NCM 112a CAHPTER IV: CARE OF CLIENTS AT RISK OR WITH INFECTIOUS DISEASES

LESSON 2- WATERBORNE DISEASES

INTRODUCTION OF THE LESSON OF THE LESSON AND PRESENTATION OF OUTCOMES

Waterborne diseases are diseases which can be transmitted via the GIT. The microorganisms
are spread thru fecal-oral route via contamination of water, milk and foods with stools or vomitus of
infected persons; and thru flies, and soiled hands and utensils.

At the end of the lesson, you must have:

1. identified the different waterborne diseases including the causative agent, mode of
transmission, incubation period, period of communicability and source of infection;
2. described thesigns and symptoms of waterborne diseases including the pathognomonic
signs;
3. discussed the various diagnostic examinations and treatment for waterborne diseases;
4. used the nursing process as framework for care of patients with waterborne diseases;
and
5. enumerated effective ways to prevent and control waterborne diseases.

WARM UP ACTIVITY:
Complete the following terms by supplying the missing letters.

C_OL_R_
_MO_B_A _I _
T_P_O_D F_V_R
O_R_L F_C_L R_U_E
W_T_R B_R _E

PRESENTATION OF LEARNING INPUTS

A. Amoebiasis/Amoebic Dysentery/Amebiasis
This refers to the infection of man by Entamoeba histolytica initially involving the colon but
which may spread to other soft tissue organs by contiguity or by hematogenous or lymphatic
dissemination most commonly to the lungs or the liver.

Risk Factors
This disease usually occurs in areas with poor sanitation and health practices. It is worldwide
in distribution and all areas of the Philippines are endemic. It seems to seasonal trend in transmission
associated with months of greater precipitation or rainfall.

Amebiasis is most common in:

• People who have traveled to tropical places that have poor sanitary conditions
• Immigrants from tropical countries that have poor sanitary conditions
• People who live in institutions that have poor sanitary conditions
• Men who have sex with men

Causative Agent Entamoeba histolytica (trophozoites/vegetative form and

cyst forms
Incubation Period 3 days in severe infection; several months in sub–acute and
chronic form (average 2–4 weeks period)
Portal of Entry Ingestion of cysts in fecal-contaminated food or water; flies
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on foods; soiled hands of infected food handlers; oral-anal

sexual contact
Period of Communicability May persist for years or if the causative agent is
present/period of cyst passing
Mode of Transmission Fecal–oral

Mode of Transmission
The parasite lives only in humans and is passed in the feces (poop) of an infected person.
Some people with amebiasis may carry the parasite for weeks to years, often without symptoms,
continually passing it in their feces. Histolytica infection can occur when a person:

• Puts anything into their mouth that has touched the feces (poop) of a person who is infected
with E. histolytica.
• Swallows something, such as water or food, that is contaminated with E. histolytica.
• Swallows E. histolytica cysts (eggs) picked up from contaminated surfaces or fingers.
• It can also be spread sexually by oral-anal contact.

Pathogenesis
When cyst is swallowed, it passes
through the stomach unharmed and
shows no activity while in an acidic
environment. When it reaches the
alkaline medium of the intestine, the
metacyst begins to move within the
cyst wall, which rapidly weakens and
tears.
The quadrinucleate amoeba
emerges and divides into amebulas
that are swept down into the cecum.
This is the first opportunity of the
organism to colonize, and its success
depends on one or more metacystic
trophozoites making contact with the
mucosa. Mature cyst in the large
intestines leaves the host in great
numbers (the host remains
asymptomatic). The cyst can remain
viable and infective in moist and cool
environment for at least 12 days, and
in water for 30 days. The cysts are
resistant to levels of chlorine
normally used for water purification.
They are rapidly killed by
purification, desiccation and
temperatures below 5 and above 40
degrees.
The metacystic trophozoites of their progenies reach the cecum and those that come in
contact with the oral mucosa penetrate or invade the epithelium by lytic digestion. The
trophozoites burrow deeper with tendency to spread laterally or continue the lysis of cells until
they reach the sub-mucosa forming flash-shape ulcers. There may be several points of

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penetration. From the primary site of invasion, secondary lesions maybe produced at the lower
level of the large intestine.
Progenies of the initial colonies are squeezed out to the lower portion of the bowel and
thus, have the opportunity to invade and produce additional ulcers. Eventually, the whole colon
may be involved. E. histolytica has been demonstrated in practically every soft organ of the body.
Trophozoites which reach the muscularis mucosa frequently erode the lymphatics or walls of the
mesenteric venules in the floor of the ulcers, and are carried to the intrahepatic portal vein. If
thrombi occur in the small branches of the portal veins, the trophozoites in thrombi cause lytic
necrosis on the wall of the vessels and digest a pathway into the lobules. The colonies increase in
size and develop into abscess.
▪ A typical liver abscess develops and consists of:
▪ Central zone necrosis
▪ Median zone of stoma only
▪ An outer zone of normal tissue newly invaded by amoeba. Most amoebic abscess of the
liver are in the right lobe. Next to the liver, the organ which is the frequent site of extra-
intestinal amoebiasis is the lungs. This commonly develops as an extension of the
hepatic abscess
▪
As the trophozoites are carried slowly toward the rectum, they are encysted and then
excreted in the feces.

Entamoeba histolytica has 2 developmental stages: a) Trophozoites/vegetative form.

Trophozoites are found in the parasitized tissues and they cannot survive outside the body. They
cause the pathogenic stage; b) Cyst form is resistant to environmental conditions thus they can
survive outside the body. They cause the infective stage.

Ingestion of
infective cyst

Excretion CA reaches small

intestines
(EXCYSTATION)

Trophozoites migrate
ENCYSTATION
to the large intestines

Trophozoites
further multiply

Figure 1: Pathogenesis of amoebiasis

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Intestinal Forms of Amoebiasis:

1. Acute amoebic dysentery. It is characterized by attacks of diarrhea alternating with
periods of constipation and often accompanied by tenesmus and colic and gaseous
distention of the lower abdomen.

2. Chronic amoebic dysentery. It is characterized by attacks of dysentery lasting for

several days to weeks, usually succeeded by a period of constipation.

3. Non–dysenteric colitis. It is a condition wherein the patient is usually asymptomatic

however is still capable of passing on the infection through excretion via the feces.

4. Amoebic colitis. It is characterized by inflammation of the intestines and its

manifestations are similar with that of appendicitis.

Diagnostic Procedures
1. Stool examination – Microscopic examination for identifying demonstrable E.H cysts or
trophozoites in stool samples is the most confirmative method for diagnosis. Trophozoites
survive only for a few hours, so the diagnosis mostly goes with the presence of cysts. But
fresh warm faeces always show trophozoites. The cysts are identified by their spherical
nature with chromatin bars and nucleus. They are noticed as brownish eggs when stained
with iodine.
2. Biopsy also can point out E.H cysts or trophozoites.
3. Culture of the stool also can guide us for diagnosis.
4. Blood tests may suggest infection which may be indicated as leucocytosis (increased level of
white blood cells), also it can indicate whether any damage to the liver has occurred or not.
5. Ultrasound scan – it should be performed when a liver abscess is suspected

Manifestations:
Only about 10% to 20% of people who are infected with E. histolytica become sick from the
infection.
1. Asymptomatic (symptomless amoebiasis)
2. Initial symptoms: diarrhea which contains specks of bloody mucus (pathognomonic sign)
secondary to lytic digestion of epithelium and mucosa, nausea and vomiting, abdominal
pain, tenesmus (sensation of the desire to defecate without the production of feces)
3. Intestinal form - acute amoebic dysentery, chronic amoebic dysentery, non-dysenteric colitis
and amoebic colitis
4. Extra-intestinal forms - hepatic, pulmonary, cutaneous and abscess of the brain and spleen.
Rarely, E. histolytica invades the liver and forms an abscess (a collection of pus). In a small
number of instances, it has been shown to spread to other parts of the body, such as the
lungs or brain, but this is very uncommon.

Common Nursing Diagnosis

▪ Altered nutrition: Less than body requirement
▪ Alteration in bowel elimination
▪ High risk for infection
▪ Anxiety
▪ Altered body temperature

Management:
1. Pharmacological

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o Tissue Amoebicides. They could be absorbed from the GIT into the bloodstream
(extraintestinal form)
▪ Metronidazole 500–75mg TID x 5–10 days
▪ Tinidazole 2g OD x 3 days
Note: when taking Metronidazole, the patient should be advised to avoid alcohol as it
may cause nausea and vomiting and headache.
o Luminal Amoebicides. They are medications which remain in the GIT (intestinal Form)
▪ Paromomycin 500mg TID x 10 days
▪ Lodoquidol 650mg TID x 20 days
2. Nutrition. Increase the caloric and fiber intake of the patient.
3. Rehydration. Administer IVF to replace fluid and electrolyte losses and increase oral fluid
intake.

Prevention:
1. Proper disposal of wastes or human feces
2. Protection of safe food and water supply such as boiling and chlorination
3. Meticulous hand washing especially after defecation and before eating
4. Sanitary preparation of food and beverages. Cover left over foods properly.
5. Careful handwashing with soap and water after using the toilet or handling soiled diapers and
proper disposal of sewage is the most important way to prevent amebiasis.
6. People with amebiasis should avoid sexual contact until the infection is treated and has
cleared.
7. When traveling to a country with poor sanitary conditions, it is important to drink water from
sources that is known to be safe such as sealed bottled water, boiled tap water, and
carbonated (bubbly) water from sealed cans. It is also important to be careful about the food:
avoid eating food from street vendors, fresh fruit or vegetables that a person did not peel by
himself/herself, and raw (unpasteurized) dairy products.

Nursing Management
1. Observe isolation and enteric precaution2.Provide health education:
▪ Boil water for drinking or use purified water;
▪ Avoid washing food from open drum or pail;
▪ Cover leftover food;
▪ Wash hands after defecation or before eating; and
▪ Avoid ground vegetables (lettuce, carrots, and the like).
2. Proper collection of stool specimen
▪ Never give paraffin or any oil preparation for at least 48 hours prior to
collectionof specimen.
▪ Instruct patient to avoid mixing urine with stools.
▪ If whole stool cannot be sent to laboratory, select as much portion as
possiblecontaining blood and mucus.
▪ Send specimen immediately to the laboratory; stool that is not fresh is
nearlyuseless for examination
▪ Label specimen properly.
3. Skin care
▪ Cleanliness, freedom from wrinkles on the sheet will be helpful with all the
usual precautionary measures against pressure sores.
4. Mouth care
5. Provide optimum comfort.
▪ Patient should be kept warm. Dysenteric patient should never be allowed
to feel,even for a moment.

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6. Diet
▪ During the acute stage, fluids should be forced.
▪ In the beginning of an attack, cereal and strained meat broths without fat
should be given.
▪ Chicken and fish maybe added when convalescence is established.
▪ Bland diet without cellulose or bulk-producing food should be maintained
for along time.

ACTIVITY 1: Enumerate at least three ways by which amoebiasis can spread to

other humans. Next is identify the two forms of the causative agent and
differentiate. Write them in the table below. When finished, kindly take a photo
of your output and post it in the discussion forum for this part of the lesson.

Ways by which the microorganism (Entamoeba histolytica) could spread:

1.
2.
3.
Developmental Stages of Entamoeba histolytica:
1.
2.

B. Cholera/ Violent dysentery

Cholera is an acute diarrheal disease characterized by projectile vomiting and massive watery
diarrhea with rapid dehydration and shock. This results from a powerful toxin elaborated by vibrio
cholera. The causative agent multiplies rapidly in the lumen of the small intestines and produces a
powerful enterotoxin that acts on the lining of the intestines to induce LBM leading to dehydration
and shock.

Causative Agent Vibrio cholera

Source of Infection
Mode of Transmission
Incubation period:
Period of Communicability
Spirillum cholera
The organisms are slightly curved rods (comma-shaped),
gram-negative and motile with a single polar flagellum
The organisms survive well at ordinary temperatures and
longer in refrigerated foods
Man
Fecal-oral route
• direct or indirect fecal contamination of water or food
supplies by soiled hands, utensils or mechanical carriers
(fingers, fomites, flies, feces)
Ingestion of contaminated water and ingestion of
contaminated raw or under cooked seafood
few hours to 5 days (an average of 1-3 days)
1-14 days as long as the causative agent is seen in the feces

Risk factors
• Environmental factors. Primary infection in humans is incidentally acquired. Risk of primary
infection is facilitated by seasonal increases in the number of organisms, possibly associated
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with changes in water temperature and algal blooms; secondary transmission occurs
through fecal-oral spread of the organism through person-to-person contact or through
contaminated water and food.
• Host factors. Malnutrition increases susceptibility to cholera. Because gastric acid can quickly
render an inoculum of V cholerae noninfectious before it reaches the site of colonization in
the small bowel, hydrochlorhydria or achlorhydria of any cause (including Helicobacter
pylori infection, gastric surgery, vagotomy, use of H2 blockers for ulcer disease) increases
susceptibility; infection rates of household contacts of cholera patients range from 20-50%.
Rates are lower in areas where infection is endemic and individuals, especially adults, may
have preexisting vibriocidal antibodies from previous encounters with the organism.

Pathogenesis
The causative agent is ingested by the susceptible host. Once it enters thru the mouth, it
adheres to the epithelial cells of the stomach and intestines. There, it multiplies and produce
enterotoxin (choleragen) which binds to a receptor on the surfaces of cell and activates intracellular
adenylates cyclase to convert to adenosine triphosphate (ATP) into cyclicadenosine monophosphate)
(CAMP). Increased CAMP activates a secretory mechanism which blocks sodium absorption and
promotes excretion of water and chloride (this mechanism is the prototype of all toxigenic diarrhea).
Toxins act through an intact epithelium on the vasculature of the bowel with resultant outpouring of
the intestinal fluids.

Manifestations:
The following are the manifestations of cholera:
a. abdominal pain. This is due to the inflammation and injury in the GIT;
b. LBM which is continuous without straining- initially, yellowish and greenish then
becomes grayish-white or RICE WATERY STOOL (pathognomonic sign) characterized as
voluminous whitish/slightly grayish mucoid without fecal matter with peculiar fishy
odor.
c. vomiting-effortless without preceding nausea;
d. signs and symptoms of dehydration such as increased thirst, muscle cramps, weakness,
poor skin turgor, oliguria and sunken fontanelle.

Mild Dehydration Moderate Dehydration Severe Dehydration

▪ Somewhat dry mucous
membranes Pale, cool skin
on arms & legs
▪ Slight tachycardia
▪ Increased capillary refill
▪ Anxiety
▪ Dry mucous membranes
Poor skin turgor
▪ Cool truncal skin
▪ Sunken fontanel/eyes
▪ Rapid, thread pulse
▪ Supine hypotension
▪ Increased thirst
▪ Restlessness, confusion, or
irritability
▪ Dry, cracked mucous
membranes Very poor skin
turgor
▪ Cold, mottled, or cyanotic
skin
▪ Sunken fontanel/ eyes
▪ Marked tachycardia &
hypotension
▪ Narrowed pulse pressure
▪ Delayed capillary refill
▪ Unconsciousness

Diagnosis:
• Stool examination. Although observed as a gram-negative organism, the characteristic
motility of Vibrio species cannot be identified on a Gram stain, but it is easily seen on direct
dark-field examination of the stool.
• Stool culture. V cholerae is not fastidious in nutritional requirements for growth; however, it
does need an adequate buffering system if fermentable carbohydrate is present because
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viability is severely compromised if the pH is less than 6, often resulting in autosterilization of

the culture.
• Serotyping and biotyping. Specific antisera can be used in immobilization tests; a positive
immobilization test result (ie, cessation of motility of the organism) is produced only if the
antiserum is specific for the Vibrio type present; the second antiserum serves as a negative
control.
• Hematologic tests. Hematocrit, serum-specific gravity, and serum protein are elevated in
dehydrated patients because of resulting hemoconcentration; when patients are first
observed, they generally have a leukocytosis without a left shift.
• Metabolic panel. Serum sodium is usually 130-135 mmol/L, reflecting the substantial loss of
sodium in the stool; serum potassium usually is normal in the acute phase of the illness,
reflecting the exchange of intracellular potassium for extracellular hydrogen ion in an effort
to correct the acidosis; hyperglycemia may be present, secondary to systemic release
of epinephrine, glucagon, and cortisol due to hypovolemia; patients have
elevated blood urea nitrogen and creatinine levels consistent with prerenal azotemia.

Cholera case is suspected if:

• in an area where the disease is not known to be present, a patient aged 5 years or more
develops severe dehydration or dies from acute watery diarrhea;
• in an area where there is a cholera epidemic, a patient aged 5 years or more develops
acute watery diarrhea, with or without vomiting.

Three Principal Deficits in Cholera:

There are three extracellular fluid volume loss in cholera and they are:
a. extracellular fluid volume loss due to intestinal loss of isotonic fluid leading to severe
dehydration and circulatory collapse or shock;
b. metabolic acidosis due to large loss f bicarbonate rich stool;
c. electrolyte imbalance (hypokalemia, hyponatremia, hypocalcemia).

Nursing Diagnosis
• Deficient fluid volume related to excessive fluid loss through the stool or emesis.
• Imbalanced Nutrition: less than body requirements related to loss of fluids through
diarrhea, inadequate intake.
• Risk for infection related to microorganisms that penetrate the gastrointestinal tract.
• Impaired Skin Integrity: perianal, related to irritation from diarrhea.
• Anxiety related to separation from parents, unfamiliar environment, a stressful
procedure.

Management:
There are three objectives in the management of cholera:
a. relief of toxemia,
b. restoration of fluid loss, and
c. prevention of complications.

As to the medical management of cholera, the following can be done:

a. prophylaxis such as the administration of cholera vaccine, 0.5 ml IM. It provides
60-80% of immunity and effective for 3-6 moths;
b. early management of fluid and electrolyte imbalance- administration of LR and
KCL to address fluid and electrolyte imbalance
c. rehydration therapy-ORS (NaCl 3.5 grams, Na bicarbonate-2.9 grams and glucose
20 grams dissolved in 1L of H20); and

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d. medications such as tetracyclines and Cotrimoxazole.

Rehydration is the first priority in the treatment of cholera. Rehydration is

accomplished in 2 phases: rehydration and maintenance.

• Rehydration phase. The goal of the rehydration phase is to restore normal hydration
status, which should take no more than 4 hours; set the rate of intravenous infusion
in severely dehydrated patients at 50-100 mL/kg/hr; Lactated Ringer solution is
preferred over isotonic sodium chloride solution because saline does not correct
metabolic acidosis.
• Maintenance phase. The goal of the maintenance phase is to maintain normal
hydration status by replacing ongoing losses; the oral route is preferred, and the use
of oral rehydration solution (ORS) at a rate of 500-1000 mL/hr is recommended.
• Cholera cots. In areas where cholera is endemic, cholera cots have been used to
assess the volume of ongoing stool losses; a cholera cot is a cot covered by a plastic
sheet with a hole in the center to allow the stool to collect in a calibrated bucket
underneath.
• Diet. Resume feeding with a normal diet when vomiting has stopped;
continue breastfeeding infants and young children.

Nursing Care:
In providing care to a client with cholera, the following can be done: 1) Isolation – enteric
precautions; 2) care of exposed persons; 3) accurate monitoring of VS, I and O; and 4) prevention
of complications.

• Assess for dehydration. Assess the status of dehydration ( skin color, temperature,
skin turgor, mucous membranes, eyes, crown, body temperature, pulse, respiration,
behavior, weight loss).
• Observe for diarrhea. Observe for a sudden attack of diarrhea, fever, anorexia,
vomiting, nausea, abdominal cramps, increased bowel sounds, and bowel
movements more than 3 times a day, with liquid stool consistency, with or without
mucus or blood.
• Assess the level of knowledge of the family. Assess for the knowledge of diarrhea at
home, dietary knowledge, and knowledge about the prevention of recurrent
diarrhea.

Prevention:
• Provision or assisting the community to access to potable and clean water resource i.e.
boiling water if not sure to be clean
• Teaching the community on proper sanitation practices, handling and preserving food
• Educating them of the importance of hand washing before handling or eating food, and after
defecating
• Proper detection of cases as part of rigid surveillance.

Complications:
Possible complications could occur in patients with cholera due to excessive diarrhea,
vomiting, and dehydration such as acidosis and shock, hypocalcemia, hypokalemia and
pneumonia.

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ACTIVITY 2: Enumerate the manifestations of cholera and highlight the

pathognomonic sign.When finished, kindly take a photo of your output and
post it in the discussion forum for this part of the lesson.
Manifestations of Cholera

C.Typhoid Fever/Enteric Fever/ Typhus Abdominalis

Typhoid fever is a bacterial infection primarily characterized diarrhea, systemic disease, and
a rash. It primarily involves the lymphoid tissue (Peyer’s patches) of the small intestines. The
infection is transmitted by contaminated water, milk, shellfish or other foods.

Causative Agent Salmonella typhi /typhosa. It is harbored inhuman excreta;

Incubation Period
Period of Communicability
Mode of Transmission
Pathognomonic Sign
Source of Infection
gram(-), motile, and non-spore forming bacillus;
pathogenic only in man; easily survives in natural habitat
like water or inorganic material.
2–3 weeks
May last for years even if the patient has become
asymptomatic as long as he is excreting the bacteria
Fecal–oral -through food and water contaminated by
infected feces and urine
Rose spots-reddish macular lesions with a diameter of 2-3
millimeters and found in the trunk of patients suffering
from typhoid fever
A person who has just recovered from the disease or has
recently taken cared of a patient with typhoid fever; stools
and vomitus.

Pathogenesis
All pathogenic Salmonella species, when present in the gut are engulfed by phagocytic cells,
which then pass them through the mucosa and present them to the macrophages in the lamina
propria.
• Salmonella typhi and paratyphi enter the host’s system primarily through the distal ileum.
• They have specialized fimbriae that adhere to the epithelium over clusters of lymphoid tissue
in the ileum (Peyer patches), the main relay point for macrophages traveling from the gut into
the lymphatic system.
• Typhoidal salmonella co-opt the macrophages’ cellular machinery for their own reproduction
as they are carried through the mesenteric lymph nodes to the thoracic duct and the
lymphatics and then through to the reticuloendothelial tissues of the liver, spleen, bone
marrow, and lymph nodes.
• Once there, they pause and continue to multiply until some critical density is reached;
afterward, the bacteria induce macrophage apoptosis, breaking out into the bloodstream to
invade the rest of the body.
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• The bacteria then infect the gallbladder via either bacteremia or direct extension of infected
bile; the result is that the organism re-enters the gastrointestinal tract in the bile and reinfects
Peyer patches.
• Bacteria that do not reinfect the host are typically shed in the stool and are then available to
infect other hosts.

Causes:
Typhoid fever is commonly acquired through an ingestion of food or water contaminated by
the urine or feces of infected carriers. While a typhoidal salmonella have no nonhuman vectors.
• Contaminated food. Paratyphi is more commonly transmitted in food from street vendors; it is
believed that some such foods provide a friendly environment for the microbe.
• Migration. Paratyphi is more common among newcomers to urban areas, probably because
they tend to be immunologically naive to it; also, travelers get little or no protection against
paratyphi fro the current typhoid vaccines, all of which target typhi.
• Decreased stomach pH. Typhoidal salmonella are able to survive a stomach pH as low as 1.5;
antacids, histamine-2 receptor antagonists (H2 blockers), proton pump inhibitors,
gastrectomy, and achlorhydria decrease stomach acidity and faciltate S typhi infection.
• Poor hygiene. As the middle class in south Asia grows, some hospitals there are seeing a large
number of typhoid fever cases among relatively well-off university students who live in group
households with poor hygiene.

Diagnostic tests
To diagnose typhoid fever, the following tests are done:
1. Typhidot. This test qualitatively detects the presence of IgM class antibodies to
Lipopolysaccharide specific to salmonella typhi in human serum or whole blood
specimens;
2. ELISA Test. It stands for enzyme-linked immune assay. It is used to detect the presence of
antibodies after having been exposed to the causative agent;
3. blood examination in which results will show leukopenia with lymphocytosis;
4. blood culture wherein it is positive with the microorganism after 1 week;
5. Urine culture which is positive with the microorganism during the first 2 weeks;
6. stool culture wherein it is positive with the organism after first week or throughout the
course of illness; done thru rectal swabbing; and
7. Widal’s Test which is a blood agglutination test done to detect the presence/absence of
serum agglutinins ( H & O) in the blood produced by the typhoid bacillus. It shows a rising
titer on the 2nd or 3rd week of the disease. Agglutination or titer of at least 1:160 against
the O antigen means the individual is in active state. Agglutination or titer of at least
1:180 against the H antigen means the individual was previously infected with typhoid
fever. A rise in the titer of the Vi antigen means the individual is a carrier.

Clinical Manifestations
The manifestations of typhoid fever are due to the systemic effects of endotoxins
and other bacterial products. These manifestations are seen in the different stages of the
disease as follows:
1. Prodromal stage (1st Week). In this stage the patient manifests fever which is
low-grade resembling a respiratory infection, malaise, somnolence
(drowsiness/sleepiness), abdominal pain, rose spots (rose colored macules early
seen on abdomen, chest, trunk and
back which disappear over a period of
3-4 days

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▪ Rose spots. The patient develops rose spots, which are salmon-colored,
blanching, truncal, maculopapules usually 1-4 cm wide and fewer than 5 in
number; these generally resolve within 2-5 days.
2. Fastigial stage or the peak of signs and symptoms). Without therapy,
temperature rises up to 40-41 degrees centigrade, severe headache, non-
productive cough, dryness of mouth, tongue covered with thick sordes (brown
collections of dried mucus and bacteria);
3. Defervescence Stage (2nd Week). In this stage, the fever becomes
remittent(temperature does not touch the baseline and remains above normal
throughout the day), PR is slow despite fever (dicrotic pulse-pulse with 2 peaks,
the 2nd is weaker)
4. other clinical S/S: enlarged liver (RUQ pain @right hypochondriac), spleen (Left
hypochondriac pain), delirium, intestinal bleeding (due to ulceration/hemorrhage
or perforation);
5. Lysis stage (3rd week). This is the stage wherein there is the abatement of signs
and symptoms; and
6. Convalescence stage. This is the stage of parenchymal repair unless
complications occur.

Nursing Diagnosis
• Risk for fluid volume deficit related to less intake, nausea, vomiting, and diarrhea.
• Imbalanced nutrition: less than body requirements related to less intake due to
nausea, vomiting, anorexia or diarrhea related to excessive output.
• Acute pain related to inflammation of the small intestine.
• Activity intolerance related to mandatory bed rest.
• Hyperthermia related to increase in metabolic rate.

Management
The management that can be employed in patients with typhoid fever can be classified as
promotive, preventive and curative.

Promotive:
1. Universal or enteric isolation
2. Special support if patient is delirious to prevent further injury
3. Safety measures
4. Cooling measures for temperature of 38.5 C or above-give antipyretics and
hydrotherapeutics
5. Increased fluid intake to prevent dehydration from sensible losses and from vomiting
6. Observe for bladder distention

Preventive
1. Good sanitation
2. Always wash hands after defecation
3. All foods from animal and fish sources should be thoroughly cooked
4. Education of general public particularly food handlers
5. Vaccination- typhoid vaccine give thru SQ followed by 2nd injection 4 weeks later then booster
dose every 3 years.
6. Abolish carrier state by routine stool culture after recovery and maybe Ampicillin

Curative
Drugs (Pharmacologic management)

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a. Chloramphenicol. This the drug of choice in typhoid fever. It acts by binding to the 50s
ribosome of bacteria thus interfering with protein synthesis in bacterial cell wall.
b. Ampicillin. It inhibits the final stage of bacterial cell wall synthesis by binding to specific
penicillin-binding proteins located inside the bacterial cell wall resulting in lysis and death of
bacteria.
c. Ciprofloxacin. It inhibits DNA-gyrase, an enzyme necessary for bacterial DNA replication and
some aspects of transcription, repair, recombination and transposition.
d. Co-trimoxazole. This drug is added in cases of relapse or in severe cases.
e. Trimethoprim sulfamethoxazole. It is given if patient is resistant to chloramphenicol

Nursing Interventions:
As part of our nursing care, we can employ the following nursing interventions.
1. Monitor fluid and electrolytes status
2. Monitor I and O
3. Increase oral fluid intake
4. Give high calorie, low residue, and non–irritating foods
5. Watch out for complications
a. Perforation of the intestines
b. Typhoid psychosis stage
• Coma vigil-a state of unconsciousness from which the patient cannot be
aroused, even by powerful stimuli.
• Subsultustendinum-an involuntary twitching of the muscles, esp. of those of
the arms and feet, causing movement of the tendons. It is thought to be a
hallmark of some febrile diseases, such as typhoid fever.
• Carphologia-describes the actions of picking or grasping at imaginary objects,
as well as the patient's own clothes or bed linens.

ACTIVITY 3: List down the stages of typhoid fever and identify the manifestations
seen in every stage. When finished, kindly take a photo of your output and post
it in the discussion forum for this part of the lesson.
Stage Manifestations
1.
2.
3.
4.
5.

D. Hepatitis A
Hepatitis A is a viral liver disease that can cause mild to severe illness caused by the
Hepatitis A virus. The hepatitis A virus (HAV) is transmitted through ingestion of
contaminated food and water or through direct contact with an infectious person.

Almost everyone recovers fully from hepatitis A with a lifelong immunity. Some
people have only a mild illness that lasts a few weeks. Others have more severe problems that
can last months. The hepatitis A virus (HAV) is transmitted through ingestion of contaminated
food and water or through direct contact with an infectious person.

The virus is primarily spread when an uninfected (and unvaccinated) person ingests
food or water that is contaminated with the feces of an infected person. The disease is

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closely associated with unsafe water or food, inadequate sanitation, poor personal hygiene
and oral-anal sex.

Unlike hepatitis B and C, hepatitis A does not cause chronic liver disease and is rarely
fatal, but it can cause debilitating symptoms and fulminant hepatitis (acute liver failure),
which is often fatal.

Hepatitis A occurs sporadically and in epidemics worldwide, with a tendency for

cyclic recurrences. The hepatitis A virus is one of the most frequent causes of foodborne
infection.

Incubation period:15–50 days with an average of 28–30 days

Risk factors
Anyone who has not been vaccinated or previously infected can get infected with the
hepatitis A virus. In areas where the virus is widespread (high endemicity), most hepatitis A infections
occur during early childhood. Risk factors include:
• poor sanitation;
• lack of safe water;
• living in a household with an infected person;
• being a sexual partner of someone with acute hepatitis A infection;
• use of recreational drugs;
• sex between men; and
• travelling to areas of high endemicity without being immunized.

Mode of Transmission
• Hepatitis A virus is transmitted by ingestion of contaminated drinking water or ice, uncooked
fruits and vegetable, and fruits and vegetables grown in or washed with contaminated water.
• It is also transmitted through fecal-oral pathway.
• The virus is transmitted also by infected food handlers.

Diagnosis
To diagnose hepatitis A, assessment/diagnostic procedures like assessment of symptoms,
liver enzymes level determination and HAV IgM antibody test or IgG Antibody test are done as
follows:
1. Assessment of symptoms like jaundice, enlargement of liver and spleen;
2. liver enzymes level determination;
3. HAV IgM antibody test.It detects the first antibody produced by the body when it is
exposed to hepatitis A. This test is used to detect early or recent infections and
to diagnose the disease in people with symptoms of acute hepatitis; and
4. IgG (immunoglobulin G) antibodies. These show up after the virus has been in your body
for a while. You may have them all your life. They protect you against hepatitis A. If you
test positive for them but not for IgM antibodies, it means you had a hepatitis A infection
in the past or had vaccinations to protect against it.

Manifestations
Majority of patients with hepatitis are anicteric and asymptomatic. However, others may
manifest symptoms such as mild, flu–like upper respiratory tract infection in the initial stage, fever,
then severe anorexia, jaundice and dark colored urine, indigestion marked by vague epigastric
distress, diarrhea, nausea, heartburn and flatulence in the later stage.

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 NCM 112a CAHPTER IV: CARE OF CLIENTS AT RISK OR WITH INFECTIOUS DISEASES

▪ Prodromal symptoms: fatigue, anorexia, malaise, headache, low-grade fever, nausea,

vomiting. Highly contagious at this time, usually 2 weeks before onset of jaundice.
▪ Icteric phase: jaundice, tea-colored urine, clay0colored stools, right upper quadrant pain
and tenderness.
▪ Symptoms often milder in children.

Prevention
Improved sanitation, food safety and immunization are the most effective ways to combat
hepatitis A. Spread of hepatitis A can be reduced by:
1. adequate supplies of safe drinking water;
2. proper disposal of sewage within communities;
3. personal hygiene practices such as regular hand-washing before meals and after going to the
bathroom
4. vaccination (Havrix and Vagta)

Management
There is no specific treatment for hepatitis A. Recovery from symptoms following infection may
be slow and may take several weeks or months. Most important is the avoidance of unnecessary
medications. Hospitalization is unnecessary in the absence of acute liver failure. Therapy is aimed at
maintaining comfort and adequate nutritional balance, including replacement of fluids that are lost
from vomiting and diarrhea.

1. bed rest during acute stage

2. frequent small feeding
3. Optimal food and fluid levels
4. gradual and progressive ambulation
5. Diet must be high in carbohydrate, low in fat, and low in protein.
6. Patient must take vitamin supplement especially the B complex group.
7. Intravenous therapy is occasionally necessary.
8. Isoprinosine (methisoprenol) may enhance the cell-mediated immunity of the T-lymphocytes.
9. Alkalies, belladonna and anti-emetics should be administered to control dyspepsia and
malaise.

Nursing Management
1. The patient must be isolated (enteric isolation).
2. Patient should be encouraged to rest during acute or symptomatic phase.
3. Improve nutritional status.
4. Utilize appropriate measures to minimize spread of the disease.
5. Observe the patient for melena and check stool for the presence of blood.
6. Provide optimum skin and oral care.
7. Increase in ability to carry out activities.
1. Encourage the patient to limit activity when fatigued.
2. Assist the client in planning periods of rest and activity.
3. Encouraged gradual resumption of activities and mild exercise during
recovery.

Prevention Control
1. Hands should be washed thoroughly every after use of toilet.
2. Travelers should avoid water and ice if unsure of their purity.
3. Food handlers should carefully be screened.
4. Safe preparation and serving of food must be practiced.

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5. The public should be educated on the mode of transmission of the disease

Complications
1. Progressive encephalopathy characterized by drowsiness and cerebral edema
2. GIT bleeding progressing to stupor and later coma. Bleeding is not responsive to parenteral
Vitamin K administration.
3. Clonus and hyperflexia are later replaced by loss of deep tendon reflexes.
4. Edema and ascitis
5. Aplastic anemia.
6. In late course of the disease, loss of corneal and papillary reflexes, elevated arterial blood,
respiratory failure, to cerebrovascular collapse may be present.

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