Dr Mohammed Malik Afroz
Oral medicine
BACTERIAL INFECTIONS – 1
1.
2.
3.
4.
5.
Scarlet Fever
Diptheria
Tuberculosis
Tetanus
Actinomycosis
BACTERIAL INFECTIONS – 2
1.
2.
3.
4.
ANUG/Noma
Cat scratch disease
Syphilis
Gonorrhea



It is a highly contagious systemic infection
occurring mostly in children
It is caused by beta- hemolytic streptococci,
st. pyogenes which produces a pyrogenic
exotoxin
There is presence of rash due to 3 exotoxins
A, B , C previously described as erythrogenic
or scarlet fever toxins.




Incubation period of 3 to 5days followed by severe
pharyngitis and tonsillitis , headache , chills . Fever
and vomiting
There is enlargement and tenderness of regional
lymph nodes
-characteristic feature – Is a appearance of diffuse,
bright, scarlet skin rash in the regions of skin folds
on the2nd or 3 rd day of illness
Scarlet rash is due to the toxic injury to vascular
endothelium which produces dilatation of small
blood vessels and consequent hyperemia
Small papules of normal color erupt through these
rashes giving a sand paper feel to the skin


The rash that is prominent in the areas of skin
folds is called pasta lines
The rash subsides after 6 or 7 days followed
by desquamation of palms and soles
•The palate and the throat is often fiery red
•The tonsils and faucal pillars are swollen and
sometimes covered with a grayish exudates.
•The early stage of the disease on the tongue is
described as “strawberry tongue” o\r “white
strawberry tongue”
In the later stage the tongue becomes deep
red , glistening and smooth except for the
swollen , hyperemic papilla and is termed as
“raspberry tongue “ or “red strawberry tongue ‘
Diagnosis – culturing the flora of intra oral lesions in
pharynx
 Dick Test – administering two different injections, one into
each arm of a patient.

 In one arm, toxin (poison) taken from a culture of scarlet fever
bacteria is injected.
 In the other arm, neutralized toxin is injected to act as a control
(a standard of comparison).
 If the toxin causes redness, tenderness and swelling after 24
hours, the person is not immune to scarlet fever. The control
normally shows no swelling for comparison.


Treatment –
Antibiotics like penicillin , dicloxacillin and cephalexin will
eliminate the disease and controls complications
Is an acute , infectious and communicable diseases of the
skin and the mucous membrane caused by toxemic
strains of corny bacterium Diptheriae
 Pathogenesis – has air borne mode of transmission and
localizes in mucous membrane of respiratory tract.
 It invades open skin lesions due to insect bites or trauma.
 Bacillus multiplies at the entry site and liberates toxins.
 Toxins induce initial edema, hyperemia  epithelial
necrosis  acute inflammation.
 Coagulation of the fibrin and purulent exudate produce a
pseudo membrane & inflammatory reaction
accompanied by vascular congestion extends into
underlying tissues

Mostly seen in children and mainly
affects the upper respiratory tract
 The characteristic feature is a
formation of a pseudo- membrane
which is seen on the tonsils
 Has a wash leather , elevated greyish
green membrane with a well defined
edge surrounded by acute
inflammation
 It manifests as a fever, sore throat ,
weakness, dysphagia , head ache
And change of voice





Formation of a passive,
diphtheritic membrane which
begins on the tonsils
This membrane contains
dead cells ,leukocytes,
bacteria overlying necrotic,
ulcerated area of the mucosa
The pseudo membrane
leaves a bleeding surface if
stripped away
Enlargement of sub mandibular and anterior
cervical nodes will give a bull
neck appearance

Prevented by prophylactic active immunization
with diphtheria toxoid
once the diseases develops it is treated with
anti- toxin usually in combination with
antibiotics
It is a specific granulomatous disease caused
by mycobacterium tuberculosis
 Commonly affects lungs and also affects the
intestines, meninges , bones , joints , lymph
glands , skin and oral mucosa
 2types –
 Primary TB
 Secondary TB





Mild symptoms – fever, chills, cough, sputum
Infected foci
granulation
scarring
calcification
Bacilli may get disseminated and involve various
organs
Main complication is loss of lung elasticity and
decrease in function.





Re – activation of infection
Is more aggressive in nature.
Multiple organ involvement is seen.
Oral tuberculosis is due to pulmonary lesion and
is contagious
Gingiva and tongue are commonly involved.







Common site –
Base of tongue – gingiva –
lip – tonsil – tooth socket –
soft palate.
Ulcers – uneven, jagged,
undermined soft borders
Lesions are painless but
purulent
Lymphadenopathy
Unilateral lymph node
involvement – scrofula
Biopsy and culture is must.
0.1cc – 5 TU of PPD
Montoux Test
Sputum examination –
Zeihl Neelson Stain
 Tissue biopsy.


Induration or redness 48 – 72hrs
+ve -> 10mm
Inconclusive –5 –9mm
- Ve -< 5mm
False – ve –cross reactivity to other
mycobacteriaor granulomatousdisease

Chest Radiograph –
apical scars with
calcifications
DOSAGES OF FIRST LINE ANTI TUBERCULOSIS DRUGS AND MAJOR
ADVERSE EFFECTS
Drug
Daily
weekly
Adverse Effects
Isoniazid 5 mg/kg
oral
(maximum
300 mg)
900 mg twice
weekly
600 mg thrice
weekly
Hepatitis, peripheral neuritis,
drug induced lupus,
seizures, and
hypersensitivity with rash
and fever. Drug interactions
with dilantin and disulfiram
Rifampic 10 mg/kg
in
oral
(maximum
600 mg)
900 mg twice
weekly
600 mg thrice
weekly
Orange body secretions, flulike syndrome, hepatitis,
thrombocytopenia, nausea,
anorexia, diarrhoea, renal
failure, and multiple drug
interactions
Dosage
Drug
Daily
weekly
Adverse Effects
Pyrazina
mide
25-30 mg/kg
oral
30-35 mg/kg
Hyperuricemia, hepatitis, rash,
nausea, and anorexia
Ethambut 25 mg/kg initial 50 mg/kg twice weekly Optic neuritis and gastrointestinal
ol
2 months, then 30 mg/kg thrice
discomfort
15 mg/kg oral weekly
Streptom
ycin
15 mg/kg IV or 15 mg/kg (maximum
IM (maximum
1.5 g) twice or thrice
1.0 g) 5 days a weekly
week
Ototoxicity, vestibular dysfunction,
nephrotoxicity, rash, and
hypersensitivity reactions
Is an acute infection of nervous system.
It is caused by clostridium tetani .
Incubation period – 2 to 14 days
Pathogenesis –
Under suitable anaerobic conditions the
bacteria germinate and produces toxins
(TETANOSPASMIN)
 It binds to peripheral motor nerve
terminal  nerve cell body 
presynaptic terminal  blocks release
of GABA – gamma amino butyric acid)





Characterized by lock jaw or trismus due
to spasm of masseter which is an initial
symptom .
 Dysphagia , stiffness or pain in the neck ,
shoulder or back muscles appear .
 Laryngeal spasm may lead to asphyxia .
 Sustained contraction of facial muscles
results in risus sardonicus .
 The contraction of muscles of the back
produces an arched back called
opisthotonus
 Cephalic tetanus characterized by trismus
and facial palsy is rare and may occur
after head injury or ear infection .





General measures : aims to remove spores at
the site of wound , prevent toxin production ,
prevent muscular spasms .
Cardiopulmonary monitoring should be
maintained .
Antibiotics should be given to eradicate
vegetative organisms .
Penicillin 10- 12 million units iv for 10 days ,
metronidazole 1gm every 12 hrs should be
administered.


Antitoxin is injected to neutralize circulating
toxin and unbound toxin within the wound .
Prophylaxis- wound debridement and
booster doses of tetanus toxoid .
A chronic granulomatous suppurative and
fibrosing disease caused by gram positive
non acid fast branched filamentous organism
namely actinomyses israelli , A.viscosus and
A. propionica
 Types – according to anatomical to location
(1) cervico- facial
(2) abdominal
(3)pulmonary forms





SWELLING DEVELOPS IN THE
FACE AND THE NECK WITH
INDURATION of tissues
Swelling  develops into 1 or
more abscess  produces pus
having a characteristic sulphur
granules .
The skin overlying the abscess
is purpulish red , indurated and
has the feel of wood or often
fluctuant
Infectious spread to mandible
or maxilla may result in
actinomycotic osteomyelitis

long standing fibrosing cases are treated by
draining the abscess  excising the sinus
tract  under a high dose of antibiotics(
penicillin and tetracycline )
Organism
Disease
Toxin
Further
Information
Clostridium tetani
Tetanus
Tetanospasmin
Blocks action of
inhibitory neurones
Corynebacterium
diphtheriae
Diphtheria
Diphtheria toxin
Inhibits elongation
factor- 2 (EF2) by
ADP ribosylation


DTaP – given for DIPHTHERIA that is often
combined with TETANUS TOXOID and
ACELLULAR PERTUSSIS as a series of injections
during infancy and childhood.
Toxoid is prepared by mixing formaldehyde with
the poisonous toxin produced by
Corynebacterium diphtheriae, rendering the
toxin harmless.