eMedicine Specialties > Dermatology > Parasitic Infections

Strongyloidiasis

Robert A Schwartz, MD, MPH, Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Mordechai M Tarlow, MD, Physician, Department of Medicine, Section of Dermatology, Kimball Medical Center

Updated: May 29, 2009

Introduction

Background

Fulleborn first described strongyloidiasis in 1926. The parasitic helminth Strongyloides stercoralis causes this disease. This nematode is unique in its ability to complete its life cycle in humans. It may cause infection over a period as long as several decades. The symptoms related to strongyloidiasis may reflect the nematode's systemic passage, its local cutaneous involvement, or both. Individuals with an intact immune system may have minimal or no symptoms. In contrast, those with a compromised immune system may develop a rapidly fatal infection (eg, hyperinfection syndrome, disseminated strongyloidiasis). During chronic uncomplicated infections, the larvae may migrate to the skin, where they can cause cutaneous strongyloidiasis, known as larva currens because of the quick migratory rate of the larva.

Consequences of captivity include health effects, including strongyloidiasis. Allied military personnel held by the Japanese during the World War II experienced deprivation, malnutrition, and exposure to tropical diseases.¹ Certain tropical diseases have persisted in these survivors, notably infections with S stercoralis, with studies 30 years or more after release documenting overall infection rates of 15%. Chronic strongyloidiasis may produce a linear urticarial larva currens rash, with such individuals at risk of fatal hyperinfection if immunity is suppressed.

Also see the eMedicine article Strongyloidiasis.²

Pathophysiology

Strongyloidiasis is typically acquired when the infective filariform larvae penetrate the skin during contact with contaminated soil, although ingestion of filariform larvae via the fecal-oral route can also result in infection. The larvae are transferred through the circulation to the lungs. From the lungs, they ascend to the glottis via the bronchi and are subsequently swallowed. In the duodenum and jejunum, the larvae burrow into the mucus membrane, where, after molting, the female worm produces eggs by parthenogenesis, which yields noninfective rhabditiform larvae. These larvae can be passed in the stool and become infective filariform larvae, or they can develop into adults in the external environment and produce rhabditiform larvae. In the external environment, the rhabditiform larvae can complete the free-living cycle, or they can become infective filariform larvae with the potential to penetrate the skin of another individual.

Autoinfection occurs when noninfective rhabditiform larvae prematurely transform into infective filariform larvae (ie, before leaving the body) and reenter the circulation by 1 of 3 methods. For the first, the larvae penetrate the mucosa of the colon and cause indirect endoautoinfection. For the second, the larvae penetrate the mucosa of the upper small intestine and cause direct endoautoinfection. For the third, the larvae penetrate the perianal skin and cause exoautoinfection. The last method has been associated with the development of larva currens.

After entering the circulation, the larvae are carried to the lungs, where the cycle repeats itself. This mechanism accounts for the chronicity and frequent recurrence of the disease in patients who no longer live in areas in which the disease is endemic.

In immunocompromised hosts, larvae may migrate beyond the normally controlled internal pathways, with widespread dissemination to the extraintestinal regions, including the CNS, heart, urinary tract, endocrine organs, and skin. Millions of filariform larvae reach the skin by means of the circulation or direct invasion from body cavities; they can migrate through all levels of the dermis and involve the subcutaneous tissue.

Frequency

United States

Strongyloidiasis is relatively uncommon. Endemic foci exist in rural areas of the southeastern United States and Appalachia, with prevalence rates close to 4%.³ Infections acquired in the United States, while not usually associated with larva currens, are not clinically silent; the infected individuals usually have a chronic relapsing illness of mild to moderate severity. Among veterans of the US military forces who served in Southeast Asia, the prevalence of larva currens in those with confirmed strongyloidiasis is high, with studies showing a range of 30-90%.^4,5

International

Strongyloidiasis is endemic in tropical and subtropical countries.⁶ The worldwide prevalence is approximately 35 million cases, and rates are as high as 40% in certain regions, including Southeast Asia, Latin America, and the Caribbean basin. The international prevalence of larva currens among patients with strongyloidiasis varies, with rates in the range of 30-90% in Southeast Asia. High rates of larva currens are also reported in Latin America. A stool and serosurvey for S stercoralis conducted in a community in the Peruvian Amazon region found strongyloidiasis due to S stercoralis in the stool of 69 (8.7%) of 792 participants.⁷

Mortality/Morbidity

In patients who are immunocompromised, disseminated strongyloidiasis may develop. If it does, it is commonly fatal; the mortality rate may be as high as 80%. Therefore, patients at risk must be identified before immunosuppressive therapy is begun.

Race

No racial predilection is recognized; however, it is highly prevalent in some tropical Aboriginal communities in Australia.⁸

Sex

No sex predilection is reported.

Age

Infection can occur in individuals at any age, although infection is more common during childhood than at other times. Advanced age is a risk factor for severe strongyloidiasis because it may be associated with an immunosuppressed state.

Clinical

History

Strongyloides infection is associated with cutaneous and systemic signs and symptoms that can be categorized by the stage of disease. Infection can be asymptomatic, can cause a wide variety of clinical syndromes, or can result in death. 

• Acute infection
  • Cutaneous features
    • The patient may report a mild eruption at the site of larval penetration, usually on the feet.
    • Most often, the area is also pruritic. This rash has been referred to as ground itch.
  • Systemic features
    • Pulmonary symptoms caused by the migration of larvae through the lungs may result in coughing, shortness of breath, and fever.
    • GI symptoms include epigastric discomfort, nausea, vomiting, and diarrhea.
• Chronic infection
  • Cutaneous features
    • Larva currens, or creeping infection, is a form of cutaneous larva migrans specific to Strongyloides infection; it is a result of autoinfection. The eruption begins in the perianal region and rapidly spreads, causing intense pruritus. Episodes usually last several hours, and patients can remain free of symptoms for weeks or months between episodes. Evidence of larva currens may appear soon after infection with Strongyloides organisms, or it may first appear many years (often decades) later. Because of autoinfection, episodes may continue for many years.
    • Excoriation and impetigo are common.
    • Chronic urticaria is also described in a small percentage of patients with strongyloidiasis. This usually resolves after 1 or 2 days.
  • Systemic features
    • Most patients are asymptomatic or have only vague abdominal complaints.
    • Symptoms may include burning or cramping, nausea, vomiting, diarrhea, constipation, and weight loss.
• Severe disseminated infection
  • Cutaneous features
    • A rapidly progressive, diffuse petechial and purpuric eruption may occur.
    • The cause is the massive migration of filariform larvae into the skin.
  • Systemic features
    • Abdominal symptoms are similar to those of chronic infection, but they are more severe.
    • Bloody stools may occur along with severe abdominal pains.
    • Pneumonitis may cause hemoptysis and difficulty in breathing.
    • An altered mental status or a stiff neck may indicate CNS involvement.
• Severe strongyloidiasis is a risk in every corticosteroid-treated patient who has traveled to a soil-infested country, even if the contact was decades earlier.^9,10 This diagnosis should be suspected with unusual GI or pulmonary symptoms or an unexplained Gram-negative bacilli sepsis.
• Cutaneous manifestations in disseminated strongyloidiasis are infrequent; characteristic purpuric periumbilical skin lesions should raise the suspicion for its diagnosis. If often portends a fatal outcome in cancer patients.¹¹

Physical

Strongyloides infection is associated with cutaneous and systemic signs and symptoms that can be categorized by the stage of disease.

• Acute infection
  • Cutaneous findings
    • A local pruritic eruption develops in the area of larval penetration, which usually occurs on the foot.
    • This eruption may consist of erythematous macules and papules or acute urticaria, and it is often accompanied by excoriation.
  • Systemic findings
    • Wheezing may occur.
    • The patient may have a fever.
    • Epigastric tenderness may be present.
• Chronic infection
  • Cutaneous findings
    • Larva currens is an intensely pruritic linear or serpiginous urticarial lesion, which typically begins within 12 cm of the anus. The lesions may consist of 1 or more such bands, which migrate intermittently and rapidly at a rate as fast as 15 cm/h.
    • Similar lesions may also occur on the groin and trunk, and areas of involvement on the thighs and upper body have been described as well.
    • Excoriation and impetiginization are common.
  • Systemic findings
    • Examination findings are usually normal.
    • Epigastric tenderness may be preset, and weight loss may occur.
• Severe disseminated infection
  • Cutaneous findings
    • Petechial and purpuric lesions rapidly expand; these may be accompanied by pink macules and papules.
    • The eruption is diffuse and may consist of serpiginous streaks in a reticulated pattern.
  • Systemic findings
    • GI findings include abdominal tenderness; distension; and hyperactive, hypoactive, or absent bowel sounds.
    • CNS infection manifests as an altered mental status or meningismus.
    • Pulmonary involvement may result in coughing, respiratory distress, wheezing, or crackles.
    • General signs of severe infection include fever, chills, and shock.
• However, most patients who are immunocompetent have few or no symptoms.

Causes

The parasite responsible for strongyloidiasis is S stercoralis. Other species in the genus Strongyloides include Strongyloides myopotami and Strongyloides procyonis. These species have animal hosts and are thus responsible for zoonotic infections.¹²

• S stercoralis infection is usually contracted by penetration of the larvae into the foot. Barefoot contact with sand or soil that is contaminated with human feces in endemic areas accounts for many infections.
• Zoonotic infections by Strongyloides species are similarly contracted by contact with sand or soil that contains infected animal droppings, including feces from raccoons and nutria.
  • Infections are reported among veterinarians and laboratory workers who work in temperate climates and are exposed to larvae from horses.
  • Zoonotic forms of Strongyloides infection can also produce creeping skin eruptions identical to those of S stercoralis infection.
• Risk factors for severe strongyloidiasis include any cause of an immunosuppressed state, including the following:
  • Use of immunosuppressive agents
  • Malignancy
  • Other infections, particularly HIV infection and other immunosuppressive infections¹³
  • Collagen-vascular disease
  • Diabetes mellitus
  • Malnutrition
  • Advanced age
• In patients who were exposed to the parasite, the likelihood of Strongyloides should be carefully assessed before immunosuppressive therapy is begun.

Differential Diagnoses

Contact Dermatitis, Allergic
Erythema Annulare Centrifugum
Scabies

Other Problems to Be Considered

Human hookworm infection with Ancylostoma duodenale or Necator americanus
Zoonotic infection with S myopotami, S procyonis, Ancylostoma braziliensis, or Ancylostoma caninum

Strongyloides colitis is an easily curable yet potentially lethal mimic of ulcerative colitis.¹⁴  One should have a high index of suspicion and should be aware of GI similarities with ulcerative colitis. Strongyloides colitis should be included in the differential diagnosis of ulcerative colitis.

Workup

Laboratory Studies

• Routine blood testing
  • The CBC count usually reveals a normal WBC count in acute and chronic strongyloidiasis. The WBC count may be elevated in severe strongyloidiasis.
  • Eosinophilia of 10-40% is common during acute infection; it may be as high as 75-80%. Eosinophilia also occurs in chronic infection, although it is intermittent and may not be found at all during severe infection.
  • The total serum immunoglobulin E (IgE) level is usually elevated.
  • Severe infection may be associated with anemia, thrombocytopenia, and a prolonged prothrombin time (PT) because of decreased levels of clotting factors.
  • Obtain blood cultures in all patients in whom Strongyloides infection is suspected because enteric pathogens often cause co-infection.
• Stool examination for ova and parasites¹⁵
  • Definitive diagnosis depends on the microscopic demonstration of S stercoralis larvae in the feces.
  • The larvae resemble those of hookworms, but they can be distinguished by their short buccal cavity.
  • Ova are almost never observed during strongyloidiasis unless severe diarrhea occurs.
  • Several fresh stool specimens may need to be examined before a positive result is found. At least 3 separate examinations on different days are recommended to achieve a sensitivity of approximately 70-80%.
  • Stool samples may be concentrated with zinc sulfate prior to examination to enhance the recovery of larvae. A modified agar plate method is superior to other techniques used for stool examination.
  • Duodenal fluid can be aspirated or examined by using the Entero-Test, or the string capsule method. This test offers a higher likelihood of larval recovery than simple stool examination.
• Serologic analysis
  • Although serologic analysis is the most sensitive test for strongyloidiasis (sensitivity, 84-92%), it is not specific, and cross-reactions with other nematode infections are possible. Therefore, microscopic analysis is also necessary for diagnosis.
  • Common serologic tests used in diagnosing strongyloidiasis include the enzyme immunoassay (EIA) and the enzyme-linked immunosorbent assay (ELISA). However, a stool and serosurvey for S stercoralis conducted in a community in the Peruvian Amazon region found the ELISA test had a negative predictive value of 98% and is an excellent screening test for strongyloidiasis.⁷
  • Gelatin particle agglutination test (GPAT) and ELISA results were evaluated in endemic regions of Thailand.¹⁶ In this work, the GPAT was judged to be more practical for screening for strongyloidiasis than the conventional ELISA.
• Often, establishing a diagnosis and confirming a cure of strongyloidiasis is difficult. Strongyloides -specific antibody levels may be used for serological follow-up for strongyloidiasis.¹⁷ They may indicate reversion to negative serostatus after successful ivermectin therapy, which is frequent.

Imaging Studies

• Systemic infection is associated with findings that may be observed with imaging studies.
  • Alveolar or interstitial infiltrates or pulmonary effusion may be visible on chest radiographs.
  • Severe infection may be associated with loss of the mucosal pattern, rigidity, and tubular narrowing, as depicted on abdominal radiographs.

Procedures

• In acute or chronic infection, skin biopsy is usually neither necessary nor sufficient because parasites are rarely visualized. When they are, speciation is difficult.
• In severe infection, skin biopsy may be useful because filariform larvae are often observed. Obtain specimens from the purpuric eruptions because these areas contain the largest amount of larvae.
• Intestinal colonoscopy may reveal multiple findings, including normal mucosa, moderate inflammation, or severe duodenitis and colitis, particularly in immunosuppressed patients. Histopathologic examination identified larvae in 71.4% of those immunosuppressed by duodenal biopsy.¹⁸ Thus, in addition to stool analysis, endoscopic observation and biopsies are very important.¹⁹
• Lumbar puncture and cerebrospinal fluid (CSF) evaluation are indicated when CNS involvement is suspected.
• In severe infections, sputum examination or bronchoalveolar lavage is appropriate for the identification of larvae.

Histologic Findings

Skin biopsy is often helpful in severe infection. Larvae can be observed in all levels of the dermis and occasionally in the subcutis. Other findings include edema, extravasated RBCs, and some lymphocytes in the superficial dermis. Larvae range from 9-15 µm in size. They contain a triradiate digestive tract.

Biopsy of the duodenum or jejunum reveals larvae in the lamina propria, where they produce edema, a cellular infiltrate, villous atrophy, or even fibrosis in prolonged infection.

Treatment

Medical Care

• The pathogen in strongyloidiasis cannot be extracted from the area of eruption because it is not localized in any single area.
• Anthelmintic therapy is the standard treatment.²⁰
• Supportive therapy should be administered as indicated.
• In instances in which co-infection with enteric bacteria is suspected, antibiotic therapy is indicated as well.
• Cyclosporine, an immunosuppressive agent, has anthelmintic activity. To date, no cases of severe strongyloidiasis development have been reported in patients receiving this agent.
• Strongyloides hyperinfection syndrome, usually precipitated by immune suppression, should be considered in patients who have resided in endemic regions. It is often caused by corticosteroidal drugs.²¹ Attempts at the detection and eradication of this infection are recommended to prevent this potentially fatal complication.

Consultations

• Consider consulting an infectious disease specialist.
• To ensure that the optimal larval-detection tests are performed, notify the local microbiology laboratory staff that strongyloidiasis is suspected.
• Physicians in the United States may obtain assistance with serologic testing from the Centers for Disease Control and Prevention (CDC). Send a serum sample with the patient's history and physical examination findings to the state public health laboratory, which will then send the data to the CDC. Be aware that this process is often lengthy.
• Several commercial laboratories in the United States can perform serologic testing within a few days. Two are listed below.
  • Parasitic Disease Consultants
    PO Box 616
    2177 Flintstone Drive, Suite J
    Tucker, GA 30084
    770-496-1370
    (This facility performs ELISA for Strongyloides detection.)
  • Specialty Laboratories
    2211 Michigan Avenue
    Santa Monica, CA 90404
    800-421-4449 or 310-828-6543
    (These laboratories perform EIA for Strongyloides detection.)

Diet

No specific diet is required.

Activity

The patient's activity does not need to be limited when a cutaneous or systemic infection exists, unless severe disseminated infection occurs.

Medication

The goals of pharmacotherapy are to eradicate the infection, reduce morbidity, and prevent complications.

The medications listed below are available from the CDC Drug Service, Centers for Disease Control and Prevention, Atlanta, GA 30333 (404-639-3670 during business hours, 404-639-2888 during evenings and weekends).

Anthelmintics

Parasitic biochemical pathways are sufficiently different from those of the human host to allow selective interference by chemotherapeutic agents in relatively small doses.

Ivermectin (Stromectol, Mectizan)

DOC for treatment of acute and chronic infection in intestinal stages. Selectively binds to glutamate-gated chloride ion channels in invertebrate nerve and muscle cells, causing paralysis and death of the organism. Half-life is 16 h; metabolized in liver.

Dosing

Adult

170-200 mcg/kg PO for 1 dose; may repeat if larvae reappear in stool; in immunocompromised patients, several treatments every q2wk may be necessary
Intestinal strongyloidiasis, nondisseminated: 200 mcg/kg PO once

Pediatric

<15 kg: Not established
>15 kg: Administer as in adults

Interactions

May interact with other ligand-gated chloride channels (eg, those gated by GABA)

Contraindications

Documented hypersensitivity; do not use in first trimester of pregnancy and avoid use until after delivery if possible

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Treat mothers who intend to breastfeed only when risk of delayed treatment outweighs possible risks to newborn (excreted in breast milk); following symptoms primarily seen with accidental intoxications from veterinary formulations, headaches, nausea, vomiting, ataxia, seizures, and mild CNS depression; may cause drowsiness; infection with Loa loa, rarely, may develop encephalopathy with ivermectin treatment; Mazzotti reaction, a severe generalized immune reaction resulting from rapidly killed microfilariae in large numbers, may occur (symptoms include intolerable pruritus, papular rashes, lymphadenopathy, fever, ocular damage, and hypotension)

Albendazole (Albenza)

Second-best agent for treatment of acute and chronic infection. High-affinity binding to free beta-tubulin in parasite cells. Causes energy depletion by inhibiting glucose uptake, immobilization, and finally death.

Dosing

Adult

400 mg/d for 3 d; repeat in 2-3 wk if necessary

Pediatric

³ 2 years: 400 mg/d PO for 3 d with food; repeat in 3 wk if necessary

Interactions

Coadministration with carbamazepine may decrease effectiveness; dexamethasone, cimetidine, and praziquantel may increase toxicity; monitor theophylline levels if coadministered

Contraindications

Documented hypersensitivity to albendazole, benzimidazole class of compounds, or any components of the product; not for use in first trimester of pregnancy and avoid use until after delivery if possible

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Discontinue use if LFT values increase significantly (resume when levels decrease to pretest values); leukopenia, thrombocytopenia (rare), anemia (rare), abdominal pain, nausea, vomiting, diarrhea, dizziness, vertigo, fever, increased intracranial pressure, and alopecia may occur; in neurocysticercosis, anticonvulsants and high-dose glucocorticoids must also be administered; increased risk of retinal damage in patients with cysticercosis (weigh risks versus benefits of therapy)

Thiabendazole (Mintezol)

DOC for treatment of hyperinfection syndrome and disseminated infection. Inhibits helminth-specific mitochondrial fumarate reductase. Useful for treatment of cutaneous larva migrans.

Dosing

Adult

>100 lb: 1 g/dose PO
>125 lb: 1.25 g/dose PO
>150 lb: 1.5 g/dose PO; not to exceed g/d
Alternatively: 50 mg/kg PO once (expect higher incidence of adverse effects)
Cutaneous larva migrans:
25 mg/kg bid for 2 to 5 d; not to exceed 3 g/d
Topical: Apply 15% extemporaneous lipophilic ointment bid for 5 d
Hyperinfection syndrome: May need to continue treatment for 7-14 d

Pediatric

Administer PO bid for 2 d using weight-based dosing
>30 lb: 0.25 g/dose
>50 lb: 0.5 g/dose
>75 lb: 0.75 g/dose
>100 lb: Administer as in adults
Severe infection: 25 mg/kg PO q12h for 7-14 d; not to exceed 3 g/d
Cutaneous larva migrans: Administer as in adults

Interactions

May elevate serum levels of theophylline, increasing toxicity (monitor serum levels and reduce dose prn)

Contraindications

Documented hypersensitivity; do not use in first trimester of pregnancy and avoid use until after delivery if possible

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Closely monitor in hepatic or renal dysfunction; pretherapeutic supportive therapy needed patients who are anemic, dehydrated, or malnourished; caution in confirmed worm infestation (not prophylactic); may cause nausea, vomiting, and mild CNS depression

Follow-up

Further Outpatient Care

• Continue serial sampling of the stool or duodenal aspirates at intervals of 2-3 months to ensure complete eradication of the parasite.
• Serologic studies can be used to monitor the response to therapy.
  • Perform these tests 4-8 months after anthelmintic therapy is completed.
  • Strongyloides titers should decrease to low or undetectable levels 6-18 months after treatment. If titer has not decreased sufficiently, additional therapy may be necessary.

Deterrence/Prevention

• Infection is prevented by avoiding direct skin contact with soil containing infective larvae. Instruct travelers to endemic areas to wear footwear when walking on the beach and other areas with soil.
• Identify patients at risk and perform appropriate diagnostic tests before they begin immunosuppressive therapy.
• No accepted prophylactic regimens exist, and no vaccines are available.
• A wise practice is to search for S stercoralis larvae before initiating immunosuppression in anyone who has traveled to an endemic area, even if it was decades earlier.¹⁰

Complications

• Cutaneous complications of strongyloidiasis include larva currens and chronic urticaria. Cutaneous complications in immunocompromised patients with severe infection include purpura and petechia.
• Many systemic complications are possible; these can be divided by system.
  • GI complications include intestinal obstruction, perforation or infarction, malabsorption, hemorrhage, ileus, jaundice, and peritonitis.
  • Respiratory complications include pneumonitis, alveolar hemorrhage, pleural effusion, exacerbation of preexisting pulmonary disease, granulomatous lung disease, and adult respiratory distress syndrome (ARDS).
  • Neurologic complications include meningitis and cerebral abscess.
  • Renal and musculoskeletal complications are rare.

Prognosis

• Acute and chronic strongyloidiasis have a good prognosis. However, untreated infection can persist for the remainder of the patient's life because of autoinfection. A patient's prolonged absence from an endemic area is no guarantee of freedom from infection.
• Severe infection or dissemination is commonly a fatal event, and it is often unresponsive to therapy.²²

Miscellaneous

Medicolegal Pitfalls

• Infected immunocompromised patients are at high risk of developing severe disseminated disease.⁸ Strongyloides infection should be excluded prior to commencing immunosuppressive therapies in patients from endemic areas. Appropriate diagnostic procedures must be performed.
• Imported strongyloidosis should be considered in travelers to and immigrants from endemic areas.²³

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Keywords

strongyloidiasis, cutaneous strongyloidiasis, cutaneous larva migrans, larva currens, racing larva, creeping eruption, creeping infection, threadworm infection, disseminated strongyloidiasis, Strongyloides stercoralis, S stercoralis

Contributor Information and Disclosures

Author

Robert A Schwartz, MD, MPH, Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi
Disclosure: Nothing to disclose.

Coauthor(s)

Mordechai M Tarlow, MD, Physician, Department of Medicine, Section of Dermatology, Kimball Medical Center
Mordechai M Tarlow, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for MOHS Surgery, American Society of Cosmetic Dermatology and Aesthetic Surgery, and Sigma Xi
Disclosure: Nothing to disclose.

Medical Editor

James J Nordlund, MD, Professor Emeritus, Department of Dermatology, University of Cincinnati College of Medicine
James J Nordlund, MD is a member of the following medical societies: American Academy of Dermatology, Sigma Xi, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

Pharmacy Editor

Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center
Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Rosalie Elenitsas, MD, Herman Beerman Associate Professor of Dermatology, University of Pennsylvania School of Medicine; Director, Penn Cutaneous Pathology Services, Department of Dermatology, University of Pennsylvania Health System
Rosalie Elenitsas, MD is a member of the following medical societies: American Academy of Dermatology and American Society of Dermatopathology
Disclosure: Nothing to disclose.

CME Editor

Glen H Crawford, MD, Assistant Clinical Professor, Department of Dermatology, University of Pennsylvania School of Medicine; Chief, Division of Dermatology, The Pennsylvania Hospital
Glen H Crawford, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Phi Beta Kappa, and Society of USAF Flight Surgeons
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

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