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SUMMARY

Mycobacterial culture was performed on colostrum, milk, and feces from 126 clinically normal cows of a single herd with high prevalence of Mycobacterium paratuberculosis infection. Thirty-six (28.6%) cows were determined to be shedding the organism in the feces. Of the 36 fecal culture-positive cows, M paratuberculosis was isolated from the colostrum of 8 (22.2%) and from the milk of 3 (8.3%). Cows that were heavy fecal shedders were more likely to shed the organism in the colostrum than were light fecal shedders.

Free access
in American Journal of Veterinary Research

Abstract

Objective

To determine whether Mycobacterium paratuberculosis could survive in colostrum after pasteurization. Additionally, this study investigated the effect pasteurization had on IgG concentration in colostrum.

Animals

Colostrum samples were collected from cattle (beef and dairy) owned by the state of Ohio.

Procedure

Colostrum was divided into aliquots and inoculated with variable concentrations of M paratuberculosis (ATCC No. 19698: 104, 103, and 102 colony-forming units/ml). Half the samples at each concentration were subjected to pasteurization temperatures (63 C) for 30 minutes and the remainder were kept at approximately 20 to 23 C. All samples were incubated (Herrold's egg yolk medium with and without mycobactin J) and observed for growth during the next 16 weeks. Additionally, the IgG concentration of colostrum was determined by radioimmunoassay before and after pasteurization. Samples that coagulated at pasteurization temperatures were mechanically resuspended before measurement of IgG concentration.

Results

Growth of M paratuberculosis was retarded but not eliminated by pasteurization. Growth was observed in all unpasteurized samples incubated on Herrold's egg yolk medium with mycobactin J but in only 2 of 18 pasteurized samples similarly cultured. Growth from pasteurized samples appeared 5 to 9 weeks after growth was observed from nonpasteurized samples.

Mean colostral IgG concentration was 44.4 g/L in nonpasteurized samples and 37.2 g/L in pasteurized sample, a decrease of 12.3%. High-quality colostrum (> 48 g of IgG/L) had a significantly greater loss of IgG concentration than did colostrum of lesser quality (P = 0.002).

Conclusions

Pasteurization lessened, but did not eliminate, growth of M paratuberculosis from experimentally inoculated colostrum samples. Pasteurization resulted in a significant decrease in colostral IgG concentration but not to an unmanageable level that would preclude the colostrum's use for passive transfer of immunity.

Clinical Relevance

Colostrum is macrophage rich and may serve as a source of M paratuberculosis infection to calves. Pasteurization of colostrum may lessen the risk of infection, but will not totally eliminate M paratuberculosis. (Am J Vet Res 1996;57:1580–1585)

Free access
in American Journal of Veterinary Research

Summary

The infectivity and pathogenic potential of a cell culture-adapted simian rotavirus was evaluated in colostrum-deprived newborn and infant cynomolgus macaques (Macaca fascicularis). Intragastric challenge exposure with the simian rotavirus strain SA11 on postpartum day 2 induced diarrhea in 5 of 5 colostrum-deprived newborn monkeys. Compared with sham-inoculated controls, 3 of the 5 inoculated monkeys also manifested reduced body weight gain during the initial 5 days after challenge exposure. Rotavirus was detected in feces of 3 challenge-exposed monkeys for up to 2 days after inoculation. Evaluation of antibody response after rotavirus inoculation was obscured by high but variable prechallenge-exposure serum titers of rotavirus-specific antibody. Preexisting serum titer of neutralizing antibody in newborn monkeys was not predictive of clinical response to inoculation with rotavirus SA11. Two 90-day-old infant monkeys with low serum neutralizing antibody titer did not have diarrhea, reduced weight gain, or antibody response after oral inoculation with rotavirus SA11. Results of these challenge-exposure studies in newborn cynomolgus monkeys were consistent with a heterologous host-rotavirus model and indicate that neonatal serum antibody of maternal origin may not be associated with resistance to rotavirus-induced disease.

Free access
in American Journal of Veterinary Research

Abstract

Objective

To investigate in vitro antigenic relations, in vivo cross-protection, and isotype antibody responses to a winter dysentery (WD) and calf diarrhea strain of bovine coronavirus (BCV).

Design and Animals

Gnotobiotic and colostrum-deprived calves were inoculated oronasally with a WD (DBA) or a calf diarrhea (DB2) BCV, and were challenge exposed with the heterologous BCV.

Procedure

Nasal swab and feces specimens and blood samples were collected. Fecal and nasal specimens were assayed for BCV shedding by antigen-capture ELISA or immune electron microscopy. Bovine coronavirus antigens were detected in nasal epithelial cells by immunofluorescence. Antibody titers to BCV in serum were assayed by virus neutralization (VN), and BCV antibody isotype titers in feces and sera were quantitated by ELISA.

Results

All calves developed diarrhea and shed BCV nasally and in feces, then recovered and were protected from BCV-associated diarrhea after challenge exposure with the heterologous BCV. After challenge exposure with either strain, fecal shedding of DBA was detected in 1 of 4 calves and nasal shedding of DB2 was detected in 2 of 4 calves. Immunoglobulin M was the principal coproantibody to BCV early, followed predominantly by IgA. Immunoglobulin G1 coproantibody titers to BCV were low, but increased after challenge exposure. Immunoglobulin G1 antibodies were predominant in serum. After challenge exposure, all serum antibody isotype titers increased except IgG2. The VN antibody responses paralleled serum IgG1, antibody responses.

Conclusions and Clinical Relevance

Immunoglobulin A coproantibodies at challenge exposure were associated with protection against diarrhea. Nasal shedding of BCV after challenge exposure confirmed field data documenting reinfection of the respiratory tract of cattle, suggesting that, in closed herds, respiratory tract infections constitute a source of BCV transmission to cows (WD) or young calves. (Am J Vet Res 1996;57:48-53)

Free access
in American Journal of Veterinary Research

SUMMARY

Colostrum-deprived calves (n = 24) were fed various amounts of colostrum, colostrum substitute, or milk replacer to establish a range in titer of passively acquired viral neutralizing antibody in serum. The calves were then challenge exposed intranasally with a virulent, noncytopathic bovine viral diarrhea virus (bvdv-890). After viral challenge exposure, calves were monitored for fever, leukopenia, thrombocytopenia, and diarrhea. In addition, viral isolation and viral titration were performed on specimens of nasal secretions, buffy coat cells, and serum obtained from the calves. Fever and systemic spread of virus were detected in calves that had viral neutralizing titer of 256 or lower. Calves that had viral neutralizing titer lower than 16 developed severe clinical disease manifested by fever, leukopenia, thrombocytopenia, and diarrhea. Severity and duration of signs of disease decreased as titers of passively acquired viral neutralizing antibody increased. These results indicate that low to intermediate titers of passively acquired viral neutralizing antibody were not sufficient to fully protect calves from virulent bovine viral diarrhea virus.

Free access
in American Journal of Veterinary Research

SUMMARY

The ability of pigs to respond immunologically to ingestion of bovine parvovirus (bpv) was tested by feeding 4 cesarean-derived, colostrum-deprived (cdcd) pigs a live virus-contaminated, liquid diet for the first 4 weeks of life. Virus-neutralizing (vn) antibodies were detected in the serum of 2 of the 4 pigs when they were 4 weeks old. Antibody titer remained at about the same level for several weeks, then decreased during the remainder of the 29-week interval of testing. The relative reactivity of these sera based on results of indirect immunofluorescence paralleled the corresponding vn titer. Neither of the other 2 pigs exposed to bpv had any appreciable immune response. The potential for passive acquisition of antibody from the diet was tested by feeding 4 other cdcd pigs bovine colostrum containing antibodies to bpv and bovine viral diarrhea virus (bvdv) for the first 2 days of life. All had serum vn antibodies for both viruses when they were tested at 2 days of age. The decay rate of the heterologous, passively acquired antibody was approximately linear; however, antibody half-life was relatively short, about 3.5 days, and titers were no longer detectable when pigs were 4 weeks (bpv) and 6 weeks (bvdv) old. An additional 4 cdcd pigs fed a liquid diet without virus or antibody remained free of any appreciable serum reactivity for either bpv or bvdv. Results supported the hypothesis that antibodies for bpv previously detected in the serum of pigs and people may reflect ingestion of virus-contaminated bovine milk or milk products.

Free access
in American Journal of Veterinary Research

SUMMARY

Three-week-old weaned and colostrum-deprived neonatal (< 1 day old) pigs were inoculated to determine the pathogenicity of 2 enterotoxigenic Escherichia coli isolates that do not express K88, K99, F41, or 987P adhesins (strains 2134 and 2171). Strains 2134 and 2171 were isolated from pigs that had diarrhea after weaning attributable to enterotoxigenic E coli infection. We found that both strains of E coli adhered in the ileum and caused diarrhea in pigs of both age groups. In control experiments, adherent bacteria were not seen in the ileum of pigs < 1 day old or 3 weeks old that were noninoculated or inoculated with a nonpathogenic strain of E coli. These control pigs did not develop diarrhea. Antisera raised against strains 2134 and 2171 and absorbed with the autologous strain, grown at 18 C, were used for bacterial-agglutination and colony-immunoblot assays. Both absorbed antisera reacted with strains 2134 and 2171, but not with strains that express K99, F41, or 987P adhesins. A cross-reaction was observed with 2 wild-type K88 strains, but not with a K12 strain that expresses K88 pili. Indirect immunofluorescence with these absorbed antisera revealed adherent bacteria in frozen sections of ileum from pigs infected with either strain. We concluded that these strains are pathogenic and express a common surface antigen that may be a novel adhesin in E coli strains that cause diarrhea in weaned pigs.

Free access
in American Journal of Veterinary Research

SUMMARY

Four colostrum-deprived calves each were immunized passively with antisera to whole Pasteurella haemolytica, leukotoxin-containing supernatants of P haemolytica, P haemolytica lipopolysaccharide, or newborn calf serum. Calves were challenge exposed intrabronchially with 5 × 109 P haemolytica, and 24 hours later, the resulting lesions were evaluated. The greatest protection against challenge exposure was provided by the antiserum to whole P haemolytica (lesion score = 6.3), whereas newborn calf serum provided the least protection (lesion score = 28.3). Calves that received antiserum to P haemolytica supernatants were moderately protected (lesion score = 16.3), and the antiserum to lipopolysaccharide provided minimal protection (lesion score = 21.8). Antibodies that were unique to whole P haemolytica antiserum and produced dense bands on immunoblots were detected to antigens at 66, 50, and 30 kd. Antibodies in the supernatant preparation that produced prominent bands reacted to antigens between 100 and 90 kd. Collectively, antibodies to these antigens may be responsible for enhancing resistance to experimentally induced pneumonic pasteurellosis. Antibodies to antigens in P haemolytica lipopolysaccharide provided little to no protection.

Free access
in American Journal of Veterinary Research

SUMMARY

Twenty-six clinically normal colostrum-fed dairy calves were allotted to 5 groups. Calves of groups 1 and 2 served as nonvaccinated controls and were challenge-exposed with variable numbers of organisms. Group-3 calves were vaccinated SC with a modified Salmonella typhimurium bacterin. The bacterin was composed of killed acid-hydrolyzed S typhimurium G30/C21 (Re-mutant) whole cells coated with alkali-hydrolyzed S typhimurium LT-2 lipopolysaccharide, as antigen, and monophosphoryl lipid A, as adjuvant. Calves of groups 4 and 5 were vaccinated with a 2% mineral oil-in-water emulsion containing lipopolysaccharide as antigen and monophosphoryl lipid A and trehalose 6-6′-dimycolate as adjuvants. Calves of groups 3-5 were vaccinated at 2 weeks of age and again at 4 or 6 weeks of age. Adverse reactions were not observed after vaccination. Calves were challenge-exposed orally at 6 or 8 weeks of age with 1.5 × 1011 (groups 1 and 4), or 3.0 × 1011 (groups 2, 3, and 5) colony-forming units of S typhimurium UCD 108-11.

Mortality after challenge exposure was 2 of 5 group-1 calves; 4 of 5 group-2 calves; 5 of 6 group-3 calves; 1 of 5 group-4 calves; and 4 of 5 group-5 calves. Statistical difference between calves of similarly challenge-exposed groups was not evident, indicating failure of either vaccine to protect calves of this age from oral challenge exposure with virulent S typhimurium.

Free access
in American Journal of Veterinary Research

SUMMARY

Conventionally raised Chinese Meishan and European Large White pigs were intragastrically challenge exposed with 2.1 × 1010 enterotoxigenic Esherichia coli strains bearing colonization factor K88, 987P, F41, or F41 plus K99. In response to challenge exposure with the K88-positive (K88+ ) organisms, 96% of Large White pigs died within 48 hours, whereas none of the Meishan pigs died. Both breeds of pigs had similar susceptibility to strains bearing 987P or F41. Lastly, Meishan pigs were found to be more susceptible than Large White pigs to a strain expressing K99 and F41. In pigs with diarrhea, challenge-exposure strains intensively colonized the jejunum (108 to 1010 bacteria/g of tissue) and, to less extent, the duodenum (except K88+ strain, which comprised 108/g). In most cases, jejunal concentrations of the challenge-exposure strains were substantially lower in pigs that did not have diarrhea. Half the resistant Meishan pigs eliminated the K88+ strain from the intestines. Colostral antibody titer that agglutinated challenge-exposure strains did not differ between Meishan and Large White gilts. Results indicate that resistance of pigs to the K88+ strain did not extend to enterotoxigenic strains bearing other well-known factors. They indicate, in addition, that genetic resistance to K88+ strains described in pigs in Europe may exist in pigs in China.

Free access
in American Journal of Veterinary Research