In healthy adult goats, closure of the esophageal groove was induced by thirst, IV administered vasopressin, and intracarotid administration of hypertonic NaCl solutions. The efficiency of stimulation was tested directly by visual inspection of the course taken by orally administered solutions through a ruminal or abomasal fistula, palpation of the lips of the esophageal groove through a ruminal fistula, and indirectly by following the glucose dynamics in the blood after oral administration of glucose solution. Esophageal groove closure was observed during drinking after a 48-hour period of water deprivation. Intracarotid administration of 1.5 ml of a saturated solution or 10.5 ml of a 1.5% solution of NaCl also stimulated groove closure; however, groove closure stimulated by administration of vasopressin is the most satisfactory procedure for passing compounds of therapeutic importance directly from the cardiac orifice to the abomasum.

In healthy adult goats, closure of the esophageal groove was induced by thirst, IV administered vasopressin, and intracarotid administration of hypertonic NaCl solutions. The efficiency of stimulation was tested directly by visual inspection of the course taken by orally administered solutions through a ruminal or abomasal fistula, palpation of the lips of the esophageal groove through a ruminal fistula, and indirectly by following the glucose dynamics in the blood after oral administration of glucose solution. Esophageal groove closure was observed during drinking after a 48-hour period of water deprivation. Intracarotid administration of 1.5 ml of a saturated solution or 10.5 ml of a 1.5% solution of NaCl also stimulated groove closure; however, groove closure stimulated by administration of vasopressin is the most satisfactory procedure for passing compounds of therapeutic importance directly from the cardiac orifice to the abomasum.

Adult Beagles were used to evaluate clinical signs and serologic response after inoculation with, or exposure to, Borrelia burgdorferi. An indirect immunofluorescent assay (IFA) and 2 ELISA were used to monitor the serologic response to B burgdorferi. Feeding infected ticks on 4 dogs (group 1) failed to cause seroconversion, and SC inoculation with 500 organisms caused minimal seroconversion in 2 of 4 dogs (group 2). At 56 days, approximately 3.01 X 10(8) B burgdorferi organisms were injected IV into group-1 dogs, and intraperitoneally into group-2 dogs. A control group of 4 dogs (group 3) had noninfected ticks feed on them, and then were given IV injection of physiologic saline solution. Increases in immunoglobulin M (IgM) titers were detected in 2 of 4 group-2 dogs approximately 7 days after the initial exposure. These titers returned to negligible values 20 days later. Immunoglobulin G titers increased approximately 10 days after the initial exposure and were mildly increased 56 days later, when dogs were exposed a second time. Both the IV and intraperitoneal injections (second exposures) resulted in increased IgM titers, which in both groups eventually returned to preexposure values after approximately 2 months. Immunoglobulin G titers increased within a week after the second exposure, and in 3 dogs monitored for 8 months, returned to negligible values after the 8-month period. One control dog had a slightly increased IgG titer 24 days after the second inoculation. The possibility of urine transmission is suggested. Clinical status, hemograms, serum biochemical profiles, ECG and results of urinalyses remained normal throughout the study. Borrelia burgdorferi was not isolated from either the blood or urine of these dogs. Gross or microscopic pathologic changes were not detected on necropsy.

Adult Beagles were used to evaluate clinical signs and serologic response after inoculation with, or exposure to, Borrelia burgdorferi. An indirect immunofluorescent assay (IFA) and 2 ELISA were used to monitor the serologic response to B burgdorferi. Feeding infected ticks on 4 dogs (group 1) failed to cause seroconversion, and SC inoculation with 500 organisms caused minimal seroconversion in 2 of 4 dogs (group 2). At 56 days, approximately 3.01 X 10(8) B burgdorferi organisms were injected IV into group-1 dogs, and intraperitoneally into group-2 dogs. A control group of 4 dogs (group 3) had noninfected ticks feed on them, and then were given IV injection of physiologic saline solution. Increases in immunoglobulin M (IgM) titers were detected in 2 of 4 group-2 dogs approximately 7 days after the initial exposure. These titers returned to negligible values 20 days later. Immunoglobulin G titers increased approximately 10 days after the initial exposure and were mildly increased 56 days later, when dogs were exposed a second time. Both the IV and intraperitoneal injections (second exposures) resulted in increased IgM titers, which in both groups eventually returned to preexposure values after approximately 2 months. Immunoglobulin G titers increased within a week after the second exposure, and in 3 dogs monitored for 8 months, returned to negligible values after the 8-month period. One control dog had a slightly increased IgG titer 24 days after the second inoculation. The possibility of urine transmission is suggested. Clinical status, hemograms, serum biochemical profiles, ECG and results of urinalyses remained normal throughout the study. Borrelia burgdorferi was not isolated from either the blood or urine of these dogs. Gross or microscopic pathologic changes were not detected on necropsy.

Peanut agglutinin (PNA) and surface immunoglobulin (SIg) were investigated as markers for T and B lymphocytes in blood and lymphoid tissues of dogs of various ages. In the blood study, 4 age groups (n = 8 dogs/group) were used. The mean (+/- SD) percentages of PNA-positive (PNA +) cells were 68.4 +/- 8.6% (group 1, < 1 year old), 70.3 +/- 9.2% (group 2, 1 to 2 years old), 72.0 +/- 3.7% (group 3, 5 to 6 years old), and 63.8 +/- 10.1% (group 4, 10 to 11 years old). The mean percentages of SIg-positive (SIg+) cells in blood were 32.1 +/- 10.6% (group 1), 43.2 +/- 7.0% (group 2), 34.3 +/- 4.8% (group 3), and 35.0 +/- 6.8% (group 4). The mean total percentages of PNA+ and SIg+ cells were 100 +/-6% (group 1), 113.5 +/- 4.9% (group 2), 106.3 +/- 5.3% (group 3), and 98.9 +/- 9.2% (group 4). The proportions of PNA+ and SIg+ cells in dogs of group 2 were significantly (P < 0.05) different from those in dogs of the other groups. Serial changes in PNA+ and SIg+ cells were investigated in blood of 6- to 29-week-old pups (n = 8). A significant (P < 0.05) transient decrease in PNA+ cells and a corresponding increase in SIg+ cells was observed in pups between 14 and 17 weeks old. Lymphoid tissue specimens and blood samples were obtained from 2- to 6-month-old dogs (n = 11) and from 6- to 12-month-old dogs (n = 10). Percentages reflected the combined data from both groups because there were no significant differences between the 2 age groups. The mean percentages of PNA+ cells were: blood, 68.4 +/- 8.6%; thymus, 86.6 +/- 16.3%; spleen, 29.5 +/-16.0%; lymph node, 48.5 +/- 16.0%; and bone marrow, 30.8 +/- 26.4%. The mean percentage of SIg+ cells were: blood, 32.1 +/- 10.6%; thymus, 3.1 +/- 5.5%; spleen, 69.3 +/-10.3%; lymph node, 55.4 +/- 15.2%; and bone marrow, 65.4 +/- 22.4%. The procedure to identify T lymphocytes in blood and lymphoid tissue was easy to perform, was reproducible, and could be performed on as few as 10(6) cells.

Peanut agglutinin (PNA) and surface immunoglobulin (SIg) were investigated as markers for T and B lymphocytes in blood and lymphoid tissues of dogs of various ages. In the blood study, 4 age groups (n = 8 dogs/group) were used. The mean (+/- SD) percentages of PNA-positive (PNA +) cells were 68.4 +/- 8.6% (group 1, < 1 year old), 70.3 +/- 9.2% (group 2, 1 to 2 years old), 72.0 +/- 3.7% (group 3, 5 to 6 years old), and 63.8 +/- 10.1% (group 4, 10 to 11 years old). The mean percentages of SIg-positive (SIg+) cells in blood were 32.1 +/- 10.6% (group 1), 43.2 +/- 7.0% (group 2), 34.3 +/- 4.8% (group 3), and 35.0 +/- 6.8% (group 4). The mean total percentages of PNA+ and SIg+ cells were 100 +/-6% (group 1), 113.5 +/- 4.9% (group 2), 106.3 +/- 5.3% (group 3), and 98.9 +/- 9.2% (group 4). The proportions of PNA+ and SIg+ cells in dogs of group 2 were significantly (P < 0.05) different from those in dogs of the other groups. Serial changes in PNA+ and SIg+ cells were investigated in blood of 6- to 29-week-old pups (n = 8). A significant (P < 0.05) transient decrease in PNA+ cells and a corresponding increase in SIg+ cells was observed in pups between 14 and 17 weeks old. Lymphoid tissue specimens and blood samples were obtained from 2- to 6-month-old dogs (n = 11) and from 6- to 12-month-old dogs (n = 10). Percentages reflected the combined data from both groups because there were no significant differences between the 2 age groups. The mean percentages of PNA+ cells were: blood, 68.4 +/- 8.6%; thymus, 86.6 +/- 16.3%; spleen, 29.5 +/- 16.0%; lymph node, 48.5 +/- 16.0%; and bone marrow, 30.8 +/- 26.4%. The mean percentage of SIg+ cells were: blood, 32.1 +/- 10.6%; thymus, 3.1 +/- 5.5%; spleen, 69.3 +/- 10.3%; lymph node, 55.4 +/- 15.2%; and bone marrow, 65.4 +/- 22.4%. The procedureto identify T lymphocytes in blood and lymphoid tissue was easy to perform, was reproducible, and could be performed on as few as 10(6) cells. Percentages of T lymphocytes identified compared favorably with those of other studies.

Foals with the Ca blood group antigen on their RBC were given colostrum with anti-Ca antibodies (6 foals) or colostrum without anti-Ca antibodies (6 foals). The PVC were determined at birth and 2, 4, and 6 days after birth for the foals in each group. Significant differences were not observed for the PCV between the 2 groups, indicating that foals were not adversely affected by ingesting colostrum with the anti-Ca antibody. Standardbred mares without the Aa blood group antigen were evaluated to determine whether production of anti-Ca antibodies influenced production of anti-Aa antibodies. Of 266 mares without the Aa antigen, 3 of 61 (5%) mares without the Ca blood group antigen produced anti-Aa antibodies and 43 of 205 (21%) with the Ca blood group antigen produced anti-Aa antibodies. These 2 groups of mares were significantly (p = 0.006) different; Ca-negative mares were less likely to produce antibodies to Aa than were mares with the Ca blood group antigen. This observation was consistent with a hypothesis of antibody-mediated immunosuppression of immune response to the As blood group antigen by antibodies to the Ca blood group antigen, ie, when a mare is exposed to her foal's RBC and already has antibodies to the Ca blood group antigen on the foal's RBC, then she is less likely to initiate an immune response to the Aa blood group antigen also on the foal's RBC.

Foals with the Ca blood group antigen on their RBC were given colostrum with anti-Ca antibodies (6 foals) or colostrum without anti-Ca antibodies (6 foals). The PVC were determined at birth and 2, 4, and 6 days after birth for the foals in each group. Significant differences were not observed for the PCV between the 2 groups, indicating that foals were not adversely affected by ingesting colostrum with the anti-Ca antibody. Standardbred mares without the Aa blood group antigen were evaluated to determine whether production of anti-Ca antibodies influenced production of anti-Aa antibodies. Of 266 mares without the Aa antigen, 3 of 61 (5%) mares without the Ca blood group antigen produced anti-Aa antibodies and 43 of 205 (21%) with the Ca blood group antigen produced anti-Aa antibodies. These 2 groups of mares were significantly (p = 0.006) different; Ca-negative mares were less likely to produce antibodies to Aa than were mares with the Ca blood group antigen. This observation was consistent with a hypothesis of antibody-mediated immunosuppression of immune response to the As blood group antigen by antibodies to the Ca blood group antigen, ie, when a mare is exposed to her foal's RBC and already has antibodies to the Ca blood group antigen on the foal's RBC, then she is less likely to initiate an immune response to the Aa blood group antigen also on the foal's RBC.

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.

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.