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Beynen AC, 2020. Diet and canine coprophagy

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Abstract

Diet and canine coprophagy Coprophagy, or stool eating, is a common behavior among dogs. For several weeks after puppies are born, bitches ingest their feces, likely for hygienic purpose. Quite a few dogs eat feces of hoofed animals, their own feces and/or that of other adult dogs. Coprophagic behavior is clinical when caused by digestive disease (1) or chronic stress (2, Note 1). Otherwise, it might be considered normal canine behavior. But dogs' risk of contracting certain parasites is increased by ingesting feces of conspecifics (Note 2). In addition, the habit of dogs eating feces disgusts many owners. A web-page survey completed by 1475 dog owners found that 16% of pet dogs engaged in frequent eating of their own or other dogs' feces (3, Note 3). The conspecific coprophagy was mainly directed at feces no more than two days old (3). The web-page survey (3) and two other questionnaire-based studies (4, 5) did not ascertain an association between type of diet and coprophagy. The paper on the large-scale study states explicitly that the vast majority of the dogs was fed on dry food (3). Thus, an association between diet and coprophagy, if there is any, was undetectable beforehand due to limited variation of diet type. Unsubstantiated theories have advanced that diet affects canine coprophagy. More specifically, high carbohydrate (starch) intake, insufficient supply of vitamin B1 (thiamine), diets with below-average digestibility and low-fiber diets have all been suggested to promote coprophagic behavior (Notes 4, 5). None of the diet factors proposed to initiate or intensify canine coprophagy is backed by available research data. As to dietary behavior, the recent web-page survey (3) shows that greedy eating is associated with coprophagy. Various dietary supplements, in the form of chewable tablets or powders, are marketed as coprophagy deterrents for dogs eating their own feces (Note 6). Presumably in response to the unsubstantiated theories on diet and canine coprophagy, several supplements contain thiamin and digestive enzymes, including alpha-amylase which breaks down starch. Most products enclose substances that allegedly make stool less appealing to dogs. A commonly used substance in coprophagy deterrents is an extract from the desert plant Yucca schidigera, but there is no convincing experimental evidence for its efficacy. Three questionnaire-based studies indicate that coprophagy-treatment products are not very successful and that preventing access to feces is the most commonly used and most effective way to stop canine coprophagy (3, 5, 6). In conclusion, there is no demonstrable evidence, in the form of outcomes of controlled studies, that even one of the proposed diet changes significantly diminishes canine coprophagy. The same holds for the coprophagy deterrents on the market. In itself, the principle of making feces repellant by a safe dietary constituent or supplement seems achievable. Clearly, its application would be primarily autocoprophagy-directed. Carbohydrate intake In 1973, Kronfeld published his diet-intervention study in a group of 16 racing sled dogs that performed poorly (7). The article states that all dogs practiced coprophagy and that it was said to be a general problem. Type of coprophagy (allo-and/or autocoprophagy) and housing (individually or in
Bonny Canteen 2020; 1: 79-88.
Anton C. Beynen
Diet and canine coprophagy
Coprophagy, or stool eating, is a common behavior among dogs. For several weeks after puppies
are born, bitches ingest their feces, likely for hygienic purpose. Quite a few dogs eat feces of
hoofed animals, their own feces and/or that of other adult dogs. Coprophagic behavior is clinical
when caused by digestive disease (1) or chronic stress (2, Note 1). Otherwise, it might be
considered normal canine behavior. But dogs’ risk of contracting certain parasites is increased by
ingesting feces of conspecifics (Note 2). In addition, the habit of dogs eating feces disgusts many
owners.
A web-page survey completed by 1475 dog owners found that 16% of pet dogs engaged in
frequent eating of their own or other dogs’ feces (3, Note 3). The conspecific coprophagy was
mainly directed at feces no more than two days old (3). The web-page survey (3) and two other
questionnaire-based studies (4, 5) did not ascertain an association between type of diet and
coprophagy. The paper on the large-scale study states explicitly that the vast majority of the dogs
was fed on dry food (3). Thus, an association between diet and coprophagy, if there is any, was
undetectable beforehand due to limited variation of diet type.
Unsubstantiated theories have advanced that diet affects canine coprophagy. More specifically,
high carbohydrate (starch) intake, insufficient supply of vitamin B1 (thiamine), diets with below-
average digestibility and low-fiber diets have all been suggested to promote coprophagic behavior
(Notes 4, 5). None of the diet factors proposed to initiate or intensify canine coprophagy is backed
by available research data. As to dietary behavior, the recent web-page survey (3) shows that
greedy eating is associated with coprophagy.
Various dietary supplements, in the form of chewable tablets or powders, are marketed as
coprophagy deterrents for dogs eating their own feces (Note 6). Presumably in response to the
unsubstantiated theories on diet and canine coprophagy, several supplements contain thiamin and
digestive enzymes, including alpha-amylase which breaks down starch. Most products enclose
substances that allegedly make stool less appealing to dogs.
A commonly used substance in coprophagy deterrents is an extract from the desert plant Yucca
schidigera, but there is no convincing experimental evidence for its efficacy. Three questionnaire-
based studies indicate that coprophagy-treatment products are not very successful and that
preventing access to feces is the most commonly used and most effective way to stop canine
coprophagy (3, 5, 6).
In conclusion, there is no demonstrable evidence, in the form of outcomes of controlled studies,
that even one of the proposed diet changes significantly diminishes canine coprophagy. The same
holds for the coprophagy deterrents on the market. In itself, the principle of making feces repellant
by a safe dietary constituent or supplement seems achievable. Clearly, its application would be
primarily autocoprophagy-directed.
Carbohydrate intake
In 1973, Kronfeld published his diet-intervention study in a group of 16 racing sled dogs that
performed poorly (7). The article states that all dogs practiced coprophagy and that it was said to be
a general problem. Type of coprophagy (allo- and/or autocoprophagy) and housing (individually or in
groups) were not mentioned. Each evening, the dogs received a single meal, consisting of
commercial dry food (68.4%), horse meat (26.3%) and corn oil (5.3%). By percentages of
metabolisable energy, the dietary protein:fat:carbohydrate ratio was 29:32:39. The carbohydrate
content was lowered from 39 to 28, through replacing part of the dry food by an isoenergetic
amount of horse meat. The coprophagy was found to cease in a few days.
The observation that coprophagy was corrected by lowering of carbohydrate intake (7) corroborates
earlier and later statements that high carbohydrate intake promotes coprophagy (Note 4). However,
the evidential value of the study is rather limited: there was no control group, the intervention
involved multiple dietary variables and reproducibility is unknown.
Kronfeld and others have further reported on sled dogs fed high- or low-carbohydrate diets, but
coprophagy was either not mentioned in relation to the study at issue (8) or not at all (9, 10). This is
surprising, not only in the light of the initial study (7), but also because group-kept, Antarctic sled
dogs have been typified by their “almost invariable coprophagy“ (11) and “voracious coprophagic
habits of hungry dogs” (12).
Vitamin B1 deficiency
It has been asserted that canine coprophagy is triggered by a deficiency of B vitamins (13). As
evidence, the following statement was presented as a fact: adding brewers yeast (which is rich in B
vitamins) to the diet stopped coprophagy within a few days (13, Note 7). That statement is not
substantiated or accompanied by cited literature, but at the time there was a supportive study in
dogs with experimentally-induced vitamin B1 deficiency (14). Furthermore, it is well known that
feces is an abundant source of microbial-synthesized B vitamins. However, for the following three
reasons it is improbable that deficiency of B vitamins plays a role in canine coprophagy.
Deficiency of B vitamins is highly unlikely in coprophagic dogs fed on a commercial, complete diet. A
vitamin deficiency prompting coprophagy requires that a low bodily status of the vitamin directs
selection of feces as an edible item being rich in the vitamin concerned. However, dietary self-
selection instructed by micronutrient-status has not been demonstrated in dogs. Furthermore, as
explained below, the observation that deficiency of vitamin B1 led to coprophagy in dogs (14)
probably is irreproducible.
The 1981 paper (14) describes that young dogs fed a thiamin-deficient, semipurified diet (Note 8)
developed progressive inappetance, lack of growth and coprophagy, followed by neurological
abnormalities. The control dogs remained healthy; they were fed the same diet, but received a
weekly intramuscular dose of thiamin hydrochloride. The authors (14) mentioned that other workers
(15) also noted coprophagy in dogs fed a thiamin-deficient diet. In fact, those other workers
suspected coprophagy in two dogs, but never directly observed it (15). A literature-based list with
common signs of thiamine deficiency in dogs does not include coprophagia (16).
Exocrine pancreatic insufficiency
In 1966, McCuistion wrote that coprophagy in dogs may be an expression of an insufficiency of
digestive enzymes, particularly amylase (17, Note 4). Exocrine pancreatic insufficiency (EPI) is a well-
known maldigestion disease due to lack of pancreatic digestive enzymes (1). The clinical signs are
weight loss, polyphagia and output of voluminous, semi-formed feces. EPI also is considered a
clinical cause of coprophagia. Primary treatment consists of supplementing each meal with
pancreatic enzyme extracts.
A questionnaire-based study has addressed the efficacy of long-term enzyme replacement in dogs
with EPI (18). The study involved German Shepherd Dogs and Rough-Coated Collies, breeds with a
high risk of EPI. The dogs were either clinically normal or had EPI and were given dietary enzyme
supplements for at least four months. According to the owners, “coprophagy (sometimes)” occurred
in 8% of the healthy (n =72) and in 18% of the affected (n =45) German Shepherds. For the Collies
these frequencies were 0% (n = 73) and 26% (n =31). It is clear that coprophagia was (still) increased
in the enzyme-treated dogs with EPI.
Hungriness and coprophagy
Perhaps, hungriness instigates coprophagy in dogs with EPI (1) and in Antartic, working sled dogs
(12). Coprophagic pet dogs were more frequently typified by their owners as greedy eaters than
were non-coprophagic dogs (3). It could be suggested that food restriction, which plausibly
strengthens hungriness and gobbling, enhances coprophagic behavior. However, there is no
evidence for that suggestion. In group-housed dogs of various breeds, the transition from ad libitum
feeding to caloric restriction and vice versa did not affect camera-monitored coprophagy (19, 20).
During regular feeding, coprophagy was uncommon in the dogs (Note 9). Possibly, they were
unreceptive to engaging in coprophagy.
Yucca schidigera
For making a claim on waste-odor control, petfoods are typically supplemented with a Yucca
schidigera preparation. There is experimental evidence that yucca substances generally reduce
group-mean odor offensiveness of dog and cat feces (21). Ten out of 13 brands of coprophagy
deterrents contain Yucca schidigera as active ingredient (Note 6). One brand states that Yucca
schidigera makes stool less appealing to a dog.
Autocoprophagic behavior in dogs can be quantified as delay in fecal excretion of orally
administered radio-opaque markers (22, Note 10). Autocoprophagic dogs (n =15) were fed a dry diet
without or with 125 mg Yucca schidigera/kg in a cross-over trial (23). After 20 days on the diets,
radio-opaque markers were given and feces collected for another 10 days. The percentages marker
recovery were 71 and 93% for the control and yucca-containing diet. The outcome, albeit statistically
non-significant (P =0.15), suggests that dietary yucca reduced coprophagy. Unfortunately, the
degree of stool eating was not visually observed so that practical meaningfulness of the yucca effect
cannot be assessed.
Note 1
Boredom has been suggested as a motivating factor for canine coprophagy (cf. 6). However,
availability of toys such as rawhide or rope were not associated with less coprophagic behavior (6).
Claw horn from calves is a valued chewing object in group-housed laboratory dogs, but its
administration increased coprophagy, possibly because feces with claw residue is more attractive to
dogs (24).
Note 2
Coprophagy can increase the risk of infection with Toxocara canis in dogs (25), but certain parasites
may produce eggs that pass through the gastrointestinal tract without being affected. The presence
of those eggs in feces of a dog, due to eating another dog’s stool, can lead to false positive outcomes
in the diagnosis of parasitic infections by fecal examination (26).
Note 3
Other studies have also quantified the occurrence canine coprophagy. In a questionnaire-based
study, 177 out of 623 owners (28%) indicated that their dogs showed coprophagic behavior (6, 27).
Dogs that consumed all feces types, only dogs’ feces or only herbivores’ feces were similar in
number (6). Interviews with owners of 70 dogs revealed that 30 dogs (43%) were coprophagic (4).
A web-page survey that was focused on coprophagic dogs comprised 802 owners with 1157 dogs of
which 862 (75%) were coprophagic (5). Within the framework of a study on helminth infections in
dogs, 561 owners of 896 dogs reported that 391 animals (44%) ate feces of unspecified origin (26).
The owners of dogs that were purchased from an animal rescue shelter, reported that 49 (9%) out of
556 dogs displayed coprophagy (28).
Note 4
Chronological order of quotes, taken from veterinary journals and books, about a causative role of
the amount of dietary carbohydrates with regard to canine coprophagy. Three authors’ statements
(13, 17, 29) are not accompanied by a literature reference. Kronfeld (7) has cited McCuistion’s article
(17).
1966 (17): “Feeding these dogs a diet high in carbohydrates, which they frequently may not be able
to digest, results in the coprophagy syndrome”. In the quote, “these dogs” refers to German
Shepherds.
1973 (7): “The appearance of tying up, the coprophagy, and the hypoglycemia of the dogs all
suggested excessive carbohydrate intake. The immediate correction of the coprophagy, the
restoration of normal blood glucose concentrations, and the progressive increase in stamina on
lowering of the carbohydrate intake supported the diagnosis”. In the quote, “the dogs” refers to
Siberian or Alaskan Huskies with some infusion of German Shepherd breeding.
1988 (29): “Diets high in carbohydrate tend to enhance the drive to eat stool”
1991 (13): “In the dog, the consuming of faeces (its own or the faeces of others) is observed mainly
with rations containing a high level of carbohydrates: cereal starch, and more especially when this
starch is not digestible enough due to inadequate cooking”.
Note 5
Chronological order of quotes, taken from veterinary journals and books, about a causative role of
food digestibility with regard to canine coprophagy.
1993 (30): “A highly-digestible low-residue diet which has a high energy density should be fed.
Occasionally, a high-fibre diet may be more effective although the reason is not clear”
1994 (31): “If the dog is eating its own faeces, feed it a highly digestible, predominantly meat diet ...”
2000 (32): “Factors associated with coprophagy. Food. Poorly digestible food. Overfeeding”
2010 (33): “Using foods with increased fiber levels has been reported to help”
Interestingly, the last quote is at odds with second to last quote, whereas both quotes are taken
from the same authors. Foods with increased fiber levels, be it insoluble or soluble fiber, generally
lower net total-tract digestion of dietary dry matter in dogs (34, 35). Thus, high-fiber foods, as
advised in the last quote, tend to be less digestible foods, which should be avoided, as implied by the
second to last quote.
Note 6
Commercially available coprophagia deterrents for dogs: product name, form, listed active
ingredients and, if provided, explanatory information about the mechanism of action and/or
efficacy.
a. FOR-BID, powder; wheat gluten and monosodium glutamate. A highly purified crystalline edible
protein fraction that produces a bad taste to the stool, deterring them from further consumption.
b. Zesty Paws Chew No Poo Bites, soft chews; vegetable blend, breath blend, glutamic acid,
digestive enzyme blend, Yucca schidigera extract, Bacillus coagulans, capsicum extract. The enzyme
blend and probiotic support healthy digestion; the capsicum extract gives stool an unpleasant taste.
c. Vetrinex Labs Probiotics. Advanced Probiotic Formula for Dogs & Cats, powder; various
Lactobacillus species, Enteroccocus faecium, Bifidobacterium. The probiotics strengthen the
digestive tract.
d. NaturVet® Coprophagia, chewable tablets; Yucca schidigera, parsley leaf, enzyme blend,
chamomile. Thiamine monohydrate is listed as inactive ingredient. The product helps deter dogs
from consuming their own stool
e. Healthy Solutions for Pets. No Stool Eating, soft chews; Yucca schidigera, parsley leaf, enzyme
blend, Bacillius coagulans, chamomile. The product makes poop taste foul. Products d and e have
identical lists of active ingredients.
f. ThomasLabs®, Stop Stool Eating, tablets; proprietary blend including Yucca schidigera extract,
Lactobacillus acidophilus fermentation product. By changing the taste and texture of the stool, the
product helps deter dogs from eating their own waste
g. NUTRI-VET Nasty Habit®, chewable tablets; Yucca schidigera, cayenne pepper, alpha-amylase,
parsley leaf, glutamic acid, chamomile, thiamine. Yucca schidigera helps reduce odors arising from
stool and urine to make them less appealing to a dog. Cayenne pepper imparts an “offensive” taste
to stop dogs from eating poop. Alpha-amylase is a digestive enzyme that helps alter the taste and
odor of stool. Glutamic acid makes stool taste very bitter to the dog when mixed with stomach acids.
h. PetNC™, Stool eating deterrent, chewables; Yucca schidigera extract, cayenne pepper, alpha
amylase, parsley leaf, glutamic acid, chamomile, thiamine monohydrate. The product creates a bitter
taste to feces to discourage dogs from consuming their own feces Products g and h have identical
lists of active ingredients.
i. PROSENSE® Poop Eater Solutions, chewable tablets; monosodium glutamate, Yucca schidigera,
thiamine hydrochloride, oleoresin capsicum. The product may help deter dogs from consuming own
feces while reducing feces odor.
j. GNC PETS MEGA STOOL NO, chewable tablets; Yucca schidigera, parsley, chamomile, proprietary
enzyme blend. Brewer’s yeast is listed as inactive ingredient. The product is formulated to facilitate
deterrence of stool eating
k. VETIQ STOOL REPEL, tablets; brewers dried yeast, alpha amylase, capsicum oleoresin. The product
makes stool less palatable and contains alpha-amylase which breaks down starches, helping to
improve digestion.
l. Well&Good, Coprophagia, chewable tablets; Yucca schidigera extract, parsley leaf,
fructooligosaccharide, chamomile flower, glutamic acid, cayenne pepper, sodium copper
chlorphyllin, thiamine monohydrate, digestive enzymes, probiotics. The product helps prevent dogs
from consuming feces.
m. ONLY NATURAL PET Stool Eating Deterrent, chewable tablets; Mojave yucca (root) extract,
brewers yeast, parsley (leaf), chlorella, niacinamide, thiamin mononitrate, riboflavin, vitamin B6
(from pyridoxine HCl), enzyme blend (fungal amylase, fungal protease, lipase, cellulose), cayenne
(fruit). The product features natural digestive enzymes; it has been suggested that stool eating may
be induced by the presence of undigested material in the stool. The product has a powerful blend of
ingredients to alter the taste and aroma of stool, making it less appealing.
a. https://www.for-bid.com/about-forbid/ and https://www.drugs.com/vet/for-bid.html and
https://www.entirelypets.com/forbidsingle.html
b. https://zestypaws.com/products/chew-no-poo-bites
c. https://vetrinexlabs.com/collections/all/products/probiotics-for-dogs-and-cats
d. https://naturvet.com/product/coprophagia-stool-eating-deterrent-chewable-tablets/
e. https://healthysolutionsforpets.com/shop/dog-supplements/stool-health-dog-supplements/stool-
eating-deterrent-soft-chew-supplement-for-dogs
f. https://www.entirelypets.com/thomas-labs-stop-stool-eating-100-tablets
g. https://www.nutri-vet.com/dog-health/dog-digestion-and-bladder-control/nasty-habit-chewables
h. https://www.amazon.com/PetNC-Natural-Care-Deterrent-Chewables/dp/B00IW1LRN8
i. http://www.prosensepet.com/solutions/poop-eater-solutions.aspx
https://www.chewy.com/pro-sense-plus-poop-eater-solutions/dp/170614
j. https://www.gnc.com/on/demandware.static/-/Sites-GNC2-
Library/default/v1593251835095/pdf/678832_lbl.pdf
k. https://markandchappell.com/vetiq/behavioural-aids/stool-repel
l. https://www.amazon.com/Well-Good-Coprophagia-Tablets-count/dp/B01MU0LG51
m. https://www.amazon.com/Only-Natural-Pet-Deterrent-Puppies/dp/B0030ZVWZE
Note 7
Apparently, the idea that thiamine deficiency causes coprophagy and that dietary brewers yeast
stops it (13) has in some way reached several manufacturers of coprophagy deterrents. Out of the
13 coprophagia deterrents (Note 6), six and two products, respectively, contain thiamin (vitamin B1)
and brewers yeast as (active) ingredients.
Note 8
The thiamin-deficient, pelleted diet consisted of 68% sucrose, 18% vitamin-free casein, 10%
vegetable oil, 4% salt mixture and supplemental vitamins, except for vitamin B1. The casein
contained 15 µg thiamin/100 g so that the diet contained 27 µg/kg (14). The adequate and
recommended amounts of thiamin for puppies after weaning are 1.08 and 1.38 mg/kg dietary dry
matter (= 4000 kcal = 16.736 MJ) (36).
Note 9
During 72 hours of camera observation, three out of 39 dogs exhibited eight incidents of
coprophagy. The dogs were housed in groups of three or four and fed a low-calorie diet at
maintenance supply or ad libitum (20).
Note 10
Autocoprophagic behavior in dogs was quantified by measuring fecal excretion of orally
administered radio-opaque markers (22). In non-coprophagic dogs, all markers were excreted within
three days, but in their coprophagic counterparts recovery amounted to about 40%.
Note 11
A manufacturer of pressed dog food had added an emulsifier (presumably glycerol
polyethyleneglycol ricinoleate) to one of its products. The inclusion percentage was not disclosed.
According to the proprietors of two different kennels, their dogs stopped practicing coprophagy
after consuming the emulsifier-containing food. To verify the observations, a controlled trial was
carried out (37).
Two complete, pressed foods either unsupplemented or supplemented with the emulsifier, but
otherwise identical, were provided by the manufacturer. Within a double-blinded, cross-over trial
with 8-week periods, the two foods were fed to 24 privately-owned, coprophagic dogs. The 16 dog
owners recorded daily whether or not their dog had eaten its own feces or that of another dog. The
percentage of days that individual dogs were observed eating feces ranged from 0 to 100%. The
mean percentages were 40 and 42% for the control and test food, indicating that the emulsifier did
not diminish coprophagy. Likewise, perceived feces consistency was not affected by the emulsifier.
Note 12
A coprophagic dog contracted thyrotoxicosis as a result of consuming the feces from a thyroxine-
treated housemate (38).
Note 13
Dogs eating their own feces were treated with citronella-spray collar or sound therapy (39). The
severity of coprophagy as reported by the dog owners was reduced most effectively by the spray
collar.
Note 14
Four out of the 13 coprophagic deterrents contain probiotics (Note 6). A study showed that
administration of Bacillus subtilis C-3102 did not affect coprophagy in dogs with chronic diarrhea
(40).
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3102 (Calsporin®) may improve feces consistency in dogs with chronic diarrhea. Res Opin Anim Vet
Sci 2016; 6: 256-260.
... (cf. 7,8). ...
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... Wanneer honden biotine alleen via de dunne darm kunnen opnemen, dan zijn ze op een biotine-vrij voeder, voor wat betreft biotinevoorziening, volledig afhankelijk van coprofagie. In dit verband kan eraan herinnerd worden dat coprofagie bij honden een veel voorkomend gedrag is (33). ...
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Biotine voor hond en kat Biotine (vitamine B7) is een wateroplosbare, essentiële stof voor het metabolisme van hond en kat. Tekort in het lichaam leidt tot huidaandoeningen. Voor de kat is een voedernorm gesteld, maar niet voor de hond. Aannemelijkerwijs wordt bij beiden de basisbehoefte doorgaans gedekt door microbieel biotine in de darm. Bij de ontdekking van biotine, alsook bij de daaropvolgende, experimenteel geïnduceerde biotinedeficiëntie, speelde rauw ei-eiwit in de voeding een hoofdrol. Dat doet het nog steeds in relatie tot de biotinenormen. Ei-eiwit bevat avidine, een glycoproteïne dat biotine in de darminhoud stevig bindt en onbeschikbaar maakt voor absorptie (Noot 1). Avidine is rijk aan het aminozuur tryptofaan en aan de suiker mannose (1, 2). Intact avidine bindt biotine middels hydrofiele en hydrofobe interacties (3). Eiwitverteringsenzymen kunnen biotine niet vrijmaken uit het avidine-biotine complex (4). Na 15 minuten bij 100 o C was avidine geïnactiveerd, maar het avidine-biotine complex was nog intact (5). Verhitting van rauw ei-eiwit elimineert niet alleen het biotine-bindend vermogen (Noot 2), maar ook de anti-trypsine aktiviteit, waardoor de verteerbaarheid ervan aanzienlijk toeneemt (Noot 3). Ontdekking Boas publiceerde in 1927 dat jonge ratten ziek werden op een voeder met 21% ei-eiwit (in de droge stof), dat bij 37 o C luchtgedroogd was (6, Noot 4). Na drie weken verloren de ratten gewicht en toonden vervolgens een exceemachtige huidontsteking, haaruitval en spastische bewegingen, gevolgd door de dood. De ratten groeiden en bleven gezond wanneer het voeder gekookt ei-eiwit bevatte (Noot 5). In 1939 liet György zien dat een fractie uit gist en lever, genaamd vitamine H, bovengenoemde symptomen genas bij ratten die een voeder met onverhit ei-eiwit kregen (7). Later bleek vitamine H identiek aan biotine, een eerder geïsoleerde groeifactor voor gist (8). H staat voor Haut. De naam biotine is afgeleid van "bios" (leven in het Grieks) en het achtervoegsel "ine", dat in veel chemische namen voorkomt (9, Noot 6). Structuur, functie, voorziening De structuur van biotine werd in 1942 bekend (10). Biotine (C10H16N2O3S) bestaat uit twee gefuseerde ringen, die twee koolstofatomen delen: een 5-ring met 4 koolstofatomen en een zwavelatoom, en een 5-ring met twee koolstof-en twee stikstofatomen, die tussenin een koolstofatoom met ketogroep hebben. De ring met zwavelatoom heeft valeriaanzuur als zijketen. Biotine is een co-factor voor carboxylases, enzymen die kooldioxyde overdragen op hun substraten. Als essentieel onderdeel van drie enzymsystemen, acetyl-CoA-, propionyl-CoA-en pyruvaat-carboxylase, is biotine vereist voor de vetzuursynthese, afbraak van een drietal aminozuren en de synthese van glucose uit melkzuur.
... If that process extends to dogs, it would mean that dogs fed a biotin-free diet rely on coprophagy with regard to biotin supply. Coprophagy is a common behavior among dogs (48). ...
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Riboflavine voor hond en kat Riboflavine (vitamine B2) is een wateroplosbare, essentiële voedingsstof voor hond en kat. Tekort veroorzaakte bij honden gebrek aan eetlust, gewichtsverlies en onvergankelijke ineenstorting. De aanbevolen hoeveelheden B2 voor hond en kat zijn marginaal onderbouwd, maar toepasbaar als aanwijzingen. Riboflavine bestaat uit ribose en flavine, ofwel een enkelvoudige suiker en drie gekoppelde ringstructuren. De naam flavine is afgeleid van flavus, Latijn voor geel. Riboflavine weerkaatst een heldergele kleur na blootstelling aan ultraviolet licht (Noot 1). Ruim voor 1900 werd uit koemelk een wateroplosbare fractie geïsoleerd, die fluorescerend geel is onder invloed van zonlicht. Koemelk en riboflavine Onafhankelijk van elkaar, in Utrecht en Cambridge, deden Pekelharing en Hopkins een vergelijkbare waarneming. Opname van een verwaarloosbare hoeveelheid koemelk maakte groei mogelijk van muizen en ratten op een experimenteel, vezelvrij, hoog verteerbaar voeder, dat bestond uit een eiwit-, koolhydraat-en vetbron, plus zoutmengsel (1, 2, Noot 2, 3). De waarnemingen zijn in 1905 en 1909 tijdens locale bijeenkomsten gepresenteerd. Een artikel uit 1933 beschrijft de werkzaamheid van een kristallijn, geel pigment dat uit koemelk was geïsoleerd (3). Als voederaanvulling herstelde de stof, lactoflavine genaamd, de stilgevallen groei van ratten die een opgezuiverde versie van bovengenoemd mengsel kregen (Noot 4, 5). Beginjaren 1930 werd de structuur van riboflavine bekend en was chemische synthese mogelijk (Noot 6). Lactoflavine was dus riboflavine, dat ook vitamine B2 werd genoemd. B1 (thiamine) was reeds bekend (4). Deficiëntie bij de hond B2-deficiëntie bij de hond is voor het eerst in 1939 door Street en Cowgill beschreven (5). Het proefvoeder bestond uit 30% caseine, 36% sucrose, 26,9% gehydrogeneerde, plantaardige olie, 0,1% linolzuur, 4% beenderas en 3% zouten. Dagelijks werden vitamines verstrekt, in de vorm van een extract van gepolijste rijst en kabeljauwleverolie (vitamines A, D en E). Eerder was bij ratten aangetoond dat het extract alle bekende B vitamines bevatte, behalve B2. Drie paar volwassen honden kregen het basisvoeder en de twee vitaminehoudende supplementen. Eén dier van elk paar kreeg dagelijks 0,025 mg zuiver B2 per kg lichaamsgewicht (Noot 7). Binnen elk paar werd de voerdosering gelijk gehouden (Noot 8). Bij de honden zonder B2-gift namen na één week voeropname en lichaamsgewicht gestaag af. Definitieve collaps trad op na 15 weken: daling van ademhaling en lichaamstemperatuur, onregelmatige hartslag, gevolgd door sterven (Noot 9). Deficiëntie bij de kat In 1959 verscheen een artikel (6) over kittens (n=11) waaraan een semisynthetisch voeder zonder B2 werd verstrekt. De voersamenstelling was als volgt: 32,1% caseine, 37,6% sucrose, 12,5% maisolie, 12,5% gehydrogeneerd vet, 1,0% kabeljauwleverolie, 4,0% zoutmengsel en 0,3% choline. Per kg
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Canine conspecific coprophagy, the tendency or predisposition of some dogs to eat their own faeces or those of other dogs, seems paradoxical because dogs typically show an aversion to conspecific faeces. In an attempt to resolve this paradox, we set out to determine the factors associated with the occurrence of this behaviour and to evaluate the efficacy of 11 products marketed for treating coprophagy as well as behaviour modification procedures. Because a large sample of dogs was needed to address these issues, two web-based surveys were utilized. One, intended to compare coprophagic dogs and non-coprophagic dogs, yielded 1552 returns. The other, yielding 1475 usable returns, specifically recruited owners of coprophagic dogs to gather information about the characteristics of coprophagy and treatment success. The findings revealed that 16% of dogs sampled engaged in frequent conspecific coprophagy, defined as having been seen eating stools at least six times. No evidence was found relating the coprophagy to diet or the dog's age. Coprophagic dogs were as easily house trained as non-coprophagic dogs, suggesting a normal aversion to faeces. Coprophagic dogs were more likely to be reported as greedy eaters than non-coprophagic dogs. The reported success rate of the commercial products and behaviour modification approaches was close to zero, indicating that the behaviour is not readily changed. The coprophagy was overwhelmingly directed at fresh stools, defined as being no more than 2 days old. A hypothesis is offered that coprophagy reflects a tendency inherited from the ancestral wolf to keep the den area free of faecal-borne intestinal parasites that might be deposited in the den resting area and would typically have parasite ova that are not initially infective, but could develop infective larvae after 2 days. An evolved parasite defence strategy to consume fresh faeces in the rest area would be adaptive.
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The influence of supplemental Bacillus subtilis C-3102 on chronic diarrhea was studied in 40 privately-owned dogs subjected to a double-blind, placebo-controlled trial. After a run-in period of one week, 20 dogs received either placebo or test tablets for four weeks. Test tablets contained 1.3 x 10 8 colony forming units (CFU) Bacillus subtilis C-3102 per tablet. Both supplements were administered at a rate of half a tablet per 100 g of air-dry habitual diet, which equals 100 ppm Calsporin in the diet. The owners scored fecal characteristics on a line from 0 to 10 cm. For each dog and each variable, the change over time versus baseline was calculated. In comparison with the control treatment, administration of the probiotic did not influence fecal consistency, color and appearance of blood and mucus. The probiotic significantly improved fecal odor (P = 0.037) and tended to reduce flatulence incidence (P = 0.082) and apparent fecal fermentation (P = 0.080). There was no treatment effect on the degree of tenesmus, failed defecation, fecal volume and coprophagy. The probiotic tended to improve coat condition (P = 0.058). Dogs with higher severity degrees of diarrhea during the run-in period showed more improvement during the test period (P = 0.002), this relationship being clearly perceptible for the dogs receiving probiotic treatment (P = 0.056). It is concluded that administration of Bacillus subtilis C-3102 is an effective adjuvant therapy to the treatment of chronic diarrhea in dogs. It is suggested that a well-formulated dog food supplemented with Bacillus subtilis C-3102 may optimally support fecal and coat quality. Keywords: To cite this article: Paap PM, JH Van der Laak, JI Smit, N Nakamura and AC Beynen, 2016. Administration of Bacillus subtilis C-3102 (Calsporin®) may improve feces consistency in dogs with chronic diarrhea. Res. Opin. Anim. Vet. Sci., 6(8): 256-260.
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Background To reduce environmental contamination with Toxocara canis eggs, the current general advice is to deworm all dogs older than six months on average four times a year. However, only a small proportion of non-juvenile household dogs actually shed T. canis eggs, and some dogs shed eggs more frequently than others. The identification of these frequent shedders and the associated risk factors is an important cornerstone for constructing evidence-based deworming regimens. The purpose of this study is to identify risk factors associated with recurrence of periods of shedding Toxocara eggs in a cohort of household dogs older than six months. Methods We performed a prospective study (July 2011 to October 2014) on shedding Toxocara eggs in a cohort of 938 household dogs older than six months from all over the Netherlands. The median follow-up time was 14 months. Monthly, owners sent faecal samples of their dogs for Toxocara testing and completed a questionnaire. Dogs were dewormed only after diagnosis of a patent infection (PI). Survival analysis was used to assess factors influencing the time to first diagnosed PIs (FPI) and the time to recurrent PIs (RPI). ResultsThe overall prevalence of PIs was 4.5 %, resulting in an estimated average incidence of 0.54 PIs/dog/year. No PI was diagnosed in 67.9 % of the dogs, 17.5 % of the dogs went through only one PI and 14.6 % had > 1 PI. Prevalence of PIs always peaked during wintertime. Increased hazards for first diagnosed PIs were associated with coprophagy, geophagy, walking off-leash for ≥ 80 % of walking time, reported worms in the faeces, feeding a commercial diet and suffering from urologic or respiratory conditions. Median time to reinfection was nine months. Factors associated with increased hazards for recurrent PIs were taking corticosteroids, changing dog’s main purpose, and proxies for veterinary care-seeking behaviours. Conclusions We concluded that targeted anthelmintic treatments in household dogs may be feasible as PIs tend to (re)occur in specific periods and in groups of dogs at high risk. Moreover, recurrent PIs appear to be influenced more by factors related to impaired immunity than environmental exposure to Toxocara eggs.
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Thirty-nine dogs were assigned to four treatment groups for weight loss. Breed, sex and initial body condition were similar across groups. Treatments included 0, 25, 40 or 50% caloric restriction, based on calculated maintenance energy requirements for the dog's estimated ideal body weight. True maintenance energy requirements and actual caloric restriction were determined retrospectively. When the dogs reached their target weight or when 16 weeks on restriction were completed, they were switched to either maintenance or ad libitum feeding. The changes in their behavior between the end of caloric restriction and the first week off restriction, and between baseline data collected before caloric restriction and data collected 10 months after the initiation of behavioral observations (5–9 months after the end of caloric restriction) were evaluated. Minimal changes in activity and time-budgets occurred as a consequence of transition from restriction to non-restriction. Slightly more change occurred between baseline and 10 months, but changes were still not substantial. Coprophagy was not altered by diet. Aggression decreased significantly between baseline and 10 months, in spite of intervening periods of the physical stress of caloric restriction.