Blk1: Bacterial, Fungal Infections & HSV Flashcards
What is the acronym MCATSS?
Margins: discrete (well-defined), or diffuse (difficult to spot where stop/start is)
Colour: red, white, red and white, blue, black brown…..
Appearance: Homogeneous (same colour and texture throughout), nonhomogeneous (varies in colour/texture)
Texture: smooth, rough, nodule, verrucous, fissured, ulcerated
Size: length, width, thickness
Site: where it is
bacteria type involved in ANUG
Gram negative bacilli
Part of the normal oral flora
o Treponema spriochetes
o Borrelia vincentii
o Fusobacterium nucleatum
o Bacteroides melanogenicus
o Prevotells intermedia
T/F Pre existing periodontal disease is a prerequisite of ANUG
FALSE
Predespositions of ANUG
Stress
Smoking
Trauma
Nutrition
Systemic conditions
- with physical and emotional stress, frequency of ANUG inc from 0.1% to 7%
Clinical Features of ANUG
o Rapid necrosis and sloughing of interdental papillae
o Marked gingival bleeding
o Interdental papillae surfaced with a grey/yellow pseudomembrane
o Halitosis
o Hyper-salivation
o Fever, malaise, and lymphadenopathy
o Metallic taste
o Painful gingiva
o *Permanent gingival destruction (loss of interdental papillae, normal anatomic contours)
Differential Diagnosis of ANUG
o Primary herpes simplex
o Acute exacerbation of chronic marginal gingivitis
o Acute periodontitis
o Erosive lichen planus (desquamative gingivitis)
- Necrosis is not normally seen in these conditions
Tx of ANUG
o Local debridement
o Rinsing with oxygenating agents (hydrogen peroxide)
o Antibiotics (metronidazole)
o Potential for recurring infection
Contributing Factors of TB
Increase in global travel and immigration from areas with high incidence of infection
Increase in # of homeless people in urban populations
Emergence in antibiotic restraints
Increase use of immunosuppressants in organ transplant pts
HIV +ve individuals are particularly susceptible
Initial Pathogenesis of TB
Aerobic Bacillus
Passes through aerosols, induces a T-cell mediated immune response of the delayed hypersensitivity type
Progression of TB
Skin test is +ve 2-3wks after contamination
Tissue then exhibits granuloma with central caseation (necrosis)
Necrotic debris (caused by macrophage destruction) is anaerobic and acidic, inhibiting growth of bacillus, controlling the infection
Infection can be dormant for years, and reactivation can lead to systemic disease or metastatic spread (can result in oral lesions into mucosa through a break in epithelium)
Oral Lesions Present with TB
o Oral lesions present as irregular, painless chronic ulcerations with undermined margins and a granular base
Ulcers are always secondarily infected with other MO’s, can spread haematologically but is unlikely
- preferred site is tongue and palate
Differential diagnosis of TB
Syphilis
Major aphthae
Traumatic ulcerative granuloma
Oral squamous cell carcinoma
Deep mycotic infections
Diagnosis and Tx of TB
Diagnosis: tb tests and biopsy
Tx: includes tx of primary disease
Primary Syphilis
o Stage 1: Primary Syphilis
Chancre, painless, non-exudative, and indurated ulcer rolled boarders
Can arise on lips, tongue, gingivae, tonsils, commissural area
Significant unilateral lymphadenopathy
Highly infective, but ulcers will heal without tx in a few weeks
Secondary Syphilis
After several weeks flu-like symptoms with mucocutaneous lesions (mucous patches) involving oral mucosa, hands, feet
Mucous patches are reddish brown and highly infectious but heal spontaneously in 6-8 weeks
Apx. 33% of people with no tx develop tertiary disease
Tertiary Syphillis
Can be years
Multiple, chronic, inflammatory necrotic lesions (gummas) developing in CNS, heart, aorta, liver
Can cause destructive lesions in palate and tongue
Actinomycosis Infection Location, Bacteria
o Found in periapical lesions and pericoronitis
o Actinomyces Israelii – gram +ve anaerobic, microaerophilic
o Infection results from predisposing factors
o Involves soft tissues, if spreads to bone causes osteoporosis
o Firm swelling with multiple draining fistulae with exudate
Acinomycosis Tx
antibiotic management with incision and draining
Candidiasis Pathological Mechanisms
o Adherence to a surface
o Invasion into surface epithelium
o Efficiency of host immune response
o Ability of organism to modulate the host response
Candidiasis Predispositions (Systemic and Local)
o Systemic: infection, nutrition, malignancies, immune deficiency, physiological (pregnancy, infancy, old age)
o Local: xerostomia, antibiotic, nutrition
Pseudomembranous Candidiasis Features
o White, wipeable patches on oral mucosa
o Burning mouth
Pseudomembranous Candidiasis Diagnosis
based on history and clinical features and possibly staining
Atrophic Candidiasis Features
Erythematous
Sore/Burning mouth
Chronic and Acute Inflammation
Denture stomatitis is a form
Atrophic Candidiasis Causes and Diagnosis
Use of tetracycline, corticosteroids, and broad spectrum antimicrobials
Diagnosis based on C. albicans in smears
Chronic Hyperplastic Candidiasis Features
o Irregular white patches (leukoplakia)
o Can be confused for dysplasia
o Nodular plaques do not wipe off
Chronic Hyperplastic Candidiasis Diagnosis
Diagnosis based on history, clinical appearance, and histopathology
Angular Chelitis Causes
o Common in denture wearers with VBL, poor hygiene, or ill fitting dentures
o Can also be associated with vitamin B12 deficiency
o Diabetes also can be a cause
o Often can be the first indication of an immune dysfunction in young healthy children
Median Rhomboid Glossitis & CC
o Raised or flat red nodule in mid-dorsum of the tongue
o May be a similar lesion on opposed soft palate
o CC: sore tongue
Median Rhomboid Glossitis Diagnosis
Visual Diagnosis
Bacterium in Median Rhomboid Glossitis
C. albicans are found in surface epithelium in 85% of lesions
Chronic Mucoccutaneous Candidiasis
associated with a cell mediated immune infection, refractory to medication
Candidiasis Treatment and Prognosis
o Depends of type of infection
o Topical antifungal agents (Nystatin, Miconazole)
o Hyperplastic (nodular-plaque) types will require long term therapy
o 0.2% Chx
o More potent topical agens (fluconazole) for serious infection in immunocompromised hosts
Herpes Simplex Virus 1/2
Gingivostomatitis
Rapid onset with a characteristic set of signs and symptoms including fever, inflammation, and in young pts erythematous marginal gingivitis, and small painful vesicles
Herpes Simplex Virus 1/2
Gingivostomatitis Diagnosis
clinical features, history of positive contact and absence of lesions
Herpes Simplex Virus 1/2
Gingivostomatitis Conditions Considered (6)
ANUG, RAU, strep, stomatitis, erythema multiforme, acute leukemia
Recurrent Oral Herpetic Causes T1/2
o Requires depression of cell-mediated immunity
o Primary infection results in lifelong latency
o Can be induced by dental trauma, UV exposure, physical trauma, fever, immunosuppression
o First symptoms are burning/tingling (predrome)
Recurrent Oral Herpetic Histology & Diagnosis
o Involved keratinized mucosae of the attached gingiva and hard palate
o Form intra epithelial vesicles with multinucleated giant cell formation
Diagnosis: In some cells, intra nuclear viral inclusions are evident and can be stained
Varicella - Zoster (HHV-3) Lesions
o Cutaneous lesions that form vesicles and pustules and rupture, crust over, and heal
o Shingles is reactivation of Chickenpox
o Lesions confined to skin innervated by a single sensory spinal nerve
More common in older individuals
Varicella-Zoster (HHV-3) Symptoms
pain, paraesthesia, dysesthesia, followed by vesicular eruption , severe neuritis (painful)
Varicella-Zoster (HHV-3) Tx
prophylactic or early intervention with anti-viral medication, and prevention of post herpetic neuralgia
Epstein-Barr Virus (HHV-4) Further Infections and Associations
o Causes infectious mononucleosis and hairy leukoplakia in HIV infections
o Associated with malignancies like burkitt’s lymphoma, hodgkins lymphoma, nasopharyngeal carcinoma
Cytomegalovirus (HHV-5) Stages
o Asymptomatic after newborn period
o After an initial infection, life-long latency is established in salivary gland epithelium, endothelium, macrophages and lymphocytes.
Cytomegalovirus (HHV-5) Reactivation
o Immunosuppression or anti-cancer medication can lead to reactivation.
o Oral lesions present in immunocompromised pts
Painful, edematous ulcerations
Human Papilloma Virus (HPV) Oncogenic Potential
disable 2 tumor suppressor genes that regulate normal cell growth and host cell DNA repair
Human Papilloma Virus (HPV) Lesions
- Oral papillomas are most common lesion
o Similar appearance to oral verrucae (warts)
o Oral warts ass’d with HPV 2,6,11,57
Oral Condyloma Acuminatum (Venereal Warts)
o HPV incduced wart transmitted by sexual contact
o HPV 6,11,16,18
o Soft pink sessile papillated masses that develop in clusters
Focal Epithelial Hyperplasia (Heck’s Disease)
o Multiple flat papules or plaques of hyperplastic epithelium
o HPV 13 & 32
o Spontaneous regression of lesions without tx
