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Parasitic Infections in the Eyes
Saleha Sungkar
Parasitic Infections in the Eyes
Helminths: - Intestinal Nematodes: Toxocara sp- Tissue Nematodes : O. volvulus, Loa loa
Protozoa: Acanthamoeba sp, Toxoplasma gondii
Arthropodes: Demodex folliculorum
Toxocariasis Causal Agent
the larvae of Toxocara canis (dog roundworm) and Toxocara cati (cat roundworm)
Two main clinical presentations : 1. Visceral Larva Migrans (VLM) 2. Ocular larva migrans (OLM)
Morphology Adult worm: nematode, 5-15 cm lenght The eggs: - fairly rounded a thin shell & albuminoid
cover- size: - 85 µm X 75 µm (T. canis)
- 85 µm X 70 µm (T.cati)
Toxocara sp.
Life cycle Definitive host: dogs / cats Humans: accidental hosts
In definitive host Infective eggs – ingested by dogs – hatch --
larvae penetrate the gut wall -- migrate through the lungs -- bronchial tree – esophagus – small intestine: adult worms develop and oviposition
In Humans: Ingestion of infective eggs in contaminated
soil -- hatch -- larvae penetrate the intestinal wall -- carried by the circulation (via blood/lymph) to tissues (liver, heart, lungs, brain, muscle, eyes)
Ingested eggs may remain viable for years. While the larvae do not develop further in
these sites -- cause severe local inflammatory reactions.
Life cycle
Ocular Larva Migrans The organism induces an inflammatory
reaction – if macula/optic nerve is involved – loss of vision
Ophthalmoscopy: anterior uveitis, vitritis, neuroretinitis, papillitis, chronic endophthalmitis and RPE (Retinal Pigment Pithelial) changes
The most common finding is a granuloma of the retina/optic disc
Retinal Pigment Epithelium (RPE)
Ocular Larva Migrans
one or more larvae become trapped in the eye -- cause a granuloma in the retina. The larvae may reside beneath/ within the retina or extend into the choroid or vitreous -- remain viable for several years
The larvae enter the eye via central retinal artery and will manifest as a peripheral granuloma
If the larvae enter via the short posterior ciliary arteries, the granuloma will likely be at the disc, macula or elsewhere in the posterior pole
PathophysiologyOcular Toxocariasis
Toxoplasma gondii Host: man, animal Mode of infection: ingestion of cyst in raw & uncooked meats ingestion of oocyst (in cat faeces) transplacental transfusion organ transplantation laboratory accident
Organ damage Depends on host age, virulence and organ
infected. CNS and eye: more severe CNS: - Meningoencephalitis- brain abscess (multiple)- aquaductus sylvii congestion
hydrocephalus- intracranial calcification- mental and motoric retardation
Ocular toxoplasmosis
The typical lesion consists of fluffy gray/white-yellow retinal infiltrates adjacent to an old pigmented scar with overlying exudation of the vitreous
Unusual presentations: papillitis, neuroretinitis, retrobulbar neuritis, outer retinal toxoplasmosis, central serous retinopathy, retinal detachment, macular edema, scleritis, and multifocal diffuse necrotizing retinitis in the elderly.
Ocular toxoplasmosis
Complications: 1. secondary glaucoma2. vascular occlusion 3. retinal neovascularization 4. choroidal neovascularization5. subretinal neovascularization
Ocular toxoplasmosis
Retinochoroiditis
Acquired Toxoplasmosis in Immunocompetent Host
Rarely detected (asymptomatic) Lymphadenopathy – self limiting Fever, headache, myalgia, sore throat,
hepatosplenomegaly Retinochoroiditis Myocarditis Encephalitis
Toxoplasmosis in Immunocompromised Host
Can be fatal Reactivation of congenital and required
infection CNS: toxoplasmic encephalitis Pulmonary involvement
Congenital ToxoplasmosisDisease in Infants
Normal at birth Hepatosplenomegaly Icterus Lymphadenopathy Erythroblastosis Hydrops foetalis Death: 5% - 15%
Congenital ToxoplasmosisDisease in Infants
Classic triad:1. Hydrocephalus2. Intracranial calcification 3. Retinochoroiditis: atrophy of retina & choroid pigmentation
+ (4) Psychomotoric retardation ⇒Tetrade Sabin
Loa loa
Loa loa
Host: human Disease: loiasis, african eye worm, fugitive swelling, calabar swelling Prevalence: 7 – 60%
Adult worm Smooth, fine, whitish, like thread Female > male 30-70 mm x 0.35-5 mm Live in subcutaneous tissue, 4-17 tahun The female produce microfilariae
Morphology & Life Cycle
Loa loa
Microfilariae
Sheathed microfilariar, live in the blood Diurnal periodicity Size 250-300 um x 6-8 um At night: pulmonary capillary
Loa loa
The vector Blood sucking
fly: Chrysops silacea & Chrysops dimidiata
Microfilaria L3: 9-12 days
Loa loa
Clinical manifestation/pathology
Adult worm migrate subcutaneous tissue Local reaction
Pass through the orbita/ across the nose nearby
Eye
Iritation Congestion Painful Eyesight disfunction
Clinical Manifestations / Pathology
Pathology Female adult worms migrate through the
subcutaneous tissue producing microfilariae
Calabar swellings develop around the adult worms.
Microfilariae do not appear in the blood until years after the adult worms appear in some cases.
Clinical Features Subconjunctival migration of an adult worm to
the eyes can occur frequently The passage over the eyeball can be sensed,
which usually < 15 min Dead worms may cause chronic abscesses
formation of granulomatous reaction & fibrosisLab: Eosinophilia
Diagnosis Microscopic examination to find microfilariae (day
time, thick smear/ concentration technique – stained with giemsa)
Subcutaneous biopsies or worm removal from the eye
Antigen detection using an immunoassay for circulating filarial antigens
Antibody detection is of limited value
Treatment and Prevention Drug of choice: Ivermectin, a macrolide,
microfilaricide Alternative: Diethylcarbamazine (DEC) Prevention involves vector control
(insecticides, repellents, netting and protective clothing)
Onchocerca volvulus(Blinding filariasis; river blindness)
Onchocerca volvulus
Host: man, chimpanze Disease: onchosercosis, onchocerciasis, blinding filariasis, river blindness
GEOGRAPHIC DISTRIBUTION
West and East Afrika , South America (Mexico, Guatemala, Venezuela ), Yaman
Onchocerca volvulus
Adult worm Filariform, whitish Female: 19-50 cm x 130-400 um Male:19-42 cm x 130-210 um, coiled tail Live in subcutaneous/muscles, 10-15 yrs The female: 1000-3000 mf/day
Onchocerca volvulus
Microfilariae Rarely found in the peripheral circulation Around or nearby the adults Morphology: unsheathed, head and tail are
unnucleated
Onchocerca volvulus
Vector Blood sucking fly
Simulium Microfilariae → L3: 6-10
days Africa: S. damnosum
and S. neavei America: S. ochraceum
Life cycleIn Human L3s are injected into human skin by the female
black fly adult worms (8 -10 months) The adults usually occur as group of tightly
coiled worms (2 to 3 females and 1 to 2 males) The gravid female releases mf, which are
distributed in the skin. They are picked up by the black fly during a blood meal
In black fly: mf gut thoracic muscle develop into L3 (6 -8 days) to the head transmitted to human.
River blindness
Onchocerca volvulus
Pathology & clinical manifestations
Skin disorders: acute & chronic Ophthalmic disorders: blindness (in 7-9 yrs) Lymphatic disorders Systemic manifestations: microfilaremia,
microfilariuria, loss of weight
Pathology Female adult worms produce microfilariae
that migrate through the subcutaneous tissue. Fibrous nodules develop around the adult worms, especially over the iliac crests
Microfilariae concentrate in the eyes, causing lesions that can lead to blindness. Some lymphatic obstruction has been documented, esp. in Africa elephantiasis results
Clinical manifestations Pruritic nodules and papules form due to
the host inflammatory response to adult worm proteins
Dermatitis, inflammatory lesions such as keratitis, iritis and chorioretinitis
Lab: Eosinophilia
Onchocerca volvulus
Diagnosis 1. Physics: subcutaneous nodules, hanging
groin, leopard skin, eye disorders2. Parasitology: skin snip microfilariae /
adult worm in the nodule3. Nodule USG: worm burden4. Oncho-150 DNA Probe: PCR
Treatment and Prevention Ivermectin is effective against microfilariae No therapy for adult worms Prevention involves vector control
(insecticides, repellents, netting and protective clothing)
Acanthamoeba castelanii Causing a rare but fatal encephalitis in the
immunocompromised host and, more frequently, a potentially blinding infection of the cornea (keratitis)
Prior to 1980's, amoebae had been reported from eye infections only rarely - these cases were associated with trauma to the eye.
Acanthamoeba castelanii In mid 1980's cases began to occur in
wearers of contact lenses. Contact lens wearers are most at risk from acanthamoeba keratitis and account for 95% of reported cases.
Poor hygiene practices such as failing to clean and disinfect lenses and rinsing them in tap water are known risk factors.
Acanthamoeba keratitis
Acanthamoeba keratitis
Diagnosis Ocular amoebic keratitis may be diagnosed
by culturing corneal scrapings on nonnutrient agar overlaid with viable Escherichia coli
direct smear of the corneal scraping – giemsa staining
Demodex folliculorum Demodex Mites (100 – 300 um ) = face mites They can badly damage the facial skin of
humans, usually starting at middle age when the immune system is weakened and their population has increased
2 species of mites: - the longer type: D. folliculorum, live in the hair
follicles- the short type: D. brevis, live in the sebaceous
glands
Clinical manifestations
blepharitis allergic conjunctivitis acne rosacea
Wassamualaikum
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