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MMI 426 > Free Living Amoebae > Flashcards

Free Living Amoebae Flashcards

1
Q

free living amoebae all belong in this group

A

Sarcodina

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2
Q

free living amoebae genera that are potentially pathogenic to humans + other vertebrates

A

Acanthamoeba
Naegleria
Balamuthia
Sappinia
Hartmannella

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3
Q

amphizoic

A

amoebae’s ability to exist within a host or in environment as free-living forms

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4
Q

T or F. Most free-living amoebaes are bacteriophagous inhabitants of soil, water, and sewage

A

T

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5
Q

most amoebae exist in two basic forms

A

trophozoite
cyst

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6
Q

some amoebae are diphasic:

A

ameboid (binary fission)
flagellated stage

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7
Q

when does amoebae encystment occurs

A

under adverse environmental conditions and allow for survival outside host

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8
Q

amoebic trophozoites

A

pseudopods

adhesion essential for locomotion and feeding

movement enhanced by higher temps (30C)

amoebastomes/”food cups” = cytoplasmic extension
- ingestion of bacteria and cell debris
- attachment to surfaces
*NO correlation w pathogenicity

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9
Q

the flagellated tage of amebae

A
  • cell changes shape = synthesizes new flagellar apparatus
    > more rigid cell, pear-shaped, sturdy shape, faster movement
  • induced by nutritional deprivation, temp or osmotic shock
  • lasts from 2 to several hrs
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10
Q

cyst stage of amoebae

A
  • environmentally hardy form
  • mucopolysaccharide double wall, resistant to biocides
  • Ostioles (pores) sealed by mucus plugs
  • cysts not formed in tissue, left behind when trophozoite emerge
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11
Q

ostioles

A

pores that allow communication that allow communication inside and outside of amoeboid cyst

not formed in tissue; left behind when trophozoites emerge

when trophozoites come out of cyst, they squeeze through this which leave intact cyst = easily seen in microscope

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12
Q

Naegleria fowleri

A

diphasic amoeba
- exist in amoeboid and flagellate form (2 to several hours)
- agent of amoebic encephalitis

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13
Q

lifecycl of Naegleeri fowleri

A

invasion via nasal passages on contact w water (ex: water slides without plugging nose)
> amoebae travel along olf nerves
> cribriform plate to brain

INHALING infested water is how you get infected; ingestion of water does nothing

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14
Q

virulence of Naegleria depends on:

A
  • Nfa1 protein (mediates amebic attachment to target cells; first step to cell invasion)
  • Feeding cups (help directly phagocytose the brain cells).
  • Nitric oxide production
  • Pore-forming proteins.
  • Cytolytic molecules like cysteine proteases, phospholipases, and phospholipolytic enzymes
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14
Q

epidemiology of N. fowlerii

A
  • ubiquitous = freshwater lakes, hot water springs, poorly chlorinated pools (NOT in seawater)
  • worldwide
  • growth enhancement at high temps (42C); thermophilic organism
  • protection = calination and chlorination (cysts more fragile than Acanthamoeba)
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15
Q

primary amoebic meningioencaphalitis

A

(PAM) FAST AND DEADLY!
N. fowleri
- extensive cell necrosis caused by amoebic trophozoites = significant hemorrhages = severe destruction of meninges, olf nerves, and brain tissue
- inflammatory exudate, edema (swelling of brain => DEATH)

16
Q

where is amoebic meningitis common?

A

new zealand/australia

17
Q

how to diagnose Naegleria fowlerii

A
  • microscopy of brain biopsy, CSF
  • in vitro culture on lab media (plain agar w lawn of bacterial growth = amoeba food)
  • molecular detection (PCR)
18
Q

Acanthamoeba culbertsoni morphology

A

troph = spine like acanthopodia; lobopodia (thick pseudopodia)
cyst = double walled
NO FLAGELATE FORM

19
Q

other Acanthamoeba species

A

A. polyphaga
A. castellani
A. astronyxis

20
Q

life cycle of Acanthamoeba

A
  • entry via resp tract, broken skin, eye, maybeee genitourinary tract
  • invasion of CNS, eye, other organs

some nasopharyngeal carriers are completely healthy

21
Q

pathogenesis of Acanthamoeba

A

slow tissue invasion (weeks to months)
- adhesion (mannose binding proteins/mannose glycoprotein receptors on cornea

  • destruction of corneal epithelium/upregulation of MMPs (matrix metalloproteinases) w release of mannose induced protein 133 + activation of phospholipases and release of collagenases and other proteases = APOPTOSIS
  • breaching Bowman’s capsule and destruction of corneal stroma

= usually does not become intraocular

22
Q

pathology of infections caused by Acanthamoebaspecies

A

Granulomatous Amebic Encephalitis (GAE) = necrotizing lesions/focal hemorrhages; MOST severe, most fatalities; slow

Eye lesions =
- inflammation
- full thickness corneal ulcers and keratitis (inflammation of the cornea)
- necrosis and full thickness destruction of the eye

Granuloma formation (skin, kidneys, liver, uterus, prostate) = necrotizing lesions/focal hemorrhages

23
Q

clinical presentation of GAE

A

granulomatous amoebic encephalitis, or meningoencephalitis

  • slow (weeks – months); unlike Naegleria
  • progressive tissue invasion and destruction in immunocompromised host
  • RARE but serious! almost always leads to death of human
  • treatment ineffective
24
Q

clinical presentation of keratitis, corneal ulcer

A

– healthy host, compromised eye (90% -contact lens, rest – eye trauma
10-15 times increase for overnight wear

25
Q

least often seen presentation of Acanthamoebae

A

Acute/chronic infection of skin, lung, uterus, prostate
(in immunocompromised host)

26
Q

ring infiltrate

A

whitish ring around pupil
Acanthamoebae

27
Q

T or F. Even if you clear acanthamoeba infection, you are still left with a scar and blindness

A

T

28
Q

epidemiology of Acanthamoeba

A

Free living and widely distributed in natural waters (ponds, lakes, hot springs, even oceans), as well as in dustand soil

Also detected in bottled mineral water, Jacuzzi tubs, recreational pools, ventilation ducts, humidifiers, air-conditioning units, shower heads and even kitchen and bathroom taps.

NOTE – Acanthamoeba spp is much more resistant to chlorination and other biocides (including radiation) than Naegleria

29
Q

T or F. Acanthamoeba can carry viruses and bacteria in their cytoplasm

A

T! (including bacteria that causes Legionnaires disease)

30
Q

lab diagnosis of Acanthamoeba

A

similar to Naegleria

Cerebrospinal fluid – very rarely!!!

Corneal scrapings, brain, skin and other tissue biopsies

Microscopy using permanent stains

In vitro culture on laboratory media (plain agar with lawn of bacterial growth)

Molecular detection (PCR)

31
Q

Balamuthia mandrillaris

A

Amoebae group

similar to Acanthamoebae (life cycle and presentation similar to GAE)
- clinical presentation = disseminated infection (skin lesion -> CNS disease in weeks to months
- often starts by involving mid-face, nose/oral cavity

32
Q
A

MMI 426 (20 decks)

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