Inherited goitre in sheep

Inherited goitre in a flock of sheep possessing a proportion of Polled Dorset blood is reported and discussed. The cases en-countered were not induced by a simple deficiency of iodine, or the presence of goitrogenic substances in their feed. Further work is recommended on the nature of the defect and its method of inheritance.     

Inherited chondrodysplasia in Texel sheep

CASE HISTORY: A skeletal disease characterised by dwarfism, limb deformity and sometimes sudden death occurred over a period of 5 years in lambs born on a commercial sheep farm in Southland. The disease showed variable expression and occurred in crossbred sheep. A genetic aetiology was supported by the birth of affected lambs over two seasons in a flock of putative carrier and affected sheep transported to Massey University. CLINICAL FINDINGS: Affected lambs appeared normal at birth but showed evidence of dwarfism, wide-based stance and exercise intolerance as early as 1 week of age. Most died within the first 3 months of life, often after developing bilateral varus deformity of the forelimbs. Some severely-affected lambs died suddenly of respiratory embarrassment, probably due to tracheal collapse. Mildly-affected individuals had a short, blocky stature and some survived to breeding age. PATHOLOGICAL FINDINGS: Gross and microscopic lesions of variable severity were present in the tracheal, articular, epiphyseal and physeal cartilages. In severe cases, articular cartilage in major joints was eroded from weight-bearing surfaces. The trachea was flaccid, abnormally kinked, and had thickened cartilaginous rings and a narrow lumen. Affected sheep that survived to breeding age eventually developed severe degenerative joint disease. Histologically, chondrocytes were disorganised, surrounded by concentric rings of abnormal fibrillar material, and the matrix often contained focal to coalescing areas of chondrolysis. DIAGNOSIS: Inherited chondrodysplasia of Texel sheep. CLINICAL RELEVANCE AND CONCLUSIONS: This chondrodysplasia differs from those previously described in sheep and is considered to be a newly-recognised, recessively-inherited genetic disease of the Texel breed. A defect in the synthesis of glycosaminoglycans in cartilage matrix is suspected. This disease of sheep may provide a suitable model for studying various forms of therapy for human chondrodysplasias.     

Inherited chondrodysplasia in Texel sheep

CASE HISTORY: A skeletal disease characterised by dwarfism, limb deformity and sometimes sudden death occurred over a period of 5 years in lambs born on a commercial sheep farm in Southland. The disease showed variable expression and occurred in crossbred sheep. A genetic aetiology was supported by the birth of affected lambs over two seasons in a flock of putative carrier and affected sheep transported to Massey University.

CLINICAL FINDINGS: Affected lambs appeared normal at birth but showed evidence of dwarfism, wide-based stance and exercise intolerance as early as 1 week of age. Most died within the first 3 months of life, often after developing bilateral varus deformity of the forelimbs. Some severely-affected lambs died suddenly of respiratory embarrassment, probably due to tracheal collapse. Mildly-affected individuals had a short, blocky stature and some survived to breeding age.

PATHOLOGICAL FINDINGS: Gross and microscopic lesions of variable severity were present in the tracheal, articular, epiphyseal and physeal cartilages. In severe cases, articular cartilage in major joints was eroded from weight-bearing surfaces. The trachea was flaccid, abnormally kinked, and had thickened cartilaginous rings and a narrow lumen. Affected sheep that survived to breeding age eventually developed severe degenerative joint disease. Histologically, chondrocytes were disorganised, surrounded by concentric rings of abnormal fibrillar material, and the matrix often contained focal to coalescing areas of chondrolysis.

DIAGNOSIS: Inherited chondrodysplasia of Texel sheep.

CLINICAL RELEVANCE AND CONCLUSIONS: This chondrodysplasia differs from those previously described in sheep and is considered to be a newly-recognised, recessively-inherited genetic disease of the Texel breed. A defect in the synthesis of glycosaminoglycans in cartilage matrix is suspected. This disease of sheep may provide a suitable model for studying various forms of therapy for human chondrodysplasias.     

Inherited abnormalities of skeletal development in sheep

Inherited diseases of the skeleton are reported less often in sheep than in most other domestic animal species but are likely to occur more frequently than the veterinary literature would suggest. Although most are lethal or semi-lethal, the gene frequency for some of these diseases has reached surprisingly high levels in defined populations, presumably due either to the founder effect or the presence of a selective advantage of heterozygous individuals. This article reviews the clinical characteristics, pathology, mode of inheritance and molecular basis of skeletal diseases known to have a genetic aetiology in sheep. Inherited skeletal diseases of sheep are potential models for studying the treatment of similar diseases in humans.     

An outbreak of severe iodine-deficiency goitre in a sheep flock in north-east Victoria

Background Several outbreaks of goitre, considered to be related to iodine deficiency, occurred in sheep flocks throughout Victoria in 2010. Objective We describe one outbreak in Merino–Border Leicester‐cross ewes and their lambs in north‐east Victoria that appeared to be associated with increased rainfall and pasture growth, particularly during the preceding summer and autumn. Results The outbreak was characterised by a four‐fold increase in neonatal lamb deaths and goitre, alopecia and poor skeletal development in the lambs. Most cases occurred in lambs born to 2‐year‐old crossbred ewes that had grazed long, lush perennial pastures throughout their entire pregnancy, whereas few cases occurred in mature crossbred or Merino ewes that had grazed shorter, annual pastures on hill country for 3 weeks in late pregnancy but were otherwise managed similarly. Conclusion Existing recommendations for south‐eastern Australia are that only spring‐lambing ewes in iodine‐deficient areas require iodine supplementation to prevent goitre in years with high autumn–winter rainfall. Aspects of this outbreak suggest that ewes lambing at other times of the year and grazing abundant pasture for prolonged periods may also require supplementation to prevent goitre, even if autumn–winter rainfall does not exceed previously established thresholds.     

Massive goitre (struma parenchymatosa) in geese.

In a goose flock consisting of 2300 birds of 6 months of age severe goitre was diagnosed. To the best of our knowledge this is the first report of naturally occurring goitre in geese, which is not related to the feeding of rapeseed meal. The major pathological findings included retarded growth and plumage development, significantly (300%) increased relative thyroid weight, fat accumulation in the mesenteric and abdominal region, and lipid infiltration of liver and kidney cells. Subsequent hormone analysis showed undetectable thyroxine (T4) levels and a dramatic drop in triiodothyronine (T3) plasma levels of the diseased geese. Thyroidal histology displayed the typical signs of struma parenchymatosa. In order to get more information about the possible causes of the goitre, 10 geese from the affected farm were transferred into the laboratories of the Central Veterinary Institute. The geese were allotted into two groups. Group I received iodine supplementation for 55 days, while the other group served as sick control (Group S). Iodine treatment caused a dramatic improvement in the birds' clinical condition except in plumage growth in Group I, while the clinical and main pathological signs of goitre remained unchanged or worsened in the untreated Group S. Contrary to this, the serum levels of thyroid hormones and responsiveness to thyrotropin releasing hormone (TRH) improved not only in Group I but also in Group S. Almost euthyroid biochemical parameters were found after 55 days of iodine treatment in Group I and, surprisingly, a considerable improvement (especially in serum T3 levels) occurred also in Group S. These findings confirm the diagnosis of goitre but also call attention to the fact that iodine deficiency was not the only factor eliciting the disorder. The underlying possible goitrogenic substance could not be traced down.     

Iodine-deficiency goitre in a bitch

Extract

A 9-year-old working bitch was presented by a freezing-works shepherd. The bitch had a history of dyspnoea, coughing and difficulty in swallowing.     

Inherited phosphofructokinase deficiency in an American cocker spaniel.

A 3-year-old female American Cocker Spaniel with a chronic hemolytic disorder and hemolytic crises was found to have M-type phosphofructokinase deficiency. This inherited erythroenzymopathy and myopathy is commonly diagnosed in English Springer Spaniels, but the family study of this Cocker Spaniel, although supporting an autosomal recessive mode of inheritance, did not reveal any English Springer Spaniel ancestors. Molecular genetic studies did, however, identify the same mutation in this dog as we previously reported in the English Springer Spaniel breed, suggesting that this mutation originated prior to the separation of these 2 breeds.     

Inherited laryngeal paralysis. Analysis in the Husky Cross

Summary

A report of inherited laryngeal paralysis of neurogenic origin in the Siberian Husky and the crossbreed Husky or Alaskan Sled dog is presented.     

Case of equine goitre

A brief review of the literature on equine goitre is presented, together with a case of congenital goitre in a foal. This animal showed localised swelling of the neck, hyperextension of the lower limbs and initial difficulty in sucking. The goitre was removed surgically and the hyperextension successfully treated with surgical shoes and bandaging. The cause was probably iodine deficiency coupled with a goitrogen in the diet.     

Toxic nodular goitre in the cat

Hyperthyroidism was diagnosed in 24 aged cats and was characterized by palpable enlargement of the thyroid gland, high circulating levels of thyroid hormones, increased thyroidal uptake of ¹²³I, and abnormal uptake and distribution of activity on thyroid scintiscans. Unilateral or bilateral thyroidectomy was performed in all cats and resulted in remission of signs in all but one case. The histological diagnosis was adenomatous hyperplasia in 23 cats and adenocarcinoma in one. Serum thyroid hormone concentrations decreased to normal or subnormal levels within 24 hours after complete removal of functioning thyroid nodules. Hypothyroidism occurred postoperatively in 16 of the 24 cats. Presumed hypoparathyroidism and hypocalcaemia occurred in 6 cases.