Viral Exanthems Flashcards
Direct Effects
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
Secondary Effects
Secondary effects
Skin lesions resulting from a systemic infection
Measles (rubeola)
Parvovirus B19 (fifth disease)
Rubella
Human herpes viruses types 6 & 7 (roseola infantum)
Dx of Viruses
- Clinical Presentation and History
- Lesions: culture, microscopic examination, detection of viral antigens and viral nucleic acid (only use if direct effect)
- Serology: good for systemic effects
Viruses that cause Macules
Macule = red lesions
Rubella EBV HHV-6 Coxsackie Echo viruses Measles Parvovirus B19
Viruses that cause Macules and Papules
Maculopapular: red raised lesions
Measles virus
Echovirus
Parvovirus B19
Viruses that cause Papules
Papules: raised lesions
Papilloma viruses
Molluscum contagiosum
HHV-8
Vesicle Forming Viruses
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
HSV: Transmission
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
HSV: Symptoms
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
Acute Herpetic Gingivostomatitis
Abrupt onset High fever Anorexia, listlessness Gingivitis Vesicular lesions Regional lymphadenopathy
Parent to child transmission
Systemic symptoms
90% are due to HSV 1
Primary HSV-1 Infection in Adults
Acute herpetic pharyngotonsillitis
Fever, malaise, sore throat
Ulcerative lesions on the tonsils and posterior pharynx
HSV Pathophysiology
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
Recurrences of HSV
Prodrome: burning, tingling or itching sensations
Clinical disease:
Small reddened areas develop in site of primary lesion
Followed by formation of blisters
Dx of HSV
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
Tx of HSV
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
HSV Complications
- Bacterial and fungal super-infections
- Skin infections:
Eczema herpeticum
Herpetic whitlow
Herpes gladiatorium - Ocular infections
Herpes keratitis: pain and light sensitivity, discharge, gritty feeling, scarring - Perinatal infections
Transmission to newborn infant
High frequency of visceral and CNS infections
Neurological sequelae - Immunosuppressed: life-threatening disease, disseminated infection
- Encephalitis
Papilloma Viruses: Transmission and Clinical Presentation
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)
Common, Plantar, Mosaic, Flat, and Butcher Warts
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
HPV: Route of Infection
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
HPV: E6 and E7
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)
Papilloma Virus Dx, Tx, and Prevention
Diagnosis: clinical presentation, histology
Treatment:
Topical application of caustic agents
Cryotherapy - liquid N
Prevention: vaccination
Molluscum contagiosum: Transmission, Pathophysiology, and Differentiation
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
Molluscum contagiosum: Tx and Complications
Treatment: curretage, cryosurgery, topical agents
Complications: none
Rubella Virus: Transmission, Clinical Presentation, Congenital Infections, Prevention, and Complications
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
HHV-6: Transmission, Symptoms, Dx, Tx, and Complications
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
Measles Virus Characteristics, Dx, and Prevention
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)
Measles: Spread, Growth, Fever, Rash, and Transmission
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
