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F Elvinger

Publications and source records attributed to F Elvinger.

24 records · Page 2Linked to original sources

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↗

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↗

Mycoplasmal mastitis in a dairy herd.

In October 1985, mycoplasmas were isolated from bulk tank milk samples in a large Florida dairy (greater than 1,400 lactating cows). At that time, measures to isolate and control the spread of infection were instituted. In an initial screening test, Mycoplasma bovis was isolated from 21 of 153 milking string samples (milk from all quarters of 10 cows/string). Composite quarter milk samples from all quarters of every individual lactating cow in the herd were obtained for culture in November 1985 and December 1985. In October, 88 of 1,535 (5.7%) cows were identified as Mycoplasma-positive. An additional 31 Mycoplasma-infected cows were identified in December. The dairy elected to maintain the infected cows in a separate Mycoplasma-positive subherd, which would be milked at the end of each milking session. Seven additional Mycoplasma-positive cows were identified at initiation of lactation. All newly identified infected cows were transferred to the Mycoplasma-positive subherd. After segregation of Mycoplasma-positive cows, bulk tank milk samples obtained routinely from the main herd remained culture negative throughout the study. From February 1986 to October 1986, quarter milk samples were obtained monthly from cows in the Mycoplasma-positive subherd. Any cow that developed clinical mastitis or substantial decrease in milk production was, at the discretion of the herdsman, culled. Of the 126 cows in the subherd, 22 (17.5%) were culled for mastitis, 35 (27.8%) were culled for low production, and 9 (7.1%) were culled for other reasons. Of the remaining 60 cows, 16 (12.7% of the 126 cows) were Mycoplasma-positive on the basis of results from one or more samples obtained after February 1986.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

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↗

Pathogenic and fecal Escherichia coil strains from turkeys in a commercial operation.

The biochemical phenotypes and antimicrobial susceptibility patterns of 105 clinical Escherichia coli isolates from flocks with colibacillosis in a turkey operation were compared with 1104 fecal E. coli isolates from 20 flocks in that operation. Clinical isolates and 194 fecal isolates with biochemical phenotypes or minimum inhibitory concentrations for gentamicin and sulfamethoxazole similar to clinical isolates were tested for somatic antigens and the potential virulence genes hylE, iss, tsh, and K1. The predominant biochemical phenotype of clinical isolates contained 21 isolates including 14 isolates belonging to serogroup 078 with barely detectable beta-D-glucuronidase activity. Thirty-five fecal isolates had biochemical phenotypes matching common phenotypes of clinical isolates. Sixty-six (63%) clinical isolates exhibited intermediate susceptibility or resistance to gentamicin and sulfamethoxazole compared with 265 (24%) fecal isolates (P < 0.001). Seventy-seven clinical isolates reacted with O-antisera, of which 51 (66%) belonged to the following serogroups: O1, O2, O8, O25, O78, O114, and O119. In comparison, 8 of 35 (23%) fecal isolates subtyped on the basis of biochemical phenotype belonged to these serogroups and four of 167 (2%) fecal isolates subtyped on the basis of their antimicrobial resistance patterns belonged to these serogroups. Iss, K1, and tsh genes were detected more often among clinical isolates than these fecal isolates (P < 0.05). In summary, a small subgroup of E. coli strains caused most colibacillosis infections in this operation. These strains existed at low concentration in normal fecal flora of healthy turkeys in intensively raised flocks. The data suggest that colibacillosis in turkey operations may be due to endogenous infections caused by specialized pathogens.

Animals↗

Ataxia and paresis with equine herpesvirus type 1 infection in a herd of riding school horses.

An outbreak of neurologic disease associated with serologic evidence of equine herpesvirus type 1 (EHV-1) infection occurred in a herd of 46 riding school horses. Ataxia and paresis were observed in 14 geldings and 5 barren mares. Eight affected horses had distal limb edema, 1 horse had a head tilt, and 3 others had urinary incontinence. Other clinical signs included fever, depression, and inappetance in 30 horses. Seven horses with neurologic signs were treated with acyclovir. Serum neutralizing antibody titers against EHV-1 increased 4-fold between acute and convalescent samples or exceeded 1:256 in 19 of 44 horses, confirming recent infection. A significantly greater proportion of horses that seroconverted were mares (P = .014). Of the 19 horses exhibiting ataxia and paresis, 17 made a complete recovery, 1 made a partial recovery, and 1 was euthanized.

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