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MICROBIOLOGY - Colloquium 1 > Lippincott chapter 8 DONE BUT WITHOUT THE FIGURES AND TABLES > Flashcards

Lippincott chapter 8 DONE BUT WITHOUT THE FIGURES AND TABLES Flashcards

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Biology 101 flashcards
1
Q

What consitute the main groups of medically important gram-positive cocci?

A

staphylococci and streptococci

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2
Q

Staphylococcus areus

A
  • one of the most common causes of bacterial infection

- important cause of food poisoning and toxic shock syndrome

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3
Q

Staphylococcus epidermidis

A
  • less virulent staphylococal species

- important cause of prosthetic implant infections

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4
Q

Staphylococcus saprophyticus

A
  • causes urinary tract infections, especially in women
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5
Q

Staphylococci is a part of the human…..

A

flora

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6
Q

Staphylococci:

A
  • stain darkly gram positive
  • round rather than oval
  • occur in bunches like grapes
  • cultured on broth and/ or blood
  • anaerobic
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7
Q

What does the staphylococci produce?

A

catalase, which is one feature that distinguish them from catalase-negative streptococci

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8
Q

What is the most virulent species of staphylococcus?

A

staphylococcus aureus

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9
Q

Staphylococcus aureus

A

almost all isolates of which secretes coagulase, an enzyme that causes citrated plasma to clot

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10
Q

Coagulase-negative staphylococci:

A

referred to species that occationally cause disease and lack coagulase

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11
Q

Folliculitis:

A

obstructed hair follicle

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12
Q

Staphylococcus aureus may be:

A
  1. largely or wholly the result of an actual invasive infection, overcomming host defense mechanisms, and the production of extracellular substances which facilitate invasion
  2. a result of toxins in the absence of invasive infection (“pure” toxinoses)
  3. a combination of invasive infection an intoxication
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13
Q

Virulence factors are……..

A

the genetic, biochemical, or structural features that enable an organism to produce disease

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14
Q

What does the clinical outcome of an infection depend on?

A

the virulence of the pathogen and the opposing effectiveness of the host defense mechanisms

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15
Q

Does staphylococcus aureus express many or few potential virulence factors?

A

many

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16
Q

PMNs =

A

polymorphonuclear neutrophils

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17
Q

What does coagulase activity result in?

A

coagulase activity results in localized clotting, which restricts access by polymorphonuclear neutrophils (PMNs) and other immune defenses. This would make coagulase a virulent factor, even tho mutants lacking the ability to make this factor remain virulent in animal models

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18
Q

What are the cell wall virluence factors?

A
  • Capsule
  • Protein A
  • Fibronectin-binding protein
  • Clumping factor
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19
Q

What does the capsule do?

A

it give an increased resistance to phagocytosis

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20
Q

Protein A:

A
  • major component of staphylococcus aureus cell wall

- binds to the Fc region of IgG, exerting an anti-opsonin (and therefore strongly antiphagocytic) effect

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21
Q

Fibronectin-binding protein (FnBP):

A
  • FnBP and other staphylococcal surface proteins promote binding to mucosal cells and tissue matrices
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22
Q

FnBP =

A

Fibronectin-binding protein

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23
Q

Clumping factor:

A
  • FnBP enhances clumping of the organisms in the presence of plasma
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24
Q

Cytolytic exotoxins:

A

α, β, γ, and δ toxins attack mammalian cell membranes, and are often referred to as hemolysins

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25
Q

α toxins:

A
  • chromosomally encoded
  • it polymerizes into tubes that pierce membranes, resulting in the loss of important molecules and, eventually, in osmotic lysis.
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26
Q

Panton-Valentine leukocidin:

A
  • this pore-forming toxin lysis PMNs
  • production of this toxin makes strains more virulent
  • is produced predominantly by community-aquired methicillin-resistant S.aureus (MRSA) strains
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27
Q

What does the superantigen exotoxins have affinity for?

A

they have affinity for the T-cell receptor-major histocompatibility complex Class II antigen complex.

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28
Q

What does the superantigen exotoxins stimulate?

A

they stimulate enhanced T-lymphocyte response (as many as 20% of T cell respond, compared with 0,01% responding to the usual processed antigens). see more page 71

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29
Q

What six major antigen types do we have? Where are they produced?

A

Enterotoxins (six major antigen types: A, B, C, D, E, and G) are produced by approximately half of all S

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30
Q

What can cause food poisoning?

A

enterotoxin in food. Toxin stimulates the vomiting center in the brain by binding to neural receptors in the upper IG tract

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31
Q

What are enterotoxins?

A
  • superantigen

- more heat-stable than S. aureus

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32
Q

Toxic shock syndrome toxin (TSST-1):

A
  • classic cause of toxic shock syndrome

- also referred to as staphylococcal enterotoxin F, although it does not cause food poisoning when ingested

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33
Q

TSST-1 =

A

Toxic shock syndrome

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34
Q

Exfoliatin (exfoliative toxin, ET)

A
  • superantigen
  • causes scalded skin syndrome in children
  • cleaves desmoglein 1. cleavage results in loss of the superficial skin layer
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35
Q

ET =

A

Exfoliatin, exfoliative toxin

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36
Q

What causes scalded skin syndrome in children?

A

exfoliatin (exfoliative toxin, ET)

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37
Q

Give examples of antigens:

A
  • enterotoxins

- exfoliatin (exfoliative toxin, ET)

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38
Q

Desmoglein 1:

A

a component of desmosomes (cell structures specialized in cell-to-cell adhesion)

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39
Q

What does the cleavage of desmoglein 1 result in?

A

cleavage results in loss of the superficial skin layer

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40
Q

What is an important complication of pneumonia?

A

staphylococcal pneumonia

41
Q

What is the localized host response to staphylococcal infection?

A

inflammation, characterized by swelling, accumulation of pus, and necrosis of tissue. Fibroblast and their products may form a wall around the inflamed area, which contains bacteria and leukocytes. This creates a characteristic pus-filled boil or abscess

42
Q

(1) Septicemia =

A
  • the presence and persistence of pathogenic microorganisms or their toxins in the blood.
  • may be rapidly fatal
  • can be caused by stephylococcal invading the blood stream
43
Q

Bacteremia =

A
  • the presence of viable bacteria circulating in the bloostream
  • may result in:
    • seeding internal abscesses
    • skin lesions
    • infections in the lung, kidney, heart, skeletal muscle, or memninges
44
Q

External hordeolum =

A

common sty

45
Q

Abscess =

A

a swollen area within body tissue, containing an accumulation of pus.

46
Q

The most common S. aureus infections are…..

A
  • small superficial abscesses involving hair follicles (folliculitis) or sweat glands or sebaceous glands
47
Q

What is the common sty (external hordeolum) created by?

A

infection of an eyelash follicle

48
Q

What can an infection of an eyelash follicle can create?

A

the common sty (external hordeolum)

49
Q

Furuncles (boils):

A
  • subcutaneous abscess

- often form around foreign bodies such as splinters

50
Q

Furuncles =

A

boils

51
Q

Boils =

A

furuncles

52
Q

Carbuncles:

A
  • larger, deeper, multiloculated skin infections that can be bacteremia and require antibiotic therapy and debridement
53
Q

Impetigo:

A
  • usually a localized, superficial, spreading crust skin lesion generally seen in children
54
Q

What causes impetigo?

A
  • can be caused by S. aureus
  • more commonly by Streptococcus pyogenes
  • or both^
55
Q

Where does the human staphylococcal infections usually remain localized?

A

at the portal of entry by normal host defenses.

56
Q

What is the most common cause of acute and chronic infection of bone marrow?

A

S. aureus

57
Q

What is the most common cause of acute infection of joint space in children (septic joint)?

A

S. aureus

58
Q

Septic joint:

A

acute infection of joint space in children that is caused by S. aureus

59
Q

What is acute endocarditis caused by?

A

it is caused by injection of contaminated preparations or by needles contaminated with S. aureus

60
Q

(2) Septicemia =

A
  • it is a generalized infection with sepsis or bacteremia taht may be associated with a known focus (for example a septic joint) or not (an occult focus)
61
Q

What can cause a severe necrotizing pneumonia?

A

S. aureus

62
Q

Nosocomial infection =

A

Originating or taking place in a hospital, acquired in a hospital, especially in reference to an infection.

63
Q

Nosocomial infections:

A

S. aureus is one of the most common causes of hospital-associated infections, often of wounds (surgical, decubital) or bacteremia associated with catheters. Progression to septicemia is often a terminal event.

64
Q

Toxinoses:

A

diseases caused by the action of a toxin, frequently when the organism that secreted the toxin is undetectable. There are toxinoses that are caused by S. aureus.

65
Q

Toxinoses caused by S. aureus include:

A
  • Toxic shock syndrome
  • Staphylococcal gastroenteritis
  • Scalded skin syndrme
66
Q

What does toxic shock syndrome result in?

A
  • High fever
  • Rash (resembling a sunburn, with diffuse errythema followed by desquamation)
  • Vomiting
  • Diarrhea
  • Hypotention
  • Multiorgan involvement (especially GI, renal, and/or hepatic damage)
67
Q

Desquamation =

A

peeling or scaling of the skin

68
Q

What causes staphylococcal gastroenteritis?

A

ingestion of food contaminated with enterotoxin-producing S. aureus.

69
Q

What are the heat-resistant toxins able to withstand?

A

subsequent reheating

70
Q

What are acute following of a short incubation period (less than 6 hours) and are triggered by local actions of the toxins of the GI tract rather than from infection?

A

Symptoms, such as nausea, vomiting, and diarrhea, are acute following of a short incubation period (less than 6 hours) and are triggered by local actions of the toxins of the GI tract rather than from infection.

71
Q

Why does the short incubation period of staphylococcal food poisoning occur?

A

the short incubation period of staphylococcal food poisoning occurs because the toxin in the food has already been formed by staphylococci before the food is ingested.

72
Q

Scalded skin syndrome

A

involves the appearance of superficial bullae resulting from the action of an exfoliative toxin that attacks the intercellular adhesive of the stratum granulosum, causing marked epithelial desquamation. the bullae may be infected or may result from toxin produced by organisms infecting a different site.

73
Q

How do we identify an isolate as a staphylococcus?

A
  • relies largely on microscopic and colony morphology and catalase positivity.
  • bacteria stain strongly gram-positive
  • frequently seen as grapelike clusters
74
Q

How is S. aureus distinguished from the coagulase-negative staphylococci?

A
  • primarily by coagulase positivity
  • in addition S. aureus colonies tend to be yellow and hemolytic rather than gray and nonhemolytic like the coagulase-negative staphylococci
  • S. aureus is mannitol-positive
75
Q

Name a bacteria that is mannitol-positive:

A

S. aureus

76
Q

Immunity (S. aureus)

A

S. aureus infections do not elicit strong or long-lasting immunity, as demonstrated by the continuing susceptibility of individuals to S. aureus infections throughout life.

77
Q

How to treat S. aureus?

A
  • it requires an aggressive treatment, including incision and drainage of localized lesions
  • systemic antibiotics
  • choice of antibiotics is complicated by the frequents presence of aquired antibiotica resistance determinants
78
Q

S. aureus being resistant:

A
  • Virtually all community and hospital-aquired S. aureus infections are now resistant to pencillin G due to pencillinase-encoding plasmids or transposons.
  • This has required the replacement of the initial agent of choice, pencillin- G, by β-lactamase-resistant pencillins, such as methicillin or oxacillin.
79
Q

What has an increased use of methicillin and related antibiotics has resulted in?

A
  • Increased use of methicillin and related antibiotics has resulted in S. aureus that is resistant to a number of β-lactam antibiotics, such as methicillin, oxacillin, and amoxicillin.
  • These strains are known as methicillin-resistant S. aureus
80
Q

MRSA =

A

Methicillin-resistant S. aureus

81
Q

What is antibiotic resistance caused by?

A

it is caused by chromosomal acquisition of the gene for a distinct pencillin-binding protein (PBP)

82
Q

PBP =

A

pencillin-binding protein

83
Q

What does the pencillin-binding protein (PBP) code for?

A

it codes for a new peptidoglycan transpeptidase with a low affinity for all currently available β-lactam antibiotics, and thus renders infections with MRSA unresponsive to β-lactam therapy

84
Q

Compare methicillin-sensetive S. aureus to MRSA:

A
  • Compared with methicillin-sensetive S. aureus, MRSA infections are associated with worse outcomes, including longer hospital and intensive care unit stays, longer durations of mechanical ventilation, and higher mortality rates.
  • MRSA strains are also frequently resistant to many other antibiotics, some being sensistive only to glycopeptides such as vancomycin.
85
Q

CA-MRSA =

A

community-aquired MRSA

86
Q

Community-aquired MRSA (CA-MRSA):

A
  • documented in mid-1990s

- occurring in individuals who had no previous risks factors for MRSA infections, such as exposure to hospital

87
Q

What is the most clinical manifistetion of CA-MRSA?

A
  • skin and soft tissue infections such as abscesses or cellulitis
  • can also causes severe diseases such as necrotizing pneumonia, osteomyelitis, and septicemia
88
Q

How doe we distinguish between CA-MRSA and hospital -associated MRSA?

A
  • CA-MRSA has a characteristic pattern of DNA fragments obtained upon enzymic cleavage and electophoresis, and it produces specific toxins.
  • CA-MRSA also exhibit a unique antibiotic resistance pattern, that is, CA-MRSA is sensitive to many antibiotics that do not show much activity against hospital-associated MRSA. These antibiotics include ciprofloxacin and clindamycin, with some CA-MRSA even sensitive to erythromycin, gentamicin, rifampin, tetracycline, and/or trimethoprim-sulfamethoxazole. P 75
89
Q

PVL =

A

Panton- Valentine leukocidin

90
Q

Vancomycin resistance:

A
  • agent of choice for treatment of life-threatening MRSA S. aureus infections
  • vancomycin resistance has increased steadily, prompting the use of alternative drugs such as quinupristin-dalfopristin, linezolid, daptomycin.
91
Q

Why is the increase of vancomycin resistance caused?

A
  • vancomycin resistance has increased steadily, prompting the use of alternative drugs such as quinupristin-dalfopristin, linezolid, daptomycin.
  • these agents have good in vitro activity against MRSA and most other clinically important gram-positive bacterial pathogens
92
Q

Are there any effective vaccines agains S.aureus?

A

nope

93
Q

What are the important coagulase-negative staphylococcal species?

A
  • S. epidermidis (most important)

- S. saprophyticus (second most important)

94
Q

Staphylococcus epidermis:

A
  • present as large numbers as part of the normal flora of the skin
  • low virulence
  • common cause of infection of implants such as heart valves and catheters
95
Q

What does Staphylococcus epidermis produce?

A

an extracellular polysaccharide material called polysaccharide intercelular adhesin (sometimes called “slime”), that facilitate adherence to bioprosthetic material surfaces, such as intravenous catheters, and acts as a barrier to antimicrobial agents

96
Q

Which bacteria causes cystitis in women?

A

S. saprophyticus. Probably related to its occurence as a part of normal vaginal flora.

97
Q

Is S. saprophyticus sensetive to most antibiotics?

A

yes. even pencillin G

98
Q

How can we distinguish S. saprophyticus from S. epidermidis and most other coagulase-negative staphylococci?

A

S. saprophyticus has a natural resistance to novovbiocin

MICROBIOLOGY - Colloquium 1 (9 decks)

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