EXAM 2 - 10 Lectures Flashcards
Chelonian (turtles) Upper Respiratory Disease - Overall Clinical Signs
ocular discharge
nasal discharge
blepharoedema - eye swelling
oral plaques
depression/lethargy
asymmetrical nares
nasal erosion
skin depigmentation
Chelonian URD - Ranavirus (FV3)
causes local outbreaks with high morbidity and mortality
survives can become carriers - consider euthanasia
Chelonian URD - Ranavirus Transmission
direct contact
indirectly through water, sediment, ingestion
Chelonian URD - Ranavirus Epidemiology
outbreaks cause 28-71% declines in focal populations
outbreaks may occur as spillover events from amphibians
survivors becoming carriers
- possible role in viral persistence in wetlands
- prolonged shedding in re-infected turtles
Chelonian URD - Ranavirus Disease Presentation
lethargy
anorexia
ophthalmic signs
nasal discharge
oropharyngeal lesions
edema
respiratory distress
mortality within 30 days of developing clinical signs
indistinguishable from mycoplasma, herpesviruses - coinfections possible
Chelonian URD - Ranavirus Pathogenesis and Treatment
pathologic changes are severe and systemically distributed
death due to multiorgan failure
treatment typically not recommended
- not often successful
- carriers
Chelonian URD - Mycoplasma
chronic upper respiratory tract disease recognized in desert and gopher tortoises
agassizii and tesudineum
tiny bacteria that lack cell walls - don’t persist in the environment
causes local outbreaks with moderate morbidity and low mortality - or can be endemic
survivors become chronically infected - disease recurs with stress
- euthanasia not recommended
Chelonian URD - Mycoplasma Transmission
direct contact
fomites
Chelonian URD - Mycoplasma Clincal Signs
nasal and ocular discharge
conjunctivitis
palpebral edema
intermittent
Chelonian URD - Mycoplasma Contributing Factors
environmental stressors
human factors
toxicant esposure
capture and release of ill animals
Chelonian URD - Herpesviruses
many different viruses affect turtles
large enveloped dsDNA
associated with respiratory disease, fibropapilloma, and other presentations
epidemiology not well understood
survivors become chronically infected
- disease recurs with stress
- euthanasia not recommended
Chelonian URD - Herpesviruses Transmission
direct
mother to offspring
URD Diagnostics
cannot be clinically distinguished
- requires diagnosis
most practical approach in live animals
- oral/cloacal swab PCR for all 3
- optimal sensitivity vs oral or cloacal swab alone
- whole blood PCR for FV3
some labs offer UR panel
postmortem histopathology and molecular testing
URD Management
treatment not recommended for FV3
herpes and mycoplasma treatment
- supportive care - heat, fluids, nutrition, nebulization
- decrease stress
- manage secondary infections
- antibiotics - mycoplasma
- antiviral - herpes
biosecurity
- gloves
- treatment order
- disinfection - remove organic debris - 3% bleach x 1 min
Ophidiomycosis (Snake Fungal Disease) Background
emerging disease in snakes worldwide
all species appear to be susceptible
impacts species of conservation concern
caused by fungus Ophidiomyces ophidiicola - snake fungal disease
- can persist in soil over wide temps and pH
- keratinophilic
- opportnistic
SFD Transmission
not fully understood
contact with infected snakes?
contact with infected soils?
at birth?
SFD Disease Presentation
general signs
- lethargy
- difficulty shedding
skin lesions
- raised and discolored scales
- necrotic scales
- pustules and granulomas
- crusts
- ulcers
additional lesions
- oclar
- ventral neck swelling
- jaw deformit
- rostrum crusting
- rostrum ulceration
secondary impacts of infection
- difficulty eating, reproducing, defecating
FSD Diagnosis
from dermal punch
- qPCR
- histopathology
- fungal culture
swab
- from qPCR
FSD Treatment
can take months to years
medication
- antifungal
- terbinafine greatest success
administration
- oral, injectable
- nebulization
monitoring
- physical exams for skin lesion improvement
- skin swabbing to detect fungus DNA every 30 days of nebulization
FSD Management
population-level impacts unclear
- need more surveillance
biosecurity
- gloves
- clean boots and equipment between sites
- disinfect natural materials before use in snake enclosures
environmental management?
Sea Turtle Fibropapillomatosis Background
likely caused by ChHV5
multifactorial etiology of tumor development and progression
mainly effects green sea turtles but reported in all marine turtle species
does not appear as a threat at population level
geographic distribution
- coastlines and continental shelf
- associated with pollution, anthropogenic impacts
Sea Turtle FP Clinical Presentation
single or multiple tumors that occur anywhere on the body
chronic condition - severity varies between individuals
histologically benign but can be detrimental based on size, location, and number
can become ulcerated and develop secondary bacterial or fungal infections
can impair vision and feeding
associated with emaciation and immunosuppresssion
Sea Turtle FP Transmission
viral shedding into the environment
potentially magnified by mechanical vectors - marine leeches
non-clinically infected turtles may also spread virus
biosecurity is important
Sea Turtle FP Diagnosis
cutaneous tumors are easily recognizable
definitive diagnosis requires histopathology
detection of ChHV5 from swabs or tissue
check for visceral disease using imaging, radiography, CT, MRI, ultrasound
Sea Turtle FP Treatment
supportive care essential
antivirals may be used but no proven efficacy
tumors can regress but is uncommon
surgical excision is most effective
- co2 laser, sharp excision, cryo, electochemo, electrocautery
possibility of tumor regrowth
Amphibians
3 major orders
- anura - frogs and toads
- urodela - salamanders and newts
- gymophiona - caecilians - not in US
defining characteristics
- vertebrates
- skin is smooth and shiny
- ectothermic
- permeable skin
- terrestrial and aquatic life stages
in US greatest diversity in southeast
Amphibian Conservation
populations declining worldwide
reasons for decline
- habitat destruction
- environmental contamination
- climate change
- introduced species
- disease
Ranivruses in Amphibians Background
large double stranded DNA
can infect all ectothermic vertebrates
conservation threat
- common frog in UK
- events in eastern box turtles
Raniviruses in Amphibians Disease Ecology
different viruses affect different species
transmission
- direct contact
- ingestion
- water exposure
Raniviruses in Amphibians Epidemiology
rapid large-scale dieoffs
90-100% mortality in tadpoles and adults
summer and spring - metamorphosis
larvae and juveniles most susceptible
Raniviruses in Amphibians Diagnosis and Mangement
diagnosis
- pcr
- virus isolation
- histopathology
- electron microscopy
no treatment
disinfection
quarantine
biosecurity
Raniviruses in Amphibians Clinical Signs
species/age dependent
abnormal behavior/lethargy
hemorrhage
edema
ulceration
death
Raniruses in Amphibians Diagnosis and management
PCR
virus isolation
histopathology
electron microscopy
no treatment
disinfection
quarantine
biosecurity
BD Chytridiomycosis Background
infectious disease of amphibians
caused by fungus Batrachochytrium dendrobatidis
name derived by blue poison dart frog
global amphibian trade
“out of asia” hypothesis
BD Pathogen Lifecycle and Transmission
infects keratinized epithelium
multiples by producing flagellated zoospores then shed into the environment - live for weeks in water
transmission
- motile zoospores via direct contact
- contact with infected water or substrate
BD Clinical Signs
vary based on species and life stage
skin thickening - impacts oxygen exchange, thermoregulation, nutrient absorption, hydration
lesions on vetrm and feet
increased skin shedding and retained shed (dysecdysis)
skin discoloration - reddening
roughened skin texture
weakness, convulsions
loss of righting ability
death
BD Diagnosis and Treatment
multiple options for detection
- swabs from live animals
- histopathology on dead animals
- wet mounts
- cytology
- PCR
treatment options
- supportive care
- baths
biosecurity is key
Salamander Chytridomycosis Background
caused by fungus Batrachochytrium salamandrivorans
host range restricted to caudate
fungus infects epidermal skin cells -> multifocal skin ulcerations
not in US yet
- higher risk in areas with more pet trade
- coast (pet trade)
- appalachia (highest species richness)
active surveillance of wild salamanders and education of owners to prevent introduction
Dermocystid Parasites Background
prostist
mostly in european anurans and urodeles
Dermocystid Parasites Presentation in Amphibians
single or multiple cutaneous lesions
observed infrequently within gastrointestinal mucosa and internal organs such as liver
Dermocystid Impacts on Hosts
host response is minimal until they rupture
complete resolution in mildly infected individuals in a few weeks
heavy infection can cause more severe clinical signs and pathologic changes
- regional edema and hemorrhage
- extensive cutaneous ulcerations
- secondary bacterial infections
- death
Dermocystid Disruption of Amphibian Skin
plays major role in osmoregulation, electrolyte balance, and defense against pathogen invasion
heavy dermocystid burdens may result in death due to fatal electrolyte disturbances
opportunistic secondary infections may contribute to morbidity and mortality
change cutaneous microbiome leading to immune dysfunction
Waterbird
bird that lives on or around water
Waterfoul
birds within the order Anseriformes - ducks, geese, swans
Avian Botulism
also called limberneck
caused by ingestion of neurotoxin produced by clostridium botulinum
- intoxication not infection
- affect neuromuscular junction
only vegetative (replicating) bacteria produce toxin
seven types
- disease syndrome similar between types
- spaces affected vary between types
- avian botulism - c (waterfowl) and e (fish eating species)
- humans - a
Avian Botulism - Clostridium botulinum
gram-positive rod
spore forming
- dormant
- adverse environmental conditions
- found in tissues of various wetland organisms
- viable for years
- resistant to heath
strict anaerobe (no oxygen)
optimal conditions for bacterial growth
- high protein substrate for energy
- 77-104 F
Avian Botulism - Botulinum Toxin
produced when spores germinate and bacteria is actively growing and multiplying
neurotoxin
prevents release of acetylcholine
reduces/blocks the passage of impulse from nerves to muscle receptors
muscles do not contract
Avian Botulism - Clinical Signs
depressed, lethargic
ascending paralysis - limberneck
paralysis of inner eyelid
death due to respiratory failure or drawing
presence of healthy, sick, and dead birds
lesions
- none
- +/- food source of toxin in GI tract
Avian Botulism Type C
primary cause of avian botulism in waterfoul - major mortality factor
C.botulinum spores widely distributed in aquatic habitats
human associated changes to environment influence outbreaks
- sewage - anaerobic in water - provide protein
- runoff
- draining and flooding
Avian Botulism Type C Toxin Production
warm temperature - summer and early fall
low dissolved oxygen - carcasses or vegetation
protein substrate - carcasses, vegetation, sewage
Avian Botulism Type C Delivery of Toxin to Birds
invertebrate food
decaying organic matter
maggots - concentrate toxins
habitat may become seeded with spores - repeated outbreaks
Avian Botulism Type E
same clinical signs as Type C
fish-eating birds - loons, gulls, diving ducks, grebes, mergansers
repeated outbreaks in great lakes
summer and fall
often associated with fish kills
though to be associated with ingestion of certain fish and mussel species
Avian Botulism Diagnosis
based on history and clinical signs
confirmation by demonstration of toxin in serum or tissues of sick birds by mouse protection test
- ethics
- look for antitoxin response
- +/- ELISA for toxin
- +/- PCR for toxin
Avian Botulism Management
minimize human influences
- maintain water quality
- minimize factors that input large amounts of decaying organic matter
outbreak management
- carcass pickup
- hazing - keep birds away
- care for sick birds
- flooding - diluting
Avian Botulism Public Health Implications
most human botulism caused by improperly canned foods - a and b
fairly resistant to c
susceptible to e - poorly cooked or smoked fish
Avian Botulism Prevention
cooking destroys toxin
PPE
Duck Plague
also called Duck Viral Enteritis
caused by alphaherpesvirus
- persistent in water
- attacks vasculature and lymphoid tissue - hemorrhage and necrosis
acutte and often fatal
carriers
- virus remains persistently latent in asymptomatic birds - in trigeminal ganglia
- stress causes reactivation
only ducks, geese, swans
- variability between species
- teal most susceptible
- pintails most resistant
most often involves captive or feral ducks
highly variable based on
- species
- age
- sex
- strain
- immune status
- inoculation/exposure
Latency
ability of a pathogenic virus to lie dormant in a cell
Duck Plague Clinical Signs - Acute
good body condition
bleeding and necrosis
bloody discharge from nares and vent
prolapsed penis
loss of wariness or cant fly
convulsions
neurologic
Duck Plague Lesions
GI hemorrhage, ulcers, inflammation
multifocal liver necrosis
heart hemorrhaging
ulcers in oropharynx under tongue - not always
microscopically seen
- intanuclear inclusion bodies seen in liver
Duck Plague Transmission
excreted by infected birds in oral secretions and feces
spread by contact with infected waterfowl or environments
- carcasses and secretions
Duck Plague Epidemiology
april-june cause 70% of outbreaks
- stress - seasonal changes, breeding, crowding
often adult birds
species differences
potentially increasing in the Atlantic flyway
Duck Plague Outbreaks
important in farmed/captive waterfoul
- global
feral ducks
sporadic outbreaks in wild waterfowl - huge
no public health implications
Duck Plague Mangement
debate on role of wild vs captive as reservoirs
carcass collection and disposal
limit contact with domestic waterfowl
euthanasia of carriers?
vaccine available for captive waterfowl
Avian Cholera
called fowl cholera or avian pasteurellosis
infection with bacterium pasteurella mulocida
- gram negative
- 16 serotypes
- 1 most prevalent in waterfowl
rapidly fatal septicemia in waterfowl
normal flora in mouths of some mammals
- bites or secretions can be source of infection in domestic birds
wide host range - susceptibility highly variable
common in waterfowl
sporadic mortality in diversity of other avian taxa
sudden onset with rapid mortality
associated with dense congregation of birds
often with arrival of specific species
- snow geese
sick birds rarely observed
- dead birds
- “fall from sky”
Avian Cholera Clinical Signs
mucoid discharge from nose or mouth
lethargy and incoordination
swimming in circles
tremors and convulsions
Avian Cholera Lesions
presence and seveity of gross lesions depend on how long bird survives beofree death
god nutritional condition
hemorrhages on surfaces of heart - common
multifocal liver necrosis - common
hemorrhages on surfaces of gizzard - variable
fibrinous casts in intestine - variable
Avian Cholera Transmission
infected birds are primary source for waterfowl
- contaminate environment
- carriers suspected
indirect transmission by inhalation or ingestion of bacteria in food or water
- contaminate environment
- poor persistence
- carcasses, nasal discharge, feces from infected birds
- bacteria present in surface waters
direct bird to bird contact
spillover into mammalian species
Avian Cholera Outbreaks
more common in central and western us
winter and spring during migration
most outbreaks in atlantic flyway
explosive outbreaks with high mortality in waterfowl
asymptomatic carriers
very infectious
low risk to humans
Avian Cholera Diagnosis
based on history and gross lesions
confirmed by culture and identification of P. multocida
- heart, liver, bonemarrow
submission of full carcass preferred to rule out other causes of acute mortality
Avian Influenza Virus
high and low path
high capacity to change
don’t ever say never or always
Genetic Drift
mutaitons
gradual, constant, accumulation of mutations - small changes
loss of immunity
Genetic Shift
reassortment
abrupt exchange of gene segments - large changes
host barrier jumps
emergence of new strains
AIV Wild Bird Reservoir System
low path
reservoir - waterfowl, gulls, terns, shorebirds
source of all subtypes
transmission - fecal oral route via water
asymptomatic infection - no lesions
high path rarely isolated from wild birds
spillover to aberrant hosts is common
AIV Spillover into Poultry
how high path emerges
requires multiple steps
not all steps may be detected
cant go back into ducks
introduction
- direct contact
- indirect - water, habitats
- fomites - poultry workers, birds, rodents
AIV in Gallinaceous Poultry
low path
- low mortality
- respiratory disease - sneeze, cough, ocular/ nasal discharge, sinuses
- reproductive disease - egg production
high path
- acute and high mortality
- severe depression
- neurologic signs
AIV Impacts on Poultry
economic loses
- depopulation and disposal
- high morbidity and mortality
- quarantine and surveillance
- indemnities
AIV Prevention and Management in Poultry in North America
understanding risk
biosecurity
testing for early detection
vaccination
- not feasible
- virus change
- shut down trade - serology
- larger amount of birds
AIV in Waterfowl
viral replication occurs primarily in epithelial cells lining the intestinal tract
- infection does not produce overt clinical disease
- rarely associated with any lesions
high concentrations excreted in feces
transmitted through indirect fecal-oral route involving water on shared habitats
- dependent on pH and temperature
peak prevalence in summer/early fall at pre-migrational staging areas
- northern US freshwater lakes
- high concentrations of juveniles
AIV Surveillance in PA Ducks
higher in juveniles than adults
higher in mallards and other dabbling ducks
AIV in Charadriiformes - Shorebirds and Gulls
extremely diverse
much less known about the biology of these species
Delaware bay - consistently found
- horseshoe crabs
one species, one location, one month
high prevalence in pre-fledge chick gulls
no clear spatial or species patterns
AIV Notable Outbreak Changes in North America
different strain
longer duration
more widespread
higher mortality in wild birds
wider diversity of wild birds
increased mammal cases
Game Bird
bird hunted for sport or food
chicken-like
wild turkeys in PA
Upland Game Bird
non-waterfowl game bird
diverse group
wild vs propagated - nonnative for hunting
migratory vs nonmigratory
Skin Lesions in Wild Turkeys
on unfeathered skin of head and legs is most common disease syndrome in wild turkeys
alone are no diagnostic
avian pox is most common cause
Avian Pox
poxvirus
- viral replication in cytoplasm of epithelial cells
- stimulate cell replication
- epidermal growth factor
diversity of species
different strains
environmentally hardy
most common cause of disease in wild turkeys in PA
not infectious in humans
Avian Pox - Dry Pox
nodules on unfeathered skin
can resolve in weeks if mild to moderate
Avian Pox Slides
hyperkeratosis
inclusion bodies
Avian Pox - Wet Pox
nodules/plaques on the mucosa of the oral cavity, esophagus, trachea
poor prognosis
more severe/virulent
Avian Pox Clinical Signs
nodules on skin or upper GI/respiratory tract
depend on size and location of nodules
weak
emaciated
blind
respiratory distress
Avian Pox Transmission
insects as mechanical vectors
inhalation or ingestion of virus containing scabs
virus can persist on surfaces and infect through mucous membranes
direct contact
Avian Pox Trends
in wild turkeys - not 100% accurate
anatomic - almost always unfeathered portions, wet pox lesions more common
seasonal - any time of year, most common in fall and winter - insect activity - time for nodules to form
Avian Pox Diagnosis
virus isolation
cytology - speed
histology - most common
- hypertrophy
- hyperplasia
- inclusion bodies
- hyperkerattosis
- ballooning degeneration
- secondary bacterial infection
Avian Pox Management
not many options for wildlife
minimize transmission from artificial sources (feeders) or fomites
treatment of individual birds is possible but not typically conducted in wildlife
disinfection
Retroviral Neoplasms in Wild Turkeys
rna virus
viral encoded reverse transcriptase creates proviral DNA from viral rna
integrate into host genome
pathogenesis
- oncogene
can have latent infections
lymphoid neoplasms
- don’t know cause
- viral associated
- spontaneous
LPVD Histopathology
infiltration of visceral organs and tissues by large numbers of pleomorphic lymphoid cells
LPVD in Domestic Turkeys
minor importance to poultry
transmission unknown
pathogenesis unknown
unknown how to propagate
common among clinically ill adult turkeys - formation of tumors is rare
Lymphoid Tumors in Wild Turkeys Clinical Signs
emaciated
weak
unable to move
unaware of surrounding
tumors in multiple organs/tissues
neoplastic lymphoid cells infiltrating internal organs
Lymphoid Tumors in Wild Turkeys Diagnosis
must identify goals of diagnosis
microscopic examination identify tumor
PCR to identify proviral DNA
LPVD Surveillance
want distal leg
most have no signs
no human health risks
Histomoniasis
also called blackhead
- blood pooling in head - uncommon
histomonas meleagridis
- protozoan parasite
initially replicate in epithelium of cecum resulting in tissue damage
- secondary bacterial infections from intestinal flora
- spread to liver
most wild and domestic galliforms susceptible
- clinical disease and parasite shedding varies
direct transmission possible but unlikely
- fragile in environment
reemergin in domestic turkeys
- no approved treatments
no human health implications
Histomoniasis Clinical Signs
weakness
emaciation
droopy wings
ruffled feathers
listlessness
sulfur yellow feces
lesions in cecum +/- liver
Histomoniasis Life Cycle
another parasite is vector
cecal worm heterakis gallinarum
- hardy eggs that survive in environment
earthworms eat eggs
chicken eats worm
Histomoniasis Diagnosis
gross lesions are suggestive
bioassay
PCR
histology
protozoa destroyed by freezing
Histomoniasis Management
limit exposure of vulnerable species to carriers
free ranging of poultry?
chicken liter as fertilizer - broiler aren’t shedding so not as many eggs
release of infected pen raised birds
Trichomoniasis
trichomonas gallinae
- protoxoan parasizte
predominately disease of columbiform birds
raptors that feed on infected doves may develop
no human health implications
upper respiratory track
young pigeons infected early with crop milk and remain carriers for life
parasite invades mucosal surface of oropharynx
Trichomoniasis Clinical Signs
weakness
respiratory distress
emaciation
swelling around oral cavity or neck
green or yellow fluid dripping from mouth
cankers in mouth - firm yellow to white masses
Trichomoniasis Transmission
direct
regurgitation feeding or ingestion of recently shed parasites in contaminated water or moist grains
poorly maintained feeder birds
platform and birdbaths
Trichomoniasis Diagnosis
gross lesions
microscopic examinations of scrapings
culture
freezing diminishes capability
differentiate from avian pox
histology
PCR
Trichomoniais Mangement
bird bath sanitation
reduce contact between carriers ad susceptible species
treatment
One Health
collaborative, multi-sectoral, transdisciplinary approach with the goal of achieving optimal health outcomes recognizing the interconnection between people, animals, plants, and their shared environment
Wildlife Health and Disease
is there a problem
can you define the problem through surveillance or research
- applied research
can you manage it
can you measure success or failure
Ruffled Grouse
bonasa umbellus
native wild galliform
young forest habitat - different stages, brush
boom or bust population cycles
declines in mid Atlantic and southeast
West Nile Virus in Wild Birds
flavivirus
arbovirus - arthropod born
broad host range
potential populaiton impats
immunity in survivors is thought to be long lived
most common sign - dead bird
neurological abnormalities
highly susceptible species
- crows, raptors, sage grouse, pelicans
mosquitoes
frequent spillover
urban - suburban
mammals are dead end host
West Nile Virus in Humans
asymptomatic to fatal neurologic disease
- most asymptomatic
flu-like symptoms
prevention focuses on limiting mosquito exposure
West Nile Surveillance
human disease
- hospital
- department of health
mosquito surveillance
horces
dead bird testing and serology
sentinels
West Nile - Is There a Problem
what data exisists
- most birds that flew into houses
- most birds don’t make it rehab centers - hard to find or die
measure fall flush rates
- brood counts impacted in mid to late summer
grouse populations can rebound in good habitat and time between outbreaks
West Nile Management
young forest habitat
elevation and drainage
grouse priority area siting tool
responsive harvest framework
population monitoring
- fall flush rates
- summer brood surveys
disease monitoring
Captive Gamebirds
primarily propagated for raise and release for hunting
if not hunted don’t survive well
Raising Captive Gamebirds
retaining wild traits is desirable
raising in captivity can be stressful for birds
most operations are multiage, multistage, multispecies - biosecurity is challenging
Captive Gamebirds Diseases
avian encephalomyelitis - epidemic tremor
marble spleen disease
quail bronchitis
gapeworm
ulcerative quail enteritis
fowl cholera
capillaria - threadworms
coccidiosis
Treatment of Disease in Gamebirds
few drugs approved/labelled for use in gamebirds species
- limited research
- few vets with knowledge
water administration
- only water available
feed administration
individual gavage or injection
none for viral disease
limited antibiotics and resistance for bacterial disease
parasitic - only dewormers for worms
Disease Prevention and Control in Captive Gamebirds
biosecurity
waterfowl are natural reservoir hosts
outdoor flight pens hard to control wild animals/pests
vaccination
density
rotation of pastures
Control of Vertically Transmitted Diseases in Captive Gamebirds
monitoring breeders
breeder nutrition - affects shell quality
frequent egg collection
next box cleanliness
hatchery sanitation
farm and hatchery biosecurity
Preventing Cannibalism in Captive Gamebirds
low light
feeder and drinker space
quality feed
appropriate temperature
appropriate bird density
beak trimming
cover to high
removal of dead or sick birds
use of blinders
ratio of males to females
Predator Control in Captive Gamebirds
netting over flight pens
noise cannons
flashing lights
trapping
wire mesh in ground
gravel rock perimeter
Raptors
birds of prey
good eyesight - depth, eyes in front
talons
hooked beak
diverse
top of food chain - biomagnification
learning morphology between species and age is important
Trauma in Raptors
diversity of causes
gunshot
hit by car
intra or interspeciees aggression
predation
Electrocution in Raptors
no lesions may be present - peracute
lesions can be subtle
- where electricity exits
signalment important
look at feathers
Anticoagulant Rodenticides in Raptors
first generation - warfarin/indanedione - less toxic
second generation - more toxic
inhibits vitamin k production - blood clotting - use of first then cant replenish
severity depends on the extent of bleeding
birds associated with agricultural settings
non-specific
weak
lethargic
unaware
most often found dead
muscle atrophy - can feel keal
hemorrhage and bruising
pale tissues
diagnosis requires gross lessons and lab testing
- exposure can occur without bleeding
- coagulation assays
treatment
- may not be feasible in wildlife
- flush gi - if not already in tissue and acute
management
- education
- other forms of pest control
Raptors - Avian Vacuolar Myelinopathy
eagle-coot disease - eagles eat coot
consistent brain lesion - vacuolar myelinopathy - white matter
on slides - neuron cell bodies and edema
- effected by autolysis - vacuolated
clinical signs develop within 5 days
not contagious
from cyanobacterium (neurotoxin) on hydrilla plant
trying to identify triggers for toxin productions
spread through human actions
- boats
limit spread of hydrilla
- carp to eat hydrilla
no impact on mammals
Lead Toxicity
also called plumbism
all birds susceptible
- mostly waterfowl
- scavengers and raptors
- loons and pelicans
result of absorption of lead into blood
in most cases due to ingestion - acidic environment
joints or inflamed tissue
sources vary with avian group
- waterfowl - lead shot
- loons - fishing lures
- albatross - lead paint
Lead Toxicity - proventriculus and gizzard
break down lead for absorption then releases into blood stream
grinding action of gizzard
low ph
smaller fragments of lead absorb faster and are harder to regurgitate
accumulate in body over time
Lead Toxicity - clinical signs
mimics calcium in various biochemical and cellular processes
disrupts normal functions of multiple organ systems
- binds enzymes
- neurotoxin and nephrotoxin
- disrupts rbc development and oxygen carrying capacity of hemoglobin
- depression of immune system
- musculoskeletal system - muscle contractions
acute, chronic, and sub-lethal syndromes
nonspecific clinical signs
- reluctant or unable to fly
- lag behind other birds
- unsteady gait
- changes in vocalization
chronic disease
- weak and lethargic
- don’t attempt to escape when captured
- emaciated
- neurological signs
Lead Toxicity - lesions
may or may not be present
very poor nutritional condition
esophageal impactions - waterfowl
green stain around vent
gall bladder distension
green stained gizzard
finding shot in gizzard
myocardial degeneration/necrosis
Lead Toxicity - environment and host
dependent on multiple factors
environment
- shallow water
- sediment
host
- diet - high carb - decreases ph
- nutritional status
- age - younger
- species
- sex
- underlying disease
very low amounts can result in toxicity
Lead Toxicity - diagnosis
suggestive based on lesions/signs and presence of lead in ventriculus
- may not be present in all cases
radiographs
lead testing required for confirmation
- liver and kidney
- whole blood - antemortem
- no concentration in a tissue can be diagnostic by itself
Lead Toxicity - treatment
possible but challenging
- expensive and time consuming
- prognosis depends on level of toxicity - often poor
- euthanasia or non releasable status
gastric lavage or surgery
chelation therapy
- form complexes with lead and eliminate in urine
- frequent treatment
supportive care
rehabs are expensive
Lead Toxicity - management and prevention
controversial in wild birds
non lead ammunition - copper - doesn’t fragment
if lead
- recovery and proper disposal of animal carcasses or parts
- bury or cover carcass or parts
education
Lead Toxicity - bald eagles
sources
- gut piles
- animals shot and not retrieved
- animals shot and left in field - groundhogs
fragmentation
- dependent on ammunition
- striking bone
- rinsing carcass doesn’t remove
Lead Toxicity - one health
personal harvest
donated venison - ethics
education
Verminous Peritonitis - eustrongylidosis
3 species cause disease in birds
- ignotus - in herons and egrets - rarely spoonbills and pelicans
- tubifex - in mergansers, loons, cormorants, herons, egrets
- excisus - ducks and waterbirds in Europe
vary large nematode parasite
adult worms encase in large masses on the wall of the proventriculus
nematodes perforating ventriculus
Verminous Peritonitis - eustrongylides ingnotus
primarily great blue heron, great egret, snowy egret, night herons, tricolor herons, American egret
sporadic disease in other fish eating mammals, birds, and reptiles
Verminous Peritonitis - transmission and life cycle
indirect transmission
2 intermediate hosts
- freshwater oligochaetes or aquatic worms
- minnows or small fish
small fish eats oligochaetes and gets infected
larvae encapsulates on inside of fish
larger fish can serve as a paratenic host
fish eating bird eats infected fish
Verminous Peritonitis - clinical signs
high mortality of nestlings
spasms of head and neck
weakness
abdominal swelling
emaciation
peritonitis with hemorrhage, necrosis and fibrosis of abdominal viscera
large shield like masses of parasites encased in extensive inflammatory reaction, most often involving the ventriculus and adjacent organs
Verminous Peritonitis - diagnosis
gross lesions are suggestive
identification from infected hosts is confirmatory
Verminous Peritonitis - impacts
wild life
- major recurrent mortality factor
- cause of overwinter losses
humans
- can be acute in people who eat raw infected fish
- aesthetic problem with infected fish
Verminous Peritonitis - management
water quality in habitats of sensitive wading bird species
be aware of feeding wild fish to sensitive captive or rehabbed speciese
Sarcocytosis
also called rice breast
protozoan parasites
- sarcocystis rileyi and other species
common in waterfowl
-macroscopic cysts commonly in dabbling ducks
- microscopic cysts are common in other ducks, geese and swans
different species infect mammals and reptiles
Sarcocytosis - transmission
indrect transmission driven by predatory prey cycle
- intermediate host - bird
- definitive host - carnivore
birds ingest eggs in environment
- form elongated cysts in the muscles
carnivore ingests the bird
Sarcocystosis - clinical signs/lesions/diagnosis
clinical signs
- none
- potentially loss of muscle tissue in severe cases - weakness and lameness
lesions
- cysts visible upon removal of skin
- resemble grains of ricee
- calcified cysts may be gritty
diagnosis
- gross appearance
- histopathology
Sarcocystosis - implications
wild life
- none
humans
- none
Avian Tick Paralysis
ixodes brunneus
- three hosot, ixodid tick
wide variety of birds - particularly songbirds
paralysis due to circulating neurotixin in bloodstream
cases throughout the year, but most common in winter and spring
Avian Tick Paralysis - clinical signs
paralysis of various skeletal muscle systems
usually noted when flight is impaired
ticks usually attacked to head or neck
no external or internal lesions
