Part 4: Paleness

By Dr. Inge Heinzl, Editor and Marisabel Caballero, Global Technical Manager Poultry

We already showed bad feathering, mouth and beak lesions, bone issues, and foot pad lesions as signs of mycotoxin contamination in the feed, but there is another indicator: paleness. Paleness can signify a low count of red blood cells resulting from blood loss or inadequate production of these cells. Other possibilities are higher bilirubin levels in the blood due to an impaired liver, leading to jaundice or missing pigmentation.

The mycotoxins mainly causing anemia are Aflatoxins, Ochratoxin, DON, and T-2 toxin

Anemia can be diagnosed using parameters such as red blood cell count, hemoglobin levels, and hematocrit/packed cell volume (PCV). Numerous studies have examined the impact of mycotoxins on hematological parameters. They reveal their propensity to affect red blood cell production by impairing the function of the spleen and inducing hematological alterations. On the other hand, anemia can be caused by blood loss. Due to affecting coagulation factors, mycotoxins can lead to internal hemorrhages. The gut wall damage, probably due to secondary infections such as coccidiosis and necrotic enteritis, can entail bloody diarrhea in various animal species.

Impact on the production of blood cells

Low values of blood parameters such as red blood cells, hemoglobin, and hematocrit can result from inadequate production due to impacted production organs. The World Health Organization (WHO, 1990) and European Commission (European Commission, 2001) have identified hematopoietic tissues as targets for necrosis caused by T-2 toxin. Chu (2003) even stated that “the major lesion of T-2 toxin is its devastating effect on the hematopoietic system in many mammals, including humans”. Pande et al. (2006) suggested that reduced hemoglobin values result from decreased protein synthesis due to mycotoxin contamination, a notion supported by Pronk et al. (2002), who described trichothecenes as potent inhibitors of protein, DNA, and RNA synthesis, particularly affecting tissues with high cell division rates. Additionally, the European Commission (2001) highlighted the sensitivity of red blood cell progenitor cells (in this trial, the cells of mice, rats, and humans) to the toxic effects of T-2 and HT-toxins. DAS also seems to attack the hematopoietic system, as shown in humans (WHO, 1990). A further cause for anemia might be low feed intake or nutrient absorption, which inhibits adequate iron absorption and leads to iron deficiency. In their case report, Bozzo et al. (2023) assumed that renal failure and a resulting impaired excretion capacity caused by OTA might even increase the half-life of the toxins. This would enhance their effects on their target organs, such as the liver and bone marrow, and lead to anemia.

Several studies utilizing different animal species and mycotoxin dosages have been conducted to assess the effects of Aflatoxins, Ochratoxin, and T-2 Toxin on hematological parameters. The following table provides a summary of some of these studies.

Table 1: The effects of different mycotoxins on hematological parameters – hematopoiesis

In their meta-analysis, Andretta et al. (2012) reported that the presence of mycotoxins in broiler diets decreased the hematocrit and the hemoglobin concentration by 5% and 15%, and aflatoxin alone decreased the parameters by 6% and 20%.

It should be evident that a simultaneous occurrence of several mycotoxins even aggravates the situation. In an experiment involving Sprague Dawley rats, administering T-2, DON, NIV, ZEA, NEO, and OTB decreased hematocrit and red blood cell counts across all mycotoxins. However, for DON, NIV, ZEN, and OTB, red blood cell values showed partial recovery after 24 hours (Chattopadhyay, 2013). Perhaps the organism learns to cope with the mycotoxins.

The examples show that Trichothecenes, such as T-2 toxin, DON, and others, as well as Ochratoxins and Aflatoxins, impact blood parameters such as hematocrit, hemoglobin, red blood cell count, and mean corpuscular volume. All these changes might lead to paleness of the skin and birds’ feet and combs.

Blood loss caused by bleeding or destruction of erythrocytes

The second possibility for anemia is blood loss due to injuries or lesions. In addition to directly causing hemorrhages, mycotoxins can promote secondary infections such as coccidiosis, which damages the gut and may produce bloody feces.

Parent-Massin (2004) e.g. reports on rapidly progressing coagulation problems after the ingestion of trichothecenes leading to septicemia and massive hemorrhages. Table 2 shows more examples of mycotoxins causing paleness due to blood loss.

Table 2: The effects of different mycotoxins on hematological parameters – blood loss

Poor pigmentation

The fourth reason for paleness can be inadequate pigmentation. According to Hy Line (2021), the so-called pale bird syndrome is characterized by poor skin and egg yolk pigmentation and is caused by reduced absorption of fat and carotenoid pigments in compromised birds. This is also the case when the diets contain pigment supplements. Tyczkowski and Hamilton (1986) observed in their experiment with chickens exposed to doses of 1-8 µg of Aflatoxins/g of diet for three weeks that aflatoxins can cause poor pigmentation in chickens, probably by impairing carotenoids absorption but also transport and deposition. Osborne et al. (1982) asserted that carotenoids were significantly (P<0.05) depressed by 2 ppm ochratoxin as well as by 2.5 ppm aflatoxin in the diet.

Another possibility is oxidative stress due to the mycotoxin challenge. As pigments also serve as antioxidants, they may be expended for this purpose and are no longer available for pigmentation.

Paleness in poultry – a reason to think about mycotoxins

Paleness can have different causes, some of which are influenced by mycotoxins. If your chickens or hens are pale, checking the feed concerning mycotoxins is always recommended. A feed analysis can give information about possible contamination (see our tool MasterRisk).

In the case of contamination, effective products binding the mycotoxins and mitigating the adverse effects of these harmful substances can help protect your birds. As paleness is usually not the only effect of mycotoxins but also a decrease in growth, toxin binders can help maintain the performance of your animals.

References:

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Andretta, I., M. Kipper, C.R. Lehnen, and P.A. Lovatto. “Meta-Analysis of the Relationship of Mycotoxins with Biochemical and Hematological Parameters in Broilers.” Poultry Science 91, no. 2 (February 2012): 376–82. https://doi.org/10.3382/ps.2011-01813.

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Chattopadhyay, Pronobesh, Amit Agnihotri, Danswerang Ghoyary, Aadesh Upadhyay, Sanjeev Karmakar, and Vijay Veer. “Comparative Hematoxicity of Fusarium Mycotoxin in Experimental Sprague-Dawley Rats.” Toxicology International 20, no. 1 (2013): 25. https://doi.org/10.4103/0971-6580.111552.

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Huff, W.E., R.B. Harvey, L.F. Kubena, and G.E. Rottinghaus. “Toxic Synergism between Aflatoxin and T-2 Toxin in Broiler Chickens.” Poultry Science 67, no. 10 (October 1988): 1418–23. https://doi.org/10.3382/ps.0671418.

Hy-Line. “Mycotoxins: How to deal with the threat of mycotoxicosis.” Hy-Line International. Accessed July 29, 2024. https://www.hyline.com/.

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Kubena, L.F., R.B. Harvey, T.S. Edrington, and G.E. Rottinghaus. “Influence of Ochratoxin A and Diacetoxyscirpenol Singly and in Combination on Broiler Chickens.” Poultry Science 73, no. 3 (March 1994): 408–15. https://doi.org/10.3382/ps.0730408.

Kubena, L.F., R.B. Harvey, W.E. Huff, D.E. Corrier, T.D. Philipps, and G.E. Rottinghaus. “Influence of Ochratoxin A and T-2 Toxin Singly and in Combination on Broiler Chickens.” Poultry Science 68, no. 7 (July 1989): 867–72. https://doi.org/10.3382/ps.0680867.

Kubena, L.F., R.B. Harvey, W.E. Huff, D.E. Corrier, T.D. Phillips, and G.E. Rottinghaus. “Influence of Ochratoxin A and T-2 Toxin Singly and in Combination on Broiler Chickens.” Poultry Science 68, no. 7 (July 1989): 867–72. https://doi.org/10.3382/ps.0680867.

Kubena, L.F., W.E. Huff, R.B. Harvey, T.D. Phillips, and G.E. Rottinghaus. “Individual and Combined Toxicity of Deoxynivalenol and T-2 Toxin in Broiler Chicks.” Poultry Science 68, no. 5 (May 1989): 622–26. https://doi.org/10.3382/ps.0680622.

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Lutsky, Irving, Natan Mor, Boris Yagen, and Avraham Z. Joffe. “The Role of T-2 Toxin in Experimental Alimentary Toxic Aleukia: A Toxicity Study in Cats.” Toxicology and Applied Pharmacology 43, no. 1 (January 1978): 111–24. https://doi.org/10.1016/s0041-008x(78)80036-2.

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Osborne, D.J., W.E. Huff, P.B. Hamilton, and H.R. Burmeister. “Comparison of Ochratoxin, Aflatoxin, and T-2 Toxin for Their Effects on Selected Parameters Related to Digestion and Evidence for Specific Metabolism of Carotenoids in Chickens,” Poultry Science 61, no. 8 (August 1982): 1646–52. https://doi.org/10.3382/ps.0611646.

Pande, Vivek, Nitin Kurkure, and A.G. Bhandarkar. “Effect of T-2 Toxin on Growth, Performance and Haematobiochemical Alterations in Broilers .” Indian Journal of Experimental Biology 44, no. 1 (February 2006): 86–88.

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Riahi, Insaf, Virginie Marquis, Anna Maria Pérez-Vendrell, Joaquim Brufau, Enric Esteve-Garcia, and Antonio J. Ramos. “Effects of Deoxynivalenol-Contaminated Diets on Metabolic and Immunological Parameters in Broiler Chickens.” Animals 11, no. 1 (January 11, 2021): 147. https://doi.org/10.3390/ani11010147.

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Stack, Jim, and Mike Carlson. “Fumonisins in Corn.” DigitalCommons@University of Nebraska – Lincoln, 2003. https://core.ac.uk/download/pdf/188054556.pdf.

Szathmary, C.I. “Trichothecene Toxicoses and Natural Occurrence in Hungary.” Essay. In Ueno, Y: Developments in Food Science IV. Trichothecenes, 229–50. New York: Elsevier, 1983.

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Tyczkowski, Juliusz K., and Pat B. Hamilton. “Altered Metabolism of Carotenoids during Aflatoxicosis in Young Chickens,” Poultry Science 66, no. 7 (July 1987): 1184–88. https://doi.org/10.3382/ps.0661184.

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Yohannes, T., A. K. Sharma, S. D. Singh, and V. Sumi. “Experimental Haematobiochemical Alterations in Broiler Chickens Fed with T-2 Toxin and Co-Infected with IBV.” Open Journal of Veterinary Medicine 03, no. 05 (2013): 252–58. https://doi.org/10.4236/ojvm.2013.35040.

Part 3: Bone disorders and foot pad lesions

By Dr. Inge Heinzl, Editor, and Marisabel Caballero, Global Technical Manager Poultry

Bone health is essential for animals and humans. Besides giving structural support, allowing movement, and protecting vital organs, the bones release hormones that are crucial for mineral homeostasis and acid balance and serve as reservoirs of energy and minerals (Guntur & Rosen, 2012; Rath, N.C. & Durairaj, 2022; Suchacki et al., 2017).

Bone disorders and foot pad lesions are considerable challenges in poultry production, especially for fast-growing birds with high final weights. Due to pain, the animals do not move, and dominant, healthy birds may restrict lame birds’ access to feed and water. In consequence, these birds are often culled. Moreover, processing these birds is problematic, and often, they must be discarded or downgraded.

Foot pad lesions, another common issue in poultry production, can also have significant economic implications. On the one hand, pain restricts birds from eating and drinking and reduces weight gain. On the other hand, for many producers, chicken feet constitute a substantial part of the economic value of the bird; therefore, discarding them represents a significant financial loss. Additionally, to push poultry production in the right direction concerning animal health and welfare, a foot pad scoring system at the processing plant is in place in European countries.

Mycotoxins affect bones in different ways

Mycotoxins, depending on their target organs, can have diverse effects on the skeleton of birds. For example, mycotoxins that target the liver can disrupt calcium metabolism, which in turn affects the mineralization of the bones (rickets) and the impairment of chondrocytes can slow down bone growth (e.g., tibial dyschondroplasia). When the kidneys are impacted, urate clearance decreases, plasma uric acid consequently increases, and urate crystals form in the synovial fluid and tendon sheaths of various joints, particularly the hock joints. These examples highlight the complex and varied ways mycotoxins can impact poultry bone health.

Inadequate bone mineralization and strength – Rickets and layer cage fatigue

Sufficient bone mineralization is essential for the stability of the skeleton. Calcium (Ca), Vitamin D, and Phosphorous (P) deficiency leads to inadequate mineralization, weakens the bone, and can cause soft and bent bones or, in the case of layers, cage fatigue – a collapse of the spinal bone- and paralysis. Inadequate bone mineralization can be caused in different ways, among them:

1. Decrease in the availability of the nutrients necessary for mineralization. This can occur if the digestibility of these nutrients deteriorates
2. Impact on the Ca/P ratio—A ratio of 1 – 2:1 is vital for adequate bone development (Loughrill et al., 2016). Mycotoxins can alter absorption and transporters for one or both elements, altering their ratio.
3. Impact on the Vitamin D receptor, affecting its expression or the transporters for Ca and P.

Aflatoxins can impair bone mineralization by different modes of action. An important one is the impairment of the digestibility of Ca and P: Kermanshahi et al. (2007) fed broilers diets with high levels of aflatoxins (0.8 to 1.2 mg AFB1/kg feed) for three weeks, which resulted in a significant reduction of Ca and P digestibility. Other researchers, however, did not find an effect on Ca and P digestibility with lower aflatoxin levels:  Bai et al. (2014) feeding diets contaminated with 96 (starter) and 157 µg Aflatoxins (grower) per kg of feed to broilers and Han et al. (2008) saw no impact on cherry valley ducks with levels of 20 and 40 µg AFB1/kg diet.

Indirectly, a decrease in the availability of Ca and P due to aflatoxin-contaminated feed can be shown by blood or tibia levels of these minerals, as demonstrated by  Zhao et al. (2010): They conducted a trial with broilers, resulting in blood serum levels of Ca and P levels significantly (P<0.05) dropped with feed contaminated with 2 mg/kg of AFB1. Another trial conducted by Bai et al. (2014) showed decreased Ca in the tibia and reduced tibial break strength.

To get more information about the effect of mycotoxins on bone mineralization and the utilization of Ca, P, and Vit. D in animal organisms, Costanzo et al. (2015) challenged osteosarcoma cells with 5 and 50 ppb of aflatoxin B1. They asserted a significant down-modulation of the expression of the Vitamin D receptor. Furthermore, they assumed an interference of AFB1 with the actions of vitamin D on calcium-binding gene expression in the kidney and intestine.  Paneru et al. (2024) could confirm this downregulation of the Vit D receptor and additionally of the Ca and P transporters in broilers with levels of ≥75 ppb AFB1. They also saw a significant reduction in tibial bone ash content at AFB1 levels >230 ppb, a decreased trabecular bone mineral content and density at AFB1 520 ppb, and a reduced bone volume and tissue volume of the cortical bone of the femur at the level of 230 ppb (see Figure 1). They concluded that AFB1 levels of already 230 ppb contribute to bone health issues in broilers.

Figure 1: Increasing doses of AFB1 (<2 ppb – 560 ppb) deteriorate bone quality (Paneru, 2024): Cross-sectional images of femoral metaphysis with increasing AFB1 levels (left to right). The outer cortical bone is shown in light grey, and the inner trabecular bone in blue. Higher levels of AFB1 (T4 and T5) show a disruption of the trabecular bone pattern (less dense blue pattern with thinner and more fragmented bone strands and with wide spaces between the trabecular bone) (shown in white).

All experiments strongly suggest that aflatoxins harm bone homeostasis. Additional liver damage, oxidative stress, and impaired cellular processes can exacerbate bone health issues.

Trichothecenes also negatively impact bone mineralization. Depending on the mycotoxin, they may affect the gut, decreasing the absorption of Ca and P and probably provoking an imbalance in the Ca/P ratio.

For instance, when T-2 toxin was fed to Yangzhou goslings at 0.4, 0.6, and 0.8 mg/kg of diet, it decreased the Ca levels (halved at 0.8 mg/kg) and increased the P levels in the blood serum, so the Ca/P ratio decreased from the adequate ratio of 1 – 2 to 0.85, 0.66, and 0.59 (P<0.05) (Gu et al., 2023). The alterations of the Ca and P levels, the resulting decreasing Ca/P ratio, and an additional increase in alkaline phosphatase (ALP) suggest that T-2 toxin negatively impacts Ca absorption, increases ALP, and, therefore, disturbs calcification and bone development.

Other studies show that serum P levels decreased in broilers fed DON-contaminated feed with levels of only 2.5 mg/kg (Keçi et al., 2019). One reason for the lower P level is probably the lower dry matter intake, affecting Ca and P intake. Ca serum level is not typically reduced, which can be explained by the fact that Ca plays many critical physiological roles (e.g., nerve communication, blood coagulation, hormonal regulation), so the body keeps the blood levels by reducing bone mineralization. Another explanation is delivered by Li et al. (2020): After their trial with broilers, they stated that dietary P deficiency is more critical for bone development than Ca deficiency or Ca & P deficiency. The results of the trial conducted by Keçi et al. with DON (see above) were reduced bone mineralization, affected bone density, ash content, and ash density in the femur and tibiotarsus with a stronger impact on the tibiotarsus than on the femur.

In line with trichothecenes effects in Ca and P absorption, Ledoux et al. (1992) suppose that diarrhea caused by intake of fumonisins leads to malabsorption or maldigestion of vitamin D, calcium and phosphorus, having birds with rickets as a secondary effect.

Ochratoxin A (OTA) impairs kidney function, negatively affects vitamin D metabolism, reduces Ca absorption, and contributes to deteriorated bone strength (Devegowda and Ravikiran, 2009). Indications from Huff et al. (1980) show decreased tibia strength after feeding chickens OTA levels of 2, 4, and 8 µ/g, and Duff et al. (1987) report similar results also in turkey poults.

A further mycotoxin possibly contributing to leg weakness is cyclopiazonic acid produced by Aspergillus and Penicillium. This mycotoxin is known for leading to eggs with thin or visibly racked shells, indicating an impairment of calcium metabolism (Devegowda and Ravikiran, 2009). Tran et al. (2023) also showed this fact with multiple mycotoxins.

The co-occurrence of different mycotoxins in the feed – the standard in praxis – increases the risk of leg issues. A trial with broiler chickens conducted by Raju and Devegowda (2000) showed a bone ash-decreasing effect of AFB1 (300 µg/kg), OTA (2 mg/kg), and T-2 toxin (3 mg/kg), fed individually but an incomparable higher effect when fed in combination.

Impairment of bone growth – tibial dyschondroplasia (TD)

In TD, the development of long bones is impaired, and abnormal cartilage development occurs. It is frequent in broilers, with a higher incidence in males than females. It happens when the bone grows, as the soft cartilage tissue is not adequately replaced by hard bone tissue. Some mycotoxins have been related to this condition: According to Sokolović et al. (2008), actively dividing cells such as bone marrow are susceptible to T-2 toxin, including the tibial growth plates, which regulate chondrocyte formation, maturation, and turnover.

T-2 toxin: In a study with primary cultures of chicken tibial growth plate chondrocytes (GPCs) and three different concentrations of T-2 toxin (5, 50, and 500 nM), He et al. (2011) found that T-2 toxin decreased cell viability, alkaline phosphatase activity, and glutathione content (P < 0.05). Additionally, it increased the level of reactive oxygen species and malondialdehyde in a dose-dependent way, which could be partly recompensated by adding an antioxidant (N-acetyl-cysteine). They concluded that T-2 toxin inhibits the proliferation and differentiation of GPCs and contributes, therefore, to the development of TD, altering cellular homeostasis. Antioxidants may help to reduce these effects.

Gu et al. (2023) investigated the closely bodyweight-related shank length and the tibia development in Yangzhou goslings fed feed with six different levels (0 to 2.0 mg/kg) of T-2 toxin for 21 days. They determined a clear dose-dependent slowed tibial length and weight growth (p<0.05), as well as abnormal morphological structures in the tibial growth plate. As tibial growth and shank length are closely related to weight gain (Gu et al., 2023; Gao et al., 2010; Ukwu et al., 2014; Yu et al., 2022), their slowdown indicates lower growth performance.

Fumonisin B1 is also a potential cause of this kind of leg issue. Feeding 100 and 200 mg/kg to day-old turkey poults for 21 days led to the development of TD (Weibking et al., 1993). Possible explanations are the reduced viability of chondrocytes, as found by Chu et al. (1995) after 48 h of exposure, or the toxicity of FB1 to splenocytes and chondrocytes, which was shown in different primary cell cultures from chicken (Wu et al., 1995).

Bacterial chondronecrosis with osteomyelitis lameness (BCO) can be triggered by DON and FUM

BCO presents a highly critical health and welfare issue in broiler production worldwide, and it is estimated that 1-2 % of condemnations in birds at the marketing age result from this disease. What is the reason? Today’s fast-growing broilers are susceptible to stress. This enables pathogenic bacteria to compromise epithelial barriers, translocate from the gastrointestinal tract or the pulmonary system into the bloodstream, and colonize osteochondrotic microfractures in the growth plate of the long bone. This can lead to bone necrosis and subsequent lameness.

In their experiment with DON and FUM in broilers, Alharbi et al. (2024) showed that these mycotoxins reduce the gut’s barrier strength and trigger immunosuppressive effects. They used contaminations of 0.76, 1.04, 0.94, and 0.93 mg DON/kg of feed and 2.40, 3.40, 3.20, and 3.50 mg FUM/kg diet in the starter, grower, finisher, and withdrawal phases, respectively. The team observed lameness on day 35; the mycotoxin groups always showed a significantly (P<0.05) higher incidence of cumulative lameness.

The increase in uric acid leads to gout

In general, mycotoxins, which damage the kidneys and, therefore, impact the renal excretion of uric acid, are potentially a factor for gout appearance.

One of these mycotoxins is T-2 toxin. With the trial mentioned before (Yangzhou goslings, 21 days of exposure), Gu et al. (2023) showed that the highest dosage of the toxin (2.0 mg/kg) significantly increased uric acid in the blood (P<0.05), possibly leading to the deposit of uric acid crystals in the joints and to gout.

Huff et al. (1975) applied Ochratoxin to chicks at 0, 0.5, 1.0, 2.0, 4.0, and 8.0 µg/g of feed during the first three weeks of life. They found ochratoxin A as a severe nephrotoxin in young broilers as it caused damage to the kidneys with doses of 1.0 µg/g and higher. At 4.0 and 8.0 µg/g doses, uric acid increased by 38 and 48%, respectively (see Figure 2). Page et al. (1980) also reported increased uric acid after feeding 0.5 or 1.0 mg/kg of Ochratoxin A to adult white Leghorn chickens.

Figure 2: Effect of Ochratoxin A on plasma uric acid (mg/100 ml) (according to Huff et al., 1975)

Foot pad lesions – a further hint of mycotoxicosis

Foot pad lesions often result from wet litter, originating from diarrhea due to harmed gut integrity. Frequently, mycotoxins impact the intestinal tract and create ideal conditions for the proliferation of diarrhea-causing microorganisms and, therefore, secondary infections. Some also negatively impact the immune defense system, allowing pathogens to settle down or aggravate existing bacterial or viral parasitic diseases. In general, mycotoxins affect the physical (intestinal cell proliferation, cell viability, cell apoptosis), chemical (mucins, AMPs), immunological, and microbial barriers of the gut, as reported by Gao et al. (2020). Here are some examples of the adverse effects of mycotoxins leading to intestinal disorders and diarrhea:

• Mycotoxins can modulate intestinal epithelial integrity and the renewal and repair of epithelial cells, negatively impacting the intestinal barrier’s intrinsic components; for instance, DON can significantly reduce the transepithelial electrical resistance (TEER)(Grenier and Applegate, 2013). A higher permeability of the epithelium and a decreased absorption of dietary proteins can lead to higher protein in the digesta in the small intestine, which serves as a nutrient for pathogens including perfringens (Antonissen et al., 2014; Antonissen et al., 2015).
• The application of Ochratoxin A (3 mg/kg) increased the number of S. typhimurium in the duodenum and ceca of White Leghorn chickens (Fukata et al., 1996). Another trial with broiler chicks at a concentration of 2 mg/kg aggravated the symptoms due to an infection by S. gallinarum (Gupta et al., 2005).
• In a trial by Grenier et al., 2016, feed contaminated with DON (1.5 mg/kg), Fumonisin B (20 mg/kg), or both mycotoxins aggravated lesions caused by coccidia.
• DON impacts the mucus layer composition by downregulating the expression of the gene coding for MUC2, as shown in a trial with human goblet cells (Pinton et al., 2015). The mucus layer prevents pathogenic bacteria in the intestinal lumen from contacting the intestinal epithelium (McGuckin et al., 2011).
• Furthermore, DON and other mycotoxins decrease the populations of lactic acid-producing bacteria, indicating a shift in the microbial balance (Antonissen et al., 2016).
• FB1 causes intestinal disturbances such as diarrhea, although it is poorly absorbed in the intestine. According to Bouhet and Oswald (2007), the main toxicological effect ascertained in vivo and in vitro is the accumulation of sphingoid bases associated with the depletion of complex sphingolipids. This negative impact on the sphingolipid biosynthesis pathway could explain other adverse effects, such as reduced intestinal epithelial cell viability and proliferation, modification of cytokine production, and impairment of intestinal physical barrier function.
• T-2 toxin can disrupt the immune response, enhance the proliferation of coli in the gut, and increase its efflux (Zhang et al., 2022).

All these mycotoxins can cause foot pad lesions by impacting gut integrity or damaging the gut mucosa. They promote pathogenic organisms and, thus, provoke diarrhea and wet litter.

Mitigating the negative impact of mycotoxins on bones and feet is crucial for performance

Healthy bones and feet are essential for animal welfare and performance. Mycotoxins can be obstructive. Consequently, the first step to protecting your animals is to monitor their feed. If the analyses show the occurrence of mycotoxins at risky levels, proactive measures must be taken to mitigate the issues and ensure the health and productivity of your poultry.

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By Marisabel Caballero, Global Technical Manager Poultry

As the planet’s climate experiences changes, new patterns affect the microbial communities colonizing crops. Recently, several areas of the planet have experienced extreme temperatures, drought, changes in the humid/dry cycles, and an increase in atmospheric carbon dioxide (1,2). As a response, the fungi affecting the crops have shifted their geographical distribution, and with this, the pattern of mycotoxin occurrence also changed. For instance, in Europe, we are looking at higher frequencies and levels of Aflatoxins (AF), Ochratoxins (OT), and Fumonisins (FUM) than ten or even five years ago (2-4).

This affects animal production, as mycotoxin challenges show increased frequency, quantity, and variety. Mainly long-living animals, such as laying hens and breeders, can have a higher risk. Moreover, mycotoxins can also be carried over to the eggs, potentially risking human health in the case of layers (table eggs) and in the case of breeder hens, hatchery performance and day-old chick (DOC) quality.

Laying hens and breeders: carryover of mycotoxins into eggs

Most mycotoxins are absorbed in the proximal part of the gastrointestinal tract (Table 1). This absorption can be high, as in the case of aflatoxins (~90%), but also very limited, as in the case of fumonisins (<1%), with a significant portion of unabsorbed toxins remaining within the lumen of the gastrointestinal tract (5).

Once mycotoxins are ingested, detoxification and excretion processes are started by the body, and at the same time, organ damage ensues. The detoxification of mycotoxins is mainly carried out by the liver (6), and their accumulation happens primarily in the liver and kidneys. However, accumulation in other tissues, such as the reproductive organs and muscles, has also been found (7-9). The detoxification process’ objective is the final excretion of the toxins, which occurs through urine, feces, and bile; often, the toxins can also reach the eggs (7-20).

Table 1: mycotoxin absorption rates for poultry and their carry-over rate into eggs

(Adapted from 5, 7-17, 19-21)

Table 1 shows carry-over rates of mycotoxins into eggs, resulting from diverse studies (7-10, 14, 16, 19). However, the same studies indicate that results can vary broadly due to different factors, as reviewed by Völkel and collaborators (26). This variability is related to the amount and source of contamination, way of application, period, and the possible co-occurrence of various mycotoxins or several metabolites. Other factors to consider are animal-related, such as species, breed, sex, age group, production level, and health status. Environmental and management factors can play a role in carry-over rates, and finally, detection limits and analytical procedures also influence these results. In summary, highly varying carry-over has been demonstrated, and the risk needs to be considered when animals are exposed.

Mycotoxins in breeder’s feed impact hatchery performance and day-old chick quality

When hens are exposed to mycotoxins, their effects on the intestine, liver, and kidney decrease egg production and quality (10, 14, 27), and, in the case of breeders, consequently, affect hatchery performance, DOC production, and DOC quality (28-30). The main effects of mycotoxins, when we speak about DOC production, are exerted in the gastrointestinal tract, the liver, and the kidneys, affecting embryos and young chicks:

• Intestine and kidneys: Mycotoxins harm the intestinal epithelium and have nephrotoxic effects, affecting calcium and vitamin D3 absorption and metabolism, necessary for eggshell quality (31). Thin and fragile shells can increase embryonic mortality, lower embryonic weight gain, and hinder hatchability (32).
• Liver: The liver plays a central role in egg production as it is responsible for vitamin D3 metabolism, the production of nutrient transporters, and the synthesis of the lipids that make up the yolk. Thus, when liver function is impaired, the internal and external quality of the egg declines, which affects DOC production (31-34).
• Embryo and young chicks: Studies (33-38) have found how mycotoxins affect the embryos. In general, there are two possibilities: the direct one, when the mycotoxin is transferred into the egg, and the indirect one, when the mycotoxin impacts egg quality and, therefore, leads to disease or death of the embryo. The result is a higher embryonic mortality or lower DOC quality. These, among others, result from the lower transfer of antioxidants and antibodies from the hen, low viability of the chick’s immune cells, and higher bacterial contamination. A lower relative weight of the bursa of Fabricio and the thymus is often found.

Qreshi’s team (29) studied the effects on the progeny of broiler breeders consuming feed highly contaminated with AFB1, finding suppression in antibody production and macrophage function in chicks after ten days. Similar results were found by other researchers (36, 37) evaluating the effects of AF and OTA as single and combined contamination. When both mycotoxins are present in the feed, the effect on hatchability and DOC quality are synergistic.

Due to mycotoxin contamination, the reproduction and immune response are impaired, resulting in decreased DOC production and increased early chick mortality, as they are more susceptible to bacterial and viral infections.

Mycotoxins impair table egg production and quality

Studies (22-24) have found mycotoxin contamination in commercial table eggs. A meta-analysis of mycotoxins’ concentration based on 11 published papers was completed recently (22): counting with data from 9509 samples, the meta-analysis reveals an overall presence of mycotoxins in 30% of the samples, being Beauvericin in the first place, followed by DON as well as AF and OTA in third and fourth place, respectively. The risk for humans depends on the intake of contaminated foods in terms of amount and frequency (25), and so far, it has not been estimated in most parts of the world.

Natural contamination in laying hens: a case report

Giancarlo Bozzo’s team (39) reported and published a veterinary case regarding natural mycotoxin contamination in commercial egg production: up to week 47 of age, production parameters were on top of the genetic standards. However, a drop in egg production started at around week 47, and at week 50, egg production was only 68% (figure 1).

Figure 1: production of laying hens fed naturally contaminated feed with AFB1 and OTA

The house with the reduced performance received feed with linseed. In other houses of the same complex, which did not include linseed in the feed, production was unaffected. Therefore, this raw material was considered a possible cause of the issue. Linseed was removed from the formula, and three weeks after (53 weeks of age), egg production was at 84%. Afterward, linseed got back into the formulation, and the laying rate dropped again to 70% (week 56), this time accompanied by a significant increase in mortality.

Samples were collected at week 56, and AFB1 and OTA were detected in feed and the kidneys and livers of the hens consuming it (table 2). While the levels in the feed were not considered high risk, evidence from necropsy and histopathology suggested either a higher or a prolonged exposure; a synergistic effect of both mycotoxins on hen’s health and productivity can be inferred.

Table 2: mycotoxin analysis results for feed and organs

The liver and kidneys were enlarged and showed signs of damage. Furthermore, urate crystals in the peritoneum and the abdominal air sac were observed, indicating renal failure. This limited the excretion of both toxins in the urine, increasing their half-life in the organism and enhancing the effects in target organs, contributing to the synergistic effect observed.

After using mycotoxin-free certified linseed, the problem receded. Though this is the best option to keep animals healthy and productive, it may not be practical in the long term due to the ubiquitous nature of the toxins and the cost and availability constraints of feed raw materials. Moreover, the mycotoxin levels present in the feed were relatively low and fell under recommended guidelines. For these reasons, in-feed toxin mitigation solutions must also be considered to reduce exposure for production animals.

In-feed intervention mitigates the effects of intermittent exposure to multiple mycotoxins

EW Nutrition conducted a study with Hy-Line W-36 layer-breeders intercalating three 10-day cycles of feed with 100ppb AFB1 + 100ppb OTA, with two 21-day cycles of non-challenged feed. An in-feed intervention (Solis Max 2.0, displayed as IFI) containing bentonite, yeast cell wall components, and a mixture of phytogenic components mitigated all effects.

Table 3: experimental groups and mycotoxin challenge

Trial design:

A total of 576 hens (18 replicates per diet, 8 hens each) and 58 roosters were randomly assigned to four diets at 28 weeks of age, as shown in Table 3. The 72-day experimental period included alternating 10-day challenge and 21-day non-challenge intervals (Figure 2). During the challenge intervals, the breeders in T-3 and T-4 were fed the mycotoxin-contaminated feed with and without the IFI.

Figure 2: trial timeline showing challenge and non-challenge intervals and days of data collection and sampling.

Mitigated effects on egg production and egg quality

The challenge decreased overall egg production (Figure 3), egg mass, and shell thickness (Table 4). The first challenge interval did not affect production, but days later, from the first non-challenge period, all parameters were lower for the challenged group.

Different letters indicate significant differences (p<0.05). Statistical tendencies (p<0.1) are indicated by (*).

Figure 3: Egg production of hens intermittently challenged with AFB1 and OTA, with and without in-feed Solis Max

The adverse effects on productivity and egg quality started after the first challenged feed was withdrawn and persisted through the following intervals until the end of the experiment. Similar effects in chronic mycotoxin challenges have been previously found (37, 39).

Table 4: Average egg quality parameters of hens intermittently challenged with AFB1+OTA, with and without an in-feed intervention (IFI)

Different letters indicate significant differences (p<0.05). Statistical tendencies (p<0.1) are indicated by (*).

Mitigated effects on the progeny in incubation trials

Three incubation trials were performed: after the first challenge and non-challenge interval and at the end of the trial period after the third challenge interval. A significant decrease in fertility and hatchability was observed for the challenged group in all incubation trials. As mycotoxins affect egg quality (22-24) and can be transferred to the eggs (10, 14, 27), the effects were also shown in the case of hatchability and offspring performance. Fertility was affected from the first challenge interval onwards, continuing to be low for the challenge group until the end of the trial. However, the hatchability of fertile eggs dropped after the withdrawal of the contaminated feed and showed the lowest value during the third challenge interval.

The in-feed supplementation of Solis Max 2.0 (IFI) resulted in the consistent recovery of egg production and egg quality throughout the whole experimental period, achieving the same levels of productivity as the non-challenged control.

Figure 4: Hatchery parameters of eggs from breeders intermittently challenged with AFB1 and OTA, with and without an in-feed intervention (IFI).

Results in hatch of fertile can be related to egg quality, as the thickness of the eggshell influences the egg’s moisture loss and exchange with the environment during the incubation period. Thinner eggshells lead to higher embryo mortality (31, 32). The group having the challenge with Solis Max showed the same performance as the non-challenged control regarding hatchery performance.

Day-old chick weight was not affected. However, weight gain and mortality after ten days were hindered for the chicks from breeders taking the mycotoxin-contaminated feed (Table 5).

Table 5: Average day- and 10-day-old chick parameters from hens intermittently challenged with AFB1+OTA, with and without an in-feed intervention (IFI)

Letters indicate significant differences (p<0.05). Statistical tendencies (p<0.1) indicated by (*)

At the end of the experiment, oxidative stress biomarkers were measured in the blood serum of 15 hens per treatment, showing significantly lower GPx, and SOD (figure 5) in the challenged group, which indicates a depletion of the mechanisms to fight oxidative stress (40), the hens taking the in-feed product did not show this depletion.

Figure 5: Antioxidants in blood serum, glutathione peroxidase (GPx), and superoxide dismutase (SOD) from breeders intermittently challenged with AFB1 and OTA, with and without an in-feed intervention (IFI).

Intermittent exposure to AFB1 and OTA negatively affected layer breeder productivity, egg quality, and hatchability and promoted oxidative stress in the birds. Intermittent mycotoxin challenges may affect animals even after the contamination is withdrawn. In-feed interventions showed effectiveness in mitigating these effects.

Climate changes bring new mycotoxin challenges – the right in-feed solutions can help

Today’s mycotoxin scenario shows increased frequency, quantity, and variety. Mainly long-living animals, such as laying hens and breeders, can be at more risk. Additionally, the contamination can be carried over to the eggs, potentially risking human health in the case of table eggs and hatchery performance and DOC quality in the case of breeders.

From case reports, we learn the consequences of real challenges and struggles in commercial production; from scientific trials based on possible commercial situations, we realize the advantages of interventions designed to tackle those challenges.

References

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Conference report

In the Poultry Academy held by EW Nutrition in the fall of last year, Judy Robberts, Technical Service Manager, Aviagen, explained that the success of a breeder flock depends on producing good quality hatching eggs with high hatchability and delivering first quality chicks. With this in mind, we have to ask two essential questions: What impact does the breeder farm have on chick quality? And What are the most overlooked areas for breeders?

Nest box hygiene

Nest box hygiene is key to good quality hatching eggs. Shortly after egg deposition, the eggshell is moist, and the cuticle is not yet an effective protection. In addition, during this period the egg is cooling down from the hen’s body temperature (41°C) to house temperature. Due to this process of cooling down, the content of the egg contracts and a vacuum is created in the egg. In compensation, air enters and forms the air cell. Together with this air, bacteria can easily penetrate the egg. For this reason, it is very important that only hatching eggs are used which have been laid in a clean nest.

Maintaining a hygienic nest environment with routine cleaning of the nest mat or frequently replacing the bedding material will reduce the risk of bacterial contamination.

Clean nests and nesting equipment are essential to avoiding contamination.

Egg collection and pick-up schedule

Collect nest eggs a minimum of 4 times a day, more frequently in hot weather, as eggs cannot cool down sufficiently in the house to interrupt embryonic development. Adjust the exact timing so that no more than 30% (any more will increase the incidence of cracked eggs) of the eggs fall in any one collection. When determining collection times, it is important to remember:

• The majority of eggs will be laid in the morning, and collection intervals should be managed accordingly.
• Eggs left in the nest or on belts longer than recommended will have an increased incidence of being cracked or soiled.
• Transition points on belts need to be smooth so eggs don’t pile up and bump into each other.
• Never leave eggs overnight in the nests or belts.
• Eggs left in conventional nests are subject to toe pecks or soiling from other hens.
• Floor eggs (eggs that were laid outside of the breeder flock’s next boxes) should be collected more often than nest eggs.

It is not advisable to collect eggs in cardboard egg trays/flats, as the fiber material absorbs egg heat, and it takes longer for them to cool down. Because the fiber trays are porous, they can also harbor unwanted organisms/bacteria/fungi and attract vermin.

Ideally hatching eggs should weigh a minimum of 50 g from a flock at least 22 weeks of age. Smaller eggs from younger flocks may be used, however, chick size and early livability will not be optimum. Remember that a chick will yield approximately 68% of the egg size. Therefore, a small egg will produce a small chick.

Egg cleanliness

Always wash hands after collecting floor eggs and before each collection of nest eggs. Floor eggs should not be placed in the nest box – even if they appear clean. Washing floor and dirty eggs removes the eggs protective coating. Always remember, a washed egg is still a dirty egg, but a clean egg is one that was never dirty.

Eggs should be treated with chemical-based antimicrobials, as scraping, rubbing, or washing the eggshell will damage the cuticle and remove the physical and antimicrobial barrier. Since the eggshell permeability increases after 24 hours and makes the eggs more susceptible to bacterial invasion, eggs should be sanitized as soon as possible. The most popular method is fogging as it is safe, the fog reaches all the eggs and the eggs do not get wet.

Floor eggs are not hatching eggs

The hatchery cannot fix mistakes from the breeder farm. Therefore, it is NOT recommended to set floor eggs – eggs that were laid outside of the breeder flock’s next boxes. Floor eggs have a higher bacterial load than nest eggs and consequently lower hatchability. They are also potential ‘bangers, or exploders’ and can cross-contaminate other eggs, especially in the same incubator.

Selection of floor eggs must be done at the farm, so that a dirty egg never enters the hatchery. Where strictly necessary, set floor or dirty eggs only if the disadvantages of setting these eggs are fully understood and accepted by the hatchery. If floor eggs are used for hatching, they should be clearly marked and stored separately from the nest eggs so that the hatchery can manage the contamination risk appropriately.

Floor eggs have a significantly higher risk of microbial contamination that will reduce hatch and chick quality.

Egg hygiene – bacterial contamination

Monitor the number of floor eggs and adjust management practices to minimize them. Floor eggs are a problem that should be tackled at the breeder level, with good breeder management and suitable housing equipment. If levels of floor eggs exceed 2-3% across the life of the flock, there is a problem. Floor eggs will be much higher at the start of production, but by peak production should be down to 1-2%.

Cracked eggs

Eggs with cracks are more likely to become infected and have low hatchability and poor chick quality.

Influence of eggshell crack types on hatchability and chick quality

Khabisi et al., 2011  ^a-c Means within a column without a common superscript differ significantly (p ≤ 0.05)

Do not set cracked eggs. Record the number of eggs with cracks, and if the frequency is unsatisfactory, investigate and eliminate possible causes.

On-farm egg storage rooms

Don’t forget that storage starts from the time of laying, not the time of receival at the hatchery.

Eggs need to be cooled below 24^oC (threshold temperature or physiological zero) as soon as possible to stop cellular growth of the embryo, until the egg is set at the hatchery. This minimizes embryo mortality, maximizes hatchability and helps to ensure chick quality. Eggs should be stored within 4 hours after collection.

On breeder farms, eggs are usually stored until being transported to the hatchery. The storage duration depends on the egg room capacity, supply of hatching eggs, hatchery capacity, and demand for day-old chicks. Don’t forget that storage starts from the time of laying, not the time of receival at the hatchery.

If the farm has an environmentally controlled egg storage room, eggs can be collected by the hatchery at least twice a week. If the farm has no dedicated egg storage room, eggs must be transported to the hatchery daily. Uncontrolled fluctuations in egg storage temperatures will cause stop-start growth of the germinal disc, which will reduce hatchability.

The temperature of the farm egg storage room should higher than the egg transport truck and the egg transport truck temperature should be higher than the hatchery egg storage room. This consistent decrease in temperature is to prevent condensation (also referred to as sweating) on the eggs. Condensation on the eggshell impairs the natural mechanisms of defense and provide an ideal environment for bacteria grow, penetrate the shell, and contaminate the egg. Condensation on eggs is more common in hot and humid climates common throughout Asia.

Egg storage rooms are important, yet they are frequently overlooked. Areas to consider include:

• Consistent temperature 24/7 (insulation will minimize variation),
• Temperature alarm system – set for a maximum temperature of 21°C and a minimum of 16-18 °C,
• Temperature and humidity sensor placement – don’t place in a direct line of temperature or humidity sources as this will lead to false readings,
• Do not place sensors against walls,
• Sensor accuracy (loggers are recommended),
• Fans to evenly distribute air,
• Do not place eggs directly against the wall or on the floor in the storage room to maximize air circulation and to ensure uniform conditions, and
• Avoid direct air flow onto eggs from fans, room coolers and/or humidifiers, as this can increase moisture loss and cause temperature variation throughout the room.

The farm is the starting point to ensure chick quality. Attention to detail and hygiene throughout the whole process is critical. Through monitoring and auditing, areas with deficiencies can be identified and corrected to continue producing high quality hatching eggs.

Conference report

At EW Nutrition’s Poultry Academy in the fall of last year, Judy Robberts, Technical Service Manager, Aviagen discussed the impact of the hatchery on chick quality. The transportation and storage of hatching eggs, preventative maintenance, and day-old chick transport all play an essential role. If mismanaged, these areas can negate the benefits of money spent and improvements made at the breeder farm or even in the hatchery itself.

Egg transport from breeder farm to hatchery

The transportation of hatching eggs from the breeder farm to the hatchery is critical: clean and disinfect the truck prior to use, to prevent pathogen spread, and only use a truck that is dedicated to transport hatching eggs. Always transport eggs small end down to avoid loose air cells.

The temperature of the farm egg storage room should higher than the egg transport truck. This decrease in temperature is to prevent condensation (also referred to as sweating) on the eggs. Condensation on the eggshell impairs the natural mechanisms of defense and provide an ideal environment for bacteria grow, penetrate the shell, and contaminate the egg. Condensation on eggs is more common in hot and humid climates common throughout Asia. Even when on-farm egg storage and truck temperatures are equal, sweating can still occur during loading and unloading, especially on warm and humid days. In such a case, a higher on-farm storage temperature of 23°C instead of the generally recommended 18-20°C can be considered.

Avoid sudden temperature changes. Use temperature loggers during transport to record any temperature fluctuations. Take internal egg temperatures at different locations within each batch received at the hatchery, to check temperature conditions during transport. The relative humidity of the truck should be set at 65-70%.

Egg storage at the hatchery

Don’t forget that storage starts from the time of laying, not the time of receival at the hatchery. Egg storage rooms are important, yet they are frequently overlooked. Areas to consider include:

• Consistent temperature 24/7 (insulation and fans will minimize variation),
• Avoid condensation,
• Do not place eggs directly against the wall or on the floor in the storage room, to maximize air circulation and to ensure uniform conditions,
• Alarm systems – set for a maximum temperature of 21°C and a minimum of 16-18°C,
• Sensor accuracy (loggers are recommended), and
• Sensor placement – don’t place in a direct line of temperature or humidity sources as this will lead to false readings. Similarly, allow for air circulation, do not place sensors against walls.

Temperature and storage time

“The holding temperature should be based on storage time,” advised Ms Robberts. Eggs which are set within 4 days of lay don’t need to be kept at a temperature below 20°C; in this case 21–22°C is regarded as optimal. This relatively high temperature promotes the thinning of the albumen, which improves the gas exchange during early incubation. On the other hand, it is low enough to maintain the vitality of the embryo. Best hatches result from eggs 3–7 days of age. Storage for longer than 7 days will require cooler temperatures to help reduce the loss of hatch due to embryo cell death and decline in internal egg quality. If the storage period is less than 7 days a storage temperature of 16-18°C is advised and if the storage period is longer, a temperature of 10-12°C is mostly recommended. The eggs of young breeder flocks are better suited for prolonged storage periods than eggs of older breeder flocks, as albumen quality in eggs of younger breeder flocks is higher.

Differences in temperature will result in the eggs reaching incubation temperature at different times and, therefore, hatching at different times, increasing the hatch window.

Relative humidity

The egg storage room should have a relative humidity of 70-80% to prevent egg dehydration and to maintain internal egg quality. The humidity should be a fine mist, so the eggs do not get wet. Humidifiers should be maintained and cleaned regularly. Dirty humidifiers can be a significant source of bacteria and lead to egg contamination. Follow the same guidelines for trolley placement, spacing, and air circulation in the hatching storage room as the farm egg storage room. Likewise, the same recommendations apply for thermometer monitoring and placement.

Don’t forget the maintenance

Maintenance is often reactive, not preventative – things are only fixed when they break down. This can compromise hatchability and chick quality. A few things to consider when setting up a maintenance plan are:

• Have a dedicated person responsible for maintenance reporting to the hatchery manager,
• Produce a list of all the equipment to be maintained including frequencies,
• Keep records on all performed maintenance,
• Maintenance includes calibration of equipment,
• Keep track of spare parts on hand, and
• Include the building structure and ancillary equipment in the program.

Day-old chick transport

Transport cannot improve the quality of the day-old chick, but it can certainly harm the chick’s welfare, growth, development and performance.

If chicks are transported outside their thermoneutral zone (32-35^oC) they will start using up the nutrients from the yolk sac at a much faster rate to maintain their core temperature (40-41°C) . A core temperature above 41°C post-hatch will lead to panting resulting to water loss with the risk of dehydration and below 39.5°C will lead to reduced activity and low feed consumption. Adjust the number of chicks per box if optimal temperature inside the chick boxes cannot be achieved due to limitations in transport equipment.

Optimizing transport conditions for day-old chicks from hatchery to farm for is beneficial for subsequent performance.

Conclusion

The modern hatchery is a major investment, so it just makes sense to pay attention to detail to maintain hatching egg quality and produce high-quality chicks. Factors such as egg storage conditions, play a significant role in achieving maximum hatchability. Through monitoring and auditing, areas with deficiencies can be identified and corrected to continue producing high quality hatching eggs. The transport of day–old chicks from should ensure that the birds arrive at the farm in the same condition in which they left the hatchery.

By Han Zhanqiang, Poultry Technical Manager, EWN China

Poultry meat accounts for more than one-third of global meat production. With increasing demand levels, the industry faces several challenges. Among them is the continuous supply of day-old chicks, which is affected by various issues. Mitigation strategies should be taken to ensure the supply of good quality day-old chicks to production farms.

Fast-growing broilers versus fit breeders

The poultry industry is challenged by the broiler-breeder paradox: on the one hand, fast-growing broilers are desirable for meat production. On the other hand, the parents of these broilers have the same genetic traits, but in order to be fit for reproduction, their body weight should be controlled. Thus, feed restriction programs, considering breeder nutritional requirements, are necessary to achieve breed standards for weight, uniformity, body structure, and reproductive system development, determining the success of day-old chick production.

Mycotoxins affect breeder productivity

During the rearing period, gut health problems such as coccidiosis, necrotic enteritis, and dysbiosis affect flocks. Also during the laying period, breeder flocks are also susceptible to disturbances in gut health, especially during stressful periods, leading to reduced egg production and an increase in off-spec eggs. One measure to restrain these challenges is the strict quality control of the feed. In this context, contamination with mycotoxins is an important topic. However, due to the nature of fungal contamination and limitations of sampling procedures, mycotoxins may not be detected or may be present at levels considered low and not risky.

Existing studies on mycotoxins in breeders indicate that mycotoxins can cause varying degrees of reduction in egg production and hatchability and are also associated with increased embryonic mortality. Recent studies have shown that low levels of mycotoxins interact with other stressors and may lead to reduced productivity. These losses are often mistaken for normal breeder lot variation. However, they cause economic losses far greater than normal flock-to-flock variability.

Mycotoxins impair the functionality of the gut

Low mycotoxin levels affect gut health. Individually and in combinations, mycotoxins such as DON, FUM, and T2 can impact gut functions such as digestion, absorption, permeability, immunity, and microbial balance. This is critical in feed-restricted flocks because it decreases body weight and uniformity, and in laying animals, egg production and egg quality can be reduced. Absorption of calcium and vitamin D3, which are critical for eggshell formation, depends on gut integrity and the efficiency of digestion and absorption. These factors can be adversely affected by even low mycotoxin levels: eggshells can become thin and brittle, thereby reducing hatching eggs and increasing early embryo mortality.

Prevention is the key to success in day-old chick production, therefore:

• avoid the use of raw materials with known mycotoxin contamination.
• use feed additives prophylactically, especially with anti-mycotoxin and antioxidant properties.

Prevention is an alternative approach to assure health and productivity in -many times unknown- mycotoxin challenges.

Figure 1: Effect of mycotoxins on eggshell quality and embryo death (Caballero, 2020)

University trial shows anti-mycotoxin product improving performance

A recent study by the University of Zagreb confirmed that long-term (13 weeks) exposure to feed contaminated with mycotoxins has an impact on egg production performance – a challenge that could be counteracted by using an anti-mycotoxin product.

The negative control (NC) was offered feed without mycotoxins. In contrast, the challenged control (CC), as well as a third group, received feed contaminated with 200ppb of T2, 100ppb of DON, and 2500ppb of FMB1. To the feed of the third group, an anti-mycotoxin feed additive (Mastersorb Gold, EW Nutrition) was given on top (CC+MG).

Figure 2: Influence of mycotoxins on feed intake and the effect of the anti-mycotoxin product Mastersorb Gold

Figure 3: The effect of mycotoxins on the cumulative number of eggs and the compensating effect of Mastersorb Gold

Figure 4: The impact of mycotoxins on the cumulative egg mass and the countereffect of Mastersorb Gold

As expected, the contaminated feed reduced feed intake, egg production, and egg weight (Fig. 2-4). Moreover, the liver and gut were affected which was evidenced in histopathological lesion scores of the organs: the control group had the lowest score, followed by the group fed Mastersorb Gold. The challenged group without any anti-mycotoxin product scored the highest.

Breeders are susceptible to mycotoxins and need our support

Broiler breeders and day-old chick production can be affected by long-term exposure to mycotoxins, which often exceeds the tolerance range of average flocks. To reduce or even prevent the potential impact of mycotoxins, a comprehensive management strategy is crucial. This includes responsible raw material procurement, storage, and feed processing leading to high feed quality, and the consideration of breeders’ nutrient demands. The inclusion of highly effective products to manage mycotoxin risk is an additional tool to maintain breeder performance.

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

Careful management of the breeders is a must to get their best reproductive efficiency. In today’s hatching egg production, factors such as stress, inflammation, body weight, and altered mating behavior lead to decreased performance, meaning fewer hatchable eggs and, therefore, fewer day-old chicks per hen (Grandhaye, 2020). The use of antibiotics to increase performance in farm animals is no longer allowed in many countries, and, since it may lead to the development of resistance, it is also not recommended. So, also in breeders, alternatives are requested to maintain animal health, welfare, and a high level of performance. 

Optimal gut health is the cornerstone for breeder performance 

As the organ responsible for digestion of the incoming feed, the absorption of nutrients, and the defense of the organism against pathogens or toxins, a healthy gut is a pre-condition for optimal performance (Shini and Bryden, 2021). A healthy gut, according to Bailey (2018), has optimally developed gut tissues, a well-functioning gut immune system, and well-balanced gut microbiota. It shows efficient functionality in terms of digestion and absorption and protects the organism against harmful agents. 

The gut directly or indirectly provides the elements for egg production 

Efficient feed digestion and absorption of nutrients are essential for the breeder hen to obtain the “material” for maintenance, growth, and egg production. Gut health is crucial since dysbacteriosis and diarrhea, characteristics of gut health challenges, increase dirty eggs, creating favorable conditions for pathogens to enter the egg and infect the embryo. 

Egg yolks consist of water (70%), proteins (10%), and lipids (20%). The yolk lipids are lipoproteins rich in triglycerides, built up in the liver and transported to the ovary. Cholesterol carried via lipoproteins to the egg yolk is also built up there, thus showing the importance of the liver in egg production. The gut plays a crucial role in protecting the liver from damage, constituting a barrier against harmful pathogens and toxins, potentially passing into the bloodstream and reaching this vital organ.  

Phytomolecules support performance in different ways 

Phytomolecules, are an excellent tool to support gut health and animal performance. Phytomolecules are plant-derived secondary metabolites that exert insect-attracting or defensive functions in the plant. They are used in their natural but also nature-identical forms in humans and animals to exert their digestive, immune-modulating, antimicrobial effects. 

Phytomolecules support gut health by balancing the gut microbiome 

Diverse examples can be found in the scientific literature, where phytomolecules improve the gut microbiome, resulting in better performance of layer and breeder hens. This support happens in two ways: 

1. Promoting beneficial bacteria

   Rabelo-Ruiz and co-workers (2021), asserted that adding garlic and onion extracts to the diet of layers led to more eggs with a bigger size, accompanied by an increase in Lactococci in the ileum and Lactobacilli in the cecum. Another example is provided by Park et al. (2016). When supplementing the diet of layers with a fermented phytogenic feed additive, egg production and weight raised with increasing dosage of the additive, and a higher number of Lactobacilli could be observed in the cecum.  
   Phytomolecules can promote the growth of certain beneficial bacteria and therefore act like prebiotics. As these changes took place in the lower gut, they assumed an improved digestibility of the feed. 

2. Lowering pathogenic bacteria

   In the study by Park et al. (2016) and in an in vitro study by Ghazanfari et al. (2019), E. coli in the cecum was reduced.  

   According to Burt (2007b), several essential oils / phytomolecules, amongst them, carvacrol, thymol, eugenol, and cinnamaldehyde, are effective against pathogens such as Listeria, Salmonella, E. coli, Shigella, and Staphylococcus. The hydrophobic essential oils can partition the lipids of the cell membranes. The resulting permeability of the membrane enables the leakage of cell content.  

3. Changing virulence factors

   Another mode of action is the change of virulence factors. Carvacrol, e.g., is known to decrease the motility of Campylobacter jejuni (Van Alphen et al., 2012); oregano and thyme oil reduced the motility of E. coli by inhibiting the synthesis of flagellin (Burt, 2007a). Vidanarachchi et al. (2005) mentioned that the hydrophobicity of microbes increases when some plant extracts are present, affecting their virulence characteristics. Also, the inhibition of defense measures such as efflux pumps in Gram-negative bacteria has been researched (Savoia, 2012). 

Phytomolecules support gut health by improving digestion 

For many years, phytomolecules have been studied and known for their digestive characteristics. In poultry and other animals, they influence feed digestion in two main ways. 

1. Stimulating enzyme secretion

   Platel and Srinivasan (2004) described different spices promoting not only the salivary flow, gastric juice and bile secretion but also the stimulation of the activity of enzymes such as pancreatic lipase, amylase, and proteases in rats. Hashemipour et al. (2013) saw the same effect in broilers supplemented with carvacrol and thymol in the diet. Research has also concluded on a higher nutrient digestibility:  Hernandez et al. (2004) and Basmacioğlu Malayoğlu, 2010 noticed that supplementing plant extracts or essential oils improved apparent whole-tract and ileal digestibility of different nutrients.). 

2. Maintaining gut integrity and enlarging the digestion area

   An intact gut with a large area for digestion guarantees optimal utilization of nutrients. Different researchers found that adding plant extracts or essential oils (Khalaji et al., 2011; Ghazanfari et al., 2015; Chowdhury et al., 2018) promotes intestinal gut morphology, reflected in higher villi and deeper crypts, which might lead to higher nutrient absorption.

   Concerning gut integrity, thymol and carvacrol showed protecting effects and mitigated gut lesions in broilers challenged with C. perfringens (Du et al., 2016). Probably, the lower pathogenic pressure due to the antimicrobial activity of phytogenic substances leads to minor damage to the gut wall and, in the end, to better absorption of the nutrients.  

Phytomolecules mitigate the effects of stress 

Environmental stress in breeders may decrease performance: the heat-stress-induced disruption of the tight junctions often leads to higher gut permeability, poor nutrient absorption, and higher electrolyte and water secretion (Abdelli, 2021). Sahin et al. (2010) achieved a linear improvement in egg production in quails when applying two doses of green tea catechin.  

Cold-stressed layers also reacted positively to supplementation of oregano essential oil, improving egg production compared to a non-supplemented control (Migliorini, 2019). 

Positive influence of phytomolecules results in higher performance 

As described, phytomolecules improve gut health and support the animal in multiply ways, allowing better utilization of resources for growth and production. Literature provides many articles showing the promoting effects of these substances on the performance of layers or breeders, some of them summarized in Table 1.  

Table 1: Benefits of phytomolecules in layers and breeders 

In-feed and in-water phytomolecules-based products show efficacy 

Much of the research done with phytomolecules focuses on essential oils (with variable inclusions of the active compounds or on single plant extracts. EW Nutrition is a research-driven company proposing phytomolecule-based solutions for the animal production industry. These products combine selected, synergistically acting phytomolecules to achieve optimal results.   

EW Nutrition has tested the combined use of  

• a microencapsulated blend of phytomolecules (Activo) for the feed and designed to maintain a good gut-health status during the whole life-cycle of the breeders, and  

• Activo Liquid, a liquid combination of phytomolecules and organic acids, which is conveniently applied on the farm via the waterline.  

1. Trial documents phytomolecules positively influencing microflora 

A trial conducted at the University of Central Queensland (Australia) showed that phytomolecules enhance beneficial bacteria such as Lactobacilli and, on the other hand, repress harmful bacteria such as Clostridium perfringens.  

For the trial, caecal microbiota of layers was used. They were grown with and without Activo Liquid in vitro, and the changes in microbiota were monitored. 

Result: The in vitro study clearly shows that Activo Liquid increases the number of lactobacilli and decreases clostridia and Enterococcus sp.  

Figure 1: Shifting intestinal balance with phytomolecules 

2.Three field trials with Activo Liquid showed an increased laying rate in breeders

 Many operations started testing phytomolecules in a farm-application-based program to reaffirm the gut health-improving activity of phytomolecules in broiler breeder performance. Especially the flexibility of assisting animals through the water for drinking during stress periods makes phytomolecules an optimal tool to support gut health.   

Two broiler breeder farms in Thailand (TH1 and TH2) and one grandparent farm in India (IN) are good examples of the effectiveness of phytomolecules. On each farm, the birds were always divided into two groups. Besides the standard management, feed, and water, one group got 200 ml Activo Liquid per 1,000 L of water. The periods when the birds received Activo in the water differed: 

TH1 & TH2: 5 days per week, during weeks 24 – 32 

IN:  5 days per week, every third week  from weeks 18 to 24 and every fourth week from 28 to 36  

The trials lasted for 9 weeks (Thailand 1 and 2) and 30 weeks (India). 

The results are shown in figure 2. The animals supplemented with Activo Liquid showed an up to 4.4 % higher laying rate and up to three more hatchable eggs per hen housed. 

Figure 2+3: Results of three trials conducted In Asia concerning laying rate and hatchable eggs 

3. Customers tell about lower breeder mortality and more DOCs due to phytomolecules 

The benefits of a tailored phytomolecule program have been demonstrated in several broiler breeder operations worldwide. For example, a combination of the in-feed (Activo) and the in-water solution (Activo Liquid) was tested in the Middle East. For the study, 75,000 23-weeks-old broiler breeders were divided into groups: 4 houses with the program, and 6 houses served as control (standard feed and water). The program, tailored to customer needs, was designed as follows: 

AC+AL group:

• Activo 100 g/ton of feed during the whole trial (weeks 23-41) + 
• Activo Liquid 250 ml/1000 L water, four days per week, weeks 23-30.  

As a result, the peak and average laying rates were higher for the flocks with the program, and laying persistency was also higher. This allowed for a significant difference of 3 total and 3.5 hatching eggs/hen housed at week 41. In both cases, an increase equivalent to 5 % compared to the control group (figure 4) could be observed. 

Figure 4: Total eggs and hatching eggs per hen housed

As fertility and hatchability were similar for both groups, the 5 % increase in hatching eggs resulted in a 5 % higher number of day-old chicks per hen housed (figure 5).

Figure 5: Number of DOSs per hen housed 

It must be mentioned that during the trial period, at 28 weeks of age, an NDV outbreak was diagnosed on the farm, which negatively impacted the overall results. However, this impact was reduced in the groups receiving the phytomolecule-based products, which also was reflected in a lower mortality rate (figure 6). 

Figure 6: Cumulative mortality rate wk 41

4. Scientific trial shows that Activo can increase post-peak productivity in breeders 

When thinking about the use of phytomolecules, most broiler breeder operations would like to consider scientific trial results in this type of animal. For EW Nutrition, it is crucial to accurately evaluate every product that reaches a market. Thus several scientific trials with broiler breeders have been performed. For one of them, Hubbard breeders (JA57 females with 80 M77 males) were divided into 2 treatments, having 5 replicate pens for each. The experiment started after the peak production period, at 34 weeks of age, and ended at week 62. To make the trial fair, the production data of 6 (pre-experimental) weeks was used to allocate the pens for each treatment, resulting in two (statistically) similar groups. 

The control group was fed the standard mash diet. For the Activo group, 100g Activo/MT was added to the diet. 

With Activo, breeders kept their high productivity after the peak, while the control group showed a steady decline from breed target values. During the experiment, Activo supplemented birds produced 3.6 more eggs than control birds (P=0.06) while consuming a similar amount of feed. As a result, a lower feed consumption per egg produced was achieved (169.9 vs. 173.6 g/egg, respectively). 

As the dietary treatment did not influence hatchability, the 3.6 extra eggs resulted in 2.9 extra day-old chicks per hen during the post-peak period, showing a positive return. 

Phytomolecules as gut health and performance promoters– antibiotics can be reduced! 

With their gut health-promoting activity, phytomolecules support breeders to better utilize nutrients. They can be invested for maintenance and the production of hatchable eggs, obtaining good quality day-old chicks.  

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Producing high-quality chicks is critical to the success of any broiler program, but it is even more important in an antibiotic-free (ABF) program. The hatchery is the perfect environment for the incubation of eggs and, consequently, bacteria and mold. This makes hatchery sanitation a very high priority in ABF production systems because of the inability to use antibiotics in the hatchery or later in production.

Chick quality can be divided into two categories:

• microbiologic
• chick vitality

The reality is many of the processes that impact these two categories are often intertwined but can be generally separated into

• sanitation practices
• setting/hatching practices

It is not helpful to set specific objective benchmarks for an individual hatchery without understanding its specific challenges. The hatchery manager must realize that the end product is a healthy, robust chick; therefore, benchmarks and numerical goals for the individual hatchery, breed, and flock age need to be established.

There are a host of measurements that can be performed and data that can be collected; however, it only makes sense to collect only information that will be used to make decisions. It is easy to over-collect and under-utilize data.

Hatchery sanitation

Bacterial contamination

Hatchery sanitation starts at the breeder farm. Eggs are a significant source of contamination in the hatchery; consequently, floor eggs should not be brought to the hatchery. If they must be hatched for egg flow needs, it is essential to at least segregate them from the regular egg flow throughout the process. It is imperative to send a clean egg pack to the hatchery (transport and store the eggs at proper temperatures and humidity). Once the eggs are at the hatchery, the focus is on proper storage, incubation, and hatching. 

Monitoring sanitation

The risk of multiplying bacteria in the hatchery is high. Hatchery equipment can be difficult to clean, there are sufficient nutrients to support microbial growth, and the environment is perfect for incubation. Developing a program to monitor the cleanliness of the hatchery is a critical step in managing sanitation. The whole hatchery must be regularly cleaned and disinfected, and the most effort should be spent on chick contact surfaces.

Egg flats must be clean and dry before returning to the breeder farm. Hatcher baskets must be clean and dry before eggs are transferred. The tray wash machine should use a detergent and disinfectant to remove and sanitize the trays (the water temperature should be 140^oF). A disinfectant with residual efficacy should be used after the tray wash. Too low of a temperature will encourage bacterial growth, and too high a temperature can damage the baskets.

When using an in ovo vaccination system, it is essential to clean and disinfect the machine after every use and prepare it for the next transfer. Chick belts, counters, chick baskets, hatchers, and setters are all areas that can harbor pathogens. Wet areas are also at risk for harboring disease: wet bulb thermometers, humidification equipment, and tray washers. All these areas should be regularly checked for cleanliness by traditional microbiology or rapid ATP testing.

It is important to monitor the hatchery air quality on a regular basis to ensure the level of bacteria and fungi is not too high. This is most effectively accomplished by placing air plates in key locations for air movement such as clean hatchers and setters and their respective halls, and plenums. The areas where vaccines are stored, mixed, and prepared should be surgical suite clean. 

Hatching practices

Chick vitality

A high-quality, active chick is one of the keys to program success. The actual profile used to hatch that bird is a mixture of breeder flock profile, hatchery equipment, climate, and experience. When evaluating a hatchery and a hatching program, it is best to start at the endpoint and work backward.

Managing chick comfort in the holding room is vital to set the chicks up for success on the farm. The chicks will tell you if they are too hot or too cold and if they have too much or too little airflow. This is determined by experience and monitoring behavior.

Tracking chick rectal temperatures is a useful way to check comfort. Remember that a small animal can change their body temperature from ideal to hyper- or hypothermic extremely quickly. On average, 103.5^oF is a good benchmark for chick internal temperature. Moving backward through the process, evaluate the vaccine spray cabinet to ensure chicks are getting the proper vaccines at the proper rate.

The next critical opportunity to monitor chick vitality is when chicks are being separated from hatch debris. The volume of chicks passing through the site allows for rapid evaluation of the flock. In this area, it is important to check for open navels, strings, red hocks, green chicks, dirty chicks, and general appearance and behavior.

Hatch debris

The egg should be pipped and broken almost exactly in half. The debris should have minimal meconium, yolk stains, and should not smell bad. Excess meconium is an indication that the hatch window is prolonged, and the chicks spent too much time in the machine before pull.

When eggshells are crushed in one’s hand they should break, but the membrane should remain intact. If the membrane also breaks, it is a sign that the chicks were potentially overheated, incubated too long, or humidity was too low. 

Chick yield

One of the most useful measures of the setting process is chick yield, which is the weight of the chick at hatch compared to the weight of the egg set. Chicks with a low yield were set with a high temperature or low humidity or were hatched for a long time before being removed from the hatcher. Chicks with a high chick yield are a result of the opposite: low temperature and high humidity incubation or did not spend enough time in the hatcher post-hatch. The ideal chick yield depends on the breed of chicken and the individual hatchery, but 67-68 % yield is a good benchmark.

Breakout

Analyzing hatch debris is a crucial tool for understanding setting and hatching efficiencies. Embryo mortality is variable but tends to follow a consistent pattern. The majority of embryo mortality is early (1-7 days), with little mortality in the middle (8-14 days), and the second increase in embryo mortality occurring from 15-18 days. Results should be recorded, and a standard developed for the hatchery. Deviations from this standard should be investigated.

When aiming to improve the data collection process, focus on building a program that prioritizes the most useful information. Breakouts and chick yields are two of the most meaningful tests to modify the hatching process. Sanitation checks and monitoring of disinfectant levels at critical sanitation steps are valuable to improve hatchery quality. When all the pieces come together, high quality egg pack, sanitation, and excellent hatchery management, the result is a high-quality chick ready to succeed on the farm.

Management in an ABF system requires extra attention – especially egg handling and sanitation. With the inability to use antibiotics in the progeny, it is critical to not bring additional pathogens into the hatchery on or in dirty eggs. A clean, well-managed egg pack will improve performance and animal welfare and significantly reduce seven-day mortality and the risk of foodborne illness.

1.      Cleanliness in the broiler breeder house and egg room

Managing egg cleanliness starts in the broiler breeder house before the first egg is laid. The house needs to be cleaned between flocks; at a minimum, water lines and nest pads should be cleaned and sanitized. The egg handling equipment and egg room should also be cleaned and disinfected. Special attention should be paid to egg contact surfaces and places where water accumulates, such as refrigeration and humidification equipment. If the previous flock had any disease issues, the houses should be thoroughly cleaned and disinfected. Between flocks, pest control is critical to reduce disease pressure: flies, rodents, and darkling beetles should be the focus as they are well-documented transmitters of disease. When adding shavings back to the house, it is important to not overfill the house to ensure there is a step between the scratch and the nest and thus help reduce the amount of litter and feces tracked into the nests.

2.      Training the birds

Once new breeders are moved to the house, it is important to train the birds on their location and not let hens learn to sleep in the nests. As hens begin to lay, training them not to lay floor eggs is an essential part of a clean egg pack.

Ensuring there are no dark spots, that any floor eggs are picked up quickly, and the scratch is walked on a regular basis are all important parts of the training to lay in nests. The temptation to set floor eggs is high, especially visibly clean eggs; the best way to eliminate this temptation is to reduce the amount of floor eggs. Visibly clean floor or slat eggs typically contain several logs more bacteria than clean nest eggs. Intestinal health is important to decrease the likelihood of soiled eggs.

High quality feed ingredients should always be used in breeder diets and the electrolyte balance carefully monitored to reduce the risk of flushing.

3.      Handling the eggs

The egg is well evolved to prevent contamination of the chick. There are multiple layers of protection: cuticle, shell, outer and inner shell membranes, and albumen. The cuticle and shell must be protected to reduce contamination. When removing minimal visible contamination, it is important to damage as little of the cuticle as possible.

3.1 Removing dirt

Dry contamination should be scraped off with a fingernail or soft plastic scraper. Wet contamination should be removed with a clean paper towel or disinfectant wipe. When removing wet contamination every effort should be made to prevent cross contamination of a larger area of the egg. Eggs should not be buffed clean since this may push dust and bacteria into the pores of the egg, limiting gas exchange and increasing contamination risk.

Any significantly soiled egg should be discarded. It is not advised to wash eggs or wet eggs for disinfection.

Gentle handling of eggs is important to reduce the risk of micro-cracks in the shell, further increasing the risk of bacterial contamination and dehydration.

3.2 Egg temperature and humidity

When packing eggs, fill the buggies from the bottom to the top. This decreases the risk of heating already cooled eggs, potentially reducing embryo viability. If egg packing equipment is used, it is important to clean the machine regularly. Special focus should be paid on the suction cups and rollers since they are in direct contact with the eggs and are very hard to clean.

As eggs cool, a slight vacuum is produced that may draw any liquid on the surface into the egg. Every effort should be made to ensure that eggs do not get wet. If they become wet, it is imperative to allow them to dry before putting them in the cooler. Egg trays and racks should be thoroughly cleaned and disinfected at the hatchery before returning them to the farm. Dirty or wet trays should not be used, they should either be thoroughly cleaned and disinfected on the farm or returned to the hatchery for cleaning.

Managing cooler temperatures is vital for hatchability. Additionally, it is important that eggs are continuously getting cooler to reduce the risk of sweating eggs. The hatchery egg cooler should be 15ºC or 59ºF, the farm egg cooler 2ºC warmer or 17ºC, and the egg transport truck in the middle (~16ºC). The humidity during storage should be 70-80% RH. Humidification devices are a high risk for microbial contamination; therefore, ensure that they are cleaned and disinfected frequently, and any mist is not directed towards the egg pack.

Conclusion

Appropriate management of the egg supply is key for any poultry company. The need for increased cleaning and disinfection is amplified in an ABF system. Clean and properly handled eggs are a fundamental step to producing high quality chicks.

Strong demand by consumers; restaurant chains and wholesalers for antibiotic-free (ABF) meat; the threat of antimicrobial resistance; and stringent regulations on the use of antibiotics – there are many good reasons for poultry producers to strive for antibiotic-free production systems. Crucially, to successfully produce poultry meat without antibiotics requires a paradigm shift that starts right at the parent stock level, with the antibiotic-free production of hatching eggs.

Broiler breeders’ gut health is linked to progeny’s performance

Broiler breeders’ performance is measured in terms of how many saleable day old chicks (DOCs) per hen they produce. However, within a sustainable ABF production system (also known as No Antibiotics Ever or NAE), this parameter is not seen in isolation. Breeder hens’ nutritional and health status not only affect the number of DOCs they can produce, but also the transfer of nutrients, antibodies, microbiota and even contaminants, e.g. mycotoxins, to the egg – and therefore, their progeny’s long-term health and performance.

This starts with egg formation, which requires several metabolic processes in the hen to function perfectly. If the hen’s intestinal integrity is compromised, for example due to mycotoxins, she will absorb fewer nutrients, which in turn affects egg formation. Mycotoxicosis has particularly insidious effects for egg formation as it can damage the liver whose biosynthetic activities strongly impact on the egg’s internal (yolk) and external (eggshell) quality.

Chick embryos depend on the maternal antibodies and nutrients deposited in the yolk, including vitamin D3, carotenoids, and fatty acids, to develop normally. Eggshell quality, among other things, affects the embryo’s access to oxygen, which is especially important when it develops body tissues.

Hens’ ability to form healthy eggs depends on their diet and health. Research indicates that, via the impact on egg formation, broiler breeders’ feeding program quantifiably influences their progeny’s immune system and intestinal health. There is indeed a direct relationship between parent and offspring’s gut health because the chick’s microbiome is in part also inherited from the hen. The impact on DOC quality is thus one of many dimensions to consider when calibrating one’s broiler breeders feeding approach.

The challenge of feeding an ABF broiler breeder

Just as their offspring, breeder hens are genetically predisposed for rapid growth and muscle development. From rearing right through to the laying period, poultry nutritionists need to carefully balance their diets and moderate weight gain in order for hens to reach their reproductive potential.

Different stages of a breeder’s life cycle come with different objectives – for example, good flock uniformity in the rearing period versus egg size and hatchability in the laying phase – and thus different requirements in terms of calories, amino acids, vitamins, and minerals. What remains constant is that the actual nutrient intake depends on intestinal health, determining both the breeders’ performance and, via the impact on egg characteristics, its progeny’s performance.

The feeding regimes adopted to avoid hens becoming overweight can have a negative effect on their gut flora. Without antibiotics as a tool to maintain or recover optimal gut function, even mild intestinal disorders can quickly become chronical impairments that negatively impact breeders’ productivity. In ABF production systems, intestinal health therefore needs to be a central focus for the feeding strategy.

Can phytomolecules improve broiler breeders’ performance?

Among the plethora of feed additives, phytomolecules, or secondary plant compounds, stand out as a class of active ingredients that may help to improve gut health and thereby reduce the use of antibiotics.  Synthesized by plants as a defense mechanism against pathogens, phytomolecules combine digestive, antimicrobial and antioxidant properties.

Some studies have shown that phytomolecules-based products can increase broilers’ body weight gain and improve laying hens’ laying rate, egg mass and egg weight. Both broilers and laying hens responded to the inclusion of phytomolecules in their diet with inclusion rate-dependent improvements in feed conversion. To evaluate if phytomolecules could similarly improve broiler breeders’ performance, two trials were conducted.

Study I: Effect of phytomolecules on laying performance during peak production

The first study was set up on a farm in Thailand. In total, 40000 Cobb broiler breeders (85% female, 15% male) were divided into two groups with 8500 hens (one house) in the control and 25500 (three houses) in the trial group. Both groups were fed standard feed. The trial group additionally received a phytomolecules-based liquid complementary feed (Activo Liquid, EW Nutrition GmbH) via the waterline from week 24 to week 32 at a rate of 200ml/1000L during 5 days per week.

Activo Liquid was found to have a positive influence on laying performance (Figure 1). The average laying rate increased by 7.2% during the trial period, resulting in almost 3 additional hatching eggs per hen housed. A further indication of the beneficial influence that this particular combination of phytomolecules had on gut health was a 0.2% lower mortality.

Figure 1: Laying rate (%) of breeder hens during first 9 weeks of production

Study II: Effect of phytomolecules on laying performance after peak production

For a second study, conducted in the Czech Republic, 800 female and 80 male Hubbard breeders (JA57 and M77, respectively) were divided into 2 groups with 5 replicate pens and 80 female and 8 male breeders per pen. The experiment started after the peak-production period, at 34 weeks of age and ended at 62 weeks of age. All animals received a standard mash diet. For one group a phytogenic premix (Activo, EW Nutrition GmbH) was added to the diet at a rate of 100g/MT.

The results indicate that Activo helped maintain the breeder hens’ egg laying performance close to the breed’s genetic potential (Figure 2). In the course of the experiment, Activo supplemented birds produced 3.6 more eggs than control birds, while consuming a similar amount of feed. As a result, feed consumption per egg produced was lower for birds receiving phytomolecules than for the control birds (169.9 versus 173.6g/d, respectively).

As hatchability was not influenced by the dietary treatment in this study (P>0.5), the 3.6 extra eggs resulted in 2.9 extra day old chicks per hen produced, during the post-peak period alone.
The microencapsulated, selected phytomolecules contained in Activo are likely to have improved gut health and feed digestibility, and thereby enhanced the animals’ feed efficiency.

Figure 2: Laying rate (%) of breeder hens week 35 till 62

Chicken or egg? Antibiotic-free poultry production looks at the bigger picture

To successfully produce antibiotic-free poultry meat requires a systematic re-think of each component of the production process. Broiler breeders’ lay the foundation for their progeny’s health and performance via the egg. Breeder hens need to be in optimal health to consistently deliver optimal eggs. Without recourse to antibiotics for maintaining or recovering intestinal functionality, an effective ABF production needs to make gut health central to its feeding approach.

The trials reviewed demonstrate that selected phytomolecules quantifiably boost breeders’ laying performance, increasing the number of hatching eggs and DOCs, while reducing mortality and feed consumption per egg produced. As part of an intelligent antibiotic reduction strategy, the right phytogenic products can be potent tools to help poultry producers achieve their NAE objectives.

by T. van Gerwe, Global Technical Director, and M. Caballero, Global Technical Manager Poultry, EW Nutrition 

References

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Ding, Jinmei, Ronghua Dai, Lingyu Yang, Chuan He, Ke Xu, Shuyun Liu, Wenjing Zhao, et al. “Inheritance and Establishment of Gut Microbiota in Chickens.” Frontiers in Microbiology 8 (October 10, 2017): 1967.

Kuttappan, Vivek A., Eduardo A. Vicuña, Juan D. Latorre, Amanda D. Wolfenden, Guillermo I. Téllez, Billy M. Hargis, and Lisa R. Bielke. “Evaluation of Gastrointestinal Leakage in Multiple Enteric Inflammation Models in Chickens.” Frontiers in Veterinary Science 2 (December 14, 2015): 66.

Moraes, Vera M. B., Edgar O. Oviedo-Rondón, Nadja S. M. Leandro, Michael J. Wineland, Ramon D. Malheiros, and Pamela Eusebio-Balcazar. “Broiler Breeder Trace Mineral Nutrition and Feeding Practices on Embryo Progeny Development.” Avian Biology Research 4, no. 3 (2011): 122–32.

Oviedo-Rondon, Edgar O., Nadja S. M. Leandro, Rizwana Ali, Matthew Koci, Vera M. B. Moraes, and John Brake. “Broiler Breeder Feeding Programs and Trace Minerals on Maternal Antibody Transfer and Broiler Humoral Immune response1.” The Journal of Applied Poultry Research 22, no. 3 (October 1, 2013): 499–510.