Microbiology Flashcards
Definition of caries
Biofilm-induced acid demineralization of enamel or dentin, mediated by saliva
Interaction of cariogenic microorganisms (M.S.) and fermentable carbohydrates (sucrose) induces demineralization
4 types of transmission of cariogenic bacteria:
- Direct saliva: kissing
- Indirect objects: sharing utensils, pacifiers
- Vertical from caregiver. MS genotype in infants identical to moms in 24-100% of pairs in 17 studies
- Horizontal from siblings/children @ daycare. One S-ECC study showed non-maternal MS genotypes in 74% children
What is colonization of bacteria related to?
Magnitude of inoculum
Frequency of inoculum
Minimum infective dose
Can MS colonize pre-dentate infants?
Yes, in furrows of tongue, associated with Bohn’s nodules.
Earlier transmission increases caries risk.
Mean age of MS colonization in dentate infants is 15.7 months
What bacteria is responsible for initiation of caries?
m.s.
What bacteria is responsible for caries progression?
Lactobacillus (opportunistic)
What bacteria may be responsible for smooth surface caries/rampant caries?
S. Sobrinus
Below what pH does demineralization occur?
5.5
What are the zones of the early carious lesion in enamel?
- Surface – relatively unaffected, 5-10% mineral loss (remin) 2. Body – 60% principal area of mineral loss (demin) 3. Dark zone – intermediate area of mineral loss (remin) 4. Translucent zone – 5-10% mineral loss, deepest zone (demin) 5. Normal enamel (remin lesion is stronger than original bc fluorhydroxyapatite is more resistant to acid erosion)
What is the caries sequence?
- Mandibular molars 2. Maxillary molars 3. Maxillary anteriors
Primary teeth have (lower/higher) mineral content and therefore (more/less) rapid progression of caries.
Lower mineral, more rapid
also thinner enamel and dentinpulp larger in relation to tooth size
flat contacts make clinical diagnosis difficult
Caries risk is increased in children with GERD because acid causes erosion of teeth
The statement and the reason are correct
The statement and the reason are incorrect
The statement is correct but the reason is incorrect
The statement is incorrect but the reason is correct
Answer: A. the statement and the reason are correct Unlike dental caries, where the demineralization is caused by an acidic environment in GERD is due to the reflux of hydrochloric acid from the stomach (Figur
What are the differences in gingival tissues between primary and permanent periodontium?
Primary dentition gingival tissues:
- Papilla well keratinized, + spacing => interdental saddle rather than col
- Marginal gingiva deeper sulcus, thicker/rounded free gingival margin, flaccid, retractable
- Attached gingiva less dense, less keratinized, 35% stippling, 85% retrocuspid papilla
- Alveolar mucosa more red, width increases with age/eruption
Primary dentition periodontium:
- PDL wider, less dense
- Alveolar bone has fewer trabeculae, larger marrow spaces, is less calcified
- Junctional epithelium thicker
- More leukocytes in connective tissue
- More dense collagen
*No differences in width of the free gingiva or thickness of epithelium
Where do retrocuspid papilla occur?
Lingual to mandibular canines
usually bilateral
considered a variation of normal
disappear with age
female predilection
Gingivitis peaks when?
At puberty (nearly universal)
increased inflammatory response to plaque
Is gingivitis reversible?
Yes there is no loss of attachment or boneYes there is no loss of attachment or bone
Etiologic factors of gingivitis
Plaque dependent
individual susceptibility
hormonal factors like pregnancy, puberty, oral contraceptives)
local factors (crowding, ortho, mouth breathing, transition)
Gingivitis bacteria in children:
“ACLS”
A - Actinomyces sp.
C - Capnocytophaga sp.
L - Leptotrichia sp.
S - Selemonas sp.
What is the treatment for a gingival abscess?
Clean sulcus / debride / CHX
Caused by embedded foreign object, abscess on marginal gingiva or interdental papilla, localized and painful
Vitamin C Deficiency presentation
Spongy, edematous, bleeds spontaneously,
impaired wound healing
Tx: treat underlying deficiency, plaque control
Necrotizing periodontal disease has a frequency of
<1% in North American and European children
2-5% in certain populations from developing areas of Africa, Asia and South America
Does NPD (necrotizing periodontal disease) present with pain?
Yes
+marginal/interproximal necrosis
fetid odor, pain, bleeding, bone loss, fever, lymphadenopathy, increase in plasma cortisol levels
What are four Diff Dx for the cause of ANUG
Neutropenia
Leukemia
HIV
Malnutrition
Treatment of NPD
Determine if underlying systemic disease
Mechanical debridement (ultrasonics effective)
OHI
NSAIDs for pain
Chlorhexidine oral rinse
10% povidone iodine, antifungals (Flaitz lecture)
Penicillin/ Metronidazole if febrile
careful follow up (q3-4 months)
Chlorhexidine MOA
Positive charge
attaches to pellicle, hydroxyapatite, mucous membranes and bacterial surface
– disrupts bacterial membranes and enzyme systems
antibacterial with gram + and – bacteria
does not reduce incidence of caries according to ADA Evidence-Based Clinical Recommendations 2011
T/F:
Topical iodine reduces risk for ECC
True
Lopez et al. 1999
antimicrobial effectiveness with 10% povidone-iodine (Betadine)
broad spectrum topical iodophor microbicide
Dose of metronidazole
30 mg/kg/day in 4 doses
Max 4 g/day
Bacteria involved in NPD (necrotizing periodontal disease) Necrotizing ulcerative gingivitis/periodontitis
SPIN
Spirochetes
P. INtermedia
Factors that predispose children to NPD:
Viral infections (including HIV)
malnutrition
stress
lack of sleep
systemic diseases
immunosuppression
smoking
local trauma
poor oral hygiene
What organism is implicated in linear gingival erythema?
Cause unknown but Candida species have been implicated
s/s: fiery red band 2-3 mm wide on marginal gingiva, petechiae or redness on mucosa; bleeding uncommon; pain rare
erythema disproportional to amt plaque
tx: plaque control; antifungals
Chronic Periodontitis:
What is the prevalence of severe attachment loss on multiple teeth in children?
0.2 – 0.5% in children
20% of 14-17 y.o. have att. loss of ≥ 2 mm in 1 or more sites
risk factors: teens who smoke and diabetes
Definition of localized chronic periodontitis
< 30% of dentition
Definition of generalized chronic periodontitis
> 30% dentition
Definition of mild chronic periodontitis
1 – 2 mm attachment loss
Definition of moderate chronic periodontitis
3 – 4 mm loss
Definition of severe chronic periodontitis
≥ 5 mm attachment loss
Localized Aggressive Periodontitis of primary dentition is associated with which bacteria and affects which teeth mostly?
- Actinobacillus actinomycetemcomitans (Aa)
- Attachment/bone loss around primary teeth, affects only some teeth; most commonly affects 1˚ molars – bilateral, symmetric
- inflammation not prominent, children otherwise healthy
- Prevalence <1%, African American disposition
- May progress to permanent dentition
- Suggested factors: leukocyte chemotactic defect, cementum defect
LAgP of permanent dentition affects which teeth?
Localized bone loss on least 2 Permanent first molars and incisors, and ≤ 2 other teeth
50% preceded by LAP of 1˚ dentition
Rapid attachment loss
May have minimal plaque/inflammation
patient otherwise systemically healthy
often first detected at age 10-15
prevalence: 0.2% in whites, 2.6% Afr Am
Tx: SRP, systemic abx; goal to eradicate Aa
Etiology and factors involved in aggressive periodontitis (localized and generalized)
LAgP – Actinobacillus actinomycetemcomitans in combo with Bacteroides-like species, eubacterium sp. in some populations; neutrophil defects (e.g. chemoaxis, phagocytosis, bactericidal activity, etc.); overreactive monocyte response
GAgP – heavy plaque and calculus
both – alterations to IgG2 (antibody reactive with Aa is of the IgG2 subclass.
Appears to be protective; i.e. high concentrations of the antibody have less attachment loss than patients who lack the antibody).
Protective antibody response is modified by genetics (African-Americans higher levels than Caucasian) and environmental factors like smoking.
GAgP involves what teeth?
At least three teeth that are not incisors or first molars, involves generalized interproximal attachment loss
prevalence in US adolescents is 0.13%
prevalence higher in males and African Americans
Marked inflammation, heavy plaque/calculus
progression of localized form
Tx: SRP, abx (culture/sensitivity)
Periodontitis as manifestation of what 8 systemic diseases?
- Hypophosphatasia (tissue non-specific alkaline phosphatase gene defect)
- Leukocyte Adhesion Defect (LAD) (AR)
- Papillon-LeFevre Syndrome (AR, rare) (cathepsin C gene defect)
- Down Syndrome (neutrophiil chemotaxis defect)
- Chediak-Higashi Syndrome (AR, rare)
- Neutropenia
- Langerhans Cell Histiocytosis
- Acute Leukemia
also agranulocytosis
*Diabetes is a significant modifier of all forms of periodontitis
Does generalized aggressive periodontitis have gingival inflammation?
Yes. Localized form has rapid bone loss and minimal gingival inflammation and little plaque/calc, while generalized form has rapid bone loss around nearly all teeth and marked gingival inflammation and heavy accumulation of plaque/calculus.
How many teeth does LagPaffect?
At least two perm first molars and incisors, and no more than 2 other teeth
How many teeth does GagP affect
At least 3 teeth that are not first molars or incisors
What bacteria are in LagP?
A.A, Bacteroides, eubacterium
Which bacteria are in GagP?
P. Gingivalis
T. Denticola
Gram negative facultative anaerobes
What is the tx for LagP?
Surgical or non-surgical debridement w/
Tetracycline and metronidazole
or Amoxicillin w/ metronidazole
GAgP does not always respond well to conventional mechanical therapy or antibiotics – alternative antibiotics may be required based upon the character of the pathogenic flora
T/F:
Localized Juvenile Spongiotic Gingival Hyperplasia (LJSGH) has a strong bacterial plaque association
False.
Cause unknown, but not a strong plaque association. Viral cause, esp HPV?
Origin: sulcular/junctional epithelium
Factors: ortho, tooth eruption, lip incompetence, mouth breathing, puberty
Average age – 12 y.o., F>M, white
Site: anterior facial gingiva especially maxillary (84%)
s/s: papillary, red nodule or velvety – granular patch; bleeds easy; nontender
does not respond to OH measures
Tx: biopsy, recurrence 6-16%, may resolve
What pathologic etiology would you suspect if child presents with no incisors and no hx of trauma?
Hypophosphatasia
(mild forms may have early loss of 1˚ tth)
Earlier presentation → more severe disease. Most likely to see childhood type out of the 4 types.
large pulp chambers, alveolar bone loss
abnormal cementum
permanent teeth often NOT affected
Etiology: defective/deficient alkaline phosphatase enzyme (levels alkaline phosphatase may be normal but function of the enzyme defective)
No treatment
Autosomal recessive
What systemic disease has early onset generalized periodontitis in 1˚ and permanent teeth and is accompanied by respiratory, skin, ear, soft tissue bacterial infections?
LAD (leukocyte adhesion defect)
Autosomal recessive
rapid bone loss around nearly ALL 1˚ tth
surface glycoprotein defect → poor leukocyte adherence
– decreased ability to move from circulation to sites of inflammation and infection
What bacteria are associated with periodontitis as a manifestation of systemic disease in children with neutrophil abnormalities?
CAPE
C – capnocytophaga sputigena
A – A. actinomycetemcomitans
P – Prevotella intermedia
E – Eikenella corrodens
Papillon-LeFevre has what additional findings?
- palmar/plantar hyperkeratosis
- *- Att loss results in premature loss of 1˚& permanent tth, hyperplastic and hemorrhagic gingiva**
- very rare
- autosomal recessive
- loss of function of cathepsin C gene
- Aa may induce leukocyte dysfunction
What is the prevalence of periodontal disease in those under 30 yrs old with Down Syndrome?
60-100% prevalence ≤ 30 yo
90% prevalence by age 30
Etiology – poor vascularization of the gingival tissues, T-cell maturation defect/PMN chemotactic defect
(“lazy leukocytes”)
Chediak-Higashi Syndrome
- Autosomal recessive, rare
- Oculocutaneous albinism, photophobia, nystagmus,
- peripheral neuropathy
- neutrophils have giant cytoplasmic granules
- *- severe gingivitis/periodontitis**
- bleeding problems
- leukemic infiltrates later
Neutropenia is caused by what, diagnosed how, and results in what?
Caused by: decreased or absent circulating PMN (neutrophils)
Diagnosed by WBC differential**
Causes frequent recurrent infections
Periodontal symptoms of neutropenia include:
Severe gingivitis with ulceration
attachment/bone loss
early loss of primary teeth
severe perio in permanent teeth
Name 3 drugs/classes of drugs that cause gingival hyperplasia
- Phenytoin (dilantin, antiseizure) – 50% prevalence
- Cyclosporine (immunosuppressant) – 25%
- Ca+ channel blockers (Nifedipine, amlodipine, diltiazem) 25%
(gingival enlargement doesn’t happen without teeth)
What form of leukemia most commonly presents with gingival enlargement (due to infiltration of leukemic cells)?
AML
gingival enlargement due to infiltration with leukemic cells (may be presenting symptom, especially with AML)
gingiva appear hyperplastic, edematous, bluish red
petechiae of mucosal ulcerations usually present
initial dx by CBC
Drugs of choice for tx of periodisease in children
Metronidazole & Amoxicillin
This agent is bactericidal against gram – and gram + bacteria, has a + charge and substantivity
CHX
Post-treatment diagnosis of periodontal disease:
Recurrent or refractory
Langerhans Cell Histiocytosis
Abnormal proliferation/dissemination of histiocytes→
Infiltration of bones, skin, liver, other organs by histiocytes and eosinophils
young children, most <10yo
10% show oral involvement, usually initial infiltration area
Jaws affected up to 20%
bone lesions produce floating teeth, PARLs
gingival swelling, ulcers, mucosal and gingival masses
Dx by biopsy
Tx: curettage, chemo
Four characteristics of inflammation
Rubor - redness
Tumor - swelling
Calor - heat
Dolor – pain
Also loss of function
Skin, cilia, mucous membranes are part of the _________ innate immunity.
anatomical
Elevated temperature, increased mucous secretion, phagocytic cells are part of the ______ innate immunity.
physiologic
Biochemical innate immunity includes:
Interferons, enzymes
Biological innate immunity is
Competitive microbial growth
Acquired immunity has two parts:
Cell mediated (T-cells) Humoral (B-cells, antibodies)
Name 2 primary humoral (B cell) immunodeficiencies
- Agammaglobulinemia (low Ig, few B-cells)
- Hyper IgM syndromes
Name the most common cellular (T-cell) immunodeficiency
- *DiGeorge syndrome**
- AD
- thymic hypoplasia bc of 3rd and 4th pharyngeal pouch maldevelopment
- 22q11.2 deletion
- *- VCFS occurs in 90% of cases
- cleft palate
- conotruncal heart disease**
“CATCH” = cardiac abnormality, abnormal facies, thymic aplasia, cleft palate, hypocalcemia/hypoparathyroidism
Name 3 combined immunodeficiencies
- SCID (severe combined immunodeficiency (x-linked)
- ANP, GVH rx to transfusion, oral ulcerations, candidiasis - Ataxia-Telangiectasia Syndrome
- diabetes mellitus, poor prognosis - Wiskott-Aldrich Syndrome (x-linked recessive)
- males mostly, thrombocytopenia, autoimmune disorders
Name 4 disorders of innate immunity.
-
Chronic Granulomatous Disease
- lots of fungal and bacterial infections, ulcerations -
LAD I
- AR, rare, infections, periodontitis, impaired wound healing, juvenile periodontitis, slow healing & scarring oral ulcers -
Cyclic neutropenia
- periodontitis, gingivitis, ulceration, desquamation -
Chediak-Higashi Syndrome (CHS)
- defective transport of bacteria to lysosomes for destruction
- partial albinism, photophobia, nystagmus
- recurrent pyogenic infections, neutropenia, anemia, thrombocytopenia
- severe gingivitis, periodontitis, premature primary tooth loss.
Type I hypersensitivity aka
Anaphylaxis, IgE mediated
FAST
mild: hives, pruritus, nausea
severe: widespread hives, vomiting/diarrhea, tongue/lip/throat swelling, wheeze/cough/stridor, anaphylactic shock, asthmatics more severe reaction
examples: anaphylaxis, atopic bronchial asthma, allergic rhinitis, urticaria, angioedema
Type II hypersensitivity
“cytotoxic” IgG, IgM
Transfusion reactions
hemolytic anemia
drug rxns
Type III hypersensitivity rxns
Immune complex, IgG (6-8 hrs)
- acute viral hepatitis
- serum sickness
Type IV hypersensitivity rxn
Cell-mediated (delayed) 48 hrs
- allergic contact dermatitis
- infectious granulomas (TB)
- tissue graft rejection
- chronic hepatitis
What % of people have bi-phasic anaphylactic reaction (and what does bi-phasic mean)?
Which Ig mediates release from mast cells and peripheral basophils to create anaphylactic reaction?
IgE
EEEEEEEEEK!!!!!
Treatment for mild anaphylaxis
Diphenhydramine
1–2 mg/kg
max 50 mg
q6h for 24h
Treatment of severe anaphylaxis
Monitor vitals
IM epi 1:1000
0.01 mg/kg epi 1:1000
repeat q5minutes or until help arrives, then q4h
diphenhydramine
IV corticosteroids if no response to epi/benadryl
Albuterol if bronchospasm
Call 911 for life-threatening
Normal value for hematocrit
35-50%
SCA 20%
Normal value for RBCs
4-6 million/mm3
Normal value for hemoglobin
12-18 g/100 mL
6-9 SCA
Normal value for platelets
140,000-340,000/mL
Normal Prothrombin time
Which pathway does PT measure?
1-18 sec.
*Measures Extrinsic Pathway
*prolonged in liver disease and impaired vitamin K production
Normal Bleeding Time: 1-6 min.
**measures factors I,II,V,VII and X
What does partial thromboplastin time measure?
Intrinsic Pathway + Congenital Clotting Disorders
**Prolonged in hemophilia A,B,C and Von Willebrand’s Disease
The normal WBC count of an infant is:
8,000 – 15,000 / mm3
Normal WBC count for 4 – 7 yo:
6,000 – 15,000 /mm3
Normal WBC count for 8 – 18 yo
4,500 – 13,500 /mm3
WBC count lowers with age
Low WBC may be indicative of:
Aplastic anemia
Drug toxicity
Certain infections
High WBC may be indicative of
Inflammation
trauma
toxicity
leukemia
WBC differential components:
Neutrophils ~ 60%
Lymphocytes ~ 30%
Eosinophils ~ 3%
Basophils ~ 1%
Monocytes ~0-9%
Lymphocytes – T-cells and B-cells
Eosinophils – increased in parasitic and allergic conditions
Basophils – full of histamine, involved in IgE response
How do you calculate ANC?
(%PMN + %bands)(total White cells)
100
Normal ANC value
>1500
**when ANC greater than 2000; don’t need antibiotic prophylaxis for dental treatment. When between 1000-2000; may need antibiotics (should consult physician)
At what ANC do you defer all treatment?
<500
When can the first dose of Hep B be given?
Birth.
Second dose at 4 wks
Third dose at least 16 weeks after first, minimum age for final dose is 24 weeks
What is the minimum age for Rotavirus,
Diphtheria/tetanus/pertussis,
H influenza,
pneumococcal,
inactivated polio, and meningococcal vaccinations?
6 weeks is the minumum age for what vacinnes?
12 months is the minimum age for what vaccines?
MMR
Varicella
Hep A
What is the minimum age for
inactivated influenza and
live attenuated influenza vaccines?
6 months and 2 years
Definition:
Meta Analysis
Statistical pooling of data from different studies
Randomized control trial
Control group (placebo or standard therapy) compared w/experimental therapy group, with random allocation. Strongest evidence of any well-designed trial
Cohort study
Longitudinal epidemiologic study
Ppl selected bc of factors that are to be examined for their effects on outcomes, e.g. effect of exposure to risk factor on eventual development of disease
Followed over time to find incidence rates in relation to original factors
Case control
Longitudinal epidemiologic study
Ppl HAVE or LACK (control) some outcome
Histories are examined for specific factors possibly associated with outcome.
Specificity vs. Sensitivity
Specificity = true negative rate (measures the proportion of negatives that are correctly identified as such)
Sensitivity = true positive rate (measures the proportion of positives that are correctly identified as such)
Statistical Definitions:
- Power
- Type I and II Error
- Power Analysis
Power = probability that the test correctly rejects the null hypothesis when the alternative hypothesis is true
Type I error = false negative rate
Type II error = false positive rate
Power analysis can be used to calculate the minimum sample size required (i.e – how many times do I need to toss a coin to conclude it is rigged)
Levels of Evidence 5 levels
1a. Systematic Review of RCT
1b. RCT
2a. Systematic review of cohort studies
2b. Cohort study
2c. Outcomes research, ecological studies
3a. Systematic review of case-control studies
3b. Case control study
4. Case series
4b. Case reports
5. Expert opinion
6. animal research
7. in vitro
When is P deemed statistically important?
P ≤ 0.05
null hypothesis rejected
probability of getting this result by chance
Cross over study
Each participant serves as his own control
Correlation coefficients
Higher coefficient means you are better able to predict one characteristic from another.
What is pearson’s correlation coefficient?
Measure of linear dependence (correlation) between two variables X and Y.
It has a value between +1 and -1 inclusive; where 1 is total positive linear correlation, 0 is no linear correlation and -1 is total negative linear correlation.
Dental water lines have the same standard as safe drinking water T/F
T. ≤ 500 CFU/mL
- must also use chemical germicide to remove/inactivate biofilms
Critical instruments require sterilization T/F
T. – penetrate soft tissues/bone, enter/contact bloodstream
- highest risk of transmitting infection
- surgical instruments, scalers, scalpels, burs
Semi critical instruments contact mucous membranes or non-intact skin. T/F
TRUE
Mouth mirror, impression trays, handpieces*
*though handpieces are semi-critical, they should be heat-sterilized b/n uses and not high-level disinfected
Non-critical instruments contact what?
Intact skin
examples:
x-ray head
pulse-ox
bp cuff
countertops
Does sterilization kill bacterial spores?
Yes. It destroys all microorganisms
Does high level disinfection kill bacterial spores?
No. It does destroy all microorganisms, but not a high number of bacterial spores.
- examples: washer-disinfector, glutaraldehyde +/- phenol
- H2O2
What level of disinfection destroys vegetative bacteria, most fungi and viruses, and inactivates Mycobacterium bovis(but does not necessarily kill spores)
Intermediate level
- labeled as tuberculocidal activity
ex)
- chlorine containing
- quaternary ammonium
- phenolics
- iodophors
use to clean non-critical surfaces that have visible blood
Do low level disinfectants kill HIV?
OSHA requires label claim of HIV killing potency
does not require label of tuberculocidal activity
Low level destroys most vegetative bacteria, some fungi/viruses, does not inactivate Mycobacterium bovis
examples: quaternary ammonium compounds, some phenolics/iodophors
use to clean noncritical surfaces without visible blood
If there is visible blood, what disinfectant do you need to use?
Intermediate level (tuberculocidal claim)
in absence of blood, can disinfect surfaces using EPA-registered hospital disinfectant that does not have tuberculocidal claim
Steam autoclave settings
121 ˚C
15 psi
15-20 minutes
(+) rapid, most materials
(-) corrosion/dulling, packages wet
Dry Heat oven settings
160˚C 2hrs
170˚C 1hr
(+) no dulling/corrosion, no toxic or hazardous chemicals
(-) long cycle time, destroys plastics
Rapid Heat Transfer settings
375˚F
12 minutes wrapped
6 minutes unwrapped
(+) short cycle, items dry, small capacity
(-) cannot sterilize liquids, damages plastic, can’t open door during cycle
Unsaturated chemical vapor settings
131˚C
20 psi
30 min
(+) short cycle, less corrosive
(-) toxic chemicals, needs special ventilation, destroys plastic
Ethylene Oxide settings
25˚C
10-16 hrs
(for heat-sensitive items)
(glutaraldehyde, H2O2)
(+) suitable for most materials including appliances
(-) very long cycle time, toxic chemicals, needs special ventilation
How do you disinfect alginates?
Immersion with caution, Short-term exposure to disinfectant (10 mins max) w/ Chlorine/iodophor
casts: spray til wet or immerse using chlorine compound/iodophor
impressions: immersion preferred
Prostheses: immerse or sterilize with ethylene oxide, rinse after 15 sec with water
Removable appliance (acrylic): chlorine/iodophor, rinse, store in dilute mouthwash
