EJ

SrctlwwaEo

MSStoMwnTssfc

tssw

U

A

1d

merging Infections in Dermatology. Mark Jackson, MD

Cutaneous infections are common in dermatology. They occur in all populations and allages. This review will focus on 3 emerging infections encountered by dermatologists;community-acquired methicillin-resistant Staphylococcus aureus, Epstein-Barr virus infec-tions, and the atypical mycobacterial infections. The background, clinical presentation,diagnosis, and treatment of each of the 3 infections will be discussed.Semin Cutan Med Surg 25:201-206 © 2006 Elsevier Inc. All rights reserved.

reswasmn(

vsloSleiwmobaoNffbntpPraf3

kin infections are commonly encountered in dermato-logic conditions, with the most common being impetigo

elated to the common species of staphylococci and strepto-occi. It is also important for the dermatologist to be aware ofhe other less-common infections that are emerging, particu-arly those with cutaneous manifestations, such as hepatitis C,hich has been well documented in other reports. This reviewill focus on 3 of these emerging infections: community-cquired methicillin-resistant Staphylococcus aureus (MRSA),pstein Barr virus cutaneous infections, and the reemergencef atypical mycobacterial infections.

ethicillin-Resistanttaphylococcus aureus

taphylococcus aureus is a common pathogen in dermatologyhat has a propensity to infect the skin. It is a common causef skin and soft-tissue abscesses and lymphadenopathy.any persons, especially in the medical field, are colonizedith S. aureus on the mucosal surfaces, most commonly theasal mucosa. Some estimates have that rate as high as 50%.1

he first strains of methicillin-resistant S. aureus were de-cribed in 1950. These early strains have mutated to form aecond strain, which is community acquired and has a dif-erent antimicrobial susceptibility profile. The first reports ofommunity acquired MRSA were reported in the 1990s.2

Methicillin is a semisynthetic penicillin that was developedo work against the beta lactamase-producing strains oftaphylococci. Over time, resistance has developed to thesetrains, and MRSA has increased in prevalence. MRSA is aell-known cause of cutaneous skin infections and, until

niversity of Louisville, Division of Dermatology, Dermatology Specialists,Louisville, KY.

ddress reprint requests to J. Mark Jackson, University of Louisville, Divi-sion of Dermatology, Dermatology Specialists, PSC, 444 S. First Street,

tLouisville, KY 40202. E-mail: kmmjackson@aol.com

085-5629/06/$-see front matter © 2006 Elsevier Inc. All rights reserved.oi:10.1016/j.sder.2006.08.003

ecently, was contracted from the hospital setting or throughxposure to hospital settings. It has been implicated in ab-cesses, central line and catheter infections, chronic openounds and ulcers, and cellulitis with resultant sepsis

nd pneumonia. It was rarely encountered in the outpatientetting until recently and has rapidly emerged as one of theost common causes of cutaneous infections. There areow 2 distinct forms of MRSA; hospital-acquired MRSAHA-MRSA) type and community-acquired MRSA (CA-MRSA).

Comparison of MRSA strains from asymptomatic carriersersus concurrently collected community-associated clinicaltrains from patients treated at local health care facilities al-owed for the identification of 3 populations of nasal strainsf MRSA: (1) endemic clones for example, ST8:C and ST59:ustained asymptomatic carriage and infection over pro-onged periods; (2) an epidemic clone, ST8:S, demonstratednhanced capacity for rapid transmission and widespreadnfections; and (3) an outbreak clone, ST30:Z (USA1100),as highly infectious but exhibited poor asymptomatic trans-ission.3 CA-MRSA developed notoriety in 20034 as a cause

f abscess formation in military barracks. Since then, it haseen implicated in causing infections in group settings suchs schools,5 football teams,6-9 wrestling teams,10 gyms,11 andther settings in which persons occupy common space.12,13

ow, it is seen spreading among family members and mani-esting with a variety of clinical presentations. Risk factorsor infection include exposure to group settings, family mem-ers with colonization, frequent antibiotic exposure, intrave-ous drug use, child-care attendance, and underlying condi-ions, such as diabetes or malignancy.14 CA-MRSA mayresent as boils or abscesses of the skin and soft tissue (Fig. 1).atients frequently recall a “spider bite.” The involved site ised, swollen, and painful and may have pus or other drain-ge. Other common presentations include furuncles (Fig. 2),olliculitis, cellulitis, or colonization of chronic wounds (Fig.). The diagnostic criteria from the Centers for Disease Con-

rol are included in Table 1.

201

aptpwsfiwcdempic

tC

tcpaw

wqvtrmmno2mmattt

tttp

Fo

Fo

Fc

T

202 J.M. Jackson

The diagnosis of CA-MRSA is made by clinical suspicionnd bacterial culture, which can display varying resistanceatterns.15 The most common culture results reveal a strainhat is resistant to the standard penicillins, semisyntheticenicillins (eg, oxacillins), cephalopsorins, and erythromycinhile showing sensitivity to the tetracyclines, trimethoprim-

ulfamethoxazole, rifampin and clindamycin (Fig. 4). The dif-culty arises when selecting antibiotic therapy to treat strainsith the aforementioned antibiotic resistance profile, be-

ause the organism can develop inducible resistance to clin-amycin, thereby making monotherapy with clindamycinssentially ineffective. Thus, it is suggested that if erythro-ycin resistance is evident on the antibiotic resistancerofile, the clinician request a double disk diffusion test; it

s the preferred method to detect inducible resistance tolindamycin.16,17

Treatment of choice for CA-MRSA depends on the presen-ation, symptoms, and culture and sensitivity results. IfA-MRSA manifests as a skin or soft-tissue abscess, then the

igure 1 CA-MRSA manifesting as carbuncle/abscess. (Color versionf figure is available online).

igure 2 CA-MRSA folliculitis. (Color version of figure is available

nline).

reatment of choice remains incision and drainage. Severalases of CA-MRSA abscesses in immunocompetent pediatricatients have been reported to respond to incision and drain-ge alone without the use of systemic antibiotics, especiallyhen the diameter of the lesion is less than 5 cm.18

If the presentation is that of folliculitis, then hibiclensashes and topical therapy with clindamycin may be ade-uate. Intranasal mupirocin ointment and bathing with po-idine iodine or chlorhexidine soap may be used to preventransmission.19 If this approach is ineffective, patients mayequire longer-term therapy with oral antibiotics such as tri-ethoprim-sulfamethoxazole or a tetracycline. Clindamycinay be used for initial control; however, as stated earlier, isot best used as monotherapy because of the potential devel-pment of resistance. The best approach is a combination ofdifferent oral therapies for at least 2 weeks such as clinda-ycin in combination with rifampin,20 trimethoprim-sulfa-ethoxazole, or a tetracycline.21 Personal experience dictatespreference for a tetracycline, as many times longer term

reatment is required and the safety and tolerability of longerm treatment with these agents has been establishedhrough their use in acne.

Prevention of spread among family members is an impor-ant part of management. The mucosal surfaces seem to behe usual area of carriage and therefore the source for con-amination. Family members can decrease colonization andotential spread of infection by applying mupirocin or poly-

igure 3 CA-MRSA colonization of chronic ulcer with secondaryellulites. (Color version of figure is available online).

able 1 Criteria for the Diagnosis of CA-MRSA13

Diagnosis made in the outpatient setting or by a culturepositive for MRSA within 48 hours after admission to thehospital.

No medical history of MRSA infection or colonization.No medical history in the past year of: hospitalization,

admission to a nursing home/skilled nursing facility orhospice, dialysis, or surgery.

No permanent indwelling catheters or medical devices that

pass through the skin into the body.

ssse

anvrr

EEhahetcoatupptilsibe

tnklpEsdimfie

iopept

rdsmiEa

oliarnFac

Fa

Fd

Emerging infections in dermatology 203

porin22 to the nasal and genital mucosa twice daily. Coun-eling family members and persons in group setting againstharing towels is also helpful. Showering immediately afterxposure to gym facilities is important as well.

It is important to remember that CA-MRSA is not the sames HA-MRSA and that intravenous antibiotics are not usuallyecessary to control the disease. Knowledge of this will pre-ent unnecessary antibiotic exposure and potential increasedesistance patterns to the usual parenteral antibiotics cur-ently in use for the treatment of HA-MRSA.

pstein-Barr Virus Infectionspstein-Barr Virus (EBV) is a human herpes virus that infectsuman mucosal epithelial cells and B lymphocytes. The prev-lence of previous exposure approaches 95% by early adult-ood. Once infection has occurred, lifelong immunity isstablished. The pathogenesis of EBV infection involvesransmission by person-to-person contact of virions on mu-osal surfaces and via blood transfusions or transplantationf EBV infected organs. Infection typically manifests initiallys a mononucleosis infection or with acute upper respiratoryract infection symptoms with self resolution. Other morenusual manifestations are seen as part of Hodgkin’s lym-homa and lymphoproliferative disorders in immunocom-romised hosts (eg, HIV and post-transplant patients). Withhe increase in number of patients living with diseases caus-ng immune suppression and the fact that patients are livingonger on improved immunosuppressive regimens, we areeeing a greater rate of EBV infections, many of which man-fest with cutaneous findings. Historically, EBV infection haseen implicated as the etiologic agent in a multitude of dis-

igure 4 Typical culture of CA-MRSA. (Color version of figure isvailable online).

ases, many with cutaneous findings. The most common is a

he morbilliform eruption associated with infectious mono-ucleosis.23 Two other common eruptions are oral hairy leu-oplakia associated with HIV disease24 and EBV-associated

ymphoproliferative diseases, including non-Hodgkin lym-homas and post-transplant lymphoproliferative disorders.BV-associated lymphoproliferative disorders tend to be as-ociated with long-term immune suppression caused by HIVisease or iatrogenic immunosuppression with cyclospor-

ne,25,26 methotrexate,27 mycophenolate mofetil, oral tacroli-us,28 and imatinib mesylate.29 Also worth mentioning is the

nding of EBV in lesions of the cutaneous inflammatory dis-ase lichen planus, among others.

The presentation of EBV-associated cutaneous conditionss variable.30 Clinical manifestations include multiple tumorsr plaques,31,32 ulcerations, lichenoid and granulomatouslaques,33 vesicular lesions,34 Kaposiform lesions,35 and eyeliddema.36 EBV-associated lymphoproliferative disorders mayresent with nonspecific ulcerations or lymphadenopa-hy.37,38

The diagnosis of EBV virus infection involves serum hete-ophile antibody titers. A titer greater than 1:40 is helpful iniagnosing acute EBV infection. Although serologies occa-ionally are helpful for viral syndromes, inaccurate resultsake their use impractical. Therefore, for a suspected EBV

nfection of the skin or subcutaneous tissue, tissue stains forBV are required for the diagnosis. This is also true for EBVssociated lymphoproliferative disorders.

Therapy for EBV associated cutaneous infections is basedn the clinical presentation. When EBV is present in theesions of cutaneous inflammation, therapy is aimed at treat-ng the underlying inflammatory disease. Patients with EBV-ssociated lymphoproliferative disorders may respond toeductions in the immunosuppression. Reduction in immu-osuppression as a treatment option is demonstrated inigs. 5 to 7, where a patient with dermatomyositis and EBV-ssociated cutaneous lymphoma responded to simple dis-ontinuation of methotrexate. Complete resolution with no

igure 5 Methotrexate-associated EBV� lymphoproliferative disor-er manifesting as a chronic skin ulcer. (Color version of figure is

vailable online).

ocmbauiap

AMTwttwammThspctsRb

aMpbdpt

Mt

smmmfiTs

aocfdtdMap

mbcacchpma1brc

Fv

F

204 J.M. Jackson

ther therapy occurred during an 8-week period. Oral acy-lovir (high dose) and alpha interferon,39 intravenous im-une globulin,40,41 and rituximab42,43 have reported to be of

enefit in some patients. Treatment with topical acyclovirlso has been reported.44 Systemic chemotherapy also may besed if the cutaneous findings do not resolve with lowering

mmune suppression. Surgical excision of localized areas isn additional option in refractory areas after immune sup-ression has been reduced.

typicalycobacterial Infections

he atypical mycobacteria initially were discovered in 1931hen presumed tuberculous infections did not respond to

he usual agents for Mycobacterium tuberculosis. Ubiquitous inhe environment, atypical mycobacteria can be found in soil,ater, dairy products, cold-blooded animals, human feces,

nd plants and other vegetation.45 Infection with atypicalycobacteria presented as abscesses, ulcerations, granulo-as, and lymphangitis with or without sporotrichoid spread.here are different clinical presentations depending on theosts’ immune status as there is a greater tendency for dis-eminated disease, abscess formation, ulcerations and multi-le lesions to be present in immunocompromised patients asompared with immune competent patients.46 The classifica-ion of the nontuberculous mycobacteria is based on theirpeed of growth and coloration when exposed to light. Theunyon classification is most commonly used to distinguishetween the bacteria and is noted in (Table 2).47,48

Mycobacterium marinum is the most frequent cutaneoustypical mycobacterial infection. The usual source for. marinum is salt water or water from lakes, swimming

ools or aquariums. M. marinum has an incubation period ofetween 2 to 8 weeks, but a range in one report of 5 to 270ays49 at which time it usually presents as an erythematousapule, or verrucous or ulcerated plaque. Most tissue cul-

igure 6 Four weeks after discontinuation of methotrexate. (Colorersion of figure is available online).

ures are held for 4 to 6 weeks, so if one is suspicious for v

. marinum it is important to inform the laboratory to holdhe cultures at least eight weeks before discarding them.

M. fortuitum and M. chelonae are rapid growers and are theecond most frequent agents implicated in cutaneous atypicalycobacterial infections. They are ubiquitous in the environ-ent and have an incubation period of three weeks to severalonths. Clinically they present as postoperative wound in-

ections,50 traumatic abrasions, and disseminated cutaneousnfections, especially in immune compromised patients.hey may occasionally result in lymphatic or “sporotrichoid”pread.51,52

The atypical mycobacteria infections have been present forlong time; however, with the longer survival of HIV and

rgan transplant patients leading to an expanding immuno-ompromised patient population, the prevalence of these in-ections is increasing. Awareness of the different types andifferent presentations is essential as the cutaneous manifes-ations may start with subtle findings that are difficult toistinguish from more common dermatologic conditions.ost notable are recent outbreaks in unusual settings, such

s an outbreak of 61 M. fortuitum infections after foot bathserformed before pedicures from a spa in Oregon.53-55

Although on occasion atypical mycobacterial infectionsay be self resolving, treatment usually involves either com-

ination antibiotic therapy with incision and drainage or ex-ision of localized lesions as clinically indicated. The mostctive antimicrobials against M. marinum are rifampin, doxy-ycline and minocycline,56 followed in descending order bylarithromycin and quinolone antibiotics. The same agentsave been used to treat patients with M. fortuitum.57,58 In theatients infected with M. fortuitum from foot baths the usualean duration to cure was 170 days. The cultures were neg-

tive in 10% of cases. Forty-eight patients were treated, and3 were untreated. The best therapy was multidrug (2 anti-iotics) therapy with doxycycline and ciprofloxacin, as highesistance rates occurred with ciprofloxacin and clarithromy-in alone.53 Surgical therapy was helpful in some cases.

igure 7 Eight weeks after discontinuation of methotrexate. (Color

ersion of figure is available online).

SCabmimdamoftcc

R

1

1

1

1

1

1

1

1

1

1

2

2

2

2

22

2

2

2

2

3

3

3

T

CCC

C

Emerging infections in dermatology 205

ummaryA-MRSA is a rapidly emerging pathogen in group settingsnd public places—oral and topical therapy can be adequate,ut surgery remains the treatment of choice for abscess for-ation. EBV-associated lymphoproliferative disorder occurs

n patients on immunosuppressive medications such asycophenolate mofetil and cyclosporine often utilized byermatologists. Clinicians should be aware of this conditionnd realized that discontinuation of the immunosuppressiveedication may result in remission and/or resolution with-

ut requiring additional therapy. M. marinum is the mostrequent cutaneous atypical mycobacterial infection. M. for-uitum and M. chelonae (rapid growers) are the second mostommon causes. All three are increasing in prevalence, espe-ially in patients with prolonged immunosuppression.

eferences1. Long SS: Principles and Practice of Pediatric Infectious Diseases. New

York, Churchill Livingstone, 19972. Embil J, Ramotar K, Romance L, et al: Methicillin-resistant Staphylo-

coccus aureus in tertiary care institutions on the Canadian prairies1990-1992. Infect Control Hosp Epidemiol 15:646-651, 1994

3. Pan ES, Binh AD, Edwin D, et al: Population dynamics of nasal strainsof methicillin-resistant Staphylococcus aureus and their relation to com-munity-associated disease activity. J Infect Dis 192:811-818, 2005

4. LaMar JE, Carr RB, Zinderman C, et al: Sentinel cases of community-acquired methicillin-resistant Staphylococcus aureus onboard a navalship. Mil Med 168:135-138, 2003

5. Adcock PM, Pator P, Medly F, et al: Methicillin-resistant Staphylococcusaureus in two child care centers. J Infect Dis 178:577-580, 1998

6. Cohen PR: Cutaneous community-acquired methicillin-resistantStaphylococcus aureus infection in participants of athletic activities.Southern Med J 98:596-602, 2005

7. Nguyen DM, Mascola L, Brancoft E: Recurring methicillin-resistantStaphylococcus aureus infections in a football team. Emerg Infect Dis11:526-532, 2005

8. Kazakova SV, Hageman JC, Matava M, et al: A clone of methicillin-resistant Staphylococcus aureus among professional football players.N Engl J Med 352:468-475, 2005

9. Begier EM, Frenette K, Barrett NL, et al: Connecticut Bioterrorism FieldEpidemiology Response Team. A high-morbidity outbreak of methicil-lin-resistant Staphylococcus aureus among players on a college footballteam, facilitated by cosmetic body shaving and turf burns. Clini InfectDis 39:1446-1453, 2004

0. Lindenmayer JM, Schoenfeld S, O’Grady R, et al: Methicillin-resistantStaphylococcus aureus in a high school wrestling team and the surround-ing community. Arch Intern Med 158:895-899, 1998

1. Moreno F, Crisp F, Jorgenson JH, et al: Methicillin-resistant Staphylo-coccus aureus as a community organism. Clin Infect Dis 21:1308-1312,1995

2. Bukharie HA, Abdelhadi MS, Saeed IA, et al: Emergence of methicillin-resistant Staphylococcus aureus as a community pathogen. Diagn Micro-biol Infect Dis 40:1-4, 2001

3. Centers for Disease Control and Prevention: Outbreaks of community-

able 2 The Modified Runyon Classification

lass I Photocromogens Yellow cololass II Scotochromogens Yellow cololass III Nonphotochromogens Nonpigmen

lass IV Rapid growers

associated methicillin-resistant Staphylococcus aureus skin infections—

Los Angeles County, California, 2002-2003 MMWR Morb Wkly Rep52:88, 2003

4. Centers for Disease Control website. Available at: www.cdc.gov.Accessed August 23, 2006

5. Chambers HF: The changing epidemiology of Staphylococcus aureus(review). Emerg Infect Dis 7:178-182, 2001

6. Okuma K, Iwakawa K, Turnidge JD, et al: Dissemination of new meth-icillin resistant Staphylococcus aureus clones in the community. J ClinMicrobiol 40:4289-4294, 2002

7. Levison ME, Fung S: Community-associated methicillin-resistantStaphylococcus aureus: reconsideration of therapeutic options. CurrInfect Dis Rep 8:23-30, 2006

8. Lee MC, Rios AM, Aten MF, et al: Management and outcome of childrenwith skin and soft tissue abscesses caused by community-acquiredmethicillin-resistant Staphylococcus aureus. Pediatric Infect Dis J 23:123-127, 2004

9. Cohen PR, Grossman ME: Management of cutaneous lesions associatedwith an emerging epidemic: community-acquired methicillin-resistantStaphylococcus aureus skin infections. J Am Acad Dermatol 51:132-135,2004

0. Martinez-Aguilar G, Hammerman WA, Mason EO Jr., et al: Clindamy-cin treatment of invasive infections caused by community-acquired,methicillin-resistant and methicillin-susceptible Staphylococcus au-reus in children. Pediatr Infect Dis J 22:593-598, 2003

1. Ruhe JJ, Monson T, Bradsher RW, et al: Use of long-acting tetracyclinesfor methicillin-resistant Staphylococcus aureus infections: case series andreview of the literature. Curr Infect Dis 40:1429-1434, 2005

2. Fung S, O’Grady S, Kennedy C, et al: The utility of polysporin ointmentin the eradication of methicillin-resistant Staphylococcus aureus coloni-zation: a pilot study. Infection Control Hosp Epidemiol 21:653-655,2000

3. McCarthy J, Hoagland RJ: Cutaneous manifestations of infectiousmononucleosis. JAMA 187:193-4, 1964

4. JI Cohen: Epstein-Barr virus infection. N Engl J Med 343:481-492, 20005. Cliff S, Pettengell R, Gharge S, et al: B-cell lymphoma developing in a

patient on cyclosporin for recalcitrant psoriasis. Br J Dermatol 140:763-765, 1999

6. Kirby B, Owen CM, Blewitt RW, et al: Cutaneous T-cell lymphomadeveloping in a patient on cyclosporin therapy. J Am Acad Dermatol47:S165-S167, 2002 (suppl 2)

7. Paul C, Le Tourneau A, Cayuela JM, et al: Epstein-Barr virus-associatedlymphoproliferative disease during methotrexate therapy for psoriasis.Arch Dermatol 133:903-904, 1997

8. Shapiro R, Nalesnik M, McCauley J, et al: Posttransplant lymphopro-liferative disorders in adult and pediatric renal transplant patients re-ceiving tacrolimus-based immunosuppression. Transplantation 68:1851-1854, 1999

9. Scheinfeld N: Imatinib mesylate and dermatology part 2: a review ofthe cutaneous side effects of imatinib mesylate. J Drugs Dermatol JDD5:228-231, 2006

0. Iwatsuki K, Ohtsuka M, Harada H, et al: Clinicopathologic manifesta-tions of Epstein-Barr virus-associated cutaneous lymphoproliferativedisorders. Arch Dermatol 133:1081-1086, 1997

1. Gilaberte M, Gallardo F, Bellosillo B, et al: Recurrent and self-healingcutaneous monoclonal plasmablastic infiltrates in a patient with AIDSand Kaposi sarcoma. Br J Dermatol 153:828-832, 2005

2. Lucioni M, Ippoliti G, Campana C, et al: EBV positive primary cutane-ous CD30� large T-cell lymphoma in a heart transplanted patient: case

ght M. kansasii M. marinume dark M. scrofulaceum

M. avium M. ulceransM. intracellulare M. haemophilumM. chelonae M. fortuitum

r in lir in thted

report. Am J Transplant 4:1915-1920, 2004

3

3

3

3

3

3

3

4

4

4

4

4

4

4

4

4

4

5

5

5

5

5

5

5

5

5

206 J.M. Jackson

3. Magro CM, Crowson AN: Lichenoid and granulomatous dermatitis. IntJ Dermatol 39:126-133, 2000

4. Cho KH, Lee SH, Kim CW, et al: Epstein-Barr virus-associated lympho-proliferative lesions presenting as a hydroa vacciniforme-like eruption:an analysis of six cases. Br J Dermatol 151:372-380, 2004

5. Fardet L, Blanche S, Brousse N, et al: Cutaneous EBV-related lympho-proliferative disorder in a 15-year-old boy with AIDS: an unusual clin-ical presentation. J Pediatr Hematol Oncol 24:666-669, 2002

6. Shirasaki F, Taniuchi K, Matsushita T, et al: Epstein-Barr virus-associ-ated T-cell lymphoma: a case of eyelid swelling and intramuscularinfiltration mimicking dermatomyositis. Br J Dermatol 1479:1244-1248, 2002

7. Tan HH, Goh CL: Viral infections affecting the skin in organ transplantrecipients: epidemiology and current management strategies. Am J ClinDermatol 7:13-29, 2006

8. Capaldi L, Robinson-Bostom L, Kerr P, et al: Localized cutaneous post-transplant Epstein-Barr virus-associated lymphoproliferative disorder.J Am Acad Dermatol 51:778-780, 2004

9. Drago F, Ranieri E, Pastorino A, et al: Epstein-Barr virus-related pri-mary cutaneous amyloidosis. Successful treatment with acyclovir andinterferon-alpha. Br J Dermatol 134:170-174, 1996

0. Krause I, Wu R, Sherer Y, et al: In vitro antiviral and antibacterialactivity of commercial intravenous immunoglobulin preparations–apotential role for adjuvant intravenous immunoglobulin therapy ininfectious diseases. Transfus Med 12:133-139, 2002

1. Green M, Reyes J, Webber S, et al: The role of antiviral and immuno-globulin therapy in the prevention of Epstein-Barr virus infection andpost-transplant lymphoproliferative disease following solid organtransplantation. Transpl Infect Dis 3:97-103, 2001

2. Zompi S, Tulliez M, Conti F, et al: Rituximab (anti-CD20 monoclonalantibody) for the treatment of patients with clonal lymphoproliferativedisorders after orthotopic liver transplantation: a report of three cases.J Hepatol 32:521-527, 2000

3. Sebire NJ, Haselden S, Malone M, et al: Isolated EBV lymphoprolifera-tive disease in a child with Wiskott-Aldrich syndrome manifesting ascutaneous lymphomatoid granulomatosis and responsive to anti-CD20immunotherapy. J Clin Pathol 56:555-557, 2003

4. Copur MS, Deshpande A, Mleczko K, et al: Full clinical recovery after

topical acyclovir treatment of Epstein-Barr virus associated cutaneous

B-cell lymphoma in patient with mycosis fungoides. Croat Med J46:458-462, 2005

5. Haugmann G, Lotti T: Atypical mycobacterial infections of the skin.Dermatol Clin 12:657-668, 1994

6. Bartralot R, Garcia-Patos V, Sitjas D, et al: Clinical patterns of cutaneousnontuberculous mycobacterial infections. Br J Dermatol 152:727-734,2005

7. Runyon EH: Anonymous mycobacteria in pulmonary disease. MedClin North Am 45:273-290, 1959

8. Timpe A, Runyon EH: The relationship of “atypical” acid fast bacteria tohuman disease: a preliminary report. J Lab Clin Med 44:202-209, 1954

9. Jernigan JA, Farr BM: Incubation period and sources of exposure forcutaneous Mycobacterium marinum infection: case report and reviewof the literature. Clin Inf Dis 31:439-443, 2000

0. Angeli K, Lacour JP, Mantoux F, et al: Mycobacterium fortuitum skininfection occurring after a facelift. Ann Dermatol Venereol 131:198-200, 2004

1. Jopp-McKay AG, Randell P: Sporotrichoid cutaneous infection due toMycobacterium chelonei in a renal transplant patient. Aust J Dermatol31:105-109, 1990

2. Murdoch ME, Leigh IM: Sporotrichoid spread of cutaneous Mycobac-terium chelonei infection. Clin Exp Dermatol 14:309-312, 1989

3. Winthrop KL, Albridge K, South D, et al: The clinical management andoutcome of nail salon-acquired Mycobacterium fortuitum skin infection.Clin Infect Dis 38:38-44, 2004

4. Murdoch ME, Leigh IM, Redbord KP, et al: Atypical Mycobacteriumfurunculosis occurring after pedicures. J Am Acad Dermatol 54:52-54,2006

5. Sniezek PJ, Graham BS, Busch HB, et al: Rapidly growing mycobacterialinfections after pedicures. Arch Dermatol 139:629-634, 2003

6. Cummins DL, Delacerda D, Tausk FA: Mycobacterium marinum withdifferent responses to second-generation tetracyclines. Int J Dermatol44:518-520, 2005

7. Fujita N, Utani A, Matsumoto F, et al: Levofloxacin alone efficientlytreated a cutaneous mycobacterium fortuitum infection. J Am AcadDermatol 29:452-454, 2002

8. Nagore E, Ramos P, Botella-Estrada R, et al: Cutaneous infection withMycobacterium fortuitum after localized microinjections treated success-fully with a triple drug regimen. Acta Dermatol Venereol 81:291-293,

2001