Organism Pathogenicity
This section delves into the pathogenicity of the major bacterial agents discussed in the context of skin, soft tissue, and bone infections. This includes understanding the etiology (causes), modes of transmission, and the key virulence mechanisms that allow these organisms to cause disease
Staphylococcus aureus
- Etiology: Staphylococcus aureus is a Gram-positive coccus, arranged in clusters, and a common cause of skin and soft tissue infections
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Transmission
- Direct Contact: Through contact with infected individuals or contaminated surfaces
- Autoinfection: Spread from the nares (where S. aureus commonly colonizes) to other body sites
- Healthcare-Associated: Transmission in healthcare settings via contaminated medical devices, hands of healthcare workers, and other sources
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Virulence Mechanisms
- Adhesins: Surface proteins that mediate adherence to host cells and tissues
- Capsule: Protects against phagocytosis
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Enzymes
- Coagulase: Clots plasma, potentially forming a protective barrier around the bacteria
- Hyaluronidase: Breaks down hyaluronic acid in connective tissue, promoting tissue invasion
- Fibrinolysin (Staphylokinase): Dissolves blood clots, facilitating spread
- Lipases: Break down lipids, aiding in colonization of the skin
- Proteases: Degrade host proteins, causing tissue damage
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Toxins
- Exfoliative Toxins (ETs): Cause staphylococcal scalded skin syndrome (SSSS), resulting in skin peeling
- Toxic Shock Syndrome Toxin-1 (TSST-1): A superantigen that causes toxic shock syndrome (TSS)
- Enterotoxins: Cause food poisoning
- Panton-Valentine Leukocidin (PVL): A pore-forming toxin associated with severe skin and soft tissue infections (SSTIs) and necrotizing pneumonia
- Biofilm Formation: Allows S. aureus to adhere to medical devices, forming a protective barrier that resists antibiotics and host defenses
Beta-Hemolytic Streptococci
- Etiology: Gram-positive cocci, arranged in chains, and categorized based on their Lancefield group (e.g., Group A Streptococcus - Streptococcus pyogenes)
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Transmission
- Direct Contact: Through contact with respiratory droplets or skin lesions from infected individuals
- Indirect Contact: Through contaminated objects
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Virulence Mechanisms
- Adhesins: M protein, F protein, and others that promote adherence to host cells
- Capsule: Composed of hyaluronic acid, which can mimic host tissues and evade immune recognition
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Enzymes
- Streptolysin S and O: Hemolysins that damage host cells
- Hyaluronidase: Breaks down hyaluronic acid, promoting tissue invasion
- Streptokinase: Dissolves blood clots, facilitating spread
- DNases: Degrade DNA, which can interfere with neutrophil extracellular traps (NETs)
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Toxins
- Streptococcal Pyrogenic Exotoxins (SPEs): Superantigens that cause scarlet fever, toxic shock syndrome, and other severe conditions
- M Protein: A major virulence factor that interferes with phagocytosis and activates the complement system
- Biofilm Formation: Can occur, aiding in persistence
Pseudomonas aeruginosa
- Etiology: Gram-negative rod, ubiquitous in the environment and an opportunistic pathogen
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Transmission
- Environmental Reservoirs: Commonly found in soil, water, and on various surfaces
- Healthcare-Associated: Transmission in healthcare settings via contaminated equipment, devices, and hands of healthcare workers
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Virulence Mechanisms
- Adhesins: Pili and flagella that promote adherence to host cells
- Capsule (Alginate): Protects against phagocytosis and contributes to biofilm formation
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Enzymes
- Proteases: Degrade host proteins, causing tissue damage
- Phospholipase C: Disrupts host cell membranes
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Toxins
- Exotoxin A: Inhibits protein synthesis, causing tissue damage and immune suppression
- Pyocyanin: A blue-green pigment that generates reactive oxygen species, causing tissue damage and immune suppression
- Pyoverdine: A siderophore that scavenges iron, essential for bacterial growth
- Biofilm Formation: Facilitates persistence and resistance to antibiotics and host defenses
Pasteurella multocida
- Etiology: Gram-negative coccobacillus, commonly found in the oral cavities of animals, particularly cats and dogs
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Transmission
- Animal Bites and Scratches: The primary mode of transmission
- Contact with Animal Saliva: Direct contact with animal saliva can also lead to infection
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Virulence Mechanisms
- Capsule: Protects against phagocytosis
- Adhesins: Promote adherence to host cells
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Enzymes
- Hyaluronidase: Breaks down hyaluronic acid, facilitating tissue invasion
- Chondroitin Sulfatase: Degrades cartilage, potentially leading to joint infections
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Toxins
- Capsular Polysaccharide: Contributes to virulence
- Lipopolysaccharide (LPS): Endotoxin that can trigger an inflammatory response
Eikenella corrodens
- Etiology: Gram-negative rod, commonly found in the human oral cavity
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Transmission
- Human Bites and Fist Fights: The primary mode of transmission
- Animal Bites: Can also be transmitted through animal bites
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Virulence Mechanisms
- Adhesins: Promote adherence to host cells
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Enzymes
- Collagenase: Degrades collagen, promoting tissue invasion
- Hyaluronidase: Breaks down hyaluronic acid, facilitating tissue invasion
- LPS: Endotoxin that can trigger an inflammatory response
- Outer Membrane Proteins: Contribute to virulence
Bacillus anthracis
- Etiology: Gram-positive rod, spore-forming bacterium that causes anthrax
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Transmission
- Cutaneous Anthrax: Through contact with spores that enter the skin via cuts or abrasions
- Inhalation Anthrax: Through inhalation of spores
- Gastrointestinal Anthrax: Through ingestion of contaminated meat
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Virulence Mechanisms
- Capsule: Inhibits phagocytosis
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Anthrax Toxin: Consists of three components:
- Protective Antigen (PA): Binds to host cell receptors, allowing the other toxins to enter
- Lethal Factor (LF): A metalloprotease that disrupts cellular signaling pathways, leading to cell death
- Edema Factor (EF): An adenylate cyclase that causes edema (fluid accumulation)
- Spore Formation: Enables survival in the environment for extended periods
Brucella spp.
- Etiology: Gram-negative coccobacilli that cause brucellosis (undulant fever)
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Transmission
- Ingestion: Consumption of contaminated animal products (e.g., unpasteurized milk, cheese)
- Contact: Direct contact with infected animals or their tissues (e.g., during slaughtering or veterinary procedures)
- Inhalation: Inhalation of aerosols
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Virulence Mechanisms
- Intracellular Survival: Brucella spp. can survive and multiply inside phagocytic cells, evading the immune system
- Lipopolysaccharide (LPS): Elicits an inflammatory response, but also has properties that contribute to immune evasion
- Type IV Secretion System: Delivers effector proteins into host cells, modulating host cell functions
Francisella tularensis
- Etiology: Gram-negative coccobacillus that causes tularemia
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Transmission
- Tick Bites: The most common mode of transmission
- Contact: Through contact with infected animals (e.g., rabbits, rodents) or their tissues
- Inhalation: Inhalation of aerosols
- Ingestion: Ingestion of contaminated water or food
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Virulence Mechanisms
- Intracellular Survival: Francisella tularensis can survive and multiply inside phagocytic cells, evading the immune system
- Capsule: Protects against phagocytosis
- Lipopolysaccharide (LPS): Modifies LPS to evade immune recognition
- Type VI Secretion System: Delivers effector proteins into host cells
Yersinia spp. (e.g., Yersinia pestis)
- Etiology: Gram-negative coccobacilli, with Yersinia pestis causing plague
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Transmission
- Bubonic Plague: Through the bite of an infected flea (e.g., Xenopsylla cheopis)
- Pneumonic Plague: Through inhalation of respiratory droplets from an infected individual
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Virulence Mechanisms
- Capsule: Protects against phagocytosis
- F1 Capsule: A major virulence factor
- Type III Secretion System (T3SS): Delivers effector proteins (Yops) into host cells, disrupting phagocytosis, inflammatory responses, and other host defenses
- Pla (Plasminogen Activator): Degrades fibrin clots, facilitating spread
- Yersiniabactin: A siderophore that scavenges iron
Key Terms
- Etiology: The cause of a disease
- Transmission: The ways in which an infectious agent spreads
- Virulence: The degree of pathogenicity of a microorganism
- Virulence Factors: Bacterial components or products that contribute to the ability of an organism to cause disease
- Adhesins: Bacterial surface proteins that mediate adherence to host cells
- Capsule: A polysaccharide layer that surrounds some bacteria, protecting them from phagocytosis
- Enzymes: Biological catalysts that break down or modify host tissues
- Toxins: Poisonous substances produced by bacteria
- Superantigens: Toxins that activate a large number of T cells, leading to excessive immune activation and inflammation
- Biofilm: A community of bacteria encased in a matrix of extracellular polymeric substances, providing protection from antibiotics and host defenses
- Spore: A dormant, highly resistant form of a bacterium
- Intracellular Survival: The ability of a bacterium to survive and multiply inside host cells
- LPS: Lipopolysaccharide, a component of the Gram-negative bacterial cell wall that can trigger an inflammatory response
- Siderophore: A molecule that binds and transports iron
- Endotoxin: A toxin that is part of the bacterial cell structure (e.g., LPS)
- Exotoxin: A toxin secreted by a bacterium
- Pili/Fimbriae: Hair-like appendages on bacteria that mediate attachment to host cells
- Phagocytosis: The process by which a cell engulfs and destroys a foreign particle (e.g., a bacterium)
- Protease: An enzyme that breaks down proteins
- Hemolysin: A substance that causes the lysis of red blood cells
- Bioterrorism: The intentional release of biological agents to cause harm