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Clostridial Necrotic Enteritis and
Magne Kaldhusdal1 and Atle Lovland2
Researcher1, Poultry specialist2
National Veterinary Institute,
From time to time clostridial enteritis turns up as a big problem in various regions. The reasons for these problems are complex, but resistance against in-feed antibacterial and anticoccidial compounds has been one of the factors involved. However, in general these compounds have been very successful in preventing necrotic enteritis, and still are. So why do we see an increasing interest in this disease complex now? One major reason is restrictions on the use of in-feed antibacterial and anticoccidial compounds that have limited the use of these preventive measures, and more restrictions are expected to come. Another reason may be that after 40 years with more or less unpredictable and sometimes severe problems, the broiler (and turkey) industry wants to find out more about how to control the disease. This paper presents some basic information and evaluations that hopefully are useful in the understanding of this important disease complex.
Clostridial enteritis and (cholangio)hepatitis is caused by Clostridium perfringens (CP). Toxin types A and C of this bacterium have been associated with disease outbreaks. The typical gut lesions have been reproduced experimentally by intraduodenal infusion of toxins produced by CP type A. The alpha toxin was most likely the factor causing the gut lesions (Al-Sheikhly and Truscott, 1977b). CP toxin type A is ubiquitous, spore forming, extremely prolific, and toxigenic. These attributes enables the bacterium to be present at almost any time and place with poultry, and then proliferate and produce toxins when the circumstances are favourable.
Necrotic enteritis has been reported in many bird species. Among chickens the disease is by far most common in broilers, but outbreaks in layer pullets and adult layer strain chickens have also been reported.
Lovland and Kaldhusdal (2001) studied the association between Clostridium perfringens infection and production performance in commercial
broiler flocks during a 2.5 years time period when clinical and subclinical necrotic enteritis was frequently seen. They found that the farmers profit on average was reduced by 33 % when comparing flocks with high and low levels of the disease. Impaired feed conversion, reduced live weight at slaughter and increased condemnation percentage were major causes of production losses associated with Clostridium perfringens infection. Subclinical clostridial enteritis has also been associated with impaired feed conversion and retarded growth in a pen trial (Kaldhusdal and Hofshagen, 1992).
The clinical appearance of clostridial enteritis may vary a lot, from no other symptoms than impaired performance to a sudden and high mortality. The disease can affect birds at almost any age, but in our experience the disease most commonly occurs in broilers two weeks of age or older. Age pattern of the disease may vary, depending on factors like immunity and management, including types and programs of in-feed additives.
Pathogenesis and predisposing factors
The pathogenesis of the natural disease is far from well understood. In our experience (Kaldhusdal et al., unpublished data) the pathogenic bacterium is usually present in numbers sufficient to induce subclinical disease, if no antibacterial compounds are added to the feed. However, the appearance of clinical disease even in flocks offered feed with antibacterial compounds, suggests that a number of interacting, known and unknown factors influence the disease process significantly. As with other clostridial diseases, feed composition and feeding practises are assumed to affect disease incidence (Kaldhusdal, 1999). Coccidial infections are assumed to be a predisposing factor in many cases. These organisms invade and damage intact mucosal gut tissue, which is likely to favour the establishment of a non-invasive bacterium like Clostridium perfringens. But necrotic enteritis no doubt can appear in the absence of coccidia.
At the molecular level, one or several factors triggering the alpha toxin production of Clostridium perfringens may be essential. Once the bacteria produce significant amounts of toxins, these toxins eventually induce gut tissue necrosis, favouring proliferation of Clostridium perfringens and further tissue damage within the mucosa.
The development of liver lesions is poorly understood. Both bacteria and toxins may be transported through a damaged gut mucosa to the liver by the blood. An ascending infection via the bile tree, and inflammatory processes obstructing the bile flow, are other possibilities.
The characteristic lesions are found in the mucosa of the small intestine. Mild lesions appear as small (in some cases barely visible to the naked eye) ulcers or light yellow spots on the surface of the mucosa, usually in the anterior part of the gut. More severe lesions may show membranes covering the entire mucosa of large segments of the small intestine, in some cases even the colorectum and the caecal tonsils.
Two types of liver lesions have been described (Onderka et al., 1990, Løvland and Kaldhusdal, 1999). An inflammation affecting the bile tree
(cholangiohepatitis) is the most common lesion type. Intrahepatic parts of the bile tree are most frequently affected, but gall bladder and extrahepatic bile duct changes may also be found. Another liver lesion type associated with CP infection is multifocal hepatitis, histologically characterized by fibrinoid necroses with or without an inflammatory response.
Experimental disease models
Numerous workers have reproduced clostridial necrotic enteritis experimentally using a challenge model (Al-Sheikhly and Truscott, 1977ab,
Prescott et al., 1978, Brennan et al., 2001). We have recently developed a necrotic enteritis model (Kaldhusdal et al., unpublished) based on the
assumption that a spontaneous CP infection sufficient to induce a natural, mild clostridial necrotic enteritis usually takes place, providing the appropriate predisposing factors are present. The average frequency of individuals with specific lesions in the eight first experiments using this model was 20.9 %. The model has already been used to test the effect of vaccines, litter types and feed additives (unpublished data) on clostridial enteritis.
Few studies on the immunity against Clostridium perfringens infection in poultry have been published. Heier et al. (2001) found that the level of maternal antibodies to CP alpha toxin in day-old broiler flocks varied considerably and was influence by parent flock age. Unpublished data from our own laboratory (Kaldhusdal et al.) indicate that levels of specific maternal antibodies can be increased substantially by vaccination of the parent hens. Further, this increase in maternal antibodies has been associated with reduced levels of spontaneous necrotic enteritis. Lovland et al. (unpublished data) have also found increased levels of specific serum antibodies in flocks with a previous experience of CP infection.
Clinical disease is best diagnosed by examination for gross intestinal lesions in birds that have died with the disease. Gross lesions are usually distinct from those of coccidiosis. In cases of doubt, direct microscopy of gut smears showing few or none coccidia will help establish the diagnosis. The presence of birds with cholangiohepatitis among bird from such flocks is another helpful indicator, although this is relatively seldom seen. If many coccidia are found in gut smears, and the gross lesions are considered ambiguous, histological and microbiological examinations may be required for a definitive diagnosis. In some cases of mixed infections, it may be impossible to verify which one is of
primary importance. Subclinical disease can best be diagnosed by random sampling of live birds in flocks with vague symptoms or suboptimal performance. Gut lesions must be looked for immediately following euthanasia of the birds. The gross lesions of the intestinal mucosa are specific, but some experience is required to detect and recognize especially the most moderate lesions.
Bacteriology is most useful if quantitative examinations are done. Gut contents or faeces should contain at least 1 million (often 100 and even 1000 millions in individual specimens) CP per gram if CP-associated necrotic enteritis is likely to be the disease cause.
Broiler flocks may be monitored for level of CP infection if reliable records of specific liver lesions at slaughter are available (Løvland and Kaldhudal, 1999). Unpublished data from our laboratory (Lovland et al.) suggest that broiler flocks may be monitored by examination of blood samples for CP specific antibodies. This method is based on the ELISA technique, and may possibly be established in laboratories using ELISA serology. However, further work is required before the method can be used on a routine basis.
At present clostridial enteritis and hepatitis is best controlled by use of in-feed antibacterial compounds.
Natural gut flora products have been shown to reduce the disease frequency and Clostridium perfringens counts in experiments (Elwinger et al 1992, Hofacre et al., 1998, Craven et al. 1999) and in a farm with recurring problems (Kaldhusdal et al., 2001).
Vaccination may become a viable alternative in the future.
1) Clostridial necrotic enteritis cannot be prevented by means of good hygiene alone.
2) Clostridial enteritis exists in subclinical as well as clinical form. Both forms affect productivity significantly.
3) The diagnosis of clinical and subclinical necrotic enteritis requires different procedures.
4) Preliminary findings at our laboratory suggest that clostridial necrotic enteritis may be monitored using an ELISA assay on blood samples from broiler flocks.
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The Elanco Global Enteritis Symposium July 9-11, 2002 Clostridial Necrotic Enteritis
and Cholangiohepatitis, Abstract, G-3 to G-8