Blk1: Bacterial, Fungal Infections & HSV

Question 1

What is the acronym MCATSS?

Answer 1

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

Question 2

bacteria type involved in ANUG

Answer 2

Gram negative bacilli
Part of the normal oral flora
o Treponema spriochetes
o Borrelia vincentii
o Fusobacterium nucleatum
o Bacteroides melanogenicus
o Prevotells intermedia

Question 3

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

Answer 3

FALSE

Question 4

Predespositions of ANUG

Answer 4

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

Question 5

Clinical Features of ANUG

Answer 5

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)

Question 6

Differential Diagnosis of ANUG

Answer 6

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

Question 7

Tx of ANUG

Answer 7

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

Question 8

Contributing Factors of TB

Answer 8

 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

Question 9

Initial Pathogenesis of TB

Answer 9

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

Question 10

Progression of TB

Answer 10

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)

Question 11

Oral Lesions Present with TB

Answer 11

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

Question 12

Differential diagnosis of TB

Answer 12

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

Question 13

Diagnosis and Tx of TB

Answer 13

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

Question 14

Primary Syphilis

Answer 14

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

Question 15

Secondary Syphilis

Answer 15

 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

Question 16

Tertiary Syphillis

Answer 16

 Can be years
 Multiple, chronic, inflammatory necrotic lesions (gummas) developing in CNS, heart, aorta, liver
 Can cause destructive lesions in palate and tongue

Question 17

Actinomycosis Infection Location, Bacteria

Answer 17

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

Question 18

Acinomycosis Tx

Answer 18

antibiotic management with incision and draining

Question 19

Candidiasis Pathological Mechanisms

Answer 19

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

Question 20

Candidiasis Predispositions (Systemic and Local)

Answer 20

o Systemic: infection, nutrition, malignancies, immune deficiency, physiological (pregnancy, infancy, old age)
o Local: xerostomia, antibiotic, nutrition

Question 21

Pseudomembranous Candidiasis Features

Answer 21

o White, wipeable patches on oral mucosa
o Burning mouth

Question 22

Pseudomembranous Candidiasis Diagnosis

Answer 22

based on history and clinical features and possibly staining

Question 23

Atrophic Candidiasis Features

Answer 23

Erythematous
Sore/Burning mouth
Chronic and Acute Inflammation
Denture stomatitis is a form

Question 24

Atrophic Candidiasis Causes and Diagnosis

Answer 24

Use of tetracycline, corticosteroids, and broad spectrum antimicrobials
Diagnosis based on C. albicans in smears

Question 25

Chronic Hyperplastic Candidiasis Features

Answer 25

o Irregular white patches (leukoplakia)
o Can be confused for dysplasia
o Nodular plaques do not wipe off

Question 26

Chronic Hyperplastic Candidiasis Diagnosis

Answer 26

Diagnosis based on history, clinical appearance, and histopathology

Question 27

Angular Chelitis Causes

Answer 27

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

Question 28

Median Rhomboid Glossitis & CC

Answer 28

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

Question 29

Median Rhomboid Glossitis Diagnosis

Answer 29

Visual Diagnosis

Question 30

Bacterium in Median Rhomboid Glossitis

Answer 30

C. albicans are found in surface epithelium in 85% of lesions

Question 31

Chronic Mucoccutaneous Candidiasis

Answer 31

associated with a cell mediated immune infection, refractory to medication

Question 32

Candidiasis Treatment and Prognosis

Answer 32

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

Question 33

Herpes Simplex Virus 1/2
Gingivostomatitis

Answer 33

Rapid onset with a characteristic set of signs and symptoms including fever, inflammation, and in young pts erythematous marginal gingivitis, and small painful vesicles

Question 34

Herpes Simplex Virus 1/2
Gingivostomatitis Diagnosis

Answer 34

clinical features, history of positive contact and absence of lesions

Question 35

Herpes Simplex Virus 1/2
Gingivostomatitis Conditions Considered (6)

Answer 35

ANUG, RAU, strep, stomatitis, erythema multiforme, acute leukemia

Question 36

Recurrent Oral Herpetic Causes T1/2

Answer 36

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)

Question 37

Recurrent Oral Herpetic Histology & Diagnosis

Answer 37

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

Question 38

Varicella - Zoster (HHV-3) Lesions

Answer 38

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

Question 39

Varicella-Zoster (HHV-3) Symptoms

Answer 39

pain, paraesthesia, dysesthesia, followed by vesicular eruption , severe neuritis (painful)

Question 40

Varicella-Zoster (HHV-3) Tx

Answer 40

prophylactic or early intervention with anti-viral medication, and prevention of post herpetic neuralgia

Question 41

Epstein-Barr Virus (HHV-4) Further Infections and Associations

Answer 41

o Causes infectious mononucleosis and hairy leukoplakia in HIV infections
o Associated with malignancies like burkitt’s lymphoma, hodgkins lymphoma, nasopharyngeal carcinoma

Question 42

Cytomegalovirus (HHV-5) Stages

Answer 42

o Asymptomatic after newborn period
o After an initial infection, life-long latency is established in salivary gland epithelium, endothelium, macrophages and lymphocytes.

Question 43

Cytomegalovirus (HHV-5) Reactivation

Answer 43

o Immunosuppression or anti-cancer medication can lead to reactivation.
o Oral lesions present in immunocompromised pts
 Painful, edematous ulcerations

Question 44

Human Papilloma Virus (HPV) Oncogenic Potential

Answer 44

disable 2 tumor suppressor genes that regulate normal cell growth and host cell DNA repair

Question 45

Human Papilloma Virus (HPV) Lesions

Answer 45

• Oral papillomas are most common lesion
  o Similar appearance to oral verrucae (warts)
  o Oral warts ass’d with HPV 2,6,11,57

Question 46

Oral Condyloma Acuminatum (Venereal Warts)

Answer 46

o HPV incduced wart transmitted by sexual contact
o HPV 6,11,16,18
o Soft pink sessile papillated masses that develop in clusters

Question 47

Focal Epithelial Hyperplasia (Heck’s Disease)

Answer 47

o Multiple flat papules or plaques of hyperplastic epithelium
o HPV 13 & 32
o Spontaneous regression of lesions without tx