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.

Cells acquired from lymph node biospy specimens obtained from 58 dogs scheduled to undergo chemotherapy for lymphoma were immunophenotyped, using a microlymphocytotoxicity (MLCT) assay comprising a panel of well-characterized monoclonal antibodies (MAB) specific for canine cell surface antigens. Cells from 54 of the dogs concurrently were tested cytofluorometrically, using surface immunoglobulin (SIg) as a marker for B cells and the MAB DT2 specific for peripheral blood T cells. The MLCT results indicated frequent coexpression of antigens identified by DT2 antibody and, to a lesser extent, by 1A1 antibody on SIg-positive cells, suggesting that these antigens may be associated with other types of less-differentiated lymphoid cells, in addition to being associated with mature T cells. Class-II major histocompatibility antigens, as recognized by MAB H81.98.71, HB10a, and H40.315.7, were detected on most SIg-positive cells, but generally were lacking on SIg-negative, DT2-negative cells. The MAB Wig4, reactive with canine monocytes, recognized relatively few cells (11 of 58). Response to chemotherapy was not correlated with reactivity to MAB DLy6 specific for resting lymphocytes or to MAB W3G10 specific for a polymorphic antigen associated with the canine major histocompatibility complex. The MLCT assay appears to be efficient, rapid, and inexpensive for immunophenotyping cells from lymphoma biopsy specimens.

Three antigens were prepared from a type-3 avian strain of Pasteurella multocida, and their chemical and immunologic characteristics were studied. An antigen, designated 2.5S, was extracted with 2.5% NaCl solution and purified by chromatography. Lipopolysaccharide (LPS) was extracted with phenol-water, and a third antigen, designated FS, was extracted in 0.3% formalin solution containing 0.85% NaCl and purified by differential centrifugation. The 2.5S and the FS antigens consisted of 40% protein and 15% carbohydrate, whereas LPS did not contain a substantial amount of protein. A major protein component with a molecular weight of 44,000 was detected in the 2.5S antigen, as well as in the FS antigen. Of the 3 antigens, LPS had thehighest activity in mouse lethality and Limulus lysate tests. Antigenic cross-reactions among the 3 antigens were demonstrated by immunodiffusion tests. The 2.5S antigen was indistinguishable from the FS antigen, as both antigens contained the LPS component of approximately 45%. Treatments with various reagents indicated that the 2.5S and FS antigens contained at least 2 antigenic determinants. The first was a heat-stable protein sensitive to protease or phenol-water, and the second was a periodate-sensitive carbohydrate, which was an major antigenic determinant on the LPS antigen.

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.

Using an avidin-biotin-peroxidase complex immunoperoxidase staining method, respiratory syncytial virus (RSV) antigen was demonstrated in glutaraldehyde-fixed, parraffin-processed lung sections from calves with induced RSV pneumonia. The virus also was detected in formalin-fixed, paraffin-processed lung sections from calves with naturally occurring RSV pneumonia. Specific immunoperoxidase staining was detected within the cytoplasm of epithelial cells and syncytia in small bronchi, bronchioli, and alveoli. Staining also was detected within exudates in airway lumina and in mononuclear and multinucleate cells within alveolar lumina. Optimal intensity of staining was achieved by proteolytic enzyme treatment of lung sections, using 0 .1% pronase and overnight incubation in diluted primary antiserum. The distribution of antigen had a close correlation with presence of lesions. Antigen-staining patterns were similar in lung tissue from calves with naturally occurring and induced RSV disease.

Ninety-nine nonclassical serogroups isolated from newborn pigs with neonatal diarrhea were tested for fimbrial antigens F4(K88), F5(K99), F6(987P), F41, and F165, and for heat-labile enterotoxin, heat-stable enterotoxin a (STa), heat-stable enterotoxin b, verocytotoxin, and cytolethal-distending toxin. Thirty-two strains, belonging mostly to serogroups O64:K"V142,", O9:K103, and O20:K101, were F5-positive and usually produced STa, although 5 strains produced only heat-stable enterotoxin b. Fifteen strains, belonging mostly to serogroups O64:K"V142" and O20:K101, were F41 positive and usually produced STa. Twenty-three strains belonging mostly to serogroups O64:K"V142," O9:K103, and O20:K101, were F6-positive and usually produced STa. Several strains produced more than one fimbrial antigen, either F5 and F41, F5 and F6, F6 and F41, F6 and F165, or F5, F6, F41, and F165. None of the strains produced heat-labile enterotoxin, verocytotoxin, or cytolethal-distending toxin. The indirect immunofluorescence test was much more sensitive than was the slide agglutination test for the detection of each of the fimbrial antigens F5, F6, F41, and F165 on strains grown in vitro. The production of F6 by certain strains for which only a low proportion of cells were F6-positive in vitro as demonstrated by immunofluorescence, was confirmed by experimental infection of newborn pigs.

Ten-day-old chicken embryos were inoculated with isolates of myeloblastosis-associated virus that induced osteopetrosis of slow or rapid onset. Bursa of Fabricius, thymus, spleen, bone marrow, kidney, liver, and lung were examined at 15, 17, and 19 days in ovo and at 7 and 25 days after hatching by histologic and immunoperoxidase techniques. Tissues from 19-day-old in ovo embryos also were examined by electron microscopy. The lymphoid organs of embryos inoculated with all isolates manifested changes suggesting inhibited development. Virus was most often associated with macrophages, heterophils, and non-lymphoid stromal cells in these organs. Viral particles and antigen were abundant in tissues from embryos inoculated with slow-onset isolates, but cell necrosis was infrequent. The kidney and bursa had especially abundant viral particles and antigen. Conversely, viral particles and antigen were minimal in tissues from embryos inoculated with the rapid-onset isolate, yet intravascular cellular thrombi, substantial cell necrosis, and increased heterophils and hemocytoblasts were found.

Various techniques were used to look for protective, non-cross-reactive antibodies in the sera of cats exposed to virulent feline infectious peritonitis virus (FIPV). Antibodies reactive with feline enteric coronavirus (FECV) from FIPV-exposed cats were adsorbed by several passages over an FECV-Sepharose column. In an ELISA against FECV and FIPV, the activity against both viruses was removed at the same rate; thus, no FIPV-specific antibodies could be identified. By gel electrophoresis-derived ELISA, the responses of cats surviving FIPV exposure were compared with those of cats succumbing to FIPV exposure to determine whether survival could be correlated with an antibody response against a particular virus protein. Results indicated that both groups responded in the same way to the matrix envelope protein and nucleocapsid proteins. Even though the response to peplomer in each group was weak, the survivor group responded better to this protein. Furthermore, the response of this group to the peplomer protein had the highest correlation with virus neutralization titer.