Tran Si Trung, PhD
EWN SEAP – Regional Technical Manager for Toxin Risk Management

1. Introduction

The global egg market is experiencing steady and robust growth, playing a vital role in food security and animal protein nutrition. According to reports from RaboResearch and the World Egg Organization, global egg production has more than doubled, rising from 46 million tonnes in 1995 to approximately 99 million tonnes in 2025. By 2035, the market is projected to expand by a further 22%, with an annual growth rate of approximately 2.0%. Asia leads with more than 64% of global output, with China and India being the largest producing countries. The global egg market value was estimated at USD 352 billion in 2025 and is expected to reach USD 585 billion by 2033, representing a CAGR of approximately 6.6%. This growth is driven by urbanization, rising incomes, demand for high-quality protein, and the widespread use of eggs in the processed food industry.

In Vietnam, the poultry industry has expanded rapidly and become one of the pillars of the agricultural sector. In 2023, poultry egg production reached approximately 19.22 billion eggs. In 2024, this figure exceeded 20 billion eggs, with chicken eggs accounting for the dominant share. Per-capita egg consumption rose from 108 eggs per year in 2017 to approximately 185–190 eggs per year in 2024, though this remains below the average of many other countries (300–350 eggs). In the near term, despite limited exports, domestic consumption is fairly stable, and the sector has the potential to achieve a value of USD 3 billion. Alongside these opportunities, the industry also faces challenges such as occasional local oversupply, price volatility, disease outbreaks, and food quality and safety issues. Among these, mycotoxins can be regarded as one of the most silent yet serious threats to egg quality and consumer health.

The principal mycotoxins include aflatoxins (AFs), ochratoxin A (OTA), zearalenone (ZEN), deoxynivalenol (DON), fumonisins (FBs), and T-2 toxin. These compounds form in feed raw materials — including maize, wheat, soybean, groundnut, and other oil seeds — under field stress conditions or during storage under inadequate conditions. In the tropical humid climates of Vietnam and much of Southeast Asia, the risk of natural contamination is particularly elevated. Mycotoxins not only reduce livestock productivity (organ damage, immune suppression, etc.) but also directly affect egg quality, nutritional value, and toxin residue levels in eggs, thereby impacting both the economic value of the product and consumer health.

2. Key Aspects of Egg Quality

Egg quality is typically assessed across multiple dimensions: external appearance (clean, intact shell, uniform shape and color), internal quality (albumen height, yolk color, Haugh unit score), nutritional value (high protein ~12–13%, lipids, vitamins A/D/E, carotenoids, choline, lutein), and food safety (freedom from microbiological contamination, antibiotic residues, mycotoxin residues, and heavy metals).

Key technical parameters include: egg weight and grade (AA, A, B); shell thickness and strength; Haugh unit (reflecting albumen freshness); yolk color (Roche scale or DSM Yolk Fan); air cell size; and absence of blood spots (meat spots). High quality ensures commercial value, shelf life, and nutritional benefit to the consumer.

Each of these quality dimensions (shell integrity, albumen height, yolk color, and residue status) is, to varying degrees, susceptible to mycotoxin insult, as the following section demonstrates.

3. Adverse Effects of Mycotoxins on Egg Quality and Value

Mycotoxins cause harm through multiple mechanisms: hepato-renal toxicity, hormonal disruption, oxidative stress, intestinal damage (reduced nutrient absorption), immune and enzyme suppression. Effects are often evident at relatively low concentrations (20–500 ppb depending on the toxin type) and are amplified when multiple mycotoxins are present simultaneously. Field surveys across Asia consistently demonstrate that co-contamination, the presence of two or more mycotoxins in a single feed ingredient or complete diet, is the norm rather than the exception, particularly in maize-based diets during wet-season harvests. Effective risk management must therefore address the full toxin spectrum rather than individual contaminants in isolation.

Table 1. Overview of principal mycotoxins, their main feed substrates, primary mechanisms of action, and key effects on poultry egg quality.

3.1. Reduced Laying Performance

AFs and OTA can reduce laying rate by 5–10% at field-relevant dietary concentrations, with greater reductions reported under conditions of more severe or prolonged contamination. ZEN, acting as a potent estrogen mimic, disrupts the hypothalamic-pituitary-gonadal (HPG) axis, reducing FSH, LH, and progesterone levels, thereby impairing follicular development and ovarian function. DON and FBs cause intestinal inflammation and reduced nutrient absorption. T-2 toxin can cause ulcerative lesions of the oral mucosa or gizzard, thereby reducing feed intake or impairing gizzard motility and feed digestion.

3.2. Impact on Eggshell Quality

Mycotoxins in general can reduce eggshell thickness and strength by inhibiting calcium absorption, vitamin D3 utilization, and carbonic anhydrase activity (zinc-dependent). In particular, AFs may induce secondary zinc deficiency through liver damage. OTA has been associated with increased incidence of cracked, thin, misshapen, and urate-spotted eggs. Experimental studies have shown that DON can reduce eggshell breaking strength by 10–15% under controlled conditions.

3.3. Impact on Internal Egg Quality

Research conducted at Kasetsart University (Thailand) demonstrates that DON and T-2 toxin can reduce albumen height and Haugh unit scores at relatively low dietary concentrations (Tables 2 and 3). Additionally, experimental data indicate that DON can impair yolk carotenoid content and yolk color score, diminishing both antioxidant value and visual appeal, at dietary concentrations as low as 2,500 ppb.

3.4. Residues and Food Safety

After mycotoxins are absorbed, the host begins detoxification and excretion processes, while organ damage simultaneously occurs. Detoxification is primarily carried out by the liver, and accumulation occurs mainly in the liver and kidneys. However, accumulation in other tissues, including meat and eggs, has also been documented. AFB1 and its liver-derived metabolites, including AFM1, have been detected in eggs at transfer rates of approximately 0.05% of the dietary AFB1 intake; OTA transfers at ~0.15%; T-2 at ~0.10%; while DON, FB1, and ZEN transfer at lower rates.

3.5. Economic and Indirect Impacts

While ZEN is considered to have limited impact on commercial broiler performance, the situation is markedly different for breeder flocks. Acting primarily through its active hepatic metabolite α-zearalenol (α-ZOL), which has a higher affinity for estrogen receptors than the parent compound, ZEN may reduce fertility (impaired semen quality in roosters) and hatchability (increased embryo mortality, reduced chick quality at hatch). More broadly, mycotoxins negatively affect animal health, growth performance, and egg quality, leading to increased culling and veterinary costs, as well as lower selling prices for substandard eggs. As a concrete example, with Vietnam producing more than 20 billion eggs per year, even a 1–2% reduction in productivity or egg quality could translate into losses of tens of millions of USD annually – a scale of impact applicable across every major egg-producing nation in the region.

4. Key Considerations for Mycotoxin Risk Management

Managing mycotoxin risks requires an increasingly comprehensive and integrated approach. The “3F – from Feedmill, Farm to Fork” process is an integrated management framework developed by EW Nutrition in the region to prevent, trace, and mitigate mycotoxin-related risks for poultry producers and egg manufacturers.

4.1. Prevention at Source (Feedmill)

• Upon raw material intake: conduct sensory inspection, then perform proper sampling and test for mycotoxins using rapid test strips or ELISA.
• Storage: pay close attention to ambient relative humidity and temperature in warehouses/silos, as these two factors directly influence the moisture content and water activity (Aw) of stored materials, creating favorable conditions for the growth of Aspergillus spp. and/or Penicillium spp. (mold species capable of producing mycotoxins such as AFs, OTA, citrinin, patulin, etc. during storage). As practical targets: keep grain moisture below 14% for maize and wheat (below 10% for groundnut meal); Aspergillus spp. can proliferate at Aw ≥ 0.80, while Penicillium spp. remain active at Aw ≥ 0.78; maintaining Aw below these thresholds is the single most effective storage intervention.
• Finished feed samples from each batch must be properly collected and analyzed for multiple mycotoxins using ELISA or chromatographic methods (HPLC, LC-MS/MS, etc.). Retained samples should be stored under cool, dry conditions for a minimum of two weeks to enable analysis and traceability in the event of a subsequent incident.
• Periodically inspect hygiene of storage facilities and equipment (e.g., mixer, cooler, feed transport trucks from feedmill to farm).
• Develop preventive strategies against the adverse effects of mycotoxins on the health and performance of commercial laying hens, including supplementation with broad-spectrum solutions (Mastersorb Gold, etc.) adsorbing a diverse range of toxins and providing antioxidant support to mitigate oxidative stress.

4.2. Prevention at Farm Level

• Establish a routine hygiene monitoring program for housing facilities, particularly feed storage areas/silos and associated equipment (e.g., automated feeders, egg and manure conveyors, etc.).
• Feed samples from each batch at the farm level should also be properly collected and retained (under cool, dry conditions) for a minimum of two weeks for analysis and traceability should any subsequent issue arise.
• When animal health or performance issues arise and mycotoxicosis is suspected, in complement to analyzing retained feed samples, the analysis of mycotoxin residues in Dried Blood Spots (DBS), a technique developed by EW Nutrition and its partner, can be a valuable complementary measurement to make a diagnosis.

4.3. Food Safety at the Table (Fork)

Vietnamese Standard TCVN 1858:2018 stipulates that commercial chicken eggs must be clean, uncracked, undistorted, and free from spoilage; air cell depth must not exceed 6 mm (depending on grade); yolk must not be visibly off-center; and no off-odors are permitted. Eggs are graded based on both external and internal quality criteria. Additionally, Circular 34/2012/TT-BNNPTNT and food safety and hygiene regulations require traceability, Salmonella control, and monitoring of specific residues. The national technical regulation QCVN 01-190:2020/BNNPTNT on animal feed sets maximum limits for mycotoxins in feed raw materials. While Vietnam serves as a concrete example, analogous frameworks are in place across Southeast and South Asia, with many producers also referencing the Codex Alimentarius maximum levels for aflatoxins in food (4 µg/kg total AFs; 2 µg/kg AFB1) and EU feed maximum limits as de facto benchmarks for export-oriented operations.

According to the International Agency for Research on Cancer (IARC), AFB1 is classified as a Group 1 carcinogen (carcinogenic to humans), while OTA, AFM1, and FB1 are classified as Group 2B (possibly carcinogenic to humans). It is of particular concern that these mycotoxins are also highly heat-stable, they are not destroyed by cooking or standard food processing temperatures. Consequently, their residues in eggs represent an important aspect to be monitored and controlled before eggs reach the consumer’s table.

5. Conclusion

Mycotoxins are a critical factor affecting egg quality across all dimensions – external appearance, internal quality, food safety, and economic value. In the context of Vietnam’s egg industry, and the broader dynamic growth of egg production across Southeast and South Asia, moving toward modernization and export competitiveness, mycotoxin control is not merely a loss-reduction measure, but a strategy for sustainable competitive advantage. The sector requires close collaboration among feed manufacturers, poultry and egg producers, regulatory authorities, and scientific researchers to turn these challenges into opportunities for development.

In line with this broader direction, EW Nutrition has developed and is actively supporting the implementation of the integrated 3F Management Process (from Feedmill, Farm to Fork), grounded in scientific evidence and technology, to help protect poultry flocks, enhance egg quality, and ensure consumer safety across the region.

About the Author

Dr. Tran Si Trung holds PhD degrees in Food Safety & Quality in France and serves as Regional Technical Manager for Toxin Risk Management at EW Nutrition, Southeast Asia and Pacific. He specializes in mycotoxin risk assessment and feed quality management. For further information or technical inquiries, please contact EW Nutrition Vietnam.

by David Sherwood, Managing Director EW Nutrition Oceania, and Christine Clark, Premium Agri Products

Colortek Yellow versus synthetic apo-ester: performance, stability, regulation, and market fit

Synthetic apo-ester has been the default yellow pigment in layer feed for decades. This axiom is no longer valid with current evidence. Regulatory caps in the EU, an outright ban in the US, and tightening scrutiny in ANZ are shrinking the headroom producers must work with. At the same time, consumer pressure toward natural ingredients continues to mount. Colortek Yellow, EW Nutrition’s marigold-derived yellow pigment, closes the performance gap that historically made natural alternatives unattractive. At 1.25 times the apo-ester dose it delivers equivalent yolk colour fan scores across all tested targets. It outperforms apo-ester on storage stability by a factor of 2.6 at three months, and it adds antioxidant protection that synthetic pigments cannot offer. This document sets out the evidence.

 KEY NUMBERS

1. Why Yolk Colour Matters

Yolk colour is the most visible quality signal an egg sends. Consumers associate a deeper, richer yolk with a healthier hen and better nutrition. The practical consequence is that yolk colour directly influences purchasing decisions across retail and foodservice.

Preferences differ by market. Northern European consumers favour lighter yellows (YCF 9-10). Central and Southern Europe sits in the YCF 11-14 range. Japan pushes as high as YCF 18, a benchmark that Melinda Hashimoto, CEO of Egg Farmers of Australia, cited in the National Poultry Newspaper (March 2026) as a demonstration of what precise feed formulation and carotenoid management can achieve. As Australian producers look to Asian export markets, that benchmark becomes commercially relevant.

 Colour is determined entirely by dietary carotenoids. Hens cannot synthesise these compounds. The pigments must be consumed in sufficient quantity, absorbed through a functional gut, transported in the bloodstream, and deposited in the developing yolk. Any failure along that chain, whether from poor pigment bioavailability, gut disruption, or hen stress, produces a pale yolk regardless of inclusion rate. This is why pigment source and hen health management are inseparable. 

2. The Australian Industry Context

Australia’s egg sector is navigating the same global shift toward natural inputs that is reshaping feed additive markets in Europe and North America. The regulatory position on synthetic canthaxanthin in ANZ already reflects this direction: it is not a permitted food colouring under Standard 1.3.1, even though it remains available in layer feed without a stated maximum. That regulatory ambiguity creates commercial risk that natural alternatives avoid.

 The biology of yolk pigmentation, and the two-phase process that produces it, is well understood by Australian nutritionists. Hashimoto’s March 2026 article in the National Poultry Newspaper described it clearly:

 This two-phase model is exactly what Colortek Yellow (yellow base) and Xarocol (red shift) deliver as a paired natural program. Both products are already sold in Australia through Premium Agriproducts.

 Hen health sits underneath all of it. When birds are under stress or fighting infection, carotenoids are diverted toward immune function and vitamin A synthesis rather than yolk deposition. A pale yolk can be a welfare signal as much as a nutrition one. Increasing synthetic pigment inclusion does not solve that problem. Choosing a high-bioavailability natural pigment, and managing flock health properly, does.

3. The Regulatory Landscape

Colortek is derived from marigold flowers, apo-ester is developed from a chemical manufacturing process.  The direction of travel is consistent across all major markets: synthetic carotenoid additives face tighter controls; natural alternatives do not. Producers who build their pigmentation programs around synthetic apo-ester are exposed to a risk that compounds over time.

In the EU, Commission Implementing Regulation 2020/1400 set the maximum inclusion rate for apo-ester at 5 mg/kg complete feed for laying hens following a re-evaluation by EFSA. The authority could not rule out inhalation risk for workers, and simultaneous use in drinking water was prohibited to prevent cumulative xanthophyll limits being exceeded. These constraints reflect the scrutiny synthetic molecules now attract routinely, not exceptionally.

In ANZ, synthetic canthaxanthin sits in an awkward position: excluded as a food colouring but not subject to a stated maximum when used in layer feed. That gap will not stay open indefinitely. Switching to Xarocol, the paprika-based natural red pigment, removes the exposure entirely.

4. Performance: The Trial Data

The historical objection to natural yellow pigments was straightforward. Traditional marigold-derived lutein and zeaxanthin required roughly three times the inclusion rate of apo-ester to achieve the same yolk colour score, because intestinal absorption is lower. The economics did not stack up.

EW Nutrition’s proprietary production process changes that. By improving carotenoid bioavailability at the manufacturing stage, Colortek Yellow reduces the dose ratio to 1.25 to 1 against apo-ester. Two independent trials confirm the result holds in commercial conditions.

IRTA trial, Spain (288 Hy-Line Brown layers, 39 weeks)

Seven weeks of xanthophyll depletion followed by four weeks of treatment. Three yolk colour fan targets tested (YCF 10, 11, 12). Colortek Yellow tested at 1.25x the apo-ester dose. Statistical significance at P<0.05.

At 1.25x the apo-ester dose, Colortek Yellow matched apo-ester across all three targets. The trial also found that standard apo-ester dosing recommendations were overestimated, producing scores roughly one point above target. Producers may already be using more synthetic pigment than they need.

Field validation, Spain (57,000 hens)

Under commercial conditions at scale, Colortek Yellow at a 1.25:1 ratio produced equivalent yolk colour scores to apo-ester (12.5 versus 12.7). The laboratory result holds in the field.

5. Stability

Lower stability in premix storage has been a legitimate concern with natural pigments. EW Nutrition addresses this through an accelerated saponification process that produces a low-moisture, high-xanthophyll product. The difference at extended storage is substantial.

Storage conditions: vitamin-mineral premix containing 12.5% choline chloride, closed bags, 30 degrees C, 75% relative humidity.

After three months, apo-ester retains 18% of active ingredient. Colortek Yellow retains 47%. For a premix manufacturer or feed mill running standard storage cycles, this is not a marginal difference. It means less product degradation between manufacture and use, more consistent on-farm results, and a lower effective cost per unit of pigmentation delivered.

6. Antioxidant Protection

Synthetic apo-ester is a synthetic colourant, only. Marigold-derived lutein and zeaxanthin colourants are also antioxidants, and that matters in the yolk because egg lipids oxidise readily, particularly during processing and extended retail.

Lutein and zeaxanthin also deposit in human tissue via consumption of enriched eggs, where their role in reducing cataract risk and age-related macular degeneration is documented (Landrum and Bone, 2001; Wang et al., 2016). This is the basis for functional egg positioning in premium markets, particularly in countries where antioxidant-enriched eggs are established retail categories. 

7. Colortek Yellow: Product Specifics

Colortek Yellow is a 10% concentrated marigold extract produced at EW Nutrition’s FAMI-QS certified facility in Spain. Key characteristics:

• Carotenoid source: Tagetes erecta (marigold) flower extract, lutein and zeaxanthin
• Concentration: 10% active carotenoids
• Dose ratio: 1.25:1 against synthetic apo-ester, confirmed in multiple independent trials
• Stability: higher 3-month recovery than apo-ester under accelerated storage conditions
• Physical form: free-flowing powder, homogeneous mixing in feed
• Certification: FAMI-QS, EU manufactured, strict control of undesirable substances
• Red pigment complement: Xarocol, paprika-based, natural alternative to synthetic canthaxanthin
• Australian distribution: Premium Agriproducts

 8. Summary

Synthetic apo-ester is under regulatory pressure in every major market and faces outright prohibition in others. The performance gap that previously justified its use has closed. Colortek Yellow delivers equivalent yolk colour at 1.25 times the dose, better stability at three months, and antioxidant protection that synthetic pigments cannot match.

For Australian producers, the benefits from use of natural pigments are supported by the current regulatory positions held on synthetic canthaxanthin and by the export opportunity in Asian markets where deep, consistent yolk colour from natural sources commands a premium. The Egg Farmers of Australia’s own guidance points to carotenoid source selection and hen health management as the foundations of a reliable pigmentation program. Colortek Yellow and Xarocol are built on exactly those foundations.

References

1. EU Commission Implementing Regulation 2020/1400, 5 October 2020.
2. Hashimoto, M. (2026). Egg yolk pigmentation: what drives colour and why it matters. National Poultry Newspaper, Vol 9 No. 3, March 2026.
3. Grashorn, M. (2008). Eiqualitat. In Legehuhnzucht und Eiererzeugung, Landbauforschung special issue 322.
4. Grashorn, M. (2016). Feed additives for influencing chicken meat and egg yolk color. In Handbook on Natural Pigments in Food and Beverages. Woodhead Publishing.
5. Landrum, J.T. and Bone, R.A. (2001). Lutein, zeaxanthin, and the macular pigment. Archives of Biochemistry and Biophysics 385(1):28-40.
6. Wang, W. et al. (2016). Antioxidant supplementation increases retinal responses in dogs. J. Nutr. Sci. 5 e18.
7. EW Nutrition internal trial data, IRTA Spain (288 layers) and commercial field trial (57,000 hens).

by Madalina Diaconu, Business Development Manager, EW Nutrition GmbH, and Maria Angeles Rodriguez, Gut Health Platform Manager, EW Nutrition GmbHABSTRACT
Avian coccidiosis, caused by intracellular protozoan parasites of the genus Eimeria, remains one of the most economically damaging diseases in commercial poultry production, costing the global industry an estimated USD 10–14 billion annually. For decades, disease management relied on seven recognized Eimeria species infecting chickens. However, the formal characterization in 2021 of three previously cryptic species – Eimeria lata, Eimeria nagambie, and Eimeria zaria – has fundamentally altered this landscape. These newly described parasites are pathogenic, capable of compromising bodyweight gain, and critically, they evade immunity induced by all currently available commercial anticoccidial vaccines. This white paper reviews the biology and epidemiology of these emerging species, examines the limitations of conventional control strategies, and presents the scientific rationale for phytogenic compounds as a complementary, resistance-resilient solution. Specific attention is given to the mechanisms of action of saponins, tannins, thymol, cinnamaldehyde, cumin, licorice, and others against Eimeria infection, intestinal inflammation, and secondary pathogen susceptibility.

1. Introduction: A shifting coccidiosis landscape

Coccidiosis, driven by Eimeria spp. infection of the intestinal epithelium, causes morbidity through hemorrhagic or malabsorptive diarrhea, disrupted gut microbiota, and impaired immune responses. Even subclinical infections exert measurable production costs through reduced bodyweight gain, deteriorated feed conversion ratios (FCR), and heightened susceptibility to secondary pathogens – most notably Clostridium perfringens (necrotic enteritis). The disease is ubiquitous: Eimeria oocysts are environmentally resilient, highly reproductive, and transmitted via fecal-oral routes in all commercial production systems.

For more than seven decades, the field recognized seven Eimeria species as the causative agents of avian coccidiosis in chickens: E. acervulina, E. brunetti, E. maxima, E. mitis, E. necatrix, E. praecox, and E. tenella. Each species infects a distinct region of the intestinal tract and produces characteristic pathological signatures. This taxonomy formed the basis for all commercial coccidiosis vaccines and the design of anticoccidial rotation programs.

In 2021, this foundational assumption was overturned. A landmark study by Blake et al. formally named three cryptic species – previously described only as operational taxonomic units (OTUs) x, y, and z – as Eimeria lata, Eimeria nagambie, and Eimeria zaria. This discovery, enabled by next-generation genomic sequencing, has critical implications for every layer of coccidiosis control: diagnostics, vaccination, and pharmacological management.Economic context
Avian coccidiosis costs the global poultry industry approximately £10.4 billion annually at 2016 prices (Blake et al., 2020). These losses include poor growth performance, treatment costs, increased feed consumption, increased replacement of chicks, and enhanced susceptibility to concurrent infections such as necrotic enteritis.

2. The three new Eimeria species: Biology, pathogenicity, and global spread

2.1 Discovery and formal classification

The three cryptic Eimeria OTUs were first identified through molecular epidemiological surveys in Australia in 2007–2008 (Cantacessi et al., 2008). Initially named OTU-X, OTU-Y, and OTU-Z, these genotypes showed consistent genetic divergence from the seven recognized species but lacked formal biological characterization. Blake et al. (2021), working at the Royal Veterinary College (UK), conducted an exhaustive characterization combining oocyst morphology, pre-patent periods, pathology, and draft genome sequence assemblies. The conclusion was unambiguous: all three OTUs possess sufficient genetic and biological diversity to constitute new species.

The three new species were named:

Eimeria lata n. sp. (formerly OTU-X): Named for its unusually wide oocyst morphology – the broadest average oocyst width of any Eimeria species infecting chickens.

Eimeria nagambie n. sp. (formerly OTU-Y): Named after Nagambie, Victoria, Australia, the location of the first isolate.

Eimeria zaria n. sp. (formerly OTU-Z): Named after Zaria, Nigeria, reflecting the geographic origin of its initial isolation.

Figure 1. Sporulated oocysts of the Eimeria Operational Taxonomic Unit (OTU) genotypes x, y, and z collected from domestic chickens (Gallus gallus domesticus). Photomicrographs of sporulated oocysts are shown for (A) OTUx, (B) OTUy and (C) OTUz. Composite line drawings are shown for (D) OTUx, (E) OTUy and (F) OTUz. RB, residual body; SB, stieda body; PG, polar granule. Scale bars = 10 µm. © 2021 Blake et al., Int J Parasitol. 2021 Jul;51(8):621–634. doi: 10.1016/j.ijpara.2020.12.004

2.2 Pathogenicity and production impact

Experimental infection trials demonstrated that all three new species are capable of compromising broiler bodyweight gain, a direct measure of economic impact. Unlike historically recognized species such as E. acervulina and E. tenella, whose pathological signatures are well-characterized, the intestinal tropism and precise pathological mechanisms of E. lata, E. nagambie, and E. zaria remain under active investigation. Their clinical presentation may overlap with existing species, complicating field diagnosis through standard lesion scoring alone.
The Eimeria-gut microbiota interaction is particularly relevant here. Research has demonstrated that Eimeria infection disrupts intestinal bacterial communities, reducing beneficial taxa and creating dysbiosis conditions that facilitate opportunistic bacterial overgrowth – most critically by C. perfringens. The bidirectional interaction between coccidiosis and necrotic enteritis leads to cumulative economic burdens. However, it remains to be determined whether the newly identified species possess distinct microbiota-modulating profiles.

2.3 Geographic distribution and diagnostic blind spots

Initially considered geographically restricted to the Southern Hemisphere, detection has since expanded significantly. One or more of the three new species have now been confirmed in Australia, multiple sub-Saharan African countries, India, Venezuela, the United States, and – as of 2023 – Europe, with the first reported detection of E. zaria in European broiler flocks (Jaramillo-Ortiz et al., 2023). The heavy reliance of existing diagnostic protocols on oocyst morphology and PCR panels developed for the original seven Eimeria species raises concerns that newly identified species are routinely underdetected in field surveillance.Critical diagnostic gap
Standard coccidiosis diagnostics – including lesion scoring, oocyst morphology, and many commercial PCR kits – were designed around the seven classical Eimeria species. E. lata, E. nagambie, and E. zaria may circulate undetected in flocks, contributing to unexplained performance losses and vaccine failures. Next-generation sequencing (NGS) targeting 18S rRNA is currently the most reliable identification tool (Blake et al., 2021).

2.4 Vaccine evasion: The central challenge

The most commercially disruptive characteristic of the three new species is their demonstrated ability to evade immunity induced by all currently available commercial anticoccidial vaccines. Live attenuated coccidiosis vaccines, the cornerstone of antibiotic-free coccidiosis control programs, are designed against the original seven species. Experimental challenge studies confirmed that prior vaccination provides no protective immunity against E. lata, E. nagambie, or E. zaria (Blake et al., 2021). This creates a significant vulnerability in integrated coccidiosis control programs, particularly in broiler production systems where vaccination programs are used as the primary long-term resistance management strategy.

The inability of current vaccines to address these new species underscores a critical need for broad-spectrum, mechanism-resilient complementary tools. Phytogenic compounds, acting through multiple simultaneous mechanisms, represent an ideal candidate for this role.

3. Current control strategies and their limitations

3.1 Chemical anticoccidials and ionophores

Chemical anticoccidials (e.g., diclazuril, toltrazuril, amprolium) and ionophore antibiotics (e.g., monensin, salinomycin) remain the primary pharmaceutical tools for coccidiosis control globally. These compounds target specific metabolic or ion transport mechanisms in Eimeria and have historically been highly effective when deployed in rotational shuttle programs. However, decades of continuous use have driven the emergence of resistance across multiple drug classes. Field resistance to monensin, robenidine, salinomycin, maduramicin, and diclazuril has been extensively documented across multiple geographic regions (Ferdji et al., 2022; Flores et al., 2022).

Resistance development occurs through multiple mechanisms: altered cell membrane permeability reducing drug uptake, use of alternative biochemical pathways, mutations at drug target sites, and genetic recombination within Eimeria populations. Crucially, resistance to one drug class does not necessarily confer resistance to compounds with different mechanisms – providing the theoretical basis for rotation programs. However, field conditions, partial compliance, and concurrent use often undermine the protective effects of rotation strategies.

3.2 Vaccines: Effective but incomplete

Live attenuated and live non-attenuated coccidiosis vaccines have represented a major advance in resistance management, offering cycle-by-cycle immunity development without driving pharmacological resistance. In broiler production, their use has grown significantly in recent years, particularly in no-anticoccidial or antibiotic-free production systems. However, as established in Section 2.4, no current commercial vaccine confers immunity against E. lata, E. nagambie, or E. zaria. This gap is not a minor caveat – it means that a vaccinated flock may be fully protected against classical species while remaining completely susceptible to the three newly described ones.

3.3 The regulatory and consumer pressure context

Across the European Union and in growing markets globally, regulatory restrictions on preventive antibiotic use, ionophore limitations in organic systems, and consumer demand for residue-free products have created strong incentives to explore alternatives. The combination of resistance pressure, vaccine limitations against new species, and regulatory trends makes the case for phytogenic integration both scientifically and commercially compelling.

4. Phytogenics as a multi-mechanism solution

4.1 Why phytogenics are relevant for coccidiosis control

Phytogenic compounds – plant-derived bioactive molecules including essential oil components, polyphenols, saponins, tannins, alkaloids, and bitter glycosides – have gained substantial scientific attention as a class of natural feed additives with demonstrated antimicrobial, antiparasitic, antioxidant, and immunomodulatory properties. Their relevance to coccidiosis management is grounded in three complementary properties: (1) direct antiparasitic action against Eimeria oocysts, sporozoites, and intracellular stages; (2) protection and restoration of intestinal mucosal integrity following Eimeria-induced damage; and (3) modulation of host immune responses to improve resilience against both Eimeria and secondary pathogens.

A key advantage of phytogenic compounds over conventional anticoccidials is their multi-target mode of action. Because each active molecule typically acts on multiple biological pathways simultaneously, the probability of resistance development through a single mutation is substantially lower than for single-target drugs. Furthermore, the inclusion of phytogenic blends in programs alongside vaccines or anticoccidials can provide synergistic or additive coverage – particularly relevant now that three new Eimeria species fall outside the protective scope of all available vaccines.

4.2 Compound-specific mechanisms of action

The following section reviews the scientific evidence for eight key phytogenic compounds relevant to coccidiosis control. A summary table is presented at the end of this section.

Saponins

Saponins are amphiphilic glycosides found in diverse plant species including Quillaja saponaria and Yucca schidigera. Their anticoccidial activity is primarily attributable to their capacity to interact with and disrupt lipid bilayer membranes. In the context of Eimeria, this membrane-disrupting action weakens the structural integrity of the parasite’s outer protective layers, rendering it more vulnerable to host immune effectors. Importantly, saponins also impair Eimeria attachment to intestinal epithelial cells, interrupting the invasion cascade. Bafundo et al. (2020) demonstrated that broilers receiving Quillaja/Yucca-derived saponin diets showed significantly reduced oocyst counts and improved weight gain compared to untreated controls challenged with Eimeria spp. Abbas et al. (2012), in a comprehensive botanical review, concluded that saponins significantly reduce both oocyst shedding and intestinal lesion scores, with efficacy approaching that of conventional anticoccidials.

Tannins

Tannins are polyphenolic compounds classified as condensed (proanthocyanidins) or hydrolysable (ellagitannins, gallotannins), found in chestnut, quebracho, and oak, among others. Their antiparasitic action against Eimeria involves protein precipitation at the parasite cell membrane – a non-specific mechanism that does not readily lend itself to resistance development. Tannins also exert strong antioxidant activity, directly reducing oxidative stress in intestinal tissue damaged by Eimeria – a crucial function given that lipid peroxidation is a primary driver of mucosal injury in coccidiosis. Masood et al. (2013) confirmed that tannin supplementation reduced intestinal oxidative stress and improved performance in broilers challenged with Eimeria. Abbas et al. (2012) further established their equivalence to chemical anticoccidials in reducing lesion severity and oocyst output.

Thymol (Thyme, Thymus vulgaris)

Thymol, the principal bioactive phenol of Thymus vulgaris essential oil, has been extensively studied for its anticoccidial properties. In vitro work by Remmal et al. (2013) demonstrated that thymol disrupts oocyst structural integrity and inhibits sporulation at concentrations of ≥2%, with maximal oocyst degeneration rates reaching 96% at 10%. At the level of intracellular parasite development, thyme essential oil was shown to inhibit the first round of schizogony in E. tenella with efficacy comparable to commercial anticoccidial drugs. Beyond direct antiparasitic action, thyme essential oil significantly downregulates pro-inflammatory mediators in Eimeria-challenged systems, reducing immune-mediated intestinal damage without suppressing protective immunity (Felici et al., 2024).

Cinnamaldehyde (Cinnamon, Cinnamomum verum)

Cinnamaldehyde, the principal aldehyde constituent of cinnamon bark, inhibits E. tenella sporozoite invasion of Madin-Darby bovine kidney (MDBK) epithelial cells in vitro, as part of a broader phenolic compound class with documented anti-invasion activity against Eimeria (Sidiropoulou et al., 2020). It reduces oocyst sporulation by approximately 79% in vitro (Remmal et al., 2013). Particularly notable is the synergistic effect between cinnamaldehyde and carvacrol (the active component of oregano oil): when used in combination, they achieve approximately 90% reduction in oocyst viability – substantially superior to either compound alone. This synergism supports the formulation of multi-compound blends. Cinnamaldehyde also demonstrates significant antimicrobial activity against Clostridium perfringens, providing simultaneous protection against the primary secondary pathogen associated with coccidiosis-driven necrotic enteritis.

Cumin (Cuminaldehyde, Cuminum cyminum)

Cumin seed contains cuminaldehyde as its primary bioactive compound, alongside cymene and other phenolic constituents. The anticoccidial relevance of cumin derives from multiple overlapping mechanisms: phenolic compounds interact with Eimeria oocyst membranes in a manner analogous to tannins, disrupting cytoplasmic membrane integrity and causing parasite cell death. Antioxidant properties protect intestinal epithelial cells from oxidative damage following Eimeria invasion. Broad-spectrum antimicrobial activity against common poultry pathogens, including C. perfringens, Salmonella spp., and E. coli, addresses the bacterial gateway mechanisms that amplify Eimeria-associated pathology. El-Shall et al. (2022) and the phytochemical coccidiosis control review (El-Shall et al., 2022) confirm cumin among the botanicals with documented anticoccidial and mucoprotective activity.

Licorice (Glycyrrhizin, Glycyrrhiza glabra)

Licorice root, through its primary bioactive compound glycyrrhizin and associated flavonoids (liquiritin, isoliquiritigenin), exerts potent immunomodulatory and anti-inflammatory effects particularly relevant to Eimeria-associated pathology. Glycyrrhizin stimulates T-cell mediated immune responses – the primary adaptive immune mechanism governing protective immunity against Eimeria – while modulating excessive inflammatory cascades that cause collateral intestinal damage. This dual action (immune stimulation + anti-inflammatory) is uniquely valuable in coccidiosis: it supports the development of parasite-specific immunity while limiting tissue destruction. Licorice compounds also support intestinal epithelium repair following Eimeria-induced villous atrophy, contributing to faster restoration of absorptive surface and productive performance. The immunomodulatory profile of licorice makes it particularly relevant as a complement to anticoccidial vaccination programs – supporting the immune priming process against classical species while potentially reinforcing innate defenses against the new, vaccine-evading species.

The right phytogenics can support coccidiosis control

Fig. 1 Lesion scores by intestinal segment. All treatments reduced lesion scores significantly compared to the positive control, but the Phytogenic was the clear winner overall, especially dominant in the caeca (E. tenella). Notably, the phytogenic products outperformed the coccidiostat on total lesion score, which is a strong result, particularly because the coccidiostat struggled against E. tenella in the caeca, where Phytogenic excelled.

Fig. 2 Microbiota recovery by day 18 pi. All four treatment groups performed similarly and dramatically better than the untreated positive control, reducing the dysbacteriosis score by roughly 45–49% compared to the positive control. The differences between the treated groups are minor and likely not statistically significant, meaning the phytogenic products performed on par with the coccidiostat in protecting gut health after Eimeria infection.

4.3 Summary: Phytogenic compound mechanisms at a glance

5. Integration into coccidiosis control programs

5.1 Phytogenics in combination with vaccines

The ideal integration model for phytogenics in the context of the new Eimeria species is as a permanent background layer within any coccidiosis control program – regardless of whether that program is vaccine-based, chemical-based, or a shuttle combination. For vaccinated flocks, phytogenics provide complementary activity against E. lata, E. nagambie, and E. zaria – species against which vaccines offer no protection – while supporting the immune priming process for species covered by the vaccine. Their immunomodulatory effects (particularly licorice and thyme) optimize T-cell responses during the vaccination window.

5.2 Phytogenics in chemical anticoccidial programs

In flocks managed with chemical anticoccidials, phytogenics serve a dual function: reducing the parasite load and oocyst environmental contamination (through saponins, tannins, cinnamaldehyde, and anise), and protecting intestinal integrity during chemotherapy-related periods when mucosal recovery is needed. Given the documented resistance issues with current chemical classes, the multi-mechanism action of phytogenic blends provides coverage that complements rather than competes with pharmacological programs.

5.3 Resistance management and sustainability

A defining advantage of multi-component phytogenic blends is their resistance resilience. Because compounds such as saponins, tannins, essential oil phenols, and bitter glycosides act on multiple biological targets simultaneously – membrane integrity, cell adhesion, sporulation, immune activation, oxidative balance – the probability of Eimeria developing resistance to a well-formulated phytogenic blend is fundamentally lower than for single-target anticoccidials. As regulatory pressure on chemical anticoccidials increases globally, particularly in the EU, phytogenic integration offers a scientifically grounded pathway to sustainable, long-term coccidiosis management.Key message for integrators and veterinarians
The characterization of E. lata, E. nagambie, and E. zaria creates a non-negotiable gap in current vaccine-based control programs. No available commercial vaccine provides protection against these three new species. Phytogenic blends – specifically those combining saponins, tannins, thymol, cinnamaldehyde, and supporting compounds (cumin, licorice, etc.) – offer the only currently available broad-spectrum complementary tool capable of addressing this gap while simultaneously managing drug-resistant classical species.

6. Conclusions

The formal naming of Eimeria lata, Eimeria nagambie, and Eimeria zaria in 2021 represents the most significant taxonomic development in avian coccidiosis in decades. Beyond nomenclature, these new species present concrete operational challenges: they are pathogenic, performance-impairing, capable of global spread, and invisible to all currently available commercial vaccines and most routine diagnostic protocols.

This discovery reinforces the case for moving beyond single-mechanism control strategies. Phytogenic compounds, through their complementary and multi-target mechanisms of action, provide a scientifically validated layer of broad-spectrum coccidiosis management. The compound portfolio reviewed in this paper – saponins, tannins, thymol, cinnamaldehyde, cumin, licorice, etc. – collectively addresses direct parasite suppression, intestinal barrier protection, immune modulation, oxidative stress reduction, and secondary pathogen control. These mechanisms operate independently of vaccine-induced immunity and without the resistance trajectories associated with conventional anticoccidials.

As the global poultry industry adapts to a coccidiosis landscape that now includes ten recognized Eimeria species infecting chickens, phytogenic integration is no longer an optional enhancement – it is a fundamental component of resilient, future-proof flock health management.

For more information on EW Nutrition’s phytogenic solutions supporting coccidiosis control,
contact your EW Nutrition regional representative or visit ew-nutrition.com

References

Abbas, R.Z., Colwell, D.D., Gilleard, J. (2012). Botanicals: an alternative approach for the control of avian coccidiosis. World’s Poultry Science Journal, 68(2), 203–215.

Abbas, R.Z., Iqbal, Z., Blake, D., Khan, M.N., Saleemi, M.K. (2011). Anticoccidial drug resistance in fowl coccidia: the state of play revisited. World’s Poultry Science Journal, 67(2), 337–350.

Bafundo, K.W., Johnson, A.B., Mathis, G.F. (2020). The effects of a combination of Quillaja saponaria and Yucca schidigera on Eimeria spp. in broiler chickens. Avian Diseases, 64(3), 300–304.

Blake, D.P., Knox, J., Dehaeck, B., Huntington, B., Rathinam, T., Ravipati, V., Ayoade, S., Gilbert, W., Adebambo, A.O., Tiambo, C.K., Tomley, F.M. (2020). Re-calculating the cost of coccidiosis in chickens. Veterinary Research, 51, 115.

Blake, D.P., Marugan-Hernandez, V., Tomley, F.M. (2021). Spotlight on avian pathology: Eimeria and the disease coccidiosis. Avian Pathology, 50(3), 209–213.

Blake, D.P., Vrba, V., Xia, D., Jatau, I.D., Spiro, S., Nolan, M.J., Underwood, G., Tomley, F.M. (2021). Genetic and biological characterisation of three cryptic Eimeria operational taxonomic units that infect chickens (Gallus gallus domesticus). International Journal for Parasitology, 51(8), 621–634.

Cantacessi, C., Riddell, S., Morris, G.M., Doran, T., Woods, W.G., Otranto, D., Gasser, R.B. (2008). Genetic characterization of three unique operational taxonomic units of Eimeria from chickens in Australia based on nuclear spacer ribosomal DNA. Veterinary Parasitology, 152(3–4), 226–234.

El-Shall, N.A., Abd El-Hack, M.E., Albaqami, N.M., Khafaga, A.F., Taha, A.E., Swelum, A.A., El-Saadony, M.T., Salem, H.M., El-Tahan, A.M., AbuQamar, S.F., El-Tarabily, K.A., Elbestawy, A.R. (2022). Phytochemical control of poultry coccidiosis: a review. Poultry Science, 101(1), 101542.

Felici, M., Tugnoli, B., De Hoest-Thompson, C., Piva, A., Grilli, E., Marugan-Hernandez, V. (2024). Thyme, oregano, and garlic essential oils and their main active compounds influence Eimeria tenella intracellular development. Animals, 14(1), 77.

Ferdji, F., Zahraoui-Mehadji, M., Baazizi, R., Meghit-Boumediene, K. (2022). Anticoccidial drug resistance in Eimeria field isolates from broiler farms in western Algeria. Veterinary Parasitology: Regional Studies and Reports, 32, 100733.

Flores, M.I., Saldana, B., Orozco, M.M., Quijada, N.M., Bersosa, F., Mateo, E. (2022). Anticoccidial resistance to chemical compounds and ionophores in Eimeria field isolates from commercial broiler farms. Poultry Science, 101(11), 102180.

Hailat, A.M., Abdelqader, A.M., Gharaibeh, M.H. (2024). Efficacy of phyto-genic products to control field coccidiosis in broiler chickens. International Journal of Veterinary Science, 13(3), 266–272.

Jaramillo-Ortiz, J.M., Burrell, C., Adeyemi, O., Werling, D., Blake, D.P. (2023). First detection and characterisation of Eimeria zaria in European chickens. Veterinary Parasitology, 323, 109857.

Masood, S., Abbas, R.Z., Iqbal, Z., Mansoor, M.K., Sindhu, Z.U.D., Zia, M.A., Khan, J.A. (2013). Role of natural antioxidants for the control of coccidiosis in poultry. Pakistan Veterinary Journal, 33(4), 401–407.

Mesa-Pineda, C., Navarro-Ruiz, J.L., Lopez-Osorio, S., Chaparro-Gutierrez, J.J., Gomez-Osorio, L.M. (2021). Chicken coccidiosis: from the parasite lifecycle to control of the disease. Frontiers in Veterinary Science, 8, 787653.

Remmal, A., Achahbar, S., Bouddine, L., Chami, F., & Chami, N. (2013). Oocysticidal effect of essential oil components against chicken Eimeria oocysts. International Journal of Veterinary Medicine: Research & Reports, 2013, 599816.

Saeed, Z., Alkheraije, K.A. (2023). Botanicals: a promising approach for controlling cecal coccidiosis in poultry. Frontiers in Veterinary Science, 10, 1157633.

Sidiropoulou, E., Skoufos, I., Marugan-Hernandez, V., Giannenas, I., Bonos, E., Aguiar-Martins, K., Lazari, D., Blake, D.P., Tzora, A. (2020). In vitro anticoccidial study of oregano and garlic essential oils and effects on growth performance, fecal oocyst output, and intestinal microbiota in vivo. Frontiers in Veterinary Science, 7, 420.

by Dr. Ruturaj Patil, EW Nutrition GmbH

Introduction

Dirty Eggs: A Biological Outcome of Intestinal Dysfunction

Dirty eggs are produced when eggshells come into contact with faecal material or contaminated cloacal secretions during or immediately after oviposition. This contamination is strongly associated with:

• Loose, watery, or sticky droppings
• Increased faecal microbial load
• Vent and cloacal inflammation or pasting
• Compromised cuticle quality due to impaired nutrient utilization

Birds suffering from subclinical enteric disorders often maintain acceptable egg numbers while producing a higher proportion of dirty eggs, making the problem economically severe yet clinically silent.

Numerous studies confirm that intestinal microbiota composition and gut integrity influence egg hygiene, not only through faecal consistency but also via environmental contamination and pathogen shedding. Dysbiosis alters fermentation patterns, increases osmotic pressure in the intestine, and promotes inflammation – conditions that directly translate into faecal instability and eggshell contamination.

Thus, dirty eggs should be viewed not only as a hygiene issue but as a sentinel indicator of underlying gut health compromise.

Gut Health as the Foundation of Egg Hygiene and Quality

Structural and Functional Integrity of the Layer Gut

The intestinal tract of laying hens is lined with rapidly renewing epithelial cells, connected by tight junction proteins that regulate permeability. A healthy gut is characterized by:

• A stable microbiota dominated by beneficial bacteria such as Lactobacillus spp.
• Optimal villus height to crypt depth (VH:CD) ratio
• Intact mucus layer and controlled immune surveillance
• Efficient digestion and nutrient absorption

Disruption of this equilibrium leads to leaky gut syndrome, maldigestion, excessive immune activation, and altered faecal output. Increased intestinal permeability allows bacterial toxins and metabolites to translocate, fueling systemic inflammation and worsening intestinal dysfunction.

In layers, these processes not only impair nutrient utilization for egg formation but also significantly affect dropping consistency and cloacal cleanliness, thereby compromising egg hygiene.

Etiological Factors Affecting Gut Health and Dirty Egg Production

Gut health disorders in laying hens arise from a complex interaction between infectious and noninfectious factors, operating across both growing and laying phases.

1. Etiological Factors During the Growing (Pullet) Phase

The pullet phase (0–18 weeks) is critical for establishing lifelong gut health resilience. Management failures during this period often result in latent intestinal weaknesses that manifest during peak lay.

a. Early Gut Microbiota Establishment

The intestinal microbiota begins colonization immediately after hatch. Chicks acquire microorganisms from:

• Feed and water
• Litter and housing environment
• Human handling and equipment

Delayed access to feed and water, poor brooding conditions, and weak biosecurity disrupt early microbial succession, predisposing birds to persistent dysbiosis later in life.

b. Feed Quality and AntiNutritional Factors

High levels of nonstarch polysaccharides (NSPs), oxidized fats, and mycotoxins during rearing impair gut maturation and digestive enzyme activity. These insults often remain subclinical but resurface during peak metabolic demand in lay as wet droppings and dirty egg problems.

c. Management Stressors

• Inadequate brooding temperatures divert energy from gut development
• High stocking density increases stress hormones, suppressing gut immunity
• Poor vaccination programs (e.g., against coccidiosis) increase intestinal damage

2. Etiological Factors During the Laying Phase

The laying period imposes extraordinary physiological demands on the hen, particularly for calcium metabolism, energy turnover, and sustained egg output.

a. Nutritional Imbalances

Excess crude protein, poor amino acid balance, or high dietary sodium and potassium increase intestinal osmotic load. Undigested nutrients draw water into the gut lumen, resulting in watery droppings and vent soiling.

b. Infectious and Dysbiotic Challenges

Subclinical infections caused by Clostridium perfringens, Escherichia coli, Salmonella spp., and Eimeria spp. damage intestinal mucosa and disrupt microbial equilibrium. These conditions increase faecal moisture and pathogen shedding, directly contaminating eggs during oviposition.

c. Aging and Extended Laying Cycles

Modern layer genetics favor extended production cycles. However, aging birds exhibit:

• Reduced antioxidant capacity
• Declining digestive efficiency
• Altered gut microbiome diversity

These changes contribute to faecal instability and increased dirty egg incidence in late lay.

Environmental and Management Drivers

Heat Stress

Heat stress reduces feed intake and redirects blood flow away from the gut, inducing intestinal hypoxia and oxidative stress. This damages epithelial integrity, increases permeability, and exacerbates diarrhea – strongly correlating with dirty egg production.

Water Quality

Water is a major yet underappreciated determinant of gut health. Poor water hygiene introduces pathogens, while high mineral load or improper pH disturbs osmotic balance and digestion, leading to diarrhoea and vent contamination.

Housing and Litter Management

Wet litter promotes pathogenic bacterial growth. In cagefree or aviary systems, increased faecaloral exposure further amplifies the impact of gut dysfunction on egg cleanliness.

Pathophysiological Link Between Gut Inflammation and Dirty Eggs

Inflamed intestines exhibit:

• Increased mucus secretion
• Sloughing of epithelial cells
• Fluid exudation into the lumen

These processes result in sticky, malformed droppings, rapid soiling of nests, and direct cloacal contamination of eggs. Moreover, chronic inflammation diverts nutrients away from eggshell and cuticle formation, promoting bacterial adhesion to shells.

PhytomoleculesBased Solutions: A MultiMode Gut Health Strategy

Definition and Rationale

Phytomolecules are standardized plantderived bioactive compounds, including essential oils, polyphenols, flavonoids, and alkaloids. Unlike conventional additives, they exert multitarget biological effects, making them particularly suitable for complex gut health challenges.

Antimicrobial Action

Phytomolecules such as carvacrol, thymol, and cinnamaldehyde:

• Disrupt bacterial cell membranes
• Interfere with quorum sensing
• Reduce virulence without fostering resistance

This selective antimicrobial action suppresses pathogens while preserving beneficial microbiota, reducing faecal pathogen load and wet droppings.

Antioxidant Action

Polyphenols and flavonoids neutralize reactive oxygen species generated by heat stress, aging, and mycotoxins. By protecting epithelial cells and tight junctions, antioxidant activity promotes stable gut morphology and firmer droppings.

AntiInflammatory Action

Phytomolecules downregulate proinflammatory cytokines (e.g., TNFα, IL6) and support mucosal immunity. Controlled inflammation prevents excessive mucus secretion and fluid leakage, breaking the gut–dirty egg cycle.

Additional Benefits Relevant to Dirty Egg Control

• Improved nutrient digestibility and shell quality
• Enhanced shortchain fatty acid (SCFA) production
• Better cloacal health and litter dryness
• Reduced environmental ammonia via improved nitrogen utilization

These combined effects make phytomoleculesbased solutions particularly effective in managing dirty egg problems in layers.

Integration into Practical Layer Management

For best results, phytomoleculesbased solutions should be:

• Introduced early during rearing to support gut maturation
• Continuously applied during lay to stabilize microbiota
• Strategically intensified during stress periods (heat, feed changes, vaccination)
• Integrated with feed, water, and environmental hygiene programs

Field Validation and Practical Integration: Evidence from Commercial and Research Trials

The practical relevance of phytomoleculesbased gut health solutions is supported by consistent responses across pullet rearing, peak lay, and extended laying periods, as demonstrated in multiple commercial and research trials using a standardized phytomolecules feed additive – ‘SPFA’ (Ventar® D from EW Nutrition GmbH, Germany).

a. Supporting Gut Health from Rearing to Lay

A commercial pullet trial in India (0–18 weeks) involving 10,000 BV300 pullets compared SPFA (100 g/t) with historical farm performance. Birds receiving the SPFA achieved target body weight (1242 g vs. 1190–1220 g), improved uniformity (+4%), and lower depletion, indicating superior early gut development and robustness – critical prerequisites for stable fecal consistency and cleaner eggs later in life.

“Overall, Ventar D has proven to be a gamechanger for our farm. The health and productivity benefits we have observed affirm our decision to continue using Ventar D.”
– Commercial layer producer, India

b. Performance and Egg Hygiene Support During Peak Lay

In a 20week controlled study with HyLine Brown layers (21–40 weeks), SPFA supplementation resulted in:

• ≈1% higher henday egg production
• 3.5 additional saleable eggs per hen housed
• Lower feed intake per egg (≈2.5 g)
• Improved feed conversion ratio (FCR)

These improvements reflect better gut efficiency and reduced inflammatory nutrient losses, directly supporting drier droppings, cleaner vents, and reduced risk of dirty egg production under commercial conditions.

c. Sustaining Persistency and Shell Quality in Late Lay

An 8week research trial in the Czech Republic (74–81 weeks) demonstrated that SPFA maintained higher laying persistency and significantly improved eggshell thickness and strength (p < 0.05). Improved shell integrity and gut nutrient utilization are particularly important in late lay, where intestinal oxidative stress and faecal instability are common contributors to dirty eggs.

Table 1. Summary of Phytomolecules Field Trial Outcomes Across Production Phases

Conclusion

Dirty egg production is fundamentally a biological outcome of impaired gut health, rather than solely a hygiene or housing issue. Nutritional imbalances, environmental stress, subclinical infections, poor water quality, and management gaps disrupt intestinal integrity, leading to dysbiosis, inflammation, and faecal instability – key contributors to eggshell contamination at lay.

Maintaining gut health throughout the entire production cycle, from pullet rearing to extended lay, is therefore essential for clean eggs and sustainable layer performance. Conventional control approaches, including antibiotics, are increasingly limited by regulatory constraints and do not adequately address the underlying causes of enteric dysfunction.

Phytomolecules‑based solutions provide a multi‑mode gut health strategy, combining antimicrobial, antioxidant, and anti‑inflammatory effects to restore intestinal balance, stabilize digestion, and normalize faecal consistency. This biological mechanism is supported by consistent field and research data demonstrating improved pullet uniformity, enhanced egg production and feed efficiency during peak lay, and maintained laying persistency with improved eggshell quality in late lay.

In summary, gut‑centric management supported by phytomolecules‑based interventions offers a scientifically validated and sustainable approach to reducing dirty egg incidence and improving long‑term layer productivity.

References available on request.

by Madalina Diaconu, Business Development Manager, EW Nutrition

Modern poultry production is currently battling a perfect storm of respiratory, enteric, and bacterial pressures. These overlapping challenges do more than just make birds sick; they actively erode performance, lead to higher condemnation rates at the plant, and squeeze already tight profit margins. To stay ahead, any practical health program must move beyond quick fixes and instead align interventions across everything from gut integrity and immunity to farm management and data collection.

Despite significant technological leaps in biosecurity and disease control, many “old” enemies remain stubbornly persistent:

• Coccidiosis: This remains the single largest financial drain on the industry, costing an estimated EUR 10.4 billion globally due to losses in weight gain and increased mortality. (Blake et al., 2020)
• Necrotic Enteritis (NE): Often triggered by coccidiosis, NE ranges from “silent” subclinical performance loss to sudden, fatal outbreaks. (Hargis, 2024; Skinner et al., 2010)
• Histomoniasis: In turkeys, this disease (often called Blackhead) frequently results in 80-100% mortality, made worse by the fact that there are currently no approved treatments in major markets. (Beer et al., 2022; Merck, 2024)
• APEC/Colibacillosis: This is a major driver of bird loss and processing plant condemnations, complicated by a high prevalence of multi-drug resistance. (Apostolakos et al., 2021; Joseph et al., 2023; Kazimierczak et al., 2025)
• Salmonella: This pathogen persists at critical production nodes, with varying strains moving through the production pyramid from breeders to the final product. (Siceloff et al., 2022)

Why a pillar-based approach?

Pillar 1: Pathogen pressure & epidemiology

Respiratory pathogens like IBV or NDV often show up as mixed infections, leading to high morbidity and more condemnations. MG and MS amplify these chronic issues. (Liu et al., 2025; El-Gazzar, 2025; CFSPH) Enteric pathogens like Eimeria (coccidiosis) create the groundwork for Clostridium perfringens (NE) to thrive. (Blake et al., 2020; Hargis, 2024; Skinner et al., 2010)

• The Phytogenic Lever: Essential oils and plant polyphenols can disrupt the membranes of bacteria like Salmonella and E. coli, lowering the overall intestinal load and reducing environmental shedding. (Gentile et al., 2025; Wickramasuriya et al., 2022)

Pillar 2: Immunity & Vaccination

Successful vaccination isn’t just about the bottle; it requires precise strain selection, prime/boost design, and correct application. This is especially true for managing AIV (Avian Influenza) under global risk-based strategies. (FAO/WOAH, 2025)

• The Phytogenic Lever: Certain plant-based additives act as immunomodulators, boosting macrophage activity and helping birds maintain resilience even when stressed by high stocking densities or heat. (Wickramasuriya et al., 2022)

Pillar 3: Microbiome & Gut Integrity

“Dysbacteriosis” is essentially a microbiome out of balance, which ruins nutrient absorption and weakens the gut barrier. (Aruwa et al., 2021; Aruwa & Sabiu, 2024) Protecting the gut is essential because clinical NE can kill birds quickly, while subclinical NE silently ruins efficiency. (Hargis, 2024; Skinner et al., 2010)

• The Phytogenic Lever: These additives support “good” bacteria like Lactobacilli while suppressing opportunists and strengthening the “tight junctions” in the gut lining. (Wickramasuriya et al., 2022) Multiple trials show reduced NE pressure when phytogenics accompany coccidiosis programs. (Wickramasuriya et al., 2022)

Pillar 4: Environment & Management

The environment plays a massive role; for instance, recycling litter beyond six cycles significantly increases the risk of Salmonella detection. (Machado et al., 2020) Proper ventilation is also key to preventing thermal stress, which can trigger gut dysbiosis. (Liu et al., 2025; Aruwa et al., 2021)

• The Phytogenic Lever: By stabilizing digestion and the microbiota, these additives can reduce wet litter and ammonia release, indirectly improving respiratory comfort. (Wickramasuriya et al., 2022; Aruwa et al., 2021)

Pillar 5: Biosecurity & Movement Control

Disease spreads through networks. Prioritizing biosecurity at “high-centrality” nodes – like hatcheries and common service routes – is more effective than a blanket approach. (Sequeira et al., 2025)

• The Phytogenic Lever: Reducing the amount of pathogens a flock sheds helps support structural biosecurity barriers by lowering the overall transmission risk within houses. (Gentile et al., 2025; Wickramasuriya et al., 2022)

Pillar 6: Water, Feed & Processing Interface

Water hygiene is a vital tool for microbiome stability, especially during the vulnerable brooding phase. (Wickramasuriya et al., 2022) At the processing plant, PAA chillers remain the most effective chemical intervention to reduce contamination. (Thames et al., 2022)

• The Phytogenic Lever: Using phytogenics in feed or water helps stabilize the upper-GI tract during feed transitions and can lower carcass pathogen loads. (Gentile et al., 2025; Wickramasuriya et al., 2022)

Pillar 7: Diagnostics, Genomics & Data Systems

Modern tools like Whole Genome Sequencing (WGS) and RT-PCR panels allow for much faster detection of APEC or respiratory viruses, enabling “precision” interventions. (Kazimierczak et al., 2025; El-Gazzar, 2025; Liu et al., 2025)

• The Phytogenic Lever: When data shows rising pathogen pressure, phytogenics offer a flexible, rapid-response alternative that helps maintain antibiotic stewardship. (Kazimierczak et al., 2025; Gentile et al., 2025)

A 12-Month Roadmap for Implementation

• Q1: Baseline & Risk Map: Map pathogen pressure using targeted PCR/WGS panels and review movement networks to prioritize high-centrality nodes. (Kazimierczak et al., 2025; El-Gazzar, 2025; Liu et al., 2025; Siceloff et al., 2022; Sequeira et al., 2025)
• Q2: Program Design: Update vaccine strains and set up co-management plans for coccidiosis and NE, including microbiome supports with clear targets. (Liu et al., 2025; El-Gazzar, 2025; Blake et al., 2020; Hargis, 2024; Wickramasuriya et al., 2022)
• Q3: Execution & Plant Linkage: Solidify water/feed hygiene SOPs and link farm Salmonella trends to plant PAA chiller performance. (Siceloff et al., 2022; Thames et al., 2022; Sequeira et al., 2025)
• Q4: Review & Scale: Audit how well the team followed the diagnostic-driven actions and refine the playbooks for the next cycle. (Kazimierczak et al., 2025)

The Integrated View

Phytogenic feed additives aren’t “silver bullets,” but they contribute across all seven pillars. Their multi-target mode of action – acting as anti-inflammatories, antioxidants, and antimicrobials – complements traditional tools like vaccines and biosecurity to build a more resilient bird. (Wickramasuriya et al., 2022; Gentile et al., 2025; Aruwa et al., 2021)

References

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Aruwa CE, et al. Poultry gut health – microbiome functions and engineering. J Anim Sci Biotechnol (2021). https://link.springer.com/article/10.1186/s40104-021-00640-9

Aruwa CE, Sabiu S. Interplay of poultry–microbiome interactions and dysbiosis. British Poultry Science (2024). https://www.tandfonline.com/doi/pdf/10.1080/00071668.2024.2356666

Beer LC, et al. Histomonosis in poultry: a comprehensive review. Front Vet Sci (2022). https://www.frontiersin.org/articles/10.3389/fvets.2022.880738/full

Blake DP, et al. Re‑calculating the cost of coccidiosis in chickens. Veterinary Research (2020). https://link.springer.com/article/10.1186/s13567-020-00837-2

CFSPH. Avian Mycoplasmosis (MG) Fact Sheet (updated). https://www.cfsph.iastate.edu/Factsheets/pdfs/avian_mycoplasmosis_mycoplasma_gallisepticum.pdf

El‑Gazzar M. Mycoplasma gallisepticum infection in poultry. MSD Veterinary Manual (rev. 2025). https://www.msdvetmanual.com/poultry/mycoplasmosis/mycoplasma-gallisepticum-infection-in-poultry

FAO/WOAH. Global Strategy for HPAI Prevention and Control (2024–2033). (2025). https://www.woah.org/app/uploads/2025/02/web-gf-tads-hpai-strategy-woah.pdf

Gentile N, et al. Emerging challenges in Salmonella control: innovative, sustainable disinfection strategies in poultry farming. Pathogens (2025). https://www.mdpi.com/2076-0817/14/9/912

Hargis BM. Necrotic enteritis in poultry. Merck Veterinary Manual (rev. 2024). https://www.merckvetmanual.com/poultry/necrotic-enteritis/necrotic-enteritis-in-poultry

Joseph J, et al. APEC in broiler breeders: an overview. Pathogens (2023). https://www.mdpi.com/2076-0817/12/11/1280

Kazimierczak J, et al. Rapid detection of APEC via minimal virulence markers (iroC, hlyF, wzx ‑ O78). BMC Microbiology (2025). https://link.springer.com/article/10.1186/s12866-025-03861-4

Liu H, et al. Review of respiratory syndromes in poultry: pathogens, prevention, and control measures. Veterinary Research (2025). https://link.springer.com/content/pdf/10.1186/s13567-025-01506-y.pdf

Machado PCJ, Chung C, Hagerman A. Modeling Salmonella spread in broiler production: determinants and control strategies. Front Vet Sci (2020). https://www.frontiersin.org/articles/10.3389/fvets.2020.00564/full

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Pant S, et al. Economic impact assessment and disease prevalence of coccidiosis in broilers. Journal of Entomology and Zoology Studies (2019). https://www.entomoljournal.com/archives/2019/vol7issue5/PartK/7-4-112-882.pdf

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by Ilinca Anghelescu, Global Director Marketing & Communications, EW Nutrition

2025 was a year defined by four converging forces for the global feed and animal production industry: an unprecedented HPAI crisis that cost American consumers alone $14.5 billion extra in egg expenditures; historic record corn production driving feed ingredient prices lower; a highly disruptive US tariff regime that reshuffled global trade flows for soybeans, corn, chicken, and pork; and accelerating regulatory pressure on antimicrobial use across Europe and globally.

The strategic imperatives from 2025 are clear: biosecurity investment is no longer optional, ingredient price volatility demands agile procurement strategies, trade compliance is a weekly operational concern, and antibiotic-free production transitions require credible, phased plans now.

KEY METRIC: Global chicken meat production reached approximately 105 million MT in 2025 (+2%), even as egg production suffered severely. The global feed market is valued at $542 billion in 2025, growing at 3.3% CAGR. Corn hit record production of 17 billion bushels in the US alone – the highest since 1936 in terms of harvested area.

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CHAPTER 1: HPAI & DISEASE LANDSCAPE 

1.1  The Ongoing H5N1 Crisis – Scale & Impact

The H5N1 clade 2.3.4.4b strain of Highly Pathogenic Avian Influenza (HPAI) continued to dominate animal health headlines in 2025. Since its reemergence in February 2022, the US outbreak alone has resulted in the confirmed loss of over 175 million birds across 1,700+ flocks – the costliest poultry disease event in recorded history.

1.2  2025-Specific Developments

United States: Early-Year Severity, Policy Response

The first six weeks of 2025 saw 28 million layers depopulated – the worst start to any calendar year on record. Ohio, Indiana, and Missouri bore the brunt. The USDA launched a five-pronged approach in February 2025 including:

• Gold-standard biosecurity assessments (948 completed Jan 20–June 26)
• Indemnity increase from $7 to $17 per lost layer hen
• Importation of 26+ million dozen shell eggs from Brazil, Honduras, Mexico, Turkey, and South Korea
• Removal of select regulatory burdens to accelerate flock repopulation
• $793 million in HPAI research proposals received in response to USDA Innovation Grand Challenge

⚠  Price Manipulation Investigation: In April 2025, the DOJ Antitrust Division launched an investigation into the largest US egg producer after it reported a 247% increase in quarterly net income. Egg producers and retailers face ongoing scrutiny over whether crisis pricing exceeded what supply constraints warranted.

Brazil: First Commercial HPAI Outbreak – May 2025

On May 15, 2025, Brazil – the world’s largest poultry exporter, responsible for nearly 30% of global exports – confirmed its first-ever commercial HPAI case at a breeder facility in Montenegro, Rio Grande do Sul (17,000 birds). This was a watershed event for global poultry trade.

Europe: Persistent Pressure

HPAI continued to circulate widely in European poultry and wild bird populations. Key 2025 events include recurrence in Australia (February), ongoing outbreaks in Germany, Hungary, Netherlands, UK, and France, and the first confirmed domestic cat HPAI death in the Netherlands (H5N1, November 2025).

CRITICAL RISK: HPAI is now classified as enzootic (endemic) in wild birds across North America by the CDC. The virus circulates year-round in wildlife reservoirs, making seasonal recurrence in commercial flocks a structural, not episodic, risk. US egg producers are 8% below their 2022 flock baseline.

1.3  Other Priority Diseases in 2025

CHAPTER 2: GLOBAL POULTRY PRODUCTION 

2.1  Global Output – 2025 Performance

Despite HPAI disruptions, global chicken meat production grew approximately 2% in 2025 to around 105 million MT (ready-to-cook), driven by demand resilience and lower feed costs for broiler production. Total global poultry meat (including turkey, duck, and others) is forecast to exceed 152 million MT for 2025, per FAO Food Outlook June 2025.

OECD-FAO 10-Year Outlook (2025–2034)

The OECD-FAO Agricultural Outlook 2025–2034, released in July 2025, projects global poultry meat production will grow by over 19% to 173.4 million MT by 2034 compared to the 2022–24 average. Poultry will account for the majority of additional meat consumption globally, driven by:

• Affordability relative to beef and pork, especially in price-sensitive emerging markets
• Population and income growth in Southeast Asia, South Asia, and Sub-Saharan Africa
• Rapid urbanization and expansion of Quick Service Restaurant (QSR) chains
• Superior feed conversion ratio (FCR) and lower greenhouse gas emissions per kg of protein

STRATEGIC NOTE: In high-income countries, per capita poultry consumption growth is flattening as consumers focus increasingly on welfare, environment, and health attributes. Growth opportunity is almost entirely in middle-income markets. Product premiumization (antibiotic-free, cage-free, organic) is the North American and European story.

2.2  Egg Production – Crisis Sector

Egg production was the sector hardest hit by HPAI globally. In the US, 75% of all HPAI-affected birds were table-egg layers, despite layers comprising less than 4% of the total poultry population. This structural vulnerability reflects longer flock lifespans and, increasingly, cage-free housing adoption.

⚠  Cage-Free Transition & Disease Vulnerability: Some analysts link cage-free housing to higher HPAI susceptibility. Regardless of epidemiological debate, the US cage-free market is now structurally undersupplied relative to corporate commitments made in 2014–2017. Producers face a squeeze: comply with welfare commitments while managing disease risk.

CHAPTER 3: FEED INGREDIENT MARKETS 

3.1  Grain & Oilseed Prices – 2025 Summary

From a feed cost perspective, 2025 was broadly favorable for livestock and poultry producers. Record US corn production and generally adequate global grain and oilseed supplies put downward pressure on the major feed commodities, offering partial relief from the margin pressure of recent years.

PROCUREMENT SIGNAL: The US/China trade tensions created windows of soybean buying opportunity as prices swung on trade deal news. China agreed to purchase US soybeans in late 2025 as part of a limited trade deal, causing a price uptick. Procurement teams should monitor US-China negotiations as a lead indicator for soybean pricing in 2026.

3.2  Global Feed Market Overview

3.3  Key Ingredient Trends to Watch

Fertilizer Cost Relief

Fertilizer prices have declined significantly from their 2022 peak. A basket of N, P, and K fertilizers averaged $437/tonne in May 2025, down from the $815/tonne peak in April 2022, per FAO Food Outlook. This benefits grain production economics and should support adequate grain supplies into 2026.

Soybean Oil Competition: Biodiesel vs. Feed

US soybean oil demand from renewable fuel programs (the 45Z credit) competed directly with feed-grade fat supplies, pushing soy oil prices up 20.8% in 2025. Feed mills formulating with added fats should evaluate alternative lipid sources. Poultry fat and palm olein remain cost-competitive in some markets.

Alternative Proteins: Insect Meal, DDGS, Algae

While adoption remains limited in volume, regulatory acceptance of insect meal in EU poultry diets continues to expand. Dried Distillers Grains with Solubles (DDGS) remain a strategically important co-product, particularly in the US and EU. Feed formulators should have up-to-date matrix values and be prepared to use them when corn prices favor inclusions.

⚠  Tariff Risk for Feed Inputs: US feed manufacturers faced effective tariff rates averaging 12%+ on key agricultural inputs from China and other countries in 2025, including herbicides, pesticides, and some micro-ingredient precursors. Amino acid supplies (predominantly Chinese-origin lysine, methionine, threonine) faced added cost and supply uncertainty.

CHAPTER 4: TRADE POLICY DISRUPTIONS 

4.1  The 2025 US Tariff Regime – Agricultural Impact

The Trump administration’s tariff policies beginning January 20, 2025, represented the most significant disruption to global agricultural trade in decades. The three largest US agricultural export markets – Mexico ($30.3B in 2024), Canada ($28.3B), and China ($24.7B) – were all targeted, triggering retaliatory measures that hit feed, grain, poultry, and pork exports.

CHINA TRADE DEAL (MAY 2025): A 90-day tariff truce agreed May 12, 2025 reduced US tariffs on Chinese goods from 145% to 30%, and China’s tariffs on US products from 125% to 10%. China agreed to purchase US soybeans. No permanent deal was signed. The limited agreement provided short-term stability but medium-term uncertainty remains.

4.2  Impact on US Agricultural Trade Flows

4.3  Strategic Trade Lessons

• Supply chain diversification is no longer a luxury: concentration of US soy exports to China created a single-point-of-failure vulnerability that became fully exposed in 2025.
• Regionalized disease zoning is a trade-preserving tool: Brazil’s rapid implementation of regionalized HPAI bans (rather than country-wide) preserved most of its export access; this is the model the industry should support with regulators globally.
• USMCA dependency is real: 70% of US corn, 60% of soybeans, 45% of poultry exports go to Mexico, Canada, China – the same three countries targeted by 2025 tariffs.
• US government announced $12B in emergency farm compensation in 2025, repeating the pattern from Trump’s first term – indicating persistent trade disruption risk.

CHAPTER 5: REGULATORY CHANGES 

5.1  EU: Feed & Food Safety Legislation Simplification

In 2025, the European Commission proposed a package to streamline EU food and feed safety legislation while maintaining high health standards. The initiative, announced mid-2025, is intended to boost competitiveness of EU producers by reducing regulatory complexity – a direct response to competitive concerns vs. non-EU producers.

5.2  EFSA 2025 Guidance on Microorganisms

On September 24, 2025, EFSA’s Scientific Committee adopted new harmonized guidance on the characterization of microorganisms in the food chain. This is a landmark shift with major implications for feed additive manufacturers, probiotics suppliers, and novel food applicants.

5.3  Antimicrobial Resistance (AMR) – Regulatory Pressure

AMR remains the defining long-term regulatory risk for the animal feed and production industry. Key 2025 actions:

• EFSA/ECDC Joint Report (March 2025): Highlighted persistently high resistance to critical antimicrobials in poultry, especially Campylobacter and Salmonella, with ‘statistically significant increasing trend 2020–2024.’ This directly fuels EU legislative pressure.
• EU Regulation 2019/6 (Veterinary Medicines) – Article 118: Banning import of animal products containing antimicrobials used for growth promotion. Application delayed to 2026, raising questions about enforcement timelines – and competitive fairness regarding imports from countries still allowing AGPs.
• EU AMR Implementation Decision 2023: New harmonized monitoring requirements for AMR in zoonotic and indicator bacteria from food-producing animals – effective January 1, 2025. All EU Member States now required to collect and report standardized AMR surveillance data.
• WOAH 10-Year HPAI Strategy (2024–2033): Promotes surveillance, vaccination programs, and timely reporting as cornerstones of international HPAI management.

BOTTOM LINE ON AMR: The regulatory trajectory is clear and irreversible – sub-therapeutic antibiotic use for growth promotion is being eliminated globally. The timeline varies by region (already banned in EU since 2006; US voluntary approach from 2017; global WHO action plan). Companies that have already invested in transition are ahead; those that have not face increasing compliance risk and market access restrictions.

5.4  US Regulatory Developments

CHAPTER 6: FEED ADDITIVE & NUTRITION STRATEGIES 

PRECISION NUTRITION SIGNAL: The industry’s shift to reduced crude protein (CP) diets, precisely supplemented with industrial amino acids (L-Lys, DL-Met, L-Thr, L-Trp, L-Val) remained the dominant reformulation strategy in 2025. Lower CP diets reduce feed cost, lower N excretion (environmental benefit), and reduce substrate for pathogenic bacteria. With amino acid prices remaining favorable, there are few economic arguments for maintaining high CP diets.

6.1  The Post-AGP Transition: Where the Industry Stands

The antibiotic-free (ABF) production movement accelerated further in 2025. With the EU ban on AGPs in place since 2006 and the US moving toward voluntary phase-out, the entire industry is in active transition. The key challenge: AGP removal creates enteric health gaps that must be addressed with alternative tools. Without effective management, removal of AGPs leads to increased necrotic enteritis, Campylobacter colonization, and poorer FCR.

6.2  Heat Stress – A Growing Production Challenge

Climate-related heat stress was a highlighted research and production topic in 2025. Modern high-performance broiler genetics have been selectively bred for rapid growth under thermoneutral conditions. Heat stress impairs feed intake, FCR, immunity, meat quality, and reproduction. Management strategies:

• Dietary electrolyte balance adjustment (increase K, Na, reduce Cl where appropriate)
• Vitamin C and E supplementation at heat stress periods
• Betaine inclusion as an osmolyte; reduces supplemental methionine requirement under heat stress
• Feed schedule adjustment (limit feeding during hottest hours; early morning/evening feeding)
• Housing design investment: tunnel ventilation, evaporative cooling, adequate air velocity

6.3  In Ovo Technology

In ovo vaccination and nutrition delivery continued to advance in 2025. Key developments include high-throughput systems (3,000 eggs/hour at 99% accuracy) for in ovo vaccination and nutritional interventions. Early-life gut programming through in ovo delivery of probiotics, nutrients, and vaccine antigens is becoming an increasingly important hatchery-level biosecurity and performance tool.

CHAPTER 7: MARKET TRENDS & CONSUMER SHIFTS 

7.1  Poultry Gaining Share vs. Other Proteins

Elevated beef prices throughout 2025 – driven by tight US cattle supply (herd at decades-long lows) and high demand – continued to push consumers toward poultry as a cost-effective protein. This dynamic is a structural tailwind for the broiler industry globally.

7.2  Cage-Free & Animal Welfare Commitments

The cage-free transition is structurally undersupplied in the US. Corporate commitments made in 2014–2017 implied a need for 220 million cage-free layers by 2025–26. Current production is well below that target. This creates both a market opportunity (premium pricing) and a risk (HPAI vulnerability concerns in cage-free systems). Producers must balance welfare compliance with biosecurity protocols.

7.3  Antibiotic-Free, Organic, and Specialty Products

Consumer and corporate buyer demand for ABF, No Antibiotics Ever (NAE), organic, and pasture-raised products continued to grow in premium markets in 2025. The pasture-raised egg segment reported 30% annual growth rates despite high price points. For integrated producers, this requires dedicated production lines with separate management protocols, supply chain segregation, and robust documentation systems.

7.4  Sustainability Pressure

Feed manufacturers and integrators are under growing pressure from retail and foodservice customers, NGOs, and regulators to demonstrate reduced environmental footprint. Key metrics under scrutiny:

• GHG emissions per kg of chicken meat produced (Scope 1, 2, and 3)
• Deforestation-free supply chains for soy (EU Deforestation Regulation – EUDR)
• Feed conversion ratio improvement as a sustainability lever
• Nitrogen and phosphorus excretion reduction (enzyme use, reduced CP diets, phytase)
• Water use per unit of animal protein produced

EUDR NOTE: The EU Deforestation Regulation requires companies to ensure that soy used in feed does not originate from recently deforested land. Implementation deadlines have been debated, but traceability requirements for soy origin – particularly from Brazil – are operationally significant for EU feed manufacturers and importers.

CHAPTER 8: STRATEGIC LESSONS & ACTION PRIORITIES 

8.1  Summary: Top 10 Lessons of 2025

8.2  Action Priority Matrix for Management Teams

8.3  Key Indicators to Monitor in 2026

• HPAI detection frequency in fall-winter 2025–26 migration season – predictor of next egg price cycle
• USDA HPAI vaccine grand challenge awards – signals timeline for commercial vaccine availability
• EU feed safety simplification package progress – potential relief on additive authorization timelines
• EUDR deforestation enforcement timeline – soy traceability compliance clock
• Brazil HPAI market re-entry for China – recovery of the world’s #1 poultry export relationship
• US corn/soy 2026 planting intentions (March) – USDA Prospective Plantings report is the key 2026 procurement signal

2025 demonstrated that the feed and animal production industry operates in an environment of simultaneous, compounding risks – biological, geopolitical, regulatory, and climatic. The companies that performed best were those with robust biosecurity infrastructure, agile procurement teams, clear AMR transition roadmaps, and diversified market exposure. There is no single silver bullet. Systematic risk management, not reactive crisis response, is the competitive differentiator going forward.

  KEY SOURCES & REFERENCES 

This article draws on data and analysis from the following sources:

Author: Ajay Bhoyar, Senior Global Technical Manager, EW Nutrition

The global use of feed enzymes has become a central feature of efficient monogastric animal production systems. Rising feed ingredient costs, tighter margins, and increasing regulatory pressure to reduce environmental impact have all accelerated enzyme innovation. At the same time, feed mills have shifted toward higher conditioning temperatures and time in pursuit of improved pellet durability, pathogen control, and throughput. However, this creates a hostile environment for most exogenous feed enzymes, which can lose significant activity under the harsh conditions of feed processing.

Historically, enzyme manufacturers have attempted to overcome heat degradation of by coating, encapsulating, or post-pelleting liquid application (PPLA) of enzymes. While these approaches provide partial solutions, they can also have limitations, including delayed enzyme activity, uneven distribution, reduced mixing uniformity, and reliance on specialized liquid enzyme applicators.

These limitations prompted a novel direction: enzymes designed or selected to be intrinsically heat-stable, capable of surviving pelleting without protective matrices.

This article highlights recent advancements in intrinsically heat-stable xylanase technology, explains its advantages over coated and post-pelleting enzyme solutions, and outlines its practical benefits for feed manufacturers, integrators, and nutritionists operating under modern high-temperature feed pelleting conditions.

Intrinsically Thermostable Enzymes

An enzyme is considered intrinsically heat-stable when its native protein structure resists unfolding and retains catalytic activity under high temperatures associated with feed processing—typically 80–95°C for 30–90 seconds. Unlike coated enzymes that rely on external protection, intrinsically thermostable enzymes depend on their internal protein architecture for heat tolerance. Enzymes from organisms living in compost, thermal springs, and geothermal soils naturally withstand temperatures of 80–100 °C or higher. Intrinsically thermostable enzymes are often sourced from thermophiles (organisms living in hot springs and deep-sea vents) or engineered for stability. They resist denaturation (loss of shape and function) at high-temperature processing.

Limitations of Current Thermostability Solutions

Coating / Encapsulation

A method of protecting enzymes from heat is to encapsulate or coat them with a protective coating. An ideal enzyme coating for animal feed needs to:

1. Protect the enzyme through steam conditioning (typically 85–90°C or higher) and through subsequent pelleting.

2. Release the enzyme from the coating quickly in the gastrointestinal tract of the target animal, to ensure optimum efficacy. (Gilbert and Cooney, 2007)

There is some evidence, however, suggesting that the coating of enzymes may reduce the efficacy of the product, compared to an uncoated version of the same product (Kwakkel et al., 2000).

Post-Pelleting Liquid Application (PPLA)

Post-pelleting liquid enzyme application requires sophisticated applicators to minimize the risk of uneven spraying or calibration errors, which is often not feasible in small or mid-size mills. Accurate application of the liquid enzyme, as with some other critical liquid micro-ingredients, requires specialized spraying equipment and, even then, consistency of accurate enzyme application can be an issue (Bedford and Cowieson, 2009). Research has shown that as much as 30% of the enzyme activity can be found in the pellet fines, and therefore, adding the enzyme before screening would result in a lower than expected dosage in the final feed and wastage of the enzyme product (Engelen, 1998). In some cases, adjusting the pelleting machines to the output of the PPLA’s spray nozzles to ensure a homogenous and even application of the enzyme on the pellets may reduce the overall pellet production rate, especially in big feed mills with very high throughput.

These limitations of the coated or PPLA technologies strengthen the value proposition of intrinsically heat-stable enzymes.

Nutritional and Commercial Benefits of Intrinsically Heat-Stable Xylanase

The use of intrinsically heat-stable xylanase delivers consistent nutritional benefits in poultry and swine feeds, including predictable non-starch polysaccharide (NSP) degradation, a significant increase in the metabolizable energy (ME) value of the feed, and enhanced gut health resilience supporting reduced antibiotic use.

From a commercial and operational perspective, this technology simplifies enzyme application, improves mixing uniformity, reduces formulation risk, and lowers feed cost per unit of meat or egg produced.

In-Vitro Thermal Stability Profile of Axxess XY

Axxess XY is a novel, intrinsically thermostable GH10 xylanase originating from Thermotoga maritima, a hyperthermophilic bacterium found in hydrothermal vents near volcanic grounds, and commercially it is produced by proprietary strain of Bacillus subtilis.

The superior heat stability of Axxess XY has been proven under various commercial pelleting conditions across different geographies. Axxess XY showed excellent post-pelleting recovery under commercial feed-milling conditions across varying temperatures and conditioning times (Fig. 2).

In one study, in addition to excellent post-pelleting recovery, Axxess XY also demonstrated high xylanase stability in pelleted feed over a 2-month feed storage period at>40°C, with humidity around 65%.

Conclusions

As feed mills continue to operate at higher conditioning temperatures and longer retention times, enzyme heat stability has become a critical success factor in modern feed production. Intrinsically heat-stable xylanase offers a practical and reliable solution to this challenge by maintaining enzyme activity through pelleting without the need for coatings or post-pelleting liquid application systems.

By relying on its native protein structure rather than external protection, intrinsically thermostable xylanase delivers consistent post-pelleting recovery, uniform distribution in feed, and predictable nutritional performance across different feed mills and processing conditions. This reliability translates into improved nutrient utilization, better gut health support, and reduced cost per kilogram of meat or eggs produced.

From an operational standpoint, intrinsically heat-stable xylanase simplifies enzyme application, reduces dependence on specialized equipment, and minimizes the need for over-formulation or safety margins. These advantages help feed manufacturers and integrators improve efficiency, lower risk, and achieve more consistent results, especially under demanding commercial pelleting conditions.

In summary, intrinsically heat-stable xylanase aligns well with the evolving needs of today’s feed industry, offering a robust, cost-effective, and future-ready enzyme solution for high-performance animal production systems.

References:

Bedford, M. R., and A. J. Cowieson. 2009. “Phytate and Phytase Interactions.” In Proceedings of the 17th European Symposium on Poultry Nutrition, 7–13. Edinburgh, UK.

Eeckhout, M., M. De Schrijver, and E. Vanderbeke. 1995. “The Influence of Process Parameters on the Stability of Feed Enzymes during Steam Pelleting.” In Proceedings of the 2nd European Symposium on Feed Enzymes, 163–169. Noordwijkerhout, The Netherlands.

Engelen, G. M. A. 1998. Technology of Liquid Additives in Post-Pelleting Applications. Wageningen, The Netherlands: Wageningen Institute of Animal Science.

Gilbert, T. C., and G. Cooney. 2011. “Thermostability of Feed Enzymes and Their Practical Application in the Feed Mill.” In Enzymes in Farm Animal Nutrition, 2nd ed., edited by M. R. Bedford and G. G. Partridge, 249–259. Wallingford, UK: CABI.

Kwakkel, R. P., P. L. van der Togt, and K. A. B. M. Holkenborg. 2000. “Bio-Efficacy of Two Phytase Formulations Supplemented to a Corn–Soybean Broiler Diet.” In Proceedings of the 3rd European Symposium on Feed Enzymes, 63–64. Noordwijkerhout, The Netherlands.

Reporting Period: November 6-12, 2025

Extracted Data by Disease Category

1. ASF in Domestic Pigs

2. ASF in Wild Boar

3. HPAI (NON-P) in Captive Birds / H5N1

4. HPAI (NON-P) in Wild Birds / H5 (N untyped)

5. HPAI (NON-P) in Wild Birds / H5N1

6. High Pathogenicity Avian Influenza Viruses (Poultry) (Inf. with) / H5N1

Summary Statistics

By Dr. Inge Heinzl, Editor EW Nutrition

Gut health is a critical factor in poultry production, influencing growth performance, feed efficiency, and overall bird health. A well-functioning digestive system ensures optimal nutrient absorption and ultimately contributes to economic sustainability in poultry farming.

However, another essential function of the gut is its significant role in immune defense, as evidenced by the fact that 80% of all active immune cells are in the gut. It is essential for the organism to keep a sensitive balance by eliminating invading pathogens while maintaining self-tolerance to avoid autoimmunity. Being 1.5 to 2.3 m long and with a big contact area to the external environment, the gut is the first line of defense when pathogens have orally entered the organism. For this purpose, the intestine has several specialized cells and a plethora of diverse microorganisms – the microbiome.

A balanced gut environment, therefore, enhances resistance to diseases, helps prevent infections, and reduces the need for antibiotics.

Which tools are available in the gut to counteract pathogenic attacks?

The gut wall, per se, has several fixed tools to fight pathogenic offenses, such as the mucus layers and the epithelium with highly specialized cells. Figure 1 shows in detail the different parts of the gut immune system.

1. Mucus layers

The mucus layers form the first host-derived line of defense. They help trap invasive bacteria and facilitate their removal via luminal flow. The protective properties may depend on whether the mucin is neutral or acidic, sialylated or sulfated (Broom and Kogut, 2018). The glycoprotein mucins forming the mucus layer (mainly MUC2 in the small and large intestine and MUC5ac in the proventriculus) are produced by the goblet cells, part of the intestinal epithelium just beneath.

2. Intestinal epithelium

The one-layered intestinal epithelium represents a physical barrier and consists of normal enterocytes, as well as specialized cells. All the cells are closely linked by tight junctions, consisting of claudin, occludin, and junctional adhesion molecules (JAM).
The following diverse specialized cells protect the organism from pathogenic attacks:

2.1 Proliferating stem cells

These cells are ready to replace damaged epithelial cells in the case of inflammation.

2.2 Paneth cells

Paneth cells are situated at the bottom of the Lieberkühn crypts, neighboring the stem cells in the jejunum and the ileum. Paneth cells have different tasks:
In normal conditions, they maintain homeostasis by regulating the microbiome’s composition via the secretion of antimicrobial peptides, which are accumulated in apically oriented secretory granules, performing phagocytosis and efferocytosis. Additionally, the Paneth cells provide niche factors for the intestinal stem cell compartment, absorb heavy metals, and preserve the integrity of the intestinal barrier. If one or more of these functions are impaired, intestinal and systemic inflammations or infections can develop (Wallaeys et al., 2022). The number of Paneth cells and their diameter can be enhanced via feeding. Agarwal et al. (2022) noticed a significant increase in the number and diameter of Paneth cells after feeding quinoa soluble fiber and/or quercetin 3-glucoside.

2.3 M cells

M cells (M coming from microfold and indicating the structure) are specialized epithelial cells localized along the antimesenteric border in the epithelium of the ileum. They are crucial for the immune system and an essential part of the gut-associated lymphoid tissue (GALT), a sub-system of the mucosa-associated lymphoid tissue (MALT).
M cells play an important role in the function of the immune system. They act as a transport system for antigens. They sample antigens (macromolecules, bacteria, viruses, small parasites) via the apical membrane. After the phagocytosis of the foreign organism/substance, the antigen gets through the cell and is consigned to cells of the adaptive immune system (e.g., the B-cells) at the basal side. The exact transport and the handover to the cells of the adaptive immune system are still unclear. It is also not clarified whether the antigens are processed inside the cells.

2.4 Dendritic cells

Dendritic cells are a kind of leucocyte derived from the bone marrow. Immature dendritic cells have a star-like shape. They are specialized to identify, uptake, transport, process, and present antigens to other immune system cells on their surface. To identify and uptake harmful substances/microbes, they carry receptors on their surface that recognize the attributes often occurring in pathogenic viruses, bacteria, and fungi. After contact with the antigen, the cell moves to secondary lymphoid tissue, and in the intestine, this is predominantly Mucosa-Associated Lymphoid Tissue (MALT). Arriving as mature and not phagocytizing dendritic cells, they present the antigens of the pathogens to the T-lymphocytes. For this purpose, they use cell surface proteins (MHC proteins). This presentation, together with co-stimulators and cytokines, activates naïve T-lymphocytes to develop into the relevant T-cell (fighting viruses, bacteria…) and proliferate, leading to the clearance of the pathogen.
On the other hand, dendritic cells can also suppress an immune reaction if the “suspicious subjects” are harmless or belong to the organism. Dendritic cells are the most potent antigen-presenting cells of the immune system.

2.5 Goblet cells

Goblet cells originate from pluripotent stem cells and are located between the enterocytes in the inner mucus layer of the intestine. Goblet cells develop and mature rapidly after hatching due to external stimuli such as environmental and dietary factors, but also intestinal microbiota (Duangnumsawang et al., 2021). They derive their name from their goblet-like appearance. The basal site is thin, but the cell gets thicker toward the apical side. In the thicker cell organisms, vesicles with mucins are stored and explosively released to the surface by exocytosis.

The mucins (MUC2) are viscous, slime-forming substances consisting of a protein string bound to many sugar chains. Due to their oligosaccharide chain structure, they offer adhesion binding sites for intestinal commensal bacteria and enhance probiotic colonization (Liu et al, 2020). They have a high water-binding capacity, which is responsible for their slimy and protective characteristics. In the case of inflammation, mucin production can increase strongly.

By providing bicarbonate for proper mucin unfolding in the small intestine, goblet cells help maintain homeostasis and the intestinal barrier function. Furthermore, goblet cells can form goblet cell-associated passages (GAPs) and deliver luminal substances to the antigen-presenting cells in the underlying lamina propria that can start an adaptive immune response (Knoop and Newberry, 2018).
As with Paneth cells, the number of goblet cells also increases by feeding quinoa soluble fibers.

2.6 Neuroendocrine cells

Enterochromaffin cells are neuroendocrine cells found in the epithelium of the whole digestive tract, mainly in the small intestine, the colon, and the ceca. They belong to the enteric endocrine system, are part of the diffuse neuroendocrine system, and produce 95% of the serotonin in the organism. Enterochromaffin cells act as chemo- and mechanosensors. They react to free fatty acids, amino acids, and other chemicals as well as physical forces occurring during peristaltic activity in the gut, thus modulating the secretion of water and electrolytes as well as gut motility and visceral sensation of pain (Linan-Rico et al., 2016; Diwakarla et al., 2018).

Serotonin, on its side, has been shown to affect the composition of the gut microbiota (Kwon et al., 2019) and to modulate bacterial physiology (Knecht et al., 2016). Gut-derived serotonin is responsible for immune responses (Baganz and Blakely, 2012) but also for the regulation of other functions such as bone development (Chabbi-Achengli et al., 2012), gut motility, and platelet aggregation (Berger et al., 2009). A deficient serotonergic system can cause psychopathological behaviors such as feather pecking.

3. Last but not least – the microbiome

The poultry gut microbiome consists of bacteria, fungi, protozoa, and viruses. Beneficial microbes, such as Lactobacillus, Bifidobacterium, and Bacteroides, contribute to gut health and immunity. 

On the one hand, microbes are involved in digestion and nutrient synthesis. They assist in breaking down fiber, producing short-chain fatty acids, and synthesizing essential vitamins. On the other hand, they contribute to immune defense:

Beneficial bacteria (BB) prevent the colonization of harmful microbes:
The bacteria inhabiting the poultry gut act against pathogens by competing with them for nutrients and binding sites at the intestinal mucosa.

Beneficial bacteria prevent/reduce inflammation and stabilize the intestinal mucosa
Abaidullah et al. (2019) showed in their review how beneficial bacteria influence the immune response to diverse viruses (AIV, IBDV, MDV, NDV).
Bacteria such as Collinsella, Faecalibacterium, Oscillibacter, etc., increase the release of IFN-α, IFN-β, and IL-22. These substances control virus replication and repair mucosal tissue damage. Other bacteria, such as Clostridium XIVa or Firmicutes, provoke T-cells to produce anti-inflammatory cytokines to suppress inflammation. By promoting the antimicrobial peptides such as MUC, TFF, ZO, and tight junction proteins comprised of claudins, occludin, and zona occludens mRNA expression, Bacteroides, Candidatus, SMB53, Parabacteroides, Lactobacillus, Paenibacillus, Enterococcus, and Streptococcus spp. inhibit pathobiont colonization and translocation, and suppress inflammation. Butyrate succinate and lactate, produced by Faecalibacterium and Blautia spp., provide energy and reduce inflammation.
Bacteroides fragilis produce bacterial polysaccharides that communicate with the immune system and influence the transformation of CD4+ (T-helper cells) and Foxp3+ cells (the master transcription factor of regulatory T cells in mammals, but also present in chicken (Burkhardt et al., 2022)). 

“Negative” bacteria increase inflammation and enhance viral shedding
Clostridium Cluster XI, Salmonella, and Shigella downregulate the anti-inflammatory and tight junction-stabilizing substances, which would be increased by the beneficial bacteria and increase IFN-γ and IF-17A to cause mucosal inflammation and tissue damage, as well as increased virus replication and fecal shedding. Further bacteria, which enhance mucosal and GIT inflammation, are Desulfovibrionaceae, producing hydrogen sulfides, Vampirovibrio, Clostridium cluster XIVb, and the genus Rumicoccus. They induce the pro-inflammatory cytokines IL-6 and IL-1β. The latter three bacteria also increase viral shedding. Salmonella typhimurium and Campylobacter jejuni also achieve higher viral shedding by decreasing viral-specific IgG and IgA production (Abaidullah et al., 2019)

Factors impairing intestinal immune defense

As the previous paragraph indicates, an imbalance of the intestinal microbiome called dysbiosis makes chickens more prone to diseases such as necrotic enteritis (Stanley et al., 2014). Several factors are disturbing the balance in the microbiome (Heinzl,  2020):

• An abrupt change of feed
• High contents of non-starch polysaccharides increase viscosity, decrease passage rate, lower the digestibility of other nutrients, and serve as nutrients for, e.g., Clostridium perfringens
• High protein levels can also serve as a substrate for pathogens and cause a shift in the balance of the intestinal flora
• Finely ground feed does not stimulate the gizzard muscles to do their work. pH increases, transit time decreases, and pathogenic microbes such as Salmonella, Campylobacter, and Clostridia proliferate.
• Stress (heat or cold stress, re-assembling of groups, high stocking densities)
• Mycotoxins

However, besides all these factors causing an overgrowth of commensal bacteria such as E. coli, ingested pathogens such as Marek’s or Newcastle Disease viruses can also cause this imbalance.

Immune defense in the gut – an interplay of different tools that must be protected

The first line of defense, the intestine, comprises different tools working together to fight pathogens and harmful substances. Besides the mucus layers and the specialized cells, the intestinal microbiome plays an essential role in immune defense by competing with pathogens for nutrients and binding sites, enhancing the secretion of anti-inflammatory substances, and stimulating the production of interferons, which fight the pathogens. However, several factors can impact the balance of the microbiome and cause dysbiosis. The best protection of this sensitive equilibrium can support the organism in defending against diseases and maintaining immunity and performance. Understanding the interplay between microbiota, immune function, and nutrition allows for effective strategies to enhance poultry health while reducing reliance on antibiotics. Future research will continue to provide insights into optimizing gut-immune interactions in poultry production.

References

Abaidullah, Muhammad, Shuwei Peng, Muhammad Kamran, Xu Song, and Zhongqiong Yin. “Current Findings on Gut Microbiota Mediated Immune Modulation against Viral Diseases in Chicken.” Viruses 11, no. 8 (July 25, 2019): 681. https://doi.org/10.3390/v11080681. 

Baganz, Nicole L., and Randy D. Blakely. “A Dialogue between the Immune System and Brain, Spoken in the Language of Serotonin.” ACS Chemical Neuroscience 4, no. 1 (December 24, 2012): 48–63. https://doi.org/10.1021/cn300186b. 

Berger, Miles, John A. Gray, and Bryan L. Roth. “The Expanded Biology of Serotonin.” Annual Review of Medicine 60, no. 1 (February 1, 2009): 355–66. https://doi.org/10.1146/annurev.med.60.042307.110802. 

Broom, Leon J., and Michael H. Kogut. “The Role of the Gut Microbiome in Shaping the Immune System of Chickens.” Veterinary Immunology and Immunopathology 204 (October 2018): 44–51. https://doi.org/10.1016/j.vetimm.2018.10.002. 

Burkhardt, Nina B, Daniel Elleder, Benjamin Schusser, Veronika Krchlíková, Thomas W Göbel, Sonja Härtle, and Bernd Kaspers. “The Discovery of Chicken Foxp3 Demands Redefinition of Avian Regulatory T Cells.” The Journal of Immunology 208, no. 5 (March 1, 2022): 1128–38. https://doi.org/10.4049/jimmunol.2000301. 

Chabbi-Achengli, Yasmine, Amélie E. Coudert, Jacques Callebert, Valérie Geoffroy, Francine Côté, Corinne Collet, and Marie-Christine de Vernejoul. “Decreased Osteoclastogenesis in Serotonin-Deficient Mice.” Proceedings of the National Academy of Sciences 109, no. 7 (January 30, 2012): 2567–72. https://doi.org/10.1073/pnas.1117792109. 

Clarke, G, S Grenham, P Scully, P Fitzgerald, R D Moloney, F Shanahan, T G Dinan, and J F Cryan. “The Microbiome-Gut-Brain Axis during Early Life Regulates the Hippocampal Serotonergic System in a Sex-Dependent Manner.” Molecular Psychiatry 18, no. 6 (June 2013): 666–73. https://doi.org/10.1038/mp.2012.77. 

Diwakarla, S., L. J. Fothergill, J. Fakhry, B. Callaghan, and J. B. Furness. “Heterogeneity of Enterochromaffin Cells within the Gastrointestinal Tract.” Neurogastroenterology &amp; Motility 29, no. 6 (May 9, 2017). https://doi.org/10.1111/nmo.13101. 

Duangnumsawang, Yada, Jürgen Zentek, and Farshad Goodarzi Boroojeni. “Development and Functional Properties of Intestinal Mucus Layer in Poultry.” Frontiers in Immunology 12 (October 4, 2021). https://doi.org/10.3389/fimmu.2021.745849. 

Heinzl, Inge. “Necrotic Enteritis: The Complete Overview.” EW Nutrition, August 8, 2023. https://ew-nutrition.com/necrotic-enteritis-complete-overview/. 

Knecht, Leslie D., Gregory O’Connor, Rahul Mittal, Xue Z. Liu, Pirouz Daftarian, Sapna K. Deo, and Sylvia Daunert. “Serotonin Activates Bacterial Quorum Sensing and Enhances the Virulence of Pseudomonas Aeruginosa in the Host.” EBioMedicine 9 (July 2016): 161–69. https://doi.org/10.1016/j.ebiom.2016.05.037. 

Kong, Shanshan, Yanhui H. Zhang, and Weiqiang Zhang. “Regulation of Intestinal Epithelial Cells Properties and Functions by Amino Acids.” BioMed Research International 2018 (2018): 1–10. https://doi.org/10.1155/2018/2819154. 

Kwon, Yun Han, Huaqing Wang, Emmanuel Denou, Jean-Eric Ghia, Laura Rossi, Michelle E. Fontes, Steve P. Bernier, et al. “Modulation of Gut Microbiota Composition by Serotonin Signaling Influences Intestinal Immune Response and Susceptibility to Colitis.” Cellular and Molecular Gastroenterology and Hepatology 7, no. 4 (2019): 709–28. https://doi.org/10.1016/j.jcmgh.2019.01.004. 

Linan-Rico, Andromeda, Fernando Ochoa-Cortes, Arthur Beyder, Suren Soghomonyan, Alix Zuleta-Alarcon, Vincenzo Coppola, and Fievos L. Christofi. “Mechanosensory Signaling in Enterochromaffin Cells and 5-HT Release: Potential Implications for Gut Inflammation.” Frontiers in Neuroscience 10 (December 19, 2016). https://doi.org/10.3389/fnins.2016.00564. 

Liu, Yang, Xinjie Yu, Jianxin Zhao, Hao Zhang, Qixiao Zhai, and Wei Chen. “The Role of MUC2 Mucin in Intestinal Homeostasis and the Impact of Dietary Components on MUC2 Expression.” International Journal of Biological Macromolecules 164 (December 2020): 884–91. https://doi.org/10.1016/j.ijbiomac.2020.07.191. 

Lyte, Mark. “Microbial Endocrinology in the Microbiome-Gut-Brain Axis: How Bacterial Production and Utilization of Neurochemicals Influence Behavior.” PLoS Pathogens 9, no. 11 (November 14, 2013). https://doi.org/10.1371/journal.ppat.1003726. 

Marcobal, A., P. C. Kashyap, T. A. Nelson, P. A. Aronov, M. S. Donia, A. Spormann, M. A. Fischbach, and J. L. Sonnenburg. “A Metabolomic View of How the Human Gut Microbiota Impacts the Host Metabolome Using Humanized and Gnotobiotic Mice.” The ISME Journal 7, no. 10 (June 6, 2013): 1933–43. https://doi.org/10.1038/ismej.2013.89. 

Stanley, Dragana, Shu-Biao Wu, Nicholas Rodgers, Robert A. Swick, and Robert J. Moore. “Differential Responses of Cecal Microbiota to Fishmeal, Eimeria and Clostridium Perfringens in a Necrotic Enteritis Challenge Model in Chickens.” PLoS ONE 9, no. 8 (August 28, 2014). https://doi.org/10.1371/journal.pone.0104739. 

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Yano, Jessica M., Kristie Yu, Gregory P. Donaldson, Gauri G. Shastri, Phoebe Ann, Liang Ma, Cathryn R. Nagler, Rustem F. Ismagilov, Sarkis K. Mazmanian, and Elaine Y. Hsiao. “Indigenous Bacteria from the Gut Microbiota Regulate Host Serotonin Biosynthesis.” Cell 163, no. 1 (September 2015): 258. https://doi.org/10.1016/j.cell.2015.09.017.

Recently, The Poultry Site’s Sarah Mikesell interviewed Predrag Persak, EW Nutrition’s Regional Technical Manager for Northern Europe. The conversation covered topics as wide as sustainability and challenges in poultry production, and as narrow as intestinal permeability. Thanks to The Poultry Site for the great talk!

Watch the video

Sarah Mikesell, The Poultry Site: Hi, this is Sarah Mikesell with The Poultry Site, and today we are here with Predrag Peršak. He is the Regional Technical Manager for Northern Europe with EW Nutrition. Thanks for being with us today, Predrag.

Predrag Peršak, EW Nutrition: Nice to be here, Sarah. Thank you for inviting me.

SM: Very good. It’s nice to visit with you. And today, Predrag and I are in Berlin, Germany, at an exclusive event for the poultry industry called Producing for the Future, which is sponsored by EW Nutrition. You are one of our speakers today, Predrag, so I’m going to ask you just a few questions to let everybody know a little bit about your presentation.

You’ve described animal nutrition as “never boring and never finished.” What makes this field so dynamic and constantly evolving for you?

PP: I’ve been in animal nutrition for about 25 years. And in those 25 years, I would say that not even half a year passed without something extraordinary happening. From genetics to animal husbandry, especially here in Europe, we also have a lot of pressure from consumers and slaughterhouses to adapt production to the needs of the customers.

Sustainability, sourcing raw materials, and the variety of raw materials available in Europe – and the constant development of new ones – make life for an animal nutritionist very, very interesting. It’s also very challenging, and through these challenges you learn a lot.

So, applying what we learned 20 years ago is simply not enough anymore. For someone who wants to be challenged every day with new things, this is definitely the right industry to be in – especially now.

SM: Excellent. Can you explain your holistic approach to animal nutrition and how considering multiple factors benefits practical applications on farms?

PP: The concept of a holistic approach in animal nutrition is not new. But for me – being both a veterinarian and a nutritionist – it means having deeper insight into the animal itself, into all the metabolic processes, and also into the external influences: husbandry, genetics, diseases, and management. Looking at how all of these interact, we can only really solve problems by looking at the animal as a whole system.

The same applies to feed production. You cannot look at a feed mill as just one compartment. You have to look at sourcing raw materials, their quality, how they are processed – milling, pelleting, and other technologies – and then see how that feed performs on the farm.

So, a holistic approach can be applied both from the animal perspective and from the feed production perspective, across all steps and processes. This is something we use and promote daily in our work with customers.

SM: Very good. You’ve worked with unconventional protein and fiber sources. We’re hearing a lot more about that recently. What are those, and what potential do they bring to animal nutrition?

PP: When I talk about unconventional protein and fiber sources, we need to remember that the global feed production scene is very diverse. What applies in the U.S. or Brazil does not necessarily apply in Europe or the Far East.

Here in Europe, we try to use not by-products but co-products of food production. For example, different fractions of rapeseed or sunflower meal, which are widely produced in Europe but not often used by mainstream nutritionists due to certain limitations. By finding the right processing methods and combining them with technologies, we can make these unconventional materials usable in mainstream nutrition.

The same goes for fiber sources. Both fermentable and structural fibers are increasingly important for intestinal and digestive development, as well as for overall animal health. So, processing fibers in ways that maximize usability while minimizing negative effects is a big part of my work.

SM: From a cost standpoint for producers, are those lower-cost inputs, or just alternatives they need to look at?

PP: In Germany we have a perfect expression for this: “yes and no.” There is always pressure on price, especially in poultry, because food must be accessible to everyone. But at the same time, food must not harm the environment or human health, and we should use all resources not fit for humans but still usable for animals.

So, it’s not only about cost – about availability and sustainability. Working with just two, three, or five raw materials for a long time is not the way forward. The way forward is to think of everything that can be used properly, for the benefit of the animals, and ultimately to produce enough food for the world.

Also, using locally available products is important. Feed production is very diverse around the world—raw materials in Southeast Asia differ completely from those in Europe, Brazil, or the U.S. Using technologies to enable the use of locally produced by-products makes production not only sustainable, but also economically viable for local communities. That’s really the core of the feed industry: using what is produced locally.

SM: Interesting. Very cool. How does your interdisciplinary work across poultry, pigs, and ruminants give you unique insights that might be missed with a narrower focus?

PP: I come from a small feed mill in a small country, Croatia. There, you don’t have deep specialization by species or even by category, as you find in larger markets. Specialization has its advantages, but it can also limit creativity and “outside-the-box” thinking.

By working with ruminants, I learned about fermentation processes – knowledge that can be applied to pigs and even to poultry. For example, fermentation can reduce anti-nutritional factors, allowing higher inclusion levels of certain raw materials in poultry diets.

With pigs, fermentation of fibers – especially in piglets – is crucial, and some of that knowledge could be applied to turkeys, where we still face health issues.

So, working across species demands a lot – it leaves little time for other things – but it opens up unique perspectives and cross-species applications that benefit the entire livestock industry.

SM: I was talking with someone yesterday about mycotoxins – there’s a lot of research in pigs but less in poultry. That’s kind of what you’re talking about, right? Applying knowledge across species?

PP: Absolutely. We’re focused now on poultry, but we can learn from poultry too – not only about feeding but also about farm management, biosecurity, and more. These lessons can also apply to pigs or ruminants.

It’s all holistic – you cannot solve everything with nutrition alone. It’s always a package.

SM: You presented today about the importance of intestinal permeability. Why is it important, and how can understanding it impact animal health and performance outcomes?

PP: Intestinal permeability is one of the key features we use to describe gut health. Personally, I’m very practical. For 20 years we’ve talked about “gut health,” but the real question for veterinarians and nutritionists is: what do we actually do with that knowledge?

In my presentation, I explained intestinal permeability as a “point of no return” in gut health. When leaky gut develops, everything else can deteriorate – faster or slower – but it won’t return to normal without intervention.

By comparing how different stressors or pathogens impact intestinal permeability, we can better understand severity and decide where to focus. Nutritionists already pay attention to thousands of factors, but we need to identify the most impactful ones. That was my key message: focus on the most important drivers.

SM: And leaky gut has really become something the whole industry is talking about, right? I’ve even seen it in human health – my doctor has posters about it.

PP: Exactly. Across cows, pigs, and poultry, leaky gut is getting a lot of attention. It’s a physiological or pathophysiological feature that marks the point of no return.

We can talk about dysbiosis and all the causes, but once you reach leaky gut, you understand where intervention is needed. And it’s not just hype. For example, recently Nature published research showing certain types of human bone marrow conditions are linked to leaky gut and microbial influence on blood processes.

So, this is not a passing trend. It’s fundamental. And once we solve one issue, another door opens. That’s why this industry is never boring.

SM: Very good. Well, thank you for all the information today, Predrag.

PP: Thank you, Sarah. It was a pleasure to talk with you.

Watch the video on The Poultry Site.