Bovine Viral Diarrhea (BVD)| Prevention| Control
Bovine viral diarrhea virus (BVDV) is a pathogen effecting cattle in almost every country
in the world where these animals are raised (Radostits et al. 2007).
The emergence of seemingly more virulent forms of the virus in the past
few decades have made this a pathogen of increasing economic importance
(Goens 2002). The bovine viral diarrhea (BVD) disease complex is one of
four diseases know as production limiting diseases in the Canadian
dairy industry (Radostits etal. 2007) and is arguably one of the most
economically important infectious diseases in the feedlot industry
(Campbell 2004). The virus’ high prevalence rate, resultant abortions,
persistent infections, and manifestations, and untreatable nature make
prevention and active management of BVD essential for cattle producers.
BVDV has been shown to infect a variety of hosts including sheep,
goats, water buffalo, and wild ruminants, but cattle are the primary
hosts and for that reason will be the only species discussed.
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| Bovine Viral Diarrhea |
Etiology
BVDV
is a member of the family Flaviviridae and genus Pestivirus,
characterized by single sense stranded RNA viruses of two biotypes. The
rare cytopathic (CP) biotype will damage tissue cultures and the much
more common non-cytopathic (NCP) will not. The disease syndromes caused
by the two biotypes differ mainly in the severity of disease that they
cause upon infection. Both biotypes can cause disease in cattle,
however, greater than 95% of BVDV infections, all of the persistent
infections, and the more severe forms of the disease are caused by the
non-cytopathic biotype (Kelling 2004).
The
BVDV can be divided into two genotypes (BVDV-1 and BVDV-2) on the basis
of antigenic and genetic differences, with each genotype containing
both the CP and NCP forms. Furthermore, both genotypes are divided into
subtypes. Both BVDV-1 and BVDV-2 have similar consequences if
infection occurs prenatal but their effects vary with postnatal
infection (Van den Hurk, 2000). Severe cases of clinical disease are
most commonly seen with the non-cytopathic BVDV-2 genotype (Kelling
2004).
Distribution, Prevalence and Transmission
BVDV
occurs world wide with an estimated 60-80% of cattle over the age of 1
year having serum-neutralizing antibodies to the virus. This number is
attributable to both persistently infected animals and vaccination
programs, with persistently infected (PI) cattle representing
about 1-2% of all animals (Radostits et al 1997). However this number
can vary greatly depending on geographical location and vaccination
programs.
Regardless of their prevalence, PI animals are typically the largest source of infection in
any
given herd (Radostits 2007) and represent a major challenge for the
management of the BVDV and its associated diseases. In close
confinement housing operation a PI animal can infect up to 90% of the
herd before it has reached 3-4 months of age (Houe 1999). Despite the
relatively low prevalence of persistently infected calves in randomly
selected western Canadian (< 0.1) (Taylor et al. 1995) and American
(4%)(Wittum et al. 2001) feedlots they remain a major source of the
virus (Campbell 2004). In general, the incidence of persistent
infection in calves less than one year of age is 1-2% in most countries
(Merk 2005).
BVDV can spread via direct or
indirect contact and can be isolated in and is widely disseminated by
nasal discharge, saliva, feces, semen, urine, tears and milk of
persistently infected animals (Radostits 2007). Viremic PI animals are
the major source of transmission of the BVDV and can remain clinically
normal for years during which time they can transmit the disease through
the aforementioned bodily fluids. Transplacental transmission from dam
to fetus is possible whether the dam is persistently or transiently
infected. Persistent infection in cattle can only be established via
transplacental transmission in the first half of fetal life (Radostits
2007). While primary infected animals (transiently viremic cattle) can
be a source of the virus, transmission to naïve animals is slow, not as
effective, and not possible via close contact (Radostits 2007).
Indirect transmission can occur via fomites, flies, and aerosolization
of the virus. In general, young and unvaccinated cattle are the
most likely to contract the virus.
Pathogenesis
As
with any other disease the pathogenesis of the BVDV virus depends on
the interaction between host, pathogen, and the environment. There
exists a wide range of clinical findings based on the host factors and
the virulence of the particular form of BVDV involved. In general, the
BVDV complex can result in subclinical benign bovine viral diarrhea,
fatal mucosal disease, peracute fatal diarrhea, immune suppression,
thrombocytopenia and hemorrhagic disease, reproductive failure, and
congenital abnormailities in calves (Radostits 2007). For simplicity
sake there will be no mention of environmental factors except to say
that in intensive agricultural settings the health status of an animal
is tied to its environment and for this reason sound housing and
sanitation practices should be adhered to. The clinical outcome of a
BVDV infection is dependent upon host factors such as age of the animal
at time in infection, age of fetus at time of transplacental infection,
immune status (passive (colostrum) vs. actively (vaccination or previous
exposure) derived), and the presence of stressors (Radostits 2007).
Pathogenesis is easily discussed in two categories of animals,
immuno-compentent non-pregnant cattle and immunocompetent pregnant
cattle.
Immunocompetent non-pregnant cattle
Suclinical
BVDV infections are by far the most common type of infection associated
with BVDV. It occurs in any class of cattle following the decline in
maternal antibodies. The infection rarely lasts more than a few days
and is characterized by inappetence, depression, mild diarrhea, and
transient leucopenia.
Peracute BVD is a severe and highly
fatal form of the disease caused by NCP BVDV-2, but it is much less
common. This form of the disease can result in thrombocytopenia (a
decrease in the number of circulating platelets) and hemorrhagic
syndrome, seen as hemorrhage from the sclera of the eyes, epistaxis
(bleeding from the nose), and abnormal bleeding from injection sites.
The same form of the virus can cause meningoenchephalitis (inflammation
of the brain and its protective lining), but so far only one such case
has been reported (Radostits 2007)
Immunosuppression resulting
from postnatal BVD infection and the subsequent potentiation of other
diseases is an important issue when considering the pathogenesis of the
BVDV. Cattle with BVD have been shown to be more susceptible to
infectious bovine rhinotracheitis, bovine respiratory disease, and
general enteritis. BVDV functions as a potentiator for these other
diseases by causing transient reductions in the number of circulating B
and T lymphocytes (Radostits 2007).
Some modified live-BVDV vaccines have also been shown to elicit similar effects.
Immunocompetent pregnant cattle
The
BVDV can cause fertilization failure, embryonic mortality, abortion, or
the birth of persistently infected calves depending on the stage of
gestation during which infection occurs. If exposure occurs during the
estrous cycle just prior to insemination a decrease in conception can
occur due to a delay or reduction in ovulation (Radostits 2007).
Insemination of naïve cattle with BVDV positive semen can result in
poor conception rates. Infection between days 0-45 of gestation seems
to have no effect on embryos. Between 45-125 days of gestation
infection of naïve animals can result in abortion, mummification,
congenital defects, or the birth of persistently infected calves, a
proportion of which will develop mucosal disease. In general
persistently infected calves will be ‘poor doers’. Those that develop
mucosal disease will do so because the NCP form of the virus with which
they were infected undergoes a mutation to the CP form. If infected
between days 125-175 numerous congenital defects can occur. Beyond day
175 of gestation the fetus is immunocompetent and the virus will likely
be eliminated without having any effects.
Clinical Findings and Lesions
Subclinical infection
is the predominant form of the disease featuring high morbidity but low
mortality rates. It is characterized by mild fever, mild diarrhea,
leucopenia, and inappetence. This form of BVDV infection will often go
undiagnosed because the signs are so mild and animals recover rapidly
after a few days.
Acute mucosal disease
can occur within BVDV positive herds in 5-25% of animals aged 6-24
months of age (Radostits 2007) with 45% morbidity and up to 100%
mortality. Infected animals are depressed, anorexic, drool profusely,
have increased heart and respiration rates, may strain to defecate and
the produce foul smelling watery diarrhea containing blood, mucous, and
occasionally fibrinous tags. Erosions or ulcers can be found in roughly
80% of cases within the oral cavity and on the muzzle of these animals
and may progress to the point where the entire oral cavity appears grey
and dead. A pus-like nasal discharge associated with irritation of the
nose is seen in most animals. A small proportion of infected cattle
may present with lameness. Death due to dehydration typically occurs
within 5-7days of the onset of signs.
Chronic mucosal disease can
develop from the acute form of mucosal disease. There will be
transient appearance of diarrhea, inappetence, emaciation, bloat, hoof
deformities, and erosive lesions of the oral cavity and skin. Scabbing
lesions of the skin in the genital and anal areas, as well as between
the legs and around the dew claws can occur. Failure of these lesions
to heal is an important clinical finding for this disease. Animals with
chronic mucosal disease can survive for up to 18 months.
Peracute bovine viral diarrhea
is a highly fatal disease reported as progressive outbreaks that can
last for several weeks. Animals suffer from severe depression,
anorexia, high fever, profuse watery diarrhea, and a decrease or lack of
milk production. Abortion may also be common. It can occur in all
ages of cattle but mortality is highest in young animals, with death
occurring a few days following the onset of symptoms.
Thrombocytopenia and hemorrhagic disease
is characterized by bloody diarrhea, spotty or generalized hemorrhage
of visible mucosa and the eye, epistaxis(bleeding from the nose), and
prolonged bleeding from injection or insect bite sites. Cattle will
also display fever, dehydration and rumen stasis. Mortality is
estimated to be 25%.
Reproductive consequences
are seen as conception failure, fetal abortion and mummification,
premature births, still births, congenital defects, stunted weak calves,
and the birth of persistently infected calves. Fetal infection rates
can reach as high as 21% in beef herds (Radostits 2007). PI calves are
generally unthrifty, smaller in body size, and may have a curly hair
coat. Congenital defects typically include abnormalities of the head
and its associated sensory structures. Problems with mentation, gait,
and general coordination are also common.
Necropsy findings
Acute
mucosal disease and peracute BVD have similar presentation upon
necropsy with the gross abnormalities being confined to the
gastrointestinal tract. Shallow erosions with little to no inflammation
can be seen in the oral cavity, esophagus and various stomach
compartments. In the abomasum these can be accompanied by hemorrhages
and edema. In the small intestine patchy and diffuse congestion can
occur but the more definitive lesions occur as 10-12cm long red-black
ovals which represent damage to the Peyer’s patches. The large
intestine congestion takes on a ‘tiger stripe’ pattern following the
normal folds of the internal surface of the colon.
Chronic mucosal disease
can be distinguished from the above by the presence of elevated,
yellow, friable(easily crumbled or pulverized) plaques, in the
gastrointestinal tract, especially the tongue and the rumen. Lesions of
the Peyer’s patches may be more difficult to identify.
Diagnosis
BVD
can be tentatively diagnosed from the history and clinical signs, but a
definitive diagnosis may require laboratory support especially during
outbreaks of mucosal disease or peracute bovine diarrhea which can
appear similar to rinderpest and malignant catarrhal fever (Merk 2005).
Laboratories can confirm BVDV using PCR, immunohistochemistry,
serology, virus isolation, and antibody ELISAs. The testing strategy
used and samples to be submitted will depend on the herd history,
vaccination status, age of the animals, cost of the test, needs of the
producer, and reason for doing the testing.
The
gold standard for diagnosing BVDV is virus isolation. It can be
attempted using nasal or ocular swabs, semen, intestinal tissues, spleen
or most other tissues, and blood samples. Blood samples are the best
option in live animals. The samples are used to inoculate cell cultures
and in positive cultures the virus is then identified via
immunoflourescence or immunoenzyme staining.
Treatment and Prevention
The
most effective means of prevention and control of BVDV is the
elimination of both PI individuals and the potential for the birth of PI
calves (Radostits 2007). To do this will require simultaneous
implementation of sound vaccination, herd-monitoring, biosecurity and
biocontainment programs. As treatment infected animals is not a viable
option (Radostits 2007), the control, prevention, and future
eradication efforts for this disease must be implemented by the cow-calf
industry (Campbell 2004) and by individual dairy barns (Brock 2004).
BVDV
biosecurity programs attempt to prevent introduction of the virus to a
naïve herd and thus are the most important aspect of BVDV prevention and
control. Dr. Kenny Brock at Auburn University has initiated the Top 10
List to prevent BVD in a herd. It is as follows:
1. Maintain a strict level of herd biosecurity.
2. Purchase only open animals that are known to be BVD-negative before purchase.
3. Isolate any new additions or animals re-entering the herd for a minimum of 30 days.
4. Test any new additions for BVD, and vaccinate during the isolation period.
5.
Maintain good sanitation and routinely disinfect contaminated areas.
Prevent contamination from outside sources by disinfection.
6. Prevent contact with neighboring cattle of unknown status.
7. Protect pregnant animals from potential sources of exposure during the first trimester.
8. Prevent mixing of animal groups immediately before breeding and during the first trimester.
9.
Conduct surveillance for BVD by performing necropsy on dead animals
and collect blood samples on any calves that are poor-doers and calves
that have respiratory disease.
10. Vaccinate the cow herd
yearly. Ensure that heifers are properly vaccinated at 6 months of age
(two doses) and are booster vaccinated before breeding.
(University of Florida IFAS Extension)
Whether
a farm/feedlot is free of the BVDV or has recovered from a BVDV
infection/outbreak a strict biosecurity program should be maintained as
recurrence is likely due to the endemic nature of the virus. Ongoing
biocontainment efforts, including vigilant vaccination programs, are
essential for any herd with previous history of infection or any herd
that imports animals or semen.
BVDV
Biocontaiment strategies attempt to control already existing disease in a
herd by minimizing the occurrence or severity of BVDV infection, or to
completely eliminate the virus from a herd. The goals of BVDV
biocontainment are to increase host immunity, remove PI cattle from the
herd, and to prevent contact between infected and susceptible animals
(Radostits 2007). As with any other aspect of cattle management, herd
monitoring is essential for the timely identification and response to
potential sources of BVDV infections, the most pertinent being PI
cattle. Along with the culling of these animals, immunization programs
to prevent further dissemination of the virus are needed. Some basic
vaccination principles outlined by the Dr. E.J. Richey of the
University of Florida follow:
1. Initiate
vaccination of calves after 4-6 months of age to avoid interference from
maternal antibodies passed to the calf during colostral feeding. When
using killed BVD vaccine, re-vaccination in 30-60 days will be required
to stimulate an adequate level of protection. The BVD vaccinations
should be completed in the calves at least 30 days before weaning.
2. Properly vaccinate all unvaccinated heifers and cows before breeding to ensure protection for the fetus.
3. Properly vaccinate all bulls before putting them out with the cows or heifers.
4. Properly vaccinate all new additions before adding them to the herd.
5.
When using killed BVD vaccine, annual boosters are required to
maintain an adequate resistance level when dealing with Type 1 BVD. If
dealing with Type 2 BVD, vaccinate using a killed BVD vaccine containing
Type 1 and Type 2 viruses or booster at three month intervals using
different company products. Breeding stock should be booster vaccinated
immediately before the breeding season to provide maximum protection to
the fetus. Even if MLV-BVD vaccine was used as the initial vaccination
agent, a booster vaccination using either MLV or killed BVD vaccine is
recommended every few years. Remember, do not booster vaccinate pregnant
cows with replicating BVD vaccine.
(University of Florida IFAS Extension)
The
continued prevalence of the BVDV and seeming failure of current
widespread vaccination efforts against BVDV may be attributable in part
to the difficulty of vaccinating for all the various genotypes of the
virus, but also to the mixing of cattle at market, during transport, and
at the feedlot prior to and immediately following vaccination (Campbell
2004).
References
Baker, JC.
(1995) The clinical manifestations of bovine viral diarrhea infection.
Vet Clin North Am Food Anim Pract. 13(3):425-54.
Brook, K.V. (2004) Strategies for the control and prevention of bovine viral diarrhea virus. Vet Clin Food Anim. 20:171-180.
Campbell, J.R. (2004) Effect of bovine diarrhea virus in the feedlot. Vet. Clin. North. Am. Food Anim. Pract. 20(1):39-50.
Goens, D.S. (2002). The evolution of bovine viral diarrhea: a review. Can. Vet. J. 43(12): 946-954.
Houe,
H. (1999) Epidemiological features and economical importance of bovine
viral diarrhea virus (BVDV) infections. Vet. Micro. 64:89-107.
Richey, E.J. Bovine Viral Diarrhea. University of Florida IFAS Extension.
Kelling
C.L. (2004). Evolution of Bovine Viral Diarrhea Virus Vaccines.
Veterinary Clinics Food Animal Practice. 20: 115-129.
Merck Veterinary Manual.
Taylor,
L.F., Van Donkersgoed, J., Dubovi, E.J, Harland, R.J, van der Hurk,
J.V., Ribble, C.S, Janzen, E.D. (1995) The prevalence of bovine viral
diarrhea virus infection is a population of feedlot calves in western
Canada. Can. J. Vet. Res. 59:87-93.
Wittum, T.E.,
Grotelueschen, D.M., Brock, K.V., Kvasnicka, W.G., Floyd, J.G, Kelling,
C.L. (2001). Persistent bovine viral diarrhoea virus infection in US
beef herds. Prev Vet Med. 49:83–94.
Van den Hurk, J. (2000). Health Management: Bovine Viral Diarrhea.
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