Gulshan Sethi Herpes simplex virus (HSV) types 1 and 2 are typically associated with oropharyngeal and genital infections, respectively. The type 2 virus rarely causes symptomatic oropharyngeal disease, and genital infection remains the most common site of infection. Although genital herpes infection is generally associated with HSV type 2, epidemiological studies have shown that up to 50% of new presentations are caused by HSV type 1 [1,2]. This may be the result of increasing numbers of people encountering this virus for the first time when they become sexually active, rather than in childhood, and also because oral sex has become more common. Symptoms of HSV1 are clinically indistinguishable from those of HSV2. The strongest risk factor for acquiring genital herpes is a person’s lifetime number of sexual partners [3]. The prevalence of HSV2 varies widely between countries and even within different populations in the same country [4,5]. The majority of people with genital herpes are unaware that they are infected because they are either asymptomatic or experience symptoms that are not recognised as being caused by HSV [6]. HSV infection is an important co‐factor in the transmission of HIV. Infection with HSV most frequently occurs following contact of the virus with mucous membranes or abraded skin. It then replicates in epidermal and dermal cells, resulting in vesiculation of the affected tissue. The virus spreads along the lymphatics to the regional lymph nodes and then to sensory or autonomic nerve root ganglia via local sensory neurones, where it lies dormant. Latency may be established after both symptomatic and asymptomatic infection. The majority of HSV2‐infected individuals intermittently reactivate their virus, leading to periods of symptomatic or asymptomatic shedding of virus from skin or mucous membrane. Both host and viral factors influence reactivation, and those who are immunosuppressed experience more severe and frequent episodes. Subclinical viral shedding may occur in over 80% of HSV2‐infected individuals [7] and is likely to be the primary mechanism by which transmission occurs. Viral shedding may continue for up to 16 days in primary infection [8]. Herpes infection manifests clinically for the first time either as a first non‐primary infection (in those who have previously been exposed to any type of HSV and who have antibodies) or as a true primary infection (in those who are sero‐negative with no previous exposure). Individuals with prior exposure to HSV may experience less severe symptoms at the initial episode than those without previous infection. After an incubation period of less than 7 days, initial primary genital infection with HSV results. Approximately 20% develop prodromal symptoms lasting from 2 to 24 hours in which there is localised tingling and/or pain. Following this, small painful papules appear, which then become vesicular and may ulcerate. Multiple lesions are usual (Figure 15.1), and on the vulva these can affect the labia, perineum, perianal, and urethral areas. Crusting and re‐epithelialisation follow, and healing generally occurs about 3 weeks later without scarring. There may also be constitutional symptoms including fever, malaise, headache, and inguinal lymphadenopathy. Sexually acquired HSV can produce extragenital lesions on the buttocks and thighs [9]. Cervical involvement can occur in up to 90% of women with first infection and presents as ulceration [10]. This can be mistaken for a cervical cancer if severe [11]. HSV2 causes an average of four recurrences a year compared to only one with HSV1. Approximately 90% of people with HSV2 will have at least one recurrence in the 12‐month period after infection [12]. Recurrent episodes tend to be milder and less widespread than the initial episode, and the period of viral shedding is shorter. The time from the initial appearance of vesicles to re‐epithelialisation is approximately 8 days. After the first 3 years, recurrences generally occur less frequently. Some patients may present with atypical symptoms including recurrent itching, fissuring, erythema, or linear ulceration [13], which can be misdiagnosed as recurrent candidiasis or dermatoses. The diagnosis of genital herpes is usually made clinically, but clinical diagnosis alone has a sensitivity of less than 40% and results in a false positive diagnosis in up to 20% of individuals [14]. It should therefore be confirmed with testing, and HSV DNA detection by polymerase chain reaction (PCR) increases HSV detection rates by 11–71% compared with viral culture [15–17]. PCR‐based testing requires less stringent conditions for sample storage and transport than viral culture, and the new real‐time PCR assays are rapid and highly specific. Virus typing to differentiate between HSV‐1 and HSV‐2 should be obtained in all patients with newly diagnosed genital herpes. Testing for HSV type‐specific antibodies can be used to diagnose HSV infection [16]. The detection of HSV1 IgG or HSV‐2 IgG or both in a single serum sample represents HSV infection with HSV at some time. It is difficult to say whether the infection is recent, as IgM detection is unreliable. Collection of serum samples a few weeks apart can be used to show seroconversion, and hence recent primary infection. HSV‐2 antibodies are indicative of genital herpes. HSV‐1 antibodies do not differentiate between genital and oropharyngeal infection [18]. Individuals with genital ulceration should always be tested for other causes of ulcers (including syphilis) as well as for sexually transmitted infections (STIs) in general. Figure 15.1 Genital herpes – grouped vesicles right labium majus. Women tend to have more severe symptoms and are more likely to have complications than men [10]. Primary genital herpes may be accompanied by both external and internal dysuria in over 80% of women. Dysuria may result from irritation caused by urine coming into contact with genital ulcers or autonomic nervous system dysfunction. Autonomic dysfunction may also result in constipation and hyperaesthesia of the perineal and sacral regions. Aseptic meningitis occurs in up to 36% of women [10]. Atypical herpes simplex infection can occur in HIV infection or those who are immunosuppressed. These lesions can often mimic malignant lesions (Figure 15.2) and indeed may coexist with tumours [19]. Prolonged antiviral therapy is required, but there are also reports of a good response to imiquimod [20
15
Genital Herpes
Epidemiology
Pathophysiology
Clinical features
Initial primary and non‐primary episodes
Recurrent episodes
Diagnosis
Complications
Hypertrophic (pseudotumoral) herpes simplex
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
