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Cardiology > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Staphylococci

GENERAL

A

Gram positive, Fac. Aerobe (prefer reduced O2), Normal microbiota, Extracellular pathogens, Catalase Positive , Coagulase positive

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2
Q

Staphylococci aureus Description

A

Pus-filled abscesses, almost every niche of the body
Nasal cavity, axilla, perineum
Small Capsule not important as virulent factor
Exotoxins are a major virulence factor
30% intermittently carry, 20% persistent
CA infections – carrier strain
HA – single strain around facility

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3
Q

Staphylococci aureus Scalded skin syndrome

A

in children < 5 caused by exfoliative toxin A; eta on gene or on a plasmid (exfoliative toxin B, etb) toxins are not active until they reach the skin. They cause skin problems by degrading desmoglein-1, a cadherin protein involved in holding desmosomes together.

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4
Q

Scalded skin syndrome Prognosis

A

most superficial, But in extensive infections, extensive amounts of fluid lost can lead to death. In older children the reaction is usually less severe and may only cause bullous impetigo (i.e. blisters).

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5
Q

Staphylococci aureus superantigen

A

A relatively small percentage of S. aureus produce superantigens, but when they do they usually make several different ones.

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6
Q

Staphylococci aureus enterotoxins

A

S. aureus enterotoxins (SEA, SEB, etc.) cause food poisoning, leading to vomiting (emesis) and cramping.extremely stable proteins. The onset 2-3 hours after ingesting.

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7
Q

Enterotoxins work?

A

also superantigens , but they don’t get into the bloodstream. could also be aerosolized and used as a biowarfare agent. don’t often kill people intoxication rather than an infection, since you can cook the food and kill the bacteria, but the toxin can remain.

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8
Q

Staphylococci aureus Infections

A

Follicullitis (hair follicles) Furuncles (boils)
Carbuncles (bunches of boils)- may have fever, chills. Stye (hordeoleum)
External:Sebaceous glands (Zeiss) Sweat glands (Moll)
Meibomian (or tarsal) glands infected
Chalazion – inflammation due to blockage of Meibomian gland
Bullous impetido
Blistering vesicles that crust over
Severe pneumonia w/ necrotic abscesses (secondary to flu)

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9
Q

Follicullitis

A

(hair follicles)

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10
Q

Furuncles

A

(boils)

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11
Q

Carbuncles

A

(bunches of boils)- may have fever, chills

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12
Q

Stye

A

(hordeoleum)

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13
Q

External: Sebaceous glands

A

(Zeiss)

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14
Q

External:Sweat glands

A

(Moll)

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15
Q

Chalazion

A

Chalazion – inflammation due to blockage of Meibomian (or tarsal) gland

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16
Q

Bullous impetido

A

Blistering vesicles that crust over

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17
Q

Staphylococci aureus Virulence Factors

A

Alpha-toxin/ cyolytic toxin, Panton-Valentine Leukocidin (PVL), Exfoliative Toxin, Enterotoxin, Surface-bound proteins - adhesins, fibronectin, collagen, laminin, etc.MSCRAMM, Hyaluronidase, PAMPs.

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18
Q

Alpha-toxin/ cyolytic toxin.

A

= pore-forming, beta-barrel toxin family. Cells die because they ions

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19
Q

Panton-Valentine Leukocidin (PVL)

A

PVL is a beta-toxin, but it also kills cells by forming pores in the membrane. PVL was transferred to S. aureus by a bacteriophage enhanced virulence CA-MRSA

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20
Q

Surface-bound proteins - Virulence Factors

A

adhesins bind host receptor molecules such as fibronectin, collagen, laminin, etc.

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21
Q

MSCRAMM

A

microbial surface components recognizing adhesive matrix molecules. Many anchored by a mechanism involving sortase.

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22
Q

Hyaluronidase:

A

secreted virulence factor/ enhancer - degrades hyaluronic acid in the connective tissue spaces making bacterial spread through tissues easier.

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23
Q

PAMPs

A

PAMPs cell wall components - stimulators of Toll-like receptors.

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24
Q

Staphylococci aureus TSST-1

A

TSST-1 on a pathogenicity island in the chromosome (can theoretically spread to other bacteria- a mobile genetic element) 5-25% for the fraction of S. aureus isolates that have the gene.

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25
Q

Staphylococci aureus Classification

A

Gram positive, Fac. Aerobe (prefer reduced O2), Normal microbiota, Extracellular pathogens.

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26
Q

Staphylococci aureus Diagnostic

A

Catalase Positive
Coagulase positive (activates pro-thrombin)
Agglutination +
Beta-Hemolytic (clear on BAP)
carotenoid pigment – appear more golden than other staph (more white color)

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27
Q

Staphylococci aureus (ACUTE Infection)

A

ACUTE Infective endocarditis (heart valves)- bulky vegetations platelets attach and fibrinogen is converted to fibrin, plasma proteins bind to these components. A vegetation is a complex biofilm.

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28
Q

Staphylococcal toxic shock syndrome

A

Staphylococcal toxic shock syndrome & tampons- a toxin called Toxic Shock Syndrome Toxin-1 or TSST-1.

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29
Q

Staphylococci epidermidis Description

A

Colonizes skin
Coagulase negative
Carriage rates ~100%

30
Q

Staphylococci epidermidis Infections

A

Indwelling catheters/ medical advices
15-40% prosthetic valve endocarditis
Ensure not a contaminant

31
Q

Staphylococci epidermidis Virulence Factors

A

Thick Capsule

Exotoxins are not as important

32
Q

Staphylococci epidermidis Classification

A 
Gram positive 
Fac. Aerobe (prefer reduced O2)
Normal microbiota
Extracellular pathogens
Catalase positive  
Coagulase negative
33
Q

Streptococci General

A

Range from harmless oral to flesh eating, Faculative anaerobes, Fastidious, grow on BAP, classify by the hemolysis & Lancefield antigen (carbohydrate antigen), Catalase negative (unlike staph), oxidase negative (not Neisseria)

34
Q

Staphylococci saprophyticus Description

A

Urinary Tract Infections
(second to E coli)
Colonizes GI tract, perineum
Coagulase negative

35
Q

Streptococci pyrogenes Description

A

Superantigens, Streptolysin O Titers (SLO), Streptolysin S Titers (SLS)

36
Q

Streptococci pyrogenes Infections

A

Pharyngitis, Scarlet Fever Puerperal Sepsis,
Erysipelas, Septicemia, Tonsilitis, Cellulitis, Impetigo, Ecthyma, Necrotizing Fasciitis (NF), TSS, Acute Rheumatic Fever,Acute Glomerulonephritis, PANDAS

37
Q

Streptococci pyrogenes Virulence Factors

A

Hemolysins,Hyalurinic acid capsule,M protein, Lipoteichoic Acid, Strep pyrogenic exotoxin A (SpeA, SpeB),Streptokinase:

38
Q

Streptococci pyrogenes Classification

A

Group A Strep

Beta-hemolytic

39
Q

Superantigens

A

stimulate a much larger fraction of the overall T cell population than would a normal antigen.

40
Q

Streptolysin O Titers (SLO)

A

oxygen sensitive, so you grow colonies below the surface of the agar to see it

41
Q

Streptolysin S Titers (SLS)

A

oxygen stable, you see hemolysis surrounding the oxygen colonies

42
Q

Pharyngitis (exudative)

A

Pharyngitis (exudative) 5-15yo, spread by droplets, 2-4 day incubation, tx to prevent ARF (not AGN).Enlarged, painful cervical lymph nodes, fever > 101F

43
Q

Scarlet Fever Puerperal Sepsis

A

1800s – Semmelweis & handwashing endometritis-puerperal fever- childbed fever)

44
Q

Erysipelas

A

cellulitis characterized by fiery-red erythema w/ rapidly advancing well-demarcated edges, often on the cheeks – pain, fever, lymphadenopathy, children & elderly

45
Q

Impetigo

A

Most common in children, may follow insect bites. Skin infecions associated w/ AGN, weeping vesicles that crust over (pictures of children – near their mouth)

46
Q

Ecthyma

A

deep impetigo, pustular capsule & ulceration

47
Q

Necrotizing Fasciitis (NF)

A

40-70% mortality, rapid spread (1 in/hr), early signs: flu, brawny edema, extreme pain out of proportion to the size of the lesion, spreading erythema, eccumosis, purple bullae can cause toxic shock, crescendo pain (ramping up the degree of pain)
Treatment: debridement, use of antibiotics, IV fluids, cardiac output
Clindamycin (inhibits proteins, does not breakdown cells walls to release more toxins to activate the immune system)

48
Q

TSS –

A

TSS – widespread shock that blanches when pressure is applied

49
Q

Acute Rheumatic Fever

A

Jones criteria: early signs: erythema marginatum, subcutaneous nodules

50
Q

Hyalurinic acid capsule

A

antiphagocytic, no antibodies against S pyrogenes capsule (see a halo in india ink)

51
Q

M protein

A

a sortase-anchored surface protein, C terminal is conserved, N-terminus is the basis for serotyping; M is a major phagocytic factor, binds fibrinogen to mask bacteria from the immune system
M protein also functions as an adhesion

52
Q

Lipoteichoic Acid:

A

adhesion (mucosal) PAMP (not as strong as LPS)

53
Q

Strep pyrogenic exotoxin A (SpeA, SpeB) =

A

superantigens  cytokine storm (TSS)

54
Q

Streptokinase:

A

converts plasminogen  plasmin & dissolves clots

55
Q

Streptococcal pyrogenic exotoxin B

A

SpeB, potent protease

56
Q

C5a peptidase –

A

specific for C5a peptidase, specific for C5a and also degrades IgG

57
Q

Streptococci pyrogenes Treatment:

A

Treatment: Penicillin (no resistance so far)
Allergies  clindamycin, azithromycin
IVIG – some use against superantigens?

58
Q

Streptococci pneumonia Infections

A

Common cause of pneuomonia w/ better prognosis (fewer toxins)

59
Q

Streptococci pneumonia Virulence Factors

A

Quelling (swelling) reaction due to antibody-induced stabilization of pneumococcal capsular material.

60
Q

Streptococci pneumonia Classification

A

Alpha-hemolysis (green)

61
Q

Streptococci agalctiae Description

A

Group B Strep

Beta-hemolysis

62
Q

Streptococci agalctiae Infections

A

Used to be the most predominant cause of septicemia & meningitis in neonates
-Major cause of pregnancy-related morbidity
-Testing/treating pregnant mothers reduced disease (screening at 35-37 weeks gestation)
Group B infections have increased in nursing homes

63
Q

Streptococci agalctiae Virulence Factors

A

Major VFs: CAPSULE Capsular Serotypes I-V (serves as an antiphagocytic factor)
Adhesions: alpha-protein & fibrinogen-binding proteins.
Surface Beta protein binds factor H, down-regulates complement deposition
B-hemolysin can damage cells
PG, LTA, Group B carbohydrates increase cytokine secretion while the capsule does not

64
Q

Streptococci agalctiae Classification

A 
Group B Beta-Hemolysis (clear) 
Diplococci
Bacitracin resistant 
Hydrolysis of bile esculin 
CAMP factor: a GBS factor that synergizes w/ S aureus to increase lysis of RBCs
65
Q

Streptococci viridans: Description

S. mitis
S. mutans
S. sanguis
S. salivarius

A

Part of the normal oral microbiota (dental plaque called biofilm)
Alpha hemolytic
Can grow at acidic pH

66
Q

Streptococci viridans: Infections

S. mitis
S. mutans
S. sanguis
S. salivarius

A

Subacute – long duration infective endocarditis - Suffice it for now to say that these infections usually form on valves damaged in some way, such as by acute rheumatic fever, or prosthetic valves.

67
Q

Streptococci viridans: Virulence Factor

S. mitis
S. mutans
S. sanguis
S. salivarius

A

Not very virulent
Cause transient bacteremia every time you brush your teeth
Can cause endocarditis
Have adhesins for fibronectin, fibrin, other host proteins that accumulate on injured calces

68
Q

Streptococci viridans: Classification

S. mitis
S. mutans
S. sanguis
S. salivarius

A

Alpha-hemolysis (green)
No Lancefield Group
Distinguish from enterococci by ability to grow in 0.5% NaCl
Distinguished from pneumococci by ability to resit optochin

69
Q

Enterococcus Faecalis / faecium are the main ones Description

A

Formerly known as Group D Streptococcus
Commensal of GI tract
Alpha or gamma hemolytic

70
Q

Enterococcus Faecalis / faecium are the main ones Infections

A

Antibiotics alter the dyanimic in favor of enterococci, that are tolerant to a variety of antibiotics.
Increasing the pH may increase enterococci
Leading cause of nosocomial infections
30% VRE.
Can gain access to lymphatics of blood.

71
Q

Enterococcus Faecalis / faecium are the main ones Virulence Factors

A

Do not make many toxins
Extremely proficient in taking up DNA and passing it along to other species
VRE brought vanc resistance to strep

72
Q

Enterococcus Faecalis / faecium are the main ones Classification

A

Group D
Alpha or gamma hemolytic
Can grow as high salt, 45C, bile esculin positive

Cardiology (10 decks)

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