EXAM 2 - 10 Lectures Flashcards

1
Q

Chelonian (turtles) Upper Respiratory Disease - Overall Clinical Signs

A

ocular discharge
nasal discharge
blepharoedema - eye swelling
oral plaques
depression/lethargy
asymmetrical nares
nasal erosion
skin depigmentation

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2
Q

Chelonian URD - Ranavirus (FV3)

A

causes local outbreaks with high morbidity and mortality

survives can become carriers - consider euthanasia

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3
Q

Chelonian URD - Ranavirus Transmission

A

direct contact
indirectly through water, sediment, ingestion

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4
Q

Chelonian URD - Ranavirus Epidemiology

A

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

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5
Q

Chelonian URD - Ranavirus Disease Presentation

A

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

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6
Q

Chelonian URD - Ranavirus Pathogenesis and Treatment

A

pathologic changes are severe and systemically distributed

death due to multiorgan failure

treatment typically not recommended
- not often successful
- carriers

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7
Q

Chelonian URD - Mycoplasma

A

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

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8
Q

Chelonian URD - Mycoplasma Transmission

A

direct contact
fomites

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9
Q

Chelonian URD - Mycoplasma Clincal Signs

A

nasal and ocular discharge
conjunctivitis
palpebral edema

intermittent

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10
Q

Chelonian URD - Mycoplasma Contributing Factors

A

environmental stressors
human factors
toxicant esposure
capture and release of ill animals

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11
Q

Chelonian URD - Herpesviruses

A

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

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12
Q

Chelonian URD - Herpesviruses Transmission

A

direct
mother to offspring

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13
Q

URD Diagnostics

A

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

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14
Q

URD Management

A

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

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15
Q

Ophidiomycosis (Snake Fungal Disease) Background

A

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

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16
Q

SFD Transmission

A

not fully understood

contact with infected snakes?
contact with infected soils?
at birth?

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17
Q

SFD Disease Presentation

A

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

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18
Q

FSD Diagnosis

A

from dermal punch
- qPCR
- histopathology
- fungal culture

swab
- from qPCR

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19
Q

FSD Treatment

A

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

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20
Q

FSD Management

A

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?

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21
Q

Sea Turtle Fibropapillomatosis Background

A

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

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22
Q

Sea Turtle FP Clinical Presentation

A

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

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23
Q

Sea Turtle FP Transmission

A

viral shedding into the environment

potentially magnified by mechanical vectors - marine leeches

non-clinically infected turtles may also spread virus

biosecurity is important

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24
Q

Sea Turtle FP Diagnosis

A

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

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25
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
26
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
27
Amphibian Conservation
populations declining worldwide reasons for decline - habitat destruction - environmental contamination - climate change - introduced species - disease
28
Ranivruses in Amphibians Background
large double stranded DNA can infect all ectothermic vertebrates conservation threat - common frog in UK - events in eastern box turtles
29
Raniviruses in Amphibians Disease Ecology
different viruses affect different species transmission - direct contact - ingestion - water exposure
30
Raniviruses in Amphibians Epidemiology
rapid large-scale dieoffs 90-100% mortality in tadpoles and adults summer and spring - metamorphosis larvae and juveniles most susceptible
31
Raniviruses in Amphibians Diagnosis and Mangement
diagnosis - pcr - virus isolation - histopathology - electron microscopy no treatment disinfection quarantine biosecurity
32
Raniviruses in Amphibians Clinical Signs
species/age dependent abnormal behavior/lethargy hemorrhage edema ulceration death
33
Raniruses in Amphibians Diagnosis and management
PCR virus isolation histopathology electron microscopy no treatment disinfection quarantine biosecurity
34
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
35
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
36
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
37
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
38
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
39
Dermocystid Parasites Background
prostist mostly in european anurans and urodeles
40
Dermocystid Parasites Presentation in Amphibians
single or multiple cutaneous lesions observed infrequently within gastrointestinal mucosa and internal organs such as liver
41
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
42
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
43
Waterbird
bird that lives on or around water
44
Waterfoul
birds within the order Anseriformes - ducks, geese, swans
45
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
46
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
47
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
48
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
49
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
50
Avian Botulism Type C Toxin Production
warm temperature - summer and early fall low dissolved oxygen - carcasses or vegetation protein substrate - carcasses, vegetation, sewage
51
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
52
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
53
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
54
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
55
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
56
Avian Botulism Prevention
cooking destroys toxin PPE
57
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
58
Latency
ability of a pathogenic virus to lie dormant in a cell
59
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
60
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
61
Duck Plague Transmission
excreted by infected birds in oral secretions and feces spread by contact with infected waterfowl or environments - carcasses and secretions
62
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
63
Duck Plague Outbreaks
important in farmed/captive waterfoul - global feral ducks sporadic outbreaks in wild waterfowl - huge no public health implications
64
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
65
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"
66
Avian Cholera Clinical Signs
mucoid discharge from nose or mouth lethargy and incoordination swimming in circles tremors and convulsions
67
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
68
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
69
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
70
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
71
Avian Influenza Virus
high and low path high capacity to change don't ever say never or always
72
Genetic Drift
mutaitons gradual, constant, accumulation of mutations - small changes loss of immunity
73
Genetic Shift
reassortment abrupt exchange of gene segments - large changes host barrier jumps emergence of new strains
74
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
75
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
76
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
77
AIV Impacts on Poultry
economic loses - depopulation and disposal - high morbidity and mortality - quarantine and surveillance - indemnities
78
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
79
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
80
AIV Surveillance in PA Ducks
higher in juveniles than adults higher in mallards and other dabbling ducks
81
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
82
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
83
Game Bird
bird hunted for sport or food chicken-like wild turkeys in PA
84
Upland Game Bird
non-waterfowl game bird diverse group wild vs propagated - nonnative for hunting migratory vs nonmigratory
85
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
86
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
87
Avian Pox - Dry Pox
nodules on unfeathered skin can resolve in weeks if mild to moderate
87
Avian Pox Slides
hyperkeratosis inclusion bodies
88
Avian Pox - Wet Pox
nodules/plaques on the mucosa of the oral cavity, esophagus, trachea poor prognosis more severe/virulent
89
Avian Pox Clinical Signs
nodules on skin or upper GI/respiratory tract depend on size and location of nodules weak emaciated blind respiratory distress
90
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
91
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
92
Avian Pox Diagnosis
virus isolation cytology - speed histology - most common - hypertrophy - hyperplasia - inclusion bodies - hyperkerattosis - ballooning degeneration - secondary bacterial infection
93
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
94
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
95
LPVD Histopathology
infiltration of visceral organs and tissues by large numbers of pleomorphic lymphoid cells
96
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
97
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
98
Lymphoid Tumors in Wild Turkeys Diagnosis
must identify goals of diagnosis microscopic examination identify tumor PCR to identify proviral DNA
99
LPVD Surveillance
want distal leg most have no signs no human health risks
100
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
101
Histomoniasis Clinical Signs
weakness emaciation droopy wings ruffled feathers listlessness sulfur yellow feces lesions in cecum +/- liver
102
Histomoniasis Life Cycle
another parasite is vector cecal worm heterakis gallinarum - hardy eggs that survive in environment earthworms eat eggs chicken eats worm
103
Histomoniasis Diagnosis
gross lesions are suggestive bioassay PCR histology protozoa destroyed by freezing
104
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
105
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
106
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
107
Trichomoniasis Transmission
direct regurgitation feeding or ingestion of recently shed parasites in contaminated water or moist grains poorly maintained feeder birds platform and birdbaths
108
Trichomoniasis Diagnosis
gross lesions microscopic examinations of scrapings culture freezing diminishes capability differentiate from avian pox histology PCR
109
Trichomoniais Mangement
bird bath sanitation reduce contact between carriers ad susceptible species treatment
110
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
111
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
112
Ruffled Grouse
bonasa umbellus native wild galliform young forest habitat - different stages, brush boom or bust population cycles declines in mid Atlantic and southeast
113
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
114
West Nile Virus in Humans
asymptomatic to fatal neurologic disease - most asymptomatic flu-like symptoms prevention focuses on limiting mosquito exposure
115
West Nile Surveillance
human disease - hospital - department of health mosquito surveillance horces dead bird testing and serology sentinels
116
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
117
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
118
Captive Gamebirds
primarily propagated for raise and release for hunting if not hunted don't survive well
119
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
120
Captive Gamebirds Diseases
avian encephalomyelitis - epidemic tremor marble spleen disease quail bronchitis gapeworm ulcerative quail enteritis fowl cholera capillaria - threadworms coccidiosis
121
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
122
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
123
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
124
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
125
Predator Control in Captive Gamebirds
netting over flight pens noise cannons flashing lights trapping wire mesh in ground gravel rock perimeter
126
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
127
Trauma in Raptors
diversity of causes gunshot hit by car intra or interspeciees aggression predation
128
Electrocution in Raptors
no lesions may be present - peracute lesions can be subtle - where electricity exits signalment important look at feathers
129
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
130
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
131
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
132
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
133
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
134
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
135
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
136
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
137
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
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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
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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
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Lead Toxicity - one health
personal harvest donated venison - ethics education
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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
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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
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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
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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
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Verminous Peritonitis - diagnosis
gross lesions are suggestive identification from infected hosts is confirmatory
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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
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Verminous Peritonitis - management
water quality in habitats of sensitive wading bird species be aware of feeding wild fish to sensitive captive or rehabbed speciese
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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
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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
150
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
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Sarcocystosis - implications
wild life - none humans - none
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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
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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