I'll ask others (though some experts may be away) and I AM ASKING ON
THE FHL but right now it looks like the concern about C. difficile (as
opposed to C. perfringens) on the Ferret Mailing List for ferrets MIGHT
be misplaced (but exceptions happen as do discoveries and bacterial
mutations). I do not personally know how species specific this
bacterium is but many bacteria are quite species specific. I have
to ask some experts about that. Notice that ferrets CAN have C.
perfringens blooms but that they are rare AND that some Clostridium
in the feces is NORMAL. That is not to say that at least two of the
Clostridium toxins in ferrets are not dangerous when it happens because
when that does happen infection or toxin can be rapidly fatal.

Notice past VETERINARY EXPERT posts (but these are beginning to get a
bit old so may or may not apply however the journal articles found do
not indicate a large threat at this time):
http://ferrethealth.org/archive/SG7489
by ferret expert veterinary pathogist, Dr. Bruce Williams:
>I'm not a fan of diagnosing Clostridium in feces. Robust bacilli are
>always present in ferret feces, and there is no way to tell if they
>are pathogenic Clostridium or not. It is a common and valid test in
>birds, but not really in ferrets.
>
>Add this to the fact that clostridiosis is a rare disease in ferrets
>(once diagnosed in a group of blackfooted ferrets as the cause of
>gastric bloat), and I have to be a bit circumspect about this
>diagnosis.

as well as these MUST READ PAST EXPERT POSTS
http://ferrethealth.org/archive/SG6286
http://ferrethealth.org/archive/SG2045

Here is one way to HELP PREVENT infection by the Clostridium species
ferrets appear to USUALLY have when they get infection:
http://edis.ifas.ufl.edu/fs101
The vegetative stage cells can be killed by reaching temperatures of
140'F or higher, BUT cells which are in the spore stage can still
survive so the population of the organism is reduced, which is
certainly a help.

A PubMed search did not bring up anything specifically ferret (and see
my post the other day for some things to read) but see this mustelid
"cousin" article, what they looked for and more importantly what they
found:

>Vet Res. 2010 Jan-Feb;41(1):1. Epub 2009 Sep 2.
>
>Enteric bacterial pathogen detection in southern sea otters (Enhydra
>lutris nereis) is associated with coastal urbanization and freshwater
>runoff.
>
>Miller MA, Byrne BA, Jang SS, Dodd EM, Dorfmeier E, Harris MD, Ames J,
>Paradies D, Worcester K, Jessup DA, Miller WA.
>
>California Department of Fish and Game, Marine Wildlife Veterinary
>Care and Research Center, 1451 Shaffer Road, Santa Cruz, CA 95060,
>
>[log in to unmask]
>
>Abstract
>Although protected for nearly a century, California's sea otters have
>been slow to recover, in part due to exposure to fecally-associated
>protozoal pathogens like Toxoplasma gondii and Sarcocystis neurona.
>However, potential impacts from exposure to fecal bacteria have not
>been systematically explored. Using selective media, we examined
>feces from live and dead sea otters from California for specific
>enteric bacterial pathogens (Campylobacter, Salmonella, Clostridium
>perfringens, C. difficile and Escherichia coli O157:H7), and pathogens
>endemic to the marine environment (Vibrio cholerae, V. parahaemolyticus
>and Plesiomonas shigelloides). We evaluated statistical associations
>between detection of these pathogens in otter feces and demographic
>or environmental risk factors for otter exposure, and found that
>dead otters were more likely to test positive for C. perfringens,
>Campylobacter and V. parahaemolyticus than were live otters. Otters
>from more urbanized coastlines and areas with high freshwater runoff
>(near outflows of rivers or streams) were more likely to test positive
>for one or more of these bacterial pathogens. Other risk factors for
>bacterial detection in otters included male gender and fecal samples
>collected during the rainy season when surface runoff is maximal.
>Similar risk factors were reported in prior studies of pathogen
>exposure for California otters and their invertebrate prey, suggesting
>that land-sea transfer and/or facilitation of pathogen survival in
>degraded coastal marine habitat may be impacting sea otter recovery.
>Because otters and humans share many of the same foods, our findings
>may also have implications for human health.
>PMID: 19720009 [PubMed - indexed for MEDLINE]
>PMCID: PMC2769548
>Free PMC Article

Full text can be found at either
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769548/?tool=pubmed
 or
<http://www.vetres.org/index.php?option=com_article&access=standard&Itemid=129&url=/articles/vetres/full_html/2010/01/v09198/v09198.html>

Wien Klin Wochenschr. 2009;121(3-4):91-5.

>Clostridium difficile: a new zoonotic agent?
>
>Indra A, Lassnig H, Baliko N, Much P, Fiedler A, Huhulescu S,
>Allerberger F.
>
>Austrian Agency for Health and Food Safety, Institute of Medical
>Microbiology and Hygiene, National Reference Center for Clostridium
>difficile, Wien, [log in to unmask]
>
>Abstract
>Clostridium difficile is mainly considered a nosocomial pathogen
>associated with diarrhea and pseudomembranous colitis in hospitalized
>patients. Austrian hospitals reported 2761 cases of C. difficile
>infection (including 277 lethal outcomes) in 2007, compared with
>777 cases (including 54 lethal outcomes) in 2003. The occurrence of
>community-acquired C. difficile infection is also increasingly
>reported. Recent studies have shown the occurrence of C. difficile in
>food and animals. The aim of the present study was to determine the
>occurrence of C. difficile in food and animals in Austria. Between
>March and July 2008, gut or fecal samples from 67 cows, 61 pigs and 59
>broiler chickens were collected at Austrian abattoirs. Between February
>and April 2008 meat samples (51 beef [25 ground], 27 pork [17 ground]
>and 6 samples of chicken meat) were purchased at retail outlets. Of the
>187 samples tested, eight yielded C. difficile: in cows 3/67 samples
>(4.5%) were positive, in pigs 2/61 (3.3%), in broiler chickens 3/59
>(5%). Six of the eight isolates yielded toxigenic C. difficile (toxins
>A and B): 2/67 (3%) cow samples, 2/61 (3.3%) pig samples, 2/59 (3.4%)
>chicken samples. Genes for the binary toxin were detected in one of
>the two pig isolates, a PCR ribotype 126 strain. None of the 84 meat
>samples yielded C. difficile. The results of this Austrian study
>suggest that animal reservoirs are possible sources, via food, of
>human C. difficile infection.
>
>PMID: 19280132 [PubMed - indexed for MEDLINE]


>Clin Microbiol Infect. 2007 May;13(5):457-9. Epub 2007 Feb 28.
>
>Is Clostridium difficile-associated infection a potentially zoonotic
>and foodborne disease?
>
>Rupnik M.
>
>Abstract
>Clostridium difficile has received much attention in recent years
>because of the increased incidence and severity of nosocomial disease
>caused by this organism, but C. difficile-associated disease has also
>been reported in the community, and C. difficile is an emerging
>pathogen in animals. Early typing comparisons did not identify animals
>as an important source for human infection, but recent reports have
>shown a marked overlap between isolates from calves and humans,
>including two of the predominant outbreak types, 027 and 017. C.
>difficile has also been found in retail meat samples, suggesting that
>food could be involved in the transmission of C. difficile from
>animals to humans.
>
>PMID: 17331126 [PubMed - indexed for MEDLINE]

Oh, and remember that cooking kills at least some types of Clostridia
(Maybe all types of Clostridia?) and if memory serves -- but no time
to check now but IF my memory serves sufficient cooking also destroys
the toxins (All Clostridium toxins or just botulism?). Yes, I have
questions that I don't have time to look into and you WILL find them
in my post! Read refs. I found
http://www.ecolab.com/PublicHealth/Cbotulinum.asp
fast but you may find better ones if you just look, please.

Note that this is a different species of Clostridium:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC172891/

>Schulman FY, Montali RJ, Hauer PJ. Gastroenteritis associated with
>Clostridium perfringens type A in black-footed ferrets (Mustela
>nigripes). Vet Pathol. 1993 May;30(3):308 - 310.[PubMed]

Full article:
http://vet.sagepub.com/content/30/3/308.long

Oh and yes, ferrets DO get botulism which I believe is from Clostridium
toxin but am not sure if I will have time to look (all species of
Clostridium? some species of Clostridium?), BTW, and info on that is in
multiple vet texts. Ah:
>Vet Rec. 1973 Dec 1;93(22):576-7.
>
>Deaths in ferrets (Mustela putorius) due to Clostridium botulinum type C.
>
>Harrison SG, Borland ED.
>
>PMID: 4594379 [PubMed - indexed for MEDLINE]

Also:
http://www.ncbi.nlm.nih.gov/pubmed/17679500 
(Shoot, I got so busy adding info that I forget which portion involves
that article so if it jumps you to a different part of the discussion
bear with my shortness of time.)

Notice, too, that tetanus involves a type of Clostridium:
http://www.angelfire.com/nj/woundedknee/zoonoses.html

<http://scienceblogs.com/aetiology/2006/05/emerging_disease_and_zoonoses_9.php>
mentions a human hospital therapy dog with C. difficile, and includes
this in relation to the genus, Clostridium, in general:

>As infections with these bacteria are increasingly in the spotlight,
>it's likely that we'll see more of them due not only to a real
>increase, but also due to reporting bias (in other words, you're much
>more likely to find what you're looking for than what you aren't).
>However, surveillance can only tell us so much. Clostridia are
>notoriously difficult to work with, making a better understanding
>of the bacterium via genetic manipulation a slow process. However,
>vaccines are in the works for the emerging Clostridia species, as
>well as drugs that bind to the toxins produced by C. difficile, and
>the NIH is urging research submissions on Clostridium.

Now, notice that I DID purposely say "might" and among others (like the
human hospital pet therapy poodle) this illustrates why I did that:
http://www.askthecatdoctor.com/zoonosis-clostridium-difficile.html
as does
<http://blogs.cdc.gov/publichealthmatters/2009/04/clostridium-difficile-an-emerging-zoonosis/>
which includes:

So, is C. difficile an emerging zoonosis

>The answer is: we don't know yet. CDC will continue to collaborate
>with various experts in food safety and veterinary medicine to
>identify research needs and learn more about C. difficile infection
>in foods. Our scientists are also working closely with USDA -- the
>government agency responsible for regulating the safety of meat --
>and sharing emerging information as it becomes available.

Here is one way to REDUCE THE RISK of infection by the Clostridium
species ferrets appear to USUALLY have when they get infection:
http://edis.ifas.ufl.edu/fs101
>Clostridium perfringens is a Gram-positive bacterial pathogen that
>has the capability of forming an endospore. The dormant spores can
>change to potentially harmful vegetative cells if exposed to cooking
>temperatures and allowed to stand at temperatures between 41°F and
>120°F, especially the temperature range of 70°F - 120°F. Clostridium
>perfringens vegetative cells are killed in foods when the foods are
>cooked at 140°F or above. However, spores may still be present after
>cooking. Spores can survive the cooking process. Clostridium
>perfringens can only thrive in conditions of very little or no oxygen:
>that is, it is an anaerobic organism. Clostridium perfringens will not
>grow at refrigeration or freezing temperatures.

See also:
<http://www.fda.gov/Food/ScienceResearch/LaboratoryMethods/BacteriologicalAnalyticalManualBAM/UCM070878>
which begins with
>Food poisoning caused by Clostridium perfringens may occur when foods
>such as meat or poultry are cooked and held without maintaining
>adequate heating or refrigeration before serving. The presence of
>small numbers of C. perfringens is not uncommon in raw meats, poultry,
>dehydrated soups and sauces, raw vegetables, and spices. Because the
>spores of some strains are resistant to temperatures as high as 100°C
>for more than l h, their presence in foods may be unavoidable.
>Furthermore, the oxygen level may be sufficiently reduced during
>cooking to permit growth of the clostridia. Spores that survive
>cooking may germinate and grow rapidly in foods that are inadequately
>refrigerated after cooking. Thus, when clinical and epidemiological
>evidence suggests that C. perfringens is the cause of a food poisoning
>outbreak, the presence of hundreds of thousands or more of these
>organisms per gram of food substantiates the diagnosis.

Wanted an easy answer? There may not be one for the question about the
risk rate of C. difficile in ferrets, but if you hear that your ferret
has a Clostridium infection FIRST make sure that what has been seen is
not just the normal level of intestinal Clostridium for ferrets, and
do NOT automatically assume that it is the species C. difficile.

[Posted in FML 6761]