AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Chorioretinitis (CR) is an exudative inflammatory process that involves the retinal vessels and is usually caused by congenital viral, bacterial, or protozoan infections in neonates. Congenital toxoplasmosis (CTP) is the most common cause of infectious chorioretinitis in immunocompetent children. Congenital cytomegalovirus (CMV) infection is the second most common etiology. Fungal infections are more frequently identified, and emergent pathogens, including West Nile virus and lymphocytic choriomeningitis virus, have been described. In rare instances, chorioretinitis is part of a systemic noninfectious process.

In the older pediatric age group, chorioretinitis is diagnosed in diverse clinical conditions and can reflect newly acquired diseases or reactivation. Chorioretinitis can result from a dissemination of Toxocara or Baylisascaris in immunocompetent patients. In severely immunodeficient patients, including those with acquired immunodeficiency syndrome (AIDS), chorioretinitis may be associated with Epstein-Barr virus (EBV), CMV, varicella-zoster virus, various fungi (eg, Candida, Aspergillus, Fusarium, dimorphic fungi), and Toxoplasma.

Pathophysiology

Chorioretinitis causes an inflammation of the retinal vessels in reaction to a generalized infection that involves multiple organ systems. Congenital disseminated infections also manifest as intrauterine growth retardation, microcephaly, microphthalmia, cataract, uveitis, hearing defect, osteomyelitis, enlarged liver and spleen, lymphadenopathy, dermal erythropoiesis, carditis, and congenital heart disease. Vessel trauma caused by lodging Toxocara or Baylisascaris larvae may be associated with severe inflammatory responses.

Although chorioretinitis that is associated with congenital viral infections tends to be stable or improves in infancy, chorioretinitis associated with asymptomatic CTP progresses for years after birth and is more likely to be clinically significant at an older age.

Frequency

United States

CTP occurs much less frequently in the United States than in several European countries. Chorioretinitis is extremely rare in children, regardless of immunologic status.

Worldwide, chorioretinitis due to CTP is more common than chorioretinitis due to symptomatic congenital CMV. The seroprevalence rate in childbearing women is estimated at 14-30%, and the estimated incidence rate of CTP is 0.1 per 1000 births.

Statistically, chorioretinitis due to CMV is more common than chorioretinitis due to CTP in the United States. Chorioretinitis occurs in approximately 14% of infants born with symptomatic congenital CMV infection. However, severely affected infants represent fewer than 10% of those with congenital infections due to maternal primoinfection with viremia during the first half of pregnancy. Chorioretinitis affects only 2% of asymptomatic infants with congenital infection.
 
Toxocara canis–associated ocular larva migrans occurs in more than 60% of symptomatic seropositive children. This zoonosis is probably one of most commonly acquired childhood eyesight impairments because of the high prevalence of young pet dogs in the United States.

International

Seroprevalence rates for CTP in childbearing women are 50-80% in European countries, and the estimated incidence rate of CTP is 1-4 cases per 1000 births. However, acquired toxoplasmosis accounts for a much higher rate of ocular infections in late childhood worldwide. The prevalence of CMV seroconversion in many parts of the world reaches almost 100% in young adults. The incidence of CMV congenital infection is not well documented.

Mortality/Morbidity

• If left untreated or if the condition does not respond to treatment, severe chorioretinitis can result in partial or total loss of vision in the affected eye.
• Morbidity is due to concurrent damage to major organ systems, especially damage to the brain (eg, developmental delays, seizures). 
• Mortality due to chorioretinitis depends on the nature and progression of the basic illness.

Age

• Congenital chorioretinitis is usually evident at birth.
• Congenital chorioretinitis associated with CTP actively progresses after birth and manifests when the individual is aged 5 years.
• Acquired chorioretinitis occurs at any age, depending on the disseminated illness.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

• In most individuals with chorioretinitis, the history may not help in establishing causal agents. For example, in patients with chorioretinitis associated with congenital infections, eliciting the maternal history of primary viral or flulike illnesses during pregnancy is usually not easy. Dietary habits (preference of raw meat) and pet care (cleaning cat litter box) may imply toxoplasmosis, whereas the lack of rubella vaccination in an immigrant may warrant investigating. However, a pregnant woman with symptomatic West Nile viral meningoencephalitis may be readily diagnosed using historical, epidemiologic, and laboratory data. 
• Many maternal primary infections due to CMV, rubella, herpes simplex virus (HSV), and syphilis occur insidiously and are not clinically apparent. 
• In patients with acquired chorioretinitis, a history of illness that relates to toxoplasmosis (eg, handling kitten wastes, eating undercooked meat) may be present. Toddlers with exposure to puppy or raccoon waste have an increased risk of developing visceral larva migrans and ocular larva migrans.
• A recent history that includes strabismus, vision loss, and CNS involvement in a toddler exposed to raccoon waste or who has a newly acquired puppy suggests zoonotic roundworm larval infestation (Baylisascaris or Toxocara).

Physical

Chorioretinitis is an inflammation of the posterior uveal tract and involves the retina and the vitreous body. If the inflammation is unilateral, the child may squint, favor the "good eye," or report an inability to see objects. Older children with chorioretinitis may present with photophobia and clumsiness with poor walking balance. The "red eye" phenomenon in snapshots of a child with chorioretinitis may reveal incongruency.

• Include an ophthalmologic examination as part of a detailed physical examination. 
• A pediatric ophthalmologist should perform a thorough examination of all visible components of the eye in an infant in whom any congenital infection is suspected.
• • This examination is electively performed and is documented with photographs of the abnormalities in the lens, uvea, and retina and an age-appropriate assessment of vision, visual acuity, and fields. 
  • Ophthalmologic examination is an integral part of monitoring treatment efficacy and disease progress. 
  • Ophthalmologic examination can reveal exudative "cotton balls" (ie, focal atrophic and pigmented scars of the retina). Vitreous inflammations can manifest as transient floating opacities. However, these findings are common in all patients with chorioretinitis regardless of etiologies.
• Because chorioretinitis is usually associated with a congenital syndrome, all other abnormal physical findings should be documented; these include intrauterine growth retardation, microcephaly, microphthalmia, cataract, uveitis, hearing defect, osteomyelitis, enlarged liver and spleen, lymphadenopathy, dermal erythropoiesis, carditis, and congenital heart disease.
• CNS involvement may manifest as abnormal muscle tone, changes in reflexes, or both. A complete neurological examination is warranted.
• If amnionitis is suspected at delivery, thorough examination and culture of amniotic fluid and placenta may elicit the pathogen.

Causes

• Congenital infection
• • In immunocompetent children, chorioretinitis is usually associated with congenital infection; acquired infection is a less likely cause.
  • Toxoplasma gondii and CMV are the leading causes of congenital infections associated with chorioretinitis.
  • Viral etiologies include vertical or perinatal infections, including HSV, rubella, varicella, EBV, lymphocytic choriomeningitis virus, and, possibly, flavivirus. Despite increasing rarity, congenital syphilis should still be considered in an infant born with chorioretinitis whose mother has human immunodeficiency virus infection and untreated or inadequately treated syphilis.
  • • Distinguishing these infections from perinatal transmission of other viral illnesses, including HIV, hepatitis B, and CMV, is important.
    • The risk of intrauterine infection is highest in infants of women with primoinfection and is much less with recurrent infections.
• Acquired chorioretinitis in immunocompetent children: Some children who ingest embryonated T canis or Baylisascaris procyonis eggs develop visceral larva migrans or ocular larva migrans.
• Immunocompromised children
• • Chorioretinitis may be associated with systemic infection due to a vast array of pathogens.
  • General infections include congenital or acquired Lyme disease, Yersinia enterocolitica, and Mycobacterium tuberculosis (MTB).
  • Invasive fungal infections may result from Candida and Cryptococcus species and histoplasmosis.
  • A species of blackfly (Simulium species) can transmit onchocerciasis (in tropical Africa, Yemen, Saudi Arabia, and parts of Latin America).
• Noninfectious disease
• • Systemic noninfectious disease, such as sarcoid, collagen vascular, and granulomatous diseases may cause chorioretinitis.
  • Other possible noninfectious processes, which mostly occur in older children or young adults, include chronic granulomatous disease (CGD), sarcoidosis, Behçet disease, and juvenile rheumatoid arthritis.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Baylisascariasis
Flavivirus

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• Routine laboratory screening
• • CBC and platelet count: Erythrocytic anemia suggests parvovirus B19 infection, whereas depression of all 3 lines (ie, erythrocytes, white cells, platelets) implies an infection that causes bone marrow depression. Platelet count can be low with some viral infections or intravascular coagulation.
  • Liver function test: Measure alanine aminotransferase, aspartate aminotransferase, gamma-glutamyltransferase, alkaline phosphatase, bilirubin (total, direct, and indirect), albumin, and total protein levels. Also obtain activated partial thromboplastin time and prothrombin time. All or some of these measurements can be abnormal in most congenital infections. 
  • Renal function test: Assess creatinine and BUN levels. Urinalysis can be helpful in the detection of hematuria or casts.
• Etiology
• • HIV, HSV (types I and II), EBV, varicella, enteroviruses, and parvovirus B19 are elicited by cultures or polymerase chain reaction (PCR) of blood, cerebral spinal fluid (CSF), or tissues. Immunoglobulin (ie, immunoglobulin M [IgM], immunoglobulin A [IgA], immunoglobulin G [IgG]) titers (from CNS fluid, serum, and other body fluids) are of uncertain value, except for screening purpose in HIV vertical infection, toxoplasmosis, and West Nile virus infection. 
  • Congenital rubella can infect infants of nonimmune individuals and is diagnosed by interpreting results of viral culture and IgM and IgG titers in both infants and mothers.
  • CMV is shed in the urine of infants who are congenitally infected, and diagnosis is indicated by positive urine culture results in infants younger than 3 weeks. In immunodeficient hosts, a CMV antigenemia test using a peripheral blood sample is helpful in establishing recurrence or infection. The CMV antigenemia uses immunofluorescent assay on buffy coat polymorphonuclear cells to detect CMV-infected cells. 
  • Toxoplasma species are detected by specific IgA, IgM, IgG, Sabin-Feldman dye test, and PCR (as a research tool). Document Toxoplasma status of pregnant women and individuals who are immunocompromised. 
  • Lyme disease is detected by using PCR assay of CSF and serum. The presence of specific IgM and IgG on Western blot result of serum may be significant for diagnosis and staging of infection.
  • Yersinia species are detected by special stool culture and acute and convalescent IgG titers.
  • Syphilis is detected by using serology tests (eg, nontreponemal rapid plasma reagent, Venereal Disease Research Laboratory test in CSF) and specific treponemal tests (eg, fluorescein treponemal antibody absorption, microhemagglutination-Treponema pallidum).
  • Mantoux skin test, acid-fast stain, and cultures of bronchial washings or biopsy samples of tissues detect MTB. MTB-PCR is available in many reference laboratories to detect the presence of MTB from biopsy and tissue samples, blood, and CSF. The quantiferon tuberculosis (TB) test, which measures lymphocyte interferon response to TB antigen, may aid in the diagnosis of TB.
  • Toxocariasis serology can be tested by using an enzyme-linked immunoabsorbent assay (ELISA) and confirmed by using a specific Western blot (available from the Centers for Disease Control and Prevention).
  • Baylisascaris tests can be performed using serum and CSF. ELISA and Western blot are available from the Department of Veterinary Pathobiology at Purdue University.
• Other studies
• • Nitroblue tetrazolium test (or flow cytometry with dihydrorhodamine) is used to detect CGD. In a healthy host, 95% or more of neutrophils produce superoxide radicals. In a host with a typical X-linked CGD, fewer than 5% of neutrophils have such ability. 
  • Angiotensin-converting enzyme analysis is used to detect sarcoid. 
  • Vertical HIV infection is suggested by hypergammaglobulinemia and a depressed CD4⁺ T-cell count. An HIV DNA PCR of the baby can be used to confirm diagnosis of HIV infection in the presence of maternal antibodies. Obtain a confirmatory PCR when the infant is aged 3-6 months in all infants at risk for vertical HIV infection. 
  • Rheumatoid factor, an anti-IgG/anti-IgM, is present in a significant number of infants with congenital CMV. 
  • Hypogammaglobulinemia syndrome is detected with quantitative immunoglobulin levels beyond the first few months of life. The usefulness of IgG isotypes has not been established.

Imaging Studies

• Perform sonography, CT scanning, and/or MRI of the CNS or specific organs in patients in whom congenital infections are suspected or in an immunocompromised host. 
• Perform chest radiography, CT scanning, or both in patients in whom TB or sarcoidosis is suspected. CT scanning is helpful in identifying sites on which to perform biopsy for diagnostic purpose. 
• Perform CT scanning of the abdomen for hepatic or splenic dissemination of disease. 
• Perform radiography or bone scanning of the skeleton in patients in whom syphilitic osteomyelitis is suspected. Radiography of long bone has not been found to be helpful in the workup for congenital syphilis. 
• Perform echocardiography in patients with congenital rubella infection.

Other Tests

• Perform a skin biopsy for rare cases of dermal hematopoiesis (blueberry muffin infant syndrome) in patients in whom CMV congenital infection is suspected.

Histologic Findings

Chorioretinitis is usually diagnosed using ophthalmologic examination and not using histologic findings of the retina. However, evidence of lymphocytic infiltrations and exudates characteristic of vasculitis is found in many sites. Granulomatous changes can be evident in biopsy samples of lymph nodes, liver, or spleen in histoplasmosis, sarcoid, and tuberculosis. Fungal elements are rarely found in biopsy or postmortem samples.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

• Medical care focuses on the establishment of specific therapies for treatable etiologies and on the stabilization of the patient with chorioretinitis to prevent further loss of vision and nosocomial infections, especially in immunocompromised infants and children. 
• Care for individuals with chorioretinitis is complex and requires thorough consideration of short-term and long-term care and goals to maintain quality of life. 
• Etiologic treatments of chorioretinitis are not usually available or effective. Specific treatments for a few conditions are as follows:
• • Antivirals, such as ganciclovir or cidofovir, may be administered in patients with CMV (see Medication section).
  • Antibiotics may be administered in patients with the following conditions:
  • • Lyme disease - Ampicillin (25-50 mg/kg/dose q6h) or ceftriaxone (50-75 mg/kg/d)
    • Yersinia species infection - Cefotaxime (50-200 mg/kg/d divided q6h) 
    • Syphilis - Penicillin G (100,000-250,000 U/kg/d divided q4h)
  • Antifungals, such as rifampicin (10-20 mg/kg/d) or 5-fluorocytosine (50-150 mg/kg/d PO divided q6h), are recommended by some infectious disease experts in certain situations. Antifungals may be administered in patients with the following conditions:
  • • Candida species infection - Fluconazole (6-12 mg/kg/d), amphotericin B (0.75-1 mg/kg/d)
    • Histoplasmosis - Amphotericin B (0.75-1 mg/kg/d)
    • Cryptococcus species infection - Amphotericin B (0.75-1 mg/kg/d)
  • Antituberculosis drugs are administered in patients with MTB and include isoniazid (10-30 mg/kg/d), rifampicin (10-20 mg/kg/d), rifabutin, pyrazinamide (30 mg/kg/d), and ethambutol (15 mg/kg/d). Many public health authorities have practiced direct observed treatment (DOT) with good success. 
  • Anthelmintics, including diethylcarbamazine (6 mg/kg/d), albendazole (400 mg PO bid), and mebendazole (100-200 mg PO bid), are usually administered with corticosteroids in patients with toxocariasis or baylisascariasis.
  • Coordinate the combination of drugs, length and interval of treatment, need for DOT, and toxicity screening of the treatment regimen with an infectious disease specialist and public health authority. 
  • Several agents are used to treat toxoplasmosis. These agents include pyrimethamine (0.5-1 mg/kg/d) and sulfadiazine (120-150 mg/kg/d divided q6h); dapsone (1 mg/kg/d), spiramycin, and experimental treatment with atovaquone (40 mg/kg/d has been used, no dosage for children); and newer macrolide antibiotics such as clarithromycin (15 mg/kg/d) or azithromycin (5 mg/kg/d). The involvement of a pediatric infectious diseases specialist is recommended for the selection of agents, the procurement process (eg, spiramycin through the US Food and Drug Administration [FDA]), and the study of toxicity profiles of drugs. 
  • Prevention of fetal infection after maternal Toxoplasma seroconversion during pregnancy is attempted with spiramycin administration. A 60% decrease has been reported in the congenital infection rate in patients who received this treatment; however, it does not ameliorate the fate of infants who are infected. 
  • Experimental treatment (eg, intraocular ganciclovir implants) has been tried in CMV chorioretinitis in patients with AIDS.  
  • Etiologic treatments may not alter the clinical course of chorioretinitis because the pathologic changes may be due to an inflammatory and/or immunologic response instead of infection. 
  • Treatment of other etiologies, such as syphilis, tuberculosis, yersiniosis, and neuroborreliosis, depends on diagnosis but is likely to be successful in most patients.
• Eye symptoms can be treated as follows:
• • Steroids may have a role in the acute management of many vasculitides, collagen vascular diseases, or sarcoids; in some infectious processes (eg, MTB); or in some incidents caused by Toxoplasma species.
  • Laser treatment of retinal lesions is used in certain conditions with good results.
  • Experimental intraocular implants of ganciclovir to treat CMV chorioretinitis in patients with AIDS are used with some degree of success.
  • Intravitreous amphotericin B (5-10 mcg) has been used to treat serious fungal chorioretinitis.
• Implement seizure control under the guidance of a pediatric neurologist if CNS involvement is evident.
• Exercise judicious use of supplemental immunoglobulin infusions for agammaglobulinemia on a patient-by-patient basis.

Surgical Care

Vitrectomy is usually not needed and is reserved for severe cases that are resistant to conservative medical treatment. Ocular cytology used to detect the presence of eosinophils, ocular antibody, and immunoglobulin E (IgE) levels should always be performed to differentiate toxocaral ocular larva migrans from malignant retinoblastoma to prevent unnecessary enucleations.

Consultations

• Involvement of the following specialists is helpful in performing diagnostic workup, determining the length of treatment, and planning the total management of a child with chorioretinitis:
• • Ophthalmologist - For determination of eye damage, treatment, and long-term follow-up care 
  • Neurologist - For seizure control and long-term follow-up care of neurologic deficits 
  • Infectious disease specialist and immunologist - For positive diagnosis workup, selection of therapeutic agents and options, investigation of potential drug toxicities, and determination of treatment length
  • Audiologist - For assessment and corrective measures to detect and treat deafness (if possible)
  • Physical therapist - For maximization of functions and range of motions of muscles and joints and for referral to an orthopedist for surgical intervention if needed
• Occasionally, genetic testing is required to investigate possible dysmorphic syndromes.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Few therapeutic options are available. Even in an individual with chorioretinitis of a known etiology with proven treatment, the impact of treatment is not always evident, probably because of the inherent problems with congenital infections. This section includes information on specific antiviral, antitoxoplasmosal, antibacterial, anthelmintics, and antifungal treatments.

Drug Category: Antivirals

Treatment of congenital viral infections with chorioretinitis, such as HSV (CNS, mucocutaneous, sepsis), CMV, or varicella-zoster virus, has resulted in lower mortality rates. Older children may benefit from intravitreal administration, which requires consultation with an ophthalmologist.

Drug Category: Antitoxoplasmosis agents

Pyrimethamine and sulfadiazine are synergistic against Toxoplasma species. Spiramycin is occasionally included in the regimen to treat congenital toxoplasmosis. Clindamycin has occasionally been administered to patients with AIDS and CNS toxoplasmosis. Other experimental treatments with atovaquone and newer macrolide antibiotics are being investigated.

Drug Category: Antifungals

Amphotericin B and its various lipid forms are the principal drugs for parenteral use. For synergy, 5 flucytosine (5FC) could be administered with amphotericin B. Azoles (chiefly fluconazole, itraconazole, and voriconazole) are agents of choice for long-term oral therapy. Caspofungin is useful in patients with susceptible fungi who cannot tolerate the side effects associated with other antifungals.

Drug Category: Anthelmintics

Parasite biochemical pathways are different from those of the human host; thus, the toxicity is directed to the parasite, egg, or larvae. The mechanism of action varies within the drug class. Antiparasitic actions may include the following:

• Inhibition of microtubules, which causes irreversible block of glucose uptake
• Tubulin polymerization inhibition
• Depolarizing neuromuscular blockade
• Cholinesterase inhibition
• Increased cell membrane permeability, resulting in intracellular calcium loss
• Vacuolization of the schistosome tegument
• Increased cell membrane permeability to chloride ions via chloride channels alteration

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Children with congenital infections and chorioretinitis face many possible handicaps, including partial or total loss of vision, deafness, seizure disorders, and mental retardation. An immunocompromised subgroup of these children may be prematurely delivered and born with HIV infections. 
• Short-term care for individuals with chorioretinitis includes diagnostic and management planning. Management planning requires participation of an intensivist, ophthalmologist, infectious disease specialist, neurologist, physiotherapist, and child development specialist.

Further Outpatient Care

• Long-term care should alleviate debilitating conditions and improve functions for patients with chorioretinitis. An involved primary care physician should work closely with the specialists, the school system, and social workers.

Prognosis

• Except when caused by CTP, prognosis for individuals with chorioretinitis depends on the originating process, but it tends to be self-limited. 
• Chorioretinitis due to CTP is progressive, and the outcome is not usually predictable.

Patient Education

• Aim educational efforts at reducing the incidence of primary toxoplasmosis in pregnant women. In the summer and fall seasons, public health measures can be used to reduce the risk of mosquito-borne viral encephalitis or tick-borne Lyme disease. 
• Screen pregnant women for the presence of toxoplasmosis IgG and educate these individuals to avoid consuming undercooked meat and handling a cat litter box.
• During peak season for mosquitos and ticks, educate pregnant women to avoid insect bites (eg, cover up, apply insecticide to clothing items) and carry out limited larvicidal spraying to control mosquito infestation.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Special Concerns

• Because the incidence of heterosexual HIV infections is still significant, pregnant women infected with HIV are at risk of reactivation of CMV and, more significantly, toxoplasmosis. Reactivation of these infections can translate into higher risk of congenital infections in their infants.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• Adelman RA, Membreno JH, Afshari NA, Stoessel KM. West Nile virus chorioretinitis. Retina. Feb 2003;23(1):100-1. [Medline].
• Boppana SB, Pass RF, Britt WJ, et al. Symptomatic congenital cytomegalovirus infection: neonatal morbidity and mortality. Pediatr Infect Dis J. Feb 1992;11(2):93-9. [Medline].
• CDC. Intrauterine West Nile virus infection--New York, 2002. MMWR Morb Mortal Wkly Rep. Dec 20 2002;51(50):1135-6. [Medline].
• Gur S, Silverstone BZ, Zylberman R, Berson D. Chorioretinitis and extrapulmonary tuberculosis. Ann Ophthalmol. Mar 1987;19(3):112-5. [Medline].
• Klotz SA, Penn CC, Negvesky GJ, Butrus SI. Fungal and parasitic infections of the eye. Clin Microbiol Rev. Oct 2000;13(4):662-85. [Medline].
• Lebech AM, Lebech M, Borme KK, Mathiesen, LR. [Toxoplasmosis-chorioretinitis: clinical course and treatment of seven patients]. Ugeskr Laeger. Jul 1 1996;158(27):3935-9. [Medline].
• Lynfield R, Guerina NG. Toxoplasmosis. In: Oski's Pediatrics. 1999:1184-93.
• Martin DF, Kuppermann BD, Wolitz RA, et al. Oral ganciclovir for patients with cytomegalovirus retinitis treated with a ganciclovir implant. Roche Ganciclovir Study Group. N Engl J Med. Apr 8 1999;340(14):1063-70. [Medline].
• Montoya JG, Remington JS. Toxoplasmic chorioretinitis in the setting of acute acquired toxoplasmosis. Clin Infect Dis. Aug 1996;23(2):277-82. [Medline].
• Murray WJ, Kazacos KR. Raccoon roundworm encephalitis. Clin Infect Dis. Nov 15 2004;39(10):1484-92. [Medline].
• Nguyen QV, Teran S, Snedeker J. Central nervous system sequelae in an infant with congenital West Nile virus infection. Infect Med. 2005;22:626-8.
• Osusky R, Kain HL. [Bilateral chorioretinitis after infection with Yersinia enterocolitica]. Fortschr Ophthalmol. 1991;88(5):446-9. [Medline].
• Park KL, Smith RE, Rao NA. Ocular manifestations of AIDS. Curr Opin Ophthalmol. Dec 1995;6(6):82-7. [Medline].
• Riddell Iv J, McNeil SA, Johnson TM, et al. Endogenous Aspergillus endophthalmitis: report of 3 cases and review of the literature. Medicine (Baltimore). Jul 2002;81(4):311-20. [Medline].
• Schulte DJ, Comer JA, Erickson BR, et al. Congenital lymphocytic choriomeningitis virus: an underdiagnosed cause of neonatal hydrocephalus. Pediatr Infect Dis J. Jun 2006;25(6):560-2. [Medline].
• Stray-Pedersen B. Toxoplasmosis in pregnancy. Baillieres Clin Obstet Gynaecol. Mar 1993;7(1):107-37. [Medline].
• Zarkovic A, MacMurray C, Deva N, Ghosh S, Whitley D, Guest S. Seropositivity rates for Bartonella henselae, Toxocara canis and Toxoplasma gondii in New Zealand blood donors. Clin Experiment Ophthalmol. Mar 2007;35(2):131-4. [Medline].

Article Last Updated: Aug 29, 2007