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| − | {{unfinished}}
| + | == Synonyms == |
| | + | encephalitic bovine herpesvirus type 5 or type 1 infection in cattle, infectious bovine rhinotracheitis, infectious pustular vulvovaginitis, |
| | | | |
| − | ===Antigenicity=== | + | == Introduction == |
| − | *Two different viruses:
| + | Bovine herpesvirus one, produces two diseases; [[Infectious Bovine Rhinotracheitis]] and [[Infectious Pustular Vulvovaginitis]]. |
| | + | <br> |
| | + | Infectious bovine rhinotracheitis (IBR) is a contagious viral disease of cattle caused by bovine herpesvirus 1 (BHV-1). This virus is also responsible for a genital disease called infectious pustular vulvovaginitis (IPV). |
| | + | <br> |
| | + | 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 such as Denmark, Sweden, Finland, Switzerland and Austria (OIE, 2005). Other countries have started similar control programmes. |
| | + | <br> |
| | | | |
| − | [[Infectious Bovine Rhinotracheitis]]
| + | The natural hosts are bovine species. 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 such as cattle and 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). |
| | + | <br> |
| | | | |
| − | [[Infectious Pustular Vulvovaginitis]]
| + | 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 by fomites can also occur. Vertical transmission occurs in cows, when the virus crosses the placenta and infects the fetus. |
| − | | + | <br> |
| − | | + | 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%. |
| − | | + | <br> |
| − | | + | 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. |
| − | 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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| − | | |
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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
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| − | Disease not reported OIE Handistatus, 2005
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| − | | |
| − | Cambodia
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| − | No information available OIE, 2009
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| − | | |
| − | China
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| − | No information available OIE, 2009
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| − | | |
| − | -Hong Kong
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| − | 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
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| − | Present OIE, 2009
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| − | | |
| − | Iran
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| − | Present OIE, 2009
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| − | | |
| − | Iraq
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| − | 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
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| − | 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
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| − | 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
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| − | 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
| |
| − | No information available OIE, 2009
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| − | | |
| − | Guatemala
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| − | Present OIE, 2009
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| − | | |
| − | Haiti
| |
| − | Disease never reported OIE, 2009
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| − | | |
| − | Honduras
| |
| − | 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
| |
| − | 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
| |
| − | Disease not reported OIE, 2009
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| − | | |
| − | Belarus
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| − | Disease not reported OIE, 2009
| |
| − | | |
| − | Belgium
| |
| − | Present OIE, 2009
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| − | | |
| − | Bosnia-Hercegovina
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| − | Last reported 2002 OIE Handistatus, 2005
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| − | | |
| − | Bulgaria
| |
| − | Present OIE, 2009
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| − | | |
| − | 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
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| − | | |
| − | Samoa
| |
| − | Disease not reported OIE Handistatus, 2005
| |
| − | | |
| − | Vanuatu
| |
| − | Serological evidence and/or isolation of the agent OIE Handistatus, 2005
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| − | | |
| − | 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)
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| − | Domesticated host
| |
| − | Bubalus bubalis (buffalo)
| |
| − | Domesticated host, Wild host
| |
| − | Capra hircus (goats)
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| − | Domesticated host, Wild host
| |
| − | Capreolus capreolus Wild host
| |
| − | Cervus dama Wild host
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| − | Cervus elaphus (red deer)
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| − | 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
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| − | Hippotragus niger Wild host
| |
| − | Kobus ellipsiprymnus Wild host
| |
| − | Kobus kob Wild host
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| − | 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
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| − | | |
| − | Systems Affected
| |
| − | | |
| − | Reproductive - Large Ruminants
| |
| − | Reproductive - Pigs
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| − | Reproductive - Small Ruminants
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| − | Respiratory - Large Ruminants
| |
| − | Respiratory - Small Ruminants
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| − | | |
| − | 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). | | 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
| + | <br> |
| − | | |
| − | 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
| |
| − | 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)
| |
| | | | |
| | + | == Pathology == |
| | 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 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. | | 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. |
| Line 819: |
Line 28: |
| | 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. | | 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). | | 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). |
| − | | + | <br> |
| − | 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). | | 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). | | 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). |
| | + | <br> |
| | | | |
| − | Infectious pustular vulvovaginitis (IPV) - infectious pustular balanoposthitis (IPB) | + | Infectious pustular vulvovaginitis (IPV) and infectious pustular balanoposthitis (IPB) is a pustular inflammation which 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). |
| − | | |
| − | 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).
| |
| − | | |
| | | | |
| | + | <br> |
| | | | |
| | + | == Clinical Signs == |
| | + | Signs of IBR include coughing, serous nasal discharge, tachypnoea and dyspnoea. There may also be signs of increased lacrimation and conjunctival reddening. The animal will usually be pyrexic and be weak, dull and depressed. It will usually have a reduced appetite and may show signs of weight loss. If in milk, the yield will be decreased. |
| | + | <br> |
| | + | In IPV, signs will include pain of the vagina or penis, reluctance to mate, mucous discharge from the vulva or penis and signs of ulcers, vesicles and erosions on the penis or vagina. The animal may be infertile and may abort or produce a stillborn calf. |
| | | | |
| − | Diagnosis
| + | <br> |
| − | Clinical diagnosis
| |
| | | | |
| | + | == 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. | | 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. |
| | + | <br> |
| | | | |
| − | Postmortem examination
| + | In a labortaotory, the virus can be diagnosed from nasal or vaginal swabs, or from triturated tissue. BHV-1 DNA can also be detected by polymerase chain reaction (PCR). |
| − | | + | <br> |
| − | 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.
| + | 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. |
| − | | |
| − | 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). | | 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). |
| | | | |
| | + | <br> |
| | | | |
| | + | == Treatment and Control == |
| | + | Supportive treatment is usually required for this condition. If secondary bacterial infection is present then antimicrobials can be used to treat this. |
| | + | Nonsteroidal anti-inflammatory compounds, such as carprofen, are recommended for treatment of pyrexia and for pain relief. |
| | + | <br> |
| | | | |
| − | | + | A vaccination is avaliable for control. 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. |
| − | Disease Course
| + | <br> |
| − | 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).
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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). | |
| − | 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). | | 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.
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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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| | + | <br> |
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| − | OIE Handistatus, 2002. World Animal Health Publication and Handistatus II (dataset for 2001). Paris, France: Office International des Epizooties.
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| − | | |
| − | OIE Handistatus, 2003. World Animal Health Publication and Handistatus II (dataset for 2002). Paris, France: Office International des Epizooties.
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| − | | |
| − | | |
| − | | |
| − | | |
| − | OIE Handistatus, 2004. World Animal Health Publication and Handistatus II (data set for 2003). Paris, France: Office International des Epizooties.
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| | OIE, 2004. Manual of Diagnostic Tests and Vaccines for Terrestrial Animals. Paris, France: World Organisation for Animal Health. http://www.oie.int/eng/normes/mmanual/A_summry.htm. | | OIE, 2004. Manual of Diagnostic Tests and Vaccines for Terrestrial Animals. Paris, France: World Organisation for Animal Health. http://www.oie.int/eng/normes/mmanual/A_summry.htm. |
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| | OIE, 2005. Terrestrial Animal Health Code. Paris, France: Office International Des Epizooties, Chapter 2.3.5. http://www.oie.int/eng/normes/mcode/en_INDEX.HTM#H. | | OIE, 2005. Terrestrial Animal Health Code. Paris, France: Office International Des Epizooties, Chapter 2.3.5. http://www.oie.int/eng/normes/mcode/en_INDEX.HTM#H. |
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| − | OIE, 2005. World Animal Health Publication and Handistatus II (data set for 2004). Paris, France: Office International des Epizooties.
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| | OIE, 2009. World Animal Health Information Database - Version: 1.4. World Animal Health Information Database. Paris, France: World Organisation for Animal Health. http://www.oie.int | | OIE, 2009. World Animal Health Information Database - Version: 1.4. World Animal Health Information Database. Paris, France: World Organisation for Animal Health. http://www.oie.int |
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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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| − | 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.
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| − | Pritchard GC, Banks M,Vernon RE, 2003. Subclinical breakdown with infectious bovine rhinotracheitis virus infection in dairy herd of high health status. Veterinary Record, 153(4):113-117.
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| − | 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.
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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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| − | Schaik Gvan, Dijkhuizen AA, Huirne RBM, Schukken YH, Nielen M, Hage HJ, 1998. Risk factors for existence of bovine herpes virus 1 antibodies on nonvaccinating Dutch dairy farms. Preventive Veterinary Medicine, 34(2/3):125-136; 20 ref.
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| − | Schwyzer M, Ackermann M, 1996. Molecular virology of ruminant herpesviruses. Veterinary Microbiology, 53(1/2):17-29; 83 ref.
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| − | Schynts F, Baranowski E, Lemaire M, Thiry E, 1999. A specific PCR to differentiate between gE negative vaccine and wildtype bovine herpesvirus type 1 strains. Veterinary Microbiology, 66(3):187-195; 33 ref.
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| − | Schynts F, Meurens F, Detry B, Vanderplasschen A, Thiry E, 2003. Rise and survival of bovine herpesvirus 1 recombinants after primary infection and reactivation from latency. Journal of Virology, 77(23):12535-12542.
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| | Six A, Banks M, Engels M, Bascunana CR, Ackermann M, 2001. Latency and reactivation of bovine herpesvirus 1 (BHV-1) in goats and of caprine herpesvirus 1 (CapHV-1) in calves. Archives of Virology, 146(7):1325-1335; 38 ref. | | Six A, Banks M, Engels M, Bascunana CR, Ackermann M, 2001. Latency and reactivation of bovine herpesvirus 1 (BHV-1) in goats and of caprine herpesvirus 1 (CapHV-1) in calves. Archives of Virology, 146(7):1325-1335; 38 ref. |
| − | | + | <br> |
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| − | Smith KC, 1997. Herpesviral abortion in domestic animals. Veterinary Journal, 153(3):253-268; many ref.
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| − | Smits CB et al., 2000. Comparison of three polymerase chain reaction methods for routine detection of bovine herpesvirus 1 DNA in fresh bull semen. Journal of Virological Methods, 85(1-2):65-73.
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| | Straub OC, 1990. Infectious bovine rhinotracheitis virus. Virus infections of ruminants., 71-108; 10 pp. of ref. | | Straub OC, 1990. Infectious bovine rhinotracheitis virus. Virus infections of ruminants., 71-108; 10 pp. of ref. |
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| | Thiry E et al., 2001. Risk evaluation of cross-infection of cattle with ruminant alphaherpesviruses related to bovine herpesvirus type 1. In: Körber R, ed. Tagungsbeiträge, 3. Internationales Symposium zur BHV-1- und BVD-Bekämpfung, Stendal, in press. | | Thiry E et al., 2001. Risk evaluation of cross-infection of cattle with ruminant alphaherpesviruses related to bovine herpesvirus type 1. In: Körber R, ed. Tagungsbeiträge, 3. Internationales Symposium zur BHV-1- und BVD-Bekämpfung, Stendal, in press. |
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| − | | + | <br> |
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| − | Thiry E, Detilleux P, Vriese Ade, Pirak M, Pastoret P-P, 1984. Infectious bovine rhinotracheitis in the neonatal period: a review and a case report. Annales de Médecine Vétérinaire, 128(1):33-40; 25 ref.
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| − | Thiry E, Dubuisson J, Pastoret PP, 1986. Pathogenesis, latency and reactivation of infections by herpesviruses. Revue scientifique et technique de l'Office international des Epizooties, 5:209-222.
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| − | Thiry E, Lemaire M, Schynts F, Meyer G, Dispas M, Gogev S, 1999. Infection of cattle with bovine herpesvirus 1. Point Vétérinaire, 30(199):279-286; 25 ref.
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| − | Tikoo SK, Campos M, Babiuk LA, 1995. Bovine herpesvirus 1 (BHV-1): biology, pathogenesis, and control. Advances in Virus Research, 45:191-223; many ref.
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| − | Vilcek S, Nettleton PF, Herring JA, Herring AJ, 1994. Rapid detection of bovine herpesvirus 1 (BHV 1) using the polymerase chain reaction. Veterinary Microbiology, 42(1):53-64; 48 ref.
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| − | Wellenberg GJ, Mars MH, Oirschot JTvan, 2001. Antibodies against bovine herpesvirus (BHV) 5 may be differentiated from antibodies against BHV1 in a BHV1 glycoprotein E blocking ELISA. Veterinary Microbiology, 78(1):79-84; 12 ref.
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| − | Wentink GH, Oirschot JTvan, Verhoeff J, 1993. Risk of infection with bovine herpesvirus 1 (BHV1): a review. Veterinary Quarterly, 15(1):30-33; 45 ref.
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| − | Whetstone CA, Seal BS, Miller JM, 1993. Variability occurs in the inverted repeat region of genomic DNA from bovine herpesvirus 1 respiratory, genital and bovine herpesvirus 5 encephalitic isolates. Veterinary Microbiology, 38(1/2):181-189; 22 ref.
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| − | Winkler MT, Doster A, Jones C, 2000. Persistence and reactivation of bovine herpesvirus 1 in the tonsils of latently infected calves. Journal of Virology, 74(11):5337-5347.
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| − | Wit JJde, Hage JJ, Brinkhof J, Westenbrink F, 1998. A comparative study of serological tests for use in the bovine herpesvirus 1 eradication programme in The Netherlands. Veterinary Microbiology, 61(3):153-163; 23 ref.
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| − | Woolums AR, Siger L, Johnson S, Gallo G, Conlon J, 2003. Rapid onset of protection following vaccination of calves with multivalent vaccines containing modified-live or modified-live and killed BHV-1 is associated with virus-specific interferon gamma production. Vaccine, 21(11/12):1158-1164.
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| − | Wuijckhuise Lvan, Bosch J, Franken P, Frankena K, Elbers ARW, 1998. Epidemiological characteristics of bovine herpesvirus 1 infections determined by bulk milk testing of all Dutch dairy herds. Veterinary Record, 142(8):181-184; 22 ref.
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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
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| − | Azerbaijan
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| − | No information available OIE Handistatus, 2005
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| − | | |
| − | Bahrain
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| − | Disease never reported OIE Handistatus, 2005
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| − | | |
| − | Bhutan
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| − | Serological evidence and/or isolation of the agent OIE Handistatus, 2005
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| − | | |
| − | Brunei Darussalam
| |
| − | Disease not reported OIE Handistatus, 2005
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| − | | |
| − | China
| |
| − |
| |
| − | -Hong Kong
| |
| − | No information available OIE Handistatus, 2005
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| − | | |
| − | Georgia (Republic of)
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| − | Last reported 1989 OIE Handistatus, 2005
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| − | | |
| − | India
| |
| − | OIE Handistatus, 2005
| |
| − | | |
| − | -Andaman and Nicobar Islands
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| − | CAB Abstracts data mining CAB ABSTRACTS Data Mining 2001
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| − | Indonesia
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| − | Reported present or known to be present OIE Handistatus, 2005
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| − | | |
| − | Iran
| |
| − | Reported present or known to be present OIE Handistatus, 2005
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| − | | |
| − | Iraq
| |
| − | Last reported 2002 OIE Handistatus, 2005
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| − | | |
| − | Israel
| |
| − | No information available OIE Handistatus, 2005
| |
| − | | |
| − | Japan
| |
| − | Reported present or known to be present OIE Handistatus, 2005
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| − | | |
| − | Jordan
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| − | Serological evidence and/or isolation of the agent OIE Handistatus, 2005
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| − | | |
| − | Kazakhstan
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| − | Disease not reported OIE Handistatus, 2005
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| − | | |
| − | Korea, DPR
| |
| − | Disease not reported OIE Handistatus, 2005
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| − | | |
| − | Korea, Republic of
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| − | Last reported 2003 OIE Handistatus, 2005
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| − | | |
| − | Kuwait
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| − | Reported present or known to be present OIE Handistatus, 2005
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| − | | |
| − | Lebanon
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| − | Disease not reported OIE Handistatus, 2005
| |
| − | | |
| − | Malaysia
| |
| − |
| |
| − | -Peninsular Malaysia
| |
| − | Disease never reported OIE Handistatus, 2005
| |
| − | | |
| − | -Sabah
| |
| − | Last reported 2001 OIE Handistatus, 2005
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| − | | |
| − | -Sarawak
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| − | 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
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| − | | |
| − | 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 review]] |