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Antigenicity
- Two different viruses:
Infectious Bovine Rhinotracheitis
Infectious Pustular Vulvovaginitis
DATASHEET containing DISEASE first then VIRUS below references
This one may be difficult as we have separate disease pages on WV, which I think is better. I would suggest creating a general virus page with links to the specific diseases from that page. Let me know if you’re not sure what I mean.
Animal Health and Production Compendium
Selected sections for: bovine herpesvirus 1 infections
Identity Pathogen/s Overview Distribution Distribution Table Hosts/Species Affected Host Animals Systems Affected List of Symptoms/Signs Epidemiology Pathology Diagnosis Disease Course Disease Treatment Prevention and Control References Images
Datasheet Type(s): Animal Disease Identity
Preferred Scientific Name bovine herpesvirus 1 infections
International Common Names
English acronym
BHV
IBR
IPB
IPV
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
Pathogen/s
bovine herpesvirus 1
Overview
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 a genital disease called infectious pustular vulvovaginitis (IPV). This viral infection has been known for a long time. 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.
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 Handistatus 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.
Distribution BHV-1 is distributed worldwide and has been diagnosed in all countries tested (Straub, 1990). In recent years, a few European countries have successfully eradicated the infection by applying a strict culling policy:Denmark, Sweden, Finland, Switzerland and Austria (OIE, 2005). Other countries have started similar control programmes.
Distribution Table
Country Distribution Last Reported Origin First Reported Invasive References Notes ASIA Afghanistan No information available OIE, 2009
Armenia Disease not reported OIE, 2009
Azerbaijan Disease not reported OIE, 2009
Bahrain Disease never reported OIE, 2009
Bangladesh Disease not reported OIE, 2009
Bhutan Disease not reported OIE, 2009
Brunei Darussalam Disease not reported OIE Handistatus, 2005
Cambodia No information available OIE, 2009
China No information available OIE, 2009
-Hong Kong No information available OIE, 2009
Georgia (Republic of) Last reported 1989 OIE Handistatus, 2005
India Restricted distribution OIE, 2009
Indonesia Present OIE, 2009
Iran Present OIE, 2009
Iraq Disease not reported OIE, 2009
Israel Disease not reported OIE, 2009
Japan Present OIE, 2009
Jordan Present OIE, 2009
Kazakhstan Disease not reported OIE, 2009
Korea, DPR Disease not reported OIE Handistatus, 2005
Korea, Republic of Disease not reported OIE, 2009
Kuwait Disease not reported OIE, 2009
Kyrgyzstan Disease not reported OIE, 2009
Laos Disease not reported OIE, 2009
Lebanon Absent, reported but not confirmed OIE, 2009
Malaysia Disease not reported OIE, 2009
-Peninsular Malaysia Disease never reported OIE Handistatus, 2005
-Sabah Last reported 2001 OIE Handistatus, 2005
-Sarawak No information available OIE Handistatus, 2005
Mongolia No information available OIE, 2009
Myanmar Disease never reported OIE, 2009
Nepal Disease not reported OIE, 2009
Oman Disease not reported OIE, 2009
Pakistan No information available OIE, 2009
Philippines Disease never reported OIE, 2009
Qatar No information available OIE, 2009
Saudi Arabia Disease not reported OIE, 2009
Singapore Disease never reported OIE, 2009
Sri Lanka Disease never reported OIE, 2009
Syria Disease not reported OIE, 2009
Taiwan Last reported 1989 OIE Handistatus, 2005
Tajikistan Disease not reported OIE, 2009
Thailand Disease not reported OIE, 2009
Turkey No information available OIE, 2009
Turkmenistan Disease not reported OIE Handistatus, 2005
United Arab Emirates Disease not reported OIE, 2009
Uzbekistan Disease not reported OIE Handistatus, 2005
Vietnam Absent, reported but not confirmed OIE, 2009
Yemen No information available OIE, 2009
AFRICA Algeria Disease not reported OIE, 2009
Angola No information available OIE, 2009
Benin Disease not reported OIE, 2009
Botswana Disease not reported OIE, 2009
Burkina Faso No information available OIE, 2009
Burundi Disease never reported OIE Handistatus, 2005
Cameroon No information available OIE Handistatus, 2005
Cape Verde Disease never reported OIE Handistatus, 2005
Central African Republic Disease not reported OIE Handistatus, 2005
Chad No information available OIE, 2009
Congo No information available OIE, 2009
Congo Democratic Republic Disease not reported OIE Handistatus, 2005
Côte d'Ivoire Last reported 1996 OIE Handistatus, 2005
Djibouti Disease not reported OIE, 2009
Egypt Disease not reported OIE, 2009
Eritrea No information available OIE, 2009
Ethiopia No information available OIE, 2009
Gabon Disease never reported OIE, 2009
Gambia No information available OIE, 2009
Ghana No information available OIE, 2009
Guinea No information available OIE, 2009
Guinea-Bissau No information available OIE, 2009
Kenya Disease never reported OIE, 2009
Lesotho Disease not reported OIE, 2009
Libya Disease never reported OIE Handistatus, 2005
Madagascar Disease never reported OIE, 2009
Malawi No information available OIE, 2009
Mali No information available OIE, 2009
Mauritius Disease not reported OIE, 2009
Morocco Disease not reported OIE, 2009
Mozambique Disease never reported OIE, 2009
Namibia Present OIE, 2009
Nigeria No information available OIE, 2009
Réunion Last reported 2003 OIE Handistatus, 2005
Rwanda Disease never reported OIE, 2009
Sao Tome and Principe No information available OIE Handistatus, 2005
Senegal No information available OIE, 2009
Seychelles Disease not reported OIE Handistatus, 2005
Somalia No information available OIE Handistatus, 2005
South Africa Present OIE, 2009
Sudan Disease not reported OIE, 2009
Swaziland No information available OIE, 2009
Tanzania No information available OIE, 2009
Togo No information available OIE, 2009
Tunisia Disease not reported OIE, 2009
Uganda No information available OIE, 2009
Zambia No information available OIE, 2009
Zimbabwe Disease not reported OIE, 2009
NORTH AMERICA Bermuda Disease not reported OIE Handistatus, 2005
Canada Present OIE, 2009
Greenland Disease never reported OIE, 2009
Mexico Present OIE, 2009
USA Present OIE, 2009
-Georgia Disease not reported OIE, 2009
CENTRAL AMERICA Barbados CAB Abstracts data mining OIE Handistatus, 2005
Belize Disease not reported OIE, 2009
British Virgin Islands Disease never reported OIE Handistatus, 2005
Cayman Islands Disease not reported OIE Handistatus, 2005
Costa Rica Present OIE, 2009
Cuba Present OIE, 2009
Curaçao Disease not reported OIE Handistatus, 2005
Dominica Disease not reported OIE Handistatus, 2005
Dominican Republic Present OIE, 2009
El Salvador No information available OIE, 2009
Guadeloupe No information available OIE, 2009
Guatemala Present OIE, 2009
Haiti Disease never reported OIE, 2009
Honduras Disease not reported OIE, 2009
Jamaica Disease not reported OIE, 2009
Martinique Present OIE, 2009
Nicaragua Present OIE, 2009
Panama Present OIE, 2009
Saint Kitts and Nevis Disease never reported OIE Handistatus, 2005
Saint Vincent and the Grenadines Disease never reported OIE Handistatus, 2005
Trinidad and Tobago Disease never reported OIE Handistatus, 2005
SOUTH AMERICA Argentina Present OIE, 2009
Bolivia Present OIE, 2009
Brazil Present OIE, 2009
Chile Present OIE, 2009
Colombia Present OIE, 2009
Ecuador Present OIE, 2009
Falkland Islands Disease never reported OIE Handistatus, 2005
French Guiana Disease not reported OIE, 2009
Guyana Disease never reported OIE Handistatus, 2005
Paraguay Reported present or known to be present OIE Handistatus, 2005
Peru Restricted distribution OIE, 2009
Uruguay Present OIE, 2009
Venezuela Present OIE, 2009
EUROPE Albania No information available OIE, 2009
Andorra Reported present or known to be present OIE Handistatus, 2005
Austria Disease not reported OIE, 2009
Belarus Disease not reported OIE, 2009
Belgium Present OIE, 2009
Bosnia-Hercegovina Last reported 2002 OIE Handistatus, 2005
Bulgaria Present OIE, 2009
Croatia Disease not reported OIE, 2009
Cyprus Present OIE, 2009
Czech Republic Disease not reported OIE, 2009
Denmark Disease not reported OIE, 2009
Estonia Present OIE, 2009
Finland Disease not reported OIE, 2009
France No information available OIE, 2009
Germany Disease not reported OIE, 2009
Greece Restricted distribution OIE, 2009
Hungary Present OIE, 2009
Iceland Disease never reported OIE, 2009
Ireland No information available OIE, 2009
Isle of Man (UK) Reported present or known to be present OIE Handistatus, 2005
Italy Disease not reported OIE, 2009
Jersey Disease never reported OIE Handistatus, 2005
Latvia Disease not reported OIE, 2009
Liechtenstein Absent, reported but not confirmed OIE, 2009
Lithuania Present OIE, 2009
Luxembourg Present OIE, 2009
Macedonia Absent, reported but not confirmed OIE, 2009
Malta Disease not reported OIE, 2009
Moldova Last reported 1992 OIE Handistatus, 2005
Montenegro Disease not reported OIE, 2009
Netherlands Present OIE, 2009
Norway Disease not reported OIE, 2009
Poland Present OIE, 2009
Portugal Present OIE, 2009
Romania Disease not reported OIE, 2009
Russian Federation Present OIE, 2009
Serbia Present OIE, 2009
Slovakia Present OIE, 2009
Slovenia Disease not reported OIE, 2009
Spain Restricted distribution OIE, 2009
Sweden Disease not reported OIE, 2009
Switzerland Disease not reported OIE, 2009
Ukraine Disease not reported OIE, 2009
United Kingdom
-Northern Ireland Reported present or known to be present OIE Handistatus, 2005
United Kingdom Present OIE, 2009
Yugoslavia (former) No information available OIE Handistatus, 2005
Yugoslavia (Serbia and Montenegro) Reported present or known to be present OIE Handistatus, 2005
OCEANIA Australia Present OIE, 2009
French Polynesia No information available OIE, 2009
New Caledonia Present OIE, 2009
New Zealand Present OIE, 2009
Samoa Disease not reported OIE Handistatus, 2005
Vanuatu Serological evidence and/or isolation of the agent OIE Handistatus, 2005
Wallis and Futuna Islands No information available OIE Handistatus, 2005
Hosts/Species Affected
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).
Host Animals
Animal name Context 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 Bubalus bubalis (buffalo) Domesticated host, Wild host Capra hircus (goats) Domesticated host, Wild host Capreolus capreolus Wild host Cervus dama Wild host Cervus elaphus (red deer) Wild host Cervus elaphus canadensis 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 Wild host Odocoileus virginianus Wild host Ovis aries (sheep) Domesticated host, Wild host Rangifer tarandus (reindeer) Wild host Redunca arundinum Wild host Redunca redunca Wild host Rupicapra rupicapra Domesticated host, Wild host Sus scrofa (pigs)
Syncerus caffer Domesticated host, Wild host Tragelaphus oryx Wild host Tragelaphus strepsiceros Wild host
Systems Affected
Reproductive - Large Ruminants Reproductive - Pigs Reproductive - Small Ruminants Respiratory - Large Ruminants Respiratory - Small Ruminants
List of Symptoms/Signs
Sign Type Cardiovascular Signs Tachycardia, rapid pulse, high heart rate Sign [C] Digestive Signs Anorexia, loss or decreased appetite, not nursing, off feed Sign [C] Excessive salivation, frothing at the mouth, ptyalism Sign [C] Grinding teeth, bruxism, odontoprisis Sign [C] Tongue weakness, paresis, paralysis Sign [C] Dysphagia, difficulty swallowing Sign [C] General Signs Abnormal proprioceptive positioning, knuckling Sign [C] Opisthotonus Sign [C] Inability to stand, downer, prostration Sign [C] Dysmetria, hypermetria, hypometria Sign [C] Ataxia, incoordination, staggering, falling Sign [C] Generalized weakness, paresis, paralysis Sign [C] Tetraparesis, weakness, paralysis all four limbs Sign [C] Paraparesis, weakness, paralysis both hind limbs Sign [C] Trembling, shivering, fasciculations, chilling Sign [C] Fever, pyrexia, hyperthermia Sign [C] Sudden death, found dead Sign [C] Nervous Signs Hyperesthesia, irritable, hyperactive Sign [C] Abnormal behavior, aggression, changing habits Sign [C] Dullness, depression, lethargy, depressed, lethargic, listless Sign [C] Head pressing Sign [C] Propulsion, aimless wandering Sign [C] Constant or increased vocalization Sign [C] Coma, stupor Sign [C] Head tilt Sign [C] Circling Sign [C] Excitement, delirium, mania Sign [C] Seizures or syncope, convulsions, fits, collapse Sign [C] Tremor Sign [C] Ophthalmology Signs Conjunctival, scleral, redness Sign [C] Conjunctival, scleral, injection, abnormal vasculature Sign [C] Lacrimation, tearing, serous ocular discharge, watery eyes Sign [C] Blindness Sign [C] Nystagmus Sign [C] Chemosis, conjunctival, scleral edema, swelling Sign [C] Pain/Discomfort Signs Colic, abdominal pain Sign [C] Pain, vulva, vagina Sign [C] Pain, penis Sign [C] Reproductive Signs Mucous discharge, vulvar, vaginal Sign [C] Abnormal length estrus cycle, long, short, irregular interestrus period Sign [C] Female infertility, repeat breeder Sign [C] Male infertility Sign [C] Abortion or weak newborns, stillbirth Sign [C] Papule, pustule, vesicle, ulcer penis or prepuce Sign [C] Purulent discharge, penis or prepuce Sign [C] Purulent discharge, vulvar, vaginal Sign [C] Vaginal or cervical ulcers, vesicles, erosions, tears, papules, pustules Sign [C] Female infertility, repeat breeder Sign [C] Respiratory Signs Mucoid nasal discharge, serous, watery Sign [C] Dyspnea, difficult, open mouth breathing, grunt, gasping Sign [C] Increased respiratory rate, polypnea, tachypnea, hyperpnea Sign [C] Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs Sign [C] Skin/Integumentary Signs Pruritus, itching skin Sign [C] Alopecia, thinning, shedding, easily epilated, loss of, hair Sign [C]
Epidemiology Transmission
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).
Risk factors
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).
Pathology
Subclinical infection
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. Although BHV-1 is associated with the multifactorial respiratory disease complex of cattle, 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).
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).
Metritis
Metroperitonitis has been observed in cows infected with BHV-1 around parturition, and especially after caesarean section (Lomba et al., 1976).
Encephalitis
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 diseases
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).
Diagnosis
Clinical diagnosis
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
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.
Laboratory diagnosis
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).
Disease Course
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).
Disease Treatment
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 Control
Vaccination
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. 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.
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Images
Picture Title Caption Copyright
Pathology An intense inflammation is observed in the nasal cavity: hyperaemia, oedema, pseudomembranes and ulcers. Etienne Thiry Pathology Tracheitis is frequently observed in clinical infectious bovine rhinotracheitis. In addition to the inflammatory signs, mucopurulent secretions and blood collection are visible in the lumen of the trachea. Etienne Thiry Pathology - cut section of a lesion in a lung affected by bovine rhinotracheitis A typical lesion in the lung of an animal affected with acute infectious bovine rhinotracheitis. On cut section this lesion is represented by the fleurettes of the inflamed terminal bronchiolar tree. Paul R. Greenough
Date of report: 03/04/2011
© CAB International 2010
Animal Health and Production Compendium
Selected sections for: bovine herpesvirus 1
Identity Taxonomic Tree Disease/s Table Distribution Table Pathogen Characteristics Host Animals References Images
Datasheet Type(s): Pathogen Identity
Preferred Scientific Name bovine herpesvirus 1
International Common Names
English acronym
BoHV-1
IBRV
English
infectious bovine rhinotracheitis virus
Taxonomic Tree
Domain: Virus Group: "dsDNA viruses" Group: "DNA viruses" Order: Caudovirales Family: Herpesviridae Genus: Varicellovirus Species: bovine herpesvirus 1
Disease/s Table
bovine herpesvirus 1 infections
granulomatous vulvitis in cattle
infectious pustular vulvovaginitis
Distribution Table
Country Distribution Last Reported Origin First Reported Invasive References Notes ASIA Azerbaijan No information available OIE Handistatus, 2005
Bahrain Disease never reported OIE Handistatus, 2005
Bhutan Serological evidence and/or isolation of the agent OIE Handistatus, 2005
Brunei Darussalam Disease not reported OIE Handistatus, 2005
China
-Hong Kong No information available OIE Handistatus, 2005
Georgia (Republic of) Last reported 1989 OIE Handistatus, 2005
India OIE Handistatus, 2005
-Andaman and Nicobar Islands CAB Abstracts data mining CAB ABSTRACTS Data Mining 2001 Indonesia Reported present or known to be present OIE Handistatus, 2005
Iran Reported present or known to be present OIE Handistatus, 2005
Iraq Last reported 2002 OIE Handistatus, 2005
Israel No information available OIE Handistatus, 2005
Japan Reported present or known to be present OIE Handistatus, 2005
Jordan Serological evidence and/or isolation of the agent OIE Handistatus, 2005
Kazakhstan Disease not reported OIE Handistatus, 2005
Korea, DPR Disease not reported OIE Handistatus, 2005
Korea, Republic of Last reported 2003 OIE Handistatus, 2005
Kuwait Reported present or known to be present OIE Handistatus, 2005
Lebanon Disease not reported OIE Handistatus, 2005
Malaysia
-Peninsular Malaysia Disease never reported OIE Handistatus, 2005
-Sabah Last reported 2001 OIE Handistatus, 2005
-Sarawak No information available OIE Handistatus, 2005
Mongolia No information available OIE Handistatus, 2005
Myanmar Disease never reported OIE Handistatus, 2005
Nepal Disease not reported OIE Handistatus, 2005
Oman Disease not reported OIE Handistatus, 2005
Philippines Disease never reported OIE Handistatus, 2005
Qatar No information available OIE Handistatus, 2005
Saudi Arabia Disease not reported OIE Handistatus, 2005
Singapore Disease never reported OIE Handistatus, 2005
Sri Lanka Disease never reported OIE Handistatus, 2005
Syria Disease not reported OIE Handistatus, 2005
Taiwan Last reported 1989 OIE Handistatus, 2005
Tajikistan No information available OIE Handistatus, 2005
Thailand Disease not reported OIE Handistatus, 2005
Turkey No information available OIE Handistatus, 2005
Turkmenistan Disease not reported OIE Handistatus, 2005
United Arab Emirates Disease not reported OIE Handistatus, 2005
Uzbekistan Disease not reported OIE Handistatus, 2005
Vietnam Disease never reported OIE Handistatus, 2005
Yemen No information available OIE Handistatus, 2005
AFRICA Algeria Last reported 1997 OIE Handistatus, 2005
Angola Disease not reported OIE Handistatus, 2005
Benin No information available OIE Handistatus, 2005
Botswana Serological evidence and/or isolation of the agent OIE Handistatus, 2005
Burkina Faso No information available OIE Handistatus, 2005
Burundi Disease never reported OIE Handistatus, 2005
Cameroon No information available OIE Handistatus, 2005
Cape Verde Disease never reported OIE Handistatus, 2005
Central African Republic Disease not reported OIE Handistatus, 2005
Chad No information available OIE Handistatus, 2005
Congo Democratic Republic Disease not reported OIE Handistatus, 2005
Côte d'Ivoire Last reported 1996 OIE Handistatus, 2005
Djibouti Disease not reported OIE Handistatus, 2005
Egypt Reported present or known to be present OIE Handistatus, 2005
Eritrea Disease not reported OIE Handistatus, 2005
Ghana Disease not reported OIE Handistatus, 2005
Guinea-Bissau No information available OIE Handistatus, 2005
Kenya Disease never reported OIE Handistatus, 2005
Libya Disease never reported OIE Handistatus, 2005
Madagascar Disease never reported OIE Handistatus, 2005
Malawi No information available OIE Handistatus, 2005
Mali No information available OIE Handistatus, 2005
Mauritius Disease not reported OIE Handistatus, 2005
Morocco Disease not reported OIE Handistatus, 2005
Mozambique No information available OIE Handistatus, 2005
Namibia Last reported 2002 OIE Handistatus, 2005
Nigeria No information available OIE Handistatus, 2005
Réunion Last reported 2003 OIE Handistatus, 2005
Rwanda No information available OIE Handistatus, 2005
Sao Tome and Principe No information available OIE Handistatus, 2005
Senegal No information available OIE Handistatus, 2005
Seychelles Disease not reported OIE Handistatus, 2005
Somalia No information available OIE Handistatus, 2005
South Africa Reported present or known to be present OIE Handistatus, 2005
Sudan Disease not reported OIE Handistatus, 2005
Swaziland Disease not reported OIE Handistatus, 2005
Tanzania No information available OIE Handistatus, 2005
Togo Disease not reported OIE Handistatus, 2005
Tunisia Disease not reported OIE Handistatus, 2005
Uganda No information available OIE Handistatus, 2005
Zambia No information available OIE Handistatus, 2005
Zimbabwe No information available OIE Handistatus, 2005
NORTH AMERICA Bermuda Disease not reported OIE Handistatus, 2005
Canada Reported present or known to be present OIE Handistatus, 2005
Mexico OIE Handistatus, 2005
USA Reported present or known to be present OIE Handistatus, 2005
CENTRAL AMERICA Barbados CAB Abstracts data mining OIE Handistatus, 2005
Belize Disease not reported OIE Handistatus, 2005
British Virgin Islands Disease never reported OIE Handistatus, 2005
Cayman Islands Disease not reported OIE Handistatus, 2005
Costa Rica Reported present or known to be present OIE Handistatus, 2005
Cuba Reported present or known to be present OIE Handistatus, 2005
Curaçao Disease not reported OIE Handistatus, 2005
Dominica Disease not reported OIE Handistatus, 2005
Dominican Republic Reported present or known to be present OIE Handistatus, 2005
El Salvador Last reported 2001 OIE Handistatus, 2005
Guadeloupe No information available OIE Handistatus, 2005
Guatemala Reported present or known to be present OIE Handistatus, 2005
Haiti Disease never reported OIE Handistatus, 2005
Honduras Serological evidence and/or isolation of the agent OIE Handistatus, 2005
Jamaica Last reported 1968 OIE Handistatus, 2005
Martinique Reported present or known to be present OIE Handistatus, 2005
Nicaragua Reported present or known to be present OIE Handistatus, 2005
Panama No information available OIE Handistatus, 2005
Saint Kitts and Nevis Disease never reported OIE Handistatus, 2005
Saint Vincent and the Grenadines Disease never reported OIE Handistatus, 2005
Trinidad and Tobago Disease never reported OIE Handistatus, 2005
SOUTH AMERICA Argentina Reported present or known to be present OIE Handistatus, 2005
Bolivia Reported present or known to be present OIE Handistatus, 2005
Brazil Reported present or known to be present OIE Handistatus, 2005
Chile Reported present or known to be present OIE Handistatus, 2005
Colombia Reported present or known to be present OIE Handistatus, 2005
Ecuador Reported present or known to be present OIE Handistatus, 2005
Falkland Islands Disease never reported OIE Handistatus, 2005
French Guiana Serological evidence and/or isolation of the agent OIE Handistatus, 2005
Guyana Disease never reported OIE Handistatus, 2005
Paraguay Reported present or known to be present OIE Handistatus, 2005
Peru Serological evidence and/or isolation of the agent OIE Handistatus, 2005
Uruguay Reported present or known to be present OIE Handistatus, 2005
Venezuela OIE Handistatus, 2005
EUROPE Andorra Reported present or known to be present OIE Handistatus, 2005
Austria Reported present or known to be present OIE Handistatus, 2005
Belarus Reported present or known to be present OIE Handistatus, 2005
Belgium No information available OIE Handistatus, 2005
Bosnia-Hercegovina Last reported 2002 OIE Handistatus, 2005
Bulgaria Last reported 1996 OIE Handistatus, 2005
Croatia No information available OIE Handistatus, 2005
Cyprus No information available OIE Handistatus, 2005
Czech Republic Reported present or known to be present OIE Handistatus, 2005
Denmark Last reported 2003 OIE Handistatus, 2005
Estonia Serological evidence and/or isolation of the agent OIE Handistatus, 2005
Europe CAB Abstracts data mining CAB ABSTRACTS Data Mining 2001 Finland Last reported 1994 OIE Handistatus, 2005
France Reported present or known to be present OIE Handistatus, 2005
Germany Reported present or known to be present OIE Handistatus, 2005
Greece Last reported 2003 OIE Handistatus, 2005
Hungary OIE Handistatus, 2005
Iceland Disease never reported OIE Handistatus, 2005
Ireland Reported present or known to be present OIE Handistatus, 2005
Isle of Man (UK) Reported present or known to be present OIE Handistatus, 2005
Italy Last reported 2002 OIE Handistatus, 2005
Jersey Disease never reported OIE Handistatus, 2005
Latvia Reported present or known to be present OIE Handistatus, 2005
Liechtenstein Disease not reported OIE Handistatus, 2005
Lithuania Serological evidence and/or isolation of the agent OIE Handistatus, 2005
Luxembourg Serological evidence and/or isolation of the agent OIE Handistatus, 2005
Macedonia Reported present or known to be present OIE Handistatus, 2005
Malta No information available OIE Handistatus, 2005
Moldova Last reported 1992 OIE Handistatus, 2005
Netherlands Reported present or known to be present OIE Handistatus, 2005
Norway Last reported 1992 OIE Handistatus, 2005
Poland Serological evidence and/or isolation of the agent OIE Handistatus, 2005
Portugal Reported present or known to be present OIE Handistatus, 2005
Romania OIE Handistatus, 2005
Russian Federation Reported present or known to be present OIE Handistatus, 2005
Slovakia Reported present or known to be present OIE Handistatus, 2005
Slovenia Serological evidence and/or isolation of the agent OIE Handistatus, 2005
Spain Reported present or known to be present OIE Handistatus, 2005
Sweden Last reported 1995 OIE Handistatus, 2005
Switzerland Reported present or known to be present OIE Handistatus, 2005
Ukraine Last reported 2002 OIE Handistatus, 2005
United Kingdom
-Northern Ireland Reported present or known to be present OIE Handistatus, 2005
United Kingdom Reported present or known to be present OIE Handistatus, 2005
Yugoslavia (former) No information available OIE Handistatus, 2005
Yugoslavia (Serbia and Montenegro) Reported present or known to be present OIE Handistatus, 2005
OCEANIA Australia Reported present or known to be present OIE Handistatus, 2005
French Polynesia Reported present or known to be present OIE Handistatus, 2005
New Caledonia Reported present or known to be present OIE Handistatus, 2005
New Zealand Reported present or known to be present OIE Handistatus, 2005
Samoa Disease not reported OIE Handistatus, 2005
Vanuatu Serological evidence and/or isolation of the agent OIE Handistatus, 2005
Wallis and Futuna Islands No information available OIE Handistatus, 2005
Pathogen Characteristics
BHV-1 belongs to the family Herpesviridae, subfamily Alphaherpesvirinae, genus Varicellovirus. BHV-1 is an enveloped virus with an icosahedric capsid made of 162 capsomeres (Schwyzer and Ackermann, 1996). The genome is double-stranded DNA. At least ten glycoproteins are present on the envelope. They can be differentiated into glycoproteins essential for virus replication like gB, gD and gH, and non essential glycoproteins like gC, gE and gI (Baranowski et al., 1996). The three major glycoproteins, i.e. the most abundant ones in the virion, are gB, gC and gD.
The virus exhibits a tropism for epithelial cells, blood mononuclear cells and neurones. Virus replication takes place in the nucleus of the infected cell.
BHV-1 has two subtypes, called subtype 1 and 2, which can be characterized by the restriction endonuclease profiles of viral DNA (Engels et al., 1987), and by a few discriminating monoclonal antibodies (Metzler et al., 1985; Rijsewijk et al., 1999). All BHV-1 strains are very close, both antigenically and genomically. Since the 1970s, strains of subtype 1 have mainly been isolated from the respiratory tract (IBR strains). Strains of subtype 2 are mainly genital viruses, which had been isolated before the 1970s (Edwards et al., 1990). However, the subtype distinction does not segregate all the respiratory strains from the genital isolates. Strains isolated from aborted foetuses mainly belong to subtype 1 (Pauli et al., 1984; Miller et al., 1991). Whatever the vaccine strain used, each subtype will successfully protect against the other one.
Previously, BHV-1 subtype 3 was assigned a virus species and is now called BHV-5 or bovine encephalitis herpesvirus (Brake and Studdert, 1985).
BHV-1 strains can also be distinguished on the basis of their virulence. Hypervirulent and attenuated strains have been characterized by the induced clinical signs in experimentally infected animals (Kaashoek et al., 1996). However, the virulence character cannot be linked to a biochemical marker.
Several alphaherpesviruses isolated from other ruminant species are closely related to BHV-1: caprine herpesvirus 1 (CapHV-1) (Engels et al., 1987), cervine herpesvirus 1 (CerHV-1) (Inglis et al., 1983), rangiferine herpesvirus 1 (RanHV-1) (Ek-Kommonen et al., 1986) and buffalo herpesvirus (Brake and Studdert, 1985). Recently, a herpesvirus related to BHV-1 was also isolated from elk (Deregt et al., 2000).
Disease(s) associated with this pathogen is/are on the list of diseases notifiable to the World Organisation for Animal Health (OIE). The distribution section contains data from OIE's Handistatus database on disease occurrence. Please see the AHPC library for further information 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 Animals
Animal name Context 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, Wild host Bubalus bubalis (buffalo) Domesticated host, Wild host Capra hircus (goats) Domesticated host, Wild host Capreolus capreolus Wild host Cervus dama Wild host Cervus elaphus (red deer) Wild host Cervus elaphus canadensis Wild host Connochaetes gnou Wild host Connochaetes taurinus Wild 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 Wild host Odocoileus virginianus Wild host Oryctolagus cuniculus (rabbits) Ovis aries (sheep) Domesticated host, Wild host Ovis musimon Domesticated host, Wild host Rangifer tarandus (reindeer) Wild host Redunca arundinum Wild host Redunca redunca Wild host Rupicapra rupicapra Domesticated host, Wild host Syncerus caffer Domesticated host, Wild host Tragelaphus oryx Wild host Tragelaphus strepsiceros Wild host
References
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.
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.
Deregt D et al., 2000. Antigenic and molecular characterization of a herpesvirus isolated from a North American elk. American Journal of Veterinary Research, 61:1614-1618.
Edwards S, White H, Nixon P, 1990. A study of the predominant genotypes of bovid herpesvirus 1 found in the UK. Veterinary Microbiology, 22(2/3):213-223; 21 ref.
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.
Engels M et al., 1987. The genome of bovine herpesvirus 1 (BHV-1) strains exhibiting a neuropathogenic potential compared to known BHV-1 strains by restriction site mapping and cross-hybridization. Virus Research, 6:57-73.
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.
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.
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.
Metzler AE et al., 1985. European isolates of bovine herpesvirus 1: a comparison of restriction endonuclease sites, polypeptides and reactivity with monoclonal antibodies. Archives of Virology, 85:57-69.
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, 2005. World Animal Health Publication and Handistatus II (data set for 2004). Paris, France: Office International des Epizooties.
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.
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.
Schwyzer M, Ackermann M, 1996. Molecular virology of ruminant herpesviruses. Veterinary Microbiology, 53(1/2):17-29; 83 ref.
Images
Picture Title Caption Copyright
Electron micrograph Electron micrograph of bovine herpesvirus 1 particles. The envelope surrounds the icosahedral capsid. Etienne Thiry Genome The Bovine herpesvirus 1 genome is subdivided in two parts covalently linked: a long unit (UL, 104 kbp) and a short unit (US, 10 kbp), flanked by two inverted repeat regions of 11 kbp (Internal Repeat (IR) and Terminal Repeat (TR)). The localization of glycoprotein genes is indicated. Etienne Thiry
Date of report: 03/04/2011
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