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Bacteriology > Staphylococci > Flashcards

Staphylococci Flashcards

1
Q

Describe the Staphylococci pathogen

A
  • Gram positive
  • Coccus shaped, haloduric (exist with salt)
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2
Q

There are 2 types of staphylococci. How are they distinguished?

A

2 ways:

  1. Slide test
    • Drop of plasma on slide, left to multiply
    • If it is coagulate positive, clumps form
    • If not, coagulate negative species
  2. Colony in tube
    • If it is the coagulate positive species, clumps form at the bottom

These tests look for coagulase, which turns fibrinogen into staphylothrombin = clotting

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3
Q

Which species a coagulase positive, which are coagulase negative?

  • Staphylococcus aureus (Latin for gold)
  • Staphylococcus epidermidis
  • Staphylococcus pseudintermedius
  • Staphylococcus lugdenensis
  • Staphylococcus saprophyticus
A
  • Coagulase positive staphylococci
    • Staphylococcus aureus (Latin for gold)
    • Staphylococcus pseudintermedius
    • Staphylococcus lugdenensis
  • Coagulase negative staphylococci
    • Staphylococcus epidermidis
    • Staphylococcus saprophyticus
    • Many others
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4
Q

Describe the coagulase negative pathogen Staphylococcus epidermidis

A
  • Not as dangerous as aureus
  • Colonises on skin (haloduric) and medical devices (catheters, prosthetics)
    • Produce a capsule, forms biofilms
  • ABx resistant
  • Colonises med
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5
Q

Describe the coagulase positive pathogen Staphylococcus pseudintermedius

A
  • Colonises dogs = canine pyoderma (pyo - pus, derma - skin; skin infection causing inflammation of pus)
  • ABx resistant
  • Can transmit to humans rarely
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6
Q

Staphylococcus aureus

Describe the coagulase positive pathogen Staphylococcus aureus

Describe the colonisation mechanism

A
  • Colonises humans asymptomatically, extracellularily in skin, mucous membranes, nose, vagina, rectum (moist skin)
    • 30% persistently colonised, 25% transiently colonised
  • Leading cause of hospital-acquired (nosocomial) infections
  • Colonisation mechanism
    • Direct or indirect contact (hands, towels, razors, bandaids; formite objects)
    • Surface proteins bind host proteins using adhesins (ex., collagen)
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7
Q

Staphylococcus aureus

What can a Staphylococcus aureus infection cause?

A
  • Infection often begins with a cut
  • Sign: abscess (heat, redness, swelling, pain caused by a collection of dead neutrophils (pus)) as body tries to wall off bacteria
    • Can occur in any organ, mostly skin
    • If bacteria escape from abscess –> major complications
    • Abscesses require draining, ABx
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8
Q

Staphylococcus aureus

Describe the local effect of staph infection: skin lesions

A
  1. Stye: infection of the eye sebaceous glands
    • Often will drain on its own with warm compress
    • Do not lance
  2. Furuncle (boil)
    • Infection of the hair follicle
    • Warm compress to drain
  3. Carbuncles (infection of several hair follicles)
    • The furuncles coalesce
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9
Q

Staphylococcus aureus

Describe the local effect of staph infection: impetigo

A
  • Non-bullous form has pimple-like lesions with pus (also caused by S. pyogenes - strep)
  • S. aureus produces proteins that cleave the peptide bonds in the skin
  • Painless, fluid filled blisters
  • Causes ecthyma: pus filled sores that turn into deep ulcers
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10
Q

Staphylococcus aureus

Describe the local effect of staph infection: deep abscesses

A
  • Not superficial but still localised (ex., cellulitis, liver, lung, kidney, tooth)
  • Can get them from wound or surgical infections but less visible
    • We look for constitutional symptoms (fever, chills)
  • Can be systemic
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11
Q

Staphylococcus aureus

Describe the systemic effect of staph infection: osteomyelitis

Cause, diagnosis, treatment?

A
  • Osyeomyelitis: infection of bone, bone marrow
  • S. aureus is the most common cause
  • Can come from hematogenous spread or local infection, fractures, joint replacement
  • Diagnosed with x-ray/CT/MRI and biopsy
  • Treatment is surgery and I.V. ABx
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12
Q

Staphylococcus aureus

Describe the systemic effect of staph infection: endocarditis

“Vegetation”? Causes?

A
  • Endocarditis: infection of heart valves
  • Occurs in damaged or prosthetic heart valves in I.V. drug users
  • Lesion is called vegetation –> bacteria grow to large numbers and “seed”, forming clots
  • Causes strokes, pulmonary embolism, fatigue, fever, murmurs, hemorrhage
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13
Q

Staphylococcus aureus

Describe the toxin-mediated disease effect of staph infection: staphylococcal food poisoning

A
  • Does not require live cells; caused by staphylococcal enterotoxins (superantigens)
  • Staph grows on food and produces heat resistant toxins
  • Symptoms include nausea, vomiting, cramps, diarrhea (do not need to ingest very much toxin)
  • Unknown mechanism but lasts 24 hours (very self limiting)
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14
Q

Staphylococcus aureus

Describe the toxin-mediated disease effect of staph infection: TSS

A
  • Fever, hypotension, rash, multi-organ dysfunction (called desquamation)
  • Can be caused by aureus (menstrual) and strep pyogenes
  • Superantigens function by turning on T cells rapidly, causing vascular leakage –> organ failure (systemic)
    • Superantigens manipulate conventional presentation by binding and FORCING interaction (not very specific)
    • Menstrual form is associated with superantigen TSS toxin-1
      • Super absorbent tampons = risk factor
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15
Q

Staphylococcus aureus

Describe the toxin-mediated disease effect of staph infection: scaled skin syndrome

A
  • Caused by exfoliative toxins
    • Proteases that cleave bonds within the skin causing skin to blister off
  • Primarily affects neonates (newborns), heals 1-2 weeks
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16
Q

Why are there so many diseases assocaited with S. aureus?

A
  • Each S. aureus has many different superantigens, toxins, etc., produces capsules and biofilms, many strains differ (many virulence factors)
  • It has immune evasion mechanisms as a virulence factor as well (staph has been evolving with us for a very long time)
17
Q

Describe the regulation of the expression of virulence factors in S. aureus

A
  • Surface virulence factors expressed during exponential growth
  • Secreted virulence factors (exotoxins) expressed during stationary phase of growth
18
Q

How does S. aureus avoid the immune system?

A
  • Neutrophils = key defense against Staph; chemokines move neutrophils to site of Staph infection
    • Staph survive neutrohpils in 2 ways
      1. Resistint antibody mediated phagocytosis
        • Staph protein A (SpA) binds to Fc protein of IgG; prevents Fc-receptor recognition by disrupting orientation
      2. Staph toxins kill leukocytes
        • Cytolytic toxins kill WBCs and RBCs (hemolysins) by forming holes in the membranes –> cell lysis
19
Q

Define HA, CA, and LA-MRSA

A
  • Associated with hospitals
    • HA-MRSA
    • Complicate treatments (such as cancer treatment)
  • Associated with communities
    • CA-MRSA
    • Not as drug resistant but higher virulence
    • May cause necrotizing pneumonia
    • Most common cause of skin/soft tissue infections (SSTI)
  • Associated with livestock
    • LA-MRSA
    • Many species are colonized due to frequent contact with humans
    • Antibiotic misuse: used as growth factor in livestock
      • Caused emergence of drug resistant strains

Bacteriology (8 decks)

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