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VBSC 409 > EXAM 3 - 8 Lectures > Flashcards

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
piebald anomaly in deer
genetic defect variable expression relative rare - <1% pelage, skeleton, organ abnormalities - scoliosis - roman nose - white patches
26
hemorrhagic disease of deer
two clinically indistinguishable diseases caused by distinct orbiviruses - epizootic hemorrhagic disease virus - bluetounge virus distributed throughout climatic regions that are suitable for vector populations
27
hemorrhagic disease of deer - host
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
28
hemorrhagic disease in deer - transmission
culicoides biting midges
29
hemorrhagic disease in deer - seasonality
predictable in late summer and early fall
30
hemorrhagic disease of deer - pathogenesis
virus-mediated endothelial injury leads to coagulopathy edema -> hemorrhagic and necrosis -> ulceration
31
hemorrhagic disease of deer - clinical signs
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
32
hemorrhagic disease in deer - chronic clinical signs and lesions
weight loss lameness emaciation secondary infection starvation and death over winter
33
hemorrhagic disease in deer - diagnosis
presumptive based on histoory and presentation virus isolation - dont freeze - whole blood, spleen, lung, lymph node PCR serology
34
hemorrhagic disease in deer - population impacts
mortality is difficult to quantify - varies outbreak - can be vary high
35
hemorrhagic disease in deer - management
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
36
hemorrhagic disease in deer - captive deer
significant source of mortality in captive deer - northern states - northern deer moved south
37
hemorrhagic disease in deer - cattle
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
38
hemorrhagic disease in deer - changing patterns
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
39
cutaneous fibroma in deer
virus induced tumor - papillomavirus transmission - arthropod vectors - contact possibly seasonal may spontaneously resolve
40
cutaneous fibroma in deer - clinical signs
smooth, dark, and hairless tumors white on cut surface significance depends on size and location - interfere w vision and walking - secondary infections if traumatized
41
cutaneous fibroma in deer - implications
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
coronavirus ecology and evolution
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
coronavirus in deer
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
animal-human transmission of coronavirus
spillover back to humans hard to monitor - who else infected in wild become severe disease in animals - public health implications
45
captive cervids
genetics, management, and nutrition to breed well-muscled deer, large and atypical antlers
46
cervids - who should regulate
wild cervids - pa game commission captive cervids - pa dept of agriculture
47
fair chase
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
chronic wasting disease
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
species barrier
natural mechanism that prevents a virus or disease from spreading from one species to another
50
cwd - hosts
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
cdw - infection
long incubation period variable clinical phase clinical signs nonspecific 100% fatal
52
cwd - treatment
none for infected animals no vaccine that prevents infection - all failed - distribution - multiple boosters - naturally occurs in body
53
cwd - diagnosis
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
cdw - shedding and transmission
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
cwd - disease spread
natural deer and elk movements human assisted movements - transport of high risk parts - captive cervids
56
cwd - population impacts
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
cwd - social impacts
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
cwd - exposure risk factors
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
cwd - amplification risk factors
increase prevalence of cwd areas with high cervid density batting and feeding urine based or other attractants
60
cwd - dma1
reduce movent, feeding, rehab, attractants, movement out of dma increased surveillance
61
furbearer
mammalian species traditionally trapped or hunted for fur
62
canine distemper
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
canine distemper - hosts
wide and continues to expand - carnivores and omnivores in eastern us most common to experience disease - raccoon - skunk - gray fox
64
canine distemper - transmission
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
canine distemper - virus replication
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
canine distemper - epidemiology
severity depends on host species, age, viral strain immune status summer/spring juveniles periodic epidemics may occur
67
canine distemper - clinical signs
10-14 days post infection non specific - fever, cough, nasal/ocular discharge, diarrhea, cns signs
68
canine distemper - lesions
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
canine distemper - diagnosis
cs nonspecifc and can look like rabies - gross lesions not definitive fluorescent antibody tests immunohisto PCR virus isolation serology rule out rabies first
70
canine distemper - impacts
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
canine distemper - management
mlv not recommended for wl - black footed ferret
72
baylisascaris spp.
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
baylisascaris procyonis
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
baylisarscaris procyonis - diagnosis
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
bylisascaris procyonis - implications
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
parvovirus
smallest viruses of vertebrates host range varies - raccoons at rebag - wild and domestic canids and felids - ferrets - mink
77
parvovirus - clinical signs and lesions
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
parvovirus - transmission
fecal oral is primary contact w contaminated feces or fomites - highly stable
79
parvovirus - diagnosis
signalment and cs fecal elisa histo immohisto virus isolation pcr serology
80
rabies
rhabdovirus single stranded rna 7 types bullet shaped
81
rabies - host range
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
rabies - molecular epidemiology
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
rabies - transmission
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
rabies - infection
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
rabies - transmission 2
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
rabies - clinical signs
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
rabies - lesions
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
rabies - diagnosis
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
rabies - implications
substantial mortality in wildlife significant and expensive
90
rabies - management
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
rabies - what constitutes exposure
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
black bears in PA
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
mange
contagious parasitic disease of the skin caused by mites - multiple species of mites vary between species syndrome - itchy, hairless, crusty skin
94
mange - clinical signs and lesions
itching, behavior changes, loss of body condition variable hair loss, thickened and crusted skin, foul smell, secondary bacteria and yeast infection
95
mange in bears
sarcoptes scabiei ursicoptes americanus demodex ursi - species specific - follicle - no disease unless immune suppression
96
sarcoptic mange - background
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
sarcoptic mange - life cycle and transmission
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
sarcoptic mange - clinical signs and lesions
due to burrowing causing destruction of skin - immune response - secondary infection variable hair loss thick and crusted skin foul smell
99
mange in bears - diagnosis
active mite infections cytology history per for mite dna prior exposure to detect antibodies
100
mange - implications
wl - canids, emerging in black bears domestic - many species, especially domestic dogs - flea and tick meds human - sarcoptes scabiei îs zoonotic
101
mange - management
euth treat w ivermectin (mult treatments doest kill eggs) bravest - last longer, expensive, wd time decrease feeding, baiting, bird feeders does problem need managed

VBSC 409 (3 decks)

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