CHAPTER

Infections of the Gastrointestinal Tract 14

INTRODUCTION
Microbial diseases of the diges ve system are second only to respiratory diseases as
causes of illness in the World. Most such diseases result from the inges on of food or water
contaminated with pathogenic microorganisms or their toxins. These pathogens usually
enter the food or water supply a er being shed in the feces of people or animals infected
with them. Therefore. microbial diseases of the diges ve system are typically transmi ed by
a fecal-oral cycle. This cycle is interrupted by e ec ve sanita on prac ces in food produc on
and handling. Modern methods of sewage treatment and disinfec on of water are essen al.
There is also an increasing awareness of the need for new tests that will rapidly and reliably
detect pathogens in foods (a perishable commodity).

LEARNING OUTCOMES
At the end of the chapter, students must have:
1. Recognized common gastrointes nal tract infec ons based on clinical manifesta ons;
2. Di eren ated invasive from non-invasive diarrhea;
3. Compared the ve hepa c infec ons;
4. Described the characteris cs of the causa ve organisms of each gastrointes nal tract
infec on;
5. Explained how the di erent gastrointes nal tract infec ons are transmi ed; and
6. Discussed the appropriate laboratory diagnosis, treatment, and preven on of each
infec on.

WARM-UP ACTIVITY
What is your POOP telling you?
Poop does a lot more than just get your waste out of your body! If you aren’t aware, your
poop is actually a good indicator of your health in a lot of ways. The Bristol stool chart
iden es seven di erent shapes of human feces and is used to medically diagnose a person
based on the shape of the stool of that person. Using this scale is a good way to di eren ate
between what a healthy stool should look like and what other shapes might mean.

Ouch!! Tell someone straight away! Exercising, drinking plenty, ea ng

veggies? Not holding your poos in?

Doing well! Wohoo! These are the “Best Poos Ever”

Angelica May DC. Mendoza, RPh, MS Page 1 of 12

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 Uh-oh, you might need some help if
thie con nues. No good, best to get Mum or Dad

Your poo is like wee! Need to get checked.

Microbiota in the small intestines

CENTRAL ACTIVITIES and large intestines
Learning Input 1 (Lecture)
De ni on of Terms
Gatri s - in amma on of the mucosal lining of the stomach
Enteri s - in amma on of the small intes nes
Coli s - in amma on of the colon (large intes ne)
Gastroenteri s - in amma on of the mucosal lining of the stomach and intes ne
Hepa s - in amma on of the liver
Dysentery - low-volume, painful, bloody diarrhea

Establishment of Infec ous Disease in the Diges ve System

1. Pharmacologic ac on - some bacteria produce toxins which may alter normal
intes nal func on without causing las ng damage to their target cells. For example,
the toxin produced by Vibrio cholerae produces voluminous, watery diarrhea due to its
ability to induce increased electrolyte secre on into the intes nes.
2. Local In amma on - invasion of the alimentary tract by microbes can lead to
in amma on. Invasion is usually limited to the epithelial layer but may spread to the
deeper ssues. In the mouth, the gums are usually a ected causing periodon s. In
the intes ne, infec ons can cause in amma on that can result to dysentery.
3. Deep Tissue Invasion - certain organisms are able to adjacent and enter the
bloodstream. For example,the parasite Strongyloides is capable of burrowing the
intes nal wall.
4. Perfora on - when the mucosal epithelium is perforated, the normal ora spills into
sterile areas and invades deep ssues, o en with serious consequence. For example,
perfora on of an in amed appendix can lead to peritoni s. butas in the intestinal lining. di
kayang lumusot
Mouth
1. Dental Caries (Tooth Decay)
• E ologic agents:
a. Streptococcus mutans - most important organism that causes dental
caries. Favors crevices or other sites on the teeth that are protected from
the shearing ac on of chewing or from the ushing ac on of saliva. The
lac c acid produced by the bacteria is not diluted or neutralized by saliva,

biofilm coating the teeth that serves

as a magnet that makes the bacteria
Angelica May DC. Mendoza, RPh, MS stay strong. Lactic acid causes dental Page 2 of 12
caries.

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prevention: Sucrose
xx
-Floss
-brushing, visiting
dentist every 6
and this breaks down the enamel of the teeth, leading to localized
months
flouride, so ening of the external enamel.
mouthwash(clorhexibi b. Ac nomyces
n) c. Lactobacilli
2. Periodental Disease - a term used to describe condi ons taht are characterized by
in amma on and degenera on of structures that support the teeth.
a. Gingivi s - the reversible in amma on of the gums, characterized by bleeding
of the gums while brushing the teeth.
• E ologic agents:
a. Streptococci
b. Ac nomyces
c. Anaerobic gram-nega ve bacteria (Prevotella, Bacteroides, and
Fusobacterium nucleatum)
b. Periodon s - a chronic gum disease that can cause bone destruc on and tooth
loss. It generally causes li le discomfort.
c. Acute Necro zing Ulcera ve Gingivi s (Vincent’s Disease/Trench Mouth) -
characterized by pain that prevents normal chewing and may be accompanied
by bad breath or halitosis.
• E ologic agent: Prevotella intermedia
• Treatment and Preven on:
a. Adequate debridement
b. Oxidizing agents
c. Miconazole
3. Oral Thrush- characterized by white patches adherent to the oral mucosa and may
occur on the tongue, lips, gums, or palate. overgrowth- thrush
• E logic agent: Candida albicans - a fungus that is part of the normal ora of the
skin, mucous membranes, and gastrointes nal tract.
• Predisposing Factors:
a. Endocrine disturbances pregnant
b. Prolonged intake of an bio cs
c. Malnutri on
d. Malignancy
e. Immunocompromised
f. Prolonged use of steroids
• Laboratory Diagnosis: examina on of scraped material under the microscope
demonstra ng the characteris cs of pseudohyphae
• Treatment and Preven on:
a. Nysta n - DOC
b. Correc ng the predisposing factors
c. Avoiding unnecessary use of an bio cs
4. Mumps (Epdemic Paro s) - a highly communicable disease characterized by painful
in amma on of the salivary glands. parotive glands
• E logic agent: Mumps virus - a member of the family Paramyxoviridae.
• Mode of Transmission: respiratory droplets
• Clinical Findings: The virus infects the salivary glands, the paro d glands
predominantly infected. A er incuba on period of 18-21 days, the pa ent

unilateral or bilateral.
Angelica May DC. Mendoza, RPh, MS Page 3 of 12
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 develops fever, malaise, anorexia followed by tender swelling of the paro d
glands and/or salivary glands. Involvement can be unilateral or bilateral.
• Complica ons:
a. Orchi s - in amma on of the testes
b. Meningi s coverings of the brain
• Laboratory Diagnosis: based on clinical manifesta ons. Virus isola on from
saliva, spinal uis, or urine can be done. Measurement of an body ters can
also be made.
• Treatment and Preven on:
a. Treatment is mainly suppor ve
b. MMR vaccine - preven on

Stomach
1. Gastri s and Pep c Ulcer Disease
• E logic agent: Helicobacter pylori - it has 2 major virulence factors: rapid
mo lity and urease produc on.
• Mode of Transmission: acquired through inges on and person-to -person
transmission may also occur.
• Clinical Findings: characterized by recurrent pain in the upper abdomen,
especially around the epigastric area. This may be complicated by bleeding into
the GIT.
• Laboratory Diagnosis: gastric biopsy specimen can be used for histologic
examina on. Culture can also be done as well as measurement of an body
levels speci c for H. pylori.
• Treatment and Preven on: triple therapy with proton pump inhibitor, -razol
-mycin macrolide, and amoxicillin for 7 to 10 days. omeprazol,
clarithromycin
Liver
1. Hepa s - in amma on of the liver is termed hepa s.
• E ologic agents:
a. Hepa s viruses - most important cause
b. Other viruses - Cytomegalovirus, Epstein Barr virus, Herpes Simplex virus,
Rubella virus, Enteroviruses, Dengue virus, and the Yellow Fever virus.
• Clinical Findings: the same, regardless of which hepa s virus is the cause. Typical
signs and symptoms include fever, anorexia, nausea, vomi ng, and jaundice. Dark
urine and pale feces are also observed. Most cases resolved sponatneously in 1 to
4 weeks.

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 Table 1. Comparison of Features of Hepa s Viruses
Feature Hepa sA Hepa sB Hepa sC Hepa sD Hepa sE

Common “Infec ous” “Serum” “Non-A, Non- “Delta agent” “Enteric non-
Name
street foods
B post- defective A, non-B)
transfusion” virus
Virus Picornavirus; Hepadnavirus Flavivirus; Viroid-like; Hepevirus;
Structure capsid RNA ; envelope, envelope, envelope, Calcivirus-like
DNA RNA circular DNA capsid
Transmission Fecal-oral Parenteral, Parenteral, Parental, Fecal-oral
sexual, sexual, sexual
insidous insidous
Incuba on 15-50 45-160 140-180+ 15-64 15-50
Period (Days)
Severity Mild Occasionally Usually sub- Co-infec on Normal
severe clinical; 70% or super pa ents,
chronicity infec on with mild;
subclinical HBV pregnant
women,
severe
Carrier State No Yes Yes Yes No

Other None Primary Primary Cirrhosis, None

Disease hepato- hepato- fulminant
Associa ons cellular cellular hepa s
carcinoma, carcinoma,
cirrhosis cirrhosis
Laboratory Symptoms Symptoms Symptoms An -HDV -
Diagnosis and an -HAV and serum and an -HCV ELISA
IgM levels of ELISA
HBsAg,
HBeAg, and
an -HBc IgM
Treatment Mainly Mainly Interferon Interferon Mainly
and suppor ve; suppor ve; alpha + alpha; HBV suppor ve
Preven on HAV Vaccine Interferon Ribavirin Vaccine
alpha; HBV
vaccine and
immunoglob
ulin
**Hepa s G Virus (HGV/GB Virus C) - not primarily hepatropic. The virus replicates within
monocytes then nds its way into the liver where it can cause a chronic type of hepa s. It
is transmi ed through sexual intercourse and blood transfusion and may occur as co-
infec on with HIV.
HGV may interfere the replication of
HIV

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 Small and Large Intes nes
1. Gastroenteri s (Diarrhea) - a change in the normal bowel habits of an individual, with
an increase in the frequency, idity, looseness, and volume of feces excreted per day
in comparison to the usual fecal output of the individual.
• Mode of Transmission: Fecal-oral transmission small intestines, no blood but
• Clinical Findings: watery
a. Non- invasive - result of disrup on of the secretory process due to the
toxin released from the bacteria. This is characterized by watery diarrhea
and the absence of blood or leukocytes in the feces.
b. Invasive - there is direct damage to the GIT ssues due to direct invasion
by the bacteria. It is characterized by fever, dysentery (blood in stools),
and leukocytes in the feces. large intestines, bloody
• E ologic Agents:
a. Escherichia coli - a gram-nega ve, mo le, encapsulated rod that is a
four virolence member of the family Enterobacteriaceae and is a member of the normal
intes nal ora.
‣ Five Pathogenic Groups
i. Enterotoxigenic E. coli (ETEC) - major cause of “traveler’s
diarrhea” or “turista” and is an imporatnt cause of diarrhea in
infants in developing coun es. Produces cholera-like toxin,
non-invasive.
ii. Enteropathogenic E. coli (EPEC) - important cause of diarrhea
in infants in developing countries. The organism adheres to
mucosal cells of the small intes ne and causes loss of
microvilli. This leads to watery diarrhea.
iii. Enteroaggrega ve/Adheren E. coli (EAEC) - causes acute and
chronic diarrhea. Produces ST-like toxin and a hemolysin.
iv. Enterohemorrhagic E. coli (EHEC) - Prodces a shiga-like toxin
shigella as that produced by Shigella. It is a verotoxin that is cytotoxic,
disenterae?? neurotoxic, and enterotoxic. It is associated with hemorrhagic
coli s. In 2011, E. coli O104:H4 caused a serious outbreak of
food borne illness in Germany.
v. Enteroinvasive E. coli (EIEC) - causes invasion of the colonic
mucosa. The disease is characterized by acute bloody diarrhea
with malaise, headache, high fever, and abdominal pain. It is
the most common cause of UTI as well as meningi s in
newborns.
• Laboratory Diagnosis: culture of organism using a di eren al
medium (EMB or MacConkey’s agar)
• Treatment and Preven on:
i. Trimethoprim + Sulfamethoxazole - given to shorten
symptoms and eliminate invasive forms
ii. Fluid and electrolyte replacement
iii. D o x y c y c l i n e , C i p r o o x a c i n , o r Tr i m e t h o p r i m +
Sulfamethoxazole - prophylaxis for Traveler’s diarrhea

Angelica May DC. Mendoza, RPh, MS Page 6 of 12

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 b. Salmonella spp- gram-nega ve, encapsulated, mo le rods that also
belongs to the family Enterobacteriaceae. The organism has 3 important
an gens - cell wall (soma c) O, agellar H, and capsular Vi (virulence)
an gens.
• Two Categories:
i. Typhoidal species - S. typhi and S. paratyphi
ii. Non-typhoidal species - S. enteri dis and S. cholerasuis)
**S. cholerasuis is most commonly involved in systemic
infec on.
• Clinical Findings:
iii. Enterocoli s - characterized by invasion of the small and large
instes ne. It begins with nausea and vomi ng which
progresses to abdominal pain and diarrhea. S. enteri dis
serotype typhimurium is the most common cause.
iv. Typhoid or Enteric fever - begins in the small intes nes but
gallblader few gastrointes nal symptoms occur. Survival and growth of
the organism in phagocy c cells is a striking feature of this
disease as well as the predilec on to invade the gallbladder,
resul ng in the establishment of a carrier state - asymptoma c
carriage of the bacteria for more than 1 year. It is commonly
caused by S. typhi but can also be caused by S. paratyphi.
v. Sep cemia - occurs in two se ngs: a pa ent with underlying
infection in the disease or acancer, or a child with enterocoli s. This is most
blood commonly caused by S. cholerasuis. Symptoms begin with
fever with li le or no enterocoli s then proceed to focal
symptoms. Osteomyeli s, pneumonia, and meningi s are the
most common sequelae.
• Laboratory Diagnosis:
i. Enterocoli s - stool exam, stool smear and stool culture
ii. Typhoid fever - organism isola on and biochemical test widal test
• Treatment and Preven on:
i. Ampicillin
ii. Trimethoprim-Sulfamethoxazole
iii. 3rd genera on cephalosporins
iv. Surgical removal of the gallbladder
v. Vaccines - preven on
c. Shigella spp- gram-nega ve, non-mo le rods which are members of the
family Enterobacteriaceae.
• Species:
i. S. sonnei
ii. S. exneri
iii. S. boydii
iv. S. dysenteriae type I (Shiga bacillus) - the most clinically
signi cant as it is responsible for epidemics with high
mortality. The major virulence factor is the Shiga toxin.
puss i the poop with fever

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 Clinical Findings: characterized by lower abdominal pain, fever, and •
bloody, mucoid diarrhea. Bowel movement is accompanied by
tenesmus or strained defeca on. A carrier state may also occur.
• Complica ons:
i. Perfora on of the colon
ii. Hemoly c-uremic syndrome
iii. Ekiri syndrome
• Laboratory Diagnosis:
i. Stool examina on revealing leukocytes and/or RBC in fresh
stool specimen
ii. Culture of feces
• Treatment and Preven on:
i. Cipro oxacin
ii. Ampicillin
iii. Doxycycline
iv. Trimethoprim-Sulfamethoxazole
d. Yersinia enterocoli ca- also a member of the family Enterobacteriaceae
meat and dairy and are gram-nega ve, urease-posi ve rods.
producs, contaminated • Clinical Findings: the organism causes in amma on and ulcera on
water by domestics in the ssues a ected. Early symptoms include fever, abdominal
animals pain, and diarrhea that is watery to bloody.
• Laboratory Diagnosis: Culture of feces - grow best with “cold
enrichment” or at low temperature of 4oC.
e. Vibrio cholerae- serogroups O1 and O139 cause cholera epidemics.
• Clinical Findings: Cholera - there is sudden onset of nausea and
pathogenic vomi ng, and profuse watery diarrhea (as much as a 20-30L/day)
only to with abdominal cramps. The stools may resemble “rice water”.
humans
There is severe dehydra on which can lead to circulatory collapse
and hypovolemic shock may result in death if the pa ent is not
treated promptly.
• Laboratory Diagnosis: Typical clinical presenta on. Microscopic
examina on using dark eld or phase contrast microscopy. Culture is
also diagnos c.
• Treatment and Preven on:
i. Rapid uid and electrolyte replacement
ii. Tetracycline - DOC
f. Clostridium perfringens- a toxin producing organism that can produce
invasive infec on. It produces numerous toxins and enzymes that result in
spreading infec on.
• Clinical Findings: Enteri s necro cans - an acute necro zing process
in the small intes nes that manifests with abdominal pain and
bloody diarrhea.
• Laboratory Diagnosis: culture under anaerobic condi ons.
• Treatment and Preven on:
i. Penicillin - DOC
ii. An toxins in the form of immune globulins

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 g. Clostridium di cile- it is the most common nosocomial cause of diarrhea.

The organism produces exotoxins that cause death of enterocytes.
• Clinical Findings: An bio c-associated pseudomembranous coli s -
clindamycin is the rst an bio c recognized as a cause of the
disease but other an bio cs are now implicated. The second and
third genera on cephalosporins are now considered as the most
common causes.
• Laboratory Diagnosis:
i. Detec on of toxins in stool specimens using ELISA or
cytotoxicity test.
ii. Sigmoidoscopy may also be done to visualize the
pseudomembrane.
• Treatment and Preven on:
i. Discon nuace of administra on of the o ending an bio c -
TOC
ii. Fluid replacement
h. Bacillus anthracis
• Clinical Findings: Gastrointes nal Anthrax - very rare and is
acquired by entry of spores through the mucous membranes or by
inges on of inproperly cooked meat from infected animals.
• Laboratory Diagnosis: microscopic examina on of specimen and
culture.
• Treatment and Preven on:
i. Cipro oxacin - DOC
ii. Doxycycline - alterna ve
i. Mycobacterium tuberculosis
• Clinical Findings:
i. TB of the GIT - caused by M. tuberculosis when it is swallowed
phlegm can transfer in a er being coughed up from the a lung lesion and by M. bovis
the stomach when it is ingested in unpasteurized milk products. It is
characterized by abdominal pain and chronic diarrhea,
accompanied by fever and weight loss. The most common site
involved is the ileocecal region.
ii. Oropharyngeal TB - tyopically presents with painless ulcer
accompanied by lymphadenopathy.
• Laboratory Diagnosis: microscopic examina on of specimen and
culture.
• Treatment and Preven on:
i. Mul drug therapy
ii. BCG vaccine
3. Viral Gastroenteri s - acute self-limited diarrhea which usually involves children. It
may cause severe dehydra on requiring hospitaliza on, especially in infants.
• E logic agents:
a. Rotavirus - the most common viral cause of gastroenteri s in children.

stage of development where

Angelica May DC. Mendoza, RPh, MS kids eat what they hold Page 9 of 12
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 b. Norwalk virus - responsible for majority of cases of non-bacterial food-

borne epidemic gastroenteri s in all age groups, most espacially in adults.
• Treatment and Preven on:
a. Management is mainly suppor ve with adequate uid and electrolyte
replacement
b. Rotavirus vaccine - preven on

Table 2. Common Viruses Associated with Acute Gastroenteri s in Humans

Virus Host Age Mode of Epidemiology
Transmission
Rotaviruses
Group A 6-24 moths Person-to-person; Single most
water important cause of
endemic severe
diarrheal illness in
infants and young
children.

Group B Adults and children Person-to-person; Outbreaks of

water diarrhea in China

Group C Children Person-to-person; Sporadic and

water occassional
outbreaks
Enteric adenoviruses Child < 2 years of age Person-to-person Second most
important viral agent
of endemic diarrhea
in infants and young
children worldwide
Caliciviruses
Norovirus Older children and Person-to-person; Causes outbreaks of
adults water; cold foods; vomi ng and
raw shell sh diarrhea in families,
communi es, and
ins tu ons

Saporovirus Infants, young Sporadic and

children, elderly occassional
outbreaks
Astroviruses Infants, young Person-to-person; Sporadic and
children, elderly water; raw shell sh occassional
outbreaks

3. Bacterial Enterocoli s (Food Poisoning) - two important features (1) similar

symptoms occur in several members of a group who shared meal, and (2) onset of
symptoms occurs a few hours a er food inges on.
• Three mechanisms of food poisoning:
i. Inges on of preformed toxin - the preformed toxin may be present in
contaminated food. Major o enders are Staphylococcus aureu, Vibrio, and

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 Clostridium perfringens. Symptoms develop within hours consis ng of

explosive diarrhea and acute abdominal pain.
ii. Infec on by toxigenic organisms - the organisms proliferate in the gut
lumen and elaborate an enterotoxin. Symptoms occur within hours
consis ng of diarrhea and dehydra on if it involves a secretory
enterotoxin, or dysentery if the primary mechanism is a cytotoxin.
enteroinvasive
iii. Infec on by entroinvasive organism - the organisms proliferate, invade,
and destroy mucosal epithelial cells, leading to dysentery.
• E ologic Agents:
a. Bacillus cereus - a gram-posi ve aerobic rod. Mildly pathogenic and of low
virulence. cereal, grains
• Clinical Findings:
i. Eme c form - manifested by nausea, vomi ng, abdominal
cramps, and occassionally diarrhea. It begins 1-5 hours a er
inges on of contaminated rice and occassionally pasta dishes.
ii. Diarrheal form - incuba on period is 1-24 hours and is
manifested by profuse diarrhea with abdominal pain and
cramps.
• Laboratory Diagnosis: culture of the isolated organism
b. Staphylococcus aureus - causes food poisoning with the shortest
incuba on period (30 minutes to 8 hours). Enterotoxins are produced
when the organism grows in food rich in carbohydrates and protein.
• Mode of Transmission: Inges on of the preformed heat-stable toxin
in contaminated food.
• Clinical Findings: vomi ng accompanied by nausea is more
prominent than diarrhea.
• Laboratory Diagnosis: culture of the isolated organism. Tes ng for
the presence of toxin on contaminated foods.
c. Clostridium perfringens - an enterotoxin produced by this organism is a
clostridium botolino- common cause of food poisoning.
canned goods • Mode of Transmission: Inges on of the preformed toxin from food
contaminated with soil containing the microorganism’s spores.
• Clinical Findings: watery-diarrhea with abdominal cramps
• Laboratory Diagnosis: isola on of the organism from food samples
d. Vibrio parahaemoly cus - a marine organism. Produces an enterotoxin
similar to the cholera toxin. It is the most common cause of bacterial
gasroenteri s with seafood. It is halophilic requiring 8% NaCl.
• Mode of Transmission: Inges on of raw or undercooked seafood,
especially shell sh such as oysters.
• Clinical Findings: mild to severe watery diarrhea, nausea, vomi ng,
abdominal cramps, and fever.
• Laboratory Diagnosis: culture of the organism
• Treatment and Preven on: Mainly suppor ve

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 Ac vity 1
You are expected to par cipate in the online lecture on December 22, 2020
(Tuesday; 8am-8:30am for Level IIA and 9am-9:30am for Level IIB).

Learning Input 2 (Laboratory)

Several factors paly important roles in the causa on of infec ous disease in the
diges ve system. The most crucial and important impediment to infec ve agents is an intact
mucosal epithelium covering all parts of the diges ve system. Early damage to the lining may
lead to manifesta ons such as nausea and vomi ng. Damage to the mucosa in the form of
ulcera ons allow the members of the normal ora to penetrate the deep ssue and
disseminate through the bloodstream to other organs. altera on of the acid barrier of the
stomach by disease, surgery or drugs increases the survival of pathogens leading to
infec on. Changes in the composi on of the normal ora allow the growth of pathogenic
organisms. Certain bacteria, viruses, and parasites can cause disease even in the absence of
predisposing factors due to their ability to produce virulence factors.

Ac vity 2
You are expected to par cipate in the online lecture on December 22, 2020
(Tuesday; 8:30am-9:00am for Level IIA and 9:30am-10:00am for Level IIB).

WRAP-UP ACTIVITY
Summarize what you have learned or how your new learnings has changed your
thoughts on the topic.

POST-ASSESSMENT

Worksheet 14 (Lecture)
You are required to accomplish the Worksheet 14. The ac vity will be posted on
December 21, 2020 (Monday) in the mVLE course page. Make sure to complete and submit
your output on or before 11:59 pm December 27, 2020 (Sunday).

Worksheet 14 (Laboratory)
You are required to accomplish the Worksheet 14. The ac vity will be posted on
December 21, 2020 (Monday) in the mVLE course page. Make sure to complete and submit
your output on or before 11:59 pm December 27, 2020 (Sunday).

Quiz 14
You are required to take the Quiz 14. The quiz will be posted on December 22,
2020(Tuesday) a er the online lecture in the mVLE course page. Make sure to complete and
submit your output on or before 11:59 pm December 22, 2020 (Tuesday).

Angelica May DC. Mendoza, RPh, MS Page 12 of 12

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