Diseases Affecting GI Tract

Chapter 3
Diseases Affecting the Gastrointestinal Tract
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 (GIT).
2. Enumerate the common GIT diseases affecting children, adults, and older adults.
3. Discuss the contributory/risk factors in the acquisition of infectious diseases of the GIT.
4. Identify the common diagnostic exams prescribed to clients with GIT infection and its relevance to
their diagnosis.
5. Implement the type of isolation needed by a specific disease condition.
6. Prepare a comprehensive nursing care plan for clients suffering from infectious diseases of the GIT.
7. Discuss the role of the nurse in preventing the spread and control of GIT infections.
The gastrointestinal (GI) tract is a series of hollow organs that form a long, twisting tube. It is made
up of the mouth (oral cavity), esophagus, stomach, small intestine, large intestine, and the anus. The liver,
pancreas, and gallbladder are solid organs that serve as the accessory organs of the digestive system.
The small intestine is divided into three parts. The first is called the duodenum. The jejunum. is in
the middle and the ileum is at the end. The large intestine includes the appendix, cecum, colon, and
rectum. The appendix is a finger-shaped pouch attached to the cecum. The cecum is the first part of the
large intestine. The colon is in the middle and the rectum is the terminal segment and extends to the anus.
The digestive system has two main purposes.

1. It breaks down food into simple substances that can be absorbed by the blood and transported to
all cells of the body.
2. It eliminates solid remnants of food consumed, as well as excretion of some water. Diseases in the
GI system usually results in signs and symptoms related to hemorrhage, altered motility, and
perforation (Neighbors and Tannehill-Jones, 2008).
Gastrointestinal infections are among the most commonly encountered concerns in primary care.
Even if they are not always severe and often resolve rapidly, they can be serious in specific settings.
Gastrointestinal infections could be viral, bacterial, protozoal, or parasitic. These infections cause
gastroenteritis, an inflammation of the gastrointestinal tract which involves the stomach and the small
intestine.
Although gastrointestinal infections can be resolved in a few day specific populations such as
newborns, infants, the immunocompromised, and elderly patients are potentially at risk.
Symptoms include:
a. Diarrhea
b. Vomiting
c. abdominal pain
d. Dehydration is the main danger associated to gastrointestinal infections, so rehydration is
paramount in managing these conditions.
AMOEBIASIS
(Amoebic dysentery)
Definition
Amoebiasis is a protozoal infection that initially involves the colon but may spread to tissues by
contiguity, or via hematogenous/lymphatic dissemination, most commonly to the liver or lungs.
Amoebiasis is more closely related to poor sanitation and low socioeconomic status than to climate. It is
the third leading cause of death from parasitic disease world.
(Fauci, 2008).
Etiologic Agent
Entamoeba histolytica
● This protozoan is prevalent in warm climates 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 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 (Kwan-Gett, 2009)
Mode of Transmission
1. Fecal-oral transmission
2. Humans most commonly acquire the disease by ingesting viable cysts from contaminated water,
food, and hands. Food or drinks may be tainted by cysts through polluted water supplies, as well as
using night soil for fertilizing vegetables. Unhygienic practices of food handlers can also transmit
the parasite.
3. A less common means of infection is through sexual contact such as orogenital, oroanal, or
proctogenital sexual activity.
4. Vectors such as flies, cockroaches, and rodents can also transmit the infection.
Sources of Infection
Human excreta
Period of Communicability
For duration of the illness.
Pathology
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
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.
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, 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 lung through the bloodstream.
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
FIGURE 3.1 Pathogenesis of amoebiasis
Pathogenesis
● 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 In the
mesenteric venules in the floor of the ulcers, and are carried to the intrahepatic part 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,
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.
Clinical Manifestations
1. 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
2. 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.
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.
● Boil water for drinking/drink purified water.
● Avoid washing food with water taken from open drums or pails.
● Cover leftover food. Wash hands after defecation or before eating
● Avoid ground vegetables (lettuce, carrots, etc.)
BACILLARY DYSENTERY (Shigellosis; Bloody flux)
Definition
Bacillary dysentery is an acute bacterial infection of the intestines characterized by diarrhea and
fever associated with bloody-mucoid stools with tenesmus.
Etiologic Agent
The causative agent is a bacterium from the genus Shigella. It is a short, non-mole, Gre negative
organism. There are four serologic groups that may cause diseases in humans.
1. Shigella flesneri (Group B) common in the Philippines, ale snolon uphill
2. S. boydii;
3. S. connei; and
4. S. dysenterae,
● considered as the most infectious
● their habitat is exclusively the GIT of humans,
● like other Gram-negative bacilli, they develop resistance against antibiotics and that
● they rarely invade the bloodstream.
Incubation Period
Seven hours to seven days with the average of three to five days
● Ingestion of contaminated food or drinking contaminated water or milk

● Transmitted by flies or other objects contaminated by the feces of the patient
● Fecal-oral transmission stew boiling
● Having sex that involves oro-anal contact
● Fruits and vegetables growing close to the ground can be contaminated if washed in polluted water
or grown in soil fertilized with human waste.
The patient is capable of transmitting the microorganisms during the acute infection until the
fecalysis result confirms negative results for the organism. Some patients remain carriers a year or two.
Pathogenesis/Pathology
● After the incubation period, the organism invades the intestinal mucosa and causse inflammation.
● They penetrate the lining of the intestine, and cause swelling, ulcerations, and severe diarrhea
containing blood and pus.
● Dirty, green fibrinous sloughing areas or ulcers start to form.
● Within a few days, the stool may contain pus, mucus, and blood.
● Fever, specially in children

● Tenesmus, nausea, vomiting, and headache
● Colicky or cramping abdominal pain associated with anorexia and body weakness
● Abdominal cramps and flatulence
● Diarrhea with bloody-mucoid stools that are watery at first
● Urgency to pass stools and the feeling of incomplete emptying
● Dehydration and rapid weight loss
● Mild cases of bacillary dysentery may last four to eight days, while severe cases may last three to six
weeks.
Diagnostic Procedures
● Fecalysis or microscopic examination of the stools

● Isolation of the causative organism from rectal swab or culture
● Peripheral blood examination
● Blood cultures
● Sheets of polymorphoneuclear leukocytes seen in staining with methylene blue
Complications
● Rectal prolapse, particularly in undernourished children Respiratory complications, such as cough

and pneumonia
● Non-suppurative arthritis and peripheral neuropathy
● If the infection of the bowel is especially virulent, the intestinal ulcerations may lead to bowel
perforation and death.
Prevention and Control
● Ensure sanitary disposal of human feces.

● Implement strict supervision of sanitary processing, preparation, and serving of food, particularly
those eaten raw. eboot bondo to bevisen hoog ni violarid
● Avoid eating foods cooked in unhygienic circumstances, such as from street vendors.
● Provide adequate safe washing facilities 26 awon oela el meilutod baco
● Drink only boiled or commercially bottled water. Do not use ice unless it is made from purified
water.
● Consider traveling with an alcohol-based hand sanitizer.nl) melland fastester
● Carry out fly control and protect food and water against contamination.
● Isolate the patient during the acute stage.
● Antibiotics such as ciprofloxacin, ofloxacin, levofloxacin, or azithromycin

● Iodoquinol and co-trimoxazole may be useful in severe cases.
● IV infusion with normal saline (with electrolyte) to prevent dehydration to bilo
● A bland diet (bananas, rice, soda crackers) is recommended. Avoid milk products.
● Anti-diarrheal drugs are contraindicated because they delay fecal excretion that can lead to
prolonged fever.
Nursing Management
● Maintain fluid and electrolyte balance to prevent profound dehydration.

● Restrict food until nausea and vomiting subsides.
● Carry out enteric isolation through medical aseptic technique.
● Maintain personal hygiene.
● Observe proper disposal of excreta.
● Implement concurrent and terminal disinfection.
BOTULISM
Definition
Botulism is a severe type of food poisoning caused by a neurotoxin released by Clostridium

botulinum. This toxin can induce serious illness and even paralysis. Even one case is considered an
emergency because of the virulence of the disease and its potential for bioterrorism (Kwan Gett, 2009).
Three Forms of Botulism in Humans
1. Food-borne (classical) botulism usually results from ingestion of inadequately cooked or boill
contaminated food, especially those with low-acid content. C. botulinum produces spores that can
survive in poorly preserved or canned foods, where they are capable of producing the toxin. When
consumed, even small amounts can cause severe poisoning.
2. Wound botulism is also known as cutaneous botulism. It is characterised by the formation of ulcers
with sharply demarcated edges and a membranous base as a result of deposition of the toxin in the
area.
3. Intestinal botulism (formerly infant botulism) usually afflicts infants aged 3-20 weeks This occurs
when the baby ingests contaminated food or soil. The spores germinate in the intestines and
produce a neurotoxin. The disease can cause hypotonic (floppy) infant syndrome, manifested by:
a. constipation
b. feeble cry
c. depressed gag reflex
d. inability to suck.
Toxins released by the organism can cause infant death by weakening or paralyzing the muscles of
the tongue and pharynx that are innervated by the cranial nerve IX to XII.
Etiologic Agent
Botulism is caused by Clostridium botulinum, which has the following characteristics:

● It is a Gram-positive, spore-forming, anaerobic organism whose natural habitat is the soil.
● The spores can withstand boiling for several hours.
● The organism produces botulinum toxin, which is the most lethal toxin known to humans. The toxin
damages the nerves by inhibiting the release of the neurotransmitter acetylcholine
Incubation Period
The usual incubation period is 12-36 hours, ranging from two hours to eight days, depending on the
following factors:
1. The amount of toxin ingested/absorbed. It follows that the more toxin absorbed, the shorter the
incubation period, and the more serious the disease will be more
2. In children, the incubation period is two to four weeks.
3. Wound botulism has longer incubation period and may take up to 10 days.
Pathogenesis
All the three forms of botulism produce disease via a final common pathway. The toxin is
disseminated to peripheral cholenergic synapses and blocks acetylcholamine, causing impaired autonomic
and voluntary neuromuscular transmission.
Clinical Characteristics
● Regardless of the source of botulinum toxin, whether it is ingested, produced in a wound or in the
infant gut, cranial nerve involvement marks the onset of symptoms manifested by diplopia,
dysarthria, and/or dysphagia.
● The somatic musculator is affected next, so that the patient may have generalized weakness.
Because the toxin is bloodborne, paralysis almost invariably displays symmetry as it descends.
Flaccid paralysis appears first and descends via the bulbar musculator. The descending paralysis can
lead to respiratory failure and death.
● Nausea, vomiting, and abdominal pain may precede or follow the onset of paralysis Dizziness,
blurred vision, dry mouth, and sore throat occur. The patient has fixed and dilated pupils.
Complications
● Hospital-acquired or aspiration pneumonia

● Urinary tract infection can occur due to Foley or indwelling catheter male
● Pulmonary embolism
● Flexion contractures
Treatment/Management
1. Supportive care with particular attention to respiratory and nutritional needs

2. In cases of food-borne botulism, emetics and gastric lavage are recommended
3. In wound botulism, exploration and debridement of the site is undertaken.
1. Health education through health instruction on proper preparation of food, specially home canning.
2. Do not give infants honey as it is a source of C. botulinum
CHOLERA
Definition
Cholera is an acute bacterial disease of the GIT characterized by profuse diarrhea, vomiting and
massive loss of fluid and electrolytes that could result in hypovolemic shock, acidosis, and death.
Pathognomonic sign
Rice-water stools
Etiologic Agent
Vibrio cholerae/Vibrio comma

● The organisms are slightly curved rods (comma-shaped), Gram-negative and motile with a
single polar flagellum.
● Vibrio survives well at ambient temperature and can grow well between 22 °C-40 °C. It can
also can survive longer in refrigerated foods.
● An enterotoxin, choleragen, is elaborated by the organism as they grow in the intestinal
tract.
Incubation Period
A few hours to five days; usually one to three days
1. Fecal-oral route via contamination of water, milk, and other foods

2. Ingestion of food or water contaminated with stools or vomitus of the patient
3. Flies, soiled hands, and utensils can also harbor V. cholerae.
The disease is communicable during the time the stool tests positive for the organism, and may
continue up to a few days after recovery. However, an occasional case may remain a carrier for several
months.
Pathogenesis and Pathology
● Fluid loss is attributed to the enterotoxin elaborated by the organism as they lie opposite to the
lining cells of the intestines.
● The toxin stimulates adenylate cyclase, resulting in conversion of the adenosine triphosphate (ATP)
to cyclic adesine monophophate (CAMP).
● This stimulates the mucosal cell to increase secretion of chloride, associated with water n and
bicarbonate loss.
● The toxin acts upon the intact epithelium on the vasculator of the bowel, resulting into outpouring
of intestinal fluids.
● Fluid loss of 5%-10% of the body weight will result in dehydration and metabolic acidosis.
● If treatment is delayed or inadequate, acute renal failure and hypokalemia become secondary
problems.
Vibrio cholerae
Enterotoxin (choleragen)
Acts upon the epithelium of the bowel, resulting outpouring of intestinal fluids
Principal Fluid Deficits
Dehydration and metabolic acidosis
Acute renal failure
Lactic acidosis
FIGURE 3.2 Pathogenesis of cholera
Principal Fluid Deficit
1. Extracellular volume - loss of intestinal fluid can lead to:

a. Severe dehydration with the appearance of "washerwoman's hand", restlessness and
excessive thirst.
b. Circulatory collapse or shock
2. Metabolic acidosis is due to loss of large volume of bicarbonate-rich stools that results in rapid
respiration with intervals of apnea (Kussmaul respiration).
3. Hypokalemia is the result of massive loss of potassium in stools. The patient may manifest
abdominal distention that could be attributed to paralytic ileus.
● There is an acute, profuse, watery diarrhea with no tenesmus or intestinal cramping. Initially, the
stools are brown and contain fecal material, but soon become pale gray, translucent and "rice-
water-like" with an inoffensive, slightly fishy odor.
● Vomiting often occurs after the diarrhea has been established.
● Diarrhea causes fluid loss amounting to 1-30 liters per day, causing dehydration and electrolyte
loss.
● Tissue turgor is poor, and the eyes are sunken into the orbit.
● The skin is cold, the fingers and toes are wrinkled, assuming the characteristic "washerwoman's
hand" appearance.
● Radial pulses become imperceptible and the blood pressure cannot be obtained.
● Cyanosis is present due to impending vascular collapse.
● The voice become hoarse and is then lost, so the patient speaks in a whisper (aphonia)
● Breathing is rapid and deep. Despite marked diminished peripheral circulation, the patient remains
conscious.
● The patient develops oliguria that may even lead to anuria.
● The temperature may be normal at the onset of the disease, but becomes subnormal in later
stages, especially if the patient is in shock.
● When the patient is in deep shock, the passage of diarrhea stops.
● Death may occur in as short as four hours after onset, but usually occurs on the first or the second
day if not properly treated.
1. Rectal swab
2. Darkfield or phase microscopy
3. Stool exam
The treatment of cholera consists in correcting the basic abnormalities without delay, as well as
restoring the circulating blood volume and blood electrolytes to normal levels.
1. Intravenous treatment involves a rapid intravenous infusion of alkaline saline solution containing
sodium, potassium, chloride, and bicarbonate ions in proportions Cest comparable to those in the
rice water stools.
2. Oral therapy - rehydration can be completed by oral route (Oresol, Hydrites) unless contraindicated
or if the patient is not vomiting.
3. Maintenance- after rehydration is completed, the volume of fluid and electrolyte loss must be
replaced. This is done by careful intake and output measurement.
4. Antibiotics
a. Tetracycline 500 mg every six hours for adults, and 125 mg/kg body weight gain for children
every six hours for 72 hours.)
b. Furazolidone - 100 mg for adults and 125 mg/kg for children, every six hours for 72 hours
c. Chloramphenicol - 500 mg for adults and 18 mg/kg for children every six hours for 72 hours
d. Co-trimoxazole - 8 mg/kg for 72 hours
Prevention
1. Protect food and water supplies from fecal contamination

2. Water should be boiled or chlorinated.
3. Milk should be pasteurized.
4. Dispose of human excreta properly.
5. Implement sanitary supervision of food handlers.
Nursing Management
1. Carry out strict medical aseptic practices as protective care.
2. Implement enteric isolation.
3. Obtain accurate vital signs and record accordingly.
4. Ensure accurate measurement of intake and output to determine the level of hydration.
5. Provide thorough and careful personal hygiene.
6. Proper disposal of excreta
7. Carry out concurrent disinfection.
8. Instruct the patient and significant others about proper preparation and storage of food.
9. Maintain environmental sanitation.
HELMINTHS
Helminths are metazoa (organisms that are comprised of different cells and have a digestive cavity
lined with special cells) that feed on a living host to gain nourishment and protection, while causing poor
nutrient absorption, weakness, and disease in the host. Adult worms and larvae commonly live in the small
bowel and are referred to as intestinal parasites.
Helminths are multicellular organisms that are often visible to the naked eye. They are usually
contracted through consuming tainted food or treading on contaminated soil in warm, humid countries
that have poor sanitation and hygiene.
All parasitic worms produce ova (eggs) for reproduction. These eggs have a strong shell that
protects the embryos against a range of environmental conditions and allows them to survive in the soil or
bodies of water for many months to years.
If an infected person or animal defecates on the ground, the helminth eggs present in their feces
contaminate the soil. These eggs hatch into larvae that grow into adult worms up to 13 mm in length.
Some species can penetrate human skin, specially if a person walks on barefoot on soil that contains the
larvae.
There are three groups of helminths that cause diseases in people. They have different
morphologies and infect humans in various ways.
Nematodes, also known as roundworms, belong to the phylum Nematoda and are found in a range
of habitats. They can exist as free-living organisms in terrestrial and aquatic environments, but some
species are parasitic to plants and animals.
● Roundworms are cylindrical and most species are dioecious, meaning the male and female are
separate. Copulation is essential to fertilization.
● Some nematodes that are parasitic to humans lay eggs that contain either a zygote or a completely
formed larva.
● Their developmental process includes the egg, larva, and adult stages.
● They can infect humans through:
a. Direct infection takes place when the eggs are transmitted through the oral-fecal route
without reaching the soil (pinworms and whipworms).
b. Modified direct infection occurs when eggs are passed in feces. Some species require
incubation time in the soil and pass the fecal-oral route (Ascaris lumbricoides). Other species
(Ancylostoma duodenale and Necator americanus) must penetrate human skin.
● Ascaris infections are rarely noticed unless adult worms are passed in the stools.
● In heavy infections, several worms may form a bolus and cause intestinal
obstruction, volvulus, or perforation.
● Worms can 'wander' around the host, obstructing ducts and diverticula, causing
biliary colic, cholangitis, liver abscess, pancreatitis, or appendicitis.
● Worms are sometimes coughed up in sputum.
Cestodes, also known as tapeworms, are segmented parasites classified under phylum
Platyhelminthes. They are hermaphroditic, which means each organism has a set of functional male and
female reproductive organs. They also possess a specialized rostellum which they use to attach to the
intestinal lining of the host.
Trematodes (flatworms or flukes) are flat, leaf-shaped, and unsegmented. They belong to the
phylum Platyhelminthes and are also hermaphroditic, except for some notable species that parasitize
humans (blood flukes, such as Schistosoma). These parasites often require several hosts; a primary host,
usually a vertebrate, and a secondary host (a mollusk, a fish, or a water plant) to complete their life cycle.
ASCARIASIS
(Roundworm infection)
Definition
Ascariasis is an infection caused by a parasitic roundworm Ascaris lumbricoides, also known as the
giant roundworm.
● Ascaris is the largest nematode parasite found in humans, reaching up to 40 cm in length. They are
elongated and cylindrical, and are tapered at the oral portion and pointed at the anal end.
● They have a creamy and pinkish yellow appearance when passed out with stool.
● Eggs are transmitted through contaminated fingers that are put into the mouth. Ingestion of food
and drinks contaminated with embryonated eggs.
Epidemiology
● Ascariasis occurs worldwide but is most common in tropical regions, especially in areas with poor
sanitation and in places where farmers use night soil as fertilizer.
● It has an infection rate of 70%-90% in poor areas of the Philippines and mostly affects children 4-12
years oldAscariasis is considered as the most prevalent form of parasitism in the Philippines.
● Children with poor nutritional status exhibit high incidence of positive ascaris in stool examination.
Pathogenesis
Infection may start from ingestion of embryonated ova in contaminated water or from eating raw
vegetables cultivated from fields where night soil is used as fertilizer. After ingestion, the eggs hatch and
the larvae penetrate the intestinal wall and reach the lungs through the bloodstream. After 10 days in the
pulmonary capillaries and alveoli, the larvae migrate to the bronchioles, the bronchi, trachea, and
epiglottis. They are then swallowed and return to the intestine where they mature and mate (Table 3.1).
TABLE 3.1 The life cycle of Ascaris lumbricoides
Developmental Stage Symptomatology
1. Embryonated ova
● Soil contamination with human
excreta
● Food, water, and other objects are
contaminated
● Ova are ingested and reach the
intestine
2. Larva ● Nausea and vomiting, poor appetite

● Penetrate the wall of the intestine ● Periumbilical pain
(duodenum) ● Right upper quadrant pain
● Picked up by lymphatics or ● Cough, fever, rales, blood-tinged
bloodstream, arrive at the liver, the sputum
heart, the stomach, esophagus, to ● Nasal pruritus if larvae reach nostrils
the upper respiratory tract
● Capillaries of the lungs, to the alveoli
where they grow and
3. Adults ● Colicky, paraumbilical pain

● In the small intestine aggravated by cold stimulation
gridbest ditleoH E
● At times they move erratically and (Nakamura sign)
go to the stomach, the esophagus, ● Intestinal obstruction may be caused
and sometimes the common bile by bolus of entangled worms (which
duct and the gallbladder may be palpable)
● They copulate in the GIT. The female ● Severe abdominal pain associated
lay eggs about 2-3 months after with vomiting
embryonated eggs are ingested.
1. The stool is examined for ova. The Kato technique is used to demonstrate fertilized or unfertilized
eggs in the stool.
2. An abdominal X-ray will reveal a dense shadow of adult ascaris which looks like strands of spaghetti,
the "dot" sign.
3. Routine blood counts show significant eosinophilia.
Complications
1. Hepatic abscess and cholangitis

2. ntestinal obstruction, perforation, and peritonitis daily.
3. In cases of biliary tract obstruction, the patient develops cholestatic jaundice.
4. Malnutrition results from damage to the intestinal mucosa, impairing the absorption of nutrients.
Treatment
1. Albendazole or mebendazole - 15 cc as a single dose

2. Piperazine citrate - 75 mg/kg, daily x two doses orally
3. Pyrantel pamoate - 1 mg/kg as a single dose, orally
Prevention
1. Improved sanitation and hygienic practices

2. Improved nutrition
3. Deworming may be advised.
Nursing Interventions
1. No isolation is needed.
2. Enforcement of preventive measures in each home and in the community
3. Health teaching must be given to all members of the family. Train them to wash the hands before
handling food, and that all fruits and vegetables eaten raw must b thoroughly washed. Instruct
them about effective sewage disposal.
4. Inspection for the availability of toilet facilities and emphasis on proper sewagelex disposal must be
reiterated.
5. The importance of personal hygiene should be emphasized.
ANCYLOSTOMIASIS
(Hookworm infection, Miner's disease, Egyptian chlorosis)
Definition
Ancylostomiasis is caused by two species of hookworms. Symptoms include diarrhea or cramps.

Hookworm infection mostly occurs in tropical and subtropical countries. According to the CDC,
ancylostomiasis mainly affects people in developing nations due to poor sanitation.
Etiologic Agents
1. Ancylostomia duodenate, the Old World hookworm, is most prevalent in Europe and Asia.
2. Necator americanus is commonly known as the New World hookworm.
Both species are pathogenic to humans and share a similar life cycle. However, they have slight
differences in the structure of the mouth. They both have piercing mechanisms (hooks) by which they
attach themselves to the intestinal mucosa.
A female hookworm may produce as many as 10,000 to 20,000 eggs per day. These are deposited
in the soil and will develop into embryos within 24-72 hours. It takes about six weeks for the embryo to
develop into mature larvae. The larvae remain viable in the soil for several weeks under favorable
conditions.
A person contracts hookworms by coming into contact with soil that contains larvae. Ground itch
may occur at the site of penetration. The larvae enter the skin, travel through the bloodstream, and enter
the lungs. They are carried to the small intestine when the person coughs them out of the lungs and are
subsequently swallowed. They can live in the small intestine for a year or more before passing through the
feces.
Most patients remain asymptomatic, but will often experience abdominal discomfort, flatulence,
anorexia, nausea, vomiting, and diarrhea that sometimes contains blood and mucus.
Incubation Period
Hookworm ova appear in the stools about four to six weeks after the larvae penetrate the skin.
● Incubation period is 40-100 days or two to eight weeks.
● Hookworms are usually directly acquired through the skin of the foot, specifically the soft skin
between the toes (ground itch).
● Ingestion of contaminated drinking water or food
● Carriers can spread the infection as long as they have the parasites in their GIT.
Symptoms
Symptoms of hookworm disease depend upon the number of worms present in the intestines.
● The worm engulfs small bits of tissue from the intestinal mucosa, causing small lesions. They feed
on the host's blood and may consume 50 mL of blood daily. The gradual blood loss results in iron
deficiency anemia.
● Other symptoms include abdominal pain, diarrhea, and allergic reactions like urticaria.
● Children infected with worms are often physically and mentally underdeveloped, Blood have a
protruding abdomen, and are lethargic. They tend to be malnourished and undersized. The pupils
are more or less dilated. Pedal edema may be present, and may also occur in other areas of the
body.
● Children with hookworm infection may also present appetite problems.
Incidence
● The incidence varies, but ancylostomiasis is still considered as the most important helminth
infection of humans.
● All persons, regardless of age, race or sex, are susceptible to hookworm disease.
● The greatest incidence of infection is found among persons between 15 and 25 years of age.
● The disease is primarily found in rural areas where sanitary disposal of human excreta is
inadequate.
● It occurs in tropical and subtropical countries where the climate is warm and humid and where
people do not wear shoes in a regular basis. These circumstances provide an environment for the
infection to flourish.
Pathology
● The larvae penetrates the unbroken skin of the feet and legs of the host, and enter through the
sudoriferous (sweat) glands and the hair follicles.
● They penetrate the blood and lymph vessels, damaging them in the process. The larvae then enter
the inferior vena cava to the right atrium, to the lungs where they pierce the capillary walls and
pass into the alveoli.
● Some may be coughed out and expectorated, while some are swallowed and reach the small
intestine where maturation occurs and egg production takes place.
● Microscopic examination of feces for the eggs

● Blood exams reveal eosinophilia.
● Pyrantel embonate (Quantrel)

● Tetrachloroethylene
● Carbon tetrachloride
Prevention
● Provide health education on the proper disposal of excreta.

● Regulations to prevent the pollution of streams and lakes with human excreta should be adopted.
● All persons in areas where hookworms are endemic should avoid walking barefoot.
● Good hygiene is extremely important.
● Animals should not be allowed to defecate on the streets or beaches where people most likely
linger.
● Use boiled or purified water for drinking.
● Vegetables should not be eaten raw.
Nursing Management
● Isolation is not necessary.

● The diet should be high in calories, vitamins, and minerals.
● Instruct the patient to maintain good personal hygiene.
TAENIASIS
(Tapeworm infection)
Definition
Tapeworms are flat, segmented worms that live in the intestines of some vertebrates. Animals can
become infected with these parasites while grazing in pastures or drinking contaminated water. Eating
undercooked meat from infected livestock or game is the main cause of tapeworm infection in people
(WebMD).
Taeniasis or intestinal tapeworm infections are usually mild, with only one or two adult tapeworms
in the intestines. However, invasive larval infections can cause serious complications.
Etiologic Agent
Taenia solium, the pork tapeworm, was once prevalent worldwide but is now rare in developed
countries. However, it is still fairly common in developing countries, such as in parts of Asia and the non-
Islamic areas in Africa.
An adult tapeworm has a scolex or head, which the parasite uses to attach itself to the host. The distal
portion of the scolex is the neck; this area is the segment where the proglottids are formed. When the
person has an intestinal tapeworm infection, the tapeworm head adheres to the intestinal wall, and the
proglottids grow and produce eggs. Adult tapeworms can live for up to 30 years inside a host.
Incubation Period
From ingestion of eggs: 10-14 weeks
The infection is transmitted through ingestion of food or water contaminated with the worm either
through direct contamination or by contaminated hands.
Signs and Symptoms

Manifestations depend on the site of infection, the size, and number of lesions and the host's
immune response.
1. Taeniasis initially appears asymptomatic, except for mild gastrointestinal symptoms such as nausea
and vague abdominal pain.
2. If tapeworm larvae migrate out of the intestine and form cysts in other tissues they can eventually
cause organ and tissue damage, resulting in cystic masses or lum as well as neurological signs and
symptoms, including seizures.
3. Visual disturbances may occur from ocular involvement to cranial nerve impairment
Complications
1. Large parasite loads and/or a strong immune response from the host can lead to a severe
manifestation of neurocysticercosis (infection of the brain by the larval form of the pork tapeworm;
larvae can form giant cysts in the brain).
2. Stroke, spinal cord compression, and encephalitis
3. Encephalitis is more common in children and young adults.
Treatment
1. Praziquantel 5-10 mg/kg body weight is used for taeniasis and other intestinal tapeworms
2. Supportive treatment includes:
a. anticonvulsants for seizures
b. treatment for intracranial hypertension should be urgent, and takes priority over
antiparasitic therapy.
Prevention
1. Practice improved sanitation and proper disposal of feces

2. Encourage handwashing after use of toilets and before eating.
3. Avoid using night soil as fertilizer.
4. Cook meats such as pork and beef thoroughly.
ENTEROBIASIS
(Pinworm infection, Oxyuriasis)
Definition
Enterobiasis (or pinworm, threadworm, seatworm) infection is one of the most common types of
human intestinal worm infections. Pinworms are tiny, narrow worms that are white in color and just about
half an inch long. Enterobiasis is an infection that occurs worldwide and most prevalent in school-aged
children ages 5-10 years in areas of high population densities.
Etiologic agent and Pathogenesis
● Enterobiasis is caused by the intestinal nematode Enterobius vermicularis. Humans are the only
known host. The lifespan of pinworms generally is 13-15 weeks.
● The adult worms live in the lumen of the ascending colon, and the female migrates down to the
anus at night to deposit her eggs on the perianal skin. The female worms and their eggs invariably
cause perianal pruritus.
● Scratching the affected area facilitates the transfer of the eggs from the fingers to the mouth of the
host. The eggs can survive for several hours on the hands of a person.
● When contaminated hands touch household objects like beddings, clothing, toilet seats, or toys, the
eggs will transfer to these. Pinworm eggs can survive on contaminated surfaces for up to three
weeks.
● The eggs are then ingested and remain in the intestines where they mature over several weeks.
● Reinfection may occur. Reinfection is the migration of the newly hatched larvae from the perianal
area up to the large intestine.
● The eggs may be transmitted to others through direct contact or transfer from infected materials,
such as linens, clothing, or food (Kwan-Gett, 2009)
● The interval from ingestion of infective eggs to oviposition by the adult females is about one month.
The life span of the adult is about two months.
Incubation Period
The ingestion of the eggs to the deposition of the next generation of ova on the perianal area takes
only three to five weeks.
Signs and Symptoms
1. Pruritus ani (itching of the anus) varies from mild to severe.

2. Excoriation of the anus secondary to bacterial infection
3. Vulvovaginitis is the inflammation of the vulva, and occurs if the worms happen to enter this area.
4. Children can present with vague symptoms, such as, restlessness, insomnia, less appetite, and
enuresis.
A tape test is the most reliable method for diagnosing a pinworm infection. This is done by taking a
piece of cellophane tape (Scotch tape), wrapping it around a tongue depressor with the adhesive side out.
The sticky side is then pressed against the skin around the anus, usually done early morning before the
child/person cleanses his/her anus. The tape is peeled off and sent to a laboratory for microscopic
examination.
The CDC recommends that the test should be done at least three times, on three consecutive
mornings, to increase the likelihood of finding pinworm eggs.
Complications
1. Peritonitis, though uncommon, occurs when the worms find their way into the peritoneal cavity.
2. Granulomatous nodules may occur in some abdominal organs due to invasion of the worms.
Prevention
1. Reiterate hygiene and cleanliness, including handwashing.

2. Wear clean clothes, change linens, and maintain sanitary conditions around the house.
Treatment
The following drugs usually are prescribed by the doctor. Since pinworm infection is very
communicable, that "if one member of the family has it, everybody will have it", it is advised that all
members of the family have to be treated. The common drugs prescribed are:
a. Albendazole is the treatment of choice given as a single oral dose (400 mg for adults 10-14 mg/kg
body weight for children.
b. Mebendazole is given as an initial single dose, 100 mg to be repeated after 2-4 weeks.
c. Pyrantel pamoate may also be given as a single oral dose 10 mg/kg body weight and is repeated
every four to six weeks until the patient is clear of the infection (Kwan-Gett 2009).
SCHISTOSOMIASIS
(Bilharziasis; Snail fever)
Definition
Schistosomiais or bilharziasis is a slow, progressive disease caused by blood flukes of class

Trematoda. It is a chronic wasting disease common among farmers and their families in certain parts of the
Philippines. After malaria and intestinal helminthiasis, schistosomiasis is the third most devastating tropical
disease in the world, being a major source of morbidity and mortality for developing countries in Africa,
South America, the Caribbean, the Middle East, and Asia. It is not only a public health concern but also a
socioeconomic problem, because by causing ill health, it reduces the agricultural productivity of people.
Etiologic Agents
The cause of the disease are three blood flukes of genus Schistosoma.
● Schistosoma japonica
○ Infects the intestinal tract. (Katayama disease)
○ The only type that is endemic in the Philippines
○ This is also known as "Oriental schistosomiasis"
● Schistosoma mansoni
○ Also affects the intestinal tract
○ Common in some parts of Africa
● Schistosoma haematobium
○ Affects the urinary tract
○ Can be found in some parts of the Middle East, like Iraq and Iran
Incubation Period
The incubation period is at least two months.
Sources of infection
1. Feces of infected individuals

2. Manure of infected animals (that can be hosts of the organism) such as dogs, pigs, carabaos, cows,
monkeys, and wild rats.
● Through ingestion of contaminated water

● Through the skin pores
● The disease is transmitted through an intermediary host, a tiny snail called Oncomelania quadrasi.
Characteristics of Oncomelania quadrasi
● The snail thrives best along riverbanks, freshwater streams, creeks, canals, and swamps.
● It can be found clinging to water hyacinths, grasses, decaying leaves, pieces of Introtting wood,
bamboo, and coconut husks.
● This species also loves to stay in areas with sandy-loam soil.
● The adult snail is greenish-brown in color and is just as big as the smallest grain of unhusked rice
(palay).
Pathogenesis/Pathology
● The larvae (cercaria) penetrates the skin or mucous membrane and eventually works their way to
the liver's venous portal circulation.
● They mature in one to three months in the portal vessels
● The mature worms live in copula in the portal vessels and migrate to some parts of the body.
● The female cercaria lay eggs in the blood vessels surrounding the large intestine or bladder.
● Ulceration in the mucosa occur and the eggs escape into the lumen of the intestine and are
excreted with the feces.
● The eggs secrete proteolytic enzymes that help them migrate to the bladder and intestines to be
shed.
● The enzymes also cause an eosinophilic inflammatory reaction when eggs get trapped in tissues or
embolize to the liver, spleen, lungs, or the brain.
● Some of the eggs are carried by the portal circulation and filtered in the liver where small lesions or
granulomas form.
● These granulomas resolve and are replaced by fibrous tissue.
● Likewise, the ulcerations in the intestines are healed and scar formation occurs.
● As the disease progresses, the liver enlarges due to increasing fibrosis.
● The flow of blood is interrupted in the intrahepatic portion, and results in portal hypertension.
● Fluid accumulates in the patient's abdomen, causing it to bulge.
● Fecalysis or direct stool exam

● Kato Katz technique or Richie technique (finding ova and cysts during stool examination) .Liver and
rectal biopsy
● Enzyme-linked immunosorbent assay (ELISA)
● Cercumoval precipetin test (COPT) is the confirmatory diagnostic test
● Antibody detection can be useful to indicate schistosome infection in people who have traveled to
areas where schistosomiasis is common and the eggs cannot be demonstrated in fecal or urine
specimens.
Many individuals do not experience symptoms; if symptoms do appear, it usually take four to six
weeks from the time of infection to manifest.
The signs and symptoms of the disease depend on the site of infection. However, the following can
be observed:
1. Twelve hours after infection, a pruritic rash develops at the site of the entrance of the
microorganism, known as "swimmer's itch".
2. Around 2-10 weeks later, low-grade fever, myalgia, and cough occur.
3. Weeks or months after the initial infection, acute schistosomiasis (Katayama fever) occurs as a
systemic reaction against the migrating schistosomulae as they pass through the bloodstream
through the lungs and on to the liver.
4. Abdominal discomfort due to hepatomegaly, splenomegaly, and lymphadenopathy is observed.
5. Bloody-mucoid, "dysentery-like" stools occur on and off for weeks. The patient becomes icteric and
jaundiced.
6. Later, the abdomen becomes distended due to the inflamed liver, which is a result of Schistosoma
eggs accumulating in that organ.
7. After some years of suffering from this chronic disease, the patient becomes weak, with marked
muscle wasting and a pale complexion.
8. If the parasite reaches the brain, the victim experiences severe headache, dizziness and
convulsions.
9. Many infections are mildly symptomatic, with anemia and malnutrition being
common in endemic areas.
Complications
● Liver cirrhosis, portal hypertension

● Genitourinary disease occurs when S. haematobium migrates to the veins around the bladder and
ureters, leading to calcification of the bladder and obstruction of the urinary tract. The client may
develop hydronephrosis with possible kidney failure.
● Cerebral granulomatous disease develops. The presence of eggs in the spinal cord can lead to
transverse myelitis with flaccid paraplegia.
Modalities of Treatment
Treatment is effective only when given early in the course of the disease.
● Praziquantel tablet for six months; one tab BID for three months, then one tab a day for another
three months
● Fuadin injection is given either IM or IV. The patient should consume 360 mg for the entire
treatment.
● If the patient continues to live in the endemic area, he/she frequently gets reinfected and has to be
retreated.
● Oxamniquine is not frequently used due to the lack of efficacy against the urogenital form of the
disease caused by S. haematobium.
The basic principle of schistomiasis prevention and control is to interrupt the life cycle of the
worms and protect people from infection. To achieve this, healthcare workers one must have The basic
principle of schistosomiasis prevention and control is to interrupt the life cycle of thorough knowledge of
how the disease spreads. This can be achieved through the following measures:
1. Submit samples stool examination.
2. Reduce the snail population by:
● clearing vegetation to expose the snail to sunshine;
● constructing drainage canals to dry.the land surface where the snail thrives; and
● improve farming by proper irrigation and drainage, crop rotation, and removal of weeds,
thus disturbing the living conditions of the snail host.
3. Diminish infection rate by:
● proper waste disposal,
● control of stray animals,
● preventing people, especially children, from bathing in infested streams/rivers,
● building foot bridges over snail-infested streams, and
● providing adequate water supply for bathing and laundering, and safe water for drinking.
4. Carry out health education on the disease process, mode of transmission, and prevention.
HEPATITIS A
(Infectious hepatitis; Catharrhal jaundice)
Definition
Hepatitis A is a vaccine-preventable liver infection caused by the hepatitis A virus. It is characterized

by inflammation of the liver that is not very severe and runs an acute course, generally starting within two
to six weeks after contact with the virus. It may last no longer than two months. Although highly
contagious, hepatitis A is self-limiting and is the most benign and harmless type of hepatitis (Neighbors and
Tannehill-Jones, 2008).
● The virus is one of several types of hepatitis viruses that cause inflammation and affect the liver's
ability to function.d
● It is known as infectious hepatitis because it spreads relatively easily from those infected to those in
close contact.
Incubation Period
Mean: 30 days ranges from 15-60 days or three to six weeks
The infected patient is capable of transmitting the organism a week before and a week after the
appearance of symptoms.
a. Fecal-oral transmission
b. Ingestion of contaminated food or water
c. From close contact with a person or object that is infected
d. Eating raw shellfish harvested from water polluted with sewagee.
e. Having oro-anal sex with someone who is infected with hepatitis A
f. sharing of needles between intravenous drug users
Signs/Symptoms
Indications of hepatitis A infection typically do not appear until the person had the virus for a few
weeks. Possible signs and symptoms are:
a. fatigue, low-grade fever, anorexia, nausea and vomiting;
b. abdominal pain or discomfort, especially on the upper right side beneath the lower ribs;
c. clay-colored stools with dark urine;
d. joint pain and/or arthralgia;
e. yellowish discoloration of the skin and the sclera;
f. intense itching; and
g. sometimes spider nevi on the trunk are noted.
Most of these symptoms may be relatively mild and disappear in a few weeks. Hepatitis A does not
lead to chronic hepatitis or cirrhosis. However, hepatitis A infection can result to a severe illness that lasts
for several months, depending upon the host's resistance.
Groups who are at risk for HAV
● Children at day care centers can transmit the infection through diapers and toys
● Troops living in crowded conditions at military camps or in the field
● Homosexuals are increasingly at risk of HAV infection from oral-anal sexual contact Victims of
events that cause the breakdown of sanitary conditions, such as after floods and other natural
disasters
● Living with a person who has hepatitis. A
● Someone who have a clotting-factor disorder, such as hemophilia
● Travelling or working in areas of the world where hepatitis A is common
Pathogenesis
The virus spreads when a person (unvaccinated) ingests food or water that is contaminated with
the feces of an infected person. The disease usually occurs in areas where inadequate sanitation and poor
personal hygienic practices are rampant.
Infection rates are low in high-income countries with good sanitary and hygienic conditions.
In middle-income countries and regions where sanitary conditions are variable, children often
escape infection in early childhood and reach adulthood without immunity. Consequently, these improved
economic and sanitary conditions may lead to accumulation of adults who have never been infected and
who have no immunity. These older age groups account for the higher disease rates during outbreaks of
the disease.
HAV
Liver
(interlobular infiltration)
Necrosis and hyperplasia of Kuffer cells
Failure of bile to reach intestines
Dark urine
Pale stools
Itchiness
FIGURE 3.5 The pathogenesis of hepatitis A
Complications
● In the fulminant type, progressive hepatic encephalopathy characterized by drowsiness, cerebral
edema may manifest.
● Cholestatic hepatitis with prolonged jaundice and fever may occur.
● Relapsing disease with acute elevation of liver enzymes may take place.
● In rare cases, hepatitis A can cause a sudden loss of liver function, especially in older adults or
people with chronic liver diseases. Acute liver failure requires hospital confinement for monitoring
and treatment.
1. HAV and HBV - complement fixation rate
2. Liver function test is used to determine the presence and extent of liver damage and to monitor
liver response.
3. Bile examination in stool and urine
4. Serum glutamic oxaloacetic transaminase (SGOT)
5. Serum glutamic pyruvic transaminase (SGPT)
6. Serum alanine transaminase (ALT)
7. IgM level
1. No specific treatment is prescribed, although bed rest is essential
2. High carbohydrate, low fat, low protein diet
3. Vitamin supplements, specially the b complex group
4. Intravenous therapy is occasionally necessary
5. Isoprinosine (methisoprinol), may enhance the cell-mediated immunity of the T-lymphocytes
6. Administer alkalies, belladonna, and antimetics to control dyspepsia and malaise
Prevention
The hepatitis A vaccine can prevent infections. It is typically given in two shouts. The first one is
given at age one year and followed by a booster shot six months later
The CDC recommends a hepatitis A vaccine for the following populations:

● All children at age one, or older children who did not receive the childhood vaccine
● Infants aged 6-11 months traveling internationally
● Laboratory workers who may come in contact with hepatitis A
● Men who have sex with men
● People with other risk factors who work or travel in parts of the world where hepatitis A is common
● People who use any type of illegal drugs, not just injected ones
● People who receive treatment with clotting-factor concentrates
● People with chronic liver disease
Other preventive measures include:
● Screen food handlers carefully

● Practice safe preparation and serving of food
● Educate the public on the mode of transmission of the disease
Thoroughly wash your hands often, especially after using the toilet or changing a diaper and before
preparing food or eating.
Follow safety precautions when traveling
If traveling to parts of the world where hepatitis A outbreaks occur, take these steps to prevent
infection:
● Wash and peel all fresh fruits and vegetables
● Never eat raw or undercooked meat and fish
● If bottled water isn’t available, boil tap water before drinking it
● Drink properly boiled or bottled water and use it when brushing teeth
● Avoid all beverages of unknown purity, with or without ice.
Nursing Management
1. Isolate the patient (enteric isolation)

2. Promote rest during acute or symptomatic phase
3. Improve nutritional status
4. Utilize appropriate measures to minimize spread of the disease
5. Observe for melena and check stools for the presence of blood
6. Provide optimum skin and oral care
7. Increase the patient’s ability to carry out activities by:
○ Encouraging the patient to limit activity when fatigued;
○ Assisting the client in planning periods of rest and activity; and
○ Promote gradual resumption of activities and mild exercise during recovery
HEPATITIS E
An infectious disease, characterized by inflammation of the liver caused by infection with the
hepatitis E virus (HEV)
HEV is a positive-sense, single-stranded,non-enveloped RNA virus.Is shed in the stools of infected

persons, and enters the human body through the GIT.
The infection is usually self-limiting and resolves within two to six weeks.Occasionally a serious
disease, known as fulminant hepatitis (acute liver failure) develops, and a number of People who contract
this can die.Fulminant hepatitis occurs more frequently when hepatitis E develops during pregnancy.
Incubation Period
● The incubation period ollowing exposure to HEV ranges from two to 10 weeks, with an average of
five to six weeks
● Infected persons are thought to excrete the virus starting around a few days before to around three
to four weeks after the onset of disease
1. Fecal-oral route
2. Drinking contaminated water
3. Ingestion of undercooked animal meat (including animal liver)
4. The ingestion of raw or uncooked shellfish may be the source of sporadic cases in endemic areas
5. Transfusion of infected blood products
6. Vertical transmission from a pregnant woman to her fetus
Risk Factors
1. The risk factors for hepatitis E are related to poor sanitation.
2. The disease is common in resource-limited countries with inadequate access to essential
water,sanitation, hygiene, and health services.
3. Pregnant women with hepatitis E, particularly those in the second or third trimester, are at an
increased risk of acute liver failure, fetal loss,and mortality. Case fatality rates as high as 20%-25%
have been reported among pregnant women in their third trimester.
4. Events/conditions that allow the virus excreted in the feces of infected people to reach drinking
water supplies
5. War zones, and in camps for refugees or internally displaced populations (IDP)
Signs and Symptoms
1. An initial phase of mild

2. Reduced appetite (anorexia),with occasional nausea and vomiting, lasting for a few days.
3. Some patients may complain of abdominal pain.
4. Skin rash, sometimes itchy but without skin lesions
5. Jaundice (yellow discoloration of the skin and sclera)
6. Dark urine and pale stools
7. Slightly enlarged, tender liver (hepatomegaly)
Prevention
1. Wash and peel all fresh fruits and vegetables
2. Do not eat raw or undercooked meat and fish
3. Drink boiled or bottled water and use it when brushing your teeth
4. Avoid all beverages of unknown purity, with or without ice
5. If bottled water is not available, boil tap water before drinking it
6. Practice hand hygiene
7. A vaccing to prevent HEV infection has been developed and is licensed in china, but is not yet
available in the Philippines at the time of writing
TYPHOID FEVER
(ENTERIC FEVER)
A bacterial infection transmitted by contaminated water, milk, shellfish or other food. It affects the
lymphoid tissues (peyer's patches) of the small intestine
Etiologic Agent
The disease is caused by an organism Salmonella typhosa/typhi with the following characteristics
● Gram-negative, motile and non-spore-forming, and is
● Pathogenic to humans only
● It is a hardy organism and can easily survive in natural habitats like water or inorganic materials
● The bacteria can survive for weeks in water or dried sewage
Incubation period
5-40 days; mean 10-20 days
Period of communicability
The period of communicability is variable. As long as the patient is excreting the microorganism,
he/she is still capable of infecting others
Sources of infection
a. Carries are persons who recovered from the disease or someone who took care of a patient with
typhoid and was infected. These individuals may become long-term carriers of the bacteria, even
though they have no symptoms. They could become the source of new outbreaks of typhoid fever
for many years.
b. Ingestion of shellfish (oysters) harvested from waters contaminated by sewage disposal
c. Stool and vomitus of infected individual
Mode of transmission
● Fecal-oral transmission
● The organism can be transmitted through the 5 F’s;
○ Feces of an infected individual and is considered the primary source
○ Flies carry the organism to the;
○ Food picked up the food by ;
○ Fingers, and the fifth f are
○ Fomites
Typhoid ileitis is the inflammation of the distal portion of the ileum where the Peyer’s patches are
located
Pathogenesis
● After the ingestion of contaminated food, the organisms invade the small intestine and enter the
bloodstream temporarily through the infected Peyer's patches of the lymphoid tissues.
● The bacteria are carried by white blood cells to the liver, spleen, and bone marrow,where they
multiply and re-enter the bloodstream.
● The pathogens invade the gallbladder, biliary system, and the lymphatic tissue of the bowel, and
pass into the intestinal tract and can be identified in stool samples.
● Patients develop symptoms including fever at this point.
● At the first week, these lymph nodes are swollen.
● During the second week, they form sloughs which are often bile-colored.
● At the third week, the sloughs separate and leave an ulcerated surface.
● Hemorrhage and perforation may occur due to extension of the lesion and continuous erosion of
the epithelial lining of the small intestine
● Since the toxin is absorbed by the bloodstream, almost all organs of the body are affected, most
commonly the heart, the liver, and the spleen. The mesenteric lymph glands become red and
swollen
I. Onset
● Headache, chilly sensation,aches all over the body
● Nausea and vomiting
● The patient manifests either constipation or diarrhea.
● All symptoms worsen by the fourth and fifth day.
● The fever starts low and increases daily, sometimes reaching as high as 40.5°C; it may be
higher in the morning than it is in the afternoon.
● The patient's breathing is accelerated, the tongue is furred, the skin is dry and hot, and the
abdomen is distended and tender.
● Rose spots appear on the abdominal wall on the seventh to the ninth day (considered as
pathognomonic to the disease).
● In the second week, symptoms become more aggravated. The temperature remains at a
uniform level. Rose spots become more prominent.
II. Later Illness

● The patient becomes delirious.
● Life-threatening complications often develop at this time.
● In some people, signs and symptoms may return up to two weeks after the fever has
subsided.
III. Typhoid State

● Intense symptoms decline in severity.
● The tongue protrudes, and becomes dry and brown.
● The teeth and lips accumulate a dirty-brown collection of dried mucus and bacteria known
as sordes, which are preventable with good nursing care.
● The patient seems to be staring blankly (coma vigil).
● Twitching of the tendon sets in, specially at the wrist (subsultus tendinum).
● The patient mutters deliriously and picks aimlessly at bedclothes with his/her fingers in
continuous fashion (carphologia).
● There is a constant tendency for the patient to slip down to the foot part of the bed.
● In severe cases, rambling delirium sets in, often ending in death.
Complications
● Intestinal hemorrhage or perforation are the two most dreaded complications.

● Ascites and peritonitis
● Bronchitis and pneumonia
● Meteorism or excessive distention of the bowels (tympanites)
● Early heart failure due to myocarditis and endocarditis
● Appearance of "typhoid spine" or neuritis
● Septicemia or sepsis occur.
● Reiter's syndrome: joint pain that can lead to chronic arthritis and eye irritation (conjunctivitis)
● Painful urination due to urinary bladder and kidney infection
● Infection and inflammation of the membranes and fluid surrounding the brain and spinal cord
(meningitis)
● Psychiatric problems, such as delirium, hallucinations and paranoid psychosis may be thomongoing
as presented by the patient.
Even after treatment with antibiotics, a number of people who recover from typhoid fever continue
to harbor the bacteria in their intestinal tracts or gallbladders, sometimes for years. These people are
called chronic carriers, who still shed bacteria in their feces and are capable of infecting others, although
they no longer have signs or symptoms of the
disease themselves.
● Typhidot-confirmatory
● Enzyme-linked immunosorbent assay (ELISA)
● Widal test
● .Rectal swab
● Chloramphenicol
● Ampicillin
● Co-trimoxazole
● Ciprofloxacin or ceftriaxone
● If patient does not respond to chloramphenicol, third and fourth generation drugs are
administered.
● Sanitary/proper disposal of excreta

● Proper supervision of food handlers
● Enteric isolation
● Adequate protection or provision of safe drinking water supply golan
● Reporting of cases to health authorities
● Vaccination in high-risk populations is the best way to control typhoid fever.
Two vaccines are available (CT vaccines). These are required before traveling to endemic
Areas.
● One is injected in a single dose at least one week before travel.

● One is given orally in four capsules, with one capsule to be taken every other day.
Because the vaccine will not provide complete protection, follow these guidelines when traveling to high-
risk areas:
1. Wash before eating or preparing food and after using the toilet. Carry an alcohol-based hand
sanitizer for times when water is not available. Frequent hand washing in hot, soapy water is the
best way to control infection.
2. Avoid drinking untreated water. Contaminated drinking water is a particular problem in areas
where typhoid fever is endemic. Drink only boiled or bottled water or canned bottled carbonated
beverages. Carbonated bottled water is safer than uncarbonate variants.
3. Go for drinks without ice. Use bottled water to brush your teeth, and try not swallow water in the
shower.
4. Avoid raw fruits and vegetables. These items may have been washed in unsafe wate Avoid items
that you cannot peel, especially lettuce and other leafy ground vegetables
5. Choose hot foods; steaming hot ones are best. Avoid those that are stored or served a room
temperature. Food from street vendors are more likely to be contaminated.
If a client is recovering from typhoid fever or about to be discharged, include these measures in your
health teaching in order to help keep others safe.
1. Advise clients to continue their antibiotics as prescribed

2. Emphasize hand washing often. This is the single most important thing to do to keep from
spreading the infection to others. Use hot, soapy water and scrub thoroughly for at least 30
seconds, especially before eating and after using the toilet.
3. Clients should avoid handling food. They should avoid preparing food for others until the doctor
says they are no longer contagious.
Nursing Management
● Maintain or restore fluid and electrolyte balance.

● Monitor the patient's vital signs.
● Prevent injury from falls in patients with typhoid psychosis.
● Maintain good personal hygiene and mouth care.
● Keep the patient warm if the patient feels chills.
● Administer cooling measures during febrile states.
● Watch for signs of intestinal bleeding.

Diseases Affecting GI Tract

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Diseases Affecting GI Tract

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Chapter 3

Diseases Affecting the Gastrointestinal Tract

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

The digestive system has two main purposes.

Two developmental stages

Usually one to four weeks but may be shorter or longer

For duration of the illness.

Ingestion of the cyst

FIGURE 3.1 Pathogenesis of amoebiasis

1. central zone necrosis

1. Acute amoebic dysentery is characterized by:

2. Chronic amoebic dysentery

1. Metronidazole (Flagyl) 800 mg TID for five days

1. Isolation, enteric precautions

● Ingestion of contaminated food or drinking contaminated water or milk

● Fever, specially in children

● Fecalysis or microscopic examination of the stools

● Rectal prolapse, particularly in undernourished children Respiratory complications, such as cough

Prevention and Control

● Ensure sanitary disposal of human feces.

● Antibiotics such as ciprofloxacin, ofloxacin, levofloxacin, or azithromycin

● Maintain fluid and electrolyte balance to prevent profound dehydration.

Botulism is a severe type of food poisoning caused by a neurotoxin released by Clostridium

Three Forms of Botulism in Humans

Botulism is caused by Clostridium botulinum, which has the following characteristics:

● Hospital-acquired or aspiration pneumonia

1. Supportive care with particular attention to respiratory and nutritional needs

Prevention and Control

Vibrio cholerae/Vibrio comma

A few hours to five days; usually one to three days

1. Fecal-oral route via contamination of water, milk, and other foods

Pathogenesis and Pathology

FIGURE 3.2 Pathogenesis of cholera

Principal Fluid Deficit

1. Extracellular volume - loss of intestinal fluid can lead to:

1. Protect food and water supplies from fecal contamination

TABLE 3.1 The life cycle of Ascaris lumbricoides

Developmental Stage Symptomatology

2. Larva ● Nausea and vomiting, poor appetite

3. Adults ● Colicky, paraumbilical pain

1. Hepatic abscess and cholangitis

1. Albendazole or mebendazole - 15 cc as a single dose

1. Improved sanitation and hygienic practices

Ancylostomiasis is caused by two species of hookworms. Symptoms include diarrhea or cramps.

● Incubation period is 40-100 days or two to eight weeks.

● Microscopic examination of feces for the eggs

● Pyrantel embonate (Quantrel)

● Provide health education on the proper disposal of excreta.

● Isolation is not necessary.

From ingestion of eggs: 10-14 weeks

Signs and Symptoms

1. Practice improved sanitation and proper disposal of feces

Etiologic agent and Pathogenesis

1. Pruritus ani (itching of the anus) varies from mild to severe.

1. Reiterate hygiene and cleanliness, including handwashing.

Schistosomiais or bilharziasis is a slow, progressive disease caused by blood flukes of class

The incubation period is at least two months.

1. Feces of infected individuals

● Through ingestion of contaminated water

Characteristics of Oncomelania quadrasi

● Fecalysis or direct stool exam

● Liver cirrhosis, portal hypertension

Hepatitis A is a vaccine-preventable liver infection caused by the hepatitis A virus. It is characterized