Tissue Protozoans

Question 1

Toxoplasma Gondii

definitive host?

lifecycle?

Answer 1

cats are the definitive host

1. oocysts excreted in cat feces contaminate food humans eat
2. bradyzoites emerge from cysts after the stomach and penetrate the gut
3. the bradyzoites enter macrophages and develop into tachyzoites
4. tachyzoites bust out and invade all cell types, developing cysts
5. bradyzoites multiply slowly in the cysts

Question 2

leishmaniasis

vector and life cycle

Answer 2

sandfly deposites promastigotes in blood

macrophages suck up promastigotes

amastigotes form/multiply in macrophages

amastigotes infect various tissue; especially reticuloendothelial

Question 2

how are leishmaniasis infections controlled by the immune system?

what is the immune response to each manifestation?

Answer 2

activated macrophages, INF-gamma, IL12, IL1, TNFa are needed to remove infeciton

Think of it like this: the body lacking a cellular response will have a more severe manifestation(visceral). The visceral bugs like to skew immune reaciton towards humoral

Question 3

ocular toxoplasmosis

Answer 3

necrosis of retina; granulomatous inflammation of choroid

causes blurred vision, pain; focal scars w/permanent vision loss

Question 4

treatment for trypanosoma cruzi infection

Answer 4

chagas disease

treatment indicated for acute disease or immunocompromised

nifurtimox and benzidazole

Question 4

cutaneous leishmaniasis manifestation

common new/old world spp.

Answer 4

lesions on surface of skin; central necrotic area; amastigotes found within macrophages in lesions

l. tropica, l. major = old world bugs(middle east, military operations)
l. mexicana, l. braziliensis = new world bugs(south america)

Question 6

treatment indications for toxoplasmosis

mechanism?

Answer 6

treat people w/severe disease, immunocompromised, neonatal

pyrimethamine + sulfadiazine

• inhibits folic acid metabolism @ 2 sites

leukovorin (folonic acid) is always given w/pyrimethamine

Spiramycin during pregnancy

Question 7

treatment for leishmaniasis

Answer 7

Visceral Treatment

• pentavelent antimony( sodium stibogluconate, meglumin antimoniate)
  
  • NV, ab pain, arthralgia, chemical pancreatitis
• liposomal AmB - treatment of choice in US
• parmycin - alternative treatment

Cutaneous - no treatment, or topical, excision, heat therapy

Question 8

clinical manifestation of chagas disease

Answer 8

Acute: 1-2 mo following transmission - Less than 1% are symptomatic

• Mononucleosis-like disease; Facial edema and nodule near bite

Chronic -20-30% have cardiac +- GI diseases;

• CHF, arrhythmias, heart block, sudden death, thromboembolism
• Megacolon, megaesophagus

Immunocompromised will commonly have reactivation and more severe disease w/brain lesions, acute myocarditis, skin lesions

you are infected for life!

Question 9

visceral leishmaniasis

primary species and manifestation

Answer 9

L. donovani

parasites in macrophages; worse for immunocompromised

attacks reticuloendothelial sites(liver, spleen, bone marrow)

hepatosplenomegaly, anemia, leukopenia, thrombocytopenia

5-10% die w/out treatment

Question 10

diagnosis of leishmaniasis

Answer 10

visceral: bmarrow/splenic aspirate; leishmanin skin test(-)
cutaneous: biopsy, aspirate, scrape for smears, culture; leishmanin skin test(+)

can use leishmanin skin test to see how treatment is progressing for visceral disease

Question 11

mucosal leishmaniasis

primary spp.

manifestation

Answer 11

L. braziliensis

immunological hyperreactivity causes damage at skin first, then lesions can appear in nasopharynx. cause disfiguration of nose.

can disseminate/relapse if immunocompromised

Question 13

describe the life cycle of trypanosoma cruzi

Answer 13

Chaga’s disease

• triatomine bugs bite and poops trypomastigotes
• you itch yourself, pushing the poopy trypomastigotes into your body
• amastigotes form w/in host cells which can kill the cell/cause inflammation
• amastigotes can develop back into trypomastigotes to complete cycle when bug bitse again

Question 14

clinical manifestation of toxoplasma gondii infection

Answer 14

• acute(healthy host): subclinical; can have lymphadenopathy and mono symptoms
  
  • uncommonly, severe disease can occur w/chorioretinitis
• chronic(tissue cysts): asymptomatic, life-long infection; constant immunity stimulation
  
  • can reactivate if immunocompromised; causes cerebral, cardiac, pulm symptoms
• congenital - mama becomes infected DURING pregnancy
  
  • miscarriage, stillbirth
  • if born: neuro, ocular, hepatospleno disease; anemia, jaundice, rash, pneumonia