Difference between revisions of "Bovine Herpesvirus 1"

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[[Infectious Pustular Vulvovaginitis]]
 
[[Infectious Pustular Vulvovaginitis]]
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DATASHEET containing DISEASE first then VIRUS below references
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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.
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Animal Health and Production Compendium
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Selected sections for: bovine herpesvirus 1 infections
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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     
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Datasheet Type(s): Animal Disease
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Identity
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Preferred Scientific Name
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bovine herpesvirus 1 infections
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International Common Names
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English acronym
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BHV
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IBR
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IPB
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IPV
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English
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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
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Pathogen/s
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bovine herpesvirus 1
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Overview
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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.
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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.
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Distribution
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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.
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Distribution Table
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Country Distribution Last Reported Origin First Reported Invasive References Notes
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ASIA
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Afghanistan
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No information available OIE, 2009
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Armenia
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Disease not reported OIE, 2009
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Azerbaijan
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Disease not reported OIE, 2009
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Bahrain
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Disease never reported OIE, 2009
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Bangladesh
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Disease not reported OIE, 2009
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Bhutan
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Disease not reported OIE, 2009
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Brunei Darussalam
 +
Disease not reported OIE Handistatus, 2005
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Cambodia
 +
No information available OIE, 2009
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China
 +
No information available OIE, 2009
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-Hong Kong
 +
No information available OIE, 2009
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Georgia (Republic of)
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Last reported 1989 OIE Handistatus, 2005
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India
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Restricted distribution OIE, 2009
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Indonesia
 +
Present OIE, 2009
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Iran
 +
Present OIE, 2009
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Iraq
 +
Disease not reported OIE, 2009
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Israel
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Disease not reported OIE, 2009
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Japan
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Present OIE, 2009
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Jordan
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Present OIE, 2009
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Kazakhstan
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Disease not reported OIE, 2009
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Korea, DPR
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Disease not reported OIE Handistatus, 2005
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Korea, Republic of
 +
Disease not reported OIE, 2009
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Kuwait
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Disease not reported OIE, 2009
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Kyrgyzstan
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Disease not reported OIE, 2009
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Laos
 +
Disease not reported OIE, 2009
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Lebanon
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Absent, reported but not confirmed OIE, 2009
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Malaysia
 +
Disease not reported OIE, 2009
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-Peninsular Malaysia
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Disease never reported OIE Handistatus, 2005
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-Sabah
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Last reported 2001 OIE Handistatus, 2005
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-Sarawak
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No information available OIE Handistatus, 2005
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Mongolia
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No information available OIE, 2009
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Myanmar
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Disease never reported OIE, 2009
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Nepal
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Disease not reported OIE, 2009
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Oman
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Disease not reported OIE, 2009
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Pakistan
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No information available OIE, 2009
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Philippines
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Disease never reported OIE, 2009
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Qatar
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No information available OIE, 2009
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Saudi Arabia
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Disease not reported OIE, 2009
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Singapore
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Disease never reported OIE, 2009
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Sri Lanka
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Disease never reported OIE, 2009
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Syria
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Disease not reported OIE, 2009
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Taiwan
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Last reported 1989 OIE Handistatus, 2005
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Tajikistan
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Disease not reported OIE, 2009
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Thailand
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Disease not reported OIE, 2009
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Turkey
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No information available OIE, 2009
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Turkmenistan
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Disease not reported OIE Handistatus, 2005
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United Arab Emirates
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Disease not reported OIE, 2009
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Uzbekistan
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Disease not reported OIE Handistatus, 2005
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Vietnam
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Absent, reported but not confirmed OIE, 2009
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Yemen
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No information available OIE, 2009
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AFRICA
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Algeria
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Disease not reported OIE, 2009
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Angola
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No information available OIE, 2009
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Benin
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Disease not reported OIE, 2009
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Botswana
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Disease not reported OIE, 2009
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Burkina Faso
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No information available OIE, 2009
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Burundi
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Disease never reported OIE Handistatus, 2005
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Cameroon
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No information available OIE Handistatus, 2005
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Cape Verde
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Disease never reported OIE Handistatus, 2005
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Central African Republic
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Disease not reported OIE Handistatus, 2005
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Chad
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No information available OIE, 2009
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Congo
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No information available OIE, 2009
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Congo Democratic Republic
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Disease not reported OIE Handistatus, 2005
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Côte d'Ivoire
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Last reported 1996 OIE Handistatus, 2005
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Djibouti
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Disease not reported OIE, 2009
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Egypt
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Disease not reported OIE, 2009
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Eritrea
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No information available OIE, 2009
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Ethiopia
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No information available OIE, 2009
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Gabon
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Disease never reported OIE, 2009
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Gambia
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No information available OIE, 2009
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Ghana
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No information available OIE, 2009
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Guinea
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No information available OIE, 2009
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Guinea-Bissau
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No information available OIE, 2009
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Kenya
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Disease never reported OIE, 2009
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Lesotho
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Disease not reported OIE, 2009
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Libya
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Disease never reported OIE Handistatus, 2005
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Madagascar
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Disease never reported OIE, 2009
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Malawi
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No information available OIE, 2009
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Mali
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No information available OIE, 2009
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Mauritius
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Disease not reported OIE, 2009
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Morocco
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Disease not reported OIE, 2009
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Mozambique
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Disease never reported OIE, 2009
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Namibia
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Present OIE, 2009
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Nigeria
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No information available OIE, 2009
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Réunion
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Last reported 2003 OIE Handistatus, 2005
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Rwanda
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Disease never reported OIE, 2009
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Sao Tome and Principe
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No information available OIE Handistatus, 2005
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Senegal
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No information available OIE, 2009
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Seychelles
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Disease not reported OIE Handistatus, 2005
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Somalia
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No information available OIE Handistatus, 2005
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South Africa
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Present OIE, 2009
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Sudan
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Disease not reported OIE, 2009
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Swaziland
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No information available OIE, 2009
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Tanzania
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No information available OIE, 2009
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Togo
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No information available OIE, 2009
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Tunisia
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Disease not reported OIE, 2009
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Uganda
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No information available OIE, 2009
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Zambia
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No information available OIE, 2009
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Zimbabwe
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Disease not reported OIE, 2009
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NORTH AMERICA
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Bermuda
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Disease not reported OIE Handistatus, 2005
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Canada
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Present OIE, 2009
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Greenland
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Disease never reported OIE, 2009
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Mexico
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Present OIE, 2009
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USA
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Present OIE, 2009
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-Georgia
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Disease not reported OIE, 2009
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CENTRAL AMERICA
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Barbados
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CAB Abstracts data mining OIE Handistatus, 2005
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Belize
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Disease not reported OIE, 2009
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British Virgin Islands
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Disease never reported OIE Handistatus, 2005
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Cayman Islands
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Disease not reported OIE Handistatus, 2005
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Costa Rica
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Present OIE, 2009
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Cuba
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Present OIE, 2009
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Curaçao
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Disease not reported OIE Handistatus, 2005
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Dominica
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Disease not reported OIE Handistatus, 2005
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Dominican Republic
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Present OIE, 2009
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El Salvador
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No information available OIE, 2009
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Guadeloupe
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No information available OIE, 2009
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Guatemala
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Present OIE, 2009
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Haiti
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Disease never reported OIE, 2009
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Honduras
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Disease not reported OIE, 2009
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Jamaica
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Disease not reported OIE, 2009
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Martinique
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Present OIE, 2009
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Nicaragua
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Present OIE, 2009
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Panama
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Present OIE, 2009
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Saint Kitts and Nevis
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Disease never reported OIE Handistatus, 2005
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Saint Vincent and the Grenadines
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Disease never reported OIE Handistatus, 2005
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Trinidad and Tobago
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Disease never reported OIE Handistatus, 2005
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SOUTH AMERICA
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Argentina
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Present OIE, 2009
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Bolivia
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Present OIE, 2009
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Brazil
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Present OIE, 2009
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Chile
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Present OIE, 2009
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Colombia
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Present OIE, 2009
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Ecuador
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Present OIE, 2009
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Falkland Islands
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Disease never reported OIE Handistatus, 2005
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French Guiana
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Disease not reported OIE, 2009
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Guyana
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Disease never reported OIE Handistatus, 2005
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Paraguay
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Reported present or known to be present OIE Handistatus, 2005
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Peru
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Restricted distribution OIE, 2009
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Uruguay
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Present OIE, 2009
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Venezuela
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Present OIE, 2009
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EUROPE
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Albania
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No information available OIE, 2009
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Andorra
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Reported present or known to be present OIE Handistatus, 2005
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Austria
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Disease not reported OIE, 2009
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Belarus
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Disease not reported OIE, 2009
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Belgium
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Present OIE, 2009
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Bosnia-Hercegovina
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Last reported 2002 OIE Handistatus, 2005
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Bulgaria
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Present OIE, 2009
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Croatia
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Disease not reported OIE, 2009
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Cyprus
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Present OIE, 2009
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Czech Republic
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Disease not reported OIE, 2009
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Denmark
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Disease not reported OIE, 2009
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Estonia
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Present OIE, 2009
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Finland
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Disease not reported OIE, 2009
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France
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No information available OIE, 2009
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Germany
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Disease not reported OIE, 2009
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Greece
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Restricted distribution OIE, 2009
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Hungary
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Present OIE, 2009
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Iceland
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Disease never reported OIE, 2009
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Ireland
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No information available OIE, 2009
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Isle of Man (UK)
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Reported present or known to be present OIE Handistatus, 2005
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Italy
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Disease not reported OIE, 2009
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Jersey
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Disease never reported OIE Handistatus, 2005
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Latvia
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Disease not reported OIE, 2009
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Liechtenstein
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Absent, reported but not confirmed OIE, 2009
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Lithuania
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Present OIE, 2009
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Luxembourg
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Present OIE, 2009
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Macedonia
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Absent, reported but not confirmed OIE, 2009
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Malta
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Disease not reported OIE, 2009
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Moldova
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Last reported 1992 OIE Handistatus, 2005
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Montenegro
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Disease not reported OIE, 2009
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Netherlands
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Present OIE, 2009
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Norway
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Disease not reported OIE, 2009
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Poland
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Present OIE, 2009
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Portugal
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Present OIE, 2009
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Romania
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Disease not reported OIE, 2009
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Russian Federation
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Present OIE, 2009
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Serbia
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Present OIE, 2009
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Slovakia
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Present OIE, 2009
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Slovenia
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Disease not reported OIE, 2009
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Spain
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Restricted distribution OIE, 2009
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Sweden
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Disease not reported OIE, 2009
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Switzerland
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Disease not reported OIE, 2009
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Ukraine
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Disease not reported OIE, 2009
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United Kingdom
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-Northern Ireland
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Reported present or known to be present OIE Handistatus, 2005
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United Kingdom
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Present OIE, 2009
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Yugoslavia (former)
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No information available OIE Handistatus, 2005
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Yugoslavia (Serbia and Montenegro)
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Reported present or known to be present OIE Handistatus, 2005
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OCEANIA
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Australia
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Present OIE, 2009
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French Polynesia
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No information available OIE, 2009
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New Caledonia
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Present OIE, 2009
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New Zealand
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Present OIE, 2009
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Samoa
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Disease not reported OIE Handistatus, 2005
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Vanuatu
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Serological evidence and/or isolation of the agent OIE Handistatus, 2005
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Wallis and Futuna Islands
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No information available OIE Handistatus, 2005
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Hosts/Species Affected
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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).
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Host Animals
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Animal name Context
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Addax nasomaculatus Wild host
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Aepyceros melampus Wild host
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Alcelaphus buselaphus Wild host
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Alces alces Wild host
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Antidorcas marsupialis Wild host
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Antilocapra americana Wild host
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Bos indicus (zebu)
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Bos taurus (cattle)
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Domesticated host
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Bubalus bubalis (buffalo)
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Domesticated host, Wild host
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Capra hircus (goats)
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Domesticated host, Wild host
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Capreolus capreolus Wild host
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Cervus dama Wild host
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Cervus elaphus (red deer)
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Wild host
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Cervus elaphus canadensis Wild host
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Connochaetes gnou Wild host
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Connochaetes taurinus Wild host
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Damaliscus dorcas dorcas Domesticated host
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Gazella thomsonii Wild host
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Giraffa camelopardalis Wild host
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Hippotragus equinus Wild host
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Hippotragus niger Wild host
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Kobus ellipsiprymnus Wild host
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Kobus kob Wild host
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Kobus leche Wild host
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Odocoileus hemionus Wild host
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Odocoileus virginianus Wild host
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Ovis aries (sheep)
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Domesticated host, Wild host
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Rangifer tarandus (reindeer) Wild host
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Redunca arundinum Wild host
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Redunca redunca Wild host
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Rupicapra rupicapra Domesticated host, Wild host
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Sus scrofa (pigs)
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Syncerus caffer Domesticated host, Wild host
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Tragelaphus oryx Wild host
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Tragelaphus strepsiceros Wild host
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Systems Affected
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Reproductive - Large Ruminants
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Reproductive - Pigs
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Reproductive - Small Ruminants
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Respiratory - Large Ruminants
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Respiratory - Small Ruminants
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List of Symptoms/Signs
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Sign Type
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Cardiovascular Signs
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Tachycardia, rapid pulse, high heart rate  Sign [C]
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Digestive Signs
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Anorexia, loss or decreased appetite, not nursing, off feed  Sign [C]
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Excessive salivation, frothing at the mouth, ptyalism  Sign [C]
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Grinding teeth, bruxism, odontoprisis  Sign [C]
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Tongue weakness, paresis, paralysis  Sign [C]
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Dysphagia, difficulty swallowing  Sign [C]
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General Signs
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Abnormal proprioceptive positioning, knuckling  Sign [C]
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Opisthotonus  Sign [C]
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Inability to stand, downer, prostration  Sign [C]
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Dysmetria, hypermetria, hypometria  Sign [C]
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Ataxia, incoordination, staggering, falling  Sign [C]
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Generalized weakness, paresis, paralysis  Sign [C]
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Tetraparesis, weakness, paralysis all four limbs  Sign [C]
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Paraparesis, weakness, paralysis both hind limbs  Sign [C]
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Trembling, shivering, fasciculations, chilling Sign [C]
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Fever, pyrexia, hyperthermia  Sign [C]
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Sudden death, found dead  Sign [C]
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Nervous Signs
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Hyperesthesia, irritable, hyperactive  Sign [C]
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Abnormal behavior, aggression, changing habits  Sign [C]
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Dullness, depression, lethargy, depressed, lethargic, listless  Sign [C]
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Head pressing  Sign [C]
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Propulsion, aimless wandering  Sign [C]
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Constant or increased vocalization  Sign [C]
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Coma, stupor  Sign [C]
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Head tilt  Sign [C]
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Circling  Sign [C]
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Excitement, delirium, mania  Sign [C]
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Seizures or syncope, convulsions, fits, collapse  Sign [C]
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Tremor  Sign [C]
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Ophthalmology Signs
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Conjunctival, scleral, redness  Sign [C]
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Conjunctival, scleral, injection, abnormal vasculature  Sign [C]
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Lacrimation, tearing, serous ocular discharge, watery eyes  Sign [C]
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Blindness  Sign [C]
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Nystagmus  Sign [C]
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Chemosis, conjunctival, scleral edema, swelling  Sign [C]
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Pain/Discomfort Signs
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Colic, abdominal pain  Sign [C]
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Pain, vulva, vagina  Sign [C]
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Pain, penis  Sign [C]
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Reproductive Signs
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Mucous discharge, vulvar, vaginal  Sign [C]
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Abnormal length estrus cycle, long, short, irregular interestrus period  Sign [C]
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Female infertility, repeat breeder  Sign [C]
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Male infertility  Sign [C]
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Abortion or weak newborns, stillbirth  Sign [C]
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Papule, pustule, vesicle, ulcer penis or prepuce  Sign [C]
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Purulent discharge, penis or prepuce  Sign [C]
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Purulent discharge, vulvar, vaginal  Sign [C]
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Vaginal or cervical ulcers, vesicles, erosions, tears, papules, pustules  Sign [C]
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Female infertility, repeat breeder  Sign [C]
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Respiratory Signs
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Mucoid nasal discharge, serous, watery  Sign [C]
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Dyspnea, difficult, open mouth breathing, grunt, gasping  Sign [C]
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Increased respiratory rate, polypnea, tachypnea, hyperpnea  Sign [C]
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Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs  Sign [C]
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Skin/Integumentary Signs
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Pruritus, itching skin  Sign [C]
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Alopecia, thinning, shedding, easily epilated, loss of, hair  Sign [C]
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Epidemiology
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Transmission
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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.
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Morbidity and mortality
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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).
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Temporal and spatial evolution
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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.
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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).
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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).
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Risk factors
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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).
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Pathology
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Subclinical infection
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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).
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Infectious bovine rhinotracheitis (IBR)
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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).
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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.
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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.
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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.
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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).
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Abortion
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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).
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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).
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Infectious pustular vulvovaginitis (IPV) - infectious pustular balanoposthitis (IPB)
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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).
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Metritis
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Metroperitonitis has been observed in cows infected with BHV-1 around parturition, and especially after caesarean section (Lomba et al., 1976).
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Encephalitis
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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).
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Neonatal diseases
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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).
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Other clinical signs
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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).
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Diagnosis
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Clinical diagnosis
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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.
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Postmortem examination
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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.
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Laboratory diagnosis
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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).
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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).
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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.
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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.
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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).
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Disease Course
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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.
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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).
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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).
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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).
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Disease Treatment
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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).
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Prevention and Control
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Vaccination
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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).
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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.
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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).
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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.
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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).
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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.
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IBR control and eradication
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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).
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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).
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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.
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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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References
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Bitsch V, 1978. The p37/24 modification of the infectious bovine rhinotracheitis virus-serum neutralisation test. Acta Veterinaria Scandinavica, 19:497-505.
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Boelaert F et al., 2000. Prevalence of bovine herpesvirus 1 in the Belgian cattle population. Preventive Veterinary Medicine, 34:285-295.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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Engels M, Ackermann M, 1996. Pathogenesis of ruminant herpesvirus infections. Veterinary Microbiology, 53(1/2):3-15; 53 ref.
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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.
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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.
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Gibbs EPJ, Rweyemamu MM, 1977. Bovine herpesviruses. Part I. Bovine herpesvirus 1. Veterinary Bulletin, 47:317-343.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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Lemaire M, Pastoret PP, Thiry E, 1994. The control of infectious bovine rhinotracheitis virus. Annales de Médecine Vétérinaire, 138(3):167-180; many ref.
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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.
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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.
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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.
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Mars MH et al., 2000. Airborne transmission of bovine herpesvirus 1 infections in calves under field conditions. Veterinary Microbiology, 76(1):1-13.
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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.
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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.
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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.
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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.
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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.
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Roels S et al., 2000. Natural case of bovine herpesvirus 1 meningo-encephalitis in an adult cow. Veterinary Record, 146:586-588.
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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.
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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.
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Smith KC, 1997. Herpesviral abortion in domestic animals. Veterinary Journal, 153(3):253-268; many ref.
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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.
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Images
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Picture Title Caption Copyright
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Pathology An intense inflammation is observed in the nasal cavity: hyperaemia, oedema, pseudomembranes and ulcers. Etienne Thiry
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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
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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
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Date of report: 03/04/2011
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© CAB International 2010
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Animal Health and Production Compendium
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Selected sections for: bovine herpesvirus 1
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Identity      Taxonomic Tree      Disease/s Table      Distribution Table      Pathogen Characteristics      Host Animals    References      Images     
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Datasheet Type(s): Pathogen
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Identity
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Preferred Scientific Name
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bovine herpesvirus 1
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International Common Names
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English acronym
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BoHV-1
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IBRV
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English
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infectious bovine rhinotracheitis virus
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Taxonomic Tree
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Domain: Virus
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Group: "dsDNA viruses"
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Group: "DNA viruses"
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Order: Caudovirales
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Family: Herpesviridae
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Genus: Varicellovirus
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Species: bovine herpesvirus 1
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Disease/s Table
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bovine herpesvirus 1 infections
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granulomatous vulvitis in cattle
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infectious pustular vulvovaginitis
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Distribution Table
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Country Distribution Last Reported Origin First Reported Invasive References Notes
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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
 +
 +
© CAB International 2010
  
  
 
[[Category:Herpesviridae]][[Category:Cattle Viruses]]
 
[[Category:Herpesviridae]][[Category:Cattle Viruses]]
 
[[Category:To_Do_-_CABI]]
 
[[Category:To_Do_-_CABI]]

Revision as of 13:00, 4 April 2011


 This article is still under construction.


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

© CAB International 2010

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