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bacterial infections and their oral manifestations
ORAL MANIFESTATIONS OF
BACTERIAL INFECTIONS
*1. Introduction
*2.bacterial morphology
*3.bacterial infections
*A) scarlet fever
*B)diptheria
*C)actinomycosis
*D) tetanus
*E) gonorrhoea
* F)syphilis
*G)leprosy
*H)anug
*I)noma
* 4.references
CONTENTS
bacterial infections and their oral manifestations
bacterial infections and their oral manifestations
bacterial infections and their oral manifestations
bacterial infections and their oral manifestations
bacterial infections and their oral manifestations
bacterial infections and their oral manifestations
SCARLET FEVER
Highly contagious systemic infection.
Beta hemolytic streptococci,
streptococcus pyogenes
Rash – exotoxin A, B, C and scarlet
fever toxin.
*
Clinical features
Severe
pharyngitis
Tonsillitis
enlarged and
tender regional
cervical lymph
nodes
Headache
vomiting
Abdominal pain
Pastia
lines
Fever
Chills
Scarlet rash
Pharyngitis
tonsillitis
Oral manifestations
Forchheimer
spots
White
coating
Edematous &
hyperemic fungiform
papillae
Strawberry tongue
Deep red, glistening and
smooth
Raspberry tongue
FORCHHEIMER SPOTS
12
3
4
Local or generalised bacterial dissemination
Hypersensitivity reactions to bacterial toxins
Peritonsillar abscess
Rhinitis
Sinusitis
Otitis media
Meningitis
Rheumatic fever
Arthritis
complications
*
clear hemolysis on colonies around blood
agar plates
Diagnosis & TREATMENT
Marked leukocytosis
Increased
neutrophillia
C reactive
proteins
Elevated ESR
CULTURE
bacterial infections and their oral manifestations
bacterial infections and their oral manifestations
bacterial infections and their oral manifestations
Bull neck Diptheric membrane
Sore throat
Cutaneous diptheria
Oral manifestations
pseudomembrane
diagnosis
Pai agar
*Diptheria antitoxin
*Antibiotics :
*Penicillin
*Erthromycin
*Maintain the airway
*Prevention :
*Prophylactic active immunization with diptheria toxoid
Treatment and prevention
ACTINOMYCOSIS
Gram positive
 Non acid fast
 Branched filamentous
 Actinomyces israelii
 A. naeslundii
 A. viscosus
 A. odontolyticus
 A. bovis : lumpy jaw (cattle) A.
meyeri, A. gerencseriae, and
Propionibacterium propionicum
Actinobacillus
actinomycetemcomitans,
Eikenella corrodens,
Enterobacteriaceae
Fusobacterium, Bacteroides,
Classification:
Cervicofacial
Abdominal
Pulmonary forms
Organism may be cultured
from:
• Carious tooth
• Non vital root canals
• Tonsillar crypts
• Dental plaque
• Gingival sulcus
• Pdl pockets
POLYMICROBIAL
Disruption of
mucosal
barrier
Acute
inflammation
• Chronic
indolent
phase
Single/multi
ple
indurations
• Central
fluctuance
• Pus
containing
neutrophils
Sulphur
granules
IUCDS
• HIV
• CHEMO
• HERPES
pathogenesis
CLINICAL FEATURES
Cervicofacial actinomycosis
Overlying skin
purplish
red,indurated
& fluctuant
Soft tissue infection
Involve maxilla or
mandible
Actinomycotic
osteomyelitis
Maxilla invaded
Cranium, meninges
& brain
diagnosis
treatment
o Draining the abscess
o Excising sinus tract with
high doses of antibiotics
to accelerate healing
o Penicillin
o Tetracycline
o Erythromycin
bacterial infections and their oral manifestations
 Acute infection of nervous
system
 Intense activity of motor
neurons
 Severe muscle spasms
 Gram positive bacillus
 Clostridium tetani
 Acts at synapse of
interneurons of inhibitary
pathways & motor neurons
to produce blockade of
spinal inhibition
bacterial infections and their oral manifestations
Clinical features
opisthotonus
Facial
tetany
*General measures:
*Remove spores at site of wound
*Cardiopulmovary monitoring
*Sedation,airway & nutrition to be maintained
*Penicillin 10-12million units IV for 10days
*Metronidazole 1gm every 12hrs
*Antitoxin injected to neutralise circulating toxin & unbound toxin with
wound.
*Prophylaxis : wound debridement & TT booster doses
*Unimmunized individuals : anti tetanus serum(ATS)
1500units or TIG 250units.
treatment
GONORRHEA
o Veneral disease
o Male & female genitourinary
Tract
o Neisseria gonorrhoeae
o Gram negative
o Nonmotile, nonspore forming
o Grows in pairsage : 15-29yrs
oIncubation pd : 1-5 days
o Oropharyngeal gonorrhoea in
20% women
Clinical features
orogenital contact
lips: acute painful
ulceration
gingiva: erythematous
tongue: red, dry
ulcerations, smooth
pharyngitis, tonsillitis
fever, lymphadenopathy
gonococcal parotitis
Oral manifestations
*
*Epididymitis
*Salpingitis
*Pelvic inflammatory disease
*Dermatitis
*Arthritis
*Risk for chlamydia
* trachomatis Infection
antibiotics
complications Diagnosis & treatment
Thayer
martin
medium
SYPHILLIS
Treponema pallidium
Episodes of active
disease interrupted by
Period of latency
Gram positive, motile
Microaerophillic
Darkfield microscope
Route of transmission:
Sexual contact
Mother to child in utero
ACQUIRED SYPHILLIS
PRIMARY STAGE
Chancre : at site of innoculation
3-90 days after infection
Solitary
m/c site males: penis
females: cervix or
vulva
95% occur in genitalia
Extragenital syphillis : increase in
altered sexual activity & contact
among
Infected homosexuals.
Oral manifestations
 Elevated,
ulcerated
nodule.
 Local
induration.
 Regional
lymphadenitis.
 Brown, crusted
appearance
Heals in 3weeks to 2
months
chancre
TONGUE TONGUE
LIPS
SECONDARY STAGE
 Skin: macules or papules,
painless
 Oral lesions: MUCOUS
PATCHES, multiple, painless
 Gray white plaques overlying
ulcerated surface.
 Tongue, gingiva, buccal
mucosa
 HIGHLY INFECTIOUS
,contain vast number of
micro-organisms
 Serologic reaction is always
+ve
 Explosive, widespread form :
LUES MAILGNA
MUCOUS PATCHES
Leão JC, Gueiros LA, Porter SR. Oral manifestations of syphilis. Clinics
(Sao Paulo). 2006 Apr;61(2):161-6. Epub 2006 Apr 25.
*Late syphilis
*Do not appear for years
*CVS & CNS
*Noninfectious
*Gumma: result of hypersensitivity
*Focal, granulomatous inflammatory
*Process with central necrosis
*i/o gumma : tongue & palate
*Firm nodular mass in tissue
*May ulcerate to deep painless ulcer
*Palate: perforation by sloughing
*Herxheimer reaction
TERTIARY SYPHILIS
Atrophic or interstitial glossitis is most characteristic &
important lesion of syphilis & is due to endarteritis obliterans
SYPHILITIC GLOSSITIS
 Tongue surface gets broken up by fissures.
 Atrophy & fibrosis of tongue musculature.
 Hyperkeratosis
 May undergo carcinomatous transformation
Transmitted to offspring by
Mother
Frontal bossae
Short maxilla
High palatal arch
Saddle nose
Mulberry molars
Higoumenakis sign
Relative protuberance of mandible
Rhagades
Saber shin
CONGENITAL
SYPHILIS
RHAGADES
FRONTAL
BOSSAE
INTERSTITIAL
KERATITIS
HIGOUMENAKIS SIGNSADDLE NOSE
SABER SHIN
Diagnosis & treatment
 Penicillin: DOC
 Surgical correction
of facial defects
gives good esthetic
LEPROSY
*Hansens disease
*Mycobacterium leprae
*Incubsation pd: 5yrs
*Affects skin, peripheral nreves,
*Upper resp tract, eyes, & testes
*Bones, muscles & joints
*ONLY BACTERIA TO INFECT
*PERIPHERAL NERVES
*Dopa oxidase activity
*Acid fastness
*Living leprosy bacilli:
*Solid staining pink rod
*Nonliving : granular
*Can be grown in mouse footpad
*& nine banded armadillo
PATHOGENESIS
Clinical features
 Hypopigmented
patches
 Total loss of
cutaneous sensation
 light touch to be
affected first
 Thickening of nerves
 Presence of acid fast
bacilli in skin or nasal
smear
GENERAL
FEATURES
 Single/ multiple
macular
erythematous
eruptions
 Dermal &
peripheral nerve
trunk involvement
 Loss of sensation
 Loss of sweating
of affected skin
Tuberculoid Leprosy
 Early erythematous
macules or papules
 Thickening of skin
 Characteristic
nodules
 Severe disfigurement
Lepromatous Leprosy
Chronic insensate patch
bacterial infections and their oral manifestations
Oral manifestations
LEPROMAS
1
Hardpalate>soft palate>labial max gingiva>tongue>lips>buccal max
gingiva>labial mand gingiva>buccal mucosa
bacterial infections and their oral manifestations
Pallagatti S, Sheikh S, Kaur A, Aggarwal A, Singh R. Oral
cavity and leprosy. Indian Dermatology Online Journal.
2012;3(2):101-104..
HISTOLOGY
DIAGNOSIS & TREATMENT
 Based on clinical &
bacteriological examination
 Organism grown in footpads
of mice & armadillos
 Nasal smears & scrapings
stained with modified ziehl
nielsen method
 Lepra bacilli >1011 gm of
tissue
 Skin biopsy
 Nerve biopsy
 Foot culture histamine test
Test for humoral response:
Monoclonal antibodies
ELISA, PCR
MDT( MULTI DRUG
THERAPY)
Rifampicin
tuberculoid
Dapsone
Clofazimine lepromatous
NECROTISING ULCERATIVE
GINGIVITIS
PAIN
INTERDEN
TAL
ULCERATI
ON
ANUG
GINGIVAL
BLEEDING
 Involves free gingival margin,
crest of gingiva, interdental
papillae
 May spread to soft palate &
tonsillar areas : vincents angina
 Necrotizing ulcerative
periodontitis
 Associated with HIV
 Common in young & adults
etiology
• Fusiform bacillus & borrelia
vincentii
• Vibrio & coccal forms
• Acc to mc donald , Bacteroides
melaninogenicus : main causative
agent
• Stress , immunosupression
,smoking
• Upper resp tract infection , local
trauma
• Poor nutritional status , poor oral
Predisposingfactors
*Loesche WJ, Syed SA, Laughon BE, Stoll J. The bacteriology of acute
necrotizing ulcerative gingivitis. J Periodontol. 1982 Apr;53(4):223-
30.
*Treponema and Selenomonas sp., 32 and 6%, respectively, of the
microscopic count;
*B. melaninogenicus ssp. intermedius and Fusobacterium sp., which
averaged 24 and 3%, respectively, of the viable count.
*Plaque samples from 22 ulcerated sites in 8 patients with ANUG.
*
Clinical features
 Painful, hyperemic gingiva, sharply
punched out crater like erosions
of interdental paillae
 Grayish green necrotic
pseudomembrane
 Fetid odour
 Inability to eat
Gingival bleeding
Incubation zone
Diagnosis based on clinical finding :
gingival pain, ulceration & bleeding
Bacterial smear from gingiva
Fusiform bacillus: elongated rod with
Tapered ends 5-14microns in length
0.5-1.0microns diameter.
Weakly gram+ve
Borrellia vincentii: gram-ve
10-15microns length
Diagnosis
A- spirochete; B- bacillus fusiformis; C-
filamentous organism; D- streptococcus;
E- vibrio; F- treponema microdentinum
treatmentFIRST VISIT:
 Medical history,
diet
background,smoking,
rest , risk factors
for HIV, stress
 Examination of
general appearance,
halitosis, fever
 Topical anesthetic6,
area swabbed with
moist cotton
 Pseudomembrane &
non attached debris
removed
 Superficial calculus
removed by
ultrasonic scaling
 Antibiotics:
Amox 500mg 6hrs for
10days
Metronidazole 500mg
twice daily for 7days
 Tooth xtraction or pdl
surgery
Postponed until 4weeks
 Rinse with equal
amount of 3% h2o2 &
warm water every
2hrs or twice daily
with CHX
 Adequate rest
 Ultrasoft brush
 NSAID for pain relief
 SECOND VISIT
 1,2 days after 1st
visit
 Diminished pain
 Gingival margins
erythematous but
without
 Pseudomembrane
 Scaling if needed
THIRD VISIT
 5 DAYS after
 Resolution of
symptoms
 Plaque control
procedures
 Counselling on
nutrition, smoking
cessation
 CHX rinses for 2-4
weeks
Reevaluation after 1
month
 Gingival contouring :
gingivoplasty
 Nutritional
supplements
bacterial infections and their oral manifestations
small ulcer of gingiva spreads
involve surrounding tissues of jaw,lip
& cheeks by gangrenous necrosis.
 rapidly spreading
 Gangrenous stomatitis
 m/c in children
 seen in persons who are
undernourished or debilated
from infection
diptheria,dysentry,tb,syphilli
s,anemia…
 Secondary complication of
systemic disease rather than
a primary disease.
 Specific infection by
vincents organisms,
ANUG…soon complicated by
secondary invasion of
streptococci, staphylococci &
Clinical features
Area of
stagnation
Around fixed
bridge or crown
Overlying skin
inflammed,edem
atous & necrotic
Large mass of
tissue slough out.
Blackening of
skin.
Subcutaneous fat
undergoes
necrosis.
Foul odour
High
temperature,sec
ondary infection,
death from
toxemia
bacterial infections and their oral manifestations
bacterial infections and their oral manifestations
ORAL MANIFESTATIONS OF
BACTERIAL INFECTIONS
*
*1.bacterial infections
*A) pericoronitis
*B) pyogenic granuloma
*C) angular chelitis
*D) cellulitis
*E) ludwigs angina
* F)sarcoidosis
*G)tuberculosis
*H)osteomyelitis
*
* 2.references
CONTENTS
PERICORONITIS
* : inflammatory lesion occuring around the
impacted or partially erupted tooth.
Mixed infection(anaerobes)
*Mand 3rd molar
*Pain & swelling
*Difficulty in opening & chewing
Mildly ill, fever & regional lymphadenopathy
Sixou JL, Magaud C, Jolivet-Gougeon A, Cormier M, Bonnaure-Mallet M. Microbiology of
mandibular third molar pericoronitis: incidence of beta-lactamase-producing bacteria. Oral
Surg Oral Med Oral Pathol Oral Radiol Endod. 2003 Jun;95(6):655-9
PERICORONITIS
Clinicalfeatures
alpha-hemolytic streptococci (26/26)
Prevotella (15/26), Veillonella (15/26),
Bacteroides (9/26), and
Capnocytophaga (9/26)
*Gently flushing area with warm water
*Entrapped food debris must be removed
*Swabbing with antiseptic after elevating flap
Gently from tooth with a scaler
*Upper tooth when involved should be
ground or extracted
*Radiograph help in assessing position of tooth
*Surgical removal after acute symptoms subside
*Antibiotics to relieve symptoms & to prevent spread of
infection.
treatment
PYOGENIC GRANULOMA
*Originate as a response of tissue
*To a nonspecific infection.
*Tumor like growth : exaggerated
*Conditioned response to minor
* trauma
 Infection staphylococci or streptococci
 Arise as a result of minor trauma to
tissues
 Pathway for invasion of nonspecific
type of micro-organism.
 Surface of pyogenic granuloma in cases
of ulceration abounds with typical
colonies of saprophytic organisms.
 Sulfhydryl radical
etiology
Clinical features
histology TREATMENT
 Surgical excision
 Laser
 Recurrence : not encapsulated
 Excising gingiva lesion, care to be
taken
 To scale adjacent tooth
 Calculus irritant for recurrence
 Recurrence rate – 15%
Endothelium lined vascular
spaces & extreme proliferation
Of fibroblasts & budding
endothelial cells.
ANGULAR CHELITIS
*Multifactorial disease affecting commissure of lips
*m/c in denture wearers
*Associated with infection
*Reduced vertical dimension of mouth
*60% : candida albicans & staphylococcus
*20%: staphylococcus
*20%: candida albicans
*Nutritional deficiencies: fe, vit B, folic acid
*Ariboflavinosis: circumoral lesions
*Seen in diabetes, neutropenia, AIDS
*Occur in both young children & adults
*Dryness, burning sensation at corners
*Wrinkled skin at commissure
*Deep fissures & cracks
*Fissures stop at mucocutaneous
junction
Clinical features
Depending on the specific cause, the following treatments may
be useful:
*Lip balm or thick emollient ointment, applied frequently.
*Topical antiseptics.
*Topical or oral antistaphylococcal antibiotic.
*Topical antifungal cream.
*Oral antifungal medication
*.ketoconazole tab 200-400mg twice daily with food for 2weeks
* Fluconazole cap 50-100mg once daily for 2-3weeks
*Nutritional supplements.
treatment
CELLULITIS
*:
*Cellulitis is a diffuse inflammation of soft tissues which is
not circumscribed or confined to one area, but which, in
contrary to the abscess, tends to spread through tissue
spaces and along fascial planes.
*Common causative agent : streptococci viridans
*Produce : streptokinase, hyaluronidase, fibrinolysins
*Prevotella & porphyromonas : destroy collagen
*As result of apical abscess, osteomyelitis, following pdl
infection
*Pericoronitis
*Injection with infected needle
CELLULITIS
bacterial infections and their oral manifestations
*Moderately ill
*Elevated temperature
*Leukocytosis
*Firm & brawny, painful swelling of soft tissues
*Inflammatory edema
*Inflammed , orange peel appearance
*Regional lymphadenitis
*Infections in maxilla perforate outer cortical layer
Of bone above buccinator attachment : swelling of upper half
of face
*Eye: cavernous sinus thrombosis
*Infection in mandible perforate outer
cortical plate below buccinator :
*diffuse swelling of lower half of face
*Spread to cervical tissue : respiratory discomfort
Clinical features
histology
 Diffusion exudation
of
Polymorphonuclear
Leukocytes,
lymphocytes
 Separation of
connective tissue or
muscle fibers
treatment
 Treatment for cellulitis depends on what
caused the infection, the severity of
symptoms and the general state of health.
 Hospital treatment may be necessary if
symptoms such as fever, nausea and
vomiting suggesting infection has spread
from skin to bloodstream or other parts of
the body.
 Antibiotics:
flucloxacillin, 25mg/kg(max 500mg) 6hr for
7days
Flucloxacillin 50mg/kg iv 6hr
Ceftriaxone 50mg/kg/dose iv 12 hr
 Drink plenty of fluids to avoid dehydration.
 NSAIDS : pain control
LUDWIG’S ANGINA
*
*Ludwig's angina, otherwise known as angina ludovici, is a
serious, potentially life-threatening cellulitis, or
connective tissue infection, of the floor of the mouth,
usually occurring in adults with concomitant dental
infections and if left untreated, may obstruct the
airways, necessitating tracheotomy.
 Acute, toxic begin in
submandibular space
* secondarily involve sublingual &
submental spaces spaces.
* dental origin
* mandibular molar : chief
source of infection
* other causes :
LUDWIG’S
ANGINA
2nd & 3rd molars: m/c
Unusual speech(hot potato in mouth)
Bilateral sublingual space infection
Bilateral submandibular space infection
Brawny edema
Elevated tongue
Airway obstruction
Paucity of pus
CLINICALFEATURES
HALLMARK SIGNS
3’F’ :
FEARED
FATAL(often)
FLUCTUANT(rarely)
bacterial infections and their oral manifestations
 Mixed infection
 Beta hemolytic
Streptococci
 Peptostreptococcus
 Streptococcus
viridans(40.9%)
 Staphylococcus aureus
(27.3%), staph epidermis
(22.7%)
 Pseudomonas, klbsiella,
e.coli
 Clostridium, enterococcus
fecalis
 Fusiform bacilli & spiral
forms
LAB FINDINGS :
TREATMENT
*Early recognition of incipient cases
*Maintenance of airway
*Intense & prolonged antibiotic therapy
*Extraction of affected tooth
*Surgical drainage
*Edema of glottis necessitates emergency
tracheostomy to prevent suffocation.
*Complications may include:
*Airway blockage
*Generalized infection (sepsis)
*Septic shock
BACTERIAL SAILADENITIS
* ETIOLOGY:
*microbial overgrowth in association with a reduction in salivary flow
*subsequent to dehydration and debilitation
*trauma to the duct system and hematogenous spread of infection from other
areas.
*The most commonly isolated organisms in parotitis : penicillin-resistant
Staphylococcus aureus, Streptococcus viridans, and Streptococcus pneumoniae
* presence of a painful swelling,
*low-grade fever
*malaise headache
*gland is extremely tender Trismus
*purulence at the duct orifice may be produced by gentle pressure on the
involved gland or duct.
* If infection is not eliminated early, suppuration may extend beyond the
limiting capsule of the parotid gland.
*Extension into surrounding tissues along fascial planes in the neck or
extension posteriorly into the external auditory canal may follow.
CLINICAL FEATURES
bacterial infections and their oral manifestations
*Laboratory studies :
*elevated erythrocyte sedimentation rale(ESR)
*leukocytosis, often with a characteristic shift to the left,
indicating acute infection.
* elimination of the causative organism
*rehydration of the patient
*drainage of purulence, if present.
*Culture and sensitivity testing of the exudate at the orifice of
the duct is the first step in antibiotic management.
*After a culture is obtained, patients empirically be placed on
regimen of a penicillinase-resistant antibiotic such as
semisynthetic penicillin. Along with rehydration and attempts
at establishing and encouraging salivary flow, moist
compresses, analgesics, and rest are in order.
*Medications containing parasympathomimetic agents, which
reduce salivary flow, should be reduced or eliminated.
Treatment & prognosis
*A biopsy and retrograde sialography should be avoided.
* may cause sinus tract formation, may allow infection to proceed beyond the
boundaries of the gland into surrounding" soft tissues.
* With prompt and effective treatment, recurrence is generally avoided.
* recurrent parotitis, considerable destructive glandular changes can be seen.
* juvenile, variant, of parotitis, intermittent unilateral or bilateral painful
swelling is accompanied by fever and malaise.
*initial attack : ages 2 and 6 years,
* neonatal form of suppurative parotitis may develop, with S. aureus being
the most common causative pathogen.
* Gross destruction of the parenchymal and ductal elements may be noted on
sialographic examination.
*Absence of secretory acinar components and a damaged ductal system with
numerous punctate globular spaces.
*Spontaneous regeneration of parotid salivary tissue.
SARCOIDOSIS
*Sarcoidosis a multisystem granulomatous disease of unknown origin
characterized by the formation of uniform ,discrete, compact, non-caseating
epithelioid granulomas. I
*blacks >>whites.
* infectious etiology : Mycobacterium and Propionibacterium
* young adults
*lesions most common in the lungs, skin, lymph nodes, salivary glands,
spleen, bones,& the mouth.
*characterized by depression of delayed-type hypersensitivity
suggesting an impaired cell-mediated immunity, and raised or
abnormal serum immunoglobulins suggesting lymphoproliferation
*interferon gamma (IFN-J) and cytokines such as TNF-D, IL-12 and
IL-18 play an important role in the formation of granulomatous
lesions
bacterial infections and their oral manifestations
bacterial infections and their oral manifestations
ERYTHEMA NODOSUM: multiple raised red
patches,in groups, occur slowly
LUPUS PERNIO
FOREHEAD
Oral manifestations
Small papular nodular
plaques, resemble
herpetic lesions or fever
blisters
Bleblike, containing
clear yellowish
fluid, or as solid
nodules
LIPS
HARD PALATE
BUCCAL MUCOSA
Intracutaneous test: kveim siltzbach test
A lip biopsy may occasionally provide evidence of sarcoid involvement of minor
salivary glands in support of a clinical impression of pulmonary disease.
* Lab assay for angiotensin I—converting enzyme
* Elevation of this enzyme in conjunction with a positive chest radiograph has a
high diagnostic reliability
* Spontaneous resolution
* Corticosteroids: doc for symptomating pulmonary sarcoidosis
* Chloroquine anti TNF agents
* Immunosuppresive drugs to those not responding to steroids
* Levamisole for arthritic symptoms
* Good prognosis
diagnosis
TREATMENT
HISTOLOGY
Nests of epitheloid cells with
multinucleated giant cells
Non caesating
Solid, amorphous,eosinophillic,
hyaline mass
*a form of sarcoidosis in which characteristically there is
firm, painless, usually bilateral enlargement of the parotid
glands, accompanied by inflammation of the uveal tracts of
the eye and cranial nerve involvement.
*The submandibular and sublingual glands may be involved
* chronic, low-grade fever lassitude, malaise and vague
gastrointestinal disturbances nausea, and vomiting.
*Xerostomia is common.
* patchy erythema of the skin
*Enlargement of the cervical lymph nodes
earliest symptom : uveitis
*
*most common nerve involvement is unilateral or bilateral
seventh nerve paralysis,in one-third to one-half of all cases
UVEOPAROTID FEVER (HEERFORDT SYNDROME)
TUBERCULOSIS
*Tuberculosis (TB) is a specific infectious granulomatous disease
caused by Mycobacterium tuberculosis
*M. tuberculosis is a rod-shaped, nonspore forming, and thin
aerobic bacteria called acid-fast bacilli,
*once stained, it cannot be decolorized by acid alcohol.
*Its acid-fastness is due to the high content of mycolic acids,
long chain cross-linked fatty acids and other cell wall lipids.
*Males are more affected than females in India though it
affects all ages, from an average of 1% in the under-five age
group.
M. tuberculosis is a facultative intracellular
atypical or opportunistic mycobacteria: pulmonary or
generalized infection in immunocompromised individuals
etiology
*M. tuberculosis is most commonly transmitted from a
person with infectious pulmonary TB by droplet nuclei,
which are aerosolized by coughing, sneezing, or speaking.
The tiny droplets dry rapidly; the smallest (<5–10 μm in
diameter) may remain suspended in the air for several
hours and may reach the terminal air passages when
inhaled. There may be as many as 3000 infectious nuclei
per cough
bacterial infections and their oral manifestations
bacterial infections and their oral manifestations
Exposure to TB
No infection(70-90%) Infection (10-30%)
Latent TB (90%) well
Never develop TB
Not infectious
Active TB (10%) ill
 5% develop TB within 2
yr
 5% develop TB many yrs
later
untreated treated
 50% die
within 5
years
 25% remain
sick
 25% recover
cured
bacterial infections and their oral manifestations
Oral manifestations
TONGUE
Undermined
edges
painful
0.05-5%
patients
Tongue>palate>lips>buccal mucosa>gingiva>frenula
PALATE
PALATE
Enlarged cervical lymphnode
BUCCAL MUCOSA
l
r
Buccal vestibule
TUBERCULAR
GINGIVITIS
Diffuse hyperemic
nodular or
papillary
proliferation
HISTOLOGY
bacterial infections and their oral manifestations
*Demonstration of organism by microbial stains
*Culture of sputum or infected tissue : lj medium middle brook media
*Presence of acid fast bacilli in sputum : gold standard
*Radiograph
*Tuberculin test
*CT scan: mediastinal or hilar lymphadenopathy
*MRI : extrapulmonary TB
*Ziehl Nielsen stain, Kinyouns stain , rhodamine staining for fluorescent
microsopy
*Minimum of 5 acidfast bacilli on fluorescent microscopy positive
*3 on ZN staining
*Rapid slide culture technique
*Radiometric culture method
*Radioimmunoassay
*ELISA
*PCR
DIAGNOSIS
TUBERCULIN TEST
CORRECT INCORRECT
bacterial infections and their oral manifestations
bacterial infections and their oral manifestations
TREATMENT
*Global TB statistics
*In 2014 1.5 million people died of TB. Of these people 0.4 million people
were HIV positive.
*TB now annually causes more deaths worldwide than HIV.
*In 2014 1.2 million people died of HIV and this includes the 0.4 million TB
deaths among HIV positive people. People who have both TB and
HIV when they die, are internationally classified as having died from HIV.
*There were an estimated 9.6 million new cases of TB in 2014.There were
an estimated 3.2 million cases and 480,000 TB deaths among women.
*There were also an estimated 1.0 million cases of TB in children and
140,000 deaths.
bacterial infections and their oral manifestations
bacterial infections and their oral manifestations
bacterial infections and their oral manifestations
* The World Health Organisation (WHO) current estimates in 2015 are that 1 million children
currently suffer from TB worldwide (<15 years), and that more than 136,000 die each year.
* 70-80% of children with TB have the disease in their lungs (pulmonary TB). The rest are
affected by TB disease in other parts of their body (extra pulmonary TB) –
* Some children are at greater risk of getting TB than others and these include: A child that
lives in the same household as a person who has been recently diagnosed with smear
positive TB
* A child less than 5 years old
* A child with HIV infection
* A child with severe malnutrition
* in children with pulmonary TB the commonest chronic symptoms are a chronic cough that
has been present for more than 21 days, a fever, and weight loss or failure to thrive.
TB & CHILDREN
*The 2010 WHO TB drug dosage guidance for children
*The major recommendations of the WHO drug dosage guidance
for children were that:
*1) The dosages of the following four TB drugs should be:
• Isoniazid(H) 10mg/kg (range 10-15 mg/kg); maximum dose 300
mg/day
• Rifampicin(R) 15mg/kg (range 10-20 mg/kg); maximum dose 600
mg/day
• Pyrazinamide(Z) 35mg/kg (30-40) mg/kg)
• Ethambutol(E) 20mg/kg (15-25 mg/kg)
*As children approach a body weight of 25kg, adult dosages can
be used.
bacterial infections and their oral manifestations
OSTEOMYELITIS
*Osteomyelitis is defined as the inflammation of bone and its
marrow contents.
* trauma and road traffic accidents;
*gunshot wounds, radiation damage, Paget’s disease, and osteopetrosis.
*Systemic conditions like malnutrition, acute leukemia, uncontrolled diabetes
mellitus, sickle cell anemia, and chronic alcoholism.
CLASSIFICATION
SUPPURATIVE NONSUPPURATIVE
ACUTE CHRONIC CHRONIC
SCLEROSI
NG
FOCAL DIFFUSEGARRE
PREDISPOSING FACTORS:
*Mixed aerobic-anaerobic infection.
*Streptococci
*Alpha hemolytic streptococci
*Anaerobic streptococci
*Fusobacterium
*Bacterioids
*Peptostreptococcus
*Others in special forms:
*Mycobacterium tuberculosis
*Treponema pallidium
*actinomyces
*
*serious sequela of periapical infection that often results in a diffuse spread
of infection throughout the medullary spaces, with subsequent necrosis of a
variable amount of bone.
*MAXILLA : well localised MANDIBLE : diffuse & widespread
* neonatal maxillitis in infants and young children
*severe pain, trismus, and paresthesia of the lips : mandibular involvement
*elevation of temperature regional lymphadenopathy.
*WBC elevated.
teeth loose and sore eating is difficult,
Pus may exude from the gingival margin.
Until periostitis develops, there is no swelling or reddening of the skin or
mucosa.
ACUTE SUPPURATIVEOSTEOMYELITIS
CLINICAL FEATURES
Chronic sclerosing
osteomyelitis
Chronic suppurative osteomyelitis
Chronic
osteomyelitis
Most infectious
(bacterial)
Varaiable pain,
swelling,
drainage
Radiolucent or
mottled
pattern
Appropriate
antibiotic,
sequestromy
Chronic
osteomyelitis
with
proliferative
periostitis
Sequelae of
tooth abscess,
extraction
Usually
associated
with lower
molar,perioste
um involved
children
Radiolucent or
mottled with
concentric
periosteal
opacities
Tooth removal,
antibiotics
Diffuse
sclerosing
osteomyelitis
Probably low
grade
infection,
pulpitis,period
ontal disease
Ocassional
pain, swelling,
drainage
mandible
Opacification
throughout jaw
Antibiotics,
find cause &
treat if
possible
Focal
sclerosing
osteitis
Low grade
focal bone
irritation
Asymptomatic,
Found on
routine
examination
Opaque mass
usually at root
apex
Treat offending
tooth
Etiology Clinical
features
Radiographs Treatment
* a reaction to mild bacterial infection entering the bone through a carious
tooth in persons who have a high degree of tissue resistance and tissue
reactivity.
 the tissues react to the infection by proliferation rather than destruction,
since infection acts as a stimulus rather than an irritant. .
MOST COMMON : CHILDREN
mandibular first molar with a large carious lesion. Endodontic treatment
or extraction
mild pain associated with an infected pulp.
CONDENSINGOSTEITIS
treatment
Medical management:
1.Systemic antibiotics- penicillin(empirical) 2-4 months
Metronidazle
Clindamycin
Cephalosporins
Vancomycin
2.Local application of antibiotics
PMMA beads- antibiotic impregnated beads
Surgical management:
Removal of necrotic foci
a) sequestrectomy- dead necrotic bone(avascular, antibiotics donot penetrate)
b) Saucerisation
c) Decortication- lateral & inferior cortical bone is removed
d) Ressection & reconstruction
MANAGEMENT
HBO THERAPY
bacterial infections and their oral manifestations
*1) Harrison’s principles of internal medicine.19th edition
*2)Scott C Kachlany. Deadly diseases and epidemics. Infectious diseases of the
mouth.2007
*3) Shafer.Hine.Levy. Textbook of OralPathology.7th edition
*4)Greenberg. Glick. Ship. Burket’s OralMedicine.11th edition
*5) Regezi.Sciubba.Jordan. OralPathologyClinical pathological correlations.4th
edition
6)Philip D Marsh. Michael V Martin. Oral Microbiology.5th edition
*7)Michael Miloro. Peterson’s Principles of Oral And Maxillofacial Surgery.2nd
edition
references
bacterial infections and their oral manifestations
bacterial infections and their oral manifestations

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bacterial infections and their oral manifestations

  • 3. *1. Introduction *2.bacterial morphology *3.bacterial infections *A) scarlet fever *B)diptheria *C)actinomycosis *D) tetanus *E) gonorrhoea * F)syphilis *G)leprosy *H)anug *I)noma * 4.references CONTENTS
  • 11. Highly contagious systemic infection. Beta hemolytic streptococci, streptococcus pyogenes Rash – exotoxin A, B, C and scarlet fever toxin.
  • 12. * Clinical features Severe pharyngitis Tonsillitis enlarged and tender regional cervical lymph nodes Headache vomiting Abdominal pain Pastia lines Fever Chills Scarlet rash Pharyngitis tonsillitis
  • 13. Oral manifestations Forchheimer spots White coating Edematous & hyperemic fungiform papillae Strawberry tongue Deep red, glistening and smooth Raspberry tongue FORCHHEIMER SPOTS
  • 15. Local or generalised bacterial dissemination Hypersensitivity reactions to bacterial toxins Peritonsillar abscess Rhinitis Sinusitis Otitis media Meningitis Rheumatic fever Arthritis complications
  • 16. * clear hemolysis on colonies around blood agar plates Diagnosis & TREATMENT Marked leukocytosis Increased neutrophillia C reactive proteins Elevated ESR CULTURE
  • 20. Bull neck Diptheric membrane Sore throat Cutaneous diptheria
  • 23. *Diptheria antitoxin *Antibiotics : *Penicillin *Erthromycin *Maintain the airway *Prevention : *Prophylactic active immunization with diptheria toxoid Treatment and prevention
  • 25. Gram positive  Non acid fast  Branched filamentous  Actinomyces israelii  A. naeslundii  A. viscosus  A. odontolyticus  A. bovis : lumpy jaw (cattle) A. meyeri, A. gerencseriae, and Propionibacterium propionicum Actinobacillus actinomycetemcomitans, Eikenella corrodens, Enterobacteriaceae Fusobacterium, Bacteroides, Classification: Cervicofacial Abdominal Pulmonary forms Organism may be cultured from: • Carious tooth • Non vital root canals • Tonsillar crypts • Dental plaque • Gingival sulcus • Pdl pockets POLYMICROBIAL
  • 26. Disruption of mucosal barrier Acute inflammation • Chronic indolent phase Single/multi ple indurations • Central fluctuance • Pus containing neutrophils Sulphur granules IUCDS • HIV • CHEMO • HERPES pathogenesis
  • 27. CLINICAL FEATURES Cervicofacial actinomycosis Overlying skin purplish red,indurated & fluctuant Soft tissue infection Involve maxilla or mandible Actinomycotic osteomyelitis Maxilla invaded Cranium, meninges & brain
  • 29. treatment o Draining the abscess o Excising sinus tract with high doses of antibiotics to accelerate healing o Penicillin o Tetracycline o Erythromycin
  • 31.  Acute infection of nervous system  Intense activity of motor neurons  Severe muscle spasms  Gram positive bacillus  Clostridium tetani  Acts at synapse of interneurons of inhibitary pathways & motor neurons to produce blockade of spinal inhibition
  • 35. *General measures: *Remove spores at site of wound *Cardiopulmovary monitoring *Sedation,airway & nutrition to be maintained *Penicillin 10-12million units IV for 10days *Metronidazole 1gm every 12hrs *Antitoxin injected to neutralise circulating toxin & unbound toxin with wound. *Prophylaxis : wound debridement & TT booster doses *Unimmunized individuals : anti tetanus serum(ATS) 1500units or TIG 250units. treatment
  • 37. o Veneral disease o Male & female genitourinary Tract o Neisseria gonorrhoeae o Gram negative o Nonmotile, nonspore forming o Grows in pairsage : 15-29yrs oIncubation pd : 1-5 days o Oropharyngeal gonorrhoea in 20% women Clinical features
  • 38. orogenital contact lips: acute painful ulceration gingiva: erythematous tongue: red, dry ulcerations, smooth pharyngitis, tonsillitis fever, lymphadenopathy gonococcal parotitis Oral manifestations
  • 39. * *Epididymitis *Salpingitis *Pelvic inflammatory disease *Dermatitis *Arthritis *Risk for chlamydia * trachomatis Infection antibiotics complications Diagnosis & treatment Thayer martin medium
  • 41. Treponema pallidium Episodes of active disease interrupted by Period of latency Gram positive, motile Microaerophillic Darkfield microscope Route of transmission: Sexual contact Mother to child in utero
  • 42. ACQUIRED SYPHILLIS PRIMARY STAGE Chancre : at site of innoculation 3-90 days after infection Solitary m/c site males: penis females: cervix or vulva 95% occur in genitalia Extragenital syphillis : increase in altered sexual activity & contact among Infected homosexuals.
  • 43. Oral manifestations  Elevated, ulcerated nodule.  Local induration.  Regional lymphadenitis.  Brown, crusted appearance Heals in 3weeks to 2 months chancre TONGUE TONGUE LIPS
  • 44. SECONDARY STAGE  Skin: macules or papules, painless  Oral lesions: MUCOUS PATCHES, multiple, painless  Gray white plaques overlying ulcerated surface.  Tongue, gingiva, buccal mucosa  HIGHLY INFECTIOUS ,contain vast number of micro-organisms  Serologic reaction is always +ve  Explosive, widespread form : LUES MAILGNA MUCOUS PATCHES Leão JC, Gueiros LA, Porter SR. Oral manifestations of syphilis. Clinics (Sao Paulo). 2006 Apr;61(2):161-6. Epub 2006 Apr 25.
  • 45. *Late syphilis *Do not appear for years *CVS & CNS *Noninfectious *Gumma: result of hypersensitivity *Focal, granulomatous inflammatory *Process with central necrosis *i/o gumma : tongue & palate *Firm nodular mass in tissue *May ulcerate to deep painless ulcer *Palate: perforation by sloughing *Herxheimer reaction TERTIARY SYPHILIS
  • 46. Atrophic or interstitial glossitis is most characteristic & important lesion of syphilis & is due to endarteritis obliterans SYPHILITIC GLOSSITIS  Tongue surface gets broken up by fissures.  Atrophy & fibrosis of tongue musculature.  Hyperkeratosis  May undergo carcinomatous transformation
  • 47. Transmitted to offspring by Mother Frontal bossae Short maxilla High palatal arch Saddle nose Mulberry molars Higoumenakis sign Relative protuberance of mandible Rhagades Saber shin CONGENITAL SYPHILIS RHAGADES FRONTAL BOSSAE INTERSTITIAL KERATITIS HIGOUMENAKIS SIGNSADDLE NOSE SABER SHIN
  • 48. Diagnosis & treatment  Penicillin: DOC  Surgical correction of facial defects gives good esthetic
  • 50. *Hansens disease *Mycobacterium leprae *Incubsation pd: 5yrs *Affects skin, peripheral nreves, *Upper resp tract, eyes, & testes *Bones, muscles & joints *ONLY BACTERIA TO INFECT *PERIPHERAL NERVES *Dopa oxidase activity *Acid fastness *Living leprosy bacilli: *Solid staining pink rod *Nonliving : granular *Can be grown in mouse footpad *& nine banded armadillo PATHOGENESIS
  • 51. Clinical features  Hypopigmented patches  Total loss of cutaneous sensation  light touch to be affected first  Thickening of nerves  Presence of acid fast bacilli in skin or nasal smear GENERAL FEATURES  Single/ multiple macular erythematous eruptions  Dermal & peripheral nerve trunk involvement  Loss of sensation  Loss of sweating of affected skin Tuberculoid Leprosy  Early erythematous macules or papules  Thickening of skin  Characteristic nodules  Severe disfigurement Lepromatous Leprosy
  • 54. Oral manifestations LEPROMAS 1 Hardpalate>soft palate>labial max gingiva>tongue>lips>buccal max gingiva>labial mand gingiva>buccal mucosa
  • 56. Pallagatti S, Sheikh S, Kaur A, Aggarwal A, Singh R. Oral cavity and leprosy. Indian Dermatology Online Journal. 2012;3(2):101-104..
  • 58. DIAGNOSIS & TREATMENT  Based on clinical & bacteriological examination  Organism grown in footpads of mice & armadillos  Nasal smears & scrapings stained with modified ziehl nielsen method  Lepra bacilli >1011 gm of tissue  Skin biopsy  Nerve biopsy  Foot culture histamine test Test for humoral response: Monoclonal antibodies ELISA, PCR MDT( MULTI DRUG THERAPY) Rifampicin tuberculoid Dapsone Clofazimine lepromatous
  • 60. PAIN INTERDEN TAL ULCERATI ON ANUG GINGIVAL BLEEDING  Involves free gingival margin, crest of gingiva, interdental papillae  May spread to soft palate & tonsillar areas : vincents angina  Necrotizing ulcerative periodontitis  Associated with HIV  Common in young & adults etiology • Fusiform bacillus & borrelia vincentii • Vibrio & coccal forms • Acc to mc donald , Bacteroides melaninogenicus : main causative agent • Stress , immunosupression ,smoking • Upper resp tract infection , local trauma • Poor nutritional status , poor oral Predisposingfactors
  • 61. *Loesche WJ, Syed SA, Laughon BE, Stoll J. The bacteriology of acute necrotizing ulcerative gingivitis. J Periodontol. 1982 Apr;53(4):223- 30. *Treponema and Selenomonas sp., 32 and 6%, respectively, of the microscopic count; *B. melaninogenicus ssp. intermedius and Fusobacterium sp., which averaged 24 and 3%, respectively, of the viable count. *Plaque samples from 22 ulcerated sites in 8 patients with ANUG. *
  • 62. Clinical features  Painful, hyperemic gingiva, sharply punched out crater like erosions of interdental paillae  Grayish green necrotic pseudomembrane  Fetid odour  Inability to eat Gingival bleeding Incubation zone
  • 63. Diagnosis based on clinical finding : gingival pain, ulceration & bleeding Bacterial smear from gingiva Fusiform bacillus: elongated rod with Tapered ends 5-14microns in length 0.5-1.0microns diameter. Weakly gram+ve Borrellia vincentii: gram-ve 10-15microns length Diagnosis A- spirochete; B- bacillus fusiformis; C- filamentous organism; D- streptococcus; E- vibrio; F- treponema microdentinum
  • 64. treatmentFIRST VISIT:  Medical history, diet background,smoking, rest , risk factors for HIV, stress  Examination of general appearance, halitosis, fever  Topical anesthetic6, area swabbed with moist cotton  Pseudomembrane & non attached debris removed  Superficial calculus removed by ultrasonic scaling  Antibiotics: Amox 500mg 6hrs for 10days Metronidazole 500mg twice daily for 7days  Tooth xtraction or pdl surgery Postponed until 4weeks  Rinse with equal amount of 3% h2o2 & warm water every 2hrs or twice daily with CHX  Adequate rest  Ultrasoft brush  NSAID for pain relief  SECOND VISIT  1,2 days after 1st visit  Diminished pain  Gingival margins erythematous but without  Pseudomembrane  Scaling if needed THIRD VISIT  5 DAYS after  Resolution of symptoms  Plaque control procedures  Counselling on nutrition, smoking cessation  CHX rinses for 2-4 weeks Reevaluation after 1 month  Gingival contouring : gingivoplasty  Nutritional supplements
  • 66. small ulcer of gingiva spreads involve surrounding tissues of jaw,lip & cheeks by gangrenous necrosis.  rapidly spreading  Gangrenous stomatitis  m/c in children  seen in persons who are undernourished or debilated from infection diptheria,dysentry,tb,syphilli s,anemia…  Secondary complication of systemic disease rather than a primary disease.  Specific infection by vincents organisms, ANUG…soon complicated by secondary invasion of streptococci, staphylococci & Clinical features
  • 67. Area of stagnation Around fixed bridge or crown Overlying skin inflammed,edem atous & necrotic Large mass of tissue slough out. Blackening of skin. Subcutaneous fat undergoes necrosis. Foul odour High temperature,sec ondary infection, death from toxemia
  • 71. * *1.bacterial infections *A) pericoronitis *B) pyogenic granuloma *C) angular chelitis *D) cellulitis *E) ludwigs angina * F)sarcoidosis *G)tuberculosis *H)osteomyelitis * * 2.references CONTENTS
  • 73. * : inflammatory lesion occuring around the impacted or partially erupted tooth. Mixed infection(anaerobes) *Mand 3rd molar *Pain & swelling *Difficulty in opening & chewing Mildly ill, fever & regional lymphadenopathy Sixou JL, Magaud C, Jolivet-Gougeon A, Cormier M, Bonnaure-Mallet M. Microbiology of mandibular third molar pericoronitis: incidence of beta-lactamase-producing bacteria. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2003 Jun;95(6):655-9 PERICORONITIS Clinicalfeatures alpha-hemolytic streptococci (26/26) Prevotella (15/26), Veillonella (15/26), Bacteroides (9/26), and Capnocytophaga (9/26)
  • 74. *Gently flushing area with warm water *Entrapped food debris must be removed *Swabbing with antiseptic after elevating flap Gently from tooth with a scaler *Upper tooth when involved should be ground or extracted *Radiograph help in assessing position of tooth *Surgical removal after acute symptoms subside *Antibiotics to relieve symptoms & to prevent spread of infection. treatment
  • 76. *Originate as a response of tissue *To a nonspecific infection. *Tumor like growth : exaggerated *Conditioned response to minor * trauma  Infection staphylococci or streptococci  Arise as a result of minor trauma to tissues  Pathway for invasion of nonspecific type of micro-organism.  Surface of pyogenic granuloma in cases of ulceration abounds with typical colonies of saprophytic organisms.  Sulfhydryl radical etiology
  • 78. histology TREATMENT  Surgical excision  Laser  Recurrence : not encapsulated  Excising gingiva lesion, care to be taken  To scale adjacent tooth  Calculus irritant for recurrence  Recurrence rate – 15% Endothelium lined vascular spaces & extreme proliferation Of fibroblasts & budding endothelial cells.
  • 80. *Multifactorial disease affecting commissure of lips *m/c in denture wearers *Associated with infection *Reduced vertical dimension of mouth *60% : candida albicans & staphylococcus *20%: staphylococcus *20%: candida albicans *Nutritional deficiencies: fe, vit B, folic acid *Ariboflavinosis: circumoral lesions *Seen in diabetes, neutropenia, AIDS
  • 81. *Occur in both young children & adults *Dryness, burning sensation at corners *Wrinkled skin at commissure *Deep fissures & cracks *Fissures stop at mucocutaneous junction Clinical features
  • 82. Depending on the specific cause, the following treatments may be useful: *Lip balm or thick emollient ointment, applied frequently. *Topical antiseptics. *Topical or oral antistaphylococcal antibiotic. *Topical antifungal cream. *Oral antifungal medication *.ketoconazole tab 200-400mg twice daily with food for 2weeks * Fluconazole cap 50-100mg once daily for 2-3weeks *Nutritional supplements. treatment
  • 84. *: *Cellulitis is a diffuse inflammation of soft tissues which is not circumscribed or confined to one area, but which, in contrary to the abscess, tends to spread through tissue spaces and along fascial planes. *Common causative agent : streptococci viridans *Produce : streptokinase, hyaluronidase, fibrinolysins *Prevotella & porphyromonas : destroy collagen *As result of apical abscess, osteomyelitis, following pdl infection *Pericoronitis *Injection with infected needle CELLULITIS
  • 86. *Moderately ill *Elevated temperature *Leukocytosis *Firm & brawny, painful swelling of soft tissues *Inflammatory edema *Inflammed , orange peel appearance *Regional lymphadenitis *Infections in maxilla perforate outer cortical layer Of bone above buccinator attachment : swelling of upper half of face *Eye: cavernous sinus thrombosis *Infection in mandible perforate outer cortical plate below buccinator : *diffuse swelling of lower half of face *Spread to cervical tissue : respiratory discomfort Clinical features
  • 87. histology  Diffusion exudation of Polymorphonuclear Leukocytes, lymphocytes  Separation of connective tissue or muscle fibers treatment  Treatment for cellulitis depends on what caused the infection, the severity of symptoms and the general state of health.  Hospital treatment may be necessary if symptoms such as fever, nausea and vomiting suggesting infection has spread from skin to bloodstream or other parts of the body.  Antibiotics: flucloxacillin, 25mg/kg(max 500mg) 6hr for 7days Flucloxacillin 50mg/kg iv 6hr Ceftriaxone 50mg/kg/dose iv 12 hr  Drink plenty of fluids to avoid dehydration.  NSAIDS : pain control
  • 89. * *Ludwig's angina, otherwise known as angina ludovici, is a serious, potentially life-threatening cellulitis, or connective tissue infection, of the floor of the mouth, usually occurring in adults with concomitant dental infections and if left untreated, may obstruct the airways, necessitating tracheotomy.  Acute, toxic begin in submandibular space * secondarily involve sublingual & submental spaces spaces. * dental origin * mandibular molar : chief source of infection * other causes : LUDWIG’S ANGINA
  • 90. 2nd & 3rd molars: m/c Unusual speech(hot potato in mouth) Bilateral sublingual space infection Bilateral submandibular space infection Brawny edema Elevated tongue Airway obstruction Paucity of pus CLINICALFEATURES HALLMARK SIGNS 3’F’ : FEARED FATAL(often) FLUCTUANT(rarely)
  • 92.  Mixed infection  Beta hemolytic Streptococci  Peptostreptococcus  Streptococcus viridans(40.9%)  Staphylococcus aureus (27.3%), staph epidermis (22.7%)  Pseudomonas, klbsiella, e.coli  Clostridium, enterococcus fecalis  Fusiform bacilli & spiral forms LAB FINDINGS : TREATMENT *Early recognition of incipient cases *Maintenance of airway *Intense & prolonged antibiotic therapy *Extraction of affected tooth *Surgical drainage *Edema of glottis necessitates emergency tracheostomy to prevent suffocation. *Complications may include: *Airway blockage *Generalized infection (sepsis) *Septic shock
  • 94. * ETIOLOGY: *microbial overgrowth in association with a reduction in salivary flow *subsequent to dehydration and debilitation *trauma to the duct system and hematogenous spread of infection from other areas. *The most commonly isolated organisms in parotitis : penicillin-resistant Staphylococcus aureus, Streptococcus viridans, and Streptococcus pneumoniae * presence of a painful swelling, *low-grade fever *malaise headache *gland is extremely tender Trismus *purulence at the duct orifice may be produced by gentle pressure on the involved gland or duct. * If infection is not eliminated early, suppuration may extend beyond the limiting capsule of the parotid gland. *Extension into surrounding tissues along fascial planes in the neck or extension posteriorly into the external auditory canal may follow. CLINICAL FEATURES
  • 96. *Laboratory studies : *elevated erythrocyte sedimentation rale(ESR) *leukocytosis, often with a characteristic shift to the left, indicating acute infection. * elimination of the causative organism *rehydration of the patient *drainage of purulence, if present. *Culture and sensitivity testing of the exudate at the orifice of the duct is the first step in antibiotic management. *After a culture is obtained, patients empirically be placed on regimen of a penicillinase-resistant antibiotic such as semisynthetic penicillin. Along with rehydration and attempts at establishing and encouraging salivary flow, moist compresses, analgesics, and rest are in order. *Medications containing parasympathomimetic agents, which reduce salivary flow, should be reduced or eliminated. Treatment & prognosis
  • 97. *A biopsy and retrograde sialography should be avoided. * may cause sinus tract formation, may allow infection to proceed beyond the boundaries of the gland into surrounding" soft tissues. * With prompt and effective treatment, recurrence is generally avoided. * recurrent parotitis, considerable destructive glandular changes can be seen. * juvenile, variant, of parotitis, intermittent unilateral or bilateral painful swelling is accompanied by fever and malaise. *initial attack : ages 2 and 6 years, * neonatal form of suppurative parotitis may develop, with S. aureus being the most common causative pathogen. * Gross destruction of the parenchymal and ductal elements may be noted on sialographic examination. *Absence of secretory acinar components and a damaged ductal system with numerous punctate globular spaces. *Spontaneous regeneration of parotid salivary tissue.
  • 99. *Sarcoidosis a multisystem granulomatous disease of unknown origin characterized by the formation of uniform ,discrete, compact, non-caseating epithelioid granulomas. I *blacks >>whites. * infectious etiology : Mycobacterium and Propionibacterium * young adults *lesions most common in the lungs, skin, lymph nodes, salivary glands, spleen, bones,& the mouth. *characterized by depression of delayed-type hypersensitivity suggesting an impaired cell-mediated immunity, and raised or abnormal serum immunoglobulins suggesting lymphoproliferation *interferon gamma (IFN-J) and cytokines such as TNF-D, IL-12 and IL-18 play an important role in the formation of granulomatous lesions
  • 102. ERYTHEMA NODOSUM: multiple raised red patches,in groups, occur slowly LUPUS PERNIO FOREHEAD
  • 103. Oral manifestations Small papular nodular plaques, resemble herpetic lesions or fever blisters Bleblike, containing clear yellowish fluid, or as solid nodules LIPS HARD PALATE BUCCAL MUCOSA
  • 104. Intracutaneous test: kveim siltzbach test A lip biopsy may occasionally provide evidence of sarcoid involvement of minor salivary glands in support of a clinical impression of pulmonary disease. * Lab assay for angiotensin I—converting enzyme * Elevation of this enzyme in conjunction with a positive chest radiograph has a high diagnostic reliability * Spontaneous resolution * Corticosteroids: doc for symptomating pulmonary sarcoidosis * Chloroquine anti TNF agents * Immunosuppresive drugs to those not responding to steroids * Levamisole for arthritic symptoms * Good prognosis diagnosis TREATMENT
  • 105. HISTOLOGY Nests of epitheloid cells with multinucleated giant cells Non caesating Solid, amorphous,eosinophillic, hyaline mass
  • 106. *a form of sarcoidosis in which characteristically there is firm, painless, usually bilateral enlargement of the parotid glands, accompanied by inflammation of the uveal tracts of the eye and cranial nerve involvement. *The submandibular and sublingual glands may be involved * chronic, low-grade fever lassitude, malaise and vague gastrointestinal disturbances nausea, and vomiting. *Xerostomia is common. * patchy erythema of the skin *Enlargement of the cervical lymph nodes earliest symptom : uveitis * *most common nerve involvement is unilateral or bilateral seventh nerve paralysis,in one-third to one-half of all cases UVEOPAROTID FEVER (HEERFORDT SYNDROME)
  • 108. *Tuberculosis (TB) is a specific infectious granulomatous disease caused by Mycobacterium tuberculosis *M. tuberculosis is a rod-shaped, nonspore forming, and thin aerobic bacteria called acid-fast bacilli, *once stained, it cannot be decolorized by acid alcohol. *Its acid-fastness is due to the high content of mycolic acids, long chain cross-linked fatty acids and other cell wall lipids. *Males are more affected than females in India though it affects all ages, from an average of 1% in the under-five age group. M. tuberculosis is a facultative intracellular atypical or opportunistic mycobacteria: pulmonary or generalized infection in immunocompromised individuals etiology
  • 109. *M. tuberculosis is most commonly transmitted from a person with infectious pulmonary TB by droplet nuclei, which are aerosolized by coughing, sneezing, or speaking. The tiny droplets dry rapidly; the smallest (<5–10 μm in diameter) may remain suspended in the air for several hours and may reach the terminal air passages when inhaled. There may be as many as 3000 infectious nuclei per cough
  • 112. Exposure to TB No infection(70-90%) Infection (10-30%) Latent TB (90%) well Never develop TB Not infectious Active TB (10%) ill  5% develop TB within 2 yr  5% develop TB many yrs later untreated treated  50% die within 5 years  25% remain sick  25% recover cured
  • 121. *Demonstration of organism by microbial stains *Culture of sputum or infected tissue : lj medium middle brook media *Presence of acid fast bacilli in sputum : gold standard *Radiograph *Tuberculin test *CT scan: mediastinal or hilar lymphadenopathy *MRI : extrapulmonary TB *Ziehl Nielsen stain, Kinyouns stain , rhodamine staining for fluorescent microsopy *Minimum of 5 acidfast bacilli on fluorescent microscopy positive *3 on ZN staining *Rapid slide culture technique *Radiometric culture method *Radioimmunoassay *ELISA *PCR DIAGNOSIS
  • 126. *Global TB statistics *In 2014 1.5 million people died of TB. Of these people 0.4 million people were HIV positive. *TB now annually causes more deaths worldwide than HIV. *In 2014 1.2 million people died of HIV and this includes the 0.4 million TB deaths among HIV positive people. People who have both TB and HIV when they die, are internationally classified as having died from HIV. *There were an estimated 9.6 million new cases of TB in 2014.There were an estimated 3.2 million cases and 480,000 TB deaths among women. *There were also an estimated 1.0 million cases of TB in children and 140,000 deaths.
  • 130. * The World Health Organisation (WHO) current estimates in 2015 are that 1 million children currently suffer from TB worldwide (<15 years), and that more than 136,000 die each year. * 70-80% of children with TB have the disease in their lungs (pulmonary TB). The rest are affected by TB disease in other parts of their body (extra pulmonary TB) – * Some children are at greater risk of getting TB than others and these include: A child that lives in the same household as a person who has been recently diagnosed with smear positive TB * A child less than 5 years old * A child with HIV infection * A child with severe malnutrition * in children with pulmonary TB the commonest chronic symptoms are a chronic cough that has been present for more than 21 days, a fever, and weight loss or failure to thrive. TB & CHILDREN
  • 131. *The 2010 WHO TB drug dosage guidance for children *The major recommendations of the WHO drug dosage guidance for children were that: *1) The dosages of the following four TB drugs should be: • Isoniazid(H) 10mg/kg (range 10-15 mg/kg); maximum dose 300 mg/day • Rifampicin(R) 15mg/kg (range 10-20 mg/kg); maximum dose 600 mg/day • Pyrazinamide(Z) 35mg/kg (30-40) mg/kg) • Ethambutol(E) 20mg/kg (15-25 mg/kg) *As children approach a body weight of 25kg, adult dosages can be used.
  • 134. *Osteomyelitis is defined as the inflammation of bone and its marrow contents. * trauma and road traffic accidents; *gunshot wounds, radiation damage, Paget’s disease, and osteopetrosis. *Systemic conditions like malnutrition, acute leukemia, uncontrolled diabetes mellitus, sickle cell anemia, and chronic alcoholism. CLASSIFICATION SUPPURATIVE NONSUPPURATIVE ACUTE CHRONIC CHRONIC SCLEROSI NG FOCAL DIFFUSEGARRE PREDISPOSING FACTORS:
  • 135. *Mixed aerobic-anaerobic infection. *Streptococci *Alpha hemolytic streptococci *Anaerobic streptococci *Fusobacterium *Bacterioids *Peptostreptococcus *Others in special forms: *Mycobacterium tuberculosis *Treponema pallidium *actinomyces
  • 136. * *serious sequela of periapical infection that often results in a diffuse spread of infection throughout the medullary spaces, with subsequent necrosis of a variable amount of bone. *MAXILLA : well localised MANDIBLE : diffuse & widespread * neonatal maxillitis in infants and young children *severe pain, trismus, and paresthesia of the lips : mandibular involvement *elevation of temperature regional lymphadenopathy. *WBC elevated. teeth loose and sore eating is difficult, Pus may exude from the gingival margin. Until periostitis develops, there is no swelling or reddening of the skin or mucosa. ACUTE SUPPURATIVEOSTEOMYELITIS CLINICAL FEATURES
  • 138. Chronic osteomyelitis Most infectious (bacterial) Varaiable pain, swelling, drainage Radiolucent or mottled pattern Appropriate antibiotic, sequestromy Chronic osteomyelitis with proliferative periostitis Sequelae of tooth abscess, extraction Usually associated with lower molar,perioste um involved children Radiolucent or mottled with concentric periosteal opacities Tooth removal, antibiotics Diffuse sclerosing osteomyelitis Probably low grade infection, pulpitis,period ontal disease Ocassional pain, swelling, drainage mandible Opacification throughout jaw Antibiotics, find cause & treat if possible Focal sclerosing osteitis Low grade focal bone irritation Asymptomatic, Found on routine examination Opaque mass usually at root apex Treat offending tooth Etiology Clinical features Radiographs Treatment
  • 139. * a reaction to mild bacterial infection entering the bone through a carious tooth in persons who have a high degree of tissue resistance and tissue reactivity.  the tissues react to the infection by proliferation rather than destruction, since infection acts as a stimulus rather than an irritant. . MOST COMMON : CHILDREN mandibular first molar with a large carious lesion. Endodontic treatment or extraction mild pain associated with an infected pulp. CONDENSINGOSTEITIS treatment
  • 140. Medical management: 1.Systemic antibiotics- penicillin(empirical) 2-4 months Metronidazle Clindamycin Cephalosporins Vancomycin 2.Local application of antibiotics PMMA beads- antibiotic impregnated beads Surgical management: Removal of necrotic foci a) sequestrectomy- dead necrotic bone(avascular, antibiotics donot penetrate) b) Saucerisation c) Decortication- lateral & inferior cortical bone is removed d) Ressection & reconstruction MANAGEMENT HBO THERAPY
  • 142. *1) Harrison’s principles of internal medicine.19th edition *2)Scott C Kachlany. Deadly diseases and epidemics. Infectious diseases of the mouth.2007 *3) Shafer.Hine.Levy. Textbook of OralPathology.7th edition *4)Greenberg. Glick. Ship. Burket’s OralMedicine.11th edition *5) Regezi.Sciubba.Jordan. OralPathologyClinical pathological correlations.4th edition 6)Philip D Marsh. Michael V Martin. Oral Microbiology.5th edition *7)Michael Miloro. Peterson’s Principles of Oral And Maxillofacial Surgery.2nd edition references