Staphylococcus aureus
Summary
TLDRStaphylococcus aureus, often found on human skin and in the nose, is a Gram-positive bacterium that can cause various infections, from skin conditions like pimples and boils to severe systemic infections like pneumonia and sepsis. It can form biofilms on medical implants and produce toxins leading to diseases like toxic shock syndrome. The bacterium has developed resistance to several antibiotics, leading to the emergence of MRSA strains, which are a significant concern in healthcare settings and the community.
Takeaways
- đ Staphylococcus aureus, often referred to as staph, is a Gram-positive, round-shaped bacterium that grows in grape-like clusters and is commonly found on human skin.
- đŹ It is named for its appearance under a microscope, where it forms sticky, purple-staining clusters due to its peptidoglycan cell wall, and its colonies exhibit a golden-yellow hue on blood agar plates.
- đ± Staphylococcus aureus is a facultative anaerobe, meaning it can survive in both aerobic and anaerobic conditions, and it does not move or form spores.
- đ§Ș Catalase production allows S. aureus to break down hydrogen peroxide into water and oxygen, a feature that can be used to differentiate it from other cocci, which are catalase-negative.
- đ Coagulase production is a key distinguishing factor for S. aureus, as it converts fibrinogen into fibrin, causing a visible clotting reaction in the presence of plasma.
- đ It is a common part of the human skin flora, colonizing about 25% of the population, usually without causing harm.
- đš Overgrowth or skin damage can lead to infections ranging from localized skin infections like pimples and boils to more serious conditions like abscesses, cellulitis, and even systemic infections.
- đ„ MRSA (Methicillin-resistant S. aureus) strains have developed resistance to many antibiotics, including methicillin, and are categorized into HA-MRSA found in healthcare settings and CA-MRSA found in the community.
- đ Treatment of S. aureus infections involves antibiotic susceptibility testing to select the most effective antibiotic, with options including clindamycin, vancomycin, and others for MRSA.
- đŹ S. aureus can produce toxins such as TSST-1, PVL, hemolysin, exfoliatin, and enterotoxins, which can cause a range of symptoms from skin conditions to food poisoning and toxic shock syndrome.
Q & A
What does the name 'Staphylococcus aureus' suggest about its appearance?
-The name 'Staphylococcus aureus' suggests a 'golden cluster of grapes', reflecting its tendency to grow in round, sticky clusters that resemble grapes and appear golden-yellow on blood agar plates.
How does the Gram stain reaction of Staphylococcus aureus contribute to its identification?
-Staphylococcus aureus is Gram positive, meaning it stains purple due to its peptidoglycan cell wall, which helps in its identification under a microscope.
What is the significance of Staphylococcus aureus being a facultative anaerobe?
-Being a facultative anaerobe means Staphylococcus aureus can survive in both aerobic and anaerobic environments, which contributes to its resilience and ability to cause infections in various conditions.
How can you differentiate Staphylococcus aureus from other catalase-negative cocci using hydrogen peroxide?
-Staphylococcus aureus is catalase positive, so when a few drops of hydrogen peroxide are added, it will foam up, unlike catalase-negative bacteria which show no reaction.
What enzyme produced by Staphylococcus aureus helps in distinguishing it from other staphylococci species?
-Staphylococcus aureus produces coagulase, an enzyme that converts fibrinogen into fibrin, which helps in clumping when mixed with plasma, distinguishing it from coagulase-negative staphylococci species.
Where is Staphylococcus aureus commonly found on the human body?
-Staphylococcus aureus is commonly found in the nostrils, groin, armpits, and other parts of the skin, often as a normal part of the skin flora.
What factors can lead to Staphylococcus aureus causing infections rather than just colonization?
-Factors such as pH, humidity, sweat levels, and the presence of other bacteria on the skin can affect the amount of Staphylococcus aureus present, leading to infections if there are high levels and breaks in the skin.
What are some of the localized skin infections that Staphylococcus aureus can cause?
-Localized skin infections caused by Staphylococcus aureus include pimples, furuncles, boils, carbuncles, impetigo, cellulitis, and subcutaneous abscesses.
How can Staphylococcus aureus infections become systemic and affect other organs?
-If Staphylococcus aureus enters the bloodstream, it can cause bacteremia, leading to systemic infections such as septic thrombophlebitis, endocarditis, osteomyelitis, and septic arthritis, and can even reach the central nervous system or cause pneumonia.
What is the role of biofilms in Staphylococcus aureus infections on medical implants?
-Biofilms are layers of 'slime' where Staphylococcus aureus can live on medical implants, making infections harder to treat as they protect the bacteria and hinder antibiotic penetration.
What are some of the toxins produced by Staphylococcus aureus that can cause severe reactions?
-Staphylococcus aureus can produce toxins such as TSST-1, PVL, hemolysin, exfoliatin, and enterotoxin, which can cause toxic shock syndrome, tissue necrosis, hemolysis, staphylococcal scalded skin syndrome, and food poisoning.
How has Staphylococcus aureus developed resistance to commonly used antibiotics?
-Staphylococcus aureus has developed resistance to antibiotics like penicillins through the production of beta lactamases and the evolution of the mecA gene, leading to MRSA strains that are resistant to methicillin and related antibiotics.
What alternative antibiotics are used to treat MRSA infections?
-Alternative antibiotics used to treat MRSA infections include glycopeptides like vancomycin, clindamycin, tetracyclines, trimethoprim/sulfamethoxazole, linezolid, tigecycline, daptomycin, and quinupristin-dalfopristin.
Outlines
đ Understanding Staphylococcus Aureus
Staphylococcus aureus, often referred to as 'staph aureus', is a Gram-positive, round-shaped bacterium that grows in grape-like clusters. It is named for its golden-yellow color when grown on blood agar plates. Staph aureus is a facultative anaerobe, meaning it can survive in both aerobic and anaerobic conditions. It is non-motile and does not form spores. The bacteria are catalase-positive, which allows them to break down hydrogen peroxide into water and oxygen, a trait that can be used to differentiate them from other cocci. Staph aureus can be identified by its coagulase enzyme, which converts fibrinogen into fibrin, causing a visible clumping reaction. It is common in human skin flora, usually found in the nostrils, groin, armpits, and other skin areas. Under normal circumstances, it does not cause harm, but it can become dominant under certain conditions and lead to infections if the skin is compromised. Staph aureus can cause a range of skin infections from pimples to abscesses and can even lead to more serious conditions if it penetrates deeper into the body, affecting organs, muscles, bones, and joints.
đ„ Invasive Potential of Staph Aureus
Staphylococcus aureus can cause serious health complications when it enters the body through breaks in the skin or directly into the bloodstream during medical procedures like surgery or dental work. It can form biofilms on medical implants, which are difficult to treat due to their protective 'slime' layer. Staph aureus can also produce toxins, including TSST-1, which can lead to toxic shock syndrome, and PVL, which can cause tissue necrosis and organ failure. Other toxins like hemolysin, exfoliatin, and enterotoxin can cause a range of symptoms from skin syndromes to food poisoning. The bacterium's ability to adapt and develop antibiotic resistance, particularly methicillin-resistant strains (MRSA), poses a significant challenge to treatment. MRSA is further classified into HA-MRSA, found in healthcare settings, and CA-MRSA, found in the community.
đ Combating Staph Aureus Infections
The treatment of Staph aureus infections has evolved due to its resistance to traditional antibiotics like penicillins. Beta lactamase inhibitors and newer beta lactam antibiotics were developed to combat resistant strains, but some strains have evolved to express a gene called mecA, which produces penicillin-binding proteins (PBPs) that are unaffected by these antibiotics, leading to the emergence of MRSA. Two types of MRSA, HA-MRSA and CA-MRSA, are particularly problematic as they cannot be treated with beta lactam antibiotics. Alternative antibiotics like vancomycin are used, but resistance to vancomycin has also emerged in strains known as VISA and VRSA. The development of new antibiotics and vaccines is ongoing to address the challenges posed by Staph aureus infections. Treatment often involves testing the bacteria against various antibiotics to select the most effective one, and hospitals may use antibiograms to guide treatment decisions.
Mindmap
Keywords
đĄStaphylococcus aureus
đĄGram-positive
đĄCatalase
đĄCoagulase
đĄBiofilm
đĄMethicillin-resistant S. aureus (MRSA)
đĄVancomycin
đĄSuperantigens
đĄEnterotoxin
đĄAntibiotic resistance
đĄSepticemia
Highlights
Staphylococcus aureus, often called staph, is a round-shaped bacterium that grows in clusters resembling grapes.
Staph aureus is Gram positive and facultative anaerobes, capable of surviving in both aerobic and anaerobic environments.
Staph aureus colonies have a distinctive golden-yellow color when grown on blood agar plates.
Catalase enzyme produced by Staph aureus helps differentiate it from other cocci like streptococci and enterococci.
Coagulase enzyme produced by Staph aureus converts fibrinogen into fibrin, aiding in its identification.
Staph aureus is commonly found in the nostrils, groin, armpits, and other parts of human skin.
Staph aureus can cause localized skin infections like pimples, furuncles, boils, and carbuncles.
Infections can spread to deeper tissues causing cellulitis, abscesses, and other severe conditions.
Staph aureus can cause systemic infections such as septic thrombophlebitis, bacteremia, and sepsis.
Staph aureus can enter the central nervous system causing meningitis or spinal epidural abscesses.
The bacterium can also cause infective endocarditis by damaging heart valves.
Staph aureus can form biofilms on medical implants, making it difficult to treat.
Staph aureus releases superantigens and toxins causing a range of diseases from skin infections to food poisoning.
Treatment of Staph aureus infections involves the use of antibiotics, but resistance is a growing problem.
Methicillin resistant Staph aureus (MRSA) strains are resistant to many antibiotics, including penicillins.
Vancomycin is used to treat MRSA, but some strains have developed resistance, known as VISA and VRSA.
The development of new antibiotics and vaccines is crucial to combat Staph aureus infections.
Antibiotic resistance in Staph aureus is a significant challenge due to overuse of antibiotics.
Transcripts
Staphylococcus aureus, sometimes called staph aureus, is coccal, or round-shaped, and grows
in clusters.
In fact, its name, broken down, means âgolden cluster of grapesâ.
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 itâs Gram positive and it resembles grapes.
As for its âgoldenâ color, when itâs 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.
Theyâre non-motile and donât 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
donât 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
thatâs made by Staph aureus, called coagulase.
Coagulase converts fibrinogen into fibrin.
So letâs say that we stir up some Staph aureus bacteria in a liquid âemulsionâ,
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 wonât.
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 itâs a normal part of our skin flora, and doesnât 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 thatâs 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, itâs 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 thatâs walled off and sometimes develops thin walls within it - called septations.
These abscesses can occur all over the body including in the mouth where theyâre called
dental abscesses, and they can develop within various organs like the liver, kidney, spleen,
and brain.
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.
Thereâs 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 itâs 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 itâs 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.
The biofilm is, essentially, a layer of âslimeâ 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 doesnât divide rapidly within these biofilms, and
itâs 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 theyâre growing on, if possible.
If all of this wasnât 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 enterotoxinâŠ
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.
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 contain 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 Ritterâs disease.
It creates painful patches of red skin, with fluid filled blisters, but it often resolves
within a few weeks.
Finally, thereâs 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.
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 arenât 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 canât 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 couldnât
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 canât 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.
Thereâs two major categories of MRSA - the health-care associated MRSA, or HA-MRSA, and
community associated MRSA, or CA-MRSA.
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, itâs not as effective and comes with problematic side effects.
To make matters worse, some Staph aureus strains have developed intermediate resistance to
vancomycin, and theyâre called âvancomycin intermediate S. aureusâ, or VISA for short.
Not the type of VISA anyone wants to get.
And strains with complete resistance are called âvancomycin resistant S. aureusâ, 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, daptomycin, and quinupristin-dalfopristin.
All right, quick recap!
S. aureus is a gram positive coccus that grows in clusters.
Itâs 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.
Weitere Àhnliche Videos ansehen
Biofilm: A New (Gross) Thing to Worry About
Infectious Diseases Overview, Animation
Septic Shock (Sepsis) | Pathophysiology and Nursing Interventions
Hipersensitivitas Tipe 1 (Immediate Hypersensitivity), Immunology
Antibiotics - What They Are, When To Use Them, Side Effects & More
Alexander Fleming and the Accidental Mould Juice â The Serendipity of Science (2/3)
5.0 / 5 (0 votes)