2. Amebiasis or amebic dysentary is
caused by the protozoan Entamoeba
histolytica. Improved sanitation and
clean water supply decrease the
incidence of amebiasis. The amount of
chlorine normally used to control
pathogens is inadequate in killing the
cysts. Drinking water can be rendered
safe by boiling or iodination with
tetraglycine hydroperiodide.
Nevertheless, drinking water is usually
not much of the problem.
3. Generalities.
Amebiasis is an intestinal infection
in which cysts are passed in the feces.
Symptoms can include fever, chills and
diarrhea, sometimes bloody or with mucus
and often with cramps. Some people may
have only mild abdominal discomfort or no
symptoms at all. Symptoms can start 2 or
more weeks after infection. Rarely,
trophozoites (the mobile amebas) may
invade the liver, lung or brain, or perforate
the colon causing septicemia.
4. E. dispar is a nonpathogenic protozoon
morphologically identical to E histolytica.
Previously reported asymptomatic infections
due to the so-called nonpathogenic strains of
E histolytica now are recognized to be due to
E. dispar. These 2 species of Entameba can
be distinguished by monoclonal antibodies.
Other morphologically distinct organisms,
such as Entamoeba coli ( E. coli ! ! ) and
Entamoeba hartmanni are also
nonpathogenic.
5. Amebiasis is the third leading
parasitic cause of death worldwide,
surpassed only by malaria and
schistosomiasis. On a global basis,
amebiasis affects approximately 50
million persons each year,
resulting in nearly 100,000 deaths.
6. Laboratory diagnosis.
An iodine-stained cyst of the pathogen
Entamoeba hystolytica with 4 nuclei is illustrated.
The harmless commensal Entamoeba coli has
larger cyts with 8 nuclei. Furthermore, recall that
E. histolytica has a lookalike E. dispars that is
harmless.
7.
8.
9. The cyst of E histolytica averages 12
µm, ranging from 5-20 µm. It has 1-4
nuclei that are morphologically similar
to the nuclei of the trophozoite. The
cyst may have iodine-stainable
glycogen clumps and chromatoid
bodies with smooth rounded edges.
The ending –oid means LIKE so
chromatoid bodies are like chromatin
in that they stain with hematoxylin.
11. Cysts
Entamoeba coli Entamoeba histolytica
10 µm - 35 µm in size 10 µm - 20 µm in size
May have 8 nuclei Never more than 4 nuclei
Karyosomes eccentric Karyosomes small, central
Nuclear chromatin clumped Chromatin finely beaded
Splintered chromatoidal bars Rounded chromatoidal bars
12. Leukocytosis and mild anemia can occur.
Erythrocyte sedimentation rate generally
is elevated. Liver function tests reveal
elevated alkaline phosphatase in 80% of
patients, elevated transaminases and
reduced albumin. Urinalysis may reveal
proteinuria.
Rectosigmoidoscopy and colonoscopy
may show small mucosal ulcers covered
with yellowish exudates. The intervening
mucosa appears normal. Biopsy results
and scrapings of ulcer edge may locate
trophozoites.
13. Symptoms and pathology.
Primary intestinal flask-shaped
(button hole) necrotic ulcers occur in
the submucosa of the large intestine,
most commonly the cecal and
sigmoidorectal regions.Ulcers contain
necrotic debris, actively feeding
trophozoites with ingested
erythrocytes, cytolyzed cells and
mucous; polymorphonuclear
leukocytes and round inflammatory
cells.
14. Extraintestinal features.
Hematogenous spread may result in
abscesses of the liver, spleen, lung or
brain. Hepatic amebiasis (abscess,
hepatitis) is the most common and
grave complication: Enlarged, tender
liver and upper abdominal pain that
may radiate to the right shoulder.
Mild jaundice may be evident,
transaminases and alkaline
phosphatase elevations may be seen.
15. Drugs for treatment.
Five pharmaceuticals are briefly noted.
Asymptomatic intestinal infection may be
treated with iodoquinol, paromomycin or
diloxanide furoate. Recommended drugs
for treatment of symptomatic intestinal
disease and for hepatic abscess are
metronidazole and tinidazole. Since these
drugs may not eliminate the cysts of the
intestine, immediately follow
metronidazole and tinidazole with
iodoquinol, paromomycin or diloxanide
furoate.
16. 1/ Metronidazole (Flagyl,
Protostat). Kills trophozoites of E.
histolytica in intestine and tissue.
Does not eradicate cysts from
intestines. Adult oral dose: 500-
750 mg 3 times per day for 10
day. Elimination is accelerated by
simultaneous use of phenytoin
and phenobarbital; clearance is
decreased by cimetidine.
17. 2/Tinidazole (Fasigyn). 5-
nitroimidazole derivative with
selective antimicrobial activity
against anaerobic bacteria and
protozoa. Not available in United
States. Adult oral dose: 600 mg
bid or 800 mg 2 times a day for 5
days. Pediatric dose 50-60 mg/kg
for 5 days, not to exceed 2 g/day.
18. 3/Paromomycin (Humatin).
Amebicidal aminoglycoside antibiotic
that is poorly absorbed. Active only
against intestinal form of amebiasis.
Used to eradicate cysts of E.
histolytica following treatment with
metronidazole or tinidazole for an
invasive disease. Adult oral dose:
25-35 mg/kg/day divided 3 times
for 7 days. Pediatric dose:
Administer as in adults.
19. 4/Diloxanide furoate (Furamid,
Entamizole, Furamide). Luminal
amebicide; acts primarily in bowel
lumen since it is poorly absorbed.
Used to eradicate cysts of E. histolytica
after treatment of invasive disease.
Available through US CDC Drug
Service (404-639-3670). Adult oral
dose 500 mg 2 times a day for 10
days. Pediatric dose 20 mg/kg/
divided twice a day for 10 days, not to
exceed 1500 mg/day.
20. 5/Iodoquinol (Yodoxin). Halogenated
hydroxyquinoline. Luminal amebicide;
acts primarily in bowel lumen since it is
poorly absorbed. Best tolerated when
given with meals. Since active only
against intraluminal form of amebiasis,
used to eradicate cysts of E. histolytica
after treatment of invasive disease. Adult
oral dose 650 mg 2 times a day for 20
days. Pediatric dose: 30-40 mg/kg/day
divided 2 times for 20 days; not to
exceed 2 g/day.
21. The control of infection.
The epidemiology of amebiasis is
folkloric, beginning with infected
foodhandlers. While elements of
truth are scattered through this
neglected syndrome, much more
can be done. Frankly, the ecology
is unknown. Are there reservoir
animals?
22. What civic water treatments kill and
which ones tolerate E. histolytica? What
part does chronic malnutrition play in
susceptibility to infection? What part
does exposure then the rise of natural
antibodies play in defense? What are the
water-borne pathogens intimately
associated with E. histolytica? Has
radioactivity been used to trace
ecological dispersion of an element like
phosphorus in a parasite? If ever, how is
E. histolytica considered in civic water
management?
23. The main point of this lecture
is to sketch E. histolytica as a
distinct pathogen differing from
E. coli and E. dispar. More,
decades pass without fruitful
reseach results. Perhaps you
find this a challenge.
Editor's Notes
Perhaps vegetables grown in untreated drainage (aguas negras) should be iodinized or treated with caution. Amebiasis, famous by transmission by foodhandlers, can be also transmitted on the surface of foods.
The larger problem is water supply & drainage, particularly in agricultural countries as in much of Latin America. Recycling scarce water is one very large civic task, and safely fertilizing crops with drainage is another. At the same time, the demand for sanitary services is increasing, because of the population explosion. Then the question can be: What is the role of E. histolytica in current and future water management problems?
Cerebral amebiasis is fatal. Cysts are spread from one person to another directly or via contaminated objects or in food or water. People are infectious as long as the cysts are being shed in their feces. When others touch the objects or eat contaminated food, they get the cysts on their hands and into their mouths. When they swallow the cysts, they get infected. Diagnosis is made by examining fecal samples under the microscope for the presence of trophozoites and cysts of Entamoeba histolytica..
In 1875 in St. Petersburg, Russia, Losch first described amebiasis, proving the ameba’s pathogenicity by infecting a dog with fecal cysts from a hospital patient. Councilman & Lafleur at Johns Hopkins University Hospital, Baltimore, Md, USA distinguished between bacillary and amebic dysentery in 1891.
Many other amebas and flagellates inhabit the human intestine, mostly harmless. Regardless, they should be recognized by anyone diagnosing fecal samples. Illustrations are through the courtesy of Chiang Mai University, Thailand: dept/parasite/image.htm.
Indications for endoscopy in suspected intestinal amebiasis include the following: a) serum antibody positive, yet feces negative, b) immediate diagnosis required and feces negative, c) high suspicion without evidence, and d) evaluation of lesions.
Patients can have chronic protracted diarrhea, dysentery (minority), cramping abdominal pain and tenderness. Fever may result from bacterial superinfections. red blood cells, neutrophils, mucus and shreds of necrotic mucosa may be seen in stool specimens.Complications include appendicitis, perforation, hemorrhage, stricture and pseudopolyposis. Chronic irritable colon or postdysenteric colitis may be experienced.
Most infections lead to uneventful recoveries. However. fulminant amebic colitis has a mortality rate of more than 50%, whereas pleuropulmonary amebiasis has a mortality rate of 15-20%, amebic pericarditis has a case fatality rate of 40%.
Have these and other drugs including the antimitotic type been adequately tested in in vitro, i. e., in trophozoite and cyst cultures? They have not. Is simple mitosis understood? It is not.
Is patient data well anaylzed by locality, income, age, sex, etc. Would questionaires help? Are these patients rural, migrant or urban? How does amebiasis relate to rural poverty? Where did certain travelers become infected? Is amebiasis a medical, a water-and-drainage or a social problem? Is underfinancing of research a problem? What distinguishes persons with antibodies against E. histolytica from others without?
