Wildlife Pathology Flashcards
Myxomatosis
1. CAUSE: ____________ (_______ virus)
- DNA or RNA virus?
- Aka: ?
2. Species affected:
- ________ (continent) rabbits (________ spp) – ___zootic, ______ disease
- _________ rabbits (?) – ____zootic, _______ disease (every pet rabbit is european)
- Australia and Brazil
- _______ (Lepus spp)…. +/-
3. Reportable to _____
Myxomatosis
1. CAUSE: Leporipoxvirus (myxoma virus)
dsDNA virus
Aka: bighead, mosquito disease (rarely used)…’mixi’
2. Species affected:
American rabbits (Sylvilagus spp) – enzootic, mild disease
European rabbits (Oryctolagus cuniculus) – epizootic, severe disease
Australia and ________
Hares (Lepus spp)…. +/-
3. Reportable to OIE
Myxomatosis: pathogenesis
- Transmitted by __________ (biting infected animals —> transmit to other animal)
- Mosquitoes (_______), fleas (________)
- Rarely through respiratory ________
- Virus infects epithelial (_______; conjuctiva, oral mucosa, nasal mucosa, skin abrasion) cells & fibroblasts and causes Local lesions (cell proliferation) and turn into tumors = pseudo-tumors, ‘myxomas’; not cancerous, but look it
Myxoma growth factor ≈ EGF (which means epithelial growth factor) –> cells proliferate and become thicker
- Virus infects lymphocytes
- Spreads to LN & systemically –> end up wth leukemia through (leukocyte trafficking)
- Severe lesions may result in death
- Emaciation (tumors around eye blindness), predation, other trauma (e.g. HBC)
- or can get Secondary bacterial infection
- when have this, it is very obvious in eyes –> Conjunctivitis
- If less severe form – particularly in american rabbits, myxoma regresses and rabbits gets better
Myxomatosis: pathogenesis
- Transmitted by arthropods
- Mosquitoes (America), fleas (Europe)
Rarely through respiratory droplets
Virus infects epithelial (mucosal) cells & fibroblasts
Local lesions (cell proliferation) = pseudo-tumors, ‘myxomas’
Myxoma growth factor ≈ EGF (which means….)
Virus infects lymphocytes
Spreads to LN & systemically
Viremia (leukocyte trafficking)
Severe lesions may result in death
Emaciation (blindness), predation, other trauma (e.g. HBC)
Secondary bacterial infection
Conjunctivitis
If less severe form – myxoma regression
Clinical signs of Myxomatosis in American rabbits (_________ spp) & hares (_____ spp):
- _____ disease
- Localized _______-tumors, _____ (__-__ days post-exposure, dpe)
- _______ (______-tumors) eventually regress (about ___ dpe) if no secondary ______ infection
Clinical signs of Myxomatosis in American rabbits (Sylvilagus spp) & hares (Lepus spp):
- Mild disease
- Localized pseudo-tumors, myxomas (4-8 days post-exposure, dpe)
- Myxomas (pseudo-tumors) eventually regress (about 40 dpe) if no secondary bacterial infection
Clinical signs of Myxomatosis in European rabbits (_______ ______):
- ______ myxomas (3-4 dpe), mostly in the face (around _____ & _____ b/c that is where mosquitos are transmitting the disease)
- Suppurative ___________, _______
- Secondary _______ infection
- _________ edema
- _____, ______ - emaciation
- viremia –> _______ spread
- _____ mortality rate
Clinical signs of Myxomatosis in European rabbits (Oryctolagus cuniculus):
- Large myxomas (3-4 dpe), mostly in the face (around eyes & nose b/c that is where mosquitos are transmitting the disease)
- Suppurative blepharoconjunctivitis, dermatitis
- Secondary bacterial infection
- Perianal edema
- Fever, anorexia - emaciation
- viremia –> Systemic spread
- High mortality rate
‘Atypical myxomatosis’ when you can have the _____ lesions and sometimes the only thing that develop is a ______ pneumonia. This type of pneumonia is _________ pneumonia.
‘Atypical myxomatosis’ when you can have the skin lesions and sometimes the only thing that develop is a Viral pneumonia. This type of pneumonia is interstitial pneumonia
moderate swelling and conjunctivitis and blephitis
European rabbits (Oryctolagus cuniculus):
Swelling & redness (inflammation) in eyelids
European rabbits (Oryctolagus cuniculus):
Secondary bacterial conjuctivitis
more severe form with purulent exudate forming
d 4 = reddening of eyelids
d 8 = some supp exu
d 11 = severe
Myxomatosis: gross findings
A. Subcutaneous ________ (______/ ______ b/c most of it is composed of _____ deposited in the dermis) masses:
- Particularly on the face (____, ____) & _____ - myxomas
B. Mucopurulent ________, nasal ______
C. Also:
- Edema of _______
- _________ in skin, heart, gastrointestinal tract, kidney, lymph nodes, & testes
- _____megaly
- Lymph node ______
- Pneumonia = _____ myxomatosis, _____
- Edema, hemorrhage –> _____ form
Myxomatosis: gross findings
A. Subcutaneous mucinous (gelatinous/ spongey b/c most of it is composed of mucin deposited in the dermis) masses:
- Particularly on the face (eyelids, nose) & perineum - myxomas
B. Mucopurulent blepharoconjunctivitis, nasal discharge
C. Also:
- Edema of perineum
- Hemorrhages in skin, heart, gastrointestinal tract, kidney, lymph nodes, & testes
- Splenomegaly
- Lymph node edema
- Pneumonia = atypical myxomatosis, interstitial
- Edema, hemorrhage –> viremic form
Subcutaneous mucinous (gelatinous) masses:
Particularly on the face (eyelids, nose) & perineum - myxomas
Mucopurulent blepharoconjunctivitis, nasal discharge
Pneumonia, interstitial
Edema, hemorrhage (atypical myxomatosis)
froth in trachea = edema
rib impressions with interstitial pneumonia
Myxomatosis: histopathology
- Epithelial _________, _______ degeneration, & large _________ _______ viral inclusions in affected epidermis and conjunctival epithelial cells
- Inclusions sometimes in _______ cells
- Myxoma cells (they are ______ cells; ______ to large _____ cell) separated by abundant myxomatous matrix in dermis
- Myxoma cells may be found in ___, ___, ___ & _____; ___ inclusion bodies (pox viruses are different from other DNA viruses that typically have ____ IB)
- Lymphoid depletion within ____ and _____ _____
- Focal areas of necrosis in lymph nodes, pneumocytes, spleen, and centrilobular hepatocytes
Myxomatosis: histopathology
- Epithelial hyperplasia, ballooning degeneration, & large eosinophilic intracytoplasmic viral inclusions in affected
epidermis and conjunctival epithelial cells
- Inclusions sometimes in myxoma cells
- Myxoma cells (they are mesenchymal cells; spindloid to large stellate cell) separated by abundant myxomatous matrix in dermis
- Myxoma cells may be found in LN, BM, repro & lungs; IC inclusion bodies (pox viruses are different from other DNA viruses that typically have IN IB)
- Lymphoid depletion within spleen and lymph nodes
- Focal areas of necrosis in lymph nodes, pneumocytes, spleen, and centrilobular hepatocytes
eyelid
Epithelial hyperplasia & dermal myxomatous matrix
thickening of epidermis with ballooning
eppidemmis is falling apart b/c in between collagen fibers and fibroblasts is mucin
Epithelial hyperplasia, ballooning degeneration
alcian blue to confirm mucin is here
Epithelial hyperplasia, ballooning degeneration , hyperkeratosis
Heterophils here
Epithelial hyperplasia,& large eosinophilic IC viral inclusions
Epithelial hyperplasia,& large eosinophilic IC viral inclusions
Epithelial hyperplasia,& large eosinophilic IC viral inclusions
spindle shaped
yellow = pointing to cell
green = pointing to inclusion body in cytoplasm
blood vessel on left; angry; lots of heterophils coming out of lumen
Myxoma cells in myxomatous matrix (dermis)
- How do you Dx Myxomatosis?
- What tests do you use to confirm your Dx?
- Characteristic clinical signs, gross lesions & histopathology
- PCR, IHC, EM, virus isolation
Myxomatosis
TEM
Dumbell shaped
Myxomatosis: prevention & control
__________ in areas with high disease prevalence - Not available everywhere
Keep ________ (or _____) away from rabbits
Is there a proper treatment protocol?
Vaccination in areas with high disease prevalence - Not available everywhere
Keep mosquitoes (or fleas) away from rabbits
No real treatment other than supportive care.
Zoonotic?
no
Snake fungal disease
- CAUSE: _________ ________
- Formerly __________ _______
- a.k.a. (ish) hibernation _____ or hibernation _____ (herpetologists)
- Species affected: pretty much ____ species, but more severe in several _______ species, particularly in ______ & _____ USA, Eastern ________ rattlesnakes (Sistrurus catenatus catenatus ) endangered (?)– _____ affected*
First ’reported’ in 2006 (other fungi, other names, before)
* Is this a bias of sampling? Is it that the populations are already in poor health/inbred?
Snake fungal disease
- CAUSE: Ophidiomyces ophiodiicola
- Formerly Chrysosporium ophiodiicola
- a.k.a. (ish) hibernation blisters or hibernation sores (herpetologists)
- Species affected: pretty much every species, but more severe in
Several rattlesnake species, particularly in Midwestern & Eastern USA
Eastern massasauga rattlesnakes (Sistrurus catenatus catenatus ) endangered (?)– most affected*
First ’reported’ in 2006 (other fungi, other names, before)
* Is this a bias of sampling? Is it that the populations are already in poor health/inbred?
Hibernate: in the fall, they go in and spend winter together where raccoons or foxes lived, and come out in spring.
Snake fungal disease: pathogenesis
- O.o. present in.. _____ but also _______;
- O.o. breaches stratum _______ (_______ usually needed)
- O.o. invades ________
- Enzymes break down ______ & ____ (in vitro evidence)– may facilitate invasion*
- Causes Release of _____ via secreting ______ - cause ______ in the skin*
- Snake mounts immune response (cell recruitment & edema)
- Cells: ________, _____, then ____
- Epidermis become _____ (____ to _____ crusts)
Crusts detach = ______/_____ (what’s the difference?)
- Fungus proliferates in ______
- +/- _____, ______, _____ & ______
- _________ in skin/deeper tissues
- ________ dissemination – rare in the wild; Why more in captive? In the wild they do not live long enough to get systemic disease
- Death –> can happen from: Emaciation, predation, secondary bacterial infection, etc
Snake fungal disease: pathogenesis
- O.o. present in.. skin but also environment; so is snake getting it from another snake or the environment?
- O.o. breaches stratum corneum (abrasion usually needed)
- O.o. invades epidermis
- Enzymes break down keratin & ECM (in vitro exidence)– may facilitate invasion*
- Causes Release of ammonia via secereting ureases - cause necrosis in the skin*
- Snake mounts immune response (cell recruitment & edema)
- Heterophils, MQ, then MGC
- Epidermis become necrotic (yellow to brown crusts)
Crusts detach = ulceration/erosion (what’s the difference?)
- Fungus proliferates in epidermis
- +/- dermis, subcutis, muscle & bone
- Granulomas in skin/deeper tissues
- Grossly see ulcers or erosions of epidermis. Due to necorsis, see crusting. Crusting dettach adn then see necrosis underneath. Fungus prolieates in the skin or it can go into subcutis –> muscle -> bone. Rarely goes into viscera.
- Systemic dissemination – rare in the wild; Why more in captive? In the wild they do not live long enough to get systemic disease
- Death –> can happen from: Emaciation, predation, secondary bacterial infection, etc
Snake fungal disease: clinical signs
A. ______ to ______ plaques
B. Increased moulting ______ bs/ since fungus starts on ______ layer of skin, increase molting.
- If effective, it may _____ infection
C. Retained ______ or ____ (_______ = problem with molting; either not shed at all or shed in pieces; _____ stays on eye = blurry)
D. Altered behavior (behavioral _____ = goes to areas that are normal so body temp _____)
E. Deformed ____
F. _______
Snake fungal disease: clinical signs
A. Yellow to brown plaques
B. Increased moulting frequency b/ since fungus sarts on superficial layer f skin, increase molting.
- If effective, it may clear infection
C. Retained spectacles or scales (dysecdysis = problem with molting; either not shed at all or shed in pieces; spectacle stays on eye = blurry)
D. Altered behavior (behavioral fever = goes to areas that are normal so body temp rises)
E. Deformed head
F. Emaciation
Snake fungal
disease:
clinical signs
Yellow to brown plaques
Deformed head
Snake fungal
disease:
gross findings
Yellow to brown plaques
Deformed head
Retained, opaque, spectacles
entered bone –> osteomyelitis
Snake fungal
disease:
gross findings
Yellow to brown plaques
Deformed head
usually die before getting to hat is pictured
Snake fungal disease: histopathology
- Epidermal ______/______
- _____ + ____ surrounded by ____, ___, ______ &, sometimes, ________
- Granulomas w/fungal _______
Snake fungal disease: histopathology
- Epidermal erosion/ulceration
- MGC + MQ surrounded by LQ, PL, heterophils &, sometimes, fibroblasts
- Granulomas w/fungal hyphae
Snake fungal
disease:
histopathology
Granulomas w/fungal hyphae allll to the right
Snake fungal
disease:
histopathology
Granulomas w/fungal hyphae
fibrous CT with fungal hyphae
MNGC and MCQ
Fungal hyphae
Stain: Silver stain or PAS
Granulomas w/fungal hyphae
Silver stain is best
- How do you Dx Snake fungal disease? diagnosis
- What tests do you need to run to Dx Snake Fungal disease?
- You also need to make sure to rule out _______ for any animal with a granulomatous response (?), because fungi can also be secondary invaders.
- Which special stain do you use to find mycobacteria in histology?
- Characteristic clinical signs, gross lesions & histopathology
- PCR +/- fungal culture (not w/o histopathology)
- Need to do PCR to confirm fungus
if you just swab skin of snake, you will have a + PCR but does not mean snake is sick - You also need to make sure to rule out mycobacteriosis for any animal wth a granulomatous response (amphibians, birds), because fungi can also be secondary invaders.
- Acid fast
Snake fungal disease: prevention & control
¿?
Field hygiene
Population health
- treatable in captivity
theory:
1. introduced from europe into NA
2. populations affected by it have a low genetic diversity
Snake fungal disease: zoonosis
Not at all
Chytridiomycosis
1. CAUSE:
- Batrachochytrium ___________ –> mostly frogs and salamanders but not as much
AND
- Batrachochytrium __________ –> disc in 2013, paper published in 2014; passive surveillance affects salamanders, some frogs
- ________ disease(s)
- Reportable to the ______
Chytridiomycosis
1. CAUSE:
- Batrachochytrium dendrobatidis –> mostly frogs and salamanders but not as much
AND
- Batrachochytrium salamandrivorans –> disc in 2013, paper published in 2014; passive surveillance affects salamanders, some frogs
- Emerging disease(s)
- Reportable to the OIE
“The impact of ________ in frogs is the most spectacular loss of vertebrate biodiversity due to disease in recorded history”
EcoHealth 2007
“The impact of chytridiomycosis in frogs is the most spectacular loss of vertebrate biodiversity due to disease in recorded history”
EcoHealth 2007
on fngi with spores tat swim
spores fnd sin of amphib or soil –> firm fkaak shape spor –> when ready come out of discharign tubes. spores infect other frogs or same frog or go into ground and live there.
there is no other species other than amphibians affected by chitrid fungus
Chytridiomycosis: pathogenesis
- ______ zoospores invade _____ (stratum ______)
- Zoosporangia develop in _________ cells (_______)
- Zoosporangia mature, & release _______
- Epidermis _____ (_______ & _______)
- Minimal or absent _________
- __________ & ________ balance are altered
- ________ impacts myocardial contractility
- Death
AND THEN:
Zoospores live in the ________ or the _____ of other amphibians
(facultative pathogen)
Chytridiomycosis: pathogenesis
- Motile zoospores invade keratin (stratum corneum)
- Zoosporangia develop in epidermal cells (keratinocytes)
- Zoosporangia mature, & release zoospores
- Epidermis thickens (hyperplasia & hyperkeratosis)
- Minimal or absent inflammation
- Respiration & electrolyte balance are altered
- Hyperkalemia impacts myocardial contractility
- Death
AND THEN:
Zoospores live in the environment or the skin of other amphibians
(facultative pathogen)
frogs have a very special type of skin.
when there is a disturbance in skin –> disturbace in electrolyte balance –> hyperkalemia that kills frogs from a heart attack.
zooospores stay in env when frog dies. once in env, never goes away
Skin ________ (_____ Leg is NOT a disease)
__________
Anorexia
_________ skin shedding
- Frogs usually _____ their sheds, but ____ when sick
- ________ (occasionally observed)
- ________ are particularly susceptible
Skin hyperemia (Red Leg is NOT a disease)
Depression
Anorexia
Increased skin shedding
Frogs usually eat their sheds, but not when sick
Seizures (occasionally observed)
Froglets are particularly susceptible
frogs shed skin and then eat that skin shed.
when sick, they do not eat skin sheds so they are stuck to their skin.
red leg = hypermeia of skin
happens with BDE, bacterial infections. it is not a disease, it is a clinical sign.
seizures usually in captive frogs.
froglets are very young frogs
Chytridiomycosis:
clinical signs
Skin hyperemia (Red Leg is NOT a disease)
Depression
Anorexia
Increased skin shedding
Frogs usually eat their sheds
Seizures (occasionally observed)
Froglets are particularly susceptible
Art: Yod Pimsen
do not see red leg as much
Skin erosion to ulceration
Depression
Anorexia
Increased skin shedding
fire salamanders
fungus was orginally discovered in this
Chytridiomycosis: gross findings, Bd
Skin _______
Or _______ at all
______ are particularly susceptible (just after metamorphosis)
Chytridiomycosis: gross findings, Bd
Skin hyperemia
Or nothing at all
Froglets are particularly susceptible (just after metamorphosis)
froglets right after metamoprhosis
keratin is only found in mouth parts because they use this to rasp vegetation to eat. as go throguh metamirphosis, do nt use this in the water b/c do not need to worry abot evap of water, so when they go throgu this process and coem out they need more protection and more waterproofness –> keratin is all over body and fungus like keratinized epi.
tadpoles –> might get deforemd jmouth parts
forglets –> infection spreads troguh entire body and die
punch marks in skin
Skin erosion to ulceration
Depression
Anorexia
Increased skin shedding
Chytridiomycosis: histopathology
A. B. dal
Epidermal ______ & ________
Occasional ________
B. B. sal
Epidermal _______ & ______ to ______
Chytridiomycosis: histopathology
A. B. dal
Epidermal hyperplasia & hyperkeratosis
Occasional inflammation
B. B. sal
Epidermal hyperplasia & erosion to ulceration
Chytridiomycosis:
histopathology
Epidermal hyperplasia & hyperkeratosis
Occasional inflammation
Epidermal hyperplasia & erosion to ulceration
Normal skin, frog
thin corneal layer on top
epidermis
glands
collagen
thickening of epidermis
some inflammatory cells
a lot of sporangia and sodospores
Epidermal hyperplasia & hyperkeratosis
Occasional inflammation
pink = apart of stratum cornueum
flask shape = sporatogorium
poison dart frog
hellbenders can get BD aka frog chitrid ‘
mostly empty sporogania
fungus spore is so tiny
- Is the condition below Bd or Bsal?
- What do you typically see in a case of Bsal?
- Bsal
- B sal grow trough entire epidermis, not just on top like other one that just stays in epidermis
- Epidermal hyperplasia, hyperkeratosis and ulceration. Usually no inflammation at all.
How do you Dx Chytridomycosis?
- PCR on skin swabs + Histopathology (for new areas AND Bsal in North America)
You can have some species that show no clinical signs evn thougb infected. Lab frogs that are aquatic can get BD infections but do not show clincal signs.
frog with clincal signs and suspect BD do above
Bsal is not present in ______
Bsal is not present in NA
Chytridiomycosis: prevention/control
1. ______ hygiene
2. Clean _____
3. ________ health
- VERY IMPORTANT for _____
respond well to _________ unless suceptible to _______ in _______ then die from that
souteast salamanders live with it and can live with it. bought in pet rade. release of these in europe –> b sal in europe.
Chytridiomycosis: prevention/control
1. Field hygiene
2. Clean trade
3. Population health
- VERY IMPORTANT for Bsal
respond well to antifungals unless suceptible to compiunds in antifungal then die from that
souteast salamanders live with it and can live with it. bought in pet rade. release of these in europe –> b sal in europe.
NA is a hotspot for biodiveristy in NA
if bsal cam here, and does what BD did to frogs, we willl use so many pops of slaamanders in the most biodiverse area int he world
Is Chytrid zoonotic?
not zoonotic
Ranavirosis
CAUSE: _________ sp (genus), family __________
- ______ virus
- _____ virus ___ (FV3) – first described, most common in _____
- Other species: CMTV, ATV, BIV, etc
- Species affected:
- All ______-blooded vertebrates
- Reportable to _______ (____)
Ranavirosis
CAUSE: Ranavirus sp (genus), family Iridoviridae
- dsDNA virus
- Frog virus 3 (FV3) – first described, most common in NA
- Other species: CMTV, ATV, BIV, etc
- Species affected:
- All cold-blooded vertebrates
- Reportable to WOAH (OIE)
Ranavirosis: significance
- Originally an ‘______’ virus
- Worldwide (first cases 1990’s)
- Mortalities in North America
- Tadpoles (___-___%)
- Population collapse, potential extirpation/ extinction
- Infection
Cannibalism
Infected water/substrate
Skin injuries
Originally an ‘orphan’ virus
Worldwide (first cases 1990’s)
Mortalities in North America
Tadpoles (98-100%)
Population collapse, potential extirpation/extinction
Infection
Cannibalism
Infected water/substrate
Skin injuries
Ranavirosis: pathogenesis
- Transmission
- ______, respiratory (________) and _________
- Virus replicates in _________ & __________
- Viremia (probably in ______)
- ________ spread
- Replication in distant _______ cells, _____ and ________ cells
- Necrosis of ________, _______ and ____ (mostly in ___)
- Death
Ranavirosis: pathogenesis
- Transmission
- Oral, respiratory (branchial) and cutaneous
- Virus replicates in epithelium & endothelium
- Viremia (probably in WBC)
- Systemic spread
- Replication in distant epithelial cells, WBCs and endothelial cells
- Necrosis of epithelia, endothelia and WBC (mostly in BM)
- Death
Ranavirosis: clinical signs
A. Reptiles
Anorexia, depression
___________ plaques in oral mucosa
_______ & _________ edema
Nasal exudate (_____ to ______)
Respiratory _______
_____ inclusions in circulating WBCs
B. Amphibians
Depression
________ skin shedding
Oral _______, skin ______ to ________ (red leg)
____ inclusions in circulating WBCs
Ranavirosis: clinical signs
A. Reptiles
Anorexia, depression
Fibrinonecrotic plaques in oral mucosa
Cervical & palpebral edema
Nasal exudate (serous to caseous)
Respiratory distress
IC inclusions in circulating WBCs
B. Amphibians
Depression
Increase skin shedding
Oral hemorrhages, skin hyperemia to hemorrhage (red leg)
IC inclusions in circulating WBCs
Ranavirosis: clinical signs
Box turtle: caseous exudate in oral cavity
Ranavirosis: clinical signs
Green frog (tadpoles) & wood frog: skin hyperemia & hemorrhage
Ranavirosis: clinical signs
Wood frog: WBC (monocyte) with IC inclusion body(ies)
Ranavirosis: gross findings
A. Reptiles
_______ exudate in oral cavity and/or _____ cavity
______ in various organs, mostly liver and kidney
B. Amphibians
_________ in oral cavity, skin, GI
_______ necrosis, pinpoint
_________
Ranavirosis: gross findings
A. Reptiles
Caseous exudate in oral cavity and/or nasal cavity
Necrosis in various organs, mostly liver and kidney
B. Amphibians
Hemorrhages in oral cavity, skin, GI
Liver necrosis, pinpoint
Splenomegaly
Ranavirosis: gross findings
Box turtle: Glossitis, fibrinonecrotizing
Ranavirosis: gross findings
Box turtle: Stomatitis, fibrinonecrotizing
Ranavirosis: gross findings
Wood frog: Hemorrhages in GI tract wall (& skin petecchia)
Ranavirosis: gross findings
Wood frog: Splenomegaly (& skin ecchymoses)
Ranavirosis: histopathology
A. Reptiles
- __________ necrosis, _______ plaques & secondary _________ infections
- Vascular fibrinoid necrosis & vasculitis
- Hepatic necrosis & biliary duct necrosis
- IC inclusion bodies in circulating WBCs
B. Amphibians
- Oral, nasal mucosal necrosis
- Vascular fibrinoid necrosis & vasculitis
- Glomerular necrosis & tubular degeneration
- BM necrosis, hepatic necrosis, splenic necrosis
- IC inclusion bodies in circulating WBCs
Ranavirosis: histopathology
A. Reptiles
- Mucosal necrosis, fibrinonecrotic plaques & secondary bacterial infections
- Vascular fibrinoid necrosis & vasculitis
- Hepatic necrosis & biliary duct necrosis
- IC inclusion bodies in circulating WBCs
B. Amphibians
- Oral, nasal mucosal necrosis
- Vascular fibrinoid necrosis & vasculitis
- Glomerular necrosis & tubular degeneration
- BM necrosis, hepatic necrosis, splenic necrosis
- IC inclusion bodies in circulating WBCs
Ranavirosis:
histopathology
Stomatitis, fibrinonecrotizing
Ranavirosis:
histopathology
Stomatitis, fibrinonecrotizing
Ranavirosis:
histopathology
Stomatitis, fibrinonecrotizing
Ranavirosis:
histopathology
Stomatitis, fibrinonecrotizing
Ranavirosis:
histopathology
Hepatitis, necrotizing
Ranavirosis:
histopathology
Biliary duct necrosis, with IC inclusions
Ranavirosis:
histopathology
Biliary duct necrosis, with IC inclusions
Ranavirosis:
histopathology
Vasculitis, necrotizing (fibrinoid necrosis)
Ranavirosis:
histopathology
Glomerular necrosis (& EMH necrosis)
Ranavirosis:
histopathology
Glomerular necrosis, with confirmatory IHC
How do you Dx Ranavirosis?
Ranavirosis: diagnosis
Characteristic clinical signs, gross lesions & histopathology + PCR, IHC, ISH, EM virus isolation
** Dx ≠:
A. Turtles
- Herpesvirus
- Mycoplasma agassizzii
B. Frogs
- Bacterial septicemia
Ranavirosis: prevention & control
1. In Captivity?
2. In Free-ranging?
- Quarantine
- Field hygiene; Avoid transportation of carriers
Ranavirosis: zoonosis
Not at all
White-nose syndrome
- CAUSE: ____________ ___________
- Formerly _________ ___________
- Species affected: _______ American (__________) ___, numerous species
White-nose syndrome
- CAUSE: Pseudogymnoascus destructans
- Formerly Geomyces destructans
- Species affected: North American (hibernating) bats, numerous species
White nose syndrome was first detected in?
White-nose syndrome
- Introduced into NA from Europe
- Howe’s cave, NY, first detection, 2006
White-nose syndrome: pathogenesis
- ____________ bats ONLY
- Transmission: _______ contact
- Fungus infects skin of _____ & _______
- [irritation] = _____ interrupted more frequently
- Energy reserves are spent ____ winter is over
- Water loss results in ________
- Bats leave hibernating site too ____ (still in ____)
- Death from _______ (no insects to feed on)
White-nose syndrome: pathogenesis
- Hibernating bats ONLY
- Transmission: direct contact
- Fungus infects skin of face & wings
- [irritation] = torpor interrupted more frequently
- Energy reserves are spent before winter is over
- Water loss results in dehydration
- Bats leave hibernating site too early (still in winter)
- Death from emaciation (no insects to feed on)
White-nose syndrome: clinical signs
- ________ bats at the entrance of caves or abandoned mines (hibernating sites)
- ___________
- Bats in caves with “…delicate, exuberant, white filaments that obscure the _________.” 1
- “White nose”
- Fuzzy growths also in ______
White-nose syndrome: clinical signs
- Dead bats at the entrance of caves or abandoned mines (hibernating sites)
- Emaciated
- Bats in caves with “…delicate, exuberant, white filaments that obscure the
muzzle.” 1
- “White nose”
- Fuzzy growths also in wings
White-nose
syndrome:
clinical signs
”White nose” = fungal growth in face & wings
White-nose
syndrome:
clinical signs
”White nose” = fungal growth in face & wings
White-nose
syndrome:
gross findings
Emaciation
Fuzzy white growth in face, wings and patagium (hibernating bats)
Discoloration or tears in wings and patagium (bats in summer)
Survivors
White-nose
syndrome:
histopathology
Hibernating bats:
Cup-like erosions of wing membrane skin w/fungal hyphae (mild) to
abundant hyphal growth and invasion of dermis (severe)
White-nose
syndrome:
histopathology
Hibernating bats:
Cup-like erosions of wing membrane skin w/fungal hyphae (mild) to
abundant hyphal growth and invasion of dermis (severe).
White-nose
syndrome:
histopathology
Non-hibernating bats (late Spring/Summer – survivors):
Dermatitis, neutrophilic, with crust formation
How do you Dx white nose syndrome?
White-nose syndrome: diagnosis
Characteristic clinical signs, gross lesions & histopathology
+
PCR, fungal culture
White-nose syndrome: prevention &
control
- Prevention?
- __________ of equipment between caves
- Control?
- Several things have been tried…______ really works
White-nose syndrome: prevention &
control
- Prevention?
- Decontamination of equipment between caves
- Control?
- Several things have been tried…nothing really works
White-nose syndrome: zoonosis
Not at all
Squirrel fibromatosis
- CAUSE: _________ (squirrel _______ virus)
- _______ virus
- Species affected:
-American _______ gray, _____ gray, ____, and _____ squirrels
- Similar to rabbit (_____) fibroma virus but different from _________ virus
- Squirrelpox virus: _________, mild in NA _____ but severe (lethal) to UK _____ squirrels
Squirrel fibromatosis
- CAUSE: Leporipoxvirus (squirrel fibroma virus)
- dsDNA virus
- Species affected:
-American eastern gray, western gray, red, and fox squirrels
- Similar to rabbit (shope) fibroma virus but different from
squirrelpox virus
- Squirrelpox virus: suppurative, mild in NA grey but severe (lethal) to UK red squirrels
Squirrel fibromatosis: pathogenesis
- Transmitted by:
- __________ (______ insects)
- _________ contact
- Virus infects _______ (______) cells & ________
- Local lesions (________ cell proliferation) = fibromas (_____________)
- Viremia or repeated exposure
- Multiple lesions
- Spontaneous regression = healing
Squirrel fibromatosis: pathogenesis
- Transmitted by:
- Arthropods (biting insects)
- Direct contact
- Virus infects epithelial (mucosal) cells & fibroblasts
- Local lesions (neoplastic cell proliferation) = fibromas (fibropapillomas)
- Viremia or repeated exposure
- Multiple lesions
- Spontaneous regression = healing
Squirrel
fibromatosis:
clinical signs &
gross findings
Nodules throughout
the skin (fibromas)
Squirrel fibromatosis: histopathology
A. Dermis:
Non-encapsulated mesenchymal cells, arranged in interweaving bundles with fine collagenous stroma, rare mitotic figures, IC
inclusions - _________
- LQ/PL inflammation
B. Epidermis:
Hyperplastic epidermis with IC inclusions, ulceration & bacterial colonies
Squirrel fibromatosis: histopathology
A. Dermis:
Non-encapsulated mesenchymal cells, arranged in interweaving bundles with fine collagenous stroma, rare mitotic figures, IC
inclusions - FIBROMAS
- LQ/PL inflammation
B. Epidermis:
Hyperplastic epidermis with IC inclusions, ulceration & bacterial colonies
Squirrel
fibromatosis:
histopathology
FIBROMAS
Squirrel
fibromatosis:
histopathology
FIBROMAS
Squirrel
fibromatosis:
histopathology
FIBROMAS
Squirrel
fibromatosis:
histopathology
FIBROMAS
Characteristic clinical signs, gross lesions & histopathology
+
PCR, virus isolation
Dx ≠:
Squirrelpox virus – deadly to UK red squirrels
Photo:DAERA
Squirrel
fibromatosis:
prevention &
control
Avoid introduction of species to non-native habitats…
For squirrelpox virus:
Avoid feeding grey and red squirrels together
Squirrel
fibromatosis:
zoonosis
Not at all
