Unit 3 Flashcards
1
Q
TF? Mature plaque is composed of gram-negative and not gram+ bacteria.
A
F. Both, greater proportion of gram -, also fungi and other organism
2
Q
How do the # of bac spp vary?
A
site to site, P2P
3
Q
Late colonizers:
A
T. denticola, P. gingivalis, A. actino… , P. intermedia, Eubacteria, S. flueggel, C. sputigena, fusobacterium nucleatum (bridge bw early and late)
4
Q
Affect bac colonization:
A
genes, age, indegenous flora/ competition, host response, food, environment
5
Q
4 habitats in mouth:
A
tongue, buccal mucosa, tooth plaque (sub and supragingival), saliva
6
Q
Cheeks, lips, palate:
A
low diversity of microflora, fac anaerobes, Strept spp mainly, some perio pathogens persists by invading the buccal CELLS
7
Q
Tongue:
A
diverse microflora, fac and obligate anaerobes, (StRAN) Strep, Rothia, Actinomyces, Neisseria, some gram - anaerobes, some anaerobic sites
8
Q
Teeth:
A
diverse microflora, many obligate anaerobes, (STAF VP) Strep, Treponema, Actinomyces, Fusobacterium, Veillonella, Prevotella, unculturable organisms, influenced by saliva and GCF
9
Q
2 most prominent cultivatable bac spp pop in saliva, buccal mucosa, tongue dorsum, and supragingival plaque
A
S oralis and S. mitis
10
Q
5 most prominent cultivatable bac pop in tongue dorsum:
A
S. oralis/ mitis/ salivarus, A. naeslundi, Haemophius spp.
11
Q
4 most prominent cultivatable bac pop in supragingival plaque:
A
A. naeslundii, A. odontolyticus, S. mutans, S. sanguinis,
12
Q
bacterial like this temp range:
A
33’-37’C, sulci: 33’-36’C, perio: 39’C
13
Q
Effect of inc temp on bac expression:
A
inc expression of some proteins
14
Q
palatal, buccal mucosa, healthy gingival crevice, & diseased gingival crevice pH
A
7.34, 6.3, 6.9, 7.4+
15
Q
critical pH:
A
5.5
16
Q
3 bac to that can survive at the highest pH
A
S. mutans, Lactobacilus, P. gingivalis,
17
Q
5 bac that can survive at the lowest pH:
A
S. mutans/ sobrinus/ sanguinis, Lactobacilus, Actinomyces (root caries)
18
Q
Most oral organisms are:
A
most anaerobic, fac or obligate anaerobes, early O2 rich, mature anaerobic
19
Q
This flow is increased in pd:
A
GCF, from circulatory system, nutrients, proteins, inflammatory cells, host defense
20
Q
Endogenous nutrient availability:
A
Saliva, GCF, bac products
21
Q
nutrients from saliva:
A
protein, glycoprotein, AA’s, peptides
22
Q
Nutrients from GCF:
A
protein, glycoprotein, albumin
23
Q
How are exogenous nutrients used in the oc?
A
up to EC polysacs or down to lactic acid
24
Q
extrapolysaccharides used for glucan and fructan synthesis:
A
glucose or fructose
25
Why are glucans/ fructans built and what are they built from?
extra food source in times of famine, extra food source, sucrose
26
Glucans, soluble or in-?
either
27
How are intracellular ps's used?
energy
28
How are extracellular ps's used?
biofilm, adhesion via S. mutans and other bac
29
Type of glucan S. mutans makes from sucrose, soluble or insoluble?
both water-soluble and water-insolube glucans
30
Uses of water-soluble glucans:
energy, lactic acid formation
31
Uses of water-insoluble glucans:
plaque accumulation (sticky, hard, cement-like)
32
Why older pts have different bac in oc:
other diseases, meds, esp. antibiotics, weak IS, dec saliva, dentures
33
Why are dentures prone to fungus accumulation?
differences bw the 2 surfaces
34
3 bac, not detectable at 3mo, detectable at 32mo:
(SPF 32) Selenomonas, P. denticola, Fusobacterium nucleatum
35
4 bac that were found in 100% of 32mo old kids:
(F*** PCP) Fusobacterium nucleatum, P. melaninogenica, Capnocytophaga, non-pigmented Prevotella
36
Bac w largest inc after tooth eruption, highest first:
(F*** PCP) Fusobacterium/ P. denticola, Capnocytophaga, P. loescheii,
37
Bac found in just after birth:
S. mitis/ S. salivarius, a. naeslundii (?)
38
Commensal bac's:
S. sanguinis, gordonii, oralis, mitis (That bloody at bitch can commence giving me head bc it's mighty good))
39
Structural formation of initial microcolonies:
columnar
40
TF? All pioneer spp. are rod shaped.
F. cocci, layer on pellicle.. Strep..COCCI
41
TF? Later plaque is comprised mainly of rod shaped bac.
T
42
Which adhere more tightly, early or late colonizers.
Late, denser, break off, disease in distant sites (harder for a pt, with the same amt of effort, to clear mature plaque than early plaque?)
43
More anaerobic bac:
P. gingivalis, T. forsythia, spirochetes like T. denticola
44
TF? In ppd, plaque is deeper in crevice, and invade INTO epi cells
T.
45
Are gram - bac capable of invading the CT and collagen?
yes
46
Define calculus:
calcium phosphate on tartar, rough surface, colonizing spot
47
After how many days of not brushing will gram - rods appear in the oral bac?
~5d
48
After how many days of not brushing will spirochettes appear in the oral bac?
~10d
49
How many days did it take to get rid of gram - bac once a person began brushing?
~5d
50
This is used as a measure of gingivitis:
gingival index
51
How many days after not brushing did gingivitis begin?
~10, same time as appearance of spirochetes
52
This bac initially inc in the 1st wk of not brushing, then dec:
S. sanguis
53
These 2 bac both inc weekly w not brushing:
A. viscosus, F. nucleatum
54
Bac found in fissures:
Strep, actinomyces, Gram +, fac anaerobes
55
Bac found in approximal areas:
Gram + & -, fac and obligate anaerobes: (SPANV-span the V shaped embrasure from tooth to tooth) Strep, Prevotella, Actinomyces, Neisseria, Veilonella
56
Bac found in gingival crevice:
Gram + & -, fac and obligate anaerobes, (SAFE TP) Strep, Actinomyces, Fusobacterium, Eubacterium, Treponema, Prevotella
57
Are cariogenic plaque bac more acid producing or acid tolerating?
both
58
TF? The proportion of S. mutans inc w caries progression.
F. dec
59
Most oral bacteria, motile or non-motile?
non-motile, no flagella, carried by salivary flow
60
Causes of expulsion or death of bac:
agglutination, mechanical shearing, antimicrobial saliva, antagonistic bac
61
Promote colonization:
adherence properties, synergistic bac, nutritional substrates, temp and moisture
62
Proteins & glycoproteins in pellicle formation:
mucins, agglutinin, PRP's, amylase, sialic acid
63
Bacterial components of pellicle:
glucan (sugar chains), glucosyltransferase (Gtf)
64
1st 3 steps in bac colonization:
assoc, adhesion, invasion
65
This is a weak, reversible attachment:
associaton
66
Is bac assoc reversible or ir-? Type of bond?
reversible, electrostatic
67
Is adhesion reversible or -ir?
irreversible
68
These are responsible for adhesion:
adhesins, complementary molecule on host surface
69
beginning of complex biofilm formation:
coaggregation
70
Adhesion is interaction bw:
bac adhesin & pellicle or cell receptor
71
Host surface receptors to which bac can attach:
glycan, glycolipid, glycoprotein, ECM glycoprotein, surface integrin, fibronectin
72
Pili or fimbriae attachment is to:
glycolipid or glycoprotein
73
Afimbrial adhesin attachment is to:
glycan, ECM glycoprotein, surface integrin, fibronectin
74
bac attach to pellicle via:
PRP's, a-amylase, sialic acid, statherin (PASS)
75
bacterial/ metabolic food chains:
complex substrates ---> 1' feeder --> product --> 2' feeder --> simpler product
76
aerobic early/ secondary colonizers:
capnophilic, facultative anaerobes
77
Autoinducer-2:
universal interspecies signal, luxS, in both gram + and - bac
78
Competence stimulating peptide (CSP):
Strep quorum sensing signal, induces genetic competence enabling exchange of free DNA to transformation-competent cells
79
Carriage of this can prevent against S. areus carriage:
S. pneumoniae
80
pneumococcal conjugate vaccine inc rate of:
Staph areus and related diseases
81
S. pneumoniae protection against S. areus can be disrupted by
vaccinating kids w pneumoccocal conjugate vaccines (red carriage of vaccine-type S. pneumoniae in nasopharynx)
82
P. gingivalis bind this weakly in suspension and tightly on surface:
S. gordonii
83
oxygen req for P. gingivalis:
obligate anaerobe, redox pot must be low, O2 scarce
84
Site of P. gingivalis attachment to plaque:
S gordonii
85
Types of viral infections that inc susceptabilty to bac infection
measles, retroviruses
86
Diseases caused by combo of 2 or more nonpathogenics
abdominal/ lung/ brain abscess or subdural empyema, 2' peritonitis, odontogenic infection, chronic otitis media or mastoiditis, liver infection, soft-tissue infection, fasciitis, bacteremia
87
TF? All polymicrobial infections depend on biofilm for resulting infection.
F. Most
88
Can single spp result in alv bone loss?
yes
89
symbiosis gone awry:
dysbiosis
90
Causes of altered commensal bac composition:
inc total commensal bac load, inc sp oral bac
91
These can be found in subgingival samples from aggressive periodontitis:
EBV, CMV, herpes, (ech...)
92
Proposed mech of interaction bw Herpes and perio bac:
Herpes lowers local defense, increasing aggressiveness of pd causing bac, bac inc virulence of herpes
93
Virus found in highest number in pd:
EBV, CMV, Herpes-1, 7, 8, 6
94
VIruses found w ANUG + malnutrition:
coinfection > CMV > EBV-1
95
Lesions S. mutans induces in animal models:
smooth, fissure and root lesions
96
Dominant bac spp. in rampant caries:
Lactobacillus spp, inc sig from initial to deep lesion
97
Is Lactobacillus found in healthy pts?
no
98
Is there a sig assoc bw S mutans and caries progression?
no
99
Bac assoc w caries progression but not found at high levels:
Propionibacterium
100
Additional candidates for progression of caries:
S. mitis, Selenomonas, Neisseria (MSN)
101
Periapical osteitis is aka:
apical peiodontitis
102
TF? Chronic endo infections are always of polymicrobial etiology.
F. Almost always
103
Routes of endo infection:
dentinal tubules, open cavity, perio sulcus via lateral canal or apical foramen, defective restoration, bacteremia
104
Cause of inflammation in apical periodontitis:
irritants seeping out of inflamed or necrotic pulp
105
Irritants that can cause inflammation:
bac, their toxins, trauma, debris added during endo
106
Apical periodontitis is aka:
granulomas (check)
107
Central zone cells of apical periodontitis:
plasma cells and lympho
108
Area beyond the central zone:
fibrous capsule (circular layer), outer margin limits bone regeneration
109
Duration for complete necrosis of pulp w granulomas and abscesses due to pulp exposure in rats:
9d+
110
This occurred 14-28d after pulp exposure in germ free rats:
dentinal bridging (?what is this?)
111
PA reaction of strep:
weak
112
Can enteroccoci survive when introduced as a single strain in apical periodontitis?
Yes
113
Result of adding single strains to apical periodontitis:
reestablishment of "8 Strain collection"
114
Root lesion bac composition, highest to lowest %:
S. anginosus, fusobacterium nucleatum, bacteroides forsythus
115
Bac NOT found in pus samples:
Actinomyces israelii, actinobacillus actinomycetemcomitans or fungal spp.
116
Bac found in endo infections:
red complex, Prevotella intermedia, Porphyromonas endodontalis, Fusobacteria, G+ anaerobic rods: filifactor alocis, actinomyces, G+ cocci: strep, enterococcus faecalis
117
Bac often found in failed root canals:
Enterococcus faecalis
118
Enterococcus faecalis:
failed root canals, in poor nutrient supply, resist meds (Ca2+ hydroxide, Na+ hypochlorite), pH, salinity & antibiotics, forms biofilm in canal
119
ANUG is aka:
Trench mouth, Vincent's gingivitis
120
These predispose to ANUG:
stress, malnutrition, smoking, immnodeficiency
121
ANUG:
necrosis of gingival margin and interdentinal papilla, pain, swelling, odor, NUP also possible
122
Bac in NUG:
fusobacterial and spirochetal forms, wide range of spp, many anaerobes
123
Potentially life-threatening cellulitis of floor of mouth, usually in adults w dental infections, can restrict airway:
Ludwig's angina
124
Ludwig's angina is aka:
Angina ludovici
125
NOMA is aka:
cancrum oris
126
NOMA:
orofacial gangrene, malnourished kids, POH, debilitating concurrent illness, begins as ulcer of mucous mem w edema of face extending out, rapidly destroys soft tissue and bone, almost always fatal wo tx
127
NOMA is attributable primarily to:
intrauterine growth retardation (check)
128
Is NOMA a primary disease?
No
129
Illnesses that predispose to NOMA:
malnutrition, measles (viral predisposing to bac infection), TB, leukemia, AIDS
130
Initial lesion of NOMA could appear as:
common cellulitis
131
Role of malnutrition in NOMA:
alters cell-mediated immune function, breaks down epi tissues, then invasion by pathogens
132
Microbial etiology of NOMA:
probably Borrelia vincentii and Fusobacterium, esp F. necrophorum, mixed w others
133
Possible role of F. necrophorum in NOMA:
rapid spread thru soft tissue bc it produces dermatotoxins
134
This creates a staging period of NOMA:
infection w endemic viruses
135
Cytokine profile shift seen in NOMA:
inflammatory to anti-inflammatory cytokines
136
Factors involved in NOMA path:
malnutrition, impaired oral mucosal immunity, immune dysfunction, infection w endemic viruses, effective structural integrity of oral mucosa, selective overgrowth of pathogenic microorganisms, inc oxidative stress, shift from inflammatory to anti-inflammatory cytokine profile
137
NOMA tx:
might be resistant to penicillin, use amoxicillin-metronidazole (last 2 letters of NOMA backwards)
138
Tx of polymicrobial infections:
debridement, incision, drainage, SRP, RCT, antibiotics, improved OH and regular visits
139
difficulty in articulating words due to disease of the central nervous system
dysarthria
140
Case: sudden dysarthria, L-sided hemiparesis, multilobar hemorrhagic lesion involving R thalamus w edema extending to brainstem, lots of periapical radiolucencies:
Brain abscess, G+, Strep intermedius, no issue in blood or Xray
141
Most common dental bac that leads to brain abscess:
Polymicrobial, then Fusobacterium spp (Gram -), Peptostreptococcus spp, Strep intermedius
142
Systemic infections w dental etiology:
Liver, brain, bone, lung, soft tissue infections, infective endocardiits
143
Bone infection is aka:
osteomyelitus
144
Soft tissue infections occur:
in muscle
145
Pts must likely to get thrush:
infants, IC, older, tumors, burns, oral prosthesis, catheters, hemodialysis, antibiotics, corticosteroids, antineoplastic or psycho-active drugs
146
% of pop that are carriers for OC:
35%
147
1st question if patients presents w oral can:
are you on antibiotics?
148
Why psycho-active drugs predispose to OC:
decrease saliva flow, predispose to oral can
149
OC:
Can really only colonize mouth, not found anywhere else, no other animals, not in soil, etc. HUMANS ONLY, been w us for a long time
150
Are neonates or infants more likely to get OC?
infants, 1-18mo (44%)
151
Why are neonates at lower risk for OC than infants?
maternal immunity
152
Where can the yeast be found in mouth?
tongue, palate, buccal mucosa, max denture, saliva, NOT man denture
153
Are candida spp normally found on the skin?
yes
154
C. albicans most to least prevalent locations in body:
mouth, vagina, resp tract, urine/pus, blood
155
2 most common Candida spp in oral cavity after albicans:
glabrata, then tropicalis
156
Projections from candida that extend into deeper layer:
hypha
157
Cationic antifungal peptides:
calprotectins, histatins
158
histatins are anti:
fungal
159
Th1 response to candidiasis:
IL12, IFNy, protective
160
Th2 response to candidiasis:
IL4, 5, 10, non-protective
161
protective response to candidiasis:
Th1 and 17 response, IL12, IFNy, IL-17, 23
162
non-protective response to candidiasis:
Th2 response, IL4, 5, 10
163
Th17 response to candidiasis:
Protective, IL-17, 23
164
Primary response to candidiasis:
TH17, protective Il-17, 23
165
Cells involved in innate immune response:
PMNs, macs
166
Localized candidiasis can focus here:
kindey, liver, spleen, endocarditis
167
Localized candidiasis w high mortality rate, difficult to treat:
spleen
168
Disseminated candidiasis is aka:
candidal septicemia
169
TF? Biopsy is an easy, effective method to dx candidiasis.
F, bc it is normally there in mouth, T if it is in another organ
170
Why have deaths due to systemic candidiasis risen since the 60s?
more ppl living w immune suppression
171
Cause of chronic mucocutaneous candidiasis:
immune dysfunction
172
Cx ind of chronic mucocutaneous candidiasis:
persistent superficial lesions
173
TF? chronic mucocutaneous candidiasis responds well to antimycotic agents.
F. poor response
174
If a person has persistent superficial lesions, what is the % likelihood that there is an oral manifestation of the disease?
90%
175
Tx for chronic mucocutaneous candidiasis:
antifungal
176
Cutaneous candidiasis can be on these body parts:
under/ around finger nails, crease of elbow, groin, moist, hidden areas
177
Acute pseudomembranous OC is aka:
thrush
178
Underlying disease assoc w OC:
leukemia, diabetes, xerostomia (radiation, drug induced), AIDS
179
OC is often diagnosed before this underlying disease is found:
leukemia
180
Tx for OC in infants:
time, antifungals
181
About __% of HIV patients will have oral Candidiasis at some point.
90
182
Cell count assoc with initial dx and severity of HIV:
CD4
183
Prevalence of candidiasis in HIV infected individuals:
9-90%
184
Dx of acute pseudomembranous candidiasis:
circumscribed white plaques, microbial smears, leaves red underlying tissue when wiped away, classic hyphae form under microscope
185
Are the colonies of acute pseudomembranous candidiasis confluent?
no
186
TF? OC can be on both the hard and soft palate.
T
187
Why is denture induced stomatitis rarely under lower denture?
attached KERATINIZED tissue
188
Which is more inflammatory, denture induced stomatitis or OC?
DIS
189
TF? There is invasion of the palatal epi in DIS.
F.
190
Type of inflammation in DIS:
diffuse sub-epi
191
Cause of inflammatory reaction in DIS:
yeast proteases, secreted
192
IR to DIS:
innate immunity, no cell mediated IR (it doesn't enter the cell!)
193
Candida spp isolated from DIS in greatest proportion:
C. albicans
194
3 Candida spp isolated from DIS:
C. albicans, C. tropicalis, C. glabrata
195
How is DIS classified?
severity of inflammation
196
Cx signs of DIS:
usually asymptomatic, itching, burning, dryness, usually not assoc w infection
197
What infection is DIS usually associated with?
None.
198
Newton Type 1 DIS:
pinpoint erythema, enlargement of palatal minor duct orifices, small localized areas of inflammation
199
Newton Type 2 DIS:
diffuse hyperemia & erythema, inflammation of denture bearing area only
200
How to know if erythema under a denture is DIS or simple irritation?
of candida present
201
Inflammation in Newton Type 2 DIS is localized here:
under max denture
202
Newton Type 3 DIS:
epi hyperplasia, granular or nodular lesion, diffuse erythema, entire palate, ground hamburger meat appearance, spongey, soft feel
203
Etiology of DIS:
yeast AND bac, prosthesis overuse/misfit, lack of saliva to affected area, (salivary antifungal histatins, re-infection from denture)
204
TF? mechanical inflammation can lead to DIS.
T. ill-fitting dentures
205
How to determine if OC is DIS or APC:
past border of denture - acute pseudomembranous candidiasis
206
Can we clean dentures with chlorhexidine?
No, it will stain them
207
Candida leukoplakia (CL) is aka:
chronic hyperplastic candidiasis
208
CL:
discrete areas, can't be removed, on buccal mucosa, assoc w tobacco use and atypia
209
candida is always:
superficial and removable w gauze
210
Angular cheilitis (AC):
fissuring, soreness, redness, may be white, may be assoc w other forms of OC
211
Tx for AC:
Nystatin, 5 X day (pid?)
212
Pts prone to AC:
overclosed pts
213
Midline glossitis (MG): is aka:
Median rhomboid glossitis, antibiotic sore tongue, papillary atrophy
214
MG:
deep red midline of tongue, not actually candida
215
2 major classes of antifungal drugs:
polyene, azole
216
MOA of polyenes:
mem disruption, perforation
217
MOA of azoles:
inhibit ergosterol synthesis, main fungal sterol
218
Toxic polyene when delivered systemically:
Amphotericin B, last resort when pt will die wo, causes kidney damage
219
Topical polyene:
Nystatin (Mycostatin) (AC)
220
Topical azole:
Clotrimazole (Mycelex, e.g. Mycelex 7- yeast infection)
221
2 systemic azoles:
Ketoconazole (Nizoral), Fluconazole (Difflucan)
222
Give this as a prophylactic to AIDS pts:
Diflucan
223
2 drugs for vaginal candidiasis:
Ketoconazole (Nizoral) (check), Fluconazole (Diflucan)
224
Issue w topical tx:
Pt must dissolve 1 tablet 5 times daily for 10d, poor compliance, vs. systemic: 1 daily for 3k
225
Adjunct therapies for candidiasis:
chlorhexidine rinse, neutral NaF
226
When to Rx chlorhexidine as prophylactic:
IC, irradiated, leukemic pts
227
When to use neutral NaF as an adjunct therapy:
while using Nystatin topical agents (AC)
228
Does chlorhexidine (0.2%) target bac or yeast more?
bac
229
Prescribe this w Nistatin/ Mycostatin for pt w teeth:
NaF (1%)
230
2 forms of topical treatment for DIS:
troche, pastilles
231
2 topical drugs to treat DIS:
Mycelex, Mycostatin
232
Which tx is a pt more likely to comply w for DIS?
mycelex, 3/d vs. 5/d
233
Overall tx for DIS:
topical, disinfect dentures, chlorhexidine rinse
234
When to prescribe prophylactic fluconazole to HIV pts:
CD4 count under 100, 1 episode of candidiasis
235
What type or candidiasis are HIV pts likely to get?
oropharyngeal candidiasis, emergence of resistant spp
236
Antifungal that is ineffective in tx of oropharyngeal candidiasis in HIV pts:
topical antifungals
237
Are pts likely to comply w Difflucan tx for OC or HIV pts?
yes, 1/d or 1 every other day
238
Key point in the treatment of any OC:
address underlying cause, prevent recurrence
239
OC arises in:
commensalism
240
Can cross infection occur w OC?
yes
241
Human cells are about __ X larger than bac and the adult human body has __ X more microbial cells than the human cell:
10, 10
242
TF? Humans are wo any microorganisms in the placenta.
T
243
First exposure to microorganisms:
vaginal canal, sterile until rupture of amniotic membrane
244
Most microbial cells inhabit:
mucosal surfaces
245
Largest microbial community in body:
colon (up to 100 trillion bac)
246
A person's microbial community is established by this age:
2
247
Strongest (?) influencing factor in a person's microbial community:
genetics, twins very similar
248
Lager health effects of gut microbial flora on body:
fat storage, obesity
249
2 lifestyles commensals can have:
commensalism, mutualism
250
Commensalism:
unidirectional, 1 benefits, other unharmed
251
Mutualism:
Synergistic, both benefit
252
Bifidobacterium longum, commensal or pathogen?
commensal, in gut, promotes health, possible role in digestion & processing of "non-digestible" plant polymers
253
Bacillus anthracis, commensal or pathogen?
pathogen, resp and skin infection
254
What type of pathogen is S. aureus?
opportunistic, multiple infections, 100,000+/yr, 30% have w no effect
255
Bacterium causing disease depends upon:
inherent virulence, host response, bac count
256
These inc inherent virulence of an organism:
virulence factors, enterotoxins
257
TF? Bac is always required in high numbers to cause disease.
F. depends on the virulence of the bac
258
prototypical biofilm:
plaque
259
factors affecting bacterial composition:
pH, O2, temp, redox potential, nutrients
260
Cause endo infection:
caries, exposure through trauma, bloodstream bac (not common), resto tooth interface, perio attachment loss, radicular dentin (?)
261
1st to discover bac:
Leeuwenhoek
262
Bac assoc with pain:
B. melaninogenicus
263
Most common bac in mouth:
actinomyces and fusobacterium naeslundii
264
Oxygen requirement of most bac in mouth:
anaerobic
265
to id Antigens sp to a bacteria
Immmunofluorescnce
266
Tolerate acidic condition and inc susceptibility to caries:
s. mutans and sobrinus
267
Red complex, new periodontal paradigm to include:
Filofactor alocis, Gram + bacilus
268
Filofactor alocis:
Gram + bacilus
269
Problems w id'ing all oral bac:
inability to cultivate, inadequate media, metabolic interdependencies
270
Strep produces ___, which is a nutrient for____
lactate, Veillonella
271
List all taxonomical groups for S. gordonii:
Bacteria, Frimuicutes, Bacilli, Lactobacilus, Streptococcacae, Streptococcus, gordonii
272
Term used instead of species to refer to a novel cluster of sequences:
phylotype, usually >2% difference in 16 sRNA sequences = distinct phenotype
273
Form the 50s subunit of rDNA:
23s and 5s (31 proteins)
274
Form the 30s subunit of rDNA:
16s (21 proteins)
275
50s and 30s subunit combine to form:
70s
276
Most evolutionarily conserved macromolecule:
16s rDNA, ued to determine relatedness
277
Which yields a more diverse view ot he oral flora, direct amplification or cultivation?
direct amlificaiton of 16s rDNA
278
Bac w a high level of genetic variation or diversity w/in individuals:
S. mitis
279
Methanobrevibacter smithii:
in gut, assoc w sever pd in mouth, health in clon, consumes end products of bacterial fermentation, combines H w CO2 to form methane
280
Non-albicans candida is most often found:
in blood
281
TF? The Th1 response will prevent candidiasis infection if the Th17 response is inhibited.
need Th17
282
Places to which candidiasis disseminates:
lungs, meninges, GI tract, dx these via culture
283
Where in mouth can candidal leukoplakia be found?
buccal mucosa only
284
Kids using asthma inhalers may get:
midline glossitis
285
pastille drug:
mycostatin (nistatin)
286
troche drug:
mycelex
287
What not to Rx for HIV pts with OC:
topicals
288
Are spirochetes free-living or symbiotic?
both
289
Only bac group w periplasmic flagella:
spirochetes
290
Ex of spirochete commensalism:
clam and termite digestive tracts
291
Causes relapsing fever:
Borrelia hermsii
292
Causes Leptospirosis:
Leptospira interrogans
293
Causes of Lyme d. and Syphillis:
Borrelia burgdorferi, T. palladium
294
Spatial distribution of P. gingivalis and T. denticola in plaque:
co-localized
295
Assoc of spirochetes w oral diseases, highest to lowest:
early onset, adult, localized juvenille periodontitis
296
TF? There are fewer spirochetes after tx than in health.
F. more
297
Most common bac in endo infection:
T. socaranskii, T. denticola, T. amylovorum, T. medium, T. maltophilum (T. madms)
298
Trep that can be cultivated:
T. denticola
299
Virulence factors of spirochetes:
cytotoxicity, tissue invasion and destruction, immnomodulation
300
Facilitates tisseu invasion by spirochetes:
chymotrypsin like protease, degrade laminin, fibronectin
301
These are being resisted in immunomodulation:
complement, neutrophils
302
T. denticola affects on fibrolasts:
degranulation, actin rearrangement, detachment
303
T. denticola affects on epi cells:
degranulation, membrane blebs, cytoskeleton, disruption and death
304
Macs, when activated by T. denticola, acitvate:
IL-1, TNF-a
305
Fxn of metalloproteinases:
disrupt gingival tissues
306
How does T. denticola avoid PMNs?
O2 production inhibition, release of enzymes like metalloproteinases
307
Fxn of cystalysin:
break cystein glutathione down to pyruvate, NH3, and H2S, which then are used for energy, to break RBCs and, promote perio lesions, anti-acid, inc oral mucosa permeability, and hydrolyze disulfide bonds of IgG, cytokines and chemokines
308
coincubation of Tmac w complement:
R chain of c3 & a-chain of C4 degrade
309
How does T. denticola inhibit neutrophil activation and migration?
MSP
