Skin infections Flashcards
Mechanisms by which bacteria attach to and colonize tissues and potentially invade and spread around the body
Adhesion to host cells (possibly invasion);
- ‘Specialized’ pili/fimbriae
- Cell wall/capsule
- Adhesins (cell adhesion; tropism) / invasins
Secretory mechanisms
- Export/deliver toxins, enzymes, invasins (invasion, spread, acquire nutrients); (see lectures on toxins)
Motility / chemotaxis
- Spread to new sites and communicate with each other e.g. Quorum sensing
Adherence
Attachment is necessary to avoid being swept away from a favourable environment or niche (e.g. GI tract, lungs, urinary tract etc)
Colonisation
Requires active replication and persistence at a specific site
Sites of attachment and colonization often associated with tissue tropism or site predilection
- Staphylococcus aureus causes disease in many tissues
Requires specific receptors (on host) and relative affinity (bacteria)
Can be species specific (N. gonorrhoeae infections limited to humans)
Adherence mechanism
2 steps: Non-specific + Specific
Adhesins (also known as Colonizing Factor Antigens) can be present at tips or all along fimbriae or on bacterial cell surface/wall
Staphyloccocus aureus has a wide range of adhesins present in its cell wall and can facilitate attachment to many different cells/tissues
Biofilms
collection of microorganisms surrounded by the slime they secrete, attached to either an inert or living surfaces
- e.g. plaque on teeth
- exists wherever surface contact water
Propionibacterium acnes
Small, Gram-positive rods found on the skin.
Produce propionic acid as a by-product of carbohydrate fermentation.
Propionibacterium acnes causes 85% of cases of acne in adolescents and young adults.
Propionibacterium acnes grows in the sebaceous oil glands of the skin; it’s growth is stimulated by sebum.
Excess sebum secreted in response to adolescent hormones (testosterone) leads to acne (see image).
This bacterium is also an opportunistic pathogen affecting medical implants.
Acne
Skin disease that causes pimples; multifactorial disorder involving excessive sebaceous secretions stimulated by hormones
Sebaceous glands become engorged/blocked and secondarily inflamed and infected
Adolescents often affected; genetics factors important
Propionibacterium acnes (S. epidermidis)
Treatment of Acne
Treatment: oral: Tetracycline, Doxycycline, Macrolides (Erythromycin); topical: Clindamycin
Staphylococcus epidermis
Gram-positive, facultative anaerobes.
Two main mechanisms Staphylococcus epidermidis uses to evade host defences:
- Structural defences against phagocytosis by secreting polysaccharide slime coat evading phagocytosis and enhancing attachment.
- Enzymes – lipases that allow it to grow on the surface of the skin and in cutaneous oil glands.
Mechanism Staphylococcus aureus use to infect + invade host
Three main mechanisms used to infect and evade host defences:
Structural defences against phagocytosis by expressing protein A which interferes with IgG binding and inhibits the complement cascade. Also possess bound coagulase which converts fibrinogen to fibrin forming a clot that surrounds the bacteria. Surface, cell wall proteins that bind host extracellular matrix (notably fibronectin). Secrete polysaccharide capsule slime coat (serotyping – pathogenic ‘strains’) evading phagocytosis and enhancing attachment.
Enzymes that breakdown fibrinogen, hyaluronic acid (ECM), lipases, β-lactamase.
Exotoxins – cytolytic (disrupt leukocytes; Panton Valentine leucocidin), exfoliative (digest desmosomes), toxic shock (super-antigen toxins), enterotoxins (food poisoning -cause diarrhoea and vomiting).
Staphyloccocus pyogenes
Group A streptococcus are Gram-positive cocci bacteria
Common cause disease when other natural flora is depleted and a large inoculum penetrates the skin.
Key structural features enable host-cell attachment and evasion of immune system phagocytosis:
- M protein – a membrane bound protein that destabilises complement; multiple variants
- Various cell wall proteins to bind to host cells and tissues
- Hyaluronic acid capsule – normally found in the body - and therefore not recognised by the immune system.
Also secrete enzymes that aid their spread through tissues:
- Streptokinases – breaks down blood clots.
- Deoxyribonucleases – breaks down DNA from dead cells softening tissue.
- C5a peptidase – breaks down complement for chemotaxis.
- Hyaluronidase – breaks down extracellular matrix.
Secrete several pyrogenic toxins (similar to S. aureus) that cause fever, rash, and toxic shock
What are the 2 adherence mechanisms
Non-specific + specific
Specific adherence
Specific adherence: ‘permanent’ attachment (“anchoring”)
Pili and fimbriae - several types (NB - often confusing nomenclature)
- common on Gram-ve bacteria
- some Gram –ve bacteria have pili that inject molecules called ‘invasins’ into a host cell causing changes in the host cell cytoskeleton to help anchoring of the bacterial cell (some strains of E.coli) or facilitate invasion into the cell (Salmonella enterica)
Non-specific adherence
Non-specific adherence: reversible attachment (“docking”)
electrostatic forces
hydrophobic interactions
trapping (biofilms)
