Bacterial skin infection

Jaber ManasiaJaber Manasia5th year medical student

Mutah University-Jordan

Jaber.manasia@gmail.com

Bacterial Skin infectionsIntact skin is one of the body’s defences

against infectionNormal flora (resident organisms) exist on

the skinNormal flora become pathogenic when

transported to alternate locationsBreak in the normal skin barrierUncomplicated skin infections usually

involve 1 or 2 pathogensPredominant organisms for skin infection

are Staphylococcus and Streptococcus spp

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Normal Skin Flora Gram Positive Staphylococcus Micrococcus Coryneforms

- Corynebacterium

- Propionibacteria

- Dermobacter

- Brevibacterium

Gram Negative Acinetobacter

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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.

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Folliculitis Pseudofolliculitis Boils Carbuncles Impetigo Infected eczema Ecthyma

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

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Folliculitis

Hot tubs Folliculitis

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DDx:Pseudofolliculitis

oTreatment:Mild folliculitis can be treated with a topical antibacterial agent, but if it is extensive a systemic antibiotic may be required.

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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.

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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)

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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

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Furuncle Furuncle: S.

aureus Soft-tissue swelling of the forehead with central abscess formation, nearing rupture.

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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

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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.

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Treatment:Moist heat, compressesDicloxacillin, Clindamycin, Erythromycin Bed rest Immobilize involved areaHand washingNeed systemic flucloxacillinIncision of abscess

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Impetigo

Worldwide distribution More frequent among economically

disadvantaged children in tropical or subtropical regions

Also prevalent in northern climates in summer months

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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

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Impetigo

• Contagious Superficial infection of the epidermis • Discrete purulent lesions• Occurs on exposed areas, well localised,

frequently multiple, bullous or non bullous in appearance initiallycharacteristic thick yellow brown crusts

• Deeply ulcerated form (extend into the dermis ) = ecthyma

• Systemic symptoms usually absent

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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).

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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.

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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

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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

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Impetigo: Treatment topical & systemic antibiotics.

flucloxacillin or 1st gen cephalosporins are preferred (eg cephalexin, cephradine)

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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.

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EtiologyStaph 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).

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• 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)

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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.

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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)

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Ecthyma A large,

circumscribed chronic ulcer with surrounding erythema in the pretibial region

Heals with scar

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DDx:ImpetigoCellulitisleshmaniasis

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Infected eczema :

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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.

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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.

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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 )

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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

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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.

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Erysipelas: Treatment

Penicillin or erythromycin

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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

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Cellulitis

Manifests clinically as erythema, oedema, heat+/- lymphangitis, peau d’orange, vesicles, bullae, petechiae/ecchymoses

Systemic: fever, tachycardia, confusion, hypotension, leucocytosis

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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

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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

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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.

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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 days52

Necrotizing Fasciitis a rare subcutaneous infection that tracks along

fascial planes and extends well beyond superficial signs of infection

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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

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Necrotizing Fasciitis

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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

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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

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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.

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History• Incubation Period

Rash appears 1 to 3 days after onset of infection.

• ExposureHousehold member(s) may be a streptococcal carrier

• Site of Infection Pharyngitis; tonsillitis. Infected surgical or other wound. Impetiginous skin lesion.

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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

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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.

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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: ErythromycinAzithromycinClarithromycin

Follow-UpReculture of throat recommended for individuals with history of rheumatic fever or if a family member has history of rheumatic fever.

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