1. This Could Happen to YOU!
Robert R. Tight, MD FACP
Bradley Kasson, DDS
Roger Schobinger
Dakota AIDS Education and Training Center

2. Human: Infecting human beings
What is HIV?
Human: Infecting human beings
Immunodeficiency: Decrease or weakness in the body’s ability to fight off infections and illnesses
Virus: A pathogen having the ability to replicate only inside a living cell
HIV stands for Human Immunodeficiency Virus. It is the virus that causes AIDS.

3. Types of HIV Virus HIV 1 HIV 2
Most common in sub-Saharan Africa and throughout the world
Groups M, N, and O
Pandemic dominated by Group M
Group M comprised of subtypes A - J
HIV 2
Most often found in West Central Africa, parts of Europe and India
Both produce the same patterns of illness. HIV2 causes a more slow progress of disease than those with HIV 1
It is important for tests to detect the HIV subtypes that are circulating in the region. Otherwise, testing may lead to false negative results.

4. Acquired: To come into possession of something new
What is AIDS?
Acquired: To come into possession of something new
Immune Deficiency: Decrease or weakness in the body’s ability to fight off infections and illnesses
Syndrome: A group of signs and symptoms that occur together and characterize a particular abnormality
HIV infection leads to a weakened immune system. This makes a person with HIV vulnerable to a group of illness, e.g., opportunistic infections, that would not as easily affect a healthy person
AIDS results when HIV infection progresses to an advanced stage, damaging the immune system to a point at which the body can no longer fight illness.
AIDS is a syndrome because it is characterized by a group of illnesses
Drugs are available which can treat HIV and AIDS.
These drugs are called antiretrovirals (ARVs). They prevent the virus from replicating and slow the progress of the disease, but there is still no cure for AIDS or vaccine to prevent HIV transmission.
AIDS is the final stage of the disease caused by infection with a type of virus called HIV.

5. HIV vs. AIDS HIV is the virus that causes AIDS
Not everyone who is infected with HIV has AIDS
Everyone with AIDS is infected with HIV
AIDS is result of the progression of HIV Infection
Anyone infected with HIV, although healthy, can still transmit the virus to another person

6. How is HIV Transmitted?
Unprotected sexual contact with an infected partner
Exposure of broken skin or wound to infected blood or body fluids
Transfusion with HIV-infected blood
Injection with contaminated objects
Mother to child during pregnancy, birth or breastfeeding

7. Basic Terms
Antigen: A substance which is recognized as foreign by the immune system. Antigens can be part of an organism or virus, e.g., envelope, core (p24) and triggers antibody production.
Antibody: A protein (immunoglobulin) made by the body’s immune system to recognize and attack foreign substances

8. Testing for Viral Infection and Immune Response
Viral Load
p24 Antigen
Immune response
Antibody (IgG, IgM)
Cellular response (CD4)
Over a period of time, HIV infects and kills white blood cells called CD4 lymphocytes or (T cells), leaving the body unable to fight off certain kinds of infections
Both T & B cells are types of white blood cells called lymphocytes
Helper T-Cells (also called T4 or CD4+ cells) help other cells destroy infective organisms.  Suppressor T-Cells (also called T8 or CD8+ cells) suppress the activity of other lymphocytes so they don't destroy normal tissue.  Killer T-Cells (also called cytotoxic T lymphocytes, or CTLs, and are another kind of T8 or CD8+ cell) recognize and destroy abnormal or infected cells.

9. Window Period
Time from initial infection with HIV until antibodies are detected by a single test
Usually 3-8 weeks before antibodies are detected
May test false-negative for HIV antibodies during this time period
Can still pass the virus to others during this period
Represents the stage when you have been infected with HIV, but your body hasn’t created antibodies.
“Seroconversion” is a term used to describe the change when antibodies are produced and the blood is tested positive.
Seroconversion occurs when your body first begins to produce antibodies to HIV. In other words, your blood may be negative to HIV antibodies during a time period after infection, but may convert to positive to HIV antibodies after a certain period. Generally 3-8 weeks after the initial infection.

10. Disease Progression
Severity of illness is determined by amount of virus in the body (increasing viral load) and the degree of immune suppression (decreasing CD4+ counts)
As the CD4 count declines, the immune function decreases.
Define viral load as the amount of HIV virus circulating in the bloodstream.
Immune suppression, measured by CD4+ cells and total lymphocyte counts, alerts us to the risk of opportunistic infections and the need for prophylactic treatment to prevent such infections from developing.

11. WHO HIV/AIDS Classification System
Stage I
Asymptomatic
Stage II
Minor
Symptoms
Stage III
Moderate Symptoms
Stage IV
AIDS
HIV infection has various stages from primary infection (or acute phase) to asymptomatic phase (or chronic phase) and late stage disease (or AIDS)
The first weeks after primary infection, seroconversion occurs and is associated with a rapid increase in circulating viral titers and a significant drop in the number of CD4+ cells.

12. Can Disease Progression Be Delayed?
Prevention and early treatment of opportunistic infections (OIs)
Antiretroviral therapy
Positive living
YES

13. HCW HIV PEP Risk Stratification
Highest risk: larger volume of blood (e.g., deep injury, large diameter hollow needle) and blood containing high titer of HIV (e.g., source patient with acute retroviral illness or end-stage AIDS)
No increased risk (e.g., solid suture needle from asymptomatic source patient)
No known risk (e.g., urine, saliva, tears)
Source patient unknown or HIV status unknown: decide on case-by-case basis, in consultation

14. HCW HIV PEP Basic (2 drug) regimen
Combivir® (ZDV/3TC) 1 tab bid or
Truvada® (TDF/FTC) 1 tab daily
Expanded regimen: Kaletra® (LPV/r)2 tabs bid
Initiate promptly: 1-2hr/<72hr/?longer
Duration: 4 wks BUAD:initial(3d), then 2 wksx2
initial supply packet
2 wks supply at a time
start on basis of preliminary +
stop if confirmatory test is negative
24 hours PEP line:

15. dendritic cells, carried to lymph node Day 0-2
Exposure to HIV at
mucosal surface (sex)
Day 0
Virus collected by
dendritic cells, carried
to lymph node
Day 0-2
HIV replicates in
CD4 cells, released
into blood
Day 4-11
Day 11 on
Virus spreads to
other organs
Kahn JO, Walker BD. N Engl J Med. 1998;339:33-39.

16. HCW HIV PEP Monitoring
Anti-HIV: baseline, 6 and 12 wks, 6 (and 12 mo. if source + HCV/HIV)
CBC, basic panel; UA: baseline, 2, 4 wks
Baseline pregnancy test

17. This Could Happen to YOU!
Robert R. Tight, MD FACP
Bradley Kasson, DDS
Roger Schobinger
Dakota AIDS Education and Training Center

18. Oral Manifestations of HIV
Dakota AIDS Education and Training Center
Bradley M Kasson, DDS
Consultant for Infection Control Office of Dentistry, Washington DC
Chief, Dental Service VA Medical Center, Fargo 18

19. Oral Manifestations of HIV
No identified unique oral lesion specific to HIV
Seldom manifest with CD4 >400
Some predict progression to AIDS
Some meet criteria for AIDS diagnosis
Casiglia JM, Mirowski GW, Oral Manifestations of Systemic Diseases. eMedicine. Oct 2006

20. Predictive Value CD4+ < 200
Major Aphthous Stomatitis 100%
NUP %
Intraoral Kaposi’s Sarcoma 93.6%
HSV (long standing) 87.0%
Oral Hairy Leukoplakia 70.3%
Oral Candidiasis %
Dental Management of the HIV-Infected Patient Supplement to JADA , December 1995

21. Candidiasis 90% of HIV patients*
Pseudomembranous
Erythematous
Angular Cheilitis
Hyperplastic
*Casiglia JM, Mirowski GW, Oral Manifestations of Systemic Diseases. eMedicine. Oct 2006

22. Angular Cheilitis (Candida)

23. Pseudomembranous Candidiasis

24. Pseudomembranous Candidiasis

25. Pseudomembranous Candidiasis

26. Pseudomembranous Candidiasis: Wikipedia

27. Erythematous Candidiasis 33yo

29. Erythematous Candidiasis

30. Hyperplastic Candidiasis

31. HIV Oral Candidiasis Treatment
Nystatin not first choice
Increasing resistance to azoles
Fluconazole
Itraconazole
Ketaconazole
Clinical recovery precedes mycologic elimination
Treat the removable denture
Clean & disinfect daily
Casiglia JM, Mirowski GW, Oral Manifestations of Systemic Diseases. eMedicine. Oct 2006

32. Necrotizing Ulcerative Periodontitis

33. Necrotizing Ulcerative Periodontitis

34. Necrotizing Ulcerative Gingivitis

35. Necrotizing Ulcerative Gingivitis post chlorhexidine therapy

36. NUG/NUP Treatment Debridement, usually with local anesthesia
Oral hygiene instruction
Chlorhexidine gluconate
Apply with toothbrush, if possible
Follow-up cleaning
Regular dental cleanings

37. Oral Hairy Leukoplakia (OHL)
Cardiac Transplant

38. Oral Hairy Leukoplakia (OHL)
33yo

39. Oral Hairy Leukoplakia (OHL)
21 yo

40. OHL Most specific oral manifestation of HIV*
Usually no treatment indicated
Usually responds to acyclovir
High recurrence rate
If symptomatic, usually indicates Candida superinfection*
*Casiglia JM, Mirowski GW, Oral Manifestations of Systemic Diseases. eMedicine. Oct 2006

41. Aphthous Stomatitis

42. RAS Treatment Recommendations, Barron
Topical is tx of 1st choice
Amlexanox (Aphthasol) most extensively studied and most cost effective of topicals
Inhibits inflammatory mediators
Levamisole
“…may prove to be the safest & most effective systemic agent for maintaining remission…”
Normalize CD4/CD8 ratio
Systemic corticosteroids
Major RAS or esophageal/GI involvement
Thalidomide
Limited to patients with severe RAS as alternative to systemic corticosteroids for esophageal/GI involvement
Significant adverse effects
Normalize CD4/CD8 ratio, inhibit cytokines & TNF
Barron RW. Treatment strategies for recurrent oral aphthous ulcers. Am J Health-Syst Phar 58(1):41-52,2001