Ocular Toxoplasmosis: Causative Agent Toxoplasma Gondi An Obligate, Intracellular Parasite

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Ocular Toxoplasmosis

Causative agent Toxoplasma gondi


An Obligate, intracellular parasite
It is the Commonest cause of retinochoroiditis and
posterior uveitis in humans
Manifest between the 2nd & 4th decades of life

Risk factors
 Immunodeficiency states
 Exposure to cats
 Eating raw or partially cooked meat

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Ocular Toxoplasmosis
Symptoms
 Blurred vision
 Floaters
 Pain
 Red eye
 Metamorphopsia
 Photophobia
Can be acquired or congenital

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Ocular Presentations
Toxoplasma necrotizing retinochoroiditis
• Is the Classical presentation of toxoplasmosis involving inner
retina
• Surrounded by oedema with contiguous inflammation of choroid
and sclera
• May be associated with dense vitritis  "headlight in the fog"
• May be associated with adjacent focal vasculitis
•  Also may be associated with Cells and flare in the anterior
chamber (rarely, mutton-fat keratic precipitates)

Immunocompetent adults:
 Unilateral, painless and unifocal retinochoroiditis
 Vision good if macula not involved
Immunocompromised adults:
 Bilateral, multifocal, severe and less vitrous reaction
 May be associated with CNS toxoplasmosis
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Toxoplasma retinochoroiditis
acute acquired toxo retinochoroiditis in an
immunocompetent adult

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Toxoplasma retinochoroiditis
Recurrence over an old scar

Active
recurrent
lesion(white)
Old scar
(pigmented)

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Toxoplasma retinochoroiditis
Active and inactive lesions

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Toxoplasma retinochoroiditis
Active and inactive lesions

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Toxoplasma Retinochoroiditis
Congenital toxoplasmosis
Results from transplacental transmission of T. gondii
Bilateral and severe
70% retinochorioditis
⅔ macula involved associated with severe visual loss
Associated with micorophthalmia, vitritis, glaucoma,
ocular palsies and other severe systemic manifestations

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Other Atypical ocular Manifestations
  
  Retrobulbar neuritis
  Rhegmatogenous retinal detachment
  Pars planitis
  Punctate outer retinitis
  Serous macular detachment
  Panuveitis

 

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Diagnosis
1. Typical Clinical signs and symptoms
2. Serologic tests
Toxoplasma-specific IgG and IgM antibodies(anti-
toxo IgG and IgM)
1. 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

Negative anti-toxo IgG excludes ocular toxoplasmosis


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Serological
2. IgM
diagnosis
Less value than IgG
A positive IgM test indicates recent infection
A negative IgM test excludes recent toxo infection
But Toxoplasma-specific IgM antibodies may be
detected up to 18 months after acute acquired infection

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Treatment
Pyrimethamine and Sulfadiazine combination
(Folinic acid needed) with or without systemic
prednisolone OR
Cotrimoxazole (Bactrim )(2 tabs bid after loading
dose) is as effective as pyrimethamine/sulfadiazine for
lesions outside fovea.
At least 6 weeks treatment needed
Corticosteroids
 Topical : depending on AC reaction.
 Depot steroid injection absolutely contraindicated
 Risk of rampant necrosis and blind, phthisical globe
 Systemic steroid adjunct to antibiotics to minimize
collateral damage from the inflammatory response
 Usually started after antibiotics are given for 3 days
 Prednisolone 1mg/kg po, tapered over 2 weeks
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Treatment
Other alternative drugs :
Clindamycine
Azithromycin + pyrimethamine
Spiramycin
Atovaquone (hydroxynaphthoquinone)

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Toxo chorioretinitis before and
after treatment with
Bactrim 2 tabs po bid for one month +Prednisolone
1mg/kg tapered over 2 weeks

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Typical Presentation & Course
Recurrence
from past scar

Inactive
scar after
treatment

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