L9: bacterial and fungal infections part 1 Flashcards

(42 cards)

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
angular cheilitis clinical feature
- erythema - fissuring, scaling - tender - irritated, raw feeling
25
cause of angular cheilitis
older px OVD decrease so saliva pools at folded corners of mouth -> favour yeast infection
26
clinical features of denture stomatitis
- varying degrees of erythema - may have petechial hemorrhage - asymptomatic
27
what kind of patient does chronic hyperplastic oral candidiasis occur in?
those on long term immunosuppressive drugs or those very immunosuppressed eg renal transplant patient, leukemia etc
28
how do lesions of chronic hyperplastic oral candidiasis look like
whitish, ddx should be candidiasis differentiation can be done as normal candidiasis can be wiped off but chronic hyperplsatic cant
29
why is it necessary to treat asymptomatic chronic erythematous candidiasis
- 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
how to dx candidiasis?
- clinical presentation - cytologic preparations (periodic acid schiff stain) - biopsy then H+E stain, PAS stain, GMS stain (show fungal hyphae)
31
common fungal infections in immunocompromised px
- aspergillus - candida - histoplasma - mucor - rhizomucor
32
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 _____
- 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
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
- 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
cause of zygomycosis
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
what is the most common type of zygomycosis
rhino-orbital-cerebral type in nose
36
zygomycosis have regional spread via ____
paranasal sinus
37
zygomycosis affects what group of px the most
diabetes mellitus
38
how does zygomycosis spread into blood
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
clinical signs of zygomycosis
- proptosis - cranial nerve defect - palatal ulcer - facial swelling - multiple clouded sinuses
40
tx of zygomycosis
- debridement - intravenous amphotericin B regime to be implemented immediately
41
what are some topical agents used for anti fungal therapy
- oral nystatin: first line, swish and spit - clotrimazole: troches, cream - itraconazole: swish and swallow - amphotericin B: rinse - CHX: rinse - povidone iodine: rinse