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Admiravision.es
Ocular Parasitic Diseases: A Review on Toxocariasis and Diffuse Unilateral Subacute Neuroretinitis
Rafael T. Cortez, MD; Gema Ramirez, MD; Lucienne Collet, MD; Gian Paolo Giuliari, MD
migratory behavior, and the host immunological re-
Parasitic infections may damage various ocular tissues,
thereby causing visual dysfunction. In 1950, Wilder de-
Visceral larva migrans is characterized by gen-
scribed the first case in which larval forms of nematodal
eralized systemic involvement due to the migration
intestinal roundworms (
Ascaridoidea:
Ascaris,
Toxocara,
capabilities of the second stage larvae of
Toxocara
Ancylostoma,
Necator, and
Strongyloides) were impli-
canis. It typically presents in children from the ages
cated as a cause of intraocular disease. This review fo-
of 6 months to 5 years. The disease is usually self-
cuses on two disorders associated with parasitic infec-
limited and subclinical; however, fever, pulmonary
tions: ocular toxocariasis and diffuse unilateral subacute
manifestations, hepatomegaly, eosinophilia, pallor,
neuroretinitis.
[J Pediatr Ophthalmol Strabismus
irritability, anorexia, and malaise can occur.6,7
On the other hand, ocular toxocariasis appears
in older patients, with an average age of 7.5 to 8.6 years.7-9 Several studies have revealed
Toxocara and
other visceral larvae migrans to be the cause of intra-
Parasitic infections may produce severe dam-
ocular inflammation in 9.4% of pediatric uveitis.10,11
age to various ocular tissues, thereby causing visual
Rarely does a patient present with both visceral larva
dysfunction. In this review, we will focus on two of
migrans and ocular toxoplasmosis at the same time
these infections, ocular toxocariasis and diffuse uni-
or even at separate intervals.3,6,12
lateral subacute neuroretinitis (DUSN). Although these diseases are not widely distributed worldwide,
Epidemiology and Life Cycle of T. canis
we believe it is of great value to the general ophthal-
The adult dog usually acquires the
T. canis parasite
mologist to be familiar with their different presenta-
by ingesting the parasite's eggs or second stage larvae
tions, due to the poor visual prognosis they carry.
found in contaminated soil, infected meat, and feces. The larvae form cysts and reactivation of the larvae
during gestation can infect the fetal puppies in the
Human infection by
Toxocara, a common
uterus. Following birth, the larvae migrate to the pup-
roundworm that infects dogs and cats, may take one
pies' lungs and then travel up the respiratory tract to
of two forms: visceral larva migrans and ocular toxo-
the pharynx, where they are swallowed. They then ma-
cariasis.1-5 The characteristics of the infection will
ture to become egg-laying adult worms in the gastroin-
depend on the number of parasites, site of infection,
testinal tract. Approximately 4 weeks after their birth,
From Centro de Cirugía Oftalmológica (RTC, GR, LC), Caracas, Venezuela; and Princess Margaret Hospital (GPG), University of Toronto, Toronto,
Ontario, Canada.
Originally submitted January 4, 2010. Accepted for publication May 3, 2010.
The authors have no financial or proprietary interest in the materials presented herein. Address correspondence to Gian Paolo Giuliari, MD, 77 Elm Street, Apt. 903, Toronto, Ontario M5G H14, Canada. E-mail: [email protected]: 10.3928/01913913-20100719-02
Journal of Pediatric Ophthalmology & Strabismus • Vol. xx, No. x, 20XX
Figure . Fundus photograph montage showing
Toxocara's pe-
Figure . Posterior pole
Toxocara granuloma. Note a traction band
ripheral granuloma with retinal fold extending from the optic
extending from the lesion to the optic disc and retinochoroidal
nerve to the retinal periphery.
worms begin laying eggs. Older dogs can harbor adult
Several ocular presentations have been recognized,
worms that do not lay eggs.13
Toxocara eggs are found
the most common of which is granulomatous inflam-
in the soil throughout tropical and temperate climate
mation in the posterior pole or periphery.14,18-20 Some
regions. In the United States and Western Europe, soil
patients may present with a more marked chronic in-
from parks and public areas has been found to carry a
flammation in the retina and the vitreous known as
contamination rate of 10% to 30%.14 In Venezuela, a
33% contamination rate was found in a metropolitan
Posterior Pole Granuloma. In the acute stage,
retinochoroiditis appears clinically as a hazy, ill-de-
Humans are primarily infected through the in-
fined white lesion with overlaying inflammatory cells
gestion of soil and food contaminated with
Toxocara
in the vitreous. As the acute inflammatory reaction
larvae. After the eggs are ingested, they develop into
subsides, the lesion appears as a well-defined elevated
second stage larvae in the small intestine. They then
mass ranging from one-half to four disc diameters in
enter the portal circulation, following hematog-
size.14,21 In some cases, traction bands may extend
enous and lymphatic routes to form cysts in tissue
from the lesion to the optic disc or to the macular
structures.15 The parasites reach the eye through the
area. In the case of chronic granulomatous inflam-
retinal, ciliary, and choroidal circulation. Humans
mation, large retinal vessels may infiltrate the mass
are not natural hosts of
Toxocara, and the parasite
and disappear into its substance, probably represent-
cannot mature into an adult worm in the intes-
ing retinochoroidal anastomosis (Fig. 1).
Peripheral Granuloma. Ocular toxocariasis
can occur as an acute inflammatory process in the
peripheral retina and ciliary body. This may either
Ocular toxocariasis is typically unilateral. Pa-
be preceded by mild acute inflammation in the an-
tients present with unilateral decrease in visual acu-
terior or posterior segment or the eye may be quiet.
ity, strabismus, or leukocoria.14,16 Cases with bilateral
The peripheral granuloma appears as a hazy, white,
involvement are extremely rare.17 Younger children
elevated mass in the peripheral fundus. It can be as-
generally do not report visual changes, even if visual
sociated with retinal folds that may extend from the
acuity is profoundly decreased, and it is common
peripheral mass to the optic nerve head or to other
that parents may seek medical attention only when
areas of the fundus. In some cases, the traction may
the signs become striking. As such, diminished visu-
lead to heterotopia of the macula, resulting in se-
al acuity is frequently detected in routine examina-
vere vision loss. It is likely that many cases of "con-
tion.14,16 Impairment of visual acuity and leukocoria
genital" retinal folds are acquired peripheral retinal
are the most common presenting manifestations.
granulomas due to
T. canis (Fig. 2).
Copyright SLACK Incorporated
Figure . Anterior segment photograph showing leukocoria in a
patient with a cicatricial peripheral inflammatory mass and a cy-
clitic membrane in a child with ocular toxocariasis.
Figure 4. Chronic
Toxocara endophthalmitis with partial retinal
Chronic Endophthalmitis. Another common
manifestation of ocular toxocariasis is chronic en-dophthalmitis (Fig. 3). This is usually associated with cyclitic membrane, retinal detachment, low
that 42% of patients with presumed retinoblastoma
grade anterior uveitis, and posterior synechiae. The
had pseudoretinoblastoma, and 16% of these had
cyclitic membrane begins to form in the peripheral
ocular toxocariasis.24,25 The clinical features that
quadrant of the fundus where the most severe in-
may help differentiate both entities are: (1) the
flammation lies and progresses across the posterior
mean age at presentation for retinoblastoma is 22
surface of the lens. Severe vitritis may also manifest
to 23 months, whereas for ocular toxocariasis it is
as leukokoria (Fig. 4).1-5 A yellow–white mass, usu-
7.5 to 8.9 years10; (2) retinoblastoma shows tumor
ally in the peripheral retina, which may resemble an
growth; (3) there is a family history; and (4) there is
endophytic retinoblastoma, can be seen through a
lack of inflammation in retinoblastoma.14
hazy vitreous.
Toxocara endophthalmitis does not
Vitreoretinal traction, signs of inflammation,
produce much pain or photophobia and external
and posterior subcapsular cataracts may be seen in
ocular examination reveals only minimal signs of in-
ocular toxocariasis. However, these signs are uncom-
flammation, usually with no ciliary flush. Hypopy-
mon in patients with retinoblastoma. Computed
on may develop in severe cases.16 A cicatricial stage
tomography and B-scan ultrasonography may show
is characterized by tractional bands that may pull
the typical tumor pattern in patients with retino-
on the retina and ciliary body. Patients with endo-
blastoma, with evidence of calcification within the
phthalmitis are usually younger than patients with
mass.26 On the other hand, endophthalmitis sec-
posterior pole granuloma.
ondary to toxocariasis does not commonly demon-
Atypical Presentation. Optic nerve granuloma,
strate a tumor pattern.14
papillitis, inflammatory iridial mass, intracorneal
Additionally, ocular toxocariasis may present
larvae, motile larvae in the vitreous and retina, and
with eosinophils in the vitreous or aqueous humor
scleritis may occur.2,19,22,23 We evaluated two cases
without evidence of malignant cells on histopatho-
that presented with vitreous hemorrhage; after the
logic examination. This may be observed in the
hemorrhage cleared up, the typical fundus changes
presence of normal levels of lactate dehydrogenase
of a posterior pole granuloma were detected.
and phosphoglucose isomerase. Other entities to be excluded are toxoplasmic retinochoroiditis, pars pla-
nitis, retinopathy of prematurity, familial exudative
Toxocara endophthalmitis may closely resemble
vitreoretinopathy, persistent fetal vasculature, Coats'
an endophytic retinoblastoma. Shields et al. found
disease, and organized vitreous hemorrhage.14
Journal of Pediatric Ophthalmology & Strabismus • Vol. xx, No. x, 20XX
dicate that this is not the case.20,30-32 The ultimate
The current gold standard to test for systemic or
utility of antihelmintic therapy remains equivocal.
ocular infection with
T. canis is the enzyme-linked
Surgical Treatment. Surgery is reserved for
immunosorbent assay (ELISA), which carries both
post-inflammatory complications such as persis-
a sensitivity and specificity rate of approximately
tent vitreous opacification, retinal detachment, and
90%.14 Although the Centers for Disease Control
epiretinal membrane formation with vitreomacular
and Prevention considers serum ELISA titers of less
or optic nerve traction (Fig. 5).The most common
than 1:32 to be insignificant for the diagnosis of
indication for surgical intervention in ocular toxo-
systemic toxocariasis, other institutions have stated
cariasis is retinal detachment.27,30,31,33 Retinal reat-
that a serum titer of 1:8, or even lower, is sufficient
tachment has been performed in 71% to 88% of
to support the diagnosis if the patient has signs and
ocular toxocariasis cases, with visual improvement
symptoms compatible with the disease.14,18,27 How-
in most patients.27,30,31,33
ever, a positive serum titer cannot be used to defini-tively confirm the diagnosis of ocular toxocariasis,
DIFFUSE UNILATERAL SUBACUTE
although the absence of serologic evidence of
Toxo-
cara presence could reduce the odds of this organ-
DUSN was first described by Gass et al.34 and
ism being the cause of ocular disease.14,18 Authors
Gass and Scelfo35 in 1978. They described 29 patients
have found that 31.8% of affected children without
between the ages of 5 and 22 years with severe visual
signs of ocular toxocariasis exhibited a serum titer
loss in one eye, vitritis, mild papillitis, and recurrent
of 1:16 or greater.14,18 ELISA testing of intraocular
crops of evanescent, gray–white lesions affecting the
fluids has been demonstrated to be of great value in
outer retina and pigment epithelium. These lesions
diagnosing ocular toxocariasis.10,14,18,19,28
are usually followed by progressive loss of visual field, optic atrophy, narrowing of the major retinal vessels,
diffuse and focal depigmentation of retinal pigment
The treatment of ocular toxocariasis depends pri-
epithelium throughout the fundus, and a moderate to
marily on the extent of inflammation at presentation
marked reduction of the b-wave amplitude on mul-
and the secondary structural changes in the vitreous
tifocal electroretinogram. Previously, this condition
and retina that are associated with the disease.14 In
was termed "unilateral wipe-out syndrome."34,35
most cases of severe nematode endophthalmitis, nu-
DUSN is most prevalent in the southeastern
merous complications ensue that frequently result in
United States and the Caribbean, although some
total blindness in the involved eye. Therefore, prompt
cases have been reported in many sections of the
treatment is justified in such cases.14
United States, Canada, the northern part of South
Medical Treatment. With ocular toxocariasis,
America, Europe, and China.36-41
the objective of treatment is to reduce inflamma-
In the United States, DUSN is probably caused
tion to prevent the formation of membranes that
by at least two different nematodes. The smaller
can consequently affect intraocular structures.
one,
Ancylostoma caninum, measures between 400
Periocular and systemic steroids (0.5 to 1 mg/kg
and 1,000 µm in length and has a diameter of ap-
prednisone daily) are the mainstays of therapy for
proximately one-twentieth of its length.36-39 It is
eyes with active vitritis. Cycloplegic agents should
mainly found in the southeastern United States, the
be employed when signs of anterior segment in-
Caribbean, and the northern part of South Amer-
volvement are present.14 There have been reports of
ica.36-39 A larger nematode,
Baylisascaris procyonis,
clinical improvements of ocular toxocariasis treated
1,500 to 2,000 µm long, is responsible for DUSN in
with antihelmintic agents thiabendazole (25 mg/kg
the northern-midwestern United States and in some
twice daily for 5 days with a maximum of 3 g per
parts of Brazil.34,38,42,43
day), albendazole (800 mg twice daily for 6 days), or mebendazole (100 to 200 mg twice daily for 5
days).14,29 Although it has been proposed that an-
Ocular findings in DUSN have been well de-
tihelmintic treatment may initiate an intraocular
scribed by Gass et al.34-39 Most patients are young
inflammation due to a hypersensitivity response to
and healthy, with ages ranging from 11 to 65 years
dead larvae, clinical and experimental evidence in-
(the mean age being 24 years) at the time of the ini-
Copyright SLACK Incorporated
Figure . (A)
Toxocara peripheral granuloma with traction fibrotic band extending to the optic nerve. (B) Fundus photograph of the same
patient 6 weeks after pars plana vitrectomy.
early stages, inflammation in the anterior segment is uncommon, although keratic precipitates and hypopyon were observed and reported in one pa-tient.34,35 Visual acuity may be reduced moderately if the condition is detected early, but it is usually markedly decreased at the time of presentation. The fundus changes, which are the most promi-nent feature of this syndrome, have been divided into early and late.34,35
The onset of DUSN is subtle and progres-
sive.34,35 Patients in the early stages of the disease may present with low vision in the affected eye, mild to moderate vitritis, optic disc swelling, and recur-rent crops of evanescent, multifocal, gray–white le-
Figure 6. Early stage of diffuse unilateral subacute neuroretinitis.
Note the vitritis, optic disc swelling, and crops of multifocal gray–
sions at the level of the outer retina (Fig. 6). The
white lesions.
lesions are typically clustered in one segment of the fundus, and successive crops of these lesions may re-cur in close proximity to previously affected areas.
tial presentation.39 For the most part, it is a unilat-
The nematode, which often assumes an S-shape
eral condition; although uncommon, bilateral cases
or coiled position, should be sought out in the vicin-
have been described.37,39,40
ity of the active lesions. In the absence of these white
Many patients, particularly children, may be
lesions, no other markers exist for the location of the
asymptomatic and visual loss is usually discovered
worm. Nematodes propel themselves by a series of
on routine eye examination. Other patients may
slow coiling and uncoiling movements, or by slith-
present with acute onset of multiple, and rapidly
ering, snake-like movements. The examining light
changing, central or paracentral scotomata, pho-
seems to stimulate movement in the nematode and
topsias, or unilateral vision loss.34,35,44-46 In the
causes it to move deeper into the subretinal space
Journal of Pediatric Ophthalmology & Strabismus • Vol. xx, No. x, 20XX
was 20/400 or worse in 69 patients (84.1%). Ad-ditionally, a subretinal nematode was identified in 33 eyes (40.2%). All of the nematodes were small, measuring approximately 400 µm in length.
As mentioned, patients with DUSN suffer pro-
gressive vision loss and seek medical attention in the late stages of the disease. Consequently, the clinician should focus on the early recognition of this syn-drome because treatment may prevent further dete-rioration of visual function and may even result in visual improvement.34,35 In patients with suspected
Figure 7. Late stage of diffuse unilateral subacute neuroretinitis.
DUSN, we first suggest an evaluation using indirect
Diffuse and focal changes of the retinal pigment epithelium. Nar-
ophthalmoscopy with a 20-diopter lens (or in some
rowing of the retinal arterioles and mild pallor of the optic nerve.
cases a 14-diopter lens) to locate the crops of evanes-
Note the intraretinal parasite superior to the fovea.
cent white lesions and to attempt to locate the nema-tode around these areas. Subsequent biomicroscopy
where the clinician may lose the opportunity to
in that area with a 78-diopter lens allows the exam-
identify it. In such cases, the light stimulus should
iner to definitely identify the nematode.34,36 In the
be discontinued for the organism to reemerge from
absence of white lesions, a careful biomicroscopic
the deeper structures.34-36,43,47
search of the entire fundus is necessary to find the
Occasionally, perivenous retinal exudation and
worm, and multiple patient visits may be required.
sheathing may be observed. In addition, cystoid
It is also possible to identify the parasite by careful
macular edema, intraretinal and subretinal hemor-
examination of fundus photographs that include the
rhages, retinal exudation, and neovascularization
suspicious areas.
may present during the early stages of the disease.34
Fluorescein angiography is not helpful in locat-
Over a period of weeks to months, late manifesta-
ing the nematode.36 Scanning laser ophthalmoscopy
tions begin to appear.36 Diffuse and focal depigmen-
using a blue light can help locate the worm due to
tation of the retinal pigment epithelium is seen. This
the provided advantage of enhancing contrast, im-
is usually less prominent in the central area. Gradual
proving visualization, and recording a videography
narrowing of the retinal vessels and an increase in
of the worms' movements.48
pallor of the optic disc will frequently result in an
Multifocal electroretinogram is subnormal in
afferent pupillary defect (Fig. 7). In general, the de-
the affected eye during all stages of the disease, with
gree of optic disc pallor and retinal vessel narrow-
b-wave being more affected than a-wave.36 Serologic
ing parallel that of central visual loss, but striking
studies, stool examination, and peripheral blood
exceptions do occur.34,35 Fluorescein angiography
smears are of little value in diagnosing DUSN.10,37
will reveal hypofluorescent lesions that turn hyper-
Toxocara and
B. procyonis antibody titers have been
fluorescent in the late stages of the test. Dye leak-
proposed as diagnostic tools to try to identify the
age occurs at the optic nerve level; active lesions and
disease.49 No serologic test is currently available for
petaloid hyperfluorescence are observed in cases of
Ancylostoma caninum. Because of the possibility of
cystoid macular edema. In more advanced stages of
commonly shared antigens by different nematodes
the disease, fluorescein angiography may reveal mul-
or seropositivity unrelated to the actual infecting
tiple hyperfluorescent lesions due to window defects
nematode, interpretation of serologic testing may be
secondary to retinal pigment epithelium alterations
subject to error.48
together with a delay in retinal circulation time.35
The clinical evaluation of 78 patients in Ven-
Etiology and Pathogenesis
ezuela39 showed the typical funduscopic late chang-
There is no consensus regarding the identifica-
es described by Gass et al.36 The mean age of these
tion of the subretinal nematode frequently found in
patients was 16.7 years; the presenting visual acuity
DUSN. Reports suggest
B. procyonis,
A. caninum,
Copyright SLACK Incorporated
Figure 8. (A) Late stage of diffuse unilateral subacute neuroretinitis. Note the parasite around the retinal vessel (arrow). (B) Fundus photo-
graph of the same patient after retinal photocoagulation of the parasite.
Dirofilaria, and a larval form of
T. canis as possible
is caused by products left in the worm's wake, and a
infectious agents involved in DUSN.50 However,
more diffuse toxic reaction affecting both the inner
the larval form of
T. canis is smaller than the worm
and outer retinal tissues ensues.36 Histopathologic
that causes DUSN and there is a lack of serologic
study of an eye believed to be affected by DUSN
evidence to support the mentioned reports. In addi-
revealed nongranulomatous vitritis and retinitis. It
tion, funduscopic manifestations are different than
also showed retinal and optic nerve perivasculitis,
those associated with other forms of ocular toxoca-
extensive degeneration of the posterior retina, mild
riasis and the high prevalence of
T. canis does not
optic atrophy, mild degenerative changes in the reti-
correlate with the scant number of DUSN cases re-
nal pigment epithelium, and a low-grade, patchy,
non-granulomatous choroiditis.34,35
A. caninum, which is a common nematode para-
site that infects dogs, is suspected of causing DUSN
because it frequently results in cutaneous larval mi-
The condition most likely to be mistaken for
grans that may later manifest signs of DUSN. The
DUSN is multiple evanescent white-dot syndrome
worm can survive for months and even years with-
(MEWDS), although in the early stages DUSN
out changing form and its infective larva measures
may resemble toxoplasmosis, cytomegalovirus, and
approximately 650 µm. This better corresponds to
bacterial abscesses. MEWDS can be distinguished
the entity described in DUSN.34,35 Scanning elec-
from DUSN by an accompanying history of flu-like
tron microscopy of a nematode excised from a case
symptoms, photophobia, wreath-like hyperfluores-
of DUSN by means of an eye wall biopsy was com-
cent dots on fluorescein angiography, blind spot
patible with, but not diagnostic for,
A. caninum.
enlargement, multiple gray or whitish outer retinal
B. procyonis is an intestinal nematode that in-
lesions, and decreased electroretinogram record-
fects raccoons and skunks. The larva measures be-
ings.51,52 Visual acuity may even return to normal
tween 300 and 2,000 µm, and it has been proposed
levels in some cases after several weeks or months.
as the larger nematode responsible for DUSN.49,50
On fluorescein angiography, the white lesions in
Nevertheless, infrequent exposure to raccoons or
DUSN block the fluorescence in the early phase,
skunks and the absence of central nervous system
whereas in MEWDS the lesions are hyperfluores-
involvement make
B. procyonis a highly unlikely
cent in the early stages of the angiogram. Rarely, one
pathogen in DUSN.
can mistake DUSN for sarcoidosis, presumed ocular
The pathogenesis of DUSN appears to involve
histoplasmosis syndrome, and multifocal choroidi-
a mechanical, inflammatory, and toxic assault on the
tis due to the appearance of focal chorioretinal scars
outer retina. A local toxic effect in the outer retina
scattered throughout the fundus.53 The absence of
Journal of Pediatric Ophthalmology & Strabismus • Vol. xx, No. x, 20XX
optic atrophy, vitritis, vessel attenuation, and the
presence of normal-looking retinal pigment epithe-
Ocular toxocariasis and DUSN may produce se-
lium between punched out lesions is more likely to
vere damage to the intraocular structures, causing sig-
be encountered in DUSN. Eyes with central retinal
nificant visual impairment. Although these diseases
artery occlusion may show some characteristics that
are not well distributed worldwide due to their poor
look like DUSN. Also, the late stages of DUSN may
visual prognosis, it is of great importance that physi-
be confused with retinitis pigmentosa, secondary
cians be aware of the variety of clinical forms in an
bone-spicules migration, and posterior subcapsular
effort to achieve an early diagnosis and treatment.
opacification, but unilaterality is characteristically a feature of DUSN.34,35 Trauma may exhibit some
DUSN characteristics such as retinal pigment epi-
1. Beaver PC, Snyder CH, Carrera GM, Dent JH, Lafferty JW.
Chronic eosinophilia due to visceral larva migrans; report of three
thelial changes and optic atrophy.34,35
cases.
Pediatrics. 1952;9:7-19.
2. Baldone JA, Clark WB, Jung RC. Nematode ophthalmitis: report
of two cases.
Am J Ophthalmol. 1964;57:763-766.
3. Nichols RL. The etiology of visceral larva migrans: I. Diagnostic
Photocoagulation of the parasite when visible,
morphology of infective second-stage Toxocara larvae.
J Parasitol.
using 200 to 500 µm, 0.2 to 0.5 second of thermal
1956;42(4 Section 1):349-362.
4. Gillespie SH. Cutaneous larva migrans.
Curr Infect Dis Rep.
laser application, is the treatment of choice36,43,47
(Fig. 8), although visual acuity does not significantly
5. Wilder HC. Nematode endophthalmitis.
Trans Am Acad Ophthal-
mol Otolaryngol. 1950;55:99-109.
improve unless the worm is killed soon after onset
6. Huntley CC, Costas MC, Lyerly A. Visceral larva migrans syn-
of visual loss.54,55 Photocoagulation does not cause
drome: clinical characteristics and immunologic studies in 51 pa-tients.
Pediatrics. 1965;36:523-536.
exacerbation of inflammation and results in prompt
7. Schantz PM, Glickman LT. Toxocaral visceral larva migrans.
N
and permanent inactivation of the disease; however,
Engl J Med. 1978;298:436-439.
the search for the nematode can become a time-con-
8. Schantz PM, Stehr-Green JK. Toxocaral larva migrans.
J Am Vet
Med Assoc. 1988;192:28-32.
suming and frustrating task.36,43,47
9. Schantz PM, Weis PE, Pollard ZF, White MC. Risk factors for
Several oral antihelmintic medications, such
toxocaral ocular larva migrans: a case-control study.
Am J Public
as thiabendazole and dietylcarbavazine, have been
10. Schantz PM, Meyer D, Glickman LT. Clinical, serologic, and epi-
used in an effort to treat this disease.36,56,57 However,
demiologic characteristics of ocular toxocariasis.
Am J Trop Med
most of the studies reported that only the subretinal
11. Benezra D, Cohen E, Maftzir G. Patterns of intraocular inflam-
worms were killed, probably due to inadequate ocu-
mation in children.
Bull Soc Belge Ophtalmol. 2001;279:35-38.
12. Paul M, Stefaniak J, Twardosz-Pawlik H, Pecold K. The co-occur-
lar penetration of the drugs. Hence, it has been sug-
rence of Toxocara ocular and visceral larva migrans syndrome: a
gested that if the worm cannot be found in a patient
case series.
Cases J. 2009;2:6881.
with a high suspicion of DUSN, a scatter pattern of
13. Vaughn J, Jordan R. Intestinal nematodes in well-cared for dogs.
Am J Trop Med Hyg. 1960;9:29-31.
laser burns in the vicinity of the multifocal active
14. Shields JA. Ocular toxocariasis: a review.
Surv Ophthalmol.
lesions can be performed to alter the blood–retinal
15. Sprent JF. The life cycles of nematodes in the family Ascarididae
barrier prior to administration of the oral medica-
Blanchard 1896.
J Parasitol. 1954;40(5, Part 1):608-617.
16. Smith PH, Greer CH. Unusual presentation of ocular Toxocara
infestation.
Br J Ophthalmol. 1971;55:317-320.
Recently, several studies have demonstrated al-
17. Benitez del Castillo JM, Herreros G, Guillen JL, Fenoy S, Banares
bendazole as a safe and beneficial treatment modal-
A, Garcia J. Bilateral ocular toxocariasis demonstrated by aqueous humor enzyme-linked immunosorbent assay.
Am J Ophthalmol.
ity for these patients.39,58 Our group published the
results of the use of oral albendazole in 6 patients
18. Ellis GS Jr, Pakalnis VA, Worley G, et al. Toxocara canis infesta-
with DUSN, following a 10-day regimen at 200
tion: clinical and epidemiological associations with seropositivity in kindergarten children.
Ophthalmology. 1986;93:1032-1037.
mg orally 3 times daily.39 The nematode was killed
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Journal of Pediatric Ophthalmology & Strabismus • Vol. xx, No. x, 20XX
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Harvard Journal of Law & Technology Volume 24, Number 2 Spring 2011 REVERSE SETTLEMENTS AS PATENT INVALIDITY SIGNALS Gregory Dolin, M.D.* TABLE OF CONTENTS I. INTRODUCTION .282 II. THE HATCH-WAXMAN ACT .286 A. The Structure and Purposes of the Act . 286 B. The Mechanics of the Hatch-Waxman Act. 290 III. REVERSE SETTLEMENTS .293
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