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Medsci 202 > Lecture 5: Staphylococcus Aureus and Disease > Flashcards

Lecture 5: Staphylococcus Aureus and Disease Flashcards

1
Q

List some general features and characteristics of staphylococci

A
  • 30 species, 3 clinically relevant
  • S. aureus, S. epidermidis, S. saprophyticus
  • gram positive
  • cocci, irregular shape, grape like clusters
  • non-motile (no flagella)
  • sometimes pigmented
  • resistant to dry condtions
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2
Q

how can staph. aureus be transmitted?

A

cracked/damaged skin/splinter
human to human transmission (shedding human lesions)
- colonises moist skin folds, oropharynx, gastrointestinal tract, and urogenital tract

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3
Q

what does it mean to say staph aureus is an opprtunistic pathogen? how many people are carriers of staph.

A

About 15% of normal healthy adults are persistant nasopharyngeal carriers of S. aureus without symptoms (opportunistic pathogen).

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4
Q

what are virulence factors

A

gene products that enable the bacteria to colonise the host, damage host tissue, spread from the site of initial infection and evade the immune response

virulentus means full of poison

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5
Q

what virulence factors does staph aureus display

A

*promote attachment to host cells (adhesins)
*help bacterium to enter host cell (invasins)
*damage host cell or tissue (e.g. cytolysins)
*help bacteria to spread from local infection (spreading factors)
*over-stimulate immune response (immunopathogenic factors)
*mediate immune evasion

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6
Q

what diagnostic lab tests are used to diagnose staphlyococcus aureus?

A

gram staining - catalase test - coagulase test - mannitol salt agar

when postive move onto next test

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7
Q

explain how adhesins helps staph aureus in pathogenesis

A

MSCRAMMS (Microbial surface components recognising adhesive matrix molecules) = large protein family that interact with ECM proteins that allow bacteria to colonise the tissue. they mediate the initial attachment of bacteria to host tissue, providing a critical step to establish infection.

  • cell wall-attached proteins in Gram-positives
  • specific binding to host extracellular matrix proteins (fibronectin, elastin laminin, vitronectin, collagen)
  • imortant for tissue colonisation
  • e.g. fibronectin binding protein, collagen binding protein
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8
Q

explain how cytolysins helps staph aureus in pathogenesis

give examples of toxins

A
  1. cytolysins
    - toxins that lyse the whole cell (bacterial spreading), erythrocytes (gaining access to iron or nutrients) or leukocytes (immune evasion)
  • alpha toxins: damage to membrane, loses osmotic barrier, swell up and burst
  • beta toxin: damage to membrane by enzymatic activity
  • delta toxin: works like detergent messes up lipid structure, interefere with integrity of lipid membrane
  • Gamma and pvl (panton-valentine leukocidin): bi-component pore forming toxins
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9
Q

explain how exfoliative toxins help staph aureus in pathogenesis

A
  • only found in staph aureus
  • serine proteins split intercellular bridges i.e. desomsomes - lose integrity of skin, upper layer peels off
  • in the stratum granulosum epidermis (exfoliative dermatitis)
  • only need toxin don’t need bacteria around
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10
Q

explain how spreading factors help staph aureus in pathogenesis

A

combination of different enzymes that allow the bacteria to move deeper in the host tissue and perhaps even the blood stream

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11
Q

give examples of spreading factors and their function

A

*Lipases: hydrolyse lipids, for invasion of cutaneous tissues
*Nucleases: hydrolyses DNA, decrease viscosity of pus
*Hyaluronidase: hydrolyses hyaluronic acid in connective tissue
*Proteases: serine protease, aureolysin (metallo-protease)
*Staphylokinase (fibrinolysin): causes fibrinolysis

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12
Q

explain how immunopathogenic factors like superantigens help staph aureus in pathogenesis

A
  • overstimulate the immune response causing systemic infalmmation
  • trigger massive release of pro-inflammatory cytokines (TNF-a, IFN-g)
  • structurally and functionally related to superantigens from S. pyogenes
  • casues damage to the immune system and can lead to toxic shock syndrome
    -can also cause food poisoning (in contrast to streptococcal SAgs)
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13
Q

list the types of immune evasion factors that help staph aureus with pathogenesis

A
  1. capsule - prevent opsonisation to prevent phagocytosis
  2. slime layer - biofilm prevents AB from access
  3. catalase - detoxidies peroxide i.e a toxin produced by immune system to kill bacteria
  4. clumping factor CIF-A (bound coagulase) - fibrinogen to fibrin forming blood clot - camouflage from immune system
  5. Protein A - embedded in cell wall, binds IgG in wrong orientation (via Fc region) to prevent opsonitation and phagocytosis
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14
Q

what are the three main disease types caused by staph

A
  1. superficial skin disease
  2. invasive disease
  3. toxigenic disease
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15
Q

give examples of superificial skin diseases

A

Impetigo: localised cutaneous infection with pus-filled vesicles, primarily affects young children
Folliculitis: impetigo involving hair follicles
Furuncles or boils: painful pus-filled cutaneous nodules
Carbuncles: coalescence of furuncles, extension into subcutaneous tissue, can lead to systemic disease, bacteremia

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16
Q

give examples of invasive diseases

A
  • pneumonia:
  • osteomyelitis:
  • septic arthritis
  • bacteremia and acute endocarditis
17
Q

pneumonia pathogenesis

A

inhaled into lungs, 2° infection after viral, reach lung through blood stream, consolidation and abscess formation in lung

18
Q

osteomyelitis pathogenesis

A

*after hematogenous dissemination to bone or secondary infection from trauma
*usually involves metaphyseal (tip) area of long bones
*more common in children
*good cure rate if treated with appropriate antibiotic

19
Q

septic arthritis pathogenesis

A

*mainly in children and young adults receiving intra-articular injections or hematogenous spread from a localised focus.
*painful erythematous joint, purulent material (pus) in joint space

20
Q

Bacteremia and Acute Endocarditis pathogenesis

A

*Spread of bacteria into the blood from a focus of infection
*>50% of cases are hospital acquired (surgery, contaminated catheters)
*bacteria can spread to other organs, particular the heart (endocarditis)
*damage to the endothelial lining of the heart, infected heart valve is coated with bacteria, platelets and cellular debris.
Perforation of heart valve mainly by secreted enzymes. Septic emboli is common.
*S. aureus (acute) endocarditis has a mortality rate of about 50%

21
Q

give examples of toxigenic diseas and explain how toxigen diseases work

A

Toxins produced by S. aureus are solely responsible for disease
1. Staphylococcal Food Poisoning
2. Staphylococcal Scalded Skin Syndrome (SSSS)
3. Toxic Shock Syndrome (TSS)

22
Q

Staphylococcal Food Poisoning pathogenesis

A

*most common foodborne illness
*results from contamination of food and improper food handling
*microbial intoxication, not infection
*caused by heat-stable enterotoxins (SEA, SEB, …)
*severe vomiting, diarrhea, abdominal pain, nausea, sweating headache
*rapid onset (hours), generally lasting for less than 24h

23
Q

Staphylococcal Scalded Skin Syndrome (SSSS) pathogenesis

A

*cutaneous blisters followed by desquamation of epithelium
*caused by action of exfoliative toxins (microbial intoxication)
*originally described by Gottfried Ritter (Ritter’s Disease)
*affects primarily neonates and young children
*low mortality rate, development of immunity

24
Q

Toxic Shock Syndrome (TSS) pathogenesis

A
  • caused by superantigen-producing strains
  • growth of superantigen-producing strain in wound
  • toxins are released into blood and cause
  • systemic disease (cytokine storm)
  • blood vessels get damaged by inflammation, blood leaks out of vessel, under skin, affect organs
  • fever, hypotension, erythematous rash, intravascular coagulation
  • multiple organ failure
25
Q

List some risk factors for staph aureus

A

*presence of a foreign body (splinter, prosthesis, catheter)
*previous surgical procedure
*poor hygiene of hospital staff
*use of antibiotics that suppress the normal microbial flora
*lack of protective antibodies

26
Q

what are the two types os toxic shock syndrome

A
  • caused by superantigen producing strains
  • menstrual TSS: growth of TSST-producing strain in vagina (Toxic Shock Syndrome Toxin is the only superantigen that can penetrate mucosal barrier), caused by prolonged use of expandable tampon
  • non-menstrual TSS: toxins released in blood cuses systemic disease and multiple physiological responses. mortality rate 30-40%

Medsci 202 (28 decks)

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