Although it’s not caused by either the HSV-1 or HSV-2 virus, herpes zoster falls under the umbrella of herpes diseases. Also known as shingles, it’s an infection caused by the varicella-zoster virus, and is characterized by the development of painful skin rashes on one side of the face or body.23 These rashes are red patches of fluid-filled blisters that tend to crack easily.24,25
When we say, “herpes” many of us are thinking about genital herpes, famously known as an incurable inconvenience. But there is more to it than being just a sexually transmitted infection. There are multiple ways that herpes can transmit but genital herpes is usually picked up from sexual contact. Apart from that, herpes can be transmitted when sharing an environment with someone who has the infection as well.
Herpes of the mouth is a viral infection. The virus HSV-1 may be transmitted by droplet spread – direct contact with saliva or even respiratory droplets. These droplets must make contact with broken skin or the mucous membranes in order to infect a person. The method of spread can involve kissing an infected person or even through touch. It can also be spread through the use of contaminated kitchen utensils. Sexual contact accounts for a small number of cases of HSV-1. Nevertheless it is a consideration when genital lesions are present. HSV-2 on the other hand is usually transmitted through sexual contact.
Antibodies that develop following an initial infection with a type of HSV prevents reinfection with the same virus type—a person with a history of orofacial infection caused by HSV-1 cannot contract herpes whitlow or a genital infection caused by HSV-1. In a monogamous couple, a seronegative female runs a greater than 30% per year risk of contracting an HSV infection from a seropositive male partner. If an oral HSV-1 infection is contracted first, seroconversion will have occurred after 6 weeks to provide protective antibodies against a future genital HSV-1 infection. Herpes simplex is a double-stranded DNA virus.
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Once a person is infected, there are no symptoms for anywhere between 2 days to 2 weeks. This is known as the incubation period and is the time during which the virus multiplies profusely. The first symptoms that are seen are the small fluid-filled blisters known as vesicles. This arises as the virus starts destroying cells at the site and causes intense localized inflammation. These small vesicles or sometimes the larger bullae may either burst resulting in ulcer or heal completely with no scarring. The virus may also travel from the site of infection and “hides” by the sensory dorsal root. Here it remains latent until is it is reactivated.
Human herpes virus 3 (HHV3) is also called varicella-zoster virus. HHV3 causes chickenpox. It can also cause a recurrent virus infection of the skin, which is called herpes zoster or shingles. Shingles occurs when dormant varicella-zoster virus from an initial bout of chickenpox becomes reactivated. Like its close relative, HHV1, herpes zoster likes to infect skin cells and nerve cells. This virus may also recur along nerve fibre pathways, causing multiple sores where nerve fibres end on skin cells. Because an entire group of nerve cells is often affected, shingles is generally much more severe than a recurrence of herpes simplex. The lesions generally appear in a band-like or belt-like pattern occurring on one side of the body and are often accompanied by itching, tingling, or even severe pain. Healing usually occurs in 2 to 4 weeks, and scars may remain. Postherpetic neuralgia is a complication of shingles where the pain associated with the infection can persist for months and even years. Most people who experience shingles once do not experience it again.
The “classic” symptoms that most people associate with genital herpes are sores, vesicles, or ulcers – all of which can also be called “lesions.” (The scientific literature on herpes uses the term “lesion” to describe any break or irregularity in the skin.) These classic lesions of genital herpes often resemble small pimples or blisters that eventually crust over and finally scab like a small cut. These lesions may take anywhere from two to four weeks to heal fully.
The risk of transmission from mother to baby is highest if the mother becomes infected around the time of delivery (30% to 60%), since insufficient time will have occurred for the generation and transfer of protective maternal antibodies before the birth of the child. In contrast, the risk falls to 3% if the infection is recurrent, and is 1–3% if the woman is seropositive for both HSV-1 and HSV-2, and is less than 1% if no lesions are visible. Women seropositive for only one type of HSV are only half as likely to transmit HSV as infected seronegative mothers. To prevent neonatal infections, seronegative women are recommended to avoid unprotected oral-genital contact with an HSV-1-seropositive partner and conventional sex with a partner having a genital infection during the last trimester of pregnancy. Mothers infected with HSV are advised to avoid procedures that would cause trauma to the infant during birth (e.g. fetal scalp electrodes, forceps, and vacuum extractors) and, should lesions be present, to elect caesarean section to reduce exposure of the child to infected secretions in the birth canal. The use of antiviral treatments, such as aciclovir, given from the 36th week of pregnancy, limits HSV recurrence and shedding during childbirth, thereby reducing the need for caesarean section.