Amebiasis.

Amebiasis.
Definition:
Infection of the colon with entamoeba
histolytica, which is commonly
asymptomatic but may produce clinical
manifestations ranging from mild
diarrhoea to severe dysentery.
 Aetiology.
It is caused by entamoeba histolytica.
E. dispar is a nonpathogenic protozoon
morphologically identical to E histolytica.
Previously reported asymptomatic
infections due to the so-called
nonpathogenic strains of E histolytica
now are recognized to be due to E.
dispar.
 Transmission.
It is a natural infection of man, that may be
transmitted by direct contact from person
to person, through the faecal-oral route,
or indirectly by food, drink and
vegetables.
 Epidemiology.
Amebiasis is the third leading parasitic
cause of death worldwide, surpassed
only by malaria and schistosomiasis. On
a global basis, amebiasis affects
approximately 50 million persons each
year, resulting in nearly 100,000 deaths.
Entamoeba life cycle

􀂃Cysts shed in faeces of carriers

􀂃Cysts transferred via contaminated food, water or
hands
Feacal-oral
Anal sex
Colonic irrigation
􀂃Excystation in the small bowel releasing
trophozoites
Cysts resistant to gastric acid but broken down by
trypsin releasing trophozoites
Entamoeba life cycle
􀂃 Trophozoites migrate to the colon and
reproduce (forming cysts)
􀂃 Within the colon trophozoites feed on
bacteria and feacal material
􀂃 If trophozoites adhere and then penetrate
the mucosa clinical infection results
􀂃 Hepatic infection if trophozoites enter
mesenteric venules
􀂃 Trophozoites and cysts are passed in the
feaces
 Pathology.
Trophozoites emerge from the cyst in
the small intestine and then pass on
the colon, where they multiply.
There is lysis and necrosis of the mucosa
by means of proteolytic enzymes
released by the trophozoites.
Rectosigmoidoscopy and colonoscopy
may show small mucosal ulcers
covered with yellowish exudates.
 Cont. pathology.
The intervening mucosa appears normal.
Biopsy results and scrapings of ulcer
edge may locate trophozoites.
Primary intestinal flask-shaped (button
hole) necrotic ulcers occur in the
submucosa of the large intestine, most
commonly the cecal and
sigmoidorectal regions.
 Cont. pathology.
Ulcers contain necrotic debris,
actively feeding trophozoites with
ingested erythrocytes, cytolyzed
cells and mucous.
polymorphonuclear leukocytes and
round inflammatory cells.
 Cont. pathology
Hematogenous spread may result in
abscesses of the liver, spleen, lung
or brain. Hepatic amebiasis
(abscess, hepatitis) is the most
common and grave complication.
 Clinical features
AMOEBIASIS (clinical presentations)
 1) assymptomatic carrier state
 2) acute amoebic dysentry
 3) amoebic liver abscess
 4) amoeboma
Clinical features
Asymptomatic
• Most common form of infestation
• “carriers”
 These people almost never develop
symptoms but can spread disease
• Spontaneously clear disease within 12
months
• If detected on stool sample should be
treated
• Risk of infection 10%/year
Clinical features
Symptomatic
 Amoebic colitis
• Subacute presentation (weeks)
 Abdominal pain/ cramping/ distention
 Diarrhoea (blood, mucus)
 Fever (40%)
 Tenesmus
 Ameobic liver abscess
Most common extraintestinal manifestation
(10% of infected patients develop liver abscesses)
 Clinical features.
Amebiasis is an intestinal infection in which
cysts are passed in the feces. Symptoms
can include fever, chills and diarrhea,
sometimes bloody or with mucus and often
with cramps. Some people may have only
mild abdominal discomfort or no symptoms
at all. Symptoms can start 2 or more weeks
after infection. Rarely, trophozoites (the
mobile amebas) may invade the liver, lung
or brain, or perforate the colon causing
septicemia.
 Cont. clinical features.
Extraintestinal features: Tender liver and
upper abdominal pain that may radiate to
the right shoulder.
Mild jaundice may be evident.
 Differential Diagnosis.
Bacillary dysentery.
Bilharziasis.
Tuberculous colitis.
Ulcerative colitis.
Cancer of the colon.
Gallbladder diseases.
 Laboratory diagnosis.
By microscopy, the diagnosis is not confirmed
until active trophozoites containing RBCs are
demonstrated from the stools.
An iodine-stained cyst of the pathogen
Entamoeba hystolytica with 4 nuclei is
illustrated.
The harmless commensal Entamoeba coli has
larger cyts with 8 nuclei.
Entamoeba histolytica trophozoite with ingested RBCs.
 Cont. lab. diagnosis
The cyst of E histolytica averages
12 m, ranging from 5-20 m.
It has 1-4 nuclei that are
morphologically similar to the
nuclei of the trophozoite.
 Trophozoites
Entamoeba coli Entamoeba histolytica
15 m - 40 m in size 10 m - 35 m size
Nondirectional motility Unidirectional motility
Multiple pseudopodia Single pseudopodia
No ingested erythrocytes Ingested erythrocytes
Cytoplasm rough looking Finely granular cytoplasm
Large, eccentric karyosome Small, central karyosome
 Cont. Diagnosis.
Leukocytosis and mild anemia can occur.
Erythrocyte sedimentation rate generally is
elevated.
Liver function tests reveal elevated alkaline
phosphatase in 80% of patients, elevated
transaminases and reduced albumin.
Urinalysis may reveal proteinuria.
Rectosigmoidoscopy and colonoscopy may show
small mucosal ulcers covered with yellowish
exudates.
The intervening mucosa appears normal.
 Drugs for treatment.
Five pharmaceuticals are briefly noted:
Asymptomatic intestinal infection may be
treated with iodoquinol, paromomycin or
diloxanide furoate.
Recommended drugs for treatment of
symptomatic intestinal disease and for
hepatic abscess are metronidazole and
tinidazole.
 Cont. treatment.
Since these drugs may not eliminate the
cysts of the intestine, immediately follow
metronidazole and tinidazole with
iodoquinol, paromomycin or diloxanide
furoate.
 Cont. treatment
1/ Metronidazole (Flagyl, Protostat). Kills
trophozoites of E. histolytica in intestine
and tissue.
Does not eradicate cysts from intestines.
Adult oral dose: 500-750 mg 3 times per
day for 10 day.
Elimination is accelerated by simultaneous
use of phenytoin and phenobarbital.
 Cont. treatment

2/Tinidazole (Fasigyn). 5-nitroimidazole

derivative with selective antimicrobial
activity against anaerobic bacteria and
protozoa. Adult oral dose: 600 mg bid or
800 mg 2 times a day for 5 days. Pediatric
dose 50-60 mg/kg for 5 days, not to
exceed 2 g/day.
 Cont. treatment

3/Paromomycin (Humatin). Amebicidal

aminoglycoside antibiotic that is poorly
absorbed. Active only against intestinal
form of amebiasis. Used to eradicate cysts
of E. histolytica following treatment with
metronidazole or tinidazole for an invasive
disease. Adult oral dose: 25-35 mg/kg/day
divided 3 times for 7 days. Pediatric dose:
Administer as in adults.
 Cont. treatment
4/Diloxanide furoate (Furamid, Entamizole,
Furamide). Luminal amebicide; acts primarily
in bowel lumen since it is poorly absorbed.
Used to eradicate cysts of E. histolytica after
treatment of invasive disease. Available
through US CDC Drug Service (404-639-
3670). Adult oral dose 500 mg 2 times a day
for 10 days. Pediatric dose 20 mg/kg/
divided twice a day for 10 days, not to
exceed 1500 mg/day.
 Cont. treatment
5/Iodoquinol (Yodoxin). Halogenated
hydroxyquinoline. Luminal amebicide; acts
primarily in bowel lumen since it is poorly
absorbed. Best tolerated when given with
meals. Since active only against intraluminal
form of amebiasis, used to eradicate cysts of E.
histolytica after treatment of invasive disease.
Adult oral dose 650 mg 2 times a day for 20
days. Pediatric dose: 30-40 mg/kg/day divided
2 times for 20 days; not to exceed 2 g/day.
Complications
􀂃 Intestinal
• Fulminant colitis
• Toxic megacolon
• Perianal disease
􀂃 Extraintestinal
• Liver abscess rupture
• Pleuro-pulmonary disease
• Bronchopulmonary fistula
• Subphrenic abscess
• Intraperitoneal rupture
• Pericardial rupture
• Secondary infection - pyogenic abscess
(usually S. aureus
Complications
􀂃 Rare
Cerebral infection
Genitourinary infection
Cutaneous infection
Amoebic liver abscess
􀂃 Trophozoites invade small vessels of the
bowel wall and reach liver via portal
circulation
􀂃 Microembolization in the portal system
causes infarction and focal areas of necrosis
􀂃 Amoeba cause lysis of neutrophils and the
edge of these lesions causing release of toxic
mediators and further hepatic necrosis
􀂃 Usually multiple small lesions coalesce
forming the “amoebic liver abscess”
Amoebic liver abscess
􀂃 Usually solitary lesion
􀂃 Right lobe more common
􀁹 80% of abscesses in right lobe
􀁹 Right lobe larger in volume and
receives most of the blood from the
caecum – where trophozoites are
commonly found
Amoebic liver abscess
Presentation
􀁹 Acute, <14d (more common)
 May have preceding amoebic colitis (20-30%)
 Fever, malaise, rigors, diaphoresis
 RUQ pain:
Sharp, constant, relieved by lying on left side
Radiating to shoulder tips and scapulae
Pleuritic component
 Hepatomegaly
􀁹 chronic presentations
 Weight loss and vague abdominal discomfort
 Can present years after amoebic colitis
Amoebic liver abscess
Rare presentations
 Pulmonary symptoms (20%)
Ameobic pulmonary abscess
Bronchopulmonary fistula
Cough, chest pain
 Jaundice (5%)
Due to large or multiple abscesses and/ or
bacterial superinfection
 Diarrhoea
Amoebic liver abscess
Examination findings
 Common
• Febrile
• Tender hepatomegaly
• Often point tenderness
• Epigastric mass (left sided disease)
 Uncommon
• Right lower lobe pneumonia
• Jaundice
• Severe sepsis - usually indicates secondary bacterial
infection
Amoebic liver abscess
Diagnosis
 Aneamia, leukocytosis, eosinophilia
 Ultrasound
 CT scan
 LFT’s
Jaundice, hypoalbuminaemia
Elevated AST (acute) and ALT (chronic)
 Serology
 Aspirate microscopy
 Stool sample
Low sensitivity (only 30% of patients have concomitant
intestinal amoebiasis)
 Response to metronidazole 750 t.i.d