Staphylococcus Notes

Staphylococcus Aureus

Trigger Words
  • Coagulase
  • Cytotoxins
  • Exfoliative toxins
  • Enterotoxins
  • Toxic shock syndrome toxin
  • MRSA
Biology and Virulence
  • Catalase-positive, gram-positive cocci arranged in clusters.
  • Characterized by coagulase and protein A presence.
  • Virulence factors:
    • Structural components for adherence to host tissues.
    • Mechanisms to avoid phagocytosis.
    • Toxins and hydrolytic enzymes (refer to Table 18.3).
  • Hospital- and community-acquired infections with MRSA are a significant worldwide problem.
Epidemiology
  • Normal flora on human skin and mucosal surfaces.
  • Can survive on dry surfaces for extended periods due to a thickened peptidoglycan layer and the absence of an outer membrane.
  • Spread through person-to-person contact or contaminated fomites such as bed linens and clothing.
  • Risk factors:
    • Foreign bodies (splinter, suture, prosthesis, catheter).
    • Previous surgical procedures.
    • Antibiotics that suppress normal microbial flora.
  • Patients at risk for specific diseases:
    • Infants (scalded skin syndrome).
    • Young children with poor hygiene (impetigo and cutaneous infections).
    • Patients with intravascular catheters (bacteremia and endocarditis) or shunts (meningitis).
    • Patients with compromised pulmonary function or a viral respiratory infection (pneumonia).
  • MRSA is now the most common cause of community-acquired skin and soft-tissue infections.
Diseases
  • Toxin-mediated diseases:
    • Food poisoning.
    • Toxic shock syndrome.
    • Scalded skin syndrome.
  • Pyogenic diseases:
    • Impetigo.
    • Folliculitis.
    • Furuncles.
    • Carbuncles.
    • Wound infections.
  • Other systemic diseases.
Diagnosis
  • Microscopy is useful for pyogenic infections but not for blood or toxin-mediated infections.
  • Staphylococci grow rapidly on nonselective media.
  • Selective media (e.g., chromogenic agar, mannitol-salt agar) can recover S.aureusS. aureus from contaminated specimens.
  • Nucleic acid amplification tests screen for MSSA and MRSA carriage.
  • Identification via biochemical tests (e.g., coagulase), molecular probes, or mass spectrometry.
Treatment, Prevention, and Control
  • Localized infections are managed by incision and drainage; systemic infections require antibiotic therapy.
  • Empirical therapy targets MRSA strains.
  • Oral antibiotics: trimethoprim-sulfamethoxazole, doxycycline/minocycline, clindamycin, or linezolid.
  • Intravenous therapy: vancomycin (drug of choice), daptomycin, tigecycline, or linezolid.
  • Treatment for food poisoning is symptomatic.
  • Proper wound cleansing and disinfectants prevent infections.
  • Thorough hand washing and covering exposed skin prevent spread.

Coagulase-Negative Staphylococci

Trigger Words
  • Opportunistic
  • Slime layer
  • Subacute
Biology and Virulence
  • Catalase-positive, coagulase-negative, gram-positive cocci arranged in clusters.
  • Relatively avirulent, but slime layer production allows adherence to foreign bodies (e.g., catheters, grafts, prosthetic valves/joints, shunts) and protection from phagocytosis and antibiotics.
Epidemiology
  • Normal human flora on skin and mucosal surfaces.
  • Can survive on dry surfaces for long periods.
  • Spread through direct contact or contaminated fomites, but most infections involve the patient’s own organisms.
  • Patients are at risk when a foreign body is present.
  • Ubiquitous, with no geographic or seasonal limitations.
Diseases
  • Infections include:
    • Subacute endocarditis.
    • Infections of foreign bodies.
    • Urinary tract infections.
Diagnosis
  • Similar to S.aureusS. aureus infections.
Treatment, Prevention, and Control
  • Oxacillin (or other penicillinase-resistant penicillin) is used, or vancomycin for oxacillin-resistant strains.
  • Removal of the foreign body is often required.
  • Prompt treatment is necessary to prevent further tissue damage or immune complex formation.

General Characteristics of Staphylococci

  • Gram-positive cocci, spherical shape, no endospores.
  • Catalase-positive (differentiates from Streptococcus and Enterococcus).
  • Grow in grape-like clusters.
  • Size: 0.5 to 1.5 µm in diameter.
  • Can grow in aerobic and anaerobic conditions, high salt concentrations (e.g., 10% sodium chloride), and temperatures from 18°C to 40°C.
  • Over 80 species and subspecies found on human skin and mucous membranes.
  • Specific niches:
    • S.aureusS. aureus: anterior nares.
    • S.capitisS. capitis: sebaceous glands (e.g., forehead).
    • S.haemolyticusS. haemolyticus and S.hominisS. hominis: apocrine glands (e.g., axilla).
  • Important human pathogens causing opportunistic infections and systemic diseases.
  • Most common species associated with human diseases: S.aureusS. aureus, S.epidermidisS. epidermidis, S.lugdunensisS. lugdunensis, and S.saprophyticusS. saprophyticus.
  • MRSA causes serious infections in hospitalized patients and healthy individuals.
  • S.aureusS. aureus colonies can have a yellow or gold color due to carotenoid pigments.
  • S.aureusS. aureus produces coagulase, which converts fibrinogen to fibrin, forming a clot when suspended in plasma.
  • Coagulase-negative staphylococci are less virulent and cause opportunistic infections.

Physiology and Structure of Staphylococci

Capsule and Slime Layer
  • Polysaccharide capsule covers the cell wall.
  • Serotypes 1 and 2: thick capsules, mucoid colonies, rarely associated with human disease.
  • Serotypes 5 and 8: associated with ~75% of human infections.
  • Capsule protects bacteria by inhibiting phagocytosis by polymorphonuclear leukocytes (PMNs).
  • Slime layer (biofilm): water-soluble film of monosaccharides, proteins, and small peptides produced by staphylococci.
  • Extracellular substance binds bacteria to tissues and foreign bodies, important for coagulase-negative staphylococci survival.
Peptidoglycan and Associated Enzymes
  • Peptidoglycan forms half the cell wall by weight.
  • Layers of glycan chains with N-acetylmuramic acid and N-acetylglucosamine subunits.
  • Oligopeptide side chains are attached to N-acetylmuramic acid subunits and cross-linked with peptide bridges.
  • Gram-positive bacteria have many cross-linked layers for rigidity.
  • Penicillin-binding proteins (PBPs) catalyze peptidoglycan layer construction and are targeted by penicillins and β-lactam antibiotics.
  • Resistance to methicillin and related antibiotics is mediated by the mecA and mecC genes encoding PBP2a, which has low affinity for these antibiotics.
  • mecA gene is on the staphylococcal cassette chromosome mec (SCCmec).
  • MRSA strains are now present in the community, not just hospitals.
  • Peptidoglycan has endotoxin-like activity, stimulating endogenous pyrogens, complement activation, IL-1 production, and PMN aggregation.
Teichoic Acids and Lipoteichoic Acids
  • Teichoic acids are species-specific, phosphate-containing polymers bound either covalently to N-acetylmuramic acid residues of the peptidoglycan layer or to lipids in the cytoplasmic membrane (lipoteichoic acids).
  • Stimulate specific antibody response when bound to peptidoglycan.
Surface Adhesion Proteins
  • Important virulence factors that adhere to host matrix proteins.
  • Designated microbial surface components recognizing adhesive matrix molecules (MSCRAMM).
  • Examples:
    • Staphylococcal protein A (spa): binds to the Fc receptor of IgG1, IgG2, and IgG4.
    • Fibronectin-binding protein A: binds fibronectin.
    • S. aureus surface protein A: undetermined function.
  • MSCRAMM proteins include staphylococcal protein A, fibronectin-binding proteins A and B, and clumping factor proteins A and B.
  • Clumping factor proteins (coagulase) bind fibrinogen and convert it to insoluble fibrin, causing staphylococci to clump/aggregate.
Cytoplasmic Membrane
  • Made up of a complex of proteins, lipids, and a small amount of carbohydrates.
  • Serves as an osmotic barrier for the cell and provides an anchorage for the cellular biosynthetic and respiratory enzymes.

Pathogenesis and Immunity

  • Ability to evade immune clearance.
  • Produce surface proteins that mediate adherence to host tissues during colonization.
  • Produce disease through specific toxins and hydrolytic enzymes, leading to tissue destruction.
  • These properties (immunologic evasion, adherence, tissue destruction) are common to most pathogenic organisms.
Regulation of Virulence Genes
  • Expression of virulence factors and biofilm formation is controlled by the accessory gene regulator (agr) operon.
  • Quorum-sensing system allows expression of adhesion proteins and promotes tissue colonization and intracellular growth when bacterial density is low, and tissue invasion/toxin production when density is high.
  • Operon encodes autoinducer peptides (AIP1 to 4) that bind to cell-surface receptors and regulate protein expression based on population density.
  • Innate immune regulation of bacterial virulence is mediated by apolipoprotein B, which binds to AIPs and suppresses agr signaling.
  • Bacterial density is maintained at a low concentration, providing the benefits of immune stimulation by colonizing staphylococci without tissue invasion/destruction.
Defenses against Innate Immunity
  • Opsonins bind to encapsulated staphylococci, but the capsule inhibits phagocytosis by PMNs.
  • Specific antibodies increase C3 binding, leading to phagocytosis.
  • Extracellular slime layer interferes with phagocytosis.
  • Protein A binds immunoglobulins, preventing antibody-mediated immune clearance and forming immune complexes.

Staphylococcal Toxins

  • S.aureusS. aureus produces:
    • 5 cytolytic or membrane-damaging toxins (alpha, beta, delta, gamma, and P-V leukocidin).
    • 2 exfoliative toxins (A and B).
    • Numerous enterotoxins (A to E, G to X, plus multiple variants).
    • TSST-1.
  • Cytolytic toxins = hemolysins, but activity is not restricted to red blood cells, and P-V leukocidin cannot lyse erythrocytes.
  • Cytotoxins can lyse neutrophils, resulting in the release of lysosomal enzymes that subsequently damage surrounding tissues.
  • P-V leukocidin is linked to severe pulmonary and cutaneous infections.
  • Exfoliative toxin A, enterotoxins, and TSST-1 are superantigens that bind to class II MHC molecules on macrophages, interacting with T-cell receptors (VβTCR).
  • This results in massive cytokine release by macrophages (IL-1β and TNF-α) and T cells (IL-2, IFN-γ, and TNF-β).
    • IL-1β is associated with fever.
    • TNF-α and TNF-β are associated with hypotension and shock.
Cytotoxins
  • Alpha toxin, encoded on the bacterial chromosome and a plasmid, is a 33,000-Da polypeptide produced by most strains causing human disease.
    • Disrupts smooth muscle in blood vessels and is toxic to erythrocytes, leukocytes, hepatocytes, and platelets.
    • Binds to the cell surface, aggregates into a heptamer with a 1- to 2-nm pore, causing rapid efflux of K+K^+ and influx of Na+Na^+, Ca2+Ca^{2+}, and other small molecules, leading to osmotic swelling and cell lysis.
    • Important mediator of tissue damage in staphylococcal disease.
  • Beta toxin (sphingomyelinase C) is a 35,000-Da heat-labile protein produced by most strains.
    • Specificity for sphingomyelin and lyso-phosphatidylcholine, toxic to erythrocytes, fibroblasts, leukocytes, and macrophages.
    • Catalyzes hydrolysis of membrane phospholipids, with lysis proportional to sphingomyelin concentration.
    • Effect on erythrocytes occurs primarily at low temperatures.
  • Delta toxin is a 3000-Da polypeptide produced by almost all S.aureusS. aureus strains and other staphylococci.
    • Wide spectrum of cytolytic activity, disrupting cellular membranes through detergent-like action.
  • Gamma toxin and P-V leukocidin:
    • Bicomponent toxins composed of two polypeptide chains: S (slow-eluting proteins) and F (fast-eluting proteins) components.
    • Three unique S proteins (HlgA, HlgC, and LukS-PV) and two F proteins (HlgB and LukF-PV) have been identified.
    • All six toxins can lyse neutrophils and macrophages.
    • Greatest hemolytic activity is associated with HlgA/HlgB, HlgC/HlgB, and HlgA/LukF-PV.
    • PV leukocidin toxin (LukS-PV/LukF-PV) is leukotoxic but has no hemolytic activity.
    • Cell lysis is mediated by pore formation, with increased permeability to cations and osmotic instability.
Exfoliative Toxins
  • SSSS is mediated by exfoliative toxins, prevalent in less than 5% of S.aureusS. aureus strains.
  • Two distinct forms: ETA (heat stable, phage-associated) and ETB (heat labile, plasmid-located).
  • Serine proteases split desmoglein-1, responsible for intercellular bridges in the stratum granulosum epidermis.
  • No cytolysis or inflammation, neither staphylococci nor leukocytes are present in the involved layer of the epidermis (diagnostic clue).
  • Protective neutralizing antibodies develop after exposure.
  • Seen mostly in young children.
Enterotoxins
  • Enterotoxin A is most commonly associated with food poisoning.
  • Enterotoxins C and D are found in contaminated milk products.
  • Enterotoxin B causes staphylococcal pseudomembranous enterocolitis.
  • Stable to heating at 100°C for 30 minutes and resistant to hydrolysis by gastric and jejunal enzymes.
  • Produced by 30% to 50% of all S.aureusS. aureus strains.
  • Superantigens capable of inducing nonspecific activation of T cells and massive cytokine release.
  • Histologic changes include neutrophil infiltration and loss of the brush border in the jejunum.
  • Stimulation of inflammatory mediator release from mast cells causes emesis.
Toxic Shock Syndrome Toxin-1
  • TSST-1 is a 22,000-Da heat- and proteolysis-resistant, chromosomally mediated exotoxin.
  • Produced by 90% of S.aureusS. aureus strains responsible for menstruation-associated TSS and half of the strains responsible for other forms of TSS.
  • Enterotoxin B and enterotoxin C are responsible for approximately half the nonmenstruation-associated TSS cases.
  • Requires elevated oxygen concentration and neutral pH.
  • Superantigen stimulating cytokine release, producing leakage of endothelial cells and cytotoxic effects.
  • Penetrates mucosal barriers, causing systemic effects.
  • Death is caused by hypovolemic shock leading to multiorgan failure.

Staphylococcal Enzymes

  • S.aureusS. aureus strains possess bound and free coagulase.
    • Bound coagulase directly converts fibrinogen to insoluble fibrin causing clumping.
    • Free coagulase reacts with a globulin plasma factor to form staphylothrombin, catalyzing the conversion of fibrinogen to insoluble fibrin.
  • Coagulase may cause fibrin layer formation, localizing infection and protecting organisms from phagocytosis.
  • Hyaluronidase hydrolyzes hyaluronic acids in connective tissue.
  • Fibrinolysin (staphylokinase) dissolves fibrin clots.
  • Lipases hydrolyze lipids.
  • Thermostable nuclease hydrolyzes deoxyribonucleic acid (DNA).

Epidemiology

  • Staphylococci are ubiquitous.
  • Coagulase-negative staphylococci are present on the skin, and transient colonization of moist skinfolds with S.aureusS. aureus is common.
  • Colonization of the umbilical stump, skin, and perineal area of neonates with S.aureusS. aureus is common.
  • S.aureusS. aureus and coagulase-negative staphylococci are found in the nares, oropharynx, gastrointestinal tract, and urogenital tract.
  • Approximately 15% of normal healthy adults are persistent nasopharyngeal carriers of S.aureusS. aureus, higher incidence for hospitalized patients, medical personnel, and those with eczematous skin diseases.
  • Adherence of the organism to the mucosal epithelium is regulated by the staphylococcal cell-surface adhesins.
  • Shedding of bacteria is common and is responsible for many hospital-acquired infections.
  • Staphylococci are susceptible to high temperatures and disinfectants but can survive on dry surfaces.
  • Transferred to susceptible persons through direct contact or fomites.
  • MRSA spread rapidly in hospitalized patients starting in the 1980s.
  • Community-acquired MRSA outbreaks were reported in 2003, with genetically unique strains.

Clinical Diseases

Staphylococcus Aureus
  • Clinical manifestations result from toxin activity (SSSS, staphylococcal food poisoning, and TSS) or proliferation of organisms (cutaneous infections, endocarditis, pneumonia, empyema, osteomyelitis, septic arthritis).
  • Introduction of small numbers of staphylococci can establish disease in the presence of a foreign body.
  • Patients with impaired chemotactic or phagocytic response are more susceptible to staphylococcal diseases.
Staphylococcal Scalded Skin Syndrome
  • Ritter disease or SSSS is characterized by the abrupt onset of perioral erythema that spreads over the entire body within 2 days.
  • Slight pressure displaces the skin (positive Nikolsky sign), and large bullae form, followed by desquamation of the epithelium.
  • Blisters contain clear fluid but no organisms or leukocytes.
  • The epithelium becomes intact again within 7 to 10 days, when antibodies against the toxin appear.
  • Scarring does not occur because only the top layer of epidermis is affected.
  • Primarily a disease of neonates and young children, with a mortality rate less than 5%.
  • Infections in adults usually occur in immunocompromised hosts or patients with renal disease.
  • Bullous impetigo is a localized form of SSSS, with specific strains of toxin-producing S.aureusS. aureus, associated with formation of superficial skin blisters.
  • S.aureusS. aureus is present in the localized blisters of patients with bullous impetigo.
  • Erythema does not extend beyond the borders of the blister, and the Nikolsky sign is not present.
  • Occurs primarily in infants and young children and is highly communicable.
Staphylococcal Food Poisoning
  • Intoxication rather than an infection, caused by bacterial toxin present in food.
  • Contaminated foods: processed meats, custard-filled pastries, potato salad, and ice cream.
  • Results from contamination of food by a human carrier.
  • After staphylococci are introduced into the food, the food must remain at room temperature or warmer for the organisms to grow and release the toxin.
  • The contaminated food will not appear or taste tainted, and subsequent heating will kill the bacteria but not inactivate the heat-stable toxin.
  • Abrupt and rapid onset, with a mean incubation period of 4 hours.
  • Severe vomiting, diarrhea, and abdominal pain or nausea are characteristic.
  • Sweating and headache may occur, but fever is not seen.
  • Diarrhea is watery and non-bloody.
  • Treatment is for relief of abdominal cramping and diarrhea and for fluid replacement; antibiotic therapy is not indicated.
  • Short-lived immunity means that second episodes can occur, particularly with serologically distinct enterotoxins.
  • Certain strains can also cause enterocolitis, manifested by watery diarrhea, abdominal cramps, and fever.
  • Enterocolitis occurs primarily in patients who have received broad-spectrum antibiotics.
  • Diagnosis is confirmed after more common causes have been excluded, and abundant S.aureusS. aureus is detected in the stool.
Toxic Shock Syndrome
  • Initiated with the localized growth of toxin-producing strains in the vagina or a wound, followed by release of the toxin into the blood.
  • Toxin production requires an aerobic atmosphere and neutral pH.
  • Clinical manifestations start abruptly and include fever, hypotension, and a diffuse, macular, erythematous rash.
  • Multiple organ systems are involved, and the entire skin desquamates.
  • Purpura fulminans is a particularly virulent form of TSS, characterized by large purpuric skin lesions, fever, hypotension, and disseminated intravascular coagulation.
  • Risk of recurrent disease is as high as 65% unless the patient is specifically treated with an effective antibiotic.
  • More than 50% of patients fail to develop protective antibodies after their disease resolves.
Cutaneous Infections
  • Localized pyogenic cutaneous infections include impetigo, folliculitis, furuncles, and carbuncles.
  • Impetigo is a superficial infection that mostly affects young children, occurring primarily on the face and limbs.
  • Folliculitis is a pyogenic infection in the hair follicles.
  • Furuncles (boils) are an extension of folliculitis.
  • Carbuncles occur when furuncles coalesce and extend into the deeper subcutaneous tissue, accompanied by chills and fevers.
  • Staphylococcal wound infections occur after a surgical procedure or trauma when organisms colonizing the skin or from an external source are introduced into the wound.
  • Infections are characterized by edema, erythema, pain, and an accumulation of purulent material.
  • MRSA strains are now the most common cause of skin and soft-tissue infections in patients presenting to U.S. hospital emergency departments.
Bacteremia and Endocarditis
  • S.aureusS. aureus is a common cause of bacteremia.
  • The initial foci of infection are not known in approximately a third of patients.
  • Acute endocarditis caused by S.aureusS. aureus is a serious disease, with a mortality rate approaching 50%.
  • Symptoms can deteriorate rapidly and include disruption of cardiac output and peripheral evidence of septic embolization.
  • The exception is S.aureusS. aureus endocarditis in parenteral drug abusers, whose disease normally involves the right side of the heart.
Pneumonia and Empyema
  • S.aureusS. aureus respiratory disease can develop after the aspiration of oral secretions or from the hematogenous spread of the organism from a distant site.
  • Radiographic examination reveals the presence of patchy infiltrates with consolidation or abscesses.
  • Community-acquired MRSA is responsible for a severe form of necrotizing pneumonia with massive hemoptysis, septic shock, and a high mortality rate.
  • Empyema occurs in 10% of patients with pneumonia, and S.aureusS. aureus is responsible for a third of all cases.
Osteomyelitis and Septic Arthritis
  • Osteomyelitis results from hematogenous dissemination to bone or a secondary infection resulting from trauma or the extension of disease from an adjacent area.
  • Hematogenous spread in children generally results from a cutaneous staphylococcal infection and usually involves the metaphyseal area of long bones.
  • In adults, it commonly occurs in the form of vertebral osteomyelitis.
  • With appropriate antibiotic therapy and surgery, the cure rate for staphylococcal osteomyelitis is excellent.
  • S.aureusS. aureus is the primary cause of septic arthritis in young children and in adults.
  • Staphylococcal arthritis is characterized by a painful erythematous joint, with purulent material obtained on aspiration.
Staphylococcus Epidermidis and Other Coagulase-Negative Staphylococci
  • S.epidermidisS. epidermidis, S.lugdunensisS. lugdunensis, can infect prosthetic and less commonly, native heart valves.
  • Infections of native valves are believed to result from the inoculation of organisms onto a damaged heart valve.
  • Catheter and shunt infections: infections of catheters and shunts are caused by coagulase-negative staphylococci.
  • Prosthetic joint infections: infections of artificial joints caused by coagulase-negative staphylococci.
  • Urinary Tract Infections: S.saprophyticusS. saprophyticus causes urinary tract infections in young, sexually active women.

Laboratory Diagnosis

Microscopy
  • Staphylococci are gram-positive cocci.
  • Successful detection depends on the type of infection and the quality of the material submitted for analysis.
Nucleic Acid–Based Tests
  • Used to detect nasal carriage of methicillin-sensitive S.aureusS. aureus (MSSA) and MRSA.
Culture
  • Clinical specimens should be inoculated onto nutritionally enriched agar media supplemented with sheep blood.
  • Staphylococci grow rapidly on nonselective media incubated aerobically or anaerobically.
Identification
  • Biochemical tests used to identify S.aureusS. aureus. Colonies resembling S.aureusS. aureus are identified in most laboratories by mixing a suspension of organisms with a drop of plasma. Mass spectrometry has been used to identify the staphylococci. Analysis of genomic DNA by pulsed-field gel electrophoresis a method for characterizing isolates. Whole genome sequencing is becoming. the preferred tool for subtyping organisms.
Antibody Detection
  • Antibodies to cell wall teichoic acids are present in many patients with long-standing S.aureusS. aureus infections.

Treatment, Prevention, and Control

  • Less than 10% of the strains are susceptible to penicillin.
  • Currently, the majority of S.aureusS. aureus responsible for hospital- and community-acquired infections are resistant to semisynthetic penicillins, and these MRSA strains are resistant to all β-lactam antibiotics.
  • Patients with localized skin and soft-tissue infections can generally be managed by incision and drainage of the abscesses.
  • Oral therapy can include trimethoprim-sulfamethoxazole, a long-acting tetracycline such as doxycycline or minocycline, clindamycin, or linezolid.
  • Vancomycin is the drug of choice for intravenous therapy, with daptomycin, tigecycline, or linezolid acceptable alternatives.
  • Isolates of S.aureusS. aureus have been found with low-level resistance which is observed in strains with a thicker, more disorganized cell wall and high-level resistance to vancomycin. Staphylococci are ubiquitous organisms present on the skin and mucous membranes.
  • The number of organisms required to establish an infection is generally large unless a foreign body is present in the wound.
  • The spread of staphylococci from person to person is more difficult to prevent.