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PubMed2002

A slow form of alpha-2-macroglobulin in diseased and healthy dogs.

Alpha-macroglobulins (AMs) function as non-specific protease inhibitors by using a so-called trapping mechanism, which is a compaction of the molecule that can be seen as a "fast" form in native polyacrylamide gel electrophoresis (PAGE). AMs also play a role in the transport and clearance of cytokines and growth factors from the circulation. In the dog, two AMs are known, alpha-1-macroglobulin (A1M) and alpha-2-macroglobulin (A2M). Using agarose and polyacrylamide gel electrophoresis of canine serum or plasma, we detected a cathodal, slow form of A2M. Upon activation with elastase, slow A2M resembled normal A2M in agarose gel electrophoresis, showing decreased negative charge at semi-saturation but not at full saturation with enzyme. In PAGE, however, slow A2M, unlike normal A2M, did not exhibit a "fast" form after short-term incubation with elastase. After incubation overnight, the "fast" form was seen, indicating a retarded reaction. Incubation of slow A2M with ammonium sulphate, a known activator of AMs, resulted in decreased negative charge in agarose gel electrophoresis and no reaction or partial reaction in PAGE. Slow A2M is present in fresh blood samples or may develop from partial alterations within a few days of storage. Moreover, it is sometimes reversible. Our findings may indicate that slow A2M is a result of an instability of the molecule, leading to a conformational change, which affects electrical charge and impairs the ability to develop into the "fast" form upon activation. This may lead to a delayed clearance of protease and inflammatory mediators from the circulation. Slow A2M was predominantly found in diseased dogs, especially in the Labrador retriever.

Animals↗
PubMedDate not supplied

DNA testing for type III von Willebrand disease in Dutch Kooiker dogs.

Von Willebrand disease type III is widespread in Dutch Kooiker dogs. To eradicate von Willebrand disease from the breed, affected dogs and nonsymptomatic carriers must be excluded from breeding. Previous efforts to detect carriers in Kooiker dogs by a von Willebrand factor antigen assay were not satisfactory because of considerable overlap of plasma concentrations in normal dogs and carriers. The aim of this study was to develop and apply a DNA test for the detection of von Willebrand disease carriers in the Kooiker breed. Two mutations in the von Willebrand factor gene in affected Kooiker dogs have been described previously, a splice site mutation at the border of intron 16 and exon 16 and a missense mutation in exon 3. We have developed polymerase chain reaction tests for both mutations in genomic DNA. The missense mutation most likely is a neutral variant and appears to be a polymorphism present in many breeds. The allele-specific oligonucleotide test for the splice site mutation was applied in the selection of animals cleared to breed by the Dutch breeding club. In a few years, the mutation has been eliminated from the breeding stock without apparent increase of inbreeding or preferential sire usage.

Animals↗
PubMed1992

Chronic tracheobronchial disease in the dog.

Tracheobronchial collapse and chronic bronchitis (CB) are the two most common forms of chronic tracheobronchial disease in dogs. These conditions may exist independently of one another, although CB and some degree of tracheobronchial collapse often co-exist in the same patient. Diagnosis of CB can be established on clinical grounds alone, whereas radiographic or bronchoscopic evidence is required to confirm the diagnosis of tracheobronchial collapse. Although glucocorticoid drug therapy remains one of the most effective methods for managing CB, surgical implantation of a prosthetic airway device may be of great benefit for some dogs with a focal area of collapsing trachea. With early diagnosis and aggressive medical and surgical management, the prognosis for many dogs with chronic tracheobronchial disease is good for reasonable quality of life.

Animals↗
PubMed1993

Adult-onset lysosomal storage disease in a Schipperke dog: clinical, morphological and biochemical studies.

An adult-onset lysosomal storage disorder was diagnosed in a 5-year-old Schipperke dog with progressive cerebellar and central vestibular signs. It was characterized by cerebellar atrophy with extensive loss of Purkinje and granular cells, and hydrocephalus. Enlarged and vacuolated neurons were observed in spinal cord and brain; pancreatic centrolobular and islet cells were also vacuolated. Ultrastructurally, enlarged secondary lysosomes laden with lamellated membrane structures were present in neurons and empty enlarged vacuoles were found in pancreatic centroacinar, ductal, and islet cells. On frozen sections neurons stained with Ricinus communis agglutinin-I and wheat germ agglutinin. On paraffin sections neurons stained with luxol fast blue, periodic acid-Schiff, Concanavalia ensiformis agglutinin, and were autofluorescent. These findings indicate an accumulation of glycolipids containing terminal beta-galactosyl and alpha-sialyl residues, and N-linked oligosaccharides. Tissue activity of lysosomal beta-galactosidase was 50% of normal and the activity of beta-hexosaminidase was elevated. Brain lipid-bound sialic acid was twice normal, with a small increase of GM1-ganglioside, but there was a significant elevation of GM2 (GD2) and GM3 (GD3). In addition, significant elevations of sialylated and non-sialylated oligosaccharides were noted. These clinical, biochemical and pathological findings are similar to those observed in human patients with adult-onset galactosialidosis.

Animals↗
PubMed1995

Human and canine cardiac troponin T and creatine kinase-MB distribution in normal and diseased myocardium. Infarct sizing using serum profiles.

OBJECTIVE: Cardiac troponin T (cTnT) has been suggested as a new, more specific marker of myocardial cellular damage. The objectives of this study were to examine the distribution of cTnT and creatine kinase (CK)-MB in normal and diseased heart tissue of dogs and humans, and to assess the use of serum cTnT for the estimation of infarct size in dogs. DESIGN: Serial serum specimens over 7 days were obtained from normal dogs (controls, n = 3) and dogs that underwent surgical coronary artery occlusion (n = 6). Heart muscle samples were obtained from the controls and after 3 weeks of occlusion in experimental dogs. Diseased human heart muscle samples were obtained at autopsy from patients who had died of acute myocardial infarction (n = 3). Normal heart muscle samples (n = 3) were obtained at autopsy from patients who died of non-cardiac-related illnesses. Tissues were sectioned and homogenized to harvest both cytosolic and myofibril-bound proteins. Serum samples and tissue homogenates were assayed for cTnT, CK-MB, and myoglobin (humans only). Total protein was assayed on homogenate samples and results were reported as milligrams per gram of total protein. RESULTS: The distributions of cTnT, CK-MB, and myoglobin were equivalent across 14 sites within normal human heart. Creatine kinase-MB and myoglobin were more than 99% cytosolic. Cardiac troponin T was 92% myofibril bound and 8% cytosolic. In the control dog hearts, cTnT was higher and CK-MB was lower in the right ventricle than in the left ventricle. While CK-MB and myoglobin were more than 99% cytosolic, cTnT was 98% myofibril bound and 2% cytosolic. Infarct sizing in dog hearts initially did not correlate well with serum cTnT or CK-MB concentrations. However, when the data were separated by infarct location (right coronary artery; left circumflex coronary artery), the correlations improved dramatically. Differences in tissue concentrations of cTnT and CK-MB between the left and right ventricle might explain the change in correlations. Coronary artery occlusion in dogs and humans resulted in decreased cytosolic and myofibril cTnT and increased CK-MB and myoglobin in diseased myocardial tissue. CONCLUSIONS: Our observed biochemical alterations suggest that the energy-producing proteins CK-MB and myoglobin are upregulated following cellular damage, while the structural and regulatory protein cTnT does not have a mechanism for replacement of lost protein following cell injury and necrosis.

Animals↗
PubMedDate not supplied

Urodynamic alterations after prostatectomy in dogs without clinical prostatic disease.

Prostatectomy in dogs with clinical prostatic disease has been associated with a high incidence of urinary incontinence. In this study, urodynamic alterations after prostatectomy in 10 dogs without clinical prostatic disease were evaluated. Measurements of residual urine volume, simultaneous urethral pressure profilometry and electromyography, and carbon dioxide cystometry were made before and 14 and 20 weeks after prostatectomy. Voiding was observed daily for 20 weeks after prostatectomy. All dogs remained continent for 20 weeks after prostatectomy, and only minor urodynamic abnormalities were noted. Castration had no effect on urodynamic changes associated with prostatectomy. Prostatectomy produced minimal functional changes in dogs without clinical prostatic disease.

Animals↗
PubMed1994

Association of age and body weight with periodontal disease in North American dogs.

Thirteen hundred and fifty dogs were examined under anesthesia at veterinary hospitals in the USA and Canada. Periodontal health was recorded in detail. Teeth were frequently absent (particularly lower third molar, upper and lower first premolars, and incisor teeth). Calculus was most extensive on the upper fourth premolar and molar teeth. Missing teeth, mobility of remaining teeth, extent of calculus and gingival inflammation, and furcation exposure and attachment loss all were more common in small dogs compared with larger dogs, and in order dogs compared with younger dogs.

Age Factors↗
PubMed2001

Spatial distribution of seropositivity to the causative agent of granulocytic ehrlichiosis in dogs in California.

OBJECTIVE: To assess spatial and temporal patterns of seroprevalence among dogs in California to the causative agent of granulocytic ehrlichiosis (GE). SAMPLE POPULATION: Sera of 1,082 clinically normal dogs from 54 of 59 counties in California in 1997 to 1998. PROCEDURES: Serum-specific IgG reactivity to Ehrlichia equi was assessed by use of an immunofluorescent antibody assay, using E. equi-infected horse neutrophils as substrate. Data were analyzed, using a geographic information system. Spatial analysis of seroprevalence included first order Bayesian analysis of seroprevalence and second order analysis of clustering by K-function and Cuzick-Edwards tests. Monthly seroprevalence among dogs was examined by use of regression on monthly densities of Ixodes pacificus adults and nymphs. RESULTS: Seroprevalence among dogs to E. equi was 8.68%. Data were seasonally bimodal with highest prevalence in winter (when adult ticks were abundant) and a secondary peak in late spring (corresponding to nymphal ticks). Humboldt County had the highest seroprevalence (47.3%), and other northern coast range counties had seroprevalence from 15 to 30%. CONCLUSIONS AND CLINICAL RELEVANCE: The patchy distribution of exposure to Ehrlichia organisms is a subset of the distribution of the tick vector. This may reflect enzootic cycles or climatic or historical factors that limited the range of the disease. Dogs, horses, and humans from north coast range counties in California are at increased risk of GE. These data provide a background for assessing risk of infection in horses and dogs, depending on geographic location. Dogs may be sentinels for assessing risk of GE in humans.

Animals↗
PubMed1998

Canine cone transducin-gamma gene and cone degeneration in the cd dog.

PURPOSE: To characterize the cDNA and the organization of the gene encoding the cone-specific gamma subunit of transducin (Tgamma c) and to examine this gene as a candidate for the recessively inherited cone photoreceptor degeneration in the cd dog. METHODS: Canine Tgamma c cDNA was cloned and sequenced. Polymerase chain reaction (PCR) was used to define the Tgamma c gene structure, northern blot analysis to examine the level of expression of Tgamma c mRNA in control and cd-affected retinas, and immunocytochemistry to determine the presence and localization of Tgamma c in normal and cd retinas. RESULTS: Immunocytochemical results showed Tgamma c localized to cone photoreceptor outer segments in the normal retina, whereas no Tgamma c immunoreactivity was observed in the cd retinas. However, the level of transcription and the primary structure of the cloned cDNA coding for the 69-amino acid protein were identical in retinas from wild-type and affected dogs. CONCLUSIONS: Although Tgamma c immunoreactivity was specifically absent in the cd dog retina, no differences were detected between normal and cd retinas in the nucleotide sequence of Tgamma c mRNA or in its synthesis. These results indicate that a mutation in the Tgamma c gene may not be causally associated with the cd dog disease. These findings suggest that possible abnormalities in posttranslational modification of Tgamma c or defective assembly of the transducin alphabetagamma complex could lead to rapid degradation of Tgamma c.

Amino Acid Sequence↗
PubMedDate not supplied

A retrospective comparison of cervical intervertebral disk disease in nonchondrodystrophic large dogs versus small dogs.

Medical records of 144 small-breed dogs (< or =15 kg) and 46 medium- to large-breed dogs (>15 kg) with surgically confirmed, Hansen type I, cervical intervertebral disk extrusions were reviewed. The most common clinical presentation was cervical hyperesthesia. The most common sites affected were the second (C(2)) to third (C(3)) cervical intervertebral disk space in small-breed dogs and the sixth (C(6)) to seventh (C(7)) cervical intervertebral disk space in the larger dogs. Following surgery, 99% of the dogs had resolution of cervical hyperesthesia and were able to ambulate unassisted. Seven (4%) dogs required a second surgery; four of these were large-breed dogs.

Animals↗
PubMed1993

Thyroxine-responsive unilateral forelimb lameness and generalized neuromuscular disease in four hypothyroid dogs.

Four dogs were examined because of unilateral forelimb lameness. For all dogs, results of physical examination, including complete neurologic examination, were unremarkable except for vague, intermittent signs of pain upon deep palpation of the affected limb. During electromyography, insertional activity, fibrillation potentials, and positive sharp waves were recorded symmetrically from all major muscle groups. Generalized neuromyopathy was diagnosed. All dogs were determined to be thyroid deficient, and L-thyroxine supplementation was initiated. The lameness resolved within 2 months in all dogs. During follow-up electromyography, abnormalities were not recorded from 3 of the dogs and were less severe in the fourth. Thyroxine supplementation was discontinued in 2 dogs, and lameness redeveloped. Lameness again resolved when supplementation was reinstituted.

Animals↗