Cervidae Flashcards
Osteopathy is common in what South American cervid?
What lesions are typically present with this disease?
- Patagonian huemul with selenium deficiency causing periodontitis
- Mandibular, maxillary, and appendicular bones – eroded alveoli, perforated maxillary & mandibular bone, exostoses and several bones, deformed hooves or phalanges
What is Alvborg Syndrome?
What species is commonly affected by this?
What nutritional deficiencies are associated with it?
What are teh gross and histologic lesions present with this disease?
- Swedish moose
- Malnutrition from overpopulation, phytotoxic substances, soil pH imbalances, viral infections
- Imbalances – low copper, increased molybdenum, abnormal levels of iron, zinc, cadmium
- Lesions – poor BCS, loss of musculature, serous atrophy of fat, fragile skin, achromotrichia, corneal opacities, cataracts, abomasal edema & hypermia, thin intestinal walls, edematous heart, osteoporosis
- Histo – edema, hemorrhage, ulceration of upper GI through abomasum, dilated lymphatic vessels in abomasum, splenic hemosiderosis, dilated heart walls, nephrosis, cerebellar abiotrophy
- Difficult to diagnose – copper levels and lesions are suggestive
How can lightning cause mass mortalities in cervids?
What lesions are present on these animals?
Herds of cervids on water-soaked ground can lead to mass mortalities
Lesions – track of singed hair from hoof to head
Describe the clinical signs and lesions associated with the following toxicities in cervids:
Fluoride
Lichen - what species?
Bracken Fern
Fluorosis
- Exposure via water, contaminated forage, vegetation contaminated with high fluoride-content soil by rain or volcanic ash
- Lesions – enamel hypoplasia, breakage, pitting, blackening, excessive wear
- Diagnosis – lesions and high fluoride concentration in bone
Lichen
- Tumbleweed Shielf Lichen (Xanthoparmelia chlorochroa)
- Red urine, ataxia, muscle weakness that progreses to recumbency and death in North American elk
- Lesions – muscle pallor and streaking (pelvic limbs especially)
- Degenerative myopathy with necrosis, rupture, and mononuclear infiltration of muscles
- Diagnosis – stomach contents and lesions
Bracken Fern
- Bracken Fern (Pteridium aquilinum)
- Hematuria, urinary bladder hemangiosarcoma, hemangioma, TCC, chronic cystitis in fallow deer
- Intestinal adenocarcinoma in sika deer
Other plant toxicities
- Wedelia glauca – SA plant causes centrilobular hepatocellular necrosis in axis deer
- Tal fescue – necrotic abdominal fat in many cervids, including Eld’s deer
- Mycotoxicosis due to fumonesin – leukoencephalomalacia in white-tailed deer
What are some common congenital defects in cervids?
Polycystic kidney disease - roe and white-tailed deer
Ocular abnormalities reported in free-ranging WTD, European red deer, Canadian moose
Ventricular septal defects – fallow and roe deer
Diverticulosis – of rectum and colon in fallow deer – of esophagus in roe deer
Describe the following antler issues in cervids:
Aberrant Antlerogenesis
Perukes
Antleroma
Cactus Buck
Perrennial Velvel Antlers
Aberrant Antlerogenesis
- Development of ectopic supernumerary pedicles or accessory antlers on frontal, nasal, or parietal bones
- Occurs in all cervids except for Rangifer spp.
- Common in roe deer, white-tailed deer, and moose; less so in red or fallow deer
Antler Malformations (Generally)
- Can occur with cryptorchidism, continued exposure of dams to estrogenic compounds, pedicle trauma, malnutrition (copper deficiency, low protein), infection (EHDV) and genetics
Perukes
- Castration produces sarcoma-like proliferations of soft bone tissue called perukes or wig antlers
Antleroma
- Antleroma – abnormal testosterone levels leads to a neoplasm – documented in WTd, fallow, roe, mule, moose
Cactus Buck
- short, abberant points – testicular & epididymal lesions following EHDV infection
Perrennial Velvel Antlers
- Inadequate circulating androgens or traumatic head injury results in permanent soft tissue antler growth
What are some causes of hoof disorder in free ranging elk?
What do their hooves look like?
What lesions are seen on histo?
- Multifactorial causes – nutritional imbalance, endophyte toxicity, mineral deficiency
- Free-ranging elk in NW US have asymmetrically curved, elongate hooves with breakage, sloughing, sole ulcers, laminar necrosis, and osteomyelitis
- Histo – suppurative, necrotizing laminitis with vasculitis and thrombosis, heel bulb and coronary band lymphoplasmacytic perivasculitis
What is the cause of cutaneous fibromas in cervids?
What are the lesions associated with this disease?
How is it diagnosed? How is it treated?
- Caused by fibroma virus, will regress with time
- Up to 25-cm diameter, smooth to verrucose, pedunculated to pendulous dermal masses mostly on the head and neck but may be on oral mucosa or legs
- Consists of neoplastic fibroblasts with a collagen matrix
- Eosinophilic to amphophilic intranuclear inclusion bodies
- Tumor regression involves lymphocyte infiltration
- Diagnosis with PCR, IFA, or IHC
Lymphoma has been well documented in cervids.
What species is it reported in?
What is the typical type?
- Reported in a variety of cervids – WTD, roe, red, and moose
- CD3+ T cell – alimentary/abdominal lymphoma is the most common – some cases have nervous involvement
- IHC identifies cells as lymphocytes
What cervid species is predposed to intestinal adenocarcinoma?
What are the lesions associated with it?
Are they suceptible to any other neoplasias?
- Farmed sika deer
- Single of multiple neoplasms in intestinal mucosa and submucosa with grey plaque like thickenings of ileocecocolic junction, proximal colon, cecum, and ileum
- These deer grazed on bracken firm which is associated with urinary bladder hemangiosarcoma, hemangioma, TCC, and cystitis in fallow deer
What are the herpesviruses of cervids? What species do they affect?
What are the associated typical signs?
What are teh typical lesions?
- Susceptible Species:
- Cervid Alphaherpesvirus 1 (CerHV-1) – red deer
- Cervid Alphaherpesvirus 2 (CerHV-2) aka Rangiferine Herpesivurs - Reindeer
- Elk Herpesvirus-1
- Etiology: Varicellovirus, Alphaherpesvirus, Herpesviridae
- Clinical signs
- CerHV-1 - conjunctivitis, eyelid edema, hypopyon, oculonasal discharge, corneal opacity
- CerHV-2 – keratoconjunctivitis, ocular exudate, periocular crusts sometimes progressing to panophthalmitis with corneal perforation, plays an important role in neonatal death and abortion
- Elk HV-1 – isolated from the semen of a healthy animal, unsure if causes disease
- Histo Lesions: Vitriol hemorrhage & fibrin deposition, conjunctivitis with edema, neutrophilic infiltration of lacrimal glands
- Diagnosis: PCR from ocular swabs or vaginal/seminal swabs
What are the poxviruses affecting cervids?
What species are susceptible?
What is the pathogenesis of this disease?
What are the clinical signs?
What are the histologic lesions - including the inclusino bodies?
- Susceptible Species:
- Red deer, reindeer, white-tailed deer, black-tailed deer
- Etiology:
- Deer Poxvirus – Cervidpoxvirus, Chordopoxvirinae, Poxviridae
- Deer Parapoxvirus – Parapoxvirus, Poxviridae
- Pathogenesis & Epidemiology :
- Direct contact and fomite transmission through breaches in keratin
- Results in high morbidity, but mortality can be high in fawns
- Clinical signs
- Pustular dermatitis of muzzle, face, ears, neck, and limbs
- Epithelial ulceration on lips, tongue, buccal cavity, and ruminal ulcers
- Histo Lesions:
- Intracytoplasmic eosinophilic inclusion bodies in keratinocytes
- Hyperkeratotis and hyperplastic dermaiitis with pustules & ulcers
- Diagnosis with PCR
What is the etiologic agent of Adenoviral Hemorrhagic Disease of Deer?
What species are susceptible?
Describe the pathogenesis of this disease.
What are the typical clinical signs and lesions?
What are the inclusion bodies?
How is this disease diagnosed?
- Susceptible Species:
- Columbian black-tailed deer, mule deer, white tailed deer, moose
- Etiology: Cervid Adenovirus, Atadenovirus, Adenoviridae
- Closely related to ovine adenovirus 7, goat adenovirus 1
- Pathogenesis & Epidemiology
- Fecal-oral route
- Endotheliotropic
- Vasculitis is seen primarily in the lungs but can lead to systemic infection and DIC
- Clinical signs & gross lesions
- Ulcerative alimentary tract disease can be diffuse or localized usually around the mouth but can occur in the forestomachs as well
- Pulmonary edema, intestinal mucosal hemorrhage
- Lymphoid depletion – retropharyngeal, mandibular, parotid, cranial cervical
- Histo Lesions
- Endothelial, eosinophilic to amphophilic intranuclear inclusion bodies
- Vasculitis, endothelial hypertrophy or necrosis
- Diagnosis – similar lesions to bluetongue & EHDV, requires virus isolation or PCR
What is the etiologic agent of necrobacillosis in cervids?
What species are susceptible?
How is it transmitted?
What are the typical clinical signs and lesions?
How is it diagnosed?
- Susceptible Species:
- Tundra reindeer, farmed fallow deer, farmed white-tailed deer, mule-deer, elk, red deer, sambar
- Etiology: Fusobacterium necrophorum
- Commensal bacterium of alimentary tract – serves as an opportunistic pathogen
- Filamentous gram-negative bacteria – anerobic
- Pathogenesis & Epidemiology
- Foot rot or oral form
- Stress of crowding or inadequate nutrition (vitamins A, E, selenium) are risk factors
- Skin abrasions serve as a portal of entry
- Coninfection with other bacteria commonly occurs
- Clinical signs
- Oral – base of tongue is often severely affected, necrosis of buccal surfaces tongue, pharynx, gingiva, periodontal tissues
- Secondary lesions in lungs and liver occur
- Histo Lesions: pyogranulomatous inflammation, mononuclear cell infiltrate, and fibrosis
- Diagnosis: culture or identification of sulfur granules
What is the etiologic agent of mandibular osteomyelitis in cervids?
What species are susceptible?
How is this transmitted?
What risk factors have been identified?
What are the clinical signs and lesions?
How is this disease diagnosed?
- Susceptible Species:
- Whtie-tailed deer, moose, caribou, red deer, fallow deer, roe deer
- Etiology: Actinomyces bovis and Trueperella pyogenes
- Gram positive bacteria – filamentous and branching in A. bovis, v-shaped pairs in facultative anaerobic T. pyogenes
- Pathogenesis & Epidemiology:
- Abrasions in skin and oral mucosa (rough feed, impacted vegetation, abnormal tooth wear) and through the dental alveoli
- Stress, poor diet, suboptimal environmental conditions, limestone-based habitat, dental fluorosis, replacement of deciduous dentition, and high population density may contribute
- Clinical signs
- Mandibular lesions result in difficulty masticating and progressive body condition loss
- Deformed and swollen mandible with purulent exudate from fistulas and tooth loss
- Pale, military, slightly gritty up to 3 mm foci called “sulfur granules”
- Histo Lesions: pyogranulomatous inflammation, mononuclear cell infiltrate, and fibrosis
- Diagnosis: culture or identification of sulfur granules
What is the the etiologic agent of suppurative meningoencaphalitis in cervids?
What species are affected?
How is this disease transmitted?
What clinical signs and lesions are typical?
How is this disease diagnosed?
- Susceptible Species:
- Free-ranging white-tailed deer in NA, roe deer in Europe
- Etiology: Trueperella pyogenes
- Gram-positive bacteria, v-shaped pairs of coccoid rods
- Pathogenesis:
- Common resident bacterium of white-tailed deer, higher in males
- Antler sparring, rubbing, and casting predispose to bacterial transmission which enters along skull sutures
- Varying virulence factors and environmental factors such as aridity lead to regional differences
- Clinical signs
- Grossly evident purulent material within cranial vault
- Abscesses range from 1-3 cm diameter with necrosis, erosion, and pitting of cranial bones near the pedicles (parietal and frontal bones)
- Histo Lesions: diffuse meningoencephalitis
- Diagnosis: Necropsy
What is the etiologic agent of dermatophilosis in cervids?
How is this disease diagnsosed?
What risk factors enhance transmission?
What are the typical clinical signs and lesinos?
How is this disease diagnosed?
- Susceptible Species:
- Roe deer, white-tailed deer, mule deer
- Etiology: Dermatophilus congolensis
- Gram-positive actinomycte, 2-6 parallel rows of cocci that look like railroad tracks
- Fungus-like life cycle and morphology - dormant zoopores are resistance to dessication
- Pathogenesis & Epidemiology:
- Direct contact, ectoparasite, or thorn bush transmission
- Humid environments (damp hair coat), skin trauma, and ectoparasites facilitate spore growth
- Clinical Signs and Gross Lesions
- Mild multi-focal erythema with crusts to severe extensive exudative lesions in the skin
- Crusts most commonly on back, tail, carpal and tarsal regions; less common on udder, scrotum, neck, and head; in white-tailed deer, crusts are usually present on face, ears, and distal limbs
- Crusts detach easily exposing moist, hairless foci with exudate and erythema
- Animals become emaciated
- Histo Lesions: Keratin debris, degenerated neutrophils, bacteria
- Diagnosis: direct smear of detached crusts
What is the etiologic agent of elk hoof disease?
What risk factors have been identified?
What are the typical lesions?
- Susceptible Species:
- Free-ranging elk
- Etiology: Treponema spp.
- Pathogenesis & Epidemiology:
- Copper and selenium deficient animals
- Accelerated hoof growth due to inflammation
- Clinical Signs & Gross Lesions
- Elongated, deformed hooves, without horn lesions
- Erosive lesions at coronary band, erosion of pedal bone, red corium
- Diagnosis: PCR – Treponema not confirmed as primary cause yet
What causes bullwinkle deer?
What species are most susceptible?
What are teh typical clinical signs and lesions?
How is this disease diagnosed?
- Susceptible Species:
- White-tailed deer
- Etiology: Mannheimia granulomatis
- Gram-negative coccobacilli – difficult to culture
- Also reported in roe deer with keratoconjunctivitis, stomatitis, glossititis, and pleuopneumonia
- Clinical Signs & Gross Lesions
- Chronic bacterial infection of skin and subcutis of the muzzle
- Histo Lesions: nodular and sclerosing pyogranulomatous and eosinophilic dermatitis and cellulitis
- Diagnosis: PCR
What are the flukes that commonly affect cervids?
What are the natural hosts?
What clinical signs and lesions occur as a result of infestation?
- Susceptible Species:
- White-tailed deer (natural host of F. magna) – others include the mule deer, black-tailed deer, and elk
- Moose are dead-end hosts
- WTD, elk, red deer, roe deer, fallow deer for F. hepatica
- White-tailed deer (natural host of F. magna) – others include the mule deer, black-tailed deer, and elk
- Etiology: Fasioloides magna (American liver fluke) & Fasciola hepatica (small liver fluke)
- Pathogenesis:
- Clinical Signs & Gross Lesions
- Fatalities (elk) due to extensive liver damage or rupture of hepatic capsule or vein
- Liver cysts – two flukes per cyst – eggs found in feces
- Diagnosis: fecal examination
What are the clinical signs associated with sarcocystis in cervids?
What species are particularly susceptible?
What are the associated lesions?
How is this diagnosed?
- Susceptible Species:
- Multiple cervid species – elk, mule deer
- Etiology: Sarcocystis spp.
- Aplicomplexa – tissue inhabiting protozoa
- Pathogenesis:
- Ingestion of sporocysts in carnivore feces
- Sporozoites excyst in small intestine, replicat in endothelial cells, and then enter muscle cells to form sarcocysts
- Clinical signs
- Pale streak in muscle
- Elk – multi-organ petechiae, pericardial, and pleural effusion
- Histo Lesions: parasitophrous vacuole that toxoplasma does not have
- Diagnosis: IHC
What are the clinical signs of besnotiosis in cervids?
What species are susceptible?
What are the classic lesions?
How is this diagnosed?
- Susceptible Species:
- Reindeer, ground caribou, mule deer, roe deer are intermediate hosts
- Etiology: Besnoitia
- Tissue-inhabiting protozoa
- Pathogenesis:
- Transmission to IH hosts directly or via vectos such as biting flies
- Merozoites develop in endothelial cells which then spread to connective tissue and fibroblasts forming cysts
- Clinical signs
- Often inapparent infections
- <1 mm diameter, firm, spherical white cysts in skin, subcutis, and underlysing tissue
- Histo Lesions: inflammation absent unless there is cyst rupture
- Diagnosis: PCR
What species of cervids are particularly susceptible to trombiculid mites?
What are the genera of mites that affect them?
What are the typical clinical signs and lesions?
How are they diagnosed?
- Susceptible Species:
- White tail deer >2 years more likely
- Etiology: Demodex spp
- Pathogenesis & Epidemiology:
- Predisposing factors – immunosuppression, concurrent infections, endocrinopathies
- Clinical signs
- Emaciation, patchy to generalized alopecia, hyperemia, hyperpigmentation, lichenification, cutaneous nodules
- Histo Lesions: Dilated hair follicles and sebaceous glands filled with mites, lymphoplasmacytic inflammation, hyperkeratosis, acanthosis
- Diagnosis: deep skin scrape, PCR
What are the clinical signs of demodicosis in cervids?
What species are particularly susceptible?
What risk factors have been identified?
What are the typical lesions?
How is this diagnosed?
- Susceptible Species:
- White tail deer >2 years more likely
- Etiology: Demodex spp
- Pathogenesis & Epidemiology:
- Predisposing factors – immunosuppression, concurrent infections, endocrinopathies
- Clinical signs
- Emaciation, patchy to generalized alopecia, hyperemia, hyperpigmentation, lichenification, cutaneous nodules
- Histo Lesions: Dilated hair follicles and sebaceous glands filled with mites, lymphoplasmacytic inflammation, hyperkeratosis, acanthosis
- Diagnosis: deep skin scrape, PCR
What is the scientific name of the winter tick?
What cervid species is particularly susceptible?
Desacribe the life cycle of the tick.
WHat are the common clinical signs in affected animals?
- Susceptible Species:
- North American cervids and reindeer, particularly moose
- Etiology: Dermacentor albopictus
- Pathogenesis:
- Ticks engorge late in winter, mate, and leave host
- Numbers can reach tens of thousands on moose (up to 178,000)
- Calves are especially vulnerable
- Clinical signs
- Poor nutritional condition, alopecia and hair breakage, anemia, hydropericardium – death can occur from severe anemia and exhaustion
- \Diagnosis: high densities of ticks in animals above 60 degrees north in America
What are the nasal bots of deer?
Describe their life cycle.
What are teh common clinical signs and lesions?
- Susceptible Species:
- Multiple NA and European cervid species
- Etiology: Cephenemyia spp – nasal, pharyngeal, head, or throat bots
- Diptera, Osstridae
- Pathogenesis:
- Female fly deposits larval packets in nostrils
- First instar larvae develop within the nasal cavity
- Second instar larvae are in the retropharyngeal pouches
- Clinical signs
- Generally, do not cause significant pathology
- Aberrant migration through the cranial has been reported
- Additionally animals with additional respiratory difficulty may suffocate as a result of these bbbots
- Histo Lesions: local eosinophilic and mastocytic inflammation
- Diagnosis: bots within nasal cavities or pharyngeal pouches
What are the keds that affect cervids?
Describe teh lifecycle of these parasites.
What are the common clinical signs associated with infestation?
What are the common lesions?
- Susceptible Species:
- White-tailed deer, moose, elk, axis, fallow, sika, mule, black-tailed deer
- Etiology: Lipoptena and Neolipoptena spp. - Hippoboscidae
- Pathogenesis:
- Hematogenous biting flies – shed wings once they find a host
- Can spread from doe to fawn during suckling
- Clinical signs
- Pathology is rarely reported
- Severe cases can result in poor nutritional condition, generalized lymphadenopathy, severe bilateral alopecia with crusting dermatitis on sheeks, ventral neck, lateral thorax, abdomen – less severe on dorsal neck, back and limbs
- Histo Lesions: orthokeratotic hyperkeratosis, epidermal hyperplasia, perivascular dermatitis with eosinophil, lymphocytes, macrophage, and plasma cell infiltrate)
- Diagnosis: presence of wingless flies on the animal
What is the etiology of chronic wasting disease in cervids?
What are the common clinical signs?
What are the typical histologic lesions?
How can this be diagnosed?
What tissues are most sensitive for testing?
- Susceptible Species:
- Elk, white-tailed deer, mule deer, moose, reindeer
- Etiology: Conversion of endogenous cellular prion protein in tissues such as brain and lymph node to abnormal protease resistant form
- Oral and nasal exposure by contact with infected animals or indirect environmental sampling during eating or rut
- Clinical signs
- Progressive weight loss and degeration of the nervous system – behavior, ataxia, excessive thirst and urination, hyporexia, teeth grinding
- Histo Lesions: neuronal vacuolation of obex, neuronal degeneration and loss, astrocytosis; gliosis
- Diagnosis:
- Early detection in lymphoid tissue – GALT, lymph nodes, tonsils
- Medial retropharyngeal lymph node and obex of the brain are the most sensitive sites for testing
Describe the antlers of cervids.
How does it differ across species?
Describe antlerogenesis.
o Defining characteristic is possession of antlers in males.
▪ Except Chinese water deer.
▪ Reindeer and caribou females also antlered.
▪ Antlers arise from frontal bones and skin and are covered with highly vascularized and sensitive skin (velvet). When mating season approaches, testosterone rises and antlers harden and velvet dries. When testosterone levels decline a layer of bone-dissolving cells invades the base of the antlers and causes them to fall off.
Describe cervid anatomy.
Where are scent glands located?
What is their typical dental formula?
Do they have a gallbladder?
What type of uterus and placentation do they have?
o Scent glands - Facial gland in front of each eye/periorbital, glands on legs.
o Dental formula – I 0/3, c 0-1/1, pm 3/3, m 3/3 x 2 = 32-34.
▪ Hydropotes, Muntiacus, Elaphodus – Maxillary canines saber-shaped, large.
▪ Tooth wear can be used for aging.
o Lack a gall bladder.
o Two pairs of mammae.
o Bicornuate uterus except Pere David’s deer and barking deer – only right uterine horn.
o Gestation variable, epitheliochorial, cotyledonary placenta.
▪ Oligocotyledonary – few caruncles compared to other polycotyledonary arteriodactyls.
▪ Most have 1-2 young, each develops in own horn, twins common.
▪ Umbilical cord contains two arteries, two veins, and an allantoic duct.
▪ Amniotic plaques incidental finding.
o Hepatic lipidosis typical in some spp during rut.
Describe the differing anatomy between cervids, tragulids, and moschids.
o Chevrotain (Tragulidae): four-chambered stomach with poorly developed omasum, have 4 toes (like pigs and hippopotami) and incomplete fusion of the 3rd and 4th metacarpals and metatarsals; lack antlers elongated upper canines (like musk deer); lack preorbital scent glands but posess a chin gland
o Musk deer (Moschidae): lack antlers, have gallbladder, one pair of mammary glands, no facial glands, but well developed preputial or musk glands
Describe housing considerations for cervids from both a enclosure and a rehabilitation standpoint.
- Special Housing (F8):
- Antlers may become caught in any form of fencing.
- Dead trees and logs act as rubbing posts when stags lose their velvet.
- Housing (MMWS):
- Diet in short term care: hay, deer pellets, local flora
- Mating season: Oct-Dec, primiparous does have 1 fawn then twins or up to 4.
- Gestation 187-222 days
- Parturition in spring, neonates are precocious
- Birth weights 2.5-4 kg, triple their weight in first month
- Weaned from 8-12 wks
- First mold in autumn - lose their spotted hair coat
- Fawns are stashed by mom during the day - true rejection indicated by frequent loud vocalization of neonate, dehydration, fly eggs
- Aging fawns:
- <1 wk old: scab over umbilicus
- Lost spots around 3-4 mo old
- Male fawns: antler pedicles develop around 4 mo, much more visibly by 7 mo
- Weight 34-38.5 kg at 6 mo and 41 kg by 1 year
- Have 4 teeth when born, grow premolars and incisors after 2 mo, have full set of adult teeth by 1.5 yr
- Pen size recommendations:
- Infant deer, pronghorn, and bighorn sheep: 4’x4’x2’ high
- Infant elk: 6’x6’x2’ high
- If umbilicus present: individually quarantine indoors, can move outdoors when umbilicus sloughs off
- Cohorts quarantined minimum 6 days and 3 negative fecals EOD
- Nursing/preweaned deer, pronghorns, bighorn sheep: 10’x15’x6’ high
- Nursing/preweaned elk: 12’x20’x6’ high
- No > 3-4 fawns/stall
- Move to large outdoor yards/paddocks when rack trained and growing: at least 8’ high
- Deer, pronghorns, bighorn sheep: min 1500 square feet
- Elk: min 4000 square feet
- Access panels to minimize human exposure
- Electric fence to keep out predators
- Max 15-20 fawns per 30’x50’ yard
- Adults: outdoor wooden paddock
- Deer, bighorn sheep: min 30’x50x’8’ high
- Elk: 50’x80’x8’ high
- Circular pens encourage running along walls rather than cornering and injuring themselves
- Pronghorns can leap long distances, bighorn sheep can leap great heights
Describe teh nutritional stategies of cervids.
Give examples of browzers and grazers.
How are cervids fed in zoo and rehab settings?
What considerations need to be made for fawns?
- Nutrition (F8):
- Musk, moose, roe deer = browsers on dicotyledonous plants
- Brachydont dentition (low-crowned) for attritional wear
- Will ingest a higher proportional content of concentrate pellets in captivity which can lead to chronic ruminal acidosis and “wasting syndrome complex“ in moose with decreased relative life expectancy
- Père David deer, fallow deer = grazers on monocotyledonous plants
- Longer retention time of fiber in the rumen and less frequent feeding needs
- Hypsodont dentition (high-crowned teeth) adapted to abrasive wear
- Excess feeding of pregnant Père David deer can result in dystocia by oversized calf
- Deer may lose up to 10% of BW because of higher energy demands in the winter season. Deer overwintered indoors will have much lower energy requirements so supplementary feeding may be greatly reduced
- Musk, moose, roe deer = browsers on dicotyledonous plants
- Diet (MMWS):
- Concentrate selectors: browse trees and shrubs
- Commercial deer diets in low-sided pans, free choice alfalfa or grass hay
- Fawns do not become fully functioning ruminants till 2 mo old, will graze at a few wks old
- Colostrum: fawns < 12-24 hr, frozen bovine or caprine colostrum or powdered colostrum supplement
- Hold bottle at 45’ angle to prevent aerophagia, neck outstretched to ensure formula flows down esophageal groove
- No > 50-66 mL/kg/feed (stomach capacity)
- Manually stimulate neonates to urinate/defecate at each feeding
- Wean around 6 wk old, D/C formula between 8-12 wk old
- Should forage exclusively natural browse at least 3 wks after weaning and prior to considering release
Describe the reproduction of cervids.
What is rut?
How long does gestation last - when does it normally occur?
What triggers the reproductive cycle? Is that true for tropical cervids?
What contraceptives are commonly used?
- Reproduction
o Rut occurs during fall season
o Gestation lasts over winter and calves born in spring. Exception: roe deer that have rut in summer and fertilized ovum doesn’t implant until the shortest day of the year so that the calf is born in spring
o Reproduction triggered by short day length which stimulates the pineal gland to initiate one or two silent ovulations. Shortened day length also stimulated luteal hormone secretion in males = activates testicular development, spermatogenesis and secretion of testosterone = antler minieralization
o Tropical deer show little or no seasonality and may breed throughout the year. When moved to temperate region, some may remain aseasonal. Javan deer exhibits reverse seasonality
- Contraception:
- Porcine zona pellucida vaccine
- GNRH vaccines
- Routine anthelminthic tx should be based on knowledge of resident helminths and their life-cycles and susceptibility of the species
- Any animals to be imported should be tested for tuberculosis and helminths before transport and quarantine after arrival
What are smoe zoonotic concerns with cervids?
How does population composition and carrying capacity affect holding decisions?
Preventative Medicine
- F8:
- Carrying capacity should be set and excess animals culled to minimize risk of contamination of infectious organisms
- Subadult males should be removed before they start to threaten the stag’s position
- Zoonotic risks (MMWS): Giardia, cryptosporidium, dermatophytosis, Dermatophilus congolensis, ticks
- Wear disposable gloves, gown, shoe covers
Describe the physical restraint of cervids.
- Physical restraint:
- Small deer can be confined in padded boxes and then restrained. Should only be restrained in lateral recumbency for short periods of 15 mins or less
- Can apply hobbles and blindoflds
- Can also use collecting funnels from paddocks
- Male cervids and both sexes of reindeer should not be restrained when antlers are in growth bc potential for major blood loss and severe pain associated w/ trauma. Once hardened the antlers should be removed if the stags are to go through a handling system
Describe the chemical restraint of cervids.
How do doses differ between free-ranging and managed cervids?
what are some preferred protocols?
How should animals be positioned?
What pre- and post-anesthetic considerations should be made?
- Chemical anesthesia:
- Prone to capture myopathy, hyperthermia, trauma
- Captive deer often have very different drug requirements very different from free-raning animals
- Relatively high doses of alpha-2 agonists needed, excitation may overcome drug’s sedative effects; can be combined with opioids to reduce excitation, muscle tremors and resp depression
- Re-narcotization can occur some hours after reversal bc shorter duration of action of some antagonists compared with opioid drug, should monitor for 72h
- Thiafentanil oxalate has the advantages of more rapid induction, equal or greater potency and shorter half-life, thus reducing likelihood of renarcotization
- Telazol has long recovery period unless zolazepam is antagonized with flumazenil
- BAM: hyperthermia is avoided, excellent respiration and good muscle relaxation in white tailed deer, but results in fallow deer have been disappointing
- After induction should position with neck extended but nose pointing slightly downward to reduce likelihood of aspiration and ruminal tympany
- Intubation aided with long laryngoscope, stylet and IV bolus of ketamine (1-2 mg/kg) or propofol (2-4 mg/kg)
- Should withhold food 24-36h prior and water 12h
- Should extubate with the cuff still partially inflated and only when swallowing reflex has returned
What neuroleptics have been used in cervids?
- Neuroleptics:
- Extrapyramidal side effects may occur
- Butyrophenones azaperone and haloperidol admin IM or IV are shorter acting (72h)
- Phenothiazines are slower in onset but longer-acting and may only be given IM
- Zuclopenthixol acetate lasts up to 4 days
- Perphenazine enanthate up to 10 days, time to onset of action is correspondingly long
Describe babesiosis in cervids.
What babesia species typically affect cervids?
What are the vectors?
What are the factos associated with disease emergence?
What are the typical clinical signs?
How is this disease diagnosed?
- F9 Ch 92 Babesiosis in Cervidae:
- Babesia capreoli, venatorum (Eu) and odocoilei (in NA)
- B. venatorum has zoonotic potential = malaria-like disease
- Primary vector in NA : Ixodes scapularis (black legged tick), but Dermacentor spp. also implicated
- Parasites induce lysis of erythrocytes à releasing parasites in circulation
- Intra and extravascular immune-mediated hemolysis
- Thrombocytopenia : immune-mediated platelet destruction or from CIVD
- Reservoir : white-tailed deer (rarely clinical unless immunosuppressed)
- Overt hemolytic disease resported in reindeer, caribou, American elk, musk oxen
- Factors involved in disease emergence :
- Climate change à more widespread tick population (seasonality)
- Migratory birds that travel ectoparasites over large territories
- Babesia capreoli, venatorum (Eu) and odocoilei (in NA)
- Clinical signs :
- Peracute : sudden death
- Acute : hemolytic disease, hemoglubinuria, hemorrhage, icterus
-
Chronic : pyrexia, anemia, emaciation
- Low-level parasitism in erythrocytes
- Subclinical : transient anemia
- Diagnosis :
- Peripheral blood smear :
- Ring-shaped organisms at periphery (accoté position)
- Nb of parasites +++ variable (removal of infected erythrocytes), not always present
- Ring-shaped organisms at periphery (accoté position)
- Peripheral blood smear :
- Hematology and Biochemistry :
- Inflammatory leukogram
- Normocytic, normochromic regenerative anemia
- Biochemistry changes as the consequence of hemolysis : azotemia (hemoglobinuric nephropathy), hepatic changes (centrolobular necrosis of hepatocytes secondary to decreased blood flow), hyperbilirubinemia (extravascular hemolysis)
- PCR on whole blood
- PCR on spleen samples (post-mortem)
A recent study experimentally inoculated mule deer with foot and mouth disease.
What is the scientific name of that species?
Why was it specifically chosen?
What were the clinical signs that developed?
What were the lesions on necropsy?
How did those signs and lesions compare to the cattle that were exposed?
FOOT-AND-MOUTH DISEASE IN EXPERIMENTALLY INFECTED MULE DEER (ODOCOILEUS HEMIONUS)
Rhyan J, McCollum M, Gidlewski T, Shalev M, Ward G, Donahue B, Arzt J, Stenfeldt C, Mohamed F, Nol P, Deng M.
Journal of wildlife diseases. 2020 Jan;56(1):93-104.
Key Points:
* The only known outbreak of FMD in the US was in mule deer.
* Following exposure, all deer and cattle developed disease (via inoculation or contact with others).
* CS - Fever, vesicles mouth and feet and inoculation sites.
* Blanching of coronary bands first sign on feet prior to vesicle formation.
* Myocarditis was more likely in mule deer, also necrotizing pancreatitis.
* Mule deer higher mortality and more severe clinical signs vs cattle.
* Most extensive oral vesicles on torus lingua - ball of the tongue.
A recent paper described winter tick associated dermatitis in wild elk.
What is the scientific name of the elk?
What is the scientific name of the winter tick?
- What is its lifecycle?
What dermatological lesions occurred on this elk?
What occurs as a result of severe tick infestation?
Calvente, E., Chinnici, N., Brown, J., Banfield, J. E., Brooks, J. W., & Yabsley, M. J. (2020).
Winter tick (Dermacentor albipictus)–associated dermatitis in a wild elk (Cervus canadensis) in Pennsylvania, USA.
Journal of wildlife diseases, 56(1), 247-250.
Key Points:
* Adult winter ticks most prevalent mid-Jan-April.
* One-host tick, remains on same host for months feeding and molting then lays eggs in environment.
* Severe tick infestation resulted in severe anemia and mortality in wild elk. Previously reported in moose.
* Hyperkeratosis, crusting, can be fatal.
A recent study described the first report of adenoviral hemorrhagic disease in Mule Deer.
What is the scientific name of mule deer?
Causative agent of deer adenovirus?
What are the typical lesions?
- What are the two forms of the disease?
Ddx? Is there a vector?
Ferguson, S. H., & Lee, J. K. (2020).
First report of adenoviral hemorrhagic disease in three mule deer (Odocoileus hemionus) in Arizona.
Journal of Zoo and Wildlife Medicine, 51(1), 232-235.
Key Points:
* Deer adenovirus (Odocoileus adenovirus 1) - Hemorrhagic disease. Ddx orbivirus infections (bluetongue and epizootic hemorrhagic dz).
* Tropism for vascular endothelium resulting in a fatal combination of severe pulmonary edema and hemorrhagic enteritis.
* Deer primary host, mule deer highly susceptible.
* High mortality rate. Two forms - systemic vasculitis and localized necrosis/ulceration of the GIT.
* Culicoides is a vector for EHDV and BTV, NOT for adenovirus.
A recent study surveilled the parasites of wild red deer.
What is the scientific name of the red deer?
What were the three most common parasites?
What was the most common lesion?
Reissig, E. C., Massone, A. R., Iovanitti, B., Gimeno, E. J., & Uzal, F. A. (2018).
A survey of parasite lesions in wild red deer (Cervus elaphus) from Argentina.
Journal of wildlife diseases, 54(4), 782-789.
Key Points:
- Fasciola – cholangiohepatitis – larvae cause granulomatous hepatitis, adults cause biliary hyperplasia & cholangitis
- Distyocaulus – congestion & hemorrhage with hyperplasia of BALT
- Sarcocystis – lymphoplasmacytic myocarditis (90%)
A recent study described lungworms in Rocky Mountain Elk.
What is the scientific name of the elk?
What is the primary lungworm of ruminants?
What new species was identified in this study?
Bangoura, B., Brinegar, B., & Creekmore, T. E. (2021).
Dictyocaulus cervi-like lungworm infection in a rocky mountain elk (cervus canadensis nelsoni) from wyoming, usa.
Journal of Wildlife Diseases, 57(1), 71-81.
Key Points:
- Lungworms in ruminants: small protostrongylids, large Dictyocaulus spp.
– Cause significant lung lesions and dz in ruminant hosts.
– Bovine: D. viviparous – Common in domestic and wild ruminants.
– Cross-transmission between cervids and domestic ruminants not described.
– Cervid: D. viviparus (considered the only species in wild ruminants in the US), D. eckerti (EU), cervi, capreolus, noerneri
– Prevalence in WY and MT elk: 0-19%
Takeaways: D. cervi elk lungworm identified, indicating a novel species in free-ranging elk in Wyoming. Possibly introduced to NA wildlife by import of captive cervids from Europe.
