Herpes Simplex Virus Infection
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FUNGI VIRUS BACTERIA DISEASE The oral focal infection theory • A concept generally negleted for several decades, is controversial yet has gained renewed interest with progress in clasification and identification of oral microorganisms. • Additionally, recent evidence associating dental with artherosclerosis and other chronic disease has also helped resurrect the focal infection theory Pathways of infection arising from oral bacteria The three pathway that may link oral bacteria to secondary disease distant from the oral nidus are : 1. Metastatic infection attributable to transient bacteria in the blood 2. Metastatic immunologic injury 3. Metastatic toxic injury The scientific evidence weak a it is best supports of first pathway of transient bacteriemias of oral origin Mechanical prosthetic valve (arrow) Odontogenic infection Caries dental pulpitis Necrosis of the pulp pulp polyp Periapical abscess Periodontal infection Periodontal abscess Gingivitis ANUG Salivary infection Mucositis Recurent Apthous Stomatitis Minor RAS Mayor Fungal infection • Are oral fungal infections common ? • No, most are associated with an underlying systemic condition immunosuppression imunodeficiency syndrome cancer therapy anemia diabetes uremia leukemia • Patients who have conditions that modify the normal oral environment are at increased risk of fungal infection Among these individuals are patients with _ xerostomia _ have taken broad spectrum antibiotics Diagnosis of oral fungal infection based on : • History • Clinical appearance • Culture • Potassium hydroxide preparation • Biopsy • What is the most common fungal infection to affect the mouth? • Oral candidiasis caused by Candida Albicans What is the typical clinical presentation of oral candidiasis ? • Pseudomembranous candidiasis • Hyperplastic candidiasis • Erythematous candidiasis • Angular cheilitis Pseudomembranous candidiasis ( Thrush ) • Most typical clinical presentation of the infection • White, cottage cheesy-looking raised lesions • Most often of tongue or palate • Can be scrapped off, leaving a painful, raw bleeding base Hyperplastic Candidiasis • Less common • As area leukoplakia at corners of the mouth or the cheeks • Unlike pseudomembranous forms, these lesions cannot be scraped off Erythematous Candidiasis • Most often present on the dorsal surface or edges tongue and palate • The degree of mucosal erythema may be variable • Patients with this form of candidiasis often complain of a burning mouth Angular cheilitis Viral infection • Are viral infections of the mouth common or rare ? Viral infections are among the most common causes of oral lesions Symptoms of acute viral infections that affects the mouth • Vesicles or rupture small ulcers • History suggesting viremia : fever, malaise, myalgia, upper respiratory symptoms, anorexia • Pain associated lesions Group of viruses for most oral infections: • HS type 1,2 • Varicella-zoster virus • The epstein-barr virus • Cytomegalovirus • Herpes virus 6,7,8 ( infectious in immunocompromisefd patient HIV HAS BEEN ISOLATED FROM BODY FLUIDS : HUMAN BLOOD. SEMEN VAGINAL SECRETIONS. BREAST MILK. TEARS. URINE. SALIVA. CEREBROSPINAL FLUID. AMNIOTIC FLUID. SAN FRANSISCO, AUG. 17, 1990 : I. CANDIDIASIS. A. Pseudomembranous candidiasis. B. Erythematous candidiasis. C. Angular cheilitis. II. GINGIVITIS / PERIODONTITIS. A. HIV – associated gingivitis. B. HIV – associated periodontitis. III. NECROTIZING STOMATITIS. IV. HERPES SIMPLEX. A. Intra oral form. B. Perioral form. V. CYTOMEGALOVIRUS. VI. VARICELLA – ZOSTER VIRUS VII. APHTHOUS ULCERATION. A. Minor. B. Mayor. C. Herpetiform. VIII. HAIRY LEUKOPLAKIA. IX. HIV SALIVARY GLAND DISEASE. X. ORAL KAPOSI SARCOMA. XI. ORAL WARTS / PAPILOMA. A. Papilloma. B. Focal epithelial hyperplasia. TREATMENT OF THE ORAL LESIONS ASSOCIATED WITH HIV INFECTION. CONDITION THERAPY I. Candidiasis Antifungal (topical and / or systemic). II. HIV- associated Plaque removal, debri- gingivitis dement, chlorhexidine, povidone iodine. CONDITION THERAPY HIV- associted Plaque removal, debri- periodontitis dement, chlorhexidine, metronidazole. Necrotizing sto- Debridement, chlorhe- matitis xidine, metronidazole. III. Herpes simplex If not self limiting, if prolonged, if frequen- tly recurrent acyclo- vir. IV. Herpes zoster Oral Acyclovir. CONDITION THERAPY V. Aphthous ulcer Topically steroid VI. Hairy leukoplakia Usually no treatment, severe acyclovir VII. Kaposi sarcoma Excision, laser, radia- tion, chemotherapy VIII. Oral wart Excisison, laser IX. Xerostomia Salivary stimulation, artificial saliva. HIV • The main targets for the virus are cells expressing the CD4 membrane reseptor, such as T4 helper lymphocyte, macrophages and monocyte • Viral replication occures within the CD4 cel, leading to its destruction and loss of function. As a result the number of CD4 cell declines, and the patient become at high risk for opportunistic infections. Many medication used to treat HIV have side effect • Abacavir oral ulceration • Flycotsine myelosuppression • Foscarnet ou &m • Ganciclovir m • Hydroxyurea ou • Interferon xerostomis,metallic taste & m • Lopinavir u & x • Pentamidine mt • Rifampin salivary discoloration • Ritonavir perioral paresthesia • Saquinavir p, neutropenia, thrombocytopenia • TMP/SMZP myelosup,ou, glositis • Dideoxycytidine my & ou Zidovudine Neutropenia VIRUS Viral infection causing, or associated with diseases of the oral mucosa : VIRUS PENYAKIT Herpes Simpleks 1 & Primary Gingivostomatitis 2 Herpetica Herpes Labialis Recurrent Herpes Intra Oral Recurrent Herpetic Whitlow Varicella - Zoster Chickenpox Herpes Zoster Coxsakie A Herpangina Hand, foot and mouth disease Viral infection causing, or associated with diseases of the oral mucosa : VIRUS PENYAKIT Cytomegalovirus Salivary gland disease Epstein Barr Hairy leukoplakia Virus Paramyxovirus Measles Papilomavirus Viral warts H I V Manifestasi oral HIV HERPES SIMPLEX VIRUS INFECTION Family herpesviridae ∗ Herpes simplex virus ––– 111 ∗ Herpes simplex virus –––222 ∗ Cytomegalovirus ∗ VaricellaVaricella----zosterzoster virus ∗ Epstein Barr virus ∗ Human herpes virusvirus----6666 ∗ Human herpes virusvirus----7777 ∗ Human herpes virusvirus----8888 Herpes Simplex virus –––111 ⇒⇒⇒ perioral, eyes Herpes Simplex virus –––222 ⇒⇒⇒ genitals TRANSMISSION : 1. Airbone droplets 2. Intimate contact HERPES SIMPLEX VIRUS INFECTION PRIMARY RECURRENT INFECTION INFECTION PRIMARY HSV-1 INFECTION : ---Seronegative for HSV ---Children, young adult --- Does not imply clinical signs & symptoms ⇒⇒⇒ subclinical ---Incubation periode : several days ––– 2 weeks --- ⇒⇒⇒ Primary Gingivostomatitis Herpetica ⇒⇒⇒ Herpetic Whitlow PRIMARY GINGIVOSTOMATITIS HERPETICA. CLINICAL APPEARANCES : ---Prodromal symptoms : fever, malaise, nausea, headache, lymphadenopathy. ---Vesicle →→→ rupture →→→ round/oval ulcers, shallow, greygrey----whitewhite pseudomembrane, surrounded by erythema area. ---Ulcers can coalescent →→→ large ulcers. ---Pain, disorders of swallowing, eating, secondarily infected. ---Location: any intra oral. ---Acute gingivitis marginalis →→→ gingiva are swollen with red edges that bleed easily. ---Heal : 10 –––12 days →→→ self limiting disease, without scar. Treatment : Goals : 1. To shorten the current attack. 2. To prevent recurrences. Medications : ♥♥♥ Analgesics. ♥♥♥ Vitamin. ♥♥♥ Anaesthetic topical. ♥♥♥ Antivirus. RECURRENT HSV INFECTION : ---Affect 20 40% 0f adult population. ---Antibody for HSV was present. ---Reactivation of latent virus by trigger factors. --- ⇒⇒⇒ Recurrent Herpes Labialis ⇒⇒⇒ Recurent Herpes Intra Oral ⇒⇒⇒ Herpetic Whitlow. RECURRENT HERPES LABIALIS. CLINICAL APPEARANCES : ---Prodromal symptoms : mild fever, tingling, burning or pain in which lesions will appear. --- Vesicles on the vermillion border of lip →→→ rupture →→→ shallow ulcer. ---Yellow crust formation. ---Problems : pain, cosmetic disfigurement, psychosocial effect. ---Heal : 1 –––2 weeks without scar. ---Recurrences is variable. RECURRENT HERPES INTRAORAL. CLINICAL APPEARANCES : ---Prodromal symptoms →→→ mild. ---Vesicles →→→ rupture →→→ ulcers. --- Intraorally. Recurrent Herpes Labialis maybe seen concurently with the intraoral lesions or they occur alone. VARICELLA –––ZOSTER VIRUS ⇒ DNA untai ganda ⇒ Neurotropic ⇒ Penularan : kontak langsung, infeksi droplet. ⇒⇒⇒ Infeksi primer dan rekuren ⇒⇒⇒ bersifat laten Varicella – zoster virus PRIMARY INFECTION RECURRENT INFECTION CHICKENPOX / HERPES ZOSTER / VARISELA SHINGLES HERPES ZOSTER : Clinical appearancess : - Gejala prodromal : parastesi, gatal, rasa terbakar, nyeri di daerah dermatom yg terlibat. - Dermatom yg terlibat : T5, C3, L1, L2, s. trigeminal ---Ruam makulopapular →→→ vesikel →→→ ulser dengan dasar eritematus →→→ krusta. - Distribusi unilateral. - Intra oral : vesikel →→→ ruptur →→→ ulkus. ∗∗∗ Cab. Maksilaris : palatum lunak, mukosa bibir atas, uvula mukosa pipi. ∗∗∗ Cab. Mandibularis : lidah, gimngiva, mukosa bibir bawah. TREATMENT : ---Bed rest. ---Local applications of heat. --- Topical anesthetic. ---Antiviral. ---Analgesics. ---tranquilizers. ORAL CANDIDIASIS A SUPERFICIAL INFECTION OF ORAL MUCOUS CAUSED BY THE YEASTLIKE FUNGUS CANDIDA ALBICANS FACTORS PREDISPOSING TO ORAL CANDIDIASIS : LOCAL FACTORS SYSTEMIC FACTORS Denture wearing Physiological Old age, infancy, pregnancy Saliva Endocrine disorders Xerostomia, low pH Diabetes Melitus Commensal flora Nutritional deficiencies Iron, folate, vit.B 12 HighHigh----carbohydratecarbohydrate diet Malignancies Leukemia Smoking tobacco Immune defects HIV / AIDS Drugs / medication