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Dr.Yogita Mistry
GMC,Surat
Ocular Parasitic Infections
Ocular parasitosis
Lesions in the eye by parasite
can be due to:
ď‚—Damage directly caused by the infectious pathogen,
ď‚—Indirect pathology caused by toxic products,
ď‚—Immune response incited by infections,
ď‚—Ectopic parasitism of the preadult or adult stages,
ď‚—Antiparasitic drug treatments.
Parts of the Eye
List of ocular parasitic
infections:
ď‚—Protozoan Eye Infection
ď‚—Acanthamoeba Keratitis
Chagas’ Disease
ď‚—Leishmaniasis
ď‚—Toxoplasmosis
ď‚—Giardiasis
ď‚—Malaria
ď‚—Microsporidiosis
ď‚—Rhinosporidiosis
ď‚—Helminthic Eye Infection
ď‚—Onchocerciasis (River Blindness)
ď‚—Loiasis
ď‚—Toxocariasis
ď‚—Angiostrongyliasis
ď‚—Bancroftian and Brugian Filariasis
ď‚—Dirofilariasis
ď‚—Cysticercosis
ď‚—Hydatid Cyst
ď‚—Fascioliasis.
ď‚—Ocular Infestation caused by Ectoparasites
ď‚—Myiasis
ď‚—Phthiriasis Palpebrum
ď‚—Tick Infestation.
ď‚—Eye Infections by Protozoa
Acanthamoeba Keratitis
ď‚—Ubiquitous free-living protozoa
ď‚—Habitat: Soil, bottled water,
eyewash stations, and air.
ď‚—Two stages in the life cycle : the
motile trophozoite (8–40 m)μ
and the dormant cyst (8–29 μm).
ď‚—Leading risk factors for
ď‚—Acanthamoeba keratitis:
ď‚—Contact-lens wear (>80%)
ď‚— Storing and handling lenses improperly
ď‚— Disinfecting lenses improperly (such as using tap water or topping off
solutions when cleaning the lenses or lens case)
ď‚— Swimming, using a hot tub, or showering while wearing lenses
ď‚— Coming into contact with contaminated water
ď‚—
ď‚—In the United States, an estimated 85% of cases occur in contact
lens users. The incidence of the disease in developed countries
is approximately one to 33 cases per million contact lens
wearers. (CDC)
ď‚—Corneal trauma
ď‚—Exposure with contaminated water in eye
Clinical manifestation of
Acanthamoeba keratitis:
ď‚—Severe pain ,
ď‚—Eyelid ptosis,
ď‚—Conjunctival hyperemia,
ď‚—Epithelial ulcers,
ď‚—Lack of discharge.
ď‚—Typically presents as a unilateral central or paracentral corneal
infiltrate, often followed by the appearance of a ring-like stromal
infiltrate in the later stages of disease.
ď‚—Acanthamoeba keratitis can progress to scleritis, and, in severe
cases, uncontrolled infections require the removal of the affected
eye.
Diagnosis:
ď‚—Provisional diagnosis: By history, clinical features
ď‚—Confirm diagnosis:
ď‚—Sample: Corneal scraping or biopsy
ď‚—Microscopy: Wet mount preparation, Giemsa or PAS
ď‚—Culture: Nutrient agar plate with washed E.coli or E.aerogens, incubate at
30ËšC.
ď‚—PCR
Treatment:
ď‚—Difficult and disappointing
ď‚—Long term topical application of propamide, Miconazole,
Neomycin
ď‚—Surgical debridment.
Chagas’disease
ď‚—Cause by hemoflagellate Trypanosoma cruzi
ď‚—Endemic disease in central and south America
ď‚—Caused by bite of Triatomine bug bite
ď‚—Usually involves reticuloendothelial system.
ď‚—Chagas disease is endemic throughout much of Mexico,
Central America, and South America where an estimated 8
million people are infected.
ď‚— The triatomine bug thrives under poor housing conditions
(for example, mud walls, thatched roofs), so in endemic
countries, people living in rural areas are at greatest risk for
acquiring infection.
ď‚—Ocular infection occurs by bite of
triatomine bug near orbit
ď‚—More common in children
ď‚—Symptoms:
ď‚— Palpebral and periorbital edema
which is painless and inflammed
(Romana’s sign).
ď‚—Fever, anorexia, malaise.
Diagnosis:
ď‚—History of bite by bug
ď‚—Blood examination:
ď‚—Wet mount examination
ď‚—Giemsa stain: Trypomastigote of T.cruzi (only in acute cases)
ď‚—Culture: Into NNN medium
ď‚—PCR: can detect as few as 1 trypomastigote in 20 ml of blood
ď‚—Xenodiagnosis: Triatomine bug are fed on patients and then
their blood is examined after 2 wks.
ď‚—Animal inoculation: Mice intraperitonially
ď‚—Serology : Not commonly used.
Treatment:
ď‚—Nifurtimox
ď‚—Benznidazole for 1 months
Leshmaniasis:
ď‚—Tissue flagellate, vector: sand fly
As an ocular
manifestation of visceral
leshmaniasis
As a cutaneous
leshmaniasis
ď‚—Rare.
ď‚—Leads to keratitis, Papillitis,
Chorioretinitis, Central
retinal vein thrombosis,
Flame shaped retinal
hemmorrage
ď‚—Glucoma after successful
treatment.
ď‚—Due to intial bite of female
sand fly near eye with
occasional spread to lacrimal
duct
ď‚—Ptosis- presenting complain
ď‚—If conjunctival mucosa
involve- mucocutaneous
leshmaniasis —sever
ulceration
Cutaneous lesions
L.Tropica L.major
ď‚—Urban cutaneous
leshmainasis/ Oriental
sore/ Delhi boil
ď‚—Less in number
ď‚—Dry
ď‚—More swollen
ď‚—Less necrotic
ď‚—Exudate: less profuse,
thick
ď‚—Rural cutaneous
leshmaniasis
ď‚—Found in area where
gerbil, fat sand rat and sand
fly are present.
ď‚—Wet lesion
ď‚—More exudative and
necrotic
ď‚—More in number
Differential diagnosis for
cutaneous leishmaniasis
ď‚—Insect site, Eczema, Malignancy,Cutaneous tuberculosis, and
other cutaneous disorders.
ď‚— Early detection of the infection is necessary in order to start
effective treatment and prevention from inappropriate
prescribing of drugs.
ď‚—In an endemic area and in a traveler from endemic area, it is
neccessary for the physician to beaware that any atypical
lesion should be surveyed for cutaneous leishmaniasis and
treated with meglumine antimonate if is necessary.
Diagnosis
Sample: Blood, Lesions: edge, Tissue biopsy
Microscopy: Amastigote form
Treatment
Pentavalent antimony, sodium stibogluconate 15–20 mg per
kg per day IM or IV for 15–20 days.
ď‚— A second or even a third treatment course with pentavalent
antimonal can be given over 6–8 weeks if healing is not
progressive.
Toxoplasmosis
ď‚—It represents commonest cause of uveitis worldwide.
ď‚—Its lifecycle passes through cats.
ď‚—Human infection occurs through ingestion of food or water
contaminated with cat faeces.
ď‚—Most commonly occurs in childhood.
Ocular toxoplasmosis
ď‚—Most cases-not present with eye signs
ď‚—In few cases- focal necrotising retinitis occasionally associated
with vascular occlusion. Usually self limiting, recover by it
self. Relapses are relatively common, occurring in around
80% of patients
ď‚—Toxoplasmosis in immunosuppressed patients- multiple,
widespread lesions of differing chronicity and look different
from classical toxoplasmosis.
ď‚—Vitritis
ď‚—Common feature
ď‚—Leads to symptomatic haze and floaters that lasts for months
after the resolution of the acute attack.
ď‚—In pregnancy:
ď‚—Congenital infection of the newborn.
ď‚—Transmission: 15-20% in first trimester ( still birth and CNS
abnormanlity), 30-45% in second( less severe) and 60-65%
in third trimester.
ď‚—Chorioretinitis
ď‚— Involvement of the macula is common in the developing
foetus and has devastating effects on central vision.
ď‚— Bilateral ocular involvement is common, and both maculae
can be affected.
Diagnosis:
ď‚—Serologic tests: Very important in the diagnosis.
ď‚—Sabin-Feldman dye test:
ď‚—Latex agglutination test
ď‚—IHA
IFAA: IgM –IFA : titre of 1:64
ď‚—IgM ELISA: titre of 1:256
ď‚—Other test:
ď‚—Microscopy: Giemsa, PAS: Tachyzoites
ď‚—Animal inoculation: mice , intraperitonially
ď‚—PCR
ď‚—Treatment:
ď‚—Pyrimethamine+ sulphadiazine
Malaria
ď‚—Ocular manifestations due to :
ď‚— Severe infection and due to chloroquine
treatment
ď‚—Signs of falciparum malaria in eye
includes:
ď‚—Retinal whitening
ď‚—Retinal heamorrage
ď‚—Papilloedema (poor outcome in children with cerebral
malaria)
ď‚—Cotton wool spots
ď‚—Study shown that retinopathy finding was
associated with subsequent death/ fatal
outcomes of patients.
Chloroquine therapy:Bull’s eye maculopathy
Microsporidiosis
ď‚—Microsporidial keratitis: Literature review and report of 2
cases in a tertiary eye care center. Hind M, Sultan A,
Sreedharan A.
ď‚—Saudi Journal Of Opthalmology, (2012) 26,199-203.
ď‚—keratoconjunctivitis form which is mostly seen in
immunocompromised individuals and stromal keratitis form
seen in immunocompetent individuals. The ocular cases
which present with superficial keratitis in acquired immune
deficiency syndrome (AIDS) patients differ from the cases
seen in immunocompetent individuals which present mainly
as deep stromal keratitis
Ocular infection
ď‚—By direct inoculation into eye structures or by dissemination
systemically.
ď‚—Ocular findings: limited to the conjunctiva and cornea.
ď‚—Diagnosis: spores have been demonstrated in most cases in
which corneal scrapings or biopsy specimens.
ď‚—Treatment: Albendazole
Giardiasis.
Ocular complications, including “salt and pepper” retinal changes.
ď‚—One study showed that asymptomatic, non progressive retinal
lesions are particularly common in younger children with
giardiasis.
ď‚—This risk does not seem to be related to the severity of the
infection, its duration, or the use of metronidazole but may reflect
a genetic predisposition.
ď‚—Diagnosis is confirmed by finding the cyst stage in the fecal smear.
ď‚—Treatment is metronidazole.
Rhinosporidiosis.
ď‚—Caused by Rhinosporidium
seeberi
ď‚—Chattisgarh South India, Sri Lanka
and tropical South America.
ď‚—Ocular infection present as
conjunctival granuloma. (15%)
ď‚—Increased tearing, Photophobia,
Pink to red polyp which bleeds
easily on manipulation.
ď‚—Diagnosis: Several round to oval
sporangia and spores
ď‚—Treatment: surgical excision.
ď‚—Some authors proposed a medical
therapy with dapsone, but the
results are not convincing.
ď‚—Antimicrobial therapy is
ineffective, and the disease may
recur after months or years.
ď‚—Ocular helminthic
infection:
Angiostrongyliasis:
ď‚—Causative agent: Angiostrongylus cantonensis.
ď‚—
ď‚—Australia and Southeast Asia.
ď‚—Its definitive host is rat (pulmonary artery, right ventricle of rat), intermediate
host is molluscs (snails, slugs)
ď‚—Human is an accident host. Human get infection by ingestion of raw or
undercooked intermediate host, water of food contaminated by third stage larva.
It causes Eosinophilic meningoencephalitis.
ď‚—Third stage larva in human are found in brain, move anterierly in orbit and finally
penetrate the eye via cribriform plate.
ď‚—Adult worm may found in anterier chamber, retina and other site.
ď‚—Symptoms: Visual impairment. No dominant affected eye can be reported due to
non specific pattern of parasitic movement.
ď‚—Diagnosis:
ď‚—Any patient with visual impairment with a history of eating
raw pila spp. snails with or without eosinophilic meningitis
should be suspected for it.
ď‚—Treatment:
ď‚—Any type of laser, surgical removal, corticosteroids show no
improvement in visual acuity. These is due to alteration of
retinal pigment epithelium/ retinal inflammation caused
directly by parasite.
ď‚—No specific anti helminthic therapy is effective.
Loiasis:
ď‚—Causative agent: Loa loa/ Eye worm
ď‚—Central & western part of tropical Africa
ď‚—Infection in human due to bite of female mango fly(Chrysops
spp.) from which larva migrate in human and converted to
mature adult worm over 1 year.
ď‚—Adult: Subcutenous and subconjunctival tissue
ď‚—Microfilaria: Blood
ď‚—Diurnal periodicity
ď‚—Ocular disease is due to both
microfilaria and presence of adult
worm.
ď‚—Worm : discomfort, edema of
eyelid, granulomata of bulbar
conjunctiva( solitary or multiple
yellow nodules), proptosis
ď‚—Diagnosis:
ď‚—Detection of microfilaria in circulation.
ď‚—Extraction of adult worm from conjunctiva confirms
diagnosis.
ď‚—Treatment:
ď‚—Mannual removal of adult worm present in conjuctiva +
Diethylcarbamazine.
ď‚—Sever hypersensitivity response may occur due to killing of
larva and adult worms.
Onchocerciasis
(River blindness)
ď‚—Human is main reservoir.
ď‚—Cause by infected female blackfly ,
Simulinum spp. that require fast
flowing water for their breeding
and development.
So disease is limited to area adjacent to River system.
ď‚—Mainly found in Sun saharan Africa and South america.
ď‚—Blackfly mainly bites over bony prominence and leads to
Onchocercoma- firm, nontender nodule.
ď‚—It releases microfilaria at the site of bite from which adult worm
develop.
ď‚—Adult: Subcutaneous connective tissue
ď‚—Microfilaria: Skin (not in blood)
ď‚—Ocular onchocerciasis:
ď‚—Due to presence and/or migration of microfilaria in and through
ocular structure as well as the host response to the migration.
ď‚—5 predominent ocular finding:
ď‚—Punctate keratitis
ď‚—Sclerosing keratitis
ď‚—Iridocyclitis
ď‚—Chorioretinitis
ď‚—Optic atrophy ( blindness)
ď‚—Diagnosis:
ď‚—Slit lamp examination: Presence of live
microfilaria in anterior chamber.
ď‚—Sclerocorneal punch biopsy: presence
of microfialria
ď‚—Provocative test (Mazzotti test): 50 mg
diethycarbamazine-development of
pruritus and rash within 24 hours.
ď‚—Rarely in blood/urine.
ď‚—PCR
ď‚—Xenodiagnosis.
ď‚—Treatment:
ď‚—Diethylcarbamazepine- Active against microfilaria only.
ď‚—Ivermectin: Drug of choice.
ď‚—Mass distribution of Ivermectin by WHO onchocerciasis
control has lead to dramatic improvement in disease control
to some extent.
Dirofilariasis.
ď‚—Parasite of dog .
ď‚—Dirofilarial zoonotic infections.
ď‚—Transmitted by mosquito vectors.
“Emergent zoonosis .
ď‚—Human cases reported in USA, Japan, subtropical and warm climates
of world with pulmonary granulomatous lesions.
ď‚—Subcutaneous nodule formation due to host inflammatory response to
worm, which are found on areas with exposed skin and are hard and
elastic.
Ocular dirofilariasis
ď‚—When nodules are near ocular area or in conjunctiva
ď‚—Development of granulomatous reaction, abcess formation
and expulsion of parasite
ď‚—The diagnosis of dirofilariasis is established
histopathologically.
ď‚— Treatment: Complete removal of larva
Toxocariasis
ď‚—Visceral larva migrans is produced by larva of Toxocara
canis.
ď‚—Important cause of unilateral visual loss and leukocoria in
infants.
ď‚—Palpebral edema with conjuctival erythema develops when
lesions developed near the eye.
ď‚—Treatment:
ď‚—Surgical removal
ď‚—Albendazole
ď‚—Topical corticosteroids
Cysticercosis
ď‚—Cause by Taenia solium.
ď‚—Worldwide in distribution
ď‚—Often asymptomatic though neurological symptoms
predominantly seizures—are the most common manifestation.
ď‚—Ocular involvement is well recognised and includes orbital,
intraocular, subretinal, and optic nerve lesions .
ď‚—Cysticercosis can be evident as a free-floating cyst with amoeboid
movements within the vitreous or anterior chamber of the eye.
ď‚— Gaze palsies may also occur secondary to intramuscular cysts or
cranial nerve lesions from intracerebral cysts.
ď‚—Diagnosis depends on imaging with ultrasound, MRI, and CT
scanning all being useful, depending on the location of the cysts.
ď‚— Serology can be useful but in cases of isolated cysts may be
negative.
ď‚—Treatment is largely with the antihelminthic albendazole.
ď‚—Antihelminthic therapy may lead to an increased inflammatory
reaction around the lesions, and for this reason corticosteroids
are often used when treating neurological or ocular disease.
ď‚—Spontaneous extrusion of cysts from the orbit may occur, and
surgery may be required for isolated ocular lesions when they are
growing and causing visual loss.
Fascioliasis.
ď‚—Fasciola hepatica is a zoonotic helminth that is prevalent in most sheep-
raising countries.
ď‚—The biliary duct of the liver is the main site of establishment of the
parasite. However, immature flukes may deviate during migration,
entering other organs, and causing an ectopic infestation.
ď‚— In humans, ectopic locations in the orbit have been reported.
Identification of the route of entry of the parasite larva into the anterior
chamber of the eye is difficult. One possible route can be via the central
retinal artery into the vitreous, causing vasculitis and endophthalmitis .
ď‚—Severe intraocular reaction, haemorrhage, diffuse vasculitis, and retinal
ischaemia of the patient may be caused as a result of the presence or
irritation of the parasite.
ď‚— Early vitrectomy and removal of the parasite resulted in a rapid
response, with reasonable final visual acuity.
Hydatid Cyst
Hydatid cysts are most commonly seen in the liver (60–
70%) and lungs (20%).
ď‚—Hydatid disease involving the orbit represents <1% of all
cases and requires surgical treatment.
ď‚—Definitive preoperative diagnosis is difficult. Laboratory and
immunologic tests are generally unhelpful.
ď‚—Orbital hydatid cysts usually appear as a well-defined, thin-
walled, oval shape lesions with fine peripheral rim
enhancement of their fibrous capsule after contrast medium
administration .
ď‚—Ocular Infestation
caused by Ectoparasites
ď‚—Myiasis
ď‚—By larvae of flies.
ď‚—Genera important to human myiasis include Dermatobia, Gasterophilus,
Oestra, Cordylobia, Chrysomia, Wohlfahrtia, Cochliomyia, and
Hypoderma.
ď‚—Ophthalmomyiasis may be categorized into three categories:
ophthalmomyiasis externa, ophthalmomyiasis interna, and orbital
myiasis.
ď‚—Ophthalmomyiasis externa is due to larvae of the sheep nasal
botfly, Oestra ovis. A crawling or wriggling sensation
accompanied by swelling and cellulitis may be seen in palpebral
myiasis.
ď‚—Ophthalmomyiasis interna is most commonly caused by a
single larva of the Hypoderma spp.
ď‚— Infection is due to invasion of the tissues, leading to uveitis. More
serious complications may include lens dislocation and retinal
detachment.
ď‚—Orbital myiasis may be due to a number of fly species and is
generally seen in patients who are unable to care for themselves.
ď‚—Diagnosis of ophthalmomyiasis is made by demonstration of
maggots, and histologic examination may show granuloma
Phthiriasis Palpebrum
ď‚—Of these, medically important species include Pediculus humanus
var. corporis, the human body louse; Pediculus humanus var. capitis, the
human head louse; Phthirus pubis, the crab louse.
ď‚—Of the species mentioned, P. pubis is most likely to involve the
eyebrows and eye lashes.
ď‚—In addition to pruritis, small erythematous papules with evidence
of excoriation may be present.
ď‚— Eyelid disease is treated with a thick layer of petrolatum twice a
day for 8 days, or the application of 1% yellow oxide of mercury
four times a day for 2 weeks
Tick Infestation
ď‚—Ticks are arthropods belonging to the class Arachnida
ď‚—Ticks have been reported to attach to ocular structures.
ď‚— In one such case, the nymph was associated with a stinging
sensation.
ď‚—Following the removal of the tick, a firm nodule,
representing a tick bite granuloma, may remain for several
weeks. This granuloma likely represents retained tick
material and generally resolves spontaneously.
Summary:
Parasite Ocular manifestation
Acanthmoeba keratitis
T.cruzi Romana’s sign
Ocular cutaneous leshmanisis L.tropica, L.major (nodules)
Ocular manifestations of visceral
leshmaniasis
L.donovani
Toxoplasmosis Uveitis, Vitritis, Chorioretinits in infants
Plasmodium Choloquine-Bull’s eye maculopathy, Sever falciparum
infection: Papilloedema, cottonwool spots
Microsporidiosis Keratoconjunctivitis
Giardiasis Salt-pepper retinopathy
Angiostrogyliasis Granulomatous bulbar conjuctivitis
Onchocerciasis River blindness
Dirofilariasis Granulomatous infection
Ectoparasite Pruritus, papule formation
References:
ď‚—Ophthalmic Parasitosis: A Review Article. Amal R. N; Ahmed
S, and Ibrahim A A.Interdisciplinary Perspectives on Infectious
Diseases. Volume 2012, Article ID 587402, 12 pages.
ď‚—Ocular Parasitic Diseases: A Review on Toxocariasis and Diffuse
Unilateral Subacute Neuroretinitis.Rafael T. C; Gema R;
Lucienne C; Gian P G. Journal of Pediatric Ophthalmology &
Strabismus.
ď‚—CDC guidelines: Acanthmoeba keratitis, Ocular Leshmaniasis,
Loaisis, Onchocerciasis.
ď‚—Microsporidial keratitis: Literature review and report of 2 cases
in a tertiary eye care center. Hind M, Sultan A, Sreedharan
A.Saudi Journal Of Opthalmology, (2012) 26,199-203.
ď‚—Thank You

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Ocular parasitic infection

  • 3. Lesions in the eye by parasite can be due to: ď‚—Damage directly caused by the infectious pathogen, ď‚—Indirect pathology caused by toxic products, ď‚—Immune response incited by infections, ď‚—Ectopic parasitism of the preadult or adult stages, ď‚—Antiparasitic drug treatments.
  • 5. List of ocular parasitic infections: ď‚—Protozoan Eye Infection ď‚—Acanthamoeba Keratitis ď‚—Chagas’ Disease ď‚—Leishmaniasis ď‚—Toxoplasmosis ď‚—Giardiasis ď‚—Malaria ď‚—Microsporidiosis ď‚—Rhinosporidiosis
  • 6. ď‚—Helminthic Eye Infection ď‚—Onchocerciasis (River Blindness) ď‚—Loiasis ď‚—Toxocariasis ď‚—Angiostrongyliasis ď‚—Bancroftian and Brugian Filariasis ď‚—Dirofilariasis ď‚—Cysticercosis ď‚—Hydatid Cyst ď‚—Fascioliasis.
  • 7. ď‚—Ocular Infestation caused by Ectoparasites ď‚—Myiasis ď‚—Phthiriasis Palpebrum ď‚—Tick Infestation.
  • 9. Acanthamoeba Keratitis ď‚—Ubiquitous free-living protozoa ď‚—Habitat: Soil, bottled water, eyewash stations, and air. ď‚—Two stages in the life cycle : the motile trophozoite (8–40 m)ÎĽ and the dormant cyst (8–29 ÎĽm).
  • 10.
  • 11. ď‚—Leading risk factors for ď‚—Acanthamoeba keratitis: ď‚—Contact-lens wear (>80%) ď‚— Storing and handling lenses improperly ď‚— Disinfecting lenses improperly (such as using tap water or topping off solutions when cleaning the lenses or lens case) ď‚— Swimming, using a hot tub, or showering while wearing lenses ď‚— Coming into contact with contaminated water ď‚— ď‚—In the United States, an estimated 85% of cases occur in contact lens users. The incidence of the disease in developed countries is approximately one to 33 cases per million contact lens wearers. (CDC) ď‚—Corneal trauma ď‚—Exposure with contaminated water in eye
  • 12. Clinical manifestation of Acanthamoeba keratitis: ď‚—Severe pain , ď‚—Eyelid ptosis, ď‚—Conjunctival hyperemia, ď‚—Epithelial ulcers, ď‚—Lack of discharge. ď‚—Typically presents as a unilateral central or paracentral corneal infiltrate, often followed by the appearance of a ring-like stromal infiltrate in the later stages of disease. ď‚—Acanthamoeba keratitis can progress to scleritis, and, in severe cases, uncontrolled infections require the removal of the affected eye.
  • 13.
  • 14. Diagnosis: ď‚—Provisional diagnosis: By history, clinical features ď‚—Confirm diagnosis: ď‚—Sample: Corneal scraping or biopsy ď‚—Microscopy: Wet mount preparation, Giemsa or PAS ď‚—Culture: Nutrient agar plate with washed E.coli or E.aerogens, incubate at 30ËšC. ď‚—PCR
  • 15. Treatment: ď‚—Difficult and disappointing ď‚—Long term topical application of propamide, Miconazole, Neomycin ď‚—Surgical debridment.
  • 16. Chagas’disease ď‚—Cause by hemoflagellate Trypanosoma cruzi ď‚—Endemic disease in central and south America ď‚—Caused by bite of Triatomine bug bite ď‚—Usually involves reticuloendothelial system.
  • 17. ď‚—Chagas disease is endemic throughout much of Mexico, Central America, and South America where an estimated 8 million people are infected. ď‚— The triatomine bug thrives under poor housing conditions (for example, mud walls, thatched roofs), so in endemic countries, people living in rural areas are at greatest risk for acquiring infection.
  • 18.
  • 19. ď‚—Ocular infection occurs by bite of triatomine bug near orbit ď‚—More common in children ď‚—Symptoms: ď‚— Palpebral and periorbital edema which is painless and inflammed (Romana’s sign). ď‚—Fever, anorexia, malaise.
  • 20. Diagnosis: ď‚—History of bite by bug ď‚—Blood examination: ď‚—Wet mount examination ď‚—Giemsa stain: Trypomastigote of T.cruzi (only in acute cases) ď‚—Culture: Into NNN medium ď‚—PCR: can detect as few as 1 trypomastigote in 20 ml of blood ď‚—Xenodiagnosis: Triatomine bug are fed on patients and then their blood is examined after 2 wks. ď‚—Animal inoculation: Mice intraperitonially ď‚—Serology : Not commonly used.
  • 21.
  • 24.
  • 25.
  • 26. As an ocular manifestation of visceral leshmaniasis As a cutaneous leshmaniasis ď‚—Rare. ď‚—Leads to keratitis, Papillitis, Chorioretinitis, Central retinal vein thrombosis, Flame shaped retinal hemmorrage ď‚—Glucoma after successful treatment. ď‚—Due to intial bite of female sand fly near eye with occasional spread to lacrimal duct ď‚—Ptosis- presenting complain ď‚—If conjunctival mucosa involve- mucocutaneous leshmaniasis —sever ulceration
  • 27. Cutaneous lesions L.Tropica L.major ď‚—Urban cutaneous leshmainasis/ Oriental sore/ Delhi boil ď‚—Less in number ď‚—Dry ď‚—More swollen ď‚—Less necrotic ď‚—Exudate: less profuse, thick ď‚—Rural cutaneous leshmaniasis ď‚—Found in area where gerbil, fat sand rat and sand fly are present. ď‚—Wet lesion ď‚—More exudative and necrotic ď‚—More in number
  • 28. Differential diagnosis for cutaneous leishmaniasis ď‚—Insect site, Eczema, Malignancy,Cutaneous tuberculosis, and other cutaneous disorders. ď‚— Early detection of the infection is necessary in order to start effective treatment and prevention from inappropriate prescribing of drugs. ď‚—In an endemic area and in a traveler from endemic area, it is neccessary for the physician to beaware that any atypical lesion should be surveyed for cutaneous leishmaniasis and treated with meglumine antimonate if is necessary.
  • 29. Diagnosis Sample: Blood, Lesions: edge, Tissue biopsy Microscopy: Amastigote form
  • 30. Treatment ď‚—Pentavalent antimony, sodium stibogluconate 15–20 mg per kg per day IM or IV for 15–20 days. ď‚— A second or even a third treatment course with pentavalent antimonal can be given over 6–8 weeks if healing is not progressive.
  • 31. Toxoplasmosis ď‚—It represents commonest cause of uveitis worldwide. ď‚—Its lifecycle passes through cats. ď‚—Human infection occurs through ingestion of food or water contaminated with cat faeces. ď‚—Most commonly occurs in childhood.
  • 32.
  • 33. Ocular toxoplasmosis ď‚—Most cases-not present with eye signs ď‚—In few cases- focal necrotising retinitis occasionally associated with vascular occlusion. Usually self limiting, recover by it self. Relapses are relatively common, occurring in around 80% of patients ď‚—Toxoplasmosis in immunosuppressed patients- multiple, widespread lesions of differing chronicity and look different from classical toxoplasmosis. ď‚—Vitritis ď‚—Common feature ď‚—Leads to symptomatic haze and floaters that lasts for months after the resolution of the acute attack.
  • 34. ď‚—In pregnancy: ď‚—Congenital infection of the newborn. ď‚—Transmission: 15-20% in first trimester ( still birth and CNS abnormanlity), 30-45% in second( less severe) and 60-65% in third trimester. ď‚—Chorioretinitis ď‚— Involvement of the macula is common in the developing foetus and has devastating effects on central vision. ď‚— Bilateral ocular involvement is common, and both maculae can be affected.
  • 35.
  • 36. Diagnosis: ď‚—Serologic tests: Very important in the diagnosis. ď‚—Sabin-Feldman dye test: ď‚—Latex agglutination test ď‚—IHA ď‚—IFAA: IgM –IFA : titre of 1:64 ď‚—IgM ELISA: titre of 1:256 ď‚—Other test: ď‚—Microscopy: Giemsa, PAS: Tachyzoites ď‚—Animal inoculation: mice , intraperitonially ď‚—PCR ď‚—Treatment: ď‚—Pyrimethamine+ sulphadiazine
  • 37. Malaria ď‚—Ocular manifestations due to : ď‚— Severe infection and due to chloroquine treatment ď‚—Signs of falciparum malaria in eye includes: ď‚—Retinal whitening ď‚—Retinal heamorrage ď‚—Papilloedema (poor outcome in children with cerebral malaria) ď‚—Cotton wool spots ď‚—Study shown that retinopathy finding was associated with subsequent death/ fatal outcomes of patients.
  • 39. Microsporidiosis ď‚—Microsporidial keratitis: Literature review and report of 2 cases in a tertiary eye care center. Hind M, Sultan A, Sreedharan A. ď‚—Saudi Journal Of Opthalmology, (2012) 26,199-203. ď‚—keratoconjunctivitis form which is mostly seen in immunocompromised individuals and stromal keratitis form seen in immunocompetent individuals. The ocular cases which present with superficial keratitis in acquired immune deficiency syndrome (AIDS) patients differ from the cases seen in immunocompetent individuals which present mainly as deep stromal keratitis
  • 40. Ocular infection ď‚—By direct inoculation into eye structures or by dissemination systemically. ď‚—Ocular findings: limited to the conjunctiva and cornea. ď‚—Diagnosis: spores have been demonstrated in most cases in which corneal scrapings or biopsy specimens. ď‚—Treatment: Albendazole
  • 41. Giardiasis. ď‚—Ocular complications, including “salt and pepper” retinal changes. ď‚—One study showed that asymptomatic, non progressive retinal lesions are particularly common in younger children with giardiasis. ď‚—This risk does not seem to be related to the severity of the infection, its duration, or the use of metronidazole but may reflect a genetic predisposition. ď‚—Diagnosis is confirmed by finding the cyst stage in the fecal smear. ď‚—Treatment is metronidazole.
  • 42. Rhinosporidiosis. ď‚—Caused by Rhinosporidium seeberi ď‚—Chattisgarh South India, Sri Lanka and tropical South America. ď‚—Ocular infection present as conjunctival granuloma. (15%) ď‚—Increased tearing, Photophobia, Pink to red polyp which bleeds easily on manipulation. ď‚—Diagnosis: Several round to oval sporangia and spores ď‚—Treatment: surgical excision. ď‚—Some authors proposed a medical therapy with dapsone, but the results are not convincing. ď‚—Antimicrobial therapy is ineffective, and the disease may recur after months or years.
  • 44. Angiostrongyliasis: ď‚—Causative agent: Angiostrongylus cantonensis. ď‚— ď‚—Australia and Southeast Asia. ď‚—Its definitive host is rat (pulmonary artery, right ventricle of rat), intermediate host is molluscs (snails, slugs) ď‚—Human is an accident host. Human get infection by ingestion of raw or undercooked intermediate host, water of food contaminated by third stage larva. It causes Eosinophilic meningoencephalitis. ď‚—Third stage larva in human are found in brain, move anterierly in orbit and finally penetrate the eye via cribriform plate. ď‚—Adult worm may found in anterier chamber, retina and other site. ď‚—Symptoms: Visual impairment. No dominant affected eye can be reported due to non specific pattern of parasitic movement.
  • 45.
  • 46.
  • 47. ď‚—Diagnosis: ď‚—Any patient with visual impairment with a history of eating raw pila spp. snails with or without eosinophilic meningitis should be suspected for it. ď‚—Treatment: ď‚—Any type of laser, surgical removal, corticosteroids show no improvement in visual acuity. These is due to alteration of retinal pigment epithelium/ retinal inflammation caused directly by parasite. ď‚—No specific anti helminthic therapy is effective.
  • 48. Loiasis: ď‚—Causative agent: Loa loa/ Eye worm ď‚—Central & western part of tropical Africa ď‚—Infection in human due to bite of female mango fly(Chrysops spp.) from which larva migrate in human and converted to mature adult worm over 1 year. ď‚—Adult: Subcutenous and subconjunctival tissue ď‚—Microfilaria: Blood ď‚—Diurnal periodicity
  • 49.
  • 50. ď‚—Ocular disease is due to both microfilaria and presence of adult worm. ď‚—Worm : discomfort, edema of eyelid, granulomata of bulbar conjunctiva( solitary or multiple yellow nodules), proptosis
  • 51.
  • 52.
  • 53. ď‚—Diagnosis: ď‚—Detection of microfilaria in circulation. ď‚—Extraction of adult worm from conjunctiva confirms diagnosis. ď‚—Treatment: ď‚—Mannual removal of adult worm present in conjuctiva + Diethylcarbamazine. ď‚—Sever hypersensitivity response may occur due to killing of larva and adult worms.
  • 54. Onchocerciasis (River blindness) ď‚—Human is main reservoir. ď‚—Cause by infected female blackfly , Simulinum spp. that require fast flowing water for their breeding and development. So disease is limited to area adjacent to River system. ď‚—Mainly found in Sun saharan Africa and South america. ď‚—Blackfly mainly bites over bony prominence and leads to Onchocercoma- firm, nontender nodule. ď‚—It releases microfilaria at the site of bite from which adult worm develop.
  • 55. ď‚—Adult: Subcutaneous connective tissue ď‚—Microfilaria: Skin (not in blood)
  • 56.
  • 57. ď‚—Ocular onchocerciasis: ď‚—Due to presence and/or migration of microfilaria in and through ocular structure as well as the host response to the migration. ď‚—5 predominent ocular finding: ď‚—Punctate keratitis ď‚—Sclerosing keratitis ď‚—Iridocyclitis ď‚—Chorioretinitis ď‚—Optic atrophy ( blindness)
  • 58. ď‚—Diagnosis: ď‚—Slit lamp examination: Presence of live microfilaria in anterior chamber. ď‚—Sclerocorneal punch biopsy: presence of microfialria ď‚—Provocative test (Mazzotti test): 50 mg diethycarbamazine-development of pruritus and rash within 24 hours. ď‚—Rarely in blood/urine. ď‚—PCR ď‚—Xenodiagnosis.
  • 59. ď‚—Treatment: ď‚—Diethylcarbamazepine- Active against microfilaria only. ď‚—Ivermectin: Drug of choice. ď‚—Mass distribution of Ivermectin by WHO onchocerciasis control has lead to dramatic improvement in disease control to some extent.
  • 60. Dirofilariasis. ď‚—Parasite of dog . ď‚—Dirofilarial zoonotic infections. ď‚—Transmitted by mosquito vectors. “Emergent zoonosis . ď‚—Human cases reported in USA, Japan, subtropical and warm climates of world with pulmonary granulomatous lesions. ď‚—Subcutaneous nodule formation due to host inflammatory response to worm, which are found on areas with exposed skin and are hard and elastic.
  • 61.
  • 62.
  • 63. Ocular dirofilariasis ď‚—When nodules are near ocular area or in conjunctiva ď‚—Development of granulomatous reaction, abcess formation and expulsion of parasite ď‚—The diagnosis of dirofilariasis is established histopathologically. ď‚— Treatment: Complete removal of larva
  • 64. Toxocariasis ď‚—Visceral larva migrans is produced by larva of Toxocara canis. ď‚—Important cause of unilateral visual loss and leukocoria in infants. ď‚—Palpebral edema with conjuctival erythema develops when lesions developed near the eye. ď‚—Treatment: ď‚—Surgical removal ď‚—Albendazole ď‚—Topical corticosteroids
  • 65. Cysticercosis ď‚—Cause by Taenia solium. ď‚—Worldwide in distribution ď‚—Often asymptomatic though neurological symptoms predominantly seizures—are the most common manifestation. ď‚—Ocular involvement is well recognised and includes orbital, intraocular, subretinal, and optic nerve lesions . ď‚—Cysticercosis can be evident as a free-floating cyst with amoeboid movements within the vitreous or anterior chamber of the eye. ď‚— Gaze palsies may also occur secondary to intramuscular cysts or cranial nerve lesions from intracerebral cysts.
  • 66.
  • 67. ď‚—Diagnosis depends on imaging with ultrasound, MRI, and CT scanning all being useful, depending on the location of the cysts. ď‚— Serology can be useful but in cases of isolated cysts may be negative. ď‚—Treatment is largely with the antihelminthic albendazole. ď‚—Antihelminthic therapy may lead to an increased inflammatory reaction around the lesions, and for this reason corticosteroids are often used when treating neurological or ocular disease. ď‚—Spontaneous extrusion of cysts from the orbit may occur, and surgery may be required for isolated ocular lesions when they are growing and causing visual loss.
  • 68. Fascioliasis. ď‚—Fasciola hepatica is a zoonotic helminth that is prevalent in most sheep- raising countries. ď‚—The biliary duct of the liver is the main site of establishment of the parasite. However, immature flukes may deviate during migration, entering other organs, and causing an ectopic infestation. ď‚— In humans, ectopic locations in the orbit have been reported. Identification of the route of entry of the parasite larva into the anterior chamber of the eye is difficult. One possible route can be via the central retinal artery into the vitreous, causing vasculitis and endophthalmitis . ď‚—Severe intraocular reaction, haemorrhage, diffuse vasculitis, and retinal ischaemia of the patient may be caused as a result of the presence or irritation of the parasite. ď‚— Early vitrectomy and removal of the parasite resulted in a rapid response, with reasonable final visual acuity.
  • 69.
  • 70. Hydatid Cyst ď‚—Hydatid cysts are most commonly seen in the liver (60– 70%) and lungs (20%). ď‚—Hydatid disease involving the orbit represents <1% of all cases and requires surgical treatment. ď‚—Definitive preoperative diagnosis is difficult. Laboratory and immunologic tests are generally unhelpful. ď‚—Orbital hydatid cysts usually appear as a well-defined, thin- walled, oval shape lesions with fine peripheral rim enhancement of their fibrous capsule after contrast medium administration .
  • 71.
  • 73. ď‚—Myiasis ď‚—By larvae of flies. ď‚—Genera important to human myiasis include Dermatobia, Gasterophilus, Oestra, Cordylobia, Chrysomia, Wohlfahrtia, Cochliomyia, and Hypoderma. ď‚—Ophthalmomyiasis may be categorized into three categories: ophthalmomyiasis externa, ophthalmomyiasis interna, and orbital myiasis.
  • 74. ď‚—Ophthalmomyiasis externa is due to larvae of the sheep nasal botfly, Oestra ovis. A crawling or wriggling sensation accompanied by swelling and cellulitis may be seen in palpebral myiasis. ď‚—Ophthalmomyiasis interna is most commonly caused by a single larva of the Hypoderma spp. ď‚— Infection is due to invasion of the tissues, leading to uveitis. More serious complications may include lens dislocation and retinal detachment. ď‚—Orbital myiasis may be due to a number of fly species and is generally seen in patients who are unable to care for themselves. ď‚—Diagnosis of ophthalmomyiasis is made by demonstration of maggots, and histologic examination may show granuloma
  • 75. Phthiriasis Palpebrum ď‚—Of these, medically important species include Pediculus humanus var. corporis, the human body louse; Pediculus humanus var. capitis, the human head louse; Phthirus pubis, the crab louse. ď‚—Of the species mentioned, P. pubis is most likely to involve the eyebrows and eye lashes. ď‚—In addition to pruritis, small erythematous papules with evidence of excoriation may be present. ď‚— Eyelid disease is treated with a thick layer of petrolatum twice a day for 8 days, or the application of 1% yellow oxide of mercury four times a day for 2 weeks
  • 76. Tick Infestation ď‚—Ticks are arthropods belonging to the class Arachnida ď‚—Ticks have been reported to attach to ocular structures. ď‚— In one such case, the nymph was associated with a stinging sensation. ď‚—Following the removal of the tick, a firm nodule, representing a tick bite granuloma, may remain for several weeks. This granuloma likely represents retained tick material and generally resolves spontaneously.
  • 77. Summary: Parasite Ocular manifestation Acanthmoeba keratitis T.cruzi Romana’s sign Ocular cutaneous leshmanisis L.tropica, L.major (nodules) Ocular manifestations of visceral leshmaniasis L.donovani Toxoplasmosis Uveitis, Vitritis, Chorioretinits in infants Plasmodium Choloquine-Bull’s eye maculopathy, Sever falciparum infection: Papilloedema, cottonwool spots Microsporidiosis Keratoconjunctivitis Giardiasis Salt-pepper retinopathy Angiostrogyliasis Granulomatous bulbar conjuctivitis Onchocerciasis River blindness Dirofilariasis Granulomatous infection Ectoparasite Pruritus, papule formation
  • 78. References: ď‚—Ophthalmic Parasitosis: A Review Article. Amal R. N; Ahmed S, and Ibrahim A A.Interdisciplinary Perspectives on Infectious Diseases. Volume 2012, Article ID 587402, 12 pages. ď‚—Ocular Parasitic Diseases: A Review on Toxocariasis and Diffuse Unilateral Subacute Neuroretinitis.Rafael T. C; Gema R; Lucienne C; Gian P G. Journal of Pediatric Ophthalmology & Strabismus. ď‚—CDC guidelines: Acanthmoeba keratitis, Ocular Leshmaniasis, Loaisis, Onchocerciasis. ď‚—Microsporidial keratitis: Literature review and report of 2 cases in a tertiary eye care center. Hind M, Sultan A, Sreedharan A.Saudi Journal Of Opthalmology, (2012) 26,199-203.