Viral diseases can reduce flock performance, productivity and profits without appearing as overt clinical disease
Viruses are therefore potentially more important than bacterial infections
Effects of viruses include: stunting, gut disease, malabsorption, respiratory disease syndromes and immune suppression
Effective vaccination programmes require healthy immune systems
Viral diseases are common, insidious, persistent and require a structured biosecurity programme using the proven virucidal disinfectant Virkon® S.
However, this is merely the tip of the iceberg. Viral challenges can be the triggers for a whole range of problems which may never even appear as clinical disease but can have an even more devastating effect on overall flock performance, production and profits.
Poultry disease can affect one or more of the birds’ body systems, the most significant of which are the respiratory tract (lungs and air sacs), the skeletal system (bones and joints) or the intestinal tract (affecting gut function).
Although other factors such as environment, nutrition and management play an important role in the full expression of diseases affecting these systems, the most significant underlying trigger is usually an infectious agent, and the most potent of these are undoubtedly viruses.
Viruses do their damage by causing primary tissue damage or by opening the gates for other infectious agents, such as bacteria and Mycoplasmas, which might also be present just waiting for a chance to act. And if that wasn’t enough, a number of avian viruses can take this insidious yet highly damaging effect up to another level by directly attacking the birds’ immune system. This can cause clinical problems in its own right or prevent the bird from recognising other harmful agents. It can also prevent birds from responding to the increasing number of vaccinations given to a range of birds.
The positive benefits of the effective control of virus diseases have been known for over 200 years since Edward Jenner’s pioneering work on small pox vaccination. In the intervening period, these concepts have been extended to animal populations worldwide. However, even in the 21st century, viral disease has continued to be a limiting factor to full expression of optimal performance in livestock species despite the emergence of large numbers of high quality vaccines.
So why are viruses potentially more important than bacteria and other infectious agents?
The first is their frequency. Common things are common. Poultry species can be exposed to a wide variety of viruses, even on high health status farms. Viruses can persist in the farm environment and diagnostic tests can be laborious, expensive and may make detection difficult.
The next important factor is their impact. Primary viral infections can open the way for other secondary bacterial infections to cause ongoing chronic and severe performance losses. Viruses are frequently subclinical and can be part of complex syndromes that are difficult to unravel and hence manage.
Finally, all these aspects make viruses difficult to control. Being subclinical and undetected, they can spread easily. They are not treatable with antibiotics. Viruses can therefore build up on farms especially if they are multi age and this can put too large a burden on vaccines which are considered by some to be the only effective defence against viruses. However, these vaccines can only work to their full potential if the majority of birds in a flock have an immune system that can respond to the vaccine and produce a robust and long lasting immunity.
To illustrate these points, it is worth considering some examples of the effects of viruses:
* Gut disease, malabsorption and stunting.
One of the most economically significant diseases of the turkey industry in recent years has been the Poult Enteritis Mortality Syndrome (PEMS). This disease can cause mortality rates up to 80 per cent and severe clinical stunting problems, poor growth and high levels of culling of birds that cannot reach market weight. Some flocks have been totally destroyed by this syndrome1.
Research has shown a variety of viruses to be involved and the most significant candidates are coronaviruses, rotaviruses and astroviruses.
Control of these viruses by terminal cleansing and disinfection using a virucidal programme has been shown to be the only truly effective measure against this syndrome. As an example, research at the South Eastern Poultry Research Laboratory, Athens, Georgia, discussed the importance of Virkon® S (Dupont Animal Health Solutions) in inactivating astroviruses. Virkon® S was shown to be superior to other products available2.
* Respiratory disease.
Respiratory disease syndromes are usually complex interactions of an assortment of infectious agents. Classically, Chronic Respiratory Disease (CRD) in broilers was associated with Infectious Bronchitis virus, Newcastle disease virus, Mycoplasma and E.coli working in tandem. In turkeys, Avian Pneumovirus (Turkey Rhinotracheitis virus), Newcastle disease virus, Mycoplasmas, Ornithobacter rhinotrachealae (ORT) and E.coli are involved in a number of respiratory complexes. Recent research has shown the importance of viral triggers in making the effects of the secondary bacterial infections more severe and long lasting by allowing them to leap frog over the birds’ defence mechanisms.
Naylor et al 19923 showed that a combination of Mycoplasma gallisepticum and Avian pneumovirus produced more severe clinical signs in infected turkey poults and increased the length of time over which clinical disease occurred than for each agent individually. Similarly, Marien et al 20054 showed that the bacterial infection ORT alone was unable to produce clinical disease in experimental turkeys but when combined with avian pneumovirus, produced significant respiratory disease which was more long lasting than Avian pneumovirus infection alone.
* An assault on the immune system.
It has been known for many years that Gumboro disease (Infectious Bursal disease, IBD) virus5, Chick Anaemia Virus6 and Marek’s Disease Virus7 can have a direct effect on the major tissues of the bird involved in producing immune defences, especially the bursa, thymus and spleen. Indeed there is evidence that combinations of two or more of these viruses can enhance their effects on birds8. In turkeys, Haemorrhagic Enteritis Virus (HEV) plays a similar role9.
Marek’s disease virus causes direct and indirect economic losses through this damage to the immune system. There may be direct mortality or increased susceptibility to common bugs such as E.coli7.
Gumboro disease virus can result in transient or long lasting damage to tissues of the Bursa of Fabricius, the organ of the bird that is the cornerstone in producing antibodies and defence against disease10.
Perhaps the clearest illustration of economic effects of subclinical disease associated with viral infection is in relation to Chick Anaemia Virus (CAV) infection. Research at the Veterinary Research Laboratory, Stormont, Belfast11 confirmed that broiler flocks affected by clinical CAV infection from a vertically transmitting parent flock had a net income per 1000 birds 17 to 19 per cent lower, average slaughter weight 3.3 per cent lower and mortality rate 2 per cent higher than that recorded in unaffected flocks. Other work suggests that the depression of average weight can be as much as 12.8 per cent.
Even more significant is the subclinical effects of CAV infection. Workers at the Veterinary Research Laboratory, Stormont12, demonstrated on a large scale trial looking at the results of 1,000,000 broilers that horizontally acquired CAV infection (i.e. persistent virus on the broiler farm) was capable of causing significant economic loss resulting from subclinical infection. Even in flocks not reporting any obvious disease signs, the infection was responsible for:
a. a 13 per cent drop in net income per 1000 birds.
b. a 2 per cent penalty in food conversion ratio (FCR).
c. a 2.5 per cent depression in average liveweight at slaughter.
Another demonstration of the severe economic effect of immuno suppression is thought to be the trigger for the largest cause of condemnation of broilers in the USA, namely infectious process, IP, a form of avian cellulitis13. This subcutaneous bacterial infection appears to gain access through skin wounds and it is considered that birds with a poorly functioning immune system are much more prone to this condition. In the USA alone, losses of US$40-50mn per annum are conservatively estimated due to avian cellulitis14.
Where do we go from here?
It is easy to demonstrate the dramatic clinical effect of viral infections on poultry flocks and there is a wealth of science confirming the insidious day in, day out effects of viral infections on bird performance without them even showing any clinical disease.
The variety of viral agents involved coupled with their frequency and persistence means that controlling viruses must be the foundation for any disease control biosecurity programme for poultry farms.
Although there is an armoury of vaccines available, it is clear that for them to work most effectively they should be given the optimal opportunity to fulfil their potential. Reducing the pressure on vaccines by reducing the viral load is the way to realise that potential. Effective measures are available with attention to structured and targeted cleansing and disinfection using disinfectant products with a proven virucidal pedigree.
In a number of livestock species, Virkon® S (DuPont Animal Health Solutions) has shown itself to be the thoroughbred in virus control with a broad spectrum of activity (including against the secondary bacteria, moulds and fungi), maintaining that activity in the presence of organic challenge.
The major economic effects of viral diseases remain below the surface – mortality and clinical disease may merely be the tip of an iceberg waiting for bird performance to flounder with “titanic” consequences.
Viruses are common, insidious and remarkably persistent. Despite the availability of a range of high quality vaccines, their efficacy is enhanced by effective reduction in viral load on farms.
Virkon® S has proven efficacy against a spectrum of viral challenges expected on poultry farms when used effectively as part of a structured biosecurity programme.
Stephen Lister BSc BVetMed CertPMP MRCVS
Qureshi et al (1997) Immune system dysfunction during exposure to Poult Enteritis Mortality Syndrome agents. Poultry Science, 76, p564 to 569
Schultz-Cherry et al (2001) Inactivation of an astrovirus associated with Poult Enteritis Mortality Syndrome. Avian Diseases, 45, p76 to 82
Naylor et al (1992) Exacerbation of Mycoplasma gallisepticum infection of turkeys by rhinotracheitis virus. Avian Pathology, 21, p295 to 305
Marien et al (2005) Synergy between avian pneumovirus and Ornithobacter rhinotrachealae in turkeys. Avian Pathology, 34, p204 to 211
Van den Berg et al (2000) Infectious Bursal Disease (Gumboro Disease). Review Sci Tech 19, p509 to 543
McNulty (1991) Chicken Anaemia Agent: a review. Avian Pathology 20, p187 to 203
Witter (1998) Control strategies for Mareks Disease: a perspective for the future. Poultry Science 77, p1197 to 1203
Balamuniga & Kataria (2006) Economically important non-oncogenic immunosuppressive viral diseases of chickens. Veterinary Research Communication, 30, p541 to 566
Saif (1998) Infectious Bursal Disease and Haemorrhagic Enteritis. Poultry Science, 77, p1186 to 1189
Lasher & Davis (1997) History of Infectious Bursal Disease in USA – the first two decades. Avian Disease, 41, p11 to 19
McIlroy et al (1992) Economic effects of clinical chicken anaemia agent infection on profitable broiler production. Avian Disease, 36, p566 to 574
McNulty et al (1991) Economic effects of sub-clinical chicken anaemia agent infection in broiler chickens. Avian Diseases, 35, p263 to 268
Avian cellulitis – beauty is only skin deep. Author: Stephen Lister. International Poultry Production, Vol 12 No 1, 2004.
Olkowski et al (2005) The role of first line of defence mechanisms in the pathogenesis of cellulites in broiler chickens: skin structural, physiological and cellular response factors. J Vet Med A Physiol Path Clin Med, 53, p517 to 524