toxoplasmosis caso clinico

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Case 3 : A Case of Ocular Toxoplasmosis Dr Johnson Tan Medical Officer Tan Tock Seng Hospital

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Page 1: toxoplasmosis Caso Clinico

Case 3 : A Case of Ocular Toxoplasmosis

Dr Johnson TanMedical Officer

Tan Tock Seng Hospital

Page 2: toxoplasmosis Caso Clinico

Mr SCHA

17/Chinese/male

c/o: RE floaters x 5 days No trauma

O/E : VA 6/7.5 OU No RAPD Colour 15/15 OU Decreased red

desaturation RE Confrontational fields

full Anterior segment NAD RTL cells 1 +

Page 3: toxoplasmosis Caso Clinico

On examination of RE,

Page 4: toxoplasmosis Caso Clinico

What were the findings?

1. Rt superior optic disc swelling superiorly

2. Superior-temporal peripapillary white lesion with indistinct edges

3. Adjacent vasculitis

What would be the next step? Take a full history

Page 5: toxoplasmosis Caso Clinico

Further questioning… No headache / neck stiffness / tinnitus No joint pains No mouth ulcers No dysuria No travel history No chronic cough / fever / constitutional

symptoms No contact history with TB

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Investigations

ESR / CRP

ANA, dsDNA ANCA

CXR / Mantoux VDRL/TPHA

Toxoplasma IgG : 18.7 IU/ml (positive) Aqueous tap for CMV/HSV/VZV/Toxoplasma /TB

PCR: not detected

NORMAL

Page 7: toxoplasmosis Caso Clinico

Ocular Toxoplasmosis Obligate, intracellular parasite Commonest cause of retinochoroiditis and posterior

uveitis Manifest between the 2nd & 4th decades of life Risk factors

Immunodeficiency states Exposure to cats Eating raw or partially cooked meat

Symptoms Blurred vision Floaters Pain Red eye Metamorphopsia Photophobia

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Ocular Presentations1. Iridocyclitis2. Unifocal superficial necrotizing retinochoroiditis

• Classical presentation involving inner retina • Surrounded by oedema with contiguous inflammation of choroid

and sclera• May be a/w dense vitritis "headlight in the fog" • May be a/w adjacent focal vasculitis kyrieleis arteriolitis

3. Jensen’s papillitis• Involvement of optic nerve from adjacent juxtapapillary retinitis• Optic nerve sheath may serve as a conduit for the direct spread

of Toxoplasma into the optic nerve from an adjacent cerebral infection optic neuritis/papillitis

4. Punctate outer retinitis - rare5. Deep retinitis - rare

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Uncommon Ocular findings

6. Ocular inflammation without necrotizing retinochoroiditis

7. Retinal and optic nerve neovascularization, usually regresses with resolution of inflammation.

• Exact aetiology not well understood• Retinal ischemia associated with severe retinal vasculitis • Inflammatory reaction

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Optic neuritis vs disc swelling from contiguous spread?

Optic neuritis Disc swelling from contiguous spread

VA ±

Colour ±

RAPD ±

VF ± ±

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Ocular ToxoplasmosisImmunocompetent adults: Unilateral, painless. unifocal Vision good if macula not involved

Neonates: Congenital toxoplasmosis Bilateral, severe 70% retinochorioditis ⅔ macula involved a/w severe visual loss Micorophthalmia, vitritis, glaucoma, ocular palsies

Immunocompromised: Bilateral, multifocal, severe May be a/w SOL of CNS Ocular palsies, nystagmus,

VF defects

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Follow-up

Bactrim 11/11 bid x 1/12

Prednisolone 1mg/kg (50mg od) tapered over 2 weeks

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Typical Presentation & Course

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Serological diagnosis

IgG: IgG seroconversion 2-4 weeks after systemic infection,

peak titres 4-6 weeks after infection Titres maintained at high levels for many months or

years. Recent infection : 4x rise in antibody titres over a 2-4

week period Clinical signs may develop before seroconversion

occurs, or after peak titres have developed. A single antibody titre is difficult to interpret and is rarely

of any value

Negative IgG excludes ocular toxoplasmosis

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Serological diagnosisIgMLess value than IgG

A negative IgM test excludes recent infectionA positive IgM test is difficult to interpret because Toxoplasma-specific IgM antibodies may be detected up to 18 months after acute acquired infection

Goldmann-Witmer coefficientRatio of Toxoplasma IgG [eye] : [serum] > 3 is generally accepted as being consistent with active ocular infection

But invasive procedure!

Aqueous humor and serum immunoblotting for immunoglobulin types G, A, M, and E in cases of

human ocular toxoplasmosis. J Clin Microbiol. 2004 Oct;42(10):4593-8.

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PCR

Presence of T. gondii in ocular fluids is detected on PCR considered to be confirmation of active eye diseaseA negative finding does not exclude ocular toxoplasmosis

Real-time PCR (Light-cycler, LC-PCR) more sensitive than nested PCR (n-PCR).

Evaluation of a Real-time PCR-based assay using the lightcycler system for detection of Toxoplasma gondii bradyzoite genes in blood specimens from patients with toxoplasmic retinochoroiditis. Int J Parasitol. 2005 Mar;35(3):275-83. Epub 2005 Jan

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Treatment: Updates Triple drug therapy :pyrimethamine, sulfadiazine, prednisolone Quadruple therapy : pyrimethamine, sulfadiazine, clindamycin, prednisolone.

Bactrim (2 tabs bid) is as effective as pyrimethamine/sulfadiazine for lesions outside fovea. 61% in classic triple therapy grp vs 59% in Bactrim grpSoheilian et al. Prospective randomised trial of Trimethoprim/sulfamethoxazole vs pyrimethamine & sulfadiazine in the

treatment of ocular toxoplasmosis. Ophthalmology. 2005 Nov;112(11):1876-82 At least 6 weeks treatment

Others: Azithromycin + pyrimethamine (AJO 2002;134:34-40)

Spiramycin (Klin Montasbl Augenheildk 1998;212:84-7)

Atovaquone (hydroxynaphthoquinone) (Ophthalmology 1999;106:148-53)

Allopurinol (Adam et al. Berlin 2000)

Corticosteroids Topical : depending on AC reaction. Depot absolutely contraindicated

Risk of rampant necrosis and blind, phthisical globe Systemic adjunct to minimize collateral damage from the inflammatory

response Usually from Day 3 @ 1mg/kg, tapered over 2 weeks

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Thank you

A presentation byA presentation byThe Eye Institute @Tan Tock Seng Hospital