Toxocara larvae can be found in any organ in humans, and many cases are discovered accidentally. Clinically the disease occurs in two forms: systemic toxocariasis and ocular toxocariasis. Both the forms rarely coexist [2, 9].

The clinical diagnosis of Toxocara is quite obvious, but still a confirmatory diagnosis is required in suspicious cases or for documentation. The larvae or its fragments may be directly visible under the microscope from tissue sections, but it’s extremely cumbersome and risky to collect samples from ocular tissues. In a Wilder’s classic study, only one larva was detected in 2300 cases examined [1]. Eosinophilia is noted in the blood of patients with systemic toxocariasis; however, the eosinophil count can be normal in patients with ocular toxocariasis [2]. The diagnosis of Toxocara can be clinched by indirect enzyme-linked immunosorbent assay (ELISA) which detects the immunogenic proteins known as Toxocara excretory-secretory (TES) antigens that are shed from the larvae [13]. A titre of 1:8 or more of ELISA along with signs and symptoms of Toxocara is sufficient to aid the diagnosis of Toxocara [2, 14]. However, there are few case reports of negative ELISA in Toxocara [15]. In literature the sensitivity for ELISA for Toxocara is variable with a range between as low as 33 % and as high as 92.2 % (depending upon the cutoff value of the titres) [2]. Detecting rising titres of anti-TES-Ag immunoglobulin E (IgE) antibody indicates acute toxocariasis. The titres return to normal after treatment and help in monitoring treatment therapy [13]. Increased IgG titres confirm a past or present infection without significant inflammation. Ultrasonography (USG) is important to differentiate it from retinoblastoma, where Toxocara appears as mass lesion and multiple vitreous membranes can be seen running from mass to disc, some of which are highly reflective. Intraocular calcification has been reported in some cases, and in that case other imaging modalities and serological test differentiate it from retinoblastoma [16]. The role of ultrasound biomicroscopy (UBM) is synergetic with USG as demonstrated by Zhou et al., where they could identify 95 % of the peripheral subtypes of toxocariasis [17]. Typical pseudocystic degeneration of the vitreous was picked up on UBM by Tran et al. [18].

Treatment of Toxocara depends upon the severity of disease. Oral steroids in a dose of 0.5–1 mg/kg body weight or periocular steroids may be required in cases of posterior uveitis along with topical steroids and cycloplegics for associated anterior uveitis [2]. The role of anthelmintic drugs (diethylcarbamazine, thiabendazole, mebendazole, albendazole) is controversial due unavailability of ocular pharmacodynamics and pharmacokinetics of these drugs. However, Barisani AT et al. [19] have treated seven eyes of five patients with oral albendazole along with steroids and have shown promising results. Ahn SJ et al. demonstrated that albendazole with steroids could reduce the recurrence to 17.4 % as compared to 54.5 % in patients who were administered only steroids by the end of 6 months, though the vision and inflammation improvement was the same in both the groups [2]. In majority of cases at the time of presentation, the parasite is dead and can be treated with steroids alone due to the inflammation caused by the dead parasite; however, in cases of live parasite, systemic albendazole can be tried/recommended (adult dose 800 mg BID, children 400 mg BID for 7–14 days) [2]. Surgical intervention is required for associated tractional or rhegmatogenous retinal detachment or endophthalmitis [20].

Gnathostomiasis is a food-borne disease caused by infection with larvae of Gnathostoma species. Intraocular infection by Gnathostoma species is quite rare but can be devastating [21].

Onchocerciasis is an infection of humans caused by filarial nematode Onchocerca species, transmitted to human beings by the bite of infected black fly of the genus Simulium [11]. Of lately there has been increasing reports of zoonotic Onchocerca, and many reports have been with infections in and around the eye [8]. It may also manifest as dermatitis, subcutaneous nodules and sclerosing lymphadenitis [35–37].

Synonyms: River blindness, sowda [38, 39].

Loiasis is caused by ‘eye worm’ Loa loa and is transmitted by an insect vector deer fly of genus Chrysops. It has predilection for ocular tissue [50].

Diffuse unilateral subacute neuroretinitis (DUSN) is a rare entity caused by a glistening white, motile nematode seen wandering in the subretinal space. It was initially known as ‘unilateral wipe-out syndrome’ [7]. The term DUSN was coined by Gass in 1978 [60].