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Purple book > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Definition of caries

A

Biofilm-induced acid demineralization of enamel or dentin, mediated by saliva

Interaction of cariogenic microorganisms (M.S.) and fermentable carbohydrates (sucrose) induces demineralization

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2
Q

4 types of transmission of cariogenic bacteria:

A
  1. Direct saliva: kissing
  2. Indirect objects: sharing utensils, pacifiers
  3. Vertical from caregiver. MS genotype in infants identical to moms in 24-100% of pairs in 17 studies
  4. Horizontal from siblings/children @ daycare. One S-ECC study showed non-maternal MS genotypes in 74% children
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3
Q

What is colonization of bacteria related to?

A

Magnitude of inoculum

Frequency of inoculum

Minimum infective dose

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4
Q

Can MS colonize pre-dentate infants?

A

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

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5
Q

What bacteria is responsible for initiation of caries?

A

m.s.

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6
Q

What bacteria is responsible for caries progression?

A

Lactobacillus (opportunistic)

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7
Q

What bacteria may be responsible for smooth surface caries/rampant caries?

A

S. Sobrinus

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8
Q

Below what pH does demineralization occur?

A

5.5

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9
Q

What are the zones of the early carious lesion in enamel?

A
  1. 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)
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10
Q

What is the caries sequence?

A
  1. Mandibular molars 2. Maxillary molars 3. Maxillary anteriors
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11
Q

Primary teeth have (lower/higher) mineral content and therefore (more/less) rapid progression of caries.

A

Lower mineral, more rapid

also thinner enamel and dentinpulp larger in relation to tooth size

flat contacts make clinical diagnosis difficult

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12
Q

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

A

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

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13
Q

What are the differences in gingival tissues between primary and permanent periodontium?

A

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

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14
Q

Where do retrocuspid papilla occur?

A

Lingual to mandibular canines

usually bilateral
considered a variation of normal
disappear with age
female predilection

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15
Q

Gingivitis peaks when?

A

At puberty (nearly universal)

increased inflammatory response to plaque

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16
Q

Is gingivitis reversible?

A

Yes there is no loss of attachment or boneYes there is no loss of attachment or bone

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17
Q

Etiologic factors of gingivitis

A

Plaque dependent
individual susceptibility
hormonal factors like pregnancy, puberty, oral contraceptives)
local factors (crowding, ortho, mouth breathing, transition)

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18
Q

Gingivitis bacteria in children:

A

“ACLS”
A - Actinomyces sp.
C - Capnocytophaga sp.
L - Leptotrichia sp.
S - Selemonas sp.

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19
Q

What is the treatment for a gingival abscess?

A

Clean sulcus / debride / CHX

Caused by embedded foreign object, abscess on marginal gingiva or interdental papilla, localized and painful

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20
Q

Vitamin C Deficiency presentation

A

Spongy, edematous, bleeds spontaneously,
impaired wound healing

Tx: treat underlying deficiency, plaque control

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21
Q

Necrotizing periodontal disease has a frequency of

A

<1% in North American and European children

2-5% in certain populations from developing areas of Africa, Asia and South America

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22
Q

Does NPD (necrotizing periodontal disease) present with pain?

A

Yes
+marginal/interproximal necrosis

fetid odor, pain, bleeding, bone loss, fever, lymphadenopathy, increase in plasma cortisol levels

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23
Q

What are four Diff Dx for the cause of ANUG

A

Neutropenia
Leukemia
HIV
Malnutrition

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24
Q

Treatment of NPD

A

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)

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25
Q

Chlorhexidine MOA

A

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

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26
Q

T/F:
Topical iodine reduces risk for ECC

A

True
Lopez et al. 1999

antimicrobial effectiveness with 10% povidone-iodine (Betadine)
broad spectrum topical iodophor microbicide

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27
Q

Dose of metronidazole

A

30 mg/kg/day in 4 doses
Max 4 g/day

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28
Q

Bacteria involved in NPD (necrotizing periodontal disease) Necrotizing ulcerative gingivitis/periodontitis

A

SPIN
Spirochetes
P. INtermedia

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29
Q

Factors that predispose children to NPD:

A

Viral infections (including HIV)
malnutrition
stress
lack of sleep
systemic diseases
immunosuppression
smoking
local trauma
poor oral hygiene

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30
Q

What organism is implicated in linear gingival erythema?

A

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

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31
Q

Chronic Periodontitis:
What is the prevalence of severe attachment loss on multiple teeth in children?

A

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

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32
Q

Definition of localized chronic periodontitis

A

< 30% of dentition

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33
Q

Definition of generalized chronic periodontitis

A

> 30% dentition

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34
Q

Definition of mild chronic periodontitis

A

1 – 2 mm attachment loss

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35
Q

Definition of moderate chronic periodontitis

A

3 – 4 mm loss

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36
Q

Definition of severe chronic periodontitis

A

≥ 5 mm attachment loss

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37
Q

Localized Aggressive Periodontitis of primary dentition is associated with which bacteria and affects which teeth mostly?

A
  • 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
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38
Q

LAgP of permanent dentition affects which teeth?

A

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

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39
Q

Etiology and factors involved in aggressive periodontitis (localized and generalized)

A

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.

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40
Q

GAgP involves what teeth?

A

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)

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41
Q

Periodontitis as manifestation of what 8 systemic diseases?

A
  1. Hypophosphatasia (tissue non-specific alkaline phosphatase gene defect)
  2. Leukocyte Adhesion Defect (LAD) (AR)
  3. Papillon-LeFevre Syndrome (AR, rare) (cathepsin C gene defect)
  4. Down Syndrome (neutrophiil chemotaxis defect)
  5. Chediak-Higashi Syndrome (AR, rare)
  6. Neutropenia
  7. Langerhans Cell Histiocytosis
  8. Acute Leukemia

also agranulocytosis

*Diabetes is a significant modifier of all forms of periodontitis

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42
Q

Does generalized aggressive periodontitis have gingival inflammation?

A

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.

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43
Q

How many teeth does LagPaffect?

A

At least two perm first molars and incisors, and no more than 2 other teeth

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44
Q

How many teeth does GagP affect

A

At least 3 teeth that are not first molars or incisors

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45
Q

What bacteria are in LagP?

A

A.A, Bacteroides, eubacterium

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46
Q

Which bacteria are in GagP?

A

P. Gingivalis
T. Denticola
Gram negative facultative anaerobes

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47
Q

What is the tx for LagP?

A

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

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48
Q

T/F:
Localized Juvenile Spongiotic Gingival Hyperplasia (LJSGH) has a strong bacterial plaque association

A

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

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49
Q

What pathologic etiology would you suspect if child presents with no incisors and no hx of trauma?

A

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

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50
Q

What systemic disease has early onset generalized periodontitis in 1˚ and permanent teeth and is accompanied by respiratory, skin, ear, soft tissue bacterial infections?

A

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

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51
Q

What bacteria are associated with periodontitis as a manifestation of systemic disease in children with neutrophil abnormalities?

A

CAPE
C – capnocytophaga sputigena
A – A. actinomycetemcomitans
P – Prevotella intermedia
E – Eikenella corrodens

52
Q

Papillon-LeFevre has what additional findings?

A
  • 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
53
Q

What is the prevalence of periodontal disease in those under 30 yrs old with Down Syndrome?

A

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”)

54
Q

Chediak-Higashi Syndrome

A
  • Autosomal recessive, rare
  • Oculocutaneous albinism, photophobia, nystagmus,
  • peripheral neuropathy
  • neutrophils have giant cytoplasmic granules
  • *- severe gingivitis/periodontitis**
  • bleeding problems
  • leukemic infiltrates later
55
Q

Neutropenia is caused by what, diagnosed how, and results in what?

A

Caused by: decreased or absent circulating PMN (neutrophils)
Diagnosed by WBC differential**
Causes frequent recurrent infections

56
Q

Periodontal symptoms of neutropenia include:

A

Severe gingivitis with ulceration
attachment/bone loss
early loss of primary teeth
severe perio in permanent teeth

57
Q

Name 3 drugs/classes of drugs that cause gingival hyperplasia

A
  1. Phenytoin (dilantin, antiseizure) – 50% prevalence
  2. Cyclosporine (immunosuppressant) – 25%
  3. Ca+ channel blockers (Nifedipine, amlodipine, diltiazem) 25%

(gingival enlargement doesn’t happen without teeth)

58
Q

What form of leukemia most commonly presents with gingival enlargement (due to infiltration of leukemic cells)?

A

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

59
Q

Drugs of choice for tx of periodisease in children

A

Metronidazole & Amoxicillin

60
Q

This agent is bactericidal against gram – and gram + bacteria, has a + charge and substantivity

A

CHX

61
Q

Post-treatment diagnosis of periodontal disease:

A

Recurrent or refractory

62
Q

Langerhans Cell Histiocytosis

A

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

63
Q

Four characteristics of inflammation

A

Rubor - redness
Tumor - swelling
Calor - heat
Dolor – pain
Also loss of function

64
Q

Skin, cilia, mucous membranes are part of the _________ innate immunity.

A

anatomical

65
Q

Elevated temperature, increased mucous secretion, phagocytic cells are part of the ______ innate immunity.

A

physiologic

66
Q

Biochemical innate immunity includes:

A

Interferons, enzymes

67
Q

Biological innate immunity is

A

Competitive microbial growth

68
Q

Acquired immunity has two parts:

A 
Cell mediated (T-cells)
Humoral (B-cells, antibodies)
69
Q

Name 2 primary humoral (B cell) immunodeficiencies

A
  • Agammaglobulinemia (low Ig, few B-cells)
  • Hyper IgM syndromes
70
Q

Name the most common cellular (T-cell) immunodeficiency

A
  • *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

71
Q

Name 3 combined immunodeficiencies

A
  1. SCID (severe combined immunodeficiency (x-linked)
    - ANP, GVH rx to transfusion, oral ulcerations, candidiasis
  2. Ataxia-Telangiectasia Syndrome
    - diabetes mellitus, poor prognosis
  3. Wiskott-Aldrich Syndrome (x-linked recessive)
    - males mostly, thrombocytopenia, autoimmune disorders
72
Q

Name 4 disorders of innate immunity.

A
  1. Chronic Granulomatous Disease
    - lots of fungal and bacterial infections, ulcerations
  2. LAD I
    - AR, rare, infections, periodontitis, impaired wound healing, juvenile periodontitis, slow healing & scarring oral ulcers
  3. Cyclic neutropenia
    - periodontitis, gingivitis, ulceration, desquamation
  4. 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.
73
Q

Type I hypersensitivity aka

A

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

74
Q

Type II hypersensitivity

A

“cytotoxic” IgG, IgM
Transfusion reactions
hemolytic anemia
drug rxns

75
Q

Type III hypersensitivity rxns

A

Immune complex, IgG (6-8 hrs)

  • acute viral hepatitis
  • serum sickness
76
Q

Type IV hypersensitivity rxn

A

Cell-mediated (delayed) 48 hrs

  • allergic contact dermatitis
  • infectious granulomas (TB)
  • tissue graft rejection
  • chronic hepatitis
77
Q

What % of people have bi-phasic anaphylactic reaction (and what does bi-phasic mean)?

A
78
Q

Which Ig mediates release from mast cells and peripheral basophils to create anaphylactic reaction?

A

IgE
EEEEEEEEEK!!!!!

79
Q

Treatment for mild anaphylaxis

A

Diphenhydramine
1–2 mg/kg
max 50 mg
q6h for 24h

80
Q

Treatment of severe anaphylaxis

A

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

81
Q

Normal value for hematocrit

A

35-50%

SCA 20%

82
Q

Normal value for RBCs

A

4-6 million/mm3

83
Q

Normal value for hemoglobin

A

12-18 g/100 mL

6-9 SCA

84
Q

Normal value for platelets

A

140,000-340,000/mL

85
Q

Normal Prothrombin time
Which pathway does PT measure?

A

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

86
Q

What does partial thromboplastin time measure?

A

Intrinsic Pathway + Congenital Clotting Disorders

**Prolonged in hemophilia A,B,C and Von Willebrand’s Disease

87
Q

The normal WBC count of an infant is:

A

8,000 – 15,000 / mm3

88
Q

Normal WBC count for 4 – 7 yo:

A

6,000 – 15,000 /mm3

89
Q

Normal WBC count for 8 – 18 yo

A

4,500 – 13,500 /mm3

WBC count lowers with age

90
Q

Low WBC may be indicative of:

A

Aplastic anemia
Drug toxicity
Certain infections

91
Q

High WBC may be indicative of

A

Inflammation
trauma
toxicity
leukemia

92
Q

WBC differential components:

A

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

93
Q

How do you calculate ANC?

A

(%PMN + %bands)(total White cells)
100

94
Q

Normal ANC value

A

>1500

**when ANC greater than 2000; don’t need antibiotic prophylaxis for dental treatment. When between 1000-2000; may need antibiotics (should consult physician)

95
Q

At what ANC do you defer all treatment?

A

<500

96
Q

When can the first dose of Hep B be given?

A

Birth.

Second dose at 4 wks

Third dose at least 16 weeks after first, minimum age for final dose is 24 weeks

97
Q

What is the minimum age for Rotavirus,
Diphtheria/tetanus/pertussis,
H influenza,
pneumococcal,
inactivated polio, and meningococcal vaccinations?

A

6 weeks is the minumum age for what vacinnes?

98
Q

12 months is the minimum age for what vaccines?

A

MMR
Varicella
Hep A

99
Q

What is the minimum age for
inactivated influenza and
live attenuated influenza vaccines?

A

6 months and 2 years

100
Q

Definition:
Meta Analysis

A

Statistical pooling of data from different studies

101
Q

Randomized control trial

A 
Control group (placebo or standard therapy) compared w/experimental therapy group, with random allocation. 
Strongest evidence of any well-designed trial
102
Q

Cohort study

A

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

103
Q

Case control

A

Longitudinal epidemiologic study
Ppl HAVE or LACK (control) some outcome
Histories are examined for specific factors possibly associated with outcome.

104
Q

Specificity vs. Sensitivity

A

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)

105
Q

Statistical Definitions:

  • Power
  • Type I and II Error
  • Power Analysis
A

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)

106
Q

Levels of Evidence 5 levels

A

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

107
Q

When is P deemed statistically important?

A

P ≤ 0.05
null hypothesis rejected
probability of getting this result by chance

108
Q

Cross over study

A

Each participant serves as his own control

109
Q

Correlation coefficients

A

Higher coefficient means you are better able to predict one characteristic from another.

110
Q

What is pearson’s correlation coefficient?

A

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.

111
Q

Dental water lines have the same standard as safe drinking water T/F

A

T. ≤ 500 CFU/mL
- must also use chemical germicide to remove/inactivate biofilms

112
Q

Critical instruments require sterilization T/F

A

T. – penetrate soft tissues/bone, enter/contact bloodstream

  • highest risk of transmitting infection
  • surgical instruments, scalers, scalpels, burs
113
Q

Semi critical instruments contact mucous membranes or non-intact skin. T/F

A

TRUE
Mouth mirror, impression trays, handpieces*

*though handpieces are semi-critical, they should be heat-sterilized b/n uses and not high-level disinfected

114
Q

Non-critical instruments contact what?

A

Intact skin

examples:
x-ray head
pulse-ox
bp cuff
countertops

115
Q

Does sterilization kill bacterial spores?

A

Yes. It destroys all microorganisms

116
Q

Does high level disinfection kill bacterial spores?

A

No. It does destroy all microorganisms, but not a high number of bacterial spores.

  • examples: washer-disinfector, glutaraldehyde +/- phenol
  • H2O2
117
Q

What level of disinfection destroys vegetative bacteria, most fungi and viruses, and inactivates Mycobacterium bovis(but does not necessarily kill spores)

A

Intermediate level
- labeled as tuberculocidal activity

ex)
- chlorine containing
- quaternary ammonium
- phenolics
- iodophors

use to clean non-critical surfaces that have visible blood

118
Q

Do low level disinfectants kill HIV?

A

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

119
Q

If there is visible blood, what disinfectant do you need to use?

A

Intermediate level (tuberculocidal claim)

in absence of blood, can disinfect surfaces using EPA-registered hospital disinfectant that does not have tuberculocidal claim

120
Q

Steam autoclave settings

A

121 ˚C
15 psi
15-20 minutes

(+) rapid, most materials
(-) corrosion/dulling, packages wet

121
Q

Dry Heat oven settings

A

160˚C 2hrs
170˚C 1hr

(+) no dulling/corrosion, no toxic or hazardous chemicals
(-) long cycle time, destroys plastics

122
Q

Rapid Heat Transfer settings

A

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

123
Q

Unsaturated chemical vapor settings

A

131˚C
20 psi
30 min

(+) short cycle, less corrosive
(-) toxic chemicals, needs special ventilation, destroys plastic

124
Q

Ethylene Oxide settings

A

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

125
Q

How do you disinfect alginates?

A

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

Purple book (10 decks)

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