February 2006, VOLUME117 /ISSUE 2

Visceral Larva Migrans Associated With Earthworm Ingestion: Clinical Evolution in an Adolescent Patient

  1. Antonella Cianferoni, MDa,
  2. Lynda Schneider, MDa,
  3. Peter M. Schantz, VMD, PhDb,
  4. Daniel Brown, MD, PhDa,
  5. LeAnne M. Fox, MD, MPHc,d
  1. Divisions ofaImmunology
  2. cInfectious Diseases, Children's Hospital, Boston, Massachusetts
  3. bDivision of Parasitic Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia
  4. dCenter for International Health and Development, Boston University, Boston, Massachusetts


A 16-year-old girl developed a cough, hypereosinophilia (absolute eosinophil count: 32000/mm3), hypergammaglobulinemia, and multiple noncavitary pulmonary nodules 1 month after having ingested an earthworm on a dare. Spirometry revealed moderate restriction and reduced gas diffusion. Parabronchial biopsy demonstrated eosinophilic organizing pneumonitis with multiple eosinophilic microabscesses, and Toxocara titers were elevated (>1:4096). Ophthalmologic examination ruled out ocular larva migrans. The patient received a 10-day course of albendazole (400 mg orally twice daily) and demonstrated significant clinical improvement with resolution of cough and pulmonary function abnormalities. Her white blood cell count and hypergammaglobulinemia normalized within 20 days, yet eosinophils (absolute eosinophil count: 1780/mm3) and Toxocara serologies (>1:4096) remained elevated 3 months after completing antihelminthic therapy. In this instance, the ingested earthworm served as the paratenic carrier of Toxocara larvae from the soil to the patient. This case highlights the clinical evolution of pulmonary visceral larva migrans infection caused by Toxocara spp. associated with a discrete ingestion in an adolescent patient. In addition, it provides a rare opportunity to define the incubation period of visceral larva migrans and emphasizes the importance of education regarding sources of Toxocara infection.

  • visceral larva migrans
  • Toxocara
  • pediatric
  • eosinophilia
  • pulmonary


A16-year-old white female with a history of asthma, urticaria, and bipolar disorder presented for evaluation to the allergy program of our hospital in mid-September 2004 with a 2-week history of progressively increasing eosinophilia associated with moderate cough, wheezing, and 5-lb weight loss. Two weeks before presentation, she had experienced nausea, a temperature to 101°F, and swelling around her eyes, cheeks, and lips and near the thenar eminence of the palm. All symptoms spontaneously resolved in 2 to 3 days.

On physical examination diffuse wheezes with moderately diminished air entry were noted on lung auscultation. Otherwise, the patient had a soft, nontender abdomen without organomegaly, no lymphadenopathy, rashes, or ocular symptoms, and a normal mental-status examination. Spirometry revealed moderate restriction (forced vital capacity [FVC]: 2.78 L at 54% of predicted [reference range: 80–100%]; forced expiratory volume in 1 second [FEV1]: 2.22 L at 58% of predicted [reference range: 80–100%]; FEV1/FVC: 107% [reference range: 80–100%]; forced expiratory flow rate between 25% and 75% of the forced vital capacity [FEF25–75]: 2.07 L/second at 55% of predicted [reference range: 70–100%]) and reduced gas diffusion (diffusion capacity of 14.63 at 58% of predicted [reference range: 80–100%]). Laboratory evaluation revealed leukocytosis, a white blood cell (WBC) count of 47800/mm3 with 67% eosinophils (absolute eosinophil count: 32000/mm3), elevated platelet count (445000/mm3), and normal hematocrit. Hypergammaglobulinemia, with increased levels of immunoglobulin (Ig)G (1870 mg/L [reference range: 639–1344 mg/L]), IgM (962 mg/L [reference range: 40–240 mg/L]), and IgE (1570 ng/L [reference range: 0–200 ng/L]), was also noted. The erythrocyte sedimentation rate, C-reactive protein, antineutrophil cytoplasmic antibody, IgA hepatic transaminase, serum urea nitrogen, and creatinine levels were within normal limits. An echocardiogram and electrocardiogram were normal.

The patient denied any history of travel. She smokes half a pack of cigarettes per day and had been taking ibuprofen once or twice daily for occasional headaches for 2 weeks before evaluation. She had a cat and guinea pig at home. She denied pica but stated that she had eaten an earthworm on a dare at the beginning of August 2004. This event occurred in a friend's backyard in which a dog and puppy frequently played. She also denied ingestion of any undercooked or raw meat or liver.

Non–contrast-enhanced chest computed tomography images demonstrated small (5-mm), noncavitary bilateral nodular opacities that were predominantly peripheral in location; several were associated with a hazy ground-glass appearance (Fig 1). Small bilateral pleural effusions were noted also. There was no evidence of pulmonary consolidation or hilar, parabronchial, or mediastinal lymphadenopathy. In addition, there was no imaging evidence of hepatic or splenic involvement or abdominal lymph node enlargement. Bronchoalveolar-lavage cultures were negative for viruses and bacteria. A parabronchial biopsy demonstrated an eosinophilic organizing pneumonitis with multiple eosinophilic microabscesses (Fig 2). No vasculitis, granulomas, or parasites were seen on biopsy. Because of concern for a malignant process, specifically acute lymphoblastic leukemia, the patient underwent a bone marrow biopsy that revealed a 70% cellular marrow, normocellular for age, with an increase in eosinophilic forms, estimated to be 50% to 60% (Fig 3).


Non–contrast-enhanced axial computed tomography image of the lungs at presentation with multifocal noncavitary pulmonary nodules (the arrow indicates 1 nodule).


Hematoxylin-eosin stain of transbronchial biopsy that demonstrates organizing eosinophilic pneumonitis.


Bone marrow biopsy, with 50% to 60% eosinophils.

Additional testing revealed that the patient was purified protein derivative–negative and had negative stool ova and parasite examinations. Serological testing for Trichinella spiralis and Strongyloides stercoralis were negative. Toxocara titers returned positive with values of >1:4096 (reference: <1:32). Ophthalmologic examination ruled out ocular larva migrans.

The patient received a 10-day course of albendazole (400 mg orally twice daily) and demonstrated significant clinical improvement with resolution of cough and pulmonary function abnormalities within several days into the course of therapy (FVC: 3.70 L at 102% of predicted [reference range: 80–100%]; FEV1: 3.25 L at 101% of predicted [reference range: 80–100%]; FEV1/FVC: 100% [reference range: 80–100%]; FEF25–75: 3.92 L/second at 100% of predicted [reference range: 70–100%]) and normal gas diffusion (diffusion capacity of 22.04 at 88% of predicted [reference range: 80–100%]). Her WBC count and hypergammaglobulinemia normalized within 20 days. Nevertheless, despite marked clinical improvement, eosinophils (WBC count: 9350 with 19% eosinophils; absolute eosinophil count: 1780/mm3) and Toxocara serologies (>1:4096) remained elevated 3 months after completing antihelminthic therapy.


To our knowledge, this is the first case report that describes the clinical course of pulmonary visceral larva migrans (VLM) caused by Toxocara spp. associated with a discrete ingestion in an adolescent patient. The majority of Toxocara infections occur in young children, 1 to 4 years of age, for whom ingestion of contaminated soil is the obvious means of infection.1 Nevertheless, among helminth infections affecting humans in developed countries, Toxocara ranks second only to pinworm infection in frequency.2

In this case, the ingested earthworm served as the paratenic carrier of Toxocara larvae from the soil to the patient. Researchers have demonstrated that Toxocara larvae are distributed in the tissues of earthworms exposed to infective Toxocara eggs and can be transmitted to animal hosts when they are fed earthworms.3 In addition, this known single-point source ingestion, in contrast to multiple instances of soil ingestion that is seen more commonly in young children, provides a rare opportunity to define the incubation period of VLM (∼4 weeks between ingestion and symptom onset in this case).

Although infection is most often clinically asymptomatic4 and self-resolving, pulmonary involvement can cause cough, wheeze, dyspnea, and infiltrates and may mimic bronchitis, pneumonia, or asthma. Adults with Toxocara spp. pulmonary infection have presented with respiratory failure,5, 6 eosinophilic pleural effusions,7, 8 pulmonary nodules, and acute and chronic eosinophilic pneumonia.9, 10 Previous reports in the pediatric literature have demonstrated varied presentations of VLM in children including chronic hypereosinophilia,11 hepatic granulomas and abdominal lymph node enlargement,12 central nervous system toxocariasis (ie, eosinophilic meningoencephalitis, cerebritis, myelitis),1316 pulmonary involvement including wheezing, coughing, respiratory distress, and pulmonary infiltration,17 myocarditis,18, 19 and, more recently, thrombocytosis.20 VLM has been associated also with pyogenic liver abscesses in children.14, 21 In addition, Toxocara infection has caused pericardial tamponade22 and has also been shown to mimic lymphoma.23

Our patient demonstrated the classic clinical findings seen with pulmonary toxocariasis, including fever, wheezing, coughing, pulmonary nodules, and eosinophilic pneumonia. In young children, fever and hepatomegaly have been shown to be common clinical signs, and abdominal ultrasound examination findings in children with Toxocara spp. infection include hepatosplenomegaly, hepatic granulomas, and abdominal lymph node enlargement.12 Nevertheless, it has been noted that hepatic nodules in VLM may not be very numerous or well defined, suggesting that such lesions might be overlooked.12 The hypergammaglobulinemia noted on laboratory evaluation suggests hepatic migration of larvae in this patient, although no clinical or radiologic hepatic abnormalities were seen. In addition, our patient demonstrated thrombocytosis on initial presentation and for 2 weeks during her illness; a laboratory manifestation of VLM that has been reported only recently.20 Because of the findings of hypereosinophilia in association with multiple pulmonary nodules, our patient underwent bone marrow biopsy to rule out a malignant process. A normocellular marrow with striking eosinophilic predominance was noted, which suggested a reactive process, as seen with a parasitic infection.

Although the definitive diagnosis of toxocariasis requires detecting Toxocara larvae in the tissues, larvae are found only rarely on pathologic examination. Alternatively, the detection of specific antibodies for Toxocara larval antigens, in the context of marked hypereosinophilia (range: 17–85%; mean: 38%),24 hypergammaglobulinemia, and negative serological results for other parasitic diseases, strongly supports the diagnosis of acute Toxocara infection. Specifically, the remarkably high enzyme-linked immunosorbent assay titer (>1: 4096) using Toxocara spp. excretory/secretory antigen from second-stage (L2) larvae in this patient who had ingested dirt while eating an earthworm, a known paratenic carrier of Toxocara larvae, in an area in which dogs and puppies had played and likely defecated, were strongly suggestive of acute infection. Antibody to the excretory-secretory Toxocara spp. antigen via the enzyme-linked immunosorbent assay method has a sensitivity of 78% and specificity of 92% at a titer of 1:32 for VLM.25 The quantity of the infecting dose and frequency of reinfection affects the distribution and survival of Toxocara spp. larvae and contributes to the marked eosinophilia and hypergammaglobulinemia seen with VLM. Infection with Toxocara spp. can produce a profound inflammatory response, not unlike atopy, and perhaps contributed to our patient's initial symptoms of swelling around the eyes, lips, and cheeks. Eosinophilia, leukocytosis,1 and Toxocara serological response16 may take months to years to resolve even when all clinical symptomatology has normalized. Given the extent of pulmonary findings in our patient associated with strongly elevated Toxocara titers, we postulate that this patient ingested a large inoculum of larvae and had a pronounced allergic and inflammatory reaction to the parasite, notwithstanding the history of an isolated ingestion of contaminated soil associated with eating an earthworm.

Previous publications have reported that VLM is a benign and self-limited illness and that treatment of mild cases is rarely necessary.4, 5 Nevertheless, severe pulmonary, myocardial, or central nervous system involvement may warrant therapy. Recommended antihelminthics, for adults and children, include albendazole 400 mg twice a day for 5 days or mebendazole 100 to 200 mg twice a day for 5 days, although the optimal duration of therapy is not known.26 Treatment with antihelminthics, particularly in cases of recent Toxocara infection, will aid in limiting additional migration of Toxocara larvae and may decrease the possibility of even a single larva migrating into the eye and causing ocular damage. There is no consensus concerning the utility of corticosteroids in the treatment of VLM, although steroids have been felt to be beneficial in cases of severe respiratory or myocardial involvement.

This case also highlights the high prevalence of Toxocara eggs in the soil environment. Numerous studies have demonstrated Toxocara eggs in substantial proportions in environmental soil samples from public parks, playgrounds, and backyards worldwide.2729 Eating earthworms, which ingest soil and are covered in soil, is certainly a risk for infection with Toxocara.

Although most pediatric patients with clinically evident VLM present with fever and hepatomegaly, this case, an adolescent patient with hypereosinophilia and nodular pulmonary disease, demonstrates the variations in clinical symptomatology in pediatric patients. Clinical recovery from pulmonary VLM may be rapid despite continued eosinophilia and consistently elevated Toxocara titers. Public education about the sources of Toxocara infection is a priority.


Dr Fox acknowledges support from the Pediatric Infectious Diseases Society Fellowship Award funded by GlaxoSmithKline.

We thank Marianna Wilson (Division of Parasitic Diseases, Centers for Disease Control and Prevention) for assistance with Toxocara testing.


    • Accepted September 9, 2005.
  • Address correspondence to LeAnne M. Fox, MD, MPH, Division of Infectious Diseases, Children's Hospital, 300 Longwood Ave, Boston, MA 02115. E-mail:{at} or lfox{at}
  • The authors have indicated they have no financial relationships relevant to this article to disclose.

FVC, forced vital capacityFEV1, forced expiratory volume in 1 secondFEF25–75, forced expiratory flow rate between 25% and 75% of the forced vital capacityWBC, white blood cellIg, immunoglobulinVLM, visceral larva migrans