Staphylococcus aureus, sometimes called staph aureus, is coccal, or round-

shaped, and grows in clusters.

In fact, its name, broken down, means “golden cluster of grapes”.

It sorta starts making sense if you look at it under a microscope - it tends to

grow in sticky clusters, and it stains purple when Gram-stained due to its
peptidoglycan cell wall, so it’s Gram positive and it resembles grapes.

As for its “golden” color, when it’s grown on blood agar plates, the colonies
have a distinctive golden-yellow color.

Staphylococcus aureus are Gram positive and facultative anaerobes,

meaning that they can survive in aerobic and anaerobic environments.

They’re non-motile and don’t form spores.

Staphylococci produce an enzyme called catalase which converts hydrogen

peroxide to water and oxygen.

Other common cocci, such as streptococci and enterococci, are catalase

negative so they don’t have this ability and we can use a few drops of
hydrogen peroxide to differentiate them.

Catalase positive bacteria will foam up, while in catalase negative bacteria,
nothing happens.

Now, a couple of other staphylococci species, like Staph epidermidis and

Staph saprophyticus are also catalase positive, so to distinguish between
them we can look for another enzyme that’s made by Staph aureus, called
coagulase.

Coagulase converts fibrinogen into fibrin.

So let’s say that we stir up some Staph aureus bacteria in a liquid “emulsion”,
and then add a few drops of plasma which contains fibrinogen. The
coagulase positive staph aureus will convert the soluble fibrinogen to sticky
fibrin, which then visibly clumps up, whereas coagulase negative bacteria
won’t.

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Staph aureus is extremely common and about a quarter of the population is
colonized by it, usually in their nostrils, groin, armpits, and other parts of
their skin.

But, most of the time it’s a normal part of our skin flora, and doesn’t cause
trouble.

The skin flora is a complex ecosystem of different bacterial species and

occasionally, Staph aureus can begin to dominate that ecosystem.

In individuals that have staph aureus colonization, a number of factors like

the pH, humidity, sweat levels of the skin, as well as presence of other
bacteria on our skin, all affect the amount of staph aureus that’s present.

If more and more Staph aureus is around on the skin, it begins to penetrate
through tiny microfissures in the skin, like you get with eczema, as well as
larger breaks in the skin like you might get after shaving.

In fact, it’s particularly troublesome in terms of causing wound infections

where there is a large break in the skin either from trauma or after a surgery.

So low levels of staph aureus with intact skin leads to colonization, whereas
high levels of Staph aureus with breaks in the skin lead to infections.

When staph aureus invades into the skin it can lead to localized skin
infections like a pimple which can evolve into a furuncle, or a boil.

A bunch of furuncles clustered together make a carbuncle.

There can also be diffuse skin infections, like superficial impetigo which is an
infection of the epidermis, or deeper-reaching cellulitis, which is an infection
of the dermis and can spread over larger surfaces rapidly.

If the infection goes deeper, it can develop into a subcutaneous abscess - a

collection of pus that’s walled off and sometimes develops thin walls within it
- called septations.

These abscesses can occur all over the body including in the mouth where
they’re called dental abscesses, and they can develop within various organs
like the liver, kidney, spleen, and brain.

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Now if the infection is overlying a muscle, it can spread into the muscle
causing a pyomyositis.

If it gets into the bone it can cause osteomyelitis, and if it gets into the joint
space it can cause septic arthritis.

Finally, if Staph aureus gets into the bloodstream, it can cause

a septic thrombophlebitis - an infected blood clot.

In addition, bacteria in the blood is called bacteremia, and it can lead to a

number of serious problems.

There’s typically a widespread immune reaction that causes the blood vessels
to expand and the blood pressure to fall. The result is hypotension and poor
perfusion to various organs - a process called sepsis.

Once it’s in the blood, Staph aureus can also get to various parts of the body.

It can get into the central nervous system - causing bacterial meningitis or
an epidural abscess in the spine.

It can get into the lungs causing a severe pneumonia.

It can start to grow on the heart valves in clumps called vegetations -

damaging the valves - a process called infective endocarditis.

Bits of the vegetations can then chip off and embolize further causing other
local infections around the body.

Now, in addition to invading the body through the skin, Staph aureus can
also enter directly into the bloodstream when a person is getting surgery or
having dental work done. These events occur infrequently, but when they do
come up it’s important to take precautions.

For example, individuals at high risk of getting serious disease with Staph
aureus - like immunocompromised individuals or those that are at risk
for infective endocarditis - should be given antibiotic prophylaxis.

Another property of our golden staph is its ability to create biofilm on

medical implants like indwelling intravenous catheters, prosthetic heart
valves, and artificial joints.

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The biofilm is, essentially, a layer of “slime” within which the Staph
aureus live. It forms when a cluster of Staph aureus adheres to a surface
either a natural one like the surface of a valve or an artificial one like the
surface of a catheter.

The bacteria start to produce extracellular matrix made of

exopolysaccharides, or EPS, and over time the cells get completely
surrounded by it.

The cells that are surrounded by the gel-like layer of exopolysaccharides, can
communicate with one other through biochemical signals and can even swap
genetic information back and forth - including antibiotic resistance genes.

In addition, Staph aureus thrives but doesn’t divide rapidly within these
biofilms, and it’s relatively hard for antibiotics to penetrate into the biofilms.

Combined that makes it much harder to get rid of these biofilm infections,
and often requires simply removing the surface that they’re growing on, if
possible.

If all of this wasn’t enough, S. aureus can also release superantigens or

toxins.

In fact, there are five major toxins related to S. aureus - toxic shock syndrome
toxin 1, or TSST-1, Panton-Valentine leukocidin toxin, hemolysin, exfoliatin,
and enterotoxin… toxin.

TSST-1 is produced at the site of infection, and can enter the bloodstream.

TSST-1 binds to major histocompatibility complex type II or MHC II, which is a

receptor found on immune cells called antigen presenting cells.

When TSST-1 binds to the MHC II receptors on these cells, it really stimulates
them, making them release loads of pro-inflammatory chemicals
called cytokines, creating a cytokine storm.

The cytokine storm results in a number of physiologic changes like fevers,

a sunburn like rash, low blood pressure, and poor end-organ perfusion that
can result in death - and together this is called toxic shock syndrome.

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Panton-Valentine leukocidin toxin, or PVL, punches holes in leukocytes - our
immune cells, killing them, and giving the toxin its name.

Leukocytes with holes in their cell membrane, die through necrosis and that
triggers inflammation.

When that happens throughout the tissue, like in a necrotizing pneumonia,

large chunks of the tissue begin to die off and the organ cannot do its job
properly leading to organ failure.

Hemolysin is another pore-forming toxin that destroys erythrocytes or red

blood cells, releasing their hemoglobin, which contains iron, into the blood.

Staph aureus uses iron in its own metabolism, so this is one way it gets
access to that coveted heavy metal.

Exfoliatin toxin causes staphylococcal scalded skin syndrome, SSSS, or Ritter’s

disease.

It creates painful patches of red skin, with fluid filled blisters, but it often
resolves within a few weeks.

Finally, there’s enterotoxin. Staph aureus might land on food and start to
generate enterotoxin.

The enterotoxin is quite stable in the environment, and can remain active
even after the bacteria are killed off by cooking. The toxin can even withstand
boiling at 100 degrees Celsius for a few minutes!

If the toxin is eaten, it can cause food poisoning - with symptoms like
vomiting and diarrhea a few hours after ingestion.

And, in rare situations, if the enterotoxin somehow gets into the

bloodstream, it can cause toxic shock syndrome, much like TSST-1.

The main treatment for infections is antibiotics, but Staph aureus adapts
quickly and has developed resistance to a number of antibiotics.

Penicillins, which are beta lactam antibiotics, were tried early on. They work
by disrupting disabling the enzyme DD-transpeptidase, which is a penicillin
binding protein, or PBP.

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PBP is in charge of crosslinking the long strands of amino polysaccharides
that make the peptidoglycan cell wall, running in parallel.

These are made of segments of N-acetylglucosamine, or NAG, and N-

acetylmuramic acid, or NAM, in an alternating pattern - so, NAG, NAM, NAG,
NAM, and so on, like a pearl necklace.

Protruding from the tips of the NAM subunits are tetrapeptide and
pentapeptide chains.

These peptide chains can link to other peptide chains from the neighboring
strands through a process known as transpeptidation.

If PBPs aren’t allowed to work, no peptidoglycan is made, and the cell wall
becomes leaky. So when the bacteria try to divide and make more cell wall -
they simply can’t and they die.

Nowadays, practically all strains of Staph aureus make beta lactamases which
allow them to simply disable beta lactam antibiotics by breaking their beta
lactam ring.

Next, antibiotics called beta lactamase inhibitors, like clavulanic acid, were
used to bind and disable the beta lactamases.

In addition, new types of beta lactam antibiotics, like methicillin, were

identified that couldn’t be easily destroyed by the beta lactamases.

Unfortunately, some S. aureus strains found a way around this as well by

evolving and expressing a gene called mecA, which encodes special PBPs -
that are unaffected by beta lactam antibiotics.

Methicillin and older penicillins can’t physically fit into them, rendering them
ineffective.

These methicillin resistant staph aureus strains are called MRSA for short -
and have become more common around the world.

There’s two major categories of MRSA - the health-care associated MRSA, or

HA-MRSA, and community associated MRSA, or CA-MRSA.

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HA-MRSA is found in places like hospitals and nursing homes, where there
are lots of chronically ill patients and a high usage of antibiotics.

CA-MRSA is found in the community, and is thought to be due to rampant

antibiotic use on factory farms, and overprescription of antibiotics.

Both HA-MRSA and CA-MRSA pose a major problem because infections with
those strains cannot be treated with beta lactam antibiotics.

As a result, another class of antibiotics - glycopeptide antibiotics,

like vancomycin, are often used instead. Unfortunately, it’s not as effective
and comes with problematic side effects.

To make matters worse, some Staph aureus strains have developed

intermediate resistance to vancomycin, and they’re called
“vancomycin intermediate S. aureus”, or VISA for short. Not the type of VISA
anyone wants to get.

And strains with complete resistance are called “vancomycin resistant S.

aureus”, or VRSA.

The search is on for new antibiotics and vaccines to prevent staph

aureus infections, but the overuse of antibiotics makes rapid resistance an
ongoing problem.

Ultimately, treatment of Staph aureus infections involves testing the bacteria

against a handful of antibiotics and then choosing the most appropriate
antibiotic from them.

Sometimes, hospitals put together an antibiogram which shows how

frequently bacteria are resistant to a particular antibiotic.

Typically when treating MRSA, antibiotics like clindamycin or vancomycin are

chosen, but alternatives include
tetracyclines, trimethoprim/sulfamethoxazole, linezolid, tigecycline, daptomy
cin, and quinupristin-dalfopristin.

Summary
All right, quick recap! S. aureus is a gram positive coccus that grows in
clusters.

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It’s a part of the normal skin and nasal flora in about a quarter of the
population, but if it overgrows or if the skin is damaged, then it can cause
disease through direct colonization, toxin production, or both.

Staph aureus is very adaptive and it has become resistant to various

antibiotics.

Methicillin resistant strains are often classified as HA-MRSA or CA-MRSA,

and vancomycin intermediate and vancomycin resistant strains are called
VISA and VRSA.

Summary

Staphylococcus aureus, also known as "staph," is a gram-positive, beta-

hemolytic, catalase, and coagulase-positive bacteria, which is known to cause
a wide range of infections in humans. Staph is normally part of the human
normal skin and nasal flora, but if it overgrows or if the skin is damaged, then
it can cause disease through direct colonization, toxin production, or both.

Staph is known to cause skin infections,

organ abscesses, pneumonia, endocarditis, septic arthritis,
and osteomyelitis. Staph infections are typically treated with antibiotics, but
in some cases, the bacteria may be resistant to the antibiotics that are
commonly used. Methicillin-resistant Staphylococcus aureus (MRSA) is a type
of staph that is resistant to many antibiotics and is a significant public health
concern.

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