Mid Staphylococcus

Front 1

What family do Staphylococci belong to?

Back 1

Micrococcaceae

Front 2

Are staphylococci intracellular or extracellular? Pyogenic or not pyogenic?

Back 2

Extracellular, pyogenic

Front 3

What does pyogenic mean?

Back 3

Pyogenic refers to bacterial infections that make pus

Front 4

How do staphylococci grow? Are they motile?

Back 4

They grow in clusters and are non-motile

Front 5

Describe the survival of staphylococci?

Back 5

They are extremely hardy and can survive for prolonged periods of time on environmental surfaces.

Front 6

What species are Staphylococci?

Back 6

aureus, epidermidis, saprophyticus

Front 7

How do you identify Staphylococci aureus in a laboratory?

Back 7

They are gram positive cocci in grape like clusters. They form round, often beta-hemolytic colonies. on agar. The aureus refers to the gold color of the colonies. They are catalase positive. Coagulase and manifold fermentation tests are used to distinguish S. aureus from other staphylococcal species.

Front 8

What is the cell wall made from?

Back 8

Alternating units of N-acetylglucosamine and N-acetyl muramic acid. The wall also includes Lipoteichoic acid and a family of structurally related surface protein that facilitate bacterial adherence to host cell surfaces.

Front 9

What can the surface proteins of staphylococcus attach to?

Back 9

Molecules of the ECM including fibronectin, fibrinogen, and collagen

Front 10

What components of staphylococcus may be responsible for sepsis?

Back 10

The combination of peptidoglycan and lipoteichoic acid

Front 11

What enzymes are secreted by S. aureus?

Back 11

Catalase, Coagular, Hyaluronidase, Beta-lactamase

Front 12

What does catalase do?

Back 12

Converts H2O2 to H2O and O2

Front 13

What does coagulase do?

Back 13

Converts fibrinogen to fibrin

Front 14

What does hyaluronidase do?

Back 14

Hydrolizes hyaluronic acid and may contribute to tissue breakdown and the spread of staphylococci across tissue barriers

Front 15

What do beta-lactamases do?

Back 15

They can hydrolize the beta-lactam ring of penicillins and cephalosporins rendering antibiotics useless

Front 16

What toxins are secreted by s. aureus?

Back 16

Superantigen family toxins and Membrane damaging toxins

Front 17

What toxins are in the superantigen family?

Back 17

Toxic shock syndrome toxin-1 (TSST-1), enterotoxins, and epidermolytic toxins

Front 18

What toxins are membrane damaging toxins?

Back 18

Leukocidin and alpha toxin

Front 19

What does Leukocidin do?

Back 19

It has been associated with soft tissue infections

Front 20

What does alpha toxin do?

Back 20

It may play a role in producing the sepsis syndrome

Front 21

What is the natural reservoir of staphylococci?

Back 21

Humans

Front 22

Where are coagulase negative staphylococci found?

Back 22

Skin flora and in the anterior nares

Front 23

What bacteria colonize the anterior nares?

Back 23

S. aureus in 20-40% of the normal population

Front 24

In what populations is carriage increased?

Back 24

Dialysis patients, diabetics, HIV infected subjects

Front 25

What is the typical cause of Staphylococcal infection?

Back 25

Autoinoculation or transmission from a carrier to a patient. Usually infections arise from a transient carrier.

Front 26

Describe the pathogenesis of staphylococci

Back 26

Staphylococci can cause disease either as the result of a mechanical breach in skin or mucosal barriers or by the elaboration of toxins

Front 27

What is neccesarry for S. aureus invasive infections?

Back 27

Some sort of trauma

Front 28

Describe the normal presence of S. aureus

Back 28

They can persist as commensals on the skin or in the nose without causing damage

Front 29

What sort of infection is caused by commensal S. aureus?

Back 29

Because of their presence as commensals on the skin and other sites,
both coagulase positive and negative bacteria frequently cause prosthetic device (e.g.
intravascular catheters) related infections.

Front 30

What sequence of events is necessary for establishment of infection?

Back 30

-Adherence
-Colonization
-Invasion
-Spread
-Host response to the process

Front 31

What facilitates adherence/bacterial attachment to host tissue surfaces?

Back 31

The staphylococcal surface proteins, e.g. fibronectin-binding protein or collagen-binding protein

Front 32

What follows adherence?

Back 32

Staphylococci elaborate enzymes that provide nutrients for the bacteria and facilitate bacterial spread to adjacent tissue as well as spread to other organs. Staphylococci are noted for their ability to spread to other tissues establishing metastatic foci of infection

Front 33

What is the primary host response to staphylococcal infection?

Back 33

The polymorphonuclear leukocyte.

Front 34

What diseases are caused by staphylococcus toxins?

Back 34

Food poisoning, toxic shock syndrome, and the scalded skin syndrome

Front 35

Do toxin diseases require infection? Give 2 examples.

Back 35

No. Food poisoning can occur even if all the bacteria are dead and the toxin remains.

TSS occurs due to vaginal colonization rather than infection. The environment changes such that the commensal organisms release toxin.

Front 36

How do superantigens work?

Back 36

They are T cell mitogens. mitogens. Disease is due to
the ability of these toxins to bind antigen presenting cells MHC 2 molecule outside the peptide groove. The superantigens then bind T cells via the variable region resulting in massive T cell activation and the release of large quantities of cytokines – a “cytokine storm” including IL-1, IL-2, TNF, and interferon gamma. The result is a multiorgan disease similar in clinical presentation to septic shock with significant morbidity and mortality.

Front 37

How are staphylococcal infections treated?

Back 37

Antibiotics

Front 38

What antibiotic is used to treat staphylococcal infections?

Back 38

The appropriate one is determined through antibiotic susceptibility testing.

Front 39

Describe staphylococcal antibiotic resistance

Back 39

Recently an increasing number of staphylococci have become resistant to the beta-lactam antibiotics. They have also become less susceptible to the second line agents such as vancomycin.

Front 40

What is the treatment for localized collection of staphylococcus, such as abscesses?

Back 40

Surgical drainage

Front 41

What approaches are available for preventing staphylococcal infections?

Back 41

Topical application of antibiotics to the nares and the development of staphylococcal vaccines

Front 42

When and why is topical application of antibiotics to the nares used?

Back 42

It is used to eliminate nasal carriage of staphylococci in high-risk groups such as hemodialysis patients.

Front 43

Describe the staphylococcus vaccines

Back 43

Candidate vaccines include
polysaccharide-protein conjugate products as well as surface ligand domain peptide vaccines

Front 44

What is the most common coagulase negative staphylococci in clinical infections?

Back 44

Staphylococcus epidermidis

Front 45

Which is more virulent, S. aureus or S. epidermidis?

Back 45

S. aureus

Front 46

Where are coagulase negative species most often encountered clinically? Why?

Back 46

In association with prosthetic devices. They have a unique ability to adhere to prosthetic material and establish infection. This appears to be in part due to the elaboration of an extracellular polysaccharide
referred to as slime or biofilm. They are among the most common causes of intravascular catheter, prosthetic valve and prosthetic hip infections.

Front 47

What is a major issue in staphylococcal diagnosis?

Back 47

An therapeutic dilemma with these species is that they are frequent contaminants. Because of their presence as part of the normal skin flora they are frequently
isolated from blood or body fluids when they are not the true pathogens. This creates some difficulty in determining whether an isolate is genuine or a contaminant.