Herpes zoster.pptx

Herpes zoster is a localised disease caused by reactivation of the varicella zoster virus that enters the cutaneous nerve endings during an earlier episode of chicken pox, travels to the dorsal root ganglia, and remains in latent form. The condition is characterised by occurrence of multiple, painful, unilateral vesicles and ulceration, and shows a typical single dermatome innervated by single dorsal root or cranial sensory ganglion.

1. HERPES ZOSTER Presented by Dr. Rahul Srivastava Professor Rama Dental College Hospital & Research Centre Kanpur

2. HERPES ZOSTER (HZ) HZ is also known as shingles, which is derived from the Latin  cingulum , meaning ‘girdle’. This is because a common presentation of HZ involves a unilateral rash that can wrap around the waist or torso like a girdle.

3. The name zoster is derived from classical Greek, referring to a belt-like binding (known as a zoster) used by warriors to secure armour . Von Bokayin , in 1988, hypothesised for the first time that chicken pox and HZ were caused by the same infectious agent.

4. Varicella is commonly known as chickenpox; it occurs in children while herpes zoster occurs in adults or the elderly. After the primary disease is healed,VZV becomes latent in the dorsal root ganglia of spinal nerves or extramedullary ganglia of cranial nerves.

5. A child without prior contact with VZV can develop chickenpox after contact with an individual with HZ. The incidence of HZ is up to 15 times higher in HIV-infected patients and it is found in 25% of patients with Hodgkin’s lymphoma.

6. Etiology Upon reactivation, the virus replicates in neuronal cell bodies and virions  shed from the cells which are carried down the nerve to the area of skin innervated by that ganglion.

7. In the skin, the virus causes local inflammation and blistering. The pain caused by zoster is due to inflammation of affected nerves with the virus. Triggers for herpes zoster include Emotional stress. Use of medications ( immunosuppressants ). Acute or chronic illness. Exposure to the virus. Presence of a malignancy.

8. PHASES OF INFECTION The three phases of the infection include: Preeruptive stage presents with abnormal skin sensations or pain within the dermatome affected. This phase appears at least 48 hours prior to any obvious lesions. At the same time, the individual may experience headaches, general malaise, and photophobia.

9. The acute eruptive phase is marked by the vesicles and the symptoms seen in the pre-eruptive phase. The lesions initially start as macules and quickly transform into painful vesicles. The vesicles often rupture, ulcerate and eventually crust over. Patients are most infectious in this stage until the lesion dry out.

10. Pain is severe during this phase and often unresponsive to traditional pain medications. The phase may last 2-4 weeks but the pain may continue.

11. Chronic infection is characterized by recurrent pain that lasts more than 4 weeks. Besides the pain, patients experience paresthesias , shock-like sensations, and dysesthesias . The pain is disabling and may last 12 months or longer.

12. Clinical Features The infection tends to involve individuals above 45 years of age, with the highest incidence among persons aged between 68 and 90 years. Among the divisions of the trigeminal nerve, the ophthalmic division is most commonly involved followed by the maxillary and mandibular divisions.

13. Involvement of the trigeminal nerve leads to lesions on the upper eyelid, forehead and scalp with V1, midface and upper lip with V2 and lower lip with V3. With the involvement of V2, patients experience a prodrome of pain, burning and tenderness, usually on the palate on one side.

14. Zoster characteristically presents with a prodrome of fever, malaise and excruciating burning pain followed by the outbreak of vesicles that appear in one to three crops over three to five days. Lesions are distributed unilaterally within a single dermatome.

15. Clinically, lesions start as closely grouped erythematous papules which, rapidly become vesicles on an erythematous and edematous base. It may occur in continuous or interrupted bands in one, two or more contiguous dermatomes unilaterally.

16. Facial and intraoral lesions occur unilaterally and are characteristic features of HZ. The lesions usually begin to dry and crustations appear after 3–5 days.

17. Total duration of the disease is generally between 7 and 10 days; however, it may take several weeks for the hypopigmented skin to return to normal. Dental complications: Osteonecrosis . Exfoliation of teeth. Periodontitis . Calcified and devitalized pulps. Periapical lesions and resorption of roots.

18. Developmental anomalies: Irregular short roots. Missing teeth.

19. Secondary bacterial infection is another common complication of HZ. Other complications such as scarring of skin, keratitis , retinal necrosis causing blindness, keratouveitis , cranial and peripheral nerve palsies, cerebral ataxia and pneumonia may lead to death.

20. Zoster sine herpete (ZSH) Zoster sine herpete (ZSH) refers to a condition in which dermatomal distribution pain occurs in the absence of an antecedent rash. First defined by Lewis, who described zoster patients with dermatomal distribution pain in areas outside that affected by zoster rash, ZSH later became a distinct disease entity when PCR provided definitive virologic confirmation. 

21. James Ramsay Hunt syndrome A special form of zoster infection of the geniculate ganglion, with the involvement of the external ear and oral mucosa, has been termed Hunt's syndrome first described in 1907 by James Ramsay−Hunt.

22. It manifests as facial paralysis as well as pain in the external auditory meatus and pinna of the ear. In addition, vesicular eruptions occur in the oral cavity and oropharynx with hoarseness, tinnitus, vertigo and occasional other disturbances.

23. When the glossopharyngeal ganglion is damaged, lesions are seen on the posterior one third of the tongue, uvula and posterior mouth along with pharyngeal pain. It can also involve the vagus nerve, which is the tenth cranial nerve leading to paralysis of the pharynx, larynx and blisters on the base of the tongue.

24. Postherpetic Neuralgia Postherpetic neuralgia (PHN) is a frequent complication of HZ characterized by intense pain. While the usual HZ pain lasts 2 to 4 weeks, PHN is defined as pain persistent after 4 or 9 weeks. Gabapentin and lidocaine patch 5% is the first line for PHN and opoid analgesics and tricyclic depressants the second line of treatments.

25. Prednisolone (administered at a dosage of 60 mg /day for first week of zoster, tapered over 21 days and given with antiviral therapy) can accelerate quality of life improvements, including return to usual activity.

26. The recommended dosages of commonly used tricyclic depressants are listed below Amitriptyline 0–25 mg orally at bedtime; increase dosage by 25 mg every 2–4 weeks until response is adequate, or to a maximum dosage of 150 mg/day Nortriptyline 0–25 mg orally at bedtime; increase dosage by 25 mg every 2–4 weeks until response is adequate, or to a maximum dosage of 125 mg/day Imipramine 25 mg orally at bedtime; increase dosage by 25 mg every 2–4 weeks until response is adequate, or to a maximum dosage of 150 mg/day Desipramine 25 mg orally at bedtime; increase dosage by 25 mg every 2–4 weeks until response is adequate

27. Diagnosis Herpes zoster is clinically diagnosed with burning pain, characteristic morphology, and typical distribution. Herpes simplex virus can occasionally produce a rash in a pattern called as zosteriform herpes simplex.

28. Tests for varicella -zoster virus  The Tzanck smear of vesicular fluid shows multinucleated giant cells. It has lower sensitivity and specificity than direct fluorescent antibody (DFA) or Polymerase chain reaction (PCR). Varicella -zoster virus-specific IgM antibody in blood is detected during the active infection of chickenpox or shingles but not  when the virus is dormant.

29. Direct fluorescent antibody testing of vesicular fluid or corneal fluid can be done when there is eye involvement. PCR testing of vesicular fluid, a corneal lesion, or blood in a case with eye involvement or disseminated infection.

30. Molecular biology tests based on in vitro nucleic acid amplification (PCR tests) are currently considered the most reliable. Nested PCR test has high sensitivity, but is susceptible to contamination leading to false-positive results. The latest real-time PCR tests are rapid, easy to perform, as sensitive as nested PCR, have a lower risk of contamination, and also have more sensitivity than viral cultures.

31. TREATMENT

32. Conventional treatment options The objective of conventional therapy in the treatment of HZ is to accelerate healing of the lesions, reduce the accompanying pain and prevent complications.

33. Topical Capsaicin Capsaicin is an alkaloid derived from cayenne pepper (Capsicum frutescens ). A well-studied compound, capsaicin is of particular importance in the treatment of PHN because of its effect on C- fibre sensory neurons.

34. These neurons release inflammatory neuropeptides such as substance P that mediate neurogenic inflammation and chemical-initiated pain. It should not be applied until skin lesions have healed. Capsaicin 0.075% cream- Apply 4 times per day. Capsaicin 8% patch- Application time of 30–90 minutes.

35. Topical lidocaine Lidocaine 5% patch - One patch can be applied to the location of pain. Up to 3 patches can be used at the same time for a maximum of 12 hours.

36. Antiviral agents  Drug Dosage Remarks Acyclovir Adults: 5 × 800 mg/day p.o . Limited bioavailability 3 × 500 mg/day i.v . In uncomplicated HZ 3–5 × 10 mg/kg/day for 10 day, usually 5–7 days In severe HZ, in case of immunosuppression Children: 3 × 10 mg/kg/day Brivudin Adults: 125 mg once a day p.o . For 5 days. Valaciclovir Adults: 3 × 1000 mg/day p.o . For 7 days Famciclovir Adults: 3 × 250–500 mg/day 2nd line in ACV-resistant patients

37. Corticosteroids Oral corticosteroids have commonly been used for pain management in HZ, although clinical trials have yielded inconsistent results for reducing development of PHN.  Oral prednisone and prednisolone , starting dose from 35 to 60 mg/day, generally tapering over 3 to 4 weeks.

38. Corticosteroids Oral corticosteroids have commonly been used for pain management in HZ, although clinical trials have yielded inconsistent results for reducing development of PHN.  Oral prednisone and prednisolone , starting dose from 35 to 60 mg/day, generally tapering over 3 to 4 weeks.

39. Pain control In patients with severe pain, use of narcotics may be indicated. Use of nerve block injections is another option in the conventional medical model. Local anaesthetic may be injected around the affected nerves, providing pain relief typically lasting 12–24 h.

40. Transcutaneous electrical nerve stimulation Use of transcutaneous electrical nerve stimulation (TENS) therapy has been beneficial in the management of PHN.  Vaccination Centers of Disease Control & Prevention (CDC) recommends two doses of chickenpox vaccine for children, adolescents, and adults who have never had chickenpox and were never vaccinated.

41. Children are routinely recommended to receive the first dose at 12 through 15 months of age and the second dose at 4 through 6 years of age. CDC recommends a single dose of Zostavax ® (zoster vaccine live) for people 60 years old or older, whether or not the person reported a prior episode of herpes zoster (shingles). 

42. References 1- Mohan RPS, Verma S, Singh U, et al. BMJ Case Rep Published online:doi:10.1136/ bcr-2013-010246 2- Patil A, Goldust M, Wollina U. Herpes zoster: A Review of Clinical Manifestations and Management. Viruses. 2022 19;14(2):192. doi : 10.3390/v14020192.

43. 3- Nair P, Gharote H, Singh P, Jain- Choudhary P. Herpes zoster on the face in the elderly. BMJ Case Rep. 2014 Oct 19;2014:bcr2013200101. doi : 10.1136/bcr-2013-200101. 4- Cohen KR, Salbu RL, Frank J, Israel I. Presentation and management of herpes zoster (shingles) in the geriatric population. P T. 2013;38(4):217-27.

44. 5- Tsai YC, Lee YP, Hwang MJ, Chiang CP. Oral herpes zoster - Case report. J Dent Sci. 2021;16(1):563-564. doi : 10.1016/j.jds.2020.10.001. 6- Peter G.E. Kennedy Neurology 2011, 76 (5) 416-417; DOI: 10.1212/WNL.0b013e31820a0d5d 7- John AR, Canaday DH. Herpes Zoster in the Older Adult. Infect Dis Clin North Am. 2017 Dec;31(4):811-826. doi : 10.1016/j.idc.2017.07.016.

45. 8- Cohen JI. Clinical practice: Herpes zoster. N Engl J Med. 2013;369(3):255–263. 9- Kawai K, Gebremeskel BG, Acosta CJ. Systematic review of incidence and complications of herpes zoster: towards a global perspective. BMJ Open. 2014;4(6):e004833.