Herpes gladiatorum

Herpes gladiatorum is one of the most infectious of herpes-caused diseases, and is transmissible by skin-to-skin contact. The disease was first described in the 1960s in the New England Journal of Medicine. It is caused by contagious infection with human herpes simplex virus type 1 (HSV-1),[1] which more commonly causes oral herpes (cold sores). Another strain, HSV-2 usually causes genital herpes, although the strains are very similar and either can cause herpes in any location.

While the disease is commonly passed through normal human contact, it is strongly associated with contact sports—outbreaks in sporting clubs being relatively common.[2] Other names for the disease are herpes rugbiorum or "scrumpox"[2] (after rugby football), "wrestler's herpes" or "mat pox" (after wrestling). In one of the largest outbreaks ever among high-school wrestlers at a four-week intensive training camp, HSV was identified in 60 of 175 wrestlers. Lesions were on the head in 73 percent of the wrestlers, the extremities in 42 percent, and the trunk in 28 percent.[3] Physical symptoms sometimes recur in the skin.[4] Previous adolescent HSV-1 seroconversion would preclude most herpes gladiatorum, but being that stress and trauma are recognized triggers, such a person would be likely to infect others.

## Signs and symptoms[edit]

Herpes gladiatorum is characterized by a rash with clusters of sometimes painful fluid-filled blisters, often on the neck, chest, face, stomach, and legs. The infection is often accompanied by lymphadenopathy (enlargement of the lymph nodes), fever, sore throat, and headache.[5] Often, the accompanying symptoms are much more of an inconvenience than the actual skin blisters and rash.[citation needed]

Each blister contains infectious virus particles (virions). Close contact, particularly abrasive contact as found in contact sports, causes the infected blisters to burst and pass the infection along. Autoinoculation (self-infection) can occur through self-contact, leading to infection at multiple sites on the body.[5]

Herpes gladiatorum symptoms may last up to a few weeks, and if they occur during the first outbreak, they can be more pronounced. In recurrences of the ailment, symptoms are milder, even if lesions still tend to occur. With recurrent infections scabs may form at 3 days yet the lesions are still considered infectious up until 6.4 days after starting oral antiviral medications.[6] Healing takes place without leaving scars. It is possible that the condition evolves asymptomatically and sores are never present.[citation needed]

## Causes[edit]

Herpes gladiatorum is a skin infection primarily caused by the herpes simplex virus. The virus infects the cells in the epidermal layer of the skin. The initial viral replication occurs at the entry site in the skin or mucous membrane.[7]

The infections caused by a HSV Type 1 virus may be primary or recurrent.[8] Studies show that even though most of the individuals who are exposed to the virus get infected, only 10% from them will develop sores as well. These types of sores appear within two to twenty days after exposure and usually do not last longer than ten days. Primary infections usually heal completely without leaving scars but the virus that caused the infection in the first place remains in the body in a latent state. This is the reason why most of the people experience recurrences even after the condition is taken care of. The virus moves to the nerve cells from where it can reactivate.[citation needed] Once the condition has recurred, it is normally a mild infection. The infection may be triggered by several external factors such as sun exposure or trauma.[vague]

Infection with either type of the HSV viruses occurs in the following way: First, the virus comes in contact with damaged skin, and then it goes to the nuclei of the cells and reproduces or replicates.[9] The blisters and ulcers formed on the skin are a result of the destruction of infected cells. In its latent form, the virus does not reproduce or replicate until recurrence is triggered by different factors.[citation needed]

## Pathophysiology[edit]

Herpes gladiatorum is transmitted by direct contact with skin lesions caused by a herpes simplex virus.[1] This is the main reason why the condition is often found in wrestlers. It is believed that the virus may be transmitted through infected wrestlers' mats, but this is still subject of research since the virus cannot live long enough outside the body in order to be able to cause an infection. Direct contact with an infected person or infected secretions is undoubtedly the main way in which this virus may be transmitted.[citation needed]

It is also believed that wearing abrasive clothing may increase the chances to get infected with this type of virus. Shirts made of polyester and cotton may cause frictions that lead to small breaks in the skin which makes it easier to contract the infection. Studies in which athletes were wearing 100% cotton shirts showed a decrease in the number of herpes gladiatorum cases.[10]

The spread is facilitated when a sore is present but it can happen in its absence as well. The patients may know that the virus is present on the skin when they experience the so-called "prodromal symptoms". These include itching or tingling on the skin, right before the blisters or lesions appear. The virus may spread since the first symptoms appear until lesions are completely healed. The incubation period is situated between 3 and 14 days. This means that a person will experience the symptoms within 14 days after he or she contracted the infection. This type of virus may be transmitted even if the symptoms are not yet present. Some individuals can have very mild symptoms that may not be taken as herpes symptoms and the patient may not recognize them. The asymptomatic transmission occurs when the infection is spread between outbreaks.[11]

### Similar infections[edit]

Herpes gladiatorum is only caused by the herpes simplex virus. Shingles, also manifesting as skin rashes with blisters, is caused by a different virus, herpes zoster. Other agents may cause skin infections, for example ringworm is primarily due to the fungal dermatophyte, T. tonsurans. Impetigo, cellulitis, folliculitis and carbuncles are usually due to Staphylococcus aureus or Beta-hemolytic streptococcus bacteria. These less common forms can be potentially more serious.[2] Anti-viral treatments will not have an effect in non-viral cases. Bacterial infections must be treated with antibiotics and fungal infections with anti-fungal medication.[2]

## Prevention[edit]

Key measures to prevent outbreaks of the disease are maintaining hygiene standards and using screening to exclude persons with suspicious infections from engaging in contact sports. A skin check performed before practice or competition takes place can identify individuals who should be evaluated, and if necessary treated by a healthcare professional.[5] In certain situations, i.e. participating in wrestling camps, consider placing participants on valacyclovir 1GM daily for the duration of camp. 10-year study has shown 89.5% reduction in outbreaks and probable prevention of contracting the virus. Medication must be started 5 days before participation to ensure proper concentrations exist.[12]

## Treatment[edit]

Herpes outbreaks should be treated with antiviral medications like Acyclovir, Valacyclovir, or Famcyclovir, each of which is available in tablet form.[2]

Oral antiviral medication is often used as a prophylactic to suppress or prevent outbreaks from occurring.[13] The recommended dosage for suppression therapy for recurrent outbreaks is 1,000 mg of valacyclovir once a day or 400 mg Acyclovir taken twice a day. In addition to preventing outbreaks, these medications greatly reduce the chance of infecting someone while the patient is not having an outbreak.[citation needed]

Often, people have regular outbreaks of anywhere from 1 to 10 times per year, but stress (because the virus lies next to the nerve cells), or a weakened immune system due to a temporary or permanent illness can also spark outbreaks. Some people become infected but fail to ever have a single outbreak, although they remain carriers of the virus and can pass the disease on to an uninfected person through asymptomatic shedding (when the virus is active on the skin but rashes or blisters do not appear).[citation needed]

The use of antiviral medications has been shown to be effective in preventing acquisition of the herpes virus.[14] Specific usage of these agents focus on wrestling camps where intense contact between individuals occur on a daily basis over several weeks. They have also been used for large outbreaks during seasonal competition, but further research needs to be performed to verify efficacy.[citation needed]

## See also[edit]

* Herpes simplex
* List of cutaneous conditions

## References[edit]

1. ^ a b Likness, LP (June 2011). "Common dermatologic infections in athletes and return-to-play guidelines". The Journal of the American Osteopathic Association. 111 (6): 373–379. doi:10.7556/jaoa.2011.111.6.373. PMID 21771922.
2. ^ a b c d e Sharp JCM (1994-06-24). "ABC of Sports Medicine: Infections in sport" (Education and Debate). BMJ. 308 (6945): 1702–1706. doi:10.1136/bmj.308.6945.1702. PMC 2540619. PMID 8025471.
3. ^ Belongia EA, Goodman JL, Holland EJ, et al. (September 1991). "An outbreak of herpes gladiatorum at a high-school wrestling camp". N. Engl. J. Med. 325 (13): 906–10. doi:10.1056/NEJM199109263251302. PMID 1652687.
4. ^ Fatahzadeh M, Schwartz RA (November 2007). "Human herpes simplex virus infections: epidemiology, pathogenesis, symptomatology, diagnosis, and management". J. Am. Acad. Dermatol. 57 (5): 737–63, quiz 764–6. doi:10.1016/j.jaad.2007.06.027. PMID 17939933.
5. ^ a b c Centers for Disease Control (CDC) (1990-02-09). "Epidemiologic Notes and Reports Herpes Gladiatorum at a High School Wrestling Camp—Minnesota". MMWR. CDC. 39 (5): 69–71. PMID 2105440.
6. ^ Anderson, BJ (September 2005). "Valacyclovir to expedite the clearance of recurrent herpes gladiatorum". Clinical Journal of Sport Medicine. 15 (5): 364–6. doi:10.1097/01.jsm.0000181468.44397.ce. PMID 16162997. S2CID 34057429.
7. ^ eMedicine Portal. "Herpes Simplex details" 2010-02-10.
8. ^ American academy of dermatology. "Herpes Simplex explained"[permanent dead link] 2010-02-10.
9. ^ Herpes Simplex Virus infection and recurrence About health online portal. Retrieved on 2010-02-10
10. ^ Ramin, Kordi (2009). Combat sports medicine. ISBN 978-1-84800-353-8.
11. ^ Herpes detailed analysis eMedicine. 2010-02-10
12. ^ Anderson BJ, McGuire D, Reed, M, Foster M, Ortiz D. Prophylactic Valacyclovir to Prevent Outbreaks of Primary Herpes Gladiatorum at a 28-day camp: a 10-year review.Clin J Sports Med. 2016. 26:4: 272–8.
13. ^ Anderson, BJ (April 1999). "The effectiveness of valacyclovir in preventing reactivation of herpes gladiatorum in wrestlers". Clinical Journal of Sport Medicine. 9 (2): 86–90. doi:10.1097/00042752-199904000-00008. PMID 10442623.
14. ^ Anderson, BJ (February 2006). "Prophylactic valacyclovir to prevent outbreaks of primary herpes gladiatorum at a 28-day wrestling camp". Japanese Journal of Infectious Diseases. 59 (1): 6–9. PMID 16495626.

* v
* t
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Skin infections, symptoms and signs related to viruses

| DNA virus|

| Herpesviridae|

| Alpha.|

| HSV|

* Herpes simplex
* Herpetic whitlow
* Herpes gladiatorum
* Herpes simplex keratitis
* Herpetic sycosis
* Neonatal herpes simplex
* Genital herpes
* Cold sore
* Eczema herpeticum
* Herpetiform esophagitis
* Herpetic gingivostomatitis

|

B virus|

* B virus infection

VZV|

* Chickenpox
* Herpes zoster
* Herpes zoster oticus
* Ophthalmic zoster
* Disseminated herpes zoster
* Zoster-associated pain
* Modified varicella-like syndrome

Beta.|

* Human herpesvirus 6/Roseolovirus
* Exanthema subitum
* Roseola vaccinia
* Cytomegalic inclusion disease

Gamma.|

* KSHV
* Kaposi's sarcoma

Poxviridae|

| Ortho.|

* Variola
* Smallpox
* Alastrim
* MoxV
* Monkeypox
* CPXV
* Cowpox
* VV
* Vaccinia
* Generalized vaccinia
* Eczema vaccinatum
* Progressive vaccinia
* Buffalopox

|

Para.|

* Farmyard pox: Milker's nodule
* Bovine papular stomatitis
* Pseudocowpox
* Orf
* Sealpox

Other|

* Yatapoxvirus: Tanapox
* Yaba monkey tumor virus
* MCV
* Molluscum contagiosum

Papillomaviridae|

| HPV|

* Wart/plantar wart
* Heck's disease
* Genital wart
* giant
* Laryngeal papillomatosis
* Butcher's wart
* Bowenoid papulosis
* Epidermodysplasia verruciformis
* Verruca plana
* Pigmented wart
* Verrucae palmares et plantares

|

* BPV
* Equine sarcoid

Parvoviridae|

* Parvovirus B19
* Erythema infectiosum
* Reticulocytopenia
* Papular purpuric gloves and socks syndrome

Polyomaviridae|

* Merkel cell polyomavirus
* Merkel cell carcinoma

RNA virus|

| Paramyxoviridae|

* MeV
* Measles

|

Matonaviridae|

* Rubella virus
* Rubella
* Congenital rubella syndrome ("German measles")

Togaviridae|

* Alphavirus infection
* Chikungunya fever

Picornaviridae|

* CAV
* Hand, foot, and mouth disease
* Herpangina
* FMDV
* Foot-and-mouth disease
* Boston exanthem disease

Ungrouped|

* Asymmetric periflexural exanthem of childhood
* Post-vaccination follicular eruption
* Lipschütz ulcer
* Eruptive pseudoangiomatosis
* Viral-associated trichodysplasia
* Gianotti–Crosti syndrome

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