Many solutions are at hand to tackle coccidiosis in poultry. One of which is the use of esterified butyrate. This could deliver the high performance level commercial producers must aim for, in an increasingly challenging environment.
By Richard Sygall, technical support & product development manager, Perstorp
Forty eight million euros per annum: that’s how much the poultry world loses in revenue as a result of coccidiosis. As the Eimeria parasite that causes the disease has a wide distribution it’s not a disease that many producers can avoid. Whether it is manifest as clinical disease or subclinical infection, coccidiosis is well recognised as a significant threat to productivity and profitability.
Unfortunately, it’s also a disease that doesn’t allow producers to rest easy at night. Even an effective coccidiosis control programme can be compromised by resistance to commonly used treatments. Resistance to anticoccidials has been an issue for the commercial poultry industry for many years and it’s a global problem. Decades of research have so far only allowed the industry to hold its ground. But there is cause for hope. Recent developments and an increasing focus on naturally derived molecules have suggested that there might be new ways to tackle avian coccidiosis.
A disease less ordinary
The lifecycle of the Eimeria parasite will be familiar to anyone who seeks to understand to control the disease. Parasitic oocysts excreted by the bird are initially not infective and must become sporulated to pose a risk to other birds. Sporulation requires warmth and humidity – conditions commercial units easily provide. Oocysts are not easily destroyed by heat, cold or even common disinfectants, so basic hygiene doesn’t always make a complete contribution to coccidiosis control.
A sporulated oocyst is consumed and releases the next parasite life stage which invades gut cells. Inside the gut cells the parasite goes through a process of replication and vast multiplication, before the cell is destroyed, releasing the next stages to re-infect another gut cell. The more oocysts that are eaten, the more severe these consequences are, with the potential for millions of gut cells to be destroyed. Furthermore, the multiplication process means millions of oocysts can be shed by infected birds.
Most birds will, under good hygienic conditions, without overcrowding or exposure to the droppings of heavily infected birds, be exposed to low levels of Eimeria parasites and develop immunity. If however there are infected birds shedding heavily into the environment, increasing challenge can overwhelm immune responses and result in clinical or subclinical disease. Any underlying disease can predispose to coccidiosis. Coccidiosis can also contribute to progression of other conditions such as necrotic enteritis due to bacterial infection by Clostridium perfringens.
So what does all this mean for control strategies? Clearly, there is a need to reduce stress and take basic hygiene seriously. The focus then has to be on treating or preventing the cause (Eimeria), and/or the consequences of the disease. The consequences in short lived birds with few opportunities to recover, such as broilers, can be serious – including poor feed conversation ratio (FCR), poor uniformity and reduced carcass quality. Most of those problems relate to gut damage and loss of function, compromising the ability to utilise nutrients in feed.
Treatment of the cause includes the use of anticoccidial drugs such as ionophores, nicarbizine or robenidine, in combination with disinfectants that destroy oocysts. Pre- and probiotics, vitamin mineral supplements and enzymes have also been reported to be of benefit.
One study examined the effects of salimomycin (an ionophore), prebiotics, probiotics, a herbal mixture and a multi-enzyme given to broiler chicks that were later challenged with Eimeria. Those chicks that received salinomycin, enzymes, pre- or probiotics all showed better FCR and body weight gain compared to infected chicks with no treatment. Uninfected chicks also showed better FCR due to salinomycin, herbal mix and prebiotics. All of the supplements reduced the severity of the lesions on the small intestine in infected chicks but only salinomycin and the herbal reduced oocyst excretion. Another study looked specifically at butyric acid as a feed additive and demonstrated an increase in carcass weight and breast meat yield. Birds given butyrate also maintained higher growth rates after challenge with coccidial oocysts. Additional weight was given to this by a paper from 2009 that showed butyric acid glycerides resulted in birds with higher carcass weights and better FCR over concentrations ranging from 0.2-1% added to feed.
One view is that these supplements may be providing substrates for caecal bacteria that digest non-starch polysaccharide (NSP). In other words, they are modulating the balance of gut microbiota. There is also a known correlation between FCR and microbiota composition. Bacterial digestion of NSPs results in an increase in short chain fatty acids (SCFA) production, particularly butyrate, that can be utilised by the intestinal epithelium.
This suggests that supporting the gut through use of appropriate feed additives is likely to be important in minimising the adverse effects of coccidiosis. But if the mechanism of action of all of these supplements depends on increasing butyrate production in the caecum, could a direct approach be more beneficial? Butyrate is increasingly recognised as a viable feed additive with the availability of esterified forms.
Butyrate – nature’s balancer
The acidic quality of butyrate has in the past limited its use as a supplement but new esterified formulations are stable, have no odour and can be used in a production setting. Esterfied butyrins are broken down by lipases and released slowly in line with natural digestive processes. Swedish feed additive producer Perstorp produces butyrate. The resulting product range of butyrins (esterified butyrate) is marketed as ProPhorce SR. Butyrate has many positive benefits that would support its use in managing gut conditions. It is a preferential energy source for colonocytes and can influence gene expression in the cell.
In addition to influencing intracellular pH and increasing cell volume, SCFAs are reported to result in increased mucosal surface area and mucosal hypertrophy, indicating increased absorptive capacity. The composition and/or enzyme activity of intestinal bacteria is affected by SCFAs, which shift the microbiota balance in favour of beneficial bacteria. Beneficial bacteria synthesize vitamins, help in the absorption of food and inhibit pathogenic bacteria. There are also positive effects on gut motility.
Improvements in gut structure and morphology may explain improvements in FCR, performance and carcass quality when butyrate is given to animals with coccidiosis. That makes sense, as a healthy gut epithelium ensures uptake of dietary nutrients.
But this may be a much more involved story. Epithelial damage by coccidiosis, necrotic enteritis or anti-nutritional factors in the diet results in poor nutrient digestion in the small intestine and therefore absorption. These undigested nutrients pass into the lower intestine and there favour the growth of bacteria that can use these simple substrates. The shift in FCR is a result of the poor nutrient absorption but so is the shift in microbiota. So although FCR and microbiota composition are correlated, it may not be a direct cause-effect relationship.
It is also known that SCFAs regulate the balance between fatty acid synthesis, fatty-acid oxidation and lipolysis in the body, essentially how energy is used in the body. A very interesting finding resulting from research in human obesity, is that lean germ free mice can be made obese by transferring microbiota from obese mice. This suggests that the bacterial population could influence energy harvesting and therefore alter FCR.
As nature intended
So, the composition of caecal microbiota correlates with the efficiency with which the host retains dietary energy but the exact mechanism may be very complex.
What does seem logical is that if coccidiosis causes gut damage, reduces nutrient digestion and absorption and reduces energy retention, an in-feed additive like butyrate that promotes the health of the gut lining, supplies and regulates energy, would counter some of these adverse effects.
Pharmacological solutions are increasingly under threat, novel molecules cannot be developed fast enough to counter resistance. There is increasing evidence to explain how butyrate might be able to right the wrongs that are at the core of diseases such as coccidiosis. Esterified butyrate could deliver the high level performance commercial producers must aim for, in an increasingly challenging environment.
References are available from the authors upon request: www.perstorp.com
[Source: World Poultry – Managing Coccidiosis, 2014]