PARAenteamoeba histolytica.ppt This power point presentation scrutinise about amoeba.

enteamoeba histolytica

2. Protozoan
◦The protozoa are a microscopic, one celled (unicellular)
organism. They are the simplest forms of animal life.
◦ Several species of protozoa are found in to intestinal tract
and few of them invade different part of human body. E.g.
blood, tissue, internal organs.
◦The protozoa are classified biologically according to their
type of locomotory organelles or according to their
habitat in the body of the host
◦ Locomotory organelles Habitat
Ameba- pseudopodia - Intestinal protozoa
Flagellate - Tissue protozoa
Ciliate - Blood protozoa

3. 
Intestinal protozoa
A number of protozoa are capable of living in the
Intestinal tract of man.
Some of the intestinal protozoa of medical
importance are
◦Amoebae
◦Flagellates
◦Ciliates and
◦sporozoan

4. PROTOZOAPROTOZOA

6. AmoebaAmoeba::
•Entamoeba histolyticaEntamoeba histolytica
•Entamoeba disparEntamoeba dispar
•Entamoeba coliEntamoeba coli
•Entamoeba Entamoeba
hartmannihartmanni
•Endolimax nanaEndolimax nana
•Iodamoeba bütschliiIodamoeba bütschlii
INTESTINAL PROTOZOAINTESTINAL PROTOZOA
ApicomplexaApicomplexa::
•Cryptosporidium Cryptosporidium
hominishominis
•Cryptosporidium parvumCryptosporidium parvum
•Cyclospora cayetanensisCyclospora cayetanensis
•Isospora belliIsospora belli
FlagellatesFlagellates::
•Giardia lambliaGiardia lamblia
•Dientamoeba fragilisDientamoeba fragilis
•Chilomastix mesniliChilomastix mesnili
•Trichomonas hominisTrichomonas hominis
•Enteromonas hominisEnteromonas hominis
•Retortamonas intestinalisRetortamonas intestinalis
Other(Cilliate)Other(Cilliate)::
•Balantidium Balantidium colicoli
•Blastocystis hominisBlastocystis hominis

7. COMMON CHARACTERSTICSCOMMON CHARACTERSTICS
TYPICAL TYPICAL FECAL-ORALFECAL-ORAL LIFE CYCLE LIFE CYCLE

8. Fecal-Oral Transmission Fecal-Oral Transmission
FactorsFactors
•Poor personal hygienePoor personal hygiene
•Food handlersFood handlers
•InstitutionsInstitutions
•Children in day care Children in day care
centerscenters
•Developing countriesDeveloping countries
•Highly endemicHighly endemic
•Poor sanitationPoor sanitation
•Travelers diarrheaTravelers diarrhea
•Water-borne epidemicsWater-borne epidemics
•Male homosexualityMale homosexuality
•Oral-anal contactOral-anal contact
•ZoonosisZoonosis
•EntamoebaEntamoeba = no = no
•CryptosporidiumCryptosporidium = yes = yes
•GiardiaGiardia = controversial = controversial

9. •Improve personal hygieneImprove personal hygiene
•Especially institutionsEspecially institutions
•Treat asymptomatic Treat asymptomatic
carrierscarriers
•Eg, family membersEg, family members
•Health educationHealth education
•Hand-washingHand-washing
•SanitationSanitation
•Food handlingFood handling
Control/Prevention
•Protect water supply
•Treat water if
questionable
•Boiling
•Iodine
•chlorine

11. Introduction
Amoeba (plural amoebae)-PAmoeba (plural amoebae)-Protists rotists that moves by that moves by
means of pseudopods means of pseudopods
Amoeba -Greek word amoeba, means changeAmoeba -Greek word amoeba, means change
-Most Amoeba are -Most Amoeba are free-living free-living widely distributed mostly widely distributed mostly
in in
aquatic environment aquatic environment
fresh water - salt water, fresh water - salt water,
wet soil, -on water plants leaveswet soil, -on water plants leaves
-Few of the parasitic and free-living amebas produce -Few of the parasitic and free-living amebas produce
human diseasehuman disease

13. TaxonomyTaxonomy
•PhylumPhylum SarcomastigophoraSarcomastigophora
• Sub-Phylum Sub-Phylum SarcodinaSarcodina
• ClassClass LoboseaLobosea
– Order AmoebidaOrder Amoebida
– Suborder TubulinaSuborder Tubulina
•GeneraGenera:: EntamoebaEntamoeba, , IodamoebaIodamoeba, , Endolimax- Endolimax-
parasiticparasitic
•Species- Entamoeba histolyticSpecies- Entamoeba histolytic
-- -- Suborder AcanthopodinaSuborder Acanthopodina
•Genera:Genera: Acanthamoeba - Free livingAcanthamoeba - Free living
– Order SchizopyrenidaOrder Schizopyrenida
•GeneraGenera: : Naegleria - Free livingNaegleria - Free living

14. Parasitic and
commensal Amoeba:
Intestinal
•Entamoeba histolytica
•Entamoeba dispar
•Entamoeba coli
•Entamoeba hartmanni
•Endolimax nana
•Iodamoeba bütschlii
Mouth
• E. gingivalis
Free living Amoeba:
Pathogenic
•Naegleria fowleri
•Acanthamoeba spp
The AmoebaThe Amoeba
Classification….

15. Classification….Classification….
1.1. pathogenicpathogenic::
intestinal amoeba: E- histolytica.intestinal amoeba: E- histolytica.
2. 2. non pathogenic/Commensalnon pathogenic/Commensal ::

►

►
Mouth amoeba: E.gingivalisMouth amoeba: E.gingivalis

►

►
intestinal amoeba: E.coli, endolimax nana, iodamoeba intestinal amoeba: E.coli, endolimax nana, iodamoeba
butschlii butschlii
3.Free living amoeba3.Free living amoeba

►

►
Naegleria fowleriNaegleria fowleri
Acanthamoeba sppAcanthamoeba spp

16. Entamoeba histolyticaEntamoeba histolytica

17. EPIDEMIOLOGY
•Cosmopolitan distribution principally
•In tropical countries with warm climates and bad sanitary
conditions (fecalism).
•It is more frequent in poorest areas with;
 Contaminated water,
 Poor management of waste,
 Poor drainage system.

18. Epidemiologic Risk Factors
Prevalence Severity
 lower socioeconomic status
 crowding
 lack of indoor plumbing
 endemic area
 institutionalization
 communal living
 promiscuity among male
homosexuals
 children, esp. neonates
 pregnancy and
postpartum states
 corticosteroid use
 malignancy
 malnutrition
Modified from Ravdin (1995) Clin. Inf. Dis. 20:1453

19. FREQUENCYFREQUENCY
•Amebiasis-Amebiasis- is the 3is the 3
rdrd
leading cause of death worldwide, leading cause of death worldwide,
~ 10% of world’s population may be ~ 10% of world’s population may be
infected withinfected with E. histolytica E. histolytica / / E. disparE. dispar. .
•worldwide incidence worldwide incidence = = 0.2-50%(tropics)0.2-50%(tropics)
• 500 million500 million people worldwide infectedpeople worldwide infected
• 100 million100 million people suffer acute symptoms people suffer acute symptoms
• 100,000 100,000 people die every yearpeople die every year
•NoteNote
•Since more survey to determine the prevalence are made on stool Since more survey to determine the prevalence are made on stool
examination which includes E. disparexamination which includes E. dispar
•Therefore, the current epidemiology of amoebiasis doesn’t show the Therefore, the current epidemiology of amoebiasis doesn’t show the
true prevalence of E histolyticatrue prevalence of E histolytica

20. Habitat and Morphology Habitat and Morphology
•E. histolytica has both trophozoite and cyst forms.E. histolytica has both trophozoite and cyst forms.
•The trophozoites are microaerophilic,The trophozoites are microaerophilic,
–dwell in the dwell in the lumen or wall of the colonlumen or wall of the colon, ,
–feed on feed on bacteria and tissue cellsbacteria and tissue cells,,
–and multiply rapidly in the anaerobic environment and multiply rapidly in the anaerobic environment
of the gut. of the gut.
–When When diarrheadiarrhea occurs, the trophozoites are occurs, the trophozoites are
passed unchanged in the liquid stool. passed unchanged in the liquid stool.

22. E. Histolytica Life Cycle
Definitive Host: Humans
Intermediate Host: None

23. •TransmissionTransmission
•Ingestion of mature cystIngestion of mature cyst
•The average infective dose exceeds 1000 organisms, The average infective dose exceeds 1000 organisms,
butbut
•Ingestion of a single cyst has been known to Ingestion of a single cyst has been known to
produce infection.produce infection.
•Location in host: Location in host:
•Colonization is most intense in areas of fecal Colonization is most intense in areas of fecal
stasis such as the cecum and recto-sigmoid but stasis such as the cecum and recto-sigmoid but
may be found throughout the large bowel.may be found throughout the large bowel.
•May be carried to liver, lungs, and other body parts May be carried to liver, lungs, and other body parts
if it perforates the intestinesif it perforates the intestines

24. L
i
f
e

c
y
c
l
e
…

26. Mature cysts can survive in envt.
•temp up to 55°C,
•Norm Chlorine conctentration
•gastric acid.
Humans are the only reservoir excreting up to 45
million cysts daily
Life cycle….

27. PATHOGENESIS AND PATHOLOGY OF AMEBIASISPATHOGENESIS AND PATHOLOGY OF AMEBIASIS
•NON-INVASIVENON-INVASIVE
–ameoba colonize on intestinal mucosaameoba colonize on intestinal mucosa
–ingest bacteria and cellular debris from the lumen.ingest bacteria and cellular debris from the lumen.
–asymptomatic cyst passed with stool.asymptomatic cyst passed with stool.
–non-dysenteric diarrhea, abdominal cramps, other GI non-dysenteric diarrhea, abdominal cramps, other GI
symptomssymptoms
•INVASIVEINVASIVE
–necrosis of mucosa necrosis of mucosa  ulcers, dysentery ulcers, dysentery
–ulcer enlargement ulcer enlargement  severe dysentery, colitis, severe dysentery, colitis,
peritonitis peritonitis
–metastasis metastasis  extraintestinal amebiasis extraintestinal amebiasis

28. 1.Trophozoites
•colonize , adhere to the mucus layer and ingest bacteria and
cellular debris from the lumen.
•Usually asymptomatic, or exhibits symptoms ranging from
mild abdominal discomfort to diarrhea and cramps..
NON-INVASIVE

29. •The non-invasive infection can persist or progress to an
invasive by
•Penetration of mucus layer
•Contact-dependent killing of epithelial cells
•Breakdown of tissues (extracellular matrix)
•Contact-dependent killing of neutrophils and other
leukocytes, etc.
INVASIVE

30. •Three key virulence factors:Three key virulence factors:
–Amebic lectin: Amebic lectin: binds parasite to galactose-binds parasite to galactose-
containing containing
sugars on host cellssugars on host cells
–Amoebapores: Amoebapores: adherence-dependent cytolysisadherence-dependent cytolysis
–Cysteine proteaseCysteine protease: cleaves antibodies and C3: cleaves antibodies and C3
–Trophozoites ingest human cellsTrophozoites ingest human cells
Dysentery -disease of lower intestine: a disease
of the lower intestine caused by infection with
bacteria, protozoans or other parasites and marked
by severe diarrhea, inflammation, and the passage
of blood and mucus

31. •ulcers with raised borders
•Mucosa between ulcers appears normal
•little inflammation between lesions

33. •‘flasked-shaped ulcer’ trophozoites at boundary of
necrotic and healthy tissue
•trophozoites ingesting host cells
•dysentery (blood and mucus in feces)
Once the lesion penetrates below the superficial epithelium, it
meets the resistance of the colonic musculature and spreads
laterally in thesubmucosa

35. ‘hematophagous’
trophozoites

37. •Ameba expand laterally and downward
into lamina propria
•Localized sloughing (ulcers coalesce)
•Perforation of intestinal wall
• Peritonitis
• 2
o
bacterial infections
• Local abscesses
•Ameboma (=amebic granuloma)
ameboma = inflammatory thickening
of intestinal wall around the abscess
(can be confused with tumor)
Ulcer Enlargement can lead to secondary
infection and extraintestinal lesions

39. Lateral and Downward Expansion
of Ameba into Lamina Propria
•localized sloughing
•perforation of intestinal wall
•ulcers coalesce

41. Gross pathology of large intestine due
to Entameba histolytica

42. •Metastasis via blood stream
•Primarily liver (portal vein)
•Other sites less frequent
•Manifested by,
•Ameba-free stools common
•High antibody titers
Extraintestinal amebiasisExtraintestinal amebiasis

44. Amebic liver abscessAmebic liver abscess
•Most common form of Most common form of
extraintestinal amebiasisextraintestinal amebiasis
•symptoms are right upper symptoms are right upper
quadrant pain and feverquadrant pain and fever
•Acute as well as chronic illness, Acute as well as chronic illness,
with gradual or sudden onsetwith gradual or sudden onset

45. Amebic Liver Abscess
•Fast growing abscess filled
with:
•chocolate-colored ‘pus’
•necrotic material
•usually bacteria free
•amoebae are found only
at borders
•lesions expand and
coalesce
•further metastasis, direct
extension or fistula

47. Amebic liver abscessAmebic liver abscess
•30-50% of patients with liver 30-50% of patients with liver
abscess show also pneumonic abscess show also pneumonic
involvementinvolvement
•Rupture is again a major threat, Rupture is again a major threat,
especially rupture into the especially rupture into the
pericardiumpericardium
•Draining abscesses is today Draining abscesses is today
only performed in extreme only performed in extreme
cases when rupture is fearedcases when rupture is feared
•Responds well to Responds well to
chemotherapychemotherapy

48. Pulmonary Amebiasis
•rarely primary
•rupture of liver abscess
through diaphragm
•2
o
bacterial infections
common
•s/s-fever, cough,
dyspnea, pain

49. Cutaneous Amebiasis
•intestinal or hepatic fistula
•mucosa bathed in fluids
containing trophozoites
•perianal ulcers
•urogenital (eg, labia,
vagina, penis)

50. •The incubation period The incubation period
–Range from a few days to months or years with 2-4 Range from a few days to months or years with 2-4
weeks being the most common. weeks being the most common.
•Transitions from one type of intestinal syndrome to Transitions from one type of intestinal syndrome to
another can occur and another can occur and
•Intestinal infections can give rise to extraintestinal Intestinal infections can give rise to extraintestinal
infections.infections.
CLINICAL MANIFESTATIONCLINICAL MANIFESTATION

51. CLINICAL MANIFESTATIONCLINICAL MANIFESTATION
•Amebiasis presents a wide range of clinical syndromesAmebiasis presents a wide range of clinical syndromes
•Depends on:Depends on:
–host’s previous exposure to parasitehost’s previous exposure to parasite
•Chronic, low-level exposure- asymptomatic.Chronic, low-level exposure- asymptomatic.
•Less frequent exposure- severe symptoms.Less frequent exposure- severe symptoms.
–on nutritional status of hoston nutritional status of host
–whatwhat organ the parasite invadesorgan the parasite invades..
•Abdominal cavityAbdominal cavity
–Peritonitis, abdominal pain, cramping, and anemiaPeritonitis, abdominal pain, cramping, and anemia
•Liver Liver
–Symptoms are similar to hepatitisSymptoms are similar to hepatitis
•Lungs, brains, or heartLungs, brains, or heart
–May cause the death of the hostMay cause the death of the host..

52. Clinical Syndromes
Associated with Amebiasis
Intestinal Disease
 asymptomatic cyst passer
 symptomatic nondysenteric
infection
 amebic dysentery
 fulminant colitis
 + perforation (peritonitis)
 ameboma (amebic granuloma)
 perianal ulceration

Extraintestinal Disease
 liver abscess
 pleuropulmonary amebiasis
 brain and other organs
 cutaneous and genital diseases

Intestinal Symptoms
range
•mild to intense
•transient to long lasting
•Non dysenteric
•Diarrhea, - cramps,
•Flatulence, - nausea
•dysenteric
•blood/mucus in stools
•cramps/pain, tenesmus
•ameboma
•palpable mass, obstruction
Liver symptoms
Symptoms are similar to hepatitis
Lungs, brains, or heart
May cause the death of the host

53. Metronidazole is the drug of choice for extra-Metronidazole is the drug of choice for extra-
intestinal amebiasisintestinal amebiasis
•Several drugs are available to clear Several drugs are available to clear
symptomatic and asymptomatic enteric symptomatic and asymptomatic enteric
(luminal) infection (luminal) infection
•Metronidazole (Flagyl) is the drug of Metronidazole (Flagyl) is the drug of
choice for invasive amoebiasis (and choice for invasive amoebiasis (and
should be combined with a lumen acting should be combined with a lumen acting
drug as it is not fully effective on luminal drug as it is not fully effective on luminal
stages)stages)
•Metronidazole is a prodrug which is Metronidazole is a prodrug which is
activated by an enzyme involved in the activated by an enzyme involved in the
microaerobic fermentation metabolism of microaerobic fermentation metabolism of
E. histolyticaE. histolytica

54. IntestinalIntestinal
1.1.Microscopic examinationMicroscopic examination
A.A.Examination of fresh dysenteric faecal specimen Examination of fresh dysenteric faecal specimen
or rectal scraping for or rectal scraping for motile trophozoites motile trophozoites
•wet mountswet mounts
–Fresh stoolFresh stool
•Permanently stained preparations (e.g. Permanently stained preparations (e.g.
trichrome).trichrome).
–Fresh stoolFresh stool
–Preserved stoolPreserved stool
Microscopy

55. Microscopic examinationMicroscopic examination
B.B.Examination of formed or semi-formed faecal Examination of formed or semi-formed faecal
specimen for specimen for cysts cysts
–Fresh stoolFresh stool
–Smear after concentrationSmear after concentration
–Preserved stoolPreserved stool

56. Characteristics used to distinguish species of Characteristics used to distinguish species of
intestinal amebaeintestinal amebae
Trophozoites Trophozoites
•MotilityMotility- progressive or nonprogressive. - progressive or nonprogressive.
•Cytoplasm Cytoplasm
–Appearance-finely granular, coarsely Appearance-finely granular, coarsely
granular, or vacuolated. granular, or vacuolated.
–Inclusions-erythrocytes, bacteria, Inclusions-erythrocytes, bacteria,
molds. molds.

57. •CystsCysts
–Nucleus Nucleus
•Nucles present. Nucles present.
•Peripheral chromatin-present or absent.Peripheral chromatin-present or absent.
–Cytoplasm Cytoplasm
•Chromatoid bodies-present or absent. Chromatoid bodies-present or absent.
•If present, the shape is important. If present, the shape is important.
•Glycogen- appearanceGlycogen- appearance. .

59. Entamoeba cysts (light microscopy)Entamoeba cysts (light microscopy)
E. coli E. histolytica

60. Prevention and control
•Personal hygiene
•Safe water supply
•Vegetable should be cooked
•Food handlers should be checked
•Access of flies and cockroach to food must be prevented
•Health education.

61. There are only two genera of Free-Living Free-Living amoebae
Naegleria fowleri
Acanthamoeba spp
Pathogenic Free-Living AmebaePathogenic Free-Living Amebae

62. General characteristicsGeneral characteristics
•Usually free livingUsually free living
•Rarely infect humansRarely infect humans
•Acquired by soil/water contactAcquired by soil/water contact
•No human to human or vector borne No human to human or vector borne
transmissiontransmission
•Causes Causes Acute/chronic Acute/chronic amebic amebic
meningoencephalitis meningoencephalitis

63. Distribution: worldwide
Habitat: Free living
Fresh water/lakes and ponds
Moist soil
Parasitic
Nasal cavity and CNS

Causes: primary amebic meningoencephalitis
(PAM)
PAM first recognized by Fowler (1965)
~ 200 documented cases worldwide
Naegleria fowleri

64. low nutrients
Distilled water
desiccat
ion
Morphology & Life cycle
Amoebofllagelate
Cyst = dormant form
Amoebid
Trophozoite =
Flagellate =
feeding and
replicating form
None feeding
Don’t replicate
•Feed on bacteria &
organic matter
•Enter nose-Infect
brain via olfactory
nerve
For dispersal
in evt.
Nutrients
restored

65. TransmissionTransmission
•Infection:-Infection:- through nasal cavity by aspiration through nasal cavity by aspiration
of water(especially warm) contaminated with of water(especially warm) contaminated with
trophozoites while;-trophozoites while;-
•bathing in stagnant fresh water/lakes/pools bathing in stagnant fresh water/lakes/pools
contaminated with sewage/decaying mattercontaminated with sewage/decaying matter
•under chlorinated swimming poolunder chlorinated swimming pool
•Snuffing water from lakes/ponds etcSnuffing water from lakes/ponds etc

67. N. fowleriN. fowleri: Pathology: Pathology
•Causes Primary Amebic Meningoencephalitis (PAM)Causes Primary Amebic Meningoencephalitis (PAM)
•Very rapidly causes the death of hostVery rapidly causes the death of host
–Rapid destruction of brain tissueRapid destruction of brain tissue
Symptoms very similar to other types of meningitis and encephalitis.Symptoms very similar to other types of meningitis and encephalitis.
•Symptoms usually seen within a few days after swimming in Symptoms usually seen within a few days after swimming in warm warm
still watersstill waters(1-14 days)(1-14 days)
•Symptoms include Symptoms include headache, lethargy, disorientation, comaheadache, lethargy, disorientation, coma
•Rapid clinical course, death in 4-5 days after onset of symptomsRapid clinical course, death in 4-5 days after onset of symptoms
•But much less common and usually mistaken for more common But much less common and usually mistaken for more common
bacterial and viral formsbacterial and viral forms
•trophozoites can be detected in trophozoites can be detected in spinal fluidspinal fluid, but diagnosis is usually at , but diagnosis is usually at
autopsyautopsy

68. Clinical symptoms Clinical symptoms
•symptoms usually seen within a few days after swimming in symptoms usually seen within a few days after swimming in
warm still waters (1-14 days) and include headache, warm still waters (1-14 days) and include headache,
lethargy, disorientation, and comalethargy, disorientation, and coma. . rapid clinical course, rapid clinical course,
death in 4-5 days after onset of symptomsdeath in 4-5 days after onset of symptoms
•The disease progresses rapidly with dramatic symptoms and The disease progresses rapidly with dramatic symptoms and
is usually fatal is usually fatal
• Incubation period 3-7 days accompanied by the prodromal Incubation period 3-7 days accompanied by the prodromal
((forewarning symptomforewarning symptom) symptoms of head ache and fever) symptoms of head ache and fever
•Frank Meningitis, Nausea, and Vomiting (Stiff-neck) Frank Meningitis, Nausea, and Vomiting (Stiff-neck)
confusion and coma-death usually occur in 3-6 day confusion and coma-death usually occur in 3-6 day
following the onset of the disease.following the onset of the disease.

69. N. fowleriN. fowleri: : Laboratory diagnosisLaboratory diagnosis
•Diagnosis is usually made at autopsy.Diagnosis is usually made at autopsy.
–Amoeba in a brain smearAmoeba in a brain smear
•May be possible to diagnose with spinal tap.May be possible to diagnose with spinal tap.
•Finding trophozoites in CSFFinding trophozoites in CSF
CSF:CSF: purulent & may contain eosinophils, purulent & may contain eosinophils,
RBC with reduced glucose and raised proteinRBC with reduced glucose and raised protein
-Indications of Naelgeria infection:-Indications of Naelgeria infection:
elevated white cell count in CSF elevated white cell count in CSF
without the successful recovery of bacteria without the successful recovery of bacteria
•Treatment is rarely given
–Amphotericin B and qinghaosu
PreventionPrevention
•Public and private swimming pools should be chlorinatedPublic and private swimming pools should be chlorinated
•Keep head above water (or use nose plugs) in thermal pools or other Keep head above water (or use nose plugs) in thermal pools or other
warm, stagnant water.warm, stagnant water.

70. AcanthameobaAcanthameoba sp. sp.
•Geographic Distribution:Geographic Distribution: Cosmopolitan Cosmopolitan
–Found in Found in freshwater freshwater almost everywhere Cannot survive in thermal almost everywhere Cannot survive in thermal
poolspools
–Has trophozoite Has trophozoite and cyst forms and cyst forms
•Definitive Host: Definitive Host: Usually Free-livingUsually Free-living
–Facultative parasite of humansFacultative parasite of humans
Mode of transmission:Mode of transmission:..
–Cyst and trophozotes are infectiveCyst and trophozotes are infective
–portal of entry unknown, possibly respiratory tract (inhalation of cysts)portal of entry unknown, possibly respiratory tract (inhalation of cysts)
–invades body through invades body through cuts and abrasions or wounds in skin/eye cuts and abrasions or wounds in skin/eye
contaminated with soilcontaminated with soil
–The brain is probably infected by trophozoites via blood stream from The brain is probably infected by trophozoites via blood stream from
infected skin or lunginfected skin or lung
•Location in HostLocation in Host:: Most common in eye and skin. Rarely invades Most common in eye and skin. Rarely invades
brain/lungbrain/lung

71. Morphology & life cycle
Typical protozoan life cycle
Exist as trophozoites and Cyst
cyst & trophozoit
are infective
Angular in shape
with three
layared wall
Wrinkled
appearance
Several yrs in soil
-Slow motility
-spiky
projection

73. AcanthameobaAcanthameoba sp: Pathology: sp: Pathology:
•Rarely causes damage in people with intact immune systems Rarely causes damage in people with intact immune systems
•Most common cause of Most common cause of corneal ulcerscorneal ulcers and and keratitiskeratitis in contact lens wearers in contact lens wearers
Mainly causesMainly causes
A- Amebic KeratitisA- Amebic Keratitis
B- chronic Granulomates meningoencephalitisB- chronic Granulomates meningoencephalitis
Amebic Keratitis-A vision threatening chronic inflammation of the Amebic Keratitis-A vision threatening chronic inflammation of the
corneacornea
•predisposing factorspredisposing factors
•ocular trauma & contact lens (contaminated cleaning solutions)ocular trauma & contact lens (contaminated cleaning solutions)
•symptomssymptoms
•ocular pain and corneal lesions (refractory to usual treatments)ocular pain and corneal lesions (refractory to usual treatments)
•diagnosisdiagnosis
•demonstration of amoebas in corneal scrapingsdemonstration of amoebas in corneal scrapings
•Treatment- difficult, limited successTreatment- difficult, limited success

74. chronic Granulomates meningoencephalitischronic Granulomates meningoencephalitis
•AIDS Patients and other immune suppressed individuals cannot fight the AIDS Patients and other immune suppressed individuals cannot fight the
amoebaamoeba
–May cause May cause skin ulcerationsskin ulcerations, , keratitiskeratitis, and , and corneal ulcerationscorneal ulcerations
–In rare cases, it can cause problems in the In rare cases, it can cause problems in the central nervous system central nervous system of of
immune suppressed individuals.immune suppressed individuals.
•Can cause meningoencephalitis like Can cause meningoencephalitis like N. fowleriN. fowleri
•associated with immunosuppressionassociated with immunosuppression
•onset is insidious with headache, personality changes, slight feveronset is insidious with headache, personality changes, slight fever
•Prolonged clinical course, weeks to months to progresses to coma and death Prolonged clinical course, weeks to months to progresses to coma and death
•amoebas not yet detected in spinal fluidamoebas not yet detected in spinal fluid
•In contrast to naegleria, both trophozoites and sometimes cysts are detected in In contrast to naegleria, both trophozoites and sometimes cysts are detected in
histological examinationhistological examination
•no human cures documentedno human cures documented
•Diagnosis is difficult usually done at autopsyDiagnosis is difficult usually done at autopsy