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Biomedical subjects

R P Natzke

Publications and source records attributed to R P Natzke.

At least 19 recordsLinked to original sources
PubMed2003

Identification of possible mediators of embryonic mortality caused by mastitis: actions of lipopolysaccharide, prostaglandin F2alpha, and the nitric oxide generator, sodium nitroprusside dihydrate, on oocyte maturation and embryonic development in cattle.

PROBLEM: Mastitis and immunization against constituents of organisms causing mastitis can reduce fertility of cattle and sheep, respectively. For the current experiments, it was hypothesized that these effects are mediated via actions of lipopolysaccharide (LPS), prostaglandin F2alpha (PGF2), and nitric oxide on oocyte maturation and embryonic development. METHOD OF STUDY: To evaluate effects on oocyte maturation, oocytes were matured with various concentrations of LPS, PGF2alpha, or the nitric oxide (NO) generator, sodium nitroprusside (SNP). Following maturation, oocytes were fertilized and cultured until day 8 after fertilization. To test effects on embryo growth, oocytes were matured and fertilized and cultured after fertilization with LPS, PGF2alpha, or SNP. RESULTS: Addition of 100 and 1000 ng/mL LPS and 50 and 100 ng/mL PGF2alpha to oocyte maturation medium reduced the proportion of oocytes that became blastocysts at day 8 after fertilization. When added after fertilization, in contrast, neither LPS nor PGF2alpha reduced development to the blastocyst stage. Unlike for LPS and PGF2alpha, addition of SNP during oocyte maturation was without effect on the proportion of oocytes that became blastocysts at day 8 after fertilization. However, addition of 10 microM SNP to culture medium after fertilization completely prevented development to the blastocyst stage while 0.1 and 1 microM SNP did not affect development. CONCLUSIONS: Results indicate that increased local concentrations of LPS, PGF2alpha, and NO can have deleterious consequences on oocyte function (LPS, PGF2alpha) and embryonic development (NO). Thus, these molecules are putative mediators of effects of infectious disease or inflammation, including mastitis, on fertility of cattle.

Animals↗
PubMed2003

Actions of tumor necrosis factor-alpha on oocyte maturation and embryonic development in cattle.

PROBLEM: Infertility can accompany mastitis in cattle. Involvement of tumor necrosis factor-alpha (TNF-alpha) in this phenomenon is suggested by observations that circulating concentrations of TNF-alpha are elevated after intramammary infection or infusion of endotoxin. It was hypothesized that (1) TNF-alpha acts on the oocyte during maturation to decrease the percent of oocytes that cleave and develop following fertilization; (2) exposure of embryos to TNF-alpha after fertilization reduces development to the blastocyst stage; and (3) TNF-alpha increases the proportion of blastomeres that undergo apoptosis in a stage-of-development dependent manner. METHOD OF STUDY: In one experiment, oocytes were matured with various concentrations of TNF-alpha and then fertilized and cultured without TNF-alpha. In another study, embryos were cultured with TNF-alpha for 8 days beginning after fertilization. Finally, embryos were collected at the two or four-cell stage (at 28-30 hr after insemination) or when > or = 9-cells (at day 4 after insemination) and cultured +/- TNF-alpha for 24 hr. The proportion of blastomeres undergoing apoptosis was then determined by the TUNEL procedure. RESULTS: Addition of TNF-alpha to maturation medium did not affect the proportion of oocytes that cleaved. However, the percent of oocytes that developed to the blastocyst stage at day 8 after insemination was reduced (P = 0.05) at all TNF-alpha concentrations tested (0.1-100 ng/mL). When added during embryo culture, there was no significant effect of TNF-alpha on the proportion of oocytes that became blastocysts. In addition, TNF-alpha did not induce apoptosis in two and four-cell embryos. For embryos > or = 9-cells, however, 10 and 100 ng/mL TNF-alpha increased (P < 0.05) the percent of blastomeres labeling as TUNEL-positive. CONCLUSION: TNF-alpha can have deleterious actions on oocyte maturation that compromise development of the resultant embryo. While exposure of fertilized embryos to TNF-alpha did not inhibit development to the blastocyst stage, TNF-alpha increased the percentage of blastomeres undergoing apoptosis when exposure occurred for embryos > or = 9-cells. Increased blastomere apoptosis could conceivably compromise subsequent embryo survival.

Animals↗
PubMed1992

Interactions of heat stress and bovine somatotropin affecting physiology and immunology of lactating cows.

During summer, 34 cows received daily injections of placebo or 25 mg of bST and were placed in a thermoregulated or a heat stress environment. Heat stress increased rectal temperatures, respiration rates, and plasma cortisol concentrations and decreased milk yield. Four of 9 bST-treated cows and none of 8 control cows became atactic on the 1st d of heat stress. When exposed to heat stress, cows treated with bST experienced higher rectal temperatures throughout the trials than cows treated with placebo. Nonetheless, bST increased milk yields in both environments. The major effect of heat stress on immune function was decreased migration of leukocytes to the mammary gland after chemotactic challenge. This effect of heat stress was not altered by bST. In summary, hyperthermia induced by heat stress and associated changes were greater for cows treated with bST. Detected effects of heat stress on the immune system were few and were not alleviated by bST. Use of bST during summer in subtropical climate zones requires careful management to avoid overexposure of bST-treated cows to heat stress.

Animals↗
PubMed1991

Actions of bovine somatotropin on polymorphonuclear leukocytes and lymphocytes in cattle.

Objectives were to determine 1) in vitro effects of bST on function of polymorphonuclear leukocytes and lymphocytes and 2) in vivo effects of bST on leukocyte function of heifers fed to maintain medium or high growth rates. When administered in vitro, bST did not affect function of polymorphonuclear leukocytes. [Methyl-3H]thymidine incorporation by resting lymphocytes was stimulated by 1000 ng/ml bST. When given in vitro, bST did not further enhance [methyl-3H]thymidine uptake by mitogen-stimulated lymphocytes cultured at 38.5 degrees C but reduced the depression of mitogen-stimulated proliferation caused by incubating cells at 42 degrees C. When bST was administered in vivo, phagocytosis and killing of Escherichia coli by polymorphonuclear leukocytes from bST-treated heifers were not different from cells of control heifers. As measured by [methyl-3H]thymidine uptake after stimulation with phytohemagglutinin, lymphocytes from bST-treated heifers responded similarly to those of control heifers when incubated at 38.5 degrees C, but the depression in [methyl-3H]thymidine uptake due to culture at 42 degrees C was less for lymphocytes obtained from bST-treated heifers. In conclusion, bST had little effect on function of polymorphonuclear leukocytes but could promote proliferation of lymphocytes in vitro and protect cells from effects of elevated temperature.

Animals↗
PubMed1991

Analysis of somatic cell count data by a peak evaluation algorithm to determine inflammation events.

Increases in SCC are an expression of inflammation events in the udder. Inflammation events are sporadic, of variable amplitude and duration, and can be analyzed by computer programs designed to evaluate pulses of hormone secretion. Baseline values for SCC, which take into account long-term trends, were calculated using the PULSAR peak evaluation algorithm. An inflammation event was defined as an increase of log2(SCC) of at least 1 unit from the preceding data point if the observed value exceeded the baseline value by a threshold value. Incidence rate, duration, and amplitude of inflammation events were calculated. Weekly composite milk SCC from individual cows from two Florida dairy farms were recorded. Data were analyzed for effects of season (summer and fall) and bST in two separate data sets. Incidence rate of inflammation events was higher in summer than in fall (4.31 and 2.91 events per cow x year). In one of two data sets only, duration of inflammation events was longer in cows treated with bST (2.4 +/- .2 vs. 1.6 +/- .2 wk). In contrast, least squares analysis of variance of log2(SCC) did not detect differences due to season or bST. The use of the peak evaluation algorithm led to the detection of seasonal and bST effects on inflammation events in cows.

Algorithms↗
PubMed1991

Modulation of function of bovine polymorphonuclear leukocytes and lymphocytes by high temperature in vitro and in vivo.

Function of polymorphonuclear leukocytes (PMNL) and proliferation of lymphocytes after stimulation with mitogens were evaluated in vitro at incubation temperatures of 38.5 and 42 C, and after in vivo heat stress of lactating Holstein cows. Cytochrome-c reduction and random migration of PMNL were reduced when cells were preincubated or incubated at 42 C, but high incubation temperature had little or no effect on phagocytosis and killing of Escherichia coli. Proliferation of lymphocytes was reduced when cells were incubated for 60 hours at 42 C after stimulation with phytohemagglutinin, pokeweed mitogen, or concanavalin A. After stimulation with phytohemagglutinin, lymphocytes were most sensitive to high temperature during the first 24 hours of the 60-hour culture period. High incubation temperature had little effect on viability of cells. In vivo heat stress had no significant effect on responses of PMNL in vitro, but the decrease in proliferation of lymphocytes in vitro at high temperature was less when cells were obtained from heat-stressed cows. Total leukocyte counts in blood and somatic cell counts in milk were higher in heat-stressed cows. Results indicate that: exposure to high temperature in vitro can depress responses of PMNL and lymphocytes; apparent adaptive mechanisms induced by in vivo heat stress provide protection from effects of high temperature seen in vitro; and evidence could not be found to support the hypothesis that reduction in immune function is the basis for increases in the incidence of mastitis during the summer.

Animals↗
PubMed1988

Consequences of diagnostic errors in mastitis therapy trials.

The effect of errors that occur in the diagnosis of intramammary infectious mastitis on the precision of experiments measuring the efficacy of mastitis therapy has been investigated. Diagnostic errors within the range found by experienced workers can create large biases in the apparent cure rate of therapy particularly at cure rates of less than 0.5. Using confirmed methods of diagnosis rather than single samples and reducing the probabilities of false positive and false negative diagnoses to 0.01 and 0.05 respectively, the biases in the apparent cure rates are reduced to acceptable levels. A method is given for calculating the rates of occurrence of false positive and false negative diagnoses from the results of trials using confirmed diagnoses. These errors cannot be calculated from therapy trial data when diagnosis is based on single milk samples. Because the bias in the measurements of the cure rate is greatest at the lowest levels of elimination, estimates of spontaneous recovery in untreated quarters have the greatest error. For this reason experiments incorporating an untreated control group of infected quarters usually reduce the precision of the therapy trials. An experiment in which the efficacy of a test product is measured relative to a reference product has advantages. It minimizes the difficulties arising from scale of measurement, diagnostic errors and herd differences in response rate, and makes possible comparisons between trials. Further investigations are required on the importance of spontaneous recovery, particularly for studies of Escherichia coli therapy and dry period therapy. The results of this investigation have relevance to all types of mastitis investigation that measure the change in mastitis status of udder quarters, i.e. new infection rates.

Animals↗
PubMed1988

Climatic effects on occurrence of clinical mastitis.

Clinical mastitis records for 6.5 yr from a large north Florida dairy and corresponding daily weather data were analyzed. Monthly incidence of clinical mastitis was expressed as percent of cow-days in milk and graphed against monthly average daily maximum temperature humidity index values and monthly total rainfall. No trends were evident with rainfall. In 3 of 6 yr, monthly incidence of clinical mastitis increased more than 50% above annual incidence, and this followed high monthly temperature-humidity values. Least squares was used to estimate regression coefficients of temperature-humidity index categories based on 999,969 Holstein records. A temperature humidity index category represented the number of days used to calculate average daily maximum temperature-humidity index value. Sources of variation in observed occurrence of clinical mastitis were cow, parity, month, year, interaction of parity by month, and continuous effects of temperature-humidity index categories 2, 6, 15, 30, 60, each to third order and 60 by parity interaction. In all temperature-humidity index categories as the temperature-humidity index value increased, occurrence of clinical mastitis increased. When values rose from 55 to 80, twice as many for 2 d cows showed signs of clinical mastitis.

Animals↗
PubMed1988

Characterization of clinical mastitis records from one herd in a subtropical environment.

Patterns of occurrence and reoccurrence of clinical mastitis, duration of episodes, and number of quarters treated in a large north Florida dairy over 6.5 yr are described. Monthly incidence of milk disposal due to clinical mastitis varied within and between years and ranged from 1.3 to 4.7% of cow-days in milk. In first parity animals, 37.6% of lactations were treated for clinical mastitis, averaging 1.4 episodes per treated lactation. Almost half of these episodes occurred by d 35 of lactation. For second, third, and fourth or greater parities, 35.5, 48.1, and 56.6% of lactations were treated. These lactations averaged 2.1, 2.3, and 2.8 episodes. In parities 2, 3, and greater than or equal to 4, episodes initiated by d 35 of lactation were 28.2, 23.9, and 20.6% of parity episodes. Seventy-two percent of episodes were treated for less than or equal to 7 d. Sixty-seven percent of episodes were treated in one quarter and treatment in two, three, or four quarters accounted for 21.6, 5.5, and 5.9% of all episodes. When two quarters were treated simultaneously, udder halves (front, rear, right, left) were treated more frequently than were diagonals.

Animals↗
PubMed1988

Effects of administration of bovine somatotropin on milk yield and composition.

Thirty-two Holstein cows were assigned to four treatment groups in a continuous lactation trial to evaluate effects of daily subcutaneous injections of 0 (A), 5.15 (B), 10.3 (C), and 20.6 mg (D) of recombinantly derived bovine somatotropin monomer. Responses were milk yield and composition, component yields, net energy intake, body weight, and somatic cell counts. Treatments began in fall, 28 to 35 d postpartum, and continued for 266 d. Base ration was corn silage and concentrate. Least squares means of milk and constituent yields and gross efficiency of milk production differed among treatments, but percentage fat and protein, energy intake, body weights, and somatic cell counts did not. Least squares means of 3.5% FCM were 21.3 (A), 25.0 (B), 26.2 (C), and 28.5 kg/d (D); fat and protein yields showed similar response to treatment. Milk yields adjusted for pretreatment yields were 21.1 (A), 25.5 (B), 26.5 (C), and 29.3 kg/d (D). Orthogonal contrasts showed lower milk and constituent yields and net energy intake for control (A) than for hormone-injected cows (B, C, D), but no differences were detected between treatments B, C, and D. Gross efficiency of production (3.5% FCM/feed net energy intake) was greater for hormone-injected cows.

Animals↗
PubMed1987

Occurrence and reoccurrence of clinical mastitis.

Clinical mastitis records for 6.5 yr (July 1977 through November 1983) from a large north Florida dairy were analyzed. Observed frequencies of clinical mastitis were calculated in 7240 Holstein and Jersey lactations. Least squares analyses used Holstein and Jersey lactations greater than 200 d and limited maximum parity to 5 (6732 lactations, 5738 episodes). Solutions for number of occurrences of clinical mastitis adjusted for month of parturition and breed effects were .47, .59, .94, 1.27, and 1.50 for parities 1 through 5. Solutions for number of occurrences across lactation in Holsteins was greater than for Jerseys (1.28 vs. .63). Solutions for occurrence of first episode in Holsteins increased from .35 in parity 1 to .71 in parity 5. Occurrence of episodes two through five increased as parity increased. Similar trends were found in Jerseys with the exception of parity 2. Correlation of residuals between specific episodes increased as episode increased. From episode 2 through 5 probability of another occurrence of clinical mastitis was greater than .75. Solutions for proportion of occurrences of clinical mastitis occurring during the first 35 d postcalving were .60, .36, .31, .30, and .28 for parities 1 through 5. Clinical mastitis in first parity cows occurred primarily during the first 35 d postcalving.

Animals↗
PubMed1987

Factors affecting days of discarded milk due to clinical mastitis and subsequent cost of discarded milk.

Records of clinical mastitis for 6.5 yr from one Florida dairy with 1050 to 1350 cows milking per month were used to predict duration of occurrence of clinical mastitis and to estimate dollar value of discarded milk per lactation with occurrences of clinical mastitis. Only 6.1% of lactations accrued more than 28 d of discarded milk and were responsible for 52.7% of days of discarded milk. Accurate maintenance of herd mastitis records enables calculation of actual days of milk available for sale and provides a useful tool for culling and treating decisions. Duration of each occurrence of clinical mastitis was modeled by fixed effects of breed, season of occurrence, current lactation history of mastitis, number of quarters with clinical signs, and average maximum temperature-humidity index for the 2 d prior to the occurrence (to second order). These effects explained 1.8% of observed variation in duration of occurrence. Random effects of cow explained 5 to 6% of variation. Prediction of duration of occurrence had a mean value of 6.6 d. When economic status of individual animals is evaluated, comparison of days of milk production available for sale is preferable to total days of milk production. Estimated average cost of discarded milk for parities 1, 2, 3, 4, and 5 ranged from $29.73 to 223.98 per lactation.

Animal Husbandry↗
PubMed1983

Cost benefit analysis of lactation therapy with somatic cell counts as indications for treatment.

Lactating dairy cows (487) from five commercial herds were in a study of benefits from lactation therapy of sub-clinical mastitis. Bacterial isolations and composite milk samples for somatic cell counts were taken from each cow each month for 15 mo. Cows (254) in the experimental group were infused with cephapirin in all quarters for two consecutive milkings if somatic cell counts rose above 400,000 cells/ml; 103 cows were so treated. Stepwise regression showed that lactation number, somatic cell counts, days in milk, and percent quarters infected explained variation in milk production, but treatment group, herd, and season did not. Also, there were no significant differences between production of infected experimental and control cows with high somatic cell counts on test dates after treatment. With the experimental program, there was a net loss of +19.65/cow. Intramammary lactation therapy based on somatic cell counts less than 400,000 cells/ml is not recommended.

Animals↗
PubMed1983

Comparison of teat dips with differing iodine concentrations in prevention of mastitis infection.

Six commercial dairy herds were used to test the relative efficacy of three concentrations of iodine as a teat dip over 12 mo. Concentrations were .1, .25, and 1% iodine with free iodine contents of 3.5, 4.0, and 1.0 ppm. Two concentrations were compared in each herd. The greatest number of new infections (71) occurred in approximately 120 cows whose teats were dipped with the 1% iodine dip, and the fewest (52) occurred in a similar number of cow quarters dipped in .1% iodine; however, differences were not significant. Clinical mastitis was highest in the 1% group. If all clinical mastitis were the result of infection, even if bacteria were not isolated from the pretreatment sample or from samples collected at the start of the study and those quarters were added to the totals, then reduction of new infection with the .1% product would be significant.

Administration, Topical↗
PubMed1982

Effect of overmilking on udder health.

This study evaluated the effect on udder health of extending the milking period with or without vacuum fluctuation. Eighty cows were allotted into treatment groups consisting of 1) Control milked with normal milking equipment and the milker removed as soon as milk flow ceases; 2) milked for 12 min with normal equipment; 3) milked 12 min with induced vacuum fluctuations; and 4) normal milking time with induced fluctuations. Groups 2 and 3 had more newly infected quarters than groups 1 and 4. However, there was no difference in the number of cows becoming infected. The increase in new infections is due to more quarters of already infected cows becoming infected rather than more new cows becoming infected. Extending the machine-on time appeared to increase the rate of cross infection presumably by lengthening the time of highest risk. Cows in groups 2 and 3 required more therapy of clinical mastitis which was a reflection of the higher new infection rate rather than of a change in trauma to the udder. Increasing the unit-on time had no apparent effect on external teat end condition.

Animals↗
PubMed1982

Predictability by somatic cell counts related to prevalence of intrammary infection within herds.

Somatic cells were counted and bacteria identified for milk samples from 719 lactating dairy cows in 12 commercial herds. These pooled data were used to look at the accuracy of alternative thresholds of somatic cell counts as indicators of intramammary infection. Sensitivity, specificity, and predictability positive and negative at alternative cell count thresholds were calculated. There was an increase of incidence of infection associated with increased cell count. Raising the cell count threshold increased predictability positive and specificity and decreased sensitivity and predictability negative. Also, the effect of prevalence of infection on predictabilities was examined for the pooled data on sensitivity and specificity at a cell count threshold of 400,000 cells/ml. As prevalence of infection increased, predictability of a positive test result also increased, but predictability negative decreased. Differences in accuracy of somatic cell count as a predictor of infection at varying prevalences of infection suggest that test results should be interpreted for individual herds.

Animals↗