Infectious Bovine Rhinotracheitis

15 Pages·2002·0.37 MB·English

Int.J.Curr.Microbiol.App.Sci (2015) 4(10): 844-858
ISSN: 2319-7706 Volume 4 Number 10 (2015) pp. 844-858
http://www.ijcmas.com
Review Article
Infectious Bovine Rhinotracheitis: An Indian Perspective
Saurabh Majumder1*, MA Ramakrishnan2 and S Nandi3
1Division of Virology, IVRI, Izatnagar, India
2Division of Virology, IVRI, Mukteswar, Uttarakhand, India
3Virology Section, CADRAD, IVRI, Izatnagar, India
*Corresponding author
A B S T R A C T
Livestock plays an important role in welfare of rural population of India and its
economy. It contributes 9% of GDP and employs 8% labor force of the country.
However, there are several infectious and non-infectious diseases, which causes
colossal economic losses to the country. Among cattle diseases, IBR is one of the
most important diseases that cause various form of clinical disease. IBR caused by
Keywords BoHV1, is a disease of domestic and wild cattle. BoHV1 is a member of the genus
Varicellovirus in the subfamily Alphaherpesvirinae, family Herpesviridae and
BoHV1, order Herpesvirales. Based on restriction endonuclease fingerprinting, BoHV1 is
IBR, classified into three subtypes, namely, BoHV1.1, BoHV1.2a and BoHV1.2b. Most
Glycoprotein, BoHV1.1 strains have been isolated from respiratory tract diseases or abortion
IPV cases and BoHV-1.2 strains from lesions of genital organs. Subtypes 1.1 and 1.2a
have been associated with severe diseases including infection of the foetus and
abortion and BoHV1.2b strains are generally involved in mild rhinitis or vaginitis.
BoHV1 infection occurs in all continents and is responsible for the significant
losses resulting from disease and trade restriction.
Introduction
suddenly and was characterized by high
The first report of disease caused by BoHV1
fever and agalactia in addition to respiratory
was made as a venereal disease in a bull and
signs. The following year, Miller (1955)
contact cows (Rychner, 1841) which was
described a disease that was first seen in a
subsequently referred to as
Colorado feedlot in the fall of 1950 and
Blaschenausschlag in German literature.
which has been present in that state ever
The viral aetiology of the disease was
since. By 1954 it was occurring in dairy
proved by Reisinger and Reimann (1928).
cattle and all ages of beef cattle both in
The first published report on respiratory IBR
feedlots and occasionally in cattle on
came from Schroeder and Moys (1954)
pasture. The actual cause was undetermined
where they described an apparently new
at that time, but the disease could be
upper respiratory disease of dairy cattle that
transmitted with tissues and exudates from
occurred in California in 1953. It appeared
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natural cases (Schroeder and Moys, 1954). 1963).Wiseman et al. (1979) concluded that
The disease was known as red nose , the losses were due to market value of fatal
necrotic rhinitis or dust pneumonia . In and culled cases, feeding cost for 1-6 wk
the year 1955, at a meeting of the US when fattening cattle did not put on weight,
livestock sanitary association, the accepted treatment cost and value of lost milk
name for the disease became infectious production. In large milking herds, the
bovine rhinotracheitis (Mckercher et al., losses varying from $ 25- $ 55/cow were
1957). estimated (Townley, 1971). In another
study, it has been shown that American
Madin et al. (1956) first isolated the livestock owners experience a loss of quarter
causative agent, and it was further of a billion dollar each year due to BoHV1
characterized by Tousimis et al. (1958). infection. Schroeder and Moys (1954)
Armstrong et al. (1961) suggested that the estimated heavy losses due to IBR in USA
IBR virus (BoHV1) belongs to the and 100% loss due to IBR was reported in
herpesvirus group. The virus was first Hungary (Bartha et al., 1974). Townley,
isolated from respiratory disease in the (1971) reported 30% morbidity and loss of $
United Kingdom in the early 1960 s 500 in an acute outbreak of respiratory form
(Darbyshire et al., 1964). Kendrick et al. of IBR in dairy herd. In India, no such
(1958) described its association with estimates have been made till date, but the
infectious pustular vulvovaginitis (IPV). epidemiological surveys indicate a
Huck et al., (1971) described its association substantial loss due to the disease. Morbidity
with panposthitis. The virus has been rate of 90% and mortality rate of 30% was
reported to be associated with infection of recorded in an outbreak of nervous form of
respiratory tract causing rhinotracheitis and disease in Australia (Gardiner et al., 1964).
conjunctivitis; reproductive tract causing Conception rate fall down from 80% to 45-
vulvovaginitis and balanoposthitis, skin 50% in majority of cows suffering from
lesions as well as neonatal infection causing herpes vulvovaginitis which are artificially
red nose, necrotic rhinitis, epididymitis, inseminated (Laveso et al., 1984). BoHV1 is
abortion, infertility, dermatitis and mastitis responsible for significant losses incurred by
(Gibbs and Rweyemamu, 1977 and Kahrs, disease and treading restriction in cattle
1977). industry.
Economic importance Disease status in India
IBR is not a highly fatal disease but it can In India, IBR/IPV is one of the endemic
cause considerable economic losses due to diseases of cattle resulting from cross-
abortion, loss of body condition, milk yield, breeding programme. The disease was first
loss of new born calves, temporary failure of reported by Mehrotra et al. (1976) who
conception, insufficient feed conversion, isolated IBR virus from cases of
secondary bacterial pneumonia and cost of keratoconjunctivitis amongst crossbred
treatment. Morbidity and mortality rates calves at an organized cattle herd in Uttar
vary considerably and were lower in dairy Pradesh. Since then the disease has been
herds (8% morbidity and 3% mortality) than reported in most of the states of India. The
in beef cattle, in feed lots in which the disease was found to be more prevalent in
mortality rate was usually 20-30% and exotic and crossbred cattle than in
rarely up to 100 (Barenfus et al., indigenous breeds. Mallick (1986) studied
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the seroprevalence of IBR disease in seven inconstant cattle serum using indirect
states and observed that 65.3% exotic, 73% ELISA kit and found an incidence rate of
crossbred and 62% indigenous cattles were 73.40% and 37.78% respectively. In
seropositive. Since then, several addition to that while indigenous crossbred,
seroprevalence studies have been carried out exotic cattle and buffaloes showed an
by different researchers and it was seen that incidence rate of 55.50%, 76.70% and
the disease is prevalent in almost all the 50.50%, respectively with a history of
states of India. The disease has been abortion, the in-contact animals showed an
recorded from states of Kerala (Sulochana et incidence rate of 40%, 36%, 66.70% and
al., 1982), Gujurat (Singh et al., 1983), 30%, respectively. Pandita and Srivastava
Tamil Nadu (Manickam and Mohan, 1987), (1995) studied the efficacy of dot ELISA
Uttar Pradesh (Mehrotra, 1977), Orissa and plate ELISA with 239 bovine serum
(Misra and Misra, 1987), Karnatak (Mohan samples from Haryana against IBR antibody
Kumar et al., 1994), West Bengal (Ganguly and 51.9% and 48.5% were positive by plate
et al., 2008) and Andhra Pradesh ELISA and dot ELISA respectively.
(Satyanarayana and Suri Babu, 1987). An
outbreak of balanoposthitis was reported Virology
from A.I. centre in U.P. (Pandey et al.,
2000). The etiological agent for IBR was first
isolated by Madin et al. (1956) and
An 8.56% of serum samples from Tamil classified subsequently as a herpesvirus and
Nadu and Andhra Pradesh were found to be BoHV1 (Tousimis et al., 1958 and
positive for IBR (Selvaraj et al., 2008). In a Armstrong et al., 1961). It belongs to
seroprevalence study carried out in three family- Herpesviridae, sub family-
south Indian states by Renukaradhya et al. Alphaherpesvirinae and genus-
(1996), 50.9% cattle and 52.5% buffalo Varicellovirus. Bovine herpesvirus 1
were found positive to BoHV1. In Gujarat, (BoHV1) is the official species name of the
Patel (1983) reported that 24 out of 32 virus. Gibbs and Rweyemamu (1977) stated
paired sera of aborted buffaloes were that the term BoHV1 refers to all virus
positive for IBR antibodies. Khan (2004) isolates that are serologically related to
from Gujarat reported 21.30% IBRV and IPVV. By DNA restriction
seroprevalence of IBR in cattle and enzyme analysis, it can be divided into
buffaloes. Seroprevalence of BoHV1 is also BoHV1.1 and BoHV1.2. Conventional
reported in yaks (Nandi and Kumar, 2010) serological assays cannot distinguish
and mithuns (Rajkhowa et al., 2004) with an between immune responses induced by
overall seroprevalence of 60.1% and 19%, BoHV1.1 from those induced by BoHV1.2.
respectively. An 32.34% seropositivity was BoHV1.1 and BoHV1.2 cause IBR and IPV,
observed in bulls by Singh et al. (1986). respectively. BoHV1.2 may be less virulent
Deka et al. (2005) observed 45.09% than BoHV1.1. BoHV1.2 can be further
seropositivity in breeding bulls and detected subdivided into BoHV1.2a and BoHV1.2b.
presence of virus in semen by isolation and BoHV1.2a causes IPV in cows and IPB in
PCR methods. The seroprevalence in bulls (Edwards et al., 1990) where as
buffalos varied from 2.75-81% (Sinha et al., BoHV1.2b is less virulent compared to the
2003). Pandita and Srivastava (1993) carried earlier one (Metzler et al., 1985). Sequence
serological survey against IBR with 94 homology between BoHV1.1 and 1.2 is
serum samples from aborted cows and 135 more than 95% (Engels et al., 1986).
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BoHV1 has an icosahedral nucleocapsid of °C within 10 days and at 22 °C within 50
95-110 nm in diameter (Armstrong et al., days (Gibbs and Rweyemamu, 1977). It may
1961 and Cruickshank et al., 1963) survive more than 30 days in feed. Virus is
consisting of 162 capsomeres each 12 nm sensitive to organic solvents such as
long and 11.5 nm wide with an axial hole of chloroform ether and acetone. It gets
3.6 nm. Nucleocapsid is surrounded by an inactivated by 0.5% NaOH, 0.01% HgCl2,
electron dense zone called tegument 1% Chlorinated lime, 1% phenolic
(Valícek and Smíd, 1976) and a lipid bilayer derivatives, 1% quaternary ammonium bases
envelope forming pleomorphic virion of and 10% Lugols iodine. Formalin (5%)
150-200 nm indiameter (Armstrong et al., inactivates the virus within 1 min (Straub,
1961). DNA is wrapped around a fibrous 1990).
spool like core, whose fibers are anchored to
the inner side of surrounding capsid. The BoHV1 Genes and their encoded proteins
virion possesses haemagglutinin activity
which is coded by a 90 kDa glycoprotein BoHV1 genome is believed to encode
(Trepanier et al., 1985). approximately 70 proteins. Electrophoretic
analysis of radiolabelled virions by
There is only one antigenic type irrespective SDSPAGE has revealed 33 structural
of whether the isolate is derived from cases proteins (Misra et al., 1981), among these 13
of IBR or IPV. The virus has a single linear are shown to be associated with viral
molecule of double stranded DNA envelope, 14 with nucleocapsid and 6 not
approximately 135-140 kbp (Wyler et al., classified. Other than these 16 non structural
1989). Buoyant density of DNA molecule is proteins are also coded by BoHV1 genome
approximately 1.730 g/mL (Russell and (Misra et al., 1981). BoHV1 glycoproteins
Crawford, 1964) and the GC ratio is 72% are homologous in structure and function to
(Plummer et al., 1969). The genome can be HSV1 glycoproteins and they are involved
divided into unique long (UL) and unique in several steps of the viral cycle such as
short (US) segment which are 102-104 kbp attachment, penetration, maturation and
and 10.5-11 kbp long, respectively. The US release of the virus. 10 genes code for
segment is bracketed by inverted internal glycoproteins and among them 6 are present
(IR) and terminal repeat (TR) regions of in UL region i.e. gK (UL53), gC (UL44), gB
approximately 24 kbp (Muylkens, 2006). (UL27), gH (UL22), gM (UL10) and gI
Majority of BoHV1 gene repertoire consists (UL1) and 4 are in Us region i.e. gG (US4),
of ORF homologous to other gD (US6), gI (US7), gE (US8). gP, gI and
alphaherpesviruses. Entire gene of BoHV1 gE possess the Fc receptor and binds with
has been sequenced by international the IgG molecule (Schwyzer and
collaboration in 1995 (Genbank accession Ackermann, 1996). UL49.5 can be
No. AJ004801). considered as a false glycoprotein. Indeed
the protein coded by UL49.5 is not
Virus is quite resistant to environmental glycosylated in BoHV1 while in other
influence. Inactivation depends on factors alphaherpesviruses it is glycosylated and is
such as temperature, pH, light, humidity, known as gN. It has conserved function and
and kind of medium harbouring the virus forms disulphide linked hetero duplex
(Gibbs and Rweyemamu, 1977). At 4 °C together with gM. The gC, gD, gE, gG, gI,
virus is stable for 1 month while gets UL49h and thymidine kinase genes are
inactivated at 56 °C within 21 minutes, at 37 involved in viral virulence (Kit et al., 1985;
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Kit et al., 1986; Smith, 1991; Smith et al., decrease in milk yield. Areas of focal
1994). necrosis are evident, often leading to serous
nasal/ocular discharge and conjunctivitis. In
Transmission both genital and respiratory form of disease
there is a focal area of epithelial cell
The virus is mainly transmitted from necrosis in which there is ballooning of
infected animal to uninfected one by contact epithelial cells. Typical herpesvirus
with mucosal droplet. Infectious virus is inclusions may be present in nucleus of
nasally shed for 10 14 days during acute periphery of necrotic foci. There is intense
respiratory infection (Gibbs and inflammatory response within the inflamed
Rweyemamu, 1977). Airborne transmission mucosa frequent with formation of
of BoHV1.1 can occur under experimental overlaying accumulation of fibrin or cellular
conditions at distances of 3.85 m, although debris (pseudomembrane). Gross lesions are
this is probably not a major route of not frequent in aborted foetus but micro
transmission (Wentink et al., 1993) and is necrotic foci are present in tissues. Liver and
dependent upon environmental temperature adrenal are affected most. It may lead to
and relative humidity (Mars et al., 1999). It secondary bacterial infection contributing to
can be mechanically transmitted between the complex syndrome called shipping fever
bulls in AI centres and virus may also be (Bovine respiratory disease complex) and
spread by artificial insemination (Van culminates in severe pneumonia caused by
Engelenburg et al., 1995) and it is the main Mannheimia haemolytica.
route of infection of the virus causing IPV.
Semen not only spread the disease but also Latency
associated with reduced fertility and
abnormal fetal development (Wyler et al., The BoHV1 causes latent infection in
1989) As the virus causes latent infection immunoprivileged sites following
animal infected once carry the virus silently productive viral infection (Rock et al., 1987;
and under some stressful conditions, shed Rock et al., 1992 and OIE 2000). Latency
the virus and infect the healthy animals of usually occurs in the body of the trigeminal
the herd. and sacral ganglia but may also occur in
tonsillar lymphoid cells and peripheral blood
Pathogenesis lymphocytes (Mweene et al., 1996). Latent
virus only produces latency-related proteins,
Virus enters through aerosol route or by which protect latently infected cells from
direct contact with the nasal secretion in apoptosis (Schang et al., 1996). Infectious
case of respiratory tract infection and by virus is not present during latent infection
direct contact or by semen containing virus (Engels and Ackermann, 1996). After
(coitus or AI) in case of genital infection. primary infection the viral capsid together
Within animal, BoHV1 is transported by with tegument are transported retrogradely
monocytes and white blood cells to target to the ophthalmic and maxillary branches of
organs. BoHV1 replicates in the nasal and the trigeminal nerve located in the
ocular epithelia during primary infection of nasopharynx and eye (respiratory tract
the respiratory tract andthen, 2-3 days post infection) or the sacral ganglia (genital tract
exposure animal develop a fever with infection) where the virus establishes a
subsequent increase in respiratory rate and lifelong latent infection. The episomal form
inappetance and in dairy cattle there is of viralgenomic DNA, transcripts
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originating from the latency-related gene Clinical signs and symptoms
(LR gene) and proteins encoded by the
latency-related gene can be detected in Incubation period of the disease varies from
trigeminal ganglia during latency (Rock et 10-12 days under natural condition. The
al., 1987). The reactivation of the virus virus mainly affects the respiratory and
occur after stressful condition like genital tracts. The infection of the
transportation, parturition and corticosteroid respiratory tract is known as IBR. It is the
treatment leading to shedding of the virus commonest form of BoHV1 infection. It
and is thought to be responsible for the occurs as a subclinical, mild or clinical
perpetuation and transmission of virus in disease. It is characterized by symptoms like
cattle population (Kutish et al., 1990). In a fever, coughing, anorexia, depression,
study carried out by Thiry et al. (1987) decreased milk production, weight loss,
showed that the stress of transport has been increase respiratory rate nasal and ocular
shown to cause viral reactivation in latently discharge which is serous at beginning and
infected cattle, leading to virus shedding become mucopurulent later and increased
from days 1-4 after the day of transport. salivation may also accompany these
Treatment with corticosteroid is done to respiratory tract problems. Nasal mucosa
eliminatethe carrier bulls from semen becomes hyperaemic and lesion progress
collection station. from pustular necrosis to large haemorrhagic
and ulcerated area covered by cream
Role of BoHV1 in viral bacterial synergy coloured diphtheritic membrane. A nasal
discharge along with nasal congestion may
Pneumonia in cattle has been a liability to develop and is referred to as red nose .
beef producers and consumers as well as a Foul breath, mouth breathing, salivation and
topic of interest and frustration for a deep bronchial cough are common.
veterinary practitioners and researchers over Animal may show the signs of bronchitis
several decades. The most important and pneumonia.
component of this complex is shipping
fever, a fibrinous pneumonia associated with Abortion is a consequence of a respiratory
pathogenic microorganisms and various BoHV1 infection. Following viraemia
stressors, especially transportation. BoHV1 BoHV1crosses the maternal fetal barrier to
is one of the most important causes of produce lethal infection to the foetus. The
respiratory disease complex called shipping route of BoHV1 from placenta to foetus is
fever (Yates, 1982 and Jones and unknown but since viral lesions are
Chowdhury, 2007). Other bacteria and virus consistently observed in fetal liver,
that are involved are BVDV, Bovine haematogenous spread most likely occurs
parainfluenzavirus 3, Bovine respiratory via umbilical vein. In typical BoHV1
syncytial virus, M. haemolytica, P. infection conjunctivitis is a predominant
multocida and Histoplasma somnis (Martin symptom which is either unilateral or
and Bohac, 1986). As a result of virus bilateral and associated with profuse
infection of the upper respiratory tract, lacrimation. Animal show photophobia,
bronchi, lower trachea and lung two epiphora and the hair beneath the eye
important events occur that increase the become heavily soiled. Secondary bacterial
colonization of the lower lung with bacterial infection is common and pus may be seen in
pathogens, leading to the development of the lacrimal discharge. Cornea usually
severe pneumonia (Babiuk et al., 1988). remains unaffected but if secondary
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bacterial infection occurs, keratitis and In the early stages, the histological picture is
corneal ulceration occur with permanent one of mild catarrhal inflammation with an
scaring of cornea (Turin and Russo, 2003). oedematous mucosa containing migrating
In uncomplicated cases symptoms regress neutrophils, a submucosa infiltrated with
within 5-10 days. A second BoHV1 lymphocytes, macrophages, and plasma
syndrome, IPV in the cow or IBP in bulls, cells, and hyperaemia and haemorrhages
causes pustular lesions of the genital tract throughout (Mckercher, 1959 and Gibbs and
and may lead to abortion. IPV is observed 1 Rweyemamu, 1977). With progression,
to 3 days after mating and often leads to there is a variable amount of epithelial
painful inflammation. The first sign of IPV necrosis in which there is ballooning of
are frequent micturition (urination) and epithelial cells (and concomitant loss of cilia
followed later by small pustules (1-2 mm) in cells so endowed) with cellular debris and
on the vulva. Pustules usually coalesce to exudates on the mucosal surface or within
form yellowish fibrinous membrane that lumina of airways, and congestion, oedema,
gradually detaches to form ulcers. Affected neutrophil infiltration, and nodular
animal develops fever, depression and mononuclear cell accumulation in the
anorexia. They avoid contact of tail with lamina propria and submucosa (Mckercher
vulva. Secondary bacterial infections are et al., 1957). Gross lesions are frequently
common and varying amount of pus is not observed in aborted foetuses, but
discharged. Lesions usually heal 10-14 days microscopic necrotic foci are present in most
after the onset of the disease but in some tissues and the liver and adrenal glands are
animals purulent vaginal discharge persists affected most consistently. The gross
for several weeks (Turin and Russo, 2003). pathology in IPV includes hyperaemia of the
Outbreaks of both the respiratory form and vulval and vaginal mucosa with focal
genital disease together are rare. haemorrhages over the lymphocytic follicles
of the submucosa. There is oedema of the
IPB also develops after 1-3 days of vulva with copious mucopurulent discharge.
infection. Lesions similar to that of IPV Small (2 3 mm) yellow coloured pock-like
appear on the penis and prepuce. Sequelae lesions replace the focal haemorrhages over
of this condition include extensive adhesion, the lymphoid follicles. The epithelium over
annular constriction and penile distortions. the lesions is lost and an ulcer is revealed.
Healing occurs in uncomplicated cases The lesions regress within 8 days in
within 10-14 days, but some animal may uncomplicated cases.
lose libido, have painful erection and
ejaculation and require several weeks to Diagnosis
resume normal mating. BoHV1 is also
associated with poor semen quality. The Currently, methods of BoHV1 detection
respiratory tract lesions in IBR are usually used in diagnostic virology laboratories
acute necrotic rhinotracheitis or ne crotizing include virus isolation, examination of
rhinitis, p haryngitis and laryngotracheo tissues by fluorescent antibody technique
bronchitis (Allan et al., 1980). There is (FAT), antigen detection by enzymelinked
serous rhinitis with mucosal hyperaemia Immunosorbent assay (ELISA) and
oedema, mucopurulent exudate, focal areas immunoperoxidase test. Virus isolation in
of necrosis, and finally overlying cell culture is a routinely used technique.
accumulation of fibrin and cellular debris However, cell lines are difficult to maintain,
which leads to pseudomembrane formation. making the process troublesome, slow and
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Int.J.Curr.Microbiol.App.Sci (2015) 4(10): 844-858
costly. The need for the viral particle to be and Southern blot hybridization (Kibenge et
infective is another inconvenience of this al., 1994 and Xia et al.1995) with
technique because in BoHV1 abortion the radioisotope (Kibenge et al., 1994 and Xia
foetus is usually autolysed and rarely is et al., 1995), labelled probes have been
expelled in a fresh state. Immunoperoxidase, applied for the detection of BoHV1 in nasal
immunofluorescence, and enzyme swabs and semen. PCR with Southern blot
immunoassays for antigen detection do not hybridization has been developed as a
require the infectiousness of the viral diagnostic in which 0.01 TCID50/100 l of
particle, but results are compromised if the BoHV1 could be detected in 1:20 diluted
virus is damaged. Thus, lack of adequate bovine semen (Kibenge et al., 1994 and Xia
sample conservation and transportation to et al., 1995). Various PCR assay for the
the laboratory adversely affect the diagnosis. detection of BoHV1 have been described
In recent years, molecular biology has using the primer of gB gene (Vilcek et al.,
contributed to the development of highly 1993a) gC gene (Van engelenburg et al.,
sensitive, new diagnostic approaches. 1993), gD gene (Wiedmann et al., 1993) and
Polymerase chain reaction (PCR) is one of (de Gee et al., 1996) and the thymidine
the molecular techniques that has been kinase (Tk) gene of BoHV1 (Kirkbride,
adopted to detect BoHV1 infection in 1992) with variable sensitivities.
aborted foetus, calves, cows, and in semen
samples (Takiuchi et al., 2005). This Control
technique has been shown to be more
sensitive and specific when compared to Control measures include normal hygienic
other diagnostic methods such as virus measures and maintaining 2-3 weeks of
isolation, immunofluorescence and nucleic quarantine period before introducing new
acid hybridization (Kataria et al., 1997). stock to the herd and precludes of virus
Realtime PCR using primers of glycoprotein positive animals, use of live attenuated or
C gene provides satisfactory reproducibility whole virus vaccines, use of semen from
as well as high specificity and sensitivity, in positive animals. Successful eradication
combination with significant reduction of prompts strict import restriction on cattle,
time for detecting amplified products, semen and embryos because the
making it a valuable alternative to the time reintroduction of the virus into these
and labour consuming virus isolation for immunologically naive populations is likely
detection of BoHV1 in extended semen to have serious consequences and lead to
(OIE, 2010). severe economic loss. Cattle are the primary
reservoir and infection is transmitted during
Recent attention in diagnostic virology has initial clinical disease or from reactivation of
been directed towards the development of latent infection with subsequent virus
nucleic acid techniques for the detection of shedding. As soon as a cow with a clinical
virus in clinical specimens. Nucleic acid BoHVl infection is diagnosed, the whole
hybridization and PCR were developed as herd may be vaccinated to protect the
ideal diagnostic tools for the detection of animals from disease, if there is a clinical
BoHV1 in clinical specimens because of outbreak of BoHVl in the close vicinity. In
their rapidity, sensitivity and specificity. such a case, cattle can be vaccinated before
Several hybridization formats such as dot- the infection finally reaches them. In order
blot hybridization (Vilcek et al., 1993a and to eliminate BoHVl from a herd, every
Vilcek et al., 1993b), in situ hybridization infected animal must be identified and
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Int.J.Curr.Microbiol.App.Sci (2015) 4(10): 844-858
removed, because of the possibility of Babiuk, L.A., Lawman, M.J., Ohmann, H.B.,
reactivation of latent virus. BoHVl infected 1988. Viral-bacterial synergistic interaction
in respiratory disease. Adv. Virus Res. 35,
animals can be identified by the presence of
219 249.
BoHVl specific antibodies in their serum.
Barenfus, M., Delliquadri, C.A., Mcintyre, R.W.,
Schroeder, R.J., 1963. Isolation of infectious
There are four kinds of vaccines namely
bovine rhinotracheitis virus from calves with
modified live virus (MLV) vaccines, meningoencephalitis. J. Am. Vet. Med.
inactivated vaccines, subunit vaccines and Assoc. 143, 725 728.
marker vaccines that are available to be used Bartha, A., Kisary, J., Belák, S., 1974. The general
febrile respiratory form of infectious bovine
in cattle against BoHV1 infections (Van
rhinotracheitis in calves. Acta Vet. Acad. Sci.
Drunen Littel-van den Hurk et al., 1993 and
Hung. 24(1), 77 83.
Nandi et al., 2009). Although, vaccines do
Chase, C.C., Letchworth, G.J., 3rd, 1994. Bovine
not prevent infection, they significantly
herpesvirus 1 gIVexpressing cells resist virus
reduce the incidence and severity of disease. penetration. J. Gen. Virol. 75 ( Pt 1),177
Importantly, breeding animals in enzootic 181.
countries, except those for export to Cruickshank, J.G., Berry, D.M., Hay, B., 1963.
The fine structure of infectious
countries free of BoHV1, should be
laryngotracheitis virus. Virology. 20, 376
vaccinated before coitus, to prevent the virus
378.
inducing abortion. In enzootic regions,
Darbyshire, J.H., Dawson, P.S., Paterson, A.B.,
vaccination to maintain population
Loosmore, R.M., 1964. Infectious Bovine
immunity is best done prior to stressful Rhinotracheitis (IBR). A clinical condition
situations such as weaning or transport. of cattle occurring in United Kingdom. Vet.
Rec. 74, 1379 1383.
Darcel, C.L., 1992. Pseudopositive ELISA results
Reference
of infectious bovine rhinotracheitis IgG
reactors in three artificial insemination studs.
Ackermann, M., Belak, S., Bitsch, V., Edwards, S.,
Can. Vet. J. 33, 407.
Moussa, A., Rockborn, G., Thiry, E., 1990.
de Gee, A.L., Wagter, L.H., Hage, J.J., 1996. The
Round table on infectious bovine
use of a polymerase chain reaction assay for
rhinotracheitis/infectious pustular
the detection of bovine herpesvirus 1 in
vulvovaginitis virus infection diagnosis and
semen during a natural outbreak of infectious
control. Vet. Microbiol. 23(1-4), 361 363.
bovine rhinotracheitis. Vet. Microbiol. 53(1-
Afshar, A., 1965. Virus disease associated with
2), 163 168.
bovine abortion and infertility. Vet. Bull. 35,
Debrauwere, H., Gendrel, C.G., Lechat, S.,
736 752.
Dutreix, M., 1997. Differences and
Allan, E.M., Pirie, H.M., Msolla, P.M., Selman,
similarities between various tandem repeat
I.E., Wiseman, A., 1980. The pathological
sequences: minisatellites and microsatellites.
features of severe cases of infectious bovine
Biochimie. 79(9-10), 577 586.
rhinotracheitis. Vet. Rec. 107, 441 445.
Deka, D., Ramneek, Maiti, N.K., Oberoi, M.S.,
Armstrong, J.A., Pereira, H.G., Andrewes, C.H.,
2005. Detection of bovine herpesvirus-1
1961. Observations on the virus of infectious
infection in breeding bull semen by virus
bovine rhinotracheitis, and its affinity with
isolation and polymerase chain reaction. Rev.
the Herpesvirus group. Virology. 14, 276
Sci. Tech. 24(3), 1085 1094.
285.
Del Médico Zajac, M.P., Romera, S.A., Ladelfa,
Babiuk, L.A., L Italien, J., van Drunen Littel-van
M.F., Kotsias, F., Thiry, J., Ziant, D.,
den Hurk, S., Zamb, T., Lawman, J.P.,
Meurens, F., Keil, G.M., Thiry, E.,
Hughes, G., Gifford, G.A., 1987. Protection
Muylkens, B., 2009. Characterization of
of cattle from bovine herpesvirus type I
interspecific recombinants generated from
(BHV-1) infection by immunization with
closely related bovine herpesviruses 1 and 5
individual viral glycoproteins. Virology.
159(1), 57 66.
852
Int.J.Curr.Microbiol.App.Sci (2015) 4(10): 844-858
through multiple PCR sequencing assays. J. Ganguly, S., Mukhopadhya, S.K., Paul, I., 2008.
Virol. Methods. 161(1), 75 83. Studies on seroprevalence of infectious
Denis, M., Slaoui, M., Keil, G., 1993. bovine rhinotracheitis in cattle population of
Identification of different target West Bengal. Ind. J. Comp. Microbiol.
glycoproteins for bovine herpesvirus-1 Immunol. Infect. Dis. 29(1-2), 12 16.
specific cytotoxic T lymphocytes depending Gardiner, M.R., Nairn, M.E., Sier, A.M., 1964.
on the method of in vitro stimulation. Viral meningoencephalitis of calves in
Immunology. 78, 7 13. western Australia. Australian Veterinary
Dunne, H.W., Griel, L.C., Cusanno, G.L., Journal. 40(6), 225 228.
Ammerrnan, E.H., Bubash, G.R., 1973. Gibbs, E.P.J., Rweyemamu, M.M., 1977. Bovine
Advances in diagnosis of bovine abortion. herpesviruses. Part I. Bovine herpesvirus 1.
77th Annual Meeting of US Animal Health Vet. Bull. 47, 317 343.
Assoc. 515 523. Gupta, P.K., Saini, M., Rai, A., 2006. Rapid and
Edwards, S., White, H., Nixon, P., 1990. A study sensitive PCR- based test for detection of
of the predominant genotypes of bovid bovine herpesvirus-1 in semen. Indian J.
herpesvirus 1 found in the U.K. Vet. Virol. 17, 23 27.
Microbiol. 22(2-3), 213 223. Huck, R.A., Millar, P.G., Evans, D.H., Stables,
El-Kholy, A.A., Abdelrahman, K.A., 2006. J.W., Ross, A., 1971. Penoposthitis
Genetic characterisation of the Egyptian associated with infectious bovine
vaccinal strain Abu-Hammad of bovine rhinotracheitisinfectious pustular
herpesvirus- 1. Rev. Off. Int. Epizoot. 25(3), vulvovaginitis (I.B.R-I.P.V.) virus in a stud
1081 1095. of bulls. Vet. Rec. 88, 292 297.
Engels, M., Ackermann, M., 1996. Pathogenesis of Hutchings, D.L., van Drunen Littel-van den Hurk,
ruminant herpesvirus infections. Vet. S., Babiuk, L.A., 1990. Lymphocyte
Microbiol. 53(1-2), 3 15. proliferative responses to separated bovine
Engels, M., Giuliani, C., Wild, P., Beck, T.M., herpesvirus 1 proteins in immune cattle. J.
Loepfe, E., Wyler, R., 1986. The genome of Virol. 64(10), 5114 5122.
bovine herpesvirus 1 (BHV-1) strains Jain, L., Kanani, A.N., Purohit, J.H., Joshi, C.G.,
exhibiting a neuropathogenic potential Rank, D.N., Kumar, V., Jain, V.K., 2009.
compared to known BHV-1 strains by Detection of bovine herpes virus-1 (BHV-1)
restriction site mapping and cross- infection in breeding bulls by serological and
hybridization. Virus Res. 6(1), 57 73. molecular methods and its characterization
Fehler, F., Herrmann, J.M., Saalmüller, A., by sequencing of PCR products. Buffalo
Mettenleiter, T.C., Keil, G.M., 1992. Bulletin. 28(2), 76 84.
Glycoprotein IV of bovine herpesvirus 1- Jan-Åke, L., Bo, S., Tomas, B., 1999. Herpes
expressing cell line complements and Simplex Virus Type 2 Glycoprotein G-
rescues a conditionally lethal viral mutant. Negative Clinical Isolates Are Generated by
J.Virol. 66(2), 831 839. Single Frameshift Mutations. J. Virol.
Fitzpatrick, D.R., Babiuk, L.A., Zamb, T.J., 1989. 73(12), 9796 9802.
Nucleotide sequence of bovine herpesvirus Jones, C., Chowdhury, S., 2007. A review of the
type 1 glycoprotein gIII, a structural model biology of bovine herpesvirus type 1 (BHV-
for gIII as a new member of the 1), its role as a cofactor in the bovine
immunoglobulin superfamily, and respiratory disease complex and
implications for the homologous development of improved vaccines. Anim.
glycoproteins of other herpesviruses. Health Res. Rev. 8(2), 187 205.
Virology. 173(1), 46 57. Kahrs, R., 1977. Infectious bovine rhinotracheitis:
Fuchs, M., Peter, H., Jan, D., Hanns, J.R., 1999. a review and update. J. Am. Vet. Med. Assoc.
Detection of bovine herpesvirus type 1 in 171, 1055 64.
blood from naturally infected cattle by using Karber, G., 1931. Beitrag zur kollektiven
a sensitive PCR that discriminates between Behandlung pharmakologischer
wild-type virus and virus lacking Reihenversuche. Arch. Exp. Path. Pharmak.
glycoprotein. E. J. Clin. Microbiol. 37, 162, 480 483.
2498 2507.
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