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Prepared by:

Melody Gay M. Igcasenza, PTRP, RN


TYPHOID FEVER
Also known as Enteric Fever, Typhus
Abdominalis
Involves the lymphoid tissues & (Peyer’s
Patches) of the small intestines.
Sources of Infection:
1. Chiefly by carriers
2. Ingestion of contaminated shellfish
3. Contaminated drug substances of
animal origin
Mode of Transmission
Ingestion of contaminated foods, milk
products, seafood, shellfish & water.
Flies – act as vectors
Asymptomatic carriers esp. Food Handlers

INCIDENCE:
• Worldwide transmission
• Endemic in areas of poor sanitation
• Occurs anytime, high from May – August
• Milder form in the young
• Evidence of foreign travel
Salmonella typhi
INCUBATION: 10 to 20
days
Period of Communicability: As long as
bacteria are excreted and present in the
stool of the patient.
DIAGNOSIS:
1.Blood exams – WBC – leukopenia
2.Cultures – blood, urine, stool
3.Widal Test (Serum Agglutination Test)
4.Bone Marrow Puncture
TREATMENT
SPECIFIC:
1.Chloramphenicol – drug of choice
2.Sulfamethoxazole + Thrimethoprim
3.Amixicillin
4.Chloramphenicol
• NON-SPECIFIC:
1.Acetaminophen
2.Prednisone
3.Plasma expanders
4.Supportive therapy
5.Sulfamethoxazole (Asymptomatic Carriers for
bacteriologic clearance)
PREVENTION & HEALTH
EDUCATION
Isolation of the patient
Typhoid Vaccine
Environmental Hygiene & Public Health
Measures
Routine Stool Culture after recovery
COMPLICATIONS
Perforation of the intestines
Intestinal Hemorrhage
Peritonitis
Toxemia, Cholecystitis, Abdominal Tympanism
Hepatitis
Respiratory Complications; pneumonia &
bronchitis
Osteoarthritis, pyelonephritis
Endocarditis, encephalitis, meningitis, psychosis
w/ alopecia
RUPTURE OF SMALL BLOOD
VESSELS IN THE ILEUM
NURSING INTERVENTIONS
1. Give supportive Care
- maintain fluid & electrolyte balance
- position to prevent aspiration
- support during toxemia, pt. may be drowsy, incontinent, delirious
- watch for bladder distention
- encourage OFI
- observe for retention of feces
- monitor body temp.
- DIET: hi-calorie, low residue. Non-gas forming & non-irritating
foods, give vit B complex

2. Watch out for symptoms of complication:


a. Intestinal perforation – sharp abdl. Pain, rigidity & shock
b. Intestinal hemorrhage – apprehensions, sweating, pallor, weak,
rapid pulse, hypotension, bloody or tarry stools
CHOLERA
A severe gastrointestinal disease resulting
from a powerful enterotoxin elaborated by
Vibrio cholerae organisms.
2 BIOTYPES:
1. Classic
2. El Tor
SOURCE: MAN
MODE OF TRANSMISSION:
1. Fecal-oral route
2. Flies, soiled hands & utensils - vectors
VIBRIO CHOLERA
INCUBATION PERIOD: 1 to 3
days
PERIOD OF COMMUNICABILITY: as long as pt’s stool is
(+) for the microorganism, carrier state may last for a
few days to mos.
CLINICAL MANIFESTATIONS:
1. Massive or profuse diarrhea – watery, voluminous,
whitish, grayish or greenish, “rice-water” stools w/
fishy odor
2. Stools are continuous w/o straining or tenesmus
3. Signs of dehydration
4. Aphonia
5. Vomiting, muscle cramps, increased exhaustion
6. Oliguria/anuria
7. Low-grade fever, Temp-subnormal (shock)
8. Tetany, abdominal distention, convulsions
Dead bodies from cholera
Cholera outbreak in
Angola
Rehydrating patients w/
cholera
Shigellosis/ Bacillary
Dysentery
Shigella
GASTROENTERITIS
- Also known as intestinal flu,
traveler’s diarrhea, viral enteritis
or food poisoning
- Is the involvement of the stomach
and the intestines in an
inflammatory process.
- Usually caused by infection but
may also result from allergic
reactions to food & drugs
Manifestations:
1. Vomiting – inflammation of the gastric
mucosa
2. Diarrhea – inflammation of the intestines,
increased motility, impaired absorption,
increased secretions
3. Nausea & abdominal cramps
4. Fever & malaise
5. Borborygmi
Common among children in
nursery schools…
Also in adults, elderly &
debilitated...
DIAGNOSIS:
1.Patient history
2.Physical assessment
3.Stool Culture by rectal
swabbing
4.Blood culture
GASTROENTERITIS
Bacterial gastroenteritis
Escherichia Coli
Mode of transmission:
Fecal-oral route
ESCHERICHIA COLI – “Traveler’s Diarrhea”
- usually a harmless microbe normally
present in the intestine.
Enterohemorrhagic E. Coli (EHEC) – highly
virulent strain present in cows. Infection
comes from partially cooked ground beef,
unpasteurized milk or other fecal-oral routes
(diapers, direct contact)
Common Bacterial
Infections Transmitted by
food
Pathogen
& water
Source Incubation Manifestations
Staphylococcus Food handlers, 1 to 7 hrs Sudden severe
Aureus inadequate cooking/ N&V, cramps,
refrigeration of custards, diarrhea,
salad dressings, cold hypothermia&
meats hypotension
Escherichia Coli Fecal contamination of 10 to 12 hrs Profuse watery
food & water diarrhea,
sometimes w/ blood
or mucus, vomiting
& abdominal
cramps

Salmonella Species Fecal contamination of 6 to 72 hrs Sudden diarrhea,


food or work surfaces, abdominal pain &
undercooked or raw fever, vomiting
eggs, poultry, shellfish
TREATMENT:
1.SUPPORTIVE – bed rest,
nutritional support, increased
fluid intake
2.IV fluid & electrolyte
replacement
3.Specific antimicrobials
EXAMPLES OF DRUGS USED IN DIGESTIVE SYSTEM DISORDERS
Classification Example Action
Antiemetic Metoclopramid Reduces vomiting from
e (Plasil) drugs, motion sickness
& radiation therapy
Antidiarrheal Loperamide Reduces intestinal
(Imodium) motility
Anti- Prednisone Reduces inflammation
inflammatory Sulfasalazine
(Aulfidine)
Acid- Ranitidine Reduces secretion of
reduction (Zantac) hydrochloric acid in the
Esomeprazole stomach
(Nexium)
CLASSIFICATION EXAMPLE ACTION
Antimicrobial Tetracycline Drugs as
Metronidazole indicated by
culture &
Clarithromycin
sensitivity
Coating agent Sucralfate Covers ulcer to
(Carafate) allow healing
Antacid Aluminum- Reduces
Magnesium hyperacidity
combinations
(Maalox)
Laxative Psyllium Increases fecal
(Metamucil) (bulk) bulk &
Docusate Na Intestinal motility
(Colace) (stool
softener)
Nursing Interventions:
 Assessment of Symptoms for signs of improvement or
worsening
 Monitor weight daily, I & O
 Patient Education
 Administer meds as ordered
 Replace lost fluids with broth, ginger ale, lemonade as
tolerated, warn pt to avoid milk & milk products
 Careful & thorough handwashing
 Warm sitz bath or witch hazel compress
 Contact public health authorities if food poisoning is the cause
COMPLICATIONS:
Severe dehydration
Electrolyte loss
Shock
Vascular Collapse
Renal failure
PARASITIC
INFECTIONS
GASTROINTESTINAL TRACT
Amoebic Dysentery
(Amoebiasis)
 Infection of man by Entamoeba Hystolytica initially involving
the colon but may spread to other soft tissue organs
commonly the liver or lungs.

Variations:
1. Acute Amoebic dysentery – stools contain blood & mucus 
amoebic hepatitis/liver abscess
2. Chronic Amoebic dysentery – recurrent attacks of diarrhea
3. Amoebic Colitis – periods of constipation & diarrhea w/
abdominal discomfort stimulating appendicitis
4. Carriers – (+) organism in stools, but are symptom-free
Entamoeba Hystolytica
ETIOLOGY
2 Developmental Stages of Entamoeba
Hystolytica:
1. Trophozoites/Vegetative form
* one-celled protozoan parasite
* found in parasitized tissues & liquid colonic
contents
* “ameboid” & absorbs food rather than
ingest it
* forms into cysts during the process of
bowel content dehydration
2. Cysts/Infective Stage
Passed out in formed/semi-formed stools
Resistant to environmental conditions

SOURCE: HUMAN EXCRETA


Period of Communicability: Duration of
illness
Incubation: 2 to 4 wks
3 days in severe infections
Mode of Transmission:
1. Direct Contact
- sexual contact by orogenital, oroanal,
proctogenital

2. Indirect Contact
- ingestion of food like uncooked vegetable
contaminated w/ fecal materials containing
viable Hystolytica cysts
- polluted water supplies, flies as vectors,
night soil fertilizers, unhygienic food handling
practices
INCIDENCE
Worldwide in distribution
Endemic in all areas of the Philippines
Higher during rainy season
More common in areas of inadequate water
supply
AMOEBIC DYSENTERY
ASCARIASIS/
Roundworm infestation
ASCARIASIS
 Ascariasis is a disease caused by a parasite, which is
an organism that depends on another organism for its
survival.
 
Caused by: Ascaris lumbricoides. 
 a type of nematode or roundworm
 giant, intestinal roundworm
 the largest intestinal roundwormfound in humans
 one of the most common parasites found in humans.
 
It currently affects more than 1-1.5 billion people
worldwide. 
Agent:
Ascaris lumbricoides
Occasionally, the swine ascarid, Ascaris suum, can infect   
 A. lumbricoides is a type of organism grouped with other
helminthes or worms. 
 Nematodes or roundworms are a type of invertebrate,
animals without backbones.  Specifically, nematodes are
characterized by their long, round bodies. 
 Common parasitic roundworms apart from A. lumbricoides
include:
 the pinworm,
 the hookworm, and the
 whipworm.    
 A.    lumbricoides gets its name from the earthworm
Lumbricus terrestrias. 
 When it was first discovered, this roundworm was called
Lumbricus teres.    
Clinical Presentation in Humans
Clinical Case Study

A 37-year-old man comes to your office after passing something in his stool
that he thought was a rubberband. He became worried when he saw the object
moving in the toilet. Apart from this occurrence, he is a healthy man and is not
taking any medications. He has had no recent change in bowel habits or stool
appearance. He has not had fever, abdominal pain, cough or rash. He does not
smoke, drink alcohol, or use recreational drugs. He has been physically active
and recently completed a weeklong backcountry hiking expedition in the
Southeastern U.S. Other than this expedition, he has not been traveling recently.
With the clinical history and presentation in mind the following are some
possible diagnoses: 1) Ascaris lumbricoides (round worm) infection
2) Toxocara(visceral larva migrans) infection
3) Trichuris (whipworm) infection
4) rubberband
ingestion.
It turned out that this patient had Ascaris lumbricoides.
General Summary of Symptom Timeline
Early phase (The early phase coincides with larval tissue-
migration.  Typically,
4-16 days after egg ingestion.)  The main symptoms include
the following:
-fever
-cough
-wheeze
Late Phase (The late phase coincides with the mechanical
effects of the worms.
These include GI symptoms from mechanical irritation. 
Typically, 6-8 weeks
after egg ingestion) The main symptoms include the following:
-vague abdominal complaints (cramping, nausea, vomiting)
-small bowel obstruction (mainly in children)
-pancreatitis (2ndary to worm migration)
-cholecystitis (2ndary to worm migration)
-appendicitis (less common, 2ndary to worm migration)
Invasion in the intestines
Transmission
 A.    lumbricoides  is transmitted primarily through fecal-oral
contamination. 
 The transmission can occur by ingesting contaminated soil,
water, or food. 
 Usually, ascariasis is caused by directly or indirectly eating
soil contaminated with feces carrying these eggs.  These
eggs mature in the body, and adult female worms can then
lay eggs that come out in the feces.  Note, however, that in
order for the eggs to be infective or embryonated, the feces
must have been infected 2-4 weeks before it is ingested. 
Infection with Ascaris eggs is so common because the eggs
are frequently
found in the environment due to poor sanitation practices
and the use of night fertilizer.    
Once embryonated, the infective egg must be swallowed to complete
the life cycle of A. lumbricoides. Bile salts and alkaline enteric juice of the
small intestine stimulate the release of the larvae from the eggs. These
second-stage larvae then travel from the small intestine to the liver. Then
the larvae migrate to the heart via pulmonary circulation. The larvae are
now third-stage larvae in the alveolar capillaries, and they enter the alveolar
spaces. Afterwards they migrate to the bronchi into the tranchea and then to
the epiglottis.
The larvae are then swallowed, and they pass once again to the
small intestine. There they molt twice and mature into adult worms. The
adult wormscan live up to one year, and the females can lay eggs in the
small intestine. However,A. lumbricoides cannot reproduce in the intestine,
and it can only lay eggs that are not yet infective.
In addition to fecal-oral transmission of A.
lumbricoides, it is also believed that ascariasis can
occur by way of transplacental transmission,
since many neonatal cases have been documented.
It should be noted that Ascaris eggs are some of the
most resistant existing microorganisms. 
Their hearty egg shells consist of four layers:
ascaroside,
chitinous,
vitelline and
uterine. 
Fertilized Egg
The eggs are not responsive to:
- chlorine, high pH, low pH, and UV irradiation. 
They are resistant to:
- high and low temperatures,
Alcohol, ether, and surfactants can inactivate
the eggs.
*** Ascaris eggs can survive for many years in
the soil.
Life Cycle

Adult worms reside in the upper part of the small intestine, where they
survive on predigested food. The worms make themselves into an S-shape
and press against the epithelium of the intestine while moving against the
peristalsis
to keep themselves in the small intestine. The female worm lays eggs, and
she can
produce up to 200,000 eggs per day. These eggs are fertilized but
nonembryonated, and the eggs are passed out with feces.
The fertilized eggs develop through embryonation in feces deposited
in the soil. The process of embryonation takes 2-4 weeks. The eggs can
survive
many months before embryonation starts, but they need a moist aerobic
environment to develop. The eggs are only infective once they are
embryonated
and have larvae in them.
Reservoir

No reservoir for this type of Ascaris exists


outside of humans. 
Pigs have their own type of Ascaris, which was
mentioned previously.

Vector
          No vector exists for Ascaris.
Incubation Period

          The appearance of early


symptoms of clinical disease can occur
anywhere between 4-16 days after
ingestion of the eggs.Fever, coughing,
and wheezing take this long to
develop. 
However, GI symptoms take 6-8 weeks
after ingestion of the eggs to develop.
Morphology

> Ascaris is a large intestinal roundworm.  It superficially


resembles the common earthworms found in the soil.  Female
worms can be as long as 20-35 cms, and males tend to be
smaller, no larger than 30 cms.  They can be anywhere from 2-
6 mm wide.  Mature worms are cylindrical, creamy white or
light brown.
 They tend to have tapered ends.
 The worms have a thick cuticle, 3 lips at its head, small teeth,
and its own digestive tract.  The fertilized eggs are oval shaped,
and they are about 65 to 40 um in size.   The eggs are brown or
yellow brown, and they have a thick shell. 
Diagnostic Test
  usually not made clinically based on signs and symptoms. 
 Sometimes it can be diagnosed using ultrasonography and
endoscopic retrograde cholangiopancreatography (ERCP). 
 Instead, diagnosis is made primarily by examining a stool
specimen.
 Infection with A. lumbricoides is determined by microscopic
identification of eggs in the stool.  Typically, the procedure
used involves the following:
 1)    collecting stool specimen 
 2) fixing specimen in 10% formalin
 3)    concentrate using formalin-ethyl acetate sedimentation
technique
 4) examine wet mount of sediment
 Occasionally, emergence of a worm in the stool or coughed up
can be used to diagnosis the patient.
Management and
Therapy
  albendazole, 400 mg once.

 mebendazole, choice drug to treat intestinal roundworm infections. 


The adult dose is 100 mg PO BID on 3  consecutive days or 500 mg
once.  A second course is administered if the patient is not cured in 3-4
weeks.  Side-effects are mild, but migratory activity has been reported
 in response to the drug.

 pyrantel pamoate. 
         
 Levamisole hydrochloride - has more side-effects than Mebendazole and
Pyrantel, and it works by paralyzing the worm. 

 piperazine salts can also be used to treat Ascaris.  Not many side-effects
have been noted, but they tend to be more common than other drugs
available.  They are often times used because they are cheap and
effective.
Public Health and Prevention Strategies
Prevention and control of Ascaris can occur on
two fronts: drug treatment and sanitation
improvement.
Mass chemotherapy programs given every 6
months can help break the cycle of constant
Ascaris infection. 
Educate people about adopting healthier
living habits.  For instance, people can avoid
eating non-cooked vegetables and fruits in
places lacking proper sanitation and areas
that use human fertilizer. 
No vaccines are currently in use to prevent
the spread of this parasite.
 1) ensuring the wide availability of  single dose antihelminthic
drugs in all health services in endemic areas

 2) ensuring good passive and active case management

 3) regularly treating at least 75% of all school-age children at


risk of morbidity by 2010

 4)regularly treating children at risk of morbidity through the


IMCI strategy

 5)improving access to safe water and sanitation through


intersectoral collaboration

 6) improving hygiene behavior by scaling up sanitation


education, targeted at high-risk groups such as school-age
children, women, and special occupation groups
DISORDERS acquired
thru the GIT

CAUSED BY
VIRUSES
poliomyelitis
POLIOMYELITIS
 Acute infectious disease affecting the AHC of
the spinal cord, Medulla, Cerebellum,
Midbrain followed by fibrile episodes with
varying degrees of muscle weakness and
progressive paralysis.
CAUSATIVE AGENT: POLIO VIRUS (Legio
Debilitants)
1. Most paralytogenic, most frequent cause
2. Next most paralytogenic
3. Least frequent cause of paralysis
3 STRAINS:
1. Brunhilde
2. Lansing
3. Leon
PERIOD OF COMMUNICABILITY:
- a few days before and after the symptoms arise when
the virus is present in the oropharynx for one week
and present in stool for three months.
MODE OF TRANSMISSION:
1. Direct Contact
2. Indirectly- Fecal-Oral
3. Droplets from respiratory secretion
4. Parenteral route
Incidence:
 Highest in infancy
 Peak older children
 INCUBATION: 7-14 DAYS (ave)
5-35 DAYS
FACTORS INCREASING THE RISK OF PARALYSIS:
1. Pregnancy
2. Old age
3. Localized trauma (tooth extraction, tonsillectomy)
4. Unusual physical exertion
Poliomyelitis/ Infantile
Paralysis/ Heine-Medin
Disease
Four Clinical Forms
1. Inapparent/Subclinical/Asymptomatic/Silent
- history of positive exposure (nurses)
2. Abortive Type/minor illness (90 to 95%)
- mild to mod. URTI w/ flu-like symptoms, fever, malaise,
HA, sore throat, pharyngitis, vomiting
- 1 to 2 days remission – child is active & playful
3. Preparalytic, Meningitic/ Major illness (5% of cases)
- higher temp., HA, vomiting, restlessness, anorexia,
lethargy, neck pain, arms, legs, abdominal muscle spasm &
back extensors.
4. Paralytic (0.5 to 1%)
- pain & stiffness
- twitching, diminished DTR’s,
paresthesia,irritability
- (+) Kernig’s sign, (+) Brudzinski sign
- weakening of muscles => paralysis
- (+) Hoyne’s sign – head falls back when
in supine & shoulders are elevated, cannot
raise his legs at ull 90deg.
THREE TYPES OF
PARALYSIS
1. Spinal – involves one or both LE or all fours
- excessive sweating (vasomotor disturbance)
- respiratory difficulty
2. Bulbar – involves the brainstem, more rapid & serious
- CN IX & X, sense of taste & swallowing, Cardiac & resp.
reflex, facial, pharyngeal, ocular muscle paralysis.
- breathing difficulties w/ periods of apnea
- anxiety & restlessness
- pulmonary edema & papilledema
- hypertension, impaired temperature regulation
- Encephalitic manifestations – facial weakness, chewing,
swallowing difficulty, regurgitation, dyspnea
3. Bulbospinal – brainstem
& Spinal Cord
COMPLICATIONS:
- respiratory paralysis - melena
- pneumonia - Htn
- myocarditis - renal calculi
- atelectasis - skeletal/ soft
tissue
deformities
DIAGNOSIS:
1. Isolation of the Virus:
Blood, Throat, Stool, CSF
2. Serologic Dx – 4X increase in antibody titer
3. CSF exam – if w/ CNS involvement, increased CHON &
glucose

TREATMENT: No specific.
1. Supportive – analgesics
2. Moist heat applications
3. Bed rest only until discomfort subsides
4. Physical therapy & rehabilitation, corrective shoes,
braces, orthopedic surgery
Iron-lung machine
Hepatitis A
HEPATITIS A Virus
Picornavirus; RNA – heparna
Most widespread of hepa viruses

HAV & Liver damage


- HAV is not directly responsible for liver
damage
- host’s own immune cells, killer T-cells
destroys HAV-infected liver cells
HAV is RESISTANT TO:
Environmental conditions – more difficult to
destroy than polioviruses
Acid – stable at a ph of 3 over 4hrs,
unaffected by gastric acid
Detergents & many solvents
Some antiviral agents
Low temperatures
High temperatures
HAV is INACTIVATED BY:
 Chlorine – only at concentrations > 1mg/L for 30mins
 Formaldehyde – 1:4000 dilution @ 37 deg. C for 72hrs
 Boiling, Autoclaving, UVR, Microwave – destroys protein
structure of the virus

MODE OF TRANSMISSION: FECAL-ORAL


VEHICLES FOR HAV TRANSMISSION:
- food & drink, fish & shellfish
- toys, cutlery, towels
- public water supplies
- food handlers
- recreational waters
RISK FACTORS for HAV
TRANSMISSION:
 Age
 Hygiene
 Travel
 Population type & size
 Other factors, natural disasters (earthquakes, typhoon,
flooding)
OTHER ROUTES FOR TRANSMISSION:
1. Parenteral – HAV in the blood is present for 3 to 5 days
2. Oro-pharyngeal secretions
3. Sexual – oral/anal contact
FOUR STAGES
1. INCUBATION – 1 month
- concentration of virus is at peak in the feces
- most infectious stage (active replication stage)
2. PRODROMAL PHASE – 1 week
- non-specific symptoms appear
- fever, N & V, loss of appetite, lethargy
- dark urine, pale stools towards the end
- jaundice develops
3. ICTERIC PHASE –few days to several weeks
- jaundice, loss of appetite, low-
fever,
itching

4. RECOVERY – liver returns to normal after


3mos.
- gradual
- weakness & lethargy => 1 yr
COMPLICATIONS
1. PROTRACTED HEP. A – longer for liver to regain normal function
2. RELAPSING HEP. A – symptoms recur 4 to 15wks after full
recovery, milder & lasts for 5 wks
3. FULMINANT HEP. A – increased sudden severe jaundice
- rapid deterioration of liver function
- drowsiness, encephalopathy, coma
- periods of excitability, insomnia, confusion & severe vomiting
4. CHOLESTATIC JAUNDICE – results from diminution of bile flow
- lasts for 3 mos.
- common in the elderly & those w/ protracted Hep. A
- fever, pruritus, prolonged jaundice, wt. loss
DIAGNOSIS
 Serum – anti-HAV IgM antibody , primary response to HAV infection
- Most useful in confirming a recent HAV infection
- Symptoms develop & concentrations increase several days and
disappears over several months
• Feces – 1st marker of HAV infection
- HAV levels are highest, most infectious before the symptoms appear
• Blood – low concentration, lasts a few days in early stages

***PAST INFECTIONS – Anti-HAV IgG antibody in serum


- appears after IgM & persists much longer
- most useful in detecting past HAV infection
- confirms natural immunity from future Hepatitis A infection
TREATMENT: no specific
effective treatment
Amantadine
Ribavarin
Interferon
Ig Administration
PREVENTION
Immunization – Hepatitis A Vaccine
Adult – not less than 720 ELISA units
Pedia – not less than 360 e.u.
Can be given as early as 1y/o, 2-doses, 6mos.
Apart
***ELISA – Enzyme-linked Immunoadsorbent
Assay
• Good Hygiene & Sanitation
Nursing interventions:
Isolation of the pt. – enteric precaution
Promote rest
Improve nutritional status – avoid alcohol,
balanced diet, encourage CHO, CHON, avoid
fried fatty foods.
Observe for changes in sensorium, abdominal
pain & tenderness
Gradual increase in ADL’s
Provide psychological support & diversional
activities