Ocular Toxoplasmosis

Notas do Editor

1. Infection with the organism in immunocompetent individuals leads to a mild or subclinical systemic disease. In some patients, the primary infection may lead to fever, fatigue, lymphadenopathy, and malaise.
2. Tachyzoits are the proliferative form of the parasite. The organism is motile with a unique cytoskeletal structure allowing it to twist, wiggle, rotate, and glide. The rostrum of the tachyzoite is known as the conoid, which can extend, retract, tilt, and rotate. These movements allow the tachyzoite to find its target host cell and to penetrate the cell, establishing an intracellular existence. Bradyzoites are slowly metabolizing organisms found in cysts formed within the tissue of the infected host. Considering that the tissue cyst incorporates elements derived from the host into its outer wall, it is easily tolerated by the host, and no inflammatory reaction is seen around it FIGURE toxoplasma bradyzoites inside cysts of tissue sections in chronically infected rabbit's retina (arrows). There were no signs of inflammation seen in the figure. it may remain for years in certain tissues, such as the eye or muscles, without provoking any inflammatory reactions. The number of organisms increases within the cyst in the retina, and once the cyst wall breaks down by mechanical stretching, the bradyzoites escape, convert into tachyzoites, and invade contiguous cells. The oocyst appears to be an important method for the transmission of toxoplasmosis. Once ingested, the oocyst wall is digested by the gastric enzymes, trypsin and pepsin, thereby liberating Toxoplasma sporozoites
3. the resistance of toxoplasmosis within chronically infected tissues of animals may lead to transmission of the disease by the ingestion of undercooked meat, including mutton, beef, pork, and chicken.
4. Toxoplasma organisms then invade intestinal mucosal cells and initiate the infection (enteroepithelial cycle). In the intestinal mucosa, the organisms undergo asexual reproduction (endodyogeny, endopolygeny, splitting, schizogony) and sexual reproduction (gametogony cycles), culminating in the formation of zygotes, which develop into oocysts. The oocysts are shed in the feces of the definitive host. Simultaneous with the enteroepithelial oocyst formation in cats, bradyzoites or sporozoites may invade and disseminate widely to all host tissue through the bloodstream or lymphatics, where they undergo an asexual cycle (extraintestinal cycle), particularly in muscle, heart, brain, lung, lymphoid tissue, retina, and central nervous system (CNS).
5. ranging from 3% to 10.8% in the United States to between 50% and 80% in France. 70% and 80% of women of childbearing age in the United States lack antibodies to T gondii, which places them at risk for contracting the disease; however, the incidence of toxoplasmosis acqUired during pregnancy is only 0.2%- 1%. overall, 40% of primary maternal infections result in congenital infection; transplacental transmission is greatest during the third trimester.
6. Previously, apparently acquired toxoplasma retinitis was thought to represent reactivation o f a Congenital infection; however recent evidence suggest thaht most patients are infected posnatally. IN ONE STUDY, acquired postnatal infection was thought to represent up to two-thirds of cases of toxoplasmic ocular diseas
7. Toxoplasmosis can be acquired congenitally via transplacental transmission from an infected mother to the fetus.
8. The area may be at the edge of an old flat atrophic scar, frequently in the macular area, or adjacent to the scar (a so-called satellite lesion). Most cases are now assumed to be acquired but can only be distinguished from congenital disease if there is no scar adjacent to a site of active inflammation or with documentation of a previously normal fundus appearance.
9. it can be supported by a positive enzyme-linked immunosorbent assay (ELISA) for Toxoplasma antibody. Because maternal lgM does not cross the placenta, finding toxoplasma-specific IgM in the infant serum is diagnostic ofcongenital infection in the infant.
10. Although the benefit of treatment has not been proven, most practitioners recommend treatment if the macula or optic nerve is involved or if massive vitritis threatens vision. The most commonly used antimicrobials are pyrimethamine and sulfadi- azine. Steroids should never be used alone without antimicrobial coverage.
11. Small extramacular lesions may be observed without treatment. Sight-threatening lesions are treated for 5-6 weeks with triple therapy pyrimethamine, sulfadiazine, and folinic acid. Prednisone in low doses of 0.5-1 mg/kg per day for 3-6 weeks may be used to reduce macular or optic nerve inflammation and can be started on day 3 of antibiotic therapy. Corticosteroids should not be used without concurrent antibiotic treatment or in immunocompromised patients due to the risk of exacerbation of the disease. Folinic acid protects against the decrease in platelets and white blood cells induced by pyrimethamine.
12. Bactrim has been shown to be equivalent to triple therapy in the treatment of ocular toxoplasmosis and may be better tolerated. Clindamycin and azythromycin can also be considered as alternative therapies. AIDS patients require chronic maintenance treatment.
13. NON CONSTITUTIONAL S/SX: Patients develop malaise, myalgia, weakness, fatigue, headache, sore throat, and maculopapular rash with sparing of the palms and soles. The course of the disease in the immunocompetent host is self-limited and often is benign. The signs and symptoms may persist for extended periods, and the generalized fatigue and malaise may occur for several months.
14. Focal condensation of vitreous and inflammatory cells may be seen overlying the pale yellow or gray-white raised lesion in the posterior pole
15. Theselesionsoccur more commonly in the posterior pole but may occasionally be seen immediately adjacent to or directly involving the optic nerve; they are sometimes mistaken for optic papillitis.
16. Toxoplasma gondii is the most common cause of infection of the retina. Ocular findings include involvement of the retina, choroid, retinal vessels, macula, optic nerve, vitreous, and anterior uvea.
17. Ocular toxoplasmosis most commonly presents as a focus of necrotizing retinitis (Fig. 7) involving the inner layers of the retina and associated with a whitish fluffy lesion surrounded by retinal edema. Cells are seen in the vitreous overlying the lesion.
18. The retina is the primary site for the multiplying parasites, whereas the choroid and sclera may be the sites of contiguous inflammation. When the choroid is involved by the inflammatory reaction, the lesion is referred to as retinochoroiditis. Severe Toxoplasma retinochoroiditis with large granuloma and overlying vitreous cells. A healed retinochoroiditic scar is seen in close proximity to the granuloma. A small focus of Toxoplasma retinochoroiditis adjacent to a healed retinochoroiditic scar near the equator in the right eye
19. Typical punched-out Toxoplasma retinochoroiditic scar surrounded by Pigmentation The central whitish area is the sclera and results from extensive necrosis of the retina and choroid.
20. Vitreous : Posterior vitreous detachment commonly is seen in patients with posterior segment inflammation from toxoplasmosis, and patients may develop precipitates of inflammatory cells on the posterior vitreous face. Anterior uveitis (granulomatous or nongranulomatous) may be associated with Toxoplasma retinochoroiditis. In immunocompetent patients, the anterior uveal inflammation is a hypersensitivity reaction to the Toxoplasma antigens.
21. Fuchs' heterochromic iridocyclitis has been described in patients who had focal necrotizing retinochoroiditis characteristic of ocular toxoplasmosis. The reason for the association of Fuchs' heterochromic iridocyclitis and toxoplasmosis is not clear. Severe anterior uveitis may lead to peripheral anterior synechiae and secondary glaucoma in patients with chronic ocular toxoplasmosis. the reason for neovascularization of the optic nerve and the retina is not well understood. Retinal ischemia associated with severe retinal vasculitis may predispose to neovascularization of the retina. On the other hand, inflammatory reactions alone may cause neovascularization of the retina.
22. The disease may be a recrudescence of a latent infection or a newly acquired toxoplasmic infection. In cases of recrudescence of the disease, it may result from rupture of the cyst and conversion of the bradyzoites into the tachyzoites within the tissue. Toxoplasmic encephalitis is a fatal disorder if not treated early or promptly. Clinical diagnosis and therapy of toxoplasmosis in patients with AIDS pose a challenge to the managing clinician.
23. n the CNS, toxoplasmic encephalitis may present as a mass lesion in the brain, toxoplasmoma. The differential diagnosis of such a focal lesion in patients with HIV infections include toxoplasmosis in 60% of the cases, primary CNS lymphoma in 25%, and multifocal leukoencephalopathy in 15%. CT scan will show Ring Enhancing Lesions with darker areas of Surounding edema that are typical of your toxoplasmosis The vasularity in the organizing wall of the abcess leads to the observed bright ring enhancement with CT and MRI Congenital toxoplasma infections can produce cerebritis with multifocal cerebral necrotizing lesions that may calcify.
24. Toxoplasmosis is becoming an important cause of mortality and morbidity in patients undergoing immunosuppressive therapy for malignancies, organ transplantation, or autoimmune disorders. Patients with impaired immunity such as those with lymphoma, leukemia, malignancies, and AIDS also are at increased risk of acquiring severe infection by T. gondii. The clinical manifestations of toxoplasmosis in the immunodeficient host may mimic other opportunistic pathogens. Diagnostic Dilemma for the Physician. Patients may present with fever, encephalitis, myocarditis, and pneumonitis, which are the most common and serious of the clinical manifestations. More than 50% of these patients have CNS involvement.