Coccidiosis is estimated to cost poultry industry US$3 billion annually, and is also a well-known predisposing factor for necrotic enteritis—widespread in broilers and responsible for losses of US$5-6 billion worldwide each year.
Mycotoxins in feeds, even at permitted levels, aggravate coccidiosis in poultry. They can facilitate Eimeria colonization in the gut, and poultry producers looking to reduce the impact of coccidiosis on their flocks would do well to monitor feed for contamination.
Gate openers to infection
Further research is required to fully understand the underlying mechanism that results in mycotoxins’ amplification of coccidiosis, however, possible explanations include increased immunosuppressive effects on modern high performing broilers, chronic low level mycotoxin exposure, and the potential for synergistic effects between mycotoxins.
Deoxynivalenol and fumonisins are known to interfere with several vital functions of cells, and disrupt intestinal cells that act as a barrier between pathogens and the birds’ bodies. These disrupted intestinal cell components can be used as a growth substrate for pathogens such as Eimeria, Clostridium and Escherischia coli.
In this way, these mycotoxins play a main role as ‘gate openers’ favoring pathogen colonization throughout the host.
Unsafe at any level
Even at concentrations allowed under European and US guidelines for mycotoxins (Table 1), deoxynivalenol, fumonisins and a combination of the two can worsen the incidence and severity of coccidiosis in challenged poultry, studies have shown.
Chickens fed mycotoxin-contaminated feed at levels well below regulatory guidelines in starter and grower diets (Table 2) displayed considerably higher lesion scores, higher numbers of oocysts in both the jejunum and in excreta, and higher lymphocyte (white blood cell) counts.
Lesion scoring in the cecum was 1.33 for the mycotoxin groups versus 0.42 for birds fed control diets (Figure 1). The number of oocysts found in the jejunum was three times higher for birds fed mycotoxins versus control. Similarly, the number of oocysts recorded in feces was 29 percent higher for the deoxynivalenol + fumonisins group and 46 percent higher for the fumonisins group.
While the poultry industry has a general awareness of the dangers linked to certain mycotoxins, the threat of the synergistic effects of deoxynivalenol and fumonisins has been largely overlooked.
Yet, these mycotoxins occur frequently in the most common poultry diet ingredients, including finished feed, maize, wheat and soybean meal.
Figure 2 reveals that deoxynivalenol was detected in 61 percent of maize, 54 percent of wheat, 71 percent of finished feed and 61 percent of soybean meal samples analyzed. Fumonisins were detected in 80 percent of maize, 27 percent of wheat, 66 percent of finished feed and 40 percent of soybean meal samples.
The implication for poultry producers looking to limit the use of antibiotics is to adopt robust mycotoxin risk management in order to protect flocks.
As animal production is shifting towards reduction of antibiotics in the near future, good farm management coupled with a mycotoxin risk management plan based on the use of authorized additives represents a winning strategy. Probiotics and phytogenic feed additives, with or without the use of coccidiostats or vaccines, can help alleviate the negative effects of coccidial infection, having been shown to reduce oocyst shedding, severity of intestinal lesions, and adverse effects on performance.