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Disease and Defense Unit III Derm & Virology > Virology > Flashcards

Virology Flashcards

1
Q

Frank Pathogen vs. Opportunistic

A

Frank pathogens can cause disease in healthy people, opportunistic need compromised host

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2
Q

Koch’s Postulates

A
  1. Specific Microbe found in disease lesions
  2. Microbes can be isolated and grown in vitro
  3. injection of Microbes into animals reproduces disease
  4. same Microbes can be re-isolated from second host
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3
Q

6 Stages of Pathogenesis

A

Encounter, Entry, Spread, Multiplication, Damage, Outcome

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4
Q

Encounter

A

how the agent meets the host, exogenously or endogenously. Mechanism of spread, route of infection.

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5
Q

Entry

A

how the agent enters the host (invasion or passive)

Colonization and adherence to body tissue

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6
Q

Spread

A

Spreading factors from infection site, includes hyaluronidase elastase or coagulase.

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7
Q

Multiplication

A

how agent multiplies in host, must exceed elimination

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8
Q

Damage

A

how agent damages tissue or how host responds. Can be direct damage or interference w/ normal physiology

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9
Q

Outcome:

A

who wins? host dies? microbe dies? mutualism?

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10
Q

Variance in microbiome

A

location on body, diet, ABX, genetics, barriers,

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11
Q

Cholera

A

Toxin-mediated pathogenesis

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12
Q

Pneumonia

A

acute inflammation pathogenesis

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13
Q

Tuberculosis

A

facultative intracellular bacteria infection pathogenesis

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14
Q

Rheumatic Fever

A

autoimmune cross-reaction pathogenesis

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15
Q

Properties of Viruses (4)

A

Submicroscopic
Obligate Parasites
No growth or division
synthesized w/in host

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16
Q

Viral survival strategies

A

Capsulation
Genome has complete infectious cycle information
Host relationships- benign to pathogenic

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17
Q

2 methods of viral classification

A 
Physical properties (genetic material, capsid structure) 
Baltimore mRNA production scheme
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18
Q

2 types of capsid structures

A

Helical or Icosahedral
Maximal contact and non-covalent interaction
Envelopes: lipid bilayers

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19
Q

DNA viruses

A

Must transcribe RNA from - strand of genome so replication is required. Most use host RNA polymerase II.
Circular genomes have reverse transcriptase

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20
Q

Poxviruses

A

Have their own RNA polyermase encoded so they use cytoplasmic replication

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21
Q

+RNA Virus

A

genomes translated by host ribosomes w/ amplification by RdRp. Anti-genome must be made by RdRp before replication occurs.

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22
Q

-RNA Virus

A

packaged RdRp to transcribe genome

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23
Q

+RNA w/ DNA intermediates

A

copy ssRNA to dsDNA via packaged reverse transcriptase, dsDNA added to host genome for transcription

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24
Q

Tissue Tropism Characteristics (4)

A

Access to tissue, receptor expression, gene expression for production, failure of host defenses
Affected by route of entry, initial replication site, spread mechanism, transmission, and pathology

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25
Acute Local Disease
Affects epithelial cells at body surface, short incubation times, many serotypes reduce IgA immunity so reinfections are common
26
Acute Systematic Disease
primary epithelial infection but viremia allows spread to secondary replication sites, longer incubation, lifetime immunity through IgG and IgA
27
Healthy Host Infections
shorter disease course, faster immune response, more pronounced immune-related symptoms, reduced shedding and transmission
28
Compromised Host Infections
longer infections, increased virus-related symptoms, more shedding and transmission
29
Persistent Infections
viruses produce new progeny over long period of time
30
Latent Infections
viruses w/ silent genomes that do not produce progeny unless reactivated
31
Slow infections
very long incubation period so symptoms take long time to develop and immunity may never develop
32
Viral Effects on Cells (7)
Nuclear shrinking, membrane proliferation, cytoplasmic vaculolization, syncytia, chromosomal margination, detachments of cells, inclusion body formation
33
Interferon Anti-Viral State
Type I IFN from all cells, Type II from T and NK cells JAK/STAT signalling of IFN I and II controls ISRE and GAS-controlled genes respectively. In this state, dsRNA reduces cell proliferation and protein synthesis through OAS and PKR
34
Primary Response ABs
Low affinity IgM
35
Secondary Response ABs
Faster, Higher Affinity, More Diverse Functions due to memory cells
36
Viral Immune Evasion Mechanisms (8)
Rapid Mutation to avoid detection by memory cells Adaption to mimic immune cells Reduced expression of viral genes in latent phase Producing inhibitor or decoy molecules Down regulation of host proteins (MHC, adhesions) Infection of immunoprivileged sites Direct infection of immune system Inhibition of apoptosis
37
Herpes Simplex Type 1 vs Type 2
Type 1 is usually orofacial | Type 2 is usually genital
38
Herpes Simplex Pathology
dsDNA Primary mucosal infection w/ latency in ganglion, 2-12 day incubation w/ painful lesions, transmitted w/ close contact
39
Herpes Simplex Treatment
Acyclovir or derivative, No vaccine
40
Varicella Zoster Pathology
dsDNA, primary mucosal, latency in ganglion 10-21 day incubation, itchy vesicular rash in crops, transmission through contact or droplets
41
Varicella Treatment
Early acyclovir or IGs. Prophylactic live attenuated vaccine available.
42
Cytomegalovirus pathology
dsDNA, primary epithelia of salivary glands or respiratory tract, latency in monocytes/lymphocytes, 2 week to 2 month incubation, F/LA/hepatitis if compromised, transmission through bodily fluids
43
CMV Treatment
Treated w/ gancyclovir or IGs, Prophlyactic w/ IVIG in compromised
44
Herpes Virus Structure
dsDNA in icosahedral capsid surrounded by glycoprotein rich envelope.
45
Causes of reactivation (5)
Illness, Sunlight, Stress, Menstruation, Immune Suppression
46
HSV Primary Infection Symptoms
gingivostomatosis, herpetic whitlow (finger), genital herpes, herpes keratitis (cornea), encephalitis
47
HSV reactivation symptoms
asymptomatic, cold sore, genital herpes, keratitis, encephalitis
48
Varicella primary symptoms
chickenpox (crops of lesions in stages)
49
Varicella reactivation symptoms
asymptomatic or shingles
50
CMV primary symptoms
asymptomatic unless immune compromised, then F, LA, hepatitis
51
CMV reactivation symptoms
asymptomatic unless compromised, then lots of itis'
52
Which herpes viruses have asymptomatic shedding?
HSV and CMV
53
Complications of Varicella
secondary cellulitis, pneumonia, necrotizing fasciitis, encephalitis, hepatitis, congenital varicella
54
Varicella Vaccines
Children: live attenuated 12-15 months w/ booster at 4-6 | Shingles vaccine is 14x more concentrated for 50+
55
3 types of vertical transmission of HSV
Skin-eye-mucous membrane CNS Disseminated
56
Congenital Varicella
Birth defects if contracted 8-20 weeks of pregnancy
57
Congenital CMV
3-5% transplacental and asymptomatic, 50% from breast feeding and birth canal contact. Low weight, hearing loss, jaundice, microcephaly
58
CMV Histology
Owl eye cells: dark nucleus w/ pale halo of intranuclear inclusions of viral proteins/virions
59
Influenza Structure
segmented ssRNA, lipid envelope w/ M1, M2, Hemagglutinin, and Neuraminidase surface glycoproteins HG binds sialic acid on host cells in respiratory tract NA helps w/ budding of enveloped virus
60
RSV Structure
non-segmented ssRNA w/ Fusion and G surface protein. F allows fusion to host membrane and syncytia. G allows binding to host membrane.
61
Influenza Pathology
Droplets or fomites contact mucosal surface, 1-3 day incubation in respiratory tract, desquamation occurs
62
RSV Pathology
invades conjuntiva or oropharynx w/ 3-5 day incubation followed by syncytia, smooth muscle constriction, bronchoconstriction, and expansion from mucous plugging
63
influenza transmission and prevention
Transmitted through droplets or fomites Live attenuated quadravalent or inactivated trivalent vaccines (70-90% effective, 30-40% in elderly) Vaccinate at 6 months + w/ priority for vulnerable
64
RSV transmission and prevention
recurrent infections common due to incomplete AB coverage, previous vaccine studies showed increased hospitalizations and higher virulence w/ injections. Very expensive IV ABs available for prophylaxis.
65
Antigenic Drift
minor point mutations in viral genome that changes the HG binding w/ sialic acid but does not change subtype
66
Antigenic Shift
only in type A influenza (it can affect multiple species) where the subtype is changed by 2 strains infecting one host and viral segments are rearranged.
67
Pandemic Criteria
new subtype that infects human w/ serious illness and has sustained human-human transmission and spreads easily

Disease and Defense Unit III Derm & Virology (2 decks)

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