Parenteral treatment of clinical mastitis with tylosin base or penethamate hydriodide in dairy cattle.

The objective of this study was to compare the clinical and bacteriological cure rates of cows with clinical mastitis following treatment with either tylosin base (5 g injected 3 times at 24-h intervals; n = 306) or penethamate hydriodide (5 g injected 3 times at 24-h intervals; n = 289). Duplicate milk samples were collected before treatment and again 14 +/- 3 and 21 +/- 3 d later for microbiological analysis. Only those quarters from which gram-positive mastitis pathogens were isolated before treatment were included in the analyses. Streptococcus uberis was the most prevalent isolate. The number of cows with clinical failure (i.e., retreated within 21 d of enrollment) did not differ between treatments (64 vs. 63, respectively). At the quarter level, there was no difference in the proportion of bacteriological cure between treatments (81.2 vs. 83.8% for penethamate hydriodide or tylosin, respectively). The proportions of clinical and bacteriological cure were influenced by age, herd, severity of mastitis, number of glands within the cow with clinical mastitis, bacterial species, and days postpartum at enrollment. There was no difference between treatment groups for SCC (4.46 vs. 4.44 +/- 0.08, mean +/- standard error of the difference in ln SCC for cows treated with penethamate hydriodide or tylosin, respectively) or production of milk solids (1.45 vs. 1.48 +/- 0.02 kg/d of milk fat + protein, for the penethamate hydriodide or tylosin treatment, respectively). Overall, there was no difference in the proportions of clinical failure (17.3 vs. 16.5% of cows treated with penethamate hydriodide or tylosin, respectively) or bacteriological cure (79.8 vs. 82.0% of cows treated with penethamate hydriodide or tylosin, respectively), or in SCC or milk production between dairy cows with clinical mastitis and those treated for clinical mastitis with 1 of 2 parenteral antibiotic therapies.

Evaluation of a liquid formulation of monensin to control bloat in pasture-fed milking cows.

AIM: To evaluate the effectiveness of a liquid formulation of monensin in reducing bloat score in milking cows grazing pasture. METHODS: A Friesian x Jersey crossbred herd which had been genetically selected for high bloat susceptibility since 1973 was used in this study. Two trials were conducted, each involving two groups of 15 cows, randomly allocated to Treated or Control groups. Trial 1 involved twice-daily administration of a novel liquid formulation of monensin given to Treated cows at morning and afternoon milkings. Trial 2 involved once-daily administration of the same product to Treated cows at the morning milking only. Control cows received no preventative treatment. The total daily dose of monensin in each trial was 300 mg per cow, given in a total volume of 100 ml of liquid. Animals were scored for bloat twice-daily whilst grazing on white-clover/ryegrass or red-clover pastures. The scoring system used a scale of 0, 1, 1.5, 2, 2.5, or 3, representing scores of increasing bloat severity as assessed by palpation of abdominal pressure on the left and right sides of the cow. RESULTS: In Trial 1, severe bloat was recorded at 9 out of 23 scoring sessions. Twelve Control cows required therapeutic treatment for bloat on at least one day, compared to 3 cows in the Treated group (p=0.003). In Trial 2, severe bloat in 3 of 9 scoring sessions led to 8/15 Control animals requiring therapeutic treatment compared to 1/14 cows in the Treated group (p=0.02). CONCLUSIONS: Oral drenching with the liquid formulation of monensin tested was effective in reducing bloat score in milking cows grazed on pasture.

A reinvestigation of the purity, isoelectric points and some kinetic properties of the aldehyde dehydrogenases from sheep liver.

1. Cytoplasmic aldehyde dehydrogenase was shown to be free of contamination by the mitochondrial enzyme by isoelectric focusing. 2. Both enzymes showed multiple banding in activity stains. The cytoplasmic enzyme gave two very close bands pI = 5.22 +/- 0.03 whereas the mitochondrial enzyme showed seven bands, a pair at pI = 5.22 and five further bands of pI 5.48 +/- 0.09, 5.56 +/- 0.07, 5.65 +/- 0.06, 5.70 +/- 0.03 and 5.76 +/- 0.02. Possible origins of the isoenzymes are discussed. 3. Disulfiram in a fourfold excess reduced the activity of the cytoplasmic enzyme to 9% of the initial value. The residual activity represents the activity of the disulfiram-modified enzyme and is not due to mitochondrial contamination. This casts doubt on the role of an essential thiol group. 4. The mitochondrial enzyme shows a low amplitude (22%) burst in the production of 4-nitrophenoxide ion during the hydrolysis of 4-nitrophenyl acetate at pH 7.6. The burst rate constant was 7.3 +/- 1 s-1 and the steady-state rate constant was 0.2 s-1, values similar to those previously reported for the cytoplasmic enzyme. 5. The mitochondrial enzyme shows a burst in the release of protons during the oxidation of propionaldehyde at pH 7.6. The burst rate constant was 6 s-1 and the amplitude was equal to half the formal enzyme concentration. The significance of these results for the steady-state mechanism is discussed.