Microbiology

2.  Amoeba are structurally simple protozoans
which have no fixed shape
 Phylum : Sarcomastigophora
 Subphylum :Sarcodina
 Super class :Rhizopoda
 Order : Amoebida

3. Amoeba
Free living
Intestinal
 Entamoeba histolytica is an intestinal
amoeba
 All intestinal amoebae are non pathogenic
except Entamoeba histolytica
 All free living amoeba are oppurtunistic
pathogens.

4.  E. histolytica was discovered by Losch in
1875
 Demonstrated the parasite in the dysenteric
feces of a patient in St.Petersburg in Russia.

5.  MORPHOLOGY
 LIFE CYCLE
 PATHOGENESIS & CLINICAL FEATURES
 LABORATORY DIAGNOSIS
 TREATMENT
 PREVENTION

6.  E.histolytica occurs in 3 forms
Trophozoite
Precyst
Cyst

7.  Vegetative or growing stage of the parasite
 Only form present in tissues
 Irregular in shape
 Size: 12-60 μm( Average 20μm)
 Large and actively motile in freshly passed
dysenteric stool, while smaller in
convalescents and carriers.
 In the lumen, commensal and small in
size(15-20 μm)-MINUTA FORM

9. Cytoplasm
Outer ectoplasm-clear,transparent,
refractile.
Inner endoplasm-finely granular
(ground glass appearance),with
nucleus
food vacuoles
erythrocytes
leucocytes(occasionally)
tissue debris

10.  Pseudopodia
Fingerlike projections formed by
sudden jerky movements of ectoplasm in one
direction, followed by the streaming in of
the whole endoplasm
 Typical amoeboid motility is a Crawling or
Gliding
 Pseudopodia formation and motility are
inhibited at low temperature

11. Nucleus
 It is spherical 4-6μm in size
 contains central karyosome,surrounded by
clear halo and anchored to the nuclear
membrane by fine radiating fibrils called the
Linin network , giving a cartwheel
appearance
 Nuclear membrane is lined by a rim of
chromatin distributed evenly as small
granules

12.  Trophozoites from acute dysentric stools
often contain phagocytosed erythrocytes-
diagnostic feature ,these are not found in
any other commensal intestinal amoeba
 These divided by binary fission in every 8
hours
 These are killed by drying, heat ,and
chemical sterilization
 Infections are not transmitted by these-
destroyed in stomach and cannot initiate
infection

13.  Trophozoites undergo encystment in the
lumen
 Before encystment,the trophozoites
extrudesits food vacuoles and become round
or oval,10-20µm in size-precyst
 Contains a large glycogen vacuole and two
chromatid bars
 It then secretes a highly retractile cyst wall
around it and become cyst

15.  Spherical ,10-20µm
 3 types of cyst
Early cyst
Binucleate cyst
mature quadrinucleate cyst
Early cyst
contains a single nucleus and two other
structures-a mass of glycogen and 1-4
chromatid bodies or chromadial bars

16.  As the cyst mature, the glycogen mass and
chromidial bars disappear and the nucleus
undergoes 2 succesive mitotic divisions to
form 2 and then 4 nuclei .
 The cyst wall is a highly resistant to gastric
juice and unfavorable environmental
conditions

17.  Infective form :mature quadrinucleate cyst
passed in feces of convalscents and carriers
 Mode of transmission :man acquires infection
by swallowing food and water contaminated
with cyst .
 Stomach –cyst wall is resistant to gastric
juice
 Exystation :cyst reaches the caecum or lower
part of ileum ,due to alkaline medium ,cyst
wall damaged by trypsin ,leading to
exystation

20.  E.histolytica causes intestinal and extra
intestinal amoebiasis
Intestinal amoebiasis -PATHOGENESIS
Lumen dwelling amoeba do not cause any
illness .They causes disease only when they
invade the intestinal tissues .
10 % -symptomatic
90% -asymptomatic

21.  Not all strains of E.histolytica are pathogenic or
invasive .
 Differentiation between pathogenic and non
pathogenic strains can be made by
 susceptibility to complement-mediated lysis
 Phagocytic activity
 by the use of genetic markers
 monoclonal antibodies
 Zymodeme analysis

22.  The metacystic trophozoites penetrate the columnar
epithelial cells of crypts of Liberkuhn
 Penetration is facilitated by
motility of the trophozoites
tissue lytic enzyme –histolysin
amoebic lectin -mediate adherence
 Mucosal penetration by amoeba produce discrete
ulcers with pinhead center and raised edges .
 Sometimes invasion remains superficial and heal
spontaneously.
 More often, the amoeba penetrates to submucosal
layer and multiplies rapidly- lytic necrosis- abscess-
ulcer

23.  Ulcer appear initially on the mucosa as raised
nodules with pouting edges .
 They breakdown discharging brownish
necrotic material contains large numbers of
trophozoites.
 The typical amoebic ulcer –flask shaped
 Multiple ulcers may coalesce to form large
necrotic lesions with ragged and undermined
edges,covered with brownish slough

24.  The ulcers generally do not extend deeper
than submucosal layer.
 Occassionally, a granulamatous
pseudotumoral growth may develop on the
intestinal wall from a chronic ulcer.This
amoebic granuloma or amoeboma may be
mistaken for are malignant tumor

25.  Small superficial ulcers involving only the mucosa
 Round or oval shaped with ragged and undermined margin
and flask-shaped in cross section
 Marked scarring of intestinal wall with thining ,dilatation
,and sacculation
 Extensive adhesions with neighboring viscera
 Formation of tumor-like masses of granulation tissue
amoeba

26.  The incubation period is highly variable from
1-4 months
 The clinical course is characterized by
prolonged latency,relapses and intermissions.
 Typical manifestation is amoebic dysentry
 Compared to bacillary desentry ,it is usually
insidious in onset and the abdominal
tenderness is less and localised.
 The stools are large, foul-smelling,and
brownish black, often with bloodstreaked
mucus intermingled with feces.

28.  The RBCs in stools are clumped and reddish
brown in color.
 Cellular exudate is scanty.
 Charcot-leyden crystals are often present.
 The patient is usually afebrile and non toxic.
 In fulminant colitis, there is confluent
ulceration and necrosis of colon-patient is
febrile and toxic.

29.  Intestinal amoebiasis not always result in
dysentry.quite often there may be only
diarrhea or vagueabdominal symptoms
popularly called uncomfortable belly or
growling abdomen.
 Chronic involvement of the caecum causes a
condition simulating appendicitis.

30.  Fulminant amoebic colitis
toxic megacolon
perianal ulceration
Amoeboma
 Extra intestinal Amoebiasis
amoebic hepatitis
amoebic liver abscess
amoebic appendicitis and peritonitis
pulmonary amoebiasis
cerebral amoebiasis
splenic abscess
cutaneous amoebiasis
genitourinary amoebiasis

33.  Hepatic Amoebiasis
 Pulmonary Amoebiasis
 Metastatic Amoebiasis
 Cutaneous Amoebiasis
 Genitourinary Amoebiasis

34.  Most common extra intestinal amoebiasis .
 The history of amoebic dysentry is absent in
more than 50% cases
 Several patients with amoebic colitis develop
an enlarged tender liver without detectable
impairment of liver function or fever.
 This acute hepatic involvement (amoebic
hepatitis) may be due to repeated invasion
by amoeba from an active colonic infection
or to toxic substance from the colon reaching
the liver.

35.  In about 5-10% of person with intestinal
amoebiasis ,liver abscesses may ensue.
 The center of the abscess contains thick
chocolate brown pus(anchovy pus),which is
liqeefied necrotic liver tissue.
 At the periphery, there is almost normal
liver tissue,which contain invading amoeba.
 Liver abscess may
multiple
solitary

36.  Usually located on right lobe of liver
 Jaundice develops
only when lesions are multiple OR
when they press on the biliary tract
 Incidenca of liver abscess is less common in
women and rare in children under age of 10

37.  It may occure by direct hematogenous spread
from colon bypassing the liver,but it most
often follows extension of hepatic abscess
through the diaphragm
 Hepatobronchial fistula usually results with
expectoration of chocolate brown sputum
 Patient presents with
severe pleuritic chest pain
dyspnea
non-productive cough

38.  Involvement of distant organs is by
hematogenous spread and through
lymphatics
 Abscess in
Kidney
Brain
Spleen
Adrenals
Spread to brain leads to severe destruction of
brain tissues and is fatal

39.  It occurs by direct extension around anus,
colostomy site,or discharging sinuses from
amoebic abscess .
 Extensive gangrenous destruction of the skin
occurs .
 The lesion may be mistaken for condyloma or
epithelioma

40.  Penile amoebiasis
prepuce and glans are affected
acquired through anal intercourse
In females
 vulva ,vagina, or cervix
 by spread from perineum
 destructive ulcerative lesions resemble
carcinoma

42. THANK YOU