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Recently, Dr. Max T. Rodibaugh met with Drs. Randy Jones, Craig
What are the most common respiratory
Rowles, Steve Dudley, and Pat Halbur to discuss swine respiratory
diseases you diagnose in your practice?
In the past 2 years, certainly we’ve had our fair share of combi-
Have you been seeing a lot more respira-
nations of PRRS and Mycoplasma
, or PRRS and influenza. Unfortu-nately in our practice area, PRV is still a viable pathogen. So we’re still
tory disease lately?
seeing a variety of viral etiologies, along with Pasteurella
, some Acti-
We have seen severe respiratory disease outbreaks lately. Most
, some Salmonella
typically at about 3–4 weeks postweaning, pigs are positive for PRRSV,
We tend to see the whole gamut. Recently in a herd where we
and have interstitial pneumonia and early Mycoplasmal pneumonia le-
instituted a Mycoplasma
/PRRS program we had Actinobacillus suis
sions. Subsequent infection with swine influenza virus (SIV), porcine
that looked like Salmonella
that was really explosive. But in our prac-
respiratory coronavirus (PRCV), or opportunistic bacteria add to the
, PRRS, and influenza are three pathogens that tend to
severity of the respiratory complex.
cause the respiratory complex that we routinely see.
My understanding was that the Mycoplasma
We’re seeing Mycoplasma
, influenza, PRRS, with some bacte-
don’t show up that early in the nursery.
ria mixed in — Streptococcus
That was my belief in the past, as well. But now we’re seeing evi-
From a diagnostic perspective, the trend has been an almost six-
dence of Mycoplasmal pneumonia earlier in the production scheme.
fold increase in PRRS cases in the last 2 years, about a threefold in-
Perhaps this is due to the sow herd stability or changing production
crease in influenza, and almost a threefold increase in Mycoplasma
withthe other pathogens staying the same or going down. It’s skewed a
Shouldn’t we focus on the the sow herd
bit in that veterinarians send in things that they have difficulty diagnos-
ing. They won’t send A. pleuropneumoniae
— they’regood at culturing those bacteria now. Certainly the three big players
That’s right. That’s a big part of the SEW thing that’s been left
from a diagnostic lab perspective are influenza, Mycoplasma
SEW is not going to work as well out here in the field where
Do you think from a diagnostic lab standpoint that any of that is
we’re starting up herds with a lot of young sows. All the research has
because of better diagnostic capabilities?
been on old sows — we’ve just sort of glossed over that.
I’d like to think we’re considerably better than we were 2–3 years
I’ve been involved in some of these discussions about not want-
ago. I think we are improving with newer technologies like immuno-
ing to vaccinate. I see no disadvantage, other than cost, to vaccinating
histochemistry. We have some better ELISA serology tests for PRRS and
the sow herd. Is there a disadvantage other than cost to vaccinate the
start-up herd, the parity-one herd, for all the respiratory pathogensyou can think of?
What tools do you use to diagnose respi-
ratory problems? How do you approach
: I can’t think of any reason other than cost. That’s going to be a
factor. Then maybe deciding to change that vaccination schedule once
a problem in the field?
that sow herd matures. But even then, some of those sow herds have
Today the use of diagnostic labs has never been more impor-
tant. Because of all these different viral etiologies that we’re dealingwith, you can’t just separate that out with a gross pathologic exam and
If 40% is our normal rollover rate, you’ve always got a start-up
culture sensitivities. We need the increased capabilities that diagnostic
herd. In the future, we’re going to bring in those gilts at 50–60 lb (23–
labs bring to the table. So not only are we doing more tissue submis-
27 kg) and get them associated with that breeding herd somehow, so
sions, we’re also doing a lot more acute/convalescent sera. It takes that
that we can try to get some natural immunity built much earlier. I think
whole battery of information before you really know what’s going on.
that’s particularly important until we have improved PRRS vaccines. Weshould be happy to have what we’ve got, but there’s a lot of room for
I certainly agree with that. We’re using some serology, some
improvement. That way you’re doubly insured — you’ve got natural
histology, and some traditional culture and sensitivity. With most of
exposure and you’ve got the vaccination.
those respiratory cases, I think what Pat has been saying is that weneed to send in more samples, we need to send in more animals, we
Swine Health and Production —
Volume 5, Number 1
need to have a statistical sampling procedure, and so we certainly want
you get out of this compared to the slaughter check. I think slaughter
to increase the sample size of how many pigs we kill and send. I don’t
checks are still valuable for atrophic rhinitis and maybe, although less
think we have changed much on serology. We send 10–12 samples for
so, for Mycoplasma
. To reflect what’s going on in the nursery pigs or
a 60- to 100-head barn, which maybe is a little on the light end. What
early grow/finish phase, I’m not sure the slaughter check is of much
we tend to see is that it’s either there or not — Mycoplasma
enza, PRRS. We also send in four to five live animals and that helps us.
So in many cases when you initially do a workup, people are fol-
The more acutely affected animal you can find, I think, the bet-
lowing those up even if they’re not having respiratory problems in the
ter. You’re going to find influenza early, and then it’s going to be gone.
herd, just as a monitoring situation.
Some of those others will hang around. I think the selection of animal
They’re definitely following up with serology and in some cases
that you get samples from is very important. You really have to decide
what pathogens are most important. Which one are you going to try tocontrol?
Do you think serology is good enough?
That’s right. That’s why I like to do these cross-sectional necrop-
What kind of procedure would you set
sies of pigs at all different stages, because then you can see what’s been
up to monitor a herd serologically?
there from the beginning and where to implement each treatment. I
We started doing a lot of serial bleedings on tagged pigs. I
like looking at healthy pigs in the same age group to see what patho-
think a lot of those are easier to interpret but take longer. So we go in
and tag a group of 3-week-old pigs and do some 9-, 14-, and 20-week-
Pat, would you describe how you suggest doing a cross-sectional
old pigs at the same time and get a cross sectional with it. Then we’ve
got the group of tagged pigs that follow. At any point when you bleedthose tagged pigs, do another cross sectional if you want to and see
In a herd of that size, we would usually start on pigs that have
what’s on either side of them. PRRS-ELISA, Mycoplasma
been weaned a week or so. Submit three or four sick pigs and one
healthy pig. Then at the end of the nursery phase, submit the samenumbers. Then a couple weeks into finishing and maybe two more
We’re doing the same thing — serially bleeding pigs. We feel
times during finishing, submit three or four pigs and one healthy pig.
pretty confident that the PRRS-ELISA is pretty accurate at monitoring
We usually end up spending $30–$50 per pig for a complete workup.
where we’re at. I’ve been a lot more confident recently now that the
That’s not a lot of money when you think about the decisions you guys
test has become more accurate. We’re still not happy
have to make in those herds, and whether to vaccinate a 500-sow herd
with the serological test for influenza. We’ll get a histopathology/
. How much would that cost?
necropsy diagnosis with influenza and still have negative animals.
If you vaccinate every pig you’re going to be looking at $10,000.
Dr. Erickson at Mount Rollins Diagnostic Laboratory says that
the younger the pigs are, the less accurate HI is. He says that there is
So you bring in 30 pigs and spend $800–$900 on diagnostics. It
some interference of the maternal antibodies with the HI test. He pre-
seems to be cost effective. At least the clients keep coming back for
fers the ELISA on young pigs, but on animals without maternal antibod-
Do you prefer that the pigs themselves be submitted, or the tis-
I’ve heard references to 1.5 as a cutoff on the ELISA for herds.
Others will say if it’s over 1.5 that’s an absolute indication of active in-
Definitely live pigs if that’s possible. The necropsy skills of veteri-
fection, and under that is perhaps just vaccine-induced. What’s your
narians are getting very good, so the vet can call and get a protocol for
interpretation of that? I worry that we’re going back into the PRV titer
It seems to me with that kind of program, if you take tissue
In pigs that we have experimentally vaccinated by intramuscular
samples in the field you need a really good recording system to keep
means we rarely get titers over 2. Then you subsequently challenge
all that straight. How many people are you seeing submit samples like
them and they’re pretty impressive — ≥ 2.5. It doesn’t make any
sense to me that it would be any different than a natural infection interms of the antibody response, but it does seem to generally hold to
We’ll get a couple submissions a week that way. Instead of spend-
that rule. But again the sequential serology is necessary because you
ing it in small pieces, they get aggressive and do it quarterly — more
don’t know whether the anitbody level has leveled off or is still on its
as a herd-health monitoring strategy than anything else.
So you are saying in some respects this might replace the slaugh-
Randy’s point on influenza serology is very well taken. We commonly
will isolate influenza out of pigs and detect it by immunohistochemistry
I don’t think there is any comparison to the useful information
and then go back to bleed penmates and titers have gone down or theywill never have developed HI titers. There are likely more antigenic
Swine Health and Production
— January and February, 1997
variants of SIV out there than we think. This makes relying on serology
Porcine respiratory disease complex
for influenza questionable. Especially if you’re going to make a deci-
(PRDC) — what do you think has
sion to vaccinate for influenza — don’t base it on serology alone.
changed that’s really warranted the
industry to come up with that acronym?
Do you feel that you should send in the serological samples indi-
vidually or wait the whole 4- to 5-month period and then send them all
In some ways we do a disservice. Obviously, we’ve stolen it
from the bovine respiratory disease complex. I think it’s important forall of us to recognize that, yes, there are a variety of etiologic agents,
It’s always best to run them all same day. It’s less an issue if you’re
but let’s not just call it PRDC and walk away like there’s nothing we can
using the ELISA, but for the IFA and tests with subjective endpoints I
do about it. You need to do the type of analyses that we’ve been de-
would want to run those the same day. I feel confident in PRRS-ELISA
scribing here, so that you can get a handle on exactly what you’re deal-
-ELISA. Every time I send a sample through that lab it
ing with. I think it’s important we don’t fall into that trap.
comes back about the same titer or S : P ratio.
Obviously the biggest challenge veterinarians have is making
What about porcine respiratory coronavirus (PRCV)?
priorities in disease-control strategies for these operations. That’s why
I’ve had the opportunity to work with a lot of PRCV isolates in
with the diagnostic information you can’t just call it a complex and
pigs — maybe half a dozen or so — that we’ve purified and put back
throw it out. The best strategy for farm, season, and situation are going
in pigs. With most of those, clinically you can’t tell you infected the
to differ and so the treatment strategies tend to differ.
pigs. There are a small percent of those that will induce transient res-
The risk is that they lump the complex into one disease then
piratory disease, like a mild influenza, but won’t damage much of the
you tend to lump your treatments into one. Whether there’s PRRS in-
lung (maybe 10%–15%). In combination with other pathogens, PRCV
volved or not, there will be treatment for PRRS. Whether there’s influ-
may be a significant part of the complex. It’s one of those things that’s
enza involved or not, there will be vaccination for influenza. Treating it
fun to diagnose, but I don’t know how to control it. It can help you ex-
as a complex is not going to be cost effective.
plain some things that are there, and if you see a pattern ofseroconversion at a certain age then maybe you could direct your
Do you think the PRRS is the major change in having to come up
medication for bacteria at that point in time. If you don’t have a serious
with this label for respiratory complex, or are there other factors you
PRRS or Mycoplasma
problem they’ll move through PRCV without any
trouble. Unfortunately the serology test is very expensive and turn-
We’ve got totally different systems than we used to have. All of a
sudden now we’re using different technologies. We have larger num-
Pat, do you think cross-sectional serology is a pretty good read-
bers of groups. We have multisite nurseries. It puts a whole different
perspective on herd health, the population, and the epidemiology ofwhat’s going on. That’s a huge factor in what we’re doing.
In your smaller herds, one- or two-site herds, I think it is. When
you deal with the kind of herds Randy does — with multiple finishing
You’ve changed exposure levels and colonization levels of
sites and multi-source nurseries going to different sites — it’s more of
a stretch to apply that to a whole system.
We have the subpopulations, we have potentially more naive
We do see differences in the same groups. Whether this is
animals, and the whole potential line variation or change in the pigs as
from lateral infection from neighboring sites or just a change in the dy-
namics of that population is hard to evaluate.
Certainly there have been changes in production style. I’m a big
It’s an interesting observation. We talk about subpopulations and
believer in different genetic susceptibilities to diseases — particularly
breeding herds, and I think now people are talking about patterns in
in PRRS. What’s new in infectious diseases that wasn’t here 5 years
subpopulations and finishers. It almost sounds as if you’ve got popula-
ago? Three things really: antigen variance of influenza, PRRS, and
tions and not really subpopulations of differences in disease exposure.
PRCV. I have a feeling that something has changed with Mycoplasma
too, because it is much more severe. Maybe it’s just the viruses that
A lot goes back to how they handle those pigs in farrowing. We
have made it that way, but I think there needs to be some serious re-
get a lot of people who want to hold pigs back. It’s like pulling teeth to
search there to see why Mycoplasma
vaccines aren’t working as well
get them either to euthanize or send those pigs on through the system.
as they had in the past. For Mycoplasma
we’re getting some seriousvaccine failures.
Swine Health and Production —
Volume 5, Number 1
How do you approach treatment of the
is really important. But because it has been less predictable, it has
various complexes or the individual
been harder for us to justify to producers to routinely do that.
diseases that make up the complex —
for example, what about PRRS?
Any further comments on influenza
treatments or preventive use of vaccine?
It really goes back now to checking the breeding herd and try-
How are you using it in the practice?
ing to stabilize the breeding herd. Herds at this time a year ago wereundergoing major seroconversion in the nurseries; now we’ve stabi-
We pretty much have stayed with the double dose in the face of
lized their sow herd and the nurseries are negative. We’ve dumped a
lot of vaccine into those herds. We’ve tried to emphasize
Is there the potential that a single dose for influenza or Myco-
acclimitization of gilts and that kind of thing too; the management
things you do to keep a herd stabilized. We basically depopulate nurs-ery sites every time we fill them. That depopulation technology is there
I think you’re counting on there being some exposure there al-
for a lot of those producers with large sow farms and nursery sites.
ready and it being a booster. I would have serious concerns, particu-
What we haven’t really done is clean up our finisher sites. You’re going
larly with the influenza vaccine. One dose will probably not protect a
to end up with some buildings there with older pigs when you put in
younger pigs. So we still get some seroconversion on the finisher. In
Do you think it could be the reverse? You dose a naive pig and
those instances we’re vaccinating pigs as feeder pigs at 40–50 lb (18–
rely on low environmental exposure to give the secondary response.
But if the exposure is heavy, you’re out of luck.
: Our experience has been the same. We felt that we had to stabi-
That’s right. The exposure dose is all important with all these viral
lize the breeding herd. In many cases once we got the breeding herd
diseases. So if you can have proper pig density and ventilation and pig
stabilized, and did some of our cross-sectional studies in finishing,
flow your dose is going to be lower. You may get by with one dose of
we’ve essentially dropped a lot of pig vaccine. We’ve experienced a
number of the antigenic variants Pat described in regards to SIV as welland that is an instance where we have had good response to vaccine.
We’ve compared two-dose versus one-dose influenza on some
One herd in particular was experiencing it all the way from nursery
sites where we’ve got four or five buildings. We’ll vaccinate some with
through finishing and in that particular instance we blanketed the sow
one dose, some with two doses, and some won’t get any vaccine. The
herd and used vaccine on that herd for a short period of time — it
biggest thing we see where we know there’s influenza is not a lot of
wasn’t permanent. By going in and blanketing the sow herd and using
death loss — just culls. Morbidity is really the problem we see with in-
a vaccine for a period of about 4–5 months we were able finally to get
fluenza where there are no other major complicating factors; e.g., ul-
it shut off. It was an influenza that would last nearly 30 days.
cers. Most of those pigs die from ulcers. So we’ve seen no differencebetween one and two doses as far as the reduction in cull rate, but you
Do you think that PRRS impairs the lungs’ ability to fight the in-
will get a reduction in cull rate in our hands with the influenza vaccine,
fluenza, or do you think it’s just a different strain of it?
even with one dose. Clinically, the pigs are coughing, but they’re still
I think more likely some of those pigs are still protected with pas-
eating and growing. We’re giving that single dose right when they come
sive antibodies and not yet susceptible. I think that’s a big part of it at
out of the nursery or a day or two after they get to the finisher —
least to 11–12 weeks of age. I also think that if they have a lot of seri-
about 8–9 weeks of age. Like you say, where there are really some
plus PRRS damage to the lung, it’s going to take them
acute problems, we’ll give a second dose and then we back down to
longer to clear influenza from herds. My impression is that influenza
one. We’ve had to go back — in some cases in late nursery — and
vaccines are being more widely used. Practitioners that I talk to on the
vaccinate for PRRS to get better control. We are also looking at Myco-
phone each day seem to be pretty happy with that product.
vaccines as well. The question of which pathogen is the mostimportant can be difficult to answer.
Vaccines are definitely being used more. I think part of it is the
frustration with the respiratory complex and not getting a response
What about Mycoplasma vaccination,
with PRRS. You find PRRS, try a vaccination, and if it doesn’t work you
treatments, and control?
jump to the next thing. Some of the increase in use in influenza would
Where we decide to make a decision to use Mycoplasma
always using two doses. We tend to recommend that we use it in an
Overall we haven’t felt that the PRRS vaccine has been terribly
early-weaned pig where they’re weaning between 14 and 18 days. We
effective. So we’re only using it in farms where there’s severe out-
like to wait 2 weeks after they’re into the nursery, give them the first
breaks. We’re trying, obviously, to get the sow herd quiet and that’s the
dose, and 2–3 weeks later hit them with the second dose. We’re also
key. We are trying to isolate some of those viruses and we have done
using some of the Lincocin® in the feed at various ages — some high
some killed vaccines in the sow herds and in certain herds that has
levels for a couple weeks, and then lowering that dosage. This combi-
helped. I think the homologous versus heterogeneous challenge model
nation of protocols has been helpful in the control of Mycoplasma
Swine Health and Production
— January and February, 1997
Where you don’t really ever expose those younger pigs back to
smaller operations to evaluate this, because there are not a lot of sub-
older pigs I think Lincocin® has really helped. Some producers just
populations to compare. So we will be looking at people in larger sys-
don’t want to give a lot of shots — it’s a labor problem. When you
tems to help with that. We’re involved in a very large system where
move that shot from the farrowing house to the nursery, there’s a big
they’re trying to evaluate just feed additives (Lincocin®) without any
difference. That’s when you really have to start convincing them they
vaccination versus vaccinations of one-dose and two-doses. We’re
keeping records on all of the 18,000–20,000 sows in that database —hopefully in a year that study will be revealing.
I think one of the things that we really need to focus on is to be
able to go in and retrospectively financially analyze what we’re doing
The problem is that a lot of this information is going to be gen-
for these herds. I think it really behooves us to get involved financially
erated internally and privately and we’re in an industry now where
in the records so that we can show them in black and white what the
there’s not a lot of publicly funded research being done on financial
economic benefits or disadvantages of doing something are. I think we
analysis, so somehow we need to figure out a way to distribute infor-
all need to work harder not just on biological or medical control, but
also financial control of what we’re doing in herds.
Craig’s right. It’s difficult, though, for people who work with
Swine Health and Production —
Volume 5, Number 1
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