Problem 3

Group 13
Gastrointestinal System Block
Tuesday, 4th Septemb er2018
Tutor : dr. Jimmy
Chief : Meilissa Christine (405160045)
Secretary: Michele Yoselin (405160077)
Writer : Jacquelien (405160112)
Member 1. Steffany Regina (405160017)
2. Felyn Gaputri (405160041)
3. Meilissa Christine (405160045)
4. Joshua (405160082)
5. Marvell Aurelinus (405160145)
6. Junius Kurrniawan (405160151)
7. Alicia (405160191)
8. Jane Roosaline (405160196)
Problem 3

A 30-year-old woman presented to family physician with six-day history of fever and diarrhea. The
fever is more prominent during the evening, and seems to worsen every night. Fever is
accompanied by headache. Today she starts complaining about difficulty to defecate. She also
complains of losing appetite and vomiting. On examination, patient looked lethargic, temperature
40°C, pulse 85-bpm. Oral mucosa was dry with coated tongue. Inspection of abdomen showed a
distended abdomen with tenderness in epigastric region and upper right quadrant.
Her son, a 1-year-old boy, just stopped his breastfeeding to start consuming formula milk,
experienced frequent watery diarrhea. He completed rotavirus vaccination and plan to have a
typhoid vaccination. His mother start to train him to walk barefooted. This family often consumes
street foods.
What can you learn from the problem?
 Mind Map
Acute diarrhea Infection Bacterial Worsen every night
30 years old woman :
Febris, lethargic, Pulse Virus
Rate: Relative
Salmonella Typhi
Bradycardia, distended
abdomen with Parasite
Chronic diarrhea
tenderness in epigastric
region & upper right
Lymph Node Hepatomegaly
quadrant.
(epigastrium) (upper right quadrant)

Work up: serology (widal)

1 year old boy Allergy Haematology routine

Intolerant
Lactose

Parasite Infection (barefoot)

Learning Issue
1. Explain anatomy, histology, physiology, biochemistry of lower GI tract
2. Explain sign of dehydration (isotonic, hypertonic, hypotonic) in adult & child
3. Explain gastroenteritis
4. Explain typhoid fever
 LI 1 Explain anatomy,
histology, physiology,
biochemistry of lower GI tract
Anatomy
JEJUNUM - ILEUM
Colon
Rectum
Histology
 • The main functions of the small intestine are
Small intestine digestion, absorption of food and production of
gastrointestinal hormones. The small intestine is
4-6 metres long in humans.
• To aid in digestion and absorption:
• the small intestine secretes enzymes and
has mucous producing glands. The pancreas and
liver also deliver their exocrine secretions into the
duodenum.
• The mucosa is highly folded.
• large circular folds called plicae circulares (shown in
the diagram to the right), most numerous in the upper
part of the small intestine
• smaller folds called villi, which are finger like mucosal
projections, about 1mm long.
• the lining columnar epithelial cells have fine
projections on their apical surfaces called microvilli.
• Together, these folds provide a huge surface
area for absorption. Between the villi there are
crypts, called crypts of Lieberkuhn, which extend
down to the muscularis mucosae. These crypts
are short glands.
 • The lamina propria which underlies the
epithelium has a rich vascular and
lymphatic network, which absorbs the
digestive products, and there is
a muscularis mucosae layer immediately
at the base of the crypts. The lymphatic
capillaries are called lacteals, and absorb
lipids. The vascular capillaries are
fenestrated to aid absorption.
• The muscularis externa layer contains
two layers of smooth muscle, an inner
circular and outer longitudinal, for
continuous peristaltic activity of the
small intestine. There are around 200 or
This is a diagram which shows the villi of the small intestine,
as indicated by the arrows in the diagram above, at higher so lymphoid aggregations called Peyer's
magnification.
patches in the mucosa.
• Lymphoid aggregations are
commonly found in the sub-
mucosa of the small intestine. The
larger aggregations of lymphoid
tissue are known as Peyer's
Patches.
• These patches are more likely to
be found in the ileum than in the
duodenum.
mucosa
Epithelium and villi
The epithelium of the villi is made up of tall columnar absorptive cells
called enterocytes, and goblet cells, which secrete mucin, for lubrication
of the intestinal contents, and protection of the epithelium.
 • The large intestine completes absorption, and
Large intestine retrieves water and sodium from the luminal
contents which become fecal residue. It
secretes large amounts of mucus, and some
hormones, but no digestive enzymes.
• The thick mucosa has deep crypts, but there
are no villi. The epithelium is formed
of columnar absorptive cells with a striated
border, many goblet cells, endocrine cells and
basal stem cells, but no Paneth cells. The
surface epithelial cells are sloughed into the
lumen, and have to be replaced around every
6 days.
• The lamina propria and submucosa are
similar to the small intestine.
• The longitudinal smooth muscle in
the muscularis externa is arranged in three
longitudinal bands called taenia coli. At the
anus, the circular muscle forms the
internal anal sphincter.
lymphoid cells in the lamina
propria layers. The pale staining
cells that line the mucosa form
tubular glands, that secrete
mucus. Some of these cells are
absorptive cells. Stem cells are
also present
Review

Wheater’s functional histology p.274

Physiology
Segmentation
Villus
INTESTINAL GASES
• Flatus – gas, primarily driven by 2 sources:
• Swallowed air
• (500 mL air during meal)
• Gas produced by bacterial fermentation in colon
• Presence of gas percolating through luminal contents  gurgling sound (borborygmi)
• Eructation (burping) removes most of swallowed air from stomach, some passes to intestine
• Little # of gas present in SI absorbed or passes on to colon + bacterial products from undigested
KH  expelled through anus
• Abdominal contraction  pressure against contracted anal sphincter  ΔP forces air out at
 velocity through slit like opening  edge of anal opening vibrates  low pitched sound
Sfingter
Carbohydrates
Protein
Lipid
Iron
Biochemistry
• Special hairlike projections on the luminal surface of the small-
intestine epithelial cells, the microvilli, form the brush border.
Contain three categories of integral proteins that function as enzyme :
• Enterokinase
• Dissacharidases (maltase, sucrase, and lactase)
• Aminopeptidase
• Biochemical balance among the stomach, pancreas, and small
intestine is normally maintained
• HCl + NaHCO3  NaCl + H2CO3
• The resultant H2CO3 decomposes into CO2 + H2O:
• H2CO3 + CO2  H2O
• Th e end products of these reactions—Na, Cl, CO2, and
• H2O—are all absorbed by the intestinal epithelium into the blood.
LI 2 Explain sign of dehydration
(isotonic, hypertonic, hypotonic)
in adult & child
Dehydration
• a state of negative fluid balance that may be caused by numerous
disease entities
Pathophysiology
• Results from decreased intake, increased output (renal, GI losses) or
fluid shift (ascites, effusion, capillary leak)
• Decrease in total body water cause reduction in both ICF & ECF
volumes
• Volume depletion will manifest clinically
• As dehydration progresses, hypovolemic shock may ensue, resulting in
end organ failure and death
Classification
• Dehydration may be isonatremic (130-150 mEq/L), hyponatremic (< 130
mEq/L), or hypernatremic (>150 mEq/L)
• Isonatremic dehydration is the most common (80%)
• Isonatremic (isotonic) dehydration: lost fluid is similar in sodium
concentration to the blood
• Hyponatremic (hypotonic) dehydration: lost fluid contains more sodium
than the blood → intravascular water shifts to the extravascular space →
intravascular volume depletion
• Hypernatremic (hypertonic) dehydration: lost fluid contains less sodium
than the blood → serum sodium is high → extravascular water shifts to the
intravascular space → minimizing intravascular volume depletion
• https://www.cdc.gov/mmwr/preview/mmwrhtml/rr5216a1.ht
mm
Etiology
• Gastroenteritis (most common; esp if diarrhea & vomit)
• Stomatitis → limit oral intake
• Diabetic Ketoacidosis → caused by osmotic diuresis
• Febrile illness → fever cause fluid loss and affect appetite
• Pharyngitis → decrease oral intake
• Burns
• GI obstruction
• Heat stroke
• Cystic Fibrosis → excessive sodium and chloride loss in sweat
• Diabetes inspidus → excessive output of very dilute urine (free water loss)
History Taking
• Intake of fluid (volume,type, • Fever
frequency) • Appetite patterns
• Urine output (frequency, • Recent weight loss
hematuria,
concentrated/diluted) • Travel history
• Method of mixing formula • Recent antibiotic use
(ration water:powder) • Possible ingestions
• Stool output (frequency,
consistency, presence of
blood/mucus)
• Vomitting (frequency, volume,
heamtemesis)
• Contact with ill people (esp
Estimated fluid deficit

Severity Infant (<10 kg) Children (> 10 kg)

Mild Dehydration 5% or 50 mL/kg 3% or 30 mL/kg

Moderate Dehydration 10% or 100mL/kg 6% or 60 mL/kg

Severe Dehydration 15% or 150 mL/kg 9% or 90 mL/kg

Procedure for fluid resucitation
• Intravenous Line
• Intraosseus line
• Orogastric / Nasogastric Tube
 Intravenous Line Intraosseus Line

https://img.medscape.com/pi/features/slideshow-
slide/intraosseous-access/fig3.jpg

https://cdn3.volusion.com/laqym.xqmps/v/vsp
files/photos/DALH84101601-2.jpg?1336944606

https://upload.wikimedia.org/wikipedia/commons/0/0d/ICU_IV_1.jpg
Nasogastric Tube
Treatment
• Hydration & nutrition
• Medications such as loperamide, opiates, anticholinergics, bismuth
subsalicylate, and adsorbents are not recommended in dehydration
because of questionable efficacy and potential adverse effects
• Severe dehydration warrants hospital admission for rehydration
with isotonic saline, as do hypernatremic or hyponatremic states
• Inability to tolerate oral rehydration therapy (ORT) may necessitate
hospital admission for nasogastric or intravenous fluid therapy
Oral Rehydration Solutions
Carbohydrate Sodium Potassium Base
Solution Osmolality
(g/dL) (mEq/L) (mEq/L) (mEq/L)

Pedialyte 2.5 45 20 30 250

Infalyte 3 50 25 30 200

Rehydralyte 2.5 75 20 30 310

WHO/UNICE
2 90 20 30 310
F*
Mild-moderate Dehydration
• Mild or moderate dehydration can usually be treated very effectively with ORT
• Vomiting is generally not a contraindication to ORT. If evidence of bowel
obstruction, ileus, or acute abdomen is noted, then intravenous rehydration is
indicated
• Calculate the fluid deficit → fluid deficit should be replaced over 4 hours
• ORS should be administered in small volumes very frequently to minimize
gastric distention and reflex vomiting → 5 mL/min is well tolerated.
• Hourly intake and output should be recorded by the caregiver
• Age appropriate diet may be started as soon as the child is able to tolerate oral
intake
Severe Dehydration
• Laboratory evaluation and intravenous rehydration are required
• Phase 1 → Focuses on emergency management!
• Severe dehydration is characterized by a state of hypovolemic shock
requiring rapid treatment
• Initial management includes placement of an intravenous or
intraosseous line and rapid administration of 20 mL/kg of an isotonic
crystalloid (eg, lactated Ringer solution, 0.9% sodium chloride)
• As intravascular volume is replenished, tachycardia, capillary refill,
urine output, and mental status all should improve
• Phase 2 → deficit replacement, provision of maintenance fluids, and
replacement of ongoing losses
•  Maintenance fluid requirements are equal to measured fluid losses
(urine, stool) plus insensible fluid losses (approx 400-500
mL/m2 body surface area)
• Daily maintenance fluid is added to the fluid deficit
• Recommended administration is one half of this volume
administered over 8 hours and administration of the remainder over
the following 16 hours
• If the child is isonatremic (130-150 mEq/L), the sodium deficit
incurred can generally be corrected by administering the fluid deficit
plus maintenance as 5% dextrose in 0.45-0.9% sodium chloride
• Rapid replacement therapy → child with severe isonatremic
dehydration is administered 20-40 mL/kg of isotonic sodium chloride
solution or lactated Ringer solution over 15-60 minutes. As perfusion
is restored, the child improves and is able to tolerate an oral
rehydration solution for the remainder of his rehydration. This
approach is not appropriate for hypernatremic or hyponatremic
dehydration.
Hyponatremic dehydration
• Phase 1 → Rapid volume expansion with 20 mL/kg of isotonic (0.9%)
sodium chloride solution or lactated Ringer, repeated until perfusion
is restored
• Phase 2
• Calculate maintanance therapy (same w/ isonatremic dehydration)
• Sodium deficit = (sodium desired - sodium actual) X volume of distribution X
weight (kg)
Hypernatremic dehydration
• Phase 1 → Rapid volume expansion with 20 mL/kg of isotonic (0.9%)
sodium chloride solution or lactated Ringer, repeated until perfusion is
restored
• Phase 2
• Reestablish intravascular volume & return serum sodium level to
reference range by not more tha 10 mEq/L/24h
• Rapid correction of hypernatremic dehydration can have disastrous
neurologic consequences, including cerebral edema and death
• Rehydration fluids should be initiated with 5% dextrose in 0.9%
sodium chloride.
Diet
• ORT may be continued at home if clear instructions are provided for
the family and if the family members can be relied upon to carry out
the hydration regimen
• Feedings are started as soon as the patient is able to tolerate oral
intake
• Diluting milk or formula is not indicated. Breast-feeding should be
resumed as soon as possible
• ßFoods that contain complex carbohydrates (eg, rice, wheat, potatoes,
bread, cereals), lean meats, fruits, and vegetables are encouraged.
Fatty foods and simple carbohydrates should be avoided.
 LI 3 Explain
gastroenteritis
Diarrhea 
• Rapid movement of fecal matter through the
intestines resulting in poor absorption of water,
nutritive elements, and electrolytes and producing
abnormally frequent watery bowel
movements. (dorland)
• Increased stooling, with stool consistency less solid
than normal, constitutes a satisfactory, if somewhat
imprecise (clevelandclinic)
Types of diarrhea
 Acute, persistent, &
chronic diarrhea
• Acute diarrhea is defined as a greater number of stools of decreased
form from the normal lasting for less than 14 days.
• If the illness persists for more than 14 days, it is called persistent.
• If the duration of symptoms is longer than 1 month, it is considered
chronic diarrhea.
Osmotic diarrhea
• osmotic force that acts in the lumen to drive water
into the gut (caused by hyperosmotic drugs (MgSO4,
Mg(OH)2), malabsorption, defect in mucosal
absorption (disacharide deficiency, glucose/galactose
malabsorption)
Secretory diarrhea
• increase in the active secretion
• inhibition of absorption.
• The most common cause of this type of diarrhea is a
cholera toxin that stimulates the secretion of anions,
especially chloride ions.
Inflammatory diarrhea
• Damage to the mucosal lining or brush
borderpassive loss of protein-rich fluids, and a
decreased ability to absorb these lost fluids.
• Features of all three of the other types of diarrhea
can be found in this type of diarrhea.
• It can be caused by bacterial infections, viral
infections, parasitic infections, or autoimmune
problems such as inflammatory bowel diseases.
• It can also be caused by tuberculosis, colon cancer,
and enteritis.
Exudative diarrhea
• Exudative diarrhea occurs with the presence of blood
and pus in the stool. This occurs with
inflammatory bowel diseases, such as Crohn's disease
or ulcerative colitis, and other severe infections
 Ethiology (infectious)
Host Cause
E. coli and viruses such as rotavirus, Minimal to moderate mucosal inflammation
Norwalk agent, and HIV

Shigella, enteroinvasive E. coli Bacteria that destroy entherocytes

Entamoeba Histolytica, Salmonella, that penetrate the mucosa, result in

Campylobacter jejuni, and Yersinia moderate to severe inflammation with or
enterocolitica without ulceration.
B. cereus, S. aureus, and Clostridium Ingestion of preformed toxin produced by
perfringens bacteria can result in acute jejunitis.

Aeromonas, Shigella, and Vibrio spp. (e.g., produce enterotoxins and also invade the
V. parahaemolyticus) intestinal mucosa.

Clostridium difficile and hemorrhagic E. coli produce inflammation from cytotoxins

0157:H7
ESCHERICHIA COLI
• Five classes of e. coli
• Enterotoxigenic E. coli (ETEC)
• Enteroinvasive E. coli (EIEC)
• Enteropathogenic E. coli (EPEC)
• Enterohemorrhagic E. coli (EHEC)
• Enteroaggregative E. coli (EAEC)
Ethiology (noninfectious)
• Inflammatory bowel disease
• Irritable bowel syndrome
• Ischemic bowel disease
• Partial small bowel obstruction
• Pelvic abscess in the rectosigmoid area
• Fecal impaction
• The ingestion of poorly absorbable sugars, such as lactulose and acute
alcohol ingestion.
Ethiology (noninfection)
STRONGYLOIDIASIS
• is an intestinal infection caused by 2 species of the parasitic
nematode Strongyloides.
• Strongyloides is classified as a soil-transmitted helminth.
• The most common and clinically important pathogenic species in humans is S
stercoralis
• S fuelleborni is found sporadically in Africa and Papua New Guinea
• Strongyloidiasis is transmitted through direct penetration of human skin by
infective larvae when in contact with soil; walking barefoot is therefore a
major risk factor for acquiring the infection.
Strongyloides stercoralis
• This roundworm,2.5 mm in length, is endemic in southern U.S.
and common in tropicsand Asia.
• Clinical manifestation:
• Skin becomes red and pruritic after penetration by larvae, which usually
occurs on feet.
• Diarrhea,
• Vomiting
• Abdominal pain
• Cough and pneumonia after migration of larvae through lung scan
• Peripheral eosinophilia may occur.
• Identification of larvae in stool isdiagnostic.
SYMPTOMS
• Abdominal pain and intermittent or persistent diarrhea), the lungs
(cough, wheezing, chronic bronchitis) or skin (pruritus, urticaria).
• The infection may be severe and life-threatening in cases of
immunodeficiency (haematological diseases, immunosuppressive
therapies).
DIAGNOSIS
• Stool specimens with enrichment and/or stool culture
• Alternative tests (serology and polymerase chain reaction)

TREATMENT
• Ivermectin, thiabendazole and albendazole are the most
effective medicines for treating the infection.
• Albendazole is considered the least effective.
• Ivermectin, the drug of choice, is not available in all
endemic countries. 
Trichuris trichiura
• T. trichiura,4-cm long whipworm, occurs most commonly in
tropical areas but is also found in subtropical areas (e.g.,
southern U.S.).
• Clinical manifestations:
• Most individuals are asymptomatic
• Diarrhea
• Tenesmus
• Weight loss
• Anemia
• Peripheral eosinophilia
• Diagnosed: by seeing eggs on microscopic stool examis
diagnostic.
Ascaris Lumbricoides
• HD : human
• Infection is by ingesting infective eggs
• Disease: Ascariasis
• Diagnosis: eggs in the stool
• Symptoms :
• Sindrom Loeffler : larvae in the lungs. Cough, pulmonary
infiltrates in the field
• GIT disorders: nausea, decreased appetite, diarrhea, constipation
• Malabsorption  malnutrition  cognitively impaired children
• Obstructive ileus
• Appendicitis
• Biliary obstruction  jaundice (rare)
Ascaris lumbricoides
• Clinical manifestations:
• Can be asymptomatic
• Mild diarrhea
• Intermittent epigastric pain
• Anorexia
• Vomiting
• Diagnosed: by identifying whitish-brown Ascaris worm,20–40
cm in length, or finding Ascaris eggs on microscopic exam of
stool is diagnostic.
Necator americanus & Ancylostoma
duodenale
• HD : human
• Disease : Necatoriasis, Ankylostomiasis
• Symptoms :
• Ground itch
• Wakana disease : ingested infective larvae  nausea,
vomiting, cough, sore throat
• Hypochromic anemia mikrositer
• Eosinophilia
• Diagnosis: eggs in the stool
• Harada Mori culture
Hookworm Infection
• Adult hookworms (N. americanus and A. duodenale)
• Clinical manifestations:
• Red, pruritic lesions on feetor between toes where larvae penetrate.
• Diarrhea
• Vomiting
• Abdominal pain
• Anemia from GI blood loss
• Peripheral eosinophilia.
• Detecting hookworm eggs on stool smear is diagnostic.
TAENIA SAGINATA
GEOGRAPHIC DISTRIBUTION GENERAL RECOGNITION FEATURES
• South america • 2-5 meters long
• Europe • 1000-2000 proglottids 
• Asia
each have 15-20 lateral
EGGS branches from the uterus
and a lateral genital pore
• 31-43 um
• Scolex has 4 suckers with a
• Brown shell
slight apical depression
• Hexacanth embryo w/ 3 pair without hooklets
of lancer shaped hooklets
• Cysticercus:
– In muscle of beef

DWELLE, T. L. :TAENIA SAGINATA, p2-8

TAENIA SAGINATA
TRANSMISSION
• Eating inadequately cooked beef
• Inadequate meat regulation
• Using raw human sewage for
fertilizer
• Inadequate human fecal sanitation
DISEASE CHARACTERISTICS
• Generally asymptomatic
• Diarrhea &abdominal cramps
• Interstinal obstruction w/ a
mass of entangled worms

DIAGNOSIS TREATMENT
• Proglottids in the stool MEDICATION ADULT PEDIATRIC

• Eggs in stool PRAZIQUANTEL 5-10 5-10 mg/kg

mg/kg once
• Scotch tape test for eggs on once
the perineum NICLOSAMIDE 2 gm 50 mg/kg
once once
• Fecal concentration techniques
• Taenia antifens in stool

DWELLE, T. L. :TAENIA SAGINATA, p2-8

TAENIA SOLIUM
GEOGRAPHIC DISTRIBUTION GENERAL RECOGNITION FEATURES
• Latin america • 2-4 meters long
• Asia • The worm attaches strongly
• Africa
to the mucosa of the upper
SIGN & SYMPTOMS small intestine by means of
its sucker and hooks
• Mild symptoms or none at all
• Scolex has 4 suckers with a
• Abdominal pain
double crown hooks,
• Distension
narrow neck
• Diarrhea
• Cysticercus:
• Nausea – In muscle of pig

GARCIA ET AL., TANEIA SOLIUM. P547-548

TAENIA SOLIUM
TRANSMISSION TREATMENT
• Eating inadequately MEDICATION ADULT PEDIATRIC
cooked pork PRAZIQUANTEL 5-10 5-10 mg/kg
mg/kg once
once
DIAGNOSIS NICLOSAMIDE 2 gm 50 mg/kg
once once
• The presence of the double
crown of hooks.
• Haematocylin-eosin straining
(proglottids)
• ELISA = detects taenia- specific
molecules in faecal samples.

GARCIA ET AL., TANEIA SOLIUM. P547-548

Cholera
• Etiology : V. cholerae
• Epidemiology : both endemic and epidemic patterns. endemic in many areas of
Asia and Africa. In Asia, cholera occurs seasonally before and after the monsoon
rains, and the incidence of disease peaks in children younger than five years, and
may occur in neonates
• Spread through contaminated water/ food, in epidemic, can spread through
contaminated stool
• Pathophysiology:
1. ingestion of V. Cholerae  the majority are killed by gastric acid  Surviving
organisms colonize the small intestine and elaborate cholera toxin
2. Cholera toxin  protein exotoxin that consists of a single A subunit associated
with five B subunits
3. the A subunit is translocated intracellularly, enzimatically activate adenylate
cyclase and elevate intracellular cAMP  leads to chloride secretion through
the apical chloride channel and secretory diarrhea
• Sign & symptons :
1. Acute watery diarrhea  “rice water” appearance
2. Nausea & vomitting
3. Dehydration
4. Electrolyte imbalance  muscle cramps & shock  most serious complication
5. In children  seizures
• Work up :
1. Isolation and identification of Vibrio cholerae serogroup O1 or O139 by
culture of a stool specimen remains the gold standard
2. Ideal for transport media  cary blair
3. Ideal for isolation & identification  thiosulfate-citrate-bile salts agar
(TCBS)
4. Stool examination  (-) stains & check under the dark field microscope
 spiral shape & shooting star motility pattern microorganism
5. Rectal swab  isolation
• Diagnosis
• a case of cholera should be suspected when:
1. a patient aged 5 years or more develops severe dehydration or dies
from acute watery diarrhea, even in an area where cholera is not
known to be present
2. a patient aged 2 years or more develops acute watery diarrhea in an
area known to have cholera
3. V. cholerae infection can be confirmed by isolation of the organism
from stool on selective media, followed by biochemical tests, as well
as serogrouping and serotyping with specific antibodies
4. Dark field microscope  rapid exam
 • Treatment
1. Rehydration
2. Antibiotics :
• Prognosis :
• Can be fatal if
don’t diagnostic
immediately

https://www.ncbi.nlm.
nih.gov/pmc/articles/P
MC3761070/table/T3/?
report=objectonly
FOOD ALLERGY
• is an abnormal response to a food triggered by your body's immune
system.
• A true food allergy is a reaction triggered by the immune system (the
part of your body that fights infection).
• Someone with two allergic parents is more likely to develop food
allergies than someone with one allergic parent.
Etiology
Although people can be allergic to any kind of food, most food allergies
are caused by:
• tree
• Nuts or peanuts
• milk, eggs, soy, wheat, fish and shellfish
These eight foods account for 90% of food allergies. Most people who
have food allergies are allergic to fewer than 4 foods.
Signs & Symptoms
• Itching or swelling in your mouth
• Vomiting, diarrhea, or abdominal cramps and pain
• Hives or eczema
• Tightening of the throat and trouble breathing
• Drop in blood pressure
Examination
• Skin test
• Prick test
• Intradermal test
• Patch test
• Blood test – IgE
Complication
• Chronic illnesses associated with food allergies are eczema and
asthma.
• The worst is anaphylaxis 
FOOD INTOLERANCE
• A variety of different mechanisms can cause foods to affect people in
this way; collectively these are known as non-IgE mediated food
hypersensitivity, 
Etiology
• Absence of an enzyme needed to fully digest a food.
• Lactose intolerance
• Irritable bowel syndrome. 
• can cause cramping, constipation and diarrhea.
• Food poisoning.
•  bacteria’s toxin in spoiled food
• Sensitivity to food additives. 
• dried fruit, canned goods and wine can trigger asthma attacks
• Recurring stress or psychological factors. 
• Celiac disease. 
• Celiac disease has some features of a true food allergy because it involves the
immune system. However, symptoms are mostly gastrointestinal, and people
with celiac disease are not at risk of anaphylaxis. This chronic digestive
condition is triggered by eating gluten, a protein found in wheat and other
grains
FOOD POISONING
• Food poisoning occurs when you swallow food or water that contains
bacteria, parasites, viruses, or the toxins made by these germs. Most
cases are caused by common bacteria such as Staphylococcus or E.
coli.
Etiology
• Hands or cooking utensils, cutting boards, and other tools hygiene
• Dairy products or food containing mayonnaise (such as coleslaw or potato salad) that
have been out of the refrigerator too long
• Frozen or refrigerated foods that are not stored at the proper temperature or are not
reheated to the right temperature
• Raw fish or oysters
• Raw fruits or vegetables that have not been washed well
• Raw vegetables or fruit juices and dairy products (look for the word "pasteurized,"
which means the food has been treated to prevent contamination)
• Undercooked meats or eggs
• Water from a well or stream, or city or town water that has not been treated
Etiology
• types of germs and toxins may cause food poisoning, including:
• Campylobacter enteritis
• Cholera
• E. coli enteritis
• Toxins in spoiled or tainted fish or shellfish
• Staphylococcus aureus
• Salmonella
• Shigella
Risk Factor
• Infants and elderly people are at the greatest risk for food poisoning.
• Having a serious medical condition, such as kidney disease, diabetes,
cancer, or HIV and/or AIDS.
• Having a weakened immune system.
• Traveling outside of the United States to areas where you are exposed
to germs that cause food poisoning.
Signs & Symptoms
• Symptoms from the most common types of food poisoning will often
start within 2 - 6 hours of eating the food.
• Abdominal cramps
• Diarrhea (may be bloody)
• Fever and chills
• Headache
• Nausea and vomiting
• Weakness (may be serious)
Exam & Test
• Tests may be done on your stools or the food you have eaten to find
out what type of germ is causing your symptoms.
• In more serious cases, your health care provider may order a
sigmoidoscopy.
Treatment
• Getting enough fluids and learning what to eat will help keep you
comfortable. You may need to:
• Manage the diarrhea
• Control nausea and vomiting
• Get plenty of rest
Prognosis & Complication
• Most people fully recover from the most common types of food
poisoning within 12 - 48 hours.
• Dehydration
• Arthritis
• Bleeding problems
• Damage to the nervous system
• Kidney problems
• Swelling or irritation in the tissue around the heart
LI 4 Typhoid Fever
The Organism
• Salmonella typhi, a Gram-negative bacterium
• Less severe disease: Salmonella serotype paratyphi A.
• S. typhi has several unique features:
• several unique clusters of genes known as pathogenicity islands (PAIs)
• S. typhi can be identified in the laboratory by several biochemical and
serological tests
• Most specific is that of polysaccharide capsule Vi
• present in about 90% of all freshly isolated S. typhi and has a protective effect against
the bactericidal action of the serum of infected patients.
• Provides the basis for one of the commercially available vaccines

Background document: The diagnosis, treatment and prevention of typhoid fever. Communicable Disease Surveillance & Response Vaccines & Biologicals. WHO
The Disease
typhoid organisms
S. typhi multiplies in
Ingestion in food or pass through the
mononuclear
water pylorus and reach
phagocytic cells.
the small intestine

rapidly penetrate the

rapidly elicit an influx
arrive in the lamina mucosal epithelium
of macrophages
propria via microfold cells or
(Mp)
enterocytes

Some bacilli remain

ingest the bacilli but
within Mp of the
do not generally kill
small intestinal
them.
lymphoid tissue
 typhoid bacilli reach
Other typhoid bacilli
the bloodstream
are drained into further multiplication
principally by lymph
mesenteric lymph and ingestion by Mp.
drainage from
nodes
mesenteric nodes,

pathogen reaches an
intracellular haven
(resides) within 24
hours after ingestion general circulation 
enter the thoracic
throughout the silent primary
duct
organs of bacteraemia
reticuloendothelial
system (spleen, liver,
bone marrow, etc.)

• The incubation period in a particular individual depends on

the quantity of inoculum
it resides during the • i.e. it decreases as the quantity of inoculum increases,
incubation period, ~8 and on host factors.
to 14 days.
• Incubation periods ranging from 3 days to more than 60
days have been reported.

Inoculation: the introduction of a pathogen or antigen into a living organism to stimulate the production of antibodies
 Typhoid Fever
Sign and symptoms
Early illness
• fever (39° to 40° C)
• feel weak
• loss of appetite.
• Headache
• Muscle aches
• Sweating
• Dry cough
• weight loss
• Abdominal pain
• Diarrhea or constipation
• In some cases, patients http://www.mayoclinic.org/diseases-conditions/typh
have a rash of flat, rose- oid-fever/basics/definition/con-20028553
colored spots. 
1st week: febris incrimetri
2nd week & 3rd week: febris continu
4th week: febris decrimenti
Factors
Factors influencing severity & overall clinical outcome of the infection:
• duration of illness before the initiation of appropriate therapy
• choice of antimicrobial treatment
• age,
• previous exposure or vaccination history
• virulence of the bacterial strain
• quantity of inoculum ingested
• host factors (e.g. HLA type, AIDS or other immunosuppression)
• taking other medications such as H2 blockers or antacids to diminish gastric acid
• HIV  significantly increased risk of clinical infection with S. typhi & S. paratyphi
• Helicobacter pylori infection  increased risk of acquiring typhoid fever
Acute non-complicated disease
• Prolonged fever
• disturbances of bowel function
• constipation in adults
• diarrhoea in children
• headache
• Malaise
• anorexia
• Bronchitic cough: common in the early stage of the illness.
• During the period of fever, up to 25% of patients show exanthem (rose
spots), on the chest, abdomen and back.
Complicated disease
• Occult blood is a common finding in the stool of 10-20% of patients, and up to
3% may have melena.
• Intestinal perforation
• Abdominal discomfort develops and increases.
• It is often restricted to the right lower quadrant but may be diffuse.
• The symptoms and signs of intestinal perforation and peritonitis sometimes
follow + sudden rise in pulse rate, hypotension, marked abdominal tenderness,
rebound tenderness and guarding, subsequent abdominal rigidity.
• Rising WBC count with a left shift
• Free air on abdominal radiographs are usually seen
• Typhoid meningitis
• encephalomyelitis,
• Guillain-Barré syndrome
• cranial or peripheral neuritis
• psychotic symptoms,
although rare, have been reported.

Other serious complications documented with typhoid fever include:

• haemorrhages (causing rapid death in some patients)
• hepatitis,
• myocarditis,
• pneumonia,
• disseminated intravascular coagulation,
• Thrombocytopenia
• Haemolytic uraemic syndrome
• Prolonged persistent fever and diseases for no clear reason.
• Genitourinary tract manifestations or relapse, and/or a chronic carrier state may
develop.
• Carrier state: 15% of patients, depending on age, become chronic carriers harbouring S.typhi in
the gallbladder.
Contamination & Transmission
• Human: only natural host & reservoir
• By Ingestion of food or water contaminated w/ feces
• Ice cream  significant risk for transmission
• Shellfish from contaminated water, raw fruit, vegs fertilized w/
sewage  sources of past outbreaks
• Dev countries: transmitted when chronic carriers contaminate food
(unsatisfactory food-related hygiene)
Diagnosis
• Definitive: isolation of S.typhi from blood, bone marrow, specific
anatomical lesion
• Presence of clinical symptoms characteristics
• Detection of specific Ab response  suggestive but not definitive
• Blood culture  mainstay of diagnosis
• Ox bile medium (Oxgall) recommended for enteric fever pathogens
(S.typhi & S.paratyphi)
• Failure to isolate organism may be caused by several
factors:
• Limitation of lab media
• Presence of AB
• Vol of specimen cultured
• Time of collection
• Patients w/ history of fever for 7-10 days
• Bone marrow aspirate: GOLD STANDARD for diagnosis
of typhoid fever
• Duodenal aspirate culture also proved highly
satisfactory diagnostic test
Ideal specimen
• 1st wk = blood (culture)
• 10-15 mL adults & adolescents
• 2-4 mL in children
• 2nd wk = serum (Ab)
• 3rd wk = stool
• 4th wk = urine
Colony Characteristics
• Blood agar
• Non-hemolytic smooth white colonies
• MacConkey agar
• Lactose non-fermenting smooth colonies
• SS agar
• Lactose non-fermenting colonies + black centers *except S.paratyphi A
Biochemical identification
Serological Procedures
• Characterized by their somatic (O) & flagellar (H) Ag
• O: w/ slide agglutination test w/ group specific antiserum + agglutination w/ factor antiserum
• H: tube agglutination test
• Organism should be motile & from a liquid culture
• Envelop Ag = Vi (virulence)
• Felix-Widal test
• Measures agglutinating Ab lvl against O & H Ag
• Doubling dilution of sera in large test tubes
• O = appear on days 6-8 after onset – disc-like pattern
• H = 10-12 after onset of disease – loose, cotton wooly clumps
• Performed on acute serum (at first contact w/ pts)
• At least 1 ml blood should be collected/time
• Moderate sensitivity & specificity
New diagnostic test
• IDL Tubex test
• Simple (1 step test) & rapid (~2 mins)
• Slide latex agglutination test
• O9 Ag – highly specific for S.typhi
(immunodominant epitope)
• Not positive for S.Paratyphi
• Detects IgM Ab
• Typhidot test
• Simple, speed, economical
• Sensitivity 85.9%, specificity
96.7%
• Detect IgM & IgG to S.typhi
• IgM dipstick test
• Detect IgM Ab in serum &
whole blood
DD
• Malaria
• Amebiasis
• Viral illnesses: dengue or EBV infection, infection w/ non-Salmonella
bacterial pathogens (Yersinia, Campylobacter, Pseudomonas)
Typhoid Fever
Typhoid Fever

• Prevention
• Vaccines
• Wash your hands
• Avoid raw fruits
and vegetables.
Prevention
• Relies on proper food handling & sanitation
• Dev countries: careful attention to separation of raw & cooked foods;
awareness to multiple ways in which cross-contamination can occur in
food preparation areas
• Monitor children to insure hand hygiene after contact w/ reptiles &
fowl
• Travel to dev countries: vaccine or parenteral capsular polysaccharide
vaccine
• 1st line: care in consumption of food & water.
• Avoid tap water, salads, uncooked vegs, unpasteurized milk & milk products
Conclusion

We had learned about anatomy, histology,

physiology, biochemistry of lower gastrointestinal
tract, we also learned about disorders and the
differential diagnostic that related to
gastroenteritis & typhoid fever.
Suggestion

 Prevent barefooted while walking

 Prevent unhygienic street food
 Wash hand before eating
References
• Mescher AJunqueira L. Junqueira's basic histology.
New York: McGraw-Hill Medical; 2013.
• Sherwood L. Introduction to human physiology. Pacific
Grove, Calif.: Brooks/Cole; 2013.
• Netter FH. Atlas of human anatomy. 4th ed.
Philadelphia: Saunders Elsevier, 2006. Longo D.
• Harrison's principles of internal medicine. New York:
McGraw-Hill; 2012.