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Ocular Toxoplasmosis
Dr. Md. Mominul
Islam
Fellow (Vitreo-Retina)
Ispahani Islamia Eye
Institute And
Hospital Dhaka
Bangladesh
Introduction
 Common zoonosis
 Caused by Toxoplasma Gondii
 Life threatening disease (newborn and
immnosuprresed patients)
 Asymptomatic in immuno competent patient
 Congenital or Acquired
 Both eye may affected
Epidemiology
Represent with posterior uveitis
 50-85% in Brazil
 25% in USA
Prevalence: (not well determind)
 0.6-2% in USA
 10-17.7% in Brazil
Transmission
 Beef
 Undercooked lamb , pork, chicken
 Environment contaminated by feces of infected cats
family
 Organ transplantation
 Blood transfusion
 Water
Biology And Life Cycle
 Obligate , intracellular protozoan
 Both sexual and asexual reproduction
 Definitive host – Members of cat family
 Intermediate host- Hundreds of species including
mammals, birds
 Host tissue - Muscle
- Retina
- Nervous tissue
- Body fluid
Contd
Three forms
Oocyte
Trachyzoite
Bradyzoit
(tissue cyst)
Genetics
Type- I
• Very
virulent
• Postnatal
acquired
ocular
infection
Type-II
• Less
virulent
• Congenital
infection
and
toxoplasmic
encephalitis
Type-III
• Less
virulent
Pathogenesis
In immunocompetent patients is characterized
histologically by
 Foci of granulomatous chorioretinal inflammation
 Coagulative necrosis of the retina with sharply
demarcated borders
 Inflammatory changes can be widespread in the eye
and involve choroid, iris, and trabecular meshwork
Contd
In Immunosuppressed
 Have both tachyzoites and tissue cysts in areas of
retinal necrosis and within retinal pigment epithelial
cells.
 Parasites can occasionally be found in the iris, choroid,
vitreous, and optic nerve
Ocular presentation
Symptoms
 Floaters
 Blurring or loss of vision
Sign (The hallmarks)
 necrotizing
retinochoroiditis
 Satellite lesion adjacent
to old hyperpigmented
scars
 Vitreous inflammation
 Anterior uveitis
 Retinal vasculitis is also
present (occationally)
Contd
New or Acute lesion
• Intensely white
• Focal lesion overlying
vitreous inflammatory
haze (head light in the
fog)
• Acute anterior uveitis
Healed lesion
• Border become more
defined
• Hyperpigmented after
several months
• Large scar will have
atrophic center
(devoid of all choroidal
retinal elements)
Investigation
 Serological test
 PCR
Differential Diagnosis
Infectious:
 Rubella
 Cytomegalovirus
 Syphilis
 Herpes simplex
 Tuberculosis
 Toxocariasis
Contd
Non-infectious:
 Retinal and choroidal coloboma
 Retinoblastoma,
 Retinopathy of prematurity
 Gyrate atrophy
 Retinal vascular membrane
 Serpiginous choroidopathy
Outcome And Complication
 Central vision will be lost
 Permanent loss of vision
 Sudden loss of vision.
Treatment and Prevention
 Available drugs do not eliminate tissue cysts and
cannot prevent chronic infection
 No treatment has proven to be superior or even more
effective than no treatment
 Antitoxoplasmic agents and systemic steroids have
never been studied in large clinical trials
“Classic” therapy:
 The combination of pyrimethamine, sulfadiazine, and
corticosteroids
Pyrimethamine:
75–100 mg loading dose given over 24 hours, followed by 25–
50 mg daily for 4–6 weeks depending on clinical response
Sulfadizine:
2.0–4.0 g loading dose initially, followed by 1.0 g given 4
times daily for 4–6 weeks, depending or clinical response
Prednisone:
40–60 mg daily for 2 to many weeks depending on clinical
response; taper off before discontinuing
pyrimethamine/sulfadiazine
Folinic acid:
5.0 mg tablet, 2–3 times weekly during pyrimethamine
therapy
Contd
Other Drugs:
Trimethoprim and sulfamethoxazole.
Systemic or intraocular clindamycin
The duration of treatment depends on the individual
clinical picture
Steroid treatment is often administered systemically and
always associated with antitoxoplasmic drugs
 Local drops are used when anterior uveitis is present
Take Whom Massage
Wrong concepts in ocular toxoplasmosis
 All cases congenital
 Must present as a “retinochoroiditis”
 Vertical transmission (pregnancy) only once in life
 Cats and meat are the only source
 No treatment to avoid recurrences
 All patients need antitoxoplasmic drugs for 4–6
weeks
 Recurrences are related only to local factors
Thank you

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Ocular toxoplasmosis

  • 1. Ocular Toxoplasmosis Dr. Md. Mominul Islam Fellow (Vitreo-Retina) Ispahani Islamia Eye Institute And Hospital Dhaka Bangladesh
  • 2. Introduction  Common zoonosis  Caused by Toxoplasma Gondii  Life threatening disease (newborn and immnosuprresed patients)  Asymptomatic in immuno competent patient  Congenital or Acquired  Both eye may affected
  • 3. Epidemiology Represent with posterior uveitis  50-85% in Brazil  25% in USA Prevalence: (not well determind)  0.6-2% in USA  10-17.7% in Brazil
  • 4. Transmission  Beef  Undercooked lamb , pork, chicken  Environment contaminated by feces of infected cats family  Organ transplantation  Blood transfusion  Water
  • 5. Biology And Life Cycle  Obligate , intracellular protozoan  Both sexual and asexual reproduction  Definitive host – Members of cat family  Intermediate host- Hundreds of species including mammals, birds  Host tissue - Muscle - Retina - Nervous tissue - Body fluid
  • 7. Genetics Type- I • Very virulent • Postnatal acquired ocular infection Type-II • Less virulent • Congenital infection and toxoplasmic encephalitis Type-III • Less virulent
  • 8. Pathogenesis In immunocompetent patients is characterized histologically by  Foci of granulomatous chorioretinal inflammation  Coagulative necrosis of the retina with sharply demarcated borders  Inflammatory changes can be widespread in the eye and involve choroid, iris, and trabecular meshwork
  • 9. Contd In Immunosuppressed  Have both tachyzoites and tissue cysts in areas of retinal necrosis and within retinal pigment epithelial cells.  Parasites can occasionally be found in the iris, choroid, vitreous, and optic nerve
  • 10.
  • 11. Ocular presentation Symptoms  Floaters  Blurring or loss of vision Sign (The hallmarks)  necrotizing retinochoroiditis  Satellite lesion adjacent to old hyperpigmented scars  Vitreous inflammation  Anterior uveitis  Retinal vasculitis is also present (occationally)
  • 12.
  • 13. Contd New or Acute lesion • Intensely white • Focal lesion overlying vitreous inflammatory haze (head light in the fog) • Acute anterior uveitis Healed lesion • Border become more defined • Hyperpigmented after several months • Large scar will have atrophic center (devoid of all choroidal retinal elements)
  • 14.
  • 16. Differential Diagnosis Infectious:  Rubella  Cytomegalovirus  Syphilis  Herpes simplex  Tuberculosis  Toxocariasis
  • 17. Contd Non-infectious:  Retinal and choroidal coloboma  Retinoblastoma,  Retinopathy of prematurity  Gyrate atrophy  Retinal vascular membrane  Serpiginous choroidopathy
  • 18. Outcome And Complication  Central vision will be lost  Permanent loss of vision  Sudden loss of vision.
  • 19. Treatment and Prevention  Available drugs do not eliminate tissue cysts and cannot prevent chronic infection  No treatment has proven to be superior or even more effective than no treatment  Antitoxoplasmic agents and systemic steroids have never been studied in large clinical trials
  • 20. “Classic” therapy:  The combination of pyrimethamine, sulfadiazine, and corticosteroids Pyrimethamine: 75–100 mg loading dose given over 24 hours, followed by 25– 50 mg daily for 4–6 weeks depending on clinical response Sulfadizine: 2.0–4.0 g loading dose initially, followed by 1.0 g given 4 times daily for 4–6 weeks, depending or clinical response Prednisone: 40–60 mg daily for 2 to many weeks depending on clinical response; taper off before discontinuing pyrimethamine/sulfadiazine Folinic acid: 5.0 mg tablet, 2–3 times weekly during pyrimethamine therapy
  • 21. Contd Other Drugs: Trimethoprim and sulfamethoxazole. Systemic or intraocular clindamycin The duration of treatment depends on the individual clinical picture Steroid treatment is often administered systemically and always associated with antitoxoplasmic drugs  Local drops are used when anterior uveitis is present
  • 22. Take Whom Massage Wrong concepts in ocular toxoplasmosis  All cases congenital  Must present as a “retinochoroiditis”  Vertical transmission (pregnancy) only once in life  Cats and meat are the only source  No treatment to avoid recurrences  All patients need antitoxoplasmic drugs for 4–6 weeks  Recurrences are related only to local factors