Download Clinical aspects of bovine virus diarrhoea virus infection

Rev. sci. tech. Off. int. Epiz., 1990, 9 (1), 25-41.
Clinical aspects of
bovine virus diarrhoea virus infection
J.C. BAKER *
Summary: Bovine virus diarrhoea virus (BVDV) infection of cattle results in
a wide range of clinical manifestations. This article reviews the clinical responses
associated with BVDV and discusses these diseases in terms of acute infection
in immunocompetent cattle, fetal infection, infection in cattle immunotolerant
to and persistently infected with BVDV and finally mucosal disease.
KEYWORDS: Abortions - Acute infection - Bovine virus diarrhoea - Bovine
virus diarrhoea virus - Congenital defects - Congenital infections Immunosuppression - Immunotolerance - Mucosal disease, acute - Mucosal
disease, chronic - Persistent infection.
Bovine virus diarrhoea virus (BVDV) was first recognised in the United States
in association with outbreaks of acute and often fatal disease characterised by
diarrhoea and erosive lesions of the digestive tract (54). Bovine virus diarrhoea virus
has a worldwide distribution. Infection with the virus is c o m m o n , as indicated by
the high prevalence of seropositive cattle (22, 2 3 , 25). T h e biology of BVDV is
complex, and multiple and diverse clinical manifestations m a y occur in cattle infected
with the virus (Table I). This diversity was difficult t o understand based on previous
explanations of pathogenesis. For example, bovine virus diarrhoea (BVD) and mucosal
disease are two clinically distinct and different diseases caused by the same virus.
Recent investigations have brought a better understanding by focusing o n cattle b o r n
immunotolerant and persistently infected with BVDV, and the role of these animals
in the pathogenesis of mucosal disease. This article will review the spectrum of clinical
responses t h a t occur in cattle following BVDV infection.
ACUTE INFECTIONS
Subclinical infections
It has been estimated t h a t 70 to 9 0 % of BVDV infections in susceptible,
immunocompetent cattle are subclinical (1). Cattle undergoing subclinical infections
m a y have a mild elevation of b o d y temperature and leukopenia that is followed by
the development of specific neutralising antibody. This form of infection undoubtedly
accounts for the high prevalence of cattle with serum antibody to BVDV without
previous history of disease (25).
* Department of Large Animal Clinical Sciences, College of Veterinary Medicine, Michigan State
University, East Lansing, Michigan 48824-1314, USA.
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TABLE I
Clinical manifestations of bovine virus diarrhoea infection in cattle
Acute bovine virus diarrhoea infection
Subclinical infections
Bovine virus diarrhoea
Venereal infections
Immunosuppression
Bovine virus diarrhoea infection in neonatal calves
Mixed infections (bovine respiratory disease)
Congenital infections
Fetal abortion, stillbirths, fetal resorption and mummification
Congenital defects
Weak and undersized calves
Normal calves born seropositive to BVDV
Calves born immunotolerant to BVDV
Chronic infections
Persistent viraemia
Mucosal disease
Acute mucosal disease
Chronic mucosal disease
Bovine virus diarrhoea
The disease referred to as bovine virus diarrhoea (BVD) represents an acute
infection in seronegative, immunocompetent cattle (14). As previously mentioned,
subclinical infection is most c o m m o n in this group. W h e n infections become clinical,
they generally do so in cattle ranging in age from six m o n t h s t o two years (7). I n
susceptible herds, morbidity may be high but mortality is low to none. The incubation
period is 5 to 7 days and is followed by transient fever and leukopenia (22). Viraemia
occurs 4 to 7 days after infection (16) a n d in some cases m a y persist u p to 15 days
(22). Clinical signs include depression, anorexia, oculonasal discharge and occasionally
oral lesions characterised by erosions or shallow ulcerations. A rapid respiratory rate
may develop secondarily to pyrexia which m a y be incorrectly diagnosed as pneumonia
(56). Diarrhoea m a y also be present, and in lactating cows milk production m a y
decrease. Virus appears to be shed in low concentrations when compared with
persistently infected cattle (22). Diagnosis can be m a d e by isolation of virus from
blood, body secretions and excretions, or by demonstration of seroconversion. Virus
neutralising antibodies generally appear in the serum two to four weeks after infection
and probably persist for life. Following the i m m u n e response it is likely that there
is life-long protection to disease caused by BVDV, but these individuals may be
susceptible to periodic reinfection (16).
Thrombocytopenia has been reported as a feature of acute BVDV infection (68).
While it could not be determined if the animals in the study were acutely infected,
or persistently infected with non-cytopathic BVDV and undergoing superinfection
with a cytopathic strain of BVDV resulting in mucosal disease, it is likely that some
were acute infections as they recovered. The thrombocytopenia resulted in clinical
signs of bleeding manifested by bloody diarrhoea, epistaxis, petechial haemorrhages,
ecchymotic haemorrhages and bleeding from injection sites. The pathogenesis of the
thrombocytopenia was not determined. However, disseminated intravascular
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coagulation was not thought t o be involved a n d most likely the thrombocytopenia
occurred as a result of BVDV-induced myelosuppression or b o n e m a r r o w necrosis.
It has been difficult to reproduce BVD in immunocompetent cattle under
experimental conditions and the reason for this is not readily apparent. Infection with
BVDV is k n o w n to cause immunosuppression (discussed later) and thus under field
conditions the addition of environmental stressors and other pathogens may result in
the manifestation of clinical disease. There is the possibility that different strains of
the virus determine the ability to produce clinical disease, but this has not been proven.
Therapy for acute BVDV infection is non-specific. Depending o n the severity of
disease, hydration should be maintained with oral or IV fluids and electrolytes.
Antimicrobial therapy m a y be considered in the presence of or for the prevention
of secondary bacterial infections. Because the virus can cause immunosuppression,
treatment with corticosteroids would be contraindicated but non-steroidal anti­
inflammatories would be a therapeutic consideration.
Venereal infections
Semen from bulls persistently infected with BVDV contains virus which is infective
to susceptible cows (6, 18, 44, 47). Semen from immunocompetent bulls undergoing
acute BVDV infection may be transiently infected (55, 91). Acceptable semen quality
and fertility has been reported for persistently infected bulls (6), although semen quality
may be affected in both persistently infected and acutely infected bulls and is charac­
terised by decreased motility and morphologic abnormalities (44, 55, 71). Significantly
reduced conception rates have been observed in seronegative cattle exposed to the virus
at the time of breeding, by serving cows with persistently infected bulls (44) and experi­
mentally by intra-uterine administration of BVDV (2, 3, 24, 92). Seronegative cows
inseminated with infective semen generally fail to conceive until they develop an immune
response to the virus (44). However, a recent report indicated that twelve seronegative
heifers inseminated with semen from a persistently infected bull all conceived, seroconverted
and gave birth to normal appearing calves, although one calf was persistently infected
with BVDV (47). The risk of venereal infection with BVDV appears to be highest with
natural service (24). Bovine virus diarrhoea virus does not appear to inhibit conception
of either seropositive or seronegative cattle when inoculated by an oral or intranasal
route or infused into the uterus of a seropositive cow at the time of breeding (92). The
adverse effect of this virus on conception is attributed to fertilisation failure (24).
Thus, BVDV may cause a herd problem characterised by repeat breeding if the
infection is by the venereal route in seronegative cows. The most notable finding would
be an increase in the number of services per conception. Such a problem will be transient
in nature (until an immune response occurs), and it may be difficult to incriminate BVDV
if there are no other concurrent signs of infection in the herd.
BVDV has been associated with ovaritis in infertile heifers (81). It was possible to
re-isolate BVDV from the ovaries many months after they had seroconverted with no
evidence of persistent viraemia. BVDV has also been incriminated in a disease similar
in appearance to pustular vulvovaginitis caused by infectious bovine rhinotracheitis virus
(1, 83). Pustular lesions have been described in the area of the vulva and vagina and
have been associated with pruritus.
Immunosuppression
The topic of BVDV-induced immunosuppression has recently been reviewed (60) and
is covered in detail elsewhere in this volume. In light of the current understanding
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of the pathogenesis of mucosal disease there m a y be a tendency to decrease the
importance of the role of BVDV in causing disease in immunocompetent, seronegative
cattle. Although the predominance of evidence indicates that most infections in such
cattle result in subclinical or mild disease, there is potential for more severe disease
because of immunosuppressive effects of the virus. T h u s , BVDV infection m a y
potentiate or enhance the pathogenicity of co-infecting pathogens, such as
parainfluenza virus type 3, infectious bovine rhinotracheitis virus, Coronavirus,
rotavirus, Pasteurella spp., Salmonella s p p . , Actinomyces pyogenes, coccidia and
helminths (1, 4, 60). Whether immunosuppression, induced by BVDV infection, leads
to the development of disease, it is undoubtedly tied to the complex interactions
between host, environment and infectious agents. If management and environmental
conditions are suboptimal and animals are in contact with a variety of potential
pathogens, BVDV m a y enhance development of a secondary disease. Even modified
live BVDV vaccines have been demonstrated to be immunosuppressive (76). Although
the use of such vaccines in unstressed, well managed cattle herds m a y pose only a
small risk, their use under some conditions (e.g. entry to a feedlot of recently weaned,
comingled, transported or otherwise stressed calves) m a y be ill-advised.
The nature of immunosuppression may differ depending on the form of BVDV
infection which the animal is undergoing. T h u s , the immunosuppression associated
with acute BVDV infection appears to be different from that described for cattle
persistently infected with BVDV. Possibly another form of immunosuppression is
associated with acute and chronic mucosal disease.
BVDV infection in neonatal calves
The importance of BVDV as a cause of neonatal calf disease has been controversial.
In light of the current understanding of the pathogenesis of BVDV infections' and
its association with the occurrence of persistently infected calves, the role of this virus
in calfhood diseases needs to be reevaluated. Calves b o r n persistently infected with
BVDV (discussed below) m a y have poor viability and succumb to early disease and
death (22). Disease in these persistently infected calves may be manifested as
pneumonia and enteritis (5, 90). Thus, it becomes important to know if calves
experiencing enteritis and p n e u m o n i a in association with BVDV are persistently
infected or are immunocompetent and undergoing an acute infection. This information
is not available in earlier reports, making it difficult to determine the importance
of acute BVDV infection in immunocompetent calves.
In general, BVDV is considered rarely to cause disease in immunocompetent calves
less t h a n six m o n t h s of age but it has been associated with and m a y contribute to
outbreaks of pneumonia and enteritis (65, 84, 87). Fetuses may become infected during
later stages of gestation or calves m a y become infected in the neonatal period and
m a y develop severe enteritis which is sometimes fatal (1). Fatal enteritis has been
experimentally produced in both colostrum-fed as well as colostrum-deprived neonatal
calves (38). In older colostrum-fed calves (4-6 months), experimental infection resulted
in mild clinical disease with rapid recovery (51). It has been suggested that BVDV
may have a major role in neonatal calf diarrhoea (37, 38) but this contention has
not been well substantiated. There is some field and experimental evidence that when
present with other infective agents, BVDV can increase the severity of neonatal
diarrhoea (89).
Passively acquired antibody in calves appears to provide protection against b o t h
systemic and respiratory infections with BVDV (27, 29, 80). Passively derived antibody
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declines to undetectable levels between 105 and 230 days, but with initial high
concentrations, antibody m a y persist u p to 398 days (19). After decay of passively
acquired antibody, titres increase following natural exposure and infection (36).
BVDV m a y have an important role in neonatal diseases of calves in the event of
failure or partial failure of passive transfer of antibody, because of the suppressive
effects of the virus on the calf's i m m u n e system. Such a problem m a y be overcome
in a herd t h r o u g h immunisation programmes in d a m s , followed by appropriate
measures to ensure adequate intake of quality colostrum.
BVDV and bovine respiratory disease
It has been controversial whether BVDV has a role, and if so, to what extent it
is involved in bovine respiratory disease. A recent review concluded that the existing
published literature failed to support the contention that BVDV has a role in the
pathogenesis of undifferentiated bovine respiratory disease (67). A l t h o u g h evidence
is only circumstantial, BVDV m a y have a role in bovine respiratory disease because
of its immunosuppressive effects on the host. T h e majority of research focusing on
viral-bacterial synergism in bovine respiratory disease has dealt with infectious bovine
rhinotracheitis virus and parainfluenza virus type 3 (94) and BVDV virus has not
been as well studied in this regard. There still remains evidence that is suggestive of
a role for BVDV in bovine respiratory disease (29, 30, 59, 69, 70, 85, 87). Despite
the fact t h a t BVDV is generally considered to be lymphotrophic and enterotrophic,
it has been identified in outbreaks of respiratory disease, usually in association with
other pathogens. In one study BVDV was the virus most often isolated from
pneumonic lungs in cases of shipping fever in feedlot cattle and was usually found
in association with Pasteurella haemolytica (70). A recent study reported BVDV to
be the most frequent virus found in association with multiple virus infection in
outbreaks of respiratory disease in calves (72). A seroepidemiologic study
demonstrated an association between antibody titres to BVDV (as well as other viruses)
and the treatment of respiratory disease (42). These findings suggest that BVDV m a y
be involved as an initiator in bovine respiratory disease.
Results of experimental attempts to reproduce respiratory disease with BVDV have
been variable. In several studies, experimental infection of calves with BVDV has
only resulted in mild interstitial p n e u m o n i a (48, 58). W h e n BVDV was administered
by aerosol exposure there was n o effect of the virus on the m e a n clearance rate of
Pasteurella haemolytica from the lung (41). In another study a synergistic association
between BVDV and P. haemolytica was demonstrated (63). Experimentally, initial
infection with BVDV impairs the ability of calves to clear infectious bovine
rhinotracheitis virus from the lung and to contain it at the infection site (62). Strains
of BVDV m a y differ in their pneumopathogenicity. In one study, cytopathic and noncytopathic strains caused respiratory tract disease when followed by inoculation with
P. haemolytica, but the cytopathic strain was associated with more severe disease (61).
In conclusion, there is data suggestive of BVDV having a role in bovine respiratory
disease, b u t further research is needed to document this contention. Such research
should include further experimental studies as well as epidemiologic field studies.
CONGENITAL
INFECTIONS
BVDV infection in an immunocompetent pregnant heifer or cow would be similar
to that described under subclinical infections and B V D . T h e m a i n importance of
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BVDV infection during pregnancy is the outcome if transplacental spread of the virus
to the conceptus occurs. Transplacental infection appears to be a probable event and
occurs with remarkable efficiency if the d a m undergoes an acute infection during
pregnancy or is persistently infected (22, 73). The main determinant of fetal response
is the gestational age of the fetus at the time of infection (74) and the most serious
consequences follow exposure during early gestation. The possible outcomes include
fetal resorption, abortion, mummification, congenital malformations and the birth
of calves weak and undersized, calves persistently infected with BVDV or normal
calves seropositive to the virus (Fig. 1).
BVDV
Abortion, stillbirths, fetal resorption,
mummification
Congenital malformations
Birth of weak, undersized calves
Persistently infected calves
Normal calves
FIG. 1
Possible outcomes of fetal infection
with bovine virus diarrhoea virus
Fetal abortion, stillbirths and mummification
BVDV does not appear to be a major cause of early embryonic death (64, 92)
but fetal infection from 50 to 100 days of gestation may result in fetal death followed
by abortion, stillbirth or mummification (17, 2 1 , 22, 32, 35, 83). Expulsion of the
fetus may occur u p to several m o n t h s after infection (34). The overall incidence of
abortion caused by BVDV appears to be low (2-7%) but in non-immune herds a higher
percentage m a y be encountered ( 1 , 23, 33, 83).
Diagnosis of abortion induced by BVDV is complicated by several factors.
Transplacental infections do not always cause abortion, therefore demonstration of
virus, viral antigen or specific antibody from an aborted fetus does not necessarily
mean the cause was BVDV. Paired serotesting of the d a m m a y be unsuccessful in
diagnosis because antibody titre may have already increased at the time of the abortion.
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Congenital defects
Infection of the fetus between approximately 100 to 150 days of gestation can
result in a variety of congenital defects (22). This period of development involves
the final stages of organogenesis of the nervous system as well as the development
of the fetal ability to m o u n t an inflammatory response. Infection during this period
may result in damage and destruction of stem cells, resulting in congenital defects
at birth. T h e teratogenic lesions recognised in association with fetal BVDV infection
have been described and are summarised in Table II (11, 12, 13, 17, 2 1 , 22, 32, 52,
66, 74, 83, 88, 93). It should also be noted that modified live BVDV vaccines when
administered to susceptible pregnant cows can cause fetal infections with the
development of congenital defects.
T A B L E II
Congenital defects associated with transplacental infection
of the fetus with BVDV
Nervous system
Microencephalopathy
Cerebellar hypoplasia
Hydranencephaly
Porencephaly
Hydrocephalus
Hypomyelinogenesis
Eye
Retinal atrophy
Optic neuritis
Cataract
Microphthalmia
Retinal dysplasia
Immune system
Thymic aplasia
Integumentary system
Hypotrichosis
Alopecia
Musculoskeletal
Brachygnathism
Growth retardation
Arthrogryposis
Respiratory system
Pulmonary hypoplasia
Calves b o r n with cerebellar hypoplasia are reluctant to stand and can only do
so with great difficulty. They have a wide base stance and are ataxic. T r e m o r is
associated with calves born with hypomyelinogenesis and is present at birth. Congenital
defect of the eye m a y result in varying degrees of blindness. Cataracts are readily
apparent u p o n ophthalmic examination. Transplacental infection with BVDV m a y
also result in retardation of fetal growth (21, 22). This is manifested by the birth
of weak, undersized calves which m a y die shortly after birth.
Normal calves born seropositive to BVDV
Infection with BVDV in the later stages of gestation, after the development of
immunocompetence, rarely causes congenital malformations. Calves m a y be
normal at birth and have neutralising antibodies to BVDV (17, 49, 53). If these
antibodies are t o be detected, serum must be obtained prior to the ingestion of
colostrum.
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Immunotolerance
Infection during early stages of fetal development, prior to the complete maturation
of the immune system, m a y result in immunotolerance to BVDV. These calves are
b o r n persistently infected with BVDV and remain so for life. Immunotolerance and
persistent infection occur naturally and have also been produced experimentally. The
precise stage of fetal development in which infection must occur to cause
immunotolerance is u n k n o w n b u t it is an u n c o m m o n outcome after 100 days of
gestation and can still occur at 125 days (18, 20, 39, 45). Thus far, immunotolerance
and persistent infection appear to be associated only with non-cytopathic strains of
BVDV (8, 43).
CHRONIC BVDV INFECTIONS
Persistent infection with BVDV
The prevalence of persistently infected cattle in the general population is not
precisely defined and there is considerable variation likely between geographical areas
and among individual herds. A study from the United States reports that 1.7 to 1.9%
of cattle in selected herds were persistently infected (8). The frequency of persistent
infection is probably overestimated in that the survey was not r a n d o m and several
of the herds were selected because of a history of BVDV infection. A study in Denmark
revealed that 0 . 9 % of healthy cattle at slaughter were viraemic, but it was not
determined if these animals were transiently or persistently infected (46). In the United
Kingdom, a prevalence of 0 . 8 % was reported for viraemia and 0.4% for persistent
infection (28) and similar findings have been reported from Germany (57). In herds
with a history of recent BVDV outbreaks, higher prevalences for viraemia and
persistent infection have been reported (46, 79).
Cattle immunotolerant and persistently infected with BVDV are viraemic,
constantly shed virus into the environment, have n o or low concentrations of specific
neutralising antibodies (with the exception of persistently infected calves that have
ingested colostrum containing specific BVDV antibody) and may appear healthy (5,
18, 20). Although persistently infected cattle are immunotolerant to BVDV, they are
immunocompetent with respect to other antigens (45). Immunotolerance appears to
be specific to the infecting non-cytopathic strain of BVDV in that persistently infected
cattle are capable of an immune response to heterologous strains (9, 10, 82). In spite
of this antibody response the persistently infecting virus continues to infect the host.
F r o m an epidemiologic standpoint, persistently infected cattle are an important
source of viral transmission to susceptible animals. Persistently infected cattle are
efficient transmitters, shed large quantities of virus into the environment over
prolonged periods of time and the spread to susceptible cattle in contact is rapid (22,
73). It appears likely that persistent infection is the major mechanism by which the
virus persists in the cattle population. If persistently infected females reach breeding
age, offspring will be persistently infected (44, 86). Affected families may thus develop
and provide a means to maintain the virus in a herd (40).
Persistently infected, immunotolerant cattle are at risk for development of mucosal
disease if superinfection with a cytopathic strain occurs (discussed under mucosal
disease). In addition to mucosal disease, persistently infected calves appear to be at
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risk to other diseases, although the pathogenesis has not been defined. Persistently
infected calves m a y have a death rate of 5 0 % in the first year of life (22) and m a y
be smaller at birth, have a slower rate of growth and m a y die or be culled from the
herd for being a " p o o r d o e r " . In one study there was a significantly higher death
rate a m o n g calves b o r n to cows k n o w n to be infected with BVDV while pregnant
than those of seropositive dams (5). Persistently infected calves m a y be predisposed
to infection by other micro-organisms which are manifested most often as enteritis
and pneumonia (5, 90). Immunosuppression has been reported in persistently infected
calves (60, 75, 77), which m a y account for the increased susceptibility to diseases
such as enteritis and pneumonia. Subclinical disease in the form of glomerulonephritis
and encephalitis has been described in persistently infected, b u t otherwise n o r m a l
appearing cattle (20).
MUCOSAL DISEASE
Mucosal disease is a sporadic form of BVDV infection in cattle generally between
the age of six m o n t h s and two years. T h e disease is characterised by severe clinical
signs, low morbidity and high case fatality. Recent studies have indicated that mucosal
disease occurs when cattle that are immunotolerant and viraemic with non-cytopathic
virus, become superinfected with a cytopathic strain of BVDV which shares close
homology with the persistently infecting non-cytopathic strain (9, 15, 43). Pathogenesis
of mucosal disease is discussed in detail elsewhere in this volume.
T h e clinical signs, clinical pathology a n d post-mortem findings associated with
the acute and chronic form of mucosal disease have been described ( 1 , 4, 7, 14, 22,
23, 26, 3 1 , 34, 50, 56, 66, 78, 83) and the following descriptions have been derived
from these references.
Acute mucosal disease
As previously mentioned, acute mucosal disease is a sporadic form of BVDV
infection and generally involves cattle ranging in age from six m o n t h s t o
two years. Usually less t h a n 5 % of the herd is affected but case fatality rate
approaches 1 0 0 % . Occasionally epizootics m a y involve u p to 2 5 % of the animals
in a herd.
Acute mucosal disease is characterised by pyrexia (40.5 t o 41 °C), depression,
weakness and anorexia. H e a r t and respiratory rate are elevated (polypnea and
tachycardia). Emaciation a n d dehydration with acidosis develop as the disease
progresses. In lactating cattle, milk production decreases.
Careful examination of the oral cavity m a y reveal erosive lesions involving the
lips, gingival margins, tongue, dental p a d , commissures of the m o u t h and posterior
part of the h a r d palate. Lesions m a y coalesce t o form large areas of necrosis and
sloughing in the oral cavity. Erosive lesions can develop o n the external nares a n d
in the nasal cavity and there are reports of similar lesions on the vulva a n d teats.
Blunting of oral papillae m a y develop.
Ptyalism (salivation) often accompanies the oral lesions which are generally found
in 75 to 8 0 % of the cases. Mucopurulent nasal discharge is often observed, with
lacrimation a n d corneal oedema being sometimes observed.
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Lameness, reluctance to move and recumbency m a y be seen, and these are
attributable to erosive lesions and necrosis of skin in the interdigital cleft. Laminitis
and coronitis m a y also be observed.
Profuse watery diarrhoea generally develops two to three days after the onset of
clinical signs, but in peracute cases death m a y occur prior to the onset of diarrhoea.
Faeces are foul-smelling and may contain variable amounts of fresh or clotted blood.
Fibrinous intestinal casts may be passed. Straining at defecation is often observed.
Ruminations are decreased and mild to moderate bloat m a y develop.
Severe leukopenia m a y be recognised in the early stages of disease. Neutropenia
without a left shift, lymphopenia and thrombocytopenia m a y develop. Secondary
bacterial infections are c o m m o n . Death m a y occur in the acute phase of the disease,
but more frequently takes place at three to ten days after onset of signs.
The distribution of lesions in mucosal disease relates
necrotising effects of BVDV o n epithelial tissues of
integument and respiratory tract. The virus also has an
of vessels, particularly in the intestines and lymphoid
to the affinity for and direct
the gastro-intestinal tract,
affinity for endothelial cells
tissue.
Post-mortem findings include erosions throughout the alimentary tract, commonly
in the oesophagus, ruminai pillars, o m a s u m , a b o m a s u m and intestines. Ruminai
papillae may be reduced in size. The pyloric portion of the a b o m a s u m is oedematous
and haemorrhagic. Bowel contents are dark, watery and foul-smelling. Catarrhal
enteritis may progress to include haemorrhage, erosions and ulcers of the intestinal
mucosa. Peyer's patches often are swollen, necrotic and haemorrhagic. The mucosa
of the large intestines may be congested often in a " s t r i p p i n g " pattern which follows
the mucosal folds.
Histologic examination reveals varying degrees of necrosis in the germinal centers
of lymph nodes and spleen. Oedema and inflammatory cell infiltration is seen in
varying degrees throughout the gastro-intestinal tract.
Chronic mucosal disease
A small proportion of cattle that develop mucosal disease do not die in the expected
time frame and become chronically affected. These cases have been referred to as
chronic BVD, but chronic mucosal disease is a more descriptive term and possibly
more accurate with respect to pathogenesis. T h e pathogenesis of chronic mucosal
disease has not been defined, but it may share similarities with that of acute mucosal
disease. As in acute mucosal disease, both non-cytopathic and cytopathic virus have
been isolated (43). It has been suggested that the differences in antigenicity of the
superinfecting cytopathic virus may give rise to different clinical responses in the
persistently infected animal (16). One extreme may be acute mucosal disease when
the superinfecting virus shares close homology with the persistently infecting noncytopathic strain. The other extreme is no clinical disease, but seroconversion occurring
when the superinfecting virus is a heterologous strain. Between these two extremes
may be the clinical entity described as chronic mucosal disease. Perhaps another form
of mucosal disease exists from which recovery is possible.
Chronic mucosal disease is characterised by inappetence, weight loss, progressive
emaciation and an overall unthrifty appearance. Diarrhoea may be continual or
intermittent. Chronic bloat may be observed. Nasal discharge and persistent ocular
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discharge are frequent findings. Areas of alopecia and hyperkeratinisation may develop,
usually on the neck. Chronic erosive lesions often are found in the mouth and involving
the skin. Areas of the skin most often affected include the perineal area, prepucial
opening, vulva, s k i n / h o r n junction, around the dewclaws, interdigital cleft and the
heels. The failure of skin lesions to heal is an important finding in chronic cases of
mucosal disease. Chronic lameness m a y develop because of laminitis, interdigital
necrosis and hoof deformities. Secondary bacterial infections are c o m m o n . Chronic
pancytopenia is characterised by anaemia, leukopenia, neutropenia and lymphopenia.
Cattle with chronic mucosal disease m a y survive u p to 18 m o n t h s and ultimately
die from severe debilitation. They should be distinguished from calves born persistently
infected, which are unthrifty and " p o o r d o e r s " from birth. Such calves m a y potentially
develop mucosal disease but, as previously discussed, may succumb to other infections
in which case the signs and lesions of mucosal disease would n o t be present.
Treatment of either form of mucosal disease is u n w a r r a n t e d . A l t h o u g h
immunomodulating drugs have sometimes been used in treatment of chronic mucosal
disease, it is unlikely that these drugs will have any long-term effect. A diagnosis
should be m a d e as rapidly as possible and the affected animal should be removed
from the herd. Testing of the herd is then indicated to determine the presence of other
persistently infected cattle which should also be removed.
*
* *
ASPECTS CLINIQUES DE L'INFECTION PAR LE VIRUS DE LA DIARRHÉE VIRALE
BOVINE. - J.C. Baker.
Résumé : L'infection des bovins par le virus de la diarrhée virale bovine (virus
BVD) se traduit par une grande variété de manifestations cliniques. Cet article
passe en revue les réponses cliniques associées au virus BVD et étudie ces maladies
sous les rubriques suivantes : infection aiguë des bovins immunocompétents,
infection du fœtus, infection des bovins immunotolérants et infectés de manière
persistante par le virus BVD et, enfin, maladie des muqueuses.
MOTS-CLÉS : Avortements - Diarrhée virale bovine - Immunosuppression Immunotolérance - Infection aiguë - Infection persistante - Infections
congénitales - Maladie des muqueuses aiguë - Maladie des muqueuses
chronique - Malformations congénitales - Virus de la diarrhée virale bovine.
*
* *
ASPECTOS CLÍNICOS DE LA INFECCIÓN POR VIRUS DE LA DIARREA VIRAL
BOVINA. - J.C. Baker.
Resumen: La infección de bovinos por virus de la diarrea viral bovina (virus
BVD) da lugar a gran cantidad de manifestaciones clínicas. Este artículo pasa
revista a las respuestas clínicas asociadas al virus BVD y estudia estas
enfermedades según la clasificación siguiente: infección aguda de los bovinos
inmunocompetentes,
infección del feto, infección de los bovinos
inmunotolerantes e infectados de manera persistente por el virus BVD y, por
último, enfermedad mucosa.
36
P A L A B R A S CLAVE: Abortos - Diarrea viral bovina - Enfermedad mucosa
aguda - Enfermedad mucosa crónica - Infección aguda - Infección persistente Infecciones congénitas - Inmunosupresión - Inmunotolerancia - Malformaciones
congénitas - Virus de la diarrea viral bovina.
*
* *
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