Nosocomial infections Flashcards

1
Q

Ignaz Semmelweiss 1847

A

-Introduced hand washing to reduce chilbed fever (puerperal sepsis) -Streptococcus pyogenes

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2
Q

Joseph Lister 1865

A
  • antiseptic phenol spray

- to reduce post-operative bacterial sepsis of wounds

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3
Q

Exogenous sources

A

other patients, medical staff, food, air, dust, water, catheters, instruments and equipment

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4
Q

Endogenous sources

A

another site within the patient

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5
Q

Hospital aquired infections

A
  • increased incidence when patients are elderly, immunocompromised etc
  • about 10% patients suffer
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6
Q

Mainly caused by opportunistic pathogens

A
  • staphylococcus aureus
  • clostridium difficile
  • norovirus (winter vomiting virus)
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7
Q

What % of nosocomial infections are preventable?

A

about 15-30%

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8
Q

Risk Factors:

A
  • age
  • length of stay in hospital
  • MRSA -previous exposure to abs
  • surgery
  • indwelling catheters
  • C.difficile
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9
Q

MRSA

A

Methicillin Resistant Staphylococcus aureus

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10
Q

Staphylococcus aureus

A
  • gram +ve coccus
  • grow in grape-like clusters
  • golden colonies
  • non-fastidious, facultative anaerobe
  • survives drying, salt tolerant
  • commonly found in nose &skin of healthy humans
  • spread by contact& airborne routes
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11
Q

Gram stained film of S.aureus would show…

A

-gram +ve cocci both intracellular and extracellular to polymorphonuclear leukocytes (PMN)

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12
Q

Virulence factors:

A

TOXINS:

  • enterotoxins(v&D)
  • toxic shock syndrome toxin (TSST)
  • ‘superantigens’, trigger cytokine release, causing ‘shock’
  • Various cell-destroying and tissue-destroying enzymes and toxins (e.g. alpha toxin, leukocidin, oxfoliative toxin, panton-valentine leukocidin)
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13
Q

Staphylococcus virulence factors:

A
  • ->Adherence -fibronectin-binding proteins etc
  • ->Anti-chemotaxis - chemotaxis inhibitory protein of staphylococci (CHIPS) , Extracellular adhesion protein (EAP)
  • -> Anti-opsonic &anti-phagocytic-
  • ->Degradative enzymes
  • -> IRON uptake systems
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14
Q

Adhesins

A

Microbial surface components recognising adhesive matrix proteins
-bind to host proteins, may aid adherence to host tissues, and serum-coated plastic

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15
Q

Capsule:

A
  • formation of biofilms

- adherence to plastic

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16
Q

what is Protein A?

A
  • evasion mechanism

- binds Fc of IgG, to prevent opsonisation

17
Q

opsonisation

A
  • immune process where particles such as bacteria are targeted for destruction by phagocyte
  • process will identify the invading particle
18
Q

Antibiotic Resistance

A

-first appeared in 1950s
–Emergence of Methicillin-resistant Staphylococcus aureus (MRSA) in the last 30years
-

19
Q

Mechanism of Resistance -Acquisition off mecA gene

A

mecA gene:

  • encodes mutant penicillin-binding protein (PBP2a) with lower affinity for Beta-lactam antibiotics
  • replaces normal penicillin binding proteins(enzymes involved in peptidoglycan synthesis) to which penicillin normally targets
20
Q

mecA gene

A

located on a transposon known as SCCmecIV (jumping gene)

  • resistant to all other B-lactam antibiotics
  • often resistant to other types of antibiotics (multiply-resistant)
21
Q

Epidemic MRSA (EMRSA)

A
  • MRSA are no more virulent than antibiotic-sensitive strains
  • they are more difficult to treat
22
Q

Community acquired MRSA

A
  • younger age group
  • severe skin infections and lethal haemolytic pneumonia
  • panton-valentine leukocidin makes pores (holes) in membranes of immune cells
23
Q

Treatment and Prevention

A
  • vancomycin
  • emergence of VISA strains: vancomycin intermediate sensitivity
  • vansomycin-resistant S.aureus (VRSA - vanA from VRE)
24
Q

Recent approach

A

screening of hospital patients and decolonisation prior to admission

25
Q

Clostridium difficile

A

-grem +ve rod
-strict anaerobe, spore-forming
-resistant to cleaning disinfectants
found in gut of:
-<1% people outside hospitals
-5-10% of hospital patients

26
Q

Clostridium difficile: Disease

A
  • diarrhoea
  • abdominal pain
    -life threatening pseudomembranous colitis
    (extensive inflammation and necrosis of the colonic mucosa)
27
Q

C. difficile infection development

A
  • disease induced by disruption of normal flora
  • broad spectrum antibiotics
  • diarhhoea, ulceration of colon, death
28
Q

Symptoms due to…

A
Toxin A (enterotoxin) cause hypersecretion of fluid
Toxin B (cytotoxin) damage and destroys cells