Blk1: Bacterial, Fungal Infections & HSV Flashcards by Jenna Jomha

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

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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

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T/F Pre existing periodontal disease is a prerequisite of ANUG

FALSE

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Predespositions of ANUG

Stress
Smoking
Trauma
Nutrition
Systemic conditions
- with physical and emotional stress, frequency of ANUG inc from 0.1% to 7%

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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)

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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

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Tx of ANUG

o Local debridement
o Rinsing with oxygenating agents (hydrogen peroxide)
o Antibiotics (metronidazole)
o Potential for recurring infection

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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

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Initial Pathogenesis of TB

Aerobic Bacillus
Passes through aerosols, induces a T-cell mediated immune response of the delayed hypersensitivity type

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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)

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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

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Differential diagnosis of TB

 Syphilis
 Major aphthae
 Traumatic ulcerative granuloma
 Oral squamous cell carcinoma
 Deep mycotic infections

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Diagnosis and Tx of TB

Diagnosis: tb tests and biopsy
Tx: includes tx of primary disease

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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

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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

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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

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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

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Acinomycosis Tx

antibiotic management with incision and draining

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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