Strategies to Manage Wet Litter

Home > Discussion Forum and Q&A

Australian Veterinary Poultry Alliance Meeting

February 2007

Stephen R. Collett,

The University of Georgia, College of Veterinary Medicine,

Poultry Diagnostic and Research Centre, 953 College Station Road, Athens,

Georgia, 30602-4875, USA

Abstract

Poultry litter becomes wet when the rate of water addition (urine/faeces/spillage) exceeds the rate of removal (evaporation). Anti-nutritional factors, toxins, pathogens and nutrient imbalances may cause wet litter directly by altering normal digestive physiology or indirectly by disturbing normal gut ecology.

Poor quality ingredients and those with excess oligosaccharides or minerals can cause a nutritionally induced polydypsia, polyuria and diarrhoea which may increase water output sufficiently to cause wet litter. If the situation
persists for long enough the ensuing inflammatory response causes mild to severe gastro enteritis which further increases water output. The damage so caused to the cytoskeleton of the gastrointestinal tract reduces the surface area for nutrient absorption and allows the opportunity for pathogen proliferation, gut colonization and even invasion and systemic disease.

It is necessary to use an integrated and holistic approach in manipulating the microbial populations and host inflammatory response to managing the gut ecology. Antibiotics, enzymes, drinking water acidification, probiotics,
prebiotics, immune modulators and mycotoxin binders have all shown promise in this regard.

Seeding the gastro-intestinal tract with bacteria at hatch and subsequently managing the gastro-intestinal environment, whilst at the same time reducing anti-nutritional factors and the use of precision diet formulation has proved advantageous in minimising the incidence of wet litter in birds whilst maintaining and improving bird performance.

Introduction

Commercial poultry housing and management practices have been designed to keep birds within their comfort-zone at all times. Apart from satisfying the primary concern for bird welfare this also minimises homeostatic activity and ensures the most efficient partitioning of energy for production. Under these carefully controlled conditions water balance is kept positive (growth) or neutral.

Water balance is compromised in healthy animals when a dietary stress exceeds homeostatic mechanism capacity and in disease when the integrity and or function of the cells responsible for water/solute transport are adversely
affected. If under such circumstances urine and faecal water loss increases to the point where the rate of water addition to the litter exceeds the rate of removal, the litter moisture content rises until it exceeds desirable levels
(25%) and at this point it is deemed “wet”.

Apart from being an indicator of gastrointestinal upset and feed conversion inefficiencies, wet litter also creates unfavourable house environment conditions.

Water Balance

Water movement across a biological membrane is solute concentration dependent and in living organisms; water balance is controlled by a combination of active and passive solute transfer, a process referred to as osmoregulation.
Since water is the biological transport medium for nutrient absorption and waste excretion, water balance is governed by solute and water movement across the gastrointestinal and renal tubule cytoskeleton.

Water balance is a crucial part of homeostasis and it involves equilibrating intake and synthesis (metabolic water) with excretion via the kidney (urine) and gastrointestinal tract (faeces) and insensible loss via the skin and
respiratory tract (evaporation). Assuming house environment control is efficient and birds remain healthy, insensible (evaporative) water loss is minimised and excretory (urine and faecal) water loss is diet dependent.
Dietary mineral content, anion-cation balance and several feed ingredient characteristics will affect water intake and feed passage time thus altering urine and faecal moisture.

Since feed is generally low in moisture (10%) and metabolic water production is limited by diet formulation (~ 0.14g/kcal of dietary energy) moisture intake is primarily controlled by drinking (~ 80%) . Water consumption is
requirement-driven and the thirst centre is stimulated by cellular dehydration (osmoreceptors), extracellular dehydration (mechanoreceptors) and angiotensin II secretion (reninangiotensin axis).

Insensible moisture loss (skin and respiratory tract) accounts for 50-80% of total loss but seldom contributes directly to litter moisture since at thermoneutrality, evaporative loss is minimised and water in the vapour form is
removed from the house relatively easily . Water loss as vapour does however increases relative humidity (RH) thus reducing the air’s litter drying capacity and could cause saturation and condensation. Once condensed, water requires additional energy (heat of evaporation) and effort (air temperature/humidity control) to remove, so homeostatic stress that increases liquid water loss (faecal and urinary) therefore poses a greater risk to litter moisture control.

Urinary excretion is somewhat unique in the avian species since firstly the ureters open into the coprodeum and secondly the urine passes retrograde up the colon to the caecae before being evacuated via the cloaca with the faeces. The content of the urine is significantly altered during its passage through the coprodeum, colon and caecae.

Urine excretion is controlled by several hormones including arginine vasotocin (antidiuretic), renin/angiotensin (diuretic/antidiuretic and natiuretic/antinatiuretic), aldosterone (antinatiuretic), atrial natriuretic peptide (diuretic and naturietic), parathyroid hormone (calcium mobilization and excretion of phosphorus).

At standard temperatures broilers will consume approximately 1.75 to 2 times more water than feed (by weight) so it is crucial that the poultry house ventilation system design and operation is efficient enough to prevent the
litter moisture content from exceeding an optimal 25%.. At stocking densities of 34kg/m2 huge amounts of water are added to the litter on a daily basis (Fig 1). At six weeks of age for example, 20,000 birds will excrete approximately 2.5t of water into the litter in one day. Relatively minor changes in water excretion rates can, very rapidly compromise litter moisture control.

Water Imbalance

Urine output increases above normal (polyuria) when intake exceeds
requirement (overcorrection of dehydration), the need for solute excretion
exceeds normal (mineral and protein loading) or when urine concentrating
mechanisms are compromised (nephrotoxins such as ochratoxin, citrinin and
oosporin). Although an increase in urine output can cause wet litter, the
condition is often incorrectly interpreted as an increase in true faecal water
consequent to diarrhoea or enteritis.

Several feed ingredient characteristics can alter faecal water content
directly by increasing ingesta osmolarity, or reducing transit time and
absorptive surface area/function thus compromising water absorption and
stimulating intake. The resultant increase in faecal water is termed diarrhoea.
This is different to enteritis, where inflammation of the gastrointestinal
lining negatively affects digestion and the consequent reduction in nutrient
and water absorption cause faecal water to increases above normal. The latter
is usually associated with pathological conditions involving gut microbiota or
feed toxins while the former is usually physiological in nature. However any
physiological perturbation that negatively affects nutrient assimilation
(intake, digestion and absorption) will increase nutrient through-flow and
could alter the microbial population of the distal gut sufficiently to cause
wet litter. Ultimately, bird health and wellbeing, food safety and the
efficient conversion of feed to food depends on the harmonious balance of the complex
gastrointestinal tract ecology.

Strategies
to Prevent Wet Litter

Preventing
Polyuria

Chickens on grain based diets (approximately 30 meq Na+/kg) excrete a lot of
NH4 +, phosphate and K+ while Na+ and Cl- together only account for just over
10% of the total osmolality. The relatively high levels of potassium in soybean
(and molasses) can also be sufficient to induce a polydipsia, polyuria and wet
litter.

Most diets will have added salt and since sodium is the primary
extracellular cation maintenance of sodium balance by the kidney is crucial to
control of extracellular fluid volume and blood pressure . When the Na+
concentration in the ration is raised threefold there is a corresponding
increase in urine Na+ and Cl- (<50% of osmotic space) at the expense of the
NH4 + while other solute concentrations change very little . Minor sodium
excess is controlled by reducing intestinal uptake but as the concentration in
the diet increases renal naturesis follows . Elevated sodium excretion
necessitates concomitant loss of an equivalent anion (usually Cl-) and water.

Provided the drinking water solute concentration does not exceed the
regulatory capacity of the kidney the bird is able to cope with relatively high
dietary salt concentrations by increasing urine output . The polyuria induced
by sodium excretion is exacerbated by chloride induced osmotic diuresis and can
to a degree be countered by partial replacement of salt derived sodium with
sodium bicarbonate thereby reducing chlorine intake.

Dietary calcium and phosphorus levels are regulated by stringent maximum and
minimum specification constraints because both the amount and ratio of these
minerals is important to productivity . Calcium is reabsorbed from the
glomerular filtrate very efficiently (>98%) by a mechanism that operates
close to maximum while phosphorus is in contrast reabsorbed fairly
inefficiently (40%) . Parathyroid hormone (PTH) secretion in response to low
blood Ca enhances intestinal absorption and reduces renal excretion . Elevated
blood Ca proportionally increases the calcium concentration of the glomerular
filtrate which easily exceeds reabsoption capacity and consequently increases
Ca excretion . PTH increases phosphorus excretion by inhibiting renal tubular
reabsorption and secretion.

Excess calcium excretion can cause renal pathology (calcinosis/urolithiasis)
resulting in compromised water retention and diuresis/wet litter . Dolomitic
limestone contains relatively high levels of magnesium (8-10%) and apart from
competing with calcium for absorption the Mg excretion can cause diuresis and
wet litter.

Mycotoxicoses are difficult to quantify as there appears to be significant
interaction and potentiation but nephrotoxins such as ochratoxin (especially
type A), citrinin and oosporin can compromise renal function causing
polyuria/polydypsia and wet litter . The avoidance of contaminated ingredients,
the dilution of contaminated ingredients with non-contaminated ingredients or
the addition of mycotoxin binders are all potential ways of limiting or
preventing toxicity.

Gut
Health management to prevent Diarrhoea and Enteritis

The integrity of the gastrointestinal absorptive membrane determines the
efficiency of the assimilation process. Development and maintenance of the
structure (anatomy) and function (physiology) has to be integrated with gut
microbial community evolution since that is the primary determinant of gut
ecological evolution. Detailed study of gut ecology with modern molecular
techniques has helped elucidate details of the gastrointestinal environment
that challenges previous dogma . Similarly gene sequencing of purported
commensals and host cascade reaction modulation studies have opened our minds
to the significance of the vast cellular communication process responsible for
balancing this eco system . As this knowledge base expands, it becomes easier
to design strategies to maintain gut health through science based gut ecology
management.

Colonization of the gut with pioneer bacteria species that are able to
modulate gene expression in the host gut epithelia to assist in creating
favourable conditions for the evolution of a stable climax (steady state)
community provides a natural form of defence against pathogen challenge. The
speed with which this “climax flora” develops appears to be important with
respect to future/sustained resilience . With this objective in mind it is
possible to identify several management opportunities to enhance gut health and
bird productivity including; seeding the hatchling gut with favorable flora; early
modification of the gut environment to promote climax flora development;
pathogen exclusion (competitive and selective); immune modulation; and
ingredient/nutrient management.

Seeding
of the gut

It was demonstrated many years ago that a “mature” gut microbial community
can reduce the prevalence of wet litter by making it more difficult for
pathogens to infiltrate . Steps to control gut health in broilers should
ideally start at the parent flock level because the first organisms to gain
access to the receptive and uninhabited environment of the hatchling gut
originate from the shell. Manipulation of parent gut flora can have a
beneficial effect on offspring resistance to pathogen colonization because even
low doses of beneficial bacteria can significantly improve resistance to
pathogen colonization if introduced at hatch . These organisms also create
conditions that shape development of the climax flora.

Similarly, dosing day-old chicks with competitive exclusion products can
reduce pathogen infection rate (95% to <5%) following low grade (<104CFU)
challenge. The proviso being, that the process of gut colonization is allowed
to proceed for at least 4 hours before challenge . Administration of
Enterococcus faecium, Lactobacillus reuteri , a combination of Lactobacillus
spp, B. bifidum, and Aspergillus oryzae , or a combination of Lactobacillus
acidophilus, Bacillus subtilis and Enterococcus faecium significantly improved
broiler performance under research conditions. Some companies have successfully
utilized continuously fed probiotics to enhance gut health and feed efficiency
on a commercial scale (Kounev, Z. 2004, personal communication).

Lactobacillus johnsonii and a mixture of Lactobacillus acidophilus and
Streptococcus faecium have shown promise in reducing the impact of low grade
necrotic enteritis on performance when used as probiotics . In one particular
study a probiotic matched an antibiotic in protecting against necrotic
enteritis induced mortality but the same organisms (Lactobacillus acidophilus
and Enterococcus faecium) proved to be less successful in an earlier study.

It would appear that by selecting specific pioneer species as probiotic
candidates it is possible to create a gut environment that accelerates the
establishment of favourable and stable climax flora communities. With this
strategy the emphasis subtly shifts from working against, to working with the
natural ecology of the gut.

Gut
environment management.

Acidification

Meta analysis and literature review indicate that water and feed
acidification have an important role to play in the avoidance of wet litter
through gut flora management. Although a fairly well researched and accepted
practice in pig production organic acids use is rapidly becoming popular in the
poultry industry as a means of relinquishing dependence on antibiotics.

The beneficial effects of commercial acid preparations are thought to arise
from the antibacterial properties of ionization. Organic acids are able to
diffuse across the bacterial cell membrane rapidly when in the undissociated
form. Once internalized the neutral pH of the cytoplasm causes dissociation,
thus raising the intracellular concentration of both protons and anions.
Bacterial proton-motive forces are exhausted in pursuance of homeostasis and
the resultant rise in cytoplasm pH interferes with bacterial cell physiology.
At low concentrations organic acids have a bacteriostatic effect but at high
concentrations they become bactericidal (when acid concentration causes
internal pH to rise to the point where denaturation of bacterial protein and
DNA occurs.)

Acid ionization varies considerably according to type, concentration and mix
of acids used and is further modified by the pH, buffering capacity and water
activity of the feed, water and gut content (Chung and Goeffert, 1970; Krause
et al., 1994). Since their activity in the gastrointestinal tract is so
variable, systematic studies of the effects of a variety of acidifiers are not
available. It is not possible to determine the overall responses to complex
acidification strategies or to compare these with other supplementation
strategies using objective analytical process (Rosen, 2003).

Nutrient
balance – Intake, absorption and excretion

The low pH of the upper gastrointestinal tract provides a competitive
advantage to the acidophilic organisms and is by contrast, relatively hostile
to many of the potential pathogens such as Clostridium perfringens and
Salmonella sp. While the lower part of the digestive tract is alkaline (pH 7-8)
and more hospitable to these potential pathogens their replication rate is
presumably limited by nutrient availability. The flora of the lower
gastrointestinal tract spend the majority of their existence in intense competition
for a limited source of nutrients . Under such conditions evolution occurs very
rapidly and continuously through mutation, selection and takeover. Any factor
that reduces digestion efficiency in the upper gastrointestinal tract changes
the nutrient supply to the lower tract and will likely favour specific
stationary phase mutants. Since many of the problem organisms such as
Clostridium perfringens are proteolytic, it is logical to expect that protein
through-flow would provide a competitive advantage to these organisms and
increase the propensity for enteritis and wet litter.

While daily feed intake in broilers has increased tremendously, feed transit
time in the small intestine has remained fairly constant . Since feed
transit-time is inversely proportional to intake this means that retention time
in the proventriculus and gizzard has declined. This is perhaps not surprising
since the primary function of the proventriculus and gizzard (feed processing)
is performed at the feed mill. What is perhaps significant is that the process
of feed acidification and pepsin activation is likely also compromised.

Any factor that accelerates feed passage couldl potentially reduce the
efficiency of digestion and absorption since this process requires time. Several
feed ingredient characteristics will affect passage time including viscosity,
particle size, digestibility (starch), and lipid or protein content. To prevent
nutrient through-flow from causing wet litter the nutritionist should consider
ingredient blend in addition to nutrient specification. Some ingredient
characteristics such as water content, viscosity and non-digestible nutrient
composition can be enhanced with concomitant enzyme and or osmolyte usage .
Water soluble non starch polysaccharides (NSP) adversely affect digestibility
by stimulating mucus production and increasing ingesta viscosity. Grains such
as wheat, rye and barley are rich in water soluble NSPs and there is ample
research to demonstrate that the use of exogenous enzymes improves digestibility
. The toxin producing capability of Clostridium perfringens is also highly
dependent on the form (mono vs disaccharide) carbohydrate substrate.

All fats and oils have the potential to become oxidised and the resulting
rancid fats have compromised digestibility and can cause gastrointestinal
disturbance and wet litter directly (steatorrhoea) or indirectly by affecting
gut flora (oxidative). Unprotected fatty acids released by oil seed processing
(grinding or chemical extraction) are very susceptible to oxidative rancidity.

The growth enhancing effect of dietary enzymes is comparable to that of the
antibiotics when tested in controlled experimental conditions, suggesting a
common mechanism of action, i.e. manipulation of the gut ecology. This may be one
of the explanations why there is individual and ingredient variation in
response to enzyme supplementation. Apart from the direct feed efficiency
implication of reduced digestion and absorption, the through flow of undigested
nutrients impacts downstream gut ecology. Potentially toxic compounds such as
ammonia, amines, phenols and indoles are generated by the proteolytic and
ureolytic activity of the caecal flora on non-digested nutrients that make
their way through to the caecal pouches. These toxic compounds affect flora
ecology in the rabbit and the same is likely true for the broiler. The
morphology of the ileocaecal junction is such that only fluid or very small
(dissolved or suspended) particles enter the caecal pouch when intra luminal
pressure increases during convergence of rectal retro peristaltic and ileal
peristaltic contractions . Since the retro peristaltic contractions of the
colon/rectum are almost continuous, 87-97% of the caecal fluid originates from
the urine. Urine derived uric acid reaching the caeca by retro peristalsis and
undigested protein from the upper gastrointestinal tract provide a source of
nitrogen for microbial amino acid synthesis. Subsequent degradation of caecal
microbial protein by for caecal microbial communities.

The amount of nitrogen reaching the caeca is influenced by the amount of
protein in the diet, the efficiency of protein digestion /absorption in the
upper gastrointestinal tract and the state of nitrogen balance. Exogenous
enzymes added to the diet to promote protein digestion affect caecal flora
communities by reducing the amount of protein nitrogen reaching the caeca.
Conversely any physiological perturbation that negatively affects nutrient
assimilation (intake, digestion and absorption) will increase caecal nitrogen
either by increasing nutrient through flow or body protein turnover rate
(nitrogen excretion via the urine).

Volatile fatty acids (VFA) are by products of uric acid degradation by
caecal flora and despite passive absorption, caecal VFA concentrations
(acetate>propionate>butyrate) are very high (125nM) . Since these weak
organic acids have antibacterial activity they likely play an important role in
balancing the caecal ecology.

Antimicrobials

Antibiotics have been an integral part of poultry feed for the past 50 years
. Decades of research and field use have established the efficiency of
antibiotics as growth promoters and in-feed antibiotics have been shown to
subtly change the composition of the normal flora. PCR-denaturant gradient gel
electrophoresis (DGGE) studies indicate that while antibiotics definitely
change the gut flora profile, microbial populations become more homogeneous.
DGGE studies are useful for tracking changes in gut flora profiles but give no
detail on actual composition. The use of 16S clone libraries have made it
possible to study specific organism profile changes in the gut. It would appear
that lactobacilli and clostridia are the two groups most significantly affected
by antibiotics.

Antibiotic growth promotion strategies have focused on manipulation of the
gut ecology of the small intestine to improve feed efficiency but the impact on
caecal flora, house flora and seeding of the hatchling gut of the next
placement has been ignored. The gut flora changes elicited by a growth
promotant are dependent on its antibacterial properties, rate of absorption,
method of inactivation/metabolism, route of excretion, the degree of luminal
(micro organism) enzyme inactivation or adsorption to ingesta. Many antibiotics
are excreted via the urine in an active form, whether metabolized or not.
Parenteral antimicrobials or those that are absorbed from the gastrointestinal
tract after oral administration are concentrated in the urine and subsequently
transported back to the caeca as illustrated by the high concentration of
antibiotic in the caecal wall. Orally administered antimicrobials that or not
absorbed also reach the caeca when the intraluminal pressure at the ileocaecal
junction increases and liquid is forced into the caecal pouches.

The extensive reviews on in-feed antibiotic use and those covering the
various alternatives, have reported on research investigating the response to
first-time-one-off use of growth promoter strategies in controlled trials under
carefully monitored experimental conditions. Broiler production is, in
contrast, a continuous system. Broiler gut flora determines the composition of
the litter/house flora which in turn acts as the seed stock for the gut flora
of the next placement . While the small-intestine ecology influences the
efficiency of digestion and absorption it is the caecal/colon/rectal flora that
gives rise to the house flora. Although there are literally thousands of
growth-promotant trials demonstrating their efficacy (or lack thereof) the
literature is devoid of data showing the long-term effect of such programs.
While the use of a growth promoter can alter the gut flora within a couple of
weeks it takes several grow-out cycles to change the house flora . This is by
no means a new concept, both rotation and shuttle programs have been used for
decades to avoid the lack of response to growth promoting antibiotics following
persistent use.

Just like penicillin many of the mycotoxins that commonly contaminate
poultry feed likely have antimicrobial properties. Mycotoxin research has
focused on host toxicity but it is possible that gut flora destabilization and
feed efficiency is affected long before symptoms of toxicity appear. Molecular
profiling using 16SrRNA library studies will likely provide more insight into
the impact that mycotoxin contamination of feed has on gut flora and help with
the understanding of exactly how these novel strategies help to control gut
health.

Selective
exclusion.

Pathogen attachment to the intestinal epithelium is a pivotal first step in
the colonisation of the gut and depends on, amongst other things, flagella,
type 1 fimbriae and pillus receptors for specific host cell docking sites .
Adherence has also been associated with mannose resistant haemagglutinins.
Scanning electron microscope studies of the caecal epithelium have shown that
the organisms of the gut flora form a tightly adherent mat over the gut
surface. These organisms are attached to each other and the epithelia by a
series of fibrils, which effectively prevents pathogenic organisms from gaining
access to epithelial receptors. The adhesive flagella of enteropathogenic E.
coli (EPEC) have been shown to be induced by animal cells. While competitive
exclusion relies on the ability of live organisms to compete for attachment
sites it is also possible to block attachment sites with decoy molecules and
change gut flora communities

Immune
response

Any immune response bears a production cost. An appropriate immune response,
adequate to contain infectious disease and minimize its impact on productivity,
is the cost of health. An inappropriate, excessive or inadequate immune
response will depress performance unnecessarily, so in a performance driven
broiler industry the prevention of wet litter should include an immune modulation
strategy.

The gastrointestinal environment is loaded with a plethora of antigens of
feed and micro-organism origin, the majority of which pose no threat of
infectious disease. An inappropriate adaptive immune response to non-pathogen
derived antigens is prevented by the innate immune system.

With systemic challenge, most (70%) of the negative impact on growth rate
and feed efficiency is attributed to reduced feed intake, while the
inefficiencies of catabolism and nutrient absorption account for the rest (30%)
. Low level antigen recognition at the gut/ingesta interface probably seldom
stimulates systemic/fever response but pro-inflammatory mediators released in
response to antigen stimulation of this nature can damage host tissue, thereby
causing localized inflammatory disease and reduced feed efficiency.

Antigen induced inflammation of the gut cytoskeleton stimulates an increase
in mucus secretion, paracellular permeability, and feed passage (peristalsis).
The cascade of events that follows is self perpetuating and provides additional
advantage to organisms such as Clostridium perfringens that are capable of
rapid multiplication thus increasing the propensity for wet litter . Both
endogenous and exogenous anti-inflammatory agents modulate the immune response
and help in the maintenance of gut health by preserving the integrity of the
host enteron/environment interface and reducing the systemic (fever) response.

Local immune response is more pronounced in the lower gastrointestinal tract
and high molecular weight proteins are more immunogenic so, apart from the
obvious inefficiencies of nutrient wastage arising from poor digestibility or
rapid feed passage, undigested proteins reaching the caeca are strongly
inflammatory and thus further reduce feed efficiency. High protein diets,
essential to attain broiler muscle tissue accretion rates, increase the risk of
downstream gut health challenges by increasing the chance of protein
throughflow. Peptic digestion is already marginal because selection for growth
rate has reduced feed retention time in the crop and gizzard, thus reducing
enzyme/nutrient contact time. This is especially so with soluble protein
because liquids pass through the digestive tract 15% faster than solids.

The nature and extent of the inflammatory response is influenced by several
nutritional factors. Dietary polyunsaturated fatty acids (PUFA) for example
provide the building blocks for cell membrane synthesis and indirectly
determine the type of immune response since the cell membrane lipids provide
the substrate for immune system communication molecule synthesis . Cereal
grains are high in linoleic acid (n-6 PUFA precursor for arachidonic acid)
which generates prostaglandins, leukotreins and thromboxanes while fish oil is
high in n-3 PUFA which generates Interleukin-1 and prostaglandin-E.

Just as the cost of an excessive or inappropriate immune response negatively
impacts performance so too does an inadequate immune response. An inadequate
immune response is usually recognized as an increase in flock mortality but has
a negative economic impact long before flock mortality rises. Specific
infectious diseases nutritional deficiencies, toxicity, and stress are all
factors that can induce sufficient immune suppression to cause an inadequate
response.

Stress only impacts performance measurably once the aggregate of each
individual stress exceeds the host’s coping mechanisms . The degree to which an
adverse stimulus or stress will negatively impact bird performance is directly
proportional to the existing stress load, so good animal husbandry, nutrition
and bio-security are prerequisites to preventing wet litter.

Immune modulation can be used to carefully manage the balance between
disease resistance and tolerance in order to maintain productivity.

Conclusion

Urine output increases above normal (polyuria) when intake exceeds
requirement (overcorrection of dehydration), the need for solute excretion
exceeds normal (mineral and protein loading) or when urine concentrating
mechanisms are compromised. Polyuria can be avoided through careful diet
formulation and ingredient management.

Gut microbial imbalance is a fundamental cause of wet litter and there are
several opportunities for intervention to enhance gut health and productivity
by managing this ecosystem:

1. Seeding of the hatchling gut begins with vertical transmission of parent
gut flora but is effectively modified with early administration of effective
probiotics or competitive exclusion products. To be successful they must
initiate the development of a primary flora which will rapidly evolve into a
stable and favorable climax flora by creating suitable gut conditions and
excluding unfavorable organisms.

2. Preparing the gut environment (pH, redox potential) for early transition
from primary to climax flora through water/feed acidification. Candidates need
to be weak acids that are buffered to withstand the neutralizing effect of
minerals dissolved in the drinking water and have dissociation characteristics
that make them active in the small intestine.

3. Excluding pathogens from colonizing the gut by competitive and selective
exclusion. It is important that the selective exclusion product is compatible
with (does not exclude) the organisms used for competitive exclusion or as a
probiotic.

4. Enhancing resilience by stimulating protective immune response while
suppressing the acute phase or fever response.

5. Decreasing nutrient through flow by enhancing nutrient digestion and
absorption (exogenous enzyme addition and nutrient modification, feeding and
lighting programs, careful use of antibiotics) to avoid caecal flora upset.

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