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H I G H L I G H T S O F A R O U N D T A B L E D I S C U S S I O N
NA
019
10 J U L Y 2 0 1 8 • D E N V E R , C O L O R A D O
P R E H A R V E S T S A L M O N E L L A C O N T R O L
R A I S I N G T H E S TA N D A R D F O R S A F E P O U LT R Y
POULTRY H E A L T HT O D A Y ®
Sponsored by
H I G H L I G H T S O F A R O U N D T A B L E D I S C U S S I O N
JON SCHAEFFER, D V M , P h D
Senior Director, US Poultry Technical Services
Zoetis
W E L C O M E
More stringent standards implemented by USDA’s Food Safety and Inspection Service
(FSIS) have put increased pressure on producers to reduce the prevalence of Salmonella in poultry
meat. It’s no longer realistic to expect processing plants to bear sole responsibility for food safety.
It’s therefore clear that preharvest Salmonella control has taken on added importance.
There are hundreds of Salmonella serotypes. Only a few affect poultry and, of those, even
fewer affect people. Nevertheless, FSIS considers all Salmonella types equal, regardless of serotype.
If live production and processing allow Salmonella Kentucky to slip through — a serotype that
poses little risk to consumers — it can just as easily leave the door open for Salmonella Enteritidis,
which does pose a food-safety risk.
As part of its Integrated Food Safety Management initiative, Zoetis is helping poultry companies
address these challenges. Toward that end, it organized a roundtable where poultry experts could
exchange ideas for improved control of Salmonella during live production. Zoetis is pleased to
share highlights from that discussion herein.
POULTRY H E A L T HT O D A Y ®
P R E H A R V E S T S A L M O N E L L A C O N T R O L
R A I S I N G T H E S T A N D A R D F O R S A F E P O U L T R Y
T A B L E O F C O N T E N T S
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P U B L I C H E A LT H I M P L I C AT I O N S
C O M P E T I N G S A L M O N E L L A S E R O V A R S
R E G U L AT I O N V E R S U S ‘ T R U E ’ F O O D S A F E T Y
L O O K T O B R E E D E R S
E L I M I N AT I N G W E A K L I N K S I N P R O D U C T I O N
V A C C I N AT I O N D E C I S I O N S
B R O I L E R V A C C I N AT I O N T R I A L S
A S S E S S I N G V A C C I N E E F F I C A C Y
S A L M O N E L L A A N D G U T H E A LT H
I M PA C T O F L I T T E R Q U A L I T Y
W AT E R A C I D I F I C AT I O N
E V A L U AT I N G I N T E R V E N T I O N S U C C E S S
P R E P R O C E S S I N G S T R E S S A N D S A L M O N E L L A
S A L M O N E L L A P R E V A L E N C E I N N A E F L O C K S
R E G U L AT O R Y C O N C E R N S
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POULTRY H E A L T HT O D A Y ®
H I G H L I G H T S O F A R O U N D T A B L E D I S C U S S I O N
K A L E N C O O K S O N , D V M
Zoetis
E L I Z A B E T H D A L E , D V M
Pilgrim’s
C H A R L E S H O F A C R E , D V M , P h D
Southern Poultry Research Group Inc.
R O B E R T O ’ C O N N O R , D V M
Foster Farms
K E N P O W E L L , D V M
Aviagen
P H I L S T A Y E R , D V M
Sanderson Farms
B R U C E S T E W A R T B R O W N , D V M
Perdue Farms
S C O T T W E S T A L L , D V M
Cobb-Vantress
M O D E R A T O R :
J E A N S A N D E R , D V M
Zoetis
P A N E L I S T S
R O B E R T O ’ C O N N O R , D V M
K A L E N C O O K S O N , D V M
E L I Z A B E T H D A L E , D V M
C H A R L E S H O F A C R E , D V M , P h D
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P R E H A R V E S T S A L M O N E L L A C O N T R O L
R A I S I N G T H E S T A N D A R D F O R S A F E P O U L T R Y
J E A N S A N D E R , D V M
P H I L S T A Y E R , D V M
B R U C E S T E W A R T B R O W N , D V MK E N P O W E L L , D V M
S C O T T W E S T A L L , D V M
POULTRY H E A L T HT O D A Y ®
H I G H L I G H T S O F A R O U N D T A B L E D I S C U S S I O N
P U B L I C H E A LT H I M P L I C AT I O N S
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S A N D E R
Let’s start by addressing why preharvest intervention is important before moving on to a discussion about your experiences and recommendations regarding Salmonella prevention and control during live production. Why is it important to reduce the load of Salmonella during live production? And is there a limit on how much Salmonella a processing plant can effectively handle? D A L E
It’s important to start taking a more
aggressive and active approach to
limiting Salmonella in live production
because ultimately, at the end of the day,
we’re engaged in food production for
people — our goal is to produce a safe,
affordable, high-quality product. That
means we’re inherently engaged in
public human health.
We’re past the point on the live side
where we can simply tell consumers to
thoroughly cook their product and wash
their knives and cutting boards. For me,
that’s why I think it’s really essential we
continue to develop Salmonella control
on the live side.
S T E W A R T B R O W N
You can get between a five- and a
seven-log reduction between the front
end of the processing plant and the other
side of the chiller. That’s pretty powerful
and often is enough to knock bacteria
down so low it’s virtually non-detectable.
It’s just not enough all the time, however.
The truth is, we don’t know when those
times are.
We’re working hard to think through that,
but the part that’s still a struggle for us, as
an industry, is to keep the pathogen load
low enough so that processing-plant
interventions can work effectively all the
time. That’s the goal, and that logically
means you’ve probably got to have
live-side intervention. Most of the industry
is working toward this end.
O ’ C O N N O R
If plant interventions don’t change at all
and suddenly your Salmonella prevalence
goes up, you almost have to assume it
wasn’t caused by the plant and that it had
something to do with the Salmonella
coming into the plant.
If you don’t reduce the levels of
Salmonella coming in, you’re leaving your
plant wide open for a lot of variability.
I have seen the prevalence of Salmonella
go up at processing depending on which
farm is being processed. The plant hasn’t
changed a thing, so I have to assume it’s
coming from the live side.
S A N D E R
What are the major types of Salmonella we need to worry about? Which serotypes pose a risk to human health? H O F A C R E
The most common serotypes for the
last 30 years in human outbreaks have
been Salmonella Enteritidis, Salmonella
Typhimurium and Salmonella Heidelberg.
Salmonella Newport and Salmonella
Infantis can also be important in
some years.
Often the other serovars are more
important one year compared to other
years, simply because they’re involved in a
large outbreak. However, S. Enteritidis, S.
Typhimurium and S. Heidelberg are the
serovars that the Centers for Disease
Control and Prevention (CDC) historically
have associated with poultry and human
foodborne illness.
?
?
P R E H A R V E S T S A L M O N E L L A C O N T R O L
R A I S I N G T H E S T A N D A R D F O R S A F E P O U L T R Y
We’re past the point on the live side where we can simply tell consumers to
thoroughly cook their product and wash their knives and cutting
boards...that’s why I think it’s really essential we continue to develop
Salmonella control on the live side. Elizabeth Dale, DVM
“”
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H I G H L I G H T S O F A R O U N D T A B L E D I S C U S S I O N
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S A N D E R
Dr. Hofacre has told us the serotypes of concern to human health. What are the Salmonella serotypes you’re most often finding? S T A Y E R
S. Kentucky seems to be the predominant
species of Salmonella a lot of us are
finding. Does anyone know why?
We find other bad actors out there, but
they’re a much smaller population than
S. Kentucky.
O ’ C O N N O R
We don’t include S. Kentucky in our
autogenous pullet vaccination. I want to
eliminate or reduce the S. Heidelbergs
and S. Typhimuriums. As an industry,
are we allowing Kentucky to become
predominant because we’re trying to
prevent the top three or top four?
S T A Y E R
We’ve been using an autogenous vaccine
for over a decade in our pullets —
sometimes with, but mostly without,
S. Kentucky. S. Kentucky’s always been our
predominant species. We haven’t really
seen a change with the vaccines we’ve
been using.
O ’ C O N N O R
We’ve been using an autogenous vaccine
since 2006, and I don’t think we’ve ever
included S. Kentucky. I want to eliminate
the other serotypes.
S T E W A R T B R O W N
We don’t focus on S. Kentucky in parents,
either, but for maybe a little different
reason. I just don’t believe vaccination is
going to do much for S. Kentucky.
H O F A C R E
S. Kentucky has a unique ability to
out-compete its neighboring Salmonellas.
It does that in the test tube and it does
it in the chicken. When we vaccinated
broilers with an S. Kentucky isolate as if it
was a vaccine and vaccinated another
group with one of the commercial
S. Typhimurium vaccines and then
challenged them all with S. Heidelberg,
there was a significant reduction in
Salmonella colonization when S. Kentucky
was used as a vaccine — although it
wasn’t as large a reduction of the
S. Heidelberg as the commercial
live vaccine.
?
P R E H A R V E S T S A L M O N E L L A C O N T R O L
R A I S I N G T H E S T A N D A R D F O R S A F E P O U L T R Y
S. Kentucky has a unique ability to out-compete its neighboring Salmonellas.
Charles Hofacre, DVM, PhD“ ”
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S A N D E R
What happens if you have a high prevalence of S. Kentucky since it’s not a major food-safety threat? D A L E
For us, there’s a place for two approaches
— decreasing the prevalence and
displacing serovars of concern. It’s the
difference between food-safety regulation
and true food safety.
You’re worried about prevalence if you
know you have a serovar known to be of
concern to the CDC — and it may be in a
tray pack where you’ve got raw product
going into consumers’ homes. Then your
goal is probably going to be getting rid
of those serovars versus worrying about
failing overall counts for S. Kentucky.
O ’ C O N N O R
I completely agree. There’s a public health
risk and then there’s a regulatory risk.
Are you going to be shut down due to a
regulatory violation or are you going to be
the cause of a human outbreak? If you
have one of the top three or four
serotypes that pose a greater risk to
people and there’s a risk of an outbreak,
that’s the bigger priority and a bigger risk
for your company.
?
P R E H A R V E S T S A L M O N E L L A C O N T R O L
R A I S I N G T H E S T A N D A R D F O R S A F E P O U L T R Y
There’s a public health risk and then there’s a regulatory risk.
Robert O’Connor, DVM“ ”
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POULTRY H E A L T HT O D A Y ®
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L O O K T O B R E E D E R S
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S A N D E R
What are some of the most common ways broilers become infected with the types of Salmonella that pose a risk to human health? Does it start with breeders? O ’ C O N N O R
It absolutely starts with the breeders. We
have a lot of data on broilers, breeders
and pullets. I can absolutely see the origin
of a serotype in our pullet population that
eventually works its way to broilers. In
every case of Salmonella I’ve had to deal
with, it always started in pullets, then
went to the breeders, then the broilers.
S T E W A R T B R O W N
For us, the breeder side is super-
important. We’re focused on the
Salmonella B and D serogroups. We
have three metrics in breeders: houses
that become positive for Bs, those that
might be Ds and those that are anything
else. The Bs and Ds go on a priority list
and are tracked heavily. It takes them
3 years to come off the list if they get on
it. They have to be negative for two
consecutive flocks before they get off
the list.
S A N D E R
How do breeders initially become infected with Salmonella?
H O F A C R E
You may source from a pullet farm that
has a mouse or darkling beetle infestation.
I’ve walked around pullet farms that have
the supplemental starter feeder full of
darkling beetles. Those chicks are going to
eat the beetles. I’ve worked with farms
where we’ve had to completely tear the
sidewalls out and the insulation to get rid
of the beetles. If you don’t, the next pullet
flock will be positive for that farm’s resi-
dent Salmonella. Even if you’ve gotten a
clean primary-breeder source, the pullet
farm can be the source.
It’s also important to know what
Salmonella serovars are from the primary
breeder. In one study, we followed
S. Kentucky back all the way from the
pedigrees through to the processing
plant. Even though S. Kentucky is seldom
transmitted vertically in the egg, it’s still
passing through, probably by fecal
contamination on the eggshell, from one
generation to the next.
? ?
P R E H A R V E S T S A L M O N E L L A C O N T R O L
R A I S I N G T H E S T A N D A R D F O R S A F E P O U L T R Y
We have three metrics in breeders: houses that become positive for
[Salmonella] Bs, those that might be Ds and those that are anything else.
The Bs and Ds go on a priority list and are tracked heavily.
Bruce Stewart-Brown, DVM
“ ”
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H I G H L I G H T S O F A R O U N D T A B L E D I S C U S S I O N
E L I M I N AT I N G W E A K L I N K S I N P R O D U C T I O N
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S A N D E R
What can be done to shore up weak links in the production system that enable Salmonella to get into a flock? P O W E L L
There’s a long list of ways that Salmonella
can get into a flock. On a daily basis, there
are three things I focus on regularly. One is
the feed contamination rate. Mainly look
for coliform levels, because that’s the
easiest to find and quantitate. The other
two are the management of gut health
and rodent control.
There are certainly other potential sources
of influx into a flock such as beetles,
dust or maybe the farm is located near
a cornfield at harvest time or hay is being
baled nearby, which stirs up dust or
rodents. Additionally, Salmonella can be
amplified the last few hours birds are in
the house during feed withdrawal.
S T E W A R T B R O W N
Focusing on some specific serogroups
(Bs and Ds) and those farms that repeat
on those higher-priority serogroups has
helped us narrow our focus on the “weak
links.” Study the repeating farms, look at
them from every angle — rodent control,
biosecurity, vaccination, etc. Don’t stop
till you break the cycle.
D A L E
A slow vertical leak, whether it’s in the
embryo or on the shell, is probably the
most dangerous. Then it gets into broilers,
and you have a higher number of birds
shedding it and the potential for
horizontal transmission.
But other things — biosecurity or the
people involved — are really key
regarding other points of introduction.
After the avian influenza breaks in 2015,
biosecurity throughout the entire industry
improved dramatically, especially with
respect to personnel and equipment.
However, I think there’s a blind spot — or
an opportunity — regarding structural
and pest-management biosecurity. We
have much stricter programs in place, but
there’s a perception among a lot of people
that if you have out bait boxes every 100
feet and you’re checking them, you have
a rodent-control program. That’s just a
monitoring program.
At some farms, and despite a producer’s
program and inspections, the job’s just
not getting done controlling some of the
vectors for Salmonella.
?
P R E H A R V E S T S A L M O N E L L A C O N T R O L
R A I S I N G T H E S T A N D A R D F O R S A F E P O U L T R Y
I think there’s a blind spot — or an opportunity — regarding structural and
pest-management biosecurity. Elizabeth Dale, DVM“ ”
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POULTRY H E A L T HT O D A Y ®
H I G H L I G H T S O F A R O U N D T A B L E D I S C U S S I O N
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S A N D E R
Most breeder flocks are vaccinated against Salmonella but that’s not the case with broilers. When should a producer consider vaccinating broilers against Salmonella with a live vaccine? An inactivated vaccine wouldn’t be used in broilers because it would have to be injected, which would adulterate the meat. H O F A C R E
I would use a live vaccine if I had
S. Enteritidis or S. Typhimurium or
S. Heidelberg in my broilers, and I needed
to get it knocked down on the broiler
farm so you have less of these serotypes
coming to the plant. The current live
vaccines are not effective against all
serovars. In other words, if I want to
lessen the amount of Salmonella
coming into the plant, then I’d consider
vaccination of broilers.
O ’ C O N N O R
Dr. Hofacre’s research has shown that a
commercial vaccine does a better job
than S. Kentucky out-competing
S. Heidelberg. That really does justify our
use of a commercial vaccine in broilers.
A lot of it comes down to cost. My pullet
population is like a tiny town. It’s not
as costly for me to use a vaccine for
that small population. But when I
exponentially multiply it into broilers, I’m
talking big money. So, I get a lot of
questions because it’s expensive to do,
but we do it and I feel we have the
science to actually show it’s a preharvest
intervention that works. W E S T A L L There are two scenarios where I would
consider vaccinating broilers against
Salmonella. One is when the plant is
having a high prevalence issue or when
you’re getting isolates of concern in
the plant that you don’t have in your
autogenous vaccine for breeders. You
might want to use a live vaccine during
that time in broilers until you get that
isolate incorporated into your autogenous
vaccine for breeders.
S T E W A R T B R O W N
If you decide there’s nothing more you
can do at the plant to lower the
prevalence of Salmonella, you have to
weigh the cost of that against the cost of
a live vaccine, which can be expensive.
It’s been a number of years, but use of a
live vaccine didn’t work well in our hands,
at least with the strains we used.
O ’ C O N N O R
When we talk about live-side
interventions, there’s no silver bullet.
It’s a “multi-hurdle” approach. If I treat
the litter, use probiotics and then
organic acids before processing and
I add a vaccine to that, I’m adding one
more hurdle. Whether or not a single
intervention, among several, is effective
is very difficult to determine. Using
prevalence as the determinant is a
very gray area.
How do we know if there are synergies
among the interventions? It’s hard to
validate the worth and what you’re
spending. If I’m in the plant, I can easily
validate. So — to your point about
spending money and making a good,
judicious decision — it’s often easier to
justify spending based on experience
at the plant instead of on the live side.
continued
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P R E H A R V E S T S A L M O N E L L A C O N T R O L
R A I S I N G T H E S T A N D A R D F O R S A F E P O U L T R Y
There are two scenarios where I would consider vaccinating broilers against Salmonella.
Scott Westall, DVM“ ”
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H I G H L I G H T S O F A R O U N D T A B L E D I S C U S S I O N
D A L E
In my experience, vaccines don’t have
an impact on prevalence. They’re more
successful at displacing specific serovars.
Now, if you’re trying to get out of Category
3, you probably need a short-term and a
long-term plan. The short-term plan may
be throwing everything in the kitchen
sink at the problem, but the long-term
plan includes a lot more, as we’ve
discussed: looking at your management
practices, your litter quality and moisture,
biosecurity, your pest control, as well as
the serovars you have, and testing and
vaccination of breeders.
C O O K S O N
It’s important to hold vaccination crews
accountable to help ensure flocks are
vaccinated properly. That’s one of the
most powerful tools we have. When they
know they’re being checked, they realize
they need to bring their A game.
V A C C I N AT I O N D E C I S I O N S
It’s important to hold vaccination crews accountable to help
ensure flocks are vaccinated properly. That’s one of the most
powerful tools we have. Kalen Cookson, DVM“ ”
B R O I L E R V A C C I N AT I O N T R I A L S
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S A N D E R
Dr. Cookson, you’ve been involved with broiler vaccination trials. What do they show? Can they help a producer get out of Category 3? C O O K S O N
In most cases, levels of Salmonella in
the plant are driven by S. Kentucky. Not
always, but if someone is in USDA’s
Category 2, going into Category 3, or the
plant is solidly in Category 3, it’s often
80% S. Kentucky-driven. There are studies
that clearly show a reduction in
S. Kentucky when broilers receive live
S. Typhimurium vaccines. In the
field, it’s a different situation than a
controlled-challenge study, but we’ve
seen reductions in positive bird rinsates.
I just don’t think the reductions are on
the same level as we see against the B
and the D serotypes, and I think there’s a
lot of science and reason for that. There
are shared antigens between the Bs
and Ds.
S A N D E R
When did these studies begin? C O O K S O N
The broiler-pen studies started about
15 years ago. Instead of challenging the
broilers, investigators relied on what we’re
talking about here — the link from
breeder to broiler. Investigators confirmed
that chick-box papers were positive for
Salmonella serotypes B and C. There was
a 30% to 60% reduction in Salmonella-
positive carcass rinsates after rehang.
S A N D E R
Haven’t there been more recent broiler trials with the live vaccine? C O O K S O N
Yes. Since then, there have been some
fairly large-scale studies that produced
similar results. In one live S. Typhimurium
vaccine trial, there was a 60% reduction in
positive rinsates at rehang. Investigators
broke it down by serotype; Salmonella C
serotypes made up about 75% of all the
isolates recovered from the unvaccinated
birds, and Bs accounted for the other 25%.
In contrast, there was a 50% reduction
of Salmonella C and no recoveries of
Salmonella B in the vaccinates.
In a second trial, investigators saw about
a 30% reduction and that included a 25%
reduction in Salmonella C serotypes and a
50% reduction in Salmonella B serotypes.
So again, limited data confirms there
were better reductions in Salmonella B
serotypes when broilers are vaccinated.
Investigators did not see much Group D.
S A N D E R
What do you recommend based on these studies regarding vaccination of broilers? C O O K S O N
There aren’t enough numbers to make
firm conclusions. But we might infer that
if you’re in USDA’s Category 3 and that’s
driven by the presence of Salmonella
serotype C, then maybe you are willing
to spend more and vaccinate your
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B R O I L E R V A C C I N AT I O N T R I A L S
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broilers. You know, the earlier you can
intervene with a vaccine — like at the
hatchery — the better the chances are
for affecting change. P O W E L L
Do you find that vaccination works better
in a small-bird or big-bird program — or
any particular program?
C O O K S O N
There isn’t enough experience yet with
birds of different sizes, but investigators
did see reductions in medium- to large-
sized birds. In pen studies, they’ve also
seen reductions in birds anywhere from
7 to 8 weeks of age.
H O F A C R E
Research shows the live S. Typhimurium
vaccines do not give as much
cross protection against Salmonella C
serotypes as they do for the B and D
serotypes. If you’re in USDA’s Category 3
or are about to go there, using a live
Salmonella vaccine for a serogroup C may
not be as effective as for B or D serotypes.
Dr. Cookson, were one or two doses used
in the broiler trials you described?
C O O K S O N
Two doses. P O W E L L
Does anyone worry that use of a live
Salmonella vaccine will show up upon
testing at the processing plant?
O ’ C O N N O R
Brilliant question. We have seen it —
very, very rarely but we have seen it. But
I don’t see it enough for me to be alarmed
about it.
P R E H A R V E S T S A L M O N E L L A C O N T R O L
R A I S I N G T H E S T A N D A R D F O R S A F E P O U L T R Y
In most cases, levels of Salmonella in the plant are driven by S. Kentucky.
Not always, but if someone is in USDA’s Category 2, going into Category 3,
or the plant is solidly in Category 3, it’s often 80% S. Kentucky-driven.
Kalen Cookson, DVM
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S A N D E R
Let’s turn to assessing vaccine efficacy. How do each of you determine if a vaccine program is effective or not? P O W E L L
I have a burning question about
monitoring a vaccination program.
How do you measure the efficacy of
killed Salmonella vaccines, especially
the autogenous bacterins for breeders?
There are obviously ELISA tests, but
none are specific.
S T E W A R T B R O W N
We get three boot-sock samples in the
course of a breeder’s life. We’ve been
doing this for about 10 years. One of the
sample sets is for pullets and two are for
hens. We get a yes/no associated with
those boot socks for Salmonella serotypes
B and D, and there’s another general
category for anything else. You put the
results on a graph and look at it monthly.
Over time, you tweak your vaccine and
watch that number. We’ve had some
cases where it moved, based on what
we believed was associated with a bad
decision in the vaccination approach.
And vice-versa. With this approach, we’ve
had a lot of success getting the
Salmonella prevalence down. But, of
course, we also worked on rodent control
and other Salmonella-control measures. P O W E L L
So you’re not measuring titers and the
vaccine efficacy itself?
H O F A C R E
No one has shown that there is a
correlation between an ELISA titer and
protection. Dr. Stewart-Brown is watching
the prevalence of Salmonella in breeders,
which will eventually show up in the
processing plant. That’s a very effective
way to monitor.
P O W E L L
What should the proportions be if
there are multiple serotypes in an
autogenous vaccine?
H O F A C R E
There’s no science.
P O W E L L
Exactly! I think such studies have merit! H O F A C R E
If you have a problem serotype you’re
most concerned about, then I would
make an autogenous vaccine for that
problem serotype. If you have two or
three problem serotypes, I would use a
vaccine for those. But I don’t like to put
more than three serotypes in a vaccine
because it’s diluting out the effectiveness.
I worked for more than 10 years trying
to use Salmonella killed vaccines
for S. Kentucky, and we were not as
successful as we had been with
autogenous S. Enteritidis or S.Heidelberg
vaccines, so this strategy may not work
as well for every Salmonella serotype.
But on S. Heidelberg, S. Enteritidis and
S. Typhimurium, they'll be fairly effective.
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No one has shown that there is a correlation between an ELISA titer and
protection. Dr. Stewart-Brown is watching the prevalence of Salmonella
in breeders, which will eventually show up in the processing plant.
That’s a very effective way to monitor. Charles Hofacre, DVM, PhD
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S A N D E R
Dr. Powell, can you tell us more about the relationship between coccidiosis and Salmonella? P O W E L L
Coccidiosis can change the gut
microflora in such a way that Salmonella
will colonize or amplify in the GI tract.
Specifically, beneficial microflora, such
as lactobacillus, decline in numbers, and
pathogenic opportunistic microflora, such
as clostridium, will proliferate.
By monitoring coccidiosis with oocyst
numbers (oocysts per gram), gross or
microscopic lesions, and with polymerase
chain reaction (PCR) to quantitate
clostridial levels in the lower intestinal
tract, I have found these numbers peak in
broiler flocks on built-up litter between
14 to 21 days of age. In antibiotic-free
production systems with total cleanouts,
you tend to see coccidial challenges later
— between 28 to 35 days of age.
To me, from a gut-health standpoint,
focusing on these times of prevalent
coccidial activity would have merit for
controlling Salmonella. S A N D E R
Do you see a difference in Salmonella
counts at processing in larger birds since they have more time to recover from a coccidial challenge compared to smaller birds? S T A Y E R
We have big and bigger chickens. We
don’t have small chickens, so we don’t
really see a difference in our Salmonella
counts relative to size. We do see
different results post-processing from
production units within 30 miles of each
other, which is probably related more to
processing-plant interventions than it
is to grow-out conditions.
D A L E
We have chickens of all sizes. We don’t
see a difference either based on cocci
cycling levels or bird size as much as a
noticeable geographic difference, as
Dr. Stayer mentioned. Whether there’s a
difference due to bird size or Eimeria
maxima, scores would be very difficult
to differentiate just because of all the
other variables — house management,
biosecurity, litter quality, the breeder
vaccination program, etc. P O W E L L
You’ve got to control coccidiosis
whether that’s in the pullet, breeder or
broiler house. A producer could have an
undetectable level of Salmonella and
then coccidiosis cycles and amplifies it.
You drop the ball on gut health, and
Salmonella is in every chicken. This is why
I focus much of the Salmonella-control
efforts on gut health.
With poor pullet immunity against
coccidiosis, it is possible to have breaks
upon the move to the breeder house,
and it wouldn’t be unusual to isolate
Salmonella in a breeder flock after that.
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A producer could have an undetectable level of Salmonella and then
coccidiosis cycles and amplifies it. You drop the ball on gut health and
Salmonella is in every chicken. This is why I focus much of the Salmonella-
control efforts on gut health. Ken Powell, DVM
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S A N D E R
Since litter quality is important for controlling coccidiosis and coccidiosis may be linked to Salmonella, would you say better litter management will help minimize Salmonella? S T E W A R T B R O W N
My favorite live-side intervention right
now is good paw health. It sounds bizarre.
But if you can have consistently good paw
health, you generally have pretty dry litter.
If you have pretty dry litter, you did a good
thing for food safety and for generally
containing bacterial contamination. Our
quantitative assessment of Salmonella
loads coming into the plant shows that
complexes with the best feet generally
have a lower Salmonella prevalence over
time. Concentrating on feet is a great
thing for animal health and for food safety.
S A N D E R
What you’re saying supports research from Mississippi State University that showed chicken feathers and feet are primary Salmonella vectors.
S T A Y E R
The point made about good paw quality
is valid since good paw health can reflect
litter dryness. But quite honestly, in our
experience, we have not seen a linkage
between paw quality — as a reflection
of litter quality — and Salmonella
at processing.
H O F A C R E
We’ve conducted several studies over
the years where we’ve looked at the
prevalence of Salmonella and
Campylobacter in broiler houses. If you
walk along the sidewall where it’s nice
and dry, you are less likely to isolate them.
If you walk in between the feeders and
drinker lines, where there’s more moisture,
you’re more apt to find Salmonella and
Campylobacter if they are in the house.
Research by Ed Mallinson 20-plus years
ago demonstrated that water activity in
the litter allows Salmonella to survive or
even multiply.
C O O K S O N
I agree that Salmonella prevalence can
relate to paw quality and litter dryness,
which we’ve sometimes seen in field
trials we’ve conducted. Prevalence can
sometimes trend up through the course
of a 14- to16-week study while other times
it may trend down, depending on whether
you’re coming into winter or summer.
Ventilation rates and litter quality are
much improved throughout most of the
country during summertime.
In Colorado, where the air is dry, we
conducted the same exact type of
Salmonella study 2 years in a row.
The first time we got a much higher
prevalence of Salmonella. The second
time we tried to keep all variables the
same, but as it turned out, the types of
pens were not exactly the same. The first
study with higher Salmonella prevalence
used solid plastic wall dividers between
pens while the second study divided
pens using mesh netting. I think that one
variable could have affected the difference
in Salmonella prevalence, with the
ventilation being better in pens with
netting so the litter dried more.
continued
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The point made about good paw quality is valid since good paw health can
reflect litter dryness. But quite honestly, in our experience, we have not seen
a linkage between paw quality — as a reflection of litter quality — and
Salmonella at processing. Phil Stayer, DVM
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I believe gut health can also affect the
prevalence of Salmonella by indirectly
affecting litter moisture. If birds have
coccidiosis and develop enteritis, for
instance, they’re going to put a lot more
moisture back into the litter, so it’s a
vicious cycle. O ’ C O N N O R
I totally agree. Enteritis goes along with
coccidiosis. I see an absolute trend upward
during January and February, which in
California are wet months. Then we hit a
very nice trough through summer, and
then interestingly, the prevalence starts to
go up again in August. Why does it go up
in August, when it’s very hot and dry?
Because that’s when we’re misting and
putting a lot of moisture into the air,
which drops on litter.
I M PA C T O F L I T T E R Q U A L I T Y
I totally agree. Enteritis goes along with coccidiosis.
I see an absolute trend upward during January and
February, which in California are wet months.
Robert O’Connor, DVM
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What about water acidification? Can it reduce the prevalence of Salmonella? S T A Y E R
We’ve tried water acidification.
Sometimes you get promising results
and sometimes not. It really depends on
where you start — where your water
pH is to begin with. It’s not consistent.
H O F A C R E
I believe one of the biggest reasons for
inconsistent results with acidification is
the pH of the water to start with, which
can vary widely between neighboring
farms. I’ve conducted studies with water
acidifiers and they work really well, but
the pH and hardness of the water need to
be tested before determining what dose
or use rate to use.
D A L E
We’ve run a lot of trials with acidification,
waterline sanitation or probiotics, and that
silver bullet does not seem to be out there
yet. Nothing is consistently effective in
every location. Part of the issue with that
is having assays that can consistently and
accurately monitor the impact.
?
W AT E R A C I D I F I C AT I O N
We’ve tried water acidification. Sometimes you get
promising results and sometimes not.
Phil Stayer, DVM“ ”
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S A N D E R
How do you measure the efficacy of your Salmonella-control efforts, whether it’s vaccination or in-house interventions? What tools do you use? O ’ C O N N O R
On the live side, we use boot socks. But
I can’t tell you why a particular region or
complex almost always runs a lower
prevalence. What I’m really looking for are
trends. If they’re normally averaging about
40% and I see them creeping up to 60%,
70%, then I think, okay, we’ve got a
problem on the live side.
We consistently use boot socks on every
farm before it processes. We do it within
2 weeks of processing. There’s probably
some inconsistency in compliance to
the protocol for sampling, but again, I’m
looking for overall trends, not results at
a specific farm.
C O O K S O N
You mentioned 2 weeks prior to
slaughter? I'm curious. Is there an ideal
time to gauge that level of Salmonella?
O ’ C O N N O R
Yes, it’s within 2 weeks of processing.
Most of us see Salmonella as an
intermittently shed bacteria, and birds
shed the most during stressful periods.
In a broiler’s life, I’d say those last 2 weeks
are going to be some of the most
competitive, stressful periods of their lives,
so that’s when we test for Salmonella.
C O O K S O N
Do you try to avoid the last 2 or 3 days
before processing?
O ’ C O N N O R
The house is denser closer to processing,
which makes it harder to get four boot
socks through the house. Again, I’m
not reacting to the boot-sock results;
I’m looking at aggregated information
and trends, not the results from one
individual farm.
H O F A C R E
In a study Roy Berghaus and I conducted
several years ago,1 we evaluated whether
boot socks or drag swabs for Salmonella
correlated to the level coming into the
plant. We looked at 3 weeks, 2 weeks and
the week the birds were processed. Only
the week the birds were processed did
the results correlate to whole birds with
feathers on rinse, so you won’t have the
culture results in time to do much about it.
D A L E
There are a few companies working
on more rapid-turnaround diagnostics
that might enable us to implement
interventions. But currently, I think drag
swabs have value, especially if you’re
looking at overall trends.
For monitoring our overall Salmonella-
control program, I still look to the overall
Enterobacteriaceae count and the
Salmonella prevalence at rehang because
that’s as close as I can get to what we’re
bringing in from the field. There’s the
stress of catching and transport, but
ultimately it’s what’s coming in the door
of your plant.
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S A N D E R
Other than boot-sock sampling and environmental testing, are there any other diagnostics used to monitor Salmonella in flocks, whether that’s for breeders or broilers? D A L E
Boot socks are of limited value. You can
pick up Salmonella with boot socks but
it’s a lot easier to test, for example,
hatch-tray residue swabs or even chick
papers. There are other sampling
methods if it’s coming out of your
breeder-source flock.
S T E W A R T B R O W N
We have been trying to work on an
“organic load” metric. These could be
super practical and simple but important
metrics — are the birds coming in clean
or not? We also have camera monitoring
in our processing plants now to judge
feather cleanliness and paw health at
the farm level. This results in a soiled-
feather score and a paw-health score.
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In a broiler’s life, I’d say those last 2 weeks are going to be some of the
most competitive, stressful periods of their lives, so that’s when we
test for Salmonella. Robert O’Connor, DVM“ ”
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1 Berghaus RD, et al. Enumeration of Salmonella and Campylobacter spp. in environmental farm samples and processing plant carcass rinses from commercial broiler chicken flocks. Appl Environ Microbiol. 2013 Jul;79(13):4106-14.
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S A N D E R
We need to address the impact of feed withdrawal. How does the timing of feed withdrawal affect the prevalence of Salmonella going into the processing plant? O ’ C O N N O R
I don’t think the 8 to 12 hours of feed
withdrawal prior to processing has
changed. But the longer birds are off the
feed, the more issues you’re probably
going to have with gut upset. You’re going
to stress them out, and they’ll shed more
Salmonella in the litter right before they’re
to be picked up.
S T E W A R T B R O W N
I agree. But there are all kinds of other
variables at play. If we get feed withdrawal
down to 6 hours, there’s no certainty
that would help reduce the prevalence of
Salmonella going into the plant.
S A N D E R
Let’s elaborate on that point because transport to processing is a big stressor for poultry and may be associated with a bigger Salmonella load going into the plant. P O W E L L
We have those concerns when we move
breeders. If it’s a rainy day or a cold day,
you can do things like cover the transport
trailer. If we’re concerned about gut health
in stressed pullets that we’re moving to
a breeder house, we use a program with
an organic acid and probiotic, often
administered simultaneously in water.
We try to preempt stresses that affect
enteric health.
S T E W A R T B R O W N
We’re looking at a new transport module
and transport system. We believe we’ll
see a significant benefit with new trailers
designed to give birds a higher level of
comfort during transport.
We also have installed a newer, full
live-haul trailer-module sanitation system.
Trailers as well as modules are fully
sanitized. The transport vehicles have
tops; the ceiling goes up and the transport
modules go on, then the ceiling comes
down. That helps with air flow. There
are also curtains. I’m excited by these
developments. These things are associated
with improved bird comfort, but I’ll be
interested to see if we get improved food
safety too.
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If we’re concerned about gut health in stressed pullets that we’re moving to
a breeder house, we use a program with an organic acid and probiotic, often
administered simultaneously in water. We try to preempt stresses that
affect enteric health. Ken Powell, DVM
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S A N D E R
Reports are mixed on the prevalence of Salmonella in poultry meat from antibiotic-free and conventional production systems. What’s been your experience with the Salmonella prevalence in flocks raised without antibiotics? S T E W A R T B R O W N
We started in 2002 moving to “no
antibiotics ever” (NAE) production in
every one of our 12 facilities. As we
progressed with the NAE program
and charted the percent positive for
Salmonellas, they were inversely
related.In other words, as NAE came in,
Salmonella came down. I’m not necessarily
attributing that to the NAE program
because we were doing a million other
things, which, by the way, I think you do
need to do.
All the breeder work had to be done
ahead of time, and that still goes on.
Gut health is really important for a million
different reasons. Gut health remains
really important not just for feed efficiency
and livability but for the food-safety
component. If you plotted our livability to
percent NAE, livability has gotten better
the last several years. But again, that’s
associated with working every aspect of
the program.
S A N D E R
Can others who have experience with both NAE and conventional flocks comment? D A L E
I can’t say that in our flocks I’ve found as
strong a consistent correlation between
NAE production and a reduced Salmonella
prevalence as Dr. Stewart-Brown has
seen. I do think that since the removal of
gentamicin from hatcheries, the industry
has seen a trend.
There are presentations at the conference
showing the difference in Salmonella loads
between NAE-type programs and in flocks
receiving BMD® after a necrotic enteritis
(NE) challenge. There are tangential or
ancillary facts associated with removing
antibiotics, but they may be related to
other health or disease conditions.
H O F A C R E
Salmonella lives primarily in the ceca. NE
occurs primarily in the small intestine. In
challenge studies where you create NE
and give Salmonella, you don’t see more
Salmonella with NE.
But when you look at what happens with
an NE flock, you get uniformity issues.
You have small birds and big birds, and
those small birds are more prone to
having crops and intestines torn, resulting
in more contamination on the carcass.
I think indirectly there’s a link for NE (gut
disease) to contribute to Salmonella, but
as Dr. Stewart-Brown said, once you learn
to control those variables and reduce your
gut-health issues, you don’t have as much
impact when you take out gentamicin.
There are ways to keep the bugs that
maintain gut health happy. The simplest
way is with an antibiotic. The more
continued
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There are ways to keep the bugs that maintain gut health happy. The
simplest way is with an antibiotic. The more expensive way to do it is
without an antibiotic, and you’re going to have to do a lot of other
things to accomplish that. Charles Hofacre, DVM, PhD
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expensive way to do it is without an
antibiotic, and you’re going to have to do
a lot of other things to accomplish that. O ’ C O N N O R We have organic flocks. We have NAE
flocks. We have conventional flocks. It
depends on who you ask and who’s giving
the answer and their biases. I don’t believe
NAE flocks are necessarily more prone to
being Salmonella-positive. And I definitely
don’t believe that if positive, they’re more
prone to have a serotype of human-health
concern. I think you’d really have to study
the data before you answer that question.
D A L E I’ll agree with that. I don’t think the hard
data is there to say one way or the other
from what we’ve seen.
O ’ C O N N O R I think there is an impact on Salmonella
prevalence in preharvest organic
production due to the restrictions on
disinfectants. If I run a probiotic, the inert
materials in it have to be organic. You are
limited more on the interventions you
can use.
S A L M O N E L L A P R E V A L E N C E I N N A E F L O C K S
I don’t believe NAE flocks are necessarily more prone to
being Salmonella-positive. And I definitely don’t believe
that if positive, they’re more prone to have a serotype of
human-health concern. Robert O’Connor, DVM
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S A N D E R
Let’s shift gears and address regulatory issues. As you know, FSIS plans to publish results of Salmonella testing for chicken parts as well as carcasses. Will this put added pressure on producers to intensify preharvest Salmonella-control programs and will it affect their relationship with their customers? O ’ C O N N O R
What they’re intending to do by
publishing results is motivate processors
to hit the standard.
S T A Y E R
If you’re in a category where you
don’t want to be, you’re going to do
everything. Then when you get where
you want to be, you’ll back down.
D A L E
I’ll echo that. You’re going to initiate a lot
of the interventions we’ve touched on and
you’re going to do more of it. The other
thing that hopefully will help us keep
moving forward will be development of
more precise assays for monitoring and
determining the impact of the different
interventions we use.
S A N D E R
Is it true that some vendor contracts specify that all their products must be sourced from Category 1 and 2 processing plants? S T E W A R T B R O W N
Sure. That’s in a number of purchasing
contracts for raw materials, generally,
based on the contracts I’ve seen.
O ’ C O N N O R
So far, I don’t feel there’s been much
customer scrutiny based on publication of
carcass findings. It’ll be interesting to see
how customers respond to publication of
results with parts.
S A N D E R
Given all the new interventions the industry has put into place, do you think we’re making progress regarding control of foodborne Salmonella?
D A L E
I have the most recent government
data here, which says that 98.5% of all
whole-chicken tests for Salmonella are
negative. That’s from large plants. Chicken
producers have reduced Salmonella in
whole chickens 66% over the past 5 years.
Those aren’t my numbers. That’s what the
government says we are doing, which is
very encouraging.
I don’t know if there’s a direct correlation
there to human cases of Salmonella,
and we’re not the only source for
those infections. But according to the
government’s own data, we are
making progress.
S A N D E R
Would you all get out your crystal ball and tell us where you think the industry will be in 5, 10 or even 15 years from now regarding Salmonella
prevention and control? D A L E
One of the most exciting aspects of this
industry for me as a veterinarian, and one
of the most enduring characteristics, is
that we have a very adaptable, progressive
industry. We’ll probably continue to
reduce Salmonella levels and maybe even
surpass what we previously thought was
impossible. Part of how we’ll be able to
do that is through better science — better
diagnostics and monitoring and hopefully
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R E G U L AT O R Y C O N C E R N S
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with better vaccines as well. It’s yet to be
determined exactly which interventions
will turn out to be the best.
S T A Y E R I’d agree. Technologies need to be in
place, and I don’t think we’ve yet figured
out which are the best interventions apart
from basic good management practices.
S T E W A R T B R O W N
I also agree with Dr. Dale, especially when
Salmonella and food-safety metrics start
to be managed like production metrics.
The industry once focused on production
management and has done a phenomenal
job. The more difficult task will be
applying that metric to Salmonella control
at the farm level, but once that’s done,
I think we’ll be amazed at what we can do.
H O F A C R E
Dr. Stewart-Brown and I can remember
the day when we didn’t have ELISA
testing, when it became routinely
available, and it changed the way we
actually established vaccination
programs once we could test, measure
and verify effectiveness.
There are a lot of companies really
pushing forward to find new ways for us
to test for Salmonella on the live side.
Once we have those tests, we’ll have the
opportunity to make more progress on
specific farms. I believe that new testing
methods will be one of the keys for
progress in the future. O ’ C O N N O R
Plus/minus is my prognosis. I’ve observed
that larger companies are being very
proactive. They’re moving ahead with
interventions. They’re trying to get things
in place, for instance, to meet the
standard. I see smaller companies that
want the parts standard eliminated, and
they are asking basic questions about
interventions. Based on my experience in
the industry, we’re sometimes better at
being reactive than proactive, but when
we get into a crisis — which might occur
if companies have trouble meeting the
parts standards — we are really good at
being reactive. I guess that’s my prognosis
for the next 5 years.
S A N D E R
Thanks to all of you for sharing an unbelievable amount of information and providing insights that will help the industry improve food safety and feed the world with an abundant and wholesome product. I’m proud to be a part of this industry.
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P R E H A R V E S T S A L M O N E L L A C O N T R O L
R A I S I N G T H E S T A N D A R D F O R S A F E P O U L T R Y
We’ll probably continue to reduce Salmonella levels and maybe even
surpass what we previously thought was impossible. Part of how we’ll be able
to do that is through better science — better diagnostics and monitoring and
hopefully with better vaccines as well. Elizabeth Dale, DVM
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