Leucoencephalomalacia and Cerebral White Matter Vacuolar Degeneration in Two Related Labrador Retriever Puppies

Two Labrador Retriever dogs from a common dam had similar neurological deficits consisting of cortical blindness, dullness, and loss of previously learned habits. Both were examined at 5 months of age, and histopathological examination revealed leucoencephalomalacia and vacuolar degeneration of the cerebral white matter. Histopathologic findings in these 2 dogs differed from those reported previously in Labrador Retrievers with spongy degeneration of central nervous system white matter. A nonlittermate full sibling to 1 of these dogs was examined at 1.5 years of age for similar clinical signs that did not progress for the next 25 months.     

Hereditary ataxia in the Jack Russell Terrier--clinical and genetic investigations

Hereditary ataxia in the Jack Russell Terrier (JRT) is characterized by a gait disturbance with symmetric generalized ataxia and hypermetric and spastic movements. Histopathology shows a disease of the entire central nervous system, predominantly an axonopathy. In the present study, 35 clinically affected dogs were examined. Gait abnormalities began at 2-9 months of age. Generalized seizures occurred in 13 dogs in addition to the ataxia, and 7 dogs developed respiratory distress. Brain stem auditory-evoked potentials (BAEPs) were abnormal in 4 of 8 examined dogs, in which only waves I and II were detected. Abnormal BAEPs suggest the possibility of hereditary ataxia in the JRT. Investigations regarding the mode of inheritance were performed by complex segregation analyses on 3 pedigrees with a total of 115 JRTs (27 clinically affected dogs and 88 unaffected littermates and ancestors). Different modes of inheritance were tested, including monogenic, mixed, and polygenic models, as well as a model with environmental effects only. Models with genetic effects explained the data significantly better than the environmental model. The monogenic model had to be rejected in this study because of an insufficient match of data when compared to that of the most general model. The polygenic and mixed major gene models explained the pedigree data best and therefore have to be regarded as possible hypotheses for the mode of inheritance of hereditary ataxia in the JRT. The polygenic model proved best suited to explain the segregation pattern in the JRT, because it had the fewest number of parameters.     

Granulomatous meningoencephalomyelitis with peripheral nervous system involvement in a dog

A 9-year-old male neutered Labrador Retriever presented with signs consistent with multifocal neurological disease. Cerebrospinal fluid analysis revealed a mononuclear pleocytosis and electromyography revealed abnormal electrical activity in distal appendicular and masticatory muscles. Treatment was declined and necropsy revealed disseminated granulomatous meningoencephalomyelitis with extensive involvement of the peripheral nervous system.     

The geographic form of retinal dysplasia in dogs is not always a congenital abnormality

To examine the congenital nature of the geographic form of focal/multifocal retinal dysplasia, we carried out a retrospective analysis of the medical records of dogs produced in a closed colony of service dogs who receive very thorough ophthalmologic examinations early in their life, and later, when they return for training. Medical records were reviewed from all dogs produced by The Seeing Eye, Inc. between October 1991 and September 1998, and which had a diagnosis of geographic retinal dysplasia coded. We identified 23 dogs of five different breeds or interbreed crosses that comprise the breeding and production program (Golden Retrievers, German Shepherds, Labrador Retrievers, Labrador Retriever/Golden Retriever cross and German Shepherd/Labrador Retriever cross) in which the results of at least two complete ophthalmic examinations were documented, the first before 10 weeks of age, and the second when the dog was a young adult. Of the 23 dogs, only one was identified as affected with the geographic form of retinal dysplasia when examined at 5–6 weeks of age. The remaining dogs were normal. Our findings indicate that, in most cases, the geographic form of retinal dysplasia is not present in dogs prior to 10 weeks of age. These findings indicate the need to revise recommendations for early screening of dogs for retinal dysplasia.     

Age-related thoracic radiographic changes in golden and labrador retriever muscular dystrophy

Golden retriever and Labrador retriever muscular dystrophy are inherited progressive degenerative myopathies that are used as models of Duchenne muscular dystrophy in man. Thoracic lesions were reported to be the most consistent radiographic finding in golden retriever dogs in a study where radiographs were performed at a single-time point. Muscular dystrophy worsens clinically over time and longitudinal studies in dogs are lacking. Thus our goal was to describe the thoracic abnormalities of golden retriever and Labrador retriever dogs, to determine the timing of first expression and their evolution with time. To this purpose, we retrospectively reviewed 390 monthly radiographic studies of 38 golden retrievers and six Labrador retrievers with muscular dystrophy. The same thoracic lesions were found in both golden and Labrador retrievers. They included, in decreasing frequency, flattened and/or scalloped diaphragmatic shape (43/44), pulmonary hyperinflation (34/44), hiatal hernia (34/44), cranial pectus excavatum (23/44), bronchopneumonia (22/44), and megaesophagus (14/44). The last three lesions were not reported in a previous radiographic study in golden retriever dogs. In all but two dogs the thoracic changes were detected between 4 and 10 months and were persistent or worsened over time. Clinically, muscular dystrophy should be included in the differential diagnosis of dogs with a combination of these thoracic radiographic findings.     

Canine storage disease characterized by hereditary progressive neurogenic muscular atrophy: breeding experiments and clinical manifestation

Progressive neurogenic muscular atrophy due to storage of a compound lipid in the lower motor neurons was diagnosed in 3 English Pointers that were littermates. Using 2 clinically normal littermates of these 3 affected dogs and 2 clinically normal dogs of the 2nd litter from the parents of the original 3 affected dogs as the initial breeding stock, a breeding experiment was performed, resulting in a breeding line of 26 dogs, 4 of which had the disease and 6 of which died before 3 months of age. Results indicated that the disease may have an autosomal recessive mode of inheritance. The clinical manifestation and electrophysiologic findings indicated lower motor neuron involvement in the affected dogs produced by breeding consistent with findings in the original 3 affected dogs. Upper motor neurons or the sensory system was not involved. The disease appeared to be distinct from other canine storage diseases previously reported.     

Evaluation of the genetic basis of tricuspid valve dysplasia in Labrador Retrievers

OBJECTIVE: To quantify inheritance of tricuspid valve dysplasia (TVD) in a population of Labrador Retrievers and evaluate the possibility of the effect of a major locus on TVD. ANIMALS: 521 Labrador Retrievers (345 with known phenotypes and 176 related dogs with unknown phenotypes). PROCEDURES: Dogs were considered normal, equivocal, and affected for TVD on the basis of echocardiographic appearance of the tricuspid valves. Information on related dogs was collected for estimation of heritability of the 3 categories of phenotype, using a threshold model. Complex segregation analysis was performed to evaluate the possibility of the effect of a major locus on TVD. RESULTS: Heritability of TVD in this population of dogs was found to be 0.71, a value sufficiently large to suggest a segregating major locus. Subsequent complex segregation analysis did not provide sufficiently strong evidence to indicate influence of a major locus on the prevalence of TVD. However, complex segregation analysis for 2 categories of phenotype (eg, equivocal dogs were grouped with affected dogs) suggested that there was a single recessive allele with a substantial impact on the expression of TVD. CONCLUSIONS AND CLINICAL RELEVANCE: In Labrador Retrievers, TVD is a heritable disorder. Affected dogs and dogs closely related to affected dogs should not be used for breeding. There was insufficient evidence to suggest the influence of a major locus on TVD, although this conclusion was affected by the classification of dogs for diagnosis of the condition.     

Canine bone shape analysis by use of a radiographic image-classification system.

A radiographic image-classification system was developed to analyze and compare the shape of the humerus of neonatal Labrador Retriever and Labrador Retriever x Beagle pups that were either phenotypically normal or affected with an ocular-skeletal dysplasia syndrome. The system consistently defined the shape of the humerus within the groups of pups studied and indicated a difference in the shape of the humerus between normal and affected pups. Results indicated that the radiographic image-classification system may be able to identify Labrador Retriever pups affected by the ocular-skeletal dysplasia syndrome at or shortly after birth.     

Dystrophin-deficient muscular dystrophy in a Labrador retriever

Sex-linked muscular dystrophy associated with dystrophin deficiency has been reported in several breeds of dogs and is best characterized in the golden retriever. In this case report, a young, male Labrador retriever with dystrophin-deficient muscular dystrophy is presented. Clinical signs included generalized weakness, lingual hypertrophy, and dysphagia. Electromyographic abnormalities including complex repetitive discharges were present. Serum creatine kinase concentration was dramatically elevated. Histopathological changes within a muscle biopsy specimen confirmed a dystrophic myopathy, and dystrophin deficiency was demonstrated by immunohistochemical staining. While X-linked muscular dystrophy has not previously been reported in the Labrador retriever, a hereditary myopathy with an autosomal recessive mode of inheritance has been characterized. A correct diagnosis and classification of these two disorders are critical for breeders and owners since both the mode of inheritance and the prognosis differ.     

Ascorbic acid deficiency and hypertrophic osteodystrophy in the dog: a rebuttal.

Plasma ascorbic acid (PAA) in normal Labrador Retriever dogs less than one year of age averaged 1.22 +/- 0.05 mg/dl (x +/- sem) and was significantly higher than the value of 0.89 +/- 0.03, for Labrador Retrievers two years of age and older. No significant diurnal variation in PAA was observed. Oral or intravenous administration of 0.5 or 1.0 g of ascorbic acid (AA) elevated PAA for less than 8 hours. Injection of ACTH caused a significant decline in PAA for the initial 2 days, with variable results thereafter. Labrador Retriever puppies fed a ration high in protein, energy and calcium developed the typical skeletal diseases of overnutrition, including hypertrophic osteodystrophy (HOD). The addition or oral AA (0.5 g twice daily) had no ameliorating effect on the skeletal lesions. Instead AA supplementation resulted in relatively higher serum calcium values which, presumably by enhanced hypercalcitoninism, decreased bone resorption. Thus, AA treatment of dogs with HOD is contraindicated, as it can only aggravate the osseous lesions of HOD. The decreased PAA reported in dogs with HOD is interpreted to be the result of stress from pain.     

Seasonal variation in the hip score of dogs as assessed by the New Zealand Veterinary Association Hip Dysplasia scheme

Abstract

AIM: To determine whether there is a seasonal variation in the phenotypic hip score of dogs born in New Zealand as assessed by the New Zealand Veterinary Association (NZVA) canine hip dysplasia (CHD) scheme.

METHODS: Data from dogs born in New Zealand between 1988 and 2009 that have been scored for CHD were retrospectively evaluated for the effect of month of birth on radiographic phenotype. Data included both the total score and the subtotal score, comprising Norberg's angle, the subluxation score and changes to the cranial acetabular edge, for each dog. Datasets were created for all breeds combined and for the four most populous breeds using the scheme (German Shepherd dog, Labrador Retriever, Golden Retriever and Rottweiler) and stratified according to month of birth and season. Due to the skewed nature of the data, a Kruskal–Wallis Rank Sum test was used to test for statistical significance. Additionally, χ² analysis was performed using the median of each dataset (proportion above/below the median). The null hypothesis was that there would be no effect of month of birth, and hence seasonality, on hip phenotype for dogs born and scored in New Zealand by the NZVA.

RESULTS: For all breeds combined, month of birth had an effect on total and subtotal NZVA CHD scores (p<0.001) with a lower total hip score in the autumn months of March and April than other months. When individual large breed data were analysed, there was an effect of month of birth on total and subtotal scores for the Labrador Retriever and the Rottweiler (p≤0.05), but not the German Shepherd dog or Golden Retriever breeds.

CONCLUSIONS: Being born in the autumn was associated with a protective effect on hip phenotype in some breeds. These results suggest that weather and/or another seasonal factor may have a significant environmental effect on the phenotype of the coxofemoral joint.

CLINICAL RELEVANCE: The protective effect of being born in autumn suggests that a decreased level of exercise during subsequent development over winter may positively impact on final coxofemoral joint conformation. Whilst statistically significant, the magnitude of the sparing effect is not likely to be clinically relevant. However, this study, in concert with other studies, may suggest that the effects of exercise can be manipulated to improve hip phenotype.     

Azoospermia in two Labrador retrievers

Azoospermia is described in two sibling Labrador Retriever dogs. Clinical investigations following failure to sire pups after normal matings revealed testicular hypoplasia and degeneration. Sperm were absent on repeated ejaculate examination in both dogs. Histopathological examination of testicular needle aspirate biopsy and whole testicle of the first dog displayed an absence of spermatids and spermatocytes. Seminiferous tubules containing Sertoli cells with or without primary spermatogonia were present in the second dog. Peritubular lymphocyte accumulation was also present in both dogs. The dogs had been conceived using frozen-thawed semen.     

Quantitative genetics of secondary hip joint osteoarthritis in a Labrador Retriever-Greyhound pedigree

OBJECTIVE: To evaluate the quantitative inheritance of secondary hip joint osteoarthritis in a canine pedigree. ANIMALS: 137 Labrador Retrievers, Greyhounds, and mixed-breed dogs. PROCEDURES: Necropsy scores ranging from 0 to 4 were obtained for each hip joint. Seven unaffected Greyhounds with normal hip joint conformation were also used for genetic modeling, but were not euthanized. Sixty-six male and 71 female dogs were allocated to 2 groups (< or = 12 months of age and > 12 months of age). Statistical models were developed to establish the inheritance pattern of hip joint osteoarthritis that developed secondary to hip dysplasia. RESULTS: 62 dogs had evidence of osteoarthritis in a hip joint, and 75 had no evidence of osteoarthritis. After sex was adjusted for, the necropsy score was found to be inherited additively but without dominance. Each Labrador Retriever allele increased the necropsy score by 0.7 to 0.9 points, compared with the Greyhound allele, and male sex increased the necropsy score 0.74 over female sex. Approximately 10% of the variation in necropsy score was attributable to the litter of puppies' origin. CONCLUSIONS AND CLINICAL RELEVANCE: Because secondary hip joint osteoarthritis is inherited additively, selection pressure could be applied to reduce its incidence. Similar statistical models can be used in linkage and association mapping to detect the genes in the underlying quantitative trait loci that contribute to hip joint osteoarthritis.     

Cutaneous neosporosis in two adult dogs on chronic immunosuppressive therapy.

Antemortem diagnosis of generalized ulcerative and pyogranulomatous dermatitis with numerous intralesional tachyzoites was made from skin biopsy specimens from 2 adult dogs on chronic immunosuppressive therapy. A 9-year-old Italian Greyhound was on long-term corticosteroid therapy for the treatment of a lupus-like systemic autoimmune disorder, and a 7-year-old Labrador Retriever had received several months of chemotherapy for lymphosarcoma. The tachyzoites were identified as Neospora caninum by immunoperoxidase immunohistochemistry. Both dogs were treated with clindamycin. Lesions in the Greyhound resolved; however, the Labrador Retriever was euthanized because of evidence of neuromuscular disease, despite improvement of the skin lesions. These 2 cases indicate that cutaneous neosporosis can occur in adult dogs on chronic immunosuppressive therapy. The disease may result from reactivation of a congenital infection and/or a recently acquired primary infection.     

Inheritance of associated ocular and skeletal dysplasia in Labrador retrievers

A breeding colony was established to investigate the inheritance of associated ocular and skeletal dysplasia in Labrador Retrievers; 124 pups were produced. These pups were evaluated for the presence of ocular lesions, including cataracts, vitreous strands, persistent hyaloid remnants, retinal folds, retinal dysplasia, peripapillary hyperreflectivity, and rhegmatogenous retinal detachments, and skeletal abnormality, which was recognized by shorter than normal forelimbs and an abnormal morphologic appearance of the radius and ulna. Analysis of the distribution of lesions in pups indicated that the syndrome is caused by one abnormal gene, which has recessive effects on the skeleton and incompletely dominant effects on the eye. This would suggest that suspect carrier dogs could be identified by test matings with a known homozygote.     

Muscular dystrophy in dogs: does the crossing of breeds influence disease phenotype?

Golden Retriever (GR) muscular dystrophy is an inherited degenerative muscle disease that provides an excellent model for Duchenne muscular dystrophy in humans. This study defined the histopathologic lesions, including the distribution of type I and II muscle fibers (FTI and FTII), in 12 dystrophic and 3 nondystrophic dogs between 7 and 15 months of age. The authors were interested in studying the influence on disease phenotype from crossing the base GR breed with Yellow Labrador Retrievers. The dystrophic dogs were divided according to breed: GRs and Golden Labrador Retrievers (GLRs). On hematoxylin and eosin staining, histopathologic lesions were more severe in GRs than GLRs. Six of eight GR muscles (75%) had a severe lesion grade (grade 3). In contrast, seven GLR muscles (87.5%) had mild lesions (grade 2), and only one had severe lesions (grade 3). Changes in fiber-type distribution were more pronounced in GRs versus GLRs. FTI:FTII ratio inversion was observed in three dystrophic GRs but only one GLR. The mean diameter of FTI and FTII was smaller in GRs and GLRs than in nondystrophic dogs (P < .01). The FTI of five GR muscles (62.5%) were larger than those of GLRs, whereas only one GLR muscle was larger (P < .05). The differential was less pronounced for FTII, with four GR muscles being larger and three GLR being larger. Observations indicate that crossing the base GR breed with Labrador Retrievers lessened the severity of the GR muscular dystrophy phenotype.     

Growth dynamics of the canine proximal tibial physis

Objective: To determine growth of the proximal tibial physis in the Labrador Retriever, a breed of dog at risk for rupture of the cranial cruciate ligament (CCL). Animals: Male Labrador Retriever dogs (n=6). Methods: Tantalum markers (0.5 mm diameter) were implanted in the right proximal tibial epiphysis and metaphysis of each dog at 16 weeks of age. Lateral and craniocaudal radiographic projections of the tibia were made monthly and longitudinal growth was assessed from radiographs; a growth curve was generated from the data. Data from dogs that had undergone proximal tibial epiphysiodesis (PTE) was compared with the growth curve to demonstrate if the growth curve accurately predicted changes in the growth associated with this procedure. Results: Growth rate of individual dogs decreased slowly and non‐linearly over the 1st year of age. Growth from the proximal tibial physis is described. Conclusions: Growth of individual dogs described here follows the model of saltation and stasis. The growth curve generated predicted the change in tibial plateau angle (TPA) for two Labrador Retrievers that had PTE (±1°).     

Clinical remission following plasmapheresis and corticosteroid treatment in a dog with acquired myasthenia gravis

A 7-year-old sexually intact male Labrador Retriever with regurgitation and generalized muscular weakness resulting from acquired myasthenia gravis received 2 plasmapheresis treatments in combination with corticosteroid treatment. Plasmapheresis was performed in an attempt to rapidly lower serum acetylcholine receptor binding antibody (AChR Ab) concentration. Seven days after the second plasmapheresis treatment, the dog's muscular strength was normal, which coincided with a 70% decrease in serum AChR Ab concentration. Because the dog also received corticosteroids, it is impossible to determine how much of the clinical improvement resulted from plasmapheresis.     

A novel movement disorder in related male Labrador Retrievers characterized by extreme generalized muscular stiffness

Objectives: To describe the clinical phenotype of a new motor disorder in Labrador Retrievers. Animals and Methods: Case series study. Seven young male Labrador Retrievers presented for evaluation of stiff gait. Results: All affected dogs had generalized muscular stiffness, persistent at rest and resulting in restricted joint movements. They showed a forward flexed posture, festinating gait, and bradykinesia. Signs developed between 2 and 16 months of age and tended to stabilize in adulthood. Needle electromyogram in the conscious state showed continuous motor unit activity in resting epaxial and proximal limb muscles. This activity was abolished by general anesthesia. Muscle and nerve histopathology was normal. In 2 dogs necropsied, astrocytosis was evident throughout the spinal cord gray matter, reticular formation and caudate nuclei. Decreased neuronal counts were selectively found in the spinal cord Rexed's lamina VII, but not in VIII and IX. Pedigree analysis showed that the affected dogs were from 5 related litters. Conclusions and Clinical Importance: This new hypertonicity syndrome in Labrador Retrievers is unique because of the selective distribution of the histological lesions, the lack of progression in adulthood, and its exclusive occurrence in male dogs. Pedigree analysis suggests an X‐linked hereditary disease, although other modes of inheritance cannot be ruled out with certainty. We hypothesize that altered output from basal nuclei and reticular formation together with motor neuron disinhibition caused by a decreased number of spinal cord interneurons leads to the muscular stiffness.