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Spread Bow Leg Syndrome in Ostrich (Struthio Camelus) Chicks Aged 2-12 Weeks Ross Gordon Cooper, Khalid Mahrose, Mohammed El-Shafei

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Spread Bow Leg Syndrome in Ostrich (Struthio Camelus) Chicks Aged 2-12 Weeks Ross Gordon Cooper, Khalid Mahrose, Mohammed El-Shafei Spread bow leg syndrome in ostrich (Struthio camelus) chicks aged 2-12 weeks Ross Gordon Cooper, Khalid Mahrose, Mohammed El-Shafei To cite this version: Ross Gordon Cooper, Khalid Mahrose, Mohammed El-Shafei. Spread bow leg syndrome in ostrich (Struthio camelus) chicks aged 2-12 weeks. British Poultry Science, Taylor & Francis, 2008, 49 (01), pp.1-6. 10.1080/00071660701744257. hal-00545323 HAL Id: hal-00545323 https://hal.archives-ouvertes.fr/hal-00545323 Submitted on 10 Dec 2010 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. British Poultry Science For Peer Review Only Spread bow leg syndrome in ostrich (Struthio camelus) chicks aged 2-12 weeks Journal: British Poultry Science Manuscript ID: CBPS-2007-040.R1 Manuscript Type: Original Manuscript Date Submitted by the 26-Mar-2007 Author: Complete List of Authors: Cooper, Ross; UCE Birmingham, Physiology MAHROSE, Khalid; Zagazig University, Poultry EL-SHAFEI, Mohammed; Gamal`s Farm for Ostriches, none Keywords: Disease, Growth, Ostrich, Physiology, Welfare E-mail: [email protected] URL: http://mc.manuscriptcentral.com/cbps Page 1 of 18 British Poultry Science 1 1 2 3 4 Struthio camelus 5 Spread bow leg syndrome in ostrich ( ) chicks aged 2-12 weeks 6 7 8 9 R.G. COOPER, K.M.A. MAHROSE 1 AND M. EL-SHAFEI 2 10 11 12 Division of Physiology, UCE Birmingham, Perry Barr, Birmingham, England, 13 14 1DepartmentFor of Poultry, Peer Faculty of Agriculture, Review Zagazig University, Only Zagazig, Sharkia and 15 16 2Gamal`s Farm for Ostriches, Belbeis, Sharkia, Egypt. 17 18 19 20 21 Running title: Bow leg syndrome in ostriches 22 23 24 25 26 27 28 Correspondence to Dr Ross Cooper, Division of Physiology, UCE Birmingham, Baker 29 30 31 Building, Room 701, Franchise Street, Perry Barr, Birmingham B42 2SU, U.K. 32 33 Phone: 00441213316227. Fax: 00441213315498. E-mail: [email protected] 34 35 Date of acceptance 15 August 2007 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 E-mail: [email protected] URL: http://mc.manuscriptcentral.com/cbps British Poultry Science Page 2 of 18 2 1 2 3 4 5 Abstract. 1. The incidence of spread bow leg syndrome and associated pathology in 15 6 7 ostrich chicks aged 2, 4, 8 and 12 weeks is reported. Measurements were made of hind 8 9 limbs: femur plus tibiotarsus; tarsometatarus; phalanx I, digit III; phalanx II, digit III plus 10 11 12 phalanx III, digit III; and phalanx IV, digit III. 13 14 2. A run wasFor constructed Peer (6 x 1.7 m) andReview subdivided into 2 mOnly sections and the time taken 15 16 to traverse it was recorded. Measurements (cm) were made of the left and right footprints; 17 18 19 the number of footprints and average stride length in 0 - 2, 3 - 4 and 5 - 6 m. Speed was 20 21 calculated using distance run (m) divided by time taken (sec). 22 23 3. The number of steps was greater in bow leg chicks aged 4 and 8 weeks by comparison 24 25 26 with healthy birds. Stride length, however, was smaller in all age groups with bow leg. 27 28 All speeds in bow leg chicks were lower than those in healthy birds, except for that 29 30 31 recorded at 2m in chicks aged 2 weeks which did not differ markedly. 32 33 4. In affected birds, feathers were sparse. Icterus was present. The tarsometatarsus was 34 35 twisted, with severely inflamed joints, eroded distal ends, thickening of the cartilage and 36 37 38 the presence of fibrous material surrounding the ligaments. Muscles in the hind limb were 39 40 emaciated. 41 42 5. The syndrome compromises the ability of chicks to keep up with adults in flocks, and 43 44 45 may compromise their ability to escape predation. 46 47 48 49 INTRODUCTION 50 51 52 53 The ostrich has specialised hind legs that minimise inertia through loss of muscle mass 54 55 (Hildebrand, 1988), while lateral digits are reduced, allowing the bird to run at high speed. 56 57 58 There are a variety of skeletal diseases, however, that severely impede this movement. 59 60 E-mail: [email protected] URL: http://mc.manuscriptcentral.com/cbps Page 3 of 18 British Poultry Science 3 1 2 3 4 5 Cooper (2007) studied the effect of tibiotarsal rotation on stride in 14-month old ostriches. 6 7 Bow leg syndrome has been previously reported in ratites (Guittin, 1986; Chang et al ., 8 9 1988) and pathology is characterized by the bowing of leg bones either inward or outward. 10 11 12 Clinical signs include abnormal posture, lameness, unable to stand, trembling and 13 14 depression (ChangFor et al.Peer, 1988). Bowing Review of the tarsometatarsus Only and thinning of compact 15 16 bone and sparse density of cancellous bone were observed. Post-mortem revealed sandy 17 18 19 pellets in the duodenum, a thickened hock joint, softening of the bone and thinning of 20 21 epiphyseal lines, plus defective mineralisation of osteoid bone. The condition may result 22 23 from an improper diet especially excess vitamin supplementation and rapid early growth 24 25 26 rates. Bow leg may result from deficiencies of calcium, manganese and niacin. There is no 27 28 suitable treatment other than to improve the diet and change the feeding programme. 29 30 31 Megamin® (Healthtech Laboratories, Centurion, South Africa) has been developed and 32 33 balanced to prevent bow leg syndrome in fast growing ostrich chicks. Personal 34 35 communications with farmers in South Africa indicated that although the condition exists, 36 37 38 it is uncommon and rarely reported in that country. 39 40 41 The aim of the present study was to examine the subtle pathological consequences 42 43 44 of bow leg syndrome in ostrich chicks and its adverse effects on locomotion. The purpose 45 46 of the gait analysis was to detect morphological and functional changes associated with the 47 48 disease. 49 50 51 52 MATERIALS AND METHODS 53 54 Case history 55 56 57 58 59 60 E-mail: [email protected] URL: http://mc.manuscriptcentral.com/cbps British Poultry Science Page 4 of 18 4 1 2 3 4 5 We studied the incidence of spread bow leg syndrome (ca. 20% pa) and associated 6 7 pathology in ostrich chicks aged between 2-12 weeks on an ostrich farm 30 km north-west 8 9 of Cairo in the Belbeis Desert, Egypt (31ºE, 13ºS). The annual rainfall is variable 10 11 12 approximating 180 mm during winter mostly during the period December to January (van 13 14 Achthoven Foret al ., 2004). Peer Water is derivedReview principally from Only the Nile from irrigation 15 16 channels. The average ambient temperature throughout the study was 38ºC and the relative 17 18 19 humidity 40-50%. Chicks were allowed access to food and water ad libitum . 20 21 Feed analysis 22 23 Inductively-coupled plasma (ICP) optical emission spectrometry (Perkin-Elmer, Norwalk, 24 25 26 CT), as described by Boss and Fredeen (1997), was used to measure calcium and 27 28 phosphorus content in the feed. Gross energy was analysed by adiabatic bomb calorimetry 29 30 31 (IKA® Works, Inc. Model c5000, Wilmington, NC). ELISA kits (SciMed Laboratories 32 33 Inc., Edmonton, Alberta), using solid phase immobilisation of a monoclonal antibody 34 35 directed against a distinct antigenic determinant on the vitamin-A molecule (retinol 36 37 38 palmitate). A second anti-vitamin-A monoclonal antibody conjugated to horseradish 39 40 peroxidase (HRP) was used as the detecting antibody in the assay mixture. The test sample 41 42 was allowed to react sequentially with the two antibodies, resulting in the vitamin-A 43 44 45 molecules being sandwiched between the solid phase and enzyme-linked antibodies. After 46 47 incubation, the wells were washed with distilled water to remove all unbound labelled 48 49 antibodies. A solution of TMB was added as a substrate, resulting in the development of a 50 51 52 blue colour and the reaction was stopped by adding 0.2 M H2SO4, changing the colour to 53 54 yellow. Vitamin A concentration is directly proportional to the colour intensity of the test 55 56 57 sample. Absorbency was measured spectrophotometrically at 450 nm. The Vitamin D3 58 59 60 E-mail: [email protected] URL: http://mc.manuscriptcentral.com/cbps Page 5 of 18 British Poultry Science 5 1 2 3 4 5 ELISA test used was based on the principle of competitive enzyme immunoassay. The 6 7 assay system utilizes a fixed number of Vitamin D3 molecules immobilised on a solid 8 9 phase. These molecules compete with an unknown number of Vitamin D3 molecules 10 11 12 extracted from feed samples for a fixed number of binding sites on enzyme labelled 13 14 monoclonalFor antibodies Peerdirected against Review Vitamin D3. As theOnly number of Vitamin D3 15 16 molecules in the sample increases, the number of bound labelled antibody molecules to 17 18 19 solid phase antigen decreases due to competition.
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