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Micro Exam 1 > Holland: Skin and Soft Tissue Infections II > Flashcards

Holland: Skin and Soft Tissue Infections II Flashcards

1
Q

HERPESVIRUSES:

General:

Fall into 3 subfamilies based on genetic and biological properties:

A

Over 100 herpesviruses known; 8 are considered human herpesviruses

Alphaherpesviruses
Betaherpesviruses
Gammaherpesviruses

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2
Q

HERPESVIRUSES

Subfamilies:
Alphaherpesviruses (3 or 4)
Betaherpesviruses (4)
Gammaherpesviruses (2)

A 
Alphaherpesviruses:
o	HSV 1
o	HSV 2
o	VZV
o	Note: B virus, a monkey alphaherpes virus, can infect humans (ie. via a bite); usually results in fatal encephalitis  
Betaherpesviruses:
o	CMV
o	HHV-6A
o	HHV-6B
o	HHV-7

Gammaherpesviruses:
o Epstein Barr Virus (EBV)
o HHV-8/Karposi’s sarcoma associated herpesvirus

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3
Q

Herpes Simplex Infections (HSV)

Incubation Period:
Primary Infection:
Recurrent Infections:

A

Incubation Period: 4-5 days on average (can be longer or shorter)

Primary Infection: takes ~2 weeks to run its course

Recurrent Infections: are typically shorter and involve fewer lesions

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4
Q

Gingivostomatitis OR
Orofacial Herpes OR
Herpes Labialis (recurrent form) OR
“Cold sores”

Typical age:
Frequency:
Usual severity:
Type:

A

Typical age:
Primary Infection: child/adolescent
Recurrent: any age

Frequency:
Very common

Usual severity:
Mild (asymptomatic) to moderate (infection with painful lesions)

Type:
1>2

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5
Q

Genital Herpes

Typical age:
Frequency:
Usual severity:
Type:

A

Typical age: Once sexually active
Frequency: Common
Usual severity: Moderate to severe
Type: 2>1

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6
Q

Keratoconjunctivitis (ocular infection)

Typical age:
Frequency:
Usual severity:
Type:

A

Typical age: Any
Frequency: Fairly common
Usual severity: Moderate to severe (can penetrate stroma and cause blindness)
Type: 1

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7
Q

Dermatitis (other than face or genitals)

Typical age:
Frequency:
Usual severity:
Type:

A

Typical age: Any
Frequency: Uncommon
Usual severity: Mild
Type: 1 or 2

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8
Q

Encephalitis

Typical age:
Frequency:
Usual severity:
Type:

A 
Typical age: Any	
Frequency: Rare
Usual severity: Severe (over 50% death rate; those that don’t die have severe SEs)
Type: 1 or 2 (in neonates)
1 (everyone else)
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9
Q

Disseminated HSV

Typical age:
Frequency:
Usual severity:
Type:

A

Typical age: Any (associated with immunosuppression)
Frequency: Rare
Usual severity: Severe
Type: 1>2

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10
Q

Neonatal Herpes (from infected mother during/after birth)

Typical age:
Frequency:
Usual severity:
Type:

A

Typical age: Newborn
Frequency: Uncommon
Usual severity: Severe (disseminates because immune system not developed yet)
Type: 2>1

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11
Q 
Herpevirus Latency (General):
Definition: 
Mechanism:
A

Definition:

  • Continued presence of viral genome
  • Absence of viral replication and viral particles

Mechanism:

  • Lytic cycle genes not expressed during latency
  • Latent virus can reactivate, causing recurrent disease or subclinical virus shedding (most common reactivation); latent viruses last lifetime of host
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12
Q

Which herpesviruses establish latent infections?

Primary herpesvirus result in:

A

All

Primary herpesvirus infections always result in latent infections
(However, different herpesviruses establish latency in different cell types)

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13
Q

HSV Latency (Specifically):

Entry into nerve cells:

Transport to nerve cell body:

Virus replication:

A

Entry into nerve cells: at primary site of infection

Transport to nerve cell body: in ganglion; via retrograde transport

  • Oral infection (trigeminal ganglion)
  • Genital infection (sacral ganglion)

Virus replication in ganglion: occurs for several days, followed by latency

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14
Q

HSV Reactivation:

Frequency depends on:

Stimuli:

Results in:

A

Frequency: depends on individual; ranges from never to monthly

Reactivation stimuli: often spontaneous; others include sunlight, menstruation, infections, compromised immune system

Reactivation results in: replication in ganglion and travel back down the axon, causing infection near site of primary infection

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15
Q

HSV Structure:

A

Large, enveloped, DNA virus (linear, dsDNA; 75-80 genes)

Icosahedral capsid

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16
Q

HSV Replication:

A

Entry

Gene expression, DNA replication, and Capsid assembly

Envelopment and release

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17
Q

Entry:

Primary and Secondary Route:

A

Primary Route: attachment to host cell via glycoproteins (on virus) and fusion of viral envelope with plasma membrane

Secondary Route: endocytosis followed by fusion with endocytic vesicle

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18
Q

Gene expression, DNA replication, and capsid assembly occurs:

A

Gene expression, DNA replication, and capsid assembly occurs in the nucleus.

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19
Q

Envelopment and Release:

How do capsids first acquire envelope?

Envelope fuses:

Capsid buds:

What release virions from the cell? How?

A

Capsids first acquire envelope by budding through inner nuclear membrane

Envelope fuses with outer nuclear membrane, and naked capsid released into cytoplasm

Capsid buds into vesicles from cytoplasmic membrane (acquires envelope again)

Enveloped virions release from cell via fusion of vesicles with plasma membrane

20
Q

Antivirals Against HSV DNA Replication:

HSV encodes its own DNA replication system:

Steps of Activation (Phosphorylation):

How does triphosphate form inhibit DNA synthesis? (2)

A

HSV encodes its own DNA replication system:

DNA polymerase is the target for most anti-herpes drugs (most are nucleoside analogs)

Steps of Activation (Phosphorylation):

  • HSV-encoded TK phosphorylates acyclovir (or other) to monophosphate-acyclovir
  • Cellular kinases synthesize di- and triphosphate forms

Triphosphate form inhibits DNA synthesis by:

  • Inhibiting viral DNA polymerase
  • Becoming incorporated into DNA, resulting in termination of strand
21
Q

Varicella-Zoster Virus

Primary VZV Infection:

Reactivation of Latent Virus:

Current vaccine:

A

Primary VZV Infection: typically manifests as varicella (chickenpox)

  • Worse in adulthood than in children
  • Latent infections established in dorsal root ganglia

Reactivation of Latent Virus: causes zoster (shingles)
- Incidence increases with age

Now use a live attenuated vaccine against VZV in the United States

22
Q

Varicella

Portal of Entry:

Viremia:
First, second stages
Lesions appear where first?
Lesion stages:
Healing

Incubation Period:

A

Portal of Entry:

  • Primary: upper respiratory tract (some replication occurs here)
  • Secondary: fluids from vesicles containing high concentrations of infectious particles

Viremia:

  • First Stage: spread to lymphoid organs (replication)
  • Second Stage: spread to epithelial tissue (lesions) and respiratory tract (more transmission)
  • Lesions appear on trunk first, spread outward (centrifugal spread)
  • Lesion stages: macule, papule, vesicle, crusting
  • Typically heal without scarring (unless secondary bacterial infection)

Incubation Period: 14-21 days

23
Q

Zoster

Reactivation of latent VZV:

Lesions:

What is possible?

A

Reactivation of latent VZV: causes unknown; can happen more than once

Prodromal syndrome may exist: nerve pain/tingling before outbreak

Lesions: generally limited to skin/mucous membranes innervated by the reactivated ganglion (sharply demarcated areas)

Post-Herpetic Neuralgia is possible: persistent nerve pain after lesions disappear (can last for months)

24
Q

Betaherpesvirus Infections:
• General:

Types:

A

Slow replication cycle (many days vs. ~24hrs for alphaherpesviruses)

Restricted host range and cell type specificity

CMV
HHV-6
HHV-7

25
Q

CMV:

A

Causes cell enlargement (cytalomegaly)

Latent infections in cells of myeloid lineage

26
Q

HHV-6:

How common?

T cell tropic?

2 subtypes:

A

Common: by 12 months of age, nearly everyone is seropositive for HHV-6

T cell tropic

2 Subtypes:

HHV-6A: not associated with disease

HHV-6B:
- Establishes latency/replicates in monocytes and macrophages

27
Q

Primary HHV-6B- Exanthem Subitum (Roseola):

Common? Age?
Incubation period:
Transmission:
Symptoms:
Complications
A
  • Common childhood infection
  • Incubation Period: 5-15 days
  • Transmission: saliva?
  • Symptoms: fever (3-5 days), rash developing over trunk/face and spreading to limbs as fever diminishes
  • Possible Complications: very high fever, neurological symptoms (convulsions, aseptic meningitis), hepatitis, mononucleosis-like syndrome
28
Q

HHV-7:

A
  • Also T cell tropic
  • Establishes latency in T cells
  • May also cause exanthem subitum (roseola)
29
Q

Gammherpesvirus Infections:

A

Epstein Barr Virus (EBV)

HHV-8/Karposi’s sarcoma associated herpesvirus

30
Q

Epstein-Barr Virus:

A
  • B cell tropic

- Latent in B cells

31
Q

HHV-8 (Kaposi’s Sarcoma Associated Herpesvirus)

Prevalence:

Associated with many forms of cancer (3):

A

Prevalence: sub-Saharan Africa and Mediterranean regions (rare elsewhere, besides in HIV-1 patients)

Associated with many forms of cancer:
o Kaposi’s Sarcoma:
o Body cavity based lymphomas
o Multicentric Castleman’s Disease (lymphoid hyperplasia)

32
Q

Kaposi’s Sarcoma: (4)

A

Classic KS:

  • Slow progression (disease you die with, not from)
  • Found in older men of Mediterranean descent
  • Nodular/plaque-like dermal lesions (often on lower leg)

Endemic-African KS:

  • More aggressive
  • LN involvement

Iatrogenic KS:

  • Caused by a medical procedure (ie. solid-organ transplant patients)
  • Also more common in those of Mediterranean descent
Lymphadenopathic KS (HIV Positive Patients):
-	Disseminated and aggressive (involvement of internal organs, viscera, LN and skin)
33
Q

HUMAN PAPILLOMA VIRUS:

General:
Structure

A

General:

  • Virus Family: papovaviraidae
  • Virus Subfamily: papilomavirinae

Structure:

  • Small, DNA virus (circular, dsDNA; 8-10 genes)
  • Nonenveloped icosahedral
34
Q

HPV-16 Genome (Carinoma-Causing):

Composed of:

Transforming Genes:

Major Capsid Protein:

Gardasil Vaccine against types:

A

Composed of 8 genes (6 early, 2 late)

Transforming Genes:
o E6: destruction of p53 TSG
o E7: inactivation of Rb TSG (primary regulator of cell cycle)

Major Capsid Protein:
o L1 gene product
o Target of virus neutralizing Abs (active component of Gardasil HPV vaccine)

Gardasil Vaccine: against types 6, 11, 16, 18

35
Q

Manifestations of HPV Infection

Cutaneous Warts (3):

A

Common Wart:

  • Painless and hyperkeratotic (hypertrophy of striatum corneum)
  • Round papules often occurring in groups
  • Caused by HPV 2, 1, 4 and others

Plantar Wart:

  • Painful, deeply set warts on weight-bearing surfaces of feet
  • Caused by HPV type 1 (most commonly)

Flat Wart:

  • Multiple flat, asymmetric, smooth papules
  • Caused by HPV types 3, 10 and others
36
Q

Manifestations of HPV Infection

Mucosal Warts (2):

A

Laryngeal, oral, conjunctivival papillomas: HPV 6 and 11 (most common)

Anogenital papillomas:

  • External genitalia, anus and near external opening of urethra
  • Types 6 and 11 most common (low risk for carcinoma)
  • Types 16, 18, 31, 33, and 35 are relatively uncommon (highest risk)
  • Risk for cervical, vulvar, penile and anal carcinoma
37
Q

Manifestations of HPV Infection

Epidermodysplasmia Verruciformis:

A

Associated with a rare uncharacterized genetic disorder

Multiple flat wart-like lesions caused by unusual HPV types

Frequent progression to cancer in sunlight exposed areas

38
Q

Clinical Outcomes of HPV Infection (4):

A
  1. Subclinical infection with viral clearance
  2. Latent infection with possible subsequent reactivation
  3. Development of warts/condylomas/low grade neoplasia
  4. Progression to high grade lesion/carcinoma/invasive carcinoma
39
Q

HPV Pathogenesis:

Transmission
Infection
Process

A

Transmission: direct contact or transfer to/from inanimate objects

Infection: requires that virus reaches basal layer of epidermis; often requires minor injuries/breaks in skin to get access to these cells

Process:
o Hyperplastic growth of basal layer cells
o Expression of HPV late genes (capsid proteins) and virion production
o Mature virus contained in highly differentiated cells at the surface of the lesion (those in basal layer are not as differentiated)

40
Q

HPV

Development to Cancer:

A

Normal Circumstances: virus replicates like an episome/plasmid in the nucleus, but does not integrate into host DNA

Molecular Accident Occurs: integration into host DNA, and cell undergoes excessive cell division

41
Q

HPV Cervical Intraepithelial Neoplasia :

Stage 1, 2,3, Invasive Carcinoma

A

Stage 1: mild dysplasia in epidermis (less than 1/3); koilcocyte may be seen in higher layers

Stage 2: moderate dysplasia in epidemis (2/3s); koilcocyte may be seen in higher layers

Stage 3: severe dysplasia (entire epidermis)

Invasive Carcinoma: cells penetrate basement membrane and invade surrounding tissue

42
Q

PICORNAVIRUSES:

• Structure:

A
  • Very small
  • Non-enveloped
  • ssRNA (plus sense)
43
Q

What type of picornaviruses cause infections of the skin/mucous membranes?

A

Coxsackieviruses, as well as Echoviruses and Enterovirus 71

44
Q

Coxsackieviruses:

A

Cause infections of the skin/mucous membranes
o Herpangina: mainly oral lesions
- Associated with certain types of Coxsackie A virus, Coxsackie B viruses, and Echoviruses
- Mistaken for herpes
o Hand, Foot and Mouth Disease

45
Q

Coxsackieviruses

Clinical Signs of Infection:

Prevalence:

Symptoms:

Lesions:

Resolution when compared to HSV:

A

Prevalence: most common in infants and children (often associated with epidemics- ie. outbreak at daycare; this is one way to differentiate from HSV)

Symptoms: fever, sore throat, headache, anorexia, lesions

Lesions:

  • Arise within 2 days of symptoms
  • Small, papulovesicular lesions on the tonsils, soft palate and tongue (can be confused with HSV lesions); enlarge within a day
  • Lesions can also occur on hands, feet and diaper area (H,F and M Disease)

Resolution: more rapid than HSV (healing of lesions in 1-5 days)

Micro Exam 1 (18 decks)

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