logging in or signing up infectious diseases in oral pathology drsundeepbhagwath Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 1055 Category: Education License: All Rights Reserved Like it (3) Dislike it (0) Added: October 26, 2010 This Presentation is Public Favorites: 4 Presentation Description No description available. Comments Posting comment... By: bero83 (9 month(s) ago) hi please i want to download this wonderful presantation Saving..... Post Reply Close Saving..... Edit Comment Close By: lsy1989 (13 month(s) ago) hi .......please i need this apresentation .... can i get it but quickly Saving..... Post Reply Close Saving..... Edit Comment Close By: iraqicataloni (14 month(s) ago) thank you very much Saving..... Post Reply Close Saving..... Edit Comment Close Premium member Presentation Transcript BACTERIAL, VIRAL & MYCOTIC INFECTIONSPrepared by:Dr Sundeep S Bhagwath : BACTERIAL, VIRAL & MYCOTIC INFECTIONSPrepared by:Dr Sundeep S Bhagwath BACTERIAL INFECTIONS : BACTERIAL INFECTIONS BACTERIAL INFECTIONS : BACTERIAL INFECTIONS Actinomycosis Syphilis Tuberculosis NOMA Scarlet fever Leprosy Slide 4: VIRAL INFECTIONS Herpes Simplex Virus ( HSV ) Chickenpox Herpes Zoster (Shingles) Herpangina Hand - Foot - Mouth Disease Infectious Mononucleosis (Glandular fever ) Measles Cytomegalovirus infection Acquired Immunodeficiency Syndrome (AIDS) Slide 5: FUNGAL / MYCOTIC INFECTIONS Candidiasis Histoplasmosis Blastomycosis Aspergillosis Toxoplasmosis ACTINOMYCOSIS : ACTINOMYCOSIS Chronic granulomatous, localized bacterial infection. AETIOLOGY :- as a result of infection by Actinomyces israelii, A. viscosus , A. Naeslundi, A.odontolyticus etc. TYPES: - according to location, - Cervicofacial actinomycosis - Thoracic actinomycosis - Abdominal actinomycosis Slide 7: CERVICOFACIAL ACTINOMYCOSIS AETIOLOGY :- as a result of infection by A.israelii , A.viscosus, and A.naeslundi CLINICAL FEATURES :- Age incidence: young adults Sex incidence: More in males Systemic manifestations: Fever , headache , vomiting dysphagia , sore throat and cervical lymphadenopathy Slide 8: Site Predilection: Submandibular, submental and cheek areas most commonly. Bacteria enter through areas of previous trauma like extraction site, periodontal pocket, non vital tooth or infected tonsil. ` : ` Signs & symptoms: Lesion begins as asymptomatic “wooden” firm area of fibrosis and later forms a central, softer area of abscess. Infection can extend to surface and drain via a fistula. Suppurative discharge may contain yellowish flecks which contain colonies of bacteria (sulfur granules) Slide 10: HISTOLOGICAL FEATURES: Characterized by formation of granulation tissue surrounding large collections of PMNL’s and colonies of bacteria. Colonies consist of club shaped filaments that form a radiating rosette pattern. With H & E stain, core of colony stains blue while periphery stains pink. SYPHILIS : SYPHILIS Chronic systemic venereal disease of bacterial etiology causing a granulomatous reaction. AETIOLOGY :- Treponema pallidum TYPES: -Acquired type ; Primary stage Secondary stage Tertiary stage - Congenital type Slide 12: TRANSMISSION: - Direct contact of a healthy patient with a diseased patient or carrier of infection (dentists/dermatologists) Unprotected sexual intercourse Transplacental (from mother to fetus) Contaminated blood or blood products ACQUIRED SYPHILIS - PRIMARY STAGE - : ACQUIRED SYPHILIS - PRIMARY STAGE - It is first stage of acquired type of syphilis Incubation period ranges from 3 – 90 days. Most infective stage Slide 14: CLINICAL FEATURES: - Age incidence: young adults Sex incidence: Males Site predilection: Oral cavity - tongue , hard palate and lips Genital organs of male and female N.B – Lesion of primary syphilis is called CHANCRE. Slide 15: Oral manifestations: Mostly solitary. Appears as painless, normal colored ulcer. Can also manifest as a vascular proliferation resembling a pyogenic granuloma. Genital manifestations: Most commonly external genitalia and anal region. Regional lymphadenopathy Slide 16: Both genital as well as extra genital lesions heal within 3 – 8 weeks if they are left untreated - SECONDARY STAGE - : - SECONDARY STAGE - Occurs 4 – 10 weeks after the initial infection. Lesion can arise before the lesions of primary syphilis have healed. In this stage, systemic symptoms are also seen. This is also a very infective stage. Slide 18: CLINICAL FEATURES: - a) Systemic symptoms: Fever, painless lymphadenopathy, sore throat , malaise, weight loss and musculoskeletal pain. Typically, diffuse, painless, maculopapular rash develops which is widespread and seen even on palmar and plantar areas. Slide 19: b) Oral manifestations: (i) Mucous patches – seen in approx 30% cases. Manifested as focal areas of intense spongiosis of oral mucosa leading to zones of whitish mucosa. (ii) Condyloma latum – appear as papillary lesions resembling viral papillomas. Lesions in secondary stage are usually multiple. Spontaneous resolution occurs within 3 – 12 weeks. - TERTIARY STAGE - : - TERTIARY STAGE - Occurs if the secondary lesion is untreated. Can occur several months to years after the secondary stage has healed. CLINICAL FEATURES: - Symptoms can be grouped as - Neurosyphilis - Cardiovascular syphilis - Diffuse gummatous lesions Slide 21: A. NEUROSYPHILIS: Characterized by infection of central and peripheral nerve tissues which manifests as - General paresis of insane, - Dementia - Tabes dorsalis, leads to ataxia and loss of deep sensations. - Psychosis Slide 22: B. CARDOVASCULAR SYPHILIS: Aneurysm of ascending aorta Stenosis and occlusion of coronary artery. Left ventricular hypertrophy Congestive cardiac failure Slide 23: C. GUMMA: Affects skin, mucosa, soft tissues and even bones. Intraoral – affects palate and tongue mostly. Presents as indurated, nodular / ulcerated lesion which can be associated with large amount of tissue destruction. Slide 24: Diffuse atrophy and loss of papillae from dorsal surface result in “luetic glossitis”. Considered premalignant condition previously, but not supported by recent research. Slide 25: CONGENITAL SYPHILIS Occurs as a result of transplacental transfer after 4th -5th months 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. Slide 26: CLINICAL FEATURES: - Three pathognomonic features described by Sir Jonathan Hutchinson (Hutchinson’s triad) - Hutchinson’s teeth - Interstitial keratitis - Eighth nerve deafness All patients may not exhibit all the features of triad. Slide 27: 1. Hutchinson’s teeth: Alteration of both anterior (Hutchinson’s incisors) as well as posterior teeth (Mulberry molars). Anterior teeth taper cervico-incisally and show a hypoplastic central notch. Molars also show similar tapering with an abnormal occlusal morphology, showing numerous globular projections. Slide 28: 2. Interstitial keratitis: Usually not seen at birth, but develops between 5 – 25 years. Affected eyes shows opacified cornea, with resultant loss of vision. 3. Other alterations: - Eighth nerve deafness - Saddle nose - Saber shin (Anterior bowing of tibia) - High arched palate Slide 29: HISTOLOGICAL FEATURES: - Non specific features. Epithelial surface in primary stage is usually ulcerated and may be either ulcerated / hyperplastic in secondary stage. Underlying CT shows predominantly perivascular inflammatory infiltrate of lymphocytes and plasma cells. Best way to diagnose syphilis is dark field examination of smear of exudate to demonstrate spirochetes. Slide 30: Oral tertiary stage lesions show surface ulceration with peripheral pseudoepithelial hyperplasia. Underlying CT shows foci of granulomatous inflammation with well circumscribed collections of macrophages and multinucleated giant cells. Slide 31: TUBERCULOSIS Chronic granulomatous systemic bacterial disease. Infection caused by Mycobacterium tuberculosis. Incidence decreased dramatically with the discovery of antibiotics in 1940’s. However, incidence increasing alarmingly since 1980’s due to various factors like association with HIV, transmission of TB in crowded or unsanitary environments etc. Slide 32: PATHOGENESIS: - Infection must be distinguished from active disease. Primary infection occurs in previously unexposed persons and almost always in lungs – leading to formation of localized, fibrocalcified nodule. Viable organisms may exist in these nodules and remain dormant for years. Only 5% - 10% patients progress from primary to active disease and immunosupression is often responsible for reactivation of dormant organisms AIDS, old age, poverty and crowded conditions are considered risk factors for progression from primary to secondary disease. Slide 33: TRANSMISSION: - - Inhalation of micro-organisms - Eating or drinking contaminated milk (bovine TB) - Direct contact with body’s fluids like blood , saliva & urine - Blood transfusion - Mother to fetus (transplacental) Slide 34: CLINICAL FEATURES:- 1. Primary TB: Usually asymptomatic. Fever and pleural effusion may occur. 2. Secondary TB: Located in apex of lungs, but can spread to many sites through lymphatics, vascular channels. Symptoms of low grade fever, night sweats, malaise, anorexia and weight loss. Extrapulmonary TB is common and can occur anywhere in body like skin (lupus vulgaris), lymph node (scrofula), bones, kidneys, GIT and head & neck also. Slide 35: ORAL LESIONS OF TB: Mostly manifest as chronic painless ulcer. May also appear nodular, granular or even leukoplakic areas. Primary TB lesions mostly involve gingiva or extraction sites. Secondary TB lesions mostly seen on palate, tongue and lip. Slide 36: Drinking milk contaminated with M.bovis can lead to non tubercular infections of cervical and oropharyngeal lymph nodes, called as Scrofula. Occasionally, significant caseous necrosis can occur and form numerous fistulas through overlying skin. Slide 37: HISTOLOGICAL FEATURES: - Classic presentation – formation of granuloma. Circumscribed collection of epitheloid macrophages, lymphocytes and langhan’s giant cells often with central caseous necrosis. Demonstration of M.tuberculosis is by acid – fast stains like Zeihl – Neelsen stain. Slide 38: CANCRUM ORIS Acute, rapidly progressing, localized, bacterial infection of the orofacial tissues and jaws Causative organisms – Fusobacterium necrophorum, F.nucleatum and Prevotella intermedia. Predisposing factors include poverty, malnutrition, poor oral hygiene & sanitation, recent illness, malignancy and immunodeficiency states like AIDS. Slide 39: CLINICAL FEATURES: - Age incidence: Predominantly children between 1 – 10 years. Sex incidence: Male Site predilection: Usually begins on gingivae as ANUG, then spreads facially / lingually to adjacent soft tissues. Slide 40: Signs & symptoms: Disease begins initially in gingivae as ANUG and later spreads to adjacent soft tissues. As necrosis extends deeper over next few days, zones of bluish-black discoloration of overlying skin develop. These zones break down into areas of yellowish necrosis that spread into adjacent bone. Other signs – fever, fetid odor, pain, malaise and regional lymphadenopathy. MYCOTIC INFECTIONS : MYCOTIC INFECTIONS Slide 42: CANDIDIASIS Refers to infection with yeast like fungal organism. Most common oral fungal infection. It is a component of normal oral flora. Can occur in persons who are debilitated by other diseases or in otherwise healthy individuals also. Slide 43: PREDISPOSING FACTORS: - a) Local Factors : - Mucosal trauma - Denture wearers - Denture hygiene - Tobacco smoking - Carbohydrate rich diet - Drugs (Broad spectrum antibiotics, steroids, immunosuppressant / cytotoxic agents) - Xerostomia Slide 44: b) Systemic factors : - Iron deficiency anaemia - Megaloblastic anaemia - Acute leukaemia - Diabetes mellitus - HIV infection - Other immunodeficiency states CLASSIFICATION OF CANDIDIASIS: - : CLASSIFICATION OF CANDIDIASIS: - Group 1 (Conditions confined to the oral mucosa): Acute - - Acute pseudomembranous candidiasis - Acute atrophic candidiasis Chronic - - Chronic atrophic candidiasis - Candida associated angular cheilitis - Chronic hyperplastic candidiasis Group 2 (oral manifestations of generalized candidiasis) - Chronic mucocutaneous candidiasis ACUTE PSEUDOMEMBRANEOUS CANDIDIASIS (THRUSH ) : ACUTE PSEUDOMEMBRANEOUS CANDIDIASIS (THRUSH ) Best recognized form of candidiasis. Characterized by development of white plaques that can be scraped off with tongue blade. Can be initiated by broad spectrum antibiotics or immune dysfunction. Slide 47: Occurs characteristically on buccal mucosa, palate and dorsal tongue. Usually asymptomatic or patients may c/o burning sensation of mucosa or unpleasant taste in mouth. Can occur in infants also. ATROPHIC CANDIDIASIS(Erythematous candidiasis) : ATROPHIC CANDIDIASIS(Erythematous candidiasis) Several presentations seen – 1. Acute atrophic candidiasis 2. Median rhomboid glossitis 3. Chronic multifocal candidiasis 4. Angular cheilitis 5. Chronic atrophic (denture sore mouth) candidiasis Slide 49: 1. ACUTE ATROPHIC CANDIDIASIS: - Also called “antibiotic sore mouth”, as it follows course of broad spectrum antibiotics. Patients c/o burning sensation of mucosae. Seen as diffuse loss of filliform papillae resulting in a bald appearance of tongue. Slide 50: 2. MEDIAN RHOMBOID GLOSSITIS: Also called central papillary atrophy of tongue. Well demarcated erythematous zone affecting midline of dorsum of tongue. Often asymptomatic. Erythema due to loss of filliform papillae. Sometimes, other areas of oral cavity like hard palate and angles of mouth also show lesions (Chronic multifocal candidiasis). Slide 51: 3. CHRONIC ATROPHIC CANDIDIASIS: - Characterized by varying degrees of erythema in denture bearing areas of usually maxillary prostheses. Usually asymptomatic. Patients give h/o wearing denture continuously. Slide 52: 4. ANGULAR CHEILITIS: - Also called perleche. Characterized by erythema, fissuring and scaling of corners of mouth. Typically occurs either along with multifocal candidiasis or in old patients with reduced vertical dimension. Saliva pools in these areas, keeping them moist and thus favoring fungal infection Slide 53: 5. CHRONIC HYPERPLASTIC CANDIDIASIS: Least common of all types. Appears as non scrapable white patch resembling leukoplakia (candidal leukoplakia) Believed that it represents candidiasis superimposed on pre-existing leukoplakia. Diagnosis confirmed by demonstration of candidal hyphae within the lesion and resolution of lesion after antifungal therapy. Slide 54: CHRONIC MUCOCUTANEOUS CANDIDIASIS: - Severe oral candidiasis can also occur as a component of a rare immunological disorder called mucocutaneous candidiasis. Autosomal recessive disorder. Immune dysfunction becomes evident in early life – patient develops candidiasis of mouth, nails, skin and other mucosae. Oral lesions appear as thick, white non scrapable patches. Slide 55: HISTOLOGICAL FEATURES: - 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. Candidal hyphae can be seen embedded in parakeratin layer and superficial spinous layer. Slide 56: EXFOLIATIVE CYTOLOGY: - Candidal hyphae can also be demonstrated by exfoliative cytology by PAS stain. Hyphae are stained magenta color by the PAS stain. RAPID DIAGNOSTIC TEST: - A 10% - 20% KOH preparation used for rapid diagnosis. KOH lyses background of epithelial cells allowing yeast and hyphae to be seen. VIRAL INFECTIONS : VIRAL INFECTIONS Slide 58: Herpes simplex infection Varicella Herpes zoster Infectious mononucleosis Enterovirus infections - Herpangina - Hand foot & mouth disease - Rubeola & Rubella - HIV HERPES SIMPLEX INFECTION : HERPES SIMPLEX INFECTION Herpes simplex virus (HSV) – DNA virus. Belongs to human herpesvirus (HHV) family, also called Herpetoviridae. Other members of this family are varicella-zoster virus, Epstein-Barr virus, Cytomegalovirus etc. Humans – only known natural reservoirs and can stay in the host for life and become periodically reactivated. TYPES OF HSV : TYPES OF HSV Herpes simplex virus – 1: Spread through saliva. Lesions above the waist, in oral, facial and ocular areas including pharynx, and skin. Herpes simplex virus – 2: Transmitted through sexual contact. Involves genitalia and skin below the waist. PATHOGENESIS : PATHOGENESIS HSV infections – 2 patterns seen. 1. Primary infection: - - Initial exposure to virus, no antibodies are produced. - Occurs in young age, often asymptomatic. - Virus taken up in sensory nerves and transported to associated ganglia. Slide 62: 2. Secondary / recurrent infection: - - Virus residing in ganglia is reactivated. - Not always symptomatic; sometimes patients only shed the virus through saliva. Predisposing factors for reactivation of virus: Old age UV light Emotional stress Trauma Menstruation Systemic diseases or malignancy Slide 63: HERPETIC GINGIVOSTOMATITIS Commonest pattern of primary HSV infection. Incubation period is 3 – 9 days. CLINICAL FEATURES: - Age incidence: 6 months – 5 years Sex incidence: Nil Site predilection: Affects movable and immovable mucosae. Primarily gingiva, labial mucosa, vermilion zone, palate. Slide 64: Signs & symptoms: Prodromal symptoms – fever with chills, nausea, anorexia and cervical lymphadenopathy. Begins as small pinhead size vesicles which coalesce and form numerous red lesions. In all cases, gingiva red, enlarged and painful. Lip lesions can extend to vermilion zone RECURRENT HERPES LABIALIS : RECURRENT HERPES LABIALIS Can occur either at primary site or in adjacent areas. Commonest sites – vermilion zone and adjacent area of lips. Multiple, small, erythematous papules develop and form clusters of fluid filled vesicles. Vesicles rupture and crust within 2 – 3 days and heal within 7 days. HERPETIC WHITLOW : HERPETIC WHITLOW Less common presentation. Infection of fingers, and thumb. Occurs due to self inoculation in children with orofacial HSV. Can also occur in medical and dental professionals who do not wear gloves and come in contact with infected patients. Slide 67: HISTOLOGICAL FEATURES: - Main effect of virus on epithelial cells. Infected epithelial cells show acantholysis, nuclear enlargement and ballooning degeneration. Nuclear fragmentation with condensation of chromatin around periphery of nucleus. These cells called – Tzanck cells. Fusion of adjacent degenerated cells – multinucleated infected cells. Intercellular edema – formation of intraepithelial vesicle. Slide 68: DIAGNOSIS: - Commonly used diagnostic procedures – cytological smear and tissue biopsy. Cytosmear is best as it is the least invasive and cost effective. Histological changes also are characteristic and only VZV produces similar changes within epithelium, but it can be differentiated easily from HSV. VARICELLA (Chickenpox) : VARICELLA (Chickenpox) VZV is similar to HSV in many respects. Chickenpox represents primary infection with VZV. Herpes zoster or Shingles represents reactivation of the latent VZV residing within the ganglia. VZV spreads through droplets or direct contact with infected persons. Incubation period is 10 – 21 days. Slide 70: CLINICAL FEATURES: - Age incidence: between 5 – 9 years. Sex incidence: Nil Site predilection: Face, trunk and extremities. Prodromal symptoms: - Fever - Malaise - Pharyngitis - Nausea - Anorexia - Headache Slide 71: Signs & symptoms: All lesions pass through phases of erythema, vesicle, pustule and crusting. Vesicle is surrounded by zone of erythema. In contrast to HSV, vesicles continue to erupt for 3 – 4 days. Thus, old crusted lesions are mixed with new vesicles. Infected persons are contagious from 2 days before appearance of vesicles until all vesicles crust. Slide 72: Oral manifestations: - Oral lesions are common and may precede skin lesions. Common sites – palate and buccal mucosa. Oral lesions begin as 3 -4 mm opaque white vesicles that rupture to form 1 – 3 mm ulcers. VZV oral lesions can be distinguished easily from HSV as VZV lesions are rarely painful. Slide 73: COMPLICATIONS: - 1.Children: - Secondary skin infections - Encephalitis - Pneumonia 2. Adults: - Varicella pneumonitis - Encephalitis - Pneumonia - Early pregnancy involvement may cause abortion or congenital defects. Slide 74: DIAGNOSIS: - H/o exposure to VZV within last 3 weeks. Characteristic vesicles. Demonstration of cytopathological changes within epithelial cells harvested from vesicular fluid. HERPES ZOSTER(Shingles) : HERPES ZOSTER(Shingles) The primary VZV infection is transported up the sensory nerves and remains latent within the dorsal spinal ganglia. Herpes zoster infection occurs by reactivation of the VZV. Unlike HSV, there is usually a single recurrence. Slide 76: PREDISPOSING FACTORS: - Immunosupression Treatment with cytotoxic drugs Radiation Presence of malignancy Alcohol abuse Dental manipulation Slide 77: CLINICAL FEATURES: - Age incidence: Middle age to old age Sex incidence: Nil Site predilection: Affects areas of skin innervated by the affected sensory nerve (dermatome). Slide 78: Signs & symptoms: Viral infection proceeds in three phases – prodromal, acute and chronic A. Prodromal: Virus replicates within ganglia, causing ganglionitis resulting in severe neuralgia (responsible for pain preceding the rash) As virus travels down the nerve, pain intensifies. Pain is accompanied by fever, malaise and headache 3 – 4 days before cutaneous / mucosal lesions develop. Typically one dermatome is affected, but two or more also can be affected Slide 79: B. Acute phase: 1 – 4 days after prodromal phase, affected skin develops clusters of vesicles on erythematous base. Within 3 – 4 days, they become pustular, ulcerate and begin to crust after 7 – 10 days. Lesion develop along the path of distribution of sensory nerve and terminate at midline. Resolution occurs within 2 – 3 weeks and usually heal by scarring. Slide 80: Oral manifestations: Oral lesion occur if trigeminal nerve involved. May occur on movable or bound mucosa. Like chickenpox, lesions appear as 1–4 mm white, opaque vesicles which rupture, forming shallow ulcers. RAMSAY HUNT SYDROME – combination of cutaneous lesions of external acoustic meatus, facial paralysis, hearing deficit and vertigo. Slide 81: DIAGNOSIS: - Clinical presentation is typical. Viral culture (takes at least 24 hours). Cytosmear to demonstrate cytopathological viral effects. Direct staining of cytosmear with fluorescent antibodies for VZV. INFECTIOUS MONONUCLEOSIS(Glandular fever) : INFECTIOUS MONONUCLEOSIS(Glandular fever) Results from exposure to Epstein-Barr virus (EBV). Transmission – intimate contact like kissing, sharing of straws, contaminated salivary transmission in children. Exposure during childhood – asymptomatic. Symptomatic infections arise in young adults. Slide 83: CLINICAL FEATURES; - Age incidence: children Sex incidence: Nil Site incidence: Apart from systemic manifestations, affects anterior and posterior cervical chain lymph nodes as well as oropharyngeal tonsils. Intra oral – hard palate and gingiva. Slide 84: Signs & symptoms: 1. Systemic = Fever, lymphadenopathy,, pharyngitis, rhinitis, cough, hepatosplenomegaly. In 90% cases, prominent, symmetric, tender enlargement of anterior and posterior cervical chain lymph nodes. 2. Oral = Petechiae on hard or soft palate and enlargement of oropharyngeal tonsils. Slide 85: DIAGNOSIS: - Diagnosis is suggested by clinical presentation WBC count is raised with differential count showing lymphocytosis as high as 70% - 90%. Classical serological finding – presence of Paul – Bunnell heterophil antibody, present in 90% of affected patients. RUBEOLA : RUBEOLA Rubeola / Measles is a viral infection produced by paramyxovirus. Incidence dramatically reduced since use of measles vaccine. Incubation period – 10 to 12 days CLINICAL FEATTURES: - Age incidence: Young children Sex incidence: Nil Site predilection: Face, trunk and extremities. Slide 87: Signs & symptoms: Most cases arise in spring and spread through respiratory droplets. Prodromal symptoms of fever, malaise, coryza and cough. Rash appears after a few days and lasts for 4 – 7 days with first appearance on face followed by trunk and extremities. Slide 88: Oral manifestations: Multiple areas of mucosal erythema on labial and buccal mucosa and soft palate (Koplik’s spots). Within these areas, bluish white macules may be seen. These spots represent areas of epithelial necrosis. Slide 89: COMPLICATIONS: - Otitis Pneumonia Persistent bronchitis Diarrhea Encephalitis HERPANGINA : HERPANGINA Caused by coxackievirus A or B or echoviruses – all these belong to enterovirus family. CLINICAL FEATURES: - Age incidence: Children & young adults. Sex incidence: Nil Site predilection: Primarily systemic disease, with oral lesions mainly in soft palate and tonsillar regions. Slide 91: Signs & symptoms:: Begins with significant sore throat, dysphagia and fever. Occasionally, vomiting, myalgia and headache. Oral lesions begins as 2-4 mm sized, red macules which form fragile vesicles that rapidly ulcerate. Systemic symptoms subside within a few days and ulcers heal within 7 – 10 days. ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS) : ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS) More than 25 million cases worldwide. Considered almost 100% fatal and no known vaccine developed so far. ROUTES OF TRANSMISSION: - Sexual contact Infected blood / blood products Intravenous drug abuse Transplacental transfer Slide 93: PATHOGENESIS: - When virus enters the body, its DNA incorporated into primary target cell i.e. CD4+ helper T lymphocyte. Similar to other viral infections, antibodies to virus are formed but are not protective. Virus can remain silent or cause cell death, as a result, decrease in helper T- cells occurs, leading to loss in immune function. There is an asymptomatic stage lasting for about 8 – 10 years after which the final symptomatic stage develops. Slide 94: CLINICAL FEATURES: - After inoculation, patient may be asymptomatic or develop acute response similar to infectious mononucleosis. Acute response – fever, generalized lymphadenopathy, sore throat, myalgia, diarrhea, maculopapular rash etc. Acute syndrome clears within a few weeks and a variable asymptomatic phase follows which may last for 8 – 10 years. Symptomatic phase – opportunistic infections (pneumonia, CMV, HSV, TB etc) and neoplastic processes (Kaposi sarcoma, Non-Hodgkin’s lymphoma etc). ORAL MANIFESTATIONS : ORAL MANIFESTATIONS Group 1 (lesions strongly associated with HIV): 1. Oral candidal infections - Erythematous - Hyperplastic - Pseudomembranous 2. Hairy leukoplakia 3.HIV associated periodontitis - HIV gingivitis - HIV periodontitis - Necrotizing ulcerative gingivitis - Necrotizing ulcerative stomatitis 4. Kaposi sarcoma 5. Non-Hodgkin’s lymphoma Slide 96: ORAL CANDIDIASIS HIV ASSOCIATED PERIODONTITIS HAIRY LEUKOPLAKIA Slide 97: HIV ASSOCIATED GINGIVITIS NECROTIZING ULCERATIVE GINGIVITIS NECROTIZING ULCERATIVE STOMATITIS Slide 98: Patch stage Plaque stage Nodular stage KAPOSI SARCOMA Slide 99: Group 2 (lesions less commonly associated with HIV): 1. Aphthous ulcers (oropharyngeal region) 2. Idiopathic thrombocytopenia 3. Salivary gland disorders - Dry mouth and decreased salivary flow - Uni or bilateral swelling of major glands 4. Viral infections (apart from EBV) - Cytomegalovirus - Herpes simplex virus - Human papilloma virus - Varicella - zoster virus Slide 100: HIV ASSOCIATED APHTHOUS ULCERS HIV ASSOCIATED HPV INFECTION HIV ASSOCIATED HERPETIC ULCERS DIAGNOSIS : DIAGNOSIS Screening test: ELISA is most commonly used test. But it can show false positive results. Western Blot test: It is a test to detect viral antibodies. More accurate than ELISA. HAIRY LEUKOPLAKIA : HAIRY LEUKOPLAKIA It is a chronic, localized viral infection Caused by Epstein-Barr virus. CLINICAL FEATURES :- Age incidence: Young age Sex incidence: Males Site predilection: Lateral borders of the tongue, bilaterally Signs and symptoms: Asymptomatic, slowly spreading. non scrapable, papillary, greyish white lesion. HISTOLOGICAL FEATURES : HISTOLOGICAL FEATURES Lesion is characterized by hyperparakeratosis and acanthosis. Epithelial cells are infected by EBV which appear as swollen cells with ballooning degeneration. Characteristic pattern of peripheral margination of nuclear chromatin is seen, called nuclear beading. BIBLIOGRAPHY : BIBLIOGRAPHY Shafer WG, Hine MK, Levy BM. A text book of oral pathology. 6th ed. Elsevier, NOIDA, 2009. Neville BW, Damm DD, Allen CM, Bouquot JE. Oral and maxillofacial pathology. 2nd ed. WB Saunders Company. Phil, London, Toronto, 2007. Cawson RA, Odell EW, Porter S. Cawson’s essentials of oral pathology and oral medicine, 7th Ed, Churchill Livingstone, 2002. Regezi JA, Sciubba JJ, Jordan RCK. Oral pathology: Clinical Pathologic Correlations. 4th ed. Saunders Company, 2003. ACKNOWLEDGEMENT: All pictures in the presentation are courtesy of the above mentioned authors. Slide 106: THANKS FOR YOUR PATIENCE ! You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.
infectious diseases in oral pathology drsundeepbhagwath Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 1055 Category: Education License: All Rights Reserved Like it (3) Dislike it (0) Added: October 26, 2010 This Presentation is Public Favorites: 4 Presentation Description No description available. Comments Posting comment... By: bero83 (9 month(s) ago) hi please i want to download this wonderful presantation Saving..... Post Reply Close Saving..... Edit Comment Close By: lsy1989 (13 month(s) ago) hi .......please i need this apresentation .... can i get it but quickly Saving..... Post Reply Close Saving..... Edit Comment Close By: iraqicataloni (14 month(s) ago) thank you very much Saving..... Post Reply Close Saving..... Edit Comment Close Premium member Presentation Transcript BACTERIAL, VIRAL & MYCOTIC INFECTIONSPrepared by:Dr Sundeep S Bhagwath : BACTERIAL, VIRAL & MYCOTIC INFECTIONSPrepared by:Dr Sundeep S Bhagwath BACTERIAL INFECTIONS : BACTERIAL INFECTIONS BACTERIAL INFECTIONS : BACTERIAL INFECTIONS Actinomycosis Syphilis Tuberculosis NOMA Scarlet fever Leprosy Slide 4: VIRAL INFECTIONS Herpes Simplex Virus ( HSV ) Chickenpox Herpes Zoster (Shingles) Herpangina Hand - Foot - Mouth Disease Infectious Mononucleosis (Glandular fever ) Measles Cytomegalovirus infection Acquired Immunodeficiency Syndrome (AIDS) Slide 5: FUNGAL / MYCOTIC INFECTIONS Candidiasis Histoplasmosis Blastomycosis Aspergillosis Toxoplasmosis ACTINOMYCOSIS : ACTINOMYCOSIS Chronic granulomatous, localized bacterial infection. AETIOLOGY :- as a result of infection by Actinomyces israelii, A. viscosus , A. Naeslundi, A.odontolyticus etc. TYPES: - according to location, - Cervicofacial actinomycosis - Thoracic actinomycosis - Abdominal actinomycosis Slide 7: CERVICOFACIAL ACTINOMYCOSIS AETIOLOGY :- as a result of infection by A.israelii , A.viscosus, and A.naeslundi CLINICAL FEATURES :- Age incidence: young adults Sex incidence: More in males Systemic manifestations: Fever , headache , vomiting dysphagia , sore throat and cervical lymphadenopathy Slide 8: Site Predilection: Submandibular, submental and cheek areas most commonly. Bacteria enter through areas of previous trauma like extraction site, periodontal pocket, non vital tooth or infected tonsil. ` : ` Signs & symptoms: Lesion begins as asymptomatic “wooden” firm area of fibrosis and later forms a central, softer area of abscess. Infection can extend to surface and drain via a fistula. Suppurative discharge may contain yellowish flecks which contain colonies of bacteria (sulfur granules) Slide 10: HISTOLOGICAL FEATURES: Characterized by formation of granulation tissue surrounding large collections of PMNL’s and colonies of bacteria. Colonies consist of club shaped filaments that form a radiating rosette pattern. With H & E stain, core of colony stains blue while periphery stains pink. SYPHILIS : SYPHILIS Chronic systemic venereal disease of bacterial etiology causing a granulomatous reaction. AETIOLOGY :- Treponema pallidum TYPES: -Acquired type ; Primary stage Secondary stage Tertiary stage - Congenital type Slide 12: TRANSMISSION: - Direct contact of a healthy patient with a diseased patient or carrier of infection (dentists/dermatologists) Unprotected sexual intercourse Transplacental (from mother to fetus) Contaminated blood or blood products ACQUIRED SYPHILIS - PRIMARY STAGE - : ACQUIRED SYPHILIS - PRIMARY STAGE - It is first stage of acquired type of syphilis Incubation period ranges from 3 – 90 days. Most infective stage Slide 14: CLINICAL FEATURES: - Age incidence: young adults Sex incidence: Males Site predilection: Oral cavity - tongue , hard palate and lips Genital organs of male and female N.B – Lesion of primary syphilis is called CHANCRE. Slide 15: Oral manifestations: Mostly solitary. Appears as painless, normal colored ulcer. Can also manifest as a vascular proliferation resembling a pyogenic granuloma. Genital manifestations: Most commonly external genitalia and anal region. Regional lymphadenopathy Slide 16: Both genital as well as extra genital lesions heal within 3 – 8 weeks if they are left untreated - SECONDARY STAGE - : - SECONDARY STAGE - Occurs 4 – 10 weeks after the initial infection. Lesion can arise before the lesions of primary syphilis have healed. In this stage, systemic symptoms are also seen. This is also a very infective stage. Slide 18: CLINICAL FEATURES: - a) Systemic symptoms: Fever, painless lymphadenopathy, sore throat , malaise, weight loss and musculoskeletal pain. Typically, diffuse, painless, maculopapular rash develops which is widespread and seen even on palmar and plantar areas. Slide 19: b) Oral manifestations: (i) Mucous patches – seen in approx 30% cases. Manifested as focal areas of intense spongiosis of oral mucosa leading to zones of whitish mucosa. (ii) Condyloma latum – appear as papillary lesions resembling viral papillomas. Lesions in secondary stage are usually multiple. Spontaneous resolution occurs within 3 – 12 weeks. - TERTIARY STAGE - : - TERTIARY STAGE - Occurs if the secondary lesion is untreated. Can occur several months to years after the secondary stage has healed. CLINICAL FEATURES: - Symptoms can be grouped as - Neurosyphilis - Cardiovascular syphilis - Diffuse gummatous lesions Slide 21: A. NEUROSYPHILIS: Characterized by infection of central and peripheral nerve tissues which manifests as - General paresis of insane, - Dementia - Tabes dorsalis, leads to ataxia and loss of deep sensations. - Psychosis Slide 22: B. CARDOVASCULAR SYPHILIS: Aneurysm of ascending aorta Stenosis and occlusion of coronary artery. Left ventricular hypertrophy Congestive cardiac failure Slide 23: C. GUMMA: Affects skin, mucosa, soft tissues and even bones. Intraoral – affects palate and tongue mostly. Presents as indurated, nodular / ulcerated lesion which can be associated with large amount of tissue destruction. Slide 24: Diffuse atrophy and loss of papillae from dorsal surface result in “luetic glossitis”. Considered premalignant condition previously, but not supported by recent research. Slide 25: CONGENITAL SYPHILIS Occurs as a result of transplacental transfer after 4th -5th months 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. Slide 26: CLINICAL FEATURES: - Three pathognomonic features described by Sir Jonathan Hutchinson (Hutchinson’s triad) - Hutchinson’s teeth - Interstitial keratitis - Eighth nerve deafness All patients may not exhibit all the features of triad. Slide 27: 1. Hutchinson’s teeth: Alteration of both anterior (Hutchinson’s incisors) as well as posterior teeth (Mulberry molars). Anterior teeth taper cervico-incisally and show a hypoplastic central notch. Molars also show similar tapering with an abnormal occlusal morphology, showing numerous globular projections. Slide 28: 2. Interstitial keratitis: Usually not seen at birth, but develops between 5 – 25 years. Affected eyes shows opacified cornea, with resultant loss of vision. 3. Other alterations: - Eighth nerve deafness - Saddle nose - Saber shin (Anterior bowing of tibia) - High arched palate Slide 29: HISTOLOGICAL FEATURES: - Non specific features. Epithelial surface in primary stage is usually ulcerated and may be either ulcerated / hyperplastic in secondary stage. Underlying CT shows predominantly perivascular inflammatory infiltrate of lymphocytes and plasma cells. Best way to diagnose syphilis is dark field examination of smear of exudate to demonstrate spirochetes. Slide 30: Oral tertiary stage lesions show surface ulceration with peripheral pseudoepithelial hyperplasia. Underlying CT shows foci of granulomatous inflammation with well circumscribed collections of macrophages and multinucleated giant cells. Slide 31: TUBERCULOSIS Chronic granulomatous systemic bacterial disease. Infection caused by Mycobacterium tuberculosis. Incidence decreased dramatically with the discovery of antibiotics in 1940’s. However, incidence increasing alarmingly since 1980’s due to various factors like association with HIV, transmission of TB in crowded or unsanitary environments etc. Slide 32: PATHOGENESIS: - Infection must be distinguished from active disease. Primary infection occurs in previously unexposed persons and almost always in lungs – leading to formation of localized, fibrocalcified nodule. Viable organisms may exist in these nodules and remain dormant for years. Only 5% - 10% patients progress from primary to active disease and immunosupression is often responsible for reactivation of dormant organisms AIDS, old age, poverty and crowded conditions are considered risk factors for progression from primary to secondary disease. Slide 33: TRANSMISSION: - - Inhalation of micro-organisms - Eating or drinking contaminated milk (bovine TB) - Direct contact with body’s fluids like blood , saliva & urine - Blood transfusion - Mother to fetus (transplacental) Slide 34: CLINICAL FEATURES:- 1. Primary TB: Usually asymptomatic. Fever and pleural effusion may occur. 2. Secondary TB: Located in apex of lungs, but can spread to many sites through lymphatics, vascular channels. Symptoms of low grade fever, night sweats, malaise, anorexia and weight loss. Extrapulmonary TB is common and can occur anywhere in body like skin (lupus vulgaris), lymph node (scrofula), bones, kidneys, GIT and head & neck also. Slide 35: ORAL LESIONS OF TB: Mostly manifest as chronic painless ulcer. May also appear nodular, granular or even leukoplakic areas. Primary TB lesions mostly involve gingiva or extraction sites. Secondary TB lesions mostly seen on palate, tongue and lip. Slide 36: Drinking milk contaminated with M.bovis can lead to non tubercular infections of cervical and oropharyngeal lymph nodes, called as Scrofula. Occasionally, significant caseous necrosis can occur and form numerous fistulas through overlying skin. Slide 37: HISTOLOGICAL FEATURES: - Classic presentation – formation of granuloma. Circumscribed collection of epitheloid macrophages, lymphocytes and langhan’s giant cells often with central caseous necrosis. Demonstration of M.tuberculosis is by acid – fast stains like Zeihl – Neelsen stain. Slide 38: CANCRUM ORIS Acute, rapidly progressing, localized, bacterial infection of the orofacial tissues and jaws Causative organisms – Fusobacterium necrophorum, F.nucleatum and Prevotella intermedia. Predisposing factors include poverty, malnutrition, poor oral hygiene & sanitation, recent illness, malignancy and immunodeficiency states like AIDS. Slide 39: CLINICAL FEATURES: - Age incidence: Predominantly children between 1 – 10 years. Sex incidence: Male Site predilection: Usually begins on gingivae as ANUG, then spreads facially / lingually to adjacent soft tissues. Slide 40: Signs & symptoms: Disease begins initially in gingivae as ANUG and later spreads to adjacent soft tissues. As necrosis extends deeper over next few days, zones of bluish-black discoloration of overlying skin develop. These zones break down into areas of yellowish necrosis that spread into adjacent bone. Other signs – fever, fetid odor, pain, malaise and regional lymphadenopathy. MYCOTIC INFECTIONS : MYCOTIC INFECTIONS Slide 42: CANDIDIASIS Refers to infection with yeast like fungal organism. Most common oral fungal infection. It is a component of normal oral flora. Can occur in persons who are debilitated by other diseases or in otherwise healthy individuals also. Slide 43: PREDISPOSING FACTORS: - a) Local Factors : - Mucosal trauma - Denture wearers - Denture hygiene - Tobacco smoking - Carbohydrate rich diet - Drugs (Broad spectrum antibiotics, steroids, immunosuppressant / cytotoxic agents) - Xerostomia Slide 44: b) Systemic factors : - Iron deficiency anaemia - Megaloblastic anaemia - Acute leukaemia - Diabetes mellitus - HIV infection - Other immunodeficiency states CLASSIFICATION OF CANDIDIASIS: - : CLASSIFICATION OF CANDIDIASIS: - Group 1 (Conditions confined to the oral mucosa): Acute - - Acute pseudomembranous candidiasis - Acute atrophic candidiasis Chronic - - Chronic atrophic candidiasis - Candida associated angular cheilitis - Chronic hyperplastic candidiasis Group 2 (oral manifestations of generalized candidiasis) - Chronic mucocutaneous candidiasis ACUTE PSEUDOMEMBRANEOUS CANDIDIASIS (THRUSH ) : ACUTE PSEUDOMEMBRANEOUS CANDIDIASIS (THRUSH ) Best recognized form of candidiasis. Characterized by development of white plaques that can be scraped off with tongue blade. Can be initiated by broad spectrum antibiotics or immune dysfunction. Slide 47: Occurs characteristically on buccal mucosa, palate and dorsal tongue. Usually asymptomatic or patients may c/o burning sensation of mucosa or unpleasant taste in mouth. Can occur in infants also. ATROPHIC CANDIDIASIS(Erythematous candidiasis) : ATROPHIC CANDIDIASIS(Erythematous candidiasis) Several presentations seen – 1. Acute atrophic candidiasis 2. Median rhomboid glossitis 3. Chronic multifocal candidiasis 4. Angular cheilitis 5. Chronic atrophic (denture sore mouth) candidiasis Slide 49: 1. ACUTE ATROPHIC CANDIDIASIS: - Also called “antibiotic sore mouth”, as it follows course of broad spectrum antibiotics. Patients c/o burning sensation of mucosae. Seen as diffuse loss of filliform papillae resulting in a bald appearance of tongue. Slide 50: 2. MEDIAN RHOMBOID GLOSSITIS: Also called central papillary atrophy of tongue. Well demarcated erythematous zone affecting midline of dorsum of tongue. Often asymptomatic. Erythema due to loss of filliform papillae. Sometimes, other areas of oral cavity like hard palate and angles of mouth also show lesions (Chronic multifocal candidiasis). Slide 51: 3. CHRONIC ATROPHIC CANDIDIASIS: - Characterized by varying degrees of erythema in denture bearing areas of usually maxillary prostheses. Usually asymptomatic. Patients give h/o wearing denture continuously. Slide 52: 4. ANGULAR CHEILITIS: - Also called perleche. Characterized by erythema, fissuring and scaling of corners of mouth. Typically occurs either along with multifocal candidiasis or in old patients with reduced vertical dimension. Saliva pools in these areas, keeping them moist and thus favoring fungal infection Slide 53: 5. CHRONIC HYPERPLASTIC CANDIDIASIS: Least common of all types. Appears as non scrapable white patch resembling leukoplakia (candidal leukoplakia) Believed that it represents candidiasis superimposed on pre-existing leukoplakia. Diagnosis confirmed by demonstration of candidal hyphae within the lesion and resolution of lesion after antifungal therapy. Slide 54: CHRONIC MUCOCUTANEOUS CANDIDIASIS: - Severe oral candidiasis can also occur as a component of a rare immunological disorder called mucocutaneous candidiasis. Autosomal recessive disorder. Immune dysfunction becomes evident in early life – patient develops candidiasis of mouth, nails, skin and other mucosae. Oral lesions appear as thick, white non scrapable patches. Slide 55: HISTOLOGICAL FEATURES: - 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. Candidal hyphae can be seen embedded in parakeratin layer and superficial spinous layer. Slide 56: EXFOLIATIVE CYTOLOGY: - Candidal hyphae can also be demonstrated by exfoliative cytology by PAS stain. Hyphae are stained magenta color by the PAS stain. RAPID DIAGNOSTIC TEST: - A 10% - 20% KOH preparation used for rapid diagnosis. KOH lyses background of epithelial cells allowing yeast and hyphae to be seen. VIRAL INFECTIONS : VIRAL INFECTIONS Slide 58: Herpes simplex infection Varicella Herpes zoster Infectious mononucleosis Enterovirus infections - Herpangina - Hand foot & mouth disease - Rubeola & Rubella - HIV HERPES SIMPLEX INFECTION : HERPES SIMPLEX INFECTION Herpes simplex virus (HSV) – DNA virus. Belongs to human herpesvirus (HHV) family, also called Herpetoviridae. Other members of this family are varicella-zoster virus, Epstein-Barr virus, Cytomegalovirus etc. Humans – only known natural reservoirs and can stay in the host for life and become periodically reactivated. TYPES OF HSV : TYPES OF HSV Herpes simplex virus – 1: Spread through saliva. Lesions above the waist, in oral, facial and ocular areas including pharynx, and skin. Herpes simplex virus – 2: Transmitted through sexual contact. Involves genitalia and skin below the waist. PATHOGENESIS : PATHOGENESIS HSV infections – 2 patterns seen. 1. Primary infection: - - Initial exposure to virus, no antibodies are produced. - Occurs in young age, often asymptomatic. - Virus taken up in sensory nerves and transported to associated ganglia. Slide 62: 2. Secondary / recurrent infection: - - Virus residing in ganglia is reactivated. - Not always symptomatic; sometimes patients only shed the virus through saliva. Predisposing factors for reactivation of virus: Old age UV light Emotional stress Trauma Menstruation Systemic diseases or malignancy Slide 63: HERPETIC GINGIVOSTOMATITIS Commonest pattern of primary HSV infection. Incubation period is 3 – 9 days. CLINICAL FEATURES: - Age incidence: 6 months – 5 years Sex incidence: Nil Site predilection: Affects movable and immovable mucosae. Primarily gingiva, labial mucosa, vermilion zone, palate. Slide 64: Signs & symptoms: Prodromal symptoms – fever with chills, nausea, anorexia and cervical lymphadenopathy. Begins as small pinhead size vesicles which coalesce and form numerous red lesions. In all cases, gingiva red, enlarged and painful. Lip lesions can extend to vermilion zone RECURRENT HERPES LABIALIS : RECURRENT HERPES LABIALIS Can occur either at primary site or in adjacent areas. Commonest sites – vermilion zone and adjacent area of lips. Multiple, small, erythematous papules develop and form clusters of fluid filled vesicles. Vesicles rupture and crust within 2 – 3 days and heal within 7 days. HERPETIC WHITLOW : HERPETIC WHITLOW Less common presentation. Infection of fingers, and thumb. Occurs due to self inoculation in children with orofacial HSV. Can also occur in medical and dental professionals who do not wear gloves and come in contact with infected patients. Slide 67: HISTOLOGICAL FEATURES: - Main effect of virus on epithelial cells. Infected epithelial cells show acantholysis, nuclear enlargement and ballooning degeneration. Nuclear fragmentation with condensation of chromatin around periphery of nucleus. These cells called – Tzanck cells. Fusion of adjacent degenerated cells – multinucleated infected cells. Intercellular edema – formation of intraepithelial vesicle. Slide 68: DIAGNOSIS: - Commonly used diagnostic procedures – cytological smear and tissue biopsy. Cytosmear is best as it is the least invasive and cost effective. Histological changes also are characteristic and only VZV produces similar changes within epithelium, but it can be differentiated easily from HSV. VARICELLA (Chickenpox) : VARICELLA (Chickenpox) VZV is similar to HSV in many respects. Chickenpox represents primary infection with VZV. Herpes zoster or Shingles represents reactivation of the latent VZV residing within the ganglia. VZV spreads through droplets or direct contact with infected persons. Incubation period is 10 – 21 days. Slide 70: CLINICAL FEATURES: - Age incidence: between 5 – 9 years. Sex incidence: Nil Site predilection: Face, trunk and extremities. Prodromal symptoms: - Fever - Malaise - Pharyngitis - Nausea - Anorexia - Headache Slide 71: Signs & symptoms: All lesions pass through phases of erythema, vesicle, pustule and crusting. Vesicle is surrounded by zone of erythema. In contrast to HSV, vesicles continue to erupt for 3 – 4 days. Thus, old crusted lesions are mixed with new vesicles. Infected persons are contagious from 2 days before appearance of vesicles until all vesicles crust. Slide 72: Oral manifestations: - Oral lesions are common and may precede skin lesions. Common sites – palate and buccal mucosa. Oral lesions begin as 3 -4 mm opaque white vesicles that rupture to form 1 – 3 mm ulcers. VZV oral lesions can be distinguished easily from HSV as VZV lesions are rarely painful. Slide 73: COMPLICATIONS: - 1.Children: - Secondary skin infections - Encephalitis - Pneumonia 2. Adults: - Varicella pneumonitis - Encephalitis - Pneumonia - Early pregnancy involvement may cause abortion or congenital defects. Slide 74: DIAGNOSIS: - H/o exposure to VZV within last 3 weeks. Characteristic vesicles. Demonstration of cytopathological changes within epithelial cells harvested from vesicular fluid. HERPES ZOSTER(Shingles) : HERPES ZOSTER(Shingles) The primary VZV infection is transported up the sensory nerves and remains latent within the dorsal spinal ganglia. Herpes zoster infection occurs by reactivation of the VZV. Unlike HSV, there is usually a single recurrence. Slide 76: PREDISPOSING FACTORS: - Immunosupression Treatment with cytotoxic drugs Radiation Presence of malignancy Alcohol abuse Dental manipulation Slide 77: CLINICAL FEATURES: - Age incidence: Middle age to old age Sex incidence: Nil Site predilection: Affects areas of skin innervated by the affected sensory nerve (dermatome). Slide 78: Signs & symptoms: Viral infection proceeds in three phases – prodromal, acute and chronic A. Prodromal: Virus replicates within ganglia, causing ganglionitis resulting in severe neuralgia (responsible for pain preceding the rash) As virus travels down the nerve, pain intensifies. Pain is accompanied by fever, malaise and headache 3 – 4 days before cutaneous / mucosal lesions develop. Typically one dermatome is affected, but two or more also can be affected Slide 79: B. Acute phase: 1 – 4 days after prodromal phase, affected skin develops clusters of vesicles on erythematous base. Within 3 – 4 days, they become pustular, ulcerate and begin to crust after 7 – 10 days. Lesion develop along the path of distribution of sensory nerve and terminate at midline. Resolution occurs within 2 – 3 weeks and usually heal by scarring. Slide 80: Oral manifestations: Oral lesion occur if trigeminal nerve involved. May occur on movable or bound mucosa. Like chickenpox, lesions appear as 1–4 mm white, opaque vesicles which rupture, forming shallow ulcers. RAMSAY HUNT SYDROME – combination of cutaneous lesions of external acoustic meatus, facial paralysis, hearing deficit and vertigo. Slide 81: DIAGNOSIS: - Clinical presentation is typical. Viral culture (takes at least 24 hours). Cytosmear to demonstrate cytopathological viral effects. Direct staining of cytosmear with fluorescent antibodies for VZV. INFECTIOUS MONONUCLEOSIS(Glandular fever) : INFECTIOUS MONONUCLEOSIS(Glandular fever) Results from exposure to Epstein-Barr virus (EBV). Transmission – intimate contact like kissing, sharing of straws, contaminated salivary transmission in children. Exposure during childhood – asymptomatic. Symptomatic infections arise in young adults. Slide 83: CLINICAL FEATURES; - Age incidence: children Sex incidence: Nil Site incidence: Apart from systemic manifestations, affects anterior and posterior cervical chain lymph nodes as well as oropharyngeal tonsils. Intra oral – hard palate and gingiva. Slide 84: Signs & symptoms: 1. Systemic = Fever, lymphadenopathy,, pharyngitis, rhinitis, cough, hepatosplenomegaly. In 90% cases, prominent, symmetric, tender enlargement of anterior and posterior cervical chain lymph nodes. 2. Oral = Petechiae on hard or soft palate and enlargement of oropharyngeal tonsils. Slide 85: DIAGNOSIS: - Diagnosis is suggested by clinical presentation WBC count is raised with differential count showing lymphocytosis as high as 70% - 90%. Classical serological finding – presence of Paul – Bunnell heterophil antibody, present in 90% of affected patients. RUBEOLA : RUBEOLA Rubeola / Measles is a viral infection produced by paramyxovirus. Incidence dramatically reduced since use of measles vaccine. Incubation period – 10 to 12 days CLINICAL FEATTURES: - Age incidence: Young children Sex incidence: Nil Site predilection: Face, trunk and extremities. Slide 87: Signs & symptoms: Most cases arise in spring and spread through respiratory droplets. Prodromal symptoms of fever, malaise, coryza and cough. Rash appears after a few days and lasts for 4 – 7 days with first appearance on face followed by trunk and extremities. Slide 88: Oral manifestations: Multiple areas of mucosal erythema on labial and buccal mucosa and soft palate (Koplik’s spots). Within these areas, bluish white macules may be seen. These spots represent areas of epithelial necrosis. Slide 89: COMPLICATIONS: - Otitis Pneumonia Persistent bronchitis Diarrhea Encephalitis HERPANGINA : HERPANGINA Caused by coxackievirus A or B or echoviruses – all these belong to enterovirus family. CLINICAL FEATURES: - Age incidence: Children & young adults. Sex incidence: Nil Site predilection: Primarily systemic disease, with oral lesions mainly in soft palate and tonsillar regions. Slide 91: Signs & symptoms:: Begins with significant sore throat, dysphagia and fever. Occasionally, vomiting, myalgia and headache. Oral lesions begins as 2-4 mm sized, red macules which form fragile vesicles that rapidly ulcerate. Systemic symptoms subside within a few days and ulcers heal within 7 – 10 days. ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS) : ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS) More than 25 million cases worldwide. Considered almost 100% fatal and no known vaccine developed so far. ROUTES OF TRANSMISSION: - Sexual contact Infected blood / blood products Intravenous drug abuse Transplacental transfer Slide 93: PATHOGENESIS: - When virus enters the body, its DNA incorporated into primary target cell i.e. CD4+ helper T lymphocyte. Similar to other viral infections, antibodies to virus are formed but are not protective. Virus can remain silent or cause cell death, as a result, decrease in helper T- cells occurs, leading to loss in immune function. There is an asymptomatic stage lasting for about 8 – 10 years after which the final symptomatic stage develops. Slide 94: CLINICAL FEATURES: - After inoculation, patient may be asymptomatic or develop acute response similar to infectious mononucleosis. Acute response – fever, generalized lymphadenopathy, sore throat, myalgia, diarrhea, maculopapular rash etc. Acute syndrome clears within a few weeks and a variable asymptomatic phase follows which may last for 8 – 10 years. Symptomatic phase – opportunistic infections (pneumonia, CMV, HSV, TB etc) and neoplastic processes (Kaposi sarcoma, Non-Hodgkin’s lymphoma etc). ORAL MANIFESTATIONS : ORAL MANIFESTATIONS Group 1 (lesions strongly associated with HIV): 1. Oral candidal infections - Erythematous - Hyperplastic - Pseudomembranous 2. Hairy leukoplakia 3.HIV associated periodontitis - HIV gingivitis - HIV periodontitis - Necrotizing ulcerative gingivitis - Necrotizing ulcerative stomatitis 4. Kaposi sarcoma 5. Non-Hodgkin’s lymphoma Slide 96: ORAL CANDIDIASIS HIV ASSOCIATED PERIODONTITIS HAIRY LEUKOPLAKIA Slide 97: HIV ASSOCIATED GINGIVITIS NECROTIZING ULCERATIVE GINGIVITIS NECROTIZING ULCERATIVE STOMATITIS Slide 98: Patch stage Plaque stage Nodular stage KAPOSI SARCOMA Slide 99: Group 2 (lesions less commonly associated with HIV): 1. Aphthous ulcers (oropharyngeal region) 2. Idiopathic thrombocytopenia 3. Salivary gland disorders - Dry mouth and decreased salivary flow - Uni or bilateral swelling of major glands 4. Viral infections (apart from EBV) - Cytomegalovirus - Herpes simplex virus - Human papilloma virus - Varicella - zoster virus Slide 100: HIV ASSOCIATED APHTHOUS ULCERS HIV ASSOCIATED HPV INFECTION HIV ASSOCIATED HERPETIC ULCERS DIAGNOSIS : DIAGNOSIS Screening test: ELISA is most commonly used test. But it can show false positive results. Western Blot test: It is a test to detect viral antibodies. More accurate than ELISA. HAIRY LEUKOPLAKIA : HAIRY LEUKOPLAKIA It is a chronic, localized viral infection Caused by Epstein-Barr virus. CLINICAL FEATURES :- Age incidence: Young age Sex incidence: Males Site predilection: Lateral borders of the tongue, bilaterally Signs and symptoms: Asymptomatic, slowly spreading. non scrapable, papillary, greyish white lesion. HISTOLOGICAL FEATURES : HISTOLOGICAL FEATURES Lesion is characterized by hyperparakeratosis and acanthosis. Epithelial cells are infected by EBV which appear as swollen cells with ballooning degeneration. Characteristic pattern of peripheral margination of nuclear chromatin is seen, called nuclear beading. BIBLIOGRAPHY : BIBLIOGRAPHY Shafer WG, Hine MK, Levy BM. A text book of oral pathology. 6th ed. Elsevier, NOIDA, 2009. Neville BW, Damm DD, Allen CM, Bouquot JE. Oral and maxillofacial pathology. 2nd ed. WB Saunders Company. Phil, London, Toronto, 2007. Cawson RA, Odell EW, Porter S. Cawson’s essentials of oral pathology and oral medicine, 7th Ed, Churchill Livingstone, 2002. Regezi JA, Sciubba JJ, Jordan RCK. Oral pathology: Clinical Pathologic Correlations. 4th ed. Saunders Company, 2003. ACKNOWLEDGEMENT: All pictures in the presentation are courtesy of the above mentioned authors. Slide 106: THANKS FOR YOUR PATIENCE !