![<![CDATA[Toxoplasmosis may be an underrecognized cause of ocular inflammation in dogs]]>](/media/3b/3b54223aff1cae6b.1280.webp)
Five-Dog Case Series Puts Toxoplasmosis on Canine Uveitis Differentials
A 5-dog case series from Jerusalem links active Toxoplasma gondii infection to uveitis, retinal detachment and what may be the first described toxoplasmosis-associated blepharitis in dogs.
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Five dogs treated at a Jerusalem veterinary teaching hospital between January 2023 and December 2025 developed ocular disease suspected to stem from active Toxoplasma gondii infection — including two dogs left blind by retinal detachment and one whose eyelid inflammation may be the first blepharitis ever described in association with the parasite.
The case series, published in Veterinary Parasitology: Regional Studies and Reports by Soueid, Ofri, Sebbag, Aroch and Pe'er (2026;75:101590), argues that toxoplasmosis belongs on the differential list for dogs presenting with uveitis or chorioretinitis — not just cats, where the parasite is a well-established cause of intraocular inflammation.
The clinical takeaway for practitioners: a dog with unexplained ocular inflammation, especially one that is systemically ill or immunocompromised, warrants T gondii serology.
What did the five dogs present with?
Researchers at the Hebrew University Veterinary Teaching Hospital retrospectively reviewed records from the ophthalmology and internal medicine services. Inclusion required ocular disease, a positive anti–T gondii IgG titer at presentation, at least one positive follow-up serologic result, and at least one ophthalmologic reexamination.
The dogs ranged from 3.5 to 8 years old; four were mixed breeds and one was a Weimaraner. Their diagnoses:
- Two dogs with bilateral anterior uveitis
- Two dogs with unilateral panuveitis, retinal detachment and blindness
- One dog with bilateral panuveitis, partial retinal detachment and acute blindness
One blind eye was enucleated because of secondary glaucoma.
Initial IgG titers, measured by indirect fluorescent antibody test, ranged from 1:256 to 1:1024 against a cutoff of ≥1:64. At recheck, three dogs showed a 4-fold titer increase consistent with seroconversion; the remaining two had persistently high titers suggestive of active infection.
Why did these dogs get sick?
Concurrent systemic disease was common. One dog was on immunosuppressive prednisone for immune-mediated thrombocytopenia, one had visceral leishmaniasis, one had atopic dermatitis intermittently treated with oclacitinib, and one was later found to have hepatic and splenic masses. The authors suggest immunosuppression — a known trigger in humans and cats — may similarly predispose dogs to active disease.
How did treatment go?
All five dogs received oral clindamycin plus topical prednisolone acetate, and all initially improved. One dog with bilateral panuveitis regained vision within 2 weeks of starting treatment. Even so, two dogs relapsed despite extended antimicrobial therapy.
The Weimaraner is the series' most instructive case. She initially presented with fever, lethargy and bilateral anterior uveitis and improved on clindamycin and corticosteroids. Roughly 3 months after clindamycin stopped, she relapsed with severe bilateral blepharitis and keratoconjunctivitis — but no intraocular inflammation — alongside rising C-reactive protein concentrations and rising anti–T gondii titers. The owners declined eyelid biopsy, so alternative causes of the blepharitis could not be excluded. Alternative therapies failed: trimethoprim-sulfamethoxazole was stopped after a severe hypersensitivity reaction, and atovaquone was stopped because of anorexia.
The second relapsing dog had been switched from a compounded veterinary clindamycin formulation to a commercial human formulation after a suboptimal response. The authors caution that the timing of the later improvement does not establish causality, but they note that variability in compounded medications is a recognized concern.
What are the diagnostic limitations?
A single IgG titer cannot distinguish active from latent infection, and T gondii–specific IgM testing was not available locally. The authors point to aqueous humor PCR and the Goldmann-Witmer coefficient as tools that improve diagnostic accuracy, and they note that PCR from Schirmer tear test strips has emerged as a noninvasive option in human medicine.
The study's limitations are those typical of the design: five dogs, retrospective review, and reliance on IgG titers plus clinical response rather than confirmatory PCR, histopathology or IgM titers.
What changes at the exam table?
For companion-animal practice, the message is to consider toxoplasmosis in dogs with uveitis or chorioretinitis — especially systemically ill or immunocompromised patients — and to expect that long-term monitoring and extended treatment may be required. No food-animal or direct public-health implication arises from this series, though T gondii remains a zoonotic agent and dog owners who are pregnant or immunocompromised should follow standard hygiene precautions around any infected animal.
The authors call for larger prospective studies focused on diagnostics, treatment regimens and long-term outcomes — work that will be needed before any consensus protocol for canine ocular toxoplasmosis can be written.
Source: dvm360.com
Grace Kim
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Staff writer covering regulation, policy and their impact on Small- and large-animal clinical practice at The Vet Scope.




