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Disease and Defense > Unit 3c > Flashcards

Unit 3c Flashcards

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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
Incubation period of CMV
2 weeks to 2 months
26
Target cell type for CMV
epithelia, monocytes, lymphocytes, others
27
Latency of CMV
-latent in monocytes, lymphocytes, others Latent for life and may be reactivated from time to time
28
Can you have asymptomatic viral shedding in CMV and HSV?
YESSSSSSSS
29
Complications associated with CMV
1) Pregnancy → child can have congenital CMV infection - Low birth weight, microcephaly, hearing loss, jaundice, skin rash 2) Immunocompromised individuals → severe disease
30
Diagnosis of CMV (5)
1) Viral culture 2) PCR 3) Fluorescent antibody staining 4) Serology (can distinguish primary vs. recurrent infection) 5) Histology
31
Serology in CMV: + IgM, - IgG → ? - IgM, -IgG → ? - IgM, +IgG → ? + IgM, + IgG → ?
+ IgM, - IgG → acute CMV disease - IgM, -IgG → never infected with CMV - IgM, +IgG → previous infection with CMV + IgM, + IgG → recent CMV reactivation
32
Histology of CMV
CMV infected cells have “owl’s eye appearance”
33
Treatment of CMV
no treatment for normal immune patients Antivirals, CMV-IG for immunocompromised
34
Prophylaxis of CMV
no available vaccine, can give CMV-IG monthly for high risk, immunocompromised patients
35
Herpes virus structure
All Herpesviruses are dsDNA viruses Icosahedral capsid Glycoprotein-rich envelope
36
Herpes virus entry into cell
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
Herpes virus replication
Organized, temporal Immediate Early Early Late Genes
38
Immediate Early genes (IE)
expressed prior to protein synthesis Required for E and L gene expression Encode transcriptional activators Brought in with the virus
39
Early Genes (E)
de novo synthesized Proteins involved in DNA replication e.g. viral DNA polymerase, helicase, etc. Many drugs target these virally encoded proteins
40
Late Genes (L)
de novo synthesized Encode structural proteins (capsid, glycoproteins)
41
Assembly of herpes virus is in...
the nucleus Capsid self-assembles with new DNA packaged in it
42
Herpes virus egress
Bud through nuclear membrane and pass through golgi → acquire glycoprotein envelope Exit cell via exocytosis or cell lysis
43
Primary infection
first infection ever - no serum Ab present when symptoms appear Primary infections may not be symptomatic, or may be more severe
44
Symptoms of influenza
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
Structure of influenza
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
Surface proteins in influenza
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
Type A influenza strain
infects other animals also Circulate in population
48
Type B influenza strain
circulates in population, can only infect humans
49
Tye C influenza strain
cause mild illness
50
RSV structure
ssRNA, non-segmented | Surface proteins
51
Surface proteins on RSV
F protein: fusion of viral envelope to host cell → Syncytia G protein: initial binding of virus to host cell
52
Which subtype of RSV (A or B) has more severe disease
A
53
Can RSV get "drift" over time like influenza?
cheeeya brah
54
_________ inhibitors are sued to treat influenza subtype A and B
Neuraminidase Tamiflu, Relenza, Rapivab (IV)
55
How is influenza transmitted? What is its incubation period?
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
How is RSV transmitted? What is its incubation period?
Invades conjunctiva/nasopharynx Incubation period: 3-5 days
57
Symptoms of RSV
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
Clinical features of RSV
People get recurrent infections because Ab/immune protection is incomplete Can predispose children to wheezing as adults Creates syncytia on cellular level
59
Influenza vaccinations (2 kinds)
Inactivated influenza vaccine Live attenuated influenza vaccine
60
Inactivated influenza vaccine (IIV) administration age quadrivalent or trivalent?
injectable (IM), killed, vaccine All individuals 6 months and older Quadrivalent or trivalent (2 A and 1 or 2 B strains)
61
Live attenuated influenza vaccine (LAIV) administration age quadrivalent or trivalent? contraindications?
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
RSV vaccine
Formalin-inactivated RSV vaccine: not protective, immunization caused worse disease in children (“priming” without immunity) Still under investigation
63
antigenic drift
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
Antigenic shift
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
Type ____ influenza virus cannot undergo antigenic shift
B can only infect humans --> can't swap genomes with other species of influenza
66
Pandemic H1N1 Influenza Virus
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
H5N1: “Avian Flu”
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
Qualities of influenza virus strain for pandemic (3)
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
2 drugs used to treat influenza that inhibit neuraminidase (NA)
Zanamivir (relenza) Oseltamivir (tamaflu) For influenza A, B, and C
70
Inhibiting Neuraminidase (NA) acts to...
Block viral budding and release Cause virus to aggregate at cell surface → Reduced viral infectivity Rare development of resistance
71
Oseltamivir administration elimination adverse reactions?
oral administration as prodrug Eliminated via renal tubular secretion Adverse reactions: minor nausea/vomiting Type C for pregnancy (don't know side effects)
72
Zanamivir Administration daily dose elimination adverse reactions?
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
You must start antivirals for influenza when?
Must start within 48 hours of symptom onset for decrease in severity/duration of symptoms
74
_______ and ______ influenza drugs act by blocking viral uncoating/entry into host cell by blocking the viral M2 proton channel
Amantadine and Rimantadine for influenza A
75
Mechanism of action of Amantadine and Rimantadine Problem?
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
Amantadine and Rimantadine are administered _______ and accumulate in ________
orally, accumulate in the lungs
77
Amantadine is excreted _________ Rimantadine is excreted ___________ both can be excreted _________
in urine hepatic elimination in breast milk
78
Acyclovir and Valacyclovir are used to treat ________. They both must be activated by ___________ in order to __________ and _________
Herpes viruses (VZV, HSV) phosphorylation by VIRAL THYMIDINE KINASE inhibit viral DNA polymerase and act as chain terminators
79
Acyclovir administration excretion
topical and IV formulations, oral absorption poor Renally excreted
80
Valacyclovir administration excretion
prodrug of acyclovir - given orally renally excreted
81
Orally administered drugs used to treat Herpes virus are effective for...
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
IV administration of drugs used to treat Herpes virus are effective for...
used for herpes simplex encephalitis, neonatal HSV infections, or serious HSV or severe VZV infections (immunocompromised)
83
Adverse reactions associated with Acyclovir and Valacyclovir
headache, nausea, vomiting, reversible renal dysfunction
84
Docosanol (Abreva) used to treat ______ by inhibiting ___________
herpes virus viral penetration/entry into cell - inhibits fusion between plasma membrane and HSV envelope
85
You must adjust the dose of Acyclovir and Valacyclovir in who?
Renal patients and neonates RENALLY EXCRETED!

Disease and Defense (11 decks)

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