Importance of genital herpes diagnostic tests
Confirmation of clinical diagnosis is important for management. A swab swing should be taken from the vesicle fluid or the base of an erosion for the HSV polymerase chain reaction test (PCR). The viral crop was previously the gold standard for the detection of HSV, but today it is rarely done in clinical practice. The PCR test is practical and useful for the diagnosis of genital herpes, with high sensitivity and specificity. A leather biopsy of a gallbladder or ulcer can be useful if the viral DNA test is not possible. Histology does not routinely distinguish between HSV-1, HSV-2 or the Varicela Zoster virus (VZV). The specific type serology can distinguish between HSV-1 and HSV-2 but cannot distinguish a primary infection from recurrent infection or differentiate oral genital HSV infection.
The specific type serology is not used routinely for the treatment of genital infections by VHS, but it can be clinically useful if a patient wants to know if he is at risk of contracting VHS of a couple with a history of genital herpes. Serological tests aimed at anti-HSV immunoglobulins confirm a primary HSV infection and discard previous viral exposure. The acute and convalescent sera are obtained within the first 3 to 4 days and several weeks after the start of the symptoms, respectively. Due to the delayed humoral response, HSV antibodies are absent from the samples taken during the acute start of HSV infection, but gradually appear;increase in the following weeks;and stay for life.
Differential diagnosis
Important differential diagnoses of genital ulceration include infectious causes (P. Eg., Syphilis, chancroid) and non -infectious (p. Eg., Ate, Behçet’s disease). Genital herpes can have atypical presentations in immunosuppressed patients (P. Eg., Persistent plate). The detection of other sexually transmitted diseases is important, in particular syphilis, hepatitis B, hepatitis C, clamidia and HIV.
Treatment
Antivirals
The objective of the treatment is to reduce the duration of the symptoms and the severity of these, accelerate the healing of the lesions and shorten viral excretion and, finally, reduce the risk of recurrences. The agents available for HSV-1 and 2 are acyclovir, valacyclovir, famciclovir and pencyclovir.
Both acyclovir and Penciclovir are inactive analogues of the Guanosine nucleosidWith the consequent inhibition of viral replication.
Once acycloviring or pencyclovir enter an infected cell, the timidine viral enzyme kinasa will convert acyclovir into acyclovir monophosphate in a first step, being "trapped" inside the cell and will then be triffoiled by other cellular enzymes of the host hosts. Finally, it will compete with the tryposphate guanosine (GTP) to be used by viral polymerase DNA with preference on the latter. That is why they are only troops in the replicative phase of the virus, when viral enzymes are active.
Acyclovir produces greater inhibition of DNA polymerase but pencyclovir presents greater intracellular concentration and for a longer time, which translates into a difference between them – and their profármacos – in bioavailability and dosage, in addition to price. The added advantage of both, over other antivirals available, is poor toxicity, since they are used by viral but non -human enzymes, so, although they penetrate healthy cells, they remain inactive and do not interfere with the synthesis of human DNA. The only authorized in children of any age is acyclovir.
Valaciclovir, although in technical file its use is authorized only for genital and ocular herpes in over 12 years, it has also been used in children over two years for the treatment of chickenpox. Its presentation in tablets limits its use, and in other countries, as in the United Kingdom, they have the possibility of making master formulations in liquid presentation crushing and dissolving the tablets. Famiclovir is not authorized in children under 18 and Penciclovir is authorized above 12 years.
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