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PID > Final > Flashcards

Final Flashcards

1
Q

What is meant by a “live” virus?

A

it is capable of replicating

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2
Q

Are attenuated vaccines capable of causing infection?

A

yes

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3
Q

What is necessary for a virus to cause disease?

A
  • must have sufficient virions to cause infection
  • the cells targeted must be accessible, susceptible, and permissive
  • the local antiviral defense must be absent or ineffective
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4
Q

What barriers are present in the respiratory tract to prevent infection

A
  • mucus, ciliated cells, mucus-secreting glands, alveolar macrophages
  • turbinates to prevent attachment
  • tonsilar lymphoid tissues
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5
Q

T/F enveloped viruses are less susceptible to drying or inactivation through different environmental factors

A

false

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6
Q

If we have a stomach bug, typically it is a (enveloped/nonenveloped) virus

A

non-enveloped

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7
Q

What is important about the M cells of the alimentary tract

A

they are constantly sampling whatever’s in the gut and passing it on to the DCs
(the king’s wine taster)

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8
Q

what is the series of events that a virus needs to go through to cause disease?

A
  • acquisition
  • primary replication
  • primary viremia
  • activation of innate response
  • incubation period
  • -> asymptomatic or prodrome
  • -> spread to secondary site
  • replication in target tisse (DISEASE)
  • secondary viremia
  • immune response
  • release (transmission)
  • resolution or persistence
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9
Q

what are the steps of viral replication for a non-enveloped virus?

A
  1. recognition: viral attachment proteins (VAPs) identify specific host cells
  2. Attachment: VAPs bind to cell receptors (proteins or carbs); these attachment sites determine host range and tissue tropism
  3. Penetration/Entry
    - non-enveloped enter by receptor-mediated endocytosis
  4. uncoating: capsid/envelope removed; DNA delivered to nucleus, RNA to cytoplasm
  5. macromolecular synethesis: synthesis of viral mRNA and proteins
    - most DNA viruses use cell RNA POL II
    - most RNA viruses encode enzymes for transcription and replication
    - all viruses depend on host ribosomes, tRNA, and post-mechanical mechanisms
  6. Assembly: DNA in nucleus, RNA and Pox in cytoplasm
  7. Release: lysis, exocytosis
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10
Q

what are the steps of viral replication for an enveloped virus?

A
  1. recognition: viral attachment proteins (VAPs) identify specific host cells
  2. Attachment: VAPs bind to cell receptors (proteins or carbs); these attachment sites determine host range and tissue tropism
  3. Penetration/Entry
    - enveloped enter by fusion of viral and cellular membranes
  4. uncoating: capsid/envelope removed; DNA delivered to nucleus, RNA to cytoplasm
  5. macromolecular synethesis: synthesis of viral mRNA and proteins
    - most DNA viruses use cell RNA POL II
    - most RNA viruses encode enzymes for transcription and replication
    - all viruses depend on host ribosomes, tRNA, and post-mechanical mechanisms
  6. Assembly: DNA in nucleus, RNA and Pox in cytoplasm
  7. Budding: viral glycoproteins delivered to cell membranes; capsid interacts with glycoprotein-membrane and surrounds capsid
    - budding occurs from plasm membrane, ER, Golgi, or nuclear membrane
  8. Release: lysis, budding, exocytosis
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11
Q

replication cycle of (+)RNA Viruses

A
  • entry
  • translation
  • transcription
  • assembly
  • release
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12
Q

replication cycle of (-) RNA viruses

A
  • mRNA transcription and replication
  • transcription
  • assembly
  • release
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13
Q

What makes retroviruses a bit slower to affect the host

A

it must integrate into the host genome-

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14
Q

how do viral mutations/recombinations/reassortments affect the virus

A
  • new virus
  • quasispecies
  • defective genomes
  • change the virulence
  • affect disease outcome
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15
Q

what is a pseudotype virus

A

proteins/capsids from one virus and genome of a different one

allows you to protect against a harmless virus while utilizing the “shell” of a dangerous one that the body can react to immensely

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16
Q

T/F mutations occur constantly in viruses

A

true

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17
Q

what is reassortment

in which viruses does it occur?

A
  • exchange of part of the genome

- occurs in all segmented viruses

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18
Q

What is viral pathogenesis outcome determined by?

A
  • virus-host interaction

- host’s response to infection

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19
Q

what do viruses need to do in order to be effective

A
  • break through barriers and invade cells
  • evade immune control
  • kill cells or trigger destructive immune reponse
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20
Q

determinants of disease

A

type of disease

  • tissue tropism
  • permissiveness of cells for replication
  • portal of entry
  • access to target tissue
  • virus strain
  • virulence factors

severity of disease

  • virus strain**
  • CPE
  • immune status
  • immunopathology
  • inoculum size
  • prior exposure
  • general health and nutrition
  • genetics
  • age
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21
Q

what is the primary determinant of disease severity

A

virus strain

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22
Q

what is the primary determinant of disease type

A

tissue tropism

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23
Q

what do virulence genes do?

A
  • affect ability of virus to replicate
  • modify host defense mechanisms
  • facilitate spread in and among hosts
  • direct toxicity
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24
Q

what are the 3 outcomes of cytopathogenesis

A
  • abortive infections
  • lytic infections
  • persistent infections
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25
Q

what are abortive infections

A

an infection in which the virus fails to replicate

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26
Q

what are lytic infections

A

“virus gets into the permissive cell and will replicate like mad and make the cell explode”

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27
Q

what are examples of persistent infections

A
  • chronic: non-lytic, productive
  • latent: limited, no virus synethesis
  • recurrent: reactivation
  • oncogenic: transforming
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28
Q

Recall the goals of immune response

A
  • respond (prevent entry and spread, eliminate virus and infected cells)
  • return to homeostasis (eliminate virus and infected cells, repair damage)
  • remember (develop memory to respond more rapidly to second exposure)
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29
Q

why are inapparent or asymptomatic individuals a major source of contagion?

A

they don’t realize that they’re infected and spread the virus to susceptible hosts

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30
Q

what is the gold standard for Virus ID?

A

PCR

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31
Q

what is the structure of a poxvirus

diseases caused?

A

dsDNA
linear
envelope

smallpox, Molluscum contagiosum

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32
Q

what is the structure of a papillomavirus

diseases caused

A

dsDNA
circular
naked

warts, epidermodysplasia verruciformis, cancer

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33
Q

what is the structure of an adenovirus

diseases caused

A

dsDNA
linear+ 5’TP
naked

respiratory, conjunctival, GI infection

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34
Q

What is the structure of a Herpesvirus

disease caused?

A

dsDNA
linear
envelope

herpes, chickenpox, zoster, mono, lymphoma, congenital syndrome, roseola, sarcoma

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35
Q

T/F poxviruses are the largest viruses

A

true

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36
Q

Where do poxviruses replicate?

what do they encode for?

A

cytoplasm

encode enzymes for mRNA and DNA synthesis

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37
Q

poxvirus tissue tropism

A

epithelial cells

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38
Q

poxvirus tranmission

A

respiratory, contact

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39
Q

T/F poxviruses has a single envelope

A

false, double envelope

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40
Q

incubation period of poxviridae

A

5-17 days

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41
Q

symptoms of smallpox

A

high fever, fatigue, severe headache, backache, malaise

red spots on tongue and mouth –> papular rash –> pustules –> scabs

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42
Q

mortality rate of smallpox

A

15-62%

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43
Q

incubation period of molluscum contagiosum

A

2-8 wk period

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44
Q

transmission of molluscum contagiosum

A

contact, fomites

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45
Q

T/F smallpox and molluscum contagiosum are strict human pathogens, while other poxviruses are asymptomatic

A

true

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46
Q

diagnosis and tx of Poxviruses

A
  • clinical: febrile prodrome, classic lesion, same stage of development
  • microscopy: Guarnieri bodies; testing at CDC
    tx: post-exp. vaccination; supportive care
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47
Q

tissue tropism of papillomaviridae

A

squamous epithelial tissue

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48
Q

transmission of papillomaviridae

A

direct contact, sexual, and vertical

oncogenic: cervical, anal, vulvar, penile, oral, laryngeal

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49
Q

what controls the replication of papillomaviridae

A

replication controlled by host cell’s transcriptional machinery

determined by differentiation of skin or mucosal epithelium

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50
Q

where are all of the genes of papillomaviridae located

A

on the (+) strand, the (-) strand is just a carrier

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51
Q

how do genital warts form?

A
  1. HPV invades the skin
  2. DNA from virus enter skin cells (makes proteins that induce epidermal growth factor)
  3. HPV causes infected skin cells to multiply and form warts
  4. Virus sheds, passing on to others
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52
Q

How does HPV lead to cancer?

A

To effectively replicate, the virus will break its own genome and integrate within the host genome, disrupting the cell cycle, thereby losing the brakes on that cell and inducing epidermal growth factor, leading to cancerous growth.

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53
Q

what are Koilocytes

A

enlarged keratinocytes with halos around shrunken nuclei

- hallmark sign of HPV(?)

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54
Q

What causes epidermodysplasia verruciformis

A

a genetic alteration in certain genes in the host, followed by contraction of HPV leads to a horny growht

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55
Q

which HPV strain causes warts

A

1-4

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56
Q

which HPV strain causes papillomas

A

6 and 11

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57
Q

which HPV strain causes Epi. verucciformis

A

5 and 8 + genetic mutation of EVER1/2

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58
Q

genital warts and cancers are caused by which strains of HPV

A

16, 18, 31, 45

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59
Q

diagnosis and tx of HPV

A

dx: visual, microscopic for hyperkeratosis; PAP smear for dysplasia; PCR for typing
tx: sx, cryotherapy, electrocautery, chemical, salicylic acid removal

Gardasil HPV vx

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60
Q

adenovirus tropism

A

mucepithelial cells, lymhpoid cells

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61
Q

adenovirus transmission

A

fecal-oral, respiratory, contact, fomites

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62
Q

what early proteins are required for replication of adenoviruses

A
  • DNA Pol
  • TP (rep. primer)

“very simply, virus recognizes receptor, enters cell, replicates, exits cell”

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63
Q

what do late proteins do to help adenovirus replication

A
  • suppress immune response

- provide capsid components

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64
Q

general path of adenoviruses

A
  • entry through respiratory mucosa (or other viable areas like eye)
  • once in, tends to go to URT, the LRT, or GIT (transports through body via blood or lymph)
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65
Q

incubation period of adenovriuses

A

~4-8 days

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66
Q

T/F adenoviruses are easily spread

A

true

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67
Q

those at risk for adenovirus infectoin

A
  • children <14 yo and people in crowded areas

- children shed virus for months

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68
Q

diagnosis and treatment of adenoviruses

A

dx: ELISA for ID; fluorescent Abs, PCR, ELISA for typing
tx: none; vaccine for type 4 and 7 for military use; CAdV2 for dogs

“you have a virus, go home and drink lots of fluids”

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69
Q

alpha-herpesviruses and site of latency

A
  • herpes simplex virus 1 (neurons)
  • herpes simplex virus 2 (neurons)
  • varicella zoster virus (Chicken pox) (neurons)
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70
Q

beta-herpesviruses and site of latency

A
  • cytomegalovirus (monocytes, lymphocytes)
  • Human herpesvirus 6 (T cells)
  • Human herpesvirus 7 (T cells)
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71
Q

gamma-herpesviruses and site of latency

A
  • Epstein-Barr virus (B cells)

- Kaposi’s sarcoma herpesvirus (B cells)

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72
Q

what kind of infections do herpesviruses typically cause

A
  • lytic, latent, persistent, or immortalizing infections
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73
Q

interesting feature of herpesviruses

A

they have their viral genome in the center, packaged inside a capsid, and keep what they need for replication (once they get into the cell) in the tegument (space btwn capsid and outer envelope

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74
Q

HSV 1 and 2 have:

A
  • multiple glycoproteins

- bind heparan sulfate and nectin-1 for membrane fusion

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75
Q

if HSV1/2 gets into the epithelial cell, what kind of infection occurs

A

lytic

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76
Q

if HSV1/2 gets into the neurons, what kind of infection occurs

A

latent

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77
Q

T/F latent-infection herpesviruses recrudesce in response to stimuli like light, stress, fever, etc.

A

true

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78
Q

HSV1 infections are generally (Above/below) the waist

A

above

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79
Q

HSV2 infections are generally (Above/below) the waist

A

below

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80
Q

HSV1/2 epidemiology

A
  • may be asymptomatic
  • once infected, infected for life
  • human disease
    HSV1: 60-90 of population
    HSV2: 20-25% of population (plus sexually active individuals and neonates)
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81
Q

HSV1/2 epidemiology

A

close contact, secretions (vesicle fluid, saliva, vaginal, semen)

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82
Q

HSV1/2 Dx and Tx

A

Dx: serology, PCR, CPE in cell culture

Tx: cell mediated immunity critical to control dz.
- Acyclovir,

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83
Q

HSV1 has a predilection for the ___

A

brain

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84
Q

HSV 2 rarely crosses into the ____ but can cause recurrent ______

A

brain

sacral meningitis

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85
Q

where does HSV1/2 establish latency

A

sensory dorsal root ganglia of the spine

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86
Q

what are the 6 childhood exanthems

A
  1. Measles
  2. Scarlet fever
  3. Rubella
  4. Chicken Pox
  5. Erythema Infectiosum
  6. Roseola infantum
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87
Q

paramyxovirus structure and diseases caused

A

ssRNA

Measles, mumps, RSV, Hendra/Nipah

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88
Q

streptococcus pyogenes structure and disease caused

A

a bacteria

scarlet fever

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89
Q

Togavirus structure and diseases caused

A

rubella (german measles)

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90
Q

herpesviruses structure and diseases caused

A

dsDNA, linear, envelope

fever blisters, genital herpes, chicken pox/zoster, mono, congenital syndrome, roseola, Kaposi Sarcoma

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91
Q

parvovirus structure and disease caused

A

ssDNA +/-, circular, naked

erythema infectiosum (Fifth disease)

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92
Q

Varicella Zoster Virvus, aka ___

A

HHV3 or VZV, chicken pox

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93
Q

where does VZV establish latency

A

in neurons (all dorsal root ganglia along the spine

94
Q

VZV transmission

A

respiratory

95
Q

typical reccurrence of VZV

A

only once

96
Q

chickenpox incubation period

A

15 days

97
Q

symptoms of chickenpox

A

sometimes mild or asymptomatic

fever, sore throat

  • *vesicular rash–> pustules –> scabs in successive crops over 3-5 days
  • most severe on trunk than extremities
  • primary infection more severe in adults with pneumonia in 20-30%
98
Q

epi of VZV

A
  • may be asymptomatic
  • once infected, infected for life
  • human disease
    chickenpox- mostly children
    zoster- older adults who had chickenpox as a child
99
Q

VZV transmission

A

respiratory, contact with vesicles, saliva

100
Q

dx and tx of VZV

A

DX: CPE in cell culture, serology, PCR

tx: acyclovir; vaccination; VZIG for IC or older people

101
Q

Cytomegalovirus is a

A

beta-herpesvirus

aka CMV or HHV5

102
Q

lytic cytomegalovirus infections target:

A

epithelial cells and macrophages

103
Q

latent cytomegalovirus infections target:

A

lymphocytes, bone marrow stromal cells

104
Q

how does CMV spread through host

how is it reactivated

A

lymphocytes

immunosuppression

105
Q

how is CMV shed?

A

urine, stool, blood, saliva, breast milk, semen, vaginal secretions, amniotic fluid, transplant organs

106
Q

what is the most common viral cause of congenital defects

A

CMV

107
Q

epidemiology of CMV

A

transmission: bodily fluids, transplacental, transfusion, transplanation

108
Q

dx and tx of CMV

A

Dx: owl’s eye intranulcear inclusion, rapid ab test for urine/blood

tx: gancyclovir, foscarnet

109
Q

HHV6 and HHV 7 infection tropisms

A

lytic: salivary glands, T cells, monocytes, epithelial cells, endothelial cells, neurons
latent: T cells and peripheral blood monocytes

110
Q

Exanthem VI

A

roseola

111
Q

symptoms/signs

A

rapid onset high fever (103-105) followed a few days later by a generalized rash lasting 24-48 hours

most common cause of febrile seizures in children 6-24 months

full recovery, no complications

if IC: pneumonitis, encephalitis, hepatitis, fever, organ rejection

112
Q

Epstein-Barr virus infection tropisms

A

AKA EBV or HHV4

lytic: B cells or nasopharyngela epithelial cells

Latent: B cells

Immortalizing: B cells

Receptor is C3d receptor

113
Q

what does mononucleosis result from

A

the battle between EBV-infected cells and activaiton/proliferation of protective T cells

114
Q

symptoms of mono

A

fever, FATIGUE, sore throat, swollen lymph nodes, and spleen

115
Q

Transmission of EBV

A

saliva

116
Q

Dx and Tx of EBV

A

Dx: clinical symptoms, atpical lymphocytes, lymphocytosis, viral antigen antibody

tx: none
vx: none

117
Q

Kaposi’s Sarcoma (AKA)

infection tropism

A

KSHV or HHV8

B cells + endothelial cells, monocytes, epithelial cells, sensory nerve cells

118
Q

Kaposi Sarcoma is ____

A

an opportunistic disease in Advanced AIDS

occurs when endothelial spindle cells proliferate

119
Q

Chilhood Exanthem #5

A

Erythema infectiosum

120
Q

what causes Erythema infectiosum?

A

parvovirus B19

121
Q

T/F parvoviruses are the smallest virus

A

True

122
Q

Parvovirus tropism

A

erythroid cells

123
Q

parvovirus transmission

A

respiratory droplets and secretions

124
Q

3 parvoviruses of concern:

A
  • parvovirus B19: Fifth’s Disease
  • Bocavirus: Resp. disease
  • Adeno-associated virus (AAV)
125
Q

Parvovirus tends to prefer which type of RBC?

A

immature RBCs

126
Q

What are the two stages of B19 infection?

A 
Febrile stage (contagious)
- killing of erythroid precursors
symptomatic stage (Not contagious)
- immune-mediated
127
Q

incubation period of EI

A

5-6 days (?)

128
Q

when does Parvo B19 typically occur?

A

late winter and spring

129
Q

Parvo B19 transmission

A

Droplets and secretions

130
Q

Childhood exanthem III

A

Rubella

131
Q

what does rubella affect

A

resp tract –> lymph nodes –> viremic spread

132
Q

T/F rubella can cross the placenta

A

true

133
Q

what does the rubella rash coincide with?

A

development of antibodies

134
Q

togavirus (rubella) transmission

A

respiratory

135
Q

rubella incubation period

A

14-21 days

136
Q

rubella symptoms in children

A

fever, 3 day rash, swollen glands

137
Q

rubella symptoms in adults

A

more severe than in children, with arthralgia and arthritis, encephalopathy

138
Q

Why do we vaccinate kids for rubella?

A

to protect unborn babies

139
Q

is there a tx for rubella?

A

no

140
Q

childhood exanthem I

A

rubeola (measles)

141
Q

what kind of virus causes measles

A

paramyxovirus

142
Q

what kind of tropism do paramyxoviruses have

A

wide range (resp tract, conjunctiva, urinary tract, small blood vessels, lymphatics, CNS)

143
Q

transmission of paramyxovirus

A

resp. droplets highly contagious

144
Q

what are the 3 rare outcomes of rubeola

A

postinfectious encephalitis (immunopathologic etiology)

subacute sclerosing panencephalitis (defective measles virus infection of CNS)

no resolutoin of acute infection caused by defective CMI (frequently fatal outcome)

145
Q

symptoms of rubeola

A

high fever, Cough, conjunctivitis, coryza, and photophobia

Koplik spots

maculopapular rash

146
Q

what is the cause of most of rubeola’s symptoms

A

cell mediated immunity

147
Q

complications from measles

A

pneumonia

encephaltis (0.5% of cases, but 15% mortality in those cases)

atypical measles (T cell deficient)

148
Q

T/F clearance of measles results in lifelong immunity

A

True

149
Q

Measles summary

A

Rubeola

Has Kolpik spots, rash behind ears

150
Q

Summary of scarlet fever

A

Caused by strep pyogenes

Only bacterial exanthem

Strawberry tongues

151
Q

Summary of measles/rubella

A

German measles

Forscheimer’s spot, rash is forehead down

152
Q

Summary of varicella

A

Chickenpox/zoster

Vesicular rash (will rupture/burst)

153
Q

Summary of erythema infectious

A

Slapped cheeks appearance

Sudden high fever

154
Q

Summary of rosella infantum

A

HHV 6 and 7

Lacy body rash

Sudden fever

155
Q

T/F few viral respiratory infections are enveloped

A

False, they are so they NEED to be wet

156
Q

Viral respiratory barriers

A

Hairs, nasal turbinates, ciliated cells, alveolar macrophages

Temperature in different sections can determine where viruses can replicate

157
Q

Approx. how many viruses can cause the “common cold”

A

200

158
Q

Where is the common cold restricted to?

A

Typically the URT

159
Q

Symptoms of the common cold are mainly due to the:

A

Immune response;

Virus binds to ICAM-1 and triggers release of inflammatory mediators

160
Q

What is the most common cause of the common cold

A

Rhinovirus (30-80%)

161
Q

Mumps is caused by a:

A

Paramyxovirus

162
Q

Mumps pathogens is

A

Inoculation of resp. Tract —> local replication —> fire is —> systemic infection

  • if spread to pancreas: may be associated w/ onset of juvenile diabetes
  • can spread to testes, ovaries, peripheral nerves, eyes, inner ear, or CNS (CNS in ~50%)
  • can spread to parotid gland: virus multiples in ducal epithelial cells, local inflammation causes marked swelling
163
Q

Mumps epidemiology

A
  • highly contagious P2P contact and droplets
  • before vx, 90% of pop. Had it
  • virus shed 7 days before symptoms; almost impossible to stop spread
164
Q

Dx and Tx of mumps

A

Dx: clinical presentation, ELISA, PCR

Tx: supportive; vx in 1967

165
Q

What causes parainfluenza

A

Paramyoxivirus; 4 stereotypes in humans

166
Q

Clinical signs of parainfluenza

A

Mild URT dz

Severe LRT dz (2nd to RSV in young children: 25%)

Laryngotracheobronchitis (croup) 2% (subglottal swelling may close airway)

Cell-mediated immune response: cell damage and protective IgA with limited memory

167
Q

Transmission of Parainfluenza

A

P2P transmission

  • usually infants and young children <5yo
  • older children and adults: mild infection, pneumonia in elderly

Treatment: nebulizers and supportive care

168
Q

What is the most common cause of fatal acute respiratory tract infection in infants and young children

A

Respiratory syncytial virus (a paramyxovirus)

169
Q

Clinical signs of RSV

A
  • common cold to pneumonia
  • direct invasion of respiratory epithelium —> immune-mediated cell injury
  • necrosis of bronchioles-> plugs of mucus, fibrin, and necrotic material in airways
  • no viremia or systemic spread
  • infection does not prevent reinfection
170
Q

Treatment of RSV

A

Supportive care

171
Q

Clinical signs of metapneumovirus

A
  • asymptomatic
  • mild URT disease + otitis media —> ~ 15% of common colds
  • severe bronchial it is and pneumonia (10% of cases)
172
Q

Where do humans often get Hendra Virus from

A

Fruit Bats

173
Q

Hendra is fatal for which species

A

Horses and humans

174
Q

Nipah Virus is fatal for which species?

What is the original host

A

Humans and pigs

Fruit bat

175
Q

Examples of picornavirus

A

Rhinovirus, enterovirus

176
Q

At what temperature do picornaviruses replicate best at?

A

33 C

177
Q

Examples of coronaviruses

A

Severe acute respiratory syndrome (SARS) and Middle East Respiratory Syndrome (MERS)

178
Q

Cold vs. flu

A

Cold:

  • rare headache
  • normal temp
  • Slight aches and pains
  • sneezing
  • runny nose
  • sore throat
  • mild to mod. Hacking cough

Flu

  • prominent headache
  • sudden onset of temp 102-104 (last 3-4 days)
  • severe aches and pains
  • extreme fatigue and weakness (lasts 2-3 weeks)
  • severe cough
  • chest discomfort
179
Q

Where does influenza A replicate?

A

Nucleus

180
Q

Why does influenza have high mutation rates?

A

Error-prone RdRP leads to high mutation rates

181
Q

Influenza symptoms

A
  • headache
  • fever
  • runny/stuffy nose
  • sore throat
  • aches
  • tiredness (muscles)
  • coughing
  • joint aches
  • vomiting
182
Q

Polio is caused by:

A

A picornavirus

183
Q

What do picornaviruses produce that blocks translation

A

Proteases that degrade cellular caps to block translation

184
Q

Picornavirus tissue tropism

A

Broad range: ICAM1, CD55, PVR

185
Q

Transmission of picornaviruses

A

Fecal-oral, respiratory

186
Q

T/F enteroviruses usually cause enteric disease

A

False

187
Q

types of picornaviruses

A
  • enteroviruses (poliovirus, Coxsackie A, Coxackie B)
  • echovirus (enteric Cytopathic human orphan virus)
  • enterovirus 68-71
  • heparnavirus —> Hepatitis A
188
Q

Pathogenesis of enteroviruses

A
  • viruses have different secondary target tissues and that determines the type of disease you see (they all enter through primary enteric tissue though, which is why they are ENTERIC viruses)
189
Q

Polio epidemiology

A
  • asymptomatic (90%) —> limited to oropharynx and gut
  • abortive poliomyelitis (5%) —> minor illness, fever, headache malaise, sore throat, vomiting
  • nonparalytic poliomyelitis or aseptic meningitis (1-2%) —> CNS and meninges; back pain, muscle spasms + other symptoms
190
Q

Paralytic polio facts

A
  • 0.1-2% of pop.
  • 3-4 days after abortive subsides
  • virus spreads from blood to anterior horn of cord and motor cortex
  • spinal or bulbar
  • asymmetrical flaccid paralysis with no sensory loss
  • Polio type 1 responsible for 85% of cases
  • bulbar: more severe (75% fatal)
191
Q

What is postpolio syndrome

A

20-40% of infected, 30-40 yrs later

Deterioration of muscles

192
Q

Epidemiology of polio

A
  • human dz w/ fecal-oral and resp. Transmission
  • asymptomatic shedding (up to 1 month)
  • often in poor sanitation and crowded conditions
193
Q

Why is paralytic polio considered a “middle class” dz

A

Infection in early childhood typically asymptomatic or mild, more severe in adults; so cleaner middle class didn’t get it until later

194
Q

Dx and to of polio

A

Dx: CSF- lymphocytes, but no neutrophils; serology or RT-PCR

Tx: pleconaril- inhibits picornavirus penetration into cell
- vx: 3 strains, stable, inexpensive, effective
- antibody is a major protective immune response
—> IgA and IgG
—> cell-mediated immunity plays role in pathogenesis

195
Q

T/F Acute Flaccid Myelitis (AFM) is polio

A

False

It is a polio-like illness, and the CDC and other orgs. Are very careful to differentiate it from polio

196
Q

Norovirus is part of which virus family

It is also known as which two names?

A

Calicivirus

Norwalk Virus

“Winter vomiting bug”

197
Q

When does clinical dz of norovirus appear

A

24-48 hrs incubation

Duration: 12-60 hrs

198
Q

Clinical symptoms of norovirus

A
  • acute onset diarrhea, nausea, vomiting, abdominal cramps

No blood

Fever occurs in ~30%

199
Q

What does norovirus do to the intestine

A

Damage to intestinal brush border which prevents absorption of water and nutrients and watery diarrhea

Gastric emptying may be delayed, causing vomiting

Blunted villi, cytoplasmic vacuolation, mononuclear cell infiltrates

Shedding for 2 was after symptoms stop

200
Q

Epidemiology of norovirus

A
  • outbreaks from a common source
  • water, shellfish, salad, food service
  • schools, resorts, hospitals, nursing homes, restaurants, cruise ships
  • fecal-oral transmission
  • 50% of all food borne GI outbreaks caused by noroviruses
201
Q

Dx and tx of norovirus

A

Dx: RT-PCR, ELISA, Serology

Tx: none; resistant to heat, pH3, detergent, chlorine
- immunity short-lived and not protective

202
Q

Rotavirus facts

A
  • reovirus family
  • small RNA viruses
  • naked, double shelled capsid
  • tissue tropism: epithelial cells
  • transmission: fecal-oral
203
Q

Rotavirus epidemiology

A
  • one of the most common causes of serious diarrhea in young children
  • 95% of children infected by 3-5 yo
  • infect many different mammals and birds
204
Q

Dx and Tx of rotavirus

A

Dx: detection of virus in stool, EIA

Tx: supportive, electrolyte replacement
- vaccines available (RotaTeq and RotaRix)

205
Q

Hepatitis overview

A
  • infect and damage the liver
  • classic symptoms: jaundice (70-80% of adults and 10% of children)
  • release of liver enzymes, fever, fatigue, nausea, loss of appetite, abdominal pain, dark urine
206
Q

People at risk for hepatitis

A
  • people who share needles

- health works who are exposed to infected blood

207
Q

Possible symptoms of hepatitis

A
  • pain in the upper right quadrant of abdomen
  • nausea and vomiting
  • loss of appetite
  • jaundice
  • fatigue
  • itching
208
Q

Hep A

  • Common Name:
  • Structure:
  • transmission:
  • Onset:
  • incubation:
  • severity:
  • mortality:
  • chronicity:
  • Other dz:
  • Lab dx:
A
  • Common Name: infectious
  • Structure: picornavirus, capsid + ssRNA
  • transmission: fecal-oral
  • Onset: abrupt
  • incubation: 15-50
  • severity: mild
  • mortality: <0.5%
  • chronicity: no
  • Other dz: none
  • Lab dx: IgM
209
Q

Hep B

  • Common Name:
  • Structure:
  • transmission:
  • Onset:
  • incubation:
  • severity:
  • mortality:
  • chronicity:
  • Other dz:
  • Lab dx:
A
  • Common Name: Serum
  • Structure: Hepadnavirus Env. CircDNA
  • transmission: parenteral; sexual
  • Onset: insidious
  • incubation: 45-160
  • severity: sometimes severe
  • mortality: 1-2%
  • chronicity: Yes
  • Other dz: carcinoma; cirrhosis
  • Lab dx: HBsAg, HBeAG, HB, IgM
210
Q

Hep C

  • Common Name:
  • Structure:
  • transmission:
  • Onset:
  • incubation:
  • severity:
  • mortality:
  • chronicity:
  • Other dz:
  • Lab dx:
A
  • Common Name: NonA, NonB, post-transfusion
  • Structure: Flavivirus env. +ssRNA
  • transmission: parenteral, sexual
  • Onset: insidious
  • incubation: 14-180
  • severity: subclinical; 70% chronic
  • mortality: ~4%
  • chronicity: yes
  • Other dz: carcinoma, cirrhosis
  • Lab dx: ELISA
211
Q

Hep D

  • Common Name:
  • Structure:
  • transmission:
  • Onset:
  • incubation:
  • severity:
  • mortality:
  • chronicity:
  • Other dz:
  • Lab dx:
A
  • Common Name: Delta Agent
  • Structure: viroid env. CircRNA-
  • transmission: Parenteral; sexual
  • Onset: abrupt
  • incubation: 15-64
  • severity: Co-HBV; severe
  • mortality: high
  • chronicity: yes
  • Other dz: Cirrhosis; fulminant
  • Lab dx: ELISA
212
Q

Hep E

  • Common Name:
  • Structure:
  • transmission:
  • Onset:
  • incubation:
  • severity:
  • mortality:
  • chronicity:
  • Other dz:
  • Lab dx:
A
  • Common Name: Enteric NonA, NonB
  • Structure: Calicivirus; capsid +ssRNA
  • transmission: fecal-oral
  • Onset: abrupt
  • incubation: 15-50
  • severity: mild; preg severe
  • mortality: 1-2%; preg 20%
  • chronicity: No
  • Other dz: None
  • Lab dx: -
213
Q

T/F Hep A is not inactivated by chlorine, formalin, UV

A

False

It is

214
Q

Where do Hep A and Hep E replicate?

When is the virus shed before symptoms show?

T/F it replicates quickly

A
  • hepatocytes and Kupffer cells
  • shed 10 days before symptoms
  • false, replicates quickly
215
Q

T/F Hep B is unusually resistant for enveloped viruses

A

True

216
Q

T/F Hep B replicates through an intermediate

A

True

217
Q

Acute Hep B infections

A
  • may be asymptomatic
  • fever, malaise, anorexia, followed by nausea, vomiting, abdominal pain, chills
  • classic symptoms: jaundice, dark urine, pale stools
218
Q

Chronic Hep B infections

A
  • 5-10% of infected
  • continued destruction of liver with cirrhosis, liver failure
  • 9-35 yrs post-infection
  • usually fatal
219
Q

What is cirrhosis

A

Replacement of liver tissue by fibrotic scare tissue and nodules

220
Q

Hep C is the predominant cause of what?

A

Non A NonB hepatitis

221
Q

Hep C tropism

A
  • hepatocytes and B cells —> tetraspanin receptors coats itself with low density lipoprotein to use LDL receptor for uptake
222
Q

Hep C transmission

A

Blood and sex (maybe)

223
Q

Where does Hep C assemble and bud?

A

At the ER

224
Q

T/F you can get rid of Hep C

A

False

225
Q

Clinical Disease of Hep C

A
  • viremia —> 1-3 wks post exp.
  • low inflammatory response
  • chronic fatigue
226
Q

What does Hep D need in order to replicate and cause dz in its host?

A

It needs the host to be actively infected with HBV

  • its a coinfection: it needs to have HBV establish an infection before HDV can replicate
  • superinfection: more rapid severe progression
227
Q

Hep A and Hep E epidemiology

A
  • 40% caused by hep A
  • 90% of infected children and 25-50% of adults have in apparent infection
  • virus shed 10-14 days before symptoms
  • fecal-oral transmission
  • common source outbreaks:
    —> sewage contamination, shellfish (clams, oysters, mussels)
  • pregnant women have high mortality with HEV (20%)
228
Q

Hep B transmission

A
  • sexual, parenteral, perinatal —> blood transfusion, needle sharing, acupuncture, ear piercing, tattooing, exchange of semen, saliva, vaginal secretions, needle sticks
229
Q

Hep C transmission and epidemiology

A

Blood-blood and sexually —> IVDU, Tatto recipients, transfusion, organ recipients, hemophiliac

  • > 90% of HIV+ IVDUs are HCV+
  • high Incidence of chronic asymptomatic infections (80-85%) —> 10-30% cirrhosis; 1-3% cirrhosis; 1-3% hepatocellular carcinoma
230
Q

Hep C treatment

A

PegIFN and ribavirin, liver transplant (50% cure rate); newer drugs, HCV type specific, 8-12 wks

  • no vx
231
Q

Hep D epidemiology

A

Causes 40% of fulminant hepatitis

  • acute liver failure
  • hepatic necrosis, encephalopathy, coagulopathy within 8 weeks
  • > 70% mortality

occurs ONLY in HBV+ people -> 5% of HBV chronic carriers

232
Q

HIV is a ?

A

Lentivirus

PID (10 decks)

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