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Microbiology Y2 > Community and Hospital Acquired Bacterial Infections > Flashcards

Community and Hospital Acquired Bacterial Infections Flashcards

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Biology 101 flashcards
1
Q

COMMON BACTERIAL VIRULENCE FACTORS (8)

A

Flagella (movement, attachment)
Pili (important adherence factors)
Capsule (protect against phagocytosis) i.e. Streptococcus pneumoniae
Endospores (metabolically dormant forms of bacteria) heat, cold, desiccation and chemically resistant i.e. Bacillus sp. and Clostridium sp.
Biofilms (organized aggregates of bacteria embedded in polysaccharide matrix – antibiotic resistant) i.e. Pseudomonas aeruginosa and Staphylococcus epidermidis
Exotoxins Neurotoxins, enterotoxins, pyrogenic toxins, tissue invasive exotoxins, misc exotoxins
Endotoxins

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2
Q

What endospores

A

(metabolically dormant forms of bacteria)

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3
Q

Example of bacteria that uses this as a virulence factor: capsule

A

Streptococcus pneumoniae

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4
Q

Example of bacteria that uses this as a virulence factor: endospores

A

Bacillus sp. and Clostridium sp.

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5
Q

Example of bacteria that uses this as a virulence factor: biofilms

A

Pseudomonas aeruginosa and Staphylococcus epidermidis

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6
Q

Example of bacteria that uses this as a virulence factor: neurotoxins

A

tetanus

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7
Q

Example of bacteria that uses this as a virulence factor: enterotoxins

A

staph aureus and E. coli

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8
Q

Example of bacteria that uses this as a virulence factor: pyrogenic exotoxins

A

staph aureus),

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9
Q

Example of bacteria that uses this as a virulence factor: tissue invasive exotoxin

A

staph aureus)

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10
Q

What type of bacteria produce endotoxins

A

Gram -ve

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11
Q

What are endotoxins functionally and where are they found

A
  • Not a protein but the lipid A moiety of LPS (on the outer lipid bilayer)
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12
Q

Why can treating gram -ve bacterial infection worsen the condition

A

when bacteria lyse they release large quantities of LPS/ Endotoxin and this can lead to Septic shock

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13
Q

WHAT CONSTITUTES AN OUTBREAK?

A

A greater-than-normal or greater-than-expected number of individuals infected or diagnosed with a particular infection in a given period of time, or a particular place, or both

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14
Q

HOW CAN AN OUTBREAK BE IDENTIFIED?

A

Surveillance systems provide an opportunity to identify outbreaks. Good and timely reporting systems are instrumental to identify them

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15
Q

What can you use to identify the strain in an outbreak?

A

PCR

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16
Q

What is haemolytic uremic syndrome characterised by? (3)

A

A triad of acute renal failure, haemolytic anaemia and thrombocytopenia

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17
Q

What causes haemolytic uremic syndrome

A

shiga toxin producing E coli

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18
Q

What toxin causes haemolytic uremic syndrome

A

shiga toxin producing E coli

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19
Q

What effect does Shiga toxin have to produce haemolytic uremic syndrome

A

Inhibits protein synthesis and affects the commensal gut flora

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20
Q

What is the virulence factor for EHEC?

A

Shiga toxin

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21
Q

What is the virulence factor for EAEC?

A

Aggregative adherence fimbriae

22
Q

What does AAF do (3)

A

Allows strong adhesion to enterocytes, stimulates strong IL-8 response, allows biofilm formation

23
Q

8 communicable diseases in Europe?

A
  1. Respiratory tract infections
  2. Sexually transmitted infections, including HIV and blood-borne viruses
  3. Food- and waterborne diseases and zoonoses
  4. Emerging and vector-borne diseases
  5. Vaccine-preventable diseases
  6. Antimicrobial resistance and healthcare-associated infections
24
Q 
LEGIONELLA PNEUMOPHILA:
Gram +ve/-ve?
Found where?
Enters body how?
Where does it grow in the body?
What does it cause?
Important virulence factor?
A
  • Gram-negative - Lives in amoeba in ponds, lakes, air conditioning units, whirlpools etc.
  • Infection route = inhalation of contaminated aerosols
  • In humans L. pneumophila will infect and grow in alveolar macrophages
    Légionnaires’ disease (legionellosis) Legionella pneumophila (Gram -)
  • Important virulence factor type IV secretion system Allows bacteria to replicate in vacuoles due to secretion of virulence factors, in a LCV (legionella containing vacuole)
25
Q 
MYCOBACTERIUM TUBERCULOSIS:
Gram +ve/-ve?
Whats different about this bacterium?
Found where?
Important virulence factor?
Time for treatment to take effect?
A
  • Gram-positive but with a very different cell wall – extra lipid layer which makes treatment more difficult
  • Difficult to treat because it has this waxy layer on the outside and it reproduces slowly which means that antibiotics have a harder time killing it.
  • Treatment of infections = antibiotics takes at least 6 months
26
Q

CHLAMYDIA TRACHOMATIS:
Why is it difficult to get a cure for chalmydia?
What does it cause?

A

Obligate intracellular pathogen – cannot culture it outside host cell
Blindness eventually

27
Q 
NEISSERIA GONORRHOEAE:
Gram +ve/-ve?
Enters body how?
Where does it grow in the body?
What does it cause?
Important virulence factor?
A
  • Gram- negative diplococcus
    STI
  • Establishes infection in the urogenital tract by interacting with non-ciliated epithelial cells
  • Important virulence factors and traits:
    pili and antigenic variation  escape detection and clearance by the immune system
28
Q 
CAMPYLOBACTER SPECIES (MOSTLY C. JEJUNI):
Enters body how?
Who does it mainly affect?
What does it cause?
Important virulence factor? (5)
A
  • Infection most likely through undercooked poultry
  • Small children 0-4 years – highest risk group
  • Virulence factors Adhesion and Invasion factors, flagella motility, type IV Secretion system, toxin
29
Q 
SALMONELLA:
Gram +ve/-ve?
Found where?
Enters body how?
Important virulence factor?
A

Gram +ve
- Undercooked poultry, enters when ate

Type III secretion systems (injection of proteins into human cells via needle like structure) encoded on pathogenicity islands (SPI):
Salmonella enterica

30
Q

VIBRIO CHOLERAE:
Gram +ve/-ve?
What does it cause?
Important virulence factor?

A

Gram -ve

  • Cholera is an acute, severe diarrheal disease
  • Without prompt rehydration, death can occur within hours of the onset of symptoms

Type IV fimbria cholera toxin carried on a phages
- Cholera toxin activates cyclase enzyme in cells which makes a small nucleotide molecule which activates a transporter that pumps Cl ions out of the cell, Na and water also then go out of the cell to compensate – diarrhoea.

31
Q 
LISTERIA MONOCYTOGENES:
Gram +ve/-ve?
Risk group?
Whats special about listeria?
What does it cause?
Important virulence factor?
A

Gram +ve
immuno-compromised, elderly, pregnant and their fetus
- Listeria can enter non-phagocytic cells and cross three tight barriers
Intestinal barrier, Blood-brain barrier and Materno-fetal barrier
- It can spread from cell to cell without ever leaving the cell, hijacks actin to transport itself

32
Q

5 most frequent HAIs?

A

surgical site infections, urinary tract infections, pneumonia, bloodstream infections and gastrointestinal infections

33
Q

3 factors that contribute to the acquisition of HAIs>

A

INTERVENTION (what is done to treat someone)
DISSEMINATION (Hospital personnel travel from one patient to another, possibly transferring pathogens from patient to patient) CONCENTRATION (Patients are very close to one another and by definition, they’re unwell)

34
Q

6 common HAIs?

A 
Enterococcus faecium 
Staphylococcus aureus 		
Clostridium difficle
Acinetobacter baumanii 
Pseudomonas aeruginosa 		
Enterobacteriaceae (E.coli, Klebsiella pneumoniae, Enterobacter sp.)
35
Q

Enterococcus faecium : Gram +ve or -ve?

A

+ve

36
Q

Staphylococcus aureus : Gram +ve or -ve?

A

+ve

37
Q

Clostridium difficile: Gram +ve or -ve?

A

+ve

38
Q

Pseudomonas aeruginosa : Gram +ve or -ve?

A

-ve

39
Q

Enterobacteriaceae (E.coli, Klebsiella pneumoniae, Enterobacter sp.): Gram +ve or -ve?

A

-ve

40
Q

Acinetobacter baumanii: Gram +ve or -ve?

A

-ve

41
Q

What is Acinetobacter baumanii resistant to?

A

High drug resistant

42
Q

What is Enterococcus faecium resistant to?

A

Vancomycin

43
Q

What is Clostridium difficile resistant to?

A

Can establish infection due to previous AB treatment

44
Q

What is Staphylococcus aureus resistant to?

A

Methicillin

45
Q

What is Pseudomonas aeruginosa resistant to?

A

Multidrug resistant (fluoroquinolone e.g.)

46
Q

What is Enterobacteriaceae resistant to?

A

Multi drug resistant

47
Q
  • Most frequent cause of community and hospital acquired UTI is?
A

E.coli

48
Q

What are E.coli resistant to

A

cephalosporsins via extended spectrum beta lactamase

49
Q

What are cephalosporins?
Target pathway?
Target protein?
Resistance?

A
  • Are a class of beta-lactam antibiotics
  • Target pathway inhibit peptidoglycan synthesis
  • Target protein inhibit the activity of penicillin binding proteins (PBPs)
  • Resistance to cephalosporins Extended spectrum beta-lactamase (ESBL) encoded on a plasmid – Mobile ESBL enzyme cleaves cephalosporin
50
Q

What are carbapenems?
Target pathway?
Target protein?
Resistance?

A
  • Are a class of beta-lactam antibiotics
  • Target pathway inhibit peptidoglycan synthesis
  • Target protein inhibit the activity of penicillin binding proteins (PBPs)
  • Resistance to carbapenems carbapenemase enzyme, blakpc, encoded on a transposon (mobile genetic element) – enzyme cleaves carbapenem
51
Q

What is methicillin?
Target pathway?
Target protein?
Resistance?

A
  • Is a beta-lactam antibiotic
  • Target pathway inhibit peptidoglycan synthesis
  • Target protein inhibit the activity of penicillin binding proteins (PBPs)
  • Resistance to methicillin Expression of additional PBP – PBP2A has low affinity for methicillin and can still function in the presence of the antibiotic – MRSA strains can synthesize peptidoglycan and survive in the presence of methicillin
52
Q

What is vancomycin?
Target pathway?
Target protein?
Resistance?

A
  • Target pathway inhibit PG synthesis
  • Target binds to PG precursor
  • Resistance to vancomycin multiple proteins / genes encoded on plasmid or transposon – Results in the synthesis of a different PG precursor meaning the vancomycin can’t bind to it properly

Microbiology Y2 (6 decks)

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