Case Study of Amoebiasis

METROPOLITAN MEDICAL CENTER
COLLEGE OF ARTS SCIENCE AND TECHNOLOGY

#1357 G. Masangkay Corner Mayhaligue Streets, Sta. Cruz, Manila
INTRODUCTION:
Amoebiasis protozoal infection of human beings initially involves the colon, but may
spread to soft tissues, most commonly to the liver or lungs, by contiguity or hematogenous or
lymphatic dissemination.
Amoebiasis is the third leading parasitic cause of death worldwide, surpassed only by
malaria and schistosomiasis. On a global basis, amoebiasis affects approximately 50 million
persons each year, resulting in nearly 100,000 deaths.
COLLEGE OF ARTS SCIENCE AND TECHNOLOGY
#1357 G. Masangkay Corner Mayhaligue Streets, Sta. Cruz, Manila
Amoebiasis is due to invasion of the intestinal wall by the protozoan parasite Entemoeba
histolytica. Amoebic colitis results from ulcerating mucosal lesions caused by the release of
parasite-derived hyaluronidases and proteases. It refers to infection of man by Entamoeba
hystolytica initially involving the colon but which may spread to other soft tissues organs by
contiguity or by hematogenous or lymphatic dissemination most commonly to the liver and
lungs.
It is a worldwide parasitic disease. It creates many medical and surgical problems.
About15 to 20 per cent of Indians are affected by the parasite. It can be acute and chronic and
can have intestinal and extra-intestinal manifestations. The causative organism is protozoa that
remains in the large intestine and can be transmitted to other organs like liver, lungs, brain,
spleen and skin. It is transmitted through contaminated food, water and infected human feces.
Amoebiasis can occur at any age. There is no gender or racial difference in the
occurrence of the disease. It is a household infection and the human being is responsible for
spreading the disease. Most of the infected people remain asymptomatic (without symptoms) and
are called as healthy carriers. If one person in a family gets infected with the parasite, other
family members are at the great risk of infection. The human carrier can discharge up to 1.5x107
cysts per day.
Pathogenic amoeba, which produce condition of a great clinical variation:
1. Acute Amoebic Dysentery

 stools contain blood and mucus, which may give rise to amoebic hepatitis or liver
abscess.
2. Chronic Amoebic Dysentery
 with recurrent attack of diarrhea or relatively mild dysentery.
3. Amoebic Colitis
 characterized by periods of constipation and diarrhea and episodes of abdominal
discomfort frequently stimulating appendicitis.
 COLLEGE OF ARTS SCIENCE AND TECHNOLOGY
 #1357 G. Masangkay Corner Mayhaligue Streets, Sta. Cruz, Manila
History of Discovery:
Human infections of the parasite are not a recent phenomenon. The earliest record of
symptoms of the disease—bloody, mucose diarrhea—was from the Sanskrit document Brigu-
samhita, written at around 1000BC. Assyrian and Babylonian texts also have references to the
diseases, with descriptions of blood in the feces, thus suggesting that amoebiasis occurred in the
Tigris-Euphrates basin before the sixth century BC. Later records were able to distinguish
bacterial infections with those of amoebic origin: epidemics of dysentery by itself are more likely
to result from bacterial infections, while dysentery that is associated with disease of the liver is
more likely to cause by amoeba. Thus, around the second century AD; there was clearer
understanding of the association between liver abscesses and amoebas.
Around the 16th century, amoebiasis became more widespread in the developed world,
mostly due to the growth of European colonies and increased world trade. There had been many
clear descriptions of the hepatic and intestinal forms of amoebiasis, considered as the cause of a
“bloody flux” spreading through Europe, Asia, Persia, and Greece. The first accurate description
of both forms of the disease came from the book Researches into the Causes, Nature and
Treatment of the More Prevalent Diseases of India and of Warm Climates Generally by James
Annersley, written in the 19th century. Considering their small size, protozoans were difficult to
identify before the invention of the microscope in the 17th century. Friedrich Losch discovered
the causal agent, Entamoeba histolytica, in Russia in 1873. His early observations came from the
case of a young farmer who had from been suffering chronic dysentery. In his diagnosis, Losch
found large numbers of amoeba in his feces and associated the amoebas to be the cause of the
dysentery.

Etiologic Agent: Enatamoeba Histolytica
 Prevalent in unsanitary areas

 Common in warm climate
 Acquired by swallowing
 Cysts survives a few days outside of the body
 Cyst passes to the large intestine and hatch into trophozoites. It passes into the mesenteric veins, to
the portal vein, to the liver, thereby forming amoebic liver abscess.
Entamoeba Histolytica has two developmental stages:

1. Trophozoites/vegetative form
 Trophozoites are facultative parasites that may invade the tissues or may be found in the
parasitized tissues and liquid colonic contents.
2. Cyst
 Cyst is passed out with formed or semi-formed stools and are resistant to environmental
conditions.
 This is considered as the infective stage in the cycle of E. histolytica
Source: Human Excreta
Incubation Period:
 The incubation period in severe infection is three days. In subacute and chronic form it
lasts for several months. In average cases the incubation period varies from three to four
weeks
Period of Communicability:
 The microorganism is communicable for the entire duration of the illness.
Modes of Transmission:
1. The disease can be passed from one person to another through fecal-oral transmission.
2. The disease can be transmitted through direct contact, through sexual contact by orogenital, oroanal,
and proctogenital sexual activity.
3. Through indirect contact, the disease can infect humans by ingestion of food especially uncooked
leafy vegetables or foods contaminated with fecal materials containing E. histolytica cysts.
Food or drinks maybe contaminated by cyst through pollution of water supplies, exposure to
flies, use of night soil for fertilizing vegetables, and through unhygienic practices of food
handlers.
Clinical Manifestations:
a. Acute amoebic dysentery
 Slight attack of diarrhea, altered with periods of constipation and often accompanied by tenesmus.
 Diarrhea, watery and foul smelling stool often containing blood-streaked mucus
 Colic and gaseous distension of the lower abdomen
 Nausea, flatulence, abdomnal distension and tenderness in the right iliac region over the colon
b. Chronic amoebic dysentery
 Attack dysentery that lasts for several days, usually succeeded by constipation
 Tenesmus accompanied by the desire to defacate
 Anorexia, weight loss, and weakness
 Liver may be enlarged
 The stool at first is semifluid but soon becomes watery, bloody, and mucoid
 Vague abdominal distress, flatulence, constipation or irregularity of bowel
 Mild toxemia, constant fatigue and lassitude
 Abdomen loses its elasticity when picked up between fingers

 On sigmoidoscopy, scattered ulceration with yellowish and erythematous border
 The gangrenous type (fatal cases) is characterized by the appearance of large sloughs of intestinal
tissues in the stool accompanied by hemorrhage.
c. Extraintestinal forms
 Hepatic
 Pain at the upper right quadrant with tenderness of the liver
 Abscess may break through the lungs, patient coughs anchovy-sauce sputum
 Jaundice
 Intermittent fever
 Loss of weight or anorexia
Clinical Features:
1. Onset is gradual
2. Diarrhea increases and stool
becomes bloody and mucoid
3. In untreated cases:

ANATOMY AND PHYSIOLOGY:
Amebiasis is an intestinal illness that is typically transmitted when someone eats or drinks
something that is contaminated with a microscopic parasite called Entamoeba histolytica (E.
histolytica). The parasite is an amoeba, a single-celled organism. That is how the illness got its
name — amebiasis.
In many cases, the parasite lives in a person’s large intestine without causing any
symptoms. But sometimes, it invades the lining of the large intestine, causing bloody diarrhea,
stomach pains, cramping, nausea, loss of appetite, or fever. In rare cases, it can spread into other
organs such as the liver, lungs, and brain.
I. Structure. The GI System consists of the oral structures, esophagus, stomach, small intestine, large
intestine and associated structures.
A. Oral Structures include the lips, teeth,
gingivae and oral mucosa, tongue, hard
palate, soft palate, pharynx and salivary
glands.
B. The esophagus is a muscular tube
extending from the pharynx to the stomach.
Esophageal openings include:
1. The upper esophageal sphincter at the

cricopharyngeal muscle.
2. The lower esophageal sphincter (LES), or cardiac sphincter, which normally remains closed
and opens only to pass food into the stomach.
C. The Stomach is a muscular pouch situated in the upper abdomen under the liver and diaphragm.
Te stomach consists of three anatomic areas: the fundus, body (i.e., corpus), and antrum (i.e.,
pylorus)
D. Sphincters. The LES allows food to enter the stomach and prevents reflux into the esophagus. The
pyloric sphincter regulates flow of stomach contents (chyme) into the duodenum.
E. The small intestine, a coiled tube, extends from the pyloric sphincter to the ileocecal valve at the
large intestine. Sections of the small intestine include the duodenum, jejunum and ileum
F. The large intestine is a shorter, wider tube beginning at the ileocecal valve and ending at
the anus. The large intestine consists of three sections:
1. The cecum is a blind pouch that extends from the ileocecal valve to the vermiform
appendix.
2. The colon, which is the main portion of the large intestine, is divided into four
anatomic sections: ascending, transverse, descending and sigmoid.
3. The rectum extends from the sigmoid colon to the anus.
G. The ileocecal valve prevents the return of feces from the cecum into the small intestine
and lies at the upper border of the cecum.
H. H. The appendix, which collects lymphoid tissues, arises from the cecum
The GI tract is composed of five layers:
1. An inner mucosal layer lubricates and protects the inner surface of the alimentary canal.
2. A submucosal layer is responsible for secreting digestive enzymes.
3. A layer of circular smooth muscle fibers is responsible for movement of the GI tract.
4. A layer of longitudinal smooth muscle fibers also facilitates movement of the GI tract.
5. The peritoneum, an outer serosal layer, covers the entire abdomen and is composed of the
parietal and visceral layers.
II. Function. The GI system performs two major body functions: digestion and elimination.
A. Digestion of food and fluid, with absorption of nutrients into the bloodstream, occurs in the
upper GI tract, stomach and small intestines.
1. Digestion begins in the mouth with chewing and the action of ptyalin, an enzyme contained
in saliva that breaks down starch.
2. Swallowed food passes through the esophagus to the stomach, where digestion continues
by several processes.
a. Secretion of gastric juice, containing hydrochloric acid and the enzymes pepsin
and lipase ( and renin in infants)
b. Mixing and churning through peristaltic action
3. From the pylorus, the mixed stomach contents (i.e. chyme) pass into the duodenum
through the pyloric valve.
4. In the small intestine, food digestion is completed, and most nutrient absorption occurs.
Digestion results from the action of numerous pancreatic and intestinal enzymes (e.g.,
trypsin, lipase, amylase, lactase, maltase, sucrose and bile).
B. Elimination of waste products through defecation occurs in the large intestines and rectum. In
the large intestine, the cecum and ascending colon absorb water and electrolytes from the now
completely digested material. The rectum stores feces for elimination.

PATHOPHYSIOLOGY:
When cyst is swallowed, it passes through the stomach unharmed and shows no activity
while in an acidic environment. When it reaches the alkaline medium of the intestine, the
metacyst begins to move within the cyst wall, which rapidly weakens and tears. The
quadrinucleate amoeba emerges and divides into amebulas that are swept down into the cecum.
This is the first opportunity of the organism to colonize, and its success depends on one or more
metacystic trophozoites making contact with the mucosa.
Mature cyst in the large intestines leaves the host in great numbers (the host remains
asymptomatic). The cyst can remain viable and infective in moist and cool environment for at
least 12 days and in water for 30 days. The cysts are resistant to levels of chlorine normally used
for water purification. Purification, desiccation and temperatures below 5 and above 40 degrees
rapidly kill them.

The metacystic trophozoites of their progenies reach the cecum and those that are
exposed to the oral mucosa penetrate or invade the epithelium by lytic digestion.
The trophozoites burrow deeper with tendency to spread laterally or continue the lysis of
cells until they reach the sub-mucosa forming flash-shape ulcers. There may be several points of
penetration.

From the primary site of invasion, secondary lesions maybe produced at the lower level
of the large intestine.
Progenies of the initial colonies are squeezed out to the lower portion of the bowel and
thus, have the opportunity to invade and produce additional ulcers. Eventually, the whole colon
may be involved.
E. histolytica has been demonstrated in practically every soft organ of the body.
Trophozoites which reach the muscularis mucosa frequently erode the lymphatics or
walls of the mesenteric venules in the floor of the ulcers, and are carried to the intrahepatic portal
vein.
If thrombi occur in the small branches of the portal veins, the trophozoites in thrombi
cause lytic necrosis on the wall of the vessels and digest a pathway into the lobules.
The colonies increase in size and develop into abscess.
A typical liver abscess develops and consists of:
 Central zone necrosis

 Median zone of stoma only
 An outer zone of normal tissue newly invaded by amoeba. Most amoebic abscess of the
liver are in the right lobe.
Next to the liver, the organ that is the frequent site of extra-intestinal amoebiasis is the
lungs. This commonly develops as an extension of the hepatic abscess.

Laboratory Diagnosis:
1. Stool exam (cyst, white and yellow pus

with plenty of amoeba)
2. Blood exam (Leukocytosis)
3. Proctoscopy/Sigmoidoscoppy
Diagnosis of amoebiasis can be very difficult.

One problem is that other parasites and cells can look
very similar to E. histolytica when seen under a microscope. Therefore, sometimes people are
told that they are infected with E. histolytica even though they are not.Entamoeba histolytica and
another ameba, Entamoeba dispar, which is about 10 times more common, look the same when
seen under a microscope. Unlike infection with E. histolytica, which sometimes makes people
sick, infection with E. dispar does not make people sick and therefore does not need to be
treated. If you have been told that you are infected with E. histolytica but you are feeling fine,
you might be infected with E. dispar instead. Unfortunately, most laboratories do not yet have
the tests that can tell whether a person is infected with E. histolytica or with E. dispar. Until these
tests become more widely available, it usually is best to assume that the parasite is E. histolytica.
A blood test is also available but is only recommended when your health care provider
thinks that your infection may have spread beyond the intestine (gut) to some other organ of your
body, such as the liver. However, this blood test may not be helpful in diagnosing your current
illness because the test may still be positive if you had amoebiasis in the past, even if you are no
longer infected now.

Complications:
1. Amebic colitis
 Fulminant or necrotizing colitis
 Toxic megacolon
 Ameboma
 Rectovaginal fistulas
2. Amebic liver abscess

 Intrathoracic or intraperitoneal rupture with or without secondary bacterial infection
 Direct extension to pleura or pericardium
3. Brain abscess
Treatment:
1. Metronidazole (Flagyl) 800mg TID X 5 days

2. Tetracyline 250 mg every 6 hours
3. Ampicillin, quinolones sulfadiazine
4. Streptomycin SO4, Chloramphenicol
5. Lost fluid and electrolytes should be replaced
Several antibiotics are available to treat amoebiasis. Treatment must be prescribed by

a physician. You will be treated with only one antibiotic if your E. histolytica infection
has not made you sick. You probably will be treated with two antibiotics (first one and then the
other) if your infection has made you sick.

Nursing Management:
1. Observe isolation and enteric precaution

2. Provide health education and instruct patient to
 Boil water for drinking or use purified water

 Avoid washing food from open drum or pail
 Cover leftover food
 Wash hands after defacation and before eating
 Avoid ground vegetables (lettuce, carrots, and the like)
3. Proper collection of stool specimen

4. Never give paraffin or any oil preparation for at least 48 hours prior to collection of
specimen.
5. Instruct patient to avoid mixing urine with stools.
6. If whole stool cannot be sent to laboratory, select as much portion as possible containing
blood and mucus.
7. Send specimen immediately to the laboratory; stool that is not fresh is nearlyuseless for
examination. Label specimen properly.
8. Skin care
9. Cleanliness, freedom from wrinkles on the sheet will be helpful with all the usual
precautionary measures against pressure sores.
a. Mouth care
b. Provide optimum comfort.
 Patient should be kept warm. Dysenteric patient should never be allowed to feel,
even for a moment.
 Diet-During the acute stage, fluids should be forced.

 In the beginning of an attack, cereal and strained meat broths without fat should
be given.
 Chicken and fish maybe added when convalescence is established.
 Bland diet without cellulose or bulk-producing food should be maintained for a
long time.
Common Nursing Diagnosis:
1. Altered nutrition: Less than body requirement

2. Alteration in bowel elimination
3. High risk for infection
4. Anxiety
5. Altered body temperature
Methods of Prevention:
1. Health education
2. Sanitary disposal of feces
3. Protect, chlorinate, and purify drinking water
4. Observe scrupulous cleanliness in food preparation and food handling
5. Detection and treatment of carriers
6. Fly control (they can serve as vector)

PUBLIC HEALTH PREVENTION
 One important public health strategy is to make sure to treat infected individuals who
appear asymptomatic, since these people also pass cysts in their stool and thus
contributed to spreading the disease.
 Good sanitation and water facilities are also important in preventing the disease.
 Food handlers, childcare workers, and health care workers with amoebiasis should not be
allowed to work until their symptoms are gone.
 If children have symptoms, they should not attend childcare centers or schools until their
symptoms are gone.
 In general, people should practice good hygiene, since the fecal matter from those
infected could contaminate food and water that is then transferred to others. This includes
careful hand washing with soap and hot running water for at least 10 seconds after going
to the toilet, as well as practice frequent hand washing in general to eliminate any parasite
that one may have picked up throughout the day.
 Travelers should take precaution
 Clean bathrooms and toilets often.
 Boil water
 Avoid uncooked foods
 Practice safe food storage and handling: thoroughly cook all raw foods, thoroughly wash
raw vegetables and fruits, and reheat food until the internal temperature of food reaches
at least 167°F.

HOME PREVENTION
 Avoidance of drinking unboiled or unbottled water in endemic areas.

 Uncooked food such as fruit and vegetables that may have been washed in local water
should also not be consumed.
 Amoebic cysts are resistant to chlorine at the levels used in water supplies, but
disinfection with iodine may be effective.
 Wash hands with soap and warm water after going to the toilet and before eating or
preparing food.
 Proper food storage and preventing its contamination with feces, flies, and contaminated
water
 Avoiding sexual practices that may lead to fecal-oral contact.

Case Study of Amoebiasis

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METROPOLITAN MEDICAL CENTER

COLLEGE OF ARTS SCIENCE AND TECHNOLOGY

Pathogenic amoeba, which produce condition of a great clinical variation:

1. Acute Amoebic Dysentery

METROPOLITAN MEDICAL CENTER

Etiologic Agent: Enatamoeba Histolytica

 Prevalent in unsanitary areas

Entamoeba Histolytica has two developmental stages:

a. Acute amoebic dysentery

b. Chronic amoebic dysentery

 Abdomen loses its elasticity when picked up between fingers

METROPOLITAN MEDICAL CENTER

ANATOMY AND PHYSIOLOGY:

Esophageal openings include:

1. The upper esophageal sphincter at the

The GI tract is composed of five layers:

METROPOLITAN MEDICAL CENTER

METROPOLITAN MEDICAL CENTER

METROPOLITAN MEDICAL CENTER

The colonies increase in size and develop into abscess.

A typical liver abscess develops and consists of:

 Central zone necrosis

METROPOLITAN MEDICAL CENTER

1. Stool exam (cyst, white and yellow pus

Diagnosis of amoebiasis can be very difficult.

METROPOLITAN MEDICAL CENTER

2. Amebic liver abscess

1. Metronidazole (Flagyl) 800mg TID X 5 days

Several antibiotics are available to treat amoebiasis. Treatment must be prescribed by

METROPOLITAN MEDICAL CENTER

1. Observe isolation and enteric precaution

 Boil water for drinking or use purified water

3. Proper collection of stool specimen

METROPOLITAN MEDICAL CENTER

Common Nursing Diagnosis:

1. Altered nutrition: Less than body requirement

METROPOLITAN MEDICAL CENTER

METROPOLITAN MEDICAL CENTER

 Avoidance of drinking unboiled or unbottled water in endemic areas.

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