Ambler Bacteria Flashcards
(47 cards)
Gram Stain
Hans Christian Gram, 1884
tells if bacteria are Gram ‘POS’ or ‘NEG’.
Gram Positives
Staphylococcus Enterococcus/Streptococcus Bacillus Clostridium Listeria Corynebacterium(Diphtheroids)
generalizations about spores
In a crux:
Bacillus and clostridium sporalate
Staph, Strep, Listeria and corynebacterium do not spore
My mnemonic: Spores, get Back in the Closet. Bacillus and Clostridium.
What GP has endotoxin?
Listeria has eNdotoxin where most GP do not
Staphylococcus
Gram Positive, catalase +, coagulase + cocci seen in Clusters.
Defenses –protein A, coagulase, hemolysins, leukocidins, penicillinase, beta-lactamases
- hyaluronidase, staphylokinase, lipase
Exotoxins
staphylococcus coagulase tests
COAGulase POS = aureus COAGulase NEG = rest, including epidermidis lugdenensis saprophyticus
Staphylococcus aureus general actions
Can infect head to toes and pretty much everything in-between
Really NEVER considered a contaminant.
Has a extracellular vesicles that carry beta lactamase into the surroundings
ie. There is a mixed abscess with ampicillin sensitive E.coli and MRSA. Some beta lactamase inhibitor needs to be included in the treatment.
Staph aureus toxins
Enterotoxin is heat stable
TSST-1: superantigen
Coagulase
Cytolytic toxin (α toxin); pore forming toxin
Panton-Valentine leukocidin (PVL); (β toxin); pore forming toxin
seen in CA-MRSA
Exfoliatins: skin exfoliating toxin (scalded skin)
staph aureus symptoms/ rx
purulent symptoms
- Boils
- septic arthritis/osteomyelitis
- Endocarditis
- Necrotizing pneumonia (salmon tinged sputum)
- intestinal
treatment is source control if possible
boils may only need I&D but many treat with abx as well.
bacteremia always treated with IV ABx
MRSA (Meth R Staph aureus)
MRSA almost universally put in Contact Isolation where MSSA is not.
Penicillin introduced to public 1941 (1942)
Methicillin 1958 (1960)
SCC MEC gene
CA-MRSA late 1990’s causes recurrent boils
Vancomycin 1958 (2002)
Linezolid 2000 (2001)
Daptomycin 2003 (2005)
VRSA
vanco resistant staph aureus
13 cases in US (first Detroit 2002). MI, PA, NY, DE
usually a history of recurrent MRSA and VRE skin/wound colonization with repeated vancomycin use (think dialyisis)
VAN-A gene from Enterococcus
VISA
vanco intermediate staph aureus
reduced vanco suceptibility
1997 Japan
Heteroresistance? Mixed MRSA with some VISA as well
mechanism is thickened cell wall
May confer some decrease daptomycin susceptibilities
Staphylococcus epidermidis
Indwelling foreign device
Usually more resistant than S.aureus = more methicillin R.
Vancomycin usually empiric choice
Treatment usually involves removal of foreign body.
Not typically as ‘virulent’ and not usually as purulent (no abscesses).
#1 cause of contaminated blood cultures
Staphylococcus saprophyticus
“Honeymoon cystitis” in women
Cause of UTI
Not resistant so PCN ok.
Enterococci
Historically Group D Strep so on micro reports, you may see strep species (gpc chains) that miraculously changes to enterococcus.
Clinically relevant are : faecalis and faecium
PYR + (pyrrolidonyl-arylamidase)
Highly resistant to many antibiotics
faecalis is usually less, highly resistant.
faecium is usually more, highly resistant
enterococci hemolysis
Usually gamma hemolysis
Can be alpha – especially some VRE
VRE (vancomycin resistant enterococci)
- Difficult to treat
- Seen in highly abx experienced patients
- Must refer to culture sensitivity but depending on the infection and site
- -linezolid
- -daptomycin
- -tetracyclines (for non-severe infections and not really urine)
- -nitrofurantoin (for urine only)
VRE
First described Europe 1980’s. felt to be from a food additive avoparcin.
Meta-analysis of 1614 enterococcal bloodstream infections had 42% VRE which has higher mortality.
Van-A, Van-B, Van-C genes
transposon. Frightened, Promiscuous bacteria!!!
(see VRSA)
Streptococci
Different classification systems have been developed.
Rebecca Lancefield classified group A-V(no I/J) and was based on the C carbohydrate on wall
We use hemolysis as well to characterize today
catalase (-) unlike staph or other aerobes/facultative anaerobes
streptococcus by hemolysis
alpha: green pneumoniae, viridans
Beta: pyogenes, agalactiae
gamma: enterococcus
Streptococcus pyogenes (symptoms, etc.)
Group A Pharyngitis (main cause of ‘strep throat’) --Red, purulent tonsils --Fever --Lymph nodes (ant cerv)
Skin infection
- -Folliculitis
- -Cellulitis
- -Impetigo (usually Staph)
- -Necrotizing disease
Scarlet fever = fever/rash
Associated with rheumatic fever Can cause Toxic shock syndrome “M” proteins (>70types) are virulence factors Cause of post strep glomerulonephritis Rapidly progressing
S. pyogenes: antibody mediated
Rheumatic Fever
- pharyngitis 2-4 weeks prior
Acute PSRPGN (post strep rapidly progressing glomerulonephritis) - skin infection or pharyngitis
Acute Rheumatic Fever
Major:
Migratory Arthritis (several joints in quick succession, each lasting days- 1 wk)
Carditis ( peri, epi, myo and dendo) and valvulitis (mitral stenosis as late complication)
CNS (Sydenham chorea)= St. Vitus dance
Erythema marginatum- rash
Subcutaneous nodules
Minor: Arthralgias Fever Acute phase reactant elevation Prolonged PR interval
Tx: symptomatic ie anti-inflammatories. Not proven to dec risk of rheumatic heart disease.
Abx even with negative throat culture – for stopping transmission
PCN for years to life
Streptococcus agalactiae
Group B
Know this causes neonatal sepsis so pregnant moms get a screening culture antepartum
Can cause occult and sporadic disease in adults including bacteremia, SSTI, pneumonia and sepsis
esp DM
PCN DOC. Some clindamycin resistance so not reliable
Group F = milleri group
another beta strep
PUS formers including abdomen, head and neck and brain abscesses! Think of CIA – sneaky fellows. Strep constellatus Strep intermedius Strep anginosus