Measures of Dispersion and Variability: Range, QD, AD and SD
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
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)
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