Bacterial Skin Infection PDF

Bacterial skin infection By dr Hanaa Haydar Infections of skin soft tissues Infections depends upon the layer of tissues involved (epiderims,dermis,subcutis,muscle) infection may involve one or several skin layers. Skin infection are associated with : swelling,tenderness,warm skin,...

Bacterial skin infection By dr Hanaa Haydar Infections of skin soft tissues Infections depends upon the layer of tissues involved (epiderims,dermis,subcutis,muscle) infection may involve one or several skin layers. Skin infection are associated with : swelling,tenderness,warm skin, blisters,ulceration,fever,headach…rarley systemic disease septicaemia. Common normal skin flora&pathogens - Saphylococci : (S.Aureus S.epidermidis ) - Propinoibateria acne (cutibacteria) - Corynebacteria minutissimum Staphylococcal skin infections 1- Non –bullous impetigo 2-Folliculitis Staph toxin 1-bullous impetigo(ET A-ETD) 2-Staphylococcal scalded skin syndrome (ET A&ETB) 3- toxic shock syndrome :menstrual(TSST1) and non menstrual (enterotoxin B and C)  Impetigo Is common ,superficial, highly contagious bacterial skin infection characterised by pustules and honey coloured crusted erosions. It is caused commonly by staphylococcus aureus and less commonly by streptococcus pyogenes(Group A beta- haemolytic streptococci). It can be classified in to: Non-bullous impetigo Bollous impetigo Non –bullous impetigo Staph.aureus &to lesser degree by group A B haemolytic streptococcus Pathogenesis due to exposes of skin protein to infection after impaired of skin barrier Early erythematous macule that rapidly evolve into short lived vesicle or pustule surrounding by erytema late superficial erosion with a typical honey colored yellow crust a circinate /annuler with peripheral extension and healing of canter may occur -Non –bullous impetigo Distribution face and the extremities usually palms and soles are not affected Mode of transmission; direct contact or indirect through fomites towels Age; infant and children Clinical course untreated lesion tend to resolve within 2 weeks in bullous impetigo heal in 3-6 weeks -Non –bullous impetigo Predisposing factors; 1-overcrowding and poor hygiene 2-Itchy skin diseases (pediuculosis, scabies,eczema) 3- hot humid climate Bullous impetigo It is caused by staph.aureus through exfoliative toxins(ETA-ETD) which a tact to desmosomal protein desmoglein 1 leading to acantholysis within epidermal granular layer Infection arises after defect in skin barrier after trauma or secondary due to underlying dermatoses (atopic ,psoriasis, blistering diseases Early small vesicles enlarge into 1-2cm Late flaccid transparent bulla measuring up to 5cm with collarets' scale but no thick crust &no surrounding erythema Distribution face ,trunk ,diaper ,extremities -Bullous impetigo Diagnosis mainly clinical Bacterial cultures can be used for confirmation of diagnosis and should obtained if methicillin resistant staph.aureus suspected (MRSA) Treatment of impetigo For patient with limited disease we can uses topical antibiotic eg.mupirocin ,fusidic acid Systemic antibiotics are indicated in the presence of fever or lymphadenopathy Azithromycin 2caps 500 mg daily for 3 days #treatment of predisposing causes Decolonizing nares and skin of the patient with recurrent staphylococcal impetigo by using mupirocin in nares and affected skin or rifampicin 600 for 10 days(for eradication) Complication of impetigo # cellulitis # ecthyma #septicemia # pneumonia # scarlet fever # guttate psoriasis #recurrence #post streptococcal glomerulonephritis  Non bullous impetigo bullous impetigo epidemiology More than 70% of all cases of 30% impetigo Age Children most often affected Neonatal period ,but children are also affected Staph aureus&to lesser Staph aureus dgree strep Pathogenesis Exofoliative toxin not Exofoliative toxin ETA-ETD elaborate Organism attach to exposed Toxin bind to desmosmol protein and cause protein Dsg 1 and cause inflammation acantholysis in granular layer Clinical lesions Initial lesion erythematous Initial lesion Small vesicles macule short lived vesicle or pustule Flaccid bullae with with collarette of scale ,usually no surrounding erythema honey colored yellow crust No honey colored yellow crust  Non bullous impetigo bullous impetigo distribution Face (around the nose and face ,trunk ,diaper ,extremitie mouth ) s And extremities Associated finding Mild lymphadenopathy may Usually no systemic but can be present be associated with weakness Clinical course Un treated lesion resolve Un treated patient heal in 3-6 within 2weeks without scar weeks Echthyma Ulcerative pyoderma of the skin mainly group A beta hemolytic streptococci Characterised by punched out ulcer healing slowly with scarring Site buttocks thighs legs Diagnosis 1- clinical. 2-skin swap. 3- rarely biopsy. Treatment Topical antibiotics , such as fusidic acid or mupirocin. Oral antibiotics, recommended in bullous impetigo such as flucloxacillin.  toxic shock syndrome Toxic shock syndrome is multisystem disease caused by release of exotoxins from staph aureus 1-menstrual toxic shock syndrome was linked to the prolonged use of highly absorbent tampons in the menstruating women. Since then manufacturers have made change to tampon production and the number of cases of tampon-induced toxic shock syndrome has dropped significantly. Its related mainly to toxic shock syndrome toxin 1(TSST1) 2-Non-menstrual toxic shock syndrome is the now common form and may occur as complication of skin wounds (surgical , traumatic ,or burn nasal packing). Cans cause by enterotoxin B&C Clinical features Fever Diffused maculopapular red rash Erythema and edema of palm an sole Erythema of the mucous membrane /tongue/eye Generlised non piting edema Low blood pressure Multiple organ involvement are the hall mark of these diseases Shedding of the skin in large sheets, especially form the palms and soles ,is usually seen 1-2 weeks after the onset of illness. diagnosis Bacterial swabs from infected site of origin. Blood cultures. Blood test: full blood count ,renal and liver function ,creatine kinase, coagulation. urine analysis. Treatment Treatment requires hospitalisation and intravenous antibiotics active against the causative organism are given to eradicate the focus of infection. Flucloxacillin ,first generation cephalosporin are the usual choice. Vancomycin can be used in patient sensitive to penicillin. Intravenous immunoglobulin Staphylococcal scalded skin syndrome superficial blistering skin disease which is characterised by detachment of the outermost skin layer (epidermis). SSSS is predominantly seen in children younger than 5 years ,or rarely in adults with weakened immune systems ,kidney disease PATHOGENESIS due to release of (exofolative toxin A nd B ). These toxins bind to specific desmosome present in the epidermis known as desmoglein -1,lead to loss of cell to cell adhesion forming large ,fragile blister that easily rupture ,this lead to wide spread skin peeling (scalded) Clinical SSSS tends to start with nonspecific symptom in children this may include irritability ,lethargy,and fever Within 24-48 hour a painful widespread red rash developed on the skin followed by the formation of large ,fragile, fluid-filled blisters(bullae).these can rupture easily leaving tender patches of skin. These rash typically started on the face and flexural regions,then spread rapidly to other part of the body including arms, legs and trunk. There is typically NO mucous membrane involvement in SSSS,which helps to distinguish it from toxic epidermal necrolysis. Diagnosis Skin swabs Blood culture Skin biopsy Treatment SSSS in some cases considered a dermatological emergency which requires hospitalisation. Fluclocillin. Ceftrixone ,clarithromycin. Supportive treatment: Pain relief Monitoring and maintaining fluid and electrolytes. Skin care Bacterial folliculitis Is an inflamed hair follicle ,lead to tender spot. Folliculitis may be superficial or deep. It can affect anywhere there are hair ,including chest ,back,buttocks,arms,and legs. Commonly caused by staphylococcus aureus. less common by yeast , fungi, viral and parasitic. Clinical features :dome –shaped ,erythematous follicular papules surmounted with pustules. Treatment: topical antibiotic for localized lesion and systemic antibiotic for extensive lesions. 1-Superficial folliculitis Its confined to the ostium. It is not always infective origin can be due to physical, chemical or other causes. 1 Bockhart IMPETIGO Small pustules or crusted papules on erythematous base 2 pseudofollcullitis of the beard Results from penetration of skin with sharp tips of shaved hair.its occurs with curley hair especially negroes 3 Acne necrotica chronic follicular necrotizing process due to staph.auerus 2-deep folliculitis 1 sycosis barbae deep folliculitis Edematous red follicular papule appears as large and tender on the beard and moustache 2 folliculitis keloidalis (acne keloid) chronic folliculitis of the nape of neck leading to hypertrophic scarring papules and plaques 3 furunculosis(boils) is adeep form bacterial folliculitis with involvement of surrounding tissue Furuncles and carbuncle Furuncles (also called boil) is adeep form bacterial folliculitis with involvement of surrounding tissue Clinical feature Boils begin as inflammatory hard tender red nodules that enlarges and become painful and fluctuant after rupturing the pain will decrease Occasionally several closely grouped boils will combine to form carbuncle usually with draining sinus tracts associated with fever headache loss of appetite Lesion often heal with scar site of infection (back of the neck,back ,thigh) Risk factors(diabetes, immunosuppression nasal /perineal carrier) diagnosis mainly clinical sometimes cultures support diagnosis Treatment In mild cases(warm compresses topical antibiotic) In certain cases systemic antibiotics and surgical incision necessary systemic antibiotics(cellulits, multiple ,no response to topical ,recurrent 1 first generation cephalosporin for 7-10 days Streptococcal skin infection Ecthyma Erysipelas and cellulitis pseudomonas aeruginosa Ecthyma gangernosum  Erysipelas Is a superficial form of cellulitis ,it is affect the upper dermis and extended into superficial cutaneous lymphatics. Most commonly by group A beta-haemolytic streptococcus Clinical feature:the affected skin has a very sharp raised border. Tender ,intensely erythematous(Bright erythema) Diagnosis: clinical ,blood test(high white cell count, raised CPR). Blood culture. Treatment :antibiotics (amoxicillin ,clavulanic acid ,cephalexin).  CELLULITS Is a common bacterial skin infection of the lower dermis and subcutaneous tissue. It is result of dull red, painful, swollen skin ,and systemic symptoms. Polymicrobial( streptococcus and others) It is usually unilateral ,the first sing of the illness is often feeling un well, with fever ,chills and rigors,(bacteraemia). Other sings : peau orange ,warmth, blistering, abscess formation. Diagnosis Blood test. Skin test. Bacterial culture. Management of cellulitis Oral antibiotics e.g.: cephalexin. Sever cases of cellulitis may require hospitalization and intravenous antibiotics.  erysipelas cellulitis etiology Streptococcus pyogenes Polymicrobial streptococcus and others pathogenesis Infection involving upper Deeper dermis and dermis and superficial subcutaneous lymphatic's clinical Bright erythema Dull red erythema site face> leg Leg>face edema less marked border Well defined Ill defined complications lymphedema Deeper necrotizing infection should be excluded when we treating cellulitis sign Positive milian sign Negative milian sign Necrotizing fasciitis Necrotizing fasciitis is a very serious bacterial infection(group A streptococcus) of the soft tissue and fascia.the bacteria multiply and release toxin and enzymes that result in thrombosis in blood vessels result in destruction of soft tissue and fascia THE present of necrosis can be detected by surgical exploration and histopathology. It is a sever disease of sudden onset that spreads rapidly. The most common affected area are the lower leg and perineum. Clinical features Symptoms may include fever ,swelling and complain of excessive pain initial skin changes are similar to cellulitis or abscess thus making the diagnosis early stage difficult. Formation of bullae ,bleeding to the skin reduced or absent of sensation skin(necrosis of underlying nerve) Fournier gangrene necrotizing changes affecting of groin ECthyma Gngernosum Cutaneous manifestation of sever invasive infection by pseudomonas aeruginosa that occurs typically in immunosuppressed patient in anogenital and extermities The characteristic lesions are hemorrhagic bullae that evolve into necrotic (black) ulcers Initial lesions appear as painless round red patches Investigations complete blood count , culture and skin biopsy (vasculitis) Treatment Intravenous fluid and iv antbiotics Consult surgical department for urgent debridement Ectyma Ulcerative pyoderma of the skin mainly group A beta hemolytic streptococci Characterized by punched out ulcer healing slowly with scarring Site buttocks thighs legs  Ecthyma gangernosum ecthyma etiology pseudomonas aeruginosa group A beta hemolytic streptococci Risk factor Marked neutropenia Non specific Immune status Immune compromised Any site anogenital and extremities buttocks thighs legs skin biopsy vasculitis Vasculitis not present clinical hemorrhagic bullae that punched out ulcer evolve into necrotic ulcers Coryneform bacterial infection Corynebacteria small gram positive cocci generally considered to be commensal organism but under certain circumstances they can cause superficial cutaneous infection( stratum corneaum and hair follicle ) risk factors warm and moist (hyperhidrosis) environment under occlusion 1 Erythrasma (corynebacterium minutissimum ,dermatophilus congolenisis) 2 pitted keratolysis (kytococuss sedentarius/micrococcus sedentarius) 3trichomycosis axillaris(corynebacterium tenius) Erythrasma Erythrasma is common skin condition affecting the skin folds under the arms,in the groin and between toes. It reported to be more prevalent in the fallowing: Worm climate ,excessive sweating ,diabetes, obesity, poor hygiene ,immunocompromised states. It is caused by Corynebacterium minutissimum. May coexist with fungal infection. Clinical feature :well-defined pink or brown patches with fine scaling, mild itching may be present,mainly on toeweb >groin>axillae  Complication :is usually self limiting ,serious complication are rare.corynebacteria have been reported to causes abscess ,cellulitis. Diagnosis is by :wood lamp (coral –red colour),swab or skin scrapings. Treatment is by antiseptic and antibiotics like fusidic acid. extensive infection can be treated by systemic antibiotics(erythromycin). Erythrasma Candidasis corynebacterium minutissimum Candida albicans well-defined pink or brown patches with Red ,moist patches fine scaling No satellite With satellite formation Asymptomatic or mild itching itchy coral –red color on wood lamp Not flouresnce Negative KOH test Positive KOH test Pitted keratolysis Also known as keratolysis plantare sulcatum or ringed keratolysis ,is superficial bacterial skin infection characterized by crater like pits and malodour. Its typicaly affect bearing areas on the soles also palms rarely affected Factors increase the risk(hyperhidrosis,keratoderma,diabetes,poor hygiene Its caused by (kytococuss sedentarius/micrococuss sedentarius) Occupations where feet are constantly wet Athletes Sailors and fishermen Military workers treatment Treat hyperhidrosis aluminum chloride or botulinum toxin(recalcitrant) Topical fusidic acid erythromycin,clindamycin Trichomycosis axillaris Crynebacterum tenius,C flavscens C propingum Superfical bacterial infection of underarm hair the disease characterized by yellow ,black or red granular nodule or concretions that stick to hair shaft. At lesser extent affect pubic hair (trichomycosis pubis),scrotal hair ,interglutel air TREATMENT Shave axillary hair Topical benzoyl peroxide OR CLINDAMYCIN