5. Medicine II_Skin and Soft Tissue Infections_2014A

SkinDr. and Soft Solante

 Immunosuppression  Presence of foreign body (IV catheter: if not change/replace within 7 days, most patient will develop phlebitis)

OUTLINE Introduction Host and Microbes Anatomy of the skin Pathophysiology Microorganisms Pyodermas a. Superficial Bacterial Skin Infections b. Folliculitis c. Furuncle d. Carbuncle e. Impetigo VII. Cellulitis VIII. Erysipelas IX. Hidradenitis suppurativa X. Treatment I. II. III. IV. V. VI.

 Most organisms causing SSTI has a virulence factor. They have the tendency to adhere to the skin and produce anti-phagocytic factors, enzymes toxins including PVL (Panton-valentine leukocidin) cytotoxin.  Important: PVL (what organism produces PVL?)  Staphylococcus aureus  Remember: Host conditions (listed in the table) is the driver why patient will develop severe SSTI.

INTRODUCTION  Among the most common disorders treated by primary care physicians (general practitioners) – because skin is the biggest and most widely exposed organ  Range from mild pyodermas to life-threatening necrotizing infections  Skin provides initial major barrier between humans and their environment  Skin infections easily detected  recognizable inflammatory changes (rubor, calor, dolor, tumor)  Overall rate of outpatient skin visits for skin infections: 48.3/1000 population  Admission rate 129/100,000 population  Always distinguish primary vs. secondary pyodermas (brought about by trauma, medications, etc.)  Early diagnosis requires a high level of suspicion in instances of unexplained fever and of pain and tenderness in the soft tissue, even in the absence of acute cutaneous inflammation [2013B]

 Severe form of skin infection: needs hospital admission 1. Necrotizing fasciitis 2. Cellulitis (can be a severe form if it involves the face)

HOST AND MICROBES        Local  Defense  Factors Bacteria l Virulenc e Factors

Host Conditio ns

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Adherence Factors Antiphagocytic Factors: Streptococcus Enzymes Toxins B-lactamase production: Gram (-) bacteria PVL (Panton-valentin leukocidin) Cytotoxin: specific for Staph. aureus Intact skin (barrier effect) Low pH concentration – prevents microorganisms from invading Relative dryness – not too dry, not too moist Antibacterial secretions of sebaceous glands Abnormalities of epidermis (eczema, dermatitis, fungal infections) – increased risk for SSTI because these conditions affect theskin barrier so, skin colonizers (e.g. Staph. aureus)can easily penetrate into the subcutaneous tissue Breaks of skin (abrasions, trauma, insect/human bites, surgical incision) Ulcers (diabetic foot pressure sores) Ischemia – patients with claudication

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ANATOMY OF THE SKIN Epidermis

 Avascular sheet of constantly renewing cells; 0.1mm on average (0.8 to 1.4mm on palms and soles)  Basal cell layer composed of keratinocytes o Divide, differentiate, slough o Also of Langerhans cells and melanocytes o Stratum corneum o Stratified, tough layer of dead cells o Protective sheath -

Disruption of this layer by burns or bites, abrasions, foreign bodies, primary dermatologic disorders (e.g., herpes simplex, varicella, ecthyma gangrenosum), surgery, or vascular or pressure ulcer allows penetration of bacteria to the deeper structures. [2013B]

o Epidermis is the initial protection against invading organism o Area where most of your organism will colonize or lodge Dermis  Several millimeters thick; separated from epidermis by basement membrane  Contains collagen and elastin embedded in glycoprotein matrix o Provides strength and resilience  Also contains blood vessels, lymphatics, fibroblasts, skin appendages, eccrine sweat glands, sebaceous glands, and hair follicles [2013B]: o o

Important that break in the skin would not go any deeper and prevent affectation of this area Rich plexus of capillaries beneath the dermal papillae provides nutrition to the stratum germinativum, and physiologic responses of this plexus produce important clinical signs and symptoms.

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Also provides bacteria with access to the circulation, thereby facilitating local spread or bacteremia. Postcapillary venules of this plexus are a major site of polymorphonuclear leukocyte sequestration, diapedesis and chemotaxis to the site of cutaneous infection. Hair follicle can serve as a portal either for components of the normal flora (e.g., Staphylococcus) or for extrinsic bacteria (e.g., Pseudomonas in hot-tub folliculitis)

varicella, ecthyma gangrenosum), surgery, or vascular or pressure ulcer allows penetration of bacteria to the deeper structures. Similarly, the hair follicle can serve as a portal either for components of the normal flora (e.g., Staphylococcus) or for extrinsic bacteria (e.g., Pseudomonas in hot-tub folliculitis). [Harrisons]

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 Associated with gaps in stratum corneum susceptible to invasion by pathogens  Thickest portion and most vascular portion of the skin.  Includes sweat glands and apocrine glands.  Layer of the skin that will induce systemic spread of infection  Intracellular infection of the squamous epithelium with vesicle formation may arise from: [2013B] o Cutaneous inoculation: herpes simplex virus (HSV) type 1 o Dermal capillary plexus: varicella and infections due to other viruses associated with viremia; o Cutaneous nerve roots: herpes zoster

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Subcutaneous Fat Thickness varies over the body Mostly contains lipid cells Cushion for the skin Beneath is the superficial fascia (cut-off for cellulitis and fasciitis) o Separates skin from underlying muscle o Provides pathway for spread of infection  Subcutaneous fat is the source of most severe type of infection

NOTE: [2013B]  Patients with systemic manifestation and cellulitis are admitted and given antibiotics since there’s a tendency of fast spread into deeper parts  In SSTI, if the infection is able to extend into muscle and fascia layer, the patient would usually complain of pain. No more erythema, warmth tenderness  have high index of suspicion that the infection has spread deeper  Edema with purple bullae, ecchymosis, and cutaneous anesthesia suggests loss of vascular integrity and necessitates exploration of the deeper structures for evidence of necrotizing fasciitis or myonecrosis.

PATHOPHYSIOLOGY  Skin infection occurs when there is a defect in the integrity of the epidermis o Colonization(presence of bacteria not yet causing a disease) tissue invasion (once barrier is broken) clinical manifestations o

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Protection against infection of the epidermis depends on the mechanical barrier afforded by the stratum corneum, since the epidermis itself is devoid of blood vessels Disruption of this layer by burns or bites, abrasions, foreign bodies, primary dermatologic disorders (e.g., herpes simplex,

Daph, Jaff, Gill, Gubs

 Physical characteristics of skin that reduce bacterial multiplication: o Relatively low pH (5.5) o Presence of natural antibacterial substances in secretions of sebaceous glands o Relative dryness of normal skin o Bacterial interference (suppressive effect of normal skin flora of the inciting organism)

MICROORGANISMS  SSTI is always caused by gram positive organism.  Skin colonizers, not pathogenic normal skin colonizers. They are not microorganisms that are potential to cause infection. o Proprionibacterium spp. o Coagulase negative Staphylococcus (CoNS) o Corynebacterium spp.  Transient colonizers - they are colonizers of your skin but they have capability to cause an infection. They can be found in your skin once your immune system or your host defense mechanism will be altered, then they become a potential pathogen. o S. aureus o B hemolytic streptococci o Enterobacteriaceae o Pseudomonas spp. o Enterococcus spp. o Anaerobes

PYODERMAS Superficial Bacterial Skin Infections  Primary superficial skin infections  Caused by B hemolytic streptococci o GAS (group A Streptococcus) Also cause pharyngitis -

and glomerulonephritis. Important to determine the possibility that the patient has sore throat then suddenly acquires SSTI

o S. aureus Mostly mild, and most do not require IV antibiotics or hospitalization – OPD treatment  Colonization of S. pyogenes or S. aureus usually precedes clinical infection

Folliculitis  One of the most common mild infection  Infection within hair follicle and apocrine glands o S. aureus – most common cause of localized folliculitis

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GNB (gram negative bacteria)

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o Candida spp.  Present as 2- to 5- mm erythematous papules that surround a hair follicle often with central postulation  Systemic manifestations rare – mostly, selflimited. Unless patient has diabetes or severely immunocompromised (antibiotics may be given)  Lesions may drain spontaneously or resolve without scarring even in the absence of antimicrobial  Sebaceous glands empty into hair follicles and ducts and, if these portals are blocked, form sebaceous cysts that may resemble staphylococcal abscesses or may become secondarily infected. [Harrisons]

Whirlpool folliculitis  Generalized fine, papular pustules  Caused by P. aeruginosa  Modified apocrine glands of the external canal of the areola are particularly susceptible o Syndrome of rash accompanied by otitis externa, mastitis, malaise, fever  Average incubation period is 2 days  Follows immersion in swimming pools or hot tubs – most important risk factor o Waters that is insufficiently chlorinated and maintained [Harrisons]

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temperature

Carbuncle    

Larger, deeper, indurated, more serious Confluent infection consisting of multiple furuncles Occur on nape, back, thighs Begin as erythematous, firm, and tender nodular lesions fluctuant mass that may drain pus spontaneously o o

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If not drained, seeks for other exit somewhere else Staph aureus in the dangerous triangle of the face: if ruptured may cause cavernous sinus thrombosis (infectious emergency)

Blood stream infection may occur Antimicrobial and drainage of lesion needed Most common risk factor: o Immunodeficiency: seen in patients with HIV, diabetic, elderly, obesity Take note of the difference between furuncle and carbuncle: o Furuncle: only one draining point o Carbuncle: more draining points

37–40°C.

 Usually self-limited Swimmer’s Itch (2013B)  Warm water temperatures and alkaline pH are suitable for mollusks (intermediate hosts) of freshwater avian schistosomes  Free-swimming schistosomal cercariae readily penetrate human hair follicles or pores but quickly die and elicit a brisk allergic reaction, causing intense itching and erythema

Furuncle

 Folliculitis extending beyond the hair follicle into subcutaneous tissues o Deeper inflammatory nodule  Usually measure 2 manifestations of inflammation (purulence, or erythema, pain,tenderness, warmth, or induration), but any cellulitis/erythema extends 1 of the following characteristics: cellulitis extending >2 cm, lymphangitic streaking, spread beneath the superficial fascia, deeptissue abscess, gangrene, and involvement of muscle, tendon, joint or bone Infection in a patient with systemic toxicity or metabolic instability (e.g., fever, chills, tachycardia, hypotension, confusion, vomiting, leukocytosis, acidosis, severe hyperglycemia, or azotemia)

Infectio n severity Uninfecte d Mild

PEDIS grade

Moderate

3

Severe

4

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MYOSITIS/MYONECROSIS  Muscle involvement can occur with viral infection (e.g., influenza, dengue, or coxsackievirus B infection) or parasitic invasion (e.g., trichinellosis, cysticercosis, or toxoplasmosis).  Anaerobic streptococcal myositis o Usually related to trauma or surgical procedure

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 Pyomyositis o Due to S. aureus o Usually monomicrobial, often in the extremity, presenting with localized pain in a single muscle group or muscle spasm and fever  Synergistic necrotizing cellulitis o Also known as necrotizing cutaneous myositis and synergistic necrotizing cellulitis o Combined involvement of superficial tissues, fascial planes and muscle groups  Fournier gangrene o Most patients are diabetic o Involves the scrotum and penis or vulva; onset can be insidious or explosive o Frequently polymcrobial  Clostridial myonecrosis o Most frequent cause of trauma-associated gas gangrene o First reliable symptom: increasingly severe pain beginning at the injury site < 24 hrs after infection – Skin may initially be pale, but can quickly change to bronze then to a purplish red – Infected region is tense and tender, and bullae filled with reddish-blue fluid could appear o Spontaneous gangrene – seen in patients with neutropenia and GI malignancy – Frequently due to C. septicum

Daph, Jaff, Gill, Gubs

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“DM FOOT” INFECTIONS Risk factors Peripheral motor neuropathy – foot anatomy Peripheral sensory neuropathy – sensation (numbness) Peripheral autonomic neuropathy – sweating Neuro-osteoarthropathic deformities (i.e., Charcot disease) or limited joint mobility Vascular (arterial) insufficiency Hyperglycemia and other metabolic derangements Patient disabilities – vision (retinopathies), mobilities Maladaptive patient behaviors - adherence Health care system failures – education & monitoring

SECONDARY OSTEOMYELITIS Contiguous source Peripheral vascular disease (PVD) in diabetics S. aureus – most frequent cause May also involve Gram negative bacilli (GNB) and anaerobes  4-6 weeks antibiotic therapy plus surgical intervention o Shorter course for superficial types  Prevention o Meticulous skin care using antibacterial soap, and washing frequently o Separate wash cloth and towel o Prolonged antibiotic treatment no more effective than 10-14 day-course in preventing recurrences o Nasal application of 2% ointment for 5 days to eliminate S.aureus colonization  o  o

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