Message Number: FHL587 | New FHL Archives Search
From: "Sukie Crandall"
Date: 2007-04-16 17:12:40 UTC
Subject: [ferrethealth] Re: pigeons as a food item - diseases found in feral (street) pigeons in urban areas
To: ferrethealth@yahoogroups.com

Well, yes and no for the natural immunity part.

On that regard there are differences between
healthy and compromised ferrets. Many things
reduce immune system action including illness,
very young age, and very old age. Well, being
honest, not just very old since immune system
action decreases in humans from middle age
onward, but does so more rapidly when very old
and that pattern appears to be echoed in
carnivores though I honestly have not personally
read any studies on that in them.

(A possible way to find if that is true for ferrets
might be in the nuances of the current avian flu
studies *IF* ferrets of multiple ages have been
used because the real problem with that flu is the
immune system cytokine storms which are an
immune system over-action which is much more
likely to occur in those with stronger immune
systems, i.e. why so many people in the prime of
life died of the bad flu in the 19-teens.)

Has anyone read any studies on immune system
changes with age in ferrets?

So, while a healthy ferret may not have problems
with certain food borne diseases, ones whose
immune systems are not as strong could, and
certainly polecat typical survival ages in the wild
are not high.

In fact, as memory serves Dr. Bruce Williams has
pointed exactly this out in relation to avian
mycobacteria infection in ferrets and that disease
is certainly able to be contracted from eating
infected birds, and well documented on that regard
for ferrets whose immune systems are not optimally
strong.

There are plenty of studies of food borne diseases
in ferrets and certainly there are FHL members' ferrets
who have had some of them. If I get time I'll hit the vet
texts. _Biology and Disease of the Ferret, second edition_
is especially good for covering many of the diseases that
ferrets can get from foods.

There also is a BFF E. coli study with a number of the
ferrets dead, and there is a study of after E. coli infection
of that particularly nasty strain (but off hand I can't recall
if that one was in domestic ferrets, though I think that it
was) which showed that even when the ferrets fought off
the infection a disproportionate later developed kidney
problems down the line, and I know the study was in a lab
animal because follow-up studies showed immediate kidney
damage which silently compromised the kidneys.

There are other long term consequences of some other
infections from food-borne diseases. I think it's either
the CDC or the FDA site which has some mentions of
these. Again, *IF* I get time I'll dig, but if anyone has
that info handy now, please, share.

Furthermore, in many animals when the bacteria-host
relationship is moving toward a symbiotic state (a very
useful condition for bacteria due to increased numbers
surviving and there are a lot of host-parasite and host-
symbiot studies on the evolution of symbiotic relationships)
there is an intermediate stage in which chronic infection
that does not usually flare exists. So, just because outward
signs of a disease which has the ability to flare up do not
always show overtly during a chronic infection that does
not mean that the infection is not there, and certainly some
ferrets with inflamed spleens have responded with splenic
size reduction to antibiotic routines that do not address
Helicobacter, so other infections could have been to blame.

Oh, I just remembered where one of those studies was:

BEGIN QUOTE
Woods, J.B., C.K. Schmitt, S.C. Darnell, K.C. Meysick, and A.
O'Brien (2002). Ferrets as a model system for renal disease
secondary to intestinal infection with Escherichia coli O157:H7
and other Shiga toxin-producing E. coli. Journal of Infectious
Diseases 185(4): 550-554. ISSN: 0022-1899.
NAL Call Number: 448.8 J821
Abstract: Ferrets were evaluated as a possible small animal
model for the development of colitis and/or signs of the
hemolytic uremic syndrome after oral infection with Escherichia
coli O157:H7 or other Shiga toxin--producing E. coli (STEC).
Ferrets treated with streptomycin (Stm) had higher counts of
E. coli O157:H7 strain 86-24 Stm-resistant (Stm(r)) or O91:H21
strain B2F1 Stm(r) in their stools than non--Stm-treated animals.
None of the animals displayed evidence of colitis, but Stm-
treated animals fed strain 86-24 Stm(r) exhibited weight loss
significantly greater than that exhibited by ferrets fed an isogenic
mutant negative for the adhesin intimin. Moreover, 11 (23%) of
the 47 Stm-treated ferrets inoculated with 86-24 Stm(r) or B2F1
Stm(r) developed hematuria and/or histological damage to
glomeruli or thrombocytopenia, compared with 0 of 14 uninfected
control animals receiving Stm in water. Thus, the ferret may serve
as a model for renal disease secondary to intestinal infection with
STEC.
Descriptors: ferrets, animal disease models, Escherichia coli
infections, Escherichia coli o157 pathogenicity, Escherichia coli
proteins, intestinal diseases, kidney diseases, shiga toxin, intestinal
diseases, streptomycin
END QUOTE

E. coli is a fecal borne disease. (When it is encountered on plant
foods that is often due to brown water irrigation which had an
infected source such as cattle field run-off, or due to unsanitary
conditions for field hands.)




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