Emerging Infections in Dermatology

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    108doient antimicrobial susceptibility profile. The first reports ofmunity acquired MRSA were reported in the 1990s.2

    Methicillin is a semisynthetic penicillin that was developedwork against the beta lactamase-producing strains ofphylococci. Over time, resistance has developed to theseains, and MRSA has increased in prevalence. MRSA is all-known cause of cutaneous skin infections and, until

    Now, it is seen spreading among family members and mani-festing with a variety of clinical presentations. Risk factorsfor infection include exposure to group settings, family mem-bers with colonization, frequent antibiotic exposure, intrave-nous drug use, child-care attendance, and underlying condi-tions, such as diabetes or malignancy.14 CA-MRSA maypresent as boils or abscesses of the skin and soft tissue (Fig. 1).Patients frequently recall a spider bite. The involved site isred, swollen, and painful and may have pus or other drain-age. Other common presentations include furuncles (Fig. 2),folliculitis, cellulitis, or colonization of chronic wounds (Fig.

    iversity of Louisville, Division of Dermatology, Dermatology Specialists,Louisville, KY.ress reprint requests to J. Mark Jackson, University of Louisville, Divi-merging Infections in DerMark Jackson, MD

    Cutaneous infections are common in dermaages. This review will focus on 3 emergingcommunity-acquired methicillin-resistant Stations, and the atypical mycobacterial infectdiagnosis, and treatment of each of the 3 inSemin Cutan Med Surg 25:201-206 2006

    kin infections are commonly encountered in dermato-logic conditions, with the most common being impetigoated to the common species of staphylococci and strepto-ci. It is also important for the dermatologist to be aware ofother less-common infections that are emerging, particu-

    ly those with cutaneous manifestations, such as hepatitis C,ich has been well documented in other reports. This reviewl focus on 3 of these emerging infections: community-uired methicillin-resistant Staphylococcus aureus (MRSA),stein Barr virus cutaneous infections, and the reemergenceatypical mycobacterial infections.

    ethicillin-Resistanttaphylococcus aureusphylococcus aureus is a common pathogen in dermatologyt has a propensity to infect the skin. It is a common causeskin and soft-tissue abscesses and lymphadenopathy.ny persons, especially in the medical field, are colonizedth S. aureus on the mucosal surfaces, most commonly thesal mucosa. Some estimates have that rate as high as 50%.1

    e first strains of methicillin-resistant S. aureus were de-3).tro

    sion of Dermatology, Dermatology Specialists, PSC, 444 S. First Street,Louisville, KY 40202. E-mail: kmmjackson@aol.com

    5-5629/06/$-see front matter 2006 Elsevier Inc. All rights reserved.:10.1016/j.sder.2006.08.003tology

    . They occur in all populations and alltions encountered by dermatologists;occus aureus, Epstein-Barr virus infec-The background, clinical presentation,s will be discussed.er Inc. All rights reserved.

    ently, was contracted from the hospital setting or throughosure to hospital settings. It has been implicated in ab-sses, central line and catheter infections, chronic openunds and ulcers, and cellulitis with resultant sepsisd pneumonia. It was rarely encountered in the outpatientting until recently and has rapidly emerged as one of thest common causes of cutaneous infections. There arew 2 distinct forms of MRSA; hospital-acquired MRSAA-MRSA) type and community-acquiredMRSA (CA-MRSA).Comparison of MRSA strains from asymptomatic carrierssus concurrently collected community-associated clinicalains from patients treated at local health care facilities al-ed for the identification of 3 populations of nasal strainsMRSA: (1) endemic clones for example, ST8:C and ST59:stained asymptomatic carriage and infection over pro-ged periods; (2) an epidemic clone, ST8:S, demonstratedhanced capacity for rapid transmission and widespreadections; and (3) an outbreak clone, ST30:Z (USA1100),s highly infectious but exhibited poor asymptomatic trans-ssion.3 CA-MRSA developed notoriety in 20034 as a causeabscess formation in military barracks. Since then, it hasen implicated in causing infections in group settings suchThe diagnostic criteria from the Centers for Disease Con-l are included in Table 1.

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    202 J.M. JacksonThe diagnosis of CA-MRSA is made by clinical suspiciond bacterial culture, which can display varying resistancetterns.15 The most common culture results reveal a straint is resistant to the standard penicillins, semisyntheticnicillins (eg, oxacillins), cephalopsorins, and erythromycinile showing sensitivity to the tetracyclines, trimethoprim-famethoxazole, rifampin and clindamycin (Fig. 4). The dif-ulty arises when selecting antibiotic therapy to treat strainsth the aforementioned antibiotic resistance profile, be-se the organism can develop inducible resistance to clin-mycin, thereby making monotherapy with clindamycinentially ineffective. Thus, it is suggested that if erythro-cin resistance is evident on the antibiotic resistancefile, the clinician request a double disk diffusion test; itthe preferred method to detect inducible resistance tondamycin.16,17

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

    re 1 CA-MRSAmanifesting as carbuncle/abscess. (Color versionfigure is available online).re 2 CA-MRSA folliculitis. (Color version of figure is availableline).

    Nopatment of choice remains incision and drainage. Severales of CA-MRSA abscesses in immunocompetent pediatrictients have been reported to respond to incision and drain-alone without the use of systemic antibiotics, especiallyen the diameter of the lesion is less than 5 cm.18

    If the presentation is that of folliculitis, then hibiclensshes and topical therapy with clindamycin may be ade-ate. Intranasal mupirocin ointment and bathing with po-ine iodine or chlorhexidine soap may be used to preventnsmission.19 If this approach is ineffective, patients mayuire longer-term therapy with oral antibiotics such as tri-thoprim-sulfamethoxazole or a tetracycline. Clindamyciny be used for initial control; however, as stated earlier, ist best used as monotherapy because of the potential devel-ment of resistance. The best approach is a combination ofifferent oral therapies for at least 2 weeks such as clinda-cin in combination with rifampin,20 trimethoprim-sulfa-thoxazole, or a tetracycline.21 Personal experience dictatesreference for a tetracycline, as many times longer termatment is required and the safety and tolerability of longm treatment with these agents has been establishedough their use in acne.Prevention of spread among family members is an impor-t part of management. The mucosal surfaces seem to beusual area of carriage and therefore the source for con-ination. Family members can decrease colonization and

    tential spread of infection by applying mupirocin or poly-

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

    le 1 Criteria for the Diagnosis of CA-MRSA13

    agnosis made in the outpatient setting or by a cultureositive for MRSA within 48 hours after admission to theospital.medical history of MRSA infection or colonization.medical history in the past year of: hospitalization,dmission to a nursing home/skilled nursing facility orospice, dialysis, or surgery.

    permanent indwelling catheters or medical devices thatass through the skin into the body.

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    Emerging infections in dermatology 203rin22 to the nasal and genital mucosa twice daily. Coun-ing family members and persons in group setting againstring towels is also helpful. Showering immediately afterosure to gym facilities is important as well.It is important to remember that CA-MRSA is not the sameHA-MRSA and that intravenous antibiotics are not usuallycessary to control the disease. Knowledge of this will pre-t unnecessary antibiotic exposure and potential increasedistance patterns to the usual parenteral antibiotics cur-tly in use for the treatment of HA-MRSA.

    stein-Barr Virus Infectionsstein-Barr Virus (EBV) is a human herpes virus that infectsmanmucosal epithelial cells and B lymphocytes. The prev-nce of previous exposure approaches 95% by early adult-od. Once infection has occurred, lifelong immunity isablished. The pathogenesis of EBV infection involvesnsmission by person-to-person contact of virions on mu-al surfaces and via blood transfusions or transplantationEBV infected organs. Infection typically manifests initiallya mononucleosis infection or with acute upper respiratoryct infection symptoms with self resolution. Other moreusual manifestations are seen as part of Hodgkins lym-oma and lymphoproliferative disorders in immunocom-mised hosts (eg, HIV and post-transplant patients). Withincrease in number of patients living with diseases caus-immune suppression and the fact that patients are livingger on improved immunosuppressive regimens, we areing a greater rate of EBV infections, many of which man-st with cutaneous findings. Historically, EBV infection has

    re 4 Typical culture of CA-MRSA. (Color version of figure isilable online).en implicated as the etiologic agent in a multitude of dis-es, many with cutaneous findings. The most common is

    deravamorbilliform eruption associated with infectious mono-cleosis.23 Two other common eruptions are oral hairy leu-plakia associated with HIV disease24 and EBV-associatedphoproliferative diseases, including non-Hodgkin lym-omas and post-transplant lymphoproliferative disorders.V-associated lymphoproliferative disorders tend to be as-iated with long-term immune suppression caused by HIVease or iatrogenic immunosuppression with cyclospor-,25,26 methotrexate,27 mycophenolate mofetil, oral tacroli-s,28 and imatinib mesylate.29 Also worthmentioning is theding of EBV in lesions of the cutaneous inflammatory dis-e lichen planus, among others.The presentation of EBV-associated cutaneous conditionsariable.30 Clinical manifestations include multiple tumorsplaques,31,32 ulcerations, lichenoid and granulomatousques,33 vesicular lesions,34 Kaposiform lesions,35 and eyelidma.36 EBV-associated lymphoproliferative disorders maysent with nonspecific ulcerations or lymphadenopa-.37,38

    The diagnosis of EBV virus infection involves serum hete-hile antibody titers. A titer greater than 1:40 is helpful ingnosing acute EBV infection. Although serologies occa-nally are helpful for viral syndromes, inaccurate resultske their use impractical. Therefore, for a suspected EBVection of the skin or subcutaneous tissue, tissue stains forV are required for the diagnosis. This is also true for EBVociated lymphoproliferative disorders.Therapy for EBV associated cutaneous infections is basedthe clinical presentation. When EBV is present in theions of cutaneous inflammation, therapy is aimed at treat-the underlying inflammatory disease. Patients with EBV-ociated lymphoproliferative disorders may respond touctions in the immunosuppression. Reduction in immu-suppression as a treatment option is demonstrated ins. 5 to 7, where a patient with dermatomyositis and EBV-ociated cutaneous lymphoma responded to simple dis-tinuation of methotrexate. Complete resolution with no

    re 5 Methotrexate-associated EBV lymphoproliferative disor-

    manifesting as a chronic skin ulcer. (Color version of figure isilable online).

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    204 J.M. Jacksoner therapy occurred during an 8-week period. Oral acy-vir (high dose) and alpha interferon,39 intravenous im-ne globulin,40,41 and rituximab42,43 have reported to be ofnefit in some patients. Treatment with topical acycloviro has been reported.44 Systemic chemotherapy alsomay bed if the cutaneous findings do not resolve with loweringmune suppression. Surgical excision of localized areas isadditional option in refractory areas after immune sup-ssion has been reduced.

    typicalycobacterial Infectionse atypical mycobacteria initially were discovered in 1931en presumed tuberculous infections did not respond tousual agents forMycobacterium tuberculosis. Ubiquitous inenvironment, atypical mycobacteria can be found in soil,ter, dairy products, cold-blooded animals, human feces,d plants and other vegetation.45 Infection with atypicalcobacteria presented as abscesses, ulcerations, granulo-s, and lymphangitis with or without sporotrichoid spread.ere are different clinical presentations depending on thests immune status as there is a greater tendency for dis-inated disease, abscess formation, ulcerations and multi-lesions to be present in immunocompromised patients aspared with immune competent patients.46 The classifica-

    n of the nontuberculous mycobacteria is based on theired of growth and coloration when exposed to light. Thenyon classification is most commonly used to distinguishtween the bacteria and is noted in (Table 2).47,48

    Mycobacterium marinum is the most frequent cutaneouspical mycobacterial infection. The usual source formarinum is salt water or water from lakes, swimmingols or aquariums.M. marinum has an incubation period oftween 2 to 8 weeks, but a range in one report of 5 to 270ys49 at which time it usually presents as an erythematous

    re 6 Four weeks after discontinuation of methotrexate. (Colorsion of figure is available online).pule, or verrucous or ulcerated plaque. Most tissue cul-es are held for 4 to 6 weeks, so if one is suspicious for

    Figuvermarinum it is important to inform the laboratory to holdcultures at least eight weeks before discarding them.

    M. fortuitum andM. chelonae are rapid growers and are theondmost frequent agents implicated in cutaneous atypicalcobacterial infections. They are ubiquitous in the environ-nt and have an incubation period of three weeks to severalnths. Clinically they present as postoperative wound in-tions,50 traumatic abrasions, and disseminated cutaneousections, especially in immune compromised patients.ey may occasionally result in lymphatic or sporotrichoidead.51,52

    The atypical mycobacteria infections have been present forong time; however, wi...

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