IBR

Infectious Bovine Rhinotracheitis

Bovine herpesvirus1 (BHV-1) virus causes two diseases in cattle: infectious bovine rhinotracheitis (IBR)
and infectious pustular vulvovaginitis (IPV). These infections occur worldwide, including in Australia and
New Zealand. The clinical signs are characterised by fever and involvement of the upper respiratory tract,
including conjunctivitis, rhinitis and tracheitis. Secondary bacterial infections may lead to pneumonia,
especially in intensively managed livestock, such as beef cattle in feedlots. The venereal forms of the disease
result in pustular lesions in the prepuce and penile epithelium of the bull male and vulva and vagina of the
cow. These lesions can impair reproduction. Strains of BHV-1 found in many countries can cause abortion
but these are not present in Australia and New Zealand. As BHV-1 is excreted in semen and can be spread
by artificial insemination, bulls entering artificial breeding centres are screened for freedom from infection.
Freedom from infection is most frequently determined by serological methods, using the virus neutralisation
test (VNT) or enzyme-linked immunosorbent assay (ELISA). Disease is diagnosed by demonstration of
seroconversion with paired sera or by virus isolation from specimens collected during the acute phase of the
disease. Semen certification is achieved by virus isolation in cell culture or by use of the polymerase chain
reaction (PCR) to detect viral DNA.

1. Aetiology

Bovine herpesvirus1 (BHV-1) virus is a member of the Family Herpesviridae (subfamily
Alphaherpesvirinae). Three subtypes of BHV-1 are recognised worldwide: BHV-1.1, BHV-1.2a and BHV-
1.2b. Subtypes 1.1 and 1.2a are present in North America and parts of Europe but do not appear to be
present in Australia1 and New Zealand2. BHV-1.2b strains are less virulent than the other strains. Viruses
from the BHV-1.1 subtype cause severe respiratory disease and can be associated with abortion. Viruses
isolated from buffaloes and goats and previously identified as BHV-1 by serological tests have a different
restriction enzyme profile to subtypes of BHV-1, are now regarded as separate viruses and have been
classified as BHV-2 and caprine herpesvirus, respectively. The bovine herpesvirus causing
meningoencephalitis (previously BHV1.3) has been classified as BHV-51. BHV-4, which was found
widespread in Israel, can cause mastitis, pneumonia, metritis, vaginitis, conjunctivitis, interdigital dermatitis
and abortion in cattle.3,4,5
2. Clinical Signs
BHV-1 infection causes an acute, contagious disease that affects either the respiratory or reproductive tracts
in the following forms:
2.1 Respiratory infection
The respiratory form of the disease is most frequently observed in cattle managed under intensive conditions
(for example, feedlots) and is not often noticed in cattle under grazing conditions. The clinical signs and
pathological changes of BHV-1 infection of cattle are not characteristic and could easily be confused with
Infectious Bovine Rhinotracheitis
Australia and New Zealand Standard Diagnostic Procedures February 2008 2 of 18
disease produced by a number of other pathogens. Laboratory confirmation is therefore essential. The
incubation period ranges from 2-7 days. If the cases are uncomplicated, the disease may be very mild with
only slight serous nasal discharge and a modest rise in body temperature over one to two days. Many cases
remain unnoticed. In more severe cases, there is pronounced pyrexia of 40-42ºC, which may last for several
days. Affected animals are depressed with an increased respiratory rate and show a decline in milk
production. The initial serous nasal discharge often becomes muco-purulent within a few days. The mucosa
of the nares becomes reddened and shallow erosions may be present. Some animals develop excessive
salivation. Oral lesions, which are uncommon, consist of shallow erosions of the oral mucosa. Some animals
develop unilateral or bilateral conjunctivitis and have a clear ocular discharge, which may later become
muco-purulent. In feedlot or other intensively managed cattle, there can be a severe necrotising laryngotracheitis
and pneumonia that is complicated by secondary bacterial infections. These infections are usually
encountered within the first 3-4 weeks of animals entering a feedlot. From time to time, there can be
outbreaks of severe pneumonia due to BHV-1 infection at later times after entry to the feedlot.
Abortion as a complication of the respiratory form of BHV-1 infection has been frequently reported in North
America and Europe but abortigenic strains of BHV-1 have not been found in Australia1,6,7,8,9 or New
Zealand2.
2.2 Genital infection
Genital infection with BHV-1 occurs in both sexes and is a more frequent manifestation of this herpesvirus
infection in cattle on pasture. The infection may result in the development of vesicles, pustules and erosions
or ulcers in the mucosa of the vulva and vagina or on the penis and prepuce 7,8.
2.2.1 Vulvovaginitis
This painful condition, which is known as infectious pustular vulvovaginitis (IPV), may be observed within
a few days of mating. Frequent micturition and raising of the tail are the first clinical signs. There may be
hyperaemia or oedema of the vulva and the posterior third of the vagina. Small red to white ulcers develop
into pustules (0.5–3 mm in diameter). There may be a thick yellow or white mucopurulent exudate,
especially in cases complicated by secondary bacterial infection.7,8
2.2.2 Balanoposthitis
The disease in bulls is known as infectious pustular balanoposthitis (IPB). After a 2–3 day incubation period,
pustules appear on the mucosal surface of the penis and prepuce.10 These pustules can progress to ulcers
with a mucopurulent discharge and may prevent a bull from serving. A proportion of infected bulls will also
excrete virus in their semen. In turn, infected semen can infect susceptible females, by natural or artificial
insemination.
2.3 Conjunctivitis
The conjunctival form of BHV-1 infection, which resembles ‘pink eye’, is relatively uncommon. There can
be occasional involvement of the cornea, and a panophthalmitis. In some cases the only sign of infection is
conjunctivitis.
3. Epidemiology
Infection occurs via the respiratory and genital routes. The virus is spread both within and between herds
mainly by horizontal transmission such as direct and indirect contact (fomites) and aerosol droplets, or from
infected bulls by coitus and in infected semen either by artificial or natural insemination. Frozen semen is
held under optimal conditions for virus survival.
As with other herpesviruses, infection with BHV-1 results in lifelong latent infection. This may occur in the
absence of clinical signs and in the absence of detectable serum antibody. Corticosteroid treatment may
induce a recrudescence of infection and excretion of virus. Natural excretion may occur following stress but
the mechanism of latency and activation has not yet been fully elucidated. BHV-1 isolates vary in virulence
in a manner unrelated to subtype. When introducing new animals into a closed herd or importing animals
from overseas, those animals with antibody should be rejected, as they will be latently infected.
Infectious Bovine Rhinotracheitis
Australia and New Zealand Standard Diagnostic Procedures February 2008 3 of 18
Seronegative animals should be checked repeatedly for antibody and should preferably be treated with
corticosteroid and sampled for virus excretion before being allowed entry to a breeding herd.
4. Occurrence and Distribution
IBR occurs worldwide. In Australia, IBR was first diagnosed in 1962 and the virus was isolated after an
outbreak of vaginitis and rhinitis in dairy herds in Victoria and Queensland. The prevalence of antibodies in
mature breeding cattle ranges from 25-40%. In Australian beef feedlots, a high proportion (>80%) of young
cattle are seronegative at entry and the prevalence of antibody rises to about 60% at slaughter.11 In New
Zealand, IBR virus is widely distributed in the cattle population and 19–82% of adult cattle have antibody
titres. Infection in young cattle or beef cattle is less common.2
5. Pathogenesis and Latent Infections
Replication of BHV-1 takes place in the mucosal epithelial surfaces of the upper respiratory tract and genital
mucosa and virus is shed in nasal and genital secretions. Semen may be contaminated during ejaculation.
Local nerve cell endings are infected and the virus is transported to trigeminal and sacral ganglia where it
establishes a lifelong latent infection. Once infected, animals become lifelong carriers of the virus. The
latent infection may be reactivated periodically, with or without clinical signs; the virus is transported back
to the site of entry and is shed with potential transmission to other animals. Most, if not all, seropositive
animals are latently infected and virus shedding can be reactivated following stress or corticosteroid
treatment. Viremia is rarely detected, but does occur.
6. Gross and Microscopic Lesions
The gross changes associated with an uncomplicated BHV-1 infection usually consist of pustular formation
and shallow ulceration of the epithelium of the upper respiratory tract (including larynx and trachea) and the
genitalia. There can be severe necrotic ulceration of the epithelium of the larynx and trachea in some cases.
When pneumonia occurs, the changes are not pathognomic and are due to a combination of the effects of the
virus and secondary bacterial infections. Histological changes that occur in uncomplicated respiratory cases
are those of acute catarrhal inflammation. There is destruction of the epithelium with necrotic foci in the
laryngeal and epiglottal mucosa. Broncho-pneumonic lesions can result from bacterial complication.
Intranuclear inclusions may be found in epithelial cells of the respiratory tract during the early stages of
infection.
7. Diagnostic Tests and Specimens
Specimens are likely to be examined for evidence of BHV-1 infection for:
(a) diagnosis of specific disease incidents;
(b) certification of the health or virus status of animals or of semen and embryos;
7.1 Disease Diagnosis
BHV-1 infection is commonly diagnosed by detection of the host response to the virus (for example,
antibodies in serum) or by direct detection of the agent.
Serological tests are frequently used for the detection of BHV-1 infection. The types of serological tests
commonly used for testing for BHV-1 antibody are:
(a) The virus neutralisation (VN) test; and
(b) The antibody ELISA.
Antibodies are detected in the serum of most animals within 2–3 weeks of infection. Maternally-derived
antibodies may be detected for up to 7 months, but usually disappear in about 4–5 months.12,13 There is no
known way of distinguishing passively transferred antibodies from those resulting from active infection