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This Could Happen to YOU!. Robert R. Tight, MD FACP Bradley Kasson, DDS Roger Schobinger Dakota AIDS Education and Training Center. What is HIV?. H uman: Infecting human beings I mmunodeficiency: Decrease or weakness in the body’s ability to fight off infections and illnesses - PowerPoint PPT Presentation

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This Could Happen to YOU!

Robert R. Tight, MD FACPBradley Kasson, DDS

Roger SchobingerDakota AIDS Education and Training Center

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

Types of HIV Virus• HIV 1

– 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

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

AIDS is the final stage of the disease caused by infection with a type of virus called HIV.

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

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

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

Testing for Viral Infection and Immune Response

• Viral infection– Viral Load– p24 Antigen

• Immune response– Antibody (IgG, IgM)– Cellular response (CD4)

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

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.

WHO HIV/AIDS Classification System

Stage I

Asymptomatic

Stage IIMinor

Symptoms

Stage IIIModerate

Symptoms

Stage IV

AIDS

Can Disease Progression Be Delayed?

• Prevention and early treatment of opportunistic infections (OIs)

• Antiretroviral therapy• Positive living

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

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: 1-888-448-4911

Kahn JO, Walker BD. N Engl J Med. 1998;339:33-39.

Exposure to HIV atmucosal surface (sex)

Virus collected by dendritic cells, carried to lymph node

HIV replicates in CD4 cells, released into blood

Virus spreads to other organs

Day 0

Day 0-2

Day 4-11

Day 11 on

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

This Could Happen to YOU!

Robert R. Tight, MD FACPBradley Kasson, DDS

Roger SchobingerDakota AIDS Education and Training Center

Robert.tight@meritcare.com

Oral Manifestations of HIV

Bradley M Kasson, DDS

Consultant for Infection Control Office of Dentistry, Washington DC

Chief, Dental Service VA Medical Center, Fargo

Dakota AIDS Education and Training Center

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 diagnosisCasiglia JM, Mirowski GW, Oral Manifestations of Systemic Diseases. eMedicine. Oct 2006

Predictive Value CD4+ < 200

Major Aphthous Stomatitis 100%NUP 95.1%Intraoral Kaposi’s Sarcoma93.6%HSV (long standing) 87.0%Oral Hairy Leukoplakia 70.3%Oral Candidiasis 69.9%

Dental Management of the HIV-Infected Patient Supplement to JADA , December 1995

Candidiasis 90% of HIV patients*

• Pseudomembranous

• Erythematous

• Angular Cheilitis

• Hyperplastic

*Casiglia JM, Mirowski GW, Oral Manifestations of Systemic Diseases. eMedicine. Oct 2006

Angular Cheilitis (Candida)

Pseudomembranous Candidiasis

Pseudomembranous Candidiasis

Pseudomembranous Candidiasis

Pseudomembranous Candidiasis: Wikipedia

Erythematous Candidiasis 33yo

Erythematous Candidiasis

Hyperplastic Candidiasis

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

Necrotizing Ulcerative Periodontitis

Necrotizing Ulcerative Periodontitis

Necrotizing Ulcerative Gingivitis

Necrotizing Ulcerative Gingivitispost chlorhexidine therapy

NUG/NUP Treatment

• Debridement, usually with local anesthesia– Oral hygiene instruction

• Chlorhexidine gluconate– Apply with toothbrush, if possible

• Follow-up cleaning– Oral hygiene instruction

• Regular dental cleanings– Oral hygiene instruction

Oral Hairy Leukoplakia (OHL)Cardiac Transplant

Oral Hairy Leukoplakia (OHL)33yo

Oral Hairy Leukoplakia (OHL)21 yo

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

Aphthous Stomatitis

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

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