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Similar to skin infections bacterial.pptx
skin infections bacterial.pptx
- 1. Bacterial Skin Infections DrSaira Niazi
- 2. Bacterial Infection ofSkin Skin is largest organ of body. Maintains homeostasis, protects underlying tissues and organs, protects body from mechanical injury, damaging substances, and ultraviolet rays of sun.
- 3. • Two microorganismsare responsible for most cutaneous infections in immunocompetent patients: • Beta-hemolytic streptococcus (groups A, B, C, G, and F) • Staphylococcus aureus, including community- acquired methicillin-resistant S. aureus (CA- MRSA).
- 4. S. aureus producesskin infection I. Direct infection of skin and adjacent tissues a. Impetigo b. Ecthyma c. Folliculitis d. Furunculosis e. Carbuncle f. Sycosis barbae II. Cutaneous disease due to effect of bacterial toxin a. Staphylococcal scalded skin syndrome b. Toxic shock syndrome
- 5. ß-hemolytic streptococcus produces skininfection I. Direct infection of skin or subcutaneous a. Impetigo (non bullous) b. Ecthyma c. Erysipelas d. Cellulitis e. Necrotizing fascitis II. Secondary infection Eczema infection
- 8. Impetigo Contagiosa • commonsuperficial contageous pyogenic skin infection. • two clinical forms – Bullous impetigo. – Non-bullous impetigo.
- 9. pathophysiology • Bullous impetigois caused by staphylococcus aureus • Non-bullous impetigo in majority caused by S. aureus but can be caused by group A beta hemolytic streptococci or both
- 10. Clinical features • non-bullousimpetigo, • the initial lesion is a thin-walled vesicle on an erythematous base which ruptures rapidly • The exudate dries to form yellowish brown crusts . Lesions enlarge and coalesce. • The crusts eventually dry and separate to leave erythema, which fades without scarring.
- 12. • In severecases regional adenitis with fever and other constitutional symptoms. Sites The face, around nose and mouth, and limbs lesions may occur anywhere on the body, especially in children with atopic eczema or scabies. tendency to spontaneous cure in 2,3 weeks
- 13. • In bullousimpetigo, the bullae are less rapidly ruptured and become much larger; persist for 2 or 3 days • some may become erosive • Regional adenitis is rare
- 19. complications of impetigo •Post-streptococcal glomerulonephritis • Lymphadenitis • Urticaria. • Erythema multiforme
- 20. Differential diagnosis • Immunobullousdiseases, • localised staphylococcal scalded skin syndrome (SSSS), • Contact dermatitis (irritant or allergic) • Herpes simplex infections.
- 21. Investigations Microbiological skin swabstaken from affected skin.
- 22. Management • Impetigo isusually self-limiting and resolves within days to weeks with the appropriate use of topical cleansers and antibiotics. • Spread to close contacts is common and relapse is more frequently seen in individuals with underlying skin diseases and in staphylococcal carriers
- 23. • General measures: Washaffected skin daily with disinfectants, e.g. chlorhexidine, povidone iodine or sodium hypochlorite. • Handwashing for patient and close contacts. • Localised disease: Topical antibiotics for 5–7 days, e.g. mupirocin, fusidic acid, or 2% clindamycin cream
- 24. • Widespread orbullous disease or local lymphadenopathy: • Systemic antibiotics for 1 week. • First-line antibiotics flucloxacillin (dicloxacillin), cephalexin, co-amoxiclav, cloxacillin and clindamycin. • Second-line antibiotics macrolides such as erythromycin and clarithromycin
- 25. Ecthyma • A pyogenicinfection of the skin characterised by ulceration with an adherent crust. • Epidemiology Extremes of age are most commonly affected. • Pathophysiology Causative organisms include GAS, Pseudomonas aeruginosa and S. aureus.
- 26. • The infectionis much deeper than in impetigo, with loss of the epidermis and dermis, ulceration and scarring. • more common in immunocompromised patients (HIV, diabetes, high humidity environments and with poor hygiene. • Pharyngeal carriers of S. pyogenes are more susceptible to recurrent disease
- 27. Predisposing factors • Poorhygiene • Malnutrition • Scabies • Minor injuries
- 28. Clinical features • Smallbullae or pustules on an erythematous base are surmounted by a hard crust of dried exudate • predominantly on the buttocks, thighs and legs. • The crust can only be removed with difficulty to reveal a purulent, irregular ulcer.
- 29. A large, circumscribedulcer with a necrotic base and surrounding erythema in the pretibial region
- 30. Multiple thickly crustedulcers on the leg
- 31. • Investigations Microbiological swabsfrom affected skin.
- 32. Management • Improved hygieneand nutrition, • treatment of scabies and any other underlying disease • Remove crust after soaking with a disinfectant and softening with an oily cream. • Topical antibiotics such as fusidic acid and mupirocin • Oral antibiotics (flucloxacillin or erythromycin) for 1–2 weeks (multiple lesions or immunocompromised patients)
- 33.
- 34. Cellulitis • Acute, subacuteor chronic inflammation of loose connective tissue
- 35. Erysipelas • bacterial infectionof the dermis and upper subcut tissue • well-defined, raised edge • reflecting more superficial (dermal) involvement
- 36. Bacteriology • Streptococci • usuallyinvolving group A • also G, C & B (esp setting of venous or lymphatic compromise) • Staphylococcus aureus • occasionally alone or with a Streptococcus • Haemophilus influenzae type b • important cause of facial cellulitis in young Children • rarely cellulitis in adults
- 37. Orbital cellulitis • usuallysecondary to sinusitis • major sinus pathogens • Streptococcus pneumoniae • Staphylococcus aureus • Haemophilus influenzae • penicillin-sensitive anaerobes
- 38. Other bacteria • Pseudomonasaeruginosa • Gangrenous cellulitis and ecthyma gangrenosum • Aeromonas hydrophila • Vibrio alginolyticus • Pasteurella multocida • Streptococcus pneumoniae • Acinetobacter calcoaceticus • Staphylococcus epidermidis • Bacteroides fragilis
- 39. Clinical features Cellulitis anderysipelas
- 40. Constant features • Erythema •Heat • Swelling • Pain or tenderness
- 41. Other features • Blistering –Esp. in erysipelas • bullae • superficial haemorrhage • dermal necrosis • Lymphangitis and lymphadenopathy
- 45.
- 46. Site • Leg •commonest site •Face • nextmost frequent
- 47. Portal of entryin Cellulitis Leg • Wound • Ulcer • T.pedis
- 48.
- 49. Cellulitis originating in furuncle:S. aureus
- 50.
- 51.
- 52.
- 53. COMPLICATIONS • fasciitis • myositis •subcutaneous abscesses • septicaemia • nephritis
- 54. Recurrent streptococcal cellulitis(or erysipelas) • Predisposing factors –lymphatic damage –Venous insufficiency –local skin damage » T.pedis • Recurrent episodes of cellulitis Is associated with post-cellulitic oedema • oedema is a risk factor for recurrent disease
- 55. Chronic lymphedema haspredisposed to cellulitis
- 56. Periorbital cellulitis • followstrauma to the eyelids or local skin sepsis . • usually streptococcal • occasionally staphylococcal. • Complications • cavernous sinus thrombosis,orbital, subperiosteal or cerebral abscess formation, or meningitis
- 57.
- 58. Investigations • Swabs canbe taken from vesicle fluid or eroded or ulcerated surfaces • blood cultures. • In facial infections the pathogen should be sought in nose, throat, conjunctiva and sinuses.
- 60. Treatment • In allcases, initial treatment should cover streptococci • for facial infections in young children initial treatment should cover, H. influenzae (ceftriaxone, ceftazidime, cefotaxime, ampicillin- sulbactam, fluoroquinolones, azithromycin)
- 61. Appropriate antibiotic(s) • intramuscularor intravenous route •more severe cases associated with septicemia, arthritis or suspected fasciitis • oral treatment •milder, uncomplicated infections
- 62. Treatment • patients withoutsystemic toxicity or co- morbidity • Flucloxacillin 500 mg four times daily • Clarithromycin 500 mg twice daily • Admitted patients • Flucloxacillin with benzylpenicillin intravenously • benzylpenicillin 600–1200 mg 6 hourly intravenously • Clarithromycin 500 mg twice I/V • clindamycin 600 mg 8 hourly intravenously • Roxithromycin
- 63. • Anticoagulant therapy •if there is associated thrombophlebitis
- 64. Recurrent cases • Predisposingfactors – lymphatic damage – Venous insufficiency – local skin damage » T.Pedis » Ulcer • long-term Antibiotic (some require lifelong) • penicillin, 500 mg to 2 g daily • Erythromycin • Treatment of any local skin damage • eg T.Pedis • Reduction of edema
- 65. Folliculitis • Subacute orchronic inflammation of hair follicles in which the inflammatory changes are confined to the ostium or extend only slightly below it • heals without scar formation.
- 66. Folliculitis • Its asuperficial inflammatory disease of hair follicle • Mostly by staphylococci • Caused by Chemical irritants Adhesive tapes, dressings Occupational Topical steroids
- 68. • Dome shapedpapules and pustules • Mostly occur on beard area , face • Can occur on thighs, buttocks and extremities
- 69. Superficial folliculitis Multiple pustulesconfined to the beard area
- 71. Treatment • Mild :Topical antiseptics • Severe : Topical antibiotics Oral antibiotics
- 72.
- 73. Furuncle • A furuncleis an acute, usually necrotic, infection of a hair follicle with S. aureus
- 74. Predisposing factors • Malnutrition •Mechanical damage to the skin •friction of collars and belts
- 75. Clinical features • small,follicular, inflammatory nodule • soon becoming pustular • then necrotic • healing after discharge of a necrotic core • leave a violaceous macule • Ultimately a permanent scar.
- 76. BACTERIAL INFECTIONS OFSKIN BOILS (FURUNCLES)
- 77.
- 79. Treatment • flucloxacillin oranother penicillinase -resistant antibiotic • Role of Rifampicin
- 80. Carbuncle Latin word fora small, fiery coal
- 81. Carbuncle • Deep infectionof a group of contiguous follicles with S. aureus • Accompanied by intense inflammatory changes in the surrounding and underlying connective tissues, including the subcutaneous fat
- 82. Predisposing factors • Middleor old age men • Underlying disease »Diabetes »Malnutrition »Cardiac failure »Drug addiction »Severe generalized dermatoses - Exfoliative dermatitis - Pemphigus • Prolonged steroid therapy
- 83. Clinical features •painful, hard,red lump •pus is discharged from the multiple follicular orifices
- 84. Most lesions areon the back of the neck, the shoulders or the hips and thighs, and although usually solitary, may be multiple SITES
- 86. Constitutional symptoms •Fevermay behigh •Malaise •Prostration
- 87. Management • Antibiotic • Swabmust be taken • Incision drainage • Diabetes and other possible underlying conditions should be sought
Editor's Notes
- #36 However, cellulitis may extend superfi cially and erysipelas deeply, so that in many cases the two processes coexist and it is impossible to make a meaningful distinction. Current usage tends to regard erysipelas as a form of cellulitis rather than a distinct entity, so that the defi nition of cellulitis would include infl ammation of dermal as well as subcutaneous tissue. The closely similar bacteriology of the two conditions [1,2], and the demonstration of streptococcal antigens in both dermis and subcutis in both conditions [1], support this view. However, the two terms are still sometimes used in the traditional sense, especially when their typical distinctive features are being contrasted.
- #61 Haemophilus influenzae produces beta-lactamases, and it is also able to modify its penicillin binding proteins, so it has gained resistance to the penicillin family of antibiotics. In severe cases cefotaxime and ceftriaxone are the elected antibiotics, delivered directly into the bloodstream, and for the less severe cases an association of ampicillin and sulbactam, cephalosporins of the second and third generation, or fluoroquinolones. Macrolide antibiotics (e.g. clarithromycin) may be used in patients with a history of allergy to beta-lactam antibiotics. [edit]Sequencing
- #85 Carbuncle