First printed in the Ranger magazine, Richard Turner discusses diagnosing and treating fatty livers.
Socrates is supposed to have said that “The only true wisdom is knowing you know nothing “but Oscar Wilde put it differently, “with age comes wisdom but sometimes age comes alone!”
I was considering these two statements the other day when presented with a case of poor production and high mortality. It seems the older I get the more I realise that what I thought was obvious is certainly less clear. There is a tendency in veterinary medicine to chase the bacteria or virus, seek the test to show exposure and name the condition. Sadly, this often leads to misdiagnosis, the wrong treatments and sometimes failure to see bird health return to normal. A recent review of the microbiological status of the human brain really challenged a lot of what I was taught. It now seems highly likely that there is a population of bacteria and viruses in the “normal“ human brain, and these microorganisms are in communication with ourselves. Where exactly they originated is not clear and whilst the same work has not been carried out to my knowledge in chicken, it would seem unlikely that humans are unique in this relationship. This takes us to the concept that bacteria in the lower gut produce dopamine if provided with a suitable nutrient source and in balance with the bird. Dopamine produces a feeling of calm in humans, does it cause the same in birds? It is clear that the use of some types of fibre in a diet, or the addition of Lucerne bales to the scratch area will affect bird aggression so the hypothesis would be that these dietary factors change birds’ behaviours. What happens I wonder if the bacteria in the gut can move closer to the brain and release neuro active chemicals which change behaviours?
Recently we have been developing management techniques to help birds live a longer productive life, and there is clear evidence across the UK and Ireland of a difference in bird behaviours. What it is remains a mystery, but we are sure feed, and therefore maybe gut/brain microbiome are involved. The challenge is how to manage the detail of the microbiome in the gut when one doesn’t have easy cheap tests. Core to long life is a healthy liver and the liver of a layer producing an egg daily is under huge pressure.
Going back to the laying birds with higher-than-normal mortality, everyone jumps at the common problems from E. coli to IB, worms and various other respiratory/oviduct pathogens such as mycoplasma. In this case the birds were all well vaccinated, red mites were under control and worming was regular. The production drops had been seen across a range of free-range sites and had started in the late summer and autumn. They were all fed from the same feed mill. The birds had pale combs and were underweight by maybe 50-100g at about 42 weeks. Egg shells were normal, but production was about 10% below target. There were no signs of respiratory disease.
These sorts of cases creep up on a farm. The early signs are not obvious and close monitoring of production parameters is essential to pick up changes early on. As always, the tendency is to wait and see. The problem becomes the longer you wait the more likely it is that the condition becomes established.
I visited the site, and the scratch area was normal, no frothy droppings and no real issue other than lighter variable birds with pale combs.
There had been smothers but the mortality was about 8/day in 32,000 birds. On postmortem the cause of death was obvious, but exact aetiology proved more of a challenge. There was clear evidence of bleeding into the gizzard with black intestinal contents and some darker crop contents. The livers were enlarged, fatty and in some cases large blood clots could be seen. We had a case of fatty liver and haemorrhage syndrome, but with gizzard ulceration was an added extra and fatty liver is usually associated with overweight birds. These birds were undereating. The rest of the intestinal tract appeared grossly normal as was the respiratory and cardiovascular system.
So, we know why they are dying, but why is it happening?
We know there is liver damage and gizzard erosion but what is the cause? Fatty Liver and Haemorrhage syndrome is normally associated with cage birds, and these were free range. The condition can be associated with either an incorrect carbohydrate source leading to build up of fat in the liver, or with an inability of the bird to produce the carrier lipoproteins needed to move fat around the blood stream. Other pathogens that damage the liver can be implicated. The lack of blood carriers might be due to lack of various B vitamins, but this is not usual. The liver produces some of the proteins essential for blood clotting, so was the gizzard bleeding due to poor clotting, probably not. There were tiny micro ulcers in the gizzard surface. These birds were underweight and not eating to target by about 15g/day, but they were free range so was this the issue? They either didn’t like the feed or had a reduced appetite for some other reason.
As is often the case in the commercial world, decisions have to be made with a lack of complete data. Viral testing is expensive and to a certain extent what is the point of testing for viral agents which cannot be controlled in a free-range environment by vaccination?
Mycotoxins are certainly a possibility but when you test feed it’s not unusual to find mycotoxins in feed fed to normal birds. The most difficult problem for a vet is the expectation from the client that there must be a diagnosis, there must be a culprit, and there must be an answer. ‘Name the culprit’ is the cry!
The diet did have a bakery waste component which I must admit, with apologies to nutritionists, is something I really don’t like. I think or rather suspect that there are issues of blood glucose level peaking quickly and also the effect of ultra processed carbohydrates on the birds’ gut flora. It doesn’t help human health so I cannot see how it can help our birds. The diet had no mycotoxin binders but that’s not unusual in GB. Personally, I think mycotoxins need to be taken more seriously as without a doubt they can not only affect the liver, but also have direct damaging effects on other organs as well as a negative impact on the gut flora, with outcomes it’s not easy to define.
The urgency of course was to stop the decline preferably with a least cost treatment and the client had no desire to spend money on laboratory work ups. We agreed to change the ration to a higher specification (which is not normal for fatty liver) and to add mycotoxin binders with added Silymarin. The birds were given Silymarin in the water for 7 days. The aim was to rule out the feed, to try to reduce the possible effects of mycotoxins and to support the liver. Silymarin is an essential oil from milk thistle which has an interesting effect on the liver and mood. We use it in birds with low performance, fatty livers and at any time when the liver is under pressure. It can be in feed (AV3) or in water (Hepamix).
What happened?
Well, production slowly returned, mortality dropped, and the client was happy. Sadly, in this case we never found out the cause, however the clinical picture fits well with mycotoxins. These are often not taken seriously enough in the UK and there is no doubt as you look at fields of cereals struggling to be harvested in a warmer wet climate that there is fungal growth. Various mycotoxin binders can be used, the effect of various mycotoxins is variable and can be insidious. The cost of prevention is not high, and it’s well to at least consider using in-feed binders to prevent a problem in the autumn.