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Amebiasis

(Amebic Dysentery)
dr Putra Hendra SpPD
UNIBA

Amebiasis
(Amebic Dysentery)
Causal agent: Entamoeba histolytica is well recognized
as a pathogenic amoeba.
History: Loosh was first described in 1875
Geographic Distribution: Worldwide, with higher
incidence of amebiasis in developing countries.
In industrialized countries, risk groups include male
homosexuals, travelers and recent immigrants, and
institutionalized populations.

Morphology

Different form of E. histolytica;

1- trophozoite

2- precyst

3- cyst(1, 2, 4 nuclei)

Trophozoite chractere

Size: 12-60m in diameter;


Non-invasive form ( minuta) / E. dispare
Invasive form (magna) contain RBC, E. histolytica

Pseudopodia:
Motility:
Ectoplasm:
Endoplasm: may be contain ingested RBC
Nucleoplasm:

Non-invasive form

invasive form

Different form of E.histolytica cyst

LIFE CYCLE

LIFE CYCLE
Entamoeba histolytica exists in two forms:
1. Cysts (infective):
can survive outside the human body.
transform to trophozoites.
2. Trophozoites (non-infective; invasive):
Can reproduce
They may feed on intestinal bacteria or
invade and ulcerate wall of large intestine,
and may migrate to liver or other tissues.
transform to cysts which are excreted in
feces.

Entamoeba histolytica Pathology


Extra-Intestinal Lesions .2
and Abscess Occurs

Entamoeba histolytica Pathology


Extra-Intestinal Lesions .2
and Abscess Occurs

A. Hepatic Amebiasis

Entamoeba histolytica Pathology


Extra-Intestinal Lesions .2
and Abscess Occurs

A. Hepatic Amebiasis

Entamoeba histolytica Pathology


Extra-Intestinal Lesions .2
and Abscess Occurs

A. Hepatic Amebiasis
B. Pulmonary
Amebiasis

Entamoeba histolytica Pathology


Extra-Intestinal Lesions .2
and Abscess Occurs

A. Hepatic Amebiasis
B. Pulmonary
Amebiasis
C. Cerebral Amebiasis

Amoebic Amebiasis of the Skin

Epidemiology

Prevalence of amebic infection varies with level of sanitation


and generally higher in tropics and subtropics than in
tempearate climates.

*Worldwide prevalence is about 10% to 50%


*Cyst passers are important source of infection

The true estimated prevalence of E. histolytica is close to 1%


worldwide.
Entamoeba histolytica is the second leading cause of
mortality due to parasitic disease in humans. (The first being
malaria). Amebiasis is the cause of an estimated 50,000100,000 deaths each year.

Transmission

1-driect contact of person to person( fecal-oral)


2- Veneral transmission among homosexual
males( oral-anal
3- Food or drink contaminated with feces containing
the E.his. cyst
4- Use of human feces (night soil) for soil fertilizer
5- contamination of foodstuffs by flies, and possibly
cockroaches

Pathogenesis

Effective factores:

1- strain virulence:

- classic strain
- non-classic strain; Laredo , Huff, .
- pathogen zymodemes

2- susceptibility of the host; nutrition status, immune-sys.

3- breakdown of immunologic barrier (tissue invasion)

Clinical symptoms
Asymptomatic infection

Symptomatic infection

Intestinal Amebiasis
Dysenteric

Non-Dysenteric colitis

Extraintestinal Amebiasis
Hepatic Pulmonary

Liver abscces

The extra foci

Acut nonsupprative

Intestinal Amebiasis symptoms: Diarrhea or dysentery, abdominal pain, cramping , anorexia,


weight loss, chronic fatigue

Clinical presentations
Asymptomatic Intestinal infection
(Carriers, passing cysts)
Mild to moderate intestinal disease
(Nondysenteric Colitis)
Severe Intestinal infection ( Dysentery)
Hepatic abscess, ameboma (localized
granulomatous lesion of colon) and other
extraintestinal disease

Extra-ntestinalAmebiasis

Pyogenic- Liver Abscess

Liver abscess

Diagnosis

Paraclinical Diagnosis:
Sigmoidoscopic examination:

precence of a grossly normal mucosa between the ulcers serves to


differentiate amebic from bacillary dysentery,( the entire mucosa being
involvoed in bacillary dysentery).

Hepatomegally
C.B.C. : leukocytosis in Amebic dys. rises above 12000 per
microliter, but counts may reach 16000 to 20000 per microliter.

Microscopy
Microscopic identification
This can be accomplished using:

Fresh stool: wet mounts and permanently stained preparations


(e.g., trichrome).

Concentrates from fresh stool: wet mounts, with or without


iodine stain, and permanently stained preparations (e.g.,
trichrome).

Trophozoites of Entamoeba histolytica /E.


dispar ( trichrome stain )

Microscopy

B
A

In the absence of erythrophagocytosis, the pathogenic E. histolytica is


morphologically indistinguishable from the nonpathogenic E. dispar!
Each trophozoite has a single nucleus, which has a centrally placed karyosome
and uniformly distributed peripheral chromatin.

Trophozoites of Entamoeba histolytica with ingested


erythrocytes (trichrome stain)

The ingested erythrocytes appear as dark inclusions.


Erythrophagocytosis is the only morphologic characteristic that can be
used to differentiate E. histolytica from the nonpathogenic E. dispar.

Cysts of Entamoeba histolytica


/E. dispar

GHI

Cysts of Entamoeba histolytica/E.


dispar, permanent preparations stained
with trichrome.

Immunodiagnosis
(Antibody Detection)

1- Antibody detection

2- Antigen detection may be useful as an adjunct to


microscopic diagnosis

The indirect hemagglutination (IHA)

The EIA test detects antibody specific for E. histolytica in


approximately 95% of patients with extraintestinal amebiasis,
70% of patients with active intestinal infection, and 10% of
asymptomatic persons who are passing cysts of E. histolytica.

Antigen Detection
Antigen detection may be useful as an adjunct to microscopic
diagnosis in detecting parasites and to distinguish between
pathogenic and nonpathogenic infections.
Recent studies indicate improved sensitivity and specificity of
fecal antigen assays with the use of monoclonal antibodies
which can distinguish between E. histolytica and E. dispar
infections.

Molecular diagnosis

In reference diagnosis laboratories, PCR is the


method of choice for discriminating between
the pathogenic species (E. histolytica) from the
(nonpathogenic species (E. dispar.

ANTIAMEBIC DRUGS
Luminal Amebicides

Tissue or systemic amebicides


Mixed Amebicides

LUMEN AMOEBICIDES
Acts on the parasites in the lumen of the bowl.
used for treatment of asymptomatic
amebiasis.
Include
Diloxanide Furoate
Iodoquinol
Antibiotics
- Paromomycin
- Tetracyclines
- Erythromycin

Tissue Amoebicides (systemic)


acts on the intestinal wall and liver (or any
other extra-intestinal tissue).
Used for treatment of systemic form of the
disease (intestinal wall infection or liver
abscesses).
Emetine
Dehydroemetine
Chloroquine (liver only)

Mixed amoebicides

Effective against both luminal and systemic


forms of the disease. Although luminal
concentration is too low for single drug
treatment.
Metronidazol
Tinidazole

METRONIDAZOLE
Mixed amoebicide.
Drug of choice for intestinal &
extraintestinal amoebiasis.
Acts on trophozoites.
Has no effect on cysts.
Nitro group of metronidazole is reduced by
protozoan leading to cytotoxic reduced
product that binds to DNA and proteins
resulting into parasite death.

Pharmacokinetics
Given orally or IV.
Absorption is rapid and complete.
Due to rapid absorption from GIT, not
reliably effective against luminal parasites.
Wide distribution to all tissues and body
fluids (CSF, saliva, milk).
Plasma protein binding is low ( < 20%).
Plasma half life is 8 h

Pharmacokinetics
Metabolized in liver by mixed function oxidase
followed by glucouroidation.
Excreted in urine as unchanged drug plus
metabolites.
Clearance is decreased in liver impairment.
Tinidazole has longer duration, simpler dosing
regimen, less toxicity, than metronidazole, but
is equally active.

Adverse effects
1. GIT:
Nausea
Vomiting
Dry mouth
Metallic taste
Diarrhoea
Oral Thrush (Moniliasis, yeast infection).

Adverse effects
2. CNS: Neurotoxicological effect
Insomnia, dizziness
peripheral neuropathy, paresthesia
encphalopathy, convulsion ( IV infusion,
rare).
3. Dysuria, dark urine.
4. Neutropenia
5. Disulfiram-like effect if taken with alcohol.

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