FIRST STEP PROGRAM 2004
DEALING WITH GI PROBLEMS …………………………………..PAGE 2
RESPIRATORY DISEASE ………………………………………….PAGE 9
ABSCESSES …………………………………………………………PAGE 16
INTRODUCTION TO FERRET MEDICINE ………………..…......PAGE 19
EXOTIC MAMMAL SURGERY………………………………….….PAGE 58
INTRODUCTION TO THE CHINCHILLA ……………………….…PAGE 73
INTRODUCTION TO THE AFRICAN PYGMY HEDGEHOG…..PAGE 76
COMMON DENTAL DISEASES……………………………………PAGE 81
DEALING WITH GI PROBLEMS
S.A. KELLEHER DVM
Broward Avian & Exotic Animal Hospital, 611 NW 31st Avenue, Pompano Beach, Florida,
FL 33069, USA
Gastrointestinal problems are by far one of the most common problems that initiate a visit to the
vet for the pet rabbit. These problems include anorexia, diarrhea, cecal dysbiosis,
gastrointestinal stasis, bloat and obstruction.
When a rabbit presents for any condition involving the GI tract, a thorough history can provide
invaluable clues as to the problem at hand. One of the best examples of this is a history of
anorexia. It is imperative to sort out from the history whether the rabbit is not eating because it
has no interest in food at all versus having a great interest in food, but just not wanting to take
food into its mouth. A complete lack of appetite is most commonly seen secondary to a severe
physiological problem such as renal failure, whereas a scenario involving a rabbit showing a keen
interest in food but not eating it is a classic presentation seen in rabbits with dental disease. It is
very important for the clinician to emphasize to him/herself that the GI tract starts with the mouth.
The most common dental disease responsible for anorexia in rabbits is misalignment of the
molars and resultant overgrowth of the crowns of the teeth. Dysfunction of the upper arcades of
cheek teeth most often involves spurs that grow into the buccal surface of the mouth, and
dysfunction of the lower arcades of cheek teeth most often involve spurs impinging on the lingual
surface. Although these statements are true over 90% of the time, there are cases that involve
lingual spurs on the upper arcade of cheek teeth and buccal spurs on the lower arcade of cheek
A cursory exam on the awake patient with an otoscope will often reveal the offending molar
spurs. However, sometimes a more thorough exam of the mouth while the patient is sedated is
necessary. If dental disease is the reason for the anorexia, it is best addressed by sedating the
rabbit and filing down the molar spurs as needed. This is most efficiently accomplished with a
small hand rasp or careful use of a dental bur. Bone ronguers can be used to clip off prominent
spurs. This instrument is appropriate because it is designed to cut sharply as opposed to cutting
by compression. Any instrument that would not cut the teeth sharply or file the spurs down
appropriately could potentially cause longitudinal microfractures in the teeth that would provide a
pathway for bacteria to seed the jaw and create a jaw abscess. When proceeding with dental
work on a rabbit in any manner, care should be taken to maintain or reproduce a normal occlusal
angle when addressing molar malocclusion (Crossley, 1996).
Other dental disease that can preclude a rabbit from eating properly is malocclusion of the
incisors. Rabbits are hypsodonts and thus, their teeth grow continuously. Since the only way to
wear any substance down is to cut it or abrade it with another substance that is as hard or harder
than it, it is essential that no matter what the rabbit chews on, it‟s teeth are properly occluded. It
is only by normal mastication of the teeth while they are properly lined up that they wear one
another down appropriately. The best way to address incisor malocclusion is to completely
extract all of the incisors. If the owner will not concede to this procedure, it will be necessary to
trim the incisors every 4-6 weeks. This is best done with a dremmel tool or dental bur. The
owner should be strongly discouraged from trimming them with nail clippers, as they are likely to
cause longitudinal fractures in the teeth.
Whenever dental disease of any form is present, it is imperative to take radiographs of the skull to
fully evaluate the extent of the disease process. Ventrodorsal, as well as right and left oblique
views are useful for evaluation of the dentition.
Signs that should incite the clinician to further investigate the teeth as the source of the problem,
other than overt molar spurs seen on initial exam, are mucopurulent discharge around the base of
any of the teeth, excessive salivation and horizontal bars across the incisor teeth. Mucopurulent
discharge is usually secondary to a tooth root abscess. Excess salivation is seen when there is
irritation of the tongue by a molar spur that may not be visible on initial exam. Horizontal bars
across the incisors are commonly seen in rabbits that have dental disease secondary to a
calcium or vitamin D deficiency (Harcourt-Brown, 1996).
True diarrhea is most often seen in young rabbits and is usually secondary to parasitism. The
most common parasites to cause diarrhea is Eimeria species of coccidia. In managing this
disease in rabbits it is important to consider environmental factors such as crowding and damp,
dirty conditions that contribute to the spread of coccidosis. For the oocysts to become infective,
they need to be exposed to oxygen for several days (Harcourt-Brown, 2002). Fastidious cleaning
as well as medical management with trimethoprim/sulfamethoxazole at a dose of 30-40mg/kg PO
q 12 hrs and supportive care are necessary to treat rabbits for this condition.
Owners will frequently report a history of diarrhea to the clinician that is not truly diarrhea, but
rather cecal dysbiosis. By carefully questioning the owner as to whether or not there are normal,
dry fecal pellets passed on the same day as the supposed diarrhea, as well as the nature and
odor of the “diarrhea” can help the clinician distinguish between true diarrhea and cecal dysbiosis.
In a case of cecal dysbiosis, rabbits do tend to continue passing normal dry faecal pellets on the
same day that they pass loose excrement. The end product that is passed as a result of cecal
dysbiosis is usually thick, pasty and has a very pungent odor.
Cecal dysbiosis occurs when the rabbit consumes a diet that is too rich in sugars and simple
carbohydrates. Owners frequently feed a ration that has whole or cracked corn as well as dried
fruits and seeds in it. Excessive amounts of fruit, crackers, cereals, and commercial “yogurt drop”
treats are often fed. If one stops to think about the way the cecum functions, it quickly becomes
obvious why this creates a problem. In the rabbit colon, large particles are propelled out and are
excreted in the form of dry, fibrous “waste” droppings. Small particles are moved retrograde back
up to the cecum where they are processed by a well-balanced population of bacteria and yeast.
The dominant bacterial population is Bacteroides species (Cheeke, 1987). The dominant yeast
is Saccharomyces guttulatus. The main end product of fermentation by the Bacteriodes
organisms is the volatile fatty acid, butyric acid. A considerable amount of energy is needed by
these hindgut tissues because the rabbit colon is extensively responsible for absorption of
electrolytes and nutrients. Butyric acid is the preferred fuel for this hindgut metabolism (Cheeke,
1987). Hence, Bacteriodes plays a significant role in the health and function of these tissues.
In cases of cecal dysbiosis, a large amount of Saccharomyces guttulatus is frequently seen on
microscopic examination of the malformed cecotropes. A hypothesis of excessive sugars and
simple carbohydrates causing this yeast overgrowth and an imbalance of the bacterial flora can
be understood if one considers how yeast react in general. Consider that when making bread or
beer it is essential to add sugar to the yeast mixture initially to “activate” the yeast. Adding
excessive sugars to the “fermentation vat” of the cecum can quickly cause an overgrowth of
yeast. Yeast overgrowth and cecal dysbiosis in general are best addressed with supportive care
as indicated by the patient‟s status, and strict diet changes. All forms of sugars and simple
carbohydrates must be eliminated from the diet and the rabbit needs to be encouraged to
consume adequate amounts of coarse fiber. It is best to eliminate concentrated nutrition sources
such as pellets at this time and put the rabbit on a diet strictly limited to hay and leafy green
Although true trichobezoars can occur in rabbits, they do not occur as commonly as one would
think. Most often a decrease in, or lack of production of faecal pellets is due to ileus or
“gastrointestinal stasis” rather than a true hairball. Due to the nature of their grooming habits,
rabbits always have some hair present in their GI tract. If they are taking in adequate amounts of
coarse fiber and water this hair is passed regularly in the faecal pellets.
Typical physical exam findings in rabbits suffering from ileus include depression, hypothermia, a
very doughy stomach and cecum, and gas filled intestinal loops. Radiographic findings include
severely gas distended intestinal loops and a very small cecum. It is not uncommon to see a gas
shadow around the gastric contents. This is especially true if the rabbit was anaesthetized with
gas for the radiographs. When a rabbits become dehydrated, they pull water from their GI tract to
keep the rest of their body hydrated. The result is very dry, compacted, doughy gastric and cecal
contents. The gas shadow around the gastric contents is most likely due to aerophagia at the
time of anesthetic induction and the dehydrated gastric contents sticking together.
Ileus is an extremely painful condition. If one considers how painful it is for an adult human to
have a small amount of intestinal gas and compare that to the degree of gas dilatation of the
loops of intestine in a small rabbit with ileus, one would be inclined to provide liberal amounts of
analgesics to a patient suffering from ileus. Useful analgesics for this condition are flunixin
meglumine at 1-2mg/kg SC q 12-24hrs (Carpenter, 2001), meloxicam at 0.1-0.2mg/kg (Harcourt-
Brown, 2002), or buprenorphine at 0.01-0.05mg/kg SC, IP, IV q 6-12 hrs (Carpenter, 2001).
Massive supportive care is often necessary to nurse a rabbit patient through a bout of ileus.
Appropriate fluids such as lactated ringers or normal saline at 100mL/kg/day given
subcutaneously as well as the syringing feeding of oral fluids will help restore normal hydration.
Syringe feeding a commercial gruel such as Oxbow Critical Care or a pureed pellet and vegetable
mix in small amounts, every few hours is necessary to avoid hepatic lipidosis. The patient should
be provided with ad lib amounts of hay and leafy greens. Pharmacological agents used in the
treatment of ileus include intestinal motility modifying drugs such as metoclopromide at 0.5mg/kg
PO, SC q 4-12 hrs. (Carpenter, 2001) and cisapride at 0.5mg/kg PO q8-12 hrs. (Carpenter,
2001). Simethicone, in the form of infant anti-gas drops are useful to help break up the gas so
that it will pass. One mL of a commercial infant anti-gas preparation such as Mylicon® PO q 4-8
hrs is helpful. Another adjunct agent to use is cholestyramine (Questran®). This product acts as
an ion exchange resin to adsorb enterotoxins that can potentially damage the liver. One-eighth
teaspoon of Questran® is added to 10mL of water and administered orally q24hrs. In case the
cholestyramine should have an affinity for any medications as well, it is best to be cautious and
administer the product several hours after other medications are given instead of at the same
time. In addition to fluid, nutritional and pharmacological support, gentle abdominal massage is
helpful to stimulate intestinal motility.
Rabbits presenting with a grossly distended, hard stomach usually have an obstruction of the
distal duodenum. Rabbits have a very tight esophageal sphincter and cannot vomit or eructate.
They produce large amounts of saliva and gastric secretions. If there is an obstruction of the
gastric outflow tract, the stomach quickly becomes distended. This condition can become life
threatening very quickly. An excessive amount of pressure is put on the diaphragm, which
compromises the rabbit‟s already small chest volume. In addition to the pressure that the
engorged stomach puts on the diaphragm, the distention of the stomach itself perpetuates the
problem by compressing the acute angle of the pyloric outflow tract. If the patient is stable
enough to be anaesthetized, a gastric tube can be passed to relieve the pressure immediately.
These cases are often obstructed because of a small mass of dehydrated ingesta. It is not
uncommon for them to respond to decompression, fluid therapy and prudent use of
metoclopromide. Appropriate pain management should be provided and if the situation is not
resolving within 2-6 hours, surgical intervention is necessary. These patients need to be
observed very closely until the condition is resolved.
The most common places for rabbits to have an obstruction in their GI tract are the distal
duodenum and the ileocolic junction. Survey radiographs are useful for making the diagnosis and
with timely surgical intervention rabbits usually recover from enterotomies quite well. Rabbits
normally have a very slow GI transit time and thus oral administration of barium for contrast
studies is often not useful. Since ileus is so common in rabbits, the main objective when
evaluating abdominal radiographs is to distinguish between a case of intestinal obstruction versus
ileus. In the case of ileus the gas pattern tends to extend all the way to the colon.
Rectal polyps are a condition seen fairly commonly on this distal aspect of the rabbit GI tract.
These are usually benign papilomas that are removed surgical if they seem to be causing a
problem such as bleeding or irritation. They are often pedunculated and removed easily by
placing a cerclage ligature around the base of the mass and excising it completely.
By understanding the normal anatomy and function of the rabbit‟s GI tract from mouth to rectum,
the veterinary practitioner can readily deal with the most common problems that rabbits are
presented for due to this organ system‟s dysfunction.
Carpenter J.W., Mashima T.Y., Rupiper D.J. Eds. Exotic Animal Formulary (second edition).
Philadelphia: W.B. Saunders, 2001; p 304.
Cheeke, P.R., Rabbit Feeding and Nutrition. Academic Press. Orlando. 1987. pp25 and 84-85.
Crossley, D.A., Vet. Rec. 1996.
Harcourt-Brown, F. Textbook of Rabbit Medicine. Oxford: Butterworth Heinemann, 2002
S.A. KELLEHER DVM
Broward Avian & Exotic Animal Hospital, 611 NW 31st Avenue, Pompano Beach, Florida, FL
Rabbits with respiratory disease may present with a variety of clinical signs. These may be as
subtle as a mild to moderate amount of discharge matted on the medial aspect of the forepaws.
This is a result of the rabbit‟s fastidious grooming behavior of cleaning its face with its forepaws.
Respiratory disease can be caused by bacterial and viral organisms, nasal foreign bodies,
neoplasia and heart disease. The most common bacterial etiology is Pasteurella multocida
(Harcourt-Brown, 2002). However, other organisms such as Staphylococcus aureus,
Enterobacter sp., and Pseudomonas aeruginosa are not uncommon pathogens cultured from
rabbits‟ respiratory tracts. Bordetella bronchiseptica has been reported as a common inhabitant
of the rabbit respiratory tract that doesn‟t usually cause clinical disease (Deeb, 1997). This
author has seen rabbits with significant upper and lower respiratory tract disease whose deep
nasal and tracheal wash cultures produced a pure growth of Bordetella bronchiseptica.
Explanations for this could include the possibility that the rabbits were immune compromised by
some other condition, the Bordetella was dominating the culture and other organisms were not
able to proliferate, or that Bordetella truly is a primary pathogen of rabbits.
Bacterial infections of the upper respiratory tract are usually characterized by a mucopurulent
discharge from one or both nasal passageways. Since the modern-day rabbit owner is usually
very vigilant, rabbits may present to the veterinarian at the earliest signs of disease such as an
increase in sneezing. At such an early stage of infection the discharge may not be evident on
the nose or even on the forepaws. However, close examination of the nasal passageways with
an otoscope cone often reveals the discharge. Culture of the discharge alone is often not fruitful
in diagnosing the causative agent. A deep nasal culture provides the best specimen. Micro-
tipped culturettes are very useful for this purpose. The culturette should be inserted at least 2cm
into the nasal cavity. Holding the rabbit in such a manner that it is on its back and slightly
tranced, or by using light sedation are two ways to make this feat possible. An otoscope also
may be used to explore the rostral aspect of the nasal passageways if the practitioner suspects
that an upper respiratory tract infection is being caused by a nasal foreign body. It is not
uncommon for a rabbit to get hay or hair up its nose. Until the foreign body is found and
removed, treatment will be futile. Rabbits with nasal foreign bodies often present with very
copious mucopurulent discharge, especially from the offending side. They also tend to paw at the
side of their nose and sneeze forcefully. If a foreign body is not recognized on the initial cursory
exam with an otoscope and the rabbit has a persistent, intractable URTI exploration of the nasal
passageways with a rigid endoscope is indicated and often very useful.
Bacteria also can be responsible for abscesses in the rabbit‟s chest. These can be very large in
size and compromise the lung capacity significantly. Clinical signs may be only tachypnea and a
mild to moderate decrease in activity level. If heart sounds are not audible on one or both sides
of the chest upon auscultation, a chest abscess or neoplastic mass should be considered as
Therapeutic agents for the treatment of respiratory infections in rabbits must be considered
carefully. Severe dysbiosis and life threatening enteritis can occur if the wrong antibiotic is
chosen. Safe antibiotic choices include the fluoroquinolones, enrofloxacin and ciprofloxacin at 5-
10mg/kg PO, SQ BID, chloramphenicol at 50mg/kg PO TID, tribrissen at 30mg/kg PO BID,
azithromycin at 50mg/kg PO QD X 10-14 days (Plumb, 2002) and parenterally administered
penicillin at 42,000-84,000IU/kg SQ, IM q 24h (Carpenter, 2001).
A very useful adjunct to systemic antibiotic therapy is the use of nebulization. Antibiotics, a
mucolytic agent, a broncodilator and saline can be combined for this therapy. The following
recipe has been very useful: 5ml of saline, 0.25cc of 20% acetylcysteine, 0.5cc of amminophylline
(25mg/ml), and 1ml of amikacin. The rabbit is nebulized with a mask over its nose. This
treatment can be repeated every 4-12 hrs. Even the most distressed rabbits seem to tolerate this
treatment quite well.
The most common viral disease that can affect the rabbit‟s respiratory tract is myxomatosis.
Rabbits infected with this virus may present with rhinitis and ocular discharge. Transmission of
the myxoma virus is vector mediated. Common vectors include fleas and mosquitoes. A vaccine
(Nobivax Myxo, Intervet) is available and affords good protection from this disease. The vaccine
protocol is injection of 0.9ml of the vaccine subcutaneously and 0.1ml of the vaccine intradermally
(Harcourt-Brown, 2002). The intradermal route utilizes the Langerhans cells in the dermis as
antigen-presenting cells that increase the activation of T-helper cells. This intradermal route also
protects the antigen by minimizing its diffusion into surrounding tissues and providing a depot
effect (Stills, 1994).
The most common neoplasias of the chest cavity include metastatic mammary adenocarcinoma
and thymomas of either lymphoid or epithelial origin. There have been several reports of surgical
removal of such masses via thoracotomy (Vernau, 1995, Clippinger, 1998., Harcourt-Brown, N.,
2002). A case is currently undergoing radiation chemotherapy at Cornell University. The rabbit‟s
chief problems were dyspnea, exercise intolerance and a moderate bulging of the eyes. Thoracic
radiographs revealed a very large mass silhouetting with the heart. After two weeks of receiving
two radiation treatments per week, a follow-up CT scan showed a 77% reduction in tumor size
Heart disease is becoming more commonly diagnosed in the pet rabbit. This is due partly to the
fact that many house rabbit owners are bringing their rabbits in for regular wellness exams before
the animals are severely clinical for disease. In the author‟s practice arrhythmias have been
auscultated more commonly than murmurs. Chest radiographs, echocardiograms and
electrocardiograms are useful diagnostic tools in managing heart disease in rabbits. Due to their
small chest size, rabbit chest radiographs can be challenging to read, but when significant heart
disease is present the heart often appears amazingly enlarged. Normal rabbit echocardiogram
measurements are presented in Table 1 (Redrobe, 2002).
Left ventricular end diastolic dimension 1.17+/- 0.19
Left ventricular end systolic dimension 0.7+/- 0.09
Shortening fraction (%D) 39.5 +/-5.39
Left ventricular ejection time (LVET) 0.08 +/- 0.01
Velocity of circumferential fiber shortening 4.74 +/- 0.45
Ejection fraction (Ej fract) 76.17 +/- 5.81
Left ventricular free wall thickness diastolic 0.31 +/- 0.08
(LVFW Th d)
Interventricular septum thickness diastolic 0.25 +/-0.05
(IVS Th d)
Left atrial dimension systolic (LAD s) 0.17+/-0.41
Left atrial to aortic root ratio (LA/Ao) 1.38 +/-0.32
Right atrial dimension systolic (RAD s) 0.61 +/- 0.08
Right atrial to aorta ratio (RA/Ao) 0.88 +/-0.17
E point septal separation (EPSS) 0.05 +/- 0.05
DE excursion (DE escurs) 0.55 +/-0.08
E to F slope (EF slope) 70.17 +/-31.82
Right ventricular outflow velocity (RVOT vel) 0.83+/-0.10
Left ventricular outflow velocity (LVOT vel) 0.65+/-0.14
It is difficult to find established rabbit dosages for heart medications in the literature. In the
author‟s practice a rabbit with dilated cardiomyopathy was managed with enalapril at 0.5mg PO
QD, digoxin at 0.03mg/kg PO BID and furosemide at 0.5-0.8mg/kg PO BID for 7 months before
decompensating and dying from heart failure. Another patient is currently being managed for
premature atrial complexes. A significant arrhythmia was detected on physical exam when the
patient presented for a mild mucopurulent discharge from his nose. Chest radiographs were
within normal limits, but an EKG showed a significant number of PACs and a heart rate of
300bpm. The only clinical sign the rabbit had other than the mild nasal discharge was minor
weakness of the rear limbs. Considering that the patient is nine years old, this change may be
associated with the cardiac disease or may be due to other changes associated with aging. The
patient was initially started on 0.75mg/kg of diltiazem given orally once daily. After it was
determined that the rabbit was tolerating the drug well (no inappetance, lethargy or other negative
changes) the dosage was increased to 0.75mg PO a.m. and 1mg/kg PO p.m. After 4 days the
dose was increased to 1mg/kg PO BID. At a recheck appointment in November 2002, the EKG
revealed a completely normal rhythm and a heart rate of 300. At the time of this visit, the right
testicle was notably enlarged. Since this change had come about extremely rapidly and the
patient was doing so well, castration was recommended. The patient was premedicated with
1.5mg of diazepam and 2mg of ketamine, intubated and maintained on isoflurane anesthesia.
The operation went well and the patient recovered and went home the same day. An EKG was
run before and after the procedure and no PACs were noted.
Another 9 year old rabbit presented for a dermatological condition. Auscultation of the chest
revealed extremely muffled heart sounds. Echocardiogram showed a large, 9cm fluid-filled mass
at the base of the heart. Approximately 60 milliliters of a dark brown fluid was removed via
ultrasound guided thoracocentesis. Cytology of the fluid was consistent with a septic effusion.
The pathologist surmised that this was possibly a liquefying abscess. A culture of the fluid grew a
coagulase negative Staphylococcus. After the thoracocentesis, the rabbit was treated with
ciprofloxacin at 10mg/kg PO BID and furosemide at 1.2mg/kg PO BID for two weeks. The mass
did not fill with fluid again and the rabbit lived for another six months.
Although bacterial infections account for the majority of respiratory diseases in pet rabbits, many
rabbits that present with clinical signs of respiratory disease often have other problems such as
neoplasia, heart disease, or a foreign body in the nose that are the primary disease process. A
thorough physical exam and diagnostic testing such as radiographs, tracheal washes, culture,
endoscopy, and ultrasound are helpful in identifying the cause of illness.
Carpenter J.W., Mashima T.Y., Rupiper D.J. Eds. Exotic Animal Formulary (second edition).
Philadelphia: W.B. Saunders, 2001; p 304.
Clippinger, T.L., Bennett, A., Alleman, R., Ginn, P.E., Bellah, J.R. Removal of a Thymoma Via
Median Sternotomy in a Rabbit with Recurrent Appendicular Neurofibrosarcoma. J AM Vet
Med Assoc. 213 , 1998, pp1140-1143.
Deeb, D. Respiratory Disease . In: Hillyer, E.V., Quesenberry, K.E., eds. Ferrets Rabbits and
Rodents – Clinical Medicine and Surgery. Philadelphia: W.B. Saunders, 1997; p198.
Harcourt-Brown, F. Textbook of Rabbit Medicine. Oxford: Butterworth Heinemann, 2002.
Harcourt-Brown, F., Harcourt-Brown, N., Surgical Removal of a Mediastinal Mass in a Rabbit.,
Exotic DVM, 4.3, ICE proceedings 2002, pp59-60.
Morrissey, J., Cornell Veterinary College, personal communication, 2002.
Plumb, D.(ed.), Veterinary Drug Handbook, Ames, Iowa, Iowa State University Press, 2002.
Redrobe, S. Imaging Techniques in Small Mammals, Seminars in Avian and Exotic Pet
Medicine, 10, 2001, pp.187-197.
Stills, H.F., Polyclonal Antibody Production. In: Manning, P.J., Ringler, D.H., Newcomer, C.E., The
Biology of The Laboratory Rabbit. New York: Academic Press, 1994; p. 437.
Vernau, K.M., Grahn, B.H., Clark-Scott, H.A., Sullivan, N. Thymoma in a Geriatric Rabbit with
Hypercalcemia and Periodic Exopthalmus. J AM Vet Med Assoc. 206 1995, pp820-822.
S.A. KELLEHER DVM
Broward Avian & Exotic Animal Hospital, 611 NW 31st Avenue, Pompano Beach, Florida,
FL 33069, USA
Rabbit abscesses can be quite the nemesis to veterinary practitioners. Rabbit‟s abscesses are
not amenable to the simple lancing and drainage that often resolve abscesses in dogs and cats.
Rabbits lack the lysosomal enzyme that breaks down dead cells into a liquid form (Brown, 2001).
This results in a very thick, caseous pus. The abscesses tend to have thick capsules around
them and often have finger like projections that extend into surrounding tissues. In order to
resolve an abscess in a rabbit, aggressive surgical resection of all affected tissue is often
required in addition to local and systemic antibiotic therapy.
Although they can occur anywhere, the most common sites for abscess formation are the jaw,
hock, nasolacrimal duct and chest. Abscesses of the jaw are most commonly associated with
tooth root abscesses. There are different theories as to why these occur so frequently in rabbits.
When rabbits are fed a diet that is mainly based on a commercial, pelleted ration that requires
very little mastication, instead of a more natural diet of grass and other vegetables that require
extensive mastication, it is theorized that the result is a disuse atrophy of the periodontal
ligaments and osteoporosis (Crossley, 1996). Alternatively, a primary calcium deficiency and
possible vitamin D deficiency due to the selective feeding habits of rabbits offered a commercial
mixed ration has been shown to correlate significantly with dental disease in pet rabbits
(Harcourt-Brown, 1996). Even though pet rabbits are offered components that should technically
meet their nutritional needs, when given the choice between high carbohydrate components in
the diets and healthy, high fiber hay, rabbits will often eat a total diet that is deficient in both
calcium and vitamin D as well as deficient in high fiber foods that require appropriate mastication
that would “exercise” their teeth. It is highly likely that a combination of these current theories is
correct in explaining the etiology of dental disease in pet rabbits.
A study of jaw abscesses in pet rabbits concluded that the most common bacterial isolates
cultured included Fusobacterium nucleatum, Prevotella heparinolytica, Prevotella spp.,
Peptostreoptococcus micros, Streptopeptococcus milleri group, Actinomyces israelii, and
Arcanobacterium haemolyticum. 100% showed sensitivity to clindamycin, 96% were susceptible
to penicillin and ceftriaxone, 54% were sensitive to ciprofloxacin, and only 7% were sensitive to
trimethoprim-sulfamethoxazole (Tyrell, 2002). When choosing antibiotics for treating jaw
abscesses, good systemic choices would be penicillin at 50,000IU/kg SC q24-72 hours, or
chloramphenicol at a dose of 50mg/kg PO q8 hrs. Even though chloramphenicol was not tested
in this study, because of the risks to humans that would be handling the medication, it does have
a broad spectrum of activity and it would be a good choice.
Abscesses of the nasolacrimal duct are most likely secondary to drainage obstruction by
overgrown maxillary incisors (Harcourt-Brown, 2002) as well as periapicle abscessation of these
roots (Crossley, 1996). Diagnosis can be made by performing contrast radiography of the
nasolacrimal duct (Harcourt-Brown, 2002).
Rabbit patients commonly present with abscesses located on the medial aspect of the tarsal joint.
Possible reasons for this particular area being affected could be bacterial emboli lodging in small
blood vessels in this area, or trauma to this area because it is not well protected by soft tissues.
Treatment is focused on excising the abscess as completely as possible and then placing
appropriate AIPMMA beads at the site.
Abscesses that occur in the chest are often not diagnosed until the rabbit is in the very end
stages of disease and decompensating for the lack of lung space. Diagnosis can be made by a
combination of radiography and ultrasound guided fine needle aspirate. A lung wash could
potentially be useful for identifying the etiologic agent. However, since rabbits tend to wall off
abscesses with a very thick capsule and this may not be fruitful. Therapy should be directed at
providing supportive care with minimal stress as well as attempting treatment with antibiotics. If
the etiologic agent cannot be assessed accurately a broad spectrum coverage that would cover
gram positive as well as gram negative aerobes and anaerobes should be chosen. This can be
accomplished with chloramphenicol or an orally administered fluoroquinolone combined with a
parenterally administered penicillin.
Abscesses can occur anywhere else on the body. The most commonly seen are abscesses in
either the maxilla or mandible. In these cases, underlying dental disease needs to be identified
and addressed in addition to providing appropriate surgical and medical management. Rabbits
also frequently present with traumatically acquired wounds that quickly develop into abscesses.
When the location is amenable to it, a complete surgical resection of all affected tissue should be
Brown, S.A., Abscesses in Rabbits. In: The Small Mammal Health Series. Veterinary
Information Network. March 2001.
Crossley, D.A., Dental Disease in Rabbits. Vet. Rec. 1996, p384.
Harcourt-Brown, F.M., Calcium Deficiency, Diet and Dental Disease in Pet Rabbits, Vet. Rec.
1996, 139, 567-671.
Harcourt-Brown, Dacryocystitis in Rabbits. Exotic DVM vol. 4.3, 2002, pp. 47-50.
Tyrell, K.C, Citron, D.M., Jenkins, J.R., Goldstein, E.J.C. and Veterinary Study Group, Periodontal
Bacteria in Rabbit Mandibular and Maxillary Abscesses,J. Clin. Micro.3, pp.1044-1047.
An Introduction to Ferret Medicine
Peter G Fisher, DVM
Pet Care Veterinary Hospital
Virginia Beach, VA
Table of Contents
Colors and Patterns 4
Basic Facts 5
Nutritional Support 6
Esophagostomy tube placement 7
Restraint, specimen collection and catheter placement 8
Intraosseus Catheterization 9
Intravenous Catheterization 9
Subcutaneous Fluids 9
Urinary Catheterization 9
Preventative Care 10
Physical Exam 10
Vaccine reactions 11
External Parasites 12
Intestinal Parasites 13
Heartworm Disease 13
Elective Surgeries 14
GI disease: Diarrhea and Vomiting 14
History and Physical Exam 14
Gastrointestinal obstruction/ foreign bodies 15
Helicobacter mustelae 16
Viral- ECE 17
Inflammatory Bowel Disease 18
Endocrine Diseases 19
Adrenal disease 19
Medical Diseases 25
Cardiac disease 25
Dental disease 27
Renal Cysts 27
Urinary Tract Inflammation (UTI) 28
Aleutian Disease 28
Estrogen toxicity 30
Neoplastic Disease 32
Suggested Text 39
The domestic ferret is believed by many to have been first domesticated about 3,000 years
ago by the ancient Egyptians. It is one of three carnivores (along with the domestic cat and dog)
that have been domesticated by man. Original ancestry of the domestic ferret is believed to be
from the European Polecat (Mustela putorius) from Northern Europe and the United Kingdom.
The domestic ferret was probably brought to North America about 300 years ago. Since the
Middle Ages, the ferret has been used primarily as a working animal, initially as a hunter of
rabbits and rats, and more recently as a construction worker, laying wire and cable in concealed
piping. During their entire history, ferrets have been kept as companion animals, but it is only
during the past 20 to 30 years that their popularity as a household pet has exploded. Current
estimates place the number of domestic ferrets kept as pets at between five and eight million
animals with several million more being used in biomedical research.
Much can be understood about the ferret by observing and recognizing its behavior patterns
and interactions displayed as it plays and communicates with humans and animals within its
home environment. Ferrets are engaging and social animals that have an affinity for people.
They are very playful and curious pets that require a lot of attention from their owners and
anecdotally require one to three hours of play daily. Well-socialized ferrets normally can
share a household with other ferrets or domestic pets; however there have been reports of
difficulties socializing with birds, small rodents or reptiles and strict supervision is
recommended during these interspecies encounters.
Kits tend to rough house a lot and be nippy. Proper socialization can be accomplished
through regular handling and interaction with the owner, thus enabling the ferret to learn more
appropriate behavior. Domestic ferrets are very intelligent and can be treated with the same
disciplinary principles that are applicable to puppies and kittens. Owners may discipline the kits
by saying a sharp, „no!‟ and perhaps scruffing to correct biting behavior if it continues. Because of
the high energy level and playful nature of ferrets, households with small children or infants
should always maintain proper supervision of the animal and child.
Greeting behavior among ferrets is similar to that of canines. Strange ferrets normally greet
each other by sniffing around the anus for a moment and then sniffing the back of the neck.
These areas contain scent glands that give information to the ferret, most importantly its sex,
relative strength and individual identity. At times, neck biting or fighting ensues as dominance
establishment takes place. It must be realized that ferret play behavior can be rough and chaotic
as well, with one ferret chasing and nipping at the other, often accompanied by jumping and
wrestling. Ferrets also signal excitement and play by displaying a hopping and bucking gait
together with a chortling vocalization.
Ferret owners are very observant and changes in the ferret‟s behavior such as sudden
listlessness, personality changes, decreased appetite, pawing at the mouth, ataxia or ptyalism,
Colors and Patterns
Sable (also termed fitch) is the most common color.
Albino White to yellowed guard hairs; red eyes; pink nose
Black Black guard hairs; black eyes; black nose
Black eyed white White guard hairs; dark red to pure black eyes; pink nose
Butterscotch Light yellow-brown guard hairs; black eyes; pink nose
Cinnamon Reddish brown cinnamon colored hairs; dark eyes; pink to brick
Chocolate Light, medium and dark brown to chocolate color guard hairs; black
eyes; pink to brick color nose
Platinum Dark guard hairs, sprinkled with white guard hairs to appear gray from
a distance; black eyes; black nose
Red Red rust guard hairs; black eyes; pink nose
Sable Dark brown (that appears almost black) guard hairs; black eyes; black
Shaded silver Evenly sprinkled silver sheen guard hairs on mostly white body; eyes
dark as possible; pink nose
Silver Appears white at a distance (almost a Black eyed white) with very light
ticking with dark hairs; eyes dark as possible; pink nose
Description of Patterns
Dalmatian Spotted ferret; eyes dark as possible; any color nose
Panda White head, neck and bib; any color guard hair; half moons under
eyes; white tipped tail and feet; dark hair in ears; dark eyes; any color
nose; spotted on head permitted but not preferred
Patches Spot(s) on head, usually irregular in shape; if white faced, half moons
or circles around eyes; mask permitted; full bib; any color coat; white
patches on knees; mitts and white tipped tail preferred
Ringneck White ring around neck; any color; dark eyes; any color nose
Shetland White faced; white stripe from top of head to neck (also known as
Siamese Distinct V mask; dark brown that appears to be black; dark colored
guard hairs and points; dark eyes; dark nose; distinct zipper on
Striped White body with dark stripe down back; dark eyes; any color nose
TriColor New color being developed, no standard yet, experimental
(Reprinted with permission from TOTALLYFerret Newsletter, June 2001)
Males = „hobs‟
Females = „jills‟
Babies = „kits‟
Puberty = 4 - 9 months of age.
Hobs typically weigh between 0.8 and 2.5 kg. Jills weigh between 0.6 and 1.2 kg. Weight is
typically lost during the Spring (longer photoperiod) and gained during the Winter. This weight
fluctuation can be up to 40% difference.
Ferrets are induced ovulators and have a gestation period of 42-44 days.
Average litter size = 8 (7-14)
Kits (baby ferrets) are weaned at 4 to 8 weeks. Their eyes open about 34 days after birth.
Fur has a fine undercoat and larger, coarser guard hairs.
Ferrets sleep very soundly and can sleep up to 18 hours per day.
Body Temperature = 37.8 - 40 degrees centigrade (100.6 - 104 degrees F)
Respiration = 33-36 breaths per minute
Heart rate = 210-245 bpm
Blood volume = 60 - 80 ml/kg (approximately 5 – 7 % body weight).
Blood Pressure (under anesthesia) is systolic 140-164, diastolic 110-125.
Urine pH = 6.5 – 7.5.
QRS complex = 1.84 +/- 0.61 mV lead II
Life span = 5 - 10 years average Eight is the most common seen „maximum‟.
Heat loss by panting = very heat intolerant. Temperatures over 90 degrees can be fatal.
Dental formula = 3131
Deciduous teeth erupt at 14 days and permanent canines at 47 - 52 days.
Vertebral column formula is C7, T15, L5 (6 or 7), S3, and Cx 18
Ferrets have a very high metabolic rate and require multiple meals throughout the day to
sustain themselves. As a result, food and fresh water should be constantly available. Commercial
ferret diets, formulated to meet the specific nutritional needs of the ferret, are now available, and
therefore ferrets should not be maintained on mink or cat food.
Water bottles are less messy and more sanitary, and therefore are preferred to water dishes.
Ferrets are true carnivores; their diet must consist mainly of meat and animal products. They
possess a very short intestinal tract that lacks a cecum and ileocolic valve, resulting in a rapid GI
transit of ingesta in as little as 3-4 hours. As a result, their digestive system cannot adequately
handle diets high in fiber or carbohydrates. Also because of this rapid transit time, ferrets need to
be fasted no longer than 5-6 hours prior to surgery.
Ferrets enjoy certain fruits, vegetables and other such treats; however, these should be fed in
moderation as they provide little in the way of nutrition and excess consumption may result in
diarrhea and create finicky eaters. Occasional pieces of cooked, boneless meat make good
A quality ferret diet should be 30 to 35% crude protein and 15 to 18% fat. When reading the
pet food label, the first several items listed should be animal proteins such as meat or poultry, or
meat or poultry meals or their by-products. Most homemade formulations should be avoided as
they fail to meet the high protein, high fat and low carbohydrate requirements, while maintaining a
healthy vitamin-mineral balance.
For maintenance, ferrets may consume between 200 and 300 kcal/kg body weight daily. For
growth and reproduction, a ration with a caloric density close to 5000 kcal/kg diet may be
necessary, and it is suggested that levels of protein and other essential nutrients be adjusted
There is some thought that excessive carbohydrate intake stimulates excessive insulin
production from the pancreas, leading to hyperplasia and eventually the neoplasia associated
with insulinoma. It has been suggested that feeding a diet high in protein (42-55%), high in fat
(18-30%), and low in carbohydrates (8-15%) and avoiding snacks high in simple sugars may
prevent insulinoma. The question pf whether this is true or whether the high protein diet would
predispose to renal disease remains to be answered.
Guaranteed Analysis of commercial ferret foods
Name Kcal/100 Crude Crude Crude
g Protein Fat Fiber
Not less Not less
Marshall’s Premium Diet 38% 18% 4%
8 in 1 Ultimate Ferret Diet 38% 15% 3%
KayTee Forti Diet 370 35% 18% 4%
Totally Ferret Adult 430 36% 22% 1.5 %
Totally Ferret Senior 400 33% 18.5% 1.5%
Mazuri 38% 20.5% 4%
Sheppard&Greene Nutri- 410 35% 20% 3%
Sheppard&Greene Maxi- 385 28% 14% 4%
Hartz Ferret Diet 30% 12% 4%
ZuPreem 472 40% 20% 2%
Hills a/d 97 8.5% 5.25% 0.5%
Nutritional support is a key element in the therapy of ferrets that are recovering from
debilitating disease. Many ferrets can be syringe fed a variety of recipes that help meet their
caloric needs. You can usually achieve 15-30 ml per feeding over a period of time. The resting
energy requirement of ferrets is 70kcal/day. The following formulas have been advocated for use
in syringe feeding ferrets.
Oxbow‟s Carnivore Critical Care
Hills a/d. A mixture of one can a/d mixed with 50 cc‟s water will give an approx. 1 kcal/ml
feeding suspension. Force-feed small amounts (3 - 5 ml) frequently (every two to four
hours) until you build up to 15-30 cc‟s with each feeding.
Duck soup. This formula was first used for a ferret named Lucky Duck and is so named.
Many adaptations of this recipe have been formulated:
1/2 cup of high quality, dry kitten food. Soften this with hot water to make
a stiff paste.
1/8 cup of Isocal (or equivalent liquid, non-dairy food supplement. Do not
use the chocolate flavored. Strawberry works well.). You can freeze the
remainder in an ice cube tray and package them in a zip lock bag and
1 1/2 inches of Nutrical or Nutristat.
1 „pump‟ of Ferretone or Linetone.
Mix all the ingredients together. Use anywhere from a thin gruel to thick
paste and force-feed small amounts (3 - 5 ml) frequently (every two to
Pureed ferret diet. Feed as with a/d.
Esophagostomy tube placement
There are many incidences where ferrets need long term nutritional support or oral
medication. Placement of esophagostomy feeding tubes has been of great benefit in serving
It is not uncommon to see debilitated ferrets secondary to chronic gastrointestinal foreign
bodies, hairballs, Epizootic Catarrhal Enteritis (ECE) virus, neoplasia, insulinoma or other
metabolic disease. Many of these ferrets also suffer from hepatic lipidosis, which develops rapidly
in anorexic ferrets. These ferrets need nutritional support not only to aid the healing process
associated with their diseases, but also to reverse the fatty changes in the liver and overall state
of malnutrition. As in our feline patients, placement of an esophagostomy feeding tube and
feeding a gruel diet will allow such nutritional support.
Esophagostomy tubes can also be used in ferrets requiring long-term oral medication. Ferrets
diagnosed with gastric ulcers, Helicobacter or who have a slow recovery from ECE may require
up to four weeks of therapy with oral medications such as antibiotics, Pepto-Bismol,
metronidazole, H2 blockers or sucralfate. Many oral medications we use in ferrets come in a
solution or suspension or can be compounded in-house or purchased from a compounding
pharmacy in liquid form for administration through an esophagostomy tube. Anyone who has tried
to give medicinal solutions to ferrets knows how difficult this can be, especially when required
long term. Placement of an esophagostomy tube ensures not only adequate dosing of
medications but ease of administration as well. Many ferrets are given nutritional support early in
the course of therapy, then once the patient is eating on its own the feeding tube is left in place so
that oral medicines can be administered for as long as necessary.
Placement of the esophagostomy tube is simple and the technique is similar to that used in
felines. A 10 French Sovereign red rubber feeding tube (Sherwood Medical) is measured from the
left side of the neck to approximately the 9-10 rib space (2/3 way to stomach). The tube is then
marked to identify this distance. The goal is to have the tube ending in the distal esophagus. Pre-
medicate the ferret with a combination of butorphanol and acepromazine and then mask down
and maintain on isoflurane or sevoflurane. Pre-anesthetic tranquilizers allow one to remove the
facemask periodically when working in the oral cavity. In severely depressed ferrets this can be
accomplished with the use of isoflorane or sevoflurane alone.
Once anesthetized, the left side of the neck is surgically prepared. A 14 cm curved Kelly
forceps is placed in the mouth and the tip passed into the proximal esophagus where it can be
palpated through the skin over the left neck just caudal to the junction of the linguofacial and
mandibular veins. A small incision with a number 10 scalpel blade is made over the tip of the
Kelly forceps and the forceps are gently forced through the incision. The tip of the red rubber tube
is placed in the jaws of the forceps and then brought out through the mouth. The tube is then
turned around 180 degrees and passed back down the esophagus. The tube sometimes kinks in
the pharyngeal area but with gentle manipulation with the Kelly forceps or the surgeons finger it
can be passed down the esophagus. The red rubber feeding tube now is manipulated from its
proximal end, which is protruding from the stab incision, and one feels for smooth gliding distally
in the esophagus. The mark indicating proper tube placement is identified and the tube is secured
to the skin with a Chinese finger trap suture pattern using 4 O nylon (Ethicon) suture. The tube is
then curved caudally over the ferrets dorsal neck and enclosed in a bandage consisting of two
inch cast padding followed by two inch Vetrap(3M). Care is taken not to place the bandaging too
tight. Triple antibiotic ointment is placed over the tube entry site prior to bandaging in order to
help control local infection. The distal end of the feeding tube can be cut so that it terminates over
the dorsal thoracic back between the shoulder blades.
Feeding tubes can be left in place for up to six weeks with weekly bandage changes. For
extended care owners can be easily taught to feed and medicate their ferrets at home. The
ferrets tolerate the feeding tubes well and do not try to physically remove them, negating the need
for any type of restraint such as Elizabethan collars. The tubes are pulled when the ferrets have
gained weight, are eating on their own, liver enzymes have returned to normal and/or when oral
medical treatment in complete.
Restraint, specimen collection and catheter placement
Most ferrets are docile and can be easily handled for routine procedures. For very active animals
or those that may bite an assistant can scruff the animal‟s skin over the back of the neck while
supporting the back legs. With this hold most ferret become very relaxed and the veterinarian
can proceed with an oral exam, ear exam and cleaning, nail trim or other procedures that require
Vena cava approach
Place the ferret on its back, extend forelimbs caudally. Enter the notch between the first rib
and manubrium on the right side. Use a 25 gauge needle (on a vacutainer or syringe) and
aim for the left hip. Advance needle slowly while applying even negative pressure until the
vena cava is pierced and blood appears in the hub. If venipuncture is unsuccessful on
advancing needle- slowly back out while maintaining slight negative pressure until blood
begins to fill the hub. Easily get 1-2 ml or more per ferret. Many veterinarians prefer to use
isoflurane or sevoflurane anesthesia in order to restrain ferrets for jugular or vena cava
Cephalic or Lateral Saphenous Veins
For small volumes of blood (i.e.; to check a blood glucose) the lateral saphenous or cephalic
veins work well using a 27ga ½ cc tuberculin syringe. For euthanasia many veterinarians
prefer to mask the patient down with an inhalant anesthetic and then use the cephalic vein for
catheter placement or a direct stick. This procedure is especially smooth when owners want
to be present at time of euthanasia.
The ferret is anesthetized and an area dorsal to the top of the femur is clipped and aseptically
cleaned. A 22 gauge 1½ “ spinal needle is lined up parallel to the shaft of the femur. The skin
over the greater trochanter is pierced and the needle advanced to the intratrochanteric fossa. The
needle is then twisted to pierce the bone and advanced. Many times the twisting results in a plug
of bone in the lumen of the needle. For this reason, you may want to „drill the hole‟ first with one
needle and then use another for the catheter. Once placed, butterfly tape the catheter and suture
to the adjacent skin.
A standard 24 or 25 gauge IV catheter can be placed in the cephalic vein of the foreleg with
relative ease. Again the ferret is anesthetized and the area is clipped and aseptically prepared. A
small skin incision is made with the tip of a 22 gauge needle. The catheter is then advanced
through the skin incision into the vein. The catheter is then carefully taped in place. Depending on
the activity level of the ferret IV catheters may be difficult to keep in place and patent. Infusion
pumps are critical in ensuring slow administration of appropriate volumes of fluid. Maintenance
fluid requirements in the adult ferret are estimated at 75-100ml/kg/day.
For non-critical cases, a bolus of maintenance fluids (either saline or LRS) can be given at
the dose of 75-100ml/kg divided q8-12h.
Urethral obstruction in the male ferret as a result of prostatic disease/hyperplasia secondary
to adrenal disease is not uncommon. Other causes of urethral obstruction include calculi or
severe crystalluria (both rare). In these cases urethral catheterization is needed to relieve the
obstruction until surgery can be performed, or underlying medical cause appropriately
Passing a urethral catheter can be a challenge in a male ferret due to the small diameter of
the urethra, the „J‟ shaped os penis, and the normal turn of the urethra over the pelvic bone.
The ferret is anesthetized. The penis is extruded and an attempt is made to „milk‟ the urethra
in hopes of dislodging any urethral obstruction. If still obstructed, a small diameter soft urethral
catheter is selected for placement. Cook Veterinary Products makes a 3.5 or 3.0 French silicone
catheter called a Slippery Sam. Venocath catheters ( 4 Fr) can also be used. Using a 22 ga
Teflon IV catheter (without needle) can be used to dilate the urethral opening which aids in initial
placement of the urinary catheter
Once placed, butterfly tape the catheter and suture to the adjacent skin.
You may need to place the ferret in a restraint collar to minimize the chewing of the catheter
Annual examinations are probably the best preventive care available. A complete physical
should evaluate the various body systems for evidence of problems such as otitis, hair loss,
weight loss, dental disease, heart disease, etc.
It is imperative to know the state laws concerning rabies vaccination in ferrets. The incidence
of rabies in ferrets is extremely low (14 cases in the last 40 years), but it is a public health
concern. There is also a lot of public opinion and misinformation about rabies in ferrets. Presently,
the only approved Rabies vaccine is Imrab3 by Merial. Vaccine reactions have been reported with
Virginia law- approved vaccine (Imrab3 - Merial ) and certificate. Incidences of ferret bite
wounds to humans can be handled on a case-by-case basis and veterinarian in charge
may decide likelihood of rabies exposure and appropriate quarantine.
Canine distemper is a highly fatal disease of ferrets. Symptoms appear 7-10 days after
exposure. The signs initially involve the upper respiratory tract resulting in a mucopurulent ocular
and nasal discharge, fever and anorexia. Facial and ventral abdominal erythema and dermatitis is
common and with time hyperplastic thickening of the footpads follows. If the ferret survives past
this point, neurological symptoms may be seen and are characterized by hyperexcitability,
muscular tremors, convulsions, hypersalivation, coma and death.
Supportive treatment can be tried (fluid replacement, anticonvulsants, antibiotics) but
distemper is 100 percent fatal. There are anecdotal reports of canine distemper survival in
ferrets treated with serum transfusions from well-vaccinated ferrets.
The manufacturer stipulates yearly vaccination of ferrets against distemper. As with dogs and
cats, there is some controversy on revaccination time interval. Owners of ferrets that have had
distemper vaccine reactions are especially concerned. Many veterinarians tell the owner what the
manufacturer states and let them make the decision. Most Ferret Shows require annual
Two approved vaccines are available: Fervac-D by United vaccines and PureVax Ferret
Distemper by Merial. Vaccine reactions are not uncommon with the Fervac-D. The PureVax
product is made via recombinant technology as to lessen vaccine reactions. It is has been on the
market since October 2001 and approval studies showed a very small vaccine reaction rate.
Canine vaccine combinations should never be used in ferrets, especially products of ferret cell or
low-passage canine cell origin. These products can cause vaccine-induced disease.
Vaccine reactions appear more commonly in ferrets than dogs and cats. A review of
treatment histories in the author‟s practice shows an occurrence of reactions of approximately 3%
in ferrets vaccinated with Fervac-D. The reactions are more typically associated with the
distemper vaccination but reactions to the rabies vaccines also occur.
The onset of vaccine reaction appears variable, with an anaphylactic-like reaction occurring
within minutes of vaccination, to delayed reactions occurring several hours post vaccination.
Delayed reactions appear less common than immediate reactions. Reactions may include
weakness, trembling, vomiting and diarrhea, respiratory distress, evidence of pulmonary edema,
erythematous skin, tail piloerection, high fever, circulatory collapse and even death.
Post-mortem lesions in ferrets succumbing to post-vaccine death support anaphylaxis.
Lesions include abnormalities consistent with shock, such as blood pooling into the intestine,
centrilobular hepatic necrosis, and scattered necrosis in the kidney. Lesions consistent with
vascular collapse include flooding of the alveoli with fluid, and histamine release from mast cells
in the lungs resulting in mass leakage from the vessels.
Treatment of vaccine reaction depends on the severity of the reaction and the symptoms
exhibited. Options include diphenhydramine hydrochloride (Benadryl, Parke Davis), (0.5-2 mg/kg
IV or IM), epinephrine (Phoenix Pharmaceutical, Inc.), (20 g/kg IV, IM, or SQ), dexamethasone
sodium phosphate (Phoenix Pharmaceutical, Inc.), (2 mg/kg IV or IM), and fluid therapy. Cases of
shock may require placement of an IV catheter and administration of crystalloid fluids.
Gastroenteritis may respond to intestinal protectants such as sucralfate (Carafate, Hoechst
Marion Rousoel) (25 mg/kg q8h PO) and drugs that inhibit gastrointestinal acid secretion such as
famotidine (Pepcid, Merck) (0.25-0.50 q24h PO or IV) or ranitidine (Zantac, Glaxo Wellcome) (24
mg/kg q8h PO). Furosemide (Lasix, Taylor Pharmaceuticals) (1-4 mg/kg q8-12h PO, SQ, IM, or
IV) can be used to treat pulmonary edema.
Note that overdoses of diphenhydramine and/or epinephrine have been documented.
Therefore, careful dilution of epinephrine and cautious dosing of both drugs is essential
Several strategies have been suggested for the management of vaccine reactions in ferrets:
1. Vaccination with PureVax and Imrab 3 followed by an in-clinic observation period. Most
practitioners recommend an observation period of at least 20 minutes, although
occasionally reactions have been reported to occur several hours after vaccination.
2. Omission of vaccination for canine distemper and rabies. The risk of death due to canine
distemper and rabies must be weighed against the risk of vaccine-induced reaction. In
addition, some communities require rabies vaccination in ferrets by law.
3. Premedication of ferrets, especially those known to have had a previous reaction, with
diphenhydramine. Some veterinarians advocate that their clients premedicate their ferrets
with oral diphenhydramine prior to arrival for vaccination appointments. If a ferret has a
history of vaccine reaction and the owner has not premedicated, a pre-vaccine injection
of diphenhydramine may alleviate problems. It is unknown whether or not this is always
beneficial, as reactions despite diphenhydramine administration have been reported.
Ferrets premedicated in this manner should still be held in the clinic for post-vaccine
Fleas (Ctenocephalides spp.)
The same fleas that can be found on dogs and cats can also be found on pet ferrets. Fleas
are spread through direct contact with other infested animals or contaminated environments.
Some infested ferrets will be clinically normal. When clinical disease does result, any combination
of the following signs may be encountered: pruritus, alopecia, erythema, scabs, and anemia.
Diagnosis is by visualization of fleas or flea feces.
The ferret, its home environment, and all infested household pets must be treated. Most
products that are safe for kittens are also safe for ferrets. As with many medications used in
exotic animal medicine, the use of most flea products in ferrets is extra-label. One exception is
imidacloprid (Advantage, Bayer Animal Health). In 2001, Bayer Animal Health published a study
showing that topical imidacloprid administered topically at a dose of 10mg/kg or one 0.4 ml 10%
pipette per ferret, was well tolerated and effective in removing established flea populations.
The same ear mites (Otodectes cynotis) that can be found on dogs and cats are also
frequently found on pet ferrets. Ear mites are spread through direct contact with other infested
animals. The vast majority of infested ferrets will be clinically normal. When clinical disease does
result, any combination of the following signs may be encountered: brown wax or crust in the ear
canals, head shaking, scratching at the ears, or erythema of the ear canal. Severe secondary
bacterial infections can occur, but are rare.
Diagnosis is by direct visualization of mites on otic exam or by identification of the mites or
mite eggs during microscropic examination of debris from the ear canal. The mere presence of
debris in the ear canal is not diagnostic of ear mites because many normal ferrets have brown,
waxy exudate in their ears.
The ferret and all infested pets must be treated. Treatment with ivermectin (Ivomec 1%
Injection for Cattle, Merck-Ag VET) is very effective. Administer 0.2-0.4 mg/kg SQ every 2 weeks
for 3-4 treatments. Topical selamectin (Revolution-Pfizer Pharmaceuticals) applied monthly has
been anecdotally used at 16 mg/kg. Milbemycin oxime (MilbeMite, Novartis) has been recently
introduced as a one-time topical ear mite treatment for dogs. It has been used anecdotally with
success in ferrets.
Intestinal parasites are fairly uncommon in pet ferrets; however, they should be included on
any complete differential diagnosis list for a ferret with diarrhea. They occur more commonly in
young ferrets at pet stores, those spending time in close proximity to infected puppies or kittens,
and those spending a lot of time outdoors.
Some ferrets infected with intestinal parasites will be clinically normal. When clinical disease
does result, any combination of the following signs may be encountered: diarrhea with or without
blood, weight loss, dehydration, decreased activity, dull hair coat, straining to defecate and rectal
Diagnosis of intestinal parasites in ferrets is made via standard laboratory techniques i.e.
microscopic examination of a fecal flotation and a fresh wet mount. Wet mounts made with saline
are superior to those made with water.
Coccidiosis is the most common internal parasitic disease of ferrets. Both Isospora (I.
laidlawi) and Eimeria (E. furonis and E. ictidea) have been identified. Infections can potentially
pass between ferrets, puppies, and kittens. Treatment is effective when using the same sulfa
drugs used in dogs and cats: ie; sulfadimethoxine or trimethoprim-sulfadiazine. Rectal prolapse
should be treated with a temporary purse-string suture. If rectal prolapse becomes a recurrent
problem a surgical colopexy can be performed. As with any disease causing diarrhea and
potential dehydration, fluid therapy and other supportive care should be included on a case-by-
Infection with intestinal helminths is rare, but can occur. Toxascaris leonina, Toxocara cati,
Ancylostoma caninum, and Dipylidium caninum have all been reported. Nematodes can
potentially pass between ferrets, puppies, and kittens and should be considered a potential
zoonosis. Treatment is effective when using the same drugs used in dogs and cats: pyrantel
pamoate, piperazine, fenbendazole, and ivermectin.
Giardiasis can potentially pass between ferrets, puppies, and kittens and should be
considered a potential zoonosis. Treatment is with metronidazole or fenbendazole.
Heartworm (Dirofilaria immitis) infection in the ferret has been reported in natural as well as
experimental settings. The lifecycle and transmission of the parasite is similar to the dog. Lower
worm burdens (1-10 adults) cause severe disease in ferrets due to the small size of the heart. All
ferrets in heartworm endemic areas are at risk of infection.
Signs of heartworm disease include dyspnea, cachexia, lethargy, pulmonary congestion,
ascites, coughing, and sudden death. The diagnosis of heartworm disease in ferrets is based on
clinical signs, radiography, echocardiography, and results of antigen and microfilaria testing.
Cardiomegaly and mild to severe pleural effusion are the most common radiographic findings.
Test sensitivities in ferrets have not been reported. Low worm burdens may cause false negative
antigen tests and peripheral microfilaremia is uncommon. ELISA antigen tests (in particular the
IDEXX Snap test, IDEXX Laboratories, Inc., Westbrook, ME) have proven useful in detection of
infected ferrets. Visualization of adult parasites in the right atrium, right ventricle and vena cava
using echocardiography has been reported.
All ferrets in heartworm endemic areas should be on year-round preventative therapy. There
are a variety of effective medications available. Ivermectin is most commonly recommended.
Proposed dosages range from 0.02-0.05 mg/kg/month PO or SQ. This higher dose has
anecdotally been reported to be safe and will not only prevent heartworm disease, but will
also slowly kill any existing heartworms that may already be present and undiagnosed. A 0.5
mg/ml suspension is easily prepared by mixing 0.5ml injectable ivermectin (Ivomec 1%
Injection for Cattle, Merck AgVET) in 9.5ml propylene glycol. This solution is dosed at
0.1ml/kg/mo to achieve the 0.05mg/kg/mo dosing level. The mixture should maintain potency
until the expiry date of the ivermectin if protected from the light.
Selamectin (Revolution) has been anecdotally dosed at 16mg/kg for heartworm prevention.
Most ferrets are descented (had their anal sacs removed) and neutered at a very young age
before they even reach the pet store. Although these surgeries will decrease their odor, it will not
eliminate their characteristic musky smell.
Ferrets should be surgically neutered for behavioral and health reasons. Neutered males will
be less aggressive. Jills are seasonally polyestrus and induced ovulators. If not mated, will
remain “in heat” for prolonged periods and succumb to anemia and/or thrombocytopenia from
Castration can be performed in similar fashion as the cat with open scrotal incisions and
ligatures around the spermatic cord. Some veterinarians prefer to perform a prescrotal closed
castration technique as that employed in the dog. The ferret ovariohysterectomy is technically
similar to the cat.
Gastrointestinal Disease: Diarrhea and Vomiting
As a general rule, diarrhea is very common in ferrets, whereas vomiting is a less common
gastrointestinal sign in ferrets.
Has there been a diet change?
Any new ferrets added to the household?
Is your ferret allowed to free-roam unsupervised?
Has your ferret been grinding its teeth or pawing at the mouth?
Is your ferret vomiting and if so how often?
What is the character of the diarrhea and how long has it been going on?
Is your ferret still eating or drinking?
hydration status - evaluate and determine best method to correct dehydration.
body temperature– subnormal temperature may be an indication for hospitalization and
use of an incubator.
abdominal palpation- check for foreign bodies, hairballs, abdominal pain, splenomegaly
or other organomegaly.
mucous membranes- color and tackiness.
fecal (floatation, direct exam, cytology) - Check for intestinal parasites and bacterial flora.
CBC and blood chemistries- important to check for hypoglycemia, metabolic disease
Radiographs- start with plain films and perform a barium series when indicated.
Ultrasonography- assess for foreign bodies, organomegaly, neoplasia.
Specific therapy depends on diagnosis, severity of signs and physical condition of the
patient. At home therapy is a viable option if the ferret is hydrated, still eating, and not
vomiting profusely. A variety of medicines may be used to help control diarrhea and
vomiting and need to be tailored to the specific case. Subcutaneous fluids can be
administered on an out patient basis. For ferrets with significant dehydration, anorexia and
lethargy, hospitalization is strongly recommended. An IV catheter should be placed and
treatment initiated, including fluid therapy and medications; based on history, physical
exam and diagnostics.
Roundworms and hookworms are possible. Diagnose this with a fecal floatation and treat
with pyrantel pamoate or fenbendazole at previously listed doses. Giardia is also possible
and can be treated with fenbendazole or metronidazole. Coccidia (Eimeria spp. and Isospora
sp) is not uncommon and can be treated with sulfa antibiotics.
Inappropriate or poor diet or dietary indiscretion can lead to diarrhea. Treatment is to correct
the diet and stop the indiscriminate offering of snacks. Antidiarrheal medications and
supportive care as needed, but many cases are self-limiting.
Diarrhea has been associated with hypoglycemia, urinary tract infections, adrenal disease
and stress. Treatment consists of diagnosing the primary illness and correcting it.
Gastrointestinal obstruction is a common problem, especially in ferrets less than one year of
age. Ferrets have a tendency to chew and ingest rubber objects of any kind, especially foam
rubber, and will occasionally ingest cloth or other foreign materials. This behavior tends to greatly
decrease in mature ferrets. In the older animal, obstruction with trichobezoars becomes a more
frequent cause of gastrointestinal obstructive disease.
In ferrets, the clinical signs associated with GI foreign bodies vary greatly. In cases of gastric
foreign bodies that are not causing acute obstructive disease, the signs can be vague and include
any combination of the following: intermittent anorexia, decreased volume of stools, tarry stools,
depression, gradual weight loss with eventual severe wasting, pawing at the mouth, teeth
grinding and salivation. Vomiting does occur, but is not as frequent a finding as in dogs or cats
with gastric foreign bodies. The ferret may become irritable and aggressive due to chronic pain.
When a complete obstruction occurs, whether it is at the pylorus or in the small intestine, the
signs are much more dramatic. The patient will exhibit severe depression and dehydration,
vomiting is more common, stools are scant and tarry and abdominal distention (caused primarily
by a gas-filled stomach) may be present. These patients also demonstrate abdominal
pain/splinting and may grind their teeth and paw at their mouths.
The differential diagnoses for gastrointestinal disease include: lymphoma or other neoplasia,
Inflammatory Bowel Disease, gastric ulcers, epizootic catarrhal enteritis, parasites, and
Helicobacter. The diagnosis is based primarily on history, physical examination and radiography.
The ferret abdomen is easily palpated and foreign material in the stomach or intestine may be
identifiable. Survey radiographs are used to look for signs of gastrointestinal tract obstruction or
the foreign body itself. Radiographic signs of gastrointestinal obstructive disease may include; a
stomach grossly dilated with air and fluid, loops of bowel distended with gas, or dense material
evident in the stomach or intestines. Be aware, that plain radiographs are non-diagnostic in many
cases and definitive diagnosis may necessitate a barium series be performed in order to outline
foreign bodies, hairballs or demonstrate a complete obstruction. The barium dosage is 12-
15ml/kg, and due to the ferret‟s short gastrointestinal transit time, a full barium series may be
completed in two hours. Any gastrointestinal barium retention greater than 30 minutes is
Exploratory surgery and subsequent gastrotomy or enterotomy is the treatment of choice for
GI foreign bodies. If surgery fails to reveal a foreign body, biopsy samples should be obtained
from representative sections of the gastrointestinal tract. Number four PDS suture material works
well to close gastrotomy or enterotomy sites. Pain medication is recommended post operatively.
Ferrets are excellent surgical candidates, and in general the prognosis is good. Supportive
care with intravenous crystalloids, electrolytes, and dextrose helps to minimize post-operative
recovery time. Many ferrets are well recovered and ready to eat within 12 hours post-operatively.
Other ferrets may require hand feeding for several days with a high calorie supplemental diet
such as Hills a/d or another enteral solution. If severely debilitated, placement of an
esophagostomy tube is a convenient way to provide nutritional support for extended periods. The
resting energy requirement (RER) of ferrets is 70 kcal/day.
Vigilant “ferret proofing” of the home, to keep potential foreign articles out of the ferret‟s
reach, and monitoring playtime will help control inadvertent ingestion of a foreign body. Hairball
remedy has been recommended every other day during heavy shedding as a preventative for
hairballs. Brush regularly and change bedding frequently to decrease the amount of loose hair in
Helicobacter is a normal inhabitant of ferret stomachs. H. mustelae colonizes nearly 100
percent of ferrets shortly after weaning, and may cause a progressive inflammatory response in
the stomach lining over the lifetime of the ferret. It is interesting to note that a different species of
this bacterium, H. pylori, has been definitively incriminated in development of ulcers in humans.
The signs of gastric ulceration can be difficult to detect. Some ferrets show subtle signs of
lethargy and poor appetite. The stools may become soft and occasional vomiting may be
seen. As the disease progresses, the ferret will start to pass dark, tarry stools indicative of
upper gastrointestinal bleeding, as well as show signs of abdominal discomfort; grinding of
the teeth and increased salivation. Anemia, more severe weakness, dehydration and
anorexia may follow. There is some thought that gastric adenocarcinoma and lymphoma may
be the result of long term antigenic stimulation associated with chronic H. mustelae infection.
GI biopsies for histopathology (Warthin-Silver stain) and culture (place biopsy specimen in 1
ml phosphate-buffered saline and store on ice until culture set up) are necessary for definitive
diagnosis and many practitioners choose to treat based on clinical signs and lab work and/or
radiographs to rule out other causes of similar GI signs. A treatment regimen similar to the
one employed for humans can be initiated on the clinician‟s discretion; amoxicillin (20 mg/kg
PO q8hr), metronidazole (20 mg/kg q8hr) and bismuth subsalicylate (pepto-bismol, 17.5
mg/kg q8hr). A H2 blocker; famotidine( pepcid, Merck 0.25-0.5mg/kg PO, IV q 24h) or
cimetidine (10 mg/kg PO q8hr) or a proton pump inhibitor; omeprazole (0.7 mg/kg q24hr)can
be used in conjunction with the antibiotics. An alternative regimen is ranitidine bismuth (24
mg/kg q8hr) and clarithromycin (50mg/kg q24h or divided q12h). The author has found good
success with a combination of amoxicillin, metronidazole and famotidine at above dosages.
With all treatment regimens continue treatment for 2 to 4 weeks.
Epizootic catarrhal enteritis (ECE), also known as “Green Slime Disease”, is a
gastrointestinal disease that has been affecting the domestic ferret since 1993, when it was first
identified in several ferret shelters in the United States and Canada. Recently, research at Purdue
University by Dr. Matti Kuipel and colleagues has definitively identified a coronavirus as the
causative agent in this disease. Unfortunately, efforts to isolate and propagate this virus have not
been successful. Histopathologic lesions seen with ECE include intestinal villar atrophy, fusion
and blunting, often with concurrent lymphoplasmacytic enteritis. Varying degrees of hepatic
lipidosis have also been reported. The disease is extremely contagious, and can be spread by
ECE is commonly diagnosed following introduction of a new ferret, often a juvenile that
serves as an asymptomatic carrier, into a household with pre-existing ferrets. In this scenario,
ferrets already living in the household may break with the disease within 2-3 days. This short
incubation period contributes to a morbidity that approaches 100% once the disease is introduced
into a household or ferret shelter. Vomiting, anorexia and lethargy are often the earliest clinical
signs, but may be missed by the owner, especially in the multi-ferret household. These early
manifestations of infection are rapidly followed by the development of a profuse, watery to
mucoid, green stool. There have also been reports of diarrhea with frank blood, or black tarry
stools, especially in older, severely affected ferrets. Melenic stools may also be seen in ferrets
with concurrent or secondary Helicobacter gastritis. Although the greenish, mucoid diarrhea is the
sign that is responsible for the layperson‟s name for this syndrome, this is not pathognomonic, as
any form of enteritis that results in rapid GI transit time can cause this type of stool in the ferret.
As the diarrhea resolves, the stool may often take on a grainy appearance, which is an indication
of intestinal malabsorption. Some ferrets may have permanent intestinal damage, leading to
continued weight loss and poor body condition.
Diagnosis of ECE is based on history of exposure to a possible carrier ferret and associated
clinical signs. Clinical pathology is nonspecific and largely related to dehydration and
inanition. Complete blood counts may be normal or show a slight elevation in WBC numbers
(10,000 – 11,000) as well as an increased PCV and total protein secondary to dehydration. In
prolonged cases there may be a monocytosis and slight anemia. Azotemia, hyperglycemia,
and elevated alanine aminotransferase (ALT) and serum alkaline phosphatase (SAP) have
been seen in affected animals. ALT, values as high as 1000 U/L, and SAP values of 200 U/L
or greater, are not uncommon when heptatic lipidosis occurs in anorexic ferrets. Abdominal
radiographs are also nonspecific; they may be completely normal or show gastric distension
or a segmental ileus that can mimic an obstructive pattern.
The cornerstone of treatment of affected animals includes subcutaneous or intravenous fluid
therapy and nutritional support, which are tailored to the severity of the disease. In the severely
dehydrated patient, intravenous fluid therapy is instituted at the rate of 100-150 ml/kg/day. If there
are significant ongoing losses from diarrhea, these rates may need to be increased to maintain
hydration. Maintenance fluid requirements in the adult ferret are estimated at 75-100 ml/kg/day. In
the older ferret with suspected or confirmed cardiovascular disease, rates should be adjusted to
avoid fluid volume overload. Tailor the administered crystalloid to electrolyte, glucose and other
clinical pathology values. If the ferret is not as severely affected, the owner may be instructed in
how to administer subcutaneous fluids at home. Total intake should be divided and given every 8-
12 hours. Most ferrets can readily absorb 30-60 ml subcutaneously, depending on size and body
condition. If the ferret must be hospitalized, strict adherence to isolation procedures is advised, as
ECE is highly contagious.
Nutritional support as described previously is extremely important. If the ferret will not accept
syringe-feeding placement of an esophagostomy tube should be considered. In addition,
some clinicians have successfully used parenteral nutrition utilizing a feline formulation
adapted to the ferret‟s increased requirement for fat and protein.
Because the causative agent has not been isolated, specific diagnostic tests and vaccines
have not been formulated against this agent. As a result, the best way to prevent ECE is to
control exposure to other ferrets or fomites that might harbor the causative agent. This
includes exposure at shelters, pet shops, or ferret shows. Affected ferrets will shed the virus
for up to six months following infection, which makes quarantine procedures impractical when
a new ferret is added to the household. As a result, veterinarians should warn owners of the
danger of this disease through the introduction of an unapparent carrier.
Inflammatory Bowel Disease
Inflammatory Bowel Disease (IBD) is a general term for a chronic inflammatory process in
the gastrointestinal tract, for which an etiologic agent in not identified. The inflammation is
primarily lymphoplasmacytic in ferrets, especially in the stomach, but about 50% of cases
may also have a lesser eosinophilic infiltrate as part of the intestinal inflammation. Possible
causes of IBD include; hypersensitivity (atopy or food), infectious disease, metabolic disease,
or any factor that can trigger an aberrant immune response.
A chronic or intermittent diarrhea is the hallmark of IBD. Stools may vary in quality from
green or mucousy, to melena, to loose “birdseed” stools, to watery. Vomiting may or may not
be seen and ferrets may show intermittent teeth grinding indicative of abdominal discomfort.
Many ferrets show somewhat subtle signs of inactivity, periodic diarrhea and weight loss.
Clinical pathology supportive of possible IBD includes; elevated lipase and globulin levels,
possible lymphocytosis, neutrophilia or eosinophilia, and/or elevated ALT and GGT.
Definitive diagnosis is based on histopathology of surgical biopsies. Full thickness
biopsies of stomach, duodenum, jejunum, as well as gastric and duodenal (peripancreatic)
lymph nodes is recommended. The liver is biopsied if serum chemistries indicate liver
inflammation. A pathologist familiar with ferrets is recommended as intense antigenic
stimulation of regional lymph nodes, as a result of chronic gastrointestinal inflammation, may
make interpretation of node microscopic architecture difficult. Lymphoma may be a sequela
of chronic untreated IBD, and those ferrets with advanced lymph node atypia need to be
monitored closely for signs consistent with systemic transformation to lymphoma.
Treatment is aimed at eliminating any underlying contributing factors such as Helicobacter
or food allergies and suppressing the inflammatory response. Any cases where biopsies
confirm bacteria morphologically consistent with Helicobacter or where gastritis and little or
no enteritis is found should be treated for Helicobacter. Food allergies can be addressed by
changing to a hypoallergenic diet with a novel protein and carbohydrate source. This may be
somewhat of a challenge in the highly carnivorous ferret. Hills z/d Feline® and IVD Duck and
Green Pea Feline® have been tried with some success. Azathioprine and prednisolone have
both been used to suppress the inflammatory response associated with IBD. Patients with
IBD often require long term or life long treatment and therefore prednisolone at the
immunosuppressing dose of 1 mg/kg or higher q24h may result in more undesirable side
effects (muscle wasting, pot belly, general decline in strength, refractory to treatment for later
onset of insulinoma or lymphoma) than azathioprine. Azathioprine is dosed at 0.9 mg/kg PO
q72 h with mild gastroenteritis, q48h with moderate gastroenteritis and q24h with severe
gastroenteritis. All patients with lymph node atypia receive azathioprine every 24 hours.
Response to azathioprine is gradual and improvement may take several months. Monitor
serum chemistries and CBC values for evidence of improvement or possible drug toxicity
Adrenal-associated endocrinopathy (hyperadrenocorticism) in ferrets is a well-known,
frequently occurring disease in ferrets. It can be caused either by adrenal hyperplasia or
neoplasia (most commonly cortical adenoma or adenocarcinoma). In many cases the enlarged
adrenal gland shows a mixed histological picture with adenocarcinoma cells being in the majority
as the disease progresses. Metastasis is very uncommon and most adrenal neoplasms tend to
be locally invasive rather than metastatic.
In humans, dogs, cats and horses the clinical signs associated with hyperadrenocorticism
(alopecia, muscle wasting and skin atrophy) are the result of increased levels of plasma cortisol.
A disparate situation occurs in the ferret where increases in plasma levels of estradiol,
androstenedione, 17 α-hydroxy progesterone and dehydroepiandrosterone sulfate (and not
cortisol) result in physical changes dominated by features of excessive production of these sex
hormones. Adrenal disease in ferrets causes an array of clinical signs, with the most common
being a bilaterally symmetrical alopecia, usually starting at or near the base of the tail and
proceeding cranially along the body, sparing the head and extremities in most cases. As a result
of seasonal hormonal changes, this alopecia may regress and the ferret return to normal coat for
a season or two before hair loss begins again. In advanced cases there may be little or no hair
remaining. Ferrets with adrenal disease may also show behavioral changes involving a return to
sexual behaviors or aggression, and in some cases these behavioral changes may be the only
clinical sign observed. Females may show an enlarged vulva, while males may have prostatic
enlargement with secondary cystitis, prostatitis and dysuria. Less common signs seen in ferrets
with adrenal disease include; polydipsia, polyuria, increased pruritus, odor, lethargy or muscular
atrophy of the hind limbs and abdominal musculature.
In the United States it has been proposed that early neutering, in many cases as early as 4-6
weeks of age, contributes to this high incidence of ferret adrenal gland disease. In The
Netherlands, where ferrets are commonly neutered at an older age of 12-18 months, adrenal
disease is also common. This is in contrast to the United Kingdom where most ferrets are left un-
neutered and ferret adrenal disease is seldom diagnosed. In 2003 Dr. Nico Schoemaker
published his thesis; Hyperadrenocorticism in Ferrets. In this thorough study of ferret adrenal
disease he found that results of previous studies revealed that characteristics of
hyperadrenocorticism in ferrets resemble those of some strains of mice in which nodular
adrenocortical hyperplasia and adrenocortical tumors occur in one or both adrenals after
neutering at an early age. This correlated with Dr Schoemaker‟s findings that suggest that
castration also plays a role in the pathogenesis of ferret hyperadrenocorticism and that the age of
neutering was found to significantly correspond with the age of onset of ferret adrenal disease.
This study of a Dutch ferret population revealed that the interval between age at neutering and
age at diagnosis of adrenal disease was 3.5 ±1.8 years and is similar to a United States
population study by Rosenthal, et al (3.3 ± 1.4 years). In the Dutch study the mean age of ferrets
with initial diagnosis of hyperadrenocorticism, 5.1 ± 1.9 years, was significantly older than those
in the American study (3.4 ± 1.4 years), which corresponds with the older age at which most
ferrets are neutered in The Netherlands.
Dr Schoemaker went on to perform immunohistochemical staining of the pituitary gland and
found that in 6 of 10 ferrets with hyperadrenocorticism, only a few cells stained positive for
gonadotropes (the granules of which secrete LH and FSH), which corresponded with what he
found in healthy intact ferrets. A possible explanation may be that hormones secreted by the
abnormal adrenal cells, such as estradiol, exert a negative feedback on pituitary gonadotropes.
Two pituitary glands had evidence of neoplasia and 8 had no abnormalities. These findings
suggest that hyperadrenocorticism in ferrets is unlikely to be the result of persistent stimulation of
the adrenal cortex as a result of a primary lesion of the pituitary gland.
Positive immunohistochemical staining confirmed the presence pf LH receptors in the
cortices of adrenal glands from healthy intact ferrets as well as ferrets with hyperadrenocorticism.
Part of Dr Schoemaker‟s thesis study involved gonadotropin releasing hormone (GnRH)
stimulation tests performed to determine the functionality of these LH receptors. Plasma
androstenedione and 17 α-hydroxyprogesterone concentrations increased after stimulation with
GnRH in 7 out of 8 hyperadrenocorticoid ferrets but only 1 out of 7 healthy neutered ferrets,
supporting the hypothesis that adrenal disease may be associated with expression of LH
receptors on those adrenocortical cells responsible for producing sex steroids. Dr Schoemaker
hypothesized that LH-R protein might be present in adrenal cortices of young, intact or neutered
ferrets, however in a desensitized nonfunctional state. Activation of this pre-existent receptor
protein into a functioning LH receptor could be associated with the metabolic/hormonal
derangement seen with the neoplastic transformation of the adrenal cortex. However, it is not
clear whether this activation is a prerequisite for hyperplasia and/or neoplasia or a consequence
of cell transformation.
Dr Schoemaker also demonstrated that lack of negative gonadal hormonal feedback on
hypothalamic GnRH, as a result of neutering, results in persistently elevated gonadotropic LH and
that persistent LH stimulation may lead to adrenocortical hyperplasia and finally autonomous
hypersecretion due to tumor transformation. This hypothesis is supported by studies in mice
where LH receptors can function as tumor promoters as a consequence of persistent hormonal
For several years veterinarians have been blaming the development of adult onset ferret
adrenal disease on the early age at which ferrets are commonly neutered in the United States.
Dr. Schoemaker‟s survey of Dutch ferret owners showed that this disease is prevalent even when
ferrets are neutered at a mature age and that there is a strong association between age at
neutering and age of onset of hyperadrenocorticism. So it appears that it is the neutering itself
that sets the stage for later development of hyperadrenocorticism versus the age at which these
ferrets are neutered. Some veterinarians would advocate that this demonstrates a strong medical
reason for leaving ferrets intact. However, we need to recall why routine neutering was originally
recommended. Ovarioysterectomy became routine in the early 1980's after publication of studies
showing estrogen induced bone marrow suppression in jills with prolonged estrus (recall ferrets
are induced ovulators). We also know that castration of hobs reduces aggression making them
more loving pets and also allowing them to be housed in groups. In both sexes, neutering
decreases the intensity of the musky odor produced by the sebaceous glands. As a result,
neutering benefits the ferrets overall health and desirability as a pet. For these reasons, the
focus now needs to be on development of alternatives to surgical neutering that accomplish the
same medical and behavioral goals without predisposing to hyperadrenocorticism. Thanks to Dr.
Schoemaker‟s detailed endocrine analysis, we now have an understanding of the pathogenesis of
ferret hyperadrenocorticism. This not only allows us to understand why and how leuprolide
therapy works in the treatment of adrenal disease, but also serves as a framework as we search
for future medical therapeutic and preventative options.
The diagnosis of adrenal disease in ferrets is frequently straightforward and can often be made
on history and clinical signs alone. A skilled practitioner may be able to palpate an enlarged
adrenal gland. Ultrasonography may identify an enlarged gland a (7.5 frequency with the near
gain turned on high), and offers the benefit of determining if right, left or both adrenals
are affected. For questionable cases, laboratory testing may be helpful. The University of
Tennessee provides an assay that measures plasma concentrations of
androstenedione, 17 α-hydroxyprogesterone and estradiol. In approximately 85% of ferrets
with hyperadrenocorticism there is unilateral adrenal enlargement, while in the other 15% of
cases bilateral enlargement is seen. Evaluations of cortisol levels are not helpful in diagnosis.
Clinical manifestation of signs may vary depending on which sex steroid is higher in
concentration, and clinical signs do not correlate with degree of adrenal gland neoplasia or in all
cases, level of hormone elevation. Seasonal alopecia in many ferrets may be a normal
physiological occurrence and should not be confused with adrenal disease. Diagnostics are
needed to confirm the presence of adrenal disease. These include the sex hormone serum panel
(University of Tennessee has the only validated test in ferrets), ultrasound or laparotomy to assess
the glands, and biopsy with histopathology.
University of Tennessee Ferret Adrenal Normal Values
hormones Normal Range
Estradiol pmol/L 30-180
17α-hydroxyprogesterone nmol/L 0-0.8
Androstenedione nmol/L 0-15
Complete blood counts and serum chemistries will be within normal limits in the vast majority
of animals, with the exception of long standing cases in which anemia and thrombocytopenia
may be seen.
In my 4 years of hormone studies, by the time there is hair loss on the tail, the
hormone levels are out of control. the idea is to keep this from happening. hair
loss is only present when estradiol ratios are higher than androstenedione. If
andros is higher, hair grows just fine. – Cathy Johnson-Delaney
Surgery. The most effective treatment for adrenal disease in ferrets has been and remains
surgical removal of the affected gland(s). For ferrets that are not surgical candidates there are
now several medical alternatives. It must be noted that these drugs do not suppress adrenal
growth, but rather block the clinical signs.
Leuprolide acetate (Lupron- TAP Pharmaceuticals) is the most effective agent currently
available. Lupron is a long-acting gonadotropin-releasing hormone analog that inhibits the release
of LH and FSH from the pituitary. It is available as a daily injection or as a 30 day, three or four
month depot. Clinical trials using the 30-day depot Lupron therapy at 100 mcg per ferret has
resulted in complete regression of clinical signs within one to four weeks of treatment . However,
regression may take up to three months to occur and can vary in these hormonally "seasonal"
animals. With long term Lupron management sonography may be used to monitor adrenal size.
An increase in adrenal gland size may indicate progression of adrenal disease with
adenocarcinoma as the majority cell and the need to increase the dose of Lupron to 200mcg or
more per ferret is not uncommon. Lupron can be divided into aliquots and frozen for at least a
year in a household freezer
Flutamide (Eulexin) is an antiandrogenic whose effects are mediated by the inhibition
of the uptake and/or nuclear binding of testosterone and dihydrotestosterone by prostatic
tissue. Seems helpful in shrinking prostate tissue in cases of prostatic hyperplasia
secondary to adrenal disease. Useful prior to adrenal/prostate surgery to help these
patients become better surgical candidates, or while waiting for Lupron to kick in. Dose is
10 mg/kg q12-24h PO.
Melatonin at 1-2 mg/ferret, given eight-nine hours after sunrise may be effective in reversing
clinical signs in some ferrets. It is believed that this increase in natural melatonin suppresses the
release of hypothalamic gonadotropin releasing hormone (GnRH), and subsequently inhibits the
release of pituitary LH. Regression of clinical signs, for up to 12 months has been reported
Insulin-secreting pancreatic islet cell tumors are among the most common neoplastic
diseases affecting ferrets. Synonyms include functional islet cell tumor, pancreatic B-cell tumor,
pancreatic endocrine tumor and insulinoma.
The disease affects both male and female ferrets between the ages of 2 and 8 years, but is
most commonly diagnosed in ferrets 4 to 5 years of age. On histopathologic examination beta cell
carcinoma is most often found, sometimes in combination with beta cell adenoma or hyperplasia.
Metastasis is uncommon; however, when it does occur it is usually to the regional lymph nodes,
spleen or liver.
The neoplastic pancreatic beta cells secrete excessive amounts of insulin. The resulting
hyperinsulinemia inhibits hepatic gluconeogenesis and glycogenolysis and stimulates the uptake
of glucose by peripheral tissues; resulting in hypoglycemia. In normal animals, low blood glucose
stimulates the release of glucagons, cortisol, epinephrine and growth hormone. These hormones
act to increase blood glucose concentrations by stimulating gluconeogenesis and glycogenolysis
in the liver and by inhibiting peripheral tissue use of glucose. In the ferret with insulinoma this
feed back mechanism is inoperable.
The rate of development, magnitude, and duration of hypoglycemia are factors determining
the severity of clinical signs that can be categorized as neuroglucopenic, adrenergic or a
combination of both. Neuroglucopenic signs result from the effect of low blood glucose on the
central nervous system and include mental dullness confusion, seizures and coma. Adrenergic
manifestations occur when blood glucose levels drop rapidly, resulting in catecholamine release
and increased sympathetic tone. Adrenergic signs include tachycardia, hypothermia, tremors,
nervousness and irritability. Prolonged, severe hypoglycemia can result in cerebral hypoxia and
possibly, irreversible cerebral lesions. Lastly, severe hypoglycemia may lead to episodic seizure
activity and coma. All of these signs may be intermittent, with varying periods of normal activity in
Some ferrets experience acute episodes of hypoglycemia with collapse into a recumbent,
non-responsive state. These episodes may last several minutes to hours with spontaneous
recovery or response to administration of an oral glucose solution. Other ferrets demonstrate
a gradual onset of weakness and lethargy over weeks to months in which the affected ferret
shows intermittent signs varying from pronounced weakness and ataxia, particularly in the
rear limbs, to hypersalivation, bruxism, pawing at the mouth and other signs of nausea
associated with hypoglycemia.
The definitive diagnosis of insulinoma depends on the histopathologic examination of
pancreatic tissue. However, in most ferrets a diagnosis of insulinoma is made before surgery, by
demonstration of hypoglycemia in association with history and clinical signs. Other causes of
hypoglycemia should be ruled out including anorexia/starvation, severe GI upset, sepsis,
neoplasia and hepatic disease.
The serum glucose concentration required for diagnosis of hypoglycemia in the ferret is a
matter of some debate. However, most clinicians agree that a 4-hour fasting glucose
concentration of less than 70mg/dl is very suggestive of insulinoma. The reference range for
normal fasting blood glucose concentrations in ferrets is 90 to 125 mg/dl. If blood glucose levels
are suspicious but inconclusive, serum or plasma insulin levels can be measured at a laboratory
that has validated the assay for ferrets. Normal ferret insulin concentrations are reported to lie
between 4.88 and 34.84 in mcU/ml. It should be noted that a normal plasma insulin level does
not rule out insulinoma and is not necessary for definitive diagnosis.
Emergency therapy of the collapsed hypoglycemic ferret involves administration of slow
boluses of 50% dextrose intravenously at the minimal amount needed to control clinical signs.
Too rapid an administration of IV dextrose may cause a rapid release of insulin, resulting in a
more severe “rebound” hyperglycemia. Hospitalization and continuous infusion of 5% dextrose
may be necessary to stabilize the patient.
Long term treatment options include dietary, medical and/or surgical management, and many
ferrets require a combination of all three to successfully control the clinical signs of hypoglycemia
associated with insulinoma. The choice of therapy depends on severity of clinical signs, the age
of the ferret, concurrent disease, and the owner preference.
Medical therapy in most cases will effectively control clinical signs of hypoglycemia, but will
not stop progression of insulinoma. Prednisone and diazoxide (Proglycem, Baker Norton
Pharmaceuticals, Inc. Miami, FL) are used singly or in combination depending on the severity of
clinical signs. Prednisone exerts its effect by promoting hepatic gluconeogenesis and reducing
cellular glucose utilization. Doses for prednisone range from 0.5 to 2 mg/kg every 12 hours. Begin
at the lowest dose and increase as needed, to control clinical signs and maintain appropriate
blood glucose levels. If clinical signs are not controlled with prednisone alone, the benzotriadizine
diuretic, diazoxide may be added to the regimen. Diazoxide works primarily by inhibiting insulin
release from pancreatic beta cells, but also reduces cellular intake of glucose and promotes
glycogenolysis and hepatic gluconeogenesis. An initial dose of 10 mg/kg divided two times daily
is added to the prednisone therapy and can gradually be increased to a maximum of 60 mg/kg
divided two times daily, if lower doses are not effective in controlling the hypoglycemia. Potential
side effects associated with diazoxide treatment include vomiting, and anorexia. The major
disadvantage of diazoxide therapy is the expense of the commercial suspension. Chemotherapy
with doxorubicin is another medical option being investigated for insulinoma therapy. Dr. Michael
Dutton has performed studies with doxorubicin therapy and found 68% (11/15) of ferrets did well
maintaining a fasting blood sugar over 80 mg/dL for at least 9 months. More studies need to be
done to see if chemotherapy is a long-term option for insulinoma control.
Dietary management is very important in controlling blood glucose levels, and indirectly
controlling insulin release. Ferrets with insulinoma should be fed many small meals
throughout the day containing high quality protein and moderate to high levels of fat. Foods
with processed sugars or high levels of simple carbohydrates (such as fruit, semi-moist
dog/cat food, cookies, etc.) should be avoided, as these can cause release of insulin and
exacerbation of clinical signs.
Long-term prognosis is determined by how quickly the insulinoma is diagnosed and by the
individual ferret‟s response to all three therapy options, alone or in combination. Ferrets that
undergo surgery generally have a longer survival time (1-3 years post op) than ferrets that
are treated with medication and dietary management alone (6 months to 1 year expected).
Regardless of which treatment option is instituted, owners need to be aware that the disease
is controlled, not cured, and that blood glucose concentrations need to be evaluated on a
Cardiology / Respiratory
Ferrets are susceptible to some types of human influenza virus and can be infected by
people. Symptoms are upper respiratory in nature and include fever, lethargy, increased tracheal
respiratory sounds, nasal discharge and anorexia. Bronchopneumonia is a rare complication.
Treatment consists of supportive care, antihistamines, cough suppressants and antibiotics (to
control secondary bacterial infections). Influenza usually runs its course in 7 - 10 days.
Diseases affecting the heart of the domestic ferret are relatively common. These diseases
include dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy (HCM), acquired valvular
disease, and myocarditis.
DCM is the most commonly encountered cardiac disease of ferrets. The cause of this
disorder is unknown. Gross pathological changes include dilation of the atria and ventricles and
thinning of the ventricular walls. Histologic examination reveals multifocal myocardial
degeneration, myocardial necrosis, and replacement fibrosis.
HCM is less common than DCM. The disease has not been sufficiently studied to establish a
cause. Gross pathological features include an abnormally thickened interventricular septum and
left free wall. Histologically, fibrous connective tissue is identified throughout the myocardium.
Valvular heart disease has been documented in the ferret. On gross exam the valves are
abnormally thickened and histologically myxomatous degeneration of the valves is recognized.
Myocarditis due to infectious disease has been reported. Multifocal myocardial necrosis due
to infection with a Toxoplasma-like organism, fibrinoid necrosis and mononuclear cell infiltration of
arterioles of the heart in Aleutian disease, and inflammatory lesions in septic ferrets have been
The signs of cardiac disease in ferrets include inappetance, weight loss, lethargy, rear limb
weakness, dyspnea, and abdominal distension. Coughing is uncommon. Physical exam findings
in ferrets with cardiac disease are similar to those in the dog and cat. Cyanosis, prolonged
capillary refill time, jugular venous distention, and pulse deficits at the femoral artery are often
detected. Left-sided holosystolic murmurs are often detected in DCM cases, whereas murmurs
are less common in HCM. Ascites may be detected.
The heart of the ferret is more caudally placed than in the dog or cat. Normal heart rate is
180-250 bpm. A pronounced sinus arrythmia is common. Be aware that scruffing the ferret will
slow the normal heart dramatically.
Diagnostic testing includes EKG, thoracic radiography, and echocardiography. The normal
EKG of ferrets has been described and several differences from the canine and feline are of note:
in lead II, the P waves are small like those of the cat whereas the R waves are large like those of
dogs. The normal mean electrical axis ranges from 70 to 97. A short QT interval and an
elevated ST segment are often seen in normal ferrets.
Thoracic radiographs may reveal an enlarged, globoid heart with increased sternal and
diaphragmatic contact in DCM but the heart may be of normal shape and size in HCM. Pleural
effusion is common, sometimes obscuring the heart. Pleural fluid analysis, including cytology, is
recommended to rule out mediastinal diseases such as lymphoma.
Echocardiography is the most sensitive and specific diagnostic test for characterization of
cardiac disease. Two-dimensional echocardiography enables objective assessment of chamber
size, shape, and function, as well as detection of pleural and pericardial masses or effusion. M-
mode echocardiography allows quantitation of chamber size and wall thickness, as well as
measuring indices of systolic function.
The principles of cardiac disease treatment in the ferret are similar to those in the canine or
feline patient. If the ferret is extremely dyspneic oxygen therapy is appropriate. Furosemide (1-
4mg/kg PO, SC, IM, IV q8-12h) is well tolerated and generic 10 mg/ml elixirs are readily available
for home therapy. Vasodilators used include nitroglycerin 2% cream (1/16-1/8 inch/animal q12-
24h) to reduce preload and aid in controlling pulmonary edema in the initial 24 hours of therapy of
heart failure. ACE inhibitors such as enalapril (0.25-0.5mg/kg PO q24h) and captopril (1/8 of
12.5mg tablet/animal PO q48h) are also mainstays of therapy. Ferrets seem to be sensitive to the
hypotensive effects of these drugs. Enalapril is usually started with every other day dosing then
increased to daily if the ferret tolerates the medication without hypotension and lethargy. Renal
function should be monitored when using ACE inhibitors. Digoxin (0.005-0.01mg/kg PO q12-24h)
is commonly used in ferrets with DCM. Pediatric elixirs are useful and well tolerated. Serum
digoxin levels should be monitored to avoid toxicity. The treatment of HCM is based on the
improvement of diastolic function and the reduction of congestion. Beta-adrenergic blocking drugs
such as atenolol (6.25mg/animal PO q24h), or calcium channel antagonists such as diltiazem
(1.5-7.5 mg/kg PO q12h) are used to reduce heart rate, improve diastolic filling, and relax the
Just like cats and dogs, ferrets may develop plaque and tartar on their teeth. Periodontal
disease has been reported and secondary bacteremia may lead to endocarditis, bronchial
disease, cystitis or kidney infections. Long-term periodontal disease may also lead to tooth loss,
gingivitis, and gum recession. Ferrets are prone to fracturing the tips of the canine teeth during
rough play, which may lead to abscessation.
Periodontal disease is often subclinical in ferrets. Routine annual physicals should include a
complete oral examination to determine the condition of the teeth and gums. Clinical signs of
periodontal disease and/or tooth root abscessation include facial swelling, pain on palpation of
the sinuses or jaw, difficulty eating, dropping food, weight loss and pawing at the mouth
Diagnosis of dental disease is based primarily on history, physical examination, and clinical
signs. Signs of periodontal disease in the ferret may mimic other diseases where nausea results
in increased salivation, pawing at the mouth, anorexia and weight loss. These diseases include:
gastric ulcerative disease, gastrointestinal obstruction, insulinoma, neoplasia, and oral ulceration
secondary to metabolic disease. Dental radiographs are recommended to determine the extent of
When tooth fracture results in exposure of the pulp, either extract the affected tooth or
perform a root canal to prevent abscessation. Tooth root abscesses of the molars and canine
teeth are treated with antibiotics prior to extraction under anesthesia. Oral clindamycin (5.5-10
mg/kg q12h) and amoxicillin-clavulinic acid (12.5 mg/kg q12h) are good choices. Standard dental
procedures practiced on cats may be applied to ferrets. Care needs to be taken during extraction
of the lower canine teeth to avoid mandibular fractures.
To prevent plaque and tartar development, recommend standard home dental care with a
finger brush or a soft child's toothbrush and an animal-approved toothpaste. Recommend
prophylactic dental scaling and polishing of the teeth as needed.
Renal cysts and polycystic kidneys have been reported in ferrets, with the incidence being
reported as high as 10-15% of ferrets necropsied. Although not uncommon, most renal cysts are
incidental findings and do not cause clinical disease. Most are found incidentally during routine
surgery, necropsy or ultrasonography (as one or more hyperechoic areas). Occasionally a ferret
presents with renal failure as a result of multiple cysts disrupting normal renal architecture,
therefore it is ideal to perform a CBC, blood chemistries and a urinalysis if renal cysts are found
There is no known specific treatment. Monitor affected ferrets with periodic palpation,
ultrasound, blood chemistries and urinalyses. There is some speculation that chronic UTI leads to
a low-grade nephritis that predisposes the kidney to cysts. For this reason, the owner should
direct immediate attention at treating UTI‟s.
Urinary Tract Inflammation (UTI)
Clinical signs of UTI include; pollakuria, stranguria, dysuria and hematuria. Another less
common finding is bruising of the genitalia. The urinalysis typically shows hematuria, pyuria and
bacteriuria. Treat with antibiotics based on cytology of urine sediment or urine culture and
sensitivity. In recurrent cases a urine culture/sensitivity should be performed and
radiographs/ultrasonography done to check for urolithiasis or prostamegaly. In addition, it is best
to rule out primary hyperadrenocorticism as cystitis and prostatitis may occur secondary to this
Uroliths are seen in ferrets and may be present in the bladder as either macroscopic calculi
or microscopic crystals. Magnesium ammonium phophate (struvite) uroliths are most common,
and urinary tact infection may or may not be present at the same time. An increased incidence
has been reported in pregnant jills. Predisposing factors may include diet, metabolic or genetic
factors and infection with urease-producing bacteria, particularly Staphylococcus and Proteus
species. Signs of urolithiasis are similar to urinary tract inflammation.
As commercial diets for pet ferrets have improved nutritionally and gained acceptance, the
incidence of urolithiasis has lessened. It is theorized that as food manufacturers have turned
away from plant-based protein diets and turned to more appropriate animal protein-based diets,
the urine pH has in turn become more acidic, and in the process discouraged formation of
magnesium ammonium phophate uroliths. Surgical removal via cystotomy is the treatment of
A fulminant, lethal infection in mink, the Aleutian Disease parvovirus is usually a chronic
latent infection in ferrets, which can cause clinical disease over a period of one to two years.
It is suspected that transmission of the virus occurs from ferret to ferret or mink to ferret by
aerolization of or direct contact with urine, saliva, blood and feces or by contacting fomites.
While the parvovirus itself causes little or no harm to the ferret host, the marked inflammatory
response generated by the ferret results in production of a large number of antigen-antibody
complexes. These circulate in the body and with time cause systemic vasculitis, most notably
in the glomerular capillaries. As the disease progresses, a marked membranous
glomerulonephritis and tubular interstitial nephritis result in eventual renal failure and death.
In addition, a marked lymphocytic-plasmacytic response interferes with bone marrow
hematopoiesis, and local accumulation of lymphocytes, plasma cells and macrophages may
result in multiple organ dysfunction and failure.
The disease was first diagnosed in ranch mink in 1946, and since mink with the autosomal
recessive Aleutian pelt color developed the most serious form of the disease, the name Aleutian
Disease was coined. Aleutian Disease was first reported in ferrets in the 1960‟s, but as recently
as 1997 a more virulent and possibly new strain of the AD parvovirus was associated with an
epizootic at a ferret rescue facility in Texas. Since then similar facility and multiple-ferret home
outbreaks have been reported in Wisconsin, Alabama, Maryland and Virginia. Despite the
increase in disease incidence, little is known about incubation, transmission, interpretation of
diagnostic tests, pathogenesis, treatment and prevention of AD in ferrets.
Aleutian Disease in ferrets can cause a wide spectrum of signs from clinically normal all the
way to death. Historically the disease is manifested by chronic, progressive weight loss, lethargy,
anemia, and melena. Other signs can include neurological (posterior paresis with progression to
an ascending paralysis, tremors, seizures, fecal and urinary incontinence), respiratory (chronic
cough, hemorrhagic interstitial pneumonia), heart disease, liver disease, and kidney failure.
Splenomegaly, mesenteric lymphadenopathy, thymic hypertrophy, and hypergammaglobulinemia
are also common. In end-stage disease, the marked hypergammaglobulinemia and vasculitis
may result in anemia and thrombocytopenia and altered platelet function with subsequent
petechial hemorrhage and clotting abnormalities. At the same time, a significant leukopenia
predisposes the ferret to secondary bacterial infections.
A presumptive diagnosis of Aleutians Disease may be based on a combination of
hypergammaglobulinemia (>20% of the total protein showing a monoclonal gammopathy),
and chronic weight loss. Ferrets with total proteins over 7.5, especially those with mildly
decreased albumins should be suspected of having AD. The diagnosis may be confirmed by
a counterimmunoelectrophoresis (CEP or CIEP) test for anti-AD virus antibodies. The CEP
test is a blood test available from United Vaccines, Madison, WI (1-800-283-6465). There is
also a new enzyme-linked immunosorbent assay (ELISA) test for antibodies to the
nonstructural proteins of the AD virus. The ELISA test can be done on either blood or saliva
and is available from Avecon Diagnostics (www. Avecon.com). All seropositive AD ferrets
should be considered persistently infected and potentially contagious.
There is no specific treatment other than supportive care at this time. Since the immune-
mediated aspects of AD cause most of the damage, immunosuppressive anti-inflammatory
therapy with prednisolone may help. Other immunosuppressive drugs such as azathioprine or
cyclophosphamide may also help, but no controlled studies have been done. In addition,
intravenous or subcutaneous fluid therapy may be needed to combat anorexia, dehydration and
kidney damage. Broad-spectrum antibiotics (Baytril, Clavamox) may be needed for opportunistic
bacterial infections, and nutritional support with Hill‟s a/d or Gerber‟s chicken or turkey baby food
is often needed.
Prognosis is guarded for this disease and depends on what extent the immune complexes
damage vital organs. Some ferrets will live for years, but unfortunately some will die within a few
months of exposure.
No vaccine against Aleutian Disease in mink or ferrets is currently available. Until an effective
vaccine becomes available, the best recommendations for preventing the spread of AD
among ferrets are: isolation of Aleutian Disease positive ferrets from Aleutian Disease
negative ferrets and environmental cleaning and disinfecting. The virus is susceptible to
mechanical cleaning as well as phenol compounds, sodium hypochlorite and quaternary
ammonium products. Mink should not be housed near ferrets. Ferret breeders, shelters and
owners of multi-ferret households should give serious consideration to testing then isolating
or culling infected ferrets.
Female ferrets are induced ovulators and roughly one half of estrous females remain in
estrus (during which time estrogen levels are high) if they are not bred or artificially stimulated to
ovulate. Ferrets are very susceptible to estrogen-induced toxicity of hematopoietic tissue. Various
manifestations of bone marrow suppression may occur including: pancytopenia,
granulocytopenia, lymphopenia, normocytic, normochromic or hypochromic, macrocytic anemia
or thrombocytopenia. Hemorrhage secondary to thrombocytopenia is a common cause of death
in these cases; therefore spaying all females not intended for breeding is highly recommended
Diagnosis is made based on a history of not being spayed, signs of estrus such as a swollen
vulva, and signs related to hematopoietic toxicity such as pale mucous membranes,
subcutaneous and mucosal petechiae and ecchymoses, melena, fever and depression. Changes
in complete blood count will also aid in diagnosis.
The goal of treatment is to bring the ferret out of estrus and provide supportive care until the
bone marrow again becomes functional (this can take days to weeks). If thrombocytopenia is not
evident and the rest of the CBC is normal, an ovariohysterectomy should be performed. If
thrombocytopenia is severe and clotting time prolonged, consider HCG at 100 U (give two doses
48 hours apart) to induce ovulation. Give supportive treatments (including supplemental iron, B
vitamins and anabolic steroids) until the ferret is in anestrus. If a subsequent CBC is normal, then
Oxyglobin (Biopure Corporation, Cambridge MA), a blood substitute, can be used safely in
ferrets for both it oxygen carrying benefits and colloidal affects. A dosing of 6 to 15 ml/kg IV over
a four-hour period has been described. Transfusion of whole blood is also possible.
Splenomegaly, a fairly common finding in ferrets, can be due to primary splenic disease, a
distant systemic disorder or may be an incidental finding. The spleen can enlarge secondary
to infectious agents, congestive states, lymphohematogenous disease, immunologic and
inflammatory diseases, storage diseases and primary and secondary neoplasms.
Splenomegaly is often present with concurrent, unrelated diseases such as insulinoma,
hyperadrenocorticism, respiratory and gastrointestinal disease. In many of these cases, the
splenic enlargement is clinically insignificant. Splenic histopathology in these cases usually
reveals extramedullary hematopoeisis or congestion or a combination of both. The cause of
extramedullary hematopoeisis in the ferret is not clear. Extramedullary hematopoiesis is
usually compensatory for myeloid insufficiency, but is commonly observed in ferrets without
evidence of anemia or other blood dyscrasias.
Clinical signs are highly variable and related to the underlying disease. Clients may describe
abdominal distention, belly dragging and decreased in activity if the spleen is large enough to
affect the ferret‟s ability to ambulate.
Rule outs for splenomegaly include: lymphoma, primary splenic disease and incidental
finding. A small percentage of ferrets with lymphoma will develop splenic involvement and
enlargement. Primary splenic tumors are rare but include hemangiosarcoma and hemangioma.
Infection with Aleutian Disease virus has been associated with splenomegaly. The presence of an
enlarged spleen may have nothing to do with the clinical signs observed or the underlying
disease found and may be an incidental finding.
A diagnostic work up of splenomegaly begins with a complete history and physical
examination. In most cases, splenomegaly is easily identified on abdominal palpation.
Irregularities on the surface (protrusions, fissures) and changes in the shape (sharp vs. rounded
edges) can often be palpated. Splenic architecture can be further characterized by ultrasound,
fine needle aspiration or biopsy.
If splenomegaly is the only abnormal physical finding on an otherwise healthy ferret a minimal
work up should include a CBC and platelet count. These values screen for hypersplenism and
may be helpful in diagnosing lymphoma. Decreased fasting blood glucose levels may indicate the
presence of an insulinoma contributing to secondary splenic enlargement. In older animals,
serum chemistries, urinalysis and full body radiographs should be performed. If diagnostics fail to
identify a concurrent disease in an apparently healthy ferret, the splenomegaly should be noted
and reexamined during future appointments. Because some diseases can be subclinical, blood
work should be repeated at least twice a year initially, especially in older patients.
Fine needle aspiration and cytological review can be used as a diagnostic tool. Be aware that this
samples a small area and may not be representative of the area of active disease. Taking fine
needle aspirations from two separate sites will provide better information. Biopsy via exploratory
surgery will provide definitive information and is recommended if primary splenic disease is high
on the differential diagnosis. The exploratory will also provide diagnostic information about
pancreatic, adrenal and other abdominal diseases.
Treatment for splenomegaly is dependent on underlying cause. Idiopathic, incidental
splenomegaly does not need to be treated unless the size of the spleen causes the ferret
consistent discomfort. A chronically enlarged spleen also increases the risk that a ferret will
suffer from a splenic rupture secondary to trauma. Clients should be warned to supervise
ferrets at play and monitor for signs of acute hemorrhage. Splenectomy is indicated in cases
of hypersplenism, splenitis, torsion, abscess, rupture and primary neoplasia. The surgical
technique is similar to that in the cat and dog.
Prognosis for ferrets with splenomegaly is variable and based on the primary underlying
disease. In many ferrets, idiopathic splenomegaly is an incidental finding. In other cases
successful treatment of underlying, maladies may correct the secondary splenomegaly.
Treatment of ferrets with hypersplenism can be rewarding, if splenectomy is performed and
cytopenias subsequently corrected. The prognosis with lymphoma varies with the ferret‟s age
and the degree of neoplastic malignancy.
Mast cell tumors or mastocytomas appear to affect both sexes equally, and present as flat
to raised, well circumscribed, tan to erythematous, hairless plaques up to 1 cm in diameter. Mast
cell tumors may be located anywhere on the body, though are most commonly found on the
trunk, neck, and shoulders. Dermatologic signs often include pruritus, alopecia, hyperkeratosis,
and the formation of a black, crusty exudates. Signs may occur intermittently. Presurgically,
these tumors may be aspirated and assessed for the presence of mast cells. On histopathology
these tumors are usually well differentiated and benign, and full excision is often curative.
Chordomas are the most common tumor of the musculoskeletal system in ferrets. They arise
from the primitive notochord and are most often seen at the tip of the tail, though they have been
uncommonly reported in the cervical and thoracic spine . The masses are usually lobulated,
smooth, firm, well demarcated, and occasionally ulcerated. While they seldom metastasize, they
are often quite invasive to the surrounding tissue. Amputation of the tail at the second
intervertebral space cranial to the mass is necessary to ensure complete removal.
Histopathology and immunohistochemistry of the mass will differentiate it from other common
musculoskeletal tumors such as chondro(sarco)ma and osteo(sarco)ma.
Apocrine gland neoplasms include cysts, adenomas, and carcinomas, and are most
commonly found on the head, neck, prepuce, and vulva. Focal swelling and alopecia are the
common presentation of all three types, while carcinomas can present with necrosis. Metastasis
of carcinomas may occur to the local lymph nodes.
Osteomas are firm, dense masses reported on the parietal bone, zygomatic arch, and
occipital bone of the skull. Osteomas are generally radiodense and lack the typical sunburst
appearance and variable lucency associated with osteosarcomas. While usually benign, they
cause disfigurement, discomfort and potentially seizures or other central nervous system signs by
exerting pressure on surrounding tissue.
Sebaceous epitheliomas and baso-squamo-sebaceous tumors are very similar clinically to
basal cell tumors, and diagnosis of specific tumor type is based upon histopathology and
cytology. These tumors are usually benign and surgery is curative.
Malignant lymphoma is a common diagnosis in pet ferrets. In a retrospective study of 574
ferrets with neoplastic disease, Li, et al found that 15.2% were hemolymphatic in origin and of
these 78% were malignant lymphomas. Clinical signs of malignant lymphoma vary with the
location of the disease as well as the age of the animal. Lymphoma can affect numerous tissues
with the visceral and peripheral lymph nodes, spleen, liver, mediastinum, bone marrow, lung,
intestine, and kidney being most commonly affected. Less frequently involved are the stomach,
pancreas, nervous system and orbit. In addition, ferrets can develop a rare form of dermal
cutaneous epitheliotropic lymphoma.
It is likely that lymphoma in ferrets, as in other species, stems from a variety of causes
including genetic, environmental and infectious etiologies. Occasional cluster outbreaks in
siblings or cohabitating ferrets suggest an infectious etiology. Erdman, et al have described
horizontal transmission of lymphoma where naive ferrets developed disseminated lymphoma
after inoculation with malignant lymphoid cells or a filtered cell-free supernatant from cultured
malignant lymphocytes, suggesting a viral etiology. A specific viral agent, however, has not
Clinical features of lymphomas in ferrets have been linked with animal age and tumor
location, both of which are useful for evaluating diagnostic and therapeutic options. The most
common form of lymphoma is a lymphocytic variant (where neoplastic cells are mature, well-
differentiated lymphocytes) seen in ferrets older than three years of age. Lymph nodes are
affected most commonly, resulting in peripheral lymphadenopathy. Visceral spread and
subsequent organ failure may occur as the disease progresses. Clinical signs vary with which
organ or systems are affected, however, most mature ferrets with lymphoma present with chronic,
non-specific abnormalities including; intermittent inappetance, lethargy and weight loss. Other
signs may include peripheral lymphadenopathy, posterior paresis, splenomegaly, chronic
vomiting and diarrhea.
A juvenile form of lymphoma, affecting ferrets 1-2 years of age, is typically an acute onset,
multicentric lymphoblastic form of lymphoma, characterized by large immature lymphocytes that
infiltrate the visceral organs early in the course of the disease. Splenomegaly, hepatomegaly and
thymic enlargement may all occur, however peripheral lymphadenopathy is not a common
finding. Clinical signs in young ferrets are often acute in nature and may mimic signs of a gastric
foreign body: vomiting, dehydration, anorexia and wasting. Ferrets with mediastinal (thymic)
lymphoma may cough and present with dyspnea. Ferrets with alimentary tract involvement may
present with varying degrees of anorexia, vomiting, or diarrhea with or without melena.
A third, relatively uncommon immunoblastic polymorphous form of lymphoma is seen in
ferrets of any age and is characterized by lymphadenopathy and visceral organ involvement with
short survival time after diagnosis.
Diagnosis of lymphoma involves biopsy of affected lymph nodes or visceral organs with
direct visualization of neoplastic cells and evaluation of cellular morphology. While cytologic
examination of lymph node, spleen, thoracic effusion, or bone marrow aspirates can provide a
preliminary diagnosis, it is generally less informative than histologic preparations, because of
disruption of tissue architecture. In addition, the large fat pads surrounding ferret peripheral
lymph nodes make obtaining an adequate sample via fine needle aspiration difficult.
Further parameters to consider when making a diagnostic and treatment plan for ferret
lymphoma include; a complete blood count, a platelet count, a serum chemistry profile, a bone
marrow aspirate, whole body radiographs (2 views) and abdominal ultrasonography. In both the
adult and juvenile forms of ferret lymphoma, absolute lymphocyte counts may be elevated,
normal or below normal. Lymphocytosis is significantly more frequent in younger ferrets and
lymphopenia is significantly more frequent in older ferrets. It should be noted that persistently
elevated lymphocyte counts may also result from chronic antigenic stimulation and the ubiquitous
nature of Helicobacter or coronavirus infection in the U.S. ferret population has tremendous
potential for inciting this non-specific change in ferrets. Mild anemia is a common finding and
hepatic enzyme activity, hypoglycemia and hypercalcemia have all been reported in ferrets with
lymphoma. Diagnostic aspirate or biopsy of the bone marrow is useful in diagnosing and
assessing the progression of diseases of the hematopoietic system, including ferret lymphoma,
and should be performed with any ferret with persistent lymphocytosis (>8,000 cells/ul).
Abdominal radiographs or ultrasonography may reveal various degrees of visceral
lymphadeopathy and organomegaly. Imaging of thymic lymphoma will often reveal pleural
effusion and a cranial thoracic mass that displaces the heart and lungs dorsally and caudally.
Lymphoma should always be considered a systemic disease even if confined to a solitary
organ, and treatment decisions should follow a careful evaluation of the patient‟s age, concurrent
diseases and therapy, type of lymphoma, and distribution and staging of tumors. Unfortunately,
classification of lymphoma is not straight forward as in the past 30 years numerous classification
schemes with a disparity of terms have been proposed, making it difficult for investigators to
compare lymphomas between species. However, objective histologic and phenotypic analysis
should facilitate inter-species comparisons. Use of the National Cancer Institute‟s Working
Formulation to classify lymphomas of ferrets into low, intermediate or high grades has proven
useful for predicting the biological progression of these tumors in ferrets and in general younger
ferrets tend to have more rapidly progressive high-grade lymphoma, whereas older ferrets may
have either high- or low-grade lymphoma. Classification of ferret lymphoma by anatomic location
may also serve as a tool in determination of disease severity, prognosis and potential response to
therapy. Stage I has been defined as involvement of a single site of tumor; stage II has been
defined as involvement of multiple sites on the same side of the diaphragm; stage III has been
defined as involvement of spleen and lymph nodes on both sides of the diaphragm; and stage IV
has been defined as involvement of multiple sites on both sides of the diaphragm. In general,
lymphomas involving the liver, intestine, stomach, and/or bone marrow, seem to respond poorly
to chemotherapy. The lymphoid cells of animals that have received glucocorticoids for an
extended period may develop resistance to the antitumoral effects of the steroids, therefore
patients receiving prednisone for insulinoma or inflammatory bowel disease may be refractory to
further chemotherapeutic treatment.
Treatment choices for ferret lymphoma include surgery, chemotherapy, radiation, alternative
therapy or combination therapy involving these modalities. Surgery may be considered as an
alternative or an adjunct to chemotherapy in those ferrets affected with a solitary abdominal mass
or cutaneous lesion. In ferrets with splenomegaly in which the spleen occupies more than 50% of
the abdominal cavity, performing a splenectomy may augment treatment and patient comfort.
Chemotherapy for ferret lymphoma involves single agent or combination drug therapy to
suppress tumor growth. The goal of most veterinary oncologists when using chemotherapy is to
control the cancer and prolong survival while maintaining a good quality of life for the patient. It is
important for the client to understand the difference between complete remission and cure.
Aggressive combination chemotherapy is based on the rationale that unrelated drugs
simultaneously attack tumor cells at different stages of the cell cycle and with different
mechanisms of action. These factors interact to prevent or delay emergence of resistant tumor
cells and result in a greater fractional kill per cycle of chemotherapy without additive host toxicity.
A number of generalizations can be made regarding the use of chemotherapeutic agents in
ferrets. The clinical status of the patient must be monitored on a frequent basis for signs of drug
toxicity and to assess physical condition. Many chemotherapeutic drugs alter the CBC and
platelet count and veterinary oncologists recommend a CBC prior to each chemotherapy to
assure a minimal level of at least 2,000 neutrophils/l and 50,000 platelets/l. In the author‟s
experience, the most common chemotherapy associated complications are lethargy, fever and
varying degrees of vomiting and diarrhea associated with leukopenia. In most cases, patients
respond favorably to supportive care including IV fluids, antibiotics, GI protectants and syringe
With any lymphoma chemotherapy protocol, remission times vary from case to case. The
response to chemotherapy depends on several factors, including the location of the disease, the
extent of disease (clinical stage), the presence or absence of clinical signs, the histologic grade,
the immunophenotype (T-Cell vs. B-cell), exposure to previous chemotherapy or corticosteroids
and subsequent development of multidrug resistance, the proliferation of rate of the tumor, and
the presence of concurrent medical problems or paraneoplastic conditions such as [adrenal
disease, inulinoma], hypercalcemia, weight loss, and liver insufficiency. As with lymphoma in
other species, treatment is not aimed at obtaining a cure of the disease, but rather a remission of
clinical signs. Remission is obtained when clinical signs improve, CBC parameters normalize,
and organ/lymph node enlargment or palpable masses decrease in size. Remissions can last
from months to years in ferrets with adult onset lymphoma, however the prognosis for ferrets with
acute-onset juvenile lymphoma remains guarded.
Caution must be exercised in handling many chemotherapeutic agents in order to minimize
risk to veterinarians and technicians. All intravenous chemotherapeutic agents should be
delivered through an IV catheter in order to minimize patient hazard. The drugs vincristine and
doxorubicin can only be given intravenously and even minimal extravasation of either drug has
the potential to cause significant harm to the surrounding tissue (e.g. sloughing or damage due to
self-mutilation). Indwelling catheters placed in the cephalic vein can be utilized to insure IV
administration. As well, subcutaneous venous access ports have been used successfully. Cost
of therapy depends on drug selection, frequency of administration, costs of testing needed to
monitor patients, and supportive care in the event of toxicity.
Numerous chemotherapy protocols have been used for the treatment of lymphoma in ferrets
and the author recommends consulting with a veterinary oncologist, preferably one who has
experience working with ferrets, for an opinion on the most up-to-date and practical protocols. It
is important to note that all published protocols have resulted in remissions of varying lengths in
ferrets with lymphoma and that becoming familiar with one or two protocols may be the most
practical approach for the practicing clinician. Unfortunately, retrospective studies of individual
chemotherapy protocols with numbers of patients, lists of toxicities and outcomes in the form of
months of remission achieved are lacking. Case reports often feature reasonably favorable
outcomes, while treatment failures are likely underreported. While combination
chemotherapeutic protocols have shown to improve patient longevity the author notes that not all
clients can afford aggressive combination therapy and prednisone (1.0mg/kg PO q12h), which
binds to cytoplasmic receptors and inhibits cell division, can be used as a single agent drug
resulting in various remission success depending on stage and type of lymphoma.
As early as 1989, Dugan et al reported on the chemotherapeutical remission of multicentric
lymphoma in a ferret using a protocol derived from various aspects of canine treatment regimens
taken from Cotter and MacEwan et al (Table 1). The case report demonstrated the use of L-
Asparaginase, oral prednisolone, and oral cyclophosphamide in bringing about complete
remission as judged by radiographic and ultrasonographic evaluation was still present after 21
weeks of chemotherapy. In 1993 Brown gave an account of a ferret chemotherapy protocol
(table 2) used successfully by oncologists at the Animal Medical Center in New York City. One
year later Rosenthal reported on another chemotherapy protocol (Table 3) that again closely
resembled those published for dogs with lymphosarcoma, and in 2000 N.Antinoff,DVM (personal
communication, August 2003) described a COP-L protocol (Table 4) based on recommendations
made by oncologists at Gulf Coast Veterinary Specialists, Houston that has been used with
success in treating ferret malignant lymphoma. In addition, Brown describes the use of
Doxorubicin at 1 mg/kg IV every 21 days for a maximum of 5 treatments, as a single-agent
chemotherapy or as a rescue therapy for patients where disease has recurred after a remission
with another protocol.
New York State College of Veterinary Medicine Ferret Lymphoma Chemotherapy Protocol
reported in 1989
1 L-Asparaginase 400 IU/kg, IP
Prednisone 1.6 mg/kg, PO, SID
2 Cyclophosphamide 336mg/ m , PO divided over
Prednisone 1.6 mg/kg, PO, SID
3 L-Asparaginase 400 IU/kg, IP
Prednisone 1.6 mg/kg, PO, SID
4,6,9,11,13 Cyclophosphamide 252mg/ m , PO divided over
Prednisone 1.6 mg/kg, PO, SID
17,20,23, 26 Cyclophosphamide 168mg/ m , PO divided over
and q3wks two days
thereafter or Prednisone 1.6mg/kg, PO SID for 36 weeks,
until relapse then every other day
Hemograms monitored prior to each treatment
Protocol developed by the Oncology Department at Animal Medical Center in New York,
Induce with L-Asparaginase at 400 IU/kg IP given once only.
Start on prednisone on the same day at 2 mg/kg divided BID and continue throughout therapy.
Start the weekly protocol 5 days after L-Asparaginase administration.
Week 1 Vincristine 0.07mg/kg, IV
Week 2 Cyclophosphamide 10mg/kg, PO
Week 3 Vincristine 0.07mg/kg ,IV
Week 4 Methotrexate 0.5mg/kg, SQ
Week 5 Vincristine 0.07mg/kg, IV
Week 6 Cyclophosphamide 10mg/kg, PO
Week 7 Vincristine 0.07mg/kg ,IV
Week 8 Methotrexate 0.5mg/kg, SQ
Repeat protocol weeks 1-8 except space out to every 2 weeks instead of weekly
University of Pennsylvania Chemotherapy Protocol
1 Vincristine 0.07 mg/kg, IV
Asparaginase 400 IU/kg, IP
Prednisone 1 mg./kg, PO, SID
2 Cyclophosphamide 10 mg/kg, SQ
Prednisone 1 mg/kg, PO, SID
3 Doxorubicin 1 mg/kg, IV
Prednisone 1 mg/kg, PO, SID
4-6 As weeks 1-3 above, but discontinue asparaginase
8 Vincristine 0.07 mg/kg, IV
Prednisone 1 mg/kg, PO, SID
10 Cyclophosphamide 10 mg/kg, SQ
Prednisone 1 mg/kg, PO, SID
12 Vincristine 0.07 mg/kg, IV
Prednisone 1 mg/kg, PO, SID
14 Methotrexate 0.5 mg/kg, IV
Prednisone 1 mg/kg, PO, SID
Protocol is continued in sequence biweekly after week 14.
Prednisone is given daily throughout the protocol.
A COP-L protocol used by Dr. Natalie Antinoff,
Gulf Coast Veterinary Specialists:
WEEK DRUG DOSE
-3 days L-asparaginase 400 IU/kg, SQ
1 Vincristine 0.10 mg/kg IV
Prednisone 1 mg/kg. PO, SID throughout therapy
Cyclophosphamide 10 mg/kg PO 24 hrs after vincristine
2 Vincristine 0.10 mg/kg IV
3 Vincristine 0.10 mg/kg IV
4 Vincristine 0.10 mg/kg, IV
Cyclophosphamide 10 mg/kg 24 hrs after Vincristine
7 Same as week 4
Continue this protocol every three weeks to maintain remission; if
leukopenia (<1,500 cell/ul) at 3 week recheck, postpone chemo and
recheck CBC in 5 – 7 days; if interval is prolonged to 4 weeks
repeatedly, consider increasing the interval for cyclophosphamide.
As with lymphoma in other species, treatment is not aimed at obtaining a cure of the disease,
but rather a remission of clinical signs. Remission is obtained when clinical signs improve, CBC
parameters normalize, and organ/lymph node enlargment or palpable masses decrease in size.
Remissions can last from months to years in ferrets with adult onset lymphoma, however the
prognosis for ferrets with acute-onset juvenile lymphoma remains guarded.
Finally, it is worth noting that cutaneous epitheliotropic lymphoma should be treated as a
separate entity from systemic lymphoma. Ferrets with this rare form of dermal lymphoma present
with; varying degrees of pruritus, alopecia, erythema and dermal excoriations, crusts and
ulcerative plaques. Palliative treatment using retinoid (isotretinoin), antibiotic and oatmeal
shampoo therapy, versus conventional lymphoma treatment, has been reported.
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EXOTIC MAMMAL SURGERY
PETER G FISHER, DVM
PET CARE VETERINARY HOSPITAL
VIRGINIA BEACH, VA
Table of Contents
I. General Considerations in Exotic Mammal Surgery 2
Suture Materials 2
Perioperative Supportive Care and Monitoring 3
Fluid Therapy 3
Pre-Anesthetic Medications 4
Anesthetic Monitoring 5
Post Operative Considerations 5
II. Surgical Conditions/Techniques 6
Adrenal Disease 6
Anal Saculectomy 7
Cutaneous Mast Cell Tumors 8
GastroIntestinal Surgery 8
Prostatic Cysts or abscesses 9
Rabbits and Guinea Pigs 10
Rabbit Ovariohysterectomy 10
Rabbit Castration 11
Ovariohysterectomy in Guinea Pigs 11
Guinea Pig Castration 12
Rat Mammary Tumors 13
Rat ovariohysterectomy 14
Sources of Surgical Equipment 14
Suggested Texts 14
I. GENERAL CONSIDERATIONS IN EXOTIC MAMMAL SURGERY
In general the surgeon can use a feline spay pack for most routine exotic mammal surgeries such
as ovarian hysterectomies, castrations and lumpectomies. A separate pack of fine, delicate instruments,
preferably developed for microsurgery is added to aid in the tissue handling of these small patients and are
prerequisite for more detailed surgery such as ferret adrenalectomies, GI surgery, or exotic mammal
cystotomies. In choosing microsurgery instruments, consider: length (5-7 inches standard), rounded
handle so they can be rolled between surgeon’s thumb and first finger, and counter balancing which allows
the instrument to rest comfortably in the surgeon’s hand, thus reducing muscle fatigue. The microsurgery
pack used for small exotic mammals should consist minimally of a microsurgical needle holder, scissors
and thumb forceps. The author prefers a ring-tipped microsurgical forceps (Sontec Instruments). The fine
ring tip provides for better holding power with minimal tissue damage. Other instruments that aid in exotic
mammal surgery include the Statinsky vascular clamp used with right sided ferret adrenalectomies and a
Hemoclip® applicator for application of ligation / hemostasis clips.
Some form of magnification is of great benefit to the exotic mammal surgeon. In patients
weighing less than 100 grams, such as hamsters, gerbils, or mice, an operating microscope should be
considered, however, in many cases, loupes can provide adequate magnification. For those on a budget,
hobby loupes provide an inexpensive form of magnification. Surgical magnification loupes such as the
Surgi-Tel® (General Scientific Corporation) are essential for surgeons (especially those over the age of
40!) looking for surgical field clarity and magnification. They have the added benefit of allowing the
surgeon to look through the lenses with the head held in an upright, ergonomically correct position.
- hemostatic clips- for vasculature and small pedicle ligation
- hemostatic agents: Gelfoam (Pharmacia)- absorbable gelatin sponge
Surgicel (J & J) oxidized regenerated cellulose
A hemostatic sandwich constructed of Gelfoam surrounded by Surgicel makes an excellent tool for control
of nonspecific hemorrhage.
The surgeon’s goal in choosing a suture material for tissue repair is to restrict loss of tissue
function and to limit the adverse effects of the repair. Absorbable suture material of sizes between 4-0 and
8-0 are generally used. Non-reactive materials (Note: rabbits are particularly prone to abdominal
adhesions) most commonly used include: PDS (polydioxanone), Vicryl (polyglactin 910), and Monocryl
(poliglecaprone). If limited to one suture, the author would choose 4-0 PDS as this is a good size and
material suitable for most small exotic mammal surgery. As a general rule, for skin closure an intradermal
suture pattern is preferred as exotic mammals, rabbits and rodents in particular, are known for their
tendency to rapidly remove external skin sutures. The author uses cyanoacrylate tissue adhesive to “neaten
up” any gaps in the intradermal closure.
Perioperative Supportive Care and Monitoring
The main goal of supportive care is to minimize the adverse physiologic effects of anesthesia,
surgery and pre-existing disease. This begins with a thorough patient history and physical exam including
the weight in grams or kilograms (depending on the size of the patient). Recommended pre-surgical
diagnostic tests vary with the case history and intended surgery. Complete blood count and serum
chemistries are ideal prior to all surgeries, but size of patient (<100 grams) and owner financial constraints
may not allow for these tests in every patient. Minimally, blood collection for PCV, total protein, and
glucose is suggested. Imaging diagnostics including radiography and/or ultrasound are recommended
Ideally, all patients are physiologically stable before anesthetic induction. Fluid therapy to correct
dehydration, electrolyte disturbances, hypoglycemia, and acid-base disturbances prior to surgery, if time
allows, is ideal. Regardless, vascular access for perioperative, pharmocologic, and fluid support is
important for any invasive procedure. Catheterization with 22 to 24 gauge indwelling IV catheters, using
the cephalic vein, is routine in ferrets, rabbits, and guinea pigs. If unsuccessful at passing an IV catheter or
if patient condition (severe dehydration, shock) precludes catheterization, an intraosseus catheter can be
placed. The author uses a 1 ½” (3.81cm) 22 gauge spinal needle in the femur of ferrets (introduced through
the trochanteric fossa), and the humerus of rabbits (introduced through the greater tubercle). Depending on
the serum chemistries, the author uses a balanced electrolyte solution, LRS or 0.9% saline, with 5%
dextrose if hypoglycemia exists. The rate of fluid administration varies with daily fluid requirements,
hydration status, presence of underlying metabolic disease (i.e.: renal or cardiac disease) and degree of
intra-op blood loss. An infusion pump is a necessity in accurate administration of fluids at rates of 6-10
mL / kg / hr. The author has used Oxyglobin in ferrets, rabbits, and guinea pigs at 10-12 mL/kg given over
two hours, when increased oxygen carrying capacity (anemia) and blood pressure maintenance with
colloids (shock, protracted fluid therapy) are needed. Oxyglobin is a great colloid choice in small
mammals. Hetastarch (10-15 ml/kg given over 2 hours) can also be used.
Hypothermia is common in small anesthetic patients due to the large surface area: patient volume,
the cooling effect of anesthetic gases, and suppression of thermoregulation by preanesthetic drugs and
analgesics. The author uses incubated cages (Snyder http://www.snydermfg.com) for pre-op warming and
post-op recovery. Another alternative is the AICU by Lyons Electric Company, Inc.
(http://www.lyonelectric.com/birds/aicu_e.html). The author also uses a surgery table with conductive heat
and the Bair Hugger® (Model 59577 or 500, Arizant Healthcare, Eden Prairie, MN) forced air warming
system for long procedures and very small patients. The Bair Hugger is a convective heater that uses
warmed forced air heat blankets and is a worthwhile investment. The advantage of convective heat vs.
radiant heat (heat lamps) or conductive heat (heated surgery tables or water circulating heating pads) is that
convective heat actually warms the patient vs only preventing heat loss. Athletic socks filled with rice and
microwaved to warm, make great portable heat blankets when anesthetized patients are in radiology or on
the pre-op prep table.
Excited or nervous patients are given pre-anesthetic sedation upon admission to the hospital for
routine out patient surgeries. Otherwise pre-anesthetics are given one-half hour prior to surgery. The
sedative effect allows for patient relaxation and makes mask induction with inhalant go more smoothly.
Some examples of pre-anesthetic drugs or combinations used in the authors practice are in the table below.
Pre-anesthetic Ferret Rabbit Guinea Pig
Butorphanol/Acepromazine (B) 0.01-0.05 mg/kg IM
(A) 0.25 mg/kg IM
Butorphanol/Medetomidine (B) 0.1 mg/kg
(M) 0.08 mg/kg
Midazolam 0.3-1mg/kg IM 1-2 mg/kg IM 1-2 mg/kg IM
Medetomidine 0.1-.02 mg/kg IM 0.25mg/kg IM
Isoflurane or Sevoflurane are used to induce anesthesia via facemask. An induction chamber can
be used in fractious or hyper-excitable patients. Most ferrets can be readily intubated using a 2.0 – 4.0 mm
endotracheal tube. Many rabbits can be intubated using a 2.0-3.0 mm uncuffed endotraceal tube and a
“blind” approach. The tracheal opening is difficult to visualize due to the rabbit’s oropharyngeal anatomy.
The thick tongue, small mouth opening, and laryngeal spasm all add to the difficulty of intubation without
the visual aid of endoscopy. A lidocaine gel (Xylocaine® 2% jelly) swabbed on the epiglottis aids
intubation. I tell my technicians that if they are not successful at rabbit intubation within five minutes then
to maintain anesthesia with use of a facemask. A dog muzzle or tape can be used to secure the mask to the
rabbit’s head and care is taken to make sure that the rabbit’s head and neck are not over extended which
compromises the airway. Facemasks are used routinely in guinea pigs and rodents due to the extreme
degree of difficulty in intubating. A 12 cc syringe case with the end cut open for an anesthetic attachment
makes a good small rodent facemask. A non-rebreathing system such as the Ayres T piece is used for
delivery of anesthetic gases. The human pediatric ones are inexpensive and can be re-used numerous times.
Oxygen flow with these systems should be two to three times the patient’s minute ventilation
It should be noted that small exotic mammals do not require an overnight fast prior to surgery. Two
to four hours fasting prior to surgery is generally adequate due to the ferrets rapid GI transit time and the
fact that rabbits and rodents do not vomit. The 2-4 hour time frame allows for herbivores to clear their
mouths of food particles, which may block the larynx during anesthesia.
All vertebrates are assumed to have nocioceptors and therefore the ability to perceive pain.
Nocioceptors and the response to pain are assessed by evaluating physiologic and muscular reaction to
painful stimuli. Recall most inhalant anesthetics produce unconciousness but are poor analgesics.
Therefore it is a good practice to incorporate analgesics into the preanesthetic protocol. Follow up with
post op analgesia at the appropriate dose, frequency and duration as determined by the surgeon. See the
chart below for some drug considerations.
analagesic Ferret Rabbit Guinea Pig
Buprenorphine (q 6-8h) 0.01-0.03 mg/kg SC 0.01-0.05 mg/kg SC 0.01-0.05 mg/kg SC
Butorphenol (q 4h) 0.05-0.5 mg/kg SC,IM 0.1-.05 mg/kg SC, IM 0.1-.05 mg/kg SC,IM
Meloxicam (q 24h) 0.3 mg/kg PO 0.3 mg/kg PO 0.3 mg/kg PO
Carprofen (q 12h) 1 mg/kg PO 2.2 mg/kg PO 1 mg/kg PO
A good veterinary technician is essential in managing the perioperative support and anesthetic depth
of these small patients as physiologic status can change rapidly. Anesthetic depth depends on drug dosage,
anesthetics/pre-anesthetics used, species, physiologic status and presence or absence of disease. Anesthetic
depth toward a surgical plane of anesthesia is assessed by: evaluating for decreased muscle tone (jaw
muscle or anal sphincter), a significant decrease in palpebral and corneal reflexes and when respirations
become regular and even. Rate, depth and pattern of respiration are the most useful indicators of anesthetic
depth. Respiratory depression (less than 4 breaths per minute) warrants concern and patient assessment. It
should be noted that anal tone and corneal reflexes are not lost at surgical anesthetic levels, but may be
difficult to assess in the small exotic mammal patient.
Tools to aid the veterinary technician in monitoring patients response to anesthesia include:
electrocardiography, Doppler flow detection and pulse oximetry. ECG standard lead positions described
for dogs and cats are used for small exotic mammals and in general the ECG tracings
of small exotic mammals resemble those of dogs and cats in general form. Doppler flow detection (Parks
medical Electronics, Inc, Aloha, OR) used for audible monitoring of blood flow, uses a probe placed as
close as possible to the blood flow in an artery or the heart. The Doppler is used wherever major arteries
are close to the skin and in small exotic mammals have been used at the ventral aspect of the tail base, the
carotid or femoral arteries, the ulnar artery (in ferrets), the auricular artery (in rabbits) or directly over the
heart. Pulse oximetry monitors blood oxygenation and in addition many pulse oximeter units will measure
heart rate, respiratory rate and CO₂ level. Potential sites for placement of transmission pulse oximeter
sensors include the ear, tongue, paw and tail.
Post Operative Considerations
Body temperature should be carefully monitored during surgery and recovery. Recovery in an
incubated cage (75-80° F or 24-27° C ) is ideal--monitor so patient is not overheated as ferrets are prone to
heat prostration. Maintenance fluids delivered via an infusion pump should be continued. Post-op
analgesia is recommended for 2-3 days. Due to the high metabolic rate of small exotic mammals, it is
important to resume food consumption as soon as the patient is adequately awake. Ferrets can eat 6-8
hours post-op for most routine procedures. Herbivores should be offered grass hay within 2-3 hours post
recovery from routine surgeries in order stimulate GI movement and prevent gut stasis. Leafy greens and
pellets can be offered the next day. Rabbits should be protected from stress related to the noise, sight, or
odor of potential predators (dogs, etc), as they are not likely to eat well if environmentally stressed.
Anorectic rabbits or guinea pigs should be syringe fed (Oxbow Critical Care® is recommended) until
eating on their own in order to prevent hepatic lipidosis and GI stasis.
II. Surgical Conditions/Techniques
Prior to surgery a complete blood cell count and serum chemistry panel should be performed.
Particular attention should be paid to the red cell count and blood glucose level, as anemia and
insulinoma are frequently concurrent. As well, the ferret should be evaluated for the presence of
For both glands a ventral midline incision is made 1-2 cm caudal to the xiphoid process and extending
caudally to allow good visualization of the cranial and mid abdomen. As in all ferret surgery, a complete
exploration of the abdomen should be performed to rule out metastasis, insulinoma, or concurrent disease.
As well, it is ideal to visually and palpably inspect both adrenals before deciding on whether to resect either
one or both. The appearance of the ferret adrenal gland is similar to other species being light pink to tan in
color and measuring 6-8 mm long and 2-3 mm wide. Abnormal adrenal glands may be a normal pink color,
brown or dark red with a variable texture; either firm or friable. Surrounding areas should also be examined
for the presence of accessory adrenal tissue. Accessory adrenal tissue was found in 11 of 135 animals
examined in one study. In light of the anatomic arrangement of the adrenal glands, a total adrenalectomy of
the ferret is difficult.
The left gland is more accessible, and may be found embedded in the fat cranial to the left kidney. To
visualize the left adrenal gland, the spleen and much of the small intestines must be gently exteriorized
and kept moist with warm isotonic saline during the surgery. Gentle manipulation will allow location
by palpation. Careful blunt and sharp dissection around the gland will allow more complete
visualization of the adrenal and its blood supply. Cotton tipped applicators may be used to tease the
adrenal away from the surrounding fat. Ligation of the vasculature using vascular clamps
[medium/large hemoclips (Weck Instruments)] aids in removal. In advanced cases, the enlarged gland
may have a more complex blood supply and care must be taken to avoid hemorrhage. In rare instances
the gland may have grown to the point where a nephrectomy must be performed.
The right adrenal gland is cranial and medial to the right kidney, and is more difficult to remove due to
its location dorsal to the caudate liver lobe and frequent adherence to the vena cava. In most cases the
hepatorenal ligament must be transected and the liver lobe elevated to expose the gland. Extreme care must
be taken to avoid damage to the blood vessel as the gland is essentially "teased" away from the vena cava.
Cotton-tipped applicators can work well for this. The neonatal Statinsky or DeBakey cardiovascular clamp
may used to partially or totally occlude the caudal vena cava while the right adrenal is being resected. Even
when performed by experienced surgeons , portions of the right adrenal or its capsule may remain, being
tightly adhered to the vena cava. Debulking the adrenal or opening the adrenal capsule and shelling out the
contents may be all that is possible without risking serious damage to the vena cava. Many times a
hemostatic clip may be placed between the adrenal and the vena cava, thus allowing its removal. Each
surgery will vary according to the size and position of the diseased adrenal gland.
If the vena cava is accidentally nicked a hemostatic material such as Surgicel® or Gelfoam® may be
used to control minor hemorrhage. Small lacerations in the vena cava can be sutured with 7-O or 8-O
nylon. Surgeons occasionally have been forced to ligate the entire vena cava because of severe lacerations
or aggressive adrenal tumors. In one unpublished study, one third of the ferrets that had their vena cava
resected died within 72 hours of the surgery from cardiovascular problems. The remaining two-thirds did
well long term. The azygous vasculature can effectively bypass the vena cava in some ferrets.
Some surgeons feel that the right adrenal gland cannot be successfully removed without resection of
part of the vena cava. For this reason some surgeons feel that cryosurgery, freezing of tissue using liquid
nitrogen, is a more effective means of removing the right adrenal gland. Obliterating the adrenal gland with
laser surgery has also been advocated.
If both glands are completely removed many surgeons administer prednisolone at 0.5-1.0 mg/ kg twice
daily for several days to weeks postoperatively. It does not impair healing and does replace the small
amount of glucocorticoid that may have been secreted by the abnormal gland. A few ferrets may develop
hypoadrenocorticism and require post-operative treatment with mineralocorticoid replacement therapy.
Clinical signs related to inadequate levels of mineralocorticoid include: acute lethargy, anorexia and
dehydration. Serum chemistries, including electrolytes, should be measured to determine if treatment is
needed. Oral fludrocortisone (florinef) and injectable desoxycorticosterone pivolate (Percorten) have both
been used successfully for treating post-surgical hypoadrenocorticism at doses extrapolated from the dog
literature. Many ferrets are not adversely affected by removal of both adrenal glands as remaining adrenal
activity may be sufficient, whether from adrenal remnants, ectopic tissue or expendable function.
Pain medication should be employed for 48-72 hours post surgery. Postoperative resolution of hair loss
may take 45 days or longer. Vulvar swelling in female ferrets will usually resolve in 7-14 days.
Position the ferret as you would for a feline perineal urethrostomy surgery and prep routinely.
Take a pair of fine hemostats and grab the tissue(including opening) right where the anal sac
opening is. Next, use a # 15 scalpel blade and carefully incise around this clamped tissue. Stay
close to hemostats, but do not cut into anal sac duct. I then pull up on the hemostats and use
side of scalpel blade to carefully “scrape” away muscular attachments that are particular strong
as you first get started. I keep pulling hemostats in varying directions (up, down, side to side) so
that I am continually working in a 360 degree fashion to isolate anal sac. Once you get beyond
the „neck‟ of the anal sac the dissection takes less effort and the remainder of sac tends to peel
out more easily (except in older ferrets, in which case muscular attachments remain throughout
the dissection). At times you have to reposition hemostats in order to get a good grasp as you
are pulling up. Repeat on opposite side and let heal by second intention. Do not suture. You
tend to be left with what appears to be two pretty large gaping holes, but they contract and close
in within a day or two. Hemorrhage is usually moderate and is usually controlled with pressure
alone. The author recommends wearing a bathers apron while doing surgery in the event of a
Cutaneous Mast Cell Tumors
Cutaneous mast cell tumors are very common and appear as well-circumscribed, raised, reddened
masses of approximately 2 mm to 1 cm in diameter. They frequently bleed if traumatized.
Treatment consists of surgical excision or cryosurgery either under general anesthesia or local
anesthesia. Temporary relief can be achieved by using a topical steroid cream.
Clients need to be aware that it is unlikely that surgery will cure the disease, and to what degree it
slows progression of clinical signs, and the need for additional medical therapy, depends on the degree of
pancreatic involvement and metastasis. An indwelling IV catheter is placed preoperatively and the ferret is
infused with maintenance fluids with added 5% dextrose.
The pancreas is an “L” shaped organ along the proximal duodenum and has a right (duodenal) and left
(splenic) limb. When doing surgery, you must be careful of the duodenal papillae. The major duodenal
papilla opens into the dorsal part of the descending duodenum about 3 cm from the pylorus. The minor
papillae, if present, are not prominent.
A ventral midline incision, similar to that described above for adrenalectomy, is made. The pancreas is
easily located adjacent to the duodenum. During surgery both lobes of the pancreas are examined visually
and manually. Inspect the spleen and liver carefully for metastastic nodules. Palpate the entire pancreas
gently between two fingers to detect very small nodules that may be single, multiple or diffuse, and range
from grossly invisible up to 2 cm in size. Solitary tumors can be resected with blunt dissection. When
infiltrative, multifocal carcinoma is suspected throughout the pancreas a partial pancreatectomy may be
preferred. Iris scissors and cotton-tipped applicators are used to carefully dissect around the abnormal
tissue. A 4-O or 5-O absorbable suture material or hemostatic clips may be used to ligate larger vessels in
the pancreas. Absorbable hemostatic material (Gelfoam® or Surgicel®) may be used to control minor
hemorrhage. Partial pancreatectomy is recommended in cases where a distinct insulinoma nodule cannot be
found and micro-metastasis throughout the pancreas is suspected. Hemostatic clips are effectively used for
this procedure, or several crushing ligatures may be used to separate the diseased tissue. Close mesentery
defects to prevent visceral entrapment. The liver, spleen, adrenal glands and mesenteric lymph nodes are
examined for abnormalities before closing. Biopsy of the liver is recommended if evidence of metastasis or
irregularities is noted.
Pain medication should be used for 48-72 hours post surgery. Ferrets are kept NPO for 12 hours post-
operative. Pancreatitis, as a sequelae to surgery is rare. Blood glucose concentrations are monitored
after cessation of the IV glucose drip to determine need for medical therapy.
GastroIntestinal Surgery: GI foreign body, hairball, neoplasia, IBD
Diagnosis is based on history, physical examination, clinical signs, and plain or barium contrast
Foreign body or hairball treatment involves the surgical removal of the object. Gastrointestinal surgery
is similar to the cat. Gastrotomy incisions are made in the greater curvature. Close gastric wall with 4-O
absorbable suture in a Cushing-Lembert pattern staying close to incision site so as not to incorporate an
inordinate amount of tissue. Enterotomy is also performed in a manner similar to the cat. Use 4-O
absorbable suture to close in simple interrupted pattern- again try to incorporate a minimum of tissue so as
not to narrow the intestinal lumen.
Biopsies of stomach, duodenum, jejunum are indicated to make a diagnosis of Inflammatory Bowel
Disease (IBD) and certain neoplasias. Stab incisions are made in the stomach great curvature and intestinal
anti-mesenteric surface. 1-2 mm by 5 mm full thickness (make sure to include mucosa) samples are taken
and close as for foreign body above.
The most common indication in ferrets is hydronephrosis that is presumed to be secondary to
inadvertent ligation of the ureter during OVH. Ferrets are usually presented because owner notices the
enlarged kidney pressing against body wall. Most ferrets are clinically normal as problem is unilateral.
Treat via nephrectomy. A mid abdominal midline incision is made. The kidney is isolated and the
peritoneum over the caudal pole of the kidneys is grasped with forceps and incised with scissors. The
surgeon expands this incision with combination of digital dissection and scissors to peel away the
peritoneal adhesions over the kidney. Dissection is continued until the kidney is free accept for attachment
of renal artery, vein and ureter. These are ligated individually or together with Hemaclips or 4-O
absorbable monofilament suture. The kidney is then removed. There is no need to close incised
peritoneum. Check for hemorrhage and close abdomen routinely.
Prostatic Cysts or abscesses
Almost all cases of prostatic cysts or abscesses are secondary to the androgenic stimulation by
underlying hyperadrenocorticism. Definitive treatment is correcting the adrenal disease.
Prostatic cysts can be drained or marsupialized to the ventral abdominal wall. Marsupialization allows
for immediate decompression of fluid-filled structures applying pressure to the urethra as well as drainage
external to the abdominal cavity. When drainage of purulent material has subsided, the stoma will heal by
Are occasionally seen in older, intact female ferrets. The symptoms are lethargy and perhaps a vaginal
discharge. Typically seen approx. 4-6 weeks post-estrus. Treatment of intact female ferrets with
progesterone containing compounds can lead to pyometra. Stump pyometras are occasionally seen
secondary to hyperadrenocorticism.
Treatment is similar to the cat: Ovariohysterectomy, fluids and antibiotics. Correct underlying adrenal
disease if present.
Splenectomy should be considered in cases of hypersplenism, selected cases of neoplasia or
when an enlarged spleen is causing discomfort or is prone to trauma due to size. If a splenectomy is
indicated make a cranial to mid abdominal incision. Gently exteriorize the spleen. Sutures or
vascular clips may be used to ligate the splenic artery and vein and the smaller vessels on the splenic
side. Either 3-O or 4-O absorbable suture material or hemoclips is used to ligate the omental side of
each vessel. The vascular clips or ligatures should be located as close to the spleen as possible so as
not to compromise circulation to the pancreas or stomach. An incision is made between the vascular
clips and/or suture ligations. The spleen is removed.
Permanent urine diversion via surgical urethostomy is required periodically in the male ferret. The
most common indications are certain neoplasms of the preputial gland and total urethral obstruction of the
penile urethra. Mechanical urethral obstruction can be secondary to gross uroliths that have entered the
urethra from the bladder and lodged at the os penis, or from gross crystalluria or viscous pyuria that
prevents urine flow. The viscous pyuria may be associated with prostatitis or cystitis secondary to adrenal
disease. If attempts at urinary catheterization of the urethra fail to relieve the obstruction, an urethrostomy
The surgical technique is similar to that in a dog and is not technically difficult. The ferret is placed in
dorsal recumbency and the urethra is palpated just caudal to the os penis. A 1-1.5 cm skin incision is made
directly over the urethra and a combination of sharp and blunt dissection is used to isolate the urethra. The
ventral midline of the urethra is incised, taking care to avoid the cavernous tissue on either side. Sectioning
of the cavernous tissue may cause significant hemorrhage. Tenotomy scissors are used to enlarge the
incision to its 1-1.5 cm length. This length may seem excessive, but after complete healing, the stoma is
approximately 1/3 to 1/2 its original length. At this point, a urinary catheter can be inserted into the bladder
to drain urine. 4-O or 5-O nonabsorbable monofilament suture material (such as nylon) is chosen for the
urethrostomy because this material incites little inflammatory reaction and has minimal tissue drag. Simple
interrupted sutures are placed at the corners of the incision to appose the urethral mucosa to the skin at the
11 and 1 position and again at the 5 and 7 position. A simple interrupted pattern is placed between the
corner sutures. In ten days the sutures are removed. The urethra stoma tends to heal nicely and stricture is
not a common problem.
Rabbits and Guinea Pigs
Rabbits can be spayed any time after 5 months of age. Immature females have very tiny
uterine horns and ovaries making identification difficult.
Indications: Ovariohysterectomy is indicated in all female rabbits to prevent pregnancy, control territorial
aggression associated with sexual related behavior, and prevent uterine neoplasia (very common) or other
uterine disorders such as pyometra or endometrial venous aneurysms.
* the cervix is bicornuate
* the flaccid vaginal body fills with urine during micturition therefore a secure transfixing
cervical ligature is required
* a substantial amount of fat may be laid down in the broad ligament and suspensory
ligament on the way
* the fallopian tube is long, convoluted, and fragile
A 2-3 cm midline incision is made approximately half way between the umbilicus and the pubic
symphysis. The linea is identified and greatly grasped and elevated with thumb forceps as a stab incision is
made into the abdomen. Great care is taken when entering the abdomen as the twin-walled cecum and
bladder often times lay directly against the ventral abdominal wall. Minimal handling of the GI and gentle
technique throughout the procedure will help minimize likelihood of the post op adhesions rabbits are prone
to. A spay hook is usually not necessary as the uterus lies dorsal to the cranial pole of the bladder and can
usually be lifted through the incision using forceps. With gentle traction, the uterus is followed to the
oviduct and infindibulum which are coiled in a large loop several times longer then that of the dog or cat.
The mesometrium of the doe is a primary site of fat storage and many times the ovaries and oviduct are
embedded in a large fat pad. Gentle digital manipulation and traction will allow identification of the ovary
which is isolated with its vasculature for ligation. There are multiple vessels associated with the ovary
which need to be identified and double-ligated (together) with transfixing sutures of PDS or Moncryl. Care
is taken to ensure all of the oviduct is removed as well. The procedure is repeated for the opposite ovary.
The uterus is now isolated and the end can be ligated cranial or caudal to the cervices. In older does, the
uterine vessels may be quite large and can be double ligated separate from the uterine body. The author
prefers to ligate and resect the uterus close to the cervix- just on the vaginal side of the cervix. Closure of the
abdomen with 4-O monofilament absorbable suture is routine: Simple interrupted pattern in linea, followed
by simple continuous patterns in SubQ and intradermal.
to control urine marking behavior
to control & minimize territorial aggressive behavior
to prevent reproduction
testicular tumors or abscesses occur occasionally
Both prescrotal and scrotal techniques have been described. The author prefers a prescrotal incision as it is
neater and is not associated with the complication of scrotal edema. A 1.5 cm incision is made on the
midline just cranial to the scrotum similar to a skin incision for canine castration. One of the testicles is
manipulated toward the incision by applying digital pressure on the scrotum. If testicles are withdrawn into
the abdomen, gentle pressure is applied to the abdomen to return testicles to their normal position. The fat
is dissected away with hemostats to expose and isolate vaginal tunic. The vaginal tunic is lifted up and the
caudal ligament of the testicle is carefully torn from its scrotal attachment, freeing the testicle and
spermatic cord. Gauze squares and traction will aid this procedure. Gentle pressure is applied to the
abdomen to ensure the testicle is isolated to the caudal aspect of the spermatic cord. The spermatic cord is
clamped distal to the testicle and close to the inguinal ring. The spermatic cord is double ligated, using
4-0 non absorbable suture, transfixed and resected. The procedure is repeated on the contra-lateral side.
Closure of the subcutaneous tissue with a simple continuous pattern is followed by a continuous
intradermal skin closure.
Post op considerations
Rabbits tend to leave intradermal skin closures alone. As with other hind gut fermentors, it is important that
rabbits return to eating soon after surgery in order to prevent GI motility problems and hepatic lipidosis.
Analgesics are recommended for several days.
Ovariohysterectomy in Guinea Pigs
- female guinea pigs can become sexually active as early as 8-12 weeks of age.
- cystic ovaries of varying degrees of size and hormonal influence are very common in older guinea pigs
- pregnancy toxemia and dystocia are common in older females
- neoplasia and pyometra are uncommon but can occur
- the suspensory and broad ligaments are sites of fat deposition
Technically guinea pig ovariohysterectomy is similar to the rabbit with two exceptions:
- The ovaries are supported by a short mesovarium making the ovary more difficult to exteriorize than rabbits or
carnivores. It may be necessary to extend the incision cranially to avoid accidentally tearing the fragile, fat-filled
suspensory ligament. As well, hemostatic clips versus suture may make for easier ovarian pedicle ligation.
- It is recommended to ligate the uterus just cranial to the cervix. In most cases, 2 transfixing sutures incorporating the
uterine blood vessels are adequate.
Guinea Pig Castration
Indications: Primarily to control reproduction and related objectionable behavior, or medical reasons such as neoplasia
Anatomical Considerations: Rodents have large epididymal fat pads within the vaginal tunic that help prevent
intestinal herniation. The spermatic cord passes through large bilateral fat bodies within the abdomen thus preventing
visceral herniation into the scrotum, but at the same time this anatomy allows the testicles to move freely from scrotum
to abdomen. As a result of this anatomy, inguinal hernia and visceral herniation are rare after castration.
Castration can be performed by a closed or open technique. The author
prefers a closed technique which will be described. In guinea pig
castration, the testicles are removed through separate incisions over each
scrotum. If either testicle is in the abdomen, gentle caudal-ventral
abdominal pressure will return the testicle to the scrotum. A 1-2 cm
incision is made through the middle of the scrotum parallel to the penis.
Care is taken not to penetrate the tunica vaginalis. Keep in mind that an
inadvertent incision into the tunic may occur while incising over the
scrotum creating an open situation. If this occurs, the tunic surrounding
the spermatic cord and vas deferens can be grasped more proximally and
still double ligated in a closed fashion.
Grasp the tunic and remove the testicle from the scrotum and gently dissect the tunic from its attachment
circumferentially. When the testicle is isolated, apply traction and gently strip the fascial attachments using a gauze
square. This allows the testicle to be exteriorized and the spermatic cord isolated proximally. Ligate the cord using
a two or three clamp technique and double ligate with transfixing absorbable suture material. Sutures are placed
close to the inguinal ring without excessive pulling of the spermatic cord. It is not necessary to remove the
epididymal fat pad and leaving it in place may prevent herniation. The technique is repeated on the opposite testicle
and the spermatic cords checked for hemorrhage. Several simple interrupted (or a short continuous) subcutaneous
sutures are utilized to appose overlying tissue followed by an intradermal closure in each scrotum.
Guinea pigs tend to leave intradermal skin closures alone. As with other hind gut fermentors, it is important that
guinea pigs return to eating soon after surgery in order to prevent GI motility problems and hepatic lipidosis.
Analgesics are recommended for several days.
Indications- cystic calculi- calcium carbonate and calcium oxolate most common in rabbits. Calcium
phosphate, and calcium oxolate most common in guinea pigs . Magnesium ammonium phosphate most
common in ferrets. Definitive causes of cystic calculi are largely unknown. Consider: nutrition, anatomy,
genetics, water intake, environment, and infection. Rabbits have unique calcium metabolism.
Anatomy- recall rabbits have a large vaginal vestibule into which the urethra empties therefore may contain
urine and not to confuse with the urinary bladder
Clinical signs: hematuria, stranguria, dysuria, incontinence, bruxism secondary to abdominal pain
Technique: Magnification very helpful for this procedure. Radiographs- two views important in gp to rule
out ureteral calculi. Multiple stones and multiple location of stones can effect therapeutic options.
As in other mammals infection and mech factors such as divertculi can predispose to calculi formation
-Ureter stones v. painful and only signs may be inappetance and decreased activity -Medical treatment has
been dissapointing and rate of recurrence is high once calculi are surgically removed. Because exact mech
of calculi foramtion are unk, dissolution and prevention of calc has not been possible in gp.
Suggested Tx options include:antibiotic for infection, pain meds, diet modific aimed at reducing Ca and
oxalate content of urine– ----avoid oxalates in spinach, parsley, celery, strawberrries, rhubarb
--timothy hay and pellets
--K citrate (150mg/kg divided q12h- reduces urinary saturation of Ca saltsby binding Ca, redcuing ion
activity and alkalinizing urine (usu alk in herb anyway). Not proven to be effective but not harmful
-“Lemonade” 4 oz conc lemon juice/ 2 liters water
-Surgery similar in all small exotic mammals.
Note: bladder wall of guinea pigs particularly thin walled. If possible, place indwelling urinary catheter in
males especially with multiple small calculi-- Tom cat catheter, 24 ga. teflon IV catheter or Slippery Sam
(Cook Medical). Ventral midline incision just cranial to the pubis. Exteriorize bladder and isolate with
saline moistened gauze squares. Make a 5-10 mm incision in ventral bladder wall, beginning at the apex.
Take sample for culture and sensitivity (calculus itself, mucosal swab or piece of excised bladder wall).
Remove calculi and flush bladder with warmed normal saline. If urinary catheter placed- flush retrograde.
If urinary catheter not placed pre-op you may pass urinary catheter normograde and flush small stones back
into bladder for removal. Close bladder wall with 4-0 to 5-0 absorbable monofilament suture in a
continuous inverting pattern (author uses Cushing-Lembert) taking care not to penetrate mucosa. Flush
surgical site. Return bladder to abdomen and close abdomen routinely.
Rat Mammary Tumors
Anatomically, the mammary gland tissue in the rat extends on either side of the ventral midline from the
axillary to the inguinal regions, and mammary gland tumors may occur anywhere in this area. Mammary
gland neoplasms are probably the most common spontaneous tumors found in the rat. Adenomas and
cystadenomas are uncommon, and carcinomas of varying types (adenocarcinomas, papillary carcinoma,
comedocarcinomas, and squamous cell carcinoma) are said to comprise less than 10% of all spontaneous
mammary gland tumors in the rat. Mammary fibroadenoma represents approximately 85-90% of all
mammary tumors in the rat. These neoplasms are most common in older rats, though may also occur in
young females and males. Overall, the biological behavior is benign; the neoplasms can become very
large, ulcerate, and infiltrate locally, but they rarely metastasize. For this reason, surgical excision is
generally curative, but additional fibroadenomas may develop in remaining mammary tissue.
Surgical removal is straightforward. Due to the size of the patient wide margins are not taken. An
elliptical incision is made around the mass. The mass is undermined and resected without penetrating the
tumor capsule. In general these tumors have limited attachments to surrounding tissue. In spite of their
large size, the vascular supply to these tumors is limited and can easily be ligated with vascular clamps
(hemaclips) or suture material. Once removed the dead space and subcutaneous tissue can be closed with
3-O to 4-O absorbable monofilament in a simple interrupted or continuous pattern (depending on size of
space to be closed). The skin is closed in a continuous intradermal suture pattern using the same suture
material. Tissue adhesive is added to seal any remaining gaps along the incision line.
Ovariohysterectomy may be performed in the rat via either the abdominal midline or dorsal midline
approach. The author prefers the abdominal approach as it allows the ability to fully visualize the
abdominal organs during the procedure. However, if the rat is obese and the gastrointestinal (GI) tract is
full, it may be difficult to perform the surgery. A midline incision is made through the skin from just
posterior to the umbilicus to just cranial to the rim of the pubis. The linea, which is very thin and
transparent at this point, is identified and incised to access the abdomen. The intestines are gently
manipulated aside with a moistened sterile cotton swab. The cotton swab is used to elevate the uterus and
isolate the reproductive tract. The abdomen of most rats contains abundant fat, whether the animal is obese
or not. The ovarian vasculature is clamped and ligated using an appropriately sized Hemoclip. The
process is repeated on the contralateral ovary. The junction of the two uterine horns and cervix is now
identified. The cervix is firmer than uterine tissue and is elevated, clamped and ligated. An appropriate-
sized Hemoclip™ can be used for ligature or double ligated using 4-O absorbable monofilament suture.
The abdominal wall is sutured in a simple interrupted pattern followed by a simple continuous intradermal
closure of the skin. Tissue glue can be used to close the gaps in the skin.. Postoperative analgesics, such as
butorphenol or buprenorphine (with or without a non-steroidal anti-inflammatory drug- meloxicam) are
recommended for pain control. The combination of analgesics and an intradermal closure are an effective
means of preventing post op chewing of sutures.
Sources of Surgical Equipment
Sontec Instruments, Englewood, CO
ASSI, Accurate Surgical & Scientific Instruments Corp., Westbury, NY
Pulling Co., Ft Washington, PA
- SurgiTel magnification loupes, General Scientific Corp., Ann Arbor, MI
A Technician’s Guide to Exotic Animal Care. AAHA Press, 2001.
Ferrets, Rabbits, and Rodents. Clinical Medicine and Surgery. Quesenberry K, Carpenter J, Saunders,
The Veterinary Clinics of North America. Small Animal Practice. Exotic Pet Medicine Edition.
Biology and Diseases of the Ferret. James G. Fox. Williams & Wilkins 1998.
Exotic Animal Formulary. James W. Carpenter. Saunders. 2001.
Exotic Companion Medicine Handbook. Cathy Johnson-Delaney, Zoologic Education Network, 1996.
Exotic DVM Magazine. Zoologic Education Network.
The Exotic Guidebook , Exotic Companion Animal Procedures. L Bartlett, T Lightfoot (eds.) Zoologic
Education Network. 2002.
Seminars in Avian and Exotic Pet Medicine. Saunders
Textbook of Rabbit Medicine. Harcourt-Brown T, Butterworth Heinemann, 2002
Cantwell,SL: Ferret, Rabbit and Rodent Anesthesia. In: Heard,D (ed) Analgesia and
Anesthesia, Veterinary Clinics of North America, Exotic Animal Practice, 4(1) pp169-
Bennett A. Preparation and Equipment Useful for Surgery Exotic Pets. In: Bennett A
(ed) Veterinary Clinics of North America, Exotic Animal Practice, 3(3) pp563-585, 2000.
Heard D. Perioperative Supportive Care and Monitoring. In: Bennett A (ed)
Veterinary Clinics of North America, Exotic Animal Practice, 3(3) pp587-615, 2000.
Jenkins J. Surgical Sterilization in Small Mammals: Spay and Castration. In: Bennett A
(ed) Veterinary Clinics of North America, Exotic Animal Practice, 3(3) pp617-627, 2000.
Mullen H. Nonreproductive Surgery in Small Mammals. . In: Bennett A (ed) Veterinary
Clinics of North America, Exotic Animal Practice, 3(3) pp629-645, 2000.
Beeber N. Abdominal Surgery in Ferrets. In: Bennett A (ed) Veterinary Clinics of North
America, Exotic Animal Practice, 3(3) pp647-662, 2000.
Rosenthal, KL (ed). Practical Exotic Animal Medicine. Veterinary Learning Systems,
Bartlett L, Lightfoot T: Ferret Surgeries. In The Exotic Guidebook, Exotic Companion Animal Procedures,
Zoological Education Network, Lake Worth, p 1-32.
Quesenberry K, Carpenter J. Ferrets Rabbits and Rodents, Clinical Medicine and Surgery, 2 nd ed.
Fisher P. Surgical Removal of Rat Mammary Tumors, Exotic DVM 4(2) p6, 2002
Johnson-Delaney K. Ovariohysterectomy in a Rat. Exotic DVM 4(4) pp17-21, 2002.
INTRODUCTION TO THE CHINCHILLA
Heidi L. Hoefer, DVM, Dip. ABVP
West Hills Animal Hospital
Huntington, New York
The chinchilla (Chinchilla lanigera) is a small rodent originating from the Andes mountains of South
America. They were first bred in California in 1923 in an attempt to establish ranch-breeding for the fur
industry. Chinchillas have been trapped to near extinction in their native countries. In the U.S., there is
estimated to be over 3,000 ranchers and a growing population of pet chinchillas.
Chinchillas are generally nocturnal and prefer a quiet environment during the day. Their lifespan is much
longer than most rodent species averaging 10 years with 18-20 years possible in some individuals. The
male averages 400-500 grams in body weight and the female is slightly larger at 500-600 grams. They are
clean, odorless, and inquisitive animals that are relatively easy to care for.
Husbandry and Diet
Chinchillas are active and require a fair amount of space. They like to jump and climb and a large
multilevel cage is recommended. A wire mesh cage is better than wood because they like to gnaw. The
mesh must be small enough to prevent foot and limb injury and part of the floor should be solid. A
hiding/sleep box is recommended.
Chinchillas are fastidious groomers and require dust as part of their daily bathing. The dust is a fine
mixture of Fuller's earth and silver sand (1:9) and is placed in a container large enough for the chinchilla to
roll around in. These baths need to be kept clean and free of feces and should be removed when not in use.
Overuse of the dust bath can lead to an irritative conjunctivitis in some chinchillas.
The chinchilla’s native habitat provides low humidity and sharp variations between daytime and evening
temperatures. High temperatures and high humidity must be avoided year-round. Chinchillas are
comfortable at cooler temperatures (>32oF) and can suffer heat stroke if the environmental temperature
climbs above 80oF, especially when coupled with high humidity. Heated hospital cages should be used
with caution in euthermic chinchillas.
Free-ranging chinchillas survived on a diet of grasses, cactus fruit, leaves, and the bark of small shrubs and
bushes. Captive chins need a diet high in fiber to prevent enteric problems. The basic chinchilla diet
consists of a good quality grass hay (timothy or orchard) and a small amount of chinchilla pellets. Because
the diet must be high in fiber, the sole feeding of pellets must be avoided. Limit pellets to 1-2 tablespoons
per day. Small amounts of greens, and fruit can be offered as treats. Any change in diet should be done
gradually and fecal output should be monitored.
Puberty for both sexes usually occurs at 10-12 months of age in the fall. The female has two uterine horns
that open separately into the cervix. There is a vaginal closure membrane that is only open during estrus
and parturition. They are seasonally polyestrous from November to May with an estrous cycle of about 40
days. Gestation period is long at 111 days and the babies are precocious. The female has a cone-shaped
clitoris that at quick glance may resemble a penis. The male has open inguinal rings and the testes are
located inguinally without a true scrotal sac. Adult male chinchillas may suffer from paraphimosis caused
by a ring of fur caught around the penis inside the prepuce ("fur ring"). The penis of all male chinchillas
should be checked during physical examination and fur rings removed. Elective neutering is usually only
performed for birth control and behavioral reasons.
Chinchillas are usually easy to handle and rarely bite. However, they can be shy and nervous and reluctant
to stay still for prolonged periods. The best approach is to gently hold the animal around the thorax.
Alternatively, the tail can be held at the base as long as the body is supported. Chinchillas that are handled
roughly will release a patch of fur, leaving the skin clean and smooth ("fur slip"). Fur regrowth may take
Chemical restraint can be used if prolonged sedation is needed. Injectable ketamine/diazepam (Valium®)
or ketamine/midazolam (Versed®) combinations work well. Isoflurane can then be delivered through an
induction chamber or a face mask. Chinchillas are very difficult to intubate; respirations and anesthetic
depth must be carefully monitored during prolonged procedures.
Similiar to other hind-gut fermenters, chinchillas rely on a complex balance of microorganisms in the
digestive tract to ferment non-digestible fiber. Any disruption in this system can change pH, interfere with
motility, and promote bacterial overgrowth. Gram-negative bacteria and clostridial overgrowths can lead to
diarrhea, enterotoxemia, and death. Antibiotics with a selective gram-positive spectrum must be avoided.
This includes the beta-lactams (penicillins and cephalosporins), clindamycin, lincomycin, and
As prey species, chinchillas are very stressed in the hospital environment. A dark, quiet cage away from
dogs must be provided. Out-patient treatments can be utilized whenever medically indicated and hospitals
stays should be kept to a minimum.
Gut Stasis and the Acute Abdomen
The chinchilla originates from an area of the Andes mountains where vegetation is tough and fibrous and
low in energy content. This type of diet requires a large amount of chewing. The cheek teeth are open-
rooted and grow continuously to compensate for this wear. Dental disease is common in chinchillas fed
inappropriate diets (see dental lecture for details).
Chinchillas are hind-gut fermenters with a relatively long gastrointestinal tract. The stomach and cecum
are large and the colon is highly sacculated. High fiber, low energy diets are the driving force behind this
herbivores' digestive physiology. Disruption in the system can result in anorexia, colic, diarrhea, hair and
fecal impaction, intussusception, mucoid enteritis, ileus, bloat, and rectal prolapse. Predisposing factors
include abrupt diet change, inappropriate antibiotic use, overcrowding and stress, and diets too low in fiber,
and too high in fat and protein. Changes in enteric pH or normal gut flora results in bacterial overgrowth
and can lead to enterotoxemia. Clostridium, E. coli, Proteus, and Pseudomonas are common isolates.
Clostridial enterotoxemia (C. perfringens) causes severe diarrhea, shock, and acute death.
Diagnosis is based on clinical signs and history. Anorexia and decreased fecal output are early warning
signs. Whole body radiographs are taken to assess both body cavities. Varying amounts of gas and ingesta
may be seen normally in hindgut fermentors and it can be difficult to determine simple gas production from
an obstructive ileus, even with barium films.
Treatment for the acute abdomen includes supportive care (fluids, temperature regulation), NSAID’s
(Banamine®) or other analgesics (buprenorphine), antibiotics, motility enhancers (cisapride), and rarely,
surgery if obstructed. Human OTC pediatric anti-gas preparations (e.g., Phazyme®) may be helpful to
decrease gas production. Keep in mind that a sick chinchilla is a poor surgical candidate and medical
management is usually indicated.
Heart murmurs are occasionally ausculted in otherwise normal young chinchillas. What role this plays, if
any, in signaling a cardiovascular problem is unknown. Heart failure can also be seen in chinchillas. These
animals present acutely dyspneic and may be difficult to distinguish from a primary respiratory condition.
Chronic respiratory infections can be caused by Bordetella, Streptococcus, and Pasteurella, often in
combination. Thoracic films and echocardiography are important to make the diagnosis of heart vs. lung
Traumatic fractures of the tibia are common. The tibia is a long straight bone in the chinchilla with very
little soft tissue covering. Tibial fractures tend to be short spiral or transverse. Soft padded bandages and
lateral splints can be applied temporarily but do not provide adequate stabilization for the active chinchilla.
Surgical repair using external fixators (KE apparatus) is recommended, but can be difficult due to the long,
thin nature of the bone.
1. Donnelly TM: Disease problems of chinchillas. In Quesenberry KQ, Carpenter JW (eds.): Ferrets,
Rabbits, and Rodents, Clinical Medicine and Surgery. Philadelphia, WB Saunders, 2004, pp 255-266.
2. Moore RW, Greenlee HH: Enterotoxaemia in chinchillas. Lab Anim 9:153-154,1975
3. Hoefer HL, Crossley DA Chinchillas. In Meredith A, Redrobe S (eds): BSAVA Manual of Exotic Pets.
Gloucester, England, British Small Animal Veterinary Association, 2002, pp 65-76.
INTRODUCTION TO THE AFRICAN PYGMY HEDGEHOG
Heidi L. Hoefer, DVM, ABVP
West Hills Animal Hospital
Huntington, New York
Hedgehogs are small mammals that belong to the order Insectivora. There are several genera and species
that are found throughout the British Isles, Europe, Asia and Africa. Hedgehogs are not native to North
America. The African pygmy hedgehog (Atelerix albiventris) originated in the African savanna, and is
now widely bred in North America for the pet industry. The European hedgehog (Erinaceus europaeus) is
a larger species, native to England and Europe and protected by law in many areas.
The African hedgehog is small, nocturnal, and spiny-coated. They have a black “peppered” appearance
with a white ventrum. The adult ranges in weight from 400-600 grams. Life expectancy averages 3-4
years in the wild but up to 10 years in captivity.
Anatomy & Physiology
Hedgehogs are characterized by the short, grooved white and dark brown spines that cover the dorsum of
the body. Color mutations can be seen (“snowflake”, albino, champagne, e.g.). The face and ventrum are
covered with soft, light-colored fur. The hedgehog can assume a defensive posture by rolling up and
erecting the spines to resemble a tight ball of sharp spines.
The dental formula is typical of insectivores and consists of 36 teeth: I 3/3; C 1/1; P 3/2; M 3/3. The teeth
are small with sharp, pointed cusps. The upper first incisors are larger than the others and spaced apart; the
lower incisors “fit” into this space when the jaw is closed. Hedgehogs have a simple stomach and no
Gender is easy to identify in hedgehogs. The male has a ventral prepuce located midway along the
abdomen. The testes are usually intra-abdominal and are not easily palpated. The female has a vulva
located close to the rectal opening. African hedgehogs breed year-round. The gestation period is 34-37
days. Litter size ranges from 1-7 with an average of 3-4 pups. The young are born blind with soft white
spines. New brown spines appear in 2-3 days and the eyes open in 2-3 weeks. Weaning occurs at 4-6
In their native habitat, a hedgehog will dig its burrow under logs, leaves, among rocks, or tree roots and
sleep most of the day. They are solitary and nocturnal, emerging at dusk to forage for insects. When
undisturbed, it moves with an unsteady, waddling gait but can run quickly. The hedgehog has a keen
olfactory and auditory sense making it an adept hunter and forager. The European species will hibernate in
the winter and the African species will aestivate in the hot, dry season. Hibernation is not essential and is
not recommended for captive hedgehogs.
Housing & Diet
Hedgehogs are usually caged alone but can be housed in groups if given enough space. They are excellent
climbers, so cages should be smooth-walled and high enough to prevent escapes. Wire flooring should be
avoided due to the potential for toe and limb injury. Newspaper or wood shavings (pine or aspen) can be
used as bedding, but it must be changed frequently. A sleeping area can be made from cardboard boxes,
hollowed logs, wooden boxes, or plastic flowerpots and filled with hay or leaves.
The native diet consists of a variety of insects, occasional small vertebrates, and carrion. Captive pets can
be fed a diet of soaked low-fat dog or cat chow, smaller amounts of mealworms or earthworms, and a small
amount of chopped fruit and vegetables. Because of the calcium-phosphorus imbalance, a diet solely of
insects must be avoided. Hedgehogs should be fed once daily in the evening. Captive hedgehogs have the
tendency to become obese; early evening exercise should be encouraged.
Physical Examination & Restraint
Hedgehogs typically roll-up making a full physical examination impossible without sedation. Light leather
gloves are recommended to protect against the sharp spines. Some individuals can be successfully scruffed
behind the ears if caught before they ball up, however, the majority of hedgehogs will need to be sedated.
The preferred method of sedation is isoflurane gas. The hedgehog is initially placed in an induction
chamber and then switched to a face mask for maintenance. Endotracheal intubation is nearly impossible.
Conversely, injectable agents can be used. Ketamine as the sole agent or in combination with diazepam or
midazolam can be administered intramuscularly. Halothane is reportedly safe to use for short procedures,
but the author prefers isoflurane for its rapid induction, recovery and safety.
Most procedures require sedation to perform, from toenail clipping to radiographs and venipuncture.
Simple treatments for hospitalized individuals can be done by subcutaneous or intramuscular injection
along the dorsum but oral administration may only be possible with weak hedgehogs. Large volumes of
replacement fluids can be given intraperitoneally or through intraosseous catheterization. Intravenous
catheters are difficult to place. Venipuncture can be accomplished in the sedated hedgehog through the
jugular vein or cranial vena cava.
Some Common Conditions And Diseases
There is a growing body of information in the literature regarding the diseases of pet African pygmy
hedgehogs. The best approach to hedgehog medicine is to apply basic medical common sense and keep in
mind that this is a wide open field and anything is possible!
Mycotic dermatitis is caused by Trichophyton and Microsporum in hedgehogs. Disease can be subclinical
or is manifested by scales, crusts, and the loss of spines. Treatment with oral griseofulvin and lime sulfur
dips weekly are helpful. Diagnosis is by fungal culture of affected skin and scales.
Mites are the most important parasitic disease of pet pygmy hedgehogs. Mite infestation is thought to be
from Caparina sp. and can be subclinical or can produce extensive disease. Acariasis can result in a severe
dermatitis characterized by scales, flaking, crusts, and loss of spines in protracted cases. Diagnosis is
through routine skin scrapes and microscopic examination. Treatment with ivermectin or acaricidal dips
(amitraz) is effective. More recently, selamectin (Revolution®) has been used for mite treatment and
anecdoctally appears to be effective and safe.
Cutaneous nodules or masses are common and can be caused by papillomas, abscesses, or neoplasias.
Granulomatous subcutaneous nodules and lymphadenitis caused by Mycobacterium have been reported.
Lymphosarcoma with peripheral lymphadenopathy is another differential. All lesions should be biopsied
Dental disease can be seen in hedgehogs on a soft food diet. Periodontitis and gingivitis have been
diagnosed in both free-ranging and captive individuals. Oral cavity food "foreign bodies" can occur with
inappropriately sized food items.
Other gastrointestinal disorders include stomatitis, esophagitis, enteritis, and colitis. Viral stomatitis with
ulcerative tongue lesions caused by foot-and-mouth disease is recognized in European hedgehogs.
Gastrointestinal parasitism is unusual but must be considered in all cases of weight loss and diarrhea.
Cryptosporidiosis can be fatal in pygmy hedgehogs. There is a high incidence of neoplasia in the
gastrointestinal tract of hedgehogs. Hepatic lipidosis is a common finding on necropsy.
Non-infectious causes of diarrhea must also be considered. Malnutrition and sudden diet changes should
be evaluated. Antibiotic use does not seem to be a factor in inducing diarrhea in the hedgehog.
As in other exotic species, respiratory disease may not be apparent until advanced stages of the disease.
Bronchopneumonia and catarrhal rhinitis caused by Bordetella bronchiseptica and Pasteurella multocida
occurs in hedgehogs. Heart disease is an important differential; dilated cardiomyopathies can present in
failure with effusion and dyspnea.
Neoplasias are very common in hedgehogs over 2 years of age. Squamous cell carcinoma of the oral cavity
seems to be over-represented and lymphosarcoma of any body part. Any system can be affected (skin,
reproductive tract, liver, lymph nodes e.g.) All lumps and bumps seen in the hedgehog should be
considered suspect and excisional biopsy is recommended. Other clinical signs to consider include chronic
weight loss, weakness, dyspnea, anorexia, and ascites.
1. Allen ME: The nutrition of insectivorous mammals. In Proceedings of the Annual Meeting of the
American Association of Zoo Veterinarians, Oakland, CA 1992, pp 113-115
2. Done LB, Dietze M, Crnafield M, et al: Necropsy lesions by body systems in African hedgehogs: Clues
to clinical diagnosis. In Proceedings of the Annual Meeting of the American Association of Zoo
Veterinarians, Oakland, CA 1992, pp 110-112
3. Gregory MW, Stocker L: Hedgehogs. In Beynon PH, Cooper JE (eds): Manual of Exotic Pets.
Gloustershire, England, British Small Animal Veterinary Association, 1991, pp 63-68
4. Hoefer HL: Hedgehogs. In Vet Clin North Am Sm Anim Pract 24 (1) pp 113-120, 1994
5. Reeve, N: Hedgehogs. T&AD Poyser Ltd, London, 1994.
TECHNIQUES IN RABBIT AND RODENT DENTISTRY
Heidi L. Hoefer, DVM, ABVP
West Hills Animal Hospital
Normal Anatomy and Physiology
The rabbit has a large mandible with a deceptively small oral cavity. The dental formula is: I
2/1, C 0/0, P 3/2 M 3/3 with all teeth continually growing and open-rooted (aradicular
hypsodont or long-crowned without an anatomical root). The second pair of upper incisors are
small "peg teeth" that sit behind the upper incisors and may be difficult to see in the normal
dental arcade. Some rabbits do not have this second pair of incisors. Unlike most rodents, rabbits
do not have pigmented enamel.
The rabbit uses its chisel-like incisors for lateral slicing movements that cut or crop grasses before
mastication by the cheek teeth. The cheek teeth are arranged in parallel rows and have a flat
occlusal surface. The jaw can move dorsal-ventral, rostro-caudal, and lateral for chewing. The
rostro-caudal action is limited (as compared to rodents) but the lateral action is extensive.
Rodents possess less incisors and cheek teeth than rabbits and tend to have pigmented (yellow)
enamel. The murine-type small rodents (rats, mice, hamsters) have a dental formula I 1/1, C 0/0,
P 0/1, M 3/3. They have open-rooted incisors but the cheek teeth have anatomical roots. This is
also true for prairie dogs and squirrels. This arrangement reflects their natural dietary habits: a
diet of grains, tubers, and roots requires less chewing and is less abrasive to the cheek teeth. The
incisors, on the other hand, are worn done from gnawing and need continual replacement.
Guinea pigs and chinchillas have the common formula of: I 1/1, C 0/0, P 1/1, M 3/3. All teeth
are open-rooted. They are true herbivores from a somewhat barren, rocky terrain of the South
American Andes Mountains. Vegetation is tough and fibrous, and its' low energy content
requires a high intake and thorough chewing. This natural diet results in the continual wear of
the cheek teeth which have a large grinding surface and no anatomical root. Unlike the rabbit
which has parallel rows of teeth, the cheek teeth in the chinchilla and the guinea pig diverge from
rostral to caudal. The mandibular cheek teeth are set wider apart than the maxillary sets.
Because of the small oral cavity and large tongue of most rabbits and rodents, a thorough oral
examination may be difficult without anesthesia. For a quick exam in an unsedated animal, an
otoscope cone with a light source can be inserted alongside the tongue and the cheek teeth. This
quick look may be obscured by salivation and food in the oral cavity. A better instrument in the
larger species is a nasal (human) speculum with an attached light source (Welch-Allyn bivalve
nasal speculum #26030). This resembles a small vaginal speculum and has the added bonus of a
light and a rechargeable handle attachment (3.5V). The blades of the speculum are used to push
the tongue aside to allow a quick look at the cheek teeth in both the awake and anesthetized
animal. Gauze strips placed around the upper and lower incisors aid in visualization by
allowing the jaw to be pulled wide open without obscuring the view.
For a complete oral examination, sedation or anesthesia will be needed in most individuals.
Isoflurane and a face mask can be used but there is the disadvantage of working around the
mask and anesthetic vapors. A short acting injectable can be used; I prefer ketamine and valium
given as a small IV bolus in the same syringe (3-5 mg/kg ketamine plus equal or double volumes
of Valium to start) or for longer procedures, ketamine can be given IM (15-20 mg/kg plus
midazolam (Versed® @ 0.5 mg/kg IM) or diazepam (Valium® @ 1-2 mg/kg IM). Other
anesthetic protocols are available in the literature. Xylazine (Rompun®), acepromazine,
tiletamine-zolazepam (Telazol®), and demetomidine (Dormitor®) have all been used.
To perform a complete dental evaluation, skull radiographs are necessary. This is especially
important in those cases that present with clinical signs of malocclusion (drooling, grinding, e.g.)
but have no obvious dental points on oral examination. Skull radiographs are important for
evaluating the occlusal surfaces as well as the roots. Check for root elongation on both
mandibular and maxillary arcades.
Most small mammals will need sedation for skull radiographs. I prefer isoflurane for this
procedure because it offers complete immobilization and rapid recovery for out-patient
procedures. A straight lateral radiograph can often provide the necessary information although
in some cases, four views might be necessary: lateral, ventro-dorsal, and 2 obliques. Use of a
film-screen combination that is suitable for radiographing extremities is preferrable. Another
alternative is mammography film (Min R). "Mammo"" film is a single emulsion film that
provides ultra-detail films, especially of boney structures. A used cassette can be purchased from
most distributors. On a typical Bennett machine, use an mAS of 10 (100mA) and KVP of 60-64 in
the chinchilla, for example. The cassette is used in the tabletop position.
Clinical signs of dental disease are what one might expect: ptyalism, grinding, selective appetite
or complete anorexia. Facial fur can become matted from salivation, and the forepaws are often
matted from facial grooming. Halitosis can be a problem in cases with abscessation. Epiphora
may be present, representing maxillary root extension into the nasolacrimal duct area. In severe
maxillary root problems, there can be upper respiratory compromise, especially in obligate nasal
breathers like the rabbit or prairie dog.
Patients with primary dental disease are still bright and alert initially and appear to be hungry.
In long-standing cases, however, these individuals can become very debilitated and suffer from
secondary problems like dehydration, cachexia, hepatic lipidosis, and in guinea pigs, the effects
of hypovitaminosis C.
Common Dental Diseases
Primary incisor malocclusion is a common dental condition seen in murine rodents, and some
dwarf breeds of rabbits. Incisor malocclusion in the guinea pig and chinchilla is usually a result
of overgrown crowns in the cheek teeth and rarely presents as a primary problem. Incisor
malocclusion in rabbits can be the result of mandibular prognathism or secondary to cheek teeth
derangement. Maloccluded rabbit incisors can become "tusk-like" in severely overgrown cases.
Rodent incisor malocclusion tends to be more subtle, with the upper teeth curling backwards into
the mouth, and the lower teeth piercing the palate in severe cases. While some individuals are
adapt at breaking off these teeth on the cage bars, the treatment for primary incisor malocclusion
involves regular cutting of the affected teeth or permanent extraction.
Care should be taken with incisor cutting. Splitting and shattering is common with certain
instruments and can lead to pain and less likely, root infection. Dental drills are probably best
but are more likely to lacerate soft tissue in the un-sedated patient.
In some chronic cases of incisor malocclusion in the rabbit, extraction may be indicated. Incisor
extraction is performed under heavy sedation or anesthesia, using a straight-tipped 1 mm
periosteal elevator to break down the interdental ligaments. The Crossley rabbit dental extractor
(Jorgensen Laboratories, www.jorvet.com) is also convenient to use, and a large gauge
hypodermic needle can facilitate extraction. All 6 incisors are removed. Care must be taken not
to pull too hard or against the natural curvature of the tooth to prevent breaks. The pocket is
cultured if infected, flushed and left open. The bunnies are given analgesics before recovery and
oral antibiotics for 10 days post extraction or longer if tooth root infection is present.
Tooth elongation affects both the root and the crown and is common in rabbits, chinchillas, and
guinea pigs on a low roughage diet. Pellets, grains, and most vegetation do not provide enough
chewing to wear down the cheek teeth, resulting in elongation. Coronal elongation in rabbits
tends to result in sharp spurs while in the guinea pig and chinchilla, crown elongation tends to
lead to tooth curvature and poor occlusion. Root extension forms palpable "bumps" on the
mandible and is readily seen on radiographs and CT scans. Maxillary root extension is difficult
to palpate but may be associated with ocular problems (epiphora, proptosis, e.g.) or upper
respiratory signs. Oral examination may show a somewhat “normal” occlusal surface and lack of
points, or the crowns may appear elongated and form sharp spurs that lacerate soft tissues in the
Crown elongation and sharp spurs can be reduced using rongeurs, files, and dental drills. The
cheek teeth need to be done under anesthesia. A small bone rongeur (Lempert) is often used to
file points but can exert enough force to damage periodontal and periapical tissues. High or low
speed hand held dental drills should be used to burr down sharp points and reduce crowns
down to gingival level. Owners should be aware of the likelihood of recurrence and the need for
regular dental care (every 6-8 weeks). Root extension is irreversible and may result in chronic
weight loss and painful mastications, especially in chinchillas. These individuals are usually on
syringe feedings and analgesics, which exacerabates the lack of wear on the crowns. Euthanasia
may be indicated for these chronically painful individuals.
Tooth root abscesses are a serious problem in any rabbit or rodent. Most of these abscesses
cannot be totally excised and recurrence is possible. Treatment consists of extraction of affected
teeth and aggressive surgical debridement. There is usually long-term follow-up care in these
patients with second and third surgical procedures possible. Radiographs must be taken before
surgery to assess the extent of tooth root involvement and evaluate for osteomyelitis of the jaw.
Once the infected area has been surgically debrided, several therapeutic options are available.
One older technique involves packing the pocket with calcium hydroxide, a dental preparation
that has a pH of 12 and essentially "nukes" everything in it's wake. This can cause severe
necrosis of normal tissues if leakage or improper placement occurs. Placement of bone matrix
materials like hydroxyapatite or bioglas (Consil® Nutrimax Labs) may enhance healing of the
affected bone following thorough debridement. Another technique involves the use of antibiotic-
impregnated polymethylmethacrylate beads into the site. Doxycycline gel (Doxyrobe® Upjohn)
can be injected into the abscess pocket. Anaerobic and aerobic cultures should be taken
whenever possible. Many of these abscesses are caused by anaerobic bacteria and appropriate
antibiotic selection is important.
Prairie dogs can have incisor tooth root aberrations that can lead to upper respiratory (nasal)
obstructions. Odontomas and other related space occupying masses can form at the tooth roots
leading to eventual encroachment on the nasal airways. Chronic trauma from cage bar chewing
may play a role in odontoma formation. These obligate nasal breathers present with non-
responsive dyspnea. Diagnosis is with radiographs or CT scan. Corrective treatment is difficult
and carries a guarded prognosis.
Analgesics and Antibiotics
The long term use of antibiotics may be indicated in some dental conditions like root abscessation
or osteomyelitis of the mandible or maxilla. Common aerobic bacterial isolates include
Streptococcus, Pasteurella, and Staphylococcus and a variety of anaerobic bacteria Antibiotic choice
based on culture and sensitivity testing is recommended whenever possible, keeping in mind, of
course, those drugs that can be safely used in rabbits and rodents. Safe antibiotics include the
quinolones (enrofloxacin/ciprofloxacin), the aminoglycosides, trimethoprim-sulfa,
chloramphenicol, and in rabbits, injectable penicillin. Because of the potential suppression of
normal enteric flora, avoid any antibiotic that has a selective gram-positive spectrum. This
includes the beta-lactams (penicillins and cephalosporins), clindamycin, lincomycin, and
Analgesia is an important part of dental disease management, especially involving the tooth roots
where pain can be chronic. Injectable agents like butorphanol (Torbugesic® @ 0.5 mg/kg IM q 6-
8 h in rabbits and large rodents), buprenorphine (Buprenex® @ 0.05 mg/kg IM q 12h in rabbits
and large rodents), and carprofen (Rimadyl® inject @ 4 mg/kg SID) are good choices. Oral
analgesics have not been extensively studied but some clinicians use a compounded carprofen
suspension (Rimadyl® @ 2 mg/kg PO q 12h or 4 mg/kg q 24 h) to manage pain short term.
References and Recommended Reading
1. Bennett RA: Management of abscesses of the head in rabbits. Proceedings, The North
American Veterinary Conference, Orlando, Jan. 1999.
2. Brown SA: Surgical removal of the incisors in the rabbit. J Small Exot Anim Med 1992, 1; 150-
3. Crossley, DA: Clinical aspects of rodent dental anatomy. J Vet Dent, 12(4):131-135, 1995
4. Crossley, DA: Clinical aspects of lagomorph dental anatomy: the rabbit. J Vet Dent, 12(4):137-
5. Crossley DA: Dental disease in chinchillas in the UK. J Sm Anim Prac, 42, 12-19, 2001
6. Harcourt-Brown, F: Textbook of Rabbit Medicine. Oxford, Butterworth Heinemann (Elsevier
Science, Ltd), 2002, pp 165-205.
7. Crossley DA, Aiken S: Small mammal dentistry. In Quesenberry KQ, Carpenter JW, (eds.):
Ferrets, Rabbits, and Rodents, Clinical Medicine and Surgery, 2 nd edition. Philadelphia, WB
Saunders, 2004, pp 370-382.
8. Legendre, LF: Oral disorders of exotic rodents. Veterinary Clinics of North America Exotic
Pet Practice, 6(3), September 2003, pp 601-628.