Sunday, December 3, 2023
| Characteristics | Total, n = 52 | No ocular involvement, n = 40 | Ocular involvement, n = 12 | p value |
|---|---|---|---|---|
| Age at infection, y, median (IQR)† | 34 (27–40) | 32 (22–38) | 43 (40–47) | <0.01 |
| ≥40 years of age† | 14 (27) | 6 (15) | 9 (75) | <0.01 |
| Sex | ||||
| M | 44 (84.6) | 33 (82.5) | 11 (91.7) | 0.50 |
| F | 8 (15.4) | 7 (17.5) | 1 (8.3) | 0.50 |
| Follow-up length, mo, median (IQR) | 36 (19–36) | 36 (12–36) | 35 (24–37) | 0.32 |
| Underlying conditions | ||||
| Arterial hypertension | 7 (13.5) | 4 (10.0) | 3 (25.0) | 0.23 |
| Diabetes mellitus | 1 (1.9) | 0 | 1 (8.3) | 0.23 |
| General signs and symptoms | ||||
| Fever | 49 (94.2) | 38 (95.0) | 11 (91.7) | 0.68 |
| Headache | 33 (63.5) | 25 (62.5) | 8 (66.7) | 0.81 |
| Myalgia | 30 (57.7) | 22 (55.0) | 8 (66.7) | 0.50 |
| Lymphadenopathy | 8 (15.4) | 7 (17.5) | 1 (8.3) | 0.50 |
| Ocular signs and symptoms | ||||
| VA at baseline, logMAR, median (IQR)†‡ | 0.0 (0.0–0.0) | 0.0 (0.0–0.0) | 0.1 (0.0–0.6) | 0.01 |
| Eye pain | 8 (15.4) | 5 (12.5) | 3 (25.0) | 0.33 |
| Self-reported recent reduction of VA† | 10 (19.2) | 1 (2.5) | 9 (75.0) | <0.01 |
| Floaters† | 3 (5.7) | 0 | 3 (25.0) | 0.01 |
Table 1. Characteristics and ocular signs and symptoms among patients with confirmed acute toxoplasmosis infection at baseline examination, Brazil*
*Values are no. (%), except as indicated. Mann-Whitney-Wilcoxon test was used to compare continuous and the mid-p exact tests for proportions between subgroups. IQR, interquartile range; logMAR, logarithm of the Minimum Angle of Resolution scale; VA, visual acuity.
†Statistical significant at α = 5%.
‡For visual acuity baseline, binocular involvement was considered the worst VA.
| Type of lesion, fundus imaging modality | Patterns of retinochoroiditis | ||
|---|---|---|---|
| Active phase, before treatment | Cicatricial phase, after treatment | ||
| Focal necrotizing retinochoroiditis Fundus photo or examination |
Dense focal retinal whitening with indistinct borders, associated with overlying vitreous haze | Initially hypopigmented retinochoroidal scar, but frequently evolving with variable degree of pigmentation and subretinal fibrosis or preretinal gliosis | |
| SD-OCT | Focal full-thickness hyper-reflectivity and disorganization of retinal layers indicating necrotizing retinitis; surrounding retinal thickening, signaling edema; numerous overlying hyper-reflective dots at the vitreous indicating vitreal inflammatory cell exudate; and underlying fusiform choroidal thickening, with loss of stromal/luminal pattern indicating reactive choroiditis | Disorganization of retinal architecture; hyper-reflectivity at the level of the scar, but without perilesional retinal thickening; resolution of choroidal thickening; marked decrease in the number of overlying vitreal hyper-reflective dots; and frequent tent-like focal detachment of the less thickened overlying posterior hyaloid | |
| FAF reflectances | Subtle hypo- or hyper-autofluorescence changes at the level of the active lesion; near infrared reflectance can indicate active focus but not as remarkably as red-free reflectance | Increased autofluorescence signal in the first weeks, then hypo-autofluorescence at the level of the scar after several months; scars less clearly delineated by near-infrared than red-free reflectance, but both reveal retinal wrinkling in the presence of epiretinal membrane | |
| FFA | Early hypofluorescence, with progressive hyperfluorescence and late leakage at the retinochoroiditis lesion; reactive changes, including hyperfluorescence, of optic disc indicating edema; staining of venular walls, signaling periphlebitis | Variable window defects and blockage at the level of the scar; staining in the presence of subretinal fibrosis and epiretinal gliosis | |
| Punctate retinochoroiditis Fundus photo or examination |
Multiple subtle, indistinct, or confluent gray-whitish punctate retinal infiltrates with minimal vitreous haze | Very subtle changes in retinal reflex, sometimes with minor hypopigmentation, but frequently with no apparent abnormality | |
| SD-OCT | Multifocal hyper-reflectivity at the inner retinal layers, demonstrating retinitis, occasionally extending to deeper layers, with surrounding retinal thickening (edema); numerous overlying hyper-reflective dots indicating vitreal inflammatory cell exudate, along with thickening and shallow detachment of the posterior hyaloid; mild choroidal thickening without apparent major change in reflectivity | Frequent normalization of the retinal architecture, sometimes with mild disruption of outer retinal layers or retinal pigment epithelium; normalization of choroidal thickening; marked decrease in the number of overlying vitreal hyper-reflective dots and frequent tent-like focal detachment of the less-thickened overlying posterior hyaloid | |
| FAF reflectances | Subtle hypo- or hyper-autofluorescence changes at the level of the punctate active lesions; near-infrared reflectance can show changes at the area of active foci but not as remarkably as red-free reflectance | Autofluorescence and reflectance changes are minimal or absent | |
| FFA | Progressive but mild hyperfluorescence or late leakage at the site of punctate lesions; reactive changes, including hyperfluorescence of optic disc, demonstrating edema; staining of venular walls indicating periphlebitis | Normal or showing minimal punctate window defects | |
Table 2. Characterization of patterns of retinochoroiditis seen in multimodal imaging among patients with toxoplasmosis treated with antiparasitic drugs and oral corticosteroids, Brazil*
*FAF, fundus autofluorescence; FFA, fundus fluorescein angiography; SD-OCT, spectral-domain optical coherence tomography.
| Age, y/sex | Baseline eye examination | Follow-up findings | Complications | Last VA, mo; result | ||
|---|---|---|---|---|---|---|
| RC | Right | Left | ||||
| 38/M† | Bilateral | VA 0.0; SLE, AV cells and AC cells (0.5+/4+); FE, multifocal PR and peripheral large FNR | VA 0.0; SLE, AV cells; FE, PR | 1 OD recurrence; month 2, satellite active lesion | None | 21; 0.0 OU |
| 47/M† | Bilateral | VA 0.2; SLE, AV cells;FE, peripheral large FNR | VA 0.0; SLE, AV cells; FE, multiple peripheral large FNR | 1 OD recurrence; month 22, new peripheral scar | Month 22, epiretinal membrane OD | 34; 0.0 OU |
| 40/M† | Bilateral | VA 0.0; SLE, AV cells; FE, multifocal PR | VA 0.0; SLE, AV cells; FE, multifocal PR and peripheral large FNR |
Multiple recurrences OU; months 11, 21, and 24, active peripheral lesions; month 27, active peripheral lesion OS |
Month 21, epiretinal membrane OD; month 27, rhegmatogenous RD OS | 36; 0.0 OD, 0.8 OS |
| 48/M† | Bilateral | VA 2.1; SL, EAV cells; FE, macular FNR | VA 0.3; SLE, AV cells; FE, peripheral FNR |
2 recurrences OS; new peripheral scar in months 12 and 15 | Month 9, epiretinal membrane OD; month 34, epiretinal membrane OS | 34; 1.9 OD, 0.4 OS |
| 43/M† | Unilateral | VA 0.0; SLE, normal; FE, Leber miliary aneurysms | VA 0.7; SLE, fine KP, AC cells 2+/4+, and AV cells; FE, peripheral large FNR | ─ | None | 36; 0.1 OS |
| 27/M | Unilateral | VA 0.0; SLE, AV cells; FE, PR | VA 0.0; normal SLE and FE | ─ | None | 23; 0.0 OD |
| 42/M† | Unilateral | VA 0.5; SLE, granulomatous KP, AC cells (3+/4+), AV cells; IOP, 28 mmHg; FE, peripheral large FNR | VA 0.0; normal SLE and FE | 1 recurrence OD; month 9, multiple active peripheral lesions OD | Baseline transient IOP elevation OD, 28mmHg | 24; 0.0 OD |
| 31/M | Unilateral | VA 0.0; normal SLE and FE | VA 0.0; SLE OS, AV cells; FE, multiple peripheral FNR | ─ | None | 8; 0.0 OS |
| 50/M† | Unilateral | VA 0.5; SLE, AV cells; FE, peripheral large FNR |
VA 0.0; normal SLE and FE | ─ | Month 6, posterior vitreous detachment OD | 37; 0.0 OD |
| 47/F† | Unilateral | VA 1.6; SLE, AV cells; FE, macular FNR | VA 0.0; normal SLE and FE | ─ | None | 37; 1.9 OD |
| 40/M† | Unilateral | VA 0.0; SLE, AV cells; FE, peripheral large FNR | VA 0.0; normal SLE and FE | ─ | None | 37; 0.0 OD |
| 45/M | Unilateral | VA 0.0; SLE, AV cells; FE, PR | VA 0.0; normal SLE and FE | ─ | None | 37; 0.0 OD |
| 15/M‡ | NA | VA 0.0; normal SLE and FE | VA 0.0; normal SLE and FE | Late ocular involvement; OD VA 0.1; month 34, new peripheral scar | None | 34; 0.1 OD |
| 28/F‡ | NA | VA 0.0; normal SLE and FE | VA 0.0; normal SLE and FE | Late ocular involvement; OD VA 0.0; month 37, peripheral FNR | None | 39; 0.0 OD |
Table 3. Ocular characteristics, recurrences, and complications of patients with ocular involvement from toxoplasmosis, Brazil*
*Age represents age at detection of first ocular lesion or scar. AC cells, grading of anterior chamber cells according to Standardization of Uveitis Nomenclature (SUN) working group[29]; AV cells, anterior vitreous cells; FE, fundus examination; FNR, focal necrotizing retinochoroiditis, large FNR is >3 disk diameters; IOP, intraocular pressure; KP, keratic precipitates; NA, not applicable; OD, oculus dexter (right eye); OS, oculus sinister (left eye); OU, oculus uterque (both eyes); PR, punctate retinochoroiditis; RC, retinochoroiditis; RD, retinal detachment; SLE, slit-lamp examination; VA, visual acuity (log MAR); –, no recurrence or no new lesion.
†Patients with severe ocular involvement, including binocular, macular, or extensive necrotizing retinochoroiditis (>3 disk diameters).
‡Patients with initial normal ophthalmic examination.
This activity is intended for infectious disease clinicians, ophthalmologists, internists, and other clinicians caring for patients with toxoplasmosis and ocular involvement.
The goal of this activity is to describe clinical and multimodal imaging findings at presentation, prevalence of and risk factors for ocular involvement, recurrences, and complications of presumed waterborne toxoplasmosis reported during an outbreak of 52 cases, with serologic evidence of acute toxoplasmosis in 2015 in Gouveia, Southeastern Brazil.
Upon completion of this activity, participants will:
As an organization accredited by the ACCME, Medscape, LLC requires everyone who is in a position to control the content of an education activity to disclose all relevant financial relationships with any commercial interest. The ACCME defines "relevant financial relationships" as financial relationships in any amount, occurring within the past 12 months, including financial relationships of a spouse or life partner, that could create a conflict of interest.
Medscape, LLC encourages Authors to identify investigational products or off-label uses of products regulated by the US Food and Drug Administration, at first mention and where appropriate in the content.
Medscape, LLC designates this Journal-based CME activity for a maximum of 1.0
AMA PRA Category 1 Credit(s)™
. Physicians should claim only the credit commensurate with the extent of their participation in the activity.
Successful completion of this CME activity, which includes participation in the evaluation component, enables the participant to earn up to 1.0 MOC points in the American Board of Internal Medicine's (ABIM) Maintenance of Certification (MOC) program. Participants will earn MOC points equivalent to the amount of CME credits claimed for the activity. It is the CME activity provider's responsibility to submit participant completion information to ACCME for the purpose of granting ABIM MOC credit.
For questions regarding the content of this activity, contact the accredited provider for this CME/CE activity noted above. For technical assistance, contact [email protected]
There are no fees for participating in or receiving credit for this online educational activity. For information on applicability
and acceptance of continuing education credit for this activity, please consult your professional licensing board.
This activity is designed to be completed within the time designated on the title page; physicians should claim only those
credits that reflect the time actually spent in the activity. To successfully earn credit, participants must complete the
activity online during the valid credit period that is noted on the title page. To receive AMA PRA Category 1 Credit™, you must receive a minimum score of 75% on the post-test.
Follow these steps to earn CME/CE credit*:
You may now view or print the certificate from your CME/CE Tracker. You may print the certificate but you cannot alter it.
Credits will be tallied in your CME/CE Tracker and archived for 6 years; at any point within this time period you can print
out the tally as well as the certificates from the CME/CE Tracker.
*The credit that you receive is based on your user profile.
CME / ABIM MOC Released: 11/19/2020
Valid for credit through: 11/19/2021, 11:59 PM EST
processing....
In 2015, an outbreak of presumed waterborne toxoplasmosis occurred in Gouveia, Brazil. We conducted a 3-year prospective study on a cohort of 52 patients from this outbreak, collected clinical and multimodal imaging findings, and determined risk factors for ocular involvement. At baseline examination, 12 (23%) patients had retinochoroiditis; 4 patients had bilateral and 2 had macular lesions. Multimodal imaging revealed 2 distinct retinochoroiditis patterns: necrotizing focal retinochoroiditis and punctate retinochoroiditis. Older age, worse visual acuity, self-reported recent reduction of visual acuity, and presence of floaters were associated with retinochoroiditis. Among patients, persons ≥40 years of age had 5 times the risk for ocular involvement. Five patients had recurrences during follow-up, a rate of 22% per person-year. Recurrences were associated with binocular involvement. Two patients had late ocular involvement that occurred ≥34 months after initial diagnosis. Patients with acquired toxoplasmosis should have long-term ophthalmic follow-up, regardless of initial ocular involvement.
Toxoplasmosis is caused by Toxoplasma gondii, an obligate intracellular apicomplexan parasite that infects up to one third of the human population[1–4]. Humans are mainly infected by ingesting tissue cysts in undercooked or raw meat or oocysts excreted in cat feces that contaminate water or food[1–4]. Ocular disease is the major clinical repercussion in immunocompetent patients; toxoplasmosis is the leading cause of infectious posterior uveitis worldwide and can potentially lead to severe ocular complications[1,3,5,6]. Although congenital toxoplasmosis more frequently leads to retinochoroiditis, postnatally acquired infection now is acknowledged as being associated with a large proportion of cases[2,3,6,7]. Association between ocular toxoplasmosis and older age is not completely understood[8], but previous studies found increased prevalence of ocular involvement in persons >30 years of age[9,10].
Toxoplasmosis outbreaks are good opportunities to clarify clinical aspects of this complex disease because patients are infected at known times, by similar routes, and presumably by parasites of the same genotype[11–19]. In 2015, an outbreak of presumed waterborne toxoplasmosis was reported in Gouveia, a small city of ≈10,000 inhabitants in the center of the state of Minas Gerais in southeastern Brazil[20]. Municipal, state, and federal health authorities investigated several cases of fever, malaise, weight loss, and lymphadenopathy. Recent toxoplasmic infection was eventually confirmed in 52 cases. All patients had the disease after drinking water from a single, presumably contaminated, source[20].
We performed complete ophthalmic examination and multimodal fundus imaging evaluation on all 52 patients. The objective of this study was to describe clinical and multimodal imaging findings and determine the prevalence of ocular involvement, incidence of recurrences and complications, and to analyze risk factors for ocular involvement in this cohort.
