Contents
Introduction
Common recurrent, lifelong STD with no cure caused by herpes simplex virus.
Aetiology
Herpes simplex virus (HSV):
HSV are linear, double stranded DNA viruses capable of establishing latency in humans. They belong to the family of Herpesviridae and more specifically to the sub-family of Alphaherpesvirinae. There are two sub-types: HSV-1 and HSV-2 that are closely related but differ slightly in tissue tropism and antigenic properties.
90% of all people worldwide have one or both viruses
- Herpes simplex virus type 1 (HSV-1) (65% prevalence)
- Herpes simplex virus type 2 (HSV-2) (15-80% prevalence)
Risk factors:
- Sexual activity at ≤ 17 years
- History of STDs
- History of undiagnosed genital lesions or discharge
- HIV infection
- Multiple sex partners
- Multiple lifetime sex partners
- Partner diagnosed with genital HSV infection
Pathophysiology
Natural history of infection:
Natural history of HSV infection includes acute or subclinical first-episode mucocutaneous infection, establishment of viral latency, and subsequent reactivation.
The herpes virus enters the body through the skin or mucous membranes by direct sexual contact with the secretions or mucosal surfaces of an infected person. The virus multiplies at the epithelial layer and then ascends along the sensory nerve roots to the dorsal root ganglion, where it becomes latent. With reactivation, the virus travels from the dorsal root ganglion back down the nerve root to create a mucocutaneous outbreak, or it may produce no detectable symptoms.
- Initial primary infection: First virus exposure in anti-HSV-1/2 IgG-negative persons
- Initial nonprimary infection: First HSV-1/HSV-2 infection in persons having IgG antibodies against the other virus type than the one causing acute infection
- Due to cross-reaction of HSV-1 and HSV-2 antibodies, initial nonprimary genital infections cause milder symptoms than initial primary infections.
Clinical features
Herpes is predominantly transmitted through sexual contact. Viral transmission by oro-genital contact is mostly HSV-1 and therefore the number of genital HSV-1 cases is on the rise. Virus shedding is more predominant in sites like mouth and mucosal surfaces such as the vagina. Contact with any one of these increases the risk of being infected with HSV.
Prodrome:
Lasting 2-24 hours characterized by localized/regional pain, tingling, and burning. Patients also may have constitutional symptoms such as headache, fever, inguinal lymphadenopathy, anorexia, and malaise.
Primary herpes:
Primary genital infections caused by HSV-1 or HSV-2 are mostly not associated with clinical symptoms and remain asymptomatic
Classic clinical picture:
- Mucous membrane lesions appearing as maculae and papules, followed by vesicles, pustules, and ulcers
- Duration: Arise within 4–7 days after sexual exposure and last up to 3 weeks
- Symptoms: Pain, itching, burning, and dysuria
- Site: Mostly presenting on external genitalia characterized by bilateral clusters
- Women: Introitus, urethral meatus, labia, and perineum.
- Men: Shaft/glans of penis
- Both: Perianal area, thighs, or buttocks
- Associated features: Lymphadenopathy, fever, cervicitis (women), and proctitis (homosexual men).
Recurrent herpes:
Following the primary eruption the virus establishes lifelong latency in sensory neural ganglions; in the case of primary genital infection the sacral ganglions are mainly involved. From here the virus can reactivate, causing recurrent infection. Viral reactivation is common in the presence of immunogenetic predisposition, though reactivations decrease with increasing age. Numerous physiological and environmental factors such as fever, UV light, menstruation, stress or trauma can function as triggers. Endogenous viral reactivations may manifest as recurrent herpes genitalis.
Compared to primary infection, symptoms of recurrence are much less severe and the clinical course shorter.
- Prodromal symptoms: Neuralgic symptoms, dysaesthesia or lumbosacral dermatome pain 1–2 days before skin and mucosal lesions erupt
Primary herpes simplex virus vesicles on the thigh. | Beauman J. G. (2005). Genital herpes: a review. American family physician, 72(8), 1527–1534. Recurrent herpes simplex virus vesicles on the penis. | Beauman J. G. (2005). Genital herpes: a review. American family physician, 72(8), 1527–1534. Recurrent herpes simplex virus erosions on the labia minora. | Beauman J. G. (2005). Genital herpes: a review. American family physician, 72(8), 1527–1534. Healing recurrent herpes simplex virus lesion with crusts. | Beauman J. G. (2005). Genital herpes: a review. American family physician, 72(8), 1527–1534.
Asymptomatic genital viral shedding:
Majority of cases endogenous viral reactivation is characterised by asymptomatic genital viral shedding.
Complications:
Immunocompromised patients including neonates are susceptible to additional systemic infections including debilitating consequences of nervous system inflammation.
Diagnosis
- Polymerase chain reaction (PCR): Viral DNA detection
- Viral cultivation in cell cultures, detection/typing using monoclonal antibodies for virus isolation
- Immunofluorescence test with monoclonal antibodies: Viral antibody detection
- Enzyme-linked immunosorbent assay (ELISA): Detection of type-specific and non-type-specific antibodies
- Indirect immunofluorescence antibody test (IFAT): Detection of non-type-specific antibodies
- Immunoblot: Detection of type-specific antibodies
Management
Currently prescribed medications, mostly nucleoside analogs, only reduce the symptoms caused by an active infection, but do not eliminate the virus or reduce latency. Therefore, no cure exists against genital herpes and infected patients suffer from periodic recurrences of disease symptoms for their entire lives.
- Acyclovir, Valacyclovir, Famciclovir, Foscarnet