5. Entamoeba histolytica
• Entamoeba histolytica infects up to 10% of the
world's population;
• endemic foci are particularly common in the
tropics, especially in areas with low
socioeconomic and sanitary standards.
• In most infected individuals, E. histolytica
parasitizes the lumen of the gastrointestinal tract
and causes few symptoms or sequelae.
• The 2 most common forms of disease caused by
E. histolytica are amebic colitis and amebic liver
abscess .
7. Etiology
• Two morphologically identical but genetically distinct
species of Entamoeba commonly infect humans.
• Entamoeba dispar, the more prevalent species, does
not cause symptomatic disease.
• E. histolytica, the pathogenic species, causes a
spectrum of disease and can become invasive.
• Patients previously described as asymptomatic carriers
of E. histolytica based on microscopy findings were
likely harboring E. dispar.
• Five other species of nonpathogenic Entamoeba can
colonize the human gastrointestinal tract: E. coli, E.
hartmanni, E. gingivalis, E. moshkovskii, and E.
polecki.
8. • Infection is acquired through the ingestion of parasite cysts.
• Cysts are resistant to harsh environmental conditions
including :
o the concentrations of chlorine commonly used in water
purification but can be killed by heating to 55C.
• After ingestion, cysts are resistant to gastric acidity and
digestive enzymes and germinate in the small intestine to
form trophozoites.
• These large, actively motile organisms colonize the lumen
of the large intestine and may invade the mucosal lining.
• Infection is not transmitted by trophozoites, as these
rapidly degenerate outside the body and are unable to
survive the low pH of the stomach if swallowed.
Etiology
9. Epidemiology
• Prevalence of infection with E. histolytica varies
greatly depending on region and socioeconomic
status.
• Most prevalence studies have not distinguished
between E. histolytica and E. dispar, and thus the
true prevalence of E. histolytica infection is not
known.
• Amebiasis is endemic to Africa, Latin America,
India, and Southeast Asia.
• It is estimated that infection with E. histolytica
leads to 50 million cases of symptomatic disease
and 40,000-110,000 deaths annually.
10. • Amebiasis is the 3rd leading parasitic cause of
death worldwide.
• Prospective studies have shown that 4-10% of
individuals infected with E. histolytica develop
amebic colitis and that <1% of infected
individuals develop disseminated disease,
including amebic liver abscess.
• In Heevi pediatrics Teaching hospital 279
patients with E. histolytica were admitted to all
pediatrics words in 2014
Epidemiology
11. Transmission
• Food or drink contaminated with Entamoeba
cysts and direct fecal-oral contact are the most
common means of infection.
• Untreated water and night soil (human feces
used as fertilizer) are important sources of
infection.
• Food handlers shedding amebic cysts play a role
in spreading infection.
• Direct contact with infected feces also results in
person-to-person transmission.
12. Pathogenesis
• Trophozoites are responsible for tissue invasion and
destruction.
• These attach to colonic epithelial cells.
• Once attached to the colonic mucosa, amebae release
proteinases that allow for penetration through the
epithelial layer.
• Once E. histolytica trophozoites invade the intestinal
mucosa, the organisms multiply and spread laterally
underneath the intestinal epithelium to produce the
characteristic flask-shaped ulcers.
• Amebae produce similar lytic lesions if they reach the liver.
• These lesions are commonly called abscesses, although
they contain no granulocytes.
• Well-established ulcers and amebic liver abscesses
demonstrate little local inflammatory response.
13. • Immunity to infection is associated with a
mucosal secretory IgA .
• Neutrophils appear to be important in initial
host defense, but E. histolytica is able to kill
neutrophils, which then release mediators
that further damage epithelial cells.
• The sequencing of the E. histolytica genome
has led to further insights into the
pathogenesis of E. histolytica disease.
Pathogenesis
14. Clinical Manifestations
• Clinical presentations range from asymptomatic cyst
passage to amebic colitis, amebic dysentery, ameboma, and
extraintestinal disease.
• E. histolytica infection is asymptomatic in about 90% of
persons but has the potential to become invasive and
should be treated.
• Severe disease is more common in young children,
pregnant women, malnourished individuals, and persons
taking corticosteroids.
• Extraintestinal disease usually involves the liver, but less
common extraintestinal manifestations include amebic
brain abscess, pleuropulmonary disease, ulcerative skin,
and genitourinary lesions.
15. Amebic Colitis
• Amebic colitis may occur within 2 wk of infection
or may be delayed for months.
• The onset is usually gradual, with colicky
abdominal pains and frequent bowel movements
.
• Diarrhea is frequently associated with tenesmus.
• Almost all stool is heme-positive, but most
patients do not present with grossly bloody
stools.
• Generalized constitutional symptoms and signs
are characteristically absent, with fever
documented in only one third of patients.
16. • Amebic colitis affects all age groups, but its
incidence is strikingly high in children 1-5 yr of
age.
• Severe amebic colitis in infants and young
children tends to be rapidly progressive with
more frequent extraintestinal involvement and
high mortality rates, particularly in tropical
countries.
• Amebic dysentery can result in dehydration and
electrolyte disturbances.
Amebic Colitis
17. Diagnosis
• A diagnosis of amebic colitis is made in the
presence of compatible symptoms with
detection of E. histolytica antigens in stool.
• This approach has a greater than 95%
sensitivity and specificity and coupled with a
positive serology test is the most accurate
means of diagnosis in developed countries.
• The E. histolytica II stool antigen detection test
(TechLab, Blacksburg) is able to distinguish E.
histolytica from E. dispar infection.
18. • Microscopic examination of stool samples has a
sensitivity of 60%. Sensitivity can be increased to 85-
95% by examining 3 stools, since excretion of cysts can
be intermittent.
• However, microscopy cannot differentiate between E.
histolytica and E. dispar unless phagocytosed
erythrocytes (specific for E. histolytica) are seen.
• In highly endemic areas, trophozoites without
phagocytosed erythrocytes may reflect co-infection
with E. dispar in a patient with another cause of colitis,
such as shigellosis.
Diagnosis
19. • Various serum antiamebic antibody tests are available.
• Serologic results are positive in 70-80% of patients with
invasive disease (colitis or liver abscess) at presentation and
in >90% of patients after 7 days of disease symptoms.
• The most sensitive serologic test, indirect
hemagglutination, yields a positive result even years after
invasive infection.
• Therefore, many uninfected adults and children in highly
endemic areas demonstrate antibodies to E. histolytica.
• Polymerase chain reaction (PCR) detection in stool of E.
histolytica is also able to distinguish E. histolytica from E.
dispar .
• Rapid antigen and antibody tests for bedside diagnosis in
the developing world have been developed and are
currently being tested.
Diagnosis
20. Differential Diagnosis
• The differential diagnosis for amebic colitis :
• bacterial (Shigella, Salmonella, enteropathogenic
Escherichia coli, Campylobacter, Yersinia, Clostridium
difficile),
• mycobacterial (tuberculosis and atypical mycobacteria),
• viral (cytomegalovirus).
• noninfectious causes such as inflammatory bowel disease
(IBD).
• The differential diagnosis for amebic liver abscess :
• Pyogenic liver abscess due to bacterial infection,
• hepatoma, and
• echinococcal cysts .
21. Complications
• Acute necrotizing colitis,
• Ameboma,
• Toxic megacolon,
• Extraintestinal extension, or
• local perforation and peritonitis.
• Less commonly, a chronic form of amebic colitis develops,
often recurring over several years.
• Amebomas are nodular foci of proliferative inflammation
that sometimes develops in the wall of the colon.
• Chronic amebiasis should be excluded before initiating
corticosteroid treatment for IBD, as corticosteroid therapy
given during active amebic colitis is associated with high
mortality rates.
22. Treatment
• Invasive amebiasis is treated with a nitroimidazole such
as metronidazole or tinidazole or Secnidazole and
then a luminal amebicide such as paromomycin
(which is preferred)
• Diloxanide furoate can also be used in children >2 yr of
age.
Tissue:
Metronidazole
Tinidazole
Secnidazole
Dehydroemetine
Chloroquine
Bowel lumen:
Paromomycin
Iodoquinol
Diloxanide furoate
23. • Asymptomatic intestinal infection with E.
histolytica should be treated preferably with
paromomycin or alternatively with either
iodoquinol or diloxanide furoate.
• For fulminant cases of amebic colitis, some
experts suggest adding dehydroemetine
(1 mg/kg/day subcutaneously or IM, never IV),
available only through the Centers for Disease
Control and Prevention.
• Dehydroemetine should be discontinued if
tachycardia, T-wave depression, arrhythmia, or
proteinuria develops.
Treatment
24. MEDICATION ADULT DOSAGE (ORAL) PEDIATRIC DOSAGE (ORAL)*
INVASIVE DISEASE
Metronidazole
Colitis or liver abscess: 750 mg tid
for 7-10 days
35-50 mg/kg/day in 3 divided doses for
7-10 days
or
Tinidazole
Colitis: 2 g once daily for 3 days
Colitis: 50 mg/kg/day once daily for 3
days
Liver abscess: 2 g once daily for 3-
5 days
Liver abscess: 50 mg/kg/day once daily
for 3-5 days
Followed by:
Paromomycin (preferred) 500 mg tid for 7 days
25-35 mg/kg/day in 3 divided doses for 7
days
or
Diloxanide furoate or 500 mg tid for 10 days
20 mg/kg/day in 3 divided doses for 7
days
Iodoquinol 650 mg tid for 20 days
30-40 mg/kg/day in 3 divided doses for
20 days
ASYMPTOMATIC INTESTINAL COLONIZATION
Paromomycin (preferred)
As for invasive disease As for invasive disease
or
Diloxanide furoate
or
Iodoquinol
25. • Broad-spectrum antibiotic therapy may be
indicated in fulminant colitis to cover possible
spillage of intestinal bacteria into the
peritoneum and translocation into the
bloodstream.
• Intestinal perforation and toxic megacolon are
indications for surgery.
Treatment
26. Secnidazole
One of Nitroimidazole
Other amebicides are given in multiple doses whereas
secnidazole has advantage of single dosage.
Due to restricted use and single dosage of secnidazole it
didn’t develop resistance as compared to other amebicides
which developed resistance due to excess use.
Children: 30 mg/kg body wt. as single dose. taken preferably
just before meal.
Treatment
28. Prognosis
• Most infections evolve to either an
asymptomatic carrier state or eradication.
• Extraintestinal infection carries about a 5%
mortality rate
29. Prevention
• Control of amebiasis can be achieved by
exercising proper sanitation and avoiding fecal-
oral transmission.
• Regular examination of food handlers and
thorough investigation of diarrheal episodes may
help identify the source of infection
• No prophylactic drug or vaccine is currently
available for amebiasis.
• Immunization has been shown to be protective to
amebic trophozoite challenge in animals.
30. • Evidence shown that use of probiotics and
Prebiotics will reduce:
• duration of diarrhea, number of stools/day,
number of vomiting/day, Rate of fever &Rate of
abdominal pain.
Probiotics &Prebiotics = Synbiotic
Probiotics Prebiotics
Live organism Food for live organism
Present in animal product Mostly in plants
Used in stomach & small intestine Reach the colon
