VIRAL INFECTIONS-IN DERMATOLOGY MD .pptx

DERMATOLOGY

1. 1 Viral infections Part 1 PRESENTED BY DR. SNEHAL KAMBLE (JUNIOR RESIDENT-1)

2. STRUCTURE Viruses are acellular organisms with genome composed of either RNA or DNA, single- or double-stranded. Viral nucleic acid is packaged in a protein coat or capsid. The combination of viral nucleic acid and surrounding protein capsid is called the nucleocapsid.

3. The capsid is composed of repeating series of structurally similar subunits, each of which in turn is composed of only a few different proteins. Viruses depend on host to multiply and replicate only inside host cell. Because of this complete dependance on host viruses are called as obligatory intracellular parasites.

4. Pathogenesis of viral disease Virus enters the host through inhalation, ingestion or contact Attaches to the cell surface through a receptor and then enters cell by endo or Phagocytosis Host cell enzymes dissolve the capsid releasing nucleic acid Host cell ribosomes translate nucleic acid into viral proteins The multiplied viral proteins cause cell damage, get released and then affect other cells

5. The next stage depends on the nature of the virus. In relatively simple ones, like enteroviruses, the RNA acts as a messenger, is infectious on its own and is immediately translatable by host ribosomes into viral proteins. More complex RNA viruses, such as influenza, have non‐infectious RNA, called negative‐strand RNA, which has to be transcribed into messenger RNA (mRNA) by a polymerase enzyme carried in the virus itself. Eg Hepatitis D Virion consists of a length of nucleic acid, either RNA or DNA, within a protein shell, the capsid.

6. The time required for new virus production in acute infections is measured in hours and the number of new virions in thousands per cell. Newly produced virions can invade adjacent cells or be carried via the bloodstream and so the infection spreads. During this process the cell itself may be destroyed by a lytic infection (e.g. enterovirus and herpes simplex) or damaged transiently (e.g. myxovirus ) With time, an immune response develops against the virus particles and processed viral proteins, which can lead to containment and clearance of the infection.

7. Some viruses infect cells that apparently remain normal and may multiply while virus replication continues within, that is persistent infection . When persistently infected cells produce no infectious virus because the replication cycle is arrested, the virus is said to be latent . From time to time, a latent virus can become active ( reactivation ), new virions are produced and other cells are infected.

8. HERPES VIRUS INFECTIONS The herpes virus group consists of relatively large, enveloped DNA viruses. More than 80 herpes viruses are known infect animals and eight of them infect humans.

9. CLASSIFICATION Classified on basis of genome similarities as- Alpha viruses - Herpes simplex virus types 1 and 2 - Varicella zoster virus (HHV 3) Beta viruses - Cytomegalo virus (HHV 5) - Roseola virus (HHV-6 and HHV-7) Gamma viruses - - Epstein–Barr virus (HHV 4) - Human herpes virus-6 (human B cell lymphotrophic virus ) - Human herpes virus-7 ( Rk virus) - Human herpes virus-8 ( kaposi sarcoma associated herpes virus)

10. Herpes simplex virus infections Herpes simplex viruses are of two types, herpes simplex virus type 1 (HSV-1) and herpes simplex virus type 2 (HSV-2). Herpetic gingivostomatitis Herpes labialis Herpes genitalis Eczema herpeticum Ocular herpes Herpetic whitlow Herpes gladiatorum Neonatal herpes

11. Epidemiology Some studies reported increased frequency of HSV-1 with genital infections, probably due to orogenital contact. Increased incidence of both HSV-1 and HSV-2 infections are noted in immunocompromised.

12. Pathology Virus invade the epithelial cells and replicate intracellularly at the primary site Travel through the periaxonal sheath of sensory nerves in a retrograde manner to the regional ganglia Persists there dormant for life They get reactivated periodically, travel down the sensory nerves to the innervated mucocutaneous sites and replicate Manifest clinical lesions

13. Herpetic Gingivostomatitis Most common clinical manifestation of HSV type 1 primary infection. Most cases occur in children between 1 and 5 years of age, mostly subclinical. After an incubation period of 2–5 days, multiple transient vesicles may appear over tongue, pharynx, buccal mucosa, and rupture in 1–2 days, causing painful superficial ulcers with a yellowish pseudomembrane

14. Preceded or accompanied by pain, burning, and paresthesias at the inoculation site Stages- prodromal , erythema , and papule, vesicle, ulcer, and hard crust (disease stage); followed by dry flaking and residual swelling (resolution stage). Associated with fever, malaise, myalgias , dysphagia , headache, anorexia, excessive dribbling of saliva, cervical and occipital lymphadenopathy

15. Herpes Simplex Labialis Herpes simplex labialis , aka fever blisters or cold sores. Most have two or lesser episodes a year, but 5%–10% have more than six attacks a year.

16. Affects vermilion border of lip with burning, pain, pruritis . Small grouped vesicles appear, rupture, and form superficial erosions, get crusted and subside in a few days, without scarring. Recurrences occur in the same region but not the same site.

17. Herpes Genitalis HSV-2 >> HSV-1 Prodrome of tingling, burning, pain, and itching and associated with fever, headache, malaise, and lymphadenopathy. Vesicles rupture gradually forming superficial ulcers, crust and subside without scar in 2–4 weeks. Recurrent infections are milder, localized and shorter with less intense viral shedding. Asymptomatic viral shedding continues to occur after clinical lesions disappear.

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19. Eczema Herpeticum Cutaneous eruption, caused by HSV, in a patient with preexisting disease ( eg Atopic dermatitis) Other eg.Burns , contact dermatitis, Darier’s disease, pemphigus foliaceous , Hailey–Hailey disease, ichthyosis vulgaris , psoriasis, drug eruption, and cosmetic procedures like dermabrasion and laser therapy.

20. Predisposing factors are high IgE levels, early onset of atopic dermatitis, low cathelicidin-LL37,low NK cell count. Widespread vesicles erupt in crops and rapidly become pustular . Confined to abnormal skin or disseminated. Severe constitutional symptoms such as fever, malaise, headache, pain, and irritability may occur. Fever subsides in 4–5 days and pustules may crust and heal with minimal scarring and may take upto 1 month.

21. Herpetic Whitlow Cutaneous herpetic infection of the distal pulp of the fingers. Health-care workers, children with primary oral herpes, and adults with genital HSV infection. Painful vesicular eruption associated with edema and erythema .

22. Herpes Gladiatorum Wrestler’s herpes, caused by the inoculation of HSV-1 through abraded skin of atheletes of contact sports like wrestling, rugby, and soccer. vesicular eruption over face, ears, neck, and arms.

23. Neonatal Herpes Vertical transmission of HSV during vaginal delivery. Manifest within first 4 weeks of life, mostly in first week Three patterns, SEM (skin, eye, and mouth disease),CNS disease and disseminated infection. Multiple vesicles, erosions and ulcers, especially at places of trauma occur.

24. Mortality of untreated neonatal herpes is---- 60–80% when treated mortality can be-- 25–30% Management Of Neonatal Herpes If active primary herpes infection present at the time of delivery c-section is indicated and prophylactic acyclovir should be considered for the neonate. Treatment of neonatal herpes---iv Acyclovir (60 mg/kg/day in three divided doses for 2–3 weeks) followed by oral acyclovir for 6 months

25. Diagnosis Cytologic smears from the base of vesicle( Tzanck smear) show multinucleated keratinocytes , molding of nuclear borders, and nuclear inclusions.

26. The virus can be grown in culture from the vesicular fluid in 24–48 hours and is the gold standard. Negative culture doesn’t rule out disease. Skin biopsy- Ballooning degenration , intra epidermal bulla, multinucleated giant cells. IgM Antibodies Polymerase chain reaction is diagnostic method of choice in encephalitis and aseptic meningitis

27. Management First Line Topical- Anesthesic mouthwash, topical agents like Acyclovir 5% , Penciclovir 1%, Cidofovir 1%, Docosanol 10%. Oral- Acyclovir 200 mg five times daily for 5 or more days But 800 mg BD has been used with success. In children, the oral suspension given at 15 mg/kg five times per day for 7 days . Valacyclovir , 1000 mg twice daily for 10 days, is of similar efficacy to acyclovir.

28. Second Line Acyclovir systemically is the treatment of choice for severe or potentially severe primary herpes simplex infection Dose is 5 mg/kg 8‐hourly IV, though twice that dose has been used for neonatal herpes and encephalitis. As the drug is excreted via the kidneys, the dose must be scaled down in renal failure. Transient rises in blood urea and creatinine may occur with bolus injections; slow infusion over 1 h in an adequately hydrated patient is recommended. Penciclovir , Phosphonoformate ( foscarnet ), Cidofovir iv, Imiquimod topical.

29. Management to suppress Recurrent Herpes Infections > 6 episodes per year Long term acyclovir prophylaxis needed 200-400 mg Acyclovir BD for six months Also therapeutic circumcision reduces genital herpes recurrence

30. Newer Treatment Modalities: Helicase Primase inhibitors- HSV-1 as well as HSV-2 ( Amenamevir , pritelivir ) Intravaginal Needle Free Mucosal Vaccine- HSV-2 Viva gel containing SPL7013- safe in Animal and Human studies.

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32. Varicella {chicken pox} Varicella is a febrile illness characterized by a generalized, pruritic vesicular rash and is most prevalent in childhood. VZV i.e HHV-3 is cause of both chicken pox ( varicella ) and zoster (shingles ) It is endemic in temperate climates, winter and spring season. Highly contagious. Its mean incubation period ranges of 10 to 23 days. A typical patient is infectious for 2 days before the exanthem appears and 5 days thereafter.

33. Age >50% primary infection before 5 years & 85% before puberty. Following an initial period of replication in the oro ‐pharynx, a viraemia causes widespread dissemination. In the skin, in varicella, cells of the Malpighian layer show ballooning of their cytoplasm by intracellular oedema Distinctive nuclear changes, comprising eosinophilic inclusions and marginated chromatin.

34. The multinucleate giant cells with up to 15 nuclei are produced mainly by cell fusion. Intracellular oedema combined with intercellular oedema forms the vesicle, the roof of which consists of the upper Malpighian and horny layers. IgG , IgM and IgA antibodies appear 2–5 days after the onset of the rash, and their levels peak during the second and third weeks.

35. Clinical features After a day or two of fever and malaise, a scarlatiniform or morbilliform erythema is followed by the development of papules which very rapidly become tense, clear, unilocular vesicles in 2-4 days. Within a few hours, the contents become turbid and the pustules are surrounded by red areolae. It then dries beginning in the center , first producing an umbilicated pustule and then a crust. Crusts fall off spontaneously in 1 to 3 weeks. A characteristic feature is the presence of lesions at different stages in each site. (Polymorphic lesions)

36. Complication of Varicella Secondary bacterial infection Neurological Complication- encephalitis, aseptic menigitis , transverse myelitis , vasculitis , hemiplegia . Pneumonia, meningitis Thrombocytopenia, purpura fulminans , DIC Acute Retinal necrosis Rhabdomyolysis , arthritis

37. Congenital Varicella Syndrome Extremely rare disorder in which affected infants have distinctive abnormalities at birth (congenital) Second Trimester infection 13-20 weeks- 2% incidence Infection in 12 th week – 0.4 % incidence Affected newborns may have a low birth weight and scaring of the skin, Limb atrophy, the brain, the eyes.

38. Clinical Features Skin- Cicatricial Scars Neurological- Microcephaly , Encephalitis, Cortical Atrophy, Spinal Cord Atrophy, Seizures Eyes- Micropthalmia , enopthalmia , Choriretinitis , Cataract, Nystagmus , Optic Atrophy. Treatment – Varicella zoster immunoglobulin to mother within 72-96 hours (dose 125U/10 kg M max 625U IM)

39. Diagnosis In most cases, the diagnosis of varicella is clinical. centripetal distribution, the polymorphism in each affected site and the rapid progression of the individual lesion from vesicle to crust A Tzanck smear showing multinucleated giant cells, epithelial cells with acidophilic intranuclear inclusion bodies. The quickest and most reliable way to confirm diagnosis is by PCR of vesicle fluid or a scraping taken from the base of a blister.

40. The virus is readily identified by electron microscopy of vesicle Fluid and can be grown in tissue culture but this takes longer and is less reliable Detection of VZV antigen by direct fluorescent antibody is an alternative method.

41. Treatment General Cold compresses, oral antihistamines and tepid baths for symptomatic relief. Antipyretics other than salicylates are recommended. Antibiotics may be used when there is bacterial infection. Antiviral Therapy oral acyclovir (20 mg/kg body weight 5 times a day for 5 days in children) In healthy adolescents and adults, who are at increased risk of severe varicella, treatment (800 mg 5 times a day for 7 days)

42. Oral acyclovir should be given for third trimester infection, when there is a chance of viral pneumonia and when there is a risk of infection spreading to the newborn . In immunocompromised adults, the dose of acyclovir is 10 mg/kg body weight IV infused at a constant rate over 1 h every 8 h for 7 days.

43. Prevention The live attenuated VZV vaccine (Oka stain) Two doses 3 months apart of (0.5 ml administered subcutaneously) at 12 to 15 months of age, detectable Ab upto 10 years. For susceptible immunocompetent older children, two doses should be given 4 to 8 weeks separated by at least 28 days.

44. High risk individuals include: (1) neonates whose mothers developed varicella within the period from 7 days before to 7 days after delivery (2) immunosuppressed children and adults (3) non-immune pregnant women; (4) preterm infants (5) patients receiving chronic chemotherapy Post-Exposure Prophylaxis VZV-specific immune globulin should be given within 10 days of exposure reduces severity, high dose acyclovir therapy (40–80 mg/kg body weight per day for 7 days starting 7–9 days after exposure) is recommended.

45. HERPES ZOSTER (shingles) Herpes zoster (HZ) is disease characterized by unilateral radicular pain and vesicular eruption limited to the dermatome. It is caused by reactivation of VZV that is lying dormant in sensory ganglia.

46. Pathogenesis VZV passes from lesions in the skin and mucosal surfaces into the endings of sensory nerves and is transported centripetally up the sensory fibers to sensory ganglia. In the ganglia, it remains latent which may be for many years. Clinical manifestations result when the virus is reactivated. The newly synthesized VZV virions are transported along the sensory nerves and released into the skin. Reactivation of the virus is triggered by immunosupression , trauma, sunburn, stress, old age, surgery, neoplasia , radiotherapy.

47. Clinical features Prodrome of symptoms: fever, malaise, paresthesia before the lesions erupt. Usually pain is the most common and 1 st symptom. Instead of pain occasionally pruritus may be an early feature of shingles. Occasionaly pain is not followed by eruptions(zoster sine eruptione ) The time between the start of pain and the onset of rash averages 1.4 days in trigeminal HZ and 3.2 days in thoracic disease. Rash is usually unilateral, dermatomal and does not cross the midline. Closely grouped red papules, rapidly becoming vesicular and then pustular, develop in a continuous or interrupted band in the area of one, occasionally two and rarely, more contiguous dermatomes.

48. The mucous membrane of the affected dermatome is also involved. The lymph nodes draining the affected area are enlarged and tender. In uncomplicated cases, the recovery is complete in 2–3 weeks in children and young adults, and 3–4 weeks in older patients The area supplied by the trigeminal nerve, particularly the ophthalmic division, and the trunk from T3 to L2 are the most frequently affected areas In the immunocompromised generalization occurs after the initial dermatomal involvement. This is known as ‘disseminated Zoster

49. Clinical Variants of H. Zoster Trigeminal nerve zoster (Herpes zoster opthalmicus ) The eye is affected in two‐thirds of cases, especially when vesicles on the side of the nose indicate involvement of the nasociliary nerve (Hutchinson sign). Ocular complications- uveitis, keratitis, conjunctivitis, conjunctival oedema ( chemosis ), ocular muscle palsies, proptosis , scleritis , retinal vascular occlusion, and . ulceration, scarring and even necrosis of the lid. Involvement of the ciliary ganglia may give rise to Argyll– Robertson pupil.

50. Zoster of the maxillary division of the trigeminal nerve produces vesicles on the uvula and tonsillar area. Mandibular division- the vesicles appear on the anterior part of the tongue, the floor of the mouth and the buccal mucous membrane. In oro ‐facial zoster, toothache may be the presenting symptom.

51. Herpes zoster oticus ‘Ramsay–Hunt syndrome’ results from reactivation of latent virus in geniculate ganglion. presents as a triad of ipsilateral facial paralysis, ear pain, and vesicles in the auditory canal and auricle . Tinnitus, vertigo and deafness due to involvement of 8 th nerve which lies in close proximity with the genniculate ganglion. It accounts for about 10% of all cases of facial palsy. Full recovery occurs in 20% of untreated cases. Complications include—permanent hearing loss,post herpetic neuralgia.

52. Complications Secondary infection Scarring zoster gangrenosum cutaneous dissemination Post herpetic neuralgia It is the commonest and most intractable sequel of zoster , generally defined as persistence or recurrence of pain more than a month after the onset of zoster.

53. It usually remits spontaneously over a period. 3 main forms--- a continuous burning pain with hyperaesthesia ---spasmodic shooting type ---- pruritic crawling parasthesia Allodynia , pain caused by normally innocuous stimuli, is often the most distressing symptom and occurs in 90% of people with post‐herpetic neuralgia.

54. Other complications The visceral complications such as encephalitis,meningitis,pneumonitis , hepatitis, esophagitis, pericarditis, gastritis, cystitis and arthritis. Acute retinal necrosis syndrome; this rare complication follows an attack of shingles affecting the ophthalmic nerve. Guillain–Barre syndrome has also been noted occasionally following zoster Scar sarcoid

55. Investigations The classical presentation presents no difficulty in the diagnosis. However, zosteriform herpes simplex may pose a problem Where the diagnosis is uncertain,confirmation is made by culture or PCR, Tzanck smear.

56. Treatment Rest and analgesics. Soothing topical preparations with dressings as blisters break can relieve discomfort Oral treatment for zoster is with aciclovir 800 mg five times a day for 7–10 days or with valaciclovir 1 g or famciclovir 250 or 500 mg three times a day for 7 days. In immunosuppression, aciclovir may be given intravenously (10 mg/kg or 500 mg/m2 8‐hourly) or 4 g/day orally in five doses. Courses of 5, 7 and 10 days have been used.

57. FOR POST HERPETIC NEURALGIA Defined as the persistence of pain for more than 1 month after the disappearance of the rash A tricyclic antidepressant such as amitriptyline or nortriptyline (or clomipramine or doxepin) is useful, especially for hyperaesthesia.

58. For stabbing pain, sodium valproate (or other anticonvulsant, (e.g. clonazepam or carbamazepine) can be given Especially in the elderly, doses should be low initially and increased every few day. Gabapentin or pregabalin can be useful analgesics for the pain. Topical capsaicin 0.025%, a substance P depletor , Topical anaesthetic may relieve pain in some patients. Use of opiates should be avoided as far as possible

59. Prevention A live attenuated (Oka/Merck stain) varicella zoster virus vaccine (“zoster vaccine”) was found to be effective in the prevention of herpes zoster and postherpetic neuralgia in older adults. The zoster vaccine boosts VZV-specific cell mediated Immunity. Given in single dose.

60. Herpes Zoster in Pregnancy Vertical transmission rare due to pre-existing maternal antibody to VZV and generally low levels of viremia that accompany reactivation of VZV infection, compared with primary infection ( varicella ). Oral acyclovir 800mg five times a day can be given during pregnancy. Initiation of antiviral therapy in a pregnant woman with severe zoster rash (e.g., >50 lesions) promote more rapid healing and in those with acute neuritis to lessen the severity and duration of pain.

61. 62 Poxviruses are complex DNA viruses that replicate in the cytoplasm of epidermal cells. They are the largest viruses, slightly smaller than bacteria. They are brick or ovoid-shaped double-stranded DNA viruses. Man is infected by three kinds of pox viruses: Orthopox viruses (variola, vaccinia), parapox viruses (ORF, Milker’s nodule), and intermediate viruses (Molluscum contagiosum, Tanapox POXVIRUSES

62. 63 Molluscum Contagiosum Molluscum contagiosum is caused by molluscum contagiosumvirus (MCV). It belongs to intermediate (unclassified) group of Poxviridae family. It mostly affects humans. Restriction endonuclease analysis of the genomes has identified four types of MC viruses I, II, III, and IV. MCV I is the commonest type that produces human infection. In one study, 96.6% infections were caused by MCV I and 3.4% were by MCV II

63. 64 MC is transmitted by direct contact with the skin of the affected individual. It may be acquired from bath towels, tattoo instruments, gymnasiums, swimming pools, and beauty parlors. It may be inoculated with minor skin trauma (e.g., from shaving). Autoinoculation can occur from the manipulation of lesions by the patient. Fomites may also play a role in acquiring the infection. In adults, MC is mostly a sexually transmitted disease. It is more prevalent with unprotected sex and in those with multiple sex partners. In AIDS, it may be the presenting complaint. MC is reported in areas treated with steroids, tacrolimus, pimecrolimus, and in those who had undergone renal transplantation. The incubation period is 2–7 weeks, but it can be as long as 6 months. Pathogenesis

64. 65 MCV produces single or multiple, umbilicated, skin-colored, opalescent, discrete, smooth, domeshaped waxy papules. They appear vesicular because of its translucent nature. The size of papules may be 2–6 mm, but it may be as large as 1 cm in immunocompromised individuals. They may be grouped forming large plaques or disseminated. They can occur anywhere on the body but mostly seen on the face, axillae, antecubital and popliteal fossae, and perineal area . Palms and soles are rarely involved. Mucosal lesions are rare and can occur in the mouth and conjunctiva. MC can present subungually . MC lesions are usually asymptomatic but rarely, they may be painful, tender, and pruritic.

65. 66 MC is diagnosed mostly on clinical grounds. MCV cannot be cultured in a laboratory. Smears made from the cheesy material expressed from the lesion by crushing between two slides and stained with Giemsa or Wright stain show homogeneous pear shaped molluscum bodies. Skin biopsy reveals epidermal hyperplasia and many epidermal cells contain large, intracytoplasmic inclusion bodies. Electron microscopy has been used to demonstrate the poxvirus structures. Immunohistochemistry using polyclonal antibody identifies

66. 67 Treatment MC is a self-limiting disease, and even if untreated, it nearly always resolves spontaneously but may take 6–9 months, and in some cases, they may persist for 3–4 years. This fact should be given due consideration, especially in young children. Some schools may not allow children with molluscum papules. Whether the lesions should be treated or left alone can be decided by the patient’s concern, persistence of the lesions, and the stigma caused by them. Common bathing, sharing towels, and use of swimming pools are to be avoided. Simple scratching of the lesion by mother may produce inflammation and the lesion may resolve. Topical tretinoin 0.05–0.1% applied twice daily showed some success. The resolution was reported in 2 weeks and mild erythema at the lesional site may occur. Topical adapalene, topical TCA 25–50%, 10% iodine, benzoyl peroxide, and liquid phenol are found useful.

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68. 69 Syn: Sheep Pox, Ecthyma Contagiosum, Scabby Mouth, and Contagious Pustular Dermatitis Etiology ORF is caused by a DNA virus, parapox virus. The disease is widespread in sheep and goats ORF

69. 70 A small, firm, tender, red papule appears, and then, target lesions may develop and slowly enlarges to form a hemorrhagic pustule or bulla. Central umbilication may occur, often with crusting. They may be single or few with the size varying from 2 to 5 cm. Fingers and hands are commonly affected. A fully developed lesion may show a grayish-white ring around central crusting, further surrounded by an erythema Pyogenic granuloma-like lesions are reported in immunocompromised. Satellite lesions are seen in children with atopic dermatitis. Regional lymphadenitis is not uncommon. Erythema multiforme and bullous pemphigoid-like lesions occasionally appear 1–2 weeks after the onset of ORF. They may resolve spontaneously or rarely require immunosuppressive treatment

70. 71 Clinical lesions with appropriate history may make the diagnosis easy. The testing of vesicular fluid is not useful as it does not contain many viruses. Skin biopsy is useful. PCR of the crust or a biopsy can detect parapox virus. Spontaneous recovery occurs in 6–8 weeks. Secondary infection is treated and spontaneous recovery is awaited. Excision of the lesion may enhance healing. Idoxiuridine (40%) has been claimed to be effective.Topical imiquimod and cidofovir have been found effective.

71. 72 Milker’s Nodule Syn: Pseudocowpox , Paravaccinia Milker’s nodule is caused by pseudocowpox virus, a parapox virus with the same morphology as that of ORF virus. The calves are affected by ring sores and ulcers on the mouth. Milker’s and veterinarians who examine the mouth of calves are infected accidentally.It can also be transmitted by contaminated fomites. Human-to-human spread does not occur. The incubation period is 1–2 weeks. Clinical Features Flat red tender papules appear initially. As they enlarge, they crust in the center with secondary erythema.Lymphangitis may occur. Lymphadenopathy is not common. Lesions regress without scarring in 4–6 weeks. They are common on hands but may be seen on face.There may be mild constitutional symptoms. They are usually solitary but multiple lesions can occur. The nodules are very vascular and are confused with pyogenic granuloma. Differentiation from ORF is difficult and history is more helpful. The lesions heal in 4–8 weeks and sometimes longer. Secondary bacterial infections, erythema multiforme, and erythema nodosum can occur. Most cases heal without scarring

72. 73 Treatment The disease is self-limited. Symptomatic treatment is given. Secondary infection is controlled. Surgical curettage of large lesions may help in a speedy recovery.

73. 74 Smallpox is an acute contagious disease caused by Variola virus, which belongs to orthopox family Smallpox (Variola) In the absence of vaccination, all humans are susceptible to infection. There is no animal reservoir. It is transmitted from person-to-person by infected aerosols and air droplets, contaminated clothes, and beddings The incubation period is 10–14 days. After a prodrome of high fever, malaise, and headache for 3–4 days, macular eruption develops and then turns into vesicles and pustules. The rash starts on the scalp and spreads caudally affecting the extremities more than the trunk. The palms and soles are frequently affected. Unlike chickenpox, here, the lesions are of the same type at the same site. After about a week, the lesions crust and heal with scarring Complications include pneumonia, encephalitis, blindness, and arthritis. Over one-third of patients have a severe disease with 25% to 40% mortality

74. 75 The treatment is supportive. No specific treatment is available. Strict isolation procedures must be observed and contacts of any infected individual are traced quickly Unlike chickenpox, here, the lesions are of the same type at the same site. After about a week, the lesions crust and heal with scarring Complications include pneumonia, encephalitis, blindness, and arthritis. Over one-third of patients have a severe disease with 25% to 40% mortality

75. 76 Vaccinia Vaccinia is caused by Poxvirus officinalis. It is invaluable for vaccination against smallpox. Though vaccination ceased in the 1970s, it should be given to investigators at special risk and military personnel. It is associated with complications like generalized vaccinia, accidental autoinoculation, infection, encephalomyelitis, myopericarditis, hypertrophic scar, and basal cell carcinoma. Eczema Vaccinatum It occurs in people with atopic eczema. Lesions occur on eczematous areas and healthy skin about 5 days after exposure to the virus. It is associated with high fever and lymphadenopathy.

76. 77 Progressive Vaccinia The incidence of progressive vaccinia was about one per million vaccinations. The ulcer at the site of vaccination fails to heal and enlarges in immunocompromised people. Antiviral treatment helps in containing the virus and causes improvement, otherwise, a fatal outcome occurs

77. 78 Buffalopox Buffalopox is caused by Buffalopox virus, closely related to Vaccinia virus. It is mainly seen in Southeast Asia. Outbreaks were reported from India, Maharashtra, Andhra Pradesh, Telangana, and Gujarat. It infects buffaloes, cattle, pigs, and humans. Clinical Features It presents as nodules, umbilicated vesicles, and pustules on the dorsae of hands. It mimics ORF, Milker’s nodule and may be difficult to differentiate clinically. The contact buffaloes may have erosions with crusting over teats and udders. Diagnosis is confirmed by viral isolation in Vero E6 cell monolayers, plaque reduction neutralization test, electron microscopy, A‐type inclusion, and C18L gene‐specific PCR and counter immunoelectrophoresis.The treatment is supportive. The awareness about hand hygiene and the use of gloves while milking may prevent this.

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