Intro To Bacteria S. Aureus Pathogenesis

Front 1

Which are the typical gram-positive bacteria?

Back 1

Bacillus anthrasis, streptococcus Pneumoniae

Front 2

Which are the typical gram negative bacteria?

Back 2

N. Gonnorhea, Pseudomonas aergunosa, E. Coli, vibrio cholera

Front 3

Which is the most clinically relevant acid-fast bacteria?

Back 3

mycoplasma tubercolisis

Front 4

Which is the most clinically relevant "gram less" bacteria.

Back 4

Mycoplasma pneumonia (and many other organisms of the Mycoplasma genus)

Front 5

Describe the steps of gram staining. What additional steps need to be taken for complex staining organisms?

Back 5

Front 6

Describe in general the characteristics of gram positive bacteria

Back 6

Front 7

Diagram the structure of the plasma membrane an cell wall of a gram positive bacterium.

Back 7

Front 8

Diagram the structure of the plasma membrane an cell wall of a gram negative bacterium.

Back 8

Front 9

Describe the structure of LPS

Back 9

Can induce immune mediated damage endotoxic shock.

Front 10

Describe the key features and significance of the O-antigen

Back 10

O antigen is the most variable among species and can be modified by environment. Differentiates bacterial serotypes.

Front 11

Describe the mechanisms of bacitracin, penicillin, cephalonsporin and vancomycin.

Back 11

Front 12

Contrast the advantages of a bacterium being gram negative vs. gram positive.

Back 12

Front 13

Describe the structure of Acid fast-staining organisms.

Back 13

Front 14

What are characteristics of "Gramles" bacteria? Give examples of these organisms.

Back 14

Front 15

What are the common structures that are recognized by the immune system to activate inflammatory signaling?

Back 15

Front 16

Describe the structure of lipopolysaccharide.

Back 16

Front 17

Describe the different classes of bacteria with respect to growth temperature and pH preference. What are factors that affect growth rate?

Back 17

Front 18

Contrast hardy bacteria with fastidious bacteria. What are key requirements for growth?

Back 18

Front 19

Which trace metals are required for bacterial growth? What are the main 4 classes of iron transporters found in bacterial cells?

Back 19

Front 20

Describe the pathogenicity and growth of S. Ares.What are the cell surface virulence factors expressed and when? What are the secreted virulence factors expressed and when are they expressed?

Back 20

Front 21

Why does growth state matter?

Back 21

Front 22

What are Robert Koch's postulates and what are they used for?

Back 22

Front 23

What are the three categories of bacteria with which humans interact? Give two examples of how an organism might with from one to another.

Back 23

Front 24

What are some of the functions os commensal bacteria?

Back 24

Front 25

Distinguish between infection and disease. What is virulence and how is it typically measured?

Back 25

Front 26

What are the steps necessary for bacterial infection?

Back 26

Front 27

Describe the pattern of disease with respect to the magnitude of symptoms for N. Gonnorhea, bacillus anthracis, and C. Difficile for men and women.

Back 27

Front 28

What are persister cells and how do they arise? Is this state permanent or transient.

Back 28

Front 29

What are the two major ways by which bacteria cause disease?

Back 29

Front 30

What are the phases of bacterial growth?

Back 30

Front 31

What are the steps in the six link chain?

Back 31

The six-linked chain is a sequence that comprise physician-patient interactions, which are:

+ history-taking

+ physical exam

+ differential diagnosis

+ tests/investigations

+ provisional/definitive diagnosis

+ management

Front 32

Describe broadly the role of Neutrophils, basophils, eosinophils, mast cells, macrophages and dendritic cells in immunity.

Back 32

Front 33

Describe the role of natural killer cells in immunity.

Back 33

Front 34

Describe the role of effector B cells, Memory B cells, T helper cells and cytotoxic T cells in immunity.

Back 34

Front 35

Describe the appearance of malaria on a CBC. What is a common symptom?

Back 35

Front 36

Describe the structures of peptidoglycan and techioc acid. What are their constituents? Where do they occur?

Back 36

Front 37

Describe the structure and identifying features of Staphyloccoci. How could you differentiate it from another bacterium?

Back 37

+ Spherical cocci

+ Arranged in irregular grape like clusters

+ Gram-positive

+ Ferments mannitol salt (yellow staining)

+ Beta-hemolytic (bright-yellow in the midst of red)

+ Catalase test positive (bubbles)

+ Coagulase test positive (the culture coagulates)

+ All staphylococci produce catalase (note that no streptococci produce catalase → you can use a “catalase test” to differentiate staph from strep. Hydrogen peroxide + staph = oxygen bubbles)

+ Catalase degrades H2O2 into O2 and H2O and is an important virulence factor

+ Bacteria that make catalase can survive the killing effect of H2O2 within neutrophils

Front 38

How does catalase and superoxide dismutase contribute to bacterial anaerobic growth?

Back 38

Allows degradation of ROS => protects the bacteria from:

Immune attacks (neutrophils, macrophages)

Products of aerobic respiration

Front 39

What are the toxigenic disease caused by S. Aureus?

Back 39

Staph food poisoning

Scalded Skin syndrome

Toxic Shock syndrome

Front 40

Describe the symptoms, progression and prognosis for toxigenic disease caused by S. Aureus: Food poisoning

Back 40

Staph food poisoning:

Acute onset (0.5-7hr)

Short duration

Vomit > diarrhea

Cause: Emetic protein

Front 41

Describe the symptoms, progression and prognosis for toxigenic disease caused by S. Aureus: Scalded Skin syndrome

Back 41

Scalded Skin Syndrome

Dermal layer separated from intercellular junctions

Occurs mainly in young children

Cause: Exfoliatin protein (ETA, ETB) - proteases!

Front 42

Describe the symptoms, progression and prognosis for toxigenic disease caused by S. Aureus: Toxic shock syndrome

Back 42

Toxic Shock Syndrome

Typical of septic shock: high fever, chills, vomiting, diarrhea, sunburn-like rash, sore throat, muscle pain, exfoliation of basilar layer of epidermis of palms and soles, hypotension and shock resulting in multi-organ failure

Cause: Toxic Shock Syndrome Toxin (TSST-1)

Front 43

Describe the symptoms, progression and prognosis for inflammatory/invasive disease caused by S. Aureus: Skin and Tissue infections

Back 43

Impetigo, pyoderma

Front 44

Describe the symptoms, progression and prognosis for inflammatory/invasive disease caused by S. Aureus: Staphylococcal pneumonia

Back 44

May follow viral respiratory infection, especially influenza in children, or occur in postoperative patients.

Front 45

Blood stream invasion (bacteremia)

Back 45

Can follow any localized lesion

Systemic responses: chill, rigor, joint pain. Can have metastatic seeding or organs, with abscess formation:

Heart valves: endocarditis

Bone and joints: osteomyelitis and septic arthritis

Front 46

Describe the cell wall and and surface component, secreted enzyme and secreted toxin virulence factors of S. Areus

Back 46

Cell wall and surface components:

Gram + cell wall

Surface bound and secreted coagulase (Converts fibrinogen to fibrin protecting bacteria from phagocytes)

Protein A- binds to Fc portion of antibodies and inhibits Fc-mediated phagocytosis

Secreted Enzymes

Catalase- H2O2--> H2O and O2

Superoxide dismutase Hyaluronidase → promote invasion

Staphylokinase → promote invasionLipases → promote invasion

Secreted Toxins

Cytolytic Toxins- lyse host cells by forming pores in or interfering with membranesLeads to release of cellular mediators that cause further damage

Front 47

Describe exfoliative, enterotoxin and any other toxins associated with S. Areus

Back 47

Exfoliative toxins

ETA and ETB: serine proteases that promote breakage of desmosomes (cell-cell junctions) in epidermisCan also act as super antigens

Staphylococcal Enterotoxins: 8 serotypes (classified by antigens present on bacteria)

Heat and acid-stable

Cause vomiting/emesis

Cause toxic shock-like syndrome by functioning as super antigens (Superantigen - class of antigens that cause non-specific activation of T-Cells and massive cytokine release)

TSST-1:Toxin that is associated with most or all menstrual-associated cases of toxic shock syndrome (Acts a super antigen)

Front 48

Explain the mechanisms by which S. Aureus evades host immunity.

Back 48

Several mechanisms

+ Surface bound and secreted coagulase

Converts fibrinogen to fibrin protecting bacteria from phagocytes

+ Protein A- binds to Fc portion of antibodies and inhibits Fc-mediated phagocytosis

+ Secreted Catalase- converts hydrogen peroxide to water and oxygen, preventing immune system attacks with ROS

Front 49

Describe the evolution of how S. aureus acquired antibiotic resistance.

Back 49

Front 50

What are the predisposing factors for invasive S. Areus disease and what are the possible treatments?

Back 50

Invasive diseases:Most often caused by local lesion leading to infection via a break in the dermal layerSharp objects (scissors, knives, needles, etc.)Sports (wrestling mats [very common], and other full contact sports) Major cause of hospital-acquired infections

Front 51

What are the predisposing factors for toxigenic S. Aureus disease and what are the possible treatments?

Back 51