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A - Neuroinfectious Diseases 2 > Parasitic Infections 1 > Flashcards

Parasitic Infections 1 Flashcards

1
Q

“Parasitic infections of the CNS” medically is a

A

Catchall expression for all non-bacterial, non-viral, and non-fungal infections

(ameba - not parasite but when get consider parasitic infection)

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2
Q

Parasitic burden

A

Tremendous burden to public health in the developing world

Increased tourism, migratory movements, and the AIDS epidemic have facilitated the spread of formerly geographically restricted parasitic infections

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3
Q

Parasites are diverse in

A

mechanisms and pathology
clinical manifestations

Difficult diagnosis
- Nonspecific symptoms, poor reliability of serological tests

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4
Q

What is a parasite

A

Organism that lives on or in a host organism from which it gets food

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5
Q

true vs accadental parasite

A

True parasite – humans are required to complete life cycle

Accidental – humans are a dead-end hosts; no benefit to either

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6
Q

Three main clinical classes of parasites

A

protozoa, helminths, and ectoparasites

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7
Q

Protozoans

A

microscopic, unicellular eukaryotes, free-living or parasitic in nature

harder to kill - more similar to own cells - anti parasitics high side effects

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8
Q

Helminths

A

large, multicellular organism, free-living or parasitic

cestodes (tapeworms); nematodes (roundworms); trematodes (flukes)

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9
Q

Ectoparasites

A

animals that attach or burrow into the skin and feed on the host for relatively long periods of time (days to weeks)

Mostly ticks, fleas, lice, and mites

vectors for pathogens - not pathogens themselves

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10
Q

Main CNS parasitic infections

A
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11
Q

most common CNS parasitic infections (3)

A
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12
Q

Amoebic that invade CNS

A

Naegleria, Acanthamoeba, and Balamuthia

Free-living, environmental organisms

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13
Q

Amoeba clinical manifestations

A
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14
Q

PAM and GAE have different

A

etiologies, risk factors, duration of illness, clinical features, and laboratory and imaging findings

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15
Q

___ survive despite treatment for Amoebic infections

A

<5%

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16
Q

PAM Naegleria fowleri (N. fowleri) can - to brain/cells

A

Fulminant (liquify brain), acute disease - necrosis of frontal lobes

N. fowleri can phagocytose entire neurons! (+ eat neurons)

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17
Q

PAM Acute inflammatory response

A

contributes to damage - no space in brain
rapid and potent

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18
Q

health status with PAM

A

Immunocompromised and immunocompetent individuals alike

heath status not matter

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19
Q

Naegleria fowleri more common in

A

warmer regions and warmer months

N. fowleri is a thermophilic protist - lake, hot spring - climate change, changing endemic areas.

Also poorly chlorinated pools, hot tubs, and thermally polluted water bodies (industrial discharge - change water temp)

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20
Q

N. fowleri life cycle

A

3 stage life cycle: amoeboid trophozoites,
flagellates, and cysts

Amebic trophozoites are the infective form

Flagellates are temporary, non-feeding, cells

Both trophozoites and flagellated forms are found in CSF

Cysts are survival form – dormant, stress resistant

Cysts never reported in brain tissue  1 case report of infection after inhalation of cysts

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21
Q

how does N. fowleri get into CNS

A

Enters CNS via the nose - swimming or diving (why main pathology - frontal lobes)

also become infected after using a neti pot or bathing with contaminated water
You CANNOT get infected by drinking or person-to- person contact

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22
Q

steps N. fowleri get into CNS

A

(adhesion) Binds to olfactory mucosa and penetrates respiratory epithelium
- Nfa1 is an adhesin localized to tips of pseudopodia - adhesion and
chemotactic behavior

Migrates through olfactory nerves into CNS [eats through, neurotropic]

Nitric oxide production and pore-forming proteins - necrosis

Several PAMPs - intense immune response

Lysis of immune cells releases more cytotoxic compounds

= significant destruction of brain parenchymal tissue = PAM

23
Q

clinical presentation of N. fowleri

A

can mimic that of bacterial meningitis, but progresses rapidly - coma and death within days

Mouse models show protective immunity can be developed - irreversible damage occurs too fast

commonality of survival - identity fast and young

24
Q

N. fowleri is suspected in cases

A

with recent history of freshwater exposure

25
Q

N. fowleri CSF analysis

A

similar to bacterial meningitis (low glucose, elevated proteins, and polymorphonuclear cells)

26
Q

N. fowleri

Visualization on CSF

Antigen detection

Serological testing

Brain imaging studies

A

Visualization on CSF can be missed on gram stains

Antigen detection assays can be performed on CSF or tissue sample, along with PCR - very few labs in US do them

Serological testing (measures antibody production) does not work as patients die too soon - no antibodies

Brain imaging studies can be normal early to findings of diffuse hemorrhages or infarctions with high inflammation later on the disease - depends on when do imaging

27
Q

Toxoplasma can infect

A

any warm-blooded animal - Present worldwide

28
Q

In immunosuppressed individuals Toxoplasma causes

A

toxoplasmosis

Multisystem disease, CNS involvement rare but most severe complication

immunosuppressed - aids, pregnant etc.

29
Q

Toxoplasma is known for its

A

altering behavior of host to promote dissemination (by host been eaten by a feline) - once infect host looks for cat even if normally hate/avoid cat

Because humans can’t be eaten by cats, we are a dead-end host (accidental parasite)

30
Q

___ are the only known reservoir of Toxoplasma

A

Felines

can undergo sexual reproduction else where - something special about GI tract in cat

31
Q

Oocysts cycle Toxoplasma

A

Oocysts shed in cat’s feces

Oocysts picked up by intermediate hosts in nature

Oocysts sporulate, infecting muscle and neural tissue

Felines eat intermediate hosts, restarting cycle again

32
Q

Ways humans get infected

A

Livestock infected by picking up oocysts from the environment

Food or water contaminated with cat feces or by contaminated environmental samples

Blood transfusion or organ transplantation

Transplacentally from mother to fetus

33
Q

Estimated that ____ of the world is infected with Toxoplasma

A

1/3

40 – 50 million people in US

34
Q

Toxoplasma is latent as

A

cysts in the muscles and the brain in health people

if in heart - very problematic

35
Q

is the leading cause of death due to foodborne illness in the United States

A

Toxoplasma
One of the 5 neglected parasitic infections of the United States

36
Q

Toxoplasma treatment

A

No current cure for infection - active infection can be treated, but latent cysts are resistant

once infected - infected for life

37
Q

how Toxoplasma infects CNS

A
38
Q

Toxoplasma CNS involvement almost always as an

A

opportunistic infections
One of the original AIDS-defining illnesses

Encephalitic syndrome - necrotic center surrounded by tachyzoites

Reactivation of cysts, which are already inside brain

Sudden fever, seizures, increased intracranial pressure, and decreased level of consciousness even coma

39
Q

____ is the most common cause of infectious

A

Toxoplasma

retinochoroiditis (eye infection)

Can also gain access to CNS as a complication

40
Q

Toxoplasma is more common in

A

hot and humid climates – oocysts are very sensitive to cold conditions

41
Q

Toxoplasma responsible for “Cat Ladies”?

A
42
Q

Most severe complication of Plasmodium falciparum infection

A

Cerebral malaria

only Plasmodium falciparum can cause CNS infection

43
Q

Cerebral malaria GCS

A

GCS - lower number less concuss

Unarousable coma (GCS ≤ 9) with the presence of malaria infected red blood cells in the peripheral circulation

44
Q

definition of CM and pathway from illness to death

A

Sudden fever - seizures - cloudiness or loss of consciousness

45
Q

P. falciparum extensively modifies the surface of

A

RBC, leading to sequestration in the brain’s microcapillaries and “rosetting“ which contributes to the pathology.

46
Q

CM clinical symptoms child vs adult

coma
sezures
SE
systemic complecations
neurological defects
retinopathy
prognosis

A
47
Q

Status epilepticus

A

is a medical emergency associated with significant morbidity and mortality. SE is defined as a continuous seizure lasting more than 30 min, or two or more seizures without full recovery of consciousness between any of them.

48
Q

Plasmodium spp species that are human pathogens

____ are ubiquitous

All the others are____

___ causes CM

A

5

P. falciparum
P. vivax
P. ovale
P. malariae
P. knowlesi

P. falciparum and P. malariae

restricted to certain geographical regions (most in Africa, Asia, or Oceania)

P. falciparum is the only one that causes CM - ~80% of all deaths from malaria

49
Q

CM Infection happens during

A

a female Anopheles mosquito bloodmeal

Depends also on climatic factors such as temperature, humidity, and rainfall

50
Q

Plasmodium spp involves ___ hosts

A

2 hosts: mosquito & animals (humans are almost exclusive for some of the Plasmodium spp)

From mosquito - liver stage (fast replication - bursts liver cells)
From liver stage - blood stage
From blood stage - mosquito

Blood stage parasites are responsible for the clinical disease

51
Q

P. falciparum infection

Neuroimaging

CSF analysis

Diagnosis is confirmed by

In children

A
52
Q

P. falciparum infection treatment

A

Quinine is the drug of choice; artemisinin and artemether can also be used together with other drugs

There is a growing problem of drug resistance

Related symptoms if untreated can be as fatal as CM: hypoglycemia, pulmonary edema, renal failure, internal bleeding, and hepatic dysfunction

53
Q

different human and environmental factors can affect P. falciparum treatment

A

immune status (pregnancy), genetics (sickle cell trait or Duffy blood group), agricultural work, deforestation, lack of housing

sickle cell - immune to malara (infectious disease influence evolution)

54
Q

Best way to control malaria

A

control de mosquito (because v hard to treat)- nonprofit efforts

A - Neuroinfectious Diseases 2 (9 decks)

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