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Rabbits were immunized with purified caprine arthritis-encephalitis virus and examined for neutralizing activity. Analysis of virus-antiserum interaction at 37 degrees C demonstrated little loss of viral infectivity after incubation with heat-inactivated rabbit antiserum for 60 min. However, sensitization of virus (as assessed by the addition of complement) occurred almost immediately and was 95% complete after 10 min. The complement-dependent neutralizing activity was associated with the immunoglobulin G fraction of rabbit antiserum. Addition of goat anti-rabbit immunoglobulin G to the immune rabbit serum-caprine arthritis-encephalitis virus mixture also resulted in neutralization of infectivity when unbound antibody was removed before addition of the anti-immunoglobulin. Serum from most caprine arthritis-encephalitis virus-infected goats contains antibody activity to the core protein p28, as demonstrated by immunodiffusion and enzyme-linked immunosorbent assay. However, attempts to demonstrate neutralizing activity in the serum of goats up to 1.5 years post-inoculation or in serum of hyperimmunized goats were unsuccessful when the sera were examined alone or in combination with complement or rabbit anti-goat immunoglobulin or both.

The transfer of circulating immunoglobulin G1 (IgG1) antibody to the gastrointestinal tract in young calves was quantified by using bovine anti-dinitrophenol IgG1 antibody labeled with 125I. The antibody was administered to newborn calves by intravenous injection, and transfer of the labeled IgG1 to the gastrointestinal tract occurred as demonstrated by excretion of protein-bound label in the feces and by the presence of the labeled IgG1 antibody in the gastrointestinal tract lumen at necropsy. Sixty-eight percent of the [125I]IgG1 clearance occurred by transfer to the gastrointestinal tract. Protein-bound 125I in the gastrointestinal tract lumen retained 65% of the specific dinitrophenol-binding ability of the labeled antibody originally administered. These results show that (i) transfer to the intestinal lumen is the major means of IgG1 clearance in calves, and (ii) this transfer results in antigen-binding antibody in the intestinal tract lumen. The potential contribution to enteric immunity of IgG1 reaching the intestinal lumen from circulation remains to be determined.

The effect of circulating passive antibody on immunity to bovine rotavirus infections in neonatal calves was investigated. In the first experiment, rotavirus antibody titers in the small intestinal lumina of 5- and 10-day-old calves with a wide range of serum rotavirus antibody titers were determined. Neutralizing antibody was present in the small intestinal lumina in titers that correlated with the calves' serum titers (r = +0.84, P less than 0.01). Immunoglobulin G1 was the predominant isotype of intestinal luminal rotavirus antibody. Calves not fed colostrum during the absorptive period lacked rotavirus antibody in circulation and in the intestinal lumen at 7 days of age, even when they were fed large volumes of colostrum with a high rotavirus antibody titer at 48 h after birth. Therefore, rotavirus antibody is not retained in the intestinal lumen for 5 days following a colostrum meal, and the luminal antibody in the 5- and 10-day-old seropositive calves were probably derived from circulating antibody. In a second experiment, calves were passively immunized by subcutaneous injection of colostral whey with a high immunoglobulin G1 rotavirus antibody titer and challenged with virulent bovine rotavirus 48 h later. The passively immunized calves were protected from rotavirus infection and diarrhea compared with calves with comparable serum immunoglobulin concentrations but with lower serum rotavirus with lower serum rotavirus antibody titers. The results of these experiments indicate that circulating immunoglobulin G1 antibody appears in the gastrointestinal tract of neonatal calves and that circulating rotavirus antibody can prevent infection and diarrhea after rotavirus challenge.

A 14- to 26-kilodalton fraction of Staphylococcus aureus exoproteins isolated by molecular sieve chromatography and electroelution from polyacrylamide gels was shown to specifically react with antibodies in milk of naturally infected dairy cows. Silver staining of the antigen preparation electrophoresed in polyacrylamide gels showed the strongest reactivity in the 24- to 26-kilodalton region with lesser staining at lower apparent molecular sizes. An enzyme-linked immunosorbent assay was developed to differentiate infected from uninfected cows for diagnostic purposes. Samples from S. aureus-infected cows reacted in the assay, and samples from uninfected cows did not. There was no correlation between numbers of somatic cells in the samples and reactivity to the antigens. Samples from cows infected with coagulase-negative staphylococci did not react with the antigens. It was found, however, that some samples from uninfected cows that were recently postpartum or producing low amounts of milk contained antibodies which bound the antigens. This was believed to be due to transport from blood to the mammary gland of antibodies which were generated by previous intramammary infections or infections at other sites.

Concentrations of immunoglobulin (Ig) G1 were measured in 590 sera from 24- to 36-hour-old lambs, and failure in passive transfer (FPT), less than 6 mg/ml, occurred in 20 lambs. Of the 20 FPT lambs, 45% died before 3 weeks of age, whereas only 5% of the 570 lambs with adequate passive transfer died before 3 weeks of age. The low percentage of FPT was attributed to management practices ensuring suckling by the lambs and possibly to influences from several years of selecting ewes on the basis of weaned lamb production. The correlation between the concentration of IgG1 in 257 postpartum, presuckle ewe colostrum samples and the IgG1 concentrations in 362 lamb sera from those ewes was low (r = 0.32). However, the mean serum IgG1 concentration in 20 lambs from ewes with the lowest postpartum, presuckle colostrum IgG1 concentrations (less than 30 mg/ml) was significantly lower (P less than 0.001) than mean serum IgG1 concentration in 24 lambs from ewes with the highest postpartum, presuckle colostrum IgG1 concentrations (greater than 110 mg/ml). Postpartum, presuckle colostrum IgG1 was measured in 7 ewes whose lambs had FPT, and the IgG1 values varied throughout the colostrum IgG1 range. Colostrum IgG1 concentrations could not be used to explain FPT or to identify ewes likely to have lambs with FPT.

Serum IgG1 concentrations of calves less than 3 weeks old and dying from infectious disease were significantly lower (P less than 0.01) than those of clinically normal calves. Fifty percent of the dead calves had serum IgG1 concentrations that were more than 2 standard deviations below the normal mean, and an additional 35% had IgG1 concentrations that were more than 1 standard deviation below the normal mean. Low IgG1 concentrations were attributed to failures in passive transfer of colostral immunoglobulin. The few calves dying of noninfectious causes generally had normal serum immunoglobulin concentrations. The results of this study emphasize the importance of adequate colostral intake and absorption to the neonatal calf. In view of the large numbers of calves that die from neonatal infection each year, it may be assumed that failure in passive transfer, as reflected by low serum immunoglobulin concentrations, is one of the most important factors influencing neonatal calf mortality.

Presuckle colostral samples and lamb serum samples taken 36 h postpartum were assayed for immunoglobulin G1 (IgG1) concentration (mg/ml) using single radial immunodiffusion. Breeds sampled included Polypay (P), Rambouillet (R), Targhee (T), Columbia (C), Finnish Landrace (F) and Finn crosses (Fx). Sources of variation examined in IgG1 concentration in colostrum (dam trait) included dam's sire breed, dam's sire, age of ewe and number of lambs born. All sources of variation were statistically significant. Least-squares means of IgG1 levels for sire breed were 80, 64, 67, 64, 72 and 69 mg/ml for P, R, T, C, F and Fx breed groups, respectively. A fetal stimulus may exist to increase the mass of IgG1 in colostrum available for multiple births (61, 69 and 77 mg/ml for single, twin and triplet, respectively). Ewe age was a significant source of variation because of a high mean concentration of IgG1 in the yearling's colostrum (100 mg/ml), whereas only slight differences occurred between the other age groups (65 to 67 mg/ml), except for the 7-yr older group (53 mg/ml). Sources of variation examined in IgG1 concentration of lamb serum at 36 h postpartum (lamb trait) included lamb's sire breed, lamb's sire, age of dam, birth type and sex, with dam's colostral IgG1 concentration and day born as covariates. Sire within breed, birth type and the two covariates were significant. Least squares means for sire breed were 36, 32, 33, 32, 31 and 32 mg/ml of serum for P, R, T, C, F and Fx groups, respectively. Lamb serum IgG1 decreased as birth type increased. The heritability of IgG1, estimated by paternal half-sib analyses, was .19 +/- .12 for colostrum and .18 +/- .06 for lamb serum.

Summary Summary. In-vitro culture of Haemophilus somnus in liquid or solid media supplemented with bovine blood or serum resulted in non-immune binding of immunoglobulin (Ig) by the organism. This binding was independent of the antigen-combining site of the Ig molecule, since binding of an IgG preparation specific for the hapten dinitrophenol was unaffected by the presence of the homologous antigen. Quantitative comparison of the binding of Ig fragments Fab and Fc demonstrated that the non-immune binding occurred in the Fc region of bovine IgG. The isotypes of Ig that became bound to H. somnus included both bovine IgG subclasses (IgG1 and IgG2), which were bound equally, and bovine IgM.

125I-labeled immunoglobulin (Ig)G1 in colostral whey was used to determine the region of maximum absorption of Ig from the small intestine of the neonatal calf and the variation in Ig absorption among calves at the intestinal level. In experiment 1, 5 segments (approx 5%, 35%, 60%, 80%, and 95% of the duodenocecal length) were formed in the small intestine of 9 colostrum-deprived calves shortly after birth. These segments were injected with colostral whey containing 125I-IgG1 4 hours after birth, and uptake, transfer, and absorption (defined as uptake plus transfer) were determined for each segment 2 hours later. Raw data were adjusted for the milligrams of IgG1 injected per gram of intestinal tissue to obtain the least squares mean (LSM) value. The LSM values for absorption of IgG1 from distal segments 3, 4, and 5 were significantly greater (P less than 0.05) than those values for proximal segments 1 and 2. The region of the maximum IgG1 absorption was the lower small intestine, 60% to 80% of the duodenocecal length. There was also an indication of independence between uptake and transfer in each of the segments. Significant differences (P less than 0.05) were present among calves in the LSM values for uptake and absorption, but not for transfer. In experiment 2, thoracic ducts of 8 newborn calves were cannulated 4 to 5 hours after birth. At 6 hours after birth, colostral whey with 125I-IgG1 was injected into an intestinal segment (approx 60% to 80% of the duodenocecal length).(ABSTRACT TRUNCATED AT 250 WORDS)

Bovine immunoglobulin G subclass (IgG1 and IgG2) antibodies were found to fix bovine complement while only IgG1 fixed guinea-pig complement in vitro. Similar results were noted when IgG1 and IgG2 antibodies were tested by passive cutaneous anaphylaxis (PCA) in that both IgG1 and IgG2 caused PCA in bovine skin while only IgG1 mediated the reaction in rat skin. In precipitation reactions IgG1 antibodies to DNP failed to cause precipitation of DNP19-ovalbumin while IgG2 antibodies to DNP precipitated DNP19-ovalbumin. Both IgG1 and IgG2 antibodies to ovalbumin precipitated ovalbumin. Surprisingly, IgG2 antibodies to equine erythrocytes caused phagocytosis by bovine neutrophils and peripheral blood monocytes while IgG1 antibodies failed to cause either phagocytosis or adherence. Results with peripheral blood monocytes cultured for 7 days demonstrated that both IgG1 and IgG2 could mediate phagocytosis.

Crias, newborn alpacas (Lama pacos), that were almost agammaglobulinemic at birth had a 70% increase in total serum proteins within 24 hours largely because of absorption of gamma globulins from colostrum. Immunoglobulin G was the isotype in highest concentration in colostrum and in serum from 24-hour-old crias. The serum IgG concentration of 10 crias increased linearly (r = 0.97) from a mean of 0.3 mg/ml (+/- 0.1 SD) for serum collected before crias suckled to a maximal mean of 30.1 mg/ml (+/- 8.1 SD) at 24 hours. The 24-hour concentration decreased by half in 10 days. Immunoglobulin M also was absorbed from colostrum and increased linearly (r = 0.99) from a mean of 0.5 mg/ml (+/- 0.1 SD) for serum collected before crias suckled to a maximal mean of 4.2 mg/ml (+/- 2.2 SD) 24 hours after birth. The 24-hour serum concentration of IgM decreased by half in 7 days. Therefore, on a weight basis, 7 times more IgG than IgM was transferred to crias; IgG accounted for greater than 85% of the passively transferred proteins in serum of 24-hour-old crias. Absorption of functional antibodies of IgG and IgM isotypes from colostrum of immunized dams by crias also was demonstrated. Immunoglobulin G and IgM antibody titers to chicken RBC increased linearly to maximal geometric mean titers of 1,139 and 843, respectively, 24 hours after birth. The 24-hour IgG and IgM antibody titers decreased by half in 6 and 3.8 days, respectively. Purified alpaca IgG had a molecular mass of 166 kilodaltons, a predominant gamma mobility, and an extinction coefficient of 14.1.(ABSTRACT TRUNCATED AT 250 WORDS)

The capacity of cells from thymus, liver, spleen, mesenteric lymph nodes, peripheral blood, and bone marrow to respond to in vitro phytolectin and allogeneic lymphocyte-stimulation was determined in 16 pony fetuses 61 to 200 days old (gestational age). Phytolectin-responsive cells were detected in the thymus at the 80th gestational day, peripheral blood at 120 days, lymph node at 160 days, and spleen at 200 days. Mixed lymphocyte culture-responsive cells were detected in thymus at 100 days and in the spleen at 200 days (gestational age). Immunoglobulins (Ig) M and IgG were quantitated by radioimmunoassay. They were detected in fetuses prior to 200 days of age. All of 50 normal newborn foals had detectable quantities of IgM (165 +/- 56 micrograms/ml of serum). Quantities of IgG in normal newborn foal serum were lower and more variable. The minimal-maximal concentrations of IgG were 2 to 170 micrograms/ml of serum with a mean and SD of 51 +/- 49 micrograms/ml. The results indicate that (1) functional T lymphocytes are present in the fetus by 100 days (gestational age), (2) functional B lymphocytes are present by 200 days, and (3) that foals are immunocompetent before birth.

Failure of passive transfer (FPT) of immunoglobulin from colostrum was demonstrated as a major determinant of mortality in newborn alpacas (Lama pacos; crias). Serum IgG concentrations of dying crias were significantly (P less than 0.0001) lower than were serum IgG concentrations of crias that lived. Of 82 crias, 10 (12%) died within 1 month of age, and 7 of these had 0 to 9 mg of IgG/ml of serum at 48 hours after birth; 5 of the 7 had evidence of infectious diseases. The serum IgG concentrations of the remaining dead crias were 12, 13, and 20 mg/ml. On the basis of serum IgG concentrations of crias that died in the first month, FPT was defined as a 48-hour serum IgG concentration less than 9 mg/ml, which was greater than 2 SD below the 48-hour mean of clinically normal crias. Using this definition, the prevalence of FPT in the 82 crias studied was 9%. Corroborative evidence of the relationship between FPT and mortality was obtained from a retrospective study of 21 dead crias. The postmortem serum IgG concentration of 5 crias that died 2 to 10 days after birth ranged from less than 1 to 3 mg/ml; all were greater than 2 SD below the mean of age matched clinically normal crias. The range of serum IgG concentration was 2.2 to 21 mg/ml in 8 crias that died 11 to 20 days after birth; serum IgG concentration in 1 cria was greater than 2 SD below the normal mean, and 6 were greater than 1 SD below the normal mean.(ABSTRACT TRUNCATED AT 250 WORDS)

Lymphoid cells from Aleutian disease virus (ADV)-infected and noninfected mink were cultured in vitro and the synthesis of Ig M, IgG, and viral-specific antibody measured. Compared to noninfected mink, lymph node cells from mink with Aleutian disease (AD) contained a higher percentage of plasma cells and immunoglobulin-bearing lymphocytes, synthesized significantly more IgG, and produced detectable quantities of ADV-specific antibody. No significant difference in IgM synthesis was observed.

Isolated equine immunoglobulin (Ig)G(T) antibodies to equine infectious anemia virus P26 antigen did not precipitate with antigen when the ratio of antibody to antigen was high. However, at lower ratios of antibody to antigen precipitation occurred. In addition, complement-fixation by IgG and P26 antigen was inhibited by high concentrations of IgG(T). The unusual reaction pattern noted with IgG(T) antibodies was still detectable by the immunodiffusion test for equine infectious anemia virus. In situations of nonprecipitability by IgG(T), the adjacent positive control line was inhibited, and this was interpreted as a positive reaction.

Selective immunoglobulin M deficiency was diagnosed in 5 foals, on the basis of reduced serum immunoglobulin M concentrations (more than 2 standard deviations below the normal mean). All 5 foals had clinical signs or lesions involving the respiratory tract. Lkebsiella sp was isolated from joint fluids, bronchial lymph nodes, or tracheal washings from the 3 foals in which such samples were available for microbiologic evaluation.

Forty-eight-hour serum concentrations of immunoglobulin G1 (IgG1) were determined for 123 female calves born on 1 farm during a 12-month period and fed 2.8 L of colostrum by esophageal feeder within 2 hours of birth. Mean monthly serum IgG1 concentrations were lowest in the winter, and increased during the spring and early summer to reach their peak in September, after which they decreased. Eight of 64 calves (12.5%) born from June through October had failure of passive transer of IgG1 (serum IgG1 less than 8 mg/ml), whereas 27 of 58 (46.5%) born from November through May had failure of passive transfer.

With regard to our studies on the functional properties of bovine IgG1 and IgG2 antibodies, the differences were minimal when homologous systems were evaluated. Both IgG1 and IgG2 fixed bovine complement by the classical pathway, caused homologous passive cutaneous anaphylaxis, caused phagocytosis of coated erythrocytes by cultured monocytes and precipitated with an antigen having multiple unique determinants (ovalbumin). In contrast to IgG2, IgG1 caused neither adherence nor phagocytosis by freshly isolated neutrophils and monocytes. Additionally, IgG2 antibodies to DNP precipitated with DNP19ovalbumin while IgG1 antibodies formed soluble complexes with this antigen.

Measurement of serum immunoglobulins in 46 foals less than 2 weeks old revealed 9 foals with hypogammaglobulinemia. The hypogammaglobulinemia was attributed to failure in transfer of immunoglobulins from dam to foal via colostrum. Three of the affected foals did not nurse at all, or only slightly, and 2 of these died of infections within a few days after birth, whereas the 3rd foal did not grow as well as normal foals. Six of the affected foals nursed in an apparently normal manner, and 5 of these had nonfatal respiratory infections between 2 and 5 weeks of age. Analysis of serum samples from surviving foals demonstrated that immunoglobulins were eventually produced. One other foal examined had hypogammaglobulinemia at 57 days of age, an age when the foal should have produced large amounts of immunoglobulin independent of passive transfer. This foal had simultaneous infections and hypogammaglobulinemia, but eventually produced normal amounts of immunoglobulin. Cellmediated immunity was normal at 3 months of age. This condition was designated transient hypogammaglobulinemia and was thought to be due to a temporary inability to make immunoglobulins.

Agammaglobulinemia was diagnosed in a 1-year-old Thoroughbred horse on the basis of the following observations: (1) absence of serum immunoglobulins M, A, and G(T); (2) small amounts of serum immunoglobulin G (16 mg/100 ml); (3) absence of specific antibody in the serum of the horse following immunization and challenge exposure to 2 antigens; (4) absence of plasma cells, primary follicles, and germinal centers in a lymph node removed after antigenic stimulation; (5) absence of "natural" serum antibodies to rabbit-erythrocytes which were easily detectable in age-matched control horse serums; and (6) increased susceptibility to infections. There was evidence of functional cell-mediated immunity which included a skin response to injected phytolectins, skin response to antigen challenge following sensitization, and in vitro proliferative response of lymph node cells to phytohemagglutinin. An intact cell-mediated immune response was also supported by the observation that the horse lived to 17 months of age without antibody production, whereas horses with an absence of both antibody production and cell-mediated immunity (combined immunodeficiency) die by 4 months of age without immunologic intervention. The known features of agammaglobulinemia in this horse are similar to those in sex-linked agammaglobulinemia in persons and are unique among the immunodeficiences described in other animals.

The transfer of immunoglobulin G (IgG) and immunoglobulin M (IgM) from ewe to lamb was quantitated to determine the occurrence of failure in passive transfer. Concentrations of IgG and IgM in ewe serum did not correlate with those in the colostrum. Colostrum from all ewes contained abundant amounts of immunoglobulins when compared with serum values, with IgG being selectively concentrated over IgM. Absorption through the intestinal tract of the lamb appeared to be a nonselective process, lacking predilection for IgG and IgM. All lambs tested 24 hours after birth absorbed colostral immunoglobulins to some extent; however, 13 (14%) of 91 clinically normal lambs demonstrated some failure of passive transfer. In contrast, failure of passive transfer was found in 27 (46%) of 59 lambs dying of natural causes between 24 hours and 5 weeks of age. Evidence presented emphasizes the importance of absorption of adequate amounts of immunoglobulins to enable the newborn lamb to survive the first few weeks of life.