(Open Table in a new window)

Mode of
Name Symptoms
Transmission

Flagellates

Contaminated Nausea, bloating, gas,

G lamblia
water, fecal-oral diarrhoea, anorexia

Previously thought
Fecal-oral,
Dientamoeba commensal; may cause
associated
fragilis diarrhoea, abdominal, pain,
with Enterobius
nausea

Amoebas

Contaminated
Colitis, dysentery, diarrhea,
Entamoeba water, fecal-oral,
liver abscess, other
histolytica contaminated
extraintestinal disease
food

Spore-forming
(Coccidia)

Immunocompetent
patients: Self-limited
Contaminated
Cryptosporidium diarrhoea
water, swimming
parvum Immunosuppressed
pools, fecal-oral
patients: Severe and
interminable diarrhea

Same as
Isospora belli Fecal-oral
in Cryptosporidium

Fecal-oral,
Cyclospora Same as
contaminated
cayetanensis in Cryptosporidium
water and food

Microsporidia Fecal-oral,
Same as
(Septata contaminated
in Cryptosporidium
intestinalis, water
Enterocytozoon
bieneusi)

Ciliates

Fecal-oral
(frequently
Balantidium coli Colitis, diarrhea
associated with
pigs)

Other

Blastocystis
Fecal-oral May cause mild diarrhea
hominis

Pathophysiology
Understanding the life cycle is essential to explain the pathophysiology of
the diseases caused by these organisms. The life cycles of intestinal
protozoa are very similar, with the exception of D fragilis, which lacks a cyst
stage.
Mechanisms of diarrhea production by intestinal protozoa are related to
direct cytotoxic effects, the ability to invade, and/or effects of the immune
response on the intestinal epithelium. No evidence suggests that intestinal
protozoa produce enterotoxins.
Entamoeba histolytica
Mature cysts are ingested via contaminated water or food. After excystation
in the small intestine, trophozoites inhabit the large intestine and can either
invade the tissue (pathogenic amoebas) or are eliminated in the stools.
Trophozoites do not survive outside the body. This parasite was named for
its remarkable ability to lyse human tissues. A prerequisite to amebic
invasion is the parasite's ability to colonize and penetrate colonic mucins
overlying the intestinal epithelium. At least 22 amebic strains or
zymodemes have been identified based on pulsed-field gel electrophoresis
patterns of the 4 isoenzymes isolated from amoeba. Nine zymodemes have
been associated inconsistently with invasiveness.
In 1982, Sargeaunt postulated that instead of pathogenic and
nonpathogenic zymodemes, 2 different amoebas were present. [3] The
concept of E histolytica as a pathogenic amoeba and E dispar as a
nonpathogenic amoeba is currently accepted. Furthermore, both
immunologic assays and amplification tests have been developed to
distinguish these two species among symptomatic and asymptomatic
patients. Upon invasion of the host, amoebas are capable of killing immune
effector cells by contact-dependent cytolysis, possibly by a calcium-
dependent mechanism. They then disseminate to the liver or other tissues.
Giardia lamblia
After ingestion of mature cysts (infective dose varies from 10-100 cysts) via
contaminated water or food, the trophozoite emerges in the small intestine,
rapidly multiplies, and attaches to the small intestinal villi. [4]Mature infective
cysts pass in faeces and complete the cycle. The pathogenesis of diarrhea
in giardiasis is thought to be related to the following factors: (1) the number
of organisms ingested, (2) specific strain ingested, (3) nonantibody
protective factors in the GI tract, and (4) the immune response of the host.
Giardia trophozoites attach to the cell surface of villi by means of a disk on
their posterior or ventral surface. Lectin, a protein on the trophozoite lining,
recognizes specific receptors on the intestinal cell and may be partly
responsible for the tight attachment between the parasite and the villi,
which is followed by mucosal damage, mechanical obstruction (only
caused in the presence of numerous organisms), and deconjugation of bile
salts. Recent data has indicated that inflammatory mast cells may interfere
with duodenal growth of G lambliatrophozoites. [5] Other inflammatory cells,
as well as CD8+ T cells, contribute to villus-shortening and crypt
hyperplasia.
Strains that infect humans are biologically diverse, as shown by differences
in antigens, restriction endonuclease patterns, DNA fingerprinting,
isoenzyme patterns, and pulsed-field gel electrophoresis patterns.
In giardiasis, secretory immunoglobulin A (IgA) is presumed to be important
in host protection because invasion of the mucosa is not part of the
pathogenic mechanism.

Spore-forming protozoa
Spore ingestion begins a life cycle that is similar in all 4 of the intestinal spore-
forming protozoa (see Table 1). The ingested spores release sporozoites that invade
enterocytes, primarily in the small intestine. The enterocyte infection progresses
through 2 stages: merogenic and sporogonic.
The merogenic (or schizogonic) stage involves the maturation and development of
meronts to reproduce and multiply in the infected cell or to infect other enterocytes.
This asexual stage allows the infection to spread to many enterocytes, even if the
host is not exposed repeatedly to the organism.
The sporogonic (ie, gametogonic, sexual) stage involves the maturation and
development of sporozoites enclosed in cysts or spores. As the infected enterocytes
die, cyst or spore shedding occurs. The spores are then excreted in the stool. The
spore-forming protozoa are obligate intracellular pathogens. Infection by these
protozoa has been associated with substantial alterations in intestinal structure and
function, but the pathogenesis of the predominant symptom, diarrhea, is not
completely understood.
Cryptosporidiosis is the best-studied spore-forming diarrhea, and its pathogenic
mechanisms can also be related to other spore-forming protozoa. The hypothesized
sequence of events is explained below.
After invasion of the enterocytes, the epithelial cells release cytokines. These
cytokinins activate phagocytes and recruit new leukocytes, which, in turn, release
soluble factors (resulting in intestinal secretion of chloride and water) and inhibit
absorption. Enterocyte damage may be a direct consequence of parasite invasion,
multiplication, and extrusion. Regardless of the specific mechanism, marked
distortion of the villus architecture is accompanied by nutrient malabsorption and
osmotic diarrhea. With the exception of the microsporidia S intestinalis, none of the
spore-forming protozoa have the ability to invade beneath the mucosal layer of the
intestine.
Dientamoeba fragilis
The exact mode of transmission of D fragilis has not been confirmed. This parasite is
speculated to be transmitted when pinworm eggs containing D fragilis trophozoites
are ingested and, by this mechanism, resist the acid pH in the stomach. It is not
invasive and mostly inhabits the large intestine. The exact mechanisms of diarrhea
are not known.
Balantidium coli
The cyst is the infectious stage and is acquired by ingestion of contaminated food or
water. After excystation in the small intestine, the trophozoites colonize the terminal
ileum and the large intestine. They can then invade tissues by mechanical action of
ciliary movement and the secretion of hyaluronidase and probably other enzymes.
Encystation occurs in the lumen of the colon or in freshly evacuated stools. As with E
histolytica,invasiveness is the hallmark of the pathophysiology of balantidiasis.
Blastocystis hominis
Many experts believe that B hominis is pathogenic only when present in large
numbers in the intestine (>5 organisms per 400X field) and when other infectious
organisms are absent. Three distinct morphologic stages are recognized: vacuolar,
granular, and ameboid. B hominis inhabits the large intestine and has no evident life
cycle in humans. Cysticlike stages are rare and have been found in patients with
acquired immunodeficiency syndrome (AIDS) and in vitro. The mechanisms of how
this parasite causes illness have not been elucidated yet

Medical Care
See the list below:
 The most important aspect of providing care for children with diarrhea
caused by intestinal protozoa includes standard pediatric
assessments.
 Evaluate the child for signs of dehydration, including tachycardia,
delayed capillary refill, decreased tears, decreased activity, decreased
urine output, and altered mental status.
  Hypovolemic shock rarely occurs with these infections but must be
recognized.
 The child must be evaluated for the adequacy of the nutritional status.
This is particularly important in cases of chronic diarrhea and possible
immunodeficiency.
 Weight must be measured and compared on the growth curve.
Appropriate interventions occur following this immediate assessment.
 Oral rehydration therapy (ORT) is the preferred approach for children
with mild-to-moderate dehydration. Intravenous rehydration should
rarely be necessary. Current recommendations for pediatric
rehydration are outlined best in The Management of Acute Diarrhea in
Children: Oral Rehydration, Maintenance, and Nutritional Therapy. [22]
 Following immediate fluid resuscitation for dehydration, the clinician
must address potential nutritional issues and provide adequate
nutrition to the child with acute or chronic diarrhea.
 Protozoal GI infections in immunocompetent patients are usually mild-
to-moderate self-limited diseases, and special precautions are not
needed.
 The hallmark for treatment of these diseases is specific antiprotozoal
therapy.
 Patients with severe amebic or balantidic colitis should not receive oral
nutrition and should be monitored for potential surgical complications.
 Consider parenteral nutrition in some patients.
 Patients with amebic liver abscess should be treated in the hospital
until potential complications have been ruled out

Amoebiasis

This is an infection usually of the colon by Entamoeba histolytica. Most of

the

people infected by Entamoeba histolytica are asymptomatic cyst carriers.

Clinical Features

Two diseases that are caused by Entamoeba histolytica are amoebic

dysentery

and amoebic liver abscess.

Amoebic dysentery: This presents as bloody diarrhoea, and depending on

the
severity of infection there may be varying degrees of dehydration.

Amoebic liver abscess: This presents as intermittent fevers, night sweats,

and

tenderness in the right hypochondrium. Some patients may have difficulty

breathing. The abscess may rupture into the chest, causing empyema or
into

the abdomen causing peritonitis.

Investigations

Stool for microscopy – Trophozoite with ingested RBC in amoebic

dysentery

Full haemogram – Liver abscess (leucocytosis, mild anaemia)

Chest x-ray – Elevation of the right hemidiaphragm liver abscess

Abdominal ultrasound will show abscess in liver

Management

Amoebic dysentery: See Section 18, on diarrhoea.

Admit if liver abscess is suspected and start treatment for amoebic liver

abscess:

Worm
 Metronidazole 30–50mg/kg/day in 3 divided doses for 7–10 days
 • Aspiration or surgical drainage of pointing liver abscesses is indicated to
 prevent spontaneous rupture in pointing abscesses.
 Asymptomatic cyst carriers:
 • Treat cyst carrier in food handlers only. Use diloxanide furoatemetronidazole (e.g.,
entamizole).