by Inge Heinzl, Editor,  Marisabel Caballero, Global Technical Manager Poultry, and Ajay Bhoyar, Global Technical Manager Poultry, EW Nutrition

In the last few months, the prices for feed grains and oilseeds such as soybeans have been climbing to multi-year heights. In part, this can be explained by high corn purchases by China and increasing export duties in Russia. The most significant cause, however, are weather events in producing countries: Just in the last year, droughts in the USA, Canada, and France raised the price of wheat by 40 %, the worst La Niña climate event in 91 years and the drought in China’s biggest corn-growing area made corn about 100 % more expensive, and soybeans carry a 40 % higher price tag because of dry conditions in Argentina.

These events are a stark reminder that for global agriculture climate change impacts are already a reality. High feed costs are an enormous challenge for the whole agricultural sector and sustainable strategies need to be adopted to enable a more efficient use of resources, both in the short and long term. This article explores possibilities to cope with the current situation. Through understanding the positions of farmers, integrators and feed millers and using targeted feed additive solutions, we can achieve a responsible use of resources that makes animal production more resilient to feed price increases.

Feed cost issues? Always start with this

The first question producers need to ask themselves is always if there is any step in the production process that could be done more effectively. Similar to biosecurity programs, the basic steps seem self-evident, but to consistently implement them in the complex on-farm reality requires regular checks.

Feeding as “exactly” as possible

In case of high prices, the feed raw materials should be used as responsibly as possible:

• Protein and energy content (but also other components, such as minerals and vitamins) must meet the requirements of the animals – age and production phase are decisive for the calculations.
• Given variations in raw material quality, it is important to exactly determine nutrient contents to avoid over- and under-supply. For this purpose, technologies like the near-infrared spectroscopy (NIR) can be used.

Using locally available sources

In the initial stages of price hikes, it is often possible to resort to locally available sources, e.g., using sunflower or flaxseed meal to replace soybeans. Unfortunately, with increasing demand, these feed materials will usually become more expensive as well, and might not be suitable alternatives anymore. In general, however, it is worth using a maximum of local ingredients: they are often cheaper and less susceptible to transport and trade difficulties.

Feed additive solutions: use what is available in the best possible way

Once these first measures are exhausted, it is time to draw on industry solutions to derive maximum value out of the available feed ingredients. Let us consider four approaches that improve feed conversion and feed quality, adjust feed composition, and optimize feed production processes.

1.   A critical goal: improving the feed conversion rate

The most direct way to better utilize feed is to improve the animals’ feed conversion rate, with the help of the right supplements. Different product groups contribute to this aim in different ways.

1.1 Phytomolecules fight on different fronts

Phytomolecules are well-known for their antimicrobial effects against pathogenic bacteria (Zhai et al., 2018). Phy­tomolecules shift the balance of the microbiome towards the beneficial side (eubiosis instead of dysbiosis) and promote gut health. A healthy gut is able to digest the feed and absorb the nutrients in an efficient way.

Another value of phy­tomolecules is their digestive effect. They stimulate the secretion of saliva, gastric juice and digestive enzymes, and favor an adequate gastrointestinal motility, which leads to improved nutrient utilization (Jones, 2001; Mendel et al., 2017).

In trials testing the phytogenic Activo product range, supplemented animals showed the following FCR improvements compared to non-supplemented control groups (Figure 1):

Figure 1: FCR improvements for animals receiving Activo

1. 2 Enzymes improve nutrient availability

Even a corn-soybean meal diet is not fully digestible for monogastric animals. However, when feed prices increases, producers likely need to include more alternative ingredients in the diet that are much less digestible. Typically, these ingredients are rich in antinutritional factors such as non-starch polysaccharides (NSPs), which can cause detrimental effects on gut health.

Another disadvantage of NSPs is their “cage effect”. The water-insoluble NSPs cellulose and hemicellulose trap nutrients such as proteins and digestible carbohydrates. Consequently, digestive enzymes cannot reach them and they are not available to the organism.

Here is the point of attack for enzymes that enable a complete nutrient utilization: Making these substances available for the animals increases the energy content of the diet and, in the end, improves FCR. An example for laying hens receiving wheat-based diets can be found in Figure 2: Axxess XY, a xylanase, significantly improved feed utilization by the hens.

Figure 2: FCR in layers receiving Axxess XY, compared to control group (kg feed / kg egg mass)

1.3 Antioxidants maintain energy content of the diet

Corn Distiller’s Dried Grains with Solubles (DDGS), a by-product of corn distillation processes, are used as an alternative to corn. In DDGS, the starch content is removed, but fat is concentrated, reaching about three times the fat level of corn. This is the reason why the energy content in DDGS and corn is similar. This makes DDGS an attractive ingredient for monogastric diets; however, fat,  especially at hot temperatures in the summer, can be oxidized. The resulting rancidity and the accompanying destruction of vitamins, pigments, and amino acid leads to a decrease in the diet’s bioavailability and energy content and to poor feed conversion.

The use of antioxidants can stabilize DDGS and other fatty ingredients in the feed, maintaining nutrient integrity and availability. Figure 3 shows the performance benefits of using antioxidant product Santoquin in pork finisher diets in the USA containing 30% of DDGS.

Figure 3: Performance results for pigs receiving Santoquin (trial with Midwest pork producer)

In  poultry production, the use of DDGS is not as common as in swine. Antioxidants, however, can still help to protect the nutrients, maintain the energy content and improving FCR. The results from an extensive 2015 field study for broilers fed a diet without DDGS (shown in Figure 4) showed a net ROI of 6.7 to 1.

Figure 4: FCR in broilers receiving Santoquin, compared to non-supplemented control group

1.4 Organic acids improve intestinal processes

Organic acids, or acidifiers, can improve the gut microbiome, feed utilization, and gut health in production animals. The gut microbiome balance is aided by lowering the population of pathogenic bacteria susceptible to low pH, such as E. coli, Salmonella, and Clostridium.

Organic acids also directly attack pathogens by entering bacterial cells and changing the internal pH. Commensal bacteria such as Lactobacilli and Bifidobacteria survive as they can tolerate lower pH conditions. As pathogens constitute nutrient competitors, eliminating them improves gut health, which, is the most important precondition for optimal nutrient utilization.

The acidifying effect of organic acids furthermore favors digestion and nutrient utilization: for example, for weaned piglets that not able to produce enough HCl in the stomach, a low stomach pH is important for the activation of the proteolytic enzyme pepsin. Besides a non-optimal use of nutrients, undigested protein arriving in the intestine leads to the proliferation of undesired pathogens, decreasing health and performance.

Organic acids, therefore, improve FCR directly, by promoting nutrient utilization through the stimulation of enzymes, and indirectly, by enhancing gut health.

2. Improving feed quality

Feed quality is not only a question of raw material quality. Feed additives play an important role in ensuring feed safety and enabling optimal utilization by the animal.

2.1 Mold inhibitors preserve the feed’s value

Molds reduce the nutrient and energy content of the feed (table 1) and have a negative impact on animals’ growth performance (table 2). Active water is the crucial point for mold growth. Compared to bacteria, which need about 0.90 – 0.97 Aw (active water), most molds require only 0.86 Aw.

Mold inhibitors contain different ingredients. Surfactants bind the free water, so that the moisture of the feed persists, but the active water important for molds is reduced. Organic acids, as already mentioned before, have antifungal properties. Together, they reduce molds and prevent the degradation of energy in the feed.

Table 1: Nutrient loss in corn infested with molds

Table 2: Comparison of 28-day-old chicks performance fed not-infested and molded corn

2.2 Mitigating the negative impact of mycotoxins

Mycotoxins contamination of grains can occur in the field, during raw material harvesting, transportation, storage, handling, and even during feed processing and storage. By mitigating the negative effects of mycotoxins – such as gut and liver inflammation, kidney degeneration or reproductive disorders – the animals’ health and performance can be maintained. In today’s contamination scenarios, it is absolutely necessary to use products that adsorb mycotoxins and contain their harmful impact on animals.

The effectivity of such products in animals is crucial. Table 3 shows an optimal experimental design and Figure 5 shows the results of its application: a total recovery of the performance pays off.

Table 3: Trial design, impact of Mastersorb Gold on broilers challenged with zearalenone and DON-contaminated feed

Figure 5: Average FCR for broilers, with or without zearalenone and DON challenge, with or without Mastersorb Gold supplementation

2.3  Surfactants for microbiological control and high pellet quality in the feed mill

Moisture is important. Too dry feed results in poor palatability and digestibility, and lower pellet quality. Also moisture loss has a direct impact on production and profitability.

The use of surfactants, makes it possible to bind the moisture to the feed, reaching a larger contact surface between water and feed particles, and improving starch gelatinization and pelleting efficiency. The improvement in starch gelatinization leads to a higher pellet quality, a lower proportion of fines and a higher content of metabolizable energy.

Moreover, moist steam has a better antimicrobial effect than dry steam, leading to lower fungal and bacterial growth and preventing the production of toxins. The pelleting temperature can also be lower, protecting the nutrients.

Figure 6 shows how the use of SURF•ACE, a synergistic blend of organic acids and surfactants, improves pellet durability, moisture content, and mold occurrence for beef and poultry pellet feed.

Figure 6: Improvements in pellet durability, moisture content and mold through using SURF•ACE

3.   Using feed alternatives in ruminants – partial replacement of protein feed by urea

Ruminal bacteria are able to synthesize amino acids and, subsequently, generate a high-quality protein out of acid amides, a group of non-proteins occurring during the synthesis and degradation of proteins. What they require to do this is enough energy, minerals, and trace elements available in the feed (Weiß et al., 2011). When the bacteria arrive in the abomasum and in the small intestine they, or rather their proteins, are degraded by enzymes together with the undegradable rumen protein into useful amino acids.

With the aid of ruminal microbes, ruminants therefore partly cover their protein requirement through non-protein nitrogen. The most well-known is urea. It is critical that the urea given to animals has a degradation rate similar to other energy sources the animal consumes. Otherwise, there will be an imbalance between the quantity of usable nitrogen and the energy required for microbial protein synthesis: The urea accumulates in the rumen, becoming toxic for the microbiota and creating metabolic disorders.

Special coating technology allows for nitrogen to be released at a rate close to that of protein degradation of the main vegetable protein sources (e.g., soybean meal). This leads to a more constant nitrogen supply for the microorganisms and results in maximal synthesis of microbial protein.

4.   Save costs in the production process

Besides high pellet quality, feed millers seek to maximize production efficiency. Factors contributing to this target are the amount of fines to be reprocessed, the utilization of steam, the pellet throughput and the energy demand. Once more, the moisture of the feed is of decisive importance. Substances can be added to the feed to achieve an optimal moisture content. These substances bind free water by generating an emulsion of dietary fat and the added water.

Besides the positive effects on pellet durability, moisture content and mold growth shown above, this leads to a better general lubrication of the machinery: The addition of feed mill processing aid SURF•ACE leads to a 10-15 % lower energy demand or a higher production output without increasing energy consumption (Figure 7), depending on the mill’s requirements. Good machinery lubrication additionally reduces wear and tear, another important dimension of production efficiency

Figure 7: Improvements in pellet output and energy efficiency through using SURF•ACE

Producers can rise to the challenge of rising feed prices

Rising feed costs pose a significant challenge to everyone in animal production. We are all compelled to look for alternatives to optimize the utilization of resources. This firstly involves a critical look at the efficiency of every step in our operations, but also includes utilizing targeted feed additives. Various measures are available for animal producers to optimize feed conversion, improve feed quality, and resort to alternative ingredients. In feed production, tools are on hand to optimize the manufacturing processes, improve feed quality, and make a positive impact on animal performance. Feed price fluctuations will continue to challenge our industry. Still, while tackling short- and medium-term difficulties, we can also strategically build resilience – and take the measures today that will contribute to our long-term ambitions for sustainable and profitable production.

References

Jones, G. “Leistungsstarke Tiere und Verbraucherschutz stehen nicht im Widerspruch – Wirkung eines phytogenen Zusatzstoffs / High-performing livestock and consumer protection are not contradictory – Impact of a phytogenic additive.” Kraftfutter/ Feed Magazine 12 (2001): 468-473.

Mendel, M., Chłopecka, M., Dziekan, N., & Karlik, W. (2017). Phytogenic feed additives as potential gut contractility modifiers—A review. Animal Feed Science and Technology, 230, 30–46. https://doi.org/10.1016/j.anifeedsci.2017.05.008.

Weiß, J.W., S. Granz, W. Pabst. Tierproduktion. Thieme Verlag (2005):155-159.

Zhai, Hengxiao, Hong Liu, Shikui Wang, Jinlong Wu, and Anna-Maria Kluenter. “Potential of Essential Oils for Poultry and Pigs.” Animal Nutrition 4, no. 2 (June 2018): 179–86. https://doi.org/10.1016/j.aninu.2018.01.005.

by EW Nutrition USA, Inc.

In the poultry industry, Necrotic Enteritis is of great interest due to the potential detrimental growth effects it may have in a flock, even at subclinical levels⁵⁰. Coccidiostats and antibiotics have been used for a long time to get the disease-causing bacterium Clostridium perfringens under control, but with increasing antimicrobial resistance, alternative approaches are required. This article aims to give an overview of the disease and the measures against it.

Clostridium perfringens – a ubiquitous, highly resilient bacterium

Clostridium perfringens is a Gram-positive, spore-forming, anaerobic, rod-shaped bacterium⁵⁰. This encapsulated, non-motile microorganism is fastidious in growth requirements⁵⁹. Most often, complex media like cooked meat or thioglycolate broth are used as enrichment³⁰.

It was Welch and Nuttall who first identified C. perfringens in 1892 as Bacillus aerogenes capsulatus¹⁸. In Great Britain, the bacterium was commonly known as C. welchii and sometimes called Frankel’s bacillus in Germany until designated C. perfringens by Bergey¹³.

Clostridium perfringens is the causal microorganism for Necrotic Enteritis (NE)¹⁴. In humans, it is one of the most common causes of foodborne illness²⁰. The Centers for Disease Control and Prevention (CDC, 2012) estimates that nearly one million people are affected every year, making C. perfringens the third most frequent source of domestically acquired foodborne illness after Norovirus and Salmonella.

Clostridium perfringens can be found everywhere

Clostridium perfringens is found in soil, water, and other organic materials. As far as poultry facilities, C. perfringens has been isolated from litter, dust, walls, floors, fans, transportation coops, feeders, and feed⁸⁹.

Additionally, C. perfringens is found in the GI tract of broiler chickens, humans, and other mammals⁴⁷. When intestinal samples of broiler chickens were analyzed for C. perfringens, 75-95 % tested positive²⁴. Drew and co-workers¹⁰ determined that C. perfringens is usually found at ~10⁴ colony-forming units (CFU)/g of broiler digesta. These results agree with Jia et al.²⁶, who stated that C. perfringens is present at low levels in healthy poultry. In humans, investigations in different parts of the world showed a prevalence of Clostridium perfringens between 57-94%³².

Different types of Clostridium perfringens with different toxins

There are five types (A-E) of C. perfringens, which can be identified through their toxin production (see table 1). All strains produce alpha-toxin. Furthermore, Clostridium perfringens has been described to produce eight other toxins, three (delta, theta, kappa) can be lethal, but these are seldom involved in disease origin³⁷.

Table 1. Different types of Clostridium perfringens

High resilience gives an advantage against competitors

Since Clostridium perfringens is a spore-forming bacterium, it is very resilient to high temperatures, slight pH variations, and toxic chemicals^{43, 7}.

Labbe et al.³⁰ established that C. perfringens can reproduce at temperatures between 15-50 °C. Hence, proper refrigeration temperatures (below 10 °C) can be an effective means of control. The optimum range is between 37-47 °C, and at these temperatures, the mean generation time – the time required for the bacterial count to double – is approximately 10-12 minutes⁴¹. These short generation times allow the bacteria to outcompete other microorganisms that may need similar resources in a certain environment.

The optimum pH range of Clostridium perfringens is between 5.5-7.0²². However, it can grow at a pH as low as 5 and as high as 9. In live broiler chickens, the pH in the small intestine has been determined to be between 6.00-7.78.

Necrotic enteritis in poultry

The disease necrotic enteritis was first described by Parish^{45, 46} in cockerels in England. Some of the symptoms include depression, reluctance to move, ruffled feathers, somnolence, diarrhea, loss of appetite, and anorexia²¹. Mortality ranges from 0-50% ⁶ have been reported in infected flocks. Since then, virtually every area that raises poultry has reported signs of necrotic enteritis.

Clostridium perfringens – How NE unravels

As already mentioned, 10⁴ colony-forming units (CFU)/g of broiler digesta¹⁰ are normal and can be found in healthy birds. C. perfringens becomes problematic when counts reach 10⁷-10⁸ CFU/g⁶.

Necrotic enteritis is caused by types A and C of Clostridium perfringens, but normally, predisposing factors “set the stage”^{24, 48}. This could be seen in an investigation where they wanted to create a model to reproduce NE in a laboratory setting. Researchers realized that inoculation of C. perfringens alone did not cause the disease found in the field⁴⁸. Therefore, it was assessed that certain cofactors must play a significant role in the pathogenicity of C. perfringens. Williams⁵⁷ reviewed concurrent infections of coccidiosis and necrotic enteritis in chickens (Figure 1). The copious interactions of these diseases with predisposing factors, control methods, sources of infection, and disease form is a testament to the complexity of this poultry industry matter.

Coccidiosis creates access

Shane et al.⁵³ noted that several authors had considered coccidiosis to be a predisposing factor for NE. They proceeded to describe the pathogenesis of Eimeria acervulina, one of the protozoa responsible for coccidiosis in poultry. When the oocysts are ingested, they quickly attach to the intestinal wall causing lesions where the protozoa reproduce numerous times. These are the lesions to which C. perfringens attaches.

What happens in the animal?

Long et al.³³ proposed the pathogenesis for NE: First, epithelial cells are vacuolated, and the epithelium lifts off the lamina propria, which is congested and edematous. These lesions can be caused by a combination of factors like toxin production and/or, as just mentioned, coccidiosis. Clostridium perfringens cells attach to the lamina propria, where they thrive. The tissue becomes necrotic as large numbers of heterophils, a type of phagocyte, flood the foci (sites of lesions).

A combination of disease-inducing factors such as bacteria proliferation, heterophil lysis, and villus’ necrosis seem to develop quickly. The inflammation zone then becomes riddled with mononuclear cells, cells containing lymphocytes, antigen-presenting cells, and eosinophilic-staining (proteinaceous) amorphous material. This necrotizing process moves from the tip of the villi to the crypt.

Chronic version

In chronic cases, villi may be found to have multiple cysts from recurrent necrosis. In birds that overcome the disease, injured epithelial cells are replaced by newly formed reticular structures. These new cells travel from the crypt to the tip of the villi and replace the old, damaged cells. The result is a short, flat villus with a reduced surface area for nutrient absorption^{44, 45, 34}. These morphologically altered villi are the necrotic lesions found in the field and some C. perfringens challenge trials (Figure 2).

Acute form

The acute form of NE results in enlarged lesions along the gut wall, and the epithelium becomes eroded and detached; consequently, a diphtheritic membrane is formed. This yellow, green, or brownish pseudo-membrane is called the “Turkish towel,” which describes the appearance of the friable, gas-filled, foul-smelling GI tract⁵⁷.

Subclinical form

Poultry producers are not only concerned with the acute form of NE. Recent studies have shown that the disease’s subclinical form can be as detrimental as the acute illness¹⁹. Lovland and co-workers³⁵ stated that this symptomless disease is often overlooked at the farm, and the effects are only noticed at the processing facility.

Subclinical NE (SNE) can cause cholangiohepatitis, a condition where the liver is enlarged with pale reticular patterns and sometimes small, pale foci. In the United Kingdom, it was estimated that 4% of broiler carcasses and 12% of livers are condemned at processing plants due to clostridial infection; thereby, reducing profit³⁶. Moreover, sparse lesions that may be found in a case of SNE may be enough to hinder growth performance; thus, resulting in an underproductive flock³⁹.

Feeding Against Necrotic Enteritis

It has been reported that diet formulation has the greatest impact on the prevalence of C. perfringens in chicken GI tracts⁶¹. The poultry industry formulates diets on a least-cost basis, which may become problematic if nutritionists do not take into consideration the pathological consequences that some ingredients may have in the GI tracts of chickens. Every feed ingredient has a specific purpose in the diet. For instance, cereal grains are fed for their energy concentration as well as fiber. Also, some grain and animal/plant meals are used for their protein content. Since these ingredients are obtained from different sources, they are highly variable in macro and micronutrients¹.

The diet provides the conditions for proliferation

There are multiple elements that affect the proliferation of C. perfringens in chicken intestines, one of the most critical factors being diet formulation^{5, 36}. Some feed ingredients have been found to exacerbate the numbers of C. perfringens in chickens’ gastrointestinal tract. Diets formulated with wheat increased NE intestinal lesion scores compared to broiler chickens fed a corn-based diet⁴. In another study, Drew et al.¹⁰ investigated the effects of different protein sources on the intestinal populations of C. perfringens in broiler chickens. Diets were formulated to contain 230, 315, and 400 g/kg of fishmeal or soy protein concentrate (SPC). The numbers of C. perfringens in the ileum and ceca increased when the amount of protein increased from 230 to 400 g/kg.

Type of grain influences the occurrence of Clostridium perfringens

Authors have studied the effects of grain inclusion on gut microbiota, and it is well established that small cereal grains such as barley, rye, and wheat tend to increase the prevalence of C. perfringens in the GI tract. Shakouri et al.⁵² investigated the influence of barley, sorghum, wheat, and corn on counts of C. perfringens in the different intestinal segments. Corn and wheat had the lowest C. perfringens counts, followed by sorghum, while barley yielded the highest counts. These findings agree with Riddell and Kong⁵¹.

Other researchers have concluded that the increase in gut viscosity and increased chyme transit time elicit the overgrowth of C. perfringens in the intestines²⁸. Grains like wheat and barley contain high amounts of non-starch polysaccharides (NSP), which increase viscosity²⁶. Furthermore, it has been alleged that, since these grains are high in NSP, the bird cannot absorb nutrients as efficiently, thereby leaving them for microbes like C. perfringens to consume³¹.

Enzymes improve nutrient availability in the presence of C. perfringens

Shakori et al.⁵² and Jia et al.²⁶ also studied the impact of several diets with the inclusion of a blend of carbohydrases such as glucanase and xylanase. Their findings suggested that enzyme addition did not affect counts of C. perfringens in the different intestinal sections. However, they did find an improvement in growth performance. They stated that enzymes improved chyme viscosity by degrading the encapsulation of nutrients in diets.

For this reason, researchers have investigated the use of enzymes in wheat and barley-based diets on the incidence of C. perfringens in chicken intestines. Jackson et al.²⁵ studied the effect of beta-mannanase addition on flocks infected with Eimeria spp. and C. perfringens. They found that feeding this enzyme significantly reduced the impact of C. perfringens on the performance of infected flocks as well as intestinal lesion scores. Moreover, the authors explained that this might be due to beta-mannanase crossing the intestinal wall to provoke an immune response. They determined that this enzyme tended to ameliorate the symptoms of necrotic enteritis, but not significantly.

MOS may have a positive impact on immunity

Hofacre et al. ²³ found similar results when birds were fed mannan-oligosaccharides. A marked effect was only found when mannan-oligosaccharides were included along with lactic acid-producing, competitive exclusion products (probiotics).

The feed form is decisive

Feed form has also been investigated on the incidence of C. perfringens. When birds were fed whole wheat compared to ground, researchers found reduced counts of C. perfringens in the gut². These results can be extrapolated to the findings of Engberg et al.¹¹. They found that when birds were fed coarse versus fine mash or pellets, C. perfringens counts were consistently higher in flocks fed mash diets. These authors concluded that feeding pellets or whole grains increases gizzard activity, which consequently triggers hydrochloric acid production and decreases pH in the GI tract. This drop in pH of approximately 0.5 units may be responsible for decreased C. perfringens counts.

Mind the protein source

Another well-established fact is that the C. perfringens population can be affected by the type of the protein source and the inclusion rates.

Potato is worse than fish

Palliyeguru et al. ⁴² studied the inclusion of protein concentrates (potato, fish, and soy) on subclinical NE. They determined that the potato-containing diet resulted in the highest incidence of C. perfringens in the gut, followed by fish and soy. Also, the potato-containing diet had the highest activity of trypsin inhibitors and lowest lipid content. Increased trypsin inhibition does not allow for the inactivation of alpha and beta toxins produced by C. perfringens, resulting in increased intestinal wall lesions.

Fish is worse than soy due to the amino acid composition

Drew et al.¹⁰ formulated diets containing fishmeal or a soy protein concentrate at different levels. Feeding dietary fishmeal resulted in a higher incidence of C. perfringens as compared to the soy protein diet. Furthermore, with increasing levels of soy and fishmeal diets, counts of C. perfringens increased as well. A notable difference in fishmeal protein concentrate compared to the soy protein concentrate was the amino acid ratio in this experiment; the methionine and glycine ratios were 1.3 times greater in fishmeal diets. Muhammed et al.⁴⁰ determined that methionine was required for C. perfringens sporulation. This may be of interest to nutritionists since some authors have estimated that 10-20 % of synthetic amino acids are not absorbed and reach the lower intestinal tract, i.e., ceca; thereby, aiding in the proliferation of C. perfringens.

Fat source – animal fat is critical

The effects of fat sources on C. perfringens population remain largely unknown. Knarreborg et al.²⁹ studied the bacterial microflora in chicken intestines after feeding different dietary fats (soy oil and a tallow and lard mix) in rations containing antibiotic growth promoters (AGP). When soy oil was fed, C. perfringens counts were significantly lower than diets containing animal fats. The authors stated that, since plant oils contain higher amounts of unsaturated fatty acids, the chyme in birds fed oil diets would have decreased viscosity, decreasing transit time. Furthermore, an additive effect was found when soy oil was provided along with AGP, which may be due to facilitated antibiotic dispersion caused by the oil’s lipophilic properties. Knarreborg et al. (2002) investigated the effects of fat sources on C. perfringens. They found that total anaerobic counts increased with animal fat addition. However, zinc bacitracin was included in their diets, specifically targeting Gram-positive microorganisms like C. perfringens; thus, potentially biasing their results.

Antibiotics and coccidiostats in the diet – helpful, but finite

Antibiotics and coccidiostats have been commonly included in poultry diets since the mid-1940s and 1950s^{61, 58}.

Prescott et al.⁴⁹ studied the inclusion of zinc bacitracin to prevent necrotic enteritis and concluded that it successfully controlled the C. perfringens challenge. Flocks in the antibiotic treatments were able to overcome disease and perform similarly to unchallenged birds. Multiple authors have replicated these results using different antibiotics such as virginiamycin and salinomycin^{17, 3, 11}.

Improvements in flock performance with the inclusion of antibiotics and coccidiostats are well understood and omnipresent in the literature. However, the potential loss of subtherapeutic antibiotic usage in livestock in the United States due to increasing concerns over antimicrobial resistance and consumer demands makes research of viable alternatives to these compounds paramount.

So, what are your alternatives?

A lot of different approaches are possible. In general, these measures should act against Clostridium perfringens while supporting gut health.

Tested substances without the desired effects

Lastly, multiple options have been studied to control C. perfringens in poultry. Some researchers have studied the inclusion of complex carbohydrates and fibers like pine shavings, guar gum, and pectin with limited success^{4, 31}. Another popular alternative is the use of competitive exclusion-based products such as prebiotics and probiotics^{27, 16}. Still, these products failed to yield consistent results.

Other options that have been investigated are the addition of lactose and organic acids^{54, 38}. Potassium diformate did not produce lowered counts of C. perfringens. Lactose reduced C. perfringens counts but resulted in undesirable ceca characteristics including, enlargement and increased fermentation⁵⁴.

Essential oils alone or in combination may be a solution

Mitsch and coworkers³⁹ investigated the efficacy of two blends of essential oils with positive effects on the reduction of C. perfringens from the gut and feces of broilers. Gaucher and coworkers¹⁵ compared growth performance and gut health of broilers fed a conventional (anticoccidials and AGPs) vs. ABF (Coccidiosis vaccine and essential oil blends) diet. They established that livability, age at slaughter, and percentage of condemnation did not change with diet type. However, average daily weight gain and FCR were negatively affected. Furthermore, NE was more prevalent in ABF flocks.  Still, many authors agree that a multifactorial approach is necessary if antibiotics should be completely replaced by these strategies³⁶.

A contemporary study by Wati et al.⁵⁶ aimed to compare AGPs to a commercial blend of essential oils fed to broilers. Authors found that chickens fed essential oils had body weights and FCRs that were statistically similar to the AGP treatment. Moreover, both AGP and essential oil treatments had statistically lower counts of Salmonella and E. coli after an oral challenge than the control group.

Conclusion

C. perfringens is a potential pathogen found in every place poultry is raised. Therefore, we must continue to identify strategies to control the development of Necrotic Enteritis. Since antibiotics alone may not always successfully control C. perfringens and have the potential for subtherapeutic use loss in the US, a multifactorial approach must be considered and investigated. Grain size, enzymes, feed form, animal protein source, fats, and feed supplements such as essential oils can affect the proliferation of C. perfringens. Nutritionists, veterinarians, and live production personnel must come together to develop the best approach for their specific complex circumstances.

Figure 1. Interaction between coccidiosis and NE with environmental factors

Solid-line arrows are beneficial in controlling disease. Dashed-line arrows impart high disease risk factors. Double-line arrows depict major disease-risk factors. AGP, antibiotic growth promoter; CIA, chick infectious anemia; CEP, competitive exclusion product; Cp, Clostridium perfringens; IBD, infectious bursal disease; MD, Marek’s disease; NE, necrotic enteritis. (Williams, R.B. 2005)

 Figure 2. Necrotic Enteritis lesions in chicken intestines

Yellowish necrotic lesions in three intestinal samples. Intestines A and C show a few marked lesions. Intestine B shows clusters of lesions typical of the “Turkish towel” syndrome. (Source: http://www.mdpi.com/2072-6651/2/7/1913/htm. Accessed: January 14, 2021).

References

1. Bedford, M.R. 1996. Interaction Between Ingested Feed and the Digestive System in Poultry. Applied Poultry Science 5:86-95.
2. Bjerrum, L., K. Pedersen, and R. M. Engberg. 2005. The Influence of Whole Wheat Feeding on Salmonella Infection and Gut Flora Composition in Broilers. Avian Disease 49:9-15.
3. Bolder, N. M., J. A. Wagenaar, F. F. Putirulan, K. T. Veldman, and M. Sommer. 1999. The Effect of Flavophospholipol (Flavomycin^R) and Salinomycin Sodium (Sacox^R) on the Excretion of Clostridium perfringens, Salmonella enteritidis, and Campylobacter jejuni in Broilers After Experimental Infection. Poultry Science 78:1681-1689.
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Vitamin E prices have spiked amid production issues and lack of availability. How can you mitigate the increased cost of vitamin E inclusion?

Vitamin E prices often see severe fluctuations caused by raw materials shortages, production or distribution issues, or regulations on some key production ingredients (such as m-cresol anti-dumping rules in China leading to a global price spike some months ago).

SANTOQUIN acts as a preservative for Vitamin E, allowing more of this vitamin to enter the tissue where it exerts its antioxidant effect. In addition, in the presence of selenium, another important cellular antioxidant mineral, SANTOQUIN can help protect or spare the Vitamin E needed for proper cell function.

The Food and Agriculture Organization of the United Nations, FAO, clearly confirms this mode of action: “Dietary deficiencies of vitamins A and E seem to be ameliorated in certain circumstances and ethoxyquin promotes higher levels of vitamin A storage in the liver. Repletion/deletion experiments show that in both monogastric and ruminant animals, a diet containing an anti-oxidant protects fat soluble vitamins throughout ingestion and metabolism. The important benefit of antioxidants most probably lies in their conservation of essential nutrients and their improved utilization by the animal. Altogether too often, it is the practice to use levels of vitamin E far above the animals’ nutrient requirement and the result is economically unfavorable. It has been shown in diets designed for chicken and turkey breeders that ethoxyquin has a vitamin E sparing effect.”

Common causes of diarrhea

Despite various electrolyte drinks available from the veterinarian or in stores, too many calves still die as a consequence of diarrhea. The economic damage for the farms is immense.

The causes of the occurrence of diarrhea are diverse. Infectious causes such as viruses, parasites, bacteria, fungi, and non-infectious causes such as insufficient colostrum supply, feeding, and housing have a significant influence.

The diet of the newborn calf has a significant influence on scours. The following factors are decisive:

• The immune status of the calves
• Inadequate/incorrect preparation of the liquids
• Inadequate drinking hygiene

The development of diarrhea

In the first three weeks of life, diarrheal diseases are the most common and economically impactful diseases in newborn calves. In the first weeks of life, 75 to 85 % of calf diseases are related to diarrhea. The reason for this is that calves are born without immune protection. Their immunity is primarily built up in the first twelve hours by the supply of colostrum. After that, the intestinal barrier is barely passable for the antibodies.

The four most important pathogens are Rotavirus and Coronavirus, Cryptosporidium, and E.coli. These pathogens damage the intestinal lining, leading to water and minerals not being absorbed from the intestine into the blood. The minerals, instead of being assimilated, are lost and eliminated through feces.

Bacteria such as E.coli attach to the intestinal wall and produce toxins. Viruses, on the other hand, penetrate the intestinal wall in order to multiply. Both of them result in damages to the intestinal wall, which can allow fluids to leak out. The result is diarrhea.

Symptoms of diarrhea

The most important symptoms are:

• Sunken eyes as an expression of dehydration
• Reduced intake of fluids
• Lying down
• Low temperature
• Cold body surface
• Apathy or even coma

Types of diarrhea

There are different types of diarrhea, mainly the secretory and the malabsorptive form. Because of frequent mixed infections, the two forms of scours are often mixed.

Secretory diarrhea

The binding of toxins to the enterocytes’ cell surface receptors activates enzyme systems that lead to increased fluid secretion in the intestine. The intestinal lining can no longer absorb this increased fluid influx. The trigger for this can be, for example, an E.coli infection.

Malabsorptive diarrhea

The erythrocytes are destroyed and the villi are reduced in size. There is a loss of the microvilli. The result is a lower enzyme activity and resorption capacity. By this reduction in villi length, less fluid can be absorbed and has to be excreted through the intestine.

Importance of the colostrum supply

Low colostrum intake or a low quality of colostrum at birth results in the failure of passive transfer (FPT) due to the inadequate ingestion of colostral immunoglobulins. FPT is associated with an increased risk of mortality and decreased health status.

Adequate transfer of maternal immunoglobulins is associated with short- and long-term health advantages. These advantages are created by reducing pre- and post-weaning mortality due to infectious diseases, as well as by increasing daily weight gain, feed efficiency, fertility, and milk production in first and second lactation.

Colostrum is the elixir of life for newborn calves. As already mentioned, calves are born without their own active immune protection. Their immune system develops slowly. In order to obtain a first passive immunization, early administration of high-quality colostrum (≥ 50 mg IgG/ml) is of the highest importance.

The colostrum should be administered to calves as early as possible, but latest 4 to 6 hours after birth. The reason for early administration of colostrum is that the amount of immunoglobulins decreases with the passage of time after birth and with an increased milking number.

By the twelfth week, the calf has fully developed its own stable immune system and is therefore able to produce its own antibodies.

Economic consequences of diarrhea

The consequences of diarrhea and the associated costs should not be underestimated. Even a mild form of diarrhea costs the farmer money:

How to avoid diarrhea in calves

It is primarily essential that the calf is protected from fluid losses and that active diarrhea is avoided. Measures can be taken in advance to prevent the newborn calves from diarrhea:

• Cleaning the calving pen after each calving
• Bringing the calves into cleaned and disinfected boxes
• Regularly checking the quality of colostrum

But the most important basic requirement for a healthy start into life is to give 2 to 4 liters of colostrum within the first six hours of life. In addition to the timing, the quality of the colostrum is crucial. To that end, EW Nutrition developed a colostrum enhancer that improves colostrum management.

IgY can bind foreign substances like bacteria or viruses in the gut, which improves gut health and increases weight gain. The natural egg immunoglobulins act like maternal colostrum and bind to the pathogen epitopes. After that, the blocked pathogens cannot bind to the intestinal wall, preventing damage to the intestinal wall. Field studies prove the product’s efficacy, showing an 18 % higher daily weight gain and a 13 % higher weaning weight compared to the control group. Additionally, the IgG contained in Globigen Colostrum help you avoid a failure of passive transfer (FPT).

The application of Globigen Colostrum is very user-friendly and simple, as it can be mixed directly into the colostrum of the mother cow.

Higher profit through improved calf performance

The benefits of Globigen Colostrum are:

• Improved calf performance
• Lower incidence of diarrhea
• Improved weight gain
• Higher profit

The timely and adequate supply of colostrum is the most important factor in preventing infection-related calf diseases. Therefore, it is necessary to ensure that calves receive sufficient antibodies from the cow’s colostrum in the first days after birth.

References available upon request

What is dysbacteriosis?

Dysbacteriosis has been defined as the presence of a qualitatively and/or quantitatively abnormal microbiota in the proximal parts of the small intestine. This abnormal microbiota produces a cascade of reactions in the gastrointestinal tract, including reduced nutrient digestibility and impaired intestinal barrier function, increasing the risk of bacterial translocation and inflammatory responses (Panneman, 2000; Van der Klis, 2000 and Lensing, 2007).  Dysbacteriosis is not a specific disease but a secondary syndrome. Along the entire GI tract, there is a diverse microbial community comprised of bacteria, yeasts, archaea, ciliate protozoa, anaerobic fungi, and bacteriophages, commonly referred to as the intestinal microbiota.

Dysbacteriosis is an imbalance in the gut microbiota as a consequence of an intestinal disruption. The impact of dysbacteriosis can be separated into economic and welfare issues (Bailey, 2010). Dysbacteriosis can lead to very wet litter and caking issues. The prolonged contact of broilers with the caked litter can result in painful ulceration of the feet and hocks (pododermatitis and hock-burn), leading to a serious welfare issue and degradation of the carcass.

Apart from these issues, a major economic impact comes from reduced growth rates, FCR, and increased veterinary treatment costs (Kizerwetter-Świda and Binek, 2008).

Causes of dysbacteriosis

It is believed that both non-infectious and infectious factors can play a role in dysbacteriosis (DeGussem, 2007).

Non-infectious causes are:

• Diet
• Brooding
• Biosecurity
• Risk periods
• Environmental conditions

Diet

Intestinal bacteria derive most of their energy from dietary compounds. Thus, diet has a major influence over the bacterial populations (Apajalahti et al., 2004). Any change in feed and feed raw materials, as well as the physical quality of feed, influence the balance of the gut microbiota. Processing significantly affects the characteristics of the feed as a substrate for the bacterial community. Perhaps the temperature and pressure of the conditioning process give its characteristic signature to the bacterial community structure.

Inappropriate brooding conditions

The provision of optimal brooding conditions is essential for ensuring optimal gut microbiota development. Birds receiving appropriate brooding develop a gut that performs well and has a greater capacity to cope with the challenges of the broiler shed. Early access to feed and water is crucial. One of the most critical factors for the occurrence of dysbacteriosis is the lack of digesta. The microbiota can change in a period of hours when nutrients are not present. The quality of water is also essential to maintain normal intestinal function and digesta pH.

Faulty biosecurity

If clean-out and disinfection procedures are improperly conducted, pathogens will be introduced into the poultry shed, and exposure to these pathogens will influence gut health and development. It has been proven that litter management regimes affect chicken gastrointestinal tract (GIT) and microbiota (Wang et al., 2016)

Risk periods

There are times during poultry production when the bird will be challenged, for example, during feed changeovers, vaccination handling and transportation, overcrowding, or placement in new housing. During these periods, the gut microbiota can fluctuate and, in some cases, if management is sub-optimal, dysbacteriosis can occur.

Environmental conditions

Achieving optimal environmental conditions will promote good gut health. Any perturbation in gastroenteric physiology or immunity of the bird, caused by temperature stress or other environmental discomforts, can cause dysbacteriosis and/or enteritis. These are associated with lower absorption of nutrients by the host. Suzuki et al. 1983 demonstrated that overcrowding and heat stress, very commonly seen in intensive poultry farming, has a significant impact on the microbiota of chickens.

Infectious agents that potentially play a role in dysbacteriosis

• Mycotoxins
• Eimeria spp.
• Clostridium perfringens
• Other bacteria producing toxic metabolites

Mycotoxins

Many mycotoxins can stimulate the secretion of several antimicrobial molecules, which have positive effects on the maintenance of intestinal homeostasis. Fumonisins inhibit the growth of fungi, Fusarium toxins exhibit different antimicrobial defensive mechanisms, and aflatoxins exhibit a moderate antimicrobial activity against Escherichia coli, Bacillus subtilis, and Enterobacter aerogenes [Bevins et al. 1999 and Wan et al.2013]. Mycotoxins such as aflatoxins, trichothecenes, zearalenone, fumonisin, and ochratoxin can alter the normal intestinal functions, such as the barrier function and nutrient absorption. Some mycotoxins, like trichothecenes and ochratoxin, affect the histomorphology of the intestine (Winnie et al., 2018). Mycotoxicosis changes the population equilibrium, which can lead to dysbacteriosis.

Eimeria spp.

Coccidiosis caused by Eimeria spp. in chickens appears to be one of the principal destabilizing agents, causing the destruction of enterocytes and affecting the integrity of the intestinal mucosa and wall. The lesions that it causes, the inflammatory process, the reduced absorption and consequent excess of nutrients in the lumen all contribute to the proliferation of certain groups of bacteria. This situation clearly predisposes birds to intestinal dysbacteriosis and/or bacterial enteritis, and in particular to necrotic enteritis.

Clostridium perfringens

Clostridium perfringens is a natural part of the habitat in the hindgut that is not dangerous under normal circumstances. If it multiplies, the bacterium produces toxic substances that damage the intestinal mucosa and cause a condition called necrotic enteritis.  The disease is characterized by necrosis and inflammation of the GIT. Without treatment, this can escalate to perforation of the intestines, hemorrhages, and eventual death from septic shock.

Signs and consequences of dysbacteriosis

Dysbacteriosis can have profound effects on the host. Dysbacteriosis alters the GIT environment and favors the growth of pathogenic bacteria. Pathogenic bacteria produce toxins that increase intestinal motility or cause alterations in the amounts of mucus produced or in its composition. They also result in modifications of gastric acidity, reduction in the production of bacteriostatic peptides in the pancreas, and reduced immunoglobulin (IgA) secretion.

Toxins released by entero-pathogens damage intestinal villi, resulting in focal ulcerations of the mucosa, tissue necrosis, and shifts in gut microorganism numbers and metabolism. The costliest condition for animal production is the chronic inflammatory response of the animal to constant minor dysbacteriosis. These chronic responses can reduce weight gain and cause low feed conversion efficiency. Coccidiosis infections and any other enteric disease can be aggravated when dysbacteriosis is prevalent. Generally, animals with dysbacteriosis have high concentrations of Clostridium that generate more toxins, leading to necrotic enteritis.

In broilers, the syndrome is generally seen between 20 and 30 days of age (Wilson et al., 2005). Clinically, the main signs are:

• pale, glistening or orange droppings with undigested food particles
• wet and greasy droppings and hence dirty feathers
• sometimes foamy caecal droppings
• reduced physical activity
• increased water intake
• decrease in feed intake with a check in weight or reduced gain rates
• increased feed conversion

(Wilson et al., 2005; De Gussem, 2007)

Wet litter is also a general outcome of dysbacteriosis that may affect the air quality of the house, leading to a higher incidence of respiratory problems.

Additionally, foodborne pathogens such as Salmonella spp. and E.coli proliferate more in the dysbiotic intestine and can become persistent residents of the hindgut.

At necropsy, the main observations are

• a thin, fragile, often translucent intestinal wall
• watery or foamy intestinal contents
• frequent orange mucus and undigested particles in the intestines
• ballooning of the gut
• intestinal inflammation

(Pattison, 2002; De Gussem,2007)

Prevention of dysbacteriosis

The most important factors to prevent dysbacteriosis are

• Minimizing environmental stress
• Maintaining good water quality
• Improving feed digestibility
• Avoiding antinutritional factors, mycotoxins, and rancidity
• Feed additives that could modulate microbial component and avoid dysbacteriosis

Growth-promoting antibiotics are well known for the inhibition of undesired microbiota and the negative effects of their metabolites, and selection for beneficial bacteria. However, the adverse result is that they diminish the natural diversity of the gut microbiota. Antibiotics can also result in animals developing bacterial resistance.

Other products have been proposed as alternatives to growth promotion, taking into consideration the increasing bacterial resistance to some antibiotic categories.

Alternate feed additive technologies that have a promising role in controlling dysbacteriosis are:

• Probiotics
• Prebiotics
• Enzymes
• Organic acids
• Essential oils and phytomolecules

Probiotics

The post-hatch period is very critical for the chicks’ intestine development. Exposure to the environment in hatchery and farm affects microbial colonization in the intestine tract. The use of selective probiotics in day-old chicks at the hatchery and on the farm immediately after placement in broiler house reduces the risk of dysbacteriosis. Probiotics work by competitive exclusion, thereby prevent the colonization of potentially pathogenic bacteria. Probiotics prevent enteric diseases, improves intestine development and digestion process.

The benefits include enhanced growth and laying performance, improved gut histomorphology, immunity, and an increase in beneficial microbiota (Rajesh Jha et al., 2020)

Prebiotics: Mannan Oligosaccharide

(MOS) mimics the properties of the cells on the gut wall to attract and bind with harmful bacteria. Rather than allowing the bad bacteria to attach to the gut wall, the MOS acts as a sticky sponge, clearing up the harmful bacteria and removing them from the digestive system. MOS play an important role in gut functionality and health, through enhanced nutrient digestibility and improved gut barrier function and local defenses. MOS is also related to long villi and shallow crypts in the intestine, so a larger surface area helped with the absorption of nutrients and improved animal performance (Chand et al., 2016b)

Enzymes

Careful choice of feed enzymes will reduce nutrients available for pathogenic bacterial growth and improve gut health. Bacterial Xylanase is showing promise by digesting both soluble and insoluble arabinoxylans and reducing the viscosity of intestinal content. It maintains gut motility, improves nutrients digestibility, and impairs the growth of pathogenic bacteria in the hindgut.

Organic acids

Organic acids ameliorate the conditions of the GIT through the reduction of GIT pH, promoting proteolytic enzyme activity, intensifying pancreatic secretions. They encourage digestive enzyme activity and nutrient digestibility. Organic acids are creating stability of the microbial population by stimulating the growth of beneficial bacteriaPapatisiros et al., 2013).

Phytomolecules

Multiple scientific studies have proven the positive effects of phytomolecules (also known as phytogenics or secondary plant compounds) on the gut health of livestock animals. These substances support digestion and improve the utilization of nutrients. This results in higher daily weight gain and better feed conversion. In addition, phytomolecules have a proven antimicrobial effect, based on different biological modes of action.

EW Nutrition offers standardized phytomolecule-based solutions (Activo and Activo Liquid) that positively influence gut health and subsequent performance parameters in poultry. In scientific studies, the Activo product line has shown a positive effect on gut pathogenic bacteria, reducing necrotic enteritis (Fig 1) and improving production performance.

Conclusion

Dysbacteriosis can have profound effects on the host. Acute dysbacteriosis can result in the proliferation of pathogenic microorganisms that become enteropathogenic. Pathogenic bacteria can produce toxins and metabolites that increase gut motility, increase fermentation with gas production, change gut pH, irritate the mucosa, cause inflammation, and increase mucous secretion. This process reduces the digestibility and absorption of nutrients.

Maintaining the equilibrium of the gut ecosystem is key to avoiding dysbacteriosis. Improving feed digestibility and using feed additives that modulate gut microflora help to maintain more stable gut ecosystems, even during periods of intestinal stress preventing dysbacteriosis. Effective prevention and control of dysbacteriosis help increase poultry operations’ economic profitability by way of improved performance, health, and welfare, and reduce foodborne pathogens and environmental impact of poultry production.

References

Apajalahti, J., Kettunen, A., and H. Graham. 2004. Characteristics of the gastrointestinal microbial communities, with special reference to the chicken. World Poultry Sci J 60:223- 232.

Bailey, Richard A. 2010. Intestinal microbiota and the pathogenesis of dysbacteriosis in broiler chickens. PhD thesis submitted to the University of East Anglia. Institute of Food Research, United Kingdom.

Bevins, C. L.; Martin-Porter, E.; Ganz, T. Defensins and innate host defence of the gastrointestinal tract. Gut, 1999, 45, 911–915.

De Gussem , M. 2007. Coccidiosis in poultry: review on diagnosis, control, prevention and interaction with overall gut health . In Proceedings of the XVI European  Symposium on Poultry Nutrition (pp. 160 169 . Strasbourg , France.

Gurrre, Philippe. 2020. Review Mycotoxin and Gut Microbiota Interactions. Toxins, 12, 769.

Jha, Rajesh, Razib Das, Sophia Oak, and Pravin Mishra, 2020. Probiotics (Direct-Fed Microbials) in Poultry Nutrition and Their Effects on Nutrient Utilization, Growth and Laying Performance, and Gut Health: A Systematic Review. Animals (Basel). 10(10): 1863.

Kizerwetter-Świda, M., and M. Binek. 2008. Bacterial microflora of the chicken embryos and newly hatched chicken. Journal of Animal and Feed Sciences 17:224-232

Panneman, H. 2000 . Clostridial enteritis/dysbacteriosis, fast diagnosis by T-RFLP, a novel diagnostic tool. In Proceedings of the Elanco Global Enteritis Symposium. Cork Ireland.

Papatisiros VG, Katsoulos PD, Koutoulis KC, Karatzia M, Dedousi A, Christodoulopoulos G. Alternatives to antibiotics for farm animals. CAB Rev Ag Vet Sci Nutr Res. (2013) 8:1–15. doi: 10.1079/PAVSNNR20138032.

Pui-Pui, Winnie, and Sabran Mohd-Redzwan. 2018. Mycotoxin: Its Impact on Gut Health and Microbiota. Frontiers in Cellular and Infection Microbiology, 8:60.

Rebel, J.M.J., Balk, F.R.M., Post, J., Van Hemert, S., Zekarias, B. and Stockhofe, N. 2006. Malabsorption syndrome in broilers. World’s Poultry Science Journal, 62: 17–29.

Saeed, Mohammad, Fawwad Ahmad, Mohammad Asif Arain, Mohamed E Abd El-Hack, Mohamed Emam, Zohaib Ahmed Bhutto and Arman Moshaven, 2017. Use of Mannen – Oligosaccharides (MOS) As a Feed Additive in Poultry Nutrition. J. World Poult. Res. 7(3): 94-103.

Suzuki, K., R. Harasawa, Y. Yoshitake, and T. Mitsuoka. 1983. Effects of crowding and heat stress on intestinal flora, body weight gain, and feed efficiency of growing rats and chicks. Nippon Juigaku Zasshi 45:331-8.

Van der Klis, J.D. and Lensing, M. 2007. Wet litter problems relate to host–microbiota interactions. World Poultry, 23: 20–22.

Wan, M. L.; Woo, C. S.; Allen, K. J.; Turner, P. C.; El-Nezami, H. Modulation of porcine-defensins 1 and 2 upon individual and combined fusarium toxin exposure in a swine jejunal epithelial cell line. App. l. Environ. Microbiol., 2013, 79(7), 2225-2232

Wang L, Lilburn M, Zhongtang Y. 2016. Intestinal microbiota of broiler chickens as affected by litter management regimens Front. Microbiol (2016).

Wilson, J., Tice, G., Brash, M.L. and St Hilaire, S. 2005. Manifestations of Clostridium perfringens and related bacterial enteritides in broiler chickens. Worlds Poultry Science Journal, 61: 435–449.

Lutein belongs to the group of carotenoids, which is divided into carotenes and xanthophylls. Lutein, chemically expressed as “3,3’-dihydroxy-α-carotene”, is a xanthophyll always accompanied by its isomer zeaxanthin. It is synthesized out of two α-carotenes through hydroxylation.

Lutein provides benefits for animals and humans

Lutein has antioxidant protective properties

Under normal conditions, the cells in the animal and human organism control ROS (reactive oxygen species) levels. Usually, there is a balance between the generation of ROS and their elimination by scavenging systems. However, the high performance levels in modern animal production can easily lead to high ROS levels, translated into oxidative stress and leading to cell damage. Cell damage contributes to the generation of cancer and early aging in humans. In animals, the negative impact of oxidative stress can be responsible for lower performance and inferiority of meat and eggs.

Antioxidants stop ROS by taking up their energy

Through the uptake of energy, molecules can get into an excited state. One example is singlet excited oxygen, a highly reactive form of oxygen able to destroy proteins, lipids, and DNA. Carotenoids can intervene in this process: by exchanging electrons, the singlet excited oxygen gets neutralized, and the carotenoid gets into this excited state with higher energy. Once able to release this energy as heat into the environment, the carotenoid gets back to its normal state and can once again start acting as an antioxidant.

In this way, carotenoids, including lutein, ‘quench’ the energy of excited molecules and prevent the adverse effects of ROS (reactive oxidative substances).

Antioxidant properties profitably used

The antioxidant character of lutein plays an important role in the treatment or prophylaxis of macular degeneration in humans (Landrum & Bone, 2001). There is also evidence that lutein can be used to improve the visual and retinal function in dogs (Wang et al., 2016). In the eye, lutein and zeaxanthin, occurring in the retina and the macula, neutralize free radicals produced due to the ultraviolet light and thereby prevent damage to the macula.

Further possible applications are against cardiovascular diseases (Dwyer et al., 2001)  and various types of cancer (e.g., breast cancer, Gong et al., 2018).

Lutein is important in infant nutrition

Lutein and its isomer zeaxanthin are the two primary carotenoids found in human milk (Giordano and Quadro, 2018). Stringham and co-workers (2019) postulate that lutein plays an important role in children’s visual and cognitive development/optimization. They report that a lutein supplementation of the mother can lead to a higher concentration of this substance in the milk and, consequently, in the child’s plasma (Sherry et al., 2014). In dairy cows, an increased level of lutein in the milk can also be observed (Xu et al., 2014), suggesting that lutein could also be essential in calf development.

Lutein stimulates the immune system

Another benefit of lutein is its positive influence on the immune system.

On the one hand, lutein stimulates the production of antibodies. In dogs, Guimarães Alarça et al. (2016) could show an increase of CD4+ and CD8+ T-lymphocyte subtypes. Kim et al. (2000) demonstrated the increase of lymphocytes and cells expressing CD5, CD4, CD8, and major histocompatibility complex class II (MHC II) molecules. Bédécarrats and Leeson (2006) provoked a higher secondary antibody response to infectious bronchitis vaccination in laying hens.

Besides, lutein acts as an anti-inflammatory agent, as shown in vitro by Chao et al. (2015) and in broiler chickens by Moraes and team (2016).

Lutein improves the attractivity of poultry products

In the marketing of poultry products, appearance and color are of central importance for evaluating quality. Egg yolk coloration is to a large extent a matter of regional preferences, however it is clear that an egg with a yolk that does not have the typical color is classified as inferior by the consumer. In areas with traditional corn growing, a white-skinned chicken is not commercially viable. Even when pullets are bought, the shanks and beaks should be yellow.

The use of xanthophylls like lutein and zeaxanthin enables producers to safely control the color of the egg yolk and of the broiler skin. It also leads to a healthy color of the shanks and beaks of the birds.

Lutein in a nutshell

Lutein is a true all-rounder: a substance that delivers benefits across the board. In plants, it helps fruits and petals become attractive for insects and other animals. It positively influences the animal, acting as an antioxidant, promoting infant development, and stimulating the immune system. As a pigment, it makes poultry and poultry products look more attractive to the consumer. Through its presence in eggs and milk, lutein provides clear and clean benefits to both animals and humans.

References

Bédécarrats, G.Y. and S. Leeson. “Dietary lutein influences immune response in laying hens.”  J. Appl. Poult. Res. 15 (2006): 183–189.

https://doi.org/10.1093/japr/15.2.183

Chao, Shih-Chun, Tommaso Vagaggini, Chan-Wei Nien, Sheng-Chieh Huang, and Hung-Yu Lin. “Effects of Lutein and Zeaxanthin on LPS-Induced Secretion of IL-8 by Uveal Melanocytes and Relevant Signal Pathways.” Journal of Ophtalmology, vol. 2015 Article ID 152854 (2015): 7 pages. https://doi.org/10.1155/2015/152854

Dwyer, James H., Mohamad Navab, Kathleen M. Dwyer, Kholood Hassan, Ping Sun, Anne Shircore, Susan Hama-Levy, Greg Hough, Xuping Wang, Thomas Drake, C. Noel Bairey Merz, and Alan M. Fogelman. “Oxygenated Carotenoid Lutein and Progression of Early Atherosclerosis.” Circulation (American Heart Association) 103, no. 24 (2001): 2922-2927.

https://doi.org/10.1161/01.CIR.103.24.2922

Gong, Xiaoming, Joshua R. Smith, Haley M. Swanson, and Lewis P. Rubin. “Carotenoid Lutein Selectively Inhibits Breast Cancer Cell Growth and Potentiates the Effect of Chemotherapeutic Agents through ROS-Mediated Mechanisms.” Molecules 23 no. 4(2018): 905.

http://dx.doi.org/10.3390/molecules23040905

Guimarães Alarça, Laís, Fabiane Yukiko Murakami, Ananda Portella Félix, Everton Luis Krabbe, Simone Gisele de Oliveira, Sebastião Aparecido Borges da Silva. “Dietary lutein supplementation on diet digestibility and blood parameters of dogs.” Cienc. Rural 46 no.12 (2016)

http://dx.doi.org/10.1590/0103-8478cr20151493

Kim, Hong Wook, Boon Chew, Teri Ann S Wong, Jean Soon Park, Bor-Chun Weng, Katherine M Byrne, Michael G Hayek, and Gregory A. Reinhart. “Dietary lutein stimulates immune response in the canine.” Veterinary Immunology and Immunopathology 74 no. 3-4 (2000): 315-327.

https://doi.org/10.1016/S0165-2427(00)00180-X

Landrum, J. T. and R.A. Bone. “Lutein, zeaxanthin, and the macular pigment.” Archives of Biochemistry and Biophysics 385 no. 1 (2001): 28–40.

https://doi.org/10.1006/abbi.2000.2171.

Moraes, M. L., A. M. L. Ribeiro, E. Santin, and K. C. Klasing. “Immunology, health, and disease: effects of conjugated linoleic acid and lutein on the growth performance and immune response of broiler chickens.” Poultry Science 95 (2016): 237–246.

http://dx.doi.org/10.3382/ps/pev325

Ochoa Becerra, Mario, Luis Mojica Contrerasa, Ming Hsieh Loa, Juan Mateos Díaz, Gustavo Castillo Herrera. “Lutein as a functional food ingredient: Stability and bioavailability.” Journal of Functional Foods 66 (2020): 103771.

https://doi.org/10.1016/j.jff.2019.103771

Sherry, Christina L.,  Jeffery S. Oliver, Lisa M. Renzi, and Barbara J. Marriage. “Lutein supplementation increases breast milk and plasma lutein concentrations in lactating women and infant plasma  concentrations but does not affect other carotenoids.” J. Nutr. 144 (2014): 1256–1263.

http://dx.doi.org/10.3945/jn.114.192914

Stringham, James M., Elizabeth J Johnson, and B Randy Hammond. “Lutein across the lifespan: From childhood cognitive performance to the aging eye and brain.” Curr Dev Nutr 3 (2019): nzz066.

http://dx.doi.org/10.1093/cdn/nzz066

Wang, Wei, Jerome Hernandez, Cecil Moore, Janet Jackson, and Kristina Narfström. “Antioxidant supplementation increases retinal responses and decreases refractive error changes in dogs.” J. Nutr. Sci. 5 e18 (2016): 7 pages

http://dx.doi.org/10.1017/jns.2016.5

Xu, C.Z., H. F. Wang, J. Y. Yang, J. H. Wang, Z. Y. Duan, C. Wang, J. X. Liu , and Y. Lao. “ Effects of feeding lutein on production performance, antioxidative status, and milk quality of high-yielding dairy cows.” J. Dairy Sci. 97;  American Dairy Science Association (2014):7144–7150

http://dx.doi.org/10.3168/jds.2014-8276

by Technical Team, EW Nutrition

_{Sub-acute acidosis (SARA) is linked to high levels of ruminal LPS. The LPS cause inflammation and contribute to different metabolic conditions and diseases. Various strategies and solutions can be applied to modulate the rumen microbiota and prevent this risk.}

_{In sub-acute rumen acidosis (SARA), the quantity of free lipopolysaccharides (LPS) coming from Gram- bacteria increases considerably. These LPS cross the ruminal wall and intestine, passing into the bloodstream. The negative consequences on the health of the animal are then reflected in decreased productive and reproductive performance.}

_{The LPS are released during the lysis of GRAM- bacteria which die due to the low pH, and these bacteria are mainly responsible for the production of propionic acid for the energy yield that is obtained. It is essential to preserve ruminal balance between Gram+ and Gram- such that there is no excess of LPS.}

Nutritional needs of lactating cows with SARA

_{In the first phase of lactation (from 1 week after calving to 80 – 100 days of lactation), the cow needs a high energy level to meet the large demand for milk production. This energy demand is often not fully satisfied and feed intake falls short. This deficit leads to the need to provide as much energy as possible per feed ration.}

_{Imagine a 650 kg live weight cow, producing about 35 kg of milk per day with a fat percentage of 3.7 and a protein percentage of 3.2. To achieve this production level and fulfill its maintenance requirements, this animal needs a feed intake of 22 kg of dry matter (DM) per day, with an energy level of 21 UFL equal to 36,000 Kcal/day of NE l (Net Energy Lactation)).}

_{To obtain an energy supply of this type, it is necessary to provide rations with a high content of cereals rich in nonstructured carbohydrates (NSC). This will allow the animals to obtain the maximum efficacy in getting the NE I from the metabolizable energy  (ME) expressed as kl*.}

*_{kl expresses the effectiveness in passing from EM to EN l net of the heat dissipated by the animal, therefore kl = ENl/EM (Van Es 1978).}

_{Compared to a diet rich in NDF (Neutral Detergent Fiber), this type of diet promotes and stimulates certain strains of bacteria to the detriment of others, shifting the balance towards a greater population of bacteria that produce propionic acid instead those which produce acetic acid. This change also determines a greater share of Gram- compared to Gram+.}

What is rumen acidosis?

_{Rumen acidosis is that “pathology” whereby the volume of SCFA (Short Chain Fatty Acids) produced by the rumen bacteria is greater than the ability of the rumen itself to absorb and neutralize them. Rumen acidosis is mainly caused by the amylolytic and saccharolytic bacteria (Streptococcus bovis; Selenomonas ruminantium, Bacteroides amylophilus, Bacteroides ruminicola and others) responsible for the production of lactic acid. Unlike the other most representative volatile fatty acids (acetic, butyric and propionic), lactic acid has a lower pKa: 7 (3.9 versus 4.7). This means that for the same amount of molecules produced, lactic acid releases a number of ions H}⁺ _{in the fluid ten times greater than other VFAs, with evident effects on the pH.}

_{Ruminal acidosis can be characterized as acute or subacute. During acute ruminal acidosis, the pH in the rumen drops below 4.8 and remains low for an extended period of time. Acute acidosis leads to complete anorexia, abdominal pain, diarrhea, lethargy, and eventually death. However, the prevalence of acute acidosis in dairy is very low.}

Consequences of rumen acidosis

_{In such situations, a series of negative consequences can be triggered in the lactating cow. Investigations (for instance, using fistulated cows) can reveal, among others, the following alteration in the rumen:}

• _{Shift in total microbiome rumen profile (density; diversity; community structure)}
• _{Shift in protozoa population (increase in ciliates protozoa after 3 weeks of SARA; increase in the GNB population)}
• _{Shift in fungi population (decreasing the fungi population with high fibrolytic enzymes, which are sensitive to low pH)}
• _{Rise in LPS rumen concentration (increasing the GNB strain and their lysis)}
• _{Influence on the third layer of Stratified Squamous Epithelium (SSE) (desmosomes and tight junctions)}
• _{Lower ruminal fiber degradation (reduction in the number of cellulolytic bacteria which are less resistant to acid pH)}
• _{Reduction of the total production of fatty acids (propionic, acetic, butyric), therefore less available energy}
• _{Lower rumen motility (also as a consequence of the smaller number of protozoa)}
• The increased acid load damages the ruminal epithelium
• _{Acid accumulation increases the osmotic pressure of the rumen inducing an higher flux of water from the blood circulation into the rumen, causing swelling and rupture of rumen papilla as well as a greater hemoconcentration}

_{The last points are extremely important, as it enables an easier passage of fluids from the blood to the pre-stomachs, greatly influencing the fermentation processes.}

_{Furthermore, with diets low in NDF, the level of chewing and salivation is certainly lower, with a consequent lower level of salivary buffers that enter the rumen and which would maintain an appropriate pH under normal conditions.}

Rumen sub-acute and acute acidosis: a fertile ground for LPS

_{Studies inducing SARA in dairy cows have shown that feeding high levels of grain causes the death and cell lysis of Gram- bacteria, resulting in higher concentration of free LPS in the rumen. In a trial conducted by Ametaj et al., in 2010 (Figure 1), a lower ruminal pH and an increase in the concentration of LPS in the rumen fluid -measured as ng / ml (nanograms / milliliter)-, was the result of increasing of NSC present in the diet (% of grains).}

_{In the rumen, the presence of Gram- is very significant, however the dietary changes towards high energy concentrates, reduce the substates necessary for them to thrive, leading to their lysis and favoring gram-positive bacteria (Gram+). Gram+ also produce bacteriocins against a wide variety of bacteria, including many Gram-. Figure 2 shows the influence of ruminal pH in the population of different bacteria, many of which are are crucial for the production of SCFA and therefore of energy.} 

_{It is therefore necessary to pay close attention to the energy level of the ration as an energy input (generally around 1500 – 1700 Kcal/kg of DM intake). At the same time, we need to ensure that the animal does receive and ingest that daily amount of DM. If ingestion is negatively influenced by acidosis (clinical or sub-clinical), this can lead to endotoxemia, with harmful consequences for the animal’s health and production performance.}

_{We can therefore note that the level of LPS (endotoxins) present in the rumen is directly correlated with the pH of the rumen itself and with a symptomatologic picture dating back to SARA. This occurs when the mortality and lysis of Gram- bacteria (GNB) is high and through the consequent imbalance created with diets containing excess fermentable starches, compared to diets with higher fiber content.}

_{In fact, it was shown that the transition from a concentrated fodder ratio of 60:40 to a more stringent ratio of 40:60 caused the level of free LPS in the rumen to go from 410 to 4.310 EU / ml.}

Endotoxemia: Pathological consequences in dairy cows

_{Once the LPS enter the bloodstream, they are transported to the liver (or other organs) for the detoxification. However, sometimes this is not enough to neutralize all the endotoxins present in blood. The remaining excess can cause issues such as the modification of the body’s homeostasis or cause that cascade of inflammatory cytokines responsible for the most common pathologies typical in cows in the first phase of lactation. The most common symptoms are the increase of somatic cells in milk or claws inflammation.}

_{Pro-inflammatory cytokines as TNF, IL6 and IL8 induced by LPS-related inflammation are able to stimulate the production of ACTH (adrenocorticotropic hormone).}

_{ACTH, together with cortisol and the interleukins, inhibit the production of GnRH and LH, with serious effects on milk production. The productivity and the fertility of the animal are thus compromised.}

_{Moreover, prostaglandins are as well stimulated by LPS, and are linked with fever, anorexia and ruminal stasis. This not only limits the amount of energy available for production and maintenance functions, but also induces a higher susceptibility to disease and adds-up to the emergence of other metabolic conditions, such as laminitis and mastitis.}

Preventing rumen acidosis

_{The solution to these massive risks is a prudent and proactive approach by the nutritionist towards all situations that can cause a rapid increase of Gram- in the rumen. It is therefore necessary to avoid cases of clinical and sub-clinical acidosis (SARA) in order to avoid the issues listed above. This would also help avoid stressful conditions for the animal that would lead to decreased performance and health.}

_{To maintain balance and a healthy status of the animal, the use of additives such as phytomolecules and binders is suggested in the first phase of lactation, starting from 15 days before giving birth.}

_{Activo Premium (a mix of phytogenic substances) has given excellent results in decreasing the acetic/propionic acid ratio, while safeguarding the population of Gram+ bacteria. This is in contrast to treatments with ionophores, which, as is well known, interfere with the Gram+ population.}

Case study. Acetic acid:propionic acid ratio with Activo Premium

_{In a study conducted at the the University of Lavras and the Agr. Res. Comp. of Minas Gerais (both Brazil), 30 Holstein cows were allocated to two groups considering parity and milk production. One group was fed the standard feed (control), the other group received standard feed containing 150mg of Activo Premium/kg of dietary dry mass (DM). The following parameters were measured or calculated: intake of DM and milk production, milk ingredients such as fat, protein, lactose every week, body weight and body condition score every two weeks, and ruminal constituents (ph and SCFAs) through oesophaeal samples at day 56.}

_{Activo Premium was able to decrease the ratio between acetic acid and propionic acid, and at the same time maintain the level of Gram+ bacteria in the rumen, thus reducing the risk of endotoxins. The same trial carried out at the University of Lavras demonstrated how the performance of the animals was superior in the group fed with Activo Premium compared to the control group (see below).}

Solution: Preserve Gram+ bacteria levels while decreasing free LPS

_{We have therefore seen how important it is to decrease the acetic:propionic ratio in the rumen to obtain a greater share of available energy. However, the level of endotoxins in the rumen must remain low in order to avoid those problems of endotoxemia linked to very specific pathologies typical of “super productive cows”. These pathologies (always linked to inflammatory manifestations) can be prevented by decreasing the level of free LPS in the rumen with a product that can irreversibly bind the LPS and thus make them inactive.}

_{In a trial with porcine intestinal cells (IPEC-J2) challenged by E. coli LPS, a decrease in the intensity of inflammation was observed when Mastersorb Gold was added. This decrease could be shown through a lower amount of phosphorylated NF-kB in an immunofluorescence trial, as well as through the reduced production of Interleukin (IL)-8 in the cells measured by ELISA.}  

_{The fact that pig intestine tissue was used does not affect the adsorption concept. In this case, these intestinal cells are only a vehicle to demonstrate that in an aqueous solution containing 50 ŋg of LPS / ml and in the same solution with the addition of Mastersorb Gold, the level of LPS actually active is decreased, as a part of the LPS was tied up by Mastersorb. The solution with a lower level of LPS gave minor “inflammatory” reactions to intestinal cells, and this can be statistically reported in dairy cows.}

_Conclusions

_{To demonstrate how the decrease in the level of LPS in the rumen is directly correlated with inflammatory states in general, a trial with a total of 60 dairy cows shows that the inclusion of 25g of Mastersorb Premium/animal/day increases milk yield and improves milk quality by decreasing somatic cell count. Adsorbing substances contained in Mastersorb Premium tie up the LPS produced in the rumen in different cow lactation phases.}

_{Normally, the rise in the level of somatic cells in milk depends on etiological agents such as Streptococcus spp, Staphylococcus spp, mycoplasma and more. LPS stress is not the sole agent responsible for raising somatic cell counts, but also other factors among which:}

• _{Lactation stage and age of the animal}
• _{Season of the year (in summer the problem is increased)}
• _{Milking plant (proper maintenance)}
• _{General management and nutrition}

 _{However, by reducing the level of LPS, Mastersorb provides an important aid to decrease somatic cell count.}

Prevent escalation with rumen balance

_{In the end, ruminant producers are, like all livestock operations, interested in producing healthy animals that can easily cope with various stressors. Ensuring a proper diet, adjusted to the energy requirements of various production stages, is a first step. Providing the animal with the ingredients that modulate the microbiota and reduce the negative impact of stress in the rumen is the next essential step in efficient production.}