EXAM 3 - 8 Lectures Flashcards

1
Q

carrying capacity

A

the number of animals and area will support

depends on quality of the habitat

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2
Q

ecologic/biologic carrying capacity

A

the number of each wildlife species that can live in an area and remain healthy and not damage the habitat

dynamic

impacted by:
habitat
animals
disease
management goals

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3
Q

wildlife acceptance capacity

A

social - how much people will put up with the animals

often the limiting factor

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4
Q

brain abscesses in deer

A

caused by multiple genera of bacteria - trueperella pyogenes in most cases
- gram positive rod

skin/mucus membrane inhabiting bacteria or environmental bacteria

enter through traumatic skin lesion, break in antler, sutures of skull bones

most cases in males older than 2

strongly seasonal - sep - april

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5
Q

brain abscesses in deer - clinical signs

A

wide variety of neurological signs depending on speed of progression and entry into brain

loss of fear
aggression
circling
head pressing,
paralysis,
emaciation +/-

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6
Q

brain abscesses in deer - lesions

A

draining tracks/pus in the skin/subcutis
inflammation in subcutis
necrosis of skull bones
abscesses in cranial vault
antler fractures
disseminated lesions

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7
Q

brain abscesses in deer - diagnosis

A

tentative based on gross lesions/clinical signs

culture and identification of bacteria to confirm

bone damage helpful with skeletal remains

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8
Q

brain abscesses in deer - wildlife implications

A

not population limiting

older bucks

source of inefficient management to increase adult male segment populations

QDMA - manage deer population for genetics, nutrition, older bucks (point restrictions)

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9
Q

brain abscesses in deer - public health and agricultural implications

A

humans may be susceptible to some of the causative bacteria
- no infections associated w deer contact
- suitable for consumption?
- wear gloves, wash hands/knives

livestock may be susceptible to some of the causative bacteria
- infected deer are not an added source for infection

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10
Q

TB in deer

A

Mycobacterium bovis
- acid-fast staining
- slow growing aerobe

national eradication program
- wildlife reservoirs make it difficult

virtually eliminated from US cattle

zoonotic
- problem in developing world
- pasteurization of milk

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11
Q

TB in deer - transmission

A

inhaltion or ingestion

bacteria secreted in sputum, urine, feces, and abscesses

persist for 5 months in cold/damp conditions

enhanced by crowding and stress

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12
Q

TB in deer - clinical signs and lesions

A

poor body condition
behavior change - away from herd
pneumonia

granulomas w m. bovis
- increase in size and become fibrotic and mineralized
- suspective but not definitive

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13
Q

TB in deer - in MI

A

extensive feeding and baiting is a risk factor
- artificially raises carrying capacity
- increases nose-nose contact and indirect contact w contaminated feed

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14
Q

meningeal worm in deer

A

parelaphostrongylus tenuis
- nematode

WTD are definitive hosts
- no disease

aberrant hosts - disease
- moose
- elk
- caribou
- llama
- domestic sheep and goat

causes damage to spinal cord and brain

often fatal

worms often don’t reach adult stage
- no shedding

elk and moose may shed larvae

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15
Q

meningeal worm in deer - life cycle

A

L1 released in feces
become L3 in snails or slugs - 30d
release L3 for ingestion
travel through spinal cord to meninges
eggs released in meninges
eggs travel to blood
become larvae in lungs
spread through gi and spread in feces

ingestion to shedding - 90d

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16
Q

meningeal worm in deer - clinical signs and lesions

A

may have yellow exudate on surface of brain and meninges

may have hemorrhages in lungs or pneumonia associated with eggs and larvae

in aberrant hosts infection results in lesions in spinal cord or brain
- small and hard to see grossly
- rarely find worms - L3

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17
Q

meningeal worm in deer - diagnosis

A

depends on doals of testing

population
- fecal exam for larvae
- necropsy and recovery of worms
- histo of lungs

individual - live
- fecal exams problematic
- PCR and serology under development

individual - clinically ill
- clinical signs
- gross lesions and microscopic examination of spinal cord/brain
- pcr

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18
Q

meningeal worm in deer - implications

A

infected animals should not be moved into areas where absent

cautious relocation of vulnerable species into endemic areas

aberrant host vulnerability in overlap w WTD
- agriculture implication

no public health implications

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19
Q

parasitism malnutrition syndrome in deer

A

parasitism is common but rarely causes disease
- can result in disease when combined with other factors - habitat, crowding, malnutrition

malnutrition reduces ability to control parasitism

significant disease associated with heavy parasite loads is indicator that a wild population has exceeded carrying capacity resulting in malnutrition

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20
Q

parasitism malnutrition syndrome in deer - large lungworm

A

dictyocaulus viviaprus
- large nematode of airways

ubiquitous distribution

wide host range
- deer
- elk
- moose
- cattle
- sheep
- goats

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21
Q

parasitism malnutrition syndrome in deer - large lungworm - life cycle

A

eggs coughed up, swallowed, larvae hatch out and defecated

larvae infective after 1wk in environment

deer or other hosts ingest larvae when feeding on low-lying vegetation

pilobolus fungus propels sporangium and larvae from fecal pat

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22
Q

parasitism malnutrition syndrome in deer - large lungworm - clinical signs and lesions

A

most not visibly sick

underweight
weak
respiratory distress
less than a yr old
heavy loads of other parasites

frothy mucus and mats of worms in airways

consolidation of individual lung lobules

bronchopneumonia +/- fibrinous pleuritis
- young deer w heavy infestations

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23
Q

parasitism malnutrition syndrome in deer - large lungworm - diagnosis

A

long slender white nematodes in the trachea, bronchi, or smaller airways are presumptive

examination of feces for larvae

histo

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24
Q

parasitism malnutrition syndrome in deer - large lungworm - implications

A

widespread and common problem in overpopulated WTD herds

common in elk in western us

young animals more vulnerable

no public health implications

many livestock species susceptible
- cross species transmission?

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25
Q

piebald anomaly in deer

A

genetic defect

variable expression

relative rare - <1%

pelage, skeleton, organ abnormalities
- scoliosis
- roman nose
- white patches

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26
Q

hemorrhagic disease of deer

A

two clinically indistinguishable diseases caused by distinct orbiviruses
- epizootic hemorrhagic disease virus
- bluetounge virus

distributed throughout climatic regions that are suitable for vector populations

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27
Q

hemorrhagic disease of deer - host

A

infection doesnt equal disease

wild ruminants
- many susceptible to infection
- in eastern north America primarily in WTD

domestic ruminants
- many susceptible to infection
- captive deer
- BTV may cause disease in sheep
- EHDV - rarely mild disease in cattle

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28
Q

hemorrhagic disease in deer - transmission

A

culicoides biting midges

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29
Q

hemorrhagic disease in deer - seasonality

A

predictable in late summer and early fall

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30
Q

hemorrhagic disease of deer - pathogenesis

A

virus-mediated endothelial injury leads to coagulopathy

edema -> hemorrhagic and necrosis -> ulceration

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31
Q

hemorrhagic disease of deer - clinical signs

A

acute or chronic

variety of clinical signs
- red skin and mucus membranes
- dull and rough coat
- appetite loss
- lethargy and depression
- swelling of head and neck
- reluctance to move to reecumbency

most often found dead

field signs
- deer mortality
- time of year
- acute lesions
- highly visible or unrecognized outbreaks

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32
Q

hemorrhagic disease in deer - chronic clinical signs and lesions

A

weight loss
lameness
emaciation
secondary infection
starvation and death over winter

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33
Q

hemorrhagic disease in deer - diagnosis

A

presumptive based on histoory and presentation

virus isolation
- dont freeze
- whole blood, spleen, lung, lymph node

PCR

serology

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34
Q

hemorrhagic disease in deer - population impacts

A

mortality is difficult to quantify
- varies outbreak
- can be vary high

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35
Q

hemorrhagic disease in deer - management

A

limited options in wild deer

rarely significant or sustained population impacts in wild deer
- can bae dramatic and concerning to public

translocation of deer from north to south

communication w agricultural sector

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36
Q

hemorrhagic disease in deer - captive deer

A

significant source of mortality in captive deer
- northern states
- northern deer moved south

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37
Q

hemorrhagic disease in deer - cattle

A

EHDV rarely associated with clincial disease

in north america often associated with large outbreak in deer

clinical signs non-specific and mimic other cattle diseases
- BVD, BTV, FMD, adenovirus
- fever, anorexia, oculonasal discharge, palpebral edema, lameness, salivation, oral hemorrhages and erosions

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38
Q

hemorrhagic disease in deer - changing patterns

A

numerous changes in epidemiology of EHD and BT in last decade
- new serotypes
- increased frequency in northern states
- increasing EHD reports in cattle around world

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39
Q

cutaneous fibroma in deer

A

virus induced tumor
- papillomavirus

transmission
- arthropod vectors
- contact possibly

seasonal

may spontaneously resolve

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40
Q

cutaneous fibroma in deer - clinical signs

A

smooth, dark, and hairless tumors

white on cut surface

significance depends on size and location
- interfere w vision and walking
- secondary infections if traumatized

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41
Q

cutaneous fibroma in deer - implications

A

no significant population impact
- severe lesions probably limited to immune-compromised animals

no public health implications form virus
- secondary bacterial infections?

no agricultural impacts

42
Q

coronavirus ecology and evolution

A

adapted over 50,000 years to virtually every species of animal including humans

rna gemone prone to error during replication

higher rates of recombination - key to cov replication

adaption into animals
- changes in the spike and receptor binding domains could alter species tropism and pathogenicity

43
Q

coronavirus in deer

A

first identified free living animal reservoir outside of humans

concides with increase in human case-rate

appear largely asymptomatic

how does spillover happen
- contaminated food/environment?
- intermediary/bridging host?

44
Q

animal-human transmission of coronavirus

A

spillover back to humans

hard to monitor - who else infected in wild

become severe disease in animals - public health implications

45
Q

captive cervids

A

genetics, management, and nutrition to breed well-muscled deer, large and atypical antlers

46
Q

cervids - who should regulate

A

wild cervids - pa game commission
captive cervids - pa dept of agriculture

47
Q

fair chase

A

ethical, sportsmanlike, and lawful pursuit and taking of free-ranging wild, native North American big game animal in a manner that does not give the hunter and improper advantage

48
Q

chronic wasting disease

A

transmissible neurologic disease

transmissible spongiform encephalopathy (tse)
- BSE in cattle
- scrapie in sheep and goats
- CJD in humans

prions
- not a living organism
- abnormal form of a protein that is normally present in the nervous and lymphatic system that induces others to change
- can be spontaneous, food-born, or infectious
- accumulate in tissues and brain leading to tissue damage and cell death

49
Q

species barrier

A

natural mechanism that prevents a virus or disease from spreading from one species to another

50
Q

cwd - hosts

A

natural hosts - cervids

cattle and other domestic ruminants appear resistant to natural infections

generally a strong species barrier for most prion diseases

no evidence to infect humans

exposure most likely through infection

51
Q

cdw - infection

A

long incubation period

variable clinical phase

clinical signs nonspecific

100% fatal

52
Q

cwd - treatment

A

none for infected animals

no vaccine that prevents infection
- all failed
- distribution
- multiple boosters
- naturally occurs in body

53
Q

cwd - diagnosis

A

sample
- post mortem
- obex - part of brainstem
- retropharyngeal lymph node
- tonsil - hard in live animal

immunohisto - gold standard
microscopic lesions - poor sens
elisa - screening assay

live animal sampling under development
- reco-anal mucosal
- tonsillar biopsies
- pcr for proteins

54
Q

cdw - shedding and transmission

A

most challenging

prions excreted in saliva, feces, urine
- months before clinical signs

prions very environmentally stable

horizontal
- most likely oral exposure
- between animals
- direct or indirect

vertical
- possible

55
Q

cwd - disease spread

A

natural deer and elk movements

human assisted movements
- transport of high risk parts
- captive cervids

56
Q

cwd - population impacts

A

not completely defines
- direct or indirect mortality
- population reductions at high prevalence due to lowered survival and changes in long term dynamics
- eastern us

57
Q

cwd - social impacts

A

loss of hunter involvement

$ for conservation acts
- pr fund
- excise tax

change hunting regulations and traditions

$ for areas relying on income
- jobs
- tax revenue

divert attention from other acts
- expensive

58
Q

cwd - exposure risk factors

A

movement of cwd to new locations

captive cervids
imports of hunter killed carcasses from cwd infected areas
urine based attracants
rehab
translocation
areas adjacent to cwd positive wl orr captive herds

59
Q

cwd - amplification risk factors

A

increase prevalence of cwd

areas with high cervid density
batting and feeding
urine based or other attractants

60
Q

cwd - dma1

A

reduce movent, feeding, rehab, attractants, movement out of dma

increased surveillance

61
Q

furbearer

A

mammalian species traditionally trapped or hunted for fur

62
Q

canine distemper

A

globally one of the most significant infectious diseases of domestic and wild carnivores

rna virus that attacks epithelial tissues

related to genus morbillivirus

not hardy and inactivates easily
- can persist in cold temperatures

63
Q

canine distemper - hosts

A

wide and continues to expand
- carnivores and omnivores

in eastern us most common to experience disease
- raccoon
- skunk
- gray fox

64
Q

canine distemper - transmission

A

viral shedding
- can begin as early as 7 days post infection and last for 90 days
- subclinical animals shed
- recover and asymptomatic shed
- excreted in all body excretions

primarily respiratory transition
- feces
- urine
- transplacental

subclinical in older animals

65
Q

canine distemper - virus replication

A

replicates in lymphoid tissue of respiratory tract

spreads to all lymphatic tissue

spreads to epithelial tissues in respiratory, gi, urogenital tracts

spreads to cns

replication in these tissues results in disease

66
Q

canine distemper - epidemiology

A

severity depends on host species, age, viral strain immune status

summer/spring
juveniles

periodic epidemics may occur

67
Q

canine distemper - clinical signs

A

10-14 days post infection

non specific
- fever, cough, nasal/ocular discharge, diarrhea, cns signs

68
Q

canine distemper - lesions

A

gross lesions
where replicates most
ocular/nasal discharge, crusty footpads, emaciation, bronchopneumonia, bronchitis, gastroenteritis

microscopic lesions
necrosis and inflammation of multiple tissues
intranuclear and cytoplasmic inclusion bodies in epithelial tissues or brain

cvd is immunosuppressive
- secondary infections

69
Q

canine distemper - diagnosis

A

cs nonspecifc and can look like rabies
- gross lesions not definitive

fluorescent antibody tests
immunohisto
PCR
virus isolation
serology

rule out rabies first

70
Q

canine distemper - impacts

A

some population level in some species in wildlife
- captive
- new hosts and locations
- endangered species
- raccoons
- skunks
- gray fox

domestic
- canids highly susceptible
- vaccination
- vaccine challenges in exotics

humans
- none

71
Q

canine distemper - management

A

mlv not recommended for wl
- black footed ferret

72
Q

baylisascaris spp.

A

intestinal roundworm
- people think earthworm

4 species in North American wildlife
- raccoons, skunks, bears, badgers

b, procyonis (raccoon) most common implicated in human disease

73
Q

baylisascaris procyonis

A

raccoon definitive host - no disease
- reside in intestines and eggs excreted in feces
- patent infection 50-76 days post infection
- eggs extremely hardy in environment
- eggs require 2-4 weeks in environment to become infections
- raccoons ingest cyst or eggs and cycle continues

larval stages can migrate though organs of paratenic host and encysts
- visceral, ocular, neural
- move to cns

common in northesast and midwest
juveniles

may cause obstruction or perorations

severity in paratenic host depends on number of eggs and location

74
Q

baylisarscaris procyonis - diagnosis

A

definitive host
- fecal examination for eggs
- recovery of adult worms from small intestine

paratenic host
- antemortem challenging - not shedding, no adults in gi
- case history and neurologic signs suggestive
- histo of spinal cord and brain to demonstrate larvae
- digestion of fresh tissue in hydrochloric acid/pepsiin to recover and identify larvae

lateral alae

75
Q

bylisascaris procyonis - implications

A

wildlife
- substantial mortality among aberrant host populations
- rehab centers
- relocations
- increase public education

human
- neural, ocular, viseral larval migrans
- fatal infections
- children
- discourage racoons and skunks as pets
- avoid feces with embryonated eggs
- ppe

domestic animals
- susceptible
- evidence of dogs as definitive host

76
Q

parvovirus

A

smallest viruses of vertebrates

host range varies
- raccoons at rebag
- wild and domestic canids and felids
- ferrets
- mink

77
Q

parvovirus - clinical signs and lesions

A

target gi
- gastroenteritis
- diarrhea, lethargy, depression, no appetite

gross lesions
- watery diarrhea
- dehydration
- brown tinged fluid w fibirn
- thin intestinal wall
- fibrinonecrotizing enteritis

histo
- small intestine most severely affected
- blunting fusion of villi
- crypt necrosis and abscesses
- ulceration and attenuation of epithelium

78
Q

parvovirus - transmission

A

fecal oral is primary

contact w contaminated feces or fomites
- highly stable

79
Q

parvovirus - diagnosis

A

signalment and cs
fecal elisa
histo
immohisto
virus isolation
pcr
serology

80
Q

rabies

A

rhabdovirus
single stranded rna
7 types
bullet shaped

81
Q

rabies - host range

A

very wide - all mammals susceptible

major wildlife reservoirs in us are omniviores and carnivores
- most often infected - keep virus circulating
- raccoon, skunk, fox, coyote, bat

82
Q

rabies - molecular epidemiology

A

multiple rabies viral variants appear to be specific to particular species

molecular technique can identify

dominant viral variants and reservoir vary w country and region

83
Q

rabies - transmission

A

infected saliva or nervous system tissue is in contact w breaks in skin or mucous membranes of eyes, nose, mouth

most from bites or scratches

sporadic
- aerosolization
- mucous membranes
- organ transplant

not considered exposure
- petting rabid animal
- blood, urine, feces

long incubation period

84
Q

rabies - infection

A

local viral replication at site of exposure in muscle

enter peripheral nerves

brain and spinal cord - variable time and asymptomatic

viral dissemination and replication once in brain and spinal cord
- clinical disease
- within 10 days of infecting brain

spreads to salivary gland
- can transmit

85
Q

rabies - transmission 2

A

mammals may have virus in their salvia and be able to transmit for a short time wo clinical signs

clinically healthy animals may be able to transmit for short time

wl - euth and test

domestic
- infected and bite human - 10 day quarantine to see if in salivary gland
- bit and don’t know if raccoon is positive - 120/46 day quarantine looking for clinical signs

86
Q

rabies - clinical signs

A

fatal encephalitis w wide variety of behavior changes
- ataxia, lethargy, seizures, tremors, unprovoked attacks, self mutilation, furious, dumb, drooling

mimic other diseases

convulsions, coma, death

87
Q

rabies - lesions

A

no gross lesions associated directly w viral infection
- self mutliation
- lesions from head pressing - deer
- porcupine, broken teeth, sticks in oral cavity

microscopic inflammation of brain
- encephalitis

negri bodies

88
Q

rabies - diagnosis

A

history and signalment

cs nonspecific - suggestive

antemortem rarely used minus serology

post moretum - brainstem/salivary gland
- don’t damage head
- no freezing - refrigerate

fluorescent antibody test
histo
ihc
PCR

always test for rabies before submitting tissues for other diagnostics

89
Q

rabies - implications

A

substantial mortality in wildlife

significant and expensive

90
Q

rabies - management

A

nealry uniformly fatal in non vax host once cs occur

no realistic treatment once cs have started in humans or domestic animals

vaccination is effective

biosafety

care for bite or scratch

post exposure treatment

doctor asap - not emergency but urgent

oral baiting to keep east

91
Q

rabies - what constitutes exposure

A

direct
- bite from rabid mammal
- scratch that breaks skin from rabid mammal
- salival or neural tissue from contagious rabid animal contacting an open wound, break in skin, mucus membranes in eyes, nose, mouth

indirect
- survives on inanimate objects till saliva/tissue is dry
- sunlight kills
- freezing and moisture preserves

92
Q

black bears in PA

A

regulated hunting
- done first
- no bait
- no dogs

bear tag
- monitor how many hunted
- monitor hibernation

restocking
- genetically same in some areas

habitat restoration

research
- understand reproduction

93
Q

mange

A

contagious parasitic disease of the skin caused by mites
- multiple species of mites vary between species

syndrome - itchy, hairless, crusty skin

94
Q

mange - clinical signs and lesions

A

itching, behavior changes, loss of body condition

variable hair loss, thickened and crusted skin, foul smell, secondary bacteria and yeast infection

95
Q

mange in bears

A

sarcoptes scabiei

ursicoptes americanus

demodex ursi
- species specific
- follicle - no disease unless immune suppression

96
Q

sarcoptic mange - background

A

sarcoptes scabiei

scabies in humans

many species of domestic and wild animals

variants named from isolated host
- species strain more severe infection but can infect other species

in north america most common in wild canids

97
Q

sarcoptic mange - life cycle and transmission

A

all life stages in outer layers of skin in same host
- create tunnels in epidermis to lay eggs

can reach high densities on infected host skin

transmission - direct and indirect
- direct is main
- indirect through environment - feeding, trapping and release, breeding, family groups, dens

bears solitary

inactive extreme hot or cold

98
Q

sarcoptic mange - clinical signs and lesions

A

due to burrowing causing destruction of skin
- immune response
- secondary infection

variable hair loss
thick and crusted skin
foul smell

99
Q

mange in bears - diagnosis

A

active mite infections

cytology
history
per for mite dna

prior exposure to detect antibodies

100
Q

mange - implications

A

wl - canids, emerging in black bears

domestic - many species, especially domestic dogs
- flea and tick meds

human
- sarcoptes scabiei îs zoonotic

101
Q

mange - management

A

euth

treat w ivermectin (mult treatments doest kill eggs)

bravest - last longer, expensive, wd time

decrease feeding, baiting, bird feeders

does problem need managed