27 - Staphylococcus

Question 1

Staphylococci

Answer 1

• Gram positive cocci
• Non motile, non spore forming
• Facultative anaerobes
• Mesophiles (8-45ºC)
• Cells divide in multiple planes to form irregular clumps
• Catalase positive, oxidase negative
• High salt and drying tolerance

Question 2

Main reservoir

Answer 2

Mammals, not generally found in nature or the environment

Question 3

Divided into two major groups

Answer 3

• Coagulase positive (mostly pathogenic, e.g. S. aureus)
• Coagulase negative (relatively non pathogenic, e.g. S. epidermidis)

Question 4

Coagulase positive staphylococci

Answer 4

• S. intermedius
• S. delphini
• S. aureus (most important human pathogen)

Question 5

Staphylococcus aureus

Answer 5

• Produces golden pigment
• Carried by population transiently or persistently
• Nostrils is most common site

Question 6

S. aureus diseases

Answer 6

• Skin and soft tissue infections (e.g. impetigo)
• Food poisoning (ingestion of pre formed enterotoxin)

Question 7

Cell associated S. aureus virulence factors

Answer 7

• Adhesins
• Microcapsule (adhesion & immune evasion)
• Cell wall teichoic acids

Question 8

Life threatening diseases of S. aureus

Answer 8

• Osteomyelitis
• Sepsis
• Acute endocarditis
• Pneumonia
• Toxic shock

Question 9

Excreted S. aureus virulence factors

Answer 9

• Enzymes such as coagulase, protease, lipase (digest host tissue to allow spread)
• Exotoxins (some superantigens, may be carried on plasmids or phages)

Question 10

Coagulase

Answer 10

• Causes blood plasma to clot
• Coagulase enzyme reacts with prothrombin
• Forms complex (staphylothrombin)
• May be free or bound

Question 11

Staphylothrombin complex

Answer 11

• Can cleave fibrinogen
• Causes formation of fibrin clot
• Fibrinogen is soluble whereas fibrin is not

Question 12

Fibrin clot

Answer 12

• Protects S. aureus from phagocytosis and other host defences
• Fibrin may also deposit onto surface of S. aureus

Question 13

Bound coagulase

Answer 13

Attached to cell walls

Question 14

Free coagulase

Answer 14

Released extracellularly

Question 15

Toxins produced by most strains of S. aureus

Answer 15

Cytotoxins (haemolysins)

Question 16

Haemolysins

Answer 16

• Alpha, beta, delta, gamma
• Not all strains have all haemolysins
• Cytolytic, damage membranes
• Involved in tissue invasion

Question 17

Toxins produced by some strains of S. aureus

Answer 17

• Exfoliative toxins A and B
• Toxic Shock Syndrome toxin
• Enterotoxins
• Panton-Valentine leucocidin (PVL)

Question 18

Alpha and gamma haemolysins

Answer 18

Forms beta barrel transmembrane pores

Question 19

Beta haemolysins

Answer 19

• Does not form pores
• Hydrolyses sphingomyelin (enzyme)

Question 20

Delta haemolysins

Answer 20

• Phenol-soluble modulins
• non-specific membrane damage or short-lived pores

Question 21

Enterotoxins

Answer 21

• Cause emesis after ingestion
• More than 20, A to E most common
• Heat and acid stable
• Genes located on mobile elements (plasmids, bacteriophages)

Question 22

A and E toxin location

Answer 22

Prophage

Question 23

B and C toxin location

Answer 23

Pathogenicity island

Question 24

D toxin location

Answer 24

Plasmid

Question 25

Superantigens

Answer 25

• SEA and SEB are superantigens
• Cause non-specific T cell activation
• Binds directly to Class II MHC
• Leads to massive cytokine release and shock

Question 26

Toxic shock syndrome

Answer 26

• Rare complication of S. aureus
• Associated with vaginal products
• As bacteria grow, Toxic Shock Syndrome Toxin released and enters bloodstream

Question 27

Epidemiology of S. aureus

Answer 27

• Hospital or community acquired
• Risk factors different according to specific disease (e.g. age, female, surgery)
• May be commensal

Question 28

S. aureus antibiotic susceptibility

Answer 28

• Originally penicillin
• Now Methicillin (MRSA emerged through mecA gene)
• Vancomycin then used (VRSA emerged through vanA and B genes)

Question 29

vanA

Answer 29

• encoded on transposon
• S. aureus either retains VRE conjugative plasmid or transposon transferred into S. aureus

Question 30

S. aureus vancomycin resistance

Answer 30

• VANC binds D-ala-
  d-alla
• Disrupts peptidoglycan assembly
• Resistance achieved by altering cell wall intermediates

Question 31

Coagulase negative staphylococci

Answer 31

• Commensal flora of human skin
• Mostly opportunistic pathogens
• May also contaminate clinical specimens

Question 32

Examples of coagulase negative staphylococci

Answer 32

• S. epidermidis, produces slime and biofilm
• S. lugdunensis, Endocarditis, high mortality rate

Question 33

S. epidermidis infections

Answer 33

• Major nosocomial pathogen (causes infections of indwelling devices)
• Leads to endocarditis, bacteraemia
• Unlikely to cause infection in health yhost

Question 34

S. epidermidis virulence factors

Answer 34

• Biofilm formation
• Slime production
• Produces phenol soluble modulins (pro-inflammatory, sometimes cytolytic)

Question 35

Slime

Answer 35

• Viscous, unorganised, extracellular polysaccharide polymer
• Loosely-adhered to bacterial cell surface, easily washed off

Question 36

Role of slime in infection

Answer 36

• Allows bacteria to adhere to smooth surfaces
• Inhibits neutrophil chemotaxis
• Reduces antibiotic effectiveness

Question 37

S. epidermidis antibiotic susceptibility

Answer 37

• Susceptible to vancomycin
• Methicillin resistance encoded on mobile genetic element (SCCmec)

Question 38

Staphylococcal cassette chromosome mec (SCCmec) in S. aureus originating from S. epidermidis

Answer 38

• S. epidermidis is a commensal therefore exposed to many different antibiotics
• S. epidermidis may be a reservoir for antibiotic resistance genes
• S. epidermidis transfers mobile genetic elements to S. aureus, but reverse does not occur (due to CRISPR)