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Abstract

Objective—To determine whether porcine genogroup 1 torque teno virus (g1-TTV) can infect and cause disease in gnotobiotic swine.

Sample Population—20 conventional baby pigs and 46 gnotobiotic baby pigs.

Procedures—Porcine g1-TTV was transmitted from conventional swine to gnotobiotic pigs via pooled leukocyte-rich plasmas (n = 18) that had positive results for g1-TTV DNA. Bone marrow–liver homogenates that had positive results for torque teno virus (TTV) were used in 4 serial passages in gnotobiotic pigs (2 pigs/passage). A pathogenesis experiment was conducted with in vivo passages of g1-TTV in various groups of gnotobiotic pigs.

Results—All g1-TTV inoculated pigs had no clinical signs but developed interstitial pneumonia, transient thymic atrophy, membranous glomerulonephropathy, and modest lymphocytic to histiocytic infiltrates in the liver after inoculation with the TTV-containing tissue homogenate; these changes were not detected in uninoculated control pigs or pigs injected with tissue homogenate devoid of TTV DNAs. In situ hybridization was used to identify g1-TTV DNAs in bone marrow mononuclear cells.

Conclusions and Clinical Relevance—Analysis of these data revealed that porcine g1-TTV was readily transmitted to TTV-naïve swine and that infection was associated with characteristic pathologic changes in gnotobiotic pigs inoculated with g1-TTV. Thus, g1-TTV could be an unrecognized pathogenic viral infectious agent of swine. This indicated a directly associated induction of lesions attributable to TTV infection in swine for a virus of the genus Anellovirus.

Full access
in American Journal of Veterinary Research

Abstract

Objective—To determine whether 2 isolates of recently isolated swine-origin Helicobacter pylori-like bacteria are pathogenic in pigs and compare the signs of gastric disease induced by these isolates with those detected in H pylori- and Helicobacter heilmannii-in fected pigs.

Animals—36 neonatal gnotobiotic pigs.

Procedure—Groups of separately housed pigs were inoculated orally with swine-origin Helicobacter-like isolates 2662 or 1268, H pylori (human gastric pathogen), or a gastric homogenate from gnotobiotic swine containing H heilmannii. Noninoculated pigs were used as control animals. Clinical signs and development of homologous and heterologous antibodies against Helicobacter organisms were assessed. After euthanasia, gastric tissues were examined grossly and microscopically; Helicobacter organisms were detected by use of Warthin-Starry and immunohistochemical stains.

Results—Both porcine Helicobacter-like isolates colonized the stomachs of swine. Isolate 2662 was highly pathogenic; in 13 isolate 2662-inoculated pigs, gastroesophageal ulcerations developed in 9 and ulceration of the gastric glandular mucosa was detected in 5. Histologically, inflammatory gastritis consisting of multifocal to diffuse lymphocytic and plasmacytic cellular infiltrates and lymphoid follicle formation in the gastric lamina propria accompanied bacterial colonization of the gastric compartment. In contrast, H heilmannii was minimally pathogenic in that only modest inflammatory cell infiltrates were seen. Gastroesophageal or mucosal ulcers were not evident in pigs inoculated with H heilmannii.

Conclusions and Clinical Relevance—These data indicate that swine-origin H pylori-like bacteria can be pathogenic in pigs and suggest that porcine gastric disease may be mediated, in part, by colonization of the stomach by swine-origin H pylori-like bacteria. (Am J Vet Res 2005;66:945–952)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To determine whether genogroup 1 porcine torque teno virus (g1-TTV) can potentiate clinical disease associated with porcine circovirus type 2 (PCV2).

Sample population—33 gnotobiotic baby pigs.

Procedures—Pigs were allocated into 7 groups: group A, 5 uninoculated control pigs from 3 litters; group B, 4 pigs oronasally inoculated with PCV2 alone; group C, 4 pigs inoculated IP with first-passage g1-TTV alone; group D, 4 pigs inoculated IP with fourth-passage g1-TTV alone; group E, 6 pigs inoculated IP with first-passage g1-TTV and then oronasally inoculated with PCV2 7 days later; group F, 6 pigs inoculated IP with fourth-passage g1-TTV and then inoculated oronasally with PCV2 7 days later; and group G, 4 pigs inoculated oro-nasally with PCV2 and then inoculated IP with fourth-passage g1-TTV 7 days later.

Results—6 of 12 pigs inoculated with g1-TTV prior to PCV2 developed acute onset of postweaning multisystemic wasting syndrome (PMWS). None of the pigs inoculated with g1-TTV alone or PCV2 alone or that were challenge exposed to g1-TTV after establishment of infection with PCV2 developed clinical illness. Uninoculated control pigs remained healthy.

Conclusions and Clinical Relevance—These data implicated g1-TTV as another viral infection that facilitates PCV2-induced PMWS. This raises the possibility that torque teno viruses in swine may contribute to disease expression currently associated with only a single infectious agent.

Full access
in American Journal of Veterinary Research

Abstract

Objective—To determine whether a combination modified-live bovine respiratory syncytial virus (BRSV) vaccine can stimulate protective immunity in young BRSV-seropositive calves following intranasal (IN) administration.

Design—Controlled challenge study.

Animals—66 Holstein bull calves, 3 to 8 days old.

Procedures—In experiment 1, BRSV-seropositive and -seronegative calves were vaccinated IN with a commercially available combination modified-live virus vaccine formulated for SC administration; calves underwent BRSV challenge 4.5 months later. In experiment 2, BRSV-seronegative calves were vaccinated IN or SC (to examine the effect of route of administration) with the same combination vaccine that instead had a 1/100 dose of BRSV (to examine the effect of dose); calves underwent BRSV challenge 21 days later.

Results—In experiment 1, BRSV challenge resulted in severe respiratory tract disease with low arterial partial pressures of oxygen and lung lesions in most calves from all groups. Maximum change in rectal temperature was significantly greater in seropositive IN vaccinated calves, compared with seronegative IN vaccinated and seropositive control calves. Number of days of BRSV shedding was significantly lower in seronegative IN vaccinated calves than in seropositive IN vaccinated and seropositive control calves. In experiment 2, maximum change in rectal temperature was significantly greater in seronegative control calves, compared with seronegative IN and SC vaccinated calves. Shedding of BRSV was significantly reduced in seronegative IN and SC vaccinated calves, compared with control calves; also, lung lesions were reduced in seronegative IN and SC vaccinated calves.

Conclusions and Clinical Relevance—Maternal antibodies may inhibit priming of protective responses by IN delivered BRSV vaccines.

Restricted access
in Journal of the American Veterinary Medical Association
in Journal of the American Veterinary Medical Association

Abstract

Objective—To determine whether feline vaccine siteassociated sarcomas (VSS) contain a higher amount of endogenous FeLV (enFeLV) RNA, compared with feline nonvaccine site-associated sarcomas (non-VSS).

Sample Population—Formalin-fixed paraffin-embedded (FFPE) tissues from 50 VSS and 50 cutaneous non-VSS.

Procedure—RNA was extracted from FFPE sections of each tumor, and regions of the long terminal repeat (LTR) and envelope (env) gene of enFeLV were amplified by use of reverse transcriptase-polymerase chain reaction (RT-PCR). The density of each RT-PCR product band for enFeLV was compared with that of a constitutively expressed gene, glyceraldehyde-3-phosphate dehydrogenase (GAPDH). An integrated density value (IDV) was determined by use of densitometry, and the IDV ratio for enFeLV to GAPDH was calculated for each enFeLV primer set.

Results—The median (interquartile range) of the IDV ratio for the enFeLV LTR primer set was 0.52 (0.26 to 1.17) for the VSS group and 0.84 (0.21 to 1.53) for the non-VSS group. The median (interquartile range) of the IDV ratio for the enFeLV env primer set was 0.60 (0.37 to 0.91) for the VSS group and 0.59 (0.36 to 1.09) for the non-VSS group.

Conclusions—Because the amount of enFeLV RNA within the LTR and env gene was not significantly different between the VSS and non-VSS groups, enFeLV replication or expression is unlikely to be involved in VSS development. (Am J Vet Res 2001;62:1990–1994)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To evaluate the use of a polymerase chain reaction (PCR) method for detection of feline immunodeficiency virus (FIV) DNA, using formalin-fixed paraffin- embedded (FFPE) tissues, and to use this method to evaluate tissues obtained from vaccine site-associated sarcomas (VSS) of cats for FIV DNA.

Sample Population—50 FFPE tissue blocks from VSS of cats and 50 FFPE tissue blocks from cutaneous non-vaccine site-associated fibrosarcomas (non-VSS) of cats.

Procedure—DNA was extracted from FFPE sections of each tumor and regions of the gag gene of FIV were amplified by a PCR, using 3 sets of primers. Sensitivity of the method was compared between frozen and FFPE tissues, using splenic tissue obtained from a cat that had been experimentally infected with FIV.

Results—We did not detect FIV DNA in VSS or non- VSS tissues. Sensitivity of the PCR method was identical for frozen or FFPE tissues.

Conclusions and Clinical Relevance—It is possible to detect FIV DNA in FFPE tissues by use of a PCR. We did not find evidence to support direct FIV involvement in the pathogenesis of VSS in cats. (Am J Vet Res 2000;61:1037–1041)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To compare antibody responses to intranasal and SC Bordetella bronchiseptica vaccines in seropositive dogs.

Design—Randomized controlled study.

Animals—40 young adult Beagles vaccinated against B bronchiseptica.

Procedure—Dogs were randomly assigned to 1 of 4 groups (intranasal vaccine, SC vaccine, intranasal and SC vaccines, no vaccine) and vaccinated on day 0. Serum and salivary B bronchiseptica-reactive antibody responses were measured on days 0 through 7, 10, 14, 21, and 28.

Results—Dogs that were vaccinated with the SC vaccine, alone or in combination with the intranasal vaccine, had a significant increase in serum concentration of B bronchiseptica-reactive IgG beginning on day 5 and persisting through day 28. Dogs that were vaccinated with the intranasal vaccine alone had a significant increase in serum concentration of B bronchiseptica- reactive IgG beginning on day 10 and persisting through day 28, but serum IgG concentration in these dogs was significantly less than concentration in dogs that received the SC vaccine. Neither vaccine had a demonstrable effect on salivary concentrations of B bronchiseptica-reactive IgA or IgG. On day 10, all vaccinated groups had significantly higher serum IgA concentrations than did unvaccinated control dogs.

Conclusions and Clinical Relevance—Results suggest that the SC B bronchiseptica vaccine may be used to stimulate antibody responses in seropositive dogs. There was no apparent benefit to administering these vaccines simultaneously. Intranasal vaccines may not be effective for booster vaccination of dogs previously exposed to or immunized against B bronchiseptica. Dogs should be vaccinated at least 5 days prior to exposure to B bronchiseptica. (J Am Vet Med Assoc 2002;220:43–48)

Restricted access
in Journal of the American Veterinary Medical Association

Abstract

Objective—To determine whether a combination modified-live bovine respiratory syncytial virus (BRSV) vaccine could stimulate protective immunity in young BRSV-seropositive calves following intranasal administration and determine the duration of clinical immunity.

Design—Controlled challenge study.

Animals—84 dairy calves (3 to 11 days old).

Procedures—Responses to BRSV challenge of seronegative calves vaccinated under licensing trial conditions were compared with those of seropositive calves 2 times after vaccination. In experiment 1, young BRSV-seronegative calves were vaccinated intranasally with a minimum immunizing dose of BRSV and challenged with BRSV approximately 7 weeks later. In experiments 2 and 3, young BRSV-seropositive calves were vaccinated intranasally with a commercially available combination modified-live virus vaccine containing the commercial dose of the BRSV fraction and challenged with BRSV 9 weeks or approximately 14 weeks later, respectively.

Results—In experiments 1 and 2, BRSV-vaccinated calves had significantly higher Pao 2, significantly fewer lung lesions, and significantly lower mortality rate than did unvaccinated calves subsequent to BRSV challenge. In contrast, in experiment 3, there were no differences in Pao 2, lung lesions, or mortality rate between vaccinated and control calves after BRSV challenge approximately 14 weeks after vaccination. Protected calves in experiment 1 consistently had significant anamnestic mucosal and systemic antibody responses after challenge, whereas in experiments 2 and 3, antibody responses after challenge were more variable.

Conclusions and Clinical Relevance—A combination BRSV vaccine administered intranasally to young calves induced protective immunity in the presence of maternal antibodies. The duration of immune responses induced by intranasal vaccination was short (≤ 4 months). Boosting immunity iatrogenically, or by natural exposure, is probably required to obtain optimal responses to neonatal intranasal vaccination.

Restricted access
in Journal of the American Veterinary Medical Association

Abstract

Objective—To evaluate a group of vaccine site-associated sarcomas (VSS) for the presence of feline foamy virus (FeFV) DNA, using polymerase chain reaction (PCR) methods.

Sample Population—50 formalin-fixed paraffin embedded (FFPE) tissue blocks from VSS of cats.

Procedure—DNA was extracted from FFPE sections of each tumor, and regions of the gag and pol genes of FeFV were amplified by use of PCR methods, using 1 primer set for each region. Sensitivity of the method was compared between fresh and FFPE cells, using mouse kidney tissue that was injected with FeFVinfected cultured cells and using agarose-cell pellets.

Results—Feline foamy virus DNA was not detected in VSS tissues. Sensitivity of the method was 10 times greater in fresh versus FFPE mouse tissues. Sensitivity of the method in fresh FeFV-infected cultured cells versus FFPE agarose-cell pellets was equal when fixation was 24 or 48 hours and 10 times greater when fixation was 72 hours or 1 week.

Conclusion and Clinical Relevance—A PCR-based method can be successfully applied to FFPE tissues for FeFV DNA detection. Results suggest there is no direct FeFV involvement in the pathogenesis of VSS in cats. (Am J Vet Res 2002;63:60–63)

Full access
in American Journal of Veterinary Research