Skin and soft tissue infections 3

M Al Madadha

Sources :

Harrisons infectious diseases 2nd edition, Oxford Handbook of Infectious Diseases and Microbiology 2nd edition

Hand foot and mouth disease

• Occurs in outbreaks, typically in schools (we had one a few months ago in nov)

• The typical disease:

• Children under 10 are mostly affected, more-so under 5

• The causative agents are• Coxsackie virus A16 (an enterovirus)

• Enterovirus 71 ( HAS BEEN ASSOCIATED WITH ENCEPHALITIS AND MYOCARDITIS)

• Atypical disease:

• Higher age groups ( adults and teenagers)

• Caused by coxsackie A6

• Can have severe presentation with fever, arthralgia and flu like symptoms with the rash as vesicles that affect (the nose, cheeks, extensor arms, elbows, thighs, buttocks, groin)

• Both typical and atypical disease are transmitted by fecooral route, or direct close contact to rash

Signs and symptoms of HFMD

Symptoms and signs:

• URT symptoms before the skin lesions occur

• With fever, malaise and pharyngitis!

• The rash is typically on the soles and palms and buttocks

• The rash:

• ORAL : football shaped (eye shaped) painful vesicles, involves the buccal mucosa and tongue. (spares posterior pharynx as opposed to herpangina that spares anterior pharynx)

• SKIN: red papules that progress to gray vesicles on the soles and palms and buttocks

https://cdn1.dailyhealthpost.com/wp-content/uploads/2016/11/hand-foot-and-mouth-disease-918x420.jpg

Rx

• Only symptomatic treatment ( treat fever, pain)

• Must maintain hydration

Consider hospital admission in severe illness (enterovirus A71) which has high morbidity and mortality

Smallpox

• • Smallpox is caused by variola virus, anي orthopoxvirus.

• There are two strains: variola major (mortality 20–50%) and variola minor

• • The last reported case was in Somalia in 1977, and the virus was declared eradicated by the WHO in 1980.

• Virus stocks exist in two laboratories, and there are concerns about its potential use as a bioterrorism agent

• • The incubation period is 10–12 days and is followed by a prodromal period of 1–2 days.

• The centrifugal rash is initially maculopapular and progresses to vesicles, pustules, and scabs over 1–2 weeks.

• Death may occur with fulminant disease.

• • Diagnosis may be confirmed by EM or PCR (to differentiate it from other poxviruses).

• • There is no specific treatment (supportive)

• Orf is caused by a DNA virus related to smallpox virus (parapoxvirus).

• Also called soremouth infection and infects the fingers of individuals who work around goats and sheep.

• Usually coming into contact with infected animals (petting, feedings, harnesses,bite) , but can also transmit between people.

• There is no treatment , however, the papules may become infected by bacteria, or immune compromised

• Can be infected multiple times through out life (each time is less severe).

• Six stages: each about a week

• Small papule nodules ulcerate and crust

http://www.farmhealthonline.com/wp-content/uploads/2015/09/Orf-MSD-animal-health.co_.uk_.jpghttp://c.ymcdn.com/sites/www.aocd.org/resource/resmgr/ddb_high/orf_1_high.jpg

Molluscum contagiosum

• virus induces flaccid vesicles on the skin of healthy and immunocompromised individuals.

• Mcc 2-11 year olds, in adults as part of STD- transmission by direct contact

• Single or small clusters of vesicles (<30) raised papules, may look like vesicles, not erythematous!, with central umbilication

• On face and trunk, pubis and rarely mucosa

• Resolve on their own (cryotherapy or other dermatologic treatments can be done) may be present for YEARS

• If associated with HIV SEVERE

https://www.healthline.com/hlcmsresource/images/galleries/Molluscum-Contagiosum/molluscum_contagiosum_adult_stomach.jpg

Infections Associated with Crusted Lesions

Impetigo •

• Caused by S. aureus and/or GASusual skin flora, with local trauma that allows colonizing bacteria to break through.

• Commonly affects children (2-5 years) in tropical/subtropical regions; also prevalent in temperate regions in summer months (so warm weather >).

• It is the most common bacterial skin infection in children

• 70% are non bullous and appear as crusted legions

• It is highly contagious (scratching, towels, clothing, autoinfection and spread in daycares)

• • Clinical features—occurs on the face and extremities.

• Lesions start as small macule or papule small vesicles (with erythema) develop into flaccid bullae rupture, releasing a yellow discharge which forms thick crusts.

• Usually seen with regional LAP

• Can cause cellulitis ( deeper infection, see later)

• Or PSGN ( post strep GN)

• • Treatment—mupirocin is the best topical agent.

Patients who have numerous lesions or who do not respond to topical treatment should receive oral antibiotics (flucloxacillin or cefalexin).

If MRSA is suspected/isolated, then treatment with doxycycline, clindamycin, or co-trimoxazole.

http://diseasespictures.com/wp-content/uploads/2013/12/Impetigo-2.jpg

Ecthyma

• • Punched-out ulcers surrounded by raised deep red/violet margins invades into the dermis and leaves highly inflamed regions on the sides

• • Caused by S. aureus or GAS. Other similar lesions (ecthyma gangrenosum) may occur with P. aeruginosa in neutropenic (reduced neutrophils in blood) patients.

• • Empiric treatment is with flucloxacillin or cephalexin (unless cultures yield streptococci alone, in which case penicillin is appropriate).

• Antipseudomonal agents, e.g. piperacillin-tazobactam, should be given for P. aeruginosa infections.

http://www.pcds.org.uk/ee/images/made/ee/images/uploads/clinical/Ecthyma_gangrenosum_pseud_bact_800_600_70_http:www.pcds.org.ukeeassetsimgwatermark.gif_0_0_80_r_b_-5_-5_.jpg

Dermatophytes

• A group of fungi capable of invading the dead keratin of skin, hair, and nails (require keratin for their growth).

• They are spread by direct contact with patients or animals or soil

• Clinical classification is by age group:

Children :

-tinea capitis (scalp hair and the commonest in children),

-tinea corporis (trunk and limbs)

-tinea faciale (face)

cont.

Adolescents:

-tinea manuum and pedis (palms and soles – athletes foot-, and the commonest overall worldwide)

-tinea unguium (nail—also known as onychomycosis)

Adults:

-tinea cruris (groin) AKA jock itch

-tinea barbae (beard area and neck)

-Tinea corporis Gladiatorum ( wrestlers)

Ringworm, corporis, circinata

https://www.news-medical.net/image.axd?picture=Ringworm%20shutterstock_484652500%5B12%5D_1.jpg

https://img.webmd.com/dtmcms/live/webmd/consumer_assets/site_images/articles/health_tools/ringworm_slideshow/dermnet_photo_of_ringworm_on_scalp.jpg?resize=646px:*&output-quality=100

http://ringwormtinea.com/wp-content/uploads/2015/02/11.jpg

Demarcation lines hint at A possible dermatophyteInfection, rather than acnevulgaris

Tinea corporis psoriasis

https://www.sporthuesca.com/piscinas-antihigienicas/

http://mulicia.pixnet.net/blog/post/26749579-%E7%94%B2%E7%99%AC-onychomycosis%EF%BC%8Ctinea-unguium

DIAGNOSIS

• The goal is to distinguish dermatophytoses from other causes of skin inflammation (such as psoriasis).

• Infections caused by bacteria, other fungi, and noninfectious disorders (psoriasis, contact dermatitis) may have similar features.

• KOH mounts of skin scrapings and infected hairs demonstrate hyphae.

• Some species fluoresce by a U.V. lamp.

• Culture is used when KOH preparations are negative.

TREATMENT AND PREVENTION

• Many local skin infections resolve spontaneously without chemotherapy.

• Topical use of tolnaftate, allylamines, or azoles is usually sufficient .

• Nail bed and more extensive skin infections require systemic therapy with griseofulvin or itraconazole and terbinafine + combined with topical therapy.

• Therapy must be continued over weeks to months, and relapses may occur.

• No specific preventive measures such as vaccines exist.

Cutaneous leishmaniasis

https://web.stanford.edu/group/parasites/ParaSites2006/Leishmaniasis/images/Cutaneous%20map2.gif

Vector and parasite

• Transmitted by sandflies• Trypanosome (single flagellae)• Has two forms: disease causing (resistant) form and infectious motile form• On CBC shows reduced cell count (red, white or all), Dx by culture• Deemed as a neglected tropical illness (causes mortality with small effort

to battle it)• Has many types (other than visceral),• 1) old world in Asia, Africa and Europe long incubation time (MONTHS

2-24)• Skin lesion(s) on the face or leg: papules become necrotic and then

pigmented scars ( papule at site of bite small nodules painLESSulcer crust (pigmented) leave ugly scars after healing (social issues)

https://www.cdc.gov/parasites/images/leishmaniasis/home_page_image_leishmaniasis.jpg

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4183486/figure/pntd-0003208-g001/

• Becoming an increasing problem in surrounding countries (syria and iraq) with poor sanitation and reduced living standards.

• L. major and L. tropics is most common

• Resolve over months, round depressed scars remain

• May resemble other skin lesions (nodular lymphangitis) caused by waterborne pathogens (such as Sporothrix schenckii, Nocardiabrasiliensis, Mycobacterium marinum, Leishmania (Viannia).

• Nodular lymphangitis- granulamatous reaction to these pathogens on the path of lymphatics

https://online.epocrates.com/data_dx/reg/920/img/920-1-hlight.jpg

• Dx of CL:

• Remove crusts and take skin scrape for microbiology

• Biopsy (punch or needle aspirate) to retrieve organism and detect under microscope.

• Rx:

• Local heat to area for 2-3 hours a day

• Pentavalent antimonials (group of chemicals given for CL)

• Others include: (Liposomal amphotericin B, Oral miltefosine, Pentamidine )

• Given for a minimum of 20 days!

Infections Associated with Bullae

• Staphylococcal scalded-skin syndrome (SSSS) in neonates is caused by a toxin (exfoliatin) from phage group II (bacteria is infected by this phage, acquires the gene to produce the toxin)

• S. aureus. SSSS must be distinguished from toxic epidermal necrolysis (TEN), which occurs primarily in adults, is drug-induced, and is associated with a higher mortality rate.

• Punch biopsy with frozen section is useful in making this distinction since the cleavage plane is the stratum corneum in SSSS and the stratum germinatum in TEN

Staphylococcal scalded-skin syndrome (SSSS)

• Due to HEMATOLOGIC (not local) spread of staphylococcal EXOTOXIN.

• That means there is a point of infection somewhere else in the body

(Otitis media, Respiratory tract infection)

• Staph aureus that carry exfoliative toxins A and B (only about 5% of all S. aureus strains do carry these toxins)

• Breaks down desmoglein-1 resulting in Acantholysis (breakage of cell to cell adhesions)

https://image.slidesharecdn.com/staphylococcalscaldedskinsyndrome-140328015508-phpapp01/95/staphylococcal-scalded-skin-syndrome-7-638.jpg?cb=1395971748

https://upload.wikimedia.org/wikipedia/commons/thumb/3/3e/OSC_Microbio_21_02_SSSS.jpg/300px-OSC_Microbio_21_02_SSSS.jpg

http://www.dermnet.com/dn2/allJPG3/Staphylococcal-Scalded-Skin-Syndrome-3.jpg

SSSS

• Symptoms:• Preceded by a prodromal illness ( URTI ) or• Otitis Media, Pharyngitis, Conjunctivitis• Then the actue phase hits: fever! + malaise (loss of fluids) and red

painful skin with bullae formation

• Signs:• Paper thin (peeling) skin• Large flaccid BLISTERS, more in the flexor creases (see image above)• Mucous membranes are SPARED!• Positive Nikolsky’s sign (detects acantholysis)

You make the bullae spread further by rubbing the side from affected skin to non affected skin

SSSS Dx and Rx

• Dx: blood cultures are often positive (remember hematologic spread of toxin –bacteremia)

• Skin biopsy will show typical acantholysis

• In lab we can do exotoxin assay

• Rx:

• MUST ADMIT THE CHILD ( burn unit or ICU!)

• Systemic IV antibiotics are given (anti MRSA or anti S. aureus) +

• Systemic steroids ( only if patient doesn’t look toxic/otherwise it is not used)

• In severe cases (IV Immunoglobulins and plasmapheresis) removal of plasma

As for TEN

• TEN, primarily seen in adults is potentially fatal.

• Intravenous γ-globulin is a promising treatment for TEN.

http://i.dailymail.co.uk/i/pix/2016/12/07/11/3B2162BB00000578-4009166-image-a-41_1481111581525.jpg

Necrotizing Fasciitis

Necrotizing fasciitis

• RAPIDLY progressing infection in the area between the fascia and deep subcutaneous tissue.

• Many risk factors increase the risk (see table next slide)

• Fibrous bands in this area prevents spread of infection• These bands are present in the head but not in the extremities ( thus

extremities are more susceptible)

• >50% in extermities

• 20% in perineum or buttocks ( esp in DM and alcoholics)

• 18% in trunk

• 9% head and neck

• Necrotizing fasciitis (GAS) and gas gangrene (anaerobic clostridialinfection) also induce bulla formation.

• In the USA, the estimated incidence of invasive GAS infection is 3.5 cases per 100000 persons—necrotizing infections account for 6% of these.

Risk factors associated with necrotizing fasciitis

Malnutrition Patient conditions

Immuno-compromised

Poor blood supply

Skin trauma in last 3 months

Breaks in mucosa of GI or GU tracts (anaerobes)

-Hypo-albuminemia

-Alcoholism

-Cirrhosis

- >50 Year olds

-Obesity

-Cancer

-Steroid therapy

-Heart disease

-PVD

-DM

-Burns-penetrating trauma-IV drugs-surgery

-colon cancer-diverticulae-hemorrhoids or fissues-urethral tears-cirrhosis

Signs and Symptoms – occur in order

• Pain/tenderness• Unexplained fever (Early diagnosis may be difficult when pain or

unexplained fever is the only presenting manifestation, remember infection is deep, might not present with pain yet )

• Swelling• Dark red induration• BULLAE, filled with blueish or purple fluid• Thrombosis of dermal blood vessels (The affected area becomes

anaesthetic as a result of small vessel thrombosis and destruction of superficial nerves)

• Extension to deep fascia with rapid spread• Most progressed symptoms : toxicity , shock and multi organ failures

Pain / redness

http://www.antimicrobe.org/new/printout/e11printout/e11cause/e11cau9.jpg

Dark red induration /swelling

Progressing to bullae /thrombosis

https://osuemed.files.wordpress.com/2012/09/diff-patient-with-blebs.jpg

http://img.medscapestatic.com/pi/meds/ckb/55/37455tn.jpg

Microbiology causes:

• A) Polymicrobial (• Type I necrotizing fasciitis involves at least one anaerobic species ( Bacteroides or Peptostreptococcus spp.), as well as one or more facultative anaerobic species (e.g. non-GAS, E. coli, Enterobacter, Klebsiella, Proteus spp.).

• usually a mix of aerobes and anaerobic bacteria ( clostridium perfringens)

• 1 - Break in Gastrointestinal or Genitourinary mucosa, typically on trunk and extremities

• 2- Fournier's Gangrene (in genitalia/perineal area)

• 3- mixed infection usually have comorbid states ( DM, PVD, immunecompromised)

Microbiology causes…cont

• B) Type II necrotizing fasciitis is usually caused by GAS alone or in combination with other species (e.g. S. aureus). Group A , Beta hemolytic strep (GAS), S. pyogenes +- S. aureus

• Strains of MRSA that produce the PantonValentine leukocidin (PVL) toxin have been reported to cause necrotizing fasciitis.

• 1) usually following trauma in otherwise healthy individual

or IV drug abusers (skin popping)

2) Fasciitis progresses to skin contusions due to seeding by transient bactermia

3) Gas production if mixed infections occurs

4) Severe toxicity and renal impairments shock

5) Myositis ( destruction of muscle tissue markedly increases CPK)

6) Mortality is high (upto 50%!)

Skin popping/drug abuse = basically SubQinjections in same area over and over

• Necrotizing fasciitis caused by mixed aerobic-anaerobic bacteria begins with a breach in the integrity of a mucous membrane barrier, such as the mucosa of the gastrointestinal or genitourinary tract.

• The portal can be a malignancy, a diverticulum, a hemorrhoid, an anal fissure, or a urethral tear.

• Other predisposing factors include peripheral vascular disease, diabetes mellitus, surgery, and penetrating injury to the abdomen.

• Leakage into the perineal area results in a syndrome called Fournier’s gangrene, characterized by massive swelling of the scrotum and penis with extension into the perineum or the abdominal wall and legs.

• In the newborn, necrotizing fasciitis may complicate omphalitis and spread to involve the abdominal wall, flanks, and chest wall.

• Fournier’s gangrene is a form of necrotizing fasciitis that affects the male genitals and is usually polymicrobial.

• Craniofacial necrotizing fasciitis is usually associated with trauma and caused by GAS.

• Cervical necrotizing fasciitis is usually associated with dental or pharyngeal infections and is polymicrobial.

https://image.slidesharecdn.com/omphalitis2-120928165437-phpapp01/95/omphalitis-2-11-728.jpg?cb=1348851384

Dx of necrotizing fasciitis

Clinical findings are suggestive + surgical exploration/sample:

a) Altered mental status

b) Soft tissue infection signs (redness/swelling/pain) 70-80% of casesBullae Pain is typically exaggerated out of examTenderness is outside the red erythematous borders (indicates further progress)

c) are only seen in ¼ of cases

d) Fever in less than 50% of the cases!

e) Low BP in 21%

f) crepitation (feeling of air pockets under skin upon examination) in 20%

Rx - empiric

• 3 drug combo/ 2 drug combo/ 1 drug ( each +MRSA coverage)

3 drug combo :

• 1- anaerobic coverage (and inhibits ribosomal production of toxins)= Clindamycin

• 2- G +ve coverage (Ampicillin-sulbactam) or ( Piperacillin-tazobactam)

• 3- G-ve coverage (Ciprofloxacin)

• 2 drug combo (Cefotaxime covers G+ and G- bacteria) + (anaerobic coverage by metronidazole or clindamycin)

• 1 drug combo ( Carbapenem 0 Imipenem, meropenem, ertapenem)

• The MRSA coverage to be added to any chosen empiric regimen includes = Vancomycin or Linezolid

• Hemorrhagic bullae may indicate presence of vibrio vulnificus, in which case doxycycline is used

Rx.

• Surgical debridement, and treatment in hospital Emergency surgical exploration and debridement confirm the diagnosis and are the mainstay of therapy.

• Reducing compartment pressure in extremities

• Prophylaxis for exposed house hold members (penicillin, rifampin, clindamycin or azirthromycin)

Gas gangrene ( Clostridium infection)

Gas production due to anaerobic bacteria

• Typically due to contaminated DEEP wounds -no oxygen- (surgery, car crash..etc) to introduce spores of G+ve clostridia into the wound

• Also progresses similarly to other types: fasciitis toxemia organ failure

• Gangrene usually occurs following muscle injury and contamination of the wound by soil or foreign material containing clostridial spores.

• C. perfringens is the predominant cause (80–95%), and its pathological effects are mediated by α and λ toxins

Cont.. etiology and pathogenesis

• Spontaneous or non-traumatic gas gangrene may occur in the absence of an obvious wound.

• This form is usually caused by C. septicum and associated with intestinal abnormalities, e.g. colonic cancer, diverticulitis, bowel infarction, necrotizing enterocolitis. •

Clinical features

• • The incubation period is usually 2–3 days but may be shorter.

• • Patients present with acute onset of excruciating pain and signs of shock (fever, tachycardia, hypotension, jaundice, renal failure).

• • Local oedema and tenderness may be the only early signs, or there may be an open wound, herniation of muscle, a serosanguinous and foul smelling discharge, crepitus, skin discoloration, and necrosis.

• • Progression is rapid, and death may occur within hours

https://clinicalscienceblogsimone.files.wordpress.com/2013/02/gangrene-pictures-3.jpg

http://blog.almawiclinic.com/wp-content/uploads/2015/07/Foot-with-gangrene.jpghttp://healthooze.com/wp-content/uploads/2012/12/wet-gangrene.jpg

Diagnosis •

• The diagnosis is usually clinical but may be confirmed by Gram stain of the wound or aspirate.

• • Liquid anaerobic cultures may be positive within 6h.

• • Plain radiographs may show gas in the affected tissues

Management •

• Emergency surgical exploration and debridement of the affected area should be performed.

• • Empirical antibiotic therapy with piperacillin–tazobactam plus vancomycin (if risk of MRSA) is appropriate, pending cultures.

• • Definitive treatment for clostridial myonecrosis is with penicillin and clindamycin.

• • Hyperbaric oxygen therapy is not recommended, as its benefit is unproven and it may delay resuscitation/surgery

Folliculitis

Folliculitis

• • A superficial infection of the hair follicles and apocrine structures.

• • Aetiology—S. aureus (commonest), P. aeruginosa (‘hot tub’ folliculitis), Enterobacteriaceae (complication of acne), Candida spp., and M. furfur (in patients taking corticosteroids). Eosinophilic pustular folliculitis occurs in AIDS patients.

• • Clinical features—lesions consist of small, erythematous, pruritic papules, often with a central pustule.

• • Treatment—empiric treatment is with PO flucloxacillin. If the clinical response is slow, consider other pathogens.

Cutaneous abscesses

• • Collections of pus within the dermis and deeper skin structures. • Usually polymicrobial containing skin/mucous membrane flora; S. aureus is the sole pathogen in 725% of cases. • Clinical features—painful, tender, fluctuant nodules, usually with an overlying pustule and surrounded by a rim of erythematous swelling. • Treatment is with incision and drainage. Antibiotics are rarely necessary, unless there is extensive infection or systemic toxicity, or the patient is immunocompromised.

Furuncles and carbuncles

• • A furuncle (boil) is a deep inflammatory nodule that usually develops from preceding folliculitis. Furuncles usually occur in areas of the hairy skin, e.g. face, neck, axillae, and buttocks. • A carbuncle is a larger, deeper lesion made of multiple abscesses extending into the subcutaneous fat. Usually occur at the nape of the neck, on the back, or on the thighs. Patients may be systemically unwell. • Outbreaks of furunculosis caused by MSSA and MRSA have been described in groups of individuals with close contact, e.g. families, prisons, and sports teams.

• • Most furuncles may be treated with application of moist heat which promotes localization and spontaneous drainage. Large lesions require surgical drainage. Systemic antibiotics are indicated if fever, cellulitis, or lesions are located near the nose or lip. Control of outbreaks may require washing with chlorhexidine soaps, no sharing of cloths or towels, laundering of clothing, towels, and bedclothes, and eradication of staphylococcal carriage in colonized persons.

• Hair follicles serve as portals for a number of bacteria, although S. aureus is the most common cause of localized folliculitis. 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. Infection of sweat glands (hidradenitis suppurativa) can also mimic infection of hair follicles, particularly in the axillae. Chronic folliculitis is uncommon except in acne vulgaris, where constituents of the normal flora (e.g., Propionibacterium acnes) may play a role.

• Diffuse folliculitis occurs in two settings. Hot-tub folliculitis is caused by Pseudomonas aeruginosa in waters that are insufficiently chlorinated and maintained at temperatures of 37–40°C. Infection is usually self-limited, although bacteremia and shock have been reported. Swimmer’s itch occurs when a skin surface is exposed to water infested with freshwater avian schistosomes. Warm water temperatures and alkaline pH are suitable for mollusks that serve as intermediate hosts between birds and humans. Freeswimmingschistosomal cercariae readily penetrate human hair follicles or pores, but quickly die and elicit a brisk allergic reaction, causing intense itching and erythema.

Erysipelas

• Erysipelas is due to S. pyogenes and is characterized by an abrupt onset of fiery-red swelling of the face or extremities.

• The distinctive features of erysipelas are well-defined indurated margins, particularly along the nasolabial fold; rapid progression; and intense pain. Flaccid bullae may develop during the second or third day of illness, but extension to deeper soft tissues is rare.

• Treatment with penicillin is effective; swelling may progress despite appropriate treatment, although fever, pain, and the intense red color diminish. Desquamation of the involved skin occurs 5–10 days into the illness. Infants and elderly adults are most commonly afflicted, and the severity of systemic toxicity varies.

Erysipelas

• • An acute spreading skin infection with prominent lymphatic involvement. Usually affects children, infants, and the elderly. Predisposing factors include skin lesions, venous stasis, paraparesis, diabetes mellitus, and alcohol abuse. • Causes—GAS (commonest), group C and G streptococci, S. aureus, or GBS. • Clinical features—painful, erythematous, oedematous lesion with an elevated, sharply demarcated border. Usually occurs on the face or legs. Systemic symptoms are common; 5% are bacteraemic. • Treatment is with flucloxacillin or clindamycin. If cultures yield streptococci, treatment with penicillin is appropriate.

Ulcers with or without Eschars

• Cutaneous anthrax begins as a pruritic papule, which develops within days into an ulcer with surrounding vesicles and edema and then into an enlarging ulcer with a black eschar. Cutaneous anthrax may cause chronic nonhealing ulcers with an overlying dirtygray membrane, although lesions may also mimic psoriasis, eczema, or impetigo. Ulceroglandular tularemia may have associated ulcerated skin lesions with painful regional adenopathy. Although buboes are the major cutaneous manifestation of plague, ulcers with eschars, papules, or pustules are also present in 25% of cases

• Mycobacterium ulcerans typically causes chronic skin ulcers on the extremities of individuals living in the tropics. Mycobacterium lepraemay be associated with cutaneous ulcerations in patients with lepromatous leprosy related to Lucio’s phenomenon, in which immune-mediated destruction of tissue bearing high 255 concentrations of M. leprae bacilli occurs, usually several months after initiation of effective therapy. Mycobacterium tuberculosis may also cause ulcerations, papules, or erythematous macular lesions of the skin in both normal and immunocompromised patients.

• Decubitus ulcers are due to tissue hypoxemia secondary to pressure-induced vascular insufficiency and may become secondarily infected with components of the skin and gastrointestinal flora, including anaerobes. Ulcerative lesions on the anterior shins may be due to pyoderma gangrenosum, which must be distinguished from similar lesions of infectious etiology by histologic evaluation of biopsy sites. Ulcerated lesions on the genitals may be either painful (chancroid) or painless (primary syphilis).

• Rickettsialpox begins after mite-bite inoculation of Rickettsia akariinto the skin.

• A papule with a central vesicle evolves to form a 1- to 2.5-cm painless crusted black eschar with an erythematous halo and proximal adenopathy. While more common in the northeastern United States and the Ukraine in 1940–1950, rickettsialpox has recently been described in Ohio, Arizona, and Utah. Blistering dactylitis is a painful, vesicular, localized S. aureus or group A streptococcal infection of the pulps of the distal digits of the hands.