GIT INFECTION

Introduction
Most such diseases result from ingesting food or water contaminated
with pathogenic microorganisms or their toxins.
These pathogens usually enter the food or water supply after being
shed in the feces of people or animals infected with them.
Microbial diseases of the digestive system are typically transmitted by
a fecaloral.
Fecaloral cycle is interrupted by effective sanitation practices in food
production and handling.
There is also a relationship between the bodys digestive system and
immune system. In consequence, an estimated 80% of the immune
system is located in the intestinal tract, especially the small intestine.
This loosely organized lymphoid tissue and structures such as lymph
nodes and Peyers patches are collectively called gut-associated
lymphoid tissue (GALT).

Normal Microbiota
Bacteria heavily populate most of the digestive system.
In the mouth, each milliliter of saliva can contain millions of bacteria.
The stomach and small intestine have relatively few microorganisms because of the
hydrochloric acid produced by the stomach and the rapid movement of food through the
small intestine.
The large intestine has enormous microbial populations, exceeding 100 billion bacteria
per gram of feces. (Up to 40% of fecal mass is microbial cell material.)
The population of the large intestine is composed mostly of anaerobes and facultative
anaerobes.
Most of these bacteria assist in the enzymatic breakdown of foods, especially many
polysaccharides that would otherwise be indigestible.
Some of them synthesize useful vitamins.
N.B:
The GI tract is adapted to absorbing nutrients passing through it. However, at the same

time that nutrients are absorbed from the GI tract, harmful microbes ingested in food
and water must be kept from invading the body.
An important factor in this defense is the high acid content of the stomach, which
eliminates many potentially harmful ingested microbes.

The small intestine also contains important antimicrobial defenses, most significantly,
millions of specialized, granule filled cells called Paneth cells. These are capable of
phagocytizing bacteria, and they also produce antibacterial proteins called defensins and
the antibacterial enzyme lysozyme.

Dental Caries (Tooth Decay):

Probably the most important causative bacterium is Streptococcus
mutans,

gram-positive

coccus

that

has

important

virulence

characteristics.
Within a couple of hours, bacteria produce a dextran.
In the production of dextran, the bacteria first hydrolyze sucrose into
its component monosaccharides, fructose and glucose.
The enzyme glucosyl transferase then assembles the glucose
molecules into dextran. The residual fructose is the primary sugar
fermented into lactic acid.
Accumulations of bacteria and dextran adhering to the teeth make up
dental plaque.

.Gastroenteritis: infections and intoxications

Definition: diseases causing inflammation of the stomach and intestinal
.mucosa
.Mode of transmission: ingestion of contaminated food
Symptoms: Diarrhea, vomiting (immune response to get rid of organism),
.abdominal cramps+/- dysentery. Diarrhea is a major factor in infant mortality
:Treatment
Oral rehydration therapy (replacement of lost fluids and
electrolytes). This is usually a solution of sodium chloride, potassium

chloride, glucose, and sodium bicarbonate to replace lost fluids and

electrolytes.
Zink tablets: to replenish losses of zinc during diarrheal episodes.

Infection

Intoxication

The pathogen enter GI

Ingestion of preformed

through M cells (microfold) to

toxin produced by organism

meet payer's patches and

as Staphylococci and

multiply causing damage in

Cl.botulinum

.intestinal wall
:Long IP as

Very short IP: few hours

Organism multiplication
Affection of intestinal
tissues
Fever

Less frequent

Other symptoms: GI

Other symptoms: GI

symptoms as

symptoms or other system

Diarrhea, vomiting (immune

symptoms according to the

response to get rid of toxin as botulinum affect CNS

organism), abdominal

.as neurotoxin

.cramps+/- dysentery

.N.B: Severe diarrhea accompanied by blood or mucus is called dysentery

Staphylococcal Food Poisoning (Staphylococcal

enterotoxicosis)

 A leading cause of gastroenteritis is ingesting an enterotoxin produced

by S. aureus.
:Risk factors
Staphylococci are resistant to drying and radiation so they survive on skin -1
surfaces, nasal passages, from which it contaminates the hands and can
.enter food
:they can grow on food due to-2
Resistance to high osmotic pressures such as cured ham, Custards,
cream pies, and ham which inhibits the growth of competitors
Resistance to heat; vegetative cells can tolerate 60C for half an hour.
temperature abuse, they reproduce and release enterotoxin into the
food. Poultry products can also harbor staphylococci if they are handled
and allowed to stand at room temperatures in which the
,These events, which lead to outbreaks of staphylococcal intoxication
:Staphylococcal exotoxin (Enterotoxin)
the toxin is of serological type A and is often correlated with the
production of coagulase enzyme that coagulates blood plasma
(coagulase positive).
The toxin itself is heat stable and can survive up to 30 minutes of
boiling. Therefore, once the toxin is formed, it is not destroyed by
reheating food, although the bacteria will be killed.
:Mechanism of action
This reaction is essentially immunological in character; the
staphylococcal enterotoxin is a model example of a SUPERANTIGEN
which triggers the brains vomiting reflex center; abdominal cramps and
usually diarrhea.
Recovery is usually complete within 24 hours with No reliable immunity
results from recovery.
The mortality rate of staphylococcal food poisoning is almost zero

:Prevention
.adequate refrigeration during storage to prevent toxin formation
Diagnosis of staphylococcal food poisoning is usually based on
Clinically: the symptoms, the short incubation time characteristic of -1
.intoxication. They cause no obvious spoilage when growing in foods
2- Specimen: If the food has not been reheated so that the bacteria are not
killed,

the pathogen can be recovered and grown on:

Nutrient agar: golden-yellow colonies
Blood agar: beta hemolysis as produce hemolysin
Mannitol salt agar: selective media for staphylococci. These bacteria

grow well in 7.5% sodium chloride,

Biochemical reactions: Pathogenic staphylococci usually ferment
mannitol, produce coagulase,
phage typing of isolated S. aureus, a method used in tracing the source
of the contamination.
3-Detecting the toxin in food samples has always been a problem; there may
be only 1 to 2 nanograms in 100 g of food. Reliable serological methods have
become commercially available only recently.

Shigellosis (Bacillary Dysentery)

The genus was named for the Japanese microbiologist Kiyoshi
Shiga Shigellosis, also known as bacillary dysentery to differentiate
it from amebic dysentery, is a severe form of diarrhea caused by a
group of
Morphology: facultatively anaerobic gram-negative rods.
There are four species of pathogenic Shigella: S. sonnei , S. dysenteriae
, S. flexneri , and S. boydii . Man is the only "reservoir".
These bacteria are residents only of the intestinal tract of humans,
apes, and monkeys.
PATHOGENESIS:

 Shigella dysenteriae is responsible for bacillary dysentery, a disease

most often associated with crowded, unsanitary conditions. Other
species of Shigella may produce milder forms of diarrheal disease. The
source in each case is unwashed hands.
This is primarily a disease of young children occurring by fecal-oral
contact. Adults can catch this disease from children, although it can be
transmitted by infected adult food handlers who contaminate food. The
source in each case is unwashed hands.
Mode of transmission: spread only from person to person via fecal
contamination of water or food. Outbreaks are most often seen in families,
day-care facilities, and similar settings.
IP: long 2 weeks.
1-the bacteria:
attach to certain epithelial cells. M cells, which, take the bacterium into
the cell. The bacteria multiply in the cell to immense numbers in the
small intestine, but the primary site of disease is the large intestine. and
soon spread to neighboring cells dysentery results from bacteria
damaging the epithelial layers lining the intestine, often with release of
mucus and blood (found in the feces) and attraction of leukocytes (also
found in the feces as "pus").
Macrophages not only fail to kill Shigella bacteria that they phagocytize,
but also are killed by them.
2-Shiga toxin
(chromosomally-encoded), which is neurotoxic, enterotoxic and cytotoxic,
plays a role. Its enterotoxicity can make the disease clinically appear as a
diarrhea. The toxin inhibits protein synthesis (acting on the 70S ribosome and
lysing 28S rRNA).
DIAGNOSIS:

 Clinical: As with other diarrheal diseases, clinical diagnosis alone is

equivocal. Diarrhea, fever and a watery bright red blood tinged stool are
classical symptoms,
Laboratory:
Shigella can be isolated from diarrheal fluid.
Microscopic ex: Shigellae are grom negative rods, non-motile
Culture media: MacConkey media which gives pale lactose
nonfermenting colonies.
Biochemical reactions: (practical), do not produce H2S.
Serological techniques may be used for epidemiological
characterization.
Treatment:
oral rehydration
In severe cases of shigellosis, antibiotic therapy as, fluoroquinolones are
the antibiotics of choice.

Salmonella (Salmonella Gastroenteritis)

The Salmonella bacteria (named for their discoverer, Daniel Salmon). Their
normal habitat is the intestinal tracts of humans and many animals.
Morphology:
gram-negative, facultatively anaerobic, nonendospore-forming rods
flagellated (motile).
Salmonellae possess 3 major antigens; the "H" or flagellar antigen
(phase 1 & 2), the "O" or somatic antigen (part of the LPS moiety) and
the "Vi" or capsular antigen (referred to as "K" in other
Enterobacteriaceae).
LPS moiety is composed of an "O" polysaccharide ("O" antigen) and "R"
core ( the endotoxic inner "Lipid A").
Salmonella are classified into:
Typhoidal salmonellae: salmonella typhisalmonella paratyphi A, B and
C.

 Nontyphoidal salmonellae, which cause the milder disease of

salmonellosis: salmonella typhimurium and salmonella enteriditis.
there are more than 2000 serotypes (or serovars). they belong to only
two species, primarily Salmonella enterica such as S. enterica serotype
Typhi murium.
Salmonella Gastroenteritis
Pathogenesis:
Mode of transmission: ingestion of contaminated food as meat
products, chickens and eggs. Meat products are susceptible to
contamination from the intestine. Hens are highly susceptible to
infection, and the bacteria contaminate the eggs (inadequately cooked
or raw eggs in foods such as cookie batter, and Caesar salad).
The bacteria have the ability to survive in the albumin, in natural
preservatives such as lysozyme and lactoferrin (which binds iron the
bacteria require).
Disease is initiated by oral ingestion of the bacteria followed by
colonization of the lower intestine then bacteria invade the intestinal
mucosa and replicate within macrophages resulting in an acute
inflammation of the mucosal cells.
activation of adenylate cyclase, which increased fluid secretion into the
intestinal lumen, resulting in diarrhea.
At M cells they enter the lymphatic and cardiovascular systems, to
affect many organs.,
Incubation period: 12 to 36 hours.
C/P: There is usually a moderate fever accompanied by nausea, abdominal
pain and cramps, and diarrhea. Endotoxins evoke fever and can activate
complement, kinin and clotting factors.
The mortality rate is very low, probably less than 1%. However, the
death rate is higher in infants and the very old; death is usually from
septic shock.
Normally, recovery will be complete in a few days.

Diagnosis
isolating the pathogen from the patients stool or from leftover food.
Culture on specialized selective and differential media; these methods
are relatively slow. (details from practical)
PCR-based tests are the best for detecting small numbers of Salmonella
in foods. They require about 5 hours and identify the most common
clinical serotypes.
Prevention
good sanitation practices to decrease contamination
proper refrigeration to prevent increases in bacterial numbers.
Proper cooking to food to destroy bacteria.
Treatment:
Antibiotic therapy is NOT USEFUL in treating salmonellosis
oral rehydration therapy.

Typhoid Fever
The most virulent serotype of Salmonella, S. typhi, causes the bacterial
disease typhoid fever. Unlike the salmonellae that cause
salmonellosis, this pathogen is not found in animals; it is spread only in
the feces of other humans. Before the days of proper sewage disposal,
water treatment, and food sanitation, typhoid was an extremely
common disease.
Incubation period: 2 or 3 weeks which is much longer than for
salmonellosis (12 to 36 hours) as S. typhi multiply within phagocytes and are
disseminated into multiple organs, especially the spleen and liver.
Clinical picture:
High fever of about 40C and continual headache.

 Diarrhea appears only during the second or third week, and the fever
then tends to decline.
In severe cases, which can be fatal, ulceration and perforation of the
intestinal wall can occur.
13%, become chronic carriers. They harbor the pathogen in the
gallbladder and continue to shed bacteria for several months. The
classic example of a typhoid carrier was Mary Mallon, also known as
Typhoid Mary.
DIAGNOSIS:
Clinical: Clinical diagnosis of the salmonelloses is often difficult because the
symptoms closely resemble other diarrheal diseases.
Laboratory: (practical)
Salmonella can be readily isolated (from blood in the first week and
from stool or urine on 2nd week onward).
Microscopic examination: gram ve rods, motile.
Culture on bacteriologic media: MacConkey media which give pale non
lactose fermenter colonies.
Rapid identification systems: latex agglutination.
S. typhi multiply within them and are disseminated into multiple organs,
especially the spleen and liver.,
Biochemical reactions: produce H2S.
Serological techniques may be used for epidemiological
characterization.
Treatment:
The most effective antityphoidal drugs are quinolones or thirdgeneration cephalosporins.
Treatment of the chronic carrier might require weeks of antibiotic
therapy.
Antibiotic resistance is a frequent problem.
Recovery from typhoid confers lifelong immunity.
Prophylaxis: Vaccines are seldom used in developed countries except for
high-risk laboratory or military personnel.

1-The vaccine that has long been in use is a killed-organism type (TAB
vaccine), which must be injected and has high rates of side effects.
2-Newer-generation vaccines have become available that are quite safe and
can be used in persons 2 years of age or older.
One, a subunit vaccine that requires a single injection, confers good
protection for at least 3 years.
Another, a live attenuated vaccine that can be taken orally in three or
four doses, protects well for as long as 7 years.

Why was typhoid fever almost entirely eliminated in developed countries

by modern sewage treatment whereas salmonellosis has not been?-4

Cholera
The causative agent is Vibrio cholerae,
Morphology: a slightly curved, gram negative rod with a single polar
flagellum.
PATHOGENESIS:
The acid sensitivity of V. cholerae means that a large dose is required to
produced disease. Indeed, 1011 vibrios given orally fail to produce illness but
if bicarbonate precedes the inoculation, then only 104 are required.
Cholera is a disease of the small intestine, unlike most other enteric
illnesses. The bacteria penetrate the mucus layer and adhere to the mucosal
cells where they subsequently produce toxin.
Transmitted by the fecal-oral route
Adheres and colonizes to the small bowel by Toxin co-regulated pili (TCP)
Secretes the cholerae enterotoxin (CT).
Mechanism of cholerae toxin:
Choleragen (cholera toxin) is chromosomally encoded. This 84 kD
protein enterotoxin is composed of 2 major domains; the A domain

controls its biologic activity while the B domain binds the toxin to
cellular receptors (GM1 receptor).
The B subunit:
binds to gangliosides on epithelial cell surfaces allowing internalization
of the A subunit.
B subunits may provide a hydrophobic channel through which A
penetrates.
The A subunit:
activates adenylate cyclase present in the cell membrane of the
epithelium of the gut increasing c-AMP in turn which stimulates massive
secretion of ions and water into the lumen.
Dehydration and death (without treatment) result. A cholera patient
may secrete 20 liters of fluid per day with 108 vibrios per ml!
They occasionally cause wound infections or sepsis, especially in people
with liver disease or who are immunosuppressed.
Prevention:
Vaccination is only partially effective and not generally recommended.
It is most commonly used by international travelers.
Treatment:
1- fluid replacement is the major component of treatment.
2- Antibiotic therapy (including tetracycline) is additionally used. Recovery
from cholera results in an effective immunity, but only to bacterial
strains of the same antigenic characteristics.
Cholera bacteria, and other members of the genus Vibrio in general,
are strongly associated with brackish (salty) waters, although they
are also readily spread in contaminated fresh water. Under
unfavorable conditions V. cholerae may become dormant; the cell
shrinks into a nonculturable, spherical state. A favorable change in
the environment causes them to revert rapidly to the culturable form.
Both forms are infectious.

Vibrio cholera serotypes:

1- classical strain O:1 named El Tor (for the El Tor quarantine camp for
pilgrims to Mecca, where it was first isolated).
2- O:139 causes widespread epidemic in India and Bangladesh.
3- non-O:1/O:139: nonepidemic strains of V. cholerae, associated with
large-scale outbreaks of cholera.
DIAGNOSIS:
Clinical: rice water stool.
Laboratory:
Identification via dark-field microscopy to detect motility like shooting
stars, inhibited by serotype-specific antiserum
Isolation of V. cholera employs thiosulfate-citrate-bile salts-sucrose (TCBS)
agar, which is selective for the organism. Live V. cholerae in stool (ca. 1.0 x
108 cells per ml)
serology by ELISA: to detect serum antibodies ; Antibacterial
antibodies( vibriocidal assays) and Antitoxin antibodies
Confirmation:
isolation of V. cholerae (serogroup 01 or 0139) from faeces, in nonepidemic areas
biochemical and serologic reactions and detection of cholera toxin
Prevention:
Vaccination is only partially effective and not generally recommended.
It is most commonly used by international travelers. An experimental
vaccine using a modified strain has been attempted. This strain, called
"Texas Star", produces a toxin that has the B domain but not the A
(biologically active) domain. Ingestion of this organism should allow
production of surface IgA against the cell-binding moiety (thereby
preventing binding) without producing overt disease

Treatment:
1- fluid replacement is the major component of treatment.
2- Antibiotic therapy (including tetracycline) is additionally used. Recovery
from cholera results in an effective immunity, but only to bacterial
strains of the same antigenic characteristics.

Noncholera Vibrios
1-Vibrio parahaemolyticus
found in salt water in many parts of the world.
The most common cause of outbreaks of gastroenteritis in humans by
ingestion of Raw oysters and crustaceans, such as shrimp and crabs.
The incubation time is normally less than 24 hours.
Clinical picture:
o abdominal pain, vomiting, a burning sensation in the stomach, and
watery stools.
Diagnosis:
o Because V. parahaemolyticus has a requirement for sodium and a
high osmotic pressure, isolation media containing 24% sodium
chloride are used in diagnosing the disease.
Treatment
o by antibiotics and rehydration is usually effective. Recovery usually
follows in a few days.
2-Vibrio vulnificus
found in estuaries.
It is halophilic and requires 1% NaCl in the media used to isolate it.
Clinical picture:
gastroenteritis in only a minority of infections.
life-threatening invasion of the bloodstream
in immuno compromised patients

 very dangerous infections of minor skin lesions incurred in coastal

sea waters.
spreading tissue destruction from these infections which may require
limb amputation.
if sepsis occurs, the fatality rate is about 25%.

Escherichia coli Gastroenteritis

E. coli are normally harmless, but certain strains can be pathogenic.
Mobile genetic elements can turn E. coli into a highly adapted pathogen
causing a range of diseases.
Morphology:
Gram-negative bacilli that ferment lactose.
Most are motile by peritrichious flagella H (flagellar) antigens that can
be used for epidemiologic purposes..
Approximately 170 different O antigens have been delineated and
some of these are cross-reactive with Shigella, Salmonella and
Klebsiella.
Escherichia also possess K (capsular) antigens similar to the Vi
antigen of Salmonella.
Enterotoxigenic strains may also display colonization factor antigens
(CFA/I, CFA/II).
Some toxin-secreting pathogenic strains can invade intestinal
epithelial cells, causing E. coli gastroenteritis. Other locations, such
as the urinary tract, bloodstream, and central nervous system, can
also be affected.
Five pathogenic varieties (pathovars) of E. coli have been well
characterized.
Enteropathogenic E. coli (EPEC):
major cause of diarrhea in developing countries and is fatal in infants.
the bacteria attach to the intestinal wall, eliminate surrounding
microvilli and stimulate host-cell actin to form pedestals beneath their
site of attachment.

 EPEC bacteria secrete a number of effector proteins that are

translocated into host cells, some contributing to diarrhea.
Enteroinvasive E. coli (EIEC):
it has the same pathogenic mechanisms of shigella.
EIEC gain access to the submucosa of the intestinal tract through M
cells in the same manner as Shigella. This invasion results in
inflammation, fever, and a Shigella-like dysentery.
Enteroaggregative E. coli (EAEC):
a group of coliforms found only in humans.
the bacteria cause a stacked-brick configuration on tissue culture
cells (aggregative).
produce an enterotoxin causing a watery diarrhea.
Enterohaemorragic E. coli (EHEC):
cause the same pedestal formation observed with EPEC,.
Most outbreaks are due to EHEC serotype O157:H7, in which a phage
encodes Shiga toxin which is released into intestinal lumen (no
invasion). Other lesser known strains include O121 and O104:H21.
Because the toxin is released upon lysis of the cell, antibiotic therapy
can worsen the attack by causing the release of more toxin.
Cattle, which are not affected by the pathogen, are the main reservoir;
infections are spread by contaminated food or water.
In humans, the Shiga toxins often cause only self-limiting diarrhea, but
in about 6% of infected people, it produces an inflammation of the
colon, profuse bleeding, called hemorrhagic colitis. Another dangerous
complication is hemolytic uremic syndrome (HUS).
Differentiation of these bacteria is done by:
inability to ferment sorbitol.
confirmed by pulsed-field gel electrophoresis (PFGE), a DNA
fingerprinting technique that subtypes bacteria. The data are entered
into a national Pulse Net database so that epidemiological information
can be compared.
enterotoxigenic E. coli (ETEC):

 secretes enterotoxins that cause diarrhea which is fatal for children

under 5.
One of the enterotoxins ETEC produces resembles the cholera toxin in
function. Adenyl cyclase is activated with production of cyclic AMP and
increased secretion of water and ions. ETEC bacteria are not invasive
and remain in the intestinal lumen.
Travelers Diarrhea
The most common bacterial cause is ETEC; the second most frequent
isolate is EAEC. Travelers diarrhea can also be caused by other
gastrointestinal pathogens, such as Salmonella, Shigella, and
Campylobacteras well as by various unidentified bacterial pathogens,
viruses, and protozoan parasites.
Treatment of traveler's diarrhea:
oral rehydration recommended for all diarrhea.
In severe cases, antimicrobial drugs may be necessary to provide some
protection;
bismuth-containing preparations, such as Pepto-Bismol, but the best
advice in risky areas is to prevent infection.
Different groups are most often delineated by serology, in particular, by
the immunogenic character of the O (somatic, LPS) and H (flagellar)
antigens
DIAGNOSIS:
Clinical: clinical diagnosis of E. coli infection is equivocal. The
enterotoxigenic and enteropathogenic forms cause a watery diarrhea and
nausea while the enteroinvasive and enterohemorrhagic forms subsequently
produce bloody stools. .
Laboratory: Specialized serotyping may be necessary for epidemiologic
studies.
CONTROL:

 Sanitary: As with other fecal-oral diseases, proper food handling and

personal hygiene are the best means for preventing infection.
Immunological: New vaccines against fimbrial antigens are possible.
Chemotherapeutic: Antibiotic therapy is not generally recommended
unless disease becomes life-threatening. Oral rehydration is the best
treatment.
Classific
ation
(Strain)
Enteroto

Site

Disease(s)

Pathoge
nic

of
Infec
Sma

Traveler's

Mechani
Enterotoxins

xigenic

ll

diarrhea

ST and LT

(ETEC)

intes

Watery

tine

stool,

Enteroin

Larg

Shigella-like

Tissue

vasive

diarrhea

invasion and

(EIEC)

intes

Fever,

destruction

Enteropa

tine
Sma

Infantile

of
Adherence

thogenic

ll

diarrhea

(EPEC)

intes

Salmonella-

tine

like

Enterohe

Lar

fever,
Hemorrhagi

SLT-I,
SLT-II
epithelial

morrhagi

ge

cytotoxins

c (EHEC,

inte

Severe

("verotoxins"

O157:H7

stin

abdominal

pain,

and
destruction

with
colitis

of

Campylobacter Gastroenteritis
Campylobacter are microaerophilic, spirally curved bacteria ("campylo",
meaning curved).

 Campylobacters possess a typical Gram-negative cell wall

containing LPS endotoxin.
There are approximately 50 heat-labile "K" (capsular) and "H" (flagellar)
antigens and 60 different heat-stable "O" (somatic) antigens associated
with different species of Campylobacter.
These organisms are able to use amino acids and citric acid cycle
intermediates for growth. C. jejuni grows best at 42.
They adapt well to the intestinal environment of animal hosts, especially
poultry, but the bacteria do not replicate in food.
Campylobacter gastroenteritis usually caused by C. jejuni.
The infective dose is fewer than a thousand bacteria.
Clinical symptoms:
It is characterized by fever, cramping , abdominal pain, and diarrhea or
dysentery.
Normally, recovery follows within a week.
C. jejuni appears to produce an enterotoxin similar to both the cholera
and Escherichia coli toxins.
DIAGNOSIS:
Clinical: Clinical diagnosis is difficult since the symptomology is nonspecific.
Laboratory: Special methods are required for isolation. Growth occurs in
5% O2, 10% CO2, 85% N2 at 42. A Gram stain of fecal material may reveal
curved ("seagull" or "comma") shaped organisms.
Treatment:
Erythromycin or tetracycline can be used for severe or prolonged
illness.

Helicobacter Peptic Ulcer Disease

A spiral-shaped, microaerophilic bacterium

 It is accepted that this microbe is responsible for most cases of peptic

ulcer disease.
Only about 15% of those infected develop ulcers, so certain host factors
are probably involved. For example, people with type O blood are more
susceptible, which is also true of cholera.
H. pylori is also designated as a carcinogenic bacterium.
Pathogenesis
The stomach mucosa contains cells that secrete gastric juice containing
proteolytic enzymes and hydrochloric acid that activates these
enzymes. Other specialized cells produce a layer of mucus that protects
the stomach
itself
from
digestion.
If this defense is disrupted, an inflammation of the stomach (gastritis)
results. This inflammation can then progress to an ulcerated area.
H. pylori can grow in the highly acidic environment of the stomach,
which is lethal for most microorganisms.
H. pylori produces large amounts of an especially efficient urease, an
enzyme that converts urea to the alkaline compound ammonia,
resulting in a locally high pH in the area of growth.
DIAGNOSIS
The most reliable diagnostic test requires a biopsy of tissue and culture
of the organism.
An interesting diagnostic approach is the urea breath test. The patient
swallows radioactively labeled urea; if the test is positive, CO2 labeled
with radioactivity can be detected in the breath within about 30
minutes. This test is most useful for determining the effectiveness of
chemotherapy because a positive test is an indication of live H. pylori.
Diagnostic tests of stools to detect antigens (not antibodies) for H. pylori
are suitable for follow-up tests following therapy.
Serological tests to detect antibodies are inexpensive but not useful in
determining eradication.
Treatment:

 The eradication of H. pylori with antimicrobial drugs usually leads to the

disappearance of peptic ulcers.
Several antibiotics, usually administered in combination, have proven
effective.
Bismuth subsalicylate (Pepto-Bismol) is also effective and is often part
of the drug regimen.

Yersinia Gastroenteritis
Other enteric pathogens being identified with increasing frequency are
Yersinia enterocolitica and Y. pseudotuberculosis .
These gram negative bacteria are intestinal inhabitants of many
domestic animals and are often transmitted in meat and milk.
These pathogens cause Yersinia gastroenteritis, or yersiniosis.
Symptoms:
diarrhea, fever, headache, and abdominal pain.
The pain is often severe enough to cause a misdiagnosis of
appendicitis.

Clostridium perfringens Gastroenteritis

A large, gram-positive, endospore-forming, obligately anaerobic rod.
This bacterium is also responsible for human gas gangrene.
The microbe grows in the intestinal tract and produces an exotoxin that
causes the typical symptoms of abdominal pain and diarrhea.
Most cases are mild and self-limiting and probably are never clinically
diagnosed.

Clostridium difficileAssociated Diarrhea

C. difficile is a gram-positive, endospore forming anaerobe found in the
stool of many healthy adults.
Produces 2 entero toxins:Toxin A -enterotoxin & Toxin B cytotoxin.
The exotoxins it produces cause a disease that manifests itself in
symptoms ranging from a mild case of diarrhea to life-threatening colitis
(inflammation of the colon).

 Occurring mostly as a nosocomial disease in hospitals and nursing

homes.

Bacillus cereus Gastroenteritis

Bacillus cereus is a large, gram-positive, endospore forming bacterium
that is very common in soil and vegetation and is generally considered
harmless.
It has, however, been identified as the cause of outbreaks of foodborne
illness.
Heating the food does not always kill the spores, which germinate as
the food cools.
Lab diagnosis Demonstration of large number of bacilli in food.
The disease is self- limiting.

Viral diseases of the digestive system

Hepatitis
Hepatitis is an inflammation of the liver.
At least five different viruses cause hepatitis, and probably more
remain to be discovered or become better known.
Hepatitis is also an occasional result of infections by other viruses
such as Epstein-Barr virus (EBV) or cytomegalovirus (CMV).
Drug and chemical toxicity can also cause acute hepatitis that is
clinically identical to viral hepatitis.

Hepatitis A
The hepatitis A virus (HAV) is the causative agent of hepatitis A.
As a member of the Enterovirus group, HAV contains a linear, positive
single-strand RNA genome and lacks an envelope.
It is also known as Enterovirus type 72 and is resistant to heat and
acid.
It can be grown in cell culture.
Pathogenesis
After a typical entrance via the oral route, HAV multiplies in the
epithelial lining of the intestinal tract.

 Viremia eventually occurs, and the virus spreads to the liver, kidneys,
and spleen.
The virus is shed in the feces and can also be detected in the blood
and urine.
The amount of virus excreted is greatest before symptoms appear
and then declines rapidly.
Therefore, a food handler responsible for spreading the virus might
not appear to be ill at the time.
The virus can probably survive for several days on such surfaces as
cutting boards.
HAV is resistant to chlorine disinfectants at concentrations ordinarily
used in water, a characteristic that enhances fecal contamination of
food or drink.
Mollusks, such as oysters, that live in contaminated waters are also a
source of infection.
At least 50% of infections with HAV are subclinical, especially in
children.
Symptoms:
In clinical cases, the initial symptoms are anorexia (loss of appetite),
malaise, nausea, diarrhea, abdominal discomfort, fever, and chills.
These symptoms are more likely to appear in adults; they last 2 to 21
days, and the mortality rate is low.
In some cases, there is also jaundice (signs are yellowing of the skin
and the whites of the eyes) and the dark urine typical of liver
infections. In these cases, the liver becomes tender and enlarged.
There is no chronic form of hepatitis A, and the virus is usually shed
only during the acute stage of disease.
The incubation time averages 4 weeks and ranges from 2 to 6
weeks, making epidemiological studies for the source of infections
difficult.
There are no animal reservoirs.
Diagnosis
An ELIZA test for detection of HAV-IgM antibody (anti-HAV-IgM) in one
serum sample is the routine diagnostic proof of HAV infection.

 The presence of IgG within the first few weeks of infection suggests a
prior infection or vaccination.
HAV-IgM antibody are detectable after onset of disease and usually
disappears within 4(6) months
Diagnosis is also made from the symptoms and the clusters of cases
that occur.
HAV infection induces life-long immunity and life-long persisting antiHAV/total antibody
Anti-HAV/total antibody: test for susceptibles before immunization
No specific treatment for the disease exists.
Hepatitis A Prevention
Passive Immune Prophylaxis Immune Globulin
Immune Globulin (IG) for intramuscular administration is 85% effective
in preventing symptomatic disease when given within 2 weeks after
exposure to HAV
In some countries the use of IG is recommended for :
Pre-exposure: travelers to intermediate and high HAV-endemic region.
Post-exposure (within 14 days)
Routine
household and other intimate contacts
Selected situations
institutions (e.g., day care centers)
common source exposure (e.g., food prepared by infected food
handler)
Vaccines
vaccine available is good (Harrix); recommended for travelers and
other high risk groups; first dose given and patient seroconverts in 4
weeks; give booster after 6 months and will achieve lifelong immunity
There is also a combined hepatitisA/hepatitis B vaccine commercially
available
in most countries the vaccines are licensed for children 2 years of
age.

Viral Gastroenteritis
Acute gastroenteritis is one of the most common diseases of humans.

 About 90% of cases of acute viral gastroenteritis are caused by either

the rotavirus or the human caliciviruses(named for the Latin calyx,
meaning cup cup-shaped depressions are visible on the viruses),
better known as the Norwalk family of viruses; or collectively, the
noroviruses.

Rotavirus
Rotavirus is probably the most common cause of viral gastroenteritis,
especially in children.
In most cases, following an incubation period of 2 to 3 days, the
patient suffers from low- grade fever, diarrhea, and vomiting, which
persists for about a week.
Rotavirus cases usually peak during the cooler winter months.
The vaccine is a live, orally administered.
Rotavirus infections are routinely diagnosed by several types of
commercially available tests, such as enzyme immunoassays.
Treatment is usually limited to oral rehydration therapy.

Norovirus
Humans become infected by fecaloral transmission from food and
water and even aerosols from vomiting.
Symptoms
Following an incubation period of 18 to 48 hours, the patient suffers
from vomiting and/or diarrhea for 2 or 3 days. Vomiting is the most
prevalent symptom in children; most adults experience diarrhea,
although many adult patients experience only vomiting.
DIAGNOSIS
To detect noroviruses in stool samples, laboratories use sensitive PCR
and EIA tests.
Treatment

 The only treatment for viral gastroenteritis is oral rehydration or, in

exceptional cases, intravenous rehydration.

Fungal diseases
Some fungi produce toxins called mycotoxins. When ingested, these
toxins cause blood diseases, nervous system disorders, kidney
damage, liver damage, and even cancer.
Diagnosis is usually based on finding the fungi or mycotoxins in the
suspected food.

Ergot Poisoning
Some mycotoxins are produced by Claviceps purpurea, a fungus
causing smut infections on grain crops.
The mycotoxins produced by C. purpurea cause ergot poisoning, or
ergotism, which results from the ingestion of rye or other cereal
grains contaminated with the fungus.
The toxin can restrict blood flow in the limbs, with resulting gangrene.
It may also cause hallucinogenic symptoms, producing bizarre
behavior similar to that caused by LSD.

Aflatoxin Poisoning
Aflatoxin is a mycotoxin produced by the fungus Aspergillus flavus, a
common mold.
Aflatoxin has been found in many foods but is particularly likely to be
found on peanuts.

Aflatoxin poisoning can cause serious damage to livestock when

their feed is contaminated with A. flavus.
Although the risk to humans is unknown, there is strong evidence that
aflatoxin contributes to cirrhosis of the liver and cancer of the liver in
parts of the world, such as India and Africa, where food is subject to
aflatoxin contamination.