PROTOZOAN

MEDICINE MADE RIDICULOUSLY SIMPLE

INTESTINAL PROTOZOA

SIKATEMA MIKE Bsc Biomed

PROTOZOA
Single-celled eukaryotic microorganisms

The single protozoa cell performs all functions such as reproduction, digestion,

respiration, excretion. etc.

Most of the protozoa are completely nonpathogenic but few may cause major
diseases such as malaria, leishmaniasis and sleeping sickness.
CLASSIFICATION
PHYLUM: SARCODINA (Sarcodina means pseudopodia present)

ORDER: AMEBOZOA OR AMEBIDA

GENUS:

● Entamoeba
● Endolimax
● Iodamoeba
STRUCTURE AND TERMINOLOGIES
TERMINOLOGIES

• Trophozoite: (trophos: nourishment): Active feeding and

growing stage of the protozoa is called the trophozoites.
It derives nutrition from the environment by diffusion,
pinocytosis and phagocytosis.

• Cyst: the non motile form which is protected by a distinct

membrane or cyst well. This is an infective stage of the
parasite.
TERMINOLOGIES

• Excystation: the process of emergence of the

trophozoite from the cyst (vs. encystation)
• Pseudopod: literally means false foot;
temporary cytoplasmic processes at the surface
of the trophozoite
Intestinal amebae free-living

• Entamoeba histolytica • Naegleria fowleri

• Entamoeba dispar • Acanthamoeba spp.
• Entamoeba coli • Balamuthia mondrillaris
• Entamoeba polecki
• Entamoeba hartmanni
• Entamoeba gingivalis
• Endolimax nana
• Iodamoeba butschlii

Note: All intestinal amebae are Note: All free-living amebae

nonpathogenic, except Entomoeba are opportunistic pathogens
histolytica
ENTAMOEBA HISTOLYTICA
E. histolytica is worldwide in prevalence, being much more common in the tropics than
elsewhere. It has been found wherever sanitation is poor.
MORPHOLOGY
E. histolytica occurs in three forms:
1. Trophozoite: Trophozoite is the vegetative or growing stage of the parasite. lt is the only
form present in tissues.
Trophozoiles survive up to 5 hours at 37°C and are killed by drying, heat and chemical
sterilization. Therefore, the infection is not transmitted by trophozoites. Even if live
trophozoites from freshly-passed stools are ingested, they are rapidly destroyed in stomach
and cannot initiate infection.
TROPHOZOITE

Morphology:
Trophozoite = vegetative stage
1. Wide clear ectoplasm, granular endoplasm.
2. Food vacuoles with ingested rbcs, not bacteria.
3. Highly motile, pseudopodia fingerlike,
progressive
4. 15 – 30μm
MORPHOLOGY
ENCYSTMENT: Trophozoites undergo encystment in the intestinal lumen.
Encystment does not occur in the tissues nor in feces outside the body.
Cyst is formed in unfavorable conditions and is usually the infective form for vertebrate host
2. Precyst
Before encystment, the trophozoite extrudes its food vacuoles and becomes round or oval, about
10-20 μmin size. This is the precystic stage of the parasite.It contains a large glycogen vacuole and
two chromatid bars. It then secretes a highly retractile cyst wall around it and becomes cyst.
CYSTE
3. Cyst
The early cyst contains a single nucleus and two other structures: (1) a mass of
glycogen and (2) 1-4 chromatoid bodies or chromidial bars. As the cyst matures,
the glycogen mass and chromidial bars disappear and the nucleus undergoes two
successive mitotic divisions to form two and then four nuclei. The mature cyst is,
thus quadrinucleate (The Infective Stage).
MORPHOLOGY

• Multiplication in the host occurs by binary fission. Nuclear

replication produces four nuclei during cyst maturation.
LIFE CYCLE

• This parasite is transmitted from human to human

Transmission:
Fecal oral route
5Fs: fingers, flies, feces,food/water, fomites
Pathogenesis and Clinical Features

• E. histolytica causes intestinal and extraintestinal

amebiasis.
• Incubation period is highly variable. On an average, it
ranges from 4 days to 4 months.
INTESTINAL AMEBIASIS
INTESTINAL AMEBIASIS
Invasion of intestinal tissues

The metacystic trophozoites penetrate the columnar epithelial cells in the crypts of
lieberkuhn in the colon. This is facilitated by the motility and amebic cystein
proteases such as histolysin.

Inflammation and tissue necrosis mediated by inflammatory cells and release of

cytokines like IL8 and TNF-alpha
INTESTINAL AMEBIASIS
Ameba penetrates the submucosal layer and multiplies rapidly causing lytic necrosis
forming abscess. Abscess breaks down to form an ulcer.

The typical amebic ulcer is flak shaped.

INTESTINAL AMEBIASIS
Occasionally a granulomatous pseudotumoral growth may develop on the
intestinal wall. This is called Ameboma.
EXTRAINTESTINAL AMEBIASIS
Amebic liver abscess
a. Liver abscess : right lobe usually (due to portal circulatory
system of the right colon)
amoebae digest wall of mesenteric venules, enter
intra hepatic portal vessels,
lytic necrosis, digests lobules
= amoebic liver abscess
= amoebic hepatitis.
EXTRAINTESTINAL AMEBIASIS
Untreated abscesses tend to rupture into the adjacent tissues through the
diaphragm into the lung or pleural cavity, pericardium, peritoneal cavity, stomach,
intestine, or inferior vena cava or externally through abdominal wall and skin
EXTRAINTESTINAL AMEBIASIS
Pulmonary amebiasis:

• Amoebae perforate diaphragm, enter right lung

and pleural cavity ( hepatobronchial fistula)
• Hepatobronchial fistula usually results with
expectoration of chocolate brown sputum
• Liver colored sputum
EXTRAINTESTINAL AMEBIASIS

Cutaneous amoebiasis: amoebiasis cutis

• Ulceration of the skin, gangrene of the epidermis.
Perianal –direct extension around anus
• Amoeboma
• Pseudocondyloma (The lesion may be mistaken for
condyloma)
EXTRAINTESTINAL AMEBIASIS

Metastatic amebiasis: Involvement of distant organs is by

hematogenous spread and through lymphatics. Abscesses
in kidney, brain, spleen and adrenals have been noticed.
● Spread to brain leads to severe destruction of brain
tissue and is fatal.
EXTRAINTESTINAL AMEBIASIS
Genitourinary amebiasis: penile amebiasis which is acquired through anal

intercourse. Similar lesions in females may occur on vulva, vagina, or cervix by

spread from perineum. The destructive ulcerative lesions resemble carcinoma.
SYMPTOMS OF AMOEBIASIS
1. Incubation period; 2-5 days
several years, expected 1-4 months
2. Vague abdominal discomfort with generalized
malaise
3. Acute: sudden attack of colitis, bloody
dysentery, rapid weight loss, dehydration,
vomiting, nausea.
SYMPTOMS OF AMOEBIASIS

4. Chronic: formed stool/diarrhea for more than

1 month, generalized indisposition.
5. Hepatitis
6. Pulmonary infection: Unproductive cough,
dyspnea, liver colored sputum
7. Amoebic brain abscess; Fatal 7-10 days
Treatment
Three classes of drug are used in Lhe treatment of amebiasis:
1. Luminal amebicides: Diloxanide furoate, iodoquinol, paromomycin and tetracycline
act in the intestinal lumen but not in tissues.
2. Tissue amebicides: Emetine, chloroquine are effective in systemic infection, but less
effective in the intestine.
3. Both luminal and tissue amebicides: Metronidazole and related compounds like
tinidazole and omidazole act on both sites and are the drug of choice for treating amebic
colitis and amebic liver abscess.
CONTROL
1. Sanitary disposal, nightsoil composting
2. Hand washing/ personal hygiene
3. Health education
4. Strict control of food handlers, protecting, food hygiene
5. Treatment of drinking water
6. Group treatment
7. Travelers: use I2 iodoquinol tablets kill cysts
NON – PATHOGENIC AMOEBAS

A. Entamoeba dispar
B. Entamoeba hartmanni
C. Entamoeba gingivalis (gums)
D. Entamoeba polecki.
E. Entamoeba moshkovskii
F. Endolimax nana.
G. Iodamoeba buetschlii.
H. Entamoeba coli
QUESTIONS