Amebiasis and Schistosomiasis
Definition of Terms:
• Amebiasis - infection of the intestine
caused by a parasite called Entamoeba
histolytica.
• Schistosomiasis - a blood fluke
(trematode worm) of the genus
Schistosoma produce an acute and
chronic parasitic illness.
• Cytopathic effect - viral infection causes
structural alterations in the host cell.
• Necrosis - death of the body tissue. It may
be triggered by chemicals, cold, trauma,
radiation or chronic conditions that impair
blood flow.
• Dysentery - an infection of the intestines
that causes diarrhea containing blood or
mucus.
• Swimmer's itch - a skin rash induced by
an allergic reaction to particular tiny
parasites that infect some birds and
mammals is known as cercarial dermatitis.
• Immunoassay - is a biochemical test that
uses an antibody or an antigen to
determine the presence or concentration
of a macromolecule or a small molecule in
a solution (sometimes).
• Periportal fibrosis - Symmers found a
chronic condition that is a late-stage
consequence of schistosomiasis infection.
• Trophozoites - is the protozoan's active,
reproductive stage that feeds on the host.
• Cercariae- is the larval form of the
trematode class of parasites.
Amebiasis
 When a parasite enters a host, there are
several possible results. First, there may
be no infection at all, because the host’s
innate immunity prevents the parasite
from establishing an infection. In this case,
the host fails to provide either the
necessary physical environment or some
important nutritional factor(s) needed for
the parasite’s survival. The host may even
produce products that are toxic to the
parasite.
 In the second possible outcome, the
parasite may invade the host, become
established, and then be killed and
eliminated by host defense mechanisms.
These events indicate that an effective
immune response has occurred. Typically,
the host remains immune to reinfection
for some time. This response requires
antibody formation and cell-mediated
immunity.
 The third possible outcome is the reverse
of the second— the parasite may
overwhelm and kill the host. Reasons for
this include an organism that multiplies so
rapidly that the host does not have time
to mobilize its defenses, the parasite
invades a vital organ(s), or the host has an
inadequate immune system.
 A fourth possible outcome is a long-lasting
infection in which the host begins to
eliminate the parasite but cannot remove
it completely. In the best case, the host
controls the disease for an extended
period and eventually overcomes and
eliminates the parasite. In the worst case,
the host ultimately succumbs to the
infection and dies.
Amebiasis and Schistosomiasis
 And, finally, a fifth possible outcome is the
host mounts a response that attacks not
only the parasite but also host tissues. The
effects of this inappropriate response
(hypersensitivity or immune disease) may
be mild or severe; often the consequences
for the parasite are minimal. In fact, most
of the pathology associated with a
parasitic infection result from the
immunologic responses to the offending
organism and may be more dangerous for
the host than the invader.
Life Cycle of Entamoeba Histolytica
 Entamoeba is a protozoan that causes
intestinal amebiasis as well as
extraintestinal manifestations.
1. Occurs by ingestion of mature cysts in
fecally contaminated food, water, or
hands. The mature Cyst is resistant to
low pH of stomach, so remain unaffected
by the gastric juices.
2. The cyst wall is then lysed by intestinal
trypsin and when the cyst reaches the
caecum or lower part of illium
excystation occurs. The neutral or
alkaline environment as well as bile
components favor excystation. The stage
in the life cycle of a parasite in which it
escapes from a cyst
3. Excystation of a cyst gives 8 trophozoites.
It is the growing and feeding stage of
parasite
4. Trophozoites are actively and carried to
large intestine by peristalsis of small
intestine. Trophozoites then gain
maturity and divide by binary fission.
asexual reproduction by a separation of
the body into two new bodies.
5. Trophozoites are released, which migrate
to the large intestine.
6. Trophozoites multiply by binary fission
and produce cysts. The trophozoites
adhere to mucus lining of intestine by
lectin and secretes proteolytic enzymes
which causes tissue destruction and
necrosis. Parasite, when gain access to
blood, migrates and causes extra-
intestinal diseases.
7. In many cases, the trophozoites remain
confined to the intestinal lumen ( A: non-
invasive infection) of individuals who are
asymptomatic carriers, passing cysts in
their stool. • In some patients the
trophozoites invade the intestinal
mucosa ( B : intestinal disease), or,
8. Pass through the bloodstream,
extraintestinal sites such as the liver,
brain, and lungs (C : extra-intestinal
disease), with resultant pathologic
manifestations..
9. When the load of trophozoites increases,
some of the trophozoites stop
multiplying and revert to cyst form by
the process of encystation.
Amebiasis and Schistosomiasis

10. Then are passed in the feces. Because of
the protection conferred by their walls,
the cysts can survive days to weeks in the
external environment and are
responsible for transmission.
(Trophozoites can also be passed in
diarrheal stools, but are rapidly
destroyed once outside the body, and if
ingested would not survive exposure to
the gastric environment.) motile
amoebae lose their characteristic
pseudopoidal movement and become
covered by a protective sheath made up
of a double layered wall.
Pathophysiology of Amebiasis
 fecal-oral route
 excystation in the small bowel and
invasion of the colon by the
trophozoites.
 E. histolytica trophozoites interact with
the host through a series of steps:
• adhesion to the target cell,
• Phagocytosis (acquires nutrients by
phagocytosis of colonic bacteria, and
phagocytosis of host cells by E)
• cytopathic effect (Trophozoites may
invade the colonic mucosa and cause
dysentery and, through spreading via
the bloodstream, may give rise to
extraintestinal lesions, mainly liver
abscesses.)
 Perspective of the host: E. histolytica
induces both humoral and cellular
immune responses; cell-mediated
immunity is the major human host
defense against this complement-
resistant cytolytic protozoan. Cell-
mediated interferon gamma (IFN-γ)
appears to provide protection from
amebiasis through its ability to activate
neutrophils and macrophages to kill the
parasite.
 Stomach acid serves as an important first
line of defense against enteropathogens
through its ability to kill acid-sensitive
microorganisms. However, infectious
amebic cysts are highly resistant and
survive passage through the acidic
environment of the stomach. In the
intestine, the next layer of innate defense
may be the mucus layer, which is thought
to act as a protective barrier, preventing
E. histolytica from invading intestinal
epithelial cells (IECs).
 Macrophages also play a crucial role in the
host response against intestinal amebiasis.
 Antigen shedding (Another mechanism of
escape involves antigen shed from the
parasite. For example, Entamoeba
histolytica can shed antigens.2 Antibody is
formed and attaches to the antigen. Since
the antigen is not attached to the
parasite, the immune response is unable
to harm the offending organism
 Mechanisms of colonization and invasion
by E. histolytica trophozoites and host
immune responses to suppress and
control amebic infection. In the lumen of
the large intestine, the IEC layer is
covered by the mucus layer (blue), which
contains secreted mucin and IgA from the
host and commensal microbiota.
Amebiasis and Schistosomiasis
 Proteases and glycosidases secreted from
the amebae are involved in the
degradation of mucin and extracellular
matrix. The pro-domain of EhCP-A5 binds
to and activate integrin and enhances the
inflammasome formation of leading to
pro-inflammatory responses. PGE2 also
secreted from the amebae causes mucin
hypersecretion and depletion of mucin
from the IECs.
 PGE2 also elicits signaling in a cascade
leading to NFκB activation in the IECs and
induces IL-8 secretion. The Gal/GalNAc
lectin (lectin) and LPPG on the ameba’s
surface binds to TLR2 and leads to NFκB
activation and pro-inflammatory cytokine
release for IEC. PGE2 also helps to disrupt
tight junction function of the epithelium
and enhances the amebic infiltration.
 Phagocytosis and trogocytosis are also
involved in removal of host cells and
invasion into the host tissue. Infiltrating
trophozoites are attacked by complement
from the circulation, ROS and NO from
neutrophils and macrophages. The
Gal/GalNAc lectin and LPPG activate CD4,
CD8 T cells, and NKT cells, and, thus,
enhances protective cellular immunity.
 CD4 T cells produce IFN-γ, IL-4, IL-5, and
IL-13, and CD8 T cells produce IL-17. IL-17
induces neutrophil infiltration and
enhances secretion of mucin,
antimicrobial peptides, and IgA into the
colonic lumen. When disseminated to the
liver, the amebae are attached and
removed by the dense mediated by IFN-γ
secreted by NKT cells.
 TNF-α secreted from hepatic
macrophages leads to abscess formation.
Solid arrows depict secretion of soluble
proteins and dotted arrows indicate
interaction or signal transduction.
Cytokines mainly beneficial for an
elimination of the amebae are shown in
black, while those involved in disease
manifestations are shown in red.
 Possible mechanisms of immune evasion
during amebiasis. Secreted or surface
proteases of the amebae degrade IgA in
the mucosal layer. PGE2 from the amebae
induces IL-10 secretion from the IECs, and
in turn stimulates mucin and IgA
secretion, which likely prevents
unnecessary inflammation.
Overstimulation of TLR causes
downregulation of NFκB activation.
 Removal of infiltrating immune cells by
phagocytosis/trogocytosis helps to reduce
immune responses. Some commensal
microbiota, namely Clostridium XIV and IV
groups and Bacteroides fragilis, induce
Treg cells to downregulate immune
responses. Polysaccharide A from B.
fragilis binds to TLR2 on CD4 T cells and
induces IL-10 production.
 The amebae in the tissues and the blood
stream evade from complement by
surface receptor capping (LPPG, lectin)
and degradation of C3a and C5a by
cysteine proteases. Cysteine proteases
also degrade IL-1β, antioxidative stress
defense by the TRX and PRX systems
fends off the attack from ROS and NO
from activated neutrophils and
macrophages. LPPG binds to TLR2 on
monocytes and macrophages, which leads
to secretion of cytokines, including IL-10
and TGF-β.
 High doses of LPPG downregulate TLR2
gene expression in monocyte and cause
negative feedback of protective immune
responses. PGE2 from the amebae and
the host causes downregulation of MHC
class II expression on macrophages in the
liver, which results in anti-inflammation.
Amebiasis and Schistosomiasis
Incubation
• 1-4 weeks or 2-4 weeks
• The incubation period varies from a few
days to a much longer time
• The area where entamoeba histolytica is
considered to be endemic so it is
impossible to determine exactly when the
exposure took place
• Normally the time frame ranges from one
to four weeks
Clinical Features
 Dysentery or bloody diarrhea
• Dysentery may last for months, it usually
varies from severe to mild, and may lead
to weight loss and prostration
• Symptoms for this includes: stomach pain
, bloody stools and fever
How we can get dysentery?
 It is by food contamination example if
someone who has dysentery and he or
she prepared foods without washing his
or her hands.. it can also be things that
are contaminated with parasite or
bacteria...
• caused by: bacteria or parasite
 Fulminating colitis
 It has different types of fulminant colitis
depends on what causes them
1. Ulcerative colitis
 It occurs when the immune system over
reacts to the bacteria in our digestive tract
Causes: inflammation and bleeding ulcer
Types:
• Proctosigmoiditis: affects the rectum and lower
portion of the colon
• Left sided ulcerative colitis: affects the left side
of the colon start at rectum
• Pancolitis: affects the entire large intestine
2. Pseudomembranous colitis
 occurs from overgrowth of the bacterium
clostridium difficile
3. Ischemic colitis
 occurs when the blood flow to the colon is cut
off or restricted, the reason for this can be
blood clot.
4. Microscopic colitis
5. Allergic colitis in infants
 occurs usually within first month of birth
 Ameboma of the colon
 rare complication amoebic colitis it may result
in low gastrointestinal bleeding and bowel
obstruction, pain, swelling sa right iliac fosa.
Laboratory Test
 It is examined by a personnel who are well
trained, because if lack of appropriate training
the lab result may lead to missed information
a. Sample Preparation/ Sample used for the test
1. When routine ova and parasite examinations
are ordered, three specimens (stool) should be
submitted for the diagnosis of intestinal
amebiasis.
2. Any examination for parasites in stool
specimens must include the use of a
permanent stained smear.
3. Presumptive identification on a wet
preparation must be confirmed by using the
permanent stained smear.
Amebiasis and Schistosomiasis
 Permanent stained smear- facilitates
detection and tropozoites, and it gives
permanent record to protozoa that is
encountered.
 Presumptive – used to differentiate mga
colony forming units
4. The six smears should be prepared at
sigmoidoscopy but should not take the
place of the ova and parasite
examination.
 Sigmoidoscopy specimens may be very
helpful. It is a test that looks checks the
rectum and lower part of the large
intestine (colon)
4. Immunoassay procedures can be
performed to confirm the presence of
the E. histolytica /E. dispar group or can
be used to differentiate pathogenic E.
histolytica from nonpathogenic E. dispar.
5. The serologic test result for antibody may
or may not be positive in intestinal
disease and is much more likely to be
positive in extraintestinal disease.
 Note that if the permanent stained smear
is quite dark, a delicate E. histolytica /E.
dispar organism may appear more like
Entamoeba coli; on a very thin, pale
smear, E. coli can appear more like E.
histolytica /E. dispar. Also, when the
organisms are dying or have been poorly
fixed, they appear more highly
vacuolated, thus looking like E. coli
trophozoites rather than E. histolytica /E.
dispar
 Not every patient infected with E.
histolytica will develop invasive amebiasis;
the outcome will depend on the
interaction between parasite virulence
factors and the host response.
Screening Tests:
 Screening test for intestinal disease is rarely
recommended unless the patient has true
dysentery; Dysentery means an infection of the
intestines that causes diarrhea containing blood
or mucus. A definitive diagnosis of intestinal
amebiasis should not be made without
demonstrating the presence of the organisms
and is not useful in the diagnosis of
asymptomatic patients. In patients suspected of
having extraintestinal disease, serologic tests
are diagnostically more effective and a valuable
tool in conjunction with either antigen or
nucleic acid–based testing.
The most frequently used tests in Amoeba
antigens and antibodies detection:
EIA (Enzyme
Immunoassay)
• A number of enzyme immunoassay reagents
are commercially available, and their specificity
and sensitivity provide excellent options for the
clinical laboratory.
• One fecal antigen test can differentiate the E.
histolytica or E. dispar and E. moshkovskii from
the rest of the Entamoeba spp., such as
nonpathogenic E. coli or E. hartmann.
• This kit requires fresh or frozen stool; fecal
preservatives have been found to interfere with
the Entamoeba spp. reagents.
Principle:
• A sensitive immunoassay that uses an enzyme
linked to an antibody or antigen as a marker for
the detection of a specific protein, especially an
antigen or antibody.
Amebiasis and Schistosomiasis
• Involves detection of “analyte” in a liquid
sample using liquid reagent (wet lab) or
dry strips (dry lab). In dry analysis, strips
can be read in reflectometry. The
quantitative reading is usually based on
detection of intensity or transmitted light
by spectrophotometry at specific
wavelength.
Indirect
Hemagglutination
Principle:
• Is the clumping of red blood cells, by
either a direct or indirect mechanism.
• If agglutination reaction is used in
immunohematology for blood group
typing (direct) or the detection of a red
cell antibody (indirect).
Indirect Fluorescent
Antibody Test
Principle:
• The antigen-specific antibody is unlabeled,
and a second antibody is conjugated to
the FITC.
• Fluorescent antibody tests are performed
using either a direct fluorescent antibody
(DFA) or an indirect fluorescent antibody
(IFA) technique. In the DFA technique,
FITC is conjugated directly to the specific
antibody.
 Immunofluorescence assays are
frequently used for detecting bacterial
and viral antigens in clinical laboratories.
In these tests, antigens in the patient
specimens are immobilized and fixed onto
glass slides with formalin, methanol,
ethanol, or acetone. Monoclonal or
polyclonal antibodies conjugated
(attached) to fluorescent dyes are applied
to the specimen.
After appropriate incubation, washing, and
counterstaining (staining of the background
with a nonspecific fluorescent stain such as
rhodamine or Evan’s blue), the slide is
viewed using a microscope equipped with a
high-intensity light source (usually halogen)
and filters to excite the fluorescent tag. Most
kits used in clinical microbiology laboratories
use fluorescein isothiocyanate (FITC) as the
fluorescent dye. FITC fluoresces a bright
apple-green
 Indirect hemagglutination and indirect
fluorescent antibody tests have been
reported positive with titers greater than
or equal to 1:256 and greater than or
equal to 1:200, respectively, in almost
100% of cases of amoebic liver abscess. In
the absence of STAT serologic tests for
amebiasis (tests with very short
turnaround times for results), the decision
on diagnosis must be made on clinical
grounds and on the basis of results of
other diagnostic tests, such as scans. In
addition, antibodies may persist for up to
10 years in patients who have had
previous incidences of invasive amebiasis,
making diagnosis complicated in
subsequent infections.
Additional antigen screening test kits are
available but are unable to determine the
species of amoebae. These tests include the:
• RIDASCREEN Entamoeba
• Triage Micro Parasite Panel
Amebiasis and Schistosomiasis

2. Maintain good food hygiene

Molecular Methods
• Nucleic acid–based amplification
• PCR
 Identify unique ribosomal ribonucleic acid
(rRNA) or specific episomal (small circular
nucleic acid) sequences to differentiate
the organisms. Suitable samples for real-
time PCR include stool, liver or brain
aspirates, cerebrospinal fluid, blood,
saliva, and urine samples.
• Multiplex assays
 Capable of detecting multiple types of
organisms including viral, bacterial, and
parasitic organisms capable of causing
gastroenteritis would significantly improve
diagnostic testing and enhance patient
care.
• Drink only boiled water or bottled water
• Purchase fresh food from hygienic and
reliable sources and Eat only thoroughly
cooked food.
• Wash and peel fruit by yourself and avoid
eating raw vegetables
Treatment
There are two classes of drugs used in the
treatment of amebic infections:
1. Luminal amebicides such as iodo-quinol
or diloxanide furoate
2. Tissue amebicides such as metronidazole,
chloroquine, or dehydroemetine.

 Nucleic acid–based amplification • Paromomycin- it is safe, well tolerated,

methods, including polymerase chain
reaction have been developed for the
identification of E. histolytica and E.
dispar.
Confirmatory Test for
Amebiasis
and effective in the treatment of intestinal
amebiasis.
• Diloxanide- it is a dichloroacetamide
derivative that is amebicidal against
trophozoite and cyst forms of E histolytica

• Microscopic observation of parasite in

stool
• Enzyme Linked-immunosorbent assay

Prevention

1. Maintain good personal hygiene

• Perform hand hygiene frequently,
especially before handling food or eating,
and after using the toilet or handling fecal
matter. To avoid contamination
• Use 70-80% alcohol hand rub as an
alternative
Amebiasis and Schistosomiasis

(D) Although yet to be fully defined, this

process may involve E-selectin:-Lewis-x
Schistosomiasis
interactions, and participation from platelets,
ICAM-1 and VCAM-1. While a large
An overview of S. mansoni egg migration.
proportion of eggs successfully penetrate the
Schistosome egg transit is facilitated by a
endothelium and reach intestinal tissue,
series of host interactions at the intestinal
many are swept to the liver or other distal
and vascular interface.
locations (e.g., brain or spinal cord). Since
schistosome eggs are unable to transit
through these organs, overwhelming tissue
pathology and inflammation may ensue. (B)
Once schistosome eggs have passed across
the host endothelium and out of the
vasculature, they must cross the multi-
layered intestinal wall. The host immune
system responds to transiting eggs via an
inflammatory granuloma response, in which
individual eggs are encapsulated by immune
cells [including alternatively activated (AA)
macrophages, Th2 cells and eosinophils] and
(A)The development of schistosomes into
extracellular matrix (ECM), which protects
sexually mature, egg-producing adults occurs
host tissues from egg-derived toxins, but
within the portal vein (~3–5 weeks post
ultimately leads to formation of fibrotic
infection) and requires the transduction of
lesions. For unknown reasons,
host-derived signals (including those from
granulomatous responses need to
the innate and adaptive immune system) to
successfully develop for effective egg
the developing worm pair.
excretion from the host.
(B)Once sexual maturity is reached, worm
Accordingly, schistosomes and their host
pairs migrate toward the mesenteric vessels,
have co-evolved a wide range of mechanisms
where the females lay approximately 300
to skew the host immune response toward
eggs per day and actively modulates the
granuloma-inducing Th2 profile.
intravascular environment to support their
long-term survival. The production of eggs at
(E) These include the ability of soluble egg
~5–6 weeks post infection is a milestone
antigens (SEA) to promote alternative
event in the schistosome life cycle, that is
activation in macrophages and to condition
characterized by induction of a marked Th2
dendritic cells (DCs) for Th2 polarization.
response and angiogenesis.
However, to prevent unwanted bystander
tissue damage and potentially fatal
(C) Notably, the generation of a Th2 response
immunopathology, schistosomes also
by the host is critical for egg passage, and
implement various strategies to dampen host
new vessel formation may favor egg transit,
immunity and expanded regulatory networks
promoting the recruitment of immune cells
(Bregs and Tregs). There remain many
and nutrients to developing granulomas.
unknowns surrounding egg migration.
Freshly deposited eggs cannot move by
themselves and must somehow attach and
extravasate the endothelium.
Amebiasis and Schistosomiasis
(F) This includes the molecules secreted by
eggs to disrupt host barriers and modulate
immune responses and, importantly, how
egg penetration and intestinal ‘leakiness'
may influence local and systemic immune
reactions.
Life Cycle
1. Schistosoma eggs are eliminated with
feces or urine, depending on species
2. Under appropriate conditions the eggs
hatch and release miracidia which swim
and penetrate specific snail intermediate
hosts
3. The stages in the snail include two
generations of sporocyst and the
production of cercariae .
4. Upon release from the snail, the infective
cercariae swim, penetrate the skin of the
human host, and shed their forked tails,
becoming schistosomulae. The
schistosomulae migrate via venous
circulation to lungs, then to the heart,
and then develop in the liver, exiting the
liver via the portal vein system when
mature.
5. Male and female adult worms copulate
and reside in the mesenteric venules, the
location of which varies by species (with
some exceptions) For instance, S.
japonicum is more frequently found in
the superior mesenteric veins draining
the small intestine, and S. mansoni
occurs more often in the inferior
mesenteric veins draining the large
intestine.
6. However, both species can occupy either
location and are capable of moving
between sites. S. intercalatum and S.
guineensis also inhabit the inferior
mesenteric plexus but lower in the bowel
than S. mansoni.
7. S. haematobium most often inhabits in
the vesicular and pelvic venous plexus of
the bladder but it can also be found in
the rectal venules. The females (size
ranges from 7–28 mm, depending on
species) deposit eggs in the small venules
of the portal and peri vesical systems.
The eggs are moved progressively toward
the lumen of the intestine (S. mansoni,S.
japonicum, S. mekongi, S.
intercalatum/guineensis) and of the
bladder and ureters (S. haematobium),
and are eliminated with feces or urine,
respectively.
Pathophysiology of
Schistosomiasis
 In humans, a wide variety of innate and
adaptive immune processes exist in
proximity to these parasites throughout
their lifespan. To survive and thrive as the
second most common parasitic disease in
humans, schistosomes have evolved many
techniques to avoid and combat these
targeted host responses. Among these
techniques are molecular mimicry
(sequence or structural resemblance of
molecules of the host and the microbe) of
host antigens
 Schistosomiasis is due to immunologic
reactions to Schistosoma eggs trapped in
tissues. Antigens released from the egg
stimulate a granulomatous reaction
involving T cells, macrophages, and
eosinophils that results in clinical disease.
Symptoms and signs depend on the
number and location of eggs trapped in
the tissues. Initially, the inflammatory
reaction is readily reversible. In the latter
stages of the disease, the pathology is
associated with collagen deposition and
fibrosis, resulting in organ damage that
may be only partially reversible.
Amebiasis and Schistosomiasis

 Adult worms release eggs in the venules

of the mesentery, and the eggs enter the
Clinical Features:
liver through the portal vein, where they
become lodged in the terminal branches  Abdominal pain
of the portal venules. The lodged eggs - enlarged liver
cause a granulomatous inflammation, and - blood in the stool or blood in the urine
the lesions are healed by periportal  Chronic infection
fibrosis. S. japonicum is more virulent than - liver fibrosis or bladder cancer
S. mansoni because its infection produces Disease: characterized by granulomatous
ten times more eggs. reaction around the parasites, eggs trapped in
 Parasitic infections, however, are chronic, tissue which can develop to severe fibrosis
because the host is rarely able to totally
eliminate the source of infection. The
immune system is forced to remain active.
Often the result is immunosuppression, Laboratory Test:
disruption of normal B-cell and T-cell
functions, and hypersensitivity reactions. a. Sample Preparation/ Sample used for the test
For example, schistosomes have
mechanisms that can down-regulate the  Stool or urine
host’s immune system. This immune
modulation promotes the parasite’s Sample: depends on what kind of species of
survival but also limits severe damage to parasite is the cause of infection
the host. As a result, adult schistomes can
live in the human host for up to 40 years Example:
before finally being eliminated. All of
these complicated mechanisms along with Examine in feces
a multitude of other evasive mechanisms • S. mansoni
either contribute to or directly cause the • S. Japonicum
pathology seen in parasitic diseases.
Examine in urine
• S. haematobium
Incubation - adult worm in lower urinary tract , eggs
are examine through urine
 If acute schistosomiasis nasa 14-84 days
ang incubation period but for chronic Screening Tests:
infection this may remain asymptomatic
for years
 Individuals infected with schistosomes have
elevated IgE and IgG4 responses, as do
patients with other helminthic infections.
Amebiasis and Schistosomiasis
 A large number of serologic tests have
been used in the diagnosis of
schistosomiasis; however, many have not
been particularly useful because of cross-
reactions with other helminth infections,
continuation of elevated titers long after
successful treatment, and slow
immunologic response of the host.
Because of the complex life cycle, a large
number of antigens have been used in
serologic tests. Only a few have been
useful.
The most frequently used tests in
Schistosoma antigens and antibodies
detection:
Circumoval
Precipitin Test
Principle:
• This method is useful for the diagnosis of
S. mansoni and S. japonicum.
• The circumoval precipitin test is based on
the patient serum precipitation with
lyophilized eggs or purified live eggs
identified under the microscope.
Procedure:
• One drop, about 0.025 mL of the
suspension containing larvae, eggs or 6-8
specimens of immature adults is put into
the well of a slide, and 3 drops, about
0.075 Ml, of serum is added.
• A cover slip is placed over the well. The
slide is incubated at 34 C. After 24 hours,
the slide is examined by microscope for
the appearance of precipitate attached to
the worms or eggs.
 Proteases and glycosidases secreted from
the amebae are involved in the
degradation of mucin and extracellular
matrix. The pro-domain of EhCP-A5 binds
to and activate integrin and enhances the
inflammasome formation of leading to
pro-inflammatory responses. PGE2 also
secreted from the amebae causes mucin
hypersecretion and depletion of mucin
from the IECs.
Cercaria-Hullen
Reaction
Principle:
• This test is simple, rapid and sensitive.
• A positive reaction is indicated by
formation of an envelope or a precracial
sheath around the cercariae when
incubated in the positive sera.
Indirect Fluorescent
Antibody Test
Principle:
• The antigen-specific antibody is unlabeled,
and a second antibody is conjugated to
the FITC.
Indirect
Hemagglutination Test
Principle:
• Is the clumping of red blood cells, by
either a direct or indirect mechanism.
ELISA
Principle:
• This test uses microwells that are coated
with Schistosoma recombinant antigen
with a reaction ending with the stop
solution, and what appears is a yellow
color instead of blue.
Amebiasis and Schistosomiasis
Procedure:
 Firstly, a diluted patient sample is
incubated in microwells and containing
antibodies which are reactive to antigen
bind to coated microwells and unbounded
antibodies are washed away by washing
step.
 Secondly, enzyme conjugate antibodies
are added and react with these
antibodies, then unbound conjugate
antibodies are washed away.
 Thirdly, substrate is added to react with
enzymes conjugated with antibodies, the
substrate color will turn yellow.
 ELISA methods using soluble adult worm
or egg antigens for the detection of
antibodies have been used as screening
tests, and infection has then been
confirmed by the enzyme-linked
immunoelectrotransfer blot (EITB) test.
 ELISA has also been used to detect
circulating schistosome antigens in the
serum and urine of infected patients and
may be one of the preferred methods of
diagnosis.
 In addition to diagnosis of infection,
antigen levels have been used to assess
disease severity in terms of intensity of
infection and to monitor the efficacy of
therapy.
Confirmatory Test
for Schistosomiasis
• Kato katz- it is the most commonly used
method for diagnosing S. japonicum in
field surveys because it is relatively simple
to perform, quantitative, and relatively
inexpensive.
• Polymerase Chain reaction (PCR)- it is a
technique used to detect the DNA of
schistosoma, by using feces, urine and
biopsies.
• PCR-based diagnoses have been shown to
be highly sensitive and specific . and
should therefore be considered as
alternative methods for the diagnosis of S.
mansoni infections.
Prevention
• Avoid swimming in freshwater
• Drink safe water, although schistosomiasis
is not transmitted by drinking water but if
the lips and mouth contracted with
parasites, the person could be infected.
• Water used for bathing should be brought
to a rolling boil for 1 minute to kill any
cercariae, and then cooled before bathing
to avoid scalding.
• Vigorous towel drying after an accidental
very brief water exposure may help to
prevent parasites from penetrating the
skin.
Treatment
1. Praziquantel- it is a drug of choice
• High efficacy
• Lack of short term and long term side
effects
• Administration as single dose
• Cheap
• Dose required is 20 mg/kg bodyweight
three times as a one day treatment, at
intervals of not less than 4 hours and not
more than 6 hours
2. Metrifonate- it is an effective drug on
schistosomiasis because the drug
exhibits high activity against the
microfilariae and some action on the
adult worms. The oral dose of 10 mg/ kg
given for 6 days to the patient
Amebiasis and Schistosomiasis

3. Oxamniquine- that is used to treat

Schistosoma mansoni, because It
prevents worms from growing or
multiplying in your body. The doses
needed to drink is 15 mg/kg of the
bodyweight or in a single oral dose of up
to 15 mg/kg of bd for 2 days, depende sa
sensitivity of Schistosoma mansoni in the
area concerned.