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AMEBIASIS

Dr. Suprakash Das.


Introduction
 Amebiasis is an infection with the intestinal
protozoan Entamoeba histolytica. About 90% of
infections are asymptomatic, and the remaining 10%
produce a spectrum of clinical syndromes ranging from
dysentery to abscesses of the liver or other organs.
 Entamoeba histolytica was first described by Losch
after being isolated in Russia from a patient with
dysenteric stools. but it was not given its Latin name
until Fritz Schaudinn described it in 1903. E.
histolytica, as its name suggests (histo–lytic = tissue
destroying).
Fritz Schaudinn
Epidemiology
 About 10% of the world’s population is infected with
Entamoeba, the majority with noninvasive Entamoeba
dispar.
 Amebiasis results from infection with E. histolytica and is
the third most common cause of death from parasitic
disease (after schistosomiasis and malaria).
 Most asymptomatic carriers, including homosexual men
and patients with AIDS, harbor E. dispar and have self-
limited infections.
 In one study, 10% of asymptomatic patients who were
colonized with E. histolytica went on to develop amebic
colitis, while the rest remained asymptomatic and cleared
the infection within 1 year.
Epidemiology
 Areas of highest incidence (due to inadequate sanitation and crowding)
include most developing countries in the tropics, particularly
 Mexico,
 India, and
 nations of Central and South America,
 tropical Asia,
 and Africa.
 In a 4-year follow-up study of preschool children in a highly endemic
area of Bangladesh, 80% of children had at least one episode of infection
with E. histolytica and 53% had more than one episode.
 The main groups at risk for amebiasis in developed countries are returned
travelers, recent immigrants, homosexual men, and inmates of
institutions.
Life cycle And Transmission

 E. histolytica is acquired by ingestion of viable cysts from fecally


contaminated water, food, or hands.
 Food-borne exposure is most prevalent and is particularly likely
when food handlers are shedding cysts or food is being grown with
feces-contaminated soil, fertilizer, or water.
 Besides the drinking of contaminated water, less common means
of transmission include oral and anal sexual practices and—in
rare instances—direct rectal inoculation through colonic irrigation
devices.
 Motile trophozoites are released from cysts in the small intestine
and, in most patients, remain as harmless commensals in the large
bowel.
 After encystation, infectious cysts are shed in the stool and can
survive for several weeks in a moist environment.
Life cycle And Transmission
 In some patients, the trophozoites invade either
the bowel mucosa, causing symptomatic colitis,
or the bloodstream, causing distant abscesses of
the liver, lungs, or brain.
 The trophozoites may not encyst in patients
withactive dysentery, and motile hematophagous
trophozoites are frequently present in fresh stools.
 Trophozoites are rapidly killed by exposure to air
or stomach acid, however, and therefore cannot
transmit infection.
Pathogenesis & Pathology
 Both trophozoites and cysts are found in the intestinal
lumen, but only trophozoites of E. histolytica invade
tissue.
 The trophozoite is 20–60 μm in diameter and contains
vacuoles and a nucleus with a characteristic central
nucleolus.
 In animals, depletion of intestinal mucus, diffuse
inflammation, and disruption of the epithelial barrier
occur before trophozoites actually come into contact
with the colonic mucosa.
 Trophozoites attach to colonic mucus and epithelial
cells by Gal/GalNAc.
Pathogenesis & Pathology
 The earliest intestinal lesions are micro-ulcerations of the
mucosa of the cecum, sigmoid colon, or rectum that release
erythrocytes, inflammatory cells, and epithelial cells.
 Proctoscopy reveals small ulcers with heaped-up margins
and normal intervening mucosa.
 Submucosal extension of ulcerations under viable-appearing
surface mucosa causes the classic “flask-shaped” ulcer
containing trophozoites at the margins of dead and viable
tissues.
 Although neutrophilic infiltrates may accompany the early
lesions in animals, human intestinal infection is marked by
a paucity of inflammatory cells, probably in part because
of the killing of neutrophils by trophozoites.
Pathogenesis & Pathology
 Rarely, intestinal infection results in the formation of a
mass lesion, or ameboma, in the bowel lumen.
 The overlying mucosa is usually thin and ulcerated, while
other layers of the wall are thickened, edematous, and
hemorrhagic; this condition results in exuberant formation
of granulation tissue with little fibrous-tissue response.
 A number of virulence factors have been linked to the
ability of E. histolytica to invade through the
interglandular epithelium.
 One consists of the extracellular cysteine proteinases
that degrade collagen, elastin, IgA, IgG, and the
anaphylatoxins C3a and C5a.
Pathogenesis & Pathology
 Other enzymes may disrupt glycoprotein bonds between
mucosal epithelial cells in the gut.
 Amebas can lyse neutrophils, monocytes, lymphocytes,
and cells of colonic and hepatic lines.
 The cytolytic effect of amebas appears to require direct
contact with target cells and may be linked to the release of
phospholipase A and pore-forming peptides.
 E. histolytica trophozoites also cause apoptosis of human
cells.
 Liver abscesses are always preceded by intestinal
colonization, which may be asymptomatic.
 Blood vessels may be compromised early by wall lysis and
thrombus formation.
Pathogenesis & Pathology
 Trophozoites invade veins to reach the liver through the portal
venous system.
 E. histolytica is resistant to complement-mediated lysis—a
property critical to survival in the bloodstream.
 Inoculation of amebas into the portal system of hamsters results in
an acute cellular infiltrate consisting predominantly of neutrophils.
Later, the neutrophils are lysed by contact with amebas, and the
release of neutrophil toxins may contribute to necrosis of
hepatocytes.
 The liver parenchyma is replaced by necrotic material that is
surrounded by a thin rim of congested liver tissue. The necrotic
contents of a liver abscess are classically described as “anchovy
paste,” although the fluid is variable in color and is composed of
bacteriologically sterile granular debris with few or no cells.
 Amebas, if seen, tend to be found near the capsule of the abscess.
Clinical Syndromes

 Intestinal Amebiasis- The most common type of amebic infection is


asymptomatic cyst passage.
 Even in highly endemic areas, most patients harbor E. dispar.
 Symptomatic amebic colitis develops 2–6 weeks after the ingestion
of infectious cysts.
 A gradual onset of lower abdominal pain and mild diarrhea is
followed by malaise,weight loss, and diffuse lower abdominal or
back pain.
 Cecal involvement may mimic acute appendicitis. Patients with full-
blown dysentery may pass 10–12 stools per day.
 The stools contain little fecal material and consist mainly of blood
and mucus.
 In contrast to those with bacterial diarrhea, fewer than 40% of
patients with amebic dysentery are febrile. Virtually all patients have
heme-positive stools.
Clinical Syndromes

 More fulminant intestinal infection, with severe


abdominal pain, high fever, and profuse diarrhea,
is rare and occurs predominantly in children.
 Patients may develop toxic megacolon, in which
there is severe bowel dilation with intramural air.
 Patients receiving glucocorticoids are at risk for
severe amebiasis.
 Uncommonly, patients develop a chronic form of
amebic colitis, which can be confused with
inflammatory bowel disease.
Clinical Syndromes

 The association between severe amebiasis complications


and glucocorticoid therapy emphasizes the importance of
excluding amebiasis when inflammatory bowel disease is
suspected.
 An occasional patient presents with only an asymptomatic
or tender abdominal mass caused by an ameboma, which is
easily confused with cancer on barium studies.
 A positive serologic test or biopsy can prevent unnecessary
surgery in this setting.
 The syndrome of postamebic colitis—persistent diarrhea
following documented cure of amebic colitis—is
controversial; no evidence of recurrent amebic infection can
be found, and re-treatment usually has no effect.
Clinical Syndromes

 Amebic Liver Abscess-


 Extraintestinal infection by E. histolytica most often
involves the liver.
 Of travelers who develop an amebic liver abscess after
leaving an endemic area, 95% do so within 5 months.
Young patients with an amebic liver abscess are more likely
than older patients to present in the acute phase with
prominent symptoms of <10 days’ duration.
 Most patients are febrile and have right-upper quadrant
pain, which may be dull or pleuritic in nature and may
radiate to the shoulder.
 Point tenderness over the liver and right-sided pleural
effusion is common. Jaundice is rare.
Clinical Syndromes

 Although the initial site of infection is the colon, fewer than one-
third of patients with an amebic abscess have active diarrhea.
 Older patients from endemic areas are more likely to have a
subacute course lasting 6 months, with weight loss and
hepatomegaly.
 About one-third of patients with chronic presentations are febrile.
 Thus, the clinical diagnosis of an amebic liver abscess may be
difficult to establish because the symptoms and signs are often
nonspecific.
 Since 10–15% of patients present only with fever, amebic liver
abscess must be considered in the differential diagnosis of fever of
unknown origin.
Clinical Syndromes

 Complications of Amebic Liver Abscess-


 Pleuropulmonary involvement, which is reported in 20–30% of patients,
is the most frequent complication of amebic liver abscess.
 Manifestations include sterile effusions, contiguous spread from the liver,
and rupture into the pleural space.
 Sterile effusions and contiguous spreadusually resolve with medical
therapy, but frank rupture into the pleural space requires drainage.
 A hepatobronchial fistula may cause cough productive of large amounts
of necrotic material that may contain amebas. This dramatic complication
carries a good prognosis.
 Abscesses that rupture into the peritoneum may present as an indolent
leak or an acute abdomen and require both percutaneous catheter drainage
and medical therapy.
 Rupture into the pericardium, usually from abscesses of the left lobe of
the liver, carries the gravest prognosis; it can occur during medical therapy
and requires surgical drainage.
Clinical Syndromes

 Other Extraintestinal Sites-


 The genitourinary tract may become involved by direct
extension of amebiasis from the colon or by
hematogenous spread of the infection.
 Painful genital ulcers, characterized by a punched-out
appearance and profuse discharge, may develop
secondary to extension from either the intestine or the
liver. Both these conditions respond well to medical
therapy.
 Cerebral involvement has been reported in fewer than
0.1% of patients in large clinical series. Symptoms and
prognosis depend on the size and location of the lesion.
Diagnosis
 Organism detection depends on collection of the correct
specimens, the number of specimens submitted, processing
methods and diagnostic tests used, and examination by personnel
who are well trained in identification of protozoa.
 The standard ova and parasite examination is the recommended
procedure for recovery and identification of E. histolytica in stool
specimens.
 Microscopic examination of a direct saline wet mount may
reveal motile trophozoites, which may contain RBCs.
 However, the number of times these trophozoites with RBCs are
present is limited.
 In many patients who do not present with acute dysentery,
trophozoites may be present but do not contain RBCs and the
organisms may be E. histolytica or E. dispar.
Diagnosis
 An asymptomatic individual may have few
trophozoites and possibly only cysts in the stool.
 Although the concentration technique is helpful in
demonstrating cysts,
 the most important technique for the recovery
and identification of protozoan organisms is the
permanent stained smear (normally stained
with trichrome or iron hematoxylin).
 A minimum of three specimens collected over a
time frame of not more than 10 days is
recommended.
Diagnosis
 Definitive diagnosis of liver abscess can be
achieved by identification of organisms from
liver aspirate material.
 Aspirated material must be aliquoted into several
different containers as it is removed from the
abscess;
 amebae may be found only in the last portion of
the aspirated material, theoretically material from
the abscess wall, not necrotic debris from the
abscess center.
Diagnosis
 Immunodetection –
 A number of enzyme immunoassay reagents are
commercially available, and their specificity and sensitivity
provide excellent options for the clinical laboratory.
 These tests can determine the presence of the E. histolytica
/E. dispar group as being distinct from the rest of the
Entamoeba species such as nonpathogenic E. coli or E.
hartmanni.
 Other test reagents can actually separate E. histolytica
from E. dispar.
 The majority of these procedures use the enzyme-linked
immunosorbent assay (ELISA) or enzyme immunoassay
(EIA) formats.
Diagnosis
 Another product is available as a cartridge format that uses an
immunochromatographic strip-based detection system for the E.
histolytica /E. dispar group, Giardia lamblia, and
Cryptosporidium spp.
 To provide clinically relevant information to physicians for
treatment of patients infected with pathogenic E. histolytica,
methods involving monoclonal antibodies, purified antigens, or
DNA probes are now available.
 Reagents have been developed to differentiate pathogenic E.
histolytica from nonpathogenic E. dispar.
 Without the use of these types of reagents, the only way to
morphologically identify true pathogenic E. histolytica would be to
observe the rare presence of trophozoites containing ingested
RBCs.
Diagnosis
 Antibody Detection –
 Serologic testing for intestinal disease is normally not
recommended unless the patient has true dysentery; even in these
cases, the titer (indirect hemagglutination as an example) may be
low and thus difficult to interpret.
 The definitive diagnosis of intestinal amebiasis should not be
made without demonstrating the organisms.
 For patients suspected of having extraintestinal disease, serologic
tests are much more relevant.
 Indirect hemagglutination and indirect fluorescent-antibody tests
have been reported positive with titers of ≥1:256 and ≥1:200,
respectively, in almost 100% of cases of amebic liver abscess.
 Positive serologic results, in addition to clinical findings, make the
diagnosis highly probable.
Diagnosis
 Histology –
 A histologic diagnosis of amebiasis can be made when
the trophozoites within the tissue are identified.
 Organisms must be differentiated from host cells,
particularly histiocytes and ganglion cells.
 Periodic acid-Schiff staining is often used to help
locate the organisms. The organisms appear bright pink
with a green-blue background (depending on the
counterstain used).
 Hematoxylin and eosin staining also allows the typical
morphology to be seen, thus allowing accurate
identification.
Difference between cyst of common
Amebea
Differential Diagnosis
 The differential diagnosis of intestinal amebiasis includes
bacterial diarrheas caused by Campylobacter ;
enteroinvasive Escherichia coli ; and species of Shigella ,
Salmonella , and Vibrio .
 Although the typical patient with amebic colitis has less
prominent fever than in these other conditions as well as
heme-positive stools with few neutrophils, correct diagnosis
requires bacterial cultures, microscopic examination of
stools, and amebic serologic testing.
 Because of the variety of presenting signs and symptoms,
amebic liver abscess can easily be confused with
pulmonary or gallbladder disease or with any febrile
illness with few localizing signs, such as malaria or
typhoid fever.
Differential Diagnosis
 Once radiographic studies have identified an
abscess in the liver, the most important
differential diagnosis is between amebic and
pyogenic abscess.
 Patients with pyogenic abscess typically are older
and have a history of underlying bowel disease or
recent surgery.
 Amebic serology is helpful, but aspiration of the
abscess, with Gram’s staining and culture of the
material, may be required for differentiation of
the two diseases.