Infections Flashcards

1
Q

Etiology of ANUG/P (including predisposing factors, causative organisms)

A

Predisposing factors:

  • Immunosuppression
  • Smoking
  • Local trauma
  • Poor OH

Causative organisms:

  • Fusobac nucleatum
  • Borrelia vincentii (spirochete)
  • Prevotella intermedia
  • Porphyromonas gingivalis

Can also occur in presence of psychologic stress - Trench mouth

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2
Q

What happens if ANUG is left untreated?

A

Can progress to ANUP if there is CAL. It can also spread to soft tissues, leading to necrotising ulcerative mucositis/stomatitis. Extension through the mucosa to the skin of the face is known as noma

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3
Q

Demographics and clinical findings of ANUG/P

A
  • More common in young and middle aged adults, rare in general population but increased in stressed or malnourished populations
  • Appears as highly inflamed interdental papillae which is erythematous, edematous and bleeds easily
  • Affected papillae are blunted with areas of “punched out”, crater-like necrosis covered by greyish pseudomembrane and necrotic gingival tissue
  • FETID ODOUR :(
  • Exquisite pain and spontaneous haemorrhage
  • Occasional lymphadenopathy, fever and malaise
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4
Q

Histopathology of ANUG/P

A
  • Thick fibrinopurulent membrane
  • Lamina propria infiltrated by inflammatory cells with extensive hyperaemia
  • Extensive BACTERIAL COLONISATION
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5
Q

Management of ANUG/P

A
  • Debridement (ScRP)
  • CHX, warm salt water, H2O2 rinses for bacterial removal
  • Systemic antibiotics if lymphadenopathy and fever present
  • Remove predisposing factors
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6
Q

Etiology of actinomycosis

A
  • Actinomycetes (normal oral flora component) infection
  • Acute, rapidly progressing infection or chronic, slowly spreading lesion ASSOCIATED WITH FIBROSIS
  • Organism enters tissue through area of prior trauma e.g. injury, perio pocket, non-fatal tooth, exo socket, infected tonsil
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7
Q

Clinical features of actinomycosis

A
  • Suppurative reaction of infection may discharge large SULFUR GRANULES that represent bacteria colonies
  • Indurated area of fibrosis forming central, softer area of abscess
  • Infection may extend to surface as sinus tract
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8
Q

Histopathologic findings of actinomycosis

A
  • Peripheral band of fibrosis encasing zone of chronically inflamed granulation tissue surrounding
  • Large collections of PMN leukocytes
  • Colonies of club-shaped filaments
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9
Q

Management of actinomycosis

A
  • Drain abscess, excise sinus tracts
  • Prolonged high antibiotic dosage to penetrate large areas of suppuration and fibrosis
  • AB: penicillin/amox or tetracycline
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10
Q

How is HSV-1 transmitted and where is it commonly observed?

A

Via infected saliva or active perioral lesions.

Seen on oral, facial and oclular areas + pharynx, i/o mucosa, lips, eyes, and skin above the waist

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11
Q

How is HSV-2 transmitted and where is it commonly observed?

A

Via sexual contact

Seen on genital zones involving genitalia and skin below the waist

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12
Q

After HSV primary infection is established, virus is taken up by sensory nerves and transported to the _________

A

Trigeminal ganglion

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13
Q

Dental condition commonly observed in people infected with HSV at early age

A

Gingivostomatitis

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14
Q

Dental condition commonly observed in people infected with HSV at later age

A

Pharyngotonsilitis

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15
Q

How does HSV recurrent infection occur?

A

Reactivation of the virus due to old age, UV light, physical/emotional stress, fatigue, heat, cold, pregnancy, allergy, trauma, dental tx, respi illness, fever, menstruation, systemic diseases and malignancy

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16
Q

Demographics and clinical findings of acute herpetic gingivostomatitis

A
  • Age: 6 months - 5 years
  • Abrupt onset, prodromal s/s 12-24h prior to appearance
  • Affected mucosa develops pinhead vesicles –> rapidly collapse to form numerous small red lesions –> enlarge and develop central ulceration covered by yellow fibrin
  • Gingiva enlarged, painful and extremely erythematous, often exhibiting punched-out erosions along midfacial FGM
  • Resolution 5-7 days (mild) to 2 weeks (severe)
17
Q

Demographics and clinical findings of herpes labialis

A
  • Prodromal signs: pain, burning, itching, tingling, localised warmth and erythema of involved epithelium 6-24h before
  • Multiple small, erythematous papules develop and form clusters of fluid-filled vesicles
  • Vesicles rupture and crust within 2 days, release virus-filled fluid may result in lesion spread
18
Q

Histopathologic findings of HSV-infected epithelial cells

A
  • Acantholysis –> Tzanck cells
  • Nuclear clearing and enlargement
  • Nuclear fragmentation with chromatin condensation around nucleus periphery
  • Multinucleated epithelial cells formed by fusion
  • Intracellular edema –> formation of intraepithelial vesicle
19
Q

Management of patients with HSV

A

Healthy: supportive and symptomatic care with topical LA, analgesics and adequate nutrition

Systemic therapy: Acyclovir (not usually given to healthy patients)

Recurrent: supportive care with topical LA, protection (vaseline, ZnO, sunscreen lip balm), topical antiviral, prophylaxis

20
Q

Where does VZV lie latent?

A

Sensory nerve ganglia

21
Q

Herpes zoster (shingles) risk factors include:

A
  • HIV infection
  • Radiation
  • Txt with cytotoxic or immunosuppressive agents
  • Presence of malignancies
  • Alcohol abuse
  • Stress
  • Old age
  • Dental manipulation
22
Q

Complications of varicella (chicken pox)?

A
  • Reye’s syndrome
  • Secondary skin infections
  • Encephalitis
  • Pneumonia
  • GI disturbances
  • Hematologic events: pancytopenia, thrombocytopenia, haemolytic anemia, sickle cell crisis
23
Q

Complication of herpes zoster (shingles)?

A
  • Ramsay Hunt syndrome –> facial paralysis, hearing deficits, vertigo
  • Post herpetic neuralgia –> pain triggered by light stroking of area persisting > 3 months after initial rash with gradual resolution, usually in >60 y/o and requires use of famacyclovir long term
24
Q

Dermatologic findings of varicella (chix pox)?

A
  • Initial: pruritic rash involving face and trunk to extremities
  • Erythema –> vesicle –> pustule –> crusting
  • Lesions continue erupting for 4-7 days, old lesions can intermix with new lesions
  • Contagious from 2 days before rash until all lesions crust
25
Oral clinical findings of varicella (chix pox)?
- Can precede skin lesions - Common: vermillion border of lips, palate, buccal mucosa, gingiva - Painless lesions - Usually affects one or more dermatome
26
Clinical findings of acute and chronic herpes zoster (shingles)?
Acute: clusters of fluid-filled vesicles on erythematous base which ulcerates --> crusting and resolves in healthy individuals Chronic: persistent pain > 3 months. Increased prevalence in older age Oral lesions: - Involving both keratinised and non-keratinised oral mucosa, occurring in conjunction with involvement of overlying skin - Devitalisation of teeth in affected quadrant - Bone necrosis due to bv damage causing focal ischemic necrosis Can also cause ocular involvement --> permanent blindness
27
Varicella's histopathologic findings
- Acantholysis with formation of Tzanck cells (similar to herpes simplex) - Virus laden epithelial cell exhibit chromatin margination and multinucleation
28
Management of varicella?
- Supportive care - No antivirals needed for healthy patients, but purified VZV Ig can be given to those immunocompromised, pregnant women and premature infants Prevention: - Live attenuated VZV virus vaccine
29
Management of herpes zoster?
- Supportive and symptomatic relief with antipyretics and antipruritics - Antivirals - Txt of post-herpetic neuralgia include early use of systemic antivirals, antidepressants, anticonvulsants and systemic steroids but lidoderm for symptomatic relief
30
How does EBV infection spread?
Intimate contact, intrafamilial spread, saliva
31
Symptoms of EBV?
Children: asymptomatic Young adults: fever, lymphadenopathy, pharyngitis and tonsillitis Older adults: fever and pharyngitis
32
What 4 conditions is EBV associated with?
1. Infectious mononucleosis 2. Oral hairy leukoplakia 3. Various lymphoproliferative disorders and lymphomas 4. Nasopharyngeal carcinoma
33
Treatment of infectious mononucleosis from EBV
Resolves within 4-6 weeks, but can use NSAIDs to minimise most common symptoms
34
Oral manifestation of CMV that can sometimes be observed intraorally?
Circumscribed ulcer
35
Treatment of CMV
Ganciclovir or valganciclovir
36
Clinical findings of herpangina
- Acute onset of sore throat, fever and dysphagia - Multiple small lesions on soft palate or tonsillar pillars - Red macules --> fragile vesicles --> rapidly ulcerate (2-4mm) --> healing (7-10 days)
37
Histopathology of herpangina and HFMD
- Affected epithelium exhibits intracellular and intercellular edema --> formation of intraepithelial vesicle - Vesicle enlarges and ruptures through epithelial nbasal cell layer with formation of subepithelial vesicle - Epithelial necrosis and ulceration soon follow
38
Management of herpangina and HFMD
- Supportive care with topical LA, analgesics and antipyretics - Monitor for systemic s/s - Usual course is 7-10 days