Caprinae Flashcards
Describe the etiology and epidemiology of capripoxviruses in nondomestic hoofstock.
What are the three viruses in the capripoxvirus genus?
What species are suceptible?
Where do these diseases occur in the wild?
How are these diseases transmitted?
Introduction/ etiology
- Genus Capripoxviruses (CaPVs) contains 3 species: sheeppox virus (SPPV), goatpox virus (GTPV), and lumpy skin disease virus (LSDV).
o Can not distinguish between species antigenically
- Domestic ruminant CaPV infections cause significant economic impact in endemic areas
- OIE notifiable diseases
Epidemiology
- SPPV and GTPV can cause very high morbidity (70-90%) and mortality rates (50-100%) in domestic animals
- LSDV morbidity typically 5-45% but can reach 100%, mortality typically <10%
- Severity of disease depends on species, age, and immune status
- Morbidity/ mortality in wild species poorly recorded
- Severe outbreak with high mortality in captive wild animals in Qatar in 2015
- Mortality rates as high as 100% in 16 ruminant species
Range and host-specificity
- CaPVs typically highly host specific but exceptions occur
o Some SPPV and GTPV strains can cause disease in both sheep and goats, and in some cases wild ruminants
- SPPV and GTPV ranges from Northern Africa, Middle East, India, and Asia
- LSDV occurs in majority of Africa into the Middle East
- Typically causes disease in domestic cattle but natural and experimental infections in severe wild species reported
- Role in wildlife not well understood
Transmission
- SPPV and GTPV highly contagious; may remain viable in crusts/ environment for several months
o Shed via secretions from ulcerated papules on mucous membranes -> transmission typically via aerosols and close contact
o Amount of viral shedding correlates with clinical disease severity -> no chronically infected carriers
- LSDV transmitted mechanically via biting insects -> virus can spread over long diseases
Describe the management of capripoxviruses in nondomestic species.
What are the clinical signs and lesions associated with these diseases?
How are they diagnosed?
How are they treated, prevented, and controlled?
Chapter 91: Capripoxviruses in nondomestic hoofstock
Clinical signs/ pathology
- Following infection, typically 8-14 day incubation period then fever with concurrent skin nodules, lymphadenopathy, lethargy, anorexia, ulcerative lesions on mucous membranes (eyes, nose, mouth, pharynx, tongue), GI signs when GI mucosa affected (most often rumen/ abomasum), lungs often develop extensive nodules
- Secondary infection and death can occur
Diagnosis
- Severe infections typically pathognomonic, mild disease more difficult to diagnose
- Can not rely on serology to differentiate, PCR with secondary sequencing most reliable
- CaPV immunity mainly cell mediated -> neutralizing antibody levels typically low
Treatment, prevention, and control
- Treatment relies on supportive care and abx therapy for secondary infections
- Isolation of sick/ exposed animals, strict quarantine, disinfectant protocols, appropriate carcass disposal, and vector control essential to prevent spread
- Vaccination via modified live vaccines in enzootic countries -> not authorized for use in nonendemic countries
- Killed vaccines available for emergency use in non-endemic countries, less effective
Bighorn sheep are commonly reported with what neoplasm?
What is the suspected etiology?
What are the lesions like?
- Free-ranging bighorn sheep
- Experimentally transmitted between bighorn and domestic sheep
- Soft, shite, gelatinous cystic masses that fill the nasal sinuses and extend into underlying bone, frontal or palatine, sinus, or nasal turbinates
- Nasal cavities may be filles with seromucinous exudate with Pasteurellacea or Mycoplasma ovipnumoniae
- Masses have deep submucosal sheets intraluminal PAS positive mucin
- Periosteal cell origin is suspected
- Tumor transmission studies suggests a viral etiology
- Separate from the enzootic nasal adenocarcinoma in domestic sheep
What is the etiologic agent of orf?
What species are susceptible?
Describe the pathogenesis and epidemiology of this disease.
What are the typical clinical signs?
What are the associated histological lesions? What are the inclusion bodies?
- Susceptible Species:
- Caprids – bighorn sheep, Dall’s sheep, mountain goats, muskoxen, takin, chamois, tahr, serow
- Also reported in blackbuck, mountain gazelle, and steenbok – experimental infection in pronghorn
- Etiology: Parapoxvirus (Poxviridae) – Orf Virus (ORFV)
- Genetic testing may be needed to differentiate from Capripoxvirus lesions in some cases
- Pathogenesis & Epidemiology :
- Infection through defects in skin or mucous membranes
- Virus shed in sloughed skin crusts but virus can remain infective in environment for long periods of time
- Outbreaks occur in higher population densities
- Young animals re most severely affected and lesions can be fatal
- Clinical signs
- Proliferative, necrotizing, and vesicular lesions on the skin and mucous membranes
- Muzzle lips, gingiva are most commonly involved – tongue, periocular region, distal limbs, interdigital cleft, heel bulb, mammary gland, vulva, prepuce and dorsal skin are other sites
- Lesions progress from papules to pustules that rupture resulting in thick crusts
- Secondary emaciation or infections leading to cellulitis, stomatitis, aspiration pneumonia, or mastitis can occur
- Histo Lesions: Intracytoplasmic eosinophilic inclusion , epidermal proliferation & swelling of stratum spinosum with intraepidermal vesicles & pustules
What is the etiologic agent of border disease?
What species are susceptible?
Describe the clinical signs and lesions.
What are the typical histo lesions?
How is this disease diagnosed?
- Susceptible Species:
- Mass mortalities in wild chamois
- Etiology: Pestivirus - Flaviviridae
- Pathogenesis:
- Persistent infections and vertical transmission
- Clinical Signs & Gross lesions
- Depression, decreased flight distance, sudden death
- Patchy to wide-spread alopecia, epidermal hyperpigmentation with secondary infections
- Histo Lesions:
- Spongiosis, perivascular edema, neuronal degeneration and necrosis, mononuclear perivascular cuffing in the brain. Follicular atrophy, tricholelemmal keratin deposition in the skin with acanthosis, melanosis, and orthokeratotic hyperkeratiosis
- Diagnosis:
- Viral antigen may be in spleen and lymph node macrophages, epithelium, kidney, rumen, or brain
- PCR, VI, ELIsA
What is the etiologic agent of epizootic pneumonia in bighorn sheep?
What other organisms contribute to disease?
How is this transmitted?
What are the clinical signs and lesions?
How is it diagnosed?
- Susceptible Species:
- Bighorn sheep
- Etiology: Mycoplasma ovipneumoniae
- Other organisms thought to be the cause – lungworm (Protostrongylus), Pasterurellacea (Bibersteinia, Mannnhemia, P. multocida)
- Pathogenesis & Epidemiology:
- Contact with domestic sheep
- In naïve population – mortality can be up to 90%
- Clinical Signs & Gross Lesions
- Penumonia-related mortality
- Acute to chronic fibrinous, suppurative or necrotizing sinusitis and bronchopneumonia with pleuritis
- Abscesses, bronchiectasis, and pleural adhesions
- Histo Lesions: neutrophilic exudate in lumina of small airways
- Diagnosis: PCR
What is the etiologic agent of infectious keratoconjunctivitis in caprids?
What species are susceptible?
How is this disease transmitted?
What are the typical clinical signs and lesions?
- Susceptible Species:
- Chamois, ibex, bighorn sheep
- Etiology: Mycoplasma conjunctivae
- Pathogenesis:
- Transmission by contact with ocular secretions or exudate or indirectly by insects; aerosols also transmitted
- Clinical signs:
- Corneal edema, erosion, ulceration, stromal necrosis with anterior synechiae or staphyloma, corneal fibrosis may occur in longterm cases
- Death typically from blindness – trauma, predation, emaciation
- Diagnosis: PCR
What species are susceptible to scrapie?
What are the class histologic lesions?
How is it diagnosed?
- Susceptible Species:
- Domestic sheep and goats – also in mouflon and other caprinids
- Histo Lesions: neuronal vacuolation of the obex
- Diagnosis: IHC, obex histo, ELISA – no reliable tests in a living animal
What are the three groups of carpinids?
Biology
- Family Bovidae, subfamily Caprinae
- Three tribes
- Ovibini – muskox & takin
- Rupricaprini – goral, serow, chamois
- Caprini – sheep, goat, tahr
- Three tribes
- 85 species
- Marked sexual dimorphism in size and shape of horns in Caprini, less pronounced in other tribes
What are important considerations in enclosure design for caprinids?
Special Housing Requirements
- Agile climbers & jumpers
- Climbing structures to promote natural behaviors & hoof wear, but care should be taken to prevent escape
Describe the nutritional strategies of caprinids.
What are some potential concerns for toxicity?
Describe the restraint of caprinids - both physically and chemically.
Restraint & Handling
- Prolonged running may induce hyperthermia & capture myopathy
- Smaller species may be restrained for short procedures
- Horns of juveniles should not be used for restraint, as the bony core may not be fused to the skull yet
- Chemical Restraint
- Opioids – ultrapotents used, butorphanol + alpha 2 seems to decrease rumen reflux
- Intubation recommended to prevent aspiration of rumen contents
- Use of stylets facilitates intubation in species with narrow muzzles
What are some of the common complications to anesthetizing caprinids?
Species Specific Physiology
· Very prone to severe hypoxemia with alpha-2 agonists – sometimes supplemental oxygen isn’t sufficient to correct this
· Prone to ruminal tympany and regurgitation during chemical restraint
Describe the physical capture techniques for wild caprinids.
Which has the lowest mortliaty rate?
Physical Capture
- Net gunning had lowest combined mortality rate (<2%), drop netting (3%), drive netting (4%), chemical immobilization (8%) had the highest mortality rate in wild animals – physical restraint is the preferred method for short procedures
- Some acepromazine with physical restraint has reduced stress of the handling
Describe the chemical restraint of caprinids?
What sites are used for vascular access?
Describe intubation techniques.
How long should these animals be fasted for?
Any tips for positioning?
Any species specific considerations?
Chemical Restraint
- Vascular Access – cephalic, jugular, saphenous
- Intubation – sternal recumbency with head extended toward sky, long laryngoscope, stylets assist in narrow mouthed species
– Administration of diazepam with ketamine, or propofol, prior to intubation is useful in providing the needed muscle relaxation for intubation
- Fasting - >24 hours to reduce tympany & regurgitation
- Monitoring – hypoxemia common with alpha-2s, hyperthermia with long catches (>41C - >106F – coldwater enema or reverse)
- Positioning – sternal recumbency or modified right lateral recumbency to reduce regurgitation
Species Specific Considerations
- Bighorn sheep
– Etorphine 3.5 mg + 50 mg xylazine
– Telazol 4.2 mg/kg + xylazine 0.5 mg/kg
- Mountain Goat
– Etorphine – 4-5 mg/animal
- Markhor – medetomidine + ketamine had more respiratory depression than etorphine-acepromazine
- Chamois – ketamine + xylazine or medetomidine
- Ibex – medetomidine + ketamine
- Muskox – large head, small mouth make intubation difficult – diazepam or guaifenesin for relaxation is crucial for intubation
What is teh cientific name of the chamois?
What are some important diseases in wild chamois?
Any diseases of zoonotic concern?
Describe their restraint.
Biology of Chamois
- Family: Bovidae Subfamily: Caprinae
- 2 species:
- Rupicapra pyreneica in Pyrenees, northern Spain
- Rupicapra rupicapra in Alps
- CITES I
- Trophy hunting trophy, meat valued, chamois leather from skin
- Females give birth May and June
- Adult males are often alone, rut is quite aggressive
Anatomy and Physiology
- Similar to domestic goats
- Horns in both sexes
Feeding and Housing
- Rarely found in zoos
- Very sensitive to high temps
- Very aggressive, esp males
- Males known to kill females during rut, Best to remove males from enclosure at this time
Reproduction
- Single kids
Restraint / Handling
- Physical restraint for newborns only
- Chemical restraint – catching them in the wild is difficult due to alps environment
- Oral sedation
- Acepromazine (short acting neurolept) not sufficient for physical restraint but good for pre-immobilization and transport
- Long acting neurolepts – Not reported
- Immobilization
- Xylazine / ketamine, doses are extremely low compared to other mountain ungulates
- Medetomidine / ketamine – superior choice
Diagnostics – same as goat
Diseases
- Endoparasites
- Eimeria specific to chamois
- Chamois kids can get clinical intestinal coccidiosis = massive ventral neck edema.
- Various cestodes are regularly demonstrated, usually not a problem, but occasionally clinical in kids
- Lungworms are extremely common, 85% Protostongylidae were detected
- GI nematode is high, Trichostrongylidae are most often detected
- Infectious Disease
- Chamois share pastures with domestic sheep and goats. Political conflict between hunters and shepherds
- Respiratory Tract
- Most important pathology in wild chamois
- Epizootics and significant die offs occur
- Manheimmia hemolytica is most frequent isolate
- Assume multifactorial etiology to die offs in additional to Manheimmia
- Some viral agents found: BVD, IBR, BRSV
- Protostrongylus
- Infectious keratoconjunctivitis
- Mycoplasma conjunctivae
- Affects goats and sheep, Chamois frequently infected
- Can be fatal in wild ungulates, where moderate dz in domestics
- Unilateral or bilateral conj or corneal inflammation
- Progresses to mucopurulent conjunctivitis and ulceration, cornea may perforate, animals are found blind
- Diagnosis: PCR
- Prevention: Prevent spill over from domestics
- Other
- Pestivirus – non specific CNS symptoms, lack of flight response to humans, high prevalence with asymptomatics. Concern for economic losses in domestic animals.
- Brucella meletensis, often described.
- Skin diseases – All three are ZOONOTIC
- Scabies – Sarcoptes scabei
- Endemic in some populations of chamois
- Cyclic outbreaks in other populations
- Head and neck, spreads over the back
- ELISA to detect asymptomatic carriers
- Easily treated
- Dermatophilosis
- Suppurative inflammatory skin disease
- Dermatophilus congolensis
- Diagnosed by demonstrating rows of coccoid bodies with a “railroad” track appearance on Geimsa
- Stress and concurrent infection likely lead to disease
- Contagious ecthyma
- Parapoxvirus
- Reported in wild and captive chamois
- Predominantly on mouth and face, but could be genital and feet
- Self limiting
- Domestic sheep and goats are reservoirs
- Vaccine available
- Scabies – Sarcoptes scabei
Neoplasms – n of 1’s, not summarized