Mycotoxins: A Problematic Puzzle

There are many stressors associated with intensive rearing practices in poultry production systems, one of which is mycotoxins. Mycotoxins are natural toxic secondary metabolites produced by fungi that can be found in feedstuffs such as cereal grains and their by-products. These compounds can negatively affect livestock through direct and indirect effects.^1–2 Mycotoxins can occur prior to harvest, as well as after harvest, transport, and storage. Once these metabolites are formed, they are chemically stable and continue to persist in the contaminated ingredient even after becoming a finished feed. Although mycotoxins can occur individually, contamination with multiple types of mycotoxins on a single feedstuff source tends to occur more frequently.^3–5 The exposure of birds to multiple mycotoxins increases risk through additive or synergistic interactions.^6–8

The Effects of Mycotoxins on the Laying Bird

Mycotoxin effects can vary depending on species, health status, age, exposure time, mycotoxin type and concentration. Consumption of mycotoxins can affect any system in the body and potentially cause lesions and clinical signs. Common types of mycotoxins that affect poultry through feedstuffs are aflatoxins (AF), ochratoxins (OTA), fumonisins (FUM), type B trichothecenes such as deoxynivalenol (DON), zearalenone (ZEA) and type A trichothecenes which include T-2/HT2 toxins.⁹ However, further advances in mycotoxin research indicate that the interactions between mycotoxins and the role of lesser-known mycotoxins have a greater impact on animal systems than previously thought.¹⁰ As a result, the impact of mycotoxins can be quite complex.

Mycotoxins have the capability to modify DNA, RNA and hinder protein synthesis which has the potential to be mutagenic, embryotoxic, teratogenic and carcinogenic.^8,11 In broiler breeders and egg layers, profitability greatly depends on the quality of the egg, including fertility and hatchability. Mycotoxins such as AF, OTA, trichothecenes, moniliformin, ZEA and FUM have been found to be toxigenic to egg production and quality.^10,12,13 Eggshell integrity, particularly eggshell thickness, shape, colour, texture, and cleanliness can be affected by mycotoxins.14 Some mycotoxins act directly on pathways that affect quality, while some act indirectly. For example, AFB1 can directly affect the eggshell by inflicting hepatic damage and thus decreasing vitamins, minerals and enzymes involved in eggshell formation(10). Indirectly, T-2 toxin and other trichothecene mycotoxins can cause eggshell quality issues through a reduction in feed intake which could lead to a decrease in available nutrients needed for the eggshell formation and an overall decrease in egg production.^10,12,15,16

Although eggshell quality may be of higher importance in table egg layers, it is also of importance in broiler breeders as the shell is involved in gas exchange and provides a natural barrier from the outside environment to keep pathogens from translocating into the egg.¹⁷ Increased number of cracks and thinner eggshells can harbour harmful pathogens that could be introduced into the incubators and increase the number of explorers, hence contaminating the rest of the batch with bacteria. Mycotoxin exposure from litter bedding systems is also important. Studies show shifts in the gastrointestinal microbiota by mycotoxins which can influence the number of dirty eggs and potentially translocate harmful pathogens into the hatchery and the progeny housing.⁵ Additionally, the presence of fungi and mycotoxins can further increase during egg storage particularly if exposed to high humidity and higher temperatures which is ideal for fungal growth. Research shows that under these conditions, there is potential for the translocation of fungi into the egg.⁵

Fertility and hatchability can be affected by mycotoxin exposure.^12,18,19 Effects are not restricted to female fertility, as male birds also show signs of dose-dependent infertility.^18,19 In males, mycotoxins such as diacetoxyscirpenol (DAS) can reduce reproductive organ weights and cause degenerative processes of the testis which leads to reduced spermatozoa quality and an overall decrease in semen quality.¹⁹ Furthermore, hatchability may be impacted simply due to changes associated with the chemical composition of the egg and not with sperm storage in the hen.