M2 | Microbiolgy > Fungi and bacteria causing infective endocarditis > Flashcards

Fungi and bacteria causing infective endocarditis Flashcards

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1
Q

Mention the important properties of “ Staphylococcus aureus “

A
  1. gram-positive cocci arranged in grapelike clusters
  2. produces a carotenoid pigment called staphyloxanthin
  3. All staphylococci produce catalase unlike streptococci they don’t have catalase
    - Bacteria that make catalase can survive the killing effect of H2O2 within neutrophils (virulent factor)
  4. S. aureus is the most important ; it’s distinguished from the others primarily by coagulase production
  5. S. aureus usually ferments mannitol and hemolyzes red blood cells (source of iron required for growth of the organism)
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2
Q

What is the function of staphyloxanthin pigment ?

A
  1. gives golden color to the colonies

2. inactivates the microbicidal effect of superoxides and other reactive oxygen species within neutrophils

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3
Q

What is the function of coagulase enzyme ?

A

an enzyme that causes plasma to clot by :

  1. activating prothrombin to form thrombin.
  2. Thrombin then catalyzes the activation of fibrinogen to form the fibrin clot
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4
Q

What are the coagulase-negative staphylococci ?

A
  1. S. epidermidis
  2. S. saprophyticus
    * Note: The coagulase-negative staphylococci do not produce protein A
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5
Q

Mention the cell wall components and antigens of “ S. aureus “ and give an explanation for each if any

A
  1. Protein A:
    1a. The major protein in the cell wall
    1b. an important virulence factor;
    - binds to the Fc portion of IgG at the complement-binding site ——> preventing the activation of complement ——> reducing opsonization and phagocytosis of the organisms
  2. endotoxin-like properties peptidoglycan :
    2a. can stimulate macrophages to produce cytokines
    2b. can activate the complement and coagulation cascades
    2c. It’s ability to cause the clinical findings of septic shock although it doesn’t possess endotoxin
  3. Teichoic acids : mediate adherence of staphylococci to mucosal cells
  4. Polysaccharide capsule :

It has antiphagocytic function

  1. Clumping factor A:

binds to fibrinogen → platelet activation, aggregation, and blood clumping

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6
Q

What is the main site of colonization of S. aureus ?

A

nose

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7
Q

State the transmission of S. aureus.

A
  1. The nose:
    is the main site of colonization
  2. The skin : ( especially of hospital personnel and patients )
    - Hand contact is an important mode of transmission.
  3. The vagina of approximately 5% of women
    - which predisposes them to toxic shock syndrome.
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8
Q

Disease caused by S. aureus is favored by:

A
  • Heavily contaminated environment.
  • Compromised immune system.
  • Diabetes.
  • Foreign bodies, such as sutures and intravenous catheters
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9
Q

Explain how s.aureus causes diseases

A

S. aureus causes disease both by:

1) Inducing pyogenic inflammation.

• The typical lesion of S. aureus infection is an abscess.

2) Producing toxins

• Several important toxins and enzymes are produced by S. aureus.

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10
Q

What are the three clinically important exotoxins ?

A
  1. Enterotoxin
  2. Toxic shock syndrome toxin.
  3. Exfoliatin
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11
Q

Define “ enterotoxin”

A

causes food poisoning characterized by prominent vomiting than diarrhea

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12
Q

Explain the mechanism of enterotoxin

A
  • It acts as a superantigen within the gastrointestinal tract to stimulate the
    release of ——> large amounts of IL-1 and IL-2 from macrophages and helper T cells, respectively.
  • The prominent vomiting appears to be caused by cytokines which ——> stimulate the enteric nervous system to ——> activate the vomiting center in the brain.
  • It is heat-resistant ; not inactivated by brief cooking. It is resistant to stomach acid and to enzymes in the stomach and jejunum.
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13
Q

What is “ Toxic shock syndrome toxin (TSST) “ ?

A
  1. causes toxic shock, especially in:

Tampon-using menstruating women or in individuals with wound infections.

  1. Patients with nasal packing used to stop bleeding from the nose.
  2. TSST is produced locally by S. aureus in the: - vagina
    - nose
    - or other infected site enters the bloodstream, causing a toxemia
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14
Q

Explain the mechanism of Toxic shock syndrome toxin .

A
  • TSST is a superantigen that triggers polyclonal T cell activation
  • causes toxic shock by stimulating the release of large amounts of IL-2, IFN-γ, and TNF-α
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15
Q

Toxic shock syndrome toxin causes toxic shock by releasing which cytokines ?

A
  1. IL-2
  2. IFN-γ
  3. TNF-α.
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16
Q

What causes “scalded skin” syndrome in young children “ ?

A

Exfoliatin

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17
Q

Explain the mechanism of “ Exfoliatin “

A

It is “epidermolytic” and acts as a protease that cleaves desmoglein in desmosomes ——> leading to the separation of the epidermis at the granular cell layer

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18
Q

Define Leukocidin.

A

pore-forming toxin that kills cells, by damaging cell membranes

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19
Q

List the enzymes that cause disease by S.aureus

A
  1. coagulase :
    - clotting plasma, serves to wall off the infected site
    - thereby retarding the migration of neutrophils into the site.
  2. Staphylokinase :
    - fibrinolysin that can lyse thrombi
  3. hyaluronidase
  4. proteases
  5. nucleases
  6. Lipases
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20
Q

Mention the two groups important for clinical manifestations caused by S. aureus

A
  1. Staphylococcus aureus pyogenic Diseases

2. Staphylococcus aureus toxin-Mediated Diseases

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21
Q

State the clinical manifestations of “ Staphylococcus aureus pyogenic Diseases “

A
  1. Skin infections are very common. These include :
    - bullous and non bullous impetigo

(vesicles or flaccid bullae, which rupture and form thin, honey colored crusts)
- skin abscess

  1. Septicemia (sepsis)
  2. Endocarditis on normal or prosthetic heart valves
  3. Osteomyelitis
  4. Postsurgical wound infections
  5. Pneumonia
  6. Conjunctivitis ( inflammation of the conjunctiva of the eye)
  7. Abscesses
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22
Q

State the clinical manifestations of “ Staphylococcus aureus toxin-Mediated Diseases “

A
  1. Food poisoning (gastroenteritis)
  2. Toxic shock syndrome
  3. Scalded-skin syndrome
  4. Large areas of skin may slough
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23
Q

In staphylococcal food poisoning, vomiting is typically more prominent than _________

A

diarrhea

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24
Q

What is the characteristic of Toxic shock syndrome ?

A
  1. fever
  2. hypotension
  3. a diffuse, macular, sunburn-like rash.
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25
What is the characteristic of Scalded-skin syndrome ?
1. fever | 2. blistering and brown crusted rash that slough off with gentle pressure (Nikolsky sign positive)
26
What is the cause of gastroenteritis ?
Food poisoning (gastroenteritis) : Ingestion of enterotoxin, which is preformed in foods - has a short incubation period (1–8 hours) - rapid onset of symptoms
27
Laboratory diagnosis ——> Smears from staphylococcal lesions reveal ?
gram-positive cocci in grapelike clusters
28
Laboratory diagnosis ——> Cultures of S. aureus typically yield ?
golden-yellow on the nutreint agar, these colonies are β-hemolytic on blood agar
29
Laboratory diagnosis ——> Mannitol-salt agar (MSA) test for S.aureus shows which color ?
S. aureus ferments mannitol —> which lowers the pH causing the agar to turn from pink to yellow
30
Laboratory diagnosis ——> Mannitol-salt agar (MSA) test for S.epidermidis shows which color ?
S. epidermidis does not ferment mannitol and the agar remains pink
31
What does “ MRSA” stands for ?
methicillin-resistant S. aureus
32
What is “MRSA”?
- These strains are commonly known as methicillin-resistant S. aureus (MRSA) or nafcillin-resistant S. aureus (NRSA) - More than 90% of S. aureus strains contain plasmids that encode β lactamase - 20% of S. aureus are resistant to the β-lactamase–resistant penicillins - Such organisms can produce outbreaks of disease, especially in hospitals
33
What is the function of “ β lactamase“?
the enzyme that degrades many, but not all penicillins * Not in the reference explanation: - β- lactamases are enzymes produced by bacteria that provide multi- resistance to β-lactam antibiotics such as penicillins, cephalosporins etc…
34
How are S.aureus resistant to the β-lactamase–resistant penicillins ?
by virtue of changes in the penicillin-binding protein (PBP) in their cell membrane.
35
State the “ Viridans group streptococci”
1- Streptococcus sanguis 2- Streptococcus mutans
36
Mention the characteristics of “Viridans group streptococci”
Characteristics: * Gram-positive cocci in chains. * α-Hemolytic colonies. * Catalase-negative. * Resistant to optochin and not dissolved by bile
37
Which bacteria gives a positive result to the optochin test ?
pneumococci - a bacterium associated with pneumonia - tests positive/ is sensitive to Optochin
38
What is the habitat for viridans group streptococci ?
human oropharynx * Organism enters bloodstream during dental procedure
39
Explain the pathogenesis of Streptococcus mutans ?
- it’s implicated in dental plaque and caries - Bacteremia from dental procedures spreads organism to damaged heart valves - Glycocalyx composed of polysaccharide enhances adhesion to heart valves - No known toxins
40
What are the clinical manifestations of Viridans group streptococci ?
Signs of endocarditis are : - fever - heart murmur - anemia - embolic events
41
What are the laboratory diagnosis of Viridans group streptococci ?
* Gram-stained smear and culture * α-Hemolytic colonies on blood agar * Growth not inhibited by bile or optochin
42
List the diseases caused by Staphylococcus epidermidis ?
* Endocarditis on prosthetic heart valves * Prosthetic hip infection * Intravascular catheter infection * Cerebrospinal fluid shunt infection
43
Mention the important properties of Staphylococcus epidermidis
- Gram-positive cocci in clusters - Coagulase negative - Catalase-positive
44
Mention the Habitat and Transmission of Staphylococcus epidermidis
——> Habitat : Normal flora of the human skin and mucous membranes ——> Transmission: mainly by patient’s own strains or from person to person via hands
45
Explain the pathogenesis of Staphylococcus epidermidis
* Glycocalyx-producing strains adhere well to foreign bodies such as prosthetic implants and catheters forming biofilm. * It is of low-virulence affects primarily immunocompromised patients and in those with implants. * It is a major cause of hospital-acquired infections. * Unlike S. aureus, no exotoxins have been identified.
46
What is the laboratory diagnosis of Staphylococcus epidermidis ?
Gram-stained smear and culture. * Whitish, nonhemolytic colonies on blood agar. * It is coagulase- negative. * Staphylococcus epidermidis is sensitive to novobiocin
47
Which bacteria is resistant to novobiocin ?
coagulase-negative —> Staphylococcus saprophyticus is resistant
48
Urinary tract and biliary tract infections are most frequent in which bacteria?
Enterococcus faecalis
49
Mention the following for Enterococcus faecalis : 1-Important properties 2- Habitat and Transmission 3- Pathogenesis 4- Laboratory Diagnosis
1- a. Gram-positive cocci in chains b. Catalase-negative 2- a.human colon b. urethra c. female genital tract d. may enter bloodstream during gastrointestinal (GI) or genitourinary tract procedures 3- No exotoxins or virulence factors identified 4- a. Gram-stained smear and culture b. α-, β-, or nonhemolytic colonies on blood agar
50
What are the “ HACEK organisms” ?
- a group of small gram-negative rods - members of the human oropharyngeal flora and can enter the bloodstream from that site - Ability to cause endocarditis - Slow growth in culture - Requirement for high CO2 levels to grow in culture
51
What does “ HÁČEK” acronym stands for?
Stands for : H ——> Haemophilus aphrophilus and Haemophilus paraphrophilus A——> Actinobacillus (Aggrigatibacter) actinomycetemcomitans C ——> Cardiobacterium hominis E——> Eikenella corrodens K———> Kingella kingae
52
State important properties of the Candida Species
* Candida albicans is an oval yeast with a single bud. * It is part of the normal flora of mucous membranes of the : - upper respiratory - gastrointestinal - and female genital tracts * In tissues it appears most often as yeasts or as pseudohyphae. * True hyphae are also formed when C. albicans invades tissues.
53
Where is C. albicans present in the body ?
It’s a member of the normal flora, already present on the skin and mucous membranes. (mouth, esophagus, vagina).
54
Explain the local infection of C. albicans
Local infection: imbalance in local flora (e.g., triggered by antibiotic use) → local mucocutaneous infection (e.g., skin, oropharyngeal infection, vaginitis)
55
Explain the systemic infection of C. albicans
Systemic infection: local mucocutaneous infection → breach of skin/mucosal barrier or translocation → bloodstream disseminated organ infection e. g. - pyelonephritis - endocarditis
56
The first line of defense against Candida infections is ?
Intact skin and mucous membranes
57
The second line of defense against Candida infections is ?
Cell mediated immunity
58
Candida infections predisposes in? a. neutropenia b. neutrophilia
a. neutropenia
59
chronic mucocutaneous candidiasis could be caused by ?
Candida infections may cause CMC for | immunosuppressed individuals
60
List the diseases that result from impaired local or systemic host defenses
1. Thrush 2. Thrush in the newborn 3. Vaginitis 4. Skin invasion 5. Diaper rash in infants 6- Right-sided endocarditis
61
What is the overgrowth of C. albicans in the mouth that produces white patches?
Thrush
62
What will possibly occur if your fingers and nails are repeatedly immersed in water (dish washers) exposing them to warm, & moist areas ?
Skin invasion
63
Why is the usage of antibiotics cause vaginitis?
Antibiotics suppress the normal flora Lactobacillus and change the pH
64
Summarize the laboratory diagnosis of | Candida Species
• In exudates or tissues : - budding yeasts and pseudohyphae appear gram-positive • In culture : - typical yeast colonies are formed that resemble large staphylococcal colonies. * Candida albicans forms germ tubes in serum at 37°C whereas most other species of Candida do not. * Chlamydospores are typically formed by C. albicans but not by most other species of Candida
M2 | Microbiolgy
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