AMEBIASIS AND INFECTION WITH
FREE LIVING AMEBAS

Dr R L Khare
Assistant Professor
Department of Medicine
Pt JNM Medical College Raipur
DEFINITION


Amebiasis is infection with intestinal pathogen

Entameba histolytica (tissue lysing ameba)


Most Infection are asymptomatic



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
multinucleate cyst

Motile Trophozoite
TRANSMISSION
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 cysts in faecally
contaminated water or food or rarely,through oralanal sexual contact
 Cysts are resistant to the acid in the stomach

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 mol. 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

PATHOGENESIS AND PATHOLOGY
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

PATHOGENESIS AND PATHOLOGY


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
Two types- Intestinal and Extra Intestinal
 Most patients harboring Entamoeba species are
asymptomatic,but individuals with E.histolytica can
develop disease
 Amebic colitis generally appear 2-6 weeks after
ingestion of the cyst of parasite
 Heme positive diarrhea and abdominal pain are the
most common complaints
 Malaise and wt.loss may be found later
 Fever is present in 40% cases
 Severe dysentry with 10-12 small volume, blood
and mucus containing stools may develop

CLINICAL MANIFESTATIONS
Fulminant amebic colitis with even profuse
diarrhea,severe
abdominal
pain,fever,and
pronounced leukocytosis are rare
 It
affects young children,pragnant women,
indivisuals treated with steroids and pts. With
diabetes and alcoholism
 Intestinal perforation occus in >75% of pts.with
fulminant disease
 Complications includes


Toxic Megacolon in .5% with severe bowel dilatation and
intraluminal air
 Ameboma-presents as abd. mass

AMEBIC LIVER ABSCESS
Most cmmon extraintestinal complication
 Disease begins when trophozoites penetrate
through the colonic mucosa, travel through the
portal circulation and reach the liver
 The classical presentation of ALA are right upper –
quadrant pain,fever and liver tenderness
 Its acute in nature lasting < 10 days
 With chronic presentation wt. loss and anorexia are
prominent
 Jaundice is uncommon

OTHER MANIFESTATIONS AND COMPLICATIONS
Rt-sided pleural effusion and atelectesis are
common in cases of ALA
 In 10% rupture of abscess through diaphragm may
cause pleuro-pulmonary amebiasis
 Sudden onset cough,pleuritic chest pain and
shortness of breath are suggestive symptom
 Hepatobronchial fistula is dramatic complication in
which pt has complaint of cough with content of liver
abscess
 Liver abscess may rupture into pericardial cavity
and can cause pericarditis with 30% mortality due to
cardiac temponade

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

DIAGNOSTIC TESTS
Diagnosis of amebic liver abscess is based on the
detection of one or more space occupying lesions
in the liver by Ultrasound and CT scan and a
positive serology
 Amebic liver abscess are classically described as
single, large and located in right lobe of liver
 When a pt. with space ahs a occupying lesion in the
liver, a positive serology is highly sensitive(>94% )
and highly specific(>95%) for the diagnosis of the
liver abscess

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 colitis should
be managed conservatively

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

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

TREATMENT
Drug

Dosage

Duration

Tinidazole

2g/day with food

3

Metronidazole

750mgtid PO or IV

5-10

Paramomycin

30mg/kg qd PO in 3
divided dose

5-10

Iodoquinol

650 mg PO tid

20

Amebic Colitis Or ALA

Luminal Infection
PREVENTION
Avoidance of ingestion of food and water
contaminated with humen feces is the only way of
prevention
 No prophylaxis
 No vaccine

Amebiasis
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Amebiasis

  • 1.
    AMEBIASIS AND INFECTIONWITH FREE LIVING AMEBAS Dr R L Khare Assistant Professor Department of Medicine Pt JNM Medical College Raipur
  • 2.
    DEFINITION  Amebiasis is infectionwith intestinal pathogen Entameba histolytica (tissue lysing ameba)  Most Infection are asymptomatic  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
  • 3.
    LIFE CYCLE ANDTRANSMISSION  E. histolytica exists in two stages multinucleate cyst Motile Trophozoite
  • 4.
    TRANSMISSION E. histolytica aremost common in areas where poor sanitation and crowding compromise the barrier to contamination of food and drinking water  Infection is acquired by ingestion of cysts in faecally contaminated water or food or rarely,through oralanal sexual contact  Cysts are resistant to the acid in the stomach 
  • 5.
  • 6.
    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 mol. 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 
  • 7.
    PATHOGENESIS AND PATHOLOGY E.histolyticacan 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 
  • 8.
    PATHOGENESIS AND PATHOLOGY  Theinterveining 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
  • 9.
  • 10.
    CLINICAL MANIFESTATIONS Two types-Intestinal and Extra Intestinal  Most patients harboring Entamoeba species are asymptomatic,but individuals with E.histolytica can develop disease  Amebic colitis generally appear 2-6 weeks after ingestion of the cyst of parasite  Heme positive diarrhea and abdominal pain are the most common complaints  Malaise and wt.loss may be found later  Fever is present in 40% cases  Severe dysentry with 10-12 small volume, blood and mucus containing stools may develop 
  • 11.
    CLINICAL MANIFESTATIONS Fulminant amebiccolitis with even profuse diarrhea,severe abdominal pain,fever,and pronounced leukocytosis are rare  It affects young children,pragnant women, indivisuals treated with steroids and pts. With diabetes and alcoholism  Intestinal perforation occus in >75% of pts.with fulminant disease  Complications includes  Toxic Megacolon in .5% with severe bowel dilatation and intraluminal air  Ameboma-presents as abd. mass 
  • 12.
    AMEBIC LIVER ABSCESS Mostcmmon extraintestinal complication  Disease begins when trophozoites penetrate through the colonic mucosa, travel through the portal circulation and reach the liver  The classical presentation of ALA are right upper – quadrant pain,fever and liver tenderness  Its acute in nature lasting < 10 days  With chronic presentation wt. loss and anorexia are prominent  Jaundice is uncommon 
  • 13.
    OTHER MANIFESTATIONS ANDCOMPLICATIONS Rt-sided pleural effusion and atelectesis are common in cases of ALA  In 10% rupture of abscess through diaphragm may cause pleuro-pulmonary amebiasis  Sudden onset cough,pleuritic chest pain and shortness of breath are suggestive symptom  Hepatobronchial fistula is dramatic complication in which pt has complaint of cough with content of liver abscess  Liver abscess may rupture into pericardial cavity and can cause pericarditis with 30% mortality due to cardiac temponade 
  • 14.
    DIAGNOSTIC TESTS Demonstration ofE.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 
  • 15.
    DIAGNOSTIC TESTS Diagnosis ofamebic liver abscess is based on the detection of one or more space occupying lesions in the liver by Ultrasound and CT scan and a positive serology  Amebic liver abscess are classically described as single, large and located in right lobe of liver  When a pt. with space ahs a occupying lesion in the liver, a positive serology is highly sensitive(>94% ) and highly specific(>95%) for the diagnosis of the liver abscess 
  • 16.
    CT SCAN LIVERWITH ALA IN RT LOBE
  • 17.
    TREATMENT The nitroimidazole compoundsare 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 colitis should be managed conservatively 
  • 18.
    TREATMENT  Aspiration of liverabscess 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
  • 19.
    TREATMENT In contrast, aspirationand 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 
  • 20.
    TREATMENT Neither metronidazole nortinidazole 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 
  • 21.
    TREATMENT Drug Dosage Duration Tinidazole 2g/day with food 3 Metronidazole 750mgtidPO or IV 5-10 Paramomycin 30mg/kg qd PO in 3 divided dose 5-10 Iodoquinol 650 mg PO tid 20 Amebic Colitis Or ALA Luminal Infection
  • 22.
    PREVENTION Avoidance of ingestionof food and water contaminated with humen feces is the only way of prevention  No prophylaxis  No vaccine 