ppt presentation

1. Dr.Prashanth Ramachandra
Dept of Oral Pathology, KCDS, Bangalore

2.  Many infections show the early signs and symptoms in the oral
cavity
 Safe guarding both the doctor and the patient
 Early intervention
 Prevention
 Prophylactic measures
 Some signs mimic dental/oral pain
 Prevention of further big complications like endocarditis etc
 Helping in collection of biological samples
 Dentists at times are first persons to diagnose

3.  Scarlet fever – group A β- hemolytic streptococci
 Diptheria – corynebacterium diptheriae
 Tuberculosis – mycobacterium tuberculosis
 Syphilis – Treponema pallidum
 Actinomycosis - Actinomyces israelii
 Tetanus – Clostridium tetany
 Noma – normal oral flora

4.  Disease caused by --group A β-hemolytic
streptococci
 Begins as tonsillitis with pharyngitis (sore
throat)
 Associated with characteristic skin rashes and
strawberry tongue

5.  Common in children 3 to 12 years
 Begins as tonsillitis and pharyngitis, painful,
erythematous, edematous with yellowish exudate
 Scattered petechiae on the palate for first two days
 Strawberry tongue
 High fever up to 103 f
 Exanthematous rash on the skin widespread

7.  White strawberry tongue-
first two days
 White coating of tongue
only fungiform papillae
projecting out
 Red strawberry tongue –
develops by fourth or fifth
day
 When white coating
desquamates

8.  Develop in first two days
and widespread in 24 hours
 Streptococcus organisms
produce erythrotoxin that
damage blood vessels
resulting in rashes
 Clears within 1 week with
desquamation

9.  Clinical signs
 Throat culture

10.  Local complications include peritonsillar and
retropharyngeal abscesses
 Systemic complications may include acute rheumatic
fever, glomerulonephritis, bacteraemia, pneumonia,
endocarditis, and meningitis
 Rare complications are Hepatitis, gallbladder hydrops
or splenomegaly
 Mucocele (hydrops) of the gallbladder is a term
denoting an overdistended gallbladder filled with
mucoid or clear and watery content.

11.  Prevention of serious complications
 Oral pencillin or erythromycin
 Treatment for fever

12.  Life threatening infection caused by
corynebacterium diptheriae
 Humans are the sole reservoirs, spread
between people by direct contact or through
the air
 The bacterium produces a lethal exotoxin
that causes tissue necrosis.

14.  high fever of above100°F with chills
 fatigue
 bluish skin coloration (cyanosis)
 sore throat, hoarseness, cough, headache
 difficulty swallowing, painful swallowing, difficulty breathing,
rapid breathing, foul-smelling and blood stained nasal discharge
and lymphadenopathy.
 Diptheria causes tissue necrosis, the dead tissues forms a thick,
gray coating that can build up in the throat or nose.
This thick gray coating is called a“PSEUDOMEMBRANE.”
It can cover tissues in the nose, tonsils, voice box, and throat,
making it very hard to breathe and swallow.

16. Associated with "barking" cough

17.  Laboratory criteria
Isolation of C. diphtheriae from a Gram stain or
throat culture from a clinical specimen
Histopathologic diagnosis of diphtheria by
Albert's stain
 Clinical criteria
Upper respiratory tract illness with sore throat
fever (above 39 °C (102 °F) is rare)
An adherent, dense, grey pseudomembrane

18.  Prevention by DPT vaccine
 Metronidazole
 Erythromycin is given (orally or by injection) for
14 days (40 mg/kg per day with a maximum of 2
g/d), or
 Procaine penicillin G is given intramuscularly for
14 days (300,000 U/d for patients weighing
<10 kg and 600,000 U/d for those weighing
>10 kg);
 patients with allergies to penicillin G or
erythromycin can use rifampin or clindamycin.

19.  Neck may swell, and breathing and swallowing are more
difficult, may require intubation or a tracheotomy
 Patients with severe cases are put in a hospital intensive
care unit and given a diphtheria antitoxin
 In cases that progress beyond a throat infection,
diphtheria toxin spreads through the blood and can lead
to potentially life-threatening complications that affect
other organs, such as the heart and kidneys

20.  Tuberculosis is a specific infectious, chronic
granulomatous disease caused by
Mycobacterium Species.
 Primary Tuberculosis mostly affects Lungs
(Primary Pulmonary TB).

21. Etiology

22. •M. tuberculosis is;
• Rod- shaped
• Non- sporing, Non- capsulated
• Facultative Aerobic
• Intracellular
• Acid fast bacillus
• Acid fastness is due to presence of complex long
chained cross-linked fatty acid (Mycolic Acid) and
other cell wall lipids.
Microbiology

23. M.tuberculosis
Acid fast staining of a smear
prepared from sputum of a
patient with tuberculosis.

24. • “Disease of Poor”
• Incidence has declined due to early & accurate
diagnosis and improved socio-economic condition.
• In developing countries, south east Asia, western
pacific and Africa accounts for 95% of cases of TB.
• HIV patients are at extremely highrisk.
Epidemiology

25. o Prevalence of Extra-pulmonary TB is increasing
nowadays.
o Most common extra-pulmonary sites in head and neck
are;
o Cervical lymph nodes
o Larynx
o Middle ear
o Less common are; nasal cavity, nasopharynx, parotid
gland, spine, esophagus and oral cavity.

26. Primary TB
is usually asymptomatic. Occasionally fever and cough
which may be productive ordry.
Usually seen in children but may occur inadults.
Secondary TB
Low grade fever, malaise, anorexia, weight loss and
night sweats
Productive cough with hemoptysis or chest pain
Clinical features

27. Episodic fever with chills andrigor
Easy fatigability and malaise
Gradual loss of weight
Persistent cough with or without hemoptysis or chest
pain.
Bilateral crackles on auscultation
Hepatosplenomegaly
Tubercular cervical lymphadenitis; tender, often shows
inflammation of overlying skin
When an actual abscess exists, typically perforate and
discharge pus.
Signs and symptoms

28. Oral lesions are realtivelyuncommon.
Lesions of oral mucosa are seldom primary, but rather
secondary to pulmonarydisease.
Most commonly affected isTongue.
Usually, an irregular, superficial or deep, painful ulcer
which tends to increase slowly in size often aroundthe
areas of trauma.
Oral manifestations

30. • Chronic ulceration orswellings
• Non healing extraction sockets
• Areas of mucosal granularity or diffuse zone ofinflammation
• Mandibular swelling with intra bonyinvolvement
• Gingiva, lips, buccal mucosa, soft palate, hard palate are other
affected sites in decreasingorder
• Primary oral TB involving gingiva present as diffuse hyperemic,
nodular or papillaryproliferation.
• Oral lesion co-exist with palpable, tender submandibular or
cervical lymphnodes;scrofula

31. Ulcerated gingiva

32. Bones of maxilla or mandible may also be involved.
Lesion produced is essentially periapical granuloma or
tuberculoma. These are usually painful andsometimes
involve considerable amount of bone by relatively
rapid extension.
Tuberculous osteomyelitis usuallyoccur in later stages
of disease and has poor prognosis.

33. Sinus formation and
discharge

34. Nonspecific.
Common findings in lungs include
 segmental or lobar airspaceconsolidation,
 ipsilateral hilar and mediastinal lymphadenopathy
 pleural effusion.
 Atelectasis may occur in primarypulmonary
tuberculosis
 Areas of nodal involvement appears as calcified
lymphnodes that may be confused withsialoliths.
Radiographic features

35. Calcified Cervical
lymph nodes.

36. Pathogenesis

37. Exposure to infected Air droplets
M. Tuberculosis bacteria is taken up by Pulmonary Alveolar
Macrophages (PAM) by receptor mediated endocytosis
In macrophages, phagosomes containg bacilli fuses with
Lysosomes; resist internal microbicidal activities and proliferates
with in macrophages
Tubercular bacilli then either freely or with in macrophages are
drained into regional lymphnodes

38. Tubercular antigens are presented to CD4+T lymphocytes viaMHC-2
complex by Antigen Presenting cells (APC’s); Macrophages
 Under influence of macrophage-secreted IL-12, CD4+T cells
differentiate into TH1 Cells which produce IFN-γ
 IFN-γ are most potent activator of Macrophages.
Activated macrophages then produces:
 TNF-α; recruits monocytes which differentiate into epithelioid cells
 Activation of ‘inducible Nitric oxide synthase’ (inos) gene; produces
Nitric Oxide; antibacterial activity
Generation of Reactive Oxygen Species; antibacterial activity

39. Thus;
 Epitheliod cells are formed by differentiation of activated
macrophages
 Activated macrophages coalesces to from multinucleated
giant cells
Production of Nitric oxide and reactive oxygen species;
which are highly oxidative causes oxidation of cellsforming
caseous necrosis
 Macrophages produced chemokines causes recruitment
of lymphocytes and fibroblast

40. Cell mediated Hypersensitivity
Oral lesions are histopathologically similar to pulmonary
lesions.
Formation of typical granuloma consistingof;
 Central caseous necrosis
 Circumscribed by epithelioid histocytes and langhans type giantcell.
 Surrounded by a rim of fibroblast and lymphocytes

41. Primary consolidation in lungs parenchyma is called as
Ghon’s Focus.
Regional lymphnodes often caseate with parenchymal
involvement; called Ghon’s complex.
In long standing cases, lymphnodes tends to calcify;
called as Ranke’s complex.

42. Photomicrograph of Histopathology of Tuberculosis
Epithelioid Cells
Langhans Type
Giant cells
Histopathological features

43. Photomicrograph of Histopathology of Pulmonary TB showing
Caseous Necrosis

44. Langhans
Type giant
cell
Epithelioi
d cells

45. Demonstration of bacilli in infected tissue or sputum
by AFB stain is gold-standard for diagnosis.
Radiographs of affected parts like chest
Tuberculine test
CT scan is used to diagnose mediastinal or hilar
lymphadenopathy, cavities and intralesional
calcification.
A high resoulation CT scan can be used to differentiate
millary TB and other diffuse form of TB from other
diffuse lungs disease.
Diagnosis

46. Also called as Mantoux Test
Principle:
 A cell mediated hypersensitivity reaction develops
against tubercular antigen.
Procedure:
 0.1ml of 5tuberculine units of purified proteins
derivatives (PPD) of siebert stabilized with Tween80
or 1tuberculine unit of PPDRT 23injected
subcutaneous into the flexor aspect offorearm.
Tuberculin test

47.  Suggestive but not diagnostic
 Readings is taken 48-72 hours later for the indurations
Size of indurations Interpretation
More than 15cm orulceration Strongly positive
More than 10cm Positive
5-9 cm intermediate
Less than 5 cm Negative

49. Treatment

50. Bacillus Calmette-Guerin (BCG) Vaccine is available to
approx. 80% of world population.
BCG is given as a single intradermal injection at the
insertion of the Deltoid muscle.
Except in neonates, a tuberculine skin test should
always be done before administering BCG.
If BCG is accidentally given subcutaneously, then a
local abscess may form (a "BCG-oma") that can
sometimes ulcerate, and may require treatmentwith
antibiotics immediately
BCG vaccine

51.  Syphilis is an infectious disease caused by a
spirochete called Treponema pallidum

52.  Sexual contact
 Mother to fetus
 Through blood transfusion ..very low

53.  Due to advent of pencillins incidence of
syphilis reduced and became almost zero
 But now, there is an upsurge in sypilitic
cases, particularly in westren world and the
cause is attributed to sexual activity among
users of crack cocaine, and particularly to the
practice of trading sex and cocaine.
 Its time for us to become alert, particularly
dentists practicing at metros.

54.  The disease proceeds in three stages,
- primary syphilis
- Secondary sypilis
- Tertiary syphilis
First two stages are highly infective .
Congenital syphilis occurs in later stages.

55.  This stage is characterized by the CHANCRE that
develops at the inoculation site .
 Becomes evident 3 to 90 days after the initial exposure
 Oral cavity is the most common extra genital site, lips
tongue, gingiva, palate and tonsils.
 It is a painless clean based ulcer with associated
lymphadenopathy.
 At this stage the organism is spreading through
lymphatic channels.
 If untreated, the ulcers heal within 3 to 8 weeks

57.  Systemic symptoms
 Maculopapular cutaneous rash
 Oral mucous patches
 Condylomata lata
 Systemic symptoms– lymphadenopathy, sore
throat, malaise (a general feeling of discomfort),
headache, weight loss, fever and myalgia.

59.  Zones of sensitive whitish mucosa , which occur due to
increased exocytosis and spongiosis (intercellular edema), which
eventually may show epithelial necrosis and sloughing with
exposure of underlying raw connective tissue

60.  Papillary lesions resembling viral papilomas

61.  Latent syphilis – free of disease from 1 to 30 years
 After the latent stage tertiary syphilis develops
 Aneurysm of aorta, ccf may happen
 CNS involvement may show psychosis, dementia, etc
 Characteristic feature of tertiary syphilis are scattered foci
of granulomatous inflammation known as ‘GUMMA’.
 Appears as indurated, nodular or ulcerated lesion, which
affect tongue or palate

63.  Hutchinson’s triad
1. Hutchinson’s teeth
2. Ocular interstitial keratitis
3. Eighth nerve deafness

65.  Not specific
 Shows a picture of chronic inflammation
 Lymphocytes and plasma cells predominate
the picture

66.  Direct visualization of the organism in tissue with
immunohistochemistry, immunofluorescence or
Warthin-Starry stain
 Dark field examination demonstrating
spirochetes from an active lesion,
 PCR testing or
 Serologic testing – VDRL, RPR, FTA-ABS, TPHA

67.  VDRL test -The VDRL is a non-treponemal serological screening
for syphilis that is also used to assess response to therapy, to
detect CNS involvement, and as an aid in the diagnosis of congenital syphilis.
The basis of the test is that an antibody produced by a patient with syphilis
reacts with an extract of ox heart (diphosphatidyl glycerol). It therefore
detects anti-cardiolipin antibodies (IgG, IgM or IgA), visualized through
foaming of the test tube fluid, or "flocculation".
 The rapid plasma reagin (RPR) test uses the same antigen as the
VDRL, but in that test, it has been bound to several other molecules,
including a carbon particle to allow visualization of the flocculation
reaction without the need of a microscope.

69.  Penicillin is the drug of choice
 Not helpful in neurosyphilis and AIDS
 Multi drug therapy
 Erythromycin and tetracyclin for patients
allergic to penicillin

70.  An infectious disease caused by
contamination of wounds from the
bacteria Clostridium tetani, or the
spores they produce that live in the
soil, and animal feces
 Greek words -“tetanos and teinein”,
meaning rigid and stretched, which
describe the condition of the muscles
affected by the toxin, tetanospasmin,
produced by Clostridium tetani

71.  Tetanus spores are found throughout the
environment, usually in soil, dust, and animal
waste.
 Tetanus is acquired through contact with the
environment; it is not transmitted from person to
person.

72.  The usual locations for the bacteria to enter the body:
 Puncture wounds (such as those
caused by rusty nails, splinters,
or insect bites.)
 Burns, any break in the skin, and
IV drug access sites are also
potential entryways for the
bacteria.

73.  Apparently trivial injuries
 Animal bites/human bites
 Open fractures
 Burns
 Gangrene
 In neonates usually via infected umbilical
stumps
 Abscess
 Parenteral drug abuse

74. 1. C. tetani enters
body from through
wound.
3. Germinates under
anaerobic conditions
and begins to multiply
and produce
tetnospasmin.
2. Stays in sporulated
form until anaerobic
conditions are
presented.
4. Tetnospasmin spreads
using blood and lymphatic
system, and binds to
motor neurons.
5. Travels along the
axons to the spinal
cord.
6. Binds to sites
responsible for inhibiting
skeletal muscle
contraction.

75. •Initially binds to peripheral
nerve terminals
•Transported within the axon and
across synaptic junctions until it
reaches the central nervous
system.
•Becomes rapidly fixed to
gangliosides at the presynaptic
inhibitory motor nerve endings,
then taken up into the axon by
endocytosis.

76. How the toxin acts?
Blocks the release of inhibitory neurotransmitters (glycine
and gamma-amino butyric acid) across the synaptic cleft,
which is required to check the nervous impulse.
If nervous impulses cannot be checked by normal
inhibitory mechanisms, it leads to unopposed muscular
contraction and spasms that are characteristic of tetanus.

77.  Risus sardonicus: Contraction of the muscles at the angle of mouth
and frontalis
 Trismus (Lock Jaw): Spasm of Masseter muscles.
 Opisthotonus: Spasm of extensor of the neck, back and legs to form
a backward curvature.
 Muscle spasticity
 Prolonged muscular action causes sudden, powerful, and painful
contractions of muscle groups. This is called tetany. These
episodes can cause fractures and muscle tears.
 If respiratory muscle is involved – apnoea.

78. Other symptoms include:
 Drooling
 Excessive sweating
 Fever
 Hand or foot spasms
 Irritability
 Swallowing difficulty
 Uncontrolled urination or defecation

79.  There are currently no blood tests that can be used to
diagnose tetanus. Diagnosis is done clinically.
Differential Diagnosis
 Masseter muscle spasm due to dental abscess
 Dystonic reaction to phenothiazine
 Rabies
 Hysteria

82.  1. Neutralization of unbound toxin with
Human tetanus immunoglobulin
 2. Prevention of further toxin production by
-Wound debridement
-Antibiotics (Metronidazole)

83.  3. Control of spasm
- Nursing in quiet environment
- avoid unnecessary stimuli
- Protecting the airway
 4. Supportive care
- Adequate hydration
- Nutrition
- Treatment of secondary infection
- prevention of bed sores.

84.  Tetanus is completely preventable
by active tetanus immunization.
 Immunization is thought to provide
protection for 10 years.
 Begins in infancy with the DTP
series of shots. The DTP vaccine is
a "3-in-1" vaccine that protects
against diphtheria, pertussis, and
tetanus.

85.  Can be achieved by active immunization by tetanus toxoid
(5 doses – 0 day, 1 month, 6 month, 1 year, 1 year).
 Older teenagers and adults who have sustained
injuries, especially puncture-type wounds, should
receive booster immunization for tetanus if more than
10 years have passed since the last booster.
 Clinical tetanus does not produce immunity to further
attacks. Therefore, even after recovery patients must
receive a full course of tetanus toxoid.

86.  Can be achieved by active immunization by tetanus toxoid
(5 doses – 0 day, 1 month, 6 month, 1 year, 1 year).
 Older teenagers and adults who have sustained
injuries, especially puncture-type wounds, should
receive booster immunization for tetanus if more than
10 years have passed since the last booster.
 Clinical tetanus does not produce immunity to further
attacks. Therefore, even after recovery patients must
receive a full course of tetanus toxoid.

87.  Chronic granulomatous, localized bacterial
infection.
 ETIO LO G Y :- as a result of infection
by Actinomyces israelii, A. viscosus , A.
Naeslundi, A.odontolyticus etc.
 TYP ES : - according to location,
- Cervicofacial actinomycosis
- Thoracic actinomycosis
- Abdominal actinomycosis

88.  It is an infection of filamentous, branching,
gram-positive anaerobic bacteria.
 Normal component of oral flora
 Actinomyces israelii is the most common
causative organism
 Colonize in the tonsillar crypts

89. Three variants
1. Cervicofacial actinomycosis
2. Thoracic actinomycosis
3. Abdominal actinomycosis
 Infection may be acute or chronic
 About 55% are cervico-facial, 25% abdominal and
15% are thoracic
 The suppurative reaction of the disease releases
a discharge with yellow granules, which are
actually bacterial colonies and called as sulphur
granules

91.  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 will be seen containing
sulphur granules.

92.  Tissue shows a peripheral
band of fibrosis encasing a
zone of chronically
inflammed granulation
tissue surrounding large
collections of PMNs and
colonies
 The colonies are club
shaped filaments that form
radiating rosette pattern
 Central area stains
basophilic and peripheral
area eosinophilic

93.  Surgical exploration with high concentration
and long term antibiotic therapy

94.  Noma is a rapidly spreading opportunistic infection
caused by normal oral flora that becomes pathogenic
during periods of compromised immune status
 Fusobacterium, Borrelia vincenti and few other
organisms are usually involved
 Predisposing factors include;
 poverty
 malnutrition
 poor oral hygiene, HIV, malignancy, etc

95.  Arises in children between 1 to 10 years of
age
 Begins as necrotizing ulcerative gingivitis
 Mucositis spreads and zones of necrosis
develops in soft tissues
 The necrosis deepens to involve bone to
cause osteomyelitis
 Other associated symptoms include fever,
malaise and regional lymphadenopathy

97.  Correcting inadequate nutrition, hydration,
electrolyte imbalance
 Penicillin and metronidazole are first line of
drugs
 Certain times require clindamycin,
gentamycin or piperacilin to combat
pseudomonas organisms

99.  HSV is a DNA virus and belong to human herpes virus
family
 Two types of HSV – HSV-1 & HSV-2
 These two are structurally similar but different
anti-genically
 HSV-1 is well adapted for oro-facial region and skin above
the waist, spreads through saliva
 HSV-2 is well adapted for genital regions and skin below
the waist, spreads through sexual contact.
 There can be exceptions to these rules.

100.  Primary infection
 Secondary infection
 PRIMARY INFECTION – the initial exposure to those who don’t have
antibodies to the HSV
 Typically occurs in young age, often asymptomatic and causes no
morbidity
 During this period, the virus is taken up by sensory nerves and taken
to associated ganglia, in HSV-1, trigeminal ganglion becomes
reservoir, where the virus remains in latent state.

101.  Occurs when re-activation of virus happens,
people show asymptomatic viral shedding in
saliva
 Affects the epithelium supplied by the
sensory ganglion
 Old age, UV light, emotional stress,
pregnancy, allergy, trauma, respiratory
illness, menstruation, systemic diseases, or
malignancy have been associated with viral
reactivation.

102.  HSV-1 is usually acquired from contaminated saliva or active peri
oral lesions
 Incidence is more in developing nations
 Initial infection usually undergoes unnoticed
 People exposed to HSV-1 at early age exhibit gingivostomatitis,
those initially exposed later in life exhibit phayngotonsilitis
 HSV is also associated with oral carcinomas, but lack substantial
evidence

103.  Primary HSV infection presents as acute herpetic
gingivostomatitis
 Arise between the ages of 6 months to 5 years, development
before 6months of age is rare because of protection from
maternal anti-HSV antibodies
 The onset is abrupt and often accompanied by cervical
lymphadenopathy, chills, fever, nausea, anorexia, irritability and
sore mouth
 Initially many pin head vesicles develop, which rapidly collapse to
form numerous red lesions. Later the lesions ulcerate and
coalesce to form bigger lesions
 The gingiva is enlarged, painful, and erythematous and exhibit
punched out erosions

104.  Labial mucosa is also affected and peri-oral
lesions are common
 Auto- inoculation of fingers, eyes and genital
areas can occur
 Lesions resolve within 2 weeks
 When primary infection occurs in adults . It
manifests as pharyngotonsilitis
 Sore throat, fever, chills, malaise with numerous
ulcerated lesions on tonsils and posterior
pharynx are seen

107.  Recurrent infections occur at the site of primary
inoculation area or adjacent epithelium supplied by the
sensory ganglion
 Most common one is herpes labialis, which occur at the
vermilion border and adjacent skin
 Prodromal symptoms occur 24 hours before the lesions
develop, which include pain, burning, itching, tingling,
etc
 Multiple small, erythematous papules develop and form
clusters of fluid filled vesicles. These vesicles rupture
and crust within 2 days. Healing occurs within 7 to 10
days

109.  Infection of thumbs and fingers in children with orofacial
herpes due to self inoculation
 Can happen in dentists also due to contamination.

110.  The virus exerts its main influence on
epithelial cells.
 Infected epithelial cells exhibit acantholysis,
nuclear clearing and nuclear enlargement ,
termed as BALLOONING DEGENERATION.
 The acantholytic cells are called TZANCK
CELLS
 Multinucleated infected epithelial cells fuse
together to form giant cells

112.  Serological tests
 Cytosmear
 Tissue biopsy

113.  Treated best symptomatically
 Prevention of auto-inoculation, particularly
eyes
 Acyclovir suspension is administered in rinse
and swallow technique for first three
symptomatic days, this prevents the
development of new lesions
 NSAIDs can help to reduce the discomfort
 Anti-viral ointments in case of herpes labialis

114.  Caused by varicella zoster virus (HHV-3)
 Chicken pox represents the primary infection
of VZV
 Recurrence due to reactivation of VZV is
called as herpes zoster
 Spread through droplets or direct contact
with the lesion
 Most cases of chicken pox arises between 5
to 9 years of age
 The incubation period is 10 to 21 days

115.  Prodromal phase – malaise, pharyngitis, rhinitis in children
and in adults additional symptoms like headache, myalgia,
nausea, anorexia and vomiting are seen
 This is followed by intense pruritic exanthem. The rash
begins on face and trunk, followed by extremities
 Each lesion progresses through stages of erythema, vesicle,
pustule and hardened crust
 The vesicular stage is described as ‘ dew drop on rose petal’ –
central vesicle surrounded by erythema
 Lesions continue to appear for 4 to 5 days , in adults the
course of the disease is more severe than children

118.  Common and appear before skin lesions
 Palate and buccal mucosa are common sites
 Painless lesions unlike herpes infection

119.  Encephalitis and pneumonia are dangerous
and life threatening
 Infection during pregnancy may result in
spontaneous abortions or congenital defects
 Infections and complications in immuno-
compromised individuals is much higher and
severe
 Few other complications include anemias, GIT
disturbances and secondary skin infections

120.  Identical to that of HSV infection

121.  Anti- viral drugs like acyclovir etc help to
reduce the severity and duration of the
infection
 In immuno-compromised and infants born
with infection use of VZIG reduces the risk of
death and improves the prognosis

122.  After initial infection with VZV, the virus resides in cranial
nerve ganglions
 Reactivation of the virus results in Herpes Zoster
 Immunosuppression, cytotoxic drugs, radiation, old age,
alcohol abuse and dental manipulation etc are pre-disposing
factors
 Commonly affected nerve is trigeminal nerve and ophthalmic
division is more common one(zoster ophthalmicus)
 Oral lesions are evident when maxillary or mandibular
division of the trigeminal nerve is affected.

123.  3 phases : prodromal, acute and chronic
 Initial replication of virus results in severe neuronal
pain, this is due to inflammation of nerves
 So intense pain precedes the rash , pain intensifies and
is described as burning, tingling, itching, prickly or
knifelike.
 The pain develops in the epithelium innervated by one
branch of the nerve, occasionally two or more branches
may be involved

124.  Clusters of vesicles develop within 3 to 4 days after
prodromal symptoms
 The vesicles become pustular, ulcerate and crust within 7 to
10 days
 Important feature is the lesions develop in the path of
innervations of affected nerve and do not cross the midline.
 The rashes resolves within 2 to 3 weeks, upon healing scar
formation may be seen

125.  Many patients do not progress into chronic
phase
 In chronic phase, neuralgia associated pain
persists longer than 3 months
 This is termed as post herpetic neuralgia
 Most of these neuralgias resolve within 1 year
of span

126.  Facial paralysis associated with cutaneous
lesions of external auditory canal, which
occurs due to involvement of ipsilateral facial
and auditory nerves
 This syndrome causes – facial paralysis
- hearing deficits
- vertigo
- other auditory and
vestibular symptoms

129.  Supportive and symptomatic measures
 Anti-viral therapy
 Topical application of capsaicin

130.  Caused by paramyxovirus
 Spread through droplets
 Affected individuals are infective from 2days before becoming
symptomatic to 4 days after appearance of rashes
 Incubation period is 10 to 12 days
 Prodromal symptoms include fever, malaise, running nose
(coryza), conjuctivitis and cough
 Rashes develop and lasts for 4 to 7 days, face is the first
sight and rashes spread downwards to involve trunk and
extremities

131.  Koplik’s spots – develops early during the
course of infection
 Multiple areas of mucosal erythema are
visible on buccal and labial mucosa or on soft
palate; within these areas numerous small
bluish – white macules are seen.

134.  Warthin – Finkeldey giant cells
 Found in the lymphoid tissue

135.  Good vaccination program – MMR vaccine
 Fluids and antipyretics
 In immunocompromised patients – ribavirin,
immunoglobulins and interferons are used

136.  Paramyxovirus infection that affects the salivary glands
 Mumps virus is transmitted through urine, saliva and
respiratory droplets
 Incubation period is 16 to 18 days
 Patients are contagious from 1 day before the clinical
appearance to 14 days after its resolution
 Prodromal symptoms: fever, headache, malaise, anorexia
and myalgia
 Parotid glands are frequently involved.

137.  Discomfort and swelling of parotid gland
 Swelling increases to its peak in 2 to 3 days
 Severe pain
 Stimulation of saliva increases the pain
 Usually unilateral
 Second common finding is EPIDIDYMOORCHITIS, which occurs
in about 30% of post pubertal males
 EPIDIDYMOORCHITIS – testicular swelling with pain and
tenderness , upon resolution atrophy occurs in the affected
testicle , sometimes leads to permanent sterility
 In females , oophoritis and mastitis can be seen

139.  Caused due to EPSTEIN-BARR VIRUS( EBV, HHV4)
 Infection spreads due to infected saliva, in children due to sharing of toys,
etc, in adults due to intimate contact, particularly kissing
 In children usually asymptomatic and in adults it is symptomatic
 Prodromal symptoms like malaise, fatigue(severe) and anorexia lasts for
about 2 weeks followed by development of pyrexia
 In adolescence and young adulthood, the disease presents with a
characteristic triad
1. Fever – usually lasting 14 days
2. Sore throat – usually severe for 3–5 days, before resolving in the next 7–10
days
3. Swollen glands – mobile; usually located around the back of the neck
(posterior cervical lymph nodes) and sometimes throughout the body.
 Splenomegaly

141.  Person's age, with highest risk at 10 to 30 years
 Medical history, such as close contact with other
people with infectious mononucleosis, and the
presence and time of onset of "mononucleosis-
like symptoms" such as fever and sore throat
 Physical examination, including palpation of
any enlarged lymph nodes in the neck,
or enlarged spleen
 Paul- Bunnell heterophile antibody test
 Peripheral smear showing atypical lymphocytes

142.  Paul- Bunnell heterophile antibody test - The heterophile
antibody test works by agglutination of red blood cells from
guinea pig, sheep and horse. This test is specific but not
particularly sensitive.
 Serologic tests detect antibodies directed against the Epstein–
Barr virus

143.  Resolves itself within 4 to 6 weeks
 NSAIDs to minimize the symptoms
 Splenic rupture is a complication, so contact
sports should be avoided

144.  Primary infection occurs during childhood and virus
establishes latency in salivary glands, endothelium,
macrophages and lymphocytes
 In infants infection occurs during delivery or feeding,
in adults through intimate contact
 In infancy infection is usually asymptomatic, but may
produce developmental tooth defects particularly
diffuse enamel hypoplasia
 In adults presents as fever, myalgia, abnormal liver
function tests and atypical peripheral lymphocytes,
but seldom causes pharyngitis and lymphadenopathy.
 Oral signs include chronic mucosal ulcerations

146.  Infected cells are swollen and show
prominent nuclei – typically called as OWL’S
EYE cell

147.  Don’t require any therapy
 In immuno-compromised , Ganciclovir is
recommended

148.  Human Immuno Deficiency Virus is the etiologic
agent of Acquired Immunodeficiency Syndrome
(AIDS).
 Characterized by severe depletion of CD4 cells.
 CD4 T lymphocytes (CD4 cells) – activate other
immune cells, such as macrophages, B
lymphocytes (B cells), and CD8 T lymphocytes
(CD8 cells), to fight infection.
 HIV weakens the immune system by destroying
CD4 cells.

151.  Sexual transmission
 Blood or blood products
 Maternal-fetal
 Infected needles
 Any blood contaminated
body fluid

152.  Group I : Acute Infection
 Group II : Chronic Asymptomatic Infections
 Group III : Persistent Generalized
Lymphadenopathy
 Group IV : Aids Related Complex

154.  Most dangerous group
 Seropositive pt who is apparently healthy
capable of infection
 Enlarged axillary glands
 Hematological & immunological abnormalities

155.  LYMPHADENOPATHY in 2 or more extra-
inguinal sites persisting for more than 3
months

156.  ARC - A prodromal phase of infection with
the human immunodeficiency virus (HIV).
 low grade fever, unexplained weight loss,
diarrhea, opportunistic infections and
generalized lymphadenopathy.
 Clinical use of this term was widely
discontinued by the year 2000

158.  OPPORTUNISTIC INFECTIONS -Pneumonia,
Cryptococcosis, Viral Infections,
Toxoplasmosis, TB etc
 NEOPLASMS – Kaposi’s Sarcoma, Lymphoma,
SCC
 NEUROLOGIC DISEASES – Meningocephalitis
 OTHERS - Encephalopathy, Purpura,
Thrombocytopenia

159.  The mode of spread of HIV also poses special danger the
dentist who works with contaminated blood, saliva and other
body fluids and has close contact with his patients.
 The dentist may possibly be the first health care provider to
diagnose the condition
 Dentists should have a good knowledge of oral lesions in HIV
/AIDS and be able to recognize and accurately diagnose such
lesions.
 Early treatment of oral lesions is also necessary to reduce
morbidity and mortality in HIV-infected patients.
 The need to maintain oral health to prevent complications
like microbial infections which may be fatal in these patients
cannot be over-emphasized.