HERPES SIMPLEX

Herpes simplex (HSV) infections are caused by two strains—HSV₁, which commonly infects skin and mucus membranes; and HSV₂ that mainly infects genital tract.

HSV₁ infections are common in early childhood in overcrowded living conditions, while HSV₂ usually infects in adolescence. A breech in skin/mucosal continuity facilitates HSV entry.

Pathogenesis of HSV infections may be divided into 3 stages—(a) primary infection, (b) latent infection, and

(c) reactivation of latent infection or secondary infection with other serotype (HSV₁ gt; HSV₂ or vice versa).

• Primary HSV infection is usually asymptomatic or limited to localized skin/mucosal lesions. Sporadic encephalitis is perhaps the only systemic manifestation of primary HSV infection.

• Latent phase: After primary infection, inactive HSV always persists life-long in ganglions as latent infection, with intermittent clinical reactivation or virus shedding.

• Re-activation is usually precipitated by external stimuli, e.g. cold or ultraviolet rays exposure or internal stimuli, e.g. fever, emotional stress and menstruation.

• Secondary infection is usually asymptomatic except the risk of perinatal transmission. All infections, whether primary, reactivation or secondary, in an immunocompromised host, i.e. newborn, mal­nutrition, malignancies and AIDS, may produce severe invasive disease.

Clinical manifestations: Grouped vesicular lesions are hallmark of primary as well as reactivated HSV disease, presenting as follows:

• Skin lesions (HSV₁) are characterized by grouped thin-wall vesicles with erythematous base, which rupture, scab and heal within 7-10 days without scarring.

- Mucosal lesions (HSV₁) manifest as—(i) herpetic gingivostomatitis, i.e. acute onset of painful oral ulcers with drooling and high fever, lasting for 7-14 days, (ii) herpes labialis, i.e. perioral grouped vesicles on or near lips, or (c) ocular lesions, e.g. keratoconjunctivitis.

- Genital lesions (HSV²) are mostly seen in adolescents as vesicles/ulcers over vulvovaginal region or penis.

- CNS infection, e.g. encephalitis or aseptic meningitis with/without mucocutaneous lesions are common even in immunocompetent children. HSV₁ is a leading cause of sporadic encephalitis in India with acute necrotizing infection of frontotemporal cortex and limbic system.

HSV in immunocompromised children may present with chronic/recurrent orogenital lesions or invasive disease, e.g. sepsis, hepatitis, DIC, pneumonitis or esophagitis.

Perinatal HSV infection is acquired in utero (lt;5%), during vaginal passage (~ 80%) or as postnatal noso­comial infection, discussed in Ch 12.15.4.

Diagnosis depends on: (a) characteristic grouped vesicular lesions, (b) virus detection by PCR or tissue

culture, (c) serology, or (d) typical histology, i.e. multi­nucleated giant cells and intranuclear inclusion bodies on Tzanck staining of vesicle scrapping, CSF or tissue biopsy. Treatment: IV Acyclovir therapy is the mainstay of treatment in HSV infections, either orally (60 mg/ kg/day q6hr for 7 days, maximum 200 mg/dose) for localized skin/mucosal lesions or intravenously (30 mg/kg/day q8hr slowly for 21 days) for encephalitis or invasive disease, apart from supportive care. Long- acting valacyclovir (500 mg BD) or famciclovir (125 mg BD) for 3-5 days may be used in adolescents with genital lesions. Half of these doses may be used for reactivation lesions (for 5 days) or prophylaxis for recurrent lesions in immunocompromised host.

10.24.2