First featured in The Ranger magazine, Richard Turner shares how a better understanding of E. coli has influenced the approach to its prevention and treatment.
E.coli infection in poultry continues to be an issue, with the source/route of infection and the options available to prevent and treat it, often confusing. Here I’ll share how our improved understanding of the routes of infection have influenced our approach to E. coli prevention and treatment and run through some of the options that are now available to producers. Identifying the source/getting to the root cause of the infection is also important – however that is a whole other article that I’ll save for another day.
Looking back
I find it interesting to recognise how our veterinary approach to a clinical case of E. coli infection has changed over the last 40 years since I qualified. With a better understanding of the routes of infection, more targeted approaches to prevent and minimise the impact that E. coli can have, are now available to us. These not only better support the health and welfare of the birds but also maximises financial returns for producers.
Looking back to the 80s and 90s, vets typically focussed on the E. coli bacteria itself. It was associated with a respiratory route of infection, and we would look at IB, TRT or Mycoplasma as the primary agent allowing the E. coli bacteria to invade.
Nowadays in the UK and Ireland, we see far fewer of these cases which has a lot to do with the quality of pullet rearing and vaccination techniques that are in place, coupled with a generally low endemic pathogen load (other than when avian influenza strikes).
The most frequent routes of infection
Therefore, with most E. coli cases having no respiratory element, the primary route of infection seems to be the intestine with some types of E. coli being able to cross the intestinal barrier and enter the bloodstream leading to peritonitis and pericarditis. This means that we must turn our attention to bird gut health and to managing the gut microbiome to tackle the E. coli challenge.
Modern human medicine now fully recognises the hugely complex relationship between the gut microflora and human mental health and overall health. With the fascinating work of, for example, Professor Steve Collett from Georgia State University, we now know that the gut health and microbiome of the mother hen is in some ways passed to the chick, as in humans. We are also on the road to better understanding the role bird gut health has on overall flock health, welfare and performance.
Approaching E. coli
Historically, treatments were antibiotic based, outcomes were not good and came with the expectation that mortality would continue. Environment-wise we were dealing with larger indoor units with a large red mite burden, an atmosphere that was affected by the deep pit of manure beneath the cages and a lot of dust – both affecting the birds’ respiratory tract. Sheds were rarely cleaned at all for many good practical reasons and the idea that E. coli was in fact a leakage from an inflamed intestine was certainly not on my mind.
Much has changed and today, we focus on managing the various microbiomes that impact birds’ performance – for example water, the house, feed, atmospheric microbiomes – and in the case of E. coli, we focus our attention on that of the gut. All these microbiomes will differ and become established. Some of these populations will have a negative effect on bird performance whilst a lot will have very positive effects. When we manage a microbiome with various products, we must now truly focus on the effect they have on the vast number of positive microorganisms that enhance our hens’ life, wellbeing and eventual performance.
Start with possible stress factors
So, turning our attention to the impact/influence gut health has on E. coli – where should we start? In a word, stress. This is because when birds are stressed, various hormones are released that change the E. coli so it can attach to the gut wall and invade, leading to gut leakage of the bacteria into the blood stream.
Often peritonitis is associated with stressors such as coming in to lay, low flying balloons, or other factor that causes issue in the flock. If the stress is short lived and there is no long-term colonisation of the gut environment, it is likely that after a week or two of higher mortality, all will return to normal. However, if the stress is longer term – such as pecking, a low fibre ration or high red mite challenge, there is likely to be a long-term E. coli infection rate.
To minimise the impact of stress on the gut, the sooner the stress factor is identified and removed, and calming products are introduced, the better.
Supporting the gut after stress
A sensible start would be a product that gives the birds a feeling a satiation. Other supplements based on minerals such as magnesium can also support the birds however there needs to be an underlying deficiency for these to be of use.
Where there is a pecking issue, adding fibre with lucerne bales or a suitable feed change should be considered. This is because we see changes in bird behaviour when some forms of fibre are added to the diet and while we don’t know the complete mechanism, it is likely that the ration changes effect the gut microbiome – and assuming that the poultry microbiome have some of the characteristics of the human microbiome – there might be changes to chemicals that change behaviour. Maintaining gut integrity by supporting the intestinal cell integrity can also help to reduce this leakage.
Once any stress influencers have been dealt with, where do we go next? Antibiotics can treat E. coli although the choice is limited to a few groups and there is often resistance. As such our approach to E. coli focuses on supporting the gut microbiome.
Probiotics
Fimbriae blockers are mainly yeast-based, in the feed and bind to the fimbriae on the E. coli surface and prevent the E. coli attaching to the gut wall. There are products that produce mucopolysaccharide, that line the gut and help to prevent the E. coli binding to the gut wall too. Some products also contain lactobacillus – a bacterial group which product acids which support intestinal integrity – which is precisely what you need when E. coli is trying to take hold.
Nutraceuticals/essential oils
As well as ‘blocking’ products, we can look to certain essential oils to kill or reduce multiplication of the E. coli. These are typically oregano based however this is a complicated area due to the vast number of products available and their varying quality. I have spent over a decade investigating every aspect of the supply chain for the products we produce and recommend, as our reputation as vets depends on good advice and products of the highest quality.
Acids in water and in feed
Finally, there are acids that are a useful addition, either on their own or after an antibiotic treatment. However much like essential oils, there are many, of varying quality available and it’s important to not base buying decisions on price alone.
The aim here is to acidify the alkaline loving bacteria – not to ‘acidify the gut’ – with the product delivered in an un dissociated form to the lower intestine where the E. coli favour the alkaline environment. Here, the short chain fatty acid (SCFA) will cross the bacterial wall and acidify the bacterial cytoplasm.
The water in the house will determine how much acid mixture is required to achieve this. The key is to select a product with the correct acid mixture and the maximum amount of buffering. A non-buffered product will lower the pH of the water too quickly, whereas a well-buffered product slows this process down, enabling more of the acid mixture to be used, which is what is needed to have action against E. coli in the gut. Buffering ensures the SCFA remains with its hydrogen ions attached to the molecule and these then are released within the bacterial cytoplasm and lead to it becoming acidic.
Acids, mainly short chain fatty acids in protected form, can also be added to the feed and support the gut bacterial flora. There are two options here. The first is adding a relatively non-buffered form to reduce the incidence of Salmonella in the feed. The second is to use a more protected form that supports the gut bacterial flora, in the same way as a buffered SCFA in water.
Vaccination
The vaccination techniques in place during the rearing phase try to minimise the incidence of E. coli in lay. There is no doubt that where a truly pathogenic E. coli is present – wherever it is established – the use of an autogenous vaccine (made from the E. coli on the farm) will provide protection. The use of the live vaccines in lay offers an additional protection, particularly where there is mortality from E. coli, however as previously mentioned, if this mortality is due to gut leakage because of stress, it’s important to remove the source of the stress first.
A tailored approach is required to assess the most effective approach to managing the impact of E. coli to make sure that the desired veterinary outcomes are achieved and deliver effective financial returns.