Case series links Toxoplasma gondii to uveitis, blindness and relapse in 5 dogs

The dogs were 3.5 to 8 years old: 4 mixed breeds and 1 Weimaraner. Two had bilateral anterior uveitis and 2 had unilateral panuveitis with retinal detachment and blindness. The fifth had bilateral panuveitis with partial retinal detachment and acute blindness. One blind eye was later removed because of secondary glaucoma.

To be included, a dog needed a positive anti-T gondii IgG titer at presentation, at least 1 positive follow-up serology result and at least 1 recheck eye exam. On indirect fluorescent antibody testing, initial titers ranged from 1:256 to 1:1024. At recheck, 3 dogs had a fourfold rise and the other 2 still had high titers.

Most dogs also had other health problems. One was on immunosuppressive prednisone for immune-mediated thrombocytopenia, 1 had visceral leishmaniasis, 1 had atopic dermatitis treated on and off with oclacitinib, and 1 was later found to have hepatic and splenic masses. The authors suggest that immunosuppression, a known risk factor in people and cats, may also make dogs more vulnerable.

All 5 dogs got oral clindamycin plus topical prednisolone acetate, and all improved at first. One dog with bilateral panuveitis had its vision back within 2 weeks. Even so, 2 dogs relapsed despite long courses of antimicrobials.

The Weimaraner had first improved on clindamycin and corticosteroids. About 3 months after clindamycin was stopped, she came back with severe bilateral blepharitis and keratoconjunctivitis but no intraocular inflammation. Her CRP and toxoplasma titers were rising. The authors think this may be the first reported case of blepharitis linked to the infection, but the owners declined an eyelid biopsy, so other causes couldn't be ruled out. Trimethoprim-sulfamethoxazole was stopped after a severe hypersensitivity reaction, and atovaquone was stopped because she stopped eating.

The other dog that relapsed was switched from compounded veterinary clindamycin to a commercial human product after responding poorly. The authors say the timing of its later improvement doesn't prove the switch helped. They note that variability in compounded drugs is a recognized concern.

A single IgG titer can't tell active infection from latent infection, and IgM testing wasn't available locally. The authors suggest aqueous humor PCR and the Goldmann-Witmer coefficient as ways to improve diagnosis. They also point to PCR on Schirmer tear test strips, a noninvasive option now being used in human medicine.

The study has clear limits: only 5 dogs, a retrospective design, and diagnosis based on IgG titers and response to treatment rather than PCR, histopathology or IgM confirmation. The authors call for larger prospective studies.