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L03 I&I Pyogenic infections (changed 12_2)

Pyogenic infections (changed 12/2)

Objectives:

  1. comparison of staphylococcus aurues and staphylococcus pyogenes
  2. discuss virulence in relation to clinical disease
    1. skin and soft tissue infection
  3. outline risk factors diagnosis and treatment

Key concuprs some commensal may bo oppertunitsin clinical prenection relatied to site of inoculation/ microbial virulence/ host factros high rates fo skin infectiros in nz

Content:

pyogenic means pus producing (aka purulent)

common in any infetions pus is bacteria nerutophils and fibrin rich exudate

most common gram positice cocci clinically staphyococcus and stretpcoccus steptococcus pyogenes staphylococcus aureus

what do thay havei ing common

  • bhaemolysis in BA
  • falcultative anaerobic gram postive
  • microbiome
  • oppertuninstix
  • cause similar infections and con co infect
  • similar cirulence factors what makes them difficult
  • s. Aureuas localised ususally
    • more antimicrobial resistant
    • catalase postivie
  • s pyogenes spreading infections
    • less Antimicro resistant
    • catalase negative

staphyocuccus aurues food poisoning eye infections joint and bone meningitis sepsis often in moist sweaty or mucous places

30% nasal carriage

aureus bc gold in ba

S aureus example list of virulence factors

toxinc auperantigens pn

enzyme (invasins) (breaks down tissue) collagenase hyaluronidase lipase coagluase

etc

immune system evasion makes fibrin capsule makes biofilms

adhesion molecules

Be aware of these virulence factors:

  • PVL (panton valentine leukocidin)
    • leukocidin - kills neutrophils
    • pore forming cytotoxin
    • necrotising pneimonia, necrotising fascitic, sepsis
    • MRSA is PVL +ve
  • Coagulase
    • free secreted and contributs to abcess fromation
      • prothrombin into thrombin
    • bound converts fibrinogen into fibrin
      • immune evasion and clumping

streptococcus pyogenes infections

  • pharyngitis
  • skin infections
  • pneumonis
  • endocarditos
  • postpartum
  • sepsis postinfectious
  • rheumatic fever
  • acute glomerulpnerphritis

5-15% pharyngeal carriage

  • disease associated with new strain or change in host statu

virulence factors invasins

toxins superantigens (cause tcells to go berserk) immune systrem evasion

  • m protein
  • capsule with hylauronic acid
  • protein g
  • biofilms surface adhesion molecules
  • f protein
  • m protein

Mprotein really important for virulence antigenic variation→< limited cross protection -ve charge repels phagocyt4es inhibits C3b prevent opsonisation through factor H bind fibronectin → adhesin

  • rheumatic fever
    • antibodies to m protein self reactive to heart
    • can cause rheumatic heart disease
  • glomerulonephritis
    • immune complex block kidneys treat pharynitis

skin and soft tissue infections common infections with staph and strept

pyodermas

  • impetigo (school sores) non bullous s aureus and s pyogenes usually around nose and mouth

bullous s aureus epidermolytic exotoxind affects all agaes anyehere on body

pretty easy to identify

  • folliculitis infection of hair follicle s aureus

  • coagulase

  • adhesins self limiting antimicrobials topical antiseptics

  • furuncles can arise from folliculitis deeper infection of follicle with pus local cellulitis

s.aureus’ coagulase adhesins

complications abcesses cellulitis risk factors

  • diabetes
  • obesity
  • immuno usppression
  • s aureuscarrige

treatment

  • surgical drainage of pus
  • oral/ IV microbials

carbuncles extensive infection of follicles usually neck bacl things usually s aureus PVL+ and coagulase systemic symptoms

risk factors age diabatas prolong sterios therapy

painful hard lump suppuration begin after around a week necrosis and ulcer

treatment

  • surgical drainage of pus
  • oral/ IV microbials

callulitis

infection in the in the dermis or hypodermis small or large little to no necrosis parin heat swelling erythema fever chills nausea leukocytosis bacteremia in 30% of cases

complicaitons abcess osteomuelitis septis arthritis sepsis nervrotixinf fasciitis

often s aureus spyogenes often a mix of bacteris invasins and toxins

risk factors- anything that reduced immunity

culture the blood or pus or aspirates antimicrobials

risk of complication so empiric therapy could be useful (treating with out knowing bacteria)

  • erysipelas only caused by s pyogenes raised bright red lesion more superficial and infeciton of lymph vessels too

necrotising fascititis high mortality rapid in the fascia >90% mortality if not treated sepsis → multi organ failure

s pyogenes and s aureus auper antigens toxins and invasins often poly micrbial

can be

Treatment pyoderma abcesses cellulitis necrotising fasciitis

s aureus >50% peniciliin resistent flucloxacillin MRSA vancomycin s pyogenes penicilline macrolides in penicillin allergy

other staphs and strepts

Summary

Graph View