A Collection of Conditions Transmitted by Insects or Ticks

Cutaneous Larva Migrans

J Ryan Jackson, DO; Felicia E. Ekpo, DO; Brianna McDaniel, DO; and Jonathan S. Crane, DO
Sampson Regional Medical Center, Clinton, North Carolina

A 67-year-old, previously healthy man presented with a pruritic eruption on his trunk, legs, and arms. The skin manifestations had appeared 1 week after he had come into contact with animal feces in stagnant water while inspecting a house. As the eruption evolved, the pruritus worsened, and the patient developed an intense burning sensation. Slowly advancing lesions appeared on the skin. 

The patient had gone to an urgent care center and had been prescribed oral fluconazole, which had minimally improved his rash. Nevertheless, the pruritus remained severe, and he had attempted to self-medicate with diphenhydramine and topical econazole cream.

At presentation, the patient denied blisters, chills, fevers, joint aches, new medications, new personal care products, or recent infections. The patient’s spouse did not have any similar symptoms. Sweating seemed to exacerbate the patient’s symptoms.

Physical examination. The man’s trunk and bilateral posterior legs and arms demonstrated largely distributed, confluent, erythematous, evanescent, edematous plaques suggestive of urticaria. There were also serpiginous, linear, tunnel-like plaques in the same areas of the body, suggestive of cutaneous larva migrans (CLM).

Discussion. CLM is a skin infection and zoodermatosis caused by helminth larvae, typically parasites of the small intestines of cats and dogs.¹ There are other canine or feline types of hookworm, but the main species for this case is Ancylostoma caninum and Ancylostoma braziliense, which are each approximately 1 cm in length.² The condition commonly occurs in tropical and subtropical areas, particularly sandy terrains that have been polluted with feces of dogs and cats.²

The diagnosis is determined by the clinical history. The characteristic signs of CLM are erythema and papules at the site of entry, followed by a winding, threadlike trail of reddish brown inflammation with a migratory pattern. The eruption usually advances a few millimeters per day. The most common sites for CLM are the feet, spaces between the toes, knees, and buttocks.³ Biopsy is of limited value in the diagnosis of CLM, because the larvae progress past the site of eruption.

Despite our patient’s widespread cutaneous presentation, his history of contact with animal feces aided in the diagnosis of CLM.⁴ This patient’s case demonstrates that urticaria can be triggered by CLM.

The severe pruritus and significant duration associated with CLM make treatment necessary.⁵ Several topical treatments have been shown to be efficacious for more localized lesions, including liquid nitrogen, electrocautery, and 10% to 15% thiabendazole solution or ointment.⁶ For more widespread CLM lesions, systemic treatment is recommended. The recommended pharmacotherapy regimens are albendazole, 400 mg/d for 3 days; ivermectin, 200 µg/kg in a single dose; or thiabendazole, 25 mg/kg/d, divided into 2 doses for 5 days.⁷

Outcome of the case. In this case, treatment with loratadine in the morning and cetirizine in the evening helped the urticaria. The 12-mg dose of ivermectin proved beneficial for our patient’s widespread presentation of CLM. Upon follow-up 22 days later, the patient’s eruption had improved by 90%.

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References:

1. Wieder S, Levitt J. Intensely pruritic eruption in a college student. JAMA. 2014;312(14):1458-1459.
2. Vano-Galvan S, Gil-Mosquera M, Truchuelo M, Jaén P. Cutaneous larva migrans: a case report. Cases J. 2009;2(1):112.
3. Lesshafft H, Schuster A, Reichert F, Talhari S, Ignatius R, Feldmeier H. Knowledge, attitudes, perceptions, and practices regarding cutaneous larva migrans in deprived communities in Manaus, Brazil. J Infect Dev Ctries. 2012;6(5):422-429.
4. Davies HD, Sakuls P, Keystone JS. Creeping eruption: a review of clinical presentation and management of 60 cases presenting to a tropical disease unit. Arch Dermatol. 1993;129(5):588-591.
5. Caumes E. Treatment of cutaneous larva migrans. Clin Infect Dis. 2000;30(5):811-814.
6. Bardazzi F, Stinchi C, Vincenzi C, Tosti A. A travelling bather’s dermatosis: cutaneous larva migrans. J Eur Acad Dermatol Venereol. 1995;4(1):82-85.
7. Meotti CD, Plates G, Nogueira LLC, et al. Cutaneous larva migrans on the scalp: atypical presentation of a common disease. An Bras Dermatol. 2014;89(2):332-333.

Human Botfly Myiasis

Anna Turner; Stephen Winfield; John Folland; and Andrew Rosenthal, MD
Memorial Regional Hospital, Hollywood, Florida

A 62-year-old man with a history of hypertension, hyperlipidemia, benign prostatic hyperplasia, and gastroesophageal reflux disease presented with a 3-week history of swelling on the dorsum of his right hand that was painful to touch. His medications included amlodipine, lovastatin, finasteride, esomeprazole, and doxazosin. His allergy status was unknown. The patient had recently immigrated to the United States from South America.

Physical examination. The man’s vital signs were within normal limits, and he was oriented to person, place, and time. Examination of the skin and extremities revealed a cystic mass on the dorsum of the right hand. The lesion was nonerythematous, raised, and compressible, and it measured 2.0 × 1.5 cm. Mild pain was elicited upon palpation, and a sinus tract was present, which produced small amounts of mucopurulent discharge upon compression. Findings from a review of all other systems were noncontributory.

Figure 1. Cyst excised from patient (left) and botfly specimen recoveryed from cyst (right).

Figure 2. Insect larva excised from the casing.

Treatment. He was taken to the operating room and underwent excision of the mass. During the procedure, a partially disrupted, thick-walled, smooth-surfaced cyst with a smooth inner lining measuring 2.0 × 1.5 × 0.8 cm was excised (Figure 1, left).

Specimens recovered from inside the cyst revealed an exoskeleton-like casing with tan-brown markings (Figure 1, right). Within the casing, there appeared to be an immature insect larva with distinct cuticle spines (Figure 2).

The man received a diagnosis of cutaneous furuncular myiasis caused by human botfly.

Discussion. Human botfly infestation, also known as human cutaneous botfly myiasis, is relatively rare in the United States. The Dermatobia hominis larvae infest the skin and live out 3 self-limiting larval stages, causing pain and discomfort to the host. The typical presentation includes a cystic nodule with a well-defined central pore.¹ Although the botfly is indigenous to Mexico and Central and South America, cases of cutaneous botfly infestation have been reported in the United States and Japan in travelers who had visited endemic areas.^2,3

The life cycle of the human botfly begins with the female botfly laying her eggs on a blood-feeding insect, most commonly a mosquito or a tick.⁴ When the insect feeds on a warm-blooded mammal—commonly dogs, cattle, cats, horses, or in some cases, humans—the eggs hatch as a result of the warmth. The larvae then burrow into the host’s skin through the bite wound or a hair follicle and anchor into the subcutaneous layer by means of small spines on their exterior surface. Once anchored, the larvae mature and remain in the host for 5 to 12 weeks.⁵ As the larvae grow, a compressible and painful lesion develops on the surface of the skin. In the United States, the diagnosis of human botfly infection often is missed or is misdiagnosed as either superficial cellulitis, an infected sebaceous cyst, or an insect bite resulting in a skin lesion.⁶

Several treatments have been described for human botfly myiasis, including injection of lidocaine, which aids in manually bringing the larvae to the skin’s surface, and application of petroleum jelly or raw meat to the area, which acts as a barrier to occlude oxygen to the larvae. The larvae then are forced to the skin surface and subsequently removed with an adhesive medium such as beeswax, paraffin, or chewing gum.^7-9 Bacon therapy even has been reported as a means to lure the larvae out of the skin.¹⁰ Surgical resection with local anesthetics, however, remains the gold-standard treatment.¹¹ 

To ensure the complete removal of the organism, excisional biopsy is recommended.¹ All biopsy specimens should be sent to a pathology laboratory for tissue analysis and definitive identification of the organism.

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References:

1. Sampson CE, MaGuire J, Eriksson E. Botfly myiasis: case report and brief review. Ann Plast Surg. 2001;46(2):150-152.
2. Lawson RD, Rizzo M. Digital infestation with the human bot fly. J Hand Surg Br. 2005;30(5): 490-491.
3. Haruki K, Hayashi T, Kobayashi M, Katagiri T, Sakurai Y, Kitajima T. Myiasis with Dermatobia hominis in a traveler returning from Costa Rica: review of 33 cases imported from South America to Japan. J Travel Med. 2005;12(5):285-288.
4. Safdar N, Young DK, Andes D. Autochthonous furuncular myiasis in the United States: case report and literature review. Clin Infect Dis. 2003;36(7):e73-e80.
5. Acha PN, Szyfres B. Myiases. In: Acha PN, Szyfres B. Zoonoses and Communicable Diseases Common to Man and Animals. Vol 3. 3rd ed. Washington, DC: Pan American Health Organization; 2003:331-345.
6. Iannini PB, Brandt D, LaForce M. Furuncular myiasis. JAMA. 1975;233(13):1375-1376.
7. Baird JK, Baird CR, Sabrosky CW. North American cuterebrid myiasis: report of seventeen new infections of human beings and review of the disease. J Am Acad Dermatol. 1989;21(4 pt 1):763-772.
8. Prasad C, Beck AR. Myiasis of the scalp from Dermatobia hominis. JAMA. 1969;210(1):133.
9. Elgart ML. Flies and myiasis. Dermatol Clin. 1990;8(2):237-244.
10. Brewer TF, Wilson ME, Gonzalez E, Felsenstein D. Bacon therapy and furuncular myiasis. JAMA. 1993;270(17):2087-2088.
11. Harrell WB, Mosely V. The surgical treatment of subdermal myiasis due to Dermatobia hominis. South Med J. 1942;35:720-723.

A Lyme Disease “Selfie”

Henry M. Feder Jr, MD
Connecticut Children’s Medical Center, Hartford, Connecticut

Gary P. Wormser, MD
New York Medical College, Valhalla, New York

Deborah Cushman
Asylum Hill Family Medicine, Hartford, Connecticut

A 58-year-old woman developed a painful red rash behind her left knee. She lived in a wooded area of Connecticut, which is moderately endemic for Lyme disease, but she had spent the day outside picking apples in a hyperendemic area of the state 8 days before the onset of her eruption. She was not aware of a tick bite.

Her rash had enlarged over 3 days and prompted a visit to her primary care physician. At that visit, she was afebrile and had no systemic complaints. Physical examination findings were unremarkable except for a slightly painful, erythematous, annular rash behind her left knee. She was thought to have erythema migrans (EM, the early localized manifestation of Lyme disease); Lyme disease serology was ordered, and doxycycline (100 mg, twice a day for 20 days) was prescribed.

The patient took 1 dose of doxycycline that evening and a second dose the next morning. She then presented for a second opinion about her rash. Her eruption had faded, and its appearance was nonspecific. An EM rash may fade quickly after just 2 doses of antibiotic therapy. She then opened her cell phone and showed a photograph that she had taken before starting the doxycycline—a “Lyme selfie” (Figure). The rash in the photograph was characteristic of Lyme disease: an erythematous ring greater than 10 cm in diameter, then clearing, then a central confluent erythema—ie, a bull’s-eye appearance. The rash completely resolved over 48 hours, and she remained well.

Discussion. Lyme disease serology, which was done by her primary care physician, came back positive. A positive Lyme disease serology is defined as a positive first-step polyvalent enzyme immunoassay (EIA) and a positive second-step immunoblot (immunoglobulin M [IgM] and/or immunoglobulin G [IgG]). An IgM immunoblot is positive if 2 of 3 (23kDa, 39kDa, and/or 41kDa) bands are present. After 4 to 6 weeks of untreated Lyme disease, the IgG immunoblot should be positive. An IgG immunoblot is positive if 5 of 10 particular bands are present.

Our patient had a positive EIA and a positive IgM immunoblot with 23kDa and 41kDa bands. No IgG bands were present. This result suggests a Borrelia burgdorferi infection of less than 6 weeks’ duration, which fits the clinical story. At the onset of EM, many patients are seronegative, and prompt treatment may even prevent seroconversion. The diagnosis of EM is clinical; routine B burgdorferi serologic testing is not needed or recommended.^1-4

The patient had a classic picture of EM: an annular, erythematous skin lesion greater than 5 cm in diameter with central erythema, that occurred in a person who had spent time outdoors in a Lyme disease–endemic area. Most patients who develop Lyme disease are not aware of a tick bite, since most tick bites go undetected.

In a prospective study of 10,936 participants in a Lyme disease vaccine trial,⁵ 147 participants developed definite Lyme disease, and 118 of the 147 (80%) presented with EM. EM begins as a red macule or papule that expands for days to weeks to form a large, annular, erythematous lesion that ranges from 5 to 70 cm in diameter (median, 15 cm). This skin lesion may be uniformly erythematous, or it may appear as a target lesion with a variable degree of central erythema. Alternatively, EM lesions may instead have central clearing. EM skin lesions can vary greatly in shape and occasionally may have a vesicular or necrotic area in the center. In the above-mentioned prospective study of 118 adult patients with EM,⁵ the lesions were homogeneously erythematous in 59%, had a target-like bull’s-eye appearance in 32%, and had central clearing in 9%.

EM usually is asymptomatic but may be pruritic or painful.¹ More than half of US patients with EM have other symptoms and/or signs such as fever, fatigue, malaise, headache, regional lymphadenopathy, stiff neck, myalgia, and arthralgia.⁴

Treatment. Doxycycline, amoxicillin, or cefuroxime axetil are the drugs of choice for the treatment of EM.⁶ Exposure to the sun should be avoided by individuals taking doxycycline, because an erythematous rash or a blistering eruption may develop in sun-exposed areas in 20% to 30% of patients taking this drug. Use of sunscreen may decrease this risk. Doxycycline usually is available in 2 formulations, doxycycline monohydrate and doxycycline hyclate. The monohydrate formulation may have better gastrointestinal tract tolerability.⁷ Amoxicillin is recommended for children younger than 8 years of age and for pregnant women. Azithromycin is an alternative for patients allergic to β-lactam antibiotics and who cannot take doxycycline, but macrolide antibiotics appear to be less effective than other agents. Most experts recommend a 14- to 21-day course of therapy for early, localized Lyme disease (except for azithromycin, which is given for 7-10 days), although evidence indicates that 10 days of doxycycline is adequate treatment in adults with uncomplicated infection. Courses shorter than 14 to 21 days have not been studied for amoxicillin or cefuroxime axetil therapy.^6,8 Objective complications following treatment of EM are extremely rare, but some patients may have mild subjective complaints (posttreatment Lyme disease symptoms) that persist for months to years following resolution of EM.⁴

Insect repellents that contain N,N-diethyl-m-toluamide (DEET) applied to the skin protect against tick bites. DEET concentrations of 20% to 30% usually are effective for 6 to 8 hours. DEET should be applied sparingly only to exposed skin, but not to skin that is either irritated or abraded. Permethrin, a synthetic pyrethroid, is available in a spray for application to clothing only; this compound kills ticks on contact.^6,9

The vector of Lyme disease is the deer tick, also called the blacklegged tick (Ixodes scapularis). After attachment, it takes at least 36 hours for deer tick infected with B burgdorferi to infect its host. Thus, tick checks and tick removal before 36 hours of attachment is a useful way to avoid infection. The overall risk of developing EM after finding an attached deer tick in areas where Lyme disease is highly endemic is 1% to 3%.⁴ 

The option of waiting, watching, and treating the EM should it occur has been suggested but may not be acceptable to an anxious patient or family members.¹⁰ In a randomized trial of antibiotic prophylaxis following deer tick bites, Lyme disease (EM) occurred in 1 of 235 (0.4%) subjects given a single 200-mg dose of doxycycline vs 8 of 247 (3.2%) of those given placebo.¹¹ Amoxicillin, 250 mg 3 times daily for 10 days, is an alternative regimen for tick-bite prophylaxis.¹² 

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References:  

1. Malane MS, Grant-Kels JM, Feder HM Jr, Luger SW.  Diagnosis of Lyme disease based on dermatologic manifestations. Ann Intern Med. 1991; 144(6):490-498.
2. Feder HM Jr, Whitaker DL. Misdiagnosis of erythema migrans. Am J Med. 1995;99(4):412-419.
3. Aguero-Rosenfeld ME, Wang G, Schwartz I, Wormser GP. Diagnosis of Lyme borreliosis. Clin Microbiol Rev. 2005;18(3):484-509.
4. Wormser GP. Clinical practice: early Lyme disease. N Engl J Med. 2006;354(26):2794-2801.
5. Smith RP, Schoen RT, Rahn DW, et al. Clinical characteristics and treatment outcome of early Lyme disease in patients with microbiologically confirmed erythema migrans. Ann Intern Med. 2002;136(6):421-428.
6. Wormser GP, Dattwyler RJ, Shapiro ED, et al. The clinical assessment, treatment, and prevention of Lyme disease, human granulocytic anaplasmosis, and babesiosis: clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis. 2006;43(9):1089-1134.
7. US Centers for Disease Control and Prevention. Medicines for the prevention of malaria while traveling: doxycycline. http://www.cdc.gov/malaria/resources/pdf/fsp/drugs/Doxycycline.pdf. Accessed May 12, 2016.
8. Wormser GP, Ramanathan R, Nowakowski J, et al. Duration of antibiotic therapy for early Lyme disease: a randomized, double-blind, placebo-controlled trial. Ann Intern Med. 2003;138(9):697-704.
9. Hayes EB, Piesman J. How can we prevent Lyme disease? N Engl J Med. 2003;348(24):2424-2430.
10. Shapiro ED. Doxycycline for tick bites—not for everyone. N Engl J Med. 2001;345(2):133-134. 
11. Nadelman RB, Nowakowski J, Fish D, et al; Tick Bite Study Group. Prophylaxis with single-dose doxycycline for the prevention of Lyme disease after an Ixodes scapularis tick bite. N Engl J Med. 2001;345(2):79-84.
12. Shapiro, ED, Gerber MA, Holabird NB, et al.  A controlled trial of antimicrobial prophylaxis for Lyme disease after deer-tick bites. N Engl J Med. 1992;327(25):1769-1773.

Strongyloidiasis

Patricia Dominguez, MD; Matthew Lincoln, DO; and Anish Patel, DO
Carl R. Darnall Army Medical Center, Fort Hood, Texas

A 51-year-old Filipino man presented for a screening colonoscopy. The patient denied any significant complaints including diarrhea, hematochezia, fever, chills, and weight changes. He reported having a good appetite. 

He had emigrated from the Philippines in his late teens, but he had served in the US Army for 25 years, including tours in Southeast Asia.

Physical examination. The man was well appearing and in no acute distress, with normal vital signs. Abdominal examination findings were unremarkable. Prior laboratory evaluation had demonstrated a normal white blood cell count and a normal eosinophil absolute count.

The patient underwent a screening colonoscopy with an excellent prep, with evidence of mild sigmoid diverticulosis. A single sessile polyp, measuring less than 5 mm in size, was found in the ascending colon and was removed by cold biopsy polypectomy. On further mucosal evaluation, multiple small (< 1 mm), scattered, punctate nodules appeared throughout the entire colon (Figure). A random biopsy was obtained for further evaluation by pathology.

Tissue biopsy results revealed a small hyperplastic polyp from the ascending colon. Random colonic biopsy of the nodules demonstrated marked eosinophilia in the surface and crypt epithelia, lamina propria, and muscularis mucosae. Expert review from the Joint Pathology Center in Washington, DC, also noted Strongyloides stercoralis in a crypt of one section of the biopsy from the ascending colon polypectomy sample.

The patient underwent treatment with ivermectin (15-mg one-time oral dose) followed by an additional 20-mg dose 2 weeks later, without any complications.

Discussion. S stercoralis is an intestinal helminth nematode considered endemic to tropical and subtropical regions that infects humans through contact with soil containing the larvae.^1,2 Strongyloidiasis has various presentations ranging from cutaneous symptoms to gastrointestinal tract symptoms but is asymptomatic in 50% or more of cases, with the only indication of disease denoted by peripheral eosinophilia.² It can lead to hyperinfection, dissemination, or death.

The World Health Organization estimates that 30 million to 100 million individuals worldwide are infected with S stercoralis.³ Infections tend to have a higher prevalence among individuals of low socioeconomic status, those with alcoholism, and men; like other soil-transmitted helminths, the risk of infection is associated with hygiene, making children especially vulnerable to infection.^3,4 Various risk factors have been associated with strongyloidiasis, including immunosuppressive therapy, malignancy, organ transplants, human immunodeficiency virus infection, human T-cell lymphotropic virus 1 infection, alcoholism, tuberculosis, impaired bowel motility, leprosy, and chronic renal failure.⁵

Strongyloidiasis is transmitted through direct penetration of human skin by infective larvae when in contact with soil; walking barefoot therefore is a major risk factor for acquiring the infection, especially in endemic areas where vegetation or soil is exposed to human excrement.³ After penetration through the skin, larvae are carried hematogenously to the lung, specifically the alveoli, where pneumonitis may occur, or the person may remain asymptomatic.^4-6 Larvae from the alveoli are expectorated, traveling up the tracheobronchial tree to the pharynx, then are swallowed. Strongyloides spp larvae reach the small intestine, where they mature into female adults and produce eggs, which hatch in the gut lumen and yield larvae that are evacuated in feces. Larvae that are not excreted transform into infectious filariform larvae and penetrate the perirectal mucosa or skin, and reenter the circulatory system, restarting the cycle, also known as autoinfection.^3-5

Strongyloides infections can vary in clinical presentation but are asymptomatic in more than 50% of cases.² The severity and duration of symptoms is closely related to the immune status of the host.⁴ Hyperinfection syndrome has been described regardless of dose, duration, or route administration of corticosteroids, and even in short courses of corticosteroids in immunocompetent patients without underlying immunosuppressive conditions.^5,6 Progression to hyperinfection can be related to the eosinophil and mast cell depletion in the intestinal mucosa.⁷ Evaluating the histopathology of the biopsies obtained from colonoscopy prior to treatment of our patient was therefore imperative, since empiric treatment with corticosteroids could have increased the parasite load, substantially increasing the risk of hyperinfection.

Eosinophilia may be the only initial presenting finding in S stercoralis infection. Eosinophilia can occur in various disorders, but the most common cause worldwide is helminthic infections. Interestingly, our patient did not present with eosinophilia (chronic or acute) but was raised in an endemic area (Southeast Asia) and likely was exposed further during his military career. Having normal eosinophil counts, therefore, does not preclude patients from having strongyloidiasis.⁸

With the devastating progression of disease, the question arises whether patients should be screened for helminthic infections even if they are asymptomatic. Patients with a history of travel to an area where strongyloidiasis is endemic and who have compatible symptoms, immunosuppressive conditions, or blood eosinophilia should be further evaluated for possible infection.² Ethanol abuse also has been shown to be important in the reactivation of strongyloidiasis, and a recent case study recommended that all alcoholics, even those who are asymptomatic, be screened.⁷ Screening high-risk patients can be performed easily by obtaining 3 different stool samples on different days and/or screening for S stercoralis serology.²

While our patient had an incidental finding on routine colonoscopy, many times strongyloidiasis is diagnosed incidentally. Health care providers should be educated about the signs and symptoms and the patient population at high risk, since 50% of the time patients with strongyloidiasis are asymptomatic. Former or active-duty members of the military stationed in endemic regions should be considered for routine screening, since infection can lay dormant for decades.

References:

1. Page KR, Zenilman J. Eosinophilia in a patient from South America. JAMA. 2008;299(4):437-444.
2. Greaves D, Coggle S, Pollard C, Aliyu SH, Moore EM. Strongyloides stercoralis infection. BMJ. 2013;347:f4610.
3. Strongyloidiasis. World Health Organization. http://www.who.int/intestinal_worms/epidemiology/strongyloidiasis/en/. Accessed May 12, 2016.
4. Rets A, Gupta R, Haseeb MA. Determinants of reactivation of inapparent Strongyloides stercoralis infection in patients hospitalized for unrelated admitting diagnosis. Eur J Gastroenterol Hepatol. 2013;25(11):1279-1285.
5. Mejia R, Nutman TB. Screening, prevention, and treatment for hyperinfection syndrome and disseminated infections caused by Strongyloides stercoralis. Curr Opin Infect Dis. 2012;25(4):458-463.
6. Chordia P, Christopher S, Abraham OC, Muliyil J, Kang G, Ajjampur SSR. Risk factors for acquiring Strongyloides stercoralis infection among patients attending a tertiary hospital in south India. Indian J Med Microbiol. 2011;29(2):147-151.
7. Teixeira MCA, Inês EJ, Pacheco FTF, et al. Asymptomatic Strongyloides stercoralis hyperinfection in an alcoholic patient with intense anemia. J Parasitol. 2010;96(4):833-835.
8. Rothenberg ME. Eosinophilia. N Engl J Med. 1998;338(22):1592-1600.