Ординатура / Офтальмология / Английские материалы / Handbook of Pediatric Eye and Systemic Disease_Wright, Spiegel, Thompson_2006

INCIDENCE

Toxocariasis is the most common nematode infection affecting the eye in the United States; however, the exact incidence of ocular toxocariasis in unknown.

ETIOLOGY

Most cases of human toxocariasis are caused by infection with the dog intestinal roundworm Toxocara canis or, rarely, the cat roundworm Toxocara catis.45,105 Ocular toxocariasis results from invasion of the eye by the secondor third-stage larva of the nematode. The dog is the definitive host and acquires the intestinal infection by several mechanisms including transplacental and transmammary transmission, ingestion of infective ova, ingestion of adults or larvae within feces or vomitus of infected puppies, and ingestion of larvae in tissues of paratenic hosts such as mice.44,113

Most puppies are infected in utero through transplacental migration of the larvae.36 Children become infected after ingestion of eggs from contaminated soil, food, or other materials. Although most children acquire the infection by ingestion of contaminated soil, contact with puppies is a significant risk factor for the disease.

CLINICAL FEATURES

Approximately 80% of children with ocular toxocariasis are less than 16 years of age. A spectrum of ocular manifestations can occur in these children although several common ocular presentations have been described. The most common presentation is a unilateral granuloma of the posterior pole or peripheral retina. The posterior pole lesion is typically round, elevated, and up to two disc diameters in size (Fig. 9-2). Vitritis is relatively common and may be severe in some cases. Peripheral granuloma are hazy white elevated lesions located in the peripheral retina. Peripheral granuloma located in the inferior retina may resemble pars planitis in some children. Vitreous membranes are often visible radiating from the peripheral lesion and may form radial retinal folds extending to the optic nerve head.

Another common manifestation is chronic endophthalmitis.113 These children often present with anterior uveitis, hypopyn, posterior synechiae, cyclitic membrane, vitritis, and retinal detachment. Leukocoria may be noted in some children

FIGURE 9-2. Ocular toxocariasis with posterior pole granuloma.

because of the severe inflammatory reaction. The inflammation may resolve without treatment in some cases revealing a more typical posterior pole or peripheral granuloma.

Children may also present to the ophthalmologist with no active inflammatory disease but instead with decreased visual acuity, amblyopia, or strabismus as a result of damage to the macula. These children may be detected during school screening examinations or as part of a routine examination.

CLINICAL ASSESSMENT

Ocular toxocariasis is a clinical diagnosis; however, serological tests are often useful when evaluating children with possible toxocariasis. Currently, ELISA tests for Toxocara spp. are the most accurate and widely used serological methods. Many laboratories report ELISA results as the number of standard deviations above a normal population. High serum titers are not common in children with ocular toxocariasis unless testing occurs during the acute phase of the disease.92 On the other hand, vitreous specimens in ocular toxocariasis have higher ELISA titers compared to serum titers.12

SYSTEMIC ASSOCIATIONS AND NATURAL HISTORY

Systemic infection with T. canis or T. catis is known as visceral larval migrans (VLM). VLM occurs most commonly in children less than 6 years of age and is characterized by eosinophilia, fever, and hepatosplenomegaly.44,45 Most infections are asymptomatic although some children may develop fulminant disease that may result in death. However, most children with ocular toxocariasis do not have VLM. In those cases where ocular disease and VLM are both present, children often present with flu-like symptoms such as cough, wheezing, fever, malaise, and weight loss.

The diagnosis of VLM should be considered in young children with eosinophilia and/or leukocytosis, and hepatomegaly. Less common manifestations include pulmonary symptoms, splenomegaly, and seizures. In most cases, a history of exposure to puppies and pica can be elicited. A definitive diagnosis requires identification of larvae in histological sections from affected tissues. Unfortunately, larvae are not apparent in many histological specimens and therefore serum ELISA tests are useful in confirming the diagnosis.

INHERITANCE

No inheritance pattern.

TREATMENT

The treatment of ocular toxocariasis must be individualized based on several factors including the severity of inflammation, macular involvement, and the visual potential of the eye. For children with active vitritis, periocular or systemic corticosteroids are useful to decrease the inflammatory response. In general, systemic corticosteroids may be the preferred therapy in children less than 10 years of age because multiple periocular corticosteroid injections are the rule in most cases. Systemic corticosteroids should be used at the lowest dosage to achieve the desired response and slowly tapered before discontinuation to avoid recurrence of inflammation. In children with associated anterior uveitis, topical corticosteroids and cycloplegic agents are useful. Thiabendazole at 50 mg/kg/day for 7 days may be considered in children who fail to respond to systemic corticosteroid therapy.34

The role of antihelminthic therapy for ocular toxocariasis remains uncertain. A number of reports have described improve-

ment in ocular toxocariasis treated with several different antihelminthic drugs including thiabendazole, diethylcarbamazine, albendazole, and mebendazole.35,72 If antihelminthic therapy is considered, consultation with a pediatric infectious disease specialist should be considered because of the potential toxicity associated with several of these agents.

Surgical procedures may be necessary in some children with ocular toxocariasis. Pars plana vitrectomy may be useful in children with refractory vitritis, vitreous membranes, epiretinal membrane, and traction or rhegmatogenous retinal detachment.49,100,115 Early vitrectomy has been advocated to reduce longterm visual morbidity in selected children.9

PROGNOSIS

The visual prognosis for children with ocular toxocariasis is dependent a number of factors. In children with inactive disease, direct damage to the retina may be evident as a macular scar, macular traction detachment, macular heterotopia, rhegmatogenous retinal detachment, and epiretinal membrane. Depending on the location, these lesions may be associated with severe visual loss, amblyopia, and strabismus. Loss of vision can also occur as a result of active posterior segment disease that is dependent on the location, severity, and duration of inflammation. The visual prognosis is also affected by complications resulting from the intraocular inflammation including glaucoma, cataract, cyclitic membrane, and phthisis.

Toxoplasmosis

Toxoplasmosis is the most common form of posterior uveitis in children and adults. In the past, most cases were thought to be caused by congenital infection, but there is increasing evidence that the acquired form of the disease is more common than previously reported.

INCIDENCE

Up to 3000 infants are born with congenital toxoplasmosis each year in the United States, and retinochoroiditic occurs in 70% to 90% of cases.77 The incidence of ocular disease in children with acquired toxoplasmosis is uncertain although recent reports have suggested that as many as 21% of all patients with acquired disease may develop retinochoroiditis.15,17

ETIOLOGY

Toxoplasma gondii is a obligate intracellular protozoan parasite found throughout the world and the etiological agent of toxoplasmosis. Cats are the definitive host for T. gondii and are initially infected by eating contaminated meat. Within the cat’s intestine, the parasite produces large numbers of oocysts that are shed in feces, thereby contaminating soil and water.96 Humans and other animals such as pigs, cattle, sheep, and poultry are infected after ingestion of contaminated food or water. The oocysts are then broken down within the intestines and sporozoites and bradyzoites are released into the cells of the intestines. Once inside the epithelial cells of the intestinal tract, these organisms are transformed into tachyzoites. Free tachyzoites are released from the epithelial cells and enter the bloodstream and lymphatic system from where they can infect any tissue or organ.

Most human infections are probably the result of ingestion of undercooked or raw meat containing tissue cysts. Other sources of human infection include contact with contaminated soil or cat litter, contact with raw meat containing tissue cysts, ingestion of unwashed fruits and vegetables, ingestion of raw eggs or unpasteurized milk, and rarely as a result of blood transfusion.54,114 Transplacental transmission occurs in women who are infected for the first time just before or during pregnancy.25

CLINICAL FEATURES

Ocular toxoplasmosis can develop following congenital or acquired infection. The most common ocular manifestation is a focal necrotizing retinitis with underlying choroiditis, vitritis, and retinal vasculitis. Toxoplasmosis retinochoroiditis is typically a recurrent disease, and most recurrent lesions develop adjacent to the border of an inactive scar. Healed toxoplasmosis scars are characterized by well-defined borders with peripheral retinal pigment epithelial hyperplasia and central chorioretinal atrophy (Fig. 9-3). Recurrent lesions may also develop in areas without chorioretinal scars as well as in the fellow eye (Fig. 9-4). A granulomatous or nongranulomatous anterior uveitis is common. Less common findings include punctate outer retinal toxoplasmosis, neuroretinitis, and papillitis.

CLINICAL ASSESSMENT

In the newborn, the clinical manifestations and serology are used to establish the diagnosis of congenital toxoplasmosis. Congenital infection is confirmed by elevated serum IgM and IgA titers in the infant. In children with recently acquired toxoplasmosis, elevated titers of IgM, IgA, and IgE are present. Follow-up serology 2 to 4 weeks later often reveals a rising IgG titer, thereby indicating a recent infection. Serum serology is less useful in recurrent disease but can be useful to confirm previous exposure to toxoplasmosis; however, serological tests should not be used in isolation to establish the diagnosis.

SYSTEMIC ASSOCIATIONS AND NATURAL HISTORY

Approximately 10% of infants with congenital infection have clinical manifestations at birth. The clinical manifestations of congenital toxoplasmosis include intracranial calcifications, hydrocephalus, microcephaly, hepatosplenomegaly, jaundice, and retinochoroiditis. Some infants may have severe disability while others are asymptomatic and may not be diagnosed until later in life.

Less information is available about children with acquired toxoplasmosis. Acquired toxoplasmosis is typically asymptomatic or results in a transient lymphadenopathic syndrome in healthy children.54 Up to 20% of all patients with acquired infections may develop ocular lesions either simultaneously with the systemic manifestations or at a later time.17,43,78

INHERITANCE

No inheritance pattern.

TREATMENT

The treatment of ocular toxoplasmosis remains somewhat controversial. However, most authorities would recommend treatment for the following: reduction in visual acuity greater than two Snellen lines, lesions within the macula, lesions near the optic nerve, lesions with severe vitritis, lesions associated with a significant hemorrhage, and any episode of retino-choroiditis during the first year of life. The most commonly used therapy for ocular toxoplasmosis is the combination of pyrimethamine with sulfonamides. Folinic acid is often used in conjunction with pyri-methamine to prevent bone marrow suppression.

following puberty. Epidemiologic studies suggest that 50% to 90% of adults in the United States have antibodies to HSV-1. Following primary infections, HSV becomes latent in the ganglia of the nerves that supply the infected area. For HSV-1, the trigeminal ganglion is most commonly involved. During periods of latency, no active virus is found in the involved areas. Recurrent infections are the hallmark of HSV and occur frequently with both HSV-1 and HSV-2. The cause of these recurrences is unknown but may be triggered by a number of factors such as stress, sunlight, fever, and local trauma. Approximately 0.15% of the U.S. population has a history of ocular infection related to HSV.

ETIOLOGY

Herpes simplex virus is a double-stranded DNA virus. The two types of HSV are classified based upon their clinical and epidemiologic patterns as well as biological and biochemical characteristics. HSV-1 is most commonly found in lesions of the oral cavity, the eye, and on the skin of the face and upper trunk. Transmission occurs by direct contact with infected oral secretions. HSV-2 is found in lesions on the genitalia and the skin of the thighs and buttocks and is spread by contact with genital secretions. However, either type of HSV may infect the mouth, eyes, skin, or the genital area. In most cases, the disease is transmitted during periods of asymptomatic shedding of the virus by infected persons.

CLINICAL FEATURES

Ocular involvement with congenital or neonatal HSV infection is not uncommon and includes conjunctivitis, keratitis, and chorioretinitis.83 Other less common ocular manifestations include optic atrophy, cataract, and microphthalmia.

Primary ocular HSV infection typically presents with a unilateral blepharoconjunctivitis. Vesicles occur on the eyelid skin or on the eyelid margin with an associated follicular conjunctivitis in most children. Preauricular lymphadenopathy is also a common finding in primary disease. In most cases the vesicles clear within 7 to 10 days without scarring. The majority of patients with primary ocular infection also develop an epithelial keratitis, either superficial punctate keratitis, geographic keratitis, or the more classic dendritic keratitis.