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SUMMARY

Ceftiofur hydrochloride was tested for effectiveness against induced colibacillosis in neonatal swine. In this model, pigs < 12 hours old were inoculated via stomach tube with a virulent, K99+, nalidixic acid-resistant strain of Escherichia coli. Six hours after challenge exposure, 1 dose of ceftiofur was administered either IM or orally in experiment 1 and orally only in experiment 2. Mortality, shedding of bacteria, fecal consistency scores, and body weight changes were monitored for 10 days. In experiment 1 (n = 383 pigs), all treatments at dosage that ranged between 0.5 and 64.0 mg of ceftiofur/kg of body weight significantly (P < 0.001) reduced mortality, bacterial shedding, and diarrhea and increased weight gain, compared with findings in untreated controls. There were no detectable differences between oral and IM routes, except that there was greater reduction in bacteria shedding associated with the oral route of administration. In experiment 2 (n = 505 pigs), ceftiofur was administered orally either once at 6 hours after challenge exposure or twice at 6 and at 48 hours after the first dose. Dosage of ceftiofur was 0, 5, 10, 20, 30, or 60 mg/kg administered once, or half the same dose was administered at each of 2 times. At the optimal dosage (10 mg/kg), a single dose was as effective as 2 doses. The single administration at all dosages reduced mortality, bacterial shedding, and diarrhea scores and increased body weight gain, compared with findings in untreated pigs (P < 0.01). In this induced infection model, the optimal treatment dosage was determined to be 10 mg/kg administered once.

Free access
in American Journal of Veterinary Research

Abstract

Objective

To test the ability of porcine respiratory coronavirus (PRCV) to induce protective immunity to antigenically related transmissible gastroenteritis virus (TGEV) in neonatal pigs.

Design

Neonatal pigs were exposed to PRCV when they were 2, 4, or 6 days old and challenge-exposed to virulent TGEV at 10 days of age.

Animals

34 hysterectomy-derived, colostrum-deprived pigs.

Procedure

After challenge exposure, clinical signs were observed, body weight, antibody response, and virus shedding were measured, and mortality was determined.

Results

After exposure to PRCV, principals had a slightly slower rate of weight gain than did controls; with 1 exception (a PRCV-exposed pig that was dyspneic for 1 day), principals and controls remained clinically normal until shortly after challenge exposure, when all pigs became listless and anorectic and developed watery diarrhea. However, by day 3, most of the pigs that had been exposed to PRCV when they were either 2 or 4 days old began to recover and most (15/18) survived. Conversely, the clinical condition of most of the other pigs worsened and most (14/16) died. Pigs exposed to PRCV when they were 2 or 4 days old also differed from all other pigs in that they had serum virus-neutralizing antibodies for PRCV and TGEV at the time of challenge exposure.

Conclusions

The PRCV can induce protective immunity to TGEV in neonatal pigs and such immunity develops at or about 6 days after exposure to PRCV. Moreover, protective immunity may be coincident with the appearance of virus-neutralizing antibody.

Clinical Relevance

Exposure to PRCV should enhance a TGE herd vaccination program.

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

The infectivity and pathogenicity of selected bovine viral diarrhea virus (bvdv) isolates were determined in gnotobiotic, colostrum-deprived neonatal lambs. Five-day-old cesarean-derived gnotobiotic lambs were exposed to 1 of 10 bvdv. isolates via aerosol suspension. These isolates were from tissues or secretions of calves or lambs affected with respiratory tract disease, weak neonatal calves, aborted bovine fetuses, or reference Singer or Draper bvdv. The pathogenicity of each isolate, relative to the others, was evaluated in lambs by measurement of the neutralizing antibody response, virus isolation from nasal secretions or tissues, and postmortem lesions. The bvdv isolates varied in their infectivity and pathogenicity. Singer, the cytopathic reference strain, was the most lymphotrophic isolate and stimulated the greatest neutralizing antibody response. Encephalitis was the most consistent lesion observed and was used as the final determinant of relative pathogenicity of the viruses. The most neuropathogenic isolates were the 2 viruses originating from lambs affected with respiratory tract disease, the 2 weak neonatal calf isolates, and 1 isolate from an aborted bovine fetus. The least pathogenic isolates were the 2 reference isolates, Draper and Singer; the 2 mucosal disease isolates; and 1 isolate originating from an aborted bovine fetus.

Free access
in American Journal of Veterinary Research

Summary

To determine whether intrauterine transmission of Borrelia burgdorferi could exist in dogs, 10 female Beagles were inoculated intradermally with approximately 1,000 B burgdorferi on day 1 of proestrus; inoculation was repeated every 2 weeks during the gestation period. Ten female control Beagles were similarly inoculated with phosphate-buffered saline solution. Prior to the start of the study, all females and 3 males used for breeding were seronegative for B burgdorferi on the basis of results of the indirect fluorescent antibody test and immunoblot (western blot) analysis. Similarly, results of culture of blood for B burgdorferi were negative. All 20 of the females were bred naturally. Blood samples were collected weekly for serologic testing and culture. Blood samples were obtained from live pups on day 1 of life, then weekly until pups were 6 weeks old when they were euthanatized. Tissues were obtained for culture and testing by use of polymerase chain reaction (pcr). Of 10 spirochete-inoculated (si) females, 8 became infected with B burgdorferi as evidenced by spirochete culture results and/or pcr-detected B burgdorferi dna in the tissues of females or their pups. Of the 10 si females, 8 delivered litters (3 to 7 pups) that had at least 1 neonatal or 6-week-old pup with B burgdorferi dna-positive tissues (by pcr), and spirochetes were cultured from tissues from pups of 2 litters. Four pups of 3 separate litters (a stillborn, a neonate that survived to 30 minutes of age, a 20- hour-old, and a 48-hour-old) had B burgdorferi-positive tissues (by pcr), and the 20-hour-old pup was also culture-positive, indicating intrauterine infection. Further evidence of intrauterine exposure was the presence of IgM antibodies to B burgdorferi detectable by western blot in 3 of 7 one-day-old pups that did not receive colostrum, indicating a primary immune response. Eight of 10 si females and 10 of 10 control females carried litters to term. Differences between si and control Beagles were seen in the duration of gestation, number of resorptions, and number of dystocias. All control females and pups remained seronegative, culture-negative, and B burgdorfer-inegative throughout the study.

Intrauterine infection by B burgdorferi does occur in dogs and is a potential means by which the spirochete can be transmitted in a breeding population in the absence of a tick vector.

Free access
in American Journal of Veterinary Research

Summary

Fecal samples were collected from 450 neonatal calves ranging from 1 to 30 days old, between May, 1988 and May, 1989 to estimate the prevalence of bovine group A rotavirus in a stratified random sample of Ohio daily herds. Calves were from 47 dairy herds chosen to be representative of Ohio herds. Bovine group A rotavirus was detected in fecal samples by a cell culture immunofluorescence test (ccif) and elisa. Of 450 samples tested, 46 (10%) were positive by ccif and 67 (15%) were positive by elisa. The agreement beyond chance between the 2 assays was good (kappa = 0.65). The overall prevalence rate of rotavirus shedding was 16.4% (74/450). Forty-three percent (29/67) of the samples positive by elisa were subgroup 1, none were subgroup 2, and the remaining 57% (38/67) could not be assigned to either subgroups 1 or 2. Thirty herds (62.5%) had at least 1 group A rotavirus-positive calf (mean number of samples per positive herd = 12.4), and 17 herds (37.5%) had no rotavirus-positive calves (mean number of samples per negative herd = 6.0). A live oral rotacoronavirus vaccine was used in neonatal calves of only 1 herd and 3 of 17 (17.6%) calves from this herd were positive for group A rotavirus. The percentage of the rotavirus-positive fecal samples from all calves (n = 450) when stratified by fecal consistency was as follows: 28.3% (13/46) had liquid feces; 25.6% (10/39) had semiliquid feces; 23.4% (22/94) had pasty feces; and 10.7% (29/271) had firm feces. Of the rotavirus-positive calves (n = 74), 17.6% (13/74) had liquid feces; 13.5% (10/74) had semiliquid feces; 29.7% (22/74) had pasty feces; and 39.2% (29/74) had firm feces. The average age of calves shedding rotavirus was 14 days (range, 1 to 30 days). Double-stranded (ds) rna extracted from 36 samples positive by 1 or both tests was examined by polyacrylamide gel electrophoresis. All samples positive by this technique (30/36) had long dsrna migration patterns, typical of group A rotaviruses, including samples from calves in the herd in which the oral vaccine was used. Moreover, the electrophoretic migration pattern of group A rotavirus dsrna in these vaccinated calves differed from that of the rotavirus vaccine strain, suggesting the rotavirus strain circulating in this herd was not the vaccine strain. All samples negative by ccif or elisa that had volumes > 5 ml (n = 323) were also subjected to dsrna extraction and polyacrylamide gel electrophoresis for detection of additional group A or nongroup A rotaviruses; none of them were positive by this technique.

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

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

Abstract

Objective

To determine patterns of cell-associated viremia and antibody responses during the early phase of ovine lentivirus (OvLV) infection in sheep.

Animals

18 neonatal lambs.

Procedures

12 lambs were inoculated intratracheally with OvLV within 24 hours after birth; 6 lambs were inoculated with noninfected cell culture supernatant. Degree of cell-associated viremia was measured every other week for 16 weeks by use of a limited dilution assay. Antibody responses to OvLV transmembrane (TM) and p25 proteins were determined weekly by use of a recombinant ELISA. Neutralizing antibody responses were measured before and 8 and 16 weeks after inoculation.

Results

Degree of cell-associated viremia peaked between 2 and 6 weeks after inoculation and then decreased. For inoculated lambs, mean anti-p25 titer peaked 5 weeks after inoculation then slowly declined, whereas mean anti-TM and neutralizing antibody titers increased steadily. Over time, mean degree of cell-associated viremia was negatively correlated with mean anti-TM titer. Maximum individual degree of cell-associated viremia was positively correlated with maximum individual anti-TM titer.

Conclusions

Results suggest that after experimental inoculation, OvLV replicates actively for several weeks and that an increase in anti-TM titer coincides with a decrease in degree of cell-associated viremia. Although the role antibodies play in protecting against lentivirus infection remains uncertain, understanding the dynamics of the antibody response may have important implications for diagnosis of OvLV infection, and antibodies may prove to be valuable markers for prediction of infection and disease. (Am J Vet Res 1998;59:563–568)

Free access
in American Journal of Veterinary Research

Summary

Pregnant gilts were exposed to porcine reproductive and respiratory syndrome virus (prrsv ) by iv inoculation at or about gestation day 30 (3 gilts), 50 (3 gilts), 70 (3 gilts), or 90 (5 gilts) to investigate the likelihood of transplacental infection with prrsvat various stages of gestation. At or about 3, 6, and 9 weeks after exposure, gilts were either euthanatized while still pregnant or allowed to farrow. Gilts and pigs were observed for clinical signs of infection, and gilts, pigs, and fetuses were tested for prrsvand homologous antibody. All gilts were healthy throughout the study, except that farrowing was sometimes difficult and prolonged, and 2 gilts failed to farrow the entire litter. One gilt farrowed on day 111 of gestation; all others farrowed on day 114 or later. Porcine reproductive and respiratory virus was isolated from significantly (x2 test, P < 0.01) more fetuses and live and stillborn pigs of the 5 gilts that were infected at 90 or 92 days of gestation than from the fetuses and live and stillborn pigs of the 9 gilts that were infected at 72 or fewer days of gestation (ie, 33 of 44, 75% vs 3 of 78,4%). After initial infection, prrsvwas isolated from gilts and their pigs for a maximum of 3 weeks and 8 to 11 weeks, respectively. Findings of this study, with regard to the temporal aspects of transplacental infection, may help explain why natural epizootics of prrsv-induced maternal reproductive failure are often recognized principally as problems of late-term gestation and neonatal survival.

Free access
in American Journal of Veterinary Research