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Infectious diseases : PowerPoint Presentation
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Infectious diseases :

Infectious diseases :

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Infectious diseases :

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  1. Infectious diseases: Fungal Diseases Viral Diseases Bacterial Diseases

  2. Syphilis • It is sexually transmitted granulomatous disease . • It is an infectious disease caused by Treponemapallidum • It is ch.ch by systemic manifestations • It appears in 3 stages: 1- Primary Syphilis(chancer) 2- Secondary Syphilis (mucous patches ). 3- Tertiary Syphilis (gumma)

  3. Ddiagnosis • Dark field microscopic exam. Of smear of genital lesion shows: (Treponemapallidium) • A blood test is the most common way to determine syphilis. (Wasserman reaction)

  4. Primary Syphilis After infection, an ulcerated lesion called a primary chancre is formed. It affects the lip. It is a painlessflat, raised margin, indurated, highly infectious ulcer with a serous Exudate. - regional lymph nodes are enlarged, firm, painless, and discrete, with a rubbery consistency. The chancre disappears spontaneously within 3 to 8 weeks.

  5. Primary Syphilis Less typical due to moisture, trauma & microbial flora. The ulcer is: Slightly painful, raised margin, covered with white film It affects the Tongue and, to a lesser extent, tIntra oral lesion: he gingivae

  6. Pimary syphilis The differential diagnosis of chancre includes: ruptured vesicles of herpes simplex, traumatic ulcers. Squamous cell carcinoma carcinoma

  7. Secondary Syphilis The signs of secondary syphilis are variable: 1- systemic symptoms including fever, headache, malaise, and general ache. 2-Acute pharyngitis. 3- generalized skin eruption. The skin lesions are found on the face, hands, feet, and genitalia and appears as dull red macular or papular spots. 4- generalized lymphadenopathy 5-Condyloma latum ,papule that erodes moist surface (genital lesion)

  8. Secodary syphilis Mucous patches mucous patches :white, glistening patches on the tongue, soft palate, tonsiland cheek (common site). The surface of these lesions is covered with a grayish membrane, which can be easily removed and contains spirochetes. It is highly infectious. The ulcers may coalesce gives (snail tracks )

  9. Tertiary Syphilis • It appears 10–30 years after infection began. In this stages, the disease damages the internal organs, including the brain, nerves, eyes, heart, blood vessels, liver and bones. • This damage can result in death.

  10. Tertiary Syphilis The lesion of this stage is called Gumma • It is localized, single or multiple granuloma, of varying in size .It breaks down to form deep ulcer. • It affects skin. Other organs involved are the cardiovascular and the nervous system

  11. Tertiary Syphilis Oral manifestations: Gumma occurs in tongue, palate. It is Rubbery in consistency, then it ulcerates. Ulcer is solitary, deep, punched out, painless and may perforate the palate, These lesions are not infective syphilitic osteomyelitis involving the mandible may occur.

  12. Teriary syphilis Atrophic or interstitial glossitis is another oral manifestation of tertiary syphilis. Clinically, there is atrophy of the filiformand fungiform papillae.

  13. Congenital Syphilis T. pallidiumcross the placental barrier. Fetus may be infected from a syphilitic mother The disease appears as: Early manifestations: (in the first 2 years) Rashes, saddle nose,, and meningitis late infection: after the second year of age: Hutchinson’s inscisors. mulberry molar. bone lesions: underdeveloped maxilla, saddle nose. Childhood gumma.

  14. Congenital SyphilisThe dental lesions of congenital syphilis As a result of infection of the developing tooth germ by T.pallidium. The permanent teeth affected. Hutchinson’s incisor The upper central incisors have crescent notches in the middle of their incisal edge. The tooth tends to be wider gingivally than at the incisaledge, ‘screwdriver’ appearance

  15. Congenital syphilis ‘mulberry molar’ The first permanent molar teeth are involved They have roughened, dirty, yellow, hypoplastic, occlusal surfaces with poorly developed cusps

  16. Differential Diagnosis Primary and secondary syphilis include candidiasis, leukoplakia, hairy leukoplakia, lichenplanus, aphthous ulcers, herpetic gingivostomatitis, erythema multiforme, TB, and trauma. The most effective drug for syphilis is procaine benzylpenicillin. Doxycycline or erythromycin can be used in patients who are sensitive to penicillin. Follow-up with regular clinical and serologic examinations is necessary for at least 2 years.

  17. END OF SYPHILIS

  18. Pathogenesis • TB is the second cause of death by infectious disease • TB is caused by acid-fast bacillus Mycobacterium tuberculosisby airborne transmission. • It grows in the pulmonary alveoli when the immune response is compromised. • So, pulmonary TB is the chief form disease, • The disease spread to other parts of the body by the lymph and blood, Miliary TB

  19. Diagnosis 1- Tuberculin skin test on the forearm with a mycobacterial antigen. If a red welt forms within 72 hours, patient have been exposed to Mycobacterium tuberculosis. 2- A chest radiograph is to look for pulmonary involvement . 3- Acid-fast bacillus test, for sputum to look for the infecting organism.

  20. OralConsiderations • Oral manifestations occur in 3% of patients . • They are secondary to pulmonary TB. • Bacilli are carried in sputum and enter mucosa through breaks . • Tongue is mostly affected. • TB lesion is irregular deep painful ulcer. • TB gingivitis is unusual form of TB which appears as diffuse hyperemic nodular gingivitis.

  21. TB infection of neck lymph nodes ( scrofula) may progress to form an abscess which perforates skin and discharge pus.

  22. Medical Management 1. There is a vaccine for TB (BCG) . 2. TB is curable in most patients, but compliance with drug regimens is critical to prevent reactivation of the disease or the development of resistance. 3.course of therapy is 6 to 9 months and involves several types of antibiotics . 4.Treatment of oral TB.is secondary to Treatment of the primary lesion.

  23. Precautions 1-Patients with active TB will be in isolation. 2-Dental treatment should be delayed until the patient is no longer considered infectious. (if they have two negative sputum cultures or have received TB treatment for at least 2 weeks).

  24. Viral diseasesHepatitis B Virus infection

  25. Hepatitis B Virus Hepatitis B is an infectious inflammatory disease of the liver caused by the hepatitis B virus. Transmission exposure to infectious blood or body fluids containing blood. From mother to child Bloodtransfusions

  26. Hepatitis B Virus • It is DNA virus lives and multiplies in hepatic cells. • The virus is identified in the serum as 3 types of antigen. 1. Surface antigen (s)HBsAg Seen in serum 6 weeks after incubation period. 2. Core antigen (c) HBcAg Present in liver cells, not detected in the serum 3. Envelop antigen (e) HBeAg -It indicate high infectivity -It appears in acute condition..

  27. Acute hepatitis B A. Prodromal phase: often preceding the onset of jaundice. The clinical features are fever, skin rash, malaise, anorexia & nausea. The symptoms often subside shortly after the onset B. Icteric phase Jaundice develops within 5 days then fever gradually subsides. yellow color of sclera, oral mucosa specially floor of the mouth and palate. 2.Hepatomegaly. 3.Spleenomegaly & Lymphadenopathy. 4.Dark urine and light colored stool.

  28. Acute Hepatitis B C. Recovery phase: it is very long . The illness lasts for a few weeks and then gradually improves. Chronic infection Hepatitis B virus either be asymptomatic or may be associated with chronic inflammation of the liver (chronic hepatitis), leading to cirrhosis over a period of several years and increases the incidence of hepatocellular carcinoma.

  29. Sequel and complication of HBV infection 1. No effect: prior immunity. 2. Subclinical50% a. recovery. 90 % b. carrier. 10% 3. Clinical: acute hepatitis 45% a. acute fulminant hepatitis 1 % b. recovery90 % c. carrier state 9 %

  30. Fate of any carrier state a. Resolution b. Chronic persistent hepatitis : HB s Ag positive & HBeAg negative c. Chronic active hepatitis : HB s Ag positive & HBe Ag positive manifestation: a) liver cirrhosis b)liver cancer

  31. Diagnosis of HBV infection 1- Clinical features. 2-Elevated liver enzymes: SGPT, SGOT. 3-Elevated Prothrombin Time, ESR. 4- Serologic tests: Antigens& antibodies

  32. Treatment of HBV infection 1. No treatment because most adults clear the infection spontaneously. 2. Antiviral for people, having aggressive course (fulminant hepatitis) or who are immunocompromised. 3. Treatment of chronic infection is to reduce the risk of cirrhosis and liver cancer.

  33. Prevention of occupationally acquired HBV 1- Vaccination. HBV & HCV were considered occupational hazards. Before Vaccination, 20% of dentists acquired the infection. 2- Booster dose for injured dentist immediately after injury. 3-Avoidance of blood and saliva contaminated blood, needle prick injury by barrier protection. 4-Screening of patients suspecting for HBV infection.

  34. Immunization .Active immunization: Vaccines are given at 0, 1 & 6 month Booster dose may be needed 5 years later. This gives protection as long as HBVs Ab is measurable. Active immunization must be given to: -Medical and Dental professional. -Infants. -Laboratories' personnel. -Pregnant ladies. - Drug abuser.

  35. Management of contaminated needle stick injury 1)If dentist is non vaccinated& subjected to needle prick injury during dealing with hepatitis B patient: a) Immediately, the dentist should get rid of blood present at the site of injuryby applying pressure to the site of injury for oozing the blood out & then clean it b) The dentist should receiveIM hepatitis B immunoglobulin (passive immunization) within 24 hour. c) Active immunization (hepatitis B vaccine) in the other deltoid muscle. d) Screen for title for HBs if negative , give vaccination at month 1 and 6

  36. Management of contaminated needle stick injury 2) If dentist is vaccinated He should receive booster dose of active immunization

  37. Hepatitis C virus infection

  38. Hepatitis C infection It is an infectious disease affecting liver, caused by hepatitis C virus (HCV). It is RNA Mode of transmission: Parentral

  39. Hepatitis C infection The virus has heat stability & ability to survive weeksto months on contaminated surfaces

  40. Hepatitis C infection The infection is asymptomatic, but chronic infection leads to cirrhosis, after many years. This may lead to liver failure, liver cancer.

  41. Diagnostic tests Detection of viral antibodies: by Enzyme Inununosorbant Assays (ELISA) b. Detection of HCV by polymerase chain reaction ( PCR ). Sequel of HCV infection 1. Acute fulminant infection < 1 % 2. Asymptomaticor mild symptoms 75 % 3. Symptomatic Both asymptomatic & symptomatic cases may lead to : a. chronic carrier state. or b. recovery

  42. Dental Implications of HCV Infection 3 major problems facing dentists when dealing with hepatitis patients: 1-Bleeding & clotting disorder. 2- Cross infection. 3-Impaired drug detoxification. So; a) Some drugs should be avoided: titracyclene, hypnotics, halothane, opium,Barbiturate and ketokenazol. b) Dose of drug should be reduced. c) G.A must be given by anaesthetist. d) Local anesthesia can be used safely.

  43. ACQUIRED IMMUNE DEFICIENCY SYNDROME (AIDS) Definition: -It is a T cell deficiency caused by human immunodeficiency virus (HIV). It is retrovirus. The infection damage immune system. so, Patients are predisposes to severe opportunistic infection & neoplasm. Immune deficiency characterized by: 1-Lymphopenia. 2-Decrease in natural killer cells (NK). 3-Diminished activity to antigen. 4-Reactive imununoglobulin(but not-neutralizing). 5-Decrease in platelets .

  44. Route of transmission • Although the virus has been isolated from all body . Transmission: only by blood & semen. through I.V. drug abuse, tattooing & acupuncture and needle stick injury • The highest conc. of virus are found in blood & semen. • Saliva is not a source of transmission, although not completely safe Treatment of AIDS : Combined medical treatment of two antiviral drugs as. a-Interferon. b-Zidovudine.

  45. Diagnosis 1) Demonstration of HIV antibodies (appear in the circulation 4-8 weeks after infection) By: a. ELISA b. Western blot: the most commonly used ,confirmatory test 2) Direct detection of HIV or one of its components Clinical manifestations: -HIV patients show a wide range of the disease that varies from asymptomaticto severe immunodeficiency. Incubation period may extent up to ten years. -Mortality rate: 3 years after diagnosis of AIDs

  46. Clinical manifestations 1.Acute self- limiting viral syndrome:one month after infection Fever,diarrhea ,weight loss, generalized lymphadenopathy, neuropathy’ oral ulceration. It lasts few weeks and passes undiagnosed. 2- Asymptomatic period: 8-10 years. Serological tests are +ve. 3-Symptomatic period: called AIDS related complex Pneumocystis carinii pneumonia (PCP): it is the cause of death. -Candidiasis, herpes, secondary neoplasm: -Kaposi's sarcoma. -Non Hodgkin' lymphoma

  47. Classification of HIV infection (CDC)systemCenter of disease control Group I acute infection: Fever, rash, lymphadenopathy, weigh loss Group II asymptomatic HIV infection: - asymptomatic for months or years andcan transmitinfection. Group IIIpersistent generalized lymphadenopathy. last for 3 months. Group IV HIV associated disease, Kaposi's sarcoma

  48. Oral manifestation Candidal infection : In AIDS patients, oral candidiasis may be an indication of immune deterioration and may precede other signs of immune deficiency and is indicators for initiating of Pneumocystispneumonia. Various forms were reported including: • Candidalleukoplakia. • Chronic pseudomembranouscandidosis. • Angular cheilitis. Treatment:Ketoconazole.