BIOL 2044 - Skin infections and dwelling diseases

primary and secondary infections

primary site of infection - mouth, catheters, implanted medical devices

secondary infections - brain, kidneys, intermembranal spaces, bones, around implanted device

examples of common implant infections

normal skin flora

• sebaceous gland secretes a lubricant fluid (rich in microbial nutrients: lactic acid, AAs, salt, lipids)

• pH of human secretion 4-6

• variety of aerobic/anaerobic bacteria, yeast, filamentous fungi

• normal flora either transeints/residents

• most transients die shortly

• residents are long term and multiply

• most skin infections are S. Aureus, S. pyogenes, P. auruginosa

• immune cells are present around hair follicles to control whats going on

• primary bacteria recovereed are mainly gr+ve bact S. epidermis, S. mitis, Micrococcus sp.

• aerobic/anaerobic corynobaceria imbalance causing secretion of subaceous glad causing acne in hormonal imbalance

• gr-ve bacteria are a minor consituent, only long term resident detected Acinetobacter Johnsonii

• thought that gr-ve ouldnt compete well with gr+ve —> is the latter is eliminated then gr-ve might thrive

skin microbiome

• each area has its own community

• 1000 species from 19 phyla

• 10m2 of skin

• major constituents from culture only male up a small constitution of flora

• were now detecting more gr-ves - proteobacteria 1.7%, bacteriodetes 6%

• P. aeruginosa thought to be a pathogen but can be mutualistic as it secretes an antibiotic which inhibits staph/strep tRNA sythetases

areas around the body

SEBACEOUS (hair/chest)

• mainly propoinibacteria and staph species

• greater species richness and more nutreints

MOIST AREAS

• crynobacteria and staphylococci

DRY AREAS

• mixture but beta proteobacteria and flabobacteria dominate

CHRONIC WOUND

• polymicrobial biofilm - many bacteria present

hip infections

• pain/arthristis lead to hip replacements

• 0.6% deep infections despite surgical procedures

• cause: pain, prolonged immobilisation, lifetime antibiotic treatment due to persistant biofilm

• treated by surgical revision —. replace joint and clean the area

  • one stage - 30% replaced

  • two stage - 60% replaced

• even surgical revision causes a 10% reinfection

how do we know about reinfections?

• 18F fluoro-deoxyglucose positron emission tomography

• activated inflammatory cells accumulate FDG

• biofilm infections in knee replacements/hip can cause secondary infection

vascular catheter

• eneters directly in to venus system

• when infected erythema and discharge omon at the exit site

catheres major cause of UTI

• difficult to keep sterile

• biofilms can have translocation - urine in catheter flows down but we usually see ascending infections as the bacteria move against flow

• can have rippling, rolling, streaming of biofilm (streaming is where long streams form and detach)

blockage of catheters

• some catheter infections cause blockage of the catheter —> requires fast treatment as theres nowhere for the urine to go

• crystalline structure deposits (magnesium ammonium phosphate) and a poorly crystalline form of apatite (hydroxylated calcium phosphate)

• bacteria on top of the crystals guide the formation of crystals

• bacteria then colonise the crystals —> caused by protens morabilis

  • highly motile and covered in flagella

  • has urease enzyme which allows it to hydrolyse urea and increase urinary pH

• as urine becomes alkaline magnesium and calcium phosphate crystals are precipitated which blocks the flow of urine

• the urea is then broken down into ammonia and hydrogen carbonate ion:

  • hydrogen carbonate ion and the calium phosphate combine whilst the ammonia combines with the magnesium

effects of crystal formation

• struvate can damage glycosaminoglycan layer of epithelium which protects the urothelial surface against infection

• P. mirabilis can cause reccurent infection - blockage of new catheter

• ascending reflux - ascends to kidneys causing pyelonephritis —> sepsisemia, endotoxic shock

• crystalline aggregates can form stones in the bladder which are resistant to antibiotics

• strategies for treatment: lower urine pH with cranberry juice, increase fluid uptake, surgically remove bladder stones

• can also cause urinary stones which penetrate down into the urinary epithelium

variations of catheters

• can we coat in antimicrobial materials

• no - silver cathters not effective

virulence factors of UTI

• E. coli causing uncomplicated UTIS

• P. mirabilis causing complicated UTIS

• both have fimbrae and pilli to help adhere to the surface

• produce toxins such as HlyA, Pic, Sat (E. coli) and Hpm (P. mirabilis)

growth environment

• latex catheters - not smooth, lots of niches

• in standard LB broth forms large collection of microcolonies whereas in urine forms swarm cells —> flagell start to swarm and form much longer finger like appendages

• if the E. coli have been able to form stones the leukocytes are unable to bind and engulf bacteria

• stones form pods and coat in europlakin

• inside a polysaccharide strain used lost of polysaccharides by the interior surface

• E. coli right in the centre

coinfection

• gerdenella vaginalis found in vaginal flora but may get into urinary tract

• debrines surface of urinary tract and exposes the surface to UTI

• a lot more E. coli infection when polymicrobial —> this suggests that E. coli does better when it’s a coinfection