SAPAN PATEL

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
VIRUS CLASSIFICATION :
Group Group VI (ssRNA-RT)

Family Retroviridae

Genus Lentivirus

Species Human immunodeficiency virus

1
Species Human immunodeficiency virus
2
HIV Structure / Morphology of HIV
 Around 120 nm in diameter (120 billionths
of a meter; around 60 times smaller than a red
blood cell)
 Roughly spherical.
Cylindrically shaped nucleoid and the
surrounding proteins, both enclosed a lipid,
fatty, envelope.
The nucleoid is composed of two proteins
known as Nucleoid Core Protein (p24) and
Matrix Core Protein (p17).
The viral membrane encloses the particle,
and has about nine or ten gp120 spikes
embedded in it which are involved in binding
and membrane fusion when the virus particle
attaches to a cell.
 The inner core is the "payload" of the virus, containing the viral RNA and some enzymes (reverse
transcriptase, protease, integrase).
Reverse transcriptase :
 Common to all retroviruses, this enzyme transcribes the viral RNA into double-stranded DNA.
Integrase :
 This enzyme integrates the DNA produced by reverse transcriptase into the host's genome.
Protease :
 A protease is any enzyme that cuts proteins into segments. HIV's gag and pol genes do not produce
their proteins in their final form, but as larger combination proteins; the specific protease used by
HIV cleaves these into separate functional units. Protease inhibitor drugs block this step.
HIV life cycle / How does HIV live ?
 HIV does not survive well outside the human body or in the outside
the environment. Therefore, HIV virus does not last very long.
 However, laboratory studies have proved that HIV can only survive
within one or two seconds. The studies also shown that drying HIV
reduces the amount of virus by nearly 95 percent within several
cases.
 The external protein of HIV (gp120) binds to the CD4 protein, which
is found on the surface of the T4 lymphocytes and macrophages.
This fact allows HIV to infect and destroy T4 lymphocytes.
 The attachment of viral particles to the
cell.
 Protein gp120 interacts with CD4 and
then with a second protein of the cell
surface (the chemokine receptor
CXCR4 or CCR5) allowing the fusion
of viral and cellular membranes
mediated by gp41.
 After membrane fusion, the viral core
enters the cell and the viral RNA is
released.
Virion interaction with CD4 receptor and CXCR4 co-
receptor
 Mode of Transmission

Sexual Contact (75%) Sharing of needles (10%)

Pregnancy & breast feeding (10 – 50%) Blood Transfusion (1%)

HIV CANNOT be transmitted
by:
 Coughing or Sneezing
 Being bitten by an insect
 Touching or Hugging
 Kissing
 Going to public bath or pool
 Using a public toilet
 Shaking hands
 Working with a person who is HIV infected
 Using telephones
 Drinking water or preparing or eating food
 Sharing cups, glasses, plates, or other utensils
CLINICAL FEATURES OF HIV INFECTION:
 AIDS is only the last stage.
 The Centers for Disease Control (USA) have classified the
clinical course of HIV infection under various groups :

Acute Retroviral Syndrome

Window Period

HIV Positive Asymptomatic Period

HIV Positive Symptomatic Period

AIDS
 HIV
STAGE OF Acute Window
positive HIV positive
retroviral asympt symptomatic AIDS
ILLNESS Syndrome Period
omatic phase
phase
AIDS defining
Prolonged fever, illness,
recurrent common Opportunistic
Fever, skin infections, TB, infections,
Symptoms rash
Nil Nil
diarrhoea, wasting
Generalized syndrome,
lymphadenopathy dementia
positive
HIV test:
ELISA/WB
From time 6-12
Within 2 -4 5-10 years after
of getting weeks About 2-5 years after
Onset weeks of
HIV after HIV HIV infection
getting HIV
infection infection
infected infection
3 ELISA or
PCR Antigen PCR or P 24 2 ELISA and 2 major 2 ELISA and AIDS
Diagnosis test antigen test
1 WB & 1
symptoms defining illness
ELISA

Transmission YES YES YES YES YES

of disease
 Clinical Symptoms
Phase I – Asymptomatic phase
 CD4 count >500 cells/ml blood
 Flu like symptoms

Phase II – Symptomatic
 CD4 count = 200 cells/ml blood
 Weight loss, fatigue,
 Diarrhea, infections, etc.

Phase – Late Symptomatic

 CD4 count <200 cells/ml blood
 Full blown AIDS
 Memory loss Heavy night
sweats
Persistent
headache Loss of
appetite
White
patches on
Chronic
tongue
Diarrhea

Swelling Fatigue &

Lymph muscle
Nodes weakness

High fever Severe

weight loss
Symptoms of HIV infection
 Cryptococcal Cytolomegalovirus
meningitis rentitis

Toxoplasmosis Herpes
encephalitis Simplex
Virus
Pulmonary
tuberculosis Oral
Candidiasis

Cryptospondiosis Kaposi’s
Sarcoma
Candida
oesophagitis
Pneumocytosis Malignant
carni pneumonia Lymphoma
AIDS related illness &
opportunistic infections
 It is known that HIV has extensive genetic flexibility causing
complications with immune responses, drug treatments, and
vaccination attempts, however, it is not known what allows for
HIV's genetic diversity among infected individuals.

 It is believed that reverse transcriptase, with its high error rate, on

average brings forth a mutation once in every 2,000 nucleotides.

 In time, several mutant HIV virions can be found within a single

infected individual, therefore, a vaccine developed for one mutant
HIV gene may not work against the others.
 CD4+ T- Lymphocyte Categories

 Category 1: > 500 cells /mm3 (or CD4% >28%)

 Category 2: 200-499 cells /mm3 (or CD4% 14-28%)

 Category 3: <200 cell/mm3 (or CD4% <14%)

Symptom Categories of the Disease

Category A
 Category A consists of one or more of the
conditions listed below in an adolescent or adult
(>13 years of age) with documented HIV
infection. Essentially, conditions listed in
Categories B and C must not have occurred
 Asymptomatic HIV infection
 Persistent generalized lymphadenopathy
 Acute (primary) infection with accompanying illness or
history of acute HIV infection
 Category B consists of symptomatic conditions
in an HIV- infected adolescent or adult that are
not included among conditions listed in clinical
category C and that meet at least one of the
following criteria:
 The conditions are attributed to HIV infection or are
indicative of a defect in cell mediated immunity OR
 The conditions are considered by physicians to have a
clinical course or to require management that is
complicated by HIV infection.
Examples of conditions in clinical category B include but are not
limited to:
 Bacillary angiomatosis
 Candidiasis, oropharyngeal (thrush)
 Candidiasis, vulvovaginal; persistent, frequent, or poorly responsive to
therapy
 Cervical dysplasia (moderate to severe)/ cervical carcinoma in situ
 Constitutional symptoms, such as fever (38.5 degrees centigrade) or
diarrhea lasting greater than 1 month
 Oral Hairy leukoplakia
 Herpes Zoster (shingles), involving at least two distinct episodes or more
than one dermatome
 Idiopathic thrombocytopenic purpura
 Listerosis
 Pelvic inflammatory disease, particularly if complicated by tubo-ovarian
abscess
 Peripheral neuropathy

 For classification purposes, Category B conditions take precedence

over those in Category A.
 For example, someone previously treated for oral or persistent
vaginal candidiasis (and who has not developed a Category C
disease) but who is now asymptomatic should be classified in
Category B.
Category C
Conditions:
 Conditions of bronchi, trachea, or lung
 Candidiasis, esophageal
 Cervical cancer, invasive
 Coccidiomycosis, disseminated or extrapulmonary
 Cryptococcosis, extrapulmonary
 Cryptosporidiosis, chronic intestinal (persisting >1 month)
 Cytomegalovirus disease (other than liver, spleen or nodes)
 Cytomegalovirus retinitis (with loss of vision)
 Encephalopathy, HIV related
 Herpes Simplex, chronic ulcers (persisting >1 month) or
bronchitis,
 pneumonitis or esophagitis
 Histoplasmosis, disseminated or extra pulmonary
 Isosporiosis, chronic intestinal (persisting >1 month)
 Kaposi’s sarcoma
 Lymphoma, Burkitt (or equivalent term)
 Lymphoma, primary of brain
 Mycobacterium aviumcomplex or
mycobacterium kansaii, disseminated or
extrapulmonary
 Mycobacterium tuberculosis, any site
(pulmonary or extra pulmonary)
 Mycobacterium other species, unidentified
species, disseminated or extrapulmonary
 Pneumocystis carnii pneumonia
 Pneumonia recurrent
 Progressive multifocal leukoencephalopathy
 Salmonella septicemia, recurrent
 Toxoplasmosis
 Wasting syndrome due to HIV
WHO Clinical Staging of HIV Disease
in Adults and Adolescents (2006
revision)

Clinical Stage I:

 Asymptomatic

 Persistent generalized lymphadenopathy

Clinical Stage II:
 Moderate unexplained weight loss (under 10% of
presumed or measured body weight)
 Recurrent respiratory tract infections (sinusitis,
tonsillitis, otitis media, pharyngitis)
 Herpes zoster
 Angular chelitis
 Recurrent oral ulceration
 Papular pruritic eruptions
 Seborrhoeic dermatitis
 Fungal nail infections
Clinical Stage III:

 Unexplained severe weight loss (over 10% of presumed or

measured body weight)
 Unexplained chronic diarrhoea for longer than one month
 Unexplained persistent fever (intermittent or constant for longer
than one month)
 Persistent oral candidiasis
 Oral hairy leukoplakia
 Pulmonary tuberculosis
 Severe bacterial infections (e.g. pneumonia, empyema,
pyomyositis, bone or joint infection, meningitis, bacteraemia)
 Acute necrotizing ulcerative stomatitis, gingivitis or periodontitis
 Unexplained anaemia (below 8 g/dl), neutropenia (below 0.5
billion/l) and/or chronic thrombocytopenia (below 50 billion/l)
Clinical Stage IV:
 HIV wasting syndrome
 Pneumocystis pneumonia
 Recurrent severe bacterial pneumonia
 Chronic herpes simplex infection (orolabial,
genital or anorectal of more than one month’s
duration or visceral at any site)
 Oesophageal candidiasis (or candidiasis of
trachea, bronchi or lungs)
 Extrapulmonary tuberculosis
 Kaposi sarcoma
 Cytomegalovirus infection (retinitis or infection of
other organs)
 Central nervous system toxoplasmosis
 HIV encephalopathy
Classification of Oral Lesions
Associated with Adult HIV Infection
(European Community-
Clearinghouse, 1993)
Group 1: Lesions strongly associated with HIV
infection
 Candidiasis
 Erythematous
 Pseudomembraneous
 Hairy leukoplakia
 Kaposi’s sarcoma
 Non-Hodgkin’s lymphoma
 Periodontal disease
 Linear gingival erythema
 Necrotizing (ulcerative) gingivitis
 Necrotizing (ulcerative) periodontitis
Group 2: Lesions less commonly associated
with HIV infection
 Bacterial infections
 Mycobacterium avium-intracellularae
 Mycobacterium tuberculosis
 Melanotic hyperpigmentation
 Necrotizing (ulcerative) stomatitis
 Salivary gland disease
 Dry mouth due to decreased salivary flow rate
 Unilateral or bilateral swelling of major salivary
glands
 Thrombocytopenia purpura
 Ulceration NOS (not otherwise specified)
 Viral infections
 Herpes simplex virus

 Human papillomavirus (warty-like) lesions

 Condyloma acuminatum
 Focal epithelial hyperplasia
 Verruca vulgaris

 Varicella-zoster virus
 Herpes zoster
 Varicella
Group 3: Lesions seen in HIV infection
 Bacterial infections
 Actinomyces israelii
 Escherichia coli
 Klebsiella pneumonia
 Cat-scratch disease
 Drug reactions (ulcerative, erythema
multiforme, lichenoid, toxic epidermolysis)
 Epithelioid (bacillary) angiomatosis
 Fungal infection other than candidiasis
 Cryptococcus neoformans
 Geotrichum candidum
 Histoplasma capsulatum
 Mucoraceae (mucormycosis zygomycosis)
 Aspergillus flavus

 Neurological disturbances
 Facial palsy
 Trigeminal neuralgia

 Recurrent aphthous stomatitis

 Viral infections
 Cytomegalovirus
 Molluscum contagiosum
CRITERIA FOR HIV ASSOCIATED
PERIODONTAL CHANGES.
 Robinson PG et al (1987)
 Erythema of the attached gingiva defined by the presence
of punctuate of diffuse erythema of the attached gingiva.

 Necrotizing periodontal disease(NUG,NUP) defined by the

presence of ulceration of one or more interdental papillae.

 Attachment loss defined by the presence of attachment

loss ≥ 4mm and where the recession is less than twice the
probing depth.

 Attachment loss with reverse architecture or interdental

cratering defined by the presence of attachment loss ≥
4mm and where the recession is greater than or equal to
twice the probing depth (excluding the midbuccal
surfaces).

 Gingivitis-inflammation manifests as change in color, of

marginal gingiva & interdental papillae edema or bleeding
on probing.
LINEAR GINGIVAL ERYTHEMA
 A persistent, linear, easily bleeding,
erythematous gingivitis
 It may or may not be the precursor of NUG
 It mimics periodontitis
 It may be localised or generalised
 The gingivitis may be extend to
 Marginal tissue
 Attached gingiva in punctate or diffuse erythema
 Alveolar mucosa
PATHOGENESIS
 Lesion commonly seen concomitantly with
candidiasis, suggesting a possible etiologic role
of candidial species in LGE.

 Some cases of LGE completely resolved with

antifungal therapy.

 Exact relation is not established.

MANAGEMENT
 They are usually unresponsive to treatment and
may go spontaneous remission
 Scaling and polishing
 Subgingival irrigation with chlorhexidine or 10%
povidone iodine
 Reevaluated after 2-3 weeks
 If patient compliance is adequate and still lesion
persist than suspect candidial infection.

 Systemic fluconazole 100mg for 10 days

 Patient is placed for 2-3 month maintenance

and check for any signs of NUG< NUP< NUS
NECROTIZING ULCERATIVE GINGIVITIS
CLINICAL FEATURES

1. Characteristic punched-out crater like depressions at

the crest of interdental papillae
2. Surface of the craters is covered by a gray,
pseudomembranous slough, demarcated from the
remainder of the gingival mucosa by a pronounced
linear erythema.
3. In some cases the lesions are denuded of the surface
pseudomembrane, exposing the gingival margin, which
is red, shiny and hemorrhagic.
4. The characteristic lesions may progressively destroy the
gingiva and underlying periodontal tissues.
5. Spontaneous gingival hemorrhage or pronounced
bleeding after the slightest stimulation.
6. Fetid odor and increased salivation.
TREATMENT FOR NUG
PRELIMNARY TREATMENT FOR NON-AMBULATORY
PATIENTS
On the 1st day:
 Gently remove the necrotic pseudomembrane
with a cotton pellet saturated with hydrogen
peroxide solution.
 Advise bed rest.
 Rinsing of mouth with hydrogen peroxide 3%
solution mixed with equal amount of warm water
2 hourly.
 Systemic antibiotics. Penicillin 250- 500mg 6
hourly.
 Metronidazole 250-500mg 8 hourly for 7 days.
 Ask the patient to report after 24 hours.
On the 2nd day:
If the condition of the patient is improved, treat like
ambulatory patient.
If no improvement: a bed side visit can be made.
At the bed side the possibility of oropharyngeal involvement
and the patient’s temperature are checked.
Involved gingiva is gently swabbed with hydrogen peroxide.
Prevoius day’s instructions repeated and patient is asked to
report after 24 hours.
TREATMENT OF AMBULATORY PATIENTS
FIRST VISIT:
 complete evaluation of the patient, including a
comprehensive medical history.
 General impression of the patient’s background.
 Vital signs including temperature and palpation for the
presence of enlarged lymph nodes, especially
submaxillary and submental lymph nodes.
 oral cavity is examined for the characteristic lesion of
NUG possible involvement of oropharyngeal region.
 Oral hygiene is evaluated with special attention to the
presence of periodontal pockets, pericoronal flaps and
local factors like poor restorations, distribution of
calculus.
 Treatment during this initial visit is confined to the acutely involved
areas.
1. The acutely involved areas are isolated with cotton rolls and dried.
2. Topical anesthetic is applied, areas are gently swabbed with a
moistened cotton pellet to remove the psuedomembrane and
nonattached surface debris.
3. Area is cleansed with warm water, the superficial calculus is removed.
Ultrasonic scalers are preferred.

 Subgingival scaling and curettage are contraindicated.

 Patients with moderate or severe NUG and local lymphadenopathy or

other systemic signs or symptoms:
antibiotic regimen of amoxicillin 500 mg orally every 6 hours for 10 days or
erythromycin 500mg every 6 hours or
metronidazole 500mg twice daily for 7 days.

 Systemic complications should subside in 1 to 3 days.

Second visit: 1 to 2 days after 1st visit.
1. Patient’s condition is usually improved. Pain is diminished.
2. The gingival margin of the involved area is erythematous but it lacks
pseudomembrane.
3. Scaling is performed and instructions given.

Third visit: 1 to 2 days after 2nd visit:

1. Patient should be usually symptom free though there may still be
erythema and gingiva may be slight painful on tactile stimulation.
2. Scaling and root planing done and plaque control procedures are
maintained
3. Hydrogen peroxide mouthwash is discontinued but chlorhexidine
gargles are continued for 2 to 3 weeks.
Additional treatment considerations:
Contouring of the gingiva as an adjunctive procedure.
Tooth extraction and any other periodontal procedures
should be postponed until 4 weeks after the acute signs and
symptoms of NUG have subsided.
Topical drug therapy is only an adjunctive measure.
Systemic antibiotics, copious fluid consumption, administration
of analgesics, vitamins should be given.
Local procedures are the keystone of the treatment of NUG.
NECROTIZING ULCERATIVE
PERIODONTITIS
 “severe and rapidly progressive disease that has
a distinctive erythema of the free gingiva,
attached gingiva, and alveolar mucosa;
extensive soft tissue necrosis; severe loss of
periodontal attachment; deep pocket
formation is not evident.”

 (1992 glossary of periodontal terms)

 It is more frequently seen in HIV patients
 It is extension of NUG
 It is characterised by soft tissue necrosis, rapid
periodontal destruction, inter proximal bone loss.
 Normally localised form is seen but severe
immune deficiency generalised form is seen
 patients were 20.8 times more likely to have
CD4+ cell counts below 200 cells/mm3 than
patients without NUP
 Some author consider a diagnosis of NUP to be
a marker for immune deterioration and
predictor for the diagnosis of AIDS.
 Others suggested that NUP may be indicator for
HIV infection in undiagnosed patients.
CLINICAL PRESENTATION
 Local ulcerations and necrosis of gingival tissue
with exposure and rapid destruction of
underlying bone, spontaneous bleeding, and
severe pain.
 Spontaneous resolution of nectrotizing lesions,
leaving painless, Deep interdental osseous
craters, that are difficult to clean and leads to
periodontitis
 Severe tooth mobility and subsequent bone loss
 Oral malodor, fever, malaise, lymphadenopathy
MANAGEMENT
 Local debridement, scaling and root planing,
irrigation with CHX or povidone-iodine.
 Pt should encourage for meticulous oral
hygiene.
 Antibiotics– metronidazole (200 mg 2 tab
immediately and then 1 tab 4 times a day for 5-
7 days)
 Fluconazole 100 mg OD for 7 days.
NECROTIZING ULCERATIVE
STOMATITIS
 Extremely painful and destructive condition.
 Affects athe soft tissue and underlying bone
 It may occur separately or extension of NUP.
 Condition is similar to cancrum oris
 Associated with severe immuno deficiency
MANAGEMENT
 Antibiotics- metronidazole
 Antiseptics- chlorhexidine
 If bone necrosis is present than removal of bone
to promote healing
Does HIV cause attachment loss?
 ROBINSON et al concluded that HIV +ve are
more likely to have chronic periodontitis than
general population(2000)

 MEALY et al concluded that incidence and

severity of chronic periodontitis are similar in HIV
positive and HIV negative individuals.(2004)
PATHOGENESIS
 Viruses play important role in periodontitis
 HIV +ve harbors greater no. viruses in
periodontal pocket than HIV –ve persons.
 Herpes virus is most commonly found.(Slots J
2001)
 These viruses increases IL-1, TNF-a secretion.
 Viruses invades tissue diffusely.
 These diffuse invasion leads to marginal
breakdown of tissue from epithelial attachment
and external oral epithelium.
 So it leads to diffuse inflammatory destruction of
soft tissue and hard tissue.
 Current antiretroviral targets
Fusion

Entry T20 Viral protease

CCR5 antag.
SQV
RNA RNA RTV
Proteins
IDV
Reverse RT NFV
transcriptase
RNA APV
RNA LPV
ZDV, ddI,
DNA FOS
ddC, d4T,
RT ATZ
3TC, ABC,
TDF, FTC DNA

DLV, NVP, DNA Provirus

Integrase
EFV
 Currently available drugs
NRTIs
Zidovudine (ZDV)
Dideoxyionisine (ddI)
Dideoxycytidine (ddC)
Stavudine (d4T)
Lamivudine (3TC)
Abacavir (ABC)
Emtricitabine (FTC)
PIs
Saquinavir (SQV)
Ritonavir (RTV)
Indinavir (IDV)
Nelfinavir (NFV)
Amprenavir (APV)
Lopinavir/Ritonavir (LPV/r)
Atazanavir (ATV)
Fos-amprenavir (f-APV)
Tipranavir

NNRTIs
Delaverdine (DLV)
Nevirapine (NVP)
Efavirenz (EFV)
Generic Antiretroviral Drugs
in India

nRTIs NNRTIs Nucleotide Protease Fusion

RTIs inhibitors inhibitors

Zidovudine(AZT) Nevirapine Tenofovir Ritonavir Enfuvirtide

Lamivudine(3TC) Efavirenz Indinavir (T20)
Didanosine(ddI) Delaviridine Saquinavir
Stavudine(d4T) Nelfinavir
Abacavir(ABC) Amprenavir
Emitricitabine(FTC) Atazanavir
Zalcitabine(ddC) Lopinavir/
Ritonavir
What to start?
NRTI

Recommended
Zidovudine NNRTI
NRTI • Nevirapine
Tenofovir
• Lamivudine • Efavirenz
Alternative
Stavudine
Abacavir
Didanosine

API –ASI ART Guidelines 2005-

2006
TREATMENT PROTOCOL
 Health status
 Infection control measures
 Goals of therapy
 Maintenance phase
 Psychological factor
HEALTH STATUS
 pt’s health status should be determined from
health history, physical evaluation, consultation
with the physician
 Treatment decisions depend upon the health of
the patients
 E.g.– delayed wound healing and postop.
Infection are possible complicating factor in AIDS
patients, but otherwise in healthy, asymptomatic,
HIV infected persons whose CD4 count is near
normal is not concerned
What is CD4 level ????
 CD4 count
 Normal 500-1600/mm3
 CD8 count
 Normal 325-1100/mm3
 CD4:CD8 – 0.9 to 1.9
 When CD4 count is less than 350/mm3,
HAART therapy is indicated.
 When CD4 count is less than 200/mm3,
patient has AIDS.
 CD4:CD8 is reversed in AIDS.
Most health care providers prescribe drugs
to prevent opportunistic infections at the
following CD4 levels:
 Less than 200: pneumocystis pneumonia (PCP)
 Less than 100: toxoplasmosis and cryptococcosis
 Less than 75: mycobacterium avium complex
(MAC).
 API –ASI-ART Guidelines 2005-
HIV infected patient 2006

History and
Physical examination

AIDS defining No symptoms

Illness/some
Non-AIDS
defining illness CD4 counts

Stabilize OIs
CD4 <200 CD4 200-350 CD4>350
CD4 counts

CD4 200-250 CD4 250-350

Recommend Monitor Defer
Confirm 4 wks
HAART PVL>100000
HCV/HIVAN
 CD4 count should be done at every 3-4 months
interval
What is current viral load ???
 Viral load– PCR method
 If over 1,00,000/ml than pt should offered
treatment
 Undetectable level means <10,000/ml count
 HAART reduces count to <50/ml
 IL1b,IL-6 and TNF-a levels among HIV-1-infected
patients with a high viral load (>10,000 copies/ml)
were higher than those from patients with a low
viral load(<400 copies/ml)
 For medical researchers, the test has been used to prove that HIV is
never "latent" but is always multiplying. Many people with no
symptoms of AIDS and high CD4 cell counts also had high viral loads.
If the virus was latent, the test wouldn't have found any HIV in the
blood.

 The test can be used for diagnosis, because it can detect a viral load
a few days after HIV infection. This is better than the standard HIV
(antibody) test, which can be "negative" for 2 to 6 months after HIV
infection.

 For prognosis, viral load can help predict how long someone will stay
healthy. The higher the viral load, the faster HIV disease progresses.

 For prevention, viral load predicts how easy it is to transmit HIV to

someone else. The higher the viral load, the higher the risk of
transmitting HIV.

 Finally, the viral load test is valuable for managing therapy, to see if
antiretroviral drugs are controlling the virus. Current guidelines suggest
measuring baseline (pre-treatment) viral load. A drug is "working" if it
lowers viral load by at least 90%; within 8 weeks. The viral load should
continue to drop to less than 50 copies within 6 months.
 The viral load should be measured within 2 to 8
weeks after treatment is started or changed,
and every 3 to 4 months after that.
INFECTION CONTROL
Standard precautions (universal work precautions) and
safe practices
 Wash hands after patient contact, removing gloves.
 Wash hands immediately if hands contaminated with body
fluids.
 Wear gloves when contamination of hands with body
substances anticipated.
 Protective eyewear and masks should be worn when splashing
with body substance is anticipated.
 Health care workers should take precautions to prevent injuries
during procedures and when cleaning or during disposal of
needles and other sharp instruments.
 Needle should not be recapped.
 Needles should not be purposely bent or broken by hand.
 Not removed from disposable syringe nor manipulated by
hand.
 After use disposable syringes and needles, scalpel blades
and other sharp items should be placed in a puncture
resistant container.
 Health care workers who have exudative lesions or
dermatitis should refrain from direct patient care and from
handling equipment.
 All needle stick injuries should be reported to infection
control officer.
 Handle and dispose of sharps safely.
 Clean & disinfect blood / body substances spills with
appropriate agents.
 Adhere to disinfection and sterilization standards.
 Regard all waste soiled with blood/body substance as
contaminated and dispose of according to relevant
standards.
 Vaccinate all clinical and laboratory workers against
hepatitis B.
 Adopt measures like double gloving, changing surgical
techniques to avoid “exposure prone” procedures, use of
needle-less systems and other safe devices.
Body Fluids To Which Universal Precautions Apply
 Blood
 Other body fluids containing visible blood
 Semen
 Vaginal secretions
 Cerebrospinal fluid (CSF)
 Synovial fluid
 Pleural fluid
Body Fluids To Which Universal Precautions Do
Not Apply

 The risk of HIV transmission is extremely low or

negligible
These Include
 Nasal secretions
 Sputum
 Sweat
 Tears Unless these contain visible blood
 Urine
 Vomit
 Saliva
 SALIVA AND HIV TRANSMISSION:
There is only a very slim responsibility that HIV may be transmitted
by saliva, for the following reasons.
 Only a small minority of HIV infected individuals harbour the virus
in whole saliva (e.g. in one study HIV was detected in mixed saliva
of 5% of infected individuals and only in one of 15 parotid saliva
samples). In any case HIV virions cannot exist in cell free State in
saliva, and estimates are that there is less than one infectious
particle of HIV per milliliter of mixed saliva.
 Saliva contains IgA group antibodies to HIV proteins (p24, gp120,
gp160) which may neutralize the infectivity of the virus and are the
basis of salivary kits used for HIV testing in epidemiological
studies.
 Other HIV inhibitory factors in saliva include high molecular weight mucins
thought to entrap the virus, proline rich proteins, and a serine protease
inhibitor termed salivary leucocyte protease inhibitor (SLPI). The latter
possibly blocks cell surface receptors needed for entry of HIV into the cells.
 The virus looses its infectivity when exposed to mixed saliva for 30 minutes.
 Animal studies have shown that it is not possible to transmit HIV by surface
application of the virus on the oral mucosa, although it was transmitted in
this manner through vaginal mucosa.
 The dose of HIV required for infection is far higher than that for hepatitis B
virus (the risk of acquiring hepatitis B infection from a contaminated needle
stick injury is 6-30%, compared with a 0.4% risk of contracting HIV
infection.
Following precautions for preventing transmission of blood-borne
pathogens in
institutional and non institutional dental practice must be strictly
pursued.

 In addition to wearing gloves for contact with oral mucous

membranes of all patients, in dental procedures in which splashing
or spattering of blood, saliva, or gingival fluids is likely, all dental
workers should wear surgical masks and protective eyewear or
chin length plastic face shields. Rubber dams, high-speed
evacuation and proper patient positioning should be utilized to
minimize generation of droplets and spatter.

 Sterilize handpieces after use with each patient, since blood,

saliva, or gingival fluid of patients often get aspirated into the
handpiece or waterline. Flush handpieces that cannot be
sterilized, their outside surface cleaned and wiped with a suitable
chemical germicide, and then rinsed. Handpieces should be
flushed at the beginning of the day and after use with each
patient. Follow manufacturers’ recommendations for use and
maintenance of waterlines and check valves and for flushing of
handpieces. Follow same precautions for ultrasonic air/water
syringes and scalers.
 Thoroughly and carefully clean all blood and saliva
from material that has been used in the mouth (e.g.
bite registration, impression materials), especially
before grinding and polishing intra-oral devices.
Contaminated materials, impressions, and intra-oral
devices should also be cleaned and disinfected
before being handled in the dental laboratory and
before they are placed in the patient’s mouth. When
using disinfection procedures, dental workers should
consult with manufacturers as to the stability of
specific materials because of the increasing variety of
dental materials used intra-orally.

 Wrap with impervious-backed paper, aluminum foil, or

clear plastic wrap those dental equipment and
surfaces which may become contaminated but are
difficult to disinfect (e.g., light cure handles or X-ray-
unit heads). Remove and discard coverings after use
with each patient and replace with clean coverings.
 Be Needle Smart
–Do NOT recap
–Do NOT bend
–Do NOT remove
–Do NOT transport
–Do NOT re-use
POST EXPOSURE PROPHYLAXIS
 Immediate measures:
 2.5% iodine solution is used for washing eyes.

 80% alcohol is used for oral contamination.

Next step :
 prompt reporting
 post-exposure treatment should begin as soon as
possible
 preferably within two hours
 not recommended after seventy -two hours
EXPOSURE CODE
Type Vol/Time/Sevr E. Code
A) Mucous a)Small vol. EC 1
membrane or few drops,
Skin integrity short duration
compromised b)Large volume
major splash, EC 2
longer duration
B)Percutaneo- a)Less severe EC 2
-us exposure (solid needle
scratch)
b)More severe
(large bore EC 3
needle, deep
puncture,visibl-
e blood)
HIV STATUS CODE
HIV Status of Source Code
a) HIV – Negative

b) HIV-Positive
Low titer (asymptomatic HIV SC 1
high CD4 count
HIV-RNA<1500/mL)
High titer (advanced AIDS HIV SC 2
low CD4 count
high viral load)
c)Status unknown HIV SC
unknown
d)Source unknown HIV SC
unknown
EVALUATION OF EXPOSURE
&EXPOSURE SOURCE

 Type of body substance involved

 Route and severity of exposure

DETERMINATION OF PEP
REGIMEN
EC HIV-SC PEP RECOMMENDATION
1 1 Consider basic 2 drug PEP
1 2 Recommend basic 2 drug PEP
2 1 -do-
2 2 Recmnd. Expnded. 3 drug PEP
3 1 or 2 -do-
Un- Consider basic 2 drug PEP
-known irrespective EC status
NO PEP RECOMMENDED
FOR

 Potentially non infectious body

material
 Intact skin exposure
 HIV negative status of source
ANTIRETROVIRAL AGENTS FOR
PEP
 NRTI : ZDV, 3TC, d4T, ABC

 NNRTI : Nevirapine, Efavirenz,

Delaviridine
 P.I. : Indinavir, Nelfinavir, Saquinavir,
Ritonavir
BASIC 2-DRUG REGIMEN
 Zidovudine(ZDV, 300mg BD) +
Lamivudine(3TC, 150mg BD)

 Lamivudine(3TC, 150mg BD) +

Stavudine(d4T, 40mg BD;
30mg for wt.<60kg)

 Didanosine(ddI, 200mg BD;

125 mg BD for wt. < 60kg) +
Stavudine(d4T, 40mg BD)
EXPANDED 3 DRUG REGIMEN
Basic regimen plus one of the following
 Indinavir (IDV) 800mg TDS
 Nelfinavir (NFV) 750 mg TDS
 Efavirenz (EFV) 600mg OD
 Abacavir (ABC) 300mg BD-careful monitoring of
hypersensitivity
REGIMEN
 Basic regimen: Zidovudine (AZT) –600 mg in
divided doses (300mg/twice a day or 200
mg/thrice a day) for 4 weeks + Lamivudine
(3TC) – 150 mg twice a day for 4 weeks

 Expanded regimen: Basic regimen (

Indinavir – 800 mg/thrice a day, or any other
(4 weeks therapy) Protease Inhibitor.
TOXICITY OF PEP

 Common
 Nausea
 Malaise
 Headache
 Anorexia
MONITORING & MANAGEMENT
OF PEP TOXICITY
Baseline and 2 wks after starting PEP
 Complete blood count
 Renal function test
 Hepatic function test
 Evidence of hyperglycemia, hematuria,
hemolytic anemia, hepatitis, crystalluria
COST OF PEP
BASIC REGIMEN:

A) ZDV(300mg) + 3TC (150mg)

 Cipla- Duovir- Rs. 274/ 10 tabs

 Zydus Bigeri-Lamuzid- Rs. 470/ 10 tabs
 Immunus Aurobindo-Zidovex L- Rs. 280 / 10 tabs
B) d4T(40 mg) + 3TC(150mg): Immunus Aurobindo
- Rs. 1020/ 60 tabs

FOR EXPANDED REGIMEN:

 Indinavir(400mg)-Immunus Aurobindo-Indivex- Rs. 1200 / 10 tabs

 Nelfinvair(250mg)-Immunus Aurobindo- Nelvex- Rs. 3600 / 90 tabs

 Efavirenz(200mg)-Immuno Aurobindo-Viranz- Rs. 3600 / 90 tabs

Testing and Counselling

The health care provider should be tested

for HIV as per the following schedule:

i) Base- line HIV test - at time of exposure

ii) Repeat HIV test - at six weeks following
exposure
iii) 2nd repeat HIV test - at twelve weeks following
exposure
Duration of PEP:

 PEP should be started, as early as possible,

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 is not unknown, 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 patient should
be referred to a physician for treatment.
GOALS OF THERAPY
 Primary goal- restoration and maintenance
of oral health, comfort, and function.
 Acute periodontal and dental infection
should be managed.
 Pt. should be motivated for meticulous oral
hygeine
 Conservative, non surgical therapy for all
periodontal conditions
 Extraction should be avoided in NUP,NUS
cases unless pt unable to maintain oral
hygeine
MAINTENANCE PHASE
 Oral hygeine
 Recall patient for every 2-3 months
Follow up - investigations
CD4 - Once in 3-6 months
Viral load- Once in 6 months
CBC- Once in 3 months
LFT- Once in 3 months