TOXOPLASMA GONDII AND STRONGYLOIDES

1. TOXOPLASMA GONDII AND
STRAONGYLOIDES

2. Toxoplasma Gondii
• Coccidian parasite
• 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.

3. Toxoplasma Gondii

4. • dry and cold 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 infection in 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 immunosuppressant individuals- 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 toxoplasmosis is 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 encephalitis of 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 of the 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.

11. SPONGYLOIDES

12. • its the only 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 hypertensive patients- 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 strongyloides hyper 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 malabsorptive cases-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.

16. THANK YOU