dermatology.Bact .inf 5th.(dr.ali)


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dermatology.Bact .inf 5th.(dr.ali)

  1. 1. Bacterial skin infectionsDR. Ali El-ethawi Specialist Dermatologist M.B.CH.B , F.I.C.M.S, C.A.B.D 5th class lecture
  2. 2. The normal skin flora• Normal skin is heavily colonized by bacterial flora (harmless commensals) such as;• coagulase negative staphylococci (e.g; S. epidermidis) .• Micrococcus species.• Aerobic coryneforms.• Anaerobic propionibacterium species, e.g. P. acnes, P. granulosum, commonly inhabit the sebaceous hair follicles.• Yeasts, pityrosporum• Protects the skin from bacterial infections through bacterial interference.• Colonization is more dense in ;intertriginous and occluded sites.
  3. 3. Predisposition to skin infection• Chronic S. aureus carrier state (nares, axillae,perineum, vagina)• Warm weather/climate, high humidity• Skin disease, especially atopic dermatitis, familial pemphigus• Social situation: poor hygiene, crowded living conditions, neglected minor trauma• Chronic disease:, diabetes mellitus, HIV/AIDS, solid organ transplant recipient & obesity• Immunodeficiency, bactericidal defects (e.g., chronic granulomatous disease)& cancer chemotherapy
  4. 4. Bacteria cause disease by• direct invasion of tissues,• by secreting toxins,• by causing immunologic consequences that result in disease.Bacteria, like viruses, may also sometimes result in exanthems (rashes).
  5. 5. The most common bacteria to cause skin infections are• Staphylococcus aureus ; – Impetigo (school sores) – Folliculitis – Furunculosis (boils) – Staphylococcal scalded skin syndrome – Toxic shock syndrome – Botryomycosis (pyoderma vegetans) Streptococcus pyogenes – Cellulitis – Erysipelas – Impetigo – Necrotising fasciitis – Scarlet fever• Overgrowth of cornebacterium spp Erythrasma Pitted Keratolysis Trichomycosis
  6. 6. Less commonly, other bacteria may cause skin infections;• Pseudomonas aeruginosa; wound infections, athletes foot, gram negative folliculitis, chronic paronychia, spa pool follic• Erysipelothrix insidosa, cause of erysipeloid (usually an animal infection)• treponema species cause syphilis (STD) , yaws and pinta• Hemophilus species ;, cause of chancroid (STD) and cellulitis in young children• Neisseria species, cause of gonorrhoea (STD) and meningococcal disease .• Calymmatobacterium granulomatis ; granuloma inguinale (STD)• Klebsiella rhinosclermatis; cause of rhinoscleroma• Bacillus anthracis ; anthrax• Clostridium perfringens and other species cause gas gangrene Calymmatobacterium granulomatis, cause of granuloma inguinale
  7. 7. IMPETIGO AND ECTHYMAEtiology: S. aureus; also, group-A streptococci (GAS)Infections of the epidermis (impetigo),Infections which may extend into the dermis (ecthyma) Clinical findings:▪ Impetigo: crusted erosions▪ Ecthyma: crusted deep erosions or ulcers. Impetigo is a common, contagious, superficial skin infection that is produced by streptococci, staphylococci, or a combination of both bacteriaThere are two different clinical presentations:bullous impetigo (primarily a staphylococcal disease)nonbullous impetigo. a streptococcal disease,but staphylococci are isolated from the majority of lesions in both bullous and nonbullous impetigoC/F : Both begin as vesicles with a very thin, fragile roof consisting only of stratum corneum. And may become pustular before rupturing to leave extending area of exudation & yellow crustingSymptoms of itching and soreness are mild; systemic symptoms are infrequent..
  8. 8. impetigoImpetigo may occur as 1ry inf. after a minor skin injury such as an insect bite or as 2ry inf. of pre-existing dermatoses, e.g. pediculosis, scabies & eczemas. course ;The disease is self-limiting, but when untreated it may last for weeks or months. complication; Post -streptococcal glomerulonephritis may follow impetigo.MANAGEMENTTreatment of predisposing causes, e.g. pediculosis & scabies.Remove the crusts: by olive oil or hydrogen peroxide.Topical antibiotic ointment;e.g. bacitracin, mupiracin or Fusidic acidSystemic antibiotics; e.g. penicillin, erythromycin & cloxacillin.are indicated especially in the presence of• fever• lymphadenopathy,• in extensive infections involving scalp, ears, eyelids• if a nephritogenic strain is suspected.
  9. 9. Ecthyma• is characterized by ulcerations that are covered by adherent crusts.• Poor hygiene is a predisposing factor.• Ecthyma has many features similar to those of impetigo But it heal with scarring• Distribution : more common on distal extremities.
  10. 10. Furuncle and CarbunclesFuruncle (abscess or boil) ;is a walled-off collection of pus that is a painful, firm, or fluctuant mass.Carbuncles ;are aggregates of infected hair follicles.The infection originates deep in the dermis and the subcutaneous tissue, forming a broad, red, swollen, slowly evolving, deep, painful mass that points and drains through multiple openings.Malaise, chills, and fever precede or occur during the active phase.Deep extension into the subcutaneous tissue may be followed by sloughing and extensive scarring.Sites ; Areas with thick dermis (i.e., the back of the neck, the back of the trunk, and the lateral aspects of the thighs) are the preferred sites.Treatment ;of an abscess, furuncle, or carbuncle is incision and drainage plus systemic antimicrobial therapy
  11. 11. ERYSIPELAS AND CELLULITIS• Acute, spreading infections of dermal and subcutaneous tissues• Characterized by a red, hot, tender area of skin• In most instances there is fever and leukocytosis .• Both may be accompanied by lymphangitis and lymphadenitis.• Often originating at the site of bacterial entry• Erysipelas involves the superficial layers of the skin and cutaneous lymphatics; cellulitis extends into the subcutaneous tissues.• Caused most frequently by group A streptococcus (erysipelas) or S. aureus .• Cellulitis is differentiated clinically from erysipelas by two physical findings: cellulitis lesions are primarily not raised, and demarcation from uninvolved skin is indistinct.• Erysipelas ;if untreated ,the condition can even be fatal ,but it responds rapidly to systemic pencillin ,some times given intravenously• Treatment of cellulites; is elevation , rest -sometime in hospital – and systemic antibiotics, sometimes given intravenously .
  12. 12. Staphylococcal scalded skin syndrome (SSSS)Etiology: S. aureus.Age: occurs mainly in newborns and infants < 2years. Also, older immunocompromised personsPathogenesis: toxin-mediated epidermolytic disease.Clinical syndromes: Erythema and widespread detachment of the superficial layers of the epidermis, resembling scaldingD. Dx; TSS, Kawasaki syndrome, drug-induced toxic epidermal necrolysis (TEN).
  13. 13. painful, tender, diffuse erythema was followed by generalized epidermalsloughing and erosions.S. aureus had colonized the nares with perioral impetigo, the site of exotoxinproduction.
  14. 14. Management:Prophylaxis ; Prevent spread of toxigenic S.aureus in neonatal care units.General Care Hospitalization is recommended for neonates and young children.Topical Therapy Baths or compresses for debridement of necrotic superficial epidermis.Topical antimicrobial agents; like for impetigo lesions: mupirocin, bacitracin, or silver sulfadiazine ointment.Systemic Antimicrobial Therapy.Adjunctive Therapy Replace significant water and electrolyte loss intravenously in severe cases.
  15. 15. TOXIC SHOCK SYNDROME (TSS)Etiology: Toxin-producing S. aureus and GAS Clinical setting▪ Staphylococcal TSS • Menstrual (MTSS) (rare after 1984) • Non menstrual (NMTSS)▪ Streptococcal TSS Clinical manifestations▪ Rapid onset of fever and hypotension▪ Skin findings • Early: generalized skin and mucosal erythema • Late: desquamation in early convalescence▪ Organ hypoperfusion and multisystem failure Management: systemic antibiotic to treat infection and stop toxin production.Irrigation of the infected site are needed . Supportive RX.
  16. 16. ERYTHRASMAFrom the Greek: “red spot”Age of Onset ; AdultsEtiology: Corynebacterium minutissimumDistribution: intertriginous areas of webspaces of feet, groins, axillae, submammary areasClinical findings: well-demarcated red or tan patches, ± scaleD.DX; from dermatophytosis and noninfectious intertrigoDiagnosis: Clinical findings, absence of fungi on direct microscopy, positive Wood lamp examination( shows coral red fluorescence )Prevention/Prophylaxis,Topical antiseptic alcohol gels: isopropyl, ethanol.Topical Therapy Preferable.Topical erythromycin or clindamycin solution twice daily for 7 days.Sodium fusidate ointment, mupirocin ointment or cream.Topical antifungal agents; clotrimazole,.Systemic Antibiotic Therapy ; A macrolide or a tetracycline for 7 days.
  17. 17. PITTED KERATOLYSIS• Etiology: Kytococcus sedentarius• Age of onset: young adults.• Sex: males > females. Distribution: plantar feet, web spaces of feet Predisposition: hyperhidrosis and Occlusive footwear• Clinical findings: eroded pits of variable depth occur as defects in thickly keratinized skin• Usually asymptomatic , but with Foot odor.
  18. 18. TRICHOMYCOSISEtiology: Corynebacterium ;gram-positive diphtheroid.age &sex ; adults, males > females.Distribution: axillae (trichomycosis axillaris), pubic hair (trichomycosis pubis)Predisposition: hyperhidrosis Clinical findings:granular concretions (yellow, black, or red) on hair shaft. Hair appears thickened, beaded, firmly adherent. Insoluble adhesive may erode cuticular and cortical keratin. Management: shave off affected hair. Benzoyl peroxide wash. Alcohol gel. Topical erythromycin or clindamycin.
  19. 19. Scarlet fever (scarlatina)Age of Onset :Children.Incidence : Much less than in the past.Etiology :Usually group A β-hemolytic S. pyogenes . Uncommonly, ET-producing S. aureus.• Incubation Period : Rash appears 1–3 days after onset of infection.• PRODROMAL AND ERUPTIVE PHASE . The sudden onset of fever and pharyngitis is followed shortly by nausea, vomiting, headache, and abdominal pain.• enlarged cervical lymph nodes .
  20. 20. Scarlet fever. Evolution of signs and symptoms.Temp> 38°C
  21. 21. Exanthem (skin rash)Face: flushed with perioral pallor.• Initial punctate lesions become confluently erythematous, i.e., scarlatiniform (Numerous papules giving a sandpaper-like texture to the skin.)• Palms/soles usually spared.• Linear petechiae (Pastia sign) occur in body folds.• Tongue• White tongue: Initially is white with scattered red, swollen papillae (white strawberry tongue).• Red strawberry tongue: By the fourth or fifth day, the hyperkeratotic membrane is sloughed, and the lingular mucosa appears bright red.Desquamation: Exanthem fades within 4–5 days and is followed by desquamationon the body and extremities and by sheet-like exfoliation on the palms/fingers and soles/toes.In subclinical or mild infections, exanthem and pharyngitis may pass unnoticed.In this case patient may seek medical advice only when exfoliation on the hand and soles is noted.
  22. 22. • 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 GAS throat carriage.• Others: cephalosporins, erythromycin , or the newer macrolides.• Follow-Up Re-culture of throat recommended for individuals with history of rheumatic fever or if a family member has history of rheumatic fever.
  23. 23. CUTANEOUS ANTHRAX Synonym : Malignant pustuleEtiology: Bacillus anthracis Zoonosis Pathogenesis: toxin-mediated Portal of entry:▪ Skin: cutaneous abrasions▪ Inhalations (woolsorters’ disease)▪ Ingestion Cutaneous anthrax accounts for 95% of anthrax cases in United States Clinical findings of cutaneous anthrax:▪ Black eschar surrounded by edema and purple vesicles• Management: Cutaneous anthrax can be self-limited, but antibiotic therapy is recommended.• Drug of choice :• Ciprofloxacin, 400 mg IV q12h, or doxycycline,100 mg IV q12h, is optimal. Alternatives : None.• Surgery for excision of eschar is contraindicated.