4 steps to improve dairy cow fertility through feeding

Group of dairy cows on meadow

by Judith Schmidt, Product Manager On-Farm Solutions

The average pregnancy rate for dairy cows has declined over the past decades. But why is my cow not getting pregnant? Is it because of feeding? These are questions we ask ourselves when things do not quite work out with the offspring in the cowshed. Economic success in the cow barn is closely related to the successful reproduction of our cattle herd.

Group of brown calves

The maintenance and possible improvement of fertility are becoming increasingly important issues for farm productivity. Infertility is still one of the main reasons for culling on dairy farms. When farmers decide to cull a cow after a few unsuccessful inseminations, they often ask themselves whether this could not have been prevented. There is no “all-encompassing” solution for achieving an optimal fertility rate, which ultimately requires excellent management. Relevant factors include oestrus monitoring and insemination timing, genetic conditions, feeding, hygiene, and climate.

How can I tell if a cow is in heat?

A cow behaves differently than usual during oestrus. She is restless and walks around more. A cow in heat stands next to other cows – head to tail. Sie also quarrels with her herd mates or sniffs at the shame of the other cows. Fertility in cows decreases during late winter and spring; the resulting absence of clear signs of oestrus makes it difficult to recognize the right time for insemination. There are several possible causes which will be reviewed below.

Possible causes of fertility problems in dairy cows

Beta-carotene deficiency

A productive herd needs to receive an optimal mineral and trace element supply. Beta-carotene, in particular, is essential for herd fertility. But why?

Beta-carotene is an orange-yellow plant pigment whose name comes from “carrot” because of its appearance. It is also a precursor of vitamin A. Both as a precursor and as vitamin A itself, it is essential for the organism of humans and animals, particularly when it comes to the fertility of dairy cows. Besides its important function as provitamin A, beta-carotene also exerts an independent effect on the ovary. It influences the quality of the follicle and the corpus luteum. Beta-carotene also protects the corpus luteum. It promotes the synthesis of the pregnancy hormone progesterone and thus enables the fertilized egg to implant successfully in the uterine lining.

A beta-carotene deficiency can lead to the following problems:

  • Smaller, not fully functional follicles
  • Altered oestrus intervals
  • Indistinct signs of oestrus
  • Decreased corpus luteum quality

Scientific trials show how much a beta-carotene deficiency influences the fertility process. With a beta-carotene deficiency, the fertilization rate after the first insemination is only 40%, whereas with a normal beta-carotene supply, the fertilization rate is about 70%.

How do I know if my herd is deficient in beta-carotene?

The easiest way is to check the color of the fresh colostrum. If it is a deep yellow to an even orange, the cows are supplied with sufficient beta-carotene. If it looks more ivory, this is a sign of a deficiency. Of course, a poor herd fertilization rate can also indicate a deficiency. If you suspect a beta-carotene deficiency, it is best to test some blood samples from your animal or use a testing device such as a carotene photometer. With such a test kit, you can determine not only the levels in the blood but also in the colostrum and the milk.

Feeding deficiencies

Feeding plays a major role in fertility issues. High input rates often have a negative effect on the health of cows. Feed quality and herd management have an impact on how long the cow loses weight after calving and at what point she gains weight again. One must always keep in mind the cows’ feeding, energy balance, and nutrient supply because cows with a negative energy balance often do not show oestrus. It is also important that the silage is of high quality – poor silage inhibits fertility.

Follicle quality

The quality of the follicle is crucial for good fertility. The quality is influenced by the energy supply during the dry period and lactation during the first days. Since the follicles are already formed in the last days of gestation, a lack of energy during this period means that the maturation of the follicles – even with a better supply later on – can no longer proceed optimally and is ultimately inferior. This inevitably leads to a reduction of oestrus symptoms and minimizes the chances of successful insemination.

Prevention is key: 4 steps to improve fertility through feeding

1) Avoid stress in the feeding environment

Well-being and a high feed intake are the basis for high milk and fattening yields as well as healthy and fertile animals. Dry cows and transit cows particularly should only experience low stress. This means no overcrowding and generous feeding space, i.e., each animal should have its own feeding space. Feeding areas that are too narrow prevent the animals from eating, rank fights occur, and feed intake decreases.

Freshly lactating cows should be separated from the group. If the cows are in calving pens or calving stables, they should always have visual contact with the herd.

2) Optimize feed quality and rations

Feed quality and feeding management determine how long the cow loses weight after calving (negative energy balance) and at what point the cow gains weight again (positive energy balance). Optimal fertility performance can only happen when a positive energy balance is achieved.

Calf drinking from cow

The cow’s fertility performance is primarily determined by nutrient supply and feeding. At the beginning of the lactation, high-quality basic feed with a high energy concentration should be fed, as feed intake is slow to get going after calving. Nevertheless, this ration should have sufficient structure. The amounts of concentrate should be divided into several individual portions and carefully increased. For high feed intakes, fresh water should be constantly available to the animals.

3) Treat diseases early to enable feeding

Diseases that lead to a reduced appetite should be treated as early as possible. In particular, attention should be paid to healthy hooves because a cow that has pain or difficulty getting up and walking is much less likely to go to the feed table.

4) Supplement vitamins, minerals, and trace elements

The needs-based supply of vitamins, minerals, and trace elements in every performance phase is a decisive success factor for good herd fertility. A sufficient supply of trace elements, especially selenium, manganese, zinc, as well as vitamin A and beta-carotene, are important for the formation of fertility hormones and optimal insemination success. At the same time, they ensure a high colostrum quality.

EW Nutrition’s Fertilgol Bolus is a long-term bolus to support fertility. The high content of beta-carotene has a positive influence on the formation of the corpus luteum, the oestrus cycle, the quality of colostrum and sperm. The release rate of the ingredients beta-carotene, selenium, vitamin A, and other trace elements takes place over at least twenty days. Fertilgol Bolus can be used for female and male breeding animals shortly before and during the breeding or insemination period.

How to reduce methane emissions in dairy cows: phytogenic solutions

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by EW Nutrition


The world demand for milk has seen a sharp rise. Today, we have just over 1 billion dairy cows in the world producing about 1.6 billion tons of milk per year. However, OECD and FAO estimate that numbers will rise up to 1.5 billion dairy cows in 2028, for a total milk production of 2 billion tons . This increase will come at a tremendous cost in terms of global warming: Each day, dairy cows can produce 250 to 500 litres of methane, a powerful greenhouse gas (Johnson and Johnson, 1995).

Dairy cows

Climate change is not the only reason for zootechnical production to adopt methane reduction strategies. Methane emissions represent an important energy loss for dairy cows, which negatively impacts production performance. In this article, we review why methanogenesis in dairy cows arises, and how the use of phytogenic product Activo Premium can help achieve efficient energy use and reduced climate impact.

Less methane: environmental, regulatory, and business pressures

Methane (CH4) is considered one of the gases that, together with CO2 (carbon dioxide) and N2O (nitrous oxide), traps heat in the atmosphere and, thus, causes global warming. While methane is generated in multiple industries, including the energy and waste sectors, much of the methane present in the atmosphere derives from livestock activities and, in particular, from ruminant farms.

About 28% of total methane emissions derive from agriculture sector and enteric fermentations (digestive processes in which feed is broken down by microorganisms) are responsible for about 65% of the total methane coming from zootechnical sector (Knapp et al., 2014). For this reason, in recent years, strategies for mitigating methane emissions in dairy cows have aroused great interest among researchers and environmentally-conscious consumers.

Regulators have also caught on: In October 2020, the European Commission presented its strategy for reducing methane emissions in Europe. Reductions are essential to achieve the Commission’s climate objectives for 2030 and climate neutrality by 2050. For the livestock sector, the Commission seeks to develop an inventory of innovative mitigating practices by the end of 2021, with a special focus on methane from enteric fermentation.

Uptake of mitigation technologies will be promoted though Member States’ and the Common Agricultural Policy’s “carbon farming” measures. Carbon-balance calculations at farm level are to be encouraged through digital tools; and the Horizon Europe strategic plan 2021-2024 will likely include targeted research on effective reduction strategies, focusing on technology, dietary factors, and nature-based solutions such as phytogenic products.


Even aside from environmental concerns, consumers demands, and regulatory steps, there is a critical business case for dairy producers to lower methane emissions. Given the ever-increasing global demand for dairy products, farmers and other operators in the sector more than ever try to maintain and indeed improve production to maximize yields, both economically and in terms of finished products. Problematically, methane production in the rumen represents a great loss of energy for the animal.

On average, about 6% of the total energy ingested by a dairy cow is transformed into methane, every single day (Succi and Hoffmann, 1993). The less methane a cow produces, the more metabolizable energy (ME) she gets out of her gross energy (GE) intake. A better ME/GE ratio translates into higher net energy of lactation (NEl). Energy losses from methanogenesis thus directly decrease the energy nutritionist can consider as usable during rationing.

Before we review the current research on how an adequate manipulation of the diet and of the rumen environment can mitigate these energy losses, we need to ask ourselves, why is methane formed in the rumen at all?

Animal physiology: how methane is formed in the rumen

Ruminants’ digestion of vegetal ingredients is linked to their rumen’s symbiotic bacterial, protozoan, and fungal flora. This microbiota has all the enzymatic properties necessary for the digestion (or rather pre-digestion) of ingested forage, including some cellulose fractions that monogastric animals cannot use.

In the rumen, the main products deriving from bacterial fermentation are volatile fatty acids and methane. The main volatile fatty acids are acetic acid, propionic and butyric acid, which are mainly absorbed and used by the animal. Meanwhile, methane helps to maintain the oxidative conditions in the rumen’ anaerobic environment, but also represents an energy loss (Czerkawski, 1988).

Methanogenesis is carried out by methanogenic bacteria and archae in the rumen (Guglielmelli, 2009). They use molecular hydrogen and carbon dioxide as a substrate for the synthesis of methane, according to the following equation:

4 H2 + CO2 → CH4 + 2 H2O

A few other chemical reactions contribute to methanogenesis, but they all have one thing in common: they require hydrogen ions in the rumen fluid to form methane from CO2. This gives us the first “point of attack” for reducing methane formation: the diet.

Increase the share of propionic acid

Propionic acid is in competition with methanogens in using hydrogen ions to reduce glucose molecules:

C6H12O6 (glucose) + 4 H → 2 C3H6O2 (propionic) + 2 H2O

It is clear that if propionic fermentations are stimulated through the diet at the expense of the pathways leading to acetate and butyrate (where hydrogen ions are transferred to the rumen environment), the availability of hydrogen for the reduction of CO2 by methanogenic bacteria decreases.

Diets with a high level of concentrates, and low levels of neutral detergent fibre, yield more propionic acid and less acetic and butyric acid. Set aside lower methane emissions, this increase in energy is desirable during peak lactation: the energy gap that follows from the decrease in ingestion by the animal requires diets with a high amount of substrate for gluconeogenesis. Furthermore, the greater production of propionate sequesters H2 in the rumen environment and, consequently, less CO2 is reduced to methane.

Optimize the protozoa count

Most methane-producing bacteria live in symbiosis with most of the protozoan species, they are located on the surface of the protozoan. It follows that optimizing the population of protozoa present in the rumen (through dietary measures) leads to a lower methanogenesis (Patra and Saxena, 2010). Naturally, a minimum amount of protozoa must be maintained to avoid excessively reducing ruminal motility (regular contractions that mix and move the rumen content), which is important for feed digestibility.

Diet is not enough: feed additives to reduce methane production

Dietary measures alone cannot considerably reduce daily methane production. In the past, antibiotic growth promoters belonging to the ionophores family were commonly administered in the EU. These antibiotics increase efficiency and daily weight gain by promoting gluconeogenesis through greater production of propionic acid in the rumen and a consequent reduction in emitted methane (Piva et al., 2014).

The emergence of bacterial forms resistant to growth-promoting antibiotics have forced the EU to ban these molecules to safeguard consumer health. Fortunately, certain feed additives can also help reduce methanogenesis and generate energy saving – without the danger of resistance.

Secondary plant extracts or phytomolecules feature relevant properties, including bactericidal, virucide, and fungicide effects. As we have seen, it is critical to encourage certain fermentations at the expense of others and possibly reduce the organisms directly and indirectly responsible (bacteria and protozoa) for methanogenic fermentations.

Activo Premium: reduce methane and preserve energy

Phytogenic product Activo Premium contains a targeted phytomolecules mix capable of influencing the rumen microbiome in this manner:

Figure 1: Anti-methanogenic properties of selected phytomolecules. Based on Lourenço et al. (2008) and Supapong et al. (2017)  

Activo Premium is a blend of phytomolecules that maximizes production results for both high- and low-energy diets. Studies show that Activo Premium’s effects on the on the rumen microbiome reduce the ratio of acetic to propionic and butyric acid and decrease the energy losses due to methane production.

Field trial: Activo Premium improves rumen fermentation processes

A trial at the University of São Paul, Brazil, sought to evaluate the impact of Activo Premium on rumen fermentation and methane emissions. Nine rumen-cannulated sheep (55 ± 3.7 kg of body weight) were divided into 3 groups, and randomly distributed in a triple 3×3 Latin square design. The animals were fed their experimental diets for 22 days (the sampling period) in the following 3 set-ups: one control group (basal diet without additives); one group receiving a basal diet with 200 mg of Activo Premium per kg of dry matter intake; and one group receiving a basal diet with 400 mg of Activo Premium per kg of dry matter intake.

Figure 2: Ratio of acetate to propionate (p = 0.03)

Figure 3: Protozoa count (p = 0.06; x 105 / ml) and methane production (p < 0.01; l per kg of dry matter). Based on Soltan et al. (2018)

As shown in figures 2 and 3, Activo Premium favourably modifies the ratio of volatile fatty acids and reduces the protozoa count, which, as to be expected, results in reduced methane emissions.

Rumen simulation trial: the more Activo Premium added, the less methane produced

A trial was conducted at the University of Hohenheim (Germany) sought to evaluate the methane-reducing effects of different inclusion rates of Activo Premium, using a continuous long-term rumen simulation technique (Rusitec). Four different inclusion levels of Activo Premium (0, 2.1, 4.2, and 8.4 mg/d) were added to a diet with a ratio of concentrates to roughages of 80% to 20%, respectively.

Five consecutive Rusitec runs with one replication of each of the four inclusion schedules were performed. The run lasted for 14 days; 7 days were used for adaptation and the later 7 days for sampling. The fermenters were heated to 39°C. During the sampling period, total gas production and methane concentration of the total gas produced were measured every 24 h.

Figure 4: Methane emission (ml / day) for increasing inclusion rates of Activo Premium

In this trial with a rumen simulation system, Activo Premium significantly reduced methane volume (Figure 4): from 231 ml/d for the diet without any Activo Premium to 172 ml/d for the highest inclusion rate of Activo Premium.

Activo Premium: reduce methane emissions, support your profits and our planet

Both in vivo and in vitro trials have shown with high statistical reliability that Activo Premium can positively modulate rumen fermentations. The strategic combination of phytomolecules appears highly effective as a natural dietary supplementation option to modulate ruminal fermentation and decrease methane emissions. Adding Activo Premium to dairy cows’ diet will likely contribute significantly to reducing their methane emissions and optimizing their energy balance – improving animal performance while curbing the climate change impact, a win-win for everyone.



Czerkawski, J. W. “Effect of Linseed Oil Fatty Acids and Linseed Oil on Rumen Fermentation in Sheep.” The Journal of Agricultural Science 81, no. 3 (1973): 517–31. https://doi.org/10.1017/s0021859600086573

Guglielmelli, Antonietta (2009) Studio sulla produzione di metano nei ruminanti: valutazione in vitro di alimenti e diete. [Tesi di dottorato] (Unpublished) http://www.fedoa.unina.it/3960/

Johnson, D.E., and K.A. Johnson. “Methane Emissions from Cattle.” Journal of Animal Science 73, no. 8 (August 1995): 2483–92. https://doi.org/10.2527/1995.7382483x

Knapp, J.R., G.L. Laur, P.A. Vadas, W.P. Weiss, and J.M. Tricarico. “Invited Review: Enteric Methane in Dairy Cattle Production: Quantifying the Opportunities and Impact of Reducing Emissions.” Journal of Dairy Science 97, no. 6 (2014): 3231–61. https://doi.org/10.3168/jds.2013-7234

Lourenço M., P. W. Cardozo, S. Calsamiglia, and V. Fievez. “Effects of Saponins, Quercetin, Eugenol, and Cinnamaldehyde on Fatty Acid Biohydrogenation of Forage Polyunsaturated Fatty Acids in Dual-Flow Continuous Culture fermenters1.” Journal of Animal Science 86, no. 11 (November 1, 2008): 3045–53. https://doi.org/10.2527/jas.2007-0708.

Patra, Amlan K., and Jyotisna Saxena. “A New Perspective on the Use of Plant Secondary Metabolites to Inhibit Methanogenesis in the Rumen.” Phytochemistry 71, no. 11-12 (August 2010): 1198–1222. https://doi.org/10.1016/j.phytochem.2010.05.010.

Piva, Jonatas Thiago, Jeferson Dieckow, Cimélio Bayer, Josiléia Acordi Zanatta, Anibal de Moraes, Michely Tomazi, Volnei Pauletti, Gabriel Barth, and Marisa de Piccolo. “Soil Gaseous N2O and CH4 Emissions and Carbon Pool Due to Integrated Crop-Livestock in a Subtropical Ferralsol.” Agriculture, Ecosystems & Environment 190 (2014): 87–93. https://doi.org/10.1016/j.agee.2013.09.008

Soltan, Y.A., A.S. Natel, R.C. Araujo, A.S. Morsy, and A.L. Abdalla. “Progressive Adaptation of Sheep to a Microencapsulated Blend of Essential Oils: Ruminal Fermentation, Methane Emission, Nutrient Digestibility, and Microbial Protein Synthesis.” Animal Feed Science and Technology 237 (March 2018): 8–18. https://doi.org/10.1016/j.anifeedsci.2018.01.004.

Supapong, C., A. Cherdthong, A. Seankamsorn, B. Khonkhaeng, M. Wanapat, S. Uriyapongson, N. Gunun, P. Gunun, P. Chanjula, and S. Polyorach. “In Vitro Fermentation, Digestibility and Methane Production as Influenced by Delonix Regia Seed Meal Containing Tannins and Saponins.” Journal of Animal and Feed Sciences 26, no. 2 (2017): 123–30. https://doi.org/10.22358/jafs/73890/2017

Succi, Giuseppe, and Inge Hoffmann. La Vacca Da Latte. Milano: Cittá Studi, 1993.

From sub-acute ruminal acidosis to endotoxins: Prevention for lactating cows

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by 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.

lactating cows

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).

Rumen endotoxins
Figure 1. The increase in the level of endotoxins in the rumen is directly correlated with an increase in ration concentrates


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. 

Gram bacteria influenced by pH
Figure 2. Activity of main bacteria in the rumen in function of pH (Daniele Cevolani Edizioni Agricole di New Business Media srl 2020)


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).

Figure 3. Effect of Activo Premium on ruminal constituents


Figure 4. Effect of Activo Premium on animal performance


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.

Immunofluorescence in PEG-J2
Figure 5. Immunofluorescence in PEG-J2: Challenge with LPS without (in the middle) and with Mastersorb Gold (right)


IL-8 AP secretion
Figure 6. IL-8 AP secretion after incubation with LPS 0111:B4 for 24h without and with Mastersorb Gold



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.

somatic cell count
Figure 7. Effect of Mastersorb Premium on 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.


Milk fever: Causes, consequences, prevention

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Nowadays, dairy cows are real top athletes. This comes with additional challenges for their health and for on-farm management. Many of these problems can be traced back to supply deficits and can be easily managed with appropriate feed supplements.

dairy cows

Milk fever is a disease that occurs mainly in cows around calving. It is caused by an insufficient amount of calcium in the blood and particularly affects cows with a very high milk yield.

The link between calcium and milk fever

Calcium performs essential functions in the body. It is particularly important for the nervous system and muscle cells, and plays a central role in muscle contraction. If the calcium content in the blood is too low, the muscles can no longer contract. When this happens, the cows cannot move or stand up.

While mild cases may not be easily detectable, they still trigger productivity loss. If undetected, long-term calcium deficiency can even lead to cardiac arrest and thus to the death of the animal.

The development of milk fever

The cause of milk fever is a lack of sufficient calcium in the blood serum (hypocalcemia). The dairy cow has to abruptly change its metabolism at the end of the dry period, going from the resting phase to a high performance phase. During the dry period, cows have a relatively low need for calcium.

When lactation starts, the need for calcium suddenly almost doubles, as large amounts of calcium are required for the production of colostrum (2.3 g/l). The calcium is generally drawn from feed or from the bones. In older cows, the mobilization mechanism often does not start quickly enough. The supply from the bones and feed is insufficient and the body draws the missing calcium from the muscles. This ultimately leads to symptoms of paralysis and overstimulation of the nervous system.

Phases of milk fever

Stage One

In the initial phase of milk fever, the initial signs are

  • muscle tremors
  • restlessness
  • stiff gait
  • slightly elevated temperature

Stage Two

At this point, the cows lie on the stomach with an extended neck or the head is lying on the flank. Early symptoms of paralysis appear:

  • fast, flat pulse
  • cold body surface
  • dilated pupils
  • flatulence

Stage Three

In the last phase of milk fever, the cow lies on its side, loses consciousness and falls into a coma. The third phase often leads to death (the mortality rate averages 2 – 5%).

While the second phase of milk fever is easy to recognize due to the clear symptoms, the consequences of a “slight” calcium deficiency (Stage One) are often underestimated. Feed intake diminishes, the negative energy and protein balance is increased, and the cows barely move. The impairment of the muscles can cause problems in the udder (mastitis) or in the gastrointestinal tract.

Prevention and solutions

As cases of hypocalcemia immediately after calving may be as high as 50% among second- or third-lactation cows, it is important to act preventively to keep potential milk fever from developing. The dairy farmer´s aim is to support the dairy cows that are at higher risk of milk fever, especially around the critical time of calving. The cows must be enabled to quickly release calcium from the bones after calving, or they must be supplied with calcium that can be easily metabolized.

Upfront prophylaxis

An energy and protein oversupply during the dry period should be avoided. In addition, an application of Vitamin D3 at the end of the pregnancy makes sense.

To stimulate the active regulatory mechanisms of calcium metabolism, the calcium content in the feed should be reduced three to four weeks before calving. In practice, however, this often is not properly observed and feed with a relatively high calcium content is still given out during this period.

There are, no doubt, farms where these above-mentioned preventive measures cannot be carried out due to operational reasons, just as there are animals that are particularly susceptible due to factors such as age, breed or healthy history.

To protect the cow from milk fever around calving, oral administration of calcium salts is widespread in practice. Vitamin D also plays a central role in calcium metabolism. It ensures that the absorption of calcium from the intestines and bones is increased.

When administering oral calcium supplements, there are three important points:

– The cow must have sufficient calcium available per dosage

– The calcium must be available immediately

– Administration must be appropriate for the animals and farmers

Methods of calcium supplementation

To support the cow, oral supplements such as pastes and gels are widely used. They are useful, however they are also relatively difficult to administer, as they require handling the animal in relatively difficult ways.

Liquids are another way of administering calcium supplements. When administering liquids, it is important to make sure the animal does not choke so that the liquids do not get into the lungs.

Boluses are probably the easiest and safest method of supplementation to prevent milk fever. The bolus must naturally be carefully inserted, however the process is easy and requires minimal handling of the animal.

EW Nutrition´s Calzogol Bolus is a dietetic mineral feed with a high level of calcium from of highly available calcium salts and vitamin D3. The Calzogol Bolus contains several calcium sources with different release rates. One major advantage is the very high mucous membrane compatibility, which helps avoid irritation of the mouth, esophagus and rumen. Furthermore, the Calzogol Bolus does not contain caustic calcium chloride. The application is simple and economical, as only one bolus per dose must be administered at the time of calving.


Milk fever is very common in dairy herds. When a cow has milk fever, the farm can incur costs of approx. €350. This is reflected in the loss of milk yield up to 600 kg, losses due to unusable milk, and veterinary and medication costs.

Time resources are also to be taken into account: The economic repercussions represent a significant factor, however they come on top of the extra workload due to the increased need for care of animals.

Cows that suffer from calcium deficiency are also much more susceptible to other diseases. For the farmer, the best strategy is to avoid losses through prophylaxis. Feeding plays a central role; to ensure the best possible production conditions, oral calcium administrations, such as Calzogol Bolus, have proven themselves in practice.


by Judith Schmidt, Product Manager, On Farm Solutions 


Rérat, M. (2005): Milchfieber bei der Milchkuh. ALP aktuell. Nr. 20.

Spiekers, H., Potthast, V. (2004): Erfolgreiche Milchviehfütterung. DLG-Verlag, Frankfurt a. M.

Kirchgeßner, M., Roth, F. X., Schwarz, F. J., Stangl, G. I. (2008): Tierernährung. 12. Auflage. DLG-Verlag, Frankfurt a. M.