HSV-1 Infections

HSV-1 Infections : 

HSV-1 Infections Dr.Gautam Srivastava, M.D.S Oral Medicine and Radiology

Contents : 

Contents Primary HSV-1 infection Latency Secondary HSV-1 infection Differential diagnosis Diagnosis Occupational hazard Precautions Patient education Treatment Prophylactic therapy

Primary HSV-1 infection : 

Primary HSV-1 infection Primary HSV-1 infection develops in people who have not been previously exposed to HSV-1. Transmission occurs via: Thigmotaxis Airborne water-droplet transmission from an infected individual Mucosal surfaces and skin with cracks are highly susceptible. The most commonly observed clinical manifestation of primary HSV-1 infection is primary herpetic gingivostomatitis or PHG.

PHG : 

PHG Primary herpetic gingivostomatitis is most often seen in children between the ages of 6 months and 5 years, and in people who are in their early 20s. Most often, exposure to HSV-1 infection in children results in a subclinical infection and the child may complain of mild flulike symptoms. Approximately 1% of patients develop primary herpetic gingivostomatitis.

Pathogenesis of PHG : 

Pathogenesis of PHG Exposure to an infected individual HSV-1 gains entry into the body via skin or mucosa with cracks The HSV-1 incubates for 1 to 26 days Nonspecific signs and symptoms such as fever (103 to 1050 F), malaise (physical discomfort), irritability, headache, chills, & cervical lymphadenopathy come The nonspecific signs and symptoms are accompanied by the appearance of vesicles, which affect any gingiva & other intraoral sites Pain due to ulcers may affect the patients ability to eat, swallow, & speak Development of viral-specific antibodies (IgM & IgG) leads to healing of lesions without scarring within 7 to 14 days The vesicles rupture to form painful, small, shallow, & round ulcers

PHG : 

PHG

Latency : 

Latency During primary infection, the newly formed HSV-1 virion comes in contact with sensory nerve endings and is transported via retrograde axonal transport to the trigeminal nerve ganglion where it establishes latency in the nerve cell bodies While latent, the HSV-1 exists in a nonreplicating state and is protected from antibody attack by the blood-brain barrier The HSV-1 remains latent until there is reactivation by reactivating factors Once, reactivated the HSV-1 is transported via anterograde transport to the epithelium where it replicates, causing lysis of keratinocytes and recurrent HSV-1 infection The limited HSV-1 replication takes place until the IgG & IgM respond and suppress it

Latency : 

Latency Red arrow Retrograde transport Green arrow Anterograde transport

Reactivating factors : 

Reactivating factors Stress Sunlight Trauma Menstruation Fever (fever blisters) Cold (cold sores) Pregnancy Immunosuppression Decompression of the trigeminal nerve Greater palatine nerve block

Animation : 

Animation Reactivation & latency

Recurrent HSV-1 infections : 

Recurrent HSV-1 infections Approximately 30 to 40% of patients who have been exposed to HSV-1 will develop recurrent HSV-1 infections. These recurrent HSV-1 infections represent reactivation & not reinfection of HSV-1. The vesicular stage of recurrent HSV-1 infection is the most contagious as the vesicles are laden with fluid containing HSV-1. However, all stages of recurrent HSV-1 infection are contagious until re-epithelialization is complete.

Types of recurrent HSV-1 infections : 

Types of recurrent HSV-1 infections Recurrent HSV-1 infections can either occur as: Recurrent intraoral herpes (RIH) Recurrent herpes labialis (RHL) RHL is the most common recurrent HSV-1 infection.

Pathogenesis of RHL : 

Pathogenesis of RHL Patient experiences prodromal signs & symptoms at the vermilion border, perioral region or ala of the nose Ulcers coalesce to form larger irregular-shaped ulcers with a crusted surface In a healthy individual, healing takes place without scarring within 7 to 14 days Within 24 hours, small macules develop, which then become papules The characteristic clinical appearance of RHL is focal clustering of vesicles The papules then become vesicles The vesicles become pustules, which then rupture & form ulcers

Prodromal signs and symptoms : 

Prodromal signs and symptoms Soreness Swelling Burning Tingling Itching

Animation : 

Animation Areas affected Focal clustering and crustations

RHL : 

RHL Characteristic focal clustering of the vesicles Crustations and healing

RIH : 

RIH Prior to the appearance of the RIH, the patient experiences prodromal signs and symptoms. RIH lesions begin as clusters of tiny vesicles that rupture quickly, resulting in erosions or ulcers. The RIH lesions affect keratinized mucosa (hard palate and attached gingiva). The pain associated with RIH may interfere with eating and speaking. In a healthy individual, the lesions heal without scarring within 7 to 14 days. RIH lesions affect the dorsum of the tongue in an immunocompromised patient.

RIH : 

RIH

Differential diagnosis : 

Differential diagnosis

Diagnostic tests – Tzanck test : 

Diagnostic tests – Tzanck test The Tzanck test (mucosal smear) is a rapid and inexpensive diagnostic aid useful in the diagnosis of HSV-1 infection. A sterile scalpel is used to unroof a vesicle, and the base of the vesicle is gently scrapped with the scalpel. The scrapping is smeared on a slide & allowed to dry in the air for couple of minutes. The scrapping is then stained with Giemsa or Wright’s stain for microscopic examination. Presence of characteristic acantholytic epithelial cells called Tzanck cells indicates a positive test. However, Tzanck cells can also be found in pemphigus vulgaris, carcinoma, and transient acantholytic dermatosis.

Tzanck cells : 

Tzanck cells Nuclear enlargement Nuclear hyperchromatism 1 2

Other diagnostic tests : 

Other diagnostic tests Other diagnostic tests, which are not routinely used, include: Tissue biopsy Viral culture Indirect immunofluorescence Direct immunofluorescence Polymerase chain reaction (PCA) ELISA

Herpetic whitlow : 

Herpetic whitlow Health care workers (HCW) are highly susceptible to an occupational hazard known as herpetic whitlow (herpetic paronychia). Herpetic whitlow is the infection in the tissues adjacent to a nail on a finger or thumb. It represents a primary HSV-1 infection.

Herpetic whitlow : 

Herpetic whitlow Before the common use of examination gloves, herpetic whitlow was very prevalent due to contact with the contaminated secretions such as saliva or vesicular fluid. Recurrences may also occur with this form of herpes infection and usually affect the same site. Recurrent lesions may result in paresthesia and permanent scarring.

Pathogenesis of herpetic whitlow : 

Pathogenesis of herpetic whitlow The virus present in contaminated secretions comes in contact with the finger or thumb HCW does not use gloves when treating a patient with a HSV-1 infection The virus gains entry into the finger or thumb via cracks in the skin & incubates for 2 to 10 days This is followed by eruption of vesicles & formation of pustules The vesicles and pustules eventually rupture to become ulcers The duration of herpetic whitlow may be as long as 4 to 6 weeks after which healing takes place They are usually accompanied by fever, axillary lymphadenitis & pain in the forearm After the incubation period, signs and symptoms such as edema, erythema, intense itching, & localized tenderness of the infected finger or thumb come

Herpetic whitlow : 

Herpetic whitlow Erythema Vesicles & pustules Ulcers and healing

Precautions : 

Precautions HCW should use gloves, face masks, and protective spectacles when examining patient infected with HSV-1 infection. Trauma to the lesion during dental care must be avoided so that healing will not be retarded. Air water sprays should not be used as transmission occurs via airborne water-droplet transmission. Airborne water-droplet transmission can be prevented by using a rubber dam.

Patient education : 

Patient education Patients should be advised not to: Squeeze or pinch the vesicles Touch their eyes or genitals (to prevent autoinoculation) unless they have washed their hands thoroughly To touch and kiss their loved ones To touch other persons Indulge in sexual activity as it can transmit HSV-1 infection to the genitals Eat acidic & spicy foods as they can aggravate the burning sensation Not to apply lipstick directly to the lesions

Patient education : 

Patient education Patients must be encouraged to maintain oral hygiene by brushing in a gentle manner. Patients with a history of RHL should be advised to wear a wide-brim hat & apply a sunscreen lotion with a sun protection factor (SPF) 15 on the lips or over the face. Towels used by the patient should be washed by the patient with hot & soapy water. Eating utensils used by the patient should be cleaned by the patient with hot & soapy water.

Symptomatic therapy for PHG & RIH : 

Symptomatic therapy for PHG & RIH NSAID can be prescribed to relieve fever and burning sensation. Cold beverages, ice creams, ice cubes & bland diet may provide temporary relief of burning sensation. The patient should be instructed to maintain adequate food & fluid intake. If severe, intravenous fluids should be administered. Palliative mouth washes can be used for 2 minutes before meals to reduce oral pain. Topical anesthetic agents such as 2% lidocaine can be used for 2 minutes before meals to reduce oral pain.

Antiviral drugs : 

Antiviral drugs Antiviral drugs that are used in the treatment of HSV-1 infection are as follows: Acyclovir (oral, topical, and intravenous) Valacyclovir (oral) Penciclovir (topical) Famciclovir (oral) Docosanol (topical) Foscarnet sodium (intravenous)

Topical antiviral ointments : 

Topical antiviral ointments Topical antiviral ointments reduce pain & healing time. Topical antiviral ointments should be used extraorally only. Topical antiviral ointments should be dabbed on rather than rubbing as it increases the duration & severity of the lesions. Dentists must advise patients to apply antiviral ointments at the first prodromal symptom.

Systemic antiviral therapy : 

Systemic antiviral therapy Systemic antiviral therapy is usually not indicated in immunocompetent patients as the primary & secondary HSV-1 lesions heal within 10 to 14 days. However, systemic antiviral therapy may be used in persistent primary & secondary HSV-1 lesions. In comparison, systemic antiviral therapy is indicated in patients who are: Immunocompromised (where the lesions are severe, widespread & prolonged (i.e., do not heal within 10 to 14 days).

Foscarnet sodium : 

Foscarnet sodium Intravenous foscarnet sodium therapy is indicated in AIDS patients with thymidine kinase-deficient HSV-1 strains. I.V foscarnet sodium therapy should be accompanied by adequate hydration to prevent toxicities such as: Seizures Somnolence (drowsiness) Confusion Elevated serum creatinine Renal failure Electrolyte imbalance

Slide 37: 

Systemic antiviral therapy for immunocompetent patient with PHG

Slide 38: 

Systemic antiviral therapy for immunocompromised patient with PHG I.V administration should be accompanied by 10% dextrose to reduce the risk of reversible renal toxicity due to crystalline nephropathy

Slide 39: 

Systemic foscarnet therapy for PHG

Topical antiviral therapy for immunocompetent & immunocompromised patients with RHL : 

Topical antiviral therapy for immunocompetent & immunocompromised patients with RHL

Systemic antiviral therapy for immunocompetent patients with RIH & RHL : 

Systemic antiviral therapy for immunocompetent patients with RIH & RHL

Systemic antiviral therapy for immunocompromised patient with RIH or RHL : 

Systemic antiviral therapy for immunocompromised patient with RIH or RHL

Slide 46: 

Systemic foscarnet therapy for RIH/RHL

Prophylactic therapy : 

Prophylactic therapy Prophylactic systemic antiviral therapy is indicated in patients: With frequent lesions (over 6 episodes per year) – Regimen 1 Before planned dental treatment – Regimen 2

Regimen - 1 : 

Regimen - 1

Regimen - 2 : 

Regimen - 2