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Micro Exam #2 > Staph and Strep > Flashcards

Staph and Strep Flashcards

1
Q

Describe the physical structure of Staphylococci?

A

G+ cocci in clusters

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2
Q

What is the catalase sensitivity of Staphylococci?

A

Catalase +

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3
Q

How does Staphylococci feel about salt?

A

Tolerant, grow up to 9%

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4
Q

What two factors are used to differentiate Staphylococci?

A

Hemolysis

Coagulase

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5
Q

Clinical presentations of Staphylococcus Aureus caused mainly by bacterial growth?

A

Fununcles
Folliculitis
Non-bullous impetigo
Bacteremia/Wound Infections

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6
Q

How are furuncles walled off?

A

Coagulase

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7
Q

What is Staphylococcus Aureus folliculitis associated with?

A

Shaving
Contact with Fomite
Complication of Acne

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8
Q

Primary cause of acne?

A

Proprionibacterium acnes

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9
Q

What is non-bullus impetigo?

A

Infection is the superficial epidermis
Most Common Bacterial Skin Disease
Crusted Blisters

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10
Q

Who usually gets non-bullus impetigo?

A

Children and Teens

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11
Q

Two most frequent causes of non-bullus impetigo?

A

Staphylococcus Aureus

Strep – Group A

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12
Q

Staphylococcus Aureus bacteremis/wound infection is a major concern in…

A

Surgical wounds

Esp. deep incisions that go into muscle, or organ space

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13
Q

Clinical presentations of Staphylococcus Aureus typically associated with exotoxin release.

A

Bullous exfoliation

Bullous impetigo

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14
Q

What is Bullous exfoliation?

A

Staphylococcal scalded skin syndrome

Intraepidermal splitting and peeling of top layers

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15
Q

Who gets bullous exfoliation?

A

Mostly Children

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16
Q

Prognosis of Staphylococcus Aureus bullous exfoliation in kids? adults?

A

Kids – Good Prognosis

Adults – Bad – Indicates Bacteremia

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17
Q

What is Staphylococcus Aureus bullous impetigo?

A

Fluid filled blisters within the epidermis

Painful

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18
Q

Who gets Staphylococcus Aureus bullous impetigo?

A

Kids under 2 years old

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19
Q

Cause of Staphylococcus Aureus bullous impetigo?

A

Exfoliative Toxin

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20
Q

What is a Staphylococcus Aureus bully?

A

A fluid filled blister in the epidermis

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21
Q

Clinical presentation of Toxic Shock Syndrome?

A

Abrupt onset fever
Rash with desquamination
Hypotension
Multisystem, DIC

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22
Q

Two types of Toxic Shock Syndrome?

A

Menstrual and Nonmen (M&F-often nosocomial)

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23
Q

Cause of Toxic Shock Syndrome?

A

TSST triggers immune rxn

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24
Q

Clinical presentation of Staphylococcus Aureus food poisoning?

A

Violent Nausea, Vomiting, Diarrhea
NO Fever
VERY quick (gone within 24)

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25
Q

Food poisoning in which you see more vomiting than diarrhea? (3)

A

B cereus
Staphylococcus Aureus
Norovirus

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26
Q

Why is there a different presentation of Toxic Shock and Food Poisoning.

A

You have lots of Tregs in the gut and few in the bloodstream

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27
Q

Typical clinical presentation of Staphylococcus epidermis?

A

Nosocomial Infections, esp. in surgery

Biofilm Formation

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28
Q

Typical clinical presentation of Staphylococcus saprophyticus?

A

UTI in young women

Has specific adhesion for UT epithelia

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29
Q

Menstrual TSS is associated with…

A

Retained tampons

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30
Q

Why can’t you eradicate Staphylococcus?

A

Its a part of the normal flora

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31
Q

Why is Staphylococcus difficult to treat?

A

Rapid multi-drug resistance development (ex. MRSA)

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32
Q

Four antigens associated with Staphylococcus?

A

PG
Teichoic Acids
Protein A
Iron Binding Proteins

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33
Q

What does Protein A do?

A

Binds to Fc part of Ab

Allows bacteria to present “self” antigens to body

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34
Q

Toxins associated with Staphylococcus? (6)

A 
Coagulase
Hyaluronidase/Streptokinase
Hemolysins
Exfoliative Toxin
TSST-1
Enterotoxins
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35
Q

What does coagulase do?

A

Walls off infection

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36
Q

What does hyaluronidase/strepto do?

A

Tissue Invasion

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37
Q

Name three types of hemolysins (and targets)

A 
alpha toxin (RBCs, plat)
beta toxin (sphingomyelin)
Leukocidin (WBC)
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38
Q

What is PVL?

A

Panton-Valentine Leukocidin

Pore forming toxin associated with MRSA, esp. USA300

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39
Q

What does Exfoliative toxin do?

A

Cleaves N Terminal of desmoglein-1 cell-cell adhesin

scalded skin syndrome, bullous impetigo

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40
Q

What is TSST-1?

A

A superantigen

Induces T cells to produce IL1, TNF

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41
Q

What are the two superantigens discussed with Staphylococcus?

A

TSST-1

Enterotoxins (Food Poisoning)

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42
Q

How are superantigen toxins spread from bacteria to bacteria?

A

On PAIs via transduction.

Horiz Gene transfer

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43
Q

What steps have been made to improve hospital MRSA control?

A

Better ahnd hygiene
Targeting catheter infections
MRSA-specific detection and decolonization

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44
Q

Give an example about how docolonization might pan out?

A

Chlorhexidine washes

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45
Q

How are recurrent Staphylococcus furuncles treated?

A

drainage and tetracycline

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46
Q

Preferred antibiotics for Staphylococcus?

A

nafcillin
oxacillin
cefazolin

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47
Q

How is MRSA typically treated?

A 
SxT
Clindamycin
Doxy
Linezolid
IF SEVERE -- Vanco
48
Q

How had MRSA treatment be optimized?

A

Susceptibility Testing

49
Q

Staphylococcus antiobiotic resistance spreads via ___ plasmids.

A

R-

50
Q

Describe the physical structure of Streptococci and enterococci.

A

G+ Cocci

May be oval in chains/Pains

51
Q

Describe the oxgen requirements of Streptococci

A

Facultative, but prefer 5-10% CO2

52
Q

Streptococci capsules are made with…

A

Group A – Hyaluronic Acid

Polysaccharide

53
Q

Classification of Streptococci is based on…

A

Hemolysis
Serotyping
Biochemistry
Colonization pattern

54
Q

Difference between alpha and beta hemolysis?

A

alpha doesn’t steal the iron

beta does steal the iron

55
Q

How does Lancefield serotyping split up Streptococci?

A

Specific amino-sugar and teichoic acid cell wall antigens

A-H, K-U

56
Q

Biochemistry informaiton you would look for in classifying Streptococci?

A

Antibiotic resistance, NaCl tolerance, Bile-esculin

57
Q

Clinical presentation of Group A Streptococci Pyogenes?

A

Invasive Infections

58
Q

Group A Streptococci Pyogenes is which kind of hemolytic?

A

Beta

59
Q

Group A Streptococci Pyogenes is sensitive to what antibiotic?

A

Bacitracin

60
Q

Examples of Group A Streptococci Pyogenes invasive infections (8)

A 
Human Erysipelas
Puerpeual Fever
Surgical Sepsis
Scarlet Fever
Streptococcal Toxic Shock Like Syndrome
Necrotizing Fasciitis
Bacteremia
Penumonia (more serious than pneumococcal)
61
Q

What is Puerpeual Fever?

A

Strep of the uterus

62
Q

Symptoms of Scarlett Fever?

A

Strep bacteremia
Characteristic Diffuse upper body
Rash, Fever, “Strawberry tongue”

63
Q

Usual initial presentation of Group A Streptococci Pyogenes Scarlet Fever?

A

Scarlet Fever

64
Q

What is necrotizing Fasciitis?

A

Deep cellulitis that spreads through sub-Q tissue into and through the deep fascia

Can be staph or strep

65
Q

Why can’t you culture fluid from a Group A Streptococci Pyogenes fluid bully.

A

Its the toxin, not the bacteria

66
Q

Examples of Group A Streptococci Pyogenes local infections (8)

A

Pharyngitis

Impetigo

67
Q

Symptoms commonly seen in Group A Streptococci Pyogenes pharyngitis.

A

Fever, Ant. Cerv. Lymphadenopathy, Tonsil Exudate
NO COUGH
Tonsilar Pus and Palletal Petachiae

68
Q

Describe the clinical presentation of Group A Streptococci Pyogenes impetigo.

A

Crusty, Purulent Blisters
Esp. on Face
ALWAYS non-bullous

69
Q

What do you need to look out for in the weeks following Group A Streptococci Pyogenes? Two manifestations?

A

Autoimmune responses
Acute Rheumatic Fever
Acute Glomerulonephritis

70
Q

What symptom might you look for in Acute Rheumatic Fever

A

Heart Valve Damage following Strep Throat

71
Q

What might you expect to see in the labs of a person with acute glomerular nephritis.

A

Blood and Protein in Urine

72
Q

Reservoirs of Group A Streptococci Pyogenes?

A

Only Humans (10-20% carrier rate)

73
Q

Epidemiology of strep throat…

How does it spread, when does it spread, who does it spread to

A

Nasal Droplets + Contact
Winter
Esp. 6-13 years

74
Q

Epidemiology of Impetigo…

How does it spread, when does it spread, who does it spread to

A

Contact, Contiguity, Fomites (Sheets, Pillows)
Summer/Early Fall
Age Peak in Preschool Children

75
Q

Epidemiology of Rheumatic fever…

How does it occur, when does it spread, who does it spread to

A

Usually 1-4 weeks after disseminated strep

76
Q

Pathogenesis of (How does it spread, when does it spread, who does it spread to) involved what toxins, Vir Factors (8)

A 
M Protein
Hyaluronic Acid Capsule
C Substance
C5a peptidase
Streptokinase
Streptodornase
Exotoxin
Hemolysins
77
Q

Effect of M protein?

A

Cause secretion of heart-reactive antibodies

78
Q

Effect of hyaluronic acid capsule?

A

Mimics host, so antiphagocytic

79
Q

What si C substance?

A

A Capsular polysaccharide that enhances invasiveness

80
Q

What is C5A peptidase

A

Antiphagocytic (anti-complement)

81
Q

What does streptokinase do?

A

Dissolves fibrin clots

82
Q

What does streptodornase do?

A

DNAse, high viscosity pus from nucleoprotein

83
Q

What is hyaluronidase?

A

Spreading Factor

84
Q

Two types of hemolysins seen in Group A Streptococci Pyogenes?

A

Streptolysin O – O2 Sensitive

Streptolysin S – not O2 Sensitive

85
Q

How is Group A Streptococci Pyogenes controlled

A

Prevent spread – pasteurize milk, isolate carriers from patients
Treat acute infections early

86
Q

How are Group A Streptococci Pyogenes treated?

A

All sensitive to PenG

If necessary, anti-inflammatories, rest

87
Q

Species that makes up Group B Strep

A

S agalactiae

88
Q

Group B strep is ____ hemolytic
It is cAMP _____
and Bacitracin _______

A

Beta
Positive
Resistant

89
Q

Clinical presentation of Group B strep is?

A

Neonatal Sepsis/Pneumonia
Neonatal Meningitis
Resp. Distress Syndrome
Bacteremia

90
Q

Who gets Group B strep?

A

Infants, IC, Elderly

91
Q

How is Group B strep usually spread?

A

Spread from infected mothers to baby in delivery

92
Q

How is Group B strep controlled?

A

Screen Before Delivery
If +, 3rd gen Ceph or Amp+Strep
Give baby prophylactics

93
Q

Group D strep consist of….

A

Enterococci and S bovis

94
Q

Group D strep are ______ hemolytic

A

Mostly Non-

Sometimes alpha

95
Q

Clinical presentation of Group D strep?

A

Nosocomial Infections
Bacteremia
Endocarditis
UTI

96
Q

How is Group D strep typically transferred?

A

Hands of hospital workers

Portal of entry — GI tract/bacteremia from colon lesions

97
Q

How is Group D strep controlled? (or not controlled)

A

Enterococci resistant to beta-lactams, SxT

Treat SYNERGISTICALLY with penicillin and aminoglycoside

98
Q

Why might you consider/not consider using vanco to treat enterococcus?

A

It should work, but there is a high frequency of vancomycin resistance in the US

99
Q

Infective endocarditis is typically caused by…

A

Staphylococci and streptococci

100
Q

Oral (Viridans) Streptococci is ___ hemolytic

optochin _________

A

Alpha

Resistant

101
Q

Most common clinical manifestation of Oral (Viridans) Streptococci?

A

Sub-acute bacterial endocarditis
(esp after tooth surgery)
Heart murmur, Weaknes, Anemia, Embolism

102
Q

Prognosis for an untreated Oral (Viridans) Streptococci infection?

A

100% fatal.

103
Q

Who would you expect to get Oral (Viridans) Streptococci infection?

A

Someone who has recently had a dental procedure

104
Q

How is Oral (Viridans) Streptococci treated?

A

Long term, High Dose antibiotic

105
Q

How is Oral (Viridans) Streptococci controlled?

A

Prophylactic antibiotics before/after oral surgery

106
Q

Strep pneumoniae is ___ hemolytic and optochin _____

A

Alpha

Sensitive

107
Q

Strep pneumoniae physical structure…

A

Diplococci with large polysaccharide capsule

108
Q

What is a quellung reaction?

A

Add polyvalent antiserum against capsule + Sputum
If Strep pneumoniae present, capsule will swell
Visualize by negative stain

109
Q

Clinical presentation of Strep pneumoniae?

A

Lobar Pneumonia with Fever, Chills, Sharp Pain
Mental Confusion
Increased Leukocytes
May spread to Middle ear (#2 otitis media)
May spread to meninges (#1 for middle age adults)

110
Q

Describe lobar pneumonia.

A

Consolidation of one+ lobes

Bronchi often open

111
Q

Describe bronchopneumonia

A

Patchy, Peribronchial Thickening

Consolidation of Alveoli

112
Q

Describe Interstitial pneumonia

A

Inflammation and edema of interstitial tissue of the lung

Fibrosis

113
Q

Three risk factors associated with Strep pneumoniae?

A

Mucus accumulation
Alcohol/Drug Use
General Debility (Flu, anemia, COPD)

114
Q

Pathogenesis of Strep pneumoniae?

A

Colonization of tissues
Polysac. capsule and debilitated host are critical
IgA Protease

115
Q

How is Strep pneumoniae controlled?

A

Vaccines available to prevent pneumococcal disease

Micro Exam #2 (15 decks)

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