VIRUS bovine viral diarrhea (BVD)
Hermelinda G. Rivera 
This article is a review of available data on the Bovine Viral Diarrhea (BVD) in relation to current concepts of pathogenesis, laboratory diagnosis and control. Hermelinda Rivera, veterinary virologist, discusses and simplifies the complex and varied knowledge in search of a flexible conceptualization of BVD and their interrelations and implications for animal health in general and Peruvian cattle in particular.
virus BVD (Bovine Virus Disease), which causes diarrhea disease Viral Bovina, is one of the most common pathogens of cattle in the world, associated with several clinical forms, ranging from unapparent infection to a fatal disease called the mucosa.1, 2.3
To understand the mechanism the disease is essential two concepts: first, two biotypes of BVD virus, cytopathogenic biotype (CP) and non-cytopathogenic (NCP), the second concept, there are two populations of cattle, persistently infected cattle and cattle " normal "infection free. Both biotypes
virus differ at the molecular level and in the laboratory for their crops celulares.4 feature, 5 The two biotypes produce disease Bovine Viral Diarrhea in its various clinical forms, but the NCP biotype is the persistent infection induced, provided the virus passes to the fetus through the placenta during the first 4 months of gestation, when this occurs, the fetus is born infected with NCP and remain infected for
lives.6
The BVD virus is a member of the genus pestivirus together with hog cholera virus and Border Disease (BD) affecting pig and sheep respectively. Until recently, the genus pestivirus was one of the Family Togavidae, but wing light of current knowledge regarding the molecular structure and mode of replication of its genome such the virus Fiaviridae family, was proposed to the International Committee for the Nomenclature of Viruses to be relocated within the family Flaviridae.7 recently been accepted the proposal and the pestivirus genus belongs to the family now Flaviridae.
The introduction of the BVD virus was apparently to Peru with the importation of cattle during the decade of 1960-1970. in 1962 - 1963 occurred in Lima and in the Mantaro Valley some imported animals cows children with severe acute diarrheal. Made by histology and serology confirmed the diagnosis of bovine viral diarrhea (De la Vega E, H Samamé, Rosadio R, personal communication). After There were probably factors such as climate, type of operation, etc. who made a living in balance, but with the frequent importation of cattle without sanitary control in recent years, may have entered finding new strains of susceptible cattle populations, another possibility is the stress they are often subjected dairy cattle helping increase the pathogenicity of the virus, and finally, newly emerging strains could be favored by antigenic pressures, whatever the case, the virus is prevalent in the country and is associated with reproductive and respiratory problems nationwide.
1. PATHOGENESIS
One of the characteristics of the BVD virus is the ability to produce multiple clinical manifestations, the most common being the following: a.
Subclinical infection.
In USA and Canada 70 to 99% of susceptible cattle develop subclinical or inapparent, but if you look carefully, the animals may have fever, leukopenia and recovery is usually rapid and complete because of the outbreak and increased levels of neutralizing antibodies in 2 to 3 weeks after exposure to the virus many times this type of infection also predisposes the animal to other infections due to immunosuppressive nature the virus.1, 9,10,11 The prevalence of over 50% of BVD found in apparently normal cattle suggest that this form is also predominant in Peru (Rivera, unpublished data). B.
Bovine Viral Diarrhea.
is the acute form of infection. In 1946, when BVD was first described, this was the most prevalent and one of the most striking sign was diarrhea, hence the name of bovine viral diarrhea, although at present it is estimated that only 1 to 5% of animals 6 months to 2 years old may have this clinical. Brownlie12 have suggested that instead of Viral Diarrhea Virus, Bovine "virus should be called mucosal disease. Clinically, the animals have developed the acute form: fever of 41 - 42 ° C, increased leukopenia, nasal and ocular discharge, oral mucosal erosions and sometimes diarrea.1, 6,10,13
c. Neonatal infection.
The calf may be infected in the perinatal period, ie in the last period of pregnancy or after birth, then developed a severe enteritis sometimes fatal, 14 thus BVD may play a role in presenting enteric disease in newborn calves. The antibodies that the calf receives from the mother colostrum and milk travésdel sell out the 105 to 230 days of age, after which the rise in titer of antibodies may be due to natural infection or
vaccination.1
d. Venereal infection.
The infected bull semen during fetal or acutely infected bulls, contains BVD virus. In this case, the spermatozoa have reduced motility and may also have abnormalities morfológicas.15 However, the virus affects fertilization, not conception, characterized by repetitions of heat and then increasing the number of services per conception. This problem may be temporary and removed when the cow acquired immunity
virus.1
The commercialization of germplasm and transfer of embryos were in potential early BVD transmission media but now these risks are minimal if the gene comes from industries with good disease control. E.
Transplacental infection.
The economic impact of fetal infection by the BVD virus is of great significance in cattle lechero10, 16. If a susceptible pregnant cow is infected with BVD virus can develop subclinical or acute, and there is great possibility that the virus crosses the placenta and infect the fetus. The effect of the virus in the fetus depends on the gestational and virus biotype infectante.1, 17 The effects of the virus in the fetus can be:
1) embryonic resorption, if the infection occurs before 45 days or so.
2) If the infection is between 50 to 100 days of life may occur fetal death followed by abortion or fetal mummification and the expulsion of the fetus is often weeks or months later.
3) If the infection is between 100 and 150 days of fetal life, birth defects occur because in this period of fetal life is completing the development of central nervous system and the ability of the immune response of the fetus, some of teratogenic lesions are microphthalmia, cataract, hydrocephalus, cerebellar hypoplasia, thymic aplasia, pulmonary hypoplasia, alopecia, etc..
4) Immune BVD virus (absence of fetal immune response), this condition occurs when the fetus is infected within 125 days of gestation, ie before the full development of the immune system.
The immune, the BVD virus leads to persistent infection and is linked to infection with the NCP biotype
5) A BVD virus infection can also lead to stunted calves which is manifested by weakness and lack of body development.
6) The BVD virus infection in the last period of pregnancy may not cause harm to the fetus, and makes it immunocompetent and can respond with antibodies neutralizing. The calf then, is normal and have antibodies to BVD virus at birth.
f. Persistent infection.
Most persistently infected calves are born susceptible than normal cows were infected with the NCP biotype during the first 4 months of gestation (120-125 days), but cows with calves are persistently infected with the same condition; can be generated in a herd of animals persistently infected clones. A calf born with persistent infection is characterized by the premature appearance, these calves are vulnerable to the respiratory and enteric, and 50% usually die during the first year of life. However, some may have normal appearance and reach reproductive age. These animals are the reservoirs and disseminators of the virus and are particularly susceptible to developing clinical form of mucosal disease, fatal in nature. Fortunately the occurrence of these calves is very rare, in USA for example, is 1 to 2%, but may be higher in some hatos20.
persistently infected animals can be identified by serology and virus isolation from leukocytes and / or blood serum collected at intervals of 3 or more weeks.20, 21,22,23
g. Mucosal disease (MD).
disease mucosa is a form of BVD is not uncommon and usually occurs in animals 6 months to 2 years old. The severe form is characterized by bloody diarrhea and mucus, dehydration, severe leukopenia and death within a few days to present the clinical findings. The most striking gross lesions in this case are ulcers and erosions in the lining of the digestive tract. Mortality can reach 50% .1,4,9,17
clinical
This form occurs when there is coinfection or superinfection with CP biotype. The source of the CP co-infecting virus can be a field virus or vaccine virus or virus that is mutating virus by NCP (within animal), causing the infection persistent. This condition apparently occurs when co-infecting virus or superinfecting CP and NCP viruses are combined perfectly. It should be pointed out that not always the associations of the NCP and CP biotypes result in mucosal disease, a concept that has been shown experimentalmente.24, 25
In Peru recently reported 2 clinical cases of disease mucous, unfortunately the studies did not permit the diagnosis (H. Andresen and R. Perales unpublished data). Invoke clinical veterinarians make all efforts to reach a definitive diagnosis.
h. Bovine viral diarrhea Chronicle.
This form is a sequel of MS or acute form of BVD and the animal is characterized by intermittent diarrhea, sores in buconasal cavity in between toes, weakness and death, after weeks or months of having the disease. '
i. The BVD virus and bovine respiratory disease complex.
The BVD virus is an important part of Bovine Respiratory Disease Complex, to be an immunosuppressive agent because of the affinity for the immune system tissue. In general, the virus causes atrophy of lymphoid tissues, profound leucopenia, impaired function of polymorphonuclear cells, suppressing the production of interferon and other dysfunctions that promote invasion and synergism of other microorganisms neumotrópicos: Pasteurella, Bovine Herpes 1 (IBR), Mycoplasma, etc.. resulting in a respiratory process agudo.1,
2,10,11,25,26 A recent study in calves from 2 days to 6 months of age with respiratory problems in different herds from the Valley of Lima, was found to BVD virus as one of the agents associated with respiratory complex with 54% prevalence, suggesting that the virus may have begun to be immunosuppressive or potentiated the effect of other pathogenic viruses such as HBV-1.
2. DIAGNOSIS
advances in understanding the biological nature of viruses, the ability to produce multiple clinical manifestations, led to confusion in the veterinary community regarding the diagnosis and interpretation of laboratory results, fortunately, the development and use of biotechnology has cleared many of these dudas.2, 27.28
In the laboratory, BVD can be diagnosed by the following: a.
Virus isolation.
In principle, this method presents no difficulty as long as the collection and transport of specimens (spleen, lymph nodes, kidney, blood with EDTA) to the laboratory is adequate and that the laboratory has to susceptible cells and endogenous BVD free and that has finally reagents of good quality. 27,29,30
Since the 2 biotypes of the virus (NCP and CP) may lead to the same clinical signs, is supposed to be isolated any of the 2 biotypes. If the biotype is CP (less common) shows the characteristic lesion in cell culture or cytopathogenic effect, if it is the NCP biotype (most common in the field) there will be no cytological lesion, therefore it is necessary to test Additionally, the immunofluorescence or immunoperoxidase.
virus isolation method is expensive and requires several days or weeks to get the result, but is very sensitive. B.
Detection of viral antigens in tissue samples.
This procedure is fast and available in most laboratories. Display consists of virus antigens (proteins) directly into a small sample of the specimen, using techniques such as immunofluorescence or immunoperoxidase, the latter also useful in samples fixed in formalin. Both techniques or methods are particularly sensitive and specific when used monoclonal antibodies and the results are obtained in a few minutos.31, 32.33,34
C. Detection of antibodies against BVD virus (serological diagnosis).
immunocompetent
When an animal is infected with the BVD virus responds producing antibodies, which are designed to neutralize and eliminate the virus from the body. These antibodies can be detected in the laboratory by virus neutralization test (standard method). This method requires the use of cell culture and laboratory strain cytopathogenic BVD, to facilitate observation of viral neutralization or as a indicator of virus neutralization by antibodies present in serum or fetal fluids in research .
Diagnosing BVD through this test in an animal or group of animals in need of a double sampling (paired sera) obtained in the acute and convalescent phase, both samples are worked in the laboratory under the same conditions to compare antibody titers in both samples. An increase in antibody titers define the diagnosis of BVD infection.
Virus neutralization method is very specific and sensitive but expensive and laborioso.27, 30,35,36
These three methods are routinely performed at the Laboratory of Virology, Faculty of Veterinary Medicine, 1 to San Marcos. In our environment it is rare to have bovine fetuses, so that often the primary culture is prepared from sheep fetuses in this case it is advisable to discard BVD / BD endogenous and should preferably be used from the third crop. D.
Other recent diagnostic tests.
These tests provide a great future, although many are not yet available. Some are:
- ELISA, used to detect BVD antibodies or antigens. Only requires monoclonal antibodies and purified antigen. The ELISA can process many samples in short time.
In our laboratory, we are standardizing the test for use in epidemiological studies of HBV-1 and possibly also for BVD.
- DNA probes (DNA Probes)
DNA probe are molecularly cloned copies of a segment of the genome of BVD and marked with a radioactive molecule or a group chemical that can be identified with a chromogenic substance, when this piece marked is added to a specimen containing the BVD virus binds to its complementary portion or alignment and that union is called hibridización.26, 27.40 But because of wide variability between BVD strains, it appears that this method is not very far confiable.27, 41
- The reaction of the polymerase chain (PCR) and flow cytometry are methods that seem to offer an alternative for speed , sensitivity and the possibility of being used in numerous samples, for example, to detect persistently infected animals in the hato.42, 43.44
3. CONTROL.
Recent advances in understanding the pathogenesis and epidemiology of BVD indicate that is unlikely to keep herds free from BVD, so the goal should be prevention and control across 3 key areas.
a. Good disease control.
The aim is to prevent the entry of virus into the herd. With this purpose to avoid a number of factors: the multiple use of hypodermic needle, contact with other ruminants, can carry the virus, the use of germplasm of dubious origin, the use of modified live virus vaccines, free entry animals in the herd without analysis, stress, etc.1, 12.30
b. Id and removal of persistently infected animals.
This is a measure of great importance since the 20 animals persistently infected (immunotolerant) are the main spreaders of the virus. Fortunately, these animals do not exceed 2%, but in some herds can reach percentages superiores.41
This should be done when there is suspicion of infection in the herd, for example: increased frequency of abortions or weak calves born congenital malformations, increased the number of cows repeating the heat. In such a situation is sampled all animals older than 6 months. If the herd is BVD, the prevalence should be high and negatives must be considered suspect and removed from the herd, if the percentage of these animals is minimal.
The other possibility is to find these animals after vaccination with killed virus vaccine to all animals older than 6 months, including the second dose recommended time, and then performed the serological analysis of all vaccinated animals those who do not respond to vaccination will be removed from the herd as soon as possible. This measure will be repeated periodically to check those animals that were not sampled (calves under 6 months) .1,12,21
c. Vaccination.
Currently there are two types of vaccines: a modified live virus and killed or inactivated virus.
The modified live virus vaccine has the advantage of producing high levels of antibodies without the need for a second dose, therefore it is suitable for extensive livestock rearing, but has the disadvantage of producing immunosuppression predisposing the animal to other infections , for example, stressed animals increases mortality due to respiratory problems, can not be used in pregnant animals and may revert to virulence causing serious problemas.46
The killed vaccine has the disadvantage of requiring a second dose to induce antibodies protective levels, but it sure is not immunosuppressive and can be used pregnant cows. Facilities management for this vaccine is recommended in intensively managed cattle. At present there are many commercial brands and the trend is the use of polyvalent killed virus vaccines with two or more strains of virus BVD.1, 20,23,30,47
Sci
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INVESTIGACIONES PECUARIAS : Enero - Junio 1993, Vol. 6 Nº 1
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