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OMOPOR > Infections > Flashcards

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
Q

Oral clinical findings of varicella (chix pox)?

A
  • Can precede skin lesions
  • Common: vermillion border of lips, palate, buccal mucosa, gingiva
  • Painless lesions
  • Usually affects one or more dermatome
26
Q

Clinical findings of acute and chronic herpes zoster (shingles)?

A

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
Q

Varicella’s histopathologic findings

A
  • Acantholysis with formation of Tzanck cells (similar to herpes simplex)
  • Virus laden epithelial cell exhibit chromatin margination and multinucleation
28
Q

Management of varicella?

A
  • 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
Q

Management of herpes zoster?

A
  • 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
Q

How does EBV infection spread?

A

Intimate contact, intrafamilial spread, saliva

31
Q

Symptoms of EBV?

A

Children: asymptomatic
Young adults: fever, lymphadenopathy, pharyngitis and tonsillitis
Older adults: fever and pharyngitis

32
Q

What 4 conditions is EBV associated with?

A
  1. Infectious mononucleosis
  2. Oral hairy leukoplakia
  3. Various lymphoproliferative disorders and lymphomas
  4. Nasopharyngeal carcinoma
33
Q

Treatment of infectious mononucleosis from EBV

A

Resolves within 4-6 weeks, but can use NSAIDs to minimise most common symptoms

34
Q

Oral manifestation of CMV that can sometimes be observed intraorally?

A

Circumscribed ulcer

35
Q

Treatment of CMV

A

Ganciclovir or valganciclovir

36
Q

Clinical findings of herpangina

A
  • 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
Q

Histopathology of herpangina and HFMD

A
  • 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
Q

Management of herpangina and HFMD

A
  • Supportive care with topical LA, analgesics and antipyretics
  • Monitor for systemic s/s
  • Usual course is 7-10 days

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