Amebiasis is a disease caused by a one-celled parasite called Entamoeba histolytica (ent-a-ME-ba his-to-LI-ti-ka). Who is at risk for amebiasis? Although anyone can have this disease, it is most common in people who live in developing countries that have poor sanitary conditions. In the United States, amebiasis is most often foundin immigrants from developing countries. It also is found in people who have traveled to developing countries and in people who live in institutions that have poor sanitary conditions. Men who have sex with men can become infected and can get sick from the infection, but they often do not have symptoms. by Mostafa Mohammadzadeh fallah (MedStudent Iran)

1. Amebiasis
M.Mohammadzadeh Fallah
December 6, 2018

2. REVIEW
EPIDEMIOLOGY
PATHOGENESIS
IMMUNE RESPONSE
CLINICAL MANIFESTATIONS
LABORATORY DIAGNOSIS
THERAPY
PREVENTION
CONCLUSION
Contents

3. Domain: Eukaryota
(unranked): Amoebozoa
Class: Tubulinea
Order: Tubulinida
Family: Amoebidae
Genus: Amoeba
3
Scientific
classification

4. • Six species of the genus Entamoeba, including the
commensals Entamoeba gingivalis, Entamoeba coli,
Entamoeba hartmanni, Entamoeba dispar, Entamoeba
moshkovskii
• the pathogen E. histolytica, occur in humans
• Entamoeba polecki, an intestinal ameba of pigs and
monkeys, is seen occasionally in humans and may cause
diarrhea
4
The Amebae

5. • possession of a vesicular nucleus with a comparatively
small karyosome located at or near its center and with
varying numbers of peripheral chromatin granules
attached to the nuclear membrane.
5
THE GENUS
ENTAMOEBA

6. Morphology
• Entamoeba histolytica occurs in 4 forms :
• Trophozoite
• Precyst
• Cyst
• Metacyst (small intestine tubage)
6
Entamoeba
histolytica

7. trophozoite
• It is the vegetative or growing stage of the parasite.
• It is irregular in shape
• The outer ectoplasm is clear, transparent and refractile.
The inner endoplasm is finely granular, having a ground
glass appearance. The endoplasm contains nucleus, food
vacuoles, erythrocytes occasionally leucocytes and
tissue debris.
• In the lumen, commensaland small in size(15-20 μm)-
MINUTA FORM
7
Entamoeba
histolytica

8. 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
8
Entamoeba
histolytica

9. Precystic stage
• Trophozoites undergo encystmentin the lumen
• Before encystment, thetrophozoites extrudesits food
vacuoles and become round or oval,10-20μm in size-
precyst
• Contains a large glycogen vacuole and two
chromatidbars
• It then secretes a highly retractile cyst wall around it and
become cyst
9
Entamoeba
histolytica

10. Cystic stage
• Spherical ,10-20μm
• 3 types of cyst
Early cyst : contains a single nucleus and two
other structures-a mass of glycogen and 1-4
chromatid bodies or chromadial bars
Binucleate cyst
mature quadrinucleate cyst
• As the cyst mature, the glycogen mass and
chromidialbars disappear and the nucleus undergoes 2
succesivemitotic divisions to form 2 and then 4 nuclei .
• The cyst wall is a highly resistant to gastric juice and
unfavorable environmental conditions
10
Entamoeba
histolytica

11. Life cycle
• 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
11
Entamoeba
histolytica

12. Life cycle
12
Entamoeba
histolytica

13. • Intestinal infection caused by E.histolytica.
• 90% of cases are asymptomatic.
• In 10%, a range of clinical syndromes from dysentery to
liver abscesses and abscesses of other organs are
observed.
13
Amebiasis

14. • highest burden of amebiasis borne by those residing in
developing countries particularly the tropics and subtropics
• Millions of people are infected with E. histolytica, making
amebic colitis a leading cause of diarrhea, estimated to kill
more than 55 000 people each year.
• Amebiasis is endemic in developing parts of Central and
South America, Africa, and Asia. In the United States, the
incidence of amebiasis is low, though amebiasis-related
deaths still routinely occur, accounting for at least 5 deaths
per year
• Data from the GeoSentinel Surveillance Network, a large
international surveillance and monitoring system, have
shown that E. histolytica is the third (after Malaria and
Schistosoma) most frequently isolated pathogen among
returning travelers with infectious gastrointestinal disease. 14
EPIDEMIOLOGY

15. • Travelers to South Asia, the Middle East, and South
America appear to have the highest risk, in particular
those volunteering as missionary workers or doing other
volunteering work.
• MSM
• Recent reports from Taiwan and Japan, for example,
have shown high rates of invasive amebiasis in HIV-
infected MSM.
• In Iran, the incidence of this disease in urban areas is
about 6 to 8 percent, and in rural areas it is reported
from 5 to 30 percent.
• The prevalence rate in the University of Tehran's
cafeteria is 2.2% , in Northern cities of the country is
12% .
• The ratio of positive cysts in males was 11.9% and in
women 22.4%. [1]
15
EPIDEMIOLOGY

16. 16

17. • Transmission occurs after the ingestion of the infectious
cyst
• This most commonly arises from fecally contaminated
hands, food, or water, but there is a new appreciation
that exposure to fecal matter may occur during sexual
contact, in particular among MSM groups [2]
• The low infectious dose and environmental stability can
predispose to the development of outbreaks
• Cysts can be killed by boiling
17
Transmission

18. A, Cyst of E. histolytica/E. dispar
stained with trichrome. Note the
chromatoid body with blunt ends (red
arrow).
B, Trophozoite of E. histolytica with
ingested erythrocytes stained with
trichrome. The ingested erythrocytes
appear as dark inclusions (red arrow).
The parasite shows nuclei that have
the typical small, centrally located
karyosome and thin, uniform
peripheral chromatin.
C, Intestinal tissue from a patient
with amebic colitis showing multiple
ulcers.
D, Classic flask-shaped ulcer of
amebiasis (courtesy of the Centers for
Disease Control and Prevention).
18

19. • E. histolytica pathogenesis can be characterized by 3
events: host cell death, inflammation, and parasite
invasion.
• Before cell adherence, trophozoites secrete immune
modulators that stimulate epithelial cells, resulting in
cytokine production and subsequent mucosal
inflammatory cell infiltration
• Adherence is mediated through the parasite Gal/GalNAc
lectin adhesion molecule
• Trophozoites are able to kill host cells by several
different mechanisms, which include inducing
programmed cell death, phagocytosis, and trogocytosis
• E. histolytica causes inflammation of the colon, termed
amebic colitis. 19
PATHOGENESIS
The parasite (blue) first attaches via its Gal/GalNAc lectin (purple) to the
target cell (green). Next, E. histolytica induces calcium influx, tyrosine
dephosphorylation andcaspase 3 activation. Finally, the killed host cell
is ingested.

20. 20

21. 21
PATHOGENESIS EhMIF
• E. histolytica, like several pathogenic
protozoa, secretes a protein homolog of
the proinflammatory cytokine macrophage
migration inhibitory factor (EhMIF).
MMPs
• EhMIF-induced inflammation results in
increased production in matrix
metalloproteinases (MMPs).
E.matrix
• MMPs break down the extracellular matrix
in the gut to promote cell migration and
are overexpressed in all infections with
protozoan parasites, including amebiasis.

22. • Interferon gamma (IFN-Ɣ) appears to provide protection
from amebiasis, as children with higher IFN-Ɣ had a
significantly lower incidence of future E.histolytica
diarrhea.
• Also, protection from amebiasis includes acquired
immunity from antibodies against the amebic antigens
Gal/GalNAc lectin and EhMIF.
• But higher TNF-α production was shown to correlate
with E. histolytica diarrhea in children.
• In response to IL-8, neutrophils infiltrate the intestinal
tract as the first cells of an innate immune response to
amebic invasion.
• neutrophils might be responsible for collateral tissue
damage during inflammation at the site of invasion. 22
IMMUNE
RESPONSE

23. • The majority of E. histolytica infections are asymptomatic;
only about 10%–20% progress to develop symptomatic
infection.
• Recently, it was found that the gut microbiome is enriched
in Prevotella copri in people with amebic diarrhea,
indicating that dysbiosis may in part contribute to
susceptibility to the development of colitis.
• Therefore, amoebic diarrhea indirectly causes rheumatoid
arthritis, diabetes, insulinity, cardiovascular disease, and so
on.
23
CLINICAL
MANIFESTATIONS

24. Intraluminal Amebiasis
• Asymptomatic infection is referred to as luminal
amebiasis.
• A gender difference in amebiasis is not seen in children,
but interestingly, in the adult population, invasive
disease is more common in males than females,
particularly for amebic liver abscess .
24
CLINICAL
MANIFESTATIONS

25. • One hallmark of amebic colitis is diarrhea, which may be
watery or bloody and present with abdominal cramps,
pain/tenderness, and weight loss.
• Amebic colitis may also present similarly to inflammatory
bowel disease (IBD).
• Disease may be limited to the ascending colon or cecum.
• Corticosteroid use has been described as a risk factor for the
development of fulminant forms of amebic colitis .
• The case fatality of fulminant amebic colitis ranges from
40% to 89%.
• Implicated risk factors for fulminant disease include
diabetes mellitus, alcoholism, malignancy/chemotherapy,
and pregnancy [4].
25
Amebic Colitis
CLINICAL
MANIFESTATIONS

26. • The only distinguishing feature was a higher median
neutrophil count in those with amebic infection
compared with those without in this series.
• The differential diagnosis of amebic colitis includes
bacterial enteric infection, such as Salmonella spp.,
Shigella spp., Campylobacter spp., enterohemorrhagic
E. coli, enteroinvasive E. coli, Clostridium difficile
infection, IBD, and other noninfectious causes of colitis.
26
Amebic Colitis
CLINICAL
MANIFESTATIONS

27. 27

28. Disseminated Amebic Disease
•Amebic liver abscess
28
CLINICAL
MANIFESTATIONS

29. A number of diagnostic
modalities are available to
assist with diagnosis, including
microscopy, antigen detection,
molecular tests, and serology
• Traditionally, microscopy has been the most widely used
but has limited diagnostic utility and is no longer
recommended as a reliable way to diagnose amebiasis.
• Stool Microscopy ; Cysts and trophozoites can be
visualized by an experienced eye, sometimes with
evidence of hemophagocytosis.
• Stool Antigen Detection ; have variable sensitivity and
specificity, particularly in low-endemic areas; The Techlab
E. histolytica II test (Blacksburg, VA), which detects E.
histolytica–derived Gal/GalNAc-specific lectin, can
exclude nonpathogenic E. dispar, as can the Cellabs
CELISA Path (Brookvale, Australia).
• Recently, an E. HISTOLYTICA QUIK CHEK
immunochromatographic (IC) assay, which is simple to
perform and has a quick turnaround time, was approved by
the US Food and Drug Administration (FDA). 29
LABORATORY
DIAGNOSIS

30. • Ultrasonography, abdominal computed tomography
(CT), and magnetic resonance imaging are all good
modalities to detect liver abscess. By ultrasound, a
cystic intrahepatic hypoechoic lesion can be found. By
CT, an abscess with a non enhancing center surrounded
by a rim of inflammation can be seen following contrast
administration. The detection of a space-occupying
lesion in the liver and positive amebic serology supports
the diagnosis of amebic liver abscess.
30
Imaging

31. This is the case of a 78
year-old woman with
Pain right
hypochondrium
referred to right
shoulder fever 100.4 F
and weight loss.
31

32. 32

33. 33
THERAPY

34. • Auranofin, a gold compound that has been used to treat
selective cases of rheumatoid arthritis, has entered into
early clinical drug development as an antiparasitic agent,
but further study is needed to determine if it will be an
effective treatment of amebiasis and whether known
safety concerns such as diarrhea, rash, and bone marrow
suppression will limit its use .
• Drainage of liver abscess, reserved for those who do not
show prompt clinical response to antiparasitic therapy
by about 72 hours or those at high risk for impending
abscess rupture, typically defined by a cavity with a
diameter >5–10 cm or by left lobe abscess, which could
rupture into the pericardium
34
THERAPY

35. • There is no vaccine to prevent amebiasis.
• The focus of primary preventative efforts, therefore,
remains food and water safety, attention to hand
hygiene, and avoidance of fecal–oral exposure,
including through sexual practices.
• Household contacts of patients with amebiasis should be
screened, as amebiasis may spread among family and
household contacts
• Use of loperamide should be avoided in amebic colitis.
35
PREVENTION

36. • Amebiasis remains one of the most significant
enteropathogens worldwide. Advances in molecular
epidemiology and pathogenesis have advanced our
understanding of this parasite; however, many gaps in
knowledge remain. In addition, although efforts are
ongoing, there is no vaccine and only a single effective
drug class. Prevention remains challenging, highlighting
the need for improved awareness of this infection and
novel therapeutic and preventative strategies.
36
CONCLUSION

37. •1.‫همکاران‬ ‫و‬ ‫کریمی‬ ‫اکبر‬‫علی‬-‫آمیبیازروده‬ ‫بیماری‬ ‫اپیدمیولوژیک‬ ‫بررسی‬‫ای‬
‫سرخس‬ ‫شهرستان‬ ‫مرزی‬ ‫درروستاهای‬
• A Review of the Global Burden, New Diagnostics, and
Current Therapeutics for Amebiasis ; Debbie-Ann T Shirley
Laura Farr Koji Watanabe Shannon Moonah
• Somlata, Nakada-Tsukui K, Nozaki T ; AGC family kinase 1
participates in trogocytosis but not in phagocytosis in
Entamoeba histolytica.
• diabetestma.org
37
Reference