Gram+ve bacteria.txt

  1. why do we want to know if an organism is gram +ve or -ve?
    • governs which antibiotic to give
    • if both G+ and G- involved then give broad spectrum antibiotic
  2. from doing a gram stain, what 3 parts of information can we gain?
    • 1. is it gram negative or positive
    • 2. shape: round = cocci; rod = bacilli
    • 3. arrangement: chains = strep; bunches = staph
  3. what are the 2 main types of G+ve cocci in chains?
    • streptococci
    • enterococci
  4. what are 2 types of streptococci?
    • alpha haemolytic: SOME digestion of RBC, see some green which is residual Hb
    • beta haemolytic: TOTAL
  5. what are the 2 broad groups of alpha haemolytic streptococci?
    1. viridans: muttons, sanguine. they are normal flora or mouth and throat (URT flora)
  6. what is potential for infection for viridans strep?
    • not in site of normal flora
    • but potential for infection where mouth flora translocates: infective endocarditis (native valve) & aspiration pneumonia from mouth to airway
  7. wherever there are mucosal surfaces, what are the most common normal flora?
    anaerobic organisms
  8. what is 99% of normal flora of gut made of? and rest?
    • anaerobes
    • 1% is E Coli
  9. when treat aspiration pneumonia, what 2 things to consider?
    • 1. treat the alpha haemolytic strep which has gone from mouth to airway
    • 2. empirically also treat anaerobic organism as they cover mucosal surfaces eg mouth so would also fall into airway
  10. why do we not see a lot of anaerobic organisms causing endocarditis?
  11. what is the chemical nature of G+ve cell wall? why is this clinically relevant?
    • this is important binding site for B-lactam antibiotics eg penicillin
  12. which 2 drugs would you use for native IE treatment?
    • 1. penicillin
    • 2. gentamicin
  13. how treat aspiration pneumonia?
    • 1. metronidazole (for anaerobes)
    • 2. penicillin eg amoxicillin for alpha streps
  14. what is drug resistance to penicillin amongst alpha streps like?
  15. what does pneumococcus look like under microscope?
    • G+ve cocci in pairs
    • area of 'non staining' or halo around each of pairs
  16. why do you get halo around pneumococcus?
    halo = capsule - thick polysaccharide capsule which does not take up gram stain
  17. what is pneumococcus' main virulence factor?
    • its capsule! as it makes it anti-phagocytic
    • phagocytes find it difficult to ingest a capsulated organism. goes to spleen for opsonisation by Ab and complement to coat organism - makes it more edible to neutrophil as on surface on neutrophil there are Ab and complement receptors
  18. what is process of making organism more tasty for neutrophils and 2 aspects to it?
    • opsonisation
    • 1. complement
    • 2. antibody coating
  19. which organ in body makes IgM that coats pneumococcus for opsonisation?
  20. what implication does this have for splenectomy?
    susceptible to overwhelming infection with capsular organisms especially pneumococcus (also meningococcus, haemophilus)
  21. if see patient with overwhelming pneumococcal infection, what do you need to check?
    • 1. ask if had splenectomy
    • 2. check spleen function
    • 3. check for sickle cell
  22. what are 2 major infectious disease process related to the pneumoncoccus?
    • pneumonia: lobar pneumonia, most important cause of CAP
    • bacterial meningitis (outside of the neonatal period)
  23. how do you protect splenctomised patients?
    • protect with penicillin prophylaxis for life
    • pneumococcal vaccine
  24. how do you treat serious pneumococcal pneumonia?
    • penicillin unless allergy or resistance. high dose benzyl-penicillin
    • emerging resistance to penicillin amongst pneumonococcus then use cefuroxime (doesn't cross BBB)
  25. how do you treat meningitis?
    • penicillin crosses the inflamed BBB very well
    • use penicillin
    • if suspect resistance eg spanish or american don't rely on penicillin so then give ceftriaxone (also penetrates BBB very well)
  26. what does beta haemolysis mean?
    • grows on blood agar
    • complete haemolysis of RBC on blood agar plate
  27. what are beta haemolytic streps grouped into? and what is this grouping based on?
    • Lancefield grouping
    • based on outer nature of the Ag carbohydrate around organism
  28. what is group A beta haemolytic strep also known as? why is it impressive?
    • strep pyogenes
    • wide range of infections
  29. what is the commonest cause of a sore throat?
  30. what is the commonest BACTERIAL cause of a sore throat?
  31. how can you tell bacterial from viral sore throat?
    • bacterial
    • looks unwell
    • fever
    • severe pain in throat
    • enlarged LN
  32. what drug used to treat empirically GAS?
    • penicillin V (oral)
    • not amoxicillin as could be glandular fever - EBV - causes RASH!
  33. if you see a child with GAS sore throat, what else may you see?
  34. what are the 2 types of impetigo? which more common
    bullous & non bullous - more common
  35. what are the 2 main features of non bullous impetigo and what causes each feature?
    • central crusting with surrounding redness
    • impetigo is usually a dual infection: staph and strep. central crusting with pus is due to staph aureus
    • peripheral erythema is due to GAStrep
  36. how do you treat a dual stroph and strep infection eg non bullous impetigo?
    • amoxicillin for GAS
    • flucloxacillin for staph aureus
  37. why do you not use amoxicillin alone in dual staph and strep infection?
    • 85% of staph worldwide make enzyme beta lactamase that destroys basic beta lactam molecule of penicillin V and amoxicillin
    • flucloxacilin - structured in a way that is beta lactamase stable
    • so if you see G+ve clusters = staph = only use fluclox
  38. what is next infection caused by GAS?
  39. if suspect cellulitis, what 2 things do you look for?
    • 1. pain +++ around lesion
    • 2. looks unwell - febrile toxic
  40. if you get cellulitis pt in A&E what to do?
    • 1. mark cellulitis to see how fast spreading
    • 2. bloods: FBC, CRP, blood cultures
    • 3. swabs from anywhere
    • 4. iv high dose ben pen & fluclox to cover staph that might inactivate penicillin
  41. what is management of necrotising fasciitis?
    • extensive surgical debridement
    • abx are only supplementary. wont work alone as blood vessels dead
    • iv ben pen & clindamycin (acts on ribosome, switch off protein synthesis so toxin production stopped)
  42. what are 2 life threatening infections of GAS?
    • 1. necrotising fasciitis
    • 2. post partum sepsis (ascends and infects raw uterine bed, causes severe toxaemia and septicaemia) high mortality
  43. which other groups of beta haemolytic strep can cause the GAS infections?
    • group C & G
    • rare and less severe
  44. what is the toxin mediated infection of GAS strep?
    • erysipelas: classic hard raised indurated lesion on face/limbs/ sub cut tissue. surrounding fluid filled blebs
    • pyrogenic exotins
  45. how do you find the organism for erysipelas?
    • swab throat or other lesion may get organism
    • not just lesion as its caused by toxin of strep so might not see the actual GAS
  46. what is treatment of erysipelas?
  47. what is the 2nd major toxin associated disease with GAS? and cause
    • scarlett fever
    • erythrogenic toxin
  48. what are features of scarlett fever? 3
    • circumoral pallor
    • fine reticular rash chest
    • strawberry tongue
  49. what is treatment of scarlet fever?
    treat with penicillin, can give amoxicilin as no association between scarlet fever and EBV (amox is easier to swallow, better absorbed from stomach, only tds as opposed to penicillin qds)
  50. what is 3rd toxin mediated infection with strep?
    toxic shock syndrome (nb originally assoc with staph but now we know also with strep too)
  51. which beta haemolytic group causes toxin associated condition?
    group A
  52. what are the different streptococcal sequalae?
    • 1. rheumatic fever: cross reaction of Ab between strep Ag and cardiac tissue Ag (autoimmune)
    • 2. post strep acute glomerulonephritis: immune complex (type 3) very big and settle on glomerular BM, attract complement and macrophages, neutrophils release potent tissue destroying enzymes so glomerular BM subjected to inflammatory reactions
  53. which types of streps are thought to cause rheumatic fever?
    sore throat causing streps
  54. which types of streps are thought to cause acute GN?
    skin and subcut causing streps
  55. what is treatment of sequelae?
    • long term abx
    • steroids
  56. what is group B beta haemolytic strep a normal flora of?
    vagina (25-30% of women)
  57. what are problems with GBS?
    pregnant: UTI, most important cause of neonatal sepsis
  58. how do you treat neonatal GBS meningitis-sepsis?
    antibiotic: penicillin
  59. what is role of gentamicin in neonatal sepsis, IE?
    • to provide anti-microbial synergy
    • penicillin attacks CELL WALL of strep
    • through cell wall gentamicin HITS RIBOSOME AND STOPS PROTEIN SYNTHESIS to over kill the organism
  60. whats the problem with antibiotic treatment in IE?
    • heart valve avascular
    • vegetation avascular
    • getting the antibiotic there depends on blood stream in heart by apposition to hit the organism
    • need quick exponential killing so have to add gentamicin for synergy
  61. which strep is related to PUS formation?
    • group F strep
    • milleri group
  62. where is group F strep?
    colonises mucosal surfaces.
  63. where do group F strep infect?
    associated with internal organ abscess tooth, sinusitis, brain, splenic, liver form gut mucosa
  64. when see strep milleri, what is Rx? due to mucosal tract relation
    • penicillin
    • metronidazole: as anaerobe also sitting there
  65. what are non-haemolytic strep known as?
  66. what are the 2 types of enterococci?
    • enterococcus faecalis
    • enterococcus faecium
  67. what is enterocci normal flora of?
  68. what are 2 differences between strep and enterococci?
    • 1. cephalosporins wont work against enterococci
    • 2. enterococci are LOW VIRULENCE, innocuous organisms that usually hang about, colonise diabetic ulcers, sacral sores
  69. what is Rx of enterocci, when do you treat?
    don't always need to treat unless some degree of immunocompromise (transplant, haem) then enterococi can cause ANYTHING from line infections, UTI, endocarditis, wound infection, septicaemia
  70. what is Rx of enterococcus?
    • 1. find out if susceptible to amoxicillin - treatment of choice
    • e. faecalis is SENSITIVE to amoxicillin
    • BUT most of e.faecium is resistant to amoxicillin
    • also give gentamicin
    • if cant use amoxicillin or cephalosporins use vancomycin or teicopleinin for serious enterococcus that doesn't respond to amoxicillin
  71. what is superbug related to enterococcus?
    • VRE: vancomycin resistant enterococus
    • then use the abx: linezolid
  72. what is so different about the treatment of strep and staph and why?
    • staph produce beta lactamase so cant use normal penicillin or amoxicillin
    • need to use beta lactamase stable penicillin
  73. what 2 groups are staph put into?
    • coagulase positive eg staph aureus
    • coagulase negative eg staph epidermidis
  74. what is the coagulase test?
    • add organism to plasma and cook it
    • if there is coagulase it will form a clot and so if you see clot it is coag+ve which is staph aureus
  75. what is staph aureus the normal flora of? why
    • its loves moisture, warmth and salt so colonises sweaty areas
    • skin: armpit, groin, hairline, nose
  76. what is a classic superficial staph aureus infection?
    • abscess. hurt themselves
    • pointy red lesion, if lance it PUS comes out
    • little pus spots on skin
    • likes to clog hair follicles, sebaceous cysts = folliculitis
  77. what are superficial pus spots caused by?
    staph aureus
  78. if person has recurrent folliculitis what do you investigate them for?
    • diabetes as neutrophils functionally not quite right
    • prone to repeated, recurrent staph infections
  79. what is a group of follicles coalesced to cause a bigger lesion called?
  80. what is a group of furuncles that coalesce to an even bigger lesion called?
  81. what is most common example of subcutaneous lesion of staph?
    lactating breast abscess as baby is colonised with staph aureus in umbilicus or in the mouth. staph goes through duct and into substance of mammary gland
  82. what is treatment of subcut staph abscess?
    • lance it
    • release pus
    • treat with flucloxacillin
  83. what are classic places that staph aureus will seed to?
    • 1. heart - endocarditis: new murmur, echo
    • 2. bone esp vertebral bodies as distribution of blood supply is such that it is a common reservoir. vertebral osteomyelitis
    • 3. psoas abscess - ask for bone and back pain
    • 4. septicaemia
    • 5. septic arthritis
  84. what is the commonest cause of osteomyelitis and septic arthritis in any age group?
    staph aureus
  85. what are the X-ray changes of osteomyelitis?
    • patchy decalcification
    • periosteal elevation
  86. what are the toxin associated syndromes in staph aureus?
    • 1. toxic shock syndrome (TSST1). menstrual tampon use; non menstrual much commoner. the staph that has infected your wound carries the gene TSST1
    • vomit, diarrhoea, rash - TSS. easily miss systemic effects of staph
    • 2. scalded skin syndrome: babies. epidermylytic toxins - peel off skin. not life threatening if no secondary infection. treat iv flucloxacillin
    • 3. food poisoning: some staph aureus have gene for enterotoxin. severe rapid onset vomiting. vomit rather than diarrhoea
    • 4. PVL: pontoon valentine leukocidin: USA who played contact sport where mixture of sweat or share gear stained with sweat - toxin destroy leucocyte and cause severe necrotising skin and lung lesions, cause death.
    • Rx: fluclox + clindamycin
  87. how do you treat MSSA?
    • mild oral fluclox,
    • severe iv fluclox + gent
  88. how do you treat MRSA?
    • flucloxacillin resistant
    • so need vancomycin, teicoplenin
    • linezolid, rifampicin are other options
  89. which is main CNS?
    staph epidermidis
  90. if see staph epidermis on culture how do you know if significant?
    • central lines
    • hickman lines
    • plastic or metal - will get colonised with skin organisms
    • prosthesis: knee joints, heart valves. so needs adequate prophylaxis, skin asepsis,
  91. how long can a peripheral cannula stay in for?
    72 hours
  92. if you see infection of a line what do you do?
    slime, biofilm, glycocalyx trap the CNS. no abx can penetrate the glycocalyx so must remove line
  93. how do you treat CNS?
    • not flucloxacillin as skin commensals get acquired resistance to it
    • so use vancomycin or teicopleinin +/- gentamicin
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Gram+ve bacteria.txt