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Flashcards in Parasitology Deck (10):

Trypanosoma brucei

-Life cycle: Tsetse fly injects into bloodstream, binary fission. Key point: extracellular
-Causes African Sleeping Sickness (African Trypanosomiasis) characterized by somnolence and demyelination
-Time scale to CNS system infection (stage 2): Gambiense (1-2 yrs); Rhodesiense (few weeks). Treat in stage 1 (lymphatics). *Waves of parasitemia


Trypanocidal drugs

Stage 1:
-Pentamidine: does not penetrate CNS, IM delivery, mild toxicity
-Suramin: slow IV admin (not practical), loss of consciousness, nephrotoxic, etc. Don't take unless have to.
-Nitroaromatics (Nifurtimox & Benznidazole): no BBB, but GI absorption. Pretty Toxic.

Stage 2:
-Arsenicals (Melarsoprol): The nasty one, extremely toxic; 5-10% encephalopathy and 1/2 of those die
-Eflornithine: trypanostatic, need long IV infusion. Not as bad toxicity as Melarsoprol. Need functional immune system. Inhibits ornithine decarboxylase

*Eflornithine + Nifurtimox is best option for late stage African trypanosomiasias.


Trypanosoma cruzi

Endemic to Latin America or Mexico (kissing bug transmission). Causes Chagas' disease. Intracellular and extracellular bloodstream stages.


Chagas' Disease

-Acute stage is mild, asymptomatic. Drugs effective
-Chronic stage (20-40%) can cause myocarditis. Can happen decades after initial infection. US transmission could occur through blood supply.


Leishmania spp.

-Req. uptake by phagocytic cell
-Transmitted by sand fly
-Causes Leishmaniasis (skin lesions, splenomegaly, mucocutaneous leishmaniasis)


Antileishmanial Drugs

Organic antimonials Sodium stibogluconate & Meglumine antimoniate
-interferes with glycolysis and fatty acid beta oxidation
-toxicity increases over time


Toxoplasma gondii

-Ingest cysts, litterbox, cats usually pick it up by eating rats and birds, cats poop. Unwashed produce and animals that we eat that ingest cysts.
-Opportunistic: the T in TORCH infections.
-Causes toxoplamosis: often occurs in basal ganglia (tremors, chorea, hemiballism)



Caused by toxoplasma gondii.
-basal ganglia
-Ocular toxoplasmosis- headlight in the fog lesion in fund. exam
-Perinatal toxoplasmosis: prego dont change litter box. Abnormal head size and neuro deficits
*Pregnant women and immunocomprompised get drugs, most don't
Treat with atovaquone and folate antagonist combo
-Spiramycin is macrolide used, need to obtain FDA if prego


Naegleria fowleri

-Thermophilic freshwater amoeba
-Normally eats bacteria
-Rarely, can consume neural tissue and penetrate to CNS
-Penetrates via the olfactory epithelium if mucosal surface fails; into the olfactory bulbs and to the meninges


What are the diagnostic hints of Primary Amebic Meningoencephalitis?

Symptoms being about 5 days post-infection:
Initially: Headache, nausea, fever, vomiting
-Stiff neck
-Lack of attention to people and surroundings
-Loss of balance, seizures
Rapid disease progression, death usually occurs within about 5 days
*75% of diagnoses are made after the death of the patient
*New experimental treatment: miltefosine (also used in Leishmania)