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Staphylococci are gram-positive aerobic organisms. Staphylococcus aureus is the most pathogenic; it typically causes skin infections and sometimes pneumonia, endocarditis, and osteomyelitis. It commonly leads to abscess formation. Some strains elaborate toxins that cause gastroenteritis, scalded skin syndrome, and toxic shock syndrome. Diagnosis is by Gram stain and culture. Treatment is usually with penicillinase-resistant β-lactams, but because antibiotic resistance is common, vancomycin or other newer antibiotics may be required. Some strains are partially or totally resistant to all but the newest antibiotics, which include linezolid, quinupristin/dalfopristin, daptomycin, telavancin, dalbavancin, tigecycline, and ceftaroline.
The ability to clot blood by producing coagulase distinguishes the virulent pathogen, Staphylococcus aureus, from the less virulent coagulase-negative staphylococcal species. Coagulase-positive S. aureus is among the most ubiquitous and dangerous human pathogens, for both its virulence and its ability to develop antibiotic resistance. Coagulase-negative species such as S. epidermidis are increasingly associated with hospital-acquired infections; S. saprophyticus causes urinary infections. S. lugdunensis, a coagulase-negative species, can cause invasive disease with virulence similar to that of S. aureus. Unlike most coagulase-negative staphylococcal species, S. lugdunensis, often remains sensitive to penicillinase-resistant β-lactam antibiotics.
Pathogenic staphylococci are ubiquitous. They are carried, usually transiently, in the anterior nares of about 30% of healthy adults and on the skin of about 20%. Rates are higher in hospital patients and personnel.
Risk factors:
Neonates and breastfeeding mothers are predisposed to staphylococcal infections, as are patients with influenza, chronic bronchopulmonary disorders (eg, cystic fibrosis, emphysema), leukemia, tumors, transplants, implanted prostheses or other foreign bodies, burns, chronic skin disorders, surgical incisions, diabetes mellitus, or indwelling intravascular plastic catheters. Patients receiving adrenal steroids, irradiation, immunosuppressants, or antitumor chemotherapy and injection drug users are also at increased risk. Predisposed patients may acquire antibiotic-resistant staphylococci from other patients, health care personnel, or inanimate objects in health care settings. Transmission via the hands of personnel is the most common means of spread, but airborne spread can also occur.
Diseases Caused by Staphylococci
Staphylococci cause disease by
S. aureus bacteremia, which frequently causes metastatic foci of infection, may occur with any localized staphylococcal infection but is particularly common with infection related to intravascular catheters or other foreign bodies. It may also occur without any obvious primary site. S. epidermidis and other coagulase-negative staphylococci increasingly cause hospital-acquired bacteremia associated with intravascular catheters and other foreign bodies because they can form biofilms on these materials. They are important causes of morbidity (especially prolongation of hospitalization) and mortality in debilitated patients. The diseases listed below are further discussed elsewhere in The Manual.
Direct invasion:
Most staphylococcal disease results from direct tissue invasion. Examples are
Skin infections are the most common form of staphylococcal disease (see Bacterial Skin Infections: Overview of Bacterial Skin Infections). Superficial infections may be diffuse, with vesicular pustules and crusting (impetigo) or sometimes cellulitis or with focal and nodular abscesses (furuncles and carbuncles). Deeper cutaneous abscesses are common. Severe necrotizing skin infections may occur. Staphylococci are commonly implicated in wound and burn infections, postoperative incision infections, and mastitis or breast abscess in breastfeeding mothers.
Neonatal infections usually appear within 6 wk after birth and include skin lesions with or without exfoliation, bacteremia, meningitis, and pneumonia.
Pneumonia that occurs in a community setting is not common but may develop in patients who have influenza, who are receiving corticosteroids or immunosuppressants, or who have chronic bronchopulmonary or other high-risk diseases. It may be a primary infection or result from hematogenous spread of S. aureus infection elsewhere in the body (eg, IV catheter infection, endocarditis, soft-tissue infection). However, S. aureus is a common cause of hospital-acquired pneumonia. Staphylococcal pneumonia is occasionally characterized by formation of lung abscesses followed by rapid development of pneumatoceles and empyema. Community-associated methicillin-resistant S. aureus (CA-MRSA) often causes severe necrotizing pneumonia.
Endocarditis can develop, particularly in IV drug abusers and patients with prosthetic heart valves. Because intravascular catheter use and implantation of cardiac devices have increased, S. aureus has become a leading cause of bacterial endocarditis. S. aureus endocarditis is an acute febrile illness often accompanied by visceral abscesses, embolic phenomena, pericarditis, subungual petechiae, subconjunctival hemorrhage, purpuric lesions, heart murmurs, and heart failure secondary to cardiac valve damage.
Osteomyelitis occurs more commonly in children, causing chills, fever, and pain over the involved bone. Subsequently, the overlying soft tissue becomes red and swollen. Articular infection may occur; it frequently results in effusion, suggesting septic arthritis rather than osteomyelitis. Most infections of the vertebrae and intervertebral disks in adults involve S. aureus.
Toxin-mediated disease:
Staphylococci may produce multiple toxins. Some have local effects; others trigger cytokine release from certain T cells, causing serious systemic effects (eg, skin lesions, shock, organ failure, death). Panton-Valentine leukocidin (PVL) is a toxin produced by strains infected with a certain bacteriophage. PVL is typically present in strains of CA-MRSA and has been thought to mediate the ability to necrotize; however, this effect has not been verified.
Toxin-mediated staphylococcal diseases include the following:
Toxic shock syndrome (see Gram-Positive Cocci: Toxic Shock Syndrome (TSS)) may result from use of vaginal tampons or complicate any type of S. aureus infection (eg, postoperative wound infection, infection of a burn, skin infection). Although most cases have been due to methicillin-susceptible S. aureus (MSSA), cases due to MRSA are becoming more frequent.
Staphylococcal scalded skin syndrome (see Bacterial Skin Infections: Staphylococcal Scalded Skin Syndrome), which is caused by several toxins termed exfoliatins, is an exfoliative dermatitis of childhood characterized by large bullae and peeling of the upper layer of skin. Eventually, exfoliation occurs. Scalded skin syndrome most commonly occurs in infants and children < 5 yr.
Staphylococcal food poisoning is caused by ingesting a preformed heat-stable staphylococcal enterotoxin. Food can be contaminated by staphylococcal carriers or people with active skin infections. In food that is incompletely cooked or left at room temperature, staphylococci reproduce and elaborate enterotoxin. Many foods can serve as growth media, and despite contamination, they have a normal taste and odor. Severe nausea and vomiting begin 2 to 8 h after ingestion, typically followed by abdominal cramps and diarrhea. The attack is brief, often lasting < 12 h.
Diagnosis
Diagnosis is by Gram stain and culture of infected material. Susceptibility tests should be done because methicillin-resistant organisms are now common and require alternative therapy.
When staphylococcal scalded skin syndrome is suspected, cultures should be obtained from blood, urine, the nasopharynx, the umbilicus, abnormal skin, or any suspected focus of infection; the intact bullae are sterile. Although the diagnosis is usually clinical, a biopsy of the affected skin may help confirm the diagnosis.
Staphylococcal food poisoning is usually suspected because of case clustering (eg, within a family, attendees of a social gathering, or customers of a restaurant). Confirmation (typically by the health department) entails isolating staphylococci from suspect food and sometimes testing for enterotoxins.
X-ray changes of osteomyelitis may not be apparent for 10 to 14 days, and bone rarefaction and periosteal reaction may not be detected for even longer. Abnormalities in MRI, CT, or radionuclide bone scans are often apparent earlier. Bone biopsy (open or percutaneous) should be done for pathogen identification and susceptibility testing.
Screening:
Some institutions that have a high incidence of MRSA nosocomial infections routinely screen admitted patients for MRSA (active surveillance) by using rapid laboratory techniques to evaluate nasal swab specimens. Some institutions screen only high-risk patients (eg, those who are admitted to the ICU, who have had previous MRSA infection, or who are about to undergo vascular, orthopedic, or cardiac surgery). Quick identification of MRSA allows carriers to be placed in contact isolation. This practice decreases the spread of MRSA and may decrease the incidence of nosocomial infections with MRSA; however, decolonization treatments (see below Gram-Positive Cocci: Prevention), although sometimes done, are not yet proved effective.
Treatment
Management includes abscess drainage, debridement of necrotic tissue, removal of foreign bodies (including intravascular catheters), and use of antibiotics. Initial choice and dosage of antibiotics depend on infection site, illness severity, and probability that resistant strains are involved. Thus, it is essential to know local resistance patterns for initial therapy (and ultimately, to know actual drug susceptibility).
Treatment of toxin-medicated staphylococcal disease (the most serious of which is toxic shock syndrome) involves decontamination of the toxin-producing area (exploration of surgical wounds, irrigation, debridement), intensive support (including IV fluids, vasopressors, and respiratory assistance), electrolyte balancing, and antimicrobials. In vitro evidence supports a preference for protein synthesis inhibitors (eg, clindamycin 900 mg IV q 8 h) over other classes of antibiotics. IV immune globulin has been beneficial in severe cases.
Antibiotic resistance:
Many staphylococcal strains produce penicillinase, an enzyme that inactivates several β-lactam antibiotics; these strains are resistant to penicillin G, ampicillin, and antipseudomonal penicillins. Community-acquired strains are often susceptible to penicillinase-resistant penicillins (eg, methicillin, oxacillin, nafcillin, cloxacillin, dicloxacillin), cephalosporins, carbapenems (eg, imipenem, meropenem, ertapenem, doripenem), macrolides, fluoroquinolones, trimethoprim/sulfamethoxazole (TMP/SMX), gentamicin, vancomycin, and teicoplanin.
MRSA isolates have become common, especially in hospitals. In addition, CA-MRSA has emerged over the past several years in most geographic regions. CA-MRSA tends to be less resistant to multiple drugs than hospital-acquired MRSA. These strains, although resistant to most β-lactams, are usually susceptible to TMP/SMX, doxycycline, or minocycline and are often susceptible to clindamycin, but there is the potential for emergence of clindamycin resistance by strains inducibly resistant to erythromycin (laboratories may report these strains as D-test positive). Vancomycin is effective against most MRSA, sometimes with rifampin and an aminoglycoside added for serious infections. An alternative drug (daptomycin, linezolid, quinupristin/dalfopristin, TMP-SMX, possibly ceftaroline) should be considered when treating MRSA strains with a vancomycin MIC of > 1.5 mcg/mL.
Vancomycin-resistant S. aureus
(VRSA; MIC > 16 mcg/mL) and vancomycin-intermediate-susceptible S. aureus (VISA; MIC 4 to 8 mcg/mL) strains have appeared in the US. These organisms require linezolid, quinupristin/dalfopristin, daptomycin, TMP/SMX, or ceftaroline.
Because incidence of MRSA has increased, initial empiric treatment for serious staphylococcal infections (particularly those that occur in a health care setting) should include a drug with reliable activity against MRSA. Thus, for proven or suspected bloodstream infections, vancomycin or daptomycin would be appropriate. For pneumonia, vancomycin or linezolid should be used because daptomycin is not reliably active in the lungs.
Table 1: Gram-Positive Cocci: Antibiotic Treatment of Staphylococcal Infections in Adults summarizes treatment options.
Prevention
Aseptic precautions (eg, thoroughly washing hands between patient examinations, sterilizing shared equipment) help decrease spread in institutions. Strict isolation procedures should be used for patients harboring resistant microbes until their infections have been cured. An asymptomatic nasal carrier need not be isolated unless the strain is MRSA or is the suspected source of an outbreak.
The organism recurs in up to 50% of carriers and frequently becomes resistant. For certain MRSA carriers (eg, preorthopedic, vascular and cardiovascular surgical patients), some experts recommend nasal decolonization with mupirocin ointment twice/day for 5 to 10 days and topical body decolonization regimens with a skin antiseptic solution (eg, chlorhexidine) or dilute bleach baths (about 5 mL/L) for 5 to 14 days. Oral antimicrobial therapy is recommended only for treatment of active infection. However, if infections recur despite topical treatments, clinicians should consider using rifampin plus either cloxacillin, dicloxacillin, TMP/SMX, or ciprofloxacin, depending on susceptibility.
Staphylococcal food poisoning can be prevented by appropriate food preparation. Patients with staphylococcal skin infections should not handle food, and food should be consumed immediately or refrigerated and not kept at room temperature.
Key Points
Last full review/revision April 2013 by Larry M. Bush, MD; Maria T. Perez, MD
Content last modified April 2013
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