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VBSC 409 > EXAM 2 - 10 Lectures > Flashcards

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
Q

Sea Turtle FP Treatment

A

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

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26
Q

Amphibians

A

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

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27
Q

Amphibian Conservation

A

populations declining worldwide

reasons for decline
- habitat destruction
- environmental contamination
- climate change
- introduced species
- disease

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28
Q

Ranivruses in Amphibians Background

A

large double stranded DNA

can infect all ectothermic vertebrates

conservation threat
- common frog in UK
- events in eastern box turtles

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29
Q

Raniviruses in Amphibians Disease Ecology

A

different viruses affect different species

transmission
- direct contact
- ingestion
- water exposure

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30
Q

Raniviruses in Amphibians Epidemiology

A

rapid large-scale dieoffs

90-100% mortality in tadpoles and adults

summer and spring - metamorphosis

larvae and juveniles most susceptible

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31
Q

Raniviruses in Amphibians Diagnosis and Mangement

A

diagnosis
- pcr
- virus isolation
- histopathology
- electron microscopy

no treatment

disinfection

quarantine

biosecurity

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32
Q

Raniviruses in Amphibians Clinical Signs

A

species/age dependent

abnormal behavior/lethargy

hemorrhage

edema

ulceration

death

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33
Q

Raniruses in Amphibians Diagnosis and management

A

PCR
virus isolation
histopathology
electron microscopy

no treatment

disinfection

quarantine

biosecurity

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34
Q

BD Chytridiomycosis Background

A

infectious disease of amphibians

caused by fungus Batrachochytrium dendrobatidis

name derived by blue poison dart frog

global amphibian trade

“out of asia” hypothesis

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35
Q

BD Pathogen Lifecycle and Transmission

A

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

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36
Q

BD Clinical Signs

A

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

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37
Q

BD Diagnosis and Treatment

A

multiple options for detection
- swabs from live animals
- histopathology on dead animals
- wet mounts
- cytology
- PCR

treatment options
- supportive care
- baths

biosecurity is key

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38
Q

Salamander Chytridomycosis Background

A

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

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39
Q

Dermocystid Parasites Background

A

prostist

mostly in european anurans and urodeles

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40
Q

Dermocystid Parasites Presentation in Amphibians

A

single or multiple cutaneous lesions

observed infrequently within gastrointestinal mucosa and internal organs such as liver

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41
Q

Dermocystid Impacts on Hosts

A

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

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42
Q

Dermocystid Disruption of Amphibian Skin

A

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

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43
Q

Waterbird

A

bird that lives on or around water

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44
Q

Waterfoul

A

birds within the order Anseriformes - ducks, geese, swans

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45
Q

Avian Botulism

A

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

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46
Q

Avian Botulism - Clostridium botulinum

A

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

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47
Q

Avian Botulism - Botulinum Toxin

A

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

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48
Q

Avian Botulism - Clinical Signs

A

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

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49
Q

Avian Botulism Type C

A

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

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50
Q

Avian Botulism Type C Toxin Production

A

warm temperature - summer and early fall

low dissolved oxygen - carcasses or vegetation

protein substrate - carcasses, vegetation, sewage

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51
Q

Avian Botulism Type C Delivery of Toxin to Birds

A

invertebrate food

decaying organic matter

maggots - concentrate toxins

habitat may become seeded with spores - repeated outbreaks

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52
Q

Avian Botulism Type E

A

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

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53
Q

Avian Botulism Diagnosis

A

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

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54
Q

Avian Botulism Management

A

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

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55
Q

Avian Botulism Public Health Implications

A

most human botulism caused by improperly canned foods - a and b

fairly resistant to c

susceptible to e - poorly cooked or smoked fish

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56
Q

Avian Botulism Prevention

A

cooking destroys toxin

PPE

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57
Q

Duck Plague

A

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

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58
Q

Latency

A

ability of a pathogenic virus to lie dormant in a cell

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59
Q

Duck Plague Clinical Signs - Acute

A

good body condition

bleeding and necrosis

bloody discharge from nares and vent

prolapsed penis

loss of wariness or cant fly

convulsions

neurologic

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60
Q

Duck Plague Lesions

A

GI hemorrhage, ulcers, inflammation

multifocal liver necrosis

heart hemorrhaging

ulcers in oropharynx under tongue - not always

microscopically seen
- intanuclear inclusion bodies seen in liver

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61
Q

Duck Plague Transmission

A

excreted by infected birds in oral secretions and feces

spread by contact with infected waterfowl or environments
- carcasses and secretions

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62
Q

Duck Plague Epidemiology

A

april-june cause 70% of outbreaks
- stress - seasonal changes, breeding, crowding

often adult birds

species differences

potentially increasing in the Atlantic flyway

63
Q

Duck Plague Outbreaks

A

important in farmed/captive waterfoul
- global

feral ducks

sporadic outbreaks in wild waterfowl - huge

no public health implications

64
Q

Duck Plague Mangement

A

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
Q

Avian Cholera

A

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
Q

Avian Cholera Clinical Signs

A

mucoid discharge from nose or mouth

lethargy and incoordination

swimming in circles

tremors and convulsions

67
Q

Avian Cholera Lesions

A

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
Q

Avian Cholera Transmission

A

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
Q

Avian Cholera Outbreaks

A

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
Q

Avian Cholera Diagnosis

A

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
Q

Avian Influenza Virus

A

high and low path

high capacity to change

don’t ever say never or always

72
Q

Genetic Drift

A

mutaitons

gradual, constant, accumulation of mutations - small changes

loss of immunity

73
Q

Genetic Shift

A

reassortment

abrupt exchange of gene segments - large changes

host barrier jumps

emergence of new strains

74
Q

AIV Wild Bird Reservoir System

A

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
Q

AIV Spillover into Poultry

A

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
Q

AIV in Gallinaceous Poultry

A

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
Q

AIV Impacts on Poultry

A

economic loses
- depopulation and disposal
- high morbidity and mortality
- quarantine and surveillance
- indemnities

78
Q

AIV Prevention and Management in Poultry in North America

A

understanding risk

biosecurity

testing for early detection

vaccination
- not feasible
- virus change
- shut down trade - serology
- larger amount of birds

79
Q

AIV in Waterfowl

A

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
Q

AIV Surveillance in PA Ducks

A

higher in juveniles than adults

higher in mallards and other dabbling ducks

81
Q

AIV in Charadriiformes - Shorebirds and Gulls

A

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
Q

AIV Notable Outbreak Changes in North America

A

different strain

longer duration

more widespread

higher mortality in wild birds

wider diversity of wild birds

increased mammal cases

83
Q

Game Bird

A

bird hunted for sport or food

chicken-like

wild turkeys in PA

84
Q

Upland Game Bird

A

non-waterfowl game bird

diverse group

wild vs propagated - nonnative for hunting

migratory vs nonmigratory

85
Q

Skin Lesions in Wild Turkeys

A

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
Q

Avian Pox

A

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
Q

Avian Pox - Dry Pox

A

nodules on unfeathered skin

can resolve in weeks if mild to moderate

87
Q

Avian Pox Slides

A

hyperkeratosis

inclusion bodies

88
Q

Avian Pox - Wet Pox

A

nodules/plaques on the mucosa of the oral cavity, esophagus, trachea

poor prognosis

more severe/virulent

89
Q

Avian Pox Clinical Signs

A

nodules on skin or upper GI/respiratory tract

depend on size and location of nodules

weak

emaciated

blind

respiratory distress

90
Q

Avian Pox Transmission

A

insects as mechanical vectors

inhalation or ingestion of virus containing scabs

virus can persist on surfaces and infect through mucous membranes

direct contact

91
Q

Avian Pox Trends

A

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
Q

Avian Pox Diagnosis

A

virus isolation

cytology - speed

histology - most common
- hypertrophy
- hyperplasia
- inclusion bodies
- hyperkerattosis
- ballooning degeneration
- secondary bacterial infection

93
Q

Avian Pox Management

A

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
Q

Retroviral Neoplasms in Wild Turkeys

A

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
Q

LPVD Histopathology

A

infiltration of visceral organs and tissues by large numbers of pleomorphic lymphoid cells

96
Q

LPVD in Domestic Turkeys

A

minor importance to poultry

transmission unknown

pathogenesis unknown

unknown how to propagate

common among clinically ill adult turkeys - formation of tumors is rare

97
Q

Lymphoid Tumors in Wild Turkeys Clinical Signs

A

emaciated

weak

unable to move

unaware of surrounding

tumors in multiple organs/tissues

neoplastic lymphoid cells infiltrating internal organs

98
Q

Lymphoid Tumors in Wild Turkeys Diagnosis

A

must identify goals of diagnosis

microscopic examination identify tumor

PCR to identify proviral DNA

99
Q

LPVD Surveillance

A

want distal leg

most have no signs

no human health risks

100
Q

Histomoniasis

A

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
Q

Histomoniasis Clinical Signs

A

weakness

emaciation

droopy wings

ruffled feathers

listlessness

sulfur yellow feces

lesions in cecum +/- liver

102
Q

Histomoniasis Life Cycle

A

another parasite is vector

cecal worm heterakis gallinarum
- hardy eggs that survive in environment

earthworms eat eggs

chicken eats worm

103
Q

Histomoniasis Diagnosis

A

gross lesions are suggestive

bioassay

PCR

histology

protozoa destroyed by freezing

104
Q

Histomoniasis Management

A

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
Q

Trichomoniasis

A

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
Q

Trichomoniasis Clinical Signs

A

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
Q

Trichomoniasis Transmission

A

direct

regurgitation feeding or ingestion of recently shed parasites in contaminated water or moist grains

poorly maintained feeder birds

platform and birdbaths

108
Q

Trichomoniasis Diagnosis

A

gross lesions

microscopic examinations of scrapings

culture

freezing diminishes capability

differentiate from avian pox

histology

PCR

109
Q

Trichomoniais Mangement

A

bird bath sanitation

reduce contact between carriers ad susceptible species

treatment

110
Q

One Health

A

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
Q

Wildlife Health and Disease

A

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
Q

Ruffled Grouse

A

bonasa umbellus

native wild galliform

young forest habitat - different stages, brush

boom or bust population cycles

declines in mid Atlantic and southeast

113
Q

West Nile Virus in Wild Birds

A

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
Q

West Nile Virus in Humans

A

asymptomatic to fatal neurologic disease
- most asymptomatic

flu-like symptoms

prevention focuses on limiting mosquito exposure

115
Q

West Nile Surveillance

A

human disease
- hospital
- department of health

mosquito surveillance

horces

dead bird testing and serology

sentinels

116
Q

West Nile - Is There a Problem

A

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
Q

West Nile Management

A

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
Q

Captive Gamebirds

A

primarily propagated for raise and release for hunting

if not hunted don’t survive well

119
Q

Raising Captive Gamebirds

A

retaining wild traits is desirable

raising in captivity can be stressful for birds

most operations are multiage, multistage, multispecies - biosecurity is challenging

120
Q

Captive Gamebirds Diseases

A

avian encephalomyelitis - epidemic tremor
marble spleen disease
quail bronchitis
gapeworm
ulcerative quail enteritis
fowl cholera
capillaria - threadworms
coccidiosis

121
Q

Treatment of Disease in Gamebirds

A

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
Q

Disease Prevention and Control in Captive Gamebirds

A

biosecurity

waterfowl are natural reservoir hosts

outdoor flight pens hard to control wild animals/pests

vaccination

density

rotation of pastures

123
Q

Control of Vertically Transmitted Diseases in Captive Gamebirds

A

monitoring breeders

breeder nutrition - affects shell quality

frequent egg collection

next box cleanliness

hatchery sanitation

farm and hatchery biosecurity

124
Q

Preventing Cannibalism in Captive Gamebirds

A

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
Q

Predator Control in Captive Gamebirds

A

netting over flight pens

noise cannons

flashing lights

trapping

wire mesh in ground

gravel rock perimeter

126
Q

Raptors

A

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
Q

Trauma in Raptors

A

diversity of causes

gunshot

hit by car

intra or interspeciees aggression

predation

128
Q

Electrocution in Raptors

A

no lesions may be present - peracute

lesions can be subtle
- where electricity exits

signalment important

look at feathers

129
Q

Anticoagulant Rodenticides in Raptors

A

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
Q

Raptors - Avian Vacuolar Myelinopathy

A

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
Q

Lead Toxicity

A

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
Q

Lead Toxicity - proventriculus and gizzard

A

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
Q

Lead Toxicity - clinical signs

A

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
Q

Lead Toxicity - lesions

A

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
Q

Lead Toxicity - environment and host

A

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
Q

Lead Toxicity - diagnosis

A

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
Q

Lead Toxicity - treatment

A

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

138
Q

Lead Toxicity - management and prevention

A

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

139
Q

Lead Toxicity - bald eagles

A

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

140
Q

Lead Toxicity - one health

A

personal harvest

donated venison - ethics

education

141
Q

Verminous Peritonitis - eustrongylidosis

A

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

142
Q

Verminous Peritonitis - eustrongylides ingnotus

A

primarily great blue heron, great egret, snowy egret, night herons, tricolor herons, American egret

sporadic disease in other fish eating mammals, birds, and reptiles

143
Q

Verminous Peritonitis - transmission and life cycle

A

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

144
Q

Verminous Peritonitis - clinical signs

A

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

145
Q

Verminous Peritonitis - diagnosis

A

gross lesions are suggestive

identification from infected hosts is confirmatory

146
Q

Verminous Peritonitis - impacts

A

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

147
Q

Verminous Peritonitis - management

A

water quality in habitats of sensitive wading bird species

be aware of feeding wild fish to sensitive captive or rehabbed speciese

148
Q

Sarcocytosis

A

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

149
Q

Sarcocytosis - transmission

A

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
Q

Sarcocystosis - clinical signs/lesions/diagnosis

A

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

151
Q

Sarcocystosis - implications

A

wild life
- none

humans
- none

152
Q

Avian Tick Paralysis

A

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

153
Q

Avian Tick Paralysis - clinical signs

A

paralysis of various skeletal muscle systems

usually noted when flight is impaired

ticks usually attacked to head or neck

no external or internal lesions

VBSC 409 (3 decks)

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