67
Human Herpesviruses
General
Herpes Simplex Viruses (HSV-1/HHV-1 and HSV-2/HHV-2)
• Ubiquitous pathogens that produce primarily orolabial (HSV-1 > HSV-2) and genital infections (HSV-2 > HSV-1) characterized by recurrent vesicular eruptions (Table 67.1).
Table 67.1
Major clinical features of classic herpes simplex virus (HSV) orolabial and genital infections.
~90% of U.S. adults are seropositive for HSV-1 and ~25–30% are seropositive for HSV-2, with an increasing seroprevalence for the latter. Treatment is outlined in Table 67.3.
* For the description of typical lesions, see text; occasionally, intact vesicles are not seen but rather grouped ulcerations with hemorrhagic crusts predominate.
EM, erythema multiforme; SJS, Stevens–Johnson syndrome; DFA, direct fluorescent antibody; H&E, hematoxylin and eosin.
• Transmission can occur during both symptomatic and asymptomatic periods of viral shedding.
• A wide range of clinical presentations exist, with asymptomatic infection being the most common.
– Onset is usually 3–7 days after exposure.
– Initial lesions: small round vesicles on an erythematous base; often painful or burning; the grouping of these vesicles is a clue to the diagnosis; vesicles may become umbilicated or pustular, followed by erosions or ulcerations with hemorrhagic crusts, often with a scalloped border; lesions resolve over 2–6 weeks (Fig. 67.1).
Fig. 67.1 Primary herpes simplex virus (HSV) infections. A Primary herpes gingivostomatitis due to HSV-1 in a child. Note the coalescing lesions with scalloped borders. B HSV-2 infection in a teenager (primary vs. non-primary initial infection). Note the scalloped borders. C Primary genital HSV infection. In addition to 1- to 2-mm hemorrhagic crusts, there are perifollicular vesicopustules. A, Courtesy, Julie V. Schaffer, MD; B, Courtesy, Jean L. Bolognia, MD; C, Courtesy, Stephen K. Tyring, MD.
– Localized prodrome of dysesthesia (e.g. burning/tingling, pain, pruritus) and tenderness.
– Mucocutaneous lesions similar as in primary but fewer in number, less severe, and shorter duration (Fig. 67.2).
Fig. 67.2 Reactivation of herpes simplex virus (HSV) infections. A Recurrent HSV-1 infection on the cheek. Occasionally such lesions are misdiagnosed as cellulitis or bullous impetigo. B Intact grouped vesicles on the penis. Note the genital wart at the base of the penis. C Grouped vesiculopustules on the buttock, a common location in women. D Healing ulcerations with scalloped borders on the penis. A, Courtesy, Kalman Watsky, MD; B, C, Courtesy, Louis A. Fragola, Jr., MD; D, Courtesy, Joseph L. Jorizzo, MD.
• In addition to the classic orolabial and genital infections, HSV can cause other infections (Table 67.2; Figs. 67.3–67.7).
Table 67.2
Major clinical features of other herpes simplex virus (HSV) infections.
Treatment is outlined in Table 67.3.
Fig. 67.3 Eczema herpeticum. Monomorphic, punched-out erosions with a scalloped border in this infant with a history of facial atopic dermatitis. Courtesy, Julie V. Schaffer, MD.
Fig. 67.4 Herpetic whitlow. On the finger of a child (A) and on the finger in an adult (B). Herpetic whitlow is sometimes misdiagnosed as cellulitis or blistering dactylitis, or, depending on the distribution, paronychia. B, Courtesy, Eugene Mirrer, MD.
Fig. 67.5 Herpes gladiatorum. Grouped vesicles and erosions on the neck of a high school wrestler. Courtesy, Louis A. Fragola, Jr., MD.
Fig. 67.6 Herpes simplex viral infections in immunocompromised hosts. A Enlarging ulcerations in a child with acute lymphocytic leukemia who was presumed to have a Rhizopus infection, and (B) in a young man with AIDS. C Coalescence of eroded, yellow-white papules and plaques on the tongue. D Chronic perianal ulcerations in an HIV-infected male. D, From Callen JP, Jorizzo JL, et al. Dermatological Signs of Internal Disease, 4th edn.; Saunders/Elsevier, 2009.
Fig. 67.7 Neonatal herpes. Grouped papulovesicles with an erythematous base on the chest. Note the scalloped borders in areas of coalescence. Courtesy, Frank Samarin, MD.
• DDx and Dx: see Table 67.1 and Fig. 67.8.
Fig. 67.8