This document summarizes amebiasis, caused by the intestinal protozoan Entamoeba histolytica. The parasite is typically acquired by ingesting cysts from fecally contaminated food, water or surfaces. In the intestines, trophozoites emerge which can invade the intestinal lining in some cases, causing a spectrum of symptoms from dysentery to liver abscesses. Amebiasis is common in developing areas with poor sanitation, though travelers and immigrants are also at risk. Diagnosis involves examining stool samples microscopically and using serology tests. Treatment involves antimicrobial drugs to eliminate the parasite from the intestines and treat extra-intestinal infections.

1. PROTOZOAL
INTESTINAL
INVASIONS

2. Amoebiasis
Amebiasis is a disease which is caused by the intestinal
protozoan Entamoeba histolytica.
- About 90 % of diseases are asymptomatic, and
the remaining 10 % produce a spectrum of clinical syndromes
ranging from dysentery to abscesses of the liver or other
organs.

3. LIFE CYCLE AND TRANSMISSION
• E. histolytica is acquired by ingestion of
viable cysts from fecally contaminated
water, food or hands.
• Less common means of transmission
include contaminated water, oral and
anal sexual practices, and in rare
instances direct rectal inoculation through
colonic irrigation devices

4. • 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.
• 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

5. EPIDEMIOLOGY
• About 10 % of the world's population is infected
with E. histolytica;
• Amebiasis is the third most common cause of
death from parasitic disease (after
schistosomiasis and malaria).
• 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.
• The main groups at risk in developed countries
are travelers, recent immigrants, homosexual
men, and inmates of institutions.

6. PATHOGENESIS AND PATHOLOGY
• Both trophozoites and cysts are found in the
intestinal lumen, but only trophozoites invade
tissue.
• The trophozoite is 20 to 60 um in diameter and
contains vacuoles and a nucleus with a
characteristic central karyosome.
• 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 a galactose-inhibitable lectin.

7. PATHOGENESIS AND
PATHOLOGY
• The earliest intestinal lesions are
microulcerations 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.

8. ETIOLOGY
Entamoeba histolytica –
forma magna, f. minuta, f.
cystica
CLINICAL SYNDROME
Intestinal Amebiasis
• The most common type of
amebic infection is
asymptomatic cyst passage.
Even in highly endemic areas,
most patients harbor
nonpathogenic strains.

9. Incubation period – some days to 3-4
months
Acute amoebiasis
• Symptomatic amebic colitis develops 2 to 6
weeks after the ingestion of infectious cysts.
• Lower abdominal pain and mild diarrhea
develop gradually and are 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
to 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.

10. • In contrast to those with bacterial
diarrhea, fewer than 40 % of patients with
amebic dysentery are febrile.
• Virtually all patients have heme-positive
stools.
• 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.

11. • Amebomas are inflammatory mass
lesions that develop owing to chronic
intestinal forms of amebiasis.
• An occasional patient presents only with
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.

12. Amebic Liver Abscess
• Extraintestinal infection by E.
histolytica most often involves the
liver. Pleuropulmonary
involvement, which is reported in
20 to 30 % of patients, is the most
frequent complication of amebic
liver abscess.
• Liver
scans, ultrasonography, computed
tomography and magnetic
resonance imaging are all useful
for detection of the round or oval
hypoechoic cyst.

13. • the typical patient with amebic colitis
has less prominent fever than in
these conditions and heme-positive
stools with few neutrophils,
• correct diagnosis requires bacterial
cultures, microscopic examination of
stools, and amebic serologic testing.

14. TREATMENT
Tissue amebicides
• Metronidazole ( Trichomonacid, Flagyl, Klion, Efloran)
tb. 0,25 gr, 30 mg/kg, 3/day, 8-10 days;
• Tinidazole (Fasigyn)
tb. 0,150, 0,5 gr, 2,o gr , 2/day, 3-5 days;
• Dehydroemetin
tb. 0,01 gr, amp. 2 ml.(0,06 gr), dose 1-1,5 mg/kg/day,
per os - 2 tb. 3 /day, i.m. - 1-1,5 mg/kg max. 90
mg/day, 3/day, 5-10 days.
• Amoebic abscesses
Dehydroemetin – Arthrochin или Chloroquin 1 gr/day,
4 х 1, 2 days and 2х1 tb 25 days,
In children - 10 mg/kg/day, 2-3 weeks, till 300
mg/day, Tetracyclin tb. 0,25 gr, 2,о gr , 4 times per
day, 10 days.
• Patients with cysts - Metronidazole, Diloxinide tb.0,5 gr
3 x1, 10 days, Dijodoquin

15. PREVENTION
• Amebic infection is spread by ingestion of food
or water contaminated with cysts.
• Since an asymptomatic carrier may excrete up
to 15 million cysts per day, prevention of
infection requires adequate sanitation and
eradication of cyst carriage.
• In high-risk areas, infection can be minimized by
the avoidance of unpeeled fruits and vegetables
and the use of bottled water.
• Because cysts are resistant to readily attainable
levels of chlorine, disinfection by iodination
(tetraglycine hydroperiodide) is recommended.
• There is no effective prophylaxis.
• Dispanserisation – 5 years with control
examinatins

16. Lambliosis
GIARDIASIS
Giardia lamblia is a cosmopolitan protozoal
parasite that inhabits the small intestines of
humans and other mammals.
Giardiasis is one of the most common parasitic
diseases worldwide and causes both endemic
and epidemic intestinal disease and diarrhea.

17. Life Cycle
• Infection
follows the
ingestion of
the
environmenta
lly hardy
cysts, which
excyst in the
small
intestine,
releasing
trophozoites
that multiply
by binary
fission

19. Lambliosis
Urticaria