Cutaneous Herpes


Chapter 50

Cutaneous Herpes



Keith A. Deardorff, Theresa A. Bedford



Definition and Epidemiology


Cutaneous infections caused by the herpes simplex virus (HSV) can be of two serologic types: HSV-1, primarily oral lesions; and HSV-2, mainly genital infections. However, either virus can cause infection at either site. Oral HSV-1 infection recurs more frequently and earlier than oral HSV-2 infection; likewise, genital HSV-2 infection recurs more frequently than genital HSV-1 infection.1,2 Both HSV-1 and HSV-2 are DNA viruses. Clinically, the lesions produced by each strain of the virus are indistinguishable.


There is a high prevalence of HSV-1 and HSV-2 throughout the world. Infection with the virus shows no seasonal variation, and there are no known animal vectors. By the fifth decade of life, 90% of adults have antibodies to HSV-1. In the United States alone, at least 50 million people have genital HSV infection.1 One third to one half of infected individuals lack clinical manifestations of infection and can shed the virus in the absence of symptoms. HSV-2 antibodies start to de­velop during puberty and correlate with the onset of sexual activity.3



Pathophysiology


Transmission of HSV occurs by direct contact with active lesions or with secretions containing the virus. HSV is a double-stranded DNA virus that may enter the host through a skin disruption (e.g., small crack in the skin) or intact mucous membranes (e.g., oropharynx, cervix, conjunctiva). The virus attaches itself to epithelial cells, enters, and replicates, exploiting cellular components. Once infected, cells die and release clear fluid, causing the formation of vesicles, which can fuse to form multinucleated giant cells. During the infection process the virus gains access to and infects regional, sensory, or autonomic nerves. The virus travels through the nerve axon to the ganglion, where it establishes a latent infection. Subsequently, the virus can reactivate and travel down the axon, where it causes a recurrent infection in the cutaneous area innervated by the affected root.3,4



Clinical Presentation


HSV infection has three distinct phases: primary, latent, and recurrent infection. An outbreak is considered to be a primary occurrence if the patient was found to be both HSV-1 and HSV-2 seronegative before the outbreak of genital lesions.5 A person’s first occurrence of HSV infection is usually the most severe and may start after an incubation period of 4 to 6 days; however, the incubation period may range anywhere from 1 to 26 days after initial exposure.6 Patients frequently report a prodrome of burning or tenderness at the site. Multiple painful round vesicles then appear at the site of infection and may be accompanied by tender lymphadenopathy in regional nodes. Fever, dysuria, vaginal discharge, or malaise may accompany the primary infection. Ulceration subsequently occurs, and lesions crust over and heal in immunocompetent patients within 2 to 3 weeks.


During the latent phase, the virus remains dormant in the ganglion of the nerve that serves the affected dermatome. The recurrent phase is characterized by virus reactivation and the reappearance of lesions in the dermatome affected during the primary infection. The outbreak may not occur at exactly the same site. Reactivation of either HSV type can be caused by local or systemic stimuli, such as immunodeficiency, trauma to mucosa, stress, depression, chronic anxiety, and poor sleep. HSV-1–specific triggers include ultraviolet light, cold weather, hot foods, lip biting, food allergy, and fever. HSV-2–specific triggers are noted to be food allergy and menses (usually 5 to 12 days before onset).5 The primary infection may last 10 to 14 days, whereas recurrent infections are shorter and usually less severe, with markedly fewer lesions.



Physical Examination


The lesions of HSV infection are distinct. Grouped round vesicles on an erythematous base appear on the lips, facial area, throat, or genital area (Fig. 50-1). The fluid contained in the vesicles turns cloudy. Vesicles rupture, leaving erosions that subsequently crust over. Regional lymphadenopathy may be associated with primary or recurrent infections but is more common with primary infections. The various stages of lesions can often make diagnosis challenging.




Diagnostics


A diagnosis of HSV infection can be made clinically with a thorough history and physical examination. However, laboratory confirmation should be considered in patients with a newly diagnosed primary infection. In addition, it is important to elicit any history of HSV infection, human immunodeficiency virus (HIV) infection, or pregnancy. The definitive test for the diagnosis of cutaneous herpes simplex infections remains viral culture. Viral cultures can take 2 to 7 days to achieve maximum sensitivity. Diagnosis may also be made with use of fluid obtained from a freshly unroofed vesicle for Tzanck preparation or by a direct fluorescent antibody (DFA) test. Both tests have lower sensitivity rates than culture. Cultures are most likely to be positive for virus when fresh, moist lesions exist; however, the DFA test result may still be positive in crusted, healing lesions.1,7


Serologic testing is available but often does not differentiate HSV-1 from HSV-2 and may only reveal previous exposure. Antigen detection tests are also of limited usefulness in primary infections because antibody development may be delayed.1,4 Polymerase chain reaction (PCR) tests are extremely sensitive and specific but are expensive and are not indicated for mucocutaneous infections. Serologic tests assessing for the specific immunoglobulin to HSV are available and are much more sensitive than viral cultures, PCR testing, and Tzanck smears.8





Management


imageImmediate physician or obstetrician consultation is indicated for pregnant women.


imagePhysician or specialist consultation for HIV co-infected patients is indicated.


Prevention is key in the management of HSV infections. Examples of prevention strategies include widespread public education about the nature of the disease and its spread, urging the use of barrier methods for prevention of sexually transmitted infections with all sexual contact and prophylactic antiviral therapy.2 According to the 2010 Centers for Disease Control and Prevention guidelines for the treatment of sexually transmitted diseases, the recommendation is to treat all patients who are experiencing initial genital herpes infections, regardless of severity, presentation, timing, or duration of symptoms, to reduce complications and possibly recurrences.1


The treatment of choice for most HSV infections remains acyclovir (Zovirax), 400 mg, given orally three times a day for 7 to 10 days; acyclovir, 200 mg, given orally five times a day for 7 to 10 days; famciclovir (Famvir), 250 mg, given orally three times a day for 7 days; or valacyclovir, 1 g, given orally twice daily for 7 to 10 days and with dosage, frequency, or duration reduced with renal impairment. It is also recommended that therapy be extended longer if indicated by incomplete healing despite treatment (Table 50-1).


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Oct 12, 2016 | Posted by in CRITICAL CARE | Comments Off on Cutaneous Herpes

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