Background

Balanced intestinal microflora help prevent necrotic enteritis

//30 Aug 2011
Necrotic enteritis is a disease affecting chickens and turkeys throughout the world. Certain factors are known to predispose birds to this disease. Keeping a healthy balance of intestinal microflora seems to be a key element in the prevention strategy. Affected flocks need to be treated to minimise death losses.

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By Dr. Tahseen Aziz, Rollins Animal Disease Diagnostic Laboratory, Raleigh, NC, USA and Dr. H. John Barnes, College of Veterinary Medicine, NC State University, Raleigh, NC, USA
Necrotic enteritis (NE) is an enteric bacterial disease of chickens, turkeys, and a few other avian species caused by Clostridium perfringens. The disease is characterised by damage to the intestinal mucosa by toxins produced by the causative bacteria. It is worldwide in distribution and causes considerable financial losses to broiler producers due to mortality and, in its milder subclinical form, poor growth and feed utilisation. In commercially raised broiler chickens, clinical disease usually occurs between 2 and 5 weeks of age.
The causative bacterium
Necrotic enteritis is caused by C. perfringens, a gram-positive, rod-shaped, spore-forming, anaerobic bacterium. C. perfringens is ubiquitous, found in used litter, soil, and intestinal tracts of healthy birds. Feed and litter contaminated with large numbers of C. perfringens have been convincingly implicated as a source of infection. The disease occurs when C. perfringens overgrows in the intestinal tract and produces potent toxins that severely damage the intestinal mucosa. Toxins absorbed from the intestinal tract produce a toxemia (toxin in blood), which is responsible for death of the bird. Thus, NE is a type of “enterotoxemia”.
 
C. perfringens is divided into five toxinotypes (A, B, C, D, and E) based on four major toxins (alpha, beta, epsilon, and iota). The majority of isolates from NE cases are type A, with a few cases caused by type C. Alpha toxin produced by types A and C, beta toxin produced by type C, and possibly other toxins produced by the organism are responsible for the damage to the intestine, enterotoxemia, and death of the bird.
A segment of small intestine from a 31-day-old broiler chicken affected with NE. There is blood-tinged fluid admixed with necrotic debris in the lumen (A). Note the necrotic, red-brown mucosa. The mucosa in figure B has a velvety appearance, a lesion characteristic of necrotic enteritis.
C. perfringens is part of the normal flora of the digestive tract of broilers. Typically, it can be found in the crop, duodenum, jejunum, ileum, and ceca of healthy birds. The population of C. perfringens in the intestine is affected by nutritional and environmental factors and health status of the gut of the bird . Molecular typing (genetic fingerprinting) has shown that isolates of C. Perfringens from the intestines of healthy birds in a flock have high genetic diversity, whereas isolates from birds in a NE outbreak are only one, or less commonly, two genetic types.
Pathogenesis is partly unclear
The pathogenesis of NE is not fully understood. There is convincing evidence that C. perfringens strains vary in virulence and that NE is caused by certain strains of the organism (“NE strains”). Why these are capable of inducing NE remains unknown. Several studies have shown that in a NE outbreak, a single virulent strain displaces the genetically heterogeneous enteric population of C. perfringens in the intestinal tract of the chicken. However, it is not clear what molecular properties or virulence factors these NE-causing strains have that enable them to effectively compete and selectively proliferate in the gut to produce tissue damage. So far, no particular genetic type of C. perfringens has been identified that causes NE. Cluster analysis of C. perfringens isolates from intestinal tracts of healthy chickens and chickens with NE did not show that NE is caused by C. Perfringens strains that belong to a specific genotypic lineage.
The small intestine from a 31-day-old chicken affected with NE is dilated and thin. Only birds that have been euthanised or died very recently can be evaluated as the changes seen here can develop postmortem as gas increases in the gut after the bird dies.
Alpha toxin, produced by C. perfringens toxinotype type A, is an important virulence factor in the pathogenicity of the organism. It is a phospholipase that hydrolyses phospholipids in membranes of red blood cells, white blood cells, platelets (thrombocytes), endothelial cells, and muscle cells; because of its hydrolytic property, the toxin is hemolytic, cytotoxic, necrotising, and potentially lethal. Large variations in the amount of alpha toxin are produced by different isolates of C. perfringens in vitro, but isolates of the same genetic type produce the same amount of alpha toxin.
However, the amount of alpha toxin produced by C. perfringens isolated from NE lesions is not significantly different from the amount of the toxin produced by isolates from the intestine of healthy birds. Recently, another novel toxin (NetB) has been identified in certain strains of C. perfringens. Initially, this toxin was thought to be the major and critical virulence factor in C. perfringens strains capable of causing NE, but recently published research indicates that NetB-negative strains are also capable of causing NE in experimentally challenged chickens. Certainly, the role of NetB as a virulence factor in the pathogenesis of NE needs further investigation.

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Source: World Poultry, Vol. 27, No. 6
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