Comparison of G-banded chromosomes from clinically normal lambs and lambs affected with ovine hereditary chondrodysplasia (spider syndrome)

Lymphocytes from 5 clinically normal lambs and 5 lambs affected with ovine hereditary chondrodysplasia (spider syndrome) were cultured, G-banded, and karyotyped. Fifty metaphase karyotypes and one heterogram were evaluated for chromosome number and morphologic features. All lambs had normal diploid (2n) chromosome numbers of 54,XX or 54,XY, and there were no apparent differences in the morphologic features of the chromosomes.     

Hereditary chondrodysplasia ("spider syndrome") in a New Zealand Suffolk lamb of American origin

The first case of hereditary chondrodysplasia ("spider syndrome") in a New Zealand Suffolk lamb of American origin is described. An imported Suffolk ram of American origin was test mated to 27 of his daughters. In one of the resulting progeny, found dead at birth, a diagnosis of hereditary chondrodysplasia was made based on the typical radiographical abnormalities of multiple centres of ossification in the anconeal process of the ulna, vertebrae, sternebrae and pelvic bones. These changes were confirmed histopathologically.     

Radiographic diagnosis of hereditary chondrodysplasia in newborn lambs

Normal appearing Suffolk lambs affected with hereditary chondrodysplasia (HC) and normal appearing unaffected lambs were radiographed at birth, and at 2, 4, and 8 weeks of age. In affected lambs, lesions were seen consistently in the elbows, shoulders, sternum, and spine. Similar lesions were not identified in unaffected lambs. A malformed Corriedale lamb was radiographed to compare its lesions to those seen in HC. The Corriedale lamb had islands of ossification of the anconeal process similar to those identified in lambs with signs of HC at birth. The islands of ossification seen in the Corriedale lamb were fused by 2 months of age, whereas elbow lesions seen in lambs with HC increased in severity during the same period.     

Insulin-like growth factor-I levels and gene expression in ovine hereditary chondrodysplasia (spider lamb syndrome).

Hereditary Chondrodysplasia or Spider Lamb Syndrome (SLS) is an inherited, semi-lethal, musculo-skeletal disease affecting lambs primarily of Suffolk or Hampshire breeding. Deformities of the limbs and spinal column along with multiple sites of ossification at the anconeal process are diagnostic for the disease. Muscle atrophy is also predominant. We have investigated the relationship between SLS and circulating levels of IGF-I and the IGF-BPs in older (50-80 d of age) animals. Serum IGF-I levels were lower (P less than 0.01) in SLS affected lambs (117 ng/ml) than in phenotypically normal lambs (188 ng/ml) while serum levels of the 32 kDa BP increased (P less than 0.01) 77% in SLS affected lambs as compared to contemporary controls. All other IGF-BPs appeared to be unaffected in this group. Gene expression of IGF-I and -II in the liver and muscle of younger (16-22 d of age) lambs was also measured. There were no differences in IGF-II expression in either muscle or liver between SLS affected and phenotypically normal control lambs. Muscle IGF-I expression also did not differ. However, liver IGF-I expression in SLS affected lambs was nearly double that of control lambs (P less than 0.01). These data suggest that the regulation of IGF-I and the IGF-BPs may be involved in the physical manifestations of this disorder.     

Congenital arthrogryposis: an inherited limb deformity in pedigree Suffolk lambs

Thirty of 52 pedigree Suffolk lambs (58 per cent) were born with arthrogryposis characterised by bilateral flexion rigidity of the metacarpophalangeal and carpal joints. The recent introduction of a breeding ram was identified as the only significant risk factor in the flock, and embryo transfer was used to test the hypothesis that the arthrogryposis was an inherited disorder associated with the introduction of this ram. Two adult ewes that had previously produced lambs with arthrogryposis by the ram and four of its affected daughters were available as donors, and 20 crossbred ewes were used as recipients. Ten Suffolk-crossed ewes that had no known familial relationship with the ram were also mated by the ram as controls and they produced 10 normal lambs. Following embryo transfer, 19 lambs were born, of which seven were stillborn; arthrogryposis was evident in 10 of the 12 live lambs. Analysis of the data suggested that in the population under study, arthrogryposis was inherited as an autosomal recessive condition.     

Acute respiratory distress syndrome (ARDS) in lambs. Hematology

Lambs suffering from Acute Respiratory Distress Syndrome (ARDS) showed elevated PCV, neutrophilia, a tendency towards lymphopenia, eosinopenia, hyperphosphatemia, hypoglycemia and extremely low serum Ca values during the first couple of days after the outbreak of symptoms. During the very early phase, plasma potassium values were mostly lowered (Figs. 1-3, Table I). The possible involvement of histamine is shortly discussed: either 1) through an atopic reaction, 2) because of acute ruminal acidosis and sudden histamine formation, or 3) involvement of endotoxins.     

Ovine progressive pneumonia (maedi-visna) in sheep

Ovine progressive pneumonia (OPP) is a multi-systemic disease of sheep caused by a nononcogenic exogenous retrovirus belonging to the Lentiviridae subfamily. Characteristics of the disease are chronic lymphocytic pneumonitis, encephalitis, arthritis, mastitis and vasculitis associated with progressive wasting, dyspnea, lameness, indurated udder and, rarely, paralysis. Any one or all of the characteristics may be manifest. Transmission of the virus is predominantly through the colostrum to newborn lambs, however, transmission can occur by contact and in utero. Treatment of the disease is only symptomatic and prevention of infection is only by avoiding the virus.     

Ovine adenovirus serotype 7-associated mortality in lambs in the United States.

Adenoviral infections were diagnosed in three neonatal lambs that died spontaneously, and no other etiologic agents were identified. Clinical signs were anorexia, weakness, abdominal distention, and sudden death. Microscopic lesions consisted of multifocal necrotizing hepatitis, multifocal subacute interstitial nephritis, and loss of enterocytes from intestinal villi. Adenovirus inclusions were identified by light microscopy in the kidneys only. Adenoviral antigen, however, was identified in the liver, kidney, and intestine of the lambs by immunohistochemical techniques. An ovine adenovirus serotype 7, not previously isolated from sheep in the United States, was characterized from these lambs.     

Acute respiratory distress syndrome (ARDS) in lambs. Clinical and pathoanatomical investigations

In the South-Western part of Norway, lambs of the Old Norwegian short tailed breed (Spael) and crosses with the Dala breed sometimes develop an Acute Respiratory Distress Syndrome (ARDS) shortly after they have been moved onto lush aftermath grazings from mountain pastures. This article covers the symptoms and pathoanatomical findings in lambs affected with ARDS (Table I). The lambs acquired ARDS 18-72 hours after change of pasture. Heavy dysphne, frothing at the mouth, elevated temperature (greater than 41 degrees C), tachycardia, urination and ruminal atony were striking symptoms (Table II). In the early phase of the disease the lambs were often in a tranquil state, depressed, sometimes atactic, and it seemed that they went into the overt dysphneic phase on exposure to physical stress. Morbidity was 1.4%, mortality 36%. Post mortem findings included frothy contents in the airways, heavy congestion and oedema in the lungs which also had emphysematous areas, subepicardial petechiae, varying degree of mottling of the myocardium, and also varying degree of paleness and spottyness of renal cortices. The lungs showed extensive focal alveolar and interstitial emphysema, septal congestion, alveolar oedema, partial collapse, and accumulations of polymorphonuclear leucocytes in vascular beds. Later, fibrillar material was found in the alveoli, alveolar macrophages accumulated, and interalveolar septa thickened because of increased fibromuscular tissue and mononuclear cells (Fig. 1, A-D). Alveolar epithelial hyperplasia was not seen in any stage. Four lambs were moderately infected with lungworms (D. filaria), three in the prepatent, one in the patent phase. Histopathological changes in other organs included granular degenerations of myocardial threads, and development of a glomerulonephritis and focal interstitial nephritis (Fig. 1, E-F). This disease entity (ARDS) in lambs seems to be unknown in literature. The disease is compared with other known diseases in ruminants. Etiology is so far unknown. Possibilities of sudden ruminal histamine formation coinciding with a hypersensitivity reaction is discussed.     

Ovine coccidiosis: heavy infection in young lambs increases resistance without causing disease

Seven groups of twin lambs, kept with their dams on pasture, were given single oral inoculations of 10,000 oocysts of Eimeria ovinoidalis and 10,000 E crandallis at one, two, four, seven, 14, 21 or 28 days after birth, respectively. All were then challenged with 100,000 of each species at 42 days of age. An eighth group was challenged without having received the earlier 'immunising' inoculum, and a ninth group was not inoculated at all. Bodyweights, faecal consistency, oocyst output, and serum coccidial antibody levels were monitored up to 12 weeks of age. No clinical response was detected to inoculation up to four days of age. Loosening of faeces and a slight setback in weight-gain occurred in lambs inoculated seven, 14 and 21 days after birth; inoculation 28 days after birth caused severe diarrhoea and weight loss. Challenge at 42 days caused severe coccidiosis with 50 per cent mortality in the 'unimmunised' group. In those that had received 'immunising' inoculations, the challenge at 42 days caused some diarrhoea and some weight loss, but much less than in the 'unimmunised' lambs. The later the 'immunisation', the less severe was the disease attributable to the challenge at 42 days. Serum antibody levels correlated fairly closely with resistance to the disease. It was concluded that very young lambs were resistant to the pathogenic effects of some coccidia, but were able to respond to them immunologically.     

Antebrachial chondrodysplasia in New Zealand white rabbits (Oryctolagus cuniculus)

Rabbits obtained from a South African rabbit breeder exhibited deformities of the distal forelimbs. The clinical, radiological and histological presentation of mid-antebrachial valgus formation (a.k.a distal foreleg curvature) in these rabbits was consistent with an autosomal recessive trait associated with a chondrodystrophic lesion of the distal ulna epiphysis 1st described in the 1960s. The impact this might have on South African farming enterprises and laboratory facilities has not been established, but the heritability and welfare implications of this condition make it a concern. Mildly affected animals can adapt to the deformity with some housing adjustments, but severely affected animals may require humane euthanasia.