PARASITOLOGY DEPARTMENT University of Sumatera …ocw.usu.ac.id/course/download/1110000121-special... · Beaver, P.C., Jung, R.C. 1984. ... Principle and practice of clinical parasitology.John

Ocular parasitiasis

Nurfida Khairina Arrasyid

PARASITOLOGY DEPARTMENT

University of Sumatera Utara

Ocular Helminthiasis

� Toxocara cani� Angiostrongylus cantonensis� Onchocerca volvulus� Onchocerca volvulus� Loa loa� Thelazia sp

Ocular toxocariasis cani

� Older children

� No history of pica

� Small dose of infection

� Posterior painless lesion near optic disc

– granuloma

– asymptomatic

– visual defects

– unilateral loss of vision

PATHOGENESIS

� Larva in an eye cause chronic inflamation of the inner chamber or retina or provoke dangerous granulomas of the retina

This reactions can lead to blindness in the � This reactions can lead to blindness in the affected eye

� Ocular involvement has been reported in 245 patients with an average age of 7.5 years

Diagnosis Treatment

� Liver biopsy – granuloma

� Laser photocoagulation

Ocular angiostrongyliasis

� Defenitive host : rodent (Rattus norvegitusand Rattus rattus)

� Habitat : pulmonary artery of rodents

� Intermediate host : snail (Achatina, Pila)� Intermediate host : snail (Achatina, Pila)

� Distribution : Southeast Asia, India, Taiwan, China, Japan, Australia and Egypt

Mode of Human Infection

� Ingested 3rd stage larvae by

consuming intermediate host

(snail) or paratenic host (exp.

crabs, fresh water shrimp).

Ingested 3rd larvae from � Ingested 3rd larvae from

water which was

contaminated by dead

mollusc/snail, or vegetables

by secretions of mollusc

Patology & Symptoms

� Larvae in eye � Ocular angiostrongyliasis � blind

� Headache and stiff neck

� Vomiting

� Severe case : paresthesia and paralysis

Eosinophilic meningitis or eosinophilic meningoencephalitis

Diagnosis

� Anamnese � eating mollusc

� Clinical signs and symptoms

� Finding larvae (young adult worm) in

spinal fluid or other organs by surgery

� Serological test

Therapy

� Supportive

� Thiabendazole, Albendazole

Prevention

� Cooking all potential intermediate

and paratenic host before eat.

Ocular onchocerciasis

� Causative agent: Onchocerca volvulus

� Insect vector: Black flies, Simulium sp.Insect vector: Black flies, Simulium sp.

� Also known as “River blindness” –5% infected are blind (2 million)

� Distribution: Tropical Africa, Central America, spread to Arabian Peninsula.

Pathology/Pathogenesis

� Live microfilaria invade many parts of the eye, but here again they cause little reaction, their death leads to lessions

� Chronic inflamatory cells with eosinophils & neutrophils surround death Chronic inflamatory cells with eosinophils & neutrophils surround death worms, follow by fibroblast proliferation & chronic inflamatory infiltrates

� The most important cause of blindness is sclerosing keratitis a hardening inflamation of the cornea

Pathology/Pathogenesis

Blindness

Any part of the eye : punctate keratitis,

sclerosing keratitis, chorioretinitis, optic

atrophy.atrophy.

Most often in savanna Africa & Guatemala

Punctate keratitis is most common –

snowflake opacities due to inflamatory

reaction to dying microfilariae

Diagnosis & Treatment

� Diagnosis– Slit-lamp examination– Serological method– Serological method– PCR has role in monitoring chemotherapy

Ocular loiasis

� Caused by the eye worm of Africa, Loa loa� Transmitted by mango flies, Chrysops sp.� Endemic only in rainforest areas of central and

west Africa – Nigeria, Cameroon, Zaire (Congo), west Africa – Nigeria, Cameroon, Zaire (Congo), Angola, Gabon, Chad & Sudan

� Mf in peripheral blood shows diurnal periodicity.� Mf has been shown in primate but has nocturnal

periodicity, probably a different species

� Occusianally adult worms migrate through the conjunctiva & cornea with swelling of the orbit

Pathology, Pathogenesis & Clinical manifestations

– Endemic patient

•Hypo-responsiveness

•90% positive for Mf

Pathology, Pathogenesis & Clinical manifestations

•90% positive for Mf

• Lower eosinophilia, parasite-specific IgG & lymphocyte proliferation

Nurfida Kh. Arrassyid

– Non-endemic population• Hyper-responsiveness

• Low positivity for Mf (10%)

• Higher level of eosinophilia (60-80%),

Pathology, Pathogenesis & Clinical manifestations

• Higher level of eosinophilia (60-80%), parasite-specific IgG & lymphocyte proliferation

• More severe & recurrent calabar swelling

Diagnosis & Treatment

� Diagnosis– Blood smear for Mf (mid-day sample)

– Biopsy– Biopsy

– Serological test (ELISA, IFA

� Treatment– DEC 8-10mg/kg in divided doses x 21 days

Ocular thelaziasis

Pathogenesis, Pathology & Symptomatology

� Thelazia produces damage to the tissues

associated with the eye.associated with the eye.

� Its presence in the conjunctival sac

provokes excess flow of lacrimal fluid.

� Its repeated migration across the corneal

conjunctiva irritates this layer & eventually

results in scarification & fibrous opacity of

the region

Pathogenesis, Pathology &

Symptomatology

� Paralysis of the muscles of the lower eyelid,

with ectropion, has been attributed to the

worms.

� The presence & movement of the parasites

in the conjunctival sac cause surprisingly

mild symptoms consisting of excessive

lacrimation, itching or pain.

Diagnosis & Treatment

Diagnosis :

� The presence of

creamy white

threaworm masses

Treatment :

Removal the worm with

forcepsthreaworm masses

coiled in the

conjunctival sac

OCULAR PROTOZOIASIS

Nurfida Khairina Arrasyid

Ocular protozoiosis

� Acanthamoeba sp

� Toxoplasma gondii

Ocular acanthamoebiasis

� Free living amoeba widely distributed in nature

� Facultative parasite of man and animal

� Causes infection :

1. CNS (Granulomatous Amebic

Encephalitis GAE)

2. Cornea (Keratitis)

3. Skin ulcers

Recent increase in the number of

cases of CNS infection as well as

cases of keratitiscases of keratitis

Problems with diagnosis and

effective treatment

Keratitis

• Inflammation of the cornea

• painful, vision threatening disease resulting

in blindness if untreatedin blindness if untreated

• painful eye, redness, photophobia

• infiltration of corneal epithelium leading to

ulceration, perineuritis, hypopyon

• very resistant to treatment resulting in tx

failure

•increasing no. of cases throughout the world

•related to contact lens wear (>80%)

•increasing usage of contact lenses but poor lens

hygienic care

•related to trauma (injury to the eyes by soil,

sand, contaminated water, mud splashing, foreign sand, contaminated water, mud splashing, foreign

bodies)

•progressive disease which resembles herpes

simplex

Risk factors

• Contact lens wear esp extended wear

• Trauma to the eye

• Use of home made saline• Use of home made saline

• Use of tap water to rinse lens

• Swimming while wearing CL

• Poor hygienic care of CL system

Diagnosis

• Hx of CL wear or injury to the eye

• Poor hygienic care of CL system

• Use of tap water or homemade saline

• Clinical presentation and finding of

perineuritisperineuritis

• Clinical spesimen is corneal scrapping or

biopsy which should be cultured onto NNA

overlay with E. coli

• Both trophozoite and cyst can be identified

• Other specimens include contact lens, CL

casing, CL saline and disinfectant, tap water

used to rinse lens

• The specimens should also be cultured for

Acanthamoeba using NNA overlay with E. Acanthamoeba using NNA overlay with E.

coli

• Examine under inverted microscope daily

until 14 days before a negative result is

confirmed

• Ocular toxoplasmosis is allegedly the

most common cause of posterior

uveitis in immunocompetent

Ocular toxoplasmosis

individuals.

• In most patients it is presumed to be

a reactivated congenital condition,

but instances of acquired infection

have also been reported.

�A white, sharp-edged but irregular neuroretinal

inflammatory focus is usually seen, frequently in

association with an old scar.

Pathogenesis, Pathology,

Symptoms

association with an old scar.

�In recurrent ocular toxoplasmosis, acute

inflammation may be restricted to a discrete

zone at the margin of an old scar.

Pathogenesis, Pathology,

Symptoms

� Chronic active or relapsing infections of

retinal cells by tachyzoites causes blinded

spot & extensive infection of the central spot & extensive infection of the central

macular area, which may lead to blindness

� Cysts & cyst rupture in the retina can also

lead to blindness

� Pathologic findings:

– necrotizing retinitis and uveitis

Signs , Symptoms,

Diagnosis & Treatment

� Acute retinochoroiditis include blurred

vission, scotoma,photophobia and pain

Pathology : coagulative necrosis of the � Pathology : coagulative necrosis of the

retina with inflamatory infiltrates & loose

granulomas in the choroid

� Funduscopic : vitritis

REFERENCE

Beaver, P.C., Jung, R.C. 1984. Clinical parasitology. 9th ed. Philadelphia, Lea & Febringer. p.292-294; 345

Gillespie, S., Pearson, R.D. 2001. Principle and practice of clinical parasitology.John Wiley & Son Ltd. p.124

Miyazaki, I. 1991. An Miyazaki, I. 1991. An illustrated book of helminthic zoonosis. Tokyo : International Medical Foundation of Japan, p. 347-353; 366; 428-434

Schimidt, G.D., Roberts, L.S. 2005. Foundation of parasitology. 7th ed. Mc Graw Hill. p. 118-119;136-137; 427-428; 458; 468-471