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.
Objective—To determine whether 2 isolates of
recently isolated swine-origin Helicobacterpylori-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)
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.
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.
Objective—To determine whether a combination viral
vaccine containing modified-live bovine herpesvirus-1
(BHV-1) would protect calves from infection with a
recent field isolate of BHV-1.
Design—Randomized controlled trial.
Animals—Sixty 4- to 6-month-old beef calves.
Procedure—Calves were inoculated with a placebo
42 and 20 days prior to challenge (group 1; n = 10) or
with the combination vaccine 42 and 20 days prior to
challenge (group 2; 10), 146 and 126 days prior to challenge
(group 3; 10), 117 and 96 days prior to challenge
(group 4; 10), 86 and 65 days prior to challenge (group
5; 10), or 126 days prior to challenge (group 6; 10). All
calves were challenged with BHV-1 via aerosol.
Clinical signs, immune responses, and nasal shedding
of virus were monitored for 14 days after challenge.
Results—Vaccination elicited increases in BHV-1–specific
IgG antibody titers. Challenge with BHV-1 resulted
in mild respiratory tract disease in all groups, but
vaccinated calves had less severe signs of clinical disease.
Extent and duration of nasal BHV-1 shedding following
challenge was significantly lower in vaccinated
calves than in control calves. In calves that received 2
doses of the vaccine, the degree of protection varied
with the interval between the last vaccination and
challenge, as evidenced by increases in risk of clinical
signs and extent and duration of viral shedding.
Conclusions and Clinical Relevance—Results suggest
that this combination vaccine provided protection from
infection with virulent BHV-1 and significantly reduced
nasal shedding of the virus for at least 126 days after vaccination.
(J Am Vet Med Assoc 2005;227:123–128)
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
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
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)
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 Pao2, 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 Pao2, 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.
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
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