Readers' Rating:

(See details)  Rate this article

In a recent survey, it was estimated that the cost of subclinical necrotic enteritis was as high as $0.05 per bird (Van der Sluis, 2000). Using these estimates and 1999 estimates on world broiler meat production, the cost of necrotic enteritis to the poultry industry globally is nearly $2 billion (Anonymous, 2000). Both clinical and subclinical necrotic enteritis is common in all poultry growing areas of the world (Van der Sluis, 2000). The disease was first described by Parish (1961) and has subsequently been reported from most areas of the world (Ficken and Wages, 1997). The causative agent of necrotic enteritis is Clostridium perfringens, a nearly ubiquitous anaerobic bacteria that can be readily found in soil, dust, feces, feed, poultry litter and in intestinal contents (Ficken and Wages, 1997).


Clostridium perfringens: the opportunist

Given the ubiquitous nature of C. perfringens, it is not surprising that we cannot attribute the clinical disease, necrotic enteritis, to only one cause.

However, it does appear that conditions that result in damage to the intestinal mucosa (coccidiosis, mycotoxicosis) or disturbance to the normal intestinal microflora predispose birds to proliferation of Clostridium (Al-Sheikhly and Al-Saieg, 1980; Elwinger et al., 1992; Ficken and Wages, 1997; Fukata et al., 1991). Smith (1965) found that manipulating the diet affected the population of C. perfringens in the intestine, suggesting necrotic enteritis may be precipitated by the diet. High levels of animal by-products, (i.e. fishmeal) wheat, barley, oats or rye, have been shown to predispose birds to the disease (Branton et al., 1987; Ficken and Wages, 1997; Kaldhusdal and Skjerve; 1996; Kaldhusdal, 2000). Therefore, in those poultry growing areas of the world that feed wheat or large amounts of fishmeal, the incidence and also the severity of the disease is more extreme than in areas that rely on a corn/maize-based ration.


Subclinical necrotic enteritis

The subclinical form of the disease may be the most economically important since it has been shown to impair feed conversion in broilers (Stutz and Lawton, 1984). Another form of subclinical necrotic enteritis is a hepatitis or cholangiohepatitis found in broilers at processing (Lovland and Kaldhusdal, 1999). It has been estimated that broiler flocks in Norway had losses due to liver condemnations as great as 20% (Schaller, 1998).


Prevention

PAST AND PRESENT METHODS

Most prevention strategies have taken the form of antibacterial feed additives, often called growth promotants, such as bacitracin, virginiamycin, avoparcin, lincomycin, tylosin and penicillin (Ficken and Wages, 1997; George et al., 1982; Hafshagan and Kaldhusdal, 1992; Maxey and Page, 1977; Stutz and Lawton, 1984, Watkins et al., 1997). Also, the ionophore anticoccidial agents have been shown to reduce the level of anaerobic bacteria such as C. perfringens (Prescott and Baggot, 1993). Dietary manipulation by lowering the level of fishmeal, wheat, or barley can also help prevent clostridial infections (Ficken and Wages, 1997; Kaldhusdal and Skjerve, 1996).

FUTURE PREVENTION STRATEGIES

In 1999, the European Union prohibited the use of the antibacterial feed additives that have most successfully controlled the incidence of both clinical and subclinical necrotic enteritis. Consequently, many countries have experienced necrotic enteritis in near epidemic proportions (25-40%) in broiler flocks (Kaldhusdal and Lovland, 2000). There are concerns by consumers and also government health officials regarding the use of these antibiotics in food producing animals due to the potential transfer of antibiotic resistance to human bacterial pathogens. The consequence of these actions is limiting or eliminating use of antibiotic growth promotants in many broiler-producing areas of the world. Therefore, new methods of prevention of necrotic enteritis must be investigated.


Probiotics and competitive exclusion

It has been well documented that disturbances in the intestinal microflora can result in elevated levels of C. perfringens, therefore the use of probiotics and competitive exclusion have been extensively investigated. Fukata et al. (1991) found that the pathogenicity of C. perfringens could be reduced by feeding chicks a monoflora of either Lactobacillus acidophilus or Streptococcus faecalis. Others have demonstrated that use of undefined competitive exclusion cultures of chicken intestinal flora, either fresh or freeze-dried, could reduce the incidence of necrotic enteritis, the cecal colonization of C. perfringens and also prevent the subclinical effects on body weight and feed efficiency in broiler chickens (Elwinger et al., 1992; Hofacre et al., 1998).


Complex carbohydrates/prebiotics

Sugars such as mannose have been used to decrease the colonization of salmonella. Recent research has demonstrated these compounds may also be effective in reducing necrotic enteritis lesions in broiler chickens (Branton et al., 1997; Kaldhusdal, 2000).


Enzymes

It is well documented that addition of enzymes to barley, wheat, or ryebased diets will increase the nutritive value of these cereals for broiler chickens. It has also been reported that these enzymes may reduce the occurrence of Clostridium-associated intestinal and hepatic conditions (Kaldhusdal, 2000).


Coccidia control

Control of coccidia, either natural infections or in controlled exposures (live vaccination), becomes more critical in those broiler growing locations that no longer use feed additive antibiotics. There is a distinct advantage to using ionophore anticoccidials due to the antibacterial effects of these products (Prescott and Baggot, 1993). It has also been demonstrated that the intestinal clostridial counts are higher (10 days post-vaccination) in chickens given an attenuated live coccidial vaccine than in the unvaccinated birds (Waldenstedt, 1998).


Recent research with competitive exclusion cultures and dietary additives

METHODS

A battery cage study using 960 male broiler chickens (Cobb) was designed to determine the efficacy of various compounds either alone or in combination in controlling necrotic enteritis caused by C. perfringens. Treatments consisted of a control, two competitive exclusion cultures (Avi-Free and All-Lac XCL) and five dietary additives including BMD, Bio-Mos (mannan oligosaccharide), fructooligosaccharide, an herbal supplement and an acid additive (Table 1). There were eight replicates of 12 male chicks per treatment. The competitive exclusion bacterial cultures were administered by coarse spray to the chicks on day 0 (0.5 ml/chick). To prevent crossing of the probiotic strains, the cages were randomized within each treatment of the respective probiotic.

Table 1. Treatment groups for necrotic enteritis prevention study.

1E. acervulina and E. maxima challenged at 15 days of age. 2Challenged with Clostridia at 18, 19, and 20 days of age. 3Mixed at 25 g/L water, applied as a coarse spray (1 L/2000 chicks)

The necrotic enteritis infection model used in the present study consisted of a solitary oral inoculation of Eimeria acervulina and E. maxima at 15 days of age followed by serial oral inoculation of C. perfringens (approximately 108 CFU/bird) days 18, 19, and 20. The basal diet offered on days 0-16 contained 26% fishmeal. Feed consumption was measured from day 0 to 15 and days 15 to 28. All birds were weighed by cage on days 0, 15, and 28.

Necropsies of all mortality from day 18 were conducted to determine cause of death. On day 22, two birds from each cage were randomly selected, sacrificed, weighed, and scored for the level of necrotic enteritis intestinal lesions (0 = none, 1 = mild, 2 = moderate, 3 = marked/severe). Remaining chicks were sacrificed, weighed and lesion-scored on day 28.


RESULTS

The challenged control had the highest mortality due to necrotic enteritis (Figure 1). Broilers treated with All-Lac XCL and Bio-Mos + All-Lac XCL had the lowest necrotic enteritis-associated mortality.

There were no significant differences between treatments in weight gain (Figure 2). However, in regard to the effects of the C. perfringens challenge on feed efficiency, the Bio-Mos + XCL broilers performed as well as those continuously treated with BMD (Figure 3).

Figure 1. Necrotic enteritis mortality (Columns with different letters are different, P< 0.05).

Figure 2. Weight gain day 0 to 28 (Columns with different letters are different, P< 0.05).

At day 28, the total intestinal gross necrotic enteritis lesion scores were highest in the group given FOS with little difference among any of the other treatments, including BMD (Figure 4). The lack of marked differences in lesion scores among the treatments is most likely due to the high mortality resulting from the necrotic enteritis challenge model prior to 28 days of age.

Figure 3. Feed conversion day 0 to 28 (Columns with different letters are different, P< 0.05).

Figure 4. Average necrotic enteritis lesion score (day 28) (Columns with different letters are different, P< 0.05).

References

Al-Sheikhly, F. and A. Al-Saieg. 1980. Role of coccidia in the occurrence of necrotic enteritis of chickens. Avian Dis. 24:324-333.

Anonymous. 2000. World growth continues. Poultry International 39, No. 1:8-14.

Branton, S.L., F.N. Reece and W.M. Hagler. 1987. Influence of a wheat diet on mortality of broiler chickens associated with necrotic enteritis. Poultry Sci. 66:1326-1330.

Branton, S.L., B.D. Lott, J.W. Deaton, W.R. Maslin, F.W. Austin, L.M. Pote, R.W. Keirs, M.A. Latour and E.J. Day. 1997. The effect of added complex carbohydrates or added dietary fiber on necrotic enteritis lesions in broiler chickens. Poultry Sci. 76:24-28.

Elwinger, K., C. Schneitz, F. Berndtson, O. Fossum, B. Teglof and B. Bagstrom. 1992. Factors affecting the incidence of necrotic enteritis, cecal carriage of Clostridium perfringens and bird performance in broiler chicks. Acta. Vet. Scand. 33:369-378.

Ficken, M.D. and D.P. Wages. 1997. Necrotic enteritis . In: Diseases of Poultry, 10th (B.W. Calnek, ed). Iowa State University Press, Ames, Iowa. pp. 261-264.

Fukata, T., Y. Hadate, E. Baba and A. Arakawa. 1991. Influence of bacteria on Clostridium perfringens infections in young chickens. Avian Dis.
35:224-227.

George, B.A., C.L. Quarles and D.J. Fagerberg. 1982. Virginiamycin effects on controlling necrotic enteritis infection in chickens. Poultry Sci. 61:447- 450.

Hofacre, C.L., R. Froyman, B. George, M.A. Goodwin and J. Brown. 1998. Use of Aviguard, virginiamycin, or bacitracin MD against Clostridium perfringens-associated necrotizing enteritis. J. Appl. Poultry Sci. 7:412- 418.

Hafshagen, M. and M. Kaldhusdal. 1992. Barley inclusion and avoparcin supplementation in broiler diets. 1. Effect on small intestinal bacterial flora and performance. Poultry Sci. 71:959-969.

Kaldhusdal, M.I. 2000. Necrotic enteritis as affected by dietary ingredients. World Poultry 16, No. 6:42-43.

Kaldhusdal, M. and E. Skjerve. 1996. Association between cereal contents in the diet and incidence of necrotic enteritis in broiler chickens in Norway. Preventive Vet. Med. 28:1-16.

Kaldhusdal, M. and A.L. Lovland. 2000. The economical impact of Clostridium perfringens is greater than anticipated. World Poultry 16, No. 8:50-51.

Lovland, A. and M. Kaldhusdal. 1999. Liver lesions seen at slaughter as an indicator of necrotic enteritis in broiler flocks. FEMS Immunol. and Med. Micro. 24:345-351.

Maxey, B.W. and R.K. Page. 1977. Efficacy of lincomycin feed medication for the control of necrotic enteritis in broiler-type chickens. Poultry Sci. 56:1909-1913.

Parish, W.E. 1961. Necrotic enteritis in the fowl. J. Comp. Path. 74:377- 393.

Prescott, J.F. and J.D. Baggot. 1993. Ionophore antibiotics. In: Antimicrobial therapy in Veterinary Medicine, 2nd ed. Iowa State University Press, Ames, Iowa. pp. 263-267.

Schaller, D. 1998. Necrotic enteritis in poultry production - the Norwegian experience. Proceedings of European Poultry Symposium, Bayer AG, Cascais, Portugal. pp. 37-42.

Smith, H.W. 1965. The development of the flora of the alimentary tract in young animals. J. Pathol. Bacteria. 90:495-513.

Stutz, M.W. and G.C. Lawton. 1984. Effects of diet and antimicrobials on growth, feed efficiency, intestinal Clostridium perfringens, and ideal weight of broilers chicks. Poultry Sci. 63:2036-2042.

Van der Sluis, W. 2000. Clostridial enteritis is an often underestimated problem. World Poultry 16, No. 7:42-43.

Waldenstedt, L. 1998. Coccidial and Clostridial infections in broiler chickensinfluence of diet composition. Doctoral thesis, Swedish University of Agricultural Sciences, Uppsala, Sweden.

Watkins, K.L., T.R. Shryock, R.N. Dearth and Y.M. Saif. 1997. In vitro antimicrobial susceptibility of Clostridium perfringens from commercial turkey and broiler chicken origin. Vet. Microbiol. 54:195-200.

Readers' Rating:

(See details)  Rate this article