Lifespan and Causes of Death in the Irish Wolfhound - Vetsuisse ...

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Fig. 3.2: Numbers of dogs of different ages at first seizure, reproduced from Casal, Munuve et al. (2006). X: age in months; Y: number of dogs. Significant differences (P0.5 suggests the presence of a major gene. However, a segregation ratio
have an independent mode of inheritance. Given that 55 out of 56 affected females were born to normal sires, an X-linked recessive inheritance is not likely, although the increased risk for males would still suggest such a model. It was concluded that epilepsy in Irish Wolfhounds is highly heritable, but genetically complex. The suggested inheritance model for all affected dogs was an incompletely penetrant recessive trait with a sex predilection for older males (Casal, Munuve et al. 2006). The authors of the quoted study chose not to provide practical breeding suggestions to control epilepsy in Irish Wolfhounds, but stress the need for the development of a genetic test. Other studies on diseases with complex modes of inheritance suggest that such diseases can be successfully addressed through estimated breeding values as long as no DNA-based testing is available (van Hagen, Janss et al. 2004). Currently, a privately funded charity is offering a risk estimation service to Wolfhound breeders over the internet (www.irishwolfhoundstudy.com). 3.9 Osteochondrosis (OC) Osteochondrosis is an orthopaedic problem that is commonly found in growing dogs. While there are no studies dealing with the condition in Irish Wolfhounds specifically, the breed is fast-growing and thus at a higher risk to develop the disease than the average dog population (Dorn 2002; Schwarz and Shires 2004 a). 3.9.1 Description OC can manifest itself in several forms, which can generally be divided into joint and growth plate problems. It is characterised by problems in the enchondral ossification process, leading to an excessive retention of cartilage that can lead to further complications (Schwarz and Shires 2004 a). 3.9.1.1 Pathophysiology Chondrocytes of the immature articular joint and/or growth plate cartilage fail to differentiate normally, which interferes with the normal process of enchondral ossification during skeletal growing. Since the cartilage continues to grow without being replaced by bone, this leads to regions with excessively thick cartilage, which is less resistant to mechanical stress than bone. Since joint cartilage nutrition is maintained through synovial diffusion, a thickening of joint cartilage results in an impaired metabolism which itself leads to degeneration and necrosis of the poorly supplied cells. This causes further weakening of the cartilage and may progress to the formation of a free cartilage flap inside the joint (Osteochondritis dissecans – OCD). Retention of cartilage in growth plates does not usually cause necrosis, but may result in asymmetric growth (Schwarz and Shires 2004 a). Some authors hypothesise that this process is also involved in the development of certain variants of elbow dysplasia (ED), which are summarised under "short radius" or "short ulna" syndrome and subsequent fracture of the anconeal or coronoid processes (Schawalder 1997). 41
Page 1 and 2: Aus der Abteilung Tierhaltung und T
Page 3 and 4: Omnia mors poscit - lex est, non po
Page 5 and 6: Table of Contents Acknowledgements
Page 7 and 8: 1 Abstract/Summary This study inves
Page 9 and 10: 1.2.3 Own Data A worldwide pedigree
Page 11 and 12: Due to the frequent bottlenecks dur
Page 13 and 14: 2 Introduction "It is impossible to
Page 15 and 16: 3 Literature Review Several disease
Page 17 and 18: previous results (Comfort 1960). No
Page 19 and 20: the average ages were significantly
Page 21 and 22: 3.2 Intrahepatic Portosystemic Shun
Page 23 and 24: Conservative therapy is also indica
Page 25 and 26: mitochondrial hyperplasia, disrupti
Page 27 and 28: there are marked individual differe
Page 29 and 30: 3.3.2 Epizootology Numbers publishe
Page 31 and 32: 2002). On the molecular level, the
Page 33 and 34: 3.4.2 Epizootology In past studies
Page 35 and 36: 3.5.1.3 Diagnosis The history and c
Page 37 and 38: 3.5.2 Epizootology A prospective st
Page 39 and 40: Differential diagnoses include recu
Page 41 and 42: 3.7.1.3 Diagnosis The definite diag
Page 43 and 44: Furthermore, the Utrecht cases also
Page 45: Figure 3.1: Survival times after fi
Page 49 and 50: 3.9.1.5 Prognosis Prognosis for OCD
Page 51 and 52: CU/dl). Of these with low values, 2
Page 53 and 54: 3.12 Miscellaneous 3.12.1 Odds Rati
Page 55 and 56: The disease is clinically character
Page 57 and 58: It is interesting to notice that ev
Page 59 and 60: 4.2.2 The SAS Program Package Stati
Page 61 and 62: 5 Results of Past Studies Revisited
Page 63 and 64: 5.1.4 Causes of Death 5.1.4.1 Influ
Page 65 and 66: 5.2 Analysis of Murphy (1991) ANOVA
Page 67 and 68: 5.2.1.3 Gender Effects As mentioned
Page 69 and 70: 5.2.2.3 Gender Effects No significa
Page 71 and 72: 6.1.2 Inbreeding Four inbreeding co
Page 73 and 74: 6.1.3 Geographical Origin Countries
Page 75 and 76: 6.2.1 Data of Living Dogs Ages at w
Page 77 and 78: Coefficient R 2 p F Coefficient R 2
Page 79 and 80: Fig. 6.8: Lifespan (GD) of direct p
Page 81 and 82: UC Excluded - Birth Cohorts Merged
Page 83 and 84: Fig. 6.10: 10-Generation Wright's I
Page 85 and 86: The individual and cumulative contr
Page 87 and 88: 6.4 Ancestor Analyses of Diseases P
Page 89 and 90: 6.4.2 Osteogenic Sarcoma 6.4.2.1 Re
Page 91 and 92: 6.4.4 Portosystemic Shunt 6.4.4.1 R
Page 93 and 94: 6.4.5.2 Dog 6844 Given that dog 684
Page 95 and 96: 6.4.5.4 Dog 6636 Dog 6636 (born 195
Page 97 and 98:
7 Discussion 7.1 Lifespan 7.1.1 Lif
Page 99 and 100:
findings of the study at hand are i
Page 101 and 102:
degree. The fact that average lifes
Page 103 and 104:
first-generation progeny. The broad
Page 105 and 106:
In this model, the degree of purgin
Page 107 and 108:
7.2.2.5 Present Study No significan
Page 109 and 110:
It is interesting to consider what
Page 111 and 112:
7.3 Ethical Considerations 7.3.1 In
Page 113 and 114:
7.3.2 Decreased Lifespan The ethica
Page 115 and 116:
(Papazoglou, Monnet et al. 2002). G
Page 117 and 118:
While there are currently no heredi
Page 119 and 120:
7.5 Future Research Prospects 7.5.1
Page 121 and 122:
8 References Ackerman, L. (1999). T
Page 123 and 124:
Deeb, B. and N. Wolf (1994). "Study
Page 125 and 126:
Kealy, R. D., D. F. Lawler, et al.
Page 127 and 128:
Rothuizen, J. (2002). Molecular Gen
Page 129 and 130:
Walker, H. (1896). Der Irish Wolfho
Page 131:
ID DR DA DR10 DA10 GR GA GR10 GA10
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