Pathophysiological changes in urine and blood from calves experimentally infected with Sarcocystit cruzi.

Two 8-week experiments were conducted to determine the relationships between nutritional stress and pathophysiological changes in male Holstein calves infected with Sarcocystis cruzi. Calves were infected by oral inoculation with 200 000 S. cruzi sporocysts. In the first experiment weight gain reduction was greatest in inoculated calves during weeks 4 and 5 after inoculation. Feed intake was reduced during the 5th week. Erythrocyte count was reduced during week 5 and haemoglobin was reduced during week 6. The 24-h excretion of urinary and urea nitrogen from the inoculated calves was increased by treatment. In the 2nd experiments, both the feed-restricted and inoculated calves lost weight during weeks 4 and 5; feed intake was lower from week 5 to 8 inclusive. Urine volume from inoculated calves was lower during week 8. Lower urine excretions of sodium and potassium resulted from S. cruzi inoculation. There was a non-significant trend for higher urinary zinc excretion in the inoculated group during week 4. Urine nitrogen excretion from inoculated calves was higher during week 6. The urinary excretion of 3-methylhistidine from the inoculated calves was higher during week 4 and excretion of guanine was higher during weeks 4, 5 and 8. S. cruzi has several specific pathophysiological effects on calves beyond those induced by nutritional stress.     

Experimental induction of the two-host life cycle of Sarcocystis cruzi between dogs and Korean native calves

Eight dogs were experimentally infected with Sarcocystis by oral inoculation of cardiac muscle from naturally infected cattle. The infected dogs commenced discharging of sporocysts in the feces after 10 to 12 days of inoculation, and continued until 20 and 35 days after inoculation. Three dogs were reinfected with cardiac muscle from the naturally infected cattle. Sporocysts reappeared in the feces on 12 to 13 days after reinfection. Sarcocystis sporocysts collected from the experimentally infected dogs were fed to each of the two 30-day-old Korean native calves. The infected calves remained clinically normal, except for the high fever (> or = 40 degrees C) and decreased hematocrit values on day 30 to 40 post inoculation. Muscular cysts of Sarcocystis were found from infected calves on day 40 post inoculation. Proliferative forms of Sarcocystis were also observed in the muscle of infected calves. These results suggest that the Sarcocystis cruzi found in Korean native cattle has a 2-host life cycle with dogs as the definitive host and Korean native calves as the intermediate host.     

Clinical and Serological Response after Experimental Inoculation with Babesia Divergens of Newborn Calves with and without Maternal Antibodies

The influence of maternal antibodies on clinical and serological response after experimental inoculation with Babesia divergens of newborn calves was studied. Five calves, born to dams seropositive for B.divergens, (Group 1) had specific maternal antibodies when tested 12 h after their first feeding of colostrum. At that point they were inoculated i.v. with B.divergens infected erythrocytes. Five other calves, born to dams seronegative for B.divergens, (Group 2) had no Babesia specific maternal antibodies when inoculated at the same age. Babesia divergens organisms were demonstrated in blood smears from calves in both groups at some point 5 to 10 days p.i. All calves in both groups had B.divergens specific IgM antibodies at 7 to 17 days p.i. as shown by a modified IF-test. Specific IgG antibodies, transferred by colostrum, were found in all calves of Group 1 before inoculation of B.divergens. The IgG titre of these animals increased by a doubling dilution step at 11–25 days p.i. Among calves of Group 2 specific IgG antibodies were found at first between day 9 and 15 p.i. Both IgM and IgG antibody titres had to be investigated since demonstrated IgG antibodies can originate both from maternally transferred antibodies and from actively produced antibodies after an infection. There was no difference in clinical parameters; parasitaemia, PCV, Hb, and rectal temperature between the groups. This experiment gives evidence that there can be a resistance to bovine babesiosis in newborn calves independent of maternal antibodies.     

Restricted dietary protein in pregnant beef cows: II. Effect on the immune response

Cows fed 0.37 Kg crude protein per day for four months before calving showed no decrease in colostral IgG, IgA, or IgM from cows fed a normal ration. Similarly, no difference in serum immunoglobulin concentration was detected in their calves. Cows in the low protein group developed significantly lower (P < 0.01) titers to Salmonella pullorum antigen than did the normal group. The data show significant positive linear regressions of calf agglutination titer to S. pullorum on the dam's colostral titers. Serum levels of IgG measured at 24 hours were significantly lower in calves from second-calf heifers than from these of other age groups. The IgA levels of serums from calves from the six-year-old cows were significantly higher than the serum levels of calves from younger dams (P < 0.01).     

Leishmania donovani: cellular and humoral immune responses after primary and challenge infections in squirrel monkeys, Saimiri sciureus

Cellular and humoral immune responses were studied in squirrel monkeys after primary and challenge infection with a Khartoum strain (WR 378) of Leishmania donovani. Each of 7 squirrel monkeys, Saimiri sciureus, was inoculated intravenously with 5 X 10(7) amastigotes/kg body weight, and one other monkey (control) was inoculated with uninfected hamster spleen homogenate. Five infected monkeys recovered from visceral leishmaniasis and two infected monkeys died. Three of the five squirrel monkeys which recovered from the primary infection demonstrated acquired resistance when challenged with an intravenous inoculation of 1.0 X 10(8) amastigotes of L. donovani/kg of body weight. Each of these same three monkeys, the two remaining monkeys which recovered from the primary infection and an uninfected control monkey, were challenged subsequently with an intradermal injection of 2.2 X 10(7) promastigotes of L. braziliensis panamensis (WR539) and developed cutaneous lesions. The reactivity of peripheral blood leukocytes from infected squirrel monkeys to phytohemagglutinin was depressed 2 to 10 weeks after infection, and the reactivity to concanavalin A was not affected. Data on responses to pokeweed mitogen were inconclusive. Reactivity to leishmanial antigens was detected at 12 weeks after infection, which coincided with a marked decrease or disappearance of parasites in liver imprints. Two of five surviving squirrel monkeys developed weak delayed skin test responses to leishmanin antigens after 23 weeks; the three remaining monkeys were anergic during the primary infection but developed strong delayed skin test responses to leishmanin antigens at 7 weeks after a challenge with L. donovani. All squirrel monkeys inoculated with L. donovani developed a hyperproteinemia, hypergammaglobulinemia, hypoalbuminemia, and a reversal of the albumin/globulin ratio between 4 to 18 weeks after infection. Plasma IgM and IgG levels were increased between 2 to 18 weeks after infection; much of this increase was due to IgG. Class-specific antileishmanial antibodies, with generally low IgM and high IgG titers, reached a maximum after 14 and 16 weeks, respectively. A correlation was observed between concentration of gamma-globulins and plasma IgM and IgG levels, but not gamma-globulin concentrations and maximum titers of class-specific antileishmanial antibodies. Squirrel monkeys challenged with L. donovani again developed hyperproteinemia, hypergammaglobulinemia, and increased concentrations of plasma IgM and IgG which correlated with high titers of IgG class-specific antileishmanial antibody 4 weeks after reinoculation.(ABSTRACT TRUNCATED AT 400 WORDS)     

Trichinella spiralis: macrophage activity and antibody response in chronic murine infection

The role of macrophages, their products, and the specific antibody response were examined during chronic Trichinella spiralis infection in BALB/c mice. Adult T. spiralis in intestines were detected from 5 to 20 dpi. Muscle larvae numbers peaked at 45 dpi and thereafter a reduction was noted. The highest numbers of macrophages in the peritoneal cavity of infected mice were obtained up to 30 dpi. The production of NO by macrophages in infected mice was suppressed at 5 dpi, and then NO release increased until 45 dpi. The levels of NO in plasma and urine were lower in infected mice during the entire experiment in comparison to control. The production of O(2)(-) in peritoneal macrophages was inhibited during the first two weeks after infection and then increased until 90 dpi. Circulating T. spiralis antigens in plasma and urine were detected from 5 to 30 dpi. Specific IgM and IgA in serum increased until 20 dpi. IgG, IgG(1), and IgG(2) levels in serum increased until 60 dpi.     

IgM neutralizing antibody responses to human herpesvirus-6 in patients with exanthem subitum or organ transplantation.

The assay for detecting IgM neutralizing (NT) antibody activity to human herpesvirus-6 (HHV-6) was developed by using pretreatment of blood sample with staphylococcal protein A. The activity was mostly present in IgM fractions of serum but not in IgA fractions separated by ultracentrifugation. The assay was used for seroepidemiological studies for HHV-6 infection. In primary HHV-6 infection, IgM NT antibodies appeared 5 to 7 days after onset of exanthem subitum, reached maximum titers at 2 to 3 weeks, and tended to decline to undetectable levels after 2 months. In contrast, reactivation of HHV-6 observed in organ transplants showed somewhat greater degree of IgM NT antibody responses that persisted for 2 to 3 months and became undetectable 5 to 6 months after transplantation. The level and persistence of NT antibody titers measured by the conventional method was generally greater than those of the IgM titers. The prevalence of the IgM NT antibodies was examined in healthy individuals. The antibody was first detected at 4 to 7 months of age (5%), reached maximum level at 8 to 11 months (40%), and was detectable by 4 to 6 years (17%). A few (4 to 5%) of adolescents and adults were positive for the antibody.     

Fasciola hepatica: IgG and IgA levels in the serum and bile of infected cattle

Bile and serum samples were collected from calves with an implanted cannula throughout a 20-week period of infection with Fasciola hepatica. Using indirect fluorescent antibody labelling and plastic-embedded sections of juvenile and adult flukes as antigens, estimates were made of the relative concentrations of IgG and IgA specific for fluke tegumental and gut antigens in the samples of serum and bile. In serum, antibodies against juvenile (t1) tegument and gut antigens reached peak concentrations 4–6 weeks postinfection and declined slowly thereafter as flukes became established in the bile ducts. IgG against adult tegument (t2) antigens appeared in the serum 6 weeks after infection, but no IgA against t2 was detected. In the bile, both IgG and IgA titres against t1 and gut antigens rose to peak values at 4–6 weeks after infection, but there was no activity against t2 antigen. The Ig levels in bile were considerably lower than in serum. Much more IgA relative to IgG occurred in bile as compared to serum (IgG/IgA ratio in serum was 16–32, in bile 1–2) suggesting a role for IgA in defence at mucosal surfaces. Comparison of the antibody profiles in bile and serum suggested that IgG in the bile was derived from circulating IgG whereas IgA may have been preferentially concentrated in the bile.     

Macromolecule absorption and cortisol secretion in newborn calves derived from in vitro produced embryos

Earlier reports indicate that calves derived from in vitro produced (IVP) embryos are more susceptible to neonatal disease than calves produced after artificial insemination (AI) or natural mating. The aims of the present study were to investigate whether calves born after IVP embryos show an altered macromolecule absorption (immunoglobulin G (IgG) and porcine serum albumin (PSA)) compared with AI calves and whether the macromolecule absorption could be related to the degree of acidosis or to the cortisol secretion around birth. Hence, IgG and PSA absorption in control AI calves (n=7) was compared with that in two groups of IVP calves (IVP-defined: SOFaa embryo culture with polyvinyl alcohol, n=6; IVP-serum: SOFaa embryo culture with serum and co-culture, n=8). The calves were fed colostrum (40ml/kg) at 2, 6 and 12h after birth. At 24h after birth, both AI and IVP calves had achieved a level of plasma IgG sufficient to provide passive immunization (>15mg/ml). When the values were adjusted for the varying colostral IgG contents and the degree of acidosis, the IVP-defined calves had significantly lower peak plasma IgG concentrations than the AI calves at 18-24h after birth (P<0.04). However, when the macromolecule marker (PSA), was fed to all calves at 2 and 12h after birth the resulting plasma PSA levels were significantly lower in the AI calves compared with the IVP calves during the whole observation period (P<0.0001). Calves with a moderate neonatal acidosis (mean pH<7.2 during the first 30min after birth) had reduced peak plasma IgG concentration at 18-24h after birth (P<0.02) compared to calves without acidosis. The basal and ACTH-stimulated cortisol levels were lower in the newborn IVP-defined calves than in the AI calves (P<0.05) and the IVP-serum calves (P<0.002). Cortisol levels shortly after birth correlated positively with birth weight (r=0.60, P<0.0001) and with gestation length (r=0.34, P<0.04). Since, the IVP calves absorbed sufficient amounts of IgG from colostrum to acquire sufficient passive immunity, we conclude that the lower viability described in IVP offspring probably is not caused by an impaired passive immunization. IVP-defined calves had significantly lower absorption efficiency of IgG compared with AI calves, whereas absorption of a non-Ig macromolecule (PSA) was higher for IVP than AI calves. This might indicate a more selective absorption in AI calves in favor of IgG. Acidosis around birth affected immunoglobulin absorption negatively. IVP-defined calves had significantly lower cortisol levels the first 3h after birth and during an ACTH-challenge and a lower IgG absorption efficiency, which might indicate a mild degree of organ dysmaturity in these calves.     

Effect of cold exposure on the metabolism of immunoglobulins in rabbits.

The effect of low environmental temperature on the metabolism of IgG and IgM was examined in unimmunized rabbits. The half-lives of both IgG and IgM were less in animals kept at 4 degrees C for 6 weeks than in animals kept at 22 degrees C. Serum concentration of IgM and GG were unaltered by cold exposure but intravascular pool sizes tended to increase as a consequence of an expanded serum volume. Fractional turnover rates of both IgM and IgG were greater in cold-exposed animals. At both 4 degrees C and 22 degrees C, the fractional catabolic rate of IgM was independent of its serum concentration whereas that of IgG was correlated directly with its serum concentration. Absolute turnover of both IgM and IgG was accelerated by cold exposure. It is suggested that increased synthesis of immunoglobulin could account for the higher levels of antibody reportedly found in cold-exposed rabbits.     

Circulating immunoglobulins and complement in mice with Hymenolepis nana infection

Changes in the circulating immunoglobulins and complement in ddY mice were assayed at various times after immunizing and challenge infections with Hymenolepis nana eggs. The levels of IgG1 and IgG2a consistently increased during 3–4 weeks after immunizing infection. The increase of these immunoglobulins after challenge infection was quicker and more intense than that following immunization. It was not possible to correlate increased levels of IgG1 and IgG2a with the onset of destruction of challenge larvae in immunized mice. IgM concentrations increased slightly during 4 days after immunization but challenge infection did not further increase IgM levels. IgA and IgG2b levels showed no significant change during the course of the infection. Serum C3 levels showed no discernible change after either immunizing or challenge infections. An attempt to specifically suppress the acquisition of resistance by administration of the complement-depleting agent, cobra venom factor (CoF), before immunization failed and depletion of complement activity with CoF that was administered just before challenge infection also failed to affect resistance. These results suggest that complement has no critical role in either induction of the response nor in the anamnestic response to H. nana infection in mice.     

Lymphoid hyperplasia resulting in immune dysregulation is caused by porcine reproductive and respiratory syndrome virus infection in neonatal pigs

Amid growing evidence that numerous viral infections can produce immunopathology, including nonspecific polyclonal lymphocyte activation, the need to test the direct impact of an infecting virus on the immune system of the host is crucial. This can best be tested in the isolator piglet model in which maternal and other extrinsic influences can be excluded. Therefore, neonatal isolator piglets were colonized with a benign Escherichia coli, or kept germfree, and then inoculated with wild-type porcine reproductive and respiratory syndrome virus (PRRSV) or sham medium. Two weeks after inoculation, serum IgM, IgG, and IgA levels were 30- to 50-, 20- to 80-, and 10- to 20-fold higher, respectively, in animals receiving virus vs sham controls, although <1% was virus specific. PRRSV-infected piglets also had bronchial tree-associated lymph nodes and submandibular lymph nodes that were 5-10 times larger than colonized, sham-inoculated animals. Size-exclusion fast performance liquid chromatography revealed that PRRSV-infected sera contained high-molecular-mass fractions that contained IgG, suggesting the presence of immune complexes. Lesions, inflammatory cell infiltration, glomerular deposits of IgG, IgM, and IgA, and Abs of all three isotypes to basement membrane and vascular endothelium were observed in the kidneys of PRRSV-infected piglets. Furthermore, autoantibodies specific for Golgi Ags and dsDNA could be detected 3-4 wk after viral inoculation. These data demonstrate that PRRSV induces B cell hyperplasia in isolator piglets that leads to immunologic injury and suggests that the isolator piglet model could serve as a useful model to determine the mechanisms of virus-induced immunopathology in this species.     

Persistent infection of chimpanzees with human T-lymphotropic virus type III/lymphadenopathy-associated virus: a potential model for acquired immunodeficiency syndrome.

The lymphadenopathy-associated virus (LAV) prototype strain of human T-lymphotropic virus type III/LAV was transmitted to juvenile chimpanzees with no prior immunostimulation by (i) intravenous injection of autologous cells infected in vitro, (ii) intravenous injection of cell-free virus, and (iii) transfusion from a previously infected chimpanzee. All five animals that received more than one 50% tissue culture infective dose were persistently infected with LAV or chimpanzee-passaged LAV for up to 18 months. During this time they developed no illnesses, but they exhibited various degrees of inguinal and axillary lymphadenopathy and significant reductions in rates of weight gain. Detailed blood chemistry and hematologic evaluations revealed no consistent abnormalities, with the exception of immunoglobulin G (IgG) hypergammaglobulinemia, which became apparent in one animal 6 months postinfection and continued at more than 1 year postinfection. Transient depressions followed by increases in the numbers of T4 cells to levels greater than normal were observed in all animals after virus inoculation. However, the number of LAV-infected peripheral blood cells decreased with time after infection. Results of enzyme immunoassays showed that all infected animals seroconverted to IgG anti-LAV within 1 month postinfection and that antibody titers remained high throughout the period of observation. In contrast, only three of the five LAV-infected chimpanzees had detectable IgM antibody responses, and these preceded IgG-specific serum antibodies by 1 to 2 weeks. Virus morphologically and serologically identical to LAV was isolated from peripheral blood mononuclear cells of all infected animals at all times tested and from bone marrow cells taken from one animal 8 months after infection. One chimpanzee that was exposed to LAV only by sharing a cage with an infected chimpanzee developed lymphadenopathy and an IgM response to LAV, both of which were transient; however, no persistent IgG antibody response to LAV developed, and no virus was recovered from peripheral blood cells during a year of follow-up. Thus, LAV readily infected chimpanzees following intravenous inoculation and persisted for extended periods despite the presence of high titers of antiviral antibodies. However, the virus was not easily transmitted from infected to uninfected chimpanzees during daily cage contact.     

Naturally acquired Pasteurella multocida infection in rabbits: immunological aspects

Natural infection with P. multocida in New Zealand White rabbits was followed in 2 to 3 weeks by development of immunoglobulin (Ig)M and IgG serum antibodies. The IgM response peaked and returned to lower levels within several weeks after infection, whereas the IgG response progressively increased and remained elevated.     

Cholera toxin modulates the systemic immune responses against Vibrio cholerae surface antigens after repeated inoculations

The immunomodulating properties of a low cholera toxin (CT) dose over the systemic antibody response against Vibrio cholerae antigens after a comparatively extensive period of time were evaluated. Groups of 10 mice were injected intraperitoneally three times at 0, 30 and 86 days with 500 microl of buffer or 10(8) viable recombinant V. cholerae bacteria (lacking cholera toxin A subunit) with or without 100 ng of CT. Sera were obtained from inoculated mice at 0, 14, 28, 37, 58, 80, 93, 114, 236 and 356 days after the first injection. Vibriocidal activity and IgM and IgG anti-lipopolysaccharide (LPS) or outer membrane protein (OMP) antibodies levels were estimated by ELISA in sera of inoculated mice. Anti-LPS IgG subclasses were measured 2 weeks after each immunization by ELISA. Treatment of mice with CT markedly influenced the immune response to LPS but not against OMP of V. cholerae. Simultaneous intraperitoneal administration of CT with V. cholerae resulted in marked enhancement of both IgM anti-LPS and vibriocidal titers which subsisted for a relatively extensive period of time after repeated antigen administration. No differences were observed in IgM and IgG anti-OMP titers after extended periods of time between CT and control treatments. A similar pattern of IgG anti-LPS subclasses was observed in the serum samples analyzed. These results suggest that long term CT administration modulates the IgM anti-V. cholerae LPS response and the serum vibriocidal activity.     

Motheaten, an immunodeficient mutant of the mouse. II. Depressed immune competence and elevated serum immunoglobulins.

Mice homozygous for the recessive mutation motheaten (me) are deficient in capacity for immune response but show an elevated level of serum immunoglobulins. In comparison to spleen cells from normal sibs, spleen cells from me/me mice have a severely depressed 19S PFC response to SRBC. In the GVH assay, spleen and thymus cells from motheaten donors caused significantly weaker reactions than like cells from normal sibs. Serum electrophoretic patterns of motheaten mice showed increased levels of alpha-, beta-, and gamma-globulins and decreased levels of albumin. Increases in quantities of all major classes of immunoglobulins were found in serum of me/me mice 5 weeks of age and older. Elevation of serum IgM was evident by 3 weeks of age and had reached 25 times the levels in normal sibs by 6 weeks of age. Immunoelectrophoresis and Ouchterlony analysis showed motheaten serum to have both kappa and lambda2 light chains. Evidence of autoimmunity was found in motheaten mice in the granular deposition of IgM and IgG in kidney glomeruli. Motheaten mice, thus, appear to have a severe immune deficiency, but the basic nature of the deficiency is not yet known.     

Taenia crassiceps: Serum and surface immunoglobulins in metacestode infections of mice

Serum levels of IgM, IgA, IgG1, IgG2a, IgG2b, and IgG3 were measured weekly for 8 weeks by radial immunodiffusion in pooled sera from female BALB/c and BDF1 mice with primary and secondary Taenia crassiceps infections and age-matched normal control mice of each strain. Although increases in levels of all immunoglobulin classes occurred during primary and secondary infections in both strains of mice, the only consistent changes common to both strains of mice were higher levels of IgG1 and IgG3 in early weeks of secondary infections as compared to primary infections, and high levels of IgG1 late in primary infections. High levels of IgG3 occurred late in primary infections in BDF1 mice but not in BALB/c mice. It was not possible to correlate increased levels of any one immunoglobulin class either with cytotoxic activity of early immune serum or with the onset of the cellular encapsulation response in secondary infections. IgM, IgA, IgG1, IgG2a, IgG2b, and IgG3 could be demonstrated on the surface of washed fixed larvae from long-term infected donor mice by the indirect fluorescent antibody method. Living T. crassiceps larvae were capable of shedding fluorescent label within 1 hr at room temperature, but not at 4 C after staining with either rabbit anti-T. crassiceps serum or rabbit anti-mouse immunoglobulin serum and fluorescein-conjugated goat anti-rabbit globulin.     

Antigen-induced rheumatoid factors. Protein and carbohydrate antigens induce different rheumatoid factor responses

Rheumatoid factors, autologous IgM anti-IgG, were produced after immunization with protein or carbohydrate antigens. After immunization with either type of antigen, the kinetics of the rheumatoid factor response reflected the kinetics of the dominant IgG isotype in the anti-antigen response. Secondary immunization with protein antigens induced an IgM rheumatoid factor response which was consistently greater than that seen after carbohydrate immunization, and almost exclusively specific for the IgG1 isotype. In contrast, primary or hyperimmunization with carbohydrate antigens gave rise to a more heterogeneous response dominated by IgM anti-IgG3, with lesser amounts of IgM anti-IgG2b and anti-IgG1. Direct immunization with immune complexes gave similar results, as complexes composed of IgG1 induced exclusively IgM anti-IgG1, whereas those complexes made up of IgG3 gave rise to IgM rheumatoid factors binding IgG3 and IgG2b. Rheumatoid factor production, with isotypic specificity defined by the immunizing antigen, appears to be a natural consequence of immunization with a variety of protein and carbohydrate antigens.     

In vivo role of lymphocyte subpopulations in the control of virus excretion and mucosal antibody responses of cattle infected with rotavirus.

T-cell control of primary rotavirus infection and mucosal antibody responses to rotavirus was studied with monoclonal antibodies (MAb) to deplete gnotobiotic calves of CD4+, CD8+, BoWC1+, or both CD4+ and CD8+ lymphocytes prior to infection with rotavirus. Injection of these MAb produced specific reductions in circulating and tissue lymphocyte subpopulations. Following infection, control calves developed fecal immunoglobulin M (IgM) and IgA antibodies and serum IgM and IgG1 antibodies; there was no IgG2 antibody produced. Anti-CD4-treated calves had reduced fecal and serum antibody responses to rotavirus compared with control calves. The IgM response was less affected than the other isotypes. Calves concurrently injected with MAb to CD4 and CD8 had antibody responses similar to those of calves injected with anti-CD4 antibody alone. No effect on serum or fecal antibody levels was seen when MAb to CD8 or BoWC1 were injected alone. Virus excretion was significantly increased in calves depleted of CD8+ cells. Depletion of CD4+ cells or BoWC1+ cells had no effect on virus excretion. Calves depleted of both CD4+ and CD8+ cells excreted amounts of virus similar to those of calves depleted of CD8+ cells alone. Onset and duration of virus excretion were not affected by any of the MAb treatments. We conclude that a CD8+ cell population is involved in limiting primary rotavirus infection, while CD4+ or BoWC1+ (gamma/delta+ TcR) lymphocytes are not. Furthermore, CD4+ lymphocytes (but not CD8+ or BoWC1+ lymphocytes) were shown to be important in the generation of mucosal, as well as systemic, antibody responses.     

Selected clinicopathologic changes associated with experimentally induced Fascioloides magna infection in white-tailed deer.

Six white-tailed deer (Odocoileus virginianus), less than one year of age, were divided into two groups of three each and administered 50, or 500 metacercariae of ascioloides magna. All six deer became infected. Three additional deer of the same age were uninoculated controls. All deer were monitored for up to 43 weeks after inoculation to investigate changes in weight, selected hematologic values, and blood chemistry values. Although clinical disease was not evident in the infected deer, a significant reduction (p less than .01) in hemoglobin and packed cell volume was detected throughout the experiment. A significant elevation (p less than .01) in the total serum protein level was detected in both infected groups from 0 to 5 months after inoculation. Increases were present in the beta and gamma globulin fractions. No differences (p greater than .05) were detected in the serum calcium, magnesium, or phosphorus levels, or in body weights between infected and uninfected control groups.