Bovine Herpesvirus 1
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Also know as: BHV-1 — Encephalitic Bovine Herpesvirus Type 5 or Type 1 infection in cattle — Infectious Bovine Rhinotracheitis — Infectious Pustular Vulvovaginitis — Infectious Pustular Balanoposthitis — IPB
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%.
BHV-1 is distributed worldwide and has been diagnosed in all countries tested.
In recent years, a few European countries have successfully eradicated the infection by applying a strict culling policy, e.g. Denmark, Sweden, Finland, Switzerland and Austria.  Other countries have started similar control programmes.
The condition is endemic in the UK.
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.
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.
Between herds transmission is a major risk of BHV-1 circulation. Airborne transmission of BHV-1 has been demonstrated over short distances and can provide an explanation of between herds transmission.
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, goats and other species belonging to the subfamily Bovidae.
Outbreaks are most often seen in cattle between 6 and 18 months of age though all ages of cattle are susceptible. Calves are usually protected by colostral antibodies until 3-4 months of age so infection before this point is uncommon.
Signs of IBR vary with each particular strain but classically include coughing, serous nasal discharge, tachypnoea and dyspnoea. There may also be signs of increased lacrimation and a marked conjunctivitis. Coughing and sneezing are observed. 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. 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. Young animals show ptyalism. In endemic dairy herds, it is not uncommon for animals to present with milk drop with or without pyrexia.
IBR may cause abortion if susceptible cows or heifers are infected during pregnancy. Abortion is usually 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. 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.
Latent infection can occur, the viral cells residing in the trigeminal nerve, and infected cattle can then shed the virus intermittently particularly after stressful episodes. Other animals recover within 14 days, due to the rise of the specific immune response. Becoming latent is a common sequelae to infection and in terms of control, all animals on an endemic farm should be considered as potential latent carriers irrespective of their antibody status. Some highly virulent BHV-1 strains induce a high mortality rate.
In IPV, signs will include pain of the vagina or penis and erythrematous swelling of this region, 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 urinate frequently and have an elevated tail.
Ulcers and redness are visible on the nasal mucosa, in the pharynx and trachea. Lesions are usually restricted to the upper respiratory tract. Bronchitis and pneumonia can also be observed, but usually as a consequence of secondary bacterial infections. Respiratory mucosae are red and oedematous, foci of ulcers are observed and some lesions are haemorrhagic. 
Infectious pustular vulvovaginitis (IPV) and infectious pustular balanoposthitis (IPB) is a pustular inflammation causing the genital mucosa to become red and oedematous with vesicles and pustules evolving into ulcers.
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.
In a laboratory, the virus can be isolated from nasal or vaginal swabs, or from triturated tissue. BHV-1 DNA can also be detected by polymerase chain reaction (PCR). In an individual animal, paired serology is useful with a raised antibody response seen two weeks after clinical signs.
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.
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. 
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 are recommended for treatment of pyrexia and for pain relief.
A vaccination is available for control and 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. Vaccinating latently infected animals may reduce the level of shedding from this group. Marker vaccines are also available and recommended. These are based on glycoprotein E (gE) deleted mutants, with detectable antibodies present to the gE antigen in marker vaccinated individuals indicating wild-type viral infection.
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- ↑ 1.0 1.1 Straub, O. C (1990) Infectious bovine rhinotracheitis virus. Virus infections of ruminants, 71-108;10
- ↑ OIE (2005) Terrestrial Animal Health Code. Paris, France: Office International Des Epizooties, Chapter 2.3.5.
- ↑ 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
- ↑ Six, A., Banks, M., Engels, M., Bascunana, C. R., 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
- ↑ Smith, K. C (1997) Herpesviral abortion in domestic animals. Vet Journal, 153(3):253-268
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- ↑ Lemaire, M., Meyer, G., Baranowski, E., Schynts, F., Wellemans, G., Kerkhofs, P., Thiry, E (2000) Effects of bovine herpesvirus type 1 infection in calves with maternal antibodies on immune response and virus latency. J Clin Microbiol, 38:1885-1894
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The datasheet was accessed on 3 April 2011.
This article has been expert reviewed by Nick Lyons MA VetMB CertCHP MRCVS
Date reviewed: 31 August 2011
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