BACTERIAL,

VIRAL &
MYCOTIC
INFECTIONS
Prepared by:
Dr Sundeep S Bhagwath
BACTERIAL INFECTIONS
 B A C T E R IA L
IN F E C T IO N S
1. Actinomycosis
2. Syphilis
3. Tuberculosis
4. NOMA
5. Scarlet fever
6. Leprosy
 V IR A L IN F E C T IO N S
2. Herpes Simplex Virus ( HSV )
3. Chickenpox

4. Herpes Zoster (Shingles)

5. Herpangina

6. Hand - Foot - Mouth Disease

7. Infectious Mononucleosis (Glandular fever )

8. Measles

9. Cytomegalovirus infection

10. Acquired Immunodeficiency Syndrome

(AIDS)
 FUNGAL / MYCOTIC
INFECTIONS
2. Candidiasis
3. Histoplasmosis
4. Blastomycosis
5. Aspergillosis
6. Toxoplasmosis
 A C T IN O M Y C O S IS
Chronic granulomatous, localized bacterial
infection.
A E T IO L O G Y :- as a result of infection
by Actinomyces israelii, A. viscosus , A.
Naeslundi, A.odontolyticus etc.
T Y P E S : - according to location,
- Cervicofacial actinomycosis
- Thoracic actinomycosis
- Abdominal actinomycosis
 C E R V IC O F A C IA L
A C T IN O M Y C O S IS
A E T IO L O G Y :- as a result of
infection by A.israelii , A.viscosus, and
A.naeslundi

C L IN IC A L F E A T U R E S :-
Ag e incide nce : young adults
Se x incide nce : More in males
Sys te mic manife s tations :
Site Pre dile ction:
Submandibular,
submental and
cheek areas most commonly.
Bacteria enter through areas of
previous trauma like extraction site,
periodontal pocket, non vital tooth
or infected tonsil.
Sig ns & s ymptoms :
Lesion begins as

asymptomatic wooden
firm area of fibrosis and
later forms a central, softer
area of abscess.
Infection can extend to
surface and drain via a
fistula.
Suppurative discharge may
contain yellowish flecks
which contain colonies of
H IS T O L O G IC A L
F E A TU R E S :
Characterized by formation

of granulation tissue
surrounding large collections
of PMNLs and colonies of
bacteria.
Colonies consist of club
shaped filaments that form a
radiating rosette pattern.
With H & E stain, core of
colony stains blue while
 S Y P H IL IS
Chronic systemic venereal disease of
bacterial etiology causing a granulomatous
reaction.

A E T IO L O G Y :- Treponema pallidum

TYP E S :
-Acquired type ;
Primary stage
Secondary stage
TRANSMISSION: -
2. Direct
contact of a healthy patient
with a diseased patient or carrier of
infection (dentists/dermatologists)
3. Unprotected sexual intercourse
4. Transplacental (from mother to
fetus)
5. Contaminated blood or blood
 A C Q U IR E D S Y P H IL IS
- P R IM A R Y S T A G E -
It is first stage of acquired type of
syphilis
Incubation period ranges from 3
90 days.
Most infective stage
C L IN IC A L F E A T U R E S : -
Ag e incide nce : young adults
Se x incide nce : Males
Site pre dile ction:
Oral cavity - tongue , hard palate and
lips
Genital organs of male and female
N.B Lesion of primary syphilis is called
CHANCRE.
Oral manife s tations :
Mostly solitary.

Appears as painless,
normal colored ulcer.
Can also manifest as a
vascular proliferation
resembling a pyogenic
granuloma.

Ge nital manife s tations :

Most commonly external

genitalia and anal region.

Both genital as well as
extra genital lesions heal
within 3 8 weeks if they
are left untreated
 - S EC O N D AR Y
Occurs
S TAG E -
4 10 weeks after the initial
infection.
Lesioncan arise before the lesions
of primary syphilis have healed.
In
this stage, systemic symptoms
are also seen.
This is also a very infective stage.
C L IN IC A L
F E ATU R E S : -
a) Sys te mic
s ymptoms :
Fever, painless
lymphadenopathy, sore
throat , malaise, weight
loss and
musculoskeletal pain.
Typically, diffuse,
painless, maculopapular
rash develops which is
b ) Oral manife s tations :
(i) Mucous patche s seen
in approx 30% cases.
Manifested as focal areas of
intense spongiosis of oral
mucosa leading to zones of
whitish mucosa.
(ii ) C o n d y lo m a la t u m
appear as papillary lesions
resembling viral papillomas.
Lesions in secondary stage
are usually multiple.
Spontaneous resolution
 - T E R T IA R Y S T A G E -
Occurs if the secondary lesion is untreated.
Can occur several months to years after the
secondary stage has healed.

C L IN IC A L F E A T U R E S : -
Symptoms can be grouped as
- Neurosyphilis
- Cardiovascular syphilis
- Diffuse gummatous lesions
A. NEUROSYPHILIS:
Characterized by infection of central
and peripheral nerve tissues which
manifests as
- General paresis of insane,
- Dementia
- Tabes dorsalis, leads to ataxia and
loss of
deep sensations.
- Psychosis
B . C AR D O VAS C U LAR
S Y P H IL IS :
An e u ry s m o f
a s c e n d in g a o r t a
S t e n o s is a n d
o c c lu s io n o f c o r o n a r y
a rte ry.
L e f t v e n t r ic u la r
h yp e rtro p h y
C o n g e s t iv e c a r d ia c
C. GUMMA:
Affects skin, mucosa,
soft tissues and even
bones.
Intraoral affects
palate and tongue
mostly.
Presents as indurated,
nodular / ulcerated
lesion which can be
 Diffuse atrophy and loss
of papillae from dorsal
surface result in luetic
glossitis.
Considered premalignant
condition previously, but
not supported by recent
research.
 CONGENITAL SYPHILIS
Occurs as a result of transplacental
transfer after 4th -5th months
The fetus may be stillborn, or die
immediately after birth or born with
the disease or become involved by
disease after a few months or
years.
C L IN IC A L F E A T U R E S : -
Three pathognomonic features

described by Sir Jonathan Hutchinson

(Hutchinsons triad)
- Hutchinsons teeth
- Interstitial keratitis
- Eighth nerve deafness
All patients may not exhibit all the
features of triad.
1 . H u t c h in s o n s
te e th :
Alteration of both anterior
( H u t c h in s o n s
in c is o r s ) as well as
posterior teeth
( M u lb e r r y m o la r s ) .
Anterior teeth taper cervico-
incisally and show a
hypoplastic central notch.
Molars also show similar
tapering with an abnormal
occlusal morphology,
2 . In t e r s t it ia l k e r a t it is :
Usually not seen at birth, but develops

between 5 25 years.
Affected eyes shows opacified cornea,
with resultant loss of vision.
3 . O t h e r a lt e r a t io n s :
- Eighth nerve deafness
- Saddle nose
- Saber shin (Anterior bowing of tibia)
- High arched palate
H IS T O L O G IC A L
F E ATU R E S : -
Non specific features.

Epithelial surface in primary

stage is usually ulcerated and
may be either ulcerated /
hyperplastic in secondary
stage.
Underlying CT shows
predominantly perivascular
inflammatory infiltrate of
lymphocytes and plasma cells.
Best way to diagnose syphilis is
 Oral tertiary stage lesions show surface
ulceration with peripheral
pseudoepithelial hyperplasia.
Underlying CT shows foci of
granulomatous inflammation with well
circumscribed collections of
macrophages and multinucleated giant
cells.
 T U B E R C U L O S IS
Chronic granulomatous systemic
bacterial disease.
Infection caused by Mycobacterium
tuberculosis.
Incidence decreased dramatically with
the discovery of antibiotics in 1940s.
However, incidence increasing
alarmingly since 1980s due to various
factors like association with HIV,
transmission of TB in crowded or
P A T H O G E N E S IS : -
Infection must be distinguished from active
disease.
Primary infection occurs in previously
unexposed persons and almost always in lungs
leading to formation of localized, fibrocalcified
nodule.
Viable organisms may exist in these nodules
and remain dormant for years.
Only 5% - 10% patients progress from primary to
active disease and immunosupression is often
responsible for reactivation of dormant
organisms
T R A N S M IS S IO N : -
- Inhalation of micro-organisms
- Eating or drinking contaminated
milk (bovine TB)
- Direct contact with bodys fluids
like blood , saliva & urine
- Blood transfusion
- Mother to fetus (transplacental)
C L IN IC A L F E A T U R E S :-
1. Primary TB: Usually asymptomatic.
Fever and pleural effusion may occur.
2. Se condary TB:
Located in apex of lungs, but can spread to
many sites through lymphatics, vascular
channels.
Symptoms of low grade fever, night
sweats, malaise, anorexia and weight loss.
Extrapulmonary TB is common and can
occur anywhere in body like skin (lupus
vulgaris), lymph node (scrofula), bones,
kidneys, GIT and head & neck also.
O R A L L E S IO N S O F
TB :
M o s t ly m a n if e s t
a s c h r o n ic
p a in le s s u lc e r .
M a y a ls o a p p e a r
n o d u la r , g r a n u la r
o r e ve n
le u k o p la k ic
a re a s .
P r im a r y T B
le s io n s m o s t ly
 Drinking milk
contaminated with M.bovis
can lead to non tubercular
infections of cervical and
oropharyngeal lymph
nodes, called as
Scrofula.
Occasionally, significant
caseous necrosis can
occur and form numerous
fistulas through overlying
H IS T O L O G IC A L
F E ATU R E S : -
Classic presentation

formation of granuloma.
Circumscribed collection of
epitheloid macrophages,
lymphocytes and langhans
giant cells often with central
caseous necrosis.
Demonstration of
M.tuberculosis is by acid
fast stains like Zeihl
 C A N C R U M O R IS
Acute, rapidly progressing, localized,
bacterial infection of the orofacial tissues
and jaws
Causative organisms Fusobacterium
necrophorum, F.nucleatum and Prevotella
intermedia.
Predisposing factors include poverty,
malnutrition, poor oral hygiene & sanitation,
recent illness, malignancy and
immunodeficiency states like AIDS.
C L IN IC A L F E A T U R E S : -
Ag e incide nce : Predominantly
children between 1 10
years.
Se x incide nce : Male
Site pre dile ction:
Usually begins on gingivae as ANUG,
then spreads facially / lingually to
adjacent soft tissues.
Sig ns & s ymptoms :
Disease begins initially in

gingivae as ANUG and later

spreads to adjacent soft tissues.
As necrosis extends deeper over
next few days, zones of bluish-
black discoloration of overlying
skin develop.
These zones break down into
areas of yellowish necrosis that
spread into adjacent bone.
Other signs fever, fetid odor,
pain, malaise and regional
MYCOTIC INFECTIONS
 C A N D ID IA S IS
Refers to infection with yeast like
fungal organism.
Most common oral fungal infection.

It is a component of normal oral

flora.
Can occur in persons who are
debilitated by other diseases or in
otherwise healthy individuals also.
P R E D IS P O S IN G F A C T O R S : -
a) Local Factors :
- Mucosal trauma
- Denture wearers
- Denture hygiene
- Tobacco smoking
- Carbohydrate rich diet
- Drugs (Broad spectrum antibiotics,
steroids, immunosuppressant /
cytotoxic agents)
- Xerostomia
b) Sys te mic factors :
- Iron deficiency anaemia
- Megaloblastic anaemia
- Acute leukaemia
- Diabetes mellitus
- HIV infection
- Other immunodeficiency states
C L A S S IF IC A T IO N O F
C A N D ID IA S IS : -
Group 1 (Conditions confine d to the
oral mucos a):
Acute -
- Acute pseudomembranous candidiasis
- Acute atrophic candidiasis
Chronic -
- Chronic atrophic candidiasis
- Candida associated angular cheilitis
- Chronic hyperplastic candidiasis

Group 2 (oral manife s tations of

g e ne ralize d candidias is )
 AC U TE
P S EU D O M EM B R AN EO U S
C A N D ID IA S IS
(T H R U S H )
Best recognized form of candidiasis.
Characterized by development of white
plaques that can be scraped off with
tongue blade.
Can be initiated by broad spectrum
antibiotics or immune dysfunction.
 Occurs
characteristically on
buccal mucosa, palate
and dorsal tongue.
Usually asymptomatic
or patients may c/o
burning sensation of
mucosa or unpleasant
taste in mouth.
Can occur in infants
 A T R O P H IC C A N D ID IA S IS
( E r y t h e m a t o u s c a n d id ia s is )

Several presentations seen

1. Acute atrophic candidiasis
2. Median rhomboid glossitis
3. Chronic multifocal candidiasis
4. Angular cheilitis
5. Chronic atrophic (denture sore
mouth) candidiasis
1 . A C U T E A T R O P H IC
C A N D ID IA S IS : -
Also called antib iotic

s ore mouth , as it
follows course of broad
spectrum antibiotics.
Patients c/o burning
sensation of mucosae.
Seen as diffuse loss of
filliform papillae resulting in
a bald appearance of
2 . M E D IA N R H O M B O ID
G L O S S IT IS :
Also called central papillary

atrophy of tongue.
Well demarcated erythematous
zone affecting midline of dorsum
of tongue.
Often asymptomatic.
Erythema due to loss of filliform
papillae.
Sometimes, other areas of oral
cavity like hard palate and angles
of mouth also show lesions
3 . C H R O N IC
A T R O P H IC
C A N D ID IA S IS : -
Characterized by varying

degrees of erythema in
denture bearing areas of
usually maxillary
prostheses.
Usually asymptomatic.
Patients give h/o wearing
denture continuously.
4 . AN G U LAR
C H E IL IT IS : -
Also called perleche.

Characterized by erythema,
fissuring and scaling of
corners of mouth.
Typically occurs either along
with multifocal candidiasis or
in old patients with reduced
vertical dimension.
Saliva pools in these areas,
keeping them moist and
5 . C H R O N IC
H Y P E R P L A S T IC
C A N D ID IA S IS :
Least common of all types.

Appears as non scrapable

white patch resembling
leukoplakia (candidal
le ukoplakia)
Believed that it represents
candidiasis superimposed on
pre-existing leukoplakia.
Diagnosis confirmed by
demonstration of candidal
C H R O N IC
M U C O C U TA N E O U S
C A N D ID IA S IS : -
Severe oral candidiasis can

also occur as a component of a

rare immunological disorder
called mucocutaneous
candidiasis.
Autosomal recessive disorder.
Immune dysfunction becomes
evident in early life patient
develops candidiasis of mouth,
nails, skin and other mucosae.
H IS T O L O G IC A L
F E A TU R E S : -
Biopsy specimen show

hyperparakeratinization,
elongation of rete ridges,
chronic inflammatory cell
infiltration of underlying CT
and small microabscesses
collection of PMNLs) within
parakeratin layer.
Candidal hyphae can be seen
embedded in parakeratin layer
EXFOLIATIVE CYTOLOGY: -
Candidal hyphae can also be
demonstrated by exfoliative cytology by
PAS stain.
Hyphae are stained magenta color by the
PAS stain.

R A P ID D IA G N O S T IC T E S T : -
A 10% - 20% KOH preparation used for

rapid diagnosis.
KOH lyses background of epithelial cells
VIRAL INFECTIONS
1. Herpes simplex infection
2. Varicella
3. Herpes zoster
4. Infectious mononucleosis
5. Enterovirus infections
- Herpangina
- Hand foot & mouth disease
- Rubeola & Rubella
- HIV
 H E R P E S S IM P L E X
IN F E C T IO N
Herpes simplex virus (HSV) DNA virus.
Belongs to human herpesvirus (HHV)
family, also called Herpetoviridae.
Other members of this family are varicella-
zoster virus, Epstein-Barr virus,
Cytomegalovirus etc.
Humans only known natural reservoirs
and can stay in the host for life and
become periodically reactivated.
 TYPES OF HSV
He rpe s s imple x virus 1:
Spread through saliva.
Lesions above the waist, in oral, facial and
ocular areas including pharynx, and skin.

He rpe s s imple x virus 2:

Transmitted through sexual contact.

Involves genitalia and skin below the

waist.
 PATHOGENESIS
HSV infections 2 patterns seen.
1. Primary infe ction: -
- Initial exposure to virus, no antibodies
are produced.
- Occurs in young age, often
asymptomatic.
- Virus taken up in sensory nerves and
transported to associated ganglia.
2. Secondary / recurrent infection: -
- Virus residing in ganglia is reactivated.
- Not always symptomatic; sometimes
patients only shed the virus through
saliva.
P r e d is p o s in g f a c t o r s f o r
r e a c t iv a t io n o f v ir u s :
5. Old age
6. UV light
7. Emotional stress
8. Trauma
 H E R P E T IC
G IN G IV O S T O M A T IT IS
Commonest pattern of primary HSV
infection.
Incubation period is 3 9 days.
C L IN IC A L F E A T U R E S : -
Ag e incide nce : 6 months 5 years
Se x incide nce : Nil
Site pre dile ction:
Affects movable and immovable mucosae.
Sig ns & s ymptoms :
Prodromal symptoms fever

with chills, nausea, anorexia

and cervical
lymphadenopathy.
Begins as small pinhead size
vesicles which coalesce and
form numerous red lesions.
In all cases, gingiva red,
enlarged and painful.
Lip lesions can extend to
vermilion zone
RECURRENT HERPES LABIALIS
Can occur either at primary
site
or in adjacent areas.
Commonest sites vermilion
zone and adjacent area of
lips.
Multiple, small, erythematous
papules develop and form
clusters of fluid filled vesicles.
Vesicles rupture and crust
within
2 3 days and heal within 7
HERPETIC WHITLOW
Less common presentation.
Infection of fingers, and
thumb.
Occurs due to self
inoculation in children with
orofacial HSV.
Can also occur in medical
and dental professionals
who do not wear gloves and
come in contact with
H IS T O L O G IC A L
F E ATU R E S : -
Main effect of virus on epithelial

cells.
Infected epithelial cells show
acantholysis, nuclear enlargement
and ballooning degeneration.
Nuclear fragmentation with
condensation of chromatin around
periphery of nucleus.
These cells called Tzanck cells.
Fusion of adjacent degenerated cells
multinucleated infected cells.
D IA G N O S IS : -
Commonly used diagnostic procedures

cytological smear and tissue biopsy.

Cytosmear is best as it is the least
invasive and cost effective.
Histological changes also are
characteristic and only VZV produces
similar changes within epithelium, but it
can be differentiated easily from HSV.
 VARICELLA
(Chickenpox)

VZV is similar to HSV in many respects.

Chickenpox represents primary infection
with VZV.
Herpes zoster or Shingles represents
reactivation of the latent VZV residing
within the ganglia.
VZV spreads through droplets or direct
contact with infected persons.
Incubation period is 10 21 days.
C L IN IC A L F E A T U R E S : -
Ag e incide nce : between 5 9 years.
Se x incide nce : Nil
Site pre dile ction: Face, trunk and
extremities.
Prodromal s ymptoms :
- Fever
- Malaise
- Pharyngitis
- Nausea
- Anorexia
Sig ns & s ymptoms :
All lesions pass through phases

of erythema, vesicle, pustule

and crusting.
Vesicle is surrounded by zone of
erythema.
In contrast to HSV, vesicles
continue to erupt for 3 4 days.
Thus, old crusted lesions are
mixed with new vesicles.
Infected persons are contagious
from 2 days before appearance
of vesicles until all vesicles
Oral manife s tations : -
Oral lesions are common and

may precede skin lesions.

Common sites palate and
buccal mucosa.
Oral lesions begin as 3 -4 mm
opaque white vesicles that
rupture to form 1 3 mm
ulcers.
VZV oral lesions can be
distinguished easily from HSV
as VZV lesions are rarely
C O M P L IC A T IO N S : -
1.Childre n:
- Secondary skin infections
- Encephalitis
- Pneumonia
2. Adults :
- Varicella pneumonitis
- Encephalitis
- Pneumonia
- Early pregnancy involvement may cause
abortion or congenital defects.
D IA G N O S IS : -
H/o exposure to VZV within last 3

weeks.
Characteristic vesicles.
Demonstration of cytopathological
changes within epithelial cells
harvested from vesicular fluid.
 HERPES ZOSTER
(Shingles)
The primary VZV infection is
transported up the sensory nerves
and remains latent within the dorsal
spinal ganglia.
Herpes zoster infection occurs by
reactivation of the VZV.
Unlike HSV, there is usually a single
recurrence.
P R E D IS P O S IN G
F AC TO R S : -
2. Immunosupression

3. Treatment with cytotoxic drugs

4. Radiation

5. Presence of malignancy
6. Alcohol abuse
7. Dental manipulation
C L IN IC A L F E A T U R E S : -
Ag e incide nce : Middle age to old
age
Se x incide nce : Nil
Site pre dile ction: Affects areas
of skin innervated
by the affected
sensory nerve
S ig n s & s y m p t o m s :
Viral infection proceeds in three phases
prodromal, acute and chronic
A. Prodromal:
Virus replicates within ganglia, causing
ganglionitis resulting in severe neuralgia
(responsible for pain preceding the rash)
As virus travels down the nerve, pain intensifies.
Pain is accompanied by fever, malaise and
headache 3 4 days before cutaneous /
mucosal lesions develop.
Typically one dermatome is affected, but two or
B. Acute phas e :
1 4 days after prodromal phase,

affected skin develops clusters of

vesicles on erythematous base.
Within 3 4 days, they become
pustular, ulcerate and begin to
crust after 7 10 days.
Lesion develop along the path of
distribution of sensory nerve and
terminate at midline.
Resolution occurs within 2 3
weeks and usually heal by
Oral manife s tations :
Oral lesion occur if trigeminal

nerve involved.
May occur on movable or bound
mucosa.
Like chickenpox, lesions appear
as 14 mm white, opaque vesicles
which rupture, forming shallow
ulcers.
R AM S AY H U N T
S Y D R O M E combination of
cutaneous lesions of external
DIAGNOSIS: -
Clinical presentation is typical.
Viral culture (takes at least 24 hours).
Cytosmear to demonstrate
cytopathological viral effects.
Direct staining of cytosmear with
fluorescent antibodies for VZV.
INFECTIOUS MONONUCLEOSIS
(Glandular fever)

Results from exposure to Epstein-Barr

virus (EBV).
Transmission intimate contact like
kissing, sharing of straws, contaminated
salivary transmission in children.
Exposure during childhood
asymptomatic.
Symptomatic infections arise in young
adults.
C L IN IC A L F E A T U R E S ; -
Ag e incide nce : children
Se x incide nce : Nil
Site incide nce :
Apart from systemic manifestations,
affects anterior and posterior cervical
chain lymph nodes as well as
oropharyngeal tonsils.
Intra oral hard palate and gingiva.
Sig ns & s ymptoms :
1 . S y s t e m ic =
Fever, lymphadenopathy,,
pharyngitis, rhinitis, cough,
hepatosplenomegaly.
In 90% cases, prominent,
symmetric, tender
enlargement of anterior and
posterior cervical chain lymph
nodes.
2 . O ra l =
Petechiae on hard or soft

palate and enlargement of

D IA G N O S IS : -
Diagnosis is suggested by clinical

presentation
WBC count is raised with differential
count showing lymphocytosis as high
as 70% - 90%.
Classical serological finding
presence of Paul Bunnell heterophil
antibody, present in 90% of affected
 RUBEOLA
Rubeola / Measles is a viral infection
produced by paramyxovirus.
Incidence dramatically reduced since use
of measles vaccine.
Incubation period 10 to 12 days
C L IN IC A L F E A T T U R E S : -
Ag e incide nce : Young children
Se x incide nce : Nil
Site pre dile ction: Face, trunk and
Sig ns & s ymptoms :
Most cases arise in spring and spread

through respiratory droplets.

Prodromal symptoms of fever,
malaise, coryza and cough.
Rash appears after a few days and
lasts for 4 7 days with first
appearance on face followed by trunk
and extremities.
Oral manife s tations :
Multiple areas of mucosal

erythema on labial and

buccal mucosa and soft
palate (Kopliks spots).
Within these areas, bluish
white macules may be
seen.
These spots represent
areas of epithelial
C O M P L IC A T IO N S : -
2. Otitis

3. Pneumonia

4. Persistent bronchitis
5. Diarrhea

6. Encephalitis
 HERPANGINA
Caused by coxackievirus A or B or
echoviruses all these belong to
enterovirus family.
C L IN IC A L F E A T U R E S : -
Ag e incide nce : Children & young adults.
Se x incide nce : Nil
Site pre dile ction:
Primarily systemic disease, with oral
lesions mainly in soft palate and tonsillar
Sig ns & s ymptoms ::
Begins with significant sore

throat, dysphagia and fever.

Occasionally, vomiting,
myalgia and headache.
Oral lesions begins as 2-4 mm
sized, red macules which form
fragile vesicles that rapidly
ulcerate.
Systemic symptoms subside
within a few days and ulcers
heal within 7 10 days.
 ACQUIRED IMMUNODEFICIENCY
SYNDROME (AIDS)
More than 25 million cases worldwide.
Considered almost 100% fatal and no
known vaccine developed so far.
R O U T E S O F T R A N S M IS S IO N :
-
4. Sexual contact

5. Infected blood / blood products

6. Intravenous drug abuse
P A T H O G E N E S IS : -
When virus enters the body, its DNA
incorporated into primary target cell i.e. CD4+
helper T lymphocyte.
Similar to other viral infections, antibodies to
virus are formed but are not protective.
Virus can remain silent or cause cell death, as a
result, decrease in helper T- cells occurs,
leading to loss in immune function.
There is an asymptomatic stage lasting for about
8 10 years after which the final symptomatic
stage develops.
C L IN IC A L F E A T U R E S : -
After inoculation, patient may be asymptomatic

or develop acute response similar to infectious

mononucleosis.
Acute response fever, generalized
lymphadenopathy, sore throat, myalgia,
diarrhea, maculopapular rash etc.
Acute syndrome clears within a few weeks and a
variable asymptomatic phase follows which may
last for 8 10 years.
Symptomatic phase opportunistic infections
(pneumonia, CMV, HSV, TB etc) and neoplastic
processes (Kaposi sarcoma, Non-Hodgkins
 ORAL MANIFESTATIONS
Group 1 (lesions strongly associated with HIV):
1. Oral candidal infections
- Erythematous
- Hyperplastic
- Pseudomembranous
2. Hairy leukoplakia
3.HIV associated periodontitis
- HIV gingivitis
- HIV periodontitis
- Necrotizing ulcerative gingivitis
- Necrotizing ulcerative stomatitis
4. Kaposi sarcoma
 ORAL CANDIDIASIS

HIV ASSOCIATED
PERIODONTITIS

HAIRY LEUKOPLAKIA
 HIV ASSOCIATED GINGIVITIS

NECROTIZING ULCERATIVE
GINGIVITIS

NECROTIZING ULCERATIVE STOMATITIS

KAPOSI SARCOMA

Patch stage

Plaque stage

Nodular stage
Group 2 (lesions less commonly associated
with HIV):
1. Aphthous ulcers (oropharyngeal region)
2. Idiopathic thrombocytopenia
3. Salivary gland disorders
- Dry mouth and decreased salivary flow
- Uni or bilateral swelling of major glands
4. Viral infections (apart from EBV)
- Cytomegalovirus
- Herpes simplex virus
- Human papilloma virus
 HIV ASSOCIATED APHTHOUS ULCERS

HIV ASSOCIATED HPV

INFECTION

HIV ASSOCIATED HERPETIC ULCERS

 DIAGNOSIS
Scre e ning te s t: ELISA is most
commonly used test. But it can
show false positive results.

We s te rn Blot te s t: It is a test
to detect viral antibodies. More
accurate than ELISA.
H A IR Y L E U K O P L A K IA
It is a chronic, localized viral infection
Caused by Epstein-Barr virus.
C L IN IC A L F E A T U R E S :-
Ag e incide nce : Young age
Se x incide nce : Males
Site pre dile ction: Lateral borders of the
tongue, bilaterally
Sig ns and s ymptoms : Asymptomatic, slowly
spreading. non scrapable,
papillary, greyish white lesion.
H IS T O L O G IC A L
F E ATU R E S
Lesion is characterized
by hyperparakeratosis
and acanthosis.
Epithelial cells are
infected by EBV which
appear as swollen cells
with ballooning
degeneration.
Characteristic pattern of
peripheral margination of
nuclear chromatin is
seen, called nucle ar
THANKS FOR YOUR PATIENCE !