adiuvante Dei gratia doctorum factionis
COMMUNICABLE DISEASE:
INFECTIOUS DIARRHEA
NORMAL PHYSIOLOGY
The GIT starts with the mouth. Does digestion starts with the mouth?
Yes, because of the salivary enzymes and the chewing mechanism of
the mouth. Then it passes to a conduit called the esophagus. Is
digestion possible in the esophagus? No, because it only creates
peristaltic movements to move food particles from the mouth to the
stomach. From the stomach, that is where most of the digestion
starts to be initiated. So, what are the parts of the gastrointestinal
tract? We have the mouth, esophagus, stomach, small intestines,
large intestines, then to the rectum and anus.
Primary function of the small intestine
 Digestion and assimilation of food nutrients.
food stays in the stomach for 4 hrs and eventually goes to
the SI absorption
Small intestine is where most of the chemical processes take place. So
what causes our chemical digestion to take place? Once food is
transported from the stomach to the small intestines, the pancreas
will be stimulated. Cholecystokinin, which is found in the small
intestinal mucosa, will be the one to stimulate pancreatic secretion.
And once pancreatic secretion takes place, you will now have the
start of digestion. The enzymes secreted by the pancreas are
stimulated by cholecystokinin so the pancreatic enzymes will now
pass to the pancreatic duct to go to the small intestine. And what are
these enzymes secreted by the pancreas to aid in digestion? Trypsin?
Trypsinogen? Now to avoid a very acidic medium in the small
intestine, what does the pancreas release to avoid an oversecretion
of acid? It will release bicarbonate. And bicarbonate is the one that
neutralize the hyperacidic state of the small intestine once it is
stimulated by the passage of food.
So the three major classes of nutrients that undergo chemical
digestion are proteins, fats and carbohydrates. So in the small
intestine, what will happen to the meat that you just took? It will be
broken down into amino acids and peptides. What about the bread
that was used for the sandwich or burger? It will be broken down into
simple sugars. What about the fats that was used to cook your burger
patty? It will be degraded to your fatty acids and glycerol. So
everything there is what we call the chyme, and the chyme is where
the three major food nutrients have been digested.
Small and large intestines
 Regulate secretion and absorption of water and electrolytes
In a single day, in a normal human, how many liters of
water, both needed and actual, do we ingest? So the
small intestine is capable of absorbing up to 10 liters of
water, both from liquid and food sources. But from the
small intestine, most of it will be absorbed and only a
hundred mL will now pass through the large intestine. So,
as you can see, what is more important in digestion will
be the small intestine because, not only nutrients but
even water is absorbed largely in the small intestine.
 Storage of intraluminal contents
 Transport of intraluminal contents aborally
normal movement is away from the mouth towards the
rectum
2014-2015
DR. FORTUNO
 Salvage of some nutrients from bacterial metabolism of
carbohydrates that are not absorbed in the small intestines
good bacteria is found in the SI and LI, the purpose is to
metabolize the carbohydrates
FUNCTIONS AT DIFFERENT ANATOMICAL LEVELS
STOMACH AND SMALL INTESTINES
So how does absorption take place in the stomach? We have 2 kinds
of movement: (1) in the stomach and small intestine, and (2) the
other kind of movement is in the large intestine
So when we talk about the movement of the stomach and small
intestine, we're talking about high amplitude propagating complexes.
So these are very fine, minute movements of the small intestine for it
to remove the undigested residue of chyme coming from the stomach
and the duodenum. The myenteric migrating motor complexes are
the ones that are primarily responsible for the movement of
undigested residue or particles from the stomach to the small
intestine. The stomach can also act as storage because in the
stomach, the food can stay there for as long as 3 hours. And in the
small intestine, it can also stay there for as long as 3 hours. So do you
think that spacing the giving of medicines at different intervals of the
day will help the patient? So your grandfather comes to you: “anak,
ang dami kong gamot. After breakfast, 5 ‘to.” Is it advisable for you to
tell your grandpa to swallow all those 5 together or should we space
them? “Oh, grandpa, inumin mo na lang ‘to ng 8, 9, 10, 11, 12.” So
pinaghiwalay mo. Is there a logic in dividing the doses of medicines if
you are going to give that? Yes or no, based on the storage time of
the stomach? No, you can just tell your patients to take them all
together. We don’t have to space them one hour apart. Because by
the time your patient has already finished the second drug, he would
have already forgotten to take the third, fourth and fifth drug. “E
nakalimutan ko na, sabi mo kasi one hour apart, doc, e nagtatrabaho
na ako.” So for you to ensure compliance to medications, just tell
your patients to take them all together because these will all be
stored, anyway, in the stomach for the next 3 hours.
So from the stomach to the small intestine, we now go to the ileum.
What is so important about the ileum that is not usually seen in the
jejunum because the jejunum is a very, very long tube? It is also
where digestion takes place but most of the important chemical
functions of the small intestine occur in the duodenum and ileum. So
what are the functions of the ileum?
1. Absorb bile acids
2. Absorb fats and cholesterol  The breakdown of fat takes place
largely in the ileum.
3. Absorption of fat-soluble vitamins, especially vitamin A and D. 
If you have a section of the ileum, you will have hypocalcemia
because of the decreased in the absorption of vitamin D.
4. Absorption of vitamin B12 is cyanocobalamin.  If you have an
elderly patient and you noticed that he is swaying while walking
or having fine tremors but is not Parkinson’s, the gait is very
poor and has difficulty standing up from sitting position, maybe
your patient has vitamin B12 deficiency. So you can give oral or
parenteral supplementation of vitamin B12.
5. Absorption of water and electrolytes (copper, zinc and sulphur)
Regular peristaltic movement
 Synchronized MMCs (myenteric motor complex) in fasting
clears nondigestible residues from the small intestines
 Ileal reservoir empties boluses
 Accommodation, mixing, transit
Stomach – 3 hours
Small bowel – 3 hours
COLON
 Irregular mixing, fermentation, absorption and transit
not controlled by MMCs but by high amplitude
propagating contractions  It can contract the entire
large intestine.
 Reservoir: ascending and transverse (15 hours)
 Conduit – connection between transverse and rectum:
descending (3 hours)
 Volitional reservoir: sigmoid and rectum
Ileocecal junction is where the small intestine will connect with the
large intestine. It is very important because there is a sudden change
in pressure from a high pressure to a low pressure structure.
Ileo - colonic storage
 Distal ileum empties intermittently by bolus movements
from the ileum to the colon  What are these intermittent
movements? These are the mass movement of the colon.
So how many times per day? There could be 3, 5 or several
times. It depends on how many times you try to move your
bowel.
 Facilitates continuous mixing, retention of residues and
formation of solid stools  The colon is where the stool
with a chyme or semi-solid consistency will become more
solid because only a hundred mL or less than a hundred mL
of water will be absorb in the colon.
Colonic motility and tone
 MMC rarely reach the colon
 HAPC
Associated with mass movements throughout the colon
Up to five times per day usually in the AM and post -
prandially
Increased frequency results in diarrhea or urgency
 Resident bacteria
Necessary in digestion of unabsorbed carbohydrates
from the small intestine
 They are there to metabolize the carbohydrates. They
cannot metabolize fats and proteins.
Also protects the colon from pathogenic bacteria
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 Now, in the small intestine, you have the resident
bacteria. And I’m sure you are very aware of
probiotics, Yakult shirota strain, and all kinds of
resident bacteria from the food. But this food must be
fermented. So what are the food sources that are rich
in probiotics? These are yogurt, kimchi and your
probiotic preparations (Yakult which has Lactobacillus
but yakult only has one strain).
 So what are the main functions of the resident
bacteria?
a. Decrease the number of pathogenic bacteria
b. Maintain intestinal integrity
DEFECATION
Angle straightening - Valsalva Manuever and position (sitting)
It is a complicated process. It involves two kinds of innervation:
intrinsic and extrinsic innervation controlled by the vagus nerve and
sacral nerve, together with the anatomical constriction of the
sigmoid. The puborectalis muscle forms a sling so that it will not be
able to make the food contents from the large intestine go down by
gravity to the rectum. But when you defecated this morning, your
puborectalis muscle relaxed, making now the curvature straight
which makes it easier for the feces to go down.
PSEUDODIARRHEA
 Pseudodiarrhea
no infection involved, not classified as diarrhea
frequent passage of small volumes of stool  with rectal
urgency  IBS and proctitis
Pseudodiarrhea is defined as the frequent passage of a small volume
of stool as opposed to diarrhea which is the frequent passage of a
large volume of stool.
What is the most common cause of pseudodiarrhea in the general
adult population (<60 years old)? It is irritable bowel syndrome and
until now there is no treatment for this because the mainstay of
treatment of irritable bowel syndrome is still psychological
counselling. Another form of pseudodiarrhea is proctitis. Proctitis is
not only common in men but also in lesbian women (basta daw ung
may nilalagay sa rectum.. hahaha). Why does this happen? Because,
sometimes, people does not sterilize the things they are putting in
the rectum or anus. Is this diarrheal? No, it is just irritation of the
external anal sphincter brought about by an inflammation or an
infection from an object inserted to the rectum.
 Fecal incontinence
Involuntary discharge of fecal contents.
Usually secondary to neuromuscular disorders and
structural anorectal problems
elderly patients, stroke; not classified as diarrhea
 Romelyn 

For the elderly population, we can observe that they keep on going to
the toilet because they cannot control their faecal movement. This is
what we call faecal incontinence. We can also see faecal incontinence
on people who have stroke and problems on the brain. They are not
able to control their defecating movements. In the past, we can also
see this on people who underwent previous surgery for
haemorrhoids.
 Overflow diarrhea
Due to Fecal impaction (patients in nursing homes 
rectal stimulation)
Not true diarrhea
Overflow diarrhea is very interesting because it is an overflow
because of constipation. It all started with constipation. So you have 2
spectrums, constipation leading to diarrhea.
Megacolon  There is accumulation of gas. We can presume that
there are faeces particles behind the gaseous colon. If you are going
to do your rectal examination, you will be able to feel faeces that are
hard at the tip of your finger.
DIARRHEA
 Passage of abnormally large liquid or unformed stools at an
increased frequency
 Stool weight increased
more than 200-250g of stool/day  diarrheic
 Diarrhea ranks second only to respiratory tract infections as
the most common illness worldwide.
Those who are thin now are the ones who had diarrhea,
and those who are fat now are those who had respiratory
tract infections.
 Range from mild annoyances to death.
most common complications: dehydration and electrolyte
abnormality (hypokalemia)
Food will travel from the mouth to the anus for 72 hours. So any food
particles that remains in the GIT for more than 72 hours, that is
already termed as constipation.
CASE 1
49 y/o female patient of medium built consults at your clinic
complaining of loose bowel movement. Patient has been defecating
for the past 5 days, 10 times per day (normal is maximum of 5 per
day). Stool is watery, non-blood streak. No rectal pain or tenesmus.
(Di ko sure kung Increase o decrease in urine output). There are
cramps. Eyeballs are sunken. Auscultation of the bowel sounds was
hyperactive. Tympanitic abdomen, nontender.
Manage or reassure the patient?
We must first classify the diarrhea according to classifications.
1. This is watery diarrhea. Watery diarrhea is the passage of a large
volume of fluid stools. If it is watery diarrhea, you have the
different organisms that are very commonly implicated in the
classification of watery diarrhea and this would be traveller’s
diarrhea, Vibrio cholera, ETEC, Salmonella and the others. Rotavirus
is very important because it is part of the very common causes of
common colds in children. Aside from that, rotavirus has the ability
to not be degraded by heat even if we keep on boiling a certain
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container of water, rotavirus will not be destroyed by heat. I think
this is the very common cause of diarrhea in children. Fortunately
for us, we do not have enough statistics of rotavirus infection
among the general adult population. So kung minsan nakikita niyo
ung mga kapatid niyo sinisipon at nagtatae. Think of rotavirus.
INFECTIOUS DIARRHEA OR BACTERIAL FOOD POISONING?
Other causes of watery diarrhea would be food poisoning and the
more commonly implicated organisms are Staphylococcus aureus,
Bacillus cereus and Clostridium perfringens. Now what is the
characteristic of food poisoning? Ask the patient how many times did
he vomit and did he vomit more than the number of times he
defecated. If the patient tells you that he is feeling nauseous and the
frequency of vomiting is more than the number he defecated, this
already gives you a clue that the patient has food poisoning.
 Adequate hydration  most important treatment
 WHO – 3.5 g sodium chloride, 2.5 g sodium bicarbonate, 1.5
g potassium chloride, 20 g glucose or 40 g sucrose + 1 liter
water
 Energy drink (e.g Gatorade)
 Severe dehydation – IV fluids – lactated ringer’s solution.
D5 LR-sugar can cause osmotic diarrhea
2. So we have classified diarrhea according to watery diarrhea or the
malabsorption state. And the malabsorption state is what we call
the steatorrheic cause of diarrhea. This is characterized by large,
pale, fatty stools. By microscopy, if we are going to let our patient
undergo fecalysis, you will see that the stools have a lot of fat
globules. Do not think of watery diarrhea. Instead, think of
malabsorption. What are the cases that are usually noted in
malabsorption? These are children who do not fit the milk formula
that is being fed to them. So if you have a patient who is a child and
whose mother is complaining to you about her child with diarrhea
and you made the patient undergo fecalysis and you took note that
there were a lot of fat globules, do not treat the patient as a case
of watery diarrhea. Instead, you think of malabsorption syndrome.
Maybe your patient is lactose intolerant. Organisms that can cause
malabsorption would be Giardia, Capillaria and Strongyloides
stercoralis.
CLASSIFICATION ACCORDING TO DURATION
 Acute – less than 2 weeks
 Persistent – between 2-4 weeks
 Chronic - more than 4 weeks
ACUTE DIARRHEA
 90% infectious etiology
 Oral-fecal transmission
 Ingestion of contaminated food and water with pathogens
from human or animal waste  Most common vector: flies
and cockroaches
 10% - medications (any drugs that contains amoxicillin -
most common), toxin ingestions, mesenteric ischemia (In
the elderly, they might complain of abdominal pain,
diarrhea, and fecalysis shows low (or no yata? Sorry di ko
madinig e) fat globules. Think of mesenteric ischemia
because it is common among the elderly) and other
conditions.
 Romelyn 
Acute infection
 Ingested agent overwhelms host’s immune and non –
immune mechanisms
Five high risk groups
1. Travelers – Latin America, Asia, Africa
 ETEC, EAEC, Campylobacter, Shigella, Norovirus,
Coronavirus, Samonella
 Visitors to Russia, mountaineers, backpackers, backwoods –
Giardia
 Nepal – Cyclospora
More commonly implicated organism is E. coli.
2. Consumers of certain foods
 Salmonella, Campylobacter – picnic, banquet, restaurants
 Shigella – undercooked chicken (abdominal pain with
dysentery)
 EHEC – undercooked hamburger
 Bacillus cereus – fried rice
diarrhea: history of last meal intake (2nd up to the 3rd
last meal)
some organisms have longer incubation period
 Bacillus cereus has very short period, usually 4-6 hours
 Staphylococcus aureus, Samonella – mayonnaise and
creams
 Salmonella – undercooked or raw eggs
 Vibrio, Salmonella, Hepatitis A – seafoods, especially raw
paragonimiasis- raw crab meat
3. Immunodeficient persons
 Primary immunodeficiency (hypogammaglobulinemia),
secondary immunodeficiency (AIDS, senescence,
pharmacologic suppression)
 Common enteric pathogens can cause a more severe and
protracted diarrheal illness
 Agents transmitted venereally: Neisseria, Treponema,
Chlamydia may contribute also to proctocolitis
4. Day Care Patients and their caregivers
 Shigella, Giardia, Cryptosporidium, Rotavirus
5. Institutionalized patients (hospital)
 C. deficile (due to antibiotic intake)
CHRONIC DIARRHEA
 Due to malabsorption, any defect in the GIT and
medications
CASE 2
52 y/o male coming from Norway who has been imprisoned in Bilibid
prison complained of bloody diarrhea for 3 days. Three days ago,
patient had abdominal colic, nausea, vomiting and low grade fever.
Bowel sounds are hyperactive. With sunken eyeballs and dry lips.
Classify this. Organism: E. coli. (ETEC, EPEC, EHEC)
PATHOGENIC MECHANISMS
 Enteric pathogens  Tactics to overcome host’s defense
systems
 Understand the virulence employed to better understand
the diagnosis and treatment
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INOCULUM SIZE
 Number or amount of organism to be ingested to cause the
disease
 Varies from species to species
 Shigella, EHEC, Giardia, Entamoeba  10 – 100 bacteria or
cysts
 Vibrio cholera – 100,000 to 100,000,000
ADHERENCE
 Organisms must adhere to the mucosa as their first step
 Can compete with the normal bowel flora, and colonize the
mucosa
 Specific cell surface proteins: attachment of the bacteria to
intestinal walls  important virulence determinants
Examples:
 Vibrio cholera
does not destroy the mucosa of the small intestine
only adheres to the brush borders of small intestinal
enterocytes
rice watery stool
most common cause of death: dehydration
 ETEC
adherence protein called colonization factor  colonizes
the upper small intestine prior to enterotoxin production
destroys the mucosa
 EPEC (young children) and EHEC (hemorrhagic colitis and
hemolytic-uremic syndrome)
produce virulence determinants that attach to the brush
borders of the intestinal epithelium  destroys the
mucosa
TOXIN PRODUCTION
 Enterotoxin
causes watery diarrhea by directly acting on the secretory
mechanisms
increase volume/fluid
Cholera toxin – causes persistent activation of the
adenylate cyclase  increased cyclic AMP  increased
chloride secretion and decreases sodium reabsorption 
diarrhea
ETEC
Produce a protein called LT (heat labile) – similar to
cholera toxin and causes secretory diarrhea using the
same mechanism
ST (heat stable) – activates guanylate cyclase and
elevation of intracellular GMP
 Cytotoxin
Cause destruction of mucosal cells
Produce dysentery (bloody stools with inflammatory
cells)
 Romelyn 
 Shigella, Clostridium, Shiga producing strains of E. coli  Mucosal immune mechanism (macrophages, natural killer
Produce outbreaks of hemorrhagic colitis cell) is the first line of defense.
tenesmus and bloody diarrhea  IgG, IgM, IgA  2nd line
 Neurotoxins
act directly on the central and peripheral NS GENETIC DETERMINANTS
causes vomiting (e.g S. aureus)
Produced by bacteria outside the host  Poorly understood
Symptoms immediately upon ingestion  Blood type O – increased susceptibility to cholera, shigella
Bacillus and Staphylococcus  vomiting and norovirus
 Polymorphism in interleukin 8 – increased risk of diarrhea
CASE 3 from EAEC

(Actually, continuation ito ng case 1) DIAGNOSTICS

Female nurse complained of cough without fever. She self-medicated
with amoxicillin. She continued to have diarrhea. She also self-  Most cases are self limited and physicians may treat these
medicated with cefuroxime and eventually, she ended with cases empirically.
clarithromycin. Despite the number of antibiotics that she had taken,  Do fecalysis.
she continued to have cough. After taking all of these, aside from
having diarrhea, she also complained now of epigastric pain. Since Amoeba
she is a nurse, she thought that it might be peptic ulcer because of  Examine fresh stools  cysts and trophozoites
the drugs she ingested. She then took omeprazole which is a proton  Storage: cool temp; up to 4 hours
pump inhibitor.  Entamoeba histolytica  ingest RBC
Metronidazole  to destroy cyst because cyst is
Note: Do not give PPI, Zantac, Maalox to patients who have diarrhea not destroyed by heat
because you are going to change the stomach and intestinal milieu Adult dose: 2g/day
from acidic to basic. Magiging conducive sa pathogenic organism ung  Entamoeba dispar (90% of the time)
condition. And the resident flora will be destroyed. No need to treat the patient. Yakult.  Kasi nga
nonpathogenic ‘to. Asymptomatic ung patient
HOST DEFENSES pero may cyst and trophozoite.

 Must combat a number of microorganisms most of the time  Do stool culture: fever and evidence of inflammatory
protection disease – Shigella, Salmonella, Campylobacter.
 Nosocomial diarrhea
NORMAL FLORA Focus on C. deficile
Stool culture useless
 Normally inhabiting bacteria in the intestinal mucosa act as Do latex agglutination tests and rapid enzyme detection
host defense (main defense mechanism) of the toxins produced(Toxin A, Toxin B)
 Less normal flora: infants, people taking antibiotics   fecalysis: (+)WBC - give antibiotics
greater risk of developing infections  fecalysis is normal: food poisoning/viral
 Majority of the normal bacteria are anaerobic organisms  etiology
acidic pH, volatile fatty acids are good resistors to enteric  Shigella, Salmonella, Campylobacter, Giardia -
pathogens. flouroquinolone and ciprofloxacin (best),
Cotrimoxazole (adverse reactions: SJS,
GASTRIC ACID dermatitis)

 Acidic pH is an important barrier. Goals of diarrhea treatment:

 Increased frequency in patients underwent gastric surgery o to destroy the organism
 Neutralization of gastric acid (H2 blockers, PPI) o to revert the patient’s hydration back to normal or to
prevent dehydration
long intake can cause diarrhea because of less acidic
environment
WHO ORS formula:
 Rotavirus can withstand acidic environment is highly stable
o 3.5 g NaCl and 2.5 g NaHCO3
in acid.
o 40 g sucrose or 20 g glucose
o 1 L of CLEAN water (baka daw kasi dirty water gamitin
INTESTINAL MOTILITY
hahaha)
 Peristalsis – major form of clearance from the proximal
If patient can’t drink this ORS, admit the patient and infuse IV fluids.
small intestine
 Impaired motility (opiates, antimotility drugs, anatomic
Racecadotril  You can give it to a spectrum of etiologies of diarrhea
abnormalities, hypomotility states) increases frequency of
whether it is infectious or non-infectious. It can decrease diarrheic
bacterial overgrowth and infection with enteric pathogens.
episodes without any change in the colonic motility.
IMMUNITY

 Cellular and antibody or humoral immunity play a role

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 Romelyn 