone types continued, however, with the net result that structural bone volumes declined throughout the laying period, resulting in osteoporosis in older birds. Comparisons between the selected lines suggested that there was little difference in structural bone mass at the onset of sexual maturity but that rate of structural bone loss was higher in the low Bone Index line during the laying period. Differences were not observed between the lines in a number of plasma characteristics, including total or ionised calcium and phosphorus. In vivo measurements of humerus and ulna radiographic densities at different ages showed that measurements at 40 weeks were highly correlated with values at 70 weeks and also with the traits used in the Bone Index.
These results show that a genetic strategy is possible to combat the problems of osteoporosis and bone fracture, although care will be needed to minimise any deleterious effects on shell quality. Although the selection was carried out in caged birds, the finding that the genetic effect on bone strength was maintained in birds housed in the aviary is important in the light of recent legislation to ban battery cages in EU. Bone fractures occur in alternative housing systems, so genetically increased bone strength will also improve welfare in these systems. It is important that measures to improve bone quality are incorporated into future selection procedures because current selection practices aimed at decreasing the age of onset of lay, and increasing persistency of lay and shell quality are likely to result in continued deterioration in bone quality of laying hens. A simplified method of selection based on metabolic criteria has not been identified yet, but application of an in vivo predictive method based on radiography of wing bones might be possible if equipment suitable for on-farm use became available.

Roslin Institute
UK-EH25 9PS Roslin - Midlothian
Tel.: +44 1315 27 42 00
Fax: +44 1314 40 04 34


    DIAS - Danish Institute of Animal Science
    Research Centre Foulum
    P.O. Box 39
    DK-8830 Tjele
    Tel.: +45 89 99 13 03
    Fax: +45 89 99 13 00

  • Karel De GREEF
    I.D. - D.L.O. - Institute for Animal Science and Health Research
    Edelhertweg 15
    P.O. Box 65
    NL-8200 AB Lelystad
    Tel.: +31 320 23 82 59
    Fax: +31 320 23 80 50

  • Dietmar FLOCK
    Lohmann Tierzucht gmbh.
    AM Seedeich 9-11
    P.O. Box 460
    D-27454 Cuxhaven
    Tel.: +49 4721 505 0114
    Fax: +49 4721 388 52
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