Staphylococcus Aureus

Staphylococcus Aureus Diagnostics

1. gram positive 2. + catalase test: distinguishes staph from strep 3. + coagulase test: distinguishes staph a. from other staph (staph epi) 4. beta hemolytic, turns agar yellow/clear 5. ferments mannitol, turns agar yellow. survives high salt/lipid conditions. 6. golden color when plated on blood agar (easy to grow)

Staphylococcus Aureus Clinical Disease

Causes a number of diseases at different host sites. Some due to toxins, others due to proliferation of staph, tissue destruction and abscess formation. • Wide variety of skin, soft tissue, and deep seated, life-threatening diseases. Some depend on production of specific microbial products. • Food intoxication-heat stable enterotoxins consumed resulting in rapid (2-6 hours) onset of symptoms such as emesis and diarrhea • Toxic Shock Syndrome- toxin shock syndrome toxin 1 or exotoxin B or C • Staphylococcal scalded skin syndrome -blistering disease caused by exfoliative toxins A or B associated with epidemics in nurseries • More invasive and disseminated disease (bacteremia, endocarditis, intraveneous catheter infection, septic arthritis, seeding of bone to cause osteomyelitis) result when tissue barriers are interrupted • An important cause of wound infection

Staphylococcus Aureus Pathogenesis (long)

Location: Nares (nose holes) Virulence factors: Capsule: 11 different capsular serotypes, which 5 and 7 being most commonly associated with infection. Prevents phagocytosis of bacterium by leukocytes and helps bacteria adhere to catheters and other synthetic materials. Important for less virulent coagulase negative staph strains that frequently colonize in-dwelling catheters. Protein A: main virulence factor, located on cell wall of most Staph A strains (but not coag - strains). binds Fc portion of Abs, preventing binding to antigen and opsonization. Thus, helps with immune evasion. Toxins: S. aureus also produces many toxins that play a role in its virulence and each contributes differently to tissue destruction. Most toxins are produced by plasmids. 1. alpha toxin: made by most strains, inserts into cell membrane and forms pores, Na+ and Ca2+ flow into cell, water follows and cell undergoes osmolysis. 2. beta toxin: sphinomyelinase enzyme present in most s. aureus strains; cleaves sphingomyelin in membranes, damaging membrane leading to lysis. 3. exfoliative toxins: ETA and ETB, present in less than 10% of S aureus strains. Proteases that digest proteins involved in cell-cell contact, leading to skin exfoliation. 4. enterotoxins: 30-50% of staph strains. associated with food poisoning. these toxins tend to be heat stable and resistant to hydrolysis by stomach and intestinal enzymes thus, if a food product is contaminated, the best thing to do is avoid it. these are thought to act as super antigens and nonspecifically activate T cells and cytokine release. Mast cell degranulation is thought to lead to emesis characteristic of staph food poisoning. 5. Toxic Shock Syndrome: toxin is very stable, superantigen that induces nonspecific and massive release of cytokines that lead to vascular permeability and falling blood pressure. In addition to toxins, Staph can produce a number of enzymes that help it penetrate tissues and spread. Coagulase enzyme helps it bind fibrin and form walled off abscesses, a major feature of S. aureus infection. In contrast, S. epidermis expresses different factors and the tissue response does not cause abscess formation.

S. Epidermis and other coagulase negative staph clinical diseases

S. epidermidis, as a very common colonizer of human skin, is frequently responsible for infections involving in-dwelling medical devices. Major considerations include: Endocarditis. Staph epi is a major cause of endocarditis of artificial heart valves. More commonly, the infection takes root at the sites where the valve is sewn into the heart. This can lead to separation of the valve at the annulus. S. epidermidis and other coag-negative staph can also infect native heart valves, but this is much less common. Catheter and shunt infections. The presence of an exopolysaccharide or 'slime layer' on staph enables efficient attachment to artificial surfaces. Thus, from 20 to 65% of all infections of indwelling catheters and shunts are due to coag-neg staph - this is a major problem because indwelling catheters are used extensively especially in debilitated patients. Such colonization leads to persistent bacteremia, and the organisms can be seeded most anywhere else in the body, leading to other localized infections. Prosthetic joint infections. Again, an important problem that is commonly associated with coag-negative staph. Importantly, patients usually have localized pain and joint failure, but lack more systemic symptoms. Urinary tract infections. S. saprophyticus is a significant cause of UTIs in sexually active women.

Staphylococcus Aureus Physiology and Structure

gram positive cocci. aerobic. Staph = grape Coccus = granule Aureus = golden thus, looks like a bunch of grapes (cluster of cocci) under the microscope. when S. aureus grows on blood agar, it appears golden. only staph species that is coagulase positive.

Staphylococcus Aureus Treatment, Prevention and Control

• Antibiotic resistance, especially the spread of MRSA, has complicated treatment. • MRSA isolates encode altered penicillin-binding proteins resulting in resistance to all β-lactam agents. • Different patterns of resistance in community-acquired and hospital-acquired strains. • MRSA has driven the use of vancomycin in hospitals, which has contributed to the spread of vancomycin-resistance among some other bacteria. • Naf for staph - naficillin for staph

Staphylococcus Aureus Pathogenesis and Immunity (Short)

• S. aureus expresses multiple virulence factors that allow it to attach to tissues, evade clearance, and invade and damage its host. Coagulase-negative Staph are much less virulent. • Expression of specific toxins by some S. aureus strains results in distinct clinical syndromes. • S. aureus infection often leads to abscess formation. • Infection may be recurrent as immunity from prior exposure is not protective.

Staphylococcus Aureus Epidemiology

• Staph colonizes human skin. For S. aureus, the external nares are the best single site to find the organism. Also found on skin that contacts the nose and in the GI and urogenital tracts. • There are persistent carriers, intermittent carriers and non-carriers. • Since on skin, spread is often due to shedding, autoinoculation and person to person. • Outbreaks of S. aureus often associated with the success and widespread dissemination of individual clones, including the currently circulating MRSA clone USA300.