Download top 10 exotic companion mammal diseases you need to know

TOP 10 EXOTIC COMPANION MAMMAL DISEASES YOU NEED TO KNOW
Dan H. Johnson, DVM, Dipl. ABVP (Exotic Companion Mammal Practice)
Avian and Exotic Animal Care
Raleigh, North Carolina, USA
[email protected]
919-844-9166
FERRET ADRENAL DISEASE
Adrenocortical disease (ACD) affects middle-aged to older ferrets with a reported prevalence of up to 25%.
Sex steroid levels may be increased as a result of adrenocortical hyperplasia, adenoma, or adenocarcinoma.
Neutering, photoperiod, and genetics are believed to play a role in the etiology. Adrenal disease typically
causes dorsocaudal alopecia in either gender. Pruritis, sexual or aggressive behavior, and a noticeable
increase in musky odor can also occur. Affected females may develop vulvar enlargement, and males may
present with stranguria or urinary obstruction secondary to prostatic hyperplasia, prostatic cysts, prostatic
abscesses, or prostatitis. Additional clinical signs may include estrogen-induced bone marrow toxicity,
mammary gland hyperplasia, cystitis, muscle atrophy, and lethargy. Clinical signs vary depending on which
sex hormones are elevated; however, clinical signs do not always correlate with the size of the affected gland
or degree of adrenal pathology. Physical exam findings of symmetrical alopecia, swollen vulva, or palpable
mass cranial to the kidney are suggestive of ACD. Elevations in plasma estradiol, androstenedione, and 17OH-progesterone are diagnostic (UT ferret adrenal hormone panel;865-974-5638). Ultrasonography can
demonstrate adrenal gland enlargement and distinguish right versus left ACD for surgical planning, and surgery
permits biopsy with histopathology. The goals of management are to reduce sex steroid production and to
provide a normal life span and a good quality of life for the patient. Surgery aims to remove or debulk the
tumor (adrenalectomy), whereas medical treatment (hormonal suppression) does not affect the tumor and is
not curative. Treatment choice depends on which gland is affected (left vs. right), surgeon’s experience,
severity of clinical signs, age of the animal, concurrent diseases, and owner finances. The GnRH agonist
leuprolide acetate was the mainstay of medical therapy for ACD until the introduction several years ago of a
longer-acting alternative, deslorelin acetate. Neutering appears to promote ACD in ferrets by removing sex
hormonal negative feedback on the hypothalamusleading to overproduction of gonadotropin-releasing hormone
(GnRH). In response, the pituitary maintains persistently elevated luteinizing hormone (LH) and folliclestimulating hormone (FSH). LH binds with functional receptors on the adrenal gland, causing it to overproduce
sex hormones and inducing hyperplastic and/or neoplastic adrenocortical enlargement. Therefore, by using
deslorelin implants as an alternative to surgical spay or castration, it may be possible to prevent ACD in ferrets.
FERRET INSULINOMA
Insulinoma is the most common neoplasm in ferrets, typically affecting thoseover 2 years of age. Islet cell
tumors secrete high levels of insulin and cause hypoglycemia. Clinical signs include lethargy, weight loss,
weakness, ptyalism, bruxism, seizures, and death. Onset of symptoms may be gradual or sudden. Appetite
may be normal or decreased, and weight loss may be noted. Advanced insulinoma results in hypoglycemia,
causing weakness, anorexia, lethargy, stupor, and seizures. The ferret’s eyes may appear “glazed” during
episodes. Hypersalivation and pawing at the mouth (presumably due to nausea, numbness, or tingling) also
occur. Affected ferrets may present with hind limb paresis or ataxia, as if nerve damage has occurred. In
patients where insulinoma is suspected but blood glucose is within normal limits (80-120 mg/dL), a carefully
monitored 3- to 4-hour fast may be required to confirm hypoglycemia. A presumptive diagnosisis made when
ferrets demonstrate fasting blood glucose of less than 60 mg/dL in the presence of clinical signs of insulinoma
and these signs cease after a feeding or intravenous administration of glucose. Histopathology of surgical
biopsy is required for definitive diagnosis. Tumors may be described as hyperplasia, adenoma, or carcinoma,
and a specific tumor may have a combination of any of these processes. Treatment modalities include medical
therapy (diazoxide, prednisolone), chemotherapy (doxorubicin), and surgery (nodulectomy, partial
pancreatectomy). Insulinoma is a disease that is likely to progress despite the best efforts of the owner and
veterinarian.Ferrets treated with surgery tend to remain symptom-free for longer and live longer than ferrets
treated with medicine alone. The etiology of insulinoma is unknown, however a nutritional hypothesis is
suspected by many. Therefore, low carbohydrate, low fiber, high protein, high fat, highly digestible meat-based
diets (including raw and whole prey diets) are recommended (but NOT proven!) to prevent insulinoma.
RABBIT UTERINE NEOPLASIA
Uterine adenocarcinoma is the most common neoplasia of female rabbits. The incidence is reported to be as
high as 80% in does over 3-4 years of age. With age, the endometrium undergoes progressive changes; from
polyp formation, to cystic hyperplasia, to adenomatous hyperplasia, to adenocarcinoma. Endometritis,
pyometra, hyperplasia, and uterine aneurysms are also reported. Adenocarcinoma is a slowly developing
tumor. Local invasion occurs as the neoplasia progresses, and metastasis typically occurs late in the disease.
Hematuria is the most common clinical sign. Serosanguinous vaginal discharge may be present. Frank blood
in the urine is most obvious and the end of urination. Cystic mammary glands may also occur. Depression,
anorexia, and dyspnea may be present in the later stages. Anemia can be severe in chronic or advanced
cases. Differentials for hematuria in rabbits include porphyuria, urolithiasis, and cystitis. Diagnostic workup
should include CBC, blood chemistry, and radiographs. Ultrasound may be important. Ovariohysterectomy is
curative if the tumor is confined to the uterus. Prevention is by client education and spaying does when they
are between 6-12 months of age.
RABBIT BLADDER SLUDGE
Rabbits absorb all of the calcium they ingest, and eliminate the excessin their urine. Sludge forms when
normal calciumsediment combines with mucus, protein and cellular debris and then comes to rest in a dense,
doughy layer along the ventral bladder wall. Sludge may lead to cystitis, bladder distension, and other
problems. High-calcium diets, inadequate water intake, lack of exercise, obesity, genetics, metabolic disorders,
bacterial or parasitic infections, and nutritional imbalances may be causative factors. Urine can vary from
normal, to cloudy, to thick and muddy; it may appear darker than usual. Hematuria is possible and may be
intermittent. Affected rabbits may be asymptomatic, urinate in an unusual area, at an unusual time, for longer
than normal, or with increased frequency. Urinary incontinence and urine scald frequently occur. Straining,
tail-bobbing, posturing, and vocalization may be mistaken for constipation. Affected rabbits may exhibit
anorexia, weight loss, decreased stool production, GI stasis, lethargy, depression, hunched posture, bruxism,
or otherwise indicate that they are in pain. Mild cases of bladder sludge may be discovered as an incidental
finding on x-rays. Abdominal radiography will reveal a diffuse to solid mineral opacity in the bladder, often
completely defining its borders. Palpation of the bladder may reveal a mass with a doughy consistency.
Bladder sludge is occasionally associated with stones; assess the bladder, kidneys, ureters, and urethra. Urine
culture is often negative. Treatment is by increasing water intake (SQ fluids, flavored drinking water, salt
block), agitating the bladder (exercise, manual massage), and bladder flushes; surgery is rarely necessary.
Prevention is through grass hay-based diet, limited pellet intake, wet leafy greens, and adequate water intake.
RABBIT HEAD TILT
Torticollis (head tilt, wry neck) is associated with disorders of the vestibular system, consisting of the vestibular
nuclei in the rostral medulla of the brainstem, the vestibular portion of the vestibulocochlear nerve (cranial nerve
VIII), and receptors in the semicircular canals (labyrinth) of the inner ear. Torticollis is the most consistent sign of
disease affecting vestibular and other closely related systems: the cerebellum, spinal cord, cerebral cortex, reticular
formation, and the extraocular eye muscles. Torticollis in the rabbit may be accompanied by ataxia, nystagmus,
anorexia (nausea), and rolling. Torticollis and ataxia usually indicate inner ear infection, vestibular disease, cranial
nerve lesions, or other central nervous system disease. In rabbits, torticollis and ataxia are most commonly caused
by pasteurellosis and other bacterial infections, encephalitozoonosis, cerebral larva migrans, or trauma to the CNS.
Head tilt resulting from otitis media or otitis interna has often been associated with Pasteurella multocida infection.
However, other bacteria cause otitis media/interna in rabbits, and these include Staphylococcus aureus,
Pseudomonas aeruginosa, Escherichia coli and Listeria monocytogenes. Encephalitozooncuniculiis considered an
opportunistic pathogen as many rabbits are reported to carry the parasite, often as a latent infection without any
clinical signs. Neurological signs caused by E. cuniculi include behavioral changes, urinary incontinence, hind limb
paresis or paralysis, ataxia, torticollis, nystagmus, rolling, or seizures. Clinical signs of E. cuniculi infection
commonly follow a period of illness or stress. Diagnosis of torticollis usually depends on physical exam,
neurological exam, skull radiographs, E. cuniculi antibody titer, and protein electrophoresis. Treatment frequently
consists of treatment for bacterial otitis (systemic antibiotics) combined with fenbendazole or ponazuril, meloxicam,
meclizine, syringe feeding gruel, and additional supportive care as needed.
DENTAL DISEASE OF SMALL HERBIVORES
Rabbits, guinea pigs, and chinchillas are adapted to a course, high-fiber diet. They graze and browse almost
continuously, chewing plant material, and gradually wearing their teeth down. To compensate, the teeth
(incisors and cheek teeth in these species) erupt throughout life at up to 2 mm per week. The rates of dental
wear and tooth eruption are in equilibrium, and if they fall out of synch, problems occur. The three main causes
proposed for dental disease are congenital, nutritional, and metabolic bone disease. The primary congenital
abnormality of teeth is incisor malocclusion, and this occurs mostly in dwarf rabbit breeds. Nutritional causes
include insufficient dietary fiber and dental wear (all species), and vitamin C deficiency (guinea pigs). Metabolic
bone disease can be due to nutritional deficiency of calcium or vitamin D, insufficient sunlight, or renal
secondary hyperthyroidism (rabbits). Of course, dental disease may occur with any process that disrupts the
teeth or bones of the skull (trauma, infection, neoplasia).Dental pathology other than congenital disease is
called acquired dental disease (ADD). Clinical signs of dental disease include changes in food preference,
decreased appetite or anorexia, drooling, and dysphagia or unusual head position while chewing. Examination
may reveal mouth odor, pus or blood, lumps or swelling on the jaw or skull. Exophthalmos, epiphora, or
blepharospasm can also be signs. If asked, owners may report that there are fewer droppings than normal,
that droppings are smaller than normal, or softer, etc. Weight loss, lethargy, and unkempt appearance are also
common. There may also be vocalization or erratic behavior due to discomfort. Diagnosis is by careful dental
examination with magnification under general anesthesia. Malocclusion or malposition of incisors and/or cheek
teeth will indicate disease. Sharp edges and spurs that form along the edges of teeth can cause lesions on
adjacent lips, buccal mucosa, gingival, or the tongue. The buccal aspect of upper cheek teeth and the lingual
aspect of lower cheek teeth are trouble spots to examine closely. Skull radiographs (V/D, lateral, and oblique
views) are important for assessing tooth apexes and reserve crowns, and for characterizing odontogenic
abscesses. CT and MRI imaging are indicated in advanced cases. Treatment requires specialized
instrumentation that is readily obtainable. Prognosis varies with the extent of disease, and complete “cure” is
rare. Most cases of ADD are gradually progressive and the goals of treatment are to maintain quality of life.
GI STASIS OF SMALL HERBIVORES
Rabbits, chinchillas, and guinea pigs are monogastric, hind-gut fermenters; all have a functional cecum and
require a high-fiber diet. Fiber is broken down in the cecum by a variety of microorganisms which are
nourished by a constant supply of water and nutrients from the stomach and small intestine. These same
microorganisms produce volatile fatty acids (VFAs) which, in turn, affect appetite and gut motility. Any
disturbance in this mutually beneficial relationship can result in gastrointestinal hypomotility—increased GI
transit time characterized by decreased frequency of cecocolonic segmental contractions. In severe cases, this
leads to ileus with little to no caudal movement of ingesta, known in practice as GI stasis. Gastrointestinal
stasis may alter large bowel ecology, threaten favorable microorganisms, and promote bacterial pathogens (E.
coli, Clostridium) and toxin production (“bacterial dysbiosis”). GI stasisis not a disease but a symptom that one
or more of the factors governing GI motility are out of order. There isno breed or gender predilection for GI
stasis and it can occur at any age. GI stasis is usually caused by insufficient dietary fiber and/or excessive
stress. Diets containing inadequate long-stemmed, course fiber promote gastrointestinal stasis. Any event
leading to inappetence or anorexia (pre-surgical fasting, sudden changes in the diet, concurrent illness,
starvation) or dehydration (sipper malfunction, bad tasting water, careless mistake) can trigger an episode.
Common stressors include dental disease (malocclusion, molar elongation, odontogenic abscesses), metabolic
disease (renal disease, liver disease), pain (oral, trauma, postoperative, urolithiasis), anxiety (dyspnea, fear,
fighting, lack of hide box), neoplasia, infection, parasitism, and environmental changes (boarding, new pets,
unfamiliar noises).Clinical signs include decreased appetite and fecal production, and feces that are smaller
than normal. Diagnosis is based upon history, physical exam, and radiographs. With complete GI stasis the
stomach may be severely distended, hard, and nondeformable. The presence of firm ingesta in the stomach of
a patient that has been anorectic for 1-3 days is compatible with the diagnosis of GI stasis. Severe distention
of the stomach with fluid and/or gas is radiographic evidence of acute small intestinal obstruction (usually with a
small matt of hair) which constitutes a surgical emergency. Treatment for GI stasis centers on basic supportive
care: warmth, stress reduction (midazolam), pain relief (meloxicam, opioids), fluid replacement and nutritional
support. Prokinetics (metoclopramide, cisapride), simethicone, antibiotics, and/or probiotics may be indicated.
BLADDER STONES IN GUINEA PIGS
Urolithiasis is particularly common in male and female guinea pigs over 2 yrs of age. Etiology is unknown, but
the alkaline pH and high mineral content of normal guinea pig urine may favor crystal formation and
precipitation. Urinary tract infections involving a variety of bacteria have been implicated, although no direct
association has been confirmed. Affected guinea pigs are more likely to be fed a high percentage of pellets/low
percentage of grass hay, vegetables, and fruits in the diet. Alfalfa-based diets have also been implicated.
Obesity and inactivity also appear to be a factor. Urolithiasis can occur anywhere along the urinary tract.
Clinical signs depend upon location and severity. Affected guinea pigs may exhibit weight loss, anorexia,
hematuria, and straining or discomfort during urination (vocalization, erratic movements). Female guinea pigs
with “urethral” stones may present with two distinct conditions: (1) bladder stones that lodge in the urethra, and
(2) calculi that form in a prepucial vestibule, the praeputium clitoridis, which lies distal to and covers the urethral
orifice. Sow with prepucial stones may show no clinical signs. Diagnosis is usually based upon clinical signs,
physical exam, urinalysis, and imaging (radiographs, ultrasound). Urinary calculi in guinea pigs are generally
radio-opaque. Treatment usually involves urethral flushing followed by surgery. In female guinea pigs,
prepucial calculi and those that lodge in the distal urethra may be removed directly via the urinary orifice.
Prevention may be possible by reducing pellets, increasing grass hay, and including a wide variety of
vegetables and fruits. Alfalfa-based diets should be avoided. Potassium citrate and hydrochlorthiazide have
been used together to prevent recurrence of stones with some clinical success.
BACTERIAL PNEUMONIA IN GUINEA PIGS
Pneumonia is considered one of the most significant diseases affecting guinea pigs; it is the number one cause
of death among guinea pigs in some surveys. Young guinea pigs are particularly at risk. Many of the organisms
that cause pneumonia are acquired by guinea pigs as babies while they are still in the breeding colony,
protected by maternal antibodies. Those with subclinical infection often continue to carry these pathogens and
only develop clinical disease later, when stress or concurrent illness occurs.The course of pneumonia can vary
from rapidly progressive and fatal, associated with respiratory failure and/or sepsis, or it can be a much milder
presentation with lethargy and subtle clinical signs. Guinea pigs are by nature very stoic and tend to hide signs
of disease, which means that pneumonia is often advanced before clinical signs are noticed.Pneumonia is
usually associated with opportunistic microbes. The two most important pathogens are Bordetella
bronchiseptica and Streptococcus pneumoniae. Other common bacteria include Klebsiella pneumonia,
Streptobaccillus moniliformis, Staphylococcus aureus, E. coli, Pasteurella pneumotropica, Pasteurella
multocida, Streptococcus zooepidemicus, Streptococcus pyogenes, Citrobacter freundii, Yersinia
pseudotuberculosis, and Pseudomonas aeruginosa. Chlamydophila psittaci can also cause pneumonia;
however, in guinea pigs it usually causes a mild, self-limiting conjunctivitis. Diagnosis is by clinical
presentation, radiographs, hemogram, nasal culture, and tracheal wash culture/cytology. Treatment usually
involves appropriate antibiotics. Nebulization is another important way to get moisture and medication into the
trachea, bronchi, and small airways. Nebulization therapy bypasses the “blood bronchus barrier”, provides
topical treatment to the airways, and helps to rehydrate the sol layer of the mucociliary escalator. Handfeeding,
fluid therapy, and vitamin C supplementation are important supportive care measures. Guinea pigs can be
vaccinated against Bordetella with commercially available vaccines.
MYCOPLASMOSIS IN RATS
Respiratory infections are the most common health problem in rats. The best-understood of these is murine
respiratory mycoplasmosis, also known as chronic respiratory disease (CRD). CRD is multifactorial, the result
of synergistic interaction between Mycoplasma pulmonis anda number of minor copathogens: cilia-associated
respiratory (CAR) bacillus, Haemophilus spp, Sendai virus (a parainfluenza virus), pneumonia virus of mice (a
paramyxovirus), rat respiratory virus (a hantavirus), and sialodacryoadenitis virus (SDA virus, a coronavirus).
Clinical signs are highly variable, and initial infection occurs without any clinical signs. Both upper and lower
respiratory tracts are involved. Signs may include snuffling, nasal discharge, red tears, rapid respiration, weight
loss, hunched posture, ruffled coat, and head tilt. CRD varies greatly in disease expression because of many
environmental, host, and organismal factors that influence the host-pathogen relationship: cage ammonia
levels, concurrent infection (Sendai virus, SDA virus, pneumonia virus of mice, rat respiratory virus, CAR
bacillus), genetic susceptibility of host, virulence of Mycoplasma strain, and vitamin A or E deficiency.
Diagnosis is by clinical presentation, physical examination, serology, radiography, and CT imaging. Antibiotic
therapy (enrofloxacin/doxycycline combination, azithromycin) will not cure CRD, but it reduces secondary
infection and alleviates clinical signs. Affected animals typically have persistent M. pulmonis infection.
Removal of cage litter and replacement daily with clean paper may help reduce ammonia levels.
Bronchodilators (aminophylline, theophylline, albuterol, etc.) and nebulization therapy are alsohelpful in the
treatment of CRD.
REFERENCES
1.
Quesenberry K, Carpenter J, eds. Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery, 3 rd
Ed. St. Louis: Elsevier 2012.
2.
Keeble E, Meredith A, eds. BSAV Manual of Rodents and Ferrets. Gloucester; British Small Animal
Veterinary Association 2009.
3.
Meredith A, Johnson-Delaney C., eds. BSAV Manual of Exotic Pets, 5th ed. Gloucester; British Small
Animal Veterinary Association, 2010.