Strategies for preventing and treating coccidiosis and necrotic enteritis

The main concern from coccidiosis is that disease is not related to a single Eimeria spp. Infections result from a mixture of Eimeria species that invade different parts of the intestine, as shown in Figure 1. The intracellular parasite invades and destroys the epithelial cells of the host, causing severe damage to the intestinal wall. Nine different Eimeria species are known in poultry, only five to seven of which are associated with diseases in commercial flocks. Whereas an E. praecox infection is generally considered to produce little pathology, an infection with E. acervulina and E. mitis can result in mild enteritis followed by fluid loss and the malabsorption of nutrients.

In more severe cases, inflammation of the intestinal wall with local bleeding (haemorrhages) and sloughing of epithelia (E. brunetti, E. maxima) or complete villar destruction resulting in extensive haemorrhage and death (E. necatrix, E. tenella) is seen in infected chickens.

Most of the highly pathogenic species invade the lower parts of the digestive tract. The life cycle of Eimeria is relatively short, from four to six days, and consists of two developmental stages; exogenous (in faecal matter) and endogenous (in host digestive tract). The exogenous stage starts after the release of unsporulated (non-infective) oocysts in the faeces. Sporulation of the oocyst occurs in the faeces and is encouraged by the right temperature, humidity and access to oxygen in the litter.

The endogenous stage starts after ingestion of the infective oocysts by the chicken. (Step 3, figure 2) In the micro-environment of the gizzard, sporozoites are released from the oocyst. Further down the digestive tract, the sporozoites invade and destroy epithelial cells and start the highly efficient reproduction cycle. This involves several rounds of asexual reproduction, followed by sexual differentiation, fertilisation and the shedding of unsporulated oocysts.

Good husbandry helps to reduce the risk of transmitting the coccidiosis-causing parasites. Additional treatments are essential, especially when the parasites cause much harm to the digestive tract of the bird. The best treatment of coccidiosis depends on contamination. Consult your vet for advice for any specific situation.

Baycox® Coccidiocide Solution, one of the drugs for the treatment and control of coccidiosis in chickens, prescribed by a vet after feacal float test. caused by Eimeria species. It is administered as a water medication. Baycox Coccidiocide contains Toltrazuril, an active constituent which destroys all intracellular stages of the pathogen’s life cycle in the intestine, without impairing the chicken’s ability to acquire lifelong natural immunity against coccidia.

Use of vaccines

Besides the number of ingested oocysts, the severity of coccidiosis highly depends on their being immunological memory for the pathogen. As early as 1923, Johnson published the first articles showing that resistance to a dose of oocysts was not agedependent, but relied on earlier exposure to the parasite. Today, we still make use of this knowledge through the application of vaccines.

Dietary treatments From a dietary point of view, different strategies can be used to fight coccidiosis. Some products act anti-microbially against Eimeria-specific species, e.g. essential oils and herbal extracts. Other products beneficially modulate the immune status of the chicken, whereas prebiotics and probiotics improve microflora in the digestive tract to reduce the chance of secondary infections (e.g. C. perfringens). Damaged intestinal tissue benefits from additional antioxidants to reduce the oxidative stress caused by damaged cells. Other products improve intestinal protection and mucosal healing, e.g. betaine, butyrate or specific amino acids.

Necrotic enteritis lesions

Coccidiosis in poultry often pre-exists or occurs concurrently with field outbreaks of necrotic enteritis. The causative agent of necrotic enteritis is Clostridium perfringens. Necrotic enteritis has long been controlled by the use of antimicrobial growth promoters (AGP). In 2006, the ban on the use of AGP’s came into force and necrotic enteritis reemerged in poultry farming. Therapeutic antimicrobial agents and anti-coccidial drugs, which not only exert an effect against Eimeria spp but also against C. perfringens, are currently used to control necrotic enteritis. To achieve the new targets for reducing the use of antibiotics in livestock farming and keeping animals healthy, research for preventive alternatives is being done for many years. Understanding the pathology and predisposing factors of necrotic enteritis is helpful in searching for preventive alternatives. Necrotic enteritis usually occurs three to four weeks after hatching. The necrotic lesions are mainly restricted to the small intestine and the infection can result in an acute clinical disease or is present in a subclinical condition. In clinical cases, there is increased flock mortality during the last weeks of rearing, often without premonitory signs. The disease is acute, with death occurring within one to two hours, and mortality rates can rise up to 50%.

Chronical damage to the intestinal mucosa leads to poor digestion and absorption of nutrients, resulting in reduced weight gain and increased feed conversion. In subclinical conditions, feed intake can be reduced by 35% during the infectious period. Although clinical outbreaks of necrotic enteritis may cause high levels of mortality, the subclinical form often stays undetected in the flock. The true impact of necrotic enteritis is not from birds that die from infection, but rather those that suffer from disease and survive the subclinical form.

Available nutrients allow proliferation

Clostridium perfringens is commonly found in the normal healthy avian gut microbiota. The virulence of a strain depends on its nature. Strains of C. perfringens are classified into five different types (A to E) on the basis of the production of four major toxins. Clostridium type A is associated with necrotic enteritis in chickens, although this type is also found in the digestive tract of healthy poultry.

As necrotic enteritis is a multifactorial disease, more predisposing factors are needed for its development. High levels of (animal) protein or poorly digestible protein sources are associated with a higher risk of necrotic enteritis, as undigested protein is a growth substrate for pathogenic bacteria such as C. perfringens. Wheat, rye, oats and barley are more often associated with necrotic enteritis, due to higher levels of indigestible, water soluble, non-starch polysaccharides, whereas maize is not. Besides the choice of raw materials, particle size also seems to influence gut health. Feed containing many small and some large-sized particles is more predisposed to necrotic enteritis than feed containing uniform particles. Changes in the feeding regime, other diseases and increased stocking density increase stress in the flock and suppress the immunological status of the chickens, making them more sensitive to necrotic enteritis infection. The intestinal damage caused by coccidiosis is one of the main factors for the development of Necrotic enteritis. C. perfringens benefits from cellular components that are released when the intestinal cells are damaged. The mucosal damage caused by Eimeria provides a favourable environment for C. perfringens to proliferate.

To date, there is no single strategy to combat C. perfringens-associated necrotic enteritis. The combination of good hygiene management in poultry houses, the use of vaccination (against C. perfringens and coccidiosis) and dietary interventions can, to some extent, be an alternative to antibiotics to maintain production and control necrotic enteritis. Low-protein diets or the use of highly digestible protein sources in combination with enzymes to break down the undigestible structural components in the diet will reduce the opportunity for C. perfingens to develop in the gut. Also, the use of additives to control coccidiosis, as earlier mentioned in this article, is a helpful tool to reduce the incidence of necrotic enteritis.

Multifarious effect of butyrate

The constant immunological challenge presented by Eimeria species, concurrently with C. perfringens, makes the barrier defence function of the gut wall extremely important. Butyrate is a short-chain fatty acid that is naturally produced in the digestive tract by the fermentation of fibres. The fatty acid is considered the most important energy source for intestinal cells and has multiple beneficial effects on vital intestinal functions. Research and practical field experience confirm that butyrate alone or in combination with other dietary strategies reduces the incidence of necrotic enteritis. In the small intestine, butyrate promotes villi development, gut morphology and function. Further on in the digestive tract, butyrate represents the preferred energy source for the cells in de large intestine and is a major precursor for lipid synthesis. These lipids are used for incorporation into the cell membranes. By supporting the cell membrane structure, butyrate contributes to the maintenance of the barrier and transporter functions in the gut. Researchers observed an important role of butyrate in intestinal wound-healing owing to its positive effect on tight junctions (connections between gut cells) and gut integrity. At low concentrations, butyrate reinforces the intestinal defence barriers by increasing the release of protective mucins in the mucus layer and the release of antimicrobial peptides. These peptides, also called host defence peptides (HDPs), possess a broad spectrum of antimicrobial activity against bacteria, protozoa, enveloped viruses and fungi. HDPs bind to the microbial membrane and cause membrane disruption, which results in microbial death.

The Belgian research group of Van Immerseel shows another antimicrobial efficacy of butyrate, whereby the fatty acid reduces the ability of pathogenic bacteria to adhere to the gut cell wall. Finally, butyrate acts as an antiinflammatory agent. Tempering the inflammatory status of the chicken is a useful tool to overcome feed intake reduction and thereby reduce the breakdown of muscle tissue during necrotic infection. Uncoated butyrate is directly absorbed in the first part of the small intestine and does not reach the lower parts of the digestive tract. Proper coating of dietary butyrate is essential for a targeted release of the fatty acid over the whole digestive tract. By testing the microencapsulated butyrate product Excential Butycoat it is shown that all butyrate passes the stomach and is gradually released in the intestinal tract.

Conclusion

Since the ban on in-feed antibiotics, necrotic enteritis caused by C. perfringens has re-emerged in avian flocks with a severe economic impact. As the occurrence of drug-resistant strains is a significant problem for public health and long-term control strategies against necrotic enteritis, solutions to control necrotic enteritis must be found in alternatives to conventional medication. Nutrition strongly influences the incidence of necrotic enteritis and the other pre-existing pathogenic infection coccidiosis. Proper micro-encapsulated butyrate in the diet ensures a targeted release of butyrate throughout the digestive tract, thus supporting intestinal cells and reinforcing the mucosal barrier function damaged by Eimeria species and C. perfringens.