Aflatoxicosis- A Silent Nuisance to Poultry Industry

Aflatoxicosis is one of the most distressing disease among both livestock and poultry caused by ingestion of contaminated feed with aflatoxins from toxigenic fungus, mainly Aspergillus spp. Aflatoxicosis is a medical condition characterized by fatty and enlarged liver, jaundice, bile duct proliferation, oedema, sudden liver failure and ultimately death (death within 24 hours of consumption of aflatoxin contaminated maize/feed is possible). Aflatoxins are commonly produced by toxigenic strains of Aspergillus flavus, Aspergillus parasiticus and Aspergillus nominus on maize, peanuts, soybeans, cottonseed, sorghum and other foods ( even in figs, tree nuts, spices) either in the field or during storage when moisture content and temperature are sufficiently high for the mould growth. Although many other species and strains of Aspergillus possess aflatoxigenic abilities, usually A. flavus contamination in food items is more frequently associated with aflatoxins. The name of the toxin was designated aflatoxin from its production by A. flavus (Aspergillus flavus toxinA-fla-toxin). Earlier recognized “mouldy corn toxicosis”, “poultry haemorrhagic syndrome” and “Aspergillus toxicosis”, may have been caused by aflatoxins. The discovery of acute dietary aflatoxin toxicity came with unknown disease named Turkey ‘X’ in England in 1960 with large number of deaths of turkey poults linked to peanut meal contaminated with aflatoxins.
Aflatoxicosis occurs in many parts of the world and affects growing poultry ,ducklings and turkey poults whereas among animals, mostly young pigs, pregnant sows, calves and dogs are the sufferers. Adult cattle, sheep and goats are relatively resistant to the acute form of the disease but are susceptible if toxic diets are fed over long periods. Contrary to long-term exposure to aflatoxins (AFs) where adverse health outcomes occur over time, dietary exposure to AFs exceeding 200 μg/kg in the short term can also be fatal for aflatoxicosis. Experimentally, all species of animals tested have shown some degree of susceptibility towards it. Dietary levels of aflatoxin (in ppb) generally tolerated are ≤30 in poultry.
Aflatoxins are cancer-causing and immunosuppressive that are associated with reduced weight gain and feed efficiency with occasional sudden deaths. Aflatoxins B1, B2, G1 and G2 are the major toxins among 16 structurally related toxins, named according to their blue or green fluorescence under UV. A. flavus produces AFB1 and AFB2 and A. parasiticus produces all the four major aflatoxins. AFB1 is produced by all the aflatoxin-positive strains and is the most hazardous, mutagenic and potent hepatocarcinogenic agent. In fact, is the most prevalent worldwide. Other known aflatoxin producers include A. nominus, A. bombycis, A. pseudotamartii and A. ochraceoroseus among the aspergilli and Emericella venezuelensis. These compounds are highly substituted coumarins and at least 18 closely related toxins are known. AFM1 is a hydroxylated product of AFB1 and it appears in milk, urine and faeces as a metabolic product in cattle and buffaloes fed on aflatoxin contaminated feed. Thus, is also of human food safety concern. AFL, AFLH1, AFQ1 and AFP1 are all derived from AFB1. AFB2 is the 2,3-dihydro form of AFB1. AFG2 is the 2,3-dihydro form of AFG1. The toxicity of the six most potent aflatoxins decreases in this given order: B1 > M1 > G1 > B2 > M2 > G2.
Structurally being the derivatives of di-furocoumarin, AFs are mainly produced as secondary metabolites of heterologous group called mycotoxins in the temperature range of 24 35°C. Temperature around 300C and water activity (aw) of 0.99 are the major conditions required for AFB1 synthesis with other environmental factors including substrate, time, CO2 levels etc. The toxic response and disease in mammals and poultry vary in relation to species, age, sex, nutritional status, level of aflatoxins in the ration and duration of intake. Avian species especially goslings, ducklings and turkey poults are highly susceptible to AFB1 toxicity. Domestic turkeys and ducks are highly sensitive to both the acute and chronic toxicity of AFB1. Chickens whereas are comparatively resistant to acute aflatoxicosis (except during the embryonic development) as compared to other poultry species. Practically, poultry are very sensitive even in a very low dose of AFB1. The order of sensitivity exists as ducks > turkey > Japanese quail > chicken.
The toxic effects of AFB1 are mainly localized in liver as manifested by hepatic necrosis, bile duct proliferation, icterus and haemorrhage. Chronic toxicity in those birds is characterized by loss of weight, diarrhoea,decline in feed efficiency, drop in egg production and increased susceptibility to infections. The incidence of hepatocellular tumours, particularly in ducklings is considered to be one of the serious consequences of aflatoxicosis. AFB1 is detrimental to cellular processes too. Synthesis of DNA, RNA and proteins are strongly inhibited in the primary hepatocytes of chicken. Mutations of G-T transversion in hepatic DNA has also been described. Risk of hepatocellular carcinoma increases many folds in humans with hepatitis B infections on chronic exposure to AFB1. Whereas, adenoma and hepatocellular carcinoma are reported in ducks. Thus, AFB1 is classified as a group I carcinogen by the International Agency for Research on Cancer.
AFB1 affects production values adversely. Dietary exposure to AFB1 and other aflatoxins lowers weight gain and hence the absolute body weights in both chickens and turkeys; as reduced feed intake and nutrient usage efficiency impair growth. AFB1 lowers the feed conversion ratio leading to more requirement of feed for muscle production in broilers and turkeys and egg production in layer birds.
In contrast, inspite of decreased feed consumption, body weight and feed conversion efficiency of quails are not altered but in ducks former two characters are reduced but not the feed efficiency. This in turn lowers the reproductive performance in poultry. The age of maturity in broilers increases and the egg quality parameters viz., total weight, shape, albumin and/or yolk percentage and shell thickness in chickens and quails adversely get affected because of AFB1 toxicity.
Moreover, AFB1 can damage the immune tissues (bursa of Fabricius, thymus and spleen) which produce mature or active leukocytes and suppress innate and adaptive immune responses. Also, immune tissue atrophy, relative bursal, spleen and thymus weight losses can be seen if AFB1 is consumed during growth period. It has been also indicated that aflatoxin can depress the phagocytic effects of heterophiles and Kupffer cells and lowers the haematological values, total basophilic and thrombocytic counts, enabling lower-resistance of the body to infection. Specific laboratory changes viz., increased AST, ALT and alkaline phosphatase, hypothrombinaemia, prolonged prothrombin and activated partial thromboplastin times, hyperbilirubinemia, hypocholesterolaemia, hypoalbuminemia and variable thrombocytopenia are prominent and frequently encountered.
Besides, nutrition also plays an important role in this context. Deficiencies of some dietary vitamins raise the aflatoxicosis in susceptible chickens. Furthermore, dietary supplementation of tryptophan helps increasing hepatoxicity of AFB1. The small intestine of the sick birds often gets targeted by lowering the length and weight of duodenum and jejunum which consequently affects the tissue morphology. Above all, transfer of aflatoxins through embryonated eggs is yet another major concern for the poultry sector. AFB1 can transmit from affected laying hen to albumin and yolk of her eggs . As a result, contaminated unfertilized eggs can be a food safety risk for human consumption. Major effects of aflatoxicosis are depicted in the given figure 1 below :
Fig 1. Prominent Effects of Aflatoxicosis
A number of aflatoxicosis outbreaks taking several human and animal lives had been encountered in Asia and Africa in the past. These incidences signify and strengthen the severity of the aflatoxin-contaminated food hazards. Even though prevention is the best medicine to control aflatoxicosis but occasionally natural contamination of crops with A. flavus becomes unavoidable. Additionally, enforcement of aflatoxin regulatory limits leads to declined markets and incomes. Methods involving physical removal or chemical inactivation of toxins in the aflatoxin contaminated feeds can be a way out for the decontamination. Some significant strategies to combat aflatoxicosis are depicted in the figure 2 below.
Fig 2. Control Measures to Resist Aflatoxicosis in Poultry
For detoxifying crops like grain, rice, maize and cottonseed, chemicals viz., ammonium hydroxide, calcium hydroxide, hydrogen peroxide, sodium hydroxide and sodium hypochlorite are useful. These chemicals play a key role in reducing aflatoxins specially AFB1 concentrations by hydrolysis which leads to production of degraded form having reduced or no toxicity. Likewise, some feed additives are employed for detoxification and strengthen the metabolic and/or immune functions of the body in order to safeguard the poultry from the effects of aflatoxicosis. Selenium supplementation is the most prominent one and highly preferred against AFB1. Also, super-activated charcoal, phenobarbital, cysteine, glutathione, beta carotene, zeolites like hydrated sodium calcium aluminosilicate, clinoptilolite and sodium bentonite and antioxidants like butylated hydroxytoluene (BHT) and turmeric have proved to reduce the effects of aflatoxicosis. On the other hand, probiotics can also aid in this process of protection. Bacteria viz., Streptococcus, Enterococcus, Lactococcus and Berevibacillus efficiently can help in vitro binding against AFB1. Works are in progress for the effective use of probiotic strains of Lactobacillus, Bifidobacterium and Propionibacterium. Above all, an effective managemental system be established till the selection of resistant lines of poultry against the same can be undertaken for farming. If in case the selection strategy has been adopted then the adverse effects can be easily controlled without any negative impacts or losses and poultry can be protected even from their day-old lives, proving it to be a gold-standard approach.
Thus, not only morbidity or mortality occurs on exposure but also aflatoxicosis in turn causes losses directly and indirectly to the poultry industry. Therefore, to save the industry and protect public health as well as poultry health, a holistic approach has to be adopted in order to mitigate all the iniquities judiciously.