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Newborn Saanen goats were orally infected with two distinct biologically cloned isolates of the caprine arthritis-encephalitis lentivirus (CAEV), designated CAEV(63) (Crawford TB, Adams DS, Cheevers WP, Cork LC: Science 207:997, 1980) and CAEV (Co) (Cork LC, Hadlow WJ, Crawford TB, Gorham JR, Piper RC: J Infect Dis 129:134, 1974; Narayan O, Clements JE, Strandberg JD, Cork LC, Griffin DE: J Gen Virol 50:69, 1980). All infected goats seroconverted for antibodies to CAEV, and there were no serologic reversions. Histologic lesions consisted of chronic inflammation of variable incidence and severity in joints and mammary gland. Clinical arthritis, estimated by enlargement of carpi, correlated with severe inflammation of radiocarpal synovium. Statistical evaluations of clinical and histologic parameters indicated that chronic joint disease was significantly more frequent and more severe in the group of goats infected with CAEV(63) than in the group infected with CAEV (Co). Thus, the severity of chronic arthritis is determined in part by the relative pathogenicity of individual CAEV isolates. Analysis of the temporal development of carpal arthritis during the first 3 years of infection indicated that (a) the extent of eventual chronic disease in individual joints was apparent relatively early after infection, (b) joints with severe chronic lesions were clinically enlarged at irregular intervals and (c) the pattern of recurrent arthritis was unique for each joint. Thus, chronic arthritis develops with a progressive course which may be promoted by recrudescent inflammation. Infectious virus was recovered 3 years after infection from selected tissues of 12 of 17 CAEV(63)-infected goats and 11 of 18 CAEV(Co)-infected goats. Virus recovery was independent of the virus isolate used for experimental infection and did not correlate with the severity of lesions.

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.

A sodium sulfite-precipitation test utilizing 3 concentrations of sodium sulfite to evaluate the immune status of neonatal calves allowed scoring of serum immunoglobulin concentrations as less than 5 mg/ml, 5 to 15 mg/ml, and greater than 15 mg/ml. Of the 54 estimations for serums that contained greater than 5 mg/ml, 96% were correct; of the 30 estimations for serums that had between 5 and 15 mg/ml, 90% were correct; and of the 42 estimations for for serums with greater than 15 mg/ml, 93% were correct. It was concluded that this test can be used under field conditions to evaluate the immune status of neonatal calves.

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.

Studies were conducted to determine the ways in which antibody regulates proliferation of lymphocytes stimulated by phytohemagglutinin (PHA) and concanavalin A (ConA). Equine lymphocytes were reacted with PHA or ConA for 1 to 10 hours, washed free of excess lectin, then cultured for 3 days and examined for proliferation and incorporation of [3H]thymidine. Both PHA and ConA induced lymphocytes to proliferate after short incubation periods. This response could be interrupted by the addition of antibody to the respective lectin. Total suppression of the proliferative response occurred if antibody was added within the first 2 hours after initial contact with PHA or ConA. Addition at times up to 48 hours produced either total or partial suppression. The removal of excess antibody 4 hours after addition to the culture did not reverse the suppression. Using radiolabeled ConA and PHA, it was observed that suppressive antibody inhibited the release of lectin from metabolically active lymphocytes and from surfaces where pinocytosis was not possible or was minimized. Antibody did not affect the rate of degradation of lectin by the cells. These results indicate that antibody attached to lectins, already bound to the lymphocyte surface, can terminate the lymphocyte response and retard the rate of release of lectin from the cell membrane.

A polysaccharide was extracted by warm aqueous phenol from the F-38 strain of mycoplasma which causes contagious caprine pleuropneumonia (CCPP). After acid hydrolysis, the polysaccharide was found to be composed of the neutral sugars glucose, galactose, mannose and fucose and the amino sugars galactosamine and glucosamine. All the sugars were present in approximately equal quantities. Unmodified goat erythrocytes bound the polysaccharide readily and the sensitised cells reacted with antibodies in sera from goats with experimental or natural CCPP. The unique composition of the F-38 polysaccharide and the specific reactivity of polysaccharide-sensitised red cells with antibodies from CCPP infected animals suggests that the polysaccharide should be useful for identification of F-38 organisms and diagnosis of the disease.

Antibodies against hemoglobulin C (alpha2beta2 6Glu leads to Lys) were produced by immunizing horses and were purified by affinity chromatography. As expected from the bivalency of both the antibody and the antigen, the purified antibodies failed to produce immunoprecipitates upon reaction with the corresponding antigens. Identification of hemoglobin C in individual erythrocytes was achieved by reacting the fluorescein isothiocyanate-conjugated antibodies with the hemoglobin antigen in fixed smears of peripheral blood. Red cells from persons having a hemoglobin C gene were labeled strongly upon reaction with anti-Hb C-FITC; there was no labeling of red cells containing normal hemoglobins or Hb S, suggesting that the anti-Hb C antibodies recognize only the amino-terminal segment of the beta chains that contain lysine in position beta6.

Persistence of virus and a marked hypergammaglobulinemia are consistent features observed in mink with Aleutian disease virus infection. These events may result from altered lymphocyte function in infected mink. To test this possibility we determined the ability of lymphocytes from infected mink to respond to phytolectins (PHA and Con A), and a specific antigen (KLH) in a lymphocyte transformation test and quantitated the number of lymphocytes bearing surface immunoglobulin. Infected mink had a significantly lower response than normal mink to PHA and Con A (P less than 0.025), and the difference in the responses increased progressively with time post-infection. Infected mink immunized with KLH also had a decreased ability to respond to this antigen when compared to normal immunized mink (P less than 0.001). The number of lymphocytes bearing surface immunoglobulin was significantly elevated in three of 10 mink infected for 10 weeks, and in all of seven mink infected 32 weeks (P less than 0.001).

Arabian horses with severe combined immunodeficiency disease (SCID) were evaluated for thymic hormone activities using thymic extracts and sera. Extracts prepared from thymus of SCID horses were able to increase the number of spleen cells responding to sheep red blood cells in irradiated, bone marrow-reconstituted mice. In addition, ultrafiltrates prepared from sera of these immunodeficient horses, which contained material with molecular weight of less than 50,000 Daltons could (a) induce a population of human bone marrow precursor cells to differentiate into cells bearing SRBC receptors and form spontaneous E-rosettes, a characteristic of T lymphocytes, and (b) stimulate cyclic adenosine monophosphate (AMP) synthesis in mouse thymocytes. Based on in vivo and in vitro effects, it was concluded that the defect of these Arabian horses with severe combined immunodeficiency disease did not involve a complete thymic hormone inadequacy.

Sixty-six cases of combined immunodeficiency (CID) in foals were studied to determine the most prevalent causes of infection and death. Lesions of the respiratory system were observed in 59 of the foals and were attributable to infection with equine adenovirus. Pneumocystis carinii, and bacteria. Significant lesions were also observed in liver, pancreas, intestines, heart, and kidneys. Maintenance of foals with CID for experimental purposes is directed at the prevention and control of these secondary infections. Adenovirus can be controlled by administration of horse plasma containing high titers of antiadenovirus antibody. Bacteria are controlled by appropriate antibiotic therapy. Pneumocystis carinii infection remains a significant problem in the maintenance of foals with CID.

Caprine arthritis-encephalitis is a retrovirus-induced disease resulting in lymphoproliferative lesions of the CNS and joints. Peripheral blood leukocytes of chronically infected goats were analyzed for the types of cells present and for their reactivity to viral antigen and polyclonal stimulants. Two of 9 infected goats had abnormal numbers of B lymphocytes--one elevated and the other deficient. Lymphocyte reactivity to viral antigens was transiently detectable by a lymphoblastogenic assay in 5 of the 9 goats. The reactive cells were peanut agglutinin-negative T lymphocytes. Concanavalin A induced more division in T lymphocytes of infected goats than in lymphocytes of noninfected goats, whereas the reactions to phytohemagglutinin, pokeweed mitogen, and bacterial lipopolysaccharide were no different in the 2 goat groups. It is concluded that goats infected by the caprine arthritis-encephalitis virus have antigen-reactive T lymphocytes and that infection promotes the response to a nonspecific T-cell stimulant.

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.

Between January 1973 and September 1979, 2,092 horses and ponies were evaluated for immunologic disorders. A total of 418 abnormalities were detected in 416 (20%) of the animals tested. Disorders encountered were failure or partial failure of colostral immunoglobulin transfer from mare to foal (228 cases), combined immunodeficiency (159 cases), selective immunoglobulin M deficiency (19 cases), agammaglobulinemia (3 cases), transient hypogammaglobulinemia (2 cases), and lymphosarcoma (7 cases). Four conclusions were drawn from the study. (1) Immunologic abnormalities occur commonly in horses and ponies. (2) Failure and partial failure of passive transfer were the most common disorders, involving 19.7% of surveyed foals at risk. (3) Combined immunodeficiency remains a disease limited to Arabian horses. (4) Considering the high frequency of immunologic disorders in horses and the availability of diagnostic tests for the disorders, older animals with recurrent infections as well as all newborn foals should be evaluated for immune disorders.

Delayed hypersensitivity (DH) responses of normal and immunodeficient horses were evaluated with antigens [dinitrochlorobenzene (DNCB), keyhole limpet hemocyanin (KLH)] and phytolectins [phytohemagglutinin (PHA), concanavalin A (Con A)]. Immunologically normal horses sensitized with 5 daily applications of 2 mg of DNCB developed positive skin reactions upon challenge with 0.4 mg of DNCB. The delayed onset of the reaction and the predominately mononuclear cell infiltration at the test site indicated these were DH reactions. Normal horses sensitized with 500 microgram of KLH and challenged with 100 microgram of KLH developed skin reactions appearing earlier and composed of neutrophils and mononuclear cells, suggesting involvement of both humor and cellular mechanisms. Arabian foals with combined immunodeficiency failed to respond visibly to either antigen. Intradermal injection of 50 microgram of PHA induced visible reactions in all normal horses tested. The slow development and the predominately mononuclear cell infiltrate of PHA reactions resembled DH responses to antigen. Reactions were induced by Con A in 15 of 16 normal adult horses and 7 of 14 normal foals. The reactions were rapid in onset and contained numerous eosinophils. All 6 foals with combined immunodeficiency failed to respond to PHA injection, whereas 5 of 6 did not respond to Con A. Based on the results of these studies, it appears that in vivo skin tests with PHA and DNCB can be used to screen horses for deficient T-lymphocyte responses.

The in vitro and in vivo effects of corticosteroids on peripheral blood lymphocytes (PBL) from ponies were studied. Prednisolone inhibited lymphocyte stimulation by phytohemagglutin (PHA) in a dose-dependent manner, without inducing lysis even at large doses. The PBL from horses heterozygous for the combined immunodeficiency trait responded to corticosteroid treatment the same as did PBL from normal ponies. Removal of the corticosteroid after incubation with PBL from normal ponies partially restored responsiveness of these cells to PHA. Chronic in vivo treatment of ponies with corticosteroids caused a marked decrease in the absolute numbers of circulating lymphocytes. Most remaining lymphocytes had detectable surface immunoglobulin and C3 receptors, suggesting a greater decrease in the T-lymphocyte population. In spite of this, there was little change in the in vitro PHA- or keyhole limpet hemocyanin-sensitized ponies. In general, the corticosteroid effects of lysis, as well as the mitogenic and antigenic responses of PBL from ponies, were similar to those previously reported for human lymphocytes.

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.

Caprine arthritis-encephalitis virus was isolated from goat milk and transmitted most efficiently to kids through both milk and colostrum. In addition, it appeared that transmissions through other secretions of the doe occurred, but were less important than transmission in milk and colostrum. Intrauterine infection may have occurred in 2 of 32 cesarean-derived goats, but postpartum horizontal transmission could not be ruled out. Transmission by the aerosol route was not demonstrated, and even short-term direct contact between virus-infected bucks and virus-free does during breeding did not result in transmission. Prolonged direct contact for over 12 months between weaned cesarean-derived goats and virus-infected goats was necessary before horizontal transmission could be demonstrated under nondairy conditions. However, when uninfected does were milked with infected does, a high percentage became infected in less than 10 months. Heat inactivation (56 C) reduced approximately 10(5) median tissue culture infective doses of caprine arthritis-encephalitis virus to below titratable levels, and virus was not transmitted to kids fed virus-infected colostrum that had been heated at 56 C for 1 hour. A program of eradication is discussed in which kids are removed from their dams at birth, fed safe sources of colostrum and milk, and isolated from other goats until weaning.

The lentiviruses, caprine arthritis-encephalitis virus (CAEV) and progressive pneumonia virus (PPV) of sheep, cause major diseases in their respective hosts; however, the infectivity of these viruses for closely related species has not been determined. Experiments were conducted to determine whether CAEV would infect sheep and whether PPV would infect goats. Upon inoculation with CAEV, lambs developed a nonsuppurative arthritis and antibody to CAEV, and the virus was isolated up to 4 months later. Exposure of 3 lambs to CAEV-infected adult goats did not lead to demonstrable infection after 18 months. Young goats inoculated with PPV replicated the virus and developed arthritis and antiviral antibody. These results demonstrate that these distinctly different lentiviruses may infect and cause diseases in species other than their accustomed host. Presently used techniques may not be effective in differentiating which lentivirus is responsible for infection of sheep and goats. Our results also indicate that mixing sheep and goats may adversely influence attempts to eradicate lentiviruses from these species.

Nine monoclonal antibodies which reacted with equine immunoglobulin (Ig)M and not other equine Ig and serum proteins were prepared. Cells producing antibodies (C 1.9) which precipitated with IgM and bound to staphylococcal protein A were triple-cloned (C 1.9/3.2) and the antibodies further characterized. Monoclonal antibody C 1.9/3.2 reacted with an IgM determinant present on serum IgM from horses of several breeds. Studies with 125I-labeled IgM revealed the presence of this determinant on all IgM molecules. The monoclonal antibody enabled quantitation of IgM in presuckling foal and adult horse sera, using rocket electrophoresis. This procedure was used because presumably it gives a positive precipitation reaction over a wide range of antigen-antibody ratios. The C 1.9/3.2 monoclonal antibody recognized an exposed mu-chain determinant on live B lymphocytes, as determined by immunofluorescence. Also, IgM-containing cells could be identified in acetone-fixed frozen sections of lymphoid tissue. Sera from several other species carry the determinant identified by C 1.9/3.2, suggesting that the reagent may be useful for IgM studies in other species.

Four methods of detecting and quantitating mink antibody against Aleutian disease (AD) virus were compared. Counterelectrophoresis, modified, counterelectrophoresis, immunofluorescence, and complement fixation were performed blindly on 274 serum samples. All four methods were reliably specific for AD antibody. Immunofluorescence was less reproducible than the other systems. Immunofluorescence complement fixation were 4- to 8-fold more sensitive than regular or modified counterelectrophoresis, but were limited by background staining and anti-complementary activity, respectively, when used to detect small amounts of antibody in undiluted sera.

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.

Laboratory methods designed to quantitate serum immunoglobulin were evaluated: single radial immunodiffusion, zinc sulfate turbidity, and serum electrophoresis. Estimation of immunoglobulin concentration in neonatle calves, using total protein measurements, was also evaluated. Single radial immunodiffusion proved useful for quantitation when either class or subclass information was needed. Zinc sulfate turbidity measurements gave accurate results for total immunoglobulin except when hemolysis was present in the sample. A correction factor for hemoglobin that will minimize errors resulting from hemolysis was presented. Serum electrophoresis was also found to be an accurate quantitation method. Large errors were encountered in attempting to estimate immunoglobulin on the basis of total protein.

Only F38 isolates of mycoplasma cause classical contagious caprine pleuropneumonia (CCPP). Therefore, research has focused on the development of a vaccine that will prevent serious epidemics of the disease in goats. Goats immunized with two doses of a lyophilized preparation of isolated F38 organisms administered 4 weeks apart were completely immune to experimentally induced CCPP. The minimum immunizing dose was 0.15 mg, and this dose was still effective after storage for 14 months at 4 C and 22 C. The duration of immunity induced by a single dose of lyophilized F38 was at least 12 months.

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.

An indirect enzyme-linked immunosorbent assay (ELISA) was developed for the detection of equine infectious anemia (EIA) antibody in horse sera. Purified P26 viral protein was the antigen; alkaline phosphatase linked to rabbit anti-horse immunoglobulin G was the conjugate. The ELISA detected EIA antibodies in horse sera as early as 11 to 14 days after experimental inoculations. There was full agreement between the results of ELISA and the agar-gel immunodiffusion tests on EIA proficiency test sera. The ELISA readily detected EIA antibody in horse sera that had weak positive reactions on agar-gel immunodiffusion.

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.

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.