Mycotoxicosis in shrimp
Mechanisms and influences

Discover the most important mycotoxins affecting shrimp health, with a special focus on aflatoxins and trichothecenes.

Al-Zahraa Mamdouh1† and Eman Zahran2*†

1Fish Diseases Department, National Institute of Oceanography and Fisheries
(NIOF), Egypt
2Department of Aquatic Animal Medicine, Faculty of Veterinary Medicine, Mansoura University, Mansoura 35516, Egypt
These authors share first authorship
*Corresponding author: [email protected]
ORCID: 0000-0003-2212-3688

Limited availability and rising costs of dietary fishmeal are among the biggest challenges faced by the shrimp aquaculture industry.

To overcome this, the use of plant-based ingredients instead of fishmeal in finished shrimp feeds has been on the rise and with success.

However, using crops in feed increases the risk of contamination with fungi and mycotoxins, as well as the incidence of mycotoxicosis in shrimp.

Mycotoxicosis negatively influences body weight, growth, disease resistance, and survivability in shrimp, leading to reduced aquaculture productivity.

Furthermore, bioaccumulation of mycotoxins can pose a risk to humans through consumption of shrimp, which means that it is a threat to food security and public health.

Additionally, mycotoxins are genotoxic, carcinogens, and immunosuppressors.

In this review, we intend to provide a review of the most important mycotoxins affecting shrimp health, namely aflatoxins and trichothecenes.

Even though research on mycotoxins has been going on since the 1960s, information about mycotoxicosis in shrimp is still lacking.

Thus, efforts should be made to monitor their level of contamination with mycotoxigenic fungi and mycotoxins.

Mycotoxins in shrimp feed
Source of contamination

Mycotoxins are secondary metabolites produced by filamentous fungi that contaminate a wide variety of food and feed products worldwide (Marroquín-Cardona et al., 2014).

Hundreds of mycotoxins are known. Among them, aflatoxins (AF), citrinin, patulin, penicillic acid, ochratoxin A (OTA), deoxynivalenol (DON), fumonisins (FUMS), and zearalenone (ZEN) are the most common contaminants in cereal grains, and most of them are produced by the three fungal genera, Aspergillus, Penicillium and Fusarium (Ismaiel y Papenbrock, 2015).

These fungi can infect a variety of crops and agricultural products, including wheat, rice, maize, nuts, corn, soybean, and sorghum, affecting many agricultural commodities before and after harvest, as well as finished feeds (Pleadin et al., 2019).

Aquaculture is one of the fastest growing food sectors worldwide and shrimp aquaculture is one of the most profitable and fastest growing sectors of the seafood industry worldwide.

According to the Food and Agriculture Organization (FAO), in 2010, global farmed shrimp production was estimated to be nearly 3.78 million tons, with production increasing over three-fold from 1.1 million tons in 2000, with an average annual growth rate of 14.5% since 1950.

The most commonly cultured shrimp species are White-leg shrimp (Litopenaeus vannamei) and Black tiger prawn (Penaeus monodon). Other minor cultivated species include Kuruma prawn (Penaeus japonicus) and Fleshy prawn (Penaeus chinensis), Indian white prawn (Penaeus indicus) and Banana prawn (Fenneropenaeus merguiensis) (Tacon et al., 2013).

White-leg shrimp (L. vannamei) was ranked first in 2010 in total farmed fish and crustacean production, with a total value of US$11.23 billion.

Shrimps have a fast growth rate, short culture period, high export value, and high market demand. As a result, the industry has rapidly grown worldwide.

However, shrimp farming faces many challenges, including the high costs of feeding programs (Ayisi et al., 2017).

Commercial compound feed is mainly required for shrimp aquaculture to provide the necessary nutrients for growth and health maintenance (Oliveira y Vasconcelos, 2020).

40.0% of all farmed fish, including shrimp, require a large amount of protein-rich aquafeeds (Tacon y Metian, 2008).

Proteins are the most expensive nutrients in diets for shrimp culture (Ayisi et al., 2017).

Fish meal is the most used protein source in commercial shrimp feed due to its high digestibility, essential amino acids, and fatty acid profile (Oujifard et al., 2012).

In 2008, shrimp industry consumed 27.2% of the fish meal used in aquafeeds, making it the largest consumer of this source of protein (Ayisi et al., 2017).

However, the increased demand for aquaculture production has resulted in an increased demand for fish meal and fish oil and the subsequent shortage of pelagic fish and other fish species used in their production (Oliveira y Vasconcelos, 2020).

Therefore, the limited availability and rising costs of dietary fish meal have resulted in the increased use of plant proteins as alternatives to fish meal and fish oil in shrimp and fish feeds (Katya et al., 2016).

Plant proteins are considered a suitable alternative to fishmeal in shrimp feed, as they are available at low prices and are highly consistent in nutrient composition (Ayisi et al., 2017).

Over the past decades, different plant protein sources have been studied to replace fish meal in shrimp feed, including soybean meal (Bulbul et al., 2015; Sharawy et al., 2016; Yang et al., 2015), canola meal, peanut meal (Bulbul et al., 2014), rice meal (Macias-Sancho et al., 2014), and sunflower oil cake (Dayal et al., 2011).

However, plant-based shrimp feed is susceptible to contamination with various fungi and mycotoxins.

The presence of mycotoxins in commercial shrimp feed has been reported in different locations around the world.

The oldest documented survey of mycotoxin occurrence was in black tiger shrimp (P. monodon) finished feed in the Philippines (Bautista et al., 1994).

Aflatoxins were detected in commercial shrimp feed in the Eastern and Southern regions of Thailand (Bintvihok et al., 2003).

In Thailand, shrimp and fish feed samples were contaminated with zearalenone and OTA, whereas in India, shrimp feed was contaminated with AF (Fegan y Spring, 2007).

In 2014, fish and shrimp feed samples from Europe (Croatia and Portugal) and South East Asia (Singapore, India, Thailand, and Myanmar) were analyzed for the detection of AF, ZEN, DON, FUM, and OTA (Gonçalves et al., 2018a), and the results showed that a higher occurrence of FUM was found in European samples than in SE Asia.

  • The remaining mycotoxins showed similar occurrence average and maximum levels for Europe and SE Asia, with mycotoxins being detected in all analyzed samples.
  • In addition, in Europe, 50% of the samples had more than one mycotoxin per sample, and in Asia, 84% of the samples were contaminated with more than one mycotoxin.

In 2015, samples of fish and shrimp feed in Europe (Denmark, Austria, Netherlands, and Germany) and SE Asia (Vietnam, Indonesia, and Myanmar) showed high DON contamination and a higher co-occurrence risk in both regions (Gonçalves et al., 2017).

In 2016, shrimp feed from India and fish feed from Indonesia, Myanmar, Taiwan, and Thailand showed mycotoxin contamination, with fish feed samples showing lower contamination than shrimp feed and relatively high contamination of DON in shrimp feed (Gonçalves et al., 2018b).

The effects of mycotoxins on shrimp health

  Mechanisms and effects on shrimp health

Aflatoxins are the most commonly found mycotoxins in shrimp feed, mainly produced by Aspergillus flavus and Aspergillus parasiticus, and to a minor extent, by Aspergillus nomius and Aspergillus bombycis, Aspergillus pseudotamari and Aspergillus ochraceoroseus (Varga et al., 2011).

They are classified according to their blue or green fluorescence under ultraviolet light in AFB1, AFB2, AFG1 and AFG2 (Dhanasekaran et al., 2011), appearing in a variety of feedstuffs, including maize, ground nuts, rice and sorghum cottonseed, spices, cereals, soybean, cocoa, and meat (Patriarca and Pinto, 2017; Vila-Donat et al., 2018).

Aflatoxins induce toxicity during their metabolism in the liver through the generation of intracellular reactive oxygen species (ROS), such as superoxide anions, hydroxyl radicals, and hydrogen peroxide (H2O2), under the action of cytochrome P450.

  • These ROS target cellular DNA, RNA, proteins, and cell membranes, leading to impaired cell function, oxidative stress, DNA damage, cytolysis, and apoptosis (Asim et al., 2011; Yang et al., 2016).
  • They can also target the p53 tumor suppressor gene, which causes hepatocarcinoma (Kew, 2013).

Aflatoxin metabolism mainly occurs in the liver under the action of cytochrome P450 in electrophilic reactive epoxides.

  • Epoxide metabolites bind to DNA, RNA, and cellular macromolecules in the liver (Abrar et al., 2013).
Aflatoxins are usually associated with the development of hepatocellular carcinoma (HCC) in humans due to their mutagenic and carcinogenic properties. Thus, they have been classified as a significant risk factor, along with hepatitis B virus (HBV) and hepatitis C virus (HCV), for HCC (Bosetti et al., 2014).


AFB1 is the most potent experimental hepatocarcinogen known in humans (Humans and Cancer, 2002), although no animal model exposed to the toxin developed HCC.

TaIt also accounts for approximately 9.2% of all new cancers worldwide (Ferlay et al., 2010). Other liver diseases, including cirrhosis (Humans, 2014) and hepatomegaly (Gong et al., 2012), have also been associated with aflatoxin toxicity in humans.


Impaired liver function and oxidative stress are the expected consequences of aflatoxicosis in fish and experimental animals.

Aflatoxins can cause severe health problems and reduce the yield of shrimp cultures.

In shrimp, AFB1 has been extensively reported to affect:

  • Growth performance
  • Blood parameters
  • Histological parameters
  • Antioxidant enzyme activity
  • The expression of transcriptome- and immune-related genes in the hepatopancreas

The hepatopancreas is the primary organ affected by dietary AFB1 as it is the main digestive organ and immune system in shrimp (Pérez-Acosta et al., 2016) and its functions are related to the synthesis and secretion of digestive enzymes and immune molecules, absorption of nutrients, storage of reserves, and excretion (Zhao et al., 2017).

Moreover, many studies have also reported that AFB1 can damage the intestinal mucosal barrier and induce an imbalance in the intestinal microbial populations (Fang et al., 2020; Wang et al., 2018).

Several studies have reported the effects of AFB1 on shrimp growth and immune response. For example:

Exposure of L. vannamei to AFB1 (500 μg/kg AFB1) for 8 weeks significantly decreased final body weight (FBW), weight gain (WG, %), and significantly increased inducible nitric oxide synthase (iNOS) activity and glutathione (GSH) and malondialdehyde (MDA) levels in the hepatopancreas (Yu et al., 2018).

Similarly, juvenile L. vannamei fed a diet containing AFB1 for 42 days had significantly decreased mean weight, feed intake, growth rate, and nitrogen retention efficiency, and significantly increased enzymatic activity of alkaline phosphatase (ALP) and glutathione S transferase (GST) in the hepatopancreas (Tapia-Salazar et al., 2022).

In the same context, exposure of L. vannamei to AFB1 for 8 weeks significantly decreased weight gain (12000 µg AFB1/kg), total antioxidant capacity (2000 µg AFB1/kg), GST, superoxide dismutase (SOD), Na and K ATPase in hepatopancreas, and significantly increased GST in the hemolymph (1600 µg AFB1/kg) (Wang et al., 2012).

L. vannamei juveniles fed diets containing grains naturally contaminated with total aflatoxins (500, 1000, and 2000 µg/kg for 28 days) showed significantly decreased weight gain and feed intake, and significantly increased feed conversion ratio.

In addition, histological analysis of the hepatopancreas revealed that B-cell activity and mitotic cell activity were significantly decreased, whereas lipid storage, tubular epithelial atrophy, and hepatopancreatocyte sloughing were significantly increased (Tapia-Salazar et al., 2012).

F. indicus fed diets containing 1600 ppb AFB1 for 8 weeks showed significantly decreased final weight, survival rate, total hemocyte count, total plasma protein and phagocytic activity and significantly increased specific growth rate.

Histopathological examination of the hepatopancreas showed atrophied R-cells, severe necrosis and shrinkage of the tubules, infiltration of haemocytes and fibroblastic cells that produced a fibrosis-like exterior aspect, cell degeneration and pyknotic nuclei in the lumen, spread necrosis and complete destruction of B cells, complete isolation of connective tissue from hepatopancreas tissue and in midgut tissue and separation between mucosal and submucosal layers (Ghaednia et al., 2013).

Ultrastructural examination of the hepatopancreas of P. monodon fed a diet containing 1000 and 2000 ppb AFB1 for 8 weeks showed nuclear vacuolation and condensation, appearance of electron-dense material, irregular shape of nucleus, loss of nuclear membrane, and fragmentation of the endoplasmic reticulum, as well as swelling of mitochondria, vacuolation and loss of organelles in a few areas, formation of vesicles in the cytoplasm, loss of microvilli, cell rounding, and extensive necrosis (Radhika et al., 2012).

Exposure of juvenile L. vannamei to 25, 50, 100, 500, and 1000 µg/kg of AFB1 induced a significant decrease in weight gain, specific growth rate, and a significant increase in survival rate, aspartate amino transferase (AST) and alanine amino transferase (ALT) levels, and serum total antioxidant activity (Zeng et al., 2016).

L. vannamei fed 15 ppm AFB1 for 8 days had a significantly decreased survival rate, significantly increased SOD, GST, glutathione peroxidase (GPx), and catalase (CAT) levels, and differential expression of 1024 genes involved in functions including peroxidase metabolism, signal transduction, transcriptional control, apoptosis, proteolysis, endocytosis, cell adhesion, and cell junction.

It also induced severe histological alterations in the shrimp hepatopancreas, including separation between the myoepithelial layer and the epithelium of the hepatopancreas, excess fat in many vacuolated cells, nuclear pyknosis, cell lysis, and cell necrosis (Zhao et al., 2017).

In a more recent study, exposure of L. vannamei to 168.3 μg/kg of AFB1 for 58 days significantly decreased weight gain, specific growth rate, survival rate, protein efficiency ratio, protein productive value, and AST and ALT levels in the serum and hepatopancreas, significantly increasing the feed conversion ratio. It also induced a significant increase in serum MDA level and GST and GPx activities, while significantly decreasing their activities in the hepatopancreas. In addition, it decreased the acid phosphatase (ACP) and alkaline phosphatase (AKP) levels in the serum and hepatopancreas.

Furthermore, AFB1 significantly downregulated the expression of immune-related genes, including myeloid differentiation factor 88 (MyD88), Dorsal, Tumor necrosis factor receptor-associated factor 6 (TRAF6), Relish, Domeless, cytochrome P450 and penaeidin 3a (Chen et al., 2020).

L. vannamei fed diets contaminated with 200 μg/kg of AFB1 for 42 days suffered from significantly reduced feed intake, growth rate, and nitrogen retention efficiency and significantly increased ALP and GST activity (García-Pérez et al., 2020).

Exposure of P. vannamei to 500 μg/kg of AFB1 for six weeks significantly decreased survival rates, weight gain, and the expression of immune-related genes in the intestine, including Rab, GST, mucin-like-PM, Dorsal, Relish and Pro-PO.

In addition, histopathological examination of the intestine showed that epithelial cells were completely detached from the basal membrane and severely destroyed. There was a significant increase in the abundance of Proteobacteria and a significant decrease in the relative abundance of Firmicutes and Bacteroidetes which is indicative of an imbalance in intestinal microbiota and the damage caused by AFB1 (Fang et al., 2020).

AFB1 induced damage to the antioxidant system and dysregulation of intestinal microbiota in L. vannamei fed a diet containing 5 ppm AFB1 for 30 days, as it induced a significant increase followed by a significant decrease in CAT, SOD, and GPX activities and a significant increase in MDA in the intestine and hepatopancreas.

In addition, an imbalance in intestinal microbiota was indicated at the phylum level, the relative abundance of Proteobacteria and Firmicutes increased, and the relative abundance of Bacteroidetes decreased.

At the genus level, the relative abundances of Vibrio and Photobacterium significantly increased, and the relative abundances of Flavobacterium_ sp_M and Tenacibaculum decreased (Wang et al., 2018).

Exposure of L. vannamei to 977.11 and 1605.61 μg/kg of AFB1 for 28 days induced significant increase in AST, ALT activities in hemolymph and the histological alternation index (HAI) value of hepatopancreas, with a significant decrease in total protein and fat (triglyceride and cholesterol) in hemolymph.

Histopathological examination of the hepatopancreas showed irregular and abnormal appearance of the hepatopancreas tubular structure, tubular cell vacuolation, separation of epithelium and myoepithelial layer, necrosis of hepatopancreatic cells and pyknotic nuclei, hepatopancreatic inflammation, and penetration of hemocytes into the space between tubules (Jamshidizadeh et al., 2019).

T-2 toxin  
  Mechanisms and effects on shrimp health

There is little information on the toxicity of other mycotoxins to aquatic invertebrates, but T-2 toxin has been reported to impair shrimp growth and immune responses in many studies.

Trichothecenes (mainly T-2 toxin) are well known for their capacity to inhibit eukaryotic protein synthesis by binding to the 60S subunit of eukaryotic ribosomes and inhibiting peptidyl transferase activity.

This leads to inhibition of the initiation, elongation, or termination of the chain elongation step in protein synthesis (Arunachalam y Doohan, 2013).

T-2 toxin can also:

  • Inhibit DNA and RNA synthesis (Minervini et al., 2004)
  • Alter cellular membrane structure (Diesing et al., 2011) and mitochondrial function
  • Arrest the cell cycle (Pestka, 2010)
  • Induce oxidative stress by increasing lipid peroxidation and altering antioxidant defenses, which eventually impairs protein synthesis and causes DNA damage (Doi and Uetsuka, 2011; Wu et al., 2014)

The effects of T-2 toxin on growth, antioxidant capacity and histopathological findings in the hepatopancreas of L. vannamei were investigated through dietary exposure to 0.5, 1.2, 2.4, 4.8, and 12.2 mg/kg of T-2 toxin for 20 days and it was reported that concentration of mT-2 in the hepatopancreas was significantly increased in a dose-dependent manner. In addition, growth and survival rates significantly decreased.

Moreover, MDA concentration was significantly increased at a dose ≥2.4 mg/kg of T-2 toxin, while SOD and GPx, total antioxidant capacity (T-AOC), and GSH content increased at a dose of 2.4–4.8 mg/kg of T-2 toxin but declined at dose 12.2 mg/kg.

Histopathological changes in the hepatopancreas were dose-dependent, with evident autophagy at the highest exposure dose (Deng et al., 2017).

T-2 toxin induced toxic effects on the hemolymph, immune system, and hepatopancreas of L. vannamei after dietary exposure to 0.5, 1.2, 2.4, and 4.8 mg/kg for 20 days, such as a significant reduction in weight gain, specific growth rate (at all doses) and survival rate (0.5 and 1.2 mg/kg). It significantly decreased phenoloxidase enzyme activity (all doses), hemocyte count (2.4 mg/kg) and albumin concentration (1.2, 2.4 and 4.8 mg/kg). Moreover, it altered the activities of the hemolymph enzymes GOT, GPT, and ALP in a dose-dependent manner.

Furthermore, T-2 toxin induced histopathological changes in hepatopancreas in a dose-dependent manner where hepatopancreas cells were swollen with a reddish-brown color and early cellular atrophy with dissolution of some areas of the basement membrane, loss of secretory cells, and partially lysed absorptive cells were evident at a dose of 0.5 mg/kg. Vacuolation of columnar cells, scattered partial dissolution of villi, with the disappearance of star-shaped polygonal structures in some hepatopancreas corpuscles were shown at a dose of 1.2 mg/kg. At 2.4 mg/kg, the damage included many vacuolated cells, excess of fat, nuclear pyknosis, some cell lysis and necrosis and a larger corpuscle diameter of the hepatopancreas, while at 4.8 mg/kg, lysis, and necrosis of many hepatopancreas cells were observed (Qiu et al., 2016).

Exposure of L. vannamei to T-2 toxin at concentrations of 0.5, 1.2, 2.4, 4.8 and 12.2 mg/kg for 20 days significantly reduced the weight gain, specific growth rate, and survival rate.

Histopathological examination of the intestine showed concentration-dependent degenerative and necrotic changes, with initial inflammation of the mucosal tissue at 0.5 and 1.2 mg/kg, progressing to the disappearance of intestinal villi and degeneration and necrosis of the submucosa at 12.2 mg/kg.

Intestinal digestive enzymes protease and amylase significantly decreased with increasing concentrations of T-2 toxin, whereas lipase activity increased with higher T-2 toxin concentrations (Huang et al., 2019).

The effect of T-2 toxin on the muscle proteins of L. vannamei was investigated through dietary exposure to 1.2, 2.4, 4.8 and 12.2 mg/kg for 20 days and it was reported that the amount of myofibrillar protein, sarcoplasmic and stroma proteins increased at the low concentration of 1.2 mg/kg T2, while higher concentrations induced significant declines in a dose-dependent manner.

Meanwhile, alkali-soluble protein showed an opposite trend, with a decrease at the low T-2 toxin concentration of 1.2 mg/ kg and an increase at higher concentrations. Moreover, T-2 toxin caused a concentration-dependent decrease in calcium (Ca2+) ATPase, magnesium (Mg2+) ATPase, and Ca2+Mg2+ATPase activities in the muscles (Huang et al., 2020).

T-2 toxin affected the fatty acid, water distribution, and muscle histopathology of L. vannamei where exposure to 0.5, 1.5, 4.5 and 13.5 mg/kg for 20 days significantly affected the muscle fatty acid composition with an initial decrease in saturated fatty acid (ΣSFA), monounsaturated fatty acids (ΣMUFA), and polyunsaturated fatty acids (ΣPUFA), followed by an increase in the high-dose groups.

In addition, T-2 toxin significantly affected water distribution in the muscle, where high doses reduced free water content resulting in a reduction in the water holding capacity and, hence, changes in shrimp muscle quality (Bi et al., 2019).

Deoxinivalenol, Fumonisins and Ochratoxin A  
   Effects on shrimp health

A few more studies have reported other mycotoxin effects on shrimp.

L. vannamei fed diets contaminated with 250, 500, and 1000 μg DON/kg for 5 weeks suffered from significantly decreased weight gain (1000 μg /kg) and significantly increased GST (500 μg /kg) and SOD activity (1000 μg /kg), while the gene expression of SOD and GPx were significantly decreased at doses of 500 and 1000 μg/kg DON. In addition, the hepatopancreas immune response related gene expression of HSP70, Toll 1 and Dorsal was higher at a dose of 250 μg DON/kg, and the expression of proPO, LGBP and PPAF was significantly higher at a dose of 1000 μg DON/kg.

Histopathological examination revealed that intestinal mucosal folds were impaired by apoptosis in intestinal epithelial cells, and B cell numbers and diameters of the hepatopancreas tubules were affected by different DON doses (Xie et al., 2018).

L. vannamei exposed to 0.5, 0.75 and 1.0 µg/g of FB1 for 18 days showed significantly decreased phenoloxidase, total hemocyte count, and superoxide anion rate.

The hepatopancreas showed histopathologic lesions, including deformation of the hepatopancreas tubules with a loss of normal cellular structure, presence of melanization, and the tubules showing severe vacuolization with cellular retraction (Mexía-Salazar et al., 2008).

Feeding P. monodon with a diet containing DON and OTA for 8 weeks significantly altered growth and immune parameters.

DON at a dose of 1000 ppb significantly reduced growth rate, specific growth rate and feeding rate, ALP, serum GOT, and GPT levels, and significantly increased weight gain. OTA reduced ALP at doses of 100, 200, and 1000 ppb and reduced serum GOT at doses of 100 and 200 ppb and GPT at 100ppb (Supamattaya et al., 2005).

Protection of shrimp against mycotoxicosis

Various strategies have been developed to reduce the toxic effects of mycotoxins in feed, such as:

  • Physical decontamination (Grenier et al., 2014; Pankaj et al., 2018)
  • Chemical decontamination (Čolović et al., 2019)
  • Biological decontamination (Shu et al., 2018)

Some of the compounds used in different studies to alleviate mycotoxin-induced toxicity in shrimp are as follows.


The use of probiotics has been shown to significantly improve the survival rate and growth performance of both aquaculture and terrestrial farmed animals (Wang et al., 2019; Zhang et al., 2019).

In shrimp aquaculture, probiotics improve the rate of digestibility and absorption and promote growth, healthy intestinal morphology and flora, a robust immune response, and resistance to diseases (Amoah et al., 2019; Azad et al., 2019; Duan et al., 2018; Zuo et al., 2019).

Supplementation of Lactobacillus pentosus HC-2 (5 × 108 CFU/g feed) to P. vannamei for 6 weeks alleviated AFB1-induced toxicity (500 μg/kg) by increasing the survival rate and percent weight gain, enhancing the intestinal morphology and community structure of intestinal microbiota by significantly increasing the abundance of Proteobacteria and decreasing the abundance of Firmicutes and Bacteroidetes. It also increased the expression of immune genes, including Rab, GST, mucin-like-PM, Dorsal and Pro-PO (Fang et al., 2020).


Other studies involved the use of antioxidants.

Curcumin supplementation was beneficial to protect L. vannamei juveniles against immune toxicity caused by AFB1 (200 μg/kg).

The addition of curcumin at dose of 0.2 g/kg increased feed intake and growth rate, while at 0.15 g/kg it increased nitrogen retention. Additionally, ALP activity was reduced at 0.15, 0.2, and 0.3 g/kg and GST activity was reduced at 0.15 and 0.2 g/kg (García-Pérez et al., 2020).

Tea polyphenols were effective in the protection of P. vannamei against the deterioration of shrimp muscle quality induced by AFB1 (1.2–2.7 mg/kg feed), where it inhibited the expansion of muscle fiber spaces and inflammation and induced a significant protective effect against the decrease in muscle nutrients and changes in the protein composition (Huang et al., 2021).

Quercetin, tea polyphenols, and rutin are widely used plant-derived antioxidants that possess antioxidant, antinflammatory, and antitumoral properties.

They reduced muscle protein deterioration in L. vannamei caused by T-2 toxin through the upregulation of target proteins involved in carbohydrate metabolism (enolase and malate dehydrogenase), protein translation (elongation factor 1-alpha and eukaryotic translation initiation factor 2 subunit alpha), and cytoskeleton components (actin 2 and fast-type skeletal muscle actin 1) (Huang et al., 2022).


The addition of clay to the diet of L. vannamei exposed to 200 μg/kg AFB1 for 42 days at doses of 4, 5, and 6 g/kg improved nitrogen retention and decreased ALP (6 g/kg) and GST (4 g /kg) activity (García-Pérez et al., 2020).


A new approach for the detoxification of mycotoxins in shrimp is the use of natural components, such as bile acids and myo-inositol.

Bile acids are detergent molecules synthesized from cholesterol in vertebrates (Šarenac and Mikov, 2018) and function as signaling molecules, regulating the detoxification and antioxidant system of mammals by activating nuclear hormone receptors (Baijal et al., 1998; Reschly et al., 2008).

Bile acids reduce the AFB1 residues in shrimp, increase the detoxification of AFB1 and decrease the levels of oxidative stress products by increasing Phase II and antioxidant systems, avoiding AFB1 induced deterioration of shrimp meat and health risks to humans (Su et al., 2022). Dietary bile acids significantly reduce AFB1 accumulation and alleviate AFB1-induced growth retardation and immunotoxicity in shrimp. CCKAR, ATR, and Relish are key mediators of the alleviating effects of bile acids (Su et al., 2023).

Myo-inositol is a vitamin-like essential nutrient that has been shown to enhance the enzymatic antioxidant capacity in carp. However, in shrimp, myo-inositol slightly (but not significantly) mitigated the negative impacts to the growth, antioxidant enzyme activities, and immune-related gene expression of L. vannamei caused by AFB1 exposure (Chen et al., 2020).


Increasing plant-based ingredients in aquafeed is considered one of the challenges in shrimp aquaculture due to the higher susceptibility to fungal contamination and mycotoxin production, which eventually impacts shrimp productivity.

Mycotoxins affect shrimp health through a variety of mechanisms that interfere with the normal physiological body functions.

Different approaches have been adopted to protect against mycotoxicosis, however, additional studies using new environmentally friendly tools to combat mycotoxin contamination are still scarce and require further investigation.

Strategies for strict monitoring of mycotoxin contamination levels in feed ingredients and commercial feeds should be implemented to avoid mycotoxicosis and improve aquaculture sustainability.


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