GIT protozoa
Ameba
Ameba:
Entamoeba histolytica
Entamoeba dispar
Entamoeba coli
Entamoeba hartmanni
Endolimax nana
Iodamoeba bütschlii
INTESTINAL PROTOZOA
unicellular eukaryotic organisms
Fecal-Oral Transmission Factors
•poor personal hygiene
• food handlers
• institutions
• children in day care centers
•developing countries
• highly endemic
• poor sanitation
• travelers diarrhea
•water-borne epidemics
•zoonosis
• Entamoeba = no
• Cryptosporidium = yes
• Giardia = controversial
Control/Prevention
• improve personal hygiene
• especially institutions
• treat asymptomatic carriers
• eg, family members
• health education
• hand-washing
• sanitation
• food handling
• protect water supply
• treat water if questionable
• boiling
• iodine
• not chlorine
Amoebiasis
 Amoebiasis is caused by Entamoeba histolytica.
 The organism formerly known as E. histolytica is now
known to consist of two distinct species: E. histolytica,
which is pathogenic, and E. dispar, which is non-
pathogenic.
 Cysts of the two species are identical, but can be
distinguished by molecular techniques after culture of
the trophozoite. E. histolytica can be distinguished
from all amoebae except E. dispar, and from other
intestinal protozoa, by microscopic appearance.
 Amoebiasis occurs world-wide, although much higher
incidence rates are found in the tropics and
subtropics.
Cont.
 The organism exists both as a motile
trophozoite and as a cyst that can survive
outside the body.
 Cysts are transmitted by ingestion of
contaminated food or water, or spread
directly by person-to-person contact.
 Trophozoites emerge from the cysts in the
small intestine and then pass on to the
colon, where they multiply.
Clinical features
 Many individuals can carry the pathogen
without obvious evidence of clinical disease
(asymptomatic cyst passers).
 This is may be due in some cases to the
misidentification of non-pathogenic E.
dispar as E. histolytica, and it is not clear
how often true E. histolytica infection is
symptomless.
 In affected people E. histolytica
trophozoites invade the colonic epithelium,
probably with the aid of their own
cytotoxins and proteolytic enzymes.
Cont.
 The parasites continue to multiply
and finally frank ulceration of the
mucosa occurs.
 If penetration continues, trophozoites
may enter the portal vein, via which
they reach the liver and cause
intrahepatic abscesses.
 This invasive form of the disease is
serious and may even be fatal.
• ulcers with raised borders
• little inflammation between lesions
Incubation period
 The incubation period of intestinal amoebiasis is
highly variable and may be as short as a few days or
as long as several months.
 The usual course is chronic, with mild intermittent
diarrhoea and abdominal discomfort. This may
progress to bloody diarrhoea with mucus, and is
sometimes accompanied by systemic symptoms such
as headache, nausea and anorexia.
 Less commonly, infection may present as acute
amoebic dysentery, resembling bacillary dysentery or
acute ulcerative colitis.
Complications
 Complications are unusual, but include toxic
dilatation of the colon, chronic infection with
stricture formation, severe haemorrhage,
amoeboma, and amoebic liver abscess.
 Amoebomas, which develop most commonly in the
caecum or rectosigmoid region, are sometimes
mistaken for carcinoma. They may bleed, cause
obstruction or intussuscept.
 Amoebic liver abscesses often develop in the absence
of a recent episode of colitis. Tender hepatomegaly, a
high swinging fever and profound malaise are
characteristic, although early in the course of the
disease both symptoms and signs may be minimal.
Diagnosis
 Microscopic examination of fresh stool or colonic
exudate obtained at sigmoidoscopy is the simplest
way of diagnosing colonic amoebic infection.
 To confirm the diagnosis motile trophozoites
containing red blood cells must be identified: the
presence of amoebic cysts alone does not imply
disease. Sigmoidoscopy and barium enema
examination may show colonic ulceration but are
rarely diagnostic.
 The amoebic fluorescent antibody test is positive in at
least 90% of patients with liver abscess and in 60-
70% with active colitis. Seropositivity is low in
asymptomatic cyst passers.
Management
 Metronidazole 800 mg three times daily for
5 days is given in amoebic colitis; a lower
dose (400 mg three times daily for 5 days)
is usually adequate in liver abscess.
 Tinidazole is also effective: dehydroemetine
and chloroquine are alternative drugs, but
are rarely used. After treatment of the
invasive disease, the bowel should be
cleared of parasites with a luminal
amoebicide such as diloxanide furoate.
prevention
 Amoebiasis is difficult to eradicate
because of the substantial human
reservoir of infection. The only
progress will be through improved
standards of hygiene and better
access to clean water.
 Cysts are destroyed by boiling, but
chlorine and iodine sterilizing tablets
are not always effective.
Thank you!!!

Intestinal amoebae

  • 1.
  • 2.
    Ameba: Entamoeba histolytica Entamoeba dispar Entamoebacoli Entamoeba hartmanni Endolimax nana Iodamoeba bütschlii INTESTINAL PROTOZOA unicellular eukaryotic organisms
  • 3.
    Fecal-Oral Transmission Factors •poorpersonal hygiene • food handlers • institutions • children in day care centers •developing countries • highly endemic • poor sanitation • travelers diarrhea •water-borne epidemics •zoonosis • Entamoeba = no • Cryptosporidium = yes • Giardia = controversial Control/Prevention • improve personal hygiene • especially institutions • treat asymptomatic carriers • eg, family members • health education • hand-washing • sanitation • food handling • protect water supply • treat water if questionable • boiling • iodine • not chlorine
  • 4.
    Amoebiasis  Amoebiasis iscaused by Entamoeba histolytica.  The organism formerly known as E. histolytica is now known to consist of two distinct species: E. histolytica, which is pathogenic, and E. dispar, which is non- pathogenic.  Cysts of the two species are identical, but can be distinguished by molecular techniques after culture of the trophozoite. E. histolytica can be distinguished from all amoebae except E. dispar, and from other intestinal protozoa, by microscopic appearance.  Amoebiasis occurs world-wide, although much higher incidence rates are found in the tropics and subtropics.
  • 5.
    Cont.  The organismexists both as a motile trophozoite and as a cyst that can survive outside the body.  Cysts are transmitted by ingestion of contaminated food or water, or spread directly by person-to-person contact.  Trophozoites emerge from the cysts in the small intestine and then pass on to the colon, where they multiply.
  • 6.
    Clinical features  Manyindividuals can carry the pathogen without obvious evidence of clinical disease (asymptomatic cyst passers).  This is may be due in some cases to the misidentification of non-pathogenic E. dispar as E. histolytica, and it is not clear how often true E. histolytica infection is symptomless.  In affected people E. histolytica trophozoites invade the colonic epithelium, probably with the aid of their own cytotoxins and proteolytic enzymes.
  • 7.
    Cont.  The parasitescontinue to multiply and finally frank ulceration of the mucosa occurs.  If penetration continues, trophozoites may enter the portal vein, via which they reach the liver and cause intrahepatic abscesses.  This invasive form of the disease is serious and may even be fatal.
  • 8.
    • ulcers withraised borders • little inflammation between lesions
  • 9.
    Incubation period  Theincubation period of intestinal amoebiasis is highly variable and may be as short as a few days or as long as several months.  The usual course is chronic, with mild intermittent diarrhoea and abdominal discomfort. This may progress to bloody diarrhoea with mucus, and is sometimes accompanied by systemic symptoms such as headache, nausea and anorexia.  Less commonly, infection may present as acute amoebic dysentery, resembling bacillary dysentery or acute ulcerative colitis.
  • 10.
    Complications  Complications areunusual, but include toxic dilatation of the colon, chronic infection with stricture formation, severe haemorrhage, amoeboma, and amoebic liver abscess.  Amoebomas, which develop most commonly in the caecum or rectosigmoid region, are sometimes mistaken for carcinoma. They may bleed, cause obstruction or intussuscept.  Amoebic liver abscesses often develop in the absence of a recent episode of colitis. Tender hepatomegaly, a high swinging fever and profound malaise are characteristic, although early in the course of the disease both symptoms and signs may be minimal.
  • 11.
    Diagnosis  Microscopic examinationof fresh stool or colonic exudate obtained at sigmoidoscopy is the simplest way of diagnosing colonic amoebic infection.  To confirm the diagnosis motile trophozoites containing red blood cells must be identified: the presence of amoebic cysts alone does not imply disease. Sigmoidoscopy and barium enema examination may show colonic ulceration but are rarely diagnostic.  The amoebic fluorescent antibody test is positive in at least 90% of patients with liver abscess and in 60- 70% with active colitis. Seropositivity is low in asymptomatic cyst passers.
  • 12.
    Management  Metronidazole 800mg three times daily for 5 days is given in amoebic colitis; a lower dose (400 mg three times daily for 5 days) is usually adequate in liver abscess.  Tinidazole is also effective: dehydroemetine and chloroquine are alternative drugs, but are rarely used. After treatment of the invasive disease, the bowel should be cleared of parasites with a luminal amoebicide such as diloxanide furoate.
  • 13.
    prevention  Amoebiasis isdifficult to eradicate because of the substantial human reservoir of infection. The only progress will be through improved standards of hygiene and better access to clean water.  Cysts are destroyed by boiling, but chlorine and iodine sterilizing tablets are not always effective.
  • 14.