BACTERIAL ETIOLOGY ORAL MANIFESTATIONS PREVENTION AND

INFECTION CONTROL
SCARLET FEVER It is a highly contagious systemic oral manifestations of scarlet fever There are no available
infection occurring mostly in have been referred to as stomatitis methods for the
(Scarlatina) children. scarlatina. prevention of scarlet
It is caused by beta- hemolytic The palate and the throat is often fiery fever.
streptococci, st. pyogenes which red. The administrat ion of
produces a pyrogenic exotoxin. The tonsils and faucal pillars are
There is presence of rash due to antibiotics like penicillin,
swollen and sometimes covered with dicloxacillin, and
3 exotoxins A, B , C previously a grayish exudates.
described as erythrogenic or cephalexin will ameliorate
The early stage of the disease on the
scarlet fever toxins. tongue is described as “strawberry the disease and also helps
Incubation period of 3 to 5days tongue” o\r “white strawberry tongue”. in controlling possible
followed by severe pharyngitis In the later stage the tongue becomes complications.
and tonsillitis , headache , chills . deep red , glistening and smooth Local applications like
Fever and vomiting. except for the swollen , hyperemic mupirocin topical
There is enlargement and papilla and is termed as “raspberry ointment also can be used
tenderness of regional lymph tongue “ or “red strawberry tongue
nodes-characteristic feature – Is to relieve discomfort.
a appearance of diffuse, bright,
scarlet skin rash in the regions of
skin folds on the.
2nd 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 subsides after 6 or 7
days followed by desquamation
of palms and soles
Diphtheria Is an acute , infectious and Formation of a passive, diphtheritic Administration of
communicable diseases of the membrane which begins on the diphtheria antitoxin
skin and the mucous membrane tonsils. neutralizes the circulating
caused by toxemic strains of This membrane contains dead cells diphtheria toxin and
cornyebacterium Diptheriae ,leukocytes, bacteria overlying
prevents the disease
Pathogenesis – has air borne necrotic, ulcerated area of the
mode of transmission and mucosa. progression.
localizes in mucous membrane of The pseudo membrane leaves a Apart from antibiotic
respiratory tract.It invades open bleeding surface if stripped away. administration usually
skin lesions due to insect bites or Enlargement of sub - mandibular and done by penicillin and
trauma. anterior cervical nodes will give a bull erythromycin;
Bacillus multiplies at the entry neck appearance maintaining the airway is
site and liberates toxins.Toxins also necessary.
induce initial edema, hyperemia  The disease may be
epithelial necrosis  acute prevented by prophylactic
inflammation.
active immunization with
Coagulation of the fibrin and
purulent exudate produce a diphtheria toxoid.
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
 BACTERIAL ETIOLOGY
INFECTION
Tuberculosis  Facultative intracellular
parasite
 Caused by Myobacterium
tuberculosis, an infectious
granulomatous
 Bovine strain may also
produce illness through
ingestion of unpasteurized
cow’s milk
 Atypical or opportunistic
mycobacteria can cause
pulmonary or generalized
infection in
immunocompromised
individuals
 It is a rodshaped,nonspore
forming, thin aerobic
bacteria called acid fast
bacilli.
 Male > Female
ORAL
MANEFESTATIONS
 Episodic fever and chills
 Easillyfaigability
 Gradual weight loss
 Lesions in base of the tongue
 Lesion in oral mucosa
 Contaminated sputum or saliva
 Lesion in palate, lips,buccal mucosa,
gingiva, frenula
 Irregular,superficial or deep,painful
ulcer which tends to increase in size
sowly.
 Occasional mucosal lesions shows
swelling, granular, nodular or fissured
lesion but noobviousclinical
ulceration.
 Gingiva diffuse, hyperemic,
nodular/papillaru proliferation of
gingival tissues.
PREVENTION &
CONTROL
 Identified through special microbial
stain and cultures of tissue or sputum
 CT scan
 Multiple drug theraphy
 Isoniazid (INH) + rifampicin for 9
months
 Isoniazid (INH)+ rifampicin +
pyrazinamide for2 months followed by
isoniazid (INH) (INH)and rifampicin for
4 months
 Other drugs are streptomycin and
ethambutol
 BACTERIAL INFECTION ETIOLOGY
Granuloma Inguinale  Caused y microorganism called Donovania
granulomatis then became Donovan bodies
but now carrying the name
CALYMMATOBACTERIUM GRANULOMATIS.
ORAL PREVENTION &
MANEFESTATIONS CONTROLU6
 Oral lesion are secondary  Tetracycline
to active genital lesins and  Chloramphenicol
appear in a variable period  Streptomycin garamycin
of timeafter primary  Cotrimoxzole
lesion, frequently months  Complete healing occurs
to several years. within 2-3 weeks
 May appear in lips, buccal
mucosa, palate.
 Types are ulcerative,
exuberant. Cicatrical.
 Fibrous scar formation
may be extensive, present
in cheek or lip and limits
mouth opening
 BACTERIAL ETIOLOGY
INFECTION
LEPROSY  M. leprae is an obligate 
(Hansen’s disease) intracellular, gram-positive,
 a chronic acid-fast bacillus. It is the
granulomatous only bacterium to infect
infection caused by peripheral nerve.
Mycobacterium leprae.
 It grows best in cooler 
 It mainly affects skin, tissues like skin, peripheral
peripheral nerves, the nerves, upper respiratory
upper respiratory tract, tract, anterior chamber of
eyes, and testes, but the eye, and testes; sparing
also affects muscles, warmer areas like axilla,
bones, and joints. groin, scalp, and midline of
 Paralysis of facial and maxillary division of
back.
 Living leprosy bacillus
appears as solid staining
pink rod whereas non-living
 Premaxilla is affected in childhood due to
leprosy bacilli may be
granular or fragmented.
 There will be a circumferential hypoplasia,
 It can be grown well in
mouse footpad and nine
banded armadillo and
ORAL PREVENTION AND CONTROL
MANIFESTATION
The oral lesions that have been reported DIAGNOSIS
generally consist of small tumor like masses  Its based mainly on clinical and
called lepromas, which develop on the bacteriological examination.
tongue, lips, or hard palate. These nodules Culturing of the organism is difficult.
show a tendency to break down and ulcerate. So far the organism has been grown
in the footpads of mice and
Gingival hyperplasia with loosening of the armadillos.
teeth has also been described, but Reichart
and his associates found that most of the TREATMENT
gingival and periodontal changes occurring in  Specific long-term chemotherapy is
a group of 30 leprosy patients were
 It consists of rifampicin, dapsone and
nonspecific.
clofazimine. The widespread use of
MDT dramatically reduces the
trigeminal nerve is reported. The dental disease burden. Rifampicin and
manifestations are described as dapsone for six months in case of
odontodysplasia leprosa. tuberculoid type and rifampicin and
dapsone along with clofazimine in
case of lepromatous type is usually
granulomatous involvement. advocated. However, drug regimen
evaluation is very difficult in certain
situations. Once the infection is
shortening of roots, usually involving
treated, the management is directed
maxillary anterior teeth. Long standing
towards the reconstruction of the
 grows at 30–33° C with a lepromatous lesions may show damage caused by this disease.
doubling time of 12 days. It granulomatous invasion of pulp and pinkish
can remain viable in the discoloration of
environment for 10 days.
 crowns.

INFECTION ETIOLOGY ORAL MANIFESTATIONS PREVENTION/CONTROL

RHINOSCLEROMA
Klebsiella  Proliferative granulomas.
rhinoscleromatis  Impairment of the sensation
(Klebsiella type 3) of taste
 Tetracycline or ciprofloxacin.
 Anesthesia of the soft
palate  If left untreated the outcome will be fatal.
- a gram-
negative non-  Enlargement of the uvula
motile bacillus and upper lip

Actinomyces  Swelling and induration of  The treatment of this disease is difficult and
the tissue in has not been uniformly successful.
ACTINOMYCOSIS - salivary glands
- anaerobic or - tongue  Long standing fibrosis cases
microaerophilic - very rarely gingiva
 gram-positive - bone
nonacid fast, - skin of the face and neck.
branched (May develop into one or more
abscesses, which tend to discharge
filamentous upon a skin surface, rarely a mucosal
bacteria.
surface, liberating pus containing the
typical ‘sulfur granules’.)Such
destructive lesions within the bone
- periapical granuloma or
cyst.
- Draining the abscess
- Excising the sinus tract with high doses of
antibiotics
 Long term high dose
- Penicillin
- Tetracycline
- Erythromycin have been used most
frequently, but the course of the disease
is still often prolonged

Bacterial Etiology Oral Manifestation Prevention and

Infection Control/Treatment
 Caused by
Tularemia the gram- Accounts for 3-4% of The disease responds well to antibiotic
all cases and are therapy. Streptomycin is the drug of
negative,
manifested as necrotic choice. It also responds to adequate
non-
ulcers of the oral cavity doses of Gentamicin and Tetracycline.
motile
pharynx, usually
bacillus
accompanied by
Francisella
severe pain.
tularensis
BACTERIAL INFECTION ETIOLOGY
BOTRYOMYCOSIS -Although an “Actinobacillus” has
(Bacterial actinophytosis, been
actinobacillosis) thought to be the one involved.
- Nevertheless, a variety of other types
of organisms have been reported.
-Many workers
believe that a number of common
bacteria such as Staphylococcus,
Streptococcus, Escherichia,
Pseudomonas and probably many
others
may serve as etiologic agents of the
disease.
NOMA -Noma appears to originate as a
(Cancrum oris, gangrenous specific infection by
stomatitis) Vincent’s organisms, an acute
necrotizing gingivostomatitis,
which is soon complicated by
secondary invasion of many
other microbial forms, including
streptococci, staphylococci,
and diphtheria bacilli.
-“Selye” that noma may not due to a
specific pathogenic agent,
due to a ‘pathogenic situation’
resulting from faulty adaptation
to a nonspecific injury or stress.
ORAL MANIFESTATIONS PREVENTION AND CONTROL
- A Localized - Treatment Is not specific but may require
granulomatous infection of antibiotic therapy and may also require
the skin or mucosa. surgical debridement.
-Firm, nodular
infiltration of the body and
base of the tongue. However,
there were no sinuses
present.
-Usually begins as a small - Antibiotics are administered before the
ulcer of patient reaches the final
the gingival mucosa which stages. Immediate treatment of any existing
rapidly spreads. malnutrition further
improves the probability of saving the patient.
-The overlying skin becomes
inflamed, edematous and
finally necrotic, with the
result that a line of
demarcation develops
between healthy and
dead tissue, and large masses
of the tissue may slough out,
leaving the jaw exposed.
 SYPHILIS a lesion known as The best way to prevent syphilis is to
Syphilis is caused by chancre develops at the  practice safe sex. Use condoms during any type of
Treponema pallidum, a site of inoculation sexual contact. In addition, it may be helpful to:
spirochete, and is approximately 3–90  Use a dental dam (a square piece of latex)
characterized by days after contact with or condoms during oral sex.
episodes of active the infection.  Avoid sharing sex toys.
disease interrupted by Primary stage  Get screened for STIs and talk to your partners about
the period of latency. occurring on the lips, their results.
This gram-positivea, tongue, palate, gingiva,  Syphilis can also be transmitted through shared
motile, microaerophilic and tonsils. even at the needles. Avoid sharing needles if using injected drugs.
spirochete is pathogenic site of a fresh extraction
Chancre of lip to humans wound. The usual
primary lesion is an
elevated, ulcerated
nodule showing local
induration and
producing regional
lymphadenitis

secondary/ metastatic
stage
Mucous patch of lip in oral lesions, called
secondary syphilis ‘mucous patches,’ are
usually multiple,
painless, grayish-white
plaques overlying an
ulcerated surface

Tertiary syphilis, also

called late syphilis
The intraoral gumma
most commonly involves
the tongue and palate.
Gumma of tongue In either situation the
lesion appears as a firm
nodular mass in the
tissue, which may
subsequently ulcerate,
to form a deep painless
ulcer.

The acquired form of

syphilis is contracted
primarily as a venereal
disease, after sexual
intercourse with an
infected partner,
although persons, such
 Acquired Syphilis as dentists, working on
infected patients in a
contagious stage, have
innocently acquired it in
many cases

Congenital syphilis is
transmitted to the
offspring only by an
infected mother and is
not inherited

 Congenital (Prenatal)
Syphilis
Bacterial Infection Etiology Oral manifestations Prevention and Control
PYOSTOMATITIS VEGETANS an uncommon inflammatory disease of the oral cavity
originally described by McCarthy in 1949. consist of large numbers of The treatment of pyostomatitis vegetans is
broad based papillary not specific, since the oral lesions are usually
The name was suggested because of the clinical projections, tiny abscesses or refractory to antibiotic therapy. It has been
similarity between the oral lesions of this disease and vegetations developing in found that the oral lesions tend to regress
the skin lesions in a dermatologic disease known as areas of intense erythema when the intestinal disturbance is brought
‘pyodermatite végetanté’. under control. However, exacerbations of
the gastrointesti nal disease frequently result
McCarthy and Shklar, who pointed out that the oral These many small in exacerbation of the oral lesions as well.
lesions are one part of a syndrome in which the projections are red or pink in
patients also manifest concomitantly ulcerative colitis color, but careful
or other gastrointestinal disturbances. examination may show tiny
pustules beneath the
In fact, the history of colitis or a gastrointestinal epithelium, which liberate
disturbance often points to the diagnosis of the oral purulent material when
lesions. ruptured. These leave areas
of ulceration, which may
Regional enteritis or regional ileitis, also known as coalesce, into large areas of
Crohn’s disease, is a granulomatous inflammation of necrosis known as snail track
the intestine of unknown etiology which is also ulcerations.
recognized as one form of gastrointestinal disturbance
that may be associated with pyostomatitis vegetans.
This has been discussed by Cataldo and his associates
who illustrated a case in which the oral lesions ulti
mately led to the diagnosis of the intestinal disease. A
few patients with liver disease also have oral
manifestations related to pyostomatitis vegetans.
Bacterial Infection Etiology
Melioidisis -caused by the bacillus
Burkholderia pseudomallei, an
aerobic, gram-negative
nonacid-fast, and rod-shaped
bacilli
Oral manifestations Prevention and Control
N/A Incision and drainage, accompanied by massive antibiotic
therapy, have proven moderately successful in treating the
disease. Tetracycline alone or in combination with
chloramphenicol were considered to be drugs of choice.

Cat-Stratch Disease -caused by N/A the disease is self-

the bacterium Bartonella limiting and regresses within a period of weeks or months.
henselae which is believed to
be spread by the cat’s saliva. Incision and drainage of the involved node may be necessary.
Antibiotic therapy is ineffective.
-This disease, occurring at an
age, but predominantly in
children and young adults, is
thought to arise after a
traumatic break in the skin
due to the scratch or bite of
the household cat.

Bacterial infection Etiology Oral manifestation Prevention and control,

Tetanus Caused by the n/a Anti toxin vaccine
clostridium tetani an To neutralize the circulating toxin and unbound the toxin
rod shaped gram Prophylaxis wound debridement and booster dose of tetanus
positive bacteria found toxcoids
in the soil globally Antibiotics such like
Penicillin 10-12 million unit intravenous for 10 days
It affect the motor
neurons of human

Muscle spasm in the

oral cavity
Trismus and facial
palsy

Pyogenic granuloma Botromycotic infection Granulation tissue Surgically excision to remove this pyogenic granuloma
Origin of this infection appear looks like
comes from horses hyperplastic macules
thought transmisible and has ulceration in
to human The gingiva and
Streptococci and tongue
staphyloccoci bacteria Connective tissue
And fungus like stroma
charcteristics in
traumatic tissue may
penetrate this
microorganism
 INFECTION ORAL MANIFESTATIONS PREVENTION/
ETIOLOGY
CONTROL

GONORRHEA Neisseria gonorrhoeae The bacterial infection establishes

-a gram-negative, nonmotile, nonspore
forming organism that grows in pairs
(diplococci).
itself in the pharynx and may be
asymptomatic (cause no
symptoms), but can cause
symptoms of sore throat and
discomfort when swallowing food.
Antibiotics (either ceftriaxone or
cefixime, azithromycin)
Use a reliable condom every time
you have vaginal, oral, or anal
sexual intercourse.
have only one sexual partner who is
uninfected and who is also sexually
monogamous