AN EMERGING WASTING SYNDROME IN PEREGRINE FALCONS(Falco peregrinus)
Richard Jones BVSc MSc MRCVS*,Neil Forbes BVetMed DipECZM(avian) FRCVS, Mark F.
Stidworthy MA VetMB PhD FRCPath MRCVS and Tristan Cogan BSc PhD
Over the past 3 years approximately 30 adult peregrine and peregrine hybrid falcons from at least
3 separate collections as well as privately owned falconry birds in the UK have succumbed to an
enteritis and ‘wasting’ syndrome apparently unresponsive to traditional treatment regimes.
Based on the results of ongoing work our current working hypothesis is that this is a form of post
infectious inflammatory bowel disease (IBD).
CLINICAL AND LABORATORY FINDINGS
Symptoms include general poor condition, weight loss (despite polyphagia), food begging
vocalisations, mucoid diarrhoea, pale feet, cere and talons, polydipsia, regurgitation and in many
cases progression to death despite culture-based antimicrobials and aggressive fluid/nutritional
support. Although no single common food item or source has been identified most of the birds
were fed mainly day old cockerels and/or quail.
Intensive ante- and post mortem investigations including faecal bacteriology and parasitology,
electron microscopy, viral culture and high-throughput molecular techniques have failed to
consistently identify any single virus, bacteria, yeast or parasite. A weak signal for Northern
Aplomado adenovirus was obtained on microarray but further PCR testing using both avian and
pan adenovirus primers failed to amplify a PCR product to support this finding.
Gross post mortem and histopathological changes mainly involved the intestinal tract, with
histological evidence of segmental chronic lymphoplasmacytic enteritis (with variable numbers of
heterophils), particularly in jejunum and ileum. Villi in these segments were wide and blunt (villous
atrophy) in comparison with reported descriptions of normal1, with occasional villous fusion. There
was crypt hyperplasia. Although classically associated with viral infection, villus atrophy and crypt
hyperplasia may be attributable to a wide variety of insults to the intestinal mucosa, including
bacterial, protozoal and metazoan infections, food allergies/intolerances and drug reactions. Some
cases remain idiopathic. No protozoa or viral inclusions were recognised in any case, but small to
excessive numbers of intraluminal bacteria of mixed morphologies were present. In one case,
membranoproliferative glomerulopathy with tubular protein loss was present in the kidneys, a
lesion typically associated with the deposition of circulating immune complexes from persistent
In parallel, biopsies were taken from the small and large intestine from selected end-stage cases
under terminal general anaesthesia. These were snap frozen or placed immediately into RNAlater.
Snap frozen biopsies were fixed in formalin, wax embedded and examined by fluorescence in situ
hybridisation to identify and localise bacterial infection. For biopsies in RNAlater, mRNA was
extracted using a Promega kit. Levels of TGF beta, IFN gamma, IL-10, TNF alpha and IL-6 were
analysed by qPCR using a Stratagene 1 step qRT-PCR kit with primers designed using available
DNA sequences for Falco
spp. from GenBank. Affected birds had large numbers of bacteria
colonising the intestinal mucosa, most of which were considered to be intestinal commensals,
although clostridia were often identified. Biopsies from affected birds showed higher levels of IFN
gamma, TNF alpha and IL-6 than those from control birds (wildlife trauma cases euthanased on
humane grounds). These are all proinflammatory cytokines, and this profile is consistent with that
seen in human IBD. The marked difference was that in humans elevated TGF beta is also seen, an
elevation absent in the affected birds. Elevated TGF beta causes excess collagen deposition in the
submucosa in humans with IBD, and is responsible for thickening of the gut wall and the
development of fibrosis2. Histology showed that affected birds did not show fibrosis. In humans,
IBD is a Th-1 disease, and the activity of these cytokines is co-regulated by the transcription factor T-bx21. Our analysis of avian genomes indicates that chickens do not have a homologue of this factor. It is likely that regulation occurs by a different mechanism that does not involve TGF beta or promote fibrosis. The clinical presentation of IBD in birds could therefore differ from that in mammals. The picture suggests that an initial inciting infection compromises intestinal barrier function before resolution/clearance. Excessive numbers of commensal bacteria remain colonising the intestinal mucosa, promoting a feedback loop of inflammation, breakdown in epithelial barrier function, further bacterial colonisation and persistent inflammation, as described for chronic human IBD3
CURRENT MANAGEMENT RECOMMENDATIONS
The authors recommend that falcons presenting with these clinical signs undergo complete
physical examination with faecal analysis for the presence of intestinal parasites, protozoa or
microbial pathogens, which should then be treated with appropriate culture-based therapeutics.
Meloxicam, oral aqueous aloe vera and probiotic/competitive exclusion products e.g. Flightpath
(Microbial Developments Ltd.) are useful adjunct therapies in such cases.
Affected birds may respond to dietary conversion to a novel protein, perhaps reflecting an
underlying hypersensitivity to antigens breaching the intestinal mucosal barrier during an
inflammatory episode. With polydipsia a common feature of this syndrome it is essential such birds
have unlimited access to fresh water to avoid dehydration. In refractory cases, based on the
hypothesis of IBD, a number of protocols including oral sulphasalazine, metronidazole,
budesonide and intramuscular dexamethasone have been attempted with varying results. Although
such therapies have proved useful in the management of acute ‘flare ups’, at the time of writing our
clinical impression is that this may be a lifelong condition. AKNOWLEDGMENTS
The authors would like to thank The Hawk Board, Honeybrook Animal Foods, Falcon Mews, M&J
Raptors, Pinmoore Animal Laboratories, Richard Ashcroft, Dr Tom Bailey, Prof. Michael Lierz,
Dr.Akbar Dastjerdi, Prof. Peter Kaiser and Dr. Arnaud Van Wettere for their input, help and support
with ongoing work. CITATION INDEX
1 Heidbrink, Stephanie. Morphological examination of the digestive tract of different raptor birds
with regard to their respective feeding habits. Doctoral thesis, Freie Universitat Berlin, 2003.
2 Guarner F. What is the role of the enteric commensal flora in IBD?.Inflammatory bowel diseases.
Vol 14, issue supplement 2. Pages S83-S84 October 2008.
3 Pucilowska J B, Williams L and Lund P K. Fibrogenesis IV. Fibrosis and inflammatory bowel
disease:cellular mediators and animal models. American Journal of Physiology. 2000. Vol. 279
number 4. G653-G659. *AUTHOR ADDRESS:
Richard Jones BVSc MSc MRCVS
Avian Veterinary Services
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