Mycotoxins and Their Effects on the Intestinal Health of Poultry06 November 2013
In a presentation to the World Veterinary Poultry Association (WVPA) Congress, Professor Siska Croubels focused on the effects of Fusarium trichothecenes on the intestinal health of poultry. Senior editor, Jackie Linden, reports.
Contamination of feeds with mycotoxins is a worldwide problem, Professor Croubels explained, with the most important for poultry being those produced by the genera, Fusarium, Aspergillus and Penicillium.
From the Faculty of Veterinary Medicine of Ghent University at Merelbeke in Belgium, Professor Croubels was addressing the WVPA Congress in the French city of Nantes in August 2013 on Fusarium trichothecenes and their impacts on the intestinal health of poultry.
Mycotoxins are a historical problem in poultry, first recognised in the 1960s as the cause of 'turkey X disease', she said.
Surveys of mycotoxin levels in poultry feeds often reveal the presence of a number of different toxins; most samples in a recent survey contained at least 10 contaminants.
Their effects on poultry health vary, depending on the type and concentration of the mycotoxins present in the feed, the age of the bird and other nutritional factors. Some of the toxins cause specific effects, while others are more generalised, as shown in the table.
|Effects of mycotoxins in poultry|
| Zearalenone (ZON)
T-2 toxin (T-2)
Ergot alkaloids (Ergot)
| Decreased hatchability
Decreased egg production
Delayed sexual maturation
|Ochratoxin A (OTA)|| Damage to the kidneys
Increased water consumption
| Gizzard lesions
| Aflatoxin B1 (AFB1)
| Fatty liver
H-2 toxin (H-2)
| Oral and dermal lesions
Inflammation of mucous membrane in oral cavity
| In the egg:
Poor egg shell quality
Blood and meat spots
The main targets of Fusarium trichothecene mycotoxins are those cells and tissues that are rapidly proliferating and differentiating, Professor Croubels explained, so those in the small intestine, liver and immune cells are particularly affected by these toxins.
Cells that line the intestine - the mucosa - form a barrier that regulates the uptake of water and nutrients. The mycotoxin, deoxynivalenol (DON), has been studied particularly because of its ability to alter normal gut and immune function; diets containing levels of DON insufficient adversely to impact bird performance have been shown to alter the morphology (structure) of the small intestine and disrupt the intestinal barrier function.
Studies of the mode of action of DON have shown that it can reduce the villus height and the crypt depth in the small intestine, thus lowering the area for the absorption of nutrients. Furthermore, Professor Croubel said, the reduction in crypt depth indicated the impairment of the regeneration of the barrier and thus also its function.
Another effect of the DON is its ability to impair protein synthesis so it appears to hasten epithelial cell death while also slowing down cell proliferation.
In turkeys, feeding a low level of T-2 toxin over a prolonged period resulted in shorter and thinner villi as well as reduced enterocyte migration, another sign of disruption to the intestinal barrier.
Research in pigs has shown that DON weakens the junctions between the intestinal lining cells and it has been suggested that it might have similar effects in poultry. What has been demonstrated in broilers is that DON changes gene expression of interleukin cells, thus impacting the immune response and causing an inflammatory reaction as well as oxidative stress in the jejunum.
Professor Croubels explained that in broilers, it has been shown that it is the intestine - rather than the liver - that plays the leading role in increasing the bioavailability of veterinary drugs and feed additives by means of active transport. The reverse process, efflux, or active removal of products from the body into the gastric lumen also occurs in the intestine. Thus DON's effect of damaging the intestinal barrier can both decrease or increase the bioavailability of drugs and feed additives.
Impaired intestinal function caused by mycotoxins can also increase the susceptibility of poultry to enteric infections, Professor Croubels said, as pathogens are more easily able to pass through the barrier where the cellular junctions are weakened.
Work at her laboratory has shown that both DON and fumonisins have an important impact on predisposing chicken to necrotic enteritis. By damaging the intestinal lining, DON increases the concentration of proteins in the small intestine, a situation that is known to promote the growth of the clostridial bacteria that are the main cause of necrotic enteritis.
In her conclusions, Professor Croubels stressed that her work has been mainly focused on DON and that there is limited research on the effects of other mycotoxins on poultry intestinal health. She considers that future research should examine the effects of other mycotoxins at low levels, both individually and in combination, as they are usually present at the same time in feeds and feed ingredients and are likely to have some synergistic effects on poultry health.
Finally, she added, the presence of masked mycotoxins and hitherto unidentified fungal metabolites may lead to underestimation of the total mycotoxin level in animal feeds. The masked forms, Professor Croubels said, are usually present as plant- or mould-derived conjugates. These are not detected by current analytical methods and it is not yet know if the conjugated forms are made active through hydrolysis in the intestine.