Toxocara Canis Myelitis

Toxocara Canis Myelitis Clinical Features, Magnetic Resonance Imaging (MRI) Findings, and Treatment Outcome in 17 Patients Rosette A. Jabbour, MD, Souha S. Kanj, MD, Raja A. Sawaya, MD, Ghassan N. Awar, MD, Mukbil H. Hourani, MD, and Samir F. Atweh, MD

Abstract: Toxocara myelitis is a rare disease. Few cases have been reported in the literature. Patients present with myelopathy, occasional eosinophilia in blood and cerebrospinal fluid (CSF), with abnormal signals on magnetic resonance imaging (MRI). In the current study we report 17 cases of isolated Toxocara myelitis from a single tertiary referral center in Lebanon, with description of the clinical presentation, laboratory data, MRI findings, and response to antihelminthic treatment. Clinical and laboratory data were collected for 17 patients who presented with evidence of spinal cord disease. The clinical presentation included sensory, motor, and autonomic dysfunction, predominantly in the lower extremities. Patients exhibited a subacute or chronic course; this was either slowly progressive or remitting-relapsing with mild to moderate disability. The patients underwent extensive blood and CSF workup as well as MRI of the spinal cord and brain. Only 2 patients had a high eosinophil count in the CSF, although blood eosinophilia was seen in 6 patients. All patients tested positive for Toxocara canis antibodies in the blood and CSF. MRI of the spinal cord revealed a single characteristic lesion in the spinal cord with fusiform enlargement that was isointense on T1-weighted images and hyperintense on T2-weighted images. Nodular enhancement was seen after gadolinium injection. Treatment with albendazole, with or without steroids, resulted in marked neurologic improvement and normalization of the MRI in all patients. The finding of a single inflammatory MRI lesion in the spinal cord with positive Toxocara canis serology in the blood and CSF in cases of subacute or chronic myelitis suggests the diagnosis of Toxocara myelitis, irrespective of the presence of eosinophilia. Antihelminthic treatment is associated with a good outcome. (Medicine 2011;90: 337Y343) Abbreviations: AI = Hauser Ambulation Index, ANA = antinuclear antibodies, CSF = cerebrospinal fluid, CNS = central nervous system, HIV = human immunodeficiency virus, MRI = magnetic resonance imaging.

From Neurology Division (RAJ), University of Balamand, Neurology at St George Hospital University Medical Center, Beirut; Infectious Diseases Division (SSK, GNA), Neurology Division (RAS, SFA), and Radiology Department (MHH), American University of Beirut Medical Center, Beirut, Lebanon. The authors have no funding or conflicts of interest to disclose. Reprints: Rosette Jabbour, MD, Saint George Hospital University Medical Center-University of Balamand, PO Box 166378, Ashrafieh Beirut 1100 2807 (e-mail: rosette.jabbour)balamand.edu.lb). Copyright * 2011 by Lippincott Williams & Wilkins ISSN: 0025-7974 DOI: 10.1097/MD.0b013e31822f63fb

Medicine

&

Volume 90, Number 5, September 2011

INTRODUCTION oxocara canis is a commonly encountered roundworm that is usually found in dogs. It may also infect humans through the consumption of contaminated rabbit, pork, beef, or chicken meat.12,13,32 In children, pica is a common source of infection. Humans can also acquire Toxocara canis by ingesting fruits and vegetables contaminated with dog feces containing Toxocara eggs. Larvae can invade several organs, including the liver, lungs, eyes, and central nervous system (CNS) via a hematogenous route.13,32 The severity of the illness depends on the number and tissue distribution of larvae. Whereas mild infection may be asymptomatic, severe infection results in malaise, anorexia, and rash. Liver involvement causes visceral larva migrans, an entity characterized by eosinophilia, hepatomegaly, and fever.12 Respiratory symptoms are common in children. Ocular symptoms can be the first and sole manifestation of the infection.6 CNS symptoms are varied, and cases of Toxocara canis myelitis have rarely been reported.8 The prevalence of Toxocara canis infection is about 2.8% in the United States and Europe.17 Surveys from Australia and the Netherlands indicate a rate of about 7%.24,36 A seroprevalence study from Lebanon revealed that 19% of the healthy population is seropositive.18 The diagnosis of toxocariasis relies on the detection of antibodies directed against the larval excretory-secretory antigens. These immunogenic glycopeptides are released from the epicuticle of migrating larvae as it is shed following the binding of specific antibodies.25 The most commonly used immunodiagnostic technique is ELISA,5 with a test sensitivity ranging between 73% and 90%.14,17 However, there has been concern about cross-reactivity with other helminths, such as Fasciola hepatica and Ascaris suum, giving the ELISA test a specificity of about 93%.14,16,26,31 The low-cost, easy-to-use ELISA method has therefore been recommended as a first-line test, but confirmatory testing by Western blot should be performed, as the latter offers comparable sensitivity and absolute specificity when considering lower molecular weight bands.4,23 Myelitis is a common condition of the CNS that presents with various degrees of motor, sensory, and autonomic deficits and may lead to permanent disabilities. The etiology of myelitis is often attributed to infectious or noninfectious inflammatory lesions of the spinal cord.2 Infectious agents affecting the spinal cord include viruses, bacteria, fungi, and rarely parasites. Autoimmune inflammatory diseases also affect the spinal cord, such as demyelinating, postinfectious, and paraneoplastic diseases. In addition, vascular and neoplastic involvement of the spinal cord may present with similar clinical pictures. The exact etiology of inflammatory myelitis remains unknown in a large number of patients who present with acute or subacute symptoms of spinal cord dysfunction. Recent advances in brain and spinal cord imaging, as well as newer chemical, microbiologic,

T

www.md-journal.com

Copyright © 2011 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

337

Clinical Manifestation

R

No

2 wk

P

Bilateral leg numbness, weakness 3/5 left leg, hyperreflexia right Babinski

3

2

34/M

R

No

2 yr

R-R

Bilateral leg numbness, weakness 3/5 left leg, hyperreflexia right Babinski

3

3

60/M

R

Dogs

1 yr

P

2

4

30/M

U

No

3 mo

P

2

5

25/M

R

No

1 yr

P

1

Albendazole, steroids

6

28/F

U

No

2 yr

R-R

1

Albendazole, steroids

7

32/M

U

Dogs

5 wk

P

1

Albendazole, steroids

8

55/M

R

No

6 mo

P

3

Albendazole, steroids

9

43/M

U

No

5 mo

P

3

Albendazole, steroids

10

41/M

U

No

1

Albendazole, steroids

11

40/M

R

No

1 mo

P

1

Albendazole, steroids

12

42/M

R

No

3 mo

P

1

Albendazole, steroids

13

23/F

U

No

8 mo

P

1

Albendazole, steroids

14

60/M

U

Dogs

1 yr

P

1

Albendazole, steroids

15

40/M

U

No

2 yr

P

2

Albendazole, steroids

16

55/M

U

No

1 yr

P

3

Albendazole, steroids

17

42/M

R

No

1.5 yr

P

Trunk & bilateral leg numbness, pollakiuria, constipation, hyperreflexia, Babinski absent Feet tingling, urinary & fecal incontinence, hyperreflexia left leg, left Babinski Bilateral leg & trunk numbness, normal reflexes, Babinski absent Fingers tingling, right leg heaviness, urinary difficulty, constipation, hyperreflexia, Babinski absent Left jaw numbness, right leg hyperesthesia, hyperreflexia, Babinski absent All limbs numbness, urinary hesitancy, constipation, 3/5 weakness right side, hyperreflexia, Babinski absent Numbness & pain right leg & trunk, urinary incontinence, 3/5 weakness bilateral legs, hyperreflexia, bilateral Babinski Left leg numbness, weakness 3/5 right side, left leg hyperreflexia, Babinski absent Bilateral leg & periumbilical numbness, urinary retention, impotence, Babinski absent Trunk & bilateral leg numbness, Lhermitte sign, Babinski absent Bilateral arm tingling, Lhermitte sign, hyperreflexia, bilateral Babinski Bilateral leg & trunk numbness, urinary difficulty, hyperreflexia, Babinski absent Bilateral leg & trunk numbness, urinary difficulty, constipation, hyperreflexia, Babinski absent Left leg lancinating pain & paresthesia, nocturia, hyperesthesia, hyperreflexia, left Babinski Right leg, abdomen numbness, urinary retention, hyperreflexia, Babinski absent

Albendazole, diethylcarbamazine, steroids Albendazole, diethylcarbamazine, steroids Albendazole, diethylcarbamazine, steroids Albendazole, steroids

2

Albendazole, steroids

45 d

P

Abbreviations: P = progressive, R = rural, R-R = remitting-relapsing, U = urban. *Gait was assessed according to Hauser Ambulation Index. AI scores range from 0 (normal gait) to 9 (unable to ambulate or transfer independently). †All patients improved on treatment.

Volume 90, Number 5, September 2011

Treatment†

42/F

&

Gait Disability*

1

Medicine

* 2011 Lippincott Williams & Wilkins

Copyright © 2011 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

www.md-journal.com

Duration of Patient Age/Sex (yr) Living Area Exposure To Pets Symptoms to Diagnosis Course of Illness

Jabbour et al

338

TABLE 1. Demographic and Clinical Characteristics of 17 Patients With Toxocara canis Myelitis

Medicine

&

Volume 90, Number 5, September 2011

and immunologic analyses of the cerebrospinal fluid (CSF), are proving helpful in reaching more accurate diagnoses of inflammatory diseases of the CNS. Myelopathy secondary to infections with parasitic agents is generally regarded as a rare and reportable entity. Several parasites have been implicated in infections of the spinal cord and are usually associated with CSF eosinophilia. Reported parasites include Gnathostoma spinigerum,19,29 Schistosoma species,1 Echinococcus granulosus, Tenia solium, Toxoplasma gondii, Acanthamoeba species, Paragonimus westermani, and Toxocara species.10,34 Infection of the CNS with Toxocara canis has been reported to induce meningoencephalitis,3 convulsions,28 subdural abscess,27 cervical arachnoiditis,38 optic neuritis,20 radiculopathy,9 and myopathy.8,9 Isolated cases of Toxocara canis myelitis have been reported.7,15,21,30,37,39

Toxocara canis Myelitis

We report here 17 cases of isolated Toxocara canis myelitis from a single tertiary medical center in Lebanon. We describe the patients’ clinical features, magnetic resonance imaging (MRI) findings, Toxocara canis serology results in blood and CSF, and clinical and radiographic response to antihelminthic treatment.

PATIENTS AND METHODS Identification and Clinical Description of Patients The 17 patients in the current report were seen and managed at the American University of Beirut Medical Center between January 2000 and December 2009. All patients presented with an isolated myelopathy including a neurologic syndrome suggestive of spinal cord disease and an abnormal MRI of the spinal cord. The patients were evaluated by at least 2

FIGURE 1. MRI of Patient 3. A1, Sagittal T1-weighted image of the dorsal spine showing the isointense fusiform enlargement of the spinal cord between T2 and T6 levels (arrow head). A2, Sagittal T2-weighted image of the same segment showing the hyperintense enlargement of the spinal cord (extent of lesion marked by straight line). A3, Sagittal, axial T1-weighted images of the T4 spinal cord after gadolinium injection showing the right anterolateral enhancing nodule (long arrow). B1, B2, and B3, The corresponding MRI images 3 months after the initiation of antihelminthic treatment, showing the resolution of the fusiform enlargement, the abnormal signal on T2-weighted image, and the gadolinium enhancement. * 2011 Lippincott Williams & Wilkins

www.md-journal.com

Copyright © 2011 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

339

Medicine

Jabbour et al

neurologists who performed full neurologic examinations, and were seen by an infectious diseases specialist. All patients were ambulatory on presentation. Gait was assessed by the Hauser Ambulation Index (AI), which measures timed walking and ability to transfer; AI scores range from 0 (normal gait) to 9 (unable to ambulate or transfer independently). After diagnosis and treatment, the patients were assessed at least monthly in follow-up visits to a neurologist where symptoms and signs were recorded. Follow-up MRI of the spinal cord was obtained at various points in time after treatment. Patients were included based on the constellation of clinical symptoms and signs of myelitis, positive serologic tests in blood and CSF as defined below, and an MRI showing a single spinal lesion. They were excluded if CSF demonstrated an increase in red blood cells or stigmata of vasculitis or systemic illnesses, or if an alternative diagnosis was reached. Eosinophilia was defined as mild (600Y1600 cells/KL), moderate (1500Y5000 cells/KL), and severe (95000 cells/KL).33

Clinical Investigations MRI of the spine and the brain, with and without intravenous gadolinium injection, was performed on all patients using an NT 1.5 Tesla Philips Gyroscan (Eindhoven, The Netherlands). Sensory evoked potentials for most patients were obtained using a Nicolet Viking IIe machine (Carefusion, Middleton, WI). Routine blood and CSF analyses were performed for all patients. Antibody titers to Toxocara canis in the blood and CSF were performed at CERBA Pasteur Laboratories in France using an ELISA kit (Bordier Affinity Products SA, Crissier, Switzerland) to detect IgG antibodies directed against the excretory-secretory antigens produced by the migrating Toxocara larvae. Positivity was confirmed using a western blot assay (LDBIO Diagnostics, Lyon, France). Many of the patients underwent serologic testing for other pathogens, such as Schistosoma mansoni, Taenia solium, Echinococcus granulosus, herpes simplex virus, varicella zoster virus, human immunodeficiency virus (HIV), hepatitis B virus, Brucella species, and Venereal Disease Research Laboratory test (VDRL). In addition, some patients had serology tests for antinuclear antibodies (ANA) and other rheumatologic tests. Stools were tested for ova and parasites in the majority of patients.

ILLUSTRATIVE CASE REPORT A 60-year-old Lebanese man, previously healthy, presented to the American University of Beirut Medical Center in June 2001 because of paresthesia in the lower extremities and unsteady gait (Table 1, Patient 3). In May 2000, he had complained of progressive numbness extending from the lower trunk, genital area, and right lower extremity. Seven months later, he developed mild left leg weakness, unsteadiness, constipation, and urinary urgency. He was admitted to another hospital where an MRI of the dorsal spine showed a fusiform enlargement of the spinal cord from T2 to T6 (Figure 1). The lesion appeared isointense on T1-weighted images and hyperintense on T2-weighted images, with an area of focal enhancement in the right lateral and anterior hemi-cord at T4 following gadolinium injection. MRI of the brain was normal. CSF analysis showed no cells, with normal glucose and protein levels. Somatosensory evoked potentials after stimulation of the posterior tibial nerves were normal bilaterally. Laboratory data showed mild eosinophilia in the blood and normal liver enzymes. Vitamin B12, cytoplasmic antineutrophil cytoplasmic antibodies, ANA, anti-dsDNA, and anticardiolipin antibodies

340

www.md-journal.com

&

Volume 90, Number 5, September 2011

were all normal. Serum angiotensin-converting enzyme and HIV serology were normal. The patient improved only partially after receiving intravenous methylprednisolone 1 g for 3 consecutive days. He presented to our clinic 3 months later for further evaluation. Neurologic examination revealed mildly unsteady gait with decreased pinprick, temperature, and touch sensation in the lower extremities and a sensory level at T10 bilaterally. Position and vibration sensation were markedly decreased in both legs with a positive Romberg sign. Deep tendon reflexes were hyperactive bilaterally in the lower extremities with ankle clonus and spastic weakness in both legs. Babinski sign was flexor bilaterally. The patient lived in a rural area and reported a history of exposure to dogs. Repeat CSF analysis was normal. The patient had persistent eosinophilia in the blood. Serum Brucella, hydatid, and Schistosoma serology were all negative. Purified protein derivative (PPD) test was negative. Stool microscopic examination for parasites was negative. Toxocara canis serology was positive in blood and CSF. The patient was treated with albendazole 400 mg twice daily and diethylcarbamazine 200 mg 3 times daily for 6 weeks. Six months after treatment, the patient’s gait improved markedly but he continued to complain of residual paresthesia. He had no evidence of recurrence 4 years later. MRI of the dorsal spine 3 months after treatment showed near total disappearance of the previously described lesions with no enhancement (see Figure 1).

RESULTS Clinical Characteristics of the 17 Patients Clinical characteristics of the 17 patients in the current study are summarized in Table 1. All patients were adults, 14 men and 3 women, ranging in age from 23 to 60 years with a mean age of 42.5 years. Patients came equally from rural (n = 8) and urban (n = 9) areas, and only 3 had a history of exposure to pets. The duration of the neurologic symptoms varied widely from 2 weeks to 2 years, with either a progressive or a remittingrelapsing course. Patients who had prolonged symptoms had been investigated on previous hospitalizations and had received long courses of steroids with little benefit. Most of the patients had a mild to moderate disability, with a predominance of sensory and autonomic symptoms. Many patients remained ambulatory even after years of being symptomatic. The signs and symptoms were mostly related to the lower extremities and the trunk, which correlated with the fact that most of the lesions were located in the upper dorsal segments of the spinal cord. Few patients had cervical lesions causing symptoms in the upper extremities. None of the patients had fever or other systemic manifestations.

Results of MRI MRI of the spine revealed a rather consistent picture characterized by swelling and enlargement of the involved spinal segment that varied in size. The lesion was isointense on T1 sequences and hyperintense on T2 and flair sequences, suggesting spinal cord inflammation and edema. Focal nodular enhancement was seen after intravenous gadolinium injection. The enhancing area was generally much smaller than the affected area and focal with a tendency to involve the posterior marginal areas of the cord. Figure 1 shows a typical lesion in 1 of the patients (Patient 3), before and after treatment. In 8 patients the lesion was in the dorsal areas, and in 7 the lesion was in the cervical areas. The lesion was below the eighth dorsal segment * 2011 Lippincott Williams & Wilkins

Copyright © 2011 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

Medicine

&

Volume 90, Number 5, September 2011

Toxocara canis Myelitis

TABLE 2. MRI Characteristics of the 17 Patients Patient 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17

Spinal Cord Appearance

Extent of Hyperintense Lesion

Lesion on T1-Weighted Images With Gadolinium

Location of Enhancing Nodule

Normal Fusiform enlargement Fusiform enlargement Fusiform enlargement Fusiform enlargement Normal Fusiform enlargement Fusiform enlargement Fusiform enlargement Fusiform enlargement Fusiform enlargement Fusiform enlargement Fusiform enlargement Fusiform enlargement Fusiform enlargement Fusiform enlargement Fusiform enlargement

T3-T7 T4-T6 T2-T6 T4-T6 T5-T6 C7-T1 C1-C3 C2-C6 T5-T8 C1-C3 C5-C7 T7-T8 C5-C6 T8-T10 T6-T7 T6-T10 C2- C6

Focal, nodular, T4 Focal, nodular, T5 Large, diffuse, T4 Focal, nodular, T5 Focal, nodular, T5 Focal, nodular, C7 Focal, nodular, C1 Focal, nodular, C4 Focal, nodular, T6 Focal, nodular, C1 Focal, nodular, C6 Focal, nodular, T7 Focal, nodular, C6 Focal, nodular, T9 Focal, nodular, T7 Focal, nodular, T6 Focal, nodular, C3

Right anterolateral Left dorsal Right anterolateral Left lateral Bilateral dorsal Right lateral Midline dorsal Right dorsolateral Central Right lateral Left dorsal Left dorsolateral Bilateral dorsal Right lateral Right lateral Right dorsal Central

in only 2 patients. Spinal MRI findings are summarized in Table 2. All patients had a normal MRI of the brain.

CSF and Blood Analyses Table 3 summarizes the relevant cell counts in blood and CSF, as well as the chemical composition of the CSF in the 17 patients on presentation. The total white cell count was often within the normal range, except in 2 cases. Peripheral eosinophilia was common but not universal. Three patients had mild eosinophilia count and 1 had moderate eosinophilia as defined above. CSF eosinophilia was much less common. Only 2 patients had significant eosinophil counts in the CSF. Total CSF protein was elevated in 4 of the 17 patients, while glucose levels were all normal. Most patients had normal CSF protein electrophoresis.

All patients had positive Toxocara canis antibody titers in the blood and the CSF. The rest of the blood chemistry, serology, collagen vascular studies, and organ functions were not revealing.

Statistical Analysis Using descriptive analysis, we found no apparent associations between MRI findings (location and extent of lesion, spinal cord appearance) and CSF eosinophilia.

Treatment Outcomes All patients showed marked improvement of neurologic function following treatment with antihelminthic agents in the form of oral albendazole (400 mg twice daily). Three patients received diethylcarbamazepime. All patients recovered normal

TABLE 3. Blood and CSF Characteristics of the 17 Patients Blood Patient 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17

CSF

WBC (/mm3 )

E (%)

E Count (/mm3 )

WBC (/mm3 )

E

P

L

M

B

Protein (g/L)

Glucose (mg/dL)

PE

13,100 7400 6900 8300 7800 10,000 6300 9000 7900 ND 9300 7700 6300 7900 10,700 15,900 4000

20 6 8 3 10 4 3 6 3 ND 6 12 3 2 11 1 1

2620 444 552 249 780 400 189 540 237 ND 558 924 189 158 1177 159 40

10 12 2 2 3 0 0 0 2 3 4 0 1 5 0 0 0

17 33 0 0 2 0 0 0 0 0 1 0 0 1 0 0 0

2 3 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

79 58 2 0 0 0 0 0 0 2 0 0 0 3 0 0 0

1 6 0 0 0 0 0 0 2 1 3 0 0 1 0 0 0

1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

0.4 0.78 0.5 0.3 0.3 0.3 0.6 0.46 0.79 0.27 0.43 0.32 0.37 0.33 0.47 0.22 0.25

61 60 52 64 68 64 62 47 52 64 76 79 62 63 50 69 58

Monoclonal Negative Negative Polyclonal Negative Negative Negative Negative Negative Suspicious Negative Negative Negative Negative Negative Negative Negative

Abbreviations: B = basophils, E = eosinophils, L = lymphocytes, M = monocytes, ND = not done, P = polymorphonuclear, PE = protein electrophoresis, WBC = white blood count.

* 2011 Lippincott Williams & Wilkins

www.md-journal.com

Copyright © 2011 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

341

Medicine

Jabbour et al

ambulation, with an AI of 0 to 1. Residual sensory complaints, spastic bladder symptoms, and mild to moderate erectile problems in men persisted in almost half the patients. Complete recovery was seen in the rest. Of note, prior to the antihelminthic agent’s intake, steroid treatment failed to relieve the symptoms or the MRI lesions. None of the patients developed any side effects from albendazole even after prolonged use. Duration of treatment varied between 2 weeks and 3 months.

DISCUSSION The diagnosis of Toxocara canis myelitis in the 17 patients in the current series was based primarily on the presence of Toxocara antibodies in the blood and CSF, the absence of any other alternative diagnosis, and the favorable response to antihelminthic treatment. The diagnosis of CSF-seropositive Toxocara canis myelitis has been reported in the literature beginning in 1992.7,8,15,21,30,39 In the only case, to our knowledge, reported before the availability of serologic tests, the diagnosis was based on isolation of the Toxocara worm from the CSF.39 The presence of eosinophilia in the CSF has been a major, if not the only, marker for a heightened suspicion of parasitic infection. Eosinophilia was present in few cases in our series and was not necessary for the diagnosis. The MRI findings in our patients, as in the previously reported cases,22,35 suggested the presence of a single inflammatory lesion of the spinal cord that caused its enlargement with edema, that was isointense on T1-weighted images and hyperintense on T2-weighted images. Focal nodular enhancement was seen mainly in the posterolateral areas following gadolinium injection. We found that this specific, single MRI finding in our patients was highly correlated with an infection with Toxocara, independent of the presence of eosinophilia. The fact that all patients responded well to antihelminthic treatment, while many failed to respond to prior treatment with steroids, strengthens the evidence for this diagnosis. In fact, several of our patients continued to be symptomatic with a persistent abnormal MRI of the spine for 1Y2 years until they received a course of albendazole treatment, which resulted in clinical improvement and normalization of the MRI. The presence of Toxocara antibody seropositivity in the blood is high in many endemic areas in the world11,12 (including a study from Lebanon18), but little is known about the incidence of positive antibody titers in the CSF. There is concern about the passive transfer of antibodies from the blood to the CSF if the blood-brain barrier is more permeable during an inflammatory disease. Although it is generally agreed that the presence of antibodies in the CSF is usually indicative of CNS infection, there is little accurate knowledge about this issue in the case of Toxocara infections; further investigations using quantitative measures of antibodies in the blood and CSF are needed. Toxocara myelitis has been reported in several parts of the world, but mostly from certain regions such as East Asia,39 Europe,15,21,30 and the United States.7 To our knowledge, before 2006 there were no published data about the incidence of Toxocara seropositivity in the Lebanese population, but it is expected that it may be endemic in the area. In a 2006 pilot study18 of 150 Lebanese patients, we found a relatively high incidence of Toxocara seropositivity in the blood (19%), with male sex and low level of education as predictors of seropositivity. The male sex was prevalent in our series. However, pet ownership, contact with soil, source of drinking water, and whether patients came from rural or urban areas were not predictive. Another point of interest is that all patients in the current study were adults in their third decade or older, which is

342

www.md-journal.com

&

Volume 90, Number 5, September 2011

similar to the cases of myelopathy previously reported in the literature.7,15,21,30,39 We found only 1 report of a child with Toxocara myelitis.37 While the domestic dog represents the definitive host, aberrant infections in humans are usually acquired through ingestion of the embryonated eggs, via contaminated soil or vegetables. In conclusion, we believe that Toxocara canis myelitis may be tremendously underestimated, especially if CSF eosinophilia is used as the only marker leading to serologic testing. Therefore we suggest that patients with idiopathic myelopathy with an MRI showing a single spinal cord inflammatory lesion should be tested for Toxocara serology in the blood and CSF. In patients with Toxocara canis myelitis, treatment with antihelminthic agents can be associated with a good outcome, unlike some other types of inflammatory myelitis. ACKNOWLEDGMENT The authors thank Dr. Zeina Kanafani for her statistical contribution. REFERENCES 1. Acute schistosomiasis with transverse myelitis in American students returning from Kenya. Centers for Disease Control (CDC). MMWR Morb Mortal Wkly Rep. 1984;33:445Y447. 2. Adams RD, Victor M, Ropper AH. Principles of Neurology. 5th ed. New York: McGraw-Hill; 1997:1237. 3. Brain L, Allan B. Encephalitis due to infection with Toxocara canis: report of a suspected case. Lancet. 1964;20:1355Y1357. 4. Courtade H, Recco P, Magnaval JF, Charlet JP, Seguela JP. EComparative study between two ELISA methods for Toxocara canis and the western-blot.^ Bull Soc Fr Parasitol. 1995;13:37Y53. 5. de Savigny DH, Voller A, Woodruff AW. Toxocariasis: serological diagnosis by enzyme immunoassay. J Clin Pathol. 1979;32:284Y288. 6. Despommier D. Toxocariasis: clinical aspects, epidemiology, medical ecology, and molecular aspects. Clin Microbiol Rev. 2003;16:265Y272. 7. Duprez TP, Bigaignon G, Delgrange E, Desfontaines P, Hermans M, Vervoort T, Sindic CJ, Buysschaert M. MRI of cervical cord lesions and their resolution in Toxocara canis myelopathy. Neuroradiology. 1996;38:792Y795. 8. Eberhardt O, Bialek R, Nagele T, Dichgans J. Eosinophilic meningomyelitis in toxocariasis: case report and review of the literature. Clin Neurol Neurosurg. 2005;107:432Y438. 9. Finsterer J, Auer H. Neurotoxocarosis. Rev Inst Med Trop Sao Paulo. 2007;49:279Y287. 10. Fishman RA. Cerebrospinal Fluid in Diseases of the Central Nervous System. 2nd ed. Philadelphia: Saunders; 1992:195. 11. Gillepsie SH. Human toxocariasis. J Appl Bacteriol. 1987;63:473Y479. 12. Gillepsie SH, Hawkey PM. Medical Parasitology. A Practical Approach. New York: IRL Press at Oxford University Press; 1995:178Y182. 13. Glickman L, Schantz PM. Epidemiology and pathogenesis of zoonotic toxocariasis. Epidemiol Rev. 1981;3:230Y250. 14. Glickman L, Schantz P, Dombroske R, Cypess R. Evaluation of serodiagnostic tests for visceral larva migrans. Am J Trop Med Hyg. 1978;27:492Y498. 15. Goffette S, Jeajean AP, Duprez TP, Bigaignon G, Sindic CJ. Eosinophilic pleocytosis and myelitis related to Toxocara canis infection. Eur J Neurol. 2000;7:703Y706. 16. Gottstein B. An immunoassay for the detection of circulating antigens in human echinococcosis. Am J Trop Med Hyg. 1984;33:1185Y1191.

* 2011 Lippincott Williams & Wilkins

Copyright © 2011 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

Medicine

&

Volume 90, Number 5, September 2011

17. Jacquier P, Gottstein B, Stingelin Y, Eckert J. Immunodiagnosis of toxocarosis in humans: Evaluation of a new enzyme-linked immunosorbent assay kit. J Clin Microbiol. 1991;8:1831Y1835. 18. Kanafani ZA, Skoury A, Araj GF, El-Khoury M, Sawaya RA, Atweh SF, Kanj SS. Seroprevalence of toxocariasis in Lebanon: a pilot study. Parasitology. 2006;132:635Y639. 19. Kawamura J, Kohri Y, Oka N. Eosinophilic meningoradiculitis caused by Gnasthostoma spinigerum. Arch Neurol. 1983;40:483Y485. 20. Komiyama A, Hasegawa O. Optic neuritis in cerebral toxocariasis. J Neurol Neurosurg Psychiatry. 1995;59:197Y198. 21. Kumar J, Kimm J. MR in Toxocara canis myelopathy. Am J Neuroradiol. 1994;15:1918Y1920.

Toxocara canis Myelitis

29. Schmutzhard E, Boongird P, Vejjajiva A. Eosinophilic meningitis and radiculomyelitis in Thailand, caused by CNS invasion of Gnasthostoma spinigerum and Angiostrongylus cantonensis. J Neurol Neurosurg Psychiatry. 1988;51:80Y87. 30. Sellal F, Picard F, Mutschler V, Marescaux C, Collard M, Magnaval JF. EMyelitis caused by toxocara canis (larva migrans).^ Rev Neurol (Paris). 1992;148:53Y55. 31. Speiser F, Gottstein B. A collaborative study on larval excretory/secretory antigens of Toxocara canis for the immunodiagnosis of human toxocariasis with ELISA. Acta Tropica. 1984;41:361Y372. 32. Sturchler D, Weiss N, Gassner M. Transmission of toxocariasis. J Infect Dis. 1990;162:571.

22. Lee IH, Kim ST, Oh DK, Kim HJ, Kim KH, Jeon P, Byun HS. MRI findings of spinal visceral larva migrans of Toxocara canis. Eur J Radiol. 2010;75:236Y240.

33. Tefferi A. Blood eosinophilia: a new paradigm in disease classification, diagnosis, and treatment. Mayo Clin Proc. 2005;80:75Y83.

23. Magnaval JF, Glickman LT, Dorchies P, Morassin B. Highlights of human toxocariasis. Korean J Parasitol. 2001;39:1Y11.

34. Tyler KL, Martin JB. Infectious Diseases of the Central Nervous System. Philadelphia: FA Davis; 1993:259Y287.

24. Nicholas WC, Stewart AC, Walker JC. Toxocariasis: a serological survey of blood donors in the Australian Capital Territory together with observations on the risks of infection. Trans R Soc Trop Med Hyg. 1986;80:217Y221.

35. Umehara F, Ookatsu H, Hayashi D, Uchida A, Douchi Y, Kawabata H, Goto R, Hashiguchi A, Matsuura E, Okubo R, Higuchi I, Arimura K, Nawa Y, Osame M. MRI studies of spinal visceral larva migrans syndrome. J Neurol Sci. 2006;249:7Y12.

25. Page AP, Rudin W, Fluri E, Blaxter ML, Maizels RM. Toxocara canis: a labile antigenic surface coat overlying the epicuticle of infective larvae. Exp Parasitol. 1992;75:72Y86.

36. Van Knapen F, Van Leusden J, Polderman AM, Franchimont JH. Visceral larva migrans: examinations by means of enzyme-linked immunosorbent assay of human sera for antibodies to excretory-secretory antigens of the second-stage larvae of Toxocara canis. Z Parasitenkd. 1983;69:113Y118.

26. Romasanta A, Romero JL, Arias M, Sanchez-Andrade R, Lopez C, Suarez JL, Diaz P, Diez-Banos P, Morrondo P, Paz-Silva A. Diagnosis of parasitic zoonoses by immunoenzymatic assaysVanalysis of cross-reactivity among the excretory/secretory antigens of Fasciola hepatica, Toxocara canis, and Ascaris suum. Immunol Invest. 2003;32:131Y142. 27. Russenger L, Schmutzhard E. Spinal toxocaral abscess. Lancet. 1989;12:398. 28. Ruttinger P, Hadidi H. MRI in cerebral toxocaral disease. J Neurol Neurosurg Psychiatry. 1991;54:361Y362.

* 2011 Lippincott Williams & Wilkins

37. Vidal JE, Sztajubock J, Seguro AC. Eosinophilic meningoencephalitis due to Toxocara canis: case report and review of the literature. Am J Trop Med Hyg. 2003;69:241Y243. 38. Villano M, Cerillo A, Narciso N, Vizioli L, De Caro D. A rare case of Toxocara canis arachnoidea. J Neurosurg Sci. 1992;36:67Y69. 39. Wang C, Huang CY, Chan PH, Preston P, Chau PY. Transverse myelitis associated with larva migrans: finding of larva in cerebrospinal fluid Eletter^. Lancet. 1983;1:423.

www.md-journal.com

Copyright © 2011 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

343