peer reviewed | Myeloperoxidase (MPO) is a specific enzyme of neutrophil azurophilic granules with a strong oxidative activity. Thanks to a radioimmunoassay of equine myeloperoxidase, the authors have observed a significantly higher plasma level of MPO in horses operated for strangulation obstruction of the large intestine (n = 6) than in horses suffering from a non-strangulating displacement of the large intestine (n = 9). For the 2 groups, 3 phases were distinguished: reception (P1), intensive care (P2) and terminal phase (P3). The mean peak values of MPO for these phases were 121.6 ng/mL (P1), 168.6 ng/mL (P2), and 107.0 ng/mL (P3) for the non-strangulating group, and 242.6 ng/mL (P1); 426.0 ng/mL (P2), and 379.5 ng/mL (P3) for the strangulation group. The variations of the mean peak values of plasma MPO were significantly different between the 2 groups and between the different phases. A significant increase of the least square means of MPO was observed between P1 and P2. A significant decrease of the least square means of the number of circulating leukocytes was observed between P1 and P3. Polymorphonuclear neutrophil activation could play a major role in the pathogenesis of acute abdominal disease and endotoxic shock.

Up to 60% of cases of equine colitis have no known cause. To improve understanding of the causes of acute colitis in horses, we hypothesized that Clostridium perfringens producing enterotoxin (CPE) and/or beta2 toxin (CPB2) are common and important causes of severe colitis in horses and/or that C. perfringens producing an as-yet-undescribed cytotoxin may also cause colitis in horses. Fecal samples from 55 horses (43 adults, 12 foals) with clinical evidence of colitis were evaluated by culture for the presence of Clostridium difficile, C. perfringens, and Salmonella. Feces were also examined by enzyme-linked immunosorbent assay (ELISA) for C. difficile A/B toxins and C. perfringens alpha toxin (CPA), beta2 toxin (CPB2), and enterotoxin (CPE). Five C. perfringens isolates per sample were genotyped for the following genes: cpa, cpb, cpb2 consensus, cpb2 atypical, cpe (enterotoxin), etx (epsilon toxin), itx (iota toxin), netB (necrotic enteritis toxin B), and tpeL (large C. perfringens cytotoxin). The supernatants of these isolates were also evaluated for toxicity for an equine cell line. All fecal samples were negative for Salmonella. Clostridium perfringens and C. difficile were isolated from 40% and 5.4% of samples, respectively. All fecal samples were negative for CPE. Clostridium perfringens CPA and CPB2 toxins were detected in 14.5% and 7.2% of fecal samples, respectively, all of which were culture-positive for C. perfringens. No isolates were cpe, etx, netB, or tpeL gene-positive. Atypical cpb2 and consensus cpb2 genes were identified in 15 (13.6%) and 4 (3.6%) of 110 isolates, respectively. All equine C. perfringens isolates showed far milder cytotoxicity effects than a CPB-producing positive control, although cpb2-positive isolates were slightly but significantly more cytotoxic than negative isolates. Based on this studied population, we were unable to confirm our hypothesis that CPE and CPB2-producing C. perfringens are common in horses with colitis in Ontario and we failed to identify cytotoxic activity in vitro in the type A isolates recovered.

High molecular weight (MW) hyaluronate (HA) is an integral part of synovial fluid (SF), regulating many important physiologic and pathophysiologic mechanisms. Many of its effects depend on, or are reflected in, the concentration and MW of HA. High-performance liquid chromatography was used to assess simultaneously the concentration and MW of HA in SF obtained from horses with various arthritides: acute traumatic arthritis; chronic traumatic arthritis, including degenerative joint disease (DJD); and infectious arthritis. The size-exclusion column was calibrated, using appropriate HA concentration and MW standards, before the high-performance liquid chromatographic assays of the SF samples. Calibration of the column disclosed that the maximal limit for MW estimation of HA was around 3 million. In control joints, MW of HA ranged from 2 to 3 X 10(6) (mean 2.5 X 10(6)) and did not differ significantly from MW of HA in SF from horses with acute or chronic traumatic arthritis (mean 2 x 10(6); range 1.5 to 3 x 10(6)). Interestingly, a small amount of HA of moderately high MW (approx 1 to 1.5 x 10(6)) was detected in chromatograms of SF from infected joints. This degree of polymerization of SF HA was significantly (P < 0.01) lower, compared with that for control joints. There was no difference in mean (+/- SD) concentration of HA between control joints and joints with acute or chronic traumatic arthritis (0.33 +/- 0.12 g/L vs 0.18 +/- 0.03 g/L or 0.23 +/- 0.12 g/L), indicating that SF HA concentration probably should not be used as a diagnostic marker for the condition. However, the SF HA concentration was significantly (P < 0.01) lower in joints with infectious arthritis (0.07 +/- 0.03 g/L) and in the joints with radiographic evidence of DJD (0.12 +/- 0.01 g/L), compared with control joints.

Sixteen healthy ponies were inoculated IV with Ehrlichia risticii-infected P388D1 mouse monocytes. Of the 16 ponies, 15 developed clinical signs of equine ehrlichial colitis. Twenty-four hours after onset of fever (rectal temperature > 38.8 degrees C), 7 ponies were treated with 25 mg of erythromycin stearate/kg of body weight and 10 mg of rifampin/kg, given orally every 12 hours for 5 days. The remaining 8 ill ponies served as nontreated controls. All ponies were observed for progression of clinical signs typical of equine ehrlichial colitis. Within 12 hours of initiation of treatment, 4 of the 7 treated ponies had rectal temperature < 38.4 C and, within 24 hours, 6 of the 7 ponies had rectal temperature < 38.3C. In contrast, all control ponies had rectal temperature > 39.2 C at 24 hours (P < 0.05). Of the 7 treated ponies, 4 no longer had signs of mental depression after the second day of treatment, and only 1 of the 7 ponies had mild signs of depression after the third day of treatment. In contrast, control ponies had high mental depression score during the observation period (P < 0.05). Feed intake improved in ponies of the treatment group, with feed intake of 4 of the 7 ponies returning to normal; the other 3 ponies were only mildly anorectic by the second day of treatment. Control ponies progressively decreased their feed intake during the observation period (P < 0.05). One control pony and 2 treated ponies developed diarrhea before the treatment/observation period began. Only 1 treated pony developed diarrhea after treatment began. Of the 8 control ponies, 7 developed diarrhea. Profound decrease in borborygmal sounds with silent periods lasting longer than 3 minutes was observed in 7 of the 8 control ponies. Only 1 of the 7 treated ponies had such profound decrease in borborygmi (P < 0.05). The decrease in borborygmal sounds progressed in the control ponies during the observation period. None of the treated ponies continued to have decreased borborygmi after treatment day 2 (P < 0.05). Of the 8 control ponies, 2 were euthanatized; all treated ponies survived. In survivors, signs lasted 8 to 17 (mean, 10) days in control ponies but only 1 to 5 (mean, 2.9) days in treated ponies.

Nineteen purebred Beagles of various ages (4, 5, 13,and 47 weeks) were inoculated with North American Trypanosoma cruzi isolates obtained from an opossum (Tc-O), armadillo (Tc-A), or a dog (Tc-D). Dogs were grouped on the basis of clinical outcome of infection. During the acute stage of disease, dogs of group 1 (n = 7 inoculated with Tc-O or Tc-A) died or were euthanatized because of the severity of disease. Dogs of group 2 (n = 5 inoculated with Tc-O or Tc-A) developed acute disease, but survived to develop chronic disease. Dogs of group 3 (n = 7Tc-D-inoculated dogs) developed neither acute nor chronic disease. Dogs of group 4 (n = 4-2 dogs 13 weeks old and 2 dogs 47 weeks old) served as noninoculated controls. Clinical signs associated with severe acute myocarditis developed in dogs of groups 1 and 2 between postinoculation day (PID) 15 and 28. Generalized lymphadenopathy and lymphocytosis were observed in all dogs of groups 1, 2, and 3 between PID 14 and 17. Serum alanine transaminase and aspartate transaminase activities and urea nitrogen concentration were high, and glucose concentration was low prior to death of dogs in group 1. Serum activities of isoenzymes of creatine kinase were significantly (P < 0.05) high in only 1 dog (group 1), whereas serum lactate dehydrogenase isoenzyme activities were not significantly high in any dog. Parasitemia was detected by examination of thick blood smears as early as PID 3, peaked by PID 17 in most dogs, and was not detected by PID 33 in dogs of groups 1 and 2. Parasitemia was documented by blood culture results in dogs of groups 2 and 3 at various times throughout the study. Dogs infected at an older age generally had lesser degree of parasitemia and higher survival rate than did dogs infected at a younger age. Dogs of group 2 did not manifest clinical signs of disease for 27 to 120 days prior to onset of chronic disease. Ventricular-based arrhythmias and exercise intolerance developed in all dogs of group 2 at various times by PID 120. Two dogs developed signs of biventricular heart failure.

acute Sarcocystis cruzi infection in calves (exper.), hematologic studies support claim that anemia is an extravascular hemolytic event, probably with immunologic basis; coagulation studies indicate that endothelial S. cruzi schizonts may cause endothelial damage, resulting in coagulation abnormalities that include disseminated intravascular coagulation

Strongylus vulgaris, massive infections of nonimmune and immune ponies, pathogenesis characterized, blood chemical and peritoneal fluid values as possible diagnostic aids

Twenty-three clinically normal Beagles were inoculated with North American Trypanosoma cruzi isolates from an opossum (Tc-O), an armadillo (Tc-A), or a dog (Te-D). The dogs were grouped according to the clinical outcome of inoculation. Group 1 consisted of 7 dogs inoculated with Tc-O or Tc-A that died or were euthanatized during acute stages of disease. Group 2 consisted of 5 dogs inoculated with Tc-O or Tc-A, that also developed acute disease, but survived to develop chronic disease. Group 3 consisted of 7 dogs inoculated with Tc-D neither developed acute nor chronic disease. Group 4 consisted of 4 dogs and served as noninoculated controls. In group 1, the gross lesions were diffusely pale myocardiums with right ventricular enlargement, hepatomegaly, and a moderate amount of modified transudate in the abdominal cavity. Severe diffuse granulomatous myocarditis with large numbers of pseudocysts and minimal fibrosis characterized the tissues from all cardiac chambers and septum. The lesions were most severe in the right atrium and ventricle. Mild multifocal myositis and pseudocysts were observed in skeletal muscles and smooth muscles of the urinary bladder and small intestine. Multifocal encephalitis and pseudocysts were in the cerebral cortex, cerebellum, and brain stem. In group 2, the gross lesions were biventricular enlargement and thinning of the ventricular free walls. The right ventricle contained the most severe microscopic changes. There were mild multifocal interstitial lymphohistiocytic cellular infiltrates, perivasculitis, and marked fibrosis in all areas of the myocardium. Mild myositis and multifocal encephalitis were seen in the skeletal muscles and brains. Pseudocysts were not observed in any tissues. In group 3, there was mild biventricular dilatation, minimal inflammation with fibrosis in cardiac tissues, and a multifocal myositis in most skeletal muscles. Multifocal encephalitis was seen in the brain stem. Pseudocysts were not observed in any tissues. Lesions were not found in group 4. Our results indicated heterogeneity between North American T cruzi isolates in lesion development in dogs, and there appeared to be a temporal relationship between acute and chronic trypanosomiasis in Tc-O- and Tc-A-inoculated dogs and the 3 phases of Chagas disease in human beings.

Six adult specific-pathogen-free cats were inoculated intraperitoneally with a cell culture-adapted strain of feline infectious peritonitis virus. Plasma samples were evaluated for antithrombin-III (AT-III) activities at post-inoculation days (PID) 0,4, and 11 and at termination on PID 16 (1 cat) or 21 (5 cats). Other hemostatic values evaluated were activated partial thromboplastin times, pro-thrombin times, thrombin times, fibrinogen, platelet counts, and fibrin/fibrinogen degradation products. Antithrombin-III activity remained within normal or above normal range (89 to 246%) in all cats, with the exception of one cat on Pid 4, 11, and 16 or 21 was 98, 162, and 130%, respectively. On PID 4 and 16 or 21, results of coagulation screening tests indicated that all cats had disseminated intravascular coagulation. Histologically, cats also had severe fibrinonecrotizing thrombovasculitis.

We evaluated the efficacy of buparvaquone in eliminating infection with Babesia equi of European origin in carrier horses and in splenectomized horses with experimentally induced acute infection. When administered at the rate of 5 mg/kg of body weight, IV, 4 times at 48-hour intervals, buparvaquone prompted rapid abatement of parasitemia. However, secondary and tertiary recrudescent parasitemias invariably returned with establishment of the carrier state. Buparvaquone, at the dosage evaluated, had transitory therapeutic efficacy against acute B equi infection in splenectomized horses, but was unable alone to clear carrier infection.