VESICULO BULLOUS DISEASE VIRAL ORIGIN- 2 HERPES ZOSTER By DR. S. KARTHIGA KANNAN. MDS PROFESSOR Oral Medicine & Radiology
LEARNING OBJECTIVES ☛ To know about those viral infections that produce vesiculo bullous lesions in orofacial area ☛ To know about their clinical features ☛ To know about their management. HE WHO STUDIES MEDICINE WITHOUT BOOKS SAILS AN UNCHARTED SEA, BUT HE WHO STUDIES MEDICINE WITHOUT PATIENTS DOES NOT GO TO SEA AT ALL. - SIR WILLIAM OSLER -
INFECTIONS BACTERIALVIRALFUNGALPARASITIC DNA VIRUS RNA VIRUS 1. Herpes viridae 2. Pox viridae 3. Adeno viridae 4. Papova viridae 5. Parvo viridae 6. Irido viridae 1. Picorno viridae 2. Orthomyxo viridae 3. Paramyxo viridae 4. Retro viridae 5. Rhabdo viridae 6. Reo viridae
HERPES VIRIDAE FAMILY - Sub Family 1. Have cytopathic effect 2. Latent infectioin in nerve ganglia Eg: HSV I, HSV II, Varicella - Sub Family 1. Infected cells show cytomegaly 2. Latent infection in salivary glands Eg: Cytomegalovirus - Sub Family 1. Grows best in lymphblastoid cells 2. Latent infection in lymphoid tissue Eg: Ebstein barr virus
A BAND OF ROSES FROM HELL HERPES ZOSTER
CHICKEN POX Primary infection of varicella virus Childhood disease Lesions appear as Erythematous macule Vesicle Pustule Ulcerate Scab Lesions widely distributed in the trunk After the primary infection, varicella virus remains dormant in the nerve ganglia
SHINGLES (HERPES ZOSTER) Recurrent infection of Varicella virus Common in old age When the virus descends down the nerve will cause prodromal pain, burning and tingling sensation in that dermatome OOccurrence of pain without the blistering lesion is called herpes sine herpes or zoster sine herpete. After Shingles, severe pain can persist and it is called POST HERPETIC NEURALGIA Lesions appear as Erythematous maculeVesicle PustuleUlcerateScab? Scars esions distributed along the course of the affected nerve, Unilaterally.
ONE WHO KNOWS SYPHILIS KNOWS MEDICINE ONE WHO KNOWS ZOSTER KNOWS CUTANEOUS NEURAL ANATOMY.
VARICELLA ZOSTER VIRUS (VZV) INFECTION Primary infection with VZV causes varicella(chicken pox). The virus then becomes latent in the ganglion of the cranial nerves. Reactivation produces Herpes Zoster Infection (HZI). Commonly affect sensory nerves like opthalmic branch of trigeminal nerve, C3,T5,L1 and L2 (Spinal nerves) HZI of facial nerve (motor) result in facial paralysis and called as Ramsay hunt syndrome
CLINICAL MANIFESTATIONS H ZI starts with prodromal symptoms of deep aching or burning pain. W ithin 2-4 days vesicles develop in a dermatomal or zosteriform pattern. T hese vesicles burst and undergo crustation with the crusts falling off after 1-2 weeks. T his pattern describes the unilateral, linear and clustered distribution of the vesicles, ulcers and scabs along the distribution of a nerve. These lesions heal within 2-4 weeks, often with scarring and hypopigmentation. One of the most important complications of HZI is post herpetic neuralgia, defined as pain that lasts for 30 days or 120 days after the development of the vesicles.
ORAL MANIFESTATIONS T he primary lesion presents as blisters turning into acute ulcerations in the mouth. I n HZI, the ophthalmic division of the trigeminal nerve is the cranial nerve most often affected. I nvolvement of the opthalmic nerve leads to lesions on the upper eyelid, forehead and scalp. W ith involvement of the maxillary division, prodromal pain, burning and tenderness, usually on the palate on one side. A few days later, painful, clustered ulcers of 1-5mm size occur on the hard palate in a unilateral pattern which then join together to form larger ulcers which heal within days. Involvement of the mandibular branch leads to formation of blisters and ulcers on the mandibular gingiva, lip and tongue.
COMPLICATIONS 1.HZ opthalmicus – can produce corneal ulcer which can lead to blindness 2.In old age HZ can result in post herpetic neuralgia 3.In immuno-suppressed patient can cause alveloar bone and pulpal necrosis and avulsion of tooth. 4.During prodromal period and in herpes sine herpes unnecessary treatments like extraction or RCT is done.
LABORATORY FINDINGS ☛ CYTOLOGICAL STUDY - Scrapings from the base of the vesicles ☛ FLUORESCENT STAINED ANTIBODY SMEAR - Using fluorescin conjugated monoclonal antibodies ☛ SEROLOGY - A rising titer of antibody in the convalescent serum ☛ VIRAL ISOLATION using cell culture is the best way to confirm a diagnosis of VZV infection. ☛ POLYMERASE CHAIN REACTION (PCR) has good sensitivity but is expensive. MANAGEMENT ☛ GENERAL MANAGEMANT ….. P ain control- Tab.Paracetamol 4 th hourly S upportive care like rest and hydration ☛ DEFINITIVE TREATMENT - Antiviral therapy ☛ Tab. Acyclovir 800mg 5 times a day for 5 days. ☛ Therapy for HZI includes Valacyclovir 1000 mg or famciclovir 500 mg three times a day for seven days which should be started within 72 hours of the disease onset.
TO BE CONTINUED…………………………………,. With my Teacher Dr.N.Gnanasundaram