CASE PRESENTATION

AMOEBIC DYSENTERY

Preceptor :
dr. Ulynar Marpaung, Sp. A

Presenter :
Ayu Wijayanti (1102009049)

DEPARTMENT OF PEDIATRIC
RADEN SAID SUKANTO POLICE CENTER HOSPITAL
FACULTY OF MEDICINE YARSI UNIVERSITY

PATIENT IDENTITY
Name

: ZRB

Birth Date

: July 1st 2012

Age

: 3 years old

Gender

: Male

Address

: Jl. H Usman No 2 RT 11/11 Kelapa Dua

Nationality

: Indonesian

Religion

: Islam

Date of admission

: April 7th 2015

Date of examination : April 7th 2015 April 9th 2015

PARENT IDENTITY

Father

Mother

Name

Mr. B

Mrs. R

Age

37 years old

32 years old

Job

Employee

Housewife

Religion

Islam

Islam

Education

Senior High School

Senior High School

HISTORY TAKING

Alloanamnesis from patients mother on the date of admission, March 24th

2015.

Chief Complain :
Diarrhea since 4 days before entering to Hospital.

Additional complains :

fever was suddenly high until 38,5C

History Of Past Illness

Pharyngitis/Tonsilitis

Bacillary Dysentry

Bronchitis

Amoeba Dysentry

Pneumonia

Diarrhea

Morbilli

Thypoid

Pertussis

Worms

Varicella

Surgery

Diphteria

Brain Concussion

Malaria

Fracture

Polio

Drug Reaction

Enteritis

PRENATAL HISTORY
Antenatal care

Antenatal check ups performed at the puskesmas by the midwife. There was
no problems during pregnancy.

No maternal illness during pregnancy

Drugs consumption : Vitamins every antenatal care

BIRTH HISTORY

Labor

: Puskesmas

Birth attendants

: midwife

Mode of delivery

: pervaginam

Gestation

: 38 weeks

Infant state

: healthy
3

Birth weight

: 3200 grams

Body length

: 47 cm

According to the mother, the baby started to cry and the baby's skin is red, no
congenital defects were reported

POST NATAL HISTORY

Examination by midwife

The state of the infant : healthy

DEVELOPMENT HISTORY

First dentition: 6 months

Psychomotor development

Head Up

: 1 month old

Smile

: 1 month old

Laughing

: 1- 2 month old

Slant

: 2,5 month old

Speech Initiation

: 5 month old

Prone Position

: 5 month old

Food Self

: 5 6 month old

Sitting

: 6 month old

Crawling

: 8 month old

Standing

: 12 month old

Walking

: 13 month old

Conclusion: Growth and development status is still in the normal limits and
was appropriate according to the patients age

HISTORY OF EATING

Breast Milk

Exclusively 6 month..

Formula milk

SGM since 1 year old

Baby biscuits

Biscuits regal

Fruit and vegetables

Banana, spinach

Solid foods and side dishes

Rice, Carrots, Potatoes

FAMILY HISTORY

Patients both parents were married when they were 24 years old and 21 years
old, and this is their first marriage.

There are not any significant illnesses or chronic illnesses in the family
declared.

History of the disease people around the patient

Around the house

People who lived around the patients house are in healthy condition

Systematic Physical Examination

Head : Normocephaly, hair (black, normal distributon, not easily removed )

sign of trauma (-), large fontanelle closed.

Eyes : Icteric sclera -/-, pale conjunctiva -/-, hyperaemia conjunctiva -/- ,
lacrimation -/-, sunken eyes -/-, pupils 3mm/3mm isokor, Direct and indirect

light response ++/++

Ears : Normal shape, no wound, no bleeding, secretion or serumen
Mouth
Lips : dry
Teeth : no carries
Mucous : moist
Tongue : not dirty
Tonsils : T1/T1, not hyperemis
Pharynx : not hyperemis
Thorax
Inspection : Symmetric when breathing , no retraction, ictus cordis is not
visible
Palpation : mass (-), tactile fremitus +/+
Percussion : sonor on both lungs
Auscultation : - Cor : regular S1-S2, murmur (-), gallop (-)
- Pulmo : vesicular +/+, Wheezing -/- , Rhonchy -/Abdomen
Inspection : Convex, epigastric retraction (-), there is no a widening of the

veins, no spider nevi.

Palpation : supple, liver and spleen not palpable, fluid wave (-), abdominal
mass (-).
Percussion : The entire field of tympanic abdomen, shifting dullness (-).
Auscultation : normal bowel sound, bruit (-).

Laboratory Investigation Hematology (April 8th 2015)

Hematology

Results

Normal Value

Haemoglobin

10,3

13-16 g/dL

Leukocytes

11.900/L

Hematocrits

31 %

Trombocytes

243.000/ L

Erythrocytes

3,50 million/L

macroscopic
colour
consistency
mucus
blood
microscopic
Leukocytes
Erythrocytes
worm eggs
Ascaris Sp
Anchilostoma Sp
Trichiuris Sp
Oxyuris Sp
Etc

5,000 10,000/
40 48 %

150,000 400,000/

4 5 million/L

brown
soft
+
+
3 4 / LPB
8 - 10 / LPB
- / LPB
- / LPB
- / LPB
- /LPB
Amoeba : +

Laboratory Investigation Hematology (April 9th 2015)

Hematology
Haemoglobin
Leukocytes
Hematocrits
Trombocytes

Results
12,0 g/dl
11.800 u/L
38%
297.000 /uL

Normal Value
13-16 g/dL
5,000 10,000/L
40 48 %
150,000 400,000/L

Differential Count (April 9th 2015)

Differential Count
(April 9th 2015)
Basophil

01

Eosinophil

13

Neutrophil Rod

2-6

Neutrophil Segment

80

50 - 70

Lymphocyte

16

20 - 40

Monocyte

2-8

Erythrocyte
Sedimentation Rate

10

<15

FOLLOW UP
April 7th 2015
S:

Diarrhea (+) : blood, mucus,

Abdominal pain (+)
Fever (+)
Vomiting and Nausea (+)
7

O:

General condition: Mild ill.

Heart rate

= 111 x/min

Respiratory rate = 26x/min

Temperature

= 36.4C

Cardio : S1/S2, reguler, no murmur, no gallop

Pulmonary : vesiculer +/+, rhonchi -/-, wheezing -/A:
P:

Amoebac Dysentery
IVFD KAEN 3B 1200 cc/24h
Inj. Cefotaxime 2x500mg
Paracetamol syr 3x1/2 cth
Lacto B 3x1 sach
Zinkid syr 1x1 cth

April 8th 2015

S:

Diarrhea (+) : blood, mucus,

Abdominal pain (+)
Fever (+)

O:

Vomiting and Nausea (+)

General condition: Mild ill.
Heart rate

= 111 x/min

Respiratory rate = 26x/min

Temperature

= 36.4C

Cardio : S1/S2, reguler, no murmur, no gallop

Pulmonary : vesiculer +/+, rhonchi -/-, wheezing -/A:
P:

Amoebac Dysentery
IVFD KAEN 3B 1200 cc/24h
Inj. Cefotaxime 2x500mg
Paracetamol syr 3x1/2 cth
Lacto B 3x1 sach
Zinkid syr 1x1 cth

LITERATURE REVIEW
1.1. DEFINITION
Dysentery is an inflammation of the intestine causing diarrhea with blood.[1][2]
Other symptoms may include fever, abdominal pain,[3] and rectal tenesmus (a
feeling of incomplete defecation).
It is caused by a number of types of infection such as bacteria, viruses, parasitic
worms, or protozoa. It is a type of gastroenteritis. The mechanism is an
inflammatory disorder of the intestine, especially of the colon.
1.2. EPIDEMIOLOGY
Amoebiasis occurs worldwide, but is mostly seen in tropical and developing
countries, which have bad sanitary and hygienic practices. Ten percent of worlds
population is estimated to be infected by the parasite (4% in USA) with an
estimated annual mortality of 40,00070,000. However, 90% of those infected are
asymptomatic, 1% may develop invasive/extraintestinal amoebiasis. Spread is
mostly through fecal-oral route, by ingestion of cysts and also through
contaminated vegetables fertilized by feces and foods and water handled by
unclean hands. Fomites and flies also have a role in the transmission.
Autoinfection through improper cleaning of hands is also reported. It is
uncommon in children below the age of 5 years. HIV infection peculiarly does
not aggravate the illness.

1.3. ETIOLOGY
Couses of Dysentery
Dysentery can have a number of causes. Bacterial infections are by far the
most common causes of dysentery. These infections include Shigella,
Campylobacter, E. coli, and Salmonella species of bacteria. The frequency of
each pathogen varies considerably in different regions of the world. For example,
shigellosis is most common in Latin America while Campylobacter is the
dominant bacteria in Southeast Asia. Dysentery is rarely caused by chemical
irritants or by intestinal worms.
Intestinal amoebiasis is caused by a protozoan parasite, Entamoeba
histolytica. The amoeba can exist for long periods of time in the large bowel
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(colon). In the vast majority of cases, amoebiasis causes no symptoms - only 10%
of infected individuals become ill. It is uncommon except in the world's tropical
zones, where it is very prevalent. People can become infected after ingesting
feces that contain somebody's excreted parasites. People are at high risk of
acquiring the parasite through food and water if the water for household use isn't
separated from waste water. The parasites can also enter through the mouth when
hands are washed in contaminated water. If people neglect to wash properly
before preparing food, the food may become contaminated. Fruits and vegetables
can be contaminated if washed in polluted water or grown in soil fertilized by
human waste.
The Shigella and Campylobacter bacteria that cause bacillary dysentery are found
all over the world. They penetrate the lining of the intestine, causing swelling,
ulcerations, and severe diarrhea containing blood and pus. Both infections are
spread by ingestion of feces within contaminated food and water. If people live or
travel in an area where poverty or overcrowding may interfere with good hygiene
and sanitation, they are at risk of being exposed to invasive bacteria. Young
children (ages 1 to 4) living in poverty are most likely to contract shigellosis,
campylobacteriosis, or salmonellosis.

1.4. PATHOGENESIS
The infective cyst form of the parasite survives passage through the stomach and
small intestine. It excysts in the bowel lumen to form motile and potentially
invasive trophozoites.
In most infections, the trophozoites aggregate in the intestinal mucin layer and
form new cysts, resulting in a self-limiting and asymptomatic infection. However,
galactose/N-acetyl-galactosamine (Gal/GalNAc) lectin-mediated adherence to
and lysis of the colonic epithelium can initiate trophozoite invasion into the colon
in some cases.
Neutrophils responding to invasion contribute to cellular damage at the site of
invasion. Once the intestinal epithelium is invaded, extraintestinal spread into the
peritoneum, liver, and other sites is possible.
Factors controlling invasion versus encystation include parasite quorum sensing
signalled by the Gal/GalNAc lectin interactions of amoebae with the bacterial

11

flora of the intestine, and host innate and acquired immune responses.
Trophozoites are always present in the gut in patients with amoebic diarrhoea and
dysentery (diarrhoea with blood or mucus), and diagnosis should concentrate on
identifying the parasite in stool by antigen detection and the serum antibody
response against the invasive parasite.
Invasion of the trophozoites through the intestinal epithelium leads to amoebic
diarrhoea and colitis. View imageView image Invasion involves a unique nibbling
process by the parasite on the intestinal lining, termed amoebic trogocytosis.
Haematogenous dissemination via the portal venous system results in amoebic
liver abscessView image and infection in other sites such as the brain,View image
although this is rare.

1.5. CLINICAL MANIFESTATIONS

The main symptom of dysentery is frequent near-liquid diarrhea flecked
with blood, mucus, or pus. Other symptoms include:

sudden onset of high fever and chills

abdominal pain

cramps and bloating

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flatulence (passing gas)

urgency to pass stool

feeling of incomplete emptying

loss of appetite

weight loss

headache

fatigue

vomiting

dehydration
Other symptoms may be intermittent and may include recurring low fevers,
abdominal cramps, increased gas, and milder and firmer diarrhea. You may feel weak
and anemic, or lose weight over a prolonged period (emaciation). Mild cases of
bacillary dysentery may last 4 to 8 days, while severe cases may last 3 to 6 weeks.
Amoebiasis usually lasts about 2 weeks.
Bacillary dysentery symptoms begin within 2 to 10 days of infection. In children, the
illness starts with fever, nausea, vomiting, abdominal cramps, and diarrhea. Episodes
of diarrhea may increase to as much as once an hour with blood, mucus, and pus in
the child's stool. Vomiting may result in rapid and severe dehydration, which may lead
to shock and death if not treated. Signs of dehydration include an extremely dry
mouth, sunken eyes, and poor skin tone. Children and infants will be thirsty, restless,
irritable, and possibly lethargic. Children may also have sunken eyes and may not be
able to produce tears or urine, the latter appearing very dark and concentrated.

1.6. EXAMINATION AND DIAGNOSIS

Diagnosis
A clinical diagnosis may be made by taking a history and doing a brief examination.
Treatment is usually started without or before confirmation by laboratory analysis.
Physical exam
The mouth, skin, and lips may appear dry due to dehydration. Lower abdominal
tenderness may also be present.
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Stool and blood test

Cultures of stool samples are examined in order to identify the organism causing
dysentery. Usually, several samples must be obtained due to the changing number of
amoeba, which changes daily.
Blood tests can be used to measure abnormalities in the levels of essential minerals
and salts.
High degree of suspicion in endemic areas is a prerequisite. Fresh liquid stool
examination showing hematophagus trophozoites with Charcot-Leyden crystals is
characteristic. Stool examination, preferably for three consecutive days is advocated.
Presence of only cysts in asymptomatic individuals is not diagnostic, since the cysts
of E. dispar, which is noninvasive and harmless are indistinguishable from those of
invasive E. histolytica. Sigmoidoscopic scrapings of ulcers showing hematophagus
trophozoites are diagnostic. So also is the finding of amoebae from the walls of
hepatic abscess.
Ultrasound (USG) scan of the abdomen helps in the delineation of hepatic abscesses.
X-ray of the chest helps in the detection of spread to the pleura, lung or pericardium.
X-ray of the abdomen is useful for the diagnosis of peritonitis and toxic megacolon.
Computed tomography/magnetic resonance imaging help in the diagnosis of
intracranial spread of amoebiasis.
Conditions to be kept in the mind are different types of E. coli and the Shigella enteric
infections in acute presentation and tuberculosis in subacute or chronic presentation.
Antibody detection at the end of 1 week of invasive amoebiasis, indirect
hemagglutination assay (IHA) and enzyme-linked immuno- sorbent assay (ELISA)
are diagnostic.
Polymerase chain reaction (PCR) in advanced centers is confirmatory.

1.7. TREATMENT

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Asymptomatic cyst shredders, need/should not be treatedWHO guidelines.

Combination therapy with luminal and tissue amoebicides is highly recommended.
Introduction of nitroimidazole derivatives has revolutionized the treatment of
amoebiasis. Usage of cardiotoxic emetine and the relatively less toxic dehydroemetine
are now of historical interest. Though metronidazole and other derivatives are highly
toxic to the vegetative forms and to a lesser extent the cysts, a course of luminal
amoebicides is recommended for complete cure.
Tissue Amoebicides

Metronidazole: 500 mg IV 8th hourly. For 710 days for extraintestinal

amoebiasis. 400 mg thrice daily orally for 710 days (4060 mg/kg body
weight in children)

Tinidazole: 2 g as single dose for 23 days. 300 mg twice daily orally for 7
days (5060 mg/kg body weight in children)

Ornidazole: 1.5 g once daily for 3 days. 500 mg twice daily orally for 710
days (40 mg/kg body weight in children)

Secnidazole: 2 g as single dose

Nitazoxanide: 500 mg twice daily for 3 days (age > 12 years), 200 mg twice
daily for 3 days (411 years) or 100 mg. Twice daily (13 years)

Chloroquine: 300 mg twice daily followed by 300 mg daily for 21 days as an

adjunct to metronidazole.

Luminal Amoebicides
These are recommended to prevent relapses following the course of tissue
amoebicides:

Diloxanide furoate: 500 mg thrice daily for 10 days (20 mg/kg body
weight in children)

Quinodocholor: 500 mg twice daily for 10 days

15

Iodochlorhydroxyquin: 500 mg twice daily for 10 days

Paromomycin: 30 mg/kg body weight thrice daily for 7 days (25

mg/kg body weight in children).

1.8. PREVENTION

Public education about personal hygiene, especially the sanitary disposal of

feces.

Education of food handlers about proper food and equipment handling and
hygiene.

Advice infected individual stoavoid food preparation.

Educate about risk of sexual practices that permit fecal-oral contact.

Test private water supplies for the presence of parasitic contamination.

Advice infected individuals against using public swimming pools.

Contaminated water can be a source of transmission of enteric pathogens.

1.9. COMPLICATIONS
These are secondary to severe toxemia, perforation of the bowel, toxic megacolon,
rupture of the hepatic abscess into pleura, lung, peritoneum, pericardium, skin and
subcutaneous tissue. Extraintes- tinal spread metastasizing in the brain and bones is
uncommon. Formation of a granuloma in the bowel wall mimicking a malignant
growth, the amoeboma, is also not common. Rarely, a large hepatic abscess producing
obstructive jaundice can occur. Fever, leukocy- tosis with elevated polymorphs, rise in
hepatic enzymes and serum bilirubin are the accompaniments of the complications.

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POINTS TO REMEMBER

Flies may act as vectors in transferring cyst-laden feces on to eatables.

Cysts remain viable for several days to months depending on the temperature
and moisture of the external atmosphere.

Cysts may survive up to 45 minutes in the fecal material lodged under the
finger nails.

Cysts are killed only by boiling water for 10 minutes and not by routine
chlorination.

Sand filters are useful.

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1.

Alberta Health and Wellness (2011). Amoebiasis: Public health notifiable disease
management guidelines. [online]. Available from
http://www.health.alberta.ca/documents/Guidelines-Amoebiasis-2011.pdf
[Accessed December, 2012].

2.

Antia FP, Desai HG, Jeejeebhoy KN, et al. (2012). Incidence of intestinal
amoebiasis. [online]. Available from http://gut.bmj.com/ content/6/5/454.full.pdf
[Accessed December, 2012].

3.

Cook GC, Alimuddin IZ. Mansions Tropical Diseases, 22nd edition.

Philadelphia: Saunders Elsevier; 2009.

4.

Dhawan VK. Current diagnosis and treatment of amoebiasis. US Infectious

Disease. 2008; 4(1):59-61.

5.

Fauci A, Braunwald E, Kasper D, et al. Harrisons principles of Internal

Medicine, 17th edition. New York: McGraw-Hill Companies; 2008.

6.

Harries J. Amoebiasis, a review. J R Soc Med. 1982;75(3):191-7.

7.

Kansas Disease Investigation Guidelines. Version 04/2009. Amebiasis (Amebic

Dysentery): Investigation Guideline. [online]. Available from
http://www.kdheks.gov/epi/Investigation_Guidelines/Amebiasis_Investigation_G
uideline.pdf [Accessed December, 2012].

8.

Rossignol JF, Kabil SM, Younis AM, et al. Nitazoxanide in the treatment of
amoebiasis. Trans R Soc Trop Med Hyg. 2007;101:1025-31.

9.

Salles JM, Salles MJ, Moraes LA. Invasive amoebiasis, an update on diagnosis
and management. Expert Rev Anti Infect Ther. 2007;5(5):893- 901.

10. Sharma SK, Munjal YP, Agarwal AK. API Textbook of Medicine, 9th edition.
New Delhi: Jaypee Brothers Medical Publishers; 2012.

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