Ferrets

Last modified on August 31, 2010

Taxonomy Genetics/nomenclature Anatomy Physiology Behavior
Common diseases

Taxonomy

European ferrets (Mustela putorius furo) were domesticated in the 4th century BC to kill rodents and snakes. Other mustelids include the mink (Mustela vision), otter, badger, skunk and weasel. The black-footed ferret, Mustela nigripes, lives in North America and is endangered. {3567} The closest living relative to the black-footed ferret is Mustela eversmanni, the Siberian polecat.{4555}

Mustela putorius furo

Mustela nigripes

Mustela nivalis

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Genetics/nomenclature

There are two varieties of common ferrets. Fitch ferrets, used for fur, are buff with black mask, feet and tails. Albino ferrets are white with pink eyes, a recessive trait. Color mutants, also recessive to fitch, include Siamese, silver and silver mitt.{3567}

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Anatomy{3567}

	Intact male ferrets are called hobs, while neutered males are called gibs; males weigh approximately 2½ pounds. Females are called jills or sprites and weigh 1½ pounds.{3767}
	Dental formula: I(3/3) C(1/1) P(4/3) M(1/2)
	Males have an os penis, but no seminal vesicles; older references claim no prostate but LAM2 says they do{4760}
	No cecum or appendix
	Poorly-developed sweat glands, therefore susceptible to heat exhaustion if the temperature exceeds 30-32°C
	Musk glands lateral to anus
	Splenic extramedullary hematopoiesis is normal and can result in splenic enlargement
	Lymphoid nodules in intestinal submucosa
	Marked seasonal variations in spermatogenesis

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Physiology

Common research uses for ferrets include cardiovascular research, toxicology (since they represent carnivores), distemper and influenza.{3567} They are also models for subacute sclerosing panencephalitis, and lymphatic filariasis caused by Brugia.

Blood can be collected from the orbit, caudal tail vein, jugular vein, or by careful cardiac puncture.{3567}

Major hematologic differences from cats and dogs include high PCV, high RBC (9.17 x 10⁶/mm³) and high reticulocyte count (mean 4.6%).{3567} Normal PCV in a ferret can go up to 60%, with 45-60% called normal.{3767}

The WBC is usually 2500-7500, but don’t worry unless it goes over 10,000. Ferrets are steroid-resistant and do not exhibit lymphocytosis as a response. Some literature maintains that lymphocytosis is a sign of lymphosarcoma, but Williams believes it is not true; lymphocytosis is more often a result of enteric infection with Helicobacter or coronaviruses.{3767}

Ferrets have essentially no important blood group antigens, so transfusions can be made safely.{3767}

Liver disease, including hepatic lipidosis, is very rare in ferrets, and is diagnosed when the ALT exceeds 1000. SGOT levels of 400-800 are common and not considered evidence of pathology.{3767}

The urine of the hob is normally very dark, which may confuse colorimetric tests such as ketones. Since their blood pressure is high, there is usually some proteinuria.{3567}

Isoflurane is the anesthetic of choice, as injectables are unpredictable. No premedications should be used. Ferrets are susceptible to hypothermia which is a common cause of postoperative mortality.{3767}

Housing, husbandry, and preventive medicine{3567}

	Ferrets are often housed in dog, cat or rabbit cages with a small nest box. Males can be housed together except during breeding season.
	To pick up a ferret, use a leather glove to grasp them around the thorax, holding the front legs together in front of them.
	Ferrets are strict carnivores, depending on meat protein and fat. Protein should be of high quality (i.e. not from plants, which have been associated with urolithiasis). They don't digest carbohydrate very well due to lack of the appropriate intestinal flora. Protein requirement for reproductively active and young ferrets is a minimum of 35%; for non-breeding adults it is 30-40%.{4536} Ferrets can be maintained on commercial mink diet, or on cat food supplemented with 5% fresh liver. They eat to maintain their caloric needs and may develop protein deficiency if the cat food isn't supplemented. They don't digest fiber, and their food passes through in only 3-4 hours.
	Vaccinate ferrets with modified live canine distemper vaccine that is of chick embryo origin (not ferret). Rabies vaccination is not approved, although ferrets are highly susceptible to rabies.
	Females should be spayed if not used for breeding, as their high endogenous estrogens can cause a fatal bone marrow depression. Males should be castrated to decrease aggressiveness and reduce their musky odor.

Reproduction{3567, 4760}

	Breeding season is March-August; males active from December-July
	Testicles decrease to prepubertal size when out of breeding season; no spermatogenesis
	Females are seasonally polyestrous. Estrus is indicated by swollen vulva; females will stay in estrus if not bred
	Bring female to male 14 days after vulvar enlargement
	Ovulation is induced; if fertilization fails they will have a 42-day pseudopregnancy
	Gestation=42 days (Siberian polecat=38 days); house females separately for 2 weeks beforehand
	Litter size=8 (2-17)
	Parturition should take 2-3 hr; dystocia is common with small litters of oversize kits; C section works well
	Placentation is zonary and endotheliochorial
	Jills return to estrus during the second-third week of lactation and should be re-bred or given hCG to terminate
	Sexing: males have os penis, prepuce opens on ventral abdomen
	Eyes and ears open at 3-5 weeks
	Wean at 6-7 weeks
	Adult weight reached at 4 months; puberty at 9-12 months depending on day length
	Lifespan 5-6 years, although pets may live longer

There are age differences in the sensitivity of both sexes to negative feedback loops between estrogen/testosterone and GNRH from the hypothalamus. After puberty, LH will rise despite the estrogen levels, if the day length is increasing.{4760}

Jills are seasonal breeders and induced ovulators. Light cycles for ferrets are critical. Short-term, ferrets can be kept at a 12:12 cycle, but if they are to be kept for more than 6 months they need lighting control. "Winter" light, 10-16 hours dark, needs to be provided for 6 weeks per year. Light cycles are manipulated to control breeding production. Jills should not be exposed to long days until they are 12 weeks of age, or they will stay in anestrus. For example, jills can be transferred from winter light to 16 hours of light at 12 weeks of age and will be in estrus at 16 weeks, whelping at 5.5 months of age. Or, ferrets born in the spring under natural lighting can be bred when they enter puberty at 7-10 months of age (the next season), and then have their light manipulated to have 3-4 litters per year for about 2 years.{4760}

Once in estrus, there are 4 possible outcomes: ovulation and pregnancy (both intromission and neck restraint are required), pseudopregnancy after infertile mating, estrogen-induced aplastic anemia which is fatal, or pharmacologic termination of estrus (50-100U hCG or 20ug GnRH repeated in 1 week if necessary).{4760}

Hyperestrogenism occurs in jills that remain in estrus for more than one month. Signs are vulvar enlargement, bilaterally symmetrical alopecia of tail and abdomen, weakness, anorexia weight loss, ADR, bacterial infection and mucopurulent vaginal discharge. Eventually, bone marrow depression occurs. Hepatic dysfunction and thrombocytopenia lead to coagulopathy, bleeding, melena, petechiation or ecchymoses, and subdural hematoma. At necropsy, the tissues are pale and there is bronchopneumonia, hemorrhage, hydrometra or pyometra and mucopurulent vaginitis. If the PCV is >25%, pharmacologic termination of estrus has a good prognosis. A 45-day pseudopregnancy should result. Repeated administration of hCG may cause sensitization and anaphylaxis, or it will just stop working. If anaphylaxis occurs, use diphenhydramine, not epinephrine.{4760}

Pregnancy toxemia can kill the jills and their kits in late gestation. It occurs more often in primiparous jills, those with large litters (i.e. 12 kits), or those exposed to environmental or dietary stress. Toxemia is of the metabolic type (characterized by abnormal fat and carbohydrate metabolism), similar to that seen in obese pregnant guinea pigs. Energy deficiency leads to mobilization of fatty acids which overwhelm the liver. The liver becomes fatty and the animal may be hypoglycemic and/or ketotic. Signs include anemia, decreased protein and calcium, azotemia, increased bilirubin and liver enzymes, and hepatic lipidosis. Glucose may be normal at presentation; hyperglycemia may be a terminal development. Ketonuria and bilirubinuria may be seen, but glucosuria may not. The jills exhibit lethargy, inappetance, dehydration and excessive shedding. Signs specific for hypocalcemia, such as those seen in ruminants with periparturient hypocalcemia, are not usually seen in jills. Histologically, hepatic lipidosis (confirmed by positive staining with oil red O) occurs. The liver may be yellow in color. Treatment must be aggressive and include nutritional supplementation (high-energy, high protein), fluids with electrolytes and glucose, C-section, and resolution of stress conditions. Agalactia in the jill is likely, so cross-fostering may be necessary.{4000}

In humans, non-obese guinea pigs, hamsters, and patas monkeys, "pregnancy toxemia" is of the vascular type. Human preeclampsia-eclampsia is caused by an ischemic event in the uterus or placenta. Patients display hypertension, edema and proteinuria, and may develop DIC and systemic thrombosis. Liver dysfunction seen in humans is of two types: hemolysis, high liver enzymes and low platelet counts (HELLP) possibly related to vascular injury; and acute fatty liver of pregnancy (AFLP), which is rare but may resemble the ferret and ruminant syndromes.{4000}

Case Report: Vaccine reaction

A 3-month old ferret received distemper vaccine from a pet store vet three days previous to presentation. Due to his anaphylactic reaction, the vet treated him with 1ml epinephrine, 1ml dexamethasone, and 20mg diphenhydramine. The ferret developed lethargy, dehydration, elevated BUN, elevated creatinine and hyperphosphatemia. He did not respond to IV fluid diuresis. Cardiac ultrasound revealed atrial enlargement, mild left ventricular dilation, and mitral valve regurgitation. He was euthanatized due to poor prognosis and an attack of cyanosis and respiratory distress. At necropsy, the kidneys had severe multifocal tubular necrosis, acute myocardial necrosis, and mild pulmonary edema.

The diagnosis was renal failure secondary to epinephrine overdose. Diphenhydramine is the recommended treatment for anaphylaxis in ferrets at 0.5-2.0mg/kg IV or IM. In severe cases, epinephrine is given at 20ug/kg IV, IM or SQ. Toxicity from epinephrine is not well-documented in animals, but it is known in humans with vasopressor overdose (dopamine, cocaine). The primary insult is to the heart, possibly via toxicity to myocytes by calcium overload or to vasoconstriction during tachycardia. Central venous pressure increases, causing pulmonary edema. Renal vasoconstriction affects renal tubular cells, which are particularly sensitive to ischemia because the medulla receives less blood flow than the cortex. Diphenhydramine exacerbates the effects of epinephrine, making it worse.

In ferrets, BUN is the most sensitive indicator of renal function. Azotemia developed in this case in response to decreased GFR. It's called uremia when azotemia is associated with clinical signs (gastroenteritis, peripheral neuropathy, or metabolic acidosis). It is difficult to diagnose isosthenuria in ferrets because the normal range of specific gravity is unknown. Fluid therapy is also not well understood, but daily requirements are estimated at 75-100ml/kg/day. IV is almost always required, as ferrets don't tolerate SQ fluids well.{4601}

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Behavior

Females can be housed together unless they have kits. Although ferrets are normally genial, moms with kits are fiercely protective.{3567}

Common Diseases {3567, 4760}

Bacterial

	Botulism (more common on fur farms)
	Clostridium perfringens type A: acute abdominal distension, dyspnea, cyanosis
	Campylobacter jejuni causes self-limiting diarrhea and mild-moderate enterocolitis
	Helicobacter mustelae colonizes 100% of ferrets after weaning and is usually asymptomatic. The ferret is the "only" animal that has naturally-occurring gastric ulcers caused by Helicobacter.{4760}
	Proliferative enteritis (Lawsonia) causes chronic green blood-tinged diarrhea, ADR, rectal prolapse. Colon is palpably thick. Treat with CHPC (50mg/kg BID po,sq, im) or metronidazole (20mg/kg BID po) for 2 weeks.{4760}
	Tuberculosis (avian, human and bovine strains)
	Abscesses due to Staphylococcus, Streptococcus, Pasteurella, Corynebacterium, Actinomyces israeli, and E. coli
	Mastitis (Staphylococcus, Streptococcus, and E. coli); treat with enrofloxacin 2.5mg/kg BID po

Viral

	Distemper: mucopurulent ocular and nasal discharge, rash; if they survive the catarrhal phase they may succumb to the CNS phase. Vaccinate with MLV vaccine of non-ferret origin
	Influenza: serous nasal discharge, low mortality, signs similar to distemper except they recover
	Aleutian disease
	Rabies
	Rotavirus

Parasitic and Fungal

	Toxoplasmosis
	Coccidiosis
	Toxascaris leonina
	Dirofilaria immitis
	Sarcoptes scabei
	Ctenocephalides
	Otodectes cynotis
	Microsporum canis

Nutritional and Metabolic

	Eclamptogenic toxemia: anorexia, incoordination, weakness, weight loss, death; not very well-documented, but give vitamins and mineral supplements during lactation
	Bone marrow depression due to high endogenous estrogen levels during estrus; prevent by spaying or by giving 50-100 IU HCG or breeding during estrus
	Urolithiasis
	Posterior paralysis
	Gastric ulcers

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Comments? Send an email to janet.rodgers@vet.ox.ac.uk