Tylosin-responsive chronic diarrhea in dogs

Fourteen dogs had shown chronic or intermittent diarrhea for more than 1 year. Diarrhea had been successfully treated with tylosin for at least 6 months but recurred when treatment was withdrawn on at least 2 occasions. Tylosin-responsive diarrhea (TRD) affects typically middle-aged, large-breed dogs and clinical signs indicate that TRD affects both the small and large intestine. Treatment with tylosin eliminated diarrhea in all dogs within 3 days and in most dogs within 24 hours. Tylosin administration controlled diarrhea in all dogs, but after it was discontinued, diarrhea reappeared in 12 (85.7%) of 14 dogs within 30 days. Prednisone given for 3 days did not completely resolve diarrhea. Probiotic Lactobacillus rhamnosus GG did not prevent the relapse of diarrhea in any of 9 dogs so treated. The etiology of TRD, a likely form of antibiotic-responsive diarrhea (ARD) is unclear. The following reasons for chronic diarrhea were excluded or found to be unlikely: parasites, exocrine pancreatic insufficiency, inflammatory bowel disease, small intestinal bacterial overgrowth, enteropathogenic bacteria (Salmonella spp., Campylobacter spp., Yersinia spp., or Lawsoni intracellularis), and Clostridium perfringens enterotoxin and Clostridium difficile A toxin. A possible etiologic factor is a specific enteropathogenic organism that is a common resident in the canine gastrointestinal tract and is sensitive to tylosin but difficult to eradicate. Additional studies are required to identify the specific cause of TRD.     

Polycythemia in dogs with chronic hypoxic pulmonary disease

BackgroundProlonged tissue hypoxia caused by chronic pulmonary disease is commonly regarded as an important mechanism in the development of secondary polycythemia, but little clinical data are available to support this hypothesis.ObjectiveTo study the prevalence and severity of erythrocytosis accompanying chronic hypoxic pulmonary disease in dogs.AnimalsForty‐seven dogs with hypoxic chronic pulmonary disease, 27 dogs with nonhypoxic chronic pulmonary disease, and 60 healthy controls.MethodsDogs with chronic pulmonary disease and chronic hypoxemia (partial pressure of arterial oxygen [PaO₂] < 80 mm Hg on at least 2 arterial blood gas measurements a minimum of 1 month apart) were identified retrospectively from patient records. Association between arterial oxygen and red blood cell parameters was analyzed using Pearson''s correlation coefficients and multivariable linear regression analysis.ResultsRed blood cell parameters measured at the end of the hypoxemia period were within the laboratory reference range in most dogs. In chronically hypoxemic dogs, hematocrit (Hct) was increased in 4/47 (8.5%; 95% confidence interval [CI], 0‐17) dogs, erythrocyte count (Erytr) was increased in 12/47 (26%; 95%CI, 13‐38) dogs and hemoglobin concentration (Hb) was increased in 3/47 (6.4%; 95%CI, 0‐14) dogs. No marked polycythemia (Hct ≥65%) was noted in any of the dogs. Red blood cell parameters were not associated with the severity of hypoxemia (correlation to PaO₂: Erytr, r = −.14; Hb, r = −.21; Hct, r = −.14; P > .05 for all).Conclusions and Clinical ImportancePolycythemia is uncommon, and usually mild if present, in dogs with chronic hypoxia caused by pulmonary disease.     

Circulating autoantibodies in dogs with chronic liver disease

Circulating autoantibodies are important diagnostic markers in human liver disease. Antinuclear antibodies, smooth muscle antibodies and liver membrane antibodies are characteristic of human autoimmune chronic active hepatitis, while antimitochondrial antibodies are most frequently found in primary biliary cirrhosis. The role of these autoantibodies in the pathogenesis and course of these diseases is not known, but they are routinely measured in order to discriminate between different liver diseases. This, in turn, helps to predict the response to different kinds of treatment. The present study reports the occurrence of circulating autoantibodies in sera of dogs with different forms of chronic hepatitis and cirrhosis, and in dogs with other liver diseases, such as acute hepatitis, liver degeneration and tumours. The results indicate several differences compared to the autoantibody patterns in human liver disease.     

Upregulation of toll-like receptors in chronic enteropathies in dogs

BACKGROUND: Inflammatory bowel disease (IBD) is thought to result from a dysregulated interaction between the host immune system and commensal microflora. Toll-like receptors (TLRs) recognize microbe-associated molecular patterns (MAMPs), but their role in enteropathies in dogs is unknown. HYPOTHESIS: That there is a dysregulation of TLRs recognizing bacterial MAMPs in dogs with IBD. ANIMALS: Sixteen healthy beagles and 12 dogs with steroid-treated (ST) and 23 dogs with food-responsive (FR) diarrhea. METHODS: Prospective, observational study. mRNA expression of canine TLR2, 4, and 9 was evaluated by quantitative real-time RT-PCR in duodenal and colonic biopsies obtained before and after standard therapy. Samples from control dogs were taken at necropsy, with additional biopsies of stomach, jejunum, ileum, and mesenteric lymph node in 6 dogs. RESULTS: There were significant differences (P< or = .017) in expression of TLR2, 4, and 9 between the 6 sampled locations in healthy control dogs (lymph node > small intestine > or = colon). Before therapy, ST expressed more mRNA than control dogs for all 3 receptors (P < .05). There were no significant differences between pretreatment and posttreatment values, even though 32/35 dogs improved clinically. No associations were found when comparing receptor mRNA expression with either histology or clinical activity scores. CONCLUSIONS AND CLINICAL IMPORTANCE: Bacteria-responsive TLR2, 4, and 9 are upregulated in duodenal and colonic mucosa in IBD. This might lead to increased inflammation through interaction with the commensal flora. The absence of significant changes after therapy despite clinical improvement might point toward the existence of a genetic predisposition to IBD as described in human IBD.     

C-reactive protein concentration in dogs with chronic valvular disease

The purpose of the study reported here was to determine whether dogs with chronic valvular disease have increased plasma C-reactive protein concentration, compared with that in clinically normal dogs. Blood was collected from 47 dogs with physical and echocardiographic evidence of chronic valvular disease and from 20 healthy controls. C-reactive protein concentration was determined with a commercial canine C-reactive protein enzyme immunoassay. Compared with controls, dogs with chronic valvular disease had higher plasma concentration of C-reactive protein (median 2.17 microg/mL [range, 0.86-33.8 microg/mL]) versus 1.43 microg/mL [range, 0.84-4.99 microg/mL]; P < .001). C-reactive protein concentration was not related to the presence of congestive heart failure or murmur grade. The results of this study suggest that increased concentration of C-reactive protein is found in dogs with chronic valvular disease.     

Hemostatic biomarkers in dogs with chronic congestive heart failure

BACKGROUND: Chronic congestive heart failure (CHF) in humans is associated with abnormal hemostasis, and abnormalities in hemostatic biomarkers carry a poor prognosis. Alterations in hemostatic pathways can be involved in the pathogenesis of CHF in dogs, and microthrombosis in the myocardium could contribute to increased mortality. HYPOTHESIS: That plasma concentration or activity of hemostatic biomarkers is altered in dogs with CHF and that these factors predict mortality. ANIMALS: Thirty-four dogs with CHF caused by either dilated cardiomyopathy (DCM, n=14) or degenerative valvular disease (CDVD, n=20) compared with 23 healthy age-matched control dogs were included in this study. Dogs with CHF were recruited from 2 referral cardiology clinics, and control dogs were owned by friends or colleagues of the investigators. METHODS: Clinical examination and echocardiography were performed in all dogs. Plasma fibrinogen and D-dimer concentrations, antithrombin and protein C activity, and thrombin-antithrombin complex (TAT) were measured in all dogs. RESULTS: Dogs with CHF had significantly higher fibrinogen (P = .04), D-dimer (P = .002), and TAT concentration (P < .0001), lower antithrombin (P < .0001) and protein C activity (P < .001) compared with control dogs. None of the hemostatic biomarkers were associated with risk of death. CONCLUSIONS AND CLINICAL IMPORTANCE: There is evidence of a procoagulant state in dogs with CHF. The lack of predictive value for survival might be due to the small number of dogs examined. Further studies are necessary to investigate the presence and importance of microthrombosis in dogs with CHF.     

Effects of castration on chronic bacterial prostatitis in dogs

An Escherichia coli bacterial prostatitis was experimentally induced in dogs to determine the effect of castration on chronic bacterial prostatitis. Two weeks after instillation of bacteria directly into the prostate gland, 17 of 22 adult mixed-breed male dogs had positive urine or prostatic fluid cultures or both. Seven of the 17 dogs were randomly chosen to be castrated, and 10 of the 17 served as sham-operated controls. At weekly intervals, urine was obtained from 17 dogs for aerobic microbiologic culturing. At each week, dogs with no bacterial growth in the cultured urine had prostatic fluid collected for aerobic microbiologic culture. Dogs with negative urine, prostatic fluid, and prostatic tissue needle biopsy culture results at week 7 were euthanatized. For remaining dogs, weekly cultures were continued until the dogs were euthanatized at week 12. None of the 7 castrated dogs and 6 of the 10 dogs subject to sham operation had prostatic infection at the time of necropsy. The castrated dogs had a mean infection duration of 4.2 weeks, which was statistically shorter than the 9.5-week mean duration of infection in the sham-operated controls. Cultures of prostatic tissue obtained immediately after euthanasia correlated 100% with urine and prostatic fluid cultures taken before euthanasia. All of the 6 dogs with positive prostatic cultures at termination had moderate to marked lymphoplasmacytic chronic prostatitis. The 11 dogs that were not infected at the end of the study had normal to moderate lymphoplasmacytic chronic prostatitis on histologic examination.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of P-wave dispersion in healthy dogs,dogs with chronic valvular disease and dogs with disturbances of supraventricular conduction

Background

P-wave dispersion (P_d) is a new ECG index used in human cardiology and veterinary medicine. It is defined as the difference between the maximum and the minimum P-wave duration recorded from multiple different ECG leads. So far no studies were performed assessing the importance of P-wave dispersion in dogs.

Methods

The current study was aimed at determining proper value of P_d in healthy dogs (group I), dogs with chronic valvular disease (group II) and dogs with disturbances of supraventricular conduction (group III). The tests were carried out in 53 healthy dogs, 23 dogs with chronic valvular disease and 12 dogs with disturbances of supraventricular conduction of various breeds, sexes and body weight from 1,5 to 80 kg, aged between 0,5 and 17 years, submitted to the ECG examination. ECG was acquired in dogs in a standing position with BTL SD-8 electrocardiographic device and analyzed once the recording was enlarged. P-wave duration was calculated in 9 ECG leads (I, II, III, aVR, aVL, aVF, V1, V2, V4) from 5 cardiac cycles.

Results

The proper P-wave dispersion in healthy dogs was determined at up to 24 ms. P-wave dispersion was statistically significant increased (p < 0.01) in dogs with chronic valvular disease and dogs with disturbances of supraventricular conduction. In dogs with the atrial enlargement the P-wave dispersion is also higher than in healthy dogs, although no significant correlation between the size of left atria and Pd was noticed (p = 0.1, r = 0,17).

Conclusions

The P-wave dispersion is a constant index in healthy dogs, that is why it can be used for evaluating P wave change in dogs with chronic valvular disease and in dogs with disturbances of supraventricular conduction.     

Quantitative assessment of urea generation and elimination in healthy dogs and in dogs with chronic kidney disease

Background: Kinetic assessment of urea, the main end product of protein metabolism, could serve to assess protein catabolism in dogs with chronic kidney disease (CKD). Protein malnutrition and catabolism are poorly documented in CKD and they often are neglected clinically because of a lack of appropriate evaluation tools. Hypothesis: Generation and excretion of urea are altered in dogs with CKD. Animals: Nine dogs with spontaneous CKD (IRIS stages 2–4) and 5 healthy research dogs. Methods: Endogenous renal clearance (Cl_renal) of urea and creatinine was measured first. Exogenous plasma clearance (Cl_plasma, total body clearance) of the 2 markers then was determined by an IV infusion of urea (250–1,000 mg/kg over 20 minutes) and an IV bolus of creatinine (40 mg/kg). Extrarenal clearance (Cl_extra) was defined as the difference between Cl_plasma and Cl_renal. Endogenous urea generation was computed assuming steady‐state conditions. Results: Median Cl_renal and Cl_extra of urea were 2.17 and 0.21 mL/min/kg in healthy dogs and 0.37 and 0.28 mL/min/kg in CKD dogs. The proportion of urea cleared by extrarenal route was markedly higher in dogs with glomerular filtration rate <1 mL/kg/min than in normal dogs, reaching up to 85% of the total clearance. A comparable pattern was observed for creatinine excretion, except in 1 dog, Cl_extra remained <20% of Cl_plasma. Conclusion: Extrarenal pathways of urea excretion are predominant in dogs with advanced CKD and justify exploring adjunctive therapies based on enteric nitrogen excretion in dogs. A trend toward increased urea generation may indicate increased catabolism in advanced CKD.     

Quantification of mucin gene expression in tracheobronchial epithelium of healthy dogs and dogs with chronic bronchitis

OBJECTIVE: To develop a real-time PCR assay for the quantification of mucin gene expression in tracheobronchial brushing specimens from dogs and compare mucin gene expression in specimens from dogs with naturally occurring chronic bronchitis with that in specimens from healthy dogs. ANIMALS: 7 healthy dogs and 5 dogs with chronic bronchitis. PROCEDURES: Primers that were designed to span the predicted intron-exon boundaries of a canine MUC5AC-like gene were used to develop a real-time PCR assay for quantification of expression of that gene. Total mRNA was isolated from tracheobronchial brushing specimens obtained from dogs with and without bronchitis during anesthesia; MUC5AC-like gene expression in those samples was quantified by use of the real-time PCR assay. RESULTS: The PCR assay was sensitive and specific for the target sequence, the predicted amino acid sequence of which had greatest homology with human, porcine, and rat MUC5AC. The assay was able to quantify the target over a wide dynamic range. Dogs with chronic bronchitis had a 3.0-fold increase in the quantity of MUC5AC-like mRNA, compared with healthy dogs. CONCLUSIONS AND CLINICAL RELEVANCE: The ability to measure mucin gene expression from tracheobronchial brushing specimens collected from client-owned dogs during routine bronchoscopy should prove to be a useful tool for the study of bronchitis in dogs and expand the usefulness of airway inflammation in dogs as a model for bronchitis in humans.