Bacterial skin infection jaber


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In this lecture, I talked about everything concerning bacterial skin infection and its management from dermatological aspect.

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  • Nape: the back of the neck
  • Mupirocin: antibiotic
  • Ecthyma: ulcerative pyoderma of the skin caused by group A beta-hemolytic streptococci
  • Omphalitis:  infection of the umbilical cord stump
  • Initially, findings of acute cellulitis (local redness, edema, heat, and pain in the involved area), typically occur on an extremity. Characteristic findings appear within 36 to 72 h after onset: the involved area becomes dusky blue in color; vesicles or bullae appear containing initially yellowish, then red-black fluid. Infection spreads rapidly along fascial planes resulting in extensive necrotic sloughs . Bullae rupture, and extensive, sharply demarcated cutaneous gangrene develops. At this point the area may be numb, and the black necrotic eschar (Fig. 22-28) with surrounding irregular border of erythema resembles a third-degree burn. The eschar sloughs off by the end of 1 week to 10 days. Peripheral areas of involvement develop about the initial site of infection.
  • Exanthem: widespread rash
  • Bacterial skin infection jaber

    1. 1. Bacterial skin infection Jaber Manasia 5th year medical student Mutah University-Jordan
    2. 2. Bacterial Skin infections Intact skin is one of the body’s defences against infection Normal flora (resident organisms) exist on the skin Normal flora become pathogenic when transported to alternate locations Break in the normal skin barrier Uncomplicated skin infections usually involve 1 or 2 pathogens Predominant organisms for skin infection are Staphylococcus and Streptococcus spp 2
    3. 3. Normal Skin Flora Gram Positive  Staphylococcus  Micrococcus  Coryneforms - Corynebacterium - Propionibacteria - Dermobacter - Brevibacterium  Gram Negative  Acinetobacter  3
    4. 4. A. Staphylococcus Aureus & Streptococcal Infections    S. aureus does not normally reside on the skin, but may be present transiently, inoculated from colonized sites such as the nares (30%), also axillae & vagina. Colonization is usually intermittent; 10 to 20% of individuals have persistent colonization Frequent hand washing reduces the risk of person-to-person transmission of cutaneous pathogens. 4
    5. 5.        Folliculitis Pseudofolliculitis Boils Carbuncles Impetigo Infected eczema Ecthyma 5
    6. 6. Folliculitis • Folliculitis is a superficial infection of the hair follicles characterized by erythematous, follicular-based papules and pustules. S. aureus is the usual pathogen, although exposure to Pseudomonas aeruginosa in hot tubs or swimming pools can lead to folliculitis. usually in scalp of children also in beard, axilla, extremities, buttocks  Causes:  Bacteria (staph.) Yeasts (pityrosporum) Chemical or physical injury • • •   6
    7. 7. Hot tubs Folliculitis Folliculitis 7
    8. 8. DDx: Pseudofolliculitis oTreatment: Mild folliculitis can be treated with a topical antibacterial agent, but if it is extensive a systemic antibiotic may be required. 8
    9. 9. Pseudofolliculitis: Also called “sycosis barbae”. Deeper folliculitis of the hair follicles of the beard area in males due to shaving. Often the lesions are sterile & poorly respond to antibiotics. 9
    10. 10. 10
    11. 11. Furuncle ( Boils ) • It is an acute, necrotic infection/abscess of a hair follicle (usually vellus). • causative agent: Staphylococcus aureus firm, red and tender papule that becomes painful and fluctuant pustule developed from preceding folliculitis deep seated occur in areas that are subject to friction and perspiration and contain hair follicles (vellus) (neck, face, axillae, buttocks) • • • • 11
    12. 12.        Precipitating factors: Poor hygiene Stress DM It may recur at intervals for no apparent cause. Such patients are carriers to the staph in the nose, axillae & groins between the attacks. Carriers may be treated with topical antibacterial applied to nostrils. They may also be helped by an antibacterial bath additives, & a prolonged course of flucloxacillin 12
    13. 13. Furuncle  Furuncle: S. aureus Soft-tissue swelling of the forehead with central abscess formation, nearing rupture. 13
    14. 14. 14
    15. 15. Carbuncle • • • • • • • causative agent: Staphylococcus aureus extend into the subcutaneous fat in areas covered by thick inelastic skin more severe and painful than furuncles multiple pustules with fever and malaise usually located at the nape, neck, back and thigh blood stream invasion may occur usually as a result of manipulation causing osteomyelitis, endocarditis or other metastatic foci 15
    16. 16. Carbuncle • Carbuncle: S. aureus A very large, inflammatory plaque studded with pustules, draining pus, on the nape of the neck. Infection extends down to the fascia and has formed from a confluence of many furuncles. 16
    17. 17. 17
    18. 18. Treatment: Moist heat, compresses Dicloxacillin, Clindamycin, Erythromycin Bed rest Immobilize involved area Hand washing Need systemic flucloxacillin Incision of abscess 18
    19. 19. Impetigo    Worldwide distribution More frequent among economically disadvantaged children in tropical or subtropical regions Also prevalent in northern climates in summer months 19
    20. 20. Impetigo      Peak incidence aged 2-5 years Older children and adults also afflicted M=F All races susceptible Nearly always caused by B-haemolytic streptococci and / or S. aureus 20
    21. 21. Impetigo • • • • • Contagious Superficial infection of the epidermis Discrete purulent lesions Occurs on exposed areas, well localised, frequently multiple, bullous or non bullous in appearance initially→characteristic thick yellow brown crusts Deeply ulcerated form (extend into the dermis ) = ecthyma Systemic symptoms usually absent 21
    22. 22. Differential Diagnosis for impetigo & ecthyma  Erosion ± Crust/Scale-Crust Excoriation, perioral dermatitis, seborrheic dermatitis, allergic contact dermatitis, herpes simplex, epidermal dermatophytosis, scabies.  Intact Bulla(e) Allergic contact dermatitis, insect bites, thermal burns, herpes simplex, herpes zoster, bullous pemphigoid, porphyria cutanea tarda (PCT) (dorsa of hands), pseudo-porphyria.  Ulcer ± Crust/Scale-Crust Chronic herpetic ulcers, excoriated insect bites, neurotic excoriations, cutaneous diphtheria, PCT, venous (stasis) and atherosclerotic ulcers (legs). 22
    23. 23.    Non-bullous impetigo is caused by S.aureus, streptococci, or both organisms together. In the nonbullous form the initial lesion is a small pustule which ruptures to leave an extending area of exudation and crusting. The crusts eventually separate to leave areas of erythema, which fade without scarring. 23
    24. 24. Non bullous Impetigo  Crusted erythematous erosions becoming confluent on the nose, cheek, lips, and chin in a child with nasal carriage of S. aureus and mild facial eczema 24
    25. 25. 25
    26. 26. 26
    27. 27. 27
    28. 28. Bullous Impetigo Scattered, discrete, intact thin-walled blisters on the thigh of a child;  Caused by strains of S. aureus that produce exotoxin causing cleavage in the superficial skin layer  28
    29. 29. Impetigo: Treatment  topical & systemic antibiotics. flucloxacillin or 1st gen cephalosporins are preferred (eg cephalexin, cephradine) 29
    30. 30. Staph Scalded Skin Syndome ((lyell’s disease): SSSS   Is a toxin mediated epidermolytic disease characterized initially by painful tender erythematous skin followed by widespread detachment of the superficial layer of the skin It occurs mainly in newborns and infants <2 years, and is rare in adults. 30
    31. 31.  Etiology Staph aureus phage group II (types 71 and 55) which produce exfoliatin toxins that disseminates systemically. The site of infection and production of the toxins is remote (Not in the skin). (purulent conjunctivitis, otitis media, omphalitis). 31
    32. 32. • Course and prognosis – With adequate antibiotic treatment the superficially denuded skin heals in 3-5 days with no scarring. – Without therapy, death occurs due to fluid and electrolyte loss and Sepsis – Treatment: – Hospitalization with IV fluid replacement and systemic antibiotics ( Flucloxacillin or 1st generation cephalosporins) 32
    33. 33. SSSS • Staphylococcal scalded-skin syndrome In this infant, painful, tender, diffuse erythema was followed by generalized epidermal sloughing and erosions. S. aureus had colonized the nares with perioral impetigo, the site of exotoxin production. 33
    34. 34. 34
    35. 35. Ecthyma      lesion of neglect—develops in excoriations; insect bites; minor trauma in diabetics, elderly patients, soldiers, and alcoholics. ( more common in debiliated patients ). Caused by strep.pyogenicus & staph Usually on upper posterior thighs or buttocks Vesiculopustule -erosion-ulcer covered by a crust Treatment (topical or Oral Abx) 35
    36. 36. Ecthyma   A large, circumscribed chronic ulcer with surrounding erythema in the pretibial region Heals with scar 36
    37. 37. DDx: Impetigo Cellulitis leshmaniasis 37
    38. 38. 38
    39. 39. Infected eczema : Eczema with exudates, crusts & inflammation. The cause is due to persistent scratching & using topical steroids. Cause: staph & strept. Treatment: weaker topical steroids & topical antibiotics, systemic antibiotics if necessary. Commonly in atopic eczema. 39
    40. 40. 40
    41. 41. Erysipelas • • • • • Diffuse spreading skin infection without underlying suppurative foci Red tender lesions raised above level of surrounding skin, clear line of demarcation of involved tissue. Usually involves lower extremities, classically butterfly area of face The patient looks ill & feverish. Cavernous sinus thrombosis is an important complication on face involvement. 41
    42. 42. Erysipelas     More common among infants, young children, and older adults Almost always caused by B-haemolytic strep (usually Group A, but can be caused by serogroups C or G) Rarely Group B streptococci or S. aureus be involved, also H.influenzae type b An area of broken skin forming portal of entry, may be found ( ex. Tenea pedis ) 42
    43. 43. Erysipelas • Erysipelas of face: group A streptococcus Painful, well-defined, shiny, erythematous, edematous plaques involving eyelids, cheeks, and the nose of an elderly febrile male. On palpation the skin is hot and tender. Portal of entry was conjunctivitis 43
    44. 44. Erysipelas • Erysipelas of leg: S. aureus The lower leg is red, hot, tender, and edematous. Erythematous plaque is well defined. The infection is recurrent with interdigital tinea pedis as the portal of entry. 44
    45. 45. Erysipelas: Treatment  Penicillin or erythromycin 45
    46. 46. 46
    47. 47. Cellulitis   Also a diffuse spreading skin infections without underlying suppurative foci Extends more deeply than erysipelas to involve subcutaneous tissues and lacks distinctive anatomical features as erysipelas 47
    48. 48. Cellulitis   Manifests clinically as erythema, oedema, heat+/- lymphangitis, peau d’orange, vesicles, bullae, petechiae/ecchymoses Systemic: fever, tachycardia, confusion, hypotension, leucocytosis 48
    49. 49. Cellulitis   Usually due to Beta Hemolytic streptococcus (commonly Gp A, less commonly from B, C or G) , also H.influenzae type b in childern S. aureus less frequently, often result from penetrating trauma including injection sites 49
    50. 50. Cellulitis • Cellulitis of cheek: H. influenzae Erythema and edema of the cheek of a young child, associated with fever and malaise. H. influenzae was isolated on culture of the nasopharynx 50
    51. 51. Cellulitis • Cellulitis of arm: S. aureus Cellulitis with abscess formation and blistering occurred as a puncture wound infection in a construction-site worker. The lower arm had to be debrided down to the facia and grafted. 51
    52. 52. Cellulitis: Investigation & Management   Blood cultures: low yield unless very severe Needle aspirations / skin biopsies unnecessary in typical cases  D.DX: Acute dermatitis, gout, herpes zoster, acute lipodermatosclerosis  Therapy: targeted at streptococci +/- S. Aureus  Flucloxacillin, clindamycin, erythromycin all suitable unless resistance common in community Severely ill pts: flucloxacillin, 1st gen cephalosporin Penicillin allergy: Clindamycin or vancomycin. In uncomplicated cases, treat for 5 days   52
    53. 53. Necrotizing Fasciitis  a rare subcutaneous infection that tracks along fascial planes and extends well beyond superficial signs of infection 53
    54. 54. Necrotizing Fasciitis      Caused by: S. pyogenes, S.aureus, and anaerobic streptococci Community acquired Present in the limbs Underlying cause: diabetes, arteriosclerotic disease, venous insufficiency Mortality is high: 50-70% in pts with hypotension and organ failure 54
    55. 55. Necrotizing Fasciitis 55
    56. 56. Necrotizing Fasciitis: Diagnosis         Suspect when there is: Failure to respond to initial antibiotic therapy Hard wooden feel of subcutaneous tissues Systemic toxicity Bullous lesions Skin necrosis or ecchymosis Appearance of tissue at operation, samples for culture best obtained from deep tissues Blood culture results 56
    57. 57. Necrotizing fasciitis: Treatment     Surgical intervention: major therapeutic modality Usually returns 24-36 hrs after first debridement, daily thereafter till no need for further debridement Aggressive fluid administration Antimicrobial therapy until operative procedures no longer needed, obvious clinical improvement and fever absent for 48-72 hours 57
    58. 58. Scarlet Fever Scarlet fever (SF) is an acute infection of the tonsils, skin, or other sites by an exotoxin-producing strain of Streptococcus pyogenes, associated with a characteristic toxigenic exanthem. Epidemiology and Etiology  Age of Onset Children.  Incidence Much less than in the past.  Etiology Usually group A -hemolytic S. pyogenes (GAS). Uncommonly S. aureus. 58
    59. 59. History • Incubation Period Rash appears 1 to 3 days after onset of infection. • Exposure Household member(s) may be a streptococcal carrier • Site of Infection Pharyngitis; tonsillitis. Infected surgical or other wound. Impetiginous skin lesion. 59
    60. 60. Physical Examination / Skin Lesions exanthem Finely punctated erythema has become confluent (scarlatiniform); petechiae can occur and have a linear configuration within the exanthem in body folds (Pastia's line). Desquamation: Exanthem fades within 4 to 5 days and is followed by browny desquamation on the body and extremities and by sheetlike exfoliation on the palms and soles 60
    61. 61. Physical Examination / Mucous Membranes  white and red strawberry tongue Bright red tongue with prominent papillae on the fifth day after onset of group A streptococcal pharyngitis in a child. The white patches at the back of the tongue represent residuals of the initial white strawberry tongue. 61
    62. 62. Management  Symptomatic Therapy Aspirin or acetaminophen for fever and/or pain.  Systemic Antimicrobial Therapy Penicillin is the drug of choice because of its efficacy in prevention of rheumatic fever. Goal is to eradicate throat carriage. For penicillin-allergic patients: Erythromycin Azithromycin Clarithromycin  Follow-Up Reculture of throat recommended for individuals with history of rheumatic fever or if a family member has history of rheumatic fever. 62
    63. 63. 63