Bacterial, Viral & Mycotic Infections

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  • This is real take it serious, who will believe that a herb can cure herpes, i navel believe that this will work i have spend a lot when getting drugs from the hospital to keep me healthy, what i was waiting for is death because i was broke, one day i hard about this great man who is well know of HIV and cancer cure, i decided to email him, unknowingly to me that this will be the end of the herpes in my body, he prepare the herb for me, and give me instruction on how to take it, at the end of the one month, he told me to go to the hospital for a check up, and i went, surprisingly after the test the doctor confirm me negative, i thought it was a joke, i went to other hospital was also negative, then i took my friend who was also herpes positive to the Dr Agumagu, after the treatment she was also confirm negative . He also have the herb to cure cancer. please i want every one with this virus to be free, that is why am dropping his email address, agumaguspelltemple@outlook.com or agumaguspelltemple@gmail.com do email him he is a great man. the government is also interested in this DR, thank you for saving my life, and I promise I will always testify for your good work call his number +233200116937..
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  • Hello I’m mariana james by name, I’m giving a testimony about Dr. Asein the great Herbalist, he has the cure to all manner of diseases, he cured my HIV disease, though I went through different website I saw different testimonies about different herbalists, I was like: “Many people have the HIV cure why are people still suffering from it?” I though of it, then I contact Dr. Asein via email, I didn’t believe him that much, I just wanted to give him a try, he replied my mail and Needed some Information about me, then I sent them to him, he prepared the CURE and sent it to me via UPS courier service, they told me that it will take 3-4 days before I’ll get the parcel, 3 days later I received the package and I started taking the medicine as prescribed by him, after 7 days of taking the medicine I went for check-up, I was tested HIV NEGATIVE… I’M GOING TO ASSIST ANYBODY THAT CONTACT HIM FOR HELP, IF YOU ARE SERIOUS YOU WILL BE CURED!!! contact him via: dr.aseinherbalhome@gmail.com or call him on +2348163904713.
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  • very infomative.good collection of slides
    Dr.N.P.Viswanathan
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Bacterial, Viral & Mycotic Infections

  1. 1. BACTERIAL, VIRAL & MYCOTIC INFECTIONS Prepared by: Dr Sundeep S Bhagwath
  2. 2. BACTERIAL INFECTIONS
  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>
  41. 41. MYCOTIC INFECTIONS
  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>
  57. 57. VIRAL INFECTIONS
  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>
  96. 96. ORAL CANDIDIASIS HIV ASSOCIATED PERIODONTITIS HAIRY LEUKOPLAKIA
  97. 97. HIV ASSOCIATED GINGIVITIS NECROTIZING ULCERATIVE GINGIVITIS NECROTIZING ULCERATIVE STOMATITIS
  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>
  100. 100. HIV ASSOCIATED APHTHOUS ULCERS HIV ASSOCIATED HPV INFECTION HIV ASSOCIATED HERPETIC ULCERS
  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>
  104. 105. THANKS FOR YOUR PATIENCE !

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