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Path > 2: herpes viruses, papillomaviruses, epidemics > Flashcards

2: herpes viruses, papillomaviruses, epidemics Flashcards

1
Q

name viruses associated with chronic infection and neoplastic transformation

A
  • HSV1
  • HSV2
  • EBV
  • CMV
  • HTLV
  • HHV8
  • papillomavirus
  • Hep B, C
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2
Q

primary and recurrent forms of HSV1 and 2

A

primary: local reaction at site of contact (can get pharyngitis)

secondary: lyses cells to form vesicles! re-activation
- inside vesicles = fluid + herpes-infected cells

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3
Q

what does scrapings of herpes lesions reveal histologically?

A

inclusion-bearing multinucleared syncytia (giant cells)

-see on Tzanck smear

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4
Q

what is a good way to differentiate this from zoster?

A

herpes is independent of skin dermatomes

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5
Q

what are herpes blisters associated with?

A

edema
ballooning degeneration
cytopathic changes
necrosis

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6
Q

what happens if you get corneal lesions w/ herpes?

A

cell infiltrates
neovascularization
scarring
blindness

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7
Q

if herpes disseminates in immunocompromised people, what can happen

A

fatal sporadic encephalitis or corneal blindness

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8
Q

congenital infections

A 
TORCH
toxo
other
rubella
CMV
herpes
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9
Q

what are the classic signs/symptoms of congenital infections that occur in 3rd trimester?

A

deafness
ataxia
blindness
developmentally delayed

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10
Q

differentiate the honey-colored crusting of herpes and impetigo

A

herpes: due to ruptured vesicles w/ serous fluid that dries
impetigo: skin ruptures, drains inflammatory fluid

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11
Q

primary and secondary infections from EBV

A

primary: infectious mononucleosis

secondary: latent infection of B cells
- Burkitt’s lymphoma
- B cell lymphomas (immunosuppressed)
- nasopharyngeal carcinoma
- sarcoidosis

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12
Q

describe infectious mononucleosis

A
  • benign, self limiting
  • transmitted by saliva
  • lymphoproliferative (hyperplasia, lymphadenopathy)
  • fatigue, headache, low grade fever, pharyngitis
  • TENDER cervical node enlargement
  • splenomegaly
  • if super widespread: hepatitis, meningoencephalitis, pneumonitis
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13
Q

pathology of infectious mononucleosis

A
  • binds to complement receptor on epithelial cells and B cells
  • spreads through oral epithelium to underlying B lymphoid tissues
  • shed in saliva
  • NONSPECIFIC POLYCLONAL AB STIMULATION
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14
Q

what will you see on peripheral blood smear?

A

ATYPICAL LYMPHOCYTES: anti-EBV T cells, not B cells

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15
Q

how does monospot test distinguish between EBV mono and CMV mono-like illness?

A

EBV- makes anti-carb Ab’s that cause polyclonal activation, so you get Ab’s of all kinds: mix pt serum with sheep RBCs and get agglutination

CMV - does not do this b/c doesn’t infect B cells like EBV does

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16
Q

what can the polyclonal activation of EBV give you a false positive for? what else gives false positive for this test?

A

false (+) VDRL

-lupus also does this

17
Q

how to differentiate infectious mononucleosis from Hodgkin’s disease

A

difficult - but mono is tender, while Hodgkin’s is non-tender

18
Q

what is diagnosis of infectious mono dependent on?

A
  • finding atypical lymphocytes
  • positive heterophile rxn
  • specific Ab’s for EBV Ag’s
19
Q

why is it really bad if a person with x-linked lymphoproliferative disease gets EBV?

A

they can die - have an absence of SAP gene: mutated protein involved in regulation of an intense CD8 cytotoxicity stimulated by EBV
-if they survive, they can develop B cell lymphomas

20
Q

what histology is associated with CMV

A

large purple nuclear or cytoplasmic inclusions

21
Q

CMV is usually a mild ish disease, unless what population gets it?

A

neonates - can mimic erythroblastosis fetalis

22
Q

what is diagnostic of neonatal CMV

A

infects renal tubules, so you see CMV infected cells in urine sediment

23
Q

most common opportunistic viral disease in AIDS patients

A

CMV (retinitis)

24
Q

when CMV presents in AIDS patients, what does it almost always present with?

A

pneumocystis infection

25
Q

what does CMV cause in immunosuppressed people

A

severe, disseminated disease associated with reactivation of viral infection from latent infection of leukocytes

26
Q

what does HPV cause

A

proliferative lesions including:

  • common warts
  • plantar warts
  • cervical dysplasia
  • cervical carcinoma/squamous cell carcinoma
27
Q

transmission of HPV

A

direct contact

28
Q

what does expression of HPV viral genes depend on

A

state of differentiation of epithelial cells

  • initially infects basal cells, but limited expression of viral genes
  • as epithelial cells differentiate, more viral genes expressed
29
Q

what are non-neoplastic strains of HPV associated with/

A

koilocytosis

30
Q

what are neoplastic strains of HPV associated with?

A

viral integration within the DNA

dysplasia

31
Q

why will papillomaviruses not grow in culture?

A

because they require terminally differentiating squamous epithelial cells (i.e. keratinocytes)

32
Q

another term for common warts

A

verruca vulgaris

33
Q

Ebola:

  • transmission
  • why important
  • where does it occur
A

-person to person transmission/considered nosocomial
-multihemorrhagic manifestations w/ DIC, shock, HIGH mortality (30-90%)
-hepatic involvement
-visceral organ necrosis
-organ damage doesn’t kill you, hemorrhage, shock, fluid
loss do

34
Q

Hanta virus:

  • transmission
  • why important
  • where does it occur
A
  • rodent urine or feces
  • acute hemorrhagic pulmonary syndrome (mortality 50%)
  • fever, acute respiratory distress, hemorrhages, DIC
  • Southwest (4 corners)
35
Q

Dengue:

  • transmission
  • why important
  • where does it occur
A
  • Aedes mosquito
  • hemorrhagic, bone breaker fever
  • myalgias, arthralgias, rashes, vomit, diarrhea, nausea
  • tropics and Africa
36
Q

West Nile virus:

  • transmission
  • why important
  • where does it occur
A
  • arbovirus transmitted by mosquitos to birds/mammals - humans are accidental hosts
  • usually asymptomatic, but when clinically infected: meningitis, encephalitis, meningoencephalitis
  • immunosuppressed and elderly at greatest risk

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