EXAM 3 - 8 Lectures Flashcards
carrying capacity
the number of animals and area will support
depends on quality of the habitat
ecologic/biologic carrying capacity
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
wildlife acceptance capacity
social - how much people will put up with the animals
often the limiting factor
brain abscesses in deer
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
brain abscesses in deer - clinical signs
wide variety of neurological signs depending on speed of progression and entry into brain
loss of fear
aggression
circling
head pressing,
paralysis,
emaciation +/-
brain abscesses in deer - lesions
draining tracks/pus in the skin/subcutis
inflammation in subcutis
necrosis of skull bones
abscesses in cranial vault
antler fractures
disseminated lesions
brain abscesses in deer - diagnosis
tentative based on gross lesions/clinical signs
culture and identification of bacteria to confirm
bone damage helpful with skeletal remains
brain abscesses in deer - wildlife implications
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)
brain abscesses in deer - public health and agricultural implications
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
TB in deer
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
TB in deer - transmission
inhaltion or ingestion
bacteria secreted in sputum, urine, feces, and abscesses
persist for 5 months in cold/damp conditions
enhanced by crowding and stress
TB in deer - clinical signs and lesions
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
TB in deer - in MI
extensive feeding and baiting is a risk factor
- artificially raises carrying capacity
- increases nose-nose contact and indirect contact w contaminated feed
meningeal worm in deer
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
meningeal worm in deer - life cycle
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
meningeal worm in deer - clinical signs and lesions
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
meningeal worm in deer - diagnosis
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
meningeal worm in deer - implications
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
parasitism malnutrition syndrome in deer
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
parasitism malnutrition syndrome in deer - large lungworm
dictyocaulus viviaprus
- large nematode of airways
ubiquitous distribution
wide host range
- deer
- elk
- moose
- cattle
- sheep
- goats
parasitism malnutrition syndrome in deer - large lungworm - life cycle
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
parasitism malnutrition syndrome in deer - large lungworm - clinical signs and lesions
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
parasitism malnutrition syndrome in deer - large lungworm - diagnosis
long slender white nematodes in the trachea, bronchi, or smaller airways are presumptive
examination of feces for larvae
histo
parasitism malnutrition syndrome in deer - large lungworm - implications
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?
piebald anomaly in deer
genetic defect
variable expression
relative rare - <1%
pelage, skeleton, organ abnormalities
- scoliosis
- roman nose
- white patches
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
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
hemorrhagic disease in deer - transmission
culicoides biting midges
hemorrhagic disease in deer - seasonality
predictable in late summer and early fall
hemorrhagic disease of deer - pathogenesis
virus-mediated endothelial injury leads to coagulopathy
edema -> hemorrhagic and necrosis -> ulceration
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
hemorrhagic disease in deer - chronic clinical signs and lesions
weight loss
lameness
emaciation
secondary infection
starvation and death over winter
hemorrhagic disease in deer - diagnosis
presumptive based on histoory and presentation
virus isolation
- dont freeze
- whole blood, spleen, lung, lymph node
PCR
serology
hemorrhagic disease in deer - population impacts
mortality is difficult to quantify
- varies outbreak
- can be vary high
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
hemorrhagic disease in deer - captive deer
significant source of mortality in captive deer
- northern states
- northern deer moved south
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
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
cutaneous fibroma in deer
virus induced tumor
- papillomavirus
transmission
- arthropod vectors
- contact possibly
seasonal
may spontaneously resolve
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
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
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
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?
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
captive cervids
genetics, management, and nutrition to breed well-muscled deer, large and atypical antlers
cervids - who should regulate
wild cervids - pa game commission
captive cervids - pa dept of agriculture
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
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
species barrier
natural mechanism that prevents a virus or disease from spreading from one species to another
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
cdw - infection
long incubation period
variable clinical phase
clinical signs nonspecific
100% fatal
cwd - treatment
none for infected animals
no vaccine that prevents infection
- all failed
- distribution
- multiple boosters
- naturally occurs in body
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
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
cwd - disease spread
natural deer and elk movements
human assisted movements
- transport of high risk parts
- captive cervids
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
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
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
cwd - amplification risk factors
increase prevalence of cwd
areas with high cervid density
batting and feeding
urine based or other attractants
cwd - dma1
reduce movent, feeding, rehab, attractants, movement out of dma
increased surveillance
furbearer
mammalian species traditionally trapped or hunted for fur
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
canine distemper - hosts
wide and continues to expand
- carnivores and omnivores
in eastern us most common to experience disease
- raccoon
- skunk
- gray fox
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
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
canine distemper - epidemiology
severity depends on host species, age, viral strain immune status
summer/spring
juveniles
periodic epidemics may occur
canine distemper - clinical signs
10-14 days post infection
non specific
- fever, cough, nasal/ocular discharge, diarrhea, cns signs
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
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
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
canine distemper - management
mlv not recommended for wl
- black footed ferret
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
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
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
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
parvovirus
smallest viruses of vertebrates
host range varies
- raccoons at rebag
- wild and domestic canids and felids
- ferrets
- mink
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
parvovirus - transmission
fecal oral is primary
contact w contaminated feces or fomites
- highly stable
parvovirus - diagnosis
signalment and cs
fecal elisa
histo
immohisto
virus isolation
pcr
serology
rabies
rhabdovirus
single stranded rna
7 types
bullet shaped
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
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
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
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
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
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
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
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
rabies - implications
substantial mortality in wildlife
significant and expensive
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
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
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
mange
contagious parasitic disease of the skin caused by mites
- multiple species of mites vary between species
syndrome - itchy, hairless, crusty skin
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
mange in bears
sarcoptes scabiei
ursicoptes americanus
demodex ursi
- species specific
- follicle - no disease unless immune suppression
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
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
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
mange in bears - diagnosis
active mite infections
cytology
history
per for mite dna
prior exposure to detect antibodies
mange - implications
wl - canids, emerging in black bears
domestic - many species, especially domestic dogs
- flea and tick meds
human
- sarcoptes scabiei îs zoonotic
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