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Second Year Microbiology > Health Care Associated Infections > Flashcards

Health Care Associated Infections Flashcards

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1
Q

What are included in HCAIs?

A
  • Acquired in the health care setting
  • Result of interventions, can become apparent after discharged
  • Includes infections among staff
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2
Q

What is the difference between prevalence and incidence?

A
  • Prevalence: number that have HCAI at any given time
  • Incidence: Risk of acquiring an HCAI within a time period
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3
Q

What kind of risk factors influences HCAI?

A

• Latrogenic

o Medical interventions cause

o Lack of removal of pathogens (hands)

o Invasive procedures

o Antibiotic use

• Organisational

o Contaminated air conditioning

o Contaminated water

o Contaminated food

o Staffing issues (patient/nurse ratio)

o Physical layout

• Patient

o Illness severity

o Underlying immunocompromised

o Length of stay

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4
Q

What links up to form the chain of infection?

A
  1. Pathogen 2. Source 3. Transmission 4. Entry 5. Host
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5
Q

What can be sources of HCAI?

A

• Humans (staff, visitors, patients)

o Acute disease

o Incubation period

o Colonised/chronic carriers

• Inanimate objects

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6
Q

What can make people at risk of HCAI?

A
  • Underlying medical conditions (compromise immune system)
  • Accident trauma
  • Surgical procedures
  • Anaesthesia
  • Invasive devices
  • Therapeutic and diagnostic procedures
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7
Q

How can HCAIs be transmitted?

A
  • Direct contact
  • Indirect contact

o Surgical instruments

o Needles

o Blood transfusion

o Fomites

o Airborne

• Vehicle transmission

o Contaminated food, water, drugs, bodily fluids, blood

  • Vector transmission
  • Self

o Endogenous

o Admitted and colonised with hospital strains of bacteria (lots of resistance)

 Skin

 Respiratory tract (gram – in URT)

 GI tract

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8
Q

What are the properties of HCAI pathogens? What are some common ones?

A
  • UTI, surgical wound, LRT, skin, blood
  • Often resistant to many antimicrobials
  • Often opportunistic
  • Viral common
  • Antibiotic resistance common and significant
  • Examples: staphylococcus aureus/epidermidis, Pseudomonas, Enterobacteria, Clostridium Difficile, Candida, Aspergillum
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9
Q

What are the features of Clostridium difficile? How does it cause illness?

A
  • Antibiotic associated diarrhoea
  • Spore forming
  • Anaerobic
  • Gram Positive Rod
  • Shed in faeces
  • Spores survive on surfaces (need bleach, need soap and water for hands, resistant to alcohol hand rub)
  • Transfer via hands (health workers)
  • Broad spectrum antibiotic treatment

o Disruption of normal gut flora, C. difficile overgrowth, mild diarrhoea, pseudo-membranous colitis

• Exotoxins

o A: enterotoxin – fluid production and mucosal damage

o B: cytopathic – ulceration

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10
Q

What can increase the risk of Clostridium diffiile infection? How can it be treated?

A
  • ICU, age, antibiotics, disease, naso-gastric tube, long time in hospital, surgery, antacids, sharing room
  • Remove antibiotics, if possible
  • Metronidazole (treats anaerobes)
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11
Q

What are the features of Staphylococcus aureus?

A
  • Superbug
  • Gram positive cocci
  • Facultative anaerobe
  • Non motile
  • Normal in URT, skin, nose, vagina, intestine
  • Adhesins for colonisation
  • Produce slime layer/biofilm
  • Infection can be serious
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12
Q

How can staphylococcus aureus cause disease? What virulence factors does it have?

A
  • Multiply, spread rapidly – disease
  • Survives drying, environment
  • Virulence factors

o Exfoliative toxins

o Enterotoxins

o Haemolysins

o Lipases

o Proteases

o DNAses

o Protein A

o Beta-lactamases

• Can cause infection of blood, heart, bone

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13
Q

What are the features of antibiotic resistance in Staphylococcus aureus? Why is it such an issue?

A
  • Penicillin
  • Methicillin (MSRA)

o Hard to treat

o Poor outcome

o Use vancomycin

  • Macrolides, tetracycline, quinolones
  • Colonises many people (25-50%)
  • Can escalate to severe illness
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14
Q

What are the features of enterococci? Which types can cause HCAI?

A
  • Gram positive cocci
  • Commensal, in GI tract
  • Can infect abdomen, urinary tract, blood (septicaemia)
  • HCAI infections: E. faecium
  • HCAI infections: E. faecalis
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15
Q

Why is E. faecium hard to treat? How can VREs be spread?

A
  • Hard to treat, lots of antimicrobial resistance
  • Intrinsic resistance

o Penicillin

o Cephalosporin

o Aminoglycosides

• Acquired resistance

o Glycopeptides/vancomycin

  • Survive well in environment
  • VRE Spread

o Faecal contamination

o Equipment

o Oral

o Hand contamination

o Fomites (handles, sinks, toilets, bed rails, surfaces)

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16
Q

What is phylogenetics? How can it be used with HCAI?

A
  • Infer phylogeny from set of taxa
  • Shows evolutionary relationships
  • In HCAI:

o Link to possible sources of infection

o Show evolution of new traits

o Show population dynamics

17
Q

What are the features of VRE? What are VSE and what relationship do they have with VRE?

A
  • First isolate, UK, 1986
  • Austin health 1994
  • Lead to outbreaks or colonisation (important if immunocompromised)
  • VSE = vancomycin sensitive enterococci
  • VSE can become VRE

o Acquire transposon with vancomycin resistant vanA/B locus (TN1549, 7 genes)

18
Q

What does vanB encode?

A

• enzyme/ligase that modifies bacterial peptidoglycan cell wall so vancomycin can’t bind

19
Q

What is the size of the VSE chromosome and vanB transposon?

A
  • VSE chromosome: 3000kbp
  • vanB transposon: 30kbp
20
Q

How might VRE be transmitted according to transmission model A?

A

• Patient arrives with VRE, spreads to surrounding environment

21
Q

How might VRE be controlled under transmission model A?

A
  • Screen patients for VRE on arrival
  • Isolate carriers to single rooms
  • Ensure good hand hygiene, protective clothing, cleaning
  • Expect eventual elimination of VRE from hospital
22
Q

What effect did hand hygiene have on Austin Health?

A
  • MRSA decrease, but VRE increase (model A not only one)
  • vanB in many anaerobic gut commensals
  • Make your own VRE from the commensals
23
Q

How does the alternative transmission model explain vanB VRE epidemiology?

A
  • Transfer vancomycin resistant genes to VSE from anaerobic bacteria in bowel flora when patient is exposed to vancomycin
  • Lateral gene transfer (vanB to VSE)
  • Environment contaminated
  • Lots of patients will carry VSE in bowel flora initial
  • VRE can emerge from de novo mutation when patient treated with broad spectrum antibiotics which select for HGT from bowel anaerobes to VSE
24
Q

What is aseptic technique?

A

• Specific practices and procedures performed under carefully controlled conditions with goal of minimising transfer of and contamination by potential pathogens

25
Q

What are standard precautions to prevent HCAI?

A
  • Universal precautions
  • Used in treatment/care of all patients, all infectious states
  • Personal Protective Equipment (PPE) when anticipate contact with bodily fluids, non intact skin, blood, mucous membranes
  • Prevent transmission
26
Q

What are additional precautions to prevent HCAI?

A

• Minimise risk of cross infection

o Transmission by air, droplet, direct, indirect contact

  • Isolation/single rooms
  • Air filtration, pressure systems
  • Respiratory masks
  • Restricted patient movement
27
Q

What are the features of hand washing? Why can’t you rely on alcohol hand rub alone?

A
  • Effective, reduce spread
  • Problem with compliance (behaviour, beliefs, equipment)
  • Alcohol hand gels available

o Still need soap and water wash to remove spores (alcohol resistant)

28
Q

What is the aim of the prudent use of antibiotics?

A
  • Avoid selecting resistant mutants
  • Avoid selecting bacteria with plasmids for multiple resistance
  • Avoid selection of certain gut bacteria
  • Minimise risk of antibiotic associated diarrhoea (C. difficile)
29
Q

Are all disinfectants sporocidal?

A

• No, bleach is

30
Q

What is the difference between biocidal and biostatic?

A
  • Biocidal – kills microorganisms (irreversible)
  • Biostatic – inhibits growth of microorganisms (reversible)
31
Q

What is involved in disinfection?

A
  • Removing some/all burden of pathogenic microorganisms from article
  • Washing, cleaning
  • Hot water/steam
  • Chemical disinfectants

o Different activity

o Don’t all kill spores (bleach is sporocidal)

32
Q

What is involved in sterilisation?

A
  • Destroying/removing all viable microorganisms, spores, infectious agents (viruses, prions) from article
  • Heat (moist or dry)
  • Filtration
  • Chemical
  • Ionising radiation
  • Required to know Type and level of contamination
  • Required to know Rate of biocidal action
  • Required to know Level of sterility assurance
33
Q

What are the requirements of chemical disinfection? When is it used?

A
  • Used in combination (before) sterilisation
  • Need appropriate agent
  • Need appropriate concentration
  • Need appropriate conditions
  • Need adequate contact (time, physical)
34
Q

How can the level of contamination be determined?

A
  • Viable count
    1. Prepare dilutions
    1. Spread on plates
    1. Incubation
    1. Count colonies
    1. Estimate microbial load
35
Q

How can you construct a killing curve? What does Dx represent?

A
    1. Initial viable count
    1. Expose to agent (X°C)
    1. Repeated viable counts
    1. Calculate Decimal Reduction Time (Dx)

o Time to reduce population 10 fold at certain temperature

36
Q

What is sterility assurance?

A
  • Probability that microorganisms remain/survive sterilisation
  • Decision depends on use (i.e. Can be higher for Band-Aids than needles)
37
Q

How can you check whether sterilisation has been effective?

A

• Physical indicators, chemical indicators, biological indicators

38
Q

What makes up the sterilisation cycle?

A
  • Preparation time
  • Sterilisation time

o Penetration time

o Holding Time

  • Safety Margin
  • Cool down/drying/aeration time
39
Q

How can heat sterilise? Which type is most effective?

A
  • Physical, chemical changes to cells
  • Moist heat

o Coagulation

o Steam under pressure more effective than dry heat

o Lower temperatures, shorter time (but corrosive)

• Dry heat

o Oxidation

o Higher temperatures, longer time (penetrates oils, solids, non-corrosive)

Second Year Microbiology (8 decks)

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