Metabolic responses to ammonium acetate infusion in exercising horses.

The relationship between elevated plasma ammonia (NH3) levels, fatigue development and muscle metabolism were examined in horses during a submaximal fatigue test. Eight Quarter Horse mares were intravenously infused prior to exercise with either sodium acetate (control) or ammonium acetate (AMINF), and exercised to fatigue on an 11% grade treadmill, carrying 27 kg of lead. Time to fatigue was not different (P greater than 0.05) between groups. Intramuscular NH3 and lactate increased (P less than 0.001) during exercise; however, the treatment did not (P greater than 0.05) affect either. A treatment by exercise interaction (P less than 0.01) occurred for plasma NH3. The reciprocal relationship between changes in plasma and intramuscular alanine (ala) and glutamate (glu) indicated activation of the glucose-alanine cycle. Plasma glutamine (gln) increased (P less than 0.001) during exercise; however intramuscular gln was not (P greater than 0.05) altered. The excretion of urea-N was depressed as a result of exercise while the orotic acid/creatinine ratio did not (P greater than 0.05) change. The amino acids and urinary metabolites were not (P greater than 0.05) affected by treatment. These results did not show any metabolic evidence for a role of increased plasma NH3 levels in fatigue development. However this study did provide insight into other aspects of nitrogen metabolism during exercise in the horse.     

Serum liver enzyme and histopathologic changes in calves with chronic and chronic-delayed Senecio jacobaea toxicosis.

Progressive changes in serum enzyme activity and liver histologic features were monitored in calves fed tansy ragwort (Senecio jacobaea)-contaminated pellets. The experiments were designed to simulate natural intoxicant ingestion conditions in relationship to the dose and duration of exposure to the toxic plant to correlate early laboratory diagnostic changes with the natural progression of the disease, thereby facilitating early diagnosis and intervention by veterinary clinicians. Eight calves were fed tansy ragwort and 4 additional calves served as controls. In group 1, 4 calves were continuously fed dried tansy ragwort mixed in a pelleted feed at a 5% concentration by dry weight until terminal liver disease developed. Serum liver enzyme (alkaline phosphatase, glutamate dehydrogenase, and gamma-glutamyltransferase) activities were monitored at weekly intervals in these calves and in the 2 controls. In group 2, 4 calves were fed the same contaminated feed for only 60 days, with return to normal feed for the duration of the trial. Two additional calves served as controls. Their liver enzyme activities were monitored every other week in conjunction with percutaneous liver biopsies. All 8 calves fed tansy ragwort-contaminated pellets developed terminal hepatopathy in either a chronic pattern (n = 6) or a chronic-delayed pattern (n = 2), with the onset of a moribund state or sudden death at 11 to 17 weeks and 27 to 51 weeks, respectively. The calves were euthanatized when classic terminal signs of hepatic encephalopathy first became evident. The clinicopathologic patterns of chronic and chronic-delayed toxicoses were typical of over 5,000 cases of field tansy toxicosis diagnosed at the diagnostic laboratory. Serum glutamate dehydrogenase was the first enzyme to increase in most animals, with a short-term increase to peak values followed by a rapid return to normal. This enzyme change was followed by increases in alkaline phosphatase and gamma-glutamyltransferase. Serum enzyme changes preceded development of recognizable histologic lesions. Vacuolar changes in hepatocyte nuclei, biliary hyperplasia, and fibrosis sequentially developed in liver biopsy specimens from each animal, whereas megalocytosis was not a predominant feature until necropsy. On the basis of our findings, we suggest that the optimal tests for diagnosis of pyrrolizidine alkaloid intoxication should consist of liver biopsy and determination of concurrent serum liver-enzyme activities.     

Polymorphism of the CD4 and CD5 differentiation antigens in cattle.

Monoclonal antibodies (mAbs) specific for bovine CD4 and CD5 antigens have been found to identify polymorphic determinants on these molecules. In the case of CD5, mAb IL-A67 recognises one allotypic form of the antigen while four other CD5-specific mAbs in the workshop (CC17, CC29, BLT-1 and 8C11) recognise a second allotype. The CD4-specific mAbs submitted to the workshop reacted with the cells of all animals tested. However, a further two mAbs (CC26 and IL-A18) specific for CD4 were found to react with cells only from about 85% of animals tested. Sequential immuno-precipitation experiments together with family studies showed that the allotypes of CD4 and CD5 are both inherited in a simple Mendelian manner and are co-dominantly expressed. One of the CD5 allotypes was not detected in Bos taurus animals while the gene frequency of the second allotype was only about 10% in the B. indicus animals tested. The gene frequency of the CD4 allotype detected by CC26 and IL-A18 was similar in the two sub-species.     

Cytogenetic analysis of a canine haemangioendothelioma: a case report.

An 8-year-old German Shepherd bitch developed a haemangioendothelioma in the mammary region. The cytogenetic characterization of the tumour cells revealed a chromosome number of 80 plus a double minute. Several aberrations were detected: trisomies 4, 35, and 38, a centric fusion 8/22 and a tandem translocation 9/23.     

Enterovirulence of enterotoxigenic Bacteroides fragilis in gnotobiotic pigs.

A porcine isolate of enterotoxigenic Bacteroides fragilis colonized the intestinal tract and caused watery, nonhemorrhagic diarrhea when given orally to 12, 1- to 2-day-old gnotobiotic pigs. Diarrhea occurred 2 to 3 days post-inoculation and continued throughout the 4 to 6 day post-inoculation period. Diarrheic pigs became mildly anorexic and dehydrated. They developed intestinal lesions characterized by swelling, vacuolation, and exfoliation of enterocytes, and crypt hyperplasia throughout the large intestine and, to a lesser extent, in the distal small intestine. Bacterial adherence to, or invasion of, the intestinal mucosa was not detected. A porcine isolate of nonenterotoxigenic B. fragilis was administered orally to six control pigs. The isolate colonized the intestinal tract, but the pigs did not develop clinical disease or intestinal lesions. The pathogenetic mechanism of the disease may involve mediation by a soluble enterotoxin (or toxins) elaborated by B. fragilis.     

Intestinal cellular reaction of cattle after infection by Fasciola hepatica]

Defence reactions of cattle against Fasciola hepatica take place not only in the liver but also on a prehepatic level. The aim of the present experiments is to identify and quantify the cellular response in the small intestine. Five groups of two bulls (Simmental x Red Holstein, 6 months old) were infected by oesophageal probe with metacercariae of F. hepatica (MC) according to two experimental procedures. Two groups of bulls served as controls. In the first experiment both infected groups received 1000 MC once or twice at an interval of five weeks. The intestinal tissue was taken before infection and 5, 10 and 19 weeks p.i., respectively 5 and 14 weeks p. reinf. (p.ri.). In the second experiment, three infected groups received 400, 2 x 400 MC (at an interval of five weeks) and 800 MC respectively. Biopsies were taken one week ante infectionem, 6, 11 and 19 weeks p.i., respectively 1, 6 and 14 weeks post reinfectionem (p. ri.). The biopsies of the small intestine were prepared for histology and the tissue sections stained as follows: Astra blue for mucosal mast cells (MMC), Lendrum for eosinophils (EOS) and Periodic Acid Schiff (PAS) for goblet cells (GC). The density of the three cell populations in the mucosa was determined microscopically and quantified. In both experiments the density of the MMC and EOS increased with each reinfection and depended on the infectious dose. There was no significant variation of the GC-numbers. The described intestinal cellular reactions suggest a participation of the small intestinal wall in the immunity against the common liver fluke.     

Effects of treatment with aspirin or aspirin/dipyridamole combination in heartworm-negative, heartworm-infected, and embolized heartworm-infected dogs.

To determine the drug dose required to inhibit platelet reactivity by at least 50%, 2 drug regimens were evaluated in heartworm-negative, heartworm-infected, and heartworm-infected dogs embolized with dead heartworms. Aspirin, or a combination of aspirin and dipyridamole, were administered to 2 groups of Beagles (n = 5 each) for 5 to 9 days; a third group of 5 Beagles served as nontreated controls. For heartworm-negative dogs, mean (+/- SD) aspirin dosage that inhibited collagen-induced platelet reactivity by at least 50% was 6 (+/- 2) mg/kg of body weight given once daily. The aspirin/diphridamole combination dosage was 1 mg of each drug/kg given every 12 hours. All dogs (n = 15) were implanted with 7 adult heartworms each and remedicated (or not treated) beginning at 21 days after heartworm implantation. In heartworm-infected dogs, mean aspirin dosage required to inhibit collagen-induced platelet reactivity greater than or equal to 50% was 10 (+/- 6) mg/kg. Mean dosage of aspirin/dipyridamole combination was 1.6 +/- (0.5) mg of each drug/kg given every 12 hours. When platelet reactivity in response to collagen was determined to be inhibited by at least 50% in all medicated dogs, each dog (n = 15) was embolized with 7 dead adult heartworms to mimic heartworm adulticidal treatment. Platelet reactivity was monitored for 21 days after treatment, and drug dose was adjusted to maintain platelet inhibition by at least 50%. In embolized dogs, mean aspirin dosage was 17 (+/- 14) mg/kg given once daily. Mean dosage of the aspirin/dipyridamole combination was 2.8 (+/- 1.3) mg of each drug/kg given every 12 hours. All dogs (n = 15) were euthanatized 21 days after heartworm embolization. Each lung lobe was evaluated for severity of lesions and presence of organized or fibrinous thrombi. Lesion severity in the aspirin- and aspirin/dipyridamole-treated dogs was not significantly different from that in control dogs.     

An abattoir survey of pneumonia and pleuritis in slaughter weight swine from 9 selected herds. IV. Bacteriological findings in chronic pneumonic lesions.

A total of 855 pig lungs were collected at slaughter and evaluated macroscopically. Bacteriological examinations were carried out on tissue samples from chronic pleuropneumonic lesions (n = 196) and from chronic bronchopneumonic lesions with suppuration (n = 14). Samples from normal lung tissue (n = 22) were also included. Pasteurella multocida was isolated from 54%, Actinobacillus (Haemophilus) pleuropneumoniae from 11%, and Streptococcus spp. from 14% of the pneumonic lesions, respectively. From normal lung tissue P. multocida was isolated from 3 (14%) of the samples, A. pleuropneumoniae was not recovered and streptococci were isolated from only 1 (5%) of these samples. The above mentioned bacterial species were recovered either in pure cultures or mixed with various other microbes. A total of 109 P. multocida strains were further characterized by capsular serotyping and testing for production of dermonecrotic toxin. Ninety-nine (91%) of the strains were capsular type A 10 (9%) were type D. Out of the type A and the type D strains 94% and 90% were toxigenic, respectively. Most of the A. pleuropneumoniae strains were serotype 2. Strains of serotypes 1 and 7 were also identified. The majority of the streptococci were identified as either Streptococcus suis or Streptococcus dysgalactiae. Actinomyces pyogenes was isolated from 14% of the lesions and anaerobic bacteria from 18%, respectively. The significance of the various bacterial species in relation to the development of chronic pneumonic lesions is discussed. Special attention is paid to P. multocida, and it is concluded that this bacterial species is probably of importance for the development of both types of chronic pneumonias.     

Evaluation of use of progesterone to counteract zearalenone toxicosis during early pregnancy in gilts.

It has been shown that zearalenone disrupts early pregnancy in swine without altering intrauterine content of estradiol 17 beta or progesterone, embryo migration, or estradiol-17 beta synthesis by blastocysts. However, serum concentrations of progesterone were reduced 2 to 3 weeks after mating in gilts that ingested zearalenone. Therefore, progesterone was administered to gilts during early pregnancy to determine whether it could counteract the detrimental actions of zearalenone on embryonic development. Thirty-two crossbred gilts (Hampshire x Chester White x Yorkshire x Duroc) were assigned randomly to a 2 x 2 factorial arrangement of treatments: zearalenone (Z); zearalenone plus progesterone (ZP); progesterone (P); or control (C). From postmating days 4 to 15, Z- and ZP-treated gilts were fed 1 mg of Z/kg of body weight, and P-treated and C gilts were fed ethanol as vehicle in a corn-soybean diet. On postmating days 3 to 15, P- and ZP-treated gilts were injected IM with 100 mg of progesterone, and C and Z-treated gilts were injected with progesterone carrier (15% ethanol, 15% benzyl alcohol, 70% propylene glycol). Blood was collected from gilts by puncture of the jugular vein daily from days 3 to 15, on alternate days from days 17 to 31, and then twice weekly until the end of the experiment. Fetal development was assessed in Z- and ZP-treated gilts on postmating day 47.6 +/- 2.9 by cesarean section and in P-treated and C gilts at slaughter on postmating days 51.2 +/- 3.2. Serum concentrations of progesterone in P-treated gilts were greater on days 7 to 8, 10 to 15, 17, and 19 than in C gilts. Serum concentrations of progesterone were greater on days 8, 10, and 12 in ZP-treated than in C gilts. However, serum concentrations of progesterone were lower in ZP-treated gilts than in C gilts on postmating days 19 to 31.(ABSTRACT TRUNCATED AT 250 WORDS)