AMOEBIASIS/AMOEBIC DYSENTERY

Other name is Amoebic Dysentery. Refers to the infection of man by Entamoeba

Hystolytica 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 liver or lungs.
Source: Human excreta
Incubation Period: The incubation periodin severe infection is three days. In sub acute
and chronic form it last for several months. In average cases in the incubation period varies from
three to four weeks.
Risk Factor
Age Children are susceptible because they have weak immune system.
Low Socio economic they can afford health services.
Nutrional malnourished children ,have weakened immune systems.
Enviroment unsanitary places.

Pathophysiology

Ingestion of Entamoeba Hystolytica

Survival of the Entamoeba Hystolytica in the Gastrointestinal Tract due to high alkaline
tolerance

Entrance of Entamoeba hystolytica into the hosts system primarily through small

Multiplication of Entamoeba Hystolytica in colon

Irritation in the mucosal lining

Colitis in the colon

Abdominal pain and cramps

Rupture of blood vessels

 Bleeding in the GIT

Mucoid blood stool (melena)

Ulceration

Necrosis of the mucosal layer

Tenesmus (painful frequent passing of stool)

Intestinal perforation

It will spread and go to the liver, lungs and then the brain

If not treated toxemia occur

Possibility of death

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
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.
Manifestation
Sudden onset of high fever and chills
Abdominal pain or cramps
Cramps and bloating
Tenesmus (painful frequent passing of stool)
Flatulence
Feeling of incomplete emptying
 Loss of appetite
Weight loss
Headache
Fatigue
Vomiting
Dehydration
Melena
Mucoid bloody stool
Clinical Features of Amoebiasis
1. Onset is gradual.
2. Diarrhea increases and stool becomes bloody and mucoid.
3. In untreated cases:
Fluid stool severe bloody mucoid stool hemorrhage intestinal perforation
peritonitis Death
Diagnostic Procedure
Stool Exam - A stool analysis is a series of tests done on a stool (feces) sample to help
diagnose certain conditions affecting the digestive tract. These conditions can include
infection (such as from parasites, viruses, or bacteria), poor nutrient absorption,
or cancer.
Proctosigmoidoscopy - It is an exam that allows a physician to look inside
the anus, rectum, and the lower part of the large intestine (colon) for the following:
o unusual growths
o swelling
o bleeding
o hemorrhoids
o It can also remove small growths and collect tissue samples (biopsy) through a
proctosigmoidoscope.
o The proctosigmoidoscope may be a rigid or a flexible lighted tube.
Aspiration from the abscess
Treatment
Diet High caloric, high fiber and increased fluid intake.
IVF PNSS
Normal Saline is a sterile, nonpyrogenic solution for fluid and electrolyte
replenishment.
It contains no antimicrobial agents.
It contains 9 g/L Sodium Chloride with an osmolarity of 308 mOsmol/L.
It contains 154 mEq/L Sodium and Chloride.
 D5LR
Hypertonic solutions are those that have an effective osmolality greater
than body fluid, these pulls the fluid on the intravascular spaces by osmosis
resulting to an increase in the intravascular fluid volume, it raises intravascular
osmotic pressure and provides fluids, electrolytes and calories for energy.

Pharmacologic Management
Methronidazole drug of choice of amoebiasis. Should be treated for 10 days. Metronidazole is
active against a variety of protozoa and bacteria. It enters the cell as a prodrug by passive
diffusion and is activated in either the cytoplasm of the bacteria or specific organelles in the
protozoa, whereas drug-resistant cells are deficient in drug activation. The metronidazole
molecule is converted to a short-lived nitroso free radical by intracellular reduction, which
includes the transfer of an electron to the nitro group of the drug. This form of the drug is
cytotoxic and can interact with the DNA molecule. The actual mechanism of action has not yet
been fully elucidated but includes the inhibition of DNA synthesis and DNA damage by
oxidation, causing single-strand and double-strand breaks that lead to DNA degradation and cell
death. The activated reduced metronidazole molecule binds nonspecifically to bacterial DNA,
inactivating the organism's DNA and enzymes and leading to a high level of DNA breakage, with
immediate action of the drug but no cell lysis.

Nursing Management
A. Isolation
Enteric Isolation
B. Promote Hygiene
Proper personal hygiene.
Wash hands after defecation or before eating.
Wash hands after going to the toilet and before eating.
C. Maintain Nutrition
Instruct to take in rich foods high in caloric, high fiber and increased fluid intake.
Administer IVF to replace fluid loss.
D. Promote Comfort
Assume a comfortable position
Elevate the head of the bed
Promote relaxation and provide adequate rest.
 Properly perform bed making
E. Prevention and Control
Proper disposal of waste
Avoid eating raw fruits and vegetables unless you can peel them yourself.
Dont eat food from street vendors.
Boil water for drinking.
F. Provide Safety
Raise side rails of the bed.
Instruct significant others do not leave the patient.
TYPHOID FEVER

Typhoid fever is caused by Salmonella typhi bacteria. Typhoid fever is rare in

industrialized countries. However, it remains a serious health threat in the developing world,
especially for children.

In the United States, it is estimated that approximately 5,700 cases occur annually. Most
cases (up to 75%) are acquired while traveling internationally. Typhoid fever is still common in
the developing world, where it affects about 21.5 million persons each year.

Typhoid fever is an acute systemic illness caused by motile, gram-negative bacilli of the
genus Salmonella usually Salmonella typhi or Salmonella enteritidis.

The organisms are gram-negative, flagellated, noncapsulated, non-sporulating, facultative

anaerobic bacilli, which have characteristic flagellar, somatic, and outer coat antigens.

Typhoid fever, the most serious human salmonellosis, is characterized by prolonged

fever, bacteremia and multiplication of the organisms within mononuclear phagocytic cells of the
liver, spleen, lymphnodes, and Payers patches.

Humans are the only natural reservoir for Salmonella typhi, and typhoid fever therefore
must be acquired from convalescing patients or from chronic carriers- especially older women
with gallstones or biliary scarring, in whom Salmonella typhi may colonize the gallbladder or
biliary tree.

Risk Factors

Typhoid fever remains a serious worldwide threat especially in the developing world
affecting an estimated 26 million or more people each year.

The disease is endemic in India, Southeast Asia, Africa, South America and many other
areas.

Worldwide, children are at greatest risk of getting the disease, although they generally
have milder symptoms than adults do.

If you live in a country where typhoid fever is rare, you're at increased risk if you: Work
in or travel to areas where typhoid fever is endemic Work as a clinical microbiologist handling
Salmonella typhi bacteria Have close contact with someone who is infected or has recently been
infected with typhoid fever Drink water contaminated by sewage that contains S. typhi.

Typhoidal salmonella have no nonhuman vectors. An inoculum as small as 100,000 organisms

of typhi causes infection in more than 50% of healthy volunteers.Paratyphi requires a much
higher inoculum to infect, and it is less endemic in rural areas. Hence, the patterns of
transmission are slightly different.
 The following are modes of transmission of typhoidal salmonella:
Oral transmission via food or beverages handled by an often asymptomatic individuala
carrierwho chronically sheds the bacteria through stool or, less commonly, urine
Hand-to-mouth transmission after using a contaminated toilet and neglecting hand
hygiene
Oral transmission via sewage-contaminated water or shellfish (especially in the
developing world).

Paratyphi is more commonly transmitted in food from street vendors. It is believed that
some such foods provide a friendly environment for the microbe.

Paratyphi is more common among newcomers to urban areas, probably because they
tend to be immunologically nave to it. Also, travellers get little or no protection
against paratyphi from the current typhoid vaccines, all of which target typhi.

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 facilitate S typhi infection.

HIV/AIDS is clearly associated with an increased risk of nontyphoidal Salmonella

infection; however, the data and opinions in the literature as to whether this is true for S typhi or
paratyphi infection are conflicting. If an association exists, it is probably minor.

Other risk factors for typhoid fever include various genetic polymorphisms. These risk
factors often also predispose to other intracellular pathogens. For instance,
PARK2 and PACGR code for a protein aggregate that is essential for breaking down the bacterial
signaling molecules that dampen the macrophage response. Polymorphisms in their shared
regulatory region are found disproportionately in persons infected with Mycobacterium
leprae and S typhi.

On the other hand, protective host mutations also exist. The fimbriae of S typhibind in
vitro to cystic fibrosis transmembrane conductance receptor (CFTR), which is expressed on the
gut membrane. Two to 5% of white persons are heterozygous for the CFTR mutation F508del,
which is associated with a decreased susceptibility to typhoid fever, as well as
to cholera and tuberculosis. The homozygous F508del mutation in CFTR is associated with
cystic fibrosis. Thus, typhoid fever may contribute to evolutionary pressure that maintains a
steady occurrence of cystic fibrosis, just as malaria maintains sickle cell disease in Africa.

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.American clinicians should keep this in mind, as members of this
cohort often come to the United States for advanced degrees.

Pathophysiology
 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. Nontyphoidal salmonellae are phagocytized throughout the distal ileum and
colon. With toll-like receptor (TLR)5 and TLR-4/MD2/CD-14 complex, macrophages
recognize pathogen-associated molecular patterns (PAMPs) such as flagella and
lipopolysaccharides. Macrophages and intestinal epithelial cells then attract T cells and
neutrophils with interleukin 8 (IL-8), causing inflammation and suppressing the infection.
In contrast to the nontyphoidal salmonellae, S 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. The bacteria then induce their
host macrophages to attract more macrophages.
S typhi has a Vi capsular antigen that masks PAMPs, avoiding neutrophil-based
inflammation, while the most common paratyphi serovar, paratyphi A, does not. This may
explain the greater infectivity of typhi compared with most of its cousins.
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.
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.
Chronic carriers are responsible for much of the transmission of the organism. While
asymptomatic, they may continue to shed bacteria in their stool for decades. The organisms
sequester themselves either as a biofilm on gallstones or gallbladder epithelium or, perhaps,
intracellularly, within the epithelium itself. The bacteria excreted by a single carrier may have
multiple genotypes, making it difficult to trace an outbreak to its origin.

Manifestation

Pathognomonic Sign: Rose Spots reddish macular lesions 2- 3 mm found in the trunk.

1. Prodromal Stage fever, malaise, somnolence, abdominal pain and rose spots.

2. Fastigial Stage without therapy temperature rises up 40 41 centrigrade, severe headache

and nonproductive cough. May suffer from convulsions. This stage is the peak of the disease.

3. Defervenscence fever becomes remittent, pulse rate slow despite fever. Other clinical s/s:
enlarged liver and spleen, delirium, intestinal bleeding.
4. Lysis stage abatement of signs and symptoms.

5. Covalescence stage of parenchymal repair.

Diagnostic Procedure

o Typhidot confirmatory
Typhidot is a medical test consisting of a dot ELISA kit that
detects IgM and IgG antibodies against the outer membrane protein (OMP) of
the Salmonella typhi. The typhidot test becomes positive within 23 days of
infection and separately identifies IgM and IgG antibodies. The test is based on
the presence of specific IgM and IgG antibodies to a specific 50Kd OMP antigen,
which is impregnated on nitrocellulose strips. IgM shows recent infection whereas
IgG signifies remote infection. The most important limitation of this test is that it
is not quantitative and result is only positive or negative. Whereas a
detailed Widal test can tell the titres of specific antibodies. However both tests
lack sensitivity and specificity. The Widal test is losing its value as it is labor-
intensive and time-consuming.It is an immunochromatographic test.

o Blood Examination (Complete Blood Count) Increased WBC (leukocytosis)

related to infection.

o Blood Culture (Culture and Sensitivity) Determine causative agent; after 1 st

week.

o Widal Test/ Agglutination Test/ Tyter Test Determine antibody against the
causative agent; (+) by the end of 2 nd week. Widal test is a tube agglutination test
employed in the serological diagnosis of enteric fever.

o Elisa - determine the presence of Antigen itself.

o Rectal Swab
A cotton swab is inserted into the rectum. The swab is rotated gently, and
removed.
A smear of the swab is placed in culture media to encourage the growth of
bacteria and other organisms. The culture is watched for growth.
The organisms can be identified when growth is seen. More tests may be
done to determine the best treatment.

Treatment

IV Fluid (D5LR)
 This helps prevent the dehydration that results from a prolonged fever and diarrhea. If
you're severely dehydrated, you may need to receive fluids through a vein (intravenously).
Hypertonic solutions are those that have an effective osmolality greater than body fluid, these
pulls the fluid on the intravascular spaces by osmosis resulting to an increase in the intravascular
fluid volume, it raises intravascular osmotic pressure and provides fluids, electrolytes and
calories for energy.

Diet
- Non bulky high calorie meals, such as those with rice or carbohydrates, and can help
replace the nutrients loss when the individual is sick with typhoid.
- Eating plenty fresh fruits and vegetables can facilitate faster recovery.

Pharmacologic Management

Chloramphenicol Drug of choice. 3-4 gm per day PO in 4 divided doses for 14 days.
Binds to 50S bacterial-ribosomal subunits and inhibits bacterial growth by inhibiting protein
synthesis. Effective against gram-negative and gram-positive bacteria.

Others: Co-Trimoxazole forte or double -strength tab twice a day PO for 14 days or
Amoxyxillin 4-6 gm per day PO in 3 divided doses for 14 days.

Nursing Management

A. Isolation
o Enteric isolation
Properly dispose human waste
B. Promote comfort
o For fever administer antipyretic medication
o Properly perform bed making
o For pain, instructed to assume comfortable position
o
C. Provide adequate nutrition
o Diet
Non bulky high calorie meals, such as those with rice or carbohydrates,
and can help replace the nutrients loss when the individual is sick with
typhoid.
Eating plenty fresh fruits and vegetables can facilitate faster recovery.

o IVF replace fluid loss.

o Increase oral fluid intake
D. Provide safety
Raise side rails of the bed

E. Monitor CBC
 To monitor red blood count.
F. Prevention and Control

Mariano Marcos State University

COLLEGE OF HEALTH SCIENCES
Department of Nursing
City of Batac

_____________________________________________________

Amoebiasis and Typhoid Fever

_____________________________________________________

Presented to:
MRS. MARILYN RACCA
Faculty, Mariano Marcos State University
College of Health Sciences
Nursing Department

_____________________________________________________

In Partial Fulfillment
Of the Requirements in the Subject
RLE 104B

_____________________________________________________

Presented by:
Jerome Clark C. Cid
Angelu Gabrielle E. Castro

BSN III-A
Group 2
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April 12, 2016