Conference Report

At the recent EW Nutrition Poultry Academy in Jakarta Indonesia, Dr Steve Leeson, Professor Emeritus, University of Guelph, Canada, defined metabolic disorders as: non-infectious, occurring with adequate diets in ‘normal’ conditions, and mostly species-specific. Their incidence is negatively correlated to productivity. Although they often have a major genetic component, genetic selection to manage the problem is often a last resort, as there is usually a negative correlation with productivity.

Ascites

First reported in the 1970s, ascites or ‘water belly’ is probably the number one metabolic issue today. It is the accumulation of fluid in the abdomen, which is caused by a cascade of events related to the need to supply high levels of oxygen to the tissues. The condition was initially most prevalent in fast-growing male broilers maintained at high altitude and where there is a degree of cold stress, but nowadays the problem can occur at any altitude. In extreme situations up to 8% mortality is seen, although 1-3% mortality is currently more common. The disorder is now re-emerging with faster growth rates, as growth rate is easily the main contributing factor.

Options to limit ascites include:

• Limit growth rate
• Feed texture (mash vs. pellets)
• Never let the temperature get below 15^oC for any age of bird
• Brooding ventilation – economics of air flow vs. temperature
• Minimize environmental contaminants, such as dust
• Lighting programs (4-6 hours of darkness)

Sudden death syndrome (SDS)

SDS almost always affects males birds close to market weight. It frequently afflicts 1-5% of the flock and from 21-35 days it will usually be the major cause of death. Afflicted birds appear healthy, are well fleshed and invariably have feed in their digestive tract. Death occurs within 1-2 minutes, the birds most frequently being found dead on their backs. There are few changes in gross pathology. The heart may contain blood clots, that are likely post-mortem in origin, and the ventricles are usually empty. Diagnosis is usually by exclusion of other diseases. The lungs are often oedematous, although this usually occurs when birds spend time on their backs and fluid drains to the lung region by gravity. There are no specific changes in the tissue or blood profile that can be used for diagnosis. The condition is precipitated by fast growth rate, and so conversely it can be prevented by varying degrees of nutrient restriction.

Spiking mortality syndrome (SMS)

SMS is characterized by severe unexplained hypoglycemia, and always occurs from 18-21 days of age. There are few post-mortem observations, so it is often misdiagnosed. Mortality can be 2-3%. Males are more susceptible than females, probably because they are growing faster. Birds fed all-vegetable diets may be more prone to SMS.  Supplementing an all-vegetable diet with milk-powder (which is high in serine), casein or serine is recommended and results in increased blood glucose.

Skeletal integrity

This disorder is not due to increased bodyweight of broilers, as the broiler is capable of supporting weight that far exceeds its own body weight. Instead, it’s due to shifting the bird’s center of gravity forward as breast muscle yields have increased, moving the legs further apart which puts torsional pressure on the head of the femur. Not only does it cause on-farm problems, but also complications with mechanical processing.

Imbalanced nutrient supply, such as excess of chloride, or infection with bacteria, viruses, and particularly mycoplasmas are involved.

Tibial dyschondroplasia (TD)

TD is due to abnormal cartilage development. Failure of normal vascularization limits mineralization. TD is characterized by enlargement of the hock, twisted metatarsi, and slipped tendons. A low electrolyte balance (<200MEq), high chloride (>0.3%), or low Ca:P or high P:Ca can precipitate TD. Adding manganese and choline to the diet will largely eliminate it.

Perosis

Now often termed Chondrodystrophy, it has manganese or choline deficiency as the classical cause, but it can also be seen with other B-vitamin deficiencies. As with TD, it can be aggravated by some grain fumigants.

Kinky back

Also known as Spondylolisthesis, it is not really a metabolic disorder, as Enterococcus infection is the most common cause. Chickens with kinky back syndrome are often seen sitting on their tail, extending their feet outward or letting them fall over to one side of their body. Once the condition stops birds from being able to walk, they are unable to reach food or water on their own and are at risk of dying from starvation. There is no treatment for kinky back.

Gizzard erosion and proventriculus

Although gizzard lesions are very common, Dr Leeson suspects their importance is overemphasized. Gizzard condition is seen in both layer and broiler chickens, but the incidence is more in broilers.

Access to grit and inclusion of at least 20% cereal particles larger than 1 mm in size in the diet will have a positive effect on the development and functioning of the gizzard and it will also reduce the frequency and severity of gizzard lesions in poultry. Ingestion of non-soluble fibers has been shown to exert strong effects on the structure and function of the gizzard. Inclusion of at least 3% coarse fibers in the feed increased the relative weight of the gizzard and reduced the pH of the gizzard contents suggesting a preventive effect of fiber.

Proventriculus appears as a very large organ and is often associated with gizzard erosion. When the proventriculus glands are affected, there is a lower secretion of hydrochloric acid and enzymes and therefore more undigested feed arrives to the intestine, where it can act as a substrate of pathogens and start digestive infections.

Breast muscle defects

Breast muscle defects are not problematic for the bird, efficiency/economics of growth, or a food safety issue. The main issue is seen at primary or secondary processing, and consumer acceptance. Due to the fast muscle growth and the enlarged muscle cells, the space between muscle fibers is reduced. This restricts the blood supply to the muscles, which can no longer reach the desired oxygen levels.

White-striping

White striping is a quality factor in chicken breast meat caused by deposits of fat in the muscle during the bird’s growth and development. It is like marbling in red meat. Dr Leeson joked that it be promoted as marbled chicken – like Wagyu beef. Because hypoxia is associated with white striping, it was thought that arginine supplementation could help with vasodilation, thus supplying the muscles with better oxygen resources.

Wooden breast (WB)

WB is an emerging quality defect. Macroscopically, it is characterized by palpably hard, pale ridge-like bulges at the caudal end, along with clear viscous fluid, small hemorrhages, and white striping, that may occur separately or together. The main cause is the high growth rate and high breast meat yield. There is no nutritional or management solution.

Wooden breast is common in male broilers >2.5 kg bodyweight, and the incidence tends to increase with the size of the breast fillet. As the incidence of wooden breast increases, the incidence of white striping tends to decrease. Due to the visual defects and hard and chewy texture, consumers have a low acceptance of WB fillets, and they are usually downgraded to use for ground products.

Reducing oxidative stress and supplying more oxygen to the cells, enabling the muscle cells to grow very fast without meat loss will reduce the incidence of WB.

 

***

EW Nutrition’s Poultry Academy took place in Jakarta and Manila in early September 2023. Dr. Steve Leeson, an expert in Poultry Nutrition & Production with nearly 50 years’ experience in the industry, was the distinguished keynote speaker.

Dr. Leeson had his Ph.D. in Poultry Nutrition in 1974 from the University of Nottingham. Over a span of 38 years, he was a Professor in the Department of Animal &Poultry Science at the University of Guelph, Canada. Since 2014, he has been Professor Emeritus at the same University. As an eminent author, he has more than 400 papers in refereed journals and 6 books on various aspects of Poultry Nutrition & Management. He also won the American Feed Manufacturer’s Association Nutrition Research Award (1981), the Canadian Society of Animal Science Fellowship Award (2001), and Novus Lifetime Achievement Award in Poultry Nutrition (2011).

By Monish Raj, Assistant Manager-Technical Services, EW Nutrition
Inge Heinzl, Editor, EW Nutrition  

Mycotoxins, toxic secondary metabolites produced by fungi, are a constant and severe threat to animal production. They can contaminate grains used for animal feed and are highly stable, invisible, and resistant to high temperatures and normal feed manufacturing processes. Mycotoxin-producing fungi can be found during plant growth and in stored grains; the prevalence of fungi species depends on environmental conditions, though in grains, we find mainly three genera: Aspergillus, Penicillium, and Fusarium. The most critical mycotoxins for poultry production and the fungi that produce them are detailed in Fig 1.

Figure 1: Fungi species and their mycotoxins of worldwide importance for poultry production (adapted from Bryden, 2012).

The effects of mycotoxins on the animal are manifold

When, usually, more than one mycotoxin enters the animal, they “cooperate” with each other, which means that they combine their effects in different ways. Also, not all mycotoxins have the same targets.

The synergistic effect: When 1+1 ≥3

Even at low concentrations, mycotoxins can display synergistic effects, which means that the toxicological consequences of two or more mycotoxins present in the same sample will be higher than the sum of the toxicological effects of the individual mycotoxins. So, disregarded mycotoxins can suddenly get important due to their additive or synergistic effect.

Table 1: Synergistic effects of mycotoxins in poultry

Synergistic interactions
	DON	ZEN	T-2	DAS
FUM	*	*	*
NIV	*	*	*
AFL			*	*

Table 2: Additive effects of mycotoxins in poultry

Additive interactions
	AFL	T2	DAS	MON
FUM	+	+	+	+
DON	+	+
OTA	+	+

Recognize the effects of mycotoxins in animals is not easy

The mode of action of mycotoxins in animals is complex and has many implications. Research so far could identify the main target organs and effects of high levels of individual mycotoxins. However, the impact of low contamination levels and interactions are not entirely understood, as they are subtle, and their identification requires diverse analytical methods and closer observation.

With regard to the gastrointestinal tract, mycotoxins can inhibit the absorption of nutrients vital for maintaining health, growth, productivity, and reproduction. The nutrients affected include amino acids, lipid-soluble vitamins (vitamins A, D, E, and K), and minerals, especially Ca and P (Devegowda and Murthy, 2005). As a result of improper absorption of nutrients, egg production, eggshell formation, fertility, and hatchability are also negatively influenced.

Most mycotoxins also have a negative impact on the immune system, causing a higher susceptibility to disease and compromising the success of vaccinations. Besides that, organs like kidneys, the liver, and lungs, but also reproduction, endocrine, and nervous systems get battered.

Mycotoxins have specific targets

Aflatoxins, fumonisins, and ochratoxin impair the liver and thus the physiological processes modulated and performed by it:

• lipid and carbohydrate metabolism and storage
• synthesis of functional proteins such as hormones, enzymes, and nutrient transporters
• metabolism of proteins, vitamins, and minerals.

For trichothecenes, the gastrointestinal tract is the main target. There, they hamper digestion, absorption, and intestinal integrity. T-2 can even produce necrosis in the oral cavity and esophagus.

Figure 2: Main target organs of important mycotoxins

How to reduce mycotoxicosis?

There are two main paths of action, depending on whether you are placed along the crop production, feed production, or animal production cycle. Essentially, you can either prevent the formation of mycotoxins on the plant on the field during harvest and storage or, if placed at a further point along the chain, mitigate their impact.

Preventing mycotoxin production means preventing mold growth

To minimize the production of mycotoxins, the development of molds must be inhibited already during the cultivation of the plants and later on throughout storage. For this purpose, different measures can be taken:

Selection of the suitable crop variety, good practices, and optimal harvesting conditions are half of the battle

Already before and during the production of the grains, actions can be taken to minimize mold growth as far as possible:

• Choose varieties of grain that are area-specific and resistant to insects and fungal attacks.
• Practice crop rotation
• Harvest proper and timely
• Avoid damage to kernels by maintaining the proper condition of harvesting equipment.

Optimal moisture of the grains and the best hygienic conditions are essential

The next step is storage. Here too, try to provide the best conditions.

• Dry properly: grains should be stored at <13% of moisture
• Control moisture: minimize chances of moisture to increase due to condensation, and rain-water leakage
• Biosecurity: clean the bins and silos routinely.
• Prevent mold growth: organic acids can help prevent mold growth and increase storage life.

Mold production does not mean that the war is lost

Even if molds and, therefore, mycotoxins occur, there is still the possibility to change tack with several actions. There are measures to improve feed and support the animal when it has already ingested the contaminated feed.

1.    Feed can sometimes be decontaminated

If a high level of mycotoxin contamination is detected, removing, replacing, or diluting contaminated raw materials is possible. However, this is not very practical, economically costly, and not always very effective, as many molds cannot be seen. Also, heat treatment does not have the desired effect, as mycotoxins are highly heat stable.

2.    Effects of mycotoxins can be mitigated

Even when mycotoxins are already present in raw materials or finished feed, you still can act. Adding products adsorbing the mycotoxins or mitigating the effects of mycotoxins in the organism has been considered a highly-effective measure to protect the animals (Galvano et al., 2001).

This type of mycotoxin mitigation happens at the animal production stage and consists of suppressing or reducing the absorption of mycotoxins in the animal. Suppose the mycotoxins get absorbed in the animal to a certain degree. In that case, mycotoxin mitigation agents help by promoting the excretion of mycotoxins, modifying their mode of action, or reducing their effects. As toxin-mitigating agents, the following are very common:

Aluminosilicates: inorganic compounds widely found in nature that are the most common agents used to mitigate the impact of mycotoxins in animals. Their layered (phyllosilicates) or porous (tectosilicates) structure helps “trap” mycotoxins and adsorbs them.

• Bentonite / Montmorillonite: classified as phyllosilicate, originated from volcanic ash. This absorbent clay is known to bind multiple toxins in vivo. Incidentally, its name derives from the Benton Shale in the USA, where large formations were discovered 150 years ago.
  Bentonite mainly consists of smectite minerals, especially montmorillonite (a layered silicate with a larger surface area and laminar structure).

• Zeolites: porous crystalline tectosilicates, consisting of aluminum, oxygen, and silicon. They have a framework structure with channels that fit cations and small molecules. The name “zeolite” means “boiling stone” in Greek, alluding to the steam this type of mineral can give off in the heat). The large pores of this material help to trap toxins.

Activated charcoal: the charcoal is “activated” when heated at very high temperatures together with gas. Afterward, it is submitted to chemical processes to remove impurities and expand the surface area. This porous, powdered, non-soluble organic compound is sometimes used as a binder, including in cases of treating acute poisoning with certain substances.

Yeast cell wall: derived from Saccharomyces cerevisiae. Yeast cell walls are widely used as adsorbing agents. Esterified glucomannan polymer extracted from the yeast cell wall was shown to bind to aflatoxin, ochratoxin, and T-2 toxin, individually and combined (Raju and Devegowda 2000).

Bacteria: In some studies, Lactic Acid Bacteria (LAB), particularly Lactobacillus rhamnosus, were found to have the ability to reduce mycotoxin contamination.

Which characteristics are crucial for an effective toxin-mitigating solution

If you are looking for an effective solution to mitigate the adverse effects of mycotoxins, you should keep some essential requirements:

1. The product must be safe to use:
   1. safe for the feed-mill workers.
   2. does not have any adverse effect on the animal
   3. does not leave residues in the animal
   4. does not bind with nutrients in the feed.
2. It must show the following effects:
   1. effectively adsorbs the toxins relevant to your operation.
   2. helps the animals to cope with the consequences of non-bound toxins.
3. It must be practical to use:
   1. cost-effective
   2. easy to store and add to the feed.

Depending on

• the challenge (one mycotoxin or several, aflatoxin or another mycotoxin),
• the animals (short-cycle or long-living animals), and
• the economical resources that can be invested,

different solutions are available on the market. The more cost-effective solutions mainly contain clay to adsorb the toxins. Higher-in-price products often additionally contain substances such as phytogenics supporting the animal to cope with the consequences of non-bound mycotoxins.

Solis – the cost-effective solution

In the case of contamination with only aflatoxin, the cost-effective solution Solis is recommended. Solis consists of well-selected superior silicates with high surface area due to its layered structure. Solis shows high adsorption of aflatoxin B1, which was proven in a trial:

Figure 3: Binding capacity of Solis for Aflatoxin

Even at a low inclusion rate, Solis effectively binds the tested mycotoxin at a very high rate of nearly 100%. It is a high-efficient, cost-effective solution for aflatoxin contamination.

Solis Max 2.0: The effective mycotoxin solution for sustainable profitability

Solis Max 2.0 has a synergistic combination of ingredients that acts by chemi- and physisorption to prevent toxic fungal metabolites from damaging the animal’s gastrointestinal tract and entering the bloodstream.

Figure 4: Composition and effects of Solis Max 2.0

Solis Max 2.0 is suitable for more complex challenges and longer-living animals: in addition to the pure mycotoxin adsorption, Solis Max 2.0 also effectively supports the liver and, thus, the animal in its fight against mycotoxins.

In an in vitro trial, the adsorption capacity of Solis Max 2.0 for the most relevant mycotoxins was tested. For the test, the concentrations of Solis Max 2.0 in the test solutions equated to 1kg/t and 2kg/t of feed.

Figure 5: Efficacy of Solis Max 2.0 against different mycotoxins relevant in poultry production

The test showed a high adsorption capacity: between 80% and 90% for Aflatoxin B1, T-2 Toxin (2kg/t), and Fumonisin B1. For OTA, DON, and Zearalenone, adsorption rates between 40% and 80% could be achieved at both concentrations (Figure 5). This test demonstrated that Solis Max 2.0 could be considered a valuable tool to mitigate the effects of mycotoxins in poultry.

Broiler trial shows improved performance in broilers

Protected and, therefore, healthier animals can use their resources for growing/laying eggs. A trial showed improved liver health and performance in broilers challenged with two different mycotoxins but supported with Solis Max 2.0.

For the trial, 480 Ross-308 broilers were divided into three groups of 160 birds each. Each group was placed in 8 pens of 20 birds in a single house. Nutrition and management were the same for all groups. If the birds were challenged, they received feed contaminated with 30 ppb of Aflatoxin B1 (AFB1) and 500 ppb of Ochratoxin Alpha (OTA).

Negative control:	no challenge	no mycotoxin-mitigating product
Challenged group:	challenge	no mycotoxin-mitigating product
Challenge + Solis Max 2.0	challenge	Solis Max 2.0, 1kg/t

The body weight and FCR performance parameters were measured, as well as the blood parameters of alanine aminotransferase and aspartate aminotransferase, both related to liver damage when increased.

Concerning performance as well as liver health, the trial showed partly even better results for the challenged group fed with Solis Max 2.0 than for the negative, unchallenged control (Figures 6 and 7):

• 6% higher body weight than the negative control and 18.5% higher body weight than the challenged group
• 12 points and 49 points better FCR than the negative control and the challenged group, respectively
• Lower levels of AST and ALT compared to the challenged group, showing a better liver health

The values for body weight, FCR, and AST, even better than the negative control, may be owed to the content of different gut and liver health-supporting phytomolecules.

Figure 6: Better performance data due to the addition of Solis Max 2.0

Figure 7: Healthier liver shown by lower values of AST and ALT

Effective toxin risk management: staying power is required

Mycotoxin mitigation requires many different approaches. Mycotoxin mitigation starts with sewing the appropriate plants and continues up to the post-ingestion moment. From various studies and field experience, we find that besides the right decisions about grain crops, storage management, and hygiene, the use of effective products which mitigate the adverse effects of mycotoxins is the most practical and effective way to maintain animals healthy and well-performing. According to Eskola and co-workers (2020), the worldwide contamination of crops with mycotoxins can be up to 80% due to the impact of climate change and the availability of sensitive technologies for analysis and detection. Using a proper mycotoxin mitigation program as a precautionary measure is, therefore, always recommended in animal production.

Toxin Risk Management

EW Nutrition’s Toxin Risk Management Program supports farmers by offering a tool (MasterRisk) that helps identify and evaluate the risk and gives recommendations concerning using toxin solutions.

By Vaibhav Gawande, Assistant Manager Technical Services, Dr. Inge Heinzl, Editor, and Marisabel Caballero, Global Technical Manager Poultry, EW Nutrition

The utility value of feed consists of the nutritional value and the quality. The first covers all characteristics concerning the essential nutrients and is important for feed formulation and the adequate supply of the animals.

Feed quality comprises all characteristics of a feed influenced by treatment, storage, conservation, hygiene, and its content of specific substances. For many factors, guidance and threshold values are available which should be met to guarantee animal health and welfare, as well as to protect public health, since some undesirable substances can be transferred to animal products such as meat, eggs, and milk.

In this article, we will focus on feed hygiene. We will talk about the consequences of low feed quality, how to understand it, its causes, and possible solutions.

What are the effects of deficient feed hygiene?

The consequences of deficient feed hygiene can be divided into two parts, impurities and spoilage.

Impurities comprise:

• the presence of soil, sand, or dust
• contamination with or residues of heavy metals, PCB, dioxins, pesticides, fertilizers, disinfectants, toxic plants, or banned feed ingredients

In the case of spoilage, we see:

• degradation of organic components by the action of molds and bacteria
• growth of pathogens such as E. coli, salmonella, etc.
• accumulation of toxins such as mycotoxins or bacterial toxins (Hoffmann, 2021)

Bad feed hygiene can also negatively impact the feed’s nutritional value by leading to a loss of energy as well as decreasing the bioavailability of vitamins A, D3, E, K, and B1.

But, how can all signs of deficient feed hygiene be recognized? Soil, sand, and probably dust can be seen in well-taken samples and impurities can be analyzed. But is it possible to spot spoilage? In this case, agglutinated particles, rancid odor, moisture, and discoloration are indicators. Sometimes, also the temperature of the feed or ingredient increases. However, spoilage is not always obvious and an analysis of the feed can give more information about the spoilage-related organisms present. It also helps to decide if the feed is safe for the animals or not. In the case of obvious alterations, the feed should not be consumed by any animal.

Different organisms decrease feed quality and impact health

Several organisms can be responsible for a decrease in feed quality. Besides the visible pests such as rats, mice, or beetles, which can easily be noticed and combatted, there are organisms whose mastering is much more difficult. In the following part, the different harmful organisms and substances are described and solutions are presented.

Enteropathogens can cause diarrhea and production losses

In poultry, different bacteria responsible for high production losses can be transferred via the feed. The most relevant of them are Clostridium perfringens, Escherichia coli, and some strains of Salmonella.

Clostridium perfringens, the cause of necrotic enteritis

Clostridium perfringens is a Gram-positive, anaerobic bacterium that is extremely resistant to environmental influences and can survive in soil, feed, and litter for several years and even reproduce. Clostridium perfringens causes necrotic enteritis mainly in 2-16 weeks old chickens and turkeys, being more critical in 3-6 weeks old chicks.

There is a clinical and a subclinical form of necrotic enteritis. The clinical form can be detected very well due to clear symptoms and mortality rates up to 50%. The subclinical form, while harder to detect, also raises production costs due to a significant decrease in performance. The best prophylaxis against clostridia is the maintenance of gut health, including feed hygiene.

Clostridia can be found in animal by-products, as can be seen in table 1.

Sr. No.	Sample details	Clostridium perfringens contamination		Total number of samples	Positivity %
		Positive	Negative
1	Meat and bone meal	39	52	91	42.86
2	Soya meal	0	3	3	0
3	Rape seed meal	0	1	1	0
4	Fish meal	21	17	38	55.26
5	Layer Feed	21	71	93	22.58
6	Dry fish	5	8	13	38.46
7	De-oiled rice bran	0	2	2	0
8	Maize	0	2	2	0
9	Bone meal	13	16	29	44.83

Table 1: Isolation of Clostridium perfringens from various poultry feed ingredients in Tamil Nadu, India (Udhayavel et al., 2017)

Salmonella is harmful to animals and humans

Salmonella is a gram-negative enterobacterium and can occur in feed. There are only two species – S. enterica and S. bongori (Lin-Hui and Cheng-Hsun, 2007), but almost 2700 serotypes. The most known poultry-specific Salmonella serotypes are S. pullorum affecting chicks and S. gallinarum affecting adult birds. The other two well-known serotypes, S. enteritidis and S. typhimurium are the most economically important ones because they can also infect humans.

Salmonella enteritidis, in particular, can be transferred via table eggs to humans. The egg content can be infected vertically as a result of a colonization of the reproductive tract of the hen (De Reu, 2015). The other possibility is a horizontal infection, as some can penetrate through the eggshell from a contaminated environment or poor egg handling.

Salmonella can also be transferred through meat. However, as there are more production steps where contamination can happen (breeder and broiler farm, slaughterhouse, processing plants, food storage…), traceability is more complicated. As feed can be vector, feed hygiene is crucial.

Moreover, different studies have found that the same Salmonella types found in feed are also detected – weeks later – in poultry farms and even further in the food chain, as reviewed by Ricke and collaborators (2019). Other researches even imply that Salmonella contamination of carcasses and eggs could be significantly reduced by minimizing the incidence of Salmonella in the feed (Shirota et al., 2000).

E. coli – some are pathogenic

E. coli is a gram-negative, not acid-resistant bacterium and most strains are inhabitants of the gut flora of birds, warm-blooded animals, and humans. Only some strains cause disease. To be infectious, the bacteria must have fimbriae to attach to the gut wall or the host must have an immune deficiency, perhaps due to stress. E. coli can be transmitted via contaminated feed or water as well as by fecal-contaminated dust.

Escherichia coli infections can be found in poultry of all ages and categories and nearly everywhere in the bird. E. coli affects the navel of chicks, the reproductive organs of hens, several parts of the gut, the respiratory tract, the bones and joints, and the skin and are part of the standard control.

The feed microbiome can contribute to a balanced gut microbial community. The origins of pathogenic E. coli in a flock can also be traced to feed contamination (Stanley & Bajagai, 2022). Especially in pre-starter/starter feeds, E. coli contamination can be critical as the day-old chick’s gut is starting to be colonized. Especially in this phase, maintaining a low microbial count in feed is crucial.

Molds cause feed spoilage and reduce nutritional value

Molds contaminate grains, both in the field and during storage, and can also grow in stored feed and even in feed stored or accumulated in storage facilities in animal production farms.

The contamination of feed by molds and their rapid growth can cause heating of the feed. As molds also need nutrients, their growth results in a reduction of energy and the availability of vitamins A, D3, E, K, and B1, thus decreasing the feed’s nutritional value. This heating occurs in most feeds with a moisture content higher than 15 /16%. Additionally, mold-contaminated feed tends to be dusty and has a bad taste impacting palatability and, as a consequence, feed intake and performance.

Molds produce spores that can, when inhaled, cause chronic respiratory disease or even death if the animals are exposed to contaminated feed for a longer time. Another consequence of mold contamination is the production of mycotoxins by several mold species. These mycotoxins can affect the animal in several ways, from decreasing performance to severe disease (Esmail, 2021; Government of Manitoba, 2023).

With effective feed hygiene management, we want to stop and prevent mold growth, as well as all its negative consequences.

Prevention is better than treatment

It is clear that when the feed is spoiled, it must be removed, and animal health supporting measures should take place. However, it is better to prevent the consequences of low feed hygiene on animals. Proper harvest and adequate storage of the feed are basic measures to stop mold growth. Additionally, different tools are available to protect the animals from feed bacterial load and other risk factors.

Solutions are available to support feed hygiene

There are several solutions to fight the organisms which decrease feed quality. Some directly act against the harmful substances / pathogens, and others act indirectly, meaning that they change the environment to a non-comfortable one for the organism.

Formaldehyde and propionic acid – an unbeatable team against bacteria

A combination of formaldehyde and propionic acid is perfect to sanitize feed. Formaldehyde results in bacterial DNA and protein damage, and propionic acid is active against bacteria and molds. Together, they improve the microbiological quality of the feed and reduce the risk of secondary diseases such as necrotic enteritis or dysbiosis on the farm. In addition to the pure hygienic aspect, organic acids support digestion.

An in-vitro trial was conducted to evaluate the effect of such a combination (Formycine Gold Px) against common poultry pathogens. Poultry feed was spiked with three different bacteria, achieving very high initial contamination of 1,000,000 CFU/g per pathogen. One batch of the contaminated feed served as a control (no additive). To the other contaminated batches, 1, 2, or 4 kg of Formycine per ton of feed were added. The results (means of triplicates) are shown in figures 1 a-c.

Figures 1 a-c: Reduction of bacterial count due to the addition of Formycine

Formycine Gold Px significantly reduced the bacterial counts in all three cases. A clear dose-response-effect can be seen and by using 2 kg of Formycine / t of feed, pathogens could not be detected anymore in the feed.

A further trial showed the positive effects of feeding Formycine Gold Px treated feed to the animals. Also here, the feed for both groups was contaminated with 1,000,000 CFU of Clostridium/g. The feed of the control group was not treated and to the treatment group, 2 kg of Formycine per t was added.

Figure 2: Preventive effect of Formycine Gold Px concerning necrotic enteritis gut lesions

Figure 3a and 3b: Performance-maintaining effect of Formycine Gold Px

The trial showed that Formycine Gold Px reduced the ingestion of the pathogen, and thus could prevent the lesions caused by necrotic enteritis (Fig. 2). The consequence of this improved gut health is a better feed conversion and higher average daily gain (Fig.3a and 3b).

Products containing formaldehyde may represent a risk for humans, however, the adequate protection equipment helps to reduce/avoid exposure.

A combination of free acids and acid salts provides optimal hygienic effects

Additionally, another blend of organic acids (Acidomix AFG) shows the best effects against representatives of relevant feed-borne pathogens in poultry. In a test, 50 µl solution containing different microorganisms (reference strains of S. enterica, E. coli, C. perfringens, C. albicans, and A. niger; concentration 10⁵ CFU/ml, respectively) were pipetted into microdilution plates together with 50 µl of increasing concentrations of a mixture of organic acids (Acidomix) After incubation, the MIC and MBC of each pathogen were calculated.

The test results show (figure 4, Minimal Bactericidal Concentration) that 0.5% of Acidomix AFG in the medium (≙ 5kg/t of feed) is sufficient to kill S. enterica, C. albicans, and A. niger and even only 2.5kg/t in the case of E. coli. If the pathogens should only be prevented to proliferate, even a lower amount of product is requested (figure 5, Minimal Inhibitory Concentration – MIC)

Figure 4: MBC of Acidomix AFG against different pathogens (%)

Figure 5: MIC of Acidomix AFG against different pathogens (%)

In addition to the direct antimicrobial effect, this product decreases the pH of the feed and reduces its buffering capacity. The combination of free acids and acid salts provides prompt and long-lasting effects.

Feed hygiene: a critical path to animal performance

Feed accounts for 65-70% of broiler and 75-80% of layer production costs. Therefore, it is essential to use the available feed to the utmost. The quality of the feed is one decisive factor for the health and performance of the animals. Proper harvesting and storage are in the hands of the farmers and the feed millers. The industry offers products to control the pathogens causing diseases and the molds producing toxins and, therefore, helps farmers save feed AND protect the health and performance of their animals.

References:

Dinev, Ivan. Diseases of Poultry: A Colour Atlas. Stara Zagora: Ceva Sante Animal, 2007.

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