EMERGING
INFECTIOUS DISEASES
Lecture 10
or
Intensive Poultry Production Systems
Click
here for selected PowerPoint slides
Picture
a Formula-one race car, the epitome of driving machines, capable of traveling
at incredible speeds. All it needs for
peak performance is an expert driver, expert maintenance, plenty of fuel, and a
smooth track. Now picture 12,000 of them
all racing around the “Old Brickyard” at 200 mph. Throw in some rain, a little moisture in the fuel mix, or a leaky
master cylinder and the result can be a disaster.
In
essence, that’s what we’ve done over the past 50 years, through aggressive
genetic selection. We have produced a
bird that is a highly specialized, finely tuned, protein producing machine
capable of great performance under a narrow set of conditions e.g., the right
feed, in the right environment, good immunity, and minimal exposure to disease
causing agents.
But
the reality is that such conditions rarely exist or they are transient at best,
in most turkey growout operations. That’s why raising healthy poultry is just
plain difficult. It’s also why figuring out disease problems on some farms is
no longer a matter of simple cause and effect.
The
purpose of this lecture is to provide an integrated view of how multiple
factors can interact to produce disease.
Identifying the various factors and understanding their relationship to
one another is essential to solving the complex health problems which qualify
as emerging infectious diseases of poultry.
It
is clear that genetic selection for performance traits has a negative effect on
immunocompetence. Chickens selected for a low antibody response to sheep red
blood cells (SRBC) have higher body weights as juveniles and better feed
efficiency than those selected for a high antibody response (1, 2,). Therefore
it’s not surprising that birds specifically bred for high body weight have
lower antibody titers to SRBC than those bred for low body weight (3). Indeed,
a genetic constitution favoring performance over antibody production appears to
increase susceptibility to mycoplasmal, viral, protozoal, and ectoparasitic
diseases (4). It has been suggested that the basis for this effect may be a
deliberate reallocation of physiologic resources towards production and away
from immune function (1, 5). In such
birds the standing levels of defense are lower and less “machinery” is dedicated
to meeting defense needs at the time a disease challenge occurs. In essence, the bird is genetically “tooled”
for growth and not biological warfare.
Resources can be reallocated, but often the response may be too little,
too late.
Figure 1. (see attached Powerpoint file)
is a schematic representation of what happens in birds programmed for “growth”.
Defenses are marginally ready in the event of a viral challenge. If the
challenge is mild, the bird will manage the “invasion” with little disruption of
the normal flow of resources. But if
the challenge is more than standing defenses can handle, a shift in the flow of
resources must occur if the bird is going to survive. This shift can be great enough to cause a reduction in growth,
activity, and bacterial defenses. However, the flow towards maintenance, e.g.,
“keeping the boiler running”, must be uninterrupted or else death will
occur. At this point, secondary
bacterial infections can become a problem. Organisms like E. coli are usually waiting in the wings for a chance like
this. So the battle begins on a second
front. If the struggle goes on long
enough, you can forget “production”. A
bird in this state is just trying to
survive. Ultimately, it’s a matter of
how long the resources will hold out. Once the bird starts dipping into its allocation for maintence,
the war is over, and the enemy doesn’t take prisoners.
Depending
on the distribution of such birds in a population, the effect on a flock can be
more or less devastating. Individuals
near the center of the “genetic” distribution e.g., the average poult, may
be able to grow and handle disease
better than those at either extreme.
Most of us have seen this effect first hand: the best growing birds are
the first to die and the runts live forever.
Nutrition has a lot to do with whether a
bird will be able to handle a disease challenge. The quantity and quality of
nutrients in feed as well as the pattern of feeding can affect health.
A good example of this would be the
occurrence of necrotic enteritis in broiler chickens. Often feed milling
operations will substitute wheat for corn because the price is better. What may
seem to be a subtle change in formulation can affect the gastrointestinal tract
dramatically. In response to the variation in carbohydrate, the microfloral
balance within the GI tract may shift in favor of Clostridia. Toxin production associated with this overgrowth can
result in the development of necrotic plaques in the mucosa.
Obviously
the microbial ecology of the GI tract is more complicated than this.
Theoretically, an overgrowth of one species of bacteria or its disappearence,
can have a ripple effect involving a multitude of interdependent organisms, not
only other bacteria but viruses, fungi, protozoa, and nematodes. An example of
this type of intricate interdependence can be found in the way dietary fiber
effects susceptibility to coronavirus infection in turkeys. Fiber is fermented
by bacterial organisms; the bi-products of this fermentation include short chain
fatty acids (SCFA’s). These SCFA’s are utilized by enterocytes as an energy
source. The availability of this energy source stimulates enterocyte
differentiation and maturation. As cells differentiate and mature, they express
receptors necessary for coronavirus target recognition. The result is increased
susceptibility to coronavirus infection.
It’s not just the addition of nutrients to the diet that can alter
the response to disease. What happens when you remove feed and water for 48
hours? You will see a decrease in the relative weights of lymphoid organs e.g.,
bursa and thymus, (6) and an increase in the ratio of circulating heterophils
to lymphocytes (7). Such changes may be the result of “perceived stress” and
not necessarily a “nutritional deficiency” but this type of physiological
response is associated with an increase in susceptibility to viral
diseases. Normally, commercial birds
would never go this long without feed in the field. But what happens when a feed delivery get messed up or when there
is feed refusal due to the presence of an unpalatable substance in the
feed? How long do birds go without feed
and water when they are moved to new surroundings i.e., from brooder to
finisher; or in the case of breeders, at the time of dark out or molting? What happens when you change from crumble to
a full pellet? What happens when water is unavailable or when it is less
palatable due to medications or contaminants? The bottom-line is that the bird
mounts a physiologic response to cope with what is perceived as an abnormal
situation. That response has short-term benefits but if there are pathogens
present in the environment, it may be just the opportunity they’ve waited for.
Nutrition is important in
determining what resources will be available to help withstand a disease
challenge (5). Diets conducive to growth in certain selected lines of broilers
actually seem to decrease their resistance to E. coli challenge (8,9) and those that contain increased levels of
animal protein seem to increase resistance to E. coli. (10).
Without question, relative
deficiencies in certain vitamins and minerals can have an effect on disease
resistance. The term relative is important here because genetic make-up is
without a doubt more important than the NRC in determining what a bird needs.
Using the same old vitamin-mineral premix in the same old amounts may not be
sufficient for this year’s genetic stock. For example, a relative deficiency in
vitamin A may compromise immunity by allowing a premature degeneration and reduced
turnover of epithelial cells which serve as one of the primary barriers to
invasion by pathogenic organisms (11). Antibody responses to Salmonella (12) and Newcastle disease
virus (13) are also reduced in cases of vitamin A deficiency. Likewise, diets relatively low in vitamin E
and selenium can also result in epithelial degeneration (14) and decreased
humoral (15) responses.
There are lots of other
examples but what’s important to remember is this: that form, content, quality,
and availability of nutrients including water can affect the ability of a bird
to successfully respond to a disease challenge either directly or indirectly.
The resource allocation model also applies here e.g., if the right nutrients
aren’t there in the right amounts, then they can’t be “rightly” allocated.
MANAGEMENT
One of the more prominent
interactions that influence the outcome of disease challenge is the environment
in which the birds are raised. Here too, there are direct and indirect affects.
Let’s use litter conditions
as an example. When litter moisture is high, molds and bacteria proliferate,
and viruses are preserved. Many of the species of bacteria present in the
litter produce ammonia as a metabolic by-product. High levels of atmospheric
ammonia reduce the trachea’s resistance
to infection with Newcastle disease virus (16,17) and impair the ability of the
mucociliary apparatus to clear the respiratory tract of bacterial pathogens like E. coli (18). In this situation our natural response as a flock manager would
be to dry the litter out. The problem
at this point is that molds depend on the drying process to disseminate their
spores. Also, if drying out the litter is taken too far, dust levels will
increase and resistance to Newcastle and E.
coli (17, 19) will be impaired once again. So we go from one extreme where
bacterial and viral numbers are high and resistance is diminished, through the
drying process where mold spore counts increase, to the other extreme where
dust does a number on the respiratory tract. The only way to avoid this
situation is vigilant, intensive,
management of the litter. Once
the litter get screwed up it’s almost too late.
Stress is the other factor
that’s important. Birds are without a
doubt, creatures of habit. Therefore, changes in the environment, adverse
conditions, noxious stimuli, and any other real or perceived threat to
“homeostasis” a.k.a. the “status quo”, may be considered stressors. Examples
would be things like bad litter conditions, equipment failures, re-assortment
of the pecking order following moving, abusive flock managers, and loud
unfamiliar noises. What may be considered a stressor in one situation may be of
no consequence in another due to the presence of modifiers such as
the severity of the stimuli, its duration, novelty, and genetic
variability within the flock (20, 21). Also important is the perception of
stress, that is to say, the amount of change detected between the current
circumstances and the new set of circumstances will determine how stressful the
new circumstances seem (22). Obviously,
birds are able physiologically to adjust to stressful situations but the
adjustment is often, albeit temporarily, at the expense of the immune system.
That’s where the problem occurs especially if a viral or mycoplasmal challenge
is looming (23). Once these pathogens get a foot-hold, bacteria like E. coli aren’t usually far behind (see
Fig. 1).
VACCINATION
As if things weren’t
complicated enough, we try to provide protection from commonly encountered
pathogens by introducing flocks to their less pathogenic (modified-live,
avirulent) cousins. At least that’s how birds see it immunologically.
For example, turkeys may be
vaccinated with an “avirulent” (live) strain of hemorrhagic enteritis virus
(HEV) or they may encounter a “virulent” field strain. Regardless of what they encounter, they
perceive it as a “viral death threat”. Its only after the infection gets
rolling that they make the unconscious decision to commit more or less of their
resources to defeat the enemy. This is
based on the magnitude of the initial antigenic exposure and the amount of
replication taking place. In the process of waging war to over-power the
organisms, they develop an immunological arsenal, cellular and humoral, that
can be used the next time this enemy or its cousin shows up. Their
immunological response may also have a “downside”as is the case with HEV. Where
the immune system’s attempt to limit the number of lymphocytic target cells
results in transient immunosuppression.
We can also hit birds too
hard or with too many things at once. Case in point: if you spray vaccinate
turkeys with B1 Newcastle, followed a week later by hemorrhagic enteritis virus
vaccine (HEV) in the water, the combined effect will open the birds up to the development
of colibacillosis (24). Part of this has to do with allocation of resources
e.g., the bird gears for a viral defense at the expense of bacterial defenses.
The other is a direct immunsuppressive effect of HEV on the immune system where
it replicates (25).
If everything else is OK
e.g., genetics, nutrition, management, minimal exposure to potential pathogens,
then the response to vaccination will be appropriate and protection will be
afforded. However, if these other factors are less than optimal, not only will
the response to vaccination be poor but the birds might actually get sick.. Try
spray vaccinating for Newcastle in a house where there is an ammonia problem or
where a low grade, subclinical, “nobody knew it was there”, Bordetella infection is simmering.
(NEW?) EMERGING, MULTIFACTORIAL, INFECTIOUS DISEASES OF POULTRY
“One agent-one disease” sure sounds nice, but it’s an archaic
axiom when it comes to today’s
intensive animal production systems. Diseases like viscerotrophic velogenic Newcastle
disease and highly pathogenic avian influenza still occur, but rarely. More and
more we’re seeing problems like Poult Enteritis Mortality Syndrome (PEMS) and
Respiratory Complex that defy elucidation by standard means i.e., Koch’s
postulates. These are representative of what I believe could be considered
“emerging diseases”.
PEMS is clinically
characterized by diarrhea, mortality (> 1% daily for 3 days and/or > 9%
total), and subsequent uneveness among young turkey poults. During an outbreak of PEMS, you may isolate
corona, astro, rota, and/or enteroviruses from affected flocks, as well as E. coli, Salmonella, Clostridia, Candida, Cochlosoma, Hexamita, and Trichomonas. Purifying the individual
agents and introducing them into naïve birds will produce varying levels of
clinical disease but not necessarily the entire syndrome. The clinical
presentation can also be altered by “non-infectious” factors as previously
described.
Is PEMS a “new” disease
caused by a yet undiscovered organism? Probably not. It is more likely a
combination of old agents interacting in a new way under a new set of
circumstances. The same can be said of Respiratory Complex which was once
thought to be just the result of a sequential infection with Mycoplasma and E. coli. Today, not only has the list of potential etiologies
grown, but respiratory complex is now considered to be more of a cascade of
events which begins with physiologic/immunologic predisposition to infection,
gains momentum from exposure to a variety of respiratory and non-respiratory
agents, and culminates in death due to overwhelming infection with
opportunists. Even organisms once
thought to be “non-pathogenic” appear to be able to get into the act.
As H.J. Barnes would say
(personal comm), the emerging infectious diseases of poultry are the result of
“too much of a good thing”. Or to put another way, they’re like the “Perfect
Storm” e.g., the right agents unwittingly brought together under the right
conditions, feeding off each other to produce devastation. In essence they are
a pestilence of our own making.
POSTLOGUE
Field experience tells us
that we have entered an era when the standard approach of vaccination and
medication either won’t continue to work or won’t be available. More and more
we are seeing sick flocks where fresh water, fresh feed, fresh air and warmth
are the only things that seem to be of any benefit. And, although we may be
able identify the etiologies for such problems as PEMS and Respiratory Complex,
my suspicion is that we will never be able to solve them unless we are willing
take a hard, repentant look at how we
breed, feed, and raise birds.
1. “Production
Diseases” are essentially “a new twist on an old idea”. They often involve
well-understood infectious agents. The “new twist” is that these “well”
defined agents, when brought together in intensive animal rearing systems,
produce syndromes for which cause and effect are difficult to establish.
The major reason for this difficulty is the sizeable number of potential
interactions that can contribute the development of clinical disease.
All of the following are examples
of such interactions EXCEPT:
a. Genetic
selection for performance traits has had a negative effect on immunocompetence,
rendering commercial poultry more susceptible to certain diseases.
b. Due
to the use of “least cost formulation”, the nutrient makeup of commercial
rations can change abruptly. This can cause shifts in the microbial ecology of
the gastrointestinal tract, which in turn can foster the overgrowth of
potential pathogens.
c. Environmental
stressors like chilling generally make birds less susceptible to viral
infection and subsequently more susceptible to secondary bacterial infections.
2. All of the following are true regarding the “Resource Allocation” model EXCEPT:
a. Bacterial
and viral defense mechanisms place different and potentially competing demands
on the resource pool.
b. Performance
characteristics like growth and reproduction are physiologically expensive and
with regard to short-term survival, expendable.
c. The
Resource Allocation model is applicable to chronic, acute, and peracute
diseases of an infectious nature.
3. Treatment, control, and prevention of disease in an intensive production setting requires that the diagnostician do all of the following EXCEPT:
a. Think
multifactorial
b. Develop
and implement a diagnostic profile for known infectious agents including
serology, histopathology, isolation and identification
c. Vaccinate
for all potential pathogens when vaccines are available
4. All of the following are TRUE regarding the physiologic response to stress EXCEPT:
a. It
can result in decreased resistance to bacterial pathogens (short term).
b. It
can cause recrudescence of latent viral pathogens like adenoviruses.
c. It
can result in decreased resistance to viral pathogens.
1. Martin,
A., E.A. Dunnington, W.B. Gross, W.E. Briles, R.W. Briles, and P.B. Siegel, 1990. Production traits and alloantigen systems in
lines of chickens selected for low antiboody responses to sheep erythrocytes.
Poultry Sci. 69:871-878.
2. Siegel,
P.B., W.B. Gross, and J.A. Cherry, 1983. Correlated responses of chickens to
selection for production of antibody to sheep erythrocytes. Anim. Blood Groups
and Biochem. Genet. 13:291-297.
3. Gross,
W.B., and P.B. Siegel, 1988. Environment-genetic influences on
immunocompetence. J. Anim. Sci. 66:2091-2094.
4. Gross,
W.B., P.B. Siegel, R.W. Hall, C.H. Domermuth, and R.T. Dubose, 1980. Production and persistence of antibodies in
chickens to sheep erythrocytes. 2. Resistance to infectious diseases. Poultry
Sci. 59:20-210.
5. Gross,
W.B., and P.B. Siegel, 1997. Why some get sick. J. Appl. Poultry Res. 6:453-460.
6. Ben
Nathan, D., E.D. Heller, and M. Perek, 1977. The effect of starvation on
antibody production of chicks. Poultry Sci. 56:1468-1471.
7. Gross,
W.B., and P.B. Siegel, 1986. Effects of initial and second periods of fasting
on heterophil/lymphocyte ratios and body weight. Avian Dis. 30:345-346.
8. Cheville,
N.F., and L.H. Arp, 1978. Comparative pathologic findings of Escherichia coli infection in birds. J.
Am. Vet. Med. Assoc. 173:584-587.
9. Cloud,
S.S., J.K. Rosenberger, P.A. Fries, R.A. Wilson, and E.M. Odor, 1985. In vitro and in vivo characterization of avian Escherichia coli. I. Serotypes, metabolic activity, and antibiotic
sensitivity. Avian Dis. 29:1084-1093.
10. Gross,
W.B., 2000. Personal Communication.
11. Scott,
M.L., M.C. Nesheim, and R.J. Young, 1982. Nutrition of the chicken. Scott and
Associates, Ithaca, NY, pp. 143-147.
12. Panda, B.,
and G.F. Combs, 1963. Impaired antibody production in chicks fed diets low in
vitamin A, pantothenic acid or riboflavin. Proc. Soc. Exp. Biol. Med.
113:530-534.
13. Davis, C.Y.,
and J.L. Sell, 1989. Immunoglobulin concentrations in serum and tissues of
vitamin A deficient broiler chicks after Newcastle disease virus vaccination.
Poultry Sci. 68:136-144.
14. Marsh,
J.A., G.F. Combs, Jr., M.E. Whitacre, and R.R. Dietert, 1986. Effect of
selenium and vitamin E dietary deficiencies on chick lymphoid organ
development. Proc. Soc. Exp. Biol. Med. 182:425-436.
15. Marsh,
J.A., R.R. Dietert, and G.F. Combs, Jr., 1981. Influence of dietary selenium
and vitamin E on the humoral immune response of the chick. Proc. Soc. Exp.
Biol. Med. 166:228-236.
16. Anderson,
D.P., C.W. Beard, and R.P. Hansen, 1964. The adverse effects of ammonia on
chickens including resistance to infection with Newcastle disease virus. Avian
Dis. 8:369-379.
17. Anderson,
D.P., C.W. Beard, and R.P. Hansen, 1966. Influence of poultry house dust,
ammonia and carbondioxide on the resistance of chickens to Newcastle disease
virus. Avian Dis. 10:177-188.
18. Nagaraja,
K.V., D.A. Emery, K.A. Jordan, V. Sivanadan, J.A. Newman, and B.S. Pomeroy,
1984. Effect of ammonia on quantitative clearance of Escherichia coli from lungs, air sacs, and livers of turkeys
aerosol vaccinated against Escherichia
coli. Am. J. Vet. Res. 45:392-395.
19. Carson,
H.C., and G.R. Whenham, 1968. Coliform bacteria in chicken broiler house dust
and their possible relationship to colisepticemia. Avian Dis. 12:297-302.
20. Dohms,
J.E., and A. Metz, 1991. Stress mechanisms of immunosuppression. Vet Immunol.
Immunopath. 30:89-109.
21. Griffin,
J.F.T., 1989. Stress and immunity: a unifying concept. Vet. Immunol.
Immunopath. 20:263-312.
22. Gross,
W.B., 1984. Effect of a range of social stress severity on Escherichia coli challenge infection. Am. J. Vet. Res.
45:2074-2077.
23. Gross,
W.B., and G. Colmano, 1969. Effect of social isolation on resistance some
infectious agents. Poultry Sci. 48:514-520.
24. Pierson,
F.W., C.T. Larsen, and C.H.
Domermuth, 1996. The production of colibacillosis in turkeys following
sequential exposure to Newcastle disease virus or Bordetella avium, avirulent hemorrhagic enteritis virus, and Escherichia coli. Avian Dis 40:837-840.
25. Pierson,
F.W., and C.H. Domermuth, 1997.
Hemorrhagic enteritis, marble spleen disease, and related infections.
In: Diseases of Poultry, 10th ed., H.J. Barnes, ed., Iowa State University
Press, Ames, IA, 1997.