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Study objective: This study aimed to determine whether the people in Australia are informed about and prepared to intervene in a cardiac emergency. Methods: A cross sectional telephone survey, which [...]

Global warming and its disproportionate impact on polar regions have led to increased iceberg populations. Southern Ocean studies in the northwest Weddell Sea have verified substantial delivery of terrestrial material accompanied by increased primary production and faunal abundance associated with free-drifting icebergs. It is hypothesized that input and utilization of macro- and micronutrients are promoted by conditions unique to free-drifting icebergs, leading to increased production, grazing, and export of organic carbon. In Arctic regions, increased freshwater input from meltwater acts to stratify and stabilize the upper water column. As has been observed in the Southern Ocean, Arctic-region icebergs should drive turbulent upwelling and reduce stratification, potentially leading to increased nitrate delivery to the local ecosystem. Increasing populations of icebergs in polar regions can potentially be important in mediating the drawdown and sequestration of CO2and can thus impact the oceanic carbon cycle.

The susceptibility of Escherichia colicultured in either iron-deplete or iron-replete media to phagocytosis by bovine neutrophils and the bactericidal activity of bovine serum was tested in vitro. Fourteen E. coliisolates from naturally occurring intramammary infections (IMI) were cultured overnight at 37°C in iron-replete media and iron-deplete media. The iron-replete media were trypticase soy broth or a chemically defined medium. The iron-deplete media were either trypticase soy broth plus 0.2mM α, α′ dipyridyl and 1mMcitrate, or the chemically defined medium plus 0.2mM α, α′ dipyridyl, and 1mMcitrate. Iron-replenished medium was the chemically defined iron-deplete medium plus 40mMferric citrate. Bacteria grown in iron-deplete media were less susceptible to phagocytosis compared with bacteria grown in iron-replete media. Replenishing the chemically defined iron-deplete medium with ferric citrate obliterated the decreased susceptibility to phagocytosis observed in iron-deplete media. The iron availability in media used to culture E. colibefore assay did not affect the bactericidal action of either the classical pathway of complement or the antibody independent alternative pathway of complement in serum. The growth of bacteria in iron-deplete medium did not alter the expression of capsule compared with growth in iron-replete medium. Iron availability during culture of E. colialtered the susceptibility of isolates to phagocytosis by neutrophils, but had no effect on the susceptibility of isolates to the bactericidal activity of serum.

The effects of immunization with the ferric citrate receptor FecA on antibody responses and on experimentally induced mastitis following intramammary challenge were investigated. Twenty-one cows were assigned to seven blocks of three cows based on expected parturition. Cows within block were randomly assigned to one of three treatments: 1) FecA immunization, 2) Escherichia coliJ5 immunization, and 3) unimmunized controls. Challenge was by infusion of approximately 60 cfu of E. coli727 into one uninfected mammary gland between 13 and 31 d after parturition. Cows within block were challenged on the same day. Cows immunized with FecA had higher immunoglobulin (Ig)G titers against FecA in serum and in mammary secretions at calving, immediately before challenge, and 7 d after challenge than did cows immunized with E. coliJ5 or control cows. Immunization with FecA also increased IgG titers against whole-cell E. coli727 in serum and in mammary secretions at calving. Serum IgM titers against FecA were higher in FecA immunized cows than in other treatment groups immediately before challenge. Bacterial counts in milk, duration of bacterial isolation in milk, rectal temperature, and milk somatic cell counts following intramammary challenge were similar among treatments. Milk production and dry matter intake did not differ among treatments. The ferric citrate receptor FecA was immunogenic in cows, but immunization had minimal effect on the clinical severity of experimentally induced E. colimastitis.

The purpose of this study was to test the hypothesis that patients whose shoulder problems are covered by workers' compensation insurance perceive worse shoulder function and health status than do comparable patients whose problem is not covered by workers' compensation. Each of 1063 consecutive patients presenting with shoulder problems to an individual consultant completed 2 questionnaires: the Simple Shoulder Test inventory of shoulder function and the Short Form 36 general health assessment. The patients were divided into 2 groups on the basis of whether care of the shoulder problem was covered by injured workers' compensation insurance. The results indicate that patients whose shoulder condition is covered by workers' compensation have significantly lower self-assessed shoulder function and health status than do those patients whose shoulder conditions are not related to on-the-job injuries. The differences between the workers' compensation and non–workers' compensation groups could not be attributed to differences in age, sex, or diagnosis. (J Shoulder Elbow Surg 2000;9:368-72.)

The efficacy of an Escherichia coliJ5 bacterin for reducing the incidence of intramammary infections and clinical signs of mastitis was tested in first lactation heifers. Ten primigravid heifers were immunized with an E. coliJ5 bacterin. Four heifers received a placebo. The bacterin and placebo were injected subcutaneously approximately 60 d prior to calving, 28 d later, and within 48h after calving. Vaccinated and placebo-injected heifers were challenged by intramammary infusion of E. coli727 in one mammary gland between 23 and 37 d after calving. All challenged quarters were diagnosed with an intramammary infection within 6h after bacteria were infused. The severity and duration of local signs of clinical mastitis were reduced in vaccinated heifers compared with placebo-injected heifers. Systemic signs of clinical mastitis were limited and did not differ between treatment groups. Bacteria counts in milk from challenged quarters were lower in vaccinated heifers than in control heifers at 12, 15, and 48h after challenge. Serum immunoglobulin G titers against whole-cell E. coliJ5 antigen at calving were higher in vaccinated heifers than they were in controls. Vaccinated heifers had higher immunoglobulin G titers than did controls in mammary secretions at calving and immediately prior to challenge. Immunization of primigravid heifers with an E. coliJ5 bacterin during the last trimester of gestation and at calving reduced the severity and duration of clinical signs following intramammary challenge with a heterologous strain of E. coli.

The ability of purified bovine immunoglobulin (Ig) G from cows immunized with ferric enterobactin receptor FepA to inhibit the growth of coliform bacteria derived from bovine intramammary infection was investigated in iron-restricted media. All isolates of Escherichia coli(n = 21) and Klebsiella pneumoniae(n = 21) were tested for growth in a chemically defined medium containing 0.5 mg/ml of apolactoferrin and in a pooled source of dry cow secretion. The addition of 4 mg/ml of purified bovine IgG directed against FepA in the synthetic medium resulted in significant growth inhibition for both E. coliand K. pneumoniaeisolates. Growth reduction of E. coliwas greater than that of K. pneumoniae. In dry cow secretions, the growth of each E. coliisolate but of less than half of K. pneumoniaeisolates (43%) was inhibited by IgG from cows immunized with FepA. Purified bovine IgG from cows immunized with E. coliJ5 had a minimal inhibitory effect on the growth of both E. coliand K. pneumoniaeisolates in the synthetic medium. In dry cow secretions, IgG from cows immunized with E. coliJ5 had no inhibitory effect on the growth of E. coliand K. pneumoniaeisolates. Supplementation with 50 μMof ferric chloride to the medium completely reversed the inhibitory effects of the antibodies and lactoferrin. Bovine IgG directed against FepA apparently inhibited the growth of coliform bacteria by interfering with the binding of the ferric enterobactin complex to the cell surface receptor FepA.

Intramammary immunization was investigated as a procedure to reduce the clinical signs of coliform mastitis. Twenty-four cows were equally distributed to the following Escherichia coliJ5 immunization schedules: 1) Subcutaneous injection 14 d prior to the end of lactation, intramammary immunization 7 d after drying off, and subcutaneous injection 30 d into the dry period; 2) subcutaneous injections at drying off, at 30 d into the dry period, and within 12h after calving; and 3) unimmunized controls. Intramammary immunizations were the infusion of vaccine via the teat canal into each of the four mammary glands. Cows were challenged by infusion of E. coli727 into one uninfected mammary quarter at approximately 30 d after calving. Intramammary immunization enhanced antibody titers against E. coliJ5 and E. coli727 compared with subcutaneous immunization. Immunoglobulin G titers against E. coliJ5 and E. coli727 in whey were greater at the time of challenge and 7 d after challenge for cows that received the intramammary immunization than for cows immunized by only subcutaneous injections. Serum IgG titers against E. coli727 were enhanced at 7 d after challenge for cows receiving intramammary immunizations compared with conventionally immunized cows. Serum IgM titers against E. coli727 were higher at calving for cows receiving intramammary immunization compared with conventionally immunized cows. Immunization schedule had minimal effect on systemic and local signs of clinical mastitis following challenge.

Bacteria counts associated with untreated organic bedding materials were compared with those of bedding treated with either an alkaline commercial bedding conditioner, acidic commercial bedding conditioner, or hydrated lime. Bedding materials were recycled manure and kiln-dried sawdust. The effects of bedding treatments on bacteria counts differed between bedding types. Each of the bedding treatments significantly reduced bacteria in recycled manure prior to use. The alkaline conditioner and hydrated lime effectively inhibited bacteria in recycled manure for 1 d. Bedding counts and teat swabs of cows housed on recycled manure treated with the alkaline conditioner were reduced on d 2. The use of the acid conditioner in recycled manure had little effect on bacteria in bedding. Sawdust differed from recycled manure in that bacteria in untreated sawdust prior to use were minimal, and populations increased rapidly during the first 2 d after use as bedding. The acid conditioner had a bacteriostatic effect in sawdust, evident by the reduction of bacteria on d 2. The alkaline conditioner and hydrated lime did not alter bacteria counts in sawdust compared with untreated sawdust. Antibacterial activity of each conditioner deteriorated between d 2 and d 6 in both beddings. The antibacterial activities of conditioners were related to the pH of bedding materials. The use of commercial bedding conditioners initially reduced bacterial counts; however, the antibacterial effects had diminished between d 2 and 6 after use in bedding.

The ability of a murine monoclonal antibody that blocks the enterobactin ligand-binding site of the ferric enterobactin receptor FepA to inhibit the growth of coliform bacteria derived from a bovine intramammary infection (IMI) was determined in an iron-restricted medium. Bacterial isolates from bovine IMI in five herds were tested by the chrome azurol sulfonate assay to detect siderophore production. Each of the isolates of Escherichia coli(n = 25) and Klebsiella pneumoniae(n = 25) were positive for siderophore production. Each isolate expressed iron-regulated outer membrane proteins when grown in trypticase soy broth plus the iron chelator α-α′-dipyridyl. Immunoblots revealed that the monoclonal antibody recognized FepA that was expressed by each of the E. coliisolates (n = 25). Only 4 of 25 K. pneumoniaeisolates produced FepA that reacted with the monoclonal antibody. This result coincided with the results of an in vitro growth assay. Growth of all E. coliisolates was significantly inhibited by the addition of monoclonal antibody to synthetic medium containing apolactoferrin. Antigenic variation in the enterobactin-binding site resulted in a low percentage of K. pneumoniaeisolates that were inhibited by the monoclonal antibody. Inhibition of bacterial growth by the monoclonal antibody was dose-dependent. As little as 50μg/ml of purified antibody had an inhibitory effect on bacterial growth in the synthetic iron-restricted medium. Monoclonal antibody specific for the enterobactin ligand-binding site of FepA inhibited the growth of E. colithat was isolated from bovine IMI.

The structure of a new polytype of zirconolite, zirconolite-4M, has been determined using X-ray and neutron powder diffraction, high resolution transmission electron microscopy, and selected area electron diffraction. Zirconolite-4M occurs when zirconolite is doped with 0.5–0.8 Nd per formula unit. Its structure consists of four hexagonal tungsten bronze (HTB) type layers interleaved alternately with layers of Ca, Zr polyhedra (as in zirconolite-2M) and Ca, Ti polyhedra (as in pyrochlore). Nd substitutes on the Ca and Zr sites. The compositions of the zirconolites were determined using an extrapolation technique based on an analysis of the impurity lines in the diffraction pattern. Cation site occupancies were determined with composition constraints applied and these were consistent with the expected zirconolite-4M cation site occupancies. Observed zirconolite-4M lattice parameters correlated with expected values for a zirconolite and pyrochlore type stacking sequence.

The serum and milk immunoglobulin (Ig) G responses of lactating dairy cows were determined following immunization with ferric enterobactin receptor FepA. Escherichia coli471 was cultured in iron-depleted medium, and outer membrane proteins were extracted by 2% N-lauroylsarcosine sodium salt and 2% Triton X-100. The FepA was isolated from the outer membrane proteins by ion-exchange chromatography. Twenty cows were assigned to four treatment groups of 5 cows blocked by breed and days in milk. Treatment groups were vaccinated with 100μg of FepA, 500μg of FepA, Escherichia coliJ5 bacterin, or sterile phosphate-buffered saline. Primary immunization was at approximately 200 d in milk, and booster immunizations were given 14 and 28 d later. Serum and whey IgG titers to FepA in cows vaccinated with FepA were significantly higher than those from cows vaccinated with either E. coliJ5 bacterin or phosphate-buffered saline. Serum and whey IgG titers to FepA were elevated by 14 d in cows vaccinated with FepA. Significant differences were not observed between doses of FepA. The degree of cross-reactivity of purified IgG from cows vaccinated with FepA to E. coliand Klebsiella pneumoniaeisolates was significantly higher than that to a control isolate that lacked FepA production. Immunization with FepA elicited an immunological response in serum and milk.

Recombinant bovine interleukin-2 was tested as adjunct therapy to intramammary infusion of antibiotics at drying off. Cows were assigned randomly within three commercial herds to either recombinant bovine interleukin-2 or PBS treatment groups at drying off. Ninety-five cows received intramammary infusions of 1mg of recombinant bovine interleukin-2 in each quarter immediately preceding intramammary infusion of a product for antibiotic therapy of dry cows. Ninety-four cows received intramammary infusion of 10ml of endotoxin-free PBS in each quarter immediately preceding the antibiotic therapy. Cure rates for IMI present at drying off did not differ between cows treated with recombinant bovine interleukin-2 and those treated with PBS. Intramammary infusion of recombinant bovine interleukin-2 did not affect the rate of new IMI during the dry period. Milk production and SCC during the first 3 mo of lactation subsequent to therapy did not differ between treatment groups. Intramammary infusion of recombinant bovine interleukin-2 was not effective as an adjunct to antibiotic therapy for dry cows.

The geometric mean bacterial count of 131 raw milk samples, using plates incubated 48 h at 30 C, was 15% higher than the geometric mean when the bacterial counts were determined at 32 C incubation. When 72 h of incubation were used, the geometric mean of samples using the lower incubation temperature was 20% higher. The mean for all 72-h raw milk counts was 31% higher than that for 48 h counts. There was no significant difference between geometric means of 51 pasteurized milk samples using plates incubated at 30 or 32 C after 48 h incubation. After 72 h of incubation, the geometric mean obtained at 30 C was 10% higher. For all 72-h counts on pasteurized milk the mean was 55% higher than for 48 h. A number of both raw and pasteurized samples showed little or no increase in count following Preliminary Incubation at 12.8 C for 18 h while others “blew up” to high levels, suggesting undesirable contamination. The International Dairy Federation procedures tended to reflect the latter better than the SPC.

We investigated a possible mechanism by which immunization against core and lipid A determinants of lipopolysaccharide reduced clinical cases of mastitis and symptoms commonly associated with heterologous Gram-negative IMI. The IgG fraction of sera from cows immunized with either Escherichia coliJ5 bacterin, E. coliJ5 lipopolysaccharide conjugate vaccine, or unimmunized controls was purified by precipitation with caprylic acid and ammonium sulfate. The degree of IgG crossreactivity with Gramnegative bacteria that were isolated from clinical quarters was greater than that with Gram-positive isolates of Staphylococcus aureus. The highest magnitude of crossreactivity was against smooth strain E. coliisolates, followed by heterologous species of Enterobacter, Serratia, and Klebsiellaisolates. Serum IgG from cows immunized with conjugate was highly crossreactive to E. coliJ5, E. coliO111:B4, Serratia marcescens, Klebsiella pneumoniae, and Salmonella typhimuriumlipopolysaccharides. The magnitude of antibody crossreactivity with lipopolysaccharides coincided with the ability of IgG to suppress the mitogenic effect of lipopolysaccharides on bovine lymphocytes.

Eighteen cows were challenged by intramammary infusion with Escherichia coli727 to determine the effects of acute clinical mastitis on α-tocopherol concentrations in plasma and milk. Cows were fed diets supplemented with 1000 IU of vitamin E/d from calving through the experimental period. At challenge, geometric mean DIM was 33 d. Each mammary quarter was diagnosed with an IMI and clinical mastitis at 24 and 48h after challenge. The α-tocopherol concentrations in milk from challenged quarters were approximately 60% greater by 24 and 48h after challenge than concentrations at prechallenge and 168h postchallenge. Plasma α-tocopherol concentrations did not change after intramammary challenge. The α-tocopherol in plasma and milk was correlated at 48 and 168h postchallenge but at prechallenge or 24h postchallenge. Milk α-tocopherol and SCC were correlated positively across all sample periods. Milk fat and milk α-tocopherol concentrations were correlated at each sample period except 24h postchallenge. Increases in milk α-tocopherol during clinical mastitis were not correlated to milk production, DMI, or BSA concentration in milk. Changes in milk α-tocopherol concentration during clinical mastitis were similar to the dynamics of milk SCC.

Efficacy of an Escherichia coli(Olll:B4) J5 bacterin was tested in an experimental challenge trial. Nineteen cows were vaccinated with an E. coliJ5 bacterin, and 10 cows were injected with a placebo containing adjuvant only. Vaccine and placebo were administered at drying off, 30 d after drying off, and within 48h after calving. Cows were challenged approximately 30 d after calving by intramammary infusion with a smooth heterologous strain of E. colipreviously shown to cause mild clinical mastitis. Vaccination with the J5 bacterin reduced duration of IMI and local signs of clinical mastitis. Concentrations of BSA in milk 24h after challenge were greater in control cows than in cows vaccinated with J5. The SCC at 7 d postchallenge were greater for cows vaccinated with the placebo than for cows vaccinated with J5. Bacterial counts were lower for cows vaccinated with the placebo than for cows vaccinated with J5 at 3, 6, and 9h postchallenge. In contrast, cows vaccinated with J5 had lower bacterial counts at 2, 3, and 4 d postchallenge than did cows vaccinated with placebo. Systemic signs of clinical mastitis were relatively mild and similar between treatment groups. Rectal temperature, DMI, and milk production did not differ between control and cows vaccinated with J5 following challenge.

Development of a lipopolysaccharide-protein conjugate vaccine and the immunological response to the vaccine were investigated. Lipopolysaccharide derived from Escherichia coliJ5 was detoxified by mild alkaline hydrolysis. Detoxification reduced endotoxin activity 2500-fold compared with that of native J5 lipopolysaccharide. The conjugate vaccine was synthesized by covalently coupling detoxified lipopolysaccharide to chicken serum albumin by reductive amination. Dairy cows were immunized with 8.35mg of conjugate (n = 3) or 5 x 109heat-killed J5 bacterin (n = 5) at 215 DIM and received a secondary immunization 14 d later. Control cows were not immunized. Immunization enhanced serum antibody titer to J5 lipopolysaccharide antigens. Whey IgG and IgM titers to J5 lipopolysaccharide were not different among treatment groups. Serum and whey IgG titers to J5 whole-cell antigens were elevated in immunized cows within treatment groups. Immunization did not enhance whey IgM to J5 whole-cell antigens. Conjugate immunization elicited an immune response comparable with or greater than that of immunized cows with J5 bacterin.

Fifteen Holstein cows were used in a trial involving intramammary challenge to determine the effects of acute clinical mastitis on the concentrations of α-tocopherol in milk and plasma and the concentrations of neutrophils in milk and blood. Cows were assigned to one of three experimental groups challenged by intramammary infusion of lipopolysaccharide, Escherichia coli, or sterile phosphate-buffered saline. All quarters infused with lipopolysaccharide or E. coliwere diagnosed with clinical mastitis on d 1 and 2 after challenge. Acute inflammation caused by intramammary infusion of lipopolysaccharide or E. coliresulted in increased concentrations of α-tocopherol in milk in challenged quarters but had no effect on concentrations of α-tocopherol in plasma. Concentrations of α-tocopherol in milk and blood neutrophils did not differ among treatment groups. Concentrations of α-tocopherol did not differ between milk and blood neutrophils. Approximately 25% of the α-tocopherol in milk from glands with clinical mastitis was associated with neutrophils, and <10% of the α-tocopherol in milk from nonmastitic glands was associated with neutrophils. A shift toward sources of α-tocopherol other than synthesized milk fat occurred during acute inflammation in the mammary gland.

The effect of an immunization schedule on responses of antibody titers was tested following vaccination with an Escherichia coliJ5 bacterin. Eighteen cows were equally distributed among three immunization schedules: 1) subcutaneous injection at 14 d prior to the end of lactation, intramammary immunization at 7 d after drying off, and subcutaneous injection at 30 d into the dry period; 2) subcutaneous injections at drying off, at 30 d into the dry period, and within 12h after calving; and 3) unimmunized controls. The E. coliJ5 bacterin consisted of 5ml of 10 9 boiled cells/ml of 0.9% NaCl plus 0.005% phenol emulsified with 5ml of Freund's incomplete adjuvant. Subcutaneous injections were administered on the upper part of the rib cage, posterior to the scapula. Intramammary immunizations of 2.5ml of bacterin were infused via the teat canal into each of the four mammary glands. Intramammary immunization increased rectal temperatures at 12h after infusion, but subcutaneous injections did not induce febrile responses. Intramammary immunization enhanced immunoglobulin G titers in serum and whey on d 0 of lactation compared with subcutaneous immunizations. Immunoglobulin G titers in serum also were greater at d 30 of the dry period and at d 14 and 21 of lactation for cows that received intramammary immunization than for cows that were vaccinated by subcutaneous injections only. Immunoglobulin M titers in whey and serum on d 21 of lactation were greater for cows that received intramammary immunizations than for cows that were immunized by subcutaneous injections only.

A natural exposure trial was conducted for 12 mo in a commercial herd of 125 lactating cows to compare the efficacy of an experimental barrier teat dip containing .55% chlorhexidine gluconate with the efficacy of a 1% iodophor for preventing new IMI and clinical mastitis. Teats of half of the cows were dipped in the experimental barrier product, and teats of the remaining half of the herd were dipped in the 1% iodophor product. Quarters dipped with the experimental barrier product had fewer new IMI caused by Escherichia coli, coagulase-negative staphylococci, or Gram-positive bacilli than did quarters dipped in the 1% iodophor. Incidence of new MI caused by Serratiaspp. and Pseudomonasspp. was greater for quarters dipped in the experimental barrier product than for quarters dipped in the 1% iodophor. Efficacy of the two teat dips against new IMI caused by Staphylococcus aureus, environmental streptococci, and Klebsiellaspp. did not differ. Incidence of bacteriologically negative clinical cases of mastitis was greater in quarters dipped in the 1% iodophor than in quarters dipped in the experimental barrier product. Incidence of clinical mastitis cases caused by Staph. aureus, environmental streptococci, E. coli, Klebsiellaspp., Serratiaspp., and Pseudomonasspp. did not differ between treatment groups.

Characteristics of environmental streptococcal IMI were investigated over a 7-yr period for a herd in total confinement. A total of 374 new environmental streptococcal IMI was detected. Approximately 50.5% of IMI were new in the dry period, and 49.5% were new in lactation. The rate of new IMI was .00312 IMI/cow day during the dry period and .00054 IMI/cow day during lactation. The percentages of cows and quarters with an environmental streptococcal IMI present at calving were 10.6 and 3.2%, respectively. The percentage of heifers with an environmental streptococcal IMI at calving was similar to that for cows. The rate of new environmental streptococcal IMI was greater during the 1st mo of lactation than during the remainder of lactation. The rate of IMI during late lactation was higher for older cows than for either heifers or cows in second lactation. The rate of environmental streptococcal IMI during the dry period and during lactation was greatest during summer. The mean days of lactation that cows were infected for all IMI was 12.3 d. Approximately 41% of IMI had a duration of <8 d. Stage of lactation, season of the year, and parity influenced the rate of new IMI.

The effects of forage to concentrate ratio and the commercial form of vitamins A and E on in vitro ruminal disappearance of retinol and α-tocopherol were studied. Ruminally fistulated cows were fed diets with either 80 or 50% forage. In vitro substrates that were similar to those fed to the donor cows were incubated with buffered ruminal fluid for 24h. Different commercial forms of vitamin E (spray-dried, silicic acid adsorbate, and lipid-encased forms) and vitamin A (gelatin beadlet and lipid-encased forms) were added to the flasks. The vitamin E was all-rac-α-tocopheryl acetate, and the vitamin A was all-trans-retinyl acetate. The amount of α-tocopherol in the flasks was not affected by diet or form of vitamin E and did not change over the 24-h incubation. Retinol disappearance was not affected by form of vitamin A but was substantially higher for the 50% forage diet than for the 80% forage diet (72 vs. 20% at 24h). These data suggest that ruminal metabolism of vitamin E is minimal and not affected by forage to concentrate ratio. Additionally, vitamin A destruction in the rumen was much higher when cows were fed a typical lactation diet than when fed a typical dry cow diet.

Sixty-six cows and heifers (Holsteins and Jerseys) were assigned to one of three treatments at 60 d before anticipated calving. Treatment 1 consisted of 100 IU/d of supplemental vitamin E during the dry period and 100 IU/d during the first 30 d of lactation. Treatment 2 was 1000 IU/d of vitamin E during the dry period and 500 IU/d during lactation. Treatment 3 was 1000 IU/d of vitamin E during the first 46 d of the dry period, 4000 IU/d during the last 14 d of the dry period, and 2000 IU/d during lactation. Plasma concentrations of α-tocopherol decreased at calving for cows fed dietary treatments with low or intermediate concentrations of vitamin E, but not for cows fed the high vitamin E treatment. High dietary vitamin E increased concentrations of α-tocopherol in blood neutrophils at parturition, but no difference was found for the other two treatments. The percentage of quarters with new infections at calving was not different (32.0%) between cows receiving treatments that contained low and intermediate concentrations of vitamin E but was reduced (11.8%) in cows receiving the high vitamin E treatment. Clinical mastitis affected 25.0, 16.7, and 2.6% of quarters during the first 7 d of lactation for cows receiving the low, intermediate, and high vitamin E treatments, respectively. Cows with plasma concentrations of α-tocopherol <3.0μg/ml at calving were 9.4 times more likely to have clinical mastitis during the first 7 d of lactation than were cows with plasma concentrations of α-tocopherol 3.0μg/ml.

Bacteria counts in untreated sawdust bedding were compared with those in sawdust bedding after the addition of lime and after daily replacement of bedding in the back one-third of the stalls. Addition of 1kg of lime to 10kg of sawdust reduced Gram-negative bacteria, coliforms, Klebsiellaspp., and streptococci prior to use as bedding. Sawdust treated with lime also showed decreased bacteria counts compared with bacteria counts for sawdust that was replaced daily and compared with bacteria counts for control bedding after 1 d in the stall. The decrease in bacterial populations was related to an increase in bedding pH. Mean pH in the sawdust treated with lime was greater prior to use and after 1 d in the stall than the pH of other treatments. After 2 and 6 d in stalls, however, bacteria counts and pH were similar among treatments. Dry matter content of bedding did not differ among bedding treatments. Bacteria counts in bedding were positively correlated with teat skin swabs. Gram-negative bacteria and Klebsiellaspp. counts on teat swabs were lower for cows housed on bedding treated with lime on d 2 compared with those for cows housed on control bedding and bedding that was replaced daily. Addition of lime to sawdust in the back one-third of tie stalls caused a decrease in exposure of teats to environmental mastitis pathogens in bedding for 1 d. Daily replacement of bedding had a minimal effect on bacteria counts in bedding and on teat skin.

Pasteurized milk poured from its original container into smaller sterile containers showed evidence that contamination occurred during the pouring process. A simple vacuum sampling apparatus was devised to transfer, aseptically, milk from the original container to smaller containers. Uniform counts and shelf-life determinations were obtained from subsamples using the vacuum apparatus.