Mycotoxicoses in poultry

Introduction

Anti-nutritional factors depress nutrient quality of the feed and hence the health and performance of poultry. Mycotoxins are one such anti-nutritional factor present in feed ingredients and complete feed. They are the secondary toxic metabolites produced by various genera of fungi. Fungi that produce mycotoxins of major significance in the poultry industry include Aspergillus, Fusarium and Penicillium. Though hundreds of mycotoxins have been implicated in animal disorders, the most significant in the Asia-Pacific region include aflatoxins, ochratoxins, citrinin, T-2 toxin, deoxynivalenol (DON), fumonisins and zearalenone (Table 1).


Table 1. Major fungi genera with associated mycotoxins.




Traditionally, aflatoxin was considered synonymous with mycotoxin because: 1) extensive data on occurrence and its adverse effects on poultry, and 2) lack of analytical procedures for other mycotoxins and therefore lack of awareness among poultry farmers about them. Today in the Asia-Pacific region, however, awareness of mycotoxins other than aflatoxin has grown and poultry farmers in some countries are considering analyzing finished feed for mycotoxins such as ochratoxin, T-2 toxin, DON, zearalenone, citrinin, and fumonisins in addition to aflatoxins.

A question still looms. Does analysis of feed for these seven mycotoxins provide a complete description? The answer is no. It is not possible to analyze for all the mycotoxins present in feed as it is time-consuming and expensive. As a result, mycotoxin-contaminated feed would have been used before the farmer received the extensive analytical report. To avoid economic losses due to mycotoxins in poultry feed, it is advisable to assume that if one mycotoxin is detected in feed then probably several others are present. Detection of aflatoxins is a certain indication of the presence of cyclopiazonic acid (CPA), as both can be produced by the same Aspergillus species, eg., Aspergillus oryzae. Similarly, the presence of T-2 toxin is a certain indication of many trichothecene mycotoxins such as diacetoxyscirpenol (DAS), HT-2 toxin, etc. Another good example of this is the co-occurrence of aflatoxin and ochratoxins. In tropical countries ochratoxins are mainly produced by Aspergillus fungi, which can also produce aflatoxins and cyclopiazonic acid (DeVries et al., 2002).


Prevalence of mycotoxins in the Asia-Pacific region

The Asia-Pacific region is now considered to be the most intensive poultry farming region in the world.

The widespread prevalence of multiple mycotoxins today in this region may be due to:

• Improved analytical procedures, which have increased the chances of mycotoxin detection in conventional ingredients and complete feed.

• Increased use of by-products and alternative feed ingredients, which are likely to have a higher incidence of mycotoxins, in an effort to reduced feed costs.

• Changes in global climatic conditions, which are more conducive to the growth of mold and subsequent mycotoxin production. Climatic conditions in the Asia-Pacific region range from tropical to semi-tropical and temperate.

• The global trade in feedstuffs, which means feedstuffs are derived from crops both grown locally and imported and hence subjected to different conditions during growing, storage and transport (Swamy, 2003).

Several recent surveys of the prevalence of mycotoxins indicate the seriousness of the mycotoxin problem in the Asia-Pacific region.


INDIA

During 2004 and 2005, a survey was conducted to study the incidence of aflatoxin, ochratoxin and T-2 toxin in various feed ingredients and finished feeds collected from different states of the country. Out of 984 samples analyzed, 824 samples were found to be positive for the presence of aflatoxin, ochratoxin and T-2 toxin (Devegowda et al., 2005) (Table 2). Of these, 91, 94, 97 and 97% of cereals, cereal by-products, oilseed meals and finished feeds, respectively, tested positive for mycotoxins. The authors reiterated that not only are aflatoxins a problem in the region; but also ochratoxins and T-2 toxin.


Table 2. Co-occurrence of aflatoxin B1, ochratoxin A and T-2 toxin in feed ingredients and finished poultry feeds in India.




Over a five-year period, Chandrasekaran et al. (2002) assayed 7,173 samples of oil cake, 3,842 samples of complete feed and 2,463 cereals for the presence of ochratoxin A (OTA), citrinin and aflatoxin. Ochratoxin was detected in all samples while aflatoxin was found in 90% of the samples (Table 3).


Table 3. Co-occurrence of ochratoxin A with aflatoxin B1 in complete feed in India.




CHINA

Wang et al. (2003) assayed complete feed samples for aflatoxin, fumonisin, OTA, T-2 toxin, DON and zearalenone. More than 90% of samples were found to contain all six mycotoxins (Table 4). The northern part of China experiences temperate weather while southern China has a tropical climate. This is the possible reason for the occurrence of aflatoxin along with Fusarium mycotoxins such as DON and zearalenone.

In another survey of Asian feed ingredient sources, 1200 raw ingredients and feed samples collected from Bengal, China, Korea, Malaysia, Pakistan, the Philippines, Singapore, Sri Lanka, Thailand and Vietnam between 1998 and 2001 were analyzed for aflatoxin B1, DON, and zearalenone. Over 70% of samples from China were contaminated with DON (Table 5).


Table 4. Mycotoxin concentrations in complete feed samples in China.




Table 5. Concentrations of aflatoxin B1, DON and zearalenone in Asian feed ingredients.




These and other surveys highlight clearly that aflatoxin is not the only mycotoxin encountered in Asian poultry feed ingredients that should be considered a threat to animal health and performance. A range of toxins including DON, zearalenone, OTA, citrinin, T-2 toxin and fumonisins are noted at significant concentrations. Since these mycotoxins rarely occur alone, any solution considered must be capable of addressing the broad range of mycotoxins expected.


Impact of increasing raw material prices on animal mycotoxicoses

Mycotoxin surveys from around the world indicate that protein sources such as rapeseed meal, cottonseed meal, groundnut cake, sunflower cake, copra meal and palm kernel meal are more susceptible to mycotoxin contamination than conventional raw materials such as soybean meal. Owing to high prices of conventional raw materials during certain years, feed manufacturers have been forced to opt for alternatives to soybean meal and this has increased the potential for mycotoxicoses for many livestock species. Similarly, the cost of maize has forced a look at other energy sources, including byproducts such as rice bran, wheat bran and screenings.

Many mycotoxins are concentrated in the outer covering of the seeds and therefore the chances of mycotoxinrelated problems are increased when such materials are used in animal rations. For example, during the milling process DON was found in the highest concentration in the bran and lowest in the flour (Lee et al., 1987). Mycotoxins from these by-products in combination with mycotoxins from more traditional ingredients can result in toxicological interactions.


Adverse effects of mycotoxins in poultry

Mycotoxins affect almost all organs in the body. The major organs and tissues affected, however, are liver, kidney, the oral cavity, gastrointestinal tract (GIT), spleen, brain and nervous system. Liver is the target organ in most cases as it is the center of detoxification of mycotoxins. Ochratoxins mainly affect the kidneys, while trichothecene mycotoxins damage the oral cavity and GIT. Symptoms of mycotoxicosis can be nonspecific and at times difficult to differentiate from viral, bacterial or parasitic diseases. In most cases, mycotoxins increase the susceptibility of animals to other disease conditions by compromising the immune system.

A delicate balance between antioxidants and prooxidants in the body in general and specifically in the cell is responsible for regulation of various metabolic pathways leading to maintenance of immunocompetence, growth, development and protection against stress conditions associated with commercial animal production (Surai, 2002). It has been postulated that mycotoxins stimulate lipid peroxidation both by enhancing free radical production and by compromising the antioxidant system. Some general effects of important mycotoxins in poultry are listed in Table 6.


Table 6. Individual effects of mycotoxins prevalent in poultry feed of Asia-Pacific origin.




Economic impact of mycotoxins

The economic effects of mycotoxins are manifested in several obvious and direct ways but also in more subtle expressions.


MORTALITY IN POULTRY

Occasionally outbreaks of mycotoxicosis around the world have resulted in devastating effects on the poultry industry. Good examples of such outbreaks are: 1) Turkey X Disease (aflatoxicosis) outbreak in turkeys in the UK, 2) outbreak of ochratoxicosis in turkeys, and 3) outbreak of T-2 toxicosis in laying hens (Devegowda and Murthy, 2005).


INCREASED HEALTH CARE AND VETERINARY COSTS

To prevent the adverse effects of mycotoxins in humans and animals, many therapeutic and preventive strategies must be put in place that add to the cost of maintaining human and animal health.


DECREASED LIVESTOCK PROFITABILITY

Livestock profitability largely depends on the amount of milk, meat or eggs produced per unit of feed consumed and/or the number of progeny produced. Mycotoxins interfere with the absorption of nutrients,
inhibit several digestive enzymes and reduce feed conversion efficiency, all of which increase production costs. Mycotoxins such as zearalenone and T-2 toxin increase embryonic mortality and reduce fertility and hatchability (Leeson et al., 1995).

Unlike in North America, where efforts have been made to accurately monitor the losses incurred in the livestock industry due to mycotoxicoses, no such detailed information is available for the Asia-Pacific region. Losses due to mycotoxicoses have been estimated at more than $1 billion in Canada and over $2.5 billion in the US during the 1990s. It is estimated that 160 million tonnes of compound feed are produced in the Asia-Pacific region each year. CAST (1989) reported that at least 25% of the total world’s feed supply is contaminated with known mycotoxins. Taking this estimate into account, about 40 million tonnes of feed in the Asia-Pacific region is either completely unfit for animal use or if fed to animals, causes loss of performance or mortality. These losses are likely to amount to more than $10 billion per annum and are conservative estimates.


LOSS OF FORAGE CROPS AND FEEDS

Mycotoxin-contaminated crops and feeds are unfit for human and animal consumption. Severely infested crops and feeds must be destroyed.


REGULATORY COSTS

To prevent human exposure to mycotoxins either through the consumption of contaminated plant or animal products, regulations are in place in many countries (ISMYCO Kagawa, 2003). When these
contaminated foods are consumed by humans, a variety of disease conditions ranging from acute toxicity (mortality) to chronic diseases (cancer) can be observed. The establishment of regulations demands large investments in monitoring and compliance. Aflatoxin B1 (10 to 50 ppb) and zearalenone (1 ppm) are the only two mycotoxins that are regulated in poultry feed in the Asia-Pacific region.


MYCOTOXIN ANALYSIS

The need to monitor mycotoxin levels in raw materials, compound feeds and animal products for human consumption indicates the severity of the issue, and underscores the problems caused by mycotoxins.


Toxicological interactions

Co-occurrence of mycotoxins is common in feed ingredients (and complete feed). The toxicity responses and clinical signs observed in poultry when more than one mycotoxin is present in feed are complex and
diverse. Symptoms typical of mycotoxicosis are often seen in poultry despite analysis of the feed indicating only very low concentrations of individual mycotoxins. Mycotoxins in combination exert a greater negative impact on health and productivity of animals than their individual effects (Swamy, 2003). Mycotoxin interactions can be additive, synergistic or antagonistic. Interaction between DON and fusaric acid, the most common Fusarium mycotoxin, is an excellent example of synergistic interaction (Smith et al., 1997). Fusaric acid by itself is not toxic to animals even at very high concentrations, but it increases the toxicity of DON when they are both present.

Interactions can alter clinical signs, resulting in a set of diagnostic characteristics that differ from the sum of individual effects. This subsequently makes field diagnosis of mycotoxin interactions difficult and
emphasizes the need to characterize mycotoxin interactions in detail.

Interactions also pose challenges to the development of uniform methodologies for remediation of mycotoxin contamination. Although a decontamination protocol may effectively reduce the detectable levels of one mycotoxin, another mycotoxin may persist at harmful concentrations. Some of the important toxicological interactions observed among various mycotoxins are given in Table 7. It is important, therefore, that a mycotoxin adsorbent should be capable of adsorbing several mycotoxins simultaneously.


Mycotoxin adsorbents

Various strategies have been identified to reduce or prevent the adverse effects of mycotoxins on animal health and production. The most practical method is the inclusion of mycotoxin adsorbents in feed. When an effective mycotoxin adsorbent is added to feed, it adsorbs mycotoxins in the GIT and they are safely excreted in feces, thereby preventing absorption and transport to target organs. The net effect is a reduction in the dose of absorbable toxin to a concentration that does not adversely affect animal performance (Swamy, 2004). Most extensively studied mycotoxin binders include clay binders and a yeast-derived glucan-based polymer (Mycosorb®).


CLAY BINDERS (HSCAS, BENTONITES, ZEOLITES)

Although mineral binders are relatively low priced, they offer very limited protection against mycotoxins for several reasons (van Kessel and Hiang-Chek, 2001).

1. Some clay binders are processed, while others are crude inorganic preparations. The efficacy of such products is variable.

2. Mineral mycotoxin binders, such as aluminosilicates, are capable of binding only one specific mycotoxin (most commonly aflatoxin). Such products are not, therefore, effective against mycotoxins of varying molecular weight and polarity. It has been repeatedly demonstrated that clay binders are not effective against T-2 toxin, ochratoxins, DON, cyclopiazonic acid, zearalenone, diacetoxyscirpenol, fumonisins and ergotamine (DeVries et al., 2002).

3. Clay binders offer low specificity and so must be used at a high level of inclusion to be effective.

4. The particles of clay binders expand as they come in contact with water. Because of this expansion, small molecules, including aflatoxins, are absorbed into the particle. This mode of action, however, has two important disadvantages. First, clay binders can bind nutrients, such as minerals and vitamins, as well as aflatoxins (Chestnut et al., 1992; Kramer et al., 1993). Secondly, aflatoxin is absorbed, as in
a sponge, but not actually bound to the mineral particle. In practice, this means that after some time toxins can again become available for absorption by the GIT.

5. Clays are not capable of adsorbing mycotoxins under the wide pH range of the GIT. One of the binding mechanisms of aflatoxins to HSCAS is by hydrogen bonding at acidic pH, but toxins are released when
pH becomes neutral or alkaline with addition of pancreatic secretions.

6. Very limited numbers of in vivo studies are available on clay binders and most of these studies have employed pure mycotoxin, which does not reflect the actual field mycotoxin problem.


Table 7. Toxicological interactions among mycotoxins.




AN ORGANIC POLYMER DERIVED FROM YEAST CELL WALL

Recent progress in yeast biotechnology and carbohydrate chemistry has opened new avenues for tackling mycotoxin problems. In 1993, researchers supplemented an aflatoxin-contaminated broiler diet with 0.05 to 0.2% live yeast (Yea-Sacc1026) and reported significant improvement in the weight gain and feed efficiency (Stanley et al., 1993). Subsequent research demonstrated that the glucan fraction of the yeast cell wall (Mycosorb®) was responsible for adsorbing mycotoxins and preventing mycotoxicoses. This yeast-derived product has a number of characteristics that make it an effective adsorbent for inclusion in animal feeds. Ability to adsorb a wide range of mycotoxins Survey data presented earlier for the Asia-Pacific region indicate clearly that mycotoxins in feed and raw materials typically comprise two or more types of mycotoxins. It is vital, hence, that the mycotoxin adsorbent be effective against multiple mycotoxins. Studies with Mycosorb®, both in vitro and in vivo have proven this adsorbent able to sequester a wide range of mycotoxins (Table 8).


Table 8. Studies of mycotoxin adsorption by Mycosorb®.




Effective at low inclusion rates over a wide pH range

For practical nutritional and economic reasons, it is preferable that a mycotoxin adsorbent be effective at a low inclusion rate. Further, pH conditions of both the GIT of monogastrics and ruminants vary considerably from the proximal to distal portions. Studies with Mycosorb® have shown it to be effective at inclusion rates as low as 0.05 to 0.1% and able to adsorb mycotoxins both at acidic and alkaline pH (Devegowda et al., 1994).


High capacity for mycotoxin adsorption

Although very high concentrations (i.e. clinically acute) of mycotoxins in feed are rare, there are many incidences of acute toxicity in animals. Under such conditions, an ideal adsorbent should have a high capacity to adsorb mycotoxins so that the concentration of unbound mycotoxin remaining is below the threshold level to cause animal toxicity. Mycosorb® has the capacity to bind as high as 2000 ppb of aflatoxin (Evans, 2000).


High affinity to adsorb mycotoxins at low concentrations

The presence of low concentrations of multiple mycotoxins is a common feature of feed ingredients. Quite often mycotoxin concentrations in the Asia-Pacific region range between 10 to 40 ppb. Whilst low levels of individually toxins may not cause clinical symptoms in animals, each contributes to synergistic effects of toxins on feed intake, weight gain, immune status and reproduction. The high affinity of Mycosorb® for toxins such as zearalenone, fumonisins, T-2 and DON when present at low concentrations means reduced synergistic toxicity.


Ability to adsorb mycotoxins rapidly

As quickly as 30 minutes after ingestion of mycotoxin contaminated material, mycotoxins are released from the feed matrix in the intestine and can be absorbed into the blood. An ideal adsorbent, therefore, should bind the maximum amount of mycotoxin possible within this short duration. Murthy and Devegowda (2004) demonstrated ability of 0.1% Mycosorb® to bind 250 and 500 ppb aflatoxin B1 within 30 minutes of feed ingestion. Any subsequent adsorption after 30 min is of little benefit as by then the majority of the mycotoxin will have been absorbed from the digestive tract and have caused organ damage and subsequent adverse effects (Figure 3).


Proven in vivo responses

Ultimately, the practical value of mycotoxin adsorbents must be proven in vivo as it is very difficult to simulate the GIT conditions in vitro (van Kessel and Hiang-Chek, 2001). Mycosorb® has proven its efficacy in a large number of in vivo trials conducted in many livestock and poultry species around the world (Table 9). Some of the recent in vivo studies are discussed in detail in the following sections.


Figure 3. Percent aflatoxin adsorbed by Mycosorb® at different time intervals in the gastrointestinal tract of broiler chickens (Murthy and Devegowda, 2004).




In vivo studies of Mycosorb® in diets containing aflatoxin, T-2 toxin, ochratoxin and zearalenone

A series of trials was conducted at the University of Agricultural Sciences, Bangalore India, to evaluate the toxicity of aflatoxin, T-2 toxin, zearalenone and OTA beginning in 1990.


AFLATOXIN, OCHRATOXINS AND T-2 TOXIN IN COMMERCIAL BROILERS

Two dietary inclusion rates of aflatoxin (0 and 0.3 mg/kg), OTA (0 and 2 mg/kg), T-2 toxin (0 and 3 mg/kg) and Mycosorb® (0 and 1 g/kg) were tested in a factorial treatment structure using a total of 960 broiler chickens from 1 to 35 days of age in an open-sided deep litter pen house. Body weight and feed intake were depressed by all the mycotoxins, OTA being the most toxic during early life (Raju and Devegowda, 2000) (Table 10). Weights of kidney and adrenals were increased by aflatoxin and OTA. Liver weight was increased by aflatoxin (17.8%), while OTA increased gizzard weight (14.6%) and reduced bone ash content (8.1%). T-2 toxin had no effect on these variables. Significant interactions were observed between any two toxins with additive effects on body weight, feed intake, bone ash content and serum GGT activity at 21 days. Simultaneous feeding of all three mycotoxins did not show increased toxicity above that seen with any two. Mycosorb® increased body weight (2.26%) and feed intake (1.6%), decreased weights of liver (32.5%) and adrenals (18.9%) and activity of serum GGT (8.7%), and increased serum protein (14.7%), cholesterol (21.9%), BUN (20.8%) and blood hemoglobin (3.1%) content, indicating its possible beneficial effect on mycotoxicosis in broiler chickens.


Table 9. List of in vivo studies conducted using Mycosorb® in poultry.




Table 10. Effect of Mycosorb® on individual and combined toxicity of aflatoxin, ochratoxin and T-2 toxin in broiler chickens.




AFLATOXIN, OCHRATOXIN, ZEARALENONE AND T-2 TOXIN MIXTURE IN BROILER CHICKENS

Commercial broiler chickens were fed diets containing a combination of 168 ppb aflatoxin, 8.4 ppb OTA, 54 ppb zearalenone and 32 ppb T-2 toxin for 35 days. Feed intake and body weight were decreased and FCR was increased significantly in birds fed contaminated diets (Table 11) (Aravind et al., 2003). Mycosorb® added at 0.05% to mycotoxin-contaminated diets ameliorated mycotoxin effects on intake, gain and efficiency.


Table 11. Effect of Mycosorb® on performance of broilers fed combinations of aflatoxin, ochratoxin, zearalenone and T-2 toxin.




AFLATOXIN AND T-2 TOXIN IN COMMERCIAL BROILERS

Twelve dietary treatments (4 x 3 factorial) consisting of two dietary levels each of aflatoxin (0 and 2 mg/kg), T-2 toxin (0 and 1 mg/kg), Mycosorb® (0 and 1 kg/ton) and hydrated sodium calcium aluminosilicate (HSCAS) (0 and 10 kg/ton) were tested using 720 commercial broiler chickens randomly assigned to 36 replicates of 20 chicks of equal sex ratio for a period of 35 days. Diets containing aflatoxin and T-2 toxin significantly reduced feed intake, weight gain and feed efficiency. Weights of thymus and bursa of Fabricius, antibody titers against Newcastle disease and infectious bursal disease were also reduced (Table 12). Mycosorb® significantly prevented these adverse effects, suggesting it protected against both aflatoxin and T-2 toxin. HSCAS showed protection only against aflatoxin with little or no effect against T-2 toxin (Girish and Devegowda, 2004).


Table 12. Effect of Mycosorb® and HSCAS on antibody titers of broilers fed individual or combination of aflatoxin and T-2 toxin.




T-2 TOXIN IN COMMERCIAL LAYING HENS

Commercial layers (192) were divided randomly into eight treatments of four replicates each. Each replicate contained six laying hens and the experimental diets were fed for three periods of 28 days. Dietary treatments consisted of four concentrations of T-2 toxin (0, 0.5, 1.0 and 2.0 ppm) and two concentrations of Mycosorb®. It was concluded that Mycosorb® reversed T-2 toxin induced suppression of egg production even at the highest concentration (Manoj and Devegowda, 2001) (Table 13).


Table 13. Effect of Mycosorb® on egg production of laying hens fed T-2 toxin.



IN VIVO STUDIES OF MYCOSORB® RESPONSE IN DIETS CONTAINING DIACETOXYSCIRPENOL (DAS) IN COMMERCIAL BROILER CHICKENS

A study was conducted to determine ability of Mycosorb® to reduce the toxicity of DAS in broiler chickens. Two dietary inclusion rates of DAS (0 and 1 ppm) and Mycosorb® (0 and 0.1%) were tested in a 2 x
2 factorial arrangement on a total of 480 broiler chickens from 1 to 42 days of age. When compared with controls, dietary DAS significantly decreased body weight (17%) and body weight gain (19%). The adverse effect of DAS on feed consumption (3%) was also observed over the entire feeding period. The addition of Mycosorb® significantly reduced the toxic effects of DAS on body weight and body weight gain. The addition of Mycosorb® to the DAS-free diet increased body weight (6%) and body weight gain (7%) compared with the control (Table 14) (Pavicic et al., 2001).


Table 14. Effect of Mycosorb® on body weight of broilers fed diacetoxyscirpenol (DAS).




IN VIVO STUDIES INVESTIGATING EFFECTS OF MYCOSORB® IN DIETS CONTAINING DON, 15-ACETYL DON, ZEARALENONE AND FUSARIC ACID

Smith and co-workers have done extensive research at University of Guelph, Canada in commercial broilers, layers, ducks and turkeys and pigs fed grains naturally contaminated with Fusarium mycotoxins. In these experimental diets, only DON, zearalenone, 15-acetyl DON and fusaric acid were found in detectable quantities among 25 different mycotoxins analyzed. This mixture of mycotoxins can also be found in temperate regions of the Asia-Pacific, especially parts of China, Australia, New Zealand and Korea.


Table 15. Effects of feeding blends of grains naturally-contaminated with Fusarium mycotoxins on weight gain and feed consumption of broiler chickens¹.




Broiler chicks were fed starter (0-3 weeks), grower (3-6 weeks) and finisher (6-8 weeks) diets in two 56-day experiments (Swamy et al., 2002; 2004a). Diets included: 1) control, 2) low level of contaminated grains, 3) high level of contaminated grains, and 4) high level of contaminated grains + 0.2% Mycosorb®. DON was found at approximately 0.5, 5.0, 9.0 and 10.0 ppm for the four diets. The concentration of 15-acetyl DON was about 0.5 ppm, zearalenone was about 0.5 ppm, and fusaric acid was about 17 ppm. There was a significant linear decrease in growth rate and feed consumption in the grower period when increasing levels of contaminated grains were fed (Swamy et al., 2004a; Table 15). No significant effect of diet was seen in the starter or finisher periods. When broilers were growing more slowly, growth depression was observed in the finisher phase (Swamy et al., 2002). At the end of the finisher phase in the earlier study, it was observed that contaminated grains elevated red blood cell count and blood concentrations of hemoglobin and uric acid. Biliary concentrations of IgA were reduced, while breast meat redness increased. Supplementation with 0.2% Mycosorb® prevented all of the above dietary effects
(Table 16).


Table 16. Effects of feeding blends of grains naturally-contaminated with Fusarium mycotoxins on hematology, serum chemistry and breast meat coloration of broiler chickens¹.




Laying hens

One hundred and forty-four 45-week-old laying hens were fed for 12 weeks diets including: 1) control, 2) contaminated grains and 3) contaminated grains + 0.2% Mycosorb®. Diets with contaminated grains had an average of 12.0 ppm DON with other three mycotoxins in the same ratios as noted in broiler trials.

Contaminated grains decreased feed consumption compared to controls in the first 4 weeks (P<0.05) (Table 17) (Chowdhury and Smith, 2004). Feed consumption increased, however, from 4 to 8 weeks and from 8 to 12 weeks. The efficiency of feed utilization (feed consumption/egg mass) decreased compared with controls in these same time periods when birds were fed contaminated grains. Supplementation with Mycosorb® decreased feed consumption and increased the efficiency of feed utilization in the period from 8 to 12 weeks.

Broilers and layers are sensitive to Fusarium mycotoxins. The adverse effects of the diets fed in the current studies are greater than literature reports based on the DON content. This is likely because of the
relatively short duration of previously reported trials. The blending of different naturally-contaminated grains, moreover, also results in a more complex mixture of mycotoxins, thereby increasing the chances of toxicological synergy.

Mycosorb® proved to be a very effective preventative approach for mycotoxicosis in poultry. The mode of action of Mycosorb® is to prevent intestinal uptake of mycotoxins and subsequent transfer of mycotoxins to sensitive target tissues such as liver, kidney, brain and reproductive tissues (Diaz and Smith, 2005). It is clear from these efficacy trials that Mycosorb® is capable of adsorbing a combination of aflatoxins, ochratoxins and Fusarium mycotoxins and minimizing the potential for toxicological synergism.


Table 17. Effects of feeding blends of grains naturally-contaminated with Fusarium mycotoxins on feed consumption and feed efficiency of laying hens.




Conclusions

Several extensive surveys of mycotoxins in feed ingredients and complete feed in the Asia-Pacific region have clearly identified the presence of ochratoxin, T-2 toxin, zearalenone, deoxynivalenol, citrinin, and
fumonisins in addition to aflatoxins.

The rising cost of the traditional mainstay ingredients, maize and soybean meal, has forced producers to consider greater use of by-products. This is likely to further increase the prevalence of mycotoxicoses since these alternative feed ingredients are more likely to contain mycotoxins. Trade in raw ingredients around the region exacerbates the problem and makes prediction of mycotoxin incidence difficult.

Livestock producers in the Asia-Pacific region can minimize the economic losses caused by mycotoxins by using an effective adsorbent. Mycosorb®, extracted from the cell wall of yeast, rapidly adsorbs a wide range of mycotoxins effectively at a low level of inclusion. In more than 25 in vivo trials conducted at universities around the world, Mycosorb® has been proven to protect poultry from adverse effects of multiple mycotoxins.


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