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Microimm 2500 > Staphylococci > Flashcards

Staphylococci Flashcards

1
Q

Where does the word staphylococci come from?

A

Staphyle - greek for bunch of grapes

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2
Q

Is Staphylococci gram positive or negative? What is the shape?

A

gram positive, coccus

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3
Q

Name a coagulase positive staphylococci

A
  • Staphylococcus aureus
  • “aureus” = Latin for gold
  • positive are more aggressive
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4
Q

Name two Coagulase Negative Staphylococci and what they are important for

A
  • Staphylococcus epidermidis
  • Staphylococcus saprophyticus
  • many other coagulase negative species
  • important causes of biofilm-associated infections
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5
Q

Staphylococcus epidermidis

A
  • found in skin
  • resistant to a number of antibiotics
  • produces a capsule (surface of polysaccharide)
  • known for forming biofilms
  • major problem for implanted devices
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6
Q

Staphylococcus aureus

A
  • an efficient colonizer of humans that doesn’t usually cause problems
  • anterior nares (nostril) and skin
  • carriers of S. aureus are healthy, asymptomatic people
  • colonization leads to greater risk of infection, but prognosis is also generally better
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7
Q

Colonization of Staphylococcus aureus

A
  • skin and mucous membranes, nose (~30% of people are persistently colonized)
  • spread person-person by direct or indirect contact
  • fomites (inanimate objects capable of transmitting an infectious disease) e.g. towels, razors, bandages
  • resistant to high salt (skin)
  • S. aureus surface proteins bind host proteins using adhesins (e.g. fibronectin, collagen and elastin binding proteins)
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8
Q

Staphylococcus aureus is a leading cause of what type of infections?

A

Nosocomial infections (hospital-acquired)

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9
Q

Is Staphyloccocus aureus extra or intracellular?

A
  • extracellular pathogen
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10
Q

what is the hallmark of S. aureus infection?

A
  • abscess
  • heat, redness, swelling, and pain
  • collection of dead neutrophils (pus) due to infection
  • a “pyogenic” or pus producing infection
  • can cause major complications if the organisms spread from the abscess
  • abscesses don’t typically heal on their own – require drainage and maybe antibiotics
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11
Q

Staphylococcus aureus Virulence factors

A
  • produces many virulence factors
  • expression of virulence factors is regulated
  • surface virulence factors expressed during exponential growth
  • secreted virulence factors (exotoxins) expressed during stationary phase
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12
Q

what is an invasive infection

A
  • isolate the organism from a location that is usually sterile
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13
Q

Generally, what are surface virulence factors for?

A

colonization purposes

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14
Q

Generally, what are secreted virulence factors for?

A

invasion and spread

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15
Q

Virulence Factors - Resistance to antibody mediated phagocytosis

A
  • Protein A
  • S. aureus surface protein
  • binds to the Fc portion of IgG
  • antibodies are bound in the incorrect orientation to be recognized by phagocyte Fc-receptor
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16
Q

Virulence Factors - toxins that kill leukocytes

A
  • can make a number of cytolytic toxins that kill white blood cells
  • “hemolysins” because they can lyse red blood cells
  • actual targets are mostly white blood cells
  • e.g. α-toxin and leukocidins
    helps to protect S. aureus in abscesses and for spreading
17
Q

Diseases due to direct effect of organism

A
  • skin lesions
  • deep abscesses
  • systemic infections
18
Q

Skin Lesions - Impetigo

A

superficial skin infection usually in young children

  • the non-bullous form has pimple-like lesions with pus (also caused by Streptococcus pyogenes)
  • the bullous form has painless, fluid filled blisters
19
Q

Skin Lesions - Stye

A
  • infection of the eye sebaceous glands
  • often will drain on its own, warm compress
  • do not lance
20
Q

Skin Lesions - Furuncle (boil)

A
  • infection of hair follicle

- warm compress to drain

21
Q

Carbuncles

A
  • infection of several hair follicles

- coalescing furuncles

22
Q

Deep Abscesses

A
  • not superficial but still localized – has a “focus” of infection
  • e.g. cellulitis, liver, lung, kidney, tooth etc
    wound or surgical infections
  • symptoms may not be obvious and may be more “constitutional” (whole body) e.g. fever, chills, malaise etc
  • deep abscesses can become systemic
23
Q

Staphylococcus aureus - Systemic Infections

A
  • often no single “focus” of infection
  • e.g. bacteremia/septicemia, pneumonia, osteomyelitis, endocarditis
  • very dangerous, often difficult to treat
24
Q

Systemic Infections: Osteomyelitis

A
  • infection of bone or bone marrow
  • S. aureus is the most common cause
  • can come from:
    hematogenous spread or local infections, fractures, joint replacement
  • diagnosed with X-ray/CT/MRI and biopsy
  • can be very difficult to treat and may require open surgery and prolonged i.v. antibiotics
25
Q

Systemic Infections: Infective Endocarditis

A
  • infection of the heart valves
  • typically occurs on damaged or prosthetic heart valves and with i.v. drug users
  • the lesion is called the “vegetation”
  • bacteria can grow to large numbers and “seed” causing strokes and pulmonary embolisms
  • fatigue, fever, heart murmurs, splinter hemorrhages
26
Q

Toxin-Mediated Diseases

A
  • infection often localized, but effects are systemic

- e.g. toxic shock syndrome, staphylococcal scalded skin syndrome, food poisoning

27
Q

Toxic Shock Syndrome (TSS)

A
  • first formally described as a systemic illness in 7 children associated with non-invasive Staphylococcus aureus infection
  • characterized by acute onset of fever, hypotension, rash, multi-organ dysfunction, (desquamation)
  • caused by both Staphylococcus aureus and Streptococcus pyogenes
  • staphylococcal TSS has menstrual and non-menstrual forms (<5% mortality)
  • streptococcal TSS occurs in association with invasive streptococcal disease (‘flesh-eating’ disease) (>40% mortality)
28
Q

Menstrual TSS

A
  • May 1980, 55 cases of TSS were reported to the CDC (52 were women, 95% were menstruating)
  • 1980 incidence of 6.2-12.3/100,000 women
  • high absorbency tampons were identified as a major risk factor and were withdrawn from the market
29
Q

How to “superantigens” contribute to TSS?

A
  • superantigens are secreted toxins
  • function to over activate large numbers of T cells and cause a systemic inflammatory response
  • produces a “cytokine storm”
  • eventually results in vascular leakage leading to shock and organ failure
  • toxic shock syndrome toxin-1 is responsible for the menstrual form
  • staphylococcal enterotoxins are also superantigens
30
Q

Staphylococcal Scalded Skin Syndrome

A
  • caused by exfoliative toxin
  • exfoliative toxins are proteases that destroy host proteins that hold cells together in the superficial layers of the skin
  • primarily affects neonates
  • cause skin peeling
  • heals in ~1-2 weeks
31
Q

Staphylococcal food-borne illness

A
  • Staphylococcal enterotoxins cause “Staph” food poisoning (proteins also function as superantigens)
  • the toxin is preformed in food – does not require the ingestion of viable staphylococci
  • 1 µg sufficient to induce “projectile” vomiting
  • mechanism remains uncharacterized
  • cats also used to study this disease
32
Q

Methicillin resistant Staphylococcus aureus

- what are the two types>

A

HA-MRSA (hospital acquired) and CA-MRSA (community- acquired)

33
Q

HA-MRSA

A
  • “hospital-associated” or “health care-associated”
  • patients generally have co-morbitidy
  • patients are usually already sick from other things
34
Q

CA-MRSA

A
  • community acquired
  • 1997 - 1999 North Dakota and Minnesota
  • 4 pediatric death from pneumonia (from S. aureus)
  • CA-MRSA strains – lack of exposure to health care setting
  • CA-MRSA are hypervirulent, but still susceptible to a number of other antibiotics
  • may cause necrotizing pneumonia
  • most common cause of skin and soft tissue infections
35
Q

“Superbug”

A
  • strains of bacteria that are resistant to the majority of antibiotics commonly used today
36
Q

Super-antigen mediated T cell activation

A
  • bind directly to MHC-II T cell receptor
  • not processed (otherwise they would be destroyed)
  • make the interaction much less specific, force the t cells to be activated when they shouldn’t, leading to cytokine storm
  • so normally where only 0.01% t cell are activated, up to 20% become activated

Microimm 2500 (8 decks)

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