Sir,

Giardiasis is a common worldwide cause of gastroenteritis. We report a case complicated by severe bilateral anterior uveitis, discussing possible mechanisms of ocular involvement.

Case report

A 57-year-old Caucasian female presented with painful visual loss in her left eye. Two weeks previously, she had developed diarrhoea and abdominal pain after returning from India. Microscopy of a stool sample demonstrated cysts of Giardia lamblia, but no evidence of Shigella spp, Campylobacter spp, Salmonella spp, or Escherichia coli spp. There was no past ophthalmic or other medical history. Oral metronidazole (400 mg t.i.d) was commenced by her general practitioner, but abandoned after she developed blurred vision which was presumed to be a side effect. However, ocular symptoms progressed despite cessation of the drug.

Visual acuity was 6/5 OD, ‘count fingers’ OS. There was marked AC activity with posterior synechiae, but no fibrin, hypopyon, or iris nodules. Vitritis obscured fundal details and rendered OCT imaging poor, but there was no evidence of cystoid macular oedema or vasculitis. The fellow eye was normal. Other than gastrointestinal upset, there were no systemic features—specifically no rash, arthritis, or conjunctivitis. Acute anterior uveitis was diagnosed and treated with hourly g. dexamethasone and g. cyclopentolate t.i.d. Oral metronidazole was restarted.

Four days later, after the patient had again stopped taking the metronidazole—still concerned it was causing her visual symptoms—acuity in her fellow eye decreased to ‘hand movements’. Bilateral anterior uveitis had developed, presumed secondary to giardiasis in the absence of other known risk factors. With a tapering course of topical steroids and a complete 7-day course of metronidazole, vision improved to 6/9 OU over 3 weeks. Neither systemic nor periocular injections of steroid were used due to the adequate response to topical steroids and oral antiprotozoal treatment. HLA-B27 status was not checked due to the confirmed diagnosis of giardiasis and the fact her condition improved on specific anti-Giardia treatment. After 3.5 months of follow-up, VA remained stable and the patient was discharged.

Comment

Protozoan infection with G. lamblia is characterised by gastroenteritis, but extraintestinal signs are frequent.1, 2 Ocular manifestations are unusual but include uveitis, retinal haemorrhages, and ‘salt and pepper’ retinal degeneration.1

Extraintestinal manifestations are considered immunologically mediated, with inflammatory infiltrates having been isolated from urticarial lesions and circulating immune complexes found in patients with ocular involvement.2, 3 Extraintestinal manifestations resolve with specific anti-Giardia therapy, other treatments being purely supportive.

While the mechanism of ocular involvement remains unclear, immunological parallels may exist with other gastroenteritides and inflammatory disorders. Enteric inflammation may lead to uveitis via a triggering agent that crosses intestinal mucosa.4 Molecular mimicry and HLA-B27 have also been implicated, whereby antigenic cross-reactivity results in antibody production against host cells.4 Similarities may exist with ocular toxoplasmosis, another protozoon that causes tissue destruction via autoimmune hypersensitivity and parasite-mediated host-cell lysis.

Appropriate anti-Giardia treatment is important in preventing ocular complications. Metronidazole can produce ophthalmic side effects including transient myopia,5 so this may be considered in patients with visual disturbance taking the drug. Furthermore, anti-Giardia treatment may lead to a temporary worsening of extraintestinal manifestations as dying parasites release antigens. However, ophthalmic opinion should be sought if considering treatment cessation, as incomplete treatment carries considerable risks.