Highlights from a roundtable discussion.
IBV in broiler breeders
IBV and immunity
Impact of no antibiotics ever
IBV evolution and spread
Role of IBV vaccination
Vaccination of broiler breeders
IBV and Newcastle disease protection
How many IBV vaccine serotypes?
Vaccine application pitfalls
Minimizing vaccine reactions
IBV Arkansas condundrum
The evolution of infectious bronchitis virus (IBV) is a continuing challenge for poultry producers and veterinarians. In broilers, this highly infectious coronavirus can present in its traditional form as respiratory disease, predisposing birds to secondary bacterial infections. Relatively newer on the scene are potentially deadly nephropathogenic IBV strains. In any form, IBV impairs animal welfare and is an important source of economic loss for poultry producers.
Vaccination is key to IBV control. Although homologous vaccines are considered to be the most effective, development of a new vaccine for every new IBV strain that emerges is difficult to impossible. Finding an effective existing vaccine or combination of vaccines that will cross-protect is a worthwhile venture, but there’s no guarantee of success.
Zoetis recently hosted a roundtable featuring renowned IBV experts as well as practitioners who shared their knowledge about IBV. These proceedings are highlights from the conversation and are provided with the hope they will help the industry achieve better control of IBV, improve animal welfare and minimize IBV’s financial burden.
JON SCHAEFFER, DVM, PhD
Director, Poultry Technical Services, Zoetis
JEAN SANDER, DVM
MARK BURLESON, DVM
KALEN COOKSON, DVM
DAVID FRENCH, DVM
MARK JACKWOOD, PhD
University of Georgia
BRIAN LADMAN, PhD
University of Delaware
MEAGAN SLATER, DVM
SARAH TILLEY, DVM
GUILLERMO ZAVALA, DVM, PhD
Avian Health International
Would practitioners on the panel briefly give us an idea about the impact of infectious bronchitis in their respective operations?
I’d say it’s our biggest respiratory issue. Bronchitis seems to be a year-long struggle — tracking variants as they arise and staying ahead of them.
IBV Arkansas tends to be a nagging problem for us. This year, we thought we had everything under control, particularly with our vaccination program, but then we had our first experience with the IBV variant DMV/1639. It caught me completely by surprise. We didn’t even know we had a respiratory disease. We were trying to explain some lost feed conversion and stumbled upon DMV/1639. So, we have it in our operation, and it’s been a new challenge to figure out how to keep it under control. That’s been our biggest issue.
Poultry flocks on the Delmarva shore have experienced quite a bit of bronchitis and continue to struggle with control of DMV/1639 — probably for the last 3, if not more, years. Prior to my position with Mountaire Farms, I worked as a consulting veterinarian in Pennsylvania where I got quite a bit of experience with DMV/1639 in broilers. We saw the impact on feed conversion and a little bit of airsacculitis. The challenge was finding a vaccination program that didn’t cause more airsacculitis than DMV/1639.
What geographic regions do your operations cover, and do the IBV serotypes you see differ from one region to another?
At Sanderson Farms, we see regional challenges that are a little different from one area to the next. We cover the Southeast from Texas all the way over to North Carolina. I would say in Texas, our biggest challenge has been Newcastle disease (ND). For IBV, our biggest challenge was with DMV/1639, which was primarily in south Georgia, although we found a little of it in Mississippi as well. In Mississippi, we mostly find GA08. So, there’s a bit of a different challenge in different regions.
We cover a lot of the Southeast from Arkansas to North Carolina and all the states in between. It’s very geographical — there are different IBV serotypes in different places. For instance, we’ve isolated DMV/1639 isolates only in south Alabama and in Arkansas.
Mountaire has isolated GA13 in North Carolina flocks. We’re going to try to do more surveillance and see what’s going on in that area. On the Delmarva shore, there’s been quite a bit of DMV/1639 as well as some GA08. It was the same in Pennsylvania when I was there.
What I’m hearing is that the IBV serotypes seen vary regionally. But given that, are you seeing an overall increase in problems with bronchitis, or is it really more of a shifting landscape?
We routinely take serum from processed flocks. In summertime, IBV calms down a bit, whereas in winter titers will increase. But generally, I’d say our titers stay relatively stable.
…if significant respiratory diseases pop up, it’s typically due to a new variant IBV.MARK BURLESON, DVM
I’d say it’s a shifting landscape. A lot of our problems with bronchitis before this past year were self-induced with vaccine application. This past year, it’s been a little bit of a different scenario with DMV/1639 and IBV evolving and then spreading. It’s been a greater concern for us this year. Maybe a little bit more of a bronchitis challenge. I expect to see a new IBV variant emerge about every 5 years.
I agree. There is a seasonal aspect to bronchitis. Generally based on my experience, summer is always better, and winter and spring tend to be the worst. However, if significant respiratory diseases pop up, it’s typically due to a new variant IBV.
Problems can also arise if someone misapplies vaccine, or maybe you decide to go to a different vaccine manufacturer and the new vaccine just doesn’t play well with your current program. But I’d say primarily the ebb and flow of variant bronchitis viruses is what we struggle with from year to year.
Are problems due to IBV usually detected during live production or at processing?
When we found DMV/1639 in Georgia, it was an interesting experience. We were off about 3 to 6 points in feed conversion and were trying to figure out why. We put together a posting session. We looked at 10 flocks of various ages. Those flocks appeared to be normal, healthy birds. There had been no mortality on the farm and no flushing, but almost every bird we opened up had a 3+ airsacculitis score.
At first, I didn’t believe what I was seeing and questioned whether the birds at posting were, in fact, normal, healthy birds. So, I went to the farm and picked out birds myself, only to find that it was real. At first, I thought it couldn’t be DMV/1639 since there was no flushing, but the virus had changed to more of a respiratory challenge. I think we just caught it early because mortality did start to pick up and got worse after about 35 to 40 days of age. We adjusted our vaccination program to correct the situation.
Has anyone else had a similar experience?
Based on my experience with GA08, GA13 and recently DMV/1639, I’d say IBV is a relatively mild virus — assuming you don’t have other confounding factors. I think it’s more of an issue at the plant than in the field. Someone in our organization once called it a silent airsacculitis where you really don’t know you have any issues until the plant calls you and says, “Hey, we’re basically shut down or our line speeds are down…with airsacculitis.”
With GA13, we didn’t have a huge increase in mortality, but the processing plant complained about airsacculitis.SARAH TILLEY, DVM
I agree that most of the impact is in the plant. With GA13, we didn’t have a huge increase in mortality, but the processing plant complained about airsacculitis.
Dr. Burleson, what are the “confounding factors” you referred to earlier?
I was thinking about the use or misapplication of aggressive respiratory vaccines, like IBV Arkansas or the Newcastle B1 strain. You’ve got a variant IBV that’s relatively mild in itself. But if you throw in other factors like aggressive respiratory vaccines, poor ventilation and farm management issues, that’s when you start seeing more clinical disease, in my experience.
What about secondary infections?
Those are primarily issues with Escherichia coli.
It was mentioned earlier that there’s a seasonality to it, and I think that has to do with the extra stress factors on the birds in wintertime. In general, if you’ve got a problem in the summertime and going into fall, you can expect to have a miserable winter. There are definitely some outside circumstances that affect respiratory challenge. And I do think E. coli’s probably the biggest secondary bacterial infection. It can be either a secondary problem or a primary pathogen, depending upon the type of E. coli creating the difficulty.
IBV in broiler breeders
We don’t have an autogenous DMV/1639 vaccine, so we used a commercial GA08 vaccine at day of age in our pullets.DAVID FRENCH, DVM
How about IBV in broiler breeders? What are you finding?
I was concerned when we found DMV/1639 was predominant in our south Georgia complex, and we didn’t have protection for that particular strain in our breeders. We heard stories about false-layer syndrome and cystic ovaries in breeders in other locations, so we’ve since included some protection in our breeder program to try and take care of that. But I was very concerned about it when I saw how widespread the challenge was in our operation in south Georgia. Those pullets are very similar in many ways to broilers and they are in the same area, so they should be exposed to the same diseases.
What changes did you implement?
We don’t have an autogenous DMV/1639 vaccine, so we used a commercial GA08 vaccine at day of age in our pullets. We’re administering a day-of-age Salmonella vaccine anyway, so we mix it with our Salmonella vaccine and give it to them before we put them in the house.
I can’t say we’ve had many issues with broiler breeders, at least with DMV/1639. I can’t say that we’ve looked extremely hard either, but we have not really seen many issues.
Whenever we see any kind of decrease in egg production, we try to correlate it with something, which is often a bit higher incidence of ND.
IBV and immunity
Dr. Zavala, what’s the role of immunity regarding infectious bronchitis and secondary infections? Are broiler flocks immunosuppressed?
That’s a compound question. Can they be immunosuppressed? Yes. However, I don’t believe that, at least in North America, immunosuppression is the reason we see bronchitis in broilers, breeders or layers. But it can happen in pockets or in particular situations. If it does happen, we surveil for infectious bursal disease (IBD) as well as chicken anemia virus and Marek’s disease. Those would be your primary infectious pathogens causing immune suppression.
As far as immunity to infectious bronchitis, the only practical way we can actually measure that is with serology. We know that a very important component of the immune system and how it responds to bronchitis vaccines and field viruses is going to be cellular immunity. Unfortunately, we don’t have a way to measure that, so we have to go with what we can see, which are antibodies on ELISA, primarily.
As far as immunity to infectious bronchitis, the only practical way we can actually measure that is with serology.GUILLERMO ZAVALA, DVM, PhD
Impact of no antibiotics ever
Our company has almost 50-50 conventional versus raised without antibiotics. I can’t say that withdrawing antibiotics is really playing a role.MARK BURLESON, DVM
This question is for the practitioners on the panel: Have you noticed more infectious bronchitis problems in flocks raised in “no antibiotics ever” (NAE) versus conventional production systems?
Our company has almost 50-50 conventional versus raised without antibiotics. I can’t say that withdrawing antibiotics is really playing a role. I think it’s more the densely populated areas where you start getting some of these viruses that start jumping around from company to company. We share our problems.
I agree with Dr. Burleson. We have only NAE production and no conventional production, but I think one of the benefits of NAE production is decreased bird density. We would argue that the birds are not as stressed, so potentially you could have less of a problem with IBV. But I think it does go back to who your neighbors are, how close they are and what they’re vaccinating with.
Dr. French, you’re in a little bit of a unique situation because you are just changing to removal of gentamicin from the hatchery. Are you seeing an increase in secondary infections?
The only difference that I can see, really, between NAE production and a traditional program is the fact that once they do break with a secondary bacterial infection, we have options with conventional production. And I’m sure that companies with NAE production have veterinarians who are allowed to treat those birds and remove them from the NAE market. But that’s the only difference.
I agree with the other speakers about infectious bronchitis. I don’t think using an antibiotic or not has any impact. I think NAE and conventional flocks are all equally susceptible.
IBV evolution and spread
Dr. Jackwood, would you please explain to us why IBV, which is a coronavirus, changes so easily?
Infectious bronchitis is an RNA virus, and the length of its genome is huge. When the virus replicates, it’s not very good at copying the genome so it has a pretty high mutation rate, and when it replicates, it’s going to make mistakes. If those mistakes translate to a gene that gives the virus a selective advantage, it means the virus may replicate quicker and may become more pathogenic. The key with controlling this is to stop IBV from replicating.
One thing we do know is that these variants tend to hang around in long-lived birds…BRIAN LADMAN, PhD
Dr. Ladman, DMV/1639 has been one of the bigger IBV problems in the Delmarva region (eastern shore of Delaware, Maryland and Virgina). Can you tell us how the variant first became apparent and how it affected flocks?
Our lab shouldn’t have named it Delmarva 1639 because it started in Pennsylvania at the end of November 2010. I always feel that fact gets lost, and everybody who grows chicken on Delmarva is now saddled with that black eye.
We see a regular invasion, if you will, of bronchitis variants from Pennsylvania into the Delmarva region. It’s been going on for quite a number of years. I think we first noted it in early 2000 or the late 1990s with IBV PA/171/99, which thankfully burned itself out. Unknown is whether DMV/1639 is the current iteration of previous viruses.
One thing we do know is that these variants tend to hang around in long-lived birds, and there are quite a few in Lancaster County (Pennsylvania), not too far from Delmarva. And so, there are viruses like PA/1220 which, for whatever reason, have really stayed in the layer population. We continue to follow that, even to this day.
DMV/1639 then is most likely rooted in layers. It didn’t cause too many problems initially. In 2011, we saw a couple of isolated cases on Delmarva, when it presented as a nephropathogenic IBV variant. Then it kind of went away, for whatever reason, then came back hard in 2014. It popped up in Georgia, although how these viruses travel is unknown. They’re likely moving via people and birds. We know they hang out in cecal tonsils.
We’ve continued to see iterations of the DMV/1639 type viruses since 2011. The vaccine that’s being used in Delmarva I believe is the 2014 version, if you will, of DMV/1639. There are some changes that we observed in 2017, and it continues to evolve today. Whether or not that’ll burn out, I don’t know. But I certainly hope at some point it will.
Is DMV/1639 genetically similar to the other circulating strains of bronchitis?
Dr. Ladman already indicated it’s rooted in a Pennsylvania virus that’s probably the progenitor of DMV/1639. So, it does have that history there, but as far as the vaccines we have available to us, none are anywhere close genetically to DMV/1639. Now there is a vaccine that Dr. French indicated they use in their birds. It does show some cross-protection, but the degree of cross-protection we get in the field is sometimes very different from what we see in a laboratory. I’ll leave it at that.
Role of IBV vaccination
Dr. Jackwood, you’ve been widely quoted as stressing the importance of vaccination to stop cycling infectious bronchitis. You’ve also said improper vaccination — particularly using the wrong vaccine — can lead to the emergence of new IBVs. Would you please explain how vaccination can either dampen or hasten the evolution of bronchitis?
There have been quite a few studies published that show vaccines can accelerate the mutation rate of these viruses. The theory behind that is that they’re trying their best to survive in a bird that’s trying to get rid of it, so they’re accumulating those mutations at a quicker rate, trying to stay ahead of the bird’s immune response to the virus. Other studies have shown if the virus is able to replicate in the field without any vaccine pressure, it will change quite rapidly and move in the field.
One of the problems we have with some of these studies — and why it can be somewhat confusing — is because we’re constantly putting attenuated live vaccines into the field. If you’re isolating an IBV Arkansas, is that an Arkansas vaccine that was just put there a month ago, a week ago or 5 days ago? Or has it been circulating for over a year in those birds and had time to change?
The bottom line is that anytime this virus replicates, it’s changing.MARK JACKWOOD, PhD
And the bottom line?
The bottom line is that anytime this virus replicates, it’s changing. Period. Whether those changes result in a virus that can have a selective advantage and start to be a problem in our birds seems to occur about every 5 years. That’s what we’ve determined. I think that if we have a homologous vaccine and do a good job of vaccinating, we get sterile immunity. I mean, we can’t even get that with flu, right? But we can with bronchitis.
In my opinion, from a scientific point of view, homologous vaccine applied properly is the best of all worlds. It absolutely is. The problem we run into is like the one we have with DMV/1639. If we start trying to make a vaccine today, it’s going to be probably 3 or 4 years until we have it on the market.
So, we vaccinate with one or more strains of bronchitis virus to get as much cross-protection as we can. We probably get a lessening of the clinical signs associated with that, and everybody congratulates each other and says we did a great job. But meanwhile, the virus is replicating under the radar until it finally gets to a point where it surfaces again.
However, it’s probably not fair to make a blanket statement that vaccine pressure will push the virus to evolve and mutate or emerge as a strain that will cause problems. I think that if we do a good job of vaccinating like we’re supposed to, I think it actually helps with keeping the virus from replicating as much, and maybe instead of 5 years we can prolong it to 8 years or 10 years. The virus mutates; that’s what this virus does and we can’t change that.
I’d just like to muddy the water a bit. We’re thinking in a single dimension here regarding the question as to whether immune pressure drives the virus to change. We know that from many viruses. But you can easily complicate the situation when you are dealing with an area heavily populated with birds from multiple companies and where eight or nine different vaccine strains are circulating simultaneously all the time.
Take northeast Georgia, for example. There are no fewer than eight different vaccine strains used every single day. Some companies spray with one serotype at the hatchery, some with two and some with three. Some even boost in the field with yet another virus. So what does that actually do to virus evolution? I don’t know; I don’t have the answer. I’m just muddying the water, as I said.
How then do we monitor for bronchitis virus? How are we going to identify all the strains that are circulating? Serology? Virus isolation? Sequencing? Direct polymerase chain reaction (PCR)?
The choices we have might not include a homologous vaccine but a vaccine that might give us some protection and relief from the clinical signs we’re seeing.DAVID FRENCH, DVM
From a laboratory standpoint, it depends on what clients are looking for, and everyone seems to be interested in something different. Right now most clients are spoiled by the rapid nature of tests. They just want answers. Sometimes it’s pressure from above that’s forcing them to seek that answer versus maybe a long-term solution. And so it depends.
The development of real-time PCR has been fantastic. Those assays that have been developed have been great tools to help producers understand what’s going on, and the benefit is that we can detect everything in a single swab. But as we start to work that up, those samples may not be ideal for additional testing such as sequencing. We sometimes tend to pull out more vaccine strains for samples if they’re in there.
Obviously, they’re highly embryo-adapted, so that’s what’s going to grow in an egg.
Next-generation sequencing seems to be fantastic, but that’s not rapid and it’s not cheap. Would you spend $700 only to find out you have an Arkansas vaccine circulating?
I think we’d all agree that in a production scenario, we just want the problem to go away. We’ve got an issue, we’ve got mortality and we’re under pressure to fix the immediate problem. The choices we have might not include a homologous vaccine but a vaccine that might give us some protection and relief from the clinical signs we’re seeing.
That’s the pressure we get. We’ve got to provide an answer to our senior management or our stockholders. We need to fix that situation as quickly as we can.
And that’s a perfect segue to our main topic: strategies for this evolving virus. Vaccination is key, but selecting the vaccines for bronchitis control in broilers can be problematic. There may not be vaccines available that match the circulating strain, or cross-protection might be too limiting. Dr. Jackwood, can you explain why cross-protection is difficult with infectious bronchitis vaccines, and does it involve genetics of the bronchitis virus circulating?
That’s a big one. Antibodies that bind to the spike protein will block infection. That’s the strong immunity we’re after here. In addition to that, cell-mediated immunity is involved in recovery from the disease, which is also very important. So, when we have spike proteins that can induce those neutralizing antibodies and also induce a good cellular immune response, we’ll get complete protection.
Different types of IBVs have different spikes. Antibodies against one spike — say, a Massachusetts-type spike — won’t bind to another spike like an Arkansas-type spike. Therefore, they won’t cross-neutralize each other.
However, there are conserved regions on spikes, so you will get antibodies to some of these more conserved regions.
Think of it as a building. The scaffolding of the building is all the same, but the surface or the top of it looks different. Some of these antibodies will bind to these conserved areas and can help block some of the infection that we see — block attachment of the virus to the host cell. When we give more than one type of IBV vaccine to birds, we’re trying to induce those antibodies, those cross-reactive antibodies, if you will.
The other difficult part with cross-reactivity is the antibodies that neutralize are against what we call conformationally dependent epitopes, which means that if you take that spike out of the virus and express it in the laboratory, it doesn’t form those epitopes anymore.
That’s why we don’t have herpesvirus of turkey-vectored vaccines for IBV. That spike has to be folded properly to be able to induce neutralizing antibodies. It is always folded properly when it’s with a virus, and that’s why we try to use attenuated live vaccines when the molecular ones won’t work. We take the protein and cut it down into small pieces and try to figure out what it is that actually induces neutralizing antibodies.
It’s been a very, very difficult chore, and nobody’s really come up with a good way of doing that yet. So, it’s that conformational epitope problem that we have, getting these neutralizing antibodies that really causes us issues with trying to get this cross-protection.
Antibodies that bind to the spike protein will block infection. That’s the strong immunity we’re after here.MARK JACKWOOD, PhD
Are the conserved regions the same?
My next question is about cross-protection. When do multiple serotypes help with cross-protection? How does that work in the field when you’re vaccinating?
It’s biology, I guess. We’re putting a foreign protein into the animal. They’re responding by making antibodies against it. We should have a vaccine virus that’s going to induce an antibody that’s going to bind to a circulating field virus in a place where it could potentially block that virus from infecting a cell. It’s like a lock and key. It might also not fit well. A conserved region between an Arkansas and a Q1 IBV have nothing in common. But we do have some conserved regions between, say, a GA08 and a DMV/1639, and we can see some cross-reaction between them. But we can’t predict it.
We now have three-dimensional structures of the spike, but we still don’t know what the amino acids are that make up that conformationally dependent epitope that induces the neutralizing antibodies and then which conserved epitopes also around that area can potentially induce antibodies that would be stereotypically protective. You can’t predict it at this point either with a computer or by just looking at the differences between the two different viruses. The bird is the only way. The bird tells us whether it will be protective or not. And that’s why we have to do vaccine challenge studies.
We produced three serials at three different times of a GA13 vaccine,
and we had really good responses.
We’re dealing with novel, new IBVs like DMV/1639 or GA13, for which there are no commercial vaccines. Dr. Tilley, did you not produce a GA13 vaccine, and what was your experience with that?
Yes, we did. We produced three serials at three different times of a GA13 vaccine, and we had really good responses. We used them during times of the year when the challenge was higher, which generally began around November/December (depending on how cold the winter was) and would continue through April/May. We continued to run surveillance to see if the virus was still circulating and vaccinated with GA13 vaccines for about 3 to 4 years on and off. When we finally stopped seeing the challenge, we stopped vaccinating. We did not want to continue to vaccinate if it was not necessary. So during that period for our birds, it worked wonderfully. It worked beautifully. It was like turning on a light switch.
Dr. French, you’ve had some experience trying to control or prevent the disease from DMV/1639. How did you manage that?
First, we had to determine whether it was in fact bronchitis; then we had to figure out what type of bronchitis it was. I have to say we got very quick response with PCR, which is a great tool, and there was already some experience with cross-protection from GA08 for control of DMV/1639.
Since we didn’t have an autogenous to draw on, we went with the quickest way we could find to solve the problem. And I have to say, it’s been a very effective response. The control we’ve gotten using that vaccine has been very good. The short-term benefits are great. I’m a little concerned about the long-term effects, but the short-term benefits are great.
Dr. Burleson, you’ve had some experiences trying to control DMV/1639. What vaccine approach did you take?
Very similar to Dr. French’s. My experience has been very limited at this point. We have had about five or six isolations across two complexes. We’re now trying to decide what to do for next winter, if it becomes an issue. I expect we’ll probably use what’s available — the same approach as Dr. French.
When I was in Pennsylvania last winter [working as a technical service representative for a vaccine distributor], I had five different companies that had DMV/1639 in multiple PCR sequences. A couple of them had really bad issues at the plant because of it. We tried multiple vaccine approaches because of company preferences. Some opted for a generic multiple-boost protection approach. Others tried both GA08 vaccines. It was kind of a wash across the board. There were breakthroughs on every program, although I think generally people were happy because it was less of a problem.
After talking a lot with the vaccine manufacturers, it sounded like the experience was generally the same elsewhere. Vaccination is going to decrease your clinical signs, but if the pressures in the environment are too high — decreased ventilation and other factors that come along with winter — it’s just not going to hold.
This roundtable is essentially about broilers. But it would be interesting to mention a few words about what the layer industry is doing and continues to do to fight this particular virus in different areas where there is no specific vaccine.
GA08 seems to have helped a lot. As a matter of fact, in northeast Georgia, there are some relatively large layer complexes that are very, very open, unfortunately — and by that I mean they don’t start vaccinating with live bronchitis vaccines until the birds are 2 to 3 weeks of age.
We’re seeing the very first cases that are possibly DMV/1639. They already have a number of flocks with cystic oviducts and false layers. Birds are peaking at 70%, where they normally peak at 96%.
So, this is one of the approaches we are copying from what’s been done up on the shore and other regions.
Vaccination is going to decrease your clinical signs, but if the
pressures in the environment are too high — decreased ventilation
and other factors that come along with winter —
it’s just not going to hold.
I don’t think there’s anyone in the industry giving only the GA08 vaccine, right? It’s always in combination. No one gives just one vaccine unless they have no challenge, although they might give just IBV Massachusetts. So, it’s GA08 plus IBV Massachusetts — up to three IBV serotypes.
Dr. Ladman, weren’t you involved with development of a DMV/1639 vaccine?
Yes, we were approached by a company on the shore. We started working on it even though it wasn’t something we were looking to do. It took 3 years to go through testing to the point where we felt we had something that could be beneficial.
Some companies have done quite well with it and others have not. Management is a factor. At the start, it seemed to work very well. It was new and more attention was likely paid to ensure proper application. Once the novelty wears off, I think people fall into a routine; perhaps there are personnel changes, results change, who knows. Although at other companies, the vaccine continues to be used with good results. I think, because somebody needs to find a problem, bronchitis is detected and it becomes the scapegoat simply because it seems like it is always there. Is it a problem to detect the vaccine in the absence of disease?
It’s been an interesting road, and I don’t know if we started down that road again today that we would be lucky enough to end up with something that was beneficial, as I think to this point that vaccine has been.
Vaccination of broiler breeders
What about IBV vaccination for broiler breeders? Dr. Zavala, is that important?
If you look at birds on an individual-flock basis, it’s important. If you look at it on an industry-wide basis, the better you can control bronchitis in one or two or multiple companies, the more benefit you’re going to find for everybody else.
I find it interesting that if you look at the composite of companies in Georgia, for example, there’s a significant proportion of companies that do not use killed vaccines for bronchitis. Most of them rely only on live vaccines. Many other areas of the world would never think about doing that, particularly in layers. But that applies to broiler breeders as well.
So, I think it’s very important to think about broiler breeders, and yes, economics is absolutely important. I think it’s very important to vaccinate. I think it’s very important to complement vaccination with killed vaccines and, of course, to use an array of strains that will help you increase broad protection, if you can.
We know that maternal-antibody transfer is not very protective for progeny. But if you look at the years when IBV Arkansas was introduced in the Southeast, it wasn’t until we introduced the Arkansas vaccine in the breeder population that things were buffered in broilers a little bit. And I think that’s an important thing to think about as well. You want to ask “How do I protect the breeder? How do I broaden the spectrum of protection?” and “How do I indirectly minimize my potential problems in the progeny?” It’s very important.
What about vaccination and false-layer syndrome? You mentioned that maternal antibody isn’t very protective. We know that some poultry companies wait until 2 weeks of age to vaccinate, yet that early infectious period is critical for the development of false-layer syndrome.
Is there anything we could be doing — whether it’s for broiler breeders or layers — that’s going to help prevent that early exposure that results in false-layer syndrome?
I would speculate that maternal immunity probably contributes partially to protecting that young bird, but it’s going to be how soon can you get it protected through active immunity versus passive immunity.
So, would using killed vaccines in breeders expand protection to broilers?
Maybe not so much expand the spectrum of protection, but you can certainly raise your antibody levels. You can also extend the longevity of that immune response, specifically in the case of the breeders through IgG (immunoglobulin G), which is really what you’re stimulating more than anything.
We know very well that when it comes to humoral immunity against IBV in broilers, it’s going to depend very much on IgA (immunoglobulin A), which is the one that’s going to essentially neutralize the virus in the respiratory tract.
But if you think about long-lived birds, it’s not just IgA. You’re trying to protect the bird against infection of the reproductive tract or even the urinary tract, for which you do need other types of antibodies and cellular immunity — IgG and cellular immunity. I wish it were very simple, but you have to use a multi-pronged approach and think in multiple dimensions. “What do I do with breeders?” “What do I do with the broilers?” And then “What do I do with the other 50% of the problem?” — which is ventilation, litter quality, drinker management and so on.
I think it’s very important to think about broiler breeders, and yes, economics is absolutely important. I think it’s very important to vaccinate.GUILLERMO ZAVALA, DVM, PhD
Will the practitioners here share your approach to vaccinating breeders against IBV to help control the disease in both breeders and broilers?
Our pullets and breeders are vaccinated with IBV strains that our breeders and broilers will encounter, as well as what our broilers will be vaccinated with later on. During the pullet-rearing stage, the birds are vaccinated at 3, 7 and 16 weeks of age with multiple live IBV strains — different combinations of Arkansas, GA98 and Massachusetts — so that they have ”seen” multiple strains before going into lay. We do split the live IBV and ND vaccinations in the pullet phase by 5 to 7 days to prevent replication-site interactions.
Once moved into the hen house, the breeders are boosted with a live IBV/NDV program every 10 weeks since we use a live program. We run routine serology at two points in the hen’s life — at 26 weeks of age and 58 weeks of age to monitor incoming immunity to IBV/NDV/IBDV/reovirus and toward the end of life to see what the hens have been exposed to. We have the ability to monitor serology both in-house and at external labs when production drops or there are shell changes.
I think Dr. Zavala did a great job explaining that there are really two reasons to consider IBV vaccination of breeders. From my point of view, it takes the edge off the vaccine that we’re going to administer to broilers. I saw first-hand what happens when you vaccinate broilers with Arkansas and you don’t have Arkansas in your breeder vaccination program. It was years and years ago, but not a mistake I would want to repeat again.
The other reason to vaccinate breeders is to protect those birds while they’re in production. We use a killed vaccine in breeders. Years ago, when I came on board and they were not getting a killed IBV vaccine, I began to see some eggshell problems. I was uncomfortable boosting with a live bronchitis virus, thinking it might contribute to more eggshell problems. So, we converted everything over to a killed vaccination program in breeders to maintain good eggshell quality.
Normally, there’s plenty of bronchitis circulating on a commercial layer operation. You have multiple ages and it’s always floating around.KALEN COOKSON, DVM
We vaccinate breeders for IBV at 2, 6, 10 and 16 weeks of age. They get nothing else for the life of the bird. We collect serology at 26 and 50 weeks and we do see some increasing titers from time to time, but we haven’t pinpointed bronchitis as being a major cause of any kind of eggshell or production issues. We try to present the hen with everything she might see during lay in that geographic area. That’s our goal.
Most of the broiler breeders in Pennsylvania when I was there were vaccinated with live primer vaccines and then at least one killed vaccine. In fact, most layers there actually received two killed vaccines before they were moved. A large percentage of companies do not boost throughout the life of the flocks, so they try to get the antibodies up front. So, for good or bad, that’s what they’re doing. It seems to be working and helping to protect against some shell-quality issues.
I think if you can have a good, diverse live program in your long-lived birds, whether they’re broiler breeders or layers, followed by a killed IBV vaccine, it works very well, in my experience. We’ve done some work with that.
Normally, there’s plenty of bronchitis circulating on a commercial layer operation. You have multiple ages and it’s always floating around. From what we’ve seen, if you have good primers up front and a good killed response, you have good immunity on board when birds are placed on the farm. The circulating IBV on the layer farm acts almost like a good autogenous booster vaccination. We conducted one layer study and saw good cross-protection well into production against an IBV serotype that wasn’t present in the killed vaccine the birds received.1
And I think the live/killed vaccination strategy also can be beneficial to the breeder side of things where you’ve got these novel variants circulating. IBV is more of an insidious disease in long-lived birds, just because they’re not under the intense stress that broilers are. It’s not always as obvious if you do have a novel bronchitis exposure, but it might be there so you’re at least hedging your bets and protecting yourself a little bit.
IBV and Newcastle disease protection
There are areas where broilers also need protection against ND. Dr. French, you mentioned that ND was a challenge in your Texas complexes. How do you balance your bronchitis and Newcastle vaccination programs for broilers?
Whether it’s an IBV or ND challenge, the more that you can reduce the respiratory stress on birds, the better off you are. We utilize recombinant Newcastle vaccines as much as we can in areas where ND is a concern, and we supplement with a very mild live Newcastle vaccine at day of age. I feel it takes a little while for the recombinant vaccines to generate enough protection, and the live vaccination at day of age helps to carry them through, regardless of maternal-antibody protection, until the recombinant protection is adequate. The birds can concentrate on responding to the bronchitis vaccine with the minimized stress of a much milder Newcastle vaccination program.
What about protection against ND and IBV in broiler breeders?
When we use a live vaccination program in broiler breeders, we’ll split up Newcastle and bronchitis vaccines 5 to 7 days apart. We don’t give them together
Whether it’s an IBV or ND challenge, the more that you can reduce the
respiratory stress on birds, the better off you are.
We have relatively little to no Newcastle challenge in our geographic areas, at least right now, fortunately, but we employ a recombinant Newcastle to try to minimize that impact of Newcastle and bronchitis reaction. And we’ve been very successful with that.
Does anyone have birds anywhere near the virulent Newcastle outbreak in California? And if so, what would be your approach to vaccinating against Newcastle and bronchitis?
I don’t know if anyone in the room has birds that close to California, but I think we would all employ the international strategy of using a more aggressive Newcastle vaccination program relative to whatever challenge is in the area. It depends on how close you are and how big a threat it is.
I think Dr. Zavala would back me up on this — why we see the killed Newcastle and bronchitis and more use of four-way vaccines when they’re giving a killed IBD/reovirus in high Newcastle challenge areas. Progeny benefit from the Newcastle maternal antibodies because velogenic Newcastle is often waiting as soon as they hit the floor in those operations. In addition, you’d probably use a recombinant and a live Newcastle at day of age.
Dr. Zavala, you do the most international travel of folks on the panel and are probably in more areas that have the more virulent Newcastle. Have you seen any strategies that you could share that might be helpful to those who will be using this information?
Yes, I’ve seen way too many strategies. I can’t say all of them are good. If you look between the Tropics of Cancer and Capricorn — the number of countries affected by Newcastle genotypes 5, 7, 13, 13A, 13B and 12 — that involves, really, a lot of countries.
Basically, the strategy in general is going to be hyperimmunization of breeders. It’s the first thing you have to do to protect breeders and egg production. But it poses a real problem with progeny. It makes it very difficult to successfully immunize broilers when they’re very young. ND maternal immunity is neutralizing, and it really makes it difficult for you to succeed with a live vaccination program.
I would say the most successful programs involve use of a recombinant
Newcastle vaccination at the hatchery, whether it’s in ovo
And the most successful programs?
I would say the most successful programs involve use of a recombinant Newcastle vaccination at the hatchery, whether it’s in ovo or subcutaneously at hatch, coupled with a mild live strain of ND virus at hatch as well. In many of these countries, they also tend to grow a pretty heavy bird. You have to boost those birds in the field, usually between 12 and 14 days of age, with live vaccines that are quite a bit stronger — the LaSota strain, for example.
If you’re in certain countries of the world, you might have to give them a killed vaccine. You’d be surprised at the vaccination devices that have been put in place for broilers and the speed at which you can vaccinate broilers with killed vaccines in the field — where you have the labor, of course. But those are the main strategies that I would say.
I get to visit companies in no less than 40 countries, and I always tell them that in the absence of catastrophic disease, the most important respiratory problem they’ll face is bronchitis. You need to focus on bronchitis and put Newcastle on the back burner, but you cannot leave yourself completely unprotected.
If you are in an area where Newcastle is constantly waiting for you to just look the other way, then you have to sustain the economic cost of vaccinating aggressively. It’s the only way you can continue to operate economically.
How many IBV vaccine serotypes?
Dr. Cookson, is there a limit on the bronchitis serotypes that can be administered?
Let me first say that, in my opinion, our best opportunity in the US for bronchitis control is in the hatchery. From what I’ve seen, focusing on hatchery vaccination has, in general, been successful.
The rule of thumb most people have adopted is no more than three IBV serotypes per dose. However, there’s some recent evidence that using up to four serotypes may have some advantages, but as an industry, we still need to figure out when that should be considered.
In one study we did, I was very surprised when we moved from two to three serotypes. We had over 90% protection in broilers against DMV/1639.2 I rarely see that kind of protection unless you have an autologous challenge vaccination program. I think even 80% protection is stellar. It will be interesting if that can be repeated, which we plan to do.
Can anyone share their experience with using four serotypes?
We recently did a study where we vaccinated birds at 1 day of age with three bronchitis virus types, and we vaccinated another group with four different types. We weren’t necessarily trying to determine whether we were going to get cross-protection or not. We were asking whether all three or four of these vaccines actually infect and replicate in the chick and if they would be protected against homologous challenge.
Using new molecular techniques, we can now see more than one bronchitis virus type in a single swab from a bird. Five days post-vaccination, we saw all three vaccines in every single bird, meaning they all got infected and the vaccines were replicating. When we gave four different serotypes, we saw all four vaccines in every single bird, and they all were replicating. We gave those vaccines by eye drop, and we gave a full dose of every single one of them.
When we challenged the birds that got three vaccines, they were protected against all three viruses they were vaccinated with. In birds that got four viruses, they were protected against all four different viruses. That was at 35 days of age.
Now that said, not all vaccines play well together. We gave Massachusetts, Arkansas, GA98 and GA08. If we would have given a Connecticut instead of one of those four, or we would have given a Delaware instead of one of those four, we might have seen some different results. I only say that because those vaccines tend to not be as aggressive as some of the others. And in our study, not all the vaccines replicated to the same titer.
We’ve done quantitative PCR, and Massachusetts replicated to the highest titer. Arkansas was the lowest. We expected that, actually. The GA98 was second lowest, and then GA08. So in progression, the lowest was Arkansas, the next was GA98, then GA08; IBV Massachusetts was the highest.
In one study we did, I was very surprised when we moved from two to three serotypes.KALEN COOKSON
We conducted similar studies a few years back looking at three serotypes, which were IBV Massachusetts, Arkansas and Delaware. It appears that Massachusetts didn’t play too well with Arkansas. We observed a difference between the replication of vaccine when given by itself versus when given with other vaccine viruses. At the end of the day, birds were protected from the challenge strains represented in the vaccines. Regardless, it was very interesting to track progression of the IBV vaccine strains in the bird. It comes back to the fact that we know that IBV has a negative impact on ND virus replication, but we haven’t paid much attention to IBV-IBV interactions. In accordance with the 9CFR regulations, the vaccines work, but a small body of work suggests that immunity is perhaps not induced at the same rate.
The other thing we have to consider with all of this is vaccine application. It’s really tough to do well. It really is. Even spray vaccinations in the hatchery, which you would think would be fairly straight-forward, can often get messed up.
Vaccine application pitfalls
Dr. Cookson, you have some tips on how to get uniform distribution of bronchitis vaccine administered by spray at the hatchery. Could you share those with us?
Yes. It’s not rocket science, but there are a lot of potential pitfalls when vaccinating. You’re in a broiler hatchery with a lot of moving parts, so you need to pay attention to details.
There are essentially two components in the hatchery: There’s the preparation of the vaccine and the application of the vaccine. As far as preparation of the vaccine, we’re dealing with a pretty fragile virus. It’s not like an IBD virus or a reovirus where there’s some forgiveness and the virus holds its titer well.
That’s really the major thing we have to be concerned about — and that’s keeping that titer as high as we can, especially when we’re spray-applying. How much of that vaccine is actually getting to the mucosal surfaces and infecting the bird? Probably less than a tenth. This is why using full doses is important — to preserve as much of the titer as we can before the bird actually sees it and responds.
The University of Georgia has done a lot of the work showing the importance of handling the temperature of the water you’re mixing with the vaccine. The cooler the water you can mix it with, the better. It should be 60° F or lower, at least when you’re mixing, and even at application would be great. When you get up above 70° F to 80° F, the titer can really start coming down quickly.
… the mechanical shearing forces we have with syringe-based spray cabinets can damage a lot of the virus if they’re not maintained well…MARK JACKWOOD, PhD
We did some studies with spray vaccination using a bronchitis vaccine as a model. Dr. Cookson is absolutely right — mixing the vaccine with cold diluent or cold distilled water is really important. If we mixed the vaccine with water that was 4° C (39° F) and we kept it at that temperature, we maintained the titer for well over 120 minutes. If you mix it with room-temperature water and let it sit at room temperature, you lose almost a log immediately. There’s literally no vaccine there after about 120 minutes. You’re not giving a full dose at that point, obviously. Dr. Brian Jordan did those studies at the Poultry Diagnostic and Research Center, University of Georgia.3
The other thing that we found is that the mechanical shearing forces we have with syringe-based spray cabinets can damage a lot of the virus if they’re not maintained well and kept in perfect working order. We have to make sure those syringes are working properly. They are disposable syringes. And that means you’re supposed to dispose of them, right? But some people use them for days on end. We need to be careful with that. We also need to watch for air in the lines. If you’re not filling that syringe completely full, you’re not giving a full dose.
One other thing I want to mention is about preparation with frozen bronchitis products. It’s a little bit different compared to a Marek’s vaccine, and the people who are preparing the bronchitis vaccine may be the same people preparing the Marek’s vaccine.
When you thaw your bronchitis vaccine, you don’t want it to get all the way thawed out because it’s sitting in water that’s 78° F (25.5° C), right? If you let it thaw completely, the temperature of the vaccine will increase to 78° F or 80° F (25.5° C or 26.7° C). That’s really important to emphasize to hatchery employees.
The other thing I see in the hatchery is that the person mixing the vaccine can be very busy and not pay close attention to all the details required for what they’re doing. If you don’t watch carefully, some may prepare the new vaccine too early, resulting in mixing too much of the old vaccine with the new vaccine, which is going to dilute the vaccine that you’re administering to the chicks.
Let’s not forget about storage. We don’t want to put thousands of dollars’ worth of vaccine into a $200 refrigerator we got on clearance at a home store because it’s dented.
Are you making sure the birds’ uptake of vaccine occurs in the appropriate amount of time? There’s definitely a checklist you go through.MEAGAN SLATER, DVM
And it shouldn’t be stored on the door shelves.
That’s right! We try to put a lot of emphasis on good storage, and we have alarms set on all of our refrigerators so the vaccine doesn’t freeze or get too warm.
Believe it or not, one of the most common problems that I see is failure to check air pressure. If the spray cabinet calls for a 50 psi and you’re using 78 psi, that along with the shear force applied with a syringe system essentially destroys the virus you’re giving to those birds.
Clogged nozzles are another big issue. I’ve seen where they’ve got two nozzles and one of them is not spraying anything.
It’s amazing. You can see these problems easily in a hatchery, and I’d say over 90% of hatcheries have a process and are supposed to be checking for these problems at least a couple times a day if not more. It’s very obvious when a nozzle is clogged if you’re looking. You’re passing a box underneath and you’re hardly getting any coverage on the paper.
One more thing that we’ve found and that’s regarding volume. Typically, hatcheries were giving 7-ml volumes.
I don’t know where 7 ml came from, but we found if you increase that to a 14-ml volume, you get more vaccine into the chicks. If you increase it to 21 ml, you get a lot of vaccine to the chicks.
Now, the combination of keeping the vaccine cold and getting 14 ml or 21 ml to the chicks in wintertime is something a lot of people don’t like to do. They think they’re going to have a chilled chick and problems with chick quality. However, our experience is that if the hatchery is managed properly and it’s warm, the chicks will dry out in less than 30 seconds and they’ll be just fine.
Dr. Slater, you’ve had some experience with educating producers on proper vaccine administration. What are some of the common mistakes with field vaccination that can be remedied, that can be fixed?
There are a lot of things that can go wrong with field vaccination. Bronchitis vaccines should theoretically be sprayed since it’s a respiratory virus, but sometimes water vaccination gets into birds better. It’s really what you think your crews can do. When I was in Pennsylvania, we had the luxury of a crew that did nothing but vaccinate birds at multiple companies. They were good at doing their job. The disadvantage is that they did every company in Pennsylvania.
That being said, if you are water vaccinating, water sanitation and preparation need to be considered such as priming the water lines and making sure they’re drained. Do you use a dye? Are you making sure the birds’ uptake of vaccine occurs in the appropriate amount of time? There’s definitely a checklist you go through.
What else do the practitioners here do regarding field vaccination to make sure bronchitis vaccines are administered effectively?
We’re not field boosting now, but we have periodically in the past. It’s difficult to double-check and see how well you’ve done. You can certainly look at routine serology to see what kind of response you’ve got.
One common mistake is not having enough people there to spray vaccinate in the field. We monitor our spray-vaccine procedure carefully. We watch how the person mixes the vaccine and how long it takes to get it out there to the birds. The best vaccinators we have know exactly how many steps it is from one end of the house to the other. They know exactly how much time it’s going to take them to vaccinate, and they finish vaccination with no vaccine left over. They don’t run out before they’re done. Those things all have to happen in order to spray vaccine properly. It’s when we take shortcuts that we get in trouble.
I‘m not a practitioner but hearing things like using a quarter dose or an eighth of a dose is mind-boggling to me. You spend millions on vaccines and then cut them, in some cases, to some fraction of a dose. May look good on paper, but how is that going to work?
We field boost our larger birds — birds that will process at 46 to 53 days of age — between 16 to 18 days of age and up to 19 days of age. We have a crew of four that field boosts with backpack sprayers. To Dr. French’s point — we actually do base the number of people vaccinating on the size of the house. In a 40-foot-wide house we’ll have two people with backpack sprayers, and for a 50-foot or wider house we’ll have three people vaccinating. One person will go through and cut the birds while the other two follow behind.
In the past, we turned off lights and fans, but then the crews would forget to turn the lights and fans back on. That’s one of those compromises and where human error can hurt you. And going back to Dr. Sander’s initial question of how to check for the effectiveness of vaccine application? I’m not sure. Perhaps it’s looking for a mild reaction 5 to 7 days after vaccination and not lingering around, causing residual airsacculitis.
We have real-time PCR that’s specific for those vaccines. We can monitor 5 or 10 days after vaccine application to see what percent of birds in that flock actually received vaccine and how much. It’s not cheap. Maybe you’re not going to do it with every single house, but if you spot check your crews every once in a while, you can be fairly sure you’re doing a good job.
Let’s not forget about storage. We don’t want to put thousands of dollars’ worth of vaccine into a $200 refrigerator we got on clearance…MARK BURLESON, DVM
Minimizing vaccine reactions
With respiratory vaccines, including bronchitis vaccines, you’re going to expect some clinical response. What is a normal response to bronchitis vaccination?
It can vary by the combination of vaccines you’re using, with your management and the type of bird you’re growing. Every location needs to develop a sense for what is within the bell-shaped curve for their flocks.
Generally speaking, a normal vaccine reaction after hatchery vaccination for bronchitis viruses will occur between 5 to 9 or 10 days of age. That’s probably when your reactions peak, and it can be quite mild, especially if you’re not also giving a live Newcastle vaccine. Even when it’s subtle, you should hear something in the flock. You may need to go in and hang out with the birds for a while and listen and observe. Some of them might shake their heads a little. That’s normal.
And a rolling reaction?
If, say, 40% to 50% of the birds are head shaking, that’s probably an excessive or rolling reaction. If you hear a lot of snicking or what I call the “frog noise,” which sounds like a wet cough or gurgle, as soon as you walk into the house, that’s excessive.
If you see too much reaction, start looking at the application and all those things we talked about. Reconsider the vaccine combinations you’re using.
A true rolling reaction is more often the result of poor application. If a significant amount of birds on the farm never got the vaccine, they’re getting it from the ones that did respond. A big problem with vaccination occurs when those vaccines have passed back into chickens and are shed back — it’s not the same as vaccinating at day of age. The amount of exposure can be higher. The shedding interval of those vaccines can be prolonged without uniform vaccination. The field challenge often comes on top of a rolling reaction and that’s a real complication.
If, say, 40% to 50% of the birds are head shaking, that’s probably an excessive or rolling reaction.KALEN COOKSON, DVM
What is the duration of the head shaking and snicking that represent a normal reaction? You said it was about 9 days?
In my experience what you see and hear occurs 5 to 9 or 10 days after vaccination. But if you’re looking at air sacs — and that’s another very important way of evaluating — that usually comes on a little bit later. That usually occurs about 9, 10 or up to even 14 or 15 days after vaccination.
The reason I ask is because I don’t know if it has anything to do with the composite of vaccines we’re using today and if it differs from what used to be used maybe 10, 12 or 14 years ago. In the past, I thought there was a lot less tolerance for vaccine reactions.
Much of the industry is vaccinating onlyonce now, at the hatchery. In the past, there was more field boosting between 12 and 14 days of age if you were producing a small bird or 14 to 18 days if you were producing a heavy bird. It was not considered acceptable to have any reactions from hatchery vaccination that lasted beyond 10 days. Today, it seems there’s a bit more tolerance and that it’s okay if birds are still snicking a little at 12 days of age. I don’t think it’s okay. I don’t know what everybody else feels about that, but I think that’s an important point.
Would anyone like to comment?
With Massachusetts vaccines you get more of a very noticeable reaction up front. But it also clears out pretty religiously, too. I think most variants cause a milder reaction, actually, and tend to persist a bit more in their presentation. We also see it with PCR and when we look at Ct values.
[Editor’s note: Using real-time PCR technology, the DNA of a virus is identified with a fluorescent signal. It can take multiple cycles to identify a virus, and the number of cycles it takes is the cycle threshold (Ct) value. When more virus is present, it takes fewer cycles to be identified with the test. When less virus is present, it takes more cycles.]
I agree. I think it depends on the vaccine.A lot of people think bronchitis vaccinesare all created equally and they’re not. We have more aggressive vaccines and we have very mild vaccines. And those vaccines and the combinations of those vaccines can push the vaccine reaction out to 12 days. I always like to say you need some vaccine reaction, because if you’re not getting any, you probably don’t have birds that are immunized. On the other hand, you don’t want production losses or severe reactions or long-lasting reactions either.
I always like to say you need some vaccine reaction, because if you’re not getting any, you probably don’t have birds that are immunized.MARK JACKWOOD, PhD
What about reactions when combining a bronchitis and Newcastle vaccine? Is there one component that causes any kind of interference or concern?
It can certainly complicate the issue. I think it makes it a bit worse. I appreciate your comments about checking air sacs, Dr. Cookson. To me, the level of airsacculitis you see in birds is critical. I expect to see it show up about 7 or 8 days after vaccination and to last for about 5 to 7 days. I don’t, however, want to see a 2+ score.
Whether you’re putting Newcastle or something else that’s really aggressive, like a laryngotracheitis vaccine, on top of a bronchitis vaccine, you start to really create problems, and birds can have a hard time getting over the response to vaccination. The more stuff you add to the vaccination, the worse the reaction gets.
IBV Arkansas condundrum
I also wonder if some of the continued problems we have with IBV Arkansas is self-induced.SARAH TILLEY, DVM
I hear concern about IBV Arkansas bronchitis vaccines leading to rolling reactions and condemnations, yet IBV Arkansas is still prevalent in the US. Does anybody have any experience in the field with managing vaccination against this serotype?
I’ve not had personal experience, but when my predecessor removed the Arkansas vaccine from the bronchitis program, everything worked well for a while, then condemnations went through the roof. He said, “No way am I ever going to do this again.”
There have been some studies, and I think it’s fairly well known that IBV Arkansas is just not very immunogenic. If you don’t use a proper dose and don’t properly prepare and administer the vaccine correctly, your best bet is a very low vaccine take, and you don’t get a robust immune response. If you are giving multiple bronchitis vaccine serotypes along with IBV Arkansas, Arkansas doesn’t compete enough and you don’t get a high enough immune response and it can persist. I also wonder if some of the continued problems we have with IBV Arkansas are self-induced.
It’s funny that when you talk to broiler veterinarians about IBV Arkansas vaccines, you get both ends of the spectrum. Some say, “Yeah, we pulled it out and we really improved our performance. Bird health got better, yaddah-yaddah.” I’m on the other end of the spectrum, where I’ve been using Arkansas now for 11 or 12 years, and we have some of the best livability and low condemnation rates — we’re in the top 25% in both of those categories. Maybe I could do a little better, but I really don’t want to touch it if it’s not broken.
Now, with the addition of these new variants, it does make you question if IBV Arkansas plays well with GA08. Can I give them together? If not, then which one do I pull? It opens up a lot of questions.
We’ve always found IBV Arkansas works great but that’s by eyedrop, and that’s not the real world. It’s always interesting to hear the woes. I don’t know whether it’s management or something specific about certain regions. It’s interesting to me because I see how it works in a lab. It’s a polarizing vaccine strain, for sure.
I think that’s complicated to some degree, for the simple reason there are several different Arkansas vaccines out there, and there’s quite a difference between them.
Is anyone aware of experience involving trouble with an IBV Arkansas who has pulled it from their program and found cross-protection against Arkansas with other bronchitis serotypes?
We’re looking at it right now. We’re trying some new combinations and are wondering if we’ll get enough protection against Arkansas to be able to pull it out. We’re as nervous as we can be about it, but that being said, I’ve never been a big fan of Arkansas vaccines anyway, so I’m kind of excited that we’re pulling it out. It’ll be interesting to see.
We did a study this year in broilers involving combinations of IBV serotypes and an IBV Arkansas challenge. The combination was Massachusetts plus GA98 or Massachusetts plus GA08. Both gave us about 50% protection, which isn’t too bad in broilers. GA08 plus GA98 gave about 30% protection. By itself, the Arkansas IBV vaccine alone gave 86% protection.4 If you’re trying to eliminate an IBV Arkansas vaccine from your program, it seems like IBV Massachusetts is a good place to start, then build from there.
The caveat is that if a bronchitis program is successful without an IBV Arkansas vaccine, it’s probably highly dependent on how much IBV Arkansas virus you actually have floating around. If the IBV Arkansas virus starts to build up, the program probably isn’t going to hold up without an IBV Arkansas vaccine. There’s no protection like IBV Arkansas against IBV Arkansas, right?
We’re almost out of time. But before we wrap up, I’d like to give everybody an opportunity to tell me where you think we might be with bronchitis control within the next 5 years. Will we still be fighting it? Are we going to see enough advances in research or vaccine technology that’s going to allow us to see some significant improvement and cut our producer losses?
I’m not so optimistic. In 5 years, I think we’ll still be in the same spot. I’d like to think within 10 years, maybe. I hope I’m not having to deal with bronchitis until I retire.
I think history has told us we can expect another wave every 3 to 5 years. I’d like to see vaccines that could be tailor-made to our challenges and that can be developed quicker than 3 years. By the time a new vaccine is developed, the virus is spreading and creating more mutations. I don’t know how tailored vaccines could be made faster, but that would be the answer to our biggest concerns.
…I think we have to be realistic and get away from the idea that we’re going to have one vaccine that’s going to cross-protect against everything. This virus just does not lend itself to a strategy like that.MARK JACKWOOD, PhD
I’m with Dr. Burleson. I think in 5 years we’re going to be at about the same place we are now. But I think we have to be realistic and get away from the idea that we’re going to have one vaccine that’s going to cross-protect against everything.
This virus just does not lend itself to a strategy like that. There are, however, some new technologies that exist today where we can create a tailor-made vaccine in a matter of months against a new IBV that we just isolated and all we have is sequence data for it. Whether USDA — and this goes back to my 5-year prediction — will allow us to license such a vaccine, which would be a recombinant, and use it in the field, remains to be seen. So it might be 10 years from now — we’ll see. But I think the future does look bright. It’s going to change.
I’ve seen good, smart people that I and many others respect retire after making significant contributions to the IBV body of knowledge, yet the disease is still here. I hate to say it, it chews people up and spits them out. I can’t say I’m as optimistic, unfortunately. We know the challenges, and we have a long way to go. Regulation is important and certainly a big challenge, probably the largest challenge of all. I think it comes down to learning how to use the tools we have in front of us, using them well and staying on top of what we’re doing.
I want to extend my thanks to each of you. This has been an informative and educational panel that should be of benefit to the industry.
1 Data on file. Study No. 06-15-7ADMJ. Zoetis LLC.
2 Cookson K, et al. Broiler challenge study evaluating different combinations of infectious bronchitis vaccines on protection against a contemporary DMV/1639 IBV challenge isolate. Am Assoc Avian Pathol. 2019.
3 Jordan B. Infectious bronchitis vaccination: How can we improve? XXIV Congreso. Centroamericano y del Caribe de Avicultura. Antigua Guatemala. November 2016.
4 Data on file. Study No. 032419-KL-70AQO-KC-5821. Zoetis LLC.
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