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Staphylococcus aureus

Staphylococcus aureus
Scanning electron micrograph of S. aureus; false color added.
Scientific classification
Domain: Bacteria
Kingdom: Eubacteria
Phylum: Firmicutes
Class: Coccus
Order: Bacillales
Family: Staphylococcaceae
Genus: Staphylococcus
Species: S. aureus
Binomial name
Staphylococcus aureus
Rosenbach 1884

Staphylococcus aureus is a gram-positive coccal bacterium that is a member of the Firmicutes, and is frequently found in the respiratory tract and on the skin forms where perspiration is present. It is often positive for catalase and nitrate reduction. Although S. aureus is not always pathogenic, it is a common cause of skin infections such as abscesses, respiratory infections such as sinusitis, and food poisoning. Pathogenic strains often promote infections by producing potent protein toxins, and expressing cell-surface proteins that bind and inactivate antibodies. The emergence of antibiotic-resistant forms of S. aureus such as MRSA is a worldwide problem in clinical medicine.

Staphylococcus was first identified in 1880 in Aberdeen, Scotland, by the surgeon Sir Alexander Ogston in pus from a surgical abscess in a knee joint.[1] This name was later appended to Staphylococcus aureus by Friedrich Julius Rosenbach, who was credited by the official system of nomenclature at the time. An estimated 20% of the human population are long-term carriers of S. aureus[2] which can be found as part of the normal skin flora and in the nostrils.[2][3] S. aureus is the most common species of Staphylococcus to cause Staph infections and is a successful pathogen due to a combination of nasal carriage and bacterial immunoevasive strategies.[2][3] S. aureus can cause a range of illnesses, from minor skin infections, such as pimples,[4] 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. Its incidence ranges from skin, soft tissue, respiratory, bone, joint, endovascular to wound infections. It is still one of the five most common causes of hospital-acquired infections and is often the cause of postsurgical wound infections. Each year, around 500,000 patients in United States' hospitals contract a staphylococcal infection like S. aureus.[5]

Staphylococcus aureus
Classification and external resources
Specialty Infectious disease
ICD-9-CM 041.11


  • Microbiology 1
  • Role in disease 2
    • Atopic dermatitis 2.1
    • Animal infections 2.2
  • Virulence factors 3
    • Enzymes 3.1
    • Toxins 3.2
    • Other immunoevasive strategies 3.3
  • Classical diagnosis 4
    • Rapid diagnosis and typing 4.1
  • Treatment and antibiotic resistance 5
    • Mechanisms of antibiotic resistance 5.1
  • Carriage of Staphylococcus aureus 6
  • Infection control 7
  • Research 8
  • See also 9
  • References 10
  • Further reading 11
  • External links 12


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 (beta hemolysis).

S. aureus (, facultative anaerobic, gram-positive coccal bacterium also known as "golden staph" and Oro staphira. In medical literature, the bacterium is often referred to as S. aureus or Staph aureus. Staphylococcus should not be confused with the similarly named and medically relevant genus Streptococcus. S. aureus appears as grape-like clusters when viewed through a microscope, and has large, round, golden-yellow colonies, often with hemolysis, when grown on blood agar plates.[6] S. aureus reproduces asexually by binary fission. The two daughter cells do not fully separate and remain attached to one another, so the cells are observed in clusters.[7]

S. aureus is catalase-positive (meaning it can produce the enzyme catalase). Catalase converts hydrogen peroxide (H
) 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[6][8] and incorrect species identification can impact effective treatment and control measures.[9]

Role in disease

SEM of methicillin-resistant S. aureus

S. aureus is responsible for many infections, but it may also occur as a commensal. The presence of S. aureus does not always indicate infection. It can survive from hours to weeks, or even months, on dry environmental surfaces, depending on strain.[10]

S. aureus can infect tissues when the skin or mucosal barriers have been breached. This can lead to many different types of infections, including boils and carbuncles (a collection of boils).

S. aureus infections can spread through contact with pus from an infected wound, skin-to-skin contact with an infected person by producing hyaluronidase that destroys tissues, and contact with objects such as towels, sheets, clothing, or athletic equipment used by an infected person. Deeply penetrating S. aureus infections can be severe. Prosthetic joints put a person at particular risk of septic arthritis, and staphylococcal endocarditis (infection of the heart valves) and pneumonia. Strains of S. aureus can host phages, such as Φ-PVL (produces Panton-Valentine leukocidin), that increase virulence.

Atopic dermatitis

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 this, Ritter's disease, can be observed in neonates.[11]

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.[12] The relationship between S. aureus and atopic dermatitis is unclear.[12] Evidence shows that attempting to control S. aureus with oral antibiotics is not efficacious.[12]

Animal infections

S. aureus can survive on dogs,[13] cats,[14] and horses,[15] and can cause Loskill, Peter; Pereira, Pedro M.; Jung, Philipp; Bischoff, Markus; Herrmann, Mathias; Pinho, Mariana G.; Jacobs, Karin (2 September 2014). "Reduction of the Peptidoglycan Crosslinking Causes a Decrease in Stiffness of the Staphylococcus aureus Cell Envelope". Biophysical Journal 107 (5): 1082–1089.  

External links

  • — Discusses how to prevent the spread of MRSA
  • — Understand what the MRSA infection is all about.
  • "Staphylococcus aureus". NCBI Taxonomy Browser. 1280. 
  • Packham, Christopher (March 16, 2015). "Successful in vivo test of breakthrough Staphylococcus aureus vaccine". Medical Press. Retrieved March 2015. 

Further reading

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  3. ^ a b Cole, A. M.; Tahk, S.; Oren, A.; Yoshioka, D.; Kim, Y. H.; Park, A.; Ganz, T (November 2001). nasal carriage"Staphylococcus aureus"Determinants of . Clin Diagn Lab Immunol 8 (6): 1064–9.  
  4. ^ "Staphylococcal Infections". MedlinePlus [Internet]. Bethesda, MD: National Library of Medicine, USA. Skin infections are the most common. They can look like pimples or boils. 
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See also

In 2015, Pfizer has commenced a Phase 2 trial with its 4-antigen Staphylococcus aureus vaccine SA4Ag.[61]

In 2010, GlaxoSmithKline (GSK) started a Phase 1 blind study to evaluate its GSK2392103A vaccine.[60]

Nabi’s enhanced Staphylococcus aureus vaccines candidate PentaStaph was sold in 2011 to GlaxoSmithKline Biologicals S.A. (GSK).[59] The current status of PentaStaph is unclear.

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 where failed.[57] Intercell’s first V710 vaccine variant was terminated during Phase II/III after higher mortality and morbidity was observed among patients who developed S. aureus infection.[58]

As of 2015, no approved vaccine exists against Staphylococcus aureus. Early clinical trials have been conducted for several vaccines candidates like Nabi’s StaphVax & PentaStaph, Intercell’s / Merck’s V710, VRi’s SA75 and others.[56]


Top common bacterium in each industry
Catering industry
Vibrio parahaemolyticus , Staphylococcus aureus, Bacillus cereus
Medical industry
Escherichia coli, Staphylococcus aureus , Pseudomonas aeruginosa[55]

These findings open the way to a biological control therapy to help in the treatment of S. aureus infections which are becoming a growing threat due to the rise of resistance to conventional antibiotic treatments.

A 2011 study[54] points to this new possible way to control S. aureus. This study was performed from observations of the nasal microbial flora of a diverse group of people. Two different strains of S. epidermidis occur, one that inhibits biofilm formation by S. aureus, S. epidermidis strain JK16 (inhibitory type), and one that does not (noninhibitory type) S. epidermidis strain JK11. Some patients were not affected by S. aureus, because these patients had S. aureus together with S. epidermis (inhibitory type), in their nasal microbial flora. This is due to an amensalistic relationship between these microorganisms, the inhibitory strain of S. epidermidis and S. aureus.

Biological control might be a new possible way to control S. aureus in body surfaces. Colonization of body surfaces (especially in the nose) by S. epidermidis (inhibitory strain JK16) impairs the establishment of S. aureus.

The non-proteinogenic amino acid L-homoarginine is a growth inhibitor of S. aureus, as well as Candida albicans. It is assumed to be an antimetabolite of arginine.

S. aureus is killed in one minute at 78 °C and in ten minutes at 64 °C.[53]

Staff or patients who are found to carry resistant strains of S. aureus may be required to undergo "eradication therapy", which may include antiseptic washes and shampoos (such as chlorhexidine) and application of topical antibiotic ointments (such as mupirocin or neomycin) to the anterior nares of the nose.

An important and previously unrecognized means of community-associated MRSA colonization and transmission is during sexual contact.[52]

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 antibacterial resistance.

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.

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;[51] polyester is the main material used in hospital privacy curtains.

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,[50] 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 and, therefore, further reduces the risk of transmission.

Infection control

The carriage of Staphylococcus 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.[2] 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.[49]

Carriage of Staphylococcus aureus

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;[46] but the first case of S. aureus truly resistant to glycopeptide antibiotics was only reported in 2002.[47] Three cases of VRSA infection had been reported in the United States as of 2005.[48]

Because of the high level of resistance to penicillins and because of the potential for MRSA to develop resistance to vancomycin, the flucloxacillin or even penicillin, as appropriate.

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 inferior.[45]

Despite this, 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.[44]

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 treatment. Methicillin was the first antibiotic in this class to be used (it was introduced in 1959), but, only two years later, the first case of MRSA was reported in England.[43]

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 bind.

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.[42] The enzyme is able to attach an adenyl moiety to the 4' hydroxyl group of many aminoglycosides, including kamamycin and gentamicin.

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.[41] There are three main mechanisms of aminoglycoside resistance mechanisms which are currently and widely accepted: aminoglycoside modifying enzymes, ribosomal mutations, and active efflux of the drug out of the bacteria.

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.

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 penicillinase.

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.

Mechanisms of antibiotic resistance

Researchers from Italy have identified a bacteriophage active against S. aureus, including MRSA, in mice and possibly humans.[40]

MRSA and often pronounced or , 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 forming. MRSA strains are most often found associated with institutions such as hospitals, but are becoming increasingly prevalent in community-acquired infections. A recent study by the Translational Genomics Research Institute showed that nearly half (47%) of the meat and poultry in U.S. grocery stores were contaminated with S. aureus, with more than half (52%) of those bacteria resistant to antibiotics.[39] This resistance is commonly caused by the widespread use of antibiotics in the husbandry of livestock, including prevention or treatment of an infection, as well as promoting growth.

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 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%.[38]

The treatment of choice for S. aureus infection is penicillin. An antibiotic derived from Penicillum fungus, 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,[35][36] but its use is controversial because of the high risk of damage to the kidneys.[37] The duration of treatment depends on the site of infection and on severity.

Treatment and antibiotic resistance

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.[34] 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.

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.[34] 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 patters 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.

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.[32] 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.[33] With these methods, it can be determined where strains of MRSA originated and also where they are currently.[34] 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.[32]

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.[30][31]

Rapid diagnosis and typing

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.

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.

Typical gram-positive cocci, in clusters, from a sputum sample, Gram stain

Classical diagnosis

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.[28] 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.[29]

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.[27] In mice, the pigmented strains cause lingering abscesses when inoculated into wounds, whereas wounds infected with the unpigmented strains quickly heal.

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.[27][28]

Staphylococcal pigments
S. aureus on trypticase soy agar: The strain is producing a yellow pigment staphyloxanthin.

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 MRSA infections.[26]

Protein A is anchored to staphylococcal peptidoglycan pentaglycine bridges (chains of five glycine residues) by the transpeptidase sortase A.[24] 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 regions.[25]

Protein A

Other immunoevasive strategies

Other toxins
Staphylococcal toxins that act on cell membranes include alpha toxin, beta toxin, delta toxin, and several bicomponent toxins. The bicomponent toxin Panton-Valentine leukocidin (PVL) is associated with severe necrotizing pneumonia in children.[22][23] The genes encoding the components of PVL are encoded on a bacteriophage found in community-associated methicillin-resistant S. aureus (MRSA) strains.
EF toxins are 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.[21]
Exfoliative toxins

(PTSAgs) have desquamation. 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 S. aureus gastroenteritis. This 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.[20][21]

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.[19]


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.[18]


Virulence factors


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