Bacterial, Viral & Mycotic Infections


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Bacterial, Viral & Mycotic Infections

  1. 1. BACTERIAL, VIRAL & MYCOTIC INFECTIONS Prepared by: Dr Sundeep S Bhagwath
  3. 3. BACTERIAL INFECTIONS <ul><li>Actinomycosis </li></ul><ul><li>Syphilis </li></ul><ul><li>Tuberculosis </li></ul><ul><li>NOMA </li></ul><ul><li>Scarlet fever </li></ul><ul><li>Leprosy </li></ul>
  4. 4. <ul><li>VIRAL INFECTIONS </li></ul><ul><li>Herpes Simplex Virus ( HSV ) </li></ul><ul><li>Chickenpox </li></ul><ul><li>Herpes Zoster (Shingles ) </li></ul><ul><li>Herpangina </li></ul><ul><li>Hand - Foot - Mouth Disease </li></ul><ul><li>Infectious Mononucleosis (Glandular fever ) </li></ul><ul><li>Measles </li></ul><ul><li>Cytomegalovirus infection </li></ul><ul><li>Acquired Immunodeficiency Syndrome (AIDS) </li></ul>
  5. 5. <ul><li>FUNGAL / MYCOTIC INFECTIONS </li></ul><ul><li>Candidiasis </li></ul><ul><li>Histoplasmosis </li></ul><ul><li>Blastomycosis </li></ul><ul><li>Aspergillosis </li></ul><ul><li>Toxoplasmosis </li></ul>
  6. 6. ACTINOMYCOSIS <ul><li>Chronic granulomatous, localized bacterial infection. </li></ul><ul><li>AETIOLOGY :- as a result of infection by Actinomyces israelii, A. viscosus , A. Naeslundi, A.odontolyticus etc. </li></ul><ul><li>TYPES: - according to location, </li></ul><ul><li>- Cervicofacial actinomycosis </li></ul><ul><li>- Thoracic actinomycosis </li></ul><ul><li>- Abdominal actinomycosis </li></ul>
  7. 7. <ul><li>CERVICOFACIAL ACTINOMYCOSIS </li></ul><ul><li>AETIOLOGY :- as a result of infection by A.israelii , A.viscosus, and A.naeslundi </li></ul><ul><li>CLINICAL FEATURES :- </li></ul><ul><li>Age incidence: young adults </li></ul><ul><li>Sex incidence: More in males </li></ul><ul><li>Systemic manifestations: </li></ul><ul><li>Fever , headache , vomiting dysphagia , sore throat and cervical lymphadenopathy </li></ul>
  8. 8. <ul><li>Site Predilection: </li></ul><ul><li>Submandibular, submental and cheek areas most commonly. </li></ul><ul><li>Bacteria enter through areas of previous trauma like extraction site, periodontal pocket, non vital tooth or infected tonsil. </li></ul>
  9. 9. <ul><li>Signs & symptoms: </li></ul><ul><li>Lesion begins as asymptomatic “wooden” firm area of fibrosis and later forms a central, softer area of abscess. </li></ul><ul><li>Infection can extend to surface and drain via a fistula. </li></ul><ul><li>Suppurative discharge may contain yellowish flecks which contain colonies of bacteria (sulfur granules) </li></ul>
  10. 10. <ul><li>HISTOLOGICAL FEATURES : </li></ul><ul><li>Characterized by formation of granulation tissue surrounding large collections of PMNL’s and colonies of bacteria. </li></ul><ul><li>Colonies consist of club shaped filaments that form a radiating rosette pattern. </li></ul><ul><li>With H & E stain, core of colony stains blue while periphery stains pink. </li></ul>
  11. 11. SYPHILIS <ul><li>Chronic systemic venereal disease of bacterial etiology causing a granulomatous reaction. </li></ul><ul><li>AETIOLOGY :- Treponema pallidum </li></ul><ul><li>TYPES : </li></ul><ul><li>-Acquired type ; </li></ul><ul><li>Primary stage </li></ul><ul><li>Secondary stage </li></ul><ul><li>Tertiary stage </li></ul><ul><li>- Congenital type </li></ul>
  12. 12. <ul><li>TRANSMISSION : - </li></ul><ul><li>Direct contact of a healthy patient with a diseased patient or carrier of infection (dentists/dermatologists) </li></ul><ul><li>Unprotected sexual intercourse </li></ul><ul><li>Transplacental (from mother to fetus) </li></ul><ul><li>Contaminated blood or blood products </li></ul>
  13. 13. ACQUIRED SYPHILIS - PRIMARY STAGE - <ul><li>It is first stage of acquired type of syphilis </li></ul><ul><li>Incubation period ranges from 3 – 90 days. </li></ul><ul><li>Most infective stage </li></ul>
  14. 14. <ul><li>CLINICAL FEATURES : - </li></ul><ul><li>Age incidence: young adults </li></ul><ul><li>Sex incidence: Males </li></ul><ul><li>Site predilection: </li></ul><ul><li>Oral cavity - tongue , hard palate and lips </li></ul><ul><li>Genital organs of male and female </li></ul><ul><li>N.B – Lesion of primary syphilis is called CHANCRE. </li></ul>
  15. 15. <ul><li>Oral manifestations: </li></ul><ul><li>Mostly solitary. </li></ul><ul><li>Appears as painless, normal colored ulcer. </li></ul><ul><li>Can also manifest as a vascular proliferation resembling a pyogenic granuloma. </li></ul><ul><li>Genital manifestations: </li></ul><ul><li>Most commonly external genitalia and anal region. </li></ul><ul><li>Regional lymphadenopathy </li></ul>
  16. 16. <ul><li>Both genital as well as extra genital lesions heal within 3 – 8 weeks if they are left untreated </li></ul>
  17. 17. - SECONDARY STAGE - <ul><li>Occurs 4 – 10 weeks after the initial infection. </li></ul><ul><li>Lesion can arise before the lesions of primary syphilis have healed. </li></ul><ul><li>In this stage, systemic symptoms are also seen. </li></ul><ul><li>This is also a very infective stage. </li></ul>
  18. 18. <ul><li>CLINICAL FEATURES : - </li></ul><ul><li>a ) Systemic symptoms: </li></ul><ul><li>Fever, painless lymphadenopathy, sore throat , malaise, weight loss and musculoskeletal pain. </li></ul><ul><li>Typically, diffuse, painless, maculopapular rash develops which is widespread and seen even on palmar and plantar areas. </li></ul>
  19. 19. <ul><li>b) Oral manifestations: </li></ul><ul><li>(i) Mucous patches – seen in approx 30% cases. Manifested as focal areas of intense spongiosis of oral mucosa leading to zones of whitish mucosa. </li></ul><ul><li>( ii) Condyloma latum – appear as papillary lesions resembling viral papillomas. </li></ul><ul><li>Lesions in secondary stage are usually multiple. </li></ul><ul><li>Spontaneous resolution occurs within 3 – 12 weeks. </li></ul>
  20. 20. - TERTIARY STAGE - <ul><li>Occurs if the secondary lesion is untreated. </li></ul><ul><li>Can occur several months to years after the secondary stage has healed. </li></ul><ul><li>CLINICAL FEATURES : - </li></ul><ul><li>Symptoms can be grouped as </li></ul><ul><li>- Neurosyphilis </li></ul><ul><li>- Cardiovascular syphilis </li></ul><ul><li>- Diffuse gummatous lesions </li></ul>
  21. 21. <ul><li>A. NEUROSYPHILIS: </li></ul><ul><li>Characterized by infection of central and peripheral nerve tissues which manifests as </li></ul><ul><li>- General paresis of insane, </li></ul><ul><li>- Dementia </li></ul><ul><li>- Tabes dorsalis, leads to ataxia and loss of </li></ul><ul><li> deep sensations. </li></ul><ul><li>- Psychosis </li></ul>
  22. 22. <ul><li>B. CARDOVASCULAR SYPHILIS: </li></ul><ul><li>Aneurysm of ascending aorta </li></ul><ul><li>Stenosis and occlusion of coronary artery. </li></ul><ul><li>Left ventricular hypertrophy </li></ul><ul><li>Congestive cardiac failure </li></ul>
  23. 23. <ul><li>C. GUMMA: </li></ul><ul><li>Affects skin, mucosa, soft tissues and even bones. </li></ul><ul><li>Intraoral – affects palate and tongue mostly. </li></ul><ul><li>Presents as indurated, nodular / ulcerated lesion which can be associated with large amount of tissue destruction. </li></ul>
  24. 24. <ul><li>Diffuse atrophy and loss of papillae from dorsal surface result in “luetic glossitis”. </li></ul><ul><li>Considered premalignant condition previously, but not supported by recent research. </li></ul>
  25. 25. <ul><li>CONGENITAL SYPHILIS </li></ul><ul><li>Occurs as a result of transplacental transfer after 4 th -5 th months </li></ul><ul><li>The fetus may be stillborn, or die immediately after birth or born with the disease or become involved by disease after a few months or years. </li></ul>
  26. 26. <ul><li>CLINICAL FEATURES : - </li></ul><ul><li>Three pathognomonic features described by Sir Jonathan Hutchinson (Hutchinson’s triad) </li></ul><ul><li>- Hutchinson’s teeth </li></ul><ul><li>- Interstitial keratitis </li></ul><ul><li>- Eighth nerve deafness </li></ul><ul><li>All patients may not exhibit all the features of triad. </li></ul>
  27. 27. <ul><li>1. Hutchinson’s teeth: </li></ul><ul><li>Alteration of both anterior (Hutchinson’s incisors) as well as posterior teeth (Mulberry molars) . </li></ul><ul><li>Anterior teeth taper cervico-incisally and show a hypoplastic central notch. </li></ul><ul><li>Molars also show similar tapering with an abnormal occlusal morphology, showing numerous globular projections. </li></ul>
  28. 28. <ul><li>2. Interstitial keratitis: </li></ul><ul><li>Usually not seen at birth, but develops between 5 – 25 years. </li></ul><ul><li>Affected eyes shows opacified cornea, with resultant loss of vision. </li></ul><ul><li>3. Other alterations: </li></ul><ul><li>- Eighth nerve deafness </li></ul><ul><li>- Saddle nose </li></ul><ul><li>- Saber shin (Anterior bowing of tibia) </li></ul><ul><li>- High arched palate </li></ul>
  29. 29. <ul><li>HISTOLOGICAL FEATURES : - </li></ul><ul><li>Non specific features. </li></ul><ul><li>Epithelial surface in primary stage is usually ulcerated and may be either ulcerated / hyperplastic in secondary stage. </li></ul><ul><li>Underlying CT shows predominantly perivascular inflammatory infiltrate of lymphocytes and plasma cells. </li></ul><ul><li>Best way to diagnose syphilis is dark field examination of smear of exudate to demonstrate spirochetes. </li></ul>
  30. 30. <ul><li>Oral tertiary stage lesions show surface ulceration with peripheral pseudoepithelial hyperplasia. </li></ul><ul><li>Underlying CT shows foci of granulomatous inflammation with well circumscribed collections of macrophages and multinucleated giant cells. </li></ul>
  31. 31. <ul><li>TUBERCULOSIS </li></ul><ul><li>Chronic granulomatous systemic bacterial disease. </li></ul><ul><li>Infection caused by Mycobacterium tuberculosis. </li></ul><ul><li>Incidence decreased dramatically with the discovery of antibiotics in 1940’s. </li></ul><ul><li>However, incidence increasing alarmingly since 1980’s due to various factors like association with HIV, transmission of TB in crowded or unsanitary environments etc. </li></ul>
  32. 32. <ul><li>PATHOGENESIS : - </li></ul><ul><li>Infection must be distinguished from active disease. </li></ul><ul><li>Primary infection occurs in previously unexposed persons and almost always in lungs – leading to formation of localized, fibrocalcified nodule. </li></ul><ul><li>Viable organisms may exist in these nodules and remain dormant for years. </li></ul><ul><li>Only 5% - 10% patients progress from primary to active disease and immunosupression is often responsible for reactivation of dormant organisms </li></ul><ul><li>AIDS, old age, poverty and crowded conditions are considered risk factors for progression from primary to secondary disease. </li></ul>
  33. 33. <ul><li>TRANSMISSION : - </li></ul><ul><li>- Inhalation of micro-organisms </li></ul><ul><li>- Eating or drinking contaminated milk (bovine TB) </li></ul><ul><li>- Direct contact with body’s fluids like blood , saliva & urine </li></ul><ul><li>- Blood transfusion </li></ul><ul><li>- Mother to fetus (transplacental) </li></ul>
  34. 34. <ul><li>CLINICAL FEATURES :- </li></ul><ul><li>1. Primary TB: Usually asymptomatic. Fever and pleural effusion may occur. </li></ul><ul><li>2. Secondary TB: </li></ul><ul><li>Located in apex of lungs, but can spread to many sites through lymphatics, vascular channels. </li></ul><ul><li>Symptoms of low grade fever, night sweats, malaise, anorexia and weight loss. </li></ul><ul><li>Extrapulmonary TB is common and can occur anywhere in body like skin (lupus vulgaris), lymph node (scrofula), bones, kidneys, GIT and head & neck also. </li></ul>
  35. 35. <ul><li>ORAL LESIONS OF TB: </li></ul><ul><li>Mostly manifest as chronic painless ulcer. </li></ul><ul><li>May also appear nodular, granular or even leukoplakic areas. </li></ul><ul><li>Primary TB lesions mostly involve gingiva or extraction sites. </li></ul><ul><li>Secondary TB lesions mostly seen on palate, tongue and lip. </li></ul>
  36. 36. <ul><li>Drinking milk contaminated with M.bovis can lead to non tubercular infections of cervical and oropharyngeal lymph nodes, called as Scrofula. </li></ul><ul><li>Occasionally, significant caseous necrosis can occur and form numerous fistulas through overlying skin. </li></ul>
  37. 37. <ul><li>HISTOLOGICAL FEATURES : - </li></ul><ul><li>Classic presentation – formation of granuloma. </li></ul><ul><li>Circumscribed collection of epitheloid macrophages, lymphocytes and langhan’s giant cells often with central caseous necrosis. </li></ul><ul><li>Demonstration of M.tuberculosis is by acid – fast stains like Zeihl – Neelsen stain. </li></ul>
  38. 38. <ul><li>CANCRUM ORIS </li></ul><ul><li>Acute, rapidly progressing, localized, bacterial infection of the orofacial tissues and jaws </li></ul><ul><li>Causative organisms – Fusobacterium necrophorum, F.nucleatum and Prevotella intermedia. </li></ul><ul><li>Predisposing factors include poverty, malnutrition, poor oral hygiene & sanitation, recent illness, malignancy and immunodeficiency states like AIDS. </li></ul>
  39. 39. <ul><li>CLINICAL FEATURES : - </li></ul><ul><li>Age incidence: Predominantly children between 1 – 10 years. </li></ul><ul><li>Sex incidence: Male </li></ul><ul><li>Site predilection: </li></ul><ul><li>Usually begins on gingivae as ANUG, then spreads facially / lingually to adjacent soft tissues. </li></ul>
  40. 40. <ul><li>Signs & symptoms: </li></ul><ul><li>Disease begins initially in gingivae as ANUG and later spreads to adjacent soft tissues. </li></ul><ul><li>As necrosis extends deeper over next few days, zones of bluish-black discoloration of overlying skin develop. </li></ul><ul><li>These zones break down into areas of yellowish necrosis that spread into adjacent bone. </li></ul><ul><li>Other signs – fever, fetid odor, pain, malaise and regional lymphadenopathy. </li></ul>
  42. 42. <ul><li>CANDIDIASIS </li></ul><ul><li>Refers to infection with yeast like fungal organism. </li></ul><ul><li>Most common oral fungal infection. </li></ul><ul><li>It is a component of normal oral flora. </li></ul><ul><li>Can occur in persons who are debilitated by other diseases or in otherwise healthy individuals also. </li></ul>
  43. 43. <ul><li>PREDISPOSING FACTORS : - </li></ul><ul><li>a) Local Factors : </li></ul><ul><li>- Mucosal trauma </li></ul><ul><li>- Denture wearers </li></ul><ul><li>- Denture hygiene </li></ul><ul><li>- Tobacco smoking </li></ul><ul><li>- Carbohydrate rich diet </li></ul><ul><li>- Drugs (Broad spectrum antibiotics, steroids, immunosuppressant / cytotoxic agents) </li></ul><ul><li>- Xerostomia </li></ul>
  44. 44. <ul><li>b) S ystemic factors : </li></ul><ul><li>- Iron deficiency anaemia </li></ul><ul><li>- Megaloblastic anaemia </li></ul><ul><li>- Acute leukaemia </li></ul><ul><li>- Diabetes mellitus </li></ul><ul><li>- HIV infection </li></ul><ul><li>- Other immunodeficiency states </li></ul>
  45. 45. CLASSIFICATION OF CANDIDIASIS : - <ul><li>Group 1 (Conditions confined to the oral mucosa): </li></ul><ul><li>Acute - </li></ul><ul><li>- Acute pseudomembranous candidiasis </li></ul><ul><li>- Acute atrophic candidiasis </li></ul><ul><li>Chronic - </li></ul><ul><li>- Chronic atrophic candidiasis </li></ul><ul><li>- Candida associated angular cheilitis </li></ul><ul><li>- Chronic hyperplastic candidiasis </li></ul><ul><li>Group 2 (oral manifestations of generalized candidiasis) </li></ul><ul><li>- Chronic mucocutaneous candidiasis </li></ul>
  46. 46. ACUTE PSEUDOMEMBRANEOUS CANDIDIASIS ( THRUSH ) <ul><li>Best recognized form of candidiasis. </li></ul><ul><li>Characterized by development of white plaques that can be scraped off with tongue blade. </li></ul><ul><li>Can be initiated by broad spectrum antibiotics or immune dysfunction. </li></ul>
  47. 47. <ul><li>Occurs characteristically on buccal mucosa, palate and dorsal tongue. </li></ul><ul><li>Usually asymptomatic or patients may c/o burning sensation of mucosa or unpleasant taste in mouth. </li></ul><ul><li>Can occur in infants also. </li></ul>
  48. 48. ATROPHIC CANDIDIASIS (Erythematous candidiasis) <ul><li>Several presentations seen – </li></ul><ul><li>1. Acute atrophic candidiasis </li></ul><ul><li>2. Median rhomboid glossitis </li></ul><ul><li>3. Chronic multifocal candidiasis </li></ul><ul><li>4. Angular cheilitis </li></ul><ul><li>5. Chronic atrophic (denture sore mouth) candidiasis </li></ul>
  49. 49. <ul><li>1. ACUTE ATROPHIC CANDIDIASIS : - </li></ul><ul><li>Also called “antibiotic sore mouth”, as it follows course of broad spectrum antibiotics. </li></ul><ul><li>Patients c/o burning sensation of mucosae. </li></ul><ul><li>Seen as diffuse loss of filliform papillae resulting in a bald appearance of tongue . </li></ul>
  50. 50. <ul><li>2. MEDIAN RHOMBOID GLOSSITIS : </li></ul><ul><li>Also called central papillary atrophy of tongue. </li></ul><ul><li>Well demarcated erythematous zone affecting midline of dorsum of tongue. </li></ul><ul><li>Often asymptomatic. </li></ul><ul><li>Erythema due to loss of filliform papillae. </li></ul><ul><li>Sometimes, other areas of oral cavity like hard palate and angles of mouth also show lesions (Chronic multifocal candidiasis). </li></ul>
  51. 51. <ul><li>3. CHRONIC ATROPHIC CANDIDIASIS : - </li></ul><ul><li>Characterized by varying degrees of erythema in denture bearing areas of usually maxillary prostheses. </li></ul><ul><li>Usually asymptomatic. </li></ul><ul><li>Patients give h/o wearing denture continuously. </li></ul>
  52. 52. <ul><li>4. ANGULAR CHEILITIS : - </li></ul><ul><li>Also called perleche. </li></ul><ul><li>Characterized by erythema, fissuring and scaling of corners of mouth. </li></ul><ul><li>Typically occurs either along with multifocal candidiasis or in old patients with reduced vertical dimension. </li></ul><ul><li>Saliva pools in these areas, keeping them moist and thus favoring fungal infection </li></ul>
  53. 53. <ul><li>5. CHRONIC HYPERPLASTIC CANDIDIASIS : </li></ul><ul><li>Least common of all types. </li></ul><ul><li>Appears as non scrapable white patch resembling leukoplakia (candidal leukoplakia) </li></ul><ul><li>Believed that it represents candidiasis superimposed on pre-existing leukoplakia. </li></ul><ul><li>Diagnosis confirmed by demonstration of candidal hyphae within the lesion and resolution of lesion after antifungal therapy. </li></ul>
  54. 54. <ul><li>CHRONIC MUCOCUTANEOUS CANDIDIASIS: - </li></ul><ul><li>Severe oral candidiasis can also occur as a component of a rare immunological disorder called mucocutaneous candidiasis. </li></ul><ul><li>Autosomal recessive disorder. </li></ul><ul><li>Immune dysfunction becomes evident in early life – patient develops candidiasis of mouth, nails, skin and other mucosae. </li></ul><ul><li>Oral lesions appear as thick, white non scrapable patches. </li></ul>
  55. 55. <ul><li>HISTOLOGICAL FEATURES : - </li></ul><ul><li>Biopsy specimen show hyperparakeratinization, elongation of rete ridges, chronic inflammatory cell infiltration of underlying CT and small microabscesses collection of PMNL’s) within parakeratin layer. </li></ul><ul><li>Candidal hyphae can be seen embedded in parakeratin layer and superficial spinous layer. </li></ul>
  56. 56. <ul><li>EXFOLIATIVE CYTOLOGY : - </li></ul><ul><li>Candidal hyphae can also be demonstrated by exfoliative cytology by PAS stain. </li></ul><ul><li>Hyphae are stained magenta color by the PAS stain. </li></ul><ul><li>RAPID DIAGNOSTIC TEST : - </li></ul><ul><li>A 10% - 20% KOH preparation used for rapid diagnosis. </li></ul><ul><li>KOH lyses background of epithelial cells allowing yeast and hyphae to be seen. </li></ul>
  58. 58. <ul><li>Herpes simplex infection </li></ul><ul><li>Varicella </li></ul><ul><li>Herpes zoster </li></ul><ul><li>Infectious mononucleosis </li></ul><ul><li>Enterovirus infections </li></ul><ul><li>- Herpangina </li></ul><ul><li>- Hand foot & mouth disease </li></ul><ul><li>- Rubeola & Rubella </li></ul><ul><li>- HIV </li></ul>
  59. 59. HERPES SIMPLEX INFECTION <ul><li>Herpes simplex virus (HSV) – DNA virus. </li></ul><ul><li>Belongs to human herpesvirus (HHV) family, also called Herpetoviridae. </li></ul><ul><li>Other members of this family are varicella-zoster virus, Epstein-Barr virus, Cytomegalovirus etc. </li></ul><ul><li>Humans – only known natural reservoirs and can stay in the host for life and become periodically reactivated. </li></ul>
  60. 60. TYPES OF HSV <ul><li>Herpes simplex virus – 1: </li></ul><ul><li>Spread through saliva. </li></ul><ul><li>Lesions above the waist, in oral, facial and ocular areas including pharynx, and skin. </li></ul><ul><li>Herpes simplex virus – 2: </li></ul><ul><li>Transmitted through sexual contact. </li></ul><ul><li>Involves genitalia and skin below the waist. </li></ul>
  61. 61. PATHOGENESIS <ul><li>HSV infections – 2 patterns seen. </li></ul><ul><li>1. Primary infection: - </li></ul><ul><li>- Initial exposure to virus, no antibodies are produced. </li></ul><ul><li>- Occurs in young age, often asymptomatic. </li></ul><ul><li>- Virus taken up in sensory nerves and transported to associated ganglia. </li></ul>
  62. 62. <ul><li>2. Secondary / recurrent infection: - </li></ul><ul><li>- Virus residing in ganglia is reactivated. </li></ul><ul><li>- Not always symptomatic; sometimes patients only shed the virus through saliva. </li></ul><ul><li>Predisposing factors for reactivation of virus : </li></ul><ul><li>Old age </li></ul><ul><li>UV light </li></ul><ul><li>Emotional stress </li></ul><ul><li>Trauma </li></ul><ul><li>Menstruation </li></ul><ul><li>Systemic diseases or malignancy </li></ul>
  63. 63. <ul><li>HERPETIC GINGIVOSTOMATITIS </li></ul><ul><li>Commonest pattern of primary HSV infection. </li></ul><ul><li>Incubation period is 3 – 9 days. </li></ul><ul><li>CLINICAL FEATURES : - </li></ul><ul><li>Age incidence: 6 months – 5 years </li></ul><ul><li>Sex incidence: Nil </li></ul><ul><li>Site predilection: </li></ul><ul><li>Affects movable and immovable mucosae. </li></ul><ul><li>Primarily gingiva, labial mucosa, vermilion zone, palate. </li></ul>
  64. 64. <ul><li>Signs & symptoms: </li></ul><ul><li>Prodromal symptoms – fever with chills, nausea, anorexia and cervical lymphadenopathy. </li></ul><ul><li>Begins as small pinhead size vesicles which coalesce and form numerous red lesions. </li></ul><ul><li>In all cases, gingiva red, enlarged and painful. </li></ul><ul><li>Lip lesions can extend to vermilion zone </li></ul>
  65. 65. RECURRENT HERPES LABIALIS <ul><li>Can occur either at primary site </li></ul><ul><li>or in adjacent areas. </li></ul><ul><li>Commonest sites – vermilion </li></ul><ul><li>zone and adjacent area of lips. </li></ul><ul><li>Multiple, small, erythematous </li></ul><ul><li>papules develop and form </li></ul><ul><li>clusters of fluid filled vesicles. </li></ul><ul><li>Vesicles rupture and crust within </li></ul><ul><li>2 – 3 days and heal within 7 </li></ul><ul><li>days. </li></ul>
  66. 66. HERPETIC WHITLOW <ul><li>Less common presentation. </li></ul><ul><li>Infection of fingers, and thumb. </li></ul><ul><li>Occurs due to self inoculation in children with orofacial HSV. </li></ul><ul><li>Can also occur in medical and dental professionals who do not wear gloves and come in contact with infected patients. </li></ul>
  67. 67. <ul><li>HISTOLOGICAL FEATURES : - </li></ul><ul><li>Main effect of virus on epithelial cells. </li></ul><ul><li>Infected epithelial cells show acantholysis, nuclear enlargement and ballooning degeneration. </li></ul><ul><li>Nuclear fragmentation with condensation of chromatin around periphery of nucleus. </li></ul><ul><li>These cells called – Tzanck cells. </li></ul><ul><li>Fusion of adjacent degenerated cells – multinucleated infected cells. </li></ul><ul><li>Intercellular edema – formation of intraepithelial vesicle. </li></ul>
  68. 68. <ul><li>DIAGNOSIS : - </li></ul><ul><li>Commonly used diagnostic procedures – cytological smear and tissue biopsy. </li></ul><ul><li>Cytosmear is best as it is the least invasive and cost effective. </li></ul><ul><li>Histological changes also are characteristic and only VZV produces similar changes within epithelium, but it can be differentiated easily from HSV. </li></ul>
  69. 69. VARICELLA (Chickenpox) <ul><li>VZV is similar to HSV in many respects. </li></ul><ul><li>Chickenpox represents primary infection with VZV. </li></ul><ul><li>Herpes zoster or Shingles represents reactivation of the latent VZV residing within the ganglia. </li></ul><ul><li>VZV spreads through droplets or direct contact with infected persons. </li></ul><ul><li>Incubation period is 10 – 21 days. </li></ul>
  70. 70. <ul><li>CLINICAL FEATURES : - </li></ul><ul><li>Age incidence: between 5 – 9 years. </li></ul><ul><li>Sex incidence: Nil </li></ul><ul><li>Site predilection: Face, trunk and extremities. </li></ul><ul><li>Prodromal symptoms: </li></ul><ul><li>- Fever </li></ul><ul><li>- Malaise </li></ul><ul><li>- Pharyngitis </li></ul><ul><li>- Nausea </li></ul><ul><li>- Anorexia </li></ul><ul><li>- Headache </li></ul>
  71. 71. <ul><li>Signs & symptoms: </li></ul><ul><li>All lesions pass through phases of erythema, vesicle, pustule and crusting. </li></ul><ul><li>Vesicle is surrounded by zone of erythema. </li></ul><ul><li>In contrast to HSV, vesicles continue to erupt for 3 – 4 days. </li></ul><ul><li>Thus, old crusted lesions are mixed with new vesicles. </li></ul><ul><li>Infected persons are contagious from 2 days before appearance of vesicles until all vesicles crust. </li></ul>
  72. 72. <ul><li>Oral manifestations: - </li></ul><ul><li>Oral lesions are common and may precede skin lesions. </li></ul><ul><li>Common sites – palate and buccal mucosa. </li></ul><ul><li>Oral lesions begin as 3 -4 mm opaque white vesicles that rupture to form 1 – 3 mm ulcers. </li></ul><ul><li>VZV oral lesions can be distinguished easily from HSV as VZV lesions are rarely painful. </li></ul>
  73. 73. <ul><li>COMPLICATIONS : - </li></ul><ul><li>1.Children: </li></ul><ul><li>- Secondary skin infections </li></ul><ul><li>- Encephalitis </li></ul><ul><li>- Pneumonia </li></ul><ul><li>2. Adults: </li></ul><ul><li>- Varicella pneumonitis </li></ul><ul><li>- Encephalitis </li></ul><ul><li>- Pneumonia </li></ul><ul><li>- Early pregnancy involvement may cause abortion or congenital defects. </li></ul>
  74. 74. <ul><li>DIAGNOSIS : - </li></ul><ul><li>H/o exposure to VZV within last 3 weeks. </li></ul><ul><li>Characteristic vesicles. </li></ul><ul><li>Demonstration of cytopathological changes within epithelial cells harvested from vesicular fluid. </li></ul>
  75. 75. HERPES ZOSTER (Shingles) <ul><li>The primary VZV infection is transported up the sensory nerves and remains latent within the dorsal spinal ganglia. </li></ul><ul><li>Herpes zoster infection occurs by reactivation of the VZV. </li></ul><ul><li>Unlike HSV, there is usually a single recurrence. </li></ul>
  76. 76. <ul><li>PREDISPOSING FACTORS : - </li></ul><ul><li>Immunosupression </li></ul><ul><li>Treatment with cytotoxic drugs </li></ul><ul><li>Radiation </li></ul><ul><li>Presence of malignancy </li></ul><ul><li>Alcohol abuse </li></ul><ul><li>Dental manipulation </li></ul>
  77. 77. <ul><li>CLINICAL FEATURES : - </li></ul><ul><li>Age incidence: Middle age to old age </li></ul><ul><li>Sex incidence: Nil </li></ul><ul><li>Site predilection: Affects areas of skin innervated by the affected sensory nerve (dermatome). </li></ul>
  78. 78. <ul><li>Signs & symptoms: </li></ul><ul><li>Viral infection proceeds in three phases – prodromal, acute and chronic </li></ul><ul><li>A. Prodromal: </li></ul><ul><li>Virus replicates within ganglia, causing ganglionitis resulting in severe neuralgia (responsible for pain preceding the rash) </li></ul><ul><li>As virus travels down the nerve, pain intensifies. </li></ul><ul><li>Pain is accompanied by fever, malaise and headache 3 – 4 days before cutaneous / mucosal lesions develop. </li></ul><ul><li>Typically one dermatome is affected, but two or more also can be affected </li></ul>
  79. 79. <ul><li>B. Acute phase: </li></ul><ul><li>1 – 4 days after prodromal phase, affected skin develops clusters of vesicles on erythematous base. </li></ul><ul><li>Within 3 – 4 days, they become pustular, ulcerate and begin to crust after 7 – 10 days. </li></ul><ul><li>Lesion develop along the path of distribution of sensory nerve and terminate at midline. </li></ul><ul><li>Resolution occurs within 2 – 3 weeks and usually heal by scarring. </li></ul>
  80. 80. <ul><li>Oral manifestations: </li></ul><ul><li>Oral lesion occur if trigeminal nerve involved. </li></ul><ul><li>May occur on movable or bound mucosa. </li></ul><ul><li>Like chickenpox, lesions appear as 1–4 mm white, opaque vesicles which rupture, forming shallow ulcers. </li></ul><ul><li>RAMSAY HUNT SYDROME – combination of cutaneous lesions of external acoustic meatus, facial paralysis, hearing deficit and vertigo. </li></ul>
  81. 81. <ul><li>DIAGNOSIS : - </li></ul><ul><li>Clinical presentation is typical. </li></ul><ul><li>Viral culture (takes at least 24 hours). </li></ul><ul><li>Cytosmear to demonstrate cytopathological viral effects. </li></ul><ul><li>Direct staining of cytosmear with fluorescent antibodies for VZV. </li></ul>
  82. 82. INFECTIOUS MONONUCLEOSIS (Glandular fever) <ul><li>Results from exposure to Epstein-Barr virus (EBV). </li></ul><ul><li>Transmission – intimate contact like kissing, sharing of straws, contaminated salivary transmission in children. </li></ul><ul><li>Exposure during childhood – asymptomatic. </li></ul><ul><li>Symptomatic infections arise in young adults. </li></ul>
  83. 83. <ul><li>CLINICAL FEATURES ; - </li></ul><ul><li>Age incidence: children </li></ul><ul><li>Sex incidence: Nil </li></ul><ul><li>Site incidence: </li></ul><ul><li>Apart from systemic manifestations, affects anterior and posterior cervical chain lymph nodes as well as oropharyngeal tonsils. </li></ul><ul><li>Intra oral – hard palate and gingiva. </li></ul>
  84. 84. <ul><li>Signs & symptoms: </li></ul><ul><li>1. Systemic = </li></ul><ul><li>Fever, lymphadenopathy,, pharyngitis, rhinitis, cough, hepatosplenomegaly. </li></ul><ul><li>In 90% cases, prominent, symmetric, tender enlargement of anterior and posterior cervical chain lymph nodes. </li></ul><ul><li>2. Oral = </li></ul><ul><li>Petechiae on hard or soft palate and enlargement of oropharyngeal tonsils. </li></ul>
  85. 85. <ul><li>DIAGNOSIS : - </li></ul><ul><li>Diagnosis is suggested by clinical presentation </li></ul><ul><li>WBC count is raised with differential count showing lymphocytosis as high as 70% - 90%. </li></ul><ul><li>Classical serological finding – presence of Paul – Bunnell heterophil antibody, present in 90% of affected patients. </li></ul>
  86. 86. RUBEOLA <ul><li>Rubeola / Measles is a viral infection produced by paramyxovirus. </li></ul><ul><li>Incidence dramatically reduced since use of measles vaccine. </li></ul><ul><li>Incubation period – 10 to 12 days </li></ul><ul><li>CLINICAL FEATTURES : - </li></ul><ul><li>Age incidence: Young children </li></ul><ul><li>Sex incidence: Nil </li></ul><ul><li>Site predilection: Face, trunk and extremities. </li></ul>
  87. 87. <ul><li>Signs & symptoms: </li></ul><ul><li>Most cases arise in spring and spread through respiratory droplets. </li></ul><ul><li>Prodromal symptoms of fever, malaise, coryza and cough. </li></ul><ul><li>Rash appears after a few days and lasts for 4 – 7 days with first appearance on face followed by trunk and extremities. </li></ul>
  88. 88. <ul><li>Oral manifestations: </li></ul><ul><li>Multiple areas of mucosal erythema on labial and buccal mucosa and soft palate (Koplik’s spots). </li></ul><ul><li>Within these areas, bluish white macules may be seen. </li></ul><ul><li>These spots represent areas of epithelial necrosis. </li></ul>
  89. 89. <ul><li>COMPLICATIONS : - </li></ul><ul><li>Otitis </li></ul><ul><li>Pneumonia </li></ul><ul><li>Persistent bronchitis </li></ul><ul><li>Diarrhea </li></ul><ul><li>Encephalitis </li></ul>
  90. 90. HERPANGINA <ul><li>Caused by coxackievirus A or B or echoviruses – all these belong to enterovirus family. </li></ul><ul><li>CLINICAL FEATURES : - </li></ul><ul><li>Age incidence: Children & young adults. </li></ul><ul><li>Sex incidence: Nil </li></ul><ul><li>Site predilection: </li></ul><ul><li>Primarily systemic disease, with oral lesions mainly in soft palate and tonsillar regions. </li></ul>
  91. 91. <ul><li>Signs & symptoms:: </li></ul><ul><li>Begins with significant sore throat, dysphagia and fever. </li></ul><ul><li>Occasionally, vomiting, myalgia and headache. </li></ul><ul><li>Oral lesions begins as 2-4 mm sized, red macules which form fragile vesicles that rapidly ulcerate. </li></ul><ul><li>Systemic symptoms subside within a few days and ulcers heal within 7 – 10 days. </li></ul>
  92. 92. ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS) <ul><li>More than 25 million cases worldwide. </li></ul><ul><li>Considered almost 100% fatal and no known vaccine developed so far. </li></ul><ul><li>ROUTES OF TRANSMISSION : - </li></ul><ul><li>Sexual contact </li></ul><ul><li>Infected blood / blood products </li></ul><ul><li>Intravenous drug abuse </li></ul><ul><li>Transplacental transfer </li></ul>
  93. 93. <ul><li>PATHOGENESIS : - </li></ul><ul><li>When virus enters the body, its DNA incorporated into primary target cell i.e. CD4+ helper T lymphocyte. </li></ul><ul><li>Similar to other viral infections, antibodies to virus are formed but are not protective. </li></ul><ul><li>Virus can remain silent or cause cell death, as a result, decrease in helper T- cells occurs, leading to loss in immune function. </li></ul><ul><li>There is an asymptomatic stage lasting for about 8 – 10 years after which the final symptomatic stage develops. </li></ul>
  94. 94. <ul><li>CLINICAL FEATURES : - </li></ul><ul><li>After inoculation, patient may be asymptomatic or develop acute response similar to infectious mononucleosis. </li></ul><ul><li>Acute response – fever, generalized lymphadenopathy, sore throat, myalgia, diarrhea, maculopapular rash etc. </li></ul><ul><li>Acute syndrome clears within a few weeks and a variable asymptomatic phase follows which may last for 8 – 10 years. </li></ul><ul><li>Symptomatic phase – opportunistic infections (pneumonia, CMV, HSV, TB etc) and neoplastic processes (Kaposi sarcoma, Non-Hodgkin’s lymphoma etc). </li></ul>
  95. 95. ORAL MANIFESTATIONS <ul><li>Group 1 (lesions strongly associated with HIV): </li></ul><ul><li>1. Oral candidal infections </li></ul><ul><li>- Erythematous </li></ul><ul><li>- Hyperplastic </li></ul><ul><li>- Pseudomembranous </li></ul><ul><li>2. Hairy leukoplakia </li></ul><ul><li>3.HIV associated periodontitis </li></ul><ul><li>- HIV gingivitis </li></ul><ul><li>- HIV periodontitis </li></ul><ul><li>- Necrotizing ulcerative gingivitis </li></ul><ul><li>- Necrotizing ulcerative stomatitis </li></ul><ul><li>4. Kaposi sarcoma </li></ul><ul><li>5. Non-Hodgkin’s lymphoma </li></ul>
  98. 98. Patch stage Plaque stage Nodular stage KAPOSI SARCOMA
  99. 99. <ul><li>Group 2 (lesions less commonly associated with HIV): </li></ul><ul><li>1. Aphthous ulcers (oropharyngeal region) </li></ul><ul><li>2. Idiopathic thrombocytopenia </li></ul><ul><li>3. Salivary gland disorders </li></ul><ul><li>- Dry mouth and decreased salivary flow </li></ul><ul><li>- Uni or bilateral swelling of major glands </li></ul><ul><li>4. Viral infections (apart from EBV) </li></ul><ul><li>- Cytomegalovirus </li></ul><ul><li>- Herpes simplex virus </li></ul><ul><li>- Human papilloma virus </li></ul><ul><li>- Varicella - zoster virus </li></ul>
  101. 101. DIAGNOSIS <ul><li>Screening test: ELISA is most commonly used test. But it can show false positive results. </li></ul><ul><li>Western Blot test: It is a test to detect viral antibodies. More accurate than ELISA. </li></ul>
  102. 102. HAIRY LEUKOPLAKIA <ul><li>It is a chronic, localized viral infection </li></ul><ul><li>Caused by Epstein-Barr virus. </li></ul><ul><li>CLINICAL FEATURES :- </li></ul><ul><li>Age incidence : Young age </li></ul><ul><li>Sex incidence : Males </li></ul><ul><li>Site predilection: Lateral borders of the tongue, bilaterally </li></ul><ul><li>Signs and symptoms: Asymptomatic, slowly spreading. non scrapable, papillary, greyish white lesion. </li></ul>
  103. 104. HISTOLOGICAL FEATURES <ul><li>Lesion is characterized by hyperparakeratosis and acanthosis. </li></ul><ul><li>Epithelial cells are infected by EBV which appear as swollen cells with ballooning degeneration. </li></ul><ul><li>Characteristic pattern of peripheral margination of nuclear chromatin is seen, called nuclear beading . </li></ul>