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CSI > CSI 3: Hospital acquired infection > Flashcards

CSI 3: Hospital acquired infection Flashcards

1
Q

What is a reservoir of an infectious agent?

A

The habitat in which the agent normally lives, grows and multiplies.

⤷ e.g. humans, animals or the environment

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2
Q

Examples of diseases without intermediaries involving human reservoirs

A

STDs, measles, mumps, streptococcal infection, diseases caused by respiratory pathogens

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3
Q

Animal reservoirs

A

Animal to animal, with humans as incidental host e.g. SARS-CoV-2

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4
Q

Why was smallpox eradicated after the last human case was identified and isolated?

A

Humans were the only reservoir for the smallpox virus.

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5
Q

What is a human carrier?

A

Someone who is with inapparent infection but is capable of transmitting the pathogen to others

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6
Q

What is the difference between a carrier and a vector?

A

A carrier is infected even if they are asymptomatic; a vector is not infected with disease even if it is on them.

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7
Q

What are the three different types of carriers?

A

Incubatory - those who can transmit the agent during the incubation period before the clinical illness begins
Convalescent - those who recovered from illness but remain capable of transmitting to others
Chronic - those who continue to harbour the causative agent for weeks and months after initial infection

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8
Q

What is zoonosis?

A

Infectious disease that is transmissible under natural conditions between vertebrate animals to humans

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9
Q

Examples of zoonosis

A

Brucellosis - cows and pigs
Anthrax - sheep
Plague - rodents
Trichnellosis/trichinosis - swine
Tularemia - rabbits
Rabies - bats, raccoons, dogs, other mammals

(Suspicions that HIV/AIDs, ebola infection, SARS came from animal hosts)

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10
Q

Examples of environmental reservoirs

A

Plants, soil, water e.g. fungal agents which cause histoplasmosis live and multiply in soil

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11
Q

What is the portal of exit?

A

Path by which pathogen leaves its host

⤷ Usually corresponds to the site where pathogen is localised

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12
Q

Examples of portals of exit (6)

A

Respiratory tract - influenza viruses, Mycobacterium tuberculosis
Urine - schistomes
Faeces - Cholera vibrios
Crossing placenta from mother to foetus - rubella, syphillois, toxoplasmosis
Cuts or needles in skin - hep B
Blood sucking arthropods - malaria

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13
Q

2 main modes of direct transmission

A

Direct contact - skin-to-skin, kissing and sexual intercourse
Droplet spread - direct spray from short range aerosols produced by sneezing, coughing or even talking

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14
Q

Examples of diseases spread by direct contact

A

Infectious mononucleosis, gonorrhoea, hookworm (direct contact with contaminated soil)

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15
Q

Examples of diseases spread by droplet spread

A

Pertussis and meningococcal infection

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16
Q

3 methods of indirect transmission

A

Airborne transmission - occurs when infectious agents are carried by dust or droplet nuclei suspended in air
Vehicle - food, water, blood and fomites (inanimate objects)
Vectors - mosquitoes, fleas, ticks

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17
Q

Examples of disease carried by vehicles

A

Hep A - carried by food and water
Clostridium botulinum - improper canned food supports production of botulinum toxin

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18
Q

Examples of diseases carried by vectors

A

Shigella - flies
Yersinia pestis - fleas

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19
Q

Different types of vector borne transmission

A

Mechanical - pathogen on vector e.g. fly moving pathogen on to a host
Biological - pathogen within vector e.g. mosquito, flea

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20
Q

What is a portal of entry? Examples

A

The manner in which a pathogen enters a susceptible host

Access to tissues
- Faecal-oral route (exit host in faeces, enter new host through mouth)
- Skin e.g. hookworm
- Mucous membranes e.g. syphilis
- Blood e.g. hep B, HIV

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21
Q

What does the susceptibility of the host depend on?

A

Genetic or constitutional factors
Specific immunity i.e. protective antibodies
Nonspecific factors that affect an individual’s ability to resist infection or to limit pathogenicity

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22
Q

6 examples of non-specific factors that defend against infection

A

Skin
Mucous membranes
Gastric acidity
Cilia in respiratory tract
Cough reflex
Non specific immune response

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23
Q

Factors that may increases susceptiblity to infection by disrupting host defences [3]

A
  • Malnutrition
  • Alcoholism
  • Disease or therapy that impairs the non specific immune response
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24
Q

How can vehicle borne transmissions be reduced?

A

Elimination or decontamination of vehicle

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25
Q

How could airborne transmissions be reduced?

A
  • Modifying ventilation or air pressure
  • Filtering or treating the air
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26
Q

How could vector borne transmission be reduced?

A

Controlling vector population, such as spraying to reduce mosquito population

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27
Q

What are interventions directed at?

A
  1. Controlling or eliminating agent at source of transmission
  2. Protecting portals of entry
  3. Increasing host’s defences
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28
Q

Examples of interventions that aim to increase host defence

A
  1. Vaccinations promote development of specific antibodies that protect against infection
  2. Prophylactic use of anti malarial drugs (visitors to malaria-endemic areas)
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29
Q

Is herd immunity acc effective?

A

In practice, not effective b/c incidence of measles and rubella is still high despite 85-90% of pop immunised

Bc people often cluster into small groups based on socioeconomic or cultural factors, hence those that are not immunised may be closer in proximity than if randomly dispersed in population

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30
Q

What kind of intervention might prevent a pathogen from entering a susceptible host?

A

Herd immunity - if there is a high enough proportion of individuals in a pop are resistant to an agent, those susceptible few will be protected by the resistant majority bc pathogen will be unlikely to ‘find’ them

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31
Q

What is a HAI?

A

An infection a patient gets while receiving treatment for medical or surgical conditions (many are preventable)

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32
Q

Where can you get a HAI? (7)

A

In all types of care settings
- Acute care hospitals
- Ambulatory surgical centers
- Dialysis facilities
- Outpatient care (e.g. physicians’ offices and health care clinics)
- Long-term care facilities (e.g. nursing homes and rehab facilities)
- GP practices
- Hospices

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33
Q

High priority HAIs flagged by the HAI objectives for Healthy people in 2020

A

Central line-associated bloodstream infection CLABSI - germs enter bloodstream through long flexible tube placed in large vein (e.g. internal jugular vein) that empties near our heart

Methicillin resistant Staphylococcus aureus MRSA - causes life threatening bloodstream infections, pneumonia, surgical site infections

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34
Q

Common types of HAI [5]

A
  1. Catheter associated urinary tract infections
  2. Surgical site infections
  3. Bloodstream infections
  4. Pneumonia
  5. Clostridium difficile

UTIs most common in US

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35
Q

What are the 4 main risk factors of HAI?

A
  • Medical procedures and antibiotic uses
  • Organisational factors
  • Patient characteristics
  • Behaviour of healthcare staff
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36
Q

How can we prevent HAIs?

A
  • Increased compliance with and adoption of best practices of healthcare workers
  • Careful insertion, maintenance and prompt removal of catheters
  • Advance development of effective prevention tools
  • Explore new prevention approaches
37
Q

Why might HAIs be more of a problem in outpatients settings?

A

Limited capacity for infection control due to patients moving in and out constantly, compared to acute care settings

38
Q

Impacts of HAIs on NHS/healthcare workers/healthcare environments

A
  1. Longer stay in hospital → bed blocking, increased backlog
  2. Strain on resources
  3. Cost of extra antibiotics being given
  4. Increased avoidable usage of antibiotics of bacterial HAIs → bacterial resistance
  5. Risk of infection to healthcare workers
    → Less staff coming into work due to illness, more strain on resources
    → Every year 62000 sick days due to HAI
  6. Guilt, difficult to tell patient
39
Q

Impacts of HAIs on patients/patient families/patient visitors

A
  1. Trust lost due to small clinical procedure going wrong
  2. Time and money spent resolving infection (coming back to hospital for further monitoring and treatment → increased disruption to life)
  3. Impact on mental health
  4. Immunosuppressive patient particularly vulnerable
  5. Patients less likely to come in until condition has escalated in fear of acquiring a HAI
  6. Increased morbidity and mortality
  7. May want to be discharged before officially decided time
  8. Families’ lives are disrupted - caring for and visiting patient despite other commitments (childcare, supporting family financially)
40
Q

What is the ‘chain of infection’?

A
  1. Infectious agent
  2. Reservoir
  3. Portal of exit
  4. Mode of transmission
  5. Portal of entry
  6. Susceptible host
41
Q

Can a susceptible host be their own reservoir?

A

Yes → commensal bacteria spreading to places it shouldn’t be in and causing more serious infections

42
Q

Hand hygiene in patient handling

A
  1. Before touching patient
  2. Before clean/aseptic procedure (e.g. catheterisation)
  3. After bodily fluid exposure risk
  4. After touching patient (e.g. hip examination)
  5. After touching patient surroundings (e.g. bedding, drug chart)
43
Q

What is elevated in a patient who has an infection?

A

CRP level, white blood cell count, respiratory rate

*Also low blood oxygen saturation

44
Q

How do you do an antibiotic sensitivity test?

A

→ Antibiotic discs diffuse on to nutrient agar with bacteria growing on it

→ Larger zone of inhibition = bacteria has a higher sensitivity to the antibiotic

45
Q

What is the difference between gram +ve and gram -ve bacteria?

A

Gram +ve → thick peptidoglycan sheath, single membrane [purple]

Gram -ve → thin layer of peptidoglycan between two lipopolysaccharide membranes [pink/red]

46
Q

What is a peptidoglycan monomer made up of?

A

→ 2 sugars - NAG, NAM

→ Amino acid chain

47
Q

How is the peptidoglycan matrix structure formed?

A

→ Sugar parts are horizontally linked with AA chains projecting outwards

→ Peptide bridges/cross links form between layers vertically

48
Q

What is the PBP (penicillin binding protein)?

A

D-alanyl-D-alanine carboxypeptidase transpeptidase

49
Q

Role of PBP

A

→ Assists with forming vertical cross links between amino acids

→ Very specific site on enzyme, where AA chain for new peptidoglycan molecule gets modified and added to another molecule

50
Q

Mode of action of penicillin

A

→ Beta lactam ring of penicillin binds to the key serine in PBP’s active site

→ Inactivates the enzyme and prevents the formation of the peptidoglycan matrix → cell bursts due to osmotic pressure

51
Q

Mechanisms of antibiotic resistance

A
  1. Altered target site → acquisition of alternative gene or gene that encodes target-modifying enzyme
  2. Inactivation of antibiotic → via enzyme degradation/alteration
  3. Altered metabolism profile → different enzyme or pathway (bypassing antibiotic’s effect or outcompeting the antibiotic inhibitor with another molecule)
  4. Decreased drug accumulation → pumping out antibiotics with efflux pumps or reducing penetration of antibiotic

NB: AIMeD

52
Q

How does MRSA show resistance to beta-lactam antibiotics?

A

→ Expresses PBP2a with an altered active site that doesn’t bind to the beta lactam ring

53
Q

How do other bacteria show resistance to beta-lactam through enzyme degradation?

A

→ Produces beta lactamase which breaks down beta lactam ring, so it can’t bind to serin residue in the active site of the PBP

→ e.g. NSM-1 codes for (new-delhi metallobeta-lactamase enzyme), which breaks down almost all known beta-lactamase drugs

54
Q

Horizontal gene transfer

A

Process in which organism transfer genetic material (plasmids) to another organism that isn’t offspring

55
Q

Vertical gene transfer

A

Transfer of genetic information including any genetic mutations from a parent to its offspring

56
Q

How can antibiotic resistance within one population of bacteria spread to another population?

A

→ Horizontal gene transfer from species with resistance to species without resistance

→ Vertical gene transfer of plasmids from one generation in species that previously did not have resistance to the next generation

57
Q

Why is the bacteria resistant to Amoxicillin but not Co-amoxiclav?

A

→ Coamoxiclav = amoxicillin but with clavulanic acid

→ Acidic group inactivates beta lactamase (enzyme inhibitor)

→ Beta lactamase can’t break down the beta lactam ring

58
Q

What is a beta lactamase inhibitor?

A

Medication used to inhibit the activity of beta-lactamases, allowing the beta-lactam antibiotic to work properly

e.g. Coamoxiclav

59
Q

Giving an example, how can antibiotics overcome bacteria that produce beta-lactamase?

A

Amoxicillin (normal antibiotic) & clavulanic (beta-lactamase inhibitor) → allowing antibiotic to inhibit PBP freely

60
Q

Give an example of allergies to penicillin and side effects of penicillin

A

Allergies → anaphylaxis, rash
Side effects → diarrhoea, vomiting

61
Q

Infection control measures for this patient

A
  1. Isolate patient in a separate side room
  2. Isolate whole bay if already affected
  3. Hand hygiene at all points throughout patient encounter
62
Q

Profuse, watery diarrhoea w/ suspicion of HAI →

A

Clostridium difficile until proven otherwise

63
Q

How do you confirm of C.difficile infection?

A

MCS → Microscopy, culture and sensitivity
Stool sample is tested

64
Q

How does C. difficile get into the body?

A

→ Most people don’t have commensal CD so is usually acquired through spores (dormant bacteria) spread by faeces

→ Spores super resilient (can live up to 5 months, aren’t affected by alcohol rubs)

65
Q

What does C.difficile do when antibiotic (Co-amoxiclav) is given?

A

Disruption of gut microbiome
→ Antibiotic eliminates other commensal bacteria, which was outcompeting the C.diff keeping it in check

Activation of toxigenic C.diff & killing of gut microbiome
→ Spores travel into gut and respond to chemical environment in gut, germinating and flourishing
→ Can produce chemicals that inhibit the growth of others

66
Q

Why does diarrhoea occur because of C.diff?

A

→ Diarrhoea disrupts the gut membrane to stop the absorption of AA which C.diff required to grow

67
Q

What are two key things you should keep in mind when apologising to patients?

A
  1. Duty of candour → legal (statutory) duty to be open and honest with patients (service users) or families when something goes wrong that appears to have caused or could lead to significant harm in the future
  2. Empathy → the ability to understand and share another person’s feelings and perspectives and use the understanding and emotion to guide future action
68
Q

What is antimicrobial resistance?

A

When microbes develop the ability to defeat the drugs designed to kill them

69
Q

What are antimicrobials?

A

Drugs used to treat infections and disease caused by microbes by killing or slowing growth of pathogens causing infection

70
Q

What are the two types of microbes?

A

Bacteria treated with antibiotics e.g. strep throat, food borne illness
Fungal treated with antifungals e.g. athlete’s foot, yeast infections

71
Q

Which bacteria has an outer layer that protects from their antibiotic drugs?

A

Gram -ve

72
Q

Antimicrobial resistance mechanisms

A
  1. Resist access of antibiotic by changing or limiting number of entry ways
  2. Get rid of antibiotics/antifungals that entered using pumps in cell wall
  3. Change or destroy the antibiotic with enzymes
  4. Change the target for antimicrobial
  5. Bypass the effects of antibiotics by modifiying metabolism to avoid using antibiotic targets
73
Q

Example of restricting access of antibiotics

A

Gram -ve bacteria with an outer layer

74
Q

Example of getting rid of antibiotics

A

Pseudomonas aeruginosa bacteria pump out fluoroquinolones, beta lactams, chloramphenicol and trimethoprim

Some Candida species pump out azoles

75
Q

Example of changing or destroying the antibiotic

A

Klebsiella pneumoniae bacteria → carbapenemases, break down carbapenem drugs and most other beta-lactam drugs

76
Q

Example of changing the antimicrobial’s target

A

E.coli with mcr-1 green can add compound to outside of cell wall → drug colistin cannot latch onto it

Aspergillus fumigatus → changes cyp1A gene so triazoles cannot bind to protein

77
Q

Example of bypassing effects of antibiotics

A

Some staphylococcus aureus bypass effects of trimethoprim

78
Q

How does antibiotic resistance move from germ to germ?

A

Plasmids - circles of DNA that can move between cells

Transposons - small pieces of DNA which can go and change the overall DNA of a cell (can move back and forth between chromosomes and genes)

Phages - virus attacks germs and carry DNA germ to germ

79
Q

How do mobile genetic elements work?

A
  1. Transduction → phage mediated transfer
  2. Conjugation → pilus mediated transfer
  3. Transformation → resistance genes released from nearby live or dead germs picked up directly
80
Q

What is sepsis?

A

Extreme response to an infection which can rapidly lead to tissue damage, organ failure and death

81
Q

What is meant by a shock?

A

Imbalances in supply and demand

82
Q

What is the sequence of septic shock?

A
  1. Hypotension - BP drops
  2. Tachycardia - high heart rate to compensate
  3. Tachypnoea - high respiratory rate
83
Q

How are antibodies administered during sepsis?

A

Intravenously bc they have a faster delivery than oral antibiotics and has a systemic effect

84
Q

What form of penicillin is suitable for oral use?

A

Penicillin V

85
Q

How can an altered metabolism profile lead to antibiotic evasion?

A

Increased production of enzyme substrate can outcompete antibiotic inhibitor or bacteria can just switch to another metabolic pathway

86
Q

Poor antibiotic stewardship

A

Mismanagement and overprescription of antibiotics
⤷ tis one of the factors driving antibiotic resistance

87
Q

What is an antimicrobial stewardship programme?

A

An organisational or healthcare system wide approach to promoting and monitoring judicious use of antimicrobials to preserve their future effectiveness

88
Q

What are the key points of antimicrobial stewardship programmes?

A
  1. Should operate across all care settings
  2. Needs to considers the resources needed to support the programme
  3. Monitor and evaluate antimicrobial prescribing and how this relates to local resistance patterns
  4. Provide regular feedback to individual prescribers about [1] their antimicrobial prescribing using professional regulatory numbers and prescriber codes and [2] patients safety incidents related to antimicrobial use.
  5. Education and training to health and social care practitioners
  6. Integrating audit into quality improvement programmes
  7. Clearly defined roles and responsibilities
  8. Involve lead health and social care practitioners in development and review of antimicrobial guidelines with national guidance and local data
  9. Provide regular e.g. yearly updates to individual prescribers abt:
    → Individual prescribing benchmarks
    → Local and national antimicrobial resistance and trends
    → Patient safety incidents
  10. Develop systems for identifying and reviewing whether hospital admission are related to prescribing decisions (inc. HAIs)

*Patient safety incidents e.g. hospital admissions for potentially avoidable life threatening infections, C.diff infections or adverse drug reactions e.g. anaphylaxis

CSI (4 decks)

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