Bacterial lesion by Dr. Gaurav Salunkhe
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Bacterial lesion by Dr. Gaurav Salunkhe

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this seminar prepared by me will be very helpful for medical and dental students. hope u like it

this seminar prepared by me will be very helpful for medical and dental students. hope u like it

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Bacterial lesion by Dr. Gaurav Salunkhe Bacterial lesion by Dr. Gaurav Salunkhe Presentation Transcript

  • Dr. Gaurav S.Salunkhe PG -Student Oral & Maxillofacial Pathology
  • Introduction  Bacteria singular: bacterium) constitute a large domain of prokaryotic microorganisms.  Typically a few micrometres in length, bacteria have a number of shapes, ranging from sphears to rods and spirals.  Bacteria were among the first life forms to appear on Earth, and are present in most of its habitats. Bacteria inhabit soil, water, acidic hot springs, radioactive waste, and the deep portions of Earth's crust.  Bacteria also live in symbiotic and parasitic relationships with plants and animals.
  • What are bacteria? Single celled organisms Very small Need a microscope to see Can be found on most materials and surfaces E. Coli O157:H7 can make you very sick. Streptococcus can cause strep throat. This E. coli helps you digest food.
  • What do they look like? Three basic shapes  Rod shaped called bacilli  Round shaped called cocci  Spiral shaped Some exist as single cells, others cluster together Bacilli Spiral Cocci Cluster of cocci
  • Ex: Streptococcus Ex: Lactobacillus Ex: Spirillium
  • A Closer Look – Helpful Bacteria Pediococcus - used in production of fermented meats Leuconostoc cremoris – used in the production of buttermilk and sour cream Lactobacillus casei – found in human intestines and mouth to improve digestion Lactobacillus bulgaricus – used in the production of yogurt www.bioweb.usu.edu
  • 1. Syphilis 2. Tuberculosis 3. Leprosy 4. Gonorrhea 5. Noma 6. Scarlet fever 7. Actinomycosis 8. Diphtheria 9. Streptococcal tonsillitis & pharyngitis 10. Tetanus 11. Cat-scratch Disease
  • Syphilis  Syphilis is a worldwide chronic infection produced by Treponema pallidum.  The organism is extremely vulnerable to drying; therefore, the primary mode of transmission are sexual contact or from mother to fetus.
  • Syphilis - Treponema pallidum on darkfield
  • Syphilis  Although the risk of infection from blood transfusion is negligible because of serological testing of donor, transmission through exposure to infected blood is theoretically possible because the organism may survive upto 5days in refrigerator blood.  Humans are the proven host for syphilis.  In patients with syphilis, the infection undergoes a characteristic evolution that classically proceeds through three stages.  A syphilitic patient is highly infectious during the first two stages but a pregnant woman may transmit the infection to the fetus, during the latent stage.
  • Syphilis  Maternal transmission during the first two stages mostly results in miscarriage, stillborn or an infant with congenital malformations.  Infection of the fetus may occur at any stage during pregnancy but the stigmata do not begin to develop until after the 4th month of gestation.  The clinical changes secondary to the fetal infection are known as congenital syphilis.
  • Syphilis  Primary syphilis: 1. It is characterized by the chancre that develops at the site of inoculation, becoming clinically evident 3 to 90 days after the initial exposure. 2. Progresses from macule to papule to ulcer 3. Typically painless, indurated, and has a clean base 4. Highly infectious 5. Heals spontaneously within 1 to 6 weeks 6. It could be solitary or multiple. 7. 25% present with multiple lesions
  • 8. The external genitalia and the anus are the most common site of infection followed by the oral cavity. 9. Oral lesion are most on the lips, but the other sites include the tongue, palate, gingiva, and tonsils. 10. Upper lip is mostly affected in males while the lower lips is mostly affected in females.
  •  The oral lesion appears as a painless, clean-based ulceration or, rarely as a vascular proliferation.  Regional lymphadenopathy which may be bilateral is seen in most of the patients.  At this time the organism spreading systemically through the lymphatic channels, setting the stage for further progression.
  • Syphilis  Secondary syphilis:  the next stage is called secondary syphilis and is discovered after 4-10 weeks of initial infection.  The lesions may arise before the primary lesion has resolve completely.  During secondary syphilis, systemic symptoms often arise.
  •  The most common systemic symptoms are 1. Painless lymphadenopathy 2. Sore throat 3. Malaise 4. Headache 5. Weight loss 6. Fever 7. Musculoskeletal pain 8. The consistent sign is a diffuse, painless, maculopapular cutaneous rash which is widespread and can even affect the palmar and plantar areas.
  •  These rashes may appear as the chancre is healing, or may be delayed several weeks after the healing process has completed.  The characteristic rash of secondary syphilis is maculo- papular (flat and slightly bumpy).  It may appear as being rough, red, or having reddish- brown spots on either the palms of the hands and/or the bottoms of the feet, which is a unique characteristic of this disease and several others. However, a rash is still a common symptom of many other diseases, which can make the diagnosis difficult. Sometimes rashes associated with secondary syphilis are so faint that they are not noticeable.
  • Syphilis  Some patients have focal areas of intense exocytosis & spongiosis of the oral mucosa leading to zone of whitish mucosa known as mucous patch.  Occasionally several adjacent patches can fuse and form a serpentine or snailtrack pattern.
  • Syphilis  Elevated mucous patches also may be centered over the crease of the oral commissure and have been termed as split papules.  Occasionally papillary lesion may resemble HPV infection and are known as Condylomata lata.
  •  In patients with compromised immunity, secondary syphilis can exhibit an explosive and widespread form known as lues maligna.  The symptoms are 1. Fever 2. Headache 3. Myalgia 4. Necrotic ulceration of face & scalp.
  • Syphilis  Tertiary syphilis:  After the secondary stage patient enters a period in which they are free of lesions and symptoms, known as latent syphilis.  This period may last from 1 to 30 years.  This stage includes the most serious complications of vascular system, CNS, ocular region.
  • Aneurysm of the ascending aorta. Left ventricle hypertrophy Aortic regurgitation Congestive heart failure General paralysis Psychosis Dementia Paresis Tabes dorsalis Death Iritis Choroidoretinitis Argyll Robertson pupil
  • Syphilis  Scattered foci of granulomatous inflammation, which may affect the skin, mucosa, soft tissue, bones, and internal organs.  This active site if granulomatous inflammation, is known as gumma.  It appears as an indurated, nodular, or ulcerated lesion that may produce extensive tissue destruction.
  •  Intraoral lesion usually affect the palate & tongue.  When the palate is involved, the ulceration usually perforates through to the nasal cavity.
  • Syphilis  The tongue may be involved diffusely with gummata and appear large, lobulated, and irregularly shaped.  This lobulated pattern is termed as intertitial glossitis.  This is thought to be caused due to contracture of the lingual musculature after healing of the gumma.  Diffused atrophy and loss of the papillae produce a condition called luetic glossitis.
  • Syphilis  Congenital syphilis:  In 1858 sir Jonathan Hutchinson described the changes found in congenital syphilis and defined the 3 pathognomic diagnostic features, known as Hutchinsons’s traid: 1. Hutchinsons’s teeth 2. Ocular intertitial keratitis 3. Eighth nerve deafness Few patients exhibits all the three features
  • Hutchinsons’s teeth
  •  Ocular intertitial keratitis means corneal scarring due to chronic inflammation of the corneal stroma.  It is not present at birth, it develops at the age of 5-25 yrs.  It may result in loss of vision.
  •  Pathophysiology  The corneal scarring is the end result of the initial invasion of blood vessels into the corneal stroma as part of the inflammatory response.  Since normal corneal tissue should be avascular and therefore clear to allow light to pass, the presence of blood vessel and the infiltration of cells as part of the inflammatory process results in scarring or hazing of the cornea
  •  Other causes  TB  Leprosy  immunological response, such as a hypersensitivity reaction.  and parasitic infections
  • Syphilis  This infection alters the formation of both anterior (Hutchinsons’s incisors) & posterior dentition (mulberry molars, Moon’s molar).  In addition to Hutchinsons’s triad, other alteration like 1. Saddle-nose deformity 2. High arch palate 3. Frontal bossing 4. Hydrocephalus 5. Mental retardation 6. Gummas & 7. Neurosyphilis may be seen.
  • Early infections treatment:  The first-choice treatment for uncomplicated syphilis remains a single dose of intramuscular penicillin G or a single dose of oral azithromycin.  Doxycycline and tetracycline are alternative choices; however, they cannot be used in pregnant women.  Antibiotic resistance has developed to a number of agents including macrolides, clindamycin, and rifampin.  Ceftriaxone, a third- generationcephalosporin antibiotic, may be as effective as penicillin based treatment.
  • Late infections treatment:  For neurosyphilis due to the poor penetration of penicillin G into the central nervous system it is recommended that those affected be given large doses of intravenous penicillin for a minimum of 10 days.  If a person is allergic, ceftriaxone may be used or penicillin desensitization attempted.  Other late presentations may be treated with once weekly intramuscular penicillin G for three weeks.  If allergic as in the case of early disease doxycycline or tetracycline may be used but for a longer duration. Treatment at this point will limit further progression but has only slight effect on damage which has already occurred
  •  Primary and Secondary Stage:  Ulcerative/ hypertrophic epithelium  Increased vascular channels in lamina propria  Intense chronic inflammatory reaction. HISTOLOGICAL FEATURES
  •  Tertiary Stage:  Pseudoepitheliomatous hyperplasia  Granulomatous inflammation  Coagulation necrosis with peripheral rim of fibrosis containing fibroblasts  Histiocytes and giant cells.
  •  Silver impregnaiton technique- Warthin Starry or Steiner Stains shows “corkscrew like spirochaetal organism”.
  •  Tuberculosis (TB) is an infectious disease caused by bacteria, Mycobacterium tuberculosis.  It was first isolated in 1882 by a German physician named Robert Koch who received the Nobel Prize for this discovery.  TB most commonly affects the lungs but also can involve almost any organ of the body.
  •  One third of the world's population is thought to have been infected with M. tuberculosis "Tuberculosis Fact sheet N°104". World Health Organization. November 2010. Retrieved 26 July 2011.  In 2007, there were an estimated 13.7 million chronic active cases globally. World Health Organization (2009). "Epidemiology".Global tuberculosis control: epidemiology, strategy, financing. pp. 6–33. ISBN 978-92-4-156380-2. Retrieved 12 November 2009.  While in 2010, there were an estimated 8.8 million new cases and 1.5 million associated deaths, mostly occurring in developing countries. The absolute number of tuberculosis cases has been decreasing since 2006, and new cases have decreased since 2002. World Health Organization (2011). "The sixteenth global report on tuberculosis"
  •  Signs and symptoms:  Tuberculosis may infect any part of the body, but most commonly occurs in the lungs (known as pulmonary tuberculosis).  Extrapulmonary TB occurs when tuberculosis develops outside of the lungs, although extrapulmonary TB may coexist with pulmonary TB as well.
  •  General signs and symptoms include 1. fever 2. chills 3. night sweats 4. loss of appetite 5. weight loss 6. Evening rise of temperature 7. and fatigue.
  • Symptoms may include chest pain and a prolonged cough producing sputum. Occasionally, people may cough up blood in small amounts, and in very rare cases, the infection may erode into the pulmonary artery, resulting in massive bleeding .
  • • Extrapulmonary TB occurs more commonly in immunosuppressed People and young children. •In those with HIV, this occurs in more than 50% of cases. Notable extrapulmonary infection sites include the pleura (in tuberculous pleurisy), the central nervous system (in tuberculous meningitis), the lymphatic system (in scrofula of the neck), the genitourinary system (in urogenital tuberculosis), and the bones and joints (in Pott's disease of the spine), among others. When it spreads to the bones, it is also known as "osseous tuberculosis". a form of osteomyelitis. •Sometimes, bursting of a tubercular abscess through skin results in tuberculous ulcer. •An ulcer originating from nearby infected lymph nodes is painless, slowly enlarging and has an appearance of "wash leather"
  •  Involvement of the skin may develop and has been called lupus valgaris.  The most common extrapulmonary sites in the head & neck are the cervical lymph nodes followed by the larynx and middle ear.  Much less common sites are nasal cavity, nasopharynx, oral cavity, parotid gland, & esophagus.  Oral TB involves the gingiva, mucobuccal fold, & extraction sites.  Secondary lesions are more common on tongue, palate & lip.
  •  A potentially more serious, widespread form of TB is called "disseminated" TB, commonly known as miliary tuberculosis.  Miliary TB makes up about 10% of extrapulmonary cases.
  • Diffuse dissemination through the vascular system may occur and often produces multiple small foci of infection that grossly and radiographically resemble millet seed, resulting in the nickname, miliary tuberculosis.
  •  Drinking contaminated milk can result in a form of mycobacterial infection known as scrofula.  Scrofula is characterized by enlargement of the oropharyngeal lymphoid tissue & cervical lymph node.  Occasionally the involved lymph node may develop caseous necrosis and form numerous sinus tracts through the overlying skin.  Radiographically it appears as calcified lymph node. 
  •  Organism enters through sputum and reaches mucosal tissue due to break in the surface. (primary lesion)  Enters through haematogenous spread and get deposited to submucosal tissue. (secondary lesion) ORAL MANIFESTATION
  •  PRIMARY TB  Gingiva- most common site, and appears as diifused, hyperemic, nodular/ papillary proliferation of gingiva.  Mucosal lesions shows swelling, granular, nodular,or fissured lesion.  SECONDARY TB  Any site in oral cavity.  Tongue most common site.  Irregular, deep, painful ulcer. ORAL MANIFESTATION
  •  BONE OF MAXILLA /MANDIBLE-  Enters by anachoretic effect/ direct migration from open pulp chamber to periapical areas.  Tuberculous periapical granuloma/ tuberculoma  Painful.  Tuberculous osteomyelitis- later case.
  •  Due to cell mediated hypersensitivity reaction  Granuloma formation. HISTOLOGICAL FEATURES
  • Treatment:  Such drugs as: 1. Isoniazid 2. Rifampin 3. Pirazinamid 4. Ethambutol 5. Streptomycin (for multidrug-resistant cases)  Combination of that drug are often used in 6-, 9-, 12- month to 2 year.
  • Leprosy HANSEN DISEASE Leprosy is a chronic infectious disease produced by Mycobacterium leprae. Leprosy takes its name from the Latin word Lepra, which means "scaly", while the term "Hansen's disease" is named after the physician Gerhard Armauer Hansen. Because of worldwide efforts coordinated by the WHO a dramatic decrease in the prevalence of leprosy has been seen over the past 15 yrs.
  • Gerhard Henrik Armauer Hansen (29 July 1841 – 12 February 1912) was a Norwegian physician, remembered for his identification of the bacterium Mycobacterium leprae in 1873 as the causative agent of leprosy.
  • However, leprosy remains a public health problem in many area of world. 82% of all current cases reported were from, 1. Brazil 2. India 3. Indonesia 4. Myanmar 5. Nigeria
  • Although the mode of transmission of leprosy remains uncertain, many think that M. leprae is usually spread from person to person in nasal droplets. Studies have shown that leprosy can be transmitted to humans by armadillos Although Humans are the major host , other animals like 1. Chimpanzee 2. Armadillo 3. Mangabey monkey
  •  Related to immune reaction to the organism leprosy can be of two types: 1. Tuberculoid leprosy 2. Lepromatous leprosy Tuberculoid leprosy- develops in patients with high immune reaction. Lepromatous leprosy – develops in patients who demonstrate a reduce cell-mediated immune reaction.
  • Clinical features  Currently, leprosy is classified into two separate categories, on the basis of clinical manifestations and skin smear results. 1. Paucibacillary leprosy 2. Multibacillary leprosy Patients showing negative smears at all sites are grouped as paucibacillary leprosy (PB), while those showing positive smears at any site are grouped as having multibacillary leprosy (MB).
  • Paucibacillary leprosy – corresponds closely to the tuberculoid pattern of leprosy . Exhibits a small number of well circumscribed, hypo pigmented skin lesion. Nerve involvement usually result in anesthesia of the affected skin, often accompanied by loss of sweating. Oral lesion are rare in this variant.
  •  Multibacillary leprosy – correspond to lepromatous pattern of leprosy.  Ill-defined macules or papules on the skin that, with time becomes thickened.  The face is the most common site.  Hairs including the eyebrows and lashes, are often lost.
  •  Nasal involvement result in nosebleeds, stuffiness, and a loss of sense of smell.  The hard tissue of the floor, septum, and bridge of nose may be affected.  Collapse of the bridge of the nose is considered pathognomomic.
  • Oral lesions are not rare in multibacillary leprosy. The locations affected in order of frequency are: 1. Hard palate 2. Soft palate 3. Labial maxillary gingiva 4. Tongue 5. Lips 6. Buccal maxillary gingiva 7. Labial mandibular gingiva 8. & buccal mucosa.
  • Affected soft tissue initially appears as yellow to red, Sessile Firm Enlarging papules that develops in ulceration and necrosis, followed by attempted healing by secondary intention. Continuous infection of an area can lead to scarring & loss of tissue. Complete loss of uvula may occur. Lingual lesion appears on anterior 1/3 as areas of erosion which develops into large nodules.
  •  Facies leprosa, a term used to describe resorption of bone in the facial region of patients with leprosy.  It is triad of lesion consisting of 1. Atrophy of the anterior nasal spine 2. Atrophy of the anterior maxillary alveolar ridge 3. Endonasal inflammatory changes.
  • Histological features:  Lepromatous type-  Sheets of lymphocytes with vacuolated macrophages called lepra cells are scattered throughout the lesion  No well formed granulomas
  • Paucibacillary leprosy -6 month regimen
  • Multibacillary leprosy – 24 month regimen
  • Patients allergic to rifampin are treated with 24 month regimen
  • 78 Multibacillary (MB or lepromatous) is a 24-month treatment of rifampicin, clofazimine, and dapsone. Paucibacillary (PB or tuberculoid) is a six-month treatment of rifampicin and dapsone.
  • Treatment After resolution of the infection, the therapy must be directed towards reconstruction of the damage , in addition to physiotherapy and patient education.
  • Impetigo  It is a highly contagious bacterial skin infection most common among pre-school children.  People who play close contact sports such as rugby, American football and wrestling are also susceptible, regardless of age. Impetigo is not as common in adults.  The name derives from the Latin impetere which means to impeach.  It is also known as school sores.
  • Impetigo  Causes  It is primarily caused by Staphylococcus aureus, and sometimes by Streptococcus pyogenes.  Either separately or together.
  • Impetigo  Transmission  The infection is spread by direct contact with lesions or with nasal carriers.  Intact epithelium is normally protective, therefore most cases arise in area of dermatitis or previous trauma such as abrasion, or cuts.  The incubation period is 1–3 days.  Dried streptococci in the air are not infectious to intact skin. Scratching may spread the lesions.
  • Classification Impetigo Impetigo contagiosa Bullous impetigo Ecthyma
  • Impetigo  Clinical features. Most commonly occurs on the skin of the face or the extremities.
  •  Impetigo contagiosa  This common form of impetigo, also called nonbullous impetigo, most often begins as a red sore near the nose or mouth which soon breaks, leaking pus or fluid, and forms a honey-colored scab, followed by a red mark which heals without leaving a scar.  Sores are not painful, but may be itchy.  Lymph nodes in the affected area may be swollen, but fever is rare. Touching or scratching the sores may easily spread the infection to other parts of the body.  Ulcerations with erythema and scarring also may result from scratching or abrading of the skin.
  •  Bullous impetig  It is mainly seen in children younger than 2 years, involves painless, fluid-filled blisters, mostly on the arms, legs and trunk, surrounded by red and itchy skin. The blisters may be large or small. After they break, they form yellow scabs.
  •  Ecthyma  In this form of impetigo, painful fluid- or pus-filled sores with redness of skin, usually on the arms and legs, become ulcers that penetrate deeper into the dermis. After they break open, they form hard, thick, gray scabs, which sometimes leave scars.  Ecthyma may be accompanied by swollen lymph nodes in the affected area.
  • Treatment  Topical or oral antibiotics are usually prescribed.  Treatment may involve washing with soap and water and letting the impetigo dry in the air.  Mild cases may be treated with bactericidal ointment, such as mupirocin, which in some countries may be available over-the-counter. More severe cases require oral antibiotics, such as dicloxacillin, flucloxacillin or erythromycin.  Alternatively amoxicillin combined with clavulanate potassium, cephalosporins (1st generation) and many others may also be used as an antibiotic treatment.
  • Erysipelas  Erysipelas Greek -red skin; also known as "Ignis sacer", "holy fire", and "St. Anthony's fire.  It is an acute infection of the upper dermis and superficial lymphatics, usually caused by streptococcus bacteria.  Erysipelas is more superficial than cellulitis, and is typically more raised and demarcated.  Also called as SAINT ANTHONY’s FIRE- because the lesion is similar to the French house of St. Anthony, which has fiery red walls.
  • Signs and symptoms  Patients typically develop symptoms including high fevers, shaking, chills, fatigue, headaches, vomitng, and general illness within 48 hours of the initial infection. The erythematous skin lesion enlarges rapidly and has a sharply demarcated raised edge.  It appears as a red, swollen, warm, hardened and painful rash, similar in consistency to an orange peel.  More severe infections can result in vesicles, bullae, and petechiae, with possible skin necrosis.  Lymph nodes may be swollen, and lymphedema may occur. Occasionally, a red streak extending to the lymph node can be seen.
  • Signs and symptoms  The infection may occur on any part of the skin including the face, arms, fingers, legs and toes, but it tends to favor the extremities.  Fat tissue is most susceptible to infection, and facial areas typically around the eyes, ears, and cheeks. Repeated infection of the extremities can lead to chronic swelling.  Butterfly shaped lesion on face, involving cheeks and bridge of nose.  Eyelids become edematous and shut.
  • Treatment  Antibiotics
  • It is a highly contageous systemic infection occuring predominantly in children. It is similar to tonsillitis & phayringitis. It is regarded as separate entity because of its nature of the toxin. A number of different strains may produce this disease.
  • Causes  The disease itself is caused by secretion of pyrogenic exotoxins by the infecting Streptococcus.  Zabriskie, J. B. (1964). "The role of temperate bacteriophage in the production of erythrogenic toxin by Group A Streptococci". J Exp Med 119 (5): 761–780  Most of the clinical features are caused by erythrogenic toxin, a substance produced by the bacterium Streptococcus pyogenes (group A strep.)
  •  Incubation period- 3 to 5 days.  Enters through pharynx.  Pharyngitis, tonsillitis, headche, chills, fever, vomiting.  Enlargement of lymph nodes.  Diffuse, bright, scarlet skin rash on 3rd day.  Occur in skin folds  Due to damage to vascular epithelium  Dilatation of blood vessels  Hyperemia. CLINICAL FEATURES
  • Samall papules of normal colour erupts through these rashes giving a characteristic “Sand paper” feel to the skin.  “Pasta lines”- rashes prominent in the areas of skin fold  Sun burn with goose pimples  Rash subsides after 6-7 days followed by desquamation of palms and soles.
  •  Stomatitis scarlatina  Palatal mucosa- congested,petechiae  Palate and throat- fiery red  Tonsils- swollen and covered with greyish white exudate.  Tongue- early in the course of the disease the tongue exhibits a white coat & the fungiform papillae are edematous projecting above the surface as small red knobs- white strawberry/ strawberry tongue.  The coating of the tongue is soon lost and this organ becomes deep red, smooth, except for the swollen papillae the tongue in this phase is called the “red strawberry/ raspberry tongue”. ORAL MANIFESTATIONS
  •  Bacterial dissemination  Hypersensitivity to bacterial toxins  Rhinitis  Sinusitis  Abscess  Arthritis etc. COMPLICATIONS
  • Treatment  Antibiotics- penicillin, cephalexin  Local applications- mupirocin relieves discomfort
  • (Strangling angel of the children)
  • Cause  Diphtheria (Greek diphthera) "pair of leather scrolls") is an upper respiratory tract illness caused by Corynebacterium diphtheriae.  A facultative anaerobic, Gram-positive bacterium.
  • PATHOGENESIS  Diphtheria is an infectious disease spread by direct physical contact or breathing the aerosolized secretions of infected individuals.
  •  Bacilli at the site of entry multiply and liberates toxins.  These toxins induce initial edema and hyperaemia followed by epithelial necrosis and acute inflammation.  Coagulation of fibrin and purulent exudates produces a pseudomembrane consist of dead cells, leukocytes, erythrocytes, and the bacteria.
  • Signs and symptoms  The symptoms of diphtheria usually begin two to seven days after infection.  Symptoms of diphtheria include 1. fever of 38°C (100.4°F), low grad fever. 2. chills, 3. fatigue, 4. bluish skin coloration (cyanosis), 5. sore throat, hoarseness, cough, 6. headache, 7. difficulty swallowing, 8. painful swallowing, 9. difficulty breathing, rapid breathing, foul-smelling 10. bloodstained nasal discharge 11. and lymphadenopathy.
  •  Diphtheric membrane- which bleeds when stripped off.  Extends to involve soft palate, buccal mucosa, tongue, lips.  Bull neck appearance.  3-5 weeks- soft palate paralysed  Nasal twang  Nasal regurgitation  Later cases- membrane extends to larynx- husky voice.  If airways not cleared- suffocation. ORAL MANIFESTATIONS
  • Diphtheritic croup  Laryngeal diphtheria can lead to a characteristic swollen neck and throat, or "bull neck".  The swollen throat is often accompanied by a serious respiratory condition, characterized by a brassy or "barking" cough, stridor, hoarseness, and difficulty breathing, and historically referred to variously as "diphtheritic croup", "true croup“, or sometimes simply as "croup“.
  • An adherent, dense, grey pseudomembrane covering the tonsils is classically seen in diphtheria
  • Diagnosis  Laboratory criteria  Isolation of Corynebacterium diphtheriae from a gram stain or throat culture from a clinical specimen.  Culture- Pai agar, Cystine tellurite agar.  Histopathologic diagnosis of diphtheria by a stain called "Albert's Stain“, Ponder’s, Neisser’s.  Clinical criteria  Upper respiratory tract illness with sore throat  Low-grade fever (>102 °F (39 °C) is rare)  An adherent, dense, grey pseudomembrane covering the posterior aspect of the pharynx. In severe cases, it can extend to cover the entire tracheobronchial tree.
  • Treatment  Antibiotics are used in patients or carriers to eradicate C. diphtheriae and prevent its transmission to others, either:  Metronidazole  Erythromycin (orally or by injection) for 14 days (40 mg/kg per day with a maximum of 2 g/d), or  Procaine penicillin G given intramuscularly for 14 days Patients with allergies to penicillin G or erythromycin can use rifampin or clindamycin.  Diphtheria antitoxin
  •  It is a chronic granulomatous suppurative & fibrous disease caused by anaerobic or microaerophilic gram+, non acid fast, branched filamentous bacteria.  Commonly isolated organisms are: A. israelii,, A. viscosus, A. odontolyticus.  Actinomyces is a common inhabitant of the oral cavity even in the absence of any specific infection, hence the organism can be cultured from tonsils, carious teeth , non vital root canals, dental plaque, calculus, gingival sulcus & periodontal pockets
  • CLASSIFICATION  Actinomycosis can be classified anatomically according to the location of the disease: Cervicofacial Abdominal Pulmonary forms
  • Epidemiology • Males > females. • Peak incidence in middle age. • Incidence has decreased due to improved oral hygiene and antibiotics.  Actinomyces is a common inhabitant of the oral cavity even in the absence of any specific infection, hence the organism can be cultured from carious teeth , non vital root canals, dental plaque, calculus, gingival sulcus & periodontal pockets
  • Pathogenesis  It is not clearly known, it appears to be endogenous infection and not communicable.  It is not an opportunistic infection.  Disruption of the mucosal barrier is the 1st step in the invasion of bacteria.  Initial acute inflammation is followed by chronic inflammation.  Lesions appears as single or multiple indurations.  Pus from the abscess shows the presence of typical ‘sulphur granules’ and neutrophils which is diagnostic of the disease.
  •  Occurs in association with HIV infection, organ transplantation, chemotherapy, herpes , & in patients with serious systemic illness. Cervicofacial Actinomycosis
  • Clinical features  Cervicofacial type is the most common.  The organism may enter through the oral mucous membrane, to the soft tissue or spread to the salivary gland, bone or even the skin of the face and neck.  It produces swelling and indurations of the tissue.
  •  These soft tissue swellings eventually develop into one or more abscesses, which tends to discharge upon a skin surface, rarely a mucosal surface, liberating pus containing the typical “sulfur granules”.
  •  The skin overlying the abscess is purplish-red, indurated, wood feel and has drained to heal.  Because of the chronicity of the disease, new abscess develop and perforate the skin surface.  The patient over a period of time, may show a great deal of scarring and disfigurement of the skin.
  •  Infection of the soft tissue may extend to the mandible-maxilla.  In maxilla it may result in actinomycotic osteomylitis, it may future result in cranium meninges or the brain itself.  In bones the destruction is more extensive, at the apex of the teeth and may result in pulp-related infections like periapical granuloma or cyst.
  •  Abdominal form-  Its an extremely serious form and carries a high mortality rate.  Fever  Chills  Nausea  Vomiting  Pain  Palpable abdominal mass
  •  Pulmonary form-  Fever  Chills  Cough  Pleural pain
  • Histological features •Typical lesion is a granulomatous one showing central abscess formation which shows characteristic colonies of microorganisms. •These colonies are floating in a sea of PNL, associated with MULTINUCLEATED GIANT CELLS & macrophages around the periphery of the lesion. •Filaments stains with haematoxylin, whereas the ends of filament show eosinophilia. •The peculiar appearance of the colonies, with the peripheral radiating filaments is called ‘ray fungus’. •Tissue surrounding the lesion exhibits fibrosis. •Methanamine silver stain can demonstrate the organism better
  • colonies of bacteria
  • Grocott-Gomori methenamine-silver nitrate stain (A) and hematoxylin- eosin stain (B), both showing a sulfur granule in a patient with actinomycosis.
  • Treatment  Draining the abscess,  Excising the sinus tract with high doses of antibiotics .  Penicillin,  Tetracycline  & Erythromycin.
  •  It is a Chronic granulomatous disease which was 1ST recognized 100 yrs ago in horse.  Caused by “Actinobacillus.
  •  Affects skin/ mucosa.  Occur in patients with impaired immunity or systemic disorder- diabetes, HIV.  Can disseminate along liver, lungs, kidney.  Mimics actinomycosis  Chronic granulomatous mass with multiple ulcers and sinuses.  Tongue- nodular swelling without sinuses. CLINICAL FEATURES
  •  Granulomatous area comprised of-  Suppurative foci containing grains and granules forming around microrganisms.  Grains and granules are eosinophilic, PAS negative and methamine negative.  Eosinophilic peripheral club formation is absent. HISTOLOGICAL FEATURES
  • Foci of suppuration
  •  Non specific, as the definite cause is not known. TREATMENT
  • Also known as Pahvant Valley plague, rabbit fever, deer fly fever, and Ohara's fever
  •  Caused by Francisella tularensis  Also called as- Bacillus/Pasteurella tularensis  Gram –ve, non motile bacillus.  Caused by contact with infected rodents and rabbits to humans, either by eating contaminated meat, bite of infected deer fly, or skinning freshly killed infected animals. CAUSE
  • Pathogenesis  F. tularensis is a facultative intracellular bacterium that is capable of infecting most cell types but primarily infects macrophages in the host organism.  F. tularensis entry into the macrophage occurs via phagocytosis and the bacterium is sequestered from the interior of the infected cell by a phagosome.  F. tularensis then breaks out of this phagosome into the cytosol and rapidly proliferates. Eventually the infected cell undergoes apoptosis, and the progeny bacteria are released to initiate new rounds of infection.
  •  F. tularensis strains produce different hemolytic agents, which may facilitate degradation of the phagosome.  Tularensis undergoes asexual replication. Bacteria will divide into two daughter cells, each of which contains identical genetic information. Genetic variation may be introduced via mutation or horizontal gene transfer.  Incubation period- 7 days.
  •  6 characteristic clinical syndromes-  Ulceroglandular (most common)  Glandular  Occuloglandular  Oropharyngeal  Pneumonic  Typhoid CLINICAL FEATURES
  •  Headache, nausea, vomiting, chills  Ulcers  A single cut or sore on the skin develops into ulcer.  Lymphatic vessels swells, painful  Enlarged lymph nodes.  OTHERS- eye involvement, conjunctivitis, pneumonia, pleuritis etc. ULCEROGLANDULAR
  • Ulceroglandular most common cutaneous ulcers
  • Occuloglandular
  • Tularaemic cervical lymphadenopathy Axillary lymphadenopathy
  •  Necrotic ulcers of oral mucosa or pharynx.  Sever Pain  Generalized stomatitis.  Regional lymphadenitis arise in submaxillary and cervical group of lymph nodes. ORAL MANIFESTATIONS
  •  Antibiotic- Streptomycin, gentamycin, tetracycline  (F. tularensis is easy to aerosolize, highly infective and no of organisms needed to infect is very less, it is considered to be “biological weapons”.) TREATMENT
  •  Bacillus Psudomonas Peudomallei  Aerobic, gram –ve, non acid fast, rod shaped bacilli. CAUSE
  •  The mode of transmission is not from man to man or from infected animal to man, organisms are abundant in soil and stagnant water.  Human infection occurs through contamination of skin abrasion by infected water or soil.  Risk factors- diabetes thalassemia  It is endemic in certain parts of east countries, like Burma, India, China, Indochina, Malaysia, Thailand.
  • Pathogenesis  Pseudomallei is a facultative intracellular pathogen that can invade and replicate inside various cells, including polymorphonuclear leukocytes and macrophages and some epithelial cell lines.  After invasion into the cell, B.pseudomallei escapes from endocytic vacuoles into the cell cytoplasm,and induction of actin polymerization at one bacterial pole leads to membrane protrusions, with cell-to-cell spread.  Additional survival factors are the ability of B. pseudomallei to form antibiotic-resistant small-colony and the ability of mucoid variants with large extracellular polysaccharide glycocalyx structures to form biofilm- encased microcolonies that are also relatively antibiotic- resistant.
  • Pathogenesis  The disease can manifest as Acute, Sub acute, and Chronic disease  Incubation may be as short as 2 – 3 days  Latent infections can occurs after months to years
  • Progress of Infection  The infection starts with non specific lesion at the inoculum, where there can be break in the skin.  Lead to septicemia  Most common form is pulmonary infection  Can lead to suppurative infection and bacterimia
  •  Acute form- fever, diarrhoea, haemoptysis, pulmonary infection  Septicemia occurs in few days to weeks.  Chronic form - develops in patients who survived acute form.  Granulomatous type  Multiple, small abscess in viscera, lymphnodes, bones which often leads to draining Sinus tracts. Clinical features
  • Respiratory Infection  The most dangerous infection can be associated with respiratory infection  Can lead to suppurative lesions.  Consolidations of upper lobe of the lung  Can mimic tuberculosis.  Progressive illness can produce cavities
  • Spreading lesions  Systemic infections spread from the primary lesions on the skin.  Can spread to lungs, Myocardium, Liver and Bone.  Can present with unexplained systemic disease.
  •  Incision and drainage  Antibiotics  Tetracycline/chloramphenicol TREATMENT
  • (LOCK JAW)
  •  Tetanus Ancient Greek: tetanos “taut”, and "to stretch") is a medical condition characterized by a prolonged contraction of skeletal muscle fibers.  Infection generally occurs through wound contamination and often involves a cut or deep puncture wound. As the infection progresses, muscle spasms develop in the jaw (thus the name lockjaw) and elsewhere in the body.
  •  Exotoxin of anaerobic, gram +ve bacillus  Clostridium.tetani  Enters through deep cuts in skin and mucosa.  Occurs always in nonimmunized individuals.  Less often in immunized.  Occur mainly in Asia because-  Umbilical cord of newborn is cut with an unsterile instrument.  Women with unsterile handling of genital tracts. CAUSE
  • How it forms…  The nonencapsulated spore-forming bacterium Clostridium tetani causes Tetanus.  Spores that gain entry can survive for months to years.  Under anaerobic conditions, these spores geminate and produce tetanospasmin. Tetanospasmin that is released by the maturing bacilli is distributed via the lymphatic and vascular circulations to the end plates of all nerves. Tetanospasmin then enters the nervous system peripherally at the myoneural junction and is transported centripetally into neurons of the central nervous system (CNS).
  • How it forms… (cont.)  These neurons become unable of neurotransmitter release. The neurons, which release gamma- aminobutyric acid (GABA) and glycine, the major inhibitory neurotransmitters, are sensitive to tetanospasmin, leading to failure of inhibition of motor reflex responses to sensory stimulation. This results in generalized contractions of the agonist and antagonist musculature characteristic of a tetanic spasm. The shortest peripheral nerves are the first to deliver the toxin to the CNS, which leads to the early symptoms of facial distortion and back and neck stiffness.
  •  Tetanus often begins with mild spasms in the jaw muscle.  The spasms can also affect the chest, neck, back, abdominal muscles, and buttocks.  Back muscle spasms often cause arching, called opisthotonos.  Sometimes the spasms affect muscles that help with breathing, which can lead to breathing problems
  • Opisthotonos.
  • Clinical features  Generalized tetanus  This is the most common type of tetanus, representing about 80% of cases.  The generalized form usually presents with a descending pattern. The first sign is trismus, or lockjaw, and the facial spasms called risus sardonicus followed by stiffness of the neck, difficulty in swallowing, and rigidity of pectoral and calf muscles.  Other symptoms include elevated temperature, sweating, elevated blood pressure, and episodic rapid heart rate.  Spasms may occur frequently and last for several minutes with the body shaped into a characteristic form called opisthotonos.  Spasms continue for up to four weeks, and complete recovery may take months.
  •  Neonatal tetanus  Neonatal tetanus is a form of generalized tetanus that occurs in newborns, usually those born to mothers who themselves have not been vaccinated. If the mother has been vaccinated against tetanus, the infants acquire passive immunity and are thus protected.  It usually occurs through infection of the unhealed umbilical stump, particularly when the stump is cut with a non-sterile instrument.
  •  Local tetanus  This is an uncommon form of the disease, in which patients have persistent contraction of muscles in the same anatomic area as the injury.  The contractions may persist for many weeks before gradually subsiding.  Local tetanus is generally milder; only about 1% of cases are fatal, but it may precede the onset of generalized tetanus.
  •  Cephalic tetanus  This is a rare form of the disease, occasionally occurring with otitis media (ear infections) in which C. tetani is present in the flora of the middle ear, or following injuries to the head.  There is involvement of the cranial nerves, especially in the facial area.
  •  General measures:  Aim is to remove –  spores at the site of the wound  prevent toxin production  Neutralize unbound toxin  Prevent muscular spasm  Maintain sedation, airway and nutrition  Antibiotics-  Penicillin 10 million units IV for 10 days. TREATMENT
  •  Antitoxin- neutralize circulating toxin  Wound debridement  Unimmunized individuals- Anti tetanus serum (ATS) 1500 units.  Active immunization- 3 doses in the first year of life and booster doses at school entry and at every 5 to 10 year intervals.
  • Causes  Gonorrhea is primarily a venereal disease affecting the male and female genitourinary tract and is sexual transmitted.  It is caused by Neisseria gonorrhoeae  gram –ve,  non-motile,  Nonspore  Grow in pairs (diplococci)
  • 170 Transmission  Efficiently transmitted by:  Male to female via semen  Female to male urethra  Rectal intercourse  Fellatio (pharyngeal infection)  Perinatal transmission (mother to infant)  Gonorrhea associated with increased transmission of and susceptibility to HIV infection Epidemiology
  • Pathogenesis  GC are ingested, and they evade host defense, and spread through subepithelial tissues.  Attachment is mediated by pili  Divides every 20-30 minutes  Leads to formation of submucosal abscess and accumulation of exudate in lumen  GC toxins damage cells
  • Clinical features  Common age group is 15-29 yrs.  It predominantly affects young persons.  Males- urethritis, dysuria, urethral discharge, prostatitis, balanitis.  Females- trichomonal or candidal vaginits, cervicitis.  Carrier symptom includes vaginal discharge, discomfort and dysuria.  It may affect the rectum, oropharynx, and the eye.
  •  Lips- painful ulcers with limited movement.  Gingiva- erythematous with or without necrosis.  Tongue- dry, red, swollen, painful erosions  Pharyngitis, tonsillitis  Vesicles or ulcers with gray or white pseudomembrane.  Oral lesions are accompanied by fever and lymphadenopathy.  Gonococcal parotitis ORAL MANIFESTATIONS
  • Treatment  Antibiotics  Preventive measure
  • Granuloma venereum/ donovanosis.
  •  Caused by chlamydia trachomatis.
  • Pathogenesis  Organisms gain entry via trauma or abrasions.  A small firm nodule containing ‘Donovan bodies’ occurs at the site of inoculation and is considered classic for the disease.  ‘Donovan bodies’ consist of large mononuclear cells in which intracytoplasmic inclusion bodies contain the bacteria.  These inclusion bodies rupture, releasing infective organisms to the surrounding tissue.
  •  PRIMARY LESION:  Occur in genitalias, anus, and in the inguinal region.  Papules, nodules which ulcerate to form clean, granular lesion with rolled margins and which shows a tendancy for peripheral enlargement.  Inguinal ulcerations begin initially as fluctuent swelling- “pseudobubo”. CLINICAL FEATURES
  •  Occurs through autoinoculation.  Lesion may occur in any oral location such as lips, buccal mucosa, or palate, or diffusely involve the mucosal surface.  3 types- ulcerative/cicatricial/exuberant.  Fibrous scar formation- limit mouth opening. ORAL MANIFESTATIONS
  •  Granulation tissue with infiltration of PMN’s and plasma cells.  Pseudoepitheliomatous hyperplasia  Large mononuclear phagocytes, containing tiny intracytoplasmic cyst.  The cyst contains “DONOVAN BODIES”-tiny, elongated, basophilic, argyrophilic rods. HISTOLOGICAL FEATURES
  •  Donovan bodies are rod-shaped, oval organisms that can be seen in the cytoplasm of mononuclear phagocytes or histiocytes in tissue samples from patients with granuloma inguinale.  They appear deep purple when stained with Wright's stain. Wright- or Giemsa-stained smears show clusters of encapsulated coccobacilli in cytoplasm of mononuclear cells called "Donovan bodies"
  •  Antibiotics  Improvement occurs in 2-3 weeks. TREATMENT
  • (CANCRUM ORIS, GANGRENOUS STOMATITIS)
  •  Noma – to devour (a spreading sore)  Occur in debilitated or nutrionally deficient persons.  Thus it is secondary complication of systemic disease, rather than a primary disease.  It originate as a specific infection by Vincent’s organism, which is complicated by streptococci, staphylococci and diphtheria bacilli. CAUSE
  • The reported predisposing factors include: malnutrition (particularly A-and B-vitamins) or dehydration poor hygiene, particularly oral unsafe drinking water proximity to unkempt livestock recent illness an immunodeficiency disease, including AIDS.
  • PATHOGENESIS  Noma starts within the oral cavity progressing from untreated Acute Necrotizing Ulcerating Gingivitis (ANUG): - halitosis, bleeding gum, painful gum and pseudomembranous ulcers.  The Bacteroides produce a range of destructive metabolites such as collagenase, fibrinolysin, endotoxins, hydrogen sulfide, Indole ammonia fatty acids, protease.  The ulcers are covered with whitish- yellow or brown fibrin and debris.  The gangrenous necrosis progressively involves the cheeks , the lips, and the adjacent bone, producing catastrophic lesions on the face.
  •  Begins as small ulcer of the gingival mucosa  Spreads to surrounding tissue of the jaws, lips, and cheeks by gangrenous necrosis.  Initial Site is an area of stagnation around a fixed bridge or crown.  Skin becomes inflamed, edematous and finally necrotic.  Line of demarcation develops between normal and dead tissue.  Large mass of tissue slough out, leaving jaw exposed.  The commencement of gangrene is denoted as Blackening of skin. CLINICAL FEATURES
  •  Subcutaneous fat and buccal fat pad undergo necrosis, in advance to other adjoining tissue.  Odor- extremely foul from the necrotic tissue.  High temperature during course of disease.  Patient die from septicemia or pneumonia.
  •  Remove the cause  Antibiotics may help if give before last stage. Treatment and Prognosis
  • Cat scratch fever Benign lymphoreticulosis Benign nonbacterial regional lymphadenitis
  • Causes  It is thought to arise after a traumatic break in the skin due to the scratch or bite of the household cats.  Rarely by dog or monkey.  It is caused by Bartonella henselae  A gram negative bacilli demonstrated by sliver stain.
  •  Children and young adults  Caused by traumatic break in the skin due to scratch or bite of the household cat.  Primary lesion- papule, pustule, vesicle at the site of injury.  1-3 weeks- regional lymphadenitis without lymphangitis. CLINICAL FEATURES
  •  Nodes- painful, several cms, drains pus, sinus formation.  Overlying skin- edematous  Lymphadenopathy may persist for 1-6 months.  Low-grade, Fever, headache, nause, malaise, abdominal pain.  Maculopapular rash  Parotid swelling  Seizures
  •  OCULOGLANDULAR SYNDROME OF PARINAUD- granuloma of eye and preauricular lymphadenopathy.  Preauricular, submaxillary or cervical lymph nodes may be involved.
  •  Initial stage- reticuloendothelial hyperplasia of lymph node.  Later stage- granulomas, suppuration, necrosis, capsular thickening  Epitheloid cells and multinucleated giant cells are rarely seen. HISTOLOGICAL FEATURES
  • Treatment and Prognosis  Incision and drainage of lymph nodes  Antibiotics- ineffective.  Prognosis is good.
  •  It is a chronic, slowly growing, localised infection.  Casused by Klebsiella rhinoscleromatosis.  Slightly more females than males are affected .  Patients are usually 10 to 30 years of age.  Affects respiratory tract, nose, lacrimal glands, orbit, skin, & sinus.  Rhinitis stage- nasal obstruction, epistaxis  Infiltrative stage- granulation tissue, larynx involvement, anaesthesia of soft palate.  Nodular stage- proliferation of nasal mass produce “HEBRA NOSE”, laryngeal and tracheal obstruction. CAUSE AND CLINICAL FEATURES
  • Hebra nose  Destruction of the nasal cartilage are also noted.  The damage may result in anaesthesia of the soft palate, enlargement of the uvula, dysphonia, and various degrees of airway obstruction.
  •  Proliferative granulomatous mass on lips, palate, tongue.  Enlargement of uvula.  Anesthesia of soft palate.  Impairment of taste sensation. ORAL MANIFESTATIONS
  • Prognosis & treatment  It is not lethal in nature and is responsive to Tetracycline or Ciprofloxacin.  However, if left untreated the disease can lead to sepsis, hemorrhage or other chronic conditions that can be fatal.
  • CAUSE and PATHOGENESIS  It is a distinctive clinical entity originating as a response of the tissues to a non-specific infection.  It is a tumor like growth that is considered and exaggerated conditioned response to minor trauma.  Synonym= Granuloma Pyogenicum.  Etiology-It is an exuberant tissue response to some local irritants or minor trauma which provides a pathway for microorganisms and show overzealous proliferation of vascular tissue.
  •  It is a vascular lesion that occurs on both mucosa and skin, and appears as an overgrowth of tissue due to irritation, physical trauma or hormonal factors.  Freedberg, et al. (2003). Fitzpatrick's Dermatology in General Medicine. (6th ed.). McGraw-Hill.  Jafarzadeh H, Sanatkhani M, Mohtasham N (December 2006). "Oral pyogenic granuloma: a review". J Oral Sci 48 (4): 167–75.
  •  SITE-It occurs on the gingiva (75% cases). Other sites are lips, tongue and buccal mucosa. More common on the facial gingiva than the lingual gingiva.  The granuloma can be smooth or lobulated. The lesion is usually elevated , pedunculated or sessile  commonly ulcerated and shows a tendency of hemorrhage. SIZE-The lesion in diiferent cases may vary in size ranging from a few millimeters to a centimeter or more in diameter. GENDER-Female (70%)>>Male. AGE-Children , young adults and pregnant women. CLINICAL FEATURES
  • It is similar to that of granulation tissue except that it is exuberant and usually well localised. The overlying epithelium is usually atrophic but maybe hyperplastic with or without ulceration. There is usually a moderately intense infiltration of polymorphonuclear leucocytes,lymphocytes and plasma cells but the finding depends on the ulceration. The connective tissue stroma is typically delicate although frequently fasiculi of collagen fibres are noted coursing through the tissue mass. Shows large amount of newly formed endothelial vascular spaces. Old lesions give a fibrous appearance. Pregnancy tumours-is histologically identical to pyogenic granuloma of the gingiva frequently occurs during pregnancy and often has been called the pregnancy tumour. HISTOLOGICAL FEATURES
  • TREATMENT AND PROGNOSIS Pyogenic granulomas can be treated by surgical excision . The lesion occasionally recurs because it is not encapsulated.
  •  Pyostomatitis vegetans is an inflammatory stomatitis and most often seen in association with inflammatory bowel disease,  Namely ulcerative colitis and Crohn's disease.  Uncommonly, it may be one of the features of orofacial granulomatosis.
  •  Broad papillary projections  Tiny vegetations/abscess in the area of erythema.  Tiny pustules may be present beneath epithelium.  Area of ulceration may coalesce to large necrosis- “SNAIL TRACK ULCERS”  BUCCAL MUCOSA SHOW- COBBLESTONE APPEARANCE. ORAL MANIFESTATIONS
  •  Papillary projection- hyperkeratotic stratified squamous epithelium  Connective tissue- plasma cells, lymphocytes, neutrophils.  Area of necrosis or microabscess formation seen intraepithelial/subepithelial. HISTOLOGICAL FEATURES
  • Treatment & Prognosis  Topical corticosteroids  Systemic steroids  Dapsone  Azathioprine