Skin and Subcutaneous Tissue Infections

·begins as small vesicles that rapidly pustulate and rupture, drying to form the characteristic “honey-colored crusts”, which may coalesce ·most common in children, and during the hot, humid summer weather. Epidemics common. ·painless; heals without scarring ·*group A strep (Strep pyogenes) most common historically, but Staph aureus just as common now ·Tx: -topical Mupirocin (Bactroban) -dicloxacillin -erythromycin -cephalexin

-distinctive type of cellulitis with prominent lymphatic involvement -almost always due to group A strep; occ. Staph aureus -historically, most common on face, now 70-80% are on the lower extremities -painful lesion with bright red, edematous, indurated appearance *sharply demarcated border from adjacent normal skin Tx: -dicloxacillin -nafcillin or oxacillin -cephalexin -cefazolin -erythromycin -Vanco, if MRSA suspected

An acute spreading infection of the skin that extends deeper than erysipelas & involves sub-Q tissues ·group A strep and Staph aureus are the most frequent organisms; other β-hemolytic strep (B, C, G) also ·Vibrio vulnificus à associated with salt water ·erythema, edema, tenderness, warmth of skin ·systemic symptoms (chills, fever, tachycardia, hypotension) common and often precede clinical findings à suggests bacteremia ·regional lymphadenopathy ·search for portal of entry

·if systemically ill-appearing, admit for blood cultures, IV abx, etc. ·Diff. Dx: -Bullous impetigo -Myositis -Skin abscesses -Chronic venous stasis -Toxin syndromes -DVT -Fasciitis -Septic arthritis/osteo ·Tx: PO amox/clav dicloxacillin,cephalexin,·clindamycin IV · ·oxacillin · ·cefazolin · ·vancomycin (if MRSA suspected) ·TMP/SMZ or erythro

Develops when an infection is not contained locally but spreads along lymphatic channels - most often group A strep, but other streptococci common; Staph aureus less common -systemic sx may develop quickly, before evidence of infection at initial site of inoculation -red, linear streaks extend toward regional LN’s, which are enlarged and tender -peripheral edema is common -bacteremia often complicates -recurrent infx common with chronic lymphedema

-pyoderma within hair follicles and apocrine glands -small (2-5mm), erythematous, sometimes pruritic papules, pustules -Staph aureus usual etiologic organism -Pseudamonas aeruginosa à “hot tub” folliculitis -enteric gram (-)’s and Candida are uncommon, but consider in immunocompromised hosts *saline compresses, topical antibacterials (mupirocin) or antifungals (clotrimazole) usually sufficient

Deep inflammatory nodule that develops from preceding folliculitis -occur along hair follicles and where we perspire (neck, face, axillae, buttocks) -Staph aureus almost invariably etiologic organism -firm, tender, red nodule that commonly becomes fluctuant and sponteously drains

More extensive process extending into sub-Q fat, where multiple septated abscesses develop -pt. may be acutely ill with systemic findings

predisposing factors:diabetes, obesity, poor hygiene are all -small lesions generally respond to warm compresses, abx -larger carbuncles may require admission, operative debridement, IV abx. Abx: -cephalexin -clindamycin -diclox -vancomycin (if MRSA) -amox/clav -TMP/SMZ -if recurrence a problem, nasal swab to rule out colonization with S. aureus (especially MRSA)

Chronic disease of apocrine glands in axillary, genital, and perineal areas -tender reddish-purple nodules that slowly become fluctuant and drain, with irregular sinus tracts and new crops of lesions developing -initially not infected, but infection frequently develops secondarily à polymicrobial *very difficult problem to take care, especially when the process is extensive -abx (based on culture results) and warm compresses may be helpful, but surgery often required

Inflammatory skin disorder of the lower legs due to chronic venous insufficiency -generally affects middle-aged to elderly folks -obesity, prior trauma/surgery, DVT, CHF are all predisposing factors -disrupted function of one-way valvular system in the deep venous plexus results in backflow to the superficial system à  venous pressure à ↓ valvular competency -precursor to more serious problems à ulcerations, episodes of cellulitis

Signs & Symptoms: -insidious onset of pruritits -history of dependent leg edema which worsens as day progresses -medial ankle most frequently + severely involved -diffuse red-brown-purple skin ∆’s -atrophic patches, loss of hair -often “weep” serous fluid **damage irreversible; key is to slow progression

*Key to most patients is to get the chronic edema under control à lifestyle modification ·compression stockings/ACE wraps (if no PVD) · bedrest even if just few hours/day ·diuretics if no contraindication ·consider admission to SAR when pt. can’t manage on their own -topical steroids to ↓ inflammation in short-term -emollients (Eucerin, etc.) long-term

Caused by varicella-zoster virus (VZV) *unilateral, vesicular eruption with dermatomal pattern -thoracic and lumbar dermatomes most common -may involve the CN’s *herpes zoster opthalmicus à sight-threatening -generally, pain precedes rash by 48-72 hrs – often misdiagnosed early. -new lesions continue to form for 3-5 days, longer in immunocompromised pts

Consider “contagious” until lesions fully scabbed over -may take a month or more for skin to return to normal -CSF analysis may show pleocytosis even without evidence of mengitis -acyclovir will ↓ amount and shorten duration of lesions *post-herpetic neuralgia (PHN) will affect >50% over 50 yo and pain can be incapacitating in some -NSAIDS/narcotics, lidocaine patches, tri- cyclics and other antidepressants, anti-Sz drugs, biofeedback, etc. have all been used -prednisone has been shown to possibly ↓ % of PHN