Pediatric Infectious Posterior

Uveitis

Dilsher S. Dhoot, MD
Daniel F. Martin, MD
Sunil K. Srivastava, MD

’ Introduction

Uveitis represents a collection of inflammatory diseases of the eye. It

occurs at a prevalence of 93 per 100,000 in adults and is a common cause
of blindness. The annual incidence ranges from 26 to 102 per 100,000.
Uveitis in the pediatric population is less common than adults, occurring
in 30 cases per 100,000, with an incidence of 4.3 to 6.9 per 100,000.1 In
most tertiary uveitis clinics, children account for 5% to 10% of all cases
observed.2 Although the majority of cases of uveitis in children are
noninfectious, infectious etiologies are responsible for up to 13% of all
pediatric uveitis cases.3 It is important to recognize the more common
cases of infectious uveitis in children as the use of immunosuppressive
therapy in these cases can lead to poor visual outcomes.
Here, we present relatively common and uncommon causes of
posterior infectious uveitis in children. Autoimmune etiologies of
pediatric uveitis are presented in a separate chapter in this series.

’ Toxoplasmosis

Toxoplasmosis is the most common etiology of infectious posterior

uveitis in all age groups.2 The causative organism is the intracellular pro-
tozoan Toxoplasma gondii. Cats are the definitive host, whereas humans
become intermediate hosts by ingesting the cyst or bradyzoite form.
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Volume 51, Number 1, 113–128
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Once ingested, the cyst form can migrate to cardiac, muscular, and
neural/retinal tissues. Rupture of the cyst then leads to release of the
active or tachyzoite form, resulting in active disease. It is believed that
congenital infection is responsible for most of human disease, with up to
40% of cases being caused by transplacental transmission. First trimester
infection can result in intracerebral calcification, hepatosplenomegaly,
hydrocephalus, seizures, and pneumonia. Infection in the second or
third trimester is associated with a milder generalized disease during
early infancy.3,4 Bilateral macular scars can be seen in congenital disease.
Among pediatric patients, toxoplasmosis is one of the most common
causes of posterior uveitis.5 Active disease adjacent to a scar is seen with
reactivation of previous infection (Fig. 1). Retinitis in the absence of
scarring is more suggestive of acquired disease. Active lesions appear as
an area of focal retinochoroiditis with an overlying vitritis that is either
mild or severe (‘‘headlight in the fog’’) (Fig. 2). In more severe cases,
anterior chamber inflammation spill-over can be seen. Retinal vasculitis
may also occur to varying degrees.6
Diagnosis is generally made based on clinical presentation. Serologic
studies are available to assist in diagnosis. Enzyme-linked immuno-
sorbent assay (ELISA), Sabin-Feldman dye study, indirect fluorescent
antibody test, complement fixation test, and indirect hemagglutination
test are various assays available for detection of serum anti-toxoplasma
antibody titers.3 Polymerase chain reaction (PCR) of aqueous and

Figure 1. Chorioretinal hyperpigmented scar with adjacent active chorioretinitis in a patient with
toxoplasmosis.

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 Pediatric Infectious Posterior Uveitis ’ 115

Figure 2. Chorioretinal scar with prominent vitritis in patient with toxoplasmosis.

vitreous specimens is highly sensitive and specific. In infants, detection

of IgM or IgA is suggestive of prenatal infection.6
Ocular toxoplasmosis is self-limited in immunocompetent indivi-
duals, with infection generally resolving in 1 to 2 months. In adult
patients, treatment is indicated when vision is threatened, that is, macula
or optic nerve involvement. Peripheral lesions can be monitored. In
children, treatment is dependent on the age of the child, the ease of
examination, location, and whether the disease is congenital or acquired.
In older children/young adults, peripheral lesions can be carefully
monitored. However, macular lesions or peripheral lesions that are
progressing warrant therapy. In younger children, where examination
may be difficult or in cases of congenital infection—treatment is
recommended.
For acquired disease, there are many treatment options. Standard
therapy includes pyrimethamine and sulfadiazine dosed by weight for
6 weeks. Folic acid supplementation is indicated to prevent leukopenia
and thrombocytopenia associated with pyrimethamine use. Platelet and
white blood cell counts should be monitored routinely while taking
pyrimethamine. Clindamycin is also an option, although its association
with gastrointestinal side-effects and its dosing regimen (twice daily or 3
times daily) make it less desirable. Azithromycin or sulfamethoxazole
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116 ’ Dhoot et al

/trimethoprim may also be used in some cases. Patients with congenital

infection require therapy for longer duration (from 2 to 12 mo) and
typically are treated with pyrimethamine and sulfadiazine. Clindamycin
may also be added to this regimen. Oral corticosteroids are used with
caution after 24 to 48 hours of antibiotic coverage has been initiated in
patients with severe inflammation.6

’ Toxocariasis

Ocular toxocariasis is a relatively common cause of retinal disease

and uveitis in children, accounting for 9.4% of all pediatric uveitis cases.7
Toxocariasis in humans is caused by the parasite Toxocara Canis. Although
T. canis can only complete its life cycle in dogs, humans are incidental
hosts. Humans are infected through ingestion of soil and contaminated
food. Ingested T. canis eggs develop into second stage larvae in the small
intestine and enter the bloodstream through the portal circulation.8
Infection can take 1 of 2 forms: visceral larva migrans or ocular
toxocariasis.
Visceral larva migrans occurs because of the systemic migration of
the second stage larvae of T. canis. Infection is usually self-limited and can
be subclinical. Typical presentation is in children of 6 months to 5 years
of age. Symptoms include fever, respiratory disease, hepatomegaly,
eosinophilia, anorexia, and malaise.9
Ocular toxocariasis occurs in patients with an average age of 7.5
to 8.6 years.9 Generally, patients present with unilateral involvement,
decreased vision, strabismus, or leukocoria. Bilateral involvement is very
rare. Posterior fundus examination reveals evidence of endophthalmitis,
posterior granuloma, or peripheral granuloma (Fig. 3). Peripheral
eosinophilia is not associated with ocular toxocariasis.6
Peripheral granuloma is the most common presentation of ocular
toxocariasis. Encysted stage II larva within the choroid are presumed to
give rise to these granulomas. Massive vitritis is also common and is
thought to result from the release of immunogenic antigens from the
dead worm.10 The granuloma has a hazy, white, elevated appearance
and ranges in size from 0.75 to 3.0 disc diameters. Associated retinal
folds extending from the optic nerve to the peripheral lesion are also
observed. Severe vision loss can result if macular traction occurs. Large
granulomas can be diagnostically difficult to separate from retino-
blastoma.3,8
Posterior pole granulomas can present as an ill-defined area of
whitening with overlaying vitritis. Over time, the lesion can become a
well-defined elevated mass. Traction bands can also extend to the optic
nerve or macula. Severe inflammation can occur in some cases of ocular
toxocariasis with the development of cyclitic membranes, vitritis, and
retinal detachment.3
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 Pediatric Infectious Posterior Uveitis ’ 117

Figure 3. Well-defined macular lesion in patient with ocular toxocariasis.

Diagnosis of T. canis can be supported by serum analysis with ELISA,

which has sensitivity and specificity of approximately 90%.11 Ocular
ultrasound is also useful in differentiating T. canis from other etiolgies.
Diagnostic vitrectomy can be used to diagnose some cases through
analysis of vitreous for toxocara antibodies. Vitrectomy is not recom-
mended for those patients where retinoblastoma is high on the
differential diagnosis.
The treatment of ocular toxocariasis involves reduction of inflam-
mation to prevent the formation of tractional membranes. Periocular
and systemic steroids are favored for patients with active vitritis. As the
differential diagnosis can include other infectious etiologies, caution is
recommended before delivering a periocular injection in these cases.
Cycloplegic agents are used when there is significant anterior segment
inflammation.
Antihelminthic agents, that is, thiabendazole, albendazole, or me-
bendazole have been reported to be helpful, but can worsen ocular
inflammation. These agents are usually not needed to treat the inflam-
mation associated with toxocara. When used, these agents should be
used concurrently with corticosteroids.8,11 Surgery is indicated in cases
of persistent vitreous opacification, epiretinal membrane formation, and
more commonly, retinal detachment.
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118 ’ Dhoot et al

’ Syphilis

Syphilis is caused by the spirochete Treponema pallidum and can be

acquired or congenital. Most organ systems can be affected by syphilis,
including the bone, central nervous system, liver, lungs, spleen, and eye.
Ocular manifestations of syphilis occur during any stage and can affect
all structures of the eye.
Congenital infection is transmitted from placenta of the infected
mother to the fetus. The rate of congenital syphilis in 2007 was 10.5 cases
per 100,000 live births.12 Children present days to weeks after birth with
fever, rash, hepatosplenomegaly, pneumonia, anemia, and generalized
lymphadenopathy. Late sequelae include Hutchinson teeth, deafness,
saddle nose, and saber shins. Choroiditis can be seen in the peripheral
retina and reveals a bone-spicule chorioretinitis or ‘‘salt-and-pepper’’
fundus. The most common early finding of congenital syphilis is uveitis,
whereas interstitial keratitis is most commonly seen in late congenital
syphilis.13 Ocular findings of syphilis can also be seen later in childhood.
Acquired syphilis is most often contracted through sexual contact
and is uncommon in children. A diffuse maculopapular rash is frequently
seen and can be associated with fever, sore throat, arthralgia, and
malaise. Uveitis is the most common ocular manifestation of acquired
syphilis. The inflammation can be granulomatous or nongranulomatous
and can be anterior, intermediate, posterior, or panuveitis. Posterior
manifestations of syphilis include retinitis (Fig. 4), chorioretintis, peri-
phlebitis, and less frequently exudative detachment. Variable degree of
vitritis is associated.
T. pallidum cannot be cultured in vitro and is not visible on gram
stain. Diagnosis is made clinically and supported by serologic testing.
Nontreponemal tests include Rapid Plasma Reagin and Venereal Disease
Research Laboratory. These tests are used to screen for active disease
and antibody quantification, but are susceptible to false positives in 1%
to 2% of patients. Treponemal tests include fluorescent treponemal
antibody absorbed and T. pallidum particle agglutination, these tests are
used to confirm previous or current infection.13,14 Direct examination
using darkfield microscopy, silver staining, and immunofluorescence
staining are used for the definitive diagnosis of T. pallidum (CDC).
The drug of choice in the treatment of all stages of syphilis is
parentally administered penicillin G. The dosing, duration, and pre-
paration depend on the stage and severity of the infection. Patients with
interstitial keratitis and uveitis can have chronic inflammation despite
therapy.
The Jarisch Herxheimer reaction result from a hypersensitivity
reaction to the treponemal antigens released in large quantity as
spirochetes are killed and usually occurs within 24 hours of treatment.
Signs include headache, fever, malaise, tachycardia, tachypnea, and
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 Pediatric Infectious Posterior Uveitis ’ 119

Figure 4. Punctate white/yellow lesions with surrounding retinitis in a patient with syphilis.

leukocytosis. Corticosteroids can be used for symptomatic relief,

although the symptoms are generally short lived.15

’ Acute Retinal Necrosis

Acute retinal necrosis (ARN) is a severe retinal infection typically

caused by the herpes virus family including herpes simplex virus 1, 2
and Varicella zoster virus. It is typically observed in immunocompetent
patients, but can also occur in immunocompromised individuals (termed
progressive outer retinal necrosis). The incidence of ARN in children is
relatively low.16–19
Patients typically present with blurred vision, photophobia, floaters,
conjunctival injection, and moderate ocular or periocular pain. Moder-
ate-to-severe vitritis, retinal vasculitis, and necrosis, along with optic
nerve inflammation and atrophy are commonly observed (Fig. 5).
Rhegmatogenous retinal detachment occurs in up to 75% of cases of
ARN.19 Contralateral eye involvement is seen in approximately one-
third of cases and is usually seen within the first 3 months of infection.6
The diagnosis of ARN is clinical. Criteria set forth by the American
Uveitis Society are based on the clinical appearance and course of
infection. The following characteristics are seen in ARN: (1) focal and
well-demarcated areas of retinal necrosis; (2) rapid circumferential
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120 ’ Dhoot et al

Figure 5. A 360-degree peripheral retinitis proceeding toward posterior pole in a patient with acute
retinal necrosis.

progression of necrosis, provided antiviral therapy has not been started;

(3) presence of occlusive vasculopathy; and (4) prominent inflammation
in the anterior chamber and vitreous. Supporting characteristics that are
not required for diagnosis, but support diagnosis include: optic atrophy,
scleritis, and pain.20 PCR of aqueous and vitreous specimens is highly
sensitive and can confirm the causative agent.21
ARN requires prompt antiviral therapy. Multiple options are
available including systemic intravenous (IV) acyclovir, oral valacyclovir,
oral famciclovir, and intravitreal injection of antiviral medications
(ganciclovir and foscarnet). Rapid therapy is warranted, thus combina-
tions of medications are typically used. Systemic IV acyclovir has
traditionally been used (dose 10 to 20 mg/kg 3 times daily for 2 to
3 wk). Oral valacyclovir can provide high-systemic doses of acyclovir and
has been reported effective in the treatment of this disease.22 Intravitreal
injections of antivirals can be used to supplement systemic therapy to
quickly provide high intraocular concentration of antiviral therapy.23,24
Systemic therapy is recommended for several months to reduce the
incidence of contralateral eye involvement.
Systemic corticosteroids are typically used after antiviral initiation to
help to decrease inflammation. Prophylactic laser photocoagulation
to the border of necrotic retina is controversial and has been advocated
to reduce the risk of retinal detachment.6 However, there is no proof
that laser actually reduces the risk of detachment.25
Retinal detachment risk is high in these patients. Repair of
detachments often require vitrectomy, scleral buckling, and silicone oil.
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 Pediatric Infectious Posterior Uveitis ’ 121

Visual acuity is limited by the high incidence of retinal detachment and

in some cases optic nerve involvement.

’ Cytomegalovirus

Cytomegalovirus (CMV) is a common viral infection in immuno-

compromised patients, including patients with acquired immunodefi-
ciency syndrome and those with iatrogenic immune suppression. The
seroprevalence of CMV is high with 50% to 80% of adults in the United
States CMV antibody positive. In healthy individuals, the virus remains
dormant; and in the immunosuppressed, the virus can become
active.26,27 CMV among pediatric patients occurs at a lower rate than
in adults.3 Congenital infection can be devastating with systemic
symptoms including microcephaly, encephalitis, deafness, and psycho-
motor retardation.28
The symptoms of CMV retinitis include decreased vision, floaters,
photopsias, and eye pain. Clinical features include mild anterior
chamber inflammation. A mild vitritis can also be seen. The fundus
appearance of CMV retinitis typically features hemorrhage and retinal
necrosis along retinal blood vessels (Fig. 6). A ‘‘brush fire’’ appearance
can also be seen with a peripheral area of retinal atrophy and a leading
edge of retinal necrosis. Multifocal lesions and periphlebitis can also
occur.

Figure 6. Hemorrhage and retinal necrosis, after the nerve fiber layer distribution, in a patient
with cytomegalovirus retinitis.

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122 ’ Dhoot et al

Diagnosis of CMV retinitis is made clinically, based on the char-

acteristic appearance. PCR analysis of anterior chamber or vitreous fluid
can be used to assist in the diagnosis. Serum CMV PCR analysis is also
helpful in the diagnosis of CMV retinitis.
Medical treatment of CMV retinitis has progressed in the past 10 to
15 years. Although parenteral therapy with ganciclovir or foscarnet can
be used initially, oral valganciclovir has been shown to be equally
effective to IV therapy.28
Local therapy of CMV retinitis is still used in selected cases in
children. Intravitreal ganciclovir (2 mg) or foscarnet (2.4 mg) can be
injected to supplement systemic therapy or temporarily treat patients
intolerant to systemic therapy. The ganciclovir intravitreal implant can
also be used in selected cases to locally treat retinitis. The median time to
progression of retinitis in eyes treated with a ganciclovir implant is 226
days (about 8 mo).29,30 In those cases where local therapy is used, oral
valganciclovir is needed to reduce the risk of contralateral eye involve-
ment or other organ involvement.31
The ultimate cure for patients with CMV retinitis is immune
recovery sufficient to stop progression of disease. In those whom
immune recovery has not occurred, long-term oral and local therapy
is required to reduce the risk of reactivation.

’ Diffuse Unilateral Subacute Neuroretinitis

Diffuse unilateral subacute neuroretinitis (DUSN) is a nematode

ocular infection first described in 1978 by Gass et al.32 DUSN is most
common in south-eastern United States and the Caribbean, although not
limited to these areas. In the United States, Ancylostoma caninum and
Baylisascaris procyonis have been implicated as causative nematodes of
DUSN. Ancylostoma caninum typically is seen in the south-eastern United
States and Latin America and typically infects dogs. Baylisascaris procyonis
typically infects raccoons and is seen in the Midwestern United States.
Patients vary in age from 11 to 65 years and are generally otherwise
healthy. DUSN is a predominantly unilateral condition with a biphasic
presentation. Patients may experience paracentral or central scotomata
early in the disease, with severe vision loss at later stages. Early clinical
presentation includes unilateral moderate-to-severe vitritis, vasculitis,
optic nerve swelling, and multifocal gray-white lesions in the posterior
pole measuring from 1200 to 1500 mm (Fig. 7). Subretinal worms can be
visualized during this stage close to active lesions. The examination light
may stimulate nematode movement and cause it to migrate deeper into
the subretinal space. In the second phase of DUSN, diffuse and focal
depigmentation of the retinal pigment epithelium is seen. Vascular
attenuation and optic nerve pallor can also occur.6,8
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 Pediatric Infectious Posterior Uveitis ’ 123

Figure 7. Multifocal depigmented lesions along with optic nerve pallor in a patient with diffuse
unilateral subacute neuroretinitis (Photo courtesy of G. Baker Hubbard, MD.).

Early diagnosis is crucial, as DUSN can lead to severe vision loss.

Clinical examination with visualization of the nematode with biomicro-
scopy is ideal, but may require multiple examinations. Fluorescein
angiography does not aid in the location of the nematode. Scanning laser
ophthalmoscopy has been used to aid in worm location.33 Multifocal
electroretinogram reveals subnormal readings at early and late stages of
the disease.8
The treatment of choice for DUSN is laser photocoagulation, using
200 to 500 mm, 0.2 to 0.5 second duration laser application.8 Unlike
ocular toxocariasis, destruction of the causative organism does not
generally result in exacerbation of inflammation. Oral antihelminthic
agents, that is, albendazole and thiabendazole, have also shown efficacy
in the treatment of DUSN.34,35

’ Lyme

Lyme disease is a multisystem disorder caused by the spirochete

Borrelia burgdorferi sensu lato. It is transmitted to humans by the
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124 ’ Dhoot et al

tick Ixodes scapularis and Ixodes pacificus. The white-footed mouse and
white-tailed deer are the preferred hosts of the I. scapularis, whereas
lizards are the preferred host for I. pacificus.6 Over 19,000 cases of
lyme disease were reported to the CDC in 2006, making it the most
common vector-borne illness in the United States. Most cases of lyme
disease occur in the Northeast, Mid-Atlantic, and upper Midwest
regions. Lyme disease is also endemic in areas of Asia and Europe.36
Despite the prevalence of lyme disease, ocular involvement is
uncommon.
Infection is divided into 3 clinical stages. Stage 1 follows infection
by the tick. A characteristic erythematous spreading rash (erythema
chronicum migrans) is seen, along with flu-like symptoms, and con-
junctivitis. Stage 2 occurs days to weeks after initial infection and is
characterized by cardiac and neurologic involvement. Cardiac involve-
ment includes acute myocarditis. Neurologic disease includes cranial
nerve palsies (7th is most common), meningitis, and radiculoneuro-
pathy. Stage 3 represents chronic disease and is associated with arthritis,
chronic fatigue, and chronic neurologic symptoms. Ocular involvement
during stage 3 includes granulomatous uveitis, vitritis, intermediate
uveitis, diffuse choroiditis, and panophthalmitis. Ischemic optic neuro-
pathy, optic papillitis, retrobulbar neuritis, and idiopathic intracranial
hypertension have also been reported.36
Diagnosis of lyme disease can be challenging given the clinical
variability. History, clinical examination, and ancillary testing are all
useful. Indirect fluorescent antibody or ELISA is used to measure
antibody titers to Borrelia burgdorferi. Confirmatory testing is performed
with Western blot for patients with positive antibody titers.
Antibiotic choice in the treatment of lyme disease depends on the
stage. Oral antibiotics are used in early stage disease, whereas IV
antibiotics are used in later stages. Ceftriaxone, penicillin, tetracycline,
doxycycline, and erythromycin have all been reported to have efficacy.
Retreatment may be necessary in cases of chronic inflammation or
recurrent infection. Topical steroids and mydriatics can be used
for anterior segment inflammation. Systemic steroid use is contro-
versial as it has been associated with an increase in antibiotic treatment
failure.6

’ Tuberculosis

Tuberculosis (TB) is caused by Mycobacterium tuberculosis, an acid-fast

bacillus. An estimated one-third of the world’s population is infected
with TB; most of these patients are in developing nations.37 TB is most
commonly transmitted through aerosolized droplets. The majority of
patients harbor subclinical disease, whereas only 10% of those infected
become symptomatic.
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 Pediatric Infectious Posterior Uveitis ’ 125

TB most commonly involves the respiratory tract but can affect

nearly every organ system in the body, including the eye. Characteristic
systemic symptoms include fever, night sweats, and weight loss. Ocular
TB can be separated into primary cases, where the eye is the source of
infection, and secondary cases, where the eye becomes infected through
hematogenous spread from a systemic source. Intraocular TB can
present as acute or chronic granulomatous uveitis. The most common
intraocular findings of TB are choroidal tubercles and tuberculomas.
Intermediate uveitis, vitritis, macular edema, retinal vasculitis, neuro-
retinitis, multifocal choroiditis, and endophthalmitis are also associated
with ocular TB.38
Timely diagnosis of ocular TB is critical, as vision loss can be
profound. The majority of patients with ocular TB do not have a history
of respiratory or systemic TB, making diagnosis difficult. Purified
protein derivative (PPD) testing is helpful when clinical suspicion is
high, although a positive test can be seen with prior exposure to TB
and is not diagnostic of active TB.6 Prior bacilli Calmette-Guerin
(BCG) vaccination can confound PPD testing, but this effect declines
over the first 7 years of life. Moreover, induration greater than 14 mm is
unlikely to be because of prior BCG vaccination.39 New testing methods
are less susceptible to the confounding effects of BCG and include
QuantiFeron-TB Gold assay and enzyme-linked immunospot assay.
These tests may be more specific than the PPD. ELISA serologic testing
and specimen PCR are alternate diagnostic assays used to aid in
diagnosis.38
Treatment of TB involves multidrug therapy for 6 to 9 months.
Isoniazid, rifampin, and pyrazinamide are administered daily for 2
months, followed by isoniazid and rifampin for an additional 4 to 7
months. Ethambutol or streptomycin can be added in cases of drug
resistance. Oral corticosteroid is often added to help to reduce the
inflammatory component of TB.6,38

’ Rare Causes of Infectious Posterior Uveitis

Brucellosis is a worldwide zoonotic disease that is seen relatively

infrequently in the United States. Human infection occurs through the
ingestion of unpasteurized milk and dairy products, and raw meat.40
Pediatric cases of brucellosis make up 3% to 10% of total reported cases
worldwide.3 Clinical presentation of brucellosis is broad and nearly
every organ system can be affected. Infection can be acute or chronic.
Symptoms include fever, chills, headache, arthralgia, myalgia, and
hepatosplenomegaly. Ophthalmic findings are also varied and include
uveitis, keratoconjunctivitis, episcleritis, optic neuritis, and endophthal-
mitis.40 Diagnosis of brucellosis is most commonly made through
serologic testing, this includes ELISA, PCR, and the agglutination test.
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126 ’ Dhoot et al

The World Health Organization recommends a multidrug antimicrobial

regimen, for adults and children above 8 years of age. This consists of
doxycycline and rifampin or doxycycline and streptomycin. For children
below 8 years of age, rifampin and trimethoprim-sulfamethoxazole is
recommended.3
Onchocerciasis, also known as river blindness, is caused by the
nematode Onchocerca volvulus. Transmission to humans results from
the bite of the Simulium exiguum fly, which breeds in fast-moving
waters. Worldwide, onchocerciasis is a public health threat, and is the
second leading cause of infectious blindness. Vision loss is because of
punctuate or sclerosing keratitis. Peripheral chorioretinal lesions,
vascular sheathing, and optic atrophy are associated clinical findings.
Diagnosis is made through identification of microfilaria in skin biopsy.
Management is with ivermectin, or suramin in those cases resistant
to ivermectin.41,42

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