Bovine alphaherpesvirus 1 & 5
Also known as
Bovine herpesvirus type 1 & 5
Both bovine herpesvirus 1 (BHV1) and bovine herpesvirus 5 (BHV5) can cause encephalitis (inflammation of the brain) in cattle, though BHV1 more commonly causes abortion, infectious bovine rhinotracheitis (“red nose”), and pustular vulvovaginitis (lesions in the reproductive tract).
BHV1 only sporadically causes meningitis (inflammation of the membranes that enclose the brain and spinal cord) in cattle because it rarely advances beyond the nerves located in the trigeminal ganglia.
This is a group of nerves at the base of the brain at the back of the head, at the top of the spine--which gathers sensory stimuli from the head and face and provides nerve stimulation to the muscles that control chewing.
By contrast, BHV5 seems to mainly prefer to attack the nervous system, and in some parts of the world, particularly South America, it is a common cause of meningoencephalitis (inflammation of the brain and its surrounding protective membrane) in cattle.
BHV5 encephalitis can cause single-animal disease or herd outbreaks, mostly in young replacement heifers. Incidence in North America appears much lower than in South America.
BHV5 meningoencephalitis may result during first exposure to the virus or from reactivation of the virus (due to stress or corticosteroid treatment) at a later time. Like most herpes viruses, BHV5 can hide in the body for long periods of time and resurface later to cause disease again.
Clinical signs generally occur approximately 1 week after initial exposure or reactivation of the virus. The virus invades the central nervous system via the olfactory mucosa (the membrane lining of the upper nasal passages) after intranasal infection or reactivation. Inflammation of the trigeminal ganglion is found in infected calves, and this is also the area of persistent infection in some individuals.
BHV5 was first isolated in 1962 from a neurological disease outbreak in Australia. It is genetically and antigenically related to bovine herpesvirus type1 and was initially thought to be a subtype of BHV-1 and was called BHV-1.3. However, the exclusive presentation of outbreaks of neurological disease suggested that this virus was a new agent capable of causing pathogenic changes in nerve tissue.
Even though both viruses can attack nerve tissue, only BHV5 is capable of replicating extensively in the central nervous system and inducing neurological disease.
Like other alpha-herpesviruses, BHV5 can establish latency in nerve tissue and due to stress factors or glucocorticoid treatment, the latent virus can be reactivated. During episodes of reactivation, the virus is excreted in nasal and genital secretions and tears (weeping eyes) and can be transmitted to other susceptible hosts.
Recently, BHV5 has been associated with infection of the reproductive tract. The virus has been isolated and the presence of viral DNA has been demonstrated in semen samples from Brazil and Australia and natural transmission of the virus through contaminated semen has also been described.
Embryos and oocytes (eggs) are susceptible to BHV5 infection and BHV5 DNA has been detected in the central nervous system of aborted fetuses.
Though the virus was first isolated in Argentina in 1962, studies of stored lab samples (nerve tissues) showed it to be present from an earlier time; it was circulating in that country long before the virus was recognized as a causative agent of neurological disorder in cattle.
Since then, the virus has been sporadically identified in cases of meningoencephalitis in other countries including the United States and Europe. The disease seems to have a high incidence in South American countries, mainly in Central and Southern Brazil and Argentina. The reasons for this restricted geographical distribution of neurological cases are unknown.
- Mild respiratory disease
- Neurologic signs that include tremors; depression
- Muscle spasms that cause backward arching of the head, neck, and spine
- Rapid eye movements
- Teeth grinding
- Recumbency (lying down and unable to get up)
The respiratory tract is the main portal of entry. Initial viral replication in the epithelium of the upper respiratory tract and in the tonsils may lead to slight respiratory signs. Virus replication at the site of entry may last for 15 days. After replication at mucosal sites, the virus reaches the central nervous system, where viral replication causes neurological damage.
Latency of BHV5 in other sites within the central nervous system is also possible. It has been suggested that viral reactivation from latency may lead to virus spread to different areas of the brain and this would be responsible for the presence of mild neurological signs during episodes of reactivation. Neurological signs begin 9 to 10 days post-infection. These signs are progressive and usually fatal.
Infection with BHV5 can show many forms, however, since it is not restricted to the central nervous system of animals with clinical signs; it can also be found in the respiratory tract. In one study, BHV5 was found in an aborted fetus from a farm where sporadic cases of abortion were recorded but no cases of neurological disease had been observed.
This virus is not confined to the respiratory tract and central nervous system.
There have been several reports describing detection of BHV-5 in bull semen. A study in 2003 showed that 6 out of 20 (30%) semen samples, previously considered positive for the presence of BHV-1 were actually BHV-5-positive, when re-evaluated by a BHV-5-specific PCR test.
In Brazil, a semen sample from an apparently healthy bull, which was identified as BHV-1-positive during virus surveillance at an AI center in 1996 was re-analyzed in 2003 and re-classified as BHV-5.
The first evidence of natural transmission of BHV-5 through contaminated semen was described in 2009 in Australia. The next year, the virus was found in frozen semen of a healthy bull. In 2009, in an outbreak of vulvovaginitis with clinical signs and lesions identical to those caused by BHV-1 the researchers determined that BHV-5 was the virus detected in the semen of the bull used for AI.
Therefore, it was suggested that BHV-5 was responsible for the outbreak of genital infections previously attributed to BHV-1.
Abortions are a common sequel of BHV-1 respiratory infection but we now realize that BHV-5 may also play a role in abortion. In Argentina, BHV-5 has been found in the central nervous system of aborted fetuses.
Further studies are needed to establish the role of the virus in reproductive tract infection and to know whether the infection of a cow with contaminated semen can lead to a latent infection or whether infection by this route can cause neurological disease.
Batches of frozen semen from bulls of accredited AI centers are normally certified negative for a number of contagious diseases. An increasing number of these centers are also certified negative for viruses like bovine leukemia virus (BLV), BHV-1 and bovine viral diarrhea virus (BVDV).
The actual role of BHV-5 in reproductive disease is still under study but the presence of the virus in bovine semen could be considered a threat for international trade of frozen semen.
BHV 5 is a potential threat when using AI for breeding since it is excreted in semen and can be transmitted to susceptible cows. To prevent the spread of the virus by AI, all semen samples, even those of apparently healthy bulls, should be analyzed.
Presently there is no treatment.