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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 www.claacanada.com and 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.

 In 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

www.claacanada.com [Articles]

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    

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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
sms14@cornell.edu

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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

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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.

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Other articles about BVD may be found at:

http://www.claacanada.com/articles.html

 

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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 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://repositories.cdlib.org/anrrec/sfrec/2004_bovine_virus_diarrhea/

 

 

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