1. Bacterial skin infectionsDR. Ali El-ethawiSpecialist Dermatologist M.B.CH.B , F.I.C.M.S, C.A.B.D5th class lecture

2. The normal skin flora Normal skin is heavily colonized by bacterial flora (harmlesscommensals) 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 bacterialinterference.Colonization is more dense in ;intertriginous and occluded sites. 3. Predisposition to skin infection Chronic S. aureus carrier state (nares, axillae,perineum,vagina) Warm weather/climate, high humidity Skin disease, especially atopic dermatitis, familialpemphigus Social situation: poor hygiene, crowded living conditions,neglected minor trauma Chronic disease:, diabetes mellitus, HIV/AIDS, solidorgan transplant recipient & obesity Immunodeficiency, bactericidal defects (e.g., chronicgranulomatous disease)& cancer chemotherapy 4. Bacteria cause disease by direct invasion of tissues, by secreting toxins, by causing immunologic consequencesthat result in disease.Bacteria, like viruses, may also sometimes result in exanthems (rashes). 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 sppErythrasmaPitted KeratolysisTrichomycosis 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 gangreneCalymmatobacterium granulomatis, cause of granuloma inguinale 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 maybecome pustular before rupturing to leave extending area of exudation & yellow crustingSymptoms of itching and soreness are mild; systemic symptoms are infrequent.. 8. impetigoImpetigo may occur as 1ry inf. after a minor skin injury such as an insect bite or as 2ry inf. ofpre-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 feverlymphadenopathy, in extensive infections involving scalp, ears, eyelids if a nephritogenic strain is suspected. 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. Furuncle and CarbunclesFuruncle (abscess or boil) ;is a walled-off collection of pusthat 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 abroad, red, swollen, slowly evolving, deep, painful mass that points and drainsthrough 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. 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 cutaneouslymphatics; 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 uninvolvedskin is indistinct. Erysipelas ;if untreated ,the condition can even be fatal ,but it respondsrapidly to systemic pencillin ,some times given intravenously Treatment of cellulites; is elevation , rest -sometime in hospital andsystemic antibiotics, sometimes given intravenously . 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-inducedtoxic epidermal necrolysis (TEN). 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. Management:Prophylaxis ; Prevent spread of toxigenic S.aureus in neonatal careunits.General Care Hospitalization is recommended for neonates and youngchildren.Topical Therapy Baths or compresses for debridement of necroticsuperficial epidermis.Topical antimicrobial agents; like for impetigo lesions: mupirocin,bacitracin, or silver sulfadiazine ointment.Systemic Antimicrobial Therapy.Adjunctive Therapy Replace significant water and electrolyte lossintravenously in severe cases. 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. ERYTHRASMAFrom the Greek: red spotAge 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. PITTED KERATOLYSIS Etiology: Kytococcus sedentarius Age of onset: young adults. Sex: males > females. Distribution: plantar feet, web spaces of feet Predisposition: hyperhidrosis and Occlusive footwearClinical findings: eroded pits of variable depth occur as defects in thicklykeratinized skin Usually asymptomatic , but with Foot odor. 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. Scarlet fever (scarlatina)Age of Onset :Children.Incidence : Much less than in the past.Etiology :Usually group A -hemolytic S. pyogenes . Uncommonly, ET-producing S. aureus. Incubation Period : Rash appears 13 days after onset ofinfection. PRODROMAL AND ERUPTIVE PHASE. The sudden onset of fever and pharyngitis is followed shortly bynausea, vomiting, headache, and abdominal pain. enlarged cervical lymph nodes . 20. Scarlet fever. Evolution of signs and symptoms.Temp> 38C 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 45 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. MANAGEMENT Symptomatic Therapy Aspirin or acetaminophen for fever and/orpain. Systemic Antimicrobial Therapy Penicillin is the drug of choicebecause of its efficacy in prevention of rheumatic fever. Goal is toeradicate GAS throat carriage. Others: cephalosporins, erythromycin , or the newer macrolides. Follow-Up Re-culture of throat recommended for individuals withhistory of rheumatic fever or if a family member has history ofrheumatic fever. 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 vesiclesManagement: Cutaneous anthrax can be self-limited, but antibiotic therapy isrecommended. 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.