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BACTERIAL INFECTIONS OF THE ORAL CAVITY

WHAT IS BACTERIA ?
Bacteria is a microscopic unicellular M.O.  spherical, rod shaped or spiral shaped. They are 0.5-5um 0.5 bacteriology  infectious diseases  Anton van leeuvenhoek in 1674  Single celled prokaryote


COLLECTION OF CLINICAL SPECIMENS

For bacteriological cultures, always use swabs with transport medium (gel or wet sponge) to prevent drying of the specimen and to preserve the bacteria

Swab with transport medium

DRY SWABS
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If anaerobic bacteria are suspected to be involved in an infectious process, prefer fine needle aspiration or tissue biopsy since most ordinary swabs are not valid transport media for these pathogens

CONTENTS
      

Impetigo Diphtheria Tuberculosis Leprosy Actinomycosis Tatanus Erysipelas

     

Syphilis Scarlet fever Gonorrhea Noma Pyogenic granuloma Sinusitis

Bacterial sinusitis
 

Bacterial sinusitis is an inflammation of the paranasal sinus mucosa. caused by bacterial overgrowth in a closed cavity. The maxillary, frontal, ethmoid, and sphenoid sinuses all drain into the nasal cavity through the ostia,which are approximately 1 to 3 mm in diameter. Obstruction of this narrow space may set up an environment for bacterial pathogens to colonize.

FACTORS PREDISPOSING TO SINUSITIS


                   

Prior upper respiratory tract infection Concurrent group A streptococcal infection Allergic rhinitis Environmental pollutants (smoke) Dental infections or extractions Hormonal changes Iatrogenic factors (mechanical ventilation, nasogastric tubes, nasal packing, dental procedures) Anatomic variations (tonsillar and adenoid hypertrophy, deviated septum, nasal polyps, cleft palate Swimming Immunodeficiency Secretory disturbances (cystic fibrosis) Immotile cilia syndrome Abnormal mucociliary clearance secondary to ciliary structural abnormalities (Kartageners syndrome) Bronchiectasis Asthma or acetylsalicylic acidasthmapolyposis triad Immature immune system Adenoidal hypertrophy

DIAGNOSTIC FACTORS PREDICTIVE OF SINUSITIS


              

Major factors Facial pain or pressure Facial congestion or fullness Nasal obstruction Nasal purulence or discolored postnasal discharge Hyposmia or anosmia Fever (acute sinusitis only) Minor factors Headache Halitosis Fatigue Dental pain Cough Ear pain, pressure, or fullness Fever (nonacute sinusitis)

PATHOGENS IN SINUSITIS
Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis.  Streptococcus pyogenes, Staphylococcus aureus, Neisseria species.  Fungi


Patient history
      

Cold present for more than 7 to 10 days. Unusually severe upper respiratory tract infection. Fever. Mucopurulent discharge (>7 days). Pain in upper teeth. Lack of response to decongestants. Dull headache.

Clinical assesment
Unilateral or bilateral tenderness in midface region.  Inspection of nasal mucosa.  Facial tenderness.  Intranasal pus.  Purulent postnasal mucus in pharynx.  Transillumination.


Diagnostic tests
          

Radiographs (Waters view) Sinus aspiration, Computed tomography Anterior rhinoscopy. Ultrasound. Magnetic resonance. Fiberoptic nasal endoscopy. Nasal mucus smear. Immunologic screen. Cultures from sinus puncture. Erythrocyte sedimentation rate.

Medical Management
           

First line Amoxicillin (Amoxil, Trimox, Wymox) 250-500 mg tid TMP-SMX (Bactrim, Septra) 160 mg/800 mg bid Second line -Lactams Cefpodoxime proxetil (Vantin) 200-400 mg bid Cefprozil (Cefzil) 250-500 mg bid Cefuroxime axetil (Ceftin) 250-500 mg bid Cefdinir (Omnicef) 300 mg bid Amoxicillin-clavulanate (Augmentin) 250-500 mg tid Third line Macrolide Azithromycin (Zithromax) 250 mg qd Clarithromycin (Biaxin) 500 mg bid

ADJUNCTIVE TREATMENTS
 

Adjunctive treatments are designed to promote ciliary function and decrease edema. nasal sprays, humidifiers, warm aerosols, steam, aromatic vapors, hot soups, and tea moisturize the nasal cavity and remove thick mucus crusts. Topical decongestants (eg, phenylephrine hydrochloride, oxymetazoline hydrochloride) relieve nasal congestion by stimulating mucosal -adrenergic receptors, thereby shrinking the edematous mucosa and relieving obstruction.

IMPETIGO


Its a superficial infection of the skin.  Causative M.O_ Streptococcus pyogens.  _ Staphlococcus aureus.  Disease arises in areas of dermatitis or previous trauma , such as cuts, abrasion or insect bites.

CLINICAL FEATURES
Commonly occurs on the skin of the face or the extremities.  2 clinical pattern seen.

 May

produce fragile vesicles that quickly rupture & are replaced by thick adherent amber crusts.  In long standing cases flacid bullous lesions develop.

IMPETIGO

CONTD CONTD
After bullae rupture , thin , light brown (honey colored) crusts develop.  Pruritis & regional lymphadenopathy may be seen.


DIAGNOSIS


It is made on clinical presentation.  Definitive diagnosis requires isolation of S.pyogens & S.aureus from culture.

TREATMENT & PROGNOSIS


Topical application of Mupirocin is effective.  For bullous type Topical antibiotics & / or systemic oral antibiotics (1 week).  The antibiotics are clindamycin , cephalexin.  Treatment with topical corticosteroids may produce resolution of the surface crusts , but infectious red raw lesions remains.


ERYSIPELAS (SAINT ANTONYS FIRE)




It is a superficial skin infection most commonly associated with Beta-hemolytic Betastreptococci Gr-(A & G) Gr Loss of integrity of the skin facilitates entry of M.O

CAUSATIVE M.O


Beta hemolytic streptococci.  S. aureus.  Pneumococcus.  Klebsiella pneumoniae.  Yersina enterocolitica.  Haemophillus influenzae.

CLINICAL FEATURES
Mainly affect young & elderly patients. some time seen in debilitated or diabetic patients.  Infection rapidly spreads through lymphatic channels which become filled with fibrin , leucocytes & streptococci.  Can be seen any where especially in areas of previous trauma.


CONTD. CONTD.
   

Increased prevalence is noted in winter & spring months. On face it is seen on cheeks , eyelids & bridge of the nose producing a butterfly shaped lesion. Occular involvement causes edematous & shut eye. Affected area is painful bright red, well circumscribed swollen indurated & warm to touch.

TREATMENT & PROGNOSIS




Diagnosis mainly done on clinical experience.  Penicillin or erythromycin.  In initiation therapy the area of skin often enlarges probably secondary to the release of toxins from the dying streptococi.  Rapid resolution is noted with in 48 hrs.

COMPLICATIONS


Abscess formation  Gangrene  Necrotizing fascitis  Toxic-shock synd. Toxic Thrombophlebitis.  Acute glomerulo nephritis.  Septicemia.  Endocarditis & death..  In recurrent case prophylaxis with oral penicillin has been used.

SCARLET FEVER


Highly contagious systemic infection.  Causative M.O is beta hemolytic streptococci , st. pyogenes.

MECHANISM OF ACTION


Disease begins as streptococcal tonsilitis with pharyngitis in which m.o elaborate an erythrogenic toxin that attacks the blood vessels & produces the characteristic skin rash.  S.pyogens which produce a pyogenic exotoxins are A,B,C (SCARLET FEVER TOXIN).

CLINICAL FEATURES
Common in children.(3-12 yrs). children.(3 Incubation period_(1-7 days). period_(1 Severe pharyngitis & tonsilitis.  Headache.  Fever &Chills.  Vomiting.  Tenderness & enlargement of regional lymphnode. Mainly cervical.


CONTD


This disease is characterized by diffuse bright scarlet skin rash appears on the 2nd & 3rd day of illness.  Rash is prominent in the area of skin folds,( PASTIAS LINE) is a result of the toxic injury to the vascular endothelium which produces dilatation of the small blood vessels & consequent hyperemia.

CONTD


Small papules of normal color erupt through these rashes giving a characteristic SAND PAPER feel of the skin.  Rash subsides after 6-7 days followed by 6desquamation of palms & soles.

ORAL MENIFESTATIONS
STOMATITIS SCARLATINASCARLATINAcharacterized by congested petechiae scattered mucosa especially soft palate & throat.  It shows a fiery red color. tonsil & faucial pillars are swollen & covered with grayish exudate.


STOMATITIS SCARLATINA

CONTD.


 

During 1st 2 days , the dorsal surface of the tongue demonstrates a white coating through which only the fungiform papillae can be seen which is called as WHITE STRAWBERRY TONGUE. It is seen at the tip & lateral margins. On 4th-5th days red strawberry tongue develops when white coating desquamates to reveal an erythematous dorsal surface with hyperplastic fungiform papillae.

Strawberry tongue

RASPBERRY TONGUE

COMPLICATIONS
    

Peritonsilar abscess Rhinitis Sinusitis Otitis media Rheumatic fever

    

Mastoiditis Meningitis Pneumonia Glomerulo nephritis Arthritis

DIAGNOSIS


Done by culturing the flora of intraoral lesions , pharynx & saliva.  Susceptibility is correlated with the results of DICK TEST

TREATMENT & PROGNOSIS


Antibiotic of choice-oral penicillin, choicedicloxacillin , cephalexin & erythromycin (in case allergic to penicillin)  Local application of mupirocin topical ointment also used.


DIPTHERIA


Its an acute, life threatening, infectious & communicable disease of skin & mucous membrane.  Causative m.o CORNYBACTERIUM DIPTHERIAE.(TOXEMIC STRAINS)  1st described in 1826.  Humans are the sole reservoir.

CORNYBACTERIUM DIPTHERIAE

MECHANISM OF ACTION


The bacterium produces a lethal exotoxin which induces initial edema & hyperemia followed by tissue necrosis there by providing nutrients for further growth & leading to peripheral spread. Coagulation of the fibrin & purulent exudates produce a pseudomembrane & the inflammatory reaction. Pseudomembrane consists of dead cells, leukocytes, erythrocytes & bacterium.

CLINICAL FEATURES
  

Symptoms arise in 1-5days after exposure 1Mainly seen in children & immunosupressive people. It is characterized by local inflammation & the formation of a grayish adherent pseudomembrane, which bleeds on removal. M.O may persist in discharge from the nose, throat, eye & skin lesions for 2-6 weeks after 2infection. Occurs in the winter months in temperature zones & throughout the year in the topical region.

SYMPTOMS


Low grade fever  Headache  Malaise  anorexia

    

Sore throat Vomiting Weakness Dysphagia Changed invoice

Diptheric membrane which is asymmetric & extends to involve the tonsil, soft palate, tongue, lips, gingiva, buccal mucosa & site of erupting teeth.  Submandibular & ant. Cervical nodes are involved.  In severe case it shows BULL NECK APP.


DIPHTHERITIC MEMBRANE

COMPLICATIONS
   

Myocarditis Polyneuritis Acute interstitial nephritis Bleeding

   

Circulatory failure Postdiptheria paralysis Pneumonia Otitis media

DIAGNOSIS


Specimen for culture should be obtained from underneath the diptheric membrane, if possible or from the surface of the membrane.  MEDIA----pai agar & cystine-tellurite agar MEDIA----pai cystine STAINS---Albert stain, ponders stain, STAINS---Albert neissers stain used to demonstrate metachromatic granules.

PREVENTION


Effective antitoxin has been available since 1913.  Can be prevented by prophylactic active immunization with diptheria toxoid.  Once disease has developed, it is treated with antitoxin. (usually in combination with antibiotics).

TREATMENT & PROGNOSIS


Antitoxins & antibiotics used to prevent further toxin production, to stop local infection & to prevent transmission  Erythromycin  Procaine penicillin or I.V penicillin.  After 4days of antibiotic therapy severity will be reduced.


CONTD


Patient is not considered negative until 3 consecutive negative culture specimens are obtained.  Before antitoxin developed mortality rate is 50% due to the cardiac & neurologic complications.  current mortality rate is less than 55%.

SYPHILIS(LUES)


The name was probably derived from a handsome & wealthy shepherd who was affected. Said to be evolved between 15000 & 3000 B.C & transported to Asia by Portuguese sailors led by Vascodagama. Extremely common infection few decades ago & its return is associated with emerging HIV infection.

Causative M.O:- Treponema pallidum M.O: It is a spirochete & is characterized by episodes of active disease interrupted by the period of latency.  Its a gram +ve, motile, microaerophilic spirochete which is pathogenic to humans & may be best demonstrated by dark field microscopy, since it stains poorly except by silver impregnation.


MICROSCOPIC APPEARANCE OF T.P

MODE OF TRANSMISSION


Primary modes are sexual contact or from mother to fetus.  May spread through infected blood transfusion because M.O may survive up to 5 days in refrigerated blood.  Cause of the disease is related to crack cocaine abuse & the barter of illegal drugs for sex.

TYPES


Broadly classified as:as:1. 2.

Acquired & Congenital

 

Initially M:F 3.5:1 Recently M:F 1:1(due to prostitution)

STAGES OF SYPHILIS

ACQUIRED
  

This form is contracted after sexual inter course with an infected partner, persons such as dentists working on infected patients in a contageous stage. It manifests as 3 distinctive stages throughout its course
1. 2. 3.

Primary Secondary Tertiary

PRIMARY SHYPHILIS


  

Characterized by chancre that develops at the site of inoculation, becoming evident 3-90 days 3after the initial exposure. Majority of chancre are solitary, may be single or multiple. Site:Site:- External genitalia & anus is most common. Affected area begins as a papular lesion, which develops a central ulceration.

Oral cavity :- Lip, tongue, palate, gingiva,tonsil :-

Oral lesion appear as a painless, clean based ulceration or rarely as a vascular proliferation resembling a pyogenic granuloma.  Lesion on the lip may have a brownish crusted appearance.  The intra oral chancre is an ulcerated lesion covered by a greyish white membrane which may be painful because of secondary infection.


Bilateral regional lymphadenopathy is seen in most patients.  If it is untreated the initial lesion heals within 3-8 weeks. 3

HISTOLOGY OF CHANCRE


Microscopically it appears as a superficial ulcer showing a rather intense inflammatory infilterate.  Plasma cells are particularly numerous.

ORAL MANIFESTATION OF PRIMARY SYPHILIS

CHANCRE

SECONDARY SYPHILIS
Also called as disseminated type.  Clinically discovered at 4-10 weeks after 4initial infection.  Lesions may be seen before the primary lesion has resolved completely.  The oral lesions called mucous patches are usually multiple painless grayish white plaques overlying an ulcerated surface.


SYMPTOMS
       

Painless lymphadenopathy Sore throat Malaise Fever Headache Weight loss Musculoskeletal pain After second stage patient are free from lesions & symptoms & they enter the latent stage which may last for 1-30 years. 1-

TERTIARY SYPHILIS
 

Also called latent syphilis. It includes the most serious of all complications:complications: 

CVS :- LVH, CHF, aneurysm of the ascending aorta. :CNS :- Tabes dorsalis, psychosis, dementia, paresis :& death.

 

Active site of granulomatous inflammation affecting skin, mucosa is called as GUMMA. It appears as an indurated, nodular or ulcerated lesion that may produce extensive tissue distruction.

Intra oral involvement is seen in palate & tongue. Palatal perforation seen.  Lobulated tongue is called as INTERSTITIAL GLOSSITIS. GLOSSITIS.  Diffuse atrophy & loss of the papillae produce a condition called LUETIC GLOSSITIS.


SYPHILITIC GLOSSITIS
The surface of the tongue gets broken up by fissures due to atrophy & fibrous of tongue musculature & hyperkeratosis frequently follows. Almost seen in males.  Incidence of malignant trasformation is 30%.


CONGENITAL SYPHILIS
Also called as prenatal syphilis.  In 1858 sir Jonathan Hutchinson described the changes found in congenital syphilis & defined the following 3 pathognomonic, diagnostic features known as HUTCHINSONS TRIAD. TRIAD.


HUTCHINSONS TRIAD:TRIAD: Hutchinsons

Teeth

 Ocular  8th

interstitial keratitis

nerve deafness

STIGMATA OF CONGENITAL SYPHILIS


      

Frontal bossing Short maxilla High arched palate Saddle nose Mulberry molars Hutchinsons incisors Cluttons joint

      

Higoumenakis sign Relative prognathism of mandible Interstitial keratitis Rhagades Saber shin 8th nerve deafness Scaphoid scapulae

SADDLE NOSE IN CONGENITAL SYPHILIS

SYPHILITIC FOOT

HISTILOGICAL FEATURES


The surface epithelium is ulcerated in primary lesions & or hyperplastic.  Underlying lamina propria may demonstrate an increase in the no. of vascular channels & an intense chronic inflammatory reaction is present.  The infiltrate is composed predominantly of lymphocytes , plasma cells & often demonstrate a perivascular pattern.

DIAGNOSIS


Best confirmed by dark field examination of a smear of the exudate of an active lesion.  False ve may be possible.  VDRL test  RPR test  After the 1st 3 weeks of infection the screening tests are +ve strongly throughout the 1st 2 stages. After latency stage the +vety decreases.

SPECIFIC TESTS:TESTS: FTA-ABS FTA TPHA




TREATMENT


Individual evaluation & a customised therapeutic approach is needed.  Antibiotic regimen therapy  Erythromycin or tetracycline is given who is allergic to penicillin.

GONORRHEA


It is primarily a veneral disease affecting male & female genitourinart tract & is trans mitted by sexual intercourse.  Causative M.O:-NEISSERIA M.O:GONORRHEA.  Disease is epidemic, especially in urban areas having a low socioeconomic status, injecting drug users, prostitutes, homosexual men & military personnel.  It is an infection of epithelium.

M.O is a gm ve, non motile, non sporing diplococci.  Disease is more widely prevalent than syphilis in India & 80% of infected women are reported to be asymtomatic carriers.  Predominantly affects young person.  Incubation period is :- 2-5 days. :

MORPHOLOGY OF N.G

COLORISED MICROGRAPH OF GONORRHEA CELLS

CLINICAL FEATURES
   

It spreads through sexual contact & most lesions occur in the genital areas. Affected areas show purulent discharge. In women the main complication is pelvic inflammatory disease. During birth infection of an infected infants eyes are called GONOCOCCAL OPTHALMIA NEONATORUM & can cause blindness

ORAL MENIFESTATIONS
Lips may develop acute painful ulceration.  Gingiva:- erythmatous with or without Gingiva:necrosis.  Tongue:- may present red, dry ulcerations Tongue:& become glazed & swollen lesions on the buccal mucosa.  Gonococcal pharyngitis & tonsillitis are also seen. Appears as vesicles or ulcers with a gray or white pseudomembrane.


COMPLICATIONS


Epididymitis.  Salpingitis.  Pelvic inflammatory disease.  Bartholinitis.  Gonococcal bacterimia leads to dermatitis & arthritis.

GONOCOCCAL EYE INFECTION

DIAGNOSIS


Gm staining of the purulent material is used. Samples can be collected with dacron or rayon swabs.  Special medias are:- Tthayer Martin Media are:or Stuart or Armies Media.  Confirmation diagnosis is made through culture & sugar fermentation tests or by a +ve fluorescent.

NEISSERIA GONORRHEA

TREATMENT


Antibiotics:Antibiotics:- ceftriaxone & doxycycline.  Pt. allergic to cephalosporin, streptomycin is used.  Re screening is recommended 1-2 months 1after therapy.  Prophylactic opthalmic erythromycin, tetracycline or silver nitrate is applied to the newborns eye to prevent the occurrence of gonococcal opthalmia neonatorum

TUBERCULOSIS


Its a chronic specific granulomatous disease.  Causative M.O:- mycobacterium M.O:tuberculosis.  In animals it is called as Bovine Tuberculosis, sometime communicated to man.

ETIOLOGY


M. Tuberculosis is a facultative intracellular parasite.  2 types of strains are seen


 

Human strains Animal strains

Human strains are responsible for many cases but the bovine type may produce illness through the ingestion of unpasteurized cows milk.

PATHOGENESIS
 

 

incidence in India accounts for nearly 1/3rd of the global burden of TB. The interaction of the bacilli & the host begins when droplet nuclei from infectious patients are inhaled. After 2-4 weeks it causes tissue damaging & 2macrophage activating responses develop. Mode of transmission is inhalation, ingestion, inoculation & transplacental route.

With the development of specific immunity & accumulation of a large number of activated macrophages at the site of primary lesion, granulomatous or tubercles are formed. The hard tubercle consists of epitheloid cells, langhans giant cells, plasma cells & fibroblasts. these response develop when host resistance is high. Tissue destruction leads to caseous necrosis. In some cases, this undergoes liquifaction & discharges into the lung leading to formation of a cavity.

PRIMARY TUBERCULOSIS


     

It occurs in previously unexposed people & almost always involves the lungs. also called as ghons complex or childhood TB SYMPTOMS:SYMPTOMS:Episodic fever & chills. Easy fatigability & malaise Gradual loss of weight Persistent cough with or without associated hemoptysis. Chest pain

PULMONARY


TUBERCULOSIS EXTRA PULMONARY

Pulmonary TB:- primary, secondary, TB:miliary  Extrapulmonary sites:- lymphnodes, sites:pleura, GIT, bones, meninges & peritonium


ORAL MANIFESTATOINS
 

Its a secondary to a pulmonary disease. Mechanism appears to be most likely that the M.O are carried in the sputum & enter the mucosal tissue through a small break on the surface. May spread through hematogenous route to the oral cavity & to be deposited on the submucosa & subequently proliferate & ulcerate the overlying mucosa. Lesions may be seen anywhere but tongue is the most common part followed by palate, lips, B.M, gingiva & frenula.

CONTD..


Chronic painless ulcers  nodular., granular or firm leukoplakic areas  Enlarged lymphnodes  Tuberculous osteomyelitis

LESION ON THE TONGUE

HISTILOGIC FEATURES


Characteristic appearance is due to the cell mediated hypersensitivity reaction  Formation of granuloma exhibiting epitheloid cells, lymphocytes & occasional multi nucleated giant cells

DIAGNOSIS


By culturing sputum in acid fast stain or Ziehl Neilsen stain we can demonstrate AFB  Roentogenographs  Tuberculin test  Ct scan  MRI in case of extrapulmonary TB

MONTOUXS TEST SHOWING POSITIVE REACTION

NEWER METHODS
Radioimmunoassay  Fluorescent tests  ELISA  DNA probes & PCR


TREATMENT & PROGNOSIS


Multiple drug therapy is often recommended as M. tuberculosis mutates & resists single drug therapy.  INH+RIFAMICIN for 9 months  INH+RIFAMICIN+PYRAZINAMIDE for 2 months followed by INH+RIFAMICIN for 4 months  Other drugs are streptomycin & etambutol


ACTINOMYCOSIS


Its a chronic granulomatous suppurative & fibrosing disease caused by anaerobic gm+ve non acid fast branched filamentous bacteria.  Its a normal component of oral flora, colon & vagina.  It seems to imply a fungal infection. So called as RAY FUNGUS.

CERVICOFACIAL ACTINOMYCOSIS

Sites of colonization in healthy patients include the tonsilar crypts, dental plaque & calculus, carious dentin, gingival sulci & periodontal pockets.  Most commonly isolated M.O is A.israelii. A.bovis produces the LUMPY JAW.


CLASSIFICATION


Actinomycosis is classified anatomically according to the location of the lesion & categorized as:- cervicofacial, abdominal, as:pulmonary & pelvic forms.

CERVICOFACIAL ACTINOMYCOSIS

EPIDEMIOLOGY


Infection occurs throughout the lifetime with peak incidence in the middle age.  Males are more affected than females possibly because of poor oral hygiene & trauma.

PATHOGENESIS


Disruption of the mucosal barrier is the main step in the invasion of bacteria.  1st acute condition followed by a chronic indolent phase.  Lesions appear as single or multiple indurations.  Central fluctuance with pus containing neutrophils & sulphur granules.

CLINICAL FEATURES


  

May be either an acute rapidly progressing infection or a chronic, slowly spreading lesion that is associated with fibrosis. 55% of case are cervicofacial, 25% abdominal & pelvic region & 15% in the pulmonary system. Remaining 5% exhibits a variety of pattern. Suppurative reaction of the infection may discharge large yellowish flecks that represent colonies of bacteria called SULFUR GRANULES.

CONTD..


Similar type is seen in case of bortryomycosis which is an unusual host reaction to S.aureus & other bacteria.  Infection may extend to the surface forming a sinus tract. Pain is minimal.  Area overlying the angle of the mandible being the most frequently affected site.

ORAL MANIFESTATIONS
    

Significant hyperplasia Tongue involvment represents as a firm, nodular of the body & base without sinus. Abscess formation in the submandibular & masseter spaces. Actinomycotic osteomyelitis of mandible & maxilla. Draining sinuses, pain & swelling are frequently reported.

INTRAORAL INVOLVEMENT

HISTILOGIC FEATURES


It demonstrates as a peripheral band of fibrosis encasing a zone of ch. Inflammatory granulation tissue surrounding a large collection of PMNs & organisms.  Colonies consists of club shaped filaments that form a radiating rosette pattern.  with H & E stains the central core stains basophilic & the peripheral portion is eosiniphilic

HISTOLOGICAL PICTURE

DIAGNOSIS


Mainly based on culture.  Culture is obtained by surgical exploration, with FNAC  Fluorescein conjugated antiserum can be used on the granules to speifically identify the Actinomyces species.

TREATMENT & PROGNOSIS


The treatment of choice is a high doses of antibiotics in association with abscess drainage and extension of sinus tracts.  Penicillin is the standard of care. Tetracyclin is also used.  Response is seen in 5-6 weeks & in deep 5seated infections may require upto 12 months.


TETANUS


Also called as LOCK-JAW. LOCK Its an acute infection of nervous system characterized by intense activity of motor neurons & resulting in severe muscle spasm.  Causative M.O:- Clostridium Tetany. M.O: M.O can enter the body through even the most trivial injury.

PATHOGENESIS


 

It is caused by exotoxin of the anaerobic gm+ve bacillus, which acts at the synapse of the interneurons of inhibitory pathways & motor neurons to produce blockade of spinal inhibition. Now a days its a rare disease. More common in males than females. It block the release of glycine and GABA which produces rigidity

CLINICAL FEATURES
It occurs after acute injuries such as laceration or abrasion.  May be acquired during farming, gardening, etc.  May also occur in patients with abscess, ulcers & gangrene. It is associated with burns, frostbite, middle ear infection, surgery, abortion & child birth.  Neonatal tetanus is fatal with a mortality rate of 80-90%. 80

Incubation period is 6-10 days. 6 Its of 2 types:- generalized & localized. types:

TREATMENT


Aim of the treatment is to remove spores at the site of wound, prevent toxin production, neutralize unbound toxins & prevent muscular spasms.  General measures should be taken.  Penicillin 10-12 million units i.v for 10 10days, metronidazole 1gm every 12hrs.  Clindamycin & erythromycin is the alternative of penicillin.

CONTD..
 

  

Antitoxin is injected to neutralize circulating toxins & unbound toxin with wound. Human tetanus immunoglobin (TIG) 3000-6000 3000units IM individual doses.500 unit is as effective as higher doses. Prophylaxis done by wound debridement & booster dose of TT In unimmunised case ATS 1500 units or TIG 250 units should be given. Active immunization requires 3 doses of triple vaccine in 1st year of life with subsequent dose at 5 years interval should be given.

NOMA
 

 

Also called as cancrum oris, gangrenous stomatitis. The name suggests that it is a devour (a spreading sore) means a rapidly spreading mutilating, gangrenous stomatitis. Usually seen in debilitated or nutritionally deficient persons. Chiefly seen in children but also found in adults

CLINICAL FEATURES


  

Predisposing factors are undernourished or debilitated from infections, poverty, poor oral hygiene, poor sanitation, malignancy, AIDS. May be considered as secondary to systemic diseases. It appears as a specific infection by vincents organisms. Normally begins as a small ulcer of the gingiva which rapidly spreads & involves the surrounding tissues of the jaw, lips & cheeks by gangrenous necrosis

FACIAL INVOLVEMENT

CONTD...


The overlying skin becomes inflamed edematous & finally necrotic with demarcation line between healthy & dead tissue.  Some time jaw is exposed. The odor is extremely foul.  High temp. is seen

TREATMENT & PROGNOSIS


Malnutrition should be cured as soon as possible.  Antibiotics should be given.


LEPROSY
   

It is a chronic infectious disease caused by ::Mycobacterium Leprae. Also called as hansens disease. The M.O is thought to require a cool host body temp for survival but still it is in controversy. Initial site of infection may be the nasal or oropharyngeal mucosa. humans are considered the major host. Lesions mainly seen in skin, nasal cavity & palate

MODE OF TRANSMISSION
Direct contact  Materno- foetal transmission Materno Transmission from milk.


CLINICAL FEATURES
 

Currently classified as paucibacillary & multibacillary. Paucibacillary leprosy is a tuberculoid type & exhibits a small no. of well circumscribed hypopigmented skin lesions. Nerve involvement usually results in anaesthesia of the affected skin often accompanied by a loss of sweating. Oral lesions are rare.

BORDERLINE TUBERCULOID LEPROSY

DEFORMED HANDS

CONTD.
  

Multibacillary leprosy corresponds to lepromatous type. Begins slowly with numerous ill defined hypopigmented macules or papules on the skin. Face is a common site of involvement & the skin enlargements can lead to a distorted facial appearance. (LEONINE FACE) Hairs including eyebrows & lashes often is lost. Nerve involvement leads to a loss of sweating & decreased light touch, pain & temp sensors. Sensory loss begins in the extremities & spreads to other part.

HYPOPIGMENTED MACULE IN T.L

FACE NODULES

FACIAL INVOLVEMENT

LOSS OF EYEBROW

ORAL MANIFESTATIONS


In order of frequency the site of involvement are hard palate, soft palate, labial max gingiva, tongue,lips, buccal max gingiva, labial mand gingiva, buccal mucosa.  Affected tissue initially appears yellowish to red, sessile, firm, enlarging papules that develop ulceration & necrosis followed by healing by secondary intention.

A condition is seen called FACCIES LEPROSA: LEPROSA:- demonstrates a triad consisting of atrophy of the ant nasal spine, atrophy of the ant maxillary alveolar ridge & endo nasal inflammatory changes


DIAGNOSIS


  

Definitive diagnosis is based on the clinical presentation & supported by the demonstration of acid-fast M.O greater than 10 to the power 11 acidgm of tissue. Other investigations are skin biopsy, nerve biopsy & foot culture histamine test. Test for humoral response are monoclonal antibodies, ELISA, PCR, etc. In children the sweat function test is used.

ACID FAST STAIN SHOWING M.L

DIFFERENTIAL DIAGNOSIS


Sarcoidosis  Leishmaniasis  Lupus vulgaris  Lymphoma  Syphilis  Yaws  Other disorders having hypopigmentation

TREATMENT & PROGNOSIS


Paucibacillary is treated with a 6 months regimen of rifampin & dapsone.  Multibacillary is treated with 24 months of rifampin, dapsone & clofazimine.  Pt. allergic to rifampin is given with a 24 months of clofazimine, ofloxacin & minocycline.


H/P OF LYMPH NODE IN LEPROMATOUS LEPROSY

TUBERCULOID LESION

 THINK  LOGIC  DONT

ASSUME  U MAKE AN ASS OF U & ME

PYOGENIC GRANULOMA


Also called as Granuloma pyogenicum. Distinctive entity which arises as a response of a tissues to a nonspecific infection. Its a tumor like growth mainly due to minor trauma. The term PG is applied based on an identical lesion on the skin thought to be caused by pyogenic M.O

 

ETIOLOGY


Due to minor trauma to the tissues, which provides a pathway for invasion of non specific types of M.O. On response there will be proliferation of vascular type of connective tissue.

CLINICAL FEATURES
Most frequent site is gingiva (75%). Maxillary ant. is common.  Other sites are lips, tongue, buccal mucosa & rarely other areas.  Characterized by an elevated, pedunculated or sessile vascular mass with a smooth, lobulated or even a warty surface which commonly is ulcerated & shows a tendency for hemorrhage either spontaneously or slight trauma


Commonly involves facial aspect than the lingual & mainly it involves interdental papillae  It is deep red or reddish purple, depending on the vascularity.  Its painless & soft in consistency. It may be brown because of hemorrhage.  Develops rapidly & reach full size in a short period. The reason of female predilection is vascular effects of female hormones.


HISTOLOGIC FEATURES


Thin epithelium ( atrophic or hyperplastic) Vast number of endothelium lined vascular spaces & the extreme proliferation of fibroblasts & budding endothelial cells. inflammatory infiltration

D.D
Pregnancy tumor  Fibroma.


TREATMENT & PROG..


Surgical excision  Occasionally recurs because it is encapsulated & difficult to determine the extent  If left untreated then leads to healed PG or fibroma.


Tularemia
 

Francisella Tularensis Pasteurella tularensis Infected rodents & rabbits Deer fly or tick

 

Classification
Cutaneous  Ophthalmic  Pleuropulmonary  Oral & abdominal


Clinical features
Incubation period 7 days  Headache,nausea,vomitting,chills,fever  Lymphnodes enlarged & painful  Cut becomes suppurative ulcer  Oculoglandular tularemia  Adults & children


CDC/Emory University/Dr. Sellers. PHIL1344

Oral manifestations
Necrotic ulcers and pain of oral mucosa & pharynx.  Nodular masses develop abcesses  Regional lymphadenitis in submaxillary & cervical nodes.


Complications


Pneumonia,pleuritis

Treatment
Streptomycin  Tetracycline


Botryomycosis


Actinobacillus,Staphylococcus,Strepto Escherichia,Pseudomonas

Clinical features
Granulomatous infection  Disseminates involving liver,lungs,kidney  Multiple Ulcers & sinuses  Tonguefirm,nodular infiltration of the Tongue body & base of tongue.


Histologic features


Suppurative foci containing grains or granules forming around Microorganisms Grains are eosinophilic

Treatment


Nonspecific

Melioidosis


Pseudomonas pseudomallei,aerobic, gram ve,non acid fast rod shaped bacilli.

Clinical features
   

Acute & chronic In acute there is high fever,acute pulmonary infection,Diarrhea,Hemoptysis Visceral involvement,septicemia Chronic is of granulomatous type,multiple,small,nonspecific abcesses ocuring subcutaneously or in viscera,lymphnodes or bones,draining sinuses Contamination of skin abrasions by soil or water

Treatment
Incision  Drainage  Tetracycline+Chloramphenicol


Granuloma Inguinale
Also called Granuloma venereum,donavanosis  Donovania Granulomitis  Popularly called Donovan bodies  Now we call Calymmatobacterium granulomitis.


Classification
Ulcerative  Exuberant  Cicatrical


Clinical features
Tropical zones  Adult blacks  External genitalia,anus,inguinal region  Manifests as papules,nodules ulcerate to form clean,granular lesions with rolled margins,peripheral enlargement.  Satellite lesions through lymphatic extension.


Inguinal ulceration arises initially as fluctuant swelling known as Pseudobubo. In OMM through Autoinoculation

Oral manifestations
      

Appear months to several years later after the primary lesion. Lips,buccal mucosa or palate. Painful,bleeding ulcerated lesions. Proliferative granular masses. OMM inflamed & edematous Cicatrization is characteristic. Fibrous scar formation is present on cheek & lips which may limit mouth opening.

Histologic Features
Granulation tissue with PMNL & plasma cell. Pseudoepitheliomatous Hyperplasia. Presence of large mononuclear phagocytes Containing intracytoplasmic cysts within which are found DONOVAN bodies. They are tiny elongated,basophilic,argyrophilic rods.

Treatment
Tetracycline  Chloramphenicol  Streptomycin  Cotrimaxazole


Rhinoslceroma
Klebsiella Rhinoscleromatis is a gm-ve gmbacilli  Mode of transmissionInfected nasal transmission exudate.  Nodular lesions are found in upper respiratory tract,nose,involves the lacrimal glands,orbit,skin,paranasal sinuses and intracranial invasion.  HEBRA NOSE;proliferative nasal masses


Oral manifestations
Proliferative granulomas  Impairment of taste sensation  Anesthesia of soft palate  Enlargement of uvula & upper lip


CatCat-scratch Disease


Bartonella Henselae GmGm-ve bacillus demonstrable with silver stain.

Clinical features
Children & young adults  Traumatic break in the skin due to a scratch or bite of cat.  Papule,pustule or vesicle  1-3 weeks later regional lymphadenitis.  Nodes are painful & several CMS in diameter.  Overlying skin inflamed.


Low grade fever,Headache,chills,nausea malaise,abdominal pain. Non pruritic rash,parotid swelling,conjunctivitis,grandmal seizures. Granuloma of the eye,preauricular lymphadenopathy.Lymphnodes become soft & fluctuant owing to necrosis & suppuration.

Abscessed Node will perforate the skin & drain. Preauricular,submaxillary nodes involved.

Differential diagnosis
Tuberculosis Tularemia Lymphogranuloma venereum Infectious Mononucleosis Hodgkins disease

Histologic features


Lymph nodes manifest reticuloendothelial hyperplasia. Destruction of lymph node architecture with focal granulomas,suppuration, necrosis,capsular thickening. Epithelioid cells & multinucleated giant cells are seen. Warthin Starry Silver stain Brown Hopps gram staining

Prognosis
Good  Self limiting & regresses  Incision & drainage  Antibiotic therapy


Pyostomatitis Vegetans
Uncommon inflammatory Disease.  Oral lesions are part of a syndrome.  Patients have ulcerative colitis or GI disturbance.  It is also associated with crohns disease.  Patients with liver disease.


Oral manifestations
Broad based papillary projections.  Tiny abscesses or vegetations develop in areas of intense erythema.  Small projections are red or pink in color.  Tiny pustules beneath the epithelium liberate purulent material when ruptured.  Areas of ulceration may coalesce into large areas of necrosis known as snail track ulcerations.


Buccal mucosa presents coblestone appearance.  Vestibular lesions appear as folds and ulcers,lips are swollen,indurated.  Gingival and alveolar mucosa lesions are granular and erythematous.  Palatal lesions appear as multiple aphthous ulcers.


Histologic features
Papillary projections show hyperplastic stratified squamous epithelium with loose connective tissue with plasma cells,lymphocytes, PMNL,eosinophils.  Focal necrosis,microabscess formation.  Areas of degeneration and necrosis of the overlying epithelium.


Treatment


Antibiotic therapy. Intestinal & GIT disturbance should be bought under control.

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