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Year : 1999  |  Volume : 47  |  Issue : 4  |  Page : 252-253

Intraocular gnathostomiasis

Regional Institute of Ophthalmology and Government Ophthalmic Hospital, Chennai, India

Correspondence Address:
K A Kannan
Regional Institute of Ophthalmology and Government Ophthalmic Hospital, Chennai
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Source of Support: None, Conflict of Interest: None

PMID: 10892485

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How to cite this article:
Kannan K A, Vasantha K, Venugopal M. Intraocular gnathostomiasis. Indian J Ophthalmol 1999;47:252-3

How to cite this URL:
Kannan K A, Vasantha K, Venugopal M. Intraocular gnathostomiasis. Indian J Ophthalmol [serial online] 1999 [cited 2023 Dec 10];47:252-3. Available from: https://journals.lww.com/ijo/pages/default.aspx/text.asp?1999/47/4/252/14900

We report a rare case of intraocular Gnathostomiasis, where a live worm, intracameral in location, was successfully removed. Its identity was confirmed by microscopy.

  Case Report Top

A 41-year-old woman presented to us with complaints of pain, redness and watering in the right eye of 2 months duration. She had noticed an itchy, tender swelling in the right axilla a month prior to the onset of eye symptoms.

On slitlamp biomicroscopy the left eye was found to be normal in all aspects with a visual acuity of 6/6. The visual acuity of the right eye was 6/18 and the intraocular pressure (IOP) was 38 mm Hg. Slitlamp biomicroscopy of the right eye showed circumdliary congestion with mild anterior chamber reaction. Few posterior synechiae were present, with a larger number found on the nasal aspect. An active live worm was seen inferonasally in the anterior chamber, with one end attached to the iris diaphragm [Figure - 1]. There were multiple full-thickness holes in the iris. The lens showed early cataractous changes. Indirect ophthalmoscopy revealed a normal fundus. On laboratory investigation, the haemogram revealed a total white cell count of 8.9109/l and a differential count of polymorphs 61%, lymphocytes 30%, and eosinophils 9%. Stool examination demonstrated Ascariasis. Ultrasound B-scan and X-ray of the orbit were within normal limits.

Under local anaesthesia, a stab incision was made at the 2 o' clock position. The anterior chamber was formed with a viscoelastic substance and the parasite was gently pulled out by its cephalic portion with a tissue-holding forceps. The live worm, which measured 3 0.5mm, was transported in normal saline for identification. It was fixed and mounted in DPX and under a light microscope (Nikon, Optiphot) and identified as the third-stage larva of Gnathostoma spinigerum.

Postoperatively, the patient was treated with topical and systemic steroids and cycloplegics. Over a period of one week the anterior segment reaction had subsided and the eye became quiet except for lens changes which caused the visual acuity to reduce to counting fingers at 1 m. Three weeks later, extra capsular cataract extraction (ECCE) with posterior chamber intraocular lens (PCIOL) implantation was done. At the final postoperative follow up 6 weeks later, the patient's best corrected visual acuity was 6/9 in the right eye.

  Discussion Top

Gnathostoma spinigerum is an intestinal nematode of the carnivores, occurring mostly in South East Asian countries. These nematodes are stout, reddish, and slightly transparent, with a cephalic swelling separated from the rest of the worm by cervical constriction. The cephalic bulb is armed with rows of hooklets, and the entire body is covered with numerous fine spines [Figure - 2].

The common definitive hosts of G. spinigerum, serving as reservoirs for human infections, are domestic cats and dogs. Other definitive hosts include wild relatives of cats and dogs. The adult worms parasitizing the stomach walls of these animals produce eggs that are liberated in the animal stools. The first-stage larvae hatch in water that has been contaminated by infected stools. The intermediate host is a copepod of genus Cyclops in which the second-stage larvae develop. After the infected Cyclops, have been ingested by the second intermediate host (a fresh water fish, eel, frog or snake) the third-stage larvae develop. When chickens, ducks or pigs consume an infected second intermediate host, the third-stage larvae excyst in their stomach and then re-encyst in their muscles. These animals are called paratenic hosts because the larvae show no morphological changes in them. When the suitable definitive host eats either the infected second larval or paratenic host the infection develops to maturity in the stomach wall in about 6 months, thus completing the life cycle.

Man can acquire the infection by eating the raw meat of either the second intermediate or paratenic host because both harbor the infective third-stage larvae. Infection may also be due to transmission through skin penetration[1] by the larva during food handling and preparation. In man the larvae can migrate to various internal organs, including the eye and subcutaneous tissue but can never become mature. Man is an incidental host and represents the dead end for the parasite.

Systemic effects include migratory cutaneous swelling, hypereoisnophilic syndrome, fatal eosinophilic encepalomyelitis,[2] gastrointestinal mass, and pleurisy. Various ocular lesions include lid oedema, orbital cellulitis, anterior uveitis[3] with or without hypopyon, secondary glaucoma, multiple iris holes, subretinal tract, and retinal detachment with multiple holes. The most common mode of presentation is anterior uveitis with or without secondary glaucoma. This patient had anterior uveitis with secondary glaucoma and multiple iris holes. The posterior segment was normal. As iris holes have not been reported with other intraocular parasites, it may be considered a diagnostic sign of this parasitic infestation.[4] Simultaneous systemic and ocular involvement was not seen in this case nor in any of the other reported cases. The larvae may migrate into the eye along the optic nerve or directly penetrate the sclera.[5] Iris holes may represent the mode of entry of the worm from posterior chamber to anterior chamber or vice versa.

As soon as the parasite is identified it should be removed, failing which structural damage and intraocular inflammation would result from its movement to different parts of the eye. An intracameral parasite can be grapsed by a forceps and removed, as was done in this case, or it may be aspirated with a large bore needle or cannula. Once the parasite is removed, inflammation subsides markedly with topical and systemic steroids. Usually prognosis is good except in cases where the central nervous system is involved.

  References Top

Daengsvang S. Infectivity of Gnathostoma spinigerum larvae in. primates. J Parasitol 1971;57;476-78.  Back to cited text no. 1
Bunnag T, Comer DS, Punyagupta S. Eosinophilic myeloencephalitis caused by Gnathostoma spinigerum, Neuropahtology of nine cases. J Neurol Sci 1970;10:419-34.  Back to cited text no. 2
Kitiiponghansa S, Prabriputaloons A, Pariyanonda S, Ritch R. Intracameral Gnathostomiasis: a cause of anterior uveitis and secondary glaucoma. By J Ophthalmol 1987;71:618-22.  Back to cited text no. 3
Biswas J, Gopal L, Sharma T, Badrinath SS. Intraocular Gnathostoma spinigerum. Retina 1994;14:438-44.  Back to cited text no. 4
Tudor RC, Blair E. Gnathostoma spinigerum: An usual cause of ocular nematodiasis in the western hemisphere. Am J Ophthalmol 1971;72:185-90.  Back to cited text no. 5


  [Figure - 1], [Figure - 2]


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