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PubMed1978

Serum complement level in dogs with neoplastic disease.

The hemolytic reactivity of complement obtained from 119 dogs with and without cancer has been determined. Dogs with cancer were divided retrospectively, into 2 groups--dogs with lymphosarcoma (37) and dogs with malignant neoplasms other than lymphosarcoma (31). Normal dogs (21) served as a control group. Also, for comparison, complement reactivity was determined on sera from a 4th group composed of a limited number (30) of dogs with serious systemic illnesses other than neoplasia. There was no significant difference among means for hemolytic complement reactivity of the 4 groups. However, when the dispersion of hemolytic complement values within each group of abnormal dogs was compared with that of normal dogs by variance ratio testing, it was found that all abnormal groups had highly significant greater variances than did normal dogs.

Animals↗
PubMed1995

Decline in glucose metabolism in the brain in neuronal ceroid lipofuscinosis (NCL) in English setter--evidence by positron emission tomography (PET).

Positron emission tomography scans were performed on brains of homozygous and heterozygous English setters with neuronal ceroid-lipofuscinosis (NCL) from 13 months of age to 24-25 months of age for homozygous dogs and to 38 months for heterozygous dogs, respectively. After iv injection of 18F-fluorodeoxyglucose (FDG), 7 coronal brain scans as well as sequential arterial blood samplings were performed for 45 min under pentobarbital anesthesia. From these data, three different functional images (DAR (standardized uptake value), FDG uptake (fractional uptake) and glucose uptake) were reconstructed and quantitatively analysed. In the age range from 13 to 15 months, glucose images were comparable for both homozygous and heterozygous dogs, so that no differentiation was possible between healthy and diseased dogs on the basis of PET findings. Between 18 and 24 months of age, a drastic decline in glucose metabolism was observed in homozygous dogs, while the decline in glucose utilization was very mild in this period for heterozygous dogs. Furthermore, in PET scans, cerebral atrophy and ventricular enlargement were clearly shown in homozygous dogs. Consequently at the age from 20 to 24 months, a clear differential diagnosis between healthy (heterozygous) and diseased (homozygous) dogs became possible even if the clinical symptoms were still not clear in the latter. We conclude that the biochemical alterations in the brain in canine NCL occurs and progresses very rapidly in the last quarter of their lives.

Aging↗
PubMedDate not supplied

Recognition and diagnosis of lysosomal storage diseases in the cat and dog.

Lysosomal storage diseases are rare, inherited disorders caused by the deficiency of 1 or more enzymes within the lysosomes of cells or by the deficiency of an activating protein or cofactor necessary for enzyme activity. The enzyme deficiency leads to a catabolic blockade and subsequent accumulation of storage material, and this in turn leads, albeit indirectly, to a wide array of clinical signs. Many features of storage diseases make them difficult to recognize and diagnose. In this review, we summarize the clinical features of these diseases and outline the steps required to confirm a diagnosis.

Animals↗
PubMed2002

Quantitation of reticulated platelets in healthy dogs and in nonthrombocytopenic dogs with clinical disease.

BACKGROUND: Thrombocytopenia is a common disorder in dogs and development of an objective diagnostic assay to measure platelets newly released from bone marrow into the blood would provide a noninvasive way to predict megakaryocytopoiesis. Reticulated platelets are newly released platelets with increased concentrations of RNA that can be detected by flow cytometric analysis of blood stained with thiazole orange (TO). OBJECTIVE: The goals of this study were to establish a reproducible method to quantitate reticulated platelets in dogs, to establish a reference interval for reticulated platelet percentages in healthy dogs, and to determine whether the percentage of reticulated platelets was nonspecifically increased in nonthrombocytopenic dogs with clinical disease. METHODS: Blood samples were obtained from healthy dogs and from nonthrombocytopenic dogs presented for a variety of disorders. An aliquot of whole blood was stained with TO and a phycoerythrin-labeled monoclonal antibody to platelet CD61, then analyzed by flow cytometry. RESULTS: The coefficients of variation were 7.8% to 15.6% (intra-assay precision) and 6.1% to 19.5% (interassay precision). Overnight storage for 18 to 26 hours, under variable conditions, resulted in an increase in the percentage of platelets staining with TO. The reference interval for reticulated platelets in the healthy control group was 0-4.3% (0-12,095/microL). No significant differences were found in the mean percentage of reticulated platelets or absolute concentration of reticulated platelets between control and affected dogs. CONCLUSIONS: These studies demonstrate a reliable, noninvasive diagnostic assay for measurement of reticulated platelets in whole blood and provide a baseline for assessment of the clinical utility of the assay.

Animals↗
PubMed1993

Granulomatous hepatitis in dogs: nine cases (1987-1990).

Granulomatous hepatitis (GH) is an uncommon histopathologic diagnosis in dogs. On the basis of clinical reports, fungal infections appear to be the most common cause of GH in dogs, but many other potential causes have been identified. The medical records and histopathologic findings for 9 dogs with GH were reviewed to identify additional specific causes of GH in dogs. Diseases associated with GH included intestinal lymphangiectasia (n = 2), lymphosarcoma (n = 1), histiocytosis (n = 1), dirofilariasis (n = 1), and histoplasmosis (n = 1). In 1 dog, no other disease process was identified. Of the remaining 2 dogs, 1 had concurrent granulomatous pneumonitis of unknown cause, and the other had periportal hepatitis and temporal muscle wasting. All 9 dogs with GH had clinical evidence of liver disease, such as hepatomegaly, icterus, and ascites, or had high serum alkaline phosphatase and alanine aminotransferase activity. Because of the wide variety of potential causes of GH in dogs, an accurate diagnosis should be sought so that appropriate treatment can be chosen and an accurate prognosis given.

Animals↗
PubMedDate not supplied

Plasma taurine concentrations in normal dogs and in dogs with heart disease.

Plasma taurine concentrations were determined in 76 dogs with dilated cardiomyopathy (DCM), 28 dogs with acquired valvular disease (AVD), and 47 normal (control) dogs. The data were collected at 2 referral centers, The Animal Medical Center, New York, NY (AMC), and the University of California, Davis (UCD), and the studies were conducted independently. Different anticoagulants (sodium citrate at AMC and lithium heparin at UCD) were used to collect the plasma samples. Paired analysis of samples showed a significant difference in plasma taurine concentrations, depending on the anticoagulant used. Consequently, results from each clinic were analyzed separately. Plasma taurine concentrations were significantly higher in dogs with AVD (median, 133 nmol/mL; range, 25 to 229 nmol/mL) than in control dogs (median, 63 nmol/mL; range 44 to 224 nmol/mL) and dogs with DCM (median, 72 nmol/mL; range, 1 to 247 nmol/mL) at AMC (P < .001). The number of dogs with AVD at UCD was too small to draw meaningful conclusions. At UCD, the median plasma taurine concentration was 98 nmol/mL (range, 28-169 nmol/mL) in dogs with AVD, 75 nmol/mL (range, 0.1-184 nmol/mL) in dogs with DCM, and 88 nmol/mL (range 52-180 nmol/mL) in control dogs. There were no significant differences in plasma taurine concentrations between dogs with DCM and the control dogs at either hospital. Congestive heart failure and administration of cardiac medication had no significant effect on plasma taurine concentrations. Plasma taurine concentration was low (< 25 nmol/mL) in 17% (13/76) of the dogs with DCM. Seven of the 13 dogs with low plasma taurine concentrations were Cocker Spaniels or Golden Retrievers.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Usefulness of intraoperative ultrasonography for two dogs with spinal disease.

Intraoperative ultrasonography was performed during spinal surgery in two dogs. An extradural lesion was demonstrated by myelography in case 1, and an extradural tumor was found during surgery. Case 2 was diagnosed with a spinal subarachnoid cyst by myelography and magnetic resonance imaging. Ultrasonographically, pathologic conditions of the spinal canal or cord were adequately imaged during surgery in both cases. Intraoperative ultrasonography was a superior method that non-invasively revealed intradural and extradural conditions and thus constitutes a valuable diagnostic mean to ensure safe and precise spinal surgery.

Animals↗
PubMed1995

Intestinal permeability testing in dogs with diet-responsive intestinal disease.

Fifteen dogs with signs of small and, or, large bowel disease that responded clinically to an exclusion diet were studied, using differential sugar absorption as an objective parameter of the mucosal response to the diet. Intestinal permeability and function were assessed by determining the urinary excretion ratios of lactulose/rhamnose and xylose/3-O-methylglucose, respectively, following oral administration of a mixture of these four sugars. Five dogs, all retrievers, were tentatively diagnosed as having dietary hypersensitivity, based upon resolution of clinical signs and normalisation of high intestinal permeability following an exclusion diet and recurrence of signs (in four of five dogs) upon challenge with the original diet. The fifth dog did not become symptomatic when challenged, but intestinal permeability increased. The remaining 10 dogs were diagnosed as having food intolerance, based upon clinical improvement on an exclusion diet, relapse on challenge with their original diet, but lack of improvement in intestinal permeability. These findings suggest that a differential sugar absorption test may be useful to determine the reasons for clinical response to exclusion diets. Demonstration of increased intestinal permeability with subsequent normalisation following an exclusion diet may be useful in the diagnosis of dietary hypersensitivity, while persistent abnormalities in intestinal permeability are suggestive of underlying intestinal disease and food intolerance.

Analysis of Variance↗
PubMed1989

Spontaneous and induced arterial disease in the dog: pathology and pathogenesis.

The spontaneous arterial diseases of the dog relevant to safety assessment studies of drugs are the extramural coronary arteritis of Hartman, intramural coronary arteriosclerosis (with amyloid deposition) occurring in older dogs with cardiac disability, intramural arteriosclerosis without amyloid deposition in the left ventricle of dogs with congenital subaortic stenosis or in the right ventricle in dogs with severe pulmonic stenosis, and necrotizing polyarteritis (nodosa). Experimentally induced lesions include right atrial necrosis and arteritis produced by minoxidil and theobromine, extramural coronary arteritis produced by positive inotropic/vasodilator drugs, intramural coronary arteriosclerosis associated with decreased peripheral resistance and tachycardia induced by hypotensive drugs (including antihypertensive and positive inotropic/vasodilator agents), and intramural arteriosclerosis associated with rapid ventricular pacing. The pathogenesis of none of these lesions is known. The left ventricular subendocardial and papillary muscle intramural coronary arterial lesions are associated with hyperdynamic activity and, in the case of drugs and subaortic stenosis, the possibility of lowered perfusion pressure and tachycardia. This has led to the supposition that these are ischemic lesions, but the evidence available either does not support or refutes that conclusion since subendocardial coronary flow and perfusion pressure are adequate with pacing tachycardia and in toxicity trials. Necrotizing polyarteritis appears to be an immune mediated disease that may appear in genetically prone beagles when they are placed under the stresses of experimental manipulation and/or a new environment. Since the right atrial minoxidil lesion can also be produced by theobromine in dogs and minoxidil can cause a left atrial lesion in swine, it is neither species nor drug specific. Its cause, however, escapes us. There appears to be little in common between the extramural coronary artery Hartman lesion and that caused by positive inotropic/vasodilator drugs. Left ventricular subendocardial and papillary muscle intramural coronary arterial lesions induced by ventricular pacing at 250 beats/min for 2 months are generally similar to those seen in toxicity trials with peripheral vasodilator drugs that induce tachycardia in electrocardiograms exceeding 200 beats/min, although in acute pacing experiments subendocardial perfusion is adequate at these heart rates. Coronary artery autoregulation may be compromised or so destabilized by the drugs that episodes of underperfusion can account for these lesions.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMedDate not supplied

Localization of cathepsin K and tartrate-resistant acid phosphatase in synovium and cranial cruciate ligament in dogs with cruciate disease.

OBJECTIVE: To localize cathepsin K and tartrate-resistant acid phosphatase (TRAP) in synovium and cranial cruciate ligament (CCL) of dogs with cruciate disease. ANIMALS: Dogs (n=15) with cruciate disease and ruptured CCL, and 12 dogs with intact CCL. METHODS: Synovium and CCL were examined histologically and cells containing cathepsin K or TRAP were identified immunohistochemically and histochemically, respectively. RESULTS: Increased cellular localization of cathepsin K and TRAP was detected in synovium and ruptured CCL in dogs with cruciate disease, when compared with tissues from dogs with intact CCL. Inflammation of synovium with TRAP+ macrophage-like cells was seen in 73% of dogs with CCL disease, but was not seen in dogs with intact CCL. The presence of cathepsin K and TRAP protein in synovium and CCL tissues was significantly correlated in dogs with CCL rupture. CONCLUSION: Inflammation of the epiligament of ruptured CCL with cathepsin K+ and TRAP+ macrophage-like cells forms part of a similar, more generalized chronic inflammatory change within the periarticular tissues of the stifle of a large proportion of dogs with CCL rupture. CLINICAL RELEVANCE: Production of matrix-degrading enzymes by the synovium may induce progressive pathologic rupture of the CCL. Therefore, these collagenolytic pathways may offer a novel target for medical therapy of joint inflammation in canine patients with cruciate disease.

Acid Phosphatase↗
PubMed1990

Systemic lupus erythematosus in dogs: association to the major histocompatibility complex class I antigen DLA-A7.

The DLA-A,B antigens and the allotypes of the fourth complement component have been determined in German shepherd dogs suffering from systemic lupus erythematosus. We have typed 26 unrelated affected dogs, 11 animals of a three generation family, and 16 dogs of a colony with a high frequency of the disease. The results obtained from the 26 unrelated diseased dogs were compared to those determined in the 23 unaffected German shepherds. The antigen DLA-A7 was found to be predominant in the diseased group with a c2 = 11.02, Pc = 0.02, and a relative risk for the carriers of 11.93. The antigens DLA-A1 and DLA-B5 were negatively associated to the disease (c2 = 14.95, Pc = 0.001, and c2 = 17.16, P = 0.0008 respectively) and thus may be of protective nature. These data were further substantiated by the typing of the three generation family and the colony.

Animals↗
PubMed1990

Ocular manifestations of systemic disease in the dog and cat. Recent developments.

The number of canine and feline clinical diseases that may be manifested as ocular dysfunction continues to increase. Veterinarians are often presented with sick patients who also have eye disease. Conversely, animals are examined for eye disease that on closer inspection also have a systemic illness. A decision must be made; is there a relationship between the observed ocular and systemic problem, or are they separate morbid processes? If they are related, can the ocular signs be used to better define the systemic illness, chart its course, or establish a prognosis? It is hoped this article will aid the clinician in gaining a better perspective on the complex relationship between the eyes and systemic disease.

Animals↗