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MCD Microbiology > Community and Hospital Acquired Bacterial Infection > Flashcards

Community and Hospital Acquired Bacterial Infection Flashcards

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1
Q

what are the examples of virulence factors?

A
  • flagella (movement and attachment)
  • pili (adherence)
  • capsule (protect against phagocytosis)
  • endospores (metabolically dormant forms of bacteria.)
  • biofilms (aggregates of bacteria embedded in polysaccharide-matrix resistant)
  • secretion systems
  • exotoxins
  • endotoxins
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2
Q

examples of bacteria using capsule

A

Streptococcus pneumoniae.

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3
Q

examples of bacteria using endospores

A

Bacillus sp. And Clostridium sp.

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4
Q

examples of bacteria using biofilms

A

Pseudomonas aeruginosa and Staphylococcus epidermidis

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5
Q

what are the exotoxins?

A
  • neurotoxins (act on nerves or motor-end-plates)
  • enterotoxins (act on GIT)
  • pyrogenic exotoxins (stimulate release of cytokines)
  • tissue invasive exotoxins (enzymes that allow bacteria to tunnel through tissue)
  • miscellaneous exotoxins (specific to certain bacteria, function not well understood)
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6
Q

examples of neurotoxins

A

Tetanus

Botulinum toxins.

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7
Q

what are the two effects of enterotoxins? what bacteria cause them?

A

 Infectious diarrhoea
– Vibrio cholera, E. coli, Shigella dysenteriae, Campylobacter jejuni.

 Food poisoning
– Bacillus cereus, Staph. aureus.

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8
Q

examples of bacteria that release pyrogenic exotoxins

A

Staph. aureus

Strep. pyogenes.

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9
Q

examples of bacteria that release tissue invasive exotoxins

A

Staph. aureus,
Strep. pyogenes
Clostridium perfringens.

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10
Q

examples of bacteria that use specific exotoxins

A

Bacillus anthracis

Corynebacterium diphtheriae.

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11
Q

where are endotoxins found?

A

only GRAM NEG

Lipid A domain of LPS , only from gram -ve bacteria, shed constantly by living bacteria

it is not a protein, but a lipid

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12
Q

what effect does treating someone with a gram -ve infection with Abx have?

A

make them worse:

Bacteria lyses –> release large quantities of LPS/endotoxins –> septic shock.

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13
Q

what is an outbreak?

A

a sudden increase in the incidence of a disease in a particular place at a particular time.

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14
Q

what is the triad of Haemolytic-uraemic syndrome? what caused this?

A
  • triad of acute renal failure, haemolytic anaemia and thrombocytopenia
  • caused by entero-aggregative E. coli (EAEC) using the Shiga-Toxin that is acquired from another strain EHEC
  • Reservoir is usually in cattle.
  • result of the fusion of Enterohaemorrhagic E. coli and Enteroaggregative E. coli.
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15
Q

what is a possible epidemic case?

A

Any person that has developed the symptoms AND has met a laboratory criteria (e.g. isolation of agent).

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16
Q

what is a probable epidemic case?

A

Any person that has met the case criteria AND has been in epidemic country, consumed possibly contaminated food, been in close contact with a confirmed epidemic case.

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17
Q

what is a confirmed epidemic case?

A

Any person meeting criteria for a possible case AND has had strain isolated.

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18
Q

how can isolates in an outbreak be screened?

A

by multiplex PCR, can be done on stool samples, determine if the strain is the outbreak strain or not

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19
Q

what does PCR reveal about the strains EHEC and EAEC?

A
  • EHEC : prophage encoding the Shiga toxin
  • EAEC:
    1) pAA-type plasmids - contain aggregative adhesion fimbrial operon.
    2) ESBL plasmids – gene encoding for extended-spectrum beta-lactamases.
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20
Q

what are the components of the Shiga Toxin?

A

o StxA is the enzymatic portion
– cleaves RNA so inhibits protein synthesis and might affect gut commensal bacteria
o StxB is the pentamer that binds to host cell receptors.

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21
Q

what encode the Shiga toxins? enables horizontal transfer

A

bacteriophages and contribute to horizontal gene transfer meaning they can be given to other bacteria types in phages.

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22
Q

what is the virulence factor of EAEC? what effect does this factor have?

A

Aggregative Adherence Fimbriae (AAF):
o AFF required for adhesion to enterocytes and stimulates IL-8 response.
o AFF also allows a biofilm formation.

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23
Q

how is an outbreak effectively identified?

A

o Surveillance.
o Good and timely reporting systems.
o PCR.

24
Q

examples of respiratory tract infections and the bacteria that cause them

A

1) Legionnaire’s disease – Legionella pneumophilia (gram-ve)
- inhalation of aerosols

2) Tuberculosis – Mycobacterium tuberculosis
- 77% success of first treatment and 54% success of second treatment
- cell wall and slow growth makes it resistant to antimicrobials

25
Q

what is the virulence factor of Legionella pneumophilia?

A

type IV secretion systems – legionella replicates in legionella containing vacuoles (LCVs) inside cells.

26
Q

what is the virulence factor of Mycobacterium tuberculosis?

A

has an extra lipid layer & can enter a dormant state for reactivation.

27
Q

examples of STIs

A

1) Chlamydia
– Chlamydia trachomatis (gram-ve obligate intracellular parasite)
- causes blindness outside of Europe
- not cultured outside host cell

2) Gonorrhoea
– Neisseria gonorrhoeae (gram-ve)
- Urogenital tract infection infecting non-ciliated epithelial cells.

28
Q

what are the virulence factors of Chlamydia trachomatis and Neisseria gonorrhoeae?

A

pili, antigenic variation mechanisms

29
Q

examples of food and waterborne diseases?

A 
1) Campylobacteriosis 
– Campylobacter sp. (mostly C. jejuni
- GI disease, high risk in kids 
- uncooked poultry 
- sporadic cases, no outbreaks
2) Salmonellosis 
– Salmonella sp. (gram-ve)
- GI disease 
- uncooked poultry 
- can cause outbreaks

3) Cholera
– Vibrio cholera (gram-ve)
- acure severe diarrhoea

4) Listeriosis
– Listeria monocytogenes (gram+ve)
- the elderly, immunocompromised, and pregnant at risk
- capable of crossing tight barrier like the materno-foetal barrier

30
Q

what are the virulence factors of Campylobacter sp.?

A

T4 secretion systems,

adhesion, invasion factors, flagella motility, toxins

31
Q

what is the virulence factor in Salmonella sp?

A

T3 secretion systems encoded on pathogenicity islands

32
Q

what is the virulence factor in vibrio cholera?

A

T4 fimbria, cholera toxin (increased cAMP –> opening of Cl- channels and expulsion of water from cells), carried on phages.

33
Q

what is the virulence factor of listeria monocytogenes?

A

actin-based cell motility

ActA and VASP

34
Q

examples of emerging and vector borne disease

A

1) Plague
– Yersina pestis (gram-ve).

2) Q fever
– Coxiella burnetti (gram-ve).

3) Smallpox (A VIRUS) – eradicated.

35
Q

examples of vaccine preventable disease and the bacteria that cause them?

A

1) Diphtheria
– Clostridium diphtheriae (gram+ve).

2) Invasive HA disease
– Haemophilus influenzae (gram-ve).

3) Invasive meningococcal disease
– Neisseria meningitides (gram-ve).

4) Invasive pneumococcal disease
– Streptococcus pneumoniae (gram+ve)

5) Pertussis
– Bordetella pertussis (gram-ve).

6) Tetanus
– Clostridium tetani (gram+ve).

36
Q

what are antimicrobials?

A

interferes with growth & reproduction of a ‘microbe’.

37
Q

what are antibacterials?

A

describes agents that reduce or eliminate harmful bacteria

antibiotics are a type of antimicrobial

38
Q

what are the most frequent HAIs?

A

surgical site infections, UTIs, pneumonia, bacteraemias, GI infections

39
Q

what is the burden of HAIs?

A
  • 3.2m a year get an HAI, 37,000 of those die of them.
  • increases the length of stay
  • HAIs cost an ~£1b extra a year.
40
Q

what are the 3 categories of causes of HAIs?

A
  • interventions
  • dissemination
  • concentration
41
Q

what interventions cause HAIs?

A
  • catheters
  • intubation
  • chemotherapy
  • prosthetics
  • lines
  • prophylactic antibiotics
  • inappropriate prescribing.
42
Q

how is dissemination a cause of HAIs?

A

carriers of the infection from person to person e.g. from staff

43
Q

how is concentration a cause of HAIs?

A

a high number of sick people in one place

44
Q

how is a HAI defined?

A

an infection acquired in a hospital setting after 48 hours from admission

45
Q

what are the “ESC(/K)APE” pathogens that cause HAIs?

A 
o Enterococcus faecium (+ve)	- Vancomycin resistant.
o Staph. aureus (+ve)
- MRSA.
o Klebsiella pneumoniae [K]
o Acinetobacter baumanii (-ve)	- Highly drug resistant.
o Pseudomonas aeruginosa (-ve)	
- MDR
o Enterobacteriaceae (-ve) 
- MDR – all the sub-types.
- Pa
thogenic e coli
- Enterobacter species
[ Clostridium difficile(+ve)
- Can infect due to previous AB treatment]
46
Q

what is pathogenic E.coli resistant to? how?

A

resistant to cephalosporins:
due to the presence of the ESBL (Extended Spectrum Beta Lactamase)
gene that produces the lactamase cleaves the cephalosporin to inactivate it

47
Q

what are cephalosporins? what is their mechanism of action?

A 
class of beta-lactams:
 that inhibit peptidoglycan synthesis by inhibiting the activity of penicillin binding protein (PBPs)
48
Q

what other antibiotic apart from cephalosporins target PBPs and therefore pathogenic e.coli?

A

carbapenems (beta lactam)
- this differs in structure and is cleaved by a different enzyme: carbapenemase (not ESBL)

pathogenic E.coli is still sensitive to carbapenems

however K.pneumonia is resistant to carbapenems

49
Q

what bacteria is the most common cause of community and HAI UTIs? what can it also cause?

A

pathogenic e.coli

also the most frequent cause of bacteraemia by g-ve bacteria

50
Q

which bacteria is resistant to carbapenems?

A

Klebsiella pneumoniae

CRKP – Carbapenem-Resistant Klebsiella pneumoniae

51
Q

what does Klebsiella pneumoniae cause and who are at risk?

A
  • UTIs and respiratory tract infections.

- immunocompromised.

52
Q

what is staphylococcus aureus resistant to? how is this resistance mediated?

A

methicillin
- MRSA expresses a different PBP (PBP2A) gene so bypasses inhibition of peptidoglycan synthesis and therefore survives as the beta lactam methicillin can’t bind

summary: PBP2A has a low affinity to methicillin so Staph aureus can still function

53
Q

who is at risk of Pseudomonas aeruginosa?

A

immunocompromised

- resistant to several antimicrobials

54
Q

which bacteria is resistant to vancomycin? how is this mediated?

A

enterococcus faecium
- VRE synthesises a different peptidoglycan precursor that is not targeted by the vancomycin.

vancoymin is a glycopeptide that will bind to the pentapeptide used in peptidoglycan synthesis

55
Q

what effect does drug resistance having on treatment options?

A

Clinicians are forced to use older, previously discarded drugs (e.g. colistin) that are associated with higher toxicities and for which there is less data on guides in dosage and duration of therapy.

56
Q

gram negative antibiotic resistance infections in the UK

A
  • pseudominas aeriginosa
    e. g. UTI, HA pneumonia
  • ESBL
    e. g. ecoli
  • Acinetobacter baumanii
57
Q

gram positive antibiotic resistant infections in the uK

A
  • MRSA

- enterococcus faecium

MCD Microbiology (6 decks)

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