Staphylococcus aureus

Categorization
Cell Wall: Gram Positive	Shape: Cocci
Biochemistry: Catalase Positive, Coagulase Positive

Associated Factors

S. aureus possesses a wide variety of factors which substantially increase its virulence in humans.

Protein A: Binds Fc Region of antibody at the complement-binding site, preventing activation of complement, and thus protecting bacteria from opsonization
Coagulase: Coagulates fibrin around bacteria protecting it from phagocytosis
Hemolysins and leukocidins: These proteins form pores in cellular membranes that lyse erythrocytes (hence S. aureus is beta-hemolytic) as well as neutrophils, macrophages, and platelets.

Penicillinase: A secreted enzyme that is a beta-lactamase thus inactivates Beta-lactam Antibiotics
Novel Penicillin Binding Protein (some strains): A version of bacterial tanspeptidase (See: Bacterial Cell Wall) that does not bind penicillin and can thus renders bacteria unaffected by penicillins and cephalosporins.

S. aureus elaborates a variety of enzymes which digest proteins, lipids, connective tissue and thus facilitates spread of the organisms from the original site of infection.

Exfoliatin: Causes skin to slough off especially in Scalded Skin Syndrome (see below)
Enterotoxins: Causes food poisoning and infectious diarrhea
Toxic Shock Syndrome toxin: Responsible for Staphylococcal Toxic Shock Syndrome

Clinical Consequences

For many individual S. aureus is just a normal part of the skin and nasal bacterial flora. However, significant pathological consequences can result from either release of exotoxins or from direct bacterial invasion into tissues.

Food Poisoning (i.e. Gastroenteritis): Infectious Diarrhea with a short incubation period of less than 8hrs characterized by nausea, vomiting, and abdominal pain. Caused by ingestion of pre-formed exotoxin produced by S. aureus growing in food prior to consumption.
Toxic Shock Syndrome:
Staphylococcal Scalded Skin Syndrome: Caused by localized skin infection with S. aureus strains that produce the exfoliatin toxin. Toxin induces cleavage of cell-cell adhesions in the middle of the epidermis. This results in the sloughing off of fine sheets that reveal erythematous areas underneath. Low mortality and generally affects neonates and Children.

Skin: S. aureus infections of the skin are very common. Minor, superficial infections may appear as impetigo. However, organisms can invade deeply, resulting in cellulitis or in extreme cases furuncles and carbuncles.
Wounds: S. aureus is an extremely common cause of wound infections and often leads to the development of abscesses in the injured tissue.
Lung: Rare but severe lobar pneumonia (both community and hospital-acquired) can be caused by S. aureus and usually follows a case of previous Influenza Virus infection. Frequently, lung abscess can result along with empyema.
Bone and Joints: Infections of bones and joints are usually due to hematogenous spread of bacteria from a local infection. S. aureus infections of the joints are the most common cause of septic arthritis in children and elderly adults over 50yo. Osteomyelitis caused by S. aureus is also common among children.
CNS: Bacterial meningitis or brain abscesses.
Heart: S. aureus can be a cause of Infective Endocarditis. This is especially true in IV drug abusers where a right-sided endocarditis results, affecting the Tricuspid Valve
Bacteremia and Sepsis: Hematogenous infection can occur due to spread from a localized infection or from an indwelling venous catheter.

Treatment

S. aureus is traditionally treated with Beta-lactam Penicillins. However, most clinical strains now possess beta-lactamases and so penicillins that are resistant to this enzyme must now be used. More recently, certain S. aureus strains have evolved with an altered transpeptidase that does not bind any Beta-lactam antibiotics. These "Methicillin-Resistant" strains must be treated with other classes of antibacterials.

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