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Clin Micro 1 > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Colony morphology of S. aureus on BAP, CNA, MAC, MSA

A

BAP: medium white to buttery pigment, smells like stinky socks, beta or gamma hemolysis
CNA: white colonies
MAC: NG
MSA: Mann POS @ 48 hrs

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2
Q

Colony morphology of S. epidermidis on BAP, CNA, MAC, MSA

A

BAP: white dome shaped colonies, almost always gamma hemolysis
CNA: white colonies
MAC: NG
MSA: mann NEG @ 48 hours

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3
Q

Colony morphology of S. saprophyticus on BAP, CNA, MAC, MSA

A

BAP: yellow or white pigment (about 50/50), almost always gamma hemolysis
CNA: white or yellow colonies
MAC: NG
MSA: mann POS or NEG; typically weaker pos rxn, may be weak pos @ 24-48 hours

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4
Q

GS rxn - Staphylococcus species

A

GPC in clusters

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5
Q

Purpose of catalase test

A

Differentiates staphs from streps

Determine if catalase enzyme is present

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6
Q

Catalase test slide method procedure

A
  1. 1 drop 3-5% H2O2 on slide
  2. Mix 3-4 colonies into H2O2 with a loop
  3. Observe rxn
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7
Q

Catalase test result interpretation

A

POSITIVE: RAPID PROFUSE BUBBLES (indicates catalase enzyme is present)
-Staph spp.

NEGATIVE: wimpy bubbles, no rxn

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8
Q

Catalase test precautions

A

False positive results may occur:
-E. faecalis may produce wimpy rxn
-RBCs will give a false pos; do not stick look into BAP plate before picking up colonies; could pick up RBCs
from media

*must use isolated colonies

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9
Q

Coagulase test purpose

A

Definitive test for Staph aureus

Determines presence of coagulase enzyme (only produced by S. aureus)

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10
Q

Coagulase test rapid slide method purpose

A

Spot test that detects cell-bound coagulase

-produced by SOME strains of S. aureus

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11
Q

Coagulase test reagents

A

Rabbit plasma

Fibrinogen

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12
Q

Coagulase test rapid slide method procedure

A

mix rabbit plasma with 3-4 colonies on a slide

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13
Q

Coagulase test rapid slide method results interpretation

A

Spot coag POS: clumps of fibrin observed; DEFINITIVE FOR S.AUREUS

Spot coag neg: must do tube method

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14
Q

Coagulase test tube method purpose

A

Detects free EC coagulase

-all strains of S. aureus

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15
Q

Coagulase test tube method procedure

A

0.5 mL rabbit plasma mixed with 3-4 colonies in a tube

Incubate 4 hrs to overnight @ 37C

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16
Q

Rapid latex kit/Staphyloside latex kit reagents & principle

A

Latex beads coated with:

  • Fibrinogen (detects cell bound coagulase)
  • IgG (protein A antibodies/receptors)

principle: antiserum mixed with sample that potentially contains its target cells; if antigenic cells are present, antibodies in the antiserum will clump (agglutinate) the antigen

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17
Q

Novobiocin susceptibility test interpretation

A

SUSCEPTIBLE: zone of inhibition; no growth around disk
-recorded as novo susc or novo S

RESISTANT: no zone of inhibition; growth up to disk
-recorded as novo res or novo R

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18
Q

Novobiocin susceptibility test results: S. saprophyticus

A

S.saprophyticus is RESISTANT to novobiocin

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19
Q

Novobiocin susceptibility test results: S. epidermidis

A

S. epidermidis is SUSCEPTIBLE to novobiocin

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20
Q

List the genera and species of the FamilyMicrococcaceae (5)

A
  • Staphylococcus aureus
    • Staphylococcus epidermidis
    • Staphylococcus saprophyticus
    • Staphylococcus haemolyticus
    • Micrococcus luteus
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21
Q

Infections caused by S. aureus (4)

A
  1. Skin infections
  2. Wounds
  3. Dissemination from local infection
  4. Toxin mediated diseases
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22
Q

Infections caused by S. aureus:

Boils

A

AKA furuncles

Begins as folliculitis

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23
Q

Infections caused by S. aureus:

Carbuncles

A

Infection from boil spreads to surrounding/deeper tissue

happens when several furuncles coalesce

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24
Q

Infections caused by S. aureus:

Impetigo

A

primarily infection of children
-common source is nose; runny nose kid

2 kinds: bolus impetigo and pustule impetigo

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25
Q

Infections caused by S. aureus:

bolus impetigo vs pustule impetigo

A

Bolus impetigo:

- blister-like 
- 80% S. aureus, 20% S. pyogenes

Pustule impetigo:

- more zit-like 
- usually S. pyogenes
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26
Q

Infections caused by S. aureus:

Dissemination from local infection - 6 conditions

A
  1. Septicemia
  2. Bacteremia
  3. Osteomyelitis
  4. Pneumonia
  5. Endocarditis
  6. Meningitis
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27
Q

Septicemia

A

Bacteria in blood multiplying & causing symptoms

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28
Q

Bacteremia

A

Bacteria in blood but no symptoms

bacteria enter bloodstream through site of infection

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29
Q

Osteomyelitis

A

Inflammation of the bone marrow and surrounding bone

Can sit in bone marrow dormant and flare back up when disturbed, usually by trauma

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30
Q

Pneumonia

A

Infection of lungs; alveoli and bronchioles become filled with fluid

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31
Q

Endocarditis

A

Infection of the inner lining of heart and potentially valves

nonspecific flu-like symptoms

Drug users

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32
Q

Meningitis

A

Inflammation of the meninges

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33
Q

Infections caused by S. aureus:

Toxin mediated diseases (3)

A
  1. Toxic shock syndrome
  2. Food poisoning
  3. Staphylococcal scalded skin syndrome
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34
Q

Infections caused by S. aureus:

Toxic shock syndrome

A

Toxin: TSST-1

- absorbed into blood stream 
- causes fever, hypotension, shock, death in some cases
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35
Q

Infections caused by S. aureus:

Food poisoning

A

Food left out at room temp 2+ hours (mayo based foods)

Enterotoxins A & D

- preformed toxins secreted by bacteria
- symptoms start in 2-8 hours

Source = carriers

food poisoning caused by enterotoxin left in food from growth of bacteria rather than by a bacterial infection

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36
Q

Infections caused by S. aureus:

Staphylococcal scalded skin syndrome

A

AKA Ritter’s disease

caused by exfoliative toxin
-causes epidermis to separate from cutaneous layer

More common in kids

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37
Q

Pathogenic mechanisms of S. aureus: (3 categories)

A
  1. Invasive mechanisms
  2. Toxin production
  3. Cytolytic toxins
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38
Q

Pathogenic mechanisms of S. aureus: Invasive mechanisms (6)

A
  1. coagulase
  2. hyaluronidase
  3. protein a
  4. lipase
  5. staphylokinase
  6. beta lactamase
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39
Q

Pathogenic mechanisms of S. aureus: Invasive mechanisms

coagulase

A

AKA clumping factor

enzyme that forms fibrin (clot) from fibrinogen

allows org to form clot around itself to protect from body defenses

***ONLY S. AUREUS SYNTHESIZES COAGULASE

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40
Q

Pathogenic mechanisms of S. aureus: Invasive mechanisms

hyaluronidase

A

AKA spreading factor

enzyme that breaks down hyaluronic acid in connective tissues and allows org to spread and break up cells

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41
Q

Pathogenic mechanisms of S. aureus: Invasive mechanisms

protein a

A

cell wall protein unique to S. aureus

prevents antibody mediated phagocytosis

can bind to FAB and Fc portion of IgG

covers Fc portion; without Fc exposed, phagocyte receptor can’t attach and phagocytosis can’t occur

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42
Q

Pathogenic mechanisms of S. aureus: Invasive mechanisms

lipase

A

breaks down oils (lipids) produced by sebaceous glands

allows staph to grow on surface of skin and in cutaneous oil glands

all staph spp. produce this

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43
Q

Pathogenic mechanisms of S. aureus: Invasive mechanisms

staphylokinase

A

acts as antagonist to coagulase

dissolves fibrin strands

allows org cells to leave clot when space and nutrients become limited

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44
Q

Pathogenic mechanisms of S. aureus: Invasive mechanisms

beta lactamase

A

AKA penicillinase

breaks down penicillin; breaks bond in lactam ring, rendering it inactive

now present in 90% of S. aureus strains

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45
Q

Pathogenic mechanisms of S. aureus: toxin production (3)

A
  1. Enterotoxin A-E
  2. Exfoliative toxin
  3. Toxin 1
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46
Q

Pathogenic mechanisms of S. aureus: toxin production

Enterotoxin A-E

A

affects lining of GI tract

stimulates intestinal muscle contractions, nausea, and intense vomiting

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47
Q

Pathogenic mechanisms of S. aureus: toxin production

Exfoliative toxin

A

AKA epidermolytic toxin

causes patients skin cells to separate from each other and slough off body

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48
Q

Pathogenic mechanisms of S. aureus: toxin production

Toxin 1

A

TSST-1

causes toxic shock syndrome

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49
Q

Pathogenic mechanisms of S. aureus: cytolytic toxins

A

alpha, beta, delta, gamma

toxic for many cells including:

  • leukocytes
  • erythrocytes
  • platelets
  • macrophages
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50
Q

CoNS (4)

A

S. epidermidis

S. saprophyticus

S. haemolyticus

S. lugdunensis

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51
Q

CoNS: S. epidermidis

A

most common aerobic bacteria on skin

cause of 70-80% of CoNS infections

Low virulence - opportunistic

Causes nosocomial infections

Slime layer is an important virulence factor for S. epi

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52
Q

CoNS: S. saprophyticus

A

UTIs in sexually active women and older males

adhere to epithelial cells lining urogenital tract
-causes cystitis

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53
Q

CoNS: S. haemolyticus

A

NF usually seen in clinical samples

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54
Q

CoNS: S. lugdunensis

A

NF on skin

can cause osteomyelitis and septicemia

most known for causing aggressive endocarditis

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55
Q

Nosocomial infection

A

hospital acquired infection (HAI)

plastic prosthetic devices, catheters, IVs
-slime layer; adherence factor

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56
Q

can report out as CoNS unless:

A

Urine or sterile sites, esp prosthetic devices

would want to work up further in these cases

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57
Q

Genera that are considered pathogenic cocci

A 
Staphylococcus
Micrococcus 
Streptococcus
Enterococcus
Neisseria
Moraxella
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58
Q

Lancefield classification scheme

A

based on components found in cell wall

causes different serological rxns

divides streps into three categories

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59
Q

3 categories of strep based on lancefield classification

A
  1. C carbohydrates
  2. Lipoteichoic acid
  3. Non-lancefield
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60
Q

Streptococcus species (7 groups)

A 
S. pyogenes
S. agalactiae
S. pneumoniae
Viridans group (S. mutans, S. sanguis, S. salivarius, S. mitis, S. milleri)
E. faecalis
E. faecium
Group D streps
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61
Q

Characteristics of Streptococcus: GS rxn

A

GPC

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62
Q

Characteristics of Streptococcus: cellular morphology

A

usually in chains

S. pneumo is diplococci

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63
Q

Characteristics of Streptococcus: Serologic groupings

A

lancefield groups

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64
Q

Characteristics of Streptococcus: colony morphology

A

non-pigmented, small colonies

ground glass

translucent

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65
Q

Characteristics of Streptococcus: hemolysis

A

alpha, beta, gamma

CAN be used for ID

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66
Q

Lancefield classifications: C carbohydrates

A

5 groups: A, B, C, F, G

-each cause different serological rxns

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67
Q

Lancefield classifications: lipoteichoic acid

A

no C carbohydrate

serological rxn caused by lipoteichoic acid

group D streps: S. bovis, S. equinus, E. faecalis, E. faecium

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68
Q

Lancefield classifications: non-lancefield

A

neither C carbs nor lipoteichoic acid serotypes

S. pneumo, viridans streps

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69
Q

Lab ID of GAS: hemolysis

A

BETA - complete lysis around individual colonies

due to streptolysin S & O

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70
Q

Lab ID of GAS: antimicrobial

A

Bacitracin susceptible (99%)

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71
Q

Streptolysin S

A

O2 stable

OK in presence of O2

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72
Q

Streptolysin O

A

O2 labile

NOT O2 tolerant

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73
Q

Criteria needed to report throat culture GAS positive (3)

A

1) strong beta hemolysis
2) streptolysin O positive
3) bacitracin susceptible

reported as: S. pyogenes or GAS

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74
Q

SXT plate

A

GAS isolation media

BAP + sulfamethoxazole + trimethroprim

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75
Q

PYR test

A

spot test - PYR enzyme

positive = RED disk after adding cinnamaldehyde reagent (2-5 min)

100% definitive for GAS

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76
Q

PYR test precautions

A

not enough organism can result in false negative

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77
Q

GAS rapid test

A

extracts C carb from swab using reagent

*IF NEGATIVE - must do culture; bacitracin + stab o

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78
Q

latex agglutination kits procedure (and what groups?)

A

for groups A-D, F, G

  1. rapid extraction of C carb and liptoteichoic acid
  2. drop each set of latex beads (A,B,C,D,F,G) on card (antibodies for each C carb and lipoteichoic acid)
  3. one drop of extracted organism
  4. tilt card for 2-3 minutes
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79
Q

Pathogenicity of GAS (6)

A

M protein

DNase

Hyaluronidase

Streptokinase

Streptolysin O and S

Pyrogenic exotoxins

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80
Q

Pathogenicity of GAS (6)

A

M protein

DNase

Hyaluronidase

Streptokinase

Streptolysin O and S

Pyrogenic exotoxins

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81
Q

Pathogenicity of GAS: m protein

A

unique to S. pyogenes

membrane protein attached to peptidoglycan

80 different serological groups
-this is why you can get it a bunch of times

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82
Q

Pathogenicity of GAS: m protein fxns

A

resists phagocytosis

adherence to mucosal cells

destabilizes complement and interferes with opsonization and lysis

*similar to S. aureus mechanisms

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83
Q

Pathogenicity of GAS: DNase

A

enzyme that breaks down DNA

gives org more room to move (pus is very viscous; makes it hard to move around/spread)

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84
Q

Pathogenicity of GAS: hyaluronidase

A

“spreading factor”

breaks down connective tissue/hyaluronic acid in connective tissue

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85
Q

Pathogenicity of GAS: streptokinase

A

breaks up fibrin clots

helps w/ spread of org

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86
Q

Pathogenicity of GAS: streptolysin O & S

A

membrane bound proteins

breaks down/lyse RBCs, WBCs, and platelets

interfere with the O2 carrying capacity of blood, immunity, and blood clotting

after GAS has been phagocytized, releases streptolysins into the cytoplasm of the phagocyte; causes lysosomes to release their contents; which lyses the phagocyte and releases the bacteria

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87
Q

Pathogenicity of GAS: pyrogenic exotoxins

A

3 toxins that cause macrophages to release cytokines

causes fever, rash, shock

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88
Q

Diseases of GAS (2 groups)

A
  1. localized infections

2. sequelae diseases

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89
Q

Diseases of GAS (2 groups)

A
  1. localized infections

2. sequelae diseases

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90
Q

Diseases of GAS: localized infections definition and examples

A

rapid onset

purulent, pus, build up of fluid

includes: pharyngitis, impetigo, erysipelas, cellulitis

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91
Q

Diseases of GAS: localized infections definition and examples

A

rapid onset

purulent, pus, build up of fluid

includes: pharyngitis, impetigo, erysipelas, cellulitis

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92
Q

Diseases of GAS: pharyngitis

A

AKA strep throat; inflammation of pharynx

abrupt sore throat

malaise, fever, headache

most prevalent ages 5-15: 90% bacterial (90% GAS), 10% viral

for adults: 10% bacterial, 90% viral

*M protein antibodies

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93
Q

Diseases of GAS: impetigo

A

usually caused by GAS

GAS can also cause bolus impetigo

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94
Q

Pyoderma

A

confined, pus-producing lesion

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95
Q

Diseases of GAS: Erysipelas

A

clear demarcations (edges of the infection well defined)

when a strep infection also involves the surrounding lymph nodes and triggers pain and inflammation

most common on faces of kids

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96
Q

Diseases of GAS: Cellulitis

A

may develop following deeper invasion of GAS following erysipelas

may be serious, even life threatening esp in cases where bacteria become septicemic

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97
Q

Diseases of GAS: sequelae diseases definition

A

post-streptococcal diseases

98
Q

Diseases of GAS: scarlet fever

A

AKA scarletina

appears 1-2 days after pharyngitis:

  • S. pyogenes releases pyogenic exotoxins
  • produces rash that usually begins on chest (goes away about a week later)
  • strawberry red tongue
  • sloughing off of skin
99
Q

Diseases of GAS: rheumatic fever cause and consequences

A

complication of untreated S. pyogenes pharyngitis

inflammation leads to damage of heart valves and muscle

thought to be caused by immune response to GAS:

  • antibodies targeting the bacteria cross react w/ heart antigens
  • bodies immune response gets confused
100
Q

Diseases of GAS: acute glomerulonephritis

A

antibody and antigen compounds not removed from blood

  • get stuck/accumulate in glomeruli of nephrons
  • causes inflammation of nephrons and reduced blood flow (results: hypertension, low urine output)
  • can lead to destruction of kidneys
101
Q

Diseases of GAS: invasive GAS disease

A

GAS secretes enzymes & toxins that destroy fascia connective tissue around muscle

*org can move ~1 inch per hour! very fast!

amputation sometimes only way to stop it; 50% of patients die

102
Q

Factors that lead to fast spread of GAS

A

DNase

hyaluronidase

exotoxins

streptokinase

(basically all virulence factors in combination)

103
Q

Diseases of GAS: streptococcal toxic shock syndrome

A

can spread from original site of infection and cause septicemia

*mostly seen in immunocompromised individuals

symptoms include: inflammation, pain, fever, chills, nausea, vomiting; can lead to shock, organ failure, death (over 40% patients die)

104
Q

Importance of diagnosing pharyngitis caused by GAS

A

consequences of GAS very serious very dangerous and can spread very rapidly without intervention

105
Q

Treatment of GAS

A

penicillin

for penicillin sensitive patients: erythromycin, cephalosporin

bacitracin (topical)

106
Q

Rapid strep ELISA steps/explanation

A

1) extraction of GAS C carb from swab

107
Q

Methicillin

A

semi-synthetic form of penicillin

not inactivated by beta lactamase

108
Q

MRSA

A

methicillin-resistant Staphylococcus aureus

109
Q

protein adhesin

A

secreted by pathogenic pneumococci

protein that mediates binding of cells to epithelial cells of the pharynx

110
Q

Sty definition

A

folliculitis that occurs at base of eyelid

111
Q

empyema definition

A

when infection from pneumonia spreads to space between lung and chest wall; pus builds up

112
Q

empyema definition

A

when infection from pneumonia spreads to space between lung and chest wall; pus builds up

113
Q

Problems associated with Vancomycin (2)

A
  1. has some serious side effects

2. takes much longer to kill the bacteria than oxacillin

114
Q

GBS

A

S. agalactiae

115
Q

GBS lab identification: GS

A

no specific pattern, pairs kinda, clusters kinda

GPC

116
Q

GBS lab identification: hemolysis

A

smoky beta hemolysis

translucent colonies

GBS does NOT have streptolysin O

117
Q

GBS lab identification: PYR

A

negative

118
Q

GBS lab identification: antimicrobials

A

bacitracin resistant

119
Q

GBS lab identification: CAMP test

A

positive (arrowhead)

120
Q

CAMP test method/reasoning

A

action of 2 enzymes:
1. beta hemolysin of S. aureus
PLUS
2. Beta hemolysin of S. agalactiae

creates an enhanced zone of hemolysis (arrowhead) after overnight incubation

121
Q

GBS lab identification: hippurate hydrolysis

A

positive (purple)

122
Q

Hippurate hydrolysis method/reasoning

A

Sodium hippurate + colonies of organism are incubated overnight @ 37C

123
Q

GBS screen reason

A

to protect pregnant mothers and newborns

124
Q

GBS method/procedure

A

done around 35-37 weeks of pregnancy

vaginal/rectal swab put into LIMs broth and incubated overnight; then plated on BAP for ID

OR

Strep B carrot broth - takes about 6 hrs

125
Q

LIMs broth ingredients

A

todd hewitt broth + colisitin + nalidixic acid

THB = enriched media for GBS
Colistin + nalidixic acid = knocks out normal flora

126
Q

Strep B carrot broth

A

chromogenic pigments for ID of GBS (pos = orange)

dont have to plate after

127
Q

Diseases of GBS/S. agalactiae (3)

A
  1. maternal septicemia
  2. neonatal infections
  3. infections of female GU tract

*part of NF in vagina for 10-30% of females

128
Q

Diseases of GBS/S. agalactiae: maternal septicemia

A

post partum infections

puerperal fever

129
Q

Diseases of GBS/S. agalactiae: neonatal infections

A

GBS responsible for ~1/3 of neonatal infections

early onset:

  • pneumonia
  • meningitis (70% of cases of meningitis in newborns is GBS)

late onset: around 3 months after birth

  • not as severe usually
  • usually acquired from environment rather than mom
130
Q

Diseases of GBS/S. agalactiae: infections of female GU tract

A

UTI

131
Q

GBS antimicrobial therapy

A

penicillin

prophylactically administered to newborns whose mothers are colonized with GBS

132
Q

S. pneumoniae lab identification: GS

A

GP diplococci

lancet shape

capsule can be seen sometimes

133
Q

S. pneumoniae lab identification: hemolysis

A

alpha hemolysis met hemoglobin!

can be used to ID S. pneumo
always recorded from BAP and CNA (never CHOC obviously)

134
Q

S. pneumoniae lab identification: colony morphology

A

pinpoint alpha on BAP, small pinpoint on CNA

“penny edge”
-autolytic enzymes dissolve and collapse center of colony

135
Q

S. pneumoniae lab identification: antimicrobials

A

optochin (p disk) susceptible

disk: ethylhydrocupreine hydrochloride

136
Q

S. pneumoniae lab identification: bile solubility test

A

positive

137
Q

bile solubility test method/purpose

A

triggers autolytic enzymes

tube method

plate method

138
Q

quelling rxn

A

rarely used today

ID S. pneumo

a type of specific capsular antigen added to the org cells which causes the cell capsule to swell; antibodies bind to the bacterial capsule

visualized microscopically

quellung = german word for swelling

139
Q

Sputum sample notes:

A

S. pneumo considered NF in URT (esophagus, larynx, and above)

LRT considered sterile

sputum collection = deep lung aspirate
-high # epis, probably just spit not sputum

140
Q

Diseases of S. pneumo (3)

A
  1. pneumonia
  2. ear and eye infections
  3. meningitis and septicemia

*S. pneumo is an opportunistic pathogen

141
Q

Diseases of S. pneumo: pneumonia

A

aka pneumococcal pneumonia

symptoms: high fever, sharp chest pains, difficulty breathing, lung congestion, rust colored sputum

142
Q

Diseases of S. pneumo: ear and eye infections

A

ear infections aka otitis media

50% of all cases due to H. flu and S. pneumo

143
Q

Diseases of S. pneumo: meningitis and septicemia (most common causative agents)

A 
#1 N. meningitidis 
#2 S. pneumo
144
Q

S. pneumo virulence factors: (4)

A
  1. capsule
  2. pneumolysin enzyme
  3. secretory IgA protease
  4. Phosphorylcholine
145
Q

S. pneumo virulence factors: capsule

A

produces polysaccharide capsule

80 different capsular antigens

colonies from virulent strains mucoid on BAP

*avirulent strains produce no capsule

146
Q

S. pneumo virulence factors: pneumolysin enzyme

A

binds to cholesterol in membranes of epithelial cells

produces transmembrane pores that result in lysis of the cell

suppresses digestion of engulfed bacteria which interferes w/ action of lysosomes

147
Q

S. pneumo virulence factors: phosphoryl choline

A

in S. pneumo cell wall

binds to receptors in lungs, meninges, & blood vessel walls; can pass across these cells and into blood

stimulates cells to engulf bacteria

148
Q

S. pneumo virulence factors: secretory IgA protease

A

body limits movement to lungs by binding active sites of secretory IgA; this then gets trapped in the mucous

protease DESTROYS IgA

149
Q

S. pneumo antimicrobial treatment

A

penicillin

erythromycin, others

150
Q

Pneumococcal vaccine

A

available for the most common serotypes of S. pneumo

consists of purified capsular material from 23 different strains (which covers about 94% of clinical isolates)

recommended for over age 65

151
Q

Enterococcus spp. and GDS lab identification: GS

A

GPC

152
Q

Enterococcus spp. and GDS lab identification: cell morphology

A

no particular morphology

can be kind of oval in shape, elongated

153
Q

Enterococcus spp. and GDS lab identification: colony morphology

A

translucent to light gray colonies

154
Q

Enterococcus spp. and GDS lab identification: hemolysis

A

beta, alpha, gamma

BUT generally gamma

155
Q

Enterococcus spp. and GDS lab identification: bile esculin hydrolysis

A

BOTH spp. positive - black color change

156
Q

bile esculin hydrolysis

A

bile - Enterococcus and GDS grow in present of bile but other orgs are inhibited by it, especially GPC

esculin - Enterococcus and GDS hydrolyze esculin

esculin –> esculetin + glucose –> reacts w/ ferric citrate in media –> BLACK color

157
Q

Enterococcus spp. and GDS lab identification: NaCl broth

A

Enterococcus POS, GDS NEG

yellow color change

158
Q

NaCl broth

A

nutrient broth + 6.5% NaCl

*set up 6.5% NaCl broth and Bile esculin broth at the same time

159
Q

Enterococcus spp. and GDS lab identification: PYR

A

enterococcus positive

GDS negative

160
Q

Enterococcus catalase rxn

A

WEAK CATALASE POSITIVE NOT TRUE POSITIVE

161
Q

important Enterococcus spp.

A

E. faecalis
E. faecium

  • N.F. in intestinal tract (entero=intestinal) and URT (upper respiratory tract)
  • common cause of nosocomial infections and UTIs
162
Q

non-enterococcus/GDS spp.

A

Streptococcus bovis
Streptococcus equinis

*zoonotic diseases

163
Q

Nosocomial infection definition

A

opportunistic org that infects an individual after 3 days of being in the hospital

164
Q

GDS antimicrobials

A

GDS susceptible to penicillin

165
Q

Enterococcus antimicrobials

A

Enterococcus resistant to penicillin

Vancomycin currently drug of choice

166
Q

VRE

A

vancomycin resistant enterococcus

167
Q

enterococcosel plate with vancomycin

A

selective and differential plating media

growth on plate would indicate RESISTANT strains of enterococcus

sometimes used with urine cultures as primary plating media

168
Q

Strep viridans spp.

A 
S. mutans
S. sanguis
S. salivarius
S. mitis 
S. milleri

major components of URT NF
not primary pathogens (low virulence) but may become opportunistic

169
Q

Viridans meaning

A

means “greening”

170
Q

Strep viridans hemolysis

A

alpha on BAP

171
Q

causative agent of tooth decay

A

S. mutans

172
Q

major disease of Strep viridans

A

bacterial endocarditis

commonly preceded by dental extraction, oral surgery, and occasionally after routine teeth cleaning

can lead to heart failure

173
Q

major disease of Strep viridans

A

bacterial endocarditis

commonly preceded by dental extraction, oral surgery, and occasionally after routine teeth cleaning

can lead to heart failure

174
Q

Group C Streps

A

frequently causes infection in many animal species but are rare causes of disease in humans

175
Q

how to determine colony forming units per mL

A

colonies x dilution factor = CFU/mL

176
Q

dilution factor for 1 microliter loop (.001 mL)

A

1000

177
Q

dilution factor for 10 microliter loop (.01 mL)

A

100

178
Q

clean catch definition

A

midstream catch

179
Q

Urine cultures interpretive and reporting guidelines: when the colony count on a plate exceeds 100 colonies, report out as ______

A

a MAXIMUM of “> 100,000 CFU/mL”

180
Q

Urine cultures interpretive and reporting guidelines: when there is a single pathogen or two potential pathogens > 20,000 CFU/mL what should you ID?

A

ID to genus and species

181
Q

Urine cultures interpretive and reporting guidelines: predominant growth of one org with 2 or 3 additional orgs, what should you ID?

A

ID predominate org and describe the others

182
Q

Urine cultures interpretive and reporting guidelines: no predominate org with 3+ org types, what should you ID?

A

probably non-clean catch sample

include:

1) CFU/mL
2) description of the colonies with GS rxn
3) # of colony types present

183
Q

Urine cultures interpretive and reporting guidelines: < 10,000 CFU/mL with 1, 2, 3, or more colony types, what should you ID?

A

probably non-clean catch sample

include:

1) CFU/mL
2) description of the colonies with GS rxn
3) # of colony types present

184
Q

Urine cultures interpretive and reporting guidelines: do not use _____ when reporting urine cultures

A

the term normal flora

185
Q

urine cultures commonly contaminated with ___?

A

urethral normal flora

CoNS, Streps, Lactobacillus, diptheroids (GPRs)

186
Q

Urine sample types: clean catch

A

pt instructed to clean genital area thoroughly before collection to reduce contamination with NF

187
Q

Urine sample types: midstream

A

pt usually instructed to begin voiding and then collect urine

helps flush out small amounts of bacteria that may be present in urethra which are not causing infection

188
Q

Urine sample types: catheterized

A

urine collected by passing a catheter through urethra into the bladder

meant to decrease contamination with urethral flora or in patients who may be unable to urinate

189
Q

Urine sample types: suprapubic aspiration

A

urine collected by passing a needle into bladder

used sometimes on infants and in other difficult cases

190
Q

Urine specimen requirements

A

urine culture should be set up within 1 hour of receipt or refrigerated

otherwise bacteria (including NF, contaminants) will quickly multiply which makes interpretation of culture difficult

191
Q

patient factors to consider when interpreting urine cultures

A

age

history

192
Q

true infections will often yield ______

A

50,000 CFU/mL or more

193
Q

you might see small numbers of orgs in _____

A

kidney infections

infant infections

UTIs in pregnant women

*should still be considered significant

194
Q

orgs to look for in urine cultures

A

CoNS (esp in young women and hospitalized patients)

Coliforms (esp E. coli) (common in all ages and hospitalized patients)

Enterococcus spp.

GBS and other types of Strep

Pseudomonas spp. and other GNBs

Yeasts such as Candida spp.

195
Q

Genus’ in the family Neisseriaceae

A

Neisseria

Moraxella

GNDC with flattened adjacent sides

196
Q

Species in the family Neisseriaceae

A

N. gonorrhoeae (very common, a leading STD)

N. meningitidis (a leading cause of meningitis, can be NF)

N. sicca, N. subflava, N. flavescens, N. mucosa, N. cinerea (typically non pathogenic)

Moraxella catarrhalis (opportunistic pathogen)

197
Q

Special requirements for Neisseria gonorrhoeae specimens: Specimen collection and transport

A

1) cannot use calcium alginate or cotton swabs (dacron or rayon swabs instead)
2) sensitive to drying during transport to lab (must be plated w/i 6 hrs; gonococcal (GC) transport media)

198
Q

Special requirements for Neisseria gonorrhoeae specimens: temp requirements

A

specimen must be kept at room temp or above

199
Q

Special requirements for Neisseria gonorrhoeae specimens: nutrient requirements

A

requires hemin (bc fastidious)

NG on BAP

WILL grow on CHOC

200
Q

Special requirements for Neisseria gonorrhoeae specimens: air requirements

A

prefers 3-5% CO2

CAPNOPHILE

201
Q

JEMBEC plate

A

sodium bicarbonate + sodium citrate disk (helps with CO2 levels)

202
Q

Specimen sources for Neisseria gonorrhoeae (4)

A

Urethra (urethral discharge), vaginal, cervical, and anal swabs

Surgical tissues from PID patients (pelvic inflammatory disease)

Throat swabs

Joint fluids

203
Q

Specimen sources for Neisseria meningitidis (2)

A

CSF (if > 1 mL, centrifuge 1500 x g for 15 min)

  • direct GS
  • plated onto CHOC

Blood

204
Q

Primary plating media for Neisseria gonorrhoeae (4)

A

Thayer Martin (TM)

Modified Thayer Martin (MTM)

New York City (NYC)

CHOC

205
Q

Precautions for plating Neisseria specimens

A

CHOC plate should always be included because 5% of N. gonorrhoeae strains are susceptible to vancomycin

Species related to Neisseria can also grow on the Neisseria plating media, specifically Kingella and Acinetobacter spp. (GNRs)

206
Q

Modified Thayer Martin composition

A

CHOC + 4 antibiotics

  1. vancomycin - inhibits GPC
  2. colistin - inhibits GNRs
  3. nystatin - inhibits yeast
  4. Trimethoprim lactate - inhibits Proteus spp.

(same as TM + one antibiotic)

207
Q

Modified Thayer Martin composition

A

CHOC + 4 antibiotics

  1. vancomycin - inhibits GPC
  2. colistin - inhibits GNRs
  3. nystatin - inhibits yeast
  4. Trimethoprim lactate - inhibits Proteus spp.

(same as TM + one antibiotic)

208
Q

New York City plate

A

transparent media w/ hemin added

4 antibiotics:

  1. vancomycin - inhibits GPCs
  2. colisitin - inhibits GNRs
  3. amphotericin B - inhibits yeast
  4. trimethoprim lactate - inhibits Proteus spp.
209
Q

Neisseria lab ID: GS rxn

A

GNDC

210
Q

Neisseria lab ID: colony morphology

A

tiny, gray, translucent @ 24 hours

N. gonorrhoeae will NOT grow on BAP

N. meningitidis WILL grow on BAP and CHOC

211
Q

Neisseria lab ID: air requirements

A

capnophile (prefers higher CO2)

212
Q

Neisseria lab ID: catalase

A

POSITIVE

213
Q

Neisseria lab ID: oxidase

A

POSITIVE

214
Q

Oxidase test reagent and methods (2)

A

reagent: N,N-dimethly-p-phenylene-diamine HCL

methods:

  1. glass slide: transfer colonies using wooden stick, add one drop of reagent onto filter paper
  2. plate method: on a 24 hr plate, actively growing culture drop reagent straight onto plate
215
Q

Oxidase test precautions (3)

A
  1. use a wooden stick to transfer colonies NOT a steel loop
  2. do NOT use MAC plate to test for oxidase, will give false negative
  3. if E. coli is used as negative control directly from fridge (cold), it will give a weak oxidase rxn
216
Q

Virulence factors of pathogenic Neisseria gonorrhoeae (5)

A
  1. Capsule
  2. Pili (fimbriae)
  3. Cell wall proteins
  4. Endotoxin
  5. IgA protease
217
Q

Virulence factors of pathogenic Neisseria gonorrhoeae: capsule

A

Functions:

  1. keep from drying out
  2. inhibit phagocytosis
  3. adherence to tissues

**N. meningitidis - 5 strains encapsulated (a, b, c, y, w135)

218
Q

Virulence factors of pathogenic Neisseria gonorrhoeae: pili (fimbriae)

A

both strains! but esp N. gonorrhoeae

Functions:

  1. inhibit phagocytosis
  2. adherence to host tissue
  3. pass genetic info from strain to strain
  • *N. gonorrhoeae have 5 strains:
  • T1 & T2 have pili - VIRULENT
  • T3, T4, T5 no pili - avirulent
219
Q

Virulence factors of pathogenic Neisseria gonorrhoeae: cell wall proteins

A

aka outer membrane proteins
basis of ELISA tests

  • Protein I
  • Protein II
  • Protein III

also inhibit phagocytosis

220
Q

Virulence factors of pathogenic Neisseria gonorrhoeae: endotoxin

A

outer portion of cell; lipoligosaccharide instead of LPS; lacks O antigen

functions:
1. inhibits phagocytosis
2. cause damage to host cell tissues

221
Q

Virulence factors of pathogenic Neisseria gonorrhoeae: IgA protease

A

breaks down IgA

mucosal cells with secretory IgA: URT, GI, urogenital, saliva, tears, breast milk

222
Q

diseases of Neisseria gonorrhoeae (3)

A
  1. gonorrhoeae
  2. PID
  3. gonococcal opthalmia
223
Q

diseases of Neisseria gonorrhoeae (3)

A
  1. gonorrhoeae
  2. PID
  3. gonococcal opthalmia (opthalmia neonatorum)
224
Q

diseases of Neisseria gonorrhoeae: gonorrhea

A

Males: acute urethritis, purulent discharge, dysuria

Females: dysuria, lower abdominal pain, vaginal bleeding

225
Q

diseases of Neisseria gonorrhoeae: PID

A

pelvic inflammatory disease

infection of uterus, fallopian tubes, and adjacent pelvic structures

caused by two types of STDs

25% of women with gonorrhea contract PID

can led to infertility or ectopic pregnancy

226
Q

diseases of N. meningitidis (2)

A
  1. meningitis

2. meningococcemia

227
Q

diseases of N. meningitidis (2)

A
  1. meningitis

2. meningococcemia

228
Q

Non pathogenic Neisseria (5)

A
  1. N. sicca
  2. N. subflava
  3. N. flavescens
  4. N. mucosa
  5. N. cinerea
229
Q

penicillin mechanism of action

A

generally effective against gram positive cell walls

interferes with synthesis of peptidoglycan

230
Q

Penicillin binding proteins (PBPs)

A

bind to the transpeptidases

231
Q

MRSE

A

methicillin resistant S. epidermidis

232
Q

VRSE

A

vancomycin resistant S. epidermidis

233
Q

Penicillin binding proteins (PBPs)

A

bind to the transpeptidases (enzymes) that bind the tetrapeptide crossbridge to the NAM molecules in GPOs during synthesis of peptidoglycan

penicillin binds directly to these PBPs and prevents the crossbridges from binding to the NAM

234
Q

beta lactamase

A

enzyme that is able to inactive penicillin

breaks apart the beta lactam ring of penicillin which produces an inactive form of the drug called penicilloic acid

~95% of S. aureus strains produce beta lactamase

235
Q

methicillin mechanism of action

A

same as penicillin; binds to transpeptidases (PBPs)

236
Q

mechanism of MRSA resistance to methicillin

A

MRSA strains have modified transpeptidases so that the drug cannot recognize the enzyme

237
Q

MRSA drug of choice

A

vancomycin

238
Q

vancomycin drawbacks (2)

A
  1. has some serious side effects

2. takes much longer to kill the bacteria than oxacillin

239
Q

VRSE

A

vancomycin resistant S. epidermidis

240
Q

benefits of oxacillin (2)

A
  1. more stable than methicillin

2. longer shelf life

241
Q

VRSA

A

vancomycin resistant S. aureus

Clin Micro 1 (3 decks)

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