Peregrine syndrome update
Dear all
We wanted to update you on the current state of play regarding ‘the peregrine syndrome’ that vets up and down the country (and indeed other parts of Europe) have been dealing with over the past 18 months.
Thankfully some of the best avian vets, pathologists and virologists in the world have donated their time and most up to date diagnostic technology to looking into this problem.
The facts as they currently stand are:
1. From our personal observations this syndrome seems only to affect peregrines or peregrine hybrids even within multi species collections.
2. Clinical signs include general poor condition, weight loss despite eating excessively, screaming, mucoid/slimy diarrhoea, pale feet and cere, vomiting and in many cases progressing to death despite culture based antibiotics.
3. Some birds with aggressive supportive therapy improve and may even breed, but recurrent relapses are typical.
4. Despite countless faecal samples and cultures no single bacteria, yeast or parasite has been consistently identified across the board suggesting that those pathogens found are secondary invaders to an already inflamed/damaged gut.
5. We have recently received results from the virologists on both tissue and faecal samples of affected birds. Viral chip technology that searches for any viral DNA present in the samples and compares it to a data base of nearly 2000 known viruses, has failed to identify a causal virus in any samples submitted over the past year.
6. A separate team at Bristol University which has been looking at tissue samples of both affected and ‘normal peregrines’ (wild casualties that have been euthanized on humane grounds) has demonstrated changes consistent with post infectious inflammatory bowel disease (IBD). This is a similar condition to ulcerative colitis in people where a historic intestinal insult be it viral, parasitic or toxic may result in an ‘autoimmune reaction’ where the bird develops antibodies to its own intestinal lining. This damages the gut allowing secondary infections to proliferate. It is thought this occurs because ‘antigens’ or protein markers on certain infectious agents (salmonella for example) may resemble similar structures found on intestinal cells. As such when antibodies are made in response to infection, they are then stored in the immune systems ‘memory’ as a permanent defence mechanism against future challenge. When under stress or hormonal influences (in a paper on ulcerative colitis in women, flare ups often occur after giving birth and rarely during pregnancy) the body can mistakenly identify intestinal cells as invading infectious agents and attack it accordingly. Also in mammals certain foods can trigger episodes. As such when a bird demonstrates clinical signs associated with certain food items it is assumed this must be carrying ‘the virus’. It is equally possible however that certain proteins cause flare ups and others don’t hence the possible response to exclusion diets (all rat for example).
Based on the above our current working hypothesis is that a historic gut insult be it a bacteria, virus, parasite or toxin results in post infectious IBD, which (as in humans) is then likely to be a lifelong problem, where flare ups are managed by identifying and removing apparent trigger factors (certain foods, parasites etc) in conjunction with supportive fluids, nutrition and medication.
The problem we are up against is by the time obvious clinical signs are apparent the inciting cause is likely long gone. We are currently working with falconers and breeders to try and identify cases at the very onset of the problem so we may have a better chance of picking up an agent.
As such if you have any concerns or queries regarding your falcon please contact your avian vet ASAP as the more information we can collect and pool together on this the better.
Best wishes
Richard Jones MRCVS and Neil Forbes FRCVS
