Bacterial Infections of the Skin

Skin barrier breakdown Host defense and inflammatory response Pathogenicity of the bacteria

3 major factors for development of bacterial skin infection

S. epidermidis: diffuse, major one 90% flora S. aureus: nose/perineum Micrococci: luteus is the main one Diphtheroids: common w/ acne Streptococci: beta hemolytic Gram - bacilli: small portion, moist intertriginous areas including Enterobacter, Klebsiella, Escherichia coli, and Proteus spp

Most common bacterial flora of the skin are as follows, where are they? S. epidermidis: S. aureus: Micrococci: Diphtheroids: Streptococci: Gram - bacilli: others are candida

Pasturella multocida

Dog bites: 80% of animal bite, 20% infected d/t polymicrobial Cats cause 50% infection d/t sharper teeth and a lot of bacteria, teeth hit bones, joints and soft tissue easily What is the most often infectious agent of cat bites

Usually penicillin for lower extremity. Oral or IV. Vancomycin for facial or if MRSA suspected. IV ceftriaxone or cefazolin. Oral erythromycin if penicillin allergic (stomach issues)

Erysipelas (superficial cellulitis) treatment for: Lower extremity: Face:

Scalded Skin Syndrome (Ritter's Disease)

Exfoliative exotoxin of S. aureus Children, infection of nares/throat/umbilicus then skin feels like sand paper and they get a rash w/ a fever Large clear bullae form then come off w/ red denuded base + Nikolskys sign Stratum granulosum*** key feature

Orbital cellulitis

Eyelid swollen +/- erythema, + deep eye pain, painful eye movement, proptosis (bulging), diplopia, visual impairment, fever

Periorbital cellulitis

Eyelid swollen +/- erythema, +/- eye pain, no proptosis, no diplopia, no vision changes, maybe fever

Toxic shock syndrome

Fever 102+ Rash diffuse macular erythroderma Desquamation palms soles 1-2 weeks Hypotension + 3 or more following: NVD, myalgia, hyperemia, BUN/Creatine 2x, hepatitis, thrombocytopenia, AMS

Papules/pustules

Follicle ruptures causing proinflammatory lipids and keratin are extruded into the surrounding dermis causing the development of an inflammatory lesion.

Mycobacterium abscessus and M. fortuitum NTM Group IV Rapid Growers

Found in water, soil, and dust. 3rd most frequently recovered respiratory NTM in US. High resistance to antibiotics. Skin infections with draining abscesses. Associated with post-surgical wounds, needle injections, and renal transplant recipients.

Tularemia

Francisella tularensis Ticks, squirrels, rabbits, beavers Lab workers, vets, farmers, hunters Transmission w/ infected animal or insect (ticks common) Fever, anorexia, malaise, HA, abdominal pain, emesis and diarrhea Fever goes away in a few days and comes back Rash can occur in multiple presentations: maculo-papular, vesiculo-papular, erythema multiforme, erythema nodosum and urticarial.

Slow growing and produce a yellow-orange pigment even when grown in dark. Mycobacterium szulgai

Group II Scotochromogens

Bacterial skin infections account for 20% of dermatology visits

How common are bacterial skin infections?

Acne

Hyperkeratosis Sebum overproduction Propionibacterium acnes proliferation Inflammation => pustules and nodules

iso-tretinoin

In general, comedones respond best to topical retinoid agents and acid products. Inflammatory lesions (papules, pustules) require either topical antibiotic agents for minor or oral antibiotics when major. Acutane is a good one to treat in general what is it

Folliculitis TX: Topical antibiotics are usually all that is needed occasionally oral antibiotics.

Infection of hair follicule Pustular (white) d/t s. aureus Can be seen w/ pseudomonas after a hot tub (pruritic papulo-pustular rash appears in moist areas or those areas covered by a bathing suit) Typically erythematous base

Carbuncle (still a boil but several hair follicles and deeper) Bacteremia is common: abx and drainage

Large abscess w/ staph in several hair follicles, can go into sub q Often nape of neck/back

Sebaceous gland

Make sebum (light yellow oily fluid) Everywhere but palms, soles and dorsa feel, lower lip React to DHT increasing their production of sebum Sebum combines with cells sloughed off in hair follicle

Topical retinoid AND Topical antimicrobial (e.g. benzoyl peroxide alone or benzoyl peroxide +/- topical antibiotic)

Mild papulopustular and mixed (comedonal and papulopustular) acne

Non-bullous impetigo

Most common form of impetigo Small vesicle ruptures w/ red moist base seen on nose, mouth, limbs Honey colored crust that sticks to lesion w/ surrounding erythema Satellite lesions appear Asymptomatic Associated w/ acute poststreptococcal glomerulonephritis. Develops 1-3 weeks following acute infections

Meningococcemia Early diagnosis and treatment are paramount! Common in closed areas dorms etc High index suspicion: neck pain fever nausea vomiting, rash means they are further along IV abx and IV acyclovir: not always sure what they have Be aggressive to prevent DIC and other severe outcomes

Neisseria meningitides Septicemia, kills faster than any other Respiratory tract spread Endotoxins in small blood vessels DIC, anoxia of organs Clinical Presentation: fever, headache, N/V, and rash. Lesions of acute infection are easily identified and virtually pathognomonic with a mixed petechial and maculo-papular rash most prevalent on the extremities and extensor surfaces. Rash starts brown stained macules then purpuric with irregular edges

Tap water is a major reservoir for most human NTM pathogens.

Non-tuberculosis Mycobacterium (NTM) reservoir?

Gram negative bacteria

Normally skin is quite dry, what does this dryness inhibit the growth of?

S. aureus

Not normal flora Colonizes the nares, perineum and axilla Invades skin and causes impetigo, folliculitis, cellulitis and furuncles Toxins made by it cause bullous impetigo and scalded skin syndrome

Intertrigio: superficial Treatment: Zinc oxide ointment (Butt Balm) Keep areas dry and frictionless. Usually reoccurs unless weight is lost. Topical antifungal or antibiotic creams as needed.

Obese F pt presents c/o submammary, axillary and gluteal fold rash w/ increased moisture that is red, itchy, and has painful fissures Can be caused by Group A/B strep, pseudomonas, fungal Dx w/ woods lamp and KOH (checking for other illnesses)

Mycobacterium marinum: Group I

Pools and fish tanks, non-chlorinated water Most common NTM, occurs at sites of minor trauma like fingers, elbows Papule/nodule -> ulcers clinical presentation and index of suspicion. Patient with salt or fresh water aquarium. Gram stain and acid fast stain, cultures.

Erysipelas (superficial cellulitis)

Pt presents w/ new onset bright red, painful, raised edematous rash w/ sharp borders that began with a fever and chills. Always group A strep Involves upper dermis and superficial lymphatics (inflammation is raised around the surrounding skin) Likes to affect the legs and face Most common cause of virulent soft tissue infection in healthy pt Improve w/ 24-48 hr of abx

Orbital cellulitis Tx: IV antibiotics Vancomyocin

Pt presents w/ proptosis, orbital pain, fever, restricted eye movement, chemosis and loss of vision. Due to S. aureus (adults); H influenza (kids) Associated w/ maxillary and ethymoid sinus infection Involves the contents of the orbit (fat and ocular muscles). Does not involve the globe Can have abscess form, be blind, not be able to move the eye THIS IS AN EMERGENCY

Periorbital Cellulitis 3x more common than orbital Tx: Now must cover both MRSA and Grp. A Strep

Pt presents w/ sinus infection and URI, they have a fever, erythema and edema of the eyelid and conjunctivia. They can see and their eye moves fine Most common w/ staph, strep (adults), H influenza (kids)

Cellulitis Rule out DVT

Pt presents with tender, red, warm, swollen leg where there was a bite previously, they have new onset malaise, fever, chills, headache and leukocytosis Spreading superficial infection of the skin via group A strep/ S. aureus Affects the deeper dermis and sub q fat Poorly defined margins w/ lymphadenopathy (Strep can cause bullous lesions)

Necrotizing fasciitis IV abx, debridement, maybe amputation Surgery is the only way to confirm it

RF: Trauma w/ tissue damage Perforation, DM, alcoholism Begins w/ fever, systemic toxicity and severe pain Affects the perinuem and extremities W/O tx = gangrene Characterized clinically by fulminant tissue destruction. Involved area is red, swollen and tender. Underlying process more extensive than what is showing. After a few days the area becomes purple, bullae develop and is followed by gangrene

Necrotizing fasciitis

Rapidly spreading cellulitis with necrosis "flesh eating disease" Mix of organisms (type I polymicrobial, II is GAS or MRSA) Spreads along fascia d/t poor blood supply Acute process Pain out of proportion w/ physical exam

Toxic Shock Syndrome

Rare, multisystem tampons, post op, IV drugs, HIV, cellulitis D/T exotoxins from S aureus Massive release of cytokines produce fever, rash, hypotension, tissue injury and shock.

Scarlet Fever (Scarlatina)

Rash from erythrogenic toxin from GAS Begins on face/neck/chest then abdomen and extremities Red erythema w/ hair follicles and sand paper texture Blanches, spares perioral, likes creases called Pastias lines 4 days later the skinsheds, tongue does too = strawberry tongue

Pseudofolliculitis barbae (razor bumps)

Reaction to hair that is cut too short and curls back into the skin Less inflammation than folliculitis Tender red papule/pustule until hair removed Cheeks and neck (axilla, pubic, legs too)

Acne

Results from a change in the keratinization pattern in the hair follicle with the keratin material becoming more dense and blocking secretion of sebum. The lesions are the result of a complex interaction between hormones, sloughed cells, and bacteria.

irritation, erythema, dryness Sun sensitivity d/t thin stratum corneum Looks worse at first then gets better

S/E retinols

Mycobacterium ulcerans group III

Site of inoculation 3rd most common, contaminated water Begins as localized lesion that ulcerates into sub q fat 3 months to happen

Group I Photochromogens Chromogen: A strongly pigmented or pigment-generating organelle, organ, or microorganism.

Slow growing with little to no pigment when grown in the dark but produce a yellow orange pigment when exposed to light. Mycobacterium marinum Mycobacterium kansasii

Gram positive toxin associated diseases

Staphylococcal Scalded Skin Syndrome Toxic Shock Syndrome Scarlet Fever

Noninflammatory lesions Open comedones: blackhead

The follicular orifice is opened with continuous distention. Densely packed keratinocytes, oxidized lipids and melanin contribute to the dark color.

Isotretinoin (Accutane) *****must do pregnancy test***** They have to be on birth control to administer it Cholesterol will go up, dry skin

The most effective tx for severe acne

Noninflammatory lesions Closed comedones: whitehead

These are an accumulation of sebum and keratinous material.

New pathogens Bacteria w/ abx resistance Immunocompromised pts

Three factors have resulted in an increase in the prevalence and virulence of bacterial infections

Exotoxins

Toxic substances secreted by bacteria and released outside the cell. Usually heat labile proteins. Found in both Gram positive and Gram negative bacteria. Usually binds to specific receptors.

Follicular hyperproliferation/abnormal desquamation retinoids, salicylic acid Increased sebum isotretinoin, birth control P. Acnes benzoyl peroxide, clindamycin Inflammation tetracycline, retinoid, steroids

Tx target areas

Ecthyma: dermal layer

Ulcerative form of impetigo Bacteria has invaded the dermis and scar Elderly and kids Distal extremities w/ regional lymphadenopathy Culture: Group A Beta-hemolytic Strep and Staph May be viral d/t sheep and goats aka farmers impetigo

Mycobacterium szulgai Group II

Unusual pathogen. Can involve skin and lungs; similar to tuberculosis. Occurs most commonly in patients with underlying lung disease. Also associated with bursitis. TX: combined high doses of isoniazid, ethambutol, and rifampin for 18-24 months.

Acne Fulminans Treatment: Systemic glucocorticoids for 4 weeks then oral isotretinoin and oral antibiotics.

A rare and severe form of acne conglobate associated with systemic symptoms. An abrupt and widespread eruption of nodules and friable hemorrhagic plaques, together with fever and arthralgia. Adolescent males, trunk Anemia, leukocytosis, elevated sed rate and proteinuria

Acne Conglobata No systemic symptoms Treatment: systemic antibiotics, intralesional glucocorticoid steroids, systemic glucocorticosteroids. Start isotretinoin after few weeks of steroids.

A severe form of nodular acne more common in males. Uncommon form of acne d/t burrowing interconnected abscesses w/ disfigurement Back, chest, butt

Folliculitis: no comedoes Rosacea: older, erythema, telangectasia, pustules Acne vulgaris has comedos but no telangestasias and is generally not central face.

Acne vs folliculitis vs rosacea

Pyodermas: Acne

Acne vulgaris Non-inflammatory: open or closed comedones Inflammatory: Papules: (less than 5 mm in diameter) Pustules: central core or purulent material Nodules: (greater than 5 mm). May become hemorrhagic or suppurative Cysts: Suppurative nodules cause epithelial-lined sinus tracts = scarring Common locations include the face, neck, upper trunk (anterior and posterior) and upper arms

Furuncle: boils

Acute deep red hot tender nodule/abscess w/ staph folliculitis Can happen in kids Likes axilla, anterior thighs, butt) Becomes fluctuant and may rupture Typically S. aureus Tx w/ warm compress

Acne Vulgaris

Affects areas w/ sebaceous glands most reactive to hormones Opened and closed comedones, also inflammatory lesions Goes from Comedo acne to Nodular acne (tender inflammatory lesions).

Gram - infections

Bartonella Infections Cat-Scratch disease Bacterial angiomatosis Trench fever Tularemia Meningococcemia

Cat Scratch Disease

Bartonella henselae Can result from cat scratch (claws infected with flea feces) bite or flea bite PRimary lesion that is small, erythematous base, papular typically self limiting Azithromycin

Bacillary Angiomatosis Associated w/ cats and immunecompromise

Bartonella henselae Vascular proliferation Angiomatous lesions, start as small red/purple papules that become pedunculated lesions/nodule bleed a lot

Trench Fever

Bartonella quintana: small gram negative rod. Spread by lice Five day fever, very contagious Close quarters Malaise, fever, HA, arthralgia of shin, splenomegaly Associated w. bacteremia, endocarditis, bacillary angiomatosis

Human bite

Bite that is serious and can become cellulitis and cause septic arthritis

topical retinoid, anti-inflammatory no sun sensitivity

Differin (adapalene)

Impetigo Causative organisms: Staphylococcal. aureus most commonly, group A -hemolytic Streptococcus or mixture of both.

Can be bullous or non-bullous Highly contagious Superficial infection of the epidermis w/ crusted erosion/ulcer: itchy and sore Primary infection more common in kids, secondary can occur whenever Name + cause

Bullous Impetigo

Caused by a Staphylococcus produced epidermolytic exotoxin. Most common in kids, hits the face most often, less lesions One or more vesicles enlarge to make a bullae, fluid goes from clear to cloudy "honey colored" crust, has a bright red inflamed base when removed w/o surrounding tissue erythema Flaccid fluid filled bullae that rupture and leave a brown crust

Erythrasma: superficial Erythromycin washing with benzoyl peroxide 2.5% gel followed by topical erythromycin solution bid for 7 days. Oral erythromycin if needed.

Caused by corynebacterium minutissimum Coral red on wood lamp Affects toes, groin, axilla Mistaken for fungal infection Red/brown w/ sharp demarcation, pruitis/burning Common skin flora but problem in: warm climates, obese, diabetes, wearing the same clothes What is it? What is the tx?

treatment of cellulitis depends on whether the clinical presentation consists of purulent or non-purulent cellulitis.

Cellulitis tx?

Mycobacterium leprae.

Chronic granulomatous disease Hypopigmented or reddish patches with definite loss of sensation. Thickened peripheral nerves. Acid-fast bacilli detected on skin smears or biopsy material. Dark skin = higher risk but lower severity Aerosol spread Skin lesions hypo-pigmented or reddish patches w/ lowered sensation

Hidradenitis Suppurativa extensive scarring. Treatment: Moist compresses, surgical drainage of fluctuant lesions and oral anti-staph antibiotics, intralesional steroids, and isotretinoin.

Chronic infection apocrine sweat glands w/ S. aureus Acilla and groin Recurrent formation -> sinus tracts Not just one, typically multiple

Topical retinoid (alternatives include salicylic acid)

Comedonal (noninflammatory) acne

Pyoderma (pus of the skin)

Very common clinical condition Primary: impetigo, folliculitis, furuncle, carbuncle, ecthyma Climate has a role Many drug resistant ones now Caused by 2 gram + cocci: Staph aureus Group A beta hemolytic strep

Acute lymphangitis Don't forget superficial thrombophlebitis. TX: antibiotics

Very common inflammatory process of lymphatic channels GAS or staph Starts w/ wound, may progress to bacteremia Red linear streak enlarged and tender to the touch

Antimicrobial peptides (AMPs)

What are released by sweat, saliva and keratinocytes that kill bacteria and activate the immune system

Primary skin infections Secondary infection of a primary disease (infected atopic dermatitis) Skin lesions d/t blood infection Reactive skin infection d/t bacteria somewhere else (e.g., erythema nodosum due to streptococcal pharyngitis).

What are the 4 major categories of skin bacterial infections?

1st degree upper 2nd is in epidermis blister 3rd degree is scarring = dermis If it goes into dermis = scar

What are the different types of burns?

Come Let's Get Sun Burned Corneum (cornified) superficial Lucidum (shiny) Granulosum (granular) Spinosum (prickle cell layer) Basale (basal cells)

What are the layers of the skin?

Maceration ( the softening and whitening of skin that is kept constantly wet) Shaving Chronic wounds Excoriation of pruitic bites Disruption of skin by other pathogens

What causes skin barrier dysfunction allowing for infection to occur?

Hemidesmosomes connects keratin in basal cells to the underlying basement membrane. Proteins called integrins.

What is affected by bullous pemphigoid

Desmosome area- Zona adherens (intermediate junction)- composed of calcium-dependent adhesion proteins called cadherins. Help to resist shearing forces. Desmosomes. Desmoglein is a type of cadherin.

What is affected by pemphigus vulgaris?

Pitted Keratolysis: superficial Tx benzoyl peroxide Drysol for the excessive sweating

Young adult male pt presents c/o sweating feet and a weird pitting foot appearance This is associated w/ micrococcus sedentarius (gram + spheres that make keratinase breaking down keratin = pits) Not contagious Tends to affect weight bearing areas of the foot on the plantar surface

Endotoxins

[[Heat stable]] lipopolysaccharide-protein complexes which form structural components of the cell wall of mostly Gram negative bacteria. Liberated only on cell lysis or death of bacteria. Specific receptors not found

Keratosis pilaris

caused by keratotic follicular plugging, patients typically present with small follicular papules on the extensor surfaces of the upper arms or thighs. Erythema may be present.

Group A beta- hemolytic streptococci

secondary invader of traumatic skin lesions and causes impetigo, erysipelas, cellulitis and lymphadenitis.