Morphologic changes developing during bovine mammary involution were examined. Quarter biopsy specimens were obtained weekly from 5 cows beginning the day milking was discontinued through parturition. Light and electron microscopic examination of mammary tissue indicated a gradual reduction in synthetic and secretory activity of alveolar epithelium as involution progressed. Light microscopic morphologic analysis revealed increases in stroma and nonactive secretory epithelium, with concomitant decreases in epithelium, lumen, and fully active secretory epithelium during the first 2 weeks of involution. Electron microscopic analysis of alveolar epithelium revealed decreased number of organelles associated with milk synthesis and secretion during this time. These changes reversed gradually beginning 2 weeks before parturition, and by the time of calving, cell structure was typical of lactating glands. Tissue from infected quarters had less synthetic and secretory ability as indicated by significantly higher percentages of stroma and nonactive cells, but lower percentages of lumen and moderately active cells, compared with uninfected quarters. Infected quarters also had more leukocytes infiltrating the epithelium, lumen, and stroma, compared with uninfected quarters. Microscopic examination of macrophages and neutrophils suggested these cells removed milk components and cellular debris during involution. Large numbers of plasma cells, with distended cisternae of rough endoplasmic reticulum, suggested local antibody production during the periparturient period.

Intramammary devices (IMD) were abraded with medium-grade emery cloth or were left smooth. One IMD of each type was inserted into a mammary quarter of each of 5 lactating cows. The remaining 2 quarters served as controls. Quarter foremilk, bucket milk, and stripping milk samples were collected for 3 consecutive days at 2 weeks after IMD insertion, and milk somatic cell counts (SCC) were determined. Milk samples also were collected immmediately after and 0.5, 1,2,4,6,8, and 11 hours after milking. All quarters were challenge exposed with 250 colony-forming units of Streptococcus uberis at 2 months after IMD insertion. Foremilk and stripping milk samples were collected for bacteriologic culture and SCC at the next 10 milkings. Mean foremilk, bucket milk, and stripping milk SCC (X 10(6) cells/ml) were 0.18, 0.07, and 0.91, respectively, for quarters with abraded IMD; 0.06, 0.05, and 0.43, respectively, for quarters with smooth IMD; and 0.03, 0.03, and 0.15, respectively, for control quarters. Mean SCC after milking (X 10(6) cells/ml) for the various intervals were 0.70, 1.29, 0.70, 0.97, 1.15, 1.17, 0.77, and 0.85 for quarters with abraded IMD; 0.43, 0.62, 0.61, 0.45, 0.64, 0.60, 0.31, and 0.26 for quarters with smooth IMD; and 0.15, 0.24, 0.15, 0.19, 0.15, 0.15, 0.14, and 0.06 for control quarters. After challenge exposure, 2 of 5 of the quarters with abraded IMD, 4 of 5 of the quarters with smooth IMD, and 8 of 9 of control quarters became infected. Results indicated that abraded IMD increased SCC in stripping milk to concentrations that provided 60% portection against challenge eexposure with S uberis.

During the 1986 lambing season, 33 Michigan sheep producers submitted all lambs that had died before weaning to the Michigan State University Diagnostic Laboratory for necropsy. Inductively coupled argon plasma emission spectroscopy was used to measure 22 elements in the liver of 888 of the lambs submitted. Mean concentrations of each element were established and compared with literature values of established deficient, normal, and toxic concentrations. Mean values in milligrams per kilogram of wet weight were as follows: A1, 3.843; As, less than 1; Ba, 0.176; Ca, 128.2; Cr, 0.778; Cu, 56.82; Fe, 491.6; Hg, less than 2; K, 2,150; Mg, 138.4; Mn, 2.776; Mo, 0.489; Na, 1,384; P, 2,583; Pb, 1,453; Sb, less than 1; Tl, less than 5; Zn, 68.31. In only 11 lambs did the liver contain As, B, Cd, Co, Hg, Sb, Se, or Tl in detectable concentrations.

To obtain synchronous infection, 10 cats were inoculated with feline herpesvirus-1 (FHV-) on the oral, nasal and conjunctival mucosa. Swab specimens of the nasal conjunctival, and pharyngeal mucosa were obtained for virus isolation from each cat before inoculation and at 3-day intervals thereafter until postinoculation day 21. Recovery of virus and evidence of clinical signs were used to document FHV-1 infection. Serum was obtained from blood samples collected sequentially from each cat between day 0 and postinoculation day 90. Virus-neutralizing antibody titer was determined in all serum specimens. Immunoprecipitation with [35S]methionine- and [14C]glucosamine-labeled viral antigens, followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, was performed on each specimen. Three precipitation bands with approximate molecular weights of 105,000, 68,000, and 60,000 were separated from [14C]glucosamine- and [35S]methionine-labeled immunoprecipitates. The concurrent detection of virus-neutralizing antibody glycoprotein-specific immunoprecipitins implied that in cats, the FHV-1 glycoproteins were important in the induction of virus-neutralizing antibodies to FHV-1.

In 5 horses, 13CO2/12CO2 ratios in expired air were determined using isotope mass spectroscopy to investigate metabolism of naturally occurring [13C]glucose. Oral glucose tolerance tests (OGTT) were performed using maize or beet glucose. Maize has a higher 13C concentration than that of most plants. The 13CO2/12CO2 ratios after OGTT was performed using maize glucose were compared with 13CO2/12CO2 ratios in expired air after OGTT was performed using beet glucose. The ratio also was determined during the period horses were not fed. Using OGTT, all horses were glucose tolerant. The OGTT performed using beet glucose led to minimal changes in 13CO2/12CO2 ratios. The 13CO2/12CO2 ratios decreased significantly (P less than 0.01) when horses were not fed. After oral dosing with maize glucose, 13CO2/12CO2 ratios reached maximal increases 5 hours after dosing and reached baseline values 15 hours after dosing.

We attempted to determine whether weaning is required for induction of diarrhea in pigs with postweaning enterotoxigenic Escherichia coli infection. Three-week-old newly weaned pigs and their suckling littermates were inoculated with the K88+ enterotoxigenic E coli strain M1823B. Fourteen of 21 weaned and 12 of 20 suckling pigs were genetically resistant to intestinal adhesion by the K88+ strain of E coli; they remained healthy, and gained weight at similar rates. Both groups of K88-resistant pigs gained weight faster, and shed fewer bacteria of strain M1823B in their feces, than did their K88-susceptible counterparts. Diarrhea developed in K88-susceptible pigs in the weaned (6 of 7 pigs) and suckling (4 of 8 pigs) groups, and 1 of the 4 affected suckling pigs died from complications resulting from diarrhea. The incidences of diarrhea, weight gain rates, and the numbers of strain M1823B shed in feces of susceptible weaned and suckling pigs were not significantly (P > 0.05) different. Diarrhea scores of susceptible weaned pigs were significantly (P < 0.02) higher than those of susceptible suckling pigs on the second day after inoculation. In this experimental model, it was concluded that weaning is not required for induction of diarrhea, but may modestly increase its severity.

Tissue drug residue research often involves the killing of an animal every time tissue concentrations are determined. To decrease the number of animals required to perform tissue depletion studies and to circumvent the statistical problems associated with determining tissue depletion kinetic properties, using multiple animals, the renal depletion profile of gentamicin from individual sheep was studied, using a bilateral renal translocation technique. Seven ewes were surgically altered, allowed to stabilize, and then allocated into 2 groups; groups-1 sheep (n = 4) were given 3 mg of gentamicin/kg, IM, q 12 h for 10 days, and group-2 sheep (n = 3) were not given gentamicin. The kidneys from all ewes were biopsied 9 times over 74 days after the termination of gentamicin treatment. The renal concentrations of gentamicin were measured by use of a validated tissue digestion procedure coupled with a liquid-phase fluorescence polarization immunoassay. On days 75 and 77 after the end of gentamicin treatment, all ewes were euthanatized and necropsied. The concentrations of gentamicin in the biopsy specimens ranged from 71.9 to 183 microgram/g on days 1 and 2 after dosing, and decreased to concentrations ranging from 3.99 to 7.35 microgram/g on days 73 and 74 after the end of dosing. The decrease in renal gentamicin concentrations was best described by a biexponential equation, The early phase half-life was 2.8 days, whereas the terminal phase half-life was 59 days (harmonic means). There was no difference in the appearance or histologic features of the kidneys from groups 1 and 2. The only lesions noticed were linear fibroses that were attributed to the biopsy procedure.

The effect of glucocorticoids on early follicular growth in sows undergoing normal estrous cycles was evaluated by administration of dexamethasone during the middle of the luteal phase. Plasma specimens were obtained for measurement of luteinizing hormone (LH), follicle-stimulating hormone (FSH), progesterone, and estradiol-17 beta concentrations. Fifteen sows were used. Control sows (n = 5) were given physiologic saline solution twice daily from day 9 to day 14 of the estrous cycle. Sows of the second group (n = 5) were given dexamethasone (30 microgram/kg of body weight, IM) similarly, and those of the third group (n = 5) were given dexamethasone plus gonadotropin-releasing hormone (GnRH+ 50 microgram at 6-hour intervals, IV). Plasma specimens, obtained twice daily from day 8 through day 26, indicated that progesterone production and luteal regression were not inhibited by any of the 3 treatment regimens. Although preovulatory plasma estradiol concentration increased in control sows, such was not observed in the sows treated with dexamethasone or dexamethasone plus GnRH (P less than 0.01). Ovulation, with formation of corpora lutea, occurred in gilts given saline solution. Dexamethasone administration resulted in persistence of 19 to 41 follicles/ovary (2 to 4 mm in diameter), and dexamethasone-plus-GnRH treatment resulted in 6 to 18 follicles/ovary (5 to 6 mm in diameter). Plasma was obtained at 15-minute intervals for 12 hours to compare the effect of treatmenton hormone concentrations on day 12 of the estrous cycle with the values on day 8. Glucocorticoid administration had no significant effect on mean concentration, final concentration excluding those hormone concentrations that constituted part of a pulse (referred to as base line), number of pulses, pulse amplitude, and area under the pulse for either gonadotropin. Addition of GnRH to dexamethasone treatment significantly (P less than 0.01) increased all plasma LH values, but only base-line concentration of FSH. For estradiol, pulse amplitude and mean pulse area were increased (P less than 0.05), and although the frequency of pulses was not significantly altered, base-line concentration in glucocorticoid-treated sows was significantly reduced, compared with that of control sows. In sows treated with GnRH plus dexamethasone, the pulse frequency of estradiol was significantly (P less than 0.01) increased, but pulse area and amplitude were similar to those of sows given saline solution. Dexamethasone treatment was associated with an increase in mean and base-line concentrations of progesterone. The results suggest that high midcycle glucocorticoid concentrations (1) do not inhibit luteal function or regression, (2) have little influence on LH and FSH secretion during the middle of the luteal phase, (3) alter the pattern of estradiol secretion, (4) are associated with the persistence of small ovarian follicles, and (5) result in the development of fewer but larger follicular structures when GnRH is administered concurrently.

Twelve Holstein calves mere used to determine the prophylactic efficacy of ivermectin against challenge exposure with gastrointestinal and pulmonary nematodes. Two groups of 6 calves (mean body weight, 205 kg) each were formed by restricted randomization according to body weight. Group-l calves served as nonmedicated controls. Each calf of group 2 was orally given one prototype sustained-release bolus designed to deliver ivermectin at a continuous daily dose of 8 mg. Third-stage nematode infective larvae were given to the calves on posttreatment days 28 and 42. The calves were euthanatized 77 or 78 days after treatment. Ivermectin was 100% effective (P < 0.05) in preventing the establishment of infection by Haemonchus placei, Ostertagia ostertagi, Cooperia spp (C punctata, C oncophora, C surnabada), Nematodirus helvetianus, Oesophagostomum radiatum, and Dictyocaulus viviparus and was > 99% effective against Trichostrongylus axei. Incidental infection by Trichuris spp was reduced by 94% (P = 0.08).