Current development

Note 15-30
Lelystad, December 23rd 2015

NECROTIC ENTERITIS: WHEN MYCOTOXINS MEET C. Perfringens

Mycotoxins are ubiquitous feed contaminants that can lead to acute or chronic effects depending on the
affected animal species. Poultry are particularly tolerant to Fusarium mycotoxins such as
deoxynivalenol (DON) and fumonisins (FBs). For instance, the EU directive requires maximum DON
concentrations of 1 and 5 ppm in complete feeds for pigs and poultry, respectively. Also, this directive
has determined the maximum tolerable levels of FBs in complete feed for pigs and poultry at 5 and 20
ppm, respectively. Hence, it is not surprising that contaminated feedstuffs are usually diverted to poultry
feed. When birds are exposed to DON and FBs in the field no acute clinical signs are observed. As a
result, these mycotoxins are sometimes considered to be of minor economic importance. Besides, it is
complicated to determine the economic impact of these mycotoxins during chronic low level exposure.
Necrotic enteritis (NE) is an important cause of production losses in the poultry industry, especially the
subclinical form, which is more prevalent in broiler flocks than the form with clinical manifestations.
The subclinical form of NE is characterized by reduced weight gain and increased feed conversion ratio.
The causative agent of NE is a pathogenic gram-positive bacterium Clostridium perfringens, which is
commonly present in the distal parts of the gastrointestinal tract of healthy poultry. Under specific
conditions that result in damaged intestinal mucosa (e.g. coccidiosis), the uptake of nutrients by the bird
will decrease. As a consequence, the increased amount of non-absorbed nutrients will become available
for proliferation of pathogenic C. perfringens in the proximal parts of the intestines, potentially
culminating in NE.
It is known that Fusarium mycotoxins DON and FBs are able to harm the gastrointestinal tract. DON
negatively affects intestinal morphology and integrity, which means less absorption of nutrients. Also,
under DON exposure, the intestines become more vulnerable to infections. FBs affect intestinal
morphology, integrity and immunity. Based on the knowledge that both mycotoxins are able to harm
the gastrointestinal tract, and that NE can develop when proliferation of pathogenic C. perfringens
increases in the proximal parts of the intestines, it can be supposed that these mycotoxins play an
important role in NE. The research group from Ghent University (Ghent, Belgium) has recently
addressed and answered this question (Antonissen et al., 2014, 2015). In two well-designed studies with
DON and FBs this research group evaluated the interaction between the pathogenic C. perfringens and
each of the mycotoxins. The studies combined in vitro and in vivo experiments.
In the first study, DON was used at concentrations below the maximum guidance level of 5 ppm for
poultry: 2.8 4.4 ppm. The authors supposed that within these levels that are considered safe, intestinal
harm caused by DON could lead to an increase in the nutrient availability for overgrowth of pathogenic
C. perfringens, thus culminating in NE. Although DON was not directly involved in pathogenic C.
perfringens growth, the presence of this myxocotin in feed increased the number of chickens affected
by NE, due to an augmented intestinal free protein concentration, and intestinal leakage.

In the second study, FBs (FB1+FB2) were used at concentrations below the maximum guidance level
of 20 ppm for poultry: 18.6 ppm. As for DON, the authors considered these levels sufficient to act as a
predisposing factor for NE development. Once more, their hypothesis was correct. Although there was
no direct correlation between Fusarium mycotoxin and pathogenic C. perfringens growth in vitro, the
ileal concentration of this bacterium was increased in broilers that were exposed to diets contaminated
with FBs. Furthermore, the presence of this myxocotin in feed negatively affected intestinal morphology
and, subsequently, the absorption of nutrients.
In conclusion, the negative effects of Fusarium mycotoxins can be extended to their role on the
proliferation of pathogenic C. perfringens, thus contributing to an increased risk of NE in broilers. This
is caused by a group of indirect factors, such as decrease in the intestinal absorption of nutrients,
intestinal leakage, and changes in the gut microbiota. The fact that feed can be contaminated with diverse
types of mycotoxins playing a role in the gut health, makes this scenario even more complex, demanding
measures to achieve a greater protection of the gastrointestinal tract, and also an awareness of the
consequences of mycotoxin contaminations in poultry feed.

Literature:
Antonissen G, Croubels S, Pasmans F, et al. 2015. Fumonisin affect the intestinal microbial homeostasis
in broiler chickens, predisposing to necrotic enteritis. Vet Res 46:98.
Antonissen G, Van Immerseel F, Pasmans F, et al. 2014. The mycotoxin deoxynivalenol predisposes
for the development of Clostridium perfrigens-induced necrotic enteritis in broiler chickens. PLOS
One 9:e108775.

Kind regards,
Schothorst Feed Research B.V.

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