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Gastrointestinal Diseases
most common in tropical countries

one of the leading causes of diarrhea in children

Outline—Diarrheal diseases
Bacterial Infections

Bacterial Food Poisoning

Viral Gastroenteritis

Prevention and Control

Bacterial Infections
Cholera

Shigellosis

Typhoid fever

Diseases caused by E. coli

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 Bacterial Food Poisoning
Intoxications — toxins produced

Staphylococci

Botulism

Infectious food poisoning

Salmonella

Campylobacter

Clostridium perfringens

Vibrio parahemolyticus

Bacillus cereus

Listeriosis

Viral Gastroenteritis
Rotavirus

Norwalk and related agents

highly contagious

Shigella

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 Serotypes:

A — S. dysenteriae, 12 serotypes

discovered by Kiyoshi Shiga

B — S. flexneri, 6 serotypes

C — S. boydii, 18 serotypes

D — S. sonnei, 1 serotype

gram-negative rods, non-motile, non-spore-forming

cannot ferment lactose, no capsule

Shigella is differentiated from E. coli on the basis of pathogenicity,

physiology

E. coli is a lactose fermenter and produces Hydrogen sulfide

S. sonnei common in US (Group D)

S. flexneri common in Third World (Group B)

Shigella is passed from the stomach and multiplies in the intestine

they spread in the large intestine, particularly in the colon

causes cramps

manifestation of Shigella disease — urea

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 Natural Reservoir and Transmission

man only "reservoir"

mostly young children

fecal to oral contact

Shigella leaves the body through human feces

the disease spreads when the bacteria from the feces of an

infected px contaminates food

children to adults

transmitted by adult food handlers

unwashed hands

small amounts of the MO — 10-200 of the MO — is sufficient to cause

infection, thus spread can occur easily

Shigellosis

Symptoms start 1-3 days after exposure

with profuse watery diarrhea

The disease can stop here

the urge to use the bathroom may be as many as 10-30 times a day →
severe dehydration

Can progress to dysentery

which is an intestinal inflammation with abdominal pain, intense diarrhea,

relatively scant stool (very small feces) with blood, mucous, and white
blood cells (pus)

Symptoms usually resolve on their own in 1 week

the disease usually goes away within 5-7 days w rest and rehydration

Rarely, an infected person becomes a carrier

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 media to selectively grow enteric bacteria

allow the differentiation of Salmonella, E. coli, Shigella

EMB, MCA, ENDO agar, Hektoen agar, SS (Salmonella-Shigella) agar

a more severe form of this disease is produced by S. dysenteriae

most virulent of all Shigella sp.

can present various complications

toxic megacolon

uremic hemolytic syndrome

small blood vessels in the kidney are damaged and inflamed

cuz of the toxin

the damage can form clots in the vessel, which can clog the
filtering system of the kidney → kidney failure

This species produces a toxin called Shiga toxin

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 the bacterium contains fimbriae, which allows for the efficient attachment
of the bacteria to the host

host and bacteria cells are both negative → repel

the fimbriae contain adhesins, which will contradict the repulsion of

the 2 negatively charged cells

characterized by phenotypes

watery diarrhea → classic dysenteric stool — little in volume

(scant) and grossly bloody

Pathogenic Factors

Ipa A, B, C, and D proteins are secreted into host cells → intracellular

growth of Shigella

Ipa — Invasion plasmid antigens

1st, bacteria invade intestinal cells by endocytosis (engulfed by the cell)

2nd, they escape from endocytotic vesicles and multiply inside the cells

3rd, directly invade adjacent cells

4th, host cells die, and mucosal abscess forms

Shiga toxin

type of exotoxin

classic A/B toxin

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 B subunit binds to cells and gets A inside the cells

B toxin — cell binding toxin component

A toxin — active toxin component

A inhibits protein synthesis

lysing 28S rRNA

cytotoxic for intestinal cells

B subunit binds to the host cell’s surface receptor — Gb3

(globotriaosylceramide)

initiate the uptake mechanism of the host cell

the toxin will now gain access in the cytoplasm

A subunit now can separate from B subunit and elicit its function

it confers the enzymatic activity of the host cell

it permanently inactivates the ribosome → inhibits the protein

synthesis complex → terminates all protein synthesis

Treatment Shigellosis

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 certain type of immunity for several years but can still be infected w other
spp and serotype of Shigella

immunity is due to the secretory IgA

manage dehydration

use of antibiotics, controversial if the case is not severe (usually self-

limiting)

for severe

Ampicillin, Bactrim (Sulfamethoxazole + Trimethoprim), Nalidixic acid,

Ciprofloxacin

patients respond to antibiotics

disease duration diminished

fluoroquinolone

Salmonella
a genus from the family Enterobacteriaceae

discovered by Daniel Salmon

>2000 antigenic O and H serotypes

O = oligosaccharide (lipopolysaccharide)

H = flagellar antigen

flagella (protein) is the H antigen

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 can differentiate serotypes based on their O and H serotypes

genetically single species

S. enterica serotype choleraesuis

the highest predilection for post-systemic infection

other serotypes infect animals

disease category

S. typhi

S. paratyphi

Natural reservoir

not humans (only infected humans), but many other animals, including birds
and reptiles

Eggs are also a risk

infected bird → feces → thrive on the shell of the egg → bacteria can
enter the egg thru the pores of the shells

improperly cooked chicken

Mode of Transmission

Transmission is by ingestion of contaminated food products (oro-fecal

route), especially poultry or dairy

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 Some transmission from person to person can occur in children, health care,
or food preparation if proper sanitation is not observed.

Salmonellosis

type of food poisoning caused by S. enterica

Gastroenteritis

nausea

vomiting

non-bloody stool mostly, sometimes bloody with fecal leukocytes

sometimes fever, abdominal cramps, malaise

self-limiting (2 — 7 days)

40,000 reported cases — 1.4 million total

identification

usually not cultured unless symptoms last a long time

Stool cultures

treatment is just fluid and salt replacement

antibiotics not recommended, with exceptions for very young, very old,
immunocompromised, debilitated

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 📌 avoid the TEMPERATURE DANGER ZONE

heating at

131 F for 1 hr

140 F for 1/2 hr

boiling for 10 mins

can eradicate the MO

Reiter’s Syndrome

Complication of Salmonellosis

aka reactive arthritis

a condition that may be triggered by a bacterial infection in the urinary or

gastrointestinal

can last for months or years → Chronic arthritis

Symptoms

Pain, swelling, and inflammation of the joints (arthritis), especially where

the pelvis attaches to the spine (sacroiliac joint) and in the fingers, toes,

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 and feet

Inflammation of the eye (iritis).

Inflammation of the urethra

Discharge from the cervix

Skin rash or small sores (ulcers), especially on the penis, on the soles of
the feet, or in the mouth.

Typhoid Fever

enteric fever

severest salmonella disease

Salmonella typhi

S. paratyphi causes a milder form of enteric fever

rare in the US — 324 cases in the US in 2005

Needs to be considered in patients with fevers who have been in endemic

areas — Latin America, the Philippines, Indian subcontinent

common ang typhoid fever in 3rd world countries

epidemics

third world

Europe (historical)

Typhoid Mary — Mary Malon

Irish cook who migrated to America

caused several typhoid outbreaks

carrier

looks healthy (no sx) but is continuously spreading the virus that could
infect other ppl

recaptured and forced to live in a seclusion

North Brother Island in New York

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 px quarantinable diseases are detained here

she lived in an isolated cottage for 23 yrs after her second capture

an outbreak of typhoid fever in a maternity hospital in Manhattan (as Mrs.

Brown)

she was sent back to the isolated island

she suffered a stroke that left her paralyzed

died at 69 yrs old

Symptoms

incubation period: 1-2 weeks

duration of illness: 3-4 weeks

poor appetite, headache, fever, lethargy, diarrhea, chest congestion, and

death can occur from overwhelming infection → intestinal bleeding,
pneumonia, intestinal perforation

Therapy

Antibiotics

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 essential

treatment must be long-lasting to eliminate the carrier state

cephalosporin like ceftriaxone

fluoroquinolone like ciprofloxacin

the optimal choice for the tx of typhoid fever

areas where bacteria is still fully sensitive to traditional first-line

drugs

chloramphenicol

amoxicillin (inexpensive)

trimethoprim (inexpensive)

sulfamethoxazole (inexpensive)

fluoroquinolones (expensive)

vaccine for visitors to endemic areas

Escherichia coli
Epidemiology and Diseases

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 sx of EHEC may vary but it usually takes 3-4 days to develop

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 bloody diarrhea (hemorrhagic), vomiting, severe stomach cramps, no to
mild fever

infection may resolve in 5-7 days

E. coli will attach to intestinal cells and produce a toxin that causes
inflammation and secretion of intestinal fluid

Enterotoxigenic E. coli

Heat labile toxin (LT)

like choleragen

Adenyl cyclase activated

the enzyme that synthesizes the cyclic adenosine monophosphate

(cyclic AMP)

cyclic AMP ⬆
cyclic adenosine monophosphate

secondary messenger that regulates diverse physiological responses,

including sugar and lipid metabolism and cell growth and
differentiation

secretion of water/ions ⬆
water is being secreted in the intestine + decrease in sugar and
lipid metabolism → diarrhea

Heat-stable toxin (ST)

Guanylate cyclase activated

cyclic GMP ⬆
cyclic guanosine monophosphate

secondary messenger

uptake water/ions ⬇
absorption of water in the colon is reduced → watery diarrhea

Enteropathogenic E. coli

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 destruction of surface microvilli

SIGNS AND SYMPTOMS

fever

diarrhea

vomiting

nausea

non-bloody stools

Enteroinvasive E. coli

dysentery

resembles shigellosis

Enterohemorrhagic E. coli

Vero toxin

“Shiga-like” toxin

Hemolysins → hemolysis → bloody diarrhea

Many strains are unable to ferment sorbitol, whereas most other E. coli do
ferment sorbitol

sorbitol = sugar alcohol

Tx for E. coli causing diarrhea

supportive care

avoid dehydration by administering fluids

antibiotic and antidiarrheal medications are specifically not recommended

for treatment (esp EHEC)

the use of these medications has been associated w severe types of illness

can lengthen the duration of diarrhea

can potentiate the effect of the Shiga toxin

increase the risk of hemolytic uremic syndrome

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 Virbrio sp. (Vibrio cholerae)
Common characteristics

Gram-negative

short, curved, rod-shaped

rapidly motile due to single polar flagellum

facultative anaerobes

growth of many vibrio strains requires or is stimulated by NaCl

well-adapted halotolerant and halophilic bacteria

culture on blood or MacConkey agar

Pathogenesis

V. cholerae is transmitted by contaminated water and food

V. cholerae has been associated w raw food, undercooked seafood

harvested from contaminated waters

No known animal reservoirs, nor animal or arthropod vectors.

Following ingestion, V. cholerae infects the small intestine

Adhesion factors are important for colonization & virulence

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 Non-invasive and causes disease by the action of the enterotoxin, cholera
toxin

cholera toxin causes the activation of adenylate cyclase by ADP-

ribosylation → outpouring of fluid into the intestine → diarrhea

Cholera

Full-blown cholera is characterized by massive loss of fluid and electrolytes

from the body

After an incubation period ranging from hours to a few days, profuse watery
diarrhea (rice-water stools)

clear watery stool w a vaguely fishy odor containing mucus

glossy appearance

Untreated, death from shock may occur in hours to days, with the death rate
exceeding 50%.

hypovolemic shock

life-threatening condition when the body doesn't have enough blood

circulating thru the system to keep the organs and tissues functioning
properly

severe diarrhea → massive loss of fluid → reduce blood volume →

shock

Treatment

Replacement of fluids & electrolytes is crucial in preventing shock, &

does not require bacteriologic diagnosis

Antibiotics such as doxycycline can shorten the duration of diarrhea and

excretion of the organism

Prevention

Public health measures that reduce fecal contamination of water supplies

and food, and adequate cooking of foods, can minimize transmission

Vibrio parahemolyticus

seafood and foods other than seafood cuz of cross-contamination

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 natural habitat

warm water

survive in sediments even if its winter

shellfish

causes gastrointestinal infections

28 sp of V. parahemolyticus

Virulence Properties

Kanagawa Reaction

most widely used in vitro test to check for the virulence of V.

parahemolyticus

most virulent types of V. parahemolyticus are the K+

K+ produces a thermostable-related hemolysin

Use human red-blood cells in Wagatsuma’s agar medium

The leading cause of FBI (foodborne infection) in Japan, the

incidence is relatively low in the US

Disease

Incubation — 3-76 hours

Duration — 1-8 Days

Symptoms

Diarrhea, cramps, weakness, nausea, chills, headache, vomiting

Treatment

self-limiting — replacement of lost fluid and electrolytes

Staphylococcus aureus
Characteristics

Gram Positive

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 Round, Clusters

Proteolytic and Lipolytic

Fastidious

Amino acids plus N source, thiamine, nicotinic acid

Facultative

Doesn’t compete well

Habitat and Distribution

well distributed

commonly present in the opening of our body surfaces

exist in low numbers in foods

can be animal origin

Illness

Scalded Skin Syndrome (SSSS)

Toxic Shock Syndrome

produce the exotoxin TSST-1

Food Toxicosis

Nausea, vomiting, abdominal cramps, diarrhea, sweating, headache

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 for a person to get sick, ingestion of the toxin is required and not the organism
as a whole

onset: 1-6 hrs after ingestion of the toxin

low mortality rate in humans, except for babies

Staphylococcal scalded skin syndrome (SSSS)

aka Ritter von Ritterschein disease (in newborns)

happens when a toxin enters the bloodstream producing a reaction all over
the skin

98% of cases of SSSS occur in children under 6yrs old

can happen to immunocompromised and those w poor kidney function

Ritter disease, and staphylococcal epidermal necrolysis, encompass a

spectrum of superficial blistering skin disorders caused by the exfoliative
toxins of some strains of Staphylococcus aureus.

acute exfoliation of the skin, typically following the erythematous

cellulitis

the severity of SSSS varies from a few blisters, localized on the site of
infection to a severe exfoliation affecting almost the whole body

a mild form of the illness involves desquamation of the skin → only on

the skin folds

severe → treated in a hospital (burn unit)

Management

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 similar to treating a child w burns

IV antibiotics

1st line = cefazoline + clindamycin

alternative for MRSA

vancomycin + clindamycin

if oral therapy

cefalexin

alternative for MRSA

sulfamethoxazole + trimethoprim for 10 days

if the baby can't eat → IV fluids to rehydrate the px

exfoliation → creams, ointment, topical agents

fusidic acid, mupirocin

pain → pain medication

NSAIDs

Incidence/Outbreaks

Wide Variety of Foods

Handmade — ice cream, milk, cheese, corn beef (high protein)

Improperly refrigerated — left-over holiday food

Prevention

KEEP OUT OF THE TEMPERATURE DANGER ZONE

40 F TO 140 F (4 – 60 C)

the optimal temperature of food where MO grow

Good Personal Hygiene

Clostridium botulinum
Characteristics

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 Gram-positive rods

Anaerobic

commonly seen in improperly processed canned goods

bloated canned goods cuz most probably contain toxins of anaerobes

Spore forming

Spores worldwide

Soil, pond, and lake sediments

Resist boiling for long periods

Destroyed by moist heat at 121°C — autoclave

Production and secretion of neurotoxin

Botulinum Toxin

Neurotoxin A-G

Type A, B — medicine → tx for muscle spasms (overactive muscle)

commercial form — Botox ® (cosmetics)

Type A, B, E, F, G

Most potent toxin known to humans (purified toxin)

1 mg is lethal for 1 human being

1 g is lethal for 1,000,000 human beings

Enzymatic Activity

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 the basis for the phenomenal potency of the botulinum toxin is
enzymatic

Zinc proteinase that could cleave (break down) neuronal vesicles

associated w the release of acetylcholine (ACh)

ACh — main neurotransmitter for muscle contraction

toxin prevents the ACh from being released in the synaptic

terminal → paralysis

can be used as a bioterrorist weapon

disseminated via the aerosol and contamination of water and food supply →
widespread casualty

the most potent toxin in a molecule of significant therapeutic utility

biological toxins for the treatment of human diseases cuz not all toxins are
very toxic

tx for Strabismus (cross-eyed) — a condition in which the eyes

don't properly align

Heat labile toxin

Rapidly destroyed by boiling

but spores are heat-resistant

Resistant to digestion in the intestinal tract

Absorbed and disseminated systemically

Proteases that degrade proteins important for neurotransmitter release (ACh)

Target cholinergic nerve endings in the neuromuscular junction and blocks

acetylcholine release → Flaccid paralysis

blockage of cholinergic terminal

Botulinum Toxin Mediated Paralysis

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 AP reaches the presynaptic terminal → influx of Ca2+→ vesicle will go to the
terminal and release ACh → ACh binds to the receptor → muscle contraction

botulinum toxin prevents the release of ACh → no NT that will stimulate the
contraction of the muscle → Flaccid paralysis (very weak, no AP in the muscle)

Botulism

Symptoms occur within 18-96 hours after ingestion

Descending flaccid paralysis

characterized by weakness, paralysis, or reduced muscle tone w/o

other obvious cause

no damage in the nerves that cause the eparalysis

Small muscles first

Double vision, blurred vision

Slurred speech

Difficulties swallowing

Respiratory paralysis results in death

Lethal in 10 – 20%

Three types of botulism

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 1. Foodborne

2. Infant

From endogenous flora in susceptible infants

From honey (< 2yrs old)

the normal flora of the intestine of infants and babies are not yet
strong so they can't fight toxins

Honey can usually harbor the botulinum toxin

3. Wound

Therapy of Botulism

Supportive care

Anti-toxin: Human

The usual type used: Trivalent vs A, B, E (most common types of

botulinum toxins)

May be most effective for Type E

Infant botulism → Reduces time in hospital, on ventilator & tube feeding

US Army anti-toxin → Heptavalent and for a bioterrorist attack

protected against all strains of the toxin

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 Patients recover after weeks to months

Prevention of Botulism

Canning or preserving foods with appropriate heat, pressure, & low pH

cuz they thrive in a vacuum space

Spores

Survive 2 hrs at 100 °C

Inactivated at 120 °C — autoclave

Toxin

Inactivated after 1 minute at 85 °C, or 5 minutes at 80 °C

Avoid exposure of infants to honey (may contain Clostridium botulinum

spores)

Immunization

Pentavalent toxoid

Used only for high-risk personnel — Laboratory workers, Military

Viral Gastroenteritis
caused by a variety of viruses

replicate in the small intestine

primary symptoms

watery diarrhea

vomiting

stomach upset

Causative agents

Rotavirus

Noroviruses (Norwalk-like viruses)

Other Causes of Viral Gastroenteritis

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 Adenoviruses

Aichi virus

Astrovirus

Calciviruses other than Noroviruses

Echovirus 22 (Human Parechovirus 1)

Torovirus

Picobirnavirus

Coronavirus

Rotavirus
the most common cause of severe dehydrating diarrhea in infants and
children less than 3 yrs old

part of the routine vaccination for children

Molecular Biology

Family: Reoviridae

Common name: Reovirus

Virus: Rotavirus

Characteristics:

Segmented, dsRNA

icosahedral capsid with no envelope

Transmission:

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 Fecal-oral

survives on inanimate objects — fomites

Disease:

Gastroenteritis in infants & children (6 mos to 2 yrs)

7 major groups (A-G)

Human strains belong to Groups A, B, C

Group A = most important pathogen

Group B = causes epidemics in China

Group C = causes sporadic disease in children

Epidemiology

Diseases

a most common cause of severe dehydrating diarrhea in infants &

children < 3 yrs old

hospitalization of

approx 55,000 children/yr in the US

Approx 30-50% of all cases of diarrhea require hospitalization

Nosocomial transmission

Death of > 600,000children/yr worldwide

causes an estimated 25% of Traveller’s diarrhea

species-specific

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 the problem with Rotavirus is similar in both developed and developing
countries

Pathology

non-invasive

acts in the small intestine from the proximal intestine to the ileum

infects & kills cells via lysis of the mature villus tips in the small intestine

may cause diarrhea due to malabsorption

However, diarrhea can occur in the absence of histopathology

even w/o stimulating adenylyl cyclase or cAMP

Cyclic nucleotide changes are not seen

Adenylyl cyclase stimulates cAMP (di iti nakikita kay Rota)

Treatment

the disease is self-limiting in patients with a normal immune system

Supportive care

oral rehydration therapy to prevent dehydration

Approx 1 in 40 affected children will require IV fluids

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 Vaccines

Live attenuated vaccines

mainly from animal viruses but are contained in a single human

Rotavirus segment

1998, RotaShield (Wyeth) → infants

withdrawn in 1999, intussusception

intestinal obstruction in which a segment of the bowel prolapse in

a more distal segment

last part of the small intestine (ileum) folds into the first part of
the large intestine (cecum)

Rotarix (GlaxoSmithKline)

Monovalent

human live attenuated

most common

po

RotaTeq (Merck)

Human or bovine live attenuated

oral pentavalent

Norwalk Virus and Norwalk-like viruses

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 Family: Caliciviridae

Common name: Calicivirus

Virus: Norwalk and Hepatitis E virus

Characteristics

Nonenveloped

icosahedral capsid surrounding ssRNA genome

causes of epidemics of viral gastroenteritis among older children & adults

named after the virus that caused the 1968 outbreak of gastroenteritis in a school in
Norwalk, Ohio

Norwalk-like viruses are closely related to Norwalk V & now called Noroviruses

Epidemiology

Seasonality:

occurs all year round

maximal outbreak frequency in winter

a major cause of epidemics of gastroenteritis (30-40%)

increasing age = slow decrease in antibody prevalence of the organism

developed countries = Norwalk virus and other Noroviruses mainly affects

older children (school-age) and adults

Transmission

Fecal/Oral

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 direct person-to-person spread

Consumption of contaminated food or water

fomite spread from aerosolized vomit

a primary attack rate of 50%

a secondary attack rate of approx 30%

Studies show infective dose = 10 virions → contagious

Diseases

cause of epidemics

Nursing homes, camps, cruise ships, & sporting events

children in densely populated areas

In developed countries

account for almost 1/2 of the epidemics of nonbacterial gastroenteritis

among older children & adult

Cause food-borne epidemics

food is contaminated by a food handler before consumption

food is often cold foods

salad, sandwiches, & baked goods

icing on a wedding cake

contaminated shellfish

oysters from contaminated waters

Cause waterborne epidemics

contamination by sewage

drinking water

recreational water

diarrhea from drinking water from swimming pools

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 Symptoms

Abrupt onset

nausea, cramps, vomiting

with or without non-bloody diarrhea

RBC & WBC not found

Children vomit more than adults

Low-grade fever is seen in > ½ of affected

disease is self-limiting

Dehydration is the most common complication so rehydration is

needed

It is most frequently seen in the young & old

Pathology

In the proximal small intestine

villus shortening & crypt hyperplasia is seen

crypt hyperplasia — grooves that are normally elongated in a normal

intestine shorten

There is a delay in gastric emptying

mild steatorrhea

fat excretion in the feces

sugar malabsorption

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 decrease in brush border enzymes

enzymes on the lining of the intestine that helps in digestion

Cyclic nucleotides are not affected

Treatment

if dehydration is severe

oral or IV fluids

Prevention

correct food handling techniques & good hygiene

Noroviruses are stable in the environment

resistant to

Chlorination

heating to 60 C

freezing (only stop the replication of the MO)

Other Causes of GI Diseases

Helicobacter pylori
gm (-) spiral bacterium

peptic ulcer disease

Associated with

90% of duodenal ulcers

70-80 % of gastric ulcers

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 Presentation

persistent or recurrent abdominal pain

Diagnosis

biopsy specimens

urea breath test

useful for both the clinical diagnosis of H. pylori and the evaluation of the
post-treatment status

urease — an enzyme that is not usually present in mammalian cells

H. pylori releases urease to promptly hydrolyze (breakdown) urea to

ammonia and CO2

ammonia is used by H. pylori in the neutralization of stomach acid

culture but it is not an easy organism to grow cuz need special

requirements for growth

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 📌 How is it performed?

pre-test: involves a person blowing into a glass tube using a

plastic straw

drink 200mL of juice and recommended urea powder sol’n

(14C or 13C urea) [C = carbon isotope]

urea will liberate carbon

14C and 13C to measure if all will be liberated

post-test: further breath samples will be collected in the same

way as the first test

measure the carbon isotope

(-) result = no CO2 in the stomach

(+) result = there will be a liberation of carbon isotope →

presence of MO in the gut

will last for around 40mins

Treatment

no need for acid suppression

no need for antacids

need to prevent the hydrogen (proton pump inhibitor — Omeprazole,

Lansoprazole)

PPI + Amoxicillin

PPI+Metronidazole/Clarithromycin

Campylobacter
The common cause of diarrhea in animals and humans

C. jejuni

C. pylori

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 now classified as Helicobacter pylori, which causes gastritis and gastric ulcer

Reservoir

animals

cattle, sheep, rodents, wild birds, poultry, dog, cat

food

poultry, milk, water

Transmission

fecal-oral route (rare)

person-to-person spread

Produces cytotoxins by C. jejuni

Diagnosis

Histopathology appearance of ulceration and inflamed bleeding in the

jejunum, ileum, and colon

Culture

slow growth compared to salmonella

Treatment

Erythromycin is the antibiotic of choice for diarrhea that is severe

Aminoglycosides for invasive infections

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 Preventive Measures

same with salmonella

No screening of food handlers because contamination of food by this route is

very uncommon

GITI

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