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PHAY00011 > Infectious disease II > Flashcards

Infectious disease II Flashcards

Bacteria, nature of bacterial resistence, HAP

1
Q

Differences between prokaryotes (P) and eukaryotes (E): Size

A

P smaller

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2
Q

Differences between prokaryotes (P) and eukaryotes (E): Nucleus

A

P: no nuclear membrane or nucleoli

E: True nucleus with nuclear membrane and nucleoli

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3
Q

Differences between prokaryotes (P) and eukaryotes (E): Membrane-enclosed organelles

A

P: present

E: absent

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4
Q

Differences between prokaryotes (P) and eukaryotes (E): Flagella

A

P: 2 protein building block

E: Complex, multiple microtubules

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5
Q

Differences between prokaryotes (P) and eukaryotes (E): Glycocalyx

A

P: present as capsule and slime layer

E: present in some cells without cell wall

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6
Q

Differences between prokaryotes (P) and eukaryotes (E): Cell wall structure

A

P: usually present, peptidoglycan, complex structure

E: Not always present, simple chemical structure, chitin and cellulose

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7
Q

Differences between prokaryotes (P) and eukaryotes (E): Cytoplasm streaming

A

P: No

E: Yes

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8
Q

Differences between prokaryotes (P) and eukaryotes (E): Plasma membrane

A

P: No sterols

E: Sterols (ergosterol and cholesterol) present

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9
Q

Differences between prokaryotes (P) and eukaryotes (E): Ribosomes

A

P: smaller in size

E: larger in size, smaller ones present in the organelles

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10
Q

Differences between prokaryotes (P) and eukaryotes (E): Chromosoms.

A

P: Single circular, no histones

E: Multiple linear with histones

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11
Q

Differences between prokaryotes (P) and eukaryotes (E): Cell division route

A

P: Binary fission

E: Mitosis involved

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12
Q

Differences between prokaryotes (P) and eukaryotes (E): Sexual recombination?

A

P: None, only DNA transfer

E: Meiosis involved

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13
Q

3 most important shapes of bacteria used for classification

A

Coccus

Bacillus

Spirochete

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14
Q

What are the different ways that can be used to classify bacteria?

A

Shape

Grouping patterns

Effects of oxygen on growth

Gram stain

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15
Q

Different grouping patterns that are used for bacteria classification.

A

Streptoccoci: chain

Tetrad

Sarcinae

Staphyloccoci: Cluster

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16
Q

Explain why some bacteria can tolerate oxygen and some cannot.

A

Presence of enzyme catalase and superoxidase dismutase (SOD)

Neutralise toxic forms of oxygen

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17
Q

Based on the effects of oxygen on growth of bacteria, what are the 5 classes of bacteria?

A

Obligate aerobes: req O2 to grow. Grow at high concentration of O2

Facultative anaerobes: grow in both but better in O2 presence

Obligate anaerobes: only grow in no O2

Aerotolerant anaerobes: start grow in anaerobic but can continue in O2 present

Microaerophiles: only grow in aerobic but low O2 concentration

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18
Q

Examples of obligate aerobes

A

Pseudomonas aeruginosa

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19
Q

Examples of falcutative anaerobes

A

Staphylococcus aureus

E.coli

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20
Q

Examples of obligate anaerobes.

A

Clostridium species

Bacteroides

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21
Q

Examples of aerotolerant anaerobes.

A

Streptococci

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22
Q

Examples of microaerophiles

A

Campylobacter

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23
Q

Based on gram-staining, how are bacteria classified?

A

Gram-positive

Gram-negative

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24
Q

Why do Gram-positive bacteria show purple stain on the staining process?

A

Thick peptidoglycan cell wall

Retain large crystal violet - iodine complex

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25
Q

Why do Gram-negative bacteria not show purple stain on the staining process?

A

Peptidoglycan cell wall is not as thick and densec -> cannot retain large crystal violet - iodine complex

Outermembrane prevents crystal to reach the cell wall

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26
Q

Explain the impact of acetone + safranin treatment on Gram-positive and Gram-negative bacteria

A

Gram-positive: remains purple - acetone dehydrate the cell wall structure - still capture complex

Gram-negative: acetone remove the membrane - allow retain safranin counterstain -> appear red

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27
Q

Name some important Gram-positive bacteria

A

Staphylococcus

Streptococcus

Bacillus

Clostridium

Lactobacillius - include enterococcus

Mycobacterium

Streptomyces

Listeria

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28
Q

Name some important Gram-negative bacteria.

A

Neisseria

Brucella

Pseudomonas

Legionella

E.coli

Salmonella

Shigella

Enterobacter

Campylobacter

Haemophillus

Chlamydia

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29
Q

What is the class of bacteria that cannot be classified by Gram-staining?

A

Mycobacteria

show weak positive or no stain at all

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30
Q

Why do mycobacteria cannot be classified by gram stain?

A

Thick cell wall

Composed of lipid and less peptidoglycan

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31
Q

Why is it harder to treat Mycobacterium?

A

Structure of cell wall

Mycolic acid layer + arabinogalactan located on top of peptidolygcan

-> effective and complex barriers

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32
Q

What is used to stain Mycobacterium? What is the result?

A

Carbol + heat then alcohol

Add methyl blue

Result: Appear as red

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33
Q

Distinguish pathogenicty and virulence

A

Pathogenicity = ability to cause disease - can only be yes or no

Virulence = relative power to cause disease - can be high or low

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34
Q

Definition of pathogen by Koch’s Postulates.

<Hint: 4 points>

A

Suspected pathogens - present in all cases + absent in healthy

Suspected pathogens - obtained and able to grow in pure culture -> can cause disease in healthy

Suspected pathogens - can be reisolated - same as the original

Antibodies against organisms - must appear

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35
Q

Explain the limitations for the Koch’s prostulates.

A

Not all bacteria can be cultured

Ethics prohibit transmission between people -> not exact mechanism

Can be caused by more than 1 microorganisms

Immunosuppression - less antibodies

Genetic disposition not considered

Infection arising from host own flora

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36
Q

Characteristic of successful pathogen.

<Hint: 6 characteristics>

A

Survive and transmit

Find entry

Attach to surface firmly

Overcome host’s defence

Ability to damage the host

Ability to replicate on the host, exit and able to infect others

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37
Q

What bacteria can produce spores?

A

Bacillus

Clostridium species

38
Q

What is the importance of spores besides reproduction?

A

Protection from harsh environment conditions

Provide resistance to harsh chemicals

39
Q

What is glycocalyx composed of?

A

Capsules and slime layers

Repeating units of carbohydrates and/or amino acids -> protection and attachment

40
Q

Distinguish the structure of capsules and slimes.

A

Capsules = distinct and gelatinous layer -> allow protection against phagocytes + attachment

Slime layer: diffused layer -> allow attachment to surface

41
Q

How are bacteria exist in the body?

A

Planktonic - floating freely

Biofilms - communities attached to solid surface

42
Q

Definition of fimbriae

A

Small fibres

Mostly protein

Protrude from cell surface

Allow adhesion to surfaces

43
Q

Definition and roles of pili

A

Elongated structure

Pilin protein

Roles:
- Allow attachment to host cells
- Passing antibiotic resistance
- Movement across the surface (some)

44
Q

How can bacteria cause damage to the host?

A

Direct damage through toxins, enzymes,..

Indirect damage - through host immune response

45
Q

Mechanism of action of coagulase

A

trigger coagulation of fibrinogen -> form clots

barriers between organism and inflammatory reactions

46
Q

Mechanism of action of streptokinase.

A

Digest fibrin to release bacteria

47
Q

Mechanism of action of hyaluronidase.

A

attack intracellular cement of connective tissues

48
Q

Mechanism of action of collagenase

A

Digest connective tissue -> promote invasion

49
Q

Mechanism of action of haemolysins

A

Lysis of RBCs

50
Q

Describe the two mechanisms through which the toxins can disrupt membrane.

A

Enzymatic lysis - released toxin to hydrolyse a component of cell membrane

Pore formation - released toxin that can induce the formation of pores -> leakage of content

51
Q

What condition is normally associated with exotoxins that induce enzymatic lysis of cellular membrane?

A

gas gangrene

alpha toxin (phospholipase C) from Clostridium perfringens -> hydrolyse phosphorylchlorine

52
Q

What condition is normally associated with exotoxins that induce pore formation of cellular membrane?

A

Tissue necrosis

Infections caused by Staphylococcus aureus

53
Q

What are A-B type toxins? How do they work?

A

Refer to toxin with 2 parts: A (actual toxin) and B (binding parts)

B components attached to host cell membrane -> enter through receptor-mediated endocytosis

Enclosed during pinocytosis

A-B separate -> A alters cell function + B released

54
Q

Examples of conditions affected by A-B toxins

A

Tetanus - A-B toxins block released of inhibitory transmitters -> spastic paralysis

Flaccid paralysis - A-B toxins blocks the release of Acetylcholine -> blockage of stimulation

55
Q

Explain how endotoxins can induce fever?

A

Macrophage ingests Gram-negative bacteria

Degradation -> release endotoxins

Endotoxins induce production of cytokines - IL-1 and TNF-alpha

Cytokines reach the hypothalamus

Induce production of PGs -> resets the thermostat to high temp -> fever

56
Q

What class of bacteria is normally associated with exotoxins and endotoxins?

A

Exotoxins - Mostly gram positive

Endotoxins - mostly gram negative

57
Q

Compare endotoxins and exotoxins: Chemical structure.

A

Exotoxins: Proteins with normally 2 parts (A and B)

Endotoxins: Lipopolysaccharides

58
Q

Compare endotoxins and exotoxins: Toxicity and lethal dose

A

Exotoxins: high toxicity -> low lethal dose

Endotoxins: low toxicity -> high lethal dose

59
Q

Compare endotoxins and exotoxins: Effects on the body.

A

Exotoxins: Specific for particular cells

Endotoxins: Fever, aches, weakness and shocks. All endotoxins produce the same effects

60
Q

Resources for antimicrobial drugs

A

Natural products from plant, insects, fungi and bacteria (majority of lead compounds)

Chemical synthesis

In silico synthesis

61
Q

Possible targets of antimicrobial drugs

<Hint: 7 targets>

A

Block the synthesis and repair of cell walls

Cause loss of permeability of cell membrane

Inhibit DNA replication or transcription

Inhibit RNA polymerase

Inhit gyrase - unwinding enzyme

Acting on ribosomes -> block initiation of protein synthesis

Block folic acid synthesis -> inhibit metabolism process

62
Q

Issues with new antibiotics development.

A

Low success rate

Long development time

Short-time conditions -> bad for business

Misuse and overuse

Resistance development shorter

Overlapping target -> resistant to one -> resistant to all

63
Q

Which factors promote rapid emergence of resistance?

A

Rapid bacterial multiplication

Capacity to exchange genetic info vertically and horizontally

Large gene pool of antibiotic resistance gene

Selective pressure provided by antibiotic use.

64
Q

Explain how widespread use of antimicrobial agents to develop resistance.

A

Vast use of Abx in hospital, community

Abx might present in herbal

Use of household products

Internet -> allow purchase without necessary and suitable

Agriculture

65
Q

Briefly explain the 4 main resistance mechanism that bacteria can develop against antibiotics.

A
  1. Decrease uptake
  2. Alteration of target
  3. Drug-modifying enzymes
  4. Efflux pump
66
Q

How can previously susceptible bacteria become resistant?

A
  1. Self-modification of genome through mutations (deletions, insertions,..)
  2. Acquisition of antibiotic resistant conferring genes
67
Q

Through which sources do bacteria acquire resistant genes?

A

Plasmids (can contain many resistance genes)

Free DNA

Conjunctive transposon

Bacteriophages

68
Q

Definition of prevalence

A

Total number of cases within a population at a given time point

Per 100,000

69
Q

Definition of Incidence

A

Number of new cases for a particular infections in a specific time period for a given population

70
Q

Definition of morbidity rate

A

Number of cases of an illness in a particular time period divided by the population at risk

71
Q

Definition of mortality rate

A

Annual number of deaths from the disease

Per 100,000 people

72
Q

Definition of endemic diseases

A

Constantly present within a given population

73
Q

Definition of epidemic diseases

A

Unusual large number of cases in population

Arise from new infectious diseases normally

74
Q

Definition of outbreak

A

Cluster of new cases occuring within a short period of time affecting particular population

Can lead to epidemic

75
Q

Definition of pandemic diseases

A

Spread to worldwide

76
Q

Definition of attack rate. What does it depend on?

A

Number of cases arising in a defined group

Depend on:
+ Infective dose
+ Immunity of population

77
Q

What factors does infective dose depend on?

A

Virulence of organism

Host factors (age, genetics, underlying diseases, immunosuppresion, surgery, transplant, other infections, physical and mental stress)

78
Q

For an infectious disease, what are the stages that a patient would go through?

A

Incubation: No symptoms, number of infectious organisms low

Prodromal period: Symptoms vague and general, increase in number of infectious organisms

Illness: Symptoms severe, number of infectious organisms peaks

Decline: Symptoms less intense, number of infectious organisms decline

Convalescence: No more symptoms

79
Q

What factors contribute to the probability of transmission?

A

Number of susceptible individuals present

Vaccinations and herd immunity

Contact between individuals

80
Q

Definition of reproductive rate in transmission.

A

Average number of secondary cases produced from 1 primary cases in optimum conditions - all members are equally susceptible

81
Q

Definition of effective rate in transmission

A

Average number of secondary cases produced from 1 primary cases in conditions considering differences in susceptibilites and previous exposure constraints

82
Q

The aim of effective rate

A

Effective rate < 1 so that infection is not sustained within the population

83
Q

Definition of hospital-associated infecitons (HAI)

A

caused by an infective agent

appears about 3 days or more after admission

appears within 3 days of discharge from the hospital

84
Q

Risk factors of HAP.

A

Direct factors - environment, dust, contaminated water supply, contact with HCPs, with other patients

Indirect factors - through contaminated objects

Unwell conditions

Extreme of age with poor immune defence

Exposure, not vaccinated

Primary or secondary infections

Defective organs

Prolonged admission

Antibiotic use

Surgical or medical procedures

85
Q

What are the common HAIs?

A

Urinary tract infections - related to catheterisation

Surgical site infections

Lower respiratory infections

Bacteraemia

86
Q

What are the organisms significantly associated with HAIs?

A

Staphylococcus aureus - blood poisoning, wound infections and pneumonia

Acinetobacter - blood poisoning in immunocompromised

Enterococcus faecalis - blood poisoning, UTIs, wound infections

E.coli - UTI, blood poisoning, diarrhoea and kidney failure

P.aeruginosa - blood poisoning, pneumonia in CF and immunocompromised

Viruses: hepatitis A, B, C, Zoster, measles

Fungi: Aspergillus species

87
Q

Explain how isolation can be used for manage HAIs.

A

Isolation of patients in room under negative pressure

Isolation of susceptible patient in room under positive pressure

88
Q

Clostridium difficile as HAIs.

A

anaerobic, Gram-positive, spore-forming rod

Found in large intestine and as spores in hospital

70% of GI hosptial-associated infection are caused by C.difficile

89
Q

How does Clostridium difficile arise?

A

From antimicrobial use.

Use of cephalosporins, ampicillin and clindamycin -> suppress normal flora

Spores of C.difficile germinate + grow + divide quickly

Produce toxin A (enterotoxin) -> fluid production and mucosal damage

Produce toxin B (cytotoxin) -> mucosal damage

90
Q

Clinical features of GI-infection caused by C.difficle.

A

Pseudomembranous colitis, characterised by:
Profuse diarrhoea + Dehydration

Superficial loss of epithelial cells - eruptions of pus on the surface

91
Q

Treatment of GI-infection caused by C.difficile (HAIs)

A

Removal of causative agent

PO vancomycin OR metronidazole

Probiotics -> restore normal GI flora.

Good hospital hygiene for prevention

92
Q

Explain why oral vancomycin is used to manage GI-infection caused by Clostridium difficile.

A

Vancomycin is poorly absorbed

High GI concentration can be achieved.

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