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Lactobin-R is a commercial hyperimmune bovine colostrum with potent anticryptosporidial activity. It was administered to a 4 year old child with AIDS and severe diarrhoea associated with cryptosporidiosis. There was significant clinical improvement in the diarrhoea and permanent elimination of the parasite from the gut as assessed through serial jejunal biopsy and stool specimens.
The feeding of colostrum to newborn calves from a bucket was found to be more effective in ensuring immune globulin uptake than leaving cow and calf together for two days post partum. A marked seasonal variation in the immune globulin status of calves, which could not readily be explained by management factors, was noted during two consecutive seasons.
The prevalence of antibodies to Mycobacterium johnei in pre-colostral lambs in a flock of sheep infected with Johne's disease was investigated. Blood from 134 ewes and their 143 lambs were collected immediately after lambing. Double immunodiffusion and counterimmunoelectrophoresis tests were used to detect antibodies to M johnei. Four (3 per cent) of 135 lambs born to 127 ewes with serological evidence of exposure to M johnei had detectable antibodies in their sera. All lambs fed colostrum from serologically positive ewes had serum antibodies.
A simple immunoassay system has been evaluated for use on farm to examine the level of maternal immunoglobin absorbed by newborn calves. Whole blood can be used in the test rather than serum. The test proved easy and reliable when used in studies on 10 farms with 650 calves. More than 50 per cent of the animals were found to be colostrum deficient and, as with other studies, such calves were subject to health breakdown and poor performance although this could be adequately offset by good management.
The aim of this study was to investigate the influence of low-dose bovine colostrum protein concentrate (CPC) supplementation on selected immune variables in cyclists. Twenty-nine highly trained male road cyclists completed an initial 40-km time trial (TT(40)) and were then randomly assigned to either a supplement (n = 14, 10 g bovine CPC/day) or placebo group (n = 15, 10 g whey protein concentrate/day). After 5 wk of supplementation, the cyclists completed a second TT(40). They then completed 5 consecutive days of high-intensity training (HIT) that included a TT(40), followed by a final TT(40) in the following week. Venous blood and saliva samples were collected immediately before and after each TT(40), and upper respiratory illness symptoms were recorded over the experimental period. Compared with the placebo group, bovine CPC supplementation significantly increased preexercise serum soluble TNF receptor 1 during the HIT period (bovine CPC = 882 +/- 233 pg/ml, placebo = 468 +/- 139 pg/ml; P = 0.039). Supplementation also suppressed the postexercise decrease in cytotoxic/suppressor T cells during the HIT period (bovine CPC = -1.0 +/- 2.7%, placebo = -9.2 +/- 2.8%; P = 0.017) and during the following week (bovine CPC = 1.4 +/- 2.9%, placebo = -8.2 +/- 2.8%; P = 0.004). Bovine CPC supplementation prevented a postexercise decrease in serum IgG(2) concentration at the end of the HIT period (bovine CPC = 4.8 +/- 6.8%, P = 0.88; placebo = -9.7 +/- 6.9%, P = 0.013). There was a trend toward reduced incidence of upper respiratory illness symptoms in the bovine CPC group (P = 0.055). In summary, low-dose bovine CPC supplementation modulates immune parameters during normal training and after an acute period of intense exercise, which may have contributed to the trend toward reduced upper respiratory illness in the bovine CPC group.
Yersinia enterocolitica enteritis in newborn, colostrum-deprived piglets fed a human milk formula caused a reduced milk intake and decreased gain in weight but not length of the body. In infected piglets, the weight of the liver was less than in controls but other abdominal organs were unaffected. The weight of the caecum and small intestinal muscle were greater, but the length and weight of the small intestine and colon were not different. In infected piglets, the RNA concentration of the small intestinal mucosa was elevated whereas the concentrations of DNA and protein were unchanged, and total lactase activity was reduced. After antibiotic therapy, the liver weight was greater and the body weight increased at the same rate as the controls but was still lower at 14 days. The body weight of the control piglets increased linearly over the 14 days after birth. The stomach, pancreas and spleen grew more rapidly, but the liver more slowly, than the body as a whole but the kidneys had a minimum relative weight at 5 days. The total lactase activity and protein and RNA concentrations of the small intestinal mucosa decreased with age, the RNA to a greater extent than the protein.
It is now well established that the CD30 glycoprotein is a surface antigen expressed by activated T cells producing T-helper (Th)-2-type lymphokines. Mounting laboratory evidence, however, suggests that CD30 expression is not confined to a functionally restricted subset of T cells, but also identifies activated cells with a Th-1 and Th-0 pattern of cytokine secretion. CD30-bearing T lymphocytes release a soluble form of the molecule (sCD30), which can be detected both in vitro and in vivo. In the present study, very high levels of sCD30 were found in colostrum from 20 puerperal women, but not in autologous and heterologous (nonpregnant women) blood samples. These data strongly support an involvement of CD30+ T cells in the immune processes which take place at the level of the mammary gland during pregnancy and lactation. Passively transferred immune components such as immunoglobulins, cytokines, macrophages, natural killer cells, granulocytes and memory/activated T cells, all of which may help the baby to fight off infections, have been revealed in human breast milk. However, how Th-2-type cytokine-secreting T cells or other T-cell types help to endow the congenitally immunocompromised newborn infant with extrinsic immunological support remains an open question.
Porcine reproductive and respiratory syndrome virus (PRRSV) antigens were detected by a streptavidin-biotin complex technique in tissues of 3-week-old colostrum-deprived pigs that had been inoculated intranasally with PRRSV and had developed moderate respiratory disease. Moderate, multifocal, tan-colored consolidation of the lungs and severe enlargement of the lymph nodes were noted at necropsy. Severe interstitial pneumonia characterized by type 2 pneumocyte proliferation, septal infiltration with mononuclear cells, and accumulation of macrophages and necrotic cells in alveolar spaces was observed at 4 and 9 days postinoculation. Moderate multifocal perivascular lymphohistiocytic myocarditis was observed at 9 days postinoculation. Marked lymphoid follicular hyperplasia and follicular necrosis in the tonsil, spleen, and lymph nodes was observed. A monoclonal antibody that recognizes a conserved epitope of PRRSV nucleocapsid protein was used as primary antibody for immunohistochemistry. Antigen was readily detected in alveolar macrophages in the lung and in endothelial cells and macrophages in the heart. Macrophages and cells resembling dendritic cells in tonsil, lymph nodes, thymus, and spleen also stained intensely positive for viral antigen. PRRSV appears to replicate primarily within macrophages in the respiratory and lymphoid systems of the pig.
Cesarean-derived, colostrum-deprived pigs (n = 23) were inoculated intranasally and subcutaneously with a low cell culture passage of type 2 porcine circovirus. In 11 pigs, a persistent fever that lasted 7-17 days began 12-15 days after inoculation with virus. Additional signs of disease in those 11 pigs included depression (11 of 11 pigs), palpable enlargement of inguinal, prefemoral, and popliteal lymph nodes (11 of 11), icterus (6 of 11), and hyperpnea (2 of 11). The remaining 12 pigs had fever that occurred intermittently for 2-4 days between days 12 and 20 postinoculation. Overt signs of disease in those pigs were limited to palpable enlargement of inguinal and popliteal lymph nodes (9 of 12 pigs). When compared with control pigs of similar age, the average daily rate of weight gain for all pigs inoculated with virus was less over a 2-week period that began 2 weeks post inoculation. At postmortem examination, lymph node enlargement was seen in 14 of 14 pigs euthanized between days 20 and 28 postinoculation. Lymph node enlargement was especially prominent in pigs that developed a persistent fever. Microscopic lesions noted in pigs that developed a persistent fever included cellular depletion in lymphoid tissues; hepatic cell necrosis; and lymphogranulomatous inflammation of lymph nodes, Peyer's patches of the intestine, liver, kidney, and heart. Virus was isolated with varying frequency from nasal, rectal, or tonsil swab specimens, buffy coat, serum, urine, and lung lavage fluid obtained antemortem or postmortem. Virus was isolated from or viral DNA was detected in a variety of tissues obtained postmortem up to 125 days postinoculation. Antibody against type 2 porcine circovirus usually was detected in serum between 15 and 20 days postinoculation; however, antibody against virus was not detected in serum from 4 pigs euthanized 20-24 days postinoculation. Direct contact with pigs inoculated with virus 42 days previously resulted in transmission of virus to 3 of 3 control pigs.
Sixteen cesarean-derived, colostrum-deprived piglets were inoculated intranasally with porcine circovirus type 2 (PCV2), originally isolated from a pig affected with postweaning multisystemic wasting syndrome (PMWS). At 1 day postinoculation (PI), 3 of the 5 piglets in the uninoculated control group were moved to the room of inoculated piglets for contact exposure. Porcine circovirus type 2 was detected by polymerase chain reaction (PCR) in swabs from inoculated piglets from 1 day PI and from contact piglets from 2 days after cohabitation. Porcine circovirus type 2 was also detected in all serum samples but not in control piglets 7 days PI. Until the end of study, PCV2 was detected in swabs and serum samples by PCR but not in the control piglets. One inoculated piglet died suddenly without clinical signs 19 days PI. Beginning at 14 days PI, 5 piglets, including 1 contact piglet, had clinical signs of depression, anorexia, and icterus, and 1 inoculated piglet died 21 days PI. Most of the piglets exhibiting the above clinical signs became moribund and were necropsied 21 and 28 days PI. In the piglets that showed clinical signs, gross lesions, including icterus of liver and hemorrhage in stomach, and typical histopathological lesions of PMWS, such as lymphoid depletion and basophilic intracytoplasmic inclusion bodies in lymph nodes and other tissues, were observed. Porcine circovirus type 2 was detected by PCR in all tissue samples except in those of the control piglets. Porcine circovirus type 2 was recovered from several tissue samples of the piglets necropsied until 35 days PI. In particular, PCV2 was recovered in high titer from most of the tissue samples of the piglets exhibiting clinical signs. Serum antibody against PCV2 was mostly detected in inoculated piglets and in contact piglets 14 and 21 days PI by an indirect fluorescence antibody test but was not detected in the piglets exhibiting clinical signs until 28 days PI. These results indicate that PCV2 was able to induce clinical PMWS in the absence of other swine pathogens and that there were significant differences in both the quantitative PCV2 distribution in tissues and the antibody response between the piglets that were infected and developed PMWS and those that were infected but remained healthy.
One hundred forty-six 5-week- old cesarean-derived, colostrum-deprived (CDCD) pigs were inoculated intranasally with 1 of 9 US porcine reproductive and respiratory syndrome virus (PRRSV) isolates. Differences were found in severity of clinical respiratory disease, rectal temperatures (P < or = 0.001), gross lung lesions (P < or = 0.001), and microscopic lung lesions (P < or = 0.05). Gross lung lesions were generally most severe 10 days postinoculation and were distributed primarily in the cranial, middle, and accessory lobes and ventromedial portion of the caudal lung lobes. Mean gross lung lesion scores estimating the percentage of lung affected by pneumonia at 10 days postinoculation ranged from 16.7% +/- 2.8% (mean +/- SEM, n = 10) for isolate ISU-51 to 62.4% +/- 5.7% (n = 10) for isolate ISU-28. Microscopic lung lesions were characterized by hyperplastic and hypertrophied type 2 pneumocytes, septal infiltration by mononuclear cells, and accumulation of necrotic alveolar exudate. Lymph node follicular hyperplasia and focal necrosis was seen with all 9 isolates. This CDCD pig model was useful for demonstration of significant differences in pathogenicity among US PRRSV isolates. This difference in pathogenicity may help explain the variation of severity of clinical disease observed in field outbreaks of porcine reproductive and respiratory syndrome and should provide for meaningful comparison of PRRSV genotypes.
Toxigenic Pasteurella multocida is the causative agent of progressive atrophic rhinitis (PAR), a serious respiratory infection of swine. Diagnosis of the disease has hitherto been based on clinical signs, pathologic findings, and subsequent isolation of the agent. The best Finnish pig breeding herds participating in the Finnish Pig Health Scheme have been surveyed for PAR since 1963, and the disease has been eradicated from these herds. In this study, a total of 5,650 colostrum samples from 188 Finnish Pig Health Scheme herds were analyzed with a new serologic screening method: an enzyme-linked immunosorbent assay (ELISA) able to detect antibodies to the toxin of P. multocida (PMT). Although the herds had been continuously controlled for PAR, 1 herd with PMT antibodies was found. The positive reactions in the ELISA were confirmed by isolating the causative organism. The origin of the infection also appeared to be obvious. The serologic ELISA is a suitable method for the detection and screening of toxigenic P. multocida-infected pig herds.
A system for the artificial rearing of colostrum-deprived neonatal piglets is described. A total of 443 piglets in 6 batches was reared. Each piglet, immediately after birth was placed in a separate incubator which was ventilated with heated filtered air. Piglets were fed hourly by an automatic system and were offered a liquid milk substitute. The mean survival rate up to the time piglets were transferred out of the rearing unit at 2 weeks of age was 78 +/- 7%. The mean daily live weight gain up to 2 weeks of age was 148 +/- 16 g/day and the dry matter intake over the same period was 154 +/- 10 g/day per piglet.
The concentration of ceruloplasmin (CP) in human milk was obtained by measuring the increased absorbance of a solution containing apotransferrin and Fe2+ at 460 nm after adding the milk. The CP concentrations in colostrum and mature milk at less than 1 month after parturition were 4.45 +/- 1.23 mg and 4.09 mg +/- 1.47 mg/100 ml, respectively. In mature milk after more than one month, the CP concentration had decreased to 1.72 +/- 0.91 mg/100 ml.
Bovine colostrum has an activity that increases the migration of WI38 fibroblasts. We evaluated the motility of fibroblasts by their ability to contract collagen gels. Part of the activity was absorbed by anion-exchange chromatography at pH 6.4, and eluted by 0.2-0.3 M sodium chloride. The activity was separated into many fractions corresponding to 20-150 kDa by gel filtration chromatography under acidic conditions. The major peak of the activity coincided with 50-70 kDa.
To determine whether pseudorabies virus (PRV) infection increases the severity of pneumonia by Mycoplasma hyopneumoniae, 18, 10-week-old Cesarean-derived, colostrum-deprived pigs were randomly assigned to 3 groups of 6 pigs each. Pigs in groups A and C were inoculated intranasally with M. hyopneumoniae at 10-week-old. At 11-week-old, pigs in groups B and C were inoculated intranasally with PRV. All pigs were initially seronegative for M. hyopneumoniae and PRV. Three pigs of each group were euthanized at 12-week-old, and remaining pigs at 14-week-old. At necropsy, gross lesions in the lung were observed in the pigs of groups A and C. On post-inoculation-week (PIW) 2 with M. hyopneumoniae (at 12-week-old), lung lesions were recognized in one of the 3 pigs in group A and all the pigs in group C. The mean percentage of the lung lesions were 0.1% in group A and 9.8% in group C. M. hyopneumoniae was isolated from broncho-alveolar lavage fluids (BALF) of pigs in group A with titer of 10(2) to 10(3) CCU/0.2 ml and in group C with titer of 10(5) to 10(6) CCU/0.2 ml. On PIW 4 (at 14-week-old), lung lesions were observed in all the pigs in groups A and C, and the mean percentage of the lung lesions were 8.3% in group A and 17.2% in group C. M. hyopneumoniae was isolated from BALF in group A with titer of 10(4) to 10(7) CCU/0.2 ml and in group C with titer of 10(6) to 10(7) CCU/0.2 ml. PRVs were isolated from nasal swab and tissue samples in groups B and C. After inoculation, antibody against M. hyopneumoniae was detected in groups A and C, and against PRV in groups B and C. Under the present experimental conditions, PRV infection appear to have effect on the severity of experimentally induced acute mycoplasmal pneumonia in young pigs.
Colostrum-deprived, neonatal, 2 days old pigs were inoculated with the attenuated HT-/SK or the virulent 90HS strain of porcine parvovirus (PPV) by the oral or subcutaneous route and sacrificed 2, 4 or 6 days after inoculation. Then, comparison was made on viral multiplication in pigs between the two strains. Pigs inoculated with the HT-/SK strain showed no detectable viremia or HI antibody responses against PPV within 6 days after inoculation. Only in pigs inoculated by the subcutaneous route, a small amount of virus was recovered from the spleen, liver, or mesenteric lymph nodes. These viruses were distinguished from the parental virulent 90HS strain, as examined for rct maker in vitro. When pigs were inoculated with the virulent 90HS strain, viremia appeared in all of them 1 day after inoculation and continued for up to the sacrificed day. Moreover, a considerable amount of virus was also detected from all tissues, including brain, lung, liver, spleen, pancreas, small intestine, and lymph node tissues, in all pigs tested. HI antibodies were first detected 6 days after inoculation.
Preweaning colibacillosis is a major cause of economic loss to the swine industry in Vietnam. The aim of this study was to examine the enteropathogenicity of representative enterotoxigenic Escherichia coli (ETEC) strains obtained during an earlier epidemiologic survey conducted in five provinces in North Vietnam. This included isolates belonging to serotype O8 that produced heat-stable and heat-labile enterotoxins but did not produce any of the recognized fimbriae (F4, F5, F6, F41, F18). In vitro hemagglutination (unique mannose-resistant hemagglutination activity with guinea pig, sheep, human, and chicken red blood cells at 37 degrees C, but not at 18 degrees C) and enterocyte brush border attachment assays suggested that the F- ETEC strains produced an unidentified colonization factor that promoted adherence to the intestinal epithelium. Colostrum-deprived 1-day-old piglets challenged with an F- strain (1-2 x 10(9) bacteria) developed acute watery diarrhea within 4 hours of inoculation and suffered up to 20% weight loss, with comparable severity to piglets challenged with conventional F4 and F5 strains. At necropsy, viable counts and histopathologic examination of intestinal sections demonstrated colonization of the duodenum, jejunum, and ileum by F4-positive strains. In comparison, the F- and F5-positive strains attached exclusively to the ileum. Transmission electron micrographs of negatively stained F- cells grown at 37 degrees C demonstrated the presence of fimbriae. These results confirm the presence of a potentially new pathogenic ETEC fimbrial type in piggeries in Vietnam, with a unique hemagglutination property and attachment characteristics similar to ETEC bearing F5 fimbriae.