USMLE gram(+)

bacteria
Phloston

Three main classifications to be aware of:

cocci, rods and filamentous rods.

Three main classifications to be aware of:

cocci, rods and filamentous rods.

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

Three main classifications to be aware of:

cocci, rods and filamentous rods.

Bacilli = rods, but on the USMLE, youll only
ever see rod or rods.
In the following slides, Ill discuss basic
classifications 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

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
fibrinogen 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
fibrinogen 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 fibrinogen. 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 differentiated 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
differentiated 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
differentiated 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 differentiated 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 differentiated 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 differentiated 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

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

know how to differentiate 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 differentiate 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. difficile,
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 nonmotile.

Gram(+) filamentous
rods

Gram(+) filamentous
rods
Weve got Nocardia and Actinomyces

Gram(+) filamentous
rods
Weve got Nocardia and Actinomyces
Nocardia is aerobic and weakly acid-fast.

Gram(+) filamentous
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 specifically

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

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 reflect 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 reflect 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 staf. 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

influenza 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

influenza 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

influenza 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. influenzae can be grown alongside S.
aureus bc S. aureus supplies NAD+ for
growth (in contrast, H. influenzae 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 specifically 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 specifically 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 biofilms that enable adhesion to

catheters

S. epidermidis
Endocarditis in prosthetic valve pts
Produces biofilms 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. saprophyticus
The only thing that comes to mind offhand 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. saprophyticus
The only thing that comes to mind offhand 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
diffuse 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 diffuse 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 alphahaemolysis.

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 alphahaemolysis.

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 Tcell response for B-cell-mediated Ab-classswitching. 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 antiserum & 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 biofilm, but it binds to tooth enamel.

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

a biofilm, 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 fibrin. 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

S. agalactiae
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. agalactiae
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. agalactiae
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 specifically for
when the penicillin is given, and its intrapartum
NOT BEFORE DELIVERY, not after, intrapartum)

S. agalactiae
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. agalactiae
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 GroupB Strep; theyll mention rupture of the
membranes w/ foul-smelling fluid. So if they
mention premature rupture of the
membranes, remember S. agalactiae.

Enterococcus
Normal GI flora 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
Lancefield grouping, which differentiates one

type of Strep from another, is based on

differences in C carbohydrate groups.

Enterococcus
Lancefield grouping, which differentiates one

type of Strep from another, is based on

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

Enterococcus
Lancefield grouping, which differentiates one

type of Strep from another, is based on

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

Enterococcus
Lancefield grouping, which differentiates one

type of Strep from another, is based on

differences 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
Lancefield grouping, which differentiates one

type of Strep from another, is based on

differences 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

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-defined 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 flaccid

paralysis

Clostridium botulinum
Produces toxin that inhibits ACh release from

presynaptic neurons, causing flaccid 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 differences
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 affected by C. botulinum. There is loss

of head control. However, constipation
precedes other Sx.

Clostridium difficile
Causes pseudomembranous colitis

secondary to clindamycin or ampicillin-use

(disruption of normal flora leads to C. difficile
overgrowth)

Clostridium difficile
Causes pseudomembranous colitis

secondary to clindamycin or ampicillin-use

(disruption of normal flora leads to C. difficile
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 difficile
The MOA of C. difficile-induced enterocytic

necrosis is CYTOSKELETAL DISRUPTION via

ACTIN DEPOLYMERIZATION. I had seen
that in two different practice questions.

Clostridium difficile
The MOA of C. difficile-induced enterocytic

necrosis is CYTOSKELETAL DISRUPTION via

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

Clostridium difficile
The MOA of C. difficile-induced enterocytic

necrosis is CYTOSKELETAL DISRUPTION via

ACTIN DEPOLYMERIZATION. I had seen
that in two different practice questions.
C. difficle, 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 flaccid
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 flaccid
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 FOURDEGREES 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 FOURDEGREES 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 FOURDEGREES 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 five 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 ADPribosylation. 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) fibrinous 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 first, 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 first, THEN the vaccine.
Cardiomyopathy is the leading cause of
death in diptheria.

Corynebacterium
diptheriae
Classically presents with GREY

OROPHARYNGEAL EXUDATES.

Actinomyces
They like you to know that it produces yellow

sulfur granules.

Actinomyces
They like you to know that it produces yellow

sulfur granules.
It causes draining facial abscesses.

Actinomyces
They like you to know that it produces yellow

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

Actinomyces
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)

Actinomyces
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(+)

filamentous 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. Wellperfused bone can support Nocardia growth.
The explanation said Nocardia can sometimes
cause osteomyelitis, but Actinomyces doesnt.
Just be aware of that. Thats it.