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Neuro Block 4 > Neuroparasitology > Flashcards

Neuroparasitology Flashcards

1
Q

Why are parasites special in terms of infectious disease?

A

they are eukaryotes that have life cycle stages that influence what sorts of symptoms they cause when.

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2
Q

What parasite causes african sleeping sickness?

A

trypanosoma brucei

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3
Q

What are the two subspecies of trypanosoma brucei and how are they different?

A

trypanosoma brucei gambiense - from west africa - less severe, longer lasting

trypanosoma brucei rhodesiense - from east africa - more acute illness

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4
Q

How is trypanosoma brucei spread?

A

transmission by tsetse fly

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5
Q

Is trypanosoma brucie always intracellualr or extracellular?

A

always extracellular

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6
Q

How does trypanosoma brucei reproduce?

A

binary fission

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7
Q

Describe the symptoms of the first stage of african sleeping sickness.

A

possible chancre at bite site, fever, headache, swollen lymph nodes, muscle and joint ahces, possibly rashes or itchiness

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8
Q

What happens in the 2nd stage of african sleeping sickness?

A

CNS involvement and neurological symptoms

especially somnolence, but also altered gait, tremors, cranial neuropathies, urinary incontinence, personality changes, abnormal GCS

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9
Q

What are the different time scales for gambiense and rhodesiense?

A

gambiense - CNS involvedment after 1-2 years, death in 3

rhodesiense: CNS involvement after a few weeks death in a few months

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10
Q

How do you diagnose trypanosomiasis?

A

you look for the organism in the blood for 1st stage and look for it in the CSF for second stage - remember it’s an extracellular organism

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11
Q

Why is trypanomiasis brucei gambiense so tricky for the immune system?

A

as they replicate, some alter their surface proteins to evade the immune system such that they come in “waves” of parasitemia

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12
Q

Why does trypanosome affect the neurological system at all?

A

it’s life cycle depends on the rodents getting eaten by cats, so it makes the rodents not run away from the smell of cats

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13
Q

How do the trypanosome reach the CNS?

A

they gain access thorugh the blood-CSF barrier, not the BBB

(so via the choroid plexus, trigeminal and dorsal root ganglia, and circum-ventricular organs)

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14
Q

What are the neurological symptoms ultimatley stem from?

A
  1. factors delivered by the trypanosomes
  2. immune response ot host in the CNS
  3. further compromise of BBB
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15
Q

At latest stages of the disease, you can get demyelination likely because of what?

A

auto-immune response against epitopes that are shared between the host and trypanosomes

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16
Q

How does Pentamidine work? Early or late stage trypanosomiasis?

A

it binds DNA minor grooves and forms tight complexes

early stages before CNS involvement (doesn’t cross BBB)

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17
Q

How does pentamidine get its specificity?

A

it’s selectively taken up by the trypanosome by protein transporters only present in tyrpanosomes

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18
Q

Is Suramin used for early or late stage trypanosomiasis? More or less toxic than pentamidine?

A

early - before CNS involvement (doesn’t cross BBB)

mechanism unknown

MORE toxic - N/V, shock, LOC, peripheral neuropathy, photophobia, urticaria, pruritis, nephrotoxicity

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19
Q

WHat are the two nitroaromatics used for treating trypanoplasmosis?

A

nifurtimox

benznidazole

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20
Q

What is the mechanism of action for nifurtimox and Benznidazole?

A

induces oxidative stress due to inhibition by NADPH-dependent dehydrogenases with subsequent impairment of the mitochondrai membrane potential

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21
Q

What is the ONLY option for trypanosomiasis that has progressed to CNS involvement for T. Brucei rhodesiense?

A

Melarsoprol

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22
Q

How does Melarsoprol have to be administered?

A

it’s liposoluble, so it can cross the BBB, but insoluble in water

thie means you have to give it IV, dissolved in propylene glycol

this is really painful

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23
Q

What are the significant toxicities of melarsoprol?

A

fever, HTN, vomiting, albuminaria, and ENCEPHALOPATHY

5-10% hav encephalopathy and half of those people will die form it

24
Q

What is the stage 2 treatment for trypanomomiasis?

A

eflornithine

it can cross the BBB, but it’s trypanostatic

25
Q

How do you have to give eflornithine

A

14 day IV infusion (becuase is has poor absorption and rapid excretion in urine)

26
Q

What is the mechanism for eflornithine?

A

it inhibits ornithine decarboxylase

it turns over rapidly in human cells, but not in trypanosomes, so you get specfcity

27
Q

What combination treatment is the best option for late stage african trypanosomiasis gabiense?

A

eflornithine + nifurtimox

28
Q

What disease is caused by the trypanosoma cruzi parasite? WHere is it endemic?

A

Chagas’ disease

latin america and mexico

29
Q

How is trypanosoma cruzi transmitted?

A

kidding bug (reduviid insect)

30
Q

Describe the two stages of Chagas’ Disease.

A
  1. acute stage: symptoms very mild or asymptomatic

20-40% of people progress to chronic disease

  1. chronic disease: myocarditic, megaesophagus, megacolon
31
Q

How is Leishmania transmitted?

A

by the sand fly

32
Q

What type of host cell is needed for Leishmania’s life cycle?

A

it requires uptake by a phagocytic cell - macrophages

33
Q

What are the three forms of leishmaniasis?

A

cutaneous (skin ulcerations)

visceral (splenomegaly)

mucocutaneous (this is the bad one)

34
Q

What is the first line treatment for leishmaniasis?

A

the organic antimonials

sodium stibogluconate

meglumine antimoniate

35
Q

What is the mechanism of action for the organic antimonials?

A

it interferes with glycolysis and fatty acid beta-oxidation in leishmania

36
Q

What two drugs can be used if the leishmaniasis is resistant to antimonial treatment?

A

liposomal amphotericin B (only for visceral)

miltefosine (mechanism unknown)

37
Q

Why is eflornithine best used in combination with another trypanocidal drug in stage 2 HAT?

A

eflornithin is trpanostatic rather than trypanocidal

38
Q

For toxoplasma gondii, what are the two life cycle stages that are transmissible to humans?

A

oocysts

tissue cysts

39
Q

What percentage of the US population is infectedw ith tooplasma?

A

25%

40
Q

How is toxoplasma gondii acquired?

A

consuming the cysts:

tissue cysts in uncooked meat

oocysts on unwashed produce

occysts form cat feces

41
Q

Although most toxoplasmosis infections are asymptomatic, what populations are vulnerable to serious disease?

A

immunocompromised individuals

fetuses - remember this is a TORCH organism

42
Q

Where in the body does toxoplasma have tropism?

A

it’s neurotropic
with intracellular encystment in host muscle and brain cells

this is because the life cycle requries the rates to be eaten by cats and this makes it so that the rats don;t run away from cat odor

43
Q

What neurotransmitter is likely altered in toxoplasma infection?

A

dopamine - probably increase in neural dopamine synthesis and release

44
Q

Describe toxoplasmosis in an immunocompromised patient.

A
  1. initial infection is most severe
  2. non-growing toxoplasma in muscle cysts can be “reactivated” and resume growth

symptoms include fver, confusion, headach,e seizures, nausea, and poor cordination

45
Q

WHat is the ultimate cause of the neurological symptoms in toxoplasmosis

A

cerebral abscesses

often in the basal ganglia, so tremore, chorea and hemiballism is common

46
Q

Besides intracranial toxoplasmosis, what is a common way it can present?

A

ocular toxoplasmosis - can be reactivated infeciton or congenital

you get toxoplasmic chorioretinitis - inflammation of the uveal tract causing redness, pain, photophobia, decrease in visual acuity

47
Q

What will you see in an ocular toxoplasmosis eye?

A

“headlight in the fog” lesion with surrounding healed chorioretinal scars

48
Q

What is the affect of toxoplasmosis on neonates?

A
  • often causes miscarriages - especially earlier on
  • abnormal head size
  • often seem normal at birth, but within first few months develop vision loss, mental disability and seizures
49
Q

Who receives treatment for tosoplasmosis?

A

most people don’t get treatment

people who do: pregnant women, newborns, those wiht ocular toxoplasmosis and immunocompromised

50
Q

What are some meds you can use for toxoplasmosis and what are they typically used for?

A

they’re mostly antimalarial combos:

atovaquone

sulfdiazine

pyrimethamine

51
Q

What experimental drug can be used for treatment of toxoplasmosis in pregnant women?

A

spiramycin - it’s a macrolide that blocks ribosome function and congregates int he placental, but doesn’t cross over the barrier to affect the fetus

great for treating ine arly infection

52
Q

What is the carnivorous amoeba that can enter the CNS after swimming in warm infected lakes?

A

naegleria fowleri

53
Q

How does naegleria penetrate the CNS?

A

It goes into the nose and enters the nasal olfactory epithelium, then travels thorugh the olfacotry nerves to the olfacotry bulb. then enters circulation to the meninges

54
Q

Describe the presentation of primary amebic meningoencephalitis?

A

symptoms begin about 5 days post-infeciton

initial symptoms include headche, nausea, fever, and vomiting

later symptoms include stiff neck, confusion, lack of attention, loss of balance, seizures, hallucinations

rapid disease progression with death usually within about 5 days

55
Q

What are the diganostic hints pointing to primary amebci meningoencephalitis?

A

june, july or august

unusually hot and dry weather

southern US freshwater

nasal saline rinsing

56
Q

What is the new experimental treatment for amebic meningoencephalitis?

A

miltefosine

57
Q
A

Neuro Block 4 (20 decks)

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