The in vitro and in vivo binding of a monoclonal antibody (MAB) that recognizes a tumor-associated carbohydrate antigen was studied in dogs. Monoclonal antibody 155H.7 was raised in response to inoculation of mice with beta-galactose(1-3)betaN-acetylgalactosamine conjugated to human serum albumin. Avidin-biotin-complex immunohistochemical staining of cryostat sections of normal and neoplastic canine tissue specimens revealed heterogenous binding of MAB 155H.7 to the cells of many canine mammary and lung carcinomas and homogenous staining of many sarcomas, including osteogenic sarcoma. In addition, there was variable staining of a variety of normal tissues including some ductual epithelium, peripheral nerve fibers, and some endothelial cells and fibroblasts. Immunoscintigraphy with 131I-labeled MAB 155H.7 was used to study the in vitro distribution of the antibody. The 131I-labeled MAB 155.H.7 was administered to 1 clinically normal dog, 7 dogs with osteogenic sarcoma, 1 dog with undifferentiated sarcoma, and 2 dogs with mammary tumor. Scintigraphy revealed concentration of radioactivity in 8 of 10 tumor sites within 24 hours after MAB administration. The ratio of 131I in tumor sites to 131I in the surrounding normal tissues, compared with the similar ratio of 99mTc-labeled erythrocytes ranged from 1.1 to 4.3 in tumor vs normal tissue with a mean value of 2, confirming tumor localization of the radiolabeled MAB in excess of that associated with enhanced tumor vascularization.

Twenty-one mixed-breed pony foals, reared and maintained under parasite-free conditions, were used to test the efficacy of ivermectin in oral drench and paste formulations (200 microgram/kg) against 11-day-old migrating larvae of Parascaris equorum. Three replicates of 4 foals and 3 replicates of 3 foals were formed on the basis of age. Foals in replicates of 4 were randomly allocated to be indicators, or to receive vehicle (control) or ivermectin paste or ivermectin liquid. Foals in replicates of 3 were randomly allocated to receive vehicle or ivermectin paste or ivermectin liquid. The recovery of larvae from the lungs, liver, and small intestines of the indicator foals showed that 99.9% of the larvae were in the lungs 11 days after inoculation (day 0 of treatment). The recoveries of larvae from lungs and small intestines of controls at 25 days after inoculation indicated that all larvae had migrated to the small intestine by this time. The mean length of larvae recovered from the lungs (11 days after inoculation) was 0.87 mm; the mean length of those recovered from the small intestine (25 days after inoculation) was 3.65 mm. Using larvae recovered from small intestinal contents for calculations, ivermectin in both formulations was 100% effective against 11-day P equorum (P less than 0.01, compared with control group geometric mean of 1498.4).

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.

Uterine response to inoculation with Streptococcus zooepidemicus organisms, 51Cr-labeled 15-micromoles microspheres, and charcoal was evaluated in 9 mares (4 resistant and 5 susceptible to endometritis) to determine mechanical and cellular clearance rates during the early postovulatory period. Mares were inoculated at estrus prior to ovulation during estrous cycles 1, 3, and 5. Uterine swab specimens for aerobic and anaerobic bacteriologic culture and serum for progesterone determination were obtained on postovulation day 3 during estrous cycle 1, on the day of ovulation during estrous cycle 3, and on postovulation day 5 during estrous cycle 5. Immediately thereafter, the uterus was irrigated with 50 ml of sterile physiologic saline solution containing tracer amounts of 125I-labeled human serum albumin. Streptococcus zooepidemicus was isolated from 10 of 15 (67%) uterine specimens collected from susceptible mares and incubated aerobically. Escherichia coli also was isolated from 2 of the 10 specimens incubated aerobically. Anaerobic bacteriologic culture of specimens from all mares yielded no growth. Chromium-labeled microspheres were recovered twice from 2 susceptible mares, on day 0 and day 5. Charcoal was retained in 5 specimens collected from 3 susceptible mares. Bacteriologic culture of specimens from resistant mares did not yield growth. On day 0, chromium-labeled microspheres and charcoal were recovered once from 1 resistant mare. Mares susceptible to end ometritis accumulated more fluid within the uterine lumen after ovulation than did resistant mares (mean +/- SEM, 52.73 +/- 15.22 ml and 7.41 +/- 1.96 ml, respectively; P less than 0.01). From this study, it appeared that uterine cellular and bactericidal mechanisms are dysfunctional during the early postovulatory period. However, there appeared to be no disruption of the mechanisms responsible for mechanical clearance of materials inoculated in the uterus.

The visceral dissemination of Borrelia burgdorferi in New Zealand White rabbits was evaluated following intradermal inoculation of 1*10 8 spirochetes. We inoculated Borrelia burgdorferi B31, B garinii KW1 and B afzelii S13, respectively, and monitored the dissemination in the experimentally infected rabbits for 28 days. In the B burgdorferi B31-challenged group, the spirochetes were com;oetely cleared in rabbits at day 1 and visceral dissemination was not demonstrated. However, B garinii KW1 and B afzelii S13 were found to successfully disseminate in visceral organs of rabbits during the experiment period of 28 days. And experimentally infection-derived immunological responses in rabbits were identified with enzyme-linked immunosorbent assay and immunoblot analysis. Based on these results, the differences in the virulence of Lymeborrelial strains were proved in rabbit model.

Twenty-one mixed-breed pony foals, reared and maintained under parasite-free conditions, were used to test the efficacy of ivermectin in oral drench and paste formulations (200 microgram/kg) against 11-day-old migrating larvae of Parascaris equorum. Three replicates of 4 foals and 3 replicates of 3 foals were formed on the basis of age. Foals in replicates of 4 were randomly allocated to be indicators, or to receive vehicle (control) or ivermectin paste or ivermectin liquid. Foals in replicates of 3 were randomly allocated to receive vehicle or ivermectin paste or ivermectin liquid. The recovery of larvae from the lungs, liver, and small intestines of the indicator foals showed that 99.9% of the larvae were in the lungs 11 days after inoculation (day 0 of treatment). The recoveries of larvae from lungs and small intestines of controls at 25 days after inoculation indicated that all larvae had migrated to the small intestine by this time. The mean length of larvae recovered from the lungs (11 days after inoculation) was 0.87 mm; the mean length of those recovered from the small intestine (25 days after inoculation) was 3.65 mm. Using larvae recovered from small intestinal contents for calculations, ivermectin in both formulations was 100% effective against 11-day P equorum (P less than 0.01, compared with control group geometric mean of 1498.4).

Thirty-two isolates of Campylobacter fetus subsp venerealis were obtained from 1 bull and 4 heifers with experimentally induced infection. When whole-cell antigens of isolates were cross titrated with antisera to the infecting strain, isolates from 3 heifers had limited antigenic variation, whereas whole-cell antigens of isolates from 2 cattle (the bull and a heifer) differed serologically from those of the infecting strain. Changes were detected specifically in 6 heat-labile antigens. Of the 6 heat-labile factors evaluated, all were initially present on the infecting parent strain, but not on early isolates obtained from 4 of the 5 cattle. Restriction enzyme analysis revealed minor variation in the DNA fingerprints of isolates obtained from individual cattle, thus implying stability of the Campylobacter genome once persistent infection is established. Isolates with identical restriction enzyme patterns expressed different heat-labile antigens. Correlation could not be found between the DNA electrophoretic pattern and the expression of heat-labile antigens.

Chicken eggs at embryonation day (ED) 18 or newly hatched chicks were inoculated with turkey herpesvirus (HVT), Marek's disease virus (MDV), or virus-free diluent and, at intervals after inoculation, tissue homogenates of virus-exposed and virus-free chickens or chicken embryos were examined for interferon (IFN) activity. Homogenates of lung thymus and spleen specimens from chickens given HVT at ED 18 had IFN activity. Activity of IFN in the lungs was studied further. Homogenates of lung specimens from chickens exposed to HVT at hatching also had IFN activity, although the concentration of IFN was lower than that in chickens given HVT at ED 18. The pathogenic isolates of MDV (JM-(MDV)), but not the atenuated (Md11/75C-(MDV)) or nonpathogenic (SB1-(MDV)) isolates, inoculates at ED 18 also induced high lung IFN activity. Exposure to a combination of HVT and SB1-MDV induced IFN activity comparable with that in chickens given HVT alone. The IFN activity in homogenates of lung specimens from virus-exposed chickens was species specific and heat and pH stable, but was destroyed by trypsin treatment. Occassionally, low IFN activity also was detected in homogenates of tissus specimens from virus-free chickens or chicken embryos. This IFN activity could have been produced constitutively or may have been induced by substances (inducers) in the environment.

Mastitis was induced in 4 lactating cows by inoculation of Klebsiella pneumoniae (10(7) organisms/ml) via the teat canal. Sterile isotonic saline solution (1 ml) was instilled into designated control quarters via the teat canal. Changes in milk leukotriene B4 and C4 (LTB4, LTC4) concentrations, milk somatic cell counts, and milk bovine serum albumin concentration were monitored over a 24-hour postinoculation period. Milk LTB4 concentration before inoculation in control quarters and quarters later to be infected was 376 +/- 45 and 326 +/- 56 pg/ml of milk, respectively. A significant (P less than 0.05) increase in milk LTB4 concentration in the infected quarters was first observed at postinoculation hour 6, and milk LTB4 concentration in infected quarters generally remained significantly high through postinoculation hour 14. Thereafter, milk LTB4 concentration in infected quarters was not significantly different from the concentration in control quarters. Measurable amounts of LTC4 were not detected in the milk of either control or infected quarters. Milk bovine serum albumin concentration in the infected quarters generally was high throughout the study, as were milk somatic cell counts. The results of this study suggested that LTB4 contributes to the pathogenesis of bovine mastitis.

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.