Phloston

Three main classications to be aware of: cocci, rods

and lamentous rods.

 Three main classications to be aware of: cocci, rods

and lamentous rods.

Bacilli = rods, but on the USMLE, youll only ever see
rod or rods.

 Three main classications to be aware of: cocci, rods

and lamentous rods.

Bacilli = rods, but on the USMLE, youll only ever see
rod or rods.
In the following slides, Ill discuss basic classications
of all of the organisms and then come back and talk
about them in more depth individually.

Gram(+) cocci

Gram(+) cocci
Main two divisions are catalase(+) and catalase(-)

Gram(+) cocci
Main two divisions are catalase(+) and catalase(-)
Of the catalase(+) cocci, theres either coagulase(+) or

coagulase(-).

Gram(+) cocci
Main two divisions are catalase(+) and catalase(-)
Of the catalase(+) cocci, theres either coagulase(+) or

coagulase(-).
S. aureus, in terms of the USMLE, is your only
catalase(+)/coagulase(+) coccus (or bacterium for
that matter). That is exceedingly high-yield.

Gram(+) cocci
Main two divisions are catalase(+) and catalase(-)
Of the catalase(+) cocci, theres either coagulase(+) or

coagulase(-).
S. aureus, in terms of the USMLE, is your only
catalase(+)/coagulase(+) coccus (or bacterium for
that matter). That is exceedingly high-yield.
In an easy question, theyll mention a coagulase(-) or
(+) organism, and youll have to know whether theyre
referring to S. aureus or not.

Gram(+) cocci
If they say coagulase(+), you know right away youre

dealing with S. aureus. If they say catalase(+) and

coagulase(-), theyre referring to S. epidermidis or S.
saprophyticus.

Gram(+) cocci
If they say coagulase(+), you know right away youre

dealing with S. aureus. If they say catalase(+) and

coagulase(-), theyre referring to S. epidermidis or S.
saprophyticus.
Therefore, S. epidermidis + saprophyticus are
catalase(+) / coagulase (-). That is very HY.

Gram(+) cocci
If they say coagulase(+), you know right away youre

dealing with S. aureus. If they say catalase(+) and

coagulase(-), theyre referring to S. epidermidis or S.
saprophyticus.
Therefore, S. epidermidis + saprophyticus are
catalase(+) / coagulase (-). That is very HY.
So the staphyloccoci, in summary, are catalase(+),
but youve gotta know that S. epidermidis +
saprophyticus are coagulase(-), but only S. aureus is
coagulase(+).

Gram(+) cocci
If theyre being nice theyll mention the coagulase or

catalase aspect directly.

Gram(+) cocci
If theyre being nice theyll mention the coagulase or

catalase aspect directly.

Ive seen in a practice question where they mentioned
a bacterial toxin + enzyme passing through a column
and binding to IgG and brinogen adsorbed to latex
beads, and then they wanted to know what the toxin
+ enzyme were.

Gram(+) cocci
If theyre being nice theyll mention the coagulase or

catalase aspect directly.

Ive seen in a practice question where they mentioned
a bacterial toxin + enzyme passing through a column
and binding to IgG and brinogen adsorbed to latex
beads, and then they wanted to know what the toxin
+ enzyme were.
S. aureus protein-A binds the Fc region of IgG;
coagulase binds brinogen. Thats how youll see
it on the real deal. I believe that was on an NBME or
free-150, which is as HY as it gets.

Gram(+) cocci
Of the catalase(+), coagulase(-) gram(+)s, S.

epidermidis is dierentiated from S. saprophyticus bc

S. epidermidis is novobiocin-sensitive, but S.
saprophyticus is novobiocin-resistant.

Gram(+) cocci
Of the catalase(-) gram(+) cocci, there are the alpha-,

beta- and gamma-haemolytics.

Gram(+) cocci
Of the catalase(-) gram(+) cocci, there are the alpha-,

beta- and gamma-haemolytics.

Alpha-haemolysis means partial haemolysis; this is
represented as a greenish zone produced on blood
agar.

Gram(+) cocci
Of the catalase(-) gram(+) cocci, there are the alpha-,

beta- and gamma-haemolytics.

Alpha-haemolysis means partial haemolysis; this is
represented as a greenish zone produced on blood
agar.
Beta-haemolysis is complete haemolysis; it is
represented as a clear zone produced on blood agar.

Gram(+) cocci
Of the catalase(-) gram(+) cocci, there are the alpha-,

beta- and gamma-haemolytics.

Alpha-haemolysis means partial haemolysis; this is
represented as a greenish zone produced on blood
agar.
Beta-haemolysis is complete haemolysis; it is
represented as a clear zone produced on blood agar.
Gamma-haemolysis is no haemolysis, or variable
haemolysis.

Gram(+) cocci
The alpha-haemolytics are S. pneumoniae and S.

viridans.

Gram(+) cocci
The alpha-haemolytics are S. pneumoniae and S.

viridans.
S. pneumoniae and S. viridans are dierentiated in
culture bc S. pneumoniae is optochin-sensitive but
S. viridans is optochin-resistant.

Gram(+) cocci
The alpha-haemolytics are S. pneumoniae and S.

viridans.
S. pneumoniae and S. viridans are dierentiated in
culture bc S. pneumoniae is optochin-sensitive but
S. viridans is optochin-resistant.
In a question, they might tell you a catalase(-),
optochin-sensitive organism or an optochin-
resistant organism that produced a green zone on
blood agar. The former and latter are S. pneumonia
and S. viridans, respectively.

Gram(+) cocci
The other thing thats important about S. pneumoniae

vs S. viridans is that S. pneumoniae cannot grow in

bile but S. viridans can. Thats a big one.

Gram(+) cocci
The other thing thats important about S. pneumoniae

vs S. viridans is that S. pneumoniae cannot grow in

bile but S. viridans can. Thats a big one.
If they mention optochin-S vs optochin-R, you got
lucky. Sometimes theyll mention that an organism
grew in bile and produced partial haemolysis S.
viridans. If the organism produced a green-zone of
haemolysis and died in bile S. pneumoniae. That
point is of moderate-yield, but the optochin S vs R is
by far the most important to remember.

Gram(+) cocci
The beta-haemolytics are S. pyogenes (group-A) and

S. agalactiae (group-B).

Gram(+) cocci
The beta-haemolytics are S. pyogenes (group-A) and

S. agalactiae (group-B).
They are dierentiated based on bacitracin, where S.
pyogenes is bacitracin-sensitive and S. agalactiae is
bacitracin-resistant.

Gram(+) cocci
The gamma-haemolytics are Enterococcus and S.

bovis.

Gram(+) cocci
The gamma-haemolytics are Enterococcus and S.

bovis.
They both grow really well in bile.

Gram(+) cocci
The gamma-haemolytics are Enterococcus and S.

bovis.
They both grow really well in bile.
Theyre dierentiated bc Enterooccus can survive in
high [NaCl] (6.5%), whereas S. bovis cant. Thats
HY.

Gram(+) cocci
The gamma-haemolytics are Enterococcus and S.

bovis.
They both grow really well in bile.
Theyre dierentiated bc Enterooccus can survive in
high [NaCl] (6.5%), whereas S. bovis cant. Thats
HY.
FA says Enterococcus has either gamma- or alpha-
haemolysis, but Ive only ever encountered questions
that have assessed Enterococcus as gamma-
haemolytic. If they refer to Enterococcus via
culturing, theyll always mention that it grows well in

Gram(+) cocci
Ive seen in a question where they wanted to know

how to dierentiate between S. viridans and

Enterococcus endocarditis (via culturing only, not pt
Hx).

Gram(+) cocci
Ive seen in a question where they wanted to know

how to dierentiate between S. viridans and

Enterococcus endocarditis (via culturing only, not pt
Hx).
Both grow well in bile, but only S. viridans is
optochin-resistant. So not only does optochin
resistance distinguish S. viridans from S. pneumoniae,
but it also distinguishes it from Enterococcus.

Gram(+) cocci
An added layer of complexity is that S. aureus, like

Enterococcus, also grows well at high [salt]. Whilst

the mentioning of salt concentration is necessary for
distinguishing Enterococcus from S. bovis in culture,
[salt] is not necessary for distinguishing S. aureus
from the other Staph bc coagulase is always used for
that. Therefore, in terms of the USMLE, if they
mention an organism growing well in salt and S.
aureus is an answer choice, be aware that it could be
right (Ive seen this show up in a couple questions).

Gram(+) rods

Gram(+) rods
Spore-forming and non-spore-forming

Gram(+) rods
Spore-forming and non-spore-forming
Spore-forming are divided into aerobic and anaerobic

Gram(+) rods
Spore-forming and non-spore-forming
Spore-forming are divided into aerobic and anaerobic
Of the aerobic spore-forming gram(+) rods, weve got

Bacillus cereus and Bacillus anthracis. B. cereus is

motile but B. anthracis is non-motile.

Gram(+) rods
Spore-forming and non-spore-forming
Spore-forming are divided into aerobic and anaerobic
Of the aerobic spore-forming gram(+) rods, weve got

Bacillus cereus and Bacillus anthracis. B. cereus is

motile but B. anthracis is non-motile.
Of the anaerobic spore-forming gram(+) rods, weve
got the Clostridia, where C. dicile, tetani and
botulinum are all motile but C. perfringens is non-
motile.

Gram(+) rods
Of the non-spore-forming gram(+) rods, weve got

Listeria monocytogenes and Corynebacterium

diptheriae.

Gram(+) rods
Of the non-spore-forming gram(+) rods, weve got

Listeria monocytogenes and Corynebacterium

diptheriae.
Listeria is motile but C. diptheriae is non-motile.

Gram(+) lamentous rods

Gram(+) lamentous rods

Weve got Nocardia and Actinomyces

Gram(+) lamentous rods

Weve got Nocardia and Actinomyces
Nocardia is aerobic and weakly acid-fast.

Gram(+) lamentous rods

Weve got Nocardia and Actinomyces
Nocardia is aerobic and weakly acid-fast.
Actinomyces is anaerobic and not acid-fast.

 Now Im going to discuss the individual organisms

more specically

S. aureus

S. aureus
S. aureus food poisoning is due to ingestion of pre-

formed toxin. Mega-HY. Theyll tell you someone

got vomiting several hours after eating potato salad
or custard, and then theyll ask you for the type of
toxin (e.g. spore, pre-formed toxin, capsule, etc.), and
youve gotta know its pre-formed toxin of S. aureus.

S. aureus
S. aureus food poisoning is due to ingestion of pre-

formed toxin. Mega-HY. Theyll tell you someone

got vomiting several hours after eating potato salad
or custard, and then theyll ask you for the type of
toxin (e.g. spore, pre-formed toxin, capsule, etc.), and
youve gotta know its pre-formed toxin of S. aureus.
S. aureus is also beta-haemolytic.

S. aureus
S. aureus food poisoning is due to ingestion of pre-

formed toxin. Mega-HY. Theyll tell you someone

got vomiting several hours after eating potato salad
or custard, and then theyll ask you for the type of
toxin (e.g. spore, pre-formed toxin, capsule, etc.), and
youve gotta know its pre-formed toxin of S. aureus.
S. aureus is also beta-haemolytic.
This means S. aureus has pore-forming ability.
Ohemgeeeee. If you lyse the RBC, youre forming a
pore in it Group A/B Strep and S. aureus all do
this.

S. aureus
It grows in clusters. Sometimes thats all theyll

mention gram(+) cocci growing in clusters

Booom! S. aureus.

S. aureus
It grows in clusters. Sometimes thats all theyll

mention gram(+) cocci growing in clusters

Booom! S. aureus.
Protein A binds the Fc region of IgG, thereby
preventing opsonization and phagocytosis. Theyll
ask you directly what the function of protein A is, and
thats the answer.

S. aureus
For SSSS (Staphylococcal scalded skin syndrome),

youve gotta know that epidermolytic toxins A+B bind

to desmoglein 1 of desmosomes, causing pemphigus
vulgaris-like Sx with a (+) Nikolsky sign; the skin
splits at the stratum granulosum.

S. aureus
For SSSS (Staphylococcal scalded skin syndrome),

youve gotta know that epidermolytic toxins A+B bind

to desmoglein 1 of desmosomes, causing pemphigus
vulgaris-like Sx with a (+) Nikolsky sign; the skin
splits at the stratum granulosum.
Dont worry, Ill break that down

S. aureus
For SSSS (Staphylococcal scalded skin syndrome),

youve gotta know that epidermolytic toxins A+B bind

to desmoglein 1 of desmosomes, causing pemphigus
vulgaris-like Sx with a (+) Nikolsky sign; the skin
splits at the stratum granulosum.
Dont worry, Ill break that down
Desmosomes are in your macula adherens of the
skin and hold adjacent keratinocytes together.
Desmogleins are important desmosomal proteins.
Nikolsky sign is sloughing of the skin with friction.

S. aureus
All of that in the prior slide is HY in one way, shape or

form. Youve gotta know that desmogleins are

components of desmosomes. Youve gotta remember
that desmosomes are sideways (holding adjacent cells
together, whereas hemidesmosomes hold cells to the
BM), and that desmosomal disruption is stratum
granulosal.

S. aureus
All of that in the prior slide is HY in one way, shape or

form. Youve gotta know that desmogleins are

components of desmosomes. Youve gotta remember
that desmosomes are sideways (holding adjacent cells
together, whereas hemidesmosomes hold cells to the
BM), and that desmosomal disruption is stratum
granulosal.
TSST-1 toxin, which causes TSS, causes
desquamation of the hands/soles after ~2wks. It is
a superantigen (bridges MHC-II to TCR; ultra-HY).

S. aureus
SSSS in a baby is called Ritter syndrome.

S. aureus
SSSS in a baby is called Ritter syndrome.
The desquamation of the hands/feet = peeling of the

skin.

S. aureus
The TSST-1 toxin is associated with packaged cotton

or tampons. That is so high-yield I want to cry.

Theyll give you a vignette of someone with a face
injury who went into shock and had had cotton-
packing in the nose, and then theyll ask you for the
immunological receptors TCR and MHC-II. That
would reect the superantigenic mechanism of the
TSST-1.

S. aureus
The TSST-1 toxin is associated with packaged cotton

or tampons. That is so high-yield I want to cry.

Theyll give you a vignette of someone with a face
injury who went into shock and had had cotton-
packing in the nose, and then theyll ask you for the
immunological receptors TCR and MHC-II. That
would reect the superantigenic mechanism of the
TSST-1.
(That is in contrast to endotoxins, which bind CD14
on macrophages also HY)

S. aureus
Dont screw that up. If the pt goes into shock and has

had packing, its not an endotoxin; its a

superantigen (TSST-1).

S. aureus
Dont screw that up. If the pt goes into shock and has

had packing, its not an endotoxin; its a

superantigen (TSST-1).
Another thing: the pre-formed toxin that causes food
poisoning is heat-resistant. Ive seen that in a
question.

S. aureus
Dont screw that up. If the pt goes into shock and has

had packing, its not an endotoxin; its a

superantigen (TSST-1).
Another thing: the pre-formed toxin that causes food
poisoning is heat-resistant. Ive seen that in a
question.
MRSA is spread in hospitals via asymptomatic
hospital sta. Carrier site is in the nares.

S. aureus
MSSA MRSA via altered PBP2a.

S. aureus
MSSA MRSA via altered PBP2a.
Youve gotta know that methicillin/nafcillin/oxacillin/

dicloxacillin resistance is via altered penicillin-

binding protein. That is so ludicrously high-yield.

S. aureus
MSSA MRSA via altered PBP2a.
Youve gotta know that methicillin/nafcillin/oxacillin/

dicloxacillin resistance is via altered penicillin-

binding protein. That is so ludicrously high-yield.
Thats because methicillin (and the others) is heavily
steric, so its already beta-lactamase resistant.
Therefore we know that if MSSA MRSA, it had
nothing to do with beta-lactamase, but instead the
PBP. Transpeptidase is a PBP. Mad high-yield.

S. aureus
Common cause of pneumonia after inuenza

infection. Theyll tell you a pt had a cold that

resolved and then he/she came down with a
pneumonia; then theyll ask for the organism S.
aureus, NOT S. pneumoniae.

S. aureus
Common cause of pneumonia after inuenza

infection. Theyll tell you a pt had a cold that

resolved and then he/she came down with a
pneumonia; then theyll ask for the organism S.
aureus, NOT S. pneumoniae.
S. aureus secretes DNAse.

S. aureus
Common cause of pneumonia after inuenza

infection. Theyll tell you a pt had a cold that

resolved and then he/she came down with a
pneumonia; then theyll ask for the organism S.
aureus, NOT S. pneumoniae.
S. aureus secretes DNAse.
H. inuenzae can be grown alongside S. aureus
bc S. aureus supplies NAD+ for growth (in
contrast, H. inuenzae cannot grow with S.
pneumoniae bc the latter produces H2O2).

S. aureus
I almost forgot to mention: the TSST-1 toxin of S.

aureus, yes, it bridges the MHC-II to TCR, but it more

specically binds the V-beta region of the TCR.
USMLE likes you to know that there are only 25 V-
beta regions on human TCRs, so toxin-induced
activation of merely a few V-betas can cause massive
lymphyocyte response.

S. aureus
I almost forgot to mention: the TSST-1 toxin of S.

aureus, yes, it bridges the MHC-II to TCR, but it more

specically binds the V-beta region of the TCR.
USMLE likes you to know that there are only 25 V-
beta regions on human TCRs, so toxin-induced
activation of merely a few V-betas can cause massive
lymphyocyte response.
Most common cause of acute bacterial endocarditis
in a pt with NO history of heart problems.

S. epidermidis
Endocarditis in prosthetic valve pts

S. epidermidis
Endocarditis in prosthetic valve pts
Produces biolms that enable adhesion to catheters

S. epidermidis
Endocarditis in prosthetic valve pts
Produces biolms that enable adhesion to catheters
Tx for S. epidermidis endocarditis is immediate

VANCOMYCIN. This is because the vast vast

majority of S. epidermidis is already methicillin-
resistant, so you immediately assume MRSE and skip
the methicillin. S. epidermidis is a common cause of
culture contamination, but if the real deal is in fact S.
epidermidis vancomycin, not methicillin.

S. saprophy9cus
The only thing that comes to mind onand is that its

the third most common cause of UTI in women and

its urease-positive, meaning it causes struvite
stones. The struvite stones are ammonium
magnesium phosphate, NOT calcium, and will be
seen as large and horn-like on ultrasound.

S. saprophy9cus
The only thing that comes to mind onand is that its

the third most common cause of UTI in women and

its urease-positive, meaning it causes struvite
stones. The struvite stones are ammonium
magnesium phosphate, NOT calcium, and will be
seen as large and horn-like on ultrasound.
Theyll tell you some chick has struvite stones and will
want you to know that Tx = acidifying the urine
(whereas all other stones abate via augmenting
basicity [e.g. cystine stones, por ejemplo, give citrate])

S. pneumoniae
Most common cause of lobar pneuomia in adults and

elderly.

S. pneumoniae
Most common cause of lobar pneuomia in adults and

elderly.
Youll see it in questions as consolidation in one of
the lobes, whereas mycoplasma interstitial (atypical)
pneumonia would be diuse crackles, for instance.

S. pneumoniae
Most common cause of lobar pneuomia in adults and

elderly.
Youll see it in questions as consolidation in one of
the lobes, whereas mycoplasma interstitial (atypical)
pneumonia would be diuse crackles, for instance.
It grows in pairs (diplococci). Crazy HY. Sometimes
theyll tell you theres a gram(+) coccus causing an
infection and then theyll show you an image. Be able
to identify the pairs. Thats a 240+ question; its HY,
but many students still wont know it.

S. pneumoniae
The USMLE also wants you to know its lancet-

shaped. Ive seen this in a couple questions, where it

literally depended on knowing that detail to get the
answer right. FA also mentions this. So lancet-
shaped diploccoci (lancet-shaped pairs).

S. pneumoniae
The USMLE also wants you to know its lancet-

shaped. Ive seen this in a couple questions, where it

literally depended on knowing that detail to get the
answer right. FA also mentions this. So lancet-
shaped diploccoci (lancet-shaped pairs).
The capsule is the most important virulence factor
when S. pneumoniae causes meningitis. Thats HY.

S. pneumoniae
The USMLE also wants you to know its lancet-

shaped. Ive seen this in a couple questions, where it

literally depended on knowing that detail to get the
answer right. FA also mentions this. So lancet-
shaped diploccoci (lancet-shaped pairs).
The capsule is the most important virulence factor
when S. pneumoniae causes meningitis. Thats HY.
Pneumolysin is what causes the alpha-haemolysis.

S. pneumoniae
The USMLE also wants you to know its lancet-

shaped. Ive seen this in a couple questions, where it

literally depended on knowing that detail to get the
answer right. FA also mentions this. So lancet-
shaped diploccoci (lancet-shaped pairs).
The capsule is the most important virulence factor
when S. pneumoniae causes meningitis. Thats HY.
Pneumolysin is what causes the alpha-haemolysis.
S. pneumonia is associated with rusty sputum.
Thats really common to see in questions.

S. pneumoniae
Since the vaccine for S. pneumoniae is developed

against the capsule, and the capsule is polysaccharidic

(T-cell independent; meaning its not displayed on
MHC-II), the resultant immune response only
produces IgM bc you need the T-cell response for B-
cell-mediated Ab-class-switching. Normally, c3b and
IgG are the immune systems major opsonins. If they
ask you for the major opsonin following vaccine
administration, you know it has to be c3b, not IgG,
because the latter isnt produced in response to the
vaccine.

S. pneumoniae
Capsule causes Quellung reaction, which is

capsule swelling after application of anti-serum &

methylene blue. just be very aware that any
mention of capsule swelling (or swelling in general) is
S. pneumoniae.

S. pneumoniae
Macrolides are the Tx of choice for outpatient

pneumonia. This is because macrolides can treat S.

pneumoniae, but they also treat the atypicals if the
pneumonia is caused by one of those.

S. pneumoniae
Macrolides are the Tx of choice for outpatient

pneumonia. This is because macrolides can treat S.

pneumoniae, but they also treat the atypicals if the
pneumonia is caused by one of those.
Meningitis pathway: 1) primary lung focus 2) blood
3) meninges

S. pneumoniae
Macrolides are the Tx of choice for outpatient

pneumonia. This is because macrolides can treat S.

pneumoniae, but they also treat the atypicals if the
pneumonia is caused by one of those.
Meningitis pathway: 1) primary lung focus 2) blood
3) meninges
Produces IgA protease, which enables lung
colonization; when the organism cleaves IgA, there
is an increased probability of its attachment to the
mucosa bc IgA obviously isnt there to clear it.

S. viridans
Like S. epidermidis, S. viridans also produces a

biolm, but it binds to tooth enamel.

S. viridans
Like S. epidermidis, S. viridans also produces a

biolm, but it binds to tooth enamel.

When S. viridans causes subacute endocarditis on
previously damaged valves, it binds to FIBRIN that is
deposited on the valve. This is because S. viridans can
produce an extracellular polysaccharide (dextran)
from sucrose/glucose that can bind brin. I was
asked this in a question.

S. pyogenes
Auto-antibodies to M-protein are responsible for

rheumatic fever (type-II HS)

S. pyogenes
Auto-antibodies to M-protein are responsible for

rheumatic fever (type-II HS)

Scarlet fever has beefy red oropharynx (they might
not mention the strawberry tongue)

S. pyogenes
Auto-antibodies to M-protein are responsible for

rheumatic fever (type-II HS)

Scarlet fever has beefy red oropharynx (they might
not mention the strawberry tongue)
Causes impetigo vesicles that turn into pustules
with honey-colored crust (bullous impetigo [NOT the
same as bullous pemphigoid] is classically S. aureus,
but for impetigo in general, S. pyogenes > S. aureus)

S. pyogenes
Auto-antibodies to M-protein are responsible for

rheumatic fever (type-II HS)

Scarlet fever has beefy red oropharynx (they might
not mention the strawberry tongue)
Causes impetigo vesicles that turn into pustules
with honey-colored crust (bullous impetigo [NOT the
same as bullous pemphigoid] is classically S. aureus,
but for impetigo in general, S. pyogenes > S. aureus)
ASO titre detects recent S. pyogenes infection

S. agalac9ae
Produces CAMP factor. **This is NOT the same as

cAMP.** CAMP stands for the four authors of the

test, but remember that CAMP test is S. agalactiae.

S. agalac9ae
Produces CAMP factor. **This is NOT the same as

cAMP.** CAMP stands for the four authors of the

test, but remember that CAMP test is S. agalactiae.
CAMP factor enlarges the area of haemolysis
produced by S. aureus. Seems like an unnecessary
detail, but Ive seen it in a question, and its in FA.

S. agalac9ae
Produces CAMP factor. **This is NOT the same as

cAMP.** CAMP stands for the four authors of the

test, but remember that CAMP test is S. agalactiae.
CAMP factor enlarges the area of haemolysis
produced by S. aureus. Seems like an unnecessary
detail, but Ive seen it in a question, and its in FA.
Pregnant women are screened for Group-B Strep at
35-37 wks; INTRAPARTUM penicillin is prophylaxis
(that is crazy HY; theyll ask you specically for when
the penicillin is given, and its intrapartum NOT
BEFORE DELIVERY, not after, intrapartum)

S. agalac9ae
Another way of assessing that the CAMP factor

enlarges the area of haemolysis caused by S. aureus, is

that theyll see if you realize that means CAMP factor
is an incomplete haemolysin.

S. agalac9ae
Another way of assessing that the CAMP factor

enlarges the area of haemolysis caused by S. aureus, is

that theyll see if you realize that means CAMP factor
is an incomplete haemolysin.
Sometimes theyll ask you for the organism that
causes stillborn fetuses, and its Group-B Strep;
theyll mention rupture of the membranes w/ foul-
smelling uid. So if they mention premature rupture
of the membranes, remember S. agalactiae.

Enterococcus
Normal GI ora that can cause endocarditis in

patients whove had URINARY TRACT

INFECTIONS. Thats a question most people will get
wrong and will get you a high score. Theyll tell you a
68 yr-old guy has had trouble micturating and then
hes got a murmur. Youve gotta know that UTIs are
common secondary to BPH, and endocarditis that
results subsequently is commonly Enterococcus.
Youre learning that now, but internalize it. If you get
a vignette of a pt with BPH UTI Enterococcus
endocarditis.

Enterococcus
Lanceeld grouping, which dierentiates one type of

Strep from another, is based on dierences in C

carbohydrate groups.

Enterococcus
Lanceeld grouping, which dierentiates one type of

Strep from another, is based on dierences in C

carbohydrate groups.
AMPICILLIN is the 1st-line Tx against Enterococci.

Enterococcus
Lanceeld grouping, which dierentiates one type of

Strep from another, is based on dierences in C

carbohydrate groups.
AMPICILLIN is the 1st-line Tx against Enterococci.
That ampicillin tidbit is really HY.

Enterococcus
Lanceeld grouping, which dierentiates one type of

Strep from another, is based on dierences in C

carbohydrate groups.
AMPICILLIN is the 1st-line Tx against Enterococci.
That ampicillin tidbit is really HY.
VRE (vancomycin-resistant Enterococcus) occurs in
hospitals, and streptogramins (dalfopristin /
quinupristin) are used to treat it.

Enterococcus
Lanceeld grouping, which dierentiates one type of

Strep from another, is based on dierences in C

carbohydrate groups.
AMPICILLIN is the 1st-line Tx against Enterococci.
That ampicillin tidbit is really HY.
VRE (vancomycin-resistant Enterococcus) occurs in
hospitals, and streptogramins (dalfopristin /
quinupristin) are used to treat it.
So for Tx, ampicillin; if resistant vancomycin; if
resistant streptogramin (-pristin drug)

Enterococcus
Enterococci are rarely resistant to DAPTOMYCIN.

Remember this drug from the antibiotics lecture? I

had seen this in a question where they mentioned the
Enterococcus was ampicillin-resistant and then
wanted to know which drug would treat it.
Daptomycin was the answer, and the explanation said
that Enterococci are rarely resistant to it. That
simple.

S. bovis
Causes endocarditis in colon cancer patients.

Thats it. Thats all you need to know (apart from the
fact that it doesnt grow well in salt, like
Enterococcus does; and remember that it does grows
well in bile, same as with Enterococcus).

Bacillus cereus
Common infection is following consumption of fried

or reheated rice.

Bacillus cereus
Common infection is following consumption of fried

or reheated rice.
USMLE wants you to know that bacteria contaminate
uncooked rice, then when the rice is heated to high
temperatures, the bacteria form protective spores.
Then, when the rice cools, toxin is liberated. It is the
toxin, NOT BACTERIUM, that causes watery
diarrhea.

Bacillus anthracis
Highest-yield = only bacterium with a protein

capsule (poly-D-glutamate).

Bacillus anthracis
Highest-yield = only bacterium with a protein

capsule (poly-D-glutamate).
Black eschar skin lesions are how youll see
cutaneous anthrax in questions. Theyll mention the
black color, and theyll mention the edematous
ring. The black color is necrosis (lethal factor); the
edematous ring is caused by edema factor.

Bacillus anthracis
Highest-yield = only bacterium with a protein

capsule (poly-D-glutamate).
Black eschar skin lesions are how youll see
cutaneous anthrax in questions. Theyll mention the
black color, and theyll mention the edematous
ring. The black color is necrosis (lethal factor); the
edematous ring is caused by edema factor.
Black eschar forms ~1 wk after rupture of ulcer. The
ulcer is painLESS. Painless! Black eschar / ulcer that
is painless, with well-dened borders.

Bacillus anthracis
Pulmonary anthrax occurs through inhalation of

spores and causes mediastinitis. Thats huge.

Remember pulmonary haemorrhage and
mediastinitis. This might be seen in a question as
widened mediastinum on CXR.

Bacillus anthracis
Pulmonary anthrax occurs through inhalation of

spores and causes mediastinitis. Thats huge.

Remember pulmonary haemorrhage and
mediastinitis. This might be seen in a question as
widened mediastinum on CXR.
Produces long chains that have a serpentine or
medusa head appearance when cultured

Clostridium botulinum
Produces toxin that inhibits ACh release from

presynaptic neurons, causing accid paralysis

Clostridium botulinum
Produces toxin that inhibits ACh release from

presynaptic neurons, causing accid paralysis

The toxin is ingested as pre-formed toxin in
ADULTS (canned foods) and as spores in BABIES
(honey). Really break down that sentence. In
ADULTS, the toxin is PRE-FORMED and is typically
ingested through improperly sterilized CANNED
GOODS; in BABIES, they ingest SPORES through
HONEY. Theyll see if you know the dierences with
this one. Most people wont remember the pre-
formed toxin vs spores in adults vs babies tidbit.

Clostridium botulinum
Floppy baby syndrome is the term given to babies

aected by C. botulinum. There is loss of head

control. However, constipation precedes other Sx.

Clostridium dicile
Causes pseudomembranous colitis secondary to

clindamycin or ampicillin-use (disruption of normal

ora leads to C. dicile overgrowth)

Clostridium dicile
Causes pseudomembranous colitis secondary to

clindamycin or ampicillin-use (disruption of normal

ora leads to C. dicile overgrowth)
The test to Dx pseudomembranous colitis is the AB-
toxin test. Theyll throw some tempting answer
choices in there (e.g. stool culture), but the answer is
stool TOXIN TEST, NOT culture.

Clostridium dicile
The MOA of C. dicile-induced enterocytic necrosis

is CYTOSKELETAL DISRUPTION via ACTIN

DEPOLYMERIZATION. I had seen that in two
dierent practice questions.

Clostridium dicile
The MOA of C. dicile-induced enterocytic necrosis

is CYTOSKELETAL DISRUPTION via ACTIN

DEPOLYMERIZATION. I had seen that in two
dierent practice questions.
C. dicle, when it becomes resistant to ampicillin,
does so via sporulation at high [antibiotic].

Clostridium dicile
The MOA of C. dicile-induced enterocytic necrosis

is CYTOSKELETAL DISRUPTION via ACTIN

DEPOLYMERIZATION. I had seen that in two
dierent practice questions.
C. dicle, when it becomes resistant to ampicillin,
does so via sporulation at high [antibiotic].
TOXIC MEGACOLON is the most serious
complication of pseudomembranous colitis.

Clostridium tetani
Producs tetanospasmin, an exotoxin causing tetanus

Clostridium tetani
Producs tetanospasmin, an exotoxin causing tetanus
The exotoxin prevents glycine (an inhibitor

neurotransmitter in the spinal cord) from exiting the

presynaptic neuron, thereby causing SPASTIC
paralysis (NOT accid paralysis).

Clostridium tetani
Producs tetanospasmin, an exotoxin causing tetanus
The exotoxin prevents glycine (an inhibitor

neurotransmitter in the spinal cord) from exiting the

presynaptic neuron, thereby causing SPASTIC
paralysis (NOT accid paralysis).
They like to ask sometimes which two organisms have
TOXINS with similar MOA, and they are C. tetani
and C. botulinum, bc both organisms TOXINS
prevent the release of a presynaptic neurotransmitter.

Clostridium tetani
The USMLE wants you to know that C. tetani

ENTERS WOUNDS. Ok? It enters wounds. The

spores germinate in the anaerobic environment of the
wound and ascend MOTOR neurons to the spinal
cord. Holy cow. MOTOR neurons. NOT sensory
neurons. MOTOR neurons.

Clostridium tetani
The USMLE wants you to know that C. tetani

ENTERS WOUNDS. Ok? It enters wounds. The

spores germinate in the anaerobic environment of the
wound and ascend MOTOR neurons to the spinal
cord. Holy cow. MOTOR neurons. NOT sensory
neurons. MOTOR neurons.
Tetanus causes TRISMUS, which is lock-jaw. Dont
confuse this with tenesmus, which is the incessant/
intractable sensation of needing to defecate. Ive seen
both as answers to the same tetanus question.

Clostridium tetani
If they mention in a question that a baby has

opisthotonos (severe arching of the back due to

spasm), and then they ask you for how the condition
occurred, it was via bacterial entry through the
umbilicus.

Clostridium perfringens
Produces gas gangrene of the skin. If they ever ask

you a question about necrosis and the skin,

particularly if there is gas (CO2) involved (or
crinkling/crunching of the skin) C. perfringens.

Clostridium perfringens
Produces gas gangrene of the skin. If they ever ask

you a question about necrosis and the skin,

particularly if there is gas (CO2) involved (or
crinkling/crunching of the skin) C. perfringens.
The toxin is a lecithinase, or phospholipase. Its
called alpha-toxin. Just memorize that. What can
you do? Just memorize it. It will come up in
questions.

Clostridium perfringens
Produces gas gangrene of the skin. If they ever ask

you a question about necrosis and the skin,

particularly if there is gas (CO2) involved (or
crinkling/crunching of the skin) C. perfringens.
The toxin is a lecithinase, or phospholipase. Its
called alpha-toxin. Just memorize that. What can
you do? Just memorize it. It will come up in
questions.
C. perfringens also causes WATERY DIARRHEA.
Thats HY.

Listeria monocytogenes
Beta-haemolytic will show a thin zone of beta-

haemolysis on blood agar. That showed up in a

question. The beta-haemolytics are most notably S.
pyogenes and S. agalactiae, but questions occasionally
in the 250+ range might ask to see if you know S.
aureus and Listeria also are.

Listeria monocytogenes
Beta-haemolytic will show a thin zone of beta-

haemolysis on blood agar. That showed up in a

question. The beta-haemolytics are most notably S.
pyogenes and S. agalactiae, but questions occasionally
in the 250+ range might ask to see if you know S.
aureus and Listeria also are.
TUMBLING motility. Thats HY. USMLE likes that.
They want you to know TUMBLING is Listeria and
SWARMING is Salmonella. Memorize that.

Listeria monocytogenes
USMLE also wants you to know (and my Gd this is

HY) that Listeria grows well at FOUR-DEGREES C.

Yersinia enterocolitica also grows well at 4C.
Remember both of those.

Listeria monocytogenes
USMLE also wants you to know (and my Gd this is

HY) that Listeria grows well at FOUR-DEGREES C.

Yersinia enterocolitica also grows well at 4C.
Remember both of those.
In a pregnant woman with Listeriosis, be aware that
nausea, diarrhea, fever + myalgias are MORE
COMMON THAN spontaneous abortion.

Listeria monocytogenes
USMLE also wants you to know (and my Gd this is

HY) that Listeria grows well at FOUR-DEGREES C.

Yersinia enterocolitica also grows well at 4C.
Remember both of those.
In a pregnant woman with Listeriosis, be aware that
nausea, diarrhea, fever + myalgias are MORE
COMMON THAN spontaneous abortion.
ONLY GRAM(+) ORGANISM WITH ENDOTOXIN

Listeria monocytogenes
Causes granulomatous infantiseptica in neonates if

the pregnant woman had Listeriosis. Youll see this in

a question as a baby with pyogenic granulomas
throughout the body.

Listeria monocytogenes
Causes granulomatous infantiseptica in neonates if

the pregnant woman had Listeriosis. Youll see this in

a question as a baby with pyogenic granulomas
throughout the body.
Pregnant women tend to get Listeria through DELI
MEET OR UNPASTEURIZED MILK. Ive seen both
in questions.

Listeria monocytogenes
Causes granulomatous infantiseptica in neonates if

the pregnant woman had Listeriosis. Youll see this in

a question as a baby with pyogenic granulomas
throughout the body.
Pregnant women tend to get Listeria through DELI
MEET OR UNPASTEURIZED MILK. Ive seen both
in questions.
Give ampicillin to Tx Listeria.

Listeria monocytogenes
Causes granulomatous infantiseptica in neonates if

the pregnant woman had Listeriosis. Youll see this in

a question as a baby with pyogenic granulomas
throughout the body.
Pregnant women tend to get Listeria through DELI
MEET OR UNPASTEURIZED MILK. Ive seen both
in questions.
Give ampicillin to Tx Listeria.
Forms actin rockets via which it moves cell to cell.

Listeria monocytogenes
They like you to know its a gram(+) rod. Theyll

mention a baby has meningitis, and then theyll

mention gram(+) rods on the lab report Listeria.
Listeria is the third most common cause of neonatal
meningitis, behind Group-B Strep and E. coli.

Listeria monocytogenes
They like you to know its a gram(+) rod. Theyll

mention a baby has meningitis, and then theyll

mention gram(+) rods on the lab report Listeria.
Listeria is the third most common cause of neonatal
meningitis, behind Group-B Strep and E. coli.
Listeria is a facultative intracellular organism. Its in
FA and Ive seen it asked in a really slick question.
Theyll imply Listeriosis in a neonate then ask you for
the mechanism of immunity, and its IMPROVED
INTRACELLULAR KILLING.

Corynebacterium diptheriae
Appears as CHINESE CHARACTERS per light

microscropy

Corynebacterium diptheriae
Appears as CHINESE CHARACTERS per light

microscropy
Youve gotta remember that the exotoxin is encoded
by a lysogenic phage (FA has the ABCDE pneumonic
for this shigA-like toxin, Botulinum, Cholera toxin,
Diptheria toxin, Erythrogenic toxin of S. pyogenes).
This has shown up in numerous questions. Know
these ve toxins are encoded by lysogenic phage.

Corynebacterium diptheriae
The toxin ADP-ribosylates EF-2 (elongation factor

2). They want you to know both C. diptheriae and P.

aeruginosa both act via this MOA. This causes
DECREASED PROTEIN SYNTHESIS. Thats HY.

Corynebacterium diptheriae
The toxin ADP-ribosylates EF-2 (elongation factor

2). They want you to know both C. diptheriae and P.

aeruginosa both act via this MOA. This causes
DECREASED PROTEIN SYNTHESIS. Thats HY.
The toxin is AB5. A-toxin causes the ADP-
ribosylation. Each of the 5 B-toxins bind to cardiac +
neural cells. Remember that B binds and A ADP-
ribosylates.

Corynebacterium diptheriae
Produces METACHROMATIC BLUE-RED

GRANULES. Thats also shown up in questions and is

in FA.

Corynebacterium diptheriae
Produces METACHROMATIC BLUE-RED

GRANULES. Thats also shown up in questions and is

in FA.
You might see that as polyphosphate granules
evident with methylene blue staining. USMLE is
slick.

Corynebacterium diptheriae
Produces METACHROMATIC BLUE-RED

GRANULES. Thats also shown up in questions and is

in FA.
You might see that as polyphosphate granules
evident with methylene blue staining. USMLE is
slick.
Grows as club-shaped rods.

Corynebacterium diptheriae
Produces METACHROMATIC BLUE-RED

GRANULES. Thats also shown up in questions and is

in FA.
You might see that as polyphosphate granules
evident with methylene blue staining. USMLE is
slick.
Grows as club-shaped rods.
Pathway of infection: 1) brinous exudate 2)
systemic circulation 3) cardiac tissue + cortical
neurons

Corynebacterium diptheriae
C. diptheriae produces K-antigen, an anti-phagocytic

capsule.

Corynebacterium diptheriae
C. diptheriae produces K-antigen, an anti-phagocytic

capsule.
In terms of Tx, the most important is diptheria
ANTITOXIN. This is >>> more important than the
DPT vaccine. DPT vaccine is preventative, but if
someone has diptheria, give the antitoxin rst, THEN
the vaccine.

Corynebacterium diptheriae
C. diptheriae produces K-antigen, an anti-phagocytic

capsule.
In terms of Tx, the most important is diptheria
ANTITOXIN. This is >>> more important than the
DPT vaccine. DPT vaccine is preventative, but if
someone has diptheria, give the antitoxin rst, THEN
the vaccine.
Cardiomyopathy is the leading cause of death in
diptheria.

Corynebacterium diptheriae
Classically presents with GREY OROPHARYNGEAL

EXUDATES.

Ac9nomyces
They like you to know that it produces yellow sulfur

granules.

Ac9nomyces
They like you to know that it produces yellow sulfur

granules.
It causes draining facial abscesses.

Ac9nomyces
They like you to know that it produces yellow sulfur

granules.
It causes draining facial abscesses.
Its anaerobic and non-acid-fast.

Ac9nomyces
They like you to know that it produces yellow sulfur

granules.
It causes draining facial abscesses.
Its anaerobic and non-acid-fast.
Treat with penicillin (SNAP Sulfonamides for
Nocardia; Actinomyces use penicillin)

Ac9nomyces
They like you to know that it produces yellow sulfur

granules.
It causes draining facial abscesses.
Its anaerobic and non-acid-fast.
Treat with penicillin (SNAP Sulfonamides for
Nocardia; Actinomyces use penicillin)
FILAMENTOUS rod

Nocardia
Weakly acid-fast and aerobic

Nocardia
Weakly acid-fast and aerobic
Can cause pulmonary infection in

immunocompromised that resembles TB. Thats

HY.

Nocardia
Weakly acid-fast and aerobic
Can cause pulmonary infection in

immunocompromised that resembles TB. Thats

HY.
The necrosis that occurs with Nocardia is caseating
(like TB).

Nocardia
Weakly acid-fast and aerobic
Can cause pulmonary infection in

immunocompromised that resembles TB. Thats

HY.
The necrosis that occurs with Nocardia is caseating
(like TB).
Treat with sulfonamides (SNAP).

Nocardia
I had seen a bizarre question once of a pt with

osteomyelitis caused by a gram(+) lamentous rod. I

was like wtf, but assumed the osseous environment is
anaerobic bc its so deep, so I went with Actinomyces
over Nocardia, but the answer was Nocardia. Well-
perfused bone can support Nocardia growth. The
explanation said Nocardia can sometimes cause
osteomyelitis, but Actinomyces doesnt. Just be aware
of that. Thats it.