Lecture 3: Skin & Subcutaneous Bacterial Infections

Staphylococcus aureus

Gram positive, catalase positive coccus

Beta hemolytic

Coagulase: clots plasma - localizes infection

Hemolysins - lyse blood cells

Leukocidin (Panton-Valentine or PVL)

Lyses leukocytes that release lysozymes for tissue destruction

Damages eukaryotic membranes – necrotic pulmonary disease

Protein A – binds Fc portion Ig; reducing opsonization

Normal flora - perineum; axillae; nares

Pseudomonas aeruginosa

Gram-negative bacilli

Opportunistic pathogen

Ubiquitous

Pyocyanin - blue pus

Pyoverdin - green fluorescent siderophore

Exotoxin A: cytotoxic activity

Extracellular, responsible for tissue damage & septicemia

Binds elongation factor – A-B exotoxin

T3SS – Type 3 secretory system – delivers exotoxin to cells

Injectosome – molecular syringe

Routes of infection for skin and soft tissue

Exogenous – disrupted integrity of skin barrier

Endogenous – opportunistic normal microbiota seeded into tissues from blood or lymph

Toxin induced – Nidus at distant site; cause pathogenesis in/near skin

Folliculitis

Staphylococcus aureus & Pseudomonas aeruginosa - water

Epidermis

Inflammation of superficial or deep portion of hair follicle

Purulent material in the epidermis

Occurs - infants, children, and adults

Folliculocentric; inflamed papules &/or pustules in hair-bearing skin

Pruritis

Folliculitis barbae

Staphylococcus aureus

Area of repeated shaving

Bearded-area (upper lip near nose)

Erythematous follicular-based papules or pustules

Rupture & leave yellow crust

Common - carriers nasal staph

Stye (hordeolum)

Staphylococcus aureus

Folliculitis of eyelid

Hair follicle of eyelid (external)

Hot Tub Folliculitis

Pseudomonas aeruginosa

Exposure - Hot tub or swimming pool

Contaminated water (inadequate chlorine, pH, bromine)

Appears in 8-48 hours

Areas of itchy maculopapular rash, some pustules

Systemic: Fever; headache; sore throat; malaise; GI distress → Possible LPS involvement

Folliculitis Treatment

S. aureus:

Mild - resolves spontaneously

If no resolution or more than one area of body involved →

Topical: mupirocin or clindamycin

Mupirocin – binds bacterial isoleucyl-tRNA synthetase

Refractory or recurrent: Oral antibiotics

MSSA – dicloxacillin (anti-beta-lactamase active)

MRSA – TMP/SMX; clindamycin; doxycycline

P. aeruginosa:

Self-limiting; resolves 7-10 days

Severe case: oral ciprofloxacin or TMP/SMX

Furuncle

Staphylococcus aureus

Epidermis, Dermis, & SubQ

Small fluctuant abscess exudes purulent material

Forms single opening – “point”

In areas where hair follicles exposed to friction and perspiration - Face, back of neck, axillae, buttocks

Starts as hard, tender, red folliculocentric nodule

Enlarges, becomes painful, & fluctuant abscess

Ruptures with decrease in pain & diminishing edema (days – weeks)

Carbuncle

Staphylococcus aureus

Epidermis, Dermis, & SubQ

Larger more serious than furuncle

Extremely painful

Aggregate of subcutaneous connected furuncles

Neck, back, and thighs

Red, indurated area

Pustules appear & drain around multiple follicles (sinus tracts)

Fever and malaise often present

Permanent scar – dense; readily evident

Furuncles and Carbuncles Treatment

Warm compresses initially

Incision and drainage – most effective

Empirically treat for MRSA – TMP/SMX or Doxycycline

Recurrent furunculosis: Mupirocin- topical

Applied to nares, axillae, and perineum for 5 days

With or w/o oral Clindamycin

Treat S aureus → prevent hematogenous spread of infection → Endocarditis; Sepsis; Osteomyelitis

Cutibacterium acnes

Acne vulgaris

Gram- positive

Pleomorphic bacilli

Common aerotolerant anaerobe

Normal skin microbiota

Especially sebaceous glands

Acne - primary bacterium

Opportunistic infections in patients with Prosthetic devices + Intravascular lines

Inflammatory vs non-inflammatory acne

Noninflammatory – follicular wall intact

Inflammatory – follicular wall lysed

Noninflammatory Acne

Begins with Microcomedo formation

Follicle opening - Partially obstructed by sebum, keratinocytes, bacteria, & hair

Comedones: small, flesh-colored, white, or dark bumps that give skin a rough texture

Found at the opening of skin pores

Solid core

Closed comedo (Whitehead):

A sebum plug in the follicular canal

Keratinocytes, bacteria, sebum increase

Open comedo:

Content reaches surface

Follicle opening dilates

Compacted melanin, keratinocytes & oxidized lipids

Black appearance (Blackheads)

Inflammatory Acne

Neutrophil hydrolytic enzymes aid in breakdown of follicular wall

Comedo contents- rupture of follicle releases free fatty acids & C. (P.) acnes into dermis → inflammatory response

Papules: Small firm pink bump

Pustules: Inflamed, visible pus, Chemical irritation - sebum

Nodules: Large & very painful, Inflamed pus-filled lesions deep within the skin

Conglobata: Severe form of nodular acne

Young males

Large draining lesions, sinus tracts, and severe scarring

Acne vulgaris treatment

Retinoids - comedolytic and anti-inflammatory

Topical – trifarotene

Antibiotics - target C. acnes

Topical and oral

Precaution – sun sensitivity

Benzoyl peroxide (topical) – antimicrobial & comedolytic

Azelaic acid (carboxylic acid): Reduce hyperpigmentation after healing of acne

Oral contraceptives

Spironolactone – anti-androgen

Nonbullous impetigo/impetigo contagiosum

S aureus and GAS

All ages w/ highest children 2 – 6 years

Exposed areas - face, arms, legs

Spread by: Autoinoculation and Contact

Superficial intraepidermal lesions

Single erythematous macule → Rapidly evolves vesicle/pustule

Ruptures → yellow crust exudate over erosion- “Honey-colored”

Pruritis

Infectious and spreads rapidly → Pathogen present in vesicle

Streptococcus pyogenes

Beta hemolytic

Gram-positive

Cocci - “string of pearls”

SPE – Streptococcal Pyrogenic Exotoxins, A-C

Erythrogenic superantigens

M protein – fimbriae/pili associated; Impede phagocytosis

DNase – reduces viscosity of lysed cell contents

Hyaluronidase – invasin

Streptokinase – dissolves blood clots- invasin

Bullous Impetigo

S. aureus - only

Exfoliative toxin A -producing strains

Digests epidermal intercellular connections

Superficial intraepidermal lesions

Begin as vesicles

Enlarge & form flaccid bullae w/ clear yellow fluid

Fluid becomes dark & turbid

Bullae rupture – thin brown crust forms

Infectious – contain S. aureus

Localized toxin does not disseminate

Ecthyma

S. aureus & GAS

Ulcerative pyoderma

Extends into dermis

Ulcers (punch-outs): Greenish-yellow crust w/ violaceous margins

Raised with induration

Buttocks, thighs, legs, ankle and feet

Pigmented scars

Rarely contagious

Impetigo and Ecthyma Treatment

Personal hygiene, Gentle debridement

Topical antibiotic: Limited Lesions

Mupirocin (isoleucine tRNA); Retapamulin (50S)

Systemic antibiotics (extensive lesions)

Cover both GAS and Staph:

First line – dicloxacillin; cephalexin

MRSA - TMP/SMX; clindamycin; doxycycline; linezolid

Only GAS - penicillin

Cellulitis

GAS or S aureus

More likely than S aureus if: No obvious portal of entry + No obvious primary site of infection - abscess

Increasing in IVDU, HIV, prisoners, athletes, military trainees, male homosexuals

Middle-aged & older adults

Uncomplicated nonnecrotizing inflammation

Deeper dermis & subcutaneous fat

With or without purulent discharge

Unilateral

Erythema and Tenderness

Skin becomes hot and swollen

Borders blend in elevation & color into surrounding tissues

Associated with intertriginous skin break w/ tinea pedis

Lymphangitis & Lymphadenitis

Possible vesicles, bullae, petechiae, & ecchymoses

Necrotizing fasciitis or Osteomyelitis or Myonecrosis

“Orange peel” or “Peau d’Orange” appearance due to edema w/ dimpling around hair follicles

Avoid NSAIDs

Erysipelas

young children & older adults

GAS

S. aureus -recurrent infection

Involves upper dermis and superficial lymphatics

Lesions raised above area of surrounding tissue

Clear line of demarcation – involved/uninvolved tissue

Milian’s ear sign – distinguishes erysipelas & facial cellulitis → Lack of deep dermis involvement of cellulitis

Butterfly Distribution

Acute onset of symptoms

Systemic manifestations including fever and chills

Acinetobacter baumannii

Cellulitis associated with trauma & use of invasive devices

Aerobic broad rods to coccobacilli

Skin & Soft Tissue disease

Multi-drug resistant & pan-resistant pathogen

Capnocytophaga canimorsus

Cellulitis

Fastidious

Slow-growing filamentous/fusiform bacilli

Oxidase and Catalase-positive

Dog bite

Infection: ≥50-yr-old males, alcoholism, splenectomy

Bacteremia and sepsis

Pasteurella multocida

Cellulitis

Facultative anaerobe, coccobacilli

Cat bite

Develops w/in 2 to 12 hr of bite

Associated purulent drainage (endotoxin; capsule)

Aeromonas hydrophila

Cellulitis

Fresh water

Facultative anaerobe motile, bacillus

Vibrio vulnificus

Cellulitis

Saltwater

Facultative anaerobe, halophile, motile, vibrio