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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
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
what are the 2 main types of G+ve cocci in chains?
what are 2 types of streptococci?
- alpha haemolytic: SOME digestion of RBC, see some green which is residual Hb
- beta haemolytic: TOTAL
what are the 2 broad groups of alpha haemolytic streptococci?
1. viridans: muttons, sanguine. they are normal flora or mouth and throat (URT flora)
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
wherever there are mucosal surfaces, what are the most common normal flora?
what is 99% of normal flora of gut made of? and rest?
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
why do we not see a lot of anaerobic organisms causing endocarditis?
because the ENVRIONMENT is NOT ANAEROBIC
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
which 2 drugs would you use for native IE treatment?
- 1. penicillin
- 2. gentamicin
how treat aspiration pneumonia?
- 1. metronidazole (for anaerobes)
- 2. penicillin eg amoxicillin for alpha streps
what is drug resistance to penicillin amongst alpha streps like?
what does pneumococcus look like under microscope?
- G+ve cocci in pairs
- area of 'non staining' or halo around each of pairs
why do you get halo around pneumococcus?
halo = capsule - thick polysaccharide capsule which does not take up gram stain
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
what is process of making organism more tasty for neutrophils and 2 aspects to it?
- 1. complement
- 2. antibody coating
which organ in body makes IgM that coats pneumococcus for opsonisation?
what implication does this have for splenectomy?
susceptible to overwhelming infection with capsular organisms especially pneumococcus (also meningococcus, haemophilus)
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
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)
how do you protect splenctomised patients?
- protect with penicillin prophylaxis for life
- pneumococcal vaccine
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)
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)
what does beta haemolysis mean?
- grows on blood agar
- complete haemolysis of RBC on blood agar plate
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
what is group A beta haemolytic strep also known as? why is it impressive?
- strep pyogenes
- wide range of infections
what is the commonest cause of a sore throat?
what is the commonest BACTERIAL cause of a sore throat?
how can you tell bacterial from viral sore throat?
- looks unwell
- severe pain in throat
- enlarged LN
what drug used to treat empirically GAS?
- penicillin V (oral)
- not amoxicillin as could be glandular fever - EBV - causes RASH!
if you see a child with GAS sore throat, what else may you see?
what are the 2 types of impetigo? which more common
bullous & non bullous - more common
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
how do you treat a dual stroph and strep infection eg non bullous impetigo?
- amoxicillin for GAS
- flucloxacillin for staph aureus
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
what is next infection caused by GAS?
if suspect cellulitis, what 2 things do you look for?
- 1. pain +++ around lesion
- 2. looks unwell - febrile toxic
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
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)
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
which other groups of beta haemolytic strep can cause the GAS infections?
- group C & G
- rare and less severe
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
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
what is treatment of erysipelas?
what is the 2nd major toxin associated disease with GAS? and cause
- scarlett fever
- erythrogenic toxin
what are features of scarlett fever? 3
- circumoral pallor
- fine reticular rash chest
- strawberry tongue
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)
what is 3rd toxin mediated infection with strep?
toxic shock syndrome (nb originally assoc with staph but now we know also with strep too)
which beta haemolytic group causes toxin associated condition?
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
which types of streps are thought to cause rheumatic fever?
sore throat causing streps
which types of streps are thought to cause acute GN?
skin and subcut causing streps
what is treatment of sequelae?
what is group B beta haemolytic strep a normal flora of?
vagina (25-30% of women)
what are problems with GBS?
pregnant: UTI, most important cause of neonatal sepsis
how do you treat neonatal GBS meningitis-sepsis?
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
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
which strep is related to PUS formation?
- group F strep
- milleri group
where is group F strep?
colonises mucosal surfaces.
where do group F strep infect?
associated with internal organ abscess tooth, sinusitis, brain, splenic, liver form gut mucosa
when see strep milleri, what is Rx? due to mucosal tract relation
- metronidazole: as anaerobe also sitting there
what are non-haemolytic strep known as?
what are the 2 types of enterococci?
- enterococcus faecalis
- enterococcus faecium
what is enterocci normal flora of?
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
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
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
what is superbug related to enterococcus?
- VRE: vancomycin resistant enterococus
- then use the abx: linezolid
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
what 2 groups are staph put into?
- coagulase positive eg staph aureus
- coagulase negative eg staph epidermidis
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
what is staph aureus the normal flora of? why
- its loves moisture, warmth and salt so colonises sweaty areas
- skin: armpit, groin, hairline, nose
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
what are superficial pus spots caused by?
if person has recurrent folliculitis what do you investigate them for?
- diabetes as neutrophils functionally not quite right
- prone to repeated, recurrent staph infections
what is a group of follicles coalesced to cause a bigger lesion called?
what is a group of furuncles that coalesce to an even bigger lesion called?
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
what is treatment of subcut staph abscess?
- lance it
- release pus
- treat with flucloxacillin
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
what is the commonest cause of osteomyelitis and septic arthritis in any age group?
what are the X-ray changes of osteomyelitis?
- patchy decalcification
- periosteal elevation
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
how do you treat MSSA?
- mild oral fluclox,
- severe iv fluclox + gent
how do you treat MRSA?
- flucloxacillin resistant
- so need vancomycin, teicoplenin
- linezolid, rifampicin are other options
which is main CNS?
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,
how long can a peripheral cannula stay in for?
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
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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