Background update:Jun 14, 2010

Target release concepts in poultry feed

An understanding of gastro-intestinal anatomy, physiology and function of the chicken is critical for achieving optimum nutritional efficiency. Here we discuss some new insights regarding the use of a mix containing coated butyrate acid, short- and medium-chained fatty acids and botanicals to target intestinal problems in poultry.

In poultry, the early development of the enteric system is considered to be one of the most crucial steps in achieving life-time performance objectives and maximum economic returns. In the immediate post-hatch period important changes occur in the physiology and function of the chick’s gastro-intestinal tract (GIT), as well as in the associated organs such as the liver and lymphoid tissue.
In size and weight the small intestine and cecum increase up to fi ve times more rapidly than most other organs, and achieve a maximum relative growth rate at 6-10 days post-hatch. The intestinal villi, crypts and enterocytes – essential for effective absorption of nutrients – develop even more rapidly, reaching a relative growth plateau at 48 hours post-hatch. In the presence of feed (nutrients) the development is increased and short- as well as long-term performance improved.
Role of microbiota
Development of the early GIT is also stimulated by the establishment of an active microbial population. However, it is not clear what the precise contribution of the microbiota is relative to that of its fermentation products. Generally a close symbiotic relationship is assumed, but competition for some nutrients between the developing tissue and the microbiota is likely. While the required substrate for microbial development is relatively well known, it is not so clear as to what the essential and signalling nutrients are that should be supplied to directly stimulate GIT development. Post-hatch colonisation of the GIT by microfl ora is also an important step in the stimulation and maturation of the immune system.
Two primary functions
The intestine is a key organ that acts upon two primary functions. It is the critical interface between the digested food and the blood circulation that carries nutrients to the cells for productive purposes. It also houses the intestinal microflora, which is important for maintenance of gut health, but can become a source of problems when the potential pathogenic bacteria gain the upper hand over the beneficial bacteria. The efficiency of the digestive function can be modified by changes in gastric pH, level and type of enzyme production, various gastric secretions, products of fermentation and overall microbial balance.
However, the condition of impaired gut health, the so-called ‘dysbacteriosis’, is a common issue in poultry today. The frequent clinical symptoms are thin, fragile and often translucent intestinal walls; ballooning of the gut; severe inflammation; watery or foamy gut contents; poorly digested feed particles at the end of the GIT; and, multicoloured oily aspect of the gut content. These gut health problems lead in most cases to reduced body weight, increased feed conversion and lower performance in general, which result in severe economical consequences for poultry producers. Besides the zootechnical losses, huge financial losses are due to wet sticky litter in the stables.
Necrotic enteritis
Although Clostridium perfringens type A is frequently found in the GIT of healthy poultry, the development of necrotic enteritis depends on the presence of predisposing factors, of which two of the most important are mucosal damage caused by coccidial pathogens, and feed containing a high level of protein. Proteolytic enzymes are thought to play a role in the early stages of lesion development. Recently, a novel poreforming toxin, netB, was identified in a C. perfringens outbreak strain. It was shown that this toxin is essential in inducing necrotic enteritis. Almost none of the C. perfringens strains isolated from healthy poultry and almost every isolate from diseased chickens carry the gene encoding for this toxin.
It is thus speculated that only a subpopulation of strains can cause disease, and the presence of such strains in a poultry house is another essential factor to induce necrotic enteritis.
In a recent study at the University of Gent, Belgium, the efficacy of coated butyrate acid, SCFA, MCFA and botanicals to control necrotic enteritis was investigated in broilers. Five groups of 25 Ross 308 broilers were fed a wheat/ rye-based (43%/7.5%) diet, with soybean meal as a protein source. Gumboro vaccine was given in the drinking water on Day 18 in all groups. From Day 19 onwards, the same diet was used with the exception that fishmeal (30%) was used as a protein source. All groups were orally challenged using a plastic tube (three times a day) with approx. 4.108 cfu C. perfringens bacteria on Days 19, 20, 21 and 22. On Day 20 all birds, except the ones in the control group, were orally inoculated with a 10-fold dose of Paracox-5TM. On Days 23, 24 and 25, eight animals of each group were euthanized by intravenous T61 (Intervet, Mechelen, Belgium) injection. Necrotic enteritis lesion scoring as described by Keyburn et al. (2006) was performed: 0 = no gross lesions; 1 = congested intestinal mucosa; 2 = small focal necrosis or ulceration (1-5 foci); 3 = focal necrosis or ulceration (6-15 foci); 4 = focal necrosis or ulceration (16 or more foci); 5 = patches of necrosis 2-3 cm long; 6 = diff use necrosis typical of field cases. Lesion scores of 2 or more were classified as positive for necrotic enteritis.
The results obtained showed no lesion in the group of birds without challenge or only with the coccidia. The birds receiving the complete challenge and no treatment had 50% lesions; however, there was a significant difference (p<0.05) with the group of birds with complete challenge and treated with 500 g/t and 1,000 g/t. The lesion scores were resp. 16% and 8%, indicating linear dose response.
No wet litter problems
A necrotic enteritis challenge (in vivo) was carried out in 2008. In two buildings of 4,400 heavy broilers poulet label jaune (all natural), birds faced enteritis problems (caused by Clostridia perfrigens) around 3-4 weeks of age; wet litter; non-uniform body weight; increased mortality; and, skin colour variances. Birds in one building remained as control with normal diets, whereas birds in the second building were fed normal diets supplemented with 500 g/t product in starter (1-28 days) and 250 g/t product in grower (29-53 days). Over the 84-day period (till slaughter), decreased mortality was observed in the product-fed group of broilers (Figure 1), along with no wet litter quality problems (Figure 2) and improved body weight (2.2 kg of birds in the control versus 2.3 kg live weight in the treated group).
Dietary interventions that provide the essential nutrients and conditions in the GIT for accelerated gut development and the establishment of a symbiotic relationship between microflora and host animal should be part of routine feeding programmes.
* References are available on request


Editor WorldPoultry

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