1) Amoebae are single-celled organisms that can change shape by extending and retracting pseudopods. They are found across eukaryotic life and include pathogens. 2) Well-known pathogenic amoebae that can infect humans include Naegleria fowleri which causes meningoencephalitis, Entamoeba histolytica which causes dysentery, and Acanthamoeba which can cause keratitis or granulomatous amoebic encephalitis. 3) Amoebae move using pseudopods, feed through phagocytosis or pinocytosis, and can form protective cysts. Their life cycles and pathogenesis depend

1. AMOEBAE
M.PRASAD NAIDU
MSc, (Medical) Ph.D. (Medical)

2. • An amoeba (also ameba, amœba or amo
eboid) is a type of cell or organism which
has the ability to alter its shape, primarily
by extending and
retracting pseudopods. Amoebae do not
form a single taxonomic group, but are
found in every
major lineage of eukaryotic organisms
(domain Eukaryota).

3. • Amoeoboid cells occur not only
among the protozoa, but
also fungi, algae and animals.
• Among microbiologists, the terms
"amoeboid" and "amoebae" are
often used interchangeably for
any organism that
exhibits amoeboid movement.

4. • The best known amoeboid protists are the
"giant amoebae" Chaos
carolinense and Amoeba proteus, both of
which are widely cultivated and studied in
classrooms and laboratories. Other well
known species include the so-called "brain-
eating amoeba" Naegleria fowleri, the
intestinal parasiteEntamoeba histolytica,
which causes amoebic dysentery, and the
multicellular "social amoeba" Dictyostelium
discoideum.

5. Naegleria fowleri :
 Primary Amoebic Meningo
Encephalitis
(PAM)
 Fowler & Carter (1965 ).

6. Amebiasis Caused by Entamoeba histolytica.
(a) Light micrographs of a trophozoite (1,000)

7. A cyst (1,000).

8. • TROPHOZOITE :
 Vegetative & Feeding stage .
 CSF &Tissue .
 10 -20 µm , Karyosome with halo .
 Actively motile (Lobopodia )
 Binary fission .

9. • Amoebae move and eat by using pseudopods,
which are bulges of cytoplasm formed by the
coordinated action
of actin microfilaments pushing out the plasma
membrane that surrounds the cell.
• Groups of amoebae are distinguished by the
appearance and internal structure of their
pseudopods.
• Amoebozoan species typically have bulbous
pseudopods, rounded at the ends and roughly
tubular in cross-section (lobose)

10. • Cercozoan amoeboids, such
as Euglypha and Gromia, have slender,
thread-like (filose)
pseudopods. Foraminiferan emit fine,
branching pseudopods that merge with
one another to form net-like (reticulose)
structures. Some groups, such as
the Radiolaria and the amoeboids loosely
called Heliozoa, have stiff, needle-like,
radiating actinopods supported from
within by bundles of microtubules

11. SHAPE,
MOVEMENT
AND
NUTRITION

12. • Free-living amoebae may be "testate"
(enclosed within a hard shell), or "naked"
(lacking any hard covering). Testate amoebae
shells are composed various substances,
including calcium, silica, chitin, or
agglutinations of found materials like small
grains of sand and the frustules of diatoms.
• To regulate osmotic pressure, most
freshwater amoebae have a
contractile vacuole which expels excess water
from the cell.

13. • This organelle is necessary because freshwater has
a lower concentration of solutes (such as salt) than
the amoeba's own internal fluids (cytosol). Because
the surrounding water is hypotonic with respect to
the contents of the cell, water is transferred across
the amoeba's cell membrane by osmosis. Without a
contractile vacuole, the cell would fill with excess
water and, eventually, burst. Marine amoebae do
not usually possess a contractile vacuole, because
the concentration of solutes within the cell are in
balance with the tonicity of the surrounding water.
• The food sources of amoebae vary. Some amoebae
are predatory and live by consuming bacteria and

14. • Some are detritivores and eat dead organic
material. Amoebae typically ingest their food
by phagocytosis, extending pseudopods to
encircle and engulf live prey or particles of
scavenged material.
• Amoeboid cells do not have a mouth
or cytostome, and there is no fixed place on
the cell at which phagocytosis normally
occurs. Some amoebae also feed
by pinocytosis, imbibing dissolved nutrients
through vesicles formed within the cell
membrane.

15. AMOEBAE IN
MULTICELLULAR
ORGANISMS: ANIMALS
AND SLIME MOLDS

16. • Amoebae in multicellular organisms: animals
and slime molds
• Some multicellular organisms have amoeboid
cells only in certain phases of life, or use
amoeboid movements for specialized
functions.
• In the immune system of humans and other
animals, amoeboid white blood cells pursue
invading organisms, such as bacteria and
pathogenic protists, and engulf them
by phagocytosis.

17. • Amoeboid stages also occur in
the multicellular fungus-like protists,
the so-called slime molds.
• Both the plasmodial slime molds,
currently classified in the
class Myxogastria, and the cellular
slime molds of the
groups Acrasida and Dictyosteliida,
live as amoebae during their feeding
stage.

18. • The cells of the former form a
giant multinucleate amoeboid
organism,while the cells of the
latter live separately until food
runs out, at which time the
amoebae aggregate to form a
multicellular migrating slug which
functions as a single organism

19. LIFE CYCLE :
ONE HOST : Man .
Asexual Generation cycle .
MOI : Swimming in Contaminated water .
Infective form : Trophozoites .
Cysts (Inhalation ) –Rare .

20. Entry : Nose
Olfactory mucosa.

Olfactory bulbs

Sub Arachnoid space.

(Multiplication)

Choroid plexus

Ventricular destruction.

Ependymitis.

22. • Trophozoites Cysts (unfavorable
conditions ) .
• PATHOGENESIS :
IP : 2 -15 days .(5 days )
Neurotropic .
Brain tissue destruction .
Acute Hemorrhagic Necrotising meningo
encephalitis .
Cysts are absent in humans .

23. CLINICAL FEATURES :
Children & Young adults .
PAM .
Rapid onset & Fulminant .

24.  Sudden severe Persistent Bifrontal /Bitemporal
Headache ,Nausea , Projectile vomiting .
 Ageusia (loss of taste function).
 Parosmia (olfactory dysfunction).
 Generalized seizures
 Photophobia
 Coma
 Death
 Poor Prognosis .(95 % death )

25. DIAGNOSIS :
• Specimen : CSF (Antemortem )
Brain Biopsy (Post
mortem ).
CSF :
• Wet mount : Plenty of Actively motile
trophozoites .

26. • Stains : Trichrome , Giemsa , Wright .
• Direct Fluorescent Antibody
staining .
• BIOPSY : IF & Immuno Peroxidase method .

27. • Serodiagnosis : Not Useful .
• Molecular methods : DNA probes & PCR .
• CSF : Features of Pyogenic
Meningitis .

28. • Treatment : Amphotericin B &
Rifampicin,Miconazole .
• Prevention :

29. Acanthamoeba
• Opportunistic pathogens .
1. A.castellani .
2. A.astronyxis .
3. A.polyphaga .
4. A.culbertsoni .

30. • HABITAT : Dust , Soil , Sand , Rivers ,
Ponds , Tap water .
• MORPHOLOGY :
2 stages .
1. Trophozoite .
2. Cyst .

31. • TROPHOZOITE :
• Variable size & shape .
• 10 -40 µm .
• Acanthopodia Characteristic feature .

32. • CYST :
Polygonal /Spherical /Star shaped .
15 -20 µm.
Double layered cyst wall .

33. • LIFE CYCLE :
• MOI : Invasion of Broken skin .
• Inhalation of Cysts & Trophozoites .
• ROUTE : Lungs to Blood stream
(Multiplication )
• CNS .
• Sites of Localisation :Basal ganglia ,
• Posterior fossa , Cerebellum .

35. • PATHOGENESIS :
• Lesions of Brain , Eye , Lungs & Skin .
• Brain: Patchy , Sub Acute lesions of
granulomatous encephalitis .
• Skin: Nodular & Ulcerative lesion. Abscess .
• Cornea : Epithelial inflammation, Hypopyon .

37. • CLINICAL MANIFESTATIONS :
 Granulomatous Amoebic Encephalitis (GAM)
 Acanthamoeba Keratitis .
 Cutaneous Lesions .

38. GAE:
• Rare .
Risk factors :
• AIDS ,
• Immunosupression,Organ transplantation
• Malnourished .

39. • Clinical features :
 Low grade fever,stiff neck ,
 Altered Mental status .
 Seizures ,
 Cranial palsies ,
 Hemiparesis , Ataxia ,
 Photophobia
 Coma ,
 Multi organ Failure ,
 Death .

40. • Acanthamoeba Keratitis :
Contact lens wearers .(trauma )
Chronic , Progressive , Ulceration .
Annular Infiltration & Congested Cornea .
Perforation .
Blindness .

41. • CUTANEOUS LESIONS :
• Face & Extremities .
• Nodules , papules & ulcers .
• Poor Prognosis .
• GAE Fatal .

42. • DIAGNOSIS :
1. Microscopy :
2. Trophozoites & Cysts In Brain Biopsy & Corneal
Smears .
3. Wet mount : Trophozoites & Cysts .

43. 1. Stains : Acridine orange , Giemsa , LCB .
2. IF .
3. Culture :
4. Serlogical tests : Not useful .
5. Molecular methods .
6. Imaging Methods .

44. • TREATMENT :
• GAE – No therapy. Sulphonamides ,
Cotrimoxazole ,
Polymyxin –B .
• Keratitis : Topical Miconazole .
• Kertoplasty .
• PROPHYLAXIS :
• Disinfecting Contact lenses .

45. Foraminiferan (Ammonia tepida)

46. Shell of the testate amoeba Difflugia
acuminata, made up of mineral particles

47. THANK
YOU