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MS > Papilloma > Flashcards

Papilloma Flashcards

1
Q

What is a koilocyte (Welle, Maulidn, JPC)

A

swollen keratinocytes with eosinophilic to lightly basophilic cytoplasm and perinuclear halo
-can have multiple nuceli

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2
Q

Name viral cytopathic effects papilloma (JPC)

A
  1. Koilocytes
  2. Intranuclear inclusion bodies
  3. Large, irregular keratohyalin granules (in exophytic types)
  4. Variable degress of ortho/para HK
  5. Degenerating KC with eosinophilic cytoplasmic inclusions (represent aggregates of keratin)- may be confused with POX!
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3
Q

How are papillomaviruses sperad

A
  1. Transplacental (FcPV-a in almost all cats from early in life)
  2. Fomites (direct and indirect contact)
  3. Skin abrasions
  4. bovine- arthropod, vertical, blood
  5. horse-flies, miking machines + co factors: malnutrition, hormonal imbalance, mutations, long term exposure to sunlight
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4
Q

Name 3 genera

A
  1. Lambda
  2. Tau
  3. Chi
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5
Q

What are the predispositions /predilections

A
  1. IgA deficiency- oral papillomatosis
  2. GC, chemotherapy
    Predilection in old animals (accumulations of spontaneous mutations throughout life)
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6
Q

Which proteins are involved in malignant transformation

A
  1. p53
  2. p16
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7
Q

How does the infection occur

A
  1. Microtrauma allows PV to intreact with BM
  2. PV enters cells after binding to alpha 6 integrin - infects KRT in SB
  3. Basal cell replication- episomal DNA spread through basal cell population and maintain infection, during this phase normal epithelial regulation not altered, infection is asymptomatic, non-infective
  4. PV to complete the life cycle - in a basal cell that undergoes terminal differentiation
  5. Replication of PV DNA dependent on host nucelus
    -key feature: ability to prevent cells from leaving the S phase (where DNA replicate , ensure that KC keep dividing, amplifies infection because every divided KC will be infected
  6. genome replication in SS and SG
  7. release new infection in keratinized squames - achantosis, HK, koilocytes in SS, giant KH granules in SG
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8
Q

PV- induced cancer. What is the critical step

A

integration od E6 and E7 genes (proteins- oncogenes) in host DNA

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9
Q

Where are early genes expressed

A

in basal and suprabasal layers

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10
Q

Where are late genes expressed

A

in SS and SG

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11
Q

Where are virions expressed

A

-upper SG and SC

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12
Q

How are infective viruses spread

A

-released due to normal cell death

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13
Q

What are the methods of evading immune system (ch infections)

A
  1. infection of immune privileged site (epidermis, HF)
  2. no idnuction of type I IFN of infected KC by CPV-2
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14
Q

Name 3 components of genes

A
  1. Early genes (E7)
  2. Late genes (L2)
  3. LCR - long control region
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15
Q

What are the oncogens

A

E5,E6,E7

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16
Q

What is the function of E1, E2

A

-regulation of viral DNA replication

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17
Q

Function of E3

A

modulates immune response of infected cells

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18
Q

Function of E4

A

disrupt cytokeratins facilitating viral release (viral replication)

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19
Q

Function of E5

A

BPV-1, BPV-2
-inhibits intercellular communication through gap junctions
-activates PDGF receptor
-down regulates MCH-1
-interactions with growth factors

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20
Q

functions of E6 and E7

A

= cell proliferation and immortalization
E6-disrupts focal adhesions, degrade p53 (accumulate various mutations)
E7-cell growth, chromosomal instability, , inhibit retinoblastoma (Rb): important tumor suppressor protein

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21
Q

What is function of late genes

A

=coded in SS and SG
L1, L2- genes encode for viral capid protein
L1- major capsid protein highly immunogenic, used to classify PV in genera

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22
Q

What are LCR (long control region)

A

-does not code proteins
-regulates viral gene transcription (when and which genes are necessary in the process of infections)

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23
Q

How can dg be made

A
  1. PCR
  2. In situ hybridization
  3. EM
  4. Rolling circle amplification
  5. IHC
  6. Histo
  7. Clinical examination
  8. Blot: southern, dot, reverse
24
Q

How is IHC used for dg PV

A

-SG: Ab detect L1 protein or increased p16
-L1 protein forms the capsid- largely produced in late process of viral repilcation
-rarely present in advanced BISC or in PV + SCC

25
Q

DDX in dogs

A
  1. IKA
  2. trichofolliculoma
  3. cutaneous horn
  4. lentigo
  5. melanocytic neoplasms
26
Q

DDX in cats

A
  1. MCT
  2. cutaneous horn
  3. dilated pore of Winer
  4. melanocytic neoplasms
27
Q

How can you differentiate pathogenic PV and asymptomatic infection in lesions of other etiology

A

p 16 protein expression
+ in PV induced skin lesions

28
Q

In bovine which animals usually develop disease

A

-young cattle
-usually regress, may lead to neoplasia + environmnetal cofactors
ch ingestion of bracken fern ( Pteris aquilina)
ch immunosupressed animals
infection with BVDV

29
Q

Which PV cause oral papilomas in dogs

A

CPV-1 (SCC) , 3, 13

30
Q

What are associations for development of oral papilomas in dogs

A
  1. IgA deficiency (beagle)
  2. GC: severe oral + generalized cutaneous in young Shar Pei
  3. CsA- anecdotal
  4. chemotherapy
  5. Imunosupressive th?
  6. UV radiation?
31
Q

Which PV cause exophtic papilloma in dogs

A

CPV-1, 2, 7, 14

32
Q

Which breeds are predisposed to exophtic PV and age ?

A
  1. Kerry blue
  2. Cocker
  3. CsA
    + OLDER DOGS
    + can udergo sponatenous remission
33
Q

What are recommedned treatments for exophytic PV in dogs

A
  1. 4-fluorouracil topical
  2. imiquimod
  3. oral etretinate
34
Q

Which PV are associated with generalised verrucosis PV

A

CPV-2, 9

35
Q

Which PV are associated with inverted papiloma and which is associated with SCC

A

CPV-1, 2, 6

CPV-2 SCC

36
Q

Which PV are associted with feline cutaneous papilloma

A

FcPV-1

-melanocytic macules-> HK pigmnted plaques, greasy
-2 Persian cats /immunosompromised

37
Q

How are caprine cutaneous PV manifested

A
  1. First form: no predilection, self cure, multiple animals
  2. Second form
    - white females that lactated at least once
    -udder, teats
    -no self cure
    -may transform to SCC
38
Q

How are ovine cutaneous PV manifested

A
  1. FILIFORM SQUAMOUS PAPILLOMAS
    -legs young,
    - scrotum rams
    - face , pinnae, legs, teats adults
    -facial can transform to SCC
  2. FIBROPAPILLOMA
    -adults
    -facial into SCC
    -Merinos may be at risk
39
Q

Are cutaneous papilomas reported in pigs

A

yes
-congenital
-face and genitalia

40
Q

In birds, where are papillomas most commonly reported

A

-cloaca
-feet, head, mm

-often proliferative,
-th: autogenous vaccines, laser

41
Q

Have PV been reported in snakes

A

yes

42
Q

Which are unique camelid PV

A
  1. viral papillomas
  2. fibropapillomas
43
Q

Name other PV in camelids

A

1,5-cauliflower like on penis
2,6-typical papillomas
2,7-congenital probable epidermal nevus
8- frond like
3, 9
5- finger like or rice grain on teat

44
Q

What does PV in rabbits cauase

A

ā€ Shope PVā€
Cotton tail rabbit PV

45
Q

What PV cause in primates

A

-warts
-epidermal hyperplasia
-oral plaques

46
Q

Which PV are associated with pigmented plaques in dogs

A

CHI
CPV-4 + 3,5, 8, 9, 16

CPV-4 pugs, viszla
-can progres to SCC (not in pugs)

47
Q

What are predilections for canine pigmented plaques

A
  1. young
  2. min Schnautzer
  3. pug - autosomal mode if inheritance
  4. Boston terrier
  5. French bulldog
  6. Viszla (genetic pred in Australia?)
  7. Chinese Shar pei
48
Q

What is recommended for canine viral plaques

A

-usually not effective
1. Tigilanol tigilate - 2 times 9 days apart
2. imiquimod

49
Q

Which PV are assocaited with viral plaques in cats?

A

FcPV-2 (BISC)
+3,5

50
Q

What are predispositions for feline pigmented plaques

A
  1. early age- Sphinx, Devon rex: highly metastatic SCC
  2. underlying immunosupersion- FIV, FeLV, Ch GCs
  3. usually middle age, old
51
Q

Feline sarcoid/feline cutaneous fibropapilloma

A

BPV-14, 1

52
Q

Equine sarcoid

A

BPV1,2, 13

53
Q

Which PV is associted with cutaneous horn

A

CPV-1

54
Q

What are other causes of cutaneous horns

A
  1. solar dermatitis
  2. skin carcinoma
  3. IKA
  4. intracutaneous epithelioma
  5. keratin cysts
  6. viral papilloma
  7. FeLV
55
Q

Name treatment options for PV

A
  1. Azytrhomicin
  2. Surgery
  3. Laser, cryosurgery, electrosurgery, CO2 laser ablation
  4. Cryotherapy ( 2 sessions)
  5. Freezing or crusing (Ag stimulation)
  6. IFN-alpha (low dose po, high dose intralesional, INF-omega)
  7. Topical 4-fluorouracil, 5-fluorouracil (no CATS- neurotoxic)
  8. Imiquimod
  9. Photodynamic th
  10. Retinoids
  11. Tatantula venom

+ VACCINE

55
Q

In wich species horn have been seen

A

-bovine, goat, ovine, rabbit

56
Q

Which vaccines have been developed for PV

A
  1. Live autologous- protective, associted with injection site SCC
  2. Modified (formalin inactivated or replication deficient)- no SCC
  3. recombinant- induce regression, may be prophylactic

MS (20 decks)

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