Herpes Simplex Type-1 Virus Infection Michaeli A
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The scope ot oral medicine practice and practitioner competencies is evoijtiorary in nature. This section ol Quintessence International is cnmrnitted to presenting evidenced-based olinical practice guidelines in collaboration with oral and nonoral health care providers. Clinical Practice Guidelines Herpes simplex type-1 virus infection Michaeli A. Huber, Oral infection caused by the herpes simplex virus represents one ot the more oommon conditions the den- tal practitioner will be oalied upon to manage. Unique in its ability to eslablish iatency and undergo subse- quent recurrence, it is an ubiquitous intectious agent for which a cure does not exist. For the immunocom- petent patient, herpes virus simplex infection typicaiiy represents nothing more than a nuisance. However, for the immunooompromised patient, this infection is associated with increased morbidity and mortality. Recentiy introduced antiviral drug regimens may reduce the morbidity and potential mortality of the herpes simplex virus, especiaiiy in immunocompromised patients. The value of antivirai therapy in the manage- ment of recurrent herpes simplex virus infection in the immunocompetent patient remains an area of con- tentious debate. (Quintessence Int 2003:34:453-467) ETIOLOGY AND EPIDEMIOLOGY 1.5% per year up to tbe age of 50.-' Witb sucb bigb prevalence rates, it is clear tbat the vast majority (over Of the more than 80 berpes viruses, at least eigbt are 90%) of primary exposures result in either asympto- known to infect man.' An important feature common matic or mildly symptomafic illness.= '*>^^ to all tbe buman berpes viruses is tbeir ability to estab- lisb latency in tbe bost.--" Both herpes simplex type-1 (HSV-l) and herpes simplex type-2 (HSV-2) are re- CLINICAL MANIFESTATIONS sponsible for primary oral herpes simplex infections, with HSV-l accounting for 75% to 90% of cases."" Primary herpetic gingivostomatitis Transmission occurs via direct contact with contami- nated secretions from an infected individual.'^'^' Of Tbe most commonly observed clinical manifestation the half million new cases per year in the United of primary HSV infection is primary acute herpetic States,'* most occur in children between tbe ages of gingivostomatitis. After an incubation period of 1 to two and tbree years of age. While prevalence rates as 26 days, initial nonspecific signs and symptoms of high as W/o have been reported, age-specific preva- moderate to high fever, malaise, irritability, headache, lence rates appear to be decreasing in industrialized and cervical lymphadenopatby occur.-'i'''^^" Witbin 1 countries. In one survey, 40'>/o of those studied be- to 3 days, tbe cbaracteristic findings of widespread tween the ages of 25 and 29 years had positive serol- vesicular eruptions and gingival inflammation are evi- ogy to HSV, and antibody prevalence rates increased dent. The vesicles affect any intraoral mucosal surface {buccal mucosa, bard/soft palate, floor of the mouth, tongue, gingiva, tonsillar pillars, pharynx) and rupture 'Assistant Professor, University ot Texas Health Science Center at San within a few days to produce painful, small, round, Antonio, Dental School, Division of Oral Medicine, Sari Antonio, Tenas. shallow ulcers (Figs 1 to 6). Often, lesions coalesce to Reprint requests; Dr Michaeii A. Huber, University of Texas Health fortn larger ¡rregular-shaped ulcérations. New vesicles Science Center at San Antonio, Dental Sctiool, Division of Oral Medicine, may erupt and break down for 3 to 5 days, but gradual Mail code 7919, 7703 Floyd Curl Drive, San Antonio, TX 78239-3900. E-rnail:[email protected] healing, without scarring, occurs within 1 to 2 weeks. Quintessence International 453 Huber The pain associated with primary herpetic gingivo- ing, tingling, or itching prior to tbe clinical appearance sfomatitis may adversely affect the patient's ability to of the recurrence, Intraorai recurrence follows a pat- eat, swallow, and speak,^"''"' In the immunocompro- fern of presentafion similar to that of RHL except the mised patient, a primary HSV infection may be more lesions arc intraorai, occur on keratinized mucosa severe and persistent, and death due to aggressive (palate or gingiva), and crusting does not occur (Fig 9), local spread or dissemination to the lungs or brain The pain associated with intraorai herpes may interfere may occur,™' Conditions that predispose to dissemi- with eafing and speaking. In the immunocompetent pa- nation include immunologie immaturity, malignancy, fient, recurrent lesions resolve uneventfully within two malnutrifion, pregnancy, organ transplantation, burns, weeks. Rarely, a recurrent infection affecting the im- corticosteroid therapy, and autoimmune deficiency munocompetent patient may mimic a primary infec- syndrome (AIDS),^«^«-^'-^' fion,^^ In the immunocompromised pafient, recurrence tends to be more severe, widespread, and prolonged. Recurrent iierpes For such a patient the clinical appearance often mimics a primary infection.''^^'**''"'* One of the more perplexing hallmarks of HSV is its ability to establish latency and undergo future reacfi- vation. During primary oral infection, the virus is DIAGNOSIS transported via retrograde axonal transport to regional sensory ganglia where it establishes latency in neu- Differentiai diagnosis ronal cell bodies. While laicnt, the virus exists in a nonreplicating immunologically shielded state in the The diagnosis of both primary and recurrent HSV in- neuron,^'' The most frequent site of latency for HSV-1 fections is typically derived from the history and clini- is the trigeminai ganglion,^^ but other potential sites cal presentation. However, other stomatologie muco- include the nodosa ganglia of the vagus nerve, dorsal cutaneous diseases should be considered in the root ganglia, sympathetic ganglia, and brain,** Viral re- differential diagnosis (Table 1), Recurrent aphthous activation does not always result in clinical recur- stomatitis (RAS) is often misdiagnosed as a HSV infec- rence, as evidenced by the fact that asymptomafic viral fion. This is most likely to occur with the uncommon shedding has been observed in 2% to 9% of the at-risk herpetiform variant of RAS. However, RAS typically population. The impact of asymptomatic viral oral does not have a prodrome of fever and malaise, there shedding on disease transmission remains unclear,^'*-' is no associated gingival erythema, and the ulcérations Numerous well-documented trigger factors are as- almost universally occur on movcablc oral mucosa. sociated with HSV recurrence. They include sunlight, Varicella zoster virus (VZV) infection (chiciien pox) trauma, menstruation, fever, immunosuppression, de- may manifest oral ulcérations similar to an HSV infec- compression of the trigeminai nerve, and irritation by fion. However, the presence of the characteristic pru- dental instruments.'^^''^^"''' While it has been postu- rific crusfing skin erupfions establishes the correct di- lated that individuals who respond to stress with more agnosis. Infrequently, an infraoral recurrent VZV emofion arc more prone to recurrence, the commonly infecfion (zoster) may occur, but the dramafic unilat- held belief that stress predisposes the pafient to recur- eral distribution and intense pain help distinguish it rence has not been confirmed through controlled from an HSV recurrence. Hand-foot-and-mouth dis- studies,^"-^''""" Ciearly, much remains to be deter- ease is disfinguished by the characteristic presence of mined concerning the understanding of the homeosta- lesions affecting the oral cavity, feet and hands. tic dynamic of primary infection, latency, and reactiva- Likewise, herpangina is characterized by oral ulcéra- tion of HSV. tions limited to the soft palate, uvula, tonsils, and pos- Recurrent infecfions are esfimated to occur in 15% terior pharyngeal wall. to 40% of individuals harboring latent HSV'^*''' Three clinical forms of recurrence are recognized: recurrent Laboratory testing herpes labialis (RHL), intraoral recurrence, and recur- rence mimicking a primary infection. RHL is clearly Tzanck smear. The Tzanck smear is a rapid and inex- the most predominant form, with an estimated 100 mil- pensive diagnostic aid. A sterile scalpel blade is used fion cases occurring each year,''^^^ RHL typically pre- to unroof a vesicle, and the base of the vesicle is gen- sents as a focal clustering of vesicles affecting the lip tly scraped to obtain the specimen. The specimen is vermilion or some other perioral site such as the skin smeared on a glass slide, allowed to air dry, and or ala of the nose (Figs 7 and 8). The vesicles quickly stained with Giemsa or Wright's stain in preparation rupture and coalesce to form the characteristic crusting for histologie interpretafion,=* Characteristic multinu- ulcer. Patients usually relate a prodrome of pain, hum- cleated epithefial cells with intranuclear inclusions 454 Voiume 34, Number 6, 2003 • Huber Figs 1 to 6 Primary herpefic gmgivcstomatitis affecting a 29-yeai-old *hife man Quintessence International 455 Huber Fig 7 ;ñ,-c,..ri..-;-it aîïccting a 32-year-old white Fig 8 Recurrent herpes labiaüs affecting a 32-year-oio' white woman (day 1). woman (day 4). TABLE 1 Differential diagnosis of oral HSV Infection Dtfterentjal diagnosis Pertinent findings Herpetiform recurrent Clustered, small, shaliow ulcérations apthous stomatitis affecting free orai mucosa, recurrent, no fever Ha nd-loot-and-mouth Aphthouslike oral ulcérations or lesions disease on hands and feef Herpangina Bandlike oral ulcération