Infectious diseases:

Fungal Diseases Viral Diseases

Bacterial Diseases

Syphilis

It is sexually transmitted granulomatous disease .

It is an infectious disease caused by Treponema pallidum

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)

Ddiagnosis

Dark field microscopic exam. Of smear of genital lesion shows: (Treponema pallidium)

A blood test is the most common way to determine syphilis. (Wasserman reaction)

Primary Syphilis

After infection, an ulcerated lesion called a primary chancre is formed.It affects the lip.It is a painless flat, 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 disappearsspontaneously within 3 to 8 weeks.

Primary Syphilis

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

Pimary syphilis

The differential diagnosis of chancre includes: ruptured vesicles of

herpes simplex, traumatic ulcers. Squamous cell

carcinoma carcinoma

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)

Secodary syphilis

Mucous patchesmucous patches : white, glistening patches on the tongue, soft palate, tonsil and 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 )

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.

Tertiary Syphilis

The lesion of this stage is called GummaIt 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

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.

Teriary syphilis

Atrophic or interstitial glossitis is another oral manifestationof tertiary syphilis. Clinically, there is atrophy of the filiform and fungiform papillae.

Congenital Syphilis

T. pallidium cross 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.

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 incisorThe upper central incisors have crescent notches in the middle of their incisal edge. The tooth tends to be wider gingivally than at the incisal edge, ‘screwdriver’ appearance

Congenital syphilis

‘mulberry molar’ The first permanent molar teeth are involved They have roughened, dirty, yellow, hypoplastic, occlusal surfaceswith poorly developed cusps

Differential Diagnosis

Primary and secondary syphilisinclude 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 inpatients who are sensitive to penicillin. Follow-up withregular clinical and serologic examinations is necessary forat least 2 years.

END OF SYPHILIS

Pathogenesis

TB is the second cause of death by infectious disease TB is caused by acid-fast bacillus Mycobacterium tuberculosis by 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

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.

Oral Considerations

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.

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

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.

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).

Viral diseasesHepatitis B Virus infection

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 Blood transfusions

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) HBsAgSeen in serum 6 weeks after incubation period.2. Core antigen (c) HBcAgPresent in liver cells, not detected in the serum3. Envelop antigen (e) HBeAg-It indicate high infectivity-It appears in acute condition..

Acute hepatitis B

A. 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 phaseJaundice 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.

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.

Sequel and complication of HBV infection

1. No effect: prior immunity.2. Subclinical 50%

a. recovery. 90 % b. carrier. 10%

3. Clinical: acute hepatitis 45%

a. acute fulminant hepatitis 1 %b. recovery 90 %c. carrier state 9 %

Fate of any carrier state

a. Resolutionb. Chronic persistent hepatitis :HB s Ag positive & HBe Ag negativec. Chronic active hepatitis : HB s Ag positive & HBe Ag positivemanifestation: a) liver cirrhosis b)liver cancer

Diagnosis of HBV infection

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

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.

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.

Immunization

.Active immunization: Vaccines are given at 0, 1 & 6 monthBooster 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.

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 injury by applying pressure to the site of injury for oozing the blood out & then clean itb) The dentist should receive IM 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

Management of contaminated needle stick injury

2) If dentist is vaccinated He should receive booster dose of active immunization

Hepatitis C virus infection

Hepatitis C infection

It is an infectious disease affecting liver, caused by hepatitis C virus (HCV). It is RNAMode of transmission: Parentral

Hepatitis C infection

The virus has heat stability & ability to survive weeks to months on contaminated surfaces

Hepatitis C infection

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

Diagnostic tests

Detection of viral antibodies:a. by Enzyme Inununosorbant Assays (ELISA)

b. Detection of HCV by polymerase chain reaction ( PCR ).Sequel of HCV infection1. Acute fulminant infection < 1 %2. Asymptomatic or mild symptoms 75 %3. SymptomaticBoth asymptomatic & symptomatic cases may lead to :a. chronic carrier state. or b. recovery

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.

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 .

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. 

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 test2) Direct detection of HIV or one of its componentsClinical manifestations:-HIV patients show a wide range of the disease that varies from asymptomatic to severe immunodeficiency.Incubation period may extent up to ten years.-Mortality rate: 3 years after diagnosis of AIDs

Clinical manifestations

1.Acute self- limiting viral syndrome: one month after infectionFever, 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 complexPneumocystis carinii pneumonia (PCP): it is the cause of death.-Candidiasis, herpes, secondary neoplasm:-Kaposi's sarcoma.-Non Hodgkin' lymphoma

Classification of HIV infection (CDC) systemCenter of disease control

Group I acute infection: Fever, rash, lymphadenopathy, weigh lossGroup II asymptomatic HIV infection:- asymptomatic for months or years and can transmit infection.Group III persistent generalized lymphadenopathy. last for 3 months.Group IV HIV associated disease, Kaposi's sarcoma

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 Pneumocystis pneumonia.

Various forms were reported including:

• Candidal leukoplakia.• Chronic pseudomembranous candidosis.• Angular cheilitis.Treatment: Ketoconazole.

• It is white keratotic lesion on the lateral sides of tongue or appears as linear striae & often has hyperkeratotic Hairy Leukoplakia: hair like projection.• EBV is the causative agent.Treatment: acyclovir

3. Kaposi's sarcoma: (due to HSV8 infection)• It is a multifocal neoplasm,with proliferation of blood vessels.• The palate and gingiva is commonly involved.It is smooth, red, maroon or bluish, highly vascular raised lesion . May be flat or form tumor

mass• Treatment: cryosurgery, sclerosing agent, chemotherapy & radiation,

HIV-RELATED PERIODONTAL DISEASE

1-linear gingival erythema . LGE is not associated with plaque, gentle probing produces bleeding 2- HIV-associated periodontitis Bone loss progresses rapidly around the tooth.3-Acute necrotizing ulcerative gingivitis:gingiva ulceration and necrosis necrosis . Treatment:

Metronidazole & Iodine, mouth wash.

Infection Control (Hepatitis & AIDS)

L General principles should be followed by the dentist which includeI .HBV vaccine to the dentist is a must.2.Proper medical history of the patient.3-Less gauge needle (30) so less amount of inoculation.4-One hand technique during anesthesia.5-Use puncture resistant and labeled waste containers.6-Proper wrapping and sealing for sterilized stored instruments.7-disposable instrument as much as you can

Thank You

2. Barrier techniques should be carried on by:-Wearing masks. -Gown.-Eye shield -Double gloves.3. Avoid holding chemicals or methacrylate by gloves as it might increase its permeability.

Cleaning, disinfection & sterilization of instruments

A. Cleaning: -Ultrasonic cleaning.-Cleaning with brush, detergent under running hot water while wearingheavy gloves and eye glasses.B. Disinfection: "By any of these chemicals"-Chlorine derivatives. -Chlorohexidine gluconate-Gluteraldehyde 2%. -Iodine (iodoform spray)

 

Treatment

The virologic response to treatment is categorized in several ways:1- The end-of-treatment response: (ETR) absence of viremia at completion of therapy; ie, the serum HCV-RNA value is below the level of detection.2- Sustained virologic response: (SVR) ie, persistent absence of serum HCV RNA for 6 months or longer after therapy.3-Relapse : an undetectable serum HCV-RNA level at the completion of therapy, with subsequent viremia.4- nonresponse: a failure to eliminate HCV RNA from the serum during therapy.

Care of laboratory material

-All materials received from dentist should be clean and disinfected (use silicone base impression material) - immersed in 2% glutaraldahyde for 10 hours without dimensional changes, before submitted to the dental technician.

-Extracted teeth should be cleaned, scaled and stored in hypochlorite (1/10) "household bleach" before submitted to dental students for cavity preparation , crown preparation or endodontic treatment

HCV antibody tests

Positive value for exposure to the hepatitis C virus.Rarely, people infected with HCV never develop antibodies to the virus and therefore, never test positive using HCV antibody screening.So, RNA testing should be considered when antibody testing is negative but suspicion of hepatitis C is high.

The presence of the virus is tested for using molecular nucleic such (PCR), transcription mediated amplification (TMA), All HCV nucleic acid molecular tests have the capacity todetect not only whether the virus is present, but also to measure the amount of virus

Oral Health ConsiderationsPrior to therapy, the clinician should attention focused on the patient’spotential for increased hemorrhage and impaired drugMetabolismlaboratory testing includes completeblood count, prothrombin time, partial thromboplastin time,international normalized ratio, bleeding time, and liver functiontests. Clinical clues of impaired

No oral lesions are specific to HIV infected patients. However, numerous oral lesions associated with the HIV-induced immunosuppression.The most strongly associated lesions are candidiasis, hairy leukoplakia, Kaposi’s sarcoma, non-Hodgkin’s lymphoma. Periodontaldisease (linear gingival erythema, necrotizing ulcerativegingivitis, necrotizing ulcerative periodontitis

Signs and symptoms

It lasts for a few weeks and then gradually improves A few people may have more severe liver disease (fulminant hepatic failure), asymptomatic and may go unrecognizedChronic infection with hepatitis B virus either may be asymptomatic or may be associated with a chronic inflammation of the liver (chronic hepatitis), leading to cirrhosis over a period of several years. increases the incidence of hepatocellular carcinoma

Hepatitis B Virus

• It is DNA virus live and multiply in hepatic cells.

• The inclusion bodies in hepatic cells called councilman bodies.

• The virus stimulates the immune system.

• The virus is identified in the serum as antigen.