D.V.M., M.Sc., A.C.P.V., Couvoir Scott Ltée, Scott, Quebec, Canada
The purpose of this paper is to try to summarize some of the observations on the reemergence of inclusion body hepatitis in the last years in Canada. Of course one must recognize that Canada is a very big place and has many differences in poultry production according to the province or the region one can work in. I will try to give an overview of the situation in Canada according to discussions with other practitioners and researchers and present more particular data for our company.
A paradigm shift
Although the United States and Canada share the longest common border and poultry consumption patterns are similar the are some major differences in the structure of the industry and its management. Canada's poultry industry is under supply management which has many effects on our perception of the industry. Because of the limit on production size there is more emphasis on maximum profit per pound or kilogram than least cost. The system also puts more emphasis on problems at the farm level since the chicken grower generally owns the quota or the right to produce chickens.
The country has ten provinces and is generally divided into three regions for chicken production. Western Canada which includes British Columbia, Alberta, Saskatchewan and Manitoba produced 314 221 000 kg in 2005. Central Canada in composed of Ontario and Quebec produced 589 894 000 kg and the Atlantic provinces produced 76 915 000 kg. Because of supply management the import and export of chicken is relatively low with 127 Mkg imported in 2005 and 94 Mkg exported the same year. Most of the production is located in southern Canada and generally within 200 km of the U.S border.
Another major difference that has helped us understand the disease is the fact that our production system sexes the males and females and sends them out to different barns. Trace backs studies help us understand the effect of the environment on the evolution of the disease.
If we look at management differences we can state a harsher winter with less disease transmitting vectors in winter. Heating costs also puts emphasis on more air tight barns that can also reduce the introduction of some insects and wild birds. The barns are cleaned out every grow-out in part because of the multi-story houses, lower bedding costs in particular for shavings and the low ventilation rates during the starter phase would permit the build-up too much ammonia with reused litter. This is especially true with breeder replacement flocks because of the pressure from industry and government on eliminating Salmonella Enteritis positive flocks.
Among the other differences that we can note are the average farm or complex size that is much smaller than in the United States, the central part of Canada uses corn-soy diets whereas western Canada and the Maritimes will tend to use more small grains in their rations, the dark out barns and corn-soy diets make the use of lighting programs frequent especially to control spiking syndrome and leg problems associated with the rapid growth of chickens. The rapid growth noted may play a role in a more rapid decline of the maternal antibody transferred from the hen to the chick.
Introduction and survey
As a form of introduction and to get an idea of the problem in Canada I called a few colleagues and asked them a few questions and here is the result of the informal survey.
The first question was do you think the IBH problematic is increasing, decreasing or stable. As of 2006 most of the respondents said that the situation was stable after the increase over the past years. This can also be observed in the data from the provincial laboratory system in Quebec with the number of cases going from unreported in 1998 to 5 in 1999 and to about 20 per year between 2000 and 2005. It was the fifth most common diagnosis out of the Quebec diagnosis laboratory system in 2005. This only represents the tip of the iceberg since once a breeder flock has been identified, practitioners often submit less birds form the same cluster of cases.
To the question in your opinion is the disease related to the hatchery or the broiler farm? Respondents say that there is a relationship to certain breeder flocks but repeat problem broiler farms exist. This tends to indicate that there are some farm factors that may aggravate the expression of the disease.
To the question is there a genetic influence on the disease? Some practitioners said they have seen it only with one breed and other have said they have seen it with all the breeds.
As for the importance of adenovirus serotype, the western veterinarians put more importance on the serotype of adenovirus whereas veterinarians from Quebec give less importance to serotype.
On the question of method of control some do nothing but most have started doing serologic tests on the breeders to evaluate their status and trying to make sure they seroconvert before they start laying.
As it can be seen there is no consensus yet on the factors affecting the clinical expression of the disease.
The "Jack in the box" disease
The disease appears in broiler flocks and can often be related to one breeder source but the breeders give no previous signs of disease in lay or hatchability. It is thus very different for EDS-76 which usually resulted in important egg drops. This makes it very difficult to try and predict flocks that will have the problem. The lack of a proven efficacious serologic test also make the prevention of the disease more difficult. Once the first flock of broilers starts having the problem trace back will tell the operator if it is breeder related. We also get isolated cases where we can identify one source of chicks but that will not repeat itself. Depending on the grower it may skip one or two placements and reappear but not much more than 6 weeks after the initial case for a breeder flock. This means by the time we see the first case in the field around 14 to 21 days of age the last case has already been placed in the incubator.
The "Clean disease"
In the same period of time as the disease has appeared, the chicken farmers of Canada introduced the safe, safer, safest on farm food safety program in 1998 which increased biosecurity, cleaning and disinfection. Although this program was intended mainly for salmonella and other food born disease control it has had an effect on the prevalence of many other diseases. Most of the steps to clean out disease start at genetic company level and trickle down to the broiler production level. More strict measures are applied to the higher levels of the production pyramid and may explain the higher incidence of adenovirus isolations in broiler flocks (up to 90% in a study by Dr Martine Boulianne) and the lower rate in breeder replacement flocks. We are also certain that the breeder suppliers have cleaned-up more than leukosis and salmonella since 1990.
The virus is reported resistant to phenol but sensitive to 1:1000 dilution of formaldehyde. For example most of our C&D protocols have eliminated phenols and replaced them with gluteraldehydes or virkon type products.
Another observation is that in Western Canada no link between infectious bursal disease and chick anemia agent could be made with the IBH cases. The number of flocks negative for infectious bursal disease gives an idea of how clean Canadian barns can become with a change of litter every flock.
Serologic results
In our company we have helped develop a dot blot assay at Dr Amer Silim's laboratory at the University of Montreal. We have also compared the results with those of the AGID and ELISA test at the university of Guelph.
The dot blot has a positive, negative or suspicious result reading and combines the results for two strains of the virus. To graph them out I give a value of 1 to positive birds 0.5 to suspicious birds and 0 to negative birds. The results are then calculated as a percent positive index and analyzed.
When we graph out the results for broilers we notice a low percentage of maternal antibodies in birds under 15 days. Almost all flocks are negative between 18 and 25 days. The data then separates out into two groups of either positive birds with more than 50% of the birds seroconverting and another group with no seroconversion. Birds with clinical symptoms seroconvert more rapidly and with a stronger reaction then their hatchmates placed on different farms. The virus seems to spread very rapidly within a pen but rather slowly between pens or floors. This can also be seen in the mortality patterns between floors and barns.
When we graph out the same data for breeders over time we can note for our company some time periods when flocks do not seroconvert as much. In our experience when the index is under 60% we can expect some problems with the progeny for IBH. When we graph out the data according to breeder age we note that the majority of our breeders do not seroconvert before 15 weeks of age. Our company has multi-age breeder complexes and the breeders are transferred at 20 weeks of age. On top of this since our clients are very demanding we do not incubate eggs under 52g. This gives most of our flocks 6 to 7 weeks to seroconvert. Some flocks did not get 60% index until 35 weeks of age and were more subject to the disease. These flocks tend to get a higher index by the time the disease stops expressing itself in the progeny.
Complicating factors
Amongst the factors thought to contribute to the expression of the disease we believe the lack of maternal antibody, the rapid dilution of maternal antibody because of rapid growth or sequestration of the antibody during omphalitis may contribute to the virus having an easier access in greater numbers to the liver. The serotype of the virus in particular if there is little cross reaction between the strains will have a similar effect. Immunosuppression which can delay the antibody response in the time period between the initial gut or respiratory tract infection and the viremia when the virus might reach the liver may also play a role. Spiking syndrome might also play a role either by a direct effect on the liver or the immunosuppression associated with the syndrome. Mycotoxins are also being investigated as an aggravating factor either by direct liver damage or another mechanism. We also believe that the use of killed vaccines in the grand parent flocks may have reduced the horizontal transmission of the disease in very clean replacement pullet grow-out barns and led to maternal antibody naïve birds. Interestingly naïve replacement pullets that seroconvert at an older age do not show clinical signs of the disease.
A model to try to put it all together
Many of the characteristics of the infection have been studied and reported. Among the factors that can be used in a model to explain the disease we can note the effect of age and virus titer on the infection, cross reactivity between some strains and the importance of route of infection of the expression of the disease. We try to demonstrate some of these theoretic models during the presentation. A two level infection model with a primary replication in the gut or trachea, interference of maternal antibody during the viremic period and a secondary infection of the liver seems promising.
Methods of control
A survey of different practitioners has given a large array of control methods starting from assaying for the presence of maternal antibody to natural contamination of problem flocks. Some have tried placing chicks from problem breeders onto non problem grow out barns. Supportive treatment goes from doing nothing to using antibiotics or vitamins that will protect the liver. Since the disease has a spike curve to the mortality treating at the peak of mortality with any product will result in a reduction in mortality.
In our experience we have had to go from serologic surveillance of negative CAA flocks to vaccinating all breeder flocks for CAA in an effort to reduce the immunosuppressive effect of CAA on this disease. Field observations tend to indicates that this has helped.
What do we need?
We need better diagnostic tools and in particular for evaluating the presence of maternal antibody, the amount of antibody under different situations and to see if the antibody persists as breeders get older.
We need a better understanding of the cross reaction of maternal antibodies with different strains of the virus.
We need more experimental infections in regards to determining if the liver is the primary site of virus replication or if it is simply overwhelmed and the relationship of the age of the bird and the decline of maternal antibody with the expression of the clinical disease.
We need vaccines and especially live vaccines that may permit early infection with the most cross reactive strains and a possible seeding of some very clean barns.
We need more research of a practical nature and the factors that permit the infection from going from sub-clinical to clinical.
We need a bigger market with the problem but we don't necessarily whish that the problem gets bigger!
Acknowledgement
The Author would like to thank Dr Amer Silim and his technician Diane Frenette at the University of Montreal, and Dr Ojkic at the University of Guelph for their comments and all the practicing veterinarians that answered his survey.
From Proceedings of the 41th National Meeting on Poultry Health and Processing, Ocean City, Maryland.
