INF1 - E. SKIN INFECTIONS-COVERED Flashcards
how do pathogens attach to and colonise tissues
- charge/electrostatic interactions
- specialised pili/fimbriae
- cell wall/capsule
- adhesins in cell wall (tropism)
- invasions (aching via injection of proteins)
- secretory mechanisms: export/deliver toxins, enzymes, invasions
- chemotaxis: spread to new sites and communicate with each other eg - Quorum sensing
what bacteria are associated with skin infections the most
S. aureus and S. Pyogenes
what are the layers of skin in order from the top
- epidermis
- dermis
- sebaceous gland and hair follicle
- sweat gland
- subcutaneous layer/hypodermis
- fascia
- muscle
- rich blood supply
explain impetigo
- superficial lesions in epidermis
- S. aureus: bullous impetigo - fluid-filled blisters with serous yellow fluid, crusted scabs if burst
- S. pyogenes: crusted, yellow lesions (scab)
- microflora infect a wound
- contagious
- spreads on face
Treatment
- topical creams: Fusidic acid, Mupirocin
- widespread: oral flucloxacillin, macrolides (clarithromycin), vancomycin, co-amoxiclav
explain furuncles (boils)/carbuncles (cluster of boils)
- furuncles: nodular, inflamed lesions affecting a hair follicle and sebaceous gland. Can develop/progress from folliculitis. Contain pus
- carbuncles: series of lesions affecting deeper regions of skin
- S. aureus
- predisposing factors: obesity, excessive perspiration, IV drug use/abuse, corticosteroids
- possibility of rupture/spread ie - toxic shock syndrome
Treatment
- hot compress to drain
- surgical debridement
- antibacterial skin washes
- topical mupirocin
- reoccurring: clindamycin, teicoplanin, vancomycin, trimethoprim-sulfamethoxazole
explain cellulitis
- spreading lesions (starts in dermis)
- red rash
- S. aureus and S. pyogenes
- heat at site due to inflammation
- pain, fever
- swabs/pus: identify micro-organism
- surgical wound, insect bite, IV drug abuse
- diabetics and elderly prone to foot and lower leg cellulitis
- Erysipelas ‘streptococcal cellulitis’ - swollen red rash, more so affects face, distinct type: S. pyogenes
Treatment
- amoxicillin, flucoxacillin, macrolides, vancomycin, co-amoxiclav
explain staphylococcus scalded skin syndrome
- exfoliation of epidermis caused by exotoxin which produce distinct lesions and desquamation
- S. aureus
- newborns - delivered, mother harbouring S. aureus and is producing exfoliating toxin
- wounds not cleaned, toxin will be produced
- scratching a chicken pox pustule
Treatment
- anti-staphylococcal agents: flucoxacillin, cephalosporins, clarithromycin, trimethoprim
explain necrotising fasciitis
- spreading lesions in fascia and subcutaneous fat
- from deep penetrating injuries or trauma to skin
- diabetics prone - esp where blood circulation/nerves damaged
- S. pyogenes (maybe E. coli) which produces pyo and pyrogenic toxins and enzymes (streptokinase, catalytic toxins, hyaluronidase)
- need to distinguish from Gangrene (Clostridia sp)
Treatment
- repeated surgical debridement
- group A strep: penicillin, clindamycin
- CA-MRSA: vancomycin
explain meningococcemia
- Neisseria meningitidis
- petechiae (endotoxin)
explain folliculitis
- infection of hair follicles after irritation or physical injury
- S. aureus (or gram -ve), heals spontaneously
- P. aueruginosa for hot tub folliculitis caused by contamination of water
explain toxic shock syndrome
- infection of wound by S. aureus and release of toxins that can spread systemically
what pathogens colonise burns
gram -ve?
S. aureus
S. epidermidis
E. coli
P. aeruginosa
Treatment for burns infections
- Topical antibiotic creams
where is S. aureus present on most people
- skin, nasal mucosa, vaginal mucosa
- harmless unless skin/mucosa damaged/underlying health issues
why is there antibiotic resistance with S. aureus
- mutations in PBP - MRSA is mecA gene in PBP2a
- production of beta-lactamases
pathogenicity factors of S. aureus
- teichoic acid and cell wall proteins: bind to host extracellular matrix (fibronectin)
- polysaccharide capsule/slime coat: evading phagocytosis, enhancing attachment
- protein A: affects IgG binding and complement cascade
- coagulase: helps blood to clot and trap bacteria
- exotoxins: cytolytic (damage RBC and leukocytes), exfoliative (digest skin cell connections), toxic shock (super-antigen toxins), enterotoxins (food-poisoning: diarrhoea and vomiting)
- enzymes: staphylokinase, hyaluronidase, lipases, beta-lactamases
what is MRSA
strains of S. aureus resistant to penicillins
what is CA-MRSA (community associated)
- MRSA strains isolated from patient in an outpatient or community setting
- tend to develop skin infections
what is HA-MRSA
- MRSA strains transmitted to and circulate between individuals who have had contact with healthcare families
- tend to suffer wound
- infection/systemic infection
where is S. pyogenes present on people
mouth and pharynx (throat infections, pharyngitis, strep throat - scarlet fever - toxin)
what antibiotics is S. pyogenes resistant to
macrolides and tetracyclines (mutations in ribosomes)
pathogenicity factors of S. pyogenes
- M protein: in membrane, destabilises complement
- cell wall proteins: bind to host cells and tissues
- hyaluronic acid capsule: not recognised by immune system
- enzymes which aid their spread:
streptokinases
deoxyribonuclease
C5a peptidase: breaks down complement for chemotaxis
hyaluronidase: breaks down extracellular matrix - secrete pyrogenic toxins that cause fever, rash, toxic shock
where is staphylococcal epidermidis found in people (gram +ve)
skin
survives in oxygenated and deoxygenated environments
pathogenicity factors of S. epidermidis
- secretes polysaccharide slime coat which evades phagocytosis and enhances attachment
- lipases allow it to grow on surface of skin and in cutaneous oil glands
- infection via catheters and implanted devices
- COAGULASE NEGATIVE, PRODUCES FEW TOXINS
how does acne vulgaris occur
- excessive sebaceous secretions stimulated by hormones
- sebaceous glands become blocked and hence inflamed and infected
