Galactose epimeraseless mutants of Salmonella typhimurium as live vaccines for calves.

The purpose of the study was to evaluate the safety and efficacy of a galactose epimeraseless mutant of Salmonella typhimurium administered as an oral vaccine to one week old calves and to investigate properties of galactose epimeraseless mutants which affect their virulence and immunogenicity. The galactose epimeraseless mutant S. typhimurium strain G30D caused diarrhea and fever in three calves to which it was administered orally at a dose of 10(10) organisms; all three calves died following challenge with virulent S. typhimurium ten days postvaccination. Mild illness developed in four calves vaccinated with a dose of 9 X 10(6) organisms and one of these calves survived challenge. Three unvaccinated calves died following challenge. The vaccine organism persisted in tissues and was shed for a prolonged period by calves which received 10(10) organisms. Studies of characteristics of galactose epimeraseless mutants of S. typhimurium showed that, in the presence of galactose, there is selection for secondary mutants which are galactose resistant. The studies indicate that galactose epimeraseless mutants of S. typhimurium are not good candidate live vaccine organisms for use in calves.     

Investigation of Caval Syndrome in Dogs Experimentally Infected With Dirofilaria immitis

Nine of 16 dogs inoculated with 200 infective heartworm larvae developed caval syndrome (CS) of heartworm disease (HWD). There was no difference between dogs that did and did not develop CS with regard to total heartworm burden, burden relative to body weight, or female heartworm burden, indicating that factors other than worm mass are involved in the pathogenesis of CS. Male dogs were twice as frequently affected as females, although this finding was not statistically significant. Dogs afflicted with CS exhibited radiographic, pathologic, and hemodynamic evidence of chronic HWD. In a model of single heartworm exposure, these findings strongly support the theory that CS develops due to retrograde migration of adult worms from the pulmonary arteries and right ventricle to the right atrium and venae cavae. Pulmonary artery pressures were dramatically and significantly greater in dogs with CS (60 +/- 18 torr) as compared to non-CS (30 +/- 4 torr) dogs with equal worm burdens.     

Interaction between Pasteurella haemolytica, sulfadiazine/trimethoprim, and bovine viral diarrhea virus

A study was designed to develop and define a sc tissue chamber as a suitable device for establishing a soft-tissue infection model in cattle and to use this model to study the interaction between Pasteurella haemolytica, sulfadiazine/trimethoprim, and bovine viral diarrhea virus (BVDV). Thermoplastic tissue chambers were implanted in the paralumbar fossae of 20 calves. At 35 days after implantation, calves were allotted to 4 groups of equal size and the calves in 2 groups were inoculated intratracheally with a New York-1 strain of BVDV. At 45 days after implantation, all chambers were inoculated with a 6-hour culture of P haemolytica serotype 1. Starting 36 hours after bacterial inoculation, sulfadiazine/trimethoprim was administered IV once a day to half of the virus-inoculated calves and to half of those calves that had not been exposed to virus. Inoculation of P haemolytica into tissue chambers resulted in the establishment of a localized soft-tissue infection, characteristic of pneumonic pasteurellosis. Despite the maintenance of chamber antimicrobial concentrations that exceeded minimal bactericidal concentrations established in vitro, the infections were not sterilized. This lack of efficacy was associated with decreased pH and increased protein concentrations in chamber fluids after inoculation. Infection with BVDV, which is thought to depress host defenses, had no effect on the response of P haemolytica to sulfadiazine/trimethoprim administration. Observation of responsive antibody titers, bacterial phagocytosis, and high leukocyte viability within P haemolytica-infected chambers documented functional host defenses within tissue chambers.     

Occurrence of 14 cases of bovine spongiform encephalopathy in a closed dairy herd

Fourteen cases of bovine spongiform encephalopathy (BSE) were diagnosed on the basis of clinical examination in a closed herd of British Friesian cows during a 9-month period from October 1987 until June 1988. The diagnosis was confirmed on histopathological examination of brain tissue from five of the six samples submitted. The main presenting clinical signs were of altered behaviour: apprehension, anxiety and hyperaesthesia. One cow was euthanized after a short period of recumbency; the remaining 13 cows were slaughtered on humane or economic grounds. No protein of animal origin had been fed to either heifers or cows in this herd during the past 5 years and there had been no direct contact with sheep. The epidemiology of BSE in this report suggests that, if the postulate of Morgan (1988) is correct, infection is ingested within the first 6 months of life and there then follows a 4-5-year period before clinical signs appear.     

Coccidial infection with Eimeria tenella and caecal defaecation in chicks.

1. The periodicity of caecal defaecation was investigated in chicks infected with Eimeria tenella. The birds were illuminated for 12 h/d (07.00-19.00) and faeces were collected at 3-h intervals for up to 21 d. 2. In uninfected birds caecal faeces were never collected during the dark period. During the periods 07.00-10.00 h, 10.00-13.00 h, 13.00-16.00 h and 16.00-19.00 h, caecal defaecation occurred on approximately 44, 19, 55 and 91% of the total number of days respectively. 3. In infected birds production of haemorrhagic caecal faeces began from between 90 and 156 h after infection and continued during both light and dark periods for between 12 and 48 h. After this period, no caecal faeces were observed for between 39 and 120 h. Normal caecal defaecation resumed from between 198 and 264 h.     

Clinical, echocardiographic, and electrocardiographic abnormalities in Boxers with cardiomyopathy and left ventricular systolic dysfunction: 48 cases (1985-2003)

OBJECTIVE: To identify clinical, echocardiographic, and electrocardiographic abnormalities in Boxers with cardiomyopathy and echocardiographic evidence of left ventricular systolic dysfunction. DESIGN: Retrospective study. ANIMALS: 48 mature Boxers. PROCEDURE: Medical records were reviewed for information on age; sex; physical examination findings; and results of electrocardiography, 24-hour ambulatory electrocardiography, thoracic radiography, and echocardiography. RESULTS: Mean age of the dogs was 6 years (range, 1 to 11 years).Twenty (42%) dogs had a systolic murmur, and 9 (19%) had ascites. Congestive heart failure was diagnosed in 24 (50%) dogs. Seventeen (35%) dogs had a history of syncope. Mean fractional shortening was 14.4% (range, 1% to 23%). Mean left ventricular systolic and diastolic diameters were 4.5 cm (range, 3 to 6.3 cm) and 5.3 cm (range, 3.9 to 7.4 cm), respectively. Twenty-eight (58%) dogs had a sinus rhythm with ventricular premature complexes (VPCs), and 20 had supraventricular arrhythmias (15 with atrial fibrillation and 5 with sinus rhythm and atrial premature complexes). Sixteen of the dogs with supraventricular arrhythmias also had occasional VPCs. Morphology of the VPCs seen on lead II ECGs was consistent with left bundle branch block in 25 dogs, right bundle branch block in 8, and both in 11. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that Boxers with cardiomyopathy and left ventricular dysfunction frequently have arrhythmias of supraventricular or ventricular origin. Whether ventricular dysfunction was preceded by electrical disturbances could not be determined from these data, and the natural history of myocardial disease in Boxers requires further study.