infection - infections on surfaces Flashcards
what is a surface?
interface between a solid & either liquid / gas
what are examples of skin micro-organisms?
- viruses: papilloma, herpes
- gram pos bac: staph aureus, coagulase neg staphylococci
- gram neg bac: enterobacteriaeceae
- fungi: yeast, dermatophytes
- parasites: mites
what are normal mucosal flora?
nasopharynx: PIM
mouth: viridans streptococci, lactobacillus, candida
stomach: helicobacter, strep, staph, lactobacilli
intestine: bacteriodes, clostridium, aerobic & anaerobic streptococci
urethra: lactobacilli, streptococci, enterobacteriaceae
vagina: lactobacilli, yeast, coagulase-neg staphylococci, enterococcus faecalis
what is microbiota?
commensals (normal flora)
micro-organisms carried on SKIN & MUCOSAL surfaces
normally HARMLESS / even beneficial
TRANSFER to other sites can be harmful
how do people get infections?
- invasion (direct, contiguous): strep pyogenes pharyngitis
- migration: E coli
- innoculation: coagulase negative staph prosthetic joint infection
- haematogenous: viridans strep (endocarditis)
what are examples of natural external surface infections?
cellulitis, pharyngitis, conjunctivitis, gastroenteritis, UTI, PNEUMONIA
what are examples of natural internal surface infections?
(think blood) endovascular: endocarditis, vasculitis septic arthritis osteomyelitis empyema
what are examples of prosthetic surface infections?
IV lines, peritoneal dialysis catheters, prosthetic joints, cardiac valves, pacing wires, endovascular grafts
what are causative organisms of prosthetic valve endocarditis?
> 1 year post-op: viridans streptococci, enterococcus faecalis, STAPH AUREUS, candida (SCEV)
<1 year post-op: COAGULASE negative, staphylococci
what are causative organisms of prosthetic joint infections and cardiac pacing wire endocarditis?
coagulase negative
staph aureus
what are the processes in the pathogenesis of infection at surfaces?
- adherence to host cells / prosthetic surface (pili / fimbriae)
- biofilm formation (come together)
- invasion & multiplication
- host response: Pyogenic (neutrophils –> pus), granulomatous (fibroblasts, lymphocytes, macrophages - nodular inflammatory lesions)
biofilm formation
- bacteria adhere to surface (pili / fimbriae)
- multiply as colony is covered in slimy matrix
- nutrients can diffuse into matrix
- close proximity of cells allows exchange of signals to regulate behaviour - antimicrobials don’t work well as only affect outer layer
- shearing forces cause cells to move together - not individually
quorum sensing
exchange of signals - ensure biofilm environment right
controls spore formation
biofilm formation
virulence factor (damage to host)
if enough bacteria then forms biofilm
signals are detached on cell surface membranes - then change gene expression
how is quorum sensing achieved
via local signalling molecules (AUTOINDUCERS) & cell surface receptors: allows bacteria to sense the diversity of local population & to coordinate behaviours to adapt via changing gene expression
changes in gene expression made across an entire colony of bacteria allow co-operative behaviours
what are examples of virulence factors? what can it lead to?
exotoxins: cytolytic, AB toxins, superantigens, enzymes
endotoxins… leading to:
host cellular damage: direct, consequent to host immune response
