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LAST EXAMMMMMM Year I > Chap8- Viral Infections > Flashcards

Chap8- Viral Infections Flashcards

1
Q

What viruses attack upper respiratory tract

A

adenovirus
rhinovirus
influenza viruses A B
Respiratory syncytial virus

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2
Q

What viruses affect the digestive tract

A 
mumps
rotavirus- childhood
norovirus
Hep A
Hep B
Hep D
Hep C
Hep E
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3
Q

What viruses cause systemic with skin eruptions

A 
measles
rubella
varicella zoster
Herpes simplex virus 1
Herpes simplex virus 2
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4
Q

What viruses cause systemic with hematopoietic disorders

A

CMV
EBV
HIV 1 and 2

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5
Q

What are the arboviral and hemorhhagic fever viruses

A

dengue virus1-4

yellow fever

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6
Q

what virus causes skin warts

A

papillomavirus

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7
Q

What viruses affect CNS

A

polio and JC

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8
Q

How do you confirm a measles Dx

A

detection of viral antigen in nasal exudate or urinary sediment

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9
Q

What type of virus is measles

A

ss RNA of the paramyxovirus family

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10
Q

What virus causes croup

A

parainfluenza virus

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11
Q

What cell R are associated with measles

A

CD46- C’ regulatroy protein that inactivates C3 converses

SLAM- involved in T cell activation

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12
Q

How does measles spread

A

respiratory droplets and from there can multuply in epithelial cells, endothelial, monocytes, macrophages, dendritic cells and lymphocytes

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13
Q

What does measles cause clinically

A

croup, pneumonia, diarrhea with protein-losing enteropathy, keratitis with scarring and blindness, encephalitis and hemorrhagic rashes in malnourished children

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14
Q

Most people develope what type immunity to measles

A

T cell, with hypersensitivity rash

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15
Q

What is the cause of measles morbiditiy and mortality rates

A

its immunosuppression resulting in secondary bacterial and viral infection

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16
Q

What are some of the late complications of measeles

A

subacute sclerosing panencephalitis and inclusion body encephalitis

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17
Q

What does the rash to measles look like and what causes it

A

blotchy reddish, brown rash on face, trunk and proximal extremities
from dilated skin vessels, edema and mononuclear perivascular infiltrate

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18
Q

What are the pathonomonic findings in measles

A

Koplik spots, ulcerated mucosal lesions in oral cavity near opening
Warthin-Finkeldey cells- multinucleate giant cells in lymphoid tissue

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19
Q

What are the 2 types of glycoproteins on the mumps virus

A

one with hemagglutinin and one with neuraminidase activities

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20
Q

Where does mump replicate

A

preferentially in activate T cells

travel in drained lymph

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21
Q

What are common signs of mumps

A

salivary gland pain and aseptic meningitis

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22
Q

Describe morphology of the parotitis in mumps

A

moist, glistening and reddish brown
diffusely infiltrated by macrophages, lymph and plasma cells which compress acini and ducts
some neutrophils and necrotic debris

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23
Q

Describe morphology mumps orchitis

A

swelling from edema and mononuclear cell infiltration with focal hemorrhages
can have ares of infarction leading to sterility

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24
Q

What does mumps look like in pancreas

A

fat necrosis and neutrophil rich inflammation

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25
Q

describe mumps encephalitis

A

causes perivenous demylination and perivascular mononuclear cuffing

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26
Q

What type of virus is polio

A

unencapsulated RNA from the enterovirus genus

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27
Q

What are the enteroviruses

A

coxsackievirus A and B, enterovirus 70, echovirus

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28
Q

How many strains are there of polio and what vaccines are available

A

3 strains

the salk formalin(killed) and sabin oral (attenuated live) have all 3

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29
Q

how is polio transmitted

A

oral fecal route

multipling in intestinal mucosa and lymph nodes

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30
Q

Why does polio only affect humans

A

uses human CD155 to gain entry

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31
Q

What group of viruses does west nile belong to

A

arbovirus of flavivirus group

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32
Q

Where does west nile replicate

A

in dendritic cells then migrating to lymph nodes where it can enter blood stream and potentially cross bbb

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33
Q

What is the double edge about CCR5

A

without it more prone to west nile

with it- can be affect by HIV

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34
Q

What are the symptoms of west nile if any

A

short lived febrile illness with HA and myalgia

maculopapular rash in some

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35
Q

What is found in brains of those who died of West nile

A

perivascular and leptomeningeal chronic inflammation with microglial nodes and neronophagia in temporal lobes and brain stem

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36
Q

what is the best way to confirm Dx of west nile

A

usually serology but viral culture and PCR used too

37
Q

what type of viruses cause viral hemorrhagic fevers and what are the 4 families

A

enveloped RNA viruses

arenaviruses, filoviruses, bunyaviruses and falviviruses

38
Q

what are the mild acute diseases cause by viral hemorrhagic fevers VHF

A

fever, HA, myalgia, rash, neutropenia and thrombocytopenia

39
Q

what are the severe diseases cause by VHF

A

hemodynamic deterioration and schock

40
Q

What immune response contributes to VHF

A

innate because activation of macrophages leads to release of mediators that modify vascular function

41
Q

What type of DNA is herpes

A

ds DNA

42
Q

what are the categories of herpes and types of cells they each infect

A

alpha group: HSV 1 and 2, VZV infecting epithelial cells and latency in neurons
lymphotropic beta group: CMV, herpes-6 and herpes-7 infect a variety of cells
-group: EBV KSHV-8 latent infections in lymphoid cells

43
Q

Where do HIV 1 and 2 replicate

A

in the skin and mucous membranes at site of entrance where they cause vesicular lesions

44
Q

What occurs during latency in HSV

A

viral DNA remains in nucleus and viral RNA trancripts are synthesized
no viral proteins are produced

45
Q

how do HSV evade CTLs

A

inhibit class I MHC and elude humoral immune defenses by producing R for the Fc domain of Ig and inhibitors of C’

46
Q

Where in the brain does HSV attack first

A

temporal lobes, orbital gyri of frontal lobes

47
Q

what do HSV cells looks like

A

large with inclusions that have intact disrupted virions with stained host cell chromatin pushed to edges of nucleus

48
Q

what is gingivostomatitis

A

children with HSV-1 that have a vesicular eruption extending from tongue to retropharynx casing cervical lymphadenopathy

49
Q

What does HSV-2 look like in neonate

A

mild, more commonly with generalized lymphadenopathy, splenomegaly and necrotic foci throughout lungs, liver, adrenals and CNS

50
Q

What type of corneal lesions does Herpes cause

A

herpes epithelial keratitis- cytolysis of superficial epithelium
herpes stromal keratitis- infiltrates of mononuclear cells around keratinocytes and endothelial cells–>neovascularization, scarring, opacificaiton of cornea and eventual blindness

51
Q

What is kaposi varicelliform eruption

A

generalized vesiculating involvement of skin

52
Q

what is eczema herpeticum

A

confluent pustular or hermorrhagic blisters with bacterial superinfection and viral dissemination to internal viscera

53
Q

how does herpes affect resp tract

A

herpes esophagitis and bronchopneumonia

54
Q

what conditions are caused by varicella zoster virus

A

chicken pox and shingles

55
Q

how is VZV transferred

A

aerosols, and causes widespread vesicular skin lesions

56
Q

Describe the recurrence of VZV

A

painful in dermatomes innervated by trigem ganglia

57
Q

How is VZV Dx confirmed

A

viral culture or detection of viral Ag in cells from superficial lesions

58
Q

what do chicken pox vesicles have in them

A

intranuclear inclusions in epithelial cells like that of HSV-1

59
Q

What is shingles

A

when VZV has been latent a long time, after having chicken pox
will infect keratinocytes that have vesicular lesions assoc with itching, burning or sharp pain

60
Q

What can VZV cause in immunocompromised patients

A

interstitial pneumonia, encephalitis, transverse myelitis, necrotizing visceral lesions

61
Q

What type of cells does CMV attack latently

A

monocytes and their bone marrow progenitors

62
Q

What does CMV cause in healthy patients? neonateS? immunocompromised?

A

asymptomatic or mononucleosis like infection with fever and lymphadenopathy, hepatomegaly
intrauterine: cytomegalic inclusion disease- growth retardation, jaundice, HSM, anemia, encephalitis, microcephaly, deafness
perinatal: interstitial pneumonitis, skin rash, hepatitis, failure to thrive
immunocompromised pneumonitis, colitis, ARDS, intestinal necrosis with formation of pseudomembranes and diarrhea

63
Q

What cells does CMV acutely affect

A

dendritic cells and impair their maturation and ability to stimulate T cells

64
Q

how does CMV elude immune system

A

downmodulates Class I and II MHC and produces homologues to TNF R, IL 10 and MHC I

65
Q

how does CMV affect NK cells

A

activate and evade NK cells by inducing ligands for activating R

66
Q

What do CMV cells look like morpho

A

enlarged

intranuclear basophillic inclusions spanning half the nuclear diameter

67
Q

what tissues and components are affected by CMV

A

glands- parenchymal epithelium
brain- neurons
lungs- alveolar macrophages
kidneys- tubular epithelium and glomerular endothelial

68
Q

What is the most common opportunistic viral pathogen in AIDS

A

cytomegalovirus

69
Q

What does HBV (HepB) cause

A

acute and chronic liver disease

70
Q

how is HBV transmitted

A

drug IV, blood, perinatally, sexually

71
Q

The cellular injury of liver from HBV occurs how

A

from immune response to infected liver cells

when the rate of infection overcomes rate that CTL can clear virus

72
Q

Patients with HBV are at increased for developing what

A

hepatocellular carcinoma

73
Q

What does EBV cause

A

infectious mononucleosis, self limited lymphoproliferative disorder
assoc with developing neoplasms like lymphomas and nasopharyngeal carcinoma

74
Q

What are the symptoms of EBV

A

fever, generalized lymphadenopaty, splenomegaly, sore throat and blood of atypical T lymphocytes

75
Q

How is EBV transmitted

A

saliva, kissing

76
Q

What type of proteins are on EBV

A

CD21 (CR2) whicis the R for C’3d on B cells

77
Q

what are the ways that B cells are infected

A

lysis of infected cells releasing virions that can infect other cells
majority just establish latent infection

78
Q

What type of disease is protective for EBV

A

X- agamaglobulinemia because don’t have B cells

79
Q

What are the gene products of EBV latency

A

EBNA1 which mediates maintenance

EBNA2 and latent membrane protein1 LMP1 that dirve proliferation

80
Q

What type of R does the LMP1 from EBV bind

A

TNFR activating pathways that mimic B cell activation by CD40

81
Q

What is used Dx for EBV

A

detection of heterophile anti-sheep red blood cell Ab

82
Q

What cells are most important against EBV

A

CD8 CTLs and NK cells

83
Q

What type of lymphomas does EBV contribute to in immunocompromised patients

A

B cell lymphomas

Burkitt lymphoma with the 8:14 translocation amplifying c-myc

84
Q

what is characteristic of EBV in peripheral smear

A

lymphocytosis with >60% WBC and many of them being atypical huge with many clear vacillations and oval indented nucleus with scattered granules

85
Q

where are lymph nodes enlarged first in EBV

A

groin, axillary and posterior cervical

86
Q

What areas of lymph nodes are expanded in EBV

A

paracortical by activated T cells

87
Q

The Dx of EBV depends on what

A

lymphocytosis with characteristic atypical lymphocytes in peripheral blood
+ heterophile Ab rxn
specific Ab for EBV Ag

88
Q

what disease if concurrent with EBV infection is fatal in 1/3 patients

A

X linked lymphoproliferation syndrome “Duncan disease”

LAST EXAMMMMMM Year I (24 decks)

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