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Questions and Answers
Which mechanism does S.aureus use to evade phagocytosis effectively?
What role does the polysaccharide capsule of S.aureus play in its pathogenesis?
What is the primary function of coagulase produced by S.aureus?
Which of the following factors is NOT a component of the S.aureus cell wall?
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How does the peptidoglycan of S.aureus contribute to its pathogenicity?
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Which statement about the virulence factors of S.aureus is accurate?
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What is a significant source of S.aureus infection among humans?
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Which enzyme produced by S.aureus helps neutralize reactive oxygen species?
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What is the primary function of hyaluronidase in bacterial virulence?
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Which toxin is specifically responsible for causing toxic shock syndrome?
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Which of the following is NOT a characteristic of superantigen exotoxins?
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What is the role of lipases produced by staphylococci?
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What effect does exfoliatin (ET) have on the skin?
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Which of the following describes the primary entry points for staphylococcal infections?
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Cytolytic exotoxins are commonly known to affect which type of cells?
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What is a significant effect of the localized host response to staphylococcal infection?
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What is the primary reason MRSA infections are unresponsive to β-lactam antibiotics?
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Which of the following is a common clinical manifestation of community-acquired MRSA (CA-MRSA)?
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What has been the effect of low-level vancomycin resistance in MRSA since its discovery in 1997?
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Which of the following is true about Staphylococcus epidermidis?
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What are the main preventive measures against S.aureus infections in hospital settings?
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Why have alternative drugs like linezolid and daptomycin been increasingly used against MRSA?
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What is a significant challenge posed by coagulase-negative staphylococci (CNS) in hospitals?
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How do MRSA infections impact patient care in hospitals?
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Which of the following statements about Staphylococcus aureus is correct?
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What distinguishes staphylococci from catalase-negative streptococci?
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Which species of staphylococci is known to cause urinary tract infections, especially cystitis in women?
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What is a common feature of Staphylococci in terms of their morphology?
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Which of the following is one of the most common causes of food poisoning?
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Which of the following describes a key characteristic of coagulase-negative staphylococci?
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What role does significant host compromise play in Staphylococcus aureus infections?
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Which feature regarding Staphylococci contributes to their ability to persist on surfaces?
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What symptom occurs within a short incubation period and is primarily caused by the action of a toxin on the gastrointestinal tract?
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Which characteristic is used to distinguish Staphylococcus aureus from coagulase-negative staphylococci?
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What is the primary reason for the shift from penicillin G to β-lactamase-resistant penicillins in treating S.aureus infections?
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In which of the following types of infections is methicillin-resistant S.aureus (MRSA) predominantly found?
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What is a common laboratory method for identifying Staphylococcus species?
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Why are strains of S.aureus resistant to methicillin becoming prevalent in hospitals?
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What morphological characteristic is typical for Staphylococcus aureus when observed under a microscope?
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What is a possible consequence of the widespread resistance of S.aureus to β-lactam antibiotics?
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Staphylococci generally stain gram negative and are oval in shape.
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Staphylococcus epidermidis is primarily associated with causing food poisoning.
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The most virulent species of staphylococcus is Staphylococcus saprophyticus.
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Coagulase-negative staphylococci (CNS) lack the enzyme coagulase and do not typically cause serious infections.
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Staphylococcus aureus infections typically require a significant host compromise, like a break in the skin.
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Staphylococci are anaerobic organisms that thrive in environments without oxygen.
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Staphylococcus aureus is known for producing toxins that can lead to toxic shock syndrome.
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All species of staphylococci are highly virulent and cause severe infections.
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MRSA infections can lead to higher mortality rates and longer hospital stays.
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Vancomycin has gained a reputation as the least effective treatment for life-threatening MRSA infections.
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Community-acquired MRSA (CA-MRSA) primarily affects individuals with prior hospital exposure.
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The protein PBP-2a has a high affinity for β-lactam antibiotics.
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Staphylococcus epidermidis is part of the normal skin flora but can also cause infections in prosthetic devices.
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The increasing incidence of vancomycin resistance among MRSA strains has led to the use of alternative drugs such as clindamycin and rifampicin.
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Polysaccharide intercellular adhesin produced by S. epidermidis helps in adherence to bioprosthetic materials.
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Necrotizing pneumonia and osteomyelitis are rare severe manifestations of CA-MRSA infections.
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The presence of a microcapsule in S.aureus is associated with increased sensitivity to phagocytosis.
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Peptidoglycan in S.aureus has no role in stimulating inflammatory responses.
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Coagulase produced by S.aureus initiates fibrin polymerization by binding to thrombin.
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Clumping factor in S.aureus promotes isolation from immune cells by converting fibrinogen to soluble fibrin.
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All S.aureus diseases are a result of both invasive infection and the production of toxins.
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The binding of IgG by Protein A in S.aureus enhances phagocytosis.
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S.aureus is carried by healthy individuals but does not pose a risk for food contamination.
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Catalase produced by S.aureus converts hydrogen peroxide to water and carbon dioxide.
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Localized skin infections caused by S.aureus may include conditions such as folliculitis, furuncles, and carbuncles.
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Toxinoses caused by S.aureus include diseases such as toxic shock syndrome and Staphylococcal gastroenteritis.
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Septicemia is primarily caused by the presence of non-viable bacteria in the bloodstream.
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S.aureus is an uncommon cause of pneumonia in patients with weakened immune systems.
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Carbuncles are small, superficial abscesses that occur around hair follicles.
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Injection of contaminated materials can lead to acute endocarditis caused by S.aureus.
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Staphylococcal gastroenteritis is caused by ingestion of food contaminated with enterotoxins produced by non-viable S.aureus.
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Furuncles are also referred to as boils and can develop around foreign bodies like splinters.
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Hyaluronidase is primarily responsible for degrading hyaluronic acid to promote the spread of bacteria.
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Cytolytic exotoxins are ineffective against mammalian cell membranes.
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The production of Panton-Valentine leukocidin decreases the virulence of staphylococcal strains.
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Enterotoxins produced by Staphylococcus aureus can lead to food poisoning upon ingestion.
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Exfoliatin (ET) is classified as an endotoxin that targets the gastrointestinal tract.
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Toxic shock syndrome toxin (TSST-1) is an example of a superantigen that can induce toxic shock syndrome.
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Lipases produced by staphylococci help to hydrolyze carbohydrates, promoting bacterial survival.
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The localized host response to staphylococcal infection is characterized by tissue necrosis and reduction of pus.
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What is the primary effect of Panton-Valentine leukocidin on polymorphonuclear leukocytes (PMNs)?
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Describe the action of superantigen exotoxins in relation to T-lymphocyte activation.
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How does hyaluronidase contribute to the spread of bacterial infections?
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What role do enterotoxins play in food poisoning associated with S.aureus?
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Explain the significance of exfoliatin (ET) in staphylococcal infections.
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What outcome results from the localized host response to staphylococcal infection?
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What is the pathogenic mechanism of fibrinolysin, also known as staphylokinase?
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Discuss the impact of superantigen-driven cytokine release in toxic shock syndrome.
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What are the typical symptoms associated with a toxin-mediated gastrointestinal disturbance caused by S.aureus?
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How can Staphylococcus aureus be distinguished from coagulase-negative staphylococci in the laboratory?
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What treatment approach is required for serious S.aureus infections, particularly when they are resistant to common antibiotics?
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What effect do penicillinase-encoding plasmids have on the treatment of S.aureus infections?
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What laboratory tests can be used to confirm the presence of S.aureus?
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What has been the trend regarding hospital-acquired methicillin-resistant S.aureus (MRSA) in recent decades?
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What is the significance of the exfoliative toxin produced by some strains of S.aureus?
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How has the increased use of methicillin changed the landscape of bacterial resistance in S.aureus?
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What distinguishes Staphylococcus aureus from other staphylococcal species in terms of virulence?
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Name two clinical implications of Staphylococcus epidermidis infections.
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How do the morphological characteristics of staphylococci assist in their identification?
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What role does the catalase enzyme play in distinguishing staphylococci from other bacteria?
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What is the significance of Staphylococcus saprophyticus in urinary tract infections?
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Explain how Staphylococcus aureus can contribute to food poisoning.
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Why are staphylococci considered hardy organisms in their environment?
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What is the general impact of host compromise on Staphylococcus aureus infections?
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What does the gene for PBP-2a contribute to in MRSA infections?
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Identify one severe disease condition that CA-MRSA can cause apart from skin infections.
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What has been a recent trend regarding vancomycin resistance in MRSA since 1997?
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What role does polysaccharide intercellular adhesin play in infections caused by Staphylococcus epidermidis?
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How have alternative treatments like linezolid and daptomycin become important against MRSA?
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What is a major strategy for controlling nosocomial S.aureus epidemics in healthcare settings?
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What is a common clinical manifestation of skin infections caused by CA-MRSA?
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What challenges does the presence of coagulase-negative staphylococci (CNS) pose in hospitals?
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What are the potential serious consequences of staphylococcal infections that invade the bloodstream?
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How do carbuncles differ from furuncles in terms of their characteristics?
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What is acute endocarditis and how is it commonly caused?
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In what way can staphylococcal gastroenteritis occur, and what type of toxin is involved?
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What are toxinoses and what significant condition is caused by S.aureus related to toxinoses?
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What role does Staphylococcus aureus play in nosocomial infections?
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Describe the process through which S.aureus can cause pneumonia.
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How do localized skin infections manifest with S.aureus and what types are most common?
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Match the following Staphylococcus species with their clinical significance:
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Match the specific effects or characteristics to the type of S.aureus infection:
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Match the following characteristics with their corresponding descriptions relating to Staphylococcus aureus:
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Match the following tests with their specific Staphylococcus identification methods:
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Match the following symptoms with their trigger related to Staphylococcus aureus:
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Match the following laboratory identification characteristics with their relevance to Staphylococcus aureus:
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Study Notes
Staphylococci
- Staphylococci are gram-positive, spherical bacteria that often appear in grape-like clusters.
- They are facultative anaerobes, meaning they can thrive in the presence or absence of oxygen.
- They are resistant to heat and drying, making them capable of surviving for long periods on surfaces.
- Staphylococcus aureus is the most virulent species and is responsible for various infections, including food poisoning, toxic shock syndrome, and abscess formation.
- Staphylococcus epidermidis is less virulent and is often a cause of infections associated with implanted medical devices, such as catheters and prosthetics.
- Staphylococcus saprophyticus is known to cause urinary tract infections, particularly cystitis, in women.
Virulence Factors of Staphylococcus aureus
-
Cell Wall Virulence Factors:
- Capsule: Provides protection against phagocytosis.
- Peptidoglycan: Plays a role in osmotic stability, triggers immune responses, and hinders phagocytosis.
- Teichoic acid: Binds to fibronectin, promoting adherence.
- Protein A: Binds to the Fc region of IgG, blocking opsonization and decreasing phagocytosis.
- Fibronectin-binding protein (FnBP): Facilitates binding to mucosal cells and tissue matrix.
- Clumping factor: Binds to fibrinogen, leading to coagulation and clumping.
-
Enzymes:
- Coagulase: Causes plasma to clot, potentially hindering phagocytosis.
- Catalase: Converts hydrogen peroxide to water and oxygen, which helps neutralize reactive oxygen species.
- Hyaluronidase: Degrades hyaluronic acid in connective tissues, facilitating bacterial spread.
- Fibrinolysin (Staphylokinase): Dissolves fibrin clots, assisting in bacterial dissemination.
- Lipases: Break down lipids, supporting survival in sebaceous areas.
- Nuclease (DNAase): Degrades DNA, possibly aiding in bacterial spread and evasion of the host's immune response.
-
Toxins:
- Cytolytic exotoxins (α, β, γ, δ Toxins): Damage cell membranes, often referred to as hemolysins.
- Panton-Valentine leukocidin: Lyses polymorphonuclear leukocytes (PMNs), contributing to virulence.
-
Superantigen exotoxins: Stimulate excessive T-cell activation, causing cytokine release and potentially leading to toxic shock syndrome.
- Enterotoxins: Cause food poisoning upon ingestion.
- Toxic shock syndrome toxin (TSST-1): The primary cause of toxic shock syndrome.
- Exfoliatin (ET): Causes scalded skin syndrome in children by disrupting intercellular adhesion.
Clinical Significance of Staphylococcus aureus
- Infections often result from entry points such as skin breaks, wounds, and the respiratory tract.
- Localized infections typically present with inflammation, swelling, pus formation, and tissue necrosis.
- Food poisoning: Associated with the ingestion of enterotoxins produced by S. aureus.
- Toxic shock syndrome (TSS): Caused by the release of TSST-1, leading to systemic inflammation and multi-organ dysfunction.
- Scalded skin syndrome: Characterized by superficial blistering due to the action of exfoliatin, which disrupts skin layers.
Laboratory Identification of Staphylococci
- Gram stain: S. aureus appears as gram-positive cocci in clusters.
- Catalase test: Positive reaction (produces bubbles) distinguishes staphylococci from streptococci.
- Coagulase test: Positive for S. aureus, indicating the presence of coagulase.
- Mannitol salt agar (MSA): S. aureus ferments mannitol, producing yellow colonies, while other staphylococci typically form white colonies.
- Automated systems: Can provide rapid identification of staphylococcal species.
Treatment
- Serious infections: Require incision and drainage of localized lesions, plus systemic antibiotics.
Antibiotic Resistance and Methicillin-Resistant Staphylococcus aureus (MRSA)
- Penicillin resistance: Common due to staphylococcal production of penicillinase.
- Methicillin and oxacillin resistance (MRSA): Develops due to the acquisition of a gene coding for a new penicillin-binding protein (PBP-2a), rendering the bacteria resistant to beta-lactam antibiotics.
- Hospital-acquired MRSA (HA-MRSA): Frequently seen in healthcare settings, associated with longer hospital stays and higher mortality rates.
- Community-acquired MRSA (CA-MRSA): Increasingly reported in individuals without prior healthcare exposure.
- Vancomycin resistance: Emerged as a significant threat, leading to the use of alternative therapies like linezolid and daptomycin.
Prevention
- Infection control measures: Disinfection of hands and surfaces is crucial for limiting transmission.
Coagulase-Negative Staphylococci (CNS)
- Staphylococcus epidermidis: Primarily a component of the skin flora, but can cause infections associated with implanted devices, often due to its ability to form biofilms.
- Polysaccharide intracellular adhesin (PIA): Produced by S. epidermidis, facilitates adherence to implanted materials and forms a protective barrier against antimicrobial agents.
Staphylococci
- Gram-positive spherical bacteria, usually arranged in grapelike clusters
- Grow on various media, ferment carbohydrates, produce pigments (white to deep yellow)
- Found in human skin and mucous membranes
- Cause abscess formation, pyogenic infections, and septicemia
Staphylococcus aureus
- One of the most common causes of bacterial infections
- Responsible for food poisoning, toxic shock syndrome
- Virulence factors include capsule, peptidoglycan, teichoic acid, protein A, fibronectin-binding protein, clumping factor, enzymes, and toxins
Staphylococcus epidermidis
- Found in human skin
- Common cause of prosthetic implant infections
Staphylococcus saprophyticus
- Causes urinary tract infections, particularly cystitis in women
- Often referred to as Coagulase Negative Staphylococci (CNS)
Virulence Factors of Staphylococcus aureus
- Capsule: Helps bacteria resist phagocytosis
- Peptidoglycan: Induces inflammation, attracts leukocytes, inhibits phagocytosis
- Teichoic acid: Binds to fibronectin
- Protein A: Binds to IgG, hindering phagocytosis
- Fibronectin-binding protein: Promotes binding to mucosal cells and tissue matrix
- Clumping factor: Binds to fibrinogen, causing bacteria to clump
Enzymes of Staphylococcus aureus
- Coagulase: Causes plasma to clot by activating prothrombin
- Catalase: Converts hydrogen peroxide to water and oxygen
- Hyaluronidase: Breaks down hyaluronic acid, allowing bacteria to spread
- Fibrinolysin: Dissolves fibrin clots
- Lipases: Hydrolyze lipids, enabling bacteria to survive in sebaceous areas
- Nuclease (DNAase): Degrades DNA, which is implicated in its virulence
Toxins of Staphylococcus aureus
- Cytolytic exotoxins (α, β, γ, δ Toxins): Damage cell membranes, including red blood cells
- Panton-Valentine leukocidin:: Lyses leukocytes, increasing strain virulence
- Superantigen exotoxins: Bind to T-cell receptors, causing enhanced T-cell response
- Enterotoxins: Contaminate food and cause staphylococcal gastroenteritis
- Toxic shock syndrome toxin (TSST-1): Cause of toxic shock syndrome
- Exfoliatin (ET): Causes scalded skin syndrome in children, disrupting skin cohesion
Clinical Significance of Staphylococcus aureus Infections
- Localized Skin Infections: Folliculitis, furuncles (boils), carbuncles, impetigo
- Deep Localized Infections: Osteomyelitis, septic arthritis
- Septicemia: Presence of bacteria in the bloodstream
- Acute Endocarditis: Caused by contaminated injections or needles
- Pneumonia: Can be severe and necrotizing
- Nosocomial Infections: Common in hospitals, affecting wounds and catheters
- Toxinoses: Diseases caused by bacterial toxins (Toxic shock syndrome, staphylococcal gastroenteritis)
Antibiotic Resistance in Staphylococcus aureus
- Methicillin-resistant Staphylococcus aureus (MRSA): Resistant to beta-lactam antibiotics (penicillin, methicillin) due to altered penicillin-binding protein (PBP-2a)
Community-Acquired MRSA (CA-MRSA)
- Occurs in individuals without previous risk factors for MRSA infections
- Causes skin and soft tissue infections (abscesses, cellulitis)
Vancomycin Resistance
- Vancomycin was a treatment for MRSA but resistance has emerged
Prevention of Staphylococcus aureus Infections
- No effective vaccine
- Disinfection of hands and fomites to control nosocomial outbreaks
Coagulase-Negative Staphylococci (CNS)
- Staphylococcus epidermidis
- Important cause of hospital-acquired infections associated with implanted devices and catheters
- Produces polysaccharide intercellular adhesin, aiding adherence to bioprosthetic materials.
Staphylococcus
- Gram-positive spherical bacteria
- Occur in grape-like clusters
- Facultatively anaerobic
- Produce catalase
- Common in skin and mucous membranes
Staphylococcus aureus
- Most virulent species of Staphylococcus
- Produces coagulase, an enzyme that clots plasma
- Common cause of bacterial infections
- Causes food poisoning and toxic shock syndrome
Staphylococcus epidermidis
- Less virulent than S. aureus
- Common cause of prosthetic implant infections
Staphylococcus saprophyticus
- Less virulent than S. aureus
- Causes urinary tract infections, especially cystitis in women
Virulence Factors of S. aureus
- Hyaluronidase (spreading factor): Degrades hyaluronic acid in connective tissues, promoting spread of bacteria
- Fibrinolysin (staphylokinase): Dissolves fibrin clots
- Lipases: Hydrolyze lipids, aiding survival in sebaceous areas
- Nuclease (DNAase): Degrades DNA
Toxins of S. aureus
- Cytolytic Exotoxins (α, β, γ, δ): Damage mammalian cell membranes, including red blood cells
- Panton-Valentine Leukocidin: Lyses neutrophils (PMNs), increasing virulence
-
Superantigen Exotoxins: Bind to T-cell receptors and MHC Class II, triggering excessive T-cell activation
- Toxic shock syndrome toxin (TSST-1): Causes toxic shock syndrome (TSS), leading to high fever, rash, vomiting, diarrhea, hypotension, and organ damage
- Exfoliatin (ET): Causes scalded skin syndrome in children, destroying skin intercellular adhesive
-
Enterotoxins: Produced by around half of S. aureus isolates
- Contaminate food and cause food poisoning upon ingestion, leading to nausea, vomiting, and diarrhea
Clinical Significance of S. aureus
- Infection causes inflammation, pus formation, and tissue necrosis
- Can invade bloodstream, causing bacteremia and septicemia
- May result in internal abscesses, skin lesions, and infections in various organs
Localized S. aureus Infections
- Folliculitis: Small abscesses involving hair follicles
- Furuncles (boils): Subcutaneous abscesses forming around foreign bodies
- Carbuncles: Large, deep, multiloculated skin infections
- Impetigo: Superficial, spreading, crusty skin lesions, common in children
Other S. aureus Infections
- Deep, localized infections: May be metastatic from superficial infections or result from trauma
- Acute endocarditis: Caused by contaminated injections or needles
- Septicemia: Generalized infection
- Pneumonia: Can cause severe, necrotizing pneumonia
- Healthcare-associated infections (nosocomial): Significant cause of hospital-acquired infections
Laboratory Identification
- Gram staining: Strongly gram-positive bacteria, often in clusters
- Catalase test: Positive
- Coagulase test: Positive in S. aureus, negative in coagulase-negative staphylococci (CNS)
- Mannitol fermentation: Positive in S. aureus
Treatment
- Incision and drainage: for localized lesions
- Systemic antibiotics: Choice is complex due to frequent antibiotic resistance
- Penicillin G: No longer the first-line treatment due to widespread penicillinase resistance
- β-Lactamase-resistant penicillins: Methicillin or oxacillin
- Methicillin-resistant S. aureus (MRSA): Resistant to many β-lactam antibiotics
MRSA
- Hospital-acquired MRSA (HA-MRSA): Common in hospital settings
- Community-acquired MRSA (CA-MRSA): Infections occur independent of hospital exposure
- Vancomycin resistance: Emergence of vancomycin-resistant MRSA strains, prompting alternative therapies
Coagulase-Negative Staphylococci (CNS)
- Important agents of healthcare-associated infections
- Infections associated with implanted prosthetic devices and catheters
Staphylococcus epidermidis
- Part of normal skin flora
- Common cause of infections of implants, such as heart valves and catheters
- Produces polysaccharide intercellular adhesin (PIA), facilitating adherence to biomaterials
Prevention
- No effective S. aureus vaccine
- Infection control measures: Hand washing, disinfection of surfaces, and fomites
Staphylococci
- Staphylococci are Gram-positive spherical bacteria, often arranged in grape-like clusters.
- They are commonly found on skin and mucous membranes.
- Staphylococci can cause a range of infections, from minor skin infections to life-threatening sepsis.
Important Species
- The most clinically significant species are Staphylococcus aureus, Staphylococcus epidermidis, and Staphylococcus saprophyticus.
- S. aureus is a major cause of bacterial infections, food poisoning, and toxic shock syndrome.
- S. epidermidis is often involved in prosthetic implant infections.
- S. saprophyticus is a frequent cause of urinary tract infections, particularly in women.
General Features
- Staphylococci are facultatively anaerobic, meaning they can grow with or without oxygen.
- They are catalase-positive, which distinguishes them from streptococci.
- S. aureus is the most virulent species and almost always produces coagulase, an enzyme that clots plasma.
- Coagulase-negative staphylococci (CNS) are less virulent and lack coagulase.
Staphylococcus aureus
- S. aureus infections often require a compromised host, like a skin break, foreign body insertion, or weakened immune system.
- S. aureus can cause infections through direct invasion, toxin production, or a combination of both.
Epidemiology
- S. aureus is commonly carried by healthy individuals on their skin and mucous membranes, making them potential carriers.
- Transmission can occur through direct contact, contaminated fomites, or contaminated food.
Pathogenesis
- S. aureus virulence depends on various factors that contribute to its ability to cause disease.
- Virulence factors include:
Cell Wall Virulence Factors
- Capsule: A thin polysaccharide layer that can hinder phagocytosis.
- Peptidoglycan: Provides structural support, stimulates inflammation, attracts leukocytes (contributes to abscess formation), and can inhibit phagocytosis.
- Teichoic acid: Binds to fibronectin, a protein found in connective tissue.
- Protein A: Binds to the Fc region of IgG antibodies, interfering with opsonization and phagocytosis.
- Fibronectin-binding protein: Promotes attachment to mucosal cells and tissue matrix.
- Clumping factor: Binds to fibrinogen, converting it to fibrin and causing staphylococci to clump together.
Enzymes
- Coagulase: Clots plasma by activating prothrombin, potentially aiding in evading phagocytosis.
- Catalase: Converts hydrogen peroxide (H2O2) to water and oxygen, detoxifying reactive oxygen species.
Infections Caused by Staphylococcus aureus
-
Localized Skin Infections:
- Folliculitis: Small abscesses in hair follicles.
- Furuncles (Boils): Subcutaneous abscesses often forming around foreign bodies (e.g., splinters).
- Carbuncles: Larger, deeper, multiloculated skin infections that can lead to bacteremia.
- Impetigo: Superficial, spreading, crusty skin lesions often seen in children.
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Deep, Localized Infections:
- Osteomyelitis: Infection of bone marrow.
- Septic Arthritis: Acute infection of joint space, particularly in children.
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Acute Endocarditis: Infection of the heart valves, often caused by contaminated injections or needles.
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Septicemia: Generalized infection with sepsis, potentially fatal.
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Pneumonia: Severe, necrotizing pneumonia.
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Nosocomial Infections: Hospital-acquired infections, frequently associated with wounds or catheters.
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Toxinoses: Disease caused by toxins:
- Toxic Shock Syndrome (TSS): High fever, rash, vomiting, diarrhea, hypotension, and multiorgan damage.
- Staphylococcal Gastroenteritis: Food poisoning caused by ingesting enterotoxin-producing S. aureus. Symptoms include nausea, vomiting, and diarrhea, onset within hours of ingestion.
- Scalded Skin Syndrome: Superficial blistering caused by an exfoliative toxin that disrupts skin layers, resulting in peeling.
Laboratory Identification
- Microscopically, S. aureus appears as Gram-positive cocci in grape-like clusters.
- Catalase Test: Positive (distinguishes from streptococci).
- Coagulase Test: Positive (distinguishes from most coagulase-negative staphylococci).
- Mannitol Fermentation: Positive (distinguishes from most coagulase-negative staphylococci).
- Automated systems like VITEK can aid in rapid identification.
Treatment
- Serious S. aureus infections: Require aggressive management with incision and drainage of abscesses and systemic antibiotics.
- Antibiotic Resistance: S. aureus frequently develops antibiotic resistance, including penicillinase production, methicillin resistance, and vancomycin resistance.
Methicillin-Resistant Staphylococcus aureus (MRSA)
- Hospital-Acquired MRSA (HA-MRSA): Common in hospitals, often resistant to many antibiotics, including methicillin and oxacillin.
- Community-Acquired MRSA (CA-MRSA): Emerged in the mid-1990s, occurring in individuals with no previous hospital exposure. Most often causes skin and soft tissue infections, but can cause severe diseases like pneumonia, osteomyelitis, and septicemia.
Vancomycin Resistance
- Vancomycin-Resistant S. aureus (VRSA): Emerged in 1997, prompting the use of alternative antibiotics like linezolid and daptomycin.
Prevention
- No effective vaccine against S. aureus.
- Infection control procedures like hand hygiene and disinfection of fomites are critical for preventing the spread of S. aureus.
Coagulase-Negative Staphylococci (CNS)
- CNS are often involved in hospital-acquired infections, primarily related to implanted prosthetic devices and catheters.
- Staphylococcus epidermidis: Commonly found on skin and can cause infections like prosthetic valve and catheter infections.
- Polysaccharide Intercellular Adhesin: Produced by S. epidermidis, facilitating adherence to prosthetic surfaces and acting as a barrier to antibiotics.
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Description
This quiz delves into the characteristics and virulence factors of Staphylococci, particularly focusing on Staphylococcus aureus and its role in various infections. Test your knowledge on the different species and their implications in medical contexts.