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Disease and Defense > Unit 3c > Flashcards

Unit 3c Flashcards

1
Q

Clinical Manifestations of HSV-1

A

1) Most common:
-Frequently asymptomatic
-Orofacial lesions
“above the belt”

2) Less common:
- (some) genital lesions
- Encephalitis - causes childhood/adult encephalitis
- Herpes whitlow (HSV on fingers)
- Herpes keratitis (HSV in eye) - can cause blindness

3) Rare
- Neonatal herpes

Usually occurs during childhood

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2
Q

Clinical Manifestations of HSV-2

A

1) Most Common:
-Asymptomatic
-Genital lesions and
“below the belt”

2) Less common:
- (some) orofacial lesions
- Herpes whitlow
- Neonatal herpes - HSV-2 is common cause

3) Rare
- Encephalitis
- Herpes keratitis

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3
Q

Transmission of HSV-1 and HSV-2

A 
HSV1 = close contact
HSV2 = close contact usually sexual
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4
Q

Target cell type in HSV-1 and 2

A

mucosal epithelium

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5
Q

Cell that HSV-1 and 2 remains latent in

A

neuron (ganglia)

Trigeminal ganglion → face
Sacral ganglion –> genitals

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6
Q

Incubation period for HSV1 and 2

A

2-12 days

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7
Q

Reactivation of HSV-1

A

Usual: Asymptomatic (most common), Herpes labialis (cold sore)

Occasional: Recurrent genital herpes, Herpes Keratitis

Rare: encephalitis

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8
Q

Reactivation of HSV-2

A

Usual: Asymptomatic (most common), Recurrent genital herpes

Occasional: Gingivostomatitis

Rare: encephalitis, herpes keratitis

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9
Q

Diagnosis of HSV1 and 2

3

A

1) Viral culture of lesions (easiest)
2) Direct fluorescent antibody stain of lesions (stain adheres to HSV antigen)
3) PCR of lesions (most expensive)

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10
Q

Treatment of HSV-1 and 2

A

Nucleoside analogs (acyclovir) -

IV acyclovir used with neonatal herpes, immunocompromised hosts, pts with encephalitis

Oral acyclovir used for HSV outbreaks

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11
Q

clinical manifestations of chicken pox (varicella)

A

Symptoms: fever, malaise, headache, cough, rash - dew drop on a rose petal (vesicle on erythematosus base)

Once rash has scabbed - no longer infectious

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12
Q

Clinical manifestations of shingles (zoster)

A

reactivation of VZV

Symptoms: radicular pain in one nerve area, lesions in grouped vesicles on an erythematous base

Do not cross midline, confined to single dermatome

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13
Q

Transmission of VZV

A

contact or respiratory route - highly contagious

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14
Q

Target cell type of VZV

A

mucosal epithelium

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15
Q

Viral pathogenesis of VZV

Primary viremia
Secondary viremia

A

Gain entry via respiratory tract → lymphoid system → viral replication occurs in regional lymph nodes (2-4 days)

Primary viremia occurs 4-6 days after initial infection
Viral replication in liver, spleen, and other organs

Secondary viremia when viral particles spread to skin 14-16 days after initial exposure → rash

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16
Q

Latency of VZV

A

neuron (ganglia)

Post primary infection, virus latent in cerebral/dorsal root ganglia

Reactivation → shingles (distributed in a dermatome)

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17
Q

Can VZV exhibit viral shedding that is asymptomatic in normal hosts?

A

NOOOOOOOOO

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18
Q

Incubation period of VZV

A

10-21 days after exposure for chickenpox

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19
Q

Chicken pox vaccination

live or killed?
what age?

A

live attenuated vaccine

Initial dose 12-15 months, booster dose at 4-6 years of age

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20
Q

Treatment of VZV

A

Antiviral therapy (within first 48-72 hours)

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21
Q

Complications associated with chickenpox

A
  • secondary infection/cellulitis
  • pneumonia
  • Necrotizing fasciitis
  • Encephalitis/ Encephalomyelitis
  • Hepatitis
  • Congenital Varicella syndrome
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22
Q

Diagnosis of VZV (3)

A

1) Direct fluorescent antibody
2) VZV PCR
3) Viral culture

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23
Q

Clinical manifestations of Cytamegalovirus (CMV)

A

Infections mononucleosis-like syndrome (fever, swollen nodes, mild hepatitis)

  • In immunocompromised → retinitis, pneumonia, colitis
  • In Newborns → congenital CMV

Primary infection usually asymptomatic

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24
Q

Transmission of CMV

A

contact with infected body fluids, blood transfusions, transplantation, congenital

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25
Q

Incubation period of CMV

A

2 weeks to 2 months

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26
Q

Target cell type for CMV

A

epithelia, monocytes, lymphocytes, others

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27
Q

Latency of CMV

A

-latent in monocytes, lymphocytes, others

Latent for life and may be reactivated from time to time

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28
Q

Can you have asymptomatic viral shedding in CMV and HSV?

A

YESSSSSSSS

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29
Q

Complications associated with CMV

A

1) Pregnancy → child can have congenital CMV infection
- Low birth weight, microcephaly, hearing loss, jaundice, skin rash

2) Immunocompromised individuals → severe disease

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30
Q

Diagnosis of CMV (5)

A

1) Viral culture
2) PCR
3) Fluorescent antibody staining
4) Serology (can distinguish primary vs. recurrent infection)
5) Histology

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31
Q

Serology in CMV:

+ IgM, - IgG → ?

  • IgM, -IgG → ?
  • IgM, +IgG → ?

+ IgM, + IgG → ?

A

+ IgM, - IgG → acute CMV disease

  • IgM, -IgG → never infected with CMV
  • IgM, +IgG → previous infection with CMV

+ IgM, + IgG → recent CMV reactivation

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32
Q

Histology of CMV

A

CMV infected cells have “owl’s eye appearance”

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33
Q

Treatment of CMV

A

no treatment for normal immune patients

Antivirals, CMV-IG for immunocompromised

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34
Q

Prophylaxis of CMV

A

no available vaccine, can give CMV-IG monthly for high risk, immunocompromised patients

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35
Q

Herpes virus structure

A

All Herpesviruses are dsDNA viruses

Icosahedral capsid

Glycoprotein-rich envelope

36
Q

Herpes virus entry into cell

A

Bind surface receptors on host cells → fusion of viral/host membranes

Release nucleocapsid into host cytoplasm → transported to nucleus on microtubules through nuclear pores

37
Q

Herpes virus replication

A

Organized, temporal

Immediate Early
Early
Late Genes

38
Q

Immediate Early genes (IE)

A

expressed prior to protein synthesis

Required for E and L gene expression

Encode transcriptional activators

Brought in with the virus

39
Q

Early Genes (E)

A

de novo synthesized

Proteins involved in DNA replication

e.g. viral DNA polymerase, helicase, etc.

Many drugs target these virally encoded proteins

40
Q

Late Genes (L)

A

de novo synthesized

Encode structural proteins (capsid, glycoproteins)

41
Q

Assembly of herpes virus is in…

A

the nucleus

Capsid self-assembles with new DNA packaged in it

42
Q

Herpes virus egress

A

Bud through nuclear membrane and pass through golgi → acquire glycoprotein envelope

Exit cell via exocytosis or cell lysis

43
Q

Primary infection

A

first infection ever - no serum Ab present when symptoms appear

Primary infections may not be symptomatic, or may be more severe

44
Q

Symptoms of influenza

A

acute, febrile respiratory disease, NOT GI upset

Acute onset of fever, chills, myalgia, headache, cough

Presentation varies with age
Infants/toddlers can have apnea, GI symptoms

45
Q

Structure of influenza

A

RNA virus with segmented genome - 8 different pieces of ssRNA

Lipid envelope lined with matrix protein on inner side

Surface proteins (H and N)

46
Q

Surface proteins in influenza

A

hemagglutinin (H), neuraminidase (N) glycoproteins

Can have variety of types H1, H2, etc. and N1, N2, etc.

Subtypes identified by combo of H and N proteins on viral coat

47
Q

Type A influenza strain

A

infects other animals also

Circulate in population

48
Q

Type B influenza strain

A

circulates in population, can only infect humans

49
Q

Tye C influenza strain

A

cause mild illness

50
Q

RSV structure

A

ssRNA, non-segmented

Surface proteins

51
Q

Surface proteins on RSV

A

F protein: fusion of viral envelope to host cell → Syncytia

G protein: initial binding of virus to host cell

52
Q

Which subtype of RSV (A or B) has more severe disease

A

A

53
Q

Can RSV get “drift” over time like influenza?

A

cheeeya brah

54
Q

_________ inhibitors are sued to treat influenza subtype A and B

A

Neuraminidase

Tamiflu, Relenza, Rapivab (IV)

55
Q

How is influenza transmitted?

What is its incubation period?

A

Respiratory

Virus lives on human hands for 5 min, steel or plastic for 24-48 hours, cloth or paper for 8-12 hours

Incubation period: 1-3 days

56
Q

How is RSV transmitted?

What is its incubation period?

A

Invades conjunctiva/nasopharynx

Incubation period: 3-5 days

57
Q

Symptoms of RSV

A

Constriction of smooth muscles in bronchioles

→ edema/inflammation of airway
→ Ventilation/perfusion mismatch (hypoxia)
→ Hyperexpansion by mucous plugging (seen on CXR)

Respiratory distress, wheezing/rhonchi, hypoxia, copious secretions

58
Q

Clinical features of RSV

A

People get recurrent infections because Ab/immune protection is incomplete

Can predispose children to wheezing as adults

Creates syncytia on cellular level

59
Q

Influenza vaccinations (2 kinds)

A

Inactivated influenza vaccine

Live attenuated influenza vaccine

60
Q

Inactivated influenza vaccine (IIV)

administration
age
quadrivalent or trivalent?

A

injectable (IM), killed, vaccine
All individuals 6 months and older

Quadrivalent or trivalent (2 A and 1 or 2 B strains)

61
Q

Live attenuated influenza vaccine (LAIV)

administration
age
quadrivalent or trivalent?
contraindications?

A

intranasal needle-free injection (fine mist in nose)

  • For healthy persons 2yrs-49yrs of age
  • Only quadrivalent (2 A and 2 B strains)
  • NOT indicated in pregnancy or immunocompromised
  • Slightly more expensive
62
Q

RSV vaccine

A

Formalin-inactivated RSV vaccine: not protective, immunization caused worse disease in children (“priming” without immunity)

Still under investigation

63
Q

antigenic drift

A

gradual change in virus through slow series of mutations, substitutions, or deletions in amino acids of H or N surface antigens

Constant and rapid change allows for repeated influenza epidemics

Adapts to antibody in host

Does NOT change the subtype of the virus (e.g. H2N2)

64
Q

Antigenic shift

A

due to reassortment of genome segments

  • Produces a new virus - swap genome segments between strains (and between strains present in other species)
  • Can create novel H or N proteins
  • Often can cause pandemics
  • Antigenic shift is less frequent, but more severe repercussions
65
Q

Type ____ influenza virus cannot undergo antigenic shift

A

B

can only infect humans –> can’t swap genomes with other species of influenza

66
Q

Pandemic H1N1 Influenza Virus

A

A/California/7/2009 (H1N1)-like virus

Caused a human pandemic in 2009-2010

“Swine Flu” - most gene segments similar to influenza viruses in pigs → Antigenic shift

Mexico, US, Canada

Highest infection among children and young adults 65 yrs (preexisting immunity?)

60 million cases, 270,000 related hospitalizations, 12,000 deaths

67
Q

H5N1: “Avian Flu”

A

Newly-emerging influenza virus

Influenza A subtype present in birds

Wild birds are asymptomatic but shed lots of virus in their stool

Currently a highly virulent strain of H5N1 circulating in bird populations
-Occasionally transmitted to humans

First noted in a goose farm in China

Infected birds found in more than 20 countries

Currently avian flu binds alpha 2,3 linkage - human viruses bind alpha 2,6 linkage → mutation in H gene may confer change in preferred binding

68
Q

Qualities of influenza virus strain for pandemic (3)

A

1) Emergence of a new influenza subtype
2) Virus must infect humans and cause serious illness
3) Virus must have sustained human-to-human transmission and spread easily (without interruption) among humans

EX) H1N1 = pandemic (meets all 3 criteria)
H5N1 = NOT pandemic (2/3 criteria)

69
Q

2 drugs used to treat influenza that inhibit neuraminidase (NA)

A

Zanamivir (relenza)

Oseltamivir (tamaflu)

For influenza A, B, and C

70
Q

Inhibiting Neuraminidase (NA) acts to…

A

Block viral budding and release
Cause virus to aggregate at cell surface
→ Reduced viral infectivity

Rare development of resistance

71
Q

Oseltamivir

administration
elimination
adverse reactions?

A

oral administration as prodrug

Eliminated via renal tubular secretion

Adverse reactions: minor nausea/vomiting
Type C for pregnancy (don’t know side effects)

72
Q

Zanamivir

Administration
daily dose
elimination
adverse reactions?

A

inhaled
Twice daily x5 days
Renal elimination

Adverse reactions: bronchospasm (asthma or COPD patients)

DO NOT USE with COPD patients

Type C for pregnancy (don’t know side effects)

73
Q

You must start antivirals for influenza when?

A

Must start within 48 hours of symptom onset for decrease in severity/duration of symptoms

74
Q

_______ and ______ influenza drugs act by blocking viral uncoating/entry into host cell by blocking the viral M2 proton channel

A

Amantadine and Rimantadine

for influenza A

75
Q

Mechanism of action of Amantadine and Rimantadine

Problem?

A

Blocks viral uncoating/entry into host cell

Block VIRALLY encoded M2 H+ channel → prevent intracellular pH change needed for uncoating → RNA not released into cytosol

HIGH RESISTANCE with mutation in proton channel - NOT USED ANYMORE

76
Q

Amantadine and Rimantadine are administered _______ and accumulate in ________

A

orally, accumulate in the lungs

77
Q

Amantadine is excreted _________

Rimantadine is excreted ___________

both can be excreted _________

A

in urine

hepatic elimination

in breast milk

78
Q

Acyclovir and Valacyclovir are used to treat ________. They both must be activated by ___________ in order to __________ and _________

A

Herpes viruses (VZV, HSV)

phosphorylation by VIRAL THYMIDINE KINASE

inhibit viral DNA polymerase and act as chain terminators

79
Q

Acyclovir

administration
excretion

A

topical and IV formulations, oral absorption poor

Renally excreted

80
Q

Valacyclovir

administration
excretion

A

prodrug of acyclovir - given orally

renally excreted

81
Q

Orally administered drugs used to treat Herpes virus are effective for…

A

shorten duration of pain in primary and recurrent genital herpes

Topical less effective

For VZV can decrease number of lesions and duration of chickenpox and shingles (requires HIGH dose)

82
Q

IV administration of drugs used to treat Herpes virus are effective for…

A

used for herpes simplex encephalitis, neonatal HSV infections, or serious HSV or severe VZV infections (immunocompromised)

83
Q

Adverse reactions associated with Acyclovir and Valacyclovir

A

headache, nausea, vomiting, reversible renal dysfunction

84
Q

Docosanol (Abreva) used to treat ______ by inhibiting ___________

A

herpes virus

viral penetration/entry into cell - inhibits fusion between plasma membrane and HSV envelope

85
Q

You must adjust the dose of Acyclovir and Valacyclovir in who?

A

Renal patients and neonates

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Disease and Defense (11 decks)

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