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Toxoplasmosis..
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05.19.06 (2 years ago)
#21
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Caused by obligatory intracellular parasite Toxoplasma gondii
Definitive host: cat
Intermediate host: mice, cattle, sheep, pigs, humans..
T. gondii has 3 forms:
oocyst, the spore form excreted in cat feaces.
bradyzoite, the inactive slowly metabolizing form encysted in tissues.
tachyzoite(trophozoite), the proliferating active form with particular affinity for neural tissue, responsible for tissue destruction & inflammation.
Modes of transmission:
Most commonly by the ingestion of raw meat.
Ingestion of oocysts is less common in humans.
Transplacental.
Three stages of toxoplasmosis:
Acute
Chronic(inactive)
Recurrent
C/F:
Acute acquired systemic toxoplasmosis
Mostly subclinical & asymptomatic..
Febrile lymphadenitis with malaise, headache, generalized lymphadenopathy presisting for about 4 wks..
Influenza-like illness with fever, malaise, headache, inertia, muscle ache lasting for about 10 days..
Occasionally meningoencephalitis with unconsciousness, convulsions, fever & lymphadenoathy..
Rarely exanthematous form with fever, chills, macular rash & cough, most serious form which may be fatal..
Congenital systemic toxoplasmosis
about 40-49% newborns acquire toxoplasmosis(active or inactive) if mother is infested during pregnancy..
The triad of Toxoplasmosis is Convulsions, Chorioretinitis & intracranial Calcification..
In active stage the typical lesion is necrotic granulomatous retinochoroiditis involving the macular region.
It may cause still birth, abortion, IUFD, hydrocephalus or microcephaly..
It may be asymptomatic at birth with discovery of bilateral healed punched out heavily pigmented chorioretinal scars in the macular area on a routine fundus examination or d/t defective vision..
Recurrent toxoplasmic retinochoroiditis
The recurrences usually take place b/w 10-35 years d/t rupture of cysts & release of tachyzoites into normal retinal cells..
It is c/b retinitis & inflammation in the iris, choroid & retinal vessels, d/t immune etiology(Ag-Ab reaction), not d/t direct infestation..
On Examination:
On SLE, AC may be quiet/non-granulomatous or granulomatous iridocyclitis..
Vitreous may show severe vitritis. The posterior vitreous may become detached & the posterior hyaloid face may be covered by inflammatory precipitates..
Characteristic fundal signs are:
Focal necrotizing retinitis: adjacent to the edge of an old inactive pigmenteed scar('satellite lesion'), mostly solitary, typically affecting post-equatorial fundus, seen as a white or yellow-white lesion with fluffy indistinct edges, with overlying vitreous haze & vitreous condensation..
Deer retinitis: seen as yellow, with more distinct borders, nost associated with overlying vitritis, the inflammatory focus being located in deeper retinal layers..
Punctate outer retinal toxoplasmosis: c/b multifocal punctate outer retinal lesions with little/no vitreous involvement, appear grey-whte, located at the level of deep retine & retinal pigment epithelium..
Massive granuloma: c/b lesions greater than 6 disc diameters with sharply defined borders & amorphus centres, may be extensive involvement of vitreous..
Papillitis: The active retinitis may be located in the juxtapapillary area (Jensen's choroiditis) & the optic nerve ead itself may be the primary site of involvement.. It is c/b white inflammatory mass on the optic disc with overlying vitreous haze..
Healing: The retinitis heals within 1-4 months, being replaced by a shrply demarcated atrophic scar surrounded by hyperpigmented border..
Causes of loss of vision in toxoplasmosis:
a) Direct involvement of fovea, papillomacular bundle or optic nerve head..
b) Cystoid macular oedema from an extrafoveal lesion..
c) Macular pucker with wrinkling of fovea..
d) Subretinal haemorrhaeg from subretinal neovascularization..
e) Secondary vitreous haemorrhage from retinal neovascularization..
f) Tractional RD d/t excessive vitreous fibrosis..
g) Rhegmatogenous RD d/t breaks occurring diring active retinitis..
Diagnosis:
ELISA
Indirect fluorescent antibody test
Haemagglutination test
Sabin-Feldman methylene blue dye test(Obsolete)
Treatment:
Indications are a lesion involving or threatening the macula or the papillomacular bundle or optic nerve head; or a very severe vitritis causing severe visual impairment, which may cause vitreous fibrosis & tractional RD..
Otherwise treatment is unnecessary as the drugs used are with potentially serious side-effects..
Steroids:
For anterior uveitis, topically or anterior sub-Tenon's injectin if severe..
For posterior uveitis, posterior sub-Tenon's injection..
Systemic therapy for vision threatening lesions, severe vitritis..
Antimicrobials:
Clindamycin: 300 mg qds for 3 weeks.
risk of pseudomembranous colitis..
Sulphonamides: Sulphadiazine 2 g loading dose f/b 1 g qds for 3-4 weeks.
risk of renal stones, allergic reactions, SJS..
Pyrimethamine: 75-150 mg loading dose f/b 25 mg/d with folinic acid 10 mg/d for 3-4 weeks.
Only 1 week course if given with clindamycin..
risk of thrombocytopenia & leucopenia, weekly blood counts are recommended..
Spiramycin
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