(Chest. 2003;123:1296-1297.)
© 2003
American College of Chest Physicians
Visceral Larva Migrans Mimicking Lymphoma*
Claude Bachmeyer, MD;
Gérard Lamarque, MD;
Rodica Morariu, MD;
Thierry Molina, MD;
Patrice Bourée, MD and
Alain Delmer, MD
* From Département de Médecine Interne (Dr. Bachmeyer) and Service de Pneumologie (Dr. Lamarque), Center Hospitalier Laënnec, Creil; Service d’Hématologie (Drs. Morariu and Delmer), Hôpital Hôtel Dieu, Paris; Laboratoire d’Anatomo-Pathologie (Dr. Molina), Hôpital Hôtel Dieu, Paris; and Laboratoire de Parasitologie (Dr. Bourée), Hôpital Bicêtre, Le Kremlin-Bicêtre, France.
Correspondence to: Claude Bachmeyer, MD, Département de Médecine Interne, Center Hospitalier Laënnec, Boulevard Laënnec, B. P. 72, F-60109 Creil Cedex, France; e-mail: claude.bachmeyer{at}ch-creil.fr
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Abstract
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We report a case of visceral larva migrans in an adult with fever, night sweats, weight loss, hilar and mediastinal lymphadenopathy, bilateral pleural effusion, and eosinophilia-mimicking lymphoma. Visceral larva migrans was diagnosed subsequently because of negative findings for malignancy and positive serologic test result for Toxocara canis. Progressive improvement was observed with albendazole therapy.
Key Words: albendazole • eosinophilia • hilar and mediastinal lymphadenopathy • visceral larva migrans
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Introduction
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Visceral larva migrans (VLM) is an infection mainly due to Toxocara canis, a common worldwide ascarid specially of children < 6 years of age.1
A wide spectrum of manifestations has been described from asymptomatic infection to fulminant disease.1
These mainly include fever, hepatomegaly, leukocytosis, eosinophilia, and hypergamma globulinemia. We report a case of VLM with hilar and mediastinal lymphadenopathy in an adult mimicking lymphoma.
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Case Report
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A 65-year-old French man with no medical history was admitted to the hospital in June 2001 for temperature of 39°C and night sweats evolving for 2 weeks. He denied ingestion of any drug and had traveled to the French West Indies 6 months previously. On hospital admission, the patient appeared fatigued and had lost 5 kg in weight. The physical examination was otherwise unremarkable. The WBC count showed 10,800/µL, with 50% neutrophils, 17% lymphocytes, and 26% eosinophils (absolute count, 2,830/µL). Erythrocyte sedimentation rate was 86 mm/h. C-reactive protein was 85 mg/L (normal > 13 mg/L). Electrolytes, liver function test results, serum creatinine level, and lactate dehydrogenase level were normal. Serum electrophoresis showed an albumin level of 32.8 g/L (normal > 39 g/L); 
2-globulin, 9.8 g/L (normal < 7 g/L); and polyclonal 
-globulinemia, 16.9 g/L (normal < 10 g/L). Search for antinuclear, anti-double-stranded DNA, antineutrophil cytoplasmic antibodies, and rheumatoid factor was negative. Infectious inquiry included blood and urine cultures and search for mycobacteria in sputum; serologic study findings for Chlamydia psittaci and Chlamydia pneumoniae, Coxiella burnetii, Legionnella pneumophilia, and Mycoplasma pneumoniae were negative. Chest radiography and thoracoabdominal CT scan showed bilateral hilar and mediastinal lymphadenopathy 2 to 5 cm in diameter, and discrete bilateral pleurisy (Fig 1
). Fiberoptic bronchoscopy demonstrated a diffuse inflammation with a nonspecific inflammation on lung biopsy; direct search for pathogens and culture findings were negative.
Treatment with ceftriaxone, amikacin, and metronidazole, then amoxicillin/clavulanic acid and ofloxacin was ineffective. Mediastinoscopy with partial lymphadenectomy was performed. Analysis of lymph nodes specimens showed destruction of their architecture with a polymorphic cellular infiltrate consisting of eosinophils, histiocytes, fibroblasts, and plasmocytes, and vascular hyperplasia. Immunophenotyping and analysis of IgH and T-cell receptor gene rearrangements failed to detect any monoclonal T-cell or B-cell population. Bacterial culture results of lymph nodes remained negative. Bone marrow biopsy results were normal. Therefore, the patient was referred to us in July of 2001. A parasitic infection was considered, and treatment with albendazole was administered at 400 mg/d for 10 days. Search for parasites in feces was negative. All helminthiasis serology results were negative, but T canis enzyme-linked immunosorbent assay serology was highly positive (optical density/optical density threshold 0.720; positive > 0.3), with antibodies directed against 24-kd and 35-kd antigens. The patient said that he had been in daily contact with a dog during the previous months. Progressive improvement of the general symptoms was observed. In August 2001, he felt well, had no fever, the eosinophil count was normal, the serology for T canis was stable, and mediastinal lymph nodes and pleurisy had almost disappeared.
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Discussion
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We report the case of a patient with fever, night sweats, weight loss, hilar and mediastinal lymphadenopathy, and eosinophilia related to VLM. This diagnosis was supported by the positive result of the enzyme-linked immunosorbent assay test for T canis and progressive improvement after treatment with albendazole. Other conditions responsible for eosinophilia, such as drug reactions, allergic diseases, autoimmune disorders, and idiopathic hypereosinophilic syndrome, were easily ruled out. Diagnosis of malignancy—particularly lymphoma—was initially suspected, but extensive investigations failed to demonstrate any neoplasm. Because of negative findings, a parasitic infection was subsequently considered.
Pulmonary symptoms mainly consist of cough and wheezing and are reported in 20 to 85% of cases in children with VLM.1
Bilateral areas of infiltration are observed in 40 to 50% of patients with pulmonary symptoms.1
Diffuse noncavitating nodules are unusual.2
Severe symptoms seem to be very rare in adults. Eosinophilic pneumonia responsible for acute respiratory disease, important pleural effusion sometimes associated with tamponade, and severe asthma have been reported.3
4
5
Mediastinal lymphadenopathy has not been reported in toxocariasis to the best of our knowledge. Conversely, hepatohilar and/or peripancreatic lymph node enlargement on ultrasound findings was observed in 78% of 18 children with VLM.6
Cervical adenitis was observed in 78% of patients with high titer of toxocara antibodies and recent clinical toxocariasis.1
VLM is usually a benign and self-limited condition, and treatment is rarely necessary. However, treatment with diethylcarbamazine, thiabendazole, mebendazole, albendazole, and now ivermectin could relieve symptoms and decrease convalescent time.1
Treatment with corticosteroids is indicated in life-threatening illnesses in association with antihelminthic drugs.3
4
Preventive measures of infection are achieved by prevention of contamination of the environment, avoidance of earth ingestion, and hand washing before meals.1
Diagnosis of VLM is often difficult in adults, requiring a high index of suspicion. Physicians should keep in mind its wide spectrum of symptoms, including hilar and mediastinal lymphadenopathy-mimicking lymphoma.
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Footnotes
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Abbreviation: VLM = visceral larva migrans
Received for publication March 21, 2002.
Accepted for publication August 1, 2002.
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References
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- Taylor, MRH, Keane, CT, O’Connor, P, et al (1988) The expanded spectrum of toxocaral disease. Lancet i,692-694
- Roig, J, Romeu, J, Riera, C, et al Acute eosinophilic pneumonia due to toxocariasis with broncho-alveolar lavage findings. Chest 1992;102,294-296[Abstract/Free Full Text]
- Jeanfaivre, T, Cimon, B, Tolstuchow, N, et al Pleural effusion and toxocariasis. Thorax 1996;51,106-107[Abstract]
- Herry, I, Philippe, B, Hennequin, C, et al Acute life-threatening toxocaral tamponade. Chest 1997;112,1692-1693[Abstract/Free Full Text]
- Feldman, GJ, Parker, HW Visceral larva migrans associated with the hypereosinophilic syndrome and the onset of severe asthma. Ann Intern Med 1992;116,838-840[ISI][Medline]
- Baldisserotto, M, Conchin, CF, Soares, MD, et al Ultrasound findings in children with toxocariasis: report on 18 cases. Pediatr Radiol 1999;29,316-319[CrossRef][Medline]
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Abstract
Introduction
