This document provides an overview of HIV/AIDS, including its types, epidemiology, structure and life cycle, transmission, diagnosis, stages of infection, and treatment. It describes how HIV infects and destroys CD4 cells, progressively weakening the immune system until opportunistic infections define AIDS. Laboratory tests for diagnosis include antibody and viral detection assays, with CD4 counts and viral load used to monitor disease progression and response to antiretroviral therapy.
2. CONTENTS
• Introduction
• Types of HIV
• Epidemiology
• Structure, Replication of Virus and Mechanism of Action of Anti-Retrovirals
• Transmission of HIV and Progression to AIDS
• Diagnostic Tests
• AIDS-Stages, Classification, AIDS related complex
• Pre Exposure Prophylaxis and Post Exposure Prophylaxis
• Management
• Oral Manifestations of AIDS
• Management of Patients in Dental Clinics
• Guidelines to prevent Transmission to dentist
• Conclusion
3. What is HIV/AIDS?
• HIV means Human immunodeficiency virus
while
• AIDS means Acquired Immunodeficiency Syndrome – It’s a
disease of the human immune system caused by the human
immunodeficiency virus (HIV).
4. H – Human – This particular virus can infect human beings.
I – Immunodeficiency – HIV weakens your immune system by
destroying important cells that fight disease and infection. A
"deficient" immune system can't protect you.
V – Virus – A virus can only reproduce itself by taking over a cell
in the body of its host.
5. A – Acquired – This means that the disease is ‘got’ and not ‘caught’.
I – Immuno – Your body's immune system includes all the organs and
cells that work to fight off infection or disease.
D – Deficiency – Immune system is "deficient," or isn't working the
way it should.
S – Syndrome – AIDS is a syndrome, rather than a single disease,
because it is a complex illness with a wide range of complications
and symptoms.
• Final stage of HIV infection.
• People at this stage of HIV disease have badly damaged immune
systems, which put them at risk for opportunistic infections.
6. Where Did HIV Come From
Scientists believe HIV came from a particular kind of chimpanzee in
Western Africa.
Humans probably came in contact with HIV when they hunted and
ate infected animals.
Recent studies indicate that HIV may have jumped from monkeys to
humans as far back as the late 1800s.
7. • The virus causing AIDS was independently identified by a team
of French scientists led by Dr. Luc Montagnier of Pasteur institute
and American scientists led by Dr. Robert C. Gallo of national
cancer institute in 1983.
• The virus has been called by different names LAV i.e.,
LYMPHADENOPATHY ASSOCIATED VIRUS by the French
and
HTLV III i.e, HUMAN T- LYMPHOCYTOTROPIC VIRUS
TYPE III by the American.
HISTORY
8. • The international committee on nomenclature of viruses named it
the “Human immune deficiency virus” (HIV) and two types.
Virus classification:
Family : Retroviridae
Genus : Lentivirus
Species : HIV 1
Species : HIV 2
13. Epidemiology
• Global Level : Approximately 35 million presently living
• Deaths – 2 million/year
• New cases – 2.5 million/year
70% - Africa
20% - Asia
10% - Rest of the World
14. STRUCTURE OF VIRUS
• ENVELOPED VIRUS
• Special Proteins – gp120, gp41 : Attachment and Fusion
16. ATTACHMENT AND FUSION
• Primary Attachment
• Conformational Change
by Interaction – Co-receptors.
CXCR4 and CCR5
• When virus 1st time enters – attaches to CCR5
• After multiple divisions - CXCR4
17. Natural immunity - against HIV
1% of Northern European population and their descendents.
HIV is present in the body for long years but there is no development
of AIDS.
– because of mutations in the gene (gene is defective and cannot
express CCR5).
27. Nucleo(t)side Reverse Transcriptase Inhibitors
(NRTIs)
• Didanosine, Lamivudine, Zidovudine false building blocks causes
Chain termination. Enzyme functioning but chain termination
occurs.
• Pseudo Nucleotides are produced.
28. Non-Nucleoside Reverse Transcriptase Inhibitors
(NNRTIs)
• Nevirapine, inhibits the function of reverse transcriptase by
binding at the active site of enzyme ( making it dysfunctional).
30. Protease Inhibitors
• Indinavir, Ritonavir directly bind to HIV protease and prevent
subsequent cleavage of polypeptides and hence the virus remains
immature.
Immature virus is not infectious. It cannot enter into other cell and virus cycle is blocked.
31. HIV exposure at
mucosal surface
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+
Path of the Virus
32. Viral transmission
Acute retro viral syndrome 2- 3 weeks
Recovery + seroconversion 2 – 4 weeks
Asymptomatic chronic HIV infection Avg. 8years.
Symptomatic HIV infection / AIDS average 5 years
Stages of HIV infection
33. Susceptibility of HIV
• Fortunately HIV is a very fragile virus. It is susceptible to heat, a
temperature of 560C for 30 minutes or boiling for few records.
• It is killed by heat, ordinary soap and water, household bleach
solutions, alcohol, hydrogen peroxide, Lysol, and the chlorine used
in swimming pools.
• Bleach kills HIV on contact; soap and alcohol require exposure of
a few minutes.
35. • Antiretroviral therapy used at the appropriate time in pregnancy
significantly reduces the risk of transmission from mother to fetus.
• Additionally, using certain methods for delivery (such as caesarian
section) also helps reduce transmission.
• Since breast milk can transmit HIV, avoiding breastfeeding further
reduces vertical transmission.
• A component of saliva helps inactivate HIV.
36. Body Fluids Containing HIV
• Blood
• Semen (cum), Pre-seminal fluid (pre-cum)
• Breast Milk
• Vaginal fluids, Rectal (anal) mucous
Healthcare workers may be exposed to some other body fluids with
high concentrations of HIV, including:
• Amniotic fluid
• Cerebrospinal fluid
• Synovial fluid
37. • Other body fluids and waste products—like feces, nasal fluid,
saliva, sweat, tears, urine, or vomit — don’t contain enough HIV to
infect you, unless they have blood mixed in them and you have
significant and direct contact with them.
38. Laboratory tests for Diagnosis of HIV
infection
After a period of 3-12 weeks, the host mounts an immune response
against the virus which is detected as antibody in the blood.
This stage is called seroconversion.
Current routine laboratory diagnosis of HIV is mainly based on the
detection of these specific anti-HIV antibodies.
The period following the entry of HIV into the body and the
appearance of detectable levels of antibodies with the available tests
is called the “WINDOW PERIOD”.
41. SEROLOGICAL SCREENING ASSAYS
a) Enzyme Linked Immunosorbent Assay [ELISA]
After several incubation and wash steps, a
color reaction occurs if HIV antibody is
present.
An automated reader gives a
measurement of optical density
(presence of color) for each well.
42. b) Home access HIV Test system/dried blood
spot
• In May 1996, the FDA approved two products for home sample
collection for HIV testing.
• The kits are marketed directly to consumers, who perform a finger
stick to obtain a dried blood specimen on filter paper.
43. Dried blood specimen on filter paper and mailing procedure
It is rapid, inexpensive, simple, does not require use of organic solvents or
extraction procedures.
Collection of sample is simplified as it requires only a small amount of blood;
and also gives high sensitivity and specificity.
44. c) Rapid tests
A. “Agglutination tests” use different types of particles to produce
clumping or settling patterns of the particles when a specimen is
positive.
• I. An “Autologous red cell agglutination” method detects HIV
antibodies with a hybrid antigen antibody reagent which
agglutinates the particles in red blood cells.
• II. “Latex particle agglutination” detects HIV antibodies by the
agglutination of minute latex particles when mixed with the
patient’s blood.
45. • B. “Flow through cassettes” or “membrane immuno concentration
devices”, capture and detect HIV antibody in a specimen flowing
through a porous membrane. A visible dot or line forms on the
membrane when HIV antibodies are present.
• C. “Solid phase tests” include dipstick “comb” assay. This assay
uses a solid plastic matrix to which an HIV antigen is fixed. When
HIV antibodies are present, a spot or dot will be visible when
processed with a signal reagent.
46. 2)Antibody Confirmatory Assays:
A) WESTERN BLOT:
Immunoblot preparation consisting of a crude lysate of HIV obtained
from tissue culture,
electrophoretically transferred onto nitrocellulose paper.
47. • In accordance with their electrophoretic migratory pattern larger
proteins are at the top of the strip and smallest proteins at the
bottom.
• A western blot for HIV-1 contains HIV-1 gp 160, gp120, gp 41,
p24, p17. HIV-2 western blots are similar but differ slightly in
terms of molecular size of the three gene products.
• If antibodies to any of these proteins are present in serum, they
bind to the immobilized HIV protein on the strip
48. B) INDIRECT IMMUNOFLUORESCENCE ASSAY:
Detection of virus antigen in clinical specimens, as well as the
detection of virus specific IgG or IgA or IgM antibody.
The technique makes use of a fluorescein labelled antibody to stain
specimens containing specific virus antigens, so that the stained cells
fluoresces under UV illumination.
49. c) Radio immunoprecipitation assay [RIPA]:
• Here the infected lymphocyte cells such as T cells are grown in
presence of amino acids radiolabelled with 35S–methionine and
35S-cystine to permit incorporation of radiolabel into HIV-1
proteins.
50. Alternative Antibody Testing Technologies
• Noninvasive methods provide alternatives to diagnostic blood tests
and have high patient acceptance, increased safety and reduced
costs.
• Currently saliva, gingival crevicular fluid, oral mucosal transudates
and urine are considered to be the alternatives to blood.
51. A. ORAL FLUIDS:
• Whole saliva, glandular duct saliva or mucosal transudates are the
specimens that can be collected for tests to detect antibody to HIV in
oral secretions.
• Several devices are commercially available for the collection of oral
mucosal transudate specimens for the detection of HIV antibodies
A. Salivette,
B. Orapette,
C. Omni-SAL,
D. OraSure.
52. B. URINE ANALYSIS:
• A high prevalence of antibodies to the glycoproteins gp120 and
gp160 in urine samples among seropositive specimens led to the
proposition of detection of antibodies specific for these
glycoproteins.
54. Additional Laboratory Tests
1. Measurement of the CD4 count in HIV-infected individuals thus
provides an estimate of how much damage has been inflicted on
the immune system by uncontrolled HIV replication and
destruction of CD4 cells.
• Following successful initiation of antiretroviral therapy, a clinically
significant rise in the CD4 count generally follows.
55. • The CD4 count should be measured regularly in patients chronically
infected with HIV, typically at least every 3-6 months.
• Closer monitoring of the CD4 count is often recommended in the
first several months following initiation of antiretroviral therapy in
order to assess the patient’s response to treatment.
56. 2. The HIV viral load represents another laboratory test commonly
performed in individuals with chronic HIV infection.
• This test simply measures the quantity of HIV virus in a single
micro litre (mL) of serum.
• Like the CD4 count, this test can be a useful marker of disease
progression and of response to antiretroviral therapy.
57. Immediately following acute (primary) infection by HIV, the viral load
is typically very high, even in the tens of millions of copies/mL.
Within weeks of initial infection, however, the viral load typically
settles into a lower level of viremia, reflecting the immune system’s
partially successful efforts to limit HIV replication.
Typically, for the HIV-infected patient not on antiretroviral therapy,
this baseline value will be in the tens of thousands of copies/mL.
58. • The most important use of the HIV viral load is to assess the
response to antiretroviral therapy.
• Ideally, this degree of virologic control is established within six
months of initiation of a properly designed antiretroviral therapy
regimen.
59.
60. Laboratory diagnosis of HIV in
Infants
• Infants born to infected women are seropositive due to passively
acquired maternal antibodies, Sensitive diagnostic tests designed to
detect small amounts of HIV antibodies, give positive results in
uninfected infants for 12 to 15 months, till they seroconvert.
• Therefore, a definitive diagnosis using traditional ELISA and
Western Blot can be made only after 18 months of age when
uninfected infants will lose all maternal antibodies and infected
infants will develop their own HIV specific antibodies.
61. How does HIV cause AIDS?
• HIV infects and destroys an important type of cell in the body’s
immune system known as the T-helper (TH) cell, also known as the
CD4 cell.
• CD4 cells direct and coordinate other cells in the immune system
to battle infections.
• When CD4 cells are destroyed, the body loses its ability to fight
off infections.
62. • Infections that develop as a result of HIV-inflicted damage to the
immune system are called “opportunistic infections” or “OIs”.
• When someone with HIV develops an opportunistic infection, they
are diagnosed with AIDS.
• Characteristically, an HIV infection can progress for eight to ten
years before the clinical syndrome (AIDS) occurs.
64. The natural history of HIV disease is divided into following stages.
1. Viral transmission
2. Primary HIV infection
3. Seroconversion
4. Clinical latent period with or without persistent generalized
lymphadenopathy (PGC)
5. Early symptomatic HIV infection
6. AIDS
7. Advanced HIV infection characterized by a CD4 count < 50 /mm3
NATURAL COURSE OF
HIV/AIDS
65. 1. Viral transmission
Sexual intercourse - exposure to contaminated blood - perinatal
transmission.
2. Primary HIV infection
-Acute HIV infection
-Time from exposure to onset of symptoms is usually 2-4 weeks.
66. Typical symptoms
• Fever
• Acute diarrhea
• Pharyngitis
• Rash (erythematous – maculo papular – 5-10mm lesions on face
trunk and sometimes extremeties including palate and soles).
• Headache
• Nausea
• Vomiting
• Splenomegaly
• Thrush
67. Laboratory findings,
1) Include lymphocytopenia
2) Followed by lymphocytosis with depletion of CD4 cells.
3) Depletion of CD8 lymphocytes.
The diagnosis best established by demonstration of P24 antigen,
Detection of HIV RNA.
68. • Acute symptoms lasts 1-4 weeks, with an average of 2 weeks and
recovery is associated with dramatic decrease in plasma HIV RNA
levels.
• At this time the lymph tissue serves as the major reservoir of HIV.
70. 4. Clinical latent period with or without persistent generalized
lymphadenopathy (PGC)
• During this period the patient is clinically asymptomatic and
generally has no findings on physical examination except for
“persistent generalized lymphadenopathy” (PGL)
• Studies of the lymphnodes at this stage of the disease shows high
concentration of HIV, as extacellular virus trapped on the follicular
dendrite cell processes within germinal centres.
71. 5. Early symptomatic HIV infection
CD4 cell count Infectious origin Non-infectious origin
> 500 mm3 1) Acute retroviral syndrome a) Persistent generalized
lymphadenopathy
b) Guillain-Barre syndrome
c) Myopathy
d) Aseptic meningitis.
200-500 mm3 a) Pneumococcal and other bacterial pneumonia.
b) Pulmonary TB
c) Herpes zoster
d) Oral candidiasis
e) Candidial
oesophagitis
f) cytosporidiosis
g) Kaposis sarcoma
h) Oval hairy leukoplakia
a) Cervical intraepithelial
neoplasia
b) Cervical cancer
c) B-cell lymphoma
Anaemia
d) ITP
e) H lymphoma
f) Mononeuritis multiplex.
72. < 200 mm3 a) Pneumocystis carinii pneumonia
b) Disseminated (chronic herpes
simplex)
c) Toxoplasmosis
d) Cryptococcus
e) Miliary extra pulmonary
tuberculosis
f) Progressive multifocal
leukoencephalopathy
g) Candidial oesophagitis.
a) Wasting
b) Peripheral neuropathy.
c) HIV associated dementia
d) Lymphoma
e) Cardiomyopathy
f) Vascular myelopathy
g) Immunoblastic lymphoma
< 50 mm3 a) Disseminated cytomegalovirus
b) Disseminated mycdxaterium avium
complex
-
73. A B C
CD4 cell categories Asymptomatic or PGL or
acute HIV infection
Symptomatic (nor A or
C)
AIDS indication
condition
1) > 500 mm3 (29%) A1 B1 C1
2) 200-499 mm3 (14-
28%)
A2 B2 C2
3) < 200 mm3 (<14%) A3 B3 C3
6. AIDS :
The most recently revised CDC classification employs 3 ranges
of CD4 cell counts.
All patients in categories A3, B3 and C l-3 are reported as AIDS
74. 7.Advanced HIV infection
• Patients with CD4 cell count of < 50 mm3.
• Patients have limited life expectancy with a median survival of 12-18
months.
75. AIDS-defining Opportunistic infections and
neoplasms
1) Protozoal and Helminthic infections
A) Pneumocytosis
B) Toxoplasmosis (pneumonia or CNS infection)
2) Fungal infections
A) Candidiasis – a) Esophageal
b) Tracheal
c) Pulmonary
B) Cryptococcosis – CNS infection
C) Histoplasmosis – (disseminated)
76. 3) Bacterial infections
A) Mycobacteriosis
B) Nocardosis – Pneumonia, meningitis
C) Salmonella
4) Viral Infections
A) CMV – a) Pulmonary
b) Intestinal
c) Retinitis
d) CNS infection
B) HSV
C) VZV
5) Neoplasms
A) Kaposi sarcoma
B) NH lymphoma
C) Primary lymphoma of brain
D) Invasive cancer of uterine cervix
77. Criteria for staging HIV infections in
adults
Stage Illness
Group I Acute infection, including illness of infection.
Group
II
Asymptomatic infection, with or without abnormal laboratory findings.
Group
III
Persistent generalized lymphadenopathy, with or without abnormal
laboratory findings.
Group
IV
Other disease
A) Constitutional disease
B) Neurological disease
C) a) Secondary infection diagnostic of AIDS
b) Other specific secondary infections.
D) Secondary cancers, including there diagnostic of AIDS.
E) Other diseases (presumed HIV, resolved).
78. Severe sequelae of chronic HIV infection
included in CDC group IV
IV A: One or more of the following constitutional symptoms.
Fever of more than 1 month duration
Weight loss of more than 10% unrelated to dieting
Diarrhoea of more than 1 month duration.
IV B : One or more of the following neurological disease
Dementia
Myelopathy
Neuropathy
79. IV C :Any secondary infection diagnostic of AIDS
Oral hairy leukoplakia
Multihematomal or generalized zoster
Salmonella bacteremia
Nocardiosis
Tuberculosis
Oral candidiasis
80. IV D – One or more neoplasia moderately indicative of a defect in
cellular immunity and known to be associated with HIV infection.
Kaposi’s sarcoma
Non-hodgkin’s lymphoma
Intracranial primary lymphoma.
IV E – Other disease or illness described as being HIV related which
presently do not fit anywhere else in the classification.
82. Goals of Antiretroviral Therapy
Control of viral replication
Prevention or delay of progressive
immunodeficiency
Delayed progression to AIDS
Prolonged Survival
83. ART Guidelines
Therapy should be initiated in following patient :
• ART should be initiated in all patients with a history of an AIDS-
defining illness or with a CD4 count <350 cells/mm3.
• ART should also be initiated, regardless of CD4 count, in patients
with the following conditions:
Pregnancy, to prevent perinatal transmission
HIV- associated nephropathy,
Active TB,
Hepatitis B virus (HBV) coinfection.
87. Nucleo(t)side Reverse Transcriptase Inhibitors
(NRTIs)
• First agents available for HIV Infection.
• Less potent than NNRTIs and PIs.
• Have activity.
Drugs
Abacavir (ABC)
Didanosine (ddI)
Emtricitabine (FTC)
Lamivudine (3TC)
Stavudine (d4T)
Tenofovir (TDF)
Zidovudine (ZDV)
88. Name Dosage Form(s) Adult Dose Adverse Events
Abacavir 300-mg tablet;
20-mg/mL oral
solution
600 mg PO qd or
300 mg PO bid
Hypersensitivity reaction (may include fever,
rash, nausea, vomiting, diarrhea, malaise,
shortness of breath, cough, pharyngitis);
patients positive for HLA-B*5701 are at
highest risk for hypersensitivity (perform
HLA screening before initiating)
Didanosine 125-mg, 200-mg,
250-mg, 400-mg
enteric-coated
capsule;
10-mg/mL
suspension
>60 kg: 400 mg PO qd
< 60 kg: 250 mg PO qd
Take 30 min ac or 2 hr
pc Oral solution: Divide
daily dose bid
Peripheral neuropathy, pancreatitis, nausea,
lactic acidosis
Emtricitabine 200-mg capsule;
10-mg/mL oral
solution
200 mg PO qd or
240 mg (24 mL) oral
solution PO qd
Minimal toxicity, hyperpigmentation
89. Name Dosage Form(s) Adult Dose Adverse Events
Lamivudine 150-mg, 300-mg tablet;
10-mg/mL solution
300 mg PO qd or
150 mg PO bid
Minimal toxicity, severe acute exacerbation of
hepatitis may occur with HBV-coinfection upon
discontinuation
Stavudine 15-mg, 20-mg, 30-mg,
40-mg capsule;
1-mg/mL oral solution
>60 kg: 40 mg PO
bid
< 60 kg: 30 mg PO
bid
Peripheral neuropathy, pancreatitis, lactic
acidosis, lipoatrophy, hyperlipidemia
Tenofovir 300-mg tablet 300 mg PO qd Nausea, vomiting, diarrhea, headache,
asthenia, renal insufficiency
Zidovudine 300-mg tablet; 100-mg
capsule;10-mg/mL oral
solution;10-mg/mL
intravenous solution
300 mg PO bid or
200 mg PO tid
Nausea, vomiting, headache, asthenia,
Anemia, granulocytopenia, myopathy, lactic
acidosis, hepatomegaly with steatosis, nail
pigmentation, lipid abnormalities, lipoatrophy,
hyperglycemia
90. Nonnucleoside Reverse Transcriptase Inhibitors
(NNRTIs)
• Were introduced in 1996 with approval of nevirapine.
• Have potent activity against HIV-1 and are part of preferred initial
regimens.
• Efavirenz, confers most significant inhibition of viral infectivity.
Drugs
Delavirdine(DLV)
Efavirenz (EFV)
Nevirapine (NVP)
Etravirine (ETR)
Rilpivirine (RPV)
91. Name Dosage Form(s) Adult Dose Adverse Events
Delavirdine 100-mg, 200-mg tab. 400 mg PO tid Rash, headache
Efavirenz 600-mg tab.;
50-mg, 200-mg caps
600 mg PO qd
Take on empty stomach
to decrease Adrs
Rash, CNS (eg, somnolence, vivid
dreams, confusion, visual
hallucinations), hyperlipidemia
Etravirine 100-mg, 200-mg
tablets
200 mg PO bid Rash, nausea
Nevirapine 200-mg tab; 400 mg
XR tab; 10-mg/mL
susp.
200 mg PO bid
XR: 400 mg PO qd
Rash, hepatitis
Rilpivirine 25-mg tablet 25 mg PO qd with meal Depressive disorders, insomnia,
headache, rash
92. Name Dosage Form(s) Adult Dose Adverse Events
Raltegravir 400-mg tablet 400 mg PO bid
With rifampin: 800
mg PO bid
Nausea, diarrhea,
headache, CK
elevations,
myopathy/rhabdomy
olysis (rare)
Elvitegravir Available in ‘quad’
pill, elvitegravir/cob
icistat/emtricitabine
/tenofovir (Stribild).
_
nausea, diarrhea,
fatigue, and
headache
Integrase Inhibitors
93. Protease Inhibitors (PIs)
Drugs
Atazanavir sulfate
Darunavir
Indinavir
lopinavir / ritonavir
Nelfinavir mesylate
Saquinavir mesylate
Tipranavir
• First introduced in 1995
• Are an integral part of treatment
94. Name Dosage Form(s) Adult Dose Adverse Events
Atazanavir 100-mg, 150-mg, 200-
mg, 300-mg capsules
400 mg PO qd or
300 mg + ritonavir 100 mg PO qd
Indirect hyperbilirubinemia,
prolonged PR interval,
hyperglycemia, skin rash (20%),
hyperlipidemia
Darunavir 75-mg, 150-mg, 300-
mg, 400-mg, 600-mg
tablets
800 mg qd + ritonavir 100 mg PO
qd or 600 mg bid + ritonavir 100
mg PO bid
Rash, nausea, diarrhea,
hyperlipidemia, hyperglycemia
Fosamprenavir 700-mg tab;
50-mg/mL oral sus.
700 mg bid + ritonavir 100 mg PO
bid or 1400 mg PO bid or 1400 mg
+ ritonavir 100-200 mg PO qd
Sus.: Take without food
with RTV: Take with food
Rash, nausea, vomiting,
diarrhea, hyperlipidemia,
hyperglycemia
Indinavir 100-mg, 200-mg, 400-
mg capsules
800 mg PO q8h
800 mg PO bid + ritonavir 100-200
mg PO bid
Take 1 h ac or 2 h pc;
Nephrolithiasis, nausea, indirect
hyperbilirubinemia,
hyperlipidemia, hyperglycemia
95. Name Dosage Form(s) Adult Dose Adverse Events
Lopinavir /
ritonavir
100-mg/25-mg, 200-
mg/50-mg tablets;
80-mg/20-mg per mL oral
solution
400 mg/100 mg PO bid or
800 mg/200 mg PO qd
Oral solution: Take with meals
Nausea, vomiting, diarrhea, asthenia,
hyperlipidemia, hyperglycemia
Nelfinavir 250-mg, 625-mg tablets,
50 mg/g oral powder
1250 mg PO bid or 750 mg PO tid
(cannot be boosted) Take with food
Diarrhea, hyperlipidemia,
hyperglycemia
Ritonavir 100-mg tablet; 100-mg soft
gelatin capsule;
80-mg/mL oral solution
Boosting dose for other PIs: 100-400 mg/d
Nonboosting dose 600 mg bid
Nausea, vomiting, diarrhea, asthenia,
hyperlipidemia, oral paresthesias,
hyperglycemia
Saquinavir 500-mg tablet;
200-mg hard gelatin
capsule
1000 mg + ritonavir 100 mg PO bid
Unboosted not recommended
Take with food, or within 2 h pc
Nausea, diarrhea, headache,
hyperlipidemia, hyperglycemia, PR
and QT interval prolongation
Tipranavir 250-mg soft gelatin
capsule
100-mg/mL oral solution
500 mg + ritonavir 200 mg PO bid
Unboosted not recommended
Hepatotoxicity, rash, hyperlipidemia,
hyperglycemia, intracranial
hemorrhage
97. 98
Drugs with Potential to Interact with
PIs or NNRTIs
• Azole antifungals
• Anticonvulsants
• Anti-TB (Rifampicin)
• Warfarin
• Clarithromycin
• Oral contraceptives
• Amitriptyline
98. Preferred regimen
NNRTI – Based regimen
• EFV/TDF/FTC
PI – Based regimen
• ATV/r + TDF/FTC
• DRV/r (OD) + TDF/FTC
INSTI – Based regimen
• RAL + TDF/FTC
Standard ART consists of 2 NRTIs in combination with an NNRTI,
PI, or integrase inhibitor.
Alternative Regimens
NNRTI-Based Regimens
EFV + ABC/3TC
RPV/TDF/FTC
RPV + ABC/3TC
PI-Based Regimens
ATV/r + ABC/3TC
DRV/r + ABC/3TC
FPV/r (once or twice daily)
+ABC/3TC or TDF/FTC
LPV/r (once or twice daily)
+ABC/3TC or TDF/FTC
INSTI-Based Regimen
RAL + ABC/3TC
99. Types of Treatment Failure:
Virologic Failure: if viral load is not <400 copies/mL after 3 months
Immunologic Failure:
The CD4 cell count persistently falls below the baseline CD4 cell
count
The CD4 cell count fails to increase by more than 25-50 cells/μL
after one year of treatment.
Clinical Failure: WHO stage 3 or 4 condition--after initiation of ART
100. Clinical Indications to Change ART due to
Toxicity
Symptom Clinical Indication
Nausea Severe discomfort or minimal intake for > 3 days
Vomiting Severe vomiting of all foods/fluids in 24 hrs, orthostatic
hypotension or need of IV fluids
Diarrhea Bloody diarrhea, orthostatic hypotension or need of IV
fluids
Fever Unexplained fever of > 39.6 C
Headache Severe or requires narcotics
Allergic
Reaction
Generalized urticaria, angioedema or anaphylaxis
Peripheral
Neuropathy
Severe discomfort, objective weakness, loss of 2-3
previously present reflexes or sensory dermatomes
Fatigue Normal activity reduced > 50%
102. PRE-EXPOSURE PROPHYLAXIS
• Pre-exposure prophylaxis, or PrEP, is a way for people who do not
have HIV to help prevent HIV infection by taking a pill every day.
• When used consistently, PrEP has been shown to greatly reduce the
risk of HIV infection in people who are at substantial risk.
• Most PrEP clinical trials have tested a combination of two
antiretroviral drugs, tenofovir 300mg, and emtricitabine 200mg – 90
days, taken in a single pill daily for HIV prevention.
104. Management of Occupational exposure and
Post Exposure Prophylaxis
• Prevention is the mainstay of strategy to avoid occupational
exposure to blood / body fluids.
• All the biosafety precautions must be practiced at all times for all
patients blood and body fluids while providing medical services.
105. Steps to be taken on exposure to HIV infected blood / body
fluids and contaminated sharps etc
A. Immediately following an exposure
B. Reporting of the exposure
C. Post exposure prophylaxis
106.
107. For the eye:
Irrigate exposed eye immediately with water or normal saline.
• Sit in a chair, tilt head back and ask a colleague to gently pour water
or normal saline over the eye.
• If wearing contact lens, leave them in place while irrigating, as they
form a barrier over the eye and will help protect it.
• Once the eye is cleaned, remove the contact lens and clean them in
the normal manner.
• Do not use soap or disinfectant on the eye.
108. For mouth:
• Spit fluid out immediately.
• Rinse the mouth thoroughly, using water or saline and spit again.
Repeat this process several times.
• Do not use soap or disinfectant in the mouth.
109.
110.
111.
112. Basic regimen : Zidovudine (AZT) – 600mg in divided doses.
Expanded regimen : Basic regimen + indinavir – 800mg/thrice a day
or any other protease inhibitor.
Testing and counseling :
The health care provider shout be tested for HIV as per the
following schedule:
• Base – line HIV test at the time of exposure.
• Repeat HIV test – at 6 weeks following exposure.
• 2nd repeat HIV test – at 12 weeks following exposure.
HIV testing should be carried act on three ERS (Elisa / Rapid /
Simple) kits or antigen preparations.
113. Duration of PEP
• Should be started, as early as possible preferably within 2hrs after
an exposure.
• It has been seen that PEP started after 72 hours of exposure is of no
use and hence is not recommended.
• The optimal course of PEP in not known, but 4 weeks of drug
therapy appears to provide protection against HIV.
• If the HIV test is found to be positive at anytime within 12 weeks,
the HCW should be referred to a physician for treatment.
115. Oral lesions in HIV positive patients may:
• Be the first sign of underlying HIV infection whose HIV status may
not be known at the time of examination.
• Serve as a potential clinical markers of the disease progression in
those who are HIV positive.
• Provide useful information on the failure ART.
116. Important steps in the diagnostic process should include:
1. A history of chief complaint
2. A detailed medical, dental and social history with special reference
to high risk behavior
3. A thorough head, neck and intra oral examination
4. Use of diagnostic aids where relevant.
117. Classification of HIV-Associated oral lesions
• In 1992 at a meeting held in London, EC-Clearing House proposed
a classification of HIV associated oral lesions based on the
frequency of their occurrence.
118. Group 1: Lesions strongly associated with HIV infection
• Candidiasis:
Pseudomembranous Candidiasis
Erythematous Candidiasis
Angular Cheilitis
• Periodontal Diseases
Linear Gingival Erythema
Necrotizing Ulcerative Gingivitis
Necrotizing (ulcerative) Periodontitis
• Non-Hodgkin’s lymphoma
• Hairy Leukoplakia
• Kaposi’s sarcoma
119. Group 2: Lesions less commonly associated with HIV infection
• Bacterial Infections:
Mycobacterium avium-intracellulare
Mycobacterium tuberculosis
• Melanotic Hyperpigmentation
• Necrotising (ulcerative) stomatitis
• Salivary Gland Disease:
Dry mouth due to decreased salivary flow rate
Unilateral or bilateral swelling of major salivary glands
• Thrombocytopenic purpura
123. Fungal Infections
• The most common fungal infection seen in association with HIV
infection is oropharyngeal candidiasis.
• Oral candidiasis - Candida albicans,- other species, such as C.
glabrata and C. tropicalis.
124. Factors predispose - infancy, old age, antibiotic therapy, steroid and
other immunosuppressive drugs, xerostomia, anemia, endocrine
disorders, and acquired immunodeficiency.
• Candida is a commensal organism in the oral cavity. It is a
dimorphic fungus which exists in two forms namely blastospores
and hyphae.
• Spores and hyphae are seen in smears from lesions and are rarely
detected in the healthy mouths in the carrier state.
125. CLINICAL MANIFESTATIONS
These are frequently observed forms of oral candidiasis:
• Erythematous candidiasis
• Pseudomembranous candidiasis
• Angular cheilitis
• Hyperplastic candidiasis
126. Pseudomembranous candidiasis
• Lesions characterised by yellow-white,
curd –like loosely adherent plaques.
• Removal of lesion leaves a red mucosa, with or without pin point
bleeding.
• Patients may complain of taste disturbances and burning mouth.
127. Erythematous Candidiasis
• Erythematous (atrophic) macular patches
on mucosal surfaces
• Dorsum of the tongue often shows
depapillation.
• Color changes from light pink to scarlet
• Patients often complain of burning and altered taste sensation.
129. Angular Cheilitis
• Angular cheilitis is characterized by fissures or linear ulcers at the
corners of the mouth unilaterally or bilaterally.
• Hyperkeratosis may often be seen peripheral to the fissures.
• Opening of the mouth becomes restricted and painful.
130. Hyperplastic Candidiasis
• This form of candidiasis,
also known as candidal leukoplakia,
is least common form of candidal
infections in HIV infected persons.
• Characterized by white patches firmly adherent to the underlying
mucosa.
• Hyperkeratosis is the predominant feature that is responsible for
the white coloured patches.
131. Diagnosis of Candidial lesions
• Clinical appearances of the lesions.
• Smears mixed with KOH or stained with PAS or Gram’s stain
• Cultures from swabs, whole saliva samples or saline rinses
• Biopsy and histological examination
• Response to antifungal therapy
132. Treatment of Fungal Infections:
• Topical therapy is used when the condition is mild and limited to the
mouth.
• Systemic therapy is used for severe oral and oropharyngeal
candidiasis.
• It is important to maintain antifungal therapy for 10-14 days even
after clinical signs and symptoms of candidiasis have resolved.
• Topical medications require that the medications are in contact with
the lesion for 20- 30 minutes.
133. • If sweetening agents are used in the medication, a concurrent
treatment of fluoride rinses daily should be considered.
• Because salivary flow in HIV infection is reduced, salivary
substitutes should be used to stimulate saliva. This helps to reduce
the occurrence and severity of oral candidiasis and dental caries.
• Maintenance (secondary prophylaxis) may be necessary as the
patient’s HIV status progresses.
• Once the acute phase of oral candidiasis has been brought under
control secondary prophylaxis may be considered. If recurrences are
frequent or severe, intermittent or chronic low dose antifungal
therapy may be necessary for maintenance.
134. • For the treatment of angular cheilitis combination creams are more
effective than antifungal agents alone.
• Combination creams consisting antifungal, antibacterial medication
with an anti-inflammatory, antipruritic agent is useful for angular
cheilitis that shows lack of response to preparations with antifungal
agents only.
135. Effect of antifungal therapy depends upon the following:
1) Patient compliance
2) Adequate saliva for the use of topical medications
3) Health status of the patient (particularly if liver disease is present
systemic use may not be effective)
4) Drug resistance
5) Use of other medications
6) Number of episodes of oral candidiasis
7) Choice of drug and timing of therapy
136. Antifungal Agents
Topical Treatment for Oral Candidiasis:
• Nystatin (Mycostatin) Oral Pastille.
1 pastille (200000U/pastille) to be dissolved in the mouth 4-5 times
a day
• Nystatin Oral Suspension (100000U/mL) used as mouth rinse with
1-5 ml of suspension held in the mouth for 5 minutes/4 times a day.
137. • Clotrimazole: As an oral troche (Mycelex)10mg. 1 troche to be
dissolved in the mouth for 15-20 minutes/5 times a day (1 troche to
be dissolved in the mouth 3 times a day for maintenance therapy).
138. Systemic Treatment:
• Ketoconazole (Nizoral) 200mg. 1 tablet daily for 2 weeks.
• Fluconazole (Diflucan)100 mg. per day for 2 weeks.
• Itraconazole (Sporonax) 200mg tabs daily with food.
• Amphotericin B: an intravenous medication that may be used for
candidiasis resistant to other medications.
139. Reasons for Antifungal Treatment Failure:
- lack of patient compliance,
- inadequate mucosal contact or
- lack of absorption of the drug
- Clinical and microbial resistance is seen in those with:
frequent episodes of candidiasis
low CD4 counts
repeated exposure to fluconazole and replacement of candida
albicans strains by other resistant fungal strains (eg: C. krusei).
140. HISTOPLASMOSIS
• Histoplasmosis is an infection caused by the fungus: Histoplasma
capsulatum.
• 30-50 percent with disseminated histoplasmosis may present with
oral lesions.
• Oral lesions appear as ulcerations
with ill defined margins and a
granulomatous appearing surface.
141. • Cervical and submandibular lymphadenopathy is a feature.
• Gingival involvement often mimics severe periodontal disease.
142. • When oral lesion is diagnosed, patient must be assessed for systemic
disease.
• Histoplasmin skin test is a useful diagnostic test.
• Liver function tests, chest X-ray and sputum culture should be
carried out in these patients.
• Diagnosis of the oral lesion requires biopsy and histological
examination of the lesion.
143. Treatment:
• Patient should be referred to HIV specialist for therapy.
• Oral lesions can be treated with Ketoconazole and Amphoterecin B
preparations.
• Analgesics and antipyretics – fever and myalgias
144. CRYPTOCOCCOSIS
• Fungus responsible for cryptococcosis is Cryptococcus neoformans.
• Nearly 10 percent of patients with cryptococcosis develop lesions
on the skin of the head and neck region.
• Oral lesions are rare.
• When they occur, oral lesions are ulcerative.
• Cryptococcosis in AIDS patients is a fatal condition.
145. • Biopsy and histological (PAS stained) examination of ulcerative
lesions should be carried out.
• A definitive diagnosis can be made on tissue culture.
• Sputum, blood and cerebrospinal fluid should also be cultured.
• Ketoconazole and Amphotericin B are the drugs of choice
146. VIRAL INFECTIONS
1. Herpes Simplex Virus infection
2. Varicella-Zoster infection
3. Human Papilloma virus infection
4. Epstein Barr virus infections
5. Cytomegalovirus infection
• Clinically these infections present lesions similar to those found in
non-HIV population.
• Response to treatment and recurrence pattern in the HIV/AIDS
population is different in HIV disease which depends on the
severity of the immunosuppression.
147. HERPES SIMPLEX VIRUS INFECTIONS
• In immunocompetent persons herpes simplex virus causes both
primary (primary herpetic gingivostomatitis) and recurrent or
secondary infection (herpes labialis or recurrent intraoral herpes
simplex infection) in the oral cavity.
• Primary infection commonly affects children.
• Secondary herpes infection is due to the reactivation of the latent
virus in the trigeminal ganglion following a primary episode.
• Causative virus in over 90 percent of oral herpes is Herpes Simplex
Virus Type-1.
148. 1. Primary Herpetic Gingivostomatitis:
• Primary HSV infection of the oral cavity is uncommon in the HIV
infected patient.
• When it occurs, its clinical presentation is not different from the
same condition in the non-HIV infected patient.
149. • Diffuse gingival swelling and pain.
• Multiple vesicles and erosions on the attached gingiva and palatal
mucosa.
• Fever, malaise cervical lymphadenopathy and halitosis.
• Primary herpetic pharyngitis is often present with diffuse erythema
of the tongue, soft palate and posterior pharynx.
150. 2. Recurrent Herpetic Infection
• Recurrent herpetic infection commonly involves the vermilion
border of the lips (herpes labialis).
• In HIV disease, intraoral involvement
of recurrent herpes and skin infection
is often seen.
• Generally intraoral lesions present as a localized crop of vesicles on
the keratinizing mucosa.
• Patient may feel pain or itching prior to the appearance of clusters of
vesicles.
151. • In HIV infected people herpetic erosions/ulcers tend to be persistent.
• In HIV infected people, herpetic ulcers are large, can occur anywhere
in the oral cavity, persist for longer periods and non –responsive to
routine antiviral therapy.
• Atypical herpetic erosions/ulcers may be the first sign of
immunosuppression, patients with these lesions who are not known to
be HIV infected should be referred to HIV counseling and testing.
152. • Diagnosis of herpetic infection is generally made on history and
clinical grounds.
• Confirmatory test include: Viral culture, mucosal smear stained
with Papanicolaou stain for cytopathic effects (viral giant cells),
biopsy for immunocytochemistry.
• Serology for antibody titres during acute and convalescent phase of
the infection is diagnostic.
153. Treatment
• Treatment to eradicate herpes simplex virus infection is not
available. Antiviral agents such as acyclovir shorten the healing time.
• Acyclovir 200 mg. capsules: 1-2 capsules 5 times a day for 10 days.
• If resolution does not occur in two weeks, seek consultation.
• Valaciclovir 500mg. per oral twice daily.
154. • Acyclovir–resistant herpes ulcerations should be considered when
ulcers with a confirmed diagnosis of HSV infection do not respond
to acyclovir.
• Treatment with Foscarnet (40mg/kg intra venous every 4 hrs for
three weeks) or Phosphonoformate is recommended for such lesions.
• Symptomatic treatment for pain is also given as required. This
includes analgesics, topical anesthetics, mucosal coating agents such
as milk of magnesia, kaolin-pectin etc.
155. VARICELLA-ZOSTER INFECTION
Herpes Zoster (Shingles):
• Caused by the reactivation of the virus Varicella (virus that causes
chicken pox) in the trigeminal ganglion.
• Herpes Zoster of the oral mucosa and facial skin is a marker of HIV
progression in HIV infected persons.
• When the facial skin is involved, the patient experiences itching,
redness, vesicle formation and eventual ulceration and crusting of
ulcers with hyperpigmentation.
156. • Lesions are unilateral in distribution following the
maxillary and/or mandibular branches of the trigeminal nerve stopping
typically at the midline.
• Prodromal symptoms with itching, burning and tenderness are
common.
• Intra-oral vesicular/erosive lesions are painful and unilateral. They
coalesce to form large ulcers.
157. • Complications of Herpes Zoster include post herpetic neuralgia and
systemic viral dissemination.
• Oral involvement may be presented as toothache or earache.
• Diagnosis is made on clinical grounds.
• Serology is useful in confirming the diagnosis.
158. Treatment
• Acyclovir 800mg five times daily for 10 days is recommended.
Acyclovir shortens the duration of infection, healing time and
reducing pain.
• Foscarnet IV for refractory cases.
• Symptomatic treatment for pain as needed.
159. HUMAN PAPILLOMA VIRUS
INFECTIONS
• Human papilloma virus (HPV) infections are characterized by
papillary projections which may be of normal mucosal color,
slightly red or white in appearance.
• Oral warts, papillomas, skin warts and genital warts are associated
with HPV.
• In HIV infected people these lesions are common.
160. • In HIV infected people, three different types of HPV lesions are
known to occur in the oral cavity.
They are:
1. Oral Warts
2. Condyloma Acuminatum
3. Focal Epithelial Hyperplasia
161. 1. Oral Warts (Verruca vulgaris)
• Oral warts are usually small (1-3 mm in diameter) asymptomatic,
nodular, warty cauliflower-like appearance.
• They may be solitary or multiple.
• Usually affect non- keratinized mucosa.
162. 2. Condyloma Acuminatum
• Condyloma acuminatum is generally a single lesion.
• It is nodular in appearance and often seen on the floor of the mouth,
labial mucosa and gingiva.
• Condyloma acuminatum is common in ano-genital regions among
HIV infected persons.
163. 3. Focal Epithelial Hyperplasia
• Focal Epithelial Hyperplasia is clinically characterized by multiple
flat pink colored nodules.
• Labial mucosa is a common site.
164. Diagnosis of HPV lesions
• Diagnosis of HPV lesions are generally made on clinical grounds and
confirmed by biopsy and histologic examination.
• Determination of the strain of HPV can be done by
immunofuorescence and immunoperoxide staining.
165. Treatment of HPV lesions
• Treatment of HPV lesions include surgical removal, carbon dioxide
laser surgery, topical application of podophyllin resin and intra
lesional injection of interferon.
• Recurrences are common.
• Surgical excision can be followed by cauterization of the base of
the lesion to avoid frequent recurrences.
166. EPSTEIN-BARR VIRUS INFECTIONS
Oral Hairy Leukoplakia (OHL)
• Oral hairy leukoplakia (OHL) is caused by Epstein-Barr virus in
those with immune deterioration.
• Presence of OHL is an indication of HIV infection and
immunodeficiency.
• becomes more common as the CD4+T-cell count drops.
167. • OHL presents as a ragged, corrugated, or irregular non- removable
“hairy” white lesion involving the lateral and/or dorso-lateral areas of
the tongue.
• Lesions may be unilateral or bilateral and asymptomatic.
• Occasionally OHL and candidiasis may co-exist.
168. Diagnosis
• Diagnosis can be made on the clinical appearance. If the lesion is
clinically consistent with OHL and the patient is known to be HIV
positive, generally no further diagnostic procedure is necessary.
• Biopsy and histological examination may be considered when
patient’s HIV status is not known.
• In situ hybridization techniques used on cytological specimen taken
from the lesion yield confirmation of EBV association with OHL.
169. Treatment
• OHL generally does not require any treatment because of its
asymptomatic nature. It responds to Acyclovir.
• High doses of Acyclovir generally eliminate OHL but lesion tends to
recur with cessation of treatment.
• Podophyllin and interferon are also used to treat OHL.
• Recurrences of OHL are common.
170. CYTOMEGALOVIRUS (CMV) INFECTION
Oral CMV Ulcers
• Oral CMV lesions seen as ulcers may occur in patients with
advanced HIV disease.
• Oral lesions due to CMV infection
can occur any where on the oral mucosa.
• Ulcers generally exhibit a white halo around the necrotic surface.
171. • Diagnosis is made from biopsy and histological examination which
show intranuclear and intracytoplasmic inclusion bodies.
• Immunohistochemistry is useful.
• CMV ulcers respond to ganciclovir.
• Patients should be referred to a physician for the treatment of
underlying CMV infection.
173. Plaque induced Gingivitis
• This condition is an immunologically mediated inflammatory
reaction to the presence of the bacterial products inside the gingival
tissue when bacteria from the plaque colonize the surfaces of the
tooth and gingival crevice.
• This reaction is confined to the marginal gingivae and is aggravated
by xerostomia in HIV patients.
174. • Prophylaxis or scaling and root planning (gingival surgery in cases
of hyperplasia) is recommended in these patients.
• Plaque control by dental flossing and tooth brushing, and appropriate
use of non alcohol based mouth washes can restore periodontal
health.
• Recall every three months is recommended.
175. Linear Gingival Erythema (LGE)
• This is also called Gingival Banding, HIV-Gingivitis or HIV induced
gingivitis.
• LGE has been defined as a lesion of the soft tissue, which presents
distinctive linear erythema of the gingival margin.
• LGE was described for the first time in the mid 1980s as a fiery red
linear erythema covering one millimeter of the gingival margin of
patients with otherwise healthy gingiva and good oral hygiene.
176. • LGE bleeds easily on brushing, flossing and probing, with some
patients complaining of burning sensation, pain or spontaneous
bleeding.
• LGE does not respond or has poor response to periodontal treatment.
• Superimposition of the common gingivitis is frequent, complicating
the diagnosis.
177. • Etiology of LGE is unknown.
• The treatment for LGE is the same as for plaque induced gingivitis.
• The use of an ultrasoft toothbrush, fine waxed dental floss, and less
abrasive toothpaste are recommended.
178. Necrotising Ulcerative Gingivitis (NUG)
• NUG has sudden onset and is very painful.
• NUG is characterized by gingival marginal necrosis, with punched out
papillae, covered by gray pseudomembrane of necrotic tissue.
• NUG starts in one area of three or four teeth and spreads rapidly
throughout the mouth.
179. • NUG is believed to be a fuso-spirochetal infection triggered by
systemic predisposing factors such as poor nutrition, stress or
immunodeficiency.
• Often there is clinical evidence of the influence of neutropenia to the
onset and recurrence of NUG.
• White blood cell count therefore must be done on patients reporting
with signs and symptoms of NUG.
180. • Patients with normal immune response always have a dramatic
response to emergency local treatment with fast improvement of the
symptoms in 24 to 48 hours followed by fast healing.
• If patient does not respond to emergency treatment, medical
evaluation must be considered.
181. • Diagnosis is based on clinical grounds.
• Treatment includes whole mouth debridement and the use of
oxygenating mouthwashes.
• When premedication is indicated, it is given always by using broad
spectrum antibiotic extended for 10 days.
182. • Initial scaling and debridement using hand and ultrasonic instruments, plus
irrigation with a 50% dilution of hydrogen peroxide in water.
Home care includes:
- the use of analgesic as needed
- high intake of liquids
- dietary supplements and solid food as soon as possible
- rest or reduced activities
- Toothbrushing after meals
- mouthwashes with water diluted hydrogen peroxide four times a day for
two days
- mouthwash with 0.12% chlorhexidine once a day before bedtime and half
hour after brushing for 15 days
183. • A follow up visit 24 or 48 hours after will allow an evaluation of
the patient’s response to the initial treatment.
• This can also be followed up by a complementary scaling and
debridement in the areas not responding to initial therapy.
• Generally, the patient should be fine to start a routine periodontal
treatment within a week.
184. Necrotizing Periodontitis (NP)
• This condition is also called Necrotizing Ulcerative Periodontitis
(NUP), HIV-Periodontitis (HIVP), and HIV Associated Periodontitis
(HIVAP)
• - There are two forms of clinical manifestations of NP, the more
common form evolves from a previous onset of NUG, the other is a
super infection of both chronic gingivitis or periodontitis.
185. Necrotizing Ulcerative Stomatitis (NUS)
• NUS is characterized by the onset of acute and painful
ulceronecrotic lesion on the oral mucosa.
• Underlying bone may be exposed and/or the lesion may extend in
to the adjoining tissues.
• Treatment is the same as recommended for NUG and NUP.
186. Bacillary Angiomatosis
• Bacillary angiomatosis is an infectious disease characterized by
proliferative vascular lesions that mainly affects HIV infected
persons.
• Causative organism is Rochalimaea Quintana or Rochalimaea
henselae.
• Oral lesions may be seen as nodular lesions. Palate is often the site
of involvement.
• Cutaneous and systemic involvement is common.
• Erythromycin (500mg. four times a day) is the drug of choice.
187. Oral Tuberculosis
• Tuberculosis is rarely seen on the oral mucosa. The disease is
caused by Mycobacterium tuberculosis.
• Occasionally oral tuberculosis appearing as persistent ulcer, firm
swelling or granulomatous growth has been reported among HIV
patients.
• Oral involvement is generally
secondary to systemic (pulmonary)
tuberculosis; hence when suspected,
a medical evaluation must be sought.
188. • Biopsy and histological examination of the oral lesion stained with
Zeil-Neelsen reagent would reveal the presence of acid fast
microorganisms.
• Chest X-ray should be obtained for all suspected cases of
tuberculosis.
• Skin tuberculin test is of importance in the diagnostic process.
• Culture studies are of diagnostic importance.
189. Mycobacterium Avium-Intracellulare (MAI)
infection
• Very rarely oral lesion presenting as granulomatous mass caused by
MAI can be seen in the oral cavity of HIV patients.
• Acid Fast Bacillus (AFB) stained histological tissue examination
and culture studies provide confirmatory evidence of the rare
infection.
190. Oral Syphilis
• Oral lesions of syphilis are uncommon. When they do occur, they
are in the form of ulcers.
• Lesions can be seen in those who have systemic involvement. In
primary syphilis chancre on the lip or tongue are reported. - rare
• In secondary syphilis oral mucous patches accompanied by
cutaneous ‘coin-like’ patches may be seen.
• Tertiary - Gumma
191. • Dark ground illumination microscopy is useful in identifying the
causative organism (Treponema pallidum).
• Serology is of diagnostic importance.
192. NEOPLASTIC LESIONS
Kaposi’s Sarcoma (KS)
• Kaposi’s sarcoma of the oral tissues is the most common neoplasm
associated with HIV infection.
• Human Herpes Virus-8 (HHV-8), a sexually transmitted virus has
been implicated to be the causative organism of KS.
• Low CD4 counts, homosexuality and CMV disease are known to
increase the probability of occurrence of KS.
193. • Oral KS may present as the first sign of AIDS.
• Oral KS presents as a flat, nodular or ulcerated mass depending on
the stage of the tumor development and time of diagnosis.
• Lesions may be multifocal and skin involvement may be seen in
association with oral KS.
• Most common in HIV infected male adults and less common in
females and children infected with HIV
194. • Palate, gingiva and tongue are most commonly involved sites.
• Early lesions are asymptomatic, flat and red or purple in color.
• Advanced lesions show nodular appearance become ulcerated and
painful and may destroy bone.
195. • Diagnosis is made on clinical signs and symptoms and confirmed
by biopsy and histological examination.
• Treatment includes surgical (or carbon dioxide laser) excision.
• Radiation therapy is indicated for large and multiple lesions.
196. • Intralesional injections of vincristine or vinblastin (One or two
injections of 0.2 mg per ml) or sodium tetradecyl as a sclerosing
agent are useful for small lesions.
• Before initiating treatment for KS of gingiva a thorough oral
prophylaxis is necessary.
• Remissions are common.
197. Non-Hodgkin’s Lymphoma
• This is of B-Lymphocyte in origin.
• Epstein–Barr virus (EBV) has been detected in the cells of NHL.
• NHL can occur anywhere in the oral cavity
• More common in males
• NHL can present as a painless soft tissue swelling with or without
ulceration
• Palate and gingival are common sites of NHL
198. • Lesion is generally single and extremely painful
• Diagnosis of NHL is made by biopsy and microscopic
examination. Biopsy should be from the centre of the lesion and
deep
• Prognosis is poor, with most patients dying within the first year
after diagnosis.
• Therapy depends on the stage of the disease: Radiation for
regional disease and systemic chemotherapy for extra nodal
disease
199. MISCELLANEOUS ORAL LESIONS
Aphthous Ulcers
• In HIV disease all three forms (Minor, Major and Herpetiform) of
recurrent aphthous ulcers (RAU) are seen.
• Generally these ulcers are seen in patients with a previous history of
recurrent aphthous stomatitis (RAS) who may report an increase in
frequency and severity of attacks.
200. Diagnosis
• Diagnosis of aphthous ulcers should be based on the characteristic
clinical presentation.
• For all ulcers not exhibiting characteristic clinical features or when
empiric therapy has failed, viral culture (isolation), mucosal smear
or biopsy may be required to rule out ulcers caused by opportunistic
infections.
• Major aphthous ulcer that is not responsive to therapy may require
biopsy to exclude malignancy or tuberculous ulcer.
201. HIV-associated Salivary Gland Disease
• HIV-Associated Salivary Gland Disease (HIV-SGD) presenting as
parotid gland enlargement has been reported in many HIV patients.
- Unilateral or mostly bilateral parotid gland enlargement is a feature.
- Salivary glands are soft but not fluctuant
- Xerostomia may be present.
202. Diagnosis:
- Clinical findings
- MRI to rule out multicystic lesions
- Biopsy to rule out lymphoma, sarcoid or lymphadenitis.
- Fine needle biopsy aids useful in this regard
• - For suppurative salivary gland lesions antibiotic use is useful.
• Microbiological identification is also to be carried out
203. Treatment:
- Generally left untreated.
- In extreme cases salivary gland enlargement can be treated with
anti-inflammatory agents, antibiotics or with steroids.
• - Xerostomia is treated with the use of salivary stimulants
204. Idiopathic Thrombocytopenia
• - Oral lesions in the form of petechiae, ecchymoses and hematoma
can be the first sign of idiopathic thrombocytopenia in HIV/AIDS
patients.
• - One of the common complaints from the patients is that they find
blood in their mouths on waking.
205. • Condition needs to be differentiated from other vascular conditions
and blood investigation for platelet counts should be carried out.
• - Invasive dental procedures should not be undertaken without
correcting the platelet count.
206. Lichenoid Reaction, Drug Induced Ulcers and Pigmentations
• In HIV patients, antibiotics and anticancer agents may cause
lichenoid reactions and ulcerations.
• There may be a history of sudden onset of these lesions following
the institution of a new drug or an increase in the dose.
207. • Erythema multiforme has been reported in HIV patients who are on
antiretroviral treatment.
• Mucosal pigmentation is frequently seen in patients receiving
antiretroviral agent Zidovudine. There is no treatment for the
pigmentation of the mucosa.
208. Dental Caries
• In HIV disease because of xerostomia and lack of maintenance of
oral health the risk for dental caries is high.
209. • In drug abusers who are also HIV positive, and in particular those
who use Methamphetamine (Meth) exhibit gross destruction of teeth
due to dental decay.
• Dental caries in these patients starts in the proximal and cervical
areas of teeth resulting in gross destruction of teeth in a short period
of time.
• Condition is referred to as Meth Mouth.
210. Inflammatory Periodontal Disease and other dental infections
• Immunodeficiency in HIV however may play a role in providing a
fertile ground for microorganisms in the periodontal tissues.
• Microorganisms may be higher in number or unusual types of
microorganisms may be found in HIV infected persons.
211. • Dental infections such as pericoronitis, dento-alveolar abscesses
and fascial infections are also not different from those occurring in
the non HIV group.
• The extent and severity of the conditions however may differ due to
immunodeficiency.
213. • Modifications of the care of patients with HIV disease is similar to
that of other medically compromised.
• In HIV patients, planning and prioritization of dental treatment are
important.
214. Treatment planning
• Alleviation of pain
• Restoration of function
• Prevention of further disease
• Consideration of esthetics
215. Antibiotic prophylaxis is required for patients with the following
conditions:
• Neutropenia (neutrophil count < 500 cells/mm3)
• CD4+ cell counts < 200
• Prevention of bacterial endocarditis
216. Bleeding Abnormalities :
• If the patient’s past medical history includes increased bleeding
tendencies or platelets are below 60,000, a conservative tooth-by-
tooth approach should be taken.
• Spontaneous bruising and bleeding may occur when platelet counts
drop below 20,000.
• All screening tests for platelet counts should be no more than 1-2
days prior to procedure, with same-day values being optimal.
217. Anemia
• Hemoglobin levels > 7g/dl, no increased complications with routine
treatment are expected.
• When hemoglobin levels drop below 7g/dl, conservative tooth-by-
tooth treatment is recommended.
• If extensive surgical treatment is needed, close consult with the
patient’s physician.
218. Pain and Anxiety Control
• Nitrous Oxide - for the temporary relief of the symptoms
• Local Anesthetics
• Non-steroidal anti-inflammatory drugs and non-narcotic and
narcotic pain relievers - acceptable for post-operative pain control.
219. Preventive Treatment
• Routine dental prophylaxis, fluoride treatment, sealants and patient
education are all essential to an effective preventive program.
• Proper home-care techniques, including daily brushing and flossing
to remove plaque and decrease bacterial load, and, where available,
the use of over-the-counter fluoride rinses to reduce caries incidence,
should be reinforced at each recall appointment.
• Asymptomatic patients should be seen for routine cleanings and
evaluation at least every 6 months.
220. Endodontic Procedures
• No substantial evidence exists to suggest that patients should not
receive endodontic therapy where indicated based on their HIV
status alone.
• Symptomatic patients with low CD4+ cell counts, extraction and
curettage followed by an appropriate course of antibiotics may
provide faster resolution of chronic infection.
221. Surgical procedures
• Pre-procedural antimicrobial mouthrinse.
• Intraoral fungal infections - An appropriate course of antifungal
therapy - prior to procedures likely to cause bleeding to reduce the
risk for systemic fungemia.
• Post-operative complications observed may be treated on a routine
outpatient basis.
222. Restorative Procedures
• Routine restorative procedures, including operative and fixed and
removable prosthodontics, may proceed as per the standard of care.
• Non-restorable (due to extensive caries) and periodontally hopeless
teeth should be removed as soon as possible to reduce bacterial and
fungal reservoirs.
223. Orthodontic Considerations
• Asymptomatic HIV patients respond to orthodontic treatment in the
same manner as do non-HIV orthodontic patients.
• Late stage AIDS , is a primary contraindication for orthodontic
treatment.
224. Conclusion
• The oral lesions are often early warning signs of HIV infection,
which highlights the key role of the dental practitioner in diagnosis.
• Early diagnosis, careful treatment planning with aggressive
prevention and frequent monitoring, as well as prompt treatment of
oral manifestations are likely to improve the quality of life of
patients with HIV/AIDS.
225. References
• Hiv/Aids in dental practice: S R Prabhu
• AIDS and oral health – NS Yadav, Rupam Sinha
• Textbook of oral medicine – burket’s
• A Textbook of Oral Pathology –Shafer’s
• Textbook of Oral Pathology –Nevielle
• Topley and Wilson’s Principles of Bacteriology, Virology and Immunity – 8th
edition (Volume-4), Virology.
• Textbook of Pathology-Robins, 7th edition.
• Microbiology in Clinical Practice – DC. Shauben
• Textbook of Microbiology – Ananthnarayan
• HIV/AIDS in Dental Care, 2002
• Manual for Dental Professions on HIV Disease.
226. • Laboratory Tests for HIV: Diagnosing, Monitoring and Managing AIDS - An
Overview- International Journal of Oral & Maxillofacial Pathology. 2011;2(1):20-
28
• Oral Lesions Associated with Human Immunodeficiency Virus. Disease Dent Clin
N Am 57 (2013) 673–698
• HIV-Positive Patients: Dental Management Considerations. Dent Clin N Am 50
(2006) 635–657
• JADA, vol 133, December 2002, 1619-1629.
• Post Exposure Prophylaxis (PEP) – NACOGuidelines
• Oral Manifestations Associated with HIV/AIDS MAY 2013
• Key to Diagnose HIV/AIDS Clinically through its Oral Manifestations-Journal of
Indian Academy of Oral Medicine and Radiology, July-September
2010;22(3):119-125
• Occupational exposure to HIV and the use of post-exposure prophylaxis-
International journal of dental clinics 2011:3(3):55-58
