Bacterial, protozoal infections V. Žampachová I. PAÚ FLORA of the ORAL CAVITY nMixed flora incl. fungal nStreptococcus, Neisseria, Staphyloccoccus, Lactobaccillus, Actinomyces, Bacteroides. nIn the epidermal layer of the cheeks, gingiva, and on the surface of teeth. nFound in saliva in large numbers Host defense mechanisms nCompetitive suppression of potential pathogens by low-virulent microorganisms nNonspecific defenses incl. antibacterial saliva, humoral (secretory IgA), and cellular (submucosal lymphocytes + plasma cells) systems. nPhagocytosis - important process nSpecific immune responses based on antibodies and specific reactions of T lymphocytes Morphologic patterns of inflammation nalterative nexsudative nserous n fibrinous, pseudomembranous nsuppurative nnecrotizing, gangrenous nproliferative nprimary (rare) x secondary n nGranulomatous inflammation n Morphologic patterns of inflammation nserous - excessive accumulation of fluid, few proteins - blister, on serous membranes commonly initial phases of inflammation nmodification - catarrhal - accumulation of mucus (salivary glands) n Morphologic patterns of inflammation nfibrinous - higher vascular permeability - exsudation of fibrinogen ® fibrin nfibrinolysis ® resolution; organization by granulation tissue ® fibrosis ® scar npseudomembranous - fibrinous pseudomembrane (diphtheria - Corynebacterium) - fibrin, necrotic mucosa, etiologic agent, neutrophiles Morphologic patterns of inflammation nsuppurative (purulent) - accumulation of neutrophillic leucocytes - formation of pus (pyogenic bacteria) ninterstitial nphlegmone – diffuse in soft tissue nabscess - localized collection nacute – border – surrounding tissue nchronic – border - pyogenic membrane npseudoabscess – pus in lumen of hollow organ (dilated salivary gland duct) nlocal complications, i.e. local spread, formation of suppurative fistule Morphologic patterns of inflammation nsystemic complications of suppurative inflammation: nbacteremia (no clinical symptoms!; danger of formation of secondary foci of inflamm. (endocarditis, meningitis) nsepsis (= massive bacteremia + toxins) - septic fever, activation of the spleen, septic shock nthrombophlebitis - secondary inflammation of the wall of a vein with subsequent thrombosis - embolization - pyemia - hematogenous abscesses (infected infarctions) nlymphangiitis, lymphadenitis n Morphologic patterns of inflammation nnecrotizing - inflammatory necrosis of the surface - ulcer (skin, oral mucosa) – necrotizing ulcerative gingivitis, noma ngangrenous - secondary modification of a necrotic focus by bacteria - humid gangrene (debilitated patients) n Infections in stomatology nSkin nOral mucosa nPharynx incl. tonsils nSinuses nSalivary glands nTeeth + surrounding structures nDeep infections (muscle, bone, …) Infections in stomatology nBacterial - nonspecific nSkin infections – impetigo, erysipelas, etc. nPharyngitis, tonsillitis nScarlet fever nDiphtheria nGonorrhea nNecrotizing ulcerative gingivitis nNoma n n n Infections in stomatology nBacterial – specific patterns nSyphilis nTuberculosis nLeprosy nActinomycosis nCat-scratch disease n Infections in stomatology nFungal – i.e. superficial pseudomembranous oral candidiasis nViral – i. e. herpetic stomatitis (HSV-1, less common HSV-2), vesicles → ulcers; herpes zoster; EBV, CMV, measles nParasitic – i. e. protozoa (toxoplasmosis) n nSialoadenitis – non-purulent viral (mumps); purulent bacterial (Stph. aureus, Str. viridans) n n Infections in stomatology nPyogenic bacteria nStreptococcus pyogenes nStaphylococcus aureus nStreptococcus pneumoniae nKlebsiella pneumoniae nothers n Streptococci nStr. pyogenes n local inf. – phlegmona, impetigo, wound inf. n erysipelas nskin erythema (lower limbs, face) + toxemia nlymphatic + blood vein thrombosis ® lymphostasis ® edema ® elephantiasis n angina (tonsillitis) ® otitis, sinusitis n scarlet fever (erythrogenic toxin) nangina + oral enanthema (raspberry tongue) + skin exanthema (face, trunk) n Impetigo nsuperficial skin infection (commonly face) nStr. /+ Staph. nin damaged skin ncontact transmission, possible epidemics in children nvesicles/bullae → pale brown crusts nusually no systemic manifestations n Impetigo n copy Impetigo copy impetigo clin impetigo micro Bullous impetigo copy copy Erysipelas nSkin + soft tissue purulent infection (cellulitis), phlegmone + local lymphatic spread, commonly bacteremia + systemic signs (fever, vomiting…) nUsually β-hemolytic streptococci nChildren, elderly, debilitated, diabetics nPainful, swollen, red, warm foci nComplications – abscess, gangrene, thrombophlebitis, shock, distant streptococcal sequelae (endocarditis, glomerulonephritis) nPossible recurrence Erysipelas nWell-demarcated cellulitis with fever and malaise nupper dermal edema lifts epidermis except fixed foci of hair follicles or sweat glands nleads to the typical „peau d'orange” appearance n copy Erysipelas ery copy Tonsillitis and pharyngitis nbacterial (Str. – 25%, Staph., Fusobacterium, dipthteria, …) nviral (EBV, influenza, adenoviruses, …) nClinical – sore throat, dysphagia, red + swollen tonsils + focal/confluent yellowish exudate, cervical lymhadenopathy, fever, malaise, … nIn viral + rhinitis, laryngitis n Tonsillitis the_appearance_of_the_thro_784 Scarlet fever nHemolytic streptococcus B group A nSystemic bacterial infection, result of an erythrogenic toxin → capillary damage nMost common in children nComplication: local spread (otitis media, abscess) nsystemic spread (pneumonia, septicemia, toxic shock syndrome); n poststreptococcal heart, kidney and joints diseases n Scarlet fever nIncubation period: 2-3days (1-7days) nUsual type: n Fever: 39°C, 1 week n Vascular dilation and damage with an erythematous macular rash on the skin ( chest area ), after 1 week desquamation. n Face →flushed except for zone of circumoral pallor n Pharyngitis, tonsillitis: red enanthema, edema, yellow exudate n Cervical lymphadenitis n n Scarlet fever nTongue: start with white coating + visible fungiform papillae – white strawberry tongue n4.-5. day – desquamation, red strawberry tongue n Soft palate: possible petechiae Scarlet fever n red8 Diphtheria nCorynebacterium diphtheriae nmostly children noutbreaks in urban poor populations, developing countries + native populations, immigrants nin immunosuppressed nwithout booster vaccination nepidemics still possible Diphtheria nPathology Pseudomembranes cover the mucosal membranes (nose, tonsils, oropharynx, larynx, genital), adherent to the tissue, bleeding by removal attempt. Progression to necrosis possible. nDamage by exotoxins to heart muscle, liver, kidneys, and adrenals. Also nerve damage resulting in paralysis of the soft palate, eye muscles or extermities. Diphtheria nClinical findings Fever, sore throat, dyspnea (obstruction by the membrane). Later on difficulties with vision, speech, swallowing, or movement of the arms or legs. Var. gravis more severe. n Pharyngeal diphtheria nThe most common type, >80%. nSites of infection: tonsils, pharynx. nSymptoms: malaise, sore throat, anorexia, vomiting and middle-grade fever. nUsually +/- systemic absorption of toxin. nWith enlarged lymph nodes in the submandibular areas of neck. n The first category is …… Pharyngeal diphtheria nOrdinary type nWithin 2-3 days, small patches of white pseudomembrane on the tonsils nTypical adherent, bluish- or greyish-white pseudomembrane forms on the congested tonsils. Diphtheria Dscn0742 copy copy Diphtheric pseudomembrane Dscn0741 copy Pharyngeal diphtheria nGrave type nSerious early symptoms, high-grade fever. nLarge, thick pseudomembrane, greyish-green or black (if bleeding), covering the tonsils, uvula, and some soft palate, odoriferous in mouth nSkin becomes pale, tachycardia, blood pressure may be normal or slightly depressed (shock). Differential diagnosis nStreptococcal pharyngitis nThe pus covering the tonsils (yellow color, easy to remove) x the pseudomembrane of diphtheria. nOral candidiasis noften in infants, in good general conditions. The membrane white, and easily removable nInfectious mononucleosis and Vincent’s angina nPossible pseudomembrane-like covering on the surface of tonsils or pharynx, removable without bleeding. n n Gonorrhea nsexually transmitted acute mucosal purulent inflammation (anogenital region, internal genital in females) nin 20% + oropharyngeal region (direct mucosal contact, rarely due to septicemia) npharynx, tonsils, uvula – erythema, edema, possible pustules nanterior oral cavity – erythema, possible → ulceration ngonococcal ophthalmia neonatorum Ophtalmia neonatorum caused by Neisseria gonorrheae Source: Microbiology Perspectives, 1999 Tissue space infections nsource from apical abscess, pericoronitis nextension along the planes of muscles/fascia naccumulation of exudate/pus ndisruption of blood supply, anaerobic space nvariable localization of facial cellulitis Tissue space infections nFacial cellulitis - flegmona ncommonly from molars ndiffuse edema (hard consistency) npain nsystemic signs (fever, leucocytosis, toxemia) ntender enlargement of cervical LN npossible fatal complications nlaryngeal edema – glottis nmediastinitis nextension to carotid artery Tissue space infections nCavernous sinus thrombosis npossibly fatal complication nsource – upper teeth, sinusitis, skin abscess nretrograde venous blood flow ncyanosis + edema of the eyelid nlimited eye movements, pain nheadache, vomiting, fever nfatal without prolonged antibiotic therapy nrapid progession Oral ulcerative lesions nAcute (traumatic, infectious, drug reactions, immunologically mediated) nChronic (vesiculobullous lesions, malignancy) nRecurrent (rec. aphthous stomatitis, etc.) n Acute ulcerative lesions nDrug reactions n Barbiturates, salicylates, phenolphthalein, quinine, digitalis, griseofulvin, dilantin, … n Acute ulcerative lesions nBacterial n Necrotizing ulcerative gingivostomatitis n Streptococcal gingivostomatitis n Oral tuberculosis n Primary syphilis n Gonococcal stomatitis n Infective gangrene nNecrotizing soft tissue infection. n - acute onset n - rapidly progressive n - deep tissue affected n1) infective conditions leading to tissue destruction: n n Bacterial infect: localized (carbuncle), n extensive (necrotizing fasciitis, etc.) n Fungal (Zygomycosis etc.) n Mixed: Fusospirochetal - Cancrum oris (noma) n n2) preexisting tissue destruction complicated by infection n n Necrotizing ulcerative gingivostomatitis nterm „acute“ not necessary – no chronic form npsychologic stress (↑ adrenal hormones →↓ immune response + local ischemia) nimportant factors: immunosuppression (incl. HIV), smoking, local trauma, poor nutrition, poor oral hygiene, inadequate sleep, recent illness (EBV) nyoung – middle-aged adults n Necrotizing ulcerative gingivostomatitis (Vincent’s disease) n„Punched out” ulcerations + necrosis, rapid onset, painful, foul, fetid odor, + event. fever, lymphadenopathy nstart in interdental papillae, → stomatitis, mucositis, nprogression to the facial skin + bone – noma (children with poor nutrition, often fatal) nFusobacterium + Borrelia vincentii (fusospirochetal complex), polymicrobial, endogenous Necrotizing ulcerative gingivostomatitis nnonspecific histopathology: fibrinopurulent pseudomembrane + cellular debris + bacteria, mixed inflammatory infiltrate. nusually quick resolution with therapy nin HIV+ persistent Necrotizing ulcerative gingivostomatitis trench1 copy Noma (cancrum oris) nrapidly progressive orofacial gangrene nin predisposed patients (immunodeficiency – HIV; malignancy - leukemia; recent illness – measles, herpes simplex, scarlet fever) nin risk populations (poverty; malnutrition + dehydratation; poor oral hygiene, poor sanitation, proximity to livestock) „Face of poverty” ncommonly starts as NUG n Noma (cancrum oris) nChildren 1-10 yrs nNoma neonatorum – low-weight infants, Pseudomonas nFatal in 70% - 90% of cases, with aggressive therapy 10%, survivors disfigured for life (healing → scar → bony fusion and tight mouth closure → microstomia) nFusobacterium necrophorum or Prevotella intermedia + Borrelia vincenti (or other bacteria – Staph., Str.) nsynergistic infection → endotoxin → gangrenous necrosis of the gingiva → extending to oral mucosa, perioral tissue and face n Noma pct_01_child noma1 copy copy copy Noma cancrumoris copy copy Granulomatous inflammation n Bacteria nTBC nleprosy nsyphilis (3rd stage) nanthropozoonoses - cat-scratch disease, n Parasites or fungi (i.e. toxoplasmosis) n Inorganic metals or dust nsilicosis, berylliosis n Foreign body nsuture (Schloffer „tumor“), prosthesis n Unknown – sarcoidosis nvasculitis (Wegener) Granulomatous inflammation ndistinctive chronic inflammation type ncell mediated immune reaction (delayed) naggregates of activated macrophages ® epithelioid cell ® multinucleated giant cells (of Langhans type x of foreign body type) nNO agent elimination but walling off nintracellulary agents (TBC) Syphilis - primary nChancre: primary lesion, hard + raised ulceration, painless. Primary complex: chancre + regional lymphadenopathy ngranulation tissue + mononuclear, predominantly plasma cell infiltrate nLips, tongue, palate, … ! highly infectious! nAverage incubation 20-30 days nSpontaneous healing in 3-6 wks n n n n . Syphilis – primary 20-03 copy Syphilis - secondary nearly generalisation (disseminated s.) nflu-like symptoms, sore throat, generalized lymphadenopathy nany time from 2 weeks to 6 months after initial chancre disappears, in 75% of untreated people nvarious cutaneous lesions – rash, typ. palms, soles; maculopapular, pustular; nmucous patches+ erosions in oral cavity; flat, broad-based wart-like papules in mouth corner - condylomata lata; multiple, infectious nnonspecific histopathology, similar to I. st., ↑ plasma cells ndisappears within 2-6 weeks n Syphilis - secondary Condylomata lata SecSyphilisRash Syphilitic rash copy Syphilis - secondary n syphilis copy Syphilis: latency period nUsually not counted as a „stage“ nDuring this period no symptoms; 5-50 years nNot transmissible by sexual contact; it can be spread by blood during this time nMuch shorter in HIV infected Syphilis - tertiary nin 1/3 of untreated patients ncardiovascular syphilis (mesaortitis), neurosyphilis (progressive paresis, dementia), nmore benign tertiary syphilis: gummas in skin, mucous membranes, bones, liver; specific granulomas – delayed hypersensitivity reaction; nhistopathology: proliferative endarteritis (endothelial hypertrophy ® intimal fibrosis ® local ischemia) + inflammation (plasma cells) n gumma – central coagulative necrosis + specific granulation tissue + fibrous tissue Syphilis - tertiary nOral cavity: npalatal ulcerations – may perforate to the nasal cavity ntongue - atrophic luetic glossitis – diffuse atrophy, loss of papils n interstitial glossitis – enlarged, irregular shape (gummata) n Syphilis - tertiary Gumma + ulceration Bone destruction copy copy Congenital syphilis n1) abortus nhepatomegaly + pancreatitis + pneumonia alba n2) infantile syphilis nchronic rhinitis (snuffles) + mucocutaneous lesions n3) late (tardive, congenital) syphilis n> 2 years duration nHutchinson triad – notched central incisors + keratitis (blindness) + deafness (injury of n. VIII) nmulberry molars + saddle nose Copyright © 2004 by Delmar Learning, a division of Thomson Learning, Inc. ALL RIGHTS RESERVED. Congenital syphilis n nHutchinson’s incisors and mulberry molars Tuberculosis nMycobacterium tuberculosis, M. bovis nPrimary – usually in lungs; possible gingiva+ cervical lymph nodes nM. bovis: contaminated milk→ scrofula (↑ oropharyngeal lymphatic tissue + cervical lymph nodes → caseous necrosis → skin fistulae nSecondary – tongue, palate, lip – painless ulcer; skin – lupus vulgaris ntypical granulomas Tuberculosis Tuberculosis with multiple fistulous tracts secondary to lymph node necrosis in patient with scrofula. Photo by Dr. I. Small Leprosy (Hansen’s disease) nM. leprae, Asia, Africa nin dermal macrophages and Schwann cells nair droplets + long contact nIncubation period: 2 to 12 years or longer nNeural, tuberculoid (anesthetic) form: Lesions on skin and peripheral nerves. Loss of pigment and sensation. High immunity → sterile lesion. nCutaneous, lepromatous form: Progressive disfiguring nodules (lepromas) in skin, invades body. Destroys skin, mucous membranes, and bone. Infectious, in ↓ cellular immunity. n n n n n n Leprosy nPaucibacillary ~ tuberculoid, low number of circumscribed hypopigmented lesions. Oral rare. nMultibacillary ~ lepromatous, start as numerous papules. Invasion → proliferation → ulceration → fibrosis. Facial skin involvment in 1/3, oral lesions in 10%. Sessile papules → necrosis → scarring TubLeprosy Source: Tropical Medicine and Parasitology, 1995 Tuberculoid leprosy lesions with depigmentation leprosy1 Source: Tropical Medicine and Parasitology, 1995 Lepromatous leprosy lesions leprosy2 Source: Diagnostic Picture Tests in Infectious Diseases, 1994 Severe bone destruction in advanced leprosy Actinomycosis nA. izraelii – actinomycosis nnormal in oral cavity, access due to local lesion (extraction, root infection, …), direct extension nfirm edematous infl. infiltrate ® fistulas, yellow „sulphur granules“, fibrosis (scar) ncervicofacial – most common (submandibular, neck) nthoracic – lung abscesses nabdominal – IUD ® salphingo-oophoritis nMicro: G+ PAS+ filamentous colonies surrounded by neutrophilic, granulomatous reaction Copyright © 2004 by Delmar Learning, a division of Thomson Learning, Inc. ALL RIGHTS RESERVED. Actinomycosis Actinomycosis Actinomycosis - impregnation Cat-scratch disease nBartonella henselae nskin inflammation - nodule, ulcer nregional lymphadenopathy in 1-3 weeks nsuppurative necrosis + histiocytic rim nself-limited Parasitic infections nToxoplasmosis – intracellular protozoan dangerous in immunocompromised patients (lymphadenopathy incl. paraoral, encephalitis, pneumonia, myositis); congenital t. nCysticercosis – frequent in developing countries, hematogenous dissemination, possible encysted taenia larvae in the mouth n n Cysticercosis copy copy nDebridement is an essential component of wound care as the presence of devitalised tissue can impede the healing process. Larval therapy has been used for the debridement of wounds for several hundred years. magggggots copy 430