Amoebiasis

Entameba

histolytica

is

an

invasive

entric

protozoan parasite that is the cause of amoebiasis.

E.dispar,

E.

moshkovkii,

E.

bangaladesi

are

parasites that are identical morphologically to E.

histolytica, of which E. dispar is non-pathogenic,
E.moshkovkii causes noninvasive diarrhoea and
E.bangaladesi is of unknown virulence.

 Most Infection are asymptomatic, although it can

cause

disease

ranging

from

Dysentry

to

extaintestinal infectons like liver absess

Most of asymptomatic infection is due to E.dispar

Endemic area Mexico,India & tropical regions of
Africa,South and Central America

Life cycle and transmission

E. histolytica exists in two stages.
The cyst form was implicated as the
infective form.
multinucleate cyst
Trophozoite

Motile

ORGANISM
Species of Entamoeba
Many Entanoeba species infect humans, but only E.
histolytica is a cause of invasive amebiasis, whereas
E.moshkovskii is associated with a noninvasive diarrhoea
E. histolytica and E. dispar genome share 90% indentity
in genic regions and E.moshkovskii is closely genetically
related.
In most industrialized countries, E. dispar is 10 times
more common than E. histolytica, but equally prevalent
in develpoing countries

Genotypes of E. histolytica
In addition to genetic differences
between the three morphologically
identical amebae E. histolytica, E.
dispar, E. moshkovskii; genetically
different strains exist with E. histolytica.
Certain genotypes are associated with
diarrhoea, others with colonization and
others with amebic liver abcess
fromation.

Life Cycle of E. histolytica

E. histolytica are most common in areas where
poor sanitation and crowding compromise the
barrier to contamination of food and drinking
water
Infection
is
acquired
by
ingestion
of
quadrinucleated cysts in faecally contaminated
water or food containing E. histolytica cyst.
Infective cyst form of the parasite survives
passage through the stomach and small intestine.

 Excystation to eight trophozoites occurs in the bowel lumen,

while motile and potentially invasive trophozoites are formed
In most infections, trophozoites aggregate in the intestinal
mucin layer and form new cyst, which results in self limited
and asymptomatic infection.
In some cases, however, adherence to and lysis of the
colonic epithilium, mediated by galactose and N-acetyl Dgalactosamine specific lectin, initiates invasion of the colon
by trophozoites
The environmental stability of the cyst and relative
resistance to chloride has resulted in waterborne outbreaks
caused by contamination of municipal water supplies.

 Neutrophils responding to invasion contribute

to cellular protection at the site of invasion.
Once intestinal epithelium is invaded,
extraintestinal spread to peritonium, liver and
other sites may follow.
Factors controlling invasion, as opposed to
encystation, probably include parasite
quorum sensing signaled by the Gal/GaINAcspecific lectin, interaction of amebae with the
bacterial floraof the intestine, and innate and
acquired immune responses of the host.

Life cycle

Pathogenesis and pathology

E. histolytica posses a potent repertoire of
adhesins, proeinases and pore forming proteins and other
molecules that enable them to lyse cells and tissue

These molecules Induce cellular necrosis and apoptosis.

Resist both innate and adaptive immunity.
E. histolytica trophozoites adhere to the colonic mucosal
epithelial cells leads to disruption
Adherence is mediated by a family of surface lectin
molecules capable of binding to galactose and Nacetylgalactosamine residues

 E.histolytica can lyse host cells upon contact through

a family of amphipathic peptides called amoebopores
E.histolytica
posses a large family of
cysteine
proteinases that are capable of lysing the
extracellular matrix between the cells and cleaving
host
defense
molecules
(complement
and
antibodies)
The ultimate effect of all these amebic virulance
factors on the human colon is the production of small
ulcers that have heaped borders and contains focal
areas of epithelial cell loss

 The interveining mucosa is normal

E.histolytica trophozoites can then invade laterally

through the submucosal layer, creating the classic
flask shaped ulcers that appear

on pathologic

examination as narrow-necked lesions broadin the

submucosal region

E.histolytica trophozoites found at the margin

between dead and the live tissues

Flask shaped ulcer

Clinical manifestations
Asymptomatic Intraluminal Amebiasis
All E. moshkovskii and E. dispar infections and upto 80% of E.
histolytica infections are asymptomatic
Asymptomatic individuals represents a risk to the community
because they are the source of new infection
Asymptomatic infection with E. histolytica also carries a small but
definite risk to the carrier for the subsequent development of
invasive amobiasis
In a study, individuals colonized with E. histolytica, 10% develpoed
invasive disease within 1 year

Amebic Diarrhea
Amebic diarrhea without dysentry is the
most common disease manifestation of
infection with E. histolytica.
Amebic diarrhea is defined as diarrhea in
an E. histolytica infected individuals (for
diagnosis of amoebic diarrhoe, mucus
need not be visible and microscopic
blood need not be present in the stool.

Amebic dysentry or colitis

Amebic dysentry or colitis is defined as diarrhoe
with mucus or visible or microscopic blood in the
patient with E. histolytica infection
Approx 15-33% of cases of E. histolytica diarrhoe
are accompanied by amebic dysentry.
Of patients with either condition, 70% have gradual
onset of symptoms over the 3 or 4 weeks after
infection
Increasing severe diarrhoe is the primary complaint
accompanied by generalized abdominal tenderness

 On occasion, onset may be acute or delayed for

several months after infestation
Fever is present only in minority of patients with
amebic colitis
Abdominal distension ans dehydration is unusual.
In young children, intussusception, perforation and
peritonitis or necrotizing colitis may develop
rapidly.
Unusual manifestation include toxic megacolon and
ameboma

Amebic liver abscess

10 times more common in men than in women and uncommon in
children.
Approx 80% of patients with amebic liver abscess have
symptoms that develop realtively quickly (within 2-4 weeks),
Fever
Cough
Constant, dull, aching abdominal pain in RUQ or epigastrium

Involvement of diaphragmatic surface of the liver may lead to

right sided pleural pain or referred shoulder pain
Associated GI symptoms, which occur in 10-35% patients include
nausea, vomiting, abdominal cramping, abdominal distension,
diarrhoe and contipation
Hepatomegaly with point tenderness over the liver, below the
ribs or in the intercostal space is typical finding.

 Approximately 90% of patients with liver abscess are male.

The abscess is usually single and is in the right lobe of the
liver in 80% of cases.
Most frequently, patients present with liver abscess but
without concurrent colitis, although a history of dysentery
within the previous year is often present.
Amebae are infrequently seen in the stool at the time of
diagnosis of liver abscess.
Liver abscess can manifest acutely (with fever and right
upper abdominal tenderness and pain) or subacutely (with
prominent weight loss and less frequent fever and
abdominal pain).

 The differential diagnosis of the lesion in

the liver includes
pyogenic abscess (less likely if the gallbladder
and ducts appear normal),
hepatoma,
echinococcal cyst.
Aspiration of the abscess is occasionally
necessary in order to diagnose amebiasis
(although amebae are visualized in the pus in
only the minority of cases; if the abscess is
pyogenic, the responsible bacteria is seen or
cultured, or both).

If a space-filling defect in the liver is observed, the

differential diagnosis includes
1. amebiasis (most common in men with a history of
travel or residence in a developing country;
2. pyogenic or bacterial abscess (suspected in women,
patients with cholecystitis, elderly patients, individuals
with diabetes, and patients with jaundice);
3. echinococcal abscess (an incidental finding, inasmuch
as echinococcal abscess should not cause pain or
fever);
4. cancer.

Diagnostic tests
Demonstration of E.histolytica or cyst in the
stool or colonic mucosa of pts with diarrhea
Antigen detection based ELISAs that can
specifically identify E.histolytica in the stool
probably represent the best choice in the
endemic areast
PCR assay for DNA in the stool samples is
currently the most sensitive and specific
method for identification but used as
research and epidemiological tool

Metastatic Amebiasis
Extra-abdominal amebiasis presumably follows direct extension from liver
abscesses rather than direct dissemination from the intestine.
Thoracic amebiasis is the most common type of extra-abdominal
amebiasis and occurs in about 10% of patients with amebic liver abscess.
Symptoms depend on the type of involvement. Empyema,
bronchohepatic fistulas, or extension of a pleuropulmonary abscess into
the pericardium may occur.
Pericardial involvement is the next most common form of extraintestinal
amebiasis and may result from rupture of a liver abscess in the left lobe
of the liver into the pericardium or through extension of the right-sided
pleural amebiasis. It is estimated to occur in 3% of patients with hepatic
abscesses. It manifests as acute pericarditis with tamponade and, on
occasion, as pneumopericardium.

 Amebic liver abscess in the left lobe also may rupture

directly into the left side of the chest. Cerebral amebic
abscesses were found in 0.66% to 4.7% of patients with
amebic liver abscess.
cerebral amebiasis, initial neurologic examination yielded
normal findings, later developed seizures.
amebic rectovesical fistula formation and involvement of
pharynx, heart, aorta, and scapula have been reported.
Cutaneous extension after the adherence of perforated,
inflamed bowel to the skin is an extremely painful but rare
complication. This situation also may arise after invasion of
the skin by trophozoites emerging from the rectum.

Investigations
1. StoolOvaandParasiteExamination
2. Culture Culture of E. histolytica from stool
samples is more sensitive than stool O&P
examination but significantly less sensitive than
antigen detection or PCR. It is also not specific
for E. histolytica, and thus an E. histolytica
specific antigen detection or PCR test must be
used on the cultured material
3. ColonoscopyandBiopsy

4. PolymeraseChainReactionTesting
forAmebiasis
5. AntigenTestingforAmebiasis The only
fecal antigen test that distinguishes E.
histolytica from E. dispar and E. moshkovskii is
the TechLab E. histolytica II enzyme-linked
immunosorbent assay (ELISA).
6. SerologicTestsforAmebiasis

Ct scan liver with ALA in Rt

lobe

Treatment
The nitroimidazole compounds are the drug of
choice
To date E.histolytica has not demonstrated
resistance to any of the compound metronidazole
and tinidazole
Tinidazole appears to be better tolerated
Whenever possible fulminant amebic
should be managed conservatively

colitis

Treatment
Neither metronidazole nor tinidazole reaches
high levels in the gut lumen therefore, patients
with amebic colitis or ALA should also receive
treatment with luminal agents (Paramomycin or
iodoquinol) to ensure eradication of infection
Paramomycin is preferred agent
Nitazoxanide, abroad spectrum antiparasitic
drug,is
efficacious
against
E.histolytica
trophozoitesin the both tissue and gut

Drug

Dosage

Side effect

Amebic liver abscess

Tinidazole

2gPO
oncedaily
5 days

Metronidazol 750mgPO
e
tid10
days

PrimarilyGIsideeffectsand
disulfiram-likeintolerance
reaction toalcoholicbeverages
for5days
anorexia, nausea,vomiting,
diarrhea, abdominaldiscomfort,
or unpleasantmetallictaste;
disulfiram-likeintolerance
reactiontoalcoholicbeverages;
neurotoxicity,includingseizures,
peripheralneuropathy,dizziness,
confusion,irritability

Followed by luminal agent

Drug

Dose

Side effect

Paromomycin

30mg/kg/dayPO
in threedivided
doses perday
5-10days

PrimarilyGIside
effects:diarrhea,
GI upset

Diloxanide furoate

500mgPOtid
10 days

PrimarilyGIside
effects:flatulence,
nausea,vomiting
Pruritus,urticaria

Drug
Amebic Colitis
Tinidazole

Dose

Side Effect

2gPOonce
daily5 days

Sameasfor
amebicliver
abscess

+
luminalagent
(sameasfor
amebicliver
abscess)
Asymptomatic
Intestinal
Colonization

Treatmentwith
luminalagentas
foramebicliver
absces

Treatment
Aspiration of liver abscess reserved for
the indivisual in whom pyogenic abscess
a bacterial superinfection is suspected but
diagnosis is uncertain,
for pts failing to respond to tinidazole or
metronidazole ( those who have fever or
abdominal pain after 4 days of treatment),
for indivisuals with large liver abscesses in
the left lobe
large abscsee with risk of rupture

Treatment
In contrast, aspiration and percutaneous
catheter
drainage
improves
outcome
in
pleuropulmonary amebiasis and empyema
Percutneous drainage or surgical drainage is
absolutely indicated in amebic pericarditis
Rupture of an amebic liver abscess in
peritoneum is managed conservatively with
medical therapy and percutaneous catheter
drainage

Prevention
Avoidance of ingestion of food and
water contaminated with humen
feces is the only way of prevention
No prophylaxis
No vaccine

GIARDIASIS

INTRODUCTION
Giardia lamblia, a flagellated enteric
protozoan, is a common cause
of sporadic, endemic, and epidemic
diarrhea throughout the world.
It is seen in waterborne outbreaks of
diarrhea, in children who live
in low-income countries, and occasionally
in foodborne outbreaks.
It is a intestinal single-celled parasite .

 Reproduce by binary fission.

Have a trophozoite and cyst phases.
Direct life cycle.
It has two nuclei and eight flagella.
Lives in duodenum and jejunum.
Typically found in lakes, streams, or ponds that
have been contaminated by human and other
animals.
It causes giardiasis.

MORPHOLOGY
Two stages:
1. Trophozoite
2. cyst

Trophozoite

SHAPE
Pear shaped,
Tennis racked shape or heart
shape(when viewed flat).
Size
Length: 10-20um
Width:
5-15um
Thickness:2-4um

Body
Bilaterally symmetrical having a peared structure.
Axostyles
Two in numbers, seen in midline as vertical lines.
Nuclei
Two or one on each side of body.
Flagella
4 pairs helping in moving.
Sucking discs
Circular in shape
Situated on ventral surfaces

CYST
Shape
Oval or ellipsoid
Size
Length: 12um
Width: 8um
Nuclei
Two nuclei in immature cyst
Four nuclei in mature cyst.
Flagella &sucking discs
may be seen in cytoplasm.

Life cycle of Giardia lamblia

Contaminate water
and food

Multiplied by
binary fission

Trophozoites

Outside
Diarrhea

Mature Cysts

Stool

Trophozoites

Duodenum, upper ileum,

gall bladder

Cysts

Outside

The lower portion

of ileum or colon

Pathogenes
G. lamblia
isinhabits in the duodenum and upper ileum
Trophozoites are attached to the mucosa
surface by sucker, reproduced by binary fission
Histology: shortening of microvilli, elongation of crypts,
and damaging the brush border of the absorptive cells

Mechanical blockage of the intestinal mucosa,

competition for nutrients, inflammation
Diarrhea, abdominal pain, bloating,
nausea, and vomiting

Habitat & transmission

Trophozites
Definitive host:
Human intestine
Cyst
Human colon & contaminated
material

Symptoms
Symptoms of giardiasis normally begin 1 to 2 weeks
(average 7
days) after becoming infected

Diarrhea
Malaise
Flatulence
Foul-smelling, greasy stools
Abdominal cramps
Bloating
Nausea
Anorexia
Weight loss
Vomiting
Fever
Urticaria
Constipation

Possible Complications
Dehydration
Malabsorption
Weight loss

Diagnosis
The diagnosis of giardiasis should be
considered in all patients with
prolonged diarrhea, particularly that
which is associated with
malabsorption or weight loss.

O&P examination
The stool should be examined fresh and after
preservation.
A saline wet mount of fresh liquid stool obtained in the
acute stages of illness may yield motile trophozoites.
In semiformed stool, trophozoites are usually not
found.
Giardia should be identified 60% to 80% of the time
after one stool, and some report over 90%
identification after three stools.

Antigen assays
Antigen assays are most helpful when giardiasis is the
leading consideration, such as during an outbreak,
when screening children in daycare, or when testing
patients for cure after the completion of treatment.
They are often less expensive than an O&P examination
85% to 98% sensitive and 90% to 100% specific
PCR is highly sensitive, has the capacity to detect as
few as one or two cysts per sample, and can identify
the assemblage

string test, duodenal aspiration, or

biopsy
Because excellent results can be obtained with an antigen detection assay
or a carefully performed stool O&P, sampling of the duodenal contents by
string test, duodenal aspiration, or biopsy is generally not needed.
However, in cases that are difficult to diagnose, these procedures may be
helpful.
The string test should yield bile-stained mucus from the duodenum, which
can be examined for trophozoites in a wet mount or after staining.
Duodenal biopsies require touch preparations, Giemsa staining, and a
careful search for trophozoites. An advantage of biopsy, particularly in
patients infected with human immunodeficiency virus or persons with
malabsorption, is the ability to identify a histologic abnormality that is not
caused by giardiasis and to detect other pathogens.
An aspirate can be sampled for small bowel overgrowth.

Testing for anti-Giardia

antibody
Testing for systemic anti-Giardia antibody is not
generally available, but it has been useful in
seroepidemiologic studies throughout the world.
IgG antibodies remain elevated for long periods,
making them less helpful diagnostically in areas
endemic for giardiasis.
It is not clear if serum anti-Giardia IgM is useful
in distinguishing current from past giardiasis.

TreatmentofGiardiasis
DRUG
Tinidazole
Metronidazole
Nitazoxanide
Albendazole
Paromomycin
Quinacrine
Furazolidone

DOSE
2 g, single dose
250 mg tid 5-7
days
500 mg bid 3 days
400 mg qd 5 days
500 mg tid 5-10
days
100 mg tid 5-7
days
100 mg qid 7-10

Prevention
Avoid water that might be contaminated.
Avoid food that might be contaminated.
Boil water before drinking.
Do not brush teeth with tap water that may be
contaminated.
Do not use ice or drink beverages made from tap water
that may be contaminated.
Wash hands before eating food etc.

THANK YOU