Bovine Viral Diarrhoea Mucosal Disease

Published Date: 02 Nov 2017

Bovine viral diarrhoea (BVD) is one of the most prevalent diseases currently affecting the British and Irish cattle industry. In terms of affecting production and economics, it is an incredibly damaging disease with mostly subclinical factors being the cause of loss to production. Important elements in the current BVD issue that will be discussed include the following; how animals become infected with BVD, the pathogenesis and different forms of the disease, how symptoms of the disease are presented and the economic effects on the cattle industry. There are many different methods of cure and prevention that had been tried and tested since the disease became prevalent.

The disease is caused by the Bovine Viral Diarrhoea Virus, which of the pestivirus genus, from the flavidiviridae family. Being a pestivirus, it has a single strand of positive sense RNA and is an enveloped virus. The virus has the ability to mutate into different variants which mostly express similar symptoms. This variation could be a possible advantage when it comes to fighting host immunity (Grimm et al, 2006). The virus strains can be split into two groups which are of different genotype, Type 1 and Type 2. (Grimm et al, 2006). Viruses from either genotype can exist as two biotypes, cytopathic (CP) and non-cytopathic (NCP) (Ahn et al, 2005). The cytopathic form exhibits itself as oral mucosal disease which will be discussed in greater detail. This symptom is more common in the Type 2 genotype. The general hypothesis for viral infection or cells is as follows; the virus enters host cells via receptor mediated endocytosis, the virus then replicates in the cell cytoplasm, and exits via receptor mediated endocytosis (Grimm et al, 2006). Following entry and contact with the mucosa of the oral or nasal cavities or the reproductive tract, BVDV replicates in epithelial cells and has a predilection for the palatine tonsil and the nasal mucosa. From here, the virus spreads to regional lymph nodes before a viraemia becomes established. The CP strain has been found to replicate in the GI tract, and in leukocytes, lymph nodes, the proximal colon and the respiratory tract, the NCP is usually found to replicate here. Type 2 genotype has been shown to have a greater virulence, and is wider spread throughout the infected animals body (Grimm et al 2006).

There are two main ways a bovine can be infected, transiently or persistently. Transient infections generally don’t result in clinical symptoms, however if the infection is severe enough mortalities can result. Transient infections are picked up either via horizontal transmission, or vertically after 150 days of pregnancy if the dam picks up the virus after this time. Any foetus infected before the 100 day mark will result in destructive lesions and the slowing in growth of organs and tissues, and will become mummified or aborted. Persistently infected (PI) animals occur when a cow is infected during 100 – 150 days of pregnancy. Calves affected during this period, when the immune system is developing become tolerised to the viral antigens, and so do not put up an immune response to the BVDV. The virus remains in their serum throughout their lives, and they shed large amounts of it in there secretions. PIs are the main problem with BVD control. PIs have a high probability of obtaining mucosal disease, with mortality rates at around half during the first year of life (Dr R Dalziel, 2012).

Transmission of BVD can be both horizontal and vertical. Horizontal transmission generally occurs via fomites. Equipment contaminated by an infected animal such as needles via blood, a bulldog/ nose tongs contaminated via nasal secretions, shared teat on a milk bucket, or even via the same rectal glove used between cows can spread the disease (Grimm et al 2006). All bodily secretions can transmit BVD, particularly if they come from a PI animal as they shed lots of the virus constantly (Transiently affected animals will transmit for a short period of time). The virus can survive outside the host body in the environment for several weeks. Vectors such as head flies and stable flies also can spread the virus. Vertical transmission occurs via a number of routes. If a cow is a PI animal, her foetus will be infected, therefore during embryo transfer will become infected if implanted into a PI cow. Infected semen can infect a cow and thus the foetus. Also, if a cow is vaccinated at the wrong stage of pregnancy with modified live vaccine, the foetus will become infected (Sayers).

Clinical signs of the disease depend on what form the disease takes. A minority of cases take on one acute form of the disease, known as Bovine Viral Diarrhoea. Some of the clinical symptoms include fever, leukopenia, depression, anorexia, occulonasal discharge, oral erosions and lesions, a drop in milk production and occasionally diarrhoea (Grimm et al, 2006). It can lower immunity for secondary infections such as IBR or Salmonella, causing severe mixed infections (Truyers, 2013). Most acute cases of the disease are sub-clinical, with no signs evident at all. These animals tend to have reproductive issues, and lower milk yields. In non pregnant animals, acute infection is followed by lifelong immunity. Mucosal disease is another form of the disease. It only occurs in PI animals that have been infected with the NCP form of the virus in-utero. The animal becomes overloaded with the cytopathic form of the virus leading to mucosal disease. It is widely hypothesised that the virus mutates in vivo - within the animal to the CP form, although there is still some doubt as to the actual pathogenesis of this. Most cases of this disease occur in animals aged between 6 months – 24 months, and this may coincide with a waning of passive immunity (Truyers, 2012). Clinical signs of the mucosal disease include the following; an acute onset depression, weight loss, pyrexia, oronasal ulceration, tacky salivation, dysentery, interdigital ulceration, dermatitis, secondary pneumonia, dehydration and usually death after 5 to 10 days.

By attempting to maintain a virus free herd, farmers will benefit enormously in both production and economics. Paying the price for good biosecurity is not as costly as having to incur loss due to BVD. Wasting money trying to get cows in calve, poorer growth rates, increased cases of disease and infection due to a lowered immune response, and reduced milk yield all cause farmers to lose money due to this disease.

Maintaining a virus free herd is a difficult proposition for any farmer in the current state of the UK farming industry. Culling PI animals is the best method for eradicating BVD from a herd, as this will reduce the large amounts of virus shed by them. Employing a policy of strict biosecurity is also an important method in maintain a BVD-free herd. Keep a closed herd when possible, and when buying in livestock by from herds that are part of a health scheme and are known to be BVD free. Ensuring farm boundaries are well maintained to prevent mixing with possibly infected stock, and ensuring bought in stock are isolated for a period before being introduced to the rest of the herd are also good principles to apply. A vaccination programme can also be implemented. There are 2 available inactivated vaccines available in the UK. The whole herd should be vaccinated, and then a booster should be administered once a year before the breeding season. Heifers should be given their primary course before being mated for the first time (Truyers, 2012). There has been some argument that PI animals could be used as natural ‘vaccinators’, by mixing them with young livestock before breeding that previously had no exposure to BVDV resulting in a life-time immunity to the virus. This has been trialled in New Zealand and appeared to have mixed results. Depending on the ratio of PI animals to healthy animals, in some cases not all animals had acquired immunity though they had run with the PI animals for an extended period of time, sometimes for as long as 600 days (Thompson, 2004).

In 2011 Pfizer Animal Health voluntarily suspended sales of PregSureBVD vaccine, and recalled the vaccine. The vaccine was recalled after 5 herds where confirmed with Bovine Neonatal Pancytopenia (BNP) that had been vaccinating with the PregSure vaccine. It was an inactivated vaccine, and the cause of the BNP was multifactorial, but there was thought to be a link with the vaccine and the BNP emergence (Pfizer, 2011). There has since been cases in Europe and the vaccine has been discontinued.

BVD virus is extremely prevalent. The disease is distributed worldwide, and its prominence varies between countries, depending on availability of vaccines, knowledge of the disease and schemes in place. It is reported that 96% of dairy herds in England and Wales where positive for BVD virus antibodies in bulk milk, with 65% of the herds likely to have suffered an outbreak in the recent past and currently having persistently infected animals in the herd (Paton et al, 1999). It is estimated that the cost of infection in a 100 cow beef herd over a ten year period is around £45,000, with the cost for a dairy herd of the same size over double that (Stephens, 2009). The majority if costs incurred are due to fertility problems such as reduced conception rates, abortions, birth of deformed calves, and embryonic losses. Lower growth rates, increased lameness and a reduced immune response also contribute to the costs of BVD. In New Zealand, 60% of herds are affected, with estimated costs to the industry totalling at about $150 million in the dairy industry every year, at $220 a cow per head.

Countries have begun to take steps to try and eradicate the problem. In Scotland a scheme has been put in place with a subsidy for mandatory testing of every herd, a ban on knowingly selling PI animals, movement restriction on BVD infected herds, pre-movement screening for BVD, and double-fencing/housing a possible requirement for herds with a persisting problem (Scottish Government, 2013). In Northern Ireland, there is a voluntary scheme started in 2013 that will become compulsory in 2014. It is based on testing ear punch samples collected using tissue sample-enabled official identity tags for BVD virus and so can identify PI calves to enable their rapid culling, eliminating shedding of the virus. Where PI calves are detected in a herd, further testing is required to identify any other PI cattle that may be present and to prevent spread through trade (Animal Health and Welfare NI, 2013).

Ultimately it can be seen from this essay that BVD, a pestivirus, is one of the most important viruses affecting cattle in the UK, and at the moment it is widespread throughout the country. It can manifest itself in many different ways, acute or persistently and can in some cases result in deaths of livestock. The main issue in the fight against BVD are PI animals. Economically, farmers are suffering large losses due to BVD particularly in relation to reproduction and fertility issues. Thankfully, countries recently have realised just how important the disease is, and so have begun to implement eradication schemes. Farmers can take their own steps to limit its spread, with vaccination programmes and strict biosecurity measures. With a joint effort from both Governments and farmers, BVD can be easily managed and hopefully in the not too distant future, eradicated.