bovine herpesvirus 1 infections
Don't need the entire report?
Generate a print friendly version containing only the sections you need.Generate report
PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- bovine herpesvirus 1 infections
International Common Names
- English: encephalitic bovine herpesvirus type 5 or type 1 infection in cattle; ibr, infectious bovine rhinotracheitis-contaminated semen; infectious bovine rhinotracheitis; infectious bovine rhinotracheitis virus, ibr, in swine; infectious bovine rhinotracheitis/infectious pustular vulvovaginitis; infectious pustular vulvovaginitis; neonatal septicemic infectious bovine rhinotracheitis, ibr
OverviewTop of page
Infectious bovine rhinotracheitis (IBR) is a contagious viral disease of cattle caused by bovine herpesvirus 1 (BHV-1) (Gibbs and Rweyemamu, 1977; Pastoret et al., 1982; Wyler et al., 1989; Tikoo et al., 1995). This virus is also responsible for infectious pustular vulvovaginitis (IPV), balanoposthitis and abortion.
IPV was the only known infection caused by BHV-1 prior to the 1950s, when the respiratory disease IBR, emerged in North America as a consequence of the intensification of cattle husbandry. The respiratory disease spread all over the world and arrived in Europe during the 1970s. The IBR form is the most frequently diagnosed BHV-1 disease.
Pathogenicity of BHV-1 can vary from mild to severe and the relative importance of each syndrome varies between countries. Although mortality is low, BHV-1 infection is economically important as it may cause a drop in production and affect trade restrictions. When animals survive, a life-long latent infection is established in sensory ganglia. Several reactivation stimuli can lead to viral re-excretion, which is responsible for the maintenance of BHV-1 within a cattle herd (Muylkens et al. 2007). The latency and reactivation cycle have a significant impact on the epidemiology and control of BHV-1. Europe has a long history of fighting against BHV-1 infections, but only a small number of countries have achieved IBR-eradication (Ackermann et al., 1990; Ackermann and Engels, 2006).
This disease is on the list of diseases notifiable to the World Organisation for Animal Health (OIE). The distribution section contains data from OIE's WAHID database on disease occurrence. Please see the AHPC library for further information on this disease from OIE, including the International Animal Health Code and the Manual of Standards for Diagnostic Tests and Vaccines. Also see the website: www.oie.int.
Host AnimalsTop of page
|Animal name||Context||Life stage||System|
|Addax nasomaculatus||Wild host|
|Aepyceros melampus||Wild host|
|Alcelaphus buselaphus||Wild host|
|Alces alces||Wild host|
|Antidorcas marsupialis||Wild host|
|Antilocapra americana||Wild host|
|Bos indicus (zebu)|
|Bos taurus (cattle)||Domesticated host||Cattle & Buffaloes: All Stages|
|Bubalus bubalis (Asian water buffalo)||Domesticated host, Wild host||Cattle & Buffaloes: All Stages|
|Capra hircus (goats)||Domesticated host, Wild host||Sheep & Goats: All Stages|
|Capreolus capreolus||Wild host|
|Cervus dama||Wild host|
|Cervus elaphus (red deer)||Wild host|
|Connochaetes gnou||Wild host|
|Connochaetes taurinus||Wild host|
|Damaliscus dorcas dorcas||Domesticated host|
|Gazella thomsonii||Wild host|
|Giraffa camelopardalis||Wild host|
|Hippotragus equinus||Wild host|
|Hippotragus niger||Wild host|
|Kobus ellipsiprymnus||Wild host|
|Kobus kob||Wild host|
|Kobus leche||Wild host|
|Odocoileus hemionus (black-tailed deer)||Wild host|
|Odocoileus virginianus||Wild host|
|Ovis aries (sheep)||Domesticated host, Wild host||Sheep & Goats: All Stages|
|Rangifer tarandus (reindeer)||Wild host|
|Redunca arundinum||Wild host|
|Redunca redunca||Wild host|
|Rupicapra rupicapra||Domesticated host, Wild host||Other: All Stages|
|Sus scrofa (pigs)|
|Syncerus caffer||Domesticated host, Wild host||Cattle & Buffaloes: All Stages|
|Tragelaphus oryx||Wild host|
|Tragelaphus strepsiceros||Wild host|
Hosts/Species AffectedTop of page
The natural hosts are bovine species. The hosts table shows the ruminant species from which BHV-1 has been isolated or when serological data have given evidence of the infection. Despite this apparent broad range, BHV-1 has a narrow species specificity. The truly susceptible species can be defined as animals in which BHV-1 can establish a latent infection: cattle, sheep (Thiry et al., 2001), goats (Six et al., 2001) and other species belonging to the subfamily Bovidae, such as wildebeest (Karstad et al., 1974).
Systems AffectedTop of page reproductive diseases of large ruminants
reproductive diseases of pigs
reproductive diseases of small ruminants
respiratory diseases of large ruminants
respiratory diseases of small ruminants
DistributionTop of page
BHV-1 is distributed worldwide and has been diagnosed in all countries tested (Straub, 1990). A few European countries have successfully eradicated the infection by applying a strict culling policy, including Denmark, Sweden, Finland, Switzerland and Austria (OIE, 2005). Other countries have started similar control programmes.
For current information on disease incidence, see OIE's WAHID Interface.
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.Last updated: 10 Jan 2020
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Algeria||Absent, No presence record(s)||OIE (2009)|
|Benin||Absent, No presence record(s)||OIE (2009)|
|Botswana||Absent, No presence record(s)||OIE (2009)|
|Burundi||Absent, No presence record(s)||OIE Handistatus (2005)|
|Cabo Verde||Absent, No presence record(s)||OIE Handistatus (2005)|
|Central African Republic||Absent, No presence record(s)||OIE Handistatus (2005)|
|Congo, Democratic Republic of the||Absent, No presence record(s)||OIE Handistatus (2005)|
|Djibouti||Absent, No presence record(s)||OIE (2009)|
|Egypt||Absent, No presence record(s)||OIE (2009)|
|Gabon||Absent, No presence record(s)||OIE (2009)|
|Kenya||Absent, No presence record(s)||OIE (2009)|
|Lesotho||Absent, No presence record(s)||OIE (2009)|
|Libya||Absent, No presence record(s)||OIE Handistatus (2005)|
|Madagascar||Absent, No presence record(s)||OIE (2009)|
|Mauritius||Absent, No presence record(s)||OIE (2009)|
|Morocco||Absent, No presence record(s)||OIE (2009)|
|Mozambique||Absent, No presence record(s)||OIE (2009)|
|Rwanda||Absent, No presence record(s)||OIE (2009)|
|Seychelles||Absent, No presence record(s)||OIE Handistatus (2005)|
|South Africa||Present||OIE (2009)|
|Sudan||Absent, No presence record(s)||OIE (2009)|
|Tunisia||Absent, No presence record(s)||OIE (2009)|
|Zimbabwe||Absent, No presence record(s)||OIE (2009)|
|Armenia||Absent, No presence record(s)||OIE (2009)|
|Azerbaijan||Absent, No presence record(s)||OIE (2009)|
|Bahrain||Absent, No presence record(s)||OIE (2009)|
|Bangladesh||Absent, No presence record(s)||OIE (2009)|
|Bhutan||Absent, No presence record(s)||OIE (2009)|
|Brunei||Absent, No presence record(s)||OIE Handistatus (2005)|
|India||Present, Localized||OIE (2009)|
|Iraq||Absent, No presence record(s)||OIE (2009)|
|Israel||Absent, No presence record(s)||OIE (2009)|
|Kazakhstan||Absent, No presence record(s)||OIE (2009)|
|Kuwait||Absent, No presence record(s)||OIE (2009)|
|Kyrgyzstan||Absent, No presence record(s)||OIE (2009)|
|Laos||Absent, No presence record(s)||OIE (2009)|
|Lebanon||Absent, Unconfirmed presence record(s)||OIE (2009)|
|Malaysia||Absent, No presence record(s)||OIE (2009)|
|-Peninsular Malaysia||Absent, No presence record(s)||OIE Handistatus (2005)|
|Myanmar||Absent, No presence record(s)||OIE (2009)|
|Nepal||Absent, No presence record(s)||OIE (2009)|
|North Korea||Absent, No presence record(s)||OIE Handistatus (2005)|
|Oman||Absent, No presence record(s)||OIE (2009)|
|Philippines||Absent, No presence record(s)||OIE (2009)|
|Saudi Arabia||Absent, No presence record(s)||OIE (2009)|
|Singapore||Absent, No presence record(s)||OIE (2009)|
|South Korea||Absent, No presence record(s)||OIE (2009)|
|Sri Lanka||Absent, No presence record(s)||OIE (2009)|
|Syria||Absent, No presence record(s)||OIE (2009)|
|Tajikistan||Absent, No presence record(s)||OIE (2009)|
|Thailand||Absent, No presence record(s)||OIE (2009)|
|Turkmenistan||Absent, No presence record(s)||OIE Handistatus (2005)|
|United Arab Emirates||Absent, No presence record(s)||OIE (2009)|
|Uzbekistan||Absent, No presence record(s)||OIE Handistatus (2005)|
|Vietnam||Absent, Unconfirmed presence record(s)||OIE (2009)|
|Andorra||Present||OIE Handistatus (2005)|
|Austria||Absent, No presence record(s)||OIE (2009)|
|Belarus||Absent, No presence record(s)||OIE (2009)|
|Croatia||Absent, No presence record(s)||OIE (2009)|
|Czechia||Absent, No presence record(s)||OIE (2009)|
|Denmark||Absent, No presence record(s)||OIE (2009)|
|Finland||Absent, No presence record(s)||OIE (2009)|
|Germany||Absent, No presence record(s)||OIE (2009)|
|Greece||Present, Localized||OIE (2009)|
|Iceland||Absent, No presence record(s)||OIE (2009)|
|Isle of Man||Present||OIE Handistatus (2005)|
|Italy||Absent, No presence record(s)||OIE (2009)|
|Jersey||Absent, No presence record(s)||OIE Handistatus (2005)|
|Latvia||Absent, No presence record(s)||OIE (2009)|
|Liechtenstein||Absent, Unconfirmed presence record(s)||OIE (2009)|
|Malta||Absent, No presence record(s)||OIE (2009)|
|Montenegro||Absent, No presence record(s)||OIE (2009)|
|North Macedonia||Absent, Unconfirmed presence record(s)||OIE (2009)|
|Norway||Absent, No presence record(s)||OIE (2009)|
|Romania||Absent, No presence record(s)||OIE (2009)|
|Serbia and Montenegro||Present||OIE Handistatus (2005)|
|Slovenia||Absent, No presence record(s)||OIE (2009)|
|Spain||Present, Localized||OIE (2009)|
|Sweden||Absent, No presence record(s)||OIE (2009)|
|Switzerland||Absent, No presence record(s)||OIE (2009)|
|Ukraine||Absent, No presence record(s)||OIE (2009)|
|United Kingdom||Present||OIE (2009)|
|-Northern Ireland||Present||OIE Handistatus (2005)|
|Barbados||Present||OIE Handistatus (2005)||CAB Abstracts Data Mining|
|Belize||Absent, No presence record(s)||OIE (2009)|
|Bermuda||Absent, No presence record(s)||OIE Handistatus (2005)|
|British Virgin Islands||Absent, No presence record(s)||OIE Handistatus (2005)|
|Cayman Islands||Absent, No presence record(s)||OIE Handistatus (2005)|
|Costa Rica||Present||OIE (2009)|
|Curaçao||Absent, No presence record(s)||OIE Handistatus (2005)|
|Dominica||Absent, No presence record(s)||OIE Handistatus (2005)|
|Dominican Republic||Present||OIE (2009)|
|Greenland||Absent, No presence record(s)||OIE (2009)|
|Haiti||Absent, No presence record(s)||OIE (2009)|
|Honduras||Absent, No presence record(s)||OIE (2009)|
|Jamaica||Absent, No presence record(s)||OIE (2009)|
|Saint Kitts and Nevis||Absent, No presence record(s)||OIE Handistatus (2005)|
|Saint Vincent and the Grenadines||Absent, No presence record(s)||OIE Handistatus (2005)|
|Trinidad and Tobago||Absent, No presence record(s)||OIE Handistatus (2005)|
|United States||Present||OIE (2009)|
|New Caledonia||Present||OIE (2009)|
|New Zealand||Present||OIE (2009)|
|Samoa||Absent, No presence record(s)||OIE Handistatus (2005)|
|Vanuatu||Present, Serological evidence and/or isolation of the agent||OIE Handistatus (2005)|
|Falkland Islands||Absent, No presence record(s)||OIE Handistatus (2005)|
|French Guiana||Absent, No presence record(s)||OIE (2009)|
|Guyana||Absent, No presence record(s)||OIE Handistatus (2005)|
|Paraguay||Present||OIE Handistatus (2005)|
|Peru||Present, Localized||OIE (2009)|
PathologyTop of page
Infectious bovine rhinotracheitis (IBR) is a sporadic viral disease. Outbreaks are observed during winter, but the incidence of the disease is low, whatever the prevalence rate in a given region. High seroprevalence without a high incidence of disease is generally explained by the circulation of hypovirulent strains, as suggested by the results of experimental inoculation of calves with strains of varying virulence (Kaashoek et al., 1996). However, subclinical infection with a BHV-1 strain normally associated with clinically severe respiratory disease has been reported in a high health status dairy herd, which had previously been seronegative for 13 years. Although over 70% of the herd had seroconverted to BHV no clinical signs were observed apart from a slight bilateral serous ocular discharge in a few cows; performance and productivity were unaffected (Pritchard et al., 2003).
Infectious bovine rhinotracheitis (IBR)
The respiratory form is the most frequently observed disease provoked by BHV-1. It affects all categories of animals. Calves are usually protected by colostral antibodies until 3-4 months of age. The severity of clinical signs varies considerably. Because of its ability to induce immune suppression, BHV-1 is an important agent in the multifactorial disorder, bovine respiratory disease complex (Jones and Chowdhury, 2010). The virus is also responsible for a typical respiratory disease called infectious bovine rhinotracheitis (IBR).
The virus is excreted in the nasal secretions as early as 24 hours after infection. After an incubation period of 2 to 4 days, nasal secretions are more profuse and evolve from sero-mucous to mucopurulent discharge. Young animals show ptyalism. Around 4 days after the beginning of excretion, elevated temperatures are recorded, and animals are depressed and anorexic. In lactating cows, the milk production suddenly drops.
Ulcers and redness are visible on the nasal mucosa, in the pharynx and trachea (see pictures). Lesions are usually restricted in the upper respiratory tract. Bronchitis and pneumonia can also be observed, but usually as a consequence of secondary bacterial infections. Coughing and sneezing are observed. Conjunctivitis is associated with the respiratory form and is manifest by increased eye secretions.
Animals recover within 14 days, due to the rise of the specific immune response. Some highly virulent BHV-1 strains induce a high mortality rate.
Lesions are almost exclusively restricted to the upper respiratory tract: rhinitis, laryngitis and tracheitis. Respiratory mucosae are red and oedematous, foci of ulcers are observed and some lesions are haemorrhagic (Gibbs and Rweyemamu, 1977; Wyler et al., 1989; Straub, 1990).
A review by Graham (2013) highlights the negative reproductive outcomes associated with BHV-1. Infection at the time of service may reduce fertility, with the potential to cause chronic necrotising endometritis and oophoritis, accompanied by a shortened oestrous cycle. Infection later in the oestrous cycle may result in a decreased conception rate, whereas infection later in pregnancy can lead to abortion.
Abortion is observed between 4 and 8 months of gestation. Early embryonic death can also occur. Abortion is a consequence of respiratory infection of pregnant cows. Viraemia allows the virus to enter the uterine artery and cross the placenta. Abortion is due to a lytic infection of the fetus. All internal organs of the fetus, especially the liver and renal cortex, show foci of necrosis. A generalized multifocal necrosis is diagnosed (Smith, 1997).
Infection of cows during the last trimester of gestation can lead to neonatal death, and death of weak calves can occur during the first 2 weeks of life (Thiry et al., 1984).
Infectious pustular vulvovaginitis (IPV) - infectious pustular balanoposthitis (IPB)
A pustular inflammation occurs in the male or female genital mucosa, together with a rise in body temperature: up to 41.5°C. The genital mucosa is red and oedematous, and vesicles and pustules evolve into ulcers. The lesions resolve within 1 to 2 weeks (Straub, 1990).
Metroperitonitis has been observed in cows infected with BHV-1 around parturition, and especially after caesarean section (Lomba et al., 1976).
Encephalitis cases have been mostly reported in calves but can also occur in older animals (Roels et al., 2000). In the case of bovine encephalitis, the distinction must be made between BHV-1 and BHV-5, the latter being the usual etiological agent of bovine encephalitis (Meyer et al., 2001).
Neonatal calves often succumb after a generalized infection. They show coughing, nasal and ocular discharge, bronchopneumonia, diarrhoea, ulcers in the digestive tract and hyperthermia. The lesions can be concentrated in the mouth, with ulcers and profuse salivation. A pure respiratory form is rarely observed in neonates. Encephalitis has been observed in 3 to 8 day-old calves (Thiry et al., 1984).
Other clinical signs
Although BHV-1 has been associated with clinical mastitis, there is little concrete evidence for its involvement in the syndrome (Gourlay et al., 1974). Isolation of BHV-1 from milk can be simply a consequence of viraemia. BHV-1 has also been isolated from ulcerative lesions of the mouth and the interdigital space (Dhennin et al., 1979), thus potentially leading to confusion with other vesicular diseases such as foot and mouth disease, vesicular stomatitis and mucosal disease (Holliman, 2005).
DiagnosisTop of page
An outbreak of acute respiratory disease with profuse nasal discharge, fever and depression suggests IBR. In a naive herd, the epidemic progresses quickly and respiratory signs are associated with neonatal deaths and abortions at 4 to 8 months of pregnancy. Hypovirulent strains can circulate without obvious clinical signs. The IPV form is suspected if animals have vesicular and pustular lesions of the genital mucosa and there is evidence of venereal transmission.
Postmortem examination can be performed in cases of fatal IBR, abortion and neonatal deaths. The IBR form is suspected when there is intense inflammation of the mucosa of the anterior respiratory tract, from the nasal cavities to the trachea. Aborted fetuses show multifocal necrosis disseminated in various internal organs. The same lesions are observed in neonates.
Virus isolation from nasal or vaginal swabs, or from triturated tissue, is performed in cell cultures, using either established cell lines like Madin-Darby Bovine Kidney cells (MDBK) or primary bovine cells of renal, lung or testicular origin. A cytopathic effect is visible, with cell rounding within 24 hours. Indirect immunofluorescence or immunoperoxidase assays confirm the presence of specific BHV-1 antigens using monoclonal antibodies against one of the major BHV-1 glycoproteins: gB, gC or gD. The restriction pattern of BHV-1 DNA is characteristic and can also discriminate between subtypes 1 and 2 (Engels et al., 1981). The use of endonucleases with a high number of cleavage sites, such as Pst1, allows strain-specific patterns to be obtained (Whetstone et al., 1993).
BHV-1 DNA can also be detected by polymerase chain reaction (PCR). Many PCR methods are reported in the literature (Vilcek et al., 1994). As viral isolation from bovine semen is difficult, PCR has also been developed for BHV-1 detection in semen (Smits et al., 2000). A specific PCR has been developed to diagnose gE negative BHV-1 strains (Schynts et al., 1999). A universal PCR combined with restriction enzyme analysis of the amplicons has been developed for detection and identification of ruminant alphaherpesviruses related to BHV-1, including BHV-5, CapHV-1, CerHV-1 and RanHV-1 (Ross and Belak, 1999). In addition, specific nested-PCR systems have also been developed, which allow the safe detection of each ruminant alphaherpesvirus without cross-reactions with heterologous viruses (Ross et al., 1999).Serological diagnosis can be performed using sero-neutralization and ELISA. Sero-neutralization requires the use of cell cultures and is rarely undertaken for diagnostic purposes. The most sensitive sero-neutralization test requires a 24-h incubation of serum with the virus at 37°C (Bitsch, 1978). Several ELISA kits are available. Blocking ELISAs have replaced most of the indirect ELISA tests. Blocking ELISAs are based on the recognition of glycoprotein gB. Glycoprotein gE blocking ELISAs are companion (DIVA – differentiation of infected from vaccinated animals) kits, used to distinguish between naturally infected animals and those immunized with a gE negative vaccine. The gB blocking ELISAs cannot distinguish between BHV-1 infection and infection with related alphaherpesviruses. A gE blocking ELISA has been shown to differentiate between BHV-1 and BHV-5 infection (Wellenberg et al., 2001).
The antigen source for most gE blocking ELISAs is a crude viral preparation in which gE is associated with other envelope glycoproteins, leading to a lack of specificity (Lehmann et al., 2002). The specificity of serological discrimination between BHV-infected animals and animals vaccinated with marker vaccines can be improved by preadsorption of serum samples with a preparation of antigen devoid of gE, prior to the blocking ELISA.
ELISAs have also been developed to detect BHV-1 antibodies in bulk milk, or in milk samples from individual cows. Milk ELISAs have been found to perform well when compared with standard serum ELISAs; there is no evidence that stage of lactation or transport or storage of the samples had a significant effect (Pritchard et al., 2002).A combination of ELISAs, for example the Danish combination test system, provides better sensitivity; (de Wit et al., 1998). It is made up of a combination of a blocking and an indirect ELISA.
In IBR control programmes, serological diagnosis aims to identify latently infected animals. However, a few animals are seronegative latent carriers (SNLC), i.e. they are latently infected with BHV-1 without detectable antibodies. Such animals can be produced experimentally by infection of neonatal calves protected with specific colostral antibodies (Lemaire et al., 2000a,b).
List of Symptoms/SignsTop of page
|Cardiovascular Signs / Tachycardia, rapid pulse, high heart rate||Sign|
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Sign|
|Digestive Signs / Dysphagia, difficulty swallowing||Sign|
|Digestive Signs / Excessive salivation, frothing at the mouth, ptyalism||Sign|
|Digestive Signs / Grinding teeth, bruxism, odontoprisis||Sign|
|Digestive Signs / Tongue weakness, paresis, paralysis||Sign|
|General Signs / Abnormal proprioceptive positioning, knuckling||Sign|
|General Signs / Ataxia, incoordination, staggering, falling||Sign|
|General Signs / Dysmetria, hypermetria, hypometria||Sign|
|General Signs / Fever, pyrexia, hyperthermia||Sign|
|General Signs / Generalized weakness, paresis, paralysis||Sign|
|General Signs / Inability to stand, downer, prostration||Sign|
|General Signs / Opisthotonus||Sign|
|General Signs / Paraparesis, weakness, paralysis both hind limbs||Sign|
|General Signs / Sudden death, found dead||Sign|
|General Signs / Tetraparesis, weakness, paralysis all four limbs||Sign|
|General Signs / Trembling, shivering, fasciculations, chilling||Sign|
|Nervous Signs / Abnormal behavior, aggression, changing habits||Sign|
|Nervous Signs / Circling||Sign|
|Nervous Signs / Coma, stupor||Sign|
|Nervous Signs / Constant or increased vocalization||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Sign|
|Nervous Signs / Excitement, delirium, mania||Sign|
|Nervous Signs / Head pressing||Sign|
|Nervous Signs / Head tilt||Sign|
|Nervous Signs / Hyperesthesia, irritable, hyperactive||Sign|
|Nervous Signs / Propulsion, aimless wandering||Sign|
|Nervous Signs / Seizures or syncope, convulsions, fits, collapse||Sign|
|Nervous Signs / Tremor||Sign|
|Ophthalmology Signs / Blindness||Sign|
|Ophthalmology Signs / Chemosis, conjunctival, scleral edema, swelling||Sign|
|Ophthalmology Signs / Conjunctival, scleral, injection, abnormal vasculature||Sign|
|Ophthalmology Signs / Conjunctival, scleral, redness||Sign|
|Ophthalmology Signs / Lacrimation, tearing, serous ocular discharge, watery eyes||Sign|
|Ophthalmology Signs / Nystagmus||Sign|
|Pain / Discomfort Signs / Colic, abdominal pain||Sign|
|Pain / Discomfort Signs / Pain, penis||Sign|
|Pain / Discomfort Signs / Pain, vulva, vagina||Sign|
|Reproductive Signs / Abnormal length estrus cycle, long, short, irregular interestrus period||Sign|
|Reproductive Signs / Abortion or weak newborns, stillbirth||Sign|
|Reproductive Signs / Female infertility, repeat breeder||Sign|
|Reproductive Signs / Female infertility, repeat breeder||Sign|
|Reproductive Signs / Male infertility||Sign|
|Reproductive Signs / Mucous discharge, vulvar, vaginal||Sign|
|Reproductive Signs / Papule, pustule, vesicle, ulcer penis or prepuce||Sign|
|Reproductive Signs / Purulent discharge, penis or prepuce||Sign|
|Reproductive Signs / Purulent discharge, vulvar, vaginal||Sign|
|Reproductive Signs / Vaginal or cervical ulcers, vesicles, erosions, tears, papules, pustules||Sign|
|Respiratory Signs / Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs||Sign|
|Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping||Sign|
|Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea||Sign|
|Respiratory Signs / Mucoid nasal discharge, serous, watery||Sign|
|Skin / Integumentary Signs / Alopecia, thinning, shedding, easily epilated, loss of, hair||Sign|
|Skin / Integumentary Signs / Pruritus, itching skin||Sign|
Disease CourseTop of page
BHV-1 is excreted in the respiratory, ocular and genital secretions of infected cattle. Nasal secretions contain high concentrations of virus and constitute the main source of infection. The virus is transmitted by direct contact, by aerosol over short distances, or by material or clothes contaminated by infectious mucus. Sperm can be infected and the virus can be transmitted genitally. As the virus is well preserved in liquid nitrogen, artificial insemination must only be made with sperm from BHV-1 free bulls. Embryo transfer is also a potential risk for BHV-1 transmission. Embryo treatment with trypsin removes the virus, which may have been adsorbed onto the pellucid membrane.
After virus replication at the portal of entry (nasal or genital mucosa),BHV-1 disseminates in the blood, the nerves and by cell-to-cell transmission inside the infected tissue. Primary infection is followed by a transient viraemia, allowing the virus to infect secondary sites such as the digestive tract, udder, fetus and ovaries (Miller et al., 1985). Infection of the neonate provokes a generalized fatal infection in the absence of specific colostral antibodies. In other animals, the infection of peripheral nerves at the site of infection induces a retrograde axonal transport of the virus to the regional nervous ganglia, i.e. the trigeminal ganglion in the case of respiratory infection and the sacral ganglion after genital infection. Other sites of latency cannot be excluded, such as the tonsils (Winkler et al., 2000).
After respiratory infection, virus is excreted in the nasal secretions at very high titres - up to 1010 tissue culture infectious doses (TCID50) - over 10 to 16 days. Virus replication is controlled by non-specific, followed by specific, immune responses (Denis et al., 1994). The virus establishes a latent infection after primary infection, re-infection or vaccination with an attenuated virus. Latent infection is lifelong and may be interrupted by virus reactivation and re-excretion. BHV-1 reactivation is provoked by several stimuli. These are transport, parturition, glucocorticoid treatment, viral superinfection and infestation with Dictyocaulus viviparus (Thiry et al., 1986). Re-excretion is usually clinically silent, but the amount of re-excreted virus can be high and the process lasts for several days. The level of re-excretion is directly related to the level of the specific immune response at the time of reactivation (Engels and Ackermann, 1996; Pastoret et al., 1984; Lemaire et al., 1994; Thiry et al., 1986, 1999).
Recombination is an important source of genetic variation in BHV-1, like other herpesviruses, and may be significant when vaccines containing deletion mutants are used. Recombination of two BHV-1 mutants lacking either glycoprotein C (gC-) or E (-gE-) was found to be a frequent event in calves coinfected with these strains. After reactivation from latency, no viruses of the originally inoculated mutants were detected, although gC+/gE- mutants, when inoculated alone, were detected after reactivation treatment (Schynts et al., 2003).
EpidemiologyTop of page
BHV-1 is transmitted by nasal or genital secretions. Transmission is mainly direct, from animal to animal, by the respiratory or the genital route. Indirect transmission via infected clothes or materials is also possible (Wentink et al., 1993). Aerosols can disseminate the virus over 4 meters in field conditions (Mars et al., 2000). Vertical transmission occurs in cows, when the virus crosses the placenta and infects the fetus.
Morbidity and mortality
The clinical consequences of BHV-1 circulation in a herd depend on the virulence of the prevalent strain. Where virulent strains circulate, morbidity rate is up to 100% in a naïve herd. Otherwise morbidity rate is approximately 20%. The mortality rate varies between 0 and 10%. Genital strains causing IPV are less virulent (Straub, 1990).
Temporal and spatial evolution
In a herd, BHV-1 circulation is initiated by virus reactivation and re-excretion in a latently infected animal already present, or more often by the introduction of an acutely or latently infected animal. In the absence of clinical signs, virus circulation is evidenced by seroconversion in young animals (van Nieuwstadt and Verhoeff, 1983). Two patterns of virus circulation are observed: rapid seroconversion of seronegative animals, most likely due to a virulent strain; or seroconversion of animals over a long period of time (several weeks to several months) usually due to hypovirulent strains (Van Nieuwstadt and Verhoeff, 1983). The basic reproduction ratio (R0) was calculated in a herd after experimental reactivation of virus in three seropositive cows. All seronegative animals seroconverted over a period of 4 weeks and an average of 7 new cases were generated by each infected animal (Hage et al., 1996). This result shows the rapid transmission of the virus in a susceptible herd.
A study of natural transmission of BHV-1 in the Netherlands involved 50 herds with 3300 head of cattle. Herds were divided into 3 groups: seronegative, vaccinated, and mixed. Three outbreaks of BHV1 occurred due to the introduction of infectious cattle, and another due to reactivation of latent BHV1 in seropositive cattle. The basic reproduction ratio within herds was estimated to be at least 4. Only one of the outbreaks led to secondary outbreaks in seronegative herds; the between herds basic reproduction ratio was estimated to be 0.6 (Hage et al., 2003).
Between herds transmission is a major risk of BHV-1 circulation. However, it can be better controlled than within herd spread. Sanitary measures can be taken to prevent the introduction of seropositive animals or animals originating from a seropositive herd. Airborne transmission of BHV-1 has been demonstrated over short distances and can provide an explanation of between herds transmission, without the introduction of any new animal (Mars et al., 1999).
The risk factors for BHV-1 infection in a herd have been studied on dairy farms. BHV-1 positive farms purchase cattle and participate in cattle shows more often than negative farms. Positive farms have also had more visitors who are less likely to use dedicated farm clothing. Positive farms are also situated closer to other cattle farms (van Schaik et al., 1998). As cattle are the main source of virus spread, risk factors for virus infection are associated with cattle movement (Wentink et al., 1993).
Impact: EconomicTop of page
The economic importance of BHV-1 infection can be envisaged from two points of view:
- At the herd level: an IBR outbreak can cause a severe epidemic of respiratory disease with direct economic losses due to death, growth retardation, decreased milk production and abortion (Hage et al., 1998). The genital IPV form is usually much less severe.
- At a regional level: the status ‘BHV-1 free’ can confer commercial advantages to a country or a region. European member states such as Denmark, Finland, Sweden and Austria are officially free of BHV-1. Only cattle, sperm and embryos from BHV-1 free herds or countries may be imported into these countries.
The impact of the infection is directly linked to the prevalence of seropositive animals. This value can vary from 0% in countries free of the disease, like Denmark and Sweden, to 67% in Belgium (Boelaert et al., 2000) and 84 % in the Netherlands (van Wuyckhuise et al., 1998). However, exact figures that describe actual losses have not been calculated.
Disease TreatmentTop of page
No antiviral drugs are used. Antimicrobial therapy is needed to overcome bacterial superinfection. The use of corticosteroids is contraindicated since these drugs provoke BHV-1 reactivation and are likely to aggravate the severity of the outbreak by increasing virus circulation. Therefore, only nonsteroidal anti-inflammatory compounds, such as carprofen, are recommended for use (Eltok and Eltok, 2004). Immunomodulators have been found to limit the spread of infection, decrease viral shedding and reduce the severity of clinical signs in experimental BHV-1 infection in calves (Castrucci et al., 2000).
Prevention and ControlTop of page
Vaccination against BHV-1 is widely used. Both inactivated and live attenuated vaccines are available. The vaccination schedule consists of two vaccinations at a 3-week interval for inactivated vaccines, starting from the age of 3-4 months to avoid interference with colostral antibodies. Live attenuated vaccines are administered either once or twice depending on the type of vaccine. Duration of immunity usually lasts from six months to one year. Vaccination is recommended for young calves to prevent clinical signs. Vaccination of calves less than 3 months of age can be achieved by intranasal administration of attenuated vaccine. This route is better for overcoming interference due to maternal immunity. Vaccinations should protect cattle clinically in case of infection and significantly reduce the shedding of field virus. It is important that the vaccines themselves do not induce disease, abortion or any other adverse reaction, and they must be genetically stable (OIE, 2005). BHV-1 is incorporated in various multivalent vaccines for cattle (for example, Ellsworth et al., 2003).
It is thought that the rapid onset of protection following vaccination of calves with multivalent vaccines containing modified-live or both modified-live and killed BHV-1 is associated with virus-specific interferon gamma production (Woolums et al., 2003). Studies have been carried out to evaluate the shedding of BHV- 1 and bovine viral diarrhoea viruses after vaccination of calves with a multivalent modified-live virus vaccine (Kleiboeker et al., 2003). Seventeen of 18 vaccinated calves seroconverted to BHV-1, but viral shedding was not detected. Pregnant in-contact cattle remained seronegative throughout the study. However, reactivation of some live attenuated vaccine viruses has been induced by administration of dexamethasone to calves three months after vaccination (Castrucci et al., 2002). The vaccine virus appears to have established latency in the host, but the calves remained clinically protected from challenge exposure.Vaccines can be effective against the genital form of BHV-1 infection, IPV. However, they must be tested specifically to protect against experimental genital infection. Most of the available BHV-1 vaccines have only been tested against respiratory infection.
Vaccination can be a tool in IBR control programmes. Repeated vaccination is needed to achieve epidemiological protection and reduce virus circulation. Indeed, in the context of control programmes, the efficacy of vaccination is not based on the reduction of clinical signs but on a decrease in the incidence of infection to reduce the prevalence of seropositive animals. Marker vaccines are recommended. The marker consists of a deletion of the glycoprotein gE gene in the vaccine strain (Kaashoek et al., 1994); such vaccines first became available in 1995 (OIE, 2005). Vaccinated animals develop an immune response against all the antigens of BHV-1, except glycoprotein gE. A DIVA (differentiation of infected from vaccinated animals) serological test (gE blocking ELISA) is used to differentiate vaccinated (gE negative) calves from those that have been naturally infected (gE positive) (Van Oirschot et al., 1996).
Experiments have been carried out to study the safety and efficacy of different immunisation protocols with marker vaccines (Kerkhofs et al., 2003). A comparison of 4 immunisation protocols based on inactivated and live attenuated marker vaccines for BHV-1 showed that cellular and humoral immune responses were highest in the groups which received at least one injection of inactivated vaccine. Virological protection was observed in all vaccinated calves after a challenge infection, but calves which received one dose of the inactivated vaccine as a booster, or two doses of the inactivated vaccine, excreted significantly less challenge virus than calves which were vaccinated only with attenuated vaccine.
Like other live attenuated strains used for vaccine production, gE-deleted mutants have been reported in field infections of cattle vaccinated with the strain several months previously (Dispas et al., 2003). BHV-1 gE-negative vaccine strains can establish latency in naive or passively immunized neonatal calves after a single intranasal inoculation. Moreover, a gE-negative vaccine, when used in passively immunized calves, has been shown to give rise to seronegative vaccine virus carriers (Lemaire et al., 2001).
Numerous recent reports describe other developments in BHV-1 vaccination technology, including DNA vaccines. Such experimental vaccines include gD alone (Castrucci et al., 2004) or fused with bovine CD154 (Manoj et al., 2004), vaccinia virus expressing gB (Huang et al., 2005), and plasmids encoding the membrane-anchored or secreted forms of gB and gD (Caselli et al., 2005). Although DNA vaccines have several advantages over conventional vaccines, particularly with regard to safety, antibody production and protection are often inadequate, particularly in single plasmid vaccine formulations, and none of the vaccines described are currently suitable for field use.
IBR control and eradication
Several European countries have initiated IBR control programmes aimed at eradicating BHV-1 infection. On other continents IBR control is not considered an important issue. Reasons for and against eradication are reviewed by Ackermann and Engels (2006). Where seroprevalence is low, the programme only consists of the identification and removal of seropositive animals. Regular serological testing of pooled serum samples or bulk tank milk can monitor the status of each farm (Hartman et al., 1997). Where seroprevalence is high, the culling of seropositive animals is too expensive. In this case the control programme starts with massive vaccination campaigns. Repeated vaccination every six months is able to reduce the circulation of the virus among animals. The use of marker gE negative vaccines helps to identify gE seropositive animals, which are latently infected with a wild-type strain. The progressive elimination of seropositive (gE positive) animals decreases the number of infected animals and reduces the seroprevalence. When it reaches a low threshold value, vaccination can be stopped and serosurveillance identifies seropositive farms from which seropositive animals are removed (Lemaire et al., 1994; Thiry et al., 1999).
A new monitoring programme for IBR, introduced in Denmark in 2004, aims to be more cost-effective and enables cases to be tracked down more rapidly. The risk-based programme tailors the monitoring programme based on factors such as type of herd, herd size, recording of separate cases or systematic sampling, time of year and proximity to known outbreaks (Chriel et al., 2005).
The effect of surveillance programmes on the spread of BHV-1 between certified cattle herds has been modelled (Graat et al., 2001). The goal of the control programmes used in many European countries is that infection in a certified herd is detected early enough to prevent spread of infection to other certified herds. The net reproduction ratio, R, (the average number of certified herds infected by one infected certified herd) should be kept below 1. The R between herds is mainly influenced by vaccination status, sampling frequency, and contacts between herds. The results showed that sampling individual cows once a year could prevent spread of infection between herds of up to 50 cattle. The frequency should be increased to twice yearly for larger herds and/or those with extensive contacts. When bulk milk is sampled, sampling should be done at least every 5 months for small herds or monthly for larger herds with more contacts.
For a country to qualify as free from IBR/IPV it must categorise the disease as notifiable, have undertaken no vaccination against BHV-1 for at least three years, and document that at least 99.8% of its herds are free from IBR/IPV (OIE, 2005). A serological survey must be carried out annually on a random sample of the cattle population of the country sufficient to provide a 99% level of confidence of detecting the infection if it is present at a prevalence higher than 0.2% of herds, and import restrictions apply (OIE, 2005). The OIE also gives requirements for certification of individual herds as IBR/IPV-free.
ReferencesTop of page
Ackermann M, Belak S, Bitsch V, Edwards S, Moussa A, Rockborn G, Thiry E, 1990. Round table on infectious bovine rhinotracheitis/infectious pustular vulvovaginitis virus infection diagnosis and control. Veterinary Microbiology, 23(1-4):361-363
Baranowski E, Keil G, Lyaku J, Rijsewijk FAM, Oirschot JTvan, Pastoret PP, Thiry E, 1996. Structural and functional analysis of bovine herpesvirus 1 minor glycoproteins. Veterinary Microbiology, 53(1/2):91-101; 73 ref
Bitsch V, 1978. The p37/24 modification of the infectious bovine rhinotracheitis virus-serum neutralisation test. Acta Veterinaria Scandinavica, 19:497-505
Boelaert, F., Biront, P., Soumare, B., Dispas, M., Vanopdenbosch, E., Vermeersch, J. P., Raskin, A., Dufey, J., Berkvens, D., Kerkhofs, P., 2000. Prevalence of bovine herpesvirus-1 in the Belgian cattle population. Preventive Veterinary Medicine, 45(3/4), 285-295. doi: 10.1016/S0167-5877(00)00128-8
Brake F, Studdert MJ, 1985. Molecular epidemiology and pathogenesis of ruminant herpesviruses including bovine, buffalo and caprine herpesviruses 1 and bovine encephalitis herpesvirus. Australian Veterinary Journal, 62(10):331-334; 21 ref
Caselli E, Boni M, Luca D di, Salvatori D, Vita A, Cassai E, 2005. A combined bovine herpesvirus 1 gB-gD DNA vaccine induces immune response in mice. Comparative Immunology, Microbiology and Infectious Diseases, 28(2):155-166
Castrucci G, Ferrari M, Marchini C, Salvatori D, Provinciali M, Tosini A, Petrini S, Sardonini Q, Dico M lo, Frigeri F, Amici A, 2004. Immunization against bovine herpesvirus-1 infection. Preliminary tests in calves with a DNA vaccine. Comparative Immunology, Microbiology and Infectious Diseases, 27(3):171-179
Castrucci G, Frigeri F, Salvatori D, Ferrari M, Dico Mlo, Rotola A, Sardonini Q, Petrini S, Cassai E, 2002. A study on latency in calves by five vaccines against bovine herpesvirus-1 infection. Comparative Immunology, Microbiology & Infectious Diseases, 25(4):205-215; 15 ref
Castrucci G, Osburn BI, Frigeri F, Ferrari M, Salvatori D, Dico Mlo, Barreca F, 2000. The use of immunomodulators in the control of infectious bovine rhinotracheitis. Comparative Immunology, Microbiology and Infectious Diseases, 23(3):163-173; 14 ref
Chriel M, Salman M, Wagner B, Nielsen J, Vestergaard P, Willeberg P, Hendriksen B, Mellergaard S, Greiner M, 2005. Risk-based monitoring of IBR in Denmark. Dansk Veterinaertidsskrift, 88(2):12-14
Denis M, Splitter G, Thiry E, Pastoret PP, Babiuk LA, 1994. Infectious bovine rhinotracheitis (bovine herpesvirus 1): helper T cells, cytotoxic T cells, and NK cells. Cell-mediated immunity in ruminants., 157-172; 109 ref
Deregt, D., Jordan, L. T., Drunen Littel-van den Hurk, S. van, Masri, S. A., Tessaro, S. V., Gilbert, S. A., 2000. Antigenic and molecular characterization of a herpesvirus isolated from a North American elk. American Journal of Veterinary Research, 61(12), 1614-1618. doi: 10.2460/ajvr.2000.61.1614
Dhennin, L., Gourreau, J. M., Calvarin, R., Kaiser, C., Corveller, M. le, Perrin, G., 1979. New clinical form of bovine infectious rhinotracheitis (cutaneous localization in the interdigital space). (Une nouvelle forme clinique de rhinotracheite infectieuse bovine). Recueil de Medecine Veterinaire, 155(11), 851-854.
Dispas M, Schynts F, Lemaire M, Letellier C, Vanopdenbosch E, Thiry E, Kerkhofs P, 2003. Isolation of a glycoprotein E-deleted bovine herpesvirus type 1 strain in the field. Veterinary Record, 153(7):209-212
Ek-Kommonen C, Pelkonen S, Nettleton PF, 1986. Isolation of a herpesvirus serologically related to bovine herpesvirus 1 from a reindeer (Rangifer tarandus). Acta Veterinaria Scandinavica, 27:299-301
Ellsworth MA, Brown MJ, Fergen BJ, Ficken MD, Tucker CM, Bierman P, TerHune TN, 2003. Safety of a modified-live combination vaccine against respiratory and reproductive diseases in pregnant cows. Veterinary Therapeutics, 4(2):120-127
Eltok B, Eltok OM, 2004. Clinical efficacy of carprofen as an adjunct to the antibacterial treatment of bovine respiratory disease. Journal of Veterinary Pharmacology and Therapeutics, 27(5):317-320
Engels M, Ackermann M, 1996. Pathogenesis of ruminant herpesvirus infections. Veterinary Microbiology, 53(1/2):3-15; 53 ref
Engels M, Loepfe E, Wild P, Schraner E, Wyler R, 1987. The genome of caprine herpesvirus 1: genome structure and relatedness to bovine herpesvirus 1. Journal of General Virology, 68(7):2019-2023; 17 ref
Engels M, Steck F, Wyler R, 1981. Comparison of the genomes of infectious bovine rhinotracheitis and infectious pustular vulvovaginitis virus strains by restriction endonuclease analysis. Archives of Virology, 67:169-174
Gibbs EPJ, Rweyemamu MM, 1977. Bovine herpesviruses. Part I. Bovine herpesvirus 1. Veterinary Bulletin, 47:317-343
Gourlay RN, Stott EJ, Espinasse J, Barle C, 1974. Isolation of Mycoplasma agalactiae var. bovis and infectious bovine rhinotracheitis virus from an outbreak of mastitis in France. Veterinary Record, 95:534-535
Graat EAM, Jong MCMde, Frankena K, Franken P, 2001. Modelling the effect of surveillance programmes on spread of bovine herpesvirus 1 between certified cattle herds. Veterinary Microbiology, 79(3):193-208; 18 ref
Graham DA, 2013. Bovine herpes virus-1 (BoHV-1) in cattle - a review with emphasis on reproductive impacts and the emergence of infection in Ireland and the United Kingdom. Irish Veterinary Journal, 66(15):(1 August 2013). http://www.irishvetjournal.org/content/66/1/15/abstract
Hage JJ, Schukken YH, Barkema HW, Benedictus G, Rijsewijk FAM, Wentink GH, 1996. Population dynamics of bovine herpesvirus 1 infection in a dairy herd. Veterinary Microbiology, 53(1/2):169-180; 23 ref
Hage JJ, Schukken YH, Dijkstra T, Barkema HW, Valkengoed PHRvan, Wentink GH, 1998. Milk production and reproduction during a subclinical bovine herpesvirus 1 infection on a dairy farm. Preventive Veterinary Medicine, 34(2/3):97-106; 21 ref
Hage JJ, Schukken YH, Schols H, Maris-Veldhuis MA, Rijsewijk FAM, Klaassen CHL, 2003. Transmission of bovine herpesvirus 1 within and between herds on an island with a BHV1 control programme. Epidemiology and Infection, 130(3):541-552
Holliman A, 2005. Differential diagnosis of diseases causing oral lesions in cattle. In Practice, 27(1):2-13
Huang Y, Babiuk LA, van Drunen Littel-van den Hurk S, 2005. Immunization with a bovine herpesvirus 1 glycoprotein B DNA vaccine induces cytotoxic T-lymphocyte responses in mice and cattle. Journal of General Virology, 86(4):887-898
Inglis DM, Bowie JM, Allan MJ, Nettleton PF, 1983. Ocular disease in red deer calves associated with a herpes virus infection. Veterinary Record, 113:182-183
Jones C, Chowdhury S, 2010. Bovine herpesvirus type 1 (BHV-1) is an important cofactor in the bovine respiratory disease complex. Veterinary Clinics of North America, Food Animal Practice, 26(2):303-321. http://www.vetfood.theclinics.com/article/S0749-0720(10)00013-7/abstract
Kaashoek MJ, Moerman A, Madic J, Rijsewijk FAM, Quak J, Gielkens ALJ, Oirschot JTvan, 1994. A conventionally attenuated glycoprotein E-negative strain of bovine herpesvirus type 1 is an efficacious and safe vaccine. Vaccine, 12(5):439-444; 19 ref
Kaashoek MJ, Straver PH, Rooij EMAvan, Quak J, Oirschot JTvan, 1996. Virulence, immunogenicity and reactivation of seven bovine herpesvirus 1.1 strains: clinical and virological aspects. Veterinary Record, 139(17):416-421; 19 ref
Karstad L, Jessett DM, Otema JC, Drevemo S, 1974. Vulvovaginitis in wildebeest caused by the virus of infectious bovine rhinotracheitis. Journal of Wildlife Diseases, 10:392-396
Kerkhofs P, Renjifo X, Toussaint JF, Letellier C, Vanopdenbosch E, Wellemans G, 2003. Enhancement of the immune response and virological protection of calves against bovine herpesvirus type 1 with an inactivated gE-deleted vaccine. Veterinary Record, 152(22):681-686
Kleiboeker SB, Lee SM, Jones CA, Estes DM, 2003. Evaluation of shedding of bovine herpesvirus 1, bovine viral diarrhea virus 1, and bovine viral diarrhea virus 2 after vaccination of calves with a multivalent modified-live virus vaccine. Journal of the American Veterinary Medical Association, 222(10):1399-1403
Lehmann D, Sodoyer R, Leterme S, Crevat D, 2002. Improvement of serological discrimination between herpesvirus-infected animals and animals vaccinated with marker vaccines. Veterinary Microbiology, 86(1/2):59-68; 12 ref
Lemaire M, Meyer G, Baranowski E, Schynts F, Wellemans G, Kerkhofs P, Thiry E, 2000. Production of bovine herpesvirus type 1-seronegative latent carriers by administration of a live-attenuated vaccine in passively immunized calves. Journal of Clinical Microbiology, 38(11):4233-4238; 43 ref
Lemaire M, Pastoret PP, Thiry E, 1994. The control of infectious bovine rhinotracheitis virus. Annales de Médecine Vétérinaire, 138(3):167-180; many ref
Lemaire M, Schynts F, Meyer G, Georgin JP, Baranowski E, Gabriel A, Ros C, Belák S, Thiry E, 2001. Latency and reactivation of a glycoprotein E negative bovine herpesvirus type 1 vaccine: influence of virus load and effect of specific maternal antibodies. Vaccine, 19(32):4795-4804; 42 ref
Lemaire, M., Weynants, V., Godfroid, J., Schynts, F., Meyer, G., Letesson, J. J., Thiry, E., 2000. Effects of bovine herpesvirus type 1 infection in calves with maternal antibodies on immune response and virus latency. Journal of Clinical Microbiology, 38(5), 1885-1894.
Lomba F, Bienfet V, Wellemans G, 1976. IBR virus and occurrence of metritis in the bovine belgian blue white breed. British Veterinary Journal, 132:178-181
Maaten MJvan der, Miller JM, Whetstone CA, 1985. Ovarian lesions induced in heifers by intravenous inoculation with modified-live infectious bovine rhinotracheitis virus on the day after breeding. American Journal of Veterinary Research, 46(9):1996-1999; 7 ref
Manoj S, Griebel PJ, Babiuk LA, van Drunen Littel-van den Hurk S, 2004. Modulation of immune responses to bovine herpesvirus-1 in cattle by immunization with a DNA vaccine encoding glycoprotein D as a fusion protein with bovine CD154. Immunology, 112(2):328-338
Mars MH, Bruschke CJM, Oirschot JTvan, 1999. Airborne transmission of BHV 1 [bovine herpesvirus 1], BRSV [bovine respiratory virus], and BVDV [bovine virus diarrhoea virus] among cattle is possible under experimental conditions. Veterinary Microbiology, 66(3):197-207; 33 ref
Mars, M. H., Jong, M. C. M. de, Maanen, C. van, Hage, J. J., Oirschot, J. T. van, 2000. Airborne transmission of bovine herpesvirus 1 infections in calves under field conditions. Veterinary Microbiology, 76(1), 1-13. doi: 10.1016/S0378-1135(00)00218-2
Metzler, A. E., Matile, H., Gassmann, U., Engels, M., Wyler, R., 1985. European isolates of bovine herpesvirus 1: a comparison of restriction endonuclease sites, polypeptides, and reactivity with monoclonal antibodies. Archives of Virology, 85(1/2), 57-69. doi: 10.1007/BF01317006
Meyer, G., Lemaire, M., Ros, C., Belak, K., Gabriel, A., Cassart, D., Coignoul, F., Belak, S., Thiry, E., 2001. Comparative pathogenesis of acute and latent infections of calves with bovine herpesvirus types 1 and 5. Archives of Virology, 146(4), 633-652. doi: 10.1007/s007050170136
Miller JM, Whetstone CA, Maaten MJvan der, 1991. Abortifacient property of bovine herpesvirus type 1 isolates that represent three subtypes determined by restriction endonuclease analysis of viral DNA. American Journal of Veterinary Research, 52(3):458-461; 36 ref
OIE Handistatus, 2002. World Animal Health Publication and Handistatus II (dataset for 2001). Paris, France: Office International des Epizooties
OIE Handistatus, 2003. World Animal Health Publication and Handistatus II (dataset for 2002). Paris, France: Office International des Epizooties
OIE Handistatus, 2004. World Animal Health Publication and Handistatus II (data set for 2003). Paris, France: Office International des Epizooties
OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (data set for 2004). Paris, France: Office International des Epizooties
OIE, 2004. Manual of Diagnostic Tests and Vaccines for Terrestrial Animals. Paris, France: World Organisation for Animal Health. http://www.oie.int/eng/normes/mmanual/A_summry.htm
OIE, 2005. Terrestrial Animal Health Code. Paris, France: Office International Des Epizooties, Chapter 2.3.5. http://www.oie.int/eng/normes/mcode/en_INDEX.HTM#H
OIE, 2009. World Animal Health Information Database - Version: 1.4. World Animal Health Information Database. Paris, France: World Organisation for Animal Health. http://www.oie.int
Oirschot JTvan, Kaashoek MJ, Rijsewijk FAM, 1996. Advances in the development and evaluation of bovine herpesvirus 1 vaccines. Veterinary Microbiology, 53(1/2):43-54; 60 ref
Pastoret PP, Thiry E, Brochier B, Derboven G, 1982. Bovid herpesvirus 1 infection of cattle: pathogenesis, latency, consequences of latency. Annales de Recherche Vétérinaire, 13:221-235
Pastoret P-P, Thiry E, Brochier B, Derboven G, Vindevogel H, 1984. The role of latency in the epizootiology of infectious bovine rhinotracheitis. Latent herpesvirus infections in veterinary medicine, 211-227; [Series: Current Topics in Veterinary Medicine and Animal Science, volume 27]; 76 ref
Pauli G, Gregersen J-P, Storz J, Ludwig H, 1984. Biology and molecular biology of latent bovine herpes virus type 1 (BHV-1). Latent herpesvirus infections in veterinary medicine, 229-239; [Series: Current Topics in Veterinary Medicine and Animal Science, volume 27]; 14 ref
Pritchard GC, Banks M, Vernon RE, 2003. Subclinical breakdown with infectious bovine rhinotracheitis virus infection in dairy herd of high health status. Veterinary Record, 153(4):113-117
Pritchard GC, Kirkwood GM, Sayers AR, 2002. Detecting antibodies to infectious bovine rhinotracheitis and BVD virus infections using milk samples from individual cows. Veterinary Record, 150(6):182-183; 12 ref
Rijsewijk FAM, Kaashoek MJ, Langeveld JPM, Meloen R, Judek J, Bienkowska-Szewczyk K, Maris-Veldhuis MA, Oirschot JTvan, 1999. Epitopes on glycoprotein C of bovine herpesvirus-1 (BHV-1) that allow differentiation between BHV-1.1 and BHV-1.2 strains. Journal of General Virology, 80(6):1477-1483; 29 ref
Roels S et al., 2000. Natural case of bovine herpesvirus 1 meningo-encephalitis in an adult cow. Veterinary Record, 146:586-588
Ros C, Belák S, 1999. Studies of genetic relationships between bovine, caprine, cervine, and rangiferine alphaherpesviruses and improved molecular methods for virus detection and identification. Journal of Clinical Microbiology, 37(5):1247-1253; 39 ref
Ros C, Riquelme ME, Forslund Kö, Belák S, 1999. Improved detection of five closely related ruminant alphaherpesviruses by specific amplification of viral genomic sequences. Journal of Virological Methods, 83(1/2):55-65; 52 ref
Schaik Gvan, Dijkhuizen AA, Huirne RBM, Schukken YH, Nielen M, Hage HJ, 1998. Risk factors for existence of bovine herpes virus 1 antibodies on nonvaccinating Dutch dairy farms. Preventive Veterinary Medicine, 34(2/3):125-136; 20 ref
Schynts F, Baranowski E, Lemaire M, Thiry E, 1999. A specific PCR to differentiate between gE negative vaccine and wildtype bovine herpesvirus type 1 strains. Veterinary Microbiology, 66(3):187-195; 33 ref
Schynts F, Meurens F, Detry B, Vanderplasschen A, Thiry E, 2003. Rise and survival of bovine herpesvirus 1 recombinants after primary infection and reactivation from latency. Journal of Virology, 77(23):12535-12542
Six A, Banks M, Engels M, Bascunana CR, Ackermann M, 2001. Latency and reactivation of bovine herpesvirus 1 (BHV-1) in goats and of caprine herpesvirus 1 (CapHV-1) in calves. Archives of Virology, 146(7):1325-1335; 38 ref
Smith KC, 1997. Herpesviral abortion in domestic animals. Veterinary Journal, 153(3):253-268; many ref
Smits, C. B., Maanen, C. van, Glas, R. D., Gee, A. L. W. de, Dijkstrab, T., Oirschot, J. T. van, Rijsewijk, F. A. M., 2000. Comparison of three polymerase chain reaction methods for routine detection of bovine herpesvirus 1 DNA in fresh bull semen. Journal of Virological Methods, 85(1/2), 65-73. doi: 10.1016/S0166-0934(99)00153-6
Straub OC, 1990. Infectious bovine rhinotracheitis virus. Virus infections of ruminants., 71-108; 10 pp. of ref
Thiry E et al, 2001. Risk evaluation of cross-infection of cattle with ruminant alphaherpesviruses related to bovine herpesvirus type 1. In: Körber R, ed. Tagungsbeiträge, 3. Internationales Symposium zur BHV-1- und BVD-Bekämpfung, Stendal, in press
Thiry E, Detilleux P, Vriese Ade, Pirak M, Pastoret P-P, 1984. Infectious bovine rhinotracheitis in the neonatal period: a review and a case report. Annales de Médecine Vétérinaire, 128(1):33-40; 25 ref
Thiry E, Dubuisson J, Pastoret PP, 1986. Pathogenesis, latency and reactivation of infections by herpesviruses. Revue scientifique et technique de l'Office international des Epizooties, 5:209-222
Thiry E, Lemaire M, Schynts F, Meyer G, Dispas M, Gogev S, 1999. Infection of cattle with bovine herpesvirus 1. Point Vétérinaire, 30(199):279-286; 25 ref
Tikoo SK, Campos M, Babiuk LA, 1995. Bovine herpesvirus 1 (BHV-1): biology, pathogenesis, and control. Advances in Virus Research, 45:191-223; many ref
Wellenberg GJ, Mars MH, Oirschot JTvan, 2001. Antibodies against bovine herpesvirus (BHV) 5 may be differentiated from antibodies against BHV1 in a BHV1 glycoprotein E blocking ELISA. Veterinary Microbiology, 78(1):79-84; 12 ref
Wentink GH, Oirschot JTvan, Verhoeff J, 1993. Risk of infection with bovine herpesvirus 1 (BHV1): a review. Veterinary Quarterly, 15(1):30-33; 45 ref
Whetstone CA, Seal BS, Miller JM, 1993. Variability occurs in the inverted repeat region of genomic DNA from bovine herpesvirus 1 respiratory, genital and bovine herpesvirus 5 encephalitic isolates. Veterinary Microbiology, 38(1/2):181-189; 22 ref
Winkler MT, Doster A, Jones C, 2000. Persistence and reactivation of bovine herpesvirus 1 in the tonsils of latently infected calves. Journal of Virology, 74(11):5337-5347
Wit JJde, Hage JJ, Brinkhof J, Westenbrink F, 1998. A comparative study of serological tests for use in the bovine herpesvirus 1 eradication programme in The Netherlands. Veterinary Microbiology, 61(3):153-163; 23 ref
Woolums AR, Siger L, Johnson S, Gallo G, Conlon J, 2003. Rapid onset of protection following vaccination of calves with multivalent vaccines containing modified-live or modified-live and killed BHV-1 is associated with virus-specific interferon gamma production. Vaccine, 21(11/12):1158-1164
Wuijckhuise Lvan, Bosch J, Franken P, Frankena K, Elbers ARW, 1998. Epidemiological characteristics of bovine herpesvirus 1 infections determined by bulk milk testing of all Dutch dairy herds. Veterinary Record, 142(8):181-184; 22 ref
Wyler R, Engels M, Schwyzer M, 1989. Infectious Bovine Rhinotracheitis/Vulvovaginitis (BHV-1). In: Wittmann G, ed. Herpesvirus Diseases of Cattle, Horse and Pigs. Massachusetts, USA: Kluwer Academic Publishers, 1-72
OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (dataset for 2004)., Paris, France: Office International des Epizooties.
OIE, 2009. World Animal Health Information Database - Version: 1.4., Paris, France: World Organisation for Animal Health. https://www.oie.int/
Distribution MapsTop of page
Unsupported Web Browser:
One or more of the features that are needed to show you the maps functionality are not available in the web browser that you are using.
Please consider upgrading your browser to the latest version or installing a new browser.
More information about modern web browsers can be found at http://browsehappy.com/