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ADULT

Herpes simplex

Herpes simplex virus may affect any body site, the most frequent patterns being discussed here. At any site, there is a primary infection following which the herpesvirus remains dormant in local nerves. This latent infection is held in check by the immune system, but local or systemic factors may cause recrudescence in the vicinity of the original infection.

Herpes labialis

Etiology and pathogenesis

After the initial bout of herpes gingivostomatitis, the herpesvirus lies dormant in the nerves of the face. During periods when the immune system is suppressed (e.g. by significant UV light) or its energies are being directed elsewhere (e.g. during a cold), a recurrence may result. Other trigger factors include dental work, fever, local trauma, mental stress, or menstruation.

Clinical

Pain or tingling followed by grouped vesicles on an erythematous base on the lip, typically centered on the vermilion border but also on nearby sites such as the nose, cheek, or chin, is characteristic. Some patients may develop secondary erythema multiforme (see Ch.11).

Differential diagnosis

For vesicular or crusted lesions around the lips and mid-face, this includes the following.

Treatment

The outbreak will run its course in 2–3 weeks. Topical antiviral drugs such as aciclovir or penciclovir are available by prescription or over the counter in some countries, but have limited value and are of no benefit unless started at the time of onset of symptoms. An oral antiviral agent will greatly shorten the healing time if given early; licensed treatments differ between countries and between patterns, site, and type of herpesvirus infection (Table 25.5). Local care with cleansing and ointments to speed healing are helpful. Prophylactic sunscreen should be used if UV is a precipitating factor.

Herpes genitalis

Etiology and pathogenesis

In the 1970s, HSV was viewed as rare, serious, and transmitted only during outbreaks. It is now understood that HSV is common, usually not serious, and is often transmitted during asymptomatic shedding. Historically, HSV-1 was almost always linked with herpes labialis and HSV-2 with genital disease, but these distinctions are increasingly blurred; HSV-1 may cause both lip and genital disease, but HSV-2 remains strongly linked with genital disease. The prevalence of HSV-2 seropositivity has risen dramatically in the past two decades and continues to rise; the percentage of US adults seropositive for HSV-2 is about 22–25%, many of whom may be asymptomatic but are still contagious. Clinically, persons infected with HSV-1 are less likely to become infected with HSV-2 and, if they do, recurrences tend to be milder and less frequent. Infection at one site with one strain makes infection at that site with another strain difficult (but not impossible).

    No matter what the viral type and no matter how infrequent the recurrences, asymptomatic viral shedding is an essential feature of HSV disease. Patients with HSV-2 will intermittently shed the virus, without any symptoms, and may therefore transmit the infection. It is known that asymptomatic shedding is more common in recently acquired disease and in the immunocompromised. The frequency of asymptomatic shedding is higher in women with more frequent symptomatic outbreaks. Longer courses of prophylactic aciclovir can decrease the amount of asymptomatic shedding.

Clinical

The classic presentation is that of pain or burning, followed after several hours by the eruption of grouped vesicles on an erythematous base in herpes simplex (Figs 25.40 – 25.43). This classic appearance may not be as common as the ‘atypical' presentations. Patients may have only edema, ulcers, crusts, fissures, erythematous patches, pustules, or fleeting ‘irritations' (Fig. 25.44). Primary infection is more severe than recurrences. As in herpes labialis, a prodrome of burning or tingling may signal the onset of a recurrence. Herpes of the buttocks is common (Fig. 25.45).

Figure 25.40 Pustular herpes simplex. After several days, the clear vesicles of herpes become pustules. Note how these lesions group together.

Figure 25.41 Herpes simplex virus after chemotherapy. It is important in an immunocompromised host to continue therapy until the infection clears.

Differential diagnosis

A variety of other sexually transmitted diseases may be suspected (Ch.20), as well as other infections, such as candidiasis, and inflammatory conditions, such as contact dermatitis. Diagnostic difficulty is greatest in those without visible vesicopustular lesions.

    Lesions on the buttocks, thighs, etc. are commonly mistaken for insect bites, although they are usually vesicular, and their recurrent nature should suggest the diagnosis. The patient should be counseled, as asymptomatic shedding may occur. Any lesions in the underwear area should be considered to be genital herpes.

    However, monolesional herpes zoster may resemble HSV infection (as can other dermatoses, such as fixed drug eruption, which is additionally a recurrent process); as the stigma of genital herpes can be immense (discussed later), it is prudent to confirm the diagnosis with virologic samples.

Figure 25.42 Scrum pox is a term used to describe herpes simplex of the face, neck, or thighs acquired during rugby.

Figure 25.43 Herpes simplex after a cold.

Figure 25.44 Crusted herpes simplex. The crusting of herpes is often mistaken for impetigo, especially in children. Always look for intact vesicles and pustules within the crust. Bacterial and viral cultures are invaluable.

Figure 25.45 Herpes simplex of buttocks. It has been theorized that women acquire herpes of the buttocks from a man with a penile lesion while spooning in bed. Others suggest that the virus can be transferred from one woman to another by a public toilet seat.

Figure 25.46 Herpetic whitlow.

Treatment

Patients should be fully aware of the infectious nature of this disease and the potential for asymptomatic shedding. Topical treatment with aciclovir or penciclovir is only minimally effective. Oral treatments are listed in Table 25.4. Suppressive therapy (Table 25.5) can significantly reduce the risk of transmission of HSV-2 to a sexual partner.

    Telling patients that they have herpes genitalis can cause myriad negative emotional and psychologic responses. Patients may feel great shame or guilt and may cry in your presence. They may articulate the belief that this is a punishment for sexual practices that are immoral or promiscuous. They may withdraw from social interactions. They may panic at the thought of telling current, past, or future sexual partners that they have herpes or they may fear sexual rejection. They may blame their partner, with accusation of infidelity, even though the episode may represent recurrence of asymptomatic infection acquired many years previously. One study found that structured psychosocial intervention that emphasized information on infection, acquisition, and transmission; identification of stressors; and stress management and other coping skills actually decreased recurrences.

Herpetic whitlow

The term herpetic whitlow refers to herpes simplex infection of a digit. Dentists, or other healthcare workers whose hands come into contact with patients' mouths or adjacent skin, are most commonly affected. Other modes of acquiring this infection include autoinfection of digits in either children with HSV gingivostomatitis or in adults with HSV genital infections. Very painful, grouped vesicles of a finger are characteristic (Figs 25.46 and 25.47). For details of treatment, see Table 25.5.

Figure 25.47 Herpetic whitlow. Lesions are seen on both the finger and the lips.

PRACTICE POINTS

Herpes zoster

Etiology and pathogenesis

Herpes zoster represents a recrudescence of the varicella zoster virus that has remained dormant after a bout of chicken pox. The virus lies dormant for decades, held in check by the body's immune system. When the immune system weakens with age or immune suppression, the virus is able to erupt. The virus is tropic for nerves, and the majority of infections occur in one or more dermatomes. A few lesions may be found outside the dermatome; more significant generalization of zoster may occur in those with decreased cellular immunity (e.g. the elderly and those with AIDS or hematologic malignancy). Such patients also have a greater risk of involvement of more than one (usually adjacent) dermatome.

    This infection can be very painful, with discomfort being felt for up to 1 month, but some patients have no pain or just minor hyperesthesia in the dermatome. Postherpetic neuralgia (PHN, defined as pain beyond 4 weeks) may occur and is a potentially debilitating sequela. The risk of developing PHN is significantly greater in those aged over 60 years.

Clinical

Groups of vesicles, each on an erythematous base scattered within a dermatome, are characteristic (Figs 25.48 – 25.52). The trunk and face are most commonly affected. The lesions stop at the midline. Intense pain may incapacitate the patient. If the genital area is involved, dysuria to the point of necessitating catheterization may occur. Constipation may result from zoster involving the sacrum.

    In mild cases, only scattered groupings of vesicles may be seen (although these can be identified as being within a dermatome if the diagnosis is suspected, and dermatomal symptoms are a diagnostic clue). In more severe cases, nearly the entire dermatome may be affected. Hemorrhage (Fig.25.53), necrosis (Fig.25.54), and even ulceration may occur (Fig.25.55). Any patient with herpes zoster involving the eye (Fig.25.56) should be referred to an ophthalmologist. Herpes zoster involving the ear may cause the Ramsay Hunt syndrome (Figs 25.57 and 25.58).

Figure 25.48 Herpes zoster. Classic appearance of grouped vesicles.

Figure 25.49 Herpes zoster. Discrete clusters of vesicles as shown here are a common pattern, especially in early lesions, but may cause diagnostic difficulty, as the dermatomal distribution may not be obvious.

Figure 25.50 Early herpes zoster mimicking herpes simplex. This patient presented with an isolated group of painful vesicles on an erythematous base. Herpes simplex was suspected. It was only when the patient returned 2 days later (Fig. 25.51) with multiple lesions scattered in a dermatome that the correct diagnosis of herpes zoster was entertained.

Figure 25.51 Herpes zoster. The same patient as in Figure 25.50, demonstrating the evolution of further lesions within the same dermatome.

Figure 25.52 Disseminated herpes zoster. Finding a few vesicles outside the affected dermatome is common and does not constitute dissemination. However, generalization of the zoster may occur, especially in those with decreased cellular immunity (e.g. the elderly and those with AIDS or hematologic malignancy).

Figure 25.53 The vesicles of herpes zoster may at times be hemorrhagic.

Figure 25.54 Necrotic herpes zoster. In debilitated patients, necrosis may occasionally occur.

Figure 25.55 Ulcerative herpes zoster. (Courtesy of Michael O. Murphy, M.D.)

    In cases of typical herpes zoster, a few scattered vesicles may occur outside the dermatome. If many are present, for example more than 20, the term disseminated herpes zoster is used (Figs 25.52 and 25.59). Dissemination of herpes zoster is more common in the immunocompromised host.

    A variety of skin changes have been reported in the affected area of skin after herpes zoster infection, including granuloma annulare, sarcoidal granuloma, granulomatous vasculitis, lymphoma, pseudolymphoma, Kaposi sarcoma, and comedones; this has been termed an isotopic response.

    HIV-positive patients who develop herpes zoster are at increased risk for major complications (27% in one study). These include meningitis, radiculitis, frank dissemination, and chronic atypical skin lesions. Also, HIV-positive patients may develop chronic, localized disease. Often, these lesions exhibit significant hyperkeratosis.

Differential diagnosis

If the presentation is classic, with vesicles limited to a dermatome, the diagnosis is clear. Very early, when only pain or erythema is present, many other diseases may be considered. For example, some patients have gone to surgery for an acute abdomen when the initial pain without a rash was extreme.

    The lesions themselves may be confused with herpes simplex and may just be viewed as non-specific in early disease. Disseminated lesions, especially in the immunosuppressed or unwell patient, may need to be differentiated from a wide variety of other infections if a dermatomal component is not apparent.

Figure 25.56 (a,b) Ophthalmologic zoster vesicles and crusting of the top and side of the nose in herpes zoster implies involvement of the nasociliary branch of the trigeminal nerve and eye involvement. Ocular scarring and loss of vision may occur. Referral to an ophthalmology specialist is mandatory. (Panel b courtesy of Michael O. Murphy, M.D.)

Figure 25.57 Ramsay Hunt syndrome. Herpes zoster of the geniculate ganglion resulting in vesicles on the ear (as shown here) and tympanic membrane occurs in Ramsay Hunt syndrome. Both seventh and eighth cranial nerve functions may be affected.

Figure 25.58 Ramsay Hunt syndrome. Patients may have tinnitus, deafness, nausea, vomiting, nystagmus, facial hemiplegia, and partial loss of taste. The patient pictured here is trying to close both eyes.)

Figure 25.59 Disseminated herpes zoster. (a,b) Note the extensive involvement of the dermatome to the point of complete erosion along with disseminated lesions on the trunk and face.

Figure 25.60 Herpes zoster occurred in this 3-year-old. She had chicken pox at age 18 months. The varicella zoster virus causes both conditions. Spontaneous resolution can be expected.

Figure 25.61 Herpes zoster in an immunocompromised host. Shingles preferentially affects those with decreased cellular immunity, for example the elderly, HIV-positive patients, and those with hematologic malignancy. This 3-year-old with leukemia developed shingles on the left arm.

Figure 25.62 (a,b) Orf. A solitary papulonodule develops at the site of inoculation of this zoonosis acquired from sheep or goats.

Treatment

If instituted early (e.g. within 72h of the onset of skin lesions), oral antiviral treatment decreases pain and shortens healing time (see Table 25.5). One study showed famciclovir 750mg once daily for 7 days was as effective as aciclovir. Such treatment is strongly recommended in those aged 50 years or over, with moderate or severe rash or pain, or in those with ophthalmologic involvement. In the immunocompromised, treatment should be given until healing occurs.

    In the patient aged 50 years or older with moderate to severe rash and pain, in whom corticosteroids are not contraindicated, prednisone (initially 60mg orally and tapered over 21 days) helps with many of the symptoms. Narcotic analgesics may be needed. Patients should be instructed that they can transmit chicken pox from the lesions until the latter scab over. The current prevailing opinion is that neither aciclovir nor prednisone significantly affects the duration or incidence of PHN.

Childhood herpes zoster

Infants and children may rarely develop herpes zoster (Figs 25.60 and 25.61). Risk factors include primary varicella zoster infection before age 12 months or any form of immunocompromise, although immunocompetent children afflicted with chicken pox after 1 year of age may also be affected. The incidence of herpes zoster is less after vaccination than after natural infection. Herpes zoster in children tends to run a benign course. PHN is rare. The thoracic dermatomes are most frequently affected. Fever, headache, and lymphadenopathy are common.

    If given within 72h of the onset of zoster, aciclovir therapy can prevent significant morbidity in children. For an adolescent seen within 72h of onset, aciclovir (80mg/kg per day in four or five divided doses, with a maximum of 4g/day) may be given. For younger children, aciclovir may be given intravenously (30mg/kg per day) or orally (40–60mg/ kg per day) until 2 days after the last lesions have developed.

Virus-associated trichodysplasia

This newly recognized disease occurs in immunosuppressed transplant patients. Patients have numerous erythematous papules concentrated in the central portion of the face. Alopecia may occur as well. The histology is characteristic, showing that the entire follicular bulb is devoted to the manufacture of inner root sheath-type keratin. Electron microscopy shows abundant viral particles consistent with papovavirus or polyoma viral infection.

    The skin of the central face is covered with 1–3-mm confluent pink papules. Some papules have spiny, keratotic excrescences. There may be alopecia. The patient is typically on immunosuppressive drug therapy to prevent rejection of a transplanted organ (e.g. kidney). Typical drugs are mycophenolate mofetil, ciclosporin, azathioprine, and prednisone.

Orf

Orf, also called ecthyma contagiosum, is a viral infection acquired from sheep or goats. The causative agent is a virus from the poxvirus group. A solitary papulonodule develops at the site of inoculation of this zoonosis (Figs 25.62 and 25.63). Fever, lymphadenopathy, lymphangitis, and erythema multiforme may accompany the lesion. If confirmation of the diagnosis is needed, one can aspirate fluid and examine by electron microscopy to identify viral particles. The development of bullous pemphigoid 2–3 weeks following orf infection has been reported in five patients. The blistering resolved in all cases with saline soaks and a potent topical steroid.

    No treatment is needed, and the lesion will usually resolve within 1–6 months. Cryotherapy is reported effective. Person-to-person transmission has not been reported.

Milker's nodule

Milker's nodule is caused by a parapoxvirus. It causes ulcerative lesions on the teats of cows and the mouths of calves.

    Human lesions are usually solitary and occur in the hands (Fig.25.64) as a verrucous nodule. They may resemble a kerion, which is also contracted from cattle. By contrast, lesions of cowpox are often more pustular or scabbed, and are often multiple.

Figure 25.63 (a,b) Orf causing erythema multiforme.

Figure 25.64 Milker’s nodule. A typical verrucous nodule on the hand of a cattle farmer.

    There is no specific treatment. Topical antiseptics such as povidone– iodine may be useful if the lesion is exposed to trauma and risk of secondary infection.

Other viral infections

Human herpesvirus 8

Human herpesvirus 8 is known to be the cause of Kaposi sarcoma, both HIV-associated and classic. See Chapter 12 and Chapter 33.

White/Cox: Diseases of the Skin, 2ed.(c) 2006, Elsevier Inc. All rights reserved.