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
For bacteriological cultures, always use swabs with transport medium (gel or wet sponge) to prevent drying of the specimen and to preserve the bacteria
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
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.
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
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.
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.
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
DIAGNOSIS
Done by culturing the flora of intraoral lesions , pharynx & saliva. Susceptibility is correlated with the results of DICK TEST
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
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
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).
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.
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
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 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 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.
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.
Teeth
Ocular 8th
interstitial keratitis
nerve deafness
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
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.
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
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.
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
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
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
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
NEWER METHODS
Radioimmunoassay Fluorescent tests ELISA DNA probes & PCR
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.
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
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.
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.
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.
DIFFERENTIAL DIAGNOSIS
Sarcoidosis Leishmaniasis Lupus vulgaris Lymphoma Syphilis Yaws Other disorders having hypopigmentation
TUBERCULOID LESION
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.
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
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
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
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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