bovine parvovirus infection
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- bovine parvovirus infection
Pathogen/sTop of page bovine parvovirus
OverviewTop of page
Parvoviruses are small, simple viruses that were first isolated in 1959 (Abinanti and Warfield, 1961) and identified as parvoviruses in the 1970s (Storz and Warren, 1970). Since then parvoviruses of veterinary importance have been found in cattle, pigs, dogs, cats, mink, geese, rats, mice, and humans. In all, more than 50 species of the family Parvoviridae have been discovered. The family is divided into 2 subfamilies, Parvovirinae and Densovirinae, and into 6 genuses, Parvovirus, Erythrovirus, Dependovirus (in the Parvovirinae), Densovirus, Iteravirus, and Brevidensovirus (in the Densovirinae).
A phylogenetic analysis of full-length genomes as well as open reading frames distinguished three evolutionary groups of parvoviruses from vertebrates: (i) the human helper-dependent adeno-associated virus (AAV) serotypes 1 to 6 and the autonomous avian parvoviruses; (ii) the bovine, chipmunk, and autonomous primate parvoviruses, including human viruses B19 and V9; and (iii) the parvoviruses from rodents (except for chipmunks), carnivores (canine and feline), and pigs. Each of these three evolutionary groups could be further subdivided, reflecting both virus-host coevolution and multiple cross-species transmissions in the evolutionary history of parvoviruses. Within the second group bovine parvovirus appeared as an outlier (Lukashov and Goudsmit, 2001). Chen et al. (1986) determined the complete nucleotide sequence of bovine parvovirus. The sequence was found to be 5491 nucleotides long. The terminal regions contained nonidentical imperfect palindromic sequences of 150 and 121 nucleotides. In the plus strand, there were three large open reading frames (left ORF, mid ORF, and right ORF) with coding capacities of 729, 255, and 685 amino acids, respectively.
Two further species of bovine parvovirus have recently been identified as contaminants of bovine serum (Allander et al., 2001). They were provisionally named bovine parvovirus 2 and 3. The viruses were identified while developing a simple and reproducible method for discovering viruses in single serum samples based on DNase treatment of the serum followed by restriction enzyme digestion and sequence-independent single primer amplification (SISPA) of the fragments. A survey of commercial sera suggests that infection by both viruses is frequent. BPV-2 occurs in calves soon after birth, whereas BPV-3 may be transmitted in utero. It remains to be investigated whether BPV-2 and BPV-3 viraemia is transient or persistent.
Bovine parvovirus was first isolated in 1959 (Abinanti and Warfield, 1961) from the intestines of calves. It was later identified as a parvovirus (Storz and Warren, 1970; Bachmann, 1971). Parvovirus has been detected in all countries where herds have been surveyed for the virus. It has been found in North America, South America, Europe, and the East Asia (see Geographical Distribution). As bovine parvovirus has little homology with the parvoviruses of other animal species it is unlikely that the antibodies detected in surveys are caused by cross reaction as a result of cross infection with non-bovine parvoviruses (Bates et al., 1972).
Host AnimalsTop of page
Hosts/Species AffectedTop of page
There appears to be no particular host characteristics such as breed, type (dairy, beef), or age that predispose towards bovine parvovirus infection.
Pigs were found to develop antibodies to bovine parvovirus after they ingested milk containing the virus. There was no evidence of disease in the pigs from the virus (Mengeling, 1990).
Systems AffectedTop of page digestive diseases of large ruminants
reproductive diseases of large ruminants
respiratory diseases of large ruminants
DistributionTop of page
Bovine parvovirus appears to have been found in all countries where cattle have been surveyed for the agent (Storz, 1990). In a large survey of 433 animals in 35 herds in western USA (Storz, 1972) antibodies were found in 243 (64.4%) of 377 animals in 29 of the herds: six of the herds were negative. Hassig et al. (1988) concluded that bovine parvovirus was widespread in cattle in Switzerland. They used the immunodot-test on serum samples taken in 1984-1986 from 295 cows in several parts of Switzerland and found antibody titres 1:28 to bovine parvovirus in 118 (40%). In 1984, 30 of 83 (36%) samples were positive, in 1985, 46 of 86 (53%), and in 1986 and 42 of 126 (23%). Of 22 calves from positive cows, 17 were positive for the virus, while 24 of 34 from negative cows were positive. In Brazil 4000 (97%) of 4096 serum samples taken from mainly dairy cattle were positive for antibodies to parvovirus (Hubner, 1996). Antibody titres varied between regions but there seemed to be no correlation between age and strength of titre. As a result of the widespread occurrence the authors concluded that bovine parvovirus was an important cause of newborn diarrhoea and of reproductive and respiratory disease in the area.
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
PathologyTop of page
The main pathological changes associated with infection are respiratory and digestive lesions. The virus has been shown to cause both respiratory and intestinal lesions. In the field, however, conditions such as diarrhoea and respiratory disease usually involve several agents and it is difficult to determine which is the primary agent. Yurov et al. (1989) inoculated the Russian field strain "B-2" of bovine parvovirus serotype 3 orally, nasally and/or intravenously into 18 calves, aged 2-3 months, after the Haden strain of serotype 1 was inoculated into 5 calves. The calves were killed and examined after 5 or 8 days. Both strains were highly pathogenic, producing lesions in the respiratory and gastrointestinal tracts. Durham et al. (1985a) orally challenged calves with bovine parvovirus, resulting in mild to moderate diarrhoea, with lymphopenia and viraemia. The virus initially infected tonsils and intestinal tract, subsequently spreading to systemic lymphoid tissues. There was moderate small intestinal villus atrophy and fusion due to crypt damage, together with lymphoid necrosis predominantly associated with the intestinal tract and thymus. Although the disease was not very severe, this may have been because the low parasite burden in the animals reduced mitotic activity in susceptible tissues. Storz et al. (1978) found that experimentally infected calves excreted the virus from 24-48 hr after infection and continued to do so for the 11 days of the experiment. The regions of the body most consistently infected were the jejunum, ileum and caecum, with highest viral titres found in the intestinal mucosa. Oral infection followed by intraveneous infection resulted in viraemia, and more serious diarrhoea. During the systemic phase of infection, cells of the adrenal cortex, thymus, lymph nodes, and heart muscle became infected.
Experimental infection of pregnant cows with the virus resulted in infection of the foetus and placenta (Storz et al., 1978). Foetuses in the first trimester of pregnancy were most susceptible. The virus was detected by immunofluorescence in the foetal adrenals, lungs, spleen, heart muscle, kidneys and thymus. Pathological examination of aborted fetuses showed them to be oedematous with increased pleural and peritoneal fluid. Intranuclear inclusions were seen in cells of the small intestines, liver, lymph nodes, and cerebellum, and lymphoid hyperplasia.
DiagnosisTop of page
The presence of bovine parvovirus can be diagnosed by viral isolation in cell culture (Storz, 1978), by combined DNA hybridization and immunodetection assay (Lederman et al., 1986), haemagglutination inhibition test (Hubner, 1996), haemagglutination assay (detecting the virus in faeces) (Elschner, 1995), enzyme linked immunosorbent assay (ELISA) (Bernhardt, 1994; Bostandjieva, 1997), electron microscopy (Biermann, 1989), and more recently DNase treatment (Allander, 2001).
Elschner (1995) found that a haemagglutination assay for bovine parvoviruses (BPV) in faecal specimens of calves was not suitable because of a high number of non-specific haemagglutinating reactions and many haemolytical specimens. A 16-fold higher sensitivity was obtained using solid-phase immune electron microscopy (SPIEM) in comparison with direct negative contrast staining for detection of BPV. Bostandjieva (1997) developed a modified sandwich ELISA with specific monovalent hyperimmune anti-bovine serum and BPV antigens. It was compared, using 103 serum samples from cows and calves with intestinal and respiratory diseases with the haemagglutination test: BPV antibodies were detected in 77 samples (74%) using ELISA and 73 samples (70.8%) using HI.
Tests such as the direct fluorescent antibody test and polymerase chain reaction are available commercially.
List of Symptoms/SignsTop of page
|Digestive Signs / Diarrhoea||Cattle & Buffaloes:Calf||Diagnosis|
|Reproductive Signs / Abortion or weak newborns, stillbirth||Cattle & Buffaloes:Calf||Diagnosis|
Disease CourseTop of page
Bovine parvovirus can cause enteritis with diarrhoea, respiratory disease and foetal death and/or abortion. Calves experimentally infected with the bovine parvovirus, either orally or intravenously developed diarrhoea 4-7 days later (Storz et al., 1978). Calves infected intravenously had more severe diarrhoea than did those infected orally (Spahn et al., 1966). Parvovirus has been detected in mixed enteric viral infections (bovine enterovirus, bovine diarrhoea virus, bovine adenovirus, bovine coronavirus). The parvoviral infection involves the host cell niche left unoccupied by intestinal coronavirus or rotavirus (Storz, 1990).
Durham et al. (1997) found that the disease course in calves experimentally infected with parvovirus was more severe in animals with sub-clinical coccidiosis. Imposition of weaning stress on coccidia-infected calves that had apparently recovered from prior infection with BPV, was found to induce severe diarrhoea with recrudescence of BPV excretion in faeces. This was in contrast to the mild diarrhoea found following weaning of control animals and animals infected with either agent alone. BPV activity and damage in the intestinal tract was probably enhanced by the extra mitotic activity induced in the region by Eimeria infection and the local effects of weaning. On the basis of these and previous findings in the field, it is suggested that BPV may play a significant role in the aetiology of post-weaning diarrhoea in calves.
EpidemiologyTop of page
Bovine parvoviruses differ antigenically from parvoviruses isolated from other species such as man, pigs, dogs, rats and rabbits. They are also antigenically related to or identical to the prototype BpoV-1 (Abinanti, 1961). Comparison of the genomic nucleotide sequences among parvoviruses showed little or no homology between rodent parvoviruses LuIII and bovine parvovirus (Banerjee, 1983). It is concluded that the lack of homology and antigenic difference suggests that antibody titres to BPV are not the result of cross-reaction following infection with parvovirus of another species (Storz, 1990). This opinion is somewhat contradicted by the finding of Bernahrdt (1994) who found neutralizing and haemagglutination inhibiting antibodies reacting with bovine parvovirus in human immunoglobulin preparations. Antibodies were also detected by ELISA and immunoblots in bovine sera which reacted with the recombinant VP 1/2 antigen of human parvovirus B19: it was concluded that a cross reaction exists between human and bovine parvovirus. Mengeling and Matthews (1990) found that newborn piglets that ingested of bovine parvovirus in the first four weeks of life developed antibody titres, and they suggested that antibodies for parvovirus previously detected in the serum of pigs and people may reflect ingestion of virus-contaminated bovine milk or milk products.
Maternal transmission of the virus has been demonstrated by detecting significant titres of antibodies in foetal serum and from the detection of the virus in tissues of aborted foetuses (Storz et al., 1972; Inaba et al., 1973). Hubner (1996) demonstrated that all of 40 calves of infected dams, tested before they ingested colostrum, were infected with bovine parvovirus at birth. In the same experiment colostral antibodies were still detectable by the haemagglutination inhibition test 180 days after birth. In a study of seasonal distribution in herds in Austria (Hinaidy, 1980) found that the highest proportion of infected calves was in February.
Impact: EconomicTop of page
There appears to be little recent study of the economic impact of bovine parvovirus. The study by Hubner (1996) which found the virus to be widespread in dairy cattle in Rio Grande de Sul, Brazil, and they concluded that it was an important cause of newborn diarrhoea, and of reproductive and respiratory diseases in the area. Bovine parvovirus is no longer contained in the mixed vaccine Lactovac (Intervet) in Europe is an indication that the virus is no longer considered an important pathogen there.
Prevention and ControlTop of page
A component against bovine parvovirus has been included in a combined vaccine to provide maternal immunity to diarrhoea in newborn calves. The combined vaccine, Lactovac, produced by Intervet (formerly by Hoescht-Roussel) contains components against coronavirus, parvovirus, rotavirus and Escherichia coli. Use of the vaccine (5 ml given to cows 6-8 weeks before parturition, followed by a second dose 4-5 weeks before parturition) in 4600 cows reduced calf sickness from 50-70% to 8-26% and calf mortality from 7-40% to 2% (Lens, 1993). The beneficial effects of the vaccine were also reported in Japan by Kohara et al. (1997), and Krdzalic et al. (1990). Tests of the vaccine in both cows and mice showed that levels of antibodies in milk to parvovirus and the other agents were sufficient to protect the newborn (Bengelsdorff, 1989). Currently in Europe, Lactovac does not contain a component for bovine parvovirus, an indication that the virus is not thought to be of much significance.
Reliable disinfection can be achieved by 0.5% chlorox or ethylene oxide in the form of the non-explosive mixture of 10% ethylene oxide and 90% carbon dioxide (Storz, 1990). Control of the virus by disinfection can be achieved by an organic acid based disinfectant disinfectant (Venno-Vet 1; Fa. Venno GmbH, Norderstedt) at 0.5% or 2%. It is also important to clean before disinfecting as serum proteins can reduce the efficacy of disinfection (Herbst, 1991).
ReferencesTop of page
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Allander T; Emerson SU; Engle SE; Purcell RH; Bukh J, 2001. A virus discovery method incorporating DNase treatment and its application to the identification of two bovine parvovirus species. Proceedings of the National Academy of Science, USA, 98(12):11609-11614.
Bachmann PA, 1971. Properties of a bovine parvovirus. Zentrabl. Veterinarmed, 18:80-81.
Banerjee PT; Olson WH; Allison DP; Bates RC; Snyder CE; Mitra S, 1983. Electron microscopic comparison of the sequences of single stranded genomes of mammalian parvoviruses by heteroduplex mapping. Journal of Molecular Biology, 166:257-272.
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Bengelsdorff HJ; Bernhardt D; Pranter W; Wieda J, 1989. Vaccination of cows against calf diarrhoea pathogens: testing efficacy in mice as on alternative to cattle. Tierärztliche Umschau, 44(6):358.364; 11 ref.
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Brauniger S; Peters J; Borchers U; Kao M, 2000. Further studies on thermal resistance of bovine parvovirus against moist and dry heat. International Journal of Hygiene and Environmental Health, 203(1):71-75.
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Hinaidy B; Messner A; Burki F, 1979. Isolation in cell culture, cytopathology and culture of bovine parvoviruses. Wiener Tierarztliche Monatsschrift, 66(12):359-364.
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Huck RA; Woods DW; Orr JP, 1975. Isolation of a bovine parvovirus in the United Kingdom. Veterinary Record, 96(7):155-156.
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Distribution MapsTop of page
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