Bovine Herpesvirus 1

Also know as: Encephalitic Bovine Herpesvirus Type 5 or Type 1 infection in cattle — Infectious Bovine Rhinotracheitis — Infectious Pustular Vulvovaginitis

Introduction

Bovine herpesvirus one, produces two diseases; Infectious Bovine Rhinotracheitis (IBR) and Infectious Pustular Vulvovaginitis (IPV) in females and Infectious Balantoposthitis in males.
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. The condition is endemic in the UK.
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).
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.
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%.
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. 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).

Signalment

Outbreaks are most often seen in cattle between six and 18 months of age though all ages of cattle are susceptible.

Clinical Signs

Signs of IBR include coughing, serous nasal discharge, tachypnoea and dyspnoea. There may also be signs of increased lacrimation and a marked conjunctivitis. 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.
IBR may cause abortion if susceptible cows or heifers are infected during pregnancy.
Not all cattle infected with the virus show obvious clinical signs. In the absence of secondary bacterial complications most animals recover from the disease.

Latent infection can occur and infected cattle can shed the virus intermittently.
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. The animal may be infertile and may abort or produce a stillborn calf.

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 excreted in the nasal secretions as early as 24 hours after infection. After an incubation period of 2 to 4 days, nasal secretions are more profuse and evolve from sero-mucous to mucopurulent discharge. Young animals show ptyalism. Around 4 days after the beginning of excretion, elevated temperatures are recorded, and animals are depressed and anorexic. In lactating cows, the milk production suddenly drops.

Ulcers and redness are visible on the nasal mucosa, in the pharynx and trachea. Lesions are usually restricted in the upper respiratory tract. Bronchitis and pneumonia can also be observed, but usually as a consequence of secondary bacterial infections. Coughing and sneezing are observed. Conjunctivitis is associated with the respiratory form and is manifest by increased eye secretions.

Animals recover within 14 days, due to the rise of the specific immune response. Some highly virulent BHV-1 strains induce a high mortality rate. Lesions are almost exclusively restricted to the upper respiratory tract: rhinitis, laryngitis and tracheitis. Respiratory mucosae are red and oedematous, foci of ulcers are observed and some lesions are haemorrhagic (Gibbs and Rweyemamu, 1977; Wyler et al., 1989; Straub, 1990).

Abortion is observed between 4 and 8 months of gestation. Early embryonic death can also occur. Abortion is a consequence of respiratory infection of pregnant cows. Viraemia allows the virus to enter the uterine artery and cross the placenta. Abortion is due to a lytic infection of the fetus. All internal organs of the fetus, especially the liver and renal cortex, show foci of necrosis. A generalized multifocal necrosis is diagnosed (Smith, 1997). Infection of cows during the last trimester of gestation can lead to neonatal death, and death of weak calves can occur during the first 2 weeks of life (Thiry et al., 1984).
Infectious pustular vulvovaginitis (IPV) 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).

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.
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).
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. Such animals can be produced experimentally by infection of neonatal calves protected with specific colostral antibodies (Lemaire et al., 2000a,b).

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.
A vaccination is available 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.
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).

References

Gibbs EPJ, Rweyemamu MM, 1977. Bovine herpesviruses. Part I. Bovine herpesvirus 1. Veterinary Bulletin, 47:317-343.
Kaashoek MJ, Moerman A, Madic J, Rijsewijk FAM, Quak J, Gielkens ALJ, Oirschot JTvan, 1994. A conventionally attenuated glycoprotein E-negative strain of bovine herpesvirus type 1 is an efficacious and safe vaccine. Vaccine, 12(5):439-444; 19 ref.
Karstad L, Jessett DM, Otema JC, Drevemo S, 1974. Vulvovaginitis in wildebeest caused by the virus of infectious bovine rhinotracheitis. Journal of Wildlife Diseases, 10:392-396.
Lemaire M et al., 2000. Effects of bovine herpesvirus type 1 infection in calves with maternal antibodies on immune response and virus latency. Journal of Clinical Microbiology, 38:1885-1894.
Lemaire M, Meyer G, Baranowski E, Schynts F, Wellemans G, Kerkhofs P, Thiry E, 2000. Production of bovine herpesvirus type 1-seronegative latent carriers by administration of a live-attenuated vaccine in passively immunized calves. Journal of Clinical Microbiology, 38(11):4233-4238; 43 ref.
Mars MH et al., 2000. Airborne transmission of bovine herpesvirus 1 infections in calves under field conditions. Veterinary Microbiology, 76(1):1-13.
Mars MH, Bruschke CJM, Oirschot JTvan, 1999. Airborne transmission of BHV 1 [bovine herpesvirus 1], BRSV [bovine respiratory virus], and BVDV [bovine virus diarrhoea virus] among cattle is possible under experimental conditions. Veterinary Microbiology, 66(3):197-207; 33 ref.
OIE, 2004. Manual of Diagnostic Tests and Vaccines for Terrestrial Animals. Paris, France: World Organisation for Animal Health. http://www.oie.int/eng/normes/mmanual/A_summry.htm.
OIE, 2005. Terrestrial Animal Health Code. Paris, France: Office International Des Epizooties, Chapter 2.3.5. http://www.oie.int/eng/normes/mcode/en_INDEX.HTM#H.
OIE, 2009. World Animal Health Information Database - Version: 1.4. World Animal Health Information Database. Paris, France: World Organisation for Animal Health. http://www.oie.int
Six A, Banks M, Engels M, Bascunana CR, Ackermann M, 2001. Latency and reactivation of bovine herpesvirus 1 (BHV-1) in goats and of caprine herpesvirus 1 (CapHV-1) in calves. Archives of Virology, 146(7):1325-1335; 38 ref.
Smith KC, 1997. Herpesviral abortion in domestic animals. Veterinary Journal, 153(3):253-268; many ref.
Straub OC, 1990. Infectious bovine rhinotracheitis virus. Virus infections of ruminants., 71-108; 10 pp. of ref.
Thiry E, Detilleux P, Vriese Ade, Pirak M, Pastoret P-P, 1984. Infectious bovine rhinotracheitis in the neonatal period: a review and a case report. Annales de Médecine Vétérinaire, 128(1):33-40; 25 ref.
Thiry E 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.
Van Oirschot JT, 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.
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.