Electrophoretic fractionation of creatine kinase isoenzymes and macroenzymes in clinically healthy dogs and cats and preliminary evaluation in central neurologic disease

Background: Information about the electrophoretic distribution of CK‐MM, CK‐MB, and CK‐BB, serum creatine kinase (CK) isoenzymes that are indicators of skeletal muscle, cardiac muscle, and brain lesions, respectively, and CK macroenzymes (macro‐CK1 and macro‐CK2) in dogs and cats with and without central neurologic disease is scant and equivocal. Objectives: The objectives of this study were to describe the electrophoretic distribution of CK isoenzymes and macroenzymes in healthy dogs and cats and to provide a preliminary assessment of the utility of CK enzymatic electrophoresis in dogs and cats with central neurologic disease. Methods: Electrophoretic separation of serum CK isoenzymes and macroenzymes was performed on freeze‐thawed serum samples from 20 healthy dogs and 3 dogs with central neurologic disease and from 14 healthy cats and 6 cats with neurologic feline infectious peritonitis (FIP). Electrophoretic separation was also performed on supernatants of homogenized brain, skeletal muscle, and cardiac muscle from both species, to assess the tissue distribution of isoenyzmes in dogs and cats. Results: CK‐MM was the predominant isoenzyme in the serum of healthy dogs and cats, followed by macro‐CK2 and CK‐BB in dogs and by both macroenzymes in cats. In dogs, CK‐MB was essentially absent from both serum and homogenized hearts. CK‐BB increased in dogs with neurologic disease. In cats, CK‐BB was essentially absent from serum, but was present in brain homogenates. Two of 6 cats with FIP had increased macro‐CK1 and increased CK‐BB activity. Conclusions: This study identified the electophoretic distribution of CK isoenzymes and macroenzymes of dogs and cats and provided encouraging data about the possible use of CK‐BB as a biomarker for canine neurologic disorders, but not for FIP.     

Serum ionized calcium in dogs with chronic renal failure and metabolic acidosis

BACKGROUND: Chronic renal failure (CRF) is a common disease in dogs, and many metabolic disorders can be observed, including metabolic acidosis and calcium and phosphorus disturbances. Acidosis may change the ionized calcium (i-Ca) fraction, usually increasing its concentration. OBJECTIVE: In this study we evaluated the influence of acidosis on the serum concentration of i-Ca in dogs with CRF and metabolic acidosis. METHODS: Dogs were studied in 2 groups: group I (control group = 40 clinically normal dogs) and group II (25 dogs with CRF and metabolic acidosis). Serum i-Ca was measured by an ion-selective electrode method; other biochemical analytes were measured using routine methods. RESULTS: The i-Ca concentration was significantly lower in dogs in group II than in group I; 56% of the dogs in group II were hypocalcemic. Hypocalcemia was observed in only 8% of dogs in group II when based on total calcium (t-Ca) concentration. No correlation between pH and i-Ca concentration was observed. A slight but significant correlation was detected between i-Ca and serum phosphorus concentration (r = -.284; P = .022), as well as between serum t-Ca and i-Ca concentration (r = .497; P < .0001). CONCLUSION: The i-Ca concentration in dogs with CRF and metabolic acidosis varied widely from that of t-Ca, showing the importance of determining the biologically active form of calcium. Metabolic acidosis did not influence the increase in i-Ca concentration, so other factors besides acidosis in CRF might alter the i-Ca fraction, such as hyperphosphatemia and other compounds that may form complexes with calcium.     

Ventilatory and Metabolic Compensation in Dogs With Acid-Base Disturbances

Ventilatory and metabolic compensation to acid-base disturbances is reviewed. The mechanisms for compensation as well as the values obtained from several studies using normal dogs and dogs with experimentally induced diseases are provided. Compensation is not the same in dogs and human beings. Dogs have a better ability to adapt to most respiratory disorders, and human beings adapt better to metabolic acidosis. In metabolic alkalosis and chronic respiratory acidosis there is no difference in compensation between these species. Ventilatory compensation for metabolic disorders in dogs is the same whether they have metabolic acidosis or metabolic alkalosis, whereas metabolic compensation in respiratory disturbances is less effective in acidosis. Values for the expected changes in PCO₂ in dogs with metabolic acidosis and metabolic alkalosis, and for bicarbonate concentration (HCO₃-) in dogs with acute and chronic respiratory alkalosis and acidosis are presented.     

Retrospective evaluation of the prognostic utility of plasma lactate concentration,base deficit,pH, and anion gap in canine and feline emergency patients

Objective

To determine the association of plasma lactate concentration, pH, base deficit (BD), and anion gap (AG) in dogs and cats on presentation to an emergency room with outcome, and to compare the prognostic significance of hyperlactatemia with a concurrent metabolic acidosis with that of hyperlactatemia and a normal metabolic acid–base balance.

Design

Retrospective study.

Setting

University teaching hospital.

Animals

Five hundred sixty‐six dogs and 185 cats that had venous blood gas analysis performed.

Interventions

None.

Measurements and Main Results

Medical records were reviewed for plasma lactate concentrations, electrolyte concentrations, and acid–base parameters obtained on emergency room admission, clinical diagnosis, and in‐hospital mortality. The primary outcome measure was all‐cause mortality for the hospitalized visit. Median plasma lactate concentration and AG were higher, BD was more negative, and pH was lower, in non‐survivor dogs and cats. The prevalence of hyperlactatemia was 53% in dogs and 30% in cats. Lactic acidosis was present in 42% and 80% of hyperlactatemic dogs and cats, respectively. Multivariate regression analyses revealed that plasma lactate concentration, BD, and pH, but not AG, were independent predictors of mortality in dogs, and that only plasma lactate concentration was an independent predictor of mortality in cats. Mortality was highest for animals with lactic acidosis, at 59.8% in dogs and 49% in cats. Mortality in dogs with lactic acidosis was significantly higher than dogs with hyperlactatemia and a normal acid–base status (P < 0.0001).

Conclusions

The presence and magnitude of hyperlactatemia on presentation to the emergency room may help identify dogs and cats with high likelihood of in‐hospital mortality, and the presence of lactic acidosis specifically may help identify dogs with yet higher risk of in‐hospital mortality.     

Increased Serum Alanine Aminotransferase Activity Associated With Muscle Necrosis in the Dog

Serum activity of alanine aminotransferase (ALT) was consistently increased in dogs with canine X-linked muscular dystrophy (CXMD), a primary myopathy characterized by profound and on-going skeletal muscle necrosis. In order to determine whether the ALT was of liver origin, serum activity of creatine kinase (CK), aspartate aminotransferase (AST), ALT, and sorbitol dehydrogenase (SDH) obtained from dystrophic dogs was compared with enzyme activity present in clinically normal dogs. In dystrophic dogs at all ages tested, serum activity of CK, AST, and ALT was increased, and significant increases were present in dogs four weeks or older. In contrast, SDH activity in dystrophic dogs was not statistically different from values in clinically normal dogs. Ultrastructural examination of liver tissue revealed no evidence of hepatic degeneration in dystrophic dogs. It was concluded that increased serum activity of ALT in the dog may be associated with severe skeletal muscle degeneration, without concurrent hepatocellular necrosis.     

Serum Erythropoietin Concentrations Measured by Radioimmunoassay in Normal, Polycythemic, and Anemic Dogs and Cats

Serum erythropoietin (Epo) concentrations were measured by radioimmunoassay (RIA) in normal, polycythemic, and anemic dogs and cats. The serum Epo concentration in normal dogs ( n = 25) ranged from 7 to 37 mU/mL (median, 20 mU/mL); and in normal cats ( n = 11) ranged from 9 to 38 mU/mL (median, 18 mU/mL). Polycythemic animals (PCV < 55% in dogs, > 45% in cats) were classified as those with primary (polycythemia vera), secondary, or polycythemia of uncertain etiology. Dogs with polycythemia vera (PV, n = 8) had a median serum Epo concentration in the normal range (17 mU/mL); cats with PV ( n = 7) also had a median serum Epo concentration that was within the normal range (10 mU/mL). In the category of secondary polycythemias, dogs ( n = 7) (median, 30.7 mU/mL) and cats ( n = 2) had normal Epo concentrations. The median serum Epoconcentration was significantly decreased ( P > .05) in dogs with PV compared with dogs with secondary polycythemias. The median serum Epo concentrations in dogs ( n = 13) and cats ( n = 5) with anemias not due to chronic renal disease were significantly increased ( P > .05) compared with normal dogs and cats. In cats with anemias due to chronic renal disease ( n = 5) the median serum Epo concentration was not significantly different from normal cats. The measurement of the serum EPO concentration may be useful in assessment of anemia or polycythemia but the overlap of values with the normal range in all groups evaluated limit its diagnostic use.     

Ureterocolonlc Anastomosis in Ten Dogs with Transitional Cell Carcinoma

Ureterocolonic anastomosis (UCA) was performed in 10 dogs with transitional cell carcinoma of the urinary bladder trigone or the urethra, or both. All grossly visible tumor was excised. All of the dogs recovered from anesthesia and surgery and had anal continence with no urine leakage. One dog died of undetermined causes 7 days after surgery. Nine dogs survived 1 to 5 months. The owners of eight of the dogs considered their dog's quality of life to be acceptable. Four dogs were euthanatized because of neurologic disease, three of which also had nausea and vomiting. The neurologic and gastrointestinal signs may have been caused by hyperammonemia, metabolic acidosis, and uremia. Blood ammonia levels were elevated in two dogs with neurologic signs. Hyperchloremic metabolic acidosis that was reversible with bicarbonate therapy was diagnosed in five dogs. All of the dogs were azotemic because of intestinal recycling of urea. Serum creatinine concentrations increased in four dogs after surgery. Drug-induced renal disease may have developed in two dogs. Pyelonephritis developed in five kidneys, two of which had outflow obstruction and two had bilateral hydroureteronephrosis before the UCA. In this small number of dogs, surgical excision of transitional cell carcinoma was not curative with six dogs having confirmed metastatic lesions at the time of death.     

Cardiac troponin I is elevated in dogs and cats with azotaemia renal failure and in dogs with non-cardiac systemic disease

OBJECTIVE: To determine if dogs and cats with renal failure, or other severe non-cardiac disease, and no antemortem evidence of cardiac disease on basic clinical evaluation, have elevated levels of cardiac troponin I (cTnI). DESIGN: Cross-sectional study using 56 dogs and 14 cats with primary non-cardiac disease (39 dogs with azotaemic renal failure, 14 cats with azotaemic renal failure, 17 dogs with non-cardiac systemic disease); 7/25 dogs and 6/14 cats had murmurs detected on physical examination. Serum or heparinised plasma was collected and analysed for cTnI. RESULTS: Cardiac troponin I concentrations were elevated above reference intervals in 70% of dogs and 70% of cats with azotaemic renal failure and in 70% of dogs with a variety of systemic non-cardiac diseases. Cardiac troponin I concentrations did not correlate with the degree of azotaemia, presence of murmurs, hypertension or type of non-cardiac illness. CONCLUSIONS: Cardiac troponin I concentration is often elevated in dogs and cats with azotaemic renal failure and in dogs with other systemic non-cardiac illness, suggesting that these conditions often result in clinically inapparent myocardial injury or possibly altered elimination of cTnI.     

北京地区犬猫弓形虫病流行病学调查

为初步调查北京地区犬猫弓形虫感染的流病学特征,用酶联免疫吸附试验(ELISA)方法检测2010年5月至2011年4月采集的家养犬猫、流浪猫血清样本.其中,家养犬血清样本1876份,家养猫血清样本561份,检测发现,家养犬动物弓形虫IgG抗体阳性率24.9％;家养猫弓形虫IgG阳性率21.2％;同时检测流浪猫样本201份,阳性率30.3％.家养犬弓形虫血清抗体阳性率不同季节间差异显著(P＜0.05),夏季最高,为30.0％,家养猫弓形虫血清抗体阳性率不同季节间无显著差异(P＞0.05).不同性别犬猫弓形虫血清抗体阳性率无显著差异(P＞0.05).随着年龄增长,犬猫弓形虫抗体阳性率均有明显增长.对25例弓形虫抗体阳性家养犬病例和37例弓形虫抗体阳性家养猫病例进行了回访调查,结果发现,该62例动物主人的弓形虫检测结果均为阴性.     

Myopathy and alterations in serum 3-methylhistidine in dogs with liver disease

Liver disease can influence the metabolism of various other organs. Regarding the influence of liver diseases on muscles, only a few studies done on people exist. The goal of our study was to investigate the influence of liver diseases on muscles in dogs. Twenty-eight dogs with different liver diseases were investigated in this study. The diagnosis of muscle alteration was based on electromyography (EMG), creatine kinase serum activity, 3-methylhistidine serum concentration and a muscle biopsy in some cases. Our results suggest that liver diseases in dogs can be accompanied with muscle alteration. 3-Methylhistidine serum concentration as a new parameter for muscle destruction in dogs was significantly increased compared to clinical healthy dogs and was comparable to those concentrations in dogs with histologically confirmed myopathy of different types. The differentiation of the liver diseases into severe hepatitis, moderate hepatitis and liver tumours showed a significant elevation of 3-methylhistidine serum concentration in cases of liver tumours (P=0.03) and a tendency in cases of severe hepatitis (P=0.07). Based on our study we can conclude that liver diseases have an influence on muscles in dogs and 3-methylhistidine could be a useful parameter for muscle destruction.     

Acid-base balance of cats with chronic renal failure: effect of deterioration in renal function

In a previous cross-sectional study of feline chronic renal failure (CRF), metabolic acidosis was identified in 52.6 per cent of animals with severe renal failure (plasma creatinine concentration >400 micromol/litre). The aim of this longitudinal study was to determine whether metabolic acidosis preceded or accompanied a deterioration in renal function in cats with CRF. Data were analysed from 55 cats with CRF that had been followed longitudinally for at least four months. Twenty-one cases showed deterioration in renal function over the period of the study, as evidenced by significant rises in their plasma creatinine concentrations and decreases in bodyweight. In five of the 21 cases, acidaemia accompanied the deterioration in renal function. Only one of these cats had evidence of metabolic acidosis before renal function deterioration. One other case developed metabolic acidosis without a rise in plasma creatinine concentration. These data suggest that biochemical evidence of metabolic acidosis does not generally occur until late in the course of feline CRF.     

Fructosamine

Fructosamines are glycated serum proteins that, depending on their life span, reflect glycemic control over the previous 2 to 3 weeks. The nitroblue tetrazolium reduction method adapted to autoanalysis appeared to be a practical means to assay fructosamine quickly, economically, and accurately. The upper limit of the reference range is 374 μmol/L in dogs (95% percentile) and 340 μmol/L in cats (95% percentile). Newly diagnosed diabetic dogs and cats that had not undergone previous insulin therapy had significantly higher fructosamine concentrations than nondiabetic animals. In diabetic dogs that were receiving insulin therapy, the fructosamine test reflected the glycemic state far more accurately than did individual blood glucose measurements. Animals with satisfactory metabolic control revealed fructosamine concentrations within the reference range, whereas fructosamine concentrations above 400 μmol/L indicated insufficient metabolic control. On the basis of fructosamine concentrations, cats with a transitory hyperglycemia and cats with diabetes mellitus were differentiated. The fructosamine test is a valuable parameter for the diagnosis and metabolic control of diabetes mellitus in dogs and cats.     

Mixed acid-base disorders

Mixed acid-base disturbances are combinations of two or more primary acid-base disturbances. Mixed acid-base disturbances may be suspected on the basis of findings obtained from the medical history, physical examination, serum electrolytes and chemistries, and anion gap. The history, physical examination, and serum biochemical profile may reveal disease processes commonly associated with acid-base disturbances. Changes in serum total CO2, serum potassium and chloride concentrations, or increased anion gap may provide clues to the existence of acid-base disorders. Blood gas analysis is usually required to confirm mixed acid-base disorders. To identify mixed acid-base disorders, blood gas analysis is used to identify primary acid-base disturbance and determine if an appropriate compensatory response has developed. Inappropriate compensatory responses (inadequate or excessive) are evidence of a mixed respiratory and metabolic disorder. The anion gap is also of value in detecting mixed acid-base disturbances. In high anion gap metabolic acidosis, the change in the anion gap should approximate the change in serum bicarbonate. Absence of this relationship should prompt consideration of a mixed metabolic acid-base disorder. Finding an elevated anion gap, regardless of serum bicarbonate concentration, suggests metabolic acidosis. In some instances, elevated anion gap is the only evidence of metabolic acidosis. In patients with hyperchloremic metabolic acidosis, increases in the serum chloride concentration should approximate the reduction in the serum bicarbonate concentration. Significant alterations from this relationship also indicate that a mixed metabolic disorder may be present. In treatment of mixed acid-base disorders, careful consideration should be given to the potential impact of therapeutically altering one acid-base disorder without correcting others.     

Suspected renal tubular acidosis in two dogs

Clinical signs of hyperventilation, muscle weakness and lethargy were recognised in a one-year-old female Bichon Frise and a three-year-old male Poodle. One dog was also hyperexcitable and pyrexic. The diagnosis of renal tubular acidosis was confirmed by demonstrating the tendency to an elevated urine pH, a low blood pH and low blood bicarbonate level, and by eliminating other causes of metabolic acidosis. Both dogs were treated with oral sodium bicarbonate resulting in improvement in their clinical condition and a return to near normal blood pH and bicarbonate levels.     

Characterization and treatment of acid-base and renal defects due to urethral obstruction in cats

In 23 cats, urinary obstruction of 24 to 48 hours' duration caused marked azotemia, hyperphosphatemia, hyperkalemia, and metabolic acidosis. The metabolic acidosis was a consistent finding and was severe in all cats (venous pH, 7.11 +/- 0.09). Serum sodium and chloride were normal. Glycosuria was found in 17 (74%) of the cats. There was no clear difference in blood pH, serum chemical values, or electrolyte concentrations between cats obstructed 24 hours and those obstructed 48 hours or longer. At a mean of 8.4 hours after relief of obstruction, acid-base status was corrected to normal, using fluid replacement and sodium bicarbonate therapy. Blood urea nitrogen serum creatinine, and serum inorganic phosphorus improved significantly (P less than 0.01) at a mean of 19.5 hours after treatment. Variation in azotemia after fluid replacement suggested variable decreases in glomerular filtration rate after relief of obstruction. Hypokalemia occasionally developed after relief of obstruction during the postobstructive diuresis. It was concluded that fluid and electrolyte therapy must be regulated in response to the postobstructive diuresis, to ensure proper medical management.     

Suspected renal tubular acidosis in two dogs

Clinical signs of hyperventilation, muscle weakness and lethargy were recognised in a one-year-old female Bichon Frise and a three-year-old male Poodle. One dog was also hyperexcitable and pyrexic. The diagnosis of renal tubular acidosis was confirmed by demonstrating the tendency to an elevated urine pH, a low blood pH and low blood bicarbonate level, and by eliminating other causes of metabolic acidosis. Both dogs were treated with oral sodium bicarbonate resulting in improvement in their clinical condition and a return to near normal blood pH and bicarbonate levels.     

Detection of biofilm formation and nanobacteria under long-term cell culture conditions in serum samples of cattle,goats, cats,and dogs

OBJECTIVE: To determine the prevalence of biofilm formation under long-term cell culture conditions in serum samples of dairy cattle, goats, cats, and dogs, and to determine whether there is an association between nanobacteria and biofilm formation. SAMPLE POPULATION: Serum samples of clinically normal animals (313 dairy cattle, 48 goats, 140 dogs, and 44 cats) and animals with various medical conditions (60 dogs and 116 cats). PROCEDURE: Serum was incubated under cell culture conditions and observed for biofilm formation by use of light microscopy, electron microscopy, and spectroscopy. A polymerase chain reaction assay was developed to identify 16S rRNA gene sequences of nanobacteria. RESULTS: Biofilm formation developed in serum samples of 304 of 313 (97%) cattle, 44 of 48 (92%) goats, 44 of 44 (100%) cats, and 126 of 140 (90%) dogs. Prevalence of serum samples with positive results for biofilm formation was not significantly different between cats or dogs with and without medical conditions associated with pathologic extraskeletal calcification processes. Scanning electron microscopy and spectroscopy of biofilm samples revealed small coccoid particles consisting mainly of calcium and phosphate. Polymerase chain reaction assay failed to amplify sequences of nanobacteria. CONCLUSIONS AND CLINICAL RELEVANCE: Under long-term cell culture conditions, biofilm made up of aggregates of calcium and phosphate crystals does form in serum samples of clinically normal dairy cattle, goats, cats, and dogs. Disease, however, does not predispose to biofilm formation in serum samples of dogs and cats. Our findings did not support the existence of nanobacteria in serum samples of cattle, goats, cats, and dogs.     

Comparative studies on serum arginase and transaminases in hepatic necrosis in various species of domestic animals

Serum concentrations of arginase, glutamic pyruvic transaminase (SGPT) and glutamic oxaloacetic transaminase (SGOT) in dogs, cats, horses, cattle, sheep and pigs were determined before and after oral administration of CCl(4) at doses known to cause hepatic necrosis. Following CCl(4) administration, serum concentration of arginase and SGOT increased to a level of diagnostic significance in all animals. SGPT increased markedly in dogs and cats and marginally in 1 of 3 cattle and 2 of 3 pigs. In the surviving animals, the serum concentration of arginase returned to normal range much earlier than SGPT or SGOT. Based on the CCl(4) experimental toxicity results of this study, an elevated level of serum arginase would appear to be a reliable indicator of hepatic necrosis in both small and large animals whereas SGPT would be a reliable indicator of hepatic necrosis only in dogs and cats.     

Occurrence, clinical features and outcome of canine pancreatitis (80 cases)

Medical records of 80 dogs diagnosed with acute pancreatitis during a 4-year period were evaluated regarding history, breed predilection, clinical signs and additional examination findings. Cases were selected if compatible clinical symptoms, increased serum activity of amylase or lipase and morphologic evidence of pancreatitis by ultrasonography, laparotomy or necropsy were all present. Like in other studies, neutered dogs had an increased risk of developing acute pancreatitis. Although breed predilection was consistent with earlier reports, some notable differences were also observed. Apart from Dachshunds, Poodles, Cocker Spaniels and Fox Terriers, the sled dogs (Laikas, Alaskan Malamutes) also demonstrated a higher risk for pancreatitis according to our results. Concurrent diseases occurred in 56 dogs (70%), diabetes mellitus (n = 29, 36%) being the most common. Clinical signs of acute pancreatitis were similar to those observed in other studies. The study group represented a dog population with severe acute pancreatitis, having a relatively high mortality rate (40%) compared to data of the literature. Breed, age, gender, neutering and body condition had no significant association with the outcome. Hypothermia (p = 0.0413) and metabolic acidosis (p = 0.0063) correlated significantly with poor prognosis and may serve as valuable markers for severity assessment in canine acute pancreatitis.     

Beta cell and insulin antibodies in treated and untreated diabetic cats

Beta cell and insulin antibodies are involved in the pathogenesis of diabetes in human patients. Beta cell antibodies have also been found in about 50% of newly diagnosed diabetic dogs. This study's objective was to examine these antibodies' role in feline diabetes. The serum of 26 newly diagnosed untreated diabetic cats, 29 cats on insulin therapy, 30 cats with diseases other than diabetes, and 30 healthy cats was examined for beta cell and insulin antibodies. For beta cell antibody testing, purified beta cells from a radiation-induced transplantable rat insulinoma were used. Serum from cats in which anti-beta cell antibodies were induced by injecting a purified beta cell suspension subcutaneously was used as a positive control. Following incubation with test sera, fluorescein-labeled anti-cat immunoglobulins were used to visualize binding between the beta cells and cat gamma globulins. Each serum was tested on two different tumor preparations. For the detection of insulin antibodies, a charcoal separation method was used. It was found that none of the healthy cats, none of the newly diagnosed, untreated diabetic cats and none of the cats with diseases other than diabetes had antibodies against beta cells or against endogenous insulin. Four diabetic cats (14%) that had been treated with different insulin preparations had insulin antibodies.It is concluded that immune-mediated processes are not causing diabetes in the cat. Further studies are needed to evaluate if antibodies directed against exogenous insulin alter the response of diabetic cats to insulin.