Ординатура / Офтальмология / Английские материалы / Clinical Ophthalmology A Systematic Approach 7th Edition_Kanski, Bowling_2011

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Fig. 11.22 Toxoplasma gondii. (A) Tissue cysts containing bradyzoites; (B) release of tachyzoites (arrow) following rupture of the cell wall

(Courtesy of J Harry – fig. A; RT Emond, PD Welsby and HA Rowland, from Colour Atlas of Infectious Diseases, Mosby 2003 – fig. B)

Mode of human infection

1Ingestion of undercooked meat (lamb, pork, beef) containing bradyzoites of an intermediate host.

2Ingestion of sporocysts following inadvertent contamination of hands when disposing of cat litter trays and then subsequent transfer on to food. Infants may also become infected by eating dirt (pica) containing sporocysts. It is likely that water contamination plays an important role in the transmission of the disease in rural areas.

3Transplacental spread of the parasite (tachyzoite) can occur if a pregnant woman becomes infected.

Congenital toxoplasmosis

Toxoplasmosis is transmitted to the fetus through the placenta when a pregnant woman becomes infected. If the mother is infected before pregnancy, the fetus will be unscathed.

1Severity of involvement of the fetus is dependent on the duration of gestation at the time of maternal infection. For example, infection during early pregnancy may result in stillbirth, whereas if it occurs during late pregnancy it may result in convulsions, paralysis, hydrocephalus (Fig. 11.23A) and visceral involvement.

2Manifestations

•Intracranial calcification seen on CT (Fig. 11.23B).

•However, just as in the acquired form, most cases of congenital systemic toxoplasmosis are subclinical. In these children, bilateral healed chorioretinal scars may be discovered later in life, either by chance or when the child is found to have defective vision.

•Infections occurring towards the end of the second trimester usually result in disease that can be detected at birth such as macular scars (Fig. 11.23B), while those occurring later in the third trimester may result in normal examination at birth, but the appearance of ocular or neurological symptoms in the future.

•The risk of disease later in life can be modified by early recognition of the transmission and long-term therapy.

3 Serological tests as previously described.

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Fig. 11.23 Congenital toxoplasmosis. (A) Hydrocephalus and right anophthalmos; (B) axial CTshows cerebral calcification; (C) macular scar

(Courtesy of M Szreter – fig. A; R T Emond, P D Welsby and HA Rowland, from Colour Atlas of Infectious Diseases, Mosby 2003 – fig. B)

Acquired toxoplasmosis

1 Immunocompetent patients may have the following manifestations:

aSubclinical is the most frequent.

bLymphadenopathic syndrome, which is uncommon and self-limiting, is characterized by cervical lymphadenopathy, fever, malaise and pharyngitis.

c Meningoencephalitis, characterized by convulsions and altered consciousness, occurs in a minority of patients.

dThe exanthematous form, resembling a rickettsial infection, is the rarest.

2In immunocompromised patients the disease may be life-threatening. The most common manifestation in AIDS patients is an intracerebral space-occupying lesion which resembles a cerebral abscess on MR.

Toxoplasma retinitis

Pathogenesis

Toxoplasmosis is the most frequent cause of infectious retinitis in immunocompetent individuals. Reactivation at previously inactive cystcontaining scars is the rule in the immunocompetent, although a small minority may represent new infection. Most quiescent lesions will have been acquired postnatally. Recurrent episodes of inflammation are common and occur when the cysts rupture and release hundreds of tachyzoites into normal retinal cells. Recurrences usually take place between the ages of 10 and 35 years (average age 25 years).

Clinical features

The diagnosis of toxoplasma retinitis is based on a compatible fundus lesion and positive serology for toxoplasma antibodies (see ‘Investigations’). Any antibody titre is significant because in recurrent ocular toxoplasmosis, no correlation exists between the titre and the activity of retinitis.

1 Presentation is with unilateral sudden onset of floaters, visual loss and photophobia.

2Signs

•‘Spill-over’ anterior uveitis, which may be granulomatous and resemble Fuchs syndrome, is common.

•Solitary inflammatory focus near an old pigmented scar (‘satellite lesion’) (Fig. 11.24A).

•Multiple foci are uncommon (Fig. 11.24B).

•Severe vitritis may greatly impair visualization of the fundus, although the inflammatory focus may still be discernible (‘headlight in the fog’ appearance) (Fig. 11.24C).

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3Atypical features that may occur particularty in immunocompromised individuals are the following:

•Extensive confluent areas of retinitis that may be bilateral and difficult to distinguish from a viral retinitis.

•Inflammatory focus not associated with a pre-existing scar implying that the infestation has been newly acquired and disseminated to the eye from extraocular sites.

4The rate of healing is dependent on the virulence of the organism, the competence of the host's immune system and (especially) the size of the lesion. In uncompromised hosts healing occurs within 6 to 8 weeks (Fig. 11.25A-C) although vitreous opacities take longer to resolve. The inflammatory focus is replaced by a sharply demarcated atrophic scar which becomes progressively pigmented starting at the edges, producing a hyperpigmented border. Resolution of anterior uveitis is a reliable sign of posterior segment healing. After the first attack, the mean recurrence rate within 3 years is about 50% and the average number of recurrent attacks per patient is 2.7. In elderly patients the course may be progressive and should be differentiated from viral retinitis and lymphoma.

Fig. 11.24 Active toxoplasma retinitis. (A) Typical ‘satellite’ lesion adjacent to an old scar; (B) two small foci; (C) severe vitreous haze and ‘headlight in the fog’ appearance

(Courtesy of C Pavésio – figs B and C)

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Fig. 11.25 Progression of toxoplasma retinitis. (A) Mild fluffy haze adjacent to an old scar at presentation; (B) after 2 weeks the area of retinitis is larger and denser;

(C) after 7 weeks the retinitis has nearly resolved.

Complications

Nearly 25% of eyes develop visual loss as a result of the following:

1Common

•Direct involvement of the macula (Fig. 11.26A).

•Secondary optic nerve head involvement due to a juxtapapillary lesion (Fig. 11.26B).

2Uncommon

•Primary optic nerve head involvement may mimic anterior ischaemic optic neuropathy.

•Occlusion of a major blood vessel by the inflammatory focus (Fig. 11.27A and B).

•Choroidal neovascularization (Fig. 11.27C and D).

•Serous retinal detachment (Fig. 11.27E and F).

•Tractional retinal detachment secondary to organization of severe vitreous opacification.

•Macular oedema.

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Fig. 11.26 Common complications of toxoplasma retinitis. (A) Scar at the fovea and a fresh lesion involving the papillomacular bundle; (B) juxtapapillary lesion involving the optic nerve head

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Fig. 11.27 Uncommon complications of toxoplasma retinitis. (A) Periarteritis resulting in branch retinal artery occlusion; (B) FA shows extensive non-perfusion at the posterior pole; (C) choroidal neovascularization adjacent to an old scar; (D) FA shows corresponding hyperfluorescence; (E) serous macular detachment; (F) FA shows hyperfluorescence due to pooling of dye

(Courtesy of C Pavésio – figs A, B, E and F; P Gili – figs C and D)

Treatment

1Aims

•To reduce the duration and severity of acute inflammation.

•To lessen the risk of permanent visual loss by reducing the size of the eventual retinochoroidal scar.

•To reduce the risk of recurrences.

2Indications. There is lack of evidence that treatment with antibiotics achieves any of the above aims although adjunctive corticosteroids may diminish the duration and severity of inflammation. Despite these reservations treatment may be considered for the following vision-threatening lesions:

•A sight-threatening lesion involving the macula, papillomacular bundle, optic nerve head or a major blood vessel.

•Very severe vitritis, because of the risk of vitreous fibrosis and tractional retinal detachment.

•In immunocompromised patients all lesions should be treated irrespective of location or severity.

3Regimen. There is no universally agreed therapeutic regimen. Systemic prednisolone (1 mg/kg) is given initially and tapered according to clinical response, but should always be used in conjunction with a specific anti-toxoplasma agent, most frequently pyrimethamine combined with sulfadiazine. Systemic steroids should be avoided or used with extreme caution in the immunocompromised.

aPyrimethamine (Daraprim) is administered as a loading dose of 50 mg followed by 25–50 mg daily for 4 weeks in combination with oral folinic acid 5 mg (mixed with orange juice) three times a week to prevent thrombocytopenia, leucopenia and folate deficiency. Weekly blood counts should be performed. In AIDS pyrimethamine is avoided because of possible pre-existing bone marrow suppression and the antagonistic effect of zidovudine when the drugs are combined.

bSulfadiazine 1 g q.i.d. for 3–4 weeks is usually given in combination with pyrimethamine. Side-effects of sulphonamides include renal stones, allergic reactions and Stevens–Johnson syndrome.

c Other systemic options include clindamycin, spiramycin, tetracyclines, atovaquone, azithromycin and clarithromycin.

dTopical steroids may be given for anterior uveitis but periocular depot injections are contraindicated as they may lead to uncontrolled progression.

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Toxocariasis

Pathogenesis

Toxocariasis is caused by an infestation with a common intestinal ascarid (roundworm) of dogs called Toxocara canis (Fig. 11.28A). About 80% of puppies between the ages of 2 and 6 months are infested with this worm. Human infestation is by accidental ingestion of soil or food contaminated with ova shed in dogs' faeces. Very young children who eat dirt (pica) or are in close contact with puppies are at particular risk of acquiring the disease. In the human intestine, the ova develop into larvae which penetrate the intestinal wall and travel to various organs, such as the liver, lungs, skin, brain and eyes (Fig. 11.28B). When the larvae die, they disintegrate and cause an inflammatory reaction followed by granulation. Clinically, human infestation can take one of the following forms:

1Visceral larva migrans (VLM) is caused by severe systemic infection which usually occurs at about the age of 2 years. The clinical features, which vary in severity, include a low-grade fever, hepatosplenomegaly, pneumonitis, convulsions and rarely, death. The blood shows leucocytosis and marked eosinophilia.

2Ocular toxocariasis differs markedly from VLM because it involves otherwise healthy individuals who have a normal white cell count with absence of eosinophilia. A history of pica is less common, and the average age at presentation is considerably older (7.5 years) compared with VLM (2 years). ELISA can be used to determine the level of serum antibodies to T. canis. When ocular toxocariasis is suspected, exact ELISA titres should be requested, including testing of undiluted serum. Any positive titre is consistent with, but not necessarily diagnostic of, toxocariasis. It must therefore be interpreted in conjunction with the clinical findings. A positive titre does not therefore exclude the possibility of retinoblastoma. Ocular toxocariasis may present as one of the following clinical forms.

Fig. 11.28 Toxocara canis. (A) Adult worms fromdog faeces; (B) larva in tissues surrounded by an inflammatory reaction

(Courtesy of CA Hart and P Shears, from Color Atlas of Medical Microbiology, Mosby 2004 – fig. B)

Chronic endophthalmitis

1Presentation is between the ages of 2 and 9 years with leukocoria (Fig. 11.29A), strabismus or unilateral visual loss.

2Signs

•Anterior uveitis and vitritis.

•In some cases, there may be a peripheral granuloma.

•The peripheral retina and pars plana may be covered by a dense greyish-white exudate, similar to the snowbanking seen in pars planitis (Fig. 11.29B).

3Ultrasonography may be useful in establishing the diagnosis in eyes with hazy media and in excluding other causes of leukocoria

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(Fig. 11.29C).

4Treatment with steroids, either periocular or systemic, may be used to reduce the inflammatory activity.

5Prognosis in most cases is very poor and some eyes eventually require enucleation. The main causes of visual loss are tractional retinal detachment and hypotony with phthisis bulbi, the latter caused by separation of the ciliary body from the sclera by contraction of a cyclitic membrane (Fig. 11.29D).

Fig. 11.29 Chronic toxocara endophthalmitis. (A) Leukocoria; (B) peripheral exudation and vitreoretinal traction bands; (C) ultrasonography shows a vitreoretinal traction band; (D) a pathological specimen shows an inflammatory mass and total retinal detachment

(Courtesy of N Rogers – figs A and C; S Lightman – fig. B; J Harry and G Misson, from Clinical Ophthalmic Pathology, ButterworthHeinemann 2001 – fig. D)

Posterior pole granuloma

1 Presentation is typically with unilateral visual impairment between the ages of 6–14 years.

2Signs

•Absence of intraocular inflammation.

•Round, yellow-white, solid granuloma which varies between one to two disc-diameters in size in the posterior fundus (Fig. 11.30A).

•Associated findings include vitreoretinal traction bands and localized tractional retinal detachment (Fig. 11.30B).

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Fig. 11.30 Toxocara granuloma. (A) Juxtapapillary granuloma: (B) posterior pole granuloma associated with a localized tractional retinal detachment; (C) peripheral granuloma with a vitreous band extending to the disc

(Courtesy of J Donald M Gass, from Stereoscopic Atlas of Macular Diseases, Mosby 1997 – fig. A)

Peripheral granuloma

1Presentation is usually in adolescence or adult life with visual impairment from distortion of the macula or retinal detachment. In uncomplicated cases, the lesion may remain undetected throughout life.

2Signs

•Absence of intraocular inflammation.

•A white hemispherical peripheral granuloma in any quadrant of the fundus that may be associated with a vitreous band extending to the disc causing ‘dragging’ (Fig. 11.30C).

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