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Introduction
Genital herpes is the most common infectious cause of genital ulceration in the developed world and the incidence of infection continues to rise. In developing countries, genital herpes is the second or third most common infective cause of genital ulceration (after chancroid and syphilis), although the prevalence of infection with the virus is considerably higher than in developed countries - HSV-2 antibody prevalence of 60 to 95% have been reported. Genital herpes plays a significant role as a co-factor for HIV transmission.

Both HSV types 1 (HSV-1) and 2 (HSV-2) can infect the genitalia, but HSV-2 causes the majority of primary and recurrent genital herpes infections. Most HSV-2 infections are asymptomatic, detected only by seroconversion; 16% of the adult population is HSV-2 seropositive. In symptomatic genital herpes, the chief clinical morbidity is painful, pruritic vesicles that may coalesce into large ulcerative lesions. Systemic symptoms, such as fever, headache, myalgia, and malaise, are reported by two thirds of patients with primary first-episode genital herpes, and serious complications such as meningitis (reported in 8%) may ensue. After initial infection, the virus enters a latent state in spinal cord ganglia. Infected persons may periodically experience viral reactivations that can be asymptomatic, characterized by viral shedding alone, or symptomatic, marked by a recurrence of signs and symptoms that are less severe than those of primary genital herpes.3 The sexual contacts of individuals with either symptomatic or asymptomatic disease are at risk of becoming infected.

In pregnant women, the rate of genital herpes reported as a maternal risk factor on birth certificates is 8.0/1,000 live births. Pregnant women with genital HSV infection can transmit the virus to their newborns. The majority (82-87%) of neonatal infections occur during delivery, but some also occur in utero or postnatally. One fourth of HSV-infected neonates develop disseminated disease and one third have encephalitis. Impairment is rare but other complications such as visual impairment or seizures occur in about 5%.13,14

Diagnostic Tests
Infection is predominantly sub clinical and individuals with unrecognized infection account for the majority of new transmission episodes to susceptible partners. There is a need for sensitive diagnostic methods to identify individuals with minimally symptomatic disease.

Viral Culture
The current standard diagnostic test is virus culture, however, it is slow and labour intensive. The sensitivity of this test is variable, however, depending upon the viral titer present, ranging in one study from 23-72%. Since the viral titer in asymptomatic shedding is 10-100 times less than that in symptomatic episodes, the sensitivity of viral culture for detecting HSV infection in asymptomatic individuals is likely to be low. In addition, conventional viral culture is time-consuming and technically demanding, and only 40-48% of positive results are available within 24 hours.

Serology
Antibody testing can accurately distinguish HSV-seropositive from HSV- seronegative persons and therefore may be useful to detect asymptomatic carriers at potential risk for transmitting disease, as well as persons susceptible to primary infection. However serological tests for HSV only indicate past infection, they cannot identify the site of infection or prove that a genital lesion is due to HSV infection. They are unreliable for distinguishing HSV-2 from HSV-1 antibodies. Antibody test results do not indicate whether the virus is currently capable of being transmitted.

Other rapid screening methods, such as cytology and direct fluorescent antibody staining, are widely available but are substantially less sensitive than is conventional viral culture.

Polymerase Chain Reaction (PCR)
PCR offers rapid, sensitive, and specific identification of HSV. It is substantially more sensitive than culture for the diagnosis of genital HSV 1& 2 infections and for detection of subclinical viral shedding. The sensitivity of Auro-HSV-PCR is more than 90%. Being a multiplex PCR it is able to detect and differentiate both HSV 1&2 PCR

Specimen
Swab
Ulcers are swabbed firmly with a cotton swab or scrapped with a wooden spatula. The cells collection with the swab or wooden spatula is then place in 1.0 ml of sterile normal saline and stored at 4°C until transportation.

References
Mosely RC, Corey L, Benjamin D, et al. Comparison of viral isolation, direct immunofluorescence, and indirect immunoperoxidase techniques for detection of genital herpes simplex virus infection. J Clin Microbiol 1981;13:913-918
Zimmerman SJ, Moses E, Sofat N, et al. Evaluation of a visual, rapid, membrane enzyme immunoassay for the detection of herpes simplex virus antigen. J Clin Microbiol 1991;29:842-845.
Espy MJ, Wold AD, Jespersen DJ, et al. Comparison of shell vials and conventional tubes seeded with rhabdomyosarcoma and MRC-5 cells for the rapid detection of herpes simplex virus. J Clin Microbiol 1991;29:2701-2703
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