Amebiasis
• Amebiasis is infection with the parasitic
intestinal protozoan Entamoeba histolytica
(the "tissue-lysing ameba").
• Most infections are probably asymptomatic.
Life Cycle and Transmission
• E. histolytica exists in two stages: a hardy multinucleate
cyst form and the motile trophozoite stage.
• Infection is acquired by ingestion of cysts contained in
fecally contaminated food or water or, more rarely,
through oral-anal sexual contact.
• Cysts survive stomach acidity and excyst within the
small intestine to form the 20- to 50-m trophozoite
stage. Trophozoites can live within the large-bowel
lumen without causing disease or can invade the
intestinal mucosa, causing amebic colitis.
• In some cases, E. histolytica trophozoites invade
through the mucosa and into the bloodstream,
traveling through the portal circulation to reach the
liver and causing amebic liver abscesses.
• Motile trophozoites may be excreted into the stool—
a diagnostically important event—but are rapidly
killed upon exposure to air or stomach acid and
therefore are not infectious.
• Trophozoite cysts within the large bowel are excreted
in the stool, continuing the life cycle.
Epidemiology
• Entamoeba dispar or Entamoeba moshkovskii.
E. dispar appears not to cause disease.
• In contrast, E. histolytica infection can cause
disease, although not all patients develop
symptoms.
• only 10% of infected patients developed
symptoms.
• amebic liver abscess, whose prevalence is 7
times higher among men than among women.
• The explanation for this difference remains
unknown, but less efficient complement-
mediated killing of amebic trophozoites by
serum from men than by serum from women
has been reported.
• E. histolytica infections are most common in
areas of the world where poor sanitation and
crowding are present.
• contamination of food and drinking water with
human feces.
Pathogenesis and Pathology
• E. histolytica trophozoites possess a potent
repertoire of adhesins, proteinases, pore-
forming proteins, and other effector
molecules that enable them to lyse cells and
tissue, induce both cellular necrosis and
apoptosis, and resist both innate and adaptive
immune defenses. Disease begins when E.
histolytica trophozoites adhere to colonic
mucosal epithelial cells
• 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, broadening in the submucosal region,
with E. histolytica trophozoites at the margins
between dead and live tissues. Ulcers tend to
stop at the muscularis layer, and full-thickness
lesions and colonic perforation are unusual.
• Amebomas, a rare complication of intestinal
disease, are granulomatous mass lesions
protruding into the bowel lumen, with a
thickened edematous and hemorrhagic bowel
wall that can cause obstructive symptoms.
• In some individuals with E. histolytica colonic
infection, trophozoites invade the portal
venous system and reach the liver, where they
cause amebic liver abscesses.
• The role of innate and adaptive immunity in
preventingE. histolytica infection or controlling
disease needs further clarification. Studies of
children in a highly endemic area have
suggested that prior E. histolytica intestinal
infection may stimulate mucosal IgA
antibodies to amebic antigens, thereby
reducing the likelihood of subsequent
infections.
CLINICAL FEATURE
• Most patients harboring Entamoeba species are
asymptomatic, but individuals with E. histolytica infection
can develop disease.
• Symptoms of amebic colitis generally appear 2–6 weeks
after ingestion of the cyst form of the parasite. Diarrhea
(classically heme-positive) and lower abdominal pain are
the most common symptoms. Malaise and weight loss
may be noted as disease progresses. Severe dysentery,
with 10–12 small-volume, blood- and mucus-containing
stools daily, may develop, but only 40% of patients are
febrile
• Fulminant amebic colitis, with even more profuse
diarrhea, severe abdominal pain (including peritoneal
signs), fever, and pronounced leukocytosis are rare,
• Paralytic ileus and colonic mucosal sloughing may be
seen; intestinal perforation occurs in >75% of patients
with this fulminant form of disease. Mortality rates
from fulminant amebic colitis exceed 40% in some
series. Recognized complications of amebic colitis also
include toxic megacolon with severe bowel dilation
and intramural air.
• Right-sided pleural effusions and atelectasis
are common in cases of amebic liver abscess
and generally require no treatment. However,
the abscess ruptures through the diaphragm
in 10% of patients, causing pleuropulmonary
amebiasis. Suggestive symptoms are sudden-
onset cough, pleuritic chest pain, and
shortness of breath.
• A dramatic complication is the development of
a hepatobronchial fistula, in which patients
can cough up the contents of the liver abscess
—copious amounts of brown sputum that may
contain E. histolytica trophozoites.
• Cerebral abscesses complicate <0.1% of cases
of amebic liver abscess and are associated
with the sudden onset of headache, vomiting,
seizures, and mental status changes and a high
mortality rate. Cutaneous amebiasis
rectovaginal fistulas, and urinary tract lesions
are rare but reported complications of
amebiasis.
DIAGNOSIS
• Examination of three stool samples improves
sensitivity for the detection of Entamoeba
species, and the presence of amebic trophozoites
containing red blood cells in a diarrheal stool is
highly suggestive of E. histolytica infection.
However, because trophozoites containing red
blood cells are not found in most patients with E.
histolytica infection, the applicability of this
finding is limited.
• PCR assay for DNA in stool samples is the most
sensitive and specific method for identifying E.
histolytica infection.
• The diagnosis of amebic liver abscess is based on the
detection (ultrasound or CT) of one or more space-
occupying lesions in the liver and a positive serologic
test for antibodies to E. histolytica antigens.
• Amebic liver abscesses are classically described as
single, large, and located in the right lobe of the liver.
When a patient has a space-occupying lesion of the
liver, a positive amebic serology is highly sensitive
(>94%) and highly specific (>95%) for the diagnosis of
amebic liver abscess.
Treatment
• Metronidazole is the drug of choice for the
treatment of amebic colitis and amebic liver
abscess. 750 mg tid PO or IV, 5–10
• Paromomycin 30 mg/kg qd PO in 3 divided
doses 5–10
Prevention
• Avoidance of the ingestion of food and water
contaminated with human feces.
• Treatment of asymptomatic persons .
Giardiasis
G.Lamblia
Life Cycle
• Cysts ingested (≥10–25 cysts) in contaminated water
or food or by direct fecal-oral transmission
• Excystation follows exposure to stomach acid and
intestinal proteases releasing trophozoite forms that
multiply by binary fission and reside in the upper small
bowel adherent to enterocytes
• Causes: Asymptomatic infection, acute diarrhea, or
chronic diarrhea and malabsorption Small bowel may
demonstrate villous blunting, crypt hypertrophy, and
mucosal inflammation
Life cycle of Giardia
Intestinal parasites 24
• Encystation occurs under conditions of bile salt
concentration changes and alkaline pH Smooth-
walled cysts can contain two trophozoites
• Cysts and trophozoites passed in the stool into
the environment
• Cysts can survive in the environment (up to
several weeks in cold water) May also infect
non-human mammalian species
• Cysts do not tolerate heating, desiccation, or
continued exposure to feces but do remain
viable for months in cold fresh water. The
number of cysts excreted varies approach 107
per gram of stool
Pathophysiology
• The lactose intolerance and significant
malabsorption are clinical signs of the loss of
brush-border enzyme activities.
Symptoms of acute giardiasis
Clinical features Patients (%)
Diarrhea 95
Weakness 76
Weight loss 68
Abdominal pain 69
Nausea 60
Steatorrhoea 56
Flatulence 35
Vomiting 29
Fever 17
Intestinal parasites 28
• Most infected persons are asymptomatic. Symptoms may develop
suddenly or gradually.
• In persons with acute giardiasis, symptoms develop after an
incubation period that lasts at least 5–6 days and usually 1–3
weeks. Prominent early symptoms include diarrhea, abdominal
pain, bloating, belching, flatus, nausea, and vomiting. Although
diarrhea is common, upper intestinal manifestations such as
nausea, vomiting, bloating, and abdominal pain may
predominate. The duration of acute giardiasis is usually >1 week.
• Individuals with chronic giardiasis may present with or without
having experienced an antecedent acute symptomatic episode.
• Diarrhea is not necessarily prominent, but increased flatus,
loose stools, sulfurous belching, and weight loss occur.
Symptoms may be continual or episodic and can persist for
years.
• Fever, the presence of blood and/or mucus in the stools
are uncommon and suggest a different diagnosis.
• Extraintestinal manifestations : urticaria, anterior uveitis,
and arthritis; whether these are caused by giardiasis or
concomitant processes is unclear
• Giardiasis can be severe in patients with
hypogammaglobulinemia.
Diagnosis
• Giardiasis is diagnosed by detection of
parasite antigens in the feces or by
identification of cysts in the feces or of
trophozoites in the feces or small intestines.
Cysts are oval, measure 8–12 m x 7–10 m, and
characteristically contain four nuclei.
Trophozoites are pear-shaped, dorsally
convex, flattened parasites with two nuclei
and four pairs of flagella.
Diagnosis of intestinal Protozoal infections
Parasite Stool O/P Fecal AFB Stool Ag Other
Giardia + +
Cryptosporidium - + +
Isospora - +
Cyclospora - +
Microsporidia - Special
stains,
Biopsy
Intestinal parasites 32
Treatment
• Cure rates with metronidazole (250 mg TID for 5 days)
are usually >90%.
• Tinidazole (2 g once by mouth) is reportedly more
effective than metronidazole.
• Paromomycin, an oral aminoglycoside that is not well
absorbed, can be given to symptomatic pregnant
woman.
• In cases refractory to multiple treatment courses,
prolonged therapy with metronidazole (750 mg thrice
daily for 21 days) has been successful.
Prevention
• consumption of non contaminated food and
water
• personal hygiene
• Boiling or filtering potentially contaminated
water.
