Pathogenesis of Staphylococcus

pathogenesis of staphylococcus
staphylococci, particularly s epidermidis, are members of the normal flora of the human skin and respiratory and gastrointestinal tracts. nasal carriage of s aureus occurs in 20–50% of humans. staphylococci are also found regularly on clothing, bed linens, and other fomites in human environments.
the pathogenic capacity of a given strain of s aureus is the combined effect of extracellular factors and toxins together with the invasive properties of the strain. at one end of the disease spectrum is staphylococcal food poisoning, attributable solely to the ingestion of preformed enterotoxin at the other end are staphylococcal bacteremia and disseminated abscesses in all organs.
pathogenic, invasive s aureus produces coagulase and tends to produce a yellow pigment and to be hemolytic. nonpathogenic, noninvasive staphylococci such as s epidermidis are coagulase-negative and tend to be nonhemolytic. such organisms rarely produce suppuration but may infect orthopedic or cardiovascular prostheses or cause disease in immunosuppressed persons. s saprophyticus is typically nonpigmented, novobiocin-resistant, and nonhemolytic it causes urinary tract infections in young women.


pathology
the prototype of a staphylococcal lesion is the furuncle or other localized abscess. groups of s aureus established in a hair follicle lead to tissue necrosis (dermonecrotic factor). coagulase is produced and coagulates fibrin around the lesion and within the lymphatics, resulting in formation of a wall that limits the process and is reinforced by the accumulation of inflammatory cells and, later, fibrous tissue. within the center of the lesion, liquefaction of the necrotic tissue occurs (enhanced by delayed hypersensitivity), and the abscess "points" in the direction of least resistance. drainage of the liquid center necrotic tissue is followed by slow filling of the cavity with granulation tissue and eventual healing.
focal suppuration (abscess) is typical of staphylococcal infection. from any one focus, organisms may spread via the lymphatics and bloodstream to other parts of the body. suppuration within veins, associated with thrombosis, is a common feature of such dissemination. in osteomyelitis, the primary focus of s aureus growth is typically in a terminal blood vessel of the metaphysis of a long bone, leading to necrosis of bone and chronic suppuration. s aureus may cause pneumonia, meningitis, empyema, endocarditis, or sepsis with suppuration in any organ. staphylococci of low invasiveness are involved in many skin infections (eg, acne, pyoderma, or impetigo). anaerobic cocci (peptostreptococcus) participate in mixed anaerobic infections.
staphylococci also cause disease through the elaboration of toxins, without apparent invasive infection. bullous exfoliation, the scalded skin syndrome, is caused by the production of exfoliative toxins. toxic shock syndrome is associated with tsst-1.
treatment
most persons harbor staphylococci on the skin and in the nose or throat. even if the skin can be cleared of staphylococci (eg, in eczema), reinfection by dropinglets will occur almost immediately. because pathogenic organisms are commonly spread from one lesion (eg, a furuncle) to other areas of the skin by fingers and clothing, scrupulous local antisepsis is important to control recurrent furunculosis.
abscesses and other closed suppurating lesions are treated by drainage, which is essential, and antimicrobial therapy.
bacteremia, endocarditis, pneumonia, and other severe infections due to s aureus require prolonged intravenous therapy with a b-lactamase-resistant penicillin. vancomycin is often reserved for use with nafcillin-resistant staphylococci.
s epidermidis infections are difficult to cure because they occur in prosthetic devices where the bacteria can sequester themselves in a biofilm. s epidermidis is more often resistant to antimicrobial drugs than is s aureus approximately 75% of s epidermidis strains are nafcillin-resistant.
penicillin g-resistant s aureus strains from clinical infections always.
newer antimicrobial agents such as linezolide, daptomycin, and quinupristin/dalfopristin are generally reserved for patients with serious staphylococcal or enterococcal infections that are resistant to the more traditional agents, who are failing clinically or who are highly allergic