SSS Week 2

Risk factors for bacterial infections

• skin barrier disruption (trauma, insect bites)

• moist, macerated environments (common in warm, occluded areas such as the axilla and groin)

• colonisation with skin flora pathogens

• impaired host defenses

What causes impaired host defenses

Metabolic - diabetes mellitus

Vascular insufficiency - Peripheral arterial disease, chronic venous insufficiency (varicose veins)

Immunodeficiency - HIV/AIDS, malignancy, immunosuppressive therapy eg. glucocorticoids

Impetigo

staph

~ most common in young children (but occurs at any age)

~ less commonly caused by strep pyogenes

~ spreads in warm moist environments with close physical contact and poor hygiene

 

Two presentations

1      Bullous (SUBCORNEAL BULLAE)

~ thin-roofed bullae with clear yellow fluid which rupture quickly leaving exudative and yellow brown crust erosions

~ more likely to have systemic symptoms of malaise, fever, and lymphadenopathy

[staph attacks intracellular adhesion molecules in stratum granulosum, causing bullae formation – explored later]

 

2      crusted or non-bullous (most common)

~ begins with a single erythematous macule which evolves into a pustule or vesicle

~ pustule or vesicle ruptures releasing serous contents which dries leaving honey-coloured crust

~ has satellite lesions due to autoinoculation

what areas of skin are prone to impetigo? broken by insect bites. superficial injury, excoriated eczema

 

complications?

Can trigger post-strep glomerulonephritis and rheumatic heart disease

 

Can grumble on for several weeks and lead to deeper ulcerated and scarring infection called Ecthyma

general measures - TREATMENT

• cover affected areas with watertight dressing to prevent spread

• hand hygiene

• school exclusion (until at least 24 hours after starting appropriate antibiotic treatment)

TOPICAL: for localised non-bullous impetigo, antiseptic recommended for 5-7 days… if ineffective or not appropriate (if around eyes) topical antibiotics can be considered (fusidic acid 1st, mupirocin - reserved for MRSA infection)

SYSTEMIC: fluclox (1st)

alternatives may include trimethoprim and sulfamethoxazole or erythromycin (for MRSA infection or if penicillin allergy)

Ecthyma

Hard crusted sores beneath which ulcers form

~ begins as a vesicle or pustule on inflamed skin

~ removal of crust reveals red, swollen, indurated ulcer oozing with pus

Community-acquired MRSA

mostly occurs

~ in overcrowded places, due to frequent contact of skin and sharing things

~ in people with draining cut or sore or that are carriers of MRSA

 

Management

~ swab for MCS

PCR

Surgical drainage if required

Clindamycin or trimethoprim/sufamethoxazole

For severe infections vancomycin is indicated

 

Clinical features of hospital acquired MRSA

~ present as skin infections (abscesses, furuncles and carbuncles, impetigo and cellultiis) or as wound infections (at trauma and surgical sites)

 

Whereas

Clinical features of community-acquired MRSA mainly presents as bacterial folliculitis, boils, impetigo

Folliculitis

Inflamed hair follicles

 

Presentation

~ tender red papule or pustule centred on a hair follicle

~ more common in hot weater

~ often occurs in macerated areas

~ look at centre of the inflammatory papule for protruding hair shaft

Shaving and waxing common triggers

 

Investigation

MCS

Skin scraping for fungus

Hair pull test (if fungal scalp involvement suspected)

 

Treatment

• Depending on the organism or cause.

• Physical factors such as occlusive clothing, grease or massage oils or in a child case nappies need to be managed.

Furuncles and carbuncles

deep form of bacterial folliculitis

~ furuncles (boils) present as single or multiple tender, red, firm or fluctuant nodules or walled-off abscesses which eventually point and discharge pus from a central core

 

~ carbuncles are when multiple furuncles coalesce and extend to the subcutis

~ carbuncles often have systemic signs (malaise, chills, fever)

 

Treatment

~ apply topical antiseptic like povidone iodine or chlorhexidine cream

Then cover with gauze

 

~ oral antibiotics: fluclox, cephalexin

 

~ incision and drainage

Acute vs chronic paronychia

Acute paronychia

~ common in nail biters and those with chronically wet hands

 

Presentation

~ nail fold becomes painful, red and swollen, sometimes yellow pus under cuticle

 

Treatment

~ drainage with sterile needle, application of a topical antibiotic, sometimes oral

 

Acute herpetic paronychia

~ caused by HSV

 

Chronic paronychia

~ chronic irritant dermatitis and C.albicans superinfection

~ may start on one and spreads to several others

~ affected nail fold is swollen and lifted off nail plate

~ becomes distorted and ridged as it grows. May become yellow or green and brittle

 

~ common in people with chronically wet hands, such as bar tenders and housewives

SSSS

~ characterised by erythematous painful blistering

~ skin looks like a burn or ‘scald’

~usually from a local infection eg. impetigo

 

Treatment: systemic antibiotics

 

Mechanism of Staph to cause SSSS

~ release of epidermolytic toxins A and B from staph

~ toxins target desmoglein-1 (a cell adhesion protein) in the stratum granulosum

~ leads to intraepidermal splitting

~ results in blistering, skin peeling and positive nikolsky sign

What is Nikolsky’s sign?

shearing stress of skin causes separation of skin, results in traumatic bulla

Toxic shock syndrome

~ caused by release of exotoxins from staph and can also be caused by s.pyogenes

~ presents with sudden high fever, widespread erythematous rash, and multi-organ involvement

~ may lead to circulatory collapse

~ classically linked to tampon use but can arise from skin or wound infections

Cellulitis vs erysipelas

Cellulitis

~ acute diffuse spreading skin infection (what ur brother had)

 

Erysipelas

~ skin infection involving upper dermis with clearly delineated borders, eg. butterfly rash

 

Both present with localised redness, pain, swelling and +/- systemic symptoms (fever)

~ usually caused by s.pyogenes (GAS)

~ if around a wound, consider staph

~ periorbital cellulitis can occur in children (like ur bro) usually S.pyogenes. his was HSV, Hib is now rare due to vaccination

 

Cellulitis presentation

~ more raised n swollen, less marginated, favours lower legs in adults, and for children, limbs and periorbital region

 

Predisposition for cellulitis

On legs (lymphoedema, tinea of feet, chronic dermatitis, poor lower leg circulation arterial and venous, wounds)

 

On face: Herpes simplex infection, dental caries, chronic sinus infection, more common in diabetics, immunosuppression)

 

Treatment:

rest and elevation of area

analgesia

oral or IV antibiotics eg. cephalexin, fluclox, penicillin-dependent on sensitivities

 

Presentation for erysipelas

~ may see lymphatic streaking

~ blisters may develop on red plaques

~ most commonly affects lower limbs

 

Treatment:

Oral antibiotics or IV if severe, usually penicillin

Necrotising fasciitis

~ infection of soft tissue and fascia

~ presents as a dusky cellulitis which progresses to extensive necrosis

~ bacteria multiplies and releases toxins and enzymes that results in thrombosis in blood vessels  destruction of soft tissues and fascia

~ due to mixture of staph, strep and anaerobes?

Erythrasma

~ in skin folds, axilla or groin or between the toes

~ macular wrinkled, slightly scaly, pink, brown or macerated

~ WOODS LIGHT: CORAL PINK

 

Treatment:

Fusidic acid cream, whitfield ointment, clindamycin solution

 

 

Trichomycosis Axillaris

Infection of underarm hair

 

~ characterised by yellow, black or red granular nodules or concretions that stick to hair shaft

~ caused by overgrowth of corynebacterium

 

~ topical antibiotics and shaving

Pitted keratolysis

~ combination of unusually sweaty feet and occlusive shoes encourages growth of microorganisms that digest keratin

~ results in honeycomb like pits in webs and toe pulps, forefott and heel

~ often with offensive odour

 

Treatment

~ keep feet dry

~ topical clindamycin, erythromycin, fuscidic acid

~ oral macrolides