Herpesvirus Infections Flashcards
(28 cards)
general characteristics of herpesviruses
large, dsDNA viruses with 4 structural features:
1. outer envelope
2. tegument
3. nucleocapsid
4. inner DNA core
Surface and integument proteins mediate cell entry and viral replication.
alpha subfamily
includes HSV1+2, VZV. (Alpha causes ulcers)
beta subfamily
includes CMV, HHV6, HHV7.
gamma subfamily
includes EBV, HHV8. (Gamma causes cancer)
tzanck smear
immunohistochemistry test for herpesviruses, especially HSV1+2, usually shows multinucleated giant cells
HSV1 primary infection
primary infection: usually in childhood, mostly asymptomatic, incubation 2-12 days. Children: gingivostomatitis; adults: exudative pharyngitis.
Resolves in 10-14 days, establishes latency in the sensory ganglia, usually trigeminal nerve (cranial nerve 5 - face sensation)
HSV1 can also cause Herpetic whitlow, herpes gladitorum, and genital HSV1 infections.
herpetic whitlow
caused by HSV1 - usually looks like a bacterial infection on the finger but is actually a herpetic lesion. Often spread by primary oral lesions and higher prevalence in dentists/pathologists, etc who have come into contact with a lesion.
herpes gladitorum
HSV1 infection from wrestling mat/rugby players. Involves face, neck, chest, arms.
recurrent HSV1 infections
due to reactivation - clinical episodes of productive viral replication with spread from neural cell to axon and then skin.
Prodromal symptoms are frequent (tingling).
Provoked by stress, fever, sun, trauma, decreased immunity, steroids.
Causes cold sores.
HSV2 primary infection
painful grouped vesicles on erythematous base - progress to pustules and then ulcers. Usually infecting the external genitalia, cervix, urethra, anus, oral/skin, and rarely the meninges.
- Incubation 2-12 days.
- Systemic sx may occur in first episodes.
- viral shedding usually 11 days, heals in 2-4 weeks.
HSV2 recurrence
88% will recur within 1 year. Less severe and less frequent over time.
- immunocomp have more recurrences and may be severe.
- treatment early (during prodrome) may prevent outbreaks
HSV1+2 treatment
acyclovir, or famciclovir, or valacyclovir
-suppressive therapy usually reserved for immunocompromised
herpes encephalitis
Due to HSV1 reactivation in the trigeminal ganglion- virus extends into temporal lobe.
Symptoms: HA, fever, behavioral changes, seizures.
CSF: shows mixed pleocytosis (increased cell count) with increased protein and RBCs in the CSF. RBCS***** important!
DX: HSV PCR of CSF or brain bx
RX: IV acyclovir
mortality 20% despite treatment
other HSV complications
neonatal herpes - meningoencephalitis, disseminated or local infection in baby.
ocular herpes - keratitis or retinitis
reactivation in immunocompromised - can cause esophagitis or organ involvement
eczema herpeticum - HSV occurs alongside active skin disease (atopic dermatitis, eczema)
primary varicella (VZV)
- chicken pox in children, more serious in adults
- disseminated disease in immunocompromised
- transmission: respiratory or contact with lesions
- incubation: 10-14 days
- prodrome: 1-2 days of fever, HA, malaise
- rash: begins on trunk, occurs in crops due to cyclic viremia; lesions progress: vesicle -> pustule -> crusted ulcer
- rash is pruritic and contagious until all lesions crust over
VZV reactivation
can cause shingles (herpes zoster) usually in dermatomes, or disseminated zoster in immunocompromised
VZV primary infection treatment
Neonates: VZIG and acyclovir
Age 2-12: No Rx necessary.
Adolescents/adults: acyclovir 800 mg QID x5 days
Pregnancy: acyclovir (IV)
herpes zoster (shingles)
- reactivation of latent varicella from a sensory ganglion
- causes painful dysthesia followed by dermatomal vesicular rash, usually in thoracic and lumbar dermatomes
- pain and burning
Treatment: famciclovir or valacyclovir within 3 days of onset. Also pain control/steroids if >50 years.
Prevention: Shingrix, series of 2 injections, 2nd one 2-6 months after 1st
EBV primary infection
ubiquitous, most infections subclinical.
- Transmission: oropharynx, primary spread from intimate contact with asymptomatic shedder.
- Virus replicates in oropharyngeal epithelial cells and local susceptible B cells - establishes latency
- Incubation: 30-50 days
Clinical manifestations of MONO: (usually in teens)
Symptoms: malaise, fatigue, sore throat, fever, pharyngitis with palatal petechiae, adenopathy, splenomegaly, hepatomegaly
-extreme tiredness lasts 2-3 weeks.
Labs: atypical lymphocytosis (>10% T CELLS!, T cells have weird shape)
Positive heterophile Ab test.
IgM VCA and EA seen in acute disease.
Treatment: REST, no contact sports, steroids if airway restricted
CMV primary infection
mimics EBV mononucleosis. Healthy young adults will have fever, malaise, adenopathy, splenomegaly. Atypical lymphocytosis but negative heterophile ab test. No specific Rx in healthy host.
congenital CMV
cytomegalic inclusion disease, caused by primary infection in mother - TORCH syndrome with jaundice, hepatomeg, rash, microcephaly, cerebral calcification, chorioretinitis, seizures.
perinatal CMV
due to acquisition at birth or from breast feeding, usually mild or no symptoms but may shed virus in urine/feces for months
CMV opportunitic infections
immunosuppressed patients. Reactivation or primary infection.
highest risk: 1-4 months post transplant.
Clinical: fever, leukopenia, direct organ involvement
CMV dx and treatment
DX: serology CMV IgM = acute; culture of blood, urine or tissue; quantitative CMV PCR of blood - may allow prediction of reactivation in transplant patients
histopathology: Owl’s eye inclusions
Treatment: ganciclovir IV, valganciclovir oral
