Wet litter is of major concern in broiler production because of its negative impact on animal health, welfare and production performance. Poor litter quality stimulates the incidence and severity of foot pad lesions which, in turn, induce pain and discomfort to the animal. As foot pad lesions are proposed as one of the main welfare indicators in the EU Broiler Directive, the severity of foot pad dermatitis in broilers will limit stocking density in the future. Jan Dirk van der Klis and Masja Lensing, Schothorst Feed Research B.V., Lelystad, the Netherlands.>/br>
By Jan Dirk van der Klis and Masja Lensing, Schothorst Feed Research B.V., Lelystad, Netherlands
The causes of wet litter in broiler houses are known to be multi-factorial, due to interactions between nutrition, management and impaired intestinal health. Until 1 January, 2006, intestinal health was controlled using antimicrobial growth promoters (AGPs) in poultry feed. Since then, however, the use of AGPs has, by law, been prohibited in the EU. This has prompted feed additive suppliers and feed manufacturers to develop alternatives for AGPs. When investigating possible alternatives, the mode of action of AGPs needs to be clarified. Several hypotheses have been proposed. It is generally assumed that the AGPs mainly exert their effects through limiting bacterial growth in the proximal intestinal tract and control growth of certain groups of micro-organisms in the intestine. It is well-accepted that bacterial overgrowth in proximal parts of the small intestine, called dysbacteriosis, induces a cascade of reactions in the gastro-intestinal tract, including reduced nutrient digestibility and impaired intestinal barrier function increasing the risk of bacterial translocation and inflammatory responses. Inflammation following infection reduces feed intake, body weight gain and bone quality.
Additionally, supplementation of AGPs resulted in an increased absorptive surface (villus length and number of villi per mm) in the small intestine; although, in general a reduced intestinal weight, intestinal length and reduced thickness of the gut wall is observed. However, an alternative mode of action was recently proposed, hypothesising that AGPs primarily limit the inflammatory response. This hypothesis introduces new ideas for developing alternative strategies to cope with bacterial challenges in the gastro-intestinal tract of broilers.
Non-infectious causes of wet litter
It is important to the health, welfare and production performance of commercial poultry that housing conditions are maintained within the comfort zone and that feed and water are available for ad libitum intake. Under these controlled conditions water excretion (urine and faeces) is closely related to moisture intake since evaporative water loss is limited. Avian osmo-regulation involves balancing water and electrolyte intake with excretion via the kidney (urine), gastrointestinal tract (faeces), skin and respiratory tract (evaporation).
Since feed is generally low in moisture (10%) and metabolic water production is limited by diet formulation (approx. 0.14 g/kcal of dietary energy), moisture intake is primarily controlled by drinking water (approx. 80%). Although an increase in urinary output can cause wet litter, the condition is usually interpreted as an increase in true faecal water, which is a result of diarrhoea or enteritis. Factors causing wet litter problems are therefore closely related to either reduced water absorption from the intestinal tract and consequently increase of faecal water content, or increased water excretion by the kidneys (so-called increase in urinary output). The main dietary causes of wet litter are:
• Dietary electrolyte levels
• Protein content and digestibility
• Fat quality
• NSP containing cereals and NSP enzymes
• Feed technology
Excess of dietary electrolyte levels stimulate mineral excretion by the kidneys, whereas uric acid excretion is increased by high protein levels or an imbalanced amino acid profile. Both factors will stimulate water excretion by the kidneys and thereby result in a higher urinary output and consequently wet litter. Non-starch polysaccharides increase intestinal viscosity which, in turn, decreases nutrient absorption rates.
Due to less efficient nutrient absorption, microbial fermentation in the intestinal tract increases because more nutrients become available for the microflora. This, in turn, enables bacteria populations to grow. As a result of a higher bacterial activity, the fat digestibility in the intestinal tract will be reduced. This effect will become more pronounced with the degree of saturation of dietary fat. A more detailed explanation of the microbial activity in the small intestine and its effect on nutrient absorption and litter quality are explained later on.
Finally, heat treatment of feedstuffs and compound feed can solubilise (e.g. non-starch polysaccharides), which increases their anti-nutritional effects. These effects can be eliminated by using NSP degrading enzymes.
Dysbacteriosis can begin as small intestinal bacterial overgrowth, which is defined as high numbers of bacteria (> 105) present per g duodenal chyme, in the absence of pathogens. As mentioned before, small intestinal bacterial overgrowth can be induced by an increase of intestinal viscosity, which decreases nutrient absorption rates. Due to less efficient nutrient absorption by the host, more nutrients become available for the microflora. This stimulates the growth of bacteria populations and the rate of fermentation of nutrients that become unavailable for the host animal. No harmful fermentation products are formed by the fermentation of carbohydrates; however, the fermentation of protein and fat can be detrimental to the host animal:
- Microbes deconjugate bile acids resulting in impaired fat digestibility, or in case of dehydroxylation even toxic metabolites can be formed.
- Fermentation of proteins results in the formation of biogenic amines, urea and ammonia, which will irritate and damage the gut wall and reduce production performance of the host animal.
Although the bacterial activity is dependent on the presence of readily available nutrients in the lumen of the intestinal tract, the effect of viscosity increasing feed components is aggravated by the intestinal microbiota themselves (Table 1). Viscosity increasing effects of highly methylated citrus (HMC) pectin were augmented through the microbiota. In germ-free birds (low bacterial activity) the effect of dietary supplementation with HMC pectin was negligible, whereas the effect in conventional chickens (high bacterial activity) was as anticipated. Due to the higher viscosity values in conventional broiler chickens, the absorption of nutrients from the intestinal lumen is reduced, and the retention time of chyme in the small intestine is increased. A higher retention time results in an increased bacterial growth in the proximal intestinal segments, whereas mucus production will be increased as a defence mechanism to improve gut barrier function. The higher viscosity values are indeed indirectly related to an increased intestinal mucus production as shown by the fact that inclusion of 2% HMC pectin in a corn/ soy diet stimulates mucus production fourfold from 15 to 58 units/g chyme. An increased bacterial growth in the proximal intestinal segments does not affect starch digestibility, but will result in a reduced fat digestibility. The apparent metabolisable energy (AME) value of the diets was reduced by 12.8% due to HMC pectin addition in chickens with an expected high bacterial pressure (conventional), whereas it was increased by 3.6% in germ-free chickens. The latter might have been due to the increased retention time (i.e. more time available for enzymatic digestion and absorption, without a negative impact of the microbiota).
In order to relate high bacterial activity to wet litter, the water absorption in a healthy broiler needs to be explained in a little more detail. Although water is absorbed from the intestinal lumen against an osmotic gradient in healthy broilers, water absorption can be hampered when the osmotic gradient from “gut lumen to blood” is increased. It is shown in Figure 1 that the chyme supernatant is hypertonic to blood plasma, which is approximately 320 mOsm/l, in all small intestinal segments. In this case, carboxy methyl cellulose (CMC) was used to increase the intestinal viscosity of the chyme and stimulate bacterial growth. It shows that graded levels of dietary