Staphylococcus

Staphylococcus grow in grape-like clusters. Catalase-positive. – Catalase is an enzyme that converts hydrogen peroxide to water and oxygen; this allows the bacteria to resist oxidative stress. Staphylococci are non-motile and do not form spores. Staphylococcus aureus is the most virulent strain of staphylococcus and is a leading cause of infectious disease. Carotenoid pigments give S. aureus a distinctive golden color. Capsule of S. aureus inhibits phagocytosis; additionally, it disrupts chemotaxis and mononuclear cell proliferation. Teichoic acids, which are anchored to the peptidoglycan of the cell wall, bind S. aureus to fibronectin of the host extracellular matrix. Lipoteichoic acid and the peptidoglycan layer have endotoxin-like effects: they trigger macrophage release of IL-1 and Tumor Necrosis Factor, which induce hypotension and cause septic shock. Cell wall Protein A binds antibodies to block complement activation and inhibit phagocytosis. Biofilm firmly adheres bacterial colonies and debris to host tissues. The biofilm reinforces adhesion to the host and shields the bacteria from immune cells and antibiotics. Cytotoxins (alpha, beta, delta, gamma, and Panton-Valentine leukocidin) that lyse red and white blood cells. Exfoliative toxins (A & B) are proteases that destroy the stratum granulosum of the epidermis. Enterotoxins stimulate T-cell and macrophage release of cytokines and trigger Mast cell degranulation, which results in peristalsis and vomiting. Toxic shock syndrome toxin -1 stimulates T cell proliferation and T cell and macrophage release of IL1, IL-2, and TNF, which causes blood vessel leakage. Superantigens Exfoliative toxin A, Enterotoxin, and TSS-1 induce massive immune responses that cause significant damage to the host. Coagulase converts fibrinogen to fibrin; by promoting clot formation and clumping, it is thought that S. aureus protects itself from host defenses. Fibrinolysin, aka, staphylokinase, has the opposite effects: it dissolves fibrin clots, potentially allowing S. aureus to spread to new niches within the host. Hyaluronidase degrades hyaluronic acids, which are present in host extracellular matrix. Lipases free fatty acids; it is thought that lipases inhibit host granulocytes, inactivate bactericidal lipids, and promote biofilm formation. Nucleases hydrolyze DNA and aid in bacterial evasion of Neutrophil Extracellular Traps (NETs). Impetigo tends to occur on the limbs and face of children; it is characterized by flat, reddened areas with pustules that crust upon rupture. Be aware that Group A streptococci also cause some forms of impetigo. Folliculitis, as its name suggests, is infection of the hair follicle; "styes" are infections of eyelash follicles. Furuncles, aka, boils, are larger, raised pus-filled nodules that can be quite painful; surgical drainage is sometimes necessary. Carbuncles are furuncles that coalesce and affect the deeper subcutaneous tissues; bacteremia leads to chills and fever. Wound infections can also be caused by S. aureus, particularly in patients with compromised immune systems. Acute endocarditis occurs when bacteria and cellular debris accumulate in vegetations and damage the cardiac valves. Blood flow can be significantly impaired, and vegetations that break free can embolize. Pneumonia with infiltrates and consolidation or abscesses caused by cell-damaging toxins and enzymes. Some patients go on to develop empyema, which is the accumulation of pus in the pleural cavity. Osteomyelitis occurs when S. aureus infects the bones; early onset is characterized by pain and fever. In children, infection involves the metaphyseal area of long bones. In adults, infection tends to occur in the vertebral bodies. In subacute osteomyelitis, localized infection within the bone can produce Brodie's abscesses. Septic arthritis typically affects the large joints. Scalded skin syndrome, aka, Ritter's disease, is caused by exfoliative toxins, and primarily affects newborns and young children. Disease onset is abrupt, and begins with perioral inflammation followed by superficial cutaneous blistering, then epithelial desquamation. Antibodies appear within 7-10 days, scarring is unusual, and mortality rate is low. Food poisoning is caused by ingestion of enterotoxins, which produces nausea, vomiting, and diarrhea. Toxic shock syndrome toxin -1 penetrates mucosal barriers and induces fever, hypotension and shock, and rash. Because it travels in the bloodstream, the toxin causes damage to multiple organ systems. The following are often associated with infections of prosthetic joints and valves as well as catheters and shunts: Staphylococcus epidermidis Staphylococcus saprophytic is associated with urinary tract infections in sexually active young women. Staphylococcus lugdunensis is particularly associated with native valve endocarditis. Staphylococcus haemolyticus