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Effect of maternal antibodies on induction

and persistence of vaccine-induced immune
responses against bovine viral diarrhea virus
type II in young calves
John Ellis, DVM, PhD, DACVP, DACVM; Keith West, DVM, PhD; Victor Cortese, DVM, PhD, DABVP;
Carrie Konoby, BSc; Dan Weigel, PhD

ith the emergence of virulent strains of bovine

viral diarrhea virus (BVDV) during the past several years, there has been a renewed interest in protecting cattle from clinical syndromes associated with
infection by these agents,1-6 particularly young cattle in
which the acute form of BVDV infection can be especially severe.5-7 Vaccination of young calves during the
early postpartum period could potentially be an important tool in minimizing the effects of BVDV infection.
From the Department of Veterinary Microbiology, Western College
of Veterinary Medicine, University of Saskatchewan, Saskatoon,
SK, Canada S7N 5B4 (Ellis, West, Cortese, Konoby); and Pfizer
Animal Health Group, 812 Springdale Dr, Exton, PA 19341-2803
(Cortese, Weigel).
Supported by a grant from Pfizer Animal Health Group.
JAVMA, Vol 219, No. 3, August 1, 2001

Materials and Methods

Calves and experimental designTwenty-four neonatal Holstein and Holstein-cross calves obtained from a local
dairy were used in the study. Calves were deprived of maternal colostrum and fed spray-dried reconstituted pooled
colostrum with a high concentration of BVDV-specific antibodiesa or pooled colostrum that tested negative for BVDV
antibodies with a BVDV-specific ELISA. Calves received 2
feedings of colostrum (1.5 L/feeding) within the first 18
hours after birth. Colostrum was administered by the dairyman, and calves were assigned to receive the reconstituted
colostrum or the pooled colostrum in alternating order. Buffy
coat samples from all calves were submitted for BVDV isolation to ensure that calves were not persistently infected with
BVDV. Calves were group housed separately from other catScientific Reports: Original Study

351

RUMINANTS

ObjectiveTo determine the effect of maternally

derived antibodies on induction of protective immune
responses against bovine viral diarrhea virus (BVDV)
type II in young calves vaccinated with a modified-live
bovine viral diarrhea virus (BVDV) type I vaccine.
DesignBlinded controlled challenge study.
Animals24 neonatal Holstein and Holstein-cross
calves that were deprived of maternal colostrum and
fed pooled colostrum that contained a high concentration of (n = 6) or no (18) antibodies to BVDV.
ProcedureAt 10 to 14 days of age, 6 seropositive
and 6 seronegative calves were given a combination
vaccine containing modified-live BVDV type I. All
calves were kept in isolation for 4.5 months. Six
calves of the remaining 12 untreated calves were vaccinated with the same combination vaccine at approximately 4 months of age. Three weeks later, all calves
were challenged intranasally with a virulent BVDV
type II.
ResultsSeronegative unvaccinated calves and
seropositive calves that were vaccinated at 2 weeks
of age developed severe disease, and 4 calves in each
of these groups required euthanasia. Seronegative
calves that were vaccinated at 2 weeks or 4 months
of age developed only mild or no clinical signs of disease.
Conclusions and Clinical RelevanceResults indicate that a single dose of a modified-live BVDV type-I
vaccine given at 10 to 14 days of age can protect susceptible young calves from virulent BVDV type II infection for at least 4 months, but high concentrations of
BVDV-specific maternally derived antibodies can block
the induction of the response. (J Am Vet Med Assoc
2001;219:351356)

Recently, it was reported that a single dose of a modified-live BVDV vaccine containing BVDV type I can
protect young seronegative calves from the clinical
effects of infection by a genetically and antigenically
disparate virulent strain of BVDV type II.8 This clearly
demonstrated that the neonatal immune system could
respond in a clinically relevant manner to vaccinal
antigens. However, the longevity of the protective
response was not determined.
One of the ongoing controversies in veterinary
medicine is the role of passively transferred antibodies
in blocking the induction of immune responses in
neonatal animals. 9 It has been reported that at least
some immune responses, for example lymphocyte
blastogenic responses, can be stimulated in young
calves in the absence of a measurable effect on antibody production10; however, such studies have rarely
involved a challenge of immunity. In a previous study,8
there was no apparent clinical benefit to vaccinating
young calves with a modified-live BVDV vaccine if they
were challenged while concentrations of passively
acquired antibodies were still high.8 The authors found
it was impossible to determine whether disease-sparing
effects were attributable to the known protective effects
of passively acquired antibodies or to some vaccinestimulated active immune response.
The purpose of the study reported here, therefore,
was to determine whether high concentrations of
maternally derived BVDV-specific antibodies can block
the induction of protective immune responses in
young calves vaccinated with a modified-live BVDV
vaccine and whether a single dose of a modified-live
BVDV vaccine given within the first 2 weeks of life can
stimulate a BVDV-specific protective immune response
that is detectable until at least 4 months of age.

RUMINANTS

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tle throughout the study. They were fed a commercial milk

replacer twice a day until approximately 7 weeks of age. A calf
starter ration, alfalfa hay, and water were available free choice.
Serum from all calves was tested within 7 days after
birth for BVDV-specific antibodies by use of an ELISA, and
calves were assigned to treatment groups on the basis of
results of this test. Group 1 consisted of seronegative unvaccinated control calves (n = 6) that did not receive any vaccine. Group 2 consisted of seropositive calves (n = 6) that
between 10 and 14 days after birth received a single dose,
intramuscularly, of a commercial vaccineb containing modified-live BVDV type I (NADL strain; plaque expanded),
bovine herpesvirus 1, parainfluenza virus 3, and bovine respiratory syncytial virus. Group 3 consisted of seronegative
calves (n = 6) that received a single dose of the same vaccine
between 10 and 14 days after birth. Group 4 consisted of
seronegative calves (n = 6) that received a single dose of the
same vaccine approximately 4 months after birth. Calves
were observed twice daily after vaccination for any local or
systemic adverse reactions.
At approximately 4.5 months of ages (3 weeks after vaccination of the group-4 calves), all calves were inoculated
intranasally with BVDV type II. Rectal temperature was measured, and a clinical score was assigned twice daily (approx
8:00 AM and 4:30 PM) for the next 14 days. A predetermined
scoring scheme (Appendix) was used to assign clinical scores;
scoring was performed by a single individual who did not
know to which group calves had been assigned. Assigning
clinical scores involved assessing appetite, severity of signs of
depression, and signs of respiratory and gastrointestinal tract
disease. Blood samples were collected prior to vaccination, on
the day of vaccination, immediately prior to challenge (day
0), and 1, 3, 5, 7, 9, 11, and 14 days after challenge.
Calves that had at least 3 of the 4 following clinical
abnormalities for more than 2 consecutive days or measurements were euthanatized by administration of a barbiturate
overdose: rectal temperature 40.6 C (105.1 F), diarrhea,
total WBC count < 2,000 cells/ml, and signs of severe depression. A complete necropsy was performed on calves that were
euthanatized or died. Samples were collected for immunohistochemical testing to confirm BVDV infection.8
Preparation of the challenge virusThe noncytopathic
BVDV isolate No. 24515c obtained from the tissues of a calf
with an acute mucosal-like disease syndrome that died during an outbreak of BVDV-associated disease in Ontario,
Canada, was used for nasal inoculation of the calves.6-8 This isolate was classified as BVDV type II on the basis of results of antigenic analyses, using type-specific monoclonal antibodies, and
genetic analyses based on sequencing of the 5' nontranslated
region of the virus.6 The virus was propagated as described in
embryonic bovine turbinate (EBT) cells,8 and virus passages 7
and 8 were used to inoculate calves. All cell lines used in the
study were tested and determined to be free of non-cytopathic
BVDV. Calves received 5 X 105 median tissue culture infective
doses of virus in 5 ml of tissue culture fluid (2.5 ml/nostril).
Virus isolationBlood samples collected from all calves
prior to enrollment in the study and on study days 0, 3, 5, 7,
9, 11, and 14 were submitted for virus isolation, which was
performed as described.8 Briefly, RBC and remaining leukocytes were washed and co-cultured in EBT cells for 7 days.
Cultures were frozen and thawed once, and aliquots of the
resulting lysates were co-cultured with Madin-Darby bovine
kidney cells for 4 days. Cells were fixed, and BVDV was identified with an immunoperoxidase technique.
Complete blood cell countsBlood samples collected
by means of jugular venipuncture into evacuated tubes containing sodium EDTA on study days 0, 1, 3, 5, 7, 9, 11, and
352

Scientific Reports: Original Study

14 were submitted for CBC. An automated cell counter and

visual assessment of blood smears were used. Manual platelet
counts were performed on samples with low platelet numbers. Granulocyte counts were determined by adding neutrophil, basophil, and eosinophil counts.
Determination of serum antibody concentrationAn
ELISA incorporating solubilized antigen was used to detect
serum antibodies to BVDV in colostrum samples and in
serum samples obtained from all calves prior to vaccination
and on study days 0, 3, 5, 7, 9, 11, and 14, as described.8
Briefly, the NADL isolate of BVDV was grown in porcine kidney cells; the cells were lysed, and soluble antigen was prepared. Control antigen was prepared in a similar fashion,
using uninfected porcine kidney cells.
Determination of virus neutralizing antibody concentrationA standard plaque reduction assay was performed as
described to quantitate BVDV-specific virus neutralizing
(VN) antibodies.8 Briefly, serial dilutions of serum samples
were created, and an aliquot of each dilution was incubated
with a standard amount (50 to 100 median tissue culture
infective doses) of either of 2 cytopathic isolates, NADL (type
I) or 125 (type II). This mixture was then used to infect EBT
cells grown in microtitration culture plates. Culture plates
were incubated for 7 days and visually examined for evidence
of virus-induced cytopathic effects. Virus neutralizing antibody concentrations were determined in a single set of assays;
serum samples were stored frozen (20 C) until analyzed.
Statistical analysisData were analyzed by use of a
general linear repeated-measures model.8 White blood cell
counts were transformed to natural logarithms prior to
analysis, and resulting estimates of least squares means for
each treatment group were then back-transformed. Similarly,
serum antibody titers were log transformed (ln [n + 1]) prior
to analysis. Virus neutralizing antibody data were transformed to the natural log scale after adding one (1) to the
antibody titer count. Data were analyzed for individual animal effects, the effects of treatment (over all days), the effects
of time, and the effects of treatment by day. Effects of treatment by day were used to assess overall significance; differences among individual days and treatment groups were then
assessed for significance. A value of P 0.05 was considered
significant. Least square means of rectal temperatures were
also determined, and the linear model procedure was used.
Differences in mortality rates were determined by use of 2
and Fisher exact tests. Differences in clinical scores were not
statistically analyzed because of the categorical nature of
these measurements.

Results
No adverse reactions were identified in the calves
that received the vaccine within the first 2 weeks after
birth. All groups of calves had an increase in mean rectal temperature on days 6 and 7. For calves in groups 3
and 4, rectal temperatures returned to baseline values;
however, for calves in groups 1 and 2, rectal temperatures remained significantly higher than those for
calves in the other groups until day 10 (group 1) or 11
(group 2; Fig 1). After challenge exposure, clinical
scores were highest for the unvaccinated control calves
(group 1) and for the seropositive calves that were vaccinated between 10 and 14 days after birth (group 2).
Calves in these groups developed various clinical signs
of disease, including signs of depression, anorexia, and
watery diarrhea, and mean clinical scores for calves in
these 2 groups were substantially higher than mean
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clinical scores for calves in groups 3 and 4 beginning

on day 7 (Fig 2). Seronegative calves that had received
a single dose of the vaccine between 10 and 14 days
after birth (group 3) or 4 months after birth (group 4)
had no clinical abnormalities or signs of only mild clinical disease, as indicated by the lower mean clinical
scores.
Four of 6 group-1 calves and 4 of 6 group-2 calves
were euthanatized because of severe disease 12 to 14
days after challenge; none of the calves in the other 2
groups died or were euthanatized. Mortality rate for
group-1 calves was not significantly different from that
for group-2 calves, and mortality rate for group-3
calves was not significantly different from that for
group-4 calves. However, mortality rates for group-1
and -2 calves were significantly higher than rates for
group-3 and -4 calves. Necropsy of euthanatized calves
revealed erosive lesions of variable severity in the oral
cavity and forestomach and bronchopneumonia.
Immunohistochemical staining revealed widespread
BVDV antigen in ileal Peyer patches of all calves that
were euthanatized, consistent with acute infection.
For all calves, results of virus isolation prior to
inclusion in the study were negative. Three control
calves (group 1), 3 group-2 calves, and 1 group-3 calf
were viremic on 1 or more days after challenge; viremia
was detected on day 5, 7, or 9. None of the group-4
calves had detectable viremia.
Mean WBC count decreased for all 4 groups of
calves after challenge (Fig 3). Mean WBC count was
significantly decreased, compared with baseline values,
JAVMA, Vol 219, No. 3, August 1, 2001

RUMINANTS

Figure 1Mean rectal temperature in 4 groups of calves (n =

6/group) after inoculation with a virulent type II isolate of bovine
viral diarrhea virus (BVDV) at 4.5 months of age (day 0). Group 1
(diamond) consisted of seronegative control calves that were
not vaccinated. Group 2 (circle) consisted of seropositive calves
that received a single dose, intramuscularly, of a commercial
vaccine containing modified-live BVDV type I between 10 and 14
days after birth. Group 3 (triangle) consisted of seronegative
calves that received a single dose of the same vaccine between
10 and 14 days after birth. Group 4 (square) consisted of
seronegative calves that received a single dose of the same vaccine approximately 4 months after birth, 3 weeks prior to inoculation with virulent BVDV.

Figure 2Mean clinical scores for 4 groups of calves after inoculation with a virulent type II isolate of BVDV at 4.5 months of
age (day 0); scores were recorded daily at 8:00 AM and 4:30 PM.
See Fig 1 for key.

Figure 3Mean WBC counts for 4 groups of calves after inoculation with a virulent type-II isolate of BVDV at 4.5 months of age
(day 0). See Fig 1 for key.

on days 3, 5, 7, 9, and 11 in group-1 calves and on days

3, 5, 7, 9, 11, and 14 in group-2 calves. In contrast,
leukopenia was transient in group-3 and -4 calves and
apparent only on day 3, day 5, or both. Paralleling
changes in the WBC count, there were prolonged significant decreases in lymphocyte and neutrophil
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Table 1Serum antibody concentrations in groups of calves (n = 6/group) at the time of vaccination
with a modified-live bovine viral diarrhea virus (BVDV) vaccine and before and after inoculation with a
virulent type-II isolate of BVDV
Mean titer (range)
Day and test

Group 1

Group 2

Group 3

Group 4

NA
ND
ND

24.5 (1629)a,b
ND
ND

0a
ND
ND

0 (01)b
ND
ND

Day of challenge (day 0)

Type I ELISA
Type I VN assay
Type II VN assay

0a
6 ( 635)a
6 ( 6108)a,b,c

0b
12 (1236)b
36 (12108)a

7 (321)a,b,c
162 (108 162)a,b
108 (18 162)b

1 (03)c
36 (1854)a
18 (12108)c

Day 3
Type I ELISA
Type I VN assay
Type II VN assay

0 (01)a
6 (054)a,b,c
6 ( 6108)a,b,c

0b
18 (1236)a
36 (12108)a

5 (023)a,b,c
54 ( 6 162)b
36 (18 162)b

1 (03)c
36 ( 6162)b
12 ( 6108)c

Day 5
Type I ELISA
Type I VN assay
Type II VN assay

0 (01)a
6 (054)a,b,c
6 (054)a,b

0b
18 (1236)a
18 (12108)a

5 (019)a,b,c
54 ( 6 162)b
36 ( 6 162)b

2 (07)a,c
36 ( 654)c
18 ( 654)

Day 7
Type I ELISA
Type I VN assay
Type II VN assay

0a
6 ( 636)a,b,c
6 ( 636)a,b

1 (01)b
18 (6108)a
36 (1854)a

11 (026)a,b
54 ( 6162)b
54 ( 6162)b

3 (019)a
18 ( 6 162)c
18 ( 6 162)a

Day 9
Type I ELISA
Type I VN assay
Type II VN assay

0a
6 ( 636)a
18 (6162)

0b,c
18 ( 6 162)b,c
18 ( 654)

37 (0121)a,b
54 ( 6 162)a,b
54 ( 6 162)

10 (093)a,c
54 ( 6 162)a,c
54 ( 6 162)

Day 11
Type I ELISA
Type I VN assay
Type II VN assay

1 (01)a
12 ( 6162)a
162

2 (07)b,c
18 (12 162)b,c
162 (54 162)

106 (72142)a,b,d
162a,b
162

26 (1062)a,c,d
162a,c
162

Day 14
Type I ELISA
Type I VN assay
Type II VN assay

1 (01)a
108 (36162)
162

2 (017)b,c
54 (12162)
162

113 (83148)a,b,c
162
162

34 (1673)a,c,d
162
162

RUMINANTS

Day of vaccination
Type I ELISA
Type I VN assay
Type II VN assay

a,b,c,d
In each row, values with the same superscript letter are significantly (P 0.05) different.
VN = Virus neutralizing. NA = Not applicable. ND = Not done.
Group 1 consisted of seronegative unvaccinated control calves that were not vaccinated. Group 2 consisted of seropositive calves that received a single dose, intramuscularly, of a commercial vaccine containing modified-live BVDV type I
between 10 and 14 days after birth. Group 3 consisted of seronegative calves that received a single dose of the same vaccine
between 10 and 14 days after birth. Group 4 consisted of seronegative calves that received a single dose of the same vaccine
approximately 4 months after birth. All calves were inoculated with a virulent strain of BVDV type II at 4.5 months of age.

counts in group-1 and -2 calves but only transient lymphopenia and neutropenia in group-3 and -4 calves.
Mean platelet count was decreased, compared with
baseline values, in group-1 calves on days 9 and 11,
group-2 calves on days 9, 11, and 14, and group-4
calves on days 5 and 7. However, platelet count was >
50,000/l in all calves at all times. Platelet count
increased during the course of the study in group-4
calves.
At the time of challenge (day 0), unvaccinated
control calves (group 1) and seropositive calves that
were vaccinated between 10 and 14 days after birth
(group 2) had no serum antibodies detectable by the
ELISA (Table 1). Tests for VN titers suggested that
some group-1 and -2 calves had suckled and had low
or moderate concentrations of antibodies reactive with
type I (NADL) or type II (125) BVDV at the time of
challenge; however, concentrations of BVDV-reactive
antibodies on day 0 were significantly lower than in
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group-3 and -4 calves. Antibody concentrations

remained unchanged or decreased (group 3) until day
9, with concentrations for group-1 calves being significantly lower than those for calves in the other groups.
On day 11, concentration of BVDV type II-reactive
antibodies in group-1 calves increased, so that concentration for group-1 calves was no longer significantly
different from concentrations for calves in the other
groups. By day 11, calves in all groups had high concentrations of circulating VN antibody reactive with
BVDV type II, and there were no significant differences
among groups in regard to VN antibody concentrations
on days 11 and 14.
Discussion
Results of the present study confirm and extend
those of a previous study,8 documenting that a modified-live BVDV type-I vaccine can protect young calves
from infection with a virulent strain of BVDV type II.
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JAVMA, Vol 219, No. 3, August 1, 2001

infection are not necessary for protection from clinical

disease.
Similarly, an early anamnestic response resulting
in production of circulating BVDV neutralizing antibodies could not explain the substantial differences in
clinical responses between group-2 calves and group-3
and -4 calves, as there was no appreciable increase in
BVDV type II-reactive VN antibodies until 11 days after
infection. Group-3 calves, which were vaccinated 10 to
14 days after birth, had significantly higher concentrations of BVDV type I antibodies than did calves that
were vaccinated at approximately 4 months of age.
This was most likely due to the longer interval between
vaccination and testing, as suggested by results of a
previous study13 in which cattle that were vaccinated
once with a modified-live BVDV type I had increasing
or stable concentrations of serum VN antibodies for up
to 18 months after vaccination.
Cell-mediated immune responses were not examined in the present study; therefore, the possibility that
cell-mediated responses had a role in protection
against clinical disease cannot be excluded. However,
in a previous study8 that involved a similar method for
challenge exposure, no relationship was found
between clinical protection and any of the cell-mediated immune responses measured, including BVDV-specific lymphocyte blastogenesis and -interferon release.
In addition, a separate study14 found that depletion of
BoCD8+ (MHC-I restricted killer T cells) had little
impact on the outcome of BVDV infection in young
calves, whereas depletion of BoCD4+ T cells, which are
thought to perform a helper function in antibody
responses, extended the duration and increased the
titer of viremia. These results, together with the likelihood that administration of a modified-live BVDV vaccine results in systemic replication of the vaccine virus,
as indicated by viremia,15 suggest that vaccine-stimulated local (mucosal) immune responses accounted for
the control of viral replication and the clinical efficacy
that was observed. Unfortunately, such responses were
not measured in the present study.
Results of this study support current immunologic dogma9 to the extent that high concentrations of
maternally derived BVDV-specific antibody apparently
prevented the induction of protective immune responses in young calves that received a single dose of a modified-live virus vaccine during the neonatal period.
Although this phenomenon is demonstrable under
controlled conditions in the laboratory in calves with
uniformly high concentrations of maternally derived
antibodies, several factors encountered in the field suggest that vaccination of calves during the neonatal period may still be a viable management tool. Most importantly, this apparent blocking effect, as with protection
from disease,11,12 is not an all-or-none phenomenon. In
a previous study,d it was found that calves with low to
moderate passive antibody titers could respond to
BVDV vaccinal antigen with a measurable increase in
antibody titer, indicating that the blocking effect is a
function of passive antibody concentration. In addition,
calves in the present study were fed high-quality
colostrum within a short time after birth, assuring a
uniformly high degree of passive transfer of BVDV-speScientific Reports: Original Study

355

RUMINANTS

Although the endpoint, or true duration, of this protective response was not determined, results did indicate that calves that were vaccinated at a young age
were protected from BVDV infection for 4 months after
vaccination. However, compared with calves vaccinated within 2 weeks after birth that had no or low concentrations of BVDV-specific antibodies at the time of
vaccination, calves with high concentrations of maternally derived antibodies at the time of vaccination
responded poorly when challenged 4 months later,
after maternally derived antibodies had decayed. This
suggests that maternally derived antibodies blocked
vaccine-induced development of protective BVDV-specific immune responses in these calves.
The duration of vaccine-induced immune responses is a topic of considerable interest and debate in veterinary medicine.8-10 Duration of immunity studies are
logistically difficult and expensive to conduct, especially in large animals, because they require long-term
isolation of vaccinated animals to ensure that natural
exposure does not occur. Although the 4.5-month period assessed in the present study is relatively short,
compared with the productive life of cattle, this period
is relevant to the times during which young dairy and
beef calves would undergo such procedures as castration, dehorning, and branding. Therefore, documenting that a single dose of this vaccine can protect calves
from infection with BVDV from the perinatal period to
early adolescence has practical application to schemes
under which many cattle are currently managed.
The immune mechanisms that conferred clinical
protection in vaccinated calves were not specifically
identified in this study. The presence of BVDV-reactive
VN serum antibodies at the time of challenge exposure
was not necessarily associated with protection,
although circulating antibody may have decreased the
sensitivity of virus isolation. Calves that had high concentrations of maternally derived antibodies when vaccinated 10 to 14 days after birth (group 2) were also
seropositive at the time of challenge. Nevertheless, all
6 developed moderate to severe clinical disease, and 4
of the 6 required euthanasia. This mortality rate was no
different from that for the unvaccinated control calves
that lacked antibody or that had residual maternally
derived antibodies that were not detected with the
ELISA. Thus, low to moderate concentrations of circulating passively acquired BVDV-reactive antibodies at
the time of infection were apparently not sufficient to
protect the calves from clinical disease, as documented
in previous studies11,12 with virulent BVDV. On the
other hand, calves in group 4 that were vaccinated 3
weeks prior to challenge also had low to moderate concentrations of type II-specific VN antibodies, and concentrations for this group were not significantly different from concentrations for group-2 calves.
Nevertheless, group-4 calves had only minimal clinical
disease subsequent to challenge exposure. The low
antibody responses of the group-4 calves were similar
to those in a previous study8 in which calves developed
no or low antibody concentrations in the 3-week interval after vaccination yet were spared from clinical disease. Taken together, these results indicate that high
concentrations of type-specific antibody at the time of

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cific antibodies. It is well documented that 40% or more

of calves, especially those in veal calf operations, may
have poor passive transfer of maternally derived antibodies for a variety or reasons,16,17 making them candidates for induction of active protective responses by
vaccination. As well, heifers, even in well-managed
operations, tend to have lower-quality colostrum than
do multiparous cows that have been repeatedly exposed
to relevant pathogens.18 In most management systems
in which vaccination of young calves is currently used
or being considered, determining which calves in any
group had partial or complete failure of passive transfer
would likely require more labor and laboratory costs
than simply vaccinating the entire population. In those
instances, revaccination of the whole group at 3 to 4
months of age, when maternally derived antibodies
have decayed, may be recommended.19
a

Headstart, Saskatoon Colostrum Co, Saskatoon, SK, Canada.

Resvac 4, Pfizer Animal Health, Exton, Pa.
Provided by Carman S, Animal Health Laboratory, Guelph, ON,
Canada.
d
Cortese VS. Clinical responses of cattle to BVDV. PhD thesis,
Department of Veterinary Microbiology, University of
Saskatchewan, Saskatoon, SK, Canada, 1999.
b

RUMINANTS

Appendix
Scoring scheme for determining severity of clinical signs of disease in calves
Variable

Criteria

Score

Depression
None
Mild anorexia or listlessness
Signs of moderate depression, slow to rise, anorectic
Recumbent
Death

0
1
2
3
4

None
Few petechiae of mucous membranes or sclera
Moderate or severe petechiation or hematomas
Large hematomas
Bloody diarrhea or epistaxis

0
1
2
3
4

Hemorrhage

Signs of respiratory tract disease

None
Clear nasal discharges or slight cough,
no treatment required
Mucopurulent discharge or severe cough with
slight increase in lung sounds, requires treatment
Severe pneumonia

0
1
2
3

Diarrhea
None
Mild ( 5% dehydration), no treatment required
Moderate (5 to 10%), oral treatment required
Severe (10%), IV treatment required

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0
1
2
3

References
1. Corapi WV, Elliot RD, French TW, et al. Thrombocytopenia
and hemorrhages in veal calves infected with bovine viral diarrhea
virus. J Am Vet Med Assoc 1990;196:590596.
2. Paisley L. Emerging acute/peracute clinical disease outbreaks
associated with BVD virus. Washington, DC: USDA, 1994.
3. Peracute bovine viral diarrhea reportedly spreading. J Am
Vet Med Assoc 1994;205:391.
4. Pollerin C, Vandershark J, Lecomte J, et al. Identification of
a new group of bovine viral diarrhea virus strains associated with
severe outbreaks and high mortalities. Virology 1994;203:260268.
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JAVMA, Vol 219, No. 3, August 1, 2001