Staphylococci

Front 1

What is the general morphology of Staph?

Back 1

Gram (+) cocci (found in clusters)

Catalase (+)

Front 2

What test would we want to use if we wanted to distinguish between different strains of Staph?

Back 2

We could use the coagulase test because ONLY S. Aureus is coagulase (+). S. epidermidis + S. saprophyticus are coagulase (-)

Front 3

How would Staph look on a gram stain?

Back 3

Would look purple (bc its gram +) cocci in clusters.

Front 4

Staphylococci are catalase ___?

Back 4

POSITIVE; All of the staphylococci would show up as catalase (+).

Front 5

What sugars does Staphylococci ferment? Based upon sugars alone, how could you use this test to distinguish between different strains of Staph?

Back 5

Glucose & mannitol

All of the strains of Staph ferment glucose, but ONLY Staph. A ferments mannitol.

Front 6

Staph is coagulase _______?

Back 6

Staph. Aureus.: Catalase positive

Staph Epidermidis: Catalase negative

Staph Saprophyticus: Coagulase negative

ONLY Staph. Aureus is coagulase positive.

Front 7

Which test could you use to isolate Staph. saprophyticus?

Back 7

Novobiocin, this strain is resistant to this drug.

Front 8

How could you isolate Staph. epidermidis?

Back 8

It is catalase +
coagulase -
ferments ONLY glucose

Front 9

What is the major player in fighting a Staph. infection? As a result of this major player, what do Staph. infections produce?

Back 9

Neutrophils; they are pus forming

Front 10

What branch of the immune system is effective in helping to fight off Staph infections? What aids the honing in of neutrophils during a Staph. infection?

Back 10

The complement system

Opsonization with AB's can assist the neutrophils in killing

Front 11

What would make a person more susceptible to a Staph infection?

Back 11

Low Ab (these help with bringing the neutrophils in because they opsonize the pathogen) --> Hypoagammaglobulinemia

Low neutrophils (these are the major players in eliminating an infection)

Front 12

What immune deficiencies would be detrimental to someone with a Staph. infection?

Back 12

Hypo or agammaglobunemia

Job's disease: high levels of IgE, which is NOT the Ab you need (need IgG).

Chronic granulomatous disease: suboptimal killing by phagocytes.

Chediak-Higashi: insufficient chemotaxis of PMN's

Diabetes

Front 13

What is the characteristic appearance of Staph. infections?

Back 13

-An abscess (well-demarcated area of necrosis containing lysed PMN's; walled off by a layer of fibrin)

Front 14

Discuss the Polysaccharide Intercellular Adhesions virulence factor + how it benefits the bacteria.

Back 14

This is how the biofilm is created which is a layer of the bacteria on a synthetic surface.

Front 15

A Polysaccharide Intercellular Adhesin is the major virulence factor for what strain of Staph?

Back 15

Staph. Epidermidis

Front 16

Surface proteins are only associated with which strain of Staph.?

Back 16

Staph. Aureus is the only strain with surface proteins.

Front 17

What is the role of Protein A in Staph A.?

Back 17

Protein A is a virulence factor; normally Ab's bind to the Fc region of an Ab during opsinozation, but Protein A blocks this function by binding to the Fc region instead of the Ab. This inhibits the process of opsinozation of the bacteria + allows it to persist.

Front 18

What is the role of clumping factor? What can the surface protein be used as a marker for?

Back 18

This causes the clumping of the organism in the presence of fibrinogen

Staph. A. because only Staph A has surface proteins.

Front 19

How is the presence of the coagulase factor provide benefit to the bacteria?

Which strains of Stap have this surface protein?

Back 19

Coagulase causes the conversion of fibrinogen to fibrin and causes the clotting of blood and PREVENTS the movement of PMN's access to the abscess.

ONLY ON STAPH. Aureus

Front 20

What can you use as a test to differentiate Staph. from Strep?

Back 20

The catalase test...Strep is catalase (-) while Staph is catalase (+).

Front 21

How do superantigens work? How so superantigens benefit the bacteria?

Back 21

-Superantigens work by binding T-cells non-specifically while it is bound to an MHC2 molecule an causing massive cytokine release(IL-1 & TNF-alpha).

This response benefits the bacteria because it causes a huge, unproductive response of the immune system and the infection isn't resolved.

Front 22

What does the release of TSST-1 cause?

Back 22

This causes desquamation of the fingers and toes.

Front 23

What does release of the exfoliatin toxin cause?

Back 23

This causes peeling of the skin; has a sun burnt appearance; blistering and loss of the superficial layer of skin

Front 24

What does the release of the staphylococcal enterotoxin cause?

Back 24

Food poisoning symptoms; these toxins will elicit vomiting

THESE ARE SUPERANTIGENS TOO

Front 25

What is the function of pore-forming toxins? List examples and what their actions may cause.

Back 25

Pore-forming toxins punch holes in human cells.

Alpha toxin --> causes pneumonia

PVL --> controversial

Front 26

Which forms of staph colonize the skin as normal flora?

Back 26

All of the coagulase (-) Staph strains are normal flora of the skin: Staph epidermidis + Staph saprophyticus

Front 27

Where does Staph. Aureus colonize?

Back 27

The nose + throat (assymptomatically)
Will not colonize intact skin

Front 28

What are 2 ways of infecting yourself with Staph?

Back 28

Autoinnoculation
Open wounds (Staph moves into them)

Front 29

What are the predominant types of infections seen with Staph Aureus? Give examples.

Back 29

Predominantly skin infections:
Folliculitis: inflammed hair follicle

Furuncle:epithelial abcsess

Carbuncle: interconnected furuncles

Cellulitis: spread to the subcutaneous or submucosal tissue

Bullous impetigo: crusty, pustular blisters

Front 30

Desribe the difference between the types of infections caused by Staph + Strep

Back 30

Staph: infections are more localized; pyogenic

Strep: these are diseases that spread (although there is some spreading that occurs with Staph)

Front 31

What mechanism allows the spread of infections in Staph?

Back 31

Virulence factors:

Proteases, nucleases, lipases, hyularonidase

Toxins: TSST-1, Exfoliatin, enterotoxins, pore-forming toxins

Front 32

What are the ways Staph Aureus spreads?

Back 32

Cellulitis: moving through tissues

Bacteremia: entering the bloodstream

Catheter: how the pathogen gains entry

Front 33

What are the metastatic infections that occur from Staph?

Back 33

Bone/joint infections:
-osteomyelitis
-septic arthritis

CV:
-endocarditis (MOST COMMON CAUSE); usually IV drug abusers

CNS: Brain abscess (MOST COMMON CAUSE of epidural abscess)


Lung:
-Nosocomial pneumonia
-emphysema

Muscle:
-Pyomyostitis (MOST COMMON CAUSE)

Front 34

What is a toxinosis?

Back 34

This is a syndrome that is caused by the toxin itself, and doesn't involve the bacterial infection in order to be infectious.

Front 35

What are the 3 toxinoses that occur with Staph Aureus? Name the toxin that is associated with the toxinoses.

Back 35

TSST-1: TSST

SSS: Exfoliatin

Food poisoning: enterotoxin

Front 36

How do metastatic infections occur?

Back 36

Via bacteremia: when the bacteria bind to vasculature, destroy the endothelial cells (endocarditis) and then move to the underlying tissue (osteomyelitis, septic arthritis etc.) or it can persist within the endothelial cells and cause persistent bacteremia.

Front 37

How does the TSST-1 work?

Back 37

Toxin is in vagina, gets released to the bloodstream. Causes fever, hypotension, peeling of skin (desquamation of epithelium).

TSST is also a superantigen and will costimulate T-cells and cause lots of cytokine release which is responsible for the clinical syndrome

Front 38

How does the exfoliatin toxin work?

Back 38

Causes the peeling of skin (superficial layer) or can cause bullae formation

Front 39

What clinical symptoms does the enterotoxin cause? How do these clinical symptoms differ from food infection?

Back 39

Food poisoning

Toxinoses: short incubation period (2-8 hours)

Enterotoxin in the MOST COMMON CAUSE food poisoning (NOT food infection)

Front 40

What characteristic of the enterotoxin allows it to persist even without the bacteria?

Back 40

Toxin is HEAT STABLE

Front 41

What are 2 reasons why a bacterial organism might be resistant to B-lactams?

Back 41

-They may have a beta-lactamase that will cleave the B-lactam ring

-they may have mutation of the penicillin binding proteins which prevents the action of the drug.

Front 42

Which drug falls under the category of glycopeptide? Why is there resistance with this drug?

Back 42

-Vancomycin
-some bacteria overproduce peptidoglycan and it makes it resistant to vancomycin moving through this thick peptidoglycan.

Front 43

What are the 2 ways staph infections are acquired?

Back 43

-Nosicomial source (MOST COMMON CAUSE OF NOSOCOMIAL BACTEREMIA)
-Autoinnoculation

Front 44

Staph saprophyticus is responsible for what type of infection? What other bacterial cell can cause this infection?

Back 44

UTI's
E. Coli (MOST COMMON)

Front 45

What is the source of Staph epidermidis infections? What is the major virulence factor this strain of Staph?

Back 45

-insertion of a foreign device (implants, catheter, joints) + cause bloodstream infections.

-the Polysaccharide Intercellular Adhesins.

VERY RESISTANT TO ANTIBIOTIC THERAPY

Front 46

Polysaccharide Intercellular Adhesin is particularly important to which strain of Staph?

Back 46

Staph. Epidermidis