1
Q
Where does the word staphylococci come from?
A
Staphyle - greek for bunch of grapes
2
Q
Is Staphylococci gram positive or negative? What is the shape?
A
gram positive, coccus
3
Q
Name a coagulase positive staphylococci
A
- Staphylococcus aureus
- “aureus” = Latin for gold
- positive are more aggressive
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
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
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
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)
8
Q
Staphylococcus aureus is a leading cause of what type of infections?
A
Nosocomial infections (hospital-acquired)
9
Q
Is Staphyloccocus aureus extra or intracellular?
A
- extracellular pathogen
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
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
12
Q
what is an invasive infection
A
- isolate the organism from a location that is usually sterile
13
Q
Generally, what are surface virulence factors for?
A
colonization purposes
14
Q
Generally, what are secreted virulence factors for?
A
invasion and spread
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
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
Systemic Infections: Infective Endocarditis
- 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
Toxin-Mediated Diseases
- infection often localized, but effects are systemic
| - e.g. toxic shock syndrome, staphylococcal scalded skin syndrome, food poisoning
27
Toxic Shock Syndrome (TSS)
- 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
Menstrual TSS
- 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
How to "superantigens" contribute to TSS?
- 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
Staphylococcal Scalded Skin Syndrome
- 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
Staphylococcal food-borne illness
- 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
Methicillin resistant Staphylococcus aureus
| - what are the two types>
HA-MRSA (hospital acquired) and CA-MRSA (community- acquired)
33
HA-MRSA
- "hospital-associated” or “health care-associated”
- patients generally have co-morbitidy
- patients are usually already sick from other things
34
CA-MRSA
- 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
"Superbug"
- strains of bacteria that are resistant to the majority of antibiotics commonly used today
36
Super-antigen mediated T cell activation
- 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
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