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microbiology year 2 > community and hospital acquired bacterial infections > Flashcards

community and hospital acquired bacterial infections Flashcards

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Biology 101 flashcards
1
Q

components of a bacterial cell

A

prokaryotic

cell wall

DNA in cytoplasm

ribosomes

surface molecules

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2
Q

list common virulence factors *

A

diverse secretion systems - to put proteins/factors into host cells

flagella - movement/attachmennt - allow them to find he niche to attach

pili - important adherence factors on surface

capsule - protect against phagocytosis - streptococcus pneumoniae

form endospores - metabolically dormant forms of bacteria - heat, cold, desiccation and chemically resistant - bacillus and clostridium

form biofilms - organised aggregates of bacteria embedded in polysaccharide matrix mean they are AB resistant ie pseudomonas aeruginosa amd staphyloccous epidermidis (staph is commensal on skin but if enter body can cause problem)

production of exotoxins

production of endotoxins

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3
Q

what are the different types of exotoxins *

A

neurotoxins - act on nerves/motor end plate - tetanus or botulinum toxins

enterotoxins - act on GIT

  • infections diarrhoa - when live organism is causing infection - vibro cholera, E coli, shigella dysenteriae, campylobacter jejuni
  • food poisening - dont need the live organism, just the exotoxin - bacillus cereus or staphy aureus

pyrogenic exotoxins - stimulate the release of cytokines = cytokine storm - staphylococcus aureus, streptococcus pyogenes

tissue invasive exotoxin - allow bacteria to destroy and tunnel through tissue - enzymes that destroy DNA, collagin, fibrin, NAD, red/white blood cells - staphyloccus aures, streptococcus pyogenes, clostridium perfringens

miscellaneous exotoxin - specific to a certain bacterium and/or func - not well understood - bacillus anthraciss and corynebacterium diphtheriae

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4
Q

describe endotoxins *

A

only produced by gram -ve bacteria

they are the lipid A moiety of LPS

shed in steady amounts from living bacteria

treating a pt who has a gram -ve infection with AB can worsen someone’s condition because it increases the sheding of LPS - they release large amounts of LPS when they lyse = septic shock

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5
Q

define 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 particular place, or both

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6
Q

how can an outbreak be identified *

A

routine surveillance provides an opportunity to identify them

good and timely reporting systems are instrumental to identify outbreaks

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7
Q

routes of communicable diseases *

A

resp tract infections

sexually transmitted

food and waterbourne and zoonoses

emerging and vector borne

vaccine preventable

angtimicrobial resistance and healthcare associated

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8
Q

examples of resp tract infections *

A

legionnaires’ disease (legionellosis) - legionella pneumophilia (gram -ve)

TB - mycobacterium tuberculosis - gram +ve

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9
Q

describe legionella pneumophilia *

A

gram -ve

lives in amoeba in ponds, lakes, air conditioning units, whirlpools

infection route - inhalation of contaminated aerosols

in humans - grows in aveolar macrophages

human infection is dead end for bacteria

important virulence factor is the type 4 secretion system

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10
Q

describe the type 4 secretion system *

A

allow bacteria to inject toxin protein from inside cytoplasm to the vacule in macorphages

allow bacteria to replicate in a bacteria containing vacule (LCV)

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11
Q

describe mycobacterium TB *

A

gram +ve

extra lipid layer in cell wall - makes treatment very difficult - hard for antimicrobials to get in

also grow slow - make treatment difficult

can enter a dormant state - latent TB - evidence of infection by immunological tests but no clinical signs and symptoms of active disease

treatment is with AB but takes 6 moths

72% success of treatment with new cases

54% success for second infection - becomes resistant

multi-drug resistant treatment success rate is 32%

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12
Q

list sexually transmitted bacteria *

A

chlamydia trachomatis infection

gonorrhoea - neisseria gonorrhoeae

symphilis - treponema pallidum

(all are gram -ve)

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13
Q

chlamydia trachomatis *

A

obligate intracellular pathogen

most frequent STI in europe

infection likely higher incidence than reported because of underreporting

in other parts of world can cause eye infection - responsible for >3% of world’s blindness

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14
Q

neisseria gonorrhoeae *

A

gram -ve

infect UGT by interacting with non-ciliated epithelial cells

pili allow adhesion to epithelium

antigenic variation mean they escape detection and clearance from the immune system

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15
Q

list food and waterbourne diseases *

A

campylobacter species - mostly c jejuni

salmonella species

vibro cholerae

listeria monocytogenes

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16
Q

campylobacter *

A

live organism is needed to cause disease

usually sporadic cases and not outbreaks

most commonly reported GI infection in EU

highest risk group is small children 0-4

through undercooked poultry

virulence factos

  • adhesion and invasion factors
  • flagella motility
  • type 4 secretion system
  • toxins
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17
Q

describe salmonella species *

A

one of most common GI infections in EU

undercooked poultry

outbreaks

highest infection rate 0-4yrs

virulence

  • type 3 secretion systems are encoded on pathogenicity islands - SPI
    • SPI1 is needed for invasion
    • SPI2 needed for intracellular accumulation
    • there are 2 membranes and a needle used to inject toxins into eukaryotic cells
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18
Q

describe vibro cholerae *

A

acute, severe diarrhoeal disease - cause death unless there is prompt rehydration

cholera was 1st infected with a phage that made the bacteria produce pili on surface - the pili had the receptor for another phage that then had the toxin on it = toxin producing strain

virulence factors

  • type 4 fimbria
  • cholera toxin
  • carried on phages
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19
Q

describe the cholera toxin *

A

A,B toxin

A subunit is enzymatic, B subunit allows toxin to enter cell

makes the cell produce a small signalling molecule - activates CFTR channel - means Cl- leaves the cell - cause Na and water to leave = diarrhoea

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20
Q

describe listeria monocytogenes *

A

risk group - immunocomp, elderly, pregnant and fetus

can enter non-phagocytic cells and cross barriers - GIT, BBB, materno-fetal

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21
Q

list vector borne bacteria *

A

plague - yersinia pestis - gram -ve

Q fever - coxiella burnetti - gram -ve

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22
Q

list vaccine preventable diseases *

A

diptheria - clostrodium diptheriae - gram +ve

invasive haemophilus influenzae disease - gram -ve

invasive meningococcal disease - neisseria meningitidis - gram -ve

invasive pneumococcal disease - streptococcus pneumonia -gram +ve

pertussis - bordetella pertussis - gram -ve

tetanus - clostridium tetani - gram +ve

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23
Q

effect of vaccines

A

they can reduce the disease level to 0

24
Q

define antimicrobial

A

interferes with growth and reproduction of a microbe

25
Q

define antibacterial

A

commonly used to describe agents to reduce or eliminate harmful bacteria - but effect the microbiota too

26
Q

define antibiotic

A

type of antimicrobial

used as medicine

originally referred to as naturally occuring compounds - now chemically synthesised but want to find more from environment

27
Q

what are hospital acquired infections *

A

healthcare assiciated infections are infections that occur after exposure to healthcare

infection starts >48hrs after admission

most frequent types are surgical site infections, UTI, pneumonia, bloodstream infections and GIT infections

28
Q

importance of HAI *

A

they cause death

increase length of stay

increase financial burden

29
Q

why do HAIs occur *

A

intervention - chemo, prophylactic AB, inappropriate prescribing, prosthetic material, catheterisation, intubation, lines (central, IV, central, arterial, CVP, pulmonary)

dissemination - good hygiene reduces this

concentration of people - so easier to spread

30
Q

what were the main bacteria that caused HAIs *

A

ESKAPE

  • Enterococcus faecium
  • Staphylococcus aureus
  • Klebsiella pneumoniae
  • Acinetobacter baumanii
  • Pseudomonas aeruginosa
  • Enterobacter species
31
Q

what are the bacteria now that cause HAIs mainly *

A

ESCAPE

  • Enterococcus faecium +ve
  • Staphylococcus aureus +ve
  • Clostridium difficile +ve
  • Acinetobacter baumanii -ve
  • Pseudomonas aeruginosa -ve
  • Enterobacteriaceae -ve (E coli, kelbsiella pneumoniae, enterobacter species)
32
Q

what is the problem with the ESKAPE bacteria *

A

they are resistant

  • Enterococcus faecium +ve vancomycin
  • Staphylococcus aureus +ve methicillin - MRSA
  • Clostridium difficile +ve develop infection because AB against previous infection has killed microbiota
  • Acinetobacter baumanii -ve highly resistant
  • Pseudomonas aeruginosa -ve multi-drug resistant (MDR) ie fluroquinolone resistance
  • Enterobacteriaceae -ve (E coli, kelbsiella pneumoniae, enterobacter species) MDR
33
Q

describe E coli *

A

most frequent bacteraemia by gram -ve bacterium

most common cause of UTI

increase in MDR strains

resistance to 3rd generation cephalosporins

most that are resistant to cephalosporins express the extended spectrum beta lactamase (ESBL)

still sensitive to carbapenems

34
Q

describe cephalosporins *

A

B-lactam AB - have B lactam ring

inhibit the activity of penicillin binding proteins (PBPs) by binding to enzyme - this inhibits peptidoglycan synthesis

PBPs are not in eukaryotic tissue so these AB dont effect self

35
Q

describe resistance to cephalosporins *

A

extended spectrum B-lactamase (ESBL) is encoded on a plasmid (means the genes are mobile so can spread between strains)

ESBL cleaves cephalosporin

36
Q

describe carbapenems *

A

B-lactems - same mechanism as cepalosporins

37
Q

describe resistance to carbenems *

A

bacteria produce carbapenemase enzyme blakpc that is encoded on a transposon - mobile genetic element

carbapenemase cleaves carbaenenem so it cant bind to the PBP and bacteria can grow again

38
Q

describe kelbsiella pneumonia *

A

cause UTI and resp tract infections

risk gp - immunocomp

high resistance to 3rd generation cephalosporins, fluroquinolones and aminoglucosides

carbapenem resistant klebsiella is the species most encounted in US

39
Q

describe pseudomonas aeruginosa *

A

important cause of infection in immunocomp

high proportion MDR

40
Q

describe methicillin resistant S. aures *

A

most important cause of antimicrobial resistant bacteria world wide

41
Q

describe methicillin *

A

B lactam

42
Q

describe resistance to methicillin *

A

acquire new gene = expression of additional PBP

PBP2 has low affinity for methicillin - still function and synthesise peptidoglycan in presence of AB

43
Q

describe vancomycin resistant enterococcus faecium *

A

3rd most frequently identified cause of nosocomial blood stream infections (BSI) in US

vacomycin resistance around 60%

44
Q

describe vancomycin *

A

inhibit peptidoglycan synthesis by binding to peptidoglycan precurser (the substrate for the production of peptidoglycan)

45
Q

describe resistance to vancomycin *

A

multiple proteins’ genes encoded on plasmid/tansposon

results in synthesis of different precurser

46
Q

describe the 2011 e coli outbreak in germany

A

Causative agent: Outbreak was caused by an entero-aggregative

Shiga-toxin producing E. coli O104:H4 strain

Illness: gastroenteritis and hemolytic-uremic syndrome (HUS)

Source: The consumption of sprouts was identified as the most likely vehicle of infection

Time frame: 1 May 2011- 4 July 2011

Scale: Total of 3816 Cases (54 death) in Germany

845 (22%) of these were with hemolytic-uremic syndrome

Smaller outbreak in France

Incubation period was around 8 days with a medium of 5 days from the onset of diarrhea to development of the hemolytic-uremic syndrome

47
Q

describe haemolytic syndrome

A

acute renal faailure, haemolytic anaemia, thrombocytopenia

found in children caused by shiga toxin produced by e coli strain O157:H7

from the EHEC strains - enterohaemorrhagic E coli

reservoir normally ruminants - mostly cattle

human infection occurs through inadvertant ingestion of feces and secondary contact with infected people

usually rare in adults

48
Q

time scale of the E coli outbreak

A

May 8th 2011: likely start of outbreak

May 19th 2011: First report to German’s national-level public health authority of three cases of the hemolytic-uremic syndrome in children admitted on the same day to a hospital in Hamburg.

May 20th 2011: a team arrived to investigate

Other authorities (i.e. food safety) were also contacted and involved to find source in order to prevent further disease

May 22th 2011 – public informed

49
Q

what do you need to identify in an outbreak *

A

people who are a possible, probable and definite case

definiate cases are identified by diagnostic tests

50
Q

how can you manage an outbreak of a new strain *

A

sequence and isoplate the organism

come up with diagnostic method to determine the confirmed cases

51
Q

describe the use of PCR in the e coli outbreak *

A

isolates screened by multiplex PCR for characteristic features

see the Stx2 strain is in new strain - shiga toxin produced by the new strain

new strain has different genetic make up to EHEC which is the normal shiga producing strain

so you can see with OCR who has ECHC and who has new strain

52
Q

describe the stain in the outbreak of e coli *

A

most similar to enteroagressive E coli (EAEC)

contains 2 plasmids

  • pAA-type of EAEC which contains the aggregative adhesion fimbrial operon - allow adhesion to GIT
  • ESBL plasmid - genes encoding fro ESBLs - this is widely distributed in pathogenic e coli strains

but the outbreak strain contained the prophage encoding the shiga toxin - characteristic of EHEC

53
Q

describe how the outbreak strain was formed *

A

phage from EHEC mobilised to EAEC stain = shiga toxin and fimbrin producing strain = very pathogenic

EHEC not normally found in bowel, but EAEC is

54
Q

describe shiga toxins

A

AB5 subunit composition

subunit A is noncovalently associated with pentamer of protein B

StxA is the enzymatically active part

  • cleaves the 28S ribosomal RNA in eukaryotic cells =inhibition of protein synthesis
  • ribosomes are also a target = decreased proliferation in suseptible bacteria = effect commensal population

effects other cell processes

StxB is the part responsible for binding to the host

they are encoded on bacteriophages so can transfer between strains - integrate in chromosomes so more strains produce the toxins - toxins highly expressed when lytic cycle of phage is activated

55
Q

describe the EAEC virulence factor *

A

genes encoding for eggregative adherence fimbriae (AAF) are on a plasmid - so are mobilised betwen strains

AAF are required for adhesion to enterocytes

they stimulate a strong IL-8 response allowing biofilm formation

additional virulence factors lead to disruption f actin cytoskeleton - exfoliations

microbiology year 2 (9 decks)

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