Coccidiosis
Management:

Better diagnostics. We need better ways to monitor the disease burden in our flocks and to make more rational decisions of when we need to rotate and make changes.

Most people would say the biggest opportunity is for better control of necrotic enteritis (NE), a bacterial disease that is directly linked to coccidiosis. It would be great if we could figure out better anticoccidials and alternatives for controlling coccidiosis, because that would help us better manage both gut diseases.

There are new technologies that I think will be beneficial. One problem with vaccination is that we don’t get 100% coverage; there’s a new water-based spray cabinet that uses a photo cell, and it may provide faster application and better coverage.

There are also new technologies coming out that will automate counting oocysts, using size and shape. That would help us. Maybe we will be able to diagnose problems earlier or at least better follow trends.

Lastly, as far as coccidiosis control, we really are still trying to figure out how and if alternative products work.

I concur with Dr. Mathis that improved vaccine administration presents a big opportunity. If you base vaccine takes on oocyst cycling at 6 or 7 days post-hatch, probably only around 15% of birds are actually cycling Eimeria maxima. They represent birds that actually received a vaccine dose of E. maxima at the hatchery. The remainder are first exposed to E. maxima via the litter during growout.  Eimeria acervulina and Eimeria tenella aren’t so much a problem, but E. maxima is the Achilles heel of the vaccination process. If only 15% of birds are getting E. maxima via vaccine, that’s a problem. If there are technologies that will improve coverage, there’s certainly a lot of room for improvement right there.

More diversification of rotation programs, which is easy to implement with good planning. In the poultry business, we tend to get rewarded for short-term returns because long-term returns are a little bit more difficult to calculate. So, the tendency is to get on an anticoccidial — an ionophore, a non-ionophore anticoccidial or whatever — and stay with it, often for too long because you’re comfortable with it and the birds are performing well.

There has to be more emphasis on preventing resistance, on managing coccidiosis over the long term and using all of the tools in the toolbox. For example, we have two categories of ionophores — monovalent and divalent — and we need to distinguish between those two, because they have different mechanisms of action. Then we have non-ionophore anticoccidials, some of which are better suited for year-round use. We need to establish sensible rotation programs that emphasize diversification.

All of us would agree that we’ve made some big strides minimizing bad actors, mostly Clostridium, that seem to accompany coccidiosis — especially since the no-antibiotics-ever (NAE) movement took place — with water acidification, decreased bird density, increased downtime and litter treatments. But there’s always room for improvement there as well.

I’ve been performing ASTs since the early 1980s, so I have good background on understanding them. Coccidia-free birds are used in the studies. We have to get samples sent in. We have to get birds for propagation, then we have to propagate. We have to sporulate the oocysts. It takes 21 days to get results starting from hatch. So, yes, it takes a long time. I think ASTs are critically important for companies that want to do them. They can speed up the process by making sure whoever is doing the ASTs is informed ahead of time so coccidia-free chicks are available.

As Dr. Schaeffer mentioned, we know that E. acervulina, E. maxima and E. tenella are the three species that we find in the field. We can probably find them in every house. Unfortunately, when we isolate, it’s quite often just E. acervulina that comes out, mostly due to its high rate of production, when we really want to concentrate on E. maxima, so that is a problem that we need to work on.

To help with isolating E. maxima, one way is not to repass it — you can’t pass it twice or you’ll get all E. acervulina. The other thing is to collect oocysts a little later. If you collect too early, you’ll be getting a lot of E. acervulina — and again, it cycles fast — and I should note that E. acervulina also isn’t a problem in vaccinated birds.

To get a useful representation of sensitivity, it is recommended to not take samples from coccidia-vaccinated chickens. These samples will have primarily vaccine strains and may not be representative of the wild strains within the house.

Correct interpretation of AST results is critical. Many factors come into play with the AST outcome and interpretation. Drug efficacy versus drug sensitivity can be complicated. The species that are in the challenge can easily influence results. Monovalent ionophores, such as salinomycin, are generally stronger against E. acervulina than divalent ionophores, such as lasalocid, which is generally stronger against E. tenella. Thus, you can see that if you have mostly E. tenella, then lasalocid will look good while salinomycin would look better if you have mostly E. acervulina. There are many such interactions. So, one must understand these factors to correctly interpret results and rely on the drug-use history to aid in your conclusions.

In all areas of research, there’s an emphasis now on reducing, refining and replacing the use of live animals. Hopefully, with all the molecular techniques coming on board, we’ll be able to come up with a quick, easier, more accurate in vitro test for assessing anticoccidial sensitivity.  Such an in vitro test would alleviate many of the issues Dr. Mathis outlined with the current in vivo AST methods.

We certainly used ASTs. We typically did them when they were sponsored by one of our allied suppliers. You had to get in the queue because ASTs are laborious and time-consuming enough that you couldn’t run one on a frequent basis and certainly not as frequently as we would like, and without the broad coverage that we would prefer to have to apply to the entire population.

ASTs are a valuable technique, but, unfortunately, I think they’re limited. That’s why I’m hoping for the day when we’ve got quicker, more accurate, in vitro techniques.

We do a ton of ASTs, and we do it in collaboration with Dr. Lorraine Fuller at the University of Georgia. We added an additional component to ASTs in that we do E. maxima micro-scoring. We don’t think gross lesions are representative of much of anything. I think micro-scoring is the most valuable part of ASTs.

You know, ASTs are a contrived experimental system. They’re run on birds that are 12 to 20 days of age and they’re raised on wire. They’re really not that representative of the commercial condition. But, as Dr. Smith said, you do the best you can. You have a limited number of birds to work with, so there’s not much ability to demonstrate statistical significance.

A lot of what AST results mean is interpretive. They’re not a perfect tool. But we do need to emphasize that E. maxima is a problem in ASTs, and quite commonly, we don’t get enough E. maxima in our challenge material to represent a sufficient challenge dose to be able to tease out differences between treatment groups. If you have no E. maxima challenge, it’s very difficult to compare and determine which anticoccidial will do the job for you.

More attention has to be paid to the collection of litter samples — both which farms are selected and the type of sample targeted. Ideally, houses are selected where active E. maxima cycling is occurring, demonstrated on bird necropsies. Also, the quality of the sample is important. Litter with fresh feces or moist litter obtained around the feed or water lines is best. Collecting only dried litter increases the likelihood that E. acervulina will predominate.

You have to do everything possible to try and get high levels of E. maxima in the collected litter. Because, as Dr. Mathis said, you don’t just take this material from the chicken house, purify and stick it in the challenge bird. You have to passage it through birds to amplify it so that you have enough material to use, and with each bird passage, E. acervulina is going to become more abundant in the challenge material.

You have to figure out which houses are actively shedding E. maxima and target them for sample collection. Going to a farm that was shedding E. maxima even a week or two prior lessens the chance of getting good samples.

Thanks for bringing that up. It’s interesting. A lot of folks sample for ASTs in the fall going into winter because wintertime is the hardest time to manage coccidiosis. So they want to know what’s going to work over the winter program.

But oftentimes coccidiosis vaccines have been used all summer. Therefore, if you take a sample for ASTs, in the fall you’re probably going to get a lot of vaccinal coccidia. We think there’s actually a good case to be made for taking samples in the spring as you’re coming off those winter programs, where the selection pressures over the course of the winter are going to give you those Eimeria strains that are most likely to cause problems the following winter. So, we’re looking for more ASTs in the spring than we are in the fall as something that might become more commonplace.

Customarily, posting sessions are done about every 6 weeks. You can increase or decrease that based on overall flock health and the need for monitoring.

Developing a meta-analysis based on posting-session results from multiple years to help determine what’s working is difficult because there are different confounding variables involved. You’ve got seasonality. Among many, you’ve got the preceding coccidiosis program and the level of leakage/challenge resulting from it and the age of birds when cycling is occurring.

We have software that can help get rid of a lot of confounding variables and enable development of trend analyses based on what’s working and what’s not working. But in the end, the most reliable indicator is what was going on in the previous posting session as compared to the current session.

I second everything that Dr. Schaeffer just said. Lesion scoring is one of the best on-the-spot tools we’ve got, but unfortunately, it’s also a pretty blunt, subjective tool. There is a correlation between lesion score and performance, but that correlation isn’t great. We also had posting sessions every 6 weeks. The selection of this frequency is somewhat empirical and is based partly on convenience and feasibility. Also, it is slightly shorter than our typical cycle so that you didn’t get the same farms at the same age every time.

I’d have to agree that our allied suppliers have done a great job of improving the collection, archiving and analysis of data. But drawing firm conclusions and making an on-the-spot decision was something we rarely did. I used it more over the long term.

When I was making anticoccidial-rotation decisions, I looked at what worked in the past. So again, as Dr. Schaeffer said, it’s looking back as much as anything. I think that’s how most people use posting sessions. I think we’re going to continue to use them, but again, my hope is for better tools that will give us a better read on the disease burden and give us more information to make rational decisions about rotations.

Personally, I haven’t done a lot of posting sessions, but I know from colleagues that if you don’t have noticeable gross lesions or micro scores but you have poor feed conversion, then maybe the issue is not coccidiosis but a nutrition, management or other disease problem.

I would say that season is a big factor. As Dr. Schaeffer mentioned, most of us would regard winter and early spring as high-challenge, difficult times, so we focus more on monitoring then. We’ll tend to try to target our stronger, more reliable alternatives to that season.

I agree. Also, a lot of anticoccidial selection is driven by marketing considerations and what theater you’re operating in, whether it’s the NAE market, the World Health Organization (WHO) guidelines or conventional production, where all FDA-approved medications may be used. That establishes the array of products you’ll have available to you.

When you start to configure an annual rotation, it’s best to start with the winter program and use products that are seasonally appropriate. In the US, for instance, nicarbazin is mostly used during the cooler months because it’s not advisable to use it in the summer. If you’re going to plan on using a vaccine, that occupies a certain number of cycles over the summer, and then you fill in the plan’s skeleton from there.

I agree that seasonality is probably the biggest driver. However, other factors come into play. Brooding time, stocking density, litter temperature and moisture drive how the vaccine coccidia will cycle — they affect timing and uniformity of immunity development, for instance. We also know that longer downtimes are going to deteriorate the coccidia oocysts to some degree, thus the coccidia-oocyst load going into the next growout will be different.

We obviously use both rotations and shuttles. I think the trick is to change things up — let the coccidial organisms see something different. There’s good evidence in the literature that periodically resting the feed medications by putting a vaccine in will restore some anticoccidial sensitivity. The evidence about rotating non-ionophore anticoccidials is a little less clear, but I think we all accept anecdotally that it has an effect. You don’t want to get on any medication and just run it forever. You’ll certainly wear it out.

I think we’ve already touched on a lot of the seasonal issues that have a big impact. We tend to use nicarbazin in the winter because it’s very reliable. It’s been very durable, but you have to use it in cool weather. We tend to use vaccines in the summer and fall. Our strategy at Fieldale was to try to mix up the non-ionophore anticoccidials and the ionophores

I’ll describe one that some of our listeners will find of interest. You know, the old classic program was to put a non-ionophore anticoccidial in a starter and follow with an ionophore. I’m not sure why we did that, but expense was probably one reason. The non-ionophores tended to be more expensive, and you used less of them in early feeds. But over the years a lot of people have found that the exact opposite strategy is actually economically more beneficial. You put an ionophore in the starter, oftentimes at a fairly low level, with the idea that it is going to leak. That promotes some immunity, and you do this at a time in the birds’ life when the economic impact of cocci cycling is less. One of the things that makes vaccines economically feasible is compensatory gain — the ability of flocks to bounce back from the short-term production losses associated with the early cycling of the live vaccines.

Then you put your stronger non-ionophore anticoccidial in the feed later to stop coccidial cycling. It’s been shown that late cycling really has the heaviest economic impact. We got excellent performance with this approach, and I would recommend producers consider trying it if they haven’t already.

There’s one thing I need to emphasize, and that’s about putting non-ionophore anticoccidials second in the rotation. With some of them, you have to be very careful. Take nicarbazin, for example. If you’re going to use it, you’d better start the birds on it. If you start using it later, you could have some serious toxicity issues.

I don’t want to sound like a broken record, but program diversification is key. You just don’t want to become enamored with one low-cost product that’s delivering efficacy and ride that train until it comes off the rails. Resistance, particularly with some non-ionophore anticoccidials and less so with ionophores, is long-lived. Once you wear out an anticoccidial tool, it’s really hard to resurrect. It’s therefore critical to diversify and use products that are available for your production system.

It’s certainly made life more difficult. I’ll be very upfront. I had great difficulty trying to use a vaccine without some sort of antibiotic coverage. We could expect a very high incidence of clinical NE when we did that. And I never found a good way to completely control NE. We tried some bioshuttles with non-ionophore anticoccidials, but that proved challenging because, in our case, the mean age of onset for the clinical signs of NE was 16 days. That doesn’t give you much time to get vaccine immunity to birds and then get an anticoccidial on board to try and short-circuit NE.

We ended up relying very heavily on the non-ionophore anticoccidials. In fact, for a long time we used them almost exclusively. We’ve already touched on why that’s difficult — their propensity to develop resistance is sometimes catastrophic — but the strategy we adopted that overall worked fairly well was to rely very heavily on the more durable medications like nicarbazin and zoalene. We would use nicarbazin heavily in the starter grower in winter and zoalene in the summer. Then we would follow up in a shuttle with what I call the more fragile chemicals.

I designed them years in advance. I came up with a proposed program that tried to avoid exposure of the more fragile drugs in the later feeds to once every 2 years or so. When you had enough options on the market, you could do that. We occasionally had supply interruptions, and that would throw a wrench in the system. But if I could lean heavily on these durable medications and then shuttle and religiously rotate the other ones on a regular, preplanned, long-term basis, you could keep it on the tracks. You didn’t always get optimum performance, but when you abandon a big part of your toolbox, that’s one of the consequences.

When the NAE movement in the US got underway around 2016, there was a lot of trepidation around about the impact on NE, which is a bacterial disease that often appears in the presence of coccidiosis. But we were lucky that zoalene had been off the market for many years due to a variety of reasons. It came back onto the market almost at the same time the NAE movement took off. So, we had a non-antibiotic anticoccidial that was pretty resilient and that hadn’t been used extensively in a good while. Zoalene has been a major go-to product for NAE production and maybe produced better outcomes over the past 4 or 5 years than we might have otherwise expected. Similarly, nicarbazin is a good tool for NAE producers, as we said, mainly for wintertime production.

I’ve looked at a lot of them and have given over 300 presentations on antibiotic alternatives, starting before the antibiotic movement. In my opinion we would not have that high percentage of alternative usage if there wasn’t something valuable.

The sapponins and essential oils are the only ones that I have tested that have a measurable amount of anticoccidial activity. However, due to limited efficacy, they should not be used as a standalone for coccidiosis control. They are not FDA-approved products. They are mostly Generally Recognized as Safe (GRASS) products.

Very negative. I have not seen one that gave me a return on investment, and that’s the bottom line.

Probably hope and desperation would be my guess.

Vaccines for NAE-production systems still present a challenge. As Dr. Smith said, without a traditional in-feed antibiotic to control clostridium while the vaccine is cycling or an ionophore as part of a bioshuttle program, they’re difficult to manage.

I think a lot of it comes back down to vaccine administration. If you can get these chicks vaccinated in the hatchery with an immunizing dose of E. maxima, they’ll go ahead and cycle those first 6 or 7 days and get a fair amount of immunity, and you’ve got less E. maxima cycling in that 16- to 24-day period, when most of this NE is occurring.

But that’s not the case. What’s happening is that most vaccinated birds are getting E. maxima doses either from the litter they’re placed on or by horizontal transmission from the few birds that did get vaccinated at the hatchery.

In some cases, the doses are overwhelming and coincide with that day 16, 17 age when NE occurs. That’s why you have to come in with ionophores to shut down that cycling.  If instead you could get these products administered at the hatchery, perhaps there wouldn’t need to be as much ionophore or chemical use in conjunction with the vaccine.

It can be demonstrated that resistance to ionophores in the field has developed to some degree. Most drug resistance, at least with poultry and Eimeria, is due to population selection, not due to a mutation. The more selection pressure there is, the more there is a chance for the predominant strain to be resistant. The stability of this resistance is variable and often not fully understood. Is ionophore resistance stable? I don’t know if current ASTs have demonstrated a change in resistance or in the degree of resistance to ionophores. Maybe Dr. Schaeffer could look at some of the Zoetis ASTs and compare them and maybe come up with field data that show a difference.

We’re in uncharted territory. There are a few producers that have gone back to using ionophores after several years of NAE production. I don’t know that we have a large enough sample size to know whether there’s been any restoration of sensitivity. My assumption is that there probably has been, but it’s also a case of “be careful what you wish for.”

We’ve grown this whole industry up the last 40 years with ionophores being the centerpiece of coccidiosis control. We’ve gone to larger and larger birds and reliance more and more on immunity developed during early growout, due to the leakage of ionophores. With sufficient immunity, producers can oftentimes eliminate anticoccidials from the later feeds, which can generate savings especially with 50- to 60-day production cycles.

As you increase sensitivity and product efficacy, it could shut down cycling more significantly so that immunity doesn’t get developed.  Then we’ve got a whole new set of problems to deal with. So only time will tell, really, on that one.

In my opinion, there are two big issues with the vaccine. One is an apparent decline in viability during storage, especially for E. maxima; it seems to “run out of gas” quickly. Unless the vaccine is very fresh, you can have some concerns about the amount of viable E. maxima there.

The other concern is spray administration. When we started spraying chicks, that method was better than anything we had before but is still inadequate. As Dr. Schaeffer has indicated, we just don’t get enough birds immunized initially in the hatchery, and when these naïve birds encounter the field challenge around 2 weeks of age, problems result.  Work is progressing on administration; the gel techniques are probably better than spray but are still marginal. Split administrations, for example in ovo and gel, or booster administrations on the feed can help, but again do not totally solve the issue and are additionally very expensive. Some novel technologies are on the horizon that may help resolve these issues.

Getting a viable dose into birds on day 1 is the issue, and that’s what we’ve got to focus on.

Coccidia provided by the vaccine cycles. And during each cycle, coccidia oocysts are shed and immunity develops. Generally, coccidia-oocyst shedding and related coccidiosis will peak around 3 weeks of age. To moderate this peak, a feed-additive anticoccidial drug or an alternative product is introduced during the peak period. This is a bioshuttle program. Coccidiosis often influences NE development. With this bioshuttle coccidiosis modulation, there’s a potentially reduced chance of flocks developing NE.

We see a lot of bioshuttles out there, mainly intended to shut down excessive coccidial cycling yet still allow enough time for immunity from the vaccine to develop. Excessive coccidial cycling is what’s often associated with NE.

I often find E. maxima on mucosal scrapings at around 28 to 30 days of age in vaccinated flocks that received an ionophore or chemical anticoccidial around 14 to 17 days of age. It’s mostly those that received an ionophore. They’re probably not vaccine E. maxima because the vaccine E. maxima is supposed to be sensitive to all the anticoccidials as part of the licensing process. You have to conclude those are wild-type E. maxima. They were in the litter to begin with, which means that the vaccine really had little effect prior to starting an anticoccidial at day 14 or 17.

I agree that if you kill off the vaccine too early by using low-level ionophores like zoalene or whichever, you might have an immunity problem. One question is whether or not you continue to keep the bioshuttle anticoccidial continously in the feed.

We ran a vaccine bioshuttle-program study using nonmedicated feed D0-18, salinomycin D18-35 then lasalocid D35-42We had very good results, due to a modulated vaccine-coccidia peak, no subsequent coccidia peaks and with the continuous antibiotic effect with inonphores. But again, if you kill off the vaccine or don’t apply it correctly, you’ve just got to control the wild strains with only your bioshuttle product.

There are many things we could consider. But unfortunately, in today’s environment, a lot of them are not economically feasible.

For instance, greatly reducing bird density would probably have an impact if you were extreme enough with it. But just a couple of percentage-points change in density is not going to have a huge impact. Greatly extending downtime is another way to reduce the prevalence of a lot of pathogens, including coccidia. But again, there’s a limit to what you can realistically do because there are economic limits.

When asked about how to make NAE production work, I advise paying close attention to detail in all production areas. Hatchery management aimed at producing a quality chick is very important. Brooding management is extremely important. Probably the big one is litter management, which goes hand in hand with ventilation. So keep good, dry, friable litter. You’ve got to be on your toes.

I’ll add to that by saying that it’s important to have an institutional emphasis on long-term coccidiosis control instead of a focus on short-term gains. That’s got to be the mindset of your operation. Also diversify your rotation programs, use all the tools available and don’t use them longer than you need to.

Remember that you cannot eradicate coccidia. It’s always going to be there. If you sanitize too much, you’re going to get what is often termed “new house effect.” This can actually increase your coccidia later, and we know having late coccidia is the worst thing you can do.

Market forces to some extent dictate what we can and can’t use for coccidiosis control. We all also know that the end consumer of our products will drive what programs we’re asked to develop: NAE, WHO, conventional. And although coccidiosis control is important, it’s not the be-all and end-all of input or production costs.

There’s always been an argument as to what triggers NE. Is it specific types of Clostridium? Is it a specific type of E. maxima? I’m of the school that it’s primarily a numbers game; very rarely do I see NE where there are not certain types of coccidia, specifically E. maxima. I would think that although the antibiotic effect has an impact on gut microflora, the biggest impact of ionophores on NE is due to their anticoccidial effect, not their antibiotic effect.

We can easily demonstrate a reduction in NE, certainly experimentally, with ionophores.

If we’re talking about sample sizes for posting sessions, we customarily go with five or six birds per farm. I don’t know that going to 10 or 15 birds per farm is going to get you any more accuracy compared to five or six. That seems to provide a good window of what’s going on across the complex, assuming you get a good cross section of flock ages brought into the posting session. Bringing in birds from 10, 15 or 20 farms is more important than necessarily the sample size from each farm.

Many coccidiosis vaccines have drug-sensitive strains. The more often you use them, the more you’ll replace wild strains, and that population should be sensitive to anticoccidials. That’s a good thing, but unfortunately, it’s temporary. As soon as you start going back onto an ionophore or a chemical program, you’re going to start killing off the sensitive coccidial-vaccine strains.

I recall an old paper reporting an increase in sensitivity with five cycles of vaccine, and then there were no more gains.

Five cycles would be about a year’s worth of vaccine, so that would really displace wild strains. Again, it wouldn’t be a permanent switch but it’s good. In studies we’ve run, the next grow-out after vaccination that received another product had a real bump in feed conversion and performance — not always but mostly. That’s always good. And those wild strains are certainly more pathogenic than vaccine strains.

No, I would not.

Over time, we actually are becoming less and less concerned about E. acervulina lesions. Unless they get really atrocious, we don’t see a big impact on performance numbers.

And once you get through an E. acervulina infection, there’s potentially some compensatory gain; the villi actually get stronger, and you do get a little bit of a recovery. I don’t think that grade-1 lesions of E. acervulina are too detrimental.

Most litter treatments are aimed at Clostridium rather than coccidial oocysts. I don’t know of a very widely marketed oocide out there that’s in common use. I think most of these litter treatments are focusing on the Clostridium and trying to minimize that challenge rather than minimize coccidia. Downtime and drier litter desiccate oocysts and make them less effective, but for the most part, most of the proactive measures I’ve seen are focusing on Clostridium.

If it’s too dry and flocking density is low, that will interfere with vaccine cycling. If it’s really, really dry, you’d have to wet the litter; otherwise, the vaccine won’t cycle. But in the US in summer, I don’t think you’re ever going to have low litter moisture or low humidity.

I want to make a point about the oocyst populations in litter. Vaccinated chicks have to have a subclinical or maybe slightly more than subclinical infection to develop immunity from the vaccine. That bird’s intestinal length is comparatively short during the first week of growout. If the vaccine cycles in birds day 0 through 6, the number of oocysts produced and contributed to the litter population is relatively small compared to a bird that first becomes exposed to those oocysts at 15, 16, 17 days of age. Those birds are bigger and have a larger intestinal length; their output is greater and so is their contribution of oocysts into the litter.

I think litter quality goes hand in hand with a lot of what we spoke about today regarding application and the lack thereof in being able to get birds immunized without complications.

A chicken that’s growing slower is not going to consume as much feed nor consume as much anticoccidial. The mg/kg of the drug concentration will drop. Lower drug levels could result in lower control.

With vaccines, most people believe that longer grow-outs pose no problem because you have that much more time for immunity development.

So, overall, slow-growing birds should be fine. Of course, I don’t know how other variables will affect immunity development such as stocking density and breeding times.

It depends on what we’re talking about with microbial load. Certainly, mycotoxins and those kinds of things are detrimental to bird health in general and to the development of immunity. As it relates to other types of microbes, we do see animal byproducts that might sometimes introduce Clostridium into the feed, but it’s hard to establish a pure cause and effect. Microflora in the litter is pretty extensive, and you’re putting birds out there shortly after hatching. I have to think that that is a far greater influence on birds than what might be in the feed.