Neutrophils from 8 Holstein heifers were evaluated for function during the periparturient period. Random migration, ingestion of bacteria, superoxide anion production, native (nonenhanced) chemiluminescence, iodination, and antibody-dependent, cell-mediated cytotoxicity by neutrophils were determined. Foremilk samples were evaluated for bacteria. Significant (P less than 0.05) increases in random migration of neutrophils, iodination, and chemiluminescence were evident 2 weeks before parturition and then decreased dramatically by the first week after parturition. These impairments of neutrophil function after parturition may be manifested as a severe cumulative deficit in the native defenses afforded by the neutrophil.

Ten Holstein heifers were fed a selenium-deficient (SeD) diet (0.04 mg of Se/kg on a total ration dry-matter basis) 3 months before calving and throughout their first lactation. A selenium-supplemented (SeS) diet (2 mg of Se/head/d) was fed to a group of 10 heifers. In about the 14th week of lactation, the cows were challenge-exposed to Escherichia coli by administering 15 to 40 colony-forming units (CFU) into 1 mammary gland. Selenium concentration microgram/ml) in blood around the time of challenge exposure was 0.033 +/-0.002 (mean +/- SEM) in SeD and 0.132 /-0.006 in SeS cows. Infections were established in all challenge-exposed quarters. The frequency of quarter atrophy and agalactia, and reduction in whole-udder milk yield in the first 4 days after challenge exposure, were greater (P < 0.05) in the SeD cows. Log10 peak bacterial concentrations in milk were higher (P < 0.05) in SeD (7.63 +/- 0.34 CFU/ml) than in SeS cows (5.57 0.66 CFU/ml). Mean log bacterial concentration was significantly higher (P < 0.05) from 12 to 20 hours after challenge exposure in SeD than in SeS cows. Duration of infection was significantly greater (P < 0.05) in SeD (162.0 +/- 12.0) than in SeS cows (114.4 +/- 18.0 hours). Milk somatic cell counts increased significantly more slowly (P < 0.05) in SeD than in SeS cows from 8 to 16 hours after challenge exposure. Ratios of milk somatic cells to bacteria in milk were significantly lower (P < 0.05) in SeD than in SeS cows at l2 and 16 hours after challenge exposure.

Infectious hematopoietic necrosis virus (IHNV) was detected in the common Mayfly (Callibaetis sp) by western immunoblot assay and was propagated in fish cells (CHSE-214) in culture. When propagated in cell culture, cytopathic effect characteristic of IHNV infection was observed. Antibody specific for IHNV was used to detect all of the major proteins of IHNV in the western immunoblot assay. When the crude lysate was subjected to electron microscopy, bullet-shaped particles (84 nm X 194 nm) characteristic of IHNV were observed. The data suggested that the Mayfly may be a factor in the dissemination of IHNV.

To determine their capacity to host Brucella abortus, face flies were examined 1 to 120 hours after feeding on broth containing bacteria and bovine erythrocytes. Brucella abortus was cultured in large numbers from whole flies for 12 hours after feeding, but not after 72 hours. Histologic analysis showed that brucellae were rapidly taken into the midgut, sequestered from erythrocytes, transiently stored, and shed in the feces; there was no evidence of bacterial replication within epithelial cells. Immunoperoxidase and immunogold techniques revealed that most brucellae in the gut were confined to the lumen by the peritrophic membrane, that brucellae were degraded in secondary lysosomes of midgut epithelial cells, and that intact brucellae passed into connective tissues surrounding the midgut. Bacterial excretion without midgut replication is consistent with transient, but not long-term, insect transmission in nature.

Gas eructation function of the gastroesophageal sphincter (GES) was investigated in 6 conscious dogs before and after a sleeve was placed around the GES and gastric cardia and during IV infusion of a beta-adrenergic amine (epinephrine). To induce eructation, nitrogen gas was insufflated (351.4 +/- 2 ml/min; mean +/- SEM) into the stomach through 1 channel of a 4-lumen catheter. After baseline studies and epinephrine infusion studies were completed in each dog, surgery was done to limit partially gastric distension by intraluminal contents by placing a silicone rubber sleeve around the GES and the first few centimeters of the cardia. Gastroesophageal sphincter pressure was 31.8 +/- 2.2 mm of Hg in baseline studies, 17.3 +/- 1.3 mm of Hg during epinephrine infusion (P less than 0.003), and 30.3 +/- 2.2 mm of Hg after the sleeve was placed around the GES and cardia. During insufflation, gastric pressures before eructation increased to 5.74 +/- 0.41 mm of Hg before and to 15.15 +/- 1.63 mm of Hg after carida sleeve placement (P less than 0.001). Eructation occurred at intervals of 1.83 +/- 0.41 minutes before cardia sleeve placement, and eructations were not observed with the sleeve in place. Before the sleeve was placed, administration of epinephrine resulted in an eructation interval of 0.84 +/- 0.09 minutes, which was significantly different from that in the same dogs given no drugs (P less than 0.004). In vitro comparison of stomachs filled with fluid or filled with fluid and gas revealed that relatively small amounts of gas added to a partially filled stomach caused marked distension of the gastric cardia in comparison with no effects when fluid only was added. Seemingly, distension of the gastric cardia was the important stimulus for eructation. Limiting this distension prevented eructation and beta-adrenergic stimulation increased eructation frequency.

Effects of xylazine HCl (0.5 mg/kg of body weight, IV) and/or butorphanol tartrate (0.04 mg/kg, IV) or neostigmine methylsulfate (0.022 mg/kg, IV) on myoelectric activity of the cecum and right ventral colon were studied in 4 conscious female ponies. Eight bipolar Ag/AgCl electrodes were sequentially placed on the seromuscular layer of the cecum (6 electrodes) and right ventral colon (2 electrodes). Recordings began 30 minutes before and continued for 90 minutes after drug administration. Each drug or drug combination was studied on 2 occasions in each pony. Two major patterns of coordinated spike bursts were identified. A series of coordinated spike bursts began at the cecal base and was conducted to the cecal apex (pattern I). A series of coordinated spike bursts began at the cecal apex, traversed the cecum, cecocolic orifice, and right ventral colon and was termed a progressive pattern (pattern II). Xylazine administration caused a significant decrease in patterns I and II for 20 minutes (P less than 0.05). Butorphanol tartrate administration caused a significant decrease in the progressive pattern for 10 minutes (P less 0.05) without affecting the orally directed pattern. Administration of the combination of xylazine/butorphanol significantly decreased the frequency of pattern I for 40 minutes (P less than 0.05) and pattern II for 30 minutes (P less than 0.05). Neostigmine administration caused a significant increase in the frequency of pattern II for 30 minutes (P less than 0.05) without affecting pattern I (P greater than 0.05). Changes in conduction velocity of pattern I or II or the duration of spiking activity were not significantly different because of any treatment.

Experiments were conducted to establish a persistent Salmonella typhimurium infection in convalescent swine, and to determine rate of shedding and distribution of the organism in internal organs. Naturally farrowed Salmonella-free pigs (n = 37) were orally exposed to S typhimurium when 7 to 8 weeks old. Fecal samples, tonsillar scrapings, and rectal swab specimens were examined bacteriologically for S typhimurium at weekly intervals after exposure until necropsy (maximum of 28 weeks after exposure). Necropsies of 1 to 4 randomly selected pigs were conducted at 2, 4, and 7 days and at 2, 4, 6, 8, 12, 16, 20, 24, and 28 weeks after exposure. The following internal organs were examined bacteriologically for S typhimurium: liver, spleen, kidney, gallbladder, heart, lung, and stomach; segments of the intestinal tract with corresponding lymph nodes; lymph nodes from lymphocenters of the head and neck, thoracic and abdominal cavities, pelvic wall, and thoracic and pelvic limbs. Fecal samples were 83 to 100% culture-positive up to postexposure (PE) week 22, then varied from 14 to 67% positive until PE week 28. At least 60% of tonsillar swab specimens and 50% of rectal swab specimens were culture-positive up to PE week 20, after which they varied from 0 to 70% positive until PE week 28. At necropsy, S typhimurium was recovered most freguently from tonsils (93.5% positive), followed by segments of the intestinal tract from caudal portion of jejunum to rectum (71% recovery from cecum), and mandibular (54.8%) and ileocolic (45.2%) lymph nodes. The organism generally did not persist beyond PE week 2 in other lymph nodes of the head and neck, lymph nodes of the abdominal wall, thoracic cavity, or limbs, or in heart, liver, or spleen. The gallbladder, kidney, and lungs of all pigs were culture-negative.

Heifers were inoculated IV with 1 of 4 modified-live bovine herpesvirus-1 vaccinal strains against infectious bovine rhinotracheitis (2 heifers/strain) on postbreeding day (PBD) 14. The effect of infection on fertility was monitored by plasma progesterone assay at 1- to 3-day intervals from the time of virus exposure until PBD 60. Infertility was detected in 4 of 8 inoculated heifers. In 2 heifers, progestrone concentrations decreased to values indicative of estrus within 10 days after inoculation (PBD 24). The 2 other heifers had evidence of embryonic death on PBD 40 and 42. Two control heifers inoculated with culture medium from noninfected cells maintained their pregnancies.

Twenty-nine healthy 17- to 29-day-old unweaned Isaeli-Friesian male calves were each given a single IV or IM injection of 10 or 20 mg of moxalactam disodium/kg of body weight. Serum concentrations were measured serially during a 12-hour period. Serum concentration vs time profiles were analyzed by use of linear least-squares regression analysis and the statistical moment theory. The elimination half-lives after IV administration were 143.7 +/- 30.2 minutes and 155.5 +/- 10.5 minutes (harmonic mean +/ SD) at dosages of 10 and 20 mg of moxalactam/kg of body weight, respectively. Corresponding mean residence time values were 153.1 +/- 26.8 minutes and 169.9 +/- 19.3 minutes (arithmetic mean +/- SD). Mean residence time values after IM administration were 200.4 +/- 17.5 minutes and 198.4 +/- 19.9 minutes at dosages of 10 and 20 mg/kg, respectively. The volumes of distribution at steady state were 0.285 +/- 0.073 L/kg and 0.313 +/- 0.020 L/kg and total body clearance values were 1.96 +/- 0.69 ml/min/kg and 1.86 +/- 0.18 ml/min/kg after administration of dosages of 10 and 20 mg/kg, respectively. Moxalactam was rapidly absorbed from the IM injection site and peak serum concentrations occurred at 1 hour. The estimated bioavailability ranged from 69.8 to 79.1%. The amount of serum protein binding was 53.4, 55.0, and 61.5% when a concentration of moxalactam was at 50, 10, and 2 micrograms/ml respectively. The minimal inhibitory concentrations of moxalactam ranged from 0.01 to 0.2 micrograms/ml against Salmonella and Escherichia coli strains and from 0.005 to 6.25 micrograms/ml against Pasteurella multocida strains.

Sixteen 7-week-old Holstein male calves were inoculated with sporulated oocysts of Eimeria zuernii. Four calves (controls) were euthanatized and necropsied at 14 and 20 days after inoculation (DAI). Two calves were treated with 20 mg of dexamethasone (IM) on 13, 14, and 15 DAI and euthanatized and necropsied 17 DAI and 2 calves were given similar treatments and necropsied 20 DAI. The 8 other calves were euthanatized and necropsied 20 DAI. Two were started on the anticoccidial drug decoquinate in feed 13 DAI; 2 others were given decoquinated on the same schedule plus dexamethasone on 13, 14, and 15 DAI. Two calves were given the antibiotic narasin in feed beginning 13 DAI and 2 calves were given parasin on the same schedule plus dexamethasone on 13, 14, and 15 DAI. All calves, except 2 controls necropsied 14 DAI and 4 calves given decoquinate, discharged moderate-to-large numbers of oocysts in feces and had moderate-to-severe changes in fecal consistency. Histologic examintions revealed large numbers of endogenous stages in tissues of calves treated or not treated with dexamethasone. Few endogenous stages were observed in tissues from calves that were given decoquinate or decoquinate plus dexamethasone. Calves given narasin or narasin plus dexamethasone had moderate-to-large numbers of endogenous stages in the tissues.