Acute Unilateral Vision Loss and Pulmonary Nodules in a Child: The Diagnostic Value of Multidisciplinary Care in a Tropical Setting

CASE A previously healthy 3-year-old boy presented to our hospital with a 2-month history of a mobile white lesion in his left eye that, 6 days before consultation, was associated with redness of the eye and decreased ipsilateral vision. No weight loss, nocturnal diaphoresis, fever or lymphadenopathy was reported. Diarrhea, abdominal pain, emesis, arthralgias or arthritis was also absent. Ophthalmologic examination revealed evidence of cells in the anterior chamber of the left eye, pupillary synechiae, leukocoria and absence of the red reflex. A diagnosis of uveitis was considered by the ophthalmologist, and topical treatment with prednisolone and tropicamide 1% eye drops was initiated. Past medical history included uncontrolled asthma. He was a native of rural Colombia (Ciénaga Santa Marta, Magdalena), where there is a lack of potable water and unpaved streets. He had frequent contact with street dogs and nonportable swamp water and used to play barefoot in the neighborhood. His parents denied consumption of crustaceans (crabs) or potable water and denied contact with anyone with suspected tuberculosis. The patient was referred to our hospital for evaluation. On arrival, his vital signs were normal, with blood pressure of 100/62 mm Hg, heart rate of 115 beats/min, respiratory rate of 98 breaths/min, oxygen saturation of 96% in ambient air, and temperature of 36°C. His weight was 14.6 kg, and he had no abnormal findings on physical examination except for the ocular findings. Ophthalmologic examination of the left eye revealed posterior synechiae, 1–2+ vitreous opacity, a healthy disc, a macula without lesions (Fig. 1), an avascular white nodular lesion behind the lower iris, and round mobile, satellite lesions compatible with anterior and intermediate uveitis (Fig. 2). An ocular ultrasound revealed vitreitis in the left eye with partial posterior vitreous detachment and a vitreous band.FIGURE 1.: Left eye, posterior pole, pink optic disc with sharp margins, macula without lesions.FIGURE 2.: Left eye, whitish inferior peripheral retinal granuloma.A complete blood count revealed leukocytosis of 15,900 mm−3 with eosinophilia (neutrophils 32.4%, lymphocytes 45.7%, eosinophils 13,7%, monocytes 7,8%, basophils 0,4%)— and platelet count of 406,000 mm−3. He had unremarkable acute phase reactants (C-reactive protein [CRP] < 0.4 mg/dL, erythrocyte sedimentation rate was slightly elevated [34 mm/h], liver function tests [total bilirubin 0.17, alanine aminotransferase 23 UI/L, aspartate aminotransferase 33 UI/L] and creatinine 0.36 mg/dL). Rheumatoid factor, antinuclear antibodies and extracellular nuclear antigens were negative. Chest radiograph revealed a pulmonary nodule in the right lower lobe (Fig. 3), and a chest computed tomography scan revealed bilateral solid nodules with ground-glass opacities, including those in the middle lobe, lower lobe, right upper lobe and left lower lobe (Fig. 4A and B). Abdominal computed tomography was normal, without hepatosplenomegaly, masses or lymphadenopathies. Serologic testing included nonreactive anti-capsid immunoglobulin (Ig)M for Epstein–Barr virus; negative Toxoplasma gondii IgA, IgM and IgG; negative fourth-generation HIV test; negative Treponema pallidum IgG and negative Mantoux test (0 mm of induration).FIGURE 3.: Anteroposterior chest radiograph showing a nodule in the right lower lobe.FIGURE 4.: A,B: Chest computed tomography with bilateral solid nodules with ground-glass opacities.Direct observation for parasites and Cepheid Xpert MTB-RIF Ultra from 3 induced sputum samples were negative. Due to no previous infections, hospitalizations or prior history suggestive of immunodeficiency, as well as with the clinical ophthalmologic findings, no immunologic evaluation was carried out. Further serologic tests revealed the diagnosis. DENOUEMENT Based on his ophthalmologic evaluation with fundoscopy suggestive of toxocariasis, treatment with high doses of albendazole at 10 mg/kg every 12 hours for 5 days and topical ocular steroids was initiated, which resulted in the resolution of eye redness and improvement of cough. After discharge, IgG antibodies for Toxocara canis came back positive (enzyme-linked immunoassay with reference values of negative results: 0–9. Positive results: >9. Result of our patient 30). The main differential diagnoses for his ocular findings included retinoblastoma and toxocariasis.1 Differentiating between these diseases is difficult, but toxocariasis is reported more frequently in children older than 5 years of age, with a reported seroprevalence of 5.1%–13% and only 8% of retinoblastoma cases occur in this age group.2 In ophthalmologic toxocariasis, posterior granulomas are the most common clinical finding, typically presenting with traction bands to the posterior pole, as in our patient.1,3 Additionally, ocular involvement in toxocariasis is almost always unilateral.3,4 It is important to note that vitreous aspiration for the purpose of obtaining ocular IgG for T. canis is contraindicated when retinoblastoma is a potential differential diagnosis, due to the risk of infraorbital dissemination that could worsen the prognosis. The presence of pulmonary nodules necessitated an expanded differential diagnosis that included malignancies and various infectious processes such as tuberculosis, syphilis and toxoplasmosis. However, these possibilities were effectively ruled out based on a negative Mantoux test, 3 negative GenXpert Ultra tests on induced sputum, and negative serologic tests for T. pallidum and toxoplasmosis.5 Furthermore, the patient displayed adequate clinical response to treatment with resolution of cough, wheezing and improvements in sight.6 Diagnosing uveitis in children presents challenges, as it is frequently asymptomatic and can lead to chronic damage to ocular structures, including cataracts, glaucoma and amblyopia.3,7 Pediatric uveitis accounts for roughly 5%–10% of all uveitis cases. Chronic idiopathic uveitis is the most common cause, followed by juvenile idiopathic arthritis. Infections are more prevalent as causes of uveitis in children compared with adults, representing up to one-third of total cases,1,3,7 particularly in tropical regions with poor sanitation and environmental exposures—such as contact with animals, contaminated soil or water, and consumption of certain foods.4,5,8–11 Ocular toxocariasis is a significant cause of acute unilateral blindness in children, transmitted through exposure to soil in contaminated playgrounds or sandboxes.11 Because many infections are restricted to ocular involvement, eosinophilia may be absent, and serum IgG could be negative. A positive IgG could indicate past exposure rather than the cause of uveitis. Despite these considerations, the measurement of IgG levels and a thorough ophthalmological examination can aid in formulating a diagnosis.4 Calcifications observed on ocular ultrasound are highly indicative of retinoblastoma, especially in children under 3 years of age, while posterior synechiae and cataracts suggest chronic uveitis. Posterior granulomas are often the most common clinical manifestation, frequently presenting with traction bands at the posterior pole.11 Treatment typically involves steroids and albendazole, although the efficacy of antiparasitic agents against intraocular parasites remains uncertain.2 In cases of pulmonary toxocariasis, over 50% of patients may be asymptomatic, with radiologic abnormalities frequently detected incidentally during routine evaluations. Common symptoms include cough, wheezing and dyspnea. Typical radiologic findings consist of bilateral ground-glass opacities, pulmonary nodules and subpleural consolidations, often affecting multiple lobes. Albendazole treatment has shown favorable responses for pulmonary lesions, unlike its effectiveness in ocular toxocariasis. Eosinophilia is observed in more than 50% of pulmonary toxocariasis cases, with differential diagnoses including cancer, paragonimiasis and tuberculosis.12,13 The initial diagnosis of human toxocariasis emerged from findings of Toxocara larvae in enucleated eyes from children suspected of having retinoblastoma, with histological examinations confirming granulomas and T. canis larvae.2,14 Toxocara canis primarily infects various canids, including dogs, wolves and coyotes, serving as definitive hosts where adult worms reside in their intestines. In humid, tropical conditions, they excrete infective eggs that can survive in soil for years. Humans become infected after ingesting the embryonated eggs through contaminated food, water or soil, resulting in larvae being released in the small intestine. These larvae can migrate to various organs, encysting as third-stage larvae without developing into adult worms, leading to a symptomatic inflammatory response.2 Public health measures to combat this neglected parasitic infection must focus on reducing infections in definitive hosts, particularly domestic pets, through regular deworming. Other preventive measures include limiting animal feces exposure in gardens and playgrounds, ensuring access to clean water, and educating communities on hygiene practices such as washing hands and vegetables before consumption.15 Antihelmintic treatment in humans has the intention to stop larvae from infecting tissues, especially the eye and central nervous system. Ocular toxocariasis is managed primarily with steroids. In summary, ocular toxocariasis can be mistaken for retinoblastoma, especially in tropical countries. It may also present with respiratory symptoms and pulmonary imaging abnormalities. An experienced multidisciplinary team, along with imaging and serological studies, is essential for distinguishing between the 2 conditions and ensuring appropriate management.