It is not easy to earn profit from growing chickens. Besides the high costs of feed ingredients and fluctuating market prices of meat and eggs, the producer has to contend with a myriad of other challenges that include nutrition, water supply and quality, biosecurity, housing, flock health management and the existence of pathogens that constantly pose disease threat to the birds.
Pathogens that are capable of causing disease to the birds are mostly opportunistic. Various factors such as immunosuppression, a change in feed quality, ingredients or nutrient levels, a lapse in biosecurity or flock health programmes, and various other critical points or stress factors, play important role in this development. Manifestations of disease can often be attributed to several causes and thus, understanding the root of the problem is imperative to overcoming the challenge.
In this article, we explore how mycotoxins, the secondary toxic metabolites produced by moulds, can harm the gastrointestinal tract (GIT) of poultry, open the gate to infectious agents and/or predispose the birds to a number of factors that could reduce performance and cause disease outbreaks.
The unique avian digestive system
The digestive system is probably the most important system in the chicken’s body, since it plays the role of converting feed into meat or eggs, oftentimes likening it to a type of feed-to-food converting machine. The avian digestive system is made up of some of the most amazing organs that are quite different from that of mammals, including a crop, a gizzard, a proventriculus, and even a pair of cul-de-sac caeca, where bacteria help to ferment and break down undigested food. This results in poultry having one of the most efficient digestive systems in the animal kingdom.
The poultry digestive tract is wondrous as it can digest feed and grain, and yet not harm or digest itself. It is the most extensively exposed surface of the body in terms of surface area and therefore functions as the most important barrier between internal and external environment. In the poultry species, more than 650 different species of bacteria and 20 different hormones within the digestive tract can be found, all responsible for digesting and absorbing a wide variety of nutrients from the raw materials in feed. The entire digestive system accounts for approximately 20% of its total energy expenditure and contributes to being the largest organ of the immune system.
A potential pitfall fallacy
The modern day poultry producer is well-informed about mycotoxins and vigilant towards its existence in poultry feed. The dangers of the different types of mycotoxins such as aflatoxins (AFL), ochratoxins, fumonisins (FUM), deoxynivalenol (DON) and zearalenone and the threats these pose towards the immune system and productivity of the entire flock are well-known. Therefore, a conscientious and diligent analyses of feed on a regular basis to detect the presence of these mycotoxins is as important as paying careful attention to detected levels in the feed, before deciding on the appropriate amount of mycotoxin deactivating product to be included in the feed formulation.
When mycotoxin risk management is discussed, it is not adequate to only consider the quantity or final concentration of mycotoxins in the feed that can cause harm or damage the birds. Oftentimes, the specific levels of mycotoxins that could lead to clinical signs or diseases symptoms in the flocks are overly concerned. The trouble is that any detected levels that fall below the higher limits of mycotoxin detection imposed by regulatory bodies such as the European Commission in the European Union and the Food &Drug Administration in the United States, are considered as having insignificant effect on livestock and the feed is considered safe.
It is misinterpret that if the level of detected mycotoxins are within regulatory limits, then it would not cause immunosuppression nor organ damage to the flocks. However, it has been found that even sub-toxic concentrations of mycotoxins in feed can cause harm to the birds, as they are able to cross the tight junction barrier or permeate even intracellularly into the systemic pathways to destroy vital organs such as the liver and kidneys. Enterocytes are the first cells to be exposed to mycotoxins and often come into contact at higher concentrations than other organ tissues. Therefore, the entire intestinal epithelia are usually compromised by the toxins even before absorption begins.
The detriments of mycotoxin exposure
Various publications have shown how different levels of mycotoxins may impact the poultry gastrointestinal tract and depress the immune system. Gut morphology studies show how feeding chickens with low levels of DON alone or in combination with other fusariotoxins may lead to a reduction in both duodenal and jejunal villi height in poultry. As a result, there will be less surface area for absorption of nutrients, which leads to impaired growth and performance.
It has also been found that mycotoxins such as DON and T-2 directly alter glucose transporters in the jejunum. This has an anti-nutritive effect, since it leads to decreased glucose absorption and may eventually limit water reabsorption, resulting in diarrhoea. Different studies investigated the effects of mycotoxins on the gastrointestinal defence system against bacterial and parasitic infections. Chicks challenged with Ochratoxin A (OTA) had more severe intestinal lesions and mucosal damage than those that were not exposed to the mycotoxin. The challenged chicks were also more susceptible to coccidiosis and had more Eimeria acervulina and E. adenoidesoocysts in their intestines than their control group counterparts. On the other hand, an experiment with DON, even at low concentrations that were considered as safe for poultry, revealed that the mycotoxin depressed the immune system, impairing the immune response and delaying intestinal recovery following a coccidiosis infection. Lymphocyte stimulation and assembly at the site of infection was inhibited, hindering the clearance of the coccidial infection.
It is wondered how a coccidiosis outbreak could still occur in a poultry flock despite the inclusion of a divalent, polyether, ionophore coccidiostat such as lasalocid within the feed. Certain experiments have shown that T-2 contamination in broiler diets could reduce the efficacy of lasalocid as an anticoccidial drug. OTA on the other hand, is able to interact with Salmonella typhimurium, and it has been proven that the number of colony forming units (cfu) increases within the duodenal and caecal contents when the animals ingested feed contaminated with OTA. Other studies have proven that DON is able to increase the intestinal inflammatory response to S. typhimurium, leading to a significant increase in both the invasion as well as the bacterial translocation of the pathogen through the intestinal barrier. It is also learnt that prolonged intestinal infection, increased intestinal colonisation, translocation of bacteria and dissemination into the lungs, liver and spleen were observed when FUM was concomitantly present with E. coli in animal diets. Besides infectious diseases, other negative impacts of mycotoxins at low levels include vaccination failure due to impediment in uptake, and loss of efficacy of various types of commonly used farm medications. Various worldwide researches confirm the negative effects of sub-toxic concentrations of mycotoxins in poultry feed and its implications on reduced productivity and profitability. Figure 2-4 indicate some of the most common issues caused by mycotoxins in the field.
Before domestication, poultry birds used to consume insects and earthworms from wild. As the first line of defence, it is only natural that the intestinal mucosal barrier is adequately reactive and able to illicit an inflammatory response to counter pathogen and foreign body invasion. In the interest of the modern day broiler producer, however, controlling this inflammation is imperative, especially to reduce wastage of nutrients such as energy and protein that are used up to generate an adequate amount of inflammatory cells to mount the immune response. Such nutrients could otherwise be directed towards faster growth and better production.
Antibiotic growth promoters (AGP) have traditionally been used to improve animal performance by somewhat reducing inflammation, but only to a certain degree of success. With the decrease in AGP usage throughout the world, it is realised that the flocks currently have little protection against the detrimental effects of pathogen invasion and the resultant intestinal inflammation.
Various studies on different animal species have proved that even at low concentrations within the feed, DON up-regulates pro-inflammatory cytokines in the intestinal epithelia, escalating the mucosal inflammatory response rate. Likewise, cytokines also regulate the opening of tight junction proteins, enabling bacterial translocation from the intestines into the bloodstream and systemic pathways. FUM may also alter the barrier function of the intestinal epithelia due to its well-known effects on sphingolipids, which play a crucial role in the maintenance of the tight junction barrier (see Figure 5). All these provide an entry portal for pathogens and an opportunity to invade the body, bypassing the first line of defence provided by the gastrointestinal tract mucosae, to cause disease and internal organ damage.
The effect of sub-toxic concentrations of mycotoxins from contaminated feed can be even more detrimental to the profits of the poultry producer than death of the bird itself, as it causes a far less noticeable form of profit drain from pockets of the producer. These include impaired nutrient uptake, immunosuppression and suboptimal performance. As a result of the poor performance, an additional sum of money is often spent on medication to treat unknown, secondary diseases, which usually result from a cascade of events that come simply from low but consistent levels of mycotoxin in the feed.
So yes, it is evident that even low levels of mycotoxins can harm poultry production. This becomes even more serious in the face of multi-mycotoxicoses, where several mycotoxins co-occur in feeds. Even at sub-toxic concentrations, the synergy created by these combinations causes detrimental effects to poultry, especially when exposed to different pathogens and other inflammatory agents.
Proper mycotoxin risk management tools are available to nullify the negative impacts of mycotoxins on poultry health and performance.
References are available from the author upon request.
Justin Tan, D.V.M., Regional Sales & Marketing Director, BIOMIN Singapore Pte Ltd
Guan Shu, Ph.D., Regional Product Manager – Mycotoxin Risk Management, BIOMIN Singapore Pte Ltd