GENERALIZED LYMPHADENOPATHY AS INITIAL PRESENTATION OF TOXOCARIASIS IN A SEVEN-YEAR-OLD BOY (1996)

The incidence of toxocariasis in the pediatric population is approximately 7 to 14%.1 Infection in the human can range from full-blown visceral larva migrans and ocular larva migrans to asymptomatic eosinophilia.2, 3 Toxocariasis should be considered in the child with chronic abdominal pain, headache and persistent cough.1, 4 We describe a 7-year-old boy with toxocariasis who presented with generalized lymphadenopathy, hemolytic anemia and mild eosinophilia. Case report. A 7-year-old, previously healthy boy was admitted to the hematology unit because of persistent generalized lymphadenopathy. Six weeks earlier he had been treated for purulent tonsillitis with trimethoprim-sulfamethoxazole. After 10 days he was sent to the regional hematologic outpatient department with suspicion of infectious mononucleosis because of recurrent fever, lymphadenopathy and hepatosplenomegaly. Atypical lymphocytes were not seen on the blood smear, and a Paul-Bunnell-Davidsohn test was negative. The boy did not improve with oral cefuroxime and doxycycline treatment. Another febrile episode was accompanied by bone pain and intense pruritus of the trunk. The boy was subsequently admitted in good condition to our department. Physical examination revealed generalized lymphadenopathy (bilaterally enlarged cervical anterior and posterior, submandibular, supraclavicular, axillary and inguinal lymph nodes 0.5 to 2 cm in diameter, firm and not matted together), hepatomegaly (0.5 cm below costal margin) and splenomegaly (2 cm below the costal margin). Laboratory findings included an erythrocyte sedimentation rate of 65 mm/h; leukocyte count of 5.8 × 109/l, platelet count 196 × 109/l and hemoglobin 11.6 g/dl. The differential count showed 43% neutrophils, 16% eosinophils, 40% lymphocytes and 1% monocytes. Thirty-three percent of the lymphocytes in the peripheral blood were B cells (1.1 × 109/l), 62% T cells (CD4+ cells, 38%; CD8+ cells, 25%; CD4:CD8 ratio, 1.5), and 5% natural killer cells. Renal and liver function studies were normal. The concentration of IgG was 28.0 g/l, IgM 1.96 g/l and IgA 5.22 g/l. Bone marrow aspirate examination excluded the diagnosis of a malignancy and revealed slight eosinophilia. Chest radiograph, abdominal ultrasound and ophthalmologic examination showed no abnormalities. Negative serologic reactions were documented for brucellosis, yersiniosis, toxoplasmosis, giardiasis, cytomegalovirus, hepatitis B virus, hepatitis C virus, Epstein-Barr virus infections, fascioliasis and trichinosis. A Mantoux test was negative. A serum specimen for detection of Toxocara-specific IgG was sent to a reference laboratory, where it was stored at -20°C. During the first month of treatment the patient had intermittent fevers to 39°C, despite sequential administration of amoxicillin, cefuroxime, doxycycline, gentamicin and trimethoprim-sulfamethoxazole. Generalized, pruritic maculopapular (morbilliform) skin eruptions were observed during the third week of treatment. Because of increasing lymphadenopathy, with matting of the lymph nodes, presence of nodes in the hilus of the spleen and markedly increased erythrocyte sedimentation rate (160 mm/h) a lymph node biopsy was performed. Histopathologic examination revealed features of hyperplastic lymphadenitis with activation of B cell and T cell zones, the presence of immunoblasts, sinus histiocytosis and vascular proliferation. The picture was consistent with that seen in viral infections or postvaccinal reactions. In the fifth week of treatment hemolysis was diagnosed on the basis of a hemoglobin of 7.5 g/dl and an increased reticulocyte count in the presence of IgG anti-erythrocyte antibodies. Prednisone 1 mg/kg was administered with good results. Blood counts normalized and lymphadenopathy diminished. Two months later we learned that in the anti-Toxocara IgG enzyme-linked immunosorbent assays with serum-diluted 1:200 extinctions were 0.95 (on 10.11.1994) and 1.109 (on 11.01.1995) (negative control, 0.239; positive control, 0.722; strong positive control, 1.069). Oral thiabendazole (25 mg/kg) was given and continued for 7 days. At the end of the treatment we did not observe recurrence of fever and skin eruptions. The lymphadenopathy decreased markedly. The anti-Toxocara enzyme-linked immunosorbent assay extinction decreased to 1.091 (negative control, 0.34; positive control, 1.18; highly positive control, 1.649). Two months after completion of treatment the specific anti-Toxocara IgG increased to 2.445, and a 7-day course of thiabendazole was repeated twice during the course of 2 months. After observation for 10 months, the patient's general condition was good, with peripheral lymph nodes <0.5 cm in diameter as the only abnormality on physical examination. Blood counts, leukocyte differential count and erythrocyte sedimentation rate were normal, and specific Toxocara antibodies were only weakly detectable. Discussion. Toxocariasis is a zoonosis transmitted to human beings by ingestion of infective eggs. Dogs are natural hosts of the parasite, especially puppies, as well as pregnant and lactating bitches. Soil sampling has revealed widespread contamination of house gardens, parks and playgrounds (sandpits) with parasite eggs.1, 5 Pica habits and poor sanitary condition favor the development of the disease.1, 6 Traditionally two clinical syndromes are described, visceral larva migrans and ocular toxocariasis.2, 7-9 Recently a third condition was distinguished, termed “covert toxocariasis” and comprising cases of infection manifested by nonspecific signs and symptoms such as chronic abdominal pain, headache, persistent cough and sleep and behavioral disturbances.10, 11 It occurs much more frequently than classically described syndromes. Sometimes moderate eosinophilia is the only abnormality. Asymptomatic toxocariasis also can occur.6, 10, 12 Generalized lymphadenopathy, a predominant feature in our patient, is rarely reported in visceral larva migrans in contrast to localized, mainly cervical, lymphadenitis.13-15 Hemolysis infrequently accompanying toxocariasis is caused by increased anti-A and anti-B agglutinin concentrations probably because of a similarity of larval surface antigens to erythrocyte glycoproteins.16 The course of toxocariasis is usually benign and symptoms subside within a few weeks, although the eosinophilia and high immunoglobulin titers may persist for years.17 Symptoms usually regress with administration of thiabendazole or fenbendazole.13 This group of patients, which includes ours, should be carefully observed, because the pathologic process may be reactivated. Our observations suggest that Toxocara canis infection should be included in the differential diagnosis of generalized lymphadenopathy, particularly when accompanied by fever, hepatosplenomegaly and mild eosinophilia. Acknowledgments. This study was supported by the Polish Scientific Committee (KBN-4-5405 047 06). The authors are grateful to Professor J. J. M. van Dongen and Dr. R. de Groot from the Departments of Immunology and Pediatrics/Division of pediatric Infectious Diseases of Erasmus University in Rotterdam for a critical reading of the manuscript. Tomasz Szczepański, M.D.; Danuta Sońta-Jakimczyk, M.D., Ph.D.; Anna Janik-Moszant, M.D.; Igor Olejnik, M.D. Department of Pediatrics and Hematology Silesian School of Medicine 41-800 Zabrze, Poland