Seminar of HIV / AIDS causes, route of transmission, diagnosis, oral manifestations and its treatment.

1. The Discussants :
Ali Alarasy Mohammed Alraei
Lotfi Alhalmi Zeyad Alawadi
Shadi Alsary Murad Aldahnoon
Ashraf Alsabahi Kais Alhetar
Seminar HIV / AIDS
Supervision:
Dr. Baleegh Alkadasi
Ibb university
Faculty of dentistry

2.  HIV : HUMAN IMMUNODEFICIENCY VIRUS.
 AIDS : ACQUIRED IMMUNO DEFICIENCY SYNDROME.
 “The greatest single public health challenge that humanity has
ever faced.” Dr. Robert Lue, Harvard University

4.  An Immunodeficiency virus weakens the immune system and
increases the risk of infection.
 Creates a Deficiency of CD4+ cells in the immune system.
 It is better to call it immunodisregulation rather that
immunodeficiency since it is in fact an alteration in T4/T8 ratio.

5. Types of HIV :
 HIV 1 : more common world wide.
 HIV 2 : found in Africa and less pathogenic.

6. Transmission of HIV by:
 Direct contact with infected blood, semen or vaginal secretions.
 Sexual contact: anal or vaginal.
 HIV-infected mothers to infants during pregnancy, delivery or
breastfeeding

7. HIV can’t transmitted by :
• Coughing, Sneezing.
• Insect bites.
• Touching.
• Hugging.
• Water, food.
• Kissing.
• Public baths/pools
• Toilets
• Handshakes
• Work or school contact
• Telephones
• Cups, glasses, plates, or other
utensils.

8. Replication

9.  HIV primarily infects CD4 T cells and cells of the macrophage
lineage.
• Monocytes
• Macrophages
• Dendritic cells (skin)
• Microglial cells (CNS)

10. Diagnosis

11.  Demonstration of HIV antibodies, it appear in the circulation 4-8
weeks after infection, by :
1. Enzyme-linked immunosorbent assay (ELISA).
• This test is usually the first one used to detect infection with
HIV. If antibodies to HIV are present (positive), the test is
usually repeated to confirm the diagnosis.
2. B- Western blot
• the most commonly used confirmatory-test.
• This test is more difficult than the ELISA to perform.

12.  Direct detection of HIV or one of its components :
1. Polymerase chain reaction (PCR).
• This test finds either the RNA of the HIV virus or the
HIV DNA in white blood cells infected with the virus.
2. CD4 count.
• CD4 count vary from 500 to more than 1,000= healthy
person .
• CD4 count becomes less than 200 =HIV infection progresses
to AIDS.
3. Viral load:
• This test measures the amount of virus in your blood.

14. Stage 1
Acute seroconversion syndrome
 Signs & Symptoms :
• Fever, weakness, diarrhea, nausea, vomiting, myalgia,
headache, Weight loss.
• Pharyngitis
• Skin rashes (roseola-like or urticarial)
• Lymphadenopathy
 CD4+ and CD8+ lymphocytes reduced in numbers, but >500
cells/μL
 The severity of the acute syndrome varies among infected persons.
 The period for seroconversion of 30% of patients without acute
symptoms varies and can be 1-6 months or longer.

15. Stage 2
Latent period (asymptomatic stage)
 Signs & Symptom :
• Median time from initial infection to onset of clinical symptoms:
8-10 years
• About 50-70% of patients develop persistent generalized
lymphadenopathy (PGL). .
 Usually a steady decline in CD4+ cell count; CD4+/CD8+ ratio.
 Viral replication is ongoing and progressive.

16. Stage 2
(Early symptomatic stage)
 Signs & Symptoms :
• fever, night sweats, fatigue, diarrhea, weight loss, weakness.
• Persistent generalized lymphadenopathy (PGL).
• Fungal infections
• Vaginal yeast and trichomonal infections
• Oral hairy leukoplakia
• Herpes zoster, Herpes simplex.
 Signs and symptoms increase as CD4+ cell count declines and
approaches 200/μL; often between 200 and 300/μL.
 Platelet count may decrease in about 10% of patients.
 The spectrum of disease changes as CD4+ cell count declines.

17. Stage 3
(AIDS)
 Signs & Symptoms :
 Opportunistic infection(s):
• Pneumocystis jiroveci pneumonia
• Cryptococcosis
• Tuberculosis
• Toxoplasmosis, Histoplasmosis
 Others Malignancies:
• Kaposi sarcoma
• Burkitt’s lymphoma, Non-Hodgkin’s lymphoma, Primary CNS
lymphoma
• Invasive cervical cancer, carcinoma of rectum
• Slim (wasting) disease

18. Stage 3
(AIDS)
 CD4+ cell count below 200/ μL.
 CD4+ cell count below 50/μL at high risk for lymphoma and death.
 Death usually occurs because of wasting, opportunistic infection, or
malignancies.
 The use of combination antiretroviral agents has slowed the death
rate, but long-term outlook must depend on vaccines for prevention
and treatment because the virus promotes resistance to these agents.

19. Classification system of HIV infection
 Two classification system are known :
• center of disease control ( CDC ) system .
• Walter Reed staging system (more precise)

20. CDC classification of HIV Infection
• Category 1: > 500 cells/mm3 or (CD4 > 28%)
• Category 2: 200-499 cells/mm3 or (CD4 14% - 28%)
• Category 3: < 200 cells/mm3 or (CD4 < 14%)
 (CD4+ T-lymphocyte counts per microliter of blood)

21. CDC system
 Group I
• acute infection :
• mononucleosis-like syndrome.
• fever, rash, lymphadenopathy.
 Group II
• asymptomatic HIV infection :
• individual may remain asymptomatic for month or years and can
transmit infection.
 Group III
• persistent generalized lymphadenopathy
• last for 3 months

22.  Group IV, HIV associated disease :
1. Constitutional disease : “Wasting syndrome”
• fever ( > one month )
• Diarrhea ( > one month )
• weight loss ( > 10% of base line )
2. Neurological disease :
• Due to neoplasm or infection .
3. Secondary infection :
• Pneumocystis carinii pneumonia ( PCP ) : it is cause death.
• Candidiasis.
4. Secondary neoplasm :
• kaposi’s sarcoma.
• primary lymphoma of brain.
• Non Hodgkin’ lymphoma.

23. Walter Reed classification
 ( WR ) According to clinical & immunological criteria
• WR0 : No detectable Ab & Ag.
• WR1 : detectable Ab & Ag.
• WR2 : Lymphadenopathy.
• WR3 : Fall in T4 level ( 400/mm3 ).
• WR4 : Impaired cell mediated immunity.
• WR5 : Thrush.
• WR6 : Other opportunistic infection.

24. Oral manifestation and local treatment
 The oral lesions may be the first clinical feature of HIV infection
and lead to diagnosis.

25.  Candidal infection :
• various clinical forms were reported including :
• Erythematous : it appears as localized punctate red lesion or
diffused erythema commonly on palate.
• candidal leukoplakia.
• chronic pseudomembranous candidosis.
• angular cheilitis.
 Treatment : ketoconazole.

26. Erythematous
palatal lesion
Angular cheilitis

27.  Oral Hairy Leukoplakia :
• Oral Hairy Leukoplakia is asymptomatic, flat, white keratotic
lesion, appears as linear striae.
• Corrugated or hairy surface, not removed with scarping.
• Occurs primarily on the lateral surface of tongue, floor of the
mouth, labial mucosa, soft palate or portions of skin.
 Treatment : Acyclovir

28.  Kaposi’s sarcoma : ( due to HSV8 infection )
• Kaposi’s sarcoma is a cancer that develops from the cells that
line lymph or blood vessels. It is multifocal neoplasm,
characterized by proliferation of blood vessels.
• Site: head, neck, tip of nose and intraoraly.
• The palate is commonly involved. smooth, red raised lesions are
distributed over the oral mucous membrane that tend to be
nodular.
• Kaposi’s sarcoma is usually asymptomatic, but occasionally
becomes painful because of ulceration or infection.
 Treatment: cryosurgery, sclerosing agent, chemotherapy
and radiation.
• there is no cured but it reduce the sale and number of lesion .

29. Multiple erythematous
lesions on the face
Multiple large, flat,
erythematous lesions
involving the palatal mucosa

30.  Periodontal disease:
A. Linear gingival erythema.
• it appears as a red band along the marginal gingiva and may
be associated with complaints of occasional bleeding.
B. Necrotizing ulcerative periodontitis ( NUP )
• NUP is associated with severe pain and bleeding ; rapid
loss of bone and soft tissue sometimes leading to exposure
and sequestration of bone ; loosening and even loss of teeth.
 Treatment: Metronidazol & Iodine povidine mouth wash.

31. Band of linear
gingival erythema
Necrotizing ulcerative
periodontitis

32. Other manifestation of AIDS are less
commonly seen such as :
 cervical lymphadenopathy:
• persistent major like ulcers.
 Parotitis and xerostomia.
 Infection:
• herpes simplex, herpes zoster, viral warts.
 Malignancy:
• squamous cell carcinoma.
 Cytomegalovirus ( CNV ) Ulcers
 Human papillomavirus lesions.

33. Systemic Treatment

34.  Anti-retroviral medicines work by stopping the HIV from making
copies of itself .
• To strengthen the immune system.
• The amount of virus in your body (viral load) is decreased.
• Allows your body to make more CD4 T cells.
• Commonly three different types of medicines are taken together.
This is called combination therapy. And that helps to prevent the
virus from becoming resistant to the medicines. These medicines are
usually taken for life.

35. The classes of anti-HIV drugs include:
 Entry or fusion inhibitors.
• These drugs block HIV's entry into CD4 cells.
 Non-nucleoside reverse transcriptase inhibitors (NNRTIs).
• It disables a protein needed by HIV to make copies of itself.
 Nucleoside reverse transcriptase inhibitors (NRTIs).
• They are faulty versions of building blocks that HIV needs to
make copies of itself.
 Integrase inhibitors.
• Raltegravir (Isentress) works by disabling integrase, a protein
that HIV uses to insert its genetic material into CD4 cells.
 Protease inhibitors (PIs).
• It disables protease, another protein that HIV needs to make
copies of itself.

36. Mechanism inhibition

37. Bibliography
 Cawson's Essentials of Oral Pathology and Oral Medicine, Elsevier.
 Sami sadek oral medicine.