India is the largest milk producer in the world since many years, but this is due to the number of animals present, not because of their productivity. One of the reasons is ignorance of importance on feed safety by our feed manufacturers and dairy farmers. Major portion of dairy animals in India lies with backyard farmers, who are least aware of the role on feed safety or food chain. Domestic waste, dry or green fodder offered to dairy animals are often moldy. As most of the cattle feed manufacturers do not have silo for raw material storage, mold gets infested during storage. Mycotoxins which are secondary metabolite of molds are produced and enter animal body. There are several mycotoxins which affect digestive, reproductive and immune systems. Mycotoxins at very low dosage in animal body creates chronic effects for a longer time. Hence, animals infected with mycotoxins has problem with liver functions and reduced immunity does not perform to any feed or fodder as per its potential and dairy farm faces economical loss. Aflatoxin B1 produced by Aspergillus flavus of mold in dairy animals milk form into Aflatoxin M1 to some extent. This Aflatoxin M1 enters food chain and becomes carcinogenic, hepatotoxic and immunosuppressive. Only way to combat this is by inhibiting the mold growth in raw material of feed by using mold inhibitors, and binding toxins with a good toxin binder which helps to expel mycotoxins out of the animal body.
In India, per animal production and reproductive performance are the major challenges for economic viability of dairy farms. Production is sub optimum due to several reasons. In past few years, a lot has been done on the improvement of breeds. Any dairy breed, be it a high yielder or low yielder, can perform only when it is healthy, and its nutrient requirement is fulfilled. Dairy animals have to synthesize milk in their body, the most wholesome edible on earth. If they don’t get it, both production and reproduction are impacted. Mold and mycotoxins that enter the animal body through feed, reduce its performance in several ways. Mold deteriorates nutrient quality of grains by utilizing the fat, protein and carbohydrates for its own propagation. Mycotoxins are produced as a secondary metabolite by certain class of fungi like Aspergillus, Fusarium and Penicillium, which infest the crop in field or during storage under optimum temperature and relative humidity conditions. Mycotoxin term was first launched in 1960 in London, England when around 1,00,000 turkeys died due to consumption of aflatoxin contaminated peanut meal, imported from Brazil. They have been regularly found responsible in toxic syndromes in humans and animals. Almost all the mycotoxins have carcinogenic, teratogenic, embryotoxic, hepatotoxic, nephrotoxic, and immunosuppressive effect. Mold and mycotoxins have ubiquitous presence, all over the globe. In last few years, demand of dairy products has increased in India, due to constantly growing population, urbanization, improved economic status of people, and increased awareness on nutrient requirements of body. To meet this ever-increasing demand, performance of dairy animals becomes crucial. Feed safety can play a major role to achieve this goal, as unsafe feed due to mycotoxins restricts animals to perform their full potential. Mycotoxins do not affect animal health and performance alone, but some part is drained into milk, meat and eggs which ultimately affects human health. Further discussion on important mycotoxins and their impact on animal health and production was detailed as below.
Aflatoxins are a group of mycotoxins produced from different species of Aspergillus, one of them is Aspergillus flavus, which gives this mycotoxin its name. These are the most studied mycotoxins associated with animal feed and human food. European countries are least bothered with the problem of Aflatoxins, due to their geographical location. Aflatoxins are a major problem of regions having hot and humid environmental conditions like Asian and African countries along with some parts of Australia. Along with adequate substrate, temperature and humidity are the most crucial parameters for production and amount of aflatoxin. Optimum temperature for the growth of Aspergillus flavus is 29 to 35°C, as aflatoxin production is maximum at 24° C and not produced at all below 13°C or above 42°C, and relative humidity below 70%. India encountered an outbreak of aflatoxicosis in 1974, which resulted in the death of around 100 people. In nature, there are more than 14 different chemical forms of aflatoxin, out of which aflatoxins B1, B2, G1 and G2 are the most dangerous forms. The suffix letters with aflatoxin, i.e. B and G represents the color these aflatoxins exhibit in ultraviolet radiation (B for blue and G for Green). Susceptibility to aflatoxicosis is maximum in young animals, but no age group is unaffected. Symptoms of aflatoxicosis depend on animal, breed, species, age, nutritional status, dose and duration of exposure to aflatoxin. Commonly observed symptoms of aflatoxicosis in all animals are gastrointestinal dysfunction, liver damage, decreased feed utilization and efficiency, reduced productive and reproductive performances, embryonic death and immunosuppression, even at very low dose. Reports revealed that reduced feed intake is mostly the first sign of aflatoxin problem. Reduction in feed efficiency in cattle is attributed to decreased ruminal function by reduction of cellulose digestion, volatile fatty acid production and motility of rumen. A part of aflatoxin B1 consumed by dairy cows through contaminated feed was drained in milk in the form of aflatoxin M1. Drainage of aflatoxin M1 in milk was more in early lactation when compared to late lactation.
Ochratoxins are produced by a species of Aspergillus and Penicillium. Ochratoxins are of three types, namely A, B and C. Ochratoxin A (OTA) is the most common and important mycotoxin, due to its impact on public and animal health. Most common sources of Ochratoxin A are grains like maize, wheat, sorghum, rice, barley, oat, rye, etc. Ochratoxin A causes renal dysfunction of animal along with various toxic effects like other potential mycotoxins, i.e. carcinogenic, teratogenic, immunosuppressive, embryotoxic and hepatotoxic. Ochratoxins alone are comparatively less toxic in cattle, perhaps due to detoxification and ruminal microbial degradation.
Fumonisins are produced from Fusarium moniliforme. Out of the sixteen different analogues of fumonisin known till date, B-series fumonisins comprises an important fumonisins like B1, B2, B3 and B4. In a recent study, Aspergillus niger was also found to produce fumonisins. Reports revealed that fumonisin B1 was the most toxic and predominant member of the family and was carcinogenic. Carcinogenic effect of fumonisin was not by direct DNA damage, rather they disrupt sphingolipid biosynthesis owing to their structural similarity with backbone precursors of sphingolipids. Fumonisin toxicity was more significant in horse, swine and rabbits as cattle and poultry are less sensitive to fumonisin toxicity. In dairy animals, fumonisins exhibit their effect by immunosuppression, damage to liver and kidney, decrease in weight gain, and increased mortality rates.
Zearalenone (earlier known as F-2 toxin) is produced by some of the Fusarium species. Zearalenone is found to cause infertility, reduction in milk yield and hyperestrogenism in cattle. Zearalenone toxicity was due to its molecular similarity to naturally occurring estrogen hormones. Higher doses of zearalenone were found to interfere with normal fertility, i.e. ovulation, conception, implantation, fetal development and survival of new born animals. Higher doses of zearalenone can result in abortions. Zearalenone toxicity can also result in reduced feed intake, reduced milk yield, increased vaginal secretions, vaginitis, poor reproductive performance, and enlarged mammary glands in heifers. In cattle, zearalenone exposure for longer duration leads to problem of follicular cysts. Maximum permissible limit of Zearalenone in diet is 250 ppb.
A large number of mycotoxins produced by different species of Fusarium are grouped under Trichothecenes. Trichothecenes and their derivatives which are more than 200 in number are classified into four types (A-D). Types A and B are most common and occurs widely in cereals. The T-2 and HT-2 toxins are included in type A trichothecenes, while deoxynivalenol (DON) is included in type B of trichothecenes. Trichothecenes use protein synthesis inhibition as their mechanism of action. They are also reported to affect leucocytes resulting in immunosuppression.
Deoxynivalenol (DON), also called as vomitoxin is the most prevalent trichothecene in grains like barley, maize, wheat, oats and rye, and less common in sorghum, rice and triticale. In feedlot, there were no reports of deoxynivalenol affecting health or performance of cattle. Even at a dose of 6 mg/kg of feed, deoxynivalenol had no negative impact on milk production or its residue in milk.
The T-2 toxins are synthesized mainly by Fusarium tricinctum. These were the first trichothecenes to be isolated as a naturally occurring contaminant in grains of United states. A lethal toxicosis by T-2 toxin in dairy cattle was reported in Wisconsin state of United states in 1970 due to consumption of moldy corn. The T-2 toxin also reported to suppress immunity in cattle by the reduction in serum levels of IgA, IgM and IgG. It also induces necrosis of lymphoid tissues. Abortion in third trimester of gestation and infertility in cattle was also stated as a consequence of T-2 toxicity. Other than the T-2 toxin, rest of the trichothecenes have no adverse effect in cattle. In other countries, association of T-2 toxins with any disorder in animals or humans were doubtful. Chances of residual T-2 toxin in edible tissue was rare, as T-2 toxin was rapidly metabolized inside the body.
Molds get entry into the crops while in field, or in feed/ feedstuff during storage. They utilize nutrients (fat, protein and carbohydrates) for their own growth resulting in reduction of nutritive value of feed stuff or feed. In the process of multiplication, molds produce secondary metabolites called mycotoxins. These molds and mycotoxins when enters the animal body through feed, results in various complications like, reduced feed intake, feed rejection, reduced milk production, reduced rumen function, diarrhea, liver damage, kidney damage, immunosuppression, reproductive problems like anestrus, abortions, and embryonic death, etc. Productivity of dairy animals in India is very low to fulfill the ever increasing demands of milk and milk products, and the performance of dairy animals needs to be optimized. Awareness on feed safety among dairy farmers and feed manufacturers can do a lot. A broad spectrum on mold inhibitor in concentrate feed will inhibit growth of molds between the interval of feed manufacture to feed consumption. No mold, no mycotoxins. A good quality toxin binder will bind any toxin entering the rumen of animal and won’t allow it to cause any damage to the animal body by excreting toxins out along with toxin binders. Thus, nutritive value of feed will be maintained, animal will be free from mycotoxin effects, and performs as per its potential. As a result, economic viability of dairy farms will be ensured.
by Dr. Vimlesh Chandra Sharma and Dr. Sudhir Kumar Singh, Kemin Industries South Asia