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Objectives: Elevated total plasma homocysteine is a risk factor for Alzheimer's disease (AD) and there is some evidence that omega-3 polyunsaturated fatty acids (n-3 PUFAs) can modulate the effects of homocysteine-lowering B vitamins on AD related pathologies. Hence we investigated the relationship between total plasma homocysteine and cortical β-amyloid (Aβ) in older adults at risk of dementia. The role of erythrocyte membrane n-3 PUFAs (omega 3 index) on this relationship was also explored. Design: This is a cross-sectional study using data from the Multidomain Alzheimer Preventive Trial (MAPT); a randomised controlled trial. Setting: French community dwellers aged 70 or over reporting subjective memory complaints, but free from a diagnosis of clinical dementia. Participants: Individuals were from the MAPT trial (n = 177) with data on total plasma homocysteine at baseline and cortical Aβ load. Measurements: Cortical-to-cerebellar standard uptake value ratios were assessed using [18F] florbetapir positron emission tomography (PET). Total baseline plasma homocysteine was measured using an enzymatic cycling assay. Baseline omega 3 index was measured using gas chromatography. Cross-sectional associations were explored using adjusted multiple linear regression models. Results: We found that total baseline plasma homocysteine was not significantly associated with cortical Aβ as demonstrated using multiple linear regression models adjusted for age, sex, education, cognitive status, time interval between baseline and PET-scan, omega-3 index, MAPT group allocation and Apolipoprotein E ε4 status (B-coefficient -0.001, 95 % CI: -0.008,0.006, p = 0.838). Exploratory analysis showed that homocysteine was however significantly associated with cortical Aβ in subjects with low baseline omega-3 index (< 4.72 %) after adjustment for Apolipoprotein E ε4 status (B-coefficient 0.041, 95 % CI: 0.017,0.066, p = 0.005, n = 10), but not in subjects with a high baseline omega-3 index (B-coefficient -0.010, 95 % CI: -0.023,0.003, p = 0.132, n = 66). Conclusions: The role of n-3 PUFAs on the relationship between homocysteine and cerebral Aβ warrants further investigation. [ABSTRACT FROM AUTHOR]

The effect of pseudorabies in a commercial farrow-to-finish operation on selected production and economic values was estimated. Pseudorabies was first diagnosed in this herd by circle testing done in March 1988, as a required part of follow up from another herd that had been diagnosed with pseudorabies in the area. A pseudorabies virus vaccination program was initiated in the herd at that time. The mean litter size of pigs born alive varied from 9.26 to 10.02 pigs/litter throughout the study period; however, there was a twofold increase in suckling pig mortality and a 2.6-fold increase in nursery pig mortality when the months of the epizootic were compared with pre-epizootic months. In the 6-month period following the epizootic, suckling pig mortality was three-fold higher than that reported in the preepizootic months. Total net loss for this operation was estimated at $99,700 from when the epizootic started until eradication, when calculating losses directly. The major economic losses (76.5% of total loss) were related to suckling pig mortality, which was $16,240 during the epizootic or $24/inventoried sow/week; $19,395 in the 6 months following the epizootic or $3.8/inventoried sow/week; and $40,628 thereafter until eradication 26 months later or $0.37/inventoried sow/week. Nursery pig mortality losses were 12.6% of total net losses; $754 during the epizootic, $357 in the 6 months after the enzootic, and $11,444 thereafter until eradication 26 months later. Sow culling and deaths accounted for 9.4% of net losses that took place from 6 months after the epizootic until eradication.(ABSTRACT TRUNCATED AT 250 WORDS)

Nine dairy herds (mean size, 149 cows) with bulk-tank milk somatic cell counts of less than 300,000 cells/ml and greater than 80% of cows with Dairy Herd Improvement Association linear somatic cell counts less than or equal to 4 were selected for study. Each herd was monitored for 12 consecutive months. Duplicate quarter-milk specimens were collected from each cow for bacteriologic culturing at beginning of lactation, cessation of lactation, and at the time of each clinical episode of mastitis. Streptococcus agalactiae was never isolated and Staphylococcus aureus was isolated from less than 1% of all quarters. There were 554 episodes of clinical mastitis. During the year of study, the incidence rate of clinical mastitis varied from 15.6 to 63.7% of cows among the 9 herds. Mean costs per cow per year in herd for mastitis prevention were: $10 for paper towels, $3 for nonlactating cow treatment, and $10 for teat disinfectants. Mean cost associated with clinical mastitis was $107/episode. Approximately 84% ($90) of the costs attributed to a clinical episode were associated with decreased milk production and nonsalable milk. Costs of medication and professional veterinary fees per clinical episode varied significantly among the 9 herds. Three of the herds did not have a veterinarian treat a clinical episode of mastitis during the year of study even though 2 of these herds had the first and third highest incidence rates of clinical mastitis. When calculated on a per cow in herd basis, mean costs of $40/cow/year were attributed to clinical mastitis.(ABSTRACT TRUNCATED AT 250 WORDS)

Bacterial counts were monitored for 1 yr in bedding materials used on nine commercial dairies. Organic materials used to bed lactating cows had significantly higher moisture content and gram-negative bacterial, coliform, Klebsiella species, and streptococcal counts than did inorganic materials. Klebsiella species counts were higher in sawdust than in chopped straw. Streptococcal counts were higher in chopped straw than sawdust. Bacterial counts did not differ between sand and crushed limestone. Gram-negative bacterial and coliform counts were higher during summer and fall than in winter and spring months. Streptococcal counts did not differ among seasons of the year. Linear relationships were significant between total rates of clinical mastitis during lactation and both gram-negative bacterial and Klebsiella species counts in lactating cow bedding. These data indicate that bacterial populations differed between both types of bedding and among seasons of the year. Rates of clinical mastitis were related to bacterial counts in bedding.

Factors associated with bulk tank milk bacterial and somatic cell counts were investigated for one year on nine well managed dairies. Geometric mean total bacterial count among dairies was 4.4 × 10 3 colony cfu/ml. Geometric mean bulk tank milk somatic cell counts among herds was 265 × 10 3 ml. Bacterial counts in bulk tank milk were correlated with rates of coliform and environmental streptococcal clinical mastitis cases. Rates of total clinical cases were also correlated with bulk tank milk somatic cell counts. Correlations were measured among bulk tank milk bacterial counts and gram-negative bacterial, coliform, Klebsiella species, and streptococcal counts in materials used to bed lactating cows. Total bacterial and staphylococcal bulk tank milk counts increased when synthetic rubber liners were used greater than 800 quarter milkings. Correlations measured indicated that monitoring bulk tank milk may be an effective means of detecting management changes in herds with low bacterial and milk somatic cell counts.

Nine commercial dairy herds, each with low herd milk somatic cell counts, were monitored for 1 yr to determine prevalence of intramammary infections and rates of clinical mastitis. Staphylococcus species was the bacterial group most frequently isolated from quarters at calving and at drying off. Environmental streptococci and coliform intramammary infections totaled less than 6% of quarters at both calving and at drying off. Staphylococcus aureus were isolated from less than 1% of quarters and Streptococcus agalactiae from 0% of quarters at both calving and drying off. A total of 646 clinical cases of mastitis were diagnosed in 548 quarters of 406 cows. Mean rate of clinical mastitis among herds was .457 clinical cases/305 cow-days. Rates of clinical mastitis ranged among herds from .273 to .748 clinical cases/305 cow-days. Coliforms and bacteriologically negative and environmental streptococci accounted for 82.3% of clinical cases. Rates of clinical mastitis and severity of clinical signs differed among herds, seasons of the year, parity groups, and stages of lactation. Rates of clinical mastitis were highest during summer, in first lactation cows, and during the first 7 d of lactation.

Serratia liquefaciens mastitis was detected and investigated in a 41-cow Holstein herd. Twenty cows were treated for mastitis over a 3-month period. Serratia liquefaciens was isolated from milk samples obtained from 8 of 12 cows tested during the epizootic. Results of an epidemiologic investigation suggested that extensive frostbite of the teats decreased the udder defense. Poor milking technique and hygiene were responsible for increased exposure of the damaged teats to potential udder pathogens. Treatment of each cow resulted in initial clinical improvement, but exacerbations occurred in 75% of the cows with documented S liquefaciens infections.