Canidae Flashcards

1
Q

Describe the general natural history and geographic distribution of canids.

Give the scientific name for the following species:

Bat-Eared Fox

Channel Island Fox

Grey Fox

Arctic Fox

Red Fox

Fennec Fox

Dhole

Coyote

Gray Wolf

Red Wolf

African Wild Dog

Maned Wolf

A

GENERAL BIOLOGY (Fowler 8)

  • 35 species of dogs, wolves, coyotes, jackals, and foxes
  • Domestic dog derived from the gray wolf through close association
  • At least one wild species present on each continent, except Antarctica
  • Red fox and gray wolf have some of the largest geographic ranges
  • 1 kg to 60 kg
  • Sexual dimorphism occurs in many species, with males being larger
  • Range from solitary to pack animals
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2
Q

Describe the unique anatomy of canids.

What is teh dental formula of canids? What are teh carnassial teeth?

What is the primary heat loss mechanism for canids?

What is teh function of the supracaudal gland?

What type of placentation do canids have?

A

UNIQUE ANATOMIC FEATURES (Fowler 8)

  • Medial position of the internal carotid artery btw entotympanic and petrosal arteries, loss of stapedial artery, and inflated entotympanic bulla divided by a partial septum
  • Insertion point of the digastric muscle is widened in several taxa, forming a subangular lobe on the horizontal ramus of the mandible
    • Rapid jaw movement
    • Prominent in foxes with complex molars and raccoon dogs
  • Dental formula: (I) 3/3, (C) 1/1, (P) 4/4, (M) 2/2
    • Maxillary fourth premolar and mandibular first molar are modified to oppose each other (carnassial or sectorial teeth)
  • Lateral nasal glands provide moisture for evaporative cooling during panting
    • primary heat loss mechanism
    • Sweat glands only present in footpads
  • Seasonal molt of pelage helps to cope with temperature extremes
  • Four digits in hindlimbs, 5 in each of the forelimbs
  • Refined senses of hearing, smell, and vision
    • Olfactory cues from urine, feces, and anal glands important in social interaction
  • Supracaudal gland (tail gland): specialized scent gland located on the dorsal surface of the tail
    • Located at 7-9 caudal vertebrae; most developed in solitary fox species
  • Raccoon dog may undergo period of seasonal torpor
    • Decreased BMR, lower levels of cortisol, insulin, and thyroid hormones
  • African wild dog lacks variation at the major histocompatibility complex (MHC)

Unique features (Terio Zoo Path)

  • Canids
    • Most have dental formula I 3/3 C 1/1 P 4/4 M2/3
    • All males have os penis
    • Placenta is zonary and circumferential; circumferential marginal hematomas are a normal feature. Histologically labyrinthine and endotheliochorial
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3
Q

Describe the ideal housing of canids.

How do social dynamics need to be considered?

What escape precautions need to be considered?

What about breeding?

A

SPECIAL HOUSING REQUIREMENTS (Fowler 8)

  • Allow for social species housed in groups to separate themselves in cases of aggression
  • Should not have sharp corners; may result in traumatic injuries, inescapability from aggressors
  • Keep in mind they are proficient diggers and skilled jumpers
    • Dig barriers
    • Height of 8 ft is recommended for most large canids
  • Periparturient dam should have multiple choices of warm and dry whelping boxes
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4
Q

Describe your preventative medicine protocol for canids.

What preventatives should be considered?

What vaccines should be considered?

Describe your choice of vaccine products.

A

PREVENTATIVE MEASURES (Fowler 8)

  • Consider heartworm preventative
  • Vaccines (Table 46-6) based on geographic location
    • Rabies, distemper, and parvo are considered core
    • Many prefer monovalent products over multivalent
    • Used modified live vaccines with caution
    • Genetically modified canary-pox vectored vaccines are a safe alternative and are commonly used (cannot induce disease)
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5
Q

Describe the physical restriant of canids.

What techniques are used for small canids? What about larger ones?

What is a common complication in canid restraint? How is it managed?

A

RESTRAINT AND HANDLING (Fowler 8)

  • Manual restraint in small canids
  • Watch muzzles for normal breathing and avoidance of hyperthermia
  • Hyperthermia commonly seen in restrained canids
    • Body temps reaching 104
    • Treat with IV cool fluids, cool slowly, sedatives
  • Larger canids (maned wolves, gray and red wolves) may be restrained using catch poles or Y shaped padded poles
    • Animals often cower when approached
    • Limited exams, U/S, blood collection, vaccination, or administration of IV injection
  • Box traps vs. foot traps vs. tranquilizer traps
  • Table 46-2: anesthetic protocols
    • Telazol: wide safety margin, however dose-dependent, prolonged, and rough recoveries are common
    • Ketamine + alpha 2 agonist: reversibility, but have concerns of spontaneous arousal and hypertension
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6
Q

Describe anesthesia of nondomestic canids.

What sites are used for vascular access?

What are some common complications with anesthesia in canids? How are they managed?

What considerations need to be made for field anesthesia?

What considerations are made for pack reintroductions?

A

Vascular access

  • Comparable with domestic dogs
  • Jugular, cephalic, lateral saphenous

Intubation

  • Not always essential, bt should be performed during prolonged procedures

Pre-anesthetic considerations

  • Respiratory depression is common, supplemental oxygen and/or intubation should be available
  • Prolonged exertion can result in hyperthermia–cooling measures should be available
  • Hypothermia occasionally occurs under cold conditions and/or prolonged immobilizations
  • Hypertension can occur with ketamine/alpha2 combos
    • Anticholinergics should be used sparingly to avoid exacerbating hypertension
  • Vomiting can occur–fast prior to anesthesia when possible
  • Seizures can occur with dissociatives but less commonly when given with benzos
  • Gastric dilation (and rarely GDV) can occur

Drug choice

  • Drug choice varies by species and situation
  • Mask induction or chamber induction also sometimes possible
  • Can become overheated in induction chambers
  • Isoflurane can be used for maintenance
  • For routine procedures on young healthy animals in a controlled environment, they recommend medetomidine/butorphanol
    • Should not be used for more invasive procedures
    • May need to add ketamine or midazolam depending on depth and working time
  • In emergency or uncontrolled situations, telazol or ketamine/medetomidine are recommended
  • If animal is ill or old, probably not advisable to use an alpha 2

Field immobilization considerations

  • Many species are nocturnal
  • Often trapped and then injected, but darting also occurs
  • Darting from helicopter or car can be done but has a higher risk of inaccuracy and trauma

Post-anesthetic challenges

  • Most canids are pack animals, reintroduction after prolonged separation can result in fighting
  • Animals should be kept with the pack as much as possible
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7
Q

Describe the most common surgeries of canids.

What types of closures should be used?

What has been associated with GDV in nondomestic canids?

A

SURGERY (Fowler 8)

  • Repair of lacerations or traumatic wounds
  • Dehiscence of body wall has been frequently seen after abdominal surgeries, may cannibalize their own surgical organs
    • Simple interrupted is preferred to close abdominal wall
    • Subcuticular skin closure
  • Social species like bushdogs and wild dogs may experience increased anxiety isolated postop
    • May not be allowed back into a social group
    • Reintegration too soon may lead to excessive grooming, licking, or biting at the incision site
  • Cystotomy for cystinuria in maned wolves
  • GDV and GD has been documented: often found on necropsy
    • Feeding an animal shortly after anesthesia anecdotally linked to GDV
  • OVH and castration often performed
    • Vasectomy has been documented in bushdogs
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8
Q

What is the etiologic agent of canine infectious hepatitis?

What species are susceptible?

What are the typical gross lesions associated with this disease?

What histologic lesions? What are the inclusion bodies?

A
  • Canine adenovirus type 1 (Canine infectious hepatitis virus)
    • Causes disease in a wide variety of canids and bears
    • Gross lesions include petechial and ecchymotic hemorrhages of serosal surfaces, lymph node and gall bladder edema, and mottled fragile liver
    • Intranuclear viral inclusion bodies which are acidophilic or basophilic are present in endothelial cells, hepatocytes, biliary epithelium and adrenal epithelium
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9
Q

What viral disease is a common cause of mortality in juvenile canids?

What are the typical clinical signs?

Describe vaccination strategies for this disease.

A
  • Canine parvovirus
    • Well documented in coyotes and wolves
    • Clinical disease similar to domestic dogs, mortality rates variable
    • GI signs, leukopenia, etc
  • Canine parvovirus
    • Likely factor in juvenile mortality
    • Significant morbidity and mortality in captive animals
    • Modified live vaccine has caused concerns, not recommended until protective titers are present after using a killed vaccine
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10
Q

What is the etiologic agent of pseudorabies?

How does it affect canids?

Does is affect other carnivores?

A
  • Pseudorabies/aujesky’s disease – caused by suid herpesvirus 1
    • “mad itch”
    • Canids can be incidentally infected
    • Non-suppurative encephalitis with intranuclear eosinophilic inclusions
    • Can also infect a variety of bear species, but clinical disease is rare
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11
Q

Describe the clinical signs associated with papillomaviruses in canids.

What are the inclusion bodies like?

A
  • Papillomaviruses
    • Oral papilomatosis of coyotes is the most common
    • Usually self limiting
    • Papilliform to cauliflower like lesions with hyperplastic basal cell layer
    • If inclusions are present they are intranuclear and basophilic
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12
Q

What is the tropism of Canine Distemper Virus?

What type of virus is this?

What are the clinical signs in affected canids?

What inclusion bodies are typically seen?

What are the classic histologic lesions of this disease?

How does this disease affect wild canids?

Describe vaccine selection in preventing this disease.

A
  • Canine distemper (CDV)
    • Epitheliotropic and neurotropic
    • Respiratory, neuro, and cutaneous signs most common, but signs variable
    • Acute lesions in non-domestic canids similar to those in domestic dogs – rhinitis with purulent nasal or occulonasal discharge and pneumonia are common
    • Eosinophilic cytoplasmic viral inclusions are most commonly found in syncytia, macrophages and bronchiolar epithelium
    • White matter demyelination is the hallmark (but not pathognomonic) nervous system lesion in CDV infections and may be multifocal or patchy; it tends to affect cerebellum most severely
    • Grey matter lesions may occur throughout the CNS
    • Nuclear or cytoplasmic eosinophilic inclusions will be present in astrocytes and neurons
    • Hyperkeratosis of the footpads is the classic cutaneous lesion, but can also been seen on the nasal planum or hair skin
    • May see diarrhea (+/- secondary cryptosporidium or E coli infections)
    • Ursids have shown serologic evidence of CDV, with few clinical cases reported
    • Vaccine induced CDV infections have been described in red pandas when modified live vaccine is used
  • Canine distemper virus (CDV)
    • Natural epizootics occur in wild populations
    • Periodic introduction and maintenance of virus in domestic dogs poses a threat to endangered species
    • CDV infection has occurred in African wild dogs despite vaccination
    • Vaccine induced CDV infection has occurred after use of modified live vaccine
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13
Q

What type of virus is the rabies virus?

How is this disease transmitted?

What are the two forms?

What are the classic lesions?

What type of inclusion bodies are present? Where are they most commonly present?

How is this disease confirmed?

This disease is a continued threat to what species of wild canids?

A
  • Rabies
    • Progressive encephalomyelitis that is typically lethal was signs are apparent
    • Transmission via saliva or open wounds
    • Dumb form and furious form
    • Non-suppurative encephalomyelitis, ganglioneuritis, adrenalitis, sialoadenitis
    • Lesions most severe from pons to hypothalamus and cervical spinal cord
    • Intracytoplasmic eosinophilic viral inclusions in neurons (negri bodies)—most common in hippocampus
    • Diagnosed off of fluorescent antibody test in unfixed samples of fresh brain including the medulla and cerebellum is most common, though PCR and DNA sequencing can provide confirmation
  • Rabies: lyssavirus in the rhabdovirus family
    • Zoonotic
    • Geographic reservoirs
    • Continued epizootic threat to survival of Ethiopian wolf and African wild dog
      • Oral vaccination of wildlife using recombinant vaccines is effective control strategy, or immunization with injectable killed rabies vaccine
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14
Q

What mycobacterium species affect canids?

How is this disease transmitted to them?

What lesions are usually present in affected canids?

A
  • Mycobacterium
    • M bovis/bovine tuberculosis – OIE reportable
      • Granulomas and granulomatous inflammation of the LN, lungs, and other organs
      • Typically a disease of ruminants but disease has been described in red foxes, gray foxes, coyotes, wolves, and fennec foxes as well as black bears
      • Transmission through infected prey or carcases
      • Granulomas with low numbers of acid fast positive bacilli, though disseminated infection with no gross or microscopic lesions has been reported in red foxes
    • Other mycobacterial species have been reported in wild carnivores including M avium paratuberculosis in red foxes and coyotes, M avium avium in a jackal, M intracellulare and M kansasii in coyotes
    • Gold standard for diagnosis is bacterial culture, though other methods are often needed
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15
Q

What is the etiologic agent that causes anthrax?

How is this disease transmitted to canids?

What canid has a high seroprevalence?

What are the two main toxins of antrhax?

A
  • Anthrax/Bacallus anthracis
    • OIE reportable, large spore forming gram positive rod with clear capsule
    • Disease most common in ruminants but can be seen in carnivores, likely through inhalation of spores from an infected carcass
    • Proteins produced by the bacteria combine to produce edema toxin and lethal toxin which cause edema and death
    • Serology of while black backed jackals shows high serum prevalence (95%), indicating high exposure and survival
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16
Q

What is the etiologic agent of lyme disease?

Clinical cases have been seen in what wild canid species?

A
  • Borrelia/lyme
    • Reported in a wild red fox – cutaneous erythema
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17
Q

What is the etiologic agent that causes Salmon poisoning?

How is it transmitted?

How are canids exposed?

Are other species also affected?

What are teh typical clinical signs and lesions?

A
  • Neorickettsia helminthoeca
    • rickettsial organism that causes salmon poisoning
    • Transmitted by Nanophyetus salmincola, an intestinal fluke of canids in NW US
    • Infected via ingestion of fish or amphibians with encysted metacercariae
  • Salmon poisoning/neorickettsia helminthoeca
    • Reported in sun bears
    • Rickettsial bacteria that infects the trematode nanophyetus salmincola – infected by eating a fish containing these trematodes
    • Clinical signs include vomiting, diarrhea, lethargy
    • Diagnosis of nanophyetus ova in feces allows a presumptive dagnosis
    • Infected bears may develop eosinophilic gastritis and enteritis
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18
Q

What are the signs typically associated with dermatophytosis in nondomestic canids?

What histologic lesions are usually present?

What are the two main species of dermatophytes that affect canids?

A
  • Dermatophytoses
    • Alopecia and scaly skin with or without crusts
    • Histo—accanthosis with orthokeratotic hyperkeratosis
    • M canis and T mentagrophytes have been described in foxes
    • M gypseum is an important cause of skin disease in red pandas
      • Lesions on the tail, extremities, muzzle, and ears
      • Typically during the warm season
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19
Q

What microsporidia have been documented to affect canids?

What species have been affected?

What lesions were found on necropsy?

A
  • Microsporidia
    • Encephalitozoon
      • Rarely described in African wild dogs and a litter of arctic foxes
      • Histo lesions seen in brain and kidney similar to that in E. cuniculi in rabbits
      • Dissemination to other organs also seen in foxes
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20
Q

What are the four lungworms that affect nondomestic canids?

What are the typical lifecycles?

What species are affected by each of these worms?

A

Metazoa

  • Oslerus osleri
    • Dog lungworm, nematode, infests the trachea mainstem bronchi of canids
    • Direct life cycle—larvae are hatched in resp tract, coughed up, swallowed, and shed via feces
    • Ingestion of infected vomit is the primary mode of transmission
    • Causes nodules within the tracheal mucosa
  • Crenosoma vulpis
    • Fox lungworm
    • Foxes, wolves, raccoons and dogs are the definitive hosts
    • Infection also reported in badgers, wolverines and black bears
    • Adults reside in the trachea, bronchi, and bronchioles
    • Larvae coughed up, swallowed, shed in feces – intermediate host is snails or slugs which are then eaten
    • Gross lesions—parenchymal consolidation with intralesional adult nematodes
  • Eucoleus aerophilus
    • Another lungworm of wild carnivores including foxes
    • Tends to infect higher in the resp tract than C vulpis
  • Angiostrongylus
    • Intravascular nematode with a wide host range including canids
    • Indirect life cycle—ingestion of larvae from environment or infected gastropods
    • A. vasorum aka French lungworm in canids and red pandas
      • Adult worms reside in the right atrium and ventricle of the heart and pulmonary arteries
    • A. gubernaculatus in island fox
    • A. raillieti in crab eating fox
    • Clinical signs include mild respiratory signs and thrombus formation
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21
Q

What two filaroid nematodes affect canids?

How are they transmitted?

What are teh typical clinical signs?

What species are affected?

A
  • Dirofilaria immitis/heartworm disease
    • Spirurid, filarial nematode
    • Canids and felids are definitive hosts
    • Other species including bears and red pandas can be infected
    • Transmission by mosquito vector
    • Pulmonary arteries and lungs
    • Severe infections cause right sided CHF and PHT or caval syndrome
  • Dirofilaria repens
    • Subcutaneous and occasionally intrabdominal, LN or intestinal infections
    • Foxes and wolves
    • Can be zoonotic
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22
Q

Describe the lesions associated with Spirocerca infestation in canids.

What is the life cycle?

What clinical signs are seen in affected animals?

What can result from chronic infestation?

A
  • Spirocerca lupi or S. artica
    • Aortic aneurysm and/or fibrotic aortic and esophageal nodules
    • reported in canids
    • indirect life cycle – intermediate host is a beetle, paratenic hosts such as poultry, lizards, nad rodents
    • infected animals may be asymptomatic or have coughing, weakness, lethargy, dysphagia or sudden death secondary to aneurysm rupture
    • Chronic infection can also cause mural hyperplasia or neoplastic transformation (fibrosarcomaa or osteosarcoma)
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23
Q

What is the giant kidney worm?

What taxa are typically affected?

Are there any canids that are commonly affected?

How is it transmitted?

What are the associated clinical signs?

A
  • Dioctophyma renale/giant kidney worm
    • Primarily in mink and dogs but reported in wild canids
      • Wolves, coyotes, jackals, foxes
      • High prevalence in free-ranging maned wolves
    • Ingestion of encysted larvae in infected raw fish, frogs, or annelid worms
    • Largest known nematode to infect mammals
    • Hematuria, ureteral obstruction and hydronephrosis
    • Unilateral infections most common, right kidney usually affected
    • Intraperitoneal parasites can be seen with aberrant migration
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24
Q

What are the most common Trichinella species?

What animals are most commonly affected?

How is this disease transmitted? Can it be transmitted to people?

What are the typical lesions?

A
  • Trichinella spp
    • OIE reportable
    • T spiralis most common, with T britovi, T pseudospiralis and T. nativa also reported
    • Foxes, bears, and wolves most commonly infected
    • Ovoviviparous nematodes
    • Zoonotic transmission through consumption of undercooked meat (pork, bear)
    • Myofiber necrosis with neutrophilic and eosinophilic inflammation
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25
Q

What is the etiologic agent of hepatozoonosis?

What canid species are commonly affected?

Describe the life cycle of this diease.

How is it transmitted?

What are the typical clinical signs?

What are the typical lesions?

A
  • Hepatozoon
    • Reported in jackalds, AWD, crab eating foxes, Pampas gray foxes, coyotes
    • Life cycle: sexual development in definitive hosts (hematophagus arthropods) and asexual development in a vertebrate host
    • Infection by ingestion of the arthropod or vertical transmission
    • Clinical signs often absent, but lesions can include anemia or leukcytosis, pneumonia, myocarditis
    • H canis has a characteristic “whell spoke” appearance with a central eosinophilic nucleus and peripheral, basophilic merozoites
    • H americanum can cause severe segmental periosteal woven-bone production in canids
26
Q

What are the four genera of piroplasms that affect canids?

What is the life cycle like?

What are teh typical clinical lesions?

What is the etiologic agent of yellow fever in dogs? What species is commonly affected?

A
  • Piroplasmosis
    • 4 genera – babesia, theileria, cytauxzoon and rangelia
    • Life cycle similar to hepatozoon
    • Infection often incidental finding, but babesia (B annae and B canis) can cause anemia +/- thrombocytopenia
      • Gross lesions can include hepatomegaly, splenomegaly, and renal petechiae
      • Histologically may see merozoites or trophozoites within RBC’s
    • Rangeliosis aka yellow fever of dogs
      • Caused by rangelia vitalli
      • Reported in pampas foxes
      • Tear dropped shaped protozoa infecting erythrocytes, leukocytes and endothelial cells
      • Causes hemolysis, GI hemorrhage, icterus, fever
      • Severe bilateral hemorrhage along the lateral margins of the pinna is characteristic
27
Q

What canid species have been affected by Toxoplasma gondii?

How does transmission occur?

A
  • Toxoplasma gondii
    • Felids are the definitive host
    • Transmission to intermediate, reservoir hosts by ingestion of infective oocysts in feces
    • Infected ursids or canids are usually asymptomatic. However, fatal infections have been reported in several fox species and giant pandas
28
Q

How is leishmania transmitted?

What canids species are commonly affected?

What are the gross and histologic lesions associated with disease?

A
  • Leishmania
    • Cutaneous and visceral disease
    • Obligate intracellular protozoa that infect monocytes and macrophages
    • Transmitted to mammalian reservoir hosts by sandflies
    • Reported in bush dogs, crab-eating foxes, golden jackals, hoary foxes, maned wolves
    • Gross - emaciation, anemia, hemorrhage, cavitary effusion, ehpatomegaly, splenomegaly, lymphadenomegaly
    • Histo - histiocytic infiltrates with intracytoplasmic amastigoes
29
Q

Neospora caninum has caused what type of disease in nondomestic canids?

What species has this disease been reported in?

A
  • Neospora caninum
    • Has caused hyperplastic dermatitis with parakeratosis in a red fox with concurrent toxoplasma infection
30
Q

What it the most common mite to affect canids?

What are teh clinical signs?

What are the two forms of the disease?

A
  • Sarcoptes scabiei
    • Widespread, contagious, pruritic disease of numerous species of canids and ursids
    • Hyperkeratotic and alopecic are the two most recognized form of the disease
    • The first form generally occurs in naïve or immunocompromised individuals
    • The second form is a hypersentivity reaction that develops in immunocompetent animals who mount a type I and type IV hypersensitivity reaction
      • In addition to alopecia they develop intense dermal eosinophilic and mast cell infiltrates with few intralesional mites
31
Q

What are the ear mites of canids?

These mites cause considerable economic damage in what farmed species?

What are teh clinical signs and lesions associated with infestation?

A
  • Otodectes cynotis
    • Ear mites
    • Has caused significant economic losses in arctic foxes and silver foxes due to scratching damaging the pelts
    • Ceruminous gland hyperplasia and subsequent tumor development occurred in ½ the population of santa Catalina island foxes with an otodectes outbreak
    • Otitis externa with hyperkeratosis and epidermal hyperplasia and ceruminous gland hyperplasia
32
Q

What pentastomid has canids as their definitve host?

Where does infection usually occur?

What clinical signs may occur as a result?

A
  • Pentastomids
    • Called “tongue worms” due to appearance
    • arthropods that infect the upper respiratory tract
    • Nasal pentastomiasis due to Linguatula serrata occurs in canids as the definitive hosts
    • Infection typically asymptomatic and found incidentally at necropsy, though URI signs can occur
33
Q

Describe the nutritional diseases observed in nondomestic canids.

What are the classic lesions associated with rickets? What species has this been reported in?

What species is nutritional secondary hyperparathyroidism common in? What lesions are seen.

Polioencephalomalacia is commonly associated with what deficiency? How would foxes get this?

A red wolf presenting with acanthosis and hyperkeratosis of footpads may have what trace element deficiency?

A
  • Nutritional
    • Starvation/nutritional insufficiency – particularly in wild animals
    • Rickets – wild arctic foxes; enlargement of costochondral junction (the “rachitic rosay”) and delayed endochondral ossification, widened physes, angular limb deformities, metaphyseal fractures
      • Also been reported in red foxes, coyote, polar bears
      • Low Vit D level may predispose, taurine deficiency may contribute
    • Nutritional secondary hyperparathyroidism—juvenile red foxes; typically emaciated with enlargement of distal epiphyses of longbones and ribs
      • Histopath confirms fibrous osteodystrophy
    • Thiamine (Vit B1) deficiency—farm raised foxes and wild red foxes. Called Chastek paralysis, caused by diet of raw fish containing thiaminase
      • Causes poliomalacia (grey matter necrosis)
      • Bilateral lesions most consistent in caudal colliculi and vestibular nuclei
      • Myocardial degeneration, hepatic lipdosis, and nephrosis also seen
    • Hyperostotic bone disease
      • Reported in a single group of captive red pandas – excessive dietary vitamin A
    • Zinc responsive dermatitis (with secondary pyoderma) has been reported in a captive red wolf – acanthosis and orthokeratotic and perakeratotic hyperkeratosis of footpads and distal limbs
34
Q

Cystinuria is common in what canid species?

What are suspected causes of this disease?

What clinical signs may occur as a result?

A
  • Cystinuria
    • common in maned wolves
    • autosomal recessive condition in humans and domestic dogs– defective transport of cystine across renal tubular epithelium
    • dibasic aminoaciduria with excretion of cysteine and lysine
    • meat based diet in captivity may predispose, but genetic component suspected
  • Cystinuria: Maned wolves, likely genetic
    • Often subclinical unless causing obstruction
    • Monitor closely for stranguria
    • Medical therapy aimed at affecting solubility of cysteine to prevent crystal precipitation
      • Urine alkalinization
      • Diet manipulation: reduce sodium intake and reducing protein from animal sources
35
Q

What are the characteristic leisons of exertional myopathy?

How common is this in canids?

A
  • Exertional myopathy
    • Less common in canids than other species but can occur
    • Monophasic necrosis of striated muscle
36
Q

Describe the effects of the following toxins in canids:

Ethylene GLycol

Rodenticides

Strychnine

Cholecalciferol

A
  • Toxic
    • Organophosphate or carbamate
      • Can occur as malicious poisoning or secondary intoxication from ingesting other species
    • Organochorline pesticids (OCP) and polychlorinated biphenyls (PCB)
      • Relatively low toxicity but tendency for bioaccumulation
      • Accumulate in fat, mobilization of adipose stores can lead to acute toxicity and death
      • Chronic exposure can cause thyroid follicular cysts and C-cell hyperplasia
      • Polar bears at high risk of bioaccumulation due to blubber stores
    • Ethylene glycol
      • Renal nephrosis with large numbers of calcium oxalate crystals in renal tubules
    • Anticogulant rodenticide
      • Hemorrhage in subcutis or body cavities
    • Strychnine
      • Convulsions and sudden death
    • Cholecaliferol poisoning
      • Described in captive foxes
      • Associated with deposits of calcium in kidney, muscle, lungs, and GIT
    • Melarsomine toxicity
      • Red panda died 24h after treatment for dirofilaria
      • Pulmonary edema secondary to direct pulmonary cellular toxicity
37
Q

For each of the following congenital disorders, describe the disease process and the canid species commonly affected:

Congenital hypotrichosis - what is this also known as?

Gingival fibromatosis

Manidbular hypoplasia

Hydrocephalus

Spongy degeneration of white matter

Lafora’s like disease

A
  • Congenital
    • Congenital hypotrichosis
      • Gray foxes, usually missing guard hairs only, otherwise normal
      • Also reported in red foxes
      • “Sampson” Fox Anomaly
        • Infrequent inherited genetic trait
        • Marked lack of guard hairs, underfur is present = fuzzy/woolly appearance
        • Occurs primarily in gray foxes (may occasionally be seen in a variety of other species)
        • Confused with mange
    • Gingival fibromatosis (hereditary hyperplastic gingivitis)
      • Autosomal recessive trait
      • Found in farm-reared silver foxes, higher prevalence in males with good fur quality
    • Mandibular hypoplasia/micrognathism
      • Reported in a population of red foxes
      • Malocclusion, supernumerary teeth, failure of tooth development may also occur
    • Hydrocephalus
      • Seen in red fox kits
      • Minimal lymphocytic meningitis
      • No link to viral infection (CDV or parvo) found, but cannot be completely ruled out
    • Spongy degeneration of white matter
      • Young captive silver foxes
      • Large cytoplasmic vacuoles in oligodendrocytes, demyelination, myelin edema
      • Brain and spinal cord affected. Bilaterally symmetrical
      • No known underlying cause
    • Lafora’s-like disease
      • Reported in one mature fennec fox with a 6 month history of seizures
      • Autosomal recessive condition characterized by intracytoplasmic accumulation of a complex polyglucosan “Lafora bodies” in neurons and various cells in other tissues. No gross lesions
38
Q

For each of teh following degenerative conditions of canids, describe the process and what canid species has been commonly affected:

Cystic endometrial hyperplasia & pyometra

Systemic amyloidosis

Degenerative heart disease

A
  • Age related/degenerative
    • Dental disease
      • Can be diet related, though in African wild dogs natural diet does not appear to be protective
    • Degenerative joint disease
      • Common in ursids especially
    • Cystic endometrial hyperplasia (CEH) and pyometra
      • Common in aged red wolves and African wild dogs
      • Can occur spontaneously, but often predisposed due to use of synthetic progestogen contraceptives
      • Prolonged cyclic exposure to endogenous steroids associated with obligate hormonal pseudopregnancy that follows ovulation in females associated with uterine pathology
        • Cystic endometrial hyperplasia-pyometra complex
        • Use of melengestrol acetate for contraception has been associated with endometrial hyperplasia, hydrometra, fibrosis, adenomyosis, uterine mineralization
    • Systemic amyloidosis
      • Well documented in free ranging island foxes – affects as many as 1/3 of the population
      • Amyloid deposition causes nephritis, can also deposit in oral tissues and spleen, causing nodules
    • Chronic renal disease
      • Common in captive bears, best described in polar bears
      • Histologic lesions show membranous and/or proliferative glomerulopathy, tubular protein and interstitial fibrosis
      • Immune complex deposition suspected but not fully investigated
    • Degenerative heart conditions
      • Rarely reported in free ranging canids
      • Valvular dysplasia in a red wolf and DCM in African wild dogs
      • Captive red pandas – cardiovascular and renal diseases are common age related findings – myocardial fibrosis and HCM most common
39
Q

Describe inflammatory bowel disease in canids.

What are the clinical signs?

What histologic findings are common?

How is this disease diagnosed and treated?

A
  • Inflammatory bowel disease
    • Cause of chronic GI disease (vomiting and diarrhea)
    • Weight loss, poor pelage, overall malaise
    • Hypoproteinemia often leading to ascites
    • Inflammatory cell infiltration of lamina propria (lymphocytes, plasma cells, eosinophils, macrophages, neutrophils)
    • Etiology: impaired immunoregulation in response of gut-associated lymphoid tissue to antigenic stimuli
    • Confirmatory diagnosis often requires gut biopsies
    • Treatment: immunomodulation, dietary modification, antibiotics, and supportive care, possibly supplementing cobalamine and folate
40
Q

For each of the following tumor types, describe the lesions and character of the neoplasia and give the canid species that is commonly affected.

Ceruminous Gland Tumors

Hepatic Tumors

Lymphoma

Nasal Adenocarcinoma

Granulosa Cell Tumors

Hemangiosarcoma

Osteosarcoma

A
  • Neoplasia
    • With a few notable exceptions, tumors are sporadic and represented by small numbers of case reports—likely that the true prevalence is underrepresented
    • Ceruminous gland tumors
      • Found in 52.2% of santa Catalina island subspecies of the island fox, 34.8% of which were considered malignant (adenocarcinomas)
      • Primarily dermal, though occasionally invaded the tympanic bullae and other bones or metastasized to LN or lung
      • Associated with ear mite infestation and chronic inflammation, but only the island foxes appear predisposed
    • Hepatic tumors
      • Relatively common in ursids and fennec foxes
      • Biliary adenoma or adenocarcinoma, hepatoma, and hepatocellular carcinoma
      • Biliary neoplasms can be extrahepatic or intrahepatic
    • Lymphoma
      • Common in one survey of red wolf mortality
      • Variable presentations/tropisms in various species, cell phenotype not thoroughly investigated
    • Nasal adenocarcinoma
      • Mexican gray wolves predisposed
    • Ovarian tumors
      • High frequency in maned wolves, most common being dysgerminoma, which is very rare in other species. These germ cell tumors are solid, multinodular with cystic cavities and are comprised of sheets of primitive round cells
      • Granulosa cell tumors—seen in maned wolves and african wild dogs
    • Malignant mammary tumors and tumors of sweat glands occasionally identified in canids
    • Hemangiosarcoma reported several times in African wild dogs, though the heart is the most common site
    • Osteosarcoma in red wolves and maned wolves
41
Q

Describe the reproduction of canids.

What type of reproductive cycle do most have?

How long is gestation typically?

What is average litter size for most canids? What species have unusually large litters?

What is pseudopregnancy? What pack members does this occur in?

A

REPRODUCTION (Fowler 8)

  • Exceptionally long proestrous and diestrous phases
  • Copulatory lock
    • May be prolonged in species like the fennec fox
  • Behavioral suppression of mating in subordinate young in a social group
  • Obligate pseudopregnancy in subordinate females
    • Pseudopregnancy: prolonged luteal phase following ovulation, may be as long as pregnancy
    • Prepare subordinate females for rearing in a pack
  • Most are seasonal breeders
42
Q

Describe the medical management of maned wolves.

What is the scientific name of the maned wolf?

What is unique about its diet?

What deficiencies and excesses are common in managed care diets?

Describe their reproduction and contraception.

What are some common diseases of wild maned wolves?

What is the pancreatic fluke that affects them?

A

Fowler 7 Ch 58 - Medical Management of Maned Wolves

Maned Wolves (Chrysocyon brachyurus)

Traits:

●Only member in this genus

●Legs long and stick-like, easy maneuvering in grasslands

●Rust red hair coat, patch of dark hair down withers and neck and often raised (‘maned’)

●Separated by Canis by one set chromosomes

●Largest canid in South America (NE brazil, No Argentina, Paraguay, Uruguay, E, Bolivia, Peru)

● Nocturnal, living in grasslands.

●Population size hard to assess due to secretive nature

●Habitat has been affected by agricultural development, and seen as road kills and poultry predator has negatively affected its numbers in the wild.

Husbandry:

●Secretive nature warrants special housing, large enclosure with tall grass, shade and hiding places

●Captive maned wolves will forage natural prey- concern for pest control and internal parasites

Nutrition:

●Omnivore ingesting 51% of diet as plant material the rest as animal protein(mammals, birds, reptiles, invertebrate).

●Taurine and amino acids deficiencies in captive animals.

●Diets too high in animal protein in captivity – consistent issue (uroliths, loose stool, unthrift)

●Zoos feed fruits veggie, whole prey items, commercial canine kibble (70% of diet)

Reproduction:

● Facultatively monogamous- pairs reunite during breeding season

● Monoestrus with 5 day cycle.

● Gestation 63-67 days.

● Give birth during dry season = Jan - March

Contraception:

●Contraception recommended as GnRH agonist (ie Deslorelin or Lupron).

●MGA shown assoc. with uterine pathology in carnivores (not recommended)

●In females – suppress pituitary LH and FSH and gonadal estradiol and progesterone.

●In males – suppress pituitary LH and FSH and gonadal testosterone.

● Reversible and useful in males and females.

Diseases of Wild Maned Wolves:

●Giant kidney worm (Dioctophyme renale) by eating fish or frogs. Migrates to right kidney causing irreversible damage. (some wolves known to survive with one kidney)

●Nematodes (Trichuris, Ancylostoma, Toxacara sp), Cestodes, Ticks and screwworms

●Exposure to domestic carnivore diseases such as parvo, lepto, toxo.

Diseases of Captive Maned Wolves:

●Canine distemper virus (morbillivirus) – neuro and respiratory signs.

-recommend vaccination (recombinant canary-pox vectored or killed distemper)

●Parvovirus- leading to debilitating diarrhea/death

  • In young use killed vaccine until serologic titer >1:80, then use mod. live for longer protection.

●Adenovirus- May have caused hepatitis in one captive

-Use available commercial vaccine products with caution.

●Rabies- should vaccinate using killed product

●Pancreatic fluke = Eurytrema procyonis

Normal host is raccoon, with arthropod intermediate host.

Clinical signs – thin, loose feces, partial anorexia

Diagnosis by fecal float or sedimentation

Treat with praziquantel and pancreatic supplement.

●Heartworm disease

Treatment and prevention as per canids.

Cystinuria is a hallmark problem of this species in captivity.

  • Also reported in wild wolves but impact unknown.
  • Possible genetic component as these canids excrete cystine in the urine.
  • Predisposing factors are high protein diet, hi levels methionine and cystine in diet

and an acidic urine.

-Males more often affected. (stranguria)

●IBD reported

●Dermatitis, atopy, lick granuloma, etc.

●Periodontal disease in captives

●Neoplasias – fibrosarcomas, osteosarcomas, ovarian dysgerminomas (intact females).

43
Q

The red fox is the major host of what zoonotic cestode?

What is teh life cycle of this cestode?

How are people affected?

A

Echinococcus Infection

  • Red foxes = major definitive host of this tiny (<1/8 in) tapeworm
    • US – red foxes & coyotes principle hosts, artic foxes in Alaska (dogs & cats can be definitive hosts)
    • Usu no clinical signs, lesions
  • Echinococcus multilocularis
    • Eggs in feces can’t be distinguished from other species of tapeworm
    • Eggs are immediately infectious when shed in feces
    • Must ID adult worm (necropsy)
  • Intermediate host = rodent
    • Dz caused by larval stage which occurs as cysts (lg proliferative cysts, most in the liver)
    • Confirmed by finding cysts in liver/organs at necropsy
  • Zoonotic – humans susceptible to larval stage
    • Alveolar hydatid disease
    • Long course of dz (10yrs), often fatal despite tx
  • Not known to occur in SE US, prevalent in red foxes & coyotes in northern plain states (important not to relocate wildlife to uninfected areas).
44
Q

Describe the conservation status and threats to African wild dogs.

What are some of the unique characteristics of AWD?

Describe the social structure of an AWD pack.

Which juveniles leave the pack?

Which individuals have the highest cortisol levels?

How does separation affect the pack?

Describe the ideal enclosure design for African wild dogs.

A

Introduction

  • Conservation status: IUCN red list priority for conservation of canid species in Africa- population 6600 animals (600 in zoos)
  • Require large ranges, live at low populations densities
  • Continuing decline due to habitat fragmentation, conflict with humans, infectious disease, predation (lions), competition (hyena)

Biology/Anatomy

  • Carnivora : Canidae – diverged from wolves in Pleistocene period, genetically distinct genus (Lycaon pictus)
  • 18-35kg, M > F, 10.3y survival in zoos (12-16y)
  • Tricolor spotted coat, large round ears, no supracaudal gland, no dew claws, intradigital webbing, similar repro anatomy (12-14 mammae), sharp large premolars (I3/3, C1/1, PM 3/4, M 3/3 = 21) and vestigial last mandibular molar

Management/Husbandry/Behavior

  • Pack- older dominant female + young dominant male, subordinates of both sexes- dominant males may be displaced
    • Juvenile males stay with pack, females often emigrate
    • Death of dominant female can lead to significant social changes and pack dispersal
  • Social management in captivity is challenging- need well-established dominant pair w/ male offspring, YOUNG F offspring
    • Females >18mo may come into conflict with dominant female
    • Unrelated individuals more likely to integrate successfully
    • If separation needed, split up as same-sex packs or with littermates <18mo
    • Contraception not successful in reducing intraspecific aggression
    • Fecal corticosteroid monitoring- useful for management- dominant animals have highest stress level
      • Behavior good indicator of social/physical well-being- establishing pack hierarchy essential
    • Permanent/temporary removal of pack member may have profound social impacts
    • Detailed planning required if pack member must be isolated- maintain olfactory/visual contact OR subdivide pack
  • Enrichment- sensory stimulants, food/behavior/habitat variance- encourage natural behaviors (dig/roll/scent mark/breed)
  • Large enclosures with ample space for exercise, prevent close contact/access from visitors, multiple heated areas if <45 F
  • Heated den if breeding planned
  • Holding space to accommodate separating animals for long period
  • High predatory drive- don’t house with other animals
  • Relocation: move in sturdy wooden/metal crates, always complete written transport plan, health evaluation, crate training
45
Q

Describe the reproduction of African wild dogs.

How long is gestation? How many pups do they have?

What contraceptives have been used? What are some common complications with contraception?

A

Reproduction/Contraception

  • Seasonally monoestrous obligate cooperative breeders, brief copulatory tie, senescence 8-9m (2y+ for successful repro)
  • Alphas produce majority of surviving pups; subordinate females often develop pseudopregnancy to lactate/care for pups
  • Estrus 6-9 days (vulvar swelling/discharge), Gestation 69-71 days, 6-8 pups (up to 21) per litter
    • Primiparous females produce more males (higher estrogen)
  • Hand-rearing NOT recommended- separate breeding pair, gradually introduce when pups emerge from nesting box
  • Newborns: 300g, open eyes at 2 weeks, emerge from den/start solid food (regurgitate) at 3w, weaned at 11-12w
  • Most captive reproduction natural (AI has been used), generally reproduce in fall; 1-2 weeks interest before breeding
    • Males: increased testicular development, spermatorrhea, semen production – increased ability to collect sperm
  • Melengestrol acetate (MGA) implant – associated with uterine pathology- GnRH agonists recommended for management
  • 23% females have reproductive pathology- CEH, pyometra, adenomycosis, adenocarcinoma, uterine rupture
    • Spay all post-reproductive females (>10yo); Deslorelin implants have variable results
46
Q

What are the most significant viral diseases of African wild dogs?

What tyep of heart disease do AWD get?

What is the most common neoplasia of the AWD?

Describe an ideal preventative medicine protocol for AWD.

How should they be vaccinated?

A

Diseases

  • VIRAL- Rabies, distemper (contribute to mortality), serology- exposure to parvo, distemper, adenovirus, rabies, coronavirus, rotavirus- contact with domestic species may increase exposure but sylvatic strains are a threat
  • BACTERIAL- Ehrlichia canis (exposure), Anthrax (low mortality)
  • PARASITIC- rare, often no clinical disease- std canine anthelmintics effective, HW testing/screening/prophylaxis
  • NON-INFECTIOUS-
    • Valvular dysplasia (genetic, mild-severe/CHF, underdiagnosed)- routine echos recommended, tx similar to dogs
    • Neoplasia- Apocrine gland tumors- surgical excision recommended; HSA, fibromatous epulis, adrenocortical adenoma/carcinoma, mammary/uterine neoplasia
    • Dental disease- fractured teeth
    • Other- Pancreatitis, diabetes, spina bifida, syringomyelia, keratitis, snake bite, trauma- often mask signs

Preventative Medicine (including preshipment and quarantine exams)

  • Complete PE- dental exam, CBC/Chem, HW test, UA, thoracic/abdominal rads, parasite screening, AUS, echos
  • Treat parasites similar to domestic dogs (pyrethrins/carbaryl for fleas/ticks, control fly/mosquito popluations)
  • Quarantine new animals- need 2 negative fecals- place microchips for identification
  • Vaccination- no universal recommended protocols- safety/efficacy not great
    • MLV Distemper- failed to produce effective antibody levels in some cases, induced distemper in others- use KV
      • Purevax Ferret vax x3 q2-3w – produced best results (1y protective titers 39-85%)
    • Imrab 3 vaccine- persistent protective rabies titers from 1 IM vaccination
    • 2006 survey- most maintain titers for 1 year, some longer
47
Q

A recent study evaluated the genes encoding P-glycoprotein in nondomestic canids.

What is the gene that encodes P-glycoprotein. What is the role of that protein?

What mutation in herding breeds alters that?

Was the mutation found in wild canids?

A

PREVALENCE OF THE ABCB1-1D GENE IN NONDOMESTIC SPECIES OF THE CANIDAE FAMILY

Journal of Zoo and Wildlife Medicine 51(4): 1007–1011, 2020

Abstract: The ABCB1 gene is responsible for encoding the P-glycoprotein (P-gp) efflux transporter that prevents accumulation of exogenous substances in the body by utilizing ATP hydrolysis to transport these substances against their concentration gradient. In dogs, homozygous or heterozygous mutations for the previously described ABCB1-1D mutation lead to ineffective P-gp efflux transport function and puts the animal at risk for potentially devastating adverse drug effects. The purpose of this study was to evaluate ABCB1-1D gene mutation status in species belonging to the Canidae family, including each of the following: maned wolf (Chrysocyon brachyurus), gray wolf (Canis lupus), red wolf (Canis rufus), coyote (Canis latrans), dingo (Canis lupus dingo), New Guinea singing dog (Canis lupus dingo), arctic fox (Vulpes lagopus), and fennec fox (Vulpes zerda). These species were chosen based on an evolutionary study conducted by Belyaev that noted foxes, bred for temperament, tended to have similar behaviors seen in the modern-day dog. Wolves, known predecessors to the modern dog, were also included. In the current study, a buccal swab was performed on each animal and then tested at Washington State University’s Veterinary Clinical Pharmacology Lab, where they were tested according to previously published methods validating buccal swab samples and polymerase chain reaction (PCR) –based genetic analysis. Knowledge of Canidae species ABCB1-1D gene mutation status allows for safe and effective therapeutic treatment of nondomestic animals, ensuring any anticipated adverse drug events are prevented. All eight species were found to have the wild-type ABCB1 gene and thus, expected to have normally functioning P-gp efflux transporters. Although these data can be used to guide clinical decision making, because of a small sample size, a more robust study is necessary to assess Canidae ABCB1-1D mutation status comprehensively.

  • The ABCB1 1 gene is responsible for encoding the P-glycoprotein (P-gp) efflux transporter that prevents toxic accumulation of exogenous substances in the brain
  • A mutation in herding breed domestic dogs causes the P-gp pump to function incorrectly, creating a risk for toxicity to a number of medications including sedatives, chemotherapy, dexamethasone, and fluoroquinolones
  • The purpose of this study was to evaluate ABCB1-1D gene mutation status in species belonging to the Canidae family

M&M

  • Animals tested: maned wolf (Chrysocyon brachyurus), gray wolf (Canis lupus), red wolf (Canis rufus), coyote (Canis latrans), dingo (Canis lupus dingo), New Guinea singing dog (Canis lupus dingo), arctic fox (Vulpes lagopus), and fennec fox (Vulpes zerda).
  • Buccal swab collected and sequencing was performed

Results and discussion

  • All eight species were found to have the wild-type ABCB1 gene and thus, expected to have normally functioning P-gp efflux transporters.
  • However, the sample size in each species was quite small (n=1 or 2) and therefore more robust analysis is warranted
48
Q

A recent study evaluated the ocular anatomy and characteristics of crab-eating foxes.

What is the scientific name of the crab-eating fox?

What is unique about its pupil shape?

How does pupil shape correspond with natural history?

A

Renzo, R., Aldrovani, M., Crivelaro, R. M., Thiesen, R., de Barros Sobrinho, A. A., da Silveira, C. P. B., … & Laus, J. L. (2020). THE EYE OF CRAB-EATING FOX (CERDOCYON THOUS): ANATOMICAL CHARACTERISTICS AND NORMATIVE VALUES OF SELECTED DIAGNOSTIC TESTS, MORPHOMETRY OF CORNEAL TISSUE, AND ARRANGEMENTS OF CORNEAL STROMAL COLLAGEN FIBERS. Journal of Zoo and Wildlife Medicine, 51(2), 280-289.

Abstract: This study aimed to evaluate the ophthalmic parameters, morphometric features of corneal tissue, and arrangements of corneal stromal collagen fibers in crab-eating fox (Cerdocyon thous), a species of neotropical wild canid. We conducted the study on six juvenile crab-eating foxes (12 eyes), whilst 16 eyes were obtained post mortem from eight adult crab-eating foxes. The research was divided into two stages. In the first stage, eye anatomical characteristics, tear production (Schirmer 1 tear test, STT1), intraocular pressure (IOP), ocular echobiometry, and specular microscopy parameters related to morphology of corneal endothelium were studied in juvenile animals. In the second stage, morphometric features of corneal tissue (central corneal thickness [CCT] and corneal epithelium thickness) and arrangements of stromal collagen fibers were studied using eyes from adult animals. The main findings were that crab-eating fox eyes have vertical-slit pupils, holangiotic retina, and reference values (mean ± SD) of 13.37 ± 3.79 mm/min for STT1 and of 10.43 ± 3.84 mmHg for IOP. The ocular echobiometric features observed in crab-eating foxes are different from those reported for domestic dogs (Canis familiaris). Conversely, the corneal endothelial parameters are similar to those of domestic dogs. The CCT measured by tissue morphometry was 0.54 ± 0.06 mm, and the corneal epithelium thickness was 60.13 ± 8.71 µm. Mean coherency related to alignment of collagen fibers was 0.66 ± 0.12. The crab-eating fox cornea had predominantly thick collagen fibers. Crab-eating fox eyes have morphofunctional peculiarities. They resemble the eyes of domestic dogs in some aspects, but diverge in others.

  • Key Points:
    • Crab-eating fox (Cerdocyon thous) – Medium-sized carnivore, canidae.
      • Widespread neotropical distribution.
    • Corneal layers of the eye.
      • Corneal epithelium protective interface with environment.
      • Endothelium fundamental to corneal homeostasis, selective barrier vs fluid entrance into the stroma.
      • Stroma determinant to transparency, shape, biomechanical properties of cornea, predominantly made of collagen fibers.
    • Eye anatomical characteristics:
      • Well-defined eyelashes on upper lid, superior and inferior lacrimal puncta, brown iris, vertical-slit pupil, nictitating membrane. Tapetum. Round optic disc.
        • Vertical slit shaped pupil similar to European red foxes, different from domestic dogs and grey wolves.
          • Facilitates stereopsis for estimating distances of object perched on the ground while enebling depth from blue to estimate distances along the ground.
          • Vertical pupils usually characteristic of nocturnal or iurnal-nocturnal predators. Herbivores tend to have horizontal pupils and most diuranal predators have round pupils.
      • Holangiotic retina with 3-4 spoke-like venules emerging from optic disc, numerous arterioles.
    • Diagnostic parameters:
      • Mean STT, IOP for juvenile crab eating foxes lower vs domestic dogs and cats.
    • Morphometry of corneal tissue:
      • All had epithelium, stroma, endothelium. Similar to dogs.
      • Epithelium had three layers – Stratum superficiale, stratum intermedium, stratum basale.
      • Crab eating foxes had lower values of axial globe length, lens thickness, vitreous chamber depth. Anterior chamber depth similar to dogs and cats.
      • CCT values of crab eating foxes determined by both noncontact specular microscopy and corneal tissue morphometry were lower than those reported for adult or juvenile domestic dogs studied with US pachymetry, confocal microscopy, or contact microscopy specular.
      • Mean value of corneal thickness lower in foxes vs dogs and cats. Also had four to five cell rows vs six to nine in dogs and cats.
  • Takeaway: Crab eating fox differs from dogs in terms of pupil shape, STT, IOP, and ocular echobiometric and corneal morphometric features. Otherwise similar.
49
Q

A recent study investigated the serological response of red foxes to Canine Distemper Vaccination.

What type of vaccine are the recombitek vaccines? Why are these used in nondomestic carnivores?

How did animals respond to vaccination?

Is this product (and the protocols described in this study) recommended for protection against CDV?

A

Hidalgo-Hermoso, E., Mathieu-Benson, C., Celis-Diez, S., Soto-Guerrero, P., Carmona-Schmidt, S., Cabello-Stom, J., & Ortiz-Tacchi, C. (2019). Safety and serological response to multivalent canine distemper virus vaccine in red foxes (vulpes vulpes). Journal of Zoo and Wildlife Medicine, 50(2), 337-341.

Abstract: Canine distemper virus (CDV) vaccination using commercial vaccines has been recommended as a useful preventive tool in zoological collections worldwide for the past 30 yr. Zoological facilities have not conducted studies to assess the effectiveness and safety of the multivalent Recombitek C6 and C8 in nondomestic carnivores. They are the only CDV recombinant vaccines available in Latin America. Seventeen clinically healthy red foxes born in Buin Zoo were divided into three groups and administered 1 ml of Recombitek C6 vaccine. Group A consisted of three animals of 9 mo of age without previous vaccination (WPV) that received a single dose. Group B consisted of four animals of 10 mo of age WPV; they received a series of three doses with a 21-day interval between doses. Group C consisted of eight animals . 1 yr of age that had received a previous vaccination 1 yr ago; they received a single-dose booster vaccination. Titers for antibodies against CDV were measured by a serum neutralization test. All animals remained clinically healthy throughout the study period and without clinical signs of disease. Only two foxes (group C) did not show any increase in the antibody titer to the vaccine. All animals of groups A and B seroconverted at 21 days after the first vaccination. Only two animals (both from group B) showed an adequate antibody protective response (titers .100) after 180 days. Absence of adverse reactions in red foxes included in this study supports the safety and apparently nondeleterious effect of CDV recombinant vaccine reported in other nondomestic carnivores. Low antibody response and lack of persistence in the serological response 6 mo after vaccination with a single dose suggested limited protective benefits in this species. Additional research is needed to confirm the antibody titer response to multiple vaccinations in this species.

Canine distemper virus:

  • Multihost pathogen
  • Abundant sympatric species can act as reservoir for infection to persist in mixed host-species population
  • Domestic canine vaccination programs ineffective to prevent CDV transmission to wildlife
  • MLV vaccines can result in vaccine-induced infections. Reports of nonseroconversion with and without booster in otters and fishers. Recombinant vaccines have been recommended as preferable
  • All animals except 2 in group C seroconverted after 21 days, but only 2 animals (group B) had adequate antibody protective response after 180 days (titers > 100)
  • No adverse effects
    • Only adverse reaction reported w/ this vaccine was erythema multiforme in a hyena
    • Presence of the other immunogens might represent a risk
  • In other fox species:
    • With canarypox-vectored CDV (Purevax) vaccine: antibody titers were more elevated and persisted over time in Fennec foxes that were vaccinated and received a booster after 21d. Had also been vaccinated w/ MLV CDV
    • Oral admin Purevax in channel island fox did not report antibody titers
  • In other carnivores:
    • African wild dogs vaccinated w/ 3 doses of Purevax only 50% had titers after 6.5 mo
    • In tigers none had detectable antibodies at day 26, only 2 had low titers at day 66
    • Case of snow leopard that developed distemper after previous immunization w/ Purevax from natural exposure
  • Further studies assessing cell-mediated immunity

Take-home

  • Single dose vaccination w/ Recombitek (multivalent CDV vaccine) ineffective in red foxes
  • Humoral immune response mounted with multiple doses but data insufficient to confirm if protective or not
50
Q

A recent study evaluated the safety and efficacy of the Recombitek Canine Distemper Vaccine in Maned Wolves.

What is the scientific name of the maned wolf?

What type of virus is CDV? What are the clinical signs? What are the reservoir species?

How did maned wolves respond to vaccination?

A

Barrett, C. A., Joyner, P. H., Anis, E., Wilkes, R. P., & Aitken-Palmer, C. (2020). Safety of and humoral immune response to the Merial Recombitek Canine Distemper Virus Vaccine in maned wolves (Chrysocyon brachyurus). Journal of Zoo and Wildlife Medicine, 50(4), 972-975.

Abstract: This study evaluated the safety of and humoral response to the Merial Recombitek® recombinant canine distemper virus (rCDV) vaccine in maned wolves (n = 9, age 2–9 yr). All maned wolves had prior history of annual vaccination with the Merial Purevax® ferret rCDV vaccine. Serum neutralization (SN) to CDV was measured prior to initial vaccination with the rCDV Recombitek vaccine followed by a booster vaccination at 4–6 wk. Final SN titers were obtained at 13 wk post initial vaccination. The maned wolves developed no observable adverse side effects through the study. Pre-Recombitek vaccination SN titers ranged from negative to 1: 8. Postvaccination CDV titers ranged from negative to 1: 8, and were therefore below the range of that considered protective in domestic dogs.

  • Maned wolves CDV seropositivity, morbidity, and mortality documented, suspect exposure in Bolivia from unvaccinated domestic dogs
  • CDV - paramyxovirus, aerosolized transmission, CS: respiratory, GI, neurologic
    • Reservoir species: domestic dogs, skunks, raccoons - may shed for months once infected
  • Maned wolf SSP strongly advises against MLV vaccines due to risk of illness and death
    • Canary-pox-vectored vaccines: Merial’s Purevax ferret distemper, Merial Recombitek

Key Points

  • No immediate or long-term adverse effects post-vaccination
  • No wolves had serum neutralization titers approaching cutoff for revaccination of domestic dogs (1:32)
    • Poor humoral response; cell-mediated immunity was not evaluated

Conclusions

  • Merial Recombitek canary-pox vectored CDV vaccine did not elicit a measurable humoral immune response in maned wolves and produced low, presumably nonprotective serum neutralizing antibody titers
51
Q

A recent study described the field immobilization of Andean foxes using ketamine and dexmedetomidine.

How quickly did induction occur?

Were there any complications?

A

Chirife, A. D., Cevidanes, A., & Millán, J. (2020). Effective Field Immobilization of Andean Fox (Lycalopex culpaeus) with Ketamine-Dexmedetomidine and Antagonism with Atipamezole. The Journal of Wildlife Diseases, 56(2), 447-451.

Abstract: A combination (mean±SD) of ketamine (4.0±1.0 mg/kg in juveniles and 3.0±0.4 in adults) and dexmedetomidine (0.055±0.01 and 0.049±0.01, respectively), reversed with atipamezole (at 10 mg/mg of dexmedetomidine), was assessed in 57 Andean foxes (Lycalopex culpaeus) in field conditions. Induction times in juveniles and adults were 4.6±3.9 min and 4.3±2.4 min, respectively. Immobilization was smooth and safe, and lasted 50±8 min in juveniles and 50±10 min in adults. Full recovery was recorded at 40±29 min in juveniles and 37±23 min in adults after atipamezole administration. Drug dose, season, body temperature, and fox sex and body condition were not related to variations in induction and recovery times, body temperature, heart rate, respiratory rate, or hemoglobin oxygen saturation. No side effects were observed other than a slight but significant decrease in mean body temperature during the procedure. This combination allowed carrying out all the typical procedures of a research project, including the collection of several biologic samples.

  • Key Points:
    • Induction time ~4 min, immobilization lasted ~50 min, generally smooth and safe.
    • No adverse physical reactions. 5 foxes started to move their head by the end of the procedure.
    • All animals maintained the palpebral reflex during the procedure.
    • No studied factors related to immobilization or recovery time.
    • Mean HR higher in females vs males.
    • Mean SpO2 higher in males vs females.
    • RR increased during procedure in juveniles, decreased in adults.
    • HR and RR markedly lower in this study compared to others using medetomidine ketamine combos in red foxes. No other signs of cardiovascular depression.
    • Decrease in mean body temp observed in this study. Similar to dogs with dexmed.
      • Contrast to hyperthermia reported with this protocol in Ethiopian wolves (Canis simensis).
    • Full recovery after atipamezole lasted ~37 min in adults and 40 min in juveniles.
  • Takeaway: Recommended combo of ketamine dexmed in Andean foxes and other SA foxes. Lower doses of ketamine should be evaluated to obtain shorter full recovery times.
52
Q

A recent study investigated the prevalence of vector borne pathogens in red foxes in France.

How commonly was a pathogen identified?

What pathogens did they identify?

A

Journal of Wildlife Diseases, 56(4): 837-850, 2020

MOLECULAR INVESTIGATION OF VECTOR-BORNE PATHOGENS IN RED FOXES (VULPES VULPES) FROM SOUTHERN FRANCE

Hacene Medkour, Younes Laidoudi, Jean-Lou Marie, Florence Fenollar, Bernard Davoust, and Oleg Mediannikov

ABSTRACT: Because of their free-ranging nature, the probability of wild animals being exposed to vector-borne pathogens is likely higher than that of humans and pets. Recently, the red fox (Vulpes vulpes) has been suspected as being a reservoir or host of several pathogens of veterinary and public health importance. We conducted a molecular survey on 93 red foxes hunted in 2008–18, in the departments of Bouches-du-Rhone and Var, in southeastern France, for pathogens including Leishmania infantum, Piroplasmida, Hepatozoon spp., nematodes, Coxiella burnetii, Borrelia spp., Rickettsia spp., and Anaplasmataceae. Spleen samples were screened for the presence of vector-borne pathogens by PCR followed by sequencing. Pathogens were detected in 94% (87/93) of red foxes, and coinfections were identified in 24% (22/93) of foxes. We identified DNA from Hepatozoon canis, L. infantum, and Babesia vogeli in 92% (86/93), 15% (14/93), and 3% (3/93) of red foxes, respectively. We also found DNA of nematodes in 3% (3/93) of foxes; Spirocerca vulpis was identified in one fox and Dirofilaria immitis in the two others. Interestingly, C. burnetii genotype 3, previously described in humans from the same region, was identified in 3% (3/93) of foxes and Anaplasma platys in 2% (2/93) of foxes. We did not detect DNA of Borrelia spp., Bartonella spp., or Rickettsia spp. In our study, the prevalence of pathogens did not vary by fox origin, sex, or tick carriage. Molecular evidence of B. vogeli, H. canis, S. vulpis, D. immitis, C. burnetii, and A. platys in red foxes has not previously, to our knowledge, been reported from southern France. We propose that red foxes are potential reservoirs for several pathogens, including major zoonotic agents such as L. infantum. They could be incidental hosts for pathogens, such C. burnetii. The high prevalence for H. canis suggests an important role of foxes in domestic dog (Canis lupus familiaris) infection. These animals may pose a threat to human and animal health.

Key Points:

  • In Europe, foxes are the most abundant wild carnivore. Main reservoir for rabies in western and central Europe.
  • Assess the prevalence of vector borne diseases (Leishmania infantum, Piroplasmida, Hepatozoon spp., nematodes, Coxiella burnetii, Borrelia spp., Rickettsia spp., and Anaplasmataceae) in spleen samples via PCR.
  • 10 years of samples collected from regulated hunting
  • 94% of foxes infected with at least one pathogen
    • 92% Hepatozoon canis
      • Reservoir for domestic canids, transmitted by Rhipicephalus sanguineus tick.
    • 15% Leishmania infantum
      • Zoonotic – visceral and cutaneous forms in humans
    • Dirofilaira immitis
      • Two cases identified. Previous studies indicated higher prevalence in foxes from irrigated areas than semiarid regions.
    • Coxiella burnetii
      • Etiologic agent of Q fever (incidental hosts)
      • Isolated same genotype that was found on a human heart valve from same region
  • No difference in prevalence of infection based on origin, sex, or tick carriage.

Take home: Wild foxes sampled in Southern France had a high prevalence of vector borne disease, most commonly Hepatozoon canis, however other notable infections included Leishmania infantum (15% of cases), dirofilatia immitis, and coxiella burnetii.

53
Q

A recent study investigated the genetic characteristics of canine distemper viruses circulating in wildlife in the United States.

What type of virus is canine distemper?

What species are affected? What are the typical clinical signs?

How is it transmitted? What receptor does it bind to? How does it affect so many taxa?

What are the lineages that have been observed in the US traditionally?

Were new strains observed?

Are vaccines sufficient to contain these strains to reservoir populations?

A

Anis, E., Needle, D. B., Stevens, B., Yan, L., & Wilkes, R. P. (2020). Genetic characteristics of canine distemper viruses circulating in wildlife in the united states. Journal of Zoo and Wildlife Medicine, 50(4), 790-797.

Abstract: Canine distemper virus (CDV) is a highly contagious disease of wild and domestic mammals. Maintenance of CDV among wildlife plays an important role in the disease epidemiology. Wild animals, including raccoons (Procyon lotor) and gray foxes (Urocyon cinereoargenteus), serve as reservoirs of CDV and hamper the control of the disease. Recently, we discovered that at least three different CDV lineages (America-3 [Edomex], America-4, and America-5] that are genetically different from the available vaccine strains are circulating in domestic dogs in the United States. Because wildlife serve as a reservoir for the virus, it is important to determine if wildlife play a role in the maintenance and spread of these lineages. To determine the genetic characteristics of circulating strains of CDV in wildlife in various geographic regions in the United States, we studied the nucleotide sequences of the hemagglutinin (H) gene of 25 CDV strains detected in nondomestic species. The species included were free-ranging wildlife: three fishers (Martes pennanti), six foxes, one skunk (Mephitis mephitis), 10 raccoons, two wolves (Canis lupus), and one mink (Neovison vison). Strains from two species in managed care, one sloth (Choloepus didactylus) and one red panda (Ailurus fulgens), were also evaluated. Phylogenetic analysis of the H genes indicated that in addition to America-3, America-4, and America-5 lineages, there are at least two other lineages circulating in US wildlife. One of these includes CDV nucleotide sequences that grouped with that of a single CDV isolate previously detected in a raccoon from Rhode Island in 2012. The other lineage is independent and genetically distinct from other CDV strains included in the analysis. Additional genetically variable strains were detected, mainly in raccoons, suggesting that this species may be the host responsible for the genetic variability of newly detected strains in the domestic dog population.

  • CDV – Morbillivirus, Paramyxoviriae, ssRNA virus.
  • Detected in all families of terrestrial carnivores – Canidae, Felidae, Mustelidae, Ursidae, Vivveridae, Hyaenidae, Procyonidae. Multihost nature, unlike some other morbilliviruses i.e. measles.
  • Respiratory, CNS, GI signs.
  • High mortality in juveniles.
  • Transmission via direct contact, air, bodily secretions, +/- fomites.
  • Mutations affecting the viral signaling lymphocytic activation molecule SLAM receptor binding region affects the ability of the virus to infect new species.
  • Maintenance within wildlife reservoirs between outbreaks hampers disease eradication and plays important role in epidemiology in domestic dogs.
  • Six CDV sequences that were detected in fox, raccoon, red panda in SE grouped with America-5 lineage. Reported in domestic dogs.
    • The red panda was a zoo animal, three other RPs died of distemper 1 month prior.
      • Was vaccinated once with RECMBITEK vaccine, need multiple boosters for protection.
    • Captive sloth from TN where another outbreak took place with American 4 lineage.
    • Three nucleotide sequences grouped with American-3 (Edomex) lineage.
    • Multiple CDV strains simultaneously circulating in domestic dogs and multiple wildlife species, adds to complexity of understanding epidemiology of CDV.
    • Likely that raccoons are the source of ‘new’ genetic lineages.

Takeaway: Recent rise in CDV cases in wildlife and detection of the same lineages circulating in domestic dogs suggests currently available vaccines are insufficient to keep these strains confined to reservoir populations. CDV distribution and epidemiology is complex.

54
Q

A recent study evaluated the risk of exposure of domestic cattle to small coccidia from wild coyote feces.

What pathogen were they concerned about?

How frequently was coccidian DNA isolated?

What pathogen was found?

A

Moreno-Torres, K. I., Sinnott, D. M., Wolfe, B. A., Marsh, A. E., Saville, W. J., Moritz, M., & Garabed, R. B. (2018). Risk of environmental exposure to small coccidia from wild canid feces in rural Ohio. American journal of veterinary research, 79(11), 1179-1187.

OBJECTIVE: To determine the extent of environmental exposure to heteroxenous coccidia from wild canid feces in southeastern Ohio.

SAMPLE: 285 presumed wild canid fecal samples collected across an ecological system in southeastern Ohio.

PROCEDURES: Morphological classification and molecular analysis were used to deter- mine the canid genus for collected fecal samples. Microscopic and molecular analysis were used to detect coccidian oocysts and DNA. Several variables were analyzed for associations with coccidian DNA detection or prevalence.

RESULTS: Coccidian DNA was detected in 51 of 285 (17.9%) fecal samples. Of those positive samples, 1% (95% confidence interval, 0.4% to 3%) had positive results for Hammondia heydorni and none had positive results for Neospora caninum, for an estimated environmental N caninum prevalence of 0% (95% confidence interval, 0% to 7%)/1-km hexagonal area evaluated. Morphological classification revealed that 78.9% (225/285) of fecal samples were from coyotes and 17.2% (49/285) were from foxes. No difference in proportions of coccidian DNA-positive fecal samples was identified among canid species. Environmental temperature and fecal freshness were associated with coccidian DNA detection. Land use type, relative canid density, and cattle density were not associated with the prevalence of coccidian DNA– positive samples.

CONCLUSIONS AND CLINICAL RELEVANCE: The low prevalence of coccidia shed in wild canid feces in this study, including the estimated 0% environmental prevalence of N caninum, suggested that the role of the oocyst environmental phase in coccidia transmission to ruminants is likely minor in rural southeastern Ohio.

  • Coyotes are suggested definitive hosts for Neospora caninum
  • Purpose was to determine role of coyote feces in transmission of coccidia that may infect livestock
  • Feces identified by morphologic identification and then confirmed with mitochondrial DNA. Oocysts confirmed by DNA extraction and PCR
  • Coccidian DNA found in 17.9% samples
    • 1% H heydorni positive and none were N caninum positive
  • Prevalence of coccidian DNA was not associated with potential risk factors (cattle density, wild canid density, and land use)
  • Role of the oocyst environmental phase in coccidia transmission to ruminants is likely minor

Take home: Role of coyote feces coccidia transmission is minimal

55
Q

A recent study investigated the effects of sarcoptic mange on endangered San Joaquin kit foxes.

What is the scientific name of the kit fox?

What wre the gross and histologic lesions associated with mange in these foxes?

What other comorbidities were seen? Are these seen in other species?

How does this differ from mange in red foxes?

What are some potential sources of exposure for these kit foxes?

A

Cypher, B. L., Rudd, J. L., Westall, T. L., Woods, L. W., Stephenson, N., Foley, J. E., … & Clifford, D. L. (2017). Sarcoptic mange in endangered kit foxes (Vulpes macrotis mutica): case histories, diagnoses, and implications for conservation. Journal of wildlife diseases, 53(1), 46-53.

Abstract: The San Joaquin kit fox (Vulpes macrotis mutica) is a federally endangered small carnivore whose distribution is limited to the San Joaquin Valley in central California. Population decline is due to profound habitat loss, and conservation of all remaining populations is critical. A robust urban population occurs in the city of Bakersfield. In spring of 2013, putative cases of mange were reported in this population. Mites from affected animals were confirmed to be Sarcoptes scabiei morphologically and by DNA sequencing. By the end of 2014, 15 cases of kit foxes with mange had been confirmed. As with other species, sarcoptic mange in kit foxes is characterized by intense pruritus and dermatitis, caused by mites burrowing into the epidermal layers, as well as alopecia, hyperkeratosis, and encrustations, secondary bacterial infections, and finally extreme morbidity and death.Of the 15 cases, six foxes were found dead, six were captured but died during attempted rehabilitation, and three were successfully treated. We have no evidence that untreated kit foxes can recover from mange. Sarcoptic mange constitutes a significant threat to the Bakersfield kit fox population and could pose an even greater threat to this imperiled species if it spreads to populations in nearby natural lands.

  • San Joaquin kit fox federally endangered, threatened in CA. 3,000-5,000 left.
  • Regional declines historically attributed to rabies and CDV.
  • This study – describes outbreak of sarcoptic mange in spring 2013, Bakersfield CA.
  • 15 cases of sarcoptic mange confirmed. 5 foxes found deceased, one humanely euthanized, 6 died within 3d of capture despite tx, 3 recovered with tx (selamectin).
  • Gross lesions – moderate to severe sarcoptic mange with dermatitis, generalized alopecia with adherent crusts, excoriations, and lichenification on the head, neck, dorsum, extremities, and tail.
  • Histo lesions – marked parakeratosis, acanthosis, intraepidermal pustules, serocellular crusts with intralesional mites and bacterial cocci.
    • Comorbidities – dermal yeast infections, peritonitis, left testicular abscess, myocarditis, esophagitis, adrenal cortical hyperplasia, encephalitis negative for CDV and WNV, pneumonia, renal mineralization, glomerulonephritis, interstitial nephritis IHC negative for lepto, lymphadenopathy. Negative for rabies.
    • 12 foxes positive for anticoagulant rodenticide exposure – brodifacoum, bromadiolone, chlorophacionone, difethialone, diphacinone.
  • Sarcoptic mange confirmed in 15 cases with skin scrapes/PCR.
    • S. scabiei commonly infects wild canids.
  • In bobcats, can cause multi-organ changes consistent with dehydration, electrolyte dysregulation, severe protein loss across skin.
  • Renal mineralization in kit foxes likely due to dehydration.
  • In Italy, mange assoc with helminth Fasciola hepatica in red foxes, not observed in this study.
  • Sarcoptic mange has a high mortality rate in San Joaquin kit foxes.
  • Without early human intervention, fatality may be as high as 100%.
  • In contrast, red foxes appear to have some capacity to recover.
  • Transmission to the kit foxes may have been from coyotes in the area or red foxes, dogs, skunks, raccoons, opossums, gray foxes.
56
Q

A recent study evaluated the climactic suitability of San Joaquin kit fox dense for transmission of Sarcoptic mange.

What was the effect of the mange outbreak in kit foxes in 2013?

How long can Sarcoptes survive off of a host? How long does it remain infective?

What methods have been tried to reduce transmission in other species?

How does the natural history of the fox affect transmission?

How long did this study suggest Sarcoptes could survive and remain infective in kit fox dens?

A

Loredo, A. I., Rudd, J. L., Foley, J. E., Clifford, D. L., & Cypher, B. L. (2020). Climatic suitability of san joaquin kit fox (vulpes macrotis mutica) dens for sarcoptic mange (sarcoptes scabiei) transmission. Journal of wildlife diseases, 56(1), 126-133.

ABSTRACT: More than 460 cases of sarcoptic mange (Sarcoptes scabiei) in endangered San Joaquin kit foxes (SJKF; Vulpes macrotis mutica) have been reported in Bakersfield, California, US. Because SJKF are a den-obligate species, their dens have been proposed as a route of transmission. We determined whether SJKF den temperatures and humidities could support mite off-host survival based on previously published estimates of off-host mite survival times. We monitored SJKF dens for 6 d in summer and winter of 2017 and 2018 using temperature- and humidity-sensing data loggers placed within the dens. Motion-triggered cameras monitored animal use of and entrances into the dens. Linear regression models were fitted to the published mite survival data to predict estimated mite survival time (EMST) in SJKF dens based on observed mean temperature and humidity of the den. Den covariates including irrigation, type of den, and season were then fitted to a mixed effects linear model to predict EMST. The average EMST across various habitats in Bakersfield was 4.8 d; the longest EMST was 7.1 d for dens in habitats with irrigated grass in the winter. Den climatic conditions in Bakersfield may support off-host mite survival through a timeframe adequate for revisitation by another fox. The finding that irrigation may enhance EMST suggested that risk to foxes varied with den type and that mitigation strategies may need to vary with den types.

  • San Joaquin kit fox - limited range in central California, federally Endangered, California Threatened species
    • Use on avg 11 dens per year throughout home range - could be route of env transmission
  • Epidemic of fatal sarcoptic mange in SJKF, first detected in Spring 2013
    • Endangered species recovery program tx: slow release flumethrin-imidacloprid, oral and injectable ivermectin, hospitalization
  • Sarcoptic mange: burrows into epidermis, numerous mammal species
    • Desiccate off host but increased survival time in lower temps (up to a month), can remain infectious 24-36h off host
    • Wombat Sarcoptic mange program: medicated flaps placed over burrows did not significantly reduce disease
    • Forced heated air to desiccate mites in environment may be effective
  • One mangy individual routinely visited up to 8 dens in the same area nightly
    • Other species that used the dens: striped skunks, CA ground squirrels, opossums, raccoons, burrowing owls.
    • SJKF observed cohabitating with skunks on 5 occasions
  • Mean den temp 29 C (summer) 12 C (winter), humidity 69% (summer), 83% (winter)
    • Significantly different microclimate than surface controls - more consistent temp, high relative humidity
  • Estimated mite survival time maximized with decreasing temp and increasing relative humidity
    • Predicted mean EMST for all dens 4.79 d (1.97 in summer, 7.38 in winter)
    • Grass dens and affected by sprinklers higher mean EMST

Takeaways:

  • Evidence that SJKF dens can support off-host survival of mites approximately 5d
    • May remain infective for at least 36-57 h
  • Max predicted EMST in grass dens in winter with higher humidity/sprinklers
    • lowest for earthen dens in summer
57
Q

A recent study investigated the prevalence of ear mites in wild foxes in Chile.

What is the scientific name of the ear mite?

What fox species did they evaluate?

Why are ear mites a concern in wild populations?

How prevalent were ear mites?

Was one species more affected than another?

A

Briceño, C., González-Acuña, D., Jiménez, J. E., Bornscheuer, M. L., Funk, S. M., & Knapp, L. A. (2020). Ear mites, otodectes cynotis, on wild foxes (pseudalopex spp.) in chile. Journal of Wildlife Diseases, 56(1), 105-112.

ABSTRACT: We found the ear mite parasite (Otodectes cynotis; Acari: Psoroptidae) in two distant insular endangered fox populations in Chile. We identified O. cynotis in both the Darwin’s fox (Pseudalopex fulvipes) from Chiloe´ and the Fuegian culpeo (Pseudalopex culpaeus lycoides) in Tierra del Fuego. These populations are approximately 2,000 km apart. Infestation rates were high for both endemic foxes: 76% (19/25) of Darwin’s foxes were affected, and 73% (11/15) of Fuegian culpeos had ear mites. Two Darwin’s foxes had abundant ear discharge, and one of these also exhibited secondary infections of Morganella morganii and Geotrichum sp. fungi. Mites were characterized molecularly as Otodectes spp. for the Fuegian culpeo samples. Genetic analyses of two mites found the O. cynotis genotype I, as well as what appeared to be a new allele sequence for O. cynotis. These results confirmed the hypothesis of aworldwide distribution species of ear mite. Introduced chilla foxes (Pseudalopex griseus; n¼11) on Tierra del Fuego Island and domestic dogs (Canis lupus familiaris; n¼379) from both islands were also sampled, but they showed no signs of infection. Our findings provided insight into the genetic diversity, the origins, and the possible impact of this globally distributed mite on endemic free-rangingpopulations of foxes.

  • Genus Pseudalopex - endemic to Chile, synonymous with Lycalopex
    • Culpeo fox (Pseudalopex culpaeus) - Andean fox, Zorro culpeo
      • Fuegian culpeo fox - distinct subspecies on Isla Grande of Tierra del Fuego, vulnerable
    • Chilla fox (Pseudalopex griseus) - South American Grey fox, grey Zorro
    • Darwin’s fox (Pseudalopex fulviceps) - Zorro Chilote *endangered
  • Mite infestation resulted in 96% mortality rate for endangered arctic fox cubs in population on Mednyi Island (Vulpes lagopus)
  • Goal: survey for Otodectes cynotis in wild foxes, domestic dogs on Chiloe and Tierra del Fuego
  • Trapped, squeeze cage for IM ketamine 20 mgkg/xylazine 1 mg/kg or ketamine 2.5 mg/kg/medetomidine 0.05 mg/kg, reversed with yohimbine 0.2 mg/kg or atipamezole 0.25 mg/kg
    • Otoscope, cotton swabs in formalin or ethanol for electron microscopy of mites and PCR to speciate mites
  • 83% Darwin’s foxes, 79% culpeos, no chilla foxes (TdF) or dogs from Chiloe had ear mites
    • Otitis appeared more severe in Darwin’s foxes than culpeos
    • Mites from two Fuegian culpeos were O. cynotis genotype 1 on PCR (100% and some 99%) as well as possible new genotypes
  • Swab of one Darwin’s fox ear duct had fungus (Geotrichum sp.) and bacilli (Morganella morganii) that was resistant to beta-lactams, doxycycline, and metronidazole

Takeaways:

  • One species of ear mite (Otodectes cynotis) with worldwide distribution
  • Ear mites and otitis found in Darwin’s foxes and culpeos but not chilla foxes in Chile (Chiloe Island and Tierra del Fuego Island)
    • Otitis more severe in Darwin’s than culpeos.
58
Q

A recent study investigated the pathology and typing units of Trypanosoma cruzi infection in coyotes and raccoons in Texas.

How is Trypanosoma transmitted?

What are the lesions associated with Chagas disease? Do all infected individuals develop these signs?

How prevalent was Trypanosoma in this study? Did prevalence vary by species?

Did the typing unit vary by species?

Were lesions seen in either species?

A

Hodo, C. L., Bañuelos, R. M., Edwards, E. E., Wozniak, E. J., & Hamer, S. A. (2020). Pathology and discrete typing unit associations of Trypanosoma cruzi infection in coyotes (Canis latrans) and raccoons (Procyon lotor) of Texas, USA. Journal of Wildlife Diseases, 56(1), 134-144.

Abstract: Trypanosoma cruzi is a vector-borne, protozoal parasite of mammals. Infected humans, dogs (Canis lupus familiaris), and nonhuman primates may remain asymptomatic or may develop Chagas disease, most commonly characterized by lymphoplasmacytic myocarditis with myocardial degeneration and fibrosis, ultimately resulting in heart failure. Although wildlife species have important roles as sylvatic reservoirs, investigations into the pathology of T. cruzi in wildlife are limited to a few studies documenting histologic lesions in opossums (Didelphis spp.) and raccoons (Procyon lotor). Pathology in coyotes (Canis latrans) has not, to our knowledge, been described, despite their recognition as a reservoir and close genetic relationship to domestic dogs. Our objectives were to perform a detailed, comparative cardiac pathology study of sympatric, naturally infected coyotes and raccoons, to characterize the overall T. cruzi infection prevalence in the heart and blood of each species via PCR, and to identify infecting discrete typing units (DTUs). We sampled hunter-harvested coyotes (n=120) and raccoons (n=24) in a 28 county region of central and south Texas, US. Raccoons were significantly more likely to have positive PCR results (P<0.001) with a prevalence of 62% (15/24), comprising DTU TcIV exclusively, with mild to no evidence of cardiac pathology. In contrast, coyotes had a lower infection prevalence (8%, 10/120), comprising DTU TcI exclusively, with lymphoplasmacytic myocarditis observed in four of the six PCR-positive animals. Many raccoons had PCR-positive blood and heart tissue simultaneously, supporting previous reports that raccoons maintain parasitemia into chronic stages of infection; in contrast, none of the PCR-positive coyotes were positive in both heart and blood. Our findings demonstrate marked differences in T. cruzi infection dynamics between coyotes and raccoons, with important implications for reservoir potential and their role in transmission cycles.

  • T. cruzi – Causative agent of Chagas dz; multiplies in hindgut of triatomine insect vectors (fam Reduviidae, subfamily Triatominae), which pass infectious trypomastigotes in their feces.
  • Complex transmission cycles involve mammalian reservoir species and triatomine vector spp.
  • 7 discrete typing units DTUs associated with different geographic regions, hosts, and vector spp.
  • Sampled 120 coyotes from 24 TX counties and 24 raccoons from 14 counties.
  • 8% coyotes, 62% raccoons PCR positive. No individuals found to harbor more than one DTU.
  • 4 coyotes had mild to moderate, multifocal, lymphoplasmacytic myocarditis with varying degrees of myocardial degeneration and fibrosis.
  • 4 other coyotes had lesions consistent with Hepatozoon americanum.
  • Many had heartworm.
  • 3 raccoons had minimal to mild lymphoplasmacytic myocarditis. 80% raccoons did not have significant inflammation in the heart.
  • Coyotes had more severe lesions and harbored DTU TcI vs DTU TcIV in raccoons.
  • Raccoons are known to maintain high levels of parasitemia into the chronic stages of infection.

Takeaway: In TX, both raccoons and coyotes had T. cruzi-positive blood and cardiac tissue, some coyotes had myocarditis. Coyotes more severe histologic lesions vs raccoons even through raccoons had a higher prevalence. All coyotes harbored DTU TcI, and all raccoons harbored DTU TcIV.

59
Q

A recent study described gastric dilatation volvulus in maned wolves.

What is the scientific name of the maned wolf?

What are som risk factors for GDV in domestic dogs?

How did these cases present?

What dietary factors may predispose animals to GDV?

A

Hinton, J. D., Padilla, L. R., Joyner, P. H., Schnellbacher, R., Walsh, T. F., & Aitken-Palmer, C. (2017). Gastric dilatation volvulus in adult maned wolves (chrysocyon brachyurus). Journal of Zoo and Wildlife Medicine, 48(2), 476-483.

Abstract: Gastric dilatation volvulus (GDV) was identified in six adult maned wolves (Chrysocyon brachyurus) housed at the Smithsonian Conservation Biology Institute in Front Royal, Virginia, and the Dickerson Park Zoo in Springfield, Missouri. Four individuals were found dead in their enclosures, and GDV was diagnosed postmortem based on radiographic and necropsy findings. Two individuals were diagnosed with GDV antemortem, with one wolf surviving following surgical intervention and supportive management. A concurrent splenic torsion was identified in three of six cases. Although GDV has been well documented in domestic dogs and is known to occur in maned wolves, objective, detailed case descriptions have been limited in this species. This report represents the first description of a surviving case of GDV in the maned wolf. Thorough species-specific documentation of any acutely fatal condition, such as GDV, is imperative for proper case recognition and medical management, with profound implications for species recovery efforts.

  • Risk factors for GDV in domestic dogs – rapid ingestion of food, amount of food ingested, abrupt diet change or dietary indiscretion, exercise behaviors, aerophagia, thoracoabdominal conformation, age, breed, genetics.
  • Reported in maned wolves, red wolves, grey wolves.
  • Cases 1-3, 6 found dead in enclosure, GDV confirmed post-mortem.
  • Case 4 – Decreased energy and appetite, next day vomited foamy fluid, rads showed GDV, OG tube was unsuccessful, ex-lap performed. 180 deg counterclockwise long-axis rotation identified and correctly.
  • Case 5 – Found laterally recumbent, GDV diagnosed on rads, went into V tach and died during ex-lap.
  • GD +/- V should be considered in any maned wolf presenting with acute abdominal signs.
  • Potential role of diet in predisposing animals to GDV.
    • Case 2 and 3 were undergoing a diet change.
    • Prompted a manufacturer adjustment to increase kibble size to try and reduce risk of GDV in captive NA maned wolves.
      • Case 5 and 6 occurred after this change.
    • Domestic dogs, it has been suggested that there is an increased risk for GDV with fat or oil as first four ingredients in the diet.
      • May result in delayed gastric emptying.
      • Domestic dog diets with soy or cereals also considered anecdotally linked to GDV.
60
Q

A recent study described trichinella infections in red foxes and golden jackals.

What two species of trichinella were evaluated?

Which trinchella species was more common to each canid species?

How prevalent was infection?

What are the risks to public health that this organism poses?

A

Dmitric, M., Vidanovic, D., Vaskovic, N., Matovic, K., Sekler, M., Debeljak, Z., & Karabasil, N. (2017). Trichinella infections in red foxes (Vulpes vulpes) and golden jackals (Canis aureus) in six districts of Serbia. Journal of Zoo and Wildlife Medicine, 48(3), 703-707.

Abstract: Wild animals, including red foxes (Vulpes vulpes) and golden jackals (Canis aureus), are the most important reservoirs of Trichinella spp. Although the red fox is considered one of the main reservoirs of Trichinella spp. in Europe, only a few animals have been examined in Serbia. The present study assessed Trichinella spp. infection in red foxes and golden jackals from the six districts in Serbia. Thirty-seven carcasses of red foxes and 13 carcasses of golden jackals shot during the official hunting season were examined. Larvae of Trichinella spp. were detected in 13 (35 % ) of 37 red foxes and in 8 (61 % ) of 13 golden jackals. Trichinella spiralis and Trichinella britovi were the only two species identified after a multiplex polymerase chain reaction analysis. Trichinella britovi infection was detected in 85 % of red foxes and in 38 % of golden jackals, and T. spiralis was detected in 15 % of red foxes and in 63 % of golden jackals. The findings emphasize the need for an active surveillance program for Trichinella spp. infection in wildlife in Serbia and the whole of the Balkans, with special attention on the red fox because it is widespread and occurs in high densities.

  • Trichinella sp 🡪 zoonotic nematode
  • Thirty-seven carcasses of red foxes and 13 carcasses of golden jackals shot during the official hunting season were examined
  • Trichinella britovi infection detected in 85 % (11/13) of red foxes and in 38 % (3/8) of golden jackals
  • T. spiralis detected in 15 % (2/13) of red foxes and in 63 % (5/8) of golden jackals
  • No mixed infections detected
  • All positive animals were adults
  • T. spiralis more common in jackals and T. britovi more common in foxes
  • No difference in prevalence between sexes
  • Trichinella spp. in wild carnivores was discovered in all six districts (12 localities), showing an increased risk to public health
61
Q

A recent study evaluated urolith submissions from multiple fox species.

What was the most common stone type in red foxes? what are these stones associated with? How do they form?

What was the most common stone type in fennec foxes? What are some potential causes for these?

A

JZWM 2022 53(3):578-82
Urolithiasis in foxes: assessment of 65 urolith submissions to the Minnesota urolith center from 1981 to 2021
Waite LA, Hahn AM, Sturgeon GL, Lulich J

ABSTRACT: This article summarizes urinary stone submissions from foxes in human care to the Minnesota Urolith Center over 40 years. A previous report documented the analysis of uroliths from foxes that were submitted between 1981 and 2007. New data compiled from 2008 to 2021 included an additional 38 stones submitted from foxes, totaling 65 fox urolith submissions from 1981 to 2021.** Struvite and cystine uroliths were most common, with the remainder comprised of calcium phosphate, calcium oxalate, compound, mixed, or miscellaneous material. Most stones were submitted from male foxes. Seventy-two percent of the stones were urocystoliths, and from 2010 to 2021, most stones were diagnosed antemortem and removed surgically. More than half of the stones were submitted from red foxes (Vulpes vulpes) and fennec foxes (Vulpes zerda).** Urolithiasis in foxes may be an underrecognized condition, and data from this study suggest that clinicians should consider routine urinalysis and diagnostic imaging as part of the preventive medicine program for fox species, especially red foxes and fennec foxes.

Key Points:
- Between 1981-2021, 65 uroliths submitted to the MN Urolith Center from foxes in human care
- Submissions from 19 red foxes, 16 fennec foxes, 5 Arctic foxes, & 25 unknown species
– Struvite (41/65 63%) & cystine (11/65 17%) uroliths most common in foxes
– Struvite uroliths form in alkaline urine oversaturated w/ Mg, ammonium, and phosphate
– In dogs, often associated with UTIs
- In dogs, cystine uroliths associated w/ a genetic renal tubular defect, cystine oversaturation, aciduria, and a high-protein diet
- No correlation w/ age & struvite uroliths; cystine uroliths more frequent in young foxes
- Most common urolith in red foxes = struvite
– Maybe predisposed b/c diets high in Mg, phosphorus, and protein vs. undiagnosed UTIs
- Most common urolith in fennec foxes = cystine
– Maybe predisposed b/c native desert environment and high-protein diets vs. selective breeding for pet and fur trade
- Most stones were submitted from male foxes (44/65 68%)
- However, male foxes overrepresented
– Male mammals more likely to show signs of urolithiasis and UO due to anatomy
- Most uroliths analyzed were from the urinary bladder (72%)
- Most stones were submitted antemortem (75%) and had been removed surgically
- Increase in urolith submissions from foxes from 2008 to 2021
- DDx: increased number of foxes in human care, more vigilant monitoring of foxes, predispositions because of limited genetic diversity, or diet and management
- Cystine urolith submissions doubled in 2008–2021 vs. 1981-2007
– Possibly due to genetic predisposition vs. androgen-dependent cystinuria

TLDR:
- Most common uroliths in foxes are struvite (especially red foxes) and cystine (especially younger fennec foxes).
- Fox uroliths are most common in the bladder and frequently removed surgically

62
Q

A recent study established the vertebral heart scores of the raccoon dog.

What is its scientific name?

How are vertebral heart scores measured?

How did they compare to domestic dogs?

A

RADIOGRAPHIC MEASUREMENT OF VERTEBRAL HEART SCALE IN KOREAN WILD RACCOON DOGS (NYCTEREUTES PROCYONOIDES KOREENSIS).
Ahn S, Lee M, Shin W, Han Y, Bae S, Choi SY, Kim JT.
Journal of Zoo and Wildlife Medicine. 2022;53(4):817-822.

Raccoon dogs (Nyctereutes procyonoides koreensis), which belong to the Canidae family, are the second most injured wildlife animals rescued by the Gangwon Wildlife Medical Rescue Center. Various imaging evaluation methods including echocardiography have been developed, but thoracic radiography remains essential for the diagnosis and management of heart disease in dogs. In particular, vertebral heart scale (VHS) measurement is usually used to evaluate the dimensions of the heart silhouette on thoracic radiographs and can measure cardiomegaly more objectively. The VHS of 50 raccoon dogs without cardiac diseases were measured using thoracic radiography in right lateral (RL) and ventrodorsal (VD) recumbent positions. The VHS in the RL view of 50 raccoon dogs was 9.03 ± 0.52 vertebrae (v), which was slightly smaller than the VHS measured in the VD view of 46 raccoon dogs (9.79 ± 0.84 v). In addition, the thoracic morphology of raccoon dogs was determined to be intermediate (thoracic depth-to-width ratio, 0.75–1.25), and thoracic morphology, gender, and weight were not significantly correlated with VHS. The VHS of raccoon dogs in this study will help veterinarians diagnose potential cardiac diseases in raccoon dogs.

Background
- Raccoon dog - family Canidae, East Asia, common rehab animal in Korea
- Radiographic vertebral heart score awake under manual restraint
– Long axis and short axis length overlaid on spine starting at T4 vertebral body - sum of number of vertebrae
– Lateral: long axis - carina of mainstem bronchus to apex of heart; short axis - perpendicular at level of caudal vena cava
– VD: long axis - line from base of heart to cardiac apex; short axis - perpendicular line

Key points
- R lat vertebral heart score lower than dogs
- Lateral slightly smaller than VD measurement but significant correlation between views
- Thoracic morphology (deep vs broad): judged as intermediate compared with dogs - likely no correlation between VHS and thoracic morphology
- No correlation of VHS with gender or body weight
- During echos found 4 cases of atrial septal defect and 1 DCM (excluded from VHS study)

Conclusions
- Raccoon dog vertebral heart score reference interval