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pathogen infection antibiotic matching Flashcards

1
Q

how can you identify whether a pathogen is gram positive or gram negative?

A

in gram positive the cell wall is made of peptidoglycan and therefore it stains purple. The inner cell wall is protected and therefore stains pink. The cell membrane is made of bilayer and therefore stains pink - staining classifys them

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2
Q

how do you identify a rod/cocci gram positive or negative?

A

gram stain positive - cocci or rods. Rods are clostridium, bacillus, corynebacteria or listeria. To identify cocci do the catylase test which if positive is stapylococcus - aureus or epidermis and if negative is streptococcus - pneumoniae or pyogenes. For gram negative the cocci are neisseria and the rods are E coli, pseudomonas etc

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3
Q

what is cocci shape?

A

they are in pairs, groups or chains

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4
Q

what is a rod shape?

A

groups, chains or solo

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5
Q

what is pencillin?

A

it is an antibiotic that is a beta lactam ring. All beta lactam rings work in a similar fashion by inhibiting cell wall synthesis - they are the oldest and most useful, safest antibiotic

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6
Q

what else can be targeted?

A

bacterial translation and protein synthesis - translation is mRNA to AA to protein - can exploit this because the bacteria and human ribosome are different

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7
Q

what types of bacteria translation and protein synthesis antibiotics are there?

A

chloramphenicol - used for conjunctivitis as eyedrops and tetracyclins

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8
Q

what does RNA synthesis and DNA replication get used for?

A

target for antibiotics as DNA to mRNA in transcription is different in different bacteria and so is DNA bacteria.

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9
Q

what is needed to make nucleotides?

A

Folate is the basic thing needed to make constituents in DNA in nucleotide synthesis

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10
Q

what types of antibiotics target cell wall?

A

penicillins, carbapenems, cephalosporins and glycopeptides

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11
Q

what antibiotics are used in translation?

A

tetracyclin, macrolides, chloramphenicol or aminoglycosides

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12
Q

what type of antibiotic are used in RNA synthesis?

A

rifamycin

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13
Q

what types of antibiotics are used in DNA replication?

A

antifolates - trimethporin and slfadrugs, quinolones and metronidazole

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14
Q

how would you test antibiotic resistance?

A

spread bacteria out of a dish and put on antibiotic discs - look at the zone of inhibition and it may take up to 6 weeks to fully wipe out bacteria

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15
Q

what should be done in the situation of a mutation?

A

change AB to avoid further resistance - can mutate and become resistant in a short amount of time

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16
Q

what are the four mechanisms of drug resistance?

A

altered target or binding site, alteration of metabolic pathways, reduced drug accumulation and drug inactivation or modification

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17
Q

how can drug inactivation work?

A

enzymes in bacteria such as E coli and carbapenemase and staph aureus with penicillinase

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18
Q

how can alteration of target work?

A

MRSA - bacteria will evolve the binding site so that AB cannot bind or staph aureus - alteration of penicillin binding protein

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19
Q

how can the alteration of metabolic pathway work?

A

sulfa resistant bugs can use preformed folic acid

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20
Q

how can reduced drug accumulation result?

A

with quinolones treatment can develop an efflux pump

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21
Q

why is co-amoxiclav used?

A

it is a component of amoxicillin (beta lactam) and clavulanic acid - acid inhibits B lactamase that often breaks down the ring in AB and then prevents amoxicillin from being degraded

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22
Q

what is a similar concept to coamoxiclav?

A

tazocin - penicillin and tazobactam

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23
Q

how have gram negative rods adapted?

A

they have B lactamase that cleaves the amoxicillin in hald

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24
Q

if MRSA is resistant to methicillin then what else will it be resistant to?

A

cyclosporin and penicillin

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25
Q

how does flucloxacillin work?

A

it inhibits cell wall synthesis - only active against gram positive bacteria such as staph aureus - binds to penicillin binding protein

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26
Q

what can be used to treat MRSA?

A

vancomycin not beta lactams

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27
Q

what are the symptoms of pneumonia?

A

fever, SOB, purulent sputum, low BP and high RR with lower consolidation on the X ray

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28
Q

what is the treatment for pneumonia?

A

depends on the CURB score (confusion, urea (<7), respiration (>30), BP (<90/60 over 65y/o). If greater than 5 use more broad spectrum as mortality increases over 65% and lower then use more targeted. Broad would be coamoxiclav and carithromycin and amoxicillin if low risk

29
Q

how can you determine the organism causing pneumonia?

A

microscopy and culture - strep pneumoniae is most common cause of community acquired and is a diplococci gram positive

30
Q

what is the most common cause of pneumonia in hospital?

A

kleibsiella and other gram negative

31
Q

what is strep pneumoniae sensitive to?

A

penicillin

32
Q

what is the best treatment?

A

the most targeted treatment

33
Q

when is C difficile common?

A

the the immunocompromised

34
Q

what are the characteristics of C difficile?

A

diarrhoea, abdo pain and vomiting

35
Q

what causes C difficile?

A

gram positive C difficile rods

36
Q

what is the basis of C difficile infection?

A

there is normal flora in the gut. When using a LT AB (worst are ciproflaxacin, cerufoxime, and co-amoxiclav) it wipes out the competition in the gut and allows the overgrowth of C difficile

37
Q

what are the symptoms in LUTI and UUTI?

A

lower is from the urethra to bladder and gives pain on urinating, frequency whereas UUTI has fever, loin pain, tachycardia and hypotension due to ascent to the kidneys

38
Q

how is LUTI managed?

A

nitrofurantoin, trimethporin and pivmecillnam - kidneys concentrate it into the urine once it has reached the collecting tubes

39
Q

what most commonly causes UTIs?

A

E coli

40
Q

`how do you manage UUTIs?

A

IV cerufoxime

41
Q

what are the symptoms of meningitis caused by neisseria meningitidis?

A

feeling unwell, confusion, fever and neck stiffness as well as struggling with bright light

42
Q

how would you manage neisseria meningitidis?

A

do CSF sample, then treat with broad spectrum antibiotic such as IV ceftriaxone - third generation cephalosporin

43
Q

what is more likely to cause meningitis in elderly patients?

A

haemophilius influenza or strep pneumoniae

44
Q

what is the difference between meningitis and meningococcal septicaemia?

A

meningitis is inflammation of the meninges in the CNS only whereas septicaemia is systematically unwell, blanching rash, low BP and tachycardia with DIC resulting in rash

45
Q

with meningitis what will you see in the meninges?

A

above the CSF there will be swollen tissue

46
Q

what is sepsis?

A

it is systemic inflammatory response syndrome and a suspected source. It has 2 of the following: temperature over 38, respiratory rate over 20, heart rate over 90 and WBC over 12.

47
Q

what is septic shock?

A

it is low blood pressure less than 90/60 and sepsis

48
Q

how do you manage sepsis?

A

BUFALO and broad spectrum ABs until have identified course and then target

49
Q

what is BUFALO?

A

blood cultures - 2 sets
Urine Output through catheterisation
Fluids - 500ml IV saline over 15 minutes. Alm 30ml/kg in 1 hour
Antibiotics - for suspected infection
lactate - arterial blood gas for lactate and pH
oxygen - 15l/min via reservoir face mask

50
Q

what is cellulitis?

A

it is a skin and soft tissue infection that results in rash, heat and swelling - could be from a scrape

51
Q

99% of the time what causes cellulitis?

A

strep pyogenes and staph aureus - gram positive cocci

52
Q

when do staph aureus symptoms appear?

A

carried on the skin of 25% of population - no issues unless has broken skin or colonised inside - transient coloniser

53
Q

how do you treat cellulitis most commonly?

A

flucloxacillin

54
Q

what is the risk of untreated cellulitis?

A

necrotising fasciitis

55
Q

what is necrotising fasciitis?

A

it is a severe skin and soft tissue infection that is caused by a polymicrobial mix, usually involving streptococcus pyogenes

56
Q

what is the advantage of strep pyogenes?

A

it is a very potent pathogen that works in anerobic environments

57
Q

what is the first line treatment of necrotising fasciitis?

A

debridement - ABs cannot penetrate the dead tissue so needs surgical removal

58
Q

what antibiotics might be used in NF?

A

clindamycin and meropenem

59
Q

what is infective endocarditis?

A

it is infection of the heart valves

60
Q

what is infective endocarditis caused by?

A

range of bugs but most commonly streptococci and staph aureus

61
Q

what is the presentation of IE?

A

fever, night sweats, splinter haemorrhage, SOB and cardiac murmur on auscultation

62
Q

what is the treatment and risk factors for IE?

A

risk factors are IV drug users and treatment is 6 weeks of AB depending on bug

63
Q

what is a complication of IE?

A

brain abscesses

64
Q

what else are risk factors or IE?

A

immunosupression, IV drug use and HIV

65
Q

what are the most common bugs for brain abscesses?

A

can be anything but strep and staph are most common

66
Q

what is the treatment for brain abscess?

A

drainage and then 4 weeks ABs depending on bug

67
Q

what is the risk of certain ABs in pregnancy?

A

quinolones - damage to cartilage such as ciprofloxacin
trimethporin - folate acid antagonist
tetracyclins - deposits and stains on bones and teeth

68
Q

what is the safest type of AB?

A

beta lactams such as penicillins, meropenems and cephalosporins - safe in pregnancy

CP (38 decks)

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