The term “wet litter” is generally used to describe, non-specific disease of the gastrointestinal or urinary tract, resulting in compromised water balance, feed conversion inefficiencies and predisposition to secondary disease. 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 the normal physiology of digestion and water balance or indirectly by disturbing normal gut ecology. An integrated and holistic approach is required to ensure that the development and maintenance of gut structure (anatomy) and function (physiology) is integrated with gut microbial community evolution. Antibiotics, enzymes, drinking water acidification, probiotics, prebiotics, immune modulators and mycotoxin binders have all shown promise in this regard.
I. 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. The term “wet litter” is generally used to describe, non-specific disease of the gastrointestinal or urinary tract, resulting in compromised water balance, feed conversion inefficiencies and predisposition to secondary disease.
II. Water balance
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 water loss is minimised and excretory 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 (Classen 1996; Leeson and Summers 2005; Refstie et al. 1999; Sell et al. 1983; Sibbald 1979; Weurding et al. 2001).
Since feed is generally low in moisture (10%) and metabolic water production is limited by diet formulation, moisture intake is primarily controlled by drinking (~ 80%) (Leeson and Summers 2005). Water consumption is requirement-driven and the thirst centre is stimulated by cellular dehydration (osmoreceptors), extracellular dehydration (mechanoreceptors) and angiotensin II secretion (renin-angiotensin axis) (Goldstein and Skadhauge 2000; Kanosue et al. 1990; Kaufman et al. 1980).
Insensible moisture loss 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 (Goldstein and Skadhauge 2000). Water loss as vapour does however increase 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) 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 (Goldstein and Skadhauge 2000). The content of the urine is significantly altered during its passage through the coprodeum, colon and caecae (Rice and Skadhauge 1982).
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% (Kellerup et al. 1965; Leeson and Summers 2005). At stocking densities of 34kg/m2 huge amounts of water are added to the litter on a daily basis. 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.
III. 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) (Leeson and Summers 2005). 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 increase above normal. The latter is usually associated with pathological conditions involving gut microbiota or feed toxins while the former is usually physiological in nature.
IV. Strategies to prevent wet litter
a) Preventing Polyuria
The relatively high levels of potassium in soybean (and molasses) can be sufficient to induce a polydipsia, polyuria and wet litter. In contrast most diets will have added salt and since sodium is the primary extracellular cation, maintenance of sodium balance by the kidney is crucial (Goldstein and Skadhauge 2000; Leeson and Summers 2005). Minor sodium excess is controlled by reducing intestinal uptake but as the concentration in the diet increases renal naturesis follows (Goldstein and Skadhauge 2000). 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 to reduce chlorine intake (Goldstein and Skadhauge 2000; Leeson and Summers 2005).
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 (Leeson and Summers 2005). Elevated blood Ca proportionally increases the calcium concentration of the glomerular filtrate which easily exceeds reabsoption capacity and consequently increases Ca excretion (Clark and Mok 1986; Wideman 1987). Excess calcium excretion can cause renal pathology (calcinosis/urolithiasis) resulting in compromised water retention and diuresis/wet litter (Shane et al. 1969; Wideman et al. 1985). In addition, 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 (Leeson and Summers 2005).
Nephrotoxins such as ochratoxin (especially type A), citrinin and oosporin, can compromise renal function causing polyuria/polydypsia and wet litter (Leeson and Summers 2005). The avoidance of contaminated ingredients, their dilution with non-contaminated ingredients or the addition of mycotoxin binders are all potential ways of limiting or preventing toxicity.
b) 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 gut structure (anatomy) and function (physiology) has to be integrated with gut microbial community evolution since they are collectively the primary determinants of gut health. Colonization of the gut with pioneer 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 (Guarner and Malagelada 2003). The speed with which this “climax flora” develops appears to be important with respect to future/sustained gut health and resilience (Hume et al. 1998; Methner et al. 1997). 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 favourable 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 (Pivnick and Nurmi 1982). Steps to control gut health in broilers should ideally start at the parent flock level because manipulation of parent gut flora can have a beneficial effect on offspring resistance to pathogen colonization (Fernandez et al. 2002). These organisms also create conditions that shape development of the climax flora (Dawson 2001).
Similarly, dosing day-old chicks with competitive exclusion products can reduce pathogen infection rate following low grade challenge provided gut colonization is allowed to proceed for at least 4 hours before challenge (Hume et al. 1998; Methner et al. 1997).
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 (Dawson 2001).
Gut environment management
1. Acidification
Meta analysis (Partanen and Mroz 1999) and literature review (Ravindran and Kornegay 1993) indicate that water and feed acidification have an important role to play in the avoidance of wet litter through gut flora management. 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 un-dissociated form (Cherrington et al. 1990; Cherrington et al. 1991). Once internalized the neutral pH of the cytoplasm causes dissociation, thus raising the intracellular concentration of both protons and anions (Cherrington et al. 1990; Cherrington et al. 1991; Davidson 2001). 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 (Davidson 2001; Ricke 2003).
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 (Ricke 2003).
2. 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 spp. The lower part of the digestive tract is alkaline (pH 7-8) and more hospitable to these potential pathogens but their dominance is limited by intense competition for a limited source of nutrients (Zinser and Kolter 2004). Under such conditions microbial evolution occurs very rapidly and continuously through mutation, selection and takeover thus increasing the propensity for pathogen dominance with nutrient through-flow (Finkel and Kolter 1999; Zambrano et al. 1993) High protein diets increase the chance of protein through-flow and downstream gut health challenges since many of the gut pathogens are proteolytic.
Feed retention time and the efficiency of digestion and absorption are reduced by several feed ingredient characteristics including viscosity, particle size, digestibility (starch), and lipid or protein content (Classen 1996; Refstie et al. 1999; Sell et al. 1983; Sibbald 1979; Weurding et al. 2001). To prevent nutrient through-flow from causing wet litter the nutritionist should consider ingredient blend in addition to nutrient specification (Bedford 1996; Collier et al. 2003; Iji 1999). Grains such as wheat, rye and barley are rich in water soluble NSPs and there is ample research to demonstrate that this improves digestibility (Choct and Annison 1992; Rosen 2000b; Rosen 2001).
Apart from the direct feed efficiency implication of reduced digestion and absorption, the through flow of undigested nutrients impacts downstream gut ecology (Leeson and Summers). 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.(Gidenne 1997). These toxic compounds affect flora ecology in the rabbit and the same is likely true for the broiler.
All fats and oils have the potential to become oxidised and the resulting rancid fats have reduced digestibility which 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(Leeson and Summers 2005).
3. Antimicrobials
Antibiotics have been an integral part of poultry feed for the past 50 years (Rosen 1995). 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. Many antibiotics are excreted via the urine in an active form, are concentrated in the urine and hence caecae, as illustrated by the high concentration of antibiotic in the caecal wall (Akester et al. 1967; Knoll et al. 1999).
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 (Collett and Dawson 2001; Hooge 2003; Rosen 1996; Rosen 2000a; Rosen 1995; Rosen 2001). 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 (Lilijebjelke et al. 2003). 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. 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 (Avellaneda et al. 2003); (Idris et al. 2003); (Lilijebjelke et al. 2003); (Schildknect et al. 2003a; 2003b).
Just like penicillin many of the mycotoxins that commonly contaminate poultry feed likely have antimicrobial properties. Mycotoxin research has focused on host toxicity (Swamy et al. 2002a; Swamy et al. 2002b) but it is possible that gut flora destabilization and feed efficiency is affected long before symptoms of toxicity appear (Kubena et al. 2001).
4. 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 (Sharon and Lis 1993; Stavric et al. 1987). 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 (Giron et al. 2002). 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 (Giron et al. 2002; Sharon and Lis 1993). The adhesive flagella of enteropathogenic E. coli (EPEC) have been shown to be induced by animal cells (Giron et al. 2002). 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.
5. Immune modulation
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 (Kelly 2004; Klasing 1998; Klasing and Barnes 1988; Klasing et al. 1987; Klipper et al. 2000; 2001).
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 (Medzhitov and Janeway 1997). Low level antigen recognition at the gut/ingesta interface probably seldom stimulates systemic/fever response but antigen stimulation of this nature can damage host tissue, thereby causing localized inflammatory disease and reduced feed efficiency (Klasing 1998; Klasing and Barnes 1988; Klasing et al. 1987; Klipper et al. 2000; 2001).
Antigen induced inflammation of the gut cytoskeleton stimulates an increase in mucus secretion, paracellular permeability, and feed passage (peristalsis) (Collier et al. 2003; Cooper 1984). 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 (Collier et al. 2003). Both endogenous and exogenous anti-inflammatory agents help to preserve the integrity of the gut and reduce the systemic (fever) response (Choct et al. 2004; Ferket et al. 2002; Grimble 2001; Kelly et al. 2004; Klasing 1998; Korver et al. 1998; Korver et al. 1997; Parks et al. 2001; Surai 2002; Sword et al. 1991).
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 (Klipper et al. 2001; 2004; Lillehoj and Trout 1996). This is especially prominent with soluble protein because liquids pass through the digestive tract 15% faster than solids (Klipper et al. 2004; Sklan et al. 1975; Sklan and Hurwitz 1980).
An inadequate immune response 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 (Ferket et al. 1999; Ferket and Qureshi 1992; Qureshi et al. 1998; Siegel 1994; Surai 2002; Swamy et al. 2002a; Swamy et al. 2002b; Sword et al. 1991).
Immune modulation can be used to carefully manage the balance between disease resistance and tolerance in order to maintain productivity (Klasing 1998; Klasing et al. 1987).
V. 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 favourable climax flora by creating suitable gut conditions and excluding unfavourable 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.
References are available on request
From Proceedings of the “19th Australian Poultry Science Symposium”, New South Wales, Australia.
S.R. COLLETT
College of Veterinary Medicine, Poultry Diagnostic and Research Centre,
University of Georgia,
Athens, Georgia,
U.S.A
