Online Textbook Bacteriology is continuously updated and includes information on Staphylococcus, MRSA, Streptococcus, E. coli, anthrax, cholera, tuberculosis, Lyme disease and other bacterial diseases of humans.
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The Online Textbook of Bacteriology is a general and medical microbiology text and includes discussion of staph, MRSA, strep, Anthrax, E. coli, cholera, tuberculosis, Lyme Disease and other bacterial pathogens.
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Tag words: Staphylococcus aureus, Staphylococcus, staph, staphylococcal, S. aureus, MRSA, CA-MRSA, superbug, staph infection, wound infection, food poisoning, toxic shock syndrome, antibiotic resistance, Staph epidermidis, normal flora, skin bacteria, bacteriology, microbiology

Staphylococcus aureus

Kingdom: Bacteria
Phylum: Firmicutes
Class: Bacilli
Order: Bacillales
Family: Staphylococcaceae
Genus: Staphylococcus
Species: S. aureus


Common References: Staphylococcus, Staph, MRSA, Superbug










Kenneth Todar currently teaches Microbiology 100 at the University of Wisconsin-Madison.  His main teaching interest include general microbiology, bacterial diversity, microbial ecology and pathogenic bacteriology.

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Staphylococcus (page 4)

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Avoidance of Host Defenses

S. aureus expresses a number of factors that have the potential to interfere with host defense mechanisms. This includes both structural and soluble elements of the bacterium.

Capsular Polysaccharide

The majority of clinical isolates of S aureus express a surface polysaccharide of either serotype 5 or 8. This has been called a microcapsule because it can be visualized only by electron microscopy unlike the true capsules of some bacteria which are readily visualized by light microscopy. S. aureus strains isolated from infections express high levels of the polysaccharide but rapidly lose the ability when cultured in the laboratory. The function of the capsule in virulence is not entirely clear. Although it does impede phagocytosis in the absence of complement, it also impedes colonization of damaged heart valves, perhaps by masking adhesins.

Protein A

Protein A is a surface protein of S. aureus which binds IgG molecules by their Fc region. In serum, the bacteria will bind IgG molecules in the wrong orientation on their surface, which disrupts opsonization and phagocytosis. Mutants of S. aureus lacking protein A are more efficiently phagocytosed in vitro, and mutants in infection models have diminished virulence.

Leukocidin

S. aureus can express a toxin that specifically acts on polymorphonuclear leukocytes. Phagocytosis is an important defense against staphylococcal infection so leukocidin should be a virulence factor.

Exotoxins

S. aureus can express several different types of protein toxins which are probably responsible for symptoms during infections. Those which damage the membranes of cells were discussed previously under Invasion. Some will lyse erythrocytes, causing hemolysis, but it is unlikely that hemolysis is a relevant determinant of virulence in vivo. Leukocidin causes membrane damage to leukocytes, but is not hemolytic.

Systemic release of alpha toxin causes septic shock, while enterotoxins and TSST-1 are superantigens that may cause toxic shock. Staphylococcal enterotoxins cause emesis (vomiting) when ingested and the bacterium is a leading cause of food poisoning (intoxication).

The exfoliatin toxin causes scalded skin syndrome in neonates, which results in widespread blistering and loss of the epidermis. There are two antigenically distinct forms of the toxin, ETA and ETB. The toxins have esterase and protease activity and apparently target a protein which is involved in maintaining the integrity of the epidermis.

Superantigens: enterotoxins and toxic shock syndrome toxin

S. aureus secretes two types of toxins with superantigen activity, enterotoxins, of which there are six antigenic types (named SE-A, B, C, D, E and G), and toxic shock syndrome toxin (TSST-1). Enterotoxins cause diarrhea and vomiting when ingested and are responsible for staphylococcal food poisoning. TSST-1 is expressed systemically and is the cause of toxic shock syndrome (TSS). When expressed systemically, enterotoxins can also cause toxic shock syndrome. In fact, enterotoxins B and C cause 50% of non-menstrual cases of TSS. TSST-1 is weakly related to enterotoxins, but it does not have emetic activity. TSST-1 is responsible for 75% of TSS, including all menstrual cases. TSS can occur as a sequel to any staphylococcal infection if an enterotoxin or TSST-1 is released systemically, and the host lacks appropriate neutralizing antibodies.

Superantigens stimulate T cells non-specifically without normal antigenic recognition (Figure 4). Up to one in five T cells may be activated, whereas only 1 in 10,000 are stimulated during a usual antigen presentation. Cytokines are released in large amounts, causing the symptoms of TSS. Superantigens bind directly to class II major histocompatibility complexes of antigen-presenting cells outside the conventional antigen-binding grove. This complex recognizes only the Vb element of the T cell receptor. Thus any T cell with the appropriate Vb element can be stimulated, whereas normally, antigen specificity is also required in binding.

Superantigens and the non-specific stimulation of T cells.

FIGURE 4. Superantigens and the non-specific stimulation of T cells. Superantigens bind directly to class II major histocompatibility complexes (MHC II) of antigen-presenting cells outside the normal antigen-binding groove. Up to one in five T cells may be activated. Cytokines are released in large amounts, causing the symptoms of toxic shock.

Exfoliatin toxin (ET) The exfoliatin toxin, associated with scalded skin syndrome, causes separation within the epidermis, between the living layers and the superficial dead layers. The separation is through the stratum granulosum of the epidermis. This is probably why healing occurs with little scarring although the risks of fluid loss and secondary infections are increased. Staphylococcal exfoliative toxin B has been shown to specifically cleave desmoglein 1, a cadherin that is found in desmosomes in the epidermis.
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Kenneth Todar has taught microbiology to undergraduate students at The University of Texas, University of Alaska and University of Wisconsin since 1969.

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