Case Study Bactegroup 3
Case Study Bactegroup 3
Escherichia coli
Submitted to:
Ansharimar Balagosa, RMT
Merryl Louise Matus, RMT
Submitted by:
November 2022
CHAPTER 1
INTRODUCTION
A bacteria known as Escherichia coli (E. coli) may be found in human and animal
intestines, the environment, and foods. Initially, it was thought to be a normal resident of the
colon's indigenous biota (Mahon, C. et al., 2019). It is currently recognized as a significant human
pathogen linked to various clinical syndromes, such as UTIs, diarrheal illnesses, and central
nervous system infections. There are several strains of E. coli, including uropathogenic E. coli
(UPEC), enterotoxigenic E. coli (ETEC), enteropathogenic E. coli (EPEC), enteroinvasive E. coli
(EIEC), enterohemorrhagic E. coli (EHEC), enteroaggregative E. coli (EAEC), and diffusely
adherent E. coli (DAEC) (Mahon, C. et al., 2019).
ETEC, also known as enterotoxigenic Escherichia coli (E. coli), is a significant contributor
to bacterial diarrheal disease. The most common cause of traveler's diarrhea and a significant
contributor to diarrheal illness in low-income nations, particularly among children, is ETEC
infection (Mahon, C. et al., 2019). When people consume food or drink water or ice tainted with
ETEC bacteria, they get infected. The primary source of ETEC contamination is human or animal
waste, such as feces. When visiting impoverished countries, travelers from industrialized nations
frequently contract ETEC. The prevalence and transmission of this disease are mainly attributed
to poor sanitation, a lack of drinking water sources, and poor hygiene (Mahon, C. et al., 2019).
According to WHO, about 75 million of the 220 million diarrhea episodes caused by ETEC are
thought to affect children under the age of five. These episodes are thought to cause between 18
700 and 42000 fatalities worldwide in children under five years old. Intense watery, nonmucoid,
nonbloody diarrhea, abdominal discomfort, nausea, vomiting, and little to no fever are typical
signs and symptoms. The disease typically lasts 3-5 days and is self-limited; however, it can
occasionally last longer than one week (Kliegman, R. et al., 2020).
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CASE PRESENTATION
In our case, a 26-year-old female with no medical history presents to her primary physician
with complaints of watery diarrhea, abdominal cramps, and nausea with no vomiting for two days.
Upon questioning, the patient stated that she visited her mother in Quezon city four days ago and
ate street foods such as isaw, Kwek Kwek, and kikiam. Physical examination showed
temperature: 37oC, P 89, RR 15 breaths per minute, BP 110/80 mmHg, Ht 5′6″, Wt
79kg, slightly distended abdomen, positive for abdominal pain, bowel sounds hyperactive and
negative for rashes and back pain. Laboratory findings showed platelet count: 155 x10 9/L, WBC
count: 13 x 109/L, Neutrophil count: 74%, Eosinophil count: 2%, Hgb: 15.0 g/dL, Sodium: 125
mmol/L, Potassium: 3.0 mmol/L, and Chloride: 87.2 mmol/L. Based on the symptoms, travel
history, and food consumed, the patient was suspected of E.coli as the causative agent of watery
diarrhea. Macroscopic examination of the stool showed color: yellow, consistency type 7, and
odor: foul odor. Microscopic examination of the stool showed negative for mucus, RBC, WBC,
ova/parasite. Moreover, stool culture is positive and on MacConkey agar, it showed a pink colony
with bile salts precipitating around and appeared green metallic sheen on EMB agar which is a
characteristic of E. coli. Biochemical tests were ruled out for a better prognosis, and it showed
glucose and lactose fermenters, indole positive, methyl red positive, Voges-Proskauer negative,
and citrate negative. Furthermore, It does not produce H2S, urease, or phenylalanine deaminase.
Based on the colony morphology and biochemical test, E. coli was confirmed to be the causative
agent of watery diarrhea. To determine the specific strain of E. coli causing the disease,
immunologic assays were ordered and showed the presence of heat-labile and heat-stable toxins,
the toxins released by Enterotoxigenic E. coli (ETEC) strains into the small intestines. Thus, the
diagnosis drawn by the physician was Traveler's diarrhea due to Enterotoxigenic E. coli (ETEC)
strains.
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CHAPTER 2
PATIENT DATA
I. Personal Data
Sex: Female
Height: 5'6
Weight: 79 kg
Address: N/A
● N/A
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○ WBC: Negative
○ Ova/Parasite: Negative
○ Stool culture: Positive
● Macroscopic examination
○ color: yellow
○ consistency: type 7
○ odor: foul odor
● Biochemical tests
○ Glucose and Lactose fermenters: Positive
○ Indole: positive
○ Methyl Red: Positive Voges-Proskauer: Negative
○ Citrate: negative
○ H2S: Negative
○ Urease: Negative
● Immunoassay
○ Heat labile toxin: Positive
○ Heat stable toxin: Positive
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CHAPTER 3
SMALL INTESTINE
I. ANATOMY
The small intestine is a convoluted tube connected from the stomach to the large
intestine. (Vasković, J., 2022). The small intestine is divided into three subdivisions;
duodenum, jejunum, and ileum. Duodenum is divided into four parts: superior,
descending, horizontal, and ascending. (Marieb and Keller, 2018). The superior part is
connected to the undersurface of the liver by the hepatoduodenal ligament (HDL). In front,
the gastroduodenal artery (GDA), portal vein, and common bile duct are located, followed
by the quadrate lobe of the liver and gallbladder (CBD). The proper hepatic artery is also
present. The right kidney and inferior vena cava are located in the rear, the transverse
mesocolon and colon are connected to the descending section in the front, which has an
upper and a lower genu (flexure), and the head of the pancreas is situated in the concavity
of the duodenal C. The ascending portion continues into the jejunum at the duodenojejunal
flexure, whereas the horizontal portion extends from right to left in front of the inferior vena
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cava, aorta, and superior mesenteric arteries.(Marieb and Keller, 2018). The jejunum is
the second region of the small intestine, runs from the duodenum to the ileum. Even
though there are no clear demarcation notes between the jejunum and ileum, the jejunum
has thicker walls and a wider lumen than the ileum and mainly occupies the upper left and
central abdomen. The ileum is the lengthiest portion of the small intestine. The terminal
ileum is situated in the lower right quadrant of the abdomen and can extend into the pelvic
cavity. The ileum terminates at the ileocecal junction, where the large intestine's cecum
begins. It has thinner walls and smaller lumens and occupies the central and right lower
abdomen and pelvis. (Marieb and Keller, 2018). The small intestine has a very high level
of nutrient absorption adaptation. Its length provides a sizable surface area and three
structural modifications significantly increasing its absorptive surface—circular folds, villi,
and microvilli. (VanPutte et al., 2013).
II. PHYSIOLOGY
The small intestine is a major constituent of the digestive system. The small
intestine is responsible for completing food digestion and absorbing nutrients. Mucus,
ions, and water comprise most small intestine mucosal secretions. Enzymes necessary
for digestion's last stages are bound to the epithelial cells' free surfaces in the small
intestine's walls. (VanPutte et al., 2013). Peptidase, an enzyme found in the small
intestine that breaks the bond present in protein to form amino acids. Disaccharidase is
an enzyme in the small intestine that breaks disaccharides, such as maltose, into their
simplest form - monosaccharide, glucose. The intestinal epithelium can absorb the amino
acids and monosaccharides. Duodenal glands and goblet cells produce mucus that is
used to help neutralize the acids produced by the stomach and help lubricate the
epithelium for the easier passage of food. (VanPutte et al., 2013). Hormones released
from the intestinal mucosa stimulate the liver and pancreatic secretions. Mixing and
propulsion of chyme happen in the small intestine. Peristalsis is a series of muscle
contractions that usually happens in the digestive system that allows moving food through
the digestive tract. Patel & Thavamani, 2022). Through peristalsis, chyme passes from the
stomach into the small intestine and allows the mix with digestive enzymes and fluids.
(Marieb and Keller, 2018).
Furthermore, most absorption occurs in the small intestine. Specifically in the
duodenum and jejunum, although some absorption also occurs in the ileum. Some
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molecules can diffuse through the intestinal wall, whereas others must be transported
across the intestinal wall. (VanPutte et al., 2013).
III. PATHOPHYSIOLOGY
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CHAPTER 4
LABORATORY RESULTS
Hematology Test/s
Platelet count:
It is important in
preventing clots
and excessive
bleeding in the
body.
Neutrophil: It is
an indication of
underlying
factors like
inflammation and
infection. It
increases when
there is a
bacterial
infection.
Eosinophil: Are
present in
parasitic
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infection
Microbiology Test/s
Macroscopic Examination
Examination
of stool
Color: Yellow Brown Fat and Bacterial The regular
Infection stool's brown
color and
Consistency: Type 3 or Type Watery, No solid consistency
Type 7 4 changing might
frequently be the
Odor: Foul Odor Odorless first sign of GI
issues.
Nevertheless, a
distinction must
be made
between this and
a potential
pathogenic
reason because
the appearance
of abnormal fecal
color may also
result from the
consumption of
highly pigmented
foods and drugs.
Microscopic
examination of
the feces is the
most crucial
Microscopic Examination stage in the
discovery of
gastrointestinal
problems and
anomalies in the
stool.
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in stool indicates
that there’s no
symptoms of
infection.
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using it.
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Biochemical Glucose and - Glucose and The majority of
tests Lactose Lactose fermenters: isolates may be
fermenters: Positive successfully
Positive Indole: positive identified to the
Indole: positive Methyl Red: species level
Methyl red: Positive Voges- with the use of
Positive Voges- Proskauer: biochemical
Proskauer: Negative testing.
Negative Citrate: negative
Citrate: negative H2S: Negative
H2S: Negative DNase: Negative
Urease: Urease: Negative
Negative
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CHAPTER 5
SUMMARY
The Travelers’ Diarrhea is an acute diarrheal illness that is generally acquired when
travelers ingest contaminated food and water. This disease is often caused by enterotoxigenic
Escherichia coli; also known as turista. This condition is characterized by profuse watery diarrhea,
abdominal cramping, fever, nausea with or without vomiting, loss of appetite, headache, and
chills. Travelers’ Diarrhea is a self‐limiting disorder that affects the gastrointestinal tract (GI) such
as the small and large intestine. The ETEC strains use an adhesin (colonization factor antigen)
to attach to the mucosal surface in the intestine. The bacterium itself doesn’t invade the surface.
Rather, it binds to a specific receptor on the intestinal microvilli and it produces either or both of
two enterotoxins: the heat-stable toxin (ST) and the heat-labile toxin (LT). The heat-labile toxins
(LT) consist of two fragments (A and B), A for the enzymatically active portion and B is the binding
portion, confers for the specificity. The B portion binds to the GM1 ganglioside of the intestinal
mucosa thus providing entry for the A portion. Both of these toxins change the net fluid transport
in the gut from absorption to secretion. During an infection, the A portion activates the adenylate
cyclase-cyclic AMP system, causing an increase in the conversion of cyclic adenosine
monophosphate (Camp) resulting in watery diarrhea similar to cholera. The heat-stable toxin (ST)
stimulates guanylate cyclase, causing increased secretion absorption of fluids and electrolytes
across the intestinal epithelium.
CONCLUSION
In this case, a 26-year-old female, was admitted to the hospital with the complaints of
watery diarrhea, an abdominal cramp, nausea without vomiting or fever. The patient, however,
has a travel history and after traveling, the patient also experiences other manifestations such as
slightly distended abdomen and hyperactive bowel sounds.Furthermore, a positive growth in the
MacConkey agar has been seen. With these clinical presentations, it is suspected that there is
Enterotoxigenic Escherichia coli infection.
Based on the laboratory findings, a stool culture sample shows an elevated level of white
blood cells (WBC) count in the stool, and immunologic assays showed a presence of heat-labile
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toxins (LT) and heat-stable toxins (ST) which are essential for the diagnosis of the infection as
part of the manifestations clinically caused by Travelers’ diarrhea. The patient shows a positive
result in MacConkey agar with pink colony growth with bile salts precipitating around it, this further
confirms that it is caused by Escherichia coli infection.
In a stool culture test, was done for ruling out other gastrointestinal pathogens and the
result is positive. Furthermore, an Immunoassays test shows there are toxin factors which are the
heat-labile toxin (LT) and heat-stable toxin (ST) indicating that indeed there is a Enterotoxigenic
Escherichia coli infection. And lastly, there is a positive growth on a MacConkey agar with a pink
colony surrounded by bile salts, as observed in this case.
The clinical manifestations presented in the patient along with the collective results of
laboratory tests are patterned to the diagnosis of Enterotoxigenic Escherichia coli infection which
is the Travelers’ Diarrhea. And the results of laboratory tests conducted have confirmed that this
disease is Travelers’ Diarrhea.
RECOMMENDATION
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CHAPTER 6
BIBLIOGRAPHY
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STUDENT CONTRIBUTION
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