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TOXOPLASMA GONDII AND STRONGYLOIDES
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- 2. Toxoplasma Gondii • Coccidianparasite • Definitive hosts- domestic cats and felines (intestine)- sexual • reproduction-fertile oocysts. • Oocysts in faeces- Highly infective to animals including humans. • Mode of transmition also through ingestion of uncooked meat. • Human infection is world wide especially in humid tropics (rarer in.
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- 4. • dry andcold climates). • adapted to intracellular survival therefore, rarely disease causing. • In immunocompetent adults- mild and self terminating attacks • with subclinical infections. • toxoplasmosis an be devastating in fetuses, babies, and • immunosuppressed individuals of all ages. • causing severe CNS damage and blindness
- 5. DEVELOPMENTAL STAGES • Schizonts •small basophilic intracellular bodies which divides rapidly to form small collection of tachyzoites. • Tissue cysts are surrounded by a thin primary cyst wall and contain 100s of basophillic bradyzoites. • Gamonts exhibit sexual differentiation, with ;microgamonts (m)apparent as multinucleate basophilic stages ultimately shedding small biflagellated microgametes; and macrogamonts (f) evident as uninucleate eosinophilic cells with a single ovoid nucleus. • Oocysts are small ovoid stage with 2 round sporocysts, each containing 4 elongate sporozoites.
- 6. • Acute infectionin normal adults- lymphademopathy with or With out fever; mimicking a lymphoma or a viral infection. Diagnosis by- examination of an incised lymph node. • Infants and children- sever acute febrile form with pneumonia, liver dysfungtion or myocarditis. • Early pregnancy - may be entirely asymptomatic; but placental involvement results in still birth or neonatal jaundice, pneumonia, myocarditis, or encephalitis. non fatal infection- braindamage, hydrocephalus, mental retardation, seizures, deafness, or other permenent neurologic deficits.
- 7. • In immunosuppressantindividuals- acute progressive encephalitis . • Toxoplasma retinochorditis - blindness and glucoma is a rare complication of chronic toxoplasmosis,sometimes seen in corticosteroid treated individuals. • The morphological pattern most often seen is lymphadentitis. suggested by the triad of follicular hyperplasia , focal proliferation of transformed, “histoid” B cells, and scattered focal accumulations of small numbers of epitheliod- type macrophages not forming well defined granulomas. cervical lymphnodes are mostly affected. Diagnosis confirmed by serological titer.
- 8. • Neonatal toxoplasmosisis characterised by destructive lesions in multiple organs, notably the Brain . lesser destructive lesions occur in severe form of acute adult toxoplasmosis.In CNS microglial nodules withmany tachyzoites appear (ventricles and aqueduct), followed by necrosis, vascular thrombosis, nd intense inflammation. obstruction of aqueduct leads to hydrocephalus. if infant survives-lesions calcify. • In infants, brain changes are preceded by liver cell necrosis and adrenal necrosis. lung and heart maybe necrotic and inflamed. there is extramedullary hematopoiesis.
- 9. • toxoplasma encephalitisof immuno suppressant patients- cysts in brain is common- which bursts to release bradyzoites to incite a microglial nodular reaction. • in toxoplasma chorioretinitis, tachyzoites destructs retina ; there will be granulomatous reaction in choroid and retina. • adult toxoplasmosis is treatable by a combination of drugs ; damage to fetus- irreversible.
- 10. SPONGYLOIDES • one ofthe smallest human pathogenic parasitic roundworm causing strongyloidiasis. • female filariform larvae-slender, fastmoving. (50 micrometer in dia., 350-600micrometer in length) • Both sexes possess a tiny buccal capsule and cylindrical esophagus with a posterior bulb. in freeliving state esophagi are rhabditiform. • males can be distinguished from females by 2 structures : spicules and gubernaculum. • S.stercoralis female buries in intestinal crypts of the duodenum or upper jejunum-its a luminal dweller-damages the absorptive surface-leading to chronic enteritis and malabsorptive syndrome.
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- 12. • its theonly common human intestinal nematode whose life cycle permits larvae to become infective both in soil and in the host intestine itself, - malnourished and immunosuppressed individuals. • Duodenal aspiration or biopsy - needed for diagnosis .
- 13. • in hypertensivepatients- larval skin penetration- urticarial eruption-fades in few days. • larval lung migration at about 7 days passes with a slight coughing episode unless infection is massive. • chronic intestinal phase- results in intermittent bouts of diarrhoea.
- 14. • endogenous strongyloideshyper infection as seen in malnourished children or in cortisone treated patients- nausea, fever, diarrhea, paralytic ileus. • concomitantly there may be gram negative sepsis, pneumonia and meningitis, to recur even after antibiotic treatment unless the underlying, strongyloidiasis is cured. • Persistant eosinophilia is the rule in moderate infection. but this decreases in hyperinfected altered host. • lesions mirrors the clinical events.in mild subclinical infectionsfocalerythema and eosinophilia of the duodenal mucosa
- 15. • in malabsorptivecases-lamina propria is heavilly infiltrated, mucosal villi are blunted, lacteals are dialated, and widespread mucosal edema. • in hyperinfection- ulceration of small bowel. • migrating filariform larvae are most frequently seen in lungs often associated with hemorrhage but with little focal inflammation. • septic bacterial foci facillitated by the hyperinfection and depressed immunity are commonly seen at this stage , and haemorrhagic pneumonia is often the final result.
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