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Skin and Soft Tissue Infections
This document provides information on skin and soft tissue infections (SSTIs). It discusses the difference between uncomplicated and complicated SSTIs, giving examples of each. It also provides short notes on specific SSTIs including impetigo, bullous impetigo, erysipelas, and cellulitis. The document further discusses the typical bacterial causes of various SSTIs and treatment approaches.
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Skin and Soft Tissue Infections
- 1. Skin and SoftTissue Infections Dr P Mahabeer Dr. N. S. Naidoo
- 2. • What isthe difference bet uncomplicated and complicated ssti. Give 2 examples of each and the bacterial causes. • Write short notes on impetigo, bullous impetigo, erysipelas, cellulitis.
- 3. The Skin • Skin: – organ system with multiple functions, incl. protection of tissues from external microbial invasion • Surface = keratinised stratified epithelium
- 4. Healthy Skin • Intactskin – physical barrier to penetration of organisms • Tight junctions bet epithelial cells • Acidic oily matrix prod by sebaceous glands coats epithelial cells • Normal skin flora prevent colonisation
- 5. How does infectionoccur? • Minor trauma that destroys the integrity and allows organisms access • Surface penetrated by ducts of pilosebaceous glands, sweat gland and hair follicles provide route of entry for microbes , esp. if ducts are obstructed
- 6. Modes of infection –Circulating microbe – Circulating toxin – Direct introduction of microbe into epithelium
- 7. Pathogenesis • To causeinfxn – organisms must penetrate barrier • Due to trauma • Symptoms incude – Pain – Warmth – Skin discolouration – Swelling – vesicles
- 8. Categories – localised orspreading – Uncomplicated – infxn of superficial layer – Complicated – infxn extending to deeper layers
- 10. • Respond todrainage and antibiotics • These include: • Minor abscess • Impetigo • Cellulitis • Erysipelas • Folliculitis • Furuncles or boils • carbuncles Uncomplicated SSTI
- 11. complicated SSTI – Involvedeeper structures – Significant surgical intervention – Infxns in pts at risk eg Diabetes; poor blood supply – These include • Gas gangrene • Necrotising cellulitis ( dermal and subcut tx) • Necrotising fascitis ( include fascia) • Pyomyositis and myonecrosis ( muscle)
- 13. Folliculitis oInfection of hair follicles oAssocwith areas of friction – neck, face, axillae, buttocks oAetiology: oS. aureus oP. aeruginosa
- 14. o Small staphylococcalabscess o Develops in region of hair follicle o Solitary or multiple Furuncles
- 15. Uncomplicated infections • Staphylococcalfuruncle better known commonly as a “ Boil”
- 16. • Spread tothe dermis and subcutaneous tissue multiloculated abscess =CARBUNCLE
- 17. Impetigo • Superficial infectionof the skin - becomes crusted • Common in childhood, poor hygiene, overcrowding • spread by sharing of clothes or towels • Aetiology • Group A Streptococci • S. aureus
- 18. Bullous impetigo • Bullousform of impetigo is caused by S. aureus • Newborns and young children • Vesicles ! rupture, leave a moist red surface ! thin, brown crusts
- 19. Erysipelas • Aetiology :S. pyogenes • Rapidly spreading infection of the deeper layers of the dermis • Assoc with pain and redness
- 20. Cellulitis • Acute spreadinginfection that extends deeper to involve the subcutaenous tissue • Aetiology: • S. pyogenes • S. aureus • Enteric gram negative bacilli • Clostridia • Anaerobes
- 21. Treatment of SSTI •Adequate drainage of infected fluid • Remove dead/necrotic tissue • Remove foreign devices • Appropriate antibiotc treatment
- 23.
- 24. Staphylococcus aureus • Manychildren and adults become transiently colonized by S. aureus. • carried in the : – Nasopharynx – skin – Clothing – perineal area. • intrapersonal transfer by aerosol and by direct contact.
- 25. Bacteriology o Gram positivecocci in clusters
- 26. o Grow onblood agar • golden colonies • some strains show ring of β- haemolysis around colonies
- 27. Pathogenesis • Colonisation byStaph aureus mediated by: – surface proteins – bind to host tissue – Fibrin – Collagen – fibronectin • Trauma , foreign matter – provide access for org to enter
- 28. Virulence factors: • Capsule –Exopolysaccharide – Prevents ingestion by PMN – Promotes adherence to host cell and prosthetic devices – Classified into 8 types based on immunotyping. • Capsular types 5 and 8 resp for up to 75% of clin infections • Vaccine ags 5 & 8 : pts with hemodialysis
- 29. Surface adhesins • Adherenceto host proteins • Microbial surface components – • acronym : MSCRAMM • Imp ones are • Clumping factor A and B • Fibronectin-binding prts • Prt A
- 30. • Protein A: –Bound to cell wall peptidoglycan – Binds Fc region of IgG – Interferes with opsonisation, ingestion by PMN • Cell wall constituents: – Teichoic acid – imp for adherence to mucosal surfaces – Peptidoglycan – rigidity & resilience – Inhibit chemotaxis
- 31. • Teichoic acidsrep 50% of wt of cell wall • They are site of attach of prts and enzymes • LTA : plasma memb-bound counterparts of teichoic acid – implicated in inflammation – triggers cytokine release
- 32. • Enzymes: – Catalase– inactivates H peroxide & free radicals prod after ingestion by PMN – Coagulase – coat bact with fibrin →resistant to opson & phagocytosis – Fibrinolysis – break down fibrin clots → spread in tissues – Hyaluronidase – hydrolyses intracellular matrix of mucopolysacc in tissue → spread – Lipases – spread in subcut tissue
- 33. • Haemolysins: – Alpha– lyses PMN , neurotoxin – Beta – sphinogomyelinase – lyse varity of cells • Panton Valentine Leucocidin (PVL): – Found in 2% of strains – Cause severe skin infections and severe haemorrhagic pneumonia in young adults and children – Encoded on a mobile phage
- 34. Staphylococcal scalded skin syndrome •SSSS (Ritter’s dx) • Skin and mucosal colonisation with a toxigenic S aureus that prod an exfoliative toxin (A or B) • Toxin genes on plasmid or phage • Toxin acts on desmoglein 1 ( transmemb desosomal glycoprotein invlv in interkeratinocyte adhesion ) in the stratum granulosum
- 35. Staphylococcal Scalded Skin Syndrome(SSSS) • Infection with S. aureus strains producing an exfoliative exotoxin • Characterized by widespread bullae and exfoliation • Common in children, especially newborns
- 36. • Superantigens • Tsst-1 •Staph enterotoxin • Are prts that do not activate the imm sys via normal Ag presenting • Attach to Vβ domain of large quan of T lymphs • Activates 20%of total poolof T cells • Normal Ag pres – 1/10000 • Massive cytokine release - shock
- 37. • Toxins: – Exfoliatin/Epidermolytictoxins: -resp for condition ‘Staph scalded skin syndrome ‘ -intercellular splitting of epidermis bet stratum spinosum and stratum granulosum Pyrogenic Toxin Superantigens: -<10 % of strains prod PTSAgs -Bind MHC II without processing -Cause massive cytokine release -Toxic shock syndrome toxin-1(TSST-1) and Enterotoxins
- 38. Staphylococcal toxic shock syndrome(TSS) •Toxin-mediated disease • Pyrogenic exotoxin • (1980’s – reported in hundreds of cases of young women using intravaginal tampons)
- 39. Streptococcus Pyogenes • Gram+ cocci in chains • Cxs – sore-throat which can lead to rheumatic heart disease – severe deep tissue infections – ‘Flesh- eating bacteria’
- 40. • Streps classifiedaccording to hemolysis – α , β ,non • β streps - serogroups based on CHO antigens in CW: – Lancefield Classification ( Group A,B,C ) • Strep pyogenes = Group A strep =GAS
- 41. Virulence factors: • Mprotein – – > 80 serotypes – Maj virulence factor – anchored in cell memb – Anti-phagocytic – Lack of M-prt = non-pathogenic • Protein F – bind to fibronectin • LTA( lipoteichoic acid) – similar to Prt F
- 42. • Adherence tonasopharynx – M protein – Protein F – LTA • Adherence to skin – M protein – keratinocytes – Protein F – Langerhans cells
- 43. Hemolysins: –Streptolysin O: • cytotoxinlysing WBC, Plts and tissue cells • toxin inserts directly into the cell memb forming pores • antigenic and antibodies ags it used for serological test ( ASOT) –Streptolysin S: – non-antigenic. – toxic to WBC
- 44. • Pyrogenic exotoxins –Erythrogenic toxin!scarlet fever(10% GAS) – Similar to pyrogenic toxins in St aureus
- 45. • Other virulencefactors contribute to spread: – Stretokinase – lyes fibrin clot – Hyaluronidase – Hyaluronic capsule - inhib phagocytosis – DNAse – C5a peptidase
- 46. • 2 immunologiccomplications of GAS infection: – Acute rheumatic fever • Antibodies to M protein bind to heart tissue- cross- react – Acute glomerulonephritis • Deposition of immune complexes in glomerulus – complement activation & inflammation
- 47. Wound infections • Secondaryto surgery, trauma or physiologic • Contributing factors : – Contaminating dose – Virulence of org – Physical condition of wound – Physiological state of wound • poor oxygenation • poor blood supply
- 48. • Sources ofinfection – Patient’s normal flora – From infected people/carriers that may reach the wound eg hands, fomites, air – From environment eg soil, clothing
- 49. Organisms • Staph aureus •Group A streptococcus/ Streptococcus pyogenes • Pseudomonas aeruginosa • Clostridium perfringens • Other gram negative bacilli – Acinetobacter spp – Klebsiella pneumoniae – Enterobacter spp
- 50. Pseudomonas aeruginosa • Pseudomonasis a gram-negative bacilli
- 51. • produce theblue- green pigment pyocyanin. • has a characteristic fruity grape-like odor.
- 52. • Epidemiology • Foundin soil, water • Has been isolated from stool • Hospitalised pts – higher colonisation rate • Most impt cause of opportunistic infection • Burns • Cystic fibrosis • Immunosuppression
- 53. • Adhesins pili (N-methyl-phenylalaninepili) polysaccharide capsule (glycocalyx) alginate slime (biofilm) • Invasins elastase hemolysins (phospholipase and lecithinase) cytotoxin (leukocidin) pyocyanin diffusible pigment
- 54. • Toxins: Exoenzyme S ExotoxinA • Lipopolysaccharide Antiphagocytic surface properties capsules, slime layers LPS Biofilm construction
- 55. Complicated SSTI • Gasgangrene is a severe condition resulting from bacteria invading healthy muscle from adjacent traumatized muscle or soft tissue. • The infection originates in a wound contaminated with bacteria of the genus CLOSTRIDIUM.
- 56. • Clostridial myonecrosisis a destructive infectious process of muscle associated with infections of the skin and soft tissues. • Caused by the anaerobic, gas-forming bacilli of the Clostridium genus. • Often occurs after • abdominal operations on the GIT , • penetrating trauma, such as gunshot wounds • frostbite, can expose muscle, fascia, and subcutaneous tissues to these organisms.
- 57. Clostridium spp. • Large,spore forming GPB • Spores resistant to heat, dessication and disinfectant • Medically impt: • C. perfringens • C. tetani
- 58. MICROSCOPY • Gram positivespore forming bacilli ‘box car shaped’
- 59. C. perfringens • Contaminationof wounds with org from own intestinal flora or spores from environment • Most common cause of gas gangrene o Culture • Grows on BA
- 60. Clostridium perfringens • Thisorganism produces collagenases and proteases that cause widespread tissue destruction • Multiple exotoxins – Most important is α-toxin-phospolipase that hydrolyses lecithin & sphingomyelin! disrupt cell membranes of various host cells
- 61. C. tetani • Contaminationof wounds • Can lead to tetanus in the unimmunised pt • Effect by neurotoxin – tetanospasmin • Blocks release of inhibitory neurotransmitters • Clinical: • Severe muscle spasm – trismus (lockjaw)
- 62. Necrotising fascitis • Severeinfection involving the subcutaneous soft tissues, particularly the superficial and deep fascia with muscle involvement • Aetiology • S. aureus • Streptococci – Group A and Strep milleri • Anaerobes • Clostridia spp • Vibrio vulnificus • Aeromonas hydrophila
- 63. Infection of otherskin layers • Infection of keratinised layers • Fungal infections: – Candida spp – Dermatophytes • Candida • Moist areas • Can be assoc with defects in cellular immunity
- 64. Dermatophyes: • Human-human transmission reqclose contact • minor lesions come in contact with dermatophyte hyphae shed from another infection. • non-living, keratinised tissues of nails, hair and stratum corneum of skin
- 65. • Low infectivity& virulence • Not painful or life-threatening • Families, locker rooms • Aetiology -3 genera • Microsporum • Trichyophyton • Epidermophyton
- 66. • Each “disease”often given its own name, eg. Tinea capitis (scalp), tinea pedis (athletes foot) • Most common – ringworm • Treatment : topical antifungals (eg azoles)
- 67. Human bites • canresult in serious soft tissue infection. • infections include – Streptococcus spp – S. aureus – Eikenella corrodens – Fusobacterium nucleatum – Prevotella melaninogenica
- 68. Dog bites • Infectionsrelated to dog bites are often polymicrobial, predominantly involving Pasteurella and Bacteroides spp.
- 70. • A historyof travel is important in the assessment of SSTIs: – Vibrio spp. infection in those exposed to sea water • Rashes in travellers may be associated with a range of infections – Tick bite fever