Infectiology & Dermatology & Family Medicine & Mucosal Medicine
Herpes labialis (HSV-1)
Herpes labialis, commonly known as «cold sores», is a recurrent mucocutaneous infection caused by herpes simplex virus type 1 (HSV-1), an enveloped double-stranded DNA alpha-herpesvirus of the Herpesviridae family. HSV-1 seroprevalence is remarkably high: around 67 % of the world's population under 50 is infected, according to WHO (Looker 2015 - PLOS ONE), with rates exceeding 80-90 % in some populations over 50. Primary infection most often occurs in childhood through direct contact with the saliva or lesions of an infected person. After primary infection - often asymptomatic or presenting as herpetic gingivostomatitis - the virus establishes a lifelong latency in the trigeminal ganglion (Gasser's ganglion). Periodic reactivations occur throughout life, typically manifesting as grouped vesicles on the vermilion lip, preceded by prodromal symptoms (burning, tingling, pruritus). HSV-1 can also infect other areas: the eyes (herpetic keratitis - the main cause of infectious corneal blindness in developed countries), fingers (herpetic panariasis), genital organs (HSV-1 now accounts for 30-50 % of primary genital infections in high-income countries), and, in severe forms, the central nervous system (herpetic encephalitis). Treatment is based on antivirals from the nucleoside analog family: aciclovir, valaciclovir (a prodrug of aciclovir) and famciclovir - effective in shortening the duration of episodes and preventing recurrences with suppressive therapy.
Virology, latency, transmission and pathophysiology
- HSV-1 characteristics, viral cycle and establishment of latency : structure and classification: HSV-1 = 152 kb linear double-stranded DNA alpha-herpesvirus → enveloped (lipid bilayer acquired during budding) → icosahedral capsid + protein integument between capsid and envelope → envelope glycoproteins (gB + gC + gD + gE + gG + gH + gI + gL) → gD : target cell-binding receptor (HVEM + nectin-1 + 3-OS-HS) + gB + gH/gL: membrane fusion → diameter: 150-200 nm → genome: 152 kb → 80 genes → two unique regions (UL + US) flanked by terminal and internal repeat sequences → lytic replication cycle: attachment (gC + gB → heparan sulfate proteoglycan) → membrane fusion (gD + gB + gH/gL) → injection of capsid into cytoplasm → retrograde axonal transport to nucleus → decoating + release of viral DNA → transcription in 3 phases: immediate early genes (α - ICP0 + ICP4 + ICP27 - inhibition of innate defenses + activation of viral transcription) → early genes (β - viral DNA polymerase + viral thymidine kinase - TKv - target of antivirals) → late genes (γ - proteins structural proteins) → viral DNA replication (viral DNA polymerase UL30 → target of aciclovir triphosphate) → assembly + envelopment + secretion + anterograde axonal transport → infection of epithelial cells → cell lysis + release of new virions ; establishment of latency in the trigeminal ganglion : after primary infection of oro-labial epithelial cells → virions → retrograde axonal transport → sensory neurons of Gasser's ganglion (V1 + V2 - ophthalmic nerve + maxilla) → in latent neurons: no lytic replication → circular viral genome (episome) in nucleus → only LAT (Latency-Associated Transcripts) are expressed → LAT : non-coding → maintenance of latency + inhibition of neuronal apoptosis (Bloom 2004 - Journal of Neurovirology) → virus persists for life → no current antiviral treatment eliminates latent viruses → reactivation : various stimuli → oxidative stress + immunodepression + UV radiation (sun) + fever + local trauma + menstruation + fatigue → activation of ganglion neurons → lytic replication → anterograde axonal transport → release into skin or mucosa → clinical vesicular lesions or asymptomatic viral excretion; two virological types - HSV-1 vs HSV-2 - clinical and epidemiological differences: HSV-1: predominant oro-labial tropism (trigeminal ganglion) → herpes labialis + gingivostomatitis + keratitis + encephalitis (temporal lobe) → increasing genital herpes (30-50 % of genital primary infections in high-income countries - Looker 2015 PLOS ONE) → genital recurrences HSV-1: less frequent than genital HSV-2 (1-2 per year vs. 4-6) → HSV-2: predominant genital tropism (sacral node S2-S4) → genital herpes → sometimes facial herpes (rare) → Mollaret's meningitis → neonatal more frequent than HSV-1 → worldwide HSV-2 seroprevalence: 11 % in children <50 years (Looker 2015); epidemiology and transmission: transmission of HSV-1: direct mucosal or cutaneous contact with active lesions or saliva of a person excreting the virus → kissing (main mode of transmission from child to child + from adult to child) + sharing utensils (glasses + cutlery + lipstick) + self-inoculation (fingers → eyes + genitals) + oro-genital sexual transmission → asymptomatic transmission: asymptomatic viral shedding (EVA) of HSV-1 in saliva → 9 % days according to Tronstein 2011 - JAMA → patient often unaware of contagious status → period of maximum contagiousness: vesicular + ulcerative phase (very high viral excretion) + during primary infection → environmental resistance of HSV-1: enveloped virus → very fragile in the environment → rapidly inactivated by: heat + desiccation + soap + common disinfectants + lipid solvents → survival on dry surfaces: only a few hours → risk of transmission by inanimate objects: low but not zero if mucous membrane/skin directly in contact (Sattar 2000 - American Journal of Infection Control)
- Pathophysiology of lesions and immune response : mechanism of vesicular lesions during recurrence : anterograde axonal transport of reactivated HSV-1 → release of virions in cutaneous or mucosal nerve endings of the lip → infection of surrounding keratinocytes → lytic replication → cell death + accumulation of intercellular serous fluid → formation of characteristic vesicles → infiltration of CD4+ and CD8+ T lymphocytes + macrophages → control of viral replication → resolution of the lesion → healing without sequelae in 7-14 days → role of resident CD8+ T lymphocytes (Trm) : Hladik 2012 - Science Translational Medicine: skin-resident CD8+ T lymphocytes (Trm) at site of recurrences → recognize infected cells → control viral spread → efficacy correlates with severity + frequency of recurrences → immunodepression → loss of Trm → more severe + prolonged recurrences + antiviral resistance possible; triggers for recurrences - known mechanisms: UV radiation: one of the most documented triggers → UV irradiation of trigeminal ganglion or skin → NF-κB activation + oxidative stress response → viral reactivation (Rooney 1992 - Journal of Infectious Diseases: UV on lip → reproducible triggering of recurrences in 25/38 subjects) → labial sunscreen protection: Spruance 1991 - Journal of Infectious Diseases: SPF 15 on lip → significant reduction in sun-induced recurrences + immunodepression: HIV (<200 CD4/mm³) + systemic corticosteroid therapy + chemotherapy + transplantation + autoimmune diseases → more frequent + severe + resistant recurrences + psychological stress: documented correlation (Glaser 1987 - Annals of Behavioral Medicine) → mechanism: cortisol → local immunosuppression + viral reactivation + intercurrent fever/infection + local trauma (dermabrasion + orofacial surgery + dental care) + menstruation (hormonal fluctuations) + chronic fatigue; asymptomatic viral shedding (EVA) - public health implication: Tronstein 2011 - JAMA: 498 HSV seropositive subjects + monitoring of viral shedding by daily salivary PCR → viral shedding detected 9 % of days (oral HSV-1) → 76 % of total shedding occurs during asymptomatic days → the vast majority of HSV-1 human-to-human transmission therefore occurs during periods with no visible lesions + implication: informing patients that carriage of the virus is chronic + that transmission is possible without visible lesion + that condoms reduce but do not eliminate the risk of genital transmission
Clinical pictures, diagnosis and management
| Clinical picture / intervention | Features, methods and procedures | Evidence and recommendations |
|---|---|---|
| Clinical pictures - primary infection and recurrence Gingivostomatitis - asymptomatic primary infection - prodromes - labial vesicles - progressive phases |
HSV-1 herpetic primary infection: frequency and age: the vast majority of primary infections occur in childhood (1-5 years) and are asymptomatic (90 % of cases) → only 10 % develop a patent clinical picture: acute herpetic gingivostomatitis → this is the most frequent manifestation of symptomatic primary infection; acute herpetic gingivostomatitis (symptomatic primary infection): clinical picture: high fever (38.5-40°C) + painful cervical adenopathies + intense oral pain → vesicles + diffuse aphthoid ulcerations on oral mucosa (gums + tongue + palate + jugal mucosa) → hypersalivation + refusal to eat (painful dysphagia) + dehydration possible in infants → duration: 7-14 days → complete resolution without sequelae → complications: dehydration in infant → hospitalization if feeding impossible → herpes labialis preceded by a few days → labial ± perioral lesions → genital HSV-1 primary infection (by oro-genital practice): picture similar to HSV-2 genital → vulvar or penile pain + vesicles + ulcerations + inguinal adenopathies + dysuria + fever + general signs → often more severe than HSV-2 primary infection (Langenberg 1999 - Annals of Internal Medicine) → ocular primary infection (herpetic keratoconjunctivitis): unilateral follicular conjunctivitis + photophobia + lacrimation + vesicles on eyelid + decreased visual acuity if corneal involvement → dendritic keratitis (slit lamp dead tree ulcer + fluorescein) → ophthalmological emergency; labial recurrences (recurrent herpes labialis): recurrence frequency: highly variable from one individual to another → 20-40 % of HSV-1-infected people have regular recurrences (1-12 episodes/year - median 2/year) → 60-80 % of infected people never or very rarely have recurrences → frequency factors: antibody titre + cellular immunity + genetic factors + individual triggers; evolutionary phases of labial recurrence: prodromal phase (0-24h before lesions): burning + tingling + pruritus + painful tension in the lip → vesicular phase (J1-J2): appearance of grouped vesicles on an erythematous base → at the vermilion edge (cutaneous-mucosal junction zone) + sometimes philtrum + perilabial zone → clear vesicles → pustular phase (J2-J4): vesicles become cloudy → serous content + confluent → ulcerative-crustal phase (J4-J9): rupture of vesicles → superficial ulcerations → formation of yellowish to brownish crusts → healing phase (J7-J14): progressive resolution → healing without sequelae in usual forms → total duration of episode: 7-14 days → shortened by early antiviral treatment; location of recurrences: vermilion edge of lip (cutaneous-mucosal junction zone): almost pathognomonic localization → same anatomical site at each recurrence in a given individual → other possible localizations: nostril + philtrum + cheek + chin → recurrent intra-oral herpes (>90 % = mouth ulcers - not herpes) → recurrent intra-oral herpes: only on keratinized mucosa (hard palate + gum) in the immunocompetent; distant cutaneous localization (recurrent cutaneous herpes): herpetic panaris: finger (healthcare professional - dentists + nurses) → intense pain + grouped vesicles + axillary adenopathies → care without gloves = risk factor → eczema herpeticum (Kaposi-Juliusberg syndrome): dissemination of HSV-1 on eczematous skin → dermatological emergency → fever + confluent vesicles on eczema patches → risk of sepsis → aciclovir IV | Epidemiology of recurrences and impact on quality of life: Fatahzadeh 2007 - American Family Physician: clinical review of recurrent herpes labialis → 14-40 % of infected adults have regular recurrences → significant psychosocial impact: shame + social avoidance + disruption of intimate + professional life → Whitley 2006 - Clinical Infectious Diseases: pathophysiology of recurrences + Spruance 1992 - Antimicrobial Agents and Chemotherapy: natural history → average duration without treatment: 8-10 days + max lesion size: correlates with severity of pain + spontaneous resolution → always complete in the immunocompetent; eczema herpeticum - emergency not to be missed: Beck 2009 - Journal of Allergy and Clinical Immunology: eczema herpeticum → severe HSV-1 complication on atopic skin → potentially high mortality without antiviral treatment → inpatient IV aciclovir → hospitalization criteria: fever + confluent lesions + altered general condition + peri-ocular involvement |
| Diagnosis - clinical, virological and serological Clinical diagnosis - HSV PCR - viral culture - IgG serology - HSV-1 vs HSV-2 typing |
Clinical diagnosis of recurrent herpes labialis: in the vast majority of cases (typical forms): clinical diagnosis without further investigations → pathognomonic picture: prodromal + vesicles grouped on vermilion border + same location with each recurrence → no further investigations required to initiate antiviral treatment; indications for virological investigations: atypical forms (persistent + non vesicular lesions + in the immunocompromised) + genital primary infection (HSV-1 vs HSV-2 typing → prognostic impact on recurrence frequency) + ocular involvement + neonatal involvement + encephalitis + eczema herpeticum + diagnostic confirmation before long-term suppressive therapy; virological tests available: HSV PCR (herpes simplex PCR): reference method → detection + quantification + typing (HSV-1 vs HSV-2) in a single test → sampling: swabbing of lesion (vesicular or ulcerous phase - before crusting) + CSF (encephalitis) + aqueous humor (keratitis) → sensitivity: 95-100 % in vesicular phase → specificity: 100 % → results in 24-48h → technique of choice → replaces viral culture in the majority of centers in Quebec + viral culture (viral isolation): still used in some laboratories + typing possible + antiviral susceptibility test (if resistance suspected) → lower sensitivity than PCR (70-80 % in vesicular phase + <30 % in crusted phase) + delay: 2-5 days → Corey 1987 - Journal of Infectious Diseases + Tzanck cytodiagnosis: smear from the base of a vesicle → Giemsa staining → multinucleated giant cells + intranuclear inclusions (Cowdry A bodies) → cytopathic effect of HSV → low sensitivity (50-60 %) → non-specific HSV-1 vs HSV-2 vs varicella-zoster → used in resource-limited settings + direct immunofluorescence (DIF): less sensitive than PCR → still available in some laboratories; HSV serology (anti-HHSV IgG antibodies): anti-HHSV IgG-1 + anti-HHSV IgG-2 (type-specific ELISA - glycoprotein gG): indications: screening in asymptomatic individuals + partner of subject with genital herpes + premarital or prenatal check-up + evaluation before suppressive treatment + prenatal screening of pregnant women at risk → sensitivity ELISA gG-specific: 97-100 % + specificity: 97-100 % → IgG positivity: 2-3 weeks after primary infection → lifetime persistence → in Quebec: anti-HSV-1 IgG serology not reimbursed for routine screening → reimbursed if documented medical indication (recurrent genital herpes workup + pregnancy + immunosuppression) → anti-HSV IgM: not recommended → frequent false positives (IgM reactivation) + non-specific HSV-1 vs HSV-2 → do not interpret in practice | Clinical interpretation and differential diagnoses: differential diagnoses to consider: impetigo (Staphylococcus aureus + Streptococcus pyogenes): honey-like crusts + no typical prodromes + may superinfest herpetic lesions + recurrent aphthae (aphthous stomatitis): non-keratinized mucosa (inner lips + cheeks + tongue) → no vesicles → round + painful ulcerations + no contagiousness + mucosal pemphigoid + pemphigus vulgaris: bulla with erythematous background + histological diagnosis + immunofluorescence + post-herpetic erythema multiforme (EM): one of the late complications post HSV-1 → target plaques on hands + lips + mucous membranes → 2-3 weeks after the herpetic episode → immuno-allergic mechanism → preventive treatment: long-term aciclovir or valaciclovir → Schofield 2016 - British Journal of Dermatology + angular cheilitis (perlachia): labial commissures → Candida ± Streptococcus → no vesicles; importance of HSV-1 vs HSV-2 typing in genital herpes: genital HSV-1 primary infection → less frequent recurrences (1-2/year) than HSV-2 (4-6/year) → less frequent asymptomatic viral shedding → lower risk of transmission → important prognostic information for the patient + Langenberg 1999 - Annals of Internal Medicine: prospective cohort → genital HSV-1 → recurrences: median 1.3/year vs genital HSV-2: median 5.1/year |
| Episodic treatment of labial recurrence Aciclovir - valaciclovir - famciclovir - topical cream - onset at prodrome - shortening of episode |
Mechanism of action of anti-HSV antivirals: nucleoside analogues (aciclovir + valaciclovir + famciclovir + penciclovir) → common mechanism: initial phosphorylation by viral thymidine kinase (TKv) → monophosphate → then by cellular kinases → active triphosphate (aciclovir-TP) → competitive inhibition of viral DNA polymerase UL30 → chain termination → arrest of viral replication → therapeutic selectivity: TKv is 300 times more efficient than cellular TK at phosphorylating aciclovir → low toxicity to uninfected host cells → resistance: TKv mutation (TK-deficient) → resistance to aciclovir + valaciclovir + famciclovir → treat with foscarnet or cidofovir (IV) → resistance rare in immunocompetent (<0.5 %) + more frequent in immunocompromised (5-10 %); episodic systemic treatments per os (recommended if moderate to severe recurrences): valaciclovir (Valtrex): prodrug of aciclovir → oral bioavailability 55 % vs aciclovir 15-20 % → recommended regimen for recurrent herpes labialis: 2 g × 2 times 12 h apart in a single day (Aoki single-dose regimen) → start at prodrome or first lesion → Spruance 2003 - Antimicrobial Agents and Chemotherapy: valaciclovir 2 g × 2 in 1 day vs placebo → reduction in episode duration by 1 day (4.4 vs 5.4 days) + reduction in maximum lesion size + 40 % of patients: abortion of episode (no lesion if treated during prodromes) → oral aciclovir (Zovirax): 200 mg × 5/d every 4h (except at night) × 5 days → or 400 mg × 3/d × 5 days → less convenient than valaciclovir (frequency of dosing) → same efficacy if started early → famciclovir (Famvir): prodrug of penciclovir → simplified regimen: 1,500 mg single dose × 1 tablet → efficacy comparable to valaciclovir → Spruance 2006 - JAMA: famciclovir 1,500 mg single dose → reduction in episode duration vs placebo; topical treatments (limited efficacy but over-the-counter): aciclovir cream 5 % (Zovirax cream): apply every 4h × 5 days → modest efficacy: reduction in duration of about 0.5-1 day → start at prodrome → Raborn 1989 - Oral Surgery: aciclovir cream vs placebo → modest reduction in duration → efficacy inferior to oral forms → penciclovir cream 1 % (Denavir): apply every 2h × 4 days → slightly superior efficacy to aciclovir cream → Spruance 1997 - JAMA: penciclovir cream → duration reduction of about 0.7 days vs placebo + pain reduction + docosanol cream 10 % (Abreva - over-the-counter): viral fusion inhibitor → modest efficacy (0.5-day reduction) → Sacks 2001 - JAMA: docosanol 10 % cream vs placebo → 17.5 h reduction in duration → accepted by the FDA → available without prescription in Canada → fundamental principle: the efficacy of all antivirals (topical and systemic) is maximal if treatment is started during the prodromal phase (burning + tingling) → if treatment is started after the vesicular phase: very limited benefit → educate the patient to have his treatment in advance + to start it immediately at the first prodromes | Choice of episodic treatment in Quebec clinical practice: Canadian Herpes Simplex Guidelines + Guide Québec: valaciclovir 2 g × 2 in 1 day = treatment of choice for convenience + efficacy → famciclovir 1,500 mg single dose = equivalent alternative → oral aciclovir 400 mg × 3/d × 5 days = less convenient alternative → creams: reserve for patients refusing the oral route or as a supplement → the oral route is superior to the topical route → RAMQ reimbursement: aciclovir (oral + topical) + valaciclovir = on the list of insured drugs (medical prescription required) → famciclovir = on the RAMQ list + patient education - key to therapeutic success: have the drug at home → recognize prodromes → start immediately → don't wait for vesicles to appear → duration can be reduced by 50 % if treated at prodrome → episode aborted in 30-40 % of cases if treated very early (Spruance 2003 - Antimicrobial Agents and Chemotherapy); antiviral interactions and precautions: aciclovir + valaciclovir: eliminated by glomerular filtration + tubular secretion → adapt dose if CKD (GFR <30 mL/min) → risk of nephrotoxicity if dehydrated + high IV doses → creatinine monitoring → neurological toxicity (headache + confusion): especially with high-dose IV aciclovir + renal failure → well tolerated per os at usual doses → pregnancy: aciclovir + valaciclovir: category B (reassuring data - aciclovir pregnancy registry Glaxo Smith Kline + Sheffield 2003 - New England Journal of Medicine) → Antiretroviral Pregnancy Registry: safety confirmed → treatment possible if indication (severe primary infection + frequent recurrences late in pregnancy) |
| Long-term suppressive therapy and complicated forms Recurrence suppression - daily valaciclovir - immunocompromised - encephalitis - keratitis - neonatal - resistance |
Suppressive (preventive) treatment of frequent labial recurrences: indications: ≥6 labial recurrences per year + severe or disabling recurrences (psychosocial + professional impact) + post-herpetic recurrent erythema multiforme + immunocompromised with frequent recurrences + healthcare professional at high risk of transmission; suppressive treatment modalities: valaciclovir 500 mg/d (1 cp/d): suppressive treatment recommended as 1st line → Rooney 1993 - Journal of Infectious Diseases: suppressive valaciclovir → 80 % reduction in frequency of recurrences + reduction in asymptomatic viral excretion → aciclovir 400 mg × 2/d. : equivalent alternative → less convenient (2 doses) → Strauss 1984 - NEJM: suppressive aciclovir → reduction in recurrences of recurrent oro-labial herpes + famciclovir 250 mg × 2/d: alternative → duration of suppressive therapy: annual reassessment → gradual discontinuation after 12 months → assess whether the number of recurrences has decreased spontaneously → some patients may reduce or discontinue suppressive therapy after 1-2 years; treatment of herpes labialis in the immunocompromised: aciclovir IV 5-10 mg/kg every 8h × 7-14 days if severe form + dissemination + encephalitis + oral valaciclovir 1 g × 2/d if less severe form in stable immunosuppressed → dose adapted according to degree of immunosuppression → prophylactic suppression: valaciclovir 500 mg × 2/d or aciclovir 400 mg × 3-5/d → suppressive therapy recommended in HIV patients with CD4 14 days under aciclovir + immunocompromised → alternative treatment: foscarnet 40-60 mg/kg IV every 8h (directly inhibits viral DNA polymerase - independent of TKv) → cidofovir 5 mg/kg IV/week × 2 then every 2 weeks + probenecid + hyperhydration → topical: cidofovir gel 1 % (compassionate use); complicated forms requiring specialized treatment: HSV-1 herpetic encephalitis: most severe neurological manifestation → absolute emergency → aciclovir IV 10 mg/kg every 8h × 14-21 days → mortality without treatment: 70 % → with treatment: 19-28 % → Whitley 1986 - NEJM : randomized trial aciclovir vs vidarabine → aciclovir superior → survival rate: 54 % vs 39 % → frequent neurological sequelae (amnesia + behavioral disorders) → HSV PCR on CSF: diagnosis + follow-up → herpetic keratitis (ocular): ophthalmological emergency → trifluridine eye drops 1 % (Viroptic) every 2h × 7-14 days (topical ocular treatment) + aciclovir ophthalmic ointment 3 % (Zovirax ophthalmic) every 4h → oral aciclovir or valaciclovir to prevent recurrences (stromal + recurrent forms) → Wilhelmus 2008 - Cochrane: preventive oral aciclovir → reduction of keratitis recurrences by 41 % → no corticosteroids alone without antiviral covering → risk of dissemination; neonatal herpes (HSV-1 or HSV-2): transmission at the time of delivery (active genital lesions) or postnatally (orofacial contact if active lesion of caregiver or parent) → 3 forms: localized (skin + eye + mouth) + CNS + disseminated → pediatric emergency → aciclovir IV 60 mg/kg/d in 3 doses × 14 (localized) to 21 days (CNS + disseminated) → Kimberlin 2001 - NEJM → mortality of disseminated form without treatment: >80 % → with aciclovir IV: 29 % → neonatal prophylaxis: maternal valaciclovir 500 mg × 2/d from 36 weeks if frequent genital recurrences (Sheffield 2006 - American Journal of Obstetrics and Gynecology) → reduction in viral excretion + recurrences at the time of delivery | Preventing recurrences - non-pharmacological measures and photoprotection: lip sun protection: SPF ≥30 on lips before prolonged sun exposure + skiing + altitude → Spruance 1991 - Journal of Infectious Diseases: lip photoprotection → significant reduction in UV exposure-induced recurrences → lip balm SPF 30 = simple, effective measure to be systematically recommended + stress management: stress reduction techniques (mindfulness + physical activity) → reduction in stress-related recurrences documented in observational studies + Glaser 1987 - Annals of Behavioral Medicine + hand hygiene: wash hands carefully after contact with lesions → avoid self-inoculation (eyes + genitals) → do not share utensils + lipstick + razors + glasses during active phase; post-herpetic recurrent erythema multiforme - specific suppressive treatment: recurrent erythema multiforme is triggered in 70 % of cases by HSV-1 → suppressive treatment with aciclovir 400 mg × 2/d or valaciclovir 500 mg/d → prevention of PE recurrence in 70-90 % of cases → Schofield 2016 - British Journal of Dermatology: anti-HSV suppressive therapy → reduction in recurrences of erythema multiforme + respond to all episodes of recurrent PE by prescribing anti-HSV suppressive therapy (even if HSV clinically absent on examination - post-infectious immunological mechanism); oral-genital HSV-1 transmission and counseling: increase in genital HSV-1 primary infections through oral-genital practices (30-50 % of genital primary infections in high-income countries - Looker 2015) → inform patients: active herpes labialis = risk of genital transmission during oral-genital practices → avoid cunnilingus + fellatio during active episodes + during prodromes → use barriers (dental dam) if practice maintained |
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The efficacy of antivirals depends on when they are administered: maximum benefit from antiviral treatment - whether oral (valaciclovir, aciclovir) or topical (aciclovir cream, penciclovir cream) - is obtained when treatment is started during the prodromal phase (burning, tingling, pins and needles), before vesicles appear. Starting treatment during the vesicular or crusting phase considerably reduces the effect. It is therefore advisable to have the medication at hand and to initiate treatment at the first prodromal signs, without waiting for a medical consultation.
Situations requiring urgent medical attention or a call to 911
Intense headache + high fever + confusion + disorientation + unusual behaviour + convulsions + memory impairment in a patient with a history or active herpes lesion → HSV-1 herpetic encephalitis → life-threatening emergency → call 911 immediately → IV aciclovir within hours → mortality without treatment: 70 % → each hour's delay worsens neurological prognosis.
Red eye + eye pain + photophobia + reduced vision + vesicles on the eyelid or periocular area → herpetic keratoconjunctivitis → ophthalmological emergency → same-day ophthalmology consultation → untreated dendritic keratitis → risk of permanent corneal blindness → do not instill ocular corticoids without antiviral.
Infant less than 3 weeks old with skin vesicles + fever + irritability + refusal to feed + convulsions in an infant whose mother has a history of genital or labial herpes → neonatal herpes → absolute pediatric emergency → pediatric emergencies → aciclovir IV → mortality of disseminated form without treatment: >80 %.
Extensive confluent vesicular rash on eczema background + fever + altered general condition in an atopic patient → eczema herpeticum (Kaposi-Juliusberg syndrome) → dermatological emergencies → aciclovir IV in hospital → do not confuse with a flare-up of superinfected eczema → VHS PCR on lesion → immediate treatment without waiting for results if suggestive picture.
Consult at Clinique Omicron
Clinique Omicron's physicians manage recurrent herpes labialis, prescribe the appropriate antivirals for episodic or suppressive treatment, carry out diagnostic tests (HSV PCR, typed serology) if necessary, and provide support for immunocompromised patients or those with complicated forms of the disease. Consultations are available at several points of service in Quebec, and via telemedicine for initial and follow-up care. To book an appointment, visit cliniqueomicron.ca.
The contents of this page are provided for information purposes only and do not replace medical advice. Any unusual herpes lesion, frequent recurrence or associated neurological or ophthalmological sign should be medically evaluated.
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