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ORO-FACIAL HERPES ZOSTER: A CASE REPORT WITH A DETAILED REVIEW OF LITERATURE

Abstract Herpes zoster or shingles is a reactivation of the Varicella zoster virus that entered the cutaneous nerve endings during an earlier episode of chicken pox, travelled to the dorsal root ganglia, and remained in a latent form. Nerves most commonly involved are C3, T5, L1, L2 and first division of trigeminal nerve. The condition is characterized by occurrence of multiple, painful, unilateral vesicles and ulceration which shows a typical single dermatome involvement. The infection usually affects elderly individuals, and if present in the younger age group, immunecompromised status such as HIV/AIDS may be suspected. In this case report we present a patient with herpes zoster involving the maxillary and mandibular divisions of the trigeminal nerve, with unilateral vesicles over the left side of lower and middle 1/3rd of face along the trigeminal nerve tract, with intraoral involvement of buccal mucosa, labial mucosa and the palate of the same side. Key Words: Herpes zoster, Shingles, Unilateral vesicular lesions, Trigeminal nerve Introduction Varicella zoster virus is a ubiquitous; DNA virus which belongs to the subfamily of human alpha herpes virus.1The association between varicella and herpes zoster was first made in 1892. It was later recognized that the pathologic changes of herpes zoster were usually limited to one dorsal root ganglion or the sensory ganglion of a cranial nerve producing pain and skin lesions along the distribution of the involved nerve. It is now well established that a herpes zoster infection (shingles) requires pre-exposure to the varicella zoster virus. The primary varicella virus infection causes an acute, generally mild infection (Chicken pox) and the virus subsequently establishes latency elsewhere within the sensory ganglia. The virus is then later reactivated to cause a herpes zoster (HZ) infection. 2 Zoster probably results most often from a failure of the immune system to contain latent virus replication. Whether
Oral & Maxillofacial Pathology Journal [ OMPJ ]

other factors such as radiation, physical trauma, medications, other infections, or stress can also trigger zoster has not been determined with certainty. Nor is it entirely clear why circulating varicella antibodies and cell-mediated immune mechanisms does not prevent recurrent overt disease, as is common 3 with most other viral illness. As Herpes zoster virus outbreak is commonly characterized by easily observed vesicular skin eruptions that follow the anatomic distribution of affected nerve or nerve branch. A few cases have even been reported without vesicular eruption, 2 making diagnosis difficult. Herpes Zoster infection of the maxillary branch of the trigeminal nerve produces vesicles on the palate, uvula and the tonsils, while in case of the involvement of the mandibular division; the vesicles appear on the anterior part of tongue, the floor of the mouth and buccal mucosa. In oro-facial herpes zoster, toothache may be the presenting symptom.4
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347 Oro-facial Herpes Zoster: A Case Report With A Detailed Review of Literature Oral manifestations of herpes zoster appear cells. Serum immunoglobulin levels, herpes when the mandibular and maxillary divisions simplex virus (HSV) antigen detection and viral culture were not done due to lack of of the trigeminal nerve are affected.5 Osseous facilities. The patient was prescribed oral and dental manifestations such as devitalized acyclovir (800 mg five times a day for 10 days), teeth, internal resorption, abnor mal with antihistaminic-anaesthetic mouth rinses d e ve l o p m e n t o f p e r m a n e n t t e e t h , and healing of lesions can be seen after 5 days spontaneous exfoliation of teeth and necrosis of the treatment. [Fig 5-8] of maxilla and mandible have been reported.6 Herpes zoster affecting the oral and maxilloThe patient showed remarkable facial region may pose a significant diagnostic improvement in the lesions and had shown no challenge and should be considered in the signs of recurrence in 3 months follow up differential diagnosis of those presenting with period. atypical odontalgia.7 Prompt management is required, especially in immune compromised individuals, to prevent complications, which 8 may cause significant morbidity.

Case Report A 53 year old male patient came to the dental hospital with the complaint of ulcerations over the left side of the face and mouth since 3 days. History revealed that the patient had fever and severe throat infection a week ago. Then he had burning sensation in the left side of the face as well as in the oral cavity. Gradually vesicles appeared 4 days back and then those vesicles ruptured to form ulcers which were very painful. All the ulcers were limited to the face and oral cavity of the left side only. Medical history was non contributory except for the fact that the patient suffered from chicken pox in the childhood. On examination multiple irregular shallow ulcerations and crusts are seen on the lips and the peri-oral skin on the left side of the face not crossing the midline. [Fig 1& 2] Intra-orally multiple shallow ulcerations, with erythematous irregular borders with tissue tags are seen on the buccal mucosa, palate and the labial mucosa unilaterally on the left side.[Fig 3& 4] No dysphagia or odynophagia was reported. T here were no other skin lesions accompanying the oro-facial lesions. Investigations included Tzanck smear, which revealed multi-nucleated giant
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Fig 1 Clinical photograph

Fig 2 Clinical photograph

Oro-facial Herpes Zoster: A Case Report With A Detailed Review of Literature

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Fig 3 Photograph showing ulcers

Fig 6 Post treatment Clinical photograph

Fig 4 Photograph showing ulcers

Fig 7 Intra oral photograph after treatment

Fig 5 Post treatment Clinical photograph Oral & Maxillofacial Pathology Journal [ OMPJ ] Vol. 4

Fig 8 Intra oral photograph after treatment No. 1 Jan - June 2013 ISSN 0976 - 1225

Oro-facial Herpes Zoster: A Case Report With A Detailed Review of Literature Discussion Varicella zoster (VZV) is a herpes virus, and, like other herpes viruses, it causes both primary and recurrent infection and remains latent in neurons present in sensory ganglia. Varicella zoster virus is responsible for two major clinical infections of humans: chicken pox (varicella) and shingles (herpes zoster). Chicken pox is a generalized primary infection that occurs the first time an individual contacts the virus. After the primary disease is heals, varicella zoster virus remains latent in the dorsal root ganglia of spinal nerves or extra medullary ganglia of cranial nerves. A child without prior contact with varicella zoster virus can develop chicken pox after contact with an individual with Herpes zoster. In 3-5 of every 1000 individuals, varicella zoster virus becomes reactivated, causing lesions of localized herpes zoster. The incidence of herpes zoster increases with age or immunosuppression.9 Herpes zoster is more commonly known as shingles, from the Latin cingulum, for girdle. This is because a common presentation of herpes zoster involves a unilateral rash that can wrap around the waist or torso like a girdle. Similarly, the name zoster is derived from classical Greek, referring to a belt-like binding (known as a zoster) used by 10 warriors to secure armour. Reactivation of VZV may occur spontaneously or when host 2,11-13 defences are compromised. Increased age, 11,12,14 physical trauma, (including dental procedures), psychological stress, 2,11,12,14 malignancy,11 radiation therapy14 and immunecompromised states including transplant recipients, steroid therapy and HIV infection15,16 are predisposing factors for VZV reactivation. Herpes zoster can affect any sensory ganglia and its cutaneous nerve.17 Most of the infections affect dermatomes of T-3 to L-3 but about 13% of the patients present with infections involving any of the three branches of the trigeminal nerve.18 Epidemiology Herpes zoster is a sporadic disease with an estimated life time incidence of 10Oral & Maxillofacial Pathology Journal [ OMPJ ]

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20%. The incidence of herpes zoster is upto 15 times higher in HIV infected patients than in uninfected patients and as many as 25% of patients with Hodgkin's lymphoma develop herpes zoster. Household transmission rates have been noted to be approximately 15%.19 The incidence of herpes zoster infection in the general population has been reported to be 5.4%.5,20 Herpes zoster infection typically occurs in individuals older than 45 years of age, with the highest incidence among persons 60-90 years old.21 Clinical Manifestations Patients with herpes zoster infections usually progress through three stages: (1) prodromal stage, (2) active stage (also called acute stage), and (3) chronic stage.17, 22 However, some patients do not develop symptoms of all stages. Some patients do not form vesicular eruptions of the active stage, but do develop pain restricted to a dermatome, and this has been termed zoster sine herpete which makes proper diagnosis 23 more difficult. The prodromal syndrome stage presents as sensations described as burning, tingling, itching, boring, prickly or knife-like occurring in the skin over the affected nerve distribution. It is believed that these sensory changes are a result of degeneration of nerve fibrils from viral infection activity. This usually precedes the rash of the active stage by a few hours to 17, 18, 22 several days. The patient may present with an odontalgia that may be the only prodromal symptom.23 The active stage is characterized by the emergence of the rash that may be accompanied by generalized malaise, headache, low grade fever, and sometimes nausea. T he rash prog resses from erythematous papules and oedema to vesicles in 12-24 hours and finally progresses to pustules within 1-7 days. The pustules begin to dry with crust formations that fall off in 1421 days, leaving erythematous macular lesions that result in hyper-pigmented or hypopigmented scarring. In severe cases, areas of epidermis and variable amounts of dermis
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350 Oro-facial Herpes Zoster: A Case Report With A Detailed Review of Literature other acute multiple lesions of the mouth, may be lost due to haemorrhagic necrosis.17, 22 which are bilateral and not preceded or Intra-oral lesions usually appear after the accompanied by pain along the course of one cutaneous rash. Pain and dysaesthesia during trigeminal nerve branch. the active stage are reported to be minimal when the rash is most active. However, there is Herpes zoster has been associated a return of pain during the crusting phase of with dental anomalies and severe scarring of the active stage but this pain subsides as the the facial skin when trigeminal herpes zoster crusts clear.17 occurs during tooth formation. Pulpal

The chronic pain syndrome stage is termed post herpetic neuralgia (PHN). PHN is defined as pain lasting beyond the period of healing of the active skin lesions. This has been described as pain lasting 1-3 months after the skin lesions have cleared but may in fact last for years and decades.17, 22 PHN pain has been described as pain consisting of three distinct components: (i) a constant, usually deep pain; (ii) a brief recurrent shooting or shocking tic-like pain; and (iii) a sharp radiating dysaesthetic sensation evoked by very light touching of the skin, termed allodynia.24 Oral Manifestations Herpes zoster involves one of the divisions of the trigeminal nerve in 18-20% of cases, but the ophthalmic branch is affected several times more frequently than are the second or third divisions. Herpes zoster of the first division can lead to blindness secondary to corneal scarring and should be managed by an ophthalmologist. Facial and intraoral lesions are characteristic of Herpes zoster involving the second and third divisions of the trigeminal nerve. The patient in our case showed involvement of all the three branches of trigeminal nerve. Vesicular eruptions with erythema was seen involving the nose, upper lip, lower lip, zygoma, malar area, temporal region and forehead, along with intraoral lesions of one of the trigeminal nerve branch. Each individual lesion of herpes zoster resembles lesions seen in herpes simplex infections. The diagnosis is based on a history of pain and the unilateral nature and segmental distribution of the lesions. When the clinical appearance is typical and the vesicles are present, oral herpes zoster can be distinguished clinically from
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necrosis and internal root resorption have also been documented with herpes zoster. In immune-compromised patients, large chronic herpes zoster lesions have been described that have led to necrosis of underlying bone and exfoliation of teeth.9 Schwartz and Kvoring reported 10 cases of herpes zoster with post herpetic complications including osteonecrosis of jaw, exfoliation of teeth, severe periodontitis and scarring of the skin.25 Wadden reported a 70 year old woman with a history of excellent oral health, who within 3 years of an attack of Shingles affecting the maxillary division of the left trigeminal nerve had multiple devitalization of four of the five teeth in the left maxillary quadrant suggesting a central source of injury 26 rather than a local cause. Complications (A) Acute complications- Cutaneous 27 varicella zoster dissemination , Bacterial superinfection, Zoster gangrenosum, Zoster haemorrhagicus, Septicemia,Meningoencephalitis, Aseptic meningitis, Cranial and Peripheral nerve palsies, Conjunctivitis, Episcleritis, Uveitis, Keratitis, Secondary glaucoma, Acute renal necrosis, Loss of corneal sensations, Optic neuropathy, Ptosis, Mydriasis, Neural Bronchitis, Pleuritis, Esophagitis, Gastritis/enterocolitis, Peritonitis, Pericarditis, Pneumonia, Hepatitis, Myocarditis, Arthritis (B) Chronic complications- Scar formation (atrophic scars, hypertrophic scars), Hypo/depigmentation, Post herpetic neuralgia (PHN), Guillain-Barre syndrome, Autonomic dysfunction, Granulomatous cerebral angiitis, Diaphragmatic paralysis, Bladder dysfunction, Sensory loss/deafness, Chorio-retinitis, Atrophy of optic nerve,
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351 Oro-facial Herpes Zoster: A Case Report With A Detailed Review of Literature Progressive outer retinal necrosis. cholelithiasis, or colitis, depending on its intensity and the location of the affected Development of herpes zoster at nerve.35 Common differential diagnoses at this cranial region has special importance. stage include pleurisy, cardiac disease, Involvement of cranial nerves has high herniated nucleus pulposus, trigeminal complication risk. The Trigeminal has three neuralgia, and Bell's palsy.19, 35 An appropriate branches; ophthalmic, maxillary, mandibular. diagnosis of HZ is aided by the appearance of In ophthalmic zoster the eye is affected in a vesicular rash with characteristic two-thirds of cases, especially when vesicles distribution. When the presentation of skin on the side of the nose indicate involvement lesions is not as clear, as may be the case with of the nasociliary nerve (Hutchinson's sign).28 immunocompromised patients, laboratory Hutchinson's sign is a powerful predictor of confir mation is recommended. The ocular inflammation and corneal denervation. polymerase chain reaction (PCR) technique is Involvement of the ciliary ganglia may give the most sensitive and specific diagnostic test, 28; 29 rise to Argyll-Robertson pupil. The facial as it can detect VZV DNA in fluid from the nerve (seventh cranial nerve) is then involved. vesicle. Availability of the PCR technique, When just the external ear is affected, it is 36 however, may pose a challenge. Viral culture 30, 31 named as herpes zoster oticus. Pressure on is possible but typically has low sensitivity. the facial nerve motor fibres may evolve into VZV is labile, resulting in difficult recovery of facial palsy. The Vestibulocochlear nerve and an adequate sample from vesicular fluid. Use the Facial nerve involvement complete the of direct immunofluorescence assay is a good classical triad of the Ramsay Hunt syndrome; alternative to PCR. It is preferred over viral herpes zoster of external ear or tympanic culture, as it is more sensitive, of lower cost, membrane, ipsilateral facial paralysis and and offers a more rapid turnaround time. In 32, 33 auditory symptoms. Compression of the the present case, Tzanck smear showed the vestibulocochlear nerve may cause auditory presence of multi-nucleated giant cells. symptoms which are sensorineural hearing Prevention And Treatment loss, tinnitus, dizziness and vertigo. Involvement of the nervus intermedius or its The varicella zoster virus Oka strain geniculate ganglion would impair taste vaccine is currently recommended by the sensation from the anterior two-thirds of the Advisory Committee on Immunization tongue and alter lacrimation. 29, 34 Herpes Practices for universal childhood vaccination zoster oticus accounts for about 10% of cases in USA. The vaccine increases cytotoxic of facial palsy. The paralysis is usually lymphocyte responses specific for varicella complete and full recovery occurs in only zoster vir us in seropositive elderly 37 about 20% of untreated cases. There is people. Early diagnosis and prompt permanent hearing loss in about one-third of treatment of the disease in the prodromal these patients. phase by the use of anti-viral agents should

Diagnosis Initial diagnosis poses a challenge during the prodromal stage of the disease, which typically lasts 1-2 days but can persist up to three weeks before the appearance of skin lesions.19 Furthermore, some individuals may only present with prodromal symptoms, never developing the telltale rash. This phenomenon is known as zoster sine herpete. Pain can be misdiagnosed as appendicitis, myocardial infarct, renal colic,
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probably be the mainstay of its management. The treatment of herpes zoster has three main objectives: (1) treatment of the acute viral infection, (2) treatment of the acute pain associated with herpes zoster and (3) prevention of post herpetic neuralgia. Antiviral agents have been shown to decrease the duration of herpes zoster rash and the severity of pain associated with the rash. However these benefits have only demonstrated in patients who received antiviral agents within
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352 Oro-facial Herpes Zoster: A Case Report With A Detailed Review of Literature 19 weeks until response is adequate, or 72 hours after the onset of the rash. The to maximum dosage of 150 mg per day recommended dosages of anti-viral agents (d) Desipramine 25 mg orally at bedtime; used in the management of herpes zoster increase dosage by 25 mg every 2-4 infection are:weeks until response is adequate, or 1. Acyclovir: 800 mg orally five times daily to maximum dosage of 150 mg per day for 7-10 days, or 10 mg per kg IV every 8 h (3) Anti convulsants for 7-10 days (a) Phenytoin 100-300 mg orally at 2. Famciclovir: 500 mg orally three times bedtime; increase dosage until response is daily for 7 days adequate, or blood drug level is 10-20 mg/ml 3. Valacyclovir: 1 g orally three times daily (b) Carbamazepine 100 mg orally at for 7 days bedtime; increase dosage by 100 mg every 3 4. Brivudin 125 mg once daily for 7 days days until dosage is 200 mg three times daily, Some newer molecules which are under or till response is adequate or blood drug level development and are found to be highly is 6-12 mg/ml potent are still on clinical trials and yet to be 38, 39 (c) Gabapentin 100-300 mg orally at approved bedtime; increase dosage by 100-300 mg every Newer medications for herpes zoster. 3 days until dosage is 300-900 mg three times 1. CMX 001 Hexadecyloxypropyl-cidofovir daily or response is adequate. 2. Valamaciclovir Nucleoside analogue The use of systemic corticosteroids to (H2G) prevent post herpetic neuralgia in patients 3. ASP2151 Helicase primase inhibitor over 50 years of age is controversial. Recent 4. FV100 Two bicyclic nucleoside review of the data indicated a reduction of analogues (BCNA) pain and disability during the first two weeks Although PHN is generally a self limiting but no effect on the incidence or severity of condition, it can last indefinitely. Treatment is PNH. Some clinicians advocate the use of a directed at pain control while waiting for the combination of intra-lesional steroids and condition to resolve. local anaesthetics to decrease healing time and prevent PNH, but a controlled study of this Treatment options for post herpetic 9 therapy has not been performed. neuralgia. (1) Topical agents Conclusion (a) Capsaicin cream: Application to the Herpes zoster infection may be affected area 3-5 times daily infrequently encountered in general dental (b) Lidocaine (xylocaine) patch: practice, however many patients do report to Application to the affected area every the dental clinic with the complications of 4-12 hours or as needed HZV infection, involving the trigeminal nerve (2) Tri-cyclic anti-depressants in about 15% cases. Diagnosing these (a) Amitriptyline 25 mg orally at complications of herpes zoster could pose a bedtime; increase dosage by 25 mg challenge to an oral physician due to their every 2-4 weeks until response is varied presentation ranging from post adequate, or to maximum dosage of herpetic neuralgia, external root resorption, 150 mg per day osteonecrosis and tooth exfoliation. (b) Nortriptyline 25 mg orally at Especially the elderly and the immune bedtime; increase dosage by 25 mg compromised patients are susceptible and every 2-4 weeks until response is hence burning sensation, pain, vesiculation, adequate, or to maximum dosage of ulceration along the course of the Trigeminal 125 mg per day nerve should be treated with HZV infection in (c) Impramine 25 mg orally at bedtime; mind. increase dosage by 25 mg every 2-4

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353 Oro-facial Herpes Zoster: A Case Report With A Detailed Review of Literature References 13. Sato T, Inoue T, Endo K, Watanabe Y, Kikuta T, Tsuda M. End-stage renal disease (ESRD) 1. Abendroth A, Arvin AM, Moffat JF. contributes to the increasing prevalence of herpes Varicella-zoster virus.1st ed. Berlin: Springer; zoster. NDT Plus. 2009;2:263-264. 2010. pp. 44-45 14. Owotude FJ, Ugboko VL, Kolude B. Herpes 2. Sigurdsson A, Jacoway JR. Herpes zoster zoster infection of the maxilla: case report. J infection presenting as an acute pulpitis. Oral Oral Maxillofac Surg. 1999;57: 1249-1251. Surg Oral Med Oral Pathol Oral Radiol 15. Buchbinder SP, Katz MH, Hessol NA, et al. Endodontics. 1995;80:92-95. Herpes zoster and human immunodeficiency 3. Edgerton G. Herpes zoster ophthalmicus: a virus infection. J Infect Dis. 1992;166:1153review of the literature. Arch Ophthalmol. 1156. 1945;34:40-62. pp. 114-153. 16. Miller GG, Dummer JS. Herpes simplex and 4. Nagington J, Rook A, Highet AS. Virus and varicella zoster viruses: forgotten but not gone. related infections. In: Rook A, Wilkinson DS, Am J Transplant. 2007;7: 741-747. Ebling FJG, Champion RH, Burton JL, 17. Strommen GL, Pucino F, Tight RR, Beck CL. editors. Textbook of Dermatology. 4th ed. Human infection with herpes zoster: etiology, Oxford: Blackwell Scientific Publications; pathophysiology, diagnosis, clinical course and 1986. p. 657-723. treatment. Pharmacotherapy. 1988;8: 52-68. 5. Mendieta C, Miranda J, Brunet LI, Gargallo J, 18. Millar EP, Troulis MJ. Herpes zoster of the Berini L. Alveolar bone necrosis and tooth trigeminal nerve: the dentist's role in diagnosis exfoliation following herpes zoster infection: a and treatment. J Can Dent Assoc. review of the literature and case report. J 1994;60:450-453. Periodontol. 2005;76:148-153. 19. Stankus S, Dlugopolski M, Packer D. 6. Volvoikar P, Patil S, Dinaker A. Tooth Management of herpes zoster (shingles) and exfoliation, osteonecrosis and neuralgia postherpetic neuralgia. Am Fam Physician. following herpes zoster of trigeminal nerve. 2000;61(8):2437-2444. Indian J Dent Res. 2002;13:11-14. 20. Hope-Simpson RE. The nature of herpes 7. Tidwell E, Hutson B, Burkhart N, Gutmann zoster. A long term study and new hypothesis. JL, Ellis CD. Herpes zoster of the trigeminal Proc R Soc Med. 1965;58:9-20. nerve third branch: a case report and review of 21. Eversole LR. Viral infections of head and neck the literature. Int Endod J. 1999;32:61-66. among HIVseropositive patients. Oral Surg 8. Mustafa MB, Arduino PG, Porter SR. Oral Med Oral Path. 1992;73:155-163. Varicella zoster virus: review of its 22. Carmichael JK. Treatment of herpes zoster and management. J Oral Pathol Med. post herpetic neuralgia. Am Fam Pract. 2009;38:673-688. 1991;44:203-210. 9. Greenberg Martin S, Glick Micheal. Burket's 23. Barratt AP, Katelaris CH, Morris JG, oral medicine diagnosis and treatment. 10th ed.; Schifter M. Zoster sine herpete of the trigeminal 2003. pp. 55-57. nerve. Oral Surg Oral Med Oral Path Oral 10. Mario Roxas ND. Herpes zoster and Radiol Endodon. 1993;75:173-175. postherpetic neuralgia: diagnosis and therapeutic 24. Rowbotham MC, Fields HL. Post herpetic c o n s i d e r a t i o n s . A l t e r n M e d R e v. neuralgia: the relation of pain complaint, 2006;11(2):102-113. sensory disturbance, and skin temperature. 11. Schmader KE, Dworkin RH. Natural history Pain. 1989;39:129-144. and treatment of herpes zoster. J Pain. 25. Schwartz O, Kvorning S. Tooth exfoliation, 2008;9:S3-S9. osteonecrosis of the jaw and neuralgia following 12. Thomas SL, Hall AJ. What does epidemiology herpes zoster of the trigeminal nerve. Int J Oral tell us about risk factors for herpes zoster? Surg. 1982;11(6):364-371. Lancet Infect Dis. 2004;4: 26-33.

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354 Oro-facial Herpes Zoster: A Case Report With A Detailed Review of Literature 26. Wadden J. Extensive endodontic involvements 33. Kim JH, Chung PW, Oh S, et al. Ramsay hunt following herpes zoster attack to facial area; syndrome complicated by a brainstem lesion. J report of a case. NW Dent. 1991;70(2):31. Clin Virol. 2007;39: 322-325. 27. Kutlubay Zekayi, Gksgr Nadir, Engin 34. Gnann JW Jr. Varicella zoster virus: atypical Burhan, Tzn Yaln. Complications of presentations and unusual complications. J herpes zoster. J Turk Acad Dermatol. Infect Dis. 2002;186:S91-S98. 2011;5(2):1-7. 35. Berkow R, Fletcher AJ, editors. Herpes zoster. 28. Womack LW, Liesegang TJ. Complications of The Merck manual. 16th ed. Rahway, NJ: herpes zoster ophthalmicus. Arch Ophthalmol. Merck Research Laboratories; 1992. p. 203. 1983;101:42-45. 36. Mounsey AL, Matthew LG, Slawson DC. 29. Atherton DJ, Gennery AR, Cant AJ. Herpes zoster and postherpetic neuralgia: Varicella-zoster virus. In: Burns T, Breathnach prevention and management. Am Fam S, Cox N, Griffiths C, editors. Rook's Physician. 2005;72:1075-1080. textbook of dermatology. 8th ed., vol. 33. 37. Brisson M, Edmunds W, Gay N, Law B, De Blackwell: Oxford;2010. p. 22-28. Serres G. Analysis of varicella vaccine 30. James WD, Berger TG, Elston DM. Zoster breakthrough rates: implications for the (Shingles, herpes zoster). Andrews' diseases of effectiveness of immunization programmes. the skin. Clinical dermatolog y. In: Vaccine. 2000;18(25):2775-2778. Philadelphia, editor. 10th ed. Saunders 38. Bowler D. The management of postherpetic Elsevier; 2006. p.379-384. neuralgia. Post Grad Med J. 31. Choo PW, Donahue JG, Manson JE, Platt R. 1997;73(864):623. The epidemiology of varicella and its 39. Basi-Kes V, Demarin V. Post herpetic complications. J InfectDis. 1995;172:706neuralgia. Acta Clin Croat. 2007;46(3):279712. 282. 32. Madkan V, Sra K, Brantlay J, Carrasco D, Mendoza N, Tyring SK. Varicella-zoster virus Source of Support - Nil (HHV-3). In: Bolognia JL,Jorizzo JL, Conflict of Interest - None declared Rapini RP, editors. Dermatology. 2nd ed. Philadelphia:Mosby; 2008. p. 1204-1208.

How to cite this article: Vineet DA, Mithra R, Baskaran Pavitra, Mishra Satyaranjan, Oro-facial herpes zoster: a case report with a detailed review of literature: Oral Max Path J, 4(1), Jan-Jun 2013: 346-354

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No. 1 Jan - June 2013 ISSN 0976 - 1225