POULTRY HEALTH HIGHLIGHTS OF A ROUNDTABLE DISCUSSION T ODAY

Optimizing fin ‘no ever’ and‘reduced use’ broiler flocks

july 2017 • INDIANAPOlIS, INDIANA P O U - 0 0 0 9 4 POULTRY HEALTH HIGHLIGHTS OF A ROUNDTABLE DISCUSSION T ODAY

Jon Schaeffer, DVM, PHD Director, Poultry Veterinary Services, Zoetis Inc. [email protected] • zoetisus.com/foodsafety

WELCOME

The growing trend toward “no antibiotics ever” and “reduced use” production systems has prompted poultry companies to rethink their traditional disease-management practices.

When flocks are raised with few or no antibiotics, they’re naturally more susceptible to diseases caused by primary or secondary infections. This has presented a huge challenge for poultry veterinarians.

alternative therapies have shown potential, but reports from the field — both scientific and anecdotal — show they’ve also been inconsistent.

Making refinements in nutrition, stocking rates and housing may help to reduce disease pressure. But in the end, finding ways to optimize immunity and give broilers more “staying power” could be the best strategy for maintaining the health and welfare of these birds.

To help the poultry industry meet this goal, we brought together an all-star team of experts with expertise in three diseases affecting the broiler’s — IBD, Marek’s and reovirus — to talk about what producers can do now to raise the bar for protection and flock welfare.

This booklet presents highlights from that lively and informative discussion. Special thanks to the participants for sharing their insights and expertise.

Sponsored by f Optimizing immunity in ‘no antibiotics ever’ and‘reduced use’ broiler flocks

TABLE OF CONTENTS

4 PANELISTS

6 BUILDING A STRONGER BIRD

9 INFECTIOUS BURSAL DISEASE

20 REOVIRUS

26 MAREK’S DISEASE

29 WRAPPING UP POULTRY HEALTH HIGHLIGHTS OF A ROUNDTABLE DISCUSSION T ODAY

MARK BURLESON, DVM KALEN COOKSON, DVM ELIZABETH DALE, DVM DARAL JACKWOOD, PHD

JEAN SANDER HOLLY SELLERS, DVM JOHN SMITH, DVM GUILLERMO ZAVALA, DVM

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PANELISTS

Mark BUrlesOn, DVM Wayne Farms kalen COOksOn, DVM Zoetis elizaBeth Dale, DVM Pilgrim’s

Daral JaCkwOOD, PhD Ohio State University hOlly sellers, DVM University of Georgia

JOhn sMith, DVM Alectryon, LLC

GUillerMO zaVala, DVM Avian Health International, LLC

MODERATOR: Jean sanDer Zoetis

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IBD is one of those diseases that will be here long after “ all of us are gone. It’s never going to go away. GUillerMO zaVala , D V M ”

SANDER reovirus is a little bit more inconsistent — control of these viruses is therefore ? Dr. Zavala, would you tell us a bit about some strains are immunosuppressive critical — and we have the tools we need how control of immunosuppressive and some are not. Immunosuppressive to protect against the immunosuppressive reoviruses, like IBD, may affect B cells. diseases they cause. We don’t always diseases such as infectious bursal They cause bursal atrophy, for example, protect birds against them 100% the way disease (IBD), reovirus and Marek’s can and reduce the ability of the bird to we’d like to, but for the most part, the help us produce a more resilient bird produce immunoglobulins against we have for use in the field are with a stronger immune system? specific disease agents. good tools.

ZAVALA Marek’s disease also affects B cells, IBD is one of those diseases that will be impairing the bird’s ability to produce SANDER here long after all of us are gone. It’s never sufficient to a number of ? Can vaccination against viral going to go away. It affects B cells and different infectious disease agents. It can diseases help reduce the incidence impairs their ability to produce specific impair the ability of T cells to function of secondary bacterial infections antibodies that have high affinity for very properly, which help coordinate the bird’s and, in that way, reduce the need specific disease agents. immune responses. for antibiotics?

Protecting birds against Marek’s disease is a fourth very, very critical immuno- JACKWOOD absolutely critical if, for example, we’re to suppressive agent is chicken infectious When we’re talking about vaccines for reduce condemnations due to neoplasia in anemia virus (caV). It can interact immunosuppressive diseases like IBD, the processing plant. It’s also critical for with any or all of these other viruses reovirus and Marek’s, I think we can do protecting the immune system. and predispose birds to secondary a better job than what we’re doing now. opportunistic infections. It can infect If we can prevent birds from becoming and destroy bone marrow cells. immune-suppressed and getting second- The result is increased bacterial ary bacterial infections, we may be able to infection and increased severity of get away with using fewer antibiotics. any infectious disease. continued

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...it’s important to manage our secondary bacterial levels, “ and even bronchitis. kalen COOksOn, DVM ”

SANDER broiler flock we knew had low reovirus SANDER ? Should efforts to build immunity titers and challenged half of them with ? Dr. Dale, according to published in broilers start with the breeder reovirus at 3 days of age and then IBD reports, Pilgrim is the second program? virus and caV at 7 days. and the results of largest producer in the uS, and that, from a viral standpoint, is that we got about 24% of your production is now SMITH about 10% weight suppression, probably “no antibiotics ever.” Have you Absolutely. The key to controlling diseases from the reovirus challenge, and 50% of seen a relationship between the like IBD or reovirus, at least under US the birds were infected with aL-2 by 2 management of these three diseases weeks of age. So IBD virus was also conditions, is hyper-immunization of the and the staying power of your flocks, probably a factor. hen using strains that are as close as and does it differ in -free possible to your resident challenge strains. production systems versus on top of that, we challenged all the birds conventional production systems? DALE with a pathogenic Escherichia coli using If the bird is immune-compromised or either a high dose of about 8 logs or a low overwhelmed by conditions in the dose of 5 logs. Well, there wasn’t much DALE difference in the high-dose E. coli birds — environment, you can use the best The management of those three diseases as if even the immune-intact birds were vaccines in the world but they’re not is just as important in our conventional just as overwhelmed by the high E. coli going to elicit an appropriate response, systems. These problems lead to morbidity challenge. But in the low-dose E. coli and a bacterial challenge will break and mortality in both types of systems. birds, we still had significant levels of through pretty easily. however, it’s not as easy to prevent E. coli disease in the virally challenged secondary bacterial issues due to birds and no E. coli in the birds that immunosuppression in antibiotic-free COOKSON weren’t immune suppressed. So I think production systems. I’ll just share a study we performed a there’s information in that, that can kind of fit into our paradigms that we’re few years ago at auburn University careful management throughout the facing today. You know, how it’s important because I think it illustrates the interaction entire production process is needed to to manage our secondary bacterial between virally induced immune ensure we get the reaction we levels, and even bronchitis. It’s still very suppression and susceptibility to bacterial need to elicit adequate immunity, whether 1 important that we manage our immune challenge. In this study, we picked a that’s in breeders, at the hatchery or in health programs, as well. the broiler house.

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SANDER you don’t have B cells reaching the sec- The key to successful breeder vaccination ? Dr. jackwood, can you expand on ondary lymphoid organs yet. They’re con- is having breeder birds that aren’t IBD and tell us more about how it centrated in the bursa, and if they’re immune-suppressed to begin with and contributes to immune suppression? destroyed, you don’t have any more cells that have a fully functioning immune to repopulate — resulting in permanent system so they can respond to vaccines. JACKWOOD immune suppression where antibodies You need to get the titers of antibodies The virus infects immature B cells in the can’t be produced. very high so breeders pass those bursa of fabricius. Ultimately, what you antibodies on to broiler chicks through end up with is a bird with a diminished It’s important to note that the T-cell the yolk. ability to produce antibodies. population is also affected by IBD so you also see some cellular immune It’s been shown fairly well that if you have however, the severity of compromise suppression in these birds. (T cells are high serum antibodies in your breeders, depends on the timing of infection. Let’s critical for fighting bacterial infections) . you will have high antibodies in the say the bird is 14 days or older. You’ll broilers when they hatch. The issue with get a depopulation of bursa B cells and vaccination of breeders, as Dr. Smith you’ll get immune suppression, but it’s a SANDER mentioned, is that you want to make sure transient suppression. Those birds will ? Can vaccination of breeders help the vaccines you use in your breeders recover because the bursa will repopulate ensure broilers will have access to match the antigenic type of virus in the field that will challenge the broilers. with lymphocytes and go on to mount an maternal antibodies during those immune response. Is it 100%? Maybe not, first 14 days? but the birds certainly do recover. It doesn’t matter how high your maternal JACKWOOD titers are in broilers — if they’re not the right antibody, the broilers are If birds are infected before 14 days of age Yes, breeder vaccination is the key to going to get infected early on in life — 14 days seems to be the cut-off — preventing permanent or severe immune and you’re going to have permanent suppression due to IBD. immune suppression.

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Vaccinating broilers before those maternal antibodies “ drop too low is really the key. Daral JaCkwOOD, PhD ”

SANDER By the time broilers are 18 to 20 days of to 12 days before you see any kind of ? let’s build on that. Some poultry age, the titers are getting pretty low. antibodies showing up in those birds. companies seem to believe IBD That’s when the IBD virus is going to have protection starts and ends with the the opportunity to infect these birds. at The intermediate, intermediate-plus or breeder program and they don’t about 3 weeks of age, we’ve got maternal hotter vaccines will break through vaccinate broilers against IBD. Others antibodies that are low enough for the maternal immunity a little bit better, so believe that both breeders and the birds to become infected with IBD field you can give them earlier when maternal broilers need to be vaccinated. Why virus unless they have active immunity. antibodies are relatively high. The timing Vaccinating broilers before those maternal depends on the individual vaccine and does this decision vary and what goes antibodies drop too low is really the key. how virulent or attenuated it is. The trade into making that decision? off with these hotter vaccines is that if they are given when maternal immunity JACKWOOD IBD VACCINE DECISIONS is very low they can produce some Let’s talk about antibodies present in the damage to the bursa and cause a transient broilers when they hit the farm. During SANDER ? immune suppression. the first 4 days, their immunoglobulin How do you decide which IBD vaccine antibody stays fairly constant because the to give broilers and when? birds are still reabsorbing yolk. afterwards, SANDER metabolism and growth start eroding JACKWOOD ? antibody titers. You’ve got to give one that matches the What about overall flock immunity? field virus, otherwise it’s not going to How does it factor in? The half-life — the amount of time it work. next you have to decide when to takes for half of the population of give the vaccine — we’re talking about a JACKWOOD immunoglobulin antibodies in that bird live, attenuated virus — and how well it It’s important. You have to consider the to be reduced by 50% — ranges can break through maternal immunity. percentage of birds that have lower or depending on the assay used to detect higher titers. You want to try and vaccinate those antibodies and the type of chicken, Some of the very mild viruses struggle to the flock when you have somewhere but by 7 days, broilers have probably lost do that, so you have to wait until maternal around 70% to 75% of birds with titers half of the antibodies they started with. antibodies are pretty low before you low enough to take with this vaccine. If it’s By 10 days, they’ve lost another half, so can use those vaccines, and you have to less than that, you’re just not going to get they’re down to 25%, and by 13 to 15 days remember that once you give the vaccine a really good immune response from your of age, they’re down to 12.5%. immunity isn’t immediate. It will take 10 vaccine. for example, if you’ve got only

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Besides making sure the correct strain is chosen, it’s important “ to make sure the vaccine is actually getting into breeders. Mark BUrlesOn, DVM ”

40% or 50% of your birds reacting to standard practice to use an intermediate This need creates an ongoing cycle of the vaccine, you’ve got half a flock that’s vaccine at around 18 days of age, usually autogenous vaccine use. We have to use still susceptible. followed by one live intermediate-plus or autogenous vaccines to meet specific strong vaccine at around 5 to 6 to weeks regional challenges and make sure the If flock titers are already too low (i.e., you of age. historically, that program worked breeders are hyper-immunized for strains waited too long to vaccinate), you end up very well for priming the immune system the broilers will be exposed to. with a population that’s very susceptible so pullets could respond well to the killed to the field virus, and they’re going to get vaccines they got later on. BURLESON infected and start shedding field viruses. Besides making sure the correct strain is Then you’ve got a flock that’s already There’ve been changes since the chosen, it’s important to make sure the getting immune-suppressed when you’re emergence of recombinants, which vaccine is actually getting into breeders. trying to administer a vaccine. certainly have a place. The recombinants Sometimes companies establish a strong will protect pullets most of the time. In IBD vaccination program and assume it’s So, I’ll reiterate — population immunity fact, they may do a better job than live being administered correctly, but I’ve seen is very important when you’re deciding vaccines when the challenge is in the first-hand that they don’t always follow when to give those vaccines. There are a 4- to 6-week period and immunity from up. If you’re using killed vaccines, you lot of variables involved in making the the recombinant is in full effect. however, have to be auditing vaccination crews decision of when to vaccinate. because a recombinant may actually and monitoring antibody titers to ensure reduce the circulating field challenge is every breeder is getting injected. all the more reason to continue to keep a SANDER strong, live vaccine in your program. SMITH ? How can the breeder-vaccination Live-priming helps improve the titer I think the substrate used to grow the program for IBD be set up to help response to the killed vaccines. virus for killed IBD vaccines makes a difference. With current technologies, ensure it protects broiler chicks? DALE the vaccines produced in bursal tissue COOKSON I also believe in live-priming followed are superior. by inactivated vaccines for breeders. First, the breeder pullet must be But we wrestle with finding appropriate I like to use a couple of high-quality adequately primed. Until the advent commercial vaccines that have bursal-derived vaccines with a variety of of recombinant vaccines, it was virtually homologous strains that match the viral , and I’ll add an autogenous field challenge. vaccine on top of that.

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JACKWOOD substrate vaccines and chicken-embryo wintertime when the challenge with I’ll agree with Dr. Smith about the use substrate vaccines, in addition to bursal- respiratory diseases such as bronchitis is of bursal-derived killed vaccines. When derived vaccines, you not only the highest. Many producers like to focus you start growing bursal disease virus in have a better chance of increasing your their live-vaccine program on bronchitis in eggs or in cell culture, mutations have to titers but you broaden the diversity of the winter for this reason. occur in order for that virus to infect cells antigens you’re actually injecting in those and replicate to a fairly high titer. Those birds. There’s a much higher likelihood for producers who use herpesvirus of mutations are subtle but can sometimes of success. turkey (hVT)-nD vaccines in the winter affect the antigenicity of those viruses. but still want IBD vaccine coverage, immune-complexed live IBD vaccines are In addition, the amount of high-quality ? SANDER a good alternative. Then the recombinant you get with bursal-derived Recombinant IBD vaccines are IBD vaccine can be reintroduced in vaccines is much higher than you can in greater use, but you can’t use off-winter months. get with egg- or cell-cultured vaccines. more than one. What do you do if That’s why the bursal-derived vaccines you also need to vaccinate against of course, if you have ILT, that’s the work better. Newcastle disease (ND) or infectious highest priority and the recombinant laryngotracheitis (IlT)? hVT-ILT vaccine appears to be the ZAVALA most effective. I agree it’s really critical to prime birds. DALE I don’t typically see recombinant vaccines T hat decision, for me, is always made AUTOGENOUS IBD VACCINATION used as a sole vaccine prior to the use of on a case-by-case basis for any individual killed vaccines in many, many places. complex and its challenge. It’s all about SANDER mitigating risk. ?How do you decide which IBD Wherever producers have attempted to strains to use if an autogenous use only recombinant vaccines followed There are times I will prioritize using a vaccine is needed? by killed vaccines, they typically go back recombinant vaccine for something else to the more traditional programs. not — for example, ILT. SMITH every country around the world has access I’ve found serology to test for IBD is a to bursal-derived products, but I think it COOKSON little less helpful and not as clear-cut as has been our common experience that if If you’re going to use a recombinant serology for, say, bronchitis or newcastle. you have the ability to use tissue-culture nD vaccine, it’s likely going to be in the continued

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I rely more on examination of bursas and I More valuable is histopathology. We split for Pcr and sequencing of VP2. now it do that two ways. one is during routine the bursa into thirds, put one-third into gets more complicated. how do you pick postmortems. I look at the bursa without formalin and freeze the other two pieces. the IBD strains that will be the best auto- fail on every postmortem and compare it The five to six bursas from a given farm are genous vaccine candidates? Basically, we to the standard for that age and bird — pooled, so we have one vial with five to look for significant changes in the hyper- essentially continuous monitoring of the six sections for histopathology, and two variable regions of VP2, and frankly we rely bursal status in the operation. frozen whirl-packs, each with five to six on the advice of experts like Drs. Jack- pooled fragments. Then we have a wood, Sellers and cookson. once it’s de- The other thing I do is arrange for periodic pathologist evaluate the formalin-fixed cided which strains to use, we retrieve the bursal surveys. Most companies have a list bursas from each sample to determine final frozen bursa pools in the freezer to that ranks their growers by performance. which samples should be tested for IBD submit to the vaccine manufacturer to I’ll get their list and select farms with virus by polymerase chain reaction (Pcr). make the autogenous vaccine. reasonably good managers who are an experienced pathologist can very still struggling with performance or accurately predict which bursas have disease problems and may have immune active infection and are good candidates SANDER suppression going on due to IBD virus. for viral detection. ? Should there be a limit on the I don’t want farms on the bottom of number of strains in an autogenous the list because those growers are not We submit one of the two frozen sample IBD vaccine? taking care of their chickens; I want the pools recommended by the pathologist farms that are low on the list in spite of SMITH reasonably good management. I don’t know of a good rule of thumb for this, but there’s a limited amount of space I’ll typically sample those selected flocks, in that emulsion for antigens. I typically try certainly at least two and sometimes to limit an autogenous vaccine to about three times, usually between 2 to 4 three different antigens. This is where I’d weeks of age, taking five to six bursas like to hear the experts talk more about per sampling. We measure the bursas, the selection process. obviously, if we although the value of that measurement could set up a challenge, that would be is likely limited, or calculate a bursa-to- the gold standard, but that’s difficult to bodyweight ratio. get done.

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In an ideal world, it would be really nice to do the animal studies and not to “ be restricted to having to use isolates from your farm or your flock. hOlly sellers, PhD ”

IBD DIAGNOSTIC AND REGULATORY You can’t really just stop there. You might to do the animal studies and not to be CHALLENGES have a field isolate that’s 98.5% similar to restricted to having to use isolates from the Delaware e strain, but amino acid your farm or your flock. You’ve got a virus SANDER changes in VP2 are in critical regions and that matches one that’s already been ? Dr. Sellers, what do you see in you’re not going to get enough protection described. These are killed vaccines. So, your laboratory that would be with the commercial vaccine. we’re just running into time issues. helpful regarding diagnostics and the decision about what type of We need to perform challenge studies to S M I T H vaccine to use? determine if commercial vaccines would I’ve got to jump in here because this provide adequate protection and to know has touched a nerve. The autogenous SELLERS what kind of IBD titers your birds need regulations found in Title 9 code of 2 What we see coming in from bursal to be able to use a commercial vaccine regulations (cfr) §113.113 really surveys, representing the highest number versus an autogenous. hamstring us. We’re trying to use these of IBD cases submitted to the lab — at vaccines for the right purpose. We’re least from the US — fall into a category Unfortunately, time is the issue. You’re trying to ensure the health and welfare where they are very similar once we taking samples, you’re 2.5 months into of our birds and decrease our reliance sequence the VP2 gene, which codes the bursal survey and you’ve got your on antibiotics, and the regulations are for the major antigenic protein of the histopathology report. Virus isolation may inhibiting us. IBD virus. take up to 3 weeks if multiple passages are needed to isolate the virus. now you’ve Dr. Sellers mentioned time. The clock They’re similar to variant viruses, but got this data and you need to make starts when you isolate the virus, then how similar is the question. We’re not decisions quickly. So maybe there’s not we’ve got all these other steps we have necessarily looking at the percentage of time or animal facilities available for to do before we can make an informed similarity, but we’re looking to see where protection studies in birds. decision and get the IBD virus into those changes occur within the VP2 the hands of the manufacturer, and protein. We then determine whether or So, we’ve done a lot of work up to a point, they’ve usually got a lead time of several not a particular group of viruses, having but now we are out of time or there months from receipt of the isolate(s) and amino acid changes in the hypervariable aren’t resources to do the type of work production and release of the first serial. region of VP2, are viruses appropriate for that needs to be done to evaluate the an autogenous vaccine. biological properties of these variant The production of an autogenous product viruses that we’re pulling out of birds. In is restricted to 15 months from the date of an ideal world, it would be really nice

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It goes back to timing when you’re trying to decide “ which field viruses to put into your breeder program. Daral JaCkwOOD, PhD ”

isolation, or 12 months from the date of from the date of harvest. So, with an initial application and considerable specific harvest of the first serial of product, term of 12 months, a secondary term of information regarding the adjacent and whichever comes first. The administrator 12 months (although the length of the non-adjacent herds. again, the agency may authorize production of additional permitted extension is not specifically has been fairly liberal and reasonable in serials under special permit, and with stated in Title 9 (cfr) §113.113) and an the application of these extensions to considerable documentation, including an expiration date of 18 months, the adjacent and non-adjacent flocks in assessment of the continued involvement maximum period of use could be up to the poultry industry, but in view of the of the flock with the originally isolated 42 months (3.5 years). These temporal structure of our industry and our organism, diagnostic work to support this provisions of the regulation appear to be objectives in using these vaccines, this assessment and evidence of efficacy of the fairly inflexible and can be problematic. process of geographical extension previously produced product. should almost be a given and could be We’re eating into the time we’re able to streamlined considerably. Simultaneously demonstrating continued use that isolate, and when it expires, involvement with the agent and efficacy you’re done with it. You’ve got to throw it If a neighbor has it, I think most of us of the previously used product is a bit out and start over. It doesn’t matter if it’s have been very collegial in giving of a catch-22 and can be problematic, still in the field, you’ve got to go and find it permission to use our isolates. We get a although the agency generally has been and get it again. little relief there, but there still are a lot accommodating in this regard. of issues with the regulations that really There’s another issue. The seed must be need to be examined, because they are The seed cannot be maintained by the isolated from sick or dead animals in inhibiting the proper and judicious and establishment beyond the time of the “herd of origin” only, but there are beneficial use of this technology. Thank authorized use in production (12 months provisions for use in adjacent herds at risk you for letting me get that off my chest! plus any extension). The expiration date of and in non-adjacent herds with special the product must not exceed 18 months permission — that requires formal DALE I’m glad Dr. Smith said that. a huge part of our frustration in the field is making a correct decision regarding which isolate to use, based on the available information we have, in a timely manner. When you’re talking about using an autogenous

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vaccine in your breeders, you’re a year out your breeder program?” or, “hey, this I want to reiterate what Dr. Sellers said. before you see protection in your broilers. is a new virus and it’s breaking through You can’t look at percent homology Too often by that time, the field challenge in broilers at 10 days of age. You’ve per se; you have to look at all of the amino may have changed. got to get this strain in your breeder acid mutations, especially in the hyper- program.” I don’t care where the variable region — the four peaks. and It’s difficult to know whether you have the mutations are — the timing is telling especially in Peak B. That’s where I think correct isolate. We see diversity sometimes me this is a problem virus. 80%, at least, of the antigen expression is even within a complex where only a being driven, from Peak B. certain percentage of the farms are now, let’s go back to mutations. as affected, and you’re trying to choose one Dr. Sellers said, these viruses can be 98.5% If you want an autogenous vaccine, you to put in your whole production system. alike and still be antigenically different probably want aL2 in it, and if you haven’t enough due to the location of the isolated aL2, which is unlikely, I would say JACKWOOD mutations. one or two amino acids in the keep pulling samples until you do. It goes back to timing when you’re trying right place can make a big difference with to decide which field viruses to put into these viruses, particularly in the field. If If you’re not going to rely on an autoge- your breeder program. it makes a difference in the laboratory nous vaccine, you probably want to build setting with vaccine-challenge studies, it’s a program that gives you solid protection When did you isolate that virus? Did you going to make an even bigger difference against the Delaware e strain of IBD and find the virus at 35 days or 14 days? If it’s a in the field. try to get aL2 cross protection as good as 14-day virus, that’s the one breaking you can from your conventional program. through maternal immunity, but you’ve COOKSON really got to look closely at the sequence I’m going to go out on a limb and guess JACKWOOD to be sure. that the vast majority of the autogenous To expand on what Dr. cookson just said formulations for IBD have the variant aL2 — when you start looking at surveys When you start to generate a database in them. across the US, you’ll see we don’t have and get to know what viruses are there, what we had years and years ago, and you can start to work with a farm. You We conducted a survey about 5 years ago that’s one virus that dominates the can say, “okay, we’ve seen this sequence that included data from hundreds of farms entire US. before and it’s never been a problem, from california to the Delmarva Peninsula. so what else might be going on with We had over 100 IBD isolates. about half were exactly aL2.

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Based on samples coming into my lab, BURLESON there are a lot of other conditions to we oftentimes see pockets of viruses The bursal surveys as Dr. Smith discussed rule out. If performance starts slipping, that have evolved because they are are helpful for assessing bursal health. we’re having late mortality or increased geographically isolated. for example, in I reserve challenge studies for when I want condemnations at the plant due to ohio, which I know the best, we’ve got to change the IBD program for breeders. opportunistic, secondary-type infections several small broiler companies that and I see colibacillosis or a secondary-type really don’t interact much with the rest of JACKWOOD respiratory infection, I look for underlying the broiler industry because they’re in Bursal surveys are an excellent way to bursal issues and conduct a bursal survey. ohio, and they have some unique bursal assess bursal health. here in the US, the disease viruses in their flocks that we IBD viruses infecting our flocks are causing RAY OF HOPE don’t see anywhere else in the world. subclinical disease — so there aren’t any clinical signs. The only way you’ll know SANDER When you start looking across the US at a you have IBD is by examining the bursa ? Does anyone anticipate an lot of the smaller farms, you’ll see a huge to see how large they are. improvement in the situation variety of IBD viruses. with autogenous vaccines? Tracking overall flock performance can be helpful. When you start seeing JACKWOOD SANDER things like uneven flocks or poor feed Let me offer a ray of hope. The USDa’s ? efficiency, slower growth — those Challenge studies would be the ideal center for Veterinary Biologics (cVB) now kinds of things — that’s a sign that it’s way to demonstrate the potential has a new licensing category for vaccines time to consider immune suppression efficacy of vaccines, but since they are — it’s called a “conditional license” for and bursal surveys. unrealistic for most producers, what platform vaccines (VS Memorandum else can be done to determine if their no. 800.213). These are genetically DALE IBD vaccine program is working? engineered vaccines. Most of the time Before we even initiate a bursal survey, they’re virus-like particles or they’re we look at overall performance. obviously,

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Before we even initiate a bursal survey, we look at “ overall performance. elizaBeth Dale , D V M ”

combinations of proteins that are This is something I think is going to SANDER assembled together, and they can be very, make a big change in the broiler ?When might these vaccines be very effective vaccines because they industry, particularly in the killed-vaccine commercially available? match exactly what the virus looks like. industry for breeders. hopefully, we’ll get away from autogenous vaccines. JACKWOOD They are essentially the outer shell of That depends on how quickly the the virus and have no genetic material SANDER cVB can approve the first one coming inside; they are non-replicating and ? What about the efficacy of through. Some of these have already behave like a killed viral vaccine. been approved and are on the market these vaccines? for swine and horses. It’s the exact same If you find that virus on a farm and you JACKWOOD licensing procedure for poultry. make a virus-like particle to it, you can then take that back to the farm and Based on what I’ve seen in not only use it in your breeder program. You our lab but in other research labs, can also take that to a farm in another vaccines produced with in vitro protein- state and use it in their breeder program expression systems are just as good as if you found that same viral sequence the bursa-derived killed products. there. You’re not limited by time on these, either. In some ways, they’re better because you don’t have to kill them with something, once you’ve found a unique IBDV strain which can alter proteins and antigens. and you’re using that conditionally They’re not live vaccines and they don’t licensed vaccine, the cVB memorandum have to be treated with any chemicals, yet states that you can use it indefinitely in you have an antigen that exactly matches your breeders. the field virus.

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REOVIRUS

2 0 f Optimizing immunity in ‘no antibiotics ever’ and‘reduced use’ broiler flocks

Humoral immunity is the cornerstone for protection against reovirus.

“”hOlly sellers, PhD

? SANDER viremia; if gut health is poor in flocks SANDER let’s turn our focus to reovirus. that are raised without any antibiotics and ?Dr. Zavala, you do a lot of international Dr. Sellers, how does this disease a pathogen comes in, it may take a higher travel. Are you seeing any kind of toll, but there’s no direct evidence there. affect the immune system? What are difference in reovirus isolations in the consequences of infection, and your travels? are they worse in flocks raised with SANDER no or fewer antibiotics? ? ZAVALA Dr. Sellers, I understand that, in I’ll second what Dr. Sellers just said. SELLERS 2011, you saw an increase in clinical It’s interesting — I was still at the Humoral immunity is the cornerstone cases of viral arthritis or tenosynovitis University of Georgia around 2011 to for protection against reovirus. however, due to reovirus. Why do you think 2013, which was my last year there and we don’t know the extent of immunosup- that occurred? when we saw a lot of reovirus cases from pression that various reoviruses cause. many companies. Some pathogenic chicken reoviruses SELLERS cause incredible lymphocyte depletion in Everyone asks that and I don’t have an In the beginning, we thought it might be the bursa. other versions of the virus answer. We know we had an increase in breed related, but then we also saw it in cause viral arthritis and tenosynovitis, yet reovirus among both chickens and in other breeds or breed crosses. I then the bursas look okay. Therefore, I don’t turkeys in the US, and an increase was also started traveling quite a bit more to other know we can say that all reoviruses have seen in asia, South america, europe, parts countries including canada, Mexico, the ability to affect the humoral immune of africa and canada.3 Peru, ecuador, chile and Brazil, and lo and system equally. behold, there were increased problems Some of the reoviruses we isolated from with reovirus. countries in north-central I don’t have any scientific evidence the US matched some of the viruses europe started having problems with it all about whether or not the consequences characterized in other countries and in of a sudden, even including countries that of reovirus infection are worse in flocks other situations. There are viruses unique never reported having clinical reovirus raised with or without antibiotics. We to geographic regions, but I don’t know tenosynovitis before. do know these viruses replicate in the where they came from. It just appears that continued gastrointestinal tract before they cause they all came at the same time.

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REOVIRUS

...there was a huge serological shift, and all of a sudden, “ we’ve got multiple new serotypes. JOhn sMith, DVM ”

We never evaluated immunosuppression. more ILT in the southeastern US and in now, all viruses mutate and it’s random. But I found it fascinating that when we some other countries after 15, perhaps What’s different is the selection. You started submitting clinical samples to Dr. 18, years of not having seen a single case get random mutations but selection for Sellers’ lab, at least from a molecular point of ILT. just certain ones. The selections are for of view, the isolates were extremely differ- mutations that give that virus the ent from what we were used to seeing, how did it get there? It’s one of those ability to survive in the environment or and they were extremely similar to the mysteries I don’t have an explanation for, out-compete its ancestors, which are variants she’d been identifying in the US, but theoretically you could, little by basically its cousins. That’s what happened canada and other countries. little, have problems with disease agents with IBD virus in the 1980s when very that can be transmitted vertically or virulent IBD virus became a problem. This When you have a problem that occurs in transported indirectly by contamination is probably what happened with reovirus. multiple countries at the same time, of egg shells or chick boxes. you’ve got to think about what things are common among those affected. I’m just SMITH REOVIRUS VACCINATION going to leave it at that. It’s remarkable and unusual that reovirus was stable for decades, and the same SANDER COOKSON vaccine worked very well. Then there ? Dr. Burleson, please describe Vertical transmission of reovirus. That’s was a huge serological shift, and all of the reovirus vaccination plan you one thing that’s very different about a sudden, we’ve got multiple new currently use. this virus versus IBD virus, and it’s what serotypes. Something has fundamentally makes reovirus even more challenging changed and I have no idea what it is. BURLESON for us to deal with, both from an I want to take care of the classic epidemiological standpoint and for JACKWOOD reoviruses first, using commercially control with vaccination. Bursal disease did the same thing. available products. We typically give Both reoviruses and IBD viruses are our live vaccines on day 1, and then at ZAVALA double-stranded rna viruses. They 2 weeks and 6 weeks of age. We then This applies to other disease agents as mutate but not like a bronchitis or avian follow that with a killed IBD-reovirus well. around 2006, we started seeing a lot influenza virus, which are single-stranded vaccine at 12 and 21 weeks of age. rna viruses that can mutate very fast compared to the double-stranded We also have a routine program with an rna viruses. autogenous reovirus vaccine that has

2 2 f Optimizing immunity in ‘no antibiotics ever’ and‘reduced use’ broiler flocks

multiple variant reovirus serotypes. What’s different now is that we are missing The 1133 is great because it grows in Whenever it comes time to make a new the homologous, live-vaccine component fibroblasts. The variants don’t grow very autogenous vaccine, I’ll typically test the (to help protect against and prime for well in fibroblasts, and if they do, the titers waters to see what contemporary isolates variant strains). are very low. replication of the variant are out there to include in our autogenous viruses in fibroblasts requires adaptation, vaccine in an effort to stay proactive. If you couple that with the timing of and you can’t predict how long this vaccination — I’m aware of vaccination process will take. again, this requires time as mentioned, when you have a problem, programs with three commercial live and you’re already at a deficit because the reovirus is bad, and it’s bad for a long time vaccinations followed by one commercial clock started ticking 3 months prior when until you get adequate protection. You plus autogenous. Some programs include the virus was isolated. have to stay on the offensive with just two live vaccinations followed by two autogenous vaccines. or three commercial plus autogenous There are just a lot of variables making this in various combinations. What you’re even more painful for the industry. couple We’ve also found we want to inject pullets trying to do is extend the duration of that with having so many different viruses as early as possible with the autogenous immunity so that you can prevent vertical in the autogenous vaccine. It’s really like a vaccine since the virus can be vertically transmission, and we know there’s a lot of rogues’ gallery. The number of reoviruses transmitted. We want protection of that that going on out there. You also want to included in autogenous vaccines varies, breeder bird as soon as possible. be sure that chicks have adequate levels of maternal-derived antibodies to protect SELLERS during the first week or so when they are I agree with Dr. Smith that our commercial most susceptible. vaccines have really been a success story because they have been so successful for We also need to look at the production decades. commercial reovirus vaccines of reovirus autogenous vaccines. Perhaps worked well and protection achieved by there’s a method of producing a reovirus priming with a live, attenuated vaccine, vaccine that’s superior, similar to what’s followed by a boost with a homologous, been said about the bursa-derived inactivated vaccine. The number of live vaccines for IBD. and inactivated vaccinations varies by company, but the strategy of live- prime/boost provided good protection.

2 3 POULTRY HEALTH HIGHLIGHTS OF A ROUNDTABLE DISCUSSION T ODAY

REOVIRUS

generally from two to four in any given for a year’s worth of autogenous vaccine. what you have on broiler farms. If you serial. Selection of the appropriate So, we’re going to leave it in there, but don’t, your other resource is to use as isolate/isolates for inclusion in an autoge- I don’t know for how long. many vaccines as possible and to nous vaccine is not always straightforward vaccinate as much as possible, and do — unless you have clinical disease in a ZAVALA something that hasn’t been said yet — complex and all the reoviruses isolated It’s interesting to see how the industry has which is really work with your crews, from those farms are the same. The dramatically sero-converted, so to speak, supervise them and conduct serologic difficulty is when there are four or five in the last few years. however, things are surveillance. That sounds very, very basic, different isolates, how do you pick the starting to get back to normal, and I think but a lot of times we don’t have time to right one? the industry is starting to abandon, little do that and we just leave it up to them. by little, the use of autogenous vaccines. It’s really complicated. and I don’t really REOVIRUS SURVEILLANCE see a change in the number of samples reovirus vaccination programs for broiler we’re receiving from clinically affected breeders is probably one of the most SANDER flocks over the course of the past 5 or 6 variable types of programs out there. ? How are companies monitoring years. What I’m seeing is a change in There are companies that use only one live for reovirus status in their flocks? the genetic and antigenic profile of the vaccine given in water, followed by one What are the best practices that can viruses. It’s shifting pretty rapidly, and killed vaccine at about 15 to 16 weeks. help ensure you’re making your it’s hard to predict or to make recommen- investment worthwhile? dations for what you need to use. It’s others give three live and two killed plus really a best guess, absent putting those one autogenous. The autogenous vaccine ZAVALA viruses back into birds, and then we will contain two or three resident strains, Serology is probably the most practical come back to the race against time. which I think is probably one of the very way to follow your flocks and determine best things that you can do. of course, if your vaccines are performing, since BURLESON there’s cost involved, but the expense is in challenge work often isn’t realistic. If you We’re not willing to take out the the broiler, so you don’t save money with follow your flocks serologically, follow autogenous vaccine now. We’ve found if your breeder program. their performance and the health status we can prevent two houses of broilers of your progeny birds and you don’t have from breaking with reovirus, we can pay You really have to be as aggressive as a significant frequency of reovirus-like possible, hoping you have strains in the problems in the field, I think for the most vaccine that are as close as possible to part that gives you a good assessment.

2 4 f Optimizing immunity in ‘no antibiotics ever’ and‘reduced use’ broiler flocks

It helps a lot to take as much wind out of the variant’s sails “ as possible before giving the killed vaccine. kalen COOksOn, DVM ”

COOKSON that’s why there’s still a big opportunity even. We also look at broiler titers and I’d want to look at seroconversion to for live-priming. sometimes actually start with broiler titers, reovirus in my flocks or just prior to the then start looking at common source first killed injection to see what the live BURLESON flocks and go back from there and try and response is. You should have a good sense The good thing about reovirus diagnostics find it. of what to expect from your pullets from is that it’s pretty classic. You know if your your live-vaccine program. vaccination program is working or not This becomes a really maddening issue because you typically have lesions — in production, and part of that reason is If you have any outliers — a variant versus maybe IBD, which is a bit tougher because it’s sporadic in terms of where reovirus challenge — it’s pretty clear you’ll — but with reovirus the tenosynovitis is you’re affected and in different regions. have a really big bump in titer response. usually obvious. and it seems to continue to change. That will give you an idea of what’s out there and how early it’s out there. Then it’s ZAVALA I’ll second Dr. Burleson’s comment that time to reconsider your program. It might That’s right. Serology in broilers, however, usually you can diagnose reovirus in the be too light on the live-vaccine side. hasn’t been mentioned, but that’s field if you start looking at the right ages another good barometer of what might — between about 2 and 4 weeks of age in Granted, all we have are conventional, be circulating. It doesn’t reflect things your broilers. however, I’ve found recently classic vaccines. But if you’re just using the 100%, but when you have a problem, this is also changing. I’ve gotten some milder vaccines that are mass-applied, seroconversion tends to be a very isolates from complexes where there are you’re not really touching that immune magnified version of what you normally no obvious gross lesions or tenosynovitis system much. It’s not really creating much have. It’s very quickly clear. at the time of active infection, but we’ve effect and resistance to variant strains. seen weight suppression and then tendon DALE ruptures at older ages. It’s getting harder It helps a lot to take as much wind out of I’ve approached it from both ends at to find the correct samples to take in the variant’s sails as possible before giving times. We look at post-live prime titers broilers because now we’re seeing more the killed vaccine. We’ve seen that even and also at post-killed vaccine titers before of these variants with much more subtle flocks infected at 6 to 8 weeks of age birds go into production. Sometimes lesions during active infection. I don’t with these variant reoviruses can end up you can catch on to something early, as know that we have looked explicitly at shedding in lay unless you have two really Dr. Zavala alluded to earlier. immunosuppression; we’re not necessarily solid autogenous vaccines in there. I think seeing secondary infections. Those titers are interesting. often your first sign of it is in the broilers or at the plant,

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MAREK’S DISEASE

2 6 f Optimizing immunity in ‘no antibiotics ever’ and‘reduced use’ broiler flocks

The dose of Marek’s vaccine that will protect against tumor expression “ may not be enough to protect the immune system. GUillerMO zaVala, DVM ”

SANDER Generally speaking, that’s how Marek’s the plant, but you may not be protecting ? Turning to Marek’s — I’d like Dr. Zavala affects the ability of the immune system to adequately against immunosuppression. to review how this disease affects the respond to just about any pathogen. If you affect B cells and T cells, you’re effectively immune system. damaging almost the entire ability of the SANDER immune system. ZAVALA ? Are you seeing variation in the It’s interesting that during the very first problems that Marek’s disease causes days post-infection in the field, the virus in different regions or different areas? SANDER is going to start replicating very actively ? in birds that aren’t properly protected. What about the consequences of ZAVALA first, B cells and their ability to produce Marek’s virus in flocks raised without Historically in the US, we’ve had antibodies are affected. Initially, immuno- antibiotics or with fewer antibiotics? geographic pockets or states where suppression is transient in a way, but then Marek’s tends to be more of a problem it becomes more of a permanent inability ZAVALA based on condemnations. That’s probably to produce immunoglobulins. As far as flocks raised in systems with the most effective barometer we have, fewer or no antibiotics, it becomes more if you will, industry-wide. Granted, after a few rounds of replication, the critical than ever to protect the immune Marek’s isn’t the only disease that leads virus is going to infect T cells. They aren’t system because that’s the only thing to condemnations, and condemnations going to be destroyed as effectively as you can do to help that baby chick and are also affected by differences in the B cells, but their function can be at least growing bird to cope with just about any inspection process at different plants. partially impaired. pathogen, whether that be a mycoplasma, a bacterium, protozoa, etc. Worldwide, Marek’s tends to be more of T cells are critical. They can coordinate a problem when companies either have other actions of the immune system, such I should note here that recent research technical problems in the way they apply as T helper cells of different kinds, and confirms something we’ve suspected for the vaccines or the way they store, they also can act as effector cells. In other a long time: The dose of Marek’s vaccine reconstitute or apply the vaccines versus words, they can directly attack either that will protect against tumor expression true vaccine failures. infected cells or pathogens themselves may not be enough to protect the or even tumor cells. immune system. In other words, when The other problem occurs when you fractionate doses of Marek’s disease companies fractionate doses to save vaccine, you may be avoiding tumors at

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MAREK’S DISEASE

Because of the efficacy of available vaccines, we’ve gotten to the point “ where Marek’s is a non-issue in our company. Mark BUrlesOn, DVM ”

money. You can fractionate doses BURLESON I’m not sure what that means exactly to a certain extent without hurting Because of the efficacy of available and I’m not sure that finding could be protection against neoplastic changes vaccines, we’ve gotten to the point where repeated, but it was an interesting or condemnations due to tumors, but Marek’s is a non-issue in our company. observation. It would be interesting to it’s very difficult to assess at what point We have a system in place where we find out exactly what dose is needed you are hurting yourself in terms of administer only hVT in half of our to protect the immune system so affecting the immune system. operations; in the other half of the you don’t have a variation in your operations, we use both hVT and SB1. condemnation rate. We just don’t deal with Marek’s SANDER condemnations anymore. JACKWOOD There was an interesting study from ? I’d like to hear your experience with SMITH Washington State University published classic Marek’s vaccination versus We’ve likewise found the recombinants to back in 19804 about how bursal disease recombinants and the degree of be effective for control of Marek’s disease. virus infection affects antibodies produced protection you get with each. to an hVT vaccine. When birds received a ZAVALA full dose of an hVT vaccine and were then DALE I’ll share something interesting. Before challenged with bursal disease virus at Most of my experience is with the I left the University of Georgia, we 1 day of age or 21 days of age, it didn’t recombinants. as Dr. Zavala noted, I’d conducted a relatively small pilot study matter — the amount of antibody advise making sure the full dose is used. to see if we could find more septicemia/ produced to Marek’s disease was lower in In addition, there are times in higher toxemia and cellulitis in birds that had less birds that got bursal disease virus. So, if challenge regions when SB1 needs to be detectable hVT vaccine in the spleen. antibody titers to hVT are being lowered added to the hVT. That seems to give There was a very clear trend. by bursal disease and not available to stop good overall coverage. the Marek’s disease infection, that could Birds with cellulitis and condemnations be one of the things that might be going due to septicemia/toxemia tended to have on. In other words, even a full dose of a lower concentration of hVT vaccine Dna hVT may not be protective if the bird is in the spleen. Birds that were healthy challenged — immune suppressed — tended to have a higher copy number of with IBD virus by 21 days of age. hVT genomes in the spleen.

2 8 WRAPPING UP

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WRAPPING UP

SANDER DALE ZAVALA ? Please sum up the impact the trend My experience has been similar and I I’ve worked with a number of poultry toward antibiotic-free production and agree; the push toward antibiotic-free companies in the US and other regions of reduced use of antibiotics has had on production has really prompted us to be the world and have found one of the first more meticulous in every aspect of the things they realize is that transitioning to the industry? entire process. even though our area of antibiotic-free production is not like BURLESON the profession has always focused on turning a switch to get instant results. It’s preventative health, this trend makes us a process that will require sometimes It’s caused poultry veterinarians to be even more so. years of hard work and standardization of more proactive in our approach. as an their procedures. example, take gentamicin. When it’s in It’s interesting that removing antibiotics your hatchery, you tend to be more seems to have a cumulative impact. By companies realize very, very quickly reactive. If mortality at 7 days is high — taking gentamicin out of the hatchery, that with the aid of antimicrobial drugs, say 1% or 1.5% — you work your way back for example, everyone’s very focused on they work with whatever birds they through the system, find the problem, fix 7-day mortality. But I believe I’ve seen get, whether it’s in the hatchery or the it and you move on. more of a difference later in life regarding broiler house. They don’t ask questions. bacterial infections and flock livability. Withdrawing antibiotics has forced the Without gentamicin, the same problem industry to be much more stringent will be much worse in terms of mortality In our case, it’s improved our hatcheries about their process and requirements in — as high as 2% to 3%. In that situation, greatly. It’s been surprising that a couple general. You can’t operate with floor eggs you find yourself thinking through issues of complexes raising birds without the way you used to. You cannot overlook and putting stronger standard operating antibiotics are top-performing in their hygienic issues in nests the way you procedures (SoPs) in place so it won’t production class. We’ve seen the same used to. happen again. So, I’d say for us, removing thing in our organic complex. It’s beating antibiotics has caused us to be more our conventional birds of the same size. It proactive versus reactive. has a lot to do with the management that’s put into place when you are raising birds without antibiotics.

3 0 f Optimizing immunity in ‘no antibiotics ever’ and‘reduced use’ broiler flocks

...if we’re honest, abandoning the use of antibiotics puts “ more pressure on us to further reduce stress. JOhn sMith, DVM ”

SANDER SMITH We know that stress is immunosuppres- ? Beyond protecting flocks from the That’s all true. There’s no magic bullet. It’s sive, so you have to do everything you immunosuppressive diseases we’ve elbow grease and hard work and attention can to reduce stress for the bird. We’d like to think we’re always doing that, but if discussed, what else can be done to to detail. we’re honest, abandoning the use of build strong immunity in flocks, It’s ventilation. It’s litter management. It’s antibiotics puts more pressure on us to especially those that are raised lighting programs and water sanitation. further reduce stress. without antibiotics? Are there other Just the nuts and bolts of raising a healthy management practices we need to chicken, including a high-quality diet. DALE consider more closely? It absolutely starts on the breeder farm, Something that I think gets overlooked and it’s all the things Dr. Smith mentioned. BURLESON is hatchery maintenance. The need for If you’re putting out a good-quality chick, Remember that it starts at the breeder cleanliness should be obvious, but you’ve it makes the whole rest of the process in farm. as I’ve mentioned, we establish SoPs also got to have the correct air flows, the life of that bird easier. that build in attention to detail. This would temperature and humidity in the hallways include egg-handling procedures at the so the machines don’t have to work I’ll echo that and reiterate Dr. Zavala’s farm as well as embryo temperatures, tray as hard. The machines have to be point that the transition to antibiotic-free wash sanitation and rectal temperatures maintained. That includes the fan blades, production is a process. Where we have of chicks coming out of the hatchers. shrouds and the turning mechanisms. been successful thus far can be attributed The SoPs that are established should be to starting the process in advance of aimed at ensuring good chick quality by The times birds are pulled need to be making the transition, with attention to making sure people do the same thing just right to make sure optimal chicks those things Dr. Smith mentioned are every time, the right way. That way, you are placed. necessary for raising a healthy chicken: know that if you put out a good chick, it ventilation, litter depth and so on. already has a good head start. I’ve found built-up litter is actually protective. I examined new versus built-up It’s true that even in a conventional litter as risk factors, and it’s quite clear that complex that’s been running on short the risk is greater with new litter.5 down time, especially for a long period of time, I can isolate viruses all day long. all Breed can have a tremendous impact. these management considerations are So can grower selection. needed and help ensure vaccines are able to do their job.

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WRAPPING UP

The choice between antibiotic-free production or reduced antibiotic use “ and conventional production should remain. elizaBeth Dale , D V M ”

If you’re transitioning to antibiotic-free poultry products the public gets. The 1 cookson K, et al. The influence of E. coli inoculum production, start early and make the industry was not selling chicken that titer and virally induced immune suppression on the incidence of cellulitis in a broiler skin challenge investment on the front end in your wasn’t wholesome. There are many other model. Proceedings of the 56th World Poultry hatcheries. Make sure all other aspects of reasons why it was decided that this is Disease conference, 2007:118-119. management are in good order. If you do the avenue to go. 2 autogenous Biologics. aPhIS.USDa.GoV. that well in advance, it should be a accessed october 27, 2017. smoother transition. DALE 3 That’s really important, and I’ll add Sellers h. Update on Variant avian reoviruses Isolated from clinical cases of Viral ZAVALA one more thing. The choice between arthritis/Tenosynovitis in Broilers. The Poultry I would like to remind everyone that antibiotic-free production or reduced Informed Professional. University of Georgia. 2013 January/february;127. antibiotic-free production is the way the antibiotic use and conventional market is going and there’s no way back, production should remain. There 4 Jen LW, cho Br. effects of infectious bursal whether we agree or disagree. We all shouldn’t be shaming within the industry disease on Marek’s disease vaccination: Suppression of antiviral immune response. avian know that. regarding the different production types. Dis. 1980;24:896-907. at my company, we have all three types It’s not, however, because the industry of systems. Let’s not have animosity 5 Van Immerseel f, Lyhs U, Pedersen K, Prescott Jf. editorial. recent breakthroughs have unveiled the was producing chickens with antibiotics, among companies for whichever many knowledge gaps in Clostridium perfringens- because there’s a withdrawal period that production system they choose. That associated necrotic enteritis in chickens: the first ensures there are no residues in the choice, hopefully, will be maintained in International conference on necrotic enteritis in Poultry. avian Pathol. 2016;45:269-270. the marketplace as well.

3 2 There’s no magic bullet. “It’s elbow grease and hard work and attention to detail.

JOhn sMith, DVM ”

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