Tracheal mucus transport rates were measured over a 10-minute period in 20 healthy horses twice in 24 hours. The mean rate was 1.93 +/- 0.55 cm/min on day 1 and 1.99 +/- 0.49 cm/min 24 hours later. The mean difference between day 1 and day 2 (0.06 +/- 0.42 cm/min) was not significant (P = 0.55). The range on day 1 was 1.12 to 2.9 cm/min and 1.11 to 2.89 cm/min on day 2.

Fifteen newborn germ-free pigs were inoculated with 2 strains, D-282 and T-15, of Streptococcus suis type II. Some pigs also were preinoculated with Bordetella bronchiseptica, which successfully predisposed them to S suis infection. The 2 streptococcal strains were differentiated by muramidase treatment, which released certain high molecular-weight proteins, termed muramidase-released proteins (MRP), from the cell wall of strain D-282, but not from the cell wall of strain T-15. Only strain D-282 (MRP-positive) induced clinical signs of disease and markedly increased neutrophil numbers in pigs. Streptococci were more frequently isolated from fecal swab specimens obtained from pigs inoculated with strain D-282 (MRP-positive) than from specimens obtained from pigs inoculated with strain T-15 (MRP-negative). Both strains were isolated from nasal swab specimens obtained from all infected pigs. Postmortem examination revealed fibrinopurulent meningitis, polyserositis, and polyarthritis in pigs inoculated with strain D-282; this strain was isolated from the CNS, serosae, visceral organs, heart, and joints. Whereas strains D-282 caused several pathologic changes, strain T-15, isolated from the lungs, caused only pneumonia. Both strains were isolated from the tonsils of all pigs. Virulence differed distinctly between the MRP-positive and the MRP-negative strains.

An avidin-biotin-peroxidase complex immunoperoxidase staining method was developed to detect Neospora caninum in formalin-fixed, paraffin-embedded tissue sections. Specific antiserum to N caninum was made in rabbits and used to probe tissues from dogs naturally and experimentally infected with N caninum. The test detected tachyzoites and bradyzoites of N caninum. A reaction was not observed to Toxoplasma gondii, Hammondia hammondi, Sarcocystis cruzi, S capricanis, S tenella, Besnoitia jellisoni, Caryospora bigenetica, Hepatazoon canis, Atoxoplasma sp, or the organism causing canine dermal coccidiosis. When antiserum made in rabbits to T gondii was used in the test, reaction to N caninum was not observed.

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.

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.

The role of bile salt in biliary lipid excretion was studied in 3 healthy ponies with chronic external biliary fistulas. After endogenous bile salt pool depletion, micelle-forming taurocholate or taurochenodeoxycholate was infused to replace excreted bile salt. Enterohepatic circulations were held open (total biliary diversion) throughout each study. Results indicated that biliary lipid excretion in ponies (113 +/- 21 nmol/in/kg of body weight) is approximately 10 times less than that reported in rodents. Although the lipid composition (4.4% cholesterol, 5.6% phospholipid, and 90% bile salt) was within the predicted range for a single phase of micellar (or vesicular) liquid in solution, it was supersaturated with cholesterol because of low absolute concentrations of bile salt and phospholipid. Ponies, like guinea pigs, were determined to have a high bile salt-independent secretion of biliary lipid with little (or no) coupling to endogenous bile salt output. However, bile salt excretion induced by higher taurocholate infusion rates (ie, those greater than the physiologic range of 61 to 125 nmol/min/kg) was positively correlated with an increase in biliary phospholipid excretion, but not cholesterol excretion, thus indicating that a threshold intracellular bile salt concentration may be associated with enchanced biliary phospholipid excretion in ponies. The apparent cholerectic effects of endogenous bile salts, taurocholate, and taurochenodenoxycholate (that is, the increment in bile flow per increment in bile salt recovered) were greater in ponies than reported for any other mammal.

Serum protein electrophoresis was performed on 71 clinically healthy juvenile and adult llamas (6 juvenile males, 7 juvenile females 25 adult males, 13 adult females, and 20 pregnant females) to determine normal serum protein concentrations. Values were reported for each of the 5 groups because the groups were not homogeneous in all 8 peaks. Although the values reported here may serve as reference values for adults, they represent only a guideline for the juveniles because of the limited number of animals in each of these groups.

A field study was performed to determine the effectiveness of benzathine cloxacillin for the treatment of infectious bovine keratoconjunctivits in cattle from 2 farms located in northern California. The study was performed between June and September of 1987. Affected calves ranging from 2 to 9 months of age were selected from the main herd when signs of corneal ulceration were observed. The study was conducted in 2 phases. For phase I, the affected calves of herd 1 (n = 21; Holsteins) and herd 2 (n = 43 Angus crossbred), were randomly assigned to 1 of 3 groups, and were either treated with 250 (n = 23) or 375 mg (n = 21) of benzathine cloxacillin, or mineral oil (n = 20) on days 1 and 4. For phase II, affected calves (n = 16; Angus crossbred, 3 to 9 months of age) from herd 2 were treated with benzathine cloxacillin (250 mg). Eight of these calves were retreated on day 4. After treatment, all calves were examined every 72 hours for 16 days. For examinations, a clinical score was assigned to each eye, and the surface areas of photographed corneal ulcers were measured. The ocular secretions were collected and examined culturally for Moraxella bovis. On days 7, 10, and 13, the calves treated with benzathine cloxacillin had significantly (P less than 0.05) lower lesion scores, compared with the controls. The percentage of day-1 area measurements on posttreatment days 4, 7, and 10 were significantly larger in the controls than in the treated calves. The mean healing times of corneal lesions in the 2 antibiotic treatment groups were significantly (P less than 0.05) shorter than in the controls. In the treated calves, the healing times of corneal ulcers less than or equal to 0.05 cm in diameter on day 1 were significantly (P less than 0.05) shorter than the healing times of larger lesions. The healing times of the corneal ulcers in the Angus crossbred calves were significantly (P less than 0.05) longer than the healing times of the Holsteins. The controls had the greatest number of nonhealed corneal ulcers on day 16. The number of calves that remained infected with M bovis on days 4, 7, 10, and 13 was significantly less in both groups of treated calves than in the controls. The scores, surface area measurements, healing times, and the M bovis isolation frequency in the calves of the 250-mg and 375-mg and 1- and 2-dose treatment groups were not significantly different. The minimal inhibitory concentrations (MIC) of penicillin, cloxacillin, and ampicillin in the day-16 isolates from benzathine cloxacillin-treated herd-2 calves were greater than in isolates from corresponding calves on observation day 1; however, twofold increases of the respective MIC of pretreatment and day-16 specimens were not observed. The highest MIC of ampicillin, cloxacillin, gentamicin, oxytetracycline, and penicillin were 0.5, 8.0, 0.5, 2, and 1 migrogram/ml, respectively, for isolates collected during the final study week.

Colostral volume and IgG and IgM concentrations were determined in 6 multiparous mares at foaling and then every 2 hours from 16 to 20 hours after parturition. Serum IgG and IgM concentrations at foaling also were determined in each mare. The rate of mammary secretion was 292 +/- 26 ml/h (range, 202 to 389 ml/h), and the colostral volume was 5.1 +/- 0.5 L (range, 3.2 to 7.0 L). The colostral IgG and IgM contents were 440 +/- 106 g (range, 199 to 855 g) and 3.1 +/- 0.9 g (range, 0.7 g to 7.1 g), respectively. There was no significant correlation between serum and initial colostral IgG and IgM concentration or between serum and total colostral IgG or IgM values. The colostral IgG and IgM concentrations at foaling correlated well with the total colostral IgG and IgM contents, respectively. The initial 250 ml of colostrum contained 10 +/- 1.4% (range, 6.0 to 13.9%) and 6 +/- 1.0% (range, 2.4 to 8.5%) of the total IgG and IgM contents, respectively, and the initial 500 ml of colostrum contained 20 +/- 2.7% (range 12.0 to 27.1%) and 14 +/- 1.2% (8.2 to 17%) of the total colostral IgG and IgM contents, respectively.