Parasitic Infections in the Eyes. Saleha Sungkar

Transcription

1 Parasitic Infections in the Eyes Saleha Sungkar

2 Parasitic Infections in the Eyes Helminths: - Intestinal Nematodes: Toxocara sp - Tissue Nematodes : O. volvulus, Loa loa Protozoa: Acanthamoeba sp, Toxoplasma gondii Arthropodes: Demodex folliculorum

3 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)

4 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)

5 Toxocara sp.

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7 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

8 Life cycle 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.

9 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

10 Retinal Pigment Epithelium (RPE)

11 Ocular Larva Migrans

12 Pathophysiology Ocular Toxocariasis 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

13 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

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16 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

17 Ocular toxoplasmosis

18 Ocular toxoplasmosis The typical lesion consists of fluffy gray/whiteyellow 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.

19 Ocular toxoplasmosis Complications: 1. secondary glaucoma 2. vascular occlusion 3. retinal neovascularization 4. choroidal neovascularization 5. subretinal neovascularization

20 Retinochoroiditis

21 Acquired Toxoplasmosis in Immunocompetent Host Rarely detected (asymptomatic) Lymphadenopathy self limiting Fever, headache, myalgia, sore throat, hepatosplenomegaly Retinochoroiditis Myocarditis Encephalitis

22 Toxoplasmosis in Immunocompromised Host Can be fatal Reactivation of congenital and required infection CNS: toxoplasmic encephalitis Pulmonary involvement

23 Congenital Toxoplasmosis Disease in Infants Normal at birth Hepatosplenomegaly Icterus Lymphadenopathy Erythroblastosis Hydrops foetalis Death: 5% - 15%

24 Congenital Toxoplasmosis Disease in Infants Classic triad: 1. Hydrocephalus 2. Intracranial calcification 3. Retinochoroiditis: atrophy of retina & choroid pigmentation + (4) Psychomotoric retardation Tetrade Sabin

25 Loa loa

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27 Loa loa Host: human Disease: loiasis, african eye worm, fugitive swelling, calabar swelling Prevalence: 7 60%

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29 Morphology & Life Cycle Adult worm Smooth, fine, whitish, like thread Female > male mm x mm Live in subcutaneous tissue, 4-17 tahun The female produce microfilariae

30 Loa loa Microfilariae Sheathed microfilariar, live in the blood Diurnal periodicity Size um x 6-8 um At night: pulmonary capillary

31 Loa loa The vector Blood sucking fly: Chrysops silacea & Chrysops dimidiata Microfilaria L3: 9-12 days

32 Loa loa Clinical manifestation/pathology Adult worm migrate subcutaneous tissue Local reaction Pass through the orbita/ across the nose nearby

33 Clinical Manifestations / Pathology Eye Iritation Congestion Painful Eyesight disfunction

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35 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.

36 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 & fibrosis Lab: Eosinophilia

37 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

38 Treatment and Prevention Drug of choice: Ivermectin, a macrolide, microfilaricide Alternative: Diethylcarbamazine (DEC) Prevention involves vector control (insecticides, repellents, netting and protective clothing)

39 Onchocerca volvulus (Blinding filariasis; river blindness)

40 Onchocerca volvulus Host: man, chimpanze Disease: onchosercosis, onchocerciasis, blinding filariasis, river blindness

41 GEOGRAPHIC DISTRIBUTION West and East Afrika, South America (Mexico, Guatemala, Venezuela ), Yaman

42 Onchocerca volvulus Adult worm Filariform, whitish Female: cm x um Male:19-42 cm x um, coiled tail Live in subcutaneous/muscles, yrs The female: mf/day

43 Onchocerca volvulus Microfilariae Rarely found in the peripheral circulation Around or nearby the adults Morphology: unsheathed, head and tail are unnucleated

44 Onchocerca volvulus Vector Blood sucking fly Simulium Microfilariae L3: 6-10 days Africa: S. damnosum and S. neavei America: S. ochraceum

45 Life cycle In 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.

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48 River blindness

49 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

50 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

51 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

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56 Onchocerca volvulus Diagnosis 1. Physics: subcutaneous nodules, hanging groin, leopard skin, eye disorders 2. Parasitology: skin snip microfilariae / adult worm in the nodule 3. Nodule USG: worm burden 4. Oncho-150 DNA Probe: PCR

57 Treatment and Prevention Ivermectin is effective against microfilariae No therapy for adult worms Prevention involves vector control (insecticides, repellents, netting and protective clothing)

58 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.

59 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.

60 Acanthamoeba keratitis

61 Acanthamoeba keratitis

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63 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

64 Demodex folliculorum Demodex Mites ( 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

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68 Clinical manifestations blepharitis allergic conjunctivitis acne rosacea

69 Wassamualaikum Thank you