Intestinal events and nutritional dynamics predispose Clostridium perfringens virulence in broilers.

Clostridium perfringensA (CPA) entering the gastrointestinal system depends on favorable conditions to develop and subsequently extend pathogenicity. Reduction in digestive dynamics progressing from the duodenum decreases lumen oxygen, leading to anaerobic conditions in the distal lumen that favor CPA. When nutritional support is concurrently provided, an expanding population threatens the mucosa. Dietary nonstarch polysaccharides that increase viscosity further impair oxygen transfer from the mucosa, improving the ability of CPA to thrive. Incompletion of feed digestion early in the small intestine along with endogenous N provide additional support for population expansion. Glucosidase versatility with mucin elicited by distal CPA concurrently erodes the villus unstirred water layer at the apex, providing access to underlying binding sites for colonization. Proteolytic destruction within the lamina propria supports colonization to create subclinical necrotic enteritis. Eventual vascular entry of CPA and toxins provides a portal path for instituting cholangiohepatitis. Liver condemnations from inspection detect acute flock infection compared with preceding marginal losses in nutrient absorption that decrease feed efficiency. Enterocyte lysis by coccidia enable CPA access to binding sites, thereby extending villus necrosis and further impairing feed conversion. Loss of BW and increased mortality follow as mucosa involvement proceeds. In practice, supplemental feed hemicellulases that reduce digesta viscosity minimize a favorable environment for CPA, while superimposing a combination of amylase, phytase, and protease avoids nutritional support. Physical dynamics of the small intestine together with characteristics of feed that modify digesta viscosity and nutritional availability are central to establishing transient CPA as a pathogen.

Basis for the diversity and extent in loss of digestible nutrients created by dietary phytin: Emphasis on fowl and swine.

Phytin is the Ca2+-Mg2+-K+ salt of phytic acid that is created and deposited in the aleurone layer and/or germ of grains and legumes. Its high presence in feedstuffs for fowl and swine diets results in it being a universal and significant impediment to optimum performance. Phytin impairs gastrointestinal recovery of a wide array of nutrients, the effect varying with the nutrient concerned. On exposure to low pH during gastric digestion, phytin dissociates into phytic acid and solubilized Ca2+. Even at low gastric pH, phytic acid is negatively charged which forms the basis of its anti-nutritive behavior. Pepsinogen has extensive basic amino acids on its activation peptide that are presented as cations at low pH which are targeted by pepsin for activation. Partially crystalized Ca2+ near the enzyme's active site further stabilizes its newly formed structure. Thus, phytic acid appears to interfere with gastric digestion by several mechanisms; interfering with pepsinogen activation by binding to the polypeptide's basic amino acids; coordinating free Ca2+, destabilizing pepsin; binding some dietary proteins directly, further compromising gastric proteolysis. Upon digesta attaining neutrality in the duodenum, Ca2+ and other cations re-bind with accessible anions, phytic acid being a significant contender. Phytate not only binds free cations but can also strip them from enzymes (e.g. Ca2+, Zn2+) which reduces their structural resistance to autolysis and ability as co-factors (e.g. Zn2+) to increase enzyme activity. Goblet cells initially employ Ca2+ as an electronic shield between mucin layers enabling granule formation and cell storage. After mucin granule release, Ca2+ is progressively displaced by Na+ to free the viscous mucins enabling its translocation. Mucin entangles with the glycocalyx of adjacent enterocytes thereby constructing the unstirred water layer (USWL). Excessive removal of Ca2+ from mucin by phytic acid increases its fluidity facilitating its loss from the USWL with its associated Na+. This partly explains increased mucin and Na+ losses noted with high phytate diets. This review suggests that phytic acid binding of Ca2+ and less so Zn2+ is the basis for the diversity in nutrient losses encountered and that such losses are in proportion to dietary phytate content.

Endogenous mucin conveyed to the mucosa with microbes can assure lumen fermentation and large intestinal security-swine versus fowl.

Endogenous protein leaving the ileum largely consists of accrued mucins from the upper gastrointestinal tract (GIT) that had resisted digestion. The amounts released rely on their mucosal generation during enteral feeding which vary with age as well as diet. These digestion resistant proteins of endogenous origin continue to be unavailable in the large intestine, whereas those of dietary origin provide amino acids that largely support the existing microbial population while denying limited amounts for absorption. Other mucins pre-exist within the large intestine as two layers at the lumen surface. A loose layer harboring a diverse microbial population is superimposed on the unstirred water layer (USWL) which simultaneously acts as an obstacle to microbes at the loose layer while performing as a molecular sieve for nutrients. The USWL is formed through interplay between enterocyte and goblet cells; however, the basis for presence of the loose layer is elusive. Large intestinal fermentation predominates within the colon of swine, whereas fowl employ their ceca. Motility within the colon of swine segregates fine materials into haustrae out-pocketings that parallel their placement within the ceca of fowl. Viscous mucins from small intestinal endogenous losses may envelop microbes within the large intestinal lumen to present successive adherents on the USWL that assemble its loose layer. The loose layer continually functions as a microbial reservoir in support of lumen fermentation. Microbial catabolism of mucin within the loose layer is known to be slow, but its proximity to the enterocyte is of advantage to enterocyte absorption with by-product amino acids fostering the USWL.

Large intestinal dynamics differ between fowl and swine: Anatomical modifications, microbial collaboration, and digestive advantages from fibrolytic enzymes.

The large intestinal systems of fowl and swine recover nutrients from ileal indigesta by a strategically different manner. Indigesta with fowl enter a short colon where retro-peristalsis using urine from the urodeum carries small particulates and solutes into both ceca while coarse materials collect in the cloaca. Fowl repetitively add fine and soluble materials into both ceca to continue fermentation until complexity of the remainder exceeds microbial action, then contents apart from faeces are entirely evacuated. Indigesta with swine initially enter a short cecum followed by a lengthy progression through to the rectal ampulla. Wall out-pocketings of circular muscle or haustrae occur throughout the length of the pig's cecum and helicoidal colon. Each pocket carries contents acquired earlier in the cecum. Motility collects fines and solutes into haustrae during their progression through the colon whereas coarse particulates assemble in the core. Haustrae contents continually ferment during movement to the distal colon with resulting volatile fatty acids (VFA) and electrolytes being absorbed. Mucin loosely covers the lumen surface in caeca as well as helicoidal colon that may capture microbes from active intestinal contents as well as release others to sustain fermentation. The microbial community continually modifies to accommodate fibre complexity as encountered. Resistant starches (RS) and simple oligosaccharides rapidly ferment to yield VFA while encouraging butyric acid in the cecum and anterior colon, whereas non-starch polysaccharides (NSP) complexity requires extended durations through the remaining colon that enhance acetic acid. Residual fibre eventually results in undue complexity for fermentation and consolidates at termination of the colon. These compact pellets are placed on core contents to form faeces having a nodular surface. Acetic, propionic, and butyric acids represent the bulk of VFA and are derived from non-digestible carbohydrates. Fibrolytic enzymes, when supplemented to feed, may increase the proportion of oligosaccharides and simpler NSP to further the rate as well as extent of fermentation. Active absorption of VFA by mucosal enterocytes employs its ionized form together with Na+, whereas direct membrane passage occurs when non-dissociated. Most absorbed VFA favour use by the host with a portion of butyric acid together with by-products from protein digestion being retained to reform mucin and sustain mucosal integrity.

Dietary free fatty acids complex with amylose creating another form of resistant starch: Gastrointestinal formation with fowl and swine.

Fat added to poultry and swine feeds often contains abundant free fatty acids (FFA) that can impair digestible energy (DE). Placement of the fatty acid (FA) hydrocarbon chain in the helix core reformed from amylose creates a complex of both nutrients. Resulting modifications create a new structure termed the V-helix that becomes resistant to α-amylase. Granules in grain naturally contain minimal amounts of these complexes with more being generated during food manufacturing when moisture and heat release amylose in the presence of FFA. A paucity of FFA usually exists in complete feeds without sources of poor-quality fat. Animal fats and by-product meals from rendering are prominent in their saturated FFA content which favorably complex within the helix. V-helix-FA complexes may arise during their concurrent encounter of FFA together with amylose during feed manufacture, particularly pelleting. FFA in the gastrointestinal tract (GIT) are speculated to further form complexes when present together with amylose. Although amylose may be dissolved in the gastric and small intestinal milieu, FFA separately coalesce into hydrophobic fat droplets along with other dietary lipids. Formation of complexes is likely restricted until FFA are released into the aqueous phase during fat digestion. Although α-amylase may be prominent, V-helix-FA complexes being resistant to enzymic attack pass into the large intestine. Subsequent microbial catabolism of V-helices may generate volatile fatty acids that are absorbed by the mucosa; however, an inability to use FFA once released leads to their excretion and basis for decreased DE. Immature microbial populations with young animals usually lack the capacity to fully catabolize the V-helix, further extending the loss in DE.

Nutrients central to maintaining intestinal absorptive efficiency and barrier integrity with fowl.

The small intestinal mucosa acts to recover nutrients from the lumen while providing a barrier against potential hazards. Its unstirred water layer (USWL) at the lumen interface involves membrane associated mucin linearly protruding from underlying microvilli that entangles secretory mucin released from local goblet cells. Both mucin sources are dominated by repetitive O-glycosylated areas dependant on threonine, serine, glycine, and proline. Secretory mucin differs from membrane attached mucin by further employing multiple cystines that interconnect these areas into a net-like molecular sieve. All of the glycosylated areas have ionizable acidic groups credited with reducing pH from that in the lumen to create a micro environment favoring enzymes finalizing digestion while optimizing nutrient terms for absorption. Erosion of the USWL and/or abuse of the membrane due to lumen threats require continuous repair. The aforementioned amino acids are necessary in substantial amounts while vitamin B6 collaborates with vitamin A as meaningful cofactors for mucin synthesis. Marginal inadequacies of these nutrients during inordinate demand are expected to impair mucin replacement. In turn, marginal increases in feed conversion likely occur while fostering the probability of necrotic enteritis together with gizzard erosions. Abuse of the absorptive membrane is of particular concern from fatty acid hydroperoxides because of their continual presence in feed and inability of the USWL to provide protection. These hydroperoxides threaten membrane integrity by their inclusion in micelles during digestive events with fat thereby permitting transit through the USWL. Once coalesced with membrane phospholipids, structural aberrations are visualized as interfering with nutrient recovery while enabling leakage of cell contents to potentiate wet excreta. Inclusion of dietary vitamin E along with vitamin A into micelles with fatty acid hydroperoxides provides relief by quenching further peroxidation. Assuring cystine, threonine, glycine, and serine that are directly available as such together with vitamins A, E, and B6 represents one approach toward optimizing maintenance of the intestinal mucosa.