Bacterial Infectionsof the Skin

General Considerations of Bacterial Diseases• Two major forms: Primary vs. 2nd manifestation in the skin

• Natural resistance of the skin:

Integrity of the skin integument

Low pH

Antibacterial substances in seb secretions

FFA (linoleic and linolenic acids)

Immunoglobulins, cellular immunity, delayed hypersensitivity

Enhanced susceptibility of immunocompromised host Relative

Dryness of nl skin

Bacterial interference

Pathogenesis of Bacterial Infection of the Skin• Pathogenicity of the microorganisms

Invasive potential (antiphagocytic surface component)

Toxin

Exotoxin

Endotoxin (LPS)

-TNF and IL1 by LPS activated microghages

-Shwartzman rxn (DIC vs. Hem necrosis)

• Portal of entry

• Specific features of host inflammatory response

Classification of Bacterial Infection of the Skin

• Etiology seems more important

• Helpful classification:

Primary infxn (Pyodermas)

Secondary infxn

Cutaneous manifestations of systemic dz

Diagnostic Strategies

• Direct examination of aspirates and biopsies (Gm and Cx)

• Special culture material

Dephtheria - Loeffler or tellurite agar

GNR - EMB or MacConkey plate

M/G - Chocolate agar or modified Thayer-Martin CO2

Anaerobic strep, clostridia, bactreroides – blood agar, O2 free

• Flourescent Ab

• Other Immunologic methods

• PCR

Antibiotic Therapy

• Dosage

• Toxicity

• Antibiotic resistance because of “ R” factor

• Topical antibacterial agents

Skin Infections Caused by Gram-Positive Organisms

Staph skin infection: Streptococcal Skin Infections

The two gram-positive cocci Staphylococcus aureus and group A beta-hemolytic streptococci account for the majority of skin and soft tissue

infections. 

• S. aureus invades skin and causes – impetigo, – folliculitis, – cellulitis, and – furuncles.

Elaboration of toxins by S. aureus causes the lesions of

– bullous impetigo and– staphylococcal scalded skin

syndrome.

• The streptococci are secondary invaders of traumatic skin lesions and cause – impetigo, – erysipelas, – cellulitis, and – lymphangitis.

Staph skin infection: • Two major groups of Staph:

coag + and coag -

• 30-50% healthy adults harbor S. aureus

• Pathogenesis:

Cellular and extracellular products - coagulase, leukocidin, alpha toxin, exotoxins (TSST-1, enterotoxins B/C, exfoliative toxins A/B)

Surface adherence

Host factors

Staph Bacteremia and Endocarditis • Secondary bacteremia

(from a defined peripheral focus of infxn), <10% endocarditis

• Primary bacteremia (no identifiable peripheral focus yet repeatedly (+) bld Cx), treated as endocarditis

• Janeway lesions, Osler’s nodes, subungual splinter hemorrhages, subconjunctival hemorrhage, Roth spots, endophthalmitis

Superficial pustular folliculitis: • = follicular or Bockhart’s

impetigo, impertigo of Bockhart

• Children: scalp; Adults: beard area, axilla, ext, buttock

• Periporitis staphylogenes = 2nd Staph infxn of neonatal miliaria

• Ddx - other infectious folliculitis, noninfectious follicular disorders

Deep folliculitis: • Sycosis barbae, Sycosis

Vulgaris, Barber’s itch

• Perifollicular, chronic, pustular, recurrent staph infxn

• Ddx – dermatophytic folliculitis (tinea barbae), pseudofollicular barbae, herpetic sycosis

• Lupoid sycosis (sycosis lupoides): a deep chronic form of pyogenic folliculitis and perifolliculitis

Treatment for folliculitis

• Antibacterial soap

• Mupirocin oint topically

• 1st gen cephalo, oxacillin, cloxacillin, dicloxacillin

• For acute inflammation, Burow’s sol diluted 1:20

• For chronic folliculitis: Drysol

• For blepharitis: antibiotic ophth oint

Furuncle-circumscribed perifollicular abscess

Carbuncle: >2 confluent furuncles

Abscess

The best, most cost-effective way to prevent hospital furunculosis is:

The best, most cost-effective way to prevent hospital furunculosis is:

Treatment for furunculosis

• Warm compresses and oral Abx

• 1st gen cephalo, oxacillin, cloxacillin, dicloxacillin

• Mupirocin oint to nares x 5 to prevent recur

• Suspect MRSA or even vanco-resistant strains

• The timing of I& D

• The cavity should be packed with iodoform or Vaseline gauze

Treatment for furunculosis-special locations

• External auditory canal: avoid irrigation and early incision; apply mupirocin; give oral Abx and heat application

• Nasal furuncles: hot saline compresses inside and outside the nostril until softening; furuncles should not be incised but steamed; local and oral Abx

• Upper lip and nose: danger of sinus thrombosis, meningitis, and septicemia; prevent trauma w dressing; local and oral Abx; incision as the last resource

Chronic furunculosis

• Due to autoinoculation and intrafamilial spread among carriers

• Daily antibacterial soap or chlorhexidine, specially to axillae, groin and perianal area

• Eradicating nasal carriage state

- Mupirocin oint bid q 4wk

- Rifampin 600mg qd x 10d combined w cloxacillin 500mg qid or clinda 150mg qd for 3 mos

- Mupirocin oint bid inside nares throughout the course of isotretinoin tx

Pyogenic paronychia: • Staph is the major cause

of acute paronychia, other bacterias including strep pyogenes, Pseudomonas, Proteus or anaerobes

• Chronic/recurrent form by C. albicans

• Predisposing factors: trauma-separation of eponychium from nail plate, chronic moisture

Treatment of paronychia: • Prevent from trauma and keep dry

• I& D for acutely inflamed absecesses

• Oral Abx (semisynthetic penicillin or 1st gen cephalosproin, if anaerobic, use Augmentin

• For chronic paronychia: fungicide and bactericide such as Neosporin soln, Vioform, 2% thymol in acetone, Castellani paint, oral azole

Staph Whitlow (Felon): • Purulent infxn/abscess @ the

bulbous distal end of the finger

• S. aureus and HSV (recurrent, hemorrhagic vesicles)

• Portal of entry: trauma, parynochia

• X-ray to r/o osteomyelitis

• Surgical drainage of loculated abscesses and IV Abx

Botryomycosis

• Rare pyogenic dz

• Nodular, crusted, purulent lesions, sinuses discharge sulfur granules

• Predisposing factors: trauma, immuno-suppression, chronic alcoholism, DM

• Skin, bone, liver

• Often genital areas

• The role of a foreign body

• Abx, surgical drainage and excision

Nonbullous Impetigo (Impertigo Contagiosa)

• Children and adults

• Face (around nares) and exts

• S. aureus > gpA strep, or both

• Bacteriocins produced by S. aureus highly bactericidal to gpA strep

• gpA beta-hemolytic strep nephritogenic strains: type 49,55,57, and 60 strains and strain M-type 2

• Tx: local and systemic Abx; soak off the crusts, prophylactic Abx oint

Bullous Impetigo

• Group 2 S. aureus phage type 71

• Exfoliatin A/B – serine protease of desmoglein 1

• 51% pts had (+) Cx from nose or throat

• Pemphigus neonatorum or Ritter’s dz

• Topical mupirocin + P.O. Abx 5-10 d (dicloxacillin, erythromycin, azithromycin, Augmentin, cephalexin, cefaclor,cefprozil,clindamycin)

Bullous Impetigo1. What is the responsible phage

type?

2. What’s exotoxin?

3. What is the target of the bacterial toxin on the skin?

4. If you see a vesicular separation on H/E, what it the level of separation?

Staph Scalded-Skin Syndrome (SSSS)

• Exfoliative (epidermolytic) toxin A/B by S. aureus phage group II

• Serine protease cleaves desmoglein 1

• Children < 5 y/o, particularly neonates

• Generalized, superficial exfoliative dz, formally known as Ritter’s dz or dermatitis exfoliativa neonatorum

• Localized form = bullous impetigo

• Abortive form: may represent mild form of toxic shock syndrome

SSSS

Bullous impetigo

SSSS

H&E: Exfoliative cytology

TEN

Staph Toxic-Shock Syndrome (STTS)

Menstrual: • TSST-1

Nonmenstrual:• TSST-1

• Enterotoxin B/C

Bulbar conjunctival hyperemia

Staph scarlatiniform eruption Recalcitrant, erythematous, desquamating disorder (RED)

Recurrent toxin-mediated perineal erythema

Streptococcal Skin Infections

• Lancefield classification A-T by C carbohydrate Ag of cell wall

• GpA strep beta-hemolytic, sensitive to bacitracin

• Subtyping of gpA strep by M-protein

• Virulence factors

Cell surface molecules

Secreted proteins

• 10% asymptomatic carriers in nl population (oropharynx)

• Acute rheumatic fever – only 2nd to pharyngitis/tonsillitis

• Acute nephritis – skin or URT (different serotype)

Ecthyma

• Neglected impetigo extends into dermis; an ulcerated staph or strep pyoderma

• Lower ext of children, elderly, DM

• Crusted, “punched out” ulcer

• Tx: same as for Staph impetigo; several wks of Abx

Superficial Pyoderma in Nonintertriginous Skin

Impetigo, nonbullous • Indistinguishable from that caused by S. aureus

• Half pts have both S. aureus and gp A strep

• GpB strep a/w impertigo in the newborn

• Tx:

Topical mupirocin

Penicillin

Erythromycin if allergic to PG

Practically, Tx should be directed at S. aureus

Strep Infxn in Intertriginous Skin Sites

Streptococcus intertrigo Streptococcus intertrigo-perianal strep cellulitis

You are asked to see a consult on the

floor, what is your impression?

Erysipelas

• Most common: gpA strep

• Occasionally, gps C, G, B strep, S. aureus

• Recurrent erysipelas a/w saphenous vein harvest and lymphedema

Cellulitis

• Most common: S. aureus

• Gp A strep, gps C, G, B strep, E. Coli and other enterobacteriaceae and anaerobes

• Extends deeper into subcut

• Ext leg > arm, thrombophlebitis

• Complicate surgical wound, pressure ulcer, animal bites

Cellulitis: Differential Diagnosis Disease Description

Anthrax (cutaneous)Edema surrounding crusted lesion. Painless or itching. Animal contact.

Calciphylaxis (calcific uremic arteriolopathy)

Affects diabetic patients with end-stage renal disease and hyperparathyroidism who are receiving renal replacement therapy. Metastatic calcification leads to small vessel vasculopathy. Early stage: presents with nonulcerating plaques in the calves. Lesions eventually become necrotic and painful ulcers develop.

Carcinoma erysipelatoides

A form of metastatic carcinoma with lymphatic involvement. Seen on anterior chest wall in breast cancer and sites of distant metastasis. No fever, slow progression. If a suspected breast infection does not resolve with antibiotics, mammography and tissue biopsy are indicated.

Contact dermatitis (acute)

Lesion sharply demarcated and constricted to the area of exposure. Pruritus present, not in cellulitis. Topical steroids effective. Systemic corticosteroids are indicated for severe cases. Secondary infection may complicate dermatitis.

Deep venous thrombophlebitis

Unilateral leg edema, warmth, or erythema. Tenderness along involved veins. Can have low-grade fever, leukocytosis. Duplex ultrasonography diagnostic.

Cellulitis: Differential Diagnosis

Disease Description

Erythema migransLyme disease rash that typically expands but clears in center. Often a single or multiple lesions occur that are round and red and expand to many centimeters but do not show central clearing.

Erythema nodosum Most common panniculitis. Raised, painful, bilateral, tender lesions located over both shins. Lesions may coalesce and resemble cellulitis.

Factitial Mechanical or chemical manipulation of skin can produce an area of erythema that resembles cellulitis.

Fixed drug eruptionA well-demarcated plaque that recurs at same site each time offending drug is taken. Itching or burning not seen in cellulitis. Most commonly affected areas are lips and genitalia.

Foreign-body granulomatous reactions (silicone injections, paraffin oils)

Material injected into skin can stimulate an overlying erythema.

Cellulitis: Differential Diagnosis

Disease Description

Gouty arthritis (acute)

Joint inflamed with overlying erythema and warmth. May lead to tendonitis and bursitis. Chills, low-grade fever, elevated leukocyte count. Typically monoarticular, lower extremity, usually first metatarsophalangeal joint or knee.

Insect stings or bites and other envenomations

Swelling that can extend over a large area; peaks within 48 hours and lasts up to 7 days. No lymphangitis. Pruritus distinguishes this lesion from infectious cellulitis. Envenomations by marine animals cause a similar picture.

Leukemia/lymphomaLymphoma diagnosed after failure of antimicrobial therapy. Persisting fever or generalized lymphadenopathy may suggest the diagnosis.

Necrotizing fasciitisA rapidly advancing erythema. Begins with fever and chills. Vesicles and bullae may form and drain fluid. Painless ulcers appear as the process spreads.

Cellulitis: Differential Diagnosis

Disease Description

Panniculitis

Pancreatic disease, either inflammatory or neoplastic, may lead to panniculitis presenting as tender, red nodules located on pretibial regions, thighs, or buttocks. Lupus panniculitis occurs on face and upper extremities. α1-Antitrypsin deficiency may present as cellulitis on trunk and proximal extremities, often precipitated by trauma. Panacinar emphysema, noninfectious hepatitis, and cirrhosis should suggest the diagnosis. Protein electrophoresis reveals low levels of α1-antitrypsin. Some patients respond to dapsone or α1-protease inhibitor concentrate. Other forms of panniculitis are Weber-Christian disease, cytophagic histiocytic panniculitis, post-steroid panniculitis, and nodular panniculitis. Deep excisional biopsies rather than punch biopsy are required to diagnose panniculitis.

Lipodermatosclerosis (chronic indurated cellulitis)

A form of panniculitis; affects middle-aged women, associated with venous insufficiency. Acute form resembles cellulitis. Painful, red, indurated, edematous area in medial aspect of leg. Lasts a few months. Superimposed cellulitis may occur. Compression therapy reduces venous hypertension and fluid extravasation.

LymphedemaNonpitting edema, erythema, induration of an extremity. No fever, no response to antibiotics. May be complicated by infection, recurrently. Lymphangioscintigraphy confirms diagnosis.

Pyoderma gangrenosum

An ulcerative cutaneous disease. Ulcers may follow trauma. An atypical form occurs on the hand. A red ulcer border may be misinterpreted as infection.

DIAGNOSIS OF CELLULITIS

• Recognizing the distinctive clinical features (erythema, warmth, edema, and pain) is the most reliable way of making an early diagnosis.

• Isolation of the etiologic agent is difficult and is usually not attempted.

• Fever, mild leukocytosis with a left shift, and a mildly increased sedimentation rate may be present.

• Patients with cellulitis of the leg often have a preexisting lesion, such as an ulcer or erosion that acts as a portal of entry for the infecting organism.

Gangrenous Cellulitis

Type II

Type I

Type I

Gangrenous Cellulitis

Type II

Type I

Type I

C. perfringens, involving more superficial subcut

C. perfringens, involving muscle w/ 2nd changes in skin

C. septicum, hem. malignancy or colon ca, 100% mortatility

Necrotizing Fasciitis NSAIDs may be contraindicated

Type II necrotizing fasciitis

• Almost always gp A strep, rarely C and G

• Gp B in newborns and postpartum

• Rarely S. pneumoniae

• Usually healthy individuals

• The location is most often an ext

• 2/3 bacteremia

• Often strep TSLS

Necrotizing Fasciitis

Type I necrotizing fasciitis

• A mix of facultative and anaerobes

• Often following Sx, bowel perf, trauma in pts with diabetes and malnutrition

• The location is often an ext, Abd, perineum, or about op wounds

• Infxn in the thigh may be 2nd to an intestinal source

• Crepitus

Necrotizing Fasciitis

Fournier’s gangrene

• Localized type I necrotizing fasciitis involving scrotum and penis

• Men 50-60 y/o with underlying dz

• Purplish discoloration -> frank gangrene

Synergistic necrotizing cellulitis

• Anaerobes and facultative bacteria

• Involve all soft-tissue structures (muscle)

• Poor prognosis related to pt population

• Small area of necrosis/blister overlying widespread destruction of deeper tissues, skin sinus draining necrotic fat

• Most common site is perineum

Progressive Bacterial Synergistic Gangrene (Meleney’s Gangrene)

• Develop in proximity to wires or other foreign bodies

• Microaerophilic or anaerobic strep at the advancing margin

• S. aureus in the central, ulcerated area

• Removal of foreign bodies, excision of necrotic tissues, zinc sulfate cream and Abx

Blistering distal dactylitis

• Gp A strep (majority)

• Occasionally gp B strep, S. aureus

• Blister over the volar skin pad of distal fingers/toes

Acute Lymphangitis

• Gp A strep (majority)

• Occasionally S. aureus; rarely, Psateurella multocida or HSV

• A portal of entry and tender regional adenopathy

• Frequently lead to bacteremia

Gp A Strep Toxic Shock-like Syndrome (TSLS) or Toxic Strep Syndrome

• Pyrogenic exotoxin (erythrogenic toxin) A > pyrogenic exotoxin B/C, strep superAg, strep mitogenic exotoxin Z

• Young (20-50 y/o), healthy pts

• 80% soft tissue site of infxn

• over half develop bacteremia

• Near 50% mortality rate

• “Septic scarlet fever” – TSLS may be a more severe form of scarlet fever

• Tx: extensive debridement, Abx, IV fluids, vasopressors, IVIG

Erythrasma

• Corynebacterium minutissimum – gram (+) rod

• More common in men

• Web spaces of feet, and intertriginous areas

• Asymptomatic or puritic

• Tx: BP wash/gel, clindamycin soln, azole cream