LEARNING OBJECTIVES:

Upon completion of this chapter, the student will be able to:

1. Define important terms related to infectious diseases affecting the gastrointestinal

tract.
2. Identify the common diagnostic exams prescribed to clients with GIT infection and its
relevance to their diagnosis.
3. Discuss the contributory/risk factors in the acquisition of infectious diseases of the
GIT.
4. Enumerate the common GIT diseases.
5. Discuss the role of the nurse in preventing the spread and control of GIT infections.

HISTORY OF AMOEBIASIS:

 Amebiasis is thought to have been discovered by Hippocrates, who described a

patient with fever and dysentery.
 1828 - The association between dysentery and amebic liver abscess was reported by
James Annesley, an Irish physician.
 1875 - E. histolytica was first isolated from a patient with dysentery by Fedor Losch, a
Russian physician.
 1903 - The organism was named Entamoeba histolytica by Fritz Schaudinn, a
German zoologist.
 1912 - Leonard Rogers, an English pathologist and tropical medicine specialist,
described the efficacy of emetine (first treatment) for the treatment of amebiasis.
 1925 - The life cycle of E. histolytica was first described by Clifford Dobell, an English
protozoologist.

AMOEBIASIS:

 Amoebiasis is a protozoal infection that initially involves the colon but may spread to
soft tissues by contiguity, 
 Amoebiasis is more closely related to poor sanitation and low socioeconomic status
than to climate.

ETOLOGIC AGENT:

Entamoeba histolytica 
 This protozoan prevalent in warm climate and areas with poor sanitation.
 The cyst can survive a few days outside the body.
 The cyst is swallowed via contaminated food or water and passes to the large
intestine.
 These hatch into trophozoites, passes into the mesenteric veins, to the portal vein,
and to the liver, forming amebic liver abscesses.

TWO DEVELOPMENTAL STAGES:

1. Trophozoites are the facultative form of the parasite that may invade tissues. They
are found in the parasitized tissues and liquid colonic contents.
2. Cysts are passed out with formed or semi-formed stools and are resistant to
environmental conditions. This is considered the infective stage in the life cycle of E.
histolytica.
INCUBATION PERIOD:

- Usually, one to four weeks but may be shorter or longer

- Hepatic amebiasis can present longer, from two to five months after exposure.

MODE OF TRANSMISSION:

1. Fecal - oral transmission

2. Humans most commonly acquire the disease by ingesting viable cysts from contaminated
water, food, and hands.

SOURCE OF INFECTION:
- Human excreta
PERIOD OF COMMUNICABILITY:
- For duration of the illness.
CLINICAL MANIFESTATION:
A. Acute amoebic dysentery is characterized by:
 Slight attack of diarrhea, alternating with periods of constipation and often
accompanied by tenesmus (painful straining defecation)
 Diarrhea, with watery and foul-smelling stools often containing blood-streaked mucus
 Colic and gaseous distension of the lower abdomen
 Nausea, flatulence, and abdominal distension, and tenderness in the right iliac region
over the colon
B. Chronic amoebic dysentery
 Attack of dysentery lasts for several days, usually followed by constipation
 Tenesmus accompanied by the desire to defecate
 Anorexia, weight loss, and weakness
 The liver may be enlarged.
  Vague abdominal distress, flatulence, constipation or irregularity of the bowel
 Mild toxemia, constant fatigue, and lassitude
 The stools are semi-fluid at first but soon become watery, bloody, and mucoid.
 The abdomen loses its elasticity when picked up between the fingers.
 Scattered ulceration with yellowish and erythematous border are observed during
sigmoidoscopy.
The gangrenous type (fatal cases) is characterized by the appearance of large sloughs
of intestinal tissue in the stools, accompanied by hemorrhage.

C. Amoebic colitis
 Amebic colitis develops two to six weeks after the ingestion of cysts.
 Lower abdominal pain and mild diarrhea develops gradually, followed by malaise and
weight loss.
 Patient may pass 10-12 stools consisting of blood and mucus with little fecal material.
 Patient may develop toxic megacolon and amebomas.

D. Extraintestinalforms
Extraintestinal amoebiasis can occur if the parasite spreads to other organs, most
commonly the liver where it causes amoebic liver abscess. Other organs may be
involved, causing pleuropulmonary, cardiac, cerebral, renal, genitourinary,
peritoneal, and cutaneous amoebic infections. Most patients develop these
symptoms within five months:
 Intermittent fever and right upper quadrant pain that radiates to the shoulders,
 Tenderness of the liver with right pleural effusion, and
 jaundice is rare.
 About 30% of the patients experience diarrhea.
 Elder patients may have weight loss and hepatomegaly.
 Abscesses may break through the lungs, and the patient coughs out anchovy sauce-
like sputum. Rupture of this abscess requires drainage.

DIAGNOSTIC PROCEDURE:
1. Stool exam (cysts, pus may be white or yellow with plenty of amoeba)
2. Blood exam (leukocytosis)
3. Liver scan via MRI
4. Proctoscopy/sigmoidoscopy is carried out by a specialized physician to prevent perforation.
5. Barium enema

TREATMENT MODALITIES:
 1. Metronidazole (Flagyl) 800 mg TID for five days
2. Tetracycline 250 mg every six hours
3. Ampicillin, quinolones, sulfadiazine
4. Streptomycin sulfate, chloramphenicol
5. Fluid and electrolytes should be replaced.

PREVENTION:
1. Health education
2. Sanitary disposal of feces
3. Protect, chlorinate, and purify drinking water.
4. Use scrupulous cleanliness in food preparation and handling.
5. Detection and treatment of carriers
6. Fly control (They can serve as vectors.)

NURSING MANAGEMENT:
1. Isolation, enteric precautions
2. Educate patients, their families and communities. Emphasize the points listed below.
3. Boil water for drinking/drink purified water.
Avoid washing food with water taken from open drums or pail.
4. Cover leftover food.
5. Wash hands after defecation or before eating.
Avoid ground vegetables (lettuce, carrots, etc).

PATHOGENES:
 The metacystic trophozoites or their progenies reach the cecum and those that come
in contact with the oral mucosa penetrate the epithelium by lytic digestion.
 The trophozoites burrow deeper and spread laterally with continuous lysis of cells
until they reach the submucosa, forming flask-shaped ulcers. There may be several
points of penetration.
 From the primary site of invasion, secondary lesions may be 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 infected.
  'Trophozoites that 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 cause lytic
necrosis on the wall of the vessels and make their way into the lobules.
 The colonies increase in size and develop into abscesses. A typical liver abscess
may consist of
1. central zone necrosis,
2. median zone of stroma only, and
3. an outer zone of normal tissue newly invaded by amoeba. Most amoebic abscesses
of the liver are in right lobe.
 Next to the liver, the most frequent site of extraintestinal amoebiasis are the lungs.
This commonly develops as an extension of the hepatic abscess.
 Extension from the liver abscess can lead to pleural and pericardial effusion.

PATHOPHYSIOLOGY:
Ingestion of the cyst

Multiplication in the intestinal mucosa

Endotoxin production affecting the lining of the small intestine, colon, and capillaries

Necrosis of the mucosal layer of the intestines

Necrotic layer sloughs off leaving an ulcer

Gangrene

Toxemia

Death

When the cyst is swallowed, it passes through the stomach unharmed and shows no activity
while in the acidic environment of the stomach. When it reaches the alkaline medium of the
intestine, the (metacys) 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.

Meanwhile, mature cysts in the large intestine leave the host in great numbers (the host
remains asymptomatic). The cyst can remain viable and infective in a moist and cool
environment for at least 12 days, and will survive in water for 30 days. Cysts are resistant to
levels of chlorine normally used for water purification. They are rapidly killed by putrefaction,
desiccation, and temperatures below 5 °C and above 40 °C.

The trophozoites remain confined to the intestinal lumen of individuals who are
asymptomatic carriers and cyst passers. In some patients, the trophozoites invade the
intestinal mucosa. The parasites may gain access to extraintestinal sites such as the liver,
brain, and lungs through the bloodstream.