Wet litter is a complicated problem caused by a number of interconnected factors, including bird management and housing, disease and diet, and gut health. It is also one of the most important factors in the development of footpad lesions (FPLs), also known as footpad dermatitis (FPD), which has become a major issue in recent years. Among all these factors, nutritional factors are of paramount importance, which include water, cereals, oil seeds, lipids, minerals, and mycotoxins.
Increased water consumption in birds, in an attempt to maintain their electrolyte balance, can lead to moist droppings if they consume too much potassium, magnesium, sodium, sulfate, or chloride in their feed or water. Mineral concentrations in the water should be examined regularly to ensure that there hasn’t been a mixing error in the feed. Diarrhea can also be caused by poor-quality or rancid fat. Furthermore, certain feed ingredients, notably those high in Non-Starch Polysaccharides (NSP), including wheat, barley, and rye, are frequently linked to wetter and more viscous excreta because these components trap water and prevent it from being reabsorbed.
Effects of nutrition on litter moisture:
- Water: Birds consume approximately twice as much water as they do feed on a weight-
for-weight basis, which emphasizes the importance of this nutrient. Since water provides the vehicle for solute movement across epithelial membranes, it is crucial to both nutrient absorption and waste excretion. Water flux across the epithelium is strongly influenced by solute content. Animals are much more sensitive to the deleterious effects of electrolytes when they are present in drinking water. High levels of sodium, magnesium, or sulfate in drinking water are purported to be associated with wet litter problems. - Cereals: Wet litter is a common consequence of including small grain cereals such as wheat, barley, oats, and rye in commercial poultry rations. These ingredients are notoriously high in water-soluble non-starch polysaccharides (NSP), which have been shown to increase fecal moisture and cause wet litter. Non-starch polysaccharide-induced flushing is thought to result from digestive upset, leading to a net efflux of water into the intestinal lumen.
High molecular weight, cell-wall-associated NSP are capable of increasing the viscosity of the intestinal aqueous phase by coalescing to form complex polymers, primarily because poultry do not possess the enzyme repertoire necessary to digest them. This polymer formation alters ingesta flow patterns, stimulates and alters mucus secretion, restricts nutrient absorption, and changes the composition of the microbial community in the small intestine. Exogenous enzyme addition to diets with high cereal inclusion rates has become standard practice to avoid the wet litter problems associated with these ingredients.
- Oilseed Meals
There is a risk of wet litter associated with feeding high levels of either animal or vegetable protein ingredients. Highly soluble protein from animal sources tends to move through the intestinal tract more rapidly than vegetable protein, which reduces the opportunity for digestion and absorption, thus increasing the chance of cecal fermentation and dysbacteriosis. In contrast, because much of the protein of vegetable origin is sequestered by the non-digestible NSP-containing cell wall, hindgut fermentation of these nutrients can also promote the development of dysbacteriosis and flushing.
- Lipid
Fats and oils provide an effective means of increasing the nutrient density of diets, as they yield more metabolizable energy than carbohydrates. From a wet litter perspective, the risk associated with lipid inclusion depends on the amount, type, and quality of lipid added. Poor lipid utilization and steatorrhea can occur if the dietary lipids are of poor quality (oxidative rancidity) or type. Certain lipids are less efficiently utilized by poultry, and rancid fats and soaps can reduce fat-soluble nutrient utilization, as well as cause intestinal inflammation (enteritis) and diarrhea. The excretion of high levels of fat can affect litter moisture directly by increasing fecal moisture and indirectly by reducing the water-holding characteristics of the litter.
- Minerals
Homeostatic control of intra- and extracellular fluid mineral balance and pH is an integral part of osmoregulation and, therefore, is very closely correlated with water balance. Sodium is the predominant extracellular cation, potassium is the dominant intracellular cation, chlorine is the most prevalent monovalent anion, and hydrogen ion concentration is critical to physiological function. Not surprisingly, the balance and movement of these four ions across the intestinal and renal tubule epithelium are pivotal to water, electrolyte, and pH balance.
The interrelationships between Na, K, and Cl are more important than their actual individual concentrations. A wide range of dietary Na and Cl requirements has been reported, and within this range, dietary salt inclusion is positively correlated with water consumption and urine output. In intensive production systems, the initially linear relationship between dietary sodium and growth rate is curtailed by the negative consequences of wet litter before salt toxicity starts to affect growth rate.
Calcium, when added to diets, can contribute to wet litter. Since calcium reabsorption from renal filtrate operates at about 98% of capacity, even a minor increase in blood calcium can overwhelm this transport mechanism, resulting in calcium loss and polyuria due to osmotic diuresis.
- Mycotoxins
Mycotoxins can be found in moldy feeds and feed additives. The contributing effect of mycotoxins should always be considered in cases of nutritionally induced wet litter. Mycotoxins, which are fungal metabolites produced by common molds found in many poultry diets, can directly affect gut integrity, resulting in lower dietary nutrient absorption and digestion, as well as increased intestinal barrier permeability, which can contribute to damp litter.
Ochratoxin A, citrinin, and oosporin are three mycotoxins known to be nephrotoxic, and they have all been associated with wet litter problems. Of the three, ochratoxin-induced wet litter has been the most commonly reported and has occurred in broilers and laying hens.
Conclusions
Inappropriate nutrition can induce wet litter by increasing urine output (polyuria), increasing fecal moisture (diarrhea), or altering the water-holding characteristics of the litter. Genetic selection has accelerated growth rates to the point where even normal physiological water balance (osmoregulatory) responses can induce wet litter in intensive production systems. Extreme care in ingredient choice and diet formulation is necessary to avert minor elevations in water loss.
by Dr Ashok Reddy, Immeureka
