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Parasitic Diseases of the Eye
Dr. Roopashree C R
JSS Hospital
Mysore
Ocular involvement is preeminent clinical feature in certain
systemic parasitic infections like
• onchocerciasis (river blindness)
• loaiasis (eye worm), and
• toxoplasmosis (retinochoroiditis).
Other systemic parasitic infections involving ocular structures are:
• microsporidia
• protozoa
• nematodes
• cestodes
• trematodes
• pentastomids
• protista
• Ectoparasites
Ocular pathology during systemic parasitic infections may be the result of:
• direct infection
• inflammation and necrosis
• space occupying lesions
• destruction secondary to migratory worms or larvae
• antiparasitic treatment
The epidemiology reflects:
• habitat of the causative parasites
• habits and health status of the patient.
Source of infection determined by:
• local sanitation
• presence of a vector for transmission
• intermitent and definitive hosts
• dietary history (food and water contamination)
• travel history to endemic areas
Classification:
I. SYSTEMIC MICROSPORIDIAL INFECTIONS:
Microsporidiosis
II.SYSTEMIC PROTOZOAL INFECTIONS:
1. Toxoplasmosis
2. Acanthamoebic infection
3. Malaria
4. African/American Trypanosomiasis
5. Leishmaniasis
6. Giardiasis
7. Rhinosporidiosis
III SYSTEMIC HELMINTHIC INFECTIONS:
A.Nematodes :
1. Onchocerciasis
2. Bancroftian and Brugian Lymphatic Filariasis
3. Loaiasis
4. Dirofilariasis
5. Toxocariasis
6. Baylisascariasis
7. Gnathostomiasis
8. Angiostrongyliasis
9. Dracunculosis
10.Ascariasis
11.Trichinosis
B. Cestodes:
1. Cysticercosis
2. Echinococcosis
3. Coenuriasis
4. Sparganosis
C. Trematodes:
1. Schistosomiasis
2. Paragonimiasis
3. Fascioliasis
IV SYSTEMIC PENTASTOMAL INFECTIONS:
1. Pentastomiasis
2. Myiasis
3. Protothecosis
Microsporidiosis
Causative agent: Encephalitozoon hellem and Nosema.
Various phases: growing–dividing (schizogenic) phase,
spore-forming (sporogenic) phase,
infectious spore phase
Mode of ocular infection: direct inoculation into eye structures
dissemination systemically (in AIDS patients).
Ocular findings: limited to the conjunctiva & cornea (epithelial surfaces)
Diagnosis: corneal scrapings or biopsy specimens (spores) & serology
Treatment: oral albendazole
Historically, severe, progressive cases of ocular microsporidiosis have resulted in enucleation.
Toxoplasmosis
Causative agent: Toxoplasma gondii
Lifecycle: cats (definitive host)
Mode of transmission: food or water contaminated with cat faeces, transplacentally or after
leukocyte transfusion & organ transplantation (Tachyzoites transported via lymphatics to eyes)
Most commonly affected age: childhood.
Ocular presentation: commonest cause of posterior uveitis worldwide.
During quiescent, asymptomatic stage: scarred, retinal lesions on fundoscopy
Most active cases are reactivation of congenital disease.
Active ocular toxoplasmosis in normal host: u/l painless DOV.
Ocular examination: u/l posterior uveitis - focal area of necrotizing chorioretinitis
hypopigmented ‘punched-out’ scar
vitritis (headlight in the fog)
lesions recur at distant site from the old scar or in the other eye
retinal tears & RD & RH
secondary glaucoma
optic neuritis
spill over anterior uveitis
Congenital toxoplasmosis: b/l, more severe (macula), microphthalmia, vitritis, glaucoma,
nystagmus, strabismus, and ocular palsies
Immunocompromised: b/l, multifocal and severe. Leading cause of necrotizing retinitis in
AIDS
Space-occupying lesions of the CNS: ocular palsies, nystagmus, and visual-field defects
Diagnosis: clinical, serology IgG or IgM, PCR and pathologic identification
Treatment: self-limited,
severe cases: combination of pyrimethamine + sulfa agents ( sulfadiazine) or
pyrimethamine and clindamycin for 3–6 weeks.
Atovaquone: active for tachyzoite and bradyzoite forms
immunocompromised: restoration of the immune system
lifelong therapy to prevent reactivation
congenital toxoplasmosis: long-term (for the first year of life) combination
therapy
pregnant women: Spiramycin
Malaria:
Causative agent: Plasmodium falciparum
Mode of transmission: Anopheles mosquito bite
Ocular findings: affects retinal vessels: retinal hemorrhages, edema & exudates at macula,
affects cerebral and ophthalmic vessels: intraocular infarction & hemorrhage
ocular palsies, ocular neuritis, cortical blindness & papilledema.
Concomitant herpes simplex keratitis
Antimalarial agent chloroquine: bull’s-eye maculopathy
Treatment: artemisinin combination therapy (ACT)
African Trypanosomiasis:
Causative agent: Sleeping sickness-Trypanosoma brucei gambiense and Trypanosoma brucei
rhodesiense
Mode of transmission: bite by infected tsetse fly (genus Glossina), infective metacyclic
trypomastigotes mature  gain access to systemic circulation eye
Ocular findings: interstitial keratitis,
uveitis
optic neuritis
conjunctival injection
mild eyelid edema
End-stage neuroencephalitis: papilledema, ophthalmoplegia, ptosis and optic neuropathy
Diagnosis: demo in aspirated lymph node fluid, blood, tissue sections or CSF and serology
Treatment: no CNS features: suramin, pentamidine or eflornithine
CNS features: melarsoprol with concomitant steroid therapy or elfornithine
American Trypanosomiasis:
Causative agent: Chaga’s disease Trypanosoma cruzi
Mode of transmission: feces of reduviid bugs while feeding  painless bite at night (face)
Ocular findings: Romaña’s sign: a painless, pronounced, unilateral, periorbital edema &
conjunctivitis (persist for many days)
lacrimal gland & preauricular & other regional lymph nodes may be enlarged
molecular mimicry by parasite antigens with rhodopsin – retinal dysfunction
Immunocompromised: reactivate as space occupying lesion of CNS  papilledema or
ophthalmoplegia
Treatment: systemic nifurtimox or benznidazole
Chronic disease refractory to therapy.
Leishmaniasis:
Causative agent: Leishmania species  systemic (visceral, kalaazar), cutaneous or
mucocutaneous (espundia)
Mode of transmission: bite of a sandfly
Ocular findings: keratitis
iritis
papillitis
chorioretinitis
b/l multifocal RH
b/l anterior uveitis
glaucoma
ulcerative lesions of the eyelids, conjunctivae & lacrimal glands
severe cases: entire eye is destroyed
Co-infected with HIV: destructive bilateral granulomatous uveitis
Treatment: liposomal amphotericin B
Acanthamoeba infection:
Ubiquitous free-living protozoa
life cycle: motile trophozoite & dormant cyst
Risk factors: contact-lens wear, corneal trauma, exposure to contaminated water
Ocular findings: Acanthamoeba keratitis with radial neuritis (severe pain disproportionate to
tissue damage)
unilateral central or paracentral corneal infiltrate (ring-shaped)
eyelid ptosis
conjunctival hyperemia
scleritis
uncontrolled infections enucleation
Diagnosis: clinical, confocal microscopy, culture(non-nutrientagar plate seeded with E coli),
histology, PCR & Giemsa or PAS.
Treatment: difficult & disappointing
Long-term topical application propamidine, miconazole & neomycin
Giardiasis:
Causative agent: Giardia lamblia
Mode of transmission: fecal–oral route
Ocular findings: iridocyclitis
choroiditis
retinal and subretinal hemorrhages
macular changes
host immunologic responses or nutritional deficiencies caused by Giardia-induced
malabsorption may have resulted in these ocular manifestations.
Onchocerciasis:
Causative agent: Onchocerca volvulus River blindness
Mode of transmission: bite of blackfly (genus Simulium), rivers and streams
Ocular findings: Microfilariae migrates: conjunctiva, cornea, anterior chamber, vitreal
humor, retina, choroid, and optic nerve
.
u/l marked inflammation  dead or dying microfilariae
anterior segment (Punctate keratitis, fluffy ‘snowflake’ corneal opacities and iritis)
posterior segment (chorioretinitis, papillitis, and optic atrophy)
granulomas
cataracts
secondary glaucoma
sclerosing keratitis (chronic, recurrent)
blindness
Diagnosis: clinical
analysis of skin snips
identification of the adult worm after surgical nodulectomy
serology
PCR
eosinophilia
On slit-lamp and fundoscopic examination: living microfilariae are transparent, coiled &
motileanterior chamber
dead microfilariae are opacified and straight
Inconclusive cases: evaluated by Mazzotti test: pruritus and inflammation develop in patients with
microfilariae after oral administration of a small dose of DEC.
Treatment: Ivermectin, single oral dose and repeated once or twice a year
Vector eradication & nodulectomy  prevention & treatment.
A large international program to limit onchocerciasis is currently under way in West Africa and is using both vector
eradication and mass chemotherapy.
Bancroftian and Brugian Lymphatic Filariasis:
Causative agent: Wuchereria bancrofti, Brugia malayi and Brugia timori
Mode of transmission: mosquitoes
Ocular findings: adult worm migrate to conjunctiva causing pain, chemosis, injection & foreign
body sensation
worms also seen in eyelid, lacrimal gland, AC, iris lens & subretina
chronic elephantiasis of the eyelid
Diagnosis: blood examination for microfilarial forms (nocturnal periodicity) & serology
Treatment: Ivermectin, albendazole, DEC (Mazzotti-type reactions)
surgical removal of the adult worm
Mansonella perstans Infection
Causative agent: M. perstans
Mode of transmission: biting of midges
Ocular findings: conjunctival nodule
proptosis
eyelid swelling
Diagnosis: microfilariae in blood or after surgical removal.
Treatment: Albendazole, mebendazole & surgical
Loaiasis:
Causative agent: Loa loa
Mode of transmission: large, day-feeding red fly Chrysops
Ocular findings: subconjunctival migration is most common (worms move -1cm/min foreign
body sensation)
mild conjunctival injection
transient visual disturbances
periorbital swelling & pruritus
adult worms in eyelid, anterior chamber, vitreous, or retina
calabar swelling of the eyelid
uveitis
Diagnosis: clinical
blood drawn btn 10.00 a.m. & 2.00 p.m  microfilariae
serology
eosinophilia
Treatment: albendazole,ivermectin,DCE,steroids,surgical removal or cryoprobes
Dirofilariasis:
Causative agent: Dirofilaria repens, Dirofilaria immitis
Definitive hosts: cats, dog. Humans are dead-end hosts
Mode of transmission: mosquitoes during feeding
Ocular findings: migratory worm in eyelid, subconjunctiva & intraocular structures foreign
body sensation, pruritus
nodule formation
uveitis
glaucoma
eyelid swelling
Diagnosis: after surgical resection of a cyst & serology
Treatment: surgical removal of the worm.
Toxocariasis:
Causative agent: Toxocara canis, Toxocara cati
Life cycle: dogs and feline-definitive hosts, humans represent a dead-end infection
Ocular findings: older children 8 -16 years
History of exposure to kittens or puppies
u/l granuloma-peripheral retina, near macula or on optic nerve
posterior pole lesions(white or gray rounded masses, 1-2 DD)
pars planitis
chronic endophthalmitis
vitritis, vitreous traction strands leading to the optic disk or granuloma
leukokoria
strabismus
TRD
CME
Diagnosis: eosinophilia, clinical features, serology (ELISA) for antibody titers
Differential diagnosis: retinoblastoma
1. unilateral mass in a young child: retinoblastoma (younger than 3 years) and
ocular toxocariasis (7 or 8 years of age or older)
2. USG, CT and MRI help to distinguish
Treatment: Asymptomatic- no chemotherapy
Albendazole, steroids
Vitreoretinal surgery
Baylisascariasis:
Causative agent: Baylisascaris procyonis
Life cycle: small birds & mammals-intermediate hosts
Mode of transmission: contaminated soil & water supplies
Ocular findings: Ocular larva migrans
retinal & subretinal tracts
retinal hemorrhages
chorioretinitis
vitritis
neuritis
Diagnosis: Serology for antigens
Treatment: Photocoagulation therapy to destroy intraretinal larvae
Gnathostomiasis:
Causative agent: Gnathostoma spinigerum
Life cycle: intermediate hosts-cyclops, fish, frogs, crayfish, crabs, eels and snakes
paratenic carrier hosts-fowl and pigs
Mode of transmission: eating raw or undercooked second intermediate or paratenic hosts
Ocular findings: edema & hemorrhage of eyelid
corneal ulcerations, iris perforation
subretinal holes, optic neuritis & retinal artery occlusion
uveitis
vitreal hemorrhage, vitritis
secondary glaucoma
CNS-cranial nerve palsies & papilledema
Diagnosis: Serology
Treatment: albendazole, ivermectin, steroids & mechanical removal
Angiostrongyliasis:
Causative agent: Angiostrongylus cantonensis (Parastrongylus cantonensis)
Life cycle: snails or slugs (intermediate hosts), transport hosts (crabs, crayfish, shrimp, cows, pigs &
humans)
Mode of transmission: ingesting snails or unwashed vegetables or intermediate transport hosts
Ocular findings: worms in AC, subretinal space & vitreous
blepharospasmlid edema
iridocyclitis
vitritis
RD, retinitis
CNS-papilledema, cranial nerve palsies or ptosis
exophthalmos extraocular palsies
neuritis both peripheral and optic
Treatment: spontaneous recovery, mebendazole, albendazole, levamisole, ivermectin, steroids and
analgesics. surgical removal
Dracunculosis:
Causative agent: Dracunculis medinensis(Guinea worm)
Mode of transmission: ingesting water contaminated with Cyclops crustacean
Ocular findings: adult female worm in conjunctiva-irritation & lacrimation
Treatment: mechanical removal of the worm, metronidazole
Ascariasis:
Causative agent: Ascaris lumbricoides
Ocular findings: rare
young adult worms present in NLD
Treatment: removed mechanically, systemic therapy with
albendazole, mebendazole, or pyrantel pamoate
Trichinosis:
Causative agent: Trichinella spiralis
Mode of transmission: ingesting infected raw or undercooked pigs & carnivores , larvae -
lymphatic & vascular circulation
Ocular findings: B/l palpebral edema
pain on eye movement
conjunctival chemosis & hemorrhages
photophobia
retinal hemorrhages
optic neuritis & edema
Diagnosis: serology or muscle biopsy
Treatment: self-limited, mebendazole, albendazole, steroids
symptomatic-cycloplegia, topical or local steroids, and cold compresses
Cysticercosis:
Causative agent: Cysticercus cellulosae, Taenia solium
Life cycle: Humans-definitive host, intermediate hosts-pigs and humans
Ocular findings: Ocular cysticercosis
cysts in vitreous, subretinal space, AC, iris, ciliary body & optic nerve
RD, retinal edema, retinal hemorrhage
chorioretinitis
vasculitis
adnexal structures-periorbital muscles, conjunctivae & lacrimal glands involved
CNS affection-cranial nerve dysfunction, ocular palsies & papilledema
Diagnosis: clinical, radiographical (CT or MRI), serological, CSF analysis & Stool examination
Treatment: Albendazole with periocular steroids, surgical removal
Echinococcosis:
Causative agent: Echinococcus granulosus, Echinococcus multilocularis
Life cycle: definitive host (canids), intermediate host (ungulate, rodent) invades via circulatory system
Ocular findings: cystic hydatid disease (cyst in orbital cavity)
bone erosion
proptosis
exposure keratitis & ulceration
conjunctival chemosis & injection
extensive lacrimation
impairment of extraocular mobility
optic atrophy
involvement of CNS-papilledema
intraocular cysts can replace the vitreous.
Diagnosis: clinical presentation, radiography & serology
Treatment: Albendazole & interventional aspiration or surgery
Coenuriasis:
Causative agent: Taenia multiceps & Taenia serialis
Life cycle: Herbivores-intermediate host
Mode of transmission: ingesting eggs passed by infected dogs
Ocular findings: space-occupying lesion(Ocular cysts) in extraocular muscles, conjunctiva &
eyelids
intraocular cysts in subretinal or intravitreal
intense inflammation
panophthalmitis
blindness
proptosis
exposure keratitis
corneal ulceration
Diagnosis: clinical presentation, radiographic imaging & histologic examination
Treatment: surgical
Sparganosis:
Causative agent: plerocercoid larvae of Spirometra species
Life cycle: Canines, felines (definitive hosts) & Cyclops, frogs, snakes & small animals
(intermediate hosts)
Mode of transmission: accidental drinking of contaminated water
eating raw or undercooked intermediate hosts
direct transfer of spargana (applied as a poultice to inflamed eyes, ulcers
or open wounds)
Ocular findings: worms in subconjunctiva & AC-pain, pruritus and lacrimation
periocular edema
proptosis
Diagnosis: after removal of the worm
Treatment: surgical removal, no systemic antiparasitic agent shown to be of benefit
Schistosomiasis:
Causative agent: blood flukes Schistosoma mansoni
Schistosoma haematobium
Schistosoma japonicum.
Life cycle: snail or mollusk intermediate hosts, eggs are released into venous circulation in humans
Ocular findings: Granulomatous responses occurs in conjunctiva, lacrimal gland, choroid and optic
nerve-optic atrophy
migrating worms- superior ophthalmic vein, AC
Diagnosis: eggs in stool, urine or biopsy material and Immunodiagnostic assays
Treatment: Praziquantel, ocular involvement is treated systemically.
Paragonimiasis:
Causative agent: Paragonimus westermani
Life cycle: definitive host (cat, dog, or primate) & intermediate hosts (snail, fresh water crabs,
shrimps or crayfish)
Mode of transmission: ingesting raw, undercooked, juices and fluids of intermediate hosts
Ocular findings: Mechanical damage by migrating worms-severe and recurrent
retinal hemorrhages
invasion of anterior chamber, eyelid and orbit
subluxation of the lens
uveitis
hypopyon
secondary glaucoma
Cerebral involvement - cranial nerve palsies & papilledema.
Diagnosis: eggs in sputum or feces, serology
Treatment: Praziquantel & surgical
Fascioliasis:
Causative agent: liver flukes Fasciola hepatica or F. gigantica
Life cycle: snail, human, animal – intermideate hosts
Ocular findings: ectopic locations in orbit
larvae in AC, vitreous viacentral retinal artery
vasculitis
endophthalmitis
intraocular haemorrhage
retinal ischaemia
Treatment: Early vitrectomy & removal of parasite, triclabendazole or bithionol
Pentastomiasis:
Causative agent: Linguatula serrate (tongue worm)
Life cycle: wormlike and arthropod-like characteristics, intermediate hosts (rodents, ungulates,
humans), humans are also dead-end definitive hosts
Ocular findings: wandering nymphs invades ocular tissues-AC
iritis
secondary glaucoma
Treatment: surgical removal
Myiasis:
Causative agent: Cochliomyia hominivorax
Gasterophilidae (‘horse bot fly’ or ‘horse warble fly’)
Wohlfahrtia magnifica (‘sheep maggot fly’)
Oestrus ovis (‘sheep bot fly’)
Chrysomyia bezziana (‘screw worm fly’)
Cordylobia anthropophaga (‘tumbu fly’)
Dermatobia hominis.
Mode of transmission: direct deposition of eggs by flies or by secondary vectors-mosquitoes
Ocular findings: larvae migrate through or across conjunctiva or eyelids
‘Ophthalmomyiasis externa’
invade deeper ocular structures ‘Ophthalmomyiasis interna’
conjunctivitis, keratitis, scleritis, iritis, vitritis, uveitis
subluxation of the lens
vitreal hemorrhage
retinal detachment, hemorrhages, retinal scarring and ‘tracks’
Treatment: Mechanical removal, laser photo-coagulation or with surgery
Topical & systemic steroids
Protothecosis:
Causative agent: Prototheca wickerhamii
Affects immunocompromised individuals
Ocular findings: vitritis
choroiditis
Diagnosis: blood culture, culture of lesion, discharge.
Treatment: involves reversal of immunosuppression
systemic amphotericin, triazole antifungal agents.
Thelaziasis:
Causative agent: T. callipaeda
Mode of transmission: nonbiting diptera that feed on the ocular secretions, tears, and
conjunctiva of animals.
Ocular findings : epiphora, conjunctivitis, keratitis, corneal opacity and ulcers,
mechanical damage to the conjunctival and corneal epithelium.
Diagnosis: after removal by morphology
Treatment: topical with thiabendazole has also, surgical
REFERENCES:
1. Albert and Jackobie
2. Amal R et al. Ophthalmic parasitosis: A review article. Hindawi journal. vol 2012,
Article ID 587402
3. Yanoff: Ophthalmology
4. Ocular microbiology by PK Mukherjee
THANK YOU

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Ophthalmic parasitology

  • 1. Parasitic Diseases of the Eye Dr. Roopashree C R JSS Hospital Mysore
  • 2. Ocular involvement is preeminent clinical feature in certain systemic parasitic infections like • onchocerciasis (river blindness) • loaiasis (eye worm), and • toxoplasmosis (retinochoroiditis).
  • 3. Other systemic parasitic infections involving ocular structures are: • microsporidia • protozoa • nematodes • cestodes • trematodes • pentastomids • protista • Ectoparasites
  • 4. Ocular pathology during systemic parasitic infections may be the result of: • direct infection • inflammation and necrosis • space occupying lesions • destruction secondary to migratory worms or larvae • antiparasitic treatment
  • 5. The epidemiology reflects: • habitat of the causative parasites • habits and health status of the patient. Source of infection determined by: • local sanitation • presence of a vector for transmission • intermitent and definitive hosts • dietary history (food and water contamination) • travel history to endemic areas
  • 6. Classification: I. SYSTEMIC MICROSPORIDIAL INFECTIONS: Microsporidiosis II.SYSTEMIC PROTOZOAL INFECTIONS: 1. Toxoplasmosis 2. Acanthamoebic infection 3. Malaria 4. African/American Trypanosomiasis 5. Leishmaniasis 6. Giardiasis 7. Rhinosporidiosis
  • 7. III SYSTEMIC HELMINTHIC INFECTIONS: A.Nematodes : 1. Onchocerciasis 2. Bancroftian and Brugian Lymphatic Filariasis 3. Loaiasis 4. Dirofilariasis 5. Toxocariasis 6. Baylisascariasis 7. Gnathostomiasis 8. Angiostrongyliasis 9. Dracunculosis 10.Ascariasis 11.Trichinosis
  • 8. B. Cestodes: 1. Cysticercosis 2. Echinococcosis 3. Coenuriasis 4. Sparganosis C. Trematodes: 1. Schistosomiasis 2. Paragonimiasis 3. Fascioliasis IV SYSTEMIC PENTASTOMAL INFECTIONS: 1. Pentastomiasis 2. Myiasis 3. Protothecosis
  • 9. Microsporidiosis Causative agent: Encephalitozoon hellem and Nosema. Various phases: growing–dividing (schizogenic) phase, spore-forming (sporogenic) phase, infectious spore phase Mode of ocular infection: direct inoculation into eye structures dissemination systemically (in AIDS patients). Ocular findings: limited to the conjunctiva & cornea (epithelial surfaces) Diagnosis: corneal scrapings or biopsy specimens (spores) & serology Treatment: oral albendazole Historically, severe, progressive cases of ocular microsporidiosis have resulted in enucleation.
  • 10.
  • 11. Toxoplasmosis Causative agent: Toxoplasma gondii Lifecycle: cats (definitive host) Mode of transmission: food or water contaminated with cat faeces, transplacentally or after leukocyte transfusion & organ transplantation (Tachyzoites transported via lymphatics to eyes) Most commonly affected age: childhood. Ocular presentation: commonest cause of posterior uveitis worldwide. During quiescent, asymptomatic stage: scarred, retinal lesions on fundoscopy Most active cases are reactivation of congenital disease. Active ocular toxoplasmosis in normal host: u/l painless DOV.
  • 12.
  • 13. Ocular examination: u/l posterior uveitis - focal area of necrotizing chorioretinitis hypopigmented ‘punched-out’ scar vitritis (headlight in the fog) lesions recur at distant site from the old scar or in the other eye retinal tears & RD & RH secondary glaucoma optic neuritis spill over anterior uveitis Congenital toxoplasmosis: b/l, more severe (macula), microphthalmia, vitritis, glaucoma, nystagmus, strabismus, and ocular palsies Immunocompromised: b/l, multifocal and severe. Leading cause of necrotizing retinitis in AIDS Space-occupying lesions of the CNS: ocular palsies, nystagmus, and visual-field defects
  • 14.
  • 15. Diagnosis: clinical, serology IgG or IgM, PCR and pathologic identification Treatment: self-limited, severe cases: combination of pyrimethamine + sulfa agents ( sulfadiazine) or pyrimethamine and clindamycin for 3–6 weeks. Atovaquone: active for tachyzoite and bradyzoite forms immunocompromised: restoration of the immune system lifelong therapy to prevent reactivation congenital toxoplasmosis: long-term (for the first year of life) combination therapy pregnant women: Spiramycin
  • 16. Malaria: Causative agent: Plasmodium falciparum Mode of transmission: Anopheles mosquito bite Ocular findings: affects retinal vessels: retinal hemorrhages, edema & exudates at macula, affects cerebral and ophthalmic vessels: intraocular infarction & hemorrhage ocular palsies, ocular neuritis, cortical blindness & papilledema. Concomitant herpes simplex keratitis Antimalarial agent chloroquine: bull’s-eye maculopathy Treatment: artemisinin combination therapy (ACT)
  • 17.
  • 18. African Trypanosomiasis: Causative agent: Sleeping sickness-Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense Mode of transmission: bite by infected tsetse fly (genus Glossina), infective metacyclic trypomastigotes mature  gain access to systemic circulation eye Ocular findings: interstitial keratitis, uveitis optic neuritis conjunctival injection mild eyelid edema End-stage neuroencephalitis: papilledema, ophthalmoplegia, ptosis and optic neuropathy Diagnosis: demo in aspirated lymph node fluid, blood, tissue sections or CSF and serology Treatment: no CNS features: suramin, pentamidine or eflornithine CNS features: melarsoprol with concomitant steroid therapy or elfornithine
  • 19. American Trypanosomiasis: Causative agent: Chaga’s disease Trypanosoma cruzi Mode of transmission: feces of reduviid bugs while feeding  painless bite at night (face) Ocular findings: Romaña’s sign: a painless, pronounced, unilateral, periorbital edema & conjunctivitis (persist for many days) lacrimal gland & preauricular & other regional lymph nodes may be enlarged molecular mimicry by parasite antigens with rhodopsin – retinal dysfunction Immunocompromised: reactivate as space occupying lesion of CNS  papilledema or ophthalmoplegia Treatment: systemic nifurtimox or benznidazole Chronic disease refractory to therapy.
  • 20.
  • 21. Leishmaniasis: Causative agent: Leishmania species  systemic (visceral, kalaazar), cutaneous or mucocutaneous (espundia) Mode of transmission: bite of a sandfly Ocular findings: keratitis iritis papillitis chorioretinitis b/l multifocal RH b/l anterior uveitis glaucoma ulcerative lesions of the eyelids, conjunctivae & lacrimal glands severe cases: entire eye is destroyed Co-infected with HIV: destructive bilateral granulomatous uveitis Treatment: liposomal amphotericin B
  • 22.
  • 23.
  • 24. Acanthamoeba infection: Ubiquitous free-living protozoa life cycle: motile trophozoite & dormant cyst Risk factors: contact-lens wear, corneal trauma, exposure to contaminated water Ocular findings: Acanthamoeba keratitis with radial neuritis (severe pain disproportionate to tissue damage) unilateral central or paracentral corneal infiltrate (ring-shaped) eyelid ptosis conjunctival hyperemia scleritis uncontrolled infections enucleation Diagnosis: clinical, confocal microscopy, culture(non-nutrientagar plate seeded with E coli), histology, PCR & Giemsa or PAS. Treatment: difficult & disappointing Long-term topical application propamidine, miconazole & neomycin
  • 25.
  • 26. Giardiasis: Causative agent: Giardia lamblia Mode of transmission: fecal–oral route Ocular findings: iridocyclitis choroiditis retinal and subretinal hemorrhages macular changes host immunologic responses or nutritional deficiencies caused by Giardia-induced malabsorption may have resulted in these ocular manifestations.
  • 27.
  • 28. Onchocerciasis: Causative agent: Onchocerca volvulus River blindness Mode of transmission: bite of blackfly (genus Simulium), rivers and streams Ocular findings: Microfilariae migrates: conjunctiva, cornea, anterior chamber, vitreal humor, retina, choroid, and optic nerve . u/l marked inflammation  dead or dying microfilariae anterior segment (Punctate keratitis, fluffy ‘snowflake’ corneal opacities and iritis) posterior segment (chorioretinitis, papillitis, and optic atrophy) granulomas cataracts secondary glaucoma sclerosing keratitis (chronic, recurrent) blindness
  • 29.
  • 30.
  • 31. Diagnosis: clinical analysis of skin snips identification of the adult worm after surgical nodulectomy serology PCR eosinophilia On slit-lamp and fundoscopic examination: living microfilariae are transparent, coiled & motileanterior chamber dead microfilariae are opacified and straight Inconclusive cases: evaluated by Mazzotti test: pruritus and inflammation develop in patients with microfilariae after oral administration of a small dose of DEC. Treatment: Ivermectin, single oral dose and repeated once or twice a year Vector eradication & nodulectomy  prevention & treatment. A large international program to limit onchocerciasis is currently under way in West Africa and is using both vector eradication and mass chemotherapy.
  • 32. Bancroftian and Brugian Lymphatic Filariasis: Causative agent: Wuchereria bancrofti, Brugia malayi and Brugia timori Mode of transmission: mosquitoes Ocular findings: adult worm migrate to conjunctiva causing pain, chemosis, injection & foreign body sensation worms also seen in eyelid, lacrimal gland, AC, iris lens & subretina chronic elephantiasis of the eyelid Diagnosis: blood examination for microfilarial forms (nocturnal periodicity) & serology Treatment: Ivermectin, albendazole, DEC (Mazzotti-type reactions) surgical removal of the adult worm
  • 33.
  • 34. Mansonella perstans Infection Causative agent: M. perstans Mode of transmission: biting of midges Ocular findings: conjunctival nodule proptosis eyelid swelling Diagnosis: microfilariae in blood or after surgical removal. Treatment: Albendazole, mebendazole & surgical
  • 35. Loaiasis: Causative agent: Loa loa Mode of transmission: large, day-feeding red fly Chrysops Ocular findings: subconjunctival migration is most common (worms move -1cm/min foreign body sensation) mild conjunctival injection transient visual disturbances periorbital swelling & pruritus adult worms in eyelid, anterior chamber, vitreous, or retina calabar swelling of the eyelid uveitis Diagnosis: clinical blood drawn btn 10.00 a.m. & 2.00 p.m  microfilariae serology eosinophilia Treatment: albendazole,ivermectin,DCE,steroids,surgical removal or cryoprobes
  • 36.
  • 37. Dirofilariasis: Causative agent: Dirofilaria repens, Dirofilaria immitis Definitive hosts: cats, dog. Humans are dead-end hosts Mode of transmission: mosquitoes during feeding Ocular findings: migratory worm in eyelid, subconjunctiva & intraocular structures foreign body sensation, pruritus nodule formation uveitis glaucoma eyelid swelling Diagnosis: after surgical resection of a cyst & serology Treatment: surgical removal of the worm.
  • 38.
  • 39. Toxocariasis: Causative agent: Toxocara canis, Toxocara cati Life cycle: dogs and feline-definitive hosts, humans represent a dead-end infection Ocular findings: older children 8 -16 years History of exposure to kittens or puppies u/l granuloma-peripheral retina, near macula or on optic nerve posterior pole lesions(white or gray rounded masses, 1-2 DD) pars planitis chronic endophthalmitis vitritis, vitreous traction strands leading to the optic disk or granuloma leukokoria strabismus TRD CME
  • 40.
  • 41. Diagnosis: eosinophilia, clinical features, serology (ELISA) for antibody titers Differential diagnosis: retinoblastoma 1. unilateral mass in a young child: retinoblastoma (younger than 3 years) and ocular toxocariasis (7 or 8 years of age or older) 2. USG, CT and MRI help to distinguish Treatment: Asymptomatic- no chemotherapy Albendazole, steroids Vitreoretinal surgery
  • 42. Baylisascariasis: Causative agent: Baylisascaris procyonis Life cycle: small birds & mammals-intermediate hosts Mode of transmission: contaminated soil & water supplies Ocular findings: Ocular larva migrans retinal & subretinal tracts retinal hemorrhages chorioretinitis vitritis neuritis Diagnosis: Serology for antigens Treatment: Photocoagulation therapy to destroy intraretinal larvae
  • 43.
  • 44. Gnathostomiasis: Causative agent: Gnathostoma spinigerum Life cycle: intermediate hosts-cyclops, fish, frogs, crayfish, crabs, eels and snakes paratenic carrier hosts-fowl and pigs Mode of transmission: eating raw or undercooked second intermediate or paratenic hosts Ocular findings: edema & hemorrhage of eyelid corneal ulcerations, iris perforation subretinal holes, optic neuritis & retinal artery occlusion uveitis vitreal hemorrhage, vitritis secondary glaucoma CNS-cranial nerve palsies & papilledema Diagnosis: Serology Treatment: albendazole, ivermectin, steroids & mechanical removal
  • 45. Angiostrongyliasis: Causative agent: Angiostrongylus cantonensis (Parastrongylus cantonensis) Life cycle: snails or slugs (intermediate hosts), transport hosts (crabs, crayfish, shrimp, cows, pigs & humans) Mode of transmission: ingesting snails or unwashed vegetables or intermediate transport hosts Ocular findings: worms in AC, subretinal space & vitreous blepharospasmlid edema iridocyclitis vitritis RD, retinitis CNS-papilledema, cranial nerve palsies or ptosis exophthalmos extraocular palsies neuritis both peripheral and optic Treatment: spontaneous recovery, mebendazole, albendazole, levamisole, ivermectin, steroids and analgesics. surgical removal
  • 46.
  • 47. Dracunculosis: Causative agent: Dracunculis medinensis(Guinea worm) Mode of transmission: ingesting water contaminated with Cyclops crustacean Ocular findings: adult female worm in conjunctiva-irritation & lacrimation Treatment: mechanical removal of the worm, metronidazole
  • 48. Ascariasis: Causative agent: Ascaris lumbricoides Ocular findings: rare young adult worms present in NLD Treatment: removed mechanically, systemic therapy with albendazole, mebendazole, or pyrantel pamoate
  • 49. Trichinosis: Causative agent: Trichinella spiralis Mode of transmission: ingesting infected raw or undercooked pigs & carnivores , larvae - lymphatic & vascular circulation Ocular findings: B/l palpebral edema pain on eye movement conjunctival chemosis & hemorrhages photophobia retinal hemorrhages optic neuritis & edema Diagnosis: serology or muscle biopsy Treatment: self-limited, mebendazole, albendazole, steroids symptomatic-cycloplegia, topical or local steroids, and cold compresses
  • 50.
  • 51. Cysticercosis: Causative agent: Cysticercus cellulosae, Taenia solium Life cycle: Humans-definitive host, intermediate hosts-pigs and humans Ocular findings: Ocular cysticercosis cysts in vitreous, subretinal space, AC, iris, ciliary body & optic nerve RD, retinal edema, retinal hemorrhage chorioretinitis vasculitis adnexal structures-periorbital muscles, conjunctivae & lacrimal glands involved CNS affection-cranial nerve dysfunction, ocular palsies & papilledema Diagnosis: clinical, radiographical (CT or MRI), serological, CSF analysis & Stool examination Treatment: Albendazole with periocular steroids, surgical removal
  • 52.
  • 53. Echinococcosis: Causative agent: Echinococcus granulosus, Echinococcus multilocularis Life cycle: definitive host (canids), intermediate host (ungulate, rodent) invades via circulatory system Ocular findings: cystic hydatid disease (cyst in orbital cavity) bone erosion proptosis exposure keratitis & ulceration conjunctival chemosis & injection extensive lacrimation impairment of extraocular mobility optic atrophy involvement of CNS-papilledema intraocular cysts can replace the vitreous. Diagnosis: clinical presentation, radiography & serology Treatment: Albendazole & interventional aspiration or surgery
  • 54.
  • 55. Coenuriasis: Causative agent: Taenia multiceps & Taenia serialis Life cycle: Herbivores-intermediate host Mode of transmission: ingesting eggs passed by infected dogs Ocular findings: space-occupying lesion(Ocular cysts) in extraocular muscles, conjunctiva & eyelids intraocular cysts in subretinal or intravitreal intense inflammation panophthalmitis blindness proptosis exposure keratitis corneal ulceration Diagnosis: clinical presentation, radiographic imaging & histologic examination Treatment: surgical
  • 56. Sparganosis: Causative agent: plerocercoid larvae of Spirometra species Life cycle: Canines, felines (definitive hosts) & Cyclops, frogs, snakes & small animals (intermediate hosts) Mode of transmission: accidental drinking of contaminated water eating raw or undercooked intermediate hosts direct transfer of spargana (applied as a poultice to inflamed eyes, ulcers or open wounds) Ocular findings: worms in subconjunctiva & AC-pain, pruritus and lacrimation periocular edema proptosis Diagnosis: after removal of the worm Treatment: surgical removal, no systemic antiparasitic agent shown to be of benefit
  • 57.
  • 58. Schistosomiasis: Causative agent: blood flukes Schistosoma mansoni Schistosoma haematobium Schistosoma japonicum. Life cycle: snail or mollusk intermediate hosts, eggs are released into venous circulation in humans Ocular findings: Granulomatous responses occurs in conjunctiva, lacrimal gland, choroid and optic nerve-optic atrophy migrating worms- superior ophthalmic vein, AC Diagnosis: eggs in stool, urine or biopsy material and Immunodiagnostic assays Treatment: Praziquantel, ocular involvement is treated systemically.
  • 59.
  • 60. Paragonimiasis: Causative agent: Paragonimus westermani Life cycle: definitive host (cat, dog, or primate) & intermediate hosts (snail, fresh water crabs, shrimps or crayfish) Mode of transmission: ingesting raw, undercooked, juices and fluids of intermediate hosts Ocular findings: Mechanical damage by migrating worms-severe and recurrent retinal hemorrhages invasion of anterior chamber, eyelid and orbit subluxation of the lens uveitis hypopyon secondary glaucoma Cerebral involvement - cranial nerve palsies & papilledema. Diagnosis: eggs in sputum or feces, serology Treatment: Praziquantel & surgical
  • 61.
  • 62. Fascioliasis: Causative agent: liver flukes Fasciola hepatica or F. gigantica Life cycle: snail, human, animal – intermideate hosts Ocular findings: ectopic locations in orbit larvae in AC, vitreous viacentral retinal artery vasculitis endophthalmitis intraocular haemorrhage retinal ischaemia Treatment: Early vitrectomy & removal of parasite, triclabendazole or bithionol
  • 63.
  • 64. Pentastomiasis: Causative agent: Linguatula serrate (tongue worm) Life cycle: wormlike and arthropod-like characteristics, intermediate hosts (rodents, ungulates, humans), humans are also dead-end definitive hosts Ocular findings: wandering nymphs invades ocular tissues-AC iritis secondary glaucoma Treatment: surgical removal
  • 65.
  • 66. Myiasis: Causative agent: Cochliomyia hominivorax Gasterophilidae (‘horse bot fly’ or ‘horse warble fly’) Wohlfahrtia magnifica (‘sheep maggot fly’) Oestrus ovis (‘sheep bot fly’) Chrysomyia bezziana (‘screw worm fly’) Cordylobia anthropophaga (‘tumbu fly’) Dermatobia hominis. Mode of transmission: direct deposition of eggs by flies or by secondary vectors-mosquitoes
  • 67. Ocular findings: larvae migrate through or across conjunctiva or eyelids ‘Ophthalmomyiasis externa’ invade deeper ocular structures ‘Ophthalmomyiasis interna’ conjunctivitis, keratitis, scleritis, iritis, vitritis, uveitis subluxation of the lens vitreal hemorrhage retinal detachment, hemorrhages, retinal scarring and ‘tracks’ Treatment: Mechanical removal, laser photo-coagulation or with surgery Topical & systemic steroids
  • 68.
  • 69. Protothecosis: Causative agent: Prototheca wickerhamii Affects immunocompromised individuals Ocular findings: vitritis choroiditis Diagnosis: blood culture, culture of lesion, discharge. Treatment: involves reversal of immunosuppression systemic amphotericin, triazole antifungal agents.
  • 70. Thelaziasis: Causative agent: T. callipaeda Mode of transmission: nonbiting diptera that feed on the ocular secretions, tears, and conjunctiva of animals. Ocular findings : epiphora, conjunctivitis, keratitis, corneal opacity and ulcers, mechanical damage to the conjunctival and corneal epithelium. Diagnosis: after removal by morphology Treatment: topical with thiabendazole has also, surgical
  • 71.
  • 72. REFERENCES: 1. Albert and Jackobie 2. Amal R et al. Ophthalmic parasitosis: A review article. Hindawi journal. vol 2012, Article ID 587402 3. Yanoff: Ophthalmology 4. Ocular microbiology by PK Mukherjee