Chapter 172 – Ocular Toxoplasmosis

Chapter 172 – Ocular Toxoplasmosis










• Intraocular inflammation due to infection with the parasite Toxoplasma gondii.



• Focal retinochoroiditis.



• Decreased vision.

• Floaters.

• Anterior uveitis.

• Vitritis.

• Retinal vasculitis and vascular occlusions.

• Retinochoroidal scars.

• Papillitis.





Ocular inflammation caused by infection with the obligate intracellular parasite Toxoplasma gondii (ocular toxoplasmosis) is the most common posterior uveitis in immunocompetent individuals.[1] [2] Although ocular toxoplasmosis usually consists of a self-limited retinochoroiditis, sight-threatening complications do occur, and in one study it was the foremost cause of unilateral vision loss in patients who have uveitis.[3] In infants and immunosuppressed individuals, ocular toxoplasmosis may be more severe and can also be associated with potentially fatal systemic toxoplasmosis.

Our understanding of ocular toxoplasmosis is changing.[4] [5] Traditionally, it was thought that toxoplasmic retinochoroiditis was almost always a reactivation of infection acquired in utero. New evidence has shown that newly acquired infection is more common than previously appreciated. The importance of the pathogenicity of specific strains of T. gondii, the role of host factors (including age and immune status), and new techniques for diagnosis and therapy of ocular toxoplasmosis are actively being researched.


T. gondii is an obligate intracellular protozoan parasite that is found worldwide and can infect most mammals and some birds. The life cycle of the organism is complex but helps explain many of the epidemiological and clinical features of the disease.[6] The sexual reproductive cycle of the parasite occurs within the small intestines of felines, the definitive hosts. The major morphological forms of T. gondii are the oocyst, tachyzoite, and tissue cyst. The oocyst is the product of sexual reproduction and is shed in the feces of cats. Oocysts can persist in soil for more than a year. Sporulation creates the infectious oocyst (containing sporozoites), which is ingested by cats and other animals, including humans, with invasion of intestinal epithelial cells and asexual proliferation of the organism as tachyzoites. Tachyzoites can disseminate throughout the host’s body in the lymph and hematological systems, carried by macrophages. Tachyzoites can penetrate virtually any nucleated cell. In the cell cytoplasm the organism is found in a parasitophorous vacuole, which protects the organism. In certain tissue types such as brain, heart, skeletal muscle, and retina, slowly metabolizing organisms (bradyzoites) form an argyrophilic, periodic acid-Schiff–positive tissue cyst in which the organism is safely isolated from the host’s immune system. When the cyst wall breaks down, bradyzoites develop into tachyzoites and can invade neighboring cells.


Human infection with T. gondii is most often acquired by eating the meat of infected animals, particularly undercooked pork and, less frequently, lamb, chicken, and beef. Exposure can also occur from contact with contaminated cat feces while cleaning a litter box or by playing in public sandboxes or dirt. Other sources of infection include eggs,[7] unpasteurized goat milk,[8] unwashed fruits and vegetables, municipal drinking water,[9] and inhalation of sporulated oocysts.[10] There is increasing evidence that acquired disease is more important as a source of ocular infection than previously recognized. [9] [10] [11] [12] [13] [14]

Most individuals who have ocular manifestations of toxoplasmosis are thought to have acquired the disease in utero. Transplacental transmission of T. gondii to the fetus occurs only with new-onset maternal infection; chronic maternal infection or recurrent disease is not thought to result in transplacental transmission and congenital infection. Primary maternal infection has been estimated to occur in 0.2–1% of pregnancies.[11] Subsequent congenital infection also depends on the stage of pregnancy in which maternal infection develops. The rate of congenital toxoplasmosis increases from 10–15% following exposure in the first trimester to 60% following third-trimester exposure.[11] Congenital disease is much more severe when acquired early in pregnancy; the low rate of congenital disease with infection in the first trimester may be due to the risk of spontaneous abortion with early infection.

The rate of ocular disease appears to vary widely in different populations. The rate of seropositivity for toxoplasmosis is estimated to be from 3% to as high as 70% of adults in the United States; this varies for different locales and age groups,[6] whereas the prevalence of ocular toxoplasmosis is less than 1%. In areas such as Micronesia, there is a high degree of seropositivity, but ocular disease is very uncommon. This suggests that either host or parasite factors, or both, are important in the development of ocular disease. In evaluating 28 strains from around the world, Sibley and Boothroyd[15] found that virulent strains had the same genotype, whereas nonvirulent strains were polymorphic, implying that specific strains are more likely to cause disease. Host factors that are important in disease pathogenesis include the individual’s immune status, which is discussed in the next section.




The primary pathological finding in active ocular toxoplasmosis is a well-demarcated coagulative retinal necrosis.[16] Viable tachyzoites and tissue cysts may be found in the infected retina.[17] An intense mononuclear inflammatory cell reaction is seen in the involved retina and vitreous, whereas a granulomatous reaction usually occurs in the contiguous choroid.

It is not known what factors are critical for the establishment of ocular disease or the triggering of recurrences. Tissue cysts may persist for years without causing an inflammatory reaction. The immune status of the host is clearly important, as demonstrated by the severe and prolonged disease course in patients who have acquired immunodeficiency syndrome (AIDS)[18] and in other immunosuppressed individuals, including those receiving corticosteroid therapy.[19] [20] Host factors that determine the outcome of infection include multiple components of the immune response to the parasites.[6] [21] [22] [23] [24] [25] Humoral immunity can play a role in lysis of the parasite when the parasites are extracellular, and antibody-coated parasites may not form a protective membrane, which is important for parasite survival in the host macrophage. However, the cellular immune response appears to be of primary importance for host defense, and both CD4 and CD8 T cells are involved in the immune defenses against T. gondii.[6]

There may be a role for autoimmunity in the pathogenesis of the ocular inflammation seen in ocular toxoplasmosis. The inflammatory response in the vitreous and anterior chamber is not associated with viable parasites in these fluids, at least in immunocompetent individuals. Further, the retinitis itself may in part be an autoimmune response and not just a response to the organism.[26] [27] Meenken et al.[28] found that the HLA-Bw62 antigen correlated with severe ocular involvement in congenital toxoplasmosis. However, despite the frequently reported association of HLA subtypes with specific autoimmune diseases, HLA genes are important in host responses to infectious agents, so an HLA association may not imply an autoimmune pathogenesis.


Active ocular infection with toxoplasmosis typically manifests as a localized necrotizing retinitis. The classic lesion is a gray-white focus of retinal necrosis at the edge of a pigmented chorioretinal scar ( Fig. 172-1 ). An adjacent choroiditis, retinal vasculitis, vitritis, iritis, and papillitis may also be seen. There is an overlying vitritis that can be so dense as to prohibit an adequate view of the posterior segment. When the white retinal lesion can just be seen through a dense vitritis, it has been described as a “headlight in the fog.” The associated iritis can be quite severe, with



Figure 172-1 Active ocular toxoplasmosis with an adjacent chorioretinal scar. From Holland GN, O’Connor GR, Belfort R, Remington JS. Toxoplasmosis. In Pepose JS, Holland GN, Wilhelmis KW, eds. Ocular infection and immunity. St. Louis: Mosby; 1996.

granulomatous features, and may be associated with increased intraocular pressure.

The patient may present with floaters (vitritis), decreased vision (vitritis, papillitis, retinal necrosis, macular edema, choroidal neovascular membranes, vascular occlusions, retinal detachment), pain, redness, and photophobia (iritis). Complications that can result in permanent loss of vision include macular inflammation resulting in a scar, choroidal neovascular membranes, vascular occlusions, optic nerve involvement, and retinal detachment.

A chorioretinal scar may not be present, particularly with recently acquired disease[14] [29] ( Fig. 172-2 ). Holland et al.[29] reported 10 patients who presented with vitritis, iritis, and retinal vasculitis without clinically apparent retinal lesions. Four of nine of these patients later developed retinochoroidal scars. The authors thought that this presentation probably represented acquired disease. Conversely, extensive retinal necrosis can be seen in elderly patients with what may also be recently acquired disease.[30]

Other forms of toxoplasmosis have been described in immunocompetent patients. Freidmann and Knox[31] classified 56% of their patients as having “large destructive lesions,” 27% as having “punctate inner lesions,” and 17% as having “punctate deep lesions.” The punctate inner lesions had less vitritis than did the large destructive lesions. The punctate deep lesions were located in the macula and had no significant vitritis. Punctate outer retinal toxoplasmosis [32] was described by Doft and Gass[33] and consists of multiple gray-white lesions less than 1000?µm in diameter at the level of the deep retina or retinal pigment epithelium. Their patients also had little vitritis. Punctate outer toxoplasmosis can be bilateral and may resolve without treatment, leaving fine white dots or small chorioretinal scars.[33] Neuroretinitis has also been attributed to infection with T. gondii. Most patients with toxoplasmic neuroretinitis have a good visual outcome with antiparasitic therapy.[34]

The most common manifestation of congenital toxoplasmosis is retinochoroiditis. Chorioretinal scars, often bilateral, are seen in about 80% of patients with congenital toxoplasmosis.[35] There is a moderate predilection for macular involvement, which may relate to fetal vascular patterns. The retinal inflammation in congenital toxoplasmosis tends to be self-limited, and the lesions may already be healed at birth or may develop months or years after birth. Other ocular manifestations include microcornea, microphthalmos, nystagmus, and strabismus.

Presumably, most individuals who are infected in utero and subsequently develop ocular toxoplasmosis do not develop clinical systemic congenital toxoplasmosis. However, acute congenital toxoplasmosis is a systemic disease and may be associated with low birth weight, fever, jaundice, maculopapular rash,



Figure 172-2 Toxoplasmosis. A, Histologic section showing an acute coagulative retinal necrosis, whereas the choroid shows a secondary diffuse granulomatous inflammation. B, A toxoplasmic cyst is present in the neural retina; note the tiny nuclei in the cyst. (From Yanoff M, Fine BS. Ocular pathology, ed 5. St. Louis: Mosby; 2002.)



pneumonia, and hepatosplenomegaly. Central nervous system involvement portends a poor outcome and may result in microcephaly, hydrocephaly, seizures, disseminated intracranial calcification, and psychomotor retardation. Severely infected infants may die within the first month of life, although infants with less severe forms of the disease may not show any signs of infection for months after birth.

In immunosuppressed and elderly patients, ocular infection can be quite severe, but perhaps more importantly, it can be associated with fatal systemic toxoplasmosis. Toxoplasmosis infection may involve the central nervous system, heart, and lungs in patients after organ transplants and in patients who have lymphomas. [19] In patients with AIDS, ocular toxoplasmosis is less common than toxoplasmic infection of other organs, in particular the central nervous system. Fifteen to 40% of individuals who have AIDS have antitoxoplasmosis antibodies in the United States, [36] and toxoplasmic encephalitis was seen in 25–50% of individuals who have AIDS and positive serologies before the era of immune reconstitution with multidrug regimens.[37] Toxoplasmic encephalitis in AIDS patients is usually a focal disease, but some patients may develop a diffuse encephalitis, which may be rapidly fatal.[38]

Ocular toxoplasmosis in individuals who have AIDS may be unilateral or bilateral, with single or multiple lesions, and it is often chronic or recurrent, requiring prolonged therapy.[18] The retinitis may be slowly progressive or very aggressive, with large areas of full-thickness retinal necrosis and severe vitritis. Patients who have AIDS have been reported to have unusual forms of ocular toxoplasmosis. Ocular toxoplasmosis presenting as an iridocyclitis without retinal involvement was confirmed by polymerase chain reaction techniques in an AIDS patient who had retinitis in the fellow eye.[39] Panophthalmitis with a presumed secondary orbititis has also been reported.[40]


The diagnosis of ocular toxoplasmosis is often made by the clinical features alone. Serological studies may be helpful in selected cases, but a positive serology does not in itself confirm the diagnosis, given the high rate of seropositive individuals found in many populations. A negative serology can, however, assist in eliminating the disease from the differential diagnosis, although false negatives do occur.

Serial tests for immunoglobulin G (IgG) and immunoglobulin M (IgM) antibodies, spaced at 3-week intervals, can identify a rise in titer levels and help point toward a recently acquired infection. Typically, IgG antibodies are produced within 2 weeks of infection, peak at 2 months, and are present for life. Detection of IgM antibody titers is usually possible within 2 weeks of infection and suggests a recently acquired infection. However, the IgM titer may be only transiently elevated; therefore, a negative titer does not rule out recent infection. Immunoglobulin A (IgA) antibodies are usually detectable for only 7 months and may be helpful in evaluating a patient for a recently acquired infection.[41] [42] Because IgM antibodies do not cross the maternal-placental blood barrier, they are especially useful in diagnosing congenital toxoplasmosis. IgA antibodies may also be useful for evaluating infants for congenital toxoplasmosis.

The standard reference study for toxoplasmosis serologies is the Sabin-Feldman dye test. This test requires live T. gondii organisms and is not readily available. Most laboratories use enzyme-linked immunosorbent assay (ELISA), immunofluorescent antibody (IFA) test, or related techniques to measure serum anti-Toxoplasma antibodies. Serologies performed using Food and Drug Administration–approved ELISA kits for the detection of IgM may vary somewhat in their sensitivity and specificity.[43] False positives in patients with rheumatoid factor or antinuclear antibodies have been reported, but this appears to be less problematic with the newer available techniques.

Diagnosis in difficult cases could require invasive techniques. Ocular tissue sections and intraocular fluids have been examined for toxoplasmic DNA by polymerase chain reaction technology. Polymerase chain reaction has proved useful in the evaluation of some difficult cases.[44] [45] Intraocular antibody production can be examined. Calculation of the Witmer Goldman coefficient is a technique used to evaluate intraocular antibody production by comparing the levels of antibody titers found in aqueous humor to those found in serum. In addition, detection of local IgA production increases the diagnostic sensitivity of aqueous humor analysis in early disease.[46]


Other diseases that must be considered in the differential diagnosis include acute retinal necrosis, sarcoidosis, pars planitis, endogenous bacterial or fungal infection, syphilis, tubercular chorioretinitis, and intraocular lymphoma. The differential diagnosis in newborn patients should include other congenital infections in the TORCH complex (toxoplasmosis, other agents, rubella, cytomegalovirus, herpes simplex), toxocariasis, macular coloboma, and retinoblastoma. Lymphocytic choriomeningitis has been described as resulting in macular scars that mimicked ocular toxoplasmosis in two otherwise normal children. [47] In AIDS patients, ocular toxoplasmosis can mimic cytomegalovirus retinopathy[48] ( Fig. 172-3 ). In toxoplasmic retinochoroiditis, the retinitis is often more sharply demarcated, without associated hemorrhage, and there is usually more vitritis than in cytomegalovirus retinitis. Syphilitic uveitis, as well as other infections and lymphoma, must also be considered in AIDS patients.


Toxoplasmic retinochoroiditis in immunocompetent individuals is often a self-limited process; therefore, not every episode requires therapeutic intervention. The potential benefits of treatment need to be balanced against the risks associated with antimicrobial therapy.[49] [50]

Criteria that have been used for the initiation of treatment of immunocompetent patients include a two-line decrease in visual acuity, lesions located within the temporal arcade or affecting the optic nerve, moderate to severe vitreous inflammation. Relative indications for treatment include lesions with active inflammation for greater than 1 month, multiple active lesions, and newly acquired infections. The size of the lesion is thought by some to be a less important criterion for treatment. It is not clear whether punctate outer retinal toxoplasmosis requires therapy.[33] [49] [50]

Many agents have been used to treat ocular toxoplasmosis ( Table 172-1 ). A triple-therapy regimen of pyrimethamine in conjunction with sulfadiazine and oral corticosteroids, or



Figure 172-3 Progressive toxoplasmic retinal necrosis in an AIDS patient. From Holland GN, O’Connor GR, Belfort R, Remington JS. Toxoplasmosis. In Pepose JS, Holland GN, Wilhelmis KW, eds. Ocular infection and immunity. St. Louis: Mosby; 1996.







Triple/Quadruple Therapy*



Loading Dose

Treatment Dose




25–50?mg qd




1.0?g qid




300?mg qid




20–80?mg qd (0.5–1.0?mg/kg qd)






Folinic acid


5?mg/3× per week


Other Agents






750?mg tid or qid




400?mg tid




250?mg qd




100?mg bid


* Numbers 1 + 2 + 4 = triple therapy; numbers 1 + 2 + 3 + 4 = quadruple therapy.

† Prednisone is started 24 hours after initiating antimicrobial therapy and is tapered before discontinuing antimicrobial therapy.





quadruple therapy with the addition of clindamycin, has traditionally been used to treat ocular toxoplasmosis. In a treatment survey, triple therapy was the most common single regimen selected; quadruple therapy was a close second.[49] [50] A prospective study comparing triple therapy to sulfadiazine, clindamycin and prednisone, trimethoprim-sulfamethoxazole and prednisone, or no treatment found that the duration of ocular inflammation and mean recurrence rate were the same for all groups.[51] Although the first two regimens resulted in smaller lesion size compared with no treatment, the difference was statistically significant only for the triple therapy group.

Sulfonamides and pyrimethamine work by inhibiting folic acid metabolism. Folinic acid is administered concurrently with pyrimethamine to prevent bone marrow suppression. A baseline complete blood count needs to be obtained before initiating treatment, followed by weekly measurements during the duration of treatment to monitor for drug toxicity. Therapy should be discontinued if the white cell count falls below 4000 cells/µl or the platelet count is less than 100,000 cells/µl, or if either decreases 25–50% below baseline.[49]

Other agents that have been used to treat infections with T. gondii are included in Table 172-1 . Atovaquone, a newer antiparasitic agent recently evaluated in a phase I trial, appears to be a well-tolerated therapeutic option.[52] Azithromycin may also be an effective agent for the treatment of acute disease, but it does not provide preventive benefits. A prospective, randomized trial comparing pyramethamine and sulfadiazine with pyramethamine and azithromycin found similar treatment efficacy but significantly less adverse drug effects with azithromycin. [53] Tetracycline, clarithromycin, and spiramycin also appear to be active against T. gondii. Combinations of medications that work by different mechanisms may have a synergistic effect. Such combinations include pyrimethamine and atovaquone or clarithromycin and minocycline.[5] According to a recent report, the use of intravitreal dexamethasone and clindamycin was thought to be effective in four eyes of four patients and may be an alternative in patients who cannot tolerate systemic therapy.[54]

Oral corticosteroids are sometimes used to control the inflammatory component of ocular toxoplasmosis, including any associated vitritis, vasculitis, and macular edema. Because increased ocular inflammation and retinal necrosis may be seen in patients receiving steroids without antimicrobial therapy, it is generally recommended that patients be treated for at least 24 hours with antiparasitic agents before beginning oral steroids. Topical steroids may be used for the anterior uveitis but have no effect on vitritis or retinochoroiditis.

In immunocompetent individuals, treatment is continued until a significant decrease in inflammation is detected and the retinochoroiditis is no longer active. This is typically in the range of 4–6 weeks, but may be longer. Steroids should be tapered before discontinuing the antimicrobial agents. A recent randomized prospective study demonstrated that in healthy individuals the rate of recurrent toxoplasmic retinochoroiditis may be reduced by the use of long-term, intermittent trimethoprim/sulfamethoxazole therapy.[55]

Treatment of pregnant women is indicated in newly acquired disease and must take into consideration the teratogenicity of standard therapeutic agents. Spiramycin is thought to be the safest agent for use in pregnancy and may reduce the rate of T. gondii transmission to the fetus. [11] As noted earlier, recurrent maternal toxoplasmic retinochoroiditis is probably not associated with transmission of the parasite to the fetus and does not require treatment unless the mother’s vision is threatened. Consideration could be given to intravitreal therapy, but the safety and effectiveness of this approach, particularly in pregnant women, have not been established. Because of the progressive nature of the ocular disease in immunosuppressed individuals with active ocular toxoplasmosis, treatment is recommended when there is any active disease in this patient population. Assessment for systemic toxoplasmosis, especially central nervous system disease, should also be pursued. The possibility of bone marrow suppression from pyrimethamine and the risk of further immunosuppression with corticosteroids are additional concerns. Long-term maintenance therapy, often with a single agent such as clindamycin, is needed to prevent recurrent disease. The role of immune reconstitution with the new antiretroviral therapies in preventing recurrences and controlling progression of toxoplasmosis in AIDS patients is not well established. It may be that with immune reconstitution it will be possible to forgo long-term therapy.

Surgical treatment with laser photocoagulation, cryotherapy, and vitrectomy has been tried, but efficacy has not been clearly demonstrated. The potential for retinal or vitreous hemorrhage and even retinal detachment when treating the acutely inflamed retina makes surgical intervention less desirable for active disease. In addition, laser or cryotherapy cannot predictably prevent disease recurrence, given that normal-appearing retina can harbor Toxoplasma tissue cysts. In cases in which vitrectomy is required to remove dense vitreous opacities, treatment



with antimicrobial agents is recommended before and after surgery.


Ocular toxoplasmosis is a self-limited process in immunocompetent patients, and most episodes resolve over a period of 1–2 months. The course can be prolonged in immunosuppressed patients, and in these individuals, as well as in infants, central nervous system and other systemic involvement may result in significant morbidity and mortality. Vision loss can be permanent from macular infection with a resultant scar or, less commonly, from optic nerve involvement, choroidal neovascular membranes, vascular occlusion, or rhegmatogenous retinal detachment.





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2 comments on “Chapter 172 – Ocular Toxoplasmosis

  1. WONDERFUL Post.thanks for share..more wait .. …

  2. Too many people automatically blame cats for transmission of this parasitic infection instead of understanding that it is mostly from contaminated meats. But don’t worry, the likelihood of you developing toxoplasmosis is very rare. However, if you do contract it, there are actually biotech companies that develop drugs, vaccines, and treatments for toxoplasmosis who need people with recent toxoplasmosis infections to donate. They actually will pay people money, like around $800 or more, or will give that money to a charity of your choice for each plasma donation. Google “get paid to donate plasma” and check it out. There are scientists who are getting closer to curing & preventing toxoplasmosis from happening so hopefully, with more people donating plasma for research, this will no longer be a concern for pregnant women

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