Staphylococcus aureus (also known as golden staph) is a Gram-positive,
round-shaped bacterium that is a member of the Firmicutes, and it is a
member of the normal flora of the body, frequently found in the nose,
respiratory tract, and on the skin. It is often positive for catalase
and nitrate reduction and is a facultative anaerobe that can grow
without the need for oxygen. Although S. aureus is not always
pathogenic (and can commonly be found existing as a commensal), it is
a common cause of skin infections including abscesses, respiratory
infections such as sinusitis, and food poisoning. Pathogenic strains
often promote infections by producing virulence factors such as potent
protein toxins, and the expression of a cell-surface protein that
binds and inactivates antibodies. The emergence of
antibiotic-resistant strains of S. aureus such as
methicillin-resistant S. aureus (MRSA) is a worldwide problem in
clinical medicine. Despite much research and development there is no
approved vaccine for S. aureus.
Staphylococcus was first identified in 1880 in Aberdeen, Scotland, by
Alexander Ogston in pus from a surgical abscess in a knee
joint. This name was later amended to
Staphylococcus aureus by
Friedrich Julius Rosenbach, who was credited by the official system
of nomenclature at the time. An estimated 20% to 30% of the human
population are long-term carriers of S. aureus which can be
found as part of the normal skin flora, in the nostrils, and as
a normal inhabitant of the lower reproductive tract of women. S.
aureus can cause a range of illnesses, from minor skin infections,
such as pimples, impetigo, boils, cellulitis, folliculitis,
carbuncles, scalded skin syndrome, and abscesses, to life-threatening
diseases such as pneumonia, meningitis, osteomyelitis, endocarditis,
toxic shock syndrome, bacteremia, and sepsis. It is still one of the
five most common causes of hospital-acquired infections and is often
the cause of wound infections following surgery. Each year, around
500,000 patients in hospitals of the United States contract a
staphylococcal infection, chiefly by S. aureus. Up to 50,000
deaths each year in the USA are linked with S. aureus infections.
Classification and external resources
[edit on Wikidata]
2 Role in health
3 Role in disease
3.1 Skin infections
3.2 Food poisoning
3.3 Bone and joint infections
3.6 Animal infections
4.3 small RNA
4.4 Strategies for post-transcriptional regulation by 3'untranslated
4.5 Other immunoevasive strategies
5 Classical diagnosis
5.1 Rapid diagnosis and typing
6.1 Antibiotic resistance
11 Further reading
12 External links
Gram stain of S. saprophyticus cells which typically occur in
clusters: The cell wall readily absorbs the crystal violet stain.
Yellow colonies of S. aureus on a blood agar plate, note regions of
clearing around colonies caused by lysis of red cells in the agar
S. aureus (/ˌstæfɪləˈkɒkəs ˈɔːriəs, -loʊ-/, Greek
σταφυλόκοκκος, "grape-cluster berry",
"golden") is a facultative anaerobic, gram-positive coccal (round)
bacterium also known as "golden staph" and "oro staphira". S. aureus
is non-motile and does not form spores. In medical literature, the
bacterium is often referred to as S. aureus, Staph aureus or Staph
A.. S. aureus appears as staphylococci (grape-like clusters) when
viewed through a microscope, and has large, round, golden-yellow
colonies, often with hemolysis, when grown on blood agar plates.
S. aureus reproduces asexually by binary fission. Complete separation
of the daughter cells is mediated by S. aureus autolysin, and in its
absence or targeted inhibition, the daughter cells remain attached to
one another and appear as clusters.
S. aureus is catalase-positive (meaning it can produce the enzyme
Catalase converts hydrogen peroxide (H
2) to water and oxygen. Catalase-activity tests are sometimes used to
distinguish staphylococci from enterococci and streptococci.
Previously, S. aureus was differentiated from other staphylococci by
the coagulase test. However, not all S. aureus strains are
coagulase-positive and incorrect species identification can
impact effective treatment and control measures.
Staphylococcus is different from the similarly named and medically
relevant genus Streptococcus.
Natural genetic transformation is a reproductive process involving DNA
transfer from one bacterium to another through the intervening medium,
and the integration of the donor sequence into the recipient genome by
homologous recombination. S. aureus was found to be capable of natural
genetic transformation, but only at low frequency under the
experimental conditions employed. Further studies suggested that
the development of competence for natural genetic transformation may
be substantially higher under appropriate conditions, yet to be
Role in health
In humans, S. aureus is part of the normal microbiota present in the
upper respiratory tract, and on skin and in the gut mucosa.
S. aureus, along with similar species that can colonize and act
symbiotically but can cause disease if they begin to take over the
tissues they have colonized or invade other tissues, have been called
Role in disease
Further information: Coagulase-positive staphylococcal infection
This 2005 scanning electron micrograph (SEM) depicts numerous clumps
of methicillin-resistant S. aureus (MRSA) bacteria.
While S. aureus usually acts as a commensal bacterium,
asymptomatically colonizing about 30% of the human population, it can
sometimes cause disease. In particular, S. aureus is one of the
most common causes of bacteremia and infective endocarditis.
Additionally, it can cause various skin and soft tissue infections,
particularly when skin or mucosal barriers have been breached.
S. aureus infections can spread through contact with pus from an
infected wound, skin-to-skin contact with an infected person, and
contact with objects used by an infected person such as towels,
sheets, clothing, or athletic equipment. Joint replacements put a
person at particular risk of septic arthritis, staphylococcal
endocarditis (infection of the heart valves), and pneumonia.
Diabetics, injection drug users, and individuals with heart
conditions, should take extra precautions to avoid coming into contact
with staphylococcus aureus, as they are at the highest risk. A couple
preventive measures are, washing hands often with soap and making sure
to bathe or shower daily.
S. aureus is a significant cause of chronic biofilm infections on
medical implants and the repressor of toxins is part of the infection
S. aureus can lay dormant in the body for years undetected. Once
symptoms begin to show, the host is contagious for another two weeks
and the overall illness lasts a few weeks. If untreated though, the
disease can be deadly.
Deeply penetrating S. aureus infections can be severe.
Skin infections are the most common form of S. aureus infection. This
can manifest in various ways, including small benign boils,
folliculitis, impetigo, cellulitis, and more severe, invasive
S. aureus is extremely prevalent in persons with atopic dermatitis. It
is mostly found in fertile, active places, including the armpits,
hair, and scalp. Large pimples that appear in those areas may
exacerbate the infection if lacerated. This can lead to staphylococcal
scalded skin syndrome, a severe form of which can be seen in
The presence of S. aureus in persons with atopic dermatitis is not an
indication to treat with oral antibiotics, as evidence has not shown
this to give benefit to the patient. The relationship between
S. aureus and atopic dermatitis is unclear.
S. aureus is also responsible for food poisoning. It is capable of
generating toxins that produce food poisoning in the human body.
Its incubation period lasts one to six hours, with the illness
itself lasting anywhere from thirty minutes to three days.
Preventative measures one can take to help prevent the spread of the
disease include washing hands thoroughly with soap and water before
preparing food. Stay away from any food if you are ill, and wear
gloves if there are any open wounds on your hands or wrists while
preparing food. If storing food for longer than 2 hours, keep the food
above 140 degrees Fahrenheit or below 40 degrees Fahrenheit.
Bone and joint infections
S. aureus is the bacterium that is commonly responsible for all major
bone and joint infections. This manifests in one of three forms:
osteomyelitis, septic arthritis and infection from a replacement joint
S. aureus is a leading cause of bloodstream infections throughout much
of the industrialized world.
Infection is generally associated
with breakages in the skin or mucosal membranes due to surgery,
injury, or use of intravascular devices such as catheters,
hemodialysis machines, or injected drugs. Once the bacteria
have entered the bloodstream, they can infect various organs, causing
infective endocarditis, septic arthritis, and osteomyelitis. This
disease is particularly prevalent and severe in the very young and
Without antibiotic treatment, S. aureus bacteremia has a case fatality
rate around 80%. With antibiotic treatment, case fatality rates
range from 15% to 50% depending on the age and health of the patient,
as well as the antibiotic resistance of the S. aureus strain.
S. aureus is often found in biofilms formed on medical devices
implanted in the body or on human tissue. It is commonly found with
another pathogen, Candida albicans, forming multispecies biofilms. The
latter is suspected to help S. aureus penetrate human tissue. A
higher mortality is linked with multispecies biofilms.
S. aureus can survive on dogs, cats, and horses, and can
cause bumblefoot in chickens. Some believe health-care workers'
dogs should be considered a significant source of antibiotic-resistant
S. aureus, especially in times of outbreak.
S. aureus is one of the causal agents of mastitis in dairy cows. Its
large polysaccharide capsule protects the organism from recognition by
the cow's immune defenses.
S. aureus produces various enzymes such as coagulase (bound and free
coagulases) which clots plasma and coats the bacterial cell, probably
to prevent phagocytosis.
Hyaluronidase (also known as spreading
factor) breaks down hyaluronic acid and helps in spreading it. S.
aureus also produces deoxyribonuclease, which breaks down the DNA,
lipase to digest lipids, staphylokinase to dissolve fibrin and aid in
spread, and beta-lactamase for drug resistance.
Depending on the strain, S. aureus is capable of secreting several
exotoxins, which can be categorized into three groups. Many of these
toxins are associated with specific diseases.
Antigens known as superantigens can induce toxic shock syndrome (TSS).
This group includes the toxins TSST-1, and enterotoxin type B, which
causes TSS associated with tampon use.
Toxic shock syndrome
Toxic shock syndrome is
characterized by fever, erythematous rash, low blood pressure, shock,
multiple organ failure, and skin peeling. Lack of antibody to TSST-1
plays a part in the pathogenesis of TSS. Other strains of S. aureus
can produce an enterotoxin that is the causative agent of a type of
gastroenteritis. This form of gastroenteritis is self-limiting,
characterized by vomiting and diarrhea one to six hours after
ingestion of the toxin, with recovery in eight to 24 hours. Symptoms
include nausea, vomiting, diarrhea, and major abdominal pain.
See also: Exfoliatin
Exfoliative toxins are exotoxins implicated in the disease
staphylococcal scalded skin syndrome (SSSS), which occurs most
commonly in infants and young children. It also may occur as epidemics
in hospital nurseries. The protease activity of the exfoliative toxins
causes peeling of the skin observed with SSSS.
Staphylococcal toxins that act on cell membranes include alpha toxin,
beta toxin, delta toxin, and several bicomponent toxins. Strains of S.
aureus can host phages, such as the prophage Φ-PVL that produces
Panton-Valentine leukocidin (PVL), to increase virulence. The
bicomponent toxin PVL is associated with severe necrotizing pneumonia
in children. The genes encoding the components of PVL are
encoded on a bacteriophage found in community-associated MRSA
There is a growing list of small RNAs involved in the control of
bacterial virulence in S.aureus. For example, RNAIII, SprD,
RsaE, SprA1, SSR42, ArtR, SprX and Teg49.
Strategies for post-transcriptional regulation by 3'untranslated
It has been shown that many mRNAs in S. aureus carry three prime
untranslated regions (3'UTR) longer than 100 nucleotides, which may
potentially have a regulatory function.
Further investigation of icaR mRNA (mRNA coding for the repressor of
the main expolysaccharidic compound of the bacteria biofilm matrix)
demonstrated that the 3'UTR binding to the 5' UTR can interfere with
the translation initiation complex and generate a double stranded
substrate for RNase III. It was shown that the interaction is between
the UCCCCUG motif in the 3'UTR and the Shine-Dalagarno region at the
5'UTR. Deletion of the motif resulted in IcaR repressor accumulation
and inhibition of biofilm development. The biofilm formation is
the main cause of
Staphylococcus implant infections.
Other immunoevasive strategies
Protein A is anchored to staphylococcal peptidoglycan pentaglycine
bridges (chains of five glycine residues) by the transpeptidase
Protein A, an IgG-binding protein, binds to the Fc
region of an antibody. In fact, studies involving mutation of genes
coding for protein A resulted in a lowered virulence of S. aureus as
measured by survival in blood, which has led to speculation that
protein A-contributed virulence requires binding of antibody Fc
Protein A in various recombinant forms has been used for decades to
bind and purify a wide range of antibodies by immunoaffinity
chromatography. Transpeptidases, such as the sortases responsible for
anchoring factors like protein A to the staphylococcal peptidoglycan,
are being studied in hopes of developing new antibiotics to target
S. aureus on trypticase soy agar: The strain is producing a yellow
Some strains of S. aureus are capable of producing staphyloxanthin —
a golden-coloured carotenoid pigment. This pigment acts as a virulence
factor, primarily by being a bacterial antioxidant which helps the
microbe evade the reactive oxygen species which the host immune system
uses to kill pathogens.
Mutant strains of S. aureus modified to lack staphyloxanthin are less
likely to survive incubation with an oxidizing chemical, such as
hydrogen peroxide, than pigmented strains.
Mutant colonies are quickly
killed when exposed to human neutrophils, while many of the pigmented
colonies survive. In mice, the pigmented strains cause lingering
abscesses when inoculated into wounds, whereas wounds infected with
the unpigmented strains quickly heal.
These tests suggest the
Staphylococcus strains use staphyloxanthin as
a defence against the normal human immune system. Drugs designed to
inhibit the production of staphyloxanthin may weaken the bacterium and
renew its susceptibility to antibiotics. In fact, because of
similarities in the pathways for biosynthesis of staphyloxanthin and
human cholesterol, a drug developed in the context of
cholesterol-lowering therapy was shown to block S. aureus pigmentation
and disease progression in a mouse infection model.
Gram-positive cocci, in clusters, from a sputum sample, Gram
Depending upon the type of infection present, an appropriate specimen
is obtained accordingly and sent to the laboratory for definitive
identification by using biochemical or enzyme-based tests. A Gram
stain is first performed to guide the way, which should show typical
Gram-positive bacteria, cocci, in clusters. Second, the isolate is
cultured on mannitol salt agar, which is a selective medium with
7–9% NaCl that allows S. aureus to grow, producing yellow-colored
colonies as a result of mannitol fermentation and subsequent drop in
the medium's pH.
Furthermore, for differentiation on the species level, catalase
(positive for all
Staphylococcus species), coagulase (fibrin clot
formation, positive for S. aureus),
DNAse (zone of clearance on DNase
agar), lipase (a yellow color and rancid odor smell), and phosphatase
(a pink color) tests are all done. For staphylococcal food poisoning,
phage typing can be performed to determine whether the staphylococci
recovered from the food were the source of infection.
Rapid diagnosis and typing
Recent activities and food that a patient has recently eaten will be
inquired about by a physician, and a physical examination is conducted
to review any symptoms. With more severe symptoms, blood tests and
stool culture may be in order. Diagnostic microbiology
laboratories and reference laboratories are key for identifying
outbreaks and new strains of S. aureus. Recent genetic advances have
enabled reliable and rapid techniques for the identification and
characterization of clinical isolates of S. aureus in real time. These
tools support infection control strategies to limit bacterial spread
and ensure the appropriate use of antibiotics.
Quantitative PCR is
increasingly being used to identify outbreaks of infection.
When observing the evolvement of S. aureus and its ability to adapt to
each modified antibiotic, two basic methods known as “band-based”
or “sequence-based” are employed. Keeping these two methods in
mind, other methods such as multilocus sequence typing (MLST),
pulsed-field gel electrophoresis (PFGE), bacteriophage typing, spa
locus typing, and SCCmec typing are often conducted more than
others. With these methods, it can be determined where strains of
MRSA originated and also where they are currently.
With MLST, this technique of typing uses fragments of several
housekeeping genes known as aroE, glpF, gmk, pta, tip, and yqiL. These
sequences are then assigned a number which give to a string of several
numbers that serve as the allelic profile. Although this is a common
method, a limitation about this method is the maintenance of the
microarray which detects newly allelic profiles, making it a costly
and time-consuming experiment.
With PFGE, a method which is still very much used dating back to its
first success in 1980s, remains capable of helping differentiate MRSA
isolates. To accomplish this, the technique uses multiple gel
electrophoresis, along with a voltage gradient to display clear
resolutions of molecules. The S. aureus fragments then transition down
the gel, producing specific band patterns that are later compared with
other isolates in hopes of identifying related strains. Limitations of
the method include practical difficulties with uniform band patterns
and PFGE sensitivity as a whole.
Spa locus typing is also considered a popular technique that uses a
single locus zone in a polymorphic region of S. aureus to distinguish
any form of mutations. Although this technique is often
inexpensive and less time-consuming, the chance of losing
discriminatory power makes it hard to differentiate between MLST CCs
exemplifies a crucial limitation.
The treatment of choice for S. aureus infection is penicillin. An
antibiotic derived from some
Penicillium fungal species, penicillin
inhibits the formation of peptidoglycan cross-linkages that provide
the rigidity and strength in a bacterial cell wall. The four-membered
β-lactam ring of penicillin is bound to enzyme DD-transpeptidase, an
enzyme that when functional, cross-links chains of peptidoglycan that
form bacterial cell walls. The binding of β-lactam to
DD-transpeptidase inhibits the enzyme’s functionality and it can no
longer catalyze the formation of the cross-links. As a result, cell
wall formation and degradation are imbalanced, thus resulting in cell
death. In most countries, however, penicillin resistance is extremely
common, and first-line therapy is most commonly a
penicillinase-resistant β-lactam antibiotic (for example, oxacillin
or flucloxacillin, both of which have the same mechanism of action as
penicillin). Combination therapy with gentamicin may be used to treat
serious infections, such as endocarditis, but its use is
controversial because of the high risk of damage to the kidneys.
The duration of treatment depends on the site of infection and on
severity. Adjunctive rifampicin has been historically used in the
management of S aureus bacteraemia, but randomised controlled trial
evidence has shown this to be of no overall benefit over standard
Antibiotic resistance in S. aureus was uncommon when penicillin was
first introduced in 1943. Indeed, the original Petri dish on which
Alexander Fleming of
Imperial College London
Imperial College London observed the
antibacterial activity of the
Penicillium fungus was growing a culture
of S. aureus. By 1950, 40% of hospital S. aureus isolates were
penicillin-resistant; by 1960, this had risen to 80%.
MRSA, often pronounced /ˈmɜːrsə/ or /ɛm ɑːr ɛs eɪ/, is one of
a number of greatly feared strains of S. aureus which have become
resistant to most β-lactam antibiotics. For this reason, vancomycin,
a glycopeptide antibiotic, is commonly used to combat MRSA. Vancomycin
inhibits the synthesis of peptidoglycan, but unlike β-lactam
antibiotics, glycopeptide antibiotics target and bind to amino acids
in the cell wall, preventing peptidoglycan cross-linkages from
MRSA strains are most often found associated with
institutions such as hospitals, but are becoming increasingly
prevalent in community-acquired infections.
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Minor skin infections can be treated with triple antibiotic
Bacterial cells of S. aureus, which is one of the causal agents of
mastitis in dairy cows: Its large capsule protects the organism from
attack by the cow's immunological defenses.
Staphylococcal resistance to penicillin is mediated by penicillinase
(a form of β-lactamase) production: an enzyme that cleaves the
β-lactam ring of the penicillin molecule, rendering the antibiotic
ineffective. Penicillinase-resistant β-lactam antibiotics, such as
methicillin, nafcillin, oxacillin, cloxacillin, dicloxacillin, and
flucloxacillin, are able to resist degradation by staphylococcal
Resistance to methicillin is mediated via the mec operon, part of the
staphylococcal cassette chromosome mec (SCCmec). Resistance is
conferred by the mecA gene, which codes for an altered
penicillin-binding protein (PBP2a or PBP2') that has a lower affinity
for binding β-lactams (penicillins, cephalosporins, and carbapenems).
This allows for resistance to all β-lactam antibiotics, and obviates
their clinical use during
MRSA infections. As such, the glycopeptide
vancomycin is often deployed against MRSA.
Aminoglycoside antibiotics, such as kanamycin, gentamicin,
streptomycin, etc., were once effective against staphylococcal
infections until strains evolved mechanisms to inhibit the
aminoglycosides' action, which occurs via protonated amine and/or
hydroxyl interactions with the ribosomal RNA of the bacterial 30S
ribosomal subunit. Three main mechanisms of aminoglycoside
resistance mechanisms are currently and widely accepted:
aminoglycoside modifying enzymes, ribosomal mutations, and active
efflux of the drug out of the bacteria.
Aminoglycoside-modifying enzymes inactivate the aminoglycoside by
covalently attaching either a phosphate, nucleotide, or acetyl moiety
to either the amine or the alcohol key functional group (or both
groups) of the antibiotic. This changes the charge or sterically
hinders the antibiotic, decreasing its ribosomal binding affinity. In
S. aureus, the best-characterized aminoglycoside-modifying enzyme is
aminoglycoside adenylyltransferase 4' IA (ANT(4')IA). This enzyme has
been solved by X-ray crystallography. The enzyme is able to attach
an adenyl moiety to the 4' hydroxyl group of many aminoglycosides,
including kamamycin and gentamicin.
Glycopeptide resistance is mediated by acquisition of the vanA gene,
which originates from the enterococci and codes for an enzyme that
produces an alternative peptidoglycan to which vancomycin will not
Today, S. aureus has become resistant to many commonly used
antibiotics. In the UK, only 2% of all S. aureus isolates are
sensitive to penicillin, with a similar picture in the rest of the
world. The β-lactamase-resistant penicillins (methicillin, oxacillin,
cloxacillin, and flucloxacillin) were developed to treat
penicillin-resistant S. aureus, and are still used as first-line
Methicillin was the first antibiotic in this class to be
used (it was introduced in 1959), but, only two years later, the first
MRSA was reported in England.
MRSA generally remained an uncommon finding, even in
hospital settings, until the 1990s, when the
MRSA prevalence in
hospitals exploded, and it is now endemic.
MRSA infections in both the hospital and community setting are
commonly treated with non-β-lactam antibiotics, such as clindamycin
(a lincosamine) and co-trimoxazole (also commonly known as
trimethoprim/sulfamethoxazole). Resistance to these antibiotics has
also led to the use of new, broad-spectrum anti-Gram-positive
antibiotics, such as linezolid, because of its availability as an oral
drug. First-line treatment for serious invasive infections due to MRSA
is currently glycopeptide antibiotics (vancomycin and teicoplanin). A
number of problems with these antibiotics occur, such as the need for
intravenous administration (no oral preparation is available),
toxicity, and the need to monitor drug levels regularly by blood
tests. Also, glycopeptide antibiotics do not penetrate very well into
infected tissues (this is a particular concern with infections of the
brain and meninges and in endocarditis). Glycopeptides must not be
used to treat methicillin-sensitive S. aureus (MSSA), as outcomes are
Because of the high level of resistance to penicillins and because of
the potential for
MRSA to develop resistance to vancomycin, the U.S.
Centers for Disease Control and Prevention has published guidelines
for the appropriate use of vancomycin. In situations where the
MRSA infections is known to be high, the attending
physician may choose to use a glycopeptide antibiotic until the
identity of the infecting organism is known. After the infection is
confirmed to be due to a methicillin-susceptible strain of S. aureus,
treatment can be changed to flucloxacillin or even penicillin], as
Vancomycin-resistant S. aureus (VRSA) is a strain of S. aureus that
has become resistant to the glycopeptides. The first case of
vancomycin-intermediate S. aureus (VISA) was reported in Japan in
1996; but the first case of S. aureus truly resistant to
glycopeptide antibiotics was only reported in 2002. Three cases of
VRSA infection had been reported in the United States as of 2005.
About 33% of the U.S. population are carriers of S. aureus and about
2% carry MRSA.
The carriage of S. aureus is an important source of hospital-acquired
infection (also called nosocomial) and community-acquired MRSA.
Although S. aureus can be present on the skin of the host, a large
proportion of its carriage is through the anterior nares of the nasal
passages and can further be present in the ears. The ability of
the nasal passages to harbour S. aureus results from a combination of
a weakened or defective host immunity and the bacterium's ability to
evade host innate immunity. Nasal carriage is also implicated in
the occurrence of staph infections.
Spread of S. aureus (including MRSA) generally is through
human-to-human contact, although recently some veterinarians have
discovered the infection can be spread through pets, with
environmental contamination thought to play a relatively unimportant
part. Emphasis on basic hand washing techniques are, therefore,
effective in preventing its transmission. The use of disposable aprons
and gloves by staff reduces skin-to-skin contact, so further reduces
the risk of transmission.
Recently, myriad cases of S. aureus have been reported in hospitals
across America. Transmission of the pathogen is facilitated in medical
settings where healthcare worker hygiene is insufficient. S. aureus is
an incredibly hardy bacterium, as was shown in a study where it
survived on polyester for just under three months; polyester is
the main material used in hospital privacy curtains.
The bacteria are transported on the hands of healthcare workers, who
may pick them up from a seemingly healthy patient carrying a benign or
commensal strain of S. aureus, and then pass it on to the next patient
being treated. Introduction of the bacteria into the bloodstream can
lead to various complications, including endocarditis, meningitis,
and, if it is widespread, sepsis.
Ethanol has proven to be an effective topical sanitizer against MRSA.
Quaternary ammonium can be used in conjunction with ethanol to
increase the duration of the sanitizing action. The prevention of
nosocomial infections involves routine and terminal cleaning.
Nonflammable alcohol vapor in CO
NAV-CO2 systems have an advantage, as they do not attack metals or
plastics used in medical environments, and do not contribute to
An important and previously unrecognized means of community-associated
MRSA colonization and transmission is during sexual contact.
S. aureus is killed in one minute at 78 °C and in ten minutes at
Certain strains of S. aureus have been described as being resistant to
Top common bacterium in each industry
Vibrio parahaemolyticus, S. aureus,
Escherichia coli, S. aureus, Pseudomonas aeruginosa
As of 2015, no approved vaccine exists against S. aureus. Early
clinical trials have been conducted for several vaccines candidates
such as Nabi’s StaphVax and PentaStaph, Intercell’s / Merck’s
V710, VRi’s SA75, and others.
While some of these vaccines candidates have shown immune responses,
other aggravated an infection by S. aureus. To date, none of these
candidates provides protection against a S. aureus infection. The
development of Nabi’s StaphVax was stopped in 2005 after phase III
trials failed. Intercell’s first V710 vaccine variant was
terminated during phase II/III after higher mortality and morbidity
were observed among patients who developed S. aureus infection.
Nabi's enhanced S. aureus vaccines candidate PentaStaph was sold in
GlaxoSmithKline Biologicals S.A. The current status of
PentaStaph is unclear. A WHO document indicates that PentaStaph is
failed in phase III trial stage.
GlaxoSmithKline started a phase 1 blind study to evaluate its
GSK2392103A vaccine. As of 2016, this vaccine is no longer under
Pfizer's S. aureus four-antigen vaccine SA4Ag was granted fast track
designation by the U.S.
Food and Drug Administration
Food and Drug Administration in February
2014. In 2015,
Pfizer has commenced a phase 2b trial regarding
the SA4Ag vaccine. Phase 1 results published in February 2017
showed a very robust and secure immunogenicity of SA4Ag.
Novartis Vaccines and Diagnostics, a former division of
now part of GlaxoSmithKline, published in 2015 promising pre-clinical
results of their four-component
Staphylococcus aureus vaccine,
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Type strain of
Staphylococcus aureus at
BacDive - the Bacterial
Firmicutes (low-G+C) Infectious diseases
Bacterial diseases: G+
primarily A00–A79, 001–041, 080–109
Viridans streptococci: S. mitis
bacitracin susceptible: S. pyogenes
Group A streptococcal infection
bacitracin resistant, CAMP test+: S. agalactiae
Group B streptococcal infection
Streptococcus iniae infection
Urinary tract infection
Staphylococcal scalded skin syndrome
Toxic shock syndrome
Clostridial necrotizing enteritis
Peptostreptococcus (non-spore forming)