4. The most common ingested material is rubber, such as shoe soles
and insoles, foam rubber, rubber dog and cat toys, and the
stuffing of furniture and mattresses. Also seen as GI FB are
pieces of towel, cotton, plastic and metal.
5. Gastric hairballs generally presents as a chronic wasting with
intermittent dark sticky stools. Melena and anemia is noted if
duodenal ulcer is present.
6. Treatment is a gastrotomy or enterotomy. Supportive care with
fluids and antibiotics and return to soft food in 24 hours.
7. Animals in good condition that have an acute but not complete
blockage may sometimes be treated medically with fluid
administration subQ and 2 - 3 cc of a feline hairball laxative
given p.o. TID. If the FB is not passed in 24 to 48 hours, or if
a crisis occurs, surgery should be performed.
B. cardiomyopathy
1. Both left ventricular hypertrophy and dilative forms are seen
generally in animals over 3 years of age.
2. Signs include a decrease in activity, stopping to rest in the
midst of vigorous play, dyspnea, splenomegally, and ascites.
3. Diagnosis by radiography and visualization of an enlarged,
rounded heart shadow and lung changes and ECG or ultrasound.
4. Treat as in the feline - in early cases, Lasix may be used
alone at .10cc/ ferret p.o. BID (dosage may be increased by
.l 0cc increments depending on the severity of the condition).
Inderol or digoxin may be used at feline dosages depending on
the nature of the disease.
5. We have seen a decrease in the number of cardiomyopathy cases
possibly due to the addition of taurine to feline diets. No
studies have been done to prove this relationship in the ferret.
C. Congenital malformations
1. Hemivertibrae are seen occasionally and can lead to
neurological deficits if severe.
2. Other defects include dark enamel on the teeth (particularly
the canines), and malformations of the feet and jaws, short
tails (this is not to be confused with tails and feet that are
bitten off accidentally by the mother at birth while cleaning
the newborn kitts)
D. Intervertebral disc disease
1. Has been reported in ferrets, diagnose by radiography and
reported response to corticosteroids.
2. Myelograms have been successfully done in ferrets
E. Anal gland impactions
1. Seen frequently - few signs early, ferrets seem to be very
"stoic". Ferret may chew at base of tail, may have thin stools
and tenesmus, may "scoot" rear end a lot. If ruptured, may
have draining lesion next to the rectum or even inside rectum.
2. Treatment is surgical drainage with antibiotic therapy followed
by bilateral anal gland removal in one to two weeks.
3. We do not consider this condition common enough to justify
routine anal gland removal in all ferrets.
F. Heat prostration - VERY COMMON - ferret: are very heat intolerant.
G. Dental disease
1. Tartar can be removed easily as in other pets.
2. Tooth root abscesses occur, particularly in the canine teeth.
Periodontal disease has also been seen.
3. Canine are difficult to remove, and if fractured can eventually
become abscessed. Repair can be done as in other species with
alloy amalgam if tooth is still viable.
H. Urolithiasis
1. Occurs in both males and females, seen infrequently in animals
on low ash diets.
2. Usually 90% magnesium ammonium phosphate hexahydrate and 10%
calcium apatite secondary to bacterial infections.
3. Surgically remove stones, use appropriate antibiotic and place
pet on low ash diet (the use of feline struvite diets have
shown poor results in causing stones to dissolve)
4. Severe blockages in the male may require a urethrostomy.
I. Aplastic anemia
1. Common in females in estrus for 1 month or longer (ferrets can
stay in estrus up to 6 months if they have not succumbed to
the anemia or related complications) - it is caused by a
hyperestrogenism leading to toxic bone marrow suppression.
2. Signs include anorexia, depression, posterior limb paresis,
lethargy; mucus membranes are very pale, the vulva is
swollen, and petechiae and ecchymoses may be present in mucous
membranes and skin. Alopecia may also be present.
3. Hematology reveals a severe nonregenerative anemia, normocytic
RBC's and nucleated RBC's, a depressed PCV (less than 25%)
and severe neutropenia, granulocytopenia and or thrombocytopenia.
4. Treatment is generally unrewarding when the PCV is 15% or less.
We recommend euthanasia these severe cases. If the PCV is
higher than 15%, the prognosis is still guarded, but therapy
may be attempted with repeated transfusions, iron, anabolic
steroids, antibiotics and other supportive care. An OHE should
be performed immediately, if possible.
5. Note: Ferrets have no apparent blood types, so repeated blood
transfusions can be performed without any problem. Approximately
20m1 of whole blood can be removed by cardiac puncture from a
healthy male ferret ( 2.5 kg or larger) with no side effects,
which can then be used immediately for transfusing.
J. Ophthalmic disease
1. Juvenile cataracts - probably hereditary. May appear before
one year of age in either one or both eyes.
2. Cataracts are also seen as an aging process in older animals
and concurrent with diseases such as adrenal neoplasia and
diabetes.
3. Retinal atrophy has been reported. Can be seen on routine eye
exam without mydriasis. Retina will appear hyperreflective.
May be related to poor taurine in the diet. No Rx.
K. Diabetes mellitus:
1. Usually created iatrogenically by too much carbohydrate -
especially refined sugar - in the diet.
2. Treat as in the feline - PZI or NPH insulin 0.5 -1 u/kg
given SID initially with increases as needed. Usually
unrewarding by the time the disease is diagnosed.
3. This disease can also be a result of insulinoma surgery
resulting from atrophied beta cells trying to regain normal
function after removal of the insulinomas. It is usually a
temporary situation, but may require short term insulin
therapy.
L. Polycystlc kidney - Unknown etiology, may result in terminal renal
disease or be an incidental finding in the older pet.
M. Eosinophylic gastroenteritis
1. Unknown e6ology - possible immune deficient disease
2. The signs are vague - lethargy, inappetence, wasting,
intermittent tarry stools, and splenomegaly.
3. Diagnosis is by intestinal biopsy or lymph node biopsy with
visualization of infiltration of eosinophils. A CBC may
reveal a peripheral absolute eosinophilia of 250 or higher.
4. Treatment is with prednisolone or prednisone at 0.50 -
2mglkg SID which will usually resolve signs
within 7 days, then slowly wean dose down to lowest effective.
This is a lifetime treatment. May need antibiotics,
supportive fluid therapy and forced feedings initially.
N. Splenomegaly
1. Splenomegaly is a very common finding in the ferret, esp. in
those over 3 years of age. It is not always possible to
find a specific reason for the enlargement, but is usually
a benign finding. However, there are a number of diseases
that are associated with splenomegaly and diagnostic tests
should be done to rule out these problems. The following
is a list of diseases to be considered in a differential.
Refer to each disease in other areas of this paper for
diagnostic procedures:
| Lymphosarcoma |
Systemic infection |
Eosinophilic gastroenteritis |
Splenitis |
| Cardiomyopathy |
Adrenal neoplasia |
Systemic mast cell neoplasia |
Insulinoma |
| Hypersplenism |
Hemangiosarcoma |
Aleutian's disease |
Colds and flu |
2. Splenitis has been responsive to a splenectomy and antibiotic
therapy. Hypersplenism is a "catch all" term that refers to
a condition that presents with a high fever, leukopenia,
erythrocytopenia and depression. The condition responds to
splenectomy and corticosteroid therapy at .50 - 2mglkg. Unknown
etiology, but it is possibly an early sign of lymphosarcoma.
O. Alopecia
1. There are several reasons for alopecia in the ferret, but
one should be thinking primarily of endocrine disease.
In very warm weather some ferrets may develop thinning of the
coat, but there should not be large alopecic areas. Dietary
problems also do not generally lead to alopecia, but rather
dry, or sparse coats. Skin parasites, other than fleas, are
a rarity.
2. The most common reason {95%) for alopecia in the neutered
pet is adrenal neoplasia. In the intact female the most
common reason is estrus alopecia. Intact males in rut may
rub their scrotums over things to mark territory, which may
wear the hair off, but this is not a true alopecia. Other
causes have been granulosa cell tumors, luteomas and
fibrosarcomas in both the intact and neutered animals. Mast
cell tumors of the integument have also been associated with
alopecia, which resolved when the tumors were surgically
removed.
3. Hair loss on the tail has been frequently observed,
particularly in the fall of the year. The alopecia occurs
only on the tail and may be total or partial. A reddish-
brown waxy deposit or black spots may also be present. The
condition resolves on its own in I - 3 months. No medications
are necessary. This is probably a response to changes in the
photoperiod. The true etiology is unknown.
IXX. NEOPLASIA
(NOTE: VVHENEVER PERFORMING EXPLORATORY SURGERY IN THE FERRET, LOOK AT
EVERYTHING, BECAUSE MULTIPLE DISEASE PROBLEMS ARE COMMON)
A. INSULINOMA (pancreatic beta cell tumor)
1. This is the most common endocrine neoplasia. Found in both
sexes 3 years of age and older. Commonly occurs concurrently
with adrenal neoplasia.
2. Signs include: Periods of lethargy, depression, staring
blankly into space, and posterior weakness that seem to
resolve spontaneously; periodic hypersalivation and pawing
at the mouth are common (an indication of nausea);
splenomegaly; periods of semiconsciousness or seizures may
occur as the disease progresses. If left untreated, this will
result in coma and death.
3. Diagnosis is based on the demonstration of low fasting blood
glucose levels. We recommend fasting no longer than 6 hours.
Blood glucose levels 65 and below are diagnostic. Levels
between 85 and 65 are highly suspicious. It may be necessary
to run more than one blood glucose test.
4. High insulin levels may also be demonstrated with this disease.
Insulin tests may be run along with a fasting blood glucose
and are recommended for borderline glucose readings. Insulin
levels over 20 are diagnostic. An amended insulin/ glucose
ratio is also helpful. If the fasting blood glucose is 65 or
less, however the insulin and AIGR will appear within normal
limits even in the presence of an insulinoma.
5. Treatment
a. Surgical removal of the tumors is the best first
choice. Although all of the tumors may not be
removed, this debulking procedure can buy medication
free time for the pet. It may prolong the life of
the ferret for up to 2 years or longer. Pancreatitis
is rarely a problem, and the larger tumors are
easily visualized. Look for metastasis in the liver,
spleen and nearby lymph nodes and biopsy as needed.
Surgery may need to be repeated at a later date.
b. Occasionally one encounters a situation where the
tumors are not easily visualized. In this instance,
resect a section of pancreas near the tip for
histopathology. Insulinoma may be diffuse, or
hyperplasia of the pancreas may be present which will
also result in hypoglycemia (may be preneoplasicic).
c. A consequence of surgery may be a transient diabetic
state, as the atrophied beta cells try to recover
their function. Glucosuria and hyperglycemia may be
present for several days to two weeks post surgically.
It is generally unnecessary to treat this condition.
PZI or NPH insulin may be used at 1 unit per ferret
if the glucose is over 300 and the pet is depressed.
d. Rarely, the diabetic condition will persist and need
to be treated with insulin for the life of the
pet.
e. Medical and dietary treatment for insulinoma also buys
quality time for the pet and may be used with or
without prior surgical intervention.
1. Prednisolone or prednisone is used at 0.25
-1 mg/kg SID initially and then increase or
decrease the dose to control the signs.
2. Proglycem (diazoxide), an insulin blocking
agent, is used at l 0mg/kg BID to start, and
can be increased to l 5mg/kg as needed. It is
a hypertensive drug, so lethargy and depression
may be noted - especially if cardiovascular
disease is present.
3. Frequent protein meals, such as meat baby food.
Sugary treats should be avoided unless being
used during a hypoglycemic episode for a quick
sugar boost. As soon as the animal is out of
danger, administer a high protein food to keep
the blood glucose level from dropping again.
4. 1 /8 tsp. of brewers yeast two times daily
mixed with a protein food (not sugar) contains
chromium which has been reported to help
stabilize blood glucose and insulin levels in
humans.
6. Prognosis is always guarded, but with surgery and medications,
ferrets have been able to have a quality life for 6 months to
over 2 years post diagnosis.
B. Adrenal neoplasia
1. This is the other most common neoplasia. This is a primary
adrenal disease usually caused by adrenal cortical adenomas
or adenocarcinomas. The pituitary does not seem to be involved
as far as we know at this time. As previously mentioned,
insulinoma and adrenal neoplasia commonly occur concurrently.
2. Signs are similar to those seen in other Cushinoid pets:
a. Bilateral alopecia, usually starting over the base
of the tail and progressing anteriorly. (7'here may
be a history of repeated alopecia and regrowth). Early
on the alopecia may respond to thyroid replacement
therapy, but eventually this will fail.
b. Thinning and softening of the skin. There may be scabs
and excoriation\rquote s present and excessive dryness
and intense pruritis.
c. Atrophy of abdominal musculature and mobilization of
fat to the abdomen leading to a "pot - bellied"
appearance.
d. Atrophy of skeletal musculature leading to hind limb
weakness.
e. Spayed females may develop an enlarged vulva as if in
estrus and / or enlarged mammary glands. Males act
as if they are intact again and try to mate with the
females or other neutered males. Males may also have
enlarged mammary glands.
f. Both genders may develop a strong body odor like that
of an intact animal. The skin may be greasier.
g. There is no noticeable polyuria or polydipsia
h. May be a neutrophilicleukocytosis and lymphopenia.
i. There is commonly a low serum T4.
4. Diagnosis is primarily made on the clinical signs. An ACTH
stimulation test or a dexamethasone suppression test can be
done using ferret protocols, but false negatives are not
uncommon. The types of hormones produced by these tumors
appear to be quite different than dogs and cats.
5. Ultrasounds and CAT scans have also been used to detect
adrenal abnormalities.
6. Surgery is the first treatment of choice. Frequently the
left adrenal is the only one affected and it can be easily
removed . The right adrenal can be difficult to remove due
to its precarious position between the vena cava and the
aorta. If both adrenals are affected, remove the left for
histopathology and for debulking. If complete removal is not
possible, then a biopsy should be performed. If pathology
results are benign, Lysodren therapy may be used on the
remaining adrenal(s). (Lysodren does not work well on
adenocarcinoma). No success has been reported with bilateral
adrenalectomies. Another reason for surgery is that
insulinoma is commonly present, but is masked on lab tests by
the excessive cortisol being produced by the adrenal. Removal
of insulinomas increases the chance of success of any medical
therapy that may need to be used post surgically.
7. After surgery on a known adrenal neoplasia ferret, whether
the adrenal is removed or not, one should use Dexamethasone
immediately post surgically at . 50mg/lb IM followed on the
next day with .25mg/kg of prednisolone SID for 5 days then
every other day for 3 doses. This eases the post surgical
transition. Fluid therapy is recommended for at least the
first 48 hours.
8. Lysodren has shown excellent results in many cases of adenoma.
The dosage is 50mg/kg (for most ferrets 50mg/ferret can be
used) SID for 7 days, then every third day for up to 8 weeks.
The dose may have to be increased or decreased in frequency
depending on the case. The drug must be compounded by a
pharmacist who must put it in the smallest gelatin capsule
possible with cornstarch as a filler. The Capsule must
swallowed hole. If the medication is mixed with another
substance or saliva. it will be ineffective. Lysodren has no
effect on the bone marrow, so routine CBCs are not required.
Its effects in other animals is primarily GI. No side effects
have been noted in ferrets at this dose.
9. The main draw back to Lysodren treatment without prior surgery
is that insulinoma is also a common concurrent disease, and
as the cortisol levels drop with therapy, the blood glucose
levels may drop also and lead to a sudden and severe
hypoglycemic crisis. It would be advisable to check fasting
blood glucose levels during Lysodren therapy unless an
exploratory had been done first.
10. Ketaconizole has had disappointing results.
C. Lymphosarcoma
1. This is another commonly seen neoplasia of ferrets. It occurs
at all ages. Research is currently being done on this disease
to try to isolate a viral agent. Information regarding this
research can be obtained from the address included at the
end of this paper.
2. Signs of disease are variable depending on the system
affected:
a. Splenomegaly
b. Peripheral and localized lymphadeopathy
c. Wasting and lethargy, despite normal eating habits.
d. Mediastinal andl or sternal Lymph node enlargement
with associated dyspnea, tacchypnea and exercise
intolerance.
e. Pyrexia and collapse
f. Masses or lumps on the skin
g. Persistent absolute lymphocytosis (over 3,500)
h. Persistent leucocytosis (10,000 or higher) with 45%
or higher lymphocyte count.
3. Diagnosis is by a variety of methods.
a. CBC may be helpful - may see leukocytosis with
abnormal circulating lymphocytes, persistent
absolute lymphocytosis, anemia, leukopenia, and /
or thrombocytopenia. However, many CBCs appear normal.
b. Lymph node removal (biopsy is difficult due to the
large amount of fat around the lymph nodes), popliteal
nodes are the easiest to remove.
c. Thoracic fluid aspirate and cytology
d. Bone marrow aspirate (femur is easiest)
e. Biopsy of mass
f. Splenic aspirate, which can be accomplished with a
25 ga needle and a 3 cc syringe through the body
wall (We find this to be of only occasional value)
4. Treatment
a. Prognosis is guarded. Young animals are poor
treatment cases. The disease spreads much faster
through their systems. Older animals with more subtle
disease are better candidates.
b. Do a complete pretreatment work up, CBC, chemistries,
and radiographs.
c. Start chemotherapy with prednisolone at 2mglkg p.o. on
the same day as the vincristine is started I.V. The
pred is continued daily throughout vincristine therapy.
The vincristine dose is 0.05mg (0.05cc) for ferrets up
to 1 kg and 0. l 0mg (0. l 0cc) for ferrets over 1 kg.
Use a butterfly catheter and a saline flush before and
after administration of vincristine. A light sedation
with ketamine as previously described or isoflurane is
recommended.
d. Vincristine therapy is continued weekly for 4 weeks
total. CBCs should be checked weekly and if thc WBC
drops below 2,000 or if severe thrombocytopenia or
anemia occurs, then vincristine is discontinued for
one or more weeks until the blood picture improves.
e. Cytoxin is given once every three weeks p.o. for 3
doses at 1/4 of a 25mg tablet per ferret. DO NOT GIVE
CYTOXIN ON TO SAME DAY AS VINCRISTINE - HAVE A THREE
DAY INTERVAL. (Some ferrets have had successful
treatment with Vincristine without the use of Cytoxin)
f. After vincristine therapy is completed, continue pred
for 4 - 5 more weeks, gradually weaning down the
dosage and doing exams and CBCs weekly.
g. Complications of chemotherapy have been similar to
those seen in other animals, including depression,
weakness, anorexia, whisker loss, hair loss, bone
marrow suppression. GI signs are uncommon.
h. Success rate for this therapy is about 70% with over 2
years remission in some cases.
i. In cases of persistent lymphocytosis, that were unable
to be confirmed as lymphoma by diagnostics, but that
histopathology calls lymphoid hyperplasia, we recommend
treating these with Alkeran (melphalan). There is great
suspicion that these may be preneoplastic lymphoma
cases. The following protocol is suggested:
1. Use in cases of persistent absolute
lymphocytosis (3500 or higher)
2. Perform CBCs weekly throughout therapy.
3. Have pharmacist make up Alkeran in small
capsules in 0.10 mg and 0.05mg amounts.
4. Start therapy with one 0.10 mg capsule per
ferret SID for two weeks.
5. Then go to one 0.50mg capsule per ferret SID for
two weeks.
6. Finally wean off using 0.50 mg capsule per
ferret every 2 days for 2 doses, then every 3
days for 2 doses, then every 4 days for 2 doses.
7. Discontinue therapy if CBC shows changes as
described under chemotherapy section.
D. Reproductive tract neoplasia
1. Granulosa cell tumors, luteomas and leiomyomas have been seen
in intact females and in remnant ovarian tissue left in spayed
females.
2. Sertoli cell tumors have been seen in intact male ferrets.
E. Miscellaneous neoplasia
1. Skin tumors are a very common neoplasia seen in the ferret 3
years of age and older. The most common is the mast cell
tumor. They appear as raised, flat, "button = like" lesions
(not unlike a human wart) that may be red or crusty due to
pruritis and scratching. They sometimes appear to come and
go. They are usually benign, but removal is recommended.
Patchy areas of alopecia have been associated &127&127 mast
cell tumors, the hair regrowing when the tumor was removed.
Systemic mast cell disease has also been seen with mast
cells being present in peripheral lymph nodes and spleen.
Multiple mast cells that are too numerous to remove may be
treated with corticosteroids.
2. Sebaceous gland adenomas, adenocarcinomas and histiocytomas
can also commonly be seen on the skin.
3. Fibrosarcoma has been seen on the extremities and in the
abdomen. One abdominal case was associated with generalized
alopecia which resolved when the tumor was removed.
4. Chondromas are common on the tip of the tail and should be
removed.
5. Other neoplasias seen are hemangiomas and hemangiosarcomas,
thymomas, mesotheliomas, osteomas, and osteosarcomes,
chordomas, gastric neoplasia and others.
NOTE: THE EXPLORATORY IS A VALID AND VALUABLE DIAGNOSTIC TOOL IN THE FERRET AND CAN BE USED SAFELY IN ROOST INSTANCES WHEN PERFORMING AN EXPLORATORY FOR ANY REASON ON A FERRET LOOK AT EVERYTHING, BECAUSE CONCURRENT DISEASES AND ABNORMALITIES ARE CONRMON.
GENERAL FERRET RESEARCH INFORMATION: LYMPHOSARCOMA RESEARCH INFORMATION:
Dr. James G. Fox Dr. Sucan Erdman
Div. of Comparatlve Medicine Div. d Comparattve Medkiae
MIT Building 45 MIT Buildlng 45
37 Vassar St 37 Vassar St
Cambridge, Mass. 02139 Cambridge, MA 02139
(6l7) 253-l722 (617) 253-l722
ALEUTIAN TESTS CAN BE SENT TO: INFO. ON RETINAL ATROPHY AND ALKERAN THERAPY
United Vaccines Dr. Thomas Kawasaki
2826 Latham Dr. Old Brldge Veterlnary Hospital
Madison, WI 53713 Woodbridge, VA
1-800-283-6465 (703)494-0094
INFO. ON HEARTWORM TREATMENT AND INFO. ON FERRET SURGERY AND CHEMOTHERAPY
DIAGNOSIS IN THE FERRET: PROCEDURES:
Dr. Deborah Kemmerer Dr. Susan Brown
West End Animal Hospital Midwest Bird and Exotc Animal Hospital
Rt 2 Box 207W 1923 S. Mannheim Rd.
Newberry, FL 32669 Westchester, IL 60559
(904) 332-4357 (708) 34&1278166
INFO. ON FERRET SURGERY AND GENERAL CARE:
Dr. Robert Ness
Glendale Pet and Blrd Clinic
1144 Maln St.
Glendale Hts. IL 60139
(708) 858-3530
REFERENCES AND RECOMMENDED READING:
1. Fox, J.G. : Biology and Diseases of the Ferret 1988
2. Hoover JP, Baldwin CA, Rupprecht CE. Seriologic Response of Domestic
Ferrets (Mustela putorius, furo) to Canine Dlstemper and Rabies Virus
Vaccines. J Am Vet Med Assoc 1989; 194: 234-238.
3. Kruger KL, Murphy JC, Fox JG. Treatment of Proliferative Colitis in Ferrets.
J Am Vd Med Assoc 1989;194: 1435 -1436
4. Rupprecht CE, Gllbert J, Pltts R, Marshall KR, Keprowski H. Evaluation
of an Inactive Rabies Vaccine in Domestic Ferrets. J Am Vd Med Assoc
l990; 196 161 a -1616.
5. Kociba GJ, Caputo CA. Aplastic Anemia Associated With Estrus In Pet
Ferrets. J Am Vd Med Assoc. 1981; 178: 1293-1294.
6. Nguyen HT, Moreland AF, Shlelds RP. Urolithiasis in Ferrets (Mustela
putorirts furo). Lab An Sci 1979; 29: 2d3 - 245.
7. Luttgen PJ, Storts RW, Rogers KS, Morton LD. Insulinoma in a Ferret.
J Am Vet Med Assoc 1986; 189: 920 - 921
8. Llberson AJ, Newcomer CE, Ackerman JI, Murphy JC, Fox JG. Mastitis
Caused by Hemolytic Escheria ecoli in the Ferret. J Am Vd Med Assoc
1983; 1 d3: 1179 -1181.
9. Dacust PY, Hunter DB. Spontaneous Aleutian Disease in ferrets.
Can Vet J 1978; 19: 133 -135.
10. Fox JG, Murphy JC, Ackrerman MS, Prostack KS, Gallagher CA, Rambow VJ.
Proliferative Colitis in Ferrets. l982; 43: 858 - 864.
ll. Stauber E, Robinette J, Basaraba R, Riggs M, Bisbop C. Mast Cell tumors
in Three Ferrets. J Am Vet Med Assoc 1990; 196: 766 - 767.
12. Garibaldi ME, Goad P, Fox JG, Sylvia TJ, Marray R. Serum Cortisol
Radioummunoassay Values In the Normal Ferret and Response to ACTH
Stimulation and Dexamethasone Supression Tests. Lab An Sd 1988;
38: 452 - 454.
13. Mannlng D, Bell J. Lack of Detectable Blood Groups In Domestic Ferrets
Implications For Transfusion. J Am Vet Med Assoa 1990; l97: 84 - 86.
14. Johnson - Delany C, Nelson W. A Rapid Proccdure for Filling Fractured
Canine Teeth in Ferrets. J of Small Exotic Animal Medidne l992; 3:
l OJ -102
15. Kawasaki T., Retinal Atrophy In the Ferret. J of Small Exotic Animal
Medidne l992; 3: l37.