Wildlife Pathology Flashcards

1
Q

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 _____

A

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

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2
Q

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

A

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

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3
Q

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
–

A

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
–

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4
Q

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
–

A

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
–

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5
Q

‘Atypical myxomatosis’ when you can have the _____ lesions and sometimes the only thing that develop is a ______ pneumonia. This type of pneumonia is _________ pneumonia.

A

‘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

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6
Q
A

moderate swelling and conjunctivitis and blephitis

European rabbits (Oryctolagus cuniculus):
– Swelling & redness (inflammation) in eyelids

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7
Q
A

European rabbits (Oryctolagus cuniculus):
– Secondary bacterial conjuctivitis

more severe form with purulent exudate forming

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8
Q
A

d 4 = reddening of eyelids
d 8 = some supp exu
d 11 = severe

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9
Q

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

A

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

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10
Q
A

– Subcutaneous mucinous (gelatinous) masses:
– Particularly on the face (eyelids, nose) & perineum - myxomas

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11
Q
A

Mucopurulent blepharoconjunctivitis, nasal discharge

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12
Q
A

– Pneumonia, interstitial
– Edema, hemorrhage (atypical myxomatosis)

froth in trachea = edema

rib impressions with interstitial pneumonia

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13
Q

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

A

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

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14
Q
A

eyelid
Epithelial hyperplasia & dermal myxomatous matrix

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15
Q
A

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

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16
Q
A

Epithelial hyperplasia, ballooning degeneration , hyperkeratosis
Heterophils here

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17
Q
A

Epithelial hyperplasia,& large eosinophilic IC viral inclusions

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18
Q
A

Epithelial hyperplasia,& large eosinophilic IC viral inclusions

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19
Q
A

Epithelial hyperplasia,& large eosinophilic IC viral inclusions

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20
Q
A

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)

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21
Q
  1. How do you Dx Myxomatosis?
  2. What tests do you use to confirm your Dx?
A
  1. Characteristic clinical signs, gross lesions & histopathology
  2. PCR, IHC, EM, virus isolation
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22
Q
A

Myxomatosis
TEM
Dumbell shaped

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23
Q

Myxomatosis: prevention & control
–
__________ in areas with high disease prevalence - Not available everywhere

Keep ________ (or _____) away from rabbits

Is there a proper treatment protocol?

A

Vaccination in areas with high disease prevalence - Not available everywhere

Keep mosquitoes (or fleas) away from rabbits

No real treatment other than supportive care.

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24
Q

Zoonotic?

A

no

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25
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.
26
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
27
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
28
Snake fungal disease: clinical signs – Yellow to brown plaques – Deformed head
29
Snake fungal disease: gross findings – Yellow to brown plaques – Deformed head – Retained, opaque, spectacles entered bone --> osteomyelitis
30
Snake fungal disease: gross findings – Yellow to brown plaques – Deformed head usually die before getting to hat is pictured
31
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
32
Snake fungal disease: histopathology – Granulomas w/fungal hyphae allll to the right
33
Snake fungal disease: histopathology – Granulomas w/fungal hyphae fibrous CT with fungal hyphae MNGC and MCQ
34
Fungal hyphae Stain: Silver stain or PAS
35
– Granulomas w/fungal hyphae Silver stain is best
36
1. How do you Dx Snake fungal disease? diagnosis 2. What tests do you need to run to Dx Snake Fungal disease? 3. You also need to make sure to rule out _______ for any animal with a granulomatous response (?), because fungi can also be secondary invaders. 4. Which special stain do you use to find mycobacteria in histology?
1. Characteristic clinical signs, gross lesions & histopathology 2. 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 3. 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. 4. Acid fast
37
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
38
Snake fungal disease: zoonosis
– Not at all
39
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
40
“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
41
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
42
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
43
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
44
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
45
do not see red leg as much – Skin erosion to ulceration – Depression – Anorexia – Increased skin shedding fire salamanders fungus was orginally discovered in this
46
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)
47
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
48
punch marks in skin – Skin erosion to ulceration – Depression – Anorexia – Increased skin shedding
49
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
50
Chytridiomycosis: histopathology – Epidermal hyperplasia & hyperkeratosis – Occasional inflammation – Epidermal hyperplasia & erosion to ulceration Normal skin, frog thin corneal layer on top epidermis glands collagen
51
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
52
hellbenders can get BD aka frog chitrid ' mostly empty sporogania fungus spore is so tiny
53
1. Is the condition below Bd or Bsal? 2. What do you typically see in a case of Bsal?
1. Bsal 2. 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.
54
How do you Dx Chytridomycosis?
1. 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
55
Bsal is not present in ______
Bsal is not present in NA
56
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.
57
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
58
Is Chytrid zoonotic?
not zoonotic
59
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)
60
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
61
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
62
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
63
Ranavirosis: clinical signs – Box turtle: caseous exudate in oral cavity
64
Ranavirosis: clinical signs – Green frog (tadpoles) & wood frog: skin hyperemia & hemorrhage
65
Ranavirosis: clinical signs – Wood frog: WBC (monocyte) with IC inclusion body(ies)
66
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
67
Ranavirosis: gross findings – Box turtle: Glossitis, fibrinonecrotizing
68
Ranavirosis: gross findings – Box turtle: Stomatitis, fibrinonecrotizing
69
Ranavirosis: gross findings – Wood frog: Hemorrhages in GI tract wall (& skin petecchia)
70
Ranavirosis: gross findings – Wood frog: Splenomegaly (& skin ecchymoses)
71
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
72
Ranavirosis: histopathology – Stomatitis, fibrinonecrotizing
73
Ranavirosis: histopathology – Stomatitis, fibrinonecrotizing
74
Ranavirosis: histopathology – Stomatitis, fibrinonecrotizing
75
Ranavirosis: histopathology – Stomatitis, fibrinonecrotizing
76
Ranavirosis: histopathology – Hepatitis, necrotizing
77
Ranavirosis: histopathology – Biliary duct necrosis, with IC inclusions
78
Ranavirosis: histopathology – Biliary duct necrosis, with IC inclusions
79
Ranavirosis: histopathology – Vasculitis, necrotizing (fibrinoid necrosis)
80
Ranavirosis: histopathology – Glomerular necrosis (& EMH necrosis)
81
Ranavirosis: histopathology – Glomerular necrosis, with confirmatory IHC
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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
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Ranavirosis: prevention & control 1. In Captivity? 2. In Free-ranging?
1. Quarantine 2. Field hygiene; Avoid transportation of carriers
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Ranavirosis: zoonosis
– Not at all
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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
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White nose syndrome was first detected in?
White-nose syndrome - Introduced into NA from Europe - Howe’s cave, NY, first detection, 2006
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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)
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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
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White-nose syndrome: clinical signs – ”White nose” = fungal growth in face & wings
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White-nose syndrome: clinical signs – ”White nose” = fungal growth in face & wings
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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
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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)
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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).
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White-nose syndrome: histopathology – Non-hibernating bats (late Spring/Summer – survivors): – Dermatitis, neutrophilic, with crust formation
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How do you Dx white nose syndrome?
White-nose syndrome: diagnosis – Characteristic clinical signs, gross lesions & histopathology + – PCR, fungal culture
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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
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White-nose syndrome: zoonosis
– Not at all
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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
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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
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Squirrel fibromatosis: clinical signs & gross findings – Nodules throughout the skin (fibromas)
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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
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Squirrel fibromatosis: histopathology – FIBROMAS
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Squirrel fibromatosis: histopathology – FIBROMAS
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Squirrel fibromatosis: histopathology – FIBROMAS
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Squirrel fibromatosis: histopathology – FIBROMAS
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– Characteristic clinical signs, gross lesions & histopathology + – PCR, virus isolation – Dx ≠: – Squirrelpox virus – deadly to UK red squirrels Photo:DAERA
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Squirrel fibromatosis: prevention & control – Avoid introduction of species to non-native habitats... – For squirrelpox virus: – Avoid feeding grey and red squirrels together
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Squirrel fibromatosis: zoonosis – Not at all