David Caudill asked about giardia.  Giardia lamblia is a protozoan parasite
that causes a foul-smelling, greasy diarrhea in humans and other mammals.
Diarrhea due to Giardia is usually does not have blood or mucus in it.
Nausea and vomiting can also accompany the illness.  It is spread by the
fecal-oral route or through contaminated food or water.  After the initial
illness, a chronic infection can set in with intermittent bouts of diarrhea.
Severe infection can cause malabsorption, which can persist for a period
after the parasite has been eradicated due to the destruction to the
intestinal microvilli.  Metronizadole (Flagyl) and some related antibiotics
can treat the infection...although ferrets typically HATE Flagyl.
 
In humans, giardia sometimes causes intestinal infection known as "beaver
fever." (Does anyone remember those Coors beer commercials from a few years
back in which Mark Harmon would be standing ankle-deep in a mountain stream,
reach down and scoop up a handful of crystal-clear mountain water and drink
it?  Well, don't *ever* do that unless you're prepared to risk the
consequences.)
 
Lisa, of Ferret Rescue of Tidewater, had some comments about the genetics
and inbreeding.  I am unfamiliar with any USDA reports about Marshall Farms
that she mentioned (was this a report available to the public?) but I can
clarify some common misunderstandings about genetics.
 
>If MF bred ferrets ONLY for laboratory testing, it wouldn't matter if
>they had a closed breeding colony, it would be preferred.  The problem lies
>in this: In order to provide animals for lab testing, the animals must be
>as genetically alike as possible, in order to prevent skewing testing
>results with different animals.
 
That's only true for certain types of research.  Not all laboratory
experiments would benefit from using genetically similar animals.  In some
cases it is more useful to study genetically diverse animals.  I know
pediatric residents who learned the techniques for intubating premature
humans infants on ferrets.  (I won't be drawn into whether this is right or
wrong.  But it *is* one research use for ferrets.) In this case, genetic
similarity either makes no difference or is a hindrance since the human
infants these MDs must eventually work on are genetically diverse.
 
>And what about the British Monarchy when brothers were marrying sisters
>and all of the sudden, hemophiliacs began popping up?
 
Oops, bad example.  First, *most* of the monarchies of Europe swapped
relatives for arranged marriages, let's not pick on just the Brits.  Second,
the intermarriages were usually at least between cousins.  I don't think any
full-blood brother-sister marriages took place.  Third, Queen Victoria
carried a sex-linked defect which probably started as a new mutation in the
egg or sperm cell of one of her parents.  (I don't recall that any male
ancestors of Victoria had hemophilia so a parent must have passed along a
de-novo mutation to her in a germ cell.) With this sort of genetic defect,
it would not have mattered whether Victoria had married Prince Albert or a
full-blooded Australian aborigine.  (Wouldn't THAT have made the headlines?
<G>) All of her half-aboriginal daughters would still have inherited the
defect (but not been affected) and all of her sons and all of her daughter's
sons would each have had a 50-50 chance of having hemophilia.  Inbreeding
had *nothing* to do with it.
 
>History generally proves out that inbreeding causes many genetic diseases,
>or at the very least, a tendency towards it.
 
Perhaps that's misstated just a bit.  Inbreeding does not *cause* genetic
diseases.  It merely allows *recessive* genetic defects to surface more
often.  In fact, in-breeding can be used to eliminate genetic defects in a
strain of animals since the appearance of a recessive mutation indicates
which parents had the defect, so that those animals are removed from the
breeding pool.  Of course, the breeder has to track all of the animals over
multiple generations to do this.  The bigger risk for so-called "congenic"
animals is not cancer, which seems to be the alleged association with MF
ferrets, but infectious disease since a microbe that is seriously infectious
to one animal, will be equally infectious to all.  And I haven't heard
anyone report that MF ferrets are more susceptible to infectious disease
than other ferrets.
 
Finally, she states that maintaining separate breeding colonies for lab
animals and for pets...
 
>would help toward solving the illnesses and diseases that our furries
>seem so susceptible to...
 
This presupposes that genetics are entirely at fault for those illnesses and
diseases.  It also ignores cases of cancers in ferrets that have not come
from Marshall Farms.  Someone in our local group has a one-year-old ferret
with suspected lymphoma (lab tests not back yet).  That ferret came from a
breeder in North Carolina, not MF.  If *non*-MF ferrets have early-onset
cancers, that should either absolve MF of charges of inbreeding or expand
the list of irresponsible breeders.  So far, however, only MF has been
targeted, even though the evidence suggests something more complicated or
subtle is going on.
 
An easy target is always nice, but genetics can't be blamed as the primary
culprit for every cancer, deformity or odd behavior.  The environment
greatly influences how genes respond.  The first human breast-cancer gene
discovered about three years ago (called "BRCA1" by geneticists) is such a
potent cancer gene that 85% of women with a defect in BRCA1 develop breast
and/or ovarian cancer before age 40.  Nonetheless, some women who definitely
have the gene lived to their late 80s and early 90s and *never* developed
breast or ovarian cancer.  Something else in their genetic make-up or in
their environment spared those women.
 
I don't believe that the evidence exists to convict Marshall Farms of
breeding ferrets with defects.  And now that so many allegations have been
lobbed against them, the information gathered about MF ferrets is almost
certainly biased.  This happens all the time in the epidemiology of genetic
diseases.  A particular defect occurs twice in a family--perhaps
coincidentally --and the family and their doctors go out of their way to
look for it, inflating the reporting rate compared with other families.  The
bias can also work the opposite way if the defect is socially embarrassing,
such as covering up a relative's cancer, diabetes or alcoholism.
 
I am hoping to begin a systematic study of this issue later this year,
although it would take several years to finish since the study would have to
follow entire litters of kits forward until they begin to die.  (If anyone
on the FML knows anything about the biostatistical issues involved in sample
selection using litters of animals, I could use your help.) I wish I could
pull an easy answer out of a hat, but it's just not possible right now.
 
--Jeff Johnston ([log in to unmask])
[Posted in FML issue 1693]