Stapylococcus – Flashcards
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Staphylococci |
-Gram positive; thick peptidoglycan cell wall typical of gram positive bacteria
– Organisms can survive long periods on dry surfaces –good hand hygiene is important to prevent spread of the organism
–Outbreaks occur in hospital as well as community |
Key Properties of Staphylococcus: Metabolism |
Metabolic
•Facultative
•Organism can grow under high salt concentration •Important in staphylococcal food poisoning
•Distinguishable from Streptococcus by the presence of catalase activity (H2O2 O2 +H2O): Staph is CATALASE POSITIVE |
Key Properties of Staphylococcus: Coagulase |
Key properties
• Forms pigmented (yellow-golden) colonies under some growth conditions (solid media; aerobic) • COAGULASE positive, as opposed to other staphylococcal species (S. epidermidis), Staphylococci are grouped into coagulase-positive and negative.
• Coagulase: enzyme that converts prothrombin to thrombin, causing fibrinogen to clot in plasma or blood. |
Where is S. aureus found? |
•Carrier state: asymptomatic colonization as many as 40% of human beings colonized. –Anterior nares •15% of normal healthy individuals •Increased incidence in patients, medical personnel -up to 90%! –All persons: transient colonization •Moist skin folds •Umbilical stump, skin, perineal area of neonates –Most persons with atopic dermatitis colonized with S. aureus |
S. aureus diseases |
• Basic lesion caused by S. aureus: ABSCESS or PYOGENIC EXUDATE
•PYOGENIC EXUDATE: Dead phagocytic cells & bacteria (pus)
•ABSCESS: “standoff” •Advantage for bacterium •Containment by host •S. aureus can escape abscess: staphylokinase similar to streptokinase: allows bacterium to dissolve fibrin •Dissemination of bacterium may follow • Important aspect of treatment: drainage of abscess |
S. aureus diseases of the skin |
•IMPETIGO : superficial infection; primarily focused on face and limbs Folliculitis: infection of hair follicle; base of follicle raised, and small collection of pus beneath the epidermal surface • Stye: at base of eyelid
Furuncles (boils): extension of folliculitis; large, painful, raised nodules with an underlying collection of dead/necrotic tissue
Carbuncles: occur when furuncles coalesce and extend to deeper tissue; patients have chills/fever indicating systemic spread via bacteremia.
Cellulitis: fever, severe pain, sometimes bacteremia
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S. aureus Pneumonia |
PNEUMONIA
• Aspiration pneumonia •Develops after the aspiration of oral secretion •Primarily observed in the very young & cystic fibrosis patients, influenza, chronic obstructive pulmonary disease. •Abscesses within lung. • Hematogenous pneumonia • Common for patients with bacteremia • Necrotizing pneumonia: community-acquired, can lead to septic shock; high mortality rate. • |
S. aureus Bacteremia |
•BACTEREMIA can lead to: ENDOCARDITIS mortality ~ 50%! – Influenza-like symptoms – Disruption of cardiac output and – Can affect otherwise healthy heart valves. – Visible sign: SEPTIC EMBOLISM |
Superantigens |
•S. aureusproduces a number of virulence factors that are superantigens • Force an association between MHC on antigen-presenting cells and T cell receptor that would not normally occur (nonspecific stimulation) •Induce cytokine release by both cell types |
Toxin Mediated Diseases: Scalded Skin Syndrome |
Toxin-mediated diseases
Scalded skin syndrome (Ritter’s disease; SSSS)
• Primarily a disease of neonates and young children
• Onset: redness and inflammation around mouth, followed by cutaneous blisters, and finally desquamation of the epithelium
• Blisters contain clear fluid but no organisms or leukocytes •Rarely fatal; fatalities usually due to secondary infection of the denuded skin areas. •Disease manifestations produced by dissemination of S. aureusexfoliative toxins A or B (ETA/ETB).
–Superantigens |
S. aureus Toxic Shock Syndrome |
•Acute disease that affects multiple systems, is mediated by toxins, and can result in multiorgan failure and death. •Forms of disease –Menstrual –Nonmenstrual •Growth of toxin-producing strains of S. aureus in vagina (menstrual) or other location (nonmenstrual) •Release and dissemination of toxin(s) (superantigen). •Nonmenstrual TSS can also occur in the absence of a wound or obvious portal of entry. –Toxins responsible: •Menstrual : TSST1 (Toxic shock syndrome toxin 1) most (~95%) of cases •Nonmenstrual: can be TSST1 (~50%), or staphylococcal enterotoxin A, B, or C (SEA, SEB, SEC)
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Clinical Features of Toxic Shock Syndrome |
Clinical features
•Superantigens induce cytokine storm.
• Fever, rash, GI symptoms, confusion, lethargy, severe myalgia lethargy, agitation, hypotension and multisystem involvement.
• Late feature: desquamation of skin. • Blood cultures: <5% positive (consistent with toxin) • Clinical features of menstrual and nonmenstrual TSS similar except: Nonmenstrual TSS: more likely acquired nosocomially Nonmenstrual TSS: more often associated with CNS manifestations (action of enterotoxin?) |
Staphylococcal Food Poisoning |
• Disease symptoms caused by a toxin (staphylococcal entero- toxin A and other enterotoxins)
These toxins aresuperantigens.
• Does not require live bacteria in contaminated food • S. auruesintroduced into food by individuals colonized/infected with S. aureus. S. aureus subsequently replicates in food and releases toxin.
• Most common foods: salted pork, custard-filled pastries potato salad, and ice cream • Symptoms: severe vomiting, diarrhea, abdominal pain/ nausea. Sweating and headache may occur but no fever is seen.
• Treatment: for relief of abdominal cramping, diarrhea, and replacement of fluids |
Penicillinase |
• Penicillinase-resistant penicillins (methicillin) were then used to treat S. aureus infections; now many strains of S. aureus are resistant to methicillin(MRSA) |
Virulence Factors of S. aureus |
1.Capsular polysaccharide – inhibits neutrophilphagocytosis and chemotaxis. Present on cell surface.
2.Protein A – binds Fc (cell receptor) portion of some forms of IgG, neutralizing the ability of phagocytic cells to recognize it. Antibody is bound to cell “in reverse.” 3. Exfoliative toxins: ETA and ETB – responsible for SSSS. Superantigens.
4. Enterotoxins: eight distinct toxins; responsible for S. aureus food poisoning. Some can take the place of TSST-1 in nonmenstrual TSS.
Stable to heat, gastric and jejunal enzymes. stimulate inflammatory mediators; stimulate vagus nerve endings, producing severe vomiting. Superantigens.
5. Toxic shock syndrome toxin (TSST-1): triggers massive release of cytokines that cause shock and death. Superantigens.
6. MSCRAMMs/Adhesins: (Microbial Surface Components Recognizing Adhesive Matrix Molecules)
Bind to extracellular matrix/host cells – many different factors are synthesized by S. aureus and allow the bacterium to adhere to a variety of host molecules.
7. Yellow pigment. Caratenoid. Protects organism from reactive oxygen species (released by neutrophils)
Cytoxins 8. Alpha, beta, gamma, delta toxins: can lysea variety of cell types (including red blood cells).
Alpha toxin: does not lyseneutrophils efficiently
9. Panton-Valentine leukocidin: Does not lyse red blood cells as efficiently as other S. aureuscytotoxins. Role in pathogenesis unclear. Encoded on the genome of most strains of CA S.aureus. 10. Peptidoglycan: component of cell wall; has endotoxin- like activity; stimulates production of endogenous pyrogens activation of complement, production of IL-1 from monocytes aggregation of neutrophils (part of abscess formation) 11. PBP2A - penicillin binding protein. Involved in cell wall biosynthesis. Mediates methicillin resistance. Encoded by mecA gene.
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