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omopor > L9: bacterial and fungal infections part 1 > Flashcards

L9: bacterial and fungal infections part 1 Flashcards

1
Q

4 bacteria causing NUG

A
  • Fusobacterium nucleatum
  • Borrelia vincetii
  • Prevotella intermedia
  • Porphyromonas gingivalis
  • polymicrobical infection by fusospirochaetal complex
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2
Q

ANUG presents in what types of ppl?

A
  • in young and middle aged adults
  • often occurs when physiologic stress present
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3
Q

predisposing factors of NUG

A
  • immunosuppression - drug induced
  • smoking
  • local trauma
  • poor nutritional status
  • poor OH
  • inadequate sleep/ rest
  • recent illness
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4
Q

clinical appearance of NUG

  • highly inflamed _____ , erythematous, edematous and bleeds easily
  • papillae are blunt and “_____”, with ______ lesions covered by greyish ________ + _____ gingival tissue
  • very distinctive _____ odor
  • ______ debri
A
  • highly inflamed interdental papillae, erythematous, edematous and bleeds easily
  • papillae are blunt and “punched out”, with ulcerative lesions covered by greyish psuedomembrane +necrotic gingival tissue
  • very distinctive fetid odor
  • necrotic debri
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5
Q

untreated NUG can progress to NUP if there is _____

A

loss of attachment

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6
Q

if NUG spreads to adjacent soft tissue, it will be known as _______

A

necrotizing ulcerative mucositis/ stomatitis

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7
Q

if the NUG necrotizing infection extends through the mucosa to the skin of the face, it is known as

A

noma: cancrum oris

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8
Q

histopatho features of NUG

  • non specific features showing ______ changes with thick ______ membrane
  • _______infiltrated by thick band of mixed _____ cells with extensive ____
  • extensive ______ present
A
  • non specific features showing ulcerative changes with thick fibrinopurulent membrane
  • lamina propria infiltrated by thick band of mixed inflam cells with extensive hyperemia
  • extensive bacterial colonisation present
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9
Q

tx for ANUG

A

there is resolution when causative bacteria is removed
- debridement
- frequent rinse with CHX, warm salt water, hydrogen peroxide
- systemic AB if lymphadenopathy and fever are present

  • improve OH
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10
Q

in recalcitrant cases of NUG, what must we rule out?

A

HIV infection or infectious mononucleosis

recalcitrant may be because of underlying immunosuppressive states

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11
Q

predisposing factors of fungal infection

A

changes in local oral flora
- may be due to AB therapy
- salivary gland dysfunction (decreased flow rate)
- removable dental appliances

changes in immunity
- local immunity: defensins, saliva, tissue injury
- immunosuppressive therapy
- medical conditions/ diseases
- cancer

inherited/ acquired autoimmune disease
- SCIDS/ DIGeroge’s syndrome/ other
- HIV/ AIDs

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12
Q

two common candida species

A
  • C albicans
  • C glabrata
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13
Q

risk factors for candidiasis

A
  • xerostomia
  • medications: AB, corticosteroid (topical/ systemic)
  • smoking
  • immune system changes
  • dentures
  • cancer
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14
Q

clinical presentation of oral candidiasis
which are red and white?

A

white – pseudomembranous candidiasis, hyperplastic candidiasis

red – erythematous, angular cheilitis, median rhomboid glossitis, denture stomatitis

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15
Q

clinical presentation of pseudomembranous candidiasis

A
  • white plaques resembling cottage cheese/ curdled milk
  • underlying mucosa is either normal or can be erythematous
  • can wipe/ scrape off
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15
Q

clinical presentation of pseudomembranous candidiasis

A
  • white plaques resembling cottage cheese/ curdled milk
  • underlying mucosa is either normal or can be erythematous
  • can wipe/ scrape off
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16
Q

symptoms of pseudomembranous candidiasis

A
  • burning sensation
  • unpleasant taste (salty/bitter)
17
Q

ddx of pseudomembranous candidiasis

A

leukoplakia and OLP
both white lesions but cant scrape off

18
Q

erythematous oral candidiasis is also known as what

A

atrophic oral candidiasis

19
Q

clinical presentation of erythematous candidiasis

A
  • red macules
  • ## smooth atrophic appearance of tongue (loss of filiform papillae, depapillation)
20
Q

location of erythematous candidiasis

A
  • buccal mucosa
  • posterior hard palate
  • dorsal tongue
  • because when we close our mouths, our tongue lies on hard palate so its likeluy to form a kissing lesion there
21
Q

what is median rhomboid glossitis

A

it is basically erythematous candidiasis but at the midline of posterior dorsal tongue

22
Q

clinical features of median rhomboid glossitis

A
  • well demarcated erythematous zone
  • atrophic mucosal areas (loss of filiform papillae). these areas are erythematous
  • smooth/lobulated surface
  • symmetrical
  • asymptomatic
23
Q

how to differentiate between benign migratory glossitis vs median rhomboid glossitis

A

benign migratory glossitis = geographic tongue
- geographic tongue is inside red outside white (patches have white rim) vs median rhomboid glossitis dont have
- geographic tongue patches move around, median rhomboid always in the middle

24
Q

angular cheilitis clinical feature

A
  • erythema
  • fissuring, scaling
  • tender
  • irritated, raw feeling
25
Q

cause of angular cheilitis

A

older px OVD decrease so saliva pools at folded corners of mouth -> favour yeast infection

26
Q

clinical features of denture stomatitis

A
  • varying degrees of erythema
  • may have petechial hemorrhage
  • asymptomatic
27
Q

what kind of patient does chronic hyperplastic oral candidiasis occur in?

A

those on long term immunosuppressive drugs
or those very immunosuppressed eg renal transplant patient, leukemia etc

28
Q

how do lesions of chronic hyperplastic oral candidiasis look like

A

whitish, ddx should be candidiasis
differentiation can be done as normal candidiasis can be wiped off but chronic hyperplsatic cant

29
Q

why is it necessary to treat asymptomatic chronic erythematous candidiasis

A
  • edematous soft tissue provides a poor base for prosthesis
  • chronic inflammation may increase bone resorption
  • may contribute to inflammatory papillary hyperplasia, which if severe may require surgical management
30
Q

how to dx candidiasis?

A
  • clinical presentation
  • cytologic preparations (periodic acid schiff stain)
  • biopsy then H+E stain, PAS stain, GMS stain (show fungal hyphae)
31
Q

common fungal infections in immunocompromised px

A
  • aspergillus
  • candida
  • histoplasma
  • mucor
  • rhizomucor
32
Q

histopatho findings of candidiasis

  • increase thickness of ______ layer with elongation of _______
  • _____ inflammatory cell infiltrate in _____ immediately subajcent to infected ______
  • small collections of _____ (microabscesses) in _____ and ______ layer
  • ______ embedded in parakeratin layer and rarely penetrate deeper, unless px severely _____
A
  • increase thickness of parakeratin layer with elongation of rete ridges
  • chronic inflammatory cell infiltrate in CT immediately subajcent to infected epithelium
  • small collections of neutrophils (microabscesses) in parakeratin and superficial spinous layer
  • hyphae embedded in parakeratin layer and rarely penetrate deeper, unless px severely immunocompromised
33
Q

histopatho findings of candidiasis

  • _______ of parakeratin layer with elongation of rete ridges
  • chronic ______ infiltrate in CT _____ (at which location)
  • small collections of neutrophils (______) in parakeratin and _______ layer
  • hyphae ______ in ______ layer and rarely penetrate deeper, unless px severely immunocompromised
A
  • increase thickness of parakeratin layer with elongation of rete ridges
  • chronic inflammatory cell infiltrate in CT immediately subajcent to infected epithelium
  • small collections of neutrophils (microabscesses) in parakeratin and superficial spinous layer
  • hyphae embedded in parakeratin layer and rarely penetrate deeper, unless px severely immunocompromised
34
Q

cause of zygomycosis

A

arise from inhalation or implantation of spores by minor trauma or insect bites
then hypersensitivity reaction produces inflammation, granulations and necrosis, causing local destruction

35
Q

what is the most common type of zygomycosis

A

rhino-orbital-cerebral type in nose

36
Q

zygomycosis have regional spread via ____

A

paranasal sinus

37
Q

zygomycosis affects what group of px the most

A

diabetes mellitus

38
Q

how does zygomycosis spread into blood

A

angioinvasive properties of the fungi lead to arterial occlusion and infarction -> causes tissue necrosis

then organism thrives in dead organic tissue, spreads along injured blood vessels (spread very fast and far)

39
Q

clinical signs of zygomycosis

A
  • proptosis
  • cranial nerve defect
  • palatal ulcer
  • facial swelling
  • multiple clouded sinuses
40
Q

tx of zygomycosis

A
  • debridement
  • intravenous amphotericin B regime to be implemented immediately
41
Q

what are some topical agents used for anti fungal therapy

A
  • oral nystatin: first line, swish and spit
  • clotrimazole: troches, cream
  • itraconazole: swish and swallow
  • amphotericin B: rinse
  • CHX: rinse
  • povidone iodine: rinse

omopor (11 decks)

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