Effects of mycotoxins in poultry

Poultry are farm animals with heterogeneous sensitivity to mycotoxins, as different species suffer different toxic effects. Ducks, geese and turkeys seem to be more susceptible to these toxic secondary metabolites compared to broilers.

In general, common aflatoxin-induced symptoms are decreases in performance - reduced weight gain and feed conversion rate (FCR) -, as well as weight and size variation of the organs such as the liver, spleen, kidneys, bursa of Fabricius and thymus. Birth hatch defects induced by aflatoxins cause an increase in the number of chicks that are rejected at the beginning of the production cycle.1 In addition, aflatoxins are immune suppressive; they affect innate, cell-mediated and humoral responses, causing symptoms such as abnormal behavior (birds standing together in groups), and other nervous syndrome related signs.2,3,4 Intoxication with aflatoxin B1 (AfB1) affects cell-mediated immunity by decreasing the concentration of albumin and globulin, and therefore it exerts an important role in the inhibition of protein synthesis.5 Additionally, impairments in major serum biochemistry parameters, gut barrier, energy and amino acid digestibility were found when feeding AfB1-contaminated feed to broiler chicks.6 AfB1-carry over was observed in eggs, tissues (kidney, liver, muscle, ova) and the blood of laying hens.7 Aflatoxin M1, classified by the International Agency for Research on Cancer (IARC) as a group 1 carcinogen (highly carcinogenic to humans), can be found in the kidneys.8

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Ergot alkaloids may induce neurotoxic effects, leading to reduced feed intake because the birds are reluctant to move and may suffer from respiratory difficulties.41 Birds affected by ergot alkaloids showed poor growth and decreased egg production. The most obvious pathological changes are gangrenous lesions on the toes, beak and claws.42

more about Ergot alkaloids

Main symptoms observed with dietary fumonisin administration were decreased body weight and average daily weight gain – due to modulation of intestinal function and disruption of gut integrity - as well as increased liver and gizzard weights, followed by increased sphinganine to sphingosine (Sa/So) ratios.30,31,32 Studies conducted in 2015 on broiler chickens revealed significant modulation of the Sa/So ratio in liver, kidneys, jejunum and caecum. Up-regulations of pro-inflammatory cytokines occurred in the small intestine, suggesting that animals were stressed.30 Fumonisins are predisposing factors for the development of necrotic enteritis in broiler chickens.31 A study from 2015 revealed that birds receiving a diet containing a mixture of fumonisins and Clostridium perfringens were more prone to develop necrotic enteritis compared to the control that received only the C. perfringens challenge.31 According to the authors, one reason could have been the involvement of fumonisins in the modulation of the gut microbiota that favored the growth of C. perfringens.31, 32 Furthermore, the group that receive the fumonisins contaminated diet showed a great alteration of the Sa/So ratio, reduced villus height and crypt depth in the ileum.33 Subacute exposure of broiler chicks to fumonisin B1 (FB1) induced liver oxidative stress concomitantly with Sa/So accumulation.28 Similar effects were observed in turkeys which seem to be even more sensitive to fumonisins.36,37 Effects on the immune system, such as a reduction in white blood cell counts in chicks fed fumonisin B1 contaminated diets, were reported as well.38 Additionally, fumonisin B1 exposure induced morphological and functional alterations (number and phagocytic ability) in the peritoneal macrophages population of chickens, implying that fumonisin B1 exposure may increase the susceptibility of chickens to bacterial infections.39 To evaluate fumonisins-carry over, 30-week-old laying hens received an intravenous (2 mg/kg BW) or an oral dose (2 mg/kg BW) of 14C-FB1 and showed no relevant residues of fumonisins (<10-15 ng fumonisin/g) in tissues, suggesting that there is no substantial contribution to human exposure.40

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Young chicks and turkeys are very sensitive to ochratoxins.4 These nephrotoxins suppress feed intake, growth, egg production and have a negative influence on eggshell quality.2 Administration of ochratoxin A (OTA) can reduce immunoglobulin concentration in birds’ sera and alter cellular, humoral and innate immune responses.28 In addition, OTA can potentiate inflammation at target sites, primarily in the kidneys, while reducing the capacity of immune cells to respond to inflammation.29

more about Ochratoxins

Type A trichothecenes

Type-A trichothecenes (T-2 toxin, HT-2 toxin, diacetoxyscirpenol) are of major concern to the poultry industry and can cause severe productivity losses. These mycotoxins are highly toxic to poultry, especially chickens, as suggested by their very low LD50 values (2 mg/kg for diacetoxyscirpenol and 4 mg/kg for T-2 toxin).4 In particular, T-2 toxin causes reduced feed intake, body weight (BW) and egg production, oral lesions and impaired nutrient absorption.9 Furthermore, T-2 toxin can reduce egg production, and increase the incidence of cracked eggs.10 T-2 toxin is cytotoxic to chicken macrophages in vitro.18

Type B trichothecenes

Deoxynivalenol (DON) had first been recognized for its pro-inflammatory and immunomodulatory activities. This mycotoxin is capable of impairing the intestinal barrier function and integrity, by affecting the intestinal surface area and function of the tight junctions.11, 12, 13 A compromised barrier function is associated with an increased epithelial permeability and translocation of pathogens and other toxic entities, as well as a non-specific inflammatory response and an overstimulation of the gut-associated immune system.11, 12, 13 In this context, several studies demonstrated that DON is a promoting factor for the development of necrotic enteritis and coccidiosis in poultry, even at concentrations that lay below the EU guidance levels.32, 45, 46

A study conducted in 2012 investigated the toxic effects of DON and its derivatives (3-ADON and 15-ADON) using in vitro (intestinal epithelial cell line), ex vivo (intestinal explants), and in vivo (animals exposed to mycotoxin-contaminated diets) models.14 The great impact of DON and its derivatives on intestinal morphology was demonstrated. DON significantly reduced the size of villi, the area for absorption and the area of the epithelial cells. Concerning the derivatives, the study concluded that 3-ADON was the less toxic form, whereas 15-ADON was capable of causing more histological lesions than DON or 3-ADON.14 Administration of feed contaminated with DON, can cause decreases in performance caused by impaired feed intake and lower weight gain, gizzard mucosa erosions and lesions, impaired hematological parameters, serum minerals and glucose levels.15 According to the literature, DON can significantly influence eggshell weight and thickness.16 Trichothecenes suppress cellular and humoral responses as well. Specifically, DON promotes leukocyte apoptosis and reduces Newcastle Disease humoral titers in 18-week old pullets.20, 21

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In comparison to other species such as Opens internal link in current windowswine, poultry are less affected by and also appear to be less sensitive to type B trichothecenes.17,18 Nevertheless, Zearalenone may have some negative effects on both fertility and hatchability of fertile eggs. In general, feeding different Fusarium toxins such as deoxynivalenol, zearalenone and fusaric acid resulted in a significant decrease in immunological parameters such as the biliary IgA level, an important line of defense against bacteria and viruses.19

more about Zearalenone

Carry over into animal products

Eggs did not contribute significantly to the dietary intake of deoxynivalenol in humans, as neither the parental compound nor the deoxynivalenol-conjugates were ever detected at significant concentrations in the egg yolk and albumen of laying hens.23 Similar conclusions can be drawn for carry-over of deoxynivalenol to turkey meat, although traces of this mycotoxin (2 ng/mL and 4 ng/mL) were detected in bile.24 Carry-over of T-2 to eggs was observed in birds fed 0.25 mg radiolabeled T-2 toxin/kg bodyweight, according to the literature.25, 26 The maximum residues in eggs were detected 24 hours after feeding, with the yolk containing 0.04% and the white 0.13% of the total dosage applied. Traces of zearalenole have been detected in bile.24,27

Synergistic effects in poultry

PoultryAflatoxin B1 (AFB1) shows synergistic interactions with ochratoxin A when fed simultaneously to broiler chicks, affecting the liver and kidneys.43 Furthermore, the literature reports that the liver tissue of broilers fed diets contaminated with ochratoxin A and AFB1 contained markedly higher concentrations of ochratoxin A compared to diets contaminated with ochratoxin A alone.33 Deoxynivalenol significantly increases the severity of T-2 toxin-induced lesions. According to the literature, interactions between fumonisins and moniliformin significantly influenced haematological parameters, whereas fumonisins and T-2 in combination with fusaric acid increased embryo mortality and enhanced oral lesions and mortality.44 Challenging broiler chicks with Eimeria spp., a pathogen responsible for coccidiosis, and a mixture of fumonisins and deoxynivalenol, results in metabolic and immunologic disturbances that amplify the severity of coccidiosis at subclinical mycotoxins levels.45

A recently conducted study investigated the impact of deoxynivalenol and fumonisins on the intestinal barrier in broiler chickens, more specifically on the mucus layer and antioxidative response to oxidative stress.46 The authors concluded that simultaneous distribution of deoxynivalenol and fumonisins at concentrations close to the European Union maximum guidance levels (5 mg deoxynivalenol and 20 mg fumonisin B1 + fumonisin B2/kg feed) had a negative influence on the intestinal mucus layer and several intestinal epithelial antioxidative mechanisms.46 Specifically, deoxynivalenol and fumonisins affected the duodenal mucus layer by suppressing the expression of intestinal mucin MUC 2 and intestinal zinc transporter ZnT1 genes; and altering the mucin monosaccharide composition.46 Furthermore, both mycotoxins interfered with the intracellular methionine homeostasis, which is important for preserving the cell’s critical antioxidant activity.46 

A summary of the synergistic and additive effects of mycotoxins in poultry is presented in Figure 1 below.

Figure 1: Synergistic and additive effects in poultry

Figure 1: Synergistic and additive effects in poultry

AFB1 – Aflatoxin B1; FB1 – Fumonisin B1; DON – Deoxynivalenol; OTA – Ochratoxin A FA – Fusaric acid; DAS – Diacetoxyscirpenol; CPA – Cyclopiazonic acid; MON - Moniliformin

Red line: synergistic effect
Dashed line: additive effect

Effects of Mycotoxins in Poultry

AFB1 – Aflatoxin B1 | AFM1 – Aflatoxin M1 | DON – Deoxynivalenol | FUM – Fumonisins | OTA – Ochratoxin A | T-2 – T-2 Toxin | HT-2 – HT-2 Toxin | ZEN - Zearalenone | Ergots – Ergot, Alkaloids

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