Compilation of
BVD Information
Various authors
Bovine
Virus Diarrhea (BVD)
An alpaca breeder's experience
(Not an RMLA Member)
Rec'd 1-5-06
Dear
Alpacasiters,
Remember
Steve McCarthy's posts where he said one of the PI crias on
his farm originated in Colorado? On Dec.1, 2005 we received
a phone call telling us that we might possibly be that farm.
Another breeder in Colorado brought the female in question to
us for stud service in October & November of 2004, subsequently
sold the bred female to a person in NY and the result was a
PI cria born at Steve’s farm in NY. Both the selling farm
and ours immediately had blood drawn on a large sampling
of our herds. Theirs came back first and was negative except
for one female that had been here for breeding at the same
time as the one they sold....so it looked like we were the ones
with the exposure.
After
getting that fateful phone call, we spent the weekend reading
everything we could find on the web via googling “BVD in alpacas”
including Nancy Carr’s excellent “Detective Story”. Our
stud service records showed that there were only 5 females
breeding at our farm in October & November of 2004: 2 of ours,
2 from the other farm that had sold the female to NY, and a
female with cria from another front range farm, here only
for about 10 days. A phone call revealed that this particular
cria had become unthrifty and died at about 7 months old. The
other "outside" female did not get pregnant, but tested positive
for BVD antibodies and later produced a healthy non-PI cria.
Our two females both had premature crias on Aug.27 (Sandman)
and Sept.5 (Snowman) that were low birth weight, with intermittent
runny noses and eyes, strange suri-like fleece for huacaya out
of well-crimped parents, and in general were "just not right".
Sandman had an incompetent immune system and fit Nancy’s
description of her PI exactly. We had already been told he would
not live much longer, so we had him put down on Dec. 5 and our
vet, Dr. Kim Gardner-Graff, sent tissue samples from major organs,
skin and blood to Dr. Dubovi at Cornell.
Snowman was healthier and gaining weight, so we waited
for his results. Meanwhile we
continued reading everything available on BVD and contacting knowledgeable
persons like Nancy Carr, Steve McCarthy and researchers
like Dr. Dubovi at Cornell, while preparing ourselves for
the worst.
On
Dec. 14, reports came back on Sandman as positively a PI [Persistently
infected] and 14 of the 15 of our herd sample tested positive
for antibodies on the serum neutralization [SN] test. Our herd
and other females here for breeding had been exposed to Sandman
over a 100 day period. Subsequent tests were positive on most
of our herd and Snowman was determined to be a PI also. We began
the very heart-rending task of calling all our 2005 breeding
clients, informing them of their alpaca’s exposure, offering
to pay for tests on their alpacas that were at our farm and
replace their breeding. We also called those farms to which
we had sold alpacas or sent alpacas for breeding, offering the
same testing for those alpacas even though little risk was involved
since we could pinpoint the initial exposure to a 10-day period
in 2004 in the female pasture and the active disease is very
short-lived.
Lest
you think this is a Colorado problem, the "outside" female that
had the presumed PI cria at her side in 2004 was bought as a
bred female from a ranch in Oregon and if you look on the ARF
website at their census, nine PI's were listed on there
as of today [last update 11/15/05] not including Steve's 2 and
our 2. Subsequent tests at the farm that brought the presumed
PI and dam for breeding have revealed another PI from a dam
purchased from the same farm in Oregon. A female bred
at our farm was sold to NY and another PI at Steve's farm originated
in Maine. Alpacas are moved around much more than cattle!
Charles
began making graphs of all our 21 females that are pregnant,
determining their vulnerability for producing a PI cria in 2006.
We began making bio-security changes at our farm, pushing construction
on an already planned doubling of our barn size to make stalls
for our herdsires nearer the breeding females. This leaves our
auxiliary barn, which is over 100 feet from the main barn,
as an isolation barn for our near-term females that are at risk
of producing PIs. We'll have foot baths for helpers going into
that area, lots of hand sanitization gel pumps, and will not
allow visitors in that area. We have offered to bring back "outside"
bred females for birthing if their owners do not have isolation
capability. Blood will be drawn on all crias at birth before
they nurse, so the dam's antibodies will not contaminate the
sample. CSU will perform the PCR tests at their lab and get
the results back to us ASAP. Any PI cria will be put down immediately.
A month has passed since Sandman was put down and our farm is
now free from active infection and by the end of 2006 will be
PI-free as well, probably one of the safest farms around with
a herd testing positive to antibodies. Meanwhile, we'll require
any cria accompanying a dam for breeding to be tested as PCR
negative to prove it is not PI prior to coming on our farm.
We'll have to make some difficult decisions, but will get through
this somehow.
Why
are we going public on this? It is imperative that breeders
take BVD seriously. It probably has been around for a long time
[think of all those stillbirths, abortions, crias that died
from failure to thrive, etc.] and we were just not testing for
it or performing the correct tests because most vets felt
that alpacas were not vulnerable to BVD. [See http://www.claacanada.com/
and http://www.alpacaresearchfoundation.org/
for testing protocol.] We have found that most cases of BVD
infection in alpacas are sub-clinical and do not involve diarrhea
or any other symptom. There was no diarrhea on our farm, no
evidence of other sickness or being “off feed” and Sandman was
producing normal pellets even on the day we put him down.
Five
weeks ago all we knew about BVD was from posts on Alpacasite
and the first question from most of our customers was “What’s
BVD?” In
September we had BVD tests performed at CSU on a stillborn
as part of the necropsy. That case just happened to be BVD negative
and we thought we didn't have a BVD problem. Wrong! That
dam was absent during our 2004 exposure. Please educate yourselves,
get samples from your herd tested to see if you have an exposure,
and consider some strict bio-security measures if you have alpacas
coming to your farm to breed. The biggest threat of exposure
is from a PI cria and PI crias can look entirely normal and
possibly grow to adulthood. [Ours just happened to look different
from our usual healthy crias.] In cattle, 93% of all BVD
infections originate with PI calves because they continue to
shed billions of viruses every day as long as they live. PI
crias have to be eliminated. That is the secret to controlling
this disease before it becomes a national epidemic.
And
please, please report any cases of PIs to ARF for
their census. I understand that there are a lot of known cases
that are not on the census because owners would not allow them
to be posted even anonymously by region! [Are we that market-driven
in this industry???] ARF has two BVD projects going: one at
Iowa and the other at Nebraska. They need to find out everything
they can about this disease and honest disclosure on the part
of breeders is the only way they will ever develop a body of
knowledge about BVD in camelids.
Snowman
is being kept alive in isolation and we have offered to donate
him to a research projects. If ARF doesn’t need him, CSU may
take Snowman and another PI from this area if funding can be
found to take advantage of this research opportunity like Tufts
is having with Copper Penny and Tag from Steve's farm.
n
addition to the articles in the 2 most recent Alpacas Magazines
and articles published in 2005 in Camelid Quarterly,
we found the following links valuable in learning about BVD:
www.diaglab.vet.cornell.edu/issues.alpacas.asp
http://www.claacanada.com/
[Articles]
http://www.alpacaresearchfoundation.org/
Our
entire herd has been tested, some more than once. The costs
of tests range from $10-$12 for a Serum Neutralization
[SN] looking for antibodies to Type 1 & 2 strains of BVD, to
$30 - $35 for a PCR test looking for the active virus.
Vet charges may vary to draw, prepare and ship the vials, and
ours is averaging about $15 for this service, plus overnight
shipping. Regardless of the costs, we need to know the herd
status and plan accordingly to isolate late-term females who
might produce PI crias this year. If there is a “silver cloud”
in all of this, our herd is now all positive for antibodies,
has no active infection that can be spread, and all the females
should be invulnerable to producing PI crias after this year…and
we are able to tell potential purchasers the BVD status of every
alpaca in our herd so that they will not have to go through
the same agonizing learning and testing process.
Charles
& Lucy Farrar
Monument,
CO
--------------------------------
December 21, 2005
Editors Notes:
Word from Alpaca Owners is that there are confirmed
cases of BVD in Alpacas in Colorado NOW!
The virus has apparently
crossed the species lines from cattle to camelids.
In lay terms: this was
intruduced from a Female, with cria at side, coming to Colorado
for breeding from the East Coast. The cria was either ill from
the infection or one of the "PI" (persistently infected) types-
think "Typhoid Mary" -a non ill carrier. The virus is
rapidly spread thru all fluids from the cria (nose, mouth, urine,
feces, etc.). Although the Title contains "diarrhea" very little,
if any diarrhea has been seen in the infected alpaca crias.
The adults are apparently immune to this.
Please read the official
info below.
-------------------------
Posted
12-26-05
Animal
Health Diagnostic Center - Emerging Issues
|
| BVD in Alpacas
|
|
|
| Bovine Virus Diarrhea virus has been isolated
from alpaca crias from sites around North America.
Dr Dubovi, our virologist, has been working with
alpaca farms on the East Coast and offers the
following comments about testing:
The extent of the problem in alpacas is unknown.
About a dozen PI crias have been identified.
The Guelph group has a paper coming out in JVDI
on the one that they had. I am not sure how
the ACE (antigen capture ELISA) is performing.
We have very weak reactions on serum -- 1 of
7 skin samples + on the one we did a necropsy
on. However, the other one that died before
it came here had an ACE skin test the equivalent
to cattle. The IHC (immunohistochemistry) tests
on most tissues are positive, but not wildly
so. Skin has been positive but the staining
pattern may be a bit different from cows. Serum
viremia levels on one were similar to calves.
I would hate to see vaccination start. I think
that this can be eradicated without vaccination.
Each herd needs to assess the issue in their
own unit. I could see having a negative PI test
before animals go to shows (Only needs to be
done once). I am recommending as a start to
test pregnant females to see what the risk is
to have a PI cria. This will give data on the
presence of BVDV in the herd. All Ab+ animals
should have the cria tested at birth (precolostrum
whole blood for virus isolation or post colostrum
whole blood for PCR). Alternatively, one can
test all crias at birth regardless of antibody
status of the dam. All PI crias should have
a complete necropsy so that we can collect data
on their response to the virus. I don't know
how long these animals will live as most are
being identified as poor doers.
I think the alpaca people need to organize
some informational meetings to get the owners
up to speed and not panic. We are starting to
see people concerned about the cost of testing
yet they risk loss of a PI cria valued at 10-20K
or abortions.
Not all cases have had a history of contact
with cattle. The initial risk appear to be contact
with cattle but once PI's are created they are
capable of causing alpaca to alpaca transmission
(if in contact with pregnant alpacas). One east
coast case that Dr Dubovi was involved with
had a history of purchasing the dam and affected
cria from the west coast. Alpacas move. Additional
biosecurity risks will occur as PI alpacas are
moved through sales, potentially shows, to other
farms for breeding or outside females coming
to a farm to be bred with a cria at its side.
Testing of crias as described above before
they attend shows, are sold or move to other
farms is highly recommended. Because we don't
know the herd prevalence, within herd testing
options depend on identification of BVD PIs
or past biosecurity risks to the farm.
- In unvaccinated herds, a single test of a
dam for antibody prior to birthing and subsequent
testing of crias born to antibody positive dams
can be use to screen herds.
- Discussions suggests that some alpaca farms
are using killed bovine vaccines. In vaccinated
herds, all dams would be expected to have antibody
so testing of all crias for PI status would
be needed if BVD cases have been identified
in the herd.
If widespread vaccination is instituted in
response to the introduction of BVD to alpacas,
testing costs and the ability to monitor the
spread of infection into alpaca herds will be
more costly. If prevalence is still low in alpacas,
the best response may be client education, heightened
awareness of biosecurity and strategic testing
to prevent introduction and further spread of
BVD infection in alpaca herds.
Sue Stehman
http://www.popmed.vet.cornell.edu/contact/index.asp?Addr=sms14@cornell.edu |
|
-----------------------------------------------------
Posted 12-22-05
BVD Virus –
A Newly Recognized
Serious Health Problem for Alpacas
By: Nancy
Carr MD and Susy Carman DVM PhD.
Bovine viral
diarrhea virus (BVD virus or BVDV), a serious problem in cattle,
has now
been proven
to also cause illness, abortions, and most important of all,
the persistently
infected (PI)
state in alpacas. The virus’s ability to produce persistently
infected cria, the
main way this
disease would be spread, and its ability to cause abortions
are extremely
important for
the alpaca industry.
At this point,
the vast majority of knowledge about BVDV and the disease that
it
causes, bovine
viral diarrhea (BVD), is about its effects in cattle, where
it is considered
one of the most
significant viral infections, causing major economic losses.
The
information
presented next is therefore what is known about BVDV in cattle;
it is likely
that most of
this applies to alpacas. Following this is the information about
BVDV and
alpacas. Despite
the name, many animals with BVD do not have diarrhea. Other
manifestations
of the virus include subclinical infections, immunosupression,
abortions,
congenital defects,
persistent infection, and mucosal disease. The majority of cows
infected are
either subclinically ill (do not appear unwell) or only mildly
unwell with low
fever and diarrhea.
Because BVDV depresses the immune system, some animals will
become ill with
other infections, usually pneumonia; others will have a classic
case of
BVD with fever,
discharge from the nose and eyes, erosions of the muzzle and
in the
mouth, and severe
diarrhea; others may have severe hemorrhagic (bloody) diarrhea
and
die. Severity
of illness is influenced by the age of the animal and its immunological
and
physiological
status, and the particular strain of the virus involved.
The most important
aspect of BVDV is its effect on the developing fetus. BVDV can
cause abortions
at any stage of gestation – from early embryo loss up to stillbirths
at
term. Even a
subclinically infected cow can abort, and abortions may occur
up to several
months after
exposure to the virus. A unique feature is that if the cow is
exposed to the
virus at a critical
phase of her gestation (approximately 40 - 120 days) and does
not abort,
she will produce
a persistently infected (PI) calf. Because the developing fetus
is not
immune competent
at that stage of development it becomes immunotolerant to the
virus
(does not recognize
the virus as foreign); it is unable to make an immune response
to rid
itself of the
virus, and once born, is a permanent carrier and sheds huge
concentrations of
the virus in
every secretion – tears, nasal discharge, saliva, urine, and
feces. PI calves
are the major
source of the spread of BVD – they shed several billion viral
particles a day
– about a thousand
times more than what is shed by an acutely infected non-PI animal.
The only way
to be PI is to be born PI. Some PI calves appear completely
normal, but
most are poor-doers
– poor weight gain, weak, and susceptible to other diseases
such as
pneumonia; many
PI calves die before they are a year old. Infection of the pregnant
cow
with BVD later
in pregnancy can result in calves that are not PI but that have
congenital
defects such
as cerebellar hypoplasia (underdevelopment of the part of the
brain that
controls balance
and co-ordination), cataracts, blindness, hypotrichosis (sparse
hair
growth) or general
growth retardation.
Acute infection
with BVDV occurs through the nose or mouth by contact with
secretions from
an infected animal (usually a PI animal) – saliva, nasal discharge,
tears,
urine or feces
– either directly from the infected animal itself or from items
that have
been contaminated
with those secretions, such as water troughs. An acutely infected
but
non-PI animal
sheds virus for a relatively short length of time (4 – 10 days,
possibly up to
2 weeks) in
comparison with a PI animal which sheds virus for its entire
life. Incubation
period is 5
to 7 days. The virus cannot survive long in the environment
– a maximum of
2 weeks. Because
it is a virus, antibiotics are of no use in treating it.
There are hundreds
of different strains of the virus, which can also be categorized
under
type 1 (BVDV1)
or type 2 (BVDV2) and by the terms cytopathic or non-cytopathic.
BVDV2 tends
to produce a more severe clinical illness than BVDV1. PI animals
always
have a non-cytopathic
strain of BVDV. An entity called mucosal disease occurs only
in
PI animals –
they become superinfected with an antigenically similar cytopathic
strain of
the virus (usually
from a mutation in their own non-cytopathic strain, or from
a modified
live vaccine);
this leads to severe diarrhea and inevitably death. Vaccines
for cattle are
available for
BVD; however they do not confer 100% immunity.
Articles published
to date on BVD and camelids have generally concluded that BVD
is not much
of a concern. In an article titled ‘A Medical Marvel’ in the
winter 1999
edition of Alpacas
Magazine Randy Larson DVM stated what was likely the commonly
held viewpoint
at that time: “BVD is an example of a significant disease of
cattle that
causes undetectable
problems in alpacas. BVD and other common cattle viruses just
do
not cause
problems in alpacas.” Medicine and Surgery of South American
Camelids
(page 469) makes
mention of BVDV only as a cause of congenital defects and impaired
immunologic
competence in calves and lambs.
In 2000, Belknap
et al. from Colorado State University reported on three cases
of
BVDV isolated
from llamas (a stillborn fetus and two sudden deaths in adults
that had
been losing
condition) and concluded that BVDV should be considered as a
cause of
death in young
and old New World camelids. The Complete Alpaca Book makes
mention
of that statement
(page 451) and also that it may be one of the causes of diarrhea
in cria
(page 400).
In 2002, Goyal
et al. in Minnesota reported on what appeared to be the first
case of
BVDV isolated
from a stillborn alpaca; there were no gross or histopathologic
changes of
any significance
seen, but BVDV was detected by reverse transcriptase polymerase
chain
reaction (rt-PCR)
from a pool of tissues, and BVDV was isolated from cell cultures.
Immunohistochemistry,
a test commonly used to detect BVDV in tissues taken at the
time of autopsies,
was negative.
In 2003 Wentz
et al. reported on the effects of experimental infection with
BVD on
llamas and their
fetuses, and on the seroprevalence of BVDV [detection of antibodies
that
would signify
the animal had been exposed to BVDV at some time in the past]
in llamas
and alpacas.
They concluded that llamas may be infected with BVDV but have
few or no
clinical signs,
and that inoculation of llamas with BVDV during gestation did
not result
in fetal infection
or PI crias. Seroprevalence in a sample of 223 llamas and alpacas
was
0.9%. They also
concluded that the most likely source of BVD infection in camelids
may
be cattle.
Dr. Donald Mattson
from Oregon State University (OSU) stated in June 2004 (personal
correspondence)
that in their llama herd at OSU there had been one sick llama
with BVD
(it had diarrhea)
but that its two herdmates did not become sick. He also knew
of a case
in southern
Oregon with a herd of 20 llamas where only one showed signs
of illness. He
stated that
they had only seen BVDV infected camelids when they had been
in contact
with cattle
that are shedding the virus, and that he had tested hundreds
of samples from
llamas and alpacas
and never found a PI camelid.
However, now
there is irrefutable proof that BVDV can cause illness, death,
abortion
and most important
of all, the PI state in alpacas. The consequences of this for
the alpaca
industry may
be profound.
The next article
in this magazine, ‘BVD Virus and Alpacas – The Detective Story’
details how
this was discovered at a farm in Ontario. There was illness,
including one
death, several
early pregnancy losses, and an aborted fetus that tested positive
for BVDV.
One of the females
who had been subclinically infected (exposure to BVDV as confirmed
by antibody
testing) at 2 months gestation subsequently delivered a persistently
infected
(PI) cria. This
is the first recorded case of a PI alpaca, but there is overwhelming
circumstantial
evidence that BVDV had been brought to the farm by another PI
cria that
died without
being tested. And it is highly likely that that cria’s mother’s
source of her
infection with
BVD during her pregnancy in Alberta (resulting in her producing
that PI
cria) would
have been from another PI alpaca.
The majority
of alpacas infected at Farm A in Ontario were subclinically
infected and it
was only apparent
by antibody testing that they had been infected. (Note: having
antibodies does
not mean that the animal is unwell or contagious; it shows that
the animal
was exposed
to the virus at some point in the past and mounted an immune
response; this
could be from
a subclinical infection (never appeared unwell), a clinical
infection
(appeared unwell)
or from immunization. For example, most of us would have
antibodies to
chickenpox from having that illness as children.) The alpacas
that were
unwell had symptoms
that ranged from having the appearance for a few days that their
mouths were
uncomfortable eating their pelletized supplement, to being off
feed and
depressed, to
one death from hepatic lipidosis (that condition would have
resulted from
decreased feed
intake). None of them had diarrhea. Many of them, even those
subclinically
infected, showed stress breaks in their fleece.
The cria who
was presumed in hindsight to be PI and the source of the infection
(he died
without being
tested) arrived at Farm A at the age of 3 months. He had been
born at full
term on Farm
B, also in Ontario, at a very low birth weight of 9 pounds.
He had done
fairly well
for the first 6 weeks of life and then developed repeated infections,
mostly
pneumonia, had
a frequent runny nose, and he had very poor weight gain. He
died at the
age of 8 months
after severe diarrhea. (This was his first episode of diarrhea
since having
a bout with
coccidia when he was much younger). Farm B, where he spent the
first three
months of his
life, had positive BVD antibody levels in alpacas that had been
in contact
with him. His
mother had been on Farms C and D, in Alberta, in her early pregnancy
(when she would
have contracted her subclinical BVD infection resulting in her
producing this
PI cria); Farm C had many abortions and Farm D had two stillbirths
and a
cria that died
at 36 hours of age in the same year that this female delivered
her presumed
PI cria. Farms
C and D have alpacas with positive BVDV antibody levels, including
the
dams of the
aborted fetuses, stillbirths and cria that died. Although it
is possible that the
mother (who
is not PI) became acutely infected at Farm D and transmitted
BVD to Farm
C during the
short time she would have been shedding virus, it is more likely
there were
separate cases
of PI animals on both those farms causing the infections. None
of the
farms involved
had any contact with cattle.
The proven PI
cria, called Gabriel, born on Farm A (to a female who had been
infected
by the above
presumed PI cria) also had a very low birth weight of 12 pounds
for the
farm he was
born on. He had excellent weight gain to 33 pounds at the time
of his
euthanization
at a little over 6 weeks of age, after two sets of blood tests
confirming he
was PI. (The
fate of all proven PI animals is to be euthanized.) He had chronic
diarrhea,
but was not
unwell with it and was perky and active.
At this point
it is unknown just how prevalent BVD is in alpacas. Alvarez
et al.
reported in
2002 that 11.5% of alpacas in a rural community of Cusco in
Peru had
antibodies to
BVDV. The other reported case of BVDV in a stillborn alpaca
fetus was in
Minnesota, and
the llama cases were in Colorado, so this is not just a Canadian
situation.
The practice
of sending females with cria at side off to other farms for
breeding is one of
the main ways
BVD would spread – a PI cria may not show any signs of being
unwell
until it is
older and yet be infecting every animal it comes in contact
with. Also, a
pregnant female
going to a new owner may be carrying a PI fetus that, once born,
will
infect all the
alpacas at the new home. This case shows how BVDV traveled
approximately
3500 kilometers (over 2000 miles) from Alberta to Ontario. Some
PI
cattle continue
to appear healthy; it is unknown how many PI alpacas may continue
to
appear normal.
It is also unknown what is the exact range of gestation in alpacas
that
infection of
the dam will result in the birth of a PI cria. Cattle have a
9 month gestation
and it is in
the period of approximately 40 –120 days of gestation that there
is the high
risk of the
fetus becoming PI if the mother is infected with BVD.
Alpacas have
a reputation for being easy aborters, and it is not unusual
to hear of poor
doing cria –
it is entirely possible that many of these cases may have been
due to BVDV.
Unless the virus
is specifically tested for there is no way of knowing that it
is present – in
both the stillborn
fetus from Minnesota and the aborted fetus from Ontario there
were no
pathological
changes to suggest BVD – it was only by testing for the presence
of the
virus itself
that it was found. In the euthanized PI cria there were no pathological
changes to suggest
he was PI – but virus isolation from blood and most tissues
was
positive. The
adult alpaca that died after what must have been an acute BVD
infection
had autopsy
findings of hepatic lipidosis, but it would have been BVD that
caused her
appetite to
decline, resulting in the hepatic lipidosis. In her case, there
would not have
been virus detected
as it would be too long after the initial acute infection –
she would
have to have
had antibody testing. It is possible that some of the unexplained
cases of
hepatic lipidosis
in alpaca herds have been caused by BVD. Schwantje and Stephen’s
paper on ‘Communicable
Disease Risks to Wildlife from Camelids in British Columbia’
reported a positive
BVDV antibody rate of 6% in a sample of 175 llamas from twelve
farms, with
the rate per farm varying from 0% for many farms to a high of
22% on one
farm. This paper
also reported on a survey of 90 llama and alpaca farms asking
about
illness and
death in the preceding year; the primary cause of death (26%
of cases) was
neonatal failure
to thrive or stillbirths. The report also reviewed the diagnoses
of llama
and alpaca submissions
to the B.C. Animal Health Centre between 1993 and 2000: 9% of
the diagnoses
were idiopathic (meaning no cause found) abortion. It is quite
possible
there is a connection
between BVDV and some of those cases of neonatal failure to
thrive, stillbirths
and abortions. Until aborted and stillborn fetuses and autopsied
animals
are tested specifically
for the presence of BVD virus or antibodies, depending on the
clinical situation,
we will not know how prevalent this is. If it is more prevalent
than has
been suspected
then probably research on the use of vaccines for BVD in camelids
will
be required.
Only a completely closed herd (no animals coming into the herd)
with good
biosecurity
measures (all visitors with footwear not contaminated by manure;
no fence
line contact
with other livestock) can be sure to be safe from BVD.
Testing for
BVDV is complicated, with different tests being used in different
situations.
Having antibodies
(blood test) to BVDV shows that the animal was exposed to the
virus
(from a clinical
or subclinical infection, or from immunization), but it is unknown
how
long antibodies
are detectable for after exposure. PI animals would not have
antibodies
(unless they
were tested as newborns soon after ingesting their mother’s
antibodycontaining
colostrum).
To detect the PI state the animal has to be tested for the virus
itself, and
there must be two positive tests three weeks apart to prove
the PI state, in case
the first positive
test was an acute infection and not from being PI. Virus isolation
is the
‘gold standard’
test for detecting BVDV – it can be done on blood (live animal)
or tissue
(dead animal).
The ELISA blood test for the virus is used to detect PI animals
over the
age of 3 months
(the maternal antibodies from colostrum interfere with the test
before
that age, and
also sometimes interfere with virus isolation.) The ELISA test
on skin
biopsies or
ear notches can be used to detect PI calves under the age of
three months.
The PCR test
(blood) is not affected by maternal antibody and is also used
to detect PI
animals under
the age of three months. Immunohistochemistry is used on formalin
fixed
tissue from
autopsies; however as noted above this test was negative in
the stillborn fetus
in Minnesota
despite BVDV being detected by PCR and virus isolation;
immunohistochemistry
was positive in the aborted fetus in Ontario. Your veterinarian
should consult
with a veterinarian virologist or with the lab that he/she uses
for BVDV
diagnosis in
cattle. Most labs doing BVDV testing are affiliated with universities,
or are
state or provincially
funded; not many private labs offer BVDV testing.
At this time,
a reasonable recommendation is that all aborted or stillborn
fetuses, all
unusually low
birth weight and ‘poor doing’ cria and all unexplained deaths
be tested for
BVD virus and/or
antibodies, depending on the case. If BVDV is found then further
testing should
be done to determine how the virus entered the herd - specifically
is there
still a PI animal
present, or has it gone back to another farm. Any cria subsequently
born
to females who
were pregnant when BVD was active in the herd should be tested
to see if
they are PI.
It is important that you bring this information to the attention
of your
veterinarian
as it will be at least a year before it is published in a veterinary
journal. It
would also be
very helpful if you or your vet notified the lab in your area
where aborted
fetuses or autopsies
are sent for testing about this, so that testing specifically
for BVDV
will become
routine in abortions, stillbirths, and unexplained deaths in
alpacas.
REFERENCES:
Alvarez
S., Rivera G.H., Pezo D., Garcia W. (2002). “Deteccion
de anticuerpos contra
pestivirus en
rumiantes de una comunidad campesina de la provincia de Canchis,
Cusco.”
Rev Investig
Vet Peru, 13(1), 46-51
Belknap
E.B., Collins J.K., Larsen R.S., Conrad
K.P. (2000). “Bovine viral diarrhea virus
in New World
camelids.” J Vet Diagn Ivest, 12(6), 568-70
Fowler,
M. (1998). Medicine and surgery of South American camelids.
Ames, Iowa:
Iowa State University
Press.
Goyal
S.M., Bouljihad M., Haugerud S., Ridpath
J.F. (2002). “Isolation of bovine viral
diarrhea virus
from an alpaca.” J Vet Diagn Ivest, 14(6), 523-5
Hoffman
E. (2003). The complete alpaca book. Santa Cruz, California:
Bonny Doon
Press.
Larson
R. DVM, “A medical marvel.” Alpacas Magazine, Winter
1999, 122
Schwantje
H., Stephen C. (2003) “Communicable Disease Risks to
Wildlife From
Camelids in
British Columbia.” [on-line]. Available:
http://wlapwww.gov.bc.ca/wld/documents/wldhealth/camelid_risk03.pdf
Wentz
P.A., Belknap E.B., Brock K.V., Collins J.K.,
Pugh D.G. (2003). “Evaluation of
bovine viral
diarrhea virus in New World camelids.” J Am Vet Med Assoc,
223 (2), 223-8
------------------------------------------------------------------------------------------
Nancy Carr MD
has alpaca farm A, Silver Cloud Alpacas, near Elginburg in eastern
Ontario, Canada.
She would like to assure readers that her herd is now completely
healthy and
not contagious, and in fact is one of the very few herds in
North America
where all the
cria have been tested to make sure they are not PI. She can
be reached at
carralpacas@sympatico.ca
or (613) 376-3389 or through her web site
www.silvercloudalpacas.com
Susy Carman
DVM PhD is in Diagnostic Virology, Animal Health Laboratory,
Laboratory Services
Division, University of Guelph, Box 3612, Guelph, Ontario, Canada
N1H 6R8. Email:
scarman@lsd.uoguelph.ca. Phone: (519) 824-4120 ext. 54551
NEED TO KNOW
- BVD virus,
a major problem in cattle, has now been shown to also cause
illness,
abortions, and,
most important of all, the persistently infected state in alpacas.
- If the alpaca
is exposed to BVDV during early pregnancy she can produce a
persistently
infected (PI) cria who sheds huge amounts of virus its whole
life and
is the major
source of the spread of BVD.
- The only way
to be PI is to be born PI.
- Because a
PI cria may not show any signs of illness for several months
or longer,
the potential
for BVD to spread between herds is significant because of the
practice of
females with cria at side going to other farms for breeding.
- It is unknown
yet how common BVD in alpacas is – this has the potential to
have
a profound impact
on the alpaca industry.
- All aborted
or stillborn fetuses and unusually low birth weight or poor
doing cria
should be tested
specifically for BVDV, as there are usually no pathological
changes to suggest
BVDV. Your veterinarian should consult with a veterinarian
virologist or
lab that does BVDV testing about the appropriate tests to be
ordered.
- Please copy
this article for your veterinarian.
------
Other articles
about BVD may be found at:
http://www.claacanada.com/articles.html
--------------------------------
April 15, 2004
Bovine Virus Diarrhea
(BVD)
Bruce
R. Hoar, School of Veterinary Medicine, Department of Medicine
and Epidemiology, University of California, Davis
ABSTRACT:
Bovine virus diarrhea (BVD) is a complicated disease to discuss
as it can result in a wide variety of disease problems from
very mild to very severe. BVD can be one of the most devastating
diseases cattle encounter and one of the hardest to get rid
of when it attacks a herd. The viruses that cause BVD have been
grouped into two genotypes, Type I and Type II. The disease
syndrome caused by the two genotypes is basically the same,
however disease caused by Type II infection is often more severe.
The various disease syndromes noted in cattle infected with
BVD virus are mainly attributed to the age of the animal when
it became infected and to certain characteristics of the virus
involved.
Diseases caused by BVD
infection
Fetal BVD infections (infection
of the unborn calf): The result of a fetal infection with the
BVD virus is usually determined by the age of the fetus at the
time of infection. The virus is capable of passing from an infected
cow to the unborn fetus which is particularly vulnerable to
the BVD virus during the first 6 months of pregnancy. Death
of the fetus is common if the infection occurs during the first
120 days of pregnancy and the cow will lose the pregnancy. However,
if the fetus survives an early infection, it will be born without
a detectable antibody titer and be persistently infected (PI)
with the BVD virus. During the first 120 days of gestation,
the fetus has an underdeveloped immune system and does not recognize
the BVD virus as foreign. The fetus does not mount an immune
response against the virus, remains infected, and does not have
a detectable anti-BVD titer. It is not uncommon for the surviving
fetus to be malformed; blindness, skeletal abnormalities and
under-developed brains are common defects noted in such calves.
A BVD PI calf may appear normal, be weak at birth, grow poorly,
be susceptible to respiratory diseases, and die before they
can be weaned. They may also grow normally, reach breeding age,
and produce more persistently BVD infected calves (The virus
is passed from generation to generation). PI carriers can only
be created by infection with BVD virus during the first 110-120
days of pregnancy. These animals shed billions of virus particles
every day in their urine, feces, and saliva, and are a source
of infection for other animals in the herd. If the fetus becomes
infected after 120 days of pregnancy, there may be an abortion
but usually, because this aged fetus has a more developed immune
system and can elicit an immune response against the BVD virus,
a healthy calf is born that has a good level of BVD antibody
titer.
Subclinical BVD infections:
Most animals that become infected with BVD never show signs
of disease caused by the virus; however infection can lower
the animal’s resistance to other infections, which could result
in illness. For example, in feedlot calves, BVD infection may
go unnoticed, but the lungs become susceptible to infection
with bacteria such as Mannheimia haemolytica (previously called
Pasteurella haemolytica) and other agents that cause “shipping
fever”. Some people believe that BVD is one of the most significant
disease organisms involved with respiratory disease of cattle.
Severe acute BVD infections: This disease syndrome is usually
(but not always) associated with Type II BVD virus infection.
The affected animals will exhibit high fevers (107-110 F), occasional
diarrhea, respiratory disease, and they will not eat. Peracute
BVD can affect cattle of all ages and often results in death
of the animal within 48 hours of disease onset regardless of
age.
Acute BVD infections: The
classic, acute form of BVD is characterized by a fever of 104-106
F, discharge from the nose and eyes, erosions of the muzzle
and in the mouth, and diarrhea that may contain mucus and blood.
Diarrhea is usually present in every herd that has an outbreak
of acute BVD, but diarrhea is not present in every animal that
has acute BVD. The percentage of the herd exhibiting clinical
disease and dying can vary extremely; however, if "secondary
infections" are controlled, most animals survive the acute disease.
This syndrome usually occurs in cattle 6 to 24 months of age.
Acute Mucosal disease: An animal persistently infected with
BVD virus is not able to mount any defense against becoming
subsequently infected with a different BVD virus. When a BVD
infection is superimposed on a PI animal, mucosal disease usually
results. Acute mucosal disease is characterized by fever, profuse,
watery diarrhea, erosions of the mouth, lack of appetite, discharge
from the eyes and nose, and occasionally lameness. Secondary
infections, such as pneumonia and mastitis, are common. Cattle
with acute mucosal disease usually die within 3 to 10 days.
Chronic Mucosal disease:
Some cattle that develop mucosal disease do not die as soon
as expected but rather become chronically infected. Cattle with
chronic mucosal disease are poor doers, and may have persistently
loose stools or intermittent diarrhea, chronic bloat, decreased
appetite, weight loss, erosions between the claws, or non-healing
skin lesions. Discharge from the eyes and nose, bald spots due
to loss of hair, and long-term lameness are also common. Cattle
with chronic mucosal disease rarely survive beyond 18 months
and ultimately die.
Treatment and Prevention
of BVD infections There is no effective treatment for infection
with BVD, but most cases are subclinical and self-limiting.
Antibiotics, fluid and supportive therapy may be indicated to
control secondary infections. Offering highly palatable feed
could tempt sick animals to eat needed nutrients. Vaccination
of susceptible cattle has been the principal approach to the
prevention and control of BVD. However, preventing the introduction
of BVD into your herd and identifying and eliminating PI animals
from your herd are important steps to take to control the disease.
Vaccinate calves: Calves
should be vaccinated twice with a modified live virus (MLV)
vaccine before leaving the herd of origin. Ideally, BVD vaccinations
should be completed in the calves at least 30 days prior to
weaning, but whatever program you initiate needs to fit with
your management system. Check with your veterinarian for specific
recommendations for your herd.
Vaccinate the cow herd:
It is difficult to provide blanket recommendations for vaccinating
the cow herd, but some general guidelines can be given. Unvaccinated
heifers and cows should be properly vaccinated before breeding
to ensure protection for the fetus. All bulls should be properly
vaccinated before putting them out with the cows or heifers
and new additions should be properly vaccinated before adding
them to the herd. Modified live virus vaccines can be safely
used in open cows (there are new MLV vaccines safe for pregnant
cows if the cows have been previously vaccinated with certain
products) and provide long-lasting protection. Killed vaccines
are safe for all cattle, but usually don’t provide as strong
an immune response and may need more frequent booster vaccinations.
Again, check with your veterinarian for specific recommendations.
Prevent introduction of
BVD into your herd: BVD virus is shed from cattle in the feces
and in secretions from the nose and mouth. BVD is also readily
transmitted by aerosol droplets and direct contact. Avoiding
contact with other cattle is therefore an important step to
take to prevent infection from entering your herd. “Good fences
make good neighbors”. It is especially important to keep pregnant
cows less than 120 days pregnant separated from other cattle.
New introductions into your herd need to be tested for PI status.
Eliminate PI animals from
your herd: Until recently, testing cattle for PI infection was
prohibitively expensive but now there are tools available making
it feasible to test for and eliminate these “typhoid Mary” animals
from the herd. There are two types of test available, one using
a skin sample and one using a blood sample: Immunohistochemistry
– for this test, a small notch of skin is taken from the edge
of the ear, easily done using a pig ear-notching tool. The triangular
piece of skin removed should be Ľ to ˝ inches per side. Depending
on the laboratory the sample will be sent to, the removed skin
is placed either in a vial containing formalin or an individual
plastic bag. All samples must be clearly labeled with the animals’
identification number. PCR – this test requires that a blood
sample in a “purple top” tube be taken and submitted. Again,
all samples must be clearly labeled with the individual animal
ID.
This has been extracted from
University of California web
site
More info is available on this
site.
http://www.rmla.com/repositories.cdlib.org/anrrec/sfrec/2004_bovine_virus_diarrhea/
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