Canine leucocyte adhesion deficiency in Irish red and white setters

Seventy-six Irish red and white setter samples were tested for the recently documented CD18 point mutation which manifests as canine leucocyte adhesion deficiency (CLAD) in Irish setters. Six carrier dogs were identified, all originating from a lineage within which sporadic deaths from symptoms consistent with CLAD had been observed. This is the first demonstration that the CLAD mutation exists outside the Irish setter population, confirming that the mutation is present in a significant minority of Irish red and white setters. Routine testing by breeders to identify carrier animals will enable the eradication of CLAD from the Irish red and white setter population.     

Molecular basis of globoid cell leukodystrophy in Irish setters

Globoid cell leukodystrophy (GLD), or Krabbe's disease, is a progressive autosomal recessive disorder of the central nervous system in man and in various other species. GLD has been shown to result from various mutations in the gene encoding galactocerebrosidase (GALC), a lysosomal enzyme. We investigated the molecular basis of GLD in a related group of Irish setters. Sequencing of the GALC cDNA from an affected individual revealed an insertion mutation of 78 base pairs (bp) consisting of 16 bp of insertion site duplication and 62 bp of sequence derived from the U4 small nuclear RNA. We implemented a PCR-based test which is useful for identifying carriers of the mutation.     

Familial non-rcd1 generalised retinal degeneration in Irish setters

Four Irish setters were diagnosed with bilateral retinal degeneration and cataracts at an age ranging from six to 11 years. In three of these dogs, progressive night blindness was reported from an age of eight to 11 years. In the fourth dog, aged six, no signs of visual impairment had been noticed. In all four dogs, the rod-cone dysplasia type 1 (rcd1) mutation was excluded as a cause, using an allele-specific PCR. From their three-generation pedigrees, a familial relationship was detected in three out of four dogs, which were also related to four additional Irish setter dogs with a history and clinical signs suggestive of late-onset progressive retinal degeneration. These results suggest the existence of a possibly hereditary, late-onset, progressive retinal atrophy in the Irish setter breed, that is distinct from rcd1.     

Immune responses to dietary antigens in gluten-sensitive enteropathy of Irish setters

This study examined whether increased intestinal permeability in Irish setters with gluten-sensitive enteropathy was associated with altered immune responses to ingested antigens, and whether a humoral immune response to gluten is involved in the pathogenesis of the condition. Affected setters reared on a wheat-containing diet were compared with littermates reared on a cereal-free diet and age-matched control setters. Measurement of serum immunoglobulins revealed increased serum IgA concentrations in affected dogs. Antibody responses to a variety of dietary antigens were measured by elisa. Antibody levels to ovalbumin, collagen I and II and soya were not significantly different from normal dogs. Anti-gliadin antibody concentrations were lower in affected dogs than controls, and correlated with immune complex formation as assessed by CIq binding. The study suggested a modified immune response in dogs with increased intestinal permeability, although there was no major systemic antibody response to dietary antigens.     

Clinical, radiological and pathological features of 12 Irish setters with canine leucocyte adhesion deficiency

The clinical, radiological and pathological findings in 12 dogs with canine leucocyte adhesion deficiency (CLAD) from six litters are described. All the dogs were younger than 15 weeks at admission, all had been febrile and 11 had been treated with antibiotics. Seven had been treated for omphalophlebitis. At admission, all had gingivitis, lymph node enlargement and profound neutrophilia. Ten dogs were radiographed and showed various skeletal lesions compatible with metaphyseal osteopathy, craniomandibular osteopathy and osteomyelitis. Four dogs had clinical signs of respiratory distress and seven exhibited a mild interstitial pneumonia at necropsy. Six dogs had skin wounds, with strikingly few neutrophils seen on stained sections. All dogs were euthanased before six months of age due to severe and incurable infections. The clinical signs, radiological features and haematology were strongly suggestive of CLAD. The diagnosis was confirmed by granulocyte function tests and flow cytometry, which revealed impaired adhesion, impaired C3b-mediated phagocytosis and absence of adhesion proteins CD11b/CD18.     

Incidence of the gene mutation causal for rod-cone dysplasia type 1 in Irish setters in the UK

A survey to establish the UK prevalence of the gene mutation causing the rod-cone dysplasia type one (rcdl) form of generalised progressive retinal atrophy (gPRA) in Irish setters was carried out. The dogs were selected by members of two Irish setter breed societies to provide examples from most of the main breeding lines in the UK. A total of 210 Irish setters were tested and one bitch was found to be a carrier of the rcdl mutation. These results show that although a confirmed case of rcdl has not been reported in Irish setters in the UK for over a decade the gene is still present in the gene pool.     

Frequency of the canine leucocyte adhesion deficiency (CLAD) mutation among Irish red setters in Germany

Canine leucocyte adhesion deficiency (CLAD) is an autosomal recessive hereditary disease occurring among Irish red setters. The genetic defect causative for this disorder was recently identified as a missense mutation in the ITGB2 gene. Irish red setters with one copy of the mutant gene appear normal, while dogs with two copies of the mutant gene manifest the disease. The present report describes the analysis of the single nucleotide polymorphism in 289 Irish red setters by DNA sequencing. The frequency of CLAD carriers in Germany is 11%.     

A review of factors influencing litter size in Irish sows

Many factors influence litter size. These include genetics, gilt management, lactation length, parity distribution, disease, stress and boar fertility. In the past 20 years, litter size in Irish sows has increased by only one pig. Born alive figures now average at 11.2 pigs per litter. In this regard, Ireland is falling behind our European competitors who have made significant advances over this time. Denmark, for example, has an average figure of 12.7 pigs born alive per litter and France an average of 12.5. The single area that could be improved immediately is sow feeding. It is important that sows are fed correctly throughout pregnancy. If over-fed during pregnancy, sows will have depressed appetite during lactation. If underfed in pregnancy, sows will be too thin at farrowing. The correct way to feed a pregnant sow is to match her feed allocation to her requirement for maintenance, body growth and growth of her developing foetuses. During lactation, sows should be given as much feed as they can eat to prevent excessive loss of body condition. Liquid-feed curves should be such that lactating sows are provided with a minimum mean daily feed supply of 6.2 kg. A small proportion of sows will eat more and this could be given as supplementary dry feed. Where dry feeding is practised in the farrowing house, it is difficult to hand-feed sows to match their appetite. Ideally ad libitum wet/dry feeders should be used. From weaning to service, sows should once again be fed ad libitum. If liquid feeding, this means giving at least 60 MJ DE (digestible energy) per day during this period. If dry feeding, at least 4 kg of lactation diet should be fed daily. The effort spent perfecting sow feeding management on units should yield high dividends in the form of increased pigs born alive per litter.     

Differential sugar absorption for the assessment of canine intestinal permeability: the cellobiose/mannitol test in gluten-sensitive enteropathy of Irish setters

Intestinal permeability was assessed in Irish setters with gluten-sensitive enteropathy by oral administration of an isotonic solution of cellobiose and mannitol, and measurement of their urinary excretion ratio. The cellobiose/mannitol ratio was increased in affected Irish setters fed a wheat-containing diet compared both with littermates reared on a cereal-free diet, with no evidence of jejunal damage, and clinically healthy Irish setters. The ratio fell following six weeks on a gluten-free diet to be comparable with control values, and subsequently increased after six weeks gluten challenge. The results indicate that the cellobiose/mannitol test may be useful for the detection of mucosal damage and for monitoring the response to therapy.     

Symmetrical onychomadesis in Norwegian Gordon and English setters

This study reports the condition onychomadesis affecting multiple claws in Norwegian Gordon and English setters. Medical records of and claw biopsies from 18 Gordon and four English setters with onychomadesis of multiple claws were obtained from July 2005 to January 2007. Only dogs with symmetrical onychomadesis and no signs of concurrent disease were included. Histopathological features varied between dogs, but typically included interface dermatitis with subepidermal cleft formation, pigment incontinence, basal cell vacuolization and necrosis, spongiosis and lymphocytic exocytosis, a lymphocytic, plasmacytic subepidermal inflammation, and fibroplasia. In two dogs, histopathological signs of a superficial infection were present. The age of onset of disease varied between 2 and 7 years with a mean of 3.9 years, and was not correlated with vaccination time. Six of the affected dogs also had siblings with the disease. Due to the close relationship of the affected dogs, pedigree map analysis was not possible. Three dogs were euthanized because of the disease and two had regrowth of normal claws. Seventeen dogs had persistent onychodystrophy that typically was nonpainful during therapy which in most dogs consisted of fatty acid supplementation or prednisolone.     

Heritability of canine hip-dysplasia score and its components in Gordon setters

Hip dysplasia (malformation of the hip joint) is an important health problem in dogs. The condition and the control scheme for Gordon Setters was organised by the British Veterinary Association (BVA) and the Kennel Club before 1976 and use hip scores. Our analyses of hip dysplasia in Gordon Setters used both hip scores and the scores for the nine components (which collectively defined the hip score). The scores for all nine components were available for 732 females and 420 males. These clinical data were merged with the Kennel Club pedigree database (animal's identity, date of birth, and also similar data for its parents, including hip scores if the parent had been tested). Regression models showed strong positive relationships between offspring and parental hip scores as well as for some component scores. The heritability of hip dysplasia (assessed using both hip scores and the major components) was significant, particularly from dams. Our research emphasizes the need for both sires and dams--particularly dams, to have zero or small hip scores. Tested parents have been used increasingly in recent years, but greater reduction in offspring hip score will require stricter selection of potential breeding stock. The models reported here provide quantitative predictions of likely health benefits from selective breeding.     

Babesiosis in a litter of pups

Babesia canis infection was diagnosed in a litter of seven 3-week-old Mastiff pups kept in a north Florida kennel. The pups were evaluated because of poor weight gain; the smallest pup also was markedly lethargic. Six of the pups were anemic and thrombocytopenic. A positive linear correlation between PCV and absolute reticulocyte count suggested that the variation in PCV may have been related more to the ability of a pup to increase erythrocyte production than to a difference in magnitude of erythrocyte destruction. All pups recovered from clinical signs and hematologic abnormalities attributable to babesiosis within 2.5 weeks after treatment with diminazene aceturate. Transient neurologic signs observed in 1 pup 3 days after treatment were believed to represent an adverse drug reaction. The dam of the litter had a serum titer of 1:640 for B canis, but appeared healthy, as did approximately 30 other adult dog in the kennel. The strain of B canis infecting dogs in the kennel caused severe illness and death in some pups, but clinically inapparent disease in adult dogs.     

Syndactyly in a litter of cats

In this case report, we describe the clinical and radiographic features of a litter of kittens affected with complex syndactyly. We also provide guidelines for the diagnosis, possible treatment and prevention of propagation of this condition. This is the first report of syndactyly in a litter of kittens and syndactyly affecting both the pectoral and pelvic limbs.     

Two cases of brachymelia in cats

In this report, two cases of brachymelia in related neonatal cats are described. The malformations are described in view of normal limb development, which is illustrated by scanning electron microscopic images. Hypoplasia and aplasia of the distal limb segments were the main disorders in both kittens. Additional malformations in the second case included fusion of the radius and ulna, congenital patella luxation and a shortened tail. Brachymelia and similar cases of feline dysmelia are poorly documented in the existing literature. Possible causes and terminology of these developmental deformations are discussed.