Some of the most common fungal toxins causing immunosuppression and depression in poultry include aflatoxins, ochratoxins, sterigmatocystin, fusaric acids, fumonisins, trichothecenes, among others, collectively known as mycotoxins. Feed contamination with aflatoxins, ochratoxins, deoxynivalenol, and fumonisins effectively interferes and antagonizes immune responses against viral and bacterial vaccines.

Immune suppression and depression due to fungal toxins:

In general, the interaction of fungal toxins and their effects on immune response is not always clear, as low doses of some toxins may indeed have beneficial effects, promoting growth. This phenomenon is termed hormesis and has been described. For example, aflatoxin B1 can both impair and enhance growth. Additionally, various fungal toxins may have different effects on immune response, gut physiology, and growth in different poultry species. Aflatoxin is the most well-known among poultry fungal toxins, although chickens are more resistant to its toxic effects compared to ducks and turkeys. After ingestion, aflatoxin B1 activates in the liver and transforms into more toxic types 8 and 9, which bind to DNA or become protein-hydrolyzing, causing cellular toxicity. The result is cell death in primary immune lymphoid organs and damage to gut structure, particularly in chickens leading to reduced humoral and cellular immune responses, although actual antibody response rates may increase during initial toxin exposure. Chicks fed diets containing aflatoxin B1 have also been observed to suffer immune function impairment when tested in their second and third weeks of age, but the duration of negative effects beyond hatching has yet to be determined. Aflatoxin B1 does not appear to affect the function of the intestinal barrier or the innate immune response, though these data are not exclusive.

A fungus genus, Fusarium, produces a number of mycotoxins such as fumonisins B1, deoxynivalenol (DON), and other trichothecenes (e.g., T-2). These mycotoxins have been linked to immune modifications in poultry. For example, administering lethal doses of DON to chickens between days 1 and 7 of age, i.e., during their first week, reduces protection from Marek's disease virus (MDV) challenge. DON inhibits DNA, RNA, and protein synthesis, affecting tissue regeneration and cellular proliferation, such as epithelial cells in the digestive tract lining and cells in immune organs. Consequently, researchers have observed increased spleen size with increased cellular proliferation, apoptosis, and DNA damage by the end of a 16-week experiment in slow-growing chickens. Other research groups have suggested that changes in gut permeability may increase bacterial challenge, leading to higher levels of IgA antibodies in chickens not fed with DON-contaminated feed compared to those with DON in their feed. Low doses of T-2 and DON have also been linked to increased IgA levels against Newcastle disease virus, while high doses suppress immune function.

Chickens fed with DON in their diets and challenged with very virulent infectious bursal disease virus (vvIBDV) developed more severe effects than those fed diets free of DON.

Zearalenone (ZEA) is a non-steroidal estrogenic fungal toxin that can bind to estrogen receptors. Limited information exists on its immunotoxicity in chickens. However, ZEA or its metabolites may potentially interfere with chicken infectious anemia virus (CIAV) since the viral enhancer/promoter is similar to the estrogen receptor. Research by Miller and colleagues suggested that estrogen binds to this enhancer/promoter in studies using the gene-regulated poultry anemia extract. So far, no published study has examined the strength of ZEA in enhancing the replication and spread of infectious anemia virus.

The interaction between trichothecenes and immune responses is complex. Low doses can stimulate immune responses by regulating cytokines and chemokines, while high doses inhibit them.

Ochratoxins (OTA) are highly toxic to several animals, including chickens, and may be found in eggs from their sources and contaminated poultry feed. Both innate and acquired immune responses are reduced by OTA, and susceptibility to disease increases in chickens fed with 1 ppm OTA and their chicks. For example, 2 ppm OTA significantly increased the mortality caused by Salmonella enterica subspecies enterica serovar Gallinarum intestinal typhoid Salmonella enterica serovar typhimurium.

Importantly, various fungal toxin compounds are often present in feed, interact with each other, and mostly enhance immune suppression effects. The presence of fungal toxins in feed and the potential for transfer to embryos have significant implications, disrupting immune function loss in commercial herds during virus-induced immune suppression or inhibition.