community and hospital acquired bacterial infections 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
define antibacterial
commonly used to describe agents to reduce or eliminate harmful bacteria - but effect the microbiota too
26
define antibiotic
type of antimicrobial used as medicine originally referred to as naturally occuring compounds - now chemically synthesised but want to find more from environment
27
what are hospital acquired infections \*
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
importance of HAI \*
they cause death increase length of stay increase financial burden
29
why do HAIs occur \*
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
what were the main bacteria that caused HAIs \*
ESKAPE * Enterococcus faecium * Staphylococcus aureus * Klebsiella pneumoniae * Acinetobacter baumanii * Pseudomonas aeruginosa * Enterobacter species
31
what are the bacteria now that cause HAIs mainly \*
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
what is the problem with the ESKAPE bacteria \*
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
describe E coli \*
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
describe cephalosporins \*
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
describe resistance to cephalosporins \*
extended spectrum B-lactamase (ESBL) is encoded on a plasmid (means the genes are mobile so can spread between strains) ESBL cleaves cephalosporin
36
describe carbapenems \*
B-lactems - same mechanism as cepalosporins
37
describe resistance to carbenems \*
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
describe kelbsiella pneumonia \*
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
describe pseudomonas aeruginosa \*
important cause of infection in immunocomp high proportion MDR
40
describe methicillin resistant S. aures \*
most important cause of antimicrobial resistant bacteria world wide
41
describe methicillin \*
B lactam
42
describe resistance to methicillin \*
acquire new gene = expression of additional PBP PBP2 has low affinity for methicillin - still function and synthesise peptidoglycan in presence of AB
43
describe vancomycin resistant enterococcus faecium \*
3rd most frequently identified cause of nosocomial blood stream infections (BSI) in US vacomycin resistance around 60%
44
describe vancomycin \*
inhibit peptidoglycan synthesis by binding to peptidoglycan precurser (the substrate for the production of peptidoglycan)
45
describe resistance to vancomycin \*
multiple proteins' genes encoded on plasmid/tansposon results in synthesis of different precurser
46
describe the 2011 e coli outbreak in germany
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
describe haemolytic syndrome
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
time scale of the E coli outbreak
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
what do you need to identify in an outbreak \*
people who are a possible, probable and definite case definiate cases are identified by diagnostic tests
50
how can you manage an outbreak of a new strain \*
sequence and isoplate the organism come up with diagnostic method to determine the confirmed cases
51
describe the use of PCR in the e coli outbreak \*
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
describe the stain in the outbreak of e coli \*
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
describe how the outbreak strain was formed \*
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
describe shiga toxins
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
describe the EAEC virulence factor \*
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