parasitic infections in the eyes

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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