Abstract
Rationale:
Toxoplasma gondii is distributed worldwide, infecting a large population. It can cause focal necrotic retinitis or retinochoroiditis in the human eyes and is one of the most common causes of posterior uveitis.
Patient concerns:
A 68-year-old patient with normal immunity was complained about blurred vision and black shadow in the right eye for 1 week.
Diagnoses:
Combined Yellow-and-white bulged lesions in the fundus of the right eye with the Goldmann-Witmer coefficient = 2 and based on the serological indicators, we considered the diagnosis of T. gondii infection-induced retinochondritis.
Interventions:
Acetylspiramycin 0.4 QID × 3 weeks, concussive 20 days treatment after 3 days, for a total of 3 months, prednisone 20 mg/day with a weekly reduction of 5 mg for 1 month.
Outcomes:
After oral acetylspiramycin, topical and systemic corticosteroids for 3 months, the retinal lesions were scarred, and inflammation of the anterior chamber and vitreum disappeared. After a 9-month follow-up, the visual acuity was 0.6, and no active lesions were observed in the fundus.
Lessons:
The immunocompetent elderly who are in contact with domestic cats may have an opportunistic infection with toxoplasmosis leading to primary retinochoroiditis. Prompt diagnosis and effective treatment can get a good clinical prognosis.
Keywords: acquired toxoplasmosis retinochoroiditis, aged, case report, diagnosis, Goldmann–Witmer, treatment
1. Introduction
Toxoplasma gondii, the most common cause of posterior uveitis worldwide, is a protozoan parasite that can infect up to one-third global population.[1] Although posterior uveitis is usually a self-limited disease, it may reduce vision secondary to the optic nerve or macular involvement and/or severe vitreous inflammation.[2] Atypical cases of ocular toxoplasmosis consist of multifocal lesions and large areas of retinal necrosis or retinochoroiditis.[3] Such cases might require a combination of periocular and oral treatment to control the inflammation. Hitherto, there is no consensus on the treatment efficiency and risk factors for the occurrence and recurrence of this eye disease.[4] In addition, the Goldmann–Witmer coefficient is useful for the diagnosis of atypical lesions by comparing the titer of IgG in aqueous humor and serum.[5]
Herein, we present an atypical toxoplasmosis retinochoroiditis in an aged, immunocompetent individual; however, it elucidates some critical principles in the diagnosis and management of this challenging condition.
2. Case presentation
The patient was a 68-year-old male, who visited the Clinical Ophthalmology Department of The Second Affiliated Hospital of Zhejiang Chinese Medical University in Hangzhou, Zhejiang, China, on September 6, 2016, and complained about blurred vision and black shadow in the right eye for 1 week. The history of systemic diseases was as follows: indirect cat exposure once for half a day, hypertension for >40 years in which, the blood pressure was controlled by drugs, prostate hyperplasia, excision of tumor of the right lung in the First Affiliated Hospital, Zhejiang University in 2006, and a smoking history of >10 years (15–20 cigarettes/day).
Ophthalmic examination showed visual acuities of 0.3 and 0.8 in the right and left eyes, respectively, and intraocular pressures of 15 and 13 mm Hg in the right and left eyes, respectively. Any obvious anomalies were not observed in the anterior segment of both eyes. The slit lamp revealed an apparent vitreous opacity in the right eye, with visible inflammatory cells. The fundus of the right eye was blurred after mydriasis. No hyperemia and edema were observed in the optic disc. Yellow-and-white bulged lesions were visible in the superior temporal area with unclear border and dilated peripheral retinal vessels, as well as subtly visible hemorrhage in the inferior retina (Fig. 1). The left eye disc was red with a distinct border, the retinal arteriovenous ratio was ∼1:3, and pigment disorders were visible in the macula.
Figure 1.
The right eye showed vitreous opacity and inflammatory cells; yellow-and-white lesions were visible in the superior temporal area, the sheath was visible in a peripheral rental artery, and dotted hemorrhage was visible in the peripheral area of the inferior retina. The left eye disc was red with a distinct border, the retinal arteriovenous ratio was ∼1:3, and pigment disorders were visible in the macula.
After 3 weeks, the yellow-and-white lesions in the fundus were significantly enlarged. Subsequently, the patient underwent further examinations, including tumor indicators, blood routine, living routine, immunization routine, TORCH (Toxoplasma, Rubella virus, Cytomegalo virus, Herpes virus), blood transfusion laboratory test, and T-spot (Detection of T cells in tuberculosis infection); Test results helpful for diagnosis and differential diagnosis are summarized in Table 1.
Table 1.
Test results helpful for diagnosis and differential diagnosis.
We hypothesized that the patient should be diagnosed with one of the following diseases: infectious retinochoroiditis, tuberculous chorioretinitis, metastatic choroidal carcinoma, or lymphoma. Combined with the clinical manifestations and fundus characteristics of the patient, we speculated that the diagnosis mainly lied in the differentiation of lymphoma and infectious retinochondritis. Therefore, we measured the IL10/IL6 value and Goldmann–Witmer coefficient of the intraocular fluid (with Prof. Tao Yong, Beijing Chao-Yang Hospital affiliated to Beijing University) and obtained the following results: IL-10/IL-6 < 1, Goldmann–Witmer coefficient = 2. On the basis of the serological indicators, we considered the diagnosis of T gondii infection induced retinochondritis. Thus, the following treatment program was adopted: acetylspiramycin 0.4 QID×3 weeks, concussive 20 days treatment after 3 days, for a total of 3 months, prednisone 20 mg/day with a weekly reduction of 5 mg for 1 month. The fundus after the treatment is shown in Fig. 2.
Figure 2.
With the application of drugs, lesions were gradually reduced, which finally led to chorioretinal atrophy with visible choroidal vessels in the fundus.
After a 9-month follow-up, the visual acuity was 0.6, and no active lesions were observed in the fundus.
The study was approved by The Second Affiliated Hospital of Zhejiang Chinese Medical University in Hangzhou, Zhejiang, China. The patient enrolled has given informed consent.
3. Discussion
Approximately 30% of the global human population is chronically infected with T gondii.[6] Human infections are primarily acquired by ingesting undercooked or raw meat containing viable tissue cysts or by ingesting food or water contaminated with T gondii oocysts.[7,8] But in this case, the only positive history was indirect cat exposure once for half a day. The primary infections in adults are mostly asymptomatic; however, lymphadenopathy or ocular toxoplasmosis is presented in some patients.[9] Severe, acute, disseminated toxoplasmosis might occur in immunocompetent individuals infected with some isolates.[10–14] This normal immunity patient had atypical ocular manifestations, which were similar with other reports, but no lymph node reaction, no severe systemic, acute, disseminated toxoplasmosis symptoms.
The diagnosis of ocular toxoplasmosis depends largely on the presence of typical lesions, with retinochoroiditis as a critical feature. However, the Goldmann–Witmer coefficient is valuable in the diagnosis of atypical lesions, which is well-validated in this case.
Currently, optimal drugs for the treatment of toxoplasmosis are lacking. The majority of the available drugs can inhibit the growth of T gondii in the proliferative stage, for example, a combination therapy of pyrimethamine and sulfadiazine. Pyrimethamine can lead to poor blood-related performances such as leukopenia and thrombocytopenia as well as gastrointestinal and skin side effects. Sulfadiazine is a sulfonamide insect-resistant drug that usually causes sudden anaphylaxis. Clinically, spiramycin combined with azithromycin is often used for the systemic treatment of T gondii infection in pregnant women, wherein remarkable effects are observed without any adverse reactions.[15] Hence, acetylspiramycin combined with hormone therapy was used for the treatment in this study. After periodic drug treatment, the serum IgM antibody was detected as negative, the topical lesions in the eye were scarred, the inflammation in the anterior chamber of the vitreum vanished, and the visual acuity improved.
In this case, we presented an immunocompetent elderly person suffered from atypical primary toxoplasmosis retinochoroiditis; we prescribed sensitive drugs and symptomatic supportive care and achieved good clinical outcomes. However, there was no direct evidence that the disease was caused by contact with domestic cats. In case of clinical suspected T gondii infection, it should be promptly confirmed by Goldmann–Witmer coefficient test, so that the patients could be treated promptly and correctly.
4. Conclusion
This case suggests that the elderly people with normal immunity may have an opportunistic infection of toxoplasmosis, and Goldmann–Witmer coefficient is valuable in the diagnosis; oral antibiotics acetylspiramycin, topical, and systemic corticosteroids can be used to obtain satisfactory clinical outcomes.
Acknowledgment
We would like to thank the native English-speaking scientists of MedSci Company (Shanghai, China) for editing our manuscript.
Author contributions
Conceptualization: Xiaoli Lv, Pingping Yu.
Data curation: Xiaoli Lv, Pingping Yu.
Formal analysis: Xiaoli Lv.
Investigation: Xiaoli Lv, Pingping Yu.
Project administration: Xiaoli Lv.
Resources: Pingping Yu.
Validation: Xiaoli Lv.
Writing – original draft: Xiaoli Lv, Pingping Yu.
Writing – review & editing: Pingping Yu.
Footnotes
Abbreviations: ESAT-6 = early secreted antigenic target-6, IgG = Immunoglobulin G, IgM = Immunoglobulin M, IL10 = interleukin-10, IL6 = interleukin-6, PPD = purified protein derivatives tuberculin, QID = qualer in die, TORCH = Toxoplasma, Rubella virus, Cytomegalovirus, Herpes virus, T-SPOT = Detection of T cells in tuberculosis infection.
The authors report no conflicts of interest.
References
- [1].Dard C, Chemla C, Fricker-Hidalgo H, et al. Late diagnosis of congenital toxoplasmosis based on serological follow-up: a case report. Parasitol Int 2017;66:186–9. [DOI] [PubMed] [Google Scholar]
- [2].Hosseini SM, Abrishami M, Mehdi Zadeh M. Intravitreal clindamycin in the treatment of unresponsive zone one toxoplasmic chorioretinitis: a case report. Iran Red Crescent Med J 2014;16:e15428. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [3].Theodoropoulou S, Schmoll C, Templeton K, et al. Atypical toxoplasmic retinochoroiditis. BMJ Case Rep 2012;2012:pii: bcr1220115419. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [4].Butler NJ, Furtado JM, Winthrop KL, et al. Ocular toxoplasmosis II: clinical features, pathology and management. Clin Exp Ophthalmol 2013;41:95–108. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [5].Hernandez-Martinez P, Dolz-Marco R, Gallego-Pinazo R, et al. [Goldmann-Witmer, definitive diagnosis in unifocal helicoid choroiditis]. Arch Soc Esp Oftalmol 2015;90:341–3. [DOI] [PubMed] [Google Scholar]
- [6].Moncada PA, Montoya JG. Toxoplasmosis in the fetus and newborn: an update on prevalence, diagnosis and treatment. Expert Rev Anti Infect Ther 2012;10:815–28. [DOI] [PubMed] [Google Scholar]
- [7].Dubey JP. The history of Toxoplasma gondii: the first 100 years. J Eukaryot Microbiol 2008;55:467–75. [DOI] [PubMed] [Google Scholar]
- [8].Tenter AM, Heckeroth AR, Weiss LM. Toxoplasma gondii: from animals to humans. Int J Parasitol 2000;30:1217–58. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [9].Paul M. Immunoglobulin G avidity in diagnosis of toxoplasmic lymphadenopathy and ocular toxoplasmosis. Clin Diagn Lab Immunol 1999;6:514–8. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [10].Cuomo G, D’Abrosca V, Rizzo V, et al. Severe polymyositis due to Toxoplasma gondii in an adult immunocompetent patient: a case report and review of the literature. Infection 2013;41:859–62. [DOI] [PubMed] [Google Scholar]
- [11].Neves Ede S, Kropf A, Bueno WF, et al. Disseminated toxoplasmosis: an atypical presentation in an immunocompetent patient. Trop Doct 2011;41:59–60. [DOI] [PubMed] [Google Scholar]
- [12].Carme B, Bissuel F, Ajzenberg D, et al. Severe acquired toxoplasmosis in immunocompetent adult patients in French Guiana. J Clin Microbiol 2002;40:4037–44. [DOI] [PMC free article] [PubMed] [Google Scholar]
- [13].Candolfi E, de Blay F, Rey D, et al. A parasitologically proven case of Toxoplasma pneumonia in an immunocompetent pregnant woman. J Infect 1993;26:79–81. [DOI] [PubMed] [Google Scholar]
- [14].Abhilash KP, Roshine MK, Vandana K, et al. A probable case of acquired toxoplasmosis presenting as pyrexia of unknown origin in an immunocompetent individual. Int J Infect Dis 2013;17:e1067–8. [DOI] [PubMed] [Google Scholar]
- [15].Tang HX, Xiong XF, Qin ZQ. [Clinical experience on treating Toxoplasma gondii infection during pregnancy by using acetyl spiramycin combined with azithromycin]. Zhongguo Xue Xi Chong Bing Fang Zhi Za Zhi 2013;25:555–6. [PubMed] [Google Scholar]