Comparison of pathophysiologic changes in the lungs of calves challenge exposed with Escherichia coli-derived endotoxin and Pasteurella haemolytica, alone or in combination

Pulmonary responses to intratracheal challenge exposure with Pasteurella haemolytica, with or without Escherichia coli-derived endotoxin, E coli endotoxin alone, or saline solution were compared in anesthetized, mechanically ventilated neonatal calves. Baseline values for dynamic compliance, total pulmonary resistance, functional residual capacity, arterial blood gas tensions, hemogram, leukogram, and systemic and pulmonary arterial pressures were recorded for each calf. After baseline data were obtained, calves were challenge exposed with logarithmic-growth phase P haemolytica organisms with or without E coli endotoxin, E coli endotoxin alone, or saline solution (0.9% NaCl). Physiologic data were obtained immediately after challenge exposure and at various intervals over the next 6 hours. Calves challenge exposed with P haemolytica alone developed sever hypoxemia, had increased alveolar-arterial oxygen difference and threefold increases in total pulmonary resistance, became hypercarbic, had decreased functional residual capacity, and developed systemic hypotension without change in pulmonary arterial pressure. At necropsy, these calves had extensive multifocal areas of necrohemorrhagic and purulent pneumonia. Ratio of extravascular lung water to lung dry weight was not significantly increased in lung specimens obtained from calves challenge exposed with P haemolytica, but ratio of lung wet weight to dry weight was increased, indicating that increased lung wet weight was attributable largely to increased solids and not to fluid alone. (Extravascular lung water measurement excludes fluid from the vascular compartment.) Intratracheal challenge exposure with endotoxin failed to alter lung function and caused minor changes in lung structure consisting of focal areas of hemorrhage and edema.(ABSTRACT TRUNCATED AT 250 WORDS)     

Heartworm in dogs in Canada in 1991

In late November 1991, 1883 clinics in Canada were sent a questionnaire to assess the status of Dirofilaria immitis in dogs in 1991 and there was a 60.0% response. There were 344,031 dogs tested for heart-worm (HW), 627 were found infected and the prevalence of HW infection was 0.18%. There were 417 dogs with HW in Ontario, 116 in Manitoba, 38 in Quebec, 53 in British Columbia, three in Alberta, and one in Nova Scotia. In British Columbia, all of the infected dogs but one were from the Okanagan valley which, as from 1991, is a new focus of infection in Canada. Most dogs with HW had not been on preventive medication in 1990, and the prevalence among dogs tested and unprotected was 0.59%. That prevalence was considerably higher in endemic areas. Companion dogs, over three years of age and maintained primarily outdoors in rural areas, were most frequently infected. One cat was diagnosed with D. immitis and 33 dogs had Dipetalonema reconditium.     

Combined Streptomycin-Isoniazid-Rifampin Therapy in the Treatment of Johne's Disease in a Goat

Johne's disease (paratuberculosis) is an insidious, invariably fatal, chronic disease of ruminants. An increasing role for the goat as a companion animal as well as its commercial use stimulated interest in attempting to treat Johne's disease in this species. The disease tends to differ both clinically and pathologically in goats compared to cattle because the former species often has less severe intestinal involvement. It was, therefore, speculated that response to therapy may differ between cattle and goats. In addition, the combination drug regime of isoniazid, rifampin and streptomycin, widely accepted for human mycobacterial infections, has not been previously employed for treatment of Mycobacterium paratuberculosis. The clinical course and pathological findings of a case of naturally occurring Johne's disease subsequent to a combined drug regime of isoniazid, rifampin and streptomycin is discussed.     

Risk factors for Thoroughbred racehorse fatality in jump starts in Victoria, Australia (1989-2004)

REASONS FOR PERFORMING STUDY: The risk of fatality is greater in jump than in flat racing in Victoria, Australia. This is the first study to identify risk factors specific to jump starts in Victoria. OBJECTIVE: To identify risk factors for fatality of Thoroughbred racehorses in jump starts on all racecourses in Victoria, Australia between 1989 and 2004. METHODS: Fatalities comprised all horses that died during or immediately after a jump (hurdle or steeplechase) race or official jump trial and all horses that were subjected to euthanasia within 24 h of an event in which an injury was sustained. The retrospective study involved 191 case starts and 2324 control starts. Univariable and multivariable backward stepwise logistic regression was used to identify risk factors for fatality at any one start. A multiple level model was used with racecourse included as a random effect. RESULTS: In the final multivariable model, the duration of the racing career of the horse, the number of flat, hurdle and steeple starts accumulated in the 60 days prior to the case or control start, the number of flat and jump starts accumulated over the racing career, if the horse had had a start between 1 and 14 days prior to the case or control start, the type of jump race (hurdle or steeple), the calendar year of the start and the location of the racecourse were associated with fatality. CONCLUSIONS: The findings highlight the need to investigate further the differences between hurdle and steeplechase events and the adverse effect of prolonged prior flat racing careers on the risk of fatality in jump starts. POTENTIAL RELEVANCE: This is the first study to examine risk factors for fatality in jump starts in Victoria. The results should shape the development of interventions to reduce the risk in jump starts in the future.     

Asymptomatic anomalous pulmonary veins in a Siberian Husky

A 2-year-old, neutered male Siberian Husky presented with depression, weight loss and an inability to prehend food and water. Cerebrospinal fluid was collected under general anaesthesia prior to euthanasia. The elevated white cell count comprised mostly mononuclear cells. Histological changes within the brain were variable and multifocal. Non-suppurative meningitis secondary to lymphoma was diagnosed. At necropsy, abnormal venous drainage of the right cranial and middle lung lobes was found. A dilated major pulmonary vein from these lobes passed across the lateral aspect of the right caudal lung lobe prior to entering the heart, and subpleural veins from the affected lobes were enlarged and tortuous. These vascular abnormalities were considered incidental. There were no apparent congenital abnormalities of the heart and the animal's clinical signs were related to lymphoma of the brain.     

γ-Amino Butyric Acid Control of Arginine Vasopressin Release from the Ewe Hypothalamus In Vitro: Sensitivity to Oestradiol

The present study aims to ascertain the influence of gamma-amino butyric acid (GABA)(A or B) receptors on arginine vasopressin (AVP) release in vitro and determine whether E(2) modulates GABA-AVP interaction. Within 10 min of ewe killing, saggital midline hypothalamic slices (from the anterior preoptic area to the mediobasal hypothalamus along with the median eminence, 2-mm thick, two per ewe) were dissected, placed in oxygenated minimum essential media (MEM)-alpha at 4 degrees C and within 2 h were singly perifused at 37 degrees C with oxygenated MEM-alpha (pH 7.4; flow rate 0.15 ml/min), either with or without E(2) (24 pg/ml). After 4-h equilibration, 10-min fractions were collected for 4 h interposed with a 10-min exposure at 60 min to a specific GABA(A or B) receptor agonist or antagonist at various doses (0.1-10 mm). GABA(A) (muscimol; no E(2), n = 7 perifusion chambers, with E(2), n = 11) or GABA(B) (baclofen; no E(2), n = 8, with E(2), n = 15) agonists (10 mm) did not influence AVP concentrations. However, AVP release increased (p < 0.05) 20-30 min after exposure to 10 mm GABA(A or B) antagonists (bicuculline, no E(2), n = 7: from 4.6 +/- 0.7 to 33.0 +/- 0.4, with E(2), n = 17: from 11.9 +/- 1.4 to 32.8 +/- 6.0; CGP52432, with E(2), n = 14: from 14.0 +/- 2.6 to 28.8 +/- 3.9 pg/ml). At the end of the collection period, hypothalamic slices responded to KCl (100 mm) with AVP efflux (p < 0.05). GABA(B) but not GABA(A) antagonist-stimulated AVP release was enhanced in the presence of E(2). In summary, AVP release is under the inhibitory influence of GABA input with further potentiation by E(2) through GABA(B) receptors in vitro.