Mustelidae/Memphitidae Flashcards
Mechanism of alfaxalone?
Mechanism of butorphanol?
High dose butorphanol-alfaxalone (5 mg/kg alfax) in ferrets vs low dose (2.5 mg/kg alfax) had what effects?
Sedative And Cardiorespiratory Effects Of Intramuscular Alfaxalone And Butorphanol At Two Dosages In Ferrets (Mustela Putorius Furo)
Matthew C. Milloway, Lysa P. Posner, and Julie A. Balko
Journal of Zoo and Wildlife Medicine 51(4): 841–847, 2020
High dose butorphanol-alfaxalone in ferrets (compared to low dose) was:
More likely to allow positioning in lateral recumbency and monitor placement
No significant difference in time to effect, induction score, recovery score, or time to recovery.
Both produced recumbency in all ferrets
Animals that were able to be monitored had mild, transient decreases SPO2, MAP, pCO2
Conclusions: Intramuscular alfaxalone and butorphanol resulted in clinically useful and dose-dependent sedation in ferrets.
Adverse effects associated with ketamine in otters?
What happened to NARO body temp throughout procedure when anesthetized with dexmed, butorphanol, and midazolam?
What was observed regarding the dose of atipamezole?
Dexmedetomidine, butorphanol, and midazolam as a reversible induction protocol in North American river otters (Lontra canadensis).
Householder HM, Henry J, Zaffarano B, Gall AJ, Nixon B, Olds JE.
Journal of Zoo and Wildlife Medicine. 2021 Jan;51(4):834-40.
Historical adverse effects of ketamine in otters:
North American river otters: apnea, hyperthermia
European otters: hyperthermia, poor myorelaxation, excitable recovery, and tachycardia in
Giant otters: bradycardia, apnea, seizures
Longer induction time in animals that were panicked/aggressive
Circulating catecholamines can outcompete alpha-2 agonists at receptors
Intubation possible in about half of otters in this study (others required isoflurane)
Body temperature decreased throughout procedure
HR, RR stable
Complications: hypothermia, apnea, cardiac arrest (n=2), vomiting on recovery (n=1)
Resedation seen in otters that received a lower dose of atipamezole (0.3 mg/kg), so increased to 1 mg/kg
Conclusions: Dexmedetomidine-butorphanol-midazolam causes rapid induction in free-ranging North American river otters without significantly affecting heart rate and respiratory rate.
In American martens anesthetized with iso, what chemistry parameter was positively correlated with lactate?
Most common complications?
Difference in induction time with facemask vs cotton ball vs induction chamber?
EFFECTS OF LIVE-TRAPPING AND ISOFLURANE ANESTHESIA ON FREE-RANGING AMERICAN MARTENS (MARTES AMERICANA)
Maria C. Spriggs, Lisa I. Muller, Paul Keenlance, Robert L. Sanders, Jill C. Witt, Debra L. Miller
J. of Wildlife Diseases, 53(3):447-458 (2017)
In american martens anesthetized with isoflurane:
Induction time: facemask > cotton ball > induction chamber
Most common complications = hyperthermia (in summer) or hypothermia
Parameters positively associated with lactate: BUN, initial temperature, ambient temperature, induction delay
BUN positively correlated with lactate
Most common physical exam abnormalities = dental disease (fractured/devitalized canines, etc.)
Conclusions: Isoflurane to anesthetize free-ranging martens can cause hyperthermia or hypothermia and lactate values are increased with BUN, initial temperature, ambient temperature, and anesthetic induction delay.
Primary vector of Yersinia pestis?
Which sex of black-footed ferrets were found to have a higher load of fleas?
FLEAS OF BLACK-FOOTED FERRETS (MUSTELA NIGRIPES) AND THEIR POTENTIAL ROLE IN THE MOVEMENT OF PLAGUE
Erica L. Mize, Shaun M. Grassel, Hugh B. Britten
Oropsylla hirsuta (flea) = primary vector of Yersinia pestis
Some O. hirsuta on prairie dogs were PCR positive for Y. pestis
Flea load in black-footed ferrets:
Males > females
Males have larger size and home ranges
Not affected by deltamethrin treatment in burrows, age, season, colony
Conclusions: Flea species Oropsylla hirsuta can transmit plague and is found on ferrets and prairie dogs.
Options for diagnosis of mycobacterium bovis in mongooses?
DIAGNOSIS AND IMPLICATIONS OF MYCOBACTERIUM BOVIS INFECTION IN BANDED MONGOOSES (MUNGOS MUNGO) IN THE KRUGER NATIONAL PARK, SOUTH AFRICA
J Wildl Dis. 2017 Jan;53(1):19-29.
Angela C. Brüns, Manfred Tanner, Mark C. Williams, Louise Botha, Amanda O’Brien, Geoffrey T. Fosgate, Paul D. van Helden, John Clarke, Anita L. Michel
Lepto, parvo, and toxoplasma seroprevalence in River Otters in NC?
What age group had highest prevalence of parvovirus?
Where was toxoplasma gondii found (which organ)? Age and sex prevalence?
LEPTOSPIRA, PARVOVIRUS, AND TOXOPLASMA IN THE NORTH AMERICAN RIVER OTTER (LONTRA CANADENSIS) IN NORTH CAROLINA, USA
Charles W. Sanders II, Colleen Olfenbuttel, Krishna Pacifici, George R. Hess, Robert S. Livingston, Christopher S. DePerno
J. of Wildlife Diseases, 56(4):791-802 (2020)
Background:
Leptospirosis = spirochete, aerobic, zoonotic bacteria
Maintained by mammals, reptiles, amphibians
Shed in urine
Toxoplasma gondii = zoonotic, protozoal parasite
Definitive host = domestic cats
Intermediate hosts = crayfish, fish, geese, mice, mussels, oysters, pigs
Transmission = ingestion of meat/water contaminated by cat feces
Major cause of death for sea otters in central CA
Key Points:
NAROs in central NC had a moderate prevalence for canine parvovirus and T. gondii
Very low leptospirosis seroprevalence
Parvovirus seropositivity highest in yearling otters had the highest prevalence of parvo in this study
No mortalities
Toxoplasma gondii found only in brain
More likely in older and female otters
Some clinical disease
Conclusions: North American river otters in central NC have not been exposed to leptospirosis and do not suffer mortality from canine parvovirus.
Most common serovars by species in leptospira in antibodies in wildlife in USA and virgin islands?
WTD?
Canids?
Raccoons, skunks?
Small Indian mongooses?
LEPTOSPIRA ANTIBODIES DETECTED IN WILDLIFE IN THE USA AND THE US VIRGIN ISLANDS
Pedersen K, Anderson TD, Maison RM, Wiscomb GW, Pipas MJ, Sinnett DR, Baroch JA, Gidlewski T
J Wildl Dis. 2018 Jul;54(3):450-459
Background:
Leptospirosis is caused by one of 250 Leptospira spp. Serovars
Wildlife species are often reservoir hosts of leptospirosis (e.g. canids and serovar Canicola)
Spirochetes from infected animals are secreted in the urine and may persist in the environment
Methods: Microagglutination test used to detect six Leptospira serovars in sera from various wildlife that interacted with USDA Wildlife Services as a part of transport/trapping procedures to reduce human-wildlife interactions.
Key Points:
Overall seroprevalence was 30%; similar to other studies
All 6 serovars were detected in all species with > 50 samples
Evidence of active/recent infection > 1:800 detected in white-tailed deer, coyotes, foxes, gray wolves, small Indian mongooses, racoon, and striped skunks
Most common serovars by species:
White tailed deer = Bratislava
Canids = Bratislava and Grippotyphosa
Raccoons and skunks = Grippotyphosa
Small Indian mongooses (all from Honolulu, HI) = Hardjo
Conclusions: Leptospirosis exposure is common across the USA in a variety of wildlife species, which may pose a public health risk.
Primary cause of death in badgers in Ontario?
Common diseases exposures?
THE OCCURRENCE OF PATHOGENS IN AN ENDANGERED POPULATION OF AMERICAN BADGERS (TAXIDEA TAXUS JACKSONI) IN ONTARIO, CANADA
Danielle M. Ethier, Joshua B. Sayers, Christopher J. Kyle, Joseph J. Nocera, Davor Ojkic, Douglas Campbell
J. of Wildlife Diseases, 53(1):73-80 (2017).
Primary cause of death in badgers in Ontario = trauma
Disease exposures that were common: Canine parvovirus (100% seropositivity), but no associated disease
Leptospirosis (most seropositive/IHC positive, but rare interstitial kidney disease)
Canine distemper virus → fatal disease in two badgers, IHC positives common
Transmission: aerosols, fomites, direct contact
100% fatal in black footed ferrets and captive badgers
No exposure to canine adenovirus
Conclusions: American badgers in Ontario are exposed to canine distemper virus, canine parvovirus, and leptospirosis, though they are more likely to die from vehicular trauma.
Seroprevalence for canine distemper, parvo, toxoplasma, lepto, and HW in american martens in Michigan?
SEROSURVEY, HEMATOLOGY, AND CAUSES OF MORTALITY OF FREE-RANGING AMERICAN MARTENS (MARTES AMERICANA) IN MICHIGAN
Maria C Spriggs, Richard W Gerhold, Rebecca P Wilkes, Paul Keenlance, Robert L Sanders, Jill Witt, Eric Clark, Debra Miller
J Zoo Wildl Med. 2018 Jun;49(2):371-383.
Background:
Infectious diseases that affect wild mustelids:
Canine distemper virus: Mustelids may have up to 100% mortality with CDV infection
Reservoirs = racoon, gray foxes, coyotes, gray wolves, dometic dogs
Toxoplasmosis: reported in black-footed ferrets, southern sea otters, and farmed mink
Canine parvovirus: Canids are natural host, but mustelids also affected
Heartworm (Dirofilaria immitis): Reported in NA river otter
Leptospirosis: Contributes to decline of European mink
Key Points:
American martens in Michigan had:
Low seropositivity for canine distemper virus and canine parvovirus
High seroprevalence of Toxoplasma gondii (58%)
Associated with higher globulin and eosinophil levels
No evidence of leptospirosis or heartworm
Most common cause of death in American martens was predation
Conclusions: American martens have exposure to toxoplasmosis, canine distemper virus, and canine parvovirus.
Prevalence of nephroliths in ASCOs (relative AZA vs wild)?
Factors associated with nephroliths?
UROLITH PREVALENCE AND RISK FACTORS IN ASIAN SMALL-CLAWED OTTERS (AONYX CINEREUS)
Yoong YT, Fujita K, Galway A, Liu MH, Cabana F.
Journal of Zoo and Wildlife Medicine. 2018 Dec;49(4):863-9.
Nephrolith prevalence = 24.5% overall
AZA (62.8%) >> EAZA (12.9%) > Asia (9.4%)
AZA diets were mostly fish/meat with commercial products
EAZA and Asian diets were mostly crustaceans
Nephroliths were more likely with increasing age and dietary calcium
Less likely with increasing dietary crude protein and dietary sodium
Not affected by sex
Conclusions: Asian small clawed otters are prone to calcium oxalate, especially in North America where they are fed fish instead of crustaceans.
Type of uroliths in Eurasian otters? Asian small-clawed otters?
Age and sex predilection?
Were uroliths in Eurasian otters associated with death? Urinary inflammation?
UROLITHIASIS IN FREE-RANGING AND CAPTIVE OTTERS (LUTRA LUTRA AND AONYX CINEREA) IN EUROPE
Bochmann M, Steinlechner S, Hesse A, Dietz HH, Weber H.
Journal of Zoo and Wildlife Medicine. 2017 Sep;48(3):725-31.
Urolithiasis prevalence: Eurasian otters (ammonium acid urate) \> Asian small-clawed otters (calcium oxalate)
Eurasian otters: Captive > free-ranging
Adults > juveniles
Not associated with sex
Uroliths not associated with death nor urinary inflammation
Some Eurasian otters had cystic changes if large or many uroliths
Conclusions: Eurasian otters get ammonium urate stones while Asian small-clawed otters get calcium oxalate.
Primary uroliths by species?
ASCO
NARO
Eurasion otter
Bottlenose dolphins
Harbor seal, CSLs, NES
West Indian manatee
Giant otters?
XANTHINE NEPHROLITHIASIS IN JUVENILE CAPTIVE GIANT OTTERS ( PTERONURA BRASILIENSIS)
Ashley Barratclough, Amanda J. Ardente, Brandon Boren, Donna Ialeggio, Michael M. Garner
Cases:
11mo F with acute lethargy and anorexia → died under anesthesia
8mo M with acute anorexia and weakness → died in anesthetic recovery
18mo M with abdominal pain → euthanized
14do F → peracute mortality
7mo F with anorexia → euthanized
All cases were genetically related and had:
Xanthine renoliths (bilateral or unilateral)
Increased BUN, Cr, P, Ca
No correlation with diet, but maybe a genetic factor
Conclusions: Giant otters get xanthine nephrolithiasis, did not find an association with diet
Is urolithiasis in ASCOs associated with hypercalcemia?
When should surgical resection of nephroliths be considered?
Management of nephrolithiasis by pyelotomy and pyeloscopy in an Asian small-clawed otter (Aonyx cinereus)
J Am Vet Med Assoc. 2019 Nov 1;255(9):1057-1063.
Mikel Sabater González, Melanie Osterwind, Jaime Fernández Colomé
Case: Adult female asian small clawed otter with episodic abdominal pain and renal pelvic calculi
Pyelotomy removed large staghorn-shaped calculus plus many small calculi from left kidney
Pyeloscopy with rigid endoscope helped find all the small calculi
Resolution of clinical signs and no progression of other calculi
Stone was primarily calcium oxalate monohydrate with ammonium urate core
Key Points:
Otters have reniculate kidneys
Urolithiasis is more common in captive otters than free-ranging otters
Calcium oxalate is most common stone in otters (primarily ASCOs)
Urolithiasis is not associated with hypercalcemia
Surgical resection should only be considered for large nephroliths with associated clinical signs
For calcium oxalate stones, consider increasing fluid intake, decreasing intake of oxalate and ascorbic, and consider supplementing with potassium citrate
Conclusions: Calcium oxalate nephrolithiasis can be resolved via pyelotomy in asian small clawed otters.
Accuracy of BUN test strips was better for what species (ferret vs rabbit)?
Which species had high sensitivity but lower specificity (more false positives)?
Utility of commercially available reagent test strips for estimation of blood urea nitrogen concentration and detection of azotemia in pet rabbits (Oryctolagus cuniculus) and ferrets (Mustela putorius furo)
Megan L Cabot, David Eshar, Hugues Beaufrère
J Am Vet Med Assoc. 2020 Feb 15;256(4):449-454.
Fair agreement between categories test strip and analyzer
Precision for detecting azotemia super high in both
Accuracy better better in ferrets
High sensitivity, lower specificity in rabbits (more false positives)
Test strips occasionally higher than analyzer
Lower sensitivity, high specificity in ferrets (more false negatives)
But 100% specificity in ferrets
Conclusions: BUN test strips are a good rule out test (high sensitivity) in rabbits and had high specificity in ferrets; still recommend gold standard chemistry analyzer.
Abnormal feces from black-footed ferrets had what compared to normal feces in a study evaluating Clostridium perfringens?
How did diet (ground meat vs whole prey) affect presence of spore-forming bacteria?
Comparison Of Fecal Cytology And Presence Of Clostridium Perfringens Enterotoxin In Captive Black-footed Ferrets (Mustela Nigripes) Based On Diet And Fecal Quality
Ferris RL, Stacy N, Stein AB, Chiles H, Goe A.
Journal of Zoo and Wildlife Medicine. 2021 Jan;51(4):814-24.
Clostridium perfringens = Gram-positive, anaerobic, spore-forming rod-shaped bacterium
Signs: diarrhea, hematochezia, dec appetite, can cause death
Spores must germinate before producing toxin
Abnormal feces from black-footed ferrets (compared to normal feces) had:
More spore-forming bacteria
Less diplococci
Abnormal bacterial microflora
Feces from black-footed ferrets fed ground meat (compared to a whole prey diet) had:
More yeast and spore-forming bacteria
Clinically abnormal ferrets (compared to healthy) had higher spore-forming bacteria
Conclusions: Spore-forming bacteria can be seen in healthy black-footed ferrets, but increases with disease, abnormal feces, and ground meat diet.
Which sample was most reliable for total mercury testing in American martens?
Mercury levels were highest in what age group and which sex?
BIOACCUMULATION OF MERCURY IN A TERRESTRIAL CARNIVORE, AMERICAN MARTEN (MARTES AMERICANA)
Jill C. Witt, Maria C. Spriggs, Timothy Veverica, Christopher Steffes, Joseph Bump
J. of Wildlife Diseases, 56(2):388-396 (2020)
Mercury levels in martens were highest in:
Hair samples (compared to kidney and liver)
Older age
Adult females (compared to juveniles and adult males)
Conclusions: Hair was most reliable for total mercury testing in American martens.
Was there a preference for flavor or shape of bait for oral rabies vx in skunks?
Did vaccination by direct oral inoculation induce titers?
Gilbert, A., Johnson, S., Walker, N., Beath, A., & VerCauteren, K. (2018). Flavor preference and efficacy of variable dose ontario rabies vaccine bait (ONRAB) delivery in striped skunks (Mephitis mephitis). Journal of wildlife diseases, 54(1), 122-132.
Results/Discussion:
• Cheese, chicken, egg flavors preferred. Preference not considered strong.
• No preference observed for shape of bait.
• All skunks challenged with rabies developed rabies.
• Incubation 10-17 days.
• Vaccination by direct oral inoculation induced robust rVNA titers in all except 1 skunk.
• In four skunks that ate the baits, only two seroconverted.
• Among direct oral vaccine groups, survival with lethal rabies challenge was 80-100%.
• High resistance to challenge observed in skunks vaccinated by the direct oral route.
• This study confirms and extends the immunogenicity and efficacy of the ONRAB vaccine by oral inoculation in skunks.
• In bait group, survival 40-50%.
• Takeaway: High resistance to challenge with rabies virus in skunks vaccinated by direct oral route with ONRAB vaccine; results with bait ingestion are variable. Further studies needed.
What factors best predicted prevalence and severity of skunk cranial worm? What is the intermediate host?
Journal of Wildlife Diseases 56(3): 597-608, 2020
PREVALENCE AND SEVERITY OF SKUNK CRANIAL WORM (SKRJABINGYLUS CHITWOODORUM) DAMAGE INCREASE WITH PRECIPITATION IN SPOTTED SKUNKS (SPILOGALE SPP.)
• Eastern spotted skunk (Spilogale putorius) and subspecies plains spotted skunk (Spilogale putorius interrupta) have experienced population declines in the past 60-70 years and are considered to be threatened or endangered throughout much of its range
o Western spotted skunk (Spilogale gracilus) has faced similar threats, however has a more stable population currently
o Parasites such as nematodes may play a role in population declines in addition to habitat loss, pesticide use, and overharvesting
• Skunks become infected with skunk cranial worm, aka sinus roundworm, by ingesting infected intermediate hosts (gastropods – snails and slugs) or infected paratenic hosts (mice, shrews, snakes, frogs)
o Skunks are definitive hosts, adults most commonly infected
o Worms migrates from mouth to frontal sinuses and molt into adults cause damage to frontal bone
o Causes abnormal behavior but overall impact poorly understood
• Precipitation the year prior to specimen collection had a positive effect on prevalence such that years with high average annual precipitation results in higher prevalence the following year
o Improved environmental conditions for intermediate hosts – snails, slugs
• Midwestern and eastern clades experienced lower prevalence and less severe infections than in western and southwestern spotted skunk clades (western severe)
o Suggests skunk cranial worm infections were not a major factor in range-wide population declines of eastern spotted skunks
o Overall infection prevalence decreased over time, but severity increased
Take home: Skunk cranial worm infection prevalence and severity in spotted skunks increases during the year following increased levels of precipitation, most likely due to improved environmental conditions for the gastropod intermediate hosts. Prevalence and severity worse in western spotted skunk clades.
What is the common name for the parasite Skrjabingylus chitwoodorum?
Lesions caused?
Hughes, M. R., Negovetich, N. J., Mayes, B. C., & Dowler, R. C. (2018). Prevalence and intensity of the sinus roundworm (skrjabingylus chitwoodorum) in rabies-negative skunks of texas, usa. Journal of wildlife diseases, 54(1), 85-94.
- Skrjabingylus chitwoodorum – Skunk Sinus Roundworm
- Several species of this genus inhabit the sinuses of mephitids and mustelids
- The migration of this worm can result in meningitis and movement within the ventricles which can result in neurologic problems for the host
- Low humidity and high temperature reduce survival of the first stage larvae in feces – the larvae can survive freezing in dry conditions but are sensitive to dessication
- Goal was to establish prevalence – skunks examined had been submitted for rabies testing – may have bias towards neurological animals
- Nematodes were rarely seen outside the sinus, but were found in the trachea, mouth, eye, and one had a mass of worms in the diastema
- A few studies show a prevalence towards the left sinus
Take Home: Abberrant migration of Skrjabingylus chitwoodorm is a differential for a neurologic skunk
Compare estimation of total solids vs total protein for ferrets and rabbits?
What was observed with refractometry vs biuret assay for both spp?
J Am Vet Med Assoc 2021;258:977–982
Comparison of plasma total solids concentration as measured by refractometry and plasma total protein concentration as measured by biuret assay in pet rabbits and ferrets
David Eshar dvm Kacey L. Solotoff dvm Hugues Beaufrère dvm, phd (Reviewed by AJC)
Key Points:
• TP measured using biuret assay in biochemistry analyzers, or is estimates as TS using refractometer
• Interferences of sample hemolysis, lipemia, colloid administration, or high sample concentrations of bilirubin, BUN, glucose, chloride or Na concretions on TS measurements by refractometer
• Objective – compare paired plasma TP (biuret) and TS (refractometer) concentrations in rabbits and ferrets
• Plasma TS values overestimated plasma TP for both ferrets and rabbits
• These two methods can not be used interchangeably for rabbits and ferrets since refractometer overestimated biuret values on average for both species
• Cholesterol, glucose, BUN, hemolysis and lipemia had significant effects on the magnitude of bias for ferrets
• BUN had a significant impact on measurement bias in rabbits
Take home:
• Plasma TS concentration as measured by refractometry overestimated and failed to adequately estimate the plasma TP concentration as measured by biuret assay for both ferrets and rabbits
Describe the nutritional diseases of mustelids.
What is the cause of thiamine deficiency?
- Thiamine is a cofactor for what important enzymes?
- What are the lesions that result from this deficiency?
What is the cause of vitamin E deficiency?
- What are the lesions associated with this deficiency?
Nutritional Diseases of Mustelids
- Hypovitaminosis A
- Vitamin E, thiamine (Chastek dz), calcium, vit D, Zn, biotin deficiencies.
- Thiamine deficiency in mink.
– Associated with thiaminase containing fish.
– Critical cofactor for production of pyruvate decarboxylase and transketolase.
– Lesion distribution parallels transketolase activity in the brain.
– Decreased activity of ATP dependent Na and water transport results in intraneuronal swelling and necrosis.
– Vascular degeneration, edema, hemorrhage.
– Bilaterally symmetrical hemorrhage and necrosis of periventricular gray matter, caudal colliculi, vestibular nuclie.
– Cardiac lesions in canids have not been described in mink.
- Vitamin E deficiency.
– Young, healthy farmed mink in summer and fall, no premonitory signs.
– Vit E deficiency associated with diets containing high levels of PUFAs, improperly stored fish.
– Steatitis, skeletal and cardiac muscle degeneration, anemia.
– Gross lesions – ‘yellow fat dz’.
– Abdominal skin thickened and doughy.
– Abdominal and SQ fat is hardened and yellow-brown with fishy odor.
– Widespread adipocyte necrosis with multifocal saponification, dystrophic mineralization, mixed suppurative and histiocytic inflammation.
– Degeneration and fibrosis of cardiac and skeletal muscle.
- Zn toxicity
- Nutritional secondary hyperparathyroidism, fibrous osteodystrophy
What are the most common GI disorders of mustelids?
Mustelid GI Diseases
- Gastric trichobezoars, dental dz
- Gastric and duodenal ulceration.
– Sea otters – typically erosions, not ulcers.
– In other mustelids, commonly present with melena.
– Contribute to morbidity and mortality through progressive, severe blood loss.
– Causal relationship proposed with Helicobacter mustelae (ferrets) and Helicobacter enhydrae (sea otter) infection.
- Gastric dilatation and torsion.
Describe the metabolic diseases of mustelids.
Urolithiasis has been documented in what species of mustelids?
- Which stone types are the most prevalent in each species?
- Ferrets?
- North American River Otters?
- Asian Small Clawed Otters?
- Giant Otters?
- Mink?
Describe the adrenal-associated endocrinopaty of ferrets
- What is the pathophysiology?
- What are the clincial signs?
- How is it diagnosed?
Mustelid Metabolic Diseases
- Metabolic diseases.
– Urolithiasis, hypocalcemia, pregnancy toxemia, agalactia, hyperestrogenism, hormonal alopecia, idiopathic hypersplenism, gastric dilatation and torsion (possibly assoc with clostridium welchii), dental and skeletal anomalies, periodontal dz, amyloidosis, hyperadrenocorcicism (ferret), insulinoma (ferret), DM (ferret), hepatic lipidosis, cardiovascular calcification, osteomalacia, degenerative joint dz.
- Urolithiasis.
– Well documented in mink, ferrets, river otters.
– Likely multifactorial.
– Metabolic, nutritional, dietary, genetic.
– Farmed mink – struvite urolithiasis is seasonal.
– Pregnant females affected in spring, males affected in fall.
– May hinder parturition in gravid females.
– May cause obstruction in males.
– Concurrent UTI with staph intermedius is common in mink.
– In ferrets, most commonly struvite, not associated with bacterial infection - recent study is cysteine
– Giant otters - xanthine
– ASCO - calcium oxalate
- Nephrolithiasis.
– Common in otters, also wolverines.
– Highest prevalence in Asian small-clawed otters.
– Age is a risk factor.
– Possibility of heritable metabolic abnormalities.
- Adrenal-associated endocrinopathy AAE
– Middle aged and older ferrets.
– In intact ferrets, seasonal GNRH from hypothalamus results in secretion of LH and FSH from pituitary, preps ovary and testis for reproduction.
– Early castration and OHE causes chronic LH secretion, loss of negative feedback, hyperplastic and potentially neoplastic proliferation of the adrenocortical cells in the juxtamedullary region.
– Hyplerplasia to carcinoma.
– CS – truncal alopecia due to inhibition of excess estrogen secretion on hair, vulvar swelling in spayed females.
– Aberrhant adrenocortical tissue may secrete estrogen, testosterone, 17OHprogesterone, others.
– Serum tests for these for dx.
– NOT excess cortisol (Cushing’s).
– Adrenocorcical nodular hyperplasia is very common in sea otters, age related. No CS or clinical pathology reported.
– Urinary obstruction following development of prostatic cysts following hyperestrogenism.
Describe the herpes and papillomaviruses of mustelids.
What are the lesions associated with mustelid herpesvirus-1?
- What species are affected?
What are teh lesions associated with mustelid herpesvirus-2?
- What species are affected?
What species are affected by herpes simplex?
What species are affected by suid alphaherpesvirus 1?
- What lesions develop?
What are the lesions associated with enhydra lutris papillomavirus-1?
Mustelid Herpesviruses
- Mustelid herpesvirus-1
– Ulcers on skin, muzzle, plantar pads.
– Basophilic to amphophilic nuclear inclusions.
– Male fisher and wild badgers.
- Mustelid herpesvirus-2
– Oral ulcers, northern sea otters Exxon Valdez spill.
– Subsequently isolated in oronasal secrstions from apparently healthy NSO.
- Necrotizing encephalitis (herpes simplex)
– Nonsuppurative.
– Neuronal and glial inclusions in striped skunk.
– Systemic necrosis experimentally, severe in liver and adrenal glands.
- Pseudorabies (Aujeszky disease – Suid Alphaherpesvirus 1)
– Causative agent neurologic dz in mink.
– Incubation 3-4 days, CS include hypersalivation, vomiting, depression, coma.
– Fibrinoid degeneration of vessels in the CNS, myocardium, oropharynx.
– Differs from the nonsuppurative encephalitis typical in other spp.
Mustelid Papillomas.
- Enhydra lutris papillomavirus-1 (EIPV-1)
– Multifocal raised, variably pigmented papillomas gingiva and lips, southern sea otters.
– Koilocytes and IN inclusions in mucosa.
Describe the bacterial diseases of mustelids.
What bacteria is associated with gastritis in ferrets? What about sea otters?
- What lesions are present?
- What special stains are used for diagnosis?
What mustelid species are reservoirs for mycobacterium?
- What lesions are typically present in affected animals?
What bacteria causes necrotizing hemorrhagic pluropneumonia and septicemia in mink?
What lesions are associated with Strep. lutetiensis?
- What species are affected?
What lesions are associated wtih Strep. delphini?
- What species are affected?
What bacteria causes bacterial pododermatitis in mink?
What bacteria causes proliferative colitis in ferrets?
- How does infection in ferrets differ from other taxa?
What species are especially susceptible to Yersinia?
- What lesions occur as a result of infection?
What species are reservoirs for leptospirosis?
- what are the lesions seen in infected animals?
Bacterial Diseases of Mustelids
Helicobacter mustelae
- Atrophic and lymphocytic gastritis
- Ferrets used as models for H. pylori infection in humas
- Hypochlorhydria, vomiting, diarrhea
- Animals > 3.5 most commonly
- Contributes to debilitation in older ferrets; lesions typically in pylorus and consist of lymphoplasmacytic gastritis with attenuation of gastric glands.
- H. mustelae has not been causally linked to gastric ulcers, a common condition in affected animals.
- Silver stains – extracellular spiral bacteria within mucous layer.
Helicobacter enhydrae sp nov – isolated from southern sea otters.
- Genetically distinct from other MM helicobacter spp.
- Severe mucosal erosions and ulcers with associated silver stain-positive bacilli.
- Not directly confirmed as cause of gastric ulcers and inflammation.
Mycobacterium spp
- Feral ferrets in NZ reservoirs of bovine TB
- Similar with badgers in UK
- Vaccination and culling to minimize livestock transmission
Mycobacterium bovis infection in wild mustelids
- Badgers – pulmonary granulomas dominate
- Ferrets – hepatic granulomas/microgranulomas
- LN granulomas common in both
- Chronic fecal shedding problematic on farms and in zoos
- Atypical mycobacteria (M. avium)
- M. celatum – granulomas in pet ferrets.
- M. avium – Eurasian badgers.
- M. Kumamotonense – stoats and weasels in UK
Pseudomonas aeruginosa
- Necrotizing hemorrhagic pleuropneumonia and septicemia, farmed mink.
- Highly contagious, spreads rapidly and causes epizootics.
- Peracute death.
- Cranioventral bronchopneumonia with copious bloody fluid on cut surface.
- Vasculitis, alveolar hemorrhage, abundant bacteria within alveoli and capillaries.
- Ddx hemolytic E. coli, but e. coli pneumonia more diffuse (entire lung), more edema than hemorrhage.
Streptococcus spp
- Often part of mixed flora infecting wounds and bite injuries.
- Lancefield group C infection valvular endocarditis in ferrets.
- S. bovis detected in mink.
- Molecular characterization is advised.
- CS – posterior paresis, suppurative intervertebral discospondylitis, myelitis, vertebral lysis or proliferation.
- Streptococcus lutetiensis sp. nov formerly S. coli.
– Northern sea otters.
– Similar strain infects southern sea otters.
– Fatal meningoencephalitis and endocarditis.
– May die acutely in good BCS with meningoencephalitis.
– Others have chornic vegetative valvular endocarditis of left AV or aortic valves, dilated left ventricle.
– Massive pulmonary edema, necrosis in myocardium, kidneys, spleen, descending aorta secondary to saddle thrombus.
– Coinfection with bartonella in sea otters.
– S. phocae and related beta hemolytic strep ID as major opportunistic pathogen of southern sea otters.
– Sepsis, abscess formation, meningoencephalitis.
- S. delphini
– Mink, badgers, ferrets consistently culture-positive for S. delphini group A.
– Hypersecretory diarrhea.
– Associated with cutaneous adenitis and mastitis in mink.
Staphylococcus spp
- Bacterial pododermatitis in farmed mink, poor husbandry.
- Chronic infections may appear as foot pad hyperkeratosis.
- S. canis, S. intermedius, S. delphini.
- Arcanobacterium phocae is associated with facilities feeding seal meat.
Lawsonia intracellulare
- Proliferative colitis in ferrets, especially young males
- Primarily associated with the colon – UNLIKE hamsters, pigs, horses (ileum).
- CS – bloody, liquid stool.
- Mucosa has thickened, corrugated appearance due to hyperplasia of colonic enterocytes.
- Silver stains – bacteria within apical cytoplasm of proliferating enterocytes.
Yersinia pestis
- Sylvatic plague
- Mortality for endangered BFF
- Primary prey for BFF is prairie dog.
- Prairie dogs and fleas are reservoir.
- Vasculitis, necrohemorrhagic inflammation, perivascular bacilli in submandibular and mesenteric LN.
- Subcutaneous hemorrhage, pulmonary edema.
- Siberian polecat model for plague in BFF.
- Idiopathic pneumonia in feral stoats in NZ
Yersinia pseudotuberculosis
- Also incidentally isolated from otters, martens, polecats, mink without lesions.
Leptospira spp.
- Striped skunk often positive, clinically silent.
- Possible reservoirs.
- Also relatively high frequency in European mustelids and European and American mink, polecats, pine martens, stone martens.
- Likely reflects high prevalence of infection in rodent prey.
- Rare sea otter deaths.
- Renal petechiae, multifocal interstitial nephritis, clumps of spiral bacteria intratubular on silver stain.
- River otters commonly seropositive but associated dz is rare.
- Chronic lepto – abortion, chronic renal dz.
A recent paper described the viral characterization of Skunk adenovirus 1 in multiple species.
What species have been rported to be affected?
what was teh most significant lesion?
Where were inclusion bodies identified?
IN SITU HYBRIDIZATION AND VIRUS CHARACTERIZATION OF SKUNK ADENOVIRUS IN NORTH AMERICAN WILDLIFE REVEALS MULTISYSTEMIC INFECTIONS IN A BROAD RANGE OF HOSTS
Journal of Wildlife Diseases, 58(2), 2022, pp. 356–367
Key Points:
- We describe and characterize the tissue distribution and lesions associated with SkAdV-1 infection in 24 wildlife diagnostic cases submitted between 2015 and 2020, including 16 North American porcupines (Erethizon dorsatum), three striped skunks (Mephitis mephitis), and five raccoons (Procyon lotor), which constitute a new host species.
- The most common lesion in all species was severe necrotizing bronchopneumonia with (n=12) or without (n=10) interstitial involvement.
- Intranuclear inclusion bodies were common in respiratory epithelium (n=21) and less often in renal tubular (n=6) and biliary epithelium (n=1).
- The most significant and common lesion was severe necrotizing bronchopneumonia or bronchointerstitial pneumonia with INIBs within sloughed airway epithelial cells.
- SkAdV-1 can cause multisystemic infections, including necrotizing tubulonephritis, hepatitis, and encephalitis
– May be able to shed via urine similar to CAdV-1
- Porcupines can recover from SkAdV-1 and be released
- SkAdv-1 can infect multiple hosts species (unique among adenoviruses) confirmed in porcupines, raccoons, gray fox and skunks
