Herpes simplex orofacial infection
Herpesviral vesicular dermatitis | |
Herpes lesion on upper lip and face |
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Herpes simplex orofacial infection On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Overview
- Infection by HSV-1 is the most common cause of herpes that affects the face and mouth (orofacial herpes), although within the recent years an increase in oral HSV-2 infections has been reported.[1]
Epidemiology
- Based on a study, lifetime prevalences of herpes simplex orofacial infection are 42.1% and 32.4%, in women and men, respectively. Moreover HSV1 prevalence was estimated 50.3%.[2]
- Another study reported herpes simplex infection rate approximately 70-80% in low socioeconomic status and 40%-60% in high socioeconomic status individuals. [3]
- Prevalence of HSV-1 estimated as 57.7% in US population. [4]
Clinical Presentations
- Early HSV infection could be asymptomatic without any obvious symptoms.[5]
- A majority of primary HSV-1 infections occur during childhood and if the virus comes into contact with the mucosa or abraded skin, it can cause acute herpetic gingivostomatitis (inflammation of the cheek's mucosa and gums) within 5–10 days. Some other symptoms may also develop, including fever and sore throat, and painful ulcers may appear.[1]
- Prodromal symptoms often precede a recurrence, which typically begins with reddening of the skin around the infected site, with eventual ulceration to form fluid-filled blisters that affect the lip (labial) tissue and the area between the lip and skin (vermillion border).[1] [6]
- Primary HSV infection in adolescents frequently manifests as severe pharyngitis with lesions developing on the cheek and gums. Some individuals develop difficulty in swallowing (dysphagia) and swollen lymph nodes (lymphadenopathy).[1] Primary HSV infections in adults often presents as pharyngitis similar to that observed in glandular fever (infectious mononucleosis), but gingivostomatitis is less likely. The symptoms of primary HSV infection generally resolve within two weeks.[1]
- Immunodeficient patients can develop sever and atypical manifestations such as linear erosions in skin creases which has a similar appearance to knife cuts(Knife-Cut Sign). [7]
Disease Progression And Recurrence
- Transmission of HSV-1 usually occurs via direct contact with skin lesions or body fluids of the involved patient (aerosol and fomite spread are rare). In orofacial infection the virus get inoculated onto oropharynx and conjunctiva or through small cracks in the skin.[8] [9]
- Some occupations such as dentists, hospital, nursery or respiratory care unit personnel are at risk of HSV-1 spread via patient's oral secretion. The aforementioned occupations are also at risk of herpes simplex infection due to hospital outbreaks.
- Outbreaks are also reported in some athletes, such as wrestlers.[10]
- Infants born to infected mothers are also at risk of catching the HSV-1 during the delivery.[11]
- HSV-1 infection can be transmitted through sexual activity especially in men who have sex with men.[12]
- Incubation period of primary infection is very short, approximately 5 days. [12]
- Once a primary oral HSV-1 infection has resolved, the HSV enters the nerves surrounding the primary lesion, migrates to the cell body of the neuron, and becomes latent in the trigeminal ganglion. In some patients, the virus reactivates to cause recurrent infection; which is more common with HSV-1 than HSV-2 oral infection.[1] [13]
- Even though trigeminal ganglion is the most common location for HSV-1 infection, inferior and superior cervical ganglia could also become infected with this serotype of herpes simplex.[14]
- After initial infection with one type of herpes simplex virus antibody development occurs which prevent another form of infection with the same type. Based on this, a patient with history of orofacial HSV-1 infection is immune against herpetic whitlow, ocular infection or genital herpes simplex caused by HSV-1. Antibody production occurs 6 months after the initial infection with HSV-1.[15]
- Even though infection with HSV-1 will not protect patients from HSV-2 infection, it will decrease the severity of HSV-2 infection.[16]
- The recurrent infection is thus often called herpes simplex labialis. Rare occasions of reinfections occur inside the mouth (intraoral HSV stomatitis), affecting the gums, alveolar ridge, hard palate, and the back of the tongue. This may be accompanied by herpes labialis.[1] [17]
- It seems that some factors are responsible for recurrent herpes simplex infection due to decreasing the cell mediated immunity (either antigen dependent or no antigen dependent). the following list contains some of these factors:[18][19]
- Other viral infections with fever
- Fatigue
- Menstural period
- Stress
- Local trauma
- Ultraviolet light
- Local injury due to high temprature or frostbite
- Oral herpes is spread by direct contact with an active sore in an infected person, for instance, by kissing. However, the virus can be transmitted through the skin in the absence of a lesion.
- Oral herpes and cold sores can sometimes be confused with canker sores.
Differential diagnosis
Herpes simplex orofacial infection must be differentiated from other diseases causing oral lesions such as leukoplakia and herpes simplex virus infection.[20]
Disease | Presentation | Risk Factors | Diagnosis | Affected Organ Systems | Important features | Picture |
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Diseases predominantly affecting the oral cavity | ||||||
Oral Candidiasis |
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Localized candidiasis
Invasive candidasis |
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Herpes simplex oral lesions | ||||||
Aphthous ulcers |
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Squamous cell carcinoma |
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Leukoplakia |
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Melanoma |
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Fordyce spots |
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Burning mouth syndrome |
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Torus palatinus |
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Diseases involving oral cavity and other organ systems | ||||||
Behcet's disease |
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Crohn's disease |
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Agranulocytosis |
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Syphilis[23] |
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Coxsackie virus |
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Chicken pox |
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Measles |
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Associated Conditions
- Leukemia:[26][27]
- Herpes simplex orofacial infection has been reported in 40% of patients with acute leukemia.
Diagnosis
- Although most orofacial infections of herpes simplex is due to HSV-1, nevertheless HSV-2 could be also responsible in some cases. Hence differentiating the two serotypes could be necessary in some occasions.
- PCR test which detects herpes simplex antibodies and immunodot glycoprotein G-specific (IgG) test are two specific tests (more than 98%) to differentiate these two different serotypes. [28]
Treatment
Acyclovir
- Based on a double-blind, placebo controlled, randomized trial done on patients with recurrent herpes simplex orofacial infection showed efficacy of 5% acyclovir cream containing propylene glycol in reducing the period of vesiculation (P = 0.016), healing time (P = 0.022) and itching duration.[29] [26]
- Another study done on 703 patients with herpes simplex keratitis demonstrated the effectiveness of acyclovir therapy for 12 months in lowering the chance of recurrent herpes simplex orofacial infection, including the ocular infection. [30]
Future or Investigational Therapies
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Bruce AJ, Rogers RS (2004) Oral manifestations of sexually transmitted diseases. Clin Dermatol 22 (6):520-7. DOI:10.1016/j.clindermatol.2004.07.005 PMID: 15596324
- ↑ Malvy D, Ezzedine K, Lançon F, Halioua B, Rezvani A, Bertrais S; et al. (2007). "Epidemiology of orofacial herpes simplex virus infections in the general population in France: results of the HERPIMAX study". J Eur Acad Dermatol Venereol. 21 (10): 1398–403. doi:10.1111/j.1468-3083.2007.02302.x. PMID 17958848.
- ↑ Chayavichitsilp P, Buckwalter JV, Krakowski AC, Friedlander SF (2009). "Herpes simplex". Pediatr Rev. 30 (4): 119–29, quiz 130. doi:10.1542/pir.30-4-119. PMID 19339385.
- ↑ Xu F, Sternberg MR, Kottiri BJ, McQuillan GM, Lee FK, Nahmias AJ; et al. (2006). "Trends in herpes simplex virus type 1 and type 2 seroprevalence in the United States". JAMA. 296 (8): 964–73. doi:10.1001/jama.296.8.964. PMID 16926356.
- ↑ Stanberry LR, Kern ER, Richards JT, Abbott TM, Overall JC (1982). "Genital herpes in guinea pigs: pathogenesis of the primary infection and description of recurrent disease". J Infect Dis. 146 (3): 397–404. doi:10.1093/infdis/146.3.397. PMID 6286797.
- ↑ Herpes Online: Exploring the "H" Community, pages 1-4 American Social Health Association 1996 Access date: 2007-03-29
- ↑ Cohen PR (2015). "The "Knife-Cut Sign" Revisited: A Distinctive Presentation of Linear Erosive Herpes Simplex Virus Infection in Immunocompromised Patients". J Clin Aesthet Dermatol. 8 (10): 38–42. PMC 4633212. PMID 26557219.
- ↑ Sen P, Barton SE (2007). "Genital herpes and its management". BMJ. 334 (7602): 1048–52. doi:10.1136/bmj.39189.504306.55. PMC 1871807. PMID 17510153.
- ↑ Perl TM, Haugen TH, Pfaller MA, Hollis R, Lakeman AD, Whitley RJ; et al. (1992). "Transmission of herpes simplex virus type 1 infection in an intensive care unit". Ann Intern Med. 117 (7): 584–6. doi:10.7326/0003-4819-117-7-584. PMID 1524332.
- ↑ Belongia EA, Goodman JL, Holland EJ, Andres CW, Homann SR, Mahanti RL; et al. (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.
- ↑ Brown ZA, Selke S, Zeh J, Kopelman J, Maslow A, Ashley RL; et al. (1997). "The acquisition of herpes simplex virus during pregnancy". N Engl J Med. 337 (8): 509–15. doi:10.1056/NEJM199708213370801. PMID 9262493.
- ↑ 12.0 12.1 Quinn TC, Corey L, Chaffee RG, Schuffler MD, Brancato FP, Holmes KK (1981). "The etiology of anorectal infections in homosexual men". Am J Med. 71 (3): 395–406. doi:10.1016/0002-9343(81)90167-4. PMID 7025620.
- ↑ Herpes Online: Exploring the "H" Community, pages 1-4 American Social Health Association 1996 Access date: 2007-03-29
- ↑ Cushing H (1983). "Landmark article April 28, 1900: A method of total extirpation of the Gasserian ganglion for trigeminal neuralgia. By a route through the temporal fossa and beneath the middle meningeal artery. By Harvey Cushing". JAMA. 250 (4): 519–28. doi:10.1001/jama.250.4.519. PMID 6345823.
- ↑ Reuven NB, Staire AE, Myers RS, Weller SK (2003). "The herpes simplex virus type 1 alkaline nuclease and single-stranded DNA binding protein mediate strand exchange in vitro". J Virol. 77 (13): 7425–33. doi:10.1128/jvi.77.13.7425-7433.2003. PMC 164775. PMID 12805441.
- ↑ Handsfield HH (2000). "Public Health Strategies to Prevent Genital Herpes: Where Do We Stand?". Curr Infect Dis Rep. 2 (1): 25–30. doi:10.1007/s11908-000-0084-y. PMID 11095834.
- ↑ Herpes Online: Exploring the "H" Community, pages 1-4 American Social Health Association 1996 Access date: 2007-03-29
- ↑ Vestey JP, Norval M, Howie S, Maingay J, Neill WA (1989). "Variation in lymphoproliferative responses during recrudescent orofacial herpes simplex virus infections". Clin Exp Immunol. 77 (3): 384–90. PMC 1542042. PMID 2553308.
- ↑ Oakley C, Epstein JB, Sherlock CH (1997). "Reactivation of oral herpes simplex virus: implications for clinical management of herpes simplex virus recurrence during radiotherapy". Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 84 (3): 272–8. doi:10.1016/s1079-2104(97)90342-5. PMID 9377190.
- ↑ Scully C (1989). "Orofacial herpes simplex virus infections: current concepts in the epidemiology, pathogenesis, and treatment, and disorders in which the virus may be implicated". Oral Surg Oral Med Oral Pathol. 68 (6): 701–10. doi:10.1016/0030-4220(89)90159-x. PMID 2556674.
- ↑ Ann M. Gillenwater, Nadarajah Vigneswaran, Hanadi Fatani, Pierre Saintigny & Adel K. El-Naggar (2013). "Proliferative verrucous leukoplakia (PVL): a review of an elusive pathologic entity!". Advances in anatomic pathology. 20 (6): 416–423. doi:10.1097/PAP.0b013e3182a92df1. PMID 24113312. Unknown parameter
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ignored (help) - ↑ Andrès E, Zimmer J, Affenberger S, Federici L, Alt M, Maloisel F. (2006). "Idiosyncratic drug-induced agranulocytosis: Update of an old disorder". Eur J Intern Med. 17 (8): 529–35. Text "pmid 17142169" ignored (help)
- ↑ title="By Internet Archive Book Images [No restrictions], via Wikimedia Commons" href="https://commons.wikimedia.org/wiki/File:A_manual_of_syphilis_and_the_venereal_diseases%2C_(1900)_(14595882378).jpg"
- ↑ Feikin DR, Lezotte DC, Hamman RF, Salmon DA, Chen RT, Hoffman RE (2000). "Individual and community risks of measles and pertussis associated with personal exemptions to immunization". JAMA. 284 (24): 3145–50. PMID 11135778.
- ↑ Ratnam S, West R, Gadag V, Williams B, Oates E (1996). "Immunity against measles in school-aged children: implications for measles revaccination strategies". Can J Public Health. 87 (6): 407–10. PMID 9009400.
- ↑ 26.0 26.1 Barrett AP (1986). "A long-term prospective clinical study of orofacial herpes simplex virus infection in acute leukemia". Oral Surg Oral Med Oral Pathol. 61 (2): 149–52. doi:10.1016/0030-4220(86)90177-5. PMID 3515270.
- ↑ Barrett AP (1988). "Chronic indolent orofacial herpes simplex virus infection in chronic leukemia: a report of three cases". Oral Surg Oral Med Oral Pathol. 66 (3): 387–90. doi:10.1016/0030-4220(88)90251-4. PMID 3050711.
- ↑ Ashley RL, Militoni J, Lee F, Nahmias A, Corey L (1988). "Comparison of Western blot (immunoblot) and glycoprotein G-specific immunodot enzyme assay for detecting antibodies to herpes simplex virus types 1 and 2 in human sera". J Clin Microbiol. 26 (4): 662–7. doi:10.1128/JCM.26.4.662-667.1988. PMC 266403. PMID 2835389.
- ↑ Van Vloten WA, Swart RN, Pot F (1983). "Topical acyclovir therapy in patients with recurrent orofacial herpes simplex infections". J Antimicrob Chemother. 12 Suppl B: 89–93. doi:10.1093/jac/12.suppl_b.89. PMID 6355055.
- ↑ "Acyclovir for the prevention of recurrent herpes simplex virus eye disease. Herpetic Eye Disease Study Group". N Engl J Med. 339 (5): 300–6. 1998. doi:10.1056/NEJM199807303390503. PMID 9696640.