Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Infection & Immunity Block > Viral Exanthems > Flashcards

Viral Exanthems Flashcards

1
Q

Direct Effects

A

Direct effects - viral replication in the epidermis

Direct inoculation of the epidermis
Papilloma viruses, Poxviruses, Primary HSV

Local spread from an internal source
Recurrent VZV, HSV

Spread from a systemic infection
Primary VZV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Secondary Effects

A

Secondary effects
Skin lesions resulting from a systemic infection
Measles (rubeola)
Parvovirus B19 (fifth disease)
Rubella
Human herpes viruses types 6 & 7 (roseola infantum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Dx of Viruses

A
  1. Clinical Presentation and History
  2. Lesions: culture, microscopic examination, detection of viral antigens and viral nucleic acid (only use if direct effect)
  3. Serology: good for systemic effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Viruses that cause Macules

A

Macule = red lesions

Rubella
EBV
HHV-6
Coxsackie
Echo viruses
Measles
Parvovirus B19
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Viruses that cause Macules and Papules

A

Maculopapular: red raised lesions

Measles virus
Echovirus
Parvovirus B19

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Viruses that cause Papules

A

Papules: raised lesions

Papilloma viruses
Molluscum contagiosum
HHV-8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Vesicle Forming Viruses

A 
HSV-1, HSV-2
VZV
Poxviruses
Coxsackie viruses
Herpangina
Enterovirus

Vesicles are fluid filled spots like blisters because virus replication causes lysis of cells causing the fluid and debris
Some viruses can present with macules first and then progression to vesicles in VZV for example

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

HSV: Transmission

A

Virus is shed in fluid from lesions
Route of transmission: close contact, mucosal surfaces, cracks in the skin
Shed in body fluids, i.e. saliva

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

HSV: Symptoms

A

1st - Primary mucocutaneous infection
2nd - Latent infection in the neuronal ganglia

Recurrent disease: viral reactivation and subsequent mucocutaneous infections

Course of disease:
Acute disease lasts 5-7 days
Symptoms subside in 2 weeks
Viral shedding may continue for 3 weeks or more

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Acute Herpetic Gingivostomatitis

A 
Abrupt onset
High fever
Anorexia, listlessness
Gingivitis
Vesicular lesions
Regional lymphadenopathy

Parent to child transmission
Systemic symptoms
90% are due to HSV 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Primary HSV-1 Infection in Adults

A

Acute herpetic pharyngotonsillitis
Fever, malaise, sore throat
Ulcerative lesions on the tonsils and posterior pharynx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

HSV Pathophysiology

A

Neurovirulence: infect neuronal tissue

Latency
HSV-1, trigeminal ganglia
HSV-2, sacral nerve root ganglia

Reactivation: where initial infection was, and then under stress the virus can be reactivated and replicate again

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Recurrences of HSV

A

Prodrome: burning, tingling or itching sensations

Clinical disease:
Small reddened areas develop in site of primary lesion
Followed by formation of blisters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Dx of HSV

A

Clinical presentation

Laboratory analysis
Isolation of virus in tissue culture
Histological appearance of lesion
Rapid detection of HSV DNA – PCR
Serology for primary sero-conversion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Tx of HSV

A

Acyclovir (ZoviraxR)
Synthetic purine nucleoside analogue

Famciclovir (FamvirR)
Prodrug that is converted to penciclovir

Valacyclovir (ValtrexR)
Prodrug rapidly converted to acyclovir

Treat the infection where all drugs target DNA polymerase that replicate viral DNA
Compounds: nucleoside analogs; these drugs can be typical nucleosides (left) or modified (right)
Must be phosphorylated by thymidine kinase, which can develop resistant to the drugs to allow virus to replicate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

HSV Complications

A
  1. Bacterial and fungal super-infections
  2. Skin infections:
    Eczema herpeticum
    Herpetic whitlow
    Herpes gladiatorium
  3. Ocular infections
    Herpes keratitis: pain and light sensitivity, discharge, gritty feeling, scarring
  4. Perinatal infections
    Transmission to newborn infant
    High frequency of visceral and CNS infections
    Neurological sequelae
  5. Immunosuppressed: life-threatening disease, disseminated infection
  6. Encephalitis
17
Q

Papilloma Viruses: Transmission and Clinical Presentation

A

Shed from skin, mucous membranes
Acquired through skin breaks

Clinical presentations:
common warts (verrucae vulgaris)
palmo-plantar warts
flat warts (verrucae plana)
epidermodysplasia verruciformis (EDV)
genital warts (condyloma acuminate)
18
Q

Common, Plantar, Mosaic, Flat, and Butcher Warts

A 
Common wart: mostly hands, genotype 2,4
Plantar wart: bottom of feet, genotype 1
Mosaic wart: hands and feet, genotype 2
Flat wart: arms, face, and knees, genotype 3, 10, 28, 41
Butcher wart: hand, genotype 7
19
Q

HPV: Route of Infection

A 
HPV: gains access through break in the skin and affects basal cells in epidermis, and these infected cells express limited amount of viral Ag, but as the cells differentiate the viral genes that are expressed will change because the virus is taking advantage of differentiation and the cells replicate abnormally and eventually release virus into the environment 
Late genes (L) are expressed on apical cells
Basal cells will continue to be infected; must eliminate basal cells to get rid of viral genome
20
Q

HPV: E6 and E7

A

E6 and E7 early genes: proteins inactivate cellular proteins; E6 blocks p53, and E7 interacts with pRB to disrupt cell cycle regulation
HPV will cause cells to make E7 and cause inactivation of retinoblastoma protein, which normally keeps the cells from replicating
P53: important for cell death when infected, but E6 causes prevention of cell death (HPV makes E6)

21
Q

Papilloma Virus Dx, Tx, and Prevention

A

Diagnosis: clinical presentation, histology

Treatment:
Topical application of caustic agents
Cryotherapy - liquid N

Prevention: vaccination

22
Q

Molluscum contagiosum: Transmission, Pathophysiology, and Differentiation

A

Transmission: skin to skin contact or fomites to skin
Shed from skin lesions
Self-limiting disease
Cluster of lesions

Pathophysiology:
Targets epidermal keratinocytes
Typical inclusion bodies

How to differentiate between this and warts: contagiosum are smooth and have “belly button”
Present with cluster of 6-8 lesions; hyperplastic response

23
Q

Molluscum contagiosum: Tx and Complications

A

Treatment: curretage, cryosurgery, topical agents
Complications: none

24
Q

Rubella Virus: Transmission, Clinical Presentation, Congenital Infections, Prevention, and Complications

A

Transmission: respiratory droplets, from mother to fetus
Initial infection in upper respiratory tract then systemic spread and replication in lymph nodes

Clinical presentation:
Mild, exanthematous disease
Low grade fever
Lymphandenopathy
Short-lived maculopapular rash

Congenital Infection: cataracts, cardiac abnormalities

Prevention – vaccination (MMR)

Complications: athralgia, encephalopathy, birth defects

25
Q

HHV-6: Transmission, Symptoms, Dx, Tx, and Complications

A

Route of transmission: respiratory tract, shed in saliva; enveloped virus
Symptoms – elevated temperature, rash
Diagnosis – clinical presentation, roseola infantum, 6th disease
Treatment – symptomatic
Complications in immunologically suppressed patients

Usually seen in infants 9-12 months of age
Abrupt onset of fever (40 C)
Lasts 3 days, development of rash: maculopapular exanthem

26
Q

Measles Virus Characteristics, Dx, and Prevention

A

Cough, coryza, conjunctivitis
Koplik’s spots: in oral cavity; gray-white spots on soft palate
Fever
Maculopapular rash

Diagnosis: clinical presentation, Ab titers, virus isolation and tissue culture, RT-PCR

Prevention: vaccination (MMR - attenuated aka makes it less virulent/harmless)

27
Q

Measles: Spread, Growth, Fever, Rash, and Transmission

A

Spread: breathing in virus containing droplets or touching contaminated surfaces
Virus grows in cells in back of throat and lungs
Fever lasts 2-4 days followed by a cough, runny nose, and red, watery eyes
Rash lasting 5-6 days appears on the face, head, torso, hands, and feet (spreads this way)
Transmission: 4 days prior to and after appearance of rash
**Reportable virus

Infection & Immunity Block (30 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions