5
Nutrition of the Ferret

James G. Fox, Carrie S. Schultz, and Brittany M. Vester Boler

Introduction

Ferrets (Mustela putorius furo), as companion animals, have increased in number in recent years in the United States, likely due to their small size, playful and endearing character, and ease of maintenance. They also serve as an animal model for cardiology, ophthalmology, pulmonary physiology and pathology, virology, bacteriology, parasitology, toxicology, neuroscience, emesis studies, developmental biology, teratology, and gastrointestinal disease research. Their use in a laboratory setting and as companion animals has demanded closer attention to the diet of these animals to help maintain health and improve longevity.

Ferrets are part of the order Carnivora and are obligate carnivores, which means that ferrets have nutritional peculiarities that are only available in animal tissue. While most nutritional requirements are well established in production animals, very little exists in comparison for many laboratory species, including the ferret. Nutritional requirements of ferrets are still lacking, and most formulators utilize the requirements of mink or felines to determine suitability in the ferret. Use of inappropriate diets in a laboratory setting could lead to incorrect research findings. In recent years, more commercially available diets for use in ferrets have been developed, and the use of inadvertently, nutritionally deplete diets in research is now uncommon. A variety of diets are now available, including natural source diets (grain-based, closed formulas) and purified diets (often open formula). Closed formulas are proprietary formulas used by a company to manufacture a diet, while open formulas provide the amount of each ingredient used within the formula.

Despite the availability of commercially prepared complete diets, the exact nutritional requirements of these animals are not known. Several diets have been formulated to contain adequate concentrations of known required nutrients based on findings from other species and practical experience but are likely oversupplemented in most cases. Furthermore, limited information is available on nutritional requirements with growing, pregnant, or lactating ferrets, and assumptions are made based on information from minks and felines. Care should be taken when feeding animals in these life stages to ensure proper nutrition during this time.

This chapter will summarize known nutritional information on ferrets for use as pets, or housed in zoos or laboratory settings. Common commercially available natural ingredient diets as well as examples of purified diets will be provided. Very little data exist regarding deficiency and toxicity symptoms in ferrets. Outcomes unique to ferrets will be discussed in this chapter, but those not mentioned are believed to be similar to other carnivorous species, in particular cats or mink.

Gastrointestinal Anatomy and Physiology of the Ferret

Digestive anatomy of most carnivores includes few molars, large canine teeth [1], a simple stomach, a short gastrointestinal tract relative to body size, and a short unsacculated colon [2]. The Mustelidae family, including ferrets, lacks a cecum [2]. The dental formula of ferrets is I3/3 C1/1 P3/3 M1/2, for 34 teeth [3], which is the same as mink, but differs from cats (I3/3 C1/1 P3/3 M1/0 = 30 teeth). Given their digestive anatomy, it would be expected that ferrets would have similar nutrient requirements to other carnivores, including felines, but due to their shorter colon, may have less ability to utilize fibrous substrates.

Their gastrointestinal anatomy is reflective of the predatory nature of these animals. Wild ferrets were reported to consume rabbits, possums, hedgehogs, birds, eggs, frogs, and eels in New Zealand, with differing prey choices based on their geographical location within the country [4,5]. A commonality between two geographical populations in New Zealand (Pukepuke Lagoon [4]; Otago and Southland, [5]) was that female ferrets, which tend to be smaller in body size [6], fed on smaller prey.

Gastrointestinal transit time is short in ferrets, but the role of diet type and composition has not been explored to date. Total tract transit time was 3 h (180 min) in adult ferrets fed a meat-based diet, 66% moisture [7] and in adult ferrets fed a kibble diet, approximately 6% moisture [8]. In comparison to other species, total transit time in cats fed a canned cat diet was 26.5 h (adult cats 3 years of age) [9]. Mink, however, were found to have a similar (187 minutes) transit time when fed the same diet as ferrets [7]. This may indicate that mustelids have a more rapid transit time than other carnivorous species. Transit time can be affected by nutrient profile and physical form of the diet [10]. Although it is still expected that ferrets would have a short transit time regardless of diet consumed, the effect of the difference in physical form of the diet and nutrient composition is not well studied.

Reduced transit time leads to fewer nutrients being able to be digested and absorbed by the animal due to this rapid passage through the gastrointestinal tract. Ferrets had lower crude protein (69.6% vs. 75.9%) and higher fat (95.8% vs. 89.4%) digestibility compared with cats fed the same diets [8]. Nitrogen-free extract and crude fiber digestibility were not different between species. The reduction in crude protein digestibility is likely due to the reduced transit time of digesta through the gut, thereby not allowing for complete breakdown of the protein sources. The authors also noted that transit time was 8–14 hours in cats and 3–4 hours in ferrets [8], which highlights the differences between the species.

Ferrets fed a high-protein raw diet containing a sig­nificant amount of fish were used to determine gastrointestinal enzyme activity along the small intestine [11]. Average amylase (6.08 vs. 66.94 mg/min/g), lipase (0.47 vs. 3.84 μmol/min/g), peptidase (3.26 vs. 4.24 mcmol/min/g), and sucrose (3.31 vs. 6.94 μmol/min/g) activities were numerically lower in ferrets compared with rats, respectively. Differences between these species would be expected as rats are omnivores, while ferrets are carnivores and would have very different natural diets. Total proteolytic activity was greatest in ferrets, 5.31 μmol /min/g. It should be noted that mink and blue fox fed the same diet had similar results to ferrets. Rats, however, had higher carbohydrate-degrading enzymes, but were fed a diet higher in carbohydrates (fed a commercially available diet—Lactamin, Stockholm, Sweden; ingredients not provided). These results do indicate that ferrets have a lower capacity to utilize available starches compared with rats [11], but further evaluation is needed regarding their ability to adapt enzyme activity to other diets.

The large intestine of mustelids differs from other carnivores as they lack a cecum and appear to have little ability to utilize fibrous substrates. The colon lies in a straight line from the liver to the rectum [12] and is unsacculated [2]. Anecdotal evidence indicates that ferrets do not have an extensive or highly functional gastrointestinal microbial population [12,13]. This belief is due in part to the reports of no gastrointestinal upset after antibiotic administration [13] and based in part on findings of a gnotobiotic ferret colony [14]. Gnotobiotic ferrets were able to survive on milk or kibble diets supplemented with vitamin K. However, the ferrets had little morphological or metabolic changes noted in other gnotobiotic animals [14], indicating that there is only minor influence of the microbiota on nutritional status. To date, evaluation of the gastrointestinal microbial populations has not been conducted in ferrets, nor has the effect of diet on the bacterial microbiome been established. Cats have an active large intestinal microbial population that allows utilization of some fiber sources, and its flora is affected by diet [15]. Alternatively, mink have total colonic bacteria counts (1 × 108 CFU/g of feces) that are two to four magnitudes lower than other mammals [16], but similar proportions of aerobic bacteria as dogs [17]. Given the more rapid transit time noted in both mink and ferrets compared with cats, a unique population of gastrointestinal microbiota would be likely compared with previously evaluated species.

Types and Forms of Diets for Ferrets

Historically, diets for ferrets used for hunting and research typically consisted of mostly animal by-products [18,19]. Previous researchers indicated that ferret diets consisted of various ingredients, including hamburger, horsemeat, cod liver oil, milk, fish, chicken, beef by-products, and dog and cat foods [6,18]. Most ferrets used for hunting today are fed a commercially prepared kibble diet as well as whole prey items, such as rabbit and rodent carcasses, tripe, and slaughter house by-products [19,20]. Laboratory settings require a consistent diet that is both economical and provides adequate nutrition during all life stages. Commercially available extruded kibble diets are now available and provide ease of feeding, adequate nutrition, and are economical.

All commercial ferret breeders should be using diets that maximize economic gain (increased litter size, number of kits weaned, etc.) while minimizing morbidity and mortality among their colony of ferrets. While diet is not a replacement for a health maintenance and vaccination program, animals on an optimal plane of nutrition are less likely to become ill and will be better able to reproduce. One ferret breeding facility, Marshall Farms (MF) USA, noted primiparous females in their colony whelp an average 10.3 ± 0.2 kits per litter, successfully wean 80% of the litter, and produce three to four litters per year [21].

In the past, traditional ferret diets included a raw meat mixture or cat food with supplemental meat. High meat diets have higher moisture levels and spoil more quickly. The ease of feeding and improved shelf life (up to 2 years) has led to a shift in many breeding facilities, which now feed ferrets an extruded kibble diet. While fish was often a source of protein and/or fat in ferret diets, feeding large amounts of fish oil or whole fish can lead to nutritional steatitis due to the large amount of polyunsaturated fatty acids (PUFAs), if adequate concentrations of vitamin E are not included in the diet [22]. Anecdotal evidence suggests that ferrets prefer the taste of avian and mammalian protein sources to that of fish [13]. Ferrets also are anecdotally more sensitive to changes in aroma and can be neophobic, developing strong preferences to certain feeds into adulthood. Additionally, fish oils become rancid more quickly; improvements in the manufacture of fish products and more potent antioxidants that are now available help minimize this issue. Natural ingredient diets also tend to be more palatable than purified diets in many species.

While there are several advantages to feeding a kibble diet, the impact on dental health should be considered. Wild ferrets, felids, and other obligate carnivores feed on carcasses, consuming mostly soft tissue from prey animals. The hardness of a kibble diet differs from what the animals were evolutionally developed to consume. Ferret teeth will wear down after long periods of consuming kibble diets, which is less problematic in dogs and cats [3]. This exaggerated wear pattern is due to the difference in internal volume of ferret teeth as compared with those of cats. This condition can be further exacerbated in some ferrets that selectively chew kibble in specific areas of the mouth, leading to more advanced dental wear in those areas [3]. Dental health should be routinely screened in ferrets to prevent excessive wear of ferrets' teeth.

Natural Ingredient Formulations for Laboratory, Captive, and Pet Ferrets

Commercial laboratory and captive ferret diets manufactured today are formulated using fixed formulation or managed formulation techniques. In fixed formulation diets, the amount of each ingredient does not change over time. Managed formulation techniques allow for ingredient composition to change slightly, keeping nutrient composition constant. Both methods are acceptable practices for diets fed to laboratory ferrets and other research species. Ingredient lists from three commercial manufacturers for laboratory or captive ferret diets are presented in Table 5.1. Diets formulated for pet ferrets may utilize managed, fixed, or least-cost formulations. A least cost formulation is utilized to adjust for costs of ingredients when manufactured. Ingredient lists from commercial manufacturers of pet ferret diets are presented in Table 5.2.

Table 5.1.  Ingredients of Extruded Diets for Laboratory and Captive Ferrets

DietManufacturerIngredients (Descending order of inclusion by as-is weight)
5M08MazuriaPoultry by-product meal, ground brown rice, dehulled soybean meal, porcine animal fat, poultry digest, poultry fat, dried beet pulp, phyridoxine hydrochloride, soybean oil, dicalcium phosphate, monocalcium phosphate, phosphoric acid, brewers dried yeast, fish oil, fish meal, salt, taurine, choline chloride, dl-methionine, calcium propionate, menadione dimethylpyrimidinol bisulfite (vitamin K), d-alpha tocopheryl acetate (vitamin E), thiamin monohydrate, vitamin A acetate, dried yucca schidigera extract, choleocalciferol (vitamin D3), biotin, folic acid, ethoxyquin, zinc oxide, vitamin B12 supplement, calcium pantothenate, riboflavin, nicotinic acid, ferrous sulfate, copper sulfate, l-lysine, manganous oxide, ferrous carbonate, zinc sulfate, calcium iodate, calcium carbonate, sodium selenite.
5L14Purina LabDietaPoultry by-product meal, porcine animal fat, ground corn, dehulled soybean meal, corn gluten meal, poultry digest, poultry fat, dried beet pulp, soybean oil, phosphoric acid, salt, brewers dried yeast, fish oil, fish meal, taurine, choline chloride, calcium propionate, pyridoxine hydrochloride, dl-methionine, menadione dimethylpyrimidinol bisulfite, thiamin mononitrate, vitamin A acetate, dl-alpha tocopheryl acetate, cholecalciferol, biotin, folic acid, ethoxyquin, zinc oxide, vitamin B12 supplement, calcium pantothenate, riboflavin, nicotinic acid, ferrous sulfate, copper sulfate, manganous oxide, ferrous carbonate, zinc sulfate, calcium iodate, calcium carbonate, cobalt carbonate, sodium selenite.
2072Harlan TekladbPoultry by-product meal, ground white rice, poultry fat, fish meal, egg product, dried beet pulp, l-lysine, brewers dried yeast, iodized salt, phosphoric acid, dl-methionine, calcium carbonate, taurine, choline chloride, vitamin E acetate, dicalcium phosphate, calcium propionate, menadione sodium bisulfite complex, ferrous sulfate, zinc oxide, calcium pantothenate, magnesium oxide, niacin, vitamin A acetate, pyridoxine hydrochloride, riboflavin, cobalt carbonate, vitamin B12 supplement, folic acid, sodium selenite, calcium iodate, biotin, vitamin D3 supplement.

aMazuri and Purina LabDiet are subsidaries of Purina Animal Nutrition LLC (St. Louis, MO).

bHarlan Laboratories, Inc. (Madison, WI).

Table 5.2.  Ingredients of Commercially Available Extruded Diets for Pet Ferrets

DietIngredients (Descending order of inclusion by as-is weight)
Marshall Premium Ferret Diet SeniorChicken by-products (organs only, including chicken liver), chicken, herring meal, corn, oatmeal, cod fish, dried beet pulp, brewer's dried yeast, cane molasses, salt, sodium propionate (a preservative), dl-methionine, l-lysine, taurine, vitamin A acetate, vitamin D3 supplement, vitamin E supplement, riboflavin supplement, niacin, biotin, choline chloride, folic acid, thiamine mononitrate, pyridoxine hydrochloride, BHA (a preservative), vitamin B12 supplement, D-calcium pantothenate, manganous oxide, inositol, ascorbic acid, iron sulfate, zinc oxide, cobalt carbonate, potassium iodide, sodium selenite.
Marshall Premium Ferret DietChicken by-products (organs only, including chicken liver), chicken, herring meal, corn, cod fish, dried beet pulp, brewer's dried yeast, cane molasses, salt, sodium propionate (a preservative), dl-methionine, l-lysine, taurine, vitamin A acetate, vitamin D3 supplement, vitamin E supplement, riboflavin supplement, niacin, biotin, choline chloride, folic acid, thiamine mononitrate, pyridoxine hydrochloride, BHA (a preservative), vitamin B12 supplement, menadione sodium bisulfate complex (a source of vitamin K), D-calcium pantothenate, manganous oxide, inositol, ascorbic acid, iron sulfate, zinc oxide, cobalt carbonate, potassium iodide, sodium selenite.
ZuPreem® Premium Ferret DietChicken meal, chicken fat, ground wheat, wheat flour, chicken, egg product, beet pulp, natural chicken flavor, brewer's dried yeast, flax seed, potassium chloride, choline chloride, iodized salt, taurine, dl-methionine, natural mixed tocopherols, rosemary extract, citric acid, ferrous sulfate, zinc oxide, copper chloride, manganous oxide, calcium iodate, sodium selenite, vitamin A supplement, vitamin D3 supplement, vitamin E supplement, thiamine, niacin, calcium pantothenate, pyridoxine hydrochloride, riboflavin, folic acid, biotin, vitamin B12 supplement.
ZuPreem® Grain-free Ferret DietChicken meal, sweet potatoes, peas, chicken fat (preserved with mixed tocopherols), potato protein, salmon, venison, natural chicken flavor, fish meal, dl-methionine, choline chloride, taurine, dried chicory root, tomatoes, blueberries, raspberries, yucca schidigera extract, dried fermentation products of Enterococcus faecium, Lactobacillus acidophilus, Lactobacillus casei, and Lactobacillus plantarum, dried Trichoderma longibrachiatum fermentation extract, vitamin E supplement, niacin, manganese proteinate, copper proteinate, zinc sulfate, manganese sulfate, copper sulfate, thiamine mononitrate (vitamin B1), vitamin A supplement, biotin, potassium iodide, calcium pantothenate, riboflavin (vitamin B2), pyridoxine hydrochloride (vitamin B6), vitamin B12 supplement, manganous oxide, sodium selenite, vitamin D supplement, folic acid.
Kaytee Fiesta MAX Ferret FoodPoultry meal, poultry by-product meal, brewers rice, ground wheat, dried egg product, poultry fat, dehulled soybean meal, soy oil, beet pulp, fish meal, soy flour, vegetable oil (preserved with BHT), feeding oatmeal, wheat middlings, ground flaxseed, wheat germ meal, corn sugar, brewer's dried yeast, salt, dried cane molasses, l-lysine, sodium bentonite, poultry digest, dl-methionine, calcium carbonate, potassium chloride, whole cell algae meal (source of omega-3 DHA), fructooligosaccharides, mixed tocopherols (a preservative), propionic acid (a preservative), taurine, yeast extract, vitamin A supplement, choline chloride, yucca schidigera extract, dicalcium phosphate, ascorbic acid, vitamin E supplement, vitamin B12 supplement, riboflavin supplement, niacin, zinc oxide, ferrous sulfate, iron proteinate, manganous oxide, menadione sodium bisulfite complex (a source of vitamin K activity), l-carnitine, rosemary extract, citric acid, calcium pantothenate, copper sulfate, copper proteinate, zinc proteinate, thiamine mononitrate, pyridoxine hydrochloride, cholecalciferol (source of vitamin D3), folic acid, calcium iodate, biotin, dried bacillus licheniformis fermentation product, dried bacillus subtilis fermentation product, cobalt carbonate, sodium selenite, artificial color, natural flavors.

All diets contain some animal protein and animal fats to meet the high-protein requirement of ferrets; however, all diets are fortified with taurine to ensure adequate concentrations after processing (extrusion). The extrusion process gelatinizes starch granules within the diet. This gelatinization of the starch allows ferrets to digest and therefore utilize starch as an energy source in the diet. Common protein sources include poultry by-product meal, fish meal, and soybean meal. Common fat sources in extruded kibble ferret diets are pork and poultry fats. Extrusion uses steam and pressure to cook starches. This process can decrease some vitamin concentrations and therefore natural ingredient diets are fortified with vitamins to account for losses during processing. Losses during processing can vary based on individual vitamin and processing conditions [23].

The calculated concentrations of various nutrients for the three commercially available laboratory and captive ferret diets are described in Table 5.3. All nutrients were provided by the manufacturer from expanded specification sheets commonly used for laboratory species diets. These values are based on known average nutrient composition of each ingredient as well as regular monitoring of certain nutrient concentrations in these ingredients by the commercial manufacturer. Because values are based on calculated values, which do not account for losses during processing, the final product should be assayed for any nutrients of interest. Protein and fat concentrations are high, and carbohydrate and fiber concentrations are low in all three commercial diets. There is little difference among diets regarding the final nutrient composition; however, different ingredients are used. All three diets have been fed successfully to ferrets in all life stages. Guaranteed analysis of commercially available pet ferret diets is presented in Table 5.4. Guaranteed analysis provides minimum concentrations of protein, fat, and moisture, and a maximum concentration of crude fiber.

Table 5.3.  Calculated Nutrient Analysis of Commercially Available Grain-Based Laboratory and Captive Diets that Appear to Meet the Needs of Ferretsa,b

c5-tbl-0003_1.jpgc5-tbl-0003_2.jpg

Table 5.4.  Guaranteed Analysis of Commercially Available Diets for Pet Ferrets

c5-tbl-0004.jpg

Use of Plant Protein

As mentioned previously, most ferret diets contain an animal protein source to meet the high-protein requirement of these animals. Amounts and the ratios of amino acids in animal protein sources more closely reflect the amino acids needed by the animal as compared with plant proteins. Plant proteins are deficient in one or more essential amino acids and are devoid of taurine, a required nutrient for ferrets and other obligate carnivores.

Semi-Purified Formulations

Semi-purified diets are available as open-source formulas; therefore, ingredient proportions should be readily available from the manufacturer. These diets contain more refined ingredients that provide one or very few nutrients from each ingredient. The main protein source in most purified diets is casein, but crystalline amino acids can be used [24,25]. Fat sources vary but include lard, coconut oil, soy oil, and others. Carbohydrate sources include maltodextrin, sucrose, and cornstarch. Semi-purified diets use refined ingredients that allow for simple depletion or addition of nutrients. This allows for testing of deficiency-repletion studies to determine requirements or toxicities of certain nutrients. Little published research to date is available that has determined the exact nutrient requirements of ferrets, but purified diets are now available that maintain ferrets [26] and examples are provided in Table 5.5.

Table 5.5.  Calculated Nutrient Analysis of Purified Diets That Appear to Meet the Needs of Ferretsa,b

Purina LabDietResearch Dietsa
1814901D93009
Ingredients
    Casein43.7334.5
    Corn starch21.9924
    Soybean oil9.960
    Cottenseed oil010.5
    Hydrogenated coconut oil010.5
    Lard50
    Sucrose50
    Powdered cellulose45
    AIN-93M mineral mix40
    Mineral mix03.5
    Maltodextrin3.3210
    Vitamin premix11
    Calcium phosphate0.970
    Choline bitartrate0.40.2
    Calcium carbonate0.350
    Taurine0.240
    l-argenine00.5
    l-methionine00.3
    Food dye0.030
    Ferric citrate0.0160
    Zinc carbonate0.00030
Calculated analysis
    Crude protein, %3931.7
    Fat (acid hydrolysis), %1521
    Carbohydratesc, %31.139.4
    Crude fiber, %45
    Metabolizable energy, kcal/gd4.154.51
Amino acids, %
    Arginine1.531.62
    Cystine0.160.13
    Glycine0.840.67
    Histidine1.130.89
    Isoleucine2.091.65
    Leucine3.782.98
    Lysine3.182.51
    Methionine1.131.19
    Phenylalanine2.091.65
    Tyrosine2.211.75
    Threonine1.691.33
    Trytophan0.480.38
    Valine2.491.97
    Serine2.411.9
    Aspartic acid2.822.22
    Glutamic acid8.937.04
    Alanine1.210.95
    Proline5.154.06
    Taurine0.240
Fatty acids, %
    Linoleic acid5.575.46
    Arachidonic acid0.010
Caloric breakdown
    Protein, %37.626.8
    Fat, %32.540
    Carbohydrates, %29.933.3

aValues from publicly available information from each company.

bAll values as-is basis.

cCalculated by difference.

dMetabolizable energy calculated using sum of the decimal fractions of protein, fat, and carbohydrate × 4, 9, and 4 kcal/g, respectively.

N/A, not available.

McLain and Roe [27] evaluated a natural, grain-based diet as well as purified diets in primiparous ferrets to determine diets that would be suitable for these animals. This purified diet was able to maintain jills during gestation and lactation, but growth and weaning rates of kits were greater in natural-ingredient fed kits. The authors suggested that the palatability of these original semi-purified diets may have led to the reduction in reproductive performance. Flavorings and higher fat diets are now available that may overcome any palatability issues noted in previous purified diet formulations.

Cat foods are frequently used as ferret food. Estimated nutrient requirements of cats, dogs, fox, and mink per 1000 kcal on a dry matter (DM) basis are provided in Table 5.6. While traditional cat diets may sustain a ferret at maintenance, levels of protein, fat, and micronutrients during demanding life stages (lactation, growth) should be ascertained to ensure nutritional adequacy.

Table 5.6.  Nutrient Requirements of Different Adult Carnivores at Maintenance Used for Extrapolation and Comparison of Dietary Nutrient Levels for the Ferret (per 1000 kcal ME)

c5-tbl-0006.jpg

Dietary Nutrients

Like all animal species, ferrets require the right proportions of amino acids, energy, fatty acids, minerals, and vitamins to meet their requirements for maintenance, growth, and reproduction. Unfortunately, compared with many other laboratory animal models, the nutrient requirements for ferrets have not been very well established. The following research-based information will provide some guidance into the general nutrient requirements for ferrets or similar species. Additional guidance can also be obtained through feed manufacturers that provide diet formulations that have successfully maintained optimal growth and health of ferrets.

Protein

Protein, per se, is not required by animals. It is actually an amino acid requirement that must be met for any life stage (maintenance, growth, or reproduction), and those requirements can only be sufficiently met by providing high-quality, highly digestible protein sources or amino acids. Unfortunately, the protein, or specific amino acid, requirements for ferrets are not well established, especially in comparison with other domestic carnivores. Data that are available for ferrets were derived using mink or cats as models for nutritional requirements.

The Nutrient Requirements of Mink and Foxes [28] recommends a dietary protein concentration of 21.8–45.7% for mink depending on the life stage, with most of these data based on nutritional research conducted in the 1950s and 1960s. Allen et al. [29] reported growth responses in mink fed diets containing varying calorie : protein (CP) ratios; this ratio appeared to have a greater influence on growth rates from 6 to 16 weeks than from 16 to 28 weeks of age. Maximal growth rates from 6 to 16 weeks of age in males were achieved with a CP ratio of 20 (5.6 kcal/28% CP) versus a ratio of 13 (4.9 kcal/37% CP) for females. Commercial diets currently on the market for ferrets appear to be adequate for growth and have an average of 4.0 cal/kg of metabolizable energy (ME; calculated using Atwater factors) and 39% crude protein, which provides a CP ratio of 10. Normal growth rates and low mortality rates (<5%) were observed in mink kits during the growing-furring phase when provided diets containing 30% of the ME as protein [30], which is slightly below that of most commercial ferret diets.

More recently, Zhang et al. [31] evaluated the effects of lower and higher protein diets supplemented with dl-methionine (MET) on growth performance of growing minks. Treatments consisted of a high-protein (HP) diet (36.3% CP, 1.1% MET; HP), low-protein (LP) diet (29% CP, 0.74% MET.; LP) and a low-protein diet with differing levels of dietary MET (LP + M1: 1.0% MET; LP + M2: 1.39% MET; and LP + M3: 1.64% MET). Final body weights of minks consuming the LP + M2 were significantly higher than those fed the HP or LP diets (p < 0.05); however, no differences were observed among those in the MET-supplemented groups. Average daily gains were also greater for kits within the MET-supplemented groups versus those in the HP or LP treatment groups, suggesting that lower protein diets may be provided as long as the diet is adequate in MET as well as other essential amino acids in minks. Similarly published literature is not available to date in ferrets, but similar responses would be expected.

Unique Amino Acid Requirements of Ferrets and Other Carnivores

Amino acids considered essential for most animals species apply to ferrets as well. Essential amino acids are those that must be supplied by the diet because the animals either cannot synthesize them de novo or at least not in quantities adequate to meet optimal growth. Generally, arginine is considered to be a nonessential amino acid; however, in mammals, it is considered to be essential or semi-essential, depending on the age and health status of the animal. Deshmukh and Shope [24] found serum ammonia levels (238–1720 μg/100 mL) were normal in young (8 weeks old) male ferrets fed an amino acid-defined, purified diet containing 0.4% or more arginine, while all ferrets receiving the same diet with 0.3% or less arginine developed hyperammonemia within 2–3 hours of consuming the diet. Recovery typically occurred with 3–4 hours post diet-induced hyperammonemia. Similar and more severe symptoms have been observed in both young and young adult cats fed an arginine-deficient diet, including hyperammonemia, sialorrhea, ataxia, emesis, and tetanic spasms [32,33]. This study demonstrated that ferrets are sensitive to arginine-deficient diets but not to the same degree as cats. As a result, the recommended minimum requirement of arginine for ferrets is 0.4%; however, most commercial diets contain between 2% and 3% total dietary arginine.

MET is generally the most limiting amino acid in natural ingredient diets for cats due to ingredients used. Zhang et al. [31] also found this to be the case when average daily gains were improved in mink provided with a low-protein diet supplemented with MET. Maximal growth was observed with a diet containing 258.5 g/kg DM protein and 13.87 g/kg DM MET. Maximal growth was also observed in mink consuming a purified diet containing 19% casein (∼0.5% MET) and supplemented with 0.25% dl-MET [34]. The total MET levels in the diet would be about 1% of the total diet, which is very similar to what is included in commercial ferret diets.

Taurine is a β-aminosulfonic acid which is an essential nutrient that must be provided in feline diets. The primary role of taurine is not only its conjugation with bile acids in the liver but also for conjugation of xenobiotic acids in the ferret [35]. A deficiency of taurine in feline diets can result in blindness, heart failure, inadequate immune response, poor neonatal growth, poor reproduction, and low survival rates of kittens [36]. Taurine deficiencies have not been described in ferrets and whether or not it is required in ferret diets is still debatable (see Chapter 19). For precautionary measures, commercial feed manufacturers formulate ferret diets to contain about 0.25% dietary taurine on average.

Energy

The caloric density of a diet can primarily be broken down into two different forms of energy, gross energy (GE), which is basically the caloric density of a particular ingredient or diet, and ME, which is the portion of GE that is actually utilized for maintenance, growth, and reproduction. GE is measured using bomb calorimetry (heat of combustion) but, unfortunately, is relatively meaningless. When evaluating a diet for the caloric density or caloric content, it is always best to refer to ME as it is the energy that will support the overall health of the animal.

Commercial diets that are available today and that appear to meet the energy requirements of ferrets have an average ME content of 4 kcal/g of diet. For maintenance, ferrets can consume between 200 and 300 kcal/kg of body weight per day. Assuming an average body weight of 1500 grams, this is approximately 130–200 kcal of ME intake/day. Because ferrets eat to meet their caloric needs [12], their average daily intake of feed would be between 33 and 50 g. Chwalibog et al. [37] evaluated energy metabolism in mink (Mustela vison) as a model for other carnivores and found that the daily energy requirement for maintenance was 125.9 kcal/kg of metabolic body weight (BWkg0.75) when in positive energy balance and a thermoneutral zone. These requirements were estimated to be slightly higher when evaluated in farm-raised, male, pastel mink, with energy for maintenance recommended at 147 kcal/BWkg0.75/day. Both recommendations fall slightly below the 200–300 kcal/kg BW that is generally recommended (196 vs. 200 kcal/kg BW); however, activity level of each individual ferret also needs to be considered as more active animals will require more calories daily than less active animals.

The energy requirements for growth and reproduction will be greater than that required for maintenance. The ME content of diets that have been shown to support reproduction in ferrets ranges from 3.89 to 4.58 kcal/g [13]. Alternatively, during lactation, even with a considerable increase in food intake, dams may not be able to consume enough energy and may have to mobilize body energy reserves depending on the litter size [38]. Intake of ME increased in lactating mink (M. vison) provided diets containing 5.0–5.3 kcal/g GE during the third trimester of gestation and the first 4 weeks of lactation compared with dams that were not mated [39]. ME intake of nonmated females at maintenance was similar to that shown by others (133.0 kcal/day), while ME intake of females during late gestation and through the fourth week of lactation increased over time and ranged from 146 to 310 kcal ME/day when provided diet ad libitum. Despite the increase in ME intake, after 2 weeks of lactation, dams were unable to sustain their energy requirements and had to mobilize fat reserves from the body, suggesting the diet was too low in ME to meet the lactational needs but adequate to meet those during gestation. The effects of energy deficiency may include, but are not limited to, stunted growth, decreased milk production, decreased reproductive deficiency, emaciation, and a rough, dull hair coat.

Fat

Dietary fat is an important component of any animal's diet as it provides essential fatty acids, is required for absorption of fat-soluble vitamins, increases palatability, and is a more concentrated form of energy as it contains 2.25 times more calories than carbohydrates or protein. Fat added to increase palatability may be more important in ferret diets as older ferrets have been known to refuse eating a diet based on taste, although other factors may also influence palatability [12]. Some animals will eat to meet a caloric need; thus, as the dietary energy increases through the addition of fat, the total intake by weight will be lower than that of an animal consuming a lower fat diet. Therefore, it is important to supplement high-fat diets with vitamins and minerals to account for the decrease in dietary intake. Depending on the fat content, increases in protein may also be needed. Because ferrets contain a short digestive tract, it is important that their diets be high-protein and high-calorie, with the majority of that energy provided by fat. Unlike other mammals, ferrets are unable to efficiently utilize carbohydrates as an energy source [12].

Commercial ferret diets generally contain 20–25% fat by weight and appear to adequately meet the needs of ferrets for maintenance, growth, and reproduction. Dietary fat levels as high as 40% have been shown to be satisfactory in mink diets [12,28]. Animals in general do not have a fat requirement per se, but rather a dietary fatty acid requirement. For optimal growth, the three essential fatty acids (EFAs) required in the diet are linoleic, linolenic, and arachidonic acid; however, the level of dietary arachidonic acid is not always specified by the feed manufacturer. Although the ferret is increasingly used as a model for cardiovascular and nonalcoholic fatty liver disease (NAFLD), the actual requirements for these essential fatty acids are relatively unknown. Commercial diets in today's market range from 2.6% to 3.7% total linoleic acid, which are comparable to levels published by Bell [13] for diets that were on the market at that time and supported reproduction in ferrets. For the five diets analyzed, linoleic levels ranged from 2.8% to 4.5%. For mink, the National Research Council (NRC) [28] recommends the diet contain 0.5% of diet DM as essential fatty acids for adult animals at maintenance and 1.5% for pregnant or lactating dams and growing kits.

Diets deficient in fat can lead to additional nutrient deficiencies. In addition, changes in the health of the skin may be the first sign of an EFA deficiency because of the important role linoleic acid plays in the transdermal water barrier [36]. Symptoms may include course, dry hair and skin lesions. Experimentally induced EFA deficiencies in other species have resulted in reduced growth rates, poor reproductive performance, alopecia, and decreased immune function.

Carbohydrates and Fiber

Ferret diets typically contain lower quantities of carbohydrates and fiber as ferrets have minimal ability to digest and process complex carbohydrates and fiber due to their shorter digestive tracts [12] and have a less diverse gut microbial flora [40]. For ferrets living in the wild, the primary source of carbohydrates and fiber will be that from killed prey, since ferrets are strict carnivores; thus, dietary energy will primarily be supplied through fat and highly digestible protein sources. A diet containing greater than 30% carbohydrates and less than 30% protein is associated with poor growth and greater propensity to acquire infectious and metabolic diseases [13]. Commercial diets for both pet and laboratory ferrets contain 20–30% total carbohydrates and less than 3% crude fiber. Purified diets fed to ferrets have as much as 40% carbohydrate and 5% fiber; however, animals are traditionally managed on these types of formulas.

Minerals

No data are currently available regarding the mineral requirements of ferrets. Some of the primary symptoms associated with any nutrient deficiency or toxicosis may include depressed intake, poor growth, poor reproductive performance, rough/dull hair coats and lethargy.

Calcium and Phosphorous

Calcium and phosphorus requirements are closely related, and must be considered together. Commercial ferret diets on the market today contain 1.4–2.2% calcium and roughly 1.3% P with a Ca : P ratio of 1.12 : 1 to 1.7 : 1. Edfors et al. [41] fed 8-week-old, domestic European ferrets (Mustela putorius furo) diets containing 0.6, 0.7, or 0.8% Ca and Ca : P ratios of 1.3 : 1 or 1 : 1.3 for 42 days and observed no adverse effects on growth or body weight and length. Femur length, weight diameter, and breaking force were also unaffected by Ca : P ratios. Further investigations are required to determine if adverse effects on growth or bone health occur when fed a diet with an inverse Ca : P ratio longer than 42 days. A ratio of 1.5 : 1 to 2 : 1 is generally accepted in the literature for most species.

While not characterized in ferrets, diets high in calcium and low in vitamin D and phosphorus in other species may produce difficulty in walking and enlargement of the bones, diuresis, depressed feed intake, elevated serum calcium, and decreased plasma magnesium. In addition, diets high in calcium and vitamin D may be associated with signs of renal impairment. Calcium deficiency may result in tetany and convulsions. Hemorrhage, a reduction in reproductive and lactation performance, spontaneous fractures, and altered metabolism or requirements for other nutrients such as magnesium may occur. Low phosphorus intake may result in slow growth rates, poor appetite, and osteomalacia in adult animals.

Iron and Copper

Severe emaciation, growth retardation, microcytic-hypochromic anemia, roughened fur, and lack of underfur pigmentation (achromotrichia) have been linked to an iron deficiency in mink [42]. This deficiency syndrome can presumably occur in ferrets consuming inadequate dietary levels of iron. Without copper, iron absorption may not be impaired, but hemoglobin cannot be formed efficiently. Excessive iron can result in anorexia, weight loss, and a decreased serum albumin level. Fortunately, commercially available ferret diets appear to contain iron and copper in amounts sufficient to prevent a deficiency.

Copper toxicity has been described in two genetically related ferrets with symptoms that included lethargy, CNS depression, and hypo- and hyperthermia [43]. However, the toxicity did not result from excess dietary copper, but rather the syndrome was suspected to be hereditary.

Sodium and Chloride

Sodium and chloride are essential for almost all forms of life and is responsible for the maintenance of osmotic and acid balance. Blood is approximately 0.9% salt and may be the only mineral compound craved by animals [44].

In mink, the requirements for sodium and chloride are met by fortifying the ration with 0.5% salt. Commercially available ferret diets provide between 0.4% and 0.6% sodium, which is equivalent to approximately 1% dietary salt, and appears to meet the requirements of ferrets. Signs of a salt deficiency in most animals may include pica, osmotic and acid–base disturbances, reduction in appetite, fatigue, slowed growth, rough hair coats, and a cessation of lactation.

Sodium and chloride toxicities can occur separately; however, when fed as sodium chloride, the effects on acid–base balance are insignificant [44].

Zinc

Commercially available ferret diets contain between 180 and 235 ppm zinc. These amounts are apparently adequate in preventing deficiency signs of alopecia, hyperkeratinization and acanthosis, disturbance in growth, anorexia, and emaciation.

Magnesium

Magnesium is essential as a cofactor for enzymatic reactions required for every major metabolic pathway in the body, including those involved with cellular respiration. The magnesium requirement for adult cats is 200 mg/kg DM (∼4 kcal ME/g) or 0.2% [36], assuming adequate levels of dietary calcium and phosphorous are present. Commercially available diets provide 0.09–0.12% magnesium, which is slightly below that of the requirement for adult felines. However, these diets appear to meet the needs of adult ferrets.

Magnesium deficiency may manifest clinically as an alteration in sodium and potassium transport, anorexia, decreased weight gain, irritability, and muscular weakness. Serum magnesium and calcium concentrations may be depressed; inorganic phosphorus levels may be elevated.

Iodine

Iodine is essential for both animals and humans as it is required for the synthesis of the thyroid hormones 3,3,5-triiodothyronine (T3) and thyroxine (T4). Iodine is needed for intermediary metabolism, reproduction, growth and development, hematopoiesis, circulation, and thermoregulation [44]. Ferrets may require a small amount of iodine for prevention of goiter. Signs of an iodine deficiency may include myxedema, skeletal deformity, delayed shedding of deciduous teeth, alopecia, dullness, apathy, drowsiness, and timidity. Commercially available diets provide approximately 2–4 ppm iodine, which appears to be adequate for preventing hypothyroidism. Hyperthyroidism is a common disease among cats [45], but to date, no information is available as to the natural incidence in pet or laboratory ferrets.

Potassium

A minimal potassium requirement has not been established for ferrets, mink, cats, or dogs. However, the NRC [36] recommends a daily allowance of potassium of 0.4% for adult dogs and 0.52% for adult felines for a diet containing 4.0 kcal ME/g. Commercial ferret diets contain between 0.5% and 0.8% potassium, which is only slightly above that of dogs and cats, and appear to meet the requirements of ferrets for growth and maintenance. Signs of deficiency include growth retardation, restlessness, muscular paralysis, dehydration, and lesions of the heart and kidney.

Vitamins

No data are available concerning the vitamin requirements of ferrets. Common vitamin deficiency and toxicity signs observed with other species are outlined in the next section, and the levels of individual vitamins contained in commercially available ferret diets are discussed.

Vitamin A

Vitamin A is required to support maintenance of epithelial cell differentiation, reproductive performance, and visual function [46]. Raila et al. [47] demonstrated through a series of studies that ferrets and dogs behave similarly with regard to vitamin A metabolism. The recommended allowance of vitamin A for adult dogs is 1.3 IU/kcal ME (5.0 IU/g DM). Commercially available diets contain 6.25–8.35 IU/kcal ME (25–33 IU/g diet) which is approximately 8- to 10-fold higher than that recommended as a daily allowance for dogs. However, most commercial diets are fortified with vitamin A and other heat-labile vitamins, to account for losses during manufacturing and storage. These concentrations are well below the safe upper limit established for dogs of 53.3 IU/kcal ME (213.3 IU/g DM) for vitamin A [36].

Feeding diets devoid of vitamin A may result in growth failure, night blindness, and muscular incoordination (particularly in the rear quarters). Eyes may be affected, with lenses becoming opaque, and the conjunctivitis is evident. Metaplasia of epithelial tissues and fatty infiltration of the liver may also occur. Symptoms of a hypervitaminosis that have been observed in dogs include loss of appetite and body weight, lethargy, irritability, and bone weakening [48].

Vitamin E

Vitamin E, one of the fat-soluble vitamins, has a fundamental role in cellular metabolism and also acts as an antioxidant and scavenger of free radicals. Commercial ferret diets contain between 185 and 250 IU/kg vitamin E, and these levels appear to meet the requirements for maintenance and growth.

Signs of a vitamin E deficiency in dogs and cats may include degeneration of skeletal muscles, reproductive failure, anorexia, depression, and steatitis. Yellow fat disease, fatty degeneration of the liver, or steatitis can also result from feeding diets containing rancid fat or high levels of unsaturated fatty acids. Additional vitamin E may be required for diets containing high levels of polyunsaturated fat. An ɑ-tocopherol : PUFA ratio (mg : g) of at least 0.6 has been recommended [28] in most species to ensure that the needs for vitamin E are met. Vitamin E is a relatively nontoxic vitamin [48], and toxicity symptoms have not been described in ferrets. Rats and chicks can withstand consuming diet with 1000 IU/kg for prolonged periods of time with no deleterious health effects. Extreme toxicity may lead to depressed growth. Absorption and metabolism of both Vitamin A and E have been characterized in the ferret in the context of the influence of micronutrients on cancer development and progression (see Chapter 32 for details).

Vitamin D

Commercially available ferret diets contain an average of 3.6 IU/g vitamin D. As with other species, the ferret's requirement for vitamin D may depend on dietary concentrations of calcium and phosphorus or on the duration of exposure to ultraviolet light. Other factors include dietary calcium : phosphorus ratio, physiologic stage of development, and sex. Rachitic changes and abnormal bone development may occur when the diet is deficient in vitamin D, calcium, or phosphorus, especially when exposure to ultraviolet light is minimized.

Vitamin K

The metabolic need for vitamin K has not been established in the ferret, but it is likely that a dry diet concentration of 1.0 mg menadione/kg would sustain normal plasma prothrombin levels in diets containing fish products. Commercial diets (Mazuri® and LabDiet®; Purina Animal Nutrition LLC, Gray Summit, MO) contain 3.3 mg/kg vitamin K (menadione) and appear to meet and safely exceed what may be required by ferrets.

A deficiency may result in hypoprothrombinemia and hemorrhage. Kernicterus and hemolytic anemia may be a manifestation of vitamin K toxicity.

Thiamin

Thiamin (B1) plays a key role in glucose metabolism and neural function. The requirements for optimal growth and fur development in mink have been estimated to be 1.2–1.5 mg/kg diet [49], while those recommended for dogs and cats are 2.25 and 5.6 mg/kg diet, respectively. Thiamin concentrations of commercially available ferret diets (Table 5.2) range from 56 to 110 (mg/kg dry diet). Commercially available diets may contain higher concentrations of thiamin than required due to the losses that occur during the extrusion process and to account for losses during the shelf life of the product.

Signs of hypervitaminosis may include restlessness, convulsions, cyanosis, and labored respiration. Death caused by depression of the respiratory center may occur with toxic doses, probably in excess of 200 mg/kg body weight.

Riboflavin

Riboflavin (B2) requirements for growth and fur production in mink are about 1.5 mg/kg of dry feed [50]. The vitamin B2 needs for most other species are met with less than 3 mg/kg. Given commercial ferret diets contain an excess of this amount, signs of deficiency are not anticipated. When manifested, however, acute deficiency may result in decreased respiratory rate, hypothermia, weakness, and coma. Chronic riboflavin deficiency may result in anorexia, muscular weakness, dermatitis, microcytic-hypochromic anemia, corneal vascularization-opacification, and reduced erythrocyte and urine riboflavin concentrations. As a water-soluble vitamin, riboflavin is relatively nontoxic when ingested orally at high doses due to its inefficient absorption. The oral LD50, as determined in rodents, was found to be more than 10 g/kg BW [48].

Pyridoxine

Pyridoxine (B6) requirements in mink were evaluated and were estimated to be 1.6 mg/kg of diet for optimal growth and the prevention of abnormal symptoms and/or tryptophan metabolism [51]. Animals receiving a diet containing 0.8 B6 mg/kg had optimal growth; however, only 9 of the 15 animals survived at 20 weeks of age. Mink fed diets containing lower concentrations of B6 exhibited signs of ataxia, acrodynia, convulsions, irritability, and apathy. Reproductive performance can also be affected by a deficiency of pyridoxine. Testes of mink fed diets devoid of vitamin B6 become atrophic, aspermatic, and degenerative, while “absorption sterility” occurs in females [52]. One milligram of vitamin B6/kg DM may be sufficient to prevent deficiency signs, and commercially available ferret diets contain more than adequate levels to allow for losses during manufacturing and storage. Very high pyridoxine concentrations led to toxicity symptoms of muscle incoordination, ataxia, convulsions, and death at very large doses in dogs and rats [48]. Toxic levels are currently unknown for ferrets, but dogs and rats are able to withstand an oral dose 1000 times their requirement before toxicity occurs.

Vitamin B12

Uncomplicated vitamin B12 deficiency has not been described in the ferret, but a macrocytic hypochromic, macrocytic normochromic, normocytic hypochromic, or normocytic normochromic anemia may be manifested with deficient vitamin B12 intake. Commercially available ferret diets contain 220–279 μg/kg of vitamin B12, which is equivalent to ∼20 μg/kg BW/day, assuming an average BW of 900 g and daily intake of 50 g, and appear to meet the requirements for both growth and maintenance. Dietary concentrations of vitamin B12 in commercial diets tend to exceed that required by the animals primarily due to the high levels of meat-based ingredients which naturally contain higher levels of this particular vitamin. Vitamin B12 appears to be relatively safe even when consumed at several hundred times the required concentrations in the diet [48].

Folic Acid

Folic acid (B9) is used as a cofactor and serves as a donor and acceptor in a variety of reactions involving amino acids and nucleotide metabolism [36]. Neither dietary requirements, nor intestinal bacterial synthesis, of folic acid have been studied in the ferret; commercially available diets range from 4.3 to 6 mg/kg DM (Table 5.2). Folic acid at a level of 0.5 mg/kg of dry feed results in a remission of folic acid deficiency symptoms in mink, but levels below this amount have not been evaluated [50]. Folate deficiency may result in erratic appetite, poor weight gain, glossitis, leukopenia, and hypochromic anemia with a tendency to microcytosis. Folic acid appears to be nontoxic even at very large doses with no adverse affects reported [48].

Biotin

Biotin (B7) is one of few vitamins that can be synthesized by gut microorganisms and absorbed by the animal. Thus, determining the dietary requirements can be difficult, although, there is some evidence that at least some level of dietary biotin should be provided as well. Egg whites have been used as a protein source in some laboratory animal diets for experimental purposes. Avidin, a glycoprotein present in egg whites, can very tightly bind biotin and create a biotin deficiency. Wehr et al. [53] were able to demonstrate biotin deficiency in mink fed a diet containing spray-dried eggs. Thus, additional biotin is required for experimental diets containing egg whites. Commercially available ferret diets contain approximately 400–500 μg biotin/kg diet (∼25.0 μg/kg BW). This level is approximately twice the level required for optimum growth in dogs [28] and recommended as a daily allowance for cats, 1.9 μg/kg BW [36]. A deficiency may result in alopecia, hyperkeratosis, graying of fur, conjunctivitis, and fatty liver. Biotin toxicity has not been reported in ferrets, but poultry and swine appear able to tolerate a dose 4 to 10 times that of their requirement [48].

Niacin

The mink, like the cat, requires dietary niacin because it cannot metabolize sufficient amounts of the precursor tryptophan to meet its niacin requirement [54]. The metabolic conversion of tryptophan to niacin has not been systematically studied in the ferret. Commercially available ferret diets provide 86–134 mg/kg dry diet, while 10–20 mg/kg diet is tentatively stated as the requirement for mink. Signs of deficiency may include anorexia, profuse salivation, diarrhea, gastrointestinal inflammation, hemorrhagic necrosis, dehydration, and emaciation. High doses of nicotinic acid may produce vasodilation, pruritus, and cutaneous desquamation.

Pantothenic Acid

Pantothenic acid is required for the normal metabolism of fatty acids, carbohydrates, and amino acids [46]. The recommended allowance for dogs and cats is 5.75 and 15.0 mg/kg DM (4 kcal ME/g diet), respectively, [36] and is below 20 mg/kg diet for most species. Calcium pantothenate is present at levels ranging from 26 to 120 mg/kg dry diet. Pantothenic acid deficiency in most species results in poor growth, possible dermatitis and alopecia, poor appetite, reduced blood cholesterol and total lipid levels, loss of conditioned reflexes, vomiting, intermittent diarrhea, gastrointestinal disorders, convulsions, and coma. Pantothenic acid appears relatively nontoxic, and dietary levels of at least 20 g pantothenic acid/kg diet are well tolerated by many species [48].

Choline

In most species, the dietary requirement for choline is markedly affected by dietary protein concentration—more specifically, by the dietary concentration of MET. Because both choline and MET may serve as labile methyl donors in metabolism, the dietary supply of one tends to spare the need for the other. Unfortunately, this interaction has not been systematically studied in ferrets, so commercial diets are supplemented with a minimum of 2500 mg choline/kg dry diet. Plasma phosphatase activity and blood prothrombin times may be elevated with a choline deficiency. Relatively high levels of dietary chlorine are needed to induce a toxicosis. If a toxicosis in induced, there may be increased alkalinization of urine and decreased ammonia excretion as well as reduced erythrocyte numbers.

Vitamin C

Ferrets are likely not to require an exogenous supply of vitamin C as it can be endogenously synthesized in all animal species studied with the exception of humans, several primates, guinea pig, a few birds, fish, and invertebrates [48]. Although physiologically essential, it is not considered an essential dietary nutrient for most domestic and laboratory animals. Thus, commercial feed suppliers do not supplement their formulations with this vitamin.

Dietary Imbalances or Toxicities

Several dietary imbalances, produced either experimentally or naturally occurring in the ferret, have been documented in the literature, and are discussed in the next section.

Use of Plant Protein

A large commercial colony experienced an outbreak of bladder calculi. Five to ten percent of pregnant jills on a diet containing mainly plant protein developed struvite bladder stones [55]. Pregnant jills were particularly susceptible to urolithiasis because of increased mobilization of minerals. Apparently any ferret on a diet having ground yellow corn as its primary ingredient can develop these urinary stones. Magnesium ammonium phosphate (struvite) crystallizes when urine pH rises above 6.4. As obligate carnivores with a normal urine pH of about 6, ferrets metabolize cysteine and MET in animal proteins and produce an acid urine. However, metabolism of organic acids in plant protein produces an alkaline urine that promotes struvite crystallization.

Urine acidifiers used in cat diets are also available for use in ferrets and should be added to a diet that leads to a more alkaline urinary pH. It should be noted, however, that urine below pH 6.3 may lead to formation of calcium oxalate crystals. Urine pH is not the only factor associated with urolithiasis, but should be a consideration when formulating ferret diets, and care to ensure optimal urinary pH in ferrets maintained for the long term is important. Other factors include water intake, mineral intake (including Ca, P, and Mg), and meal-feeding versus ad libitum.

Nutritional Steatitis

Nutritional steatitis, or yellow fat disease, has been described in ferrets fed a high level of dietary polyunsaturated fat [22]. In all species in which the disease has been reported (the mink being particularly sensitive), the disease is caused by feeding a diet high in polyunsaturated fats and/or deficient in vitamin E.

Epizootiology and Control

In carnivores, including mustelids, this disease if often associated with feeding excessive quantities of oily marine fish [56,57]. Polyunsaturated fats are highly susceptible to oxidation within the food source as well as within the host's tissue, and vitamin E is a critical nutritional component in protecting tissue lipids from oxidative injury [22]. In an outbreak of steatitis in New Zealand ferrets, the PUFA concentration of the ferrets' diet, 7.7%, was considered excessive, although vitamin E levels of 13 mg/ferret/day would be considered adequate for a low-PUFA diet of mink [58]. The squid in the ferrets' diet consisted of 17.9% PUFA and is not recommended in any diet formulation for ferrets or mink [22]. Young growing ferrets are more susceptible to the disease, and dietary management is particularly important for this age group. The toxic effects of PUFA are prevented or modified by vitamin E, which acts as an electron donor to prevent oxidation and scavenges free radicals within fat tissue. In the New Zealand outbreak of steatitis, a daily vitamin E intake of 13 mg/animal did not protect the ferret, and a dietary supplement of 75–150 mg/ferret/day (similar to mink recommendation) is advised when feeding ferrets a high-PUFA diet [22]. The high level of selenium found in the liver of ferrets with steatitis did not reduce the toxicity of the high-PUFA content of the feed, even though selenium does protect tissue against lipoperioxidases.

Clinical Signs

Young growing kits are found dead or affected kits are depressed, cry out when handled, and are reluctant to move. Affected kits have diffuse firm swellings under the skin, and prominent subcutaneous lumps in the inguinal areas. Hematologic studies reveal a marked neutrophilia with a left shift, and a mild microcytic normochromic anemia [22]. Clinical diagnosis is based on clinical signs and on a history of feeding a high-PUFA diet.

Pathologic Findings

Fat in the subcutaneous and abdominal areas is yellow-brown and of a coarse and granular texture. Histologically, fat is infiltrated with large macrophages, mononuclear cells, and fibroblasts. Focal neutrophilic infiltrates are also noted [22]. Dense deposits of periodic acid–Schiff (PAS)-positive fluorescent lipopigment within macrophages is also prominent in affected tissue.

Treatment

Immediate removal of the offending diet is recommended, and affected animals should be injected with 10 IU vitamin E daily for 2 days [22]. Vitamin E is added to the feed at 30 mg (30 IU)/ferret/day for 10 days, 15 mg for another 5 days, and 10 mg/ferret/day as a maintenance diet.

Osteodystrophia Fibrosa (Nutritional Hyperparathyroidism)

Although ferrets may be susceptible to true rickets (hy­­pophosphorosis and/or hypovitaminosis), the condition evidently has not been reported in this species. Hyperphosphorosis, associated with feeding an all-meat diet, with no calcium supplementation, has been documented in ferrets [59].

Epizootiology and Control

The prevalence and susceptibility of the ferret to this nutritional deficiency is unknown; it has, however, been diagnosed in two ferret farms in New Zealand. The disease can be prevented by ensuring adequate calcium intake and a proper calcium:phosphorus (1 : 1). Natural product diets should be supplemented with 5–10% ground bone or an all-meat diet fortified with 2% bone meal or 2% dicalcium phosphate should be given [59].

Clinical Signs

All ages are susceptible, but rapid growth predisposes ferrets to the disease. Despite an adequate diet, animals will lose weight. Affected ferrets are reluctant to move and support their weight; typical posture is abduction of the forelegs. The bones are soft and pliable, and fractures may be present.

Pathologic Findings

Grossly, bones are soft and rubberlike, and fractures of bones may be noted. Parathyroid glands are hyperplastic. Microscopically, bones are osteoporotic with typical lesions of osteodystrophia fibrosa.

Thiamine Deficiency

The disease is caused by ingestion of a diet, usually fish, that contains excess thiaminase. Feeding of raw eggs may also predispose ferrets to the disease.

Epizootiology and Control

The prevalence is unknown but is related to dietary management. The disease has been reported on ferret farms in New Zealand where the diet consisted of fish containing thiaminase: paddle crabs, gray mullet, and dogfish [59].

Clinical Signs and Diagnosis

The disease is seen in weanling growing animals or adults. Anorexia is marked, with accompanying lethargy. Advanced cases have marked dyspnea, prostration, and convulsions. Signs regress and disappear after parenteral injection of vitamin B complex (5 mg daily for 3 days); this occurs within 1–4 hours in mild cases, and usually within 8 hours in ferrets presenting with CNS symptoms [59].

Pathology

The classic lesion noted in thiaminase deficiency is laminar necrosis in the brain cortex.

Mercury Toxicity

Experimentally, the ferret is susceptible to overt mercury poisoning by ingestion of tissues from chickens [60]. Methyl mercury-dressed wheat (used in crop production) was fed to chickens, and tissues of chicken carcasses, primarily muscles (10 mg/kg) and liver (40 mg/kg), were ingested by adult female ferrets. The total intake of muscle and liver/animal during the experiment was 2500 and 200 g/per ferret, respectively.

Epizootiology and Control

To our knowledge, the disease has not been reported under natural conditions. If natural product diets are used, care should be taken to ensure that meats, including fish products, are not contaminated with mercury [61,62].

Clinical Signs

Anorexia and weight loss are noted during the clinical course of the disease. Weakness, trembling, and muscle twitching are followed by ataxia, paralysis, and generalized apathy. Periodic episodes of excitation and circling have also been observed [60].

Pathologic Findings

Muscle atrophy is generalized. All experimental ferrets had subacute ventricular dilatation. Slight to marked fatty degeneration is observed in skeletal and cardiac muscle, hepatic cells, and renal proximal tubular epithelium [60]. The most suspicious histologic changes are confined to the central and peripheral nervous systems. Focal myelin degeneration, with enlarged (focally disintegrated) axon cylinders, are consistently seen in peripheral nerves. Neuronal demyelinization and vacuolization are present in the cerebellar medulla and pons. High levels of mercury are found in the liver, kidneys, and central nervous system. Significant levels are also present in muscle tissue.

Treatment

Other than supportive therapy, there is no effective treatment. A grave prognosis is warranted and, if a definitive diagnosis of mercury poisoning has been made, clinically affected ferrets should be euthanized.

Salt Poisoning

The disease is caused by feeding a diet of 100% salted fish.

Epizootiology and Control

The disease in ferrets is caused by feeding an exclusive diet of tuna that has been stored in brine [59]. Of 30 ferrets ingesting the salted tuna, 9 were clinically affected, and 8 died. In the reported outbreak, control was achieved by reducing the amount of salted tuna in the diet to 30%. Adequate water intake must also be ensured.

Clinical Signs

Clinical signs of salt poisoning are typical of those seen in other species, particularly pigs, affected with the disease. Animals are markedly depressed and have periodic choriform spasms, seen 24–96 hours after ingestion of excessive salty diets. Death ensues shortly thereafter.

Pathologic Findings

Diagnosis is based on clinical and pathologic findings, coupled with analysis of dietary management. Pathology is restricted to the brain, which is edematous and shows coning of the cerebellum. A nonsuppurative eosinophilic meningitis is also present.

Arginine-Free Diet

Epizootiology and Control

Although this is unlikely to be found as a result of dietary deficiency in commercially prepared diets, an arginine-free diet in ferrets can result in profound clinical and pathologic abnormalities. Most young mammals require dietary arginine for optimum growth. Young ferrets, however, fasted for 16 hours and fed an arginine-free diet, will develop hyperammonemia and encephalopathy within 2–3 hours after ingesting such a diet [25]. It is speculated that young ferrets cannot synthesize sufficient amounts of ornithine from precursors other than arginine and become depleted of precursors needed to detoxify ammonia [63]. There is also an increase in serum liver enzyme levels as well as in serum-free fatty acids and liver lipids.

Clinical Signs

Clinically, the development of encephalopathy involves lethargy, or uncharacteristic combativeness early in the course of the disease, followed by prostration, coma, and death. Unlike Reye's syndrome in children, repetitive vomiting is not seen.

Pathologic Findings

Histologically, the liver has accumulations of lipid droplets and swollen mitochondria. These results are accentuated in young ferrets challenged experimentally with influenza virus and treated with aspirin [63,64].

Treatment

Adult ferrets (18 months) do not develop hyperammonemia and encephalopathy when fed an arginine-free diet. The disease is easily preventable by feeding adequate arginine in the diet. The course of the disease, once clinically apparent, can be abbreviated by ornithine injections. Sodium benzoate administered intraperitoneally to young ferrets fed an arginine-free diet fails to decrease serum ammonia levels (Thomas and Deshmukh [25] #197).

Summary

Ferrets serve as an important laboratory species and popular companion animals. Also, they are still used for hunting in some countries. Maintaining healthy animals and breeding groups requires an understanding of the needs of these animals. Owing to their requirements as obligate carnivores with very rapid gastrointestinal transit time, ferrets require diets with highly digestible protein and available energy with minimal fiber. There is little currently known regarding ferret nutrient requirements and feeding practices that might improve health or reduce disease incidence. Additional studies this area would benefit ferrets used both for research and kept as companion or hunting animals. Additional research into product form and hardness of feed is also warranted.

Acknowledgments

The authors wish to acknowledge the contribution of Daniel E. McLain, who was responsible for portions of the text which appeared in the second edition of this book.

References

  1.   1.  Savage RJG (1977) Evolution in carnivorous mammals. Palaeontology 20: 237–271.
  2.   2.  Stevens CE, Hume ID (2004) The mammalian gastrointestinal tract. In: Stevens CE, Hume ID, eds. Comparative physiology of the vertebrate digestive system, 2nd ed. New York: Cambridge University Press, pp. 46–93.
  3.   3.  Church RB (2007) The impact of diet on the dentition of the domestic ferret. Exot DVM 9: 30–39.
  4.   4.  Roser RJ, Lavers RB (1976) Food habits of the ferret (Mustela putorius furo L.) at Pukepuke Lagoon, New Zealand. NZ J Zool 3: 269–275.
  5.   5.  Smith GP, Ragg JR, Moller H, Waldrup KA (1995) Diet of feral ferrets (Mustela furo) from pastoral habitats in Otago and Southland, New Zealand. NZ J Zool 22: 363–369.
  6.   6.  Shump AU, Shump KA, Jr. (1978) Growth and development of the European ferret (Mustela putorius). Lab Anim Sci 28: 89–91.
  7.   7.  Bleavins MR, Aulerich RJ (1981) Feed consumption and food passage in mink (Mustela vison) and European ferrets (Mustela putorius furo). Lab Anim Sci 31: 268–269.
  8.   8.  Fekete SG, Fodor K, Proháczik A, Andrásofszky E (2005) Comparison of feed preference and digestion of three different commercial diets for cats and ferrets. J Anim Physiol Anim Nutr (Berl) 89: 199–202.
  9.   9.  Peachey SE, Dawson JM, Harper EJ (2000) Gastrointestinal transit times in young and old cats. Comp Biochem Physiol A 126: 85–90.
  10. 10.  Clemens ET, Stevens CE (1980) A comparison of gastrointestinal transit time in ten species of mammal. J Agric Sci 94: 735–737.
  11. 11.  Oleinik VM (1995) Distribution of digestive enzyme activities along the intestine of blue fox, mink, ferret, and rat. Comp Biochem Physiol 112A: 55–58.
  12. 12.  Bell JA (1996) Ensuring proper nutrition in ferrets. Vet Med 91: 1098–1103.
  13. 13.  Bell JA (1999) Ferret nutrition. Vet Clin North Am Exot Anim Pract 2: 169–192.
  14. 14.  Manning DD, Bell JA (1990) Derivation of gnotobiotic ferrets: perinatal diet and hand-rearing requirements. Lab Anim Sci 40: 51–55.
  15. 15.  Barry KA, Wojcicki BJ, Bauer LL, Middelbos IS, Vester Boler BM, Swanson KS, Fahey GC, Jr. (2011) Adaptation of healthy adult cats to select dietary fibers in vivo affects gas and short-chain fatty acid production from fiber fermentation in vitro. J Anim Sci 89: 3163–3169.
  16. 16.  Williams C, Elnif J, Buddington RK (1998) The gastrointestinal bacteria of mink (Mustela vison L.): influence of age and diet. Acta Vet Scand 39: 473–482.
  17. 17.  Buddington RK (2003) Postnatal changes in bacterial populations in the gastrointestinal tract of dogs. Am J Vet Res 64: 646–651.
  18. 18.  Willis LA, Barrow MA (1971) The ferret (Mustela putorius furo L.) as a laboratory animal. Lab Anim Sci 21: 712–716.
  19. 19.  Oyarzun SE, Self K, Valdes EV, Chavez ER (1995) An evaluation of the nutritional adequacy of the feeding program of the black-footed ferret (Mustela nigripes) at the Metropolitan Toronto Zoo. Proc Nutr Advisory Group 1: 104–123.
  20. 20.  Porter V, Brown N (2007) The complete book of ferrets. London: Pelham Books.
  21. 21.  McLain DE, Harper SM, Roe DA (1985) Congenital malformations and variations in reproductive performance in the ferret: effect of maternal age, color, and parity. Lab Anim Sci 35: 251–255.
  22. 22.  Brooks HV, Rammell CG, Hoogenboom JJL, Taylor DES (1985) Observations on an outbreak of nutritional steatitis (yellow fat disease) in fitch (Mustella putorius furo). N Z Vet J 33: 141–145.
  23. 23.  Tobin G, Stevens KA, Russell RJ (2007) Nutrition. In: Fox JG, Barthold SW, Davisson MT, Newcomer CE, Quimby FW, Smith AL, eds. The mouse in biomedical research: V. 3, Normative biology, husbandry and models, 2nd ed. Boston: Academic Press, pp. 343–344.
  24. 24.  Deshmukh DR, Shope TC (1983) Arginine requirement and ammonia toxicity in ferrets. J Nutr 14: 1664–1667.
  25. 25.  Thomas PE, Deshmukh DR (1986) Effect of arginine-free diet on ammonia metabolism in young and adult ferrets. J Nutr 116: 545–551.
  26. 26.  White WS, Peck KA, Ulman EA, Erdman JW (1993) The ferret as a model for evaluation of the bioavailabilities of all-trans-beta-carotene and its isomers. J Nutr 123: 1129–1139.
  27. 27.  McLain DE, Roe DA (1983) Reproductive response in ferrets consuming purified diet ingredients. Fed Proc 43A: 1318.
  28. 28.  National Research Council (NRC) (1982) The nutrient requirements of mink and foxes, 2nd rev. ed. Washington, DC: National Academies Press, p. 33.
  29. 29.  Allen MR, Evans EV, Sibbald IR (1963) Energy:protein relationships in the diets of growing mink. Can J Physiol Pharmacol 42: 733–744.
  30. 30.  Damgaard BM, Clausen TN, Dietz HH (1998) Effect of dietary protein levels on growth performance, mortality rate and clinical blood parameters in mink (Mustela vison). Acta Agric Scand 48: 38–48.
  31. 31.  Zhang HH, Li GY, Ren EJ, Xing XM, Wu Q, Yang FH (2012) Effects of diets with different protein and DL-methionine levels on the growth performance and N-balance of growing minks. J Anim Physiol Anim Nutr (Berl) 96: 436–441.
  32. 32.  Morris JG, Rogers QR (1978) Arginine: an essential amino acid for the cat. J Nutr 108: 1944–1953.
  33. 33.  Rogers QR, Morris JG (1979) Essentiality of amino acids for the growing kitten. J Nutr 109: 718–723.
  34. 34.  Leoschke WL, Elvehjem CA (1959a) The importance of arginine and methionine for the growth and fur development of mink fed purified diets. J Nutr 69: 147–150.
  35. 35.  Emudianughe ES, Caldwell J, Smith RL (1983) The utilization of exogenous taurine for the conjugation of xenobiotic acids in the ferret. Xenobiotica 3: 133–138.
  36. 36.  National Research Council (NRC) (2006) Nutrient requirements of dogs and cats, 1st ed. Washington, DC: National Academies Press, p. 135.
  37. 37.  Chwalibog A, Glem-Hansen N, Henckel S, Thorbek G. 1980. Energy metabolism in adult mink in relation to protein energy levels and environmental temperature. In: Proceedings of the 8th Symposium on Energy Metabolism. EAAP Publ. 26: 283–286.
  38. 38.  Fink R, Tauson A, Hansen KB, Wamberg S, Kristensen NB (2001) Energy intake and milk production in mink (Mustela vison)—effect of litter size. Arch Anim Nutr 55: 221–242.
  39. 39.  Tauson AH, Sorensen HJ, Wamberg S, Chwalibog A (1998) Energy metabolism, nutrient oxidation and water turnover in the lactating mink (Mustela vison). J Nutr 128: 2615S–2617S.
  40. 40.  Brown S 2001. Rethinking the ferret diet. Small Mammal Health Series. http:/www.veterinarypartner.com/Content.plx?P=A&S=0&C=0&A=479 (accessed November 2013).
  41. 41.  Edfors CH, Ullray DE, Aulerich RJ (1990) Effects of dietary calcium concentration and calcium-phosphorous ratio on growth and selected plasma and bone measures in young European ferrets (Mustela putorius furo). J Zoo Wildl Med 21: 185–191.
  42. 42.  Stout FM, Adair J, Oldfield JE (1960) Aberrant iron metabolism and the cotton fur abnormality in mink. J Nutr 72: 46–52.
  43. 43.  Fox JG, Zeman DH, Mortimer JD (1994) Copper toxicity in sibling ferrets. J Am Vet Med Assoc 205: 1154–1156.
  44. 44.  National Research Council (NRC) (2005) Mineral tolerance of animals, 2nd ed. Washington, DC: National Academies Press.
  45. 45.  Zicker SC, Ford RB, Nelson RW, Kirk CA (2000) Endocrine and lipid disorders. In: Hand MS, Thatcher CD, Remillard RL, Roudebush P, eds. Small animal clinical nutrition, 4th ed. Topeka, KS: Mark Morris Institute, pp. 849–886.
  46. 46.  Combs GF, Jr. (1998) The vitamins: fundamental aspects in nutrition and health, 2nd ed. San Diego, CA: Academic Press.
  47. 47.  Raila J, Gomez C, Schweigert FJ (2002) The ferret as a model for vitamin A metabolism in carnivores. J Nutr 132: 1787S–1789S.
  48. 48.  National Research Council (NRC) (1987) Vitamin tolerance of animals. Washington, DC: National Academies Press.
  49. 49.  Leoschke WL, Elvehjem CA (1959b) The thiamine requirement of the mink for growth and fur development. J Nutr 69: 211–213.
  50. 50.  Leoschke WL (1960) Mink nutrition research at the University of Wisconsin, Madison. Res Bull (Sun Chiwawitthaya thang Thale Phuket) 222.
  51. 51.  Bowman AL, Travis HF, Warner RG, Hogue DE (1968) Vitamin B6 requirement of the mink. J Nutr 95: 554–562.
  52. 52.  Helgebostad R, Ender F (1963) Sterility in mink induced experimentally by deficiency of vitamin B6. Acta Vet Scand 4: 228–237.
  53. 53.  Wehr NB, Adair J, Oldfield JE (1980) Biotin defi­­ciency in mink fed spray-dried eggs. J Anim Sci 50: 877–885.
  54. 54.  Warner RG, Travis FHF, Bassett CF, McCarthy B, Abernathy RP (1968) Niacin requirement of growing mink. J Nutr 95: 563–568.
  55. 55.  Bell JA (1997) Periparturient and neonatal diseases. In: Hillyer EV, Quesenberry KE, eds. Ferrets, rabbits, and rodents: clinical medicine and surgery. Philadelphia: WB Sanders, pp. 50–57.
  56. 56.  Lalor RJ, Leoschke WL, Elvehjem CA (1951) Yellow fat in the mink. J Nutr 45: 183.
  57. 57.  Mason KE, Hartsough GR (1951) Steatitis or yellow fat in mink and its relation to dietary fats and inadequacy of vitamin E. J Am Vet Med Assoc 119: 72.
  58. 58.  Stowe HD, Whitehair CK (1963) Gross and microscopic pathology of tochopherol-deficient mink. J Nutr 81: 287.
  59. 59.  Field and Laboratory Service Veterinary Staff (1984) Diseases of the fitch. Surveillance 11: 28.
  60. 60.  Hanko E, Erne K, Wanntorp H, et al. (1970) Poisoning in ferrets by tissues of alkyl mercury-fed chickens. Acta Vet Scand 11: 268.
  61. 61.  Borg K, Wanntorp H, Hanko EE (1966) Mercury poisoning in Swedish wildlife. J Appl Ecol 3: 171.
  62. 62.  Smart NA, Lloyd MK (1963) Mercury residues in eggs flesh and livers of hens fed on wheat treated with methyl mercury dicyanodiamide. J Sci Food Agric 14: 734.
  63. 63.  Deshmukh DR, Thomas PE (1985) Arginine deficiency hyperammonemia and Reye's syndrome in ferrets. Lab Anim Sci 35: 242.
  64. 64.  Deshmukh DR, Thomas PE, McArthur B, et al. (1985) Serum glutamate-dehydrogenase and ornithine carbamyl transferase in Reye's syndrome. Enzyme 33: 171.