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A - Neuroinfectious Diseases 2 > Parasitic Infections 2 > Flashcards

Parasitic Infections 2 Flashcards

1
Q

Trypanosomiasis

_____ from genus ____

A

Parasitic flagellate protozoa

Trypanosoma

true parasite

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2
Q

Trypanosomiasis

Infect variety of hosts – 2 of them cause fatal human diseases known as

A

African trypanosomiasis (sleeping
sickness)

American trypanosomiasis (Chagas disease)

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3
Q

neglected parasitic infections targeted by CDC

A
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4
Q

Chagas caused by

A

T. cruzi – mostly rural areas of Latin America

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5
Q

Sleeping sickness caused by

A

T. brucei – mostly rural Africa

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6
Q

Trypanosoma cruzi is transmitted to animals and people by

A

insect vectors found only in the Americas

  • Blood-sucking “kissing bugs” of the subfamily Triatominae
  • Nocturnal, bite you while you are asleep prefer to bite on face - attracted to face - breathing - warm air
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7
Q

Trypanosoma cruzi routs of infections

A

vectorborne (bight), contaminated food and drinks (sugary drinks - attract bugs), congenital transmission (placenta), and (rarely) blood transfusions or organ transplants

No direct contact transmission

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8
Q

Trypanosoma cruzi Vectors are endemic from

A

Mexico, Central America, and South America, but Chagas disease have occurred worldwide

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9
Q

T. cruzi infection cycles

A
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10
Q

mobile vs non-mobile T. cruzi

A
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11
Q

T. cruzi can infect any ___ cell

A

nucleated

Bad luck: cardiomyocytes, smooth muscle cells, neurons

cells w/o nuclei - platlets, red blood cells

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12
Q

vsg protein

A

Variant surface glycoprotein - temporary skins - undergo recombination of pieces of genes - diff types of glycoproteins

there are several large polymorphic glycoproteins on their surface (all tropsamsomes) - Over 1,100 possible versions!

allows for chronic infections that can last a lifetime - by time antibodies devoloped for one another grows back

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13
Q

why vsg protein makes it so hard to diagnose

A

hapen to take sample when low paracetemia - wont see it - need to take multiple samples

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14
Q

T. cruzi is not a true neurotropic pathogen unlike

A

its close homologue T. brucei

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15
Q

How does T. cruzi enter the CNS

A

choroid plexi
CNS only when uncontrolled for a very long time (high levels, high chance into CNS)

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16
Q

T. cruzi has an acute and a chronic phase

A

if untreated, infection is lifelong - immune can kill 99% but that last 1% comes back

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17
Q

Acute phase of T. cruzi

A

mostly asymptomatic or mild, general symptoms

Chagomas or Romaña’s sign are unique to Chagas (swelling of the eyelids on the side of the face near the bite wound or where the bug poop was accidentally rubbed into the eye) high inflammation at site of entry

Mostly in children, and immune status will determine if it develops severe complications (cardiac or CNS infection)

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18
Q

chronic phase of T. cruzi infection

A

After the acute phase resolves, even with treatment it enters a chronic phase

Most people remain asymptomatic (chronic indeterminate)

~30% will develop life-threatening symptoms (chronic determinate): cardiac, intestinal, or nervous infection

Most deaths are due to hearth failure – 1/3rd are due to clinical meningoencephalitis

Congenital and non-vectorborne infections are considered acute

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19
Q

diagnosis of T. cruzi

A

Acute phase – direct visualization of parasites on blood smears

Chronic phase – serologic testing since parasites are no longer detectable

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20
Q

Acute phase can be treated - chronic phase

A

has no treatment - treat symptoms

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21
Q

T. cruzi treatment

A

Two drugs are used – side effects are common and increase in severity with age

Not recommended for adults (>18 years)
drug - depends on age and health conditions

Chronic phase - treatment by cardiologist, gastroenterologist, or neurologist - always have escapes - cannot take drugs forever

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22
Q

sleeping sickness is caused by

A

two subspecies of Trypanosoma brucei

> 90% of cases caused by T. brucei gambiense - west - less pathogenic

rest by T. brucei rhodesiense. - east - neurotropic - also in flies - change behavior - inc hunger, inc food, inc chance transmit

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23
Q

African trypanosomiasis is transmitted by

A

the tsetse fly, which is found only in rural Africa

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24
Q

resuvars for African trypanosomiasis

A

large resuvars - hard to control

Animals, especially livestock, can also be infected

Only way of infection is vectorborne, but animals represent an important reservoir - implicated on dissemination

Rare reports of transplacental infection

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25
Q

If untreated both African trypanosomiasis are

A

fatal

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26
Q

tale tale symptom of CNS African trypanosomiasis

A

disrupt 24hr sleep cycle

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27
Q

T. brucei cycle

A
28
Q

T. brucei and VSG

A

Also have cycling expression of VSG, expressing only one at any given time

Larger repertoire, >1,500 versions of VSG can be expressed

29
Q

T. brucei neurotropism

A

shows neurotropism - CSF is preferred fluid for replication

Initially enters the Choroid plexus through fenestrated capillaries (later on BBB collapses)

Expresses metalloproteinases that degrade basal lamina of the BCSFB - side effect they lose their VSG coat - induces great inflammatory response - disregulated - BBB colapses

because neurotropic - all infections involve CNS

30
Q

T. brucei infection involves 2 stages

A

Hemolymphatic phase – dividing blood and lymph - parasite is found in the peripheral circulation (mild, general symptoms), but it has not yet invaded the CNS

Neurological phase – parasites have invaded the CNS

31
Q

Subspecies of T. brucei radically different

A

T. b. rhodesiense - east
reaches neurological phase in days/weeks - death within months

b. gambiense - west
stays on hemolymphatic phase for months/years, with CNS invasion usually ~3 years after - death ensues 6 – 7 years if untreated

32
Q

T. brucei diagnosis

A

is direct visualization of parasite – loads of T.b. rhodesiense are substantially higher than T.b. gambiense in any fluid

Serologic testing for T.b. gambiense works, but is used for screening purposes only and the definitive diagnosis is visualization on CSF (difficult to find on blood smears)

33
Q

T. brucei treatment

A

Therapy depends on the subspecies involved (east vs west) and on the stage of the disease - follow up examinations for up to 2 – 3 years are necessary to prevent relapse

  • Reason there are different therapies is the nature of the BBB!
  • Second phase drug can cause seizures

Both first and second stage drugs are highly effective

34
Q

Helminth CNS manifestations

A

Can produce various CNS manifestations: meningoencephalitis, brain abscesses (granulomas), and cerebral vasculitis

35
Q

Helminth infections from

A

contaminated food or water

Nematodes (roundworms) - Trichinella spiralis

Trematodes (flukes) - Schistosoma spp

Cestodes (tapeworms) - Taenia solium

36
Q

neurotropic helminths

A

most are not true neurotropic - easier to treat - but also a lot of general symptoms

True neurotropic: Angiostrongylus, Baylisascaris, Toxocara – less
common - Higher mortality due to delayed diagnosis - because they are neurotropic!

37
Q

helmith immune response

A
38
Q

Schistosoma spp (Schistosomiasis) most by

A

Most infections by S. japonicum, S. mansoni, or S. haematobium

Another of CDC’s neglected tropical diseases

In terms of socioeconomical burden, 2nd only to malaria

39
Q

Schistosoma spp complete life cycle in

A

in snale

expose - snale infeted by body of water

Water-borne – contaminated freshwater
Intermediate host, water snails, needed for cycle

40
Q

Schistosoma spp areas at risk

A
41
Q

Schistosoma spp cycle

A
42
Q

Schistosoma spp Symptoms are caused by

A

body’s reaction to eggs

Eggs that become lodged in tissues cause inflammation and scarring

Larvae may also migrate to the spinal cord or the cerebral
vasculature and shed eggs there - neuroinflammation

43
Q

Repeated Schistosoma spp infections cause

A

anemia, malnutrition – without treatment can persist for years

44
Q

Schistosoma spp Spectrum of neurological manifestations is

A

species dependent

Brain infection is most frequent S. japonicum

Other two species, although rarely, can affect the spinal cord and eventually the brain

45
Q

Neuroschistosomiasis

A
46
Q

Neuroschistosomiasis damage

A

Chronic phase is characterized by seizures, focal signs, and intracranial hypertension due to single or multiple brain granulomas.

Intracranial hemorrhages may occur  damage of small leptomeningeal or parenchymal blood vessels induced by parasites (worm not go into parachima but eggs can)

Another example of CNS disease NOT caused by pathogen invading the CNS

47
Q

S. mansoni and S. haematobium

A

almost never CNS - when is, in spinal cord

Transverse myelitis - intense inflammation around parasite

Usually lower levels of spinal cord - flaccid paralysis, sphincter dysfunction and sensory loss

May develop into abscesses - low back pain, saddle anesthesia, sphincter dysfunction, and weakness or paralysis of lower limbs

Rarely, acute paraplegia due to occlusion of the anterior spinal artery by the parasite

48
Q

S. mansoni and S. haematobium clinical manifestations

A

Most are due to uncontrolled inflammatory response against the eggs, the worm is killed

49
Q

Schistosomiasis diagnosis

A

Symptoms are general – most cases do not involve CNS

Diagnosed through the detection of parasite eggs in stool or urine specimens

50
Q

Schistosomiasis risk factors

A

Commonly places with poor sanitation
School-age children at risk
Women doing domestic chores involving water at risk
Eco-tourism and popularity of “exploring off the normal areas”

51
Q

S. japonicum is restricted to

A

(most probable to cause CNS infection)

restricted to Indonesia and parts of China and Southeast Asia (none in japan)

Other Schistosoma spp are also restricted geographically

52
Q

Schistosomiasis treatment

A

Safe and effective medication is available: Praziquantel

taken for 1-2 days to treat all Schistosoma infections

CNS involvement - Praziquantel associated with corticosteroids

Surgical decompression of the spinal canal is still an option in some cases to treat transverse myelitis

53
Q

Schistosomiasis prevention

A

large-scale treatment of at-risk population groups, access to safe water, improved sanitation, hygiene education, and snail control

54
Q

Neurocysticercosis is caused by

A

By larva form of Taenia solium

Larvae ≠ tapeworm

55
Q

common CNS parasitic infection

A

T. solium (neurocysticercosis)

Another of CDC’s neglected tropical diseases [disease of immigrants - when immigrated already infected with disease]

56
Q

T. solium Larvae vs tapeworm

A

tapeworm - grow in intestine to very long

larva can infect any organ, but clinical manifestation are always due to CNS infection

57
Q

T. solium area

A

Most common cause of focal onset epilepsy in Central and South America

58
Q

T. solium life cycle

A

Pigs and humans become infected by ingesting eggs [humans ingest undercooked pork containing cysticerci]

**Eggs hatch **in the intestine, invade the intestinal wall and reach vasculature - dissemination

[taeniasis (infection by adult tapeworm]

Once reach other tissues, they **develop into cysticerci **

Cysts in the brain results in neurocysticercosis.

Once attached, progottids are released in feces in great numbers for long periods of time

59
Q

progottid

A

small segment of worm

every progottid release lots of eggs all the time

60
Q

Cysts, (cysticerci), can develop in

A

the muscles, the eyes, the brain, and/or the spinal cord.

Generally, only cysts in brain and/or spinal cord will cause symptoms

61
Q

Neurocysticercosis symptoms

A

only cysts in brain and/or spinal cord will cause symptoms

Cause seizures and/or headaches (these are more common)

[get in parenchyma] Confusion, difficulty with balance, brain swelling, and excess fluid around the brain (these are less common) [block canalls - hydrosephilus]

62
Q

what determines Neurocysticercosis severity

A

Parasite load will determine severity  low loads will be asymptomatic

Usually not fatal, but brain damage is irreversible [lots of cysts - can be fatal]

63
Q

Cysticerci are

A

liquid-filled vesicles including an invaginated scolex

64
Q

Neurocysticercosis cysts in CNS

A

may be located anywhere within the CNS: Parenchymal brain cysticerci, subarachnoid and ventricular cysticerci, or spinal cord cysticerci

Not clear how they enter the CNS – accepted notion is bloodstream

65
Q

___ cysts can get very large due to ___

A

Extraparenchymal

osmosis

The cysts are eventually killed, and they become calcified

66
Q

Neurocysticercosis diagnosis

A

Symptoms are general – parasite material not readily accessible

Preferred criteria - brain imagining techniques [Cysts can be easily seen on brain imagining techniques - if calcified - have been infected for years]
Histological
Serological
Epidemiological

67
Q

Neurocysticercosis treatment

A

has to be individualized [b/c symptoms could be due to many reasons]

Live cysticerci can be treated with albendazole or praziquantel

Seizures can be treated with anticonvulsants

Hydrocephalus can be treated surgically

Excessive inflammation with corticosteroids

A - Neuroinfectious Diseases 2 (9 decks)

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