Doubletree Tape \# 2

3-6-02

**Dr. McCaw (continued)**

\--spread of PRRSV and other bacterial problems that cause disease that
we can't recreate in our experimental models. Our experimental models
are like what we are staying in, each one of us probably has two beds in
our room we've got our own toilet facilities. You know, we don't have to
share anything with anybody and that's the way pigs often times are held
anymore in research facilities. They're not like what we deal with in
the real world of hog production. So we're dealing with large
populations again, potential social interaction factors as with mixed
pigs, move pigs to hospital pens maybe some people are still intent on
having all the pigs the same size in pens so we move them, you force
them to fight. As Brad pointed out, we have poor ventilation control in
these facilities, size is certainly a part of it, lack of investments
another part, trying to be a least cost production. So, we've got some
systems that are very, very marginal in their ability to meet the needs
of the pig and also what we can't, what we don't usually recreate
experimentally is persistent exposure to bacteria and virus because
these pigs are living with these other pigs day in, day out seven days a
week, 30 days a month etcetera. Whereas experimentally usually we give
them the virus on day one and we give them the bacteria on day five and
if they happen to, if the infection takes then they actually get
constant exposure but otherwise it's just a point exposure and then
lastly, most of the experiments we work on are pigs that are not
compromised or stressed on entry. Again, that's probably not the real
world situation.

Okay, enough of PRRSV, enough on, on facilities. What are the challenges
in antibiotic therapy and I was reaching for a bridge to, to this
audience today to, to your conference here but I'll talk about what I
kind of think might be a rule for PRRSV and particularly in the nursery
finisher to be a challenge for antibiotic use and effectiveness quite
frankly. Again, do we see more finishing disease then in the past. I'm
not sure we see more but we certainly see it changed and often times
this may be more dramatic then we used to see, it's less endemic, less
subtle, sometimes it's more it's often times more explosive and it seems
to have almost increased the use of antibiotics and again I yield to
Brad and others, I do not get on the farm and I don't make, as much as I
used to, and I don't make decisions much anymore in my role at NC State
but what I do think is happening and what I do hear from the producers I
work with and I do work a lot with farrowing house and the nursery phase
is complaints that the antibiotics aren't working. That was that the
bacteria changed and yes that's a whole different story in itself that
they certainly do get resistance and get smarter but what we've found is
we have to use antibiotics for a much longer duration to get the desired
effect and if that doesn't work the producers just end up withdrawing
the antibiotic in frustration from certain groups of pigs because it's
not effective in treating the problem. They not getting positive results
ie the pigs becoming more healthy and they decide to so called cut their
losses and stop using antibiotics.

What does PRRSV maybe have to play in that with that so called
antibiotic failure, PRRSV is infecting alveolar macrophages and it's
also pulmonary intra-vascular macrophages and Eileen's probably going to
talk about that pretty extensively so I'm not going to go very far into
that but by that infection it decreases that, that cells ability to
phagocytize and kill bacteria you know, and that's a key part of the
pig's immune system to fight off disease, this ends up with impaired
bacteria clearance mechanisms for that pig. And also, I don't know if we
fully investigated and Carlos, if you would maybe chime in on this, the
role potentially of PMN's as well in, in clearing the bacterial
infections from the pig and what role PRRSV may have in, in that
particular aspect of the immune system but either way the efficacy of
bacteria or antibiotics I should say probably are being reduced by the
pig's inability to effectively clear the bacteria. The antibiotics are
not killing the bacteria at least not all the bacteria inside the pig
itself. It may work great on a petri plate. It may work great in a MIC
environment but those are foreign environments to the bacteria. The
bacteria has evolved oreons to be inside the thing and without the pig's
immune system, antibiotics have a much tougher road to hoe to
successfully clear that pig of the infections probably not any different
from the physicians in our hospitals trying to help AIDS patients with
obviously antibiotics and other antimicrobial. So, the challenge that we
see then is a dramatically changed animal flow in some, in our industry
and the challenges that we're seeing now with antibiotic use,
dramatically changed animal flow patterns that we've now created nearly
naive populations as the result in epidemic disease conditions often
times if that infection is transmitted and if we don't meet the needs of
the pigs along the way. We've seen amino compromised barrow infections
that are becoming very common in the nursery in finishing pigs. Again
PRRSV, Mycoplasma Eileen's show has got immuno compromising capabilities
as well as Dick, in years past. SIV, it's got a role in there and PRCV
or porcine circle virus has got a role as well.

And then the antibiotics a fear then in the end to be less effective
against bacterial diseases such as *M. hyo*., during these infections
that involve immuno suppressive viruses like PRRSV and again Circovirus.
Wish we could achieve nirvana by a way a want, we can't we're here in
the real world and hopefully some of the answers will come out from the
efforts of all of us over the next few years, for the producer and for
the hog. Thank you very much. (applause)

(Dr. Punderson)

Any questions for Dr.? Okay, we're then we're going to break early.

(a lot of noise)

(Dr. Punderson)

Is our taping fellow gone because I'm really getting a lot of feedback
and you say you can't hear it over there? Our next speaker will be Dr.
Eric Bush. He's a veterinary epidemiologist with the Center for
Epidemiology and Animal Health in Fort Collins, Colorado. He's been
there since 1993 and he's going to discuss the NAHMS Mycoplasma data.
Thank you.

# Dr. Eric Bush

Well, I'll provide a little different perspective then Brad and Monty
did and actually in both, in my history my paths have crossed with both
of them so I was at Michigan State for a while for vet school and then I
went down and did a Masters in Epidemiology in North Carolina where
Monty was the venerable swine professor there. Did want you to wait 10
years to get honored Monty. So, I'll definitely provide a different
prospective so mine's more of the epidemiological prospective and just
like you know, Brad and Monty are up there on the farm every day or
every week and they rely heavily on the input of the producer or the
manager I rely heavily on the input that you all provide us as we kind
of analyze the data at the industry level and many of you actually are
my clients whether it's the FDA wanting to know what percent of pigs are
dying from respiratory disease or what's the prevalence of respiratory
pathogens or the, those of you from the pharmaceutical companies that
use are data lot for similar purpose, to understand. What are our
producers doing out there as far as controlling micro plasma, is it
relying on management practices like all in, all out or relying on
antibiotics or natural port board using our data as well. So, my clients
are represented here but I really would like you to provide as I speak
or write it down and jot it down and e-mail it to me later as far as how
to further analyze the status. I'll be presenting a lot of the initial
descriptive epidiological look at micoplasma but we definitely want to
do more with the information later on.

So, one of our key objectives in the Swine 2000 national study that we
conducted was to address the issue of (inaudible) per disease complex.
In our needs assessment phase for the study, when we met with our
clients, those of you in the room as well as interviewing producers
micro plasma was definitely one of the top concerns as well as emergent
diseases of swine influenza virus age three and two. So we wanted to
estimate the prevalence of these primary pathogens on an industry wide
basis and we also wanted to try to get a handle for you know, this is
kind of a, a quasi disease, I mean it's kind of a syndrome or complex so
what's it really mean and how severe is it really? So, we wanted to try
address that concern. Different ways of measuring that severity would be
to look at the mortality due to respiratory illness, the age of on-set
of respiratory illness in the grower- finishers and then we also wanted
to have a better understanding of, well what are our producers doing to
try to control horse and respiratory disease complex and then eventually
relate all these together. So, on just a real quick overview of our
setty design we did three face to face interviews with producers, the
first ones done by the National Agricultural Statistical Service and
that's, those done in about 2500 producers that were randomly selected
across the country, that was done in the summer of 2000 then they turn
over half of those names to our agency, Veterinary Services and we
signed up about 900 of those for two additional interviews by state and
Federal veterinary medical officers and then besides these management
questionnaires and we also collected biological data on either of these
two visits. So, we'll be looking at that biological sampling results
too. If you want more information, sorry, the reference is down here,
part one, this is what it looks like. You should have all received a
copy, if your name isn't on our mailing list just give me a call and
I'll make sure you get on the mailing list and it has several of the
issues that have already come up like all in, all out versus continuous
flow. You know, you can look in here and see that well, 15% of all grow
finisher hogs are on sites that have continuous flow so that's actually
not very many compared to previous studies and it has other information
like that about industry so in the back it has civic design information.

Another key objective is to create a serum bank so, which allows us to
collect biological samples particularly blood, we wanted to create the
serum bank so that we can do an epidiological analysis of particular
diseases whether they're endemic diseases like micro plasma, they are
still of extreme concern to the industry or whether it's to look at
emerging diseases down the future and to understand the natural history
of those diseases as they arise.

As far as a study designed for this part of the, this objective, this
portion now of the study was, was voluntary so we randomly selected
those producers that I mentioned so for those 900 and we have selection
probabilities and then we can play some statistical games with those and
generate weights and apply the management data that we get from those
interviews back to the national population. Now, we offer them various
biological sampling protocols as an incentive for them to participate,
they can pick or choose that however they like. So, we no longer have
randomly selected them and so it's all voluntary so, the implication is
the results from that will not be rated.

We collected a maximum of 30 samples from breeding females on these
farms that had them. We instructed the data collectors to do that via
corda sampling or (inaudible), get a third of the samples from young
parody, a third from mid parody and a third from older parody. So, we
tried to spread them out. And then as far as finishers go, we collected
a maximum of 15 finisher samples from those farms, that had finishers
and we tried to collect those across the different pens, so they weren't
all from one pen and we collected those from late finishers which our
definition is more then 20 weeks of age and then these were all shipped
overnight to NVSL where they were processed and then allocated out into
eight sets of sera and then one of those sets was shipped to different
lab, to Eileen Thacker's lab. Okay.

So, the testing that was done regarding (inaudible) respiratory disease
complex, PRRSV was one set of the cerous stayed there at NVSL and
Sabrina Swenson's lab tested it for PRRSV, using the ELISA test. Another
set of the cerous was shipped to Eileen Thacker, it was probably just
drove over there and they tested between 20 ELIZA, between 20 and those
samples and ELIZA and those samples and we want to thank Faiser for
their contribution to their lab to do that and then we she was done with
them, those were again, probably driven over to VI, Vet Medica where
they tested it for micro plasma using the new idex ELISA test and so we
want to thank Idexx for providing those test kits to VI vet medica as
well as the labor that they provided and then we tested SIV, that was
also tested by, at Sabrina Swenson's lab by the Idexx ELISA test kit
that they provided and then a subset of those samples were shipped to
Chris Alson at the University of Wisconsin and those were tested for,
using the HI test for SIV and we want to thank Schering Plough for
funding that. And then we've, so we've used several sets already but we
still have five sets for future use.

So, let's first look at the blood collection and again this is not
weighted so it's not necessarily going to represent the national
population. So, we had 506 production sites that said sure, let's, we
would like to participate in the blood collection phase of the, of the
NAHMS study so 200 of those sites had only finishers, 111 of them had
only breeding females and no finishers and then 195 had both. So, we
collected a total of 8,466 samples from sows and guilds on these 603
sites that had them and a total of 5,862 finisher samples on the 395
sites ahead at least some finishers.

So, and here's the results. Site prevalence or herd prevalence for those
with finishers, 82% of them had at least one positive sample. For
breeding, about like 95% of them had at least one breeding female that
was positive. Regarding the animal prevalence, finishers about half of
the finisher samples are positive, just under half and a little under a
third of the breeding female were positive. You can kind of put those
together and guess what the, within herd prevalence would be might be a
good epidemiological pop quiz here. So, given that this is the
finisher's little lower site prevalence but higher animals prevalence so
what would we expect within herd prevalence to look like? Any takers?

Okay, we'll look at those graphs later but you can, you would expect
with fewer sites and many finishers you are going to have a lot of sites
that have positive animals or sites that don't have any positive animals
whereas with the sows, that within herd distribution would probably look
more something like you have a lot of sites that are positive but not as
many animals are positive that means you are going to have a lot of
sites with very few animals that are positive so it gives us an idea of
what within herd preference would look like. So, that's epidemiology and
Mycoplasma. Any questions? Well, I have some. First let's look at the
herd prevalence, just some basic questions this is just going to be
fairly descriptive again, you'll help me out tremendously if you can
write some ideas down or yell them out and I'll write them down as far
as how would we want to look at this down in the future beyond just
these basic descriptions. So, let's look at herd prevalence by region
and then we'll look at my type of animal, how herd prevalence varies by
type of animal, type of site, the size of the site, vaccine status of
course, some of these were vaccinated and some of them weren't. And then
by I don't want to say season necessarily but as I said blood was
collected on one or two visits and so you know, does it vary between
those two visits?

So, first by region, this is again herd prevalence or site prevalence
and I have it broken out for finishers and sows and gilts and this is
our definition of the regions so basically it's kind of longitudinal. We
have the northern region and then we have the southern region and then
we split the central region in half, it's kind of the mid east or the
east, the west central and the east central. So, starting here and
working around, 74% of the finishers are positive in the east, west
central states compared to you know, 81% in the northern states. 86% in
the east central and 89%. It still kind of increases as you, as you kind
of go around clockwise. It's you know, roughly you go that, I guess when
you compare the, this region with this region it's fairly, it's
significantly different. As far as sows and gilts if you remember the
herd prevalence there was pretty high so I mean almost everybody had it
so we're not going to see too much change, you see a little bit, 90% of
the herds with breeding females in the northern tier and the west
central were positive whereas it's closer to a hundred percent both in
these states and the southern states.

What about, how did site prevalence vary by type? So, for those that had
just finishers, just your finisher floor, about 77% of those are
positive, 77% of those sites had at least one positive finisher compared
to those with just breeding animals, 97% of those were positive. Of
course, if they had both they can't go below the 97.3 so, it's basically
the same. And then came the average for herd prevalence for all sites
regardless the types of sample that was collected was about 89%.

So, how does the herd prevalence vary by inventory, size really doesn't
too much so we have on the top sites with finishers broken out by total
inventory so less then 2000 total head. 2000 to 9000, well just under
10,000 and then 10,000 and above. So, the way these as far as the herd
prevalence goes really doesn't vary. Herd problems for breeding females
that's same total, same size break outs by total inventory and it
doesn't vary a whole lot maybe the medium size farms have a slightly
higher herd prevalence.

Q (inaudible) numbers are those of all the pigs on those sites or is it
finisher pigs?

Dr. Eric Bush: Yeah, that's, this is total inventory, so it's whatever
animals are on the farm so if it's a one site then it's going to be you
know, the sows and the, I mean the pigs and the, so it's not necessarily
the pigs at risk. So, I did the analysis by pigs at risk and it really
didn't make much difference you kind of saw the same so I just left it
the way we tend to publish it which is by total inventory.

Dr. Monte McCaw: (inaudible) our work, were very daunting to farrowing,
nursery, finisher(inaudible) it is a single site, all we use on one site
versus (inaudible)?

Dr. Eric Bush: At the least for herd prevalence and didn't make any
difference and stuff because I did look that but I just left it this
way. But yeah, that's a great question Monty, thanks. And then the
vaccination status, like I said some of them are vaccinated and some of
them aren't for mycoplasma and so how's the herd prevalence vary for
that so 88% of those sites that were vaccinating the finishers were, had
at least one positive animal compared to 77% of those that don't
vaccinate. So, that's a fairly good difference. You don't see quite as
much difference with the breeding females. About 98% of those sites with
breeding females that do vaccinate them were positive compared to 93%.

Q What do mean by vaccinate (inaudible)?

Dr. Eric Bush: Yes, this is a, when we collected this information for
sampling we had some animal level questions or sample level questions
and so one of them was, if these animals were vac, if the finisher was
vaccinated. So, we asked that for each animal. So, if they had said yeah
at least one of the samples that we collect from, finisher samples that
we collect was from the vaccinated animal then we just labeled the
finishing four as vaccinated.

Q I don't think it means that they were vaccinated as finishers.
(Inaudible)

Dr. Eric Bush: Yeah, yeah, yeah, sorry I misunderstood the question.
Yeah, when we collected the data, the sample, the blood sample though we
wanted to know if that finisher had been vaccinated before, yeah. I'll
get, later as far was when are they vaccinating but yes, sorry I
misunderstood the question.

And then, I don't know, this is probably a bad surrogate for season but
it's all really presented by visit but that first visit if you remember,
we collected the blood between August and November so kind of fall,
fallish whereas the second visit we collected the blood from basically
December through March so more of a winter. So, how does that vary? It's
kind of that you see an opposite pattern with the finishers versus sow.
So there it's, it was higher 88% versus 80% going from the first to
second visit whereas in sows the herd prevalence went the other
direction. It went up instead of down between visits. So, it's about
set, and that's a fairly significant difference, a big difference. So,
76% of the sites that we collected blood from in the first visit for
breeding females was for positive (inaudible) positive compared to 95%
of them and I had now idea why it would be. Part of this is just, like I
said going to raise additional questions so, if you have any ideas let
me know and we can look at that. So, that's herd prevalence and just
looking at the basic findings there, the next kind of question is to
look within herd prevalence so-

Q (inaudible)

Dr. Eric Bush: No they were, because we were trying to get the results
back to the producers so as the, well, actually Eileen can answer that
better.

Dr. Eileen Thacker: It was really only about a six month, I mean they
came in but they were always in groups of oh, a hundred to two hundred
or more that you did and it was pretty uniformly (inaudible). It was
less then a year.

Dr. Eric Bush

No, definitely.

Dr. Eileen Thacker:

It was like six to eight months maybe.

Dr. Eric Bush

Yeah, I think we started probably late September at least for us getting
the first results and we were probably done by March, so.

Dr. Eileen Thacker:

We did them pretty steadily then you know, because of the number of
samples.

Q (inaudible)

Dr. Eileen Thacker:

No, I think they just came in kind of randomly.

Dr. Eric Bush:

Yeah whenever they were collected. There was like a, we had like a six
week or four week window between the first and second visit. So-

Q Have you just added the easy Idexx test for the (inaudible)?

Dr. Eric Bush: Sorry, thanks John, I should have said that up front. I
had it in one of the initial slides and then I quit putting it in there
but yeah, all these results are from twin 20, Idex test I mean the---

(several people talking at the same time.)

Dr. Punderson:

Could you repeat the question so everyone can hear?

Dr. Eric Bush

Yeah, John's question was which test was are we presenting here. So,
because we did both the twin 20 as well as the Idexx ELISA so all of
these results are from twin 20 tests. The Idexx ELISA results were still
being merged and those will actually be compared in a graduate project
that Fred and Eileen are doing, with the grad students. So, I won't
present any of that today.

Dr. Eileen Thacker:

The Idexx kits didn't come in as fast and like Eric said he wanted the
results up today. So, we, since we were (inaudible) I was up and running
then they, they were based on (inaudible) after we got them. I believe
they done then.

Dr. Eric Bush:

Yeah, oh yeah, they were all done and we had the results and yeah we
just need to finish cleaning them up a little bit before merge and
(inaudible) these. So that's the site prevalence so now we have the,
within herd prevalence so we'll look at that separately for finishers
and breeding females. This is the distribution of the number of positive
finishers so, and we basically have, like I said for finishers we had a
maximum of 15 positives and so this is just saying how many farms had
zero positives, one to three positives, four to six, seven to nine, ten
to 12 or 13 to 15 positives so you see kind of this bi-model pattern
were the finisher fours are either basically negative or maybe a few
positives or they're very positive. So we could have deduced that kind
of from looking at the animal prevalence. At least that you'd have a lot
like this. So the, within herd prevalence or distribution of positives
within herd of breeding females is just the opposite really, it's not
really normal, it's skewed to the left a lot so basically you have a lot
of herds that have a low number of positives so again with the breeding
females 30 was the maximum number of samples we would have collected so
this is just broken down again between zero and the one to, you know
going up by threes basically looking at the distribution so the, I had
the mean written down, I think its, oh good, yeah 37.4. (laughter) So,
and then we want to look at animal prevalence, some of the same basic
questions there. Again, you'll help me out a lot if you'll jot down some
ideas, most of this is probably just going to raise more questions
really. So, let's look at animal prevalence by each of those. First we
have percent of animals positive now, by region so again, for finishers
and sows and guilt so same regions of course. 43% of the finishers were
positive in the west central compared to 50% in east central, 48% in the
northern states and 57% in the southern states.

So, you've got some variation there. Again, the biggest differences are
between the west central and the southern. And then as far as the animal
prevalence for finishers is, animal prevalence for sows and gilts that
varies from 36, 37, 38, 41 and again, the biggest difference is between
those in the west central and the southern states.

Q Does it make sense to divide as you've done by states whereas in fact
(inaudible)? For example in Oklahoma and Texas panhandle there's a lot
of farms there, they are all pretty much farms and, and so (inaudible) I
don't really understand why categories differ (inaudible)?

Dr. Eric Bush: I might say high density would be another way of doing
it. So, (inaudible) try to remember. How we determine our herd size
break outs we do before we really look at any results, any particular
results and so then we just set them and keep them for the whole study
so, what we do is once we get out initial data set in and how many
respondents we have we kind of divide them up so that we have equivalent
number of respondents in each of these regions. It's not going to be
exact but we don't want to divide up the regions so that you end up,
some regions that might make more sense but then you'd only have 20
producers in that one region and so we wanted to try and get, if we're
going to do regional estimates then we want roughly equal balance and I
don't know this is kind of how we've done it in the past and stuff. I
have some, I have defined some other regional definitions but I haven't
used them in analysis yet so as far as like hog density, that would be
another one to look, like you said, to look at. We actually sample that
way, based on hog density and so. I think in the future we'll look at
that.

Q (inaudible)

Dr. Eric Bush: No, I haven't done that and I wrote that down.

Q \--compounded so much you really couldn't tell.

Dr. Eric Bush: Yeah, oh yeah you mean as far as the use of all in and
all out by how that varies by region? Yeah that shouldn't, all in and
all out versus continuous vary too much by region now maybe the type of
all in, all out does maybe and I'm just throwing this out as an idea but
they maybe in some regions, they do all in, all out by sight versus
other regions, they do all in all out by room and so that may, that
might change.

So, this is animal prevalence by size so it doesn't vary too much, maybe
goes down a little bit as far as the finisher animal prevalence goes
down a little. You see a trend that goes down in size, it doesn't vary a
whole lot though, I mean going from 50 to 45. As far as breeding
females, you see the opposite trend that it tends to go up. So it goes
up from 36 to 38 to 47%. So, and this kind of makes sense so like one
question that pops into my mind at least is well, how does the parody
distribution vary on the smaller farms versus larger farms. Do larger
farms have a lower parody distribution because they have a higher turn
over and stuff like that and as we'll look at in a minute, we want to
look at how the animal prevalence varies by parity and stuff and so
we'll see that. Oh yeah, okay so there's more of the younger animals do
tend to be positive and so that shouldn't be too surprising given that.
Okay.

This is finisher prevalence broken out by gender just gilts, 46% of the
gilts are positive. 51% of the ferals are positive. So, of course the
average is in between. So, this is parodies, it's kind of a little
different way of presenting but I mean it's just taken straight out of
(inaudible) I just cut and paste the graph but so, this is the results
over here. I can't read that but we have negative, suspect and positive
and then down here we have parody. So, with the negative animals you
kind of see, it's almost normal distribution of parity skewed a little
bit to the left which we, it has a big long tail. Whereas with the
positive animals this is a parody issued region for that. So, that's no
where near normal and it's like I already alluded to, it's very skewed
to the left so you have a basically a lot of the younger parody animals
are, are positive.

This is the animal prevalence by vaccination status. So, you know 56% of
the finishers that were vaccinated now this is again, you get back to
the herd counted before sometimes they had been vaccinated because
they're an animal. It doesn't mean they were vaccinated while they were
an actual finisher or in the finishing stage but 56% of those were
positive compared to 43 of the non vaccinates. For sows and gilts 50% of
the vaccinates were positive as compared to less then a third. So that's
basically the initial results of the serological testing that was done
using the tween 20 ELISA tests so obviously a lot of the fun stuff will
come later too, to start looking at that to you know, build some models
off that and look at other factors like all in and all out and what not.
So, I want to present some of the information we had gathered from the
questionnaires. Now, this will be national estimates, not just based on
those that we got blood samples from.

First we asked the producer in that interview what diseases had been
diagnosed on that farm or were present on that farm in the previous 12
months. Then we asked that by production phase and so this is for the
nursery phase. Actually we asked that by age of pig and weight because
we wanted to take into account those that had a true nursery site versus
a weaned to finished site. So we asked for nursery aged pigs. So, this
is for nursery aged pigs by herd size, it's kind of a busy slide but we
can start with APP, the green is the small sites again based on total
inventory and then the medium sites and the large sites. So, generally
speaking the larger the sites the more apt they were to report a disease
present in that site in the previous 12 months. You can see right off in
the nursery strepsueus is the top disease regardless of site of
production. So, for the smaller, you know smaller sites you can see it's
you know, the highest bar, same for the medium, it's definitely the
highest bar and same for large. So, regardless of herd size *Strep.
suis* is the top most prevalent disease in the nursery pigs. After that
it kind of varies for the medium and large sites, mycoplasma was right
up there, it was number three followed by PRRSV, it kind of depended
actually. So, PRRSV and *Mycoplasma* are right up there the second and
third most common diseases. Very un-common is APP, if fact that's the
least common disease diagnosed in the nursery or present in nursery aged
pigs. And then the other one to point out is the SIV old and new
traditional H1, N1 versus the new H3 and 2 so traditional or the new one
not being nearly as common maybe half as common as the traditional.

Q (inaudible)

These are just reported by the producer. So, yeah that's definitely a
limitation. Now, we did ask a follow up question because that's of
course what you are always wondering well, you know, how soft or hard
are these and so we asked and also to be more comparable the way we've
asked it in previous studies but we asked a follow up question, okay was
the diagnosis made by a vet or lab and so we have those estimates too to
kind of give us an idea of how soft or how hard some of these are. So
yeah, because it's in, kind of interesting actually with PMWS, I mean
that's pretty soft estimate because hardly any of them said yeah, vet or
lab reported that and so I think it's a lot of producers just kind of
looking at it and reading, oh yes the disease of the day and so we have
it. So, some of the other ones you know, like this where you had a much
higher percentage and that were actually diagnosed by a vet or lab.
Okay.

So, this is the same for grower-finisher, I mean the same question but
now just for grower-finisher aged pigs and so you see generally speaking
more respiratory disease then we just did in the nursery and but now you
also see ileitis as the, really the top one. it's kind of neck and neck
with *Mycoplasma* for all herd size groups. It's got a little edge in
the smaller one. It's equal with the medium size and it's got the edge
with the large ones too. But still a lot of *Mycoplasma* on those number
two disease and then you see now a little more equivalence between the
prevalence of SIV old traditional and the new SIV but the old SIV still
has a little edge and then not quite as much PMWS as you'd except again,
APP is down there in prevalence as far, as far as a respiratory disease.

So, vaccinations and now we want to move into the control, this will
take care of all the prevalence stuff so what's being done to control
*Mycoplasma* on the farm. So, this is looking at vaccination of the
breeding females first so we broke it out by kill, deltagenist and don't
know and sometimes we were interviewing somebody and say we'll I know he
vaccinated but I'm not sure which product we're using. And so by size
basically only 15% of smaller sites, now this is breeding female
inventory now that we switched to but only 15% of the small sites are
vaccinating for *Mycoplasma* compared to a little under 40%. Again, this
is percent in sites, not percents in animals. And you see, I don't know
a fair amount of autogenous use I don't know what a fair amount is but
it's, this shows up at least and but it seems to be just a primarily the
medium size operations that are using the atagenous vaccine. Okay.

So, and then we asked about the timing of the vaccinations so and we've,
actually there were like six different categories but I've lumped them
into three. So, they could be prior to entry and again this is not
vaccinating in the breeding herd but of those that are in the breeding
herd, when were they vaccinated? So, that could be prior to entry, or at
entry when they're in the isolation unit or in the herd and in the herd
we asked, we broke it out into four or five different categories and but
I've collapsed that all here, the in herd. So, you see that for well,
for a large, for actually this is getting three vaccinations before that
first litter basically so about a fourth of the sites were doing that.
The most common time other wise was to just give one vaccination and
that was prior to entry. This is basically three vaccinations before
that first litter. These next three they are getting two either prior to
entry or at entry or prior to entry and in the herd or at entry and in
the herd and in these last three are they are only getting one
vaccination. So, and in the next slide kind of summarize that and it's a
little easier to look at.

We reduced some of the information but basically this is if they are
getting one, two or three vaccinations of *Mycoplasma* in the breeding
females so as herd size goes up they're more apt to use two or more
vaccinations in the breeding females.

This is for vaccination of the finishers now. So, in this can answer
your questions earlier as far as when are they vaccinating at, they're
not vaccinating really when they're out of the nursery, our cut off for
the nursery aged pig versus grower-finished aged pig was 70 pounds so
they're vaccinating them when they're less then 70 pounds or in the
nursery. So this is the rates again you see the smaller producers based
on total inventory are less apt to vaccinate. Closer to 55, 60% of the
medium and large size operations were vaccinating the finishers or
vaccinating weaned market pigs.

So, this is just asking well, how many vaccinations were they receiving?
So, again like we just saw the, as far as none, the smaller ones were
more apt not to be vaccinating, only a third of them were. Most, the
medium and large size farms that were vaccinating were using one, one
dose compared to two. Again, it's percent sites not percent animals. So,
and then the get more at the timing for vaccination of the weaned market
pigs, when we asked about the age the timing actually varied whether
they did the one dose versus the two doses so if they were just doing
one dose, the average age if they were vaccinated at was about seven,
seven and a half weeks of age. So, it varied a little bit by herd size.

Okay, if they were doing two doses then the average age of that first
dose was more around three and a half, four weeks of age and then the
second dose was and this is what really varied by herd size was when
that second dose was given, if they were vaccinating with two doses. So,
there's three weeks later if they were a small farm. It was four weeks
later if they were a medium sized farm. It was six weeks later if they
were a large farm. So how else are they, producers trying to control
*Mycoplasma* besides vaccinations?

So, that was another question we asked again, sorry it's kind of busy
because we like to break it out by herd size but let's start from the
bottom. Any, any strategy so, I mean upwards of 90% of the producers are
saying I'm doing something specifically to control micoplasma because we
didn't ask them if they were just doing all in, all out or early
weaning. We asked them what are you doing to specifically control
*Mycoplasma*? So a big issue for producers, which I'm sure you all know.

So, what are they doing? Now, we can go back to the top. This is early
weaning without antibiotics we defined early weaning as 16 days in this
case. This is medicated early weaning so it's early weaning less then 16
days with antibiotics. This is weaning otherwise, after 16 days with
antibiotics. This is an all out, all in, using an all in, all out in the
farrowing room. So, that's very strongly associated with herd size there
and the very common strategy being employed. All in, all out nursery it
kind of goes hand in hand with that again strongly associated with herd
size and very commonly employed up to two thirds of the large sites said
they were doing that specifically to control micoplasma. What about,
then we, the other strategy being employed is this treating for
respiratory disease. So, we have two strategies there basically that we
broke down. Are you just treating the pigs with respiratory disease or
are you treating the pigs with respiratory disease plus all those in the
same air space. So, that's what this one is treating ill pigs, that's
the most common strategy being employed is to treat for respiratory
disease. Around 70% of the medium and large sites. You get about a third
of them that say yeah, we also treat the whole air space so then that
may help us, give us some measure of severity on these farms --

**(End of Side A, Tape 2 of Day 1)**

**Dr. Eric Bush**: The state and federal veterinary medical officers
that were out there on the farm collecting the data, National Veterinary
Services laboratory, we can skip the rest because I did food safety. The
National Pork Board and swine practitioners that gave input and then I
had already mentioned Pfizer and Vet Medica and Idexx and
Schering-Plough (inaudible) all contributed to the testing of these
primary pathogens for PRDC and the rest are for food safety. There\'s no
more I think on there. So, if you have any questions or again, if you
jotted down some noted for us to look at then please send those to me.
We\'ll have a second report coming out probably in two, two weeks that
will have a lot of this information in it, not the serology but all the
other information will be in that report that comes out in two weeks.
So, I\'m going to be available on a website, instead of giving you a
long government website just search for knobs and swine and you\'ll find
it.

(Dr. Punderson)

Thank you Dr. Bush. (applause) Our next speaker is Dr. Kent Schwartz
that comes to us from the Iowa State Veterinary Diagnostic lab where
he\'s been for the last 15 years, prior to that he was a practitioner in
the Midwest and even now lives on a pig farm. Dr. Schwartz will discuss
gross pathology and histopathology used in the diagnosis of mycoplasma
pneumonia.

(conversation)

**Dr. Kent Schwartz**

I forgot what I was going to say. Okay, well anyway, no jokes. I thank
you for the opportunity to be here. It\'s been pretty enlightening and I
tell you when to hit the slide right? When I sit in the diagnostic lab I
get to see most, or quite a bit of dirty laundry. I don\'t get to see
very many healthy pigs and as I would walk out my door every morning to
go and look at my pigs I find out that I\'m not very good manager
either. I can pretty well identify things that we do wrong, at least
that I, I do wrong. So, anyway I\'d like to probably spend most of the
time here augmenting what\'s been previously stated and maybe just
highlighting a few things from the perspective of a diagnostician. Okay.

I too, kind of like history. I\'m not very good at it, Brad, but you
know, history to me is, is kind of important to determine whether we\'re
really dealing with something new or if we just have new people looking
at an old problem differently. Recently, I had a chance to go to China
and you talk about people think in side or out side the box or their
view point, perception or their experience. It was in some of these
smaller farms in Hunan province pigs cough and pigs scratch and that\'s
normal okay, my guess is that\'s about how it was in 1900, we ignored
the fact that they scratched, they have mange. We pretty much ignored
the cough unless it got out of hand and then we\'d have to look for is
it ascarids, along comes swine influenza in 1918 and that created great
consternation among veterinarians because they had three things to
choose from now. But at any rate, you know the early years of pathology
where relatively easy and even when I started in the diagnostic lab or
graduated from vet school, you only had a few choices and I felt fairly
confident on gross diagnosis, clinical diagnosis. Now, I\'ve in the last
15 years had to expand my dartboard you know, so it covers a whole wall
in terms of trying to establish a diagnosis, what to look for, you know,
what\'s the target I\'m trying to hit with a specific test. So, I think
we ought to keep that in mind that our knowledge is evolving but I think
a lot of what we\'re looking at today probably wasn\'t there in the old
days. Next slide.

Pigs scratch, pigs raised out doors, a great way to raise pigs enteric
disease was much more of a problem, mange a problem, mycoplasmal
pneumonia was Enzootic and truly probably not a huge problem. Next.

A finer rendition of these slides in a zip disk in my briefcase so in my
procrastination here you\'re looking at the first go through on putting
some slides together but anyway what happened then through the you know
60\'s, 70\'s, 80\'s, even since the great depression. A lot of changes
in nutrition, a lot of machination, farms got large. After World War II
we have a lot more science we can apply, define agents, mycoplasma was
isolated well, characterized, Pseudorabies emerged as a problem,
bacterial embasilis pearl pneumonia but we had antibiotics, no problem.
And if we could grow it, we could make a vaccine so that helped us even
more. Next.

And we\'ve come a long ways in controlling enteric disease I think and
parasites with out modern facilities. We still, you know obviously the
pervading thought here this morning is respiratory disease is still a
challenge and we can blame environment, I\'m not sure that environment
is certainly the whole answer because we\'ve made a lot of other
changes. Next.

I\'d like to look at it as an area of altered ecology of host agent. You
know, we\'ve changed the genotype. We\'ve got segregated rearing. All
these wonderful opportunities to have larger herds, produce pork more
efficiently albeit the net profit per animal has stayed the same since
1950 but be that as it may you know, large populations do allow us to
produce protein pretty efficiently. *Mycoplasma*, flu, APP remain and
you know in the last ten years we\'ve certainly seen a lot more of the,
of these early colonizers Carlos, you know I think those bugs are not
necessarily new but certainly we changed the ecology of how they
interact with, with the host, i.e. pig. Probably you're impressed by now
that equally as huge is the emergence of new pathogens, porcine
respiratory corona virus is probably now an issue but I always wonder
when you add things together if it wouldn\'t make things, make disease
worse and there is good evidence that PRRSV will do that, Circovirus
doesn\'t make things better I\'ll guarantee you that in the right
situation, marcera types or sub types of swine influenza are available,
so now we have this condition, you know, we call it porcine respiratory
disease complex. The old *Mycoplasma* from years gone by added to that,
a few bacteria that capitalize on *Mycoplasma's* ability to create the
environment for multiplication and then throw a few viruses in, we're
talking PRDC, terms get confusing but PRDC is really the culmination of
what, what this respiratory challenge is and that's what we see a lot
of. Next.

I like to think of it in terms of immune confusion because any
immunology is confusing for me, Eileen. It really, unless you can
simplify.

Dr. Eileen Thacker:

It is (inaudible).

Dr. Kent Schwartz: Yeah, yeah, if you can simplify on the other side of
that complexity that would help me but you know, a respiratory tract
would like to be sterile. It would like to not have bugs in it. But now
it's kind of a mixing vessel for those systemic infections like PRRSV,
Circovirus, some of the systemic bacteria, for those respiratory
pathogens we keep shooting at it and certainly *Mycoplasma* that's been
their all the time. I think herd immunity is, is variable. The stability
of a sow herd in terms of infection, immunity, maternal immunity that
(inaudible) parts as well as piglet infection status, I think Monty was
getting to that very, very nicely. All pigs aren't the same. We put
names like premium, standard farms out there, standard being, we think
as an accountant we can produce uniform product each and every time.
With age segregation every week's worth of pigs is, is the same and from
where I sit they're not. That population is extremely variable and it's
infectious, infection and immune status you know, and, and as I look at
pigs placed in my barn you know, I look *Mycoplasma* for example, going
through, this is another slant on epidemiology by the way. Epidemiology
to me is kind of looking at a defined population that I can get my hands
around and you know, when *Mycoplasma* goes through my barn it, it kind
of, or flu or whatever disease, it's kind of like the wave that you'd
see at a football game or in a stadium, the wave, starts and grows and
maybe continues to grow or diminished and maybe it comes, you want to
try that Carlos, just to see how that works? Start the wave, start the
wave. Start the wave, start the wave. Go ahead, Go ahead. Gosh it got
pretty bad back here, okay. You know a couple of you never even got
infected or coughed or were immune or whatever. Some of you got it
pretty bad. Now, I'm thinking clinically, that's what I see. I'm
thinking pathologically that's what I see, is not everybody's affected
equally. Some have lots of lesions, some have very few lesions. Some are
escorted out of the stadium for whatever reason because of you know,
concurrent more severe infections so, go ahead.

*Mycoplasma* central and primary in my mind and you know, not because
this is a *Mycoplasma* conference. You know, I really have a lot of
respect for bugs that can stay a long time. Swine influenza in and out,
a weeks time, two weeks time basically gone. PRRSV, 30 days, 60 days,
you can get in bar fights over long that persists, right? It's the same
way with micoplasma, that persists a long time and creates a huge window
of opportunity for something bad to happen and that's why I really think
micoplasma is central to respiratory disease to PRDC. It's common we
know that, it persists. I mean in the long those sillied just don't
function, don't clear debris nearly as well, causes immune confusion in
another sense which Eileen is going to expand on but pretty ineffective
immune response sometimes, pretty, pretty privileged site out there on
the cilia, not able to get antibiotics to it very well, you know not
able to get inflammatory cells to it very well, so it's able to hang out
for a long time. Not a good thing. And it does create that synergy or at
least allows opportunists to become apparent. Go ahead.

*Mycoplasma* by itself I think is kind of hard to assess as a disease
because it really doesn't make pigs all that sick, no fevers, I mean
I've been involved in a few cases where we, we need to establish a fever
of 104, 105, 106 or something and then we can call it *Mycoplasma*,
that's really not going to happen. Pigs might be, lose their bloom and
if you're a clinician you knows, know what that means. A lot of people
don't see bloom but they, you know when you walk in a building and pigs
are boofy, you know they feels good and when they're hip boofy they
don't do a lot of coughing they just feel good. Micoplasma takes that
edge off of them, in my view. Clinical assessment is very subjective, no
fever, cough, to me it's kind of a smokers cough. You know you stir them
up, they aren't really sick but they do cough for a while, go to the
feeder, that's if you're out there at five in the morning. If you're out
there at noon, not much happens when you stir them up. Okay, a very
subjective type of index or yeah subjective type of way to evaluate
severity. Moderate morbidity, it really varies you know, in some rooms
like this you get a hundred percent of people in the wave, right? Other
rooms, kind of like Carlos, reluctant to get sick. So, okay next.

Enzootic Pneumonia I think most defined is having some bacteria with it,
we've pretty well been through that but there we start to get some
fever, you know those pigs that do have a fever and are coughing may
have some mild expiratory dismea or thumping. The outcome of that may be
they recover or maybe stunt it or may die. We do know I think that
strategic intervention with medication will treat those pigs and, and
the number of those pigs generated in a *Mycoplasma* outbreak will be
decreased by some prophylactic intervention. Next.

Where we get in major problems it seems, is when we have some viruses.
Some of those confusing, immune confusion type viruses with it. Most
cases I don't care what you do to them you're not going to make them
die. In those cases you know, we can approach 20% mortality, rapid loss
of condition, a lot of thumping, a lot of high fever, severe depression.
We've had outbreaks of PRDC where the producer would suck out all the
feed in the feeder because he thought they were all intoxicated with
some bad toxin. Okay, very abrupt on-set, it can be anyway, it doesn't
have to be certainly but the point is it can be pretty dramatic, pretty
severe and pretty refractory to intervention. Okay.

So, what I'm, let's see I'm supposed to talk a little bit about
pathology. By way of review, to be bronchopneumonia we use that term
frequently, generally seen as grossly anyway as cranioventral
bronchogenic type pneumonia, gravity and the way lungs function allow
petri dates to settle and so most of those things that effect airways
first will tend to be cranial ventral, become firm maybe have some
exudating airways as opposed to another general term, (inaudible)
pneumonia, diffusely modeled more lung involvement, not hard, firm
edema, foamy type stuff in the airways but usually not a lot of pus or
mucus. Both can occur simultaneously and in chronic cases both are
likely to be present if you've got mixed infection. So, gross pathology
to me is a good way like Brad said to get an idea of how bad is this
pneumonia, histopath probably isn't a way to define the extent, the
severity. Gross pathology, digital imaging of lesions, that type of
thing, great way to assess how, how bad that pig is effected. Okay,
next.

Something that I think probably came from one of Eileen's slide sets
because I have never seen, no I won't, rarely do you see normal lungs in
pigs in a diagnostic lab but you know, you've got the caudal lobes and
the middle lobes and the cranial lobes and you know they're all normal,
pink, collapse nicely when you open the lung, next.

Contrast this to something we're not talking about and that's
*Actinobacillus pleuropneumoniae* but you really get nasty pneumonia
there and that's why Brad can make his decision today on whether he's
going to treat this group of pigs or not. I'm not talking about that
type of lesion here. With APP, you do get dramatic disease, pathology is
useful, temperatures are useful, mortality is useful. That's not what
we're talking about today. Next.

You can have pure bacterial bronchogenic pneumonia, *Bordetella* being a
really go example of that, hard, firm, red angry lung with a pure
bacterial infection. And that would be you know, kind of a classic
example of a broncogenic pneumonia where you didn't have a lot of other
co-factors including *Mycoplasma* involved appearing in younger pigs. Go
ahead.

Interstitial pneumonia on the other hand, you know, tends, the lung
tends not to collapse, multiple lobials are involved and because of
gravity and physiology and blood flow it tends to be a little worse
looking in the cranial ventral parts but again not hard from firm
consolidation. We try to make that, in an acute case anyway, you try to
make that distinction, bronchial pneumonia, interstitial pneumonia.
Next.

*Mycoplasma* tends to be a cranial ventral distribution, tends to effect
individual lobules and, and will gradually expand primarily by occlusion
of airways and causing atalectasis of everything downstream from that.
Can be fairly subtle, fairly mild, in some cases can be you know, 20 to
30% of the lung. Next.

Again, just trying to illustrate just some lobules that are becoming a
little atalectasis, early in the course of disease they tend to be just
a little bit juicier and red. As time goes on it becomes great and the
surface of the lung tends to, to be depressed from the adjacent, normal
lung. Next.

Less I give you the impression, well, the swine influenza can certainly
cause a lobular distribution with cranial ventral firmness as well of
bronchial pneumonia. Next.

I guess what I'm trying to get to here is, is gross lesions are not the
pathognomic, it's very rarely. APP, that could be asues so even now it's
not, right? But when it comes to some of these early, early changes of
bronchial pneumonia I really honestly cannot tell the difference between
flu micoplama purged with bacteria whatever, you know, I could when I
graduated from vet school and you know, but I had a, less choices and b,
I didn't have to prove it with laboratory backup. Next.

This doesn't show up quite as brightly but the typical presentation out
of Enzootic Pneumonia is a, is a gray, firm atalectasis cranial
ventrally, clearly demarcated from lung dorsal coddly that is more
normal or is normal, that clear demarcation is fairly typical but the
extent of the lesion can vary from just a few lobules in one corner to a
couple of corners of the lung to a general migration of the entire lung.
Most of the time it was going to have *Pasteurella* or some secondary
bacteria with it, that's also expanding that lesion. Okay.

Then again, just another example, see Dr. Ross is nodding off here
because they all look alike don't they, you just can't tell by looking
and I guess I've made my point then right? The more severe they are, the
more likely they are to have some viral involvement, even more typical
of PRDC. Next.

Same kind of a deal. This one's clearly demarcated, typically Enzootic
Pneumonia but it's probably made worse by the presence of PRRSV. Next.

Over time and I don't know how much time lesions can resolve and they
can resolve completely with *Mycoplasma* I think probably has a lot to
do with how bad they were to start with, what was the extent of the
lesions to start with, the extent of the secondary infections and when
you look at them, I mean you so slaughter checks in some herds and you
don't sight see evidence of *Mycoplasma* but we don't know if that's
because mycoplasmal pneumonia wasn't an issue in that herd or if it
occurred late nursery, early in the finisher, most of them healed up.
The opposite is also true, if you do a slaughter check and find a lot of
lesions, you know that could just reflect micoplasma late in that growth
stage, grow finish stage. So, slaughter checks aren't a great way to
assess the herd severity of mycoplasmal pneumonia infection. It kind of
depends what question you are trying to ask. If you are trying to ask is
it, and this is my simple mind, if I want to know if it's there, that's
a different question then how bad is it? Or is it important? You know,
there's two different issues. Next.

And again, I didn't have a great picture of something resolving here but
these lungs are depressed, they are atalectic. They'll gradually over
time, move all the goo out of those lungs, they'll re-inflate and be
pretty normal. You may be left with a, a few fissures that look kind of
like this, up, the area up in here that are left here or there but even
that will go away. And, if there's some bacteria involvement sometimes
there will be a crinkled lobe you know, but the resolution can be fairly
complete, totally complete if uncomplicated. Next.

So, progression, I think for gross examination anyway, really don't see
much for at least ten days usually it's closer to three weeks. You get a
cranioventral firm redness. As time goes on a little more clear
demarcation becomes a little grayer, a little more atalectasis. As time
goes on, airways can even become a little more prominent as we get the
lymphoplasmacytic simply cuffing those airways and you see these little
white dots on a cut surface and then resolution. Again, I guess I'd like
to emphasize that a population of animals even if it's just one weeks
production in a barn of a thousand, they're supposed to be peas in a pod
can have lesions all over the board in clinical stages all over the
board so that's my basic take home message today is, is variability is a
huge issue in the swine production industry. It is you know, the 21 pigs
that Brad sent in. There is variability in that diagnosis, so, next.

Histopath basics, again we're kind of back down to the bronchial
pneumonia, interstition pneumonia classification. Bronchial pneumonia
usually starts in larger airways, expands from there, some damage,
inflammation, exudates occurs, we call it bronchiolitis. Usually it will
extend into the adjacent alveoli and interstitium and you have bronchial
pneumonia to start with that expands into an interstitial component,
alternatively an interstitial pneumonia has kind of the same problem, it
starts in the septa, the PIMs and PAMs and the epithelium of the
alveoli, serum exudation congestion. Well, most times it\'s not
something, something bads happening there and it wants to get out, it\'s
going to traverse the airways out and you\'re going to end up with
bronchial pneumonia secondary to interstitial pneumonia. So, clearer
distinctions in my view are really hard to make unless you specifically
define the stage and the age that you\'re dealing with, chronic lesions
all start looking alike. Next.

I know there\'s been at least a dozen respiratory agents mentioned
today, pathogens and to me that, that allows a whole lot of different
permutations of organisms that can infect the lung. Our textbooks are
laden with classic lesions of a particular disease, that\'s usually an
experimental infection at a particular stage of disease we see those
occasionally, but not very often. Most of the time we are dealing with
quite a few, a large portion of those 12 different agents that are
attacking the lung and hence we don\'t have lesions that are path
gnomonic. An honest histopathologist which I\'m not a histopathologist
but try to be honest, will report a lot of these lesions as compatible
with but not specific for, and that\'s usually about as good as I get
with histopathology and that\'s probably good enough for Brad a lot of
the times because we got another way to find out the agents that are
there. Now, is this lesion compatible with that agent? You\'re happy
right? And I think sometimes the perception is that pathologists have
the final say and, and they can look on a slide and there, these little
organisms are carrying signs that say we\'re here. No, it\'s trying to
balance all of the information you\'ve got and, and I guess what I\'m
really skeptical of is, is a pathologist like me that sometimes look at
one thumb nail size of tissue on a slide and try to make some herd
assessment you know? That\'s kind of troubling. Next.

So, histopath-wise, probably the earliest lesion is the recruitment of
mononuclear cells, lymphocytes to the areas around some of the
intermediate sized airways, that\'s just what micoplasma likes to do,
attract those inflammatory cells primarily the mononuclear, create a
little inflammation, paralyze the cilia if you will, so that they don\'t
function as well. So, we\'ve got more debris and less ability to clear
it. So, the early lesion reflects that. Mucus, neutrophils are part of
that change and collect creating some atalechtisis plugging airways.
Over time that lymphoplasmacytic infiltrate gets more severe and we
actually get some frank hyperplasia of that bronchial associated
lymphoid tissue and end up with lymphoid nodules and those may remain
even though the lung looks grossly normal. So, a lot of hyperplasia of
BALT might indicate previous insult with *Mycoplasma.* Compatible with
but not specific for, okay? Again, a population has animals in at all
stages of this infection. What else can look like *Mycoplasma*? Again,
Dr, Thacker alluded to, saw the acute influenza can really look like
really, micoplasma and you know, our training, the training I got anyway
was fairly dogmatic and so there are pathologists out there that, that
really think they can tell them apart. They didn\'t work on diagnostic
lab I\'ll say that because you tend to get humbled frequently if you get
too dogmatic working on a diagnostic lab. Ascarid migrations, chronic
bacteria pneumonia, persistence of antigen and it is difficult to
demonstrate the organisms in the chronic lesions so that\'s why we try
to emphasize to our clients to get us tissues from pigs early in the
course of disease. Next.

One of the, one of the tests that, that we use frequently for a variety
of regions is immunohistochemistry and I mean you can only take pictures
of the really good ones but this gives you an idea of where that
*Mycoplasma* is located in an airway and the debris that\'s built up in
there and can\'t get whooshed out, you do see just a little bit of
inflammatory infiltrate around the outside of that airway and some
scattered neutrophils and edema, etcetera in the adjacent alveoli here.
As I said we only take pictures of the really good ones, the problems
with this test is the same as with FA test is that you\'ve got to have
the right airway at the right stage and so the sensitivity isn\'t that
great. I guess, in my view, when we\'re looking at gross lesions,
microscopic lesions of 21 pigs and if they would all be consistent with
*Mycoplasma* consistent with but not specific for and we can find these
just once in a while in one of those 21 pigs that\'s good enough for me,
okay? Doesn\'t have to be in every pig and it\'s very difficult to
confirm with FA or immuno histo chemistry the presence of *Mycoplasma*
in every pig even though we are pretty darn sure it\'s there. It\'s
better to confirm it in one pig okay, to be sure that it is. Next.

FA says, FA is doing the same thing only usually on fresh tissue. Next.

As time goes on this, this could be an example of airway a little bit
earlier in the course of infection but it\'s not, it\'s (inaudible) and
then here\'s one a little later with, with lymphoid hyperplasia and you
go, if my section didn\'t include this, I just looked at this I\'d say
well, I think you\'re two and a half weeks into infection. If my section
only includes this, well, that\'s been there a while. The fallability of
histopathology depends upon what section we\'re looking at. Taken in
total it\'s pretty indicative of *Mycoplasma* however. Next.

More of the same, let\'s go again. Key points on pathological diagnosis,
gross lesions, now more then ever are compatible with but certainly not
specific for micoplasma involvement, we need further tests. Microscopic
lesions now more then ever are compatible with but not specific for
*Mycoplasma hyopneumoniae*. We need further testing. They are valuable.
Histopath and gross assessment are valuable because of that compatible
with statement and because it also helps to find severity and it also
helps rule out presence of other stuff that might be going on that you
forgot to look for. Okay. So, I don\'t want to knock it down totally but
it\'s a tool. Pathology is a tool. Most field cases are mixed infections
which is just emphasizes what I\'ve been trying to say I think. Time for
resolutional vary, with a severity and the extended initial lesion and
the presence of co-pathogens. Next.

If we go to etiologic diagnosis then we demonstrate a specific agent
within a lesion, oh, works for me. Isolation, really tedious, really
hard, difficult to do. We\'re not going to do it are we Eileen? No,
we\'re not going to do it. Very, very difficult to do. So, we need to,
since we can\'t isolate the bug we need to find it some other way.
Immuno histo chemistry and FA tests are what we use most frequently on a
routine diagnostic investigation. PCR, I think is about to just, well, I
think Carlos is probably going to talk about this. I think it\'s about
to emerge as a huge, huge tool in, in answering the question, is it
there? Okay. Confirming, yes it is there. It probably won\'t answer the
question is it important to that pig but that might not be the question
you are trying to ask. You might be trying to ask is this bug present in
the herd. That might be important on a herd basis. So, diagnostic
investigation needs to be framed in what you are trying to answer. What
you questions are and, and what kind of results we can get. Serology
confirms presence of antibody, as we all know it\'s not definitive for
an edologic diagnosis. I don\'t even think it tells us whether it\'s
maternal active antibody or, or maternal passive antibody or active
antibody, you know? Put it in the right hands it's a tool. Next.

Okay. It seems to me with, with a disease like *Mycoplasma* that does
have such variability in a population naturally or perhaps even La Sonia
you know, it seems to me that infection models do offer pretty good
opportunity to assess interventions where you can be looking at a
relatively consistent innoculum given to a pig, all pigs simultaneously
you know, so that everybody\'s kind of at the same stage and in terms of
just determining if something\'s going to work that seems to me a
pretty, pretty good approach. We have controlled infection, controlled
specimen collection. I guess I didn\'t really hit that very hard but
where do you take your pieces of lung make a difference on what we\'ll
find, okay? So, research setting allows you to control for that. Plus
you have the benefit of a standardized evaluation performed all in the
same day or the same set, same technique with a fairly predictable
outcome and some valid measures to go with that. In fewer cases the
variability is uncontrolled and that\'s what I think is huge in terms
of, of maybe what we\'re about here today. The population varies that
wave is going through and which pig you\'re going to pick. If I pick
Carlos, he\'s not a very good candidate you know? Dr. Johnson, he got
into it, he did, okay? But, but that\'s really the point, is that it\'s
really dependent on which pig we pick, what we\'re going to find and how
bad it is. So, a descriptive pathology does have it\'s values but it has
it\'s limitation, our goal I think is to demonstrate an agent associated
with a lesion. I feel a whole lot better about that. We have to know
what specimens to take, at what age of animal, what stage of disease and
the context of what interventions may have been there. For me making a
diagnosis of Salmonella septicemia can be really hard when that, or here
Erysipelas can be really hard when a half hour before the pig died he
got a shot of penicillin you know? Just a little thing like that can
really louse up your protocol, your outcome or your ability to confirm a
diagnosis. And, and probably you know, from where I sit, I\'m supposed
to give you the answer by looking at a slide but, but I, I really like
guys like Brad who will provide the clinical science, the history and
the record assessment and the population dynamics and couple that with
diagnostic investigation, pathology findings, histopathology findings
and age identification. It takes all that I think, to make that herd
diagnosis. Don\'t take one piece of information and run with it. Next.

I think that\'s what I just said. I guess that\'s okay, though isn\'t
it, clinical science history diagnose, production records, lesions, yeah
lesions. If redundancy is a good thing for learning, I think we\'ve had
a lot of that here. But that\'s okay. Choosing the right tests, mentor
and good friend of mine, Bob Block once told me don\'t do a test unless
you\'re prepared to interpret the result. I think that\'s very, very
good advise to all of us. Frequently we get calls from people, well,
what does this mean? Well, I don\'t know. I don\'t know, throw it out.
If you hadn\'t done it we wouldn\'t have to worry about it. Okay, the
point being is be very careful in, in applying tests or interpreting
tests because there are a lot of pitfalls along the way. Next.

I think we\'re in the summary area, I hope. Mixed agents, duration,
population variability makes definitive diagnosis a challenge but yet if
we get the right specimens with the right history I think we\'re going
to do a pretty good job of finding what\'s there, what you expected to
find, maybe a few things you didn\'t expect to find. Next.

Oh, yes. And time changes things. What they had a month ago is really
irrelevant. Today, [I did a cerla]{.mark} (?), I mean, classic is
Pseudorabies, they were all negative a month ago when we did our test.
Well, we\'ve got dots on the liver, let\'s see I don\'t think that\'s
useful information anymore. Time changes things, it changes the, the
permutations of what organisms are interacting, new introductions,
populations, age, that type of thing, so I don\'t think we can take to
the bank information from last month or last year in terms of what\'s
happening today. I think there\'s a minority of people in here that
actually get into hog buildings and, and I think it\'s a worthwhile
experience to see what I mean by this variability to assess pigs in
their environment you know, with the management\'s that\'s in place, I
appreciate Eric\'s ability to look at a globe, a national herd, I
appreciate that but I also have a lot of respect for those clinicians,
Monty and Brad and whoever, that actually can go into a hog barn and fix
a problem and that\'s what I think we\'re about. I think, I hope we\'re
done here.

The summary keeps on going doesn't it? You know, we had some time for
questions, right? And discussion, whatever, would that be a good time?
Because I don\'t think I\'m going any place new. Okay. Questions for the
entire group, right?

Q Any questions?

Q (inaudible)

**Dr. Schwartz:** I can give you an answer. I can give you an answer in
24 hours. I love that advertisement. I can give you an answer but if you
want it accurate that\'s another issue.

Q Dr. Nabil Anis: (inaudible)

**Dr. Schwartz:** If the pathology is not pathognomic why do, you speak
like a microbiologist, if we find it must be important and a lot of
these bugs are present in all herds but they\'re not important.
Pathology is, is what allows you to say yes this bug is important
because it\'s creating a lesion, creating a disease, having an effect.
Otherwise you get mislead, if you just, if you take Carlos\', Carlos\'
tap here and just do PCR for everything and never looked at pigs,
you\'re going to find\--

**Dr. Carlos Pijoan:** Hey, you told you about that?

**Dr. Kent Schwartz:** You\'re going to find all the agents, you\'re
going to find the flora of the herd but you\'ll have no idea if they\'re
important or not you know? And then you\'ll have misused the information
too, as a producer I don\'t want you spending my money on stuff that\'s
not important. You know, as a taxpayer I don\'t want you spending my tax
money on stuff that\'s not important. So, I think, I think pathology is
one of the tools that comes in there to help assess relative importance
of what it is you finding microbiologically. Brad?

**Dr. Brad Thacker**: Yes, I guess I have a follow up to that question
and then a question for you but I think that I think one of the things I
said in my slides is the concept of framing the situation and it\'s kind
of like a puzzle and if we work within perfect information we\'re, we
never have enough information to make perfect decisions and that\'s
really kind of counter into, to the way many veterinarians are trained
now. I\'m going to say something that was a benefit for me going to the
University of Minnesota was Carlo, Carl Osborne, small animal clinician
that taught us the problem (inaudible) in medical record system and we
were drilled to the point of shame that we could only define things to
the point we could define them right? And you know, so extrapolation
beyond that was not allowed. Now, you still made decisions on that but
you recognize the, the value or the accuracy in, of your information all
striving for better information. So, the question I have for Kent is, is
something that I struggle with and, and is my case that I mentioned, you
know, I had Jeff haul 21 pigs over to the diagnostic lab which if I
wanted real answer I haul 21 pigs to the lab, I don\'t necropsy 21 pigs
on the, on the farm and try and do the knee croppsies myself so what is
your opinion of the strategy for sample submission? Live pigs versus
parts?

**Dr. Kent Schwartz:** If we\'re trying to investigate an acute problem,
my strategy is just a little bit different then a chronic problem I\'d
agree more information is better then less because we can always throw
out the extraneous stuff and so, in terms of a strategy for an acute
outbreak of something there\'s certainly a lot of value in having live
pigs delivered to the lab so that we can fully appreciate the spectrum
of lesions, of clinical signs that are present and can fully collect all
appropriate specimens for testing either today or in the near future so
on an acute problem I think we\'re talking generally three or four pigs
delivered to a laboratory to, to tear apart. On those chronic problems
Enzootic problems can\'t, I mean the acute problem I\'m talking about is
something that is different. Is this new or is this different to this
farm? This is, this is new and different versus something we\'ve
struggled with for the last two years so that that new and different
thing requires a pretty aggressive, pretty aggressive diagnostic workup
to see if we do have a new flu strain or a APP, or a, you know, ileitis
where we\'ve never seen it before, whatever. The, the chronic thing I
think requires even a little greater diagnostic intervention because
we\'re, we\'re sort of locked into some of the production problems, some
of the management problems that are being manifested as disease
problems. There I think we\'re looking at frequently a cross sectional
type of examination, looking at pigs at various stages of production to
see what bugs are present where, what diseases are present where. I say
that for the microbiologists, what bugs are present, is not the same as
what disease is present. Acrost, across the various age groups and
that\'s going to vary you know, that strategy will vary whether you are
all in, all out, multi site, blah, blah, blah but frequently we will get
you know, three pigs at three week, six weeks, two weeks into the
grower, 16 weeks of age and then we get a 20 weeks of age and we have a
fairly good idea, you know, that\'s a lot of pigs but some of these
problems are fairly significant economically and so you frame the
problem and then submit the, submit the appropriate pigs, for the
appropriate testing. Cross sectional serology is a whole lot easier or
longitudinal, that would be following the same group of pigs and then
picking off samples as, as they matriculate through the system but I
don\'t think this is meaningful because again, serology is about like
microbiology doesn\'t tell us if it\'s important. It tells us if it\'s
there. Is that where you want, is that where you were going or?

**Dr. Brad Thacker:** So, I guess specifically what is the value of
sending in two tissues from pigs versus sending the whole pig to a
diagnostician?

**Dr. Kent Schwartz:** Again, it depends on the question you are asking.
There are practitioners out there that want to know if it's there. Is
PRRSV in this lung? If we do BAL PCR, one test, we\'ve answered that
question. What he does with the information you know, it\'s his business
he\'s got a plan. So, there is value in shooting a rifle, diagnostically
if you will but there\'s also value in shooting the shotgun, get a broad
scatter because we have practitioners who are tunnel visioned on PRRSV
and do forget\--

(End of tape 2)