Infections of

Gastrointestinal Tract

At the end of this chapter, the student should be able to:

1. recognize common gastrointestinal tract infections based on clinical manifestations;
2. differentiate invasive from non-invasive diarrhea;
3. compare the five hepatitis infections;
4. describe the characteristics of the causative organisms of each gastrointestinal tract

5. explain how the different gastrointestinal tract infections are transmitted; and
6. discuss the appropriate laboratory diagnosis, treatment, and prevention ofeach infection.

Definitions of Terms
1. Gastritis — inflammation of the mucosal lining of the stomach
2. Enteritis — inflammation of the small intestines
3. Colitis — inflammation ofthe colon (large intestines)
4. Gastroenteritis — inflammation of the mucosal lining of the stomach and intestine
5. Hepatitis — inflammation of the liver
6. Dysentery - low-volume, painful, bloody diarrhea
 o
e) Microbiology and Parasitology: A Textbook and Laboratory Manual for the Health Sciences

The digestive system is inhabited by many microorganisms. From the mouth down to the
colon, these different ecosystems arc occupied by site-specific microbial POPUlations

The stomach, due to its acidity, acts as an effective sterilization chamber that limits the
entry Of microorganisms to the small intestines. Infections Of the digestive system range
from asymptomatic infections to life-threatening loss of fluids and electrolytes, or severe
ulceration accompanied by intestinal perforation and hemorrhage. The clinical
manifestations vary from one another.

Establishment of Infectious Disease

in the Digestive System
Several factors play important roles in thc causation of infectious disease in the
digestive system. The most crucial and important impediment to infective agents is an intact
mucosal epithelium covering all parts of the digestive system. Early damage to the lining
may lead to manifestations such as nausea and vomiting. Damage to the mucosa in the form
Of ulcerations allow the members of the normal flora to penetrate the deep tissue and
disseminate through the bloodstream to other organs. Alteration of the acid barrier of the
stomach by disease, SUrgery or drugs increases the survival of pathogens leading to
infection. Changes in the composition of the normal flora allow the growth of pathogenic
organisms. Certain bacteria, viruses, and parasites can cause disease even in the absence of
predisposing factors due to their ability to produce virulence factors (e.g., toxin production).
Signs and symptoms of infections in the gastrointestinal tract are produced in several
ways.
These mechanisms include:
1. Pharmacologic action
Some bacteria produce toxins which may alter normal intestinal function
without causing lasting damage to their target cells. For example, the toxin produced
by Vibrio cholerae produces voluminous, watery diarrhea due to its ability to induce
increased electrolyte secretion into the intestines.
2. Local inflammation
Invasion of the alimentary tract by microbes can lead to inflammation. Invasion
is usually limited to the epithelial layer but may spread to the deeper tissues. In the
mouth, the gums are usually affected causing periodontitis. In the intestines,
infections can cause inflammation that can result to dysentery.
3. Deep tissue invasion
Certain organisms are able to spread to adjacent tissues and enter the
bloodstream• For example, the parasite Strongyloides is capable of burrowing
through the intestinal wall. The parasite is often colonized by gut bacteria and as a
result, infection by this worm can Icad to polymicrobial septicemia.
 Infections of Gastrointestinal Tract G150

4. Perforationo When the mucosal epithelium is perforated, the normal flora spills into
sterile and invades deep tissues, often with serious consequence. For example,

Mouth
Dental Caries (Tooth Decay)
Unlike other exterior surfaces, the teeth are hard and do not shed surface cells
allowing accumulation of masses of microorganisms and their products. These
accumulations are dental plaques and are involved in the formation of dental caries or
tooth decay. older, calcified deposits of plaque are called dental calculus or tartar. The
most important organism that causes dental caries is Streptococcus mutans, although other
microorganisms may also be involved (e.g., Actinomyces, Lactobacilli). S. mutans favors
crevices or other sites on the teeth that are protected from the shearing action of chewing
or from the flushing action of saliva. The lactic acid produced by the bacteria is not
diluted or neutralized by saliva, and this breaks down the enamel of the teeth, leading to
localized softening of the external enamel. If the initial penetration of the enamel by caries
remains untreated, bacteria can penetrate the interior of the tooth eventually advancing
into the pulp of the tooth.
Preventive measures against the development of dental caries include minimal ingestion of
sucrose, brushing, and flossing, regular dental visits to remove plaque, and the use of fluoride.
The use of mouthwash may be effective, with chlorhexidine being the most effective.

Periodontal Disease
Periodontal disease is a term used to describe conditions that are characterized by
inflammation and degeneration of structures that support the teeth. Gingivitis is the reversible
inflammation of the gingivae or gums, characterized by bleeding of the gums while brushing the
teeth. This is due to overgrowth of supra-gingival plaque causing irritation to the tissues of the
gums. Organisms involved are varied and include streptococci, actinomycetes, and anaerobic
gram-negative bacteria (Prevotella, Bacteroides, and Fusobacterium nucleatum).
Periodontitis is a chronic gum disease that can cause bone destruction and tooth loss. It
generally causes little discomfort. The gums are inflamed and bleed easily. As the infection
Progresses, the bone and tissue that supports the teeth are destroyed, leading to loosening
and loss of teeth. Numerous bacteria may be involved in the infection.
 Acute necrotizing ulcerative gingivitis or Vincent's disease or trench mouth is also another
common serious infection of the mouth. It is characterized by pain that prevents
 O
c31F_) Microbiology and Parasitology: A Textbook and Laboratory Manual for the Health Sciences

normal chewing and may be accompanied by bad breath or halitosis. The most common
organism involved is Prevotel/a intermedia. The condition is treated by adequate debridement,
oxidizing agents, and administration of mctronidazolc.

Oral Thrush
The organism that causes this condition is Candida albicans, a fungus that is part of the
normal flora of the skin, mucous membranes, and gastrointestinal tract. The condition
consists of white patches adherent to the oral mucosa and may occur on the tongue, lips,
gums, or palate.
Factors that predispose the development of oral thrush include endocrine disturbances
(e.g., diabetes), prolonged intake of antibiotics, malnutrition, malignancy, immunosuppression,
and prolonged use of steroids. Diagnosis can usually be made by inspection and confirmed by
examination of scraped material under the microscope demonstrating the characteristic
pseudchyphae. Treatment consists primarily of correcting the predisposing factor and avoiding
unnecessary use of antibiotics. Topical antifungal agents may be used. The drug of choice is
nystatin.

Mumps (Epidemic Parotitis)

Mumps is a highly communicable disease characterized by painful inflammation of the
salivary glands. This infection is caused by the mumps virus, a member of the family
Paramyxoviridae and there is only one serotype. Humans are the natural hosts. The disease
occurs worldwide, affecting people who have not been vaccinated before the age of 15.
Lifelong

immunity occurs in persons who have had the disease.

Mode of Transmission
Mumps virus is transmitted via respiratory droplets.
Clinical Findings
The virus infects salivary glands, with the parotid
glands predominantly infected. After an incubation
period of 18—21 days, the patient develops fever,
malaise, and anorexia followed by tender swelling of the
parotid glands and/or other salivary glands. Involvement
can be
develops, especially when drinking citrus juices. The disease is Figure 18.1 Epidemic parotitis or
benign and resolves spontaneously within a week. mumps showing unilateral
enlargement of the parotid gland
unilateral or bilateral. A characteristic increase in
parotid pain
 Infections of Gastrointestinal Tract

Complications
There are two significant complications—orchitis and meningitis. Orchitis is
inflammation f the testis. This complication is significant if it occurs in post-pubertal males
and if the

involvement is bilateral. Bilateral orchitis can lead to sterility. Meningitis is usually

benign and self-limited.

Laboratory Diagnosis
Diagnosis is usually based on clinical manifestations. Virus isolation from saliva, spinal
fluid, or urine can be done. Measurement of antibody titers can also be made.

Treatment and Prevention

Treatment is mainly supportive. Prevention consists of immunization with the live,
attenuated vaccine (MMR) given at 15 months of age. Administration of immune globulin
does not prevent development of orchitis.

Stomach
The major pathologies involving the stomach are inflammatory in nature and consist of
two conditions—gastritis and peptic ulcer disease. The predominant organism involved is
Helicobacter pylori, the most common cause of chronic gastritis and peptic ulcers (gastric and
duodenal). It has two major virulence factors: rapid motility and urease production. Its rapid
motility enables it to penetrate the mucus blanket lining the stomach. Urease produced by the
organism leads to production of large amounts of ammonia from urea that leads to
neutralization of gastric acid.
The natural habitat of the organism is the stomach but it may also be found in saliva. It is
likely acquired through ingestion and person-to-person transmission may also occur. Infection
with H. pylori is a risk factor for gastric carcinoma and MALT (mucosa-associated lymphoid
tissue) B cell lymphomas.

Clinical Findings
Gastritis and peptic ulcer disease are characterized by recurrent pain in the upper abdomen,
specifically around the epigastric area. This may be complicated by bleeding into the
gastrointestinal tract. The acute symptoms may last for less than one week until about two
weeks, however, the infection can persist for years.
 o c31?J Microbiology and Parasitology: A Textbook and Laboratory Manual for the Health Sciences

Laboratory Diagnosis
Gastric biopsy specimens can be used for histologic examination. Culture can also be
done as well as measurement of antibody levels specific for H. pylori.

Treatment
Treatment involves triple therapy with proton pump inhibitor (omeprazole), macrolide
(clarithromycin) and amoxicillin for 7 to 10 days. Proton pump inhibitors directly inhibit H.
pylori.

Ldver
Inflammation of the liver is termed hepatitis. Hepatitis can be caused by varied organisms
such as bacteria, viruses, and parasites. The most important causes of hepatitis are the Hepatitis
viruses. Cytomegalovirus, Epstein Barr virus, Herpes Simplex virus, and Rubella virus
Enteroviruses, Dengue virus, and the Yellow Fever virus are associated with sporadic hepatitis.
The clinical findings of hepatitis are virtually the same, regardless of which hepatitis virus is the
cause. Typical signs and symptoms include fever, anorexia, nausea, vomiting, and jaundice. Dark
urine and pale feces are also observed. Most cases resolve spontaneously in 2—4 weeks. Table
18.1 provides a summary of important clinical features ofthe Hepatitis viruses.

Hepatitis A Virus (HAV)

HAV causes infectious hepatitis. There is only one serotype of Hepatitis A virus. It is
transmitted mainly by the fecal-oral route. Sexual transmission is possible but rare. The
virus appears in the feces two weeks before the appearance of symptoms. Children are the
most frequently infected, and outbreaks may occur. The common source of outbreaks arise
from water and food contaminated with feces.
HAV has a short incubation period (3—4 weeks) and most patients with HAV
infection are asymptomatic. Fulminating infection may occur in a small number of patients.
No chronic hepatitis or chronic carrier state occurs. There is no predisposition to
hepatocellular carcinoma or cancer of the liver.
Diagnosis is confirmed by detection of antibodies directed against the virus. An increase
in anti-HAV IgM antibody signifies active infection while the presence of anti-HAV lgG
antibody suggests previous infection.
Treatment is mainly supportive. Active immunization with a vaccine containing
inactivated HAV is available. Two doses are given—an initial dose followed by a booster
dose
6—12 months later. It is recommended for those travelling to developing countries, children
ages 2—18 years
 Infections of Gastrointestinal Tract O
319
0 d active individuals. Passive immunization can be given to individuals exposed patients
and is given 14 days after exposure. other preventive measures include proper hygiene such
as proper sewage disposal and thorough hand washing after movement. The virus can be
inactivated by heating food for at least 1 minute to above

Hepatitis B Virus (HB\/)

I-I BY causes serum hepatitis. It is the only DNA virus among the hepatitis viruses. The
three main modes of transmission are through blood, during sexual intercourse, and from
mother to newborn during birth or breast feeding. The most efficient method oftransmitting the
virus is through injection into the bloodstream. It is found worldwide.
Majority of patients are asymptomatic, however, present symptoms are more severe than
hepatitis A infection. Hepatitis B can also present with extrahepatic manifestations like
polyarthritis, polyarteritis nodosa, rashes and glomerulonephritis. Fulminant infection can occur
as well as chronic hepatitis which can lead to cirrhosis and death. some patients can become
carriers, especially infants born to hepatitis positive mothers. HBV is also associated with the
development ofhepatocellular carcinoma.
Diagnosis can be confirmed by means of serology. Treatment is mainly supportive although
interferon-alpha can be useful for the treatment of chronic infection. Prevention involves the use
of either the vaccine or hyper-immune globulin or both. All blood for transfusion should be
screened for HBV.

Hepatitis C Virus (HCV)

HCV causes parenteral hepatitis. It is the predominant cause of non-A, non-B (NAI\IB)
hepatitis worldwide and the most common cause of post-transfusion hepatitis among IV
drug abusers. Humans are the reservoir for the virus and is transmitted primarily via blood.
At present, injection drug use accounts for almost all new HCV infections. Sexual
transmission and transmission from mother to child may occur. In addition, HCV has been
found to occur as a co-infection with HIV. Approximately 90% of patients with HIV
infection are also positive for HCV-RNA.
HCV primarily infects hepatocytes and remains inside the hepatocytes throughout. As a
result, chronic and persistent hepatitis is the hallmark of infection. It resembles HBV as far as
the ensuing chronic liver disease, cirrhosis, and the predisposition to hepatocellular carcinoma
are concerned. Alcoholism greatly enhances the development of hepatocellular carcinoma in
HCV-infected individuals.
C329) Microbiology and Parasitology: A Textbook and Laboratory Manual for the Health Sciences

Diagnosis is confirmed by detecting antibodies to HCV. A combination of interferon_

alpha and ribavirin is the treatment Of choice for chronic hepatitis C. Preventive measures
includes proper screening Of blood products prior to transfusion. Reducing or completely
avoiding consumption of alcoholic beverages also reduces the risk of developing
hepatocellular carcinoma and cirrhosis.

Hepatitis D Virus (HDV/Delta Virus)

HDV causes delta hepatitis. It is an unusual virus in that it is considered as a defective
virus for it cannot replicate on its own and can only do so in cells also infected with HBV.
As such, it is considered as a viral parasite. It uses the surface antigen of HBV as its
envelope. It is therefore transmitted by the same means as HBV.
HDV can occur as co-infection and superinfection. In co-infection, the patient is infected
with both HDV and HBV at the same time. In a superinfection, a person previously infected
with HBV (carrier) becomes infected with HDV. Acute hepatitis resulting from a co-
infection is more severe than in those infected with HBV alone. Hepatitis in chronic carriers
of HBV who become superinfected with HDV is more severe with greater incidence of
fulminating hepatitis, chronic hepatitis, and liver failure.
Diagnosis rests on detection of either delta antigen or antibody to delta antigen in the
patient's serum. Administration of alpha interferon may minimize some of the effects of
chronic hepatitis, however, it does not eradicate the chronic carrier state. Vaccination for
hepatitis B may prevent the occurrence of delta infection because HDV cannot replicate
unless HBV infection also occurs.

Hepatitis E Virus (HEV)

HEV is the major cause of enteric hepatitis. It is transmitted purely through the fecal-oral
route. Clinical manifestations are similar to hepatitis A, with the exception of a high mortality
rate in pregnant women. There is no chronic hepatitis or a prolonged carrier state. Diagnosis is
made by excluding HAV and other causes. There is no antiviral drug or vaccine available to
prevent infection.

Hepatitis G Virus (HGV/GB Virus C)

HGV is not primarily hepatotropic. The virus replicates within monocytes then finds its way
into the liver where it can cause a chronic type of hepatitis. It is transmitted through sexual
intercourse and blood transfusion and may occur as a co-infection with HIV. It has been noted
that patients co-infected with HIV and HGV have lower mortality rate and have less
HIV in their blood than those infected with HIV alone. In vitro studies haye shown that HGV
may interfere with the replication of HIV.
 Infections of Gastrointestinal
Tract 3210
fable 18.1 Comparison of features of hepatitis viruses
Hepatitis
A Hepatitis B
"Infectious" "Serum" Hepatitis C
"Non-A Hepatitis D Hepatitis E
"Delta agent"
common non-B "Enteric non-
name Picornavirus; Hepadnavirus; posttransfusion" A, non-B
capsid RNA envelope, DNA
Flavivirus; Viroid-like; Hepevirus;
Virus envelope, RNA envelope, Caliciviruslike
structure Fecal-oral Parenteral, circular RNA capsid
sexual, Parenteral, Parenteral, Fecal-oral
Transmission insidious sexual, sexual
Incubation 15-50
45-160 insidious
period (days)
14—180+ 15-64 15-50
Severity Mild
Occasionally
severe Usually Co-infection Normal
subclinical; or patients, mild;
70% superinfection pregnant
with
chronicity women,
HBV severe
Chronicity/ No Yes Yes
Carrier state
Yes No
Other None Primary Primary hepato-
disease Cirrhosis,
hepato-cellular cellular None
associations fulminant
carcinoma, carcinoma,
cirrhosis cirrhosis hepatitis

Laboratory Symptoms Symptoms Symptoms Anti-HDV ELISA

diagnosis and anti-HAVand serum and anti-HCV
lgM levels of ELISA
HBsAg,
HBeAg, and
anti-HBc IgM
Sma00 and Large Ontestdnes
Diarrhea
In most cases, diarrhea is defined as a change in the normal bowel habits of an individual,
with an increase in the frequency, fluidity, looseness, and volume of feces excreted per day
in COmparison to the usual fecal output of the individual. In a normal adult, the average
daily stool weight is less than 200 grams, Of which 65% to 85% is water. Diarrhea implies
daily stool production in excess of 250 grams, containing 70% to 95% water. It is the final
common
Pathway of intestinal responses to many inciting agents and serves as an adaptive mechanism
developed by the body to get rid of noxious material.
 o
c32?) Microbiology and Parasitology: A Textbook and Laboratory Manual for the Health sciences

Depending on the causative agent, diarrhea may be classified as invasive or

Non-invasive diarrhea is the result of disruption of the secretory process due to th
released from the bacteria. This is characterized by watery diarrhea and the
absence or leukocytes in the feces. In invasive diarrhea there is direct damage to
the tissues duc to direct invasion by the bacteria. It is characterized by fever,
dysentery (blood
stools), and leukocytes in the feces. Table 18.2 summarizes the major differences between
thin two types.

Table 18.2 Differences between invasive and non-invasive types of diarrhea

(blood, mucus
cells)

(cramping; tenesmus)
intestine)

Adapted from Lecture Guide in Microbiology, Department of Microbiology, College of Medicine, Our Lady
of Fatima Unrverslty, 2018

Children and the elderly are more susceptible to dehydration from diarrhea.
Rehydration or replacement of the fluid and electrolyte lost is necessary for the
management of any form of diarrhea. Fluid replacement can be done by drinking more
fluids or oral rehydration solution (ORS) or through IV depending on the severity of the
dehydration. Some suggest giving of zinc supplement reduces the severity of diarrhea. A
new concept in the management of diarrhea is the use ofprobiotics. Some claim that
probiotics are helpful in preventing traveler's diarrhea in children and antibiotic-
associated diarrhea.
 Education of the public is vital in reducing the incidence of diarrhea. Preventive
measures include having a proper waste water and sewage disposal system, maintenance
of clean and safe food sources and drinking water, and good hygienic practices. In
addition, studies have shown that breastfeeding for the first six months after birth is
effective in preventing diarrhea in newborns and infants.

Mode of Transmission

The most common mode of transmission is fecal-oral transmission. This includes (1)
person-to-person transmission, usually in association with overcrowding and poor
personal hygiene, (2) ingestion of contaminated meat, poultry products or seafood, (3)
contamination of food during or after cooking.
 Infections of Gastrointestinal Tract O
3230
Viral Gastroenteritis
Acute, self-limited infectious diarrhea which usually involves children, is most commonly by
enteric It may cause severe dehydration requiring hospitalization, especially Table 18.3
summarizes the common gastrointestinal viruses causing gastroenteritis.

Table 18.3 Common viruses associated with acute gastroenteritis in humans

Rotaviruses
Group A
6-24 months
Single most important
cause of endemic
Group B
Person-to-person; water severe diarrheal
Adults and illness in infants and
Group C
children young children
Outbreaks of diarrhea in
Children Person-to-person; water China
Sporadic and occasional
Person-to-person; water outbreaks
Enteric Child < 2 years Person-to-person Second most important
adenoviruses of age viral agent of endemic
(Group F or diarrhea in infants and
serotypes 40 young children worldwide
and 41)
Caliciviruses Person-to-person, water, cold
Older children and foods, raw shellfish Causes outbreaks of
Norovirus
adults vomiting and diarrhea in
families, communities, and
institutions
Infants, young Sporadic and occasional
Saporovirus
children, elderly outbreaks
Astroviruses Infants, young Person-to-person, water, raw Sporadic and occasional
children, elderly shellfish outbreaks
Adapted from Jawetz, Melnick & Adelberg's Medical Microbiology 26th ed., McGraw-Hill Education, 2013, p. 547

Rotavirus is the most common viral cause of gastroenteritis in children. Infants and young
Children are most commonly affected although debilitated adults may also be susceptible. It
destroys mature enterocytes leading to loss of absorptive function of the small intestine with net
secretion of water and electrolytes. After an Outbreaks incubation may period occur of
approximately in the pediatric 2 days, population vomitingin hospitals and day care centers.
and watery diarrhea will occur for several days.
 o
C32±) Microbiology and Parasitology: A Textbook and Laboratory Manual for the Health Sciences

Norwalk virus is responsible for majority of cases of non-bacterial food-borne epidemic

gastroenteritis in all age groups, most especially in adults. The virus causes epidemic
gastroenteritis with watery diarrhea, abdominal pain, nausea, and vomiting. OUtbreaks occur
following exposure of multiple individuals to a common source. Majority of outbreaksmay
be seen in nursing homes. can
There is no specific treatment for viral gastroenteritis. Management is mainly SUPportive
with adequate fluid and electrolyte replacement.

BacterjaO Onfectdons
Bacterial Enterocolitis (Food Poisoning)
A classic case of food poisoning has two important features: (1) similar symptoms occur
in several members of a group who shared the same meal, and (2) onset of symptoms occurs a
few hours after food ingestion. Food poisoning may occur due to either of three mechanisms:

1. Ingestion ofpreformed toxin — the preformed toxin may be present in contaminated

food. Major offenders are Staphylococcus aureus, Vibrio, and Clostridium
Perfringens. Symptoms develop within hours consisting of explosive diarrhea and
acute abdominal pain.
2. Infection by toxigenic organisms — the organisms proliferate in the gut lumen and
elaborate an enterotoxin. Symptoms occur within hours consisting of diarrhea and
dehydration if it involves a secretory enterotoxin, or dysentery if the primary
mechanism is a cytotoxin.
3. Infection by enteroinvasive organism — the organisms proliferate, invade, and
destroy mucosal epithelial cells, leading to dysentery.
As a rule, the incubation period is less than 12 hours after ingestion of preformed
toxins. Longer incubation period indicates ingestion of live bacteria that must first
proliferate before producing the signs and symptoms of infection. Identification of the
causative agent requires isolation of the infectious agent or detection of the toxin in
contaminated food. Management is mainly supportive and in most cases, antibiotic
therapy is not required. Table 18.4 summarizes the important clinical and epidemiologic
features of the more important and common organisms that cause food poisoning.
 Infections of Gastrointestinal Tract
3.
o
18.4 clinical and epidemiologic features of food poisoning
Incubation
Clinical
anism period
presentation
(hours) Characteristic foods
Bacillus
reus 1-6 Vomiting
6-24 Watery diarrhea Re-warmed fried rice
Meat, poultry, vegetable
botulinum 12-17 Neuromuscular Canned foods, smoked fish,
paralysis unpasteurized honey
aureus 2-4 Vomiting, diarrhea Meats, custard, salads
aemolyticus 10-24 Watery diarrhea Shellfish
perfringens 9-15 Watery diarrhea Meat, poultry
Clostridium

Staphylococcus
Vibrio parah
Clostridium
Adapted from Lecture Guide in Microbiology, Department of Microbiology, College of Medicine, Our Lady of Fatima

University

Baci//us cereus
The organism is a gram-positive aerobic rod or bacillus. Bacillus cereus is mildly
pathogenic and of low virulence hence an opportunistic pathogen. Food poisoning caused by
B. cereus has two distinct forms: the emetic type, associated with fried rice, and the diarrheal
type, associated with meat dishes and sauces. The organism produces toxins that cause
disease that is more of an intoxication than a food-borne infection.

Clinical Findings
The emetic form is manifested by nausea, vomiting, abdominal cramps, and occasionally
diarrhea. It is self-limited with recovery occurring within 24 hours. It begins 1—5 hours after
ingestion of contaminated rice and occasionally pasta dishes. The diarrheal form has an
incubation period of 1—24 hours and is manifested by profuse diarrhea with abdominal pain
and cramps. Vomiting may occur but is uncommon. The enterotoxin may be preformed or
produced in the intestine.
 Laboratory Diagnosis
Laboratory diagnostic procedures are usually not done, although isolation of the organism
from the suspected food samples followed by culture can be performed.

Treatment and Prevention

No antibiotic therapy is required since the infection is self-limiting. Preventive measures
include preventing contamination of food by soil since the organism is usually found in soil.
Rice should also not be kept warm for long periods.
o
c32f_) Microbiology and Parasitology: A Textbook and Laboratory Manual for the Health Sciences

Staphylococcus aureus
S. aureus is an important cause of food poisoning and causes food poisoning With
shortest incubation period (30 minutes to 8 hours, average of 2 hours). the
produced when the organism grows in food rich in carbohydrates and protein.are

Mode of Transmission
The major mode of transmission for staphylococcal food poisoning is ingestion
preformed heat-stable toxin in contaminated food, especially salads, custards, milk
and processed meat. The bacteria can grow in high salt concentration hence its
association productsWith processed meats. The food does not taste spoiled making it
difficult to detect contamination. The bacteria can be killed by reheating the food,
however, it does not destroy the toxin. The chief sources of infection are carriers and
those individuals shedding human lesio fomites contaminated from such lesions, and
the human respiratory tract and skin.

Cinical Findings
Vomiting accompanied by nausea is more prominent than diarrhea. The emetic
effect is probably the result of stimulation of the vomiting center in the central nervous
system after the toxin acts on neural receptors in the gut. There is no fever and rapid
convalescence is the rule.

Laboratory Diagnosis
Isolation of the organism from the suspected food samples followed by culture can be
performed to confirm the diagnosis. Contaminated food can also be tested for the presence
of toxin, however, this is seldom done.
 Treatment and Prevention
Management is mainly supportive with the replacement of lost fluid and
electrolytes as a mainstay. No antibiotic therapy is required since the infection is self-
limited. Cleanliness, hygiene, and aseptic management of lesions can control the
spread of staphylococci from skin lesions.

C/ostridium perfringens
C. Perfringens is a large, rectangular gram-positive rod. It is anaerobic and rarely produces
spores. An enterotoxin produced by this microorganism is a common cause offood poisoning•
Infections of Gastrointestinal Tract

327t
o de of Transmission of preformed toxin from food contaminated with soil containing the

such as reheated foods like meat dishes is the most common means by
Which the otvanism is acquired.

Clinical Findings
The incubation period is 8—24 hours. The disease is characterized by watery diarrhea
with cramps. Vomiting may also occur but it is not common. The disease usually
resolves in 24 hours,

Laboratory Diagnosis
Large numbers of the organism can be isolated from food samples. There is no assay for
the

Treatment and Prevention

No antibiotic therapy is needed and management is mainly supportive. Food should be
adequately cooked before consumption to kill the organism and prevent infection.

Vibrio parahaemo/yticus
V. parahaemolyticus is a marine organism. It is a curved, gram-negative coccobacillus. Virulent
strains produce Kanagawa hemolysin, an enterotoxin similar to the cholera toxin.
It possesses polar flagella and pili. V.parahaemolyticus is the most common cause of bacterial
gastroenteritis associated with seafood.
Mode of Transmission
The infection is acquired through ingestion of raw or undercooked seafood, especially shellfish
such as oysters.

Clinical Findings
The manifestations vary from mild to severe watery diarrhea, nausea, vomiting, abdominal
cramps, and fever.The illness is self-limited, lasting about three days.

Laboratory Diagnosis
Diagnosis can be confirmed by culture. The organism is halophilic, requiring 8% sodium
chloride (NaC1) solution for growth.
 c32Y Microbiology and Parasitology: A Textbook and Laboratory Manual for the Health sciences

Treatment and Prevention

Antibiotic therapy is not necessary because the disease is relatively mild and selfiim•
Disease is prevented by proper refrigeration and cooking of seafood.

Gastroenteritis (Diarrhea)
Infectious diarrhea may result from multiplication of the microorganism in

gastrointestinal tract and the mobilization of host defenses as it attempts to eli

invading organism. All diarrhea-producing bacteria adhere to intestinal mucosal cells

by of fimbriae. Once bacteria start to proliferate, they can (1) induce structural
abnormali0'es intestinal resulting mucosa.to increased excretion of fluids and electrolytes;
(2) release toxins; or (3) invade

Bacteria producing diarrhea may be classified into invasive and non-invasive b

Non-invasive bacteria produce diarrhea by producing enterotoxins or cytotoxins.
stimulate adenylate cyclase causing fluid secretion, leading to a watery type of
Cytofoxins can cause tissue damage leading to inflammation and blood loss. Invasive
bactGa penetrate the bowel epithelium, stimulating intense inflammation. There is direct
damage to the intestinal mucosa resulting in dysenteric type of diarrhea.

Table 18.5 Features of specific types of non-invasive bacterial diarrhea

Escherichia Ye
enteroco
Shige//a spp. coli Salmonella spp.
Incubation (hours) 1-
24-72 24-72 8-48
Abdominal cramps

Vomiting

Fever
Vibrio Escherichia Clostridium Bacillus Staphylococcus
aureus
cholera coli perfringens cereus
 Incubation (hours) 12-72 24-72 6-12 3-8 1-6

Abdominal
cramps
Vomiting

Adapted from Lecture Guide in Microbiology, Department of Microbiology, College of Medicine, Our Lady
of Fatima University

Table 18.6 Features of specific types of invasive bacterial diarrhea

\dapted from Lecture Guide in Microbiology, Department of Microbiology, College of Medicine, our Lady Of
Fatima Iniversity)
 Infections of Gastrointestinal Tract

Noninvasive diarrhea diarrhea is usually is more usually severe self-limited and requires and
does aggressive not require therapy. specific Table antibiotic 18.7 summarizestherapy.

causes ofbacterial diarrhea.

fable 18.7 Major causes of bacterial diarrhea

Pathogenic
organism Mechanism Source
Escherichia coli
Clinical Features
ETEC+
Cholera-like Traveler's diarrhea
toxin, no Food, water Watery diarrhea
invasion Shiga- Hemorrhagic colitis,
like toxin, Undercooked HUS*
EPEC+
no invasion beef products Watery diarrhea
Attachment,
enterocyte Weaning foods, water
effacement
Cheese, water, Fever, pain, diarrhea,
Invasion, local spread
person- to-person dysentery
Salmonella Milk, beef, eggs, Fever, pain,
spp.
Invasion, dissemination poultry diarrhea or
dysentery,
bacteremia,
extraintestinal
infection
hige//a spp. Invasion, local spread Person-to-person, Fever, pain, diarrhea,
low inoculum dysentery, epidemic
spread
Yersinia Invasion, dissemination Milk, pork Fever, pain, diarrhea,
enteroco/itica extra-intestinal
infection
Vibrio cholerae Enterotoxin, no Water, shellfish, Watery diarrhea,
invasion person-to- pandemic spread
person
Clostridium Cytotoxin, Nosocomial spread Fever, pain,
diffici/e bloody diarrhea,
following
antibiotic use
 enterohemorrhagicE. coli; EPEC entero-pathogenic
coli; EHEC coli;
ETEC enterotoxigenic

Clostridium Enterotoxin, no invasion Meat, poultry, fish Watery diarrhea,

perfringens food sources
Mycobacterium Invasion, Contaminated Chronic abdominal
uberculosis inflammation with milk, pain; complications
necrosis and scarring swallowing of of malabsorption,
coughed-up stricture,
organisms perforation, fistulae,
hemorrhage
EIEC - enteroinvasive
HUS - hemolytic-uremic syndrome
330 Microbiology and Parasitology: A Textbook and Laboratory Manual for the Health Sciences

Escherichia co/i
E. coli is a gram-negative, motile, encapsulated rod that is a member of the
Enterobacteriaceae and is a member of the normal intestinal flora. There are 5 mily
groups of E. coli namely: (1) enterotoxigenic E. coli (ETEC), (2) enteropathogenic
OgenicE

E. coli (EAEC), (4) E. coli (EHEC)coli

E. coli only produces disease when it reaches the tissues outside of their normal flora
ETEC, EPEC, and EAEC are primarily associated with secretory diarrhea involving
the intestines while EHEC and EIEC involve the large intestines. E. coli is the most
cause of urinary tract infection and gram-negative sepsis. It is the most common cause of
neonatal meningitis and is most frequently associated with "traveler's diarrhea." It also used
 index of fecal contamination of water. as The microorganism has several components
that contribute to its ability to produce disease These include the presence of pili (for
adherence), capsule (anti-phagocytic), endotoxin and enterotoxins (two that cause watery
diarrhea and one that causes bloody diarrhea and hemolytic-uremic syndrome).

Mode of Transmission
is acquired through ingesting of food or water contaminated by human feces.
EHEC is usually associated with ingestion of undercooked meat (e.g., undercooked
hamburgers).

Enterotoxigenic E. coli (E TEC)

ETEC is the major cause of "traveler's diarrhea" or turista" and is an important cause
of diarrhea in infants in developing countries. Some strains produce a heat-labile (LT)
exotoxin that causes intense and prolonged hypersecretion of water and chlorides and
inhibits sodium re-absorption. Some produce a heat-stable (ST) enterotoxin that
stimulates fluid secretion. Strains with both toxins produce severe watery diarrhea.
ETEC-induced diarrhea is characterized by abrupt onset of diarrhea which is self-
limiting. A more serious infection may be observed in infants.

Enteropathogenic E. coli (EPEC)

EPEC is an important cause of diarrhea in infants in developing countries. It was
previously associated with outbreaks of diarrhea in nurseries in developed countries•
The organism adheres to mucosal cells of the small intestine and causes loss of
microvilli• This leads to watery diarrhea that is usually self-limited but can be chronic.
Dehydration, electrolyte imbalance, and other complications may cause death so that
antibiotic therapy is necessarY•
Infections of Gastrointestinal Tract

o E. coli (EAEC)
EAEC causes acute and chronic diarrhea. These are common causes of food-borne illness
dustrialized countries. EAEC produces ST-like toxin and a hemolysin.

Enteroinvasive E. coli (EIEC)

EIEC causes invasion of the colonic mucosa. The disease occurs most commonly in
dildren and travellers in developing countries. The disease characterized by acute bloody
b.arrhea with malaise, headache, high fever, and abdominal pain. It is an occasional cause
 of occasional outbreaks of dysentery and sporadic infection. It is the most common cause
of urinary tract infection as well as meningitis in newborns.

Enterohemorrhagic E. coli (EHEC)

EHEC produces a shiga-like toxin as that produced by Shigella. It is a verotoxin that is
cytotoxic, neurotoxic, and enterotoxic. The main source of infection is undercooked meat,
especially undercooked hamburgers in fastfood restaurants. It is associated with
hemorrhagic colitis, a severe type of diarrhea which initially presents with bloody diarrhea,
vomiting, and severe abdominal pain. It is also associated with hemolytic-uremic
syndrome, a disease resulting in acute renal failure, hemolytic anemia, and
thrombocytopenia (low platelet count). E. coli serotype 0157:H7 is the most common. In
2011, E. coli 0104:H4 caused a serious outbreak of food borne illness resulting in 35
deaths out of 3,000 persons in Germany.

Laboratory Diagnosis
Diagnosis can be confirmed by culture of organism from stool specimen using a
differential medium (EMB or MacConkey's agar). On EMB agar, E. coli colonies have a
characteristic greenish metallic sheen. E. coli can ferment lactose. Biochemical tests
should be done to differentiate it from the other members of Enterobacteriaceae.

Treatment and Prevention

Antibiotic therapy is usually not indicated in E. coli diarrheal diseases.
Trimethroprimsulfamethoxazole can be given to shorten symptoms and eliminate the
invasive forms of the organism. Fluid and electrolyte replacement is essential. Traveler's
diarrhea can sometimes be prevented by the prophylactic use of doxycycline, ciprofloxacin,
or trimethoprimsulfamethoxazole. Ingesting uncooked foods and unpurified water should
be avoided while traveling in certain countries.
 o
c33& Microbiology and Parasitology: A Textbook and Laboratory Manual for the Health sciences

Sa/mone//a spp.

Enterobacteriaceae. Salmonellae are The gram-negative, organism has encapsulated, three

important motile antigens—cell rods that also wall be(somatic) long to O,the family

H, and capsular Vi (virulence) antigens. The H antigen is responsible for the invasiveness
organism while the Vi antigen is anti-phagocytic. Gastric acid is an important host defense

Clinically, the Salmonella species can be classified into two categories,

(1) the typhoidal species (S. typhi and S. paratyphi), and (2) the non-typhoidal
(S. enteritidis and S. cholerasuis). S. cholerasuis is most commonly involved in systemic
infection.species

Mode of Transmission
Ingestion of food and water contaminated by human and animal wastes is the major
mode of transmission. S. typhi is transmitted only by humans. All other species have both
animal and human reservoirs. The most frequent animal sources are dairy products,
poultry, and eggs, however, inadequately cooked meat products have also been
implicated.

Clinical Findings
1. Enterocolitis — characterized by invasion of the small and large intestine. It begins
with nausea and vomiting which progresses to abdominal pain and diarrhea (mild to
severe, with or without blood). The disease usually lasts a few days and is self-
limited. In the U.S., S. enteritidis serotype typhimurium is the most common cause.
This is the most common manifestation of salmonella infection.
2. Typhoid or enteric fever — begins in the small intestines but few gastrointestinal
symptoms occur. Survival and growth of the organism in phagocytic cells is a
striking feature of this disease as well as the predilection to invade the gallbladder,
resulting in the establishment of a carrier state—asymptomatic carriage of the
bacteria for more than 1 year.
Typhoid fever is most commonly caused by S. typhi but can also be caused by S.
paratyphi. The illness is characterized by slow onset with fever, bradycardia and
constipation rather than vomiting and diarrhea. After the first week, as the bacteremia
becomes sustained, high fever, delirium, tenderness in the abdomen, and splenomegaly
may occur. Rose spots which is characterized by rose-colored macules on the abdomen
or chest may occur in typhoid fever. The disease begins to resolve by the 3rd week
 Complications such as intestinal hemorrhage or perforation can also occur. The carrier
state is more common in women, especially those with previous gallbladder disease
and gallstones.
Infections of Gastrointestinal Tract

o
— occurs in one of two settings: a patient with an underlying disease (e.g., sickle
3. cell anemia) or cancer, or a child with enterocolitis. Septicemia is most commonly caused by
S. cholerasuis. Symptoms begin with fever with little or no cntcrocolitis then proceed

to focal symptoms. Osteomyelitis, pneumonia, and meningitis arc the most common
sequelae.

Figure 18.2 The typical rose spots seen on the

chest of a patient with typhoid fever

Laboratory Diagnosis
I. Enterocolitis — stool exam, stool smear, stool culture
2. Typhoid Fever or Enteric Fever
a. Isolation and identification
Culture is the best method (EMB or MacConkey's agar)
• Blood or bone marrow— 1st to 3rd week of illness
• Stool or rectal swab — incubation period; 2nd to 4th week of illness
• Urine — first two weeks
b. Serology — Widal Test
• Positive only in 24%—60%; positive after the first week of illness
• Measures level of antibodies against the O, H, and Vi antigens (4-fold rise in antibody
titer)
• Interpretation:
Antibody against O Ag — acute infection
Antibody against H Ag — recovery or previous vaccination
 Antibody against Vi Ag — carrier
c. Typhidot — detects specific IgM and lgG antibodies against Salmonella
3. Biochemical tests are done to differentiate from other Enterobacteriaceae
334 Microbiology and Parasitology: A Textbook and Laboratory Manual for the Health Sciences

Treatment and Prevention

Enteric fevers and bactercmia require antimicrobial treatment, however, the of
cases of enterocolitis do not. Clinical symptoms and excretion of the organism vast
majoriyb prolonged by antimicrobial therapy in enterocolitis. Antimicrobial therapy for

cephalosporin. In most carriers, surgical removal of the gallbladder (cholecystectomy)

Sanitary measures must be undertaken to prevent contamination of food and

Thorough cooking of infected poultry, meat, and eggs must be done. Carriers must
be promptly and not be allowed to handle food, as well as observe strict hygienic
precautions Vaccines are available to prevent the infection, especially in endemic areas.

Shige//a spp.
Shigellae are gram-negative, non-motile, non-encapsulated rods which are members
ofthe family Enterobacteriaceae. The natural habitat is limited to the intestinal tracts of
humans and other primates. There are four important species of Shigella, namely S.
sonnei, S.flexneri, S. boydii, and S dysenteriae type 1 (Shiga bacillus). Of the four
species, S. dysenteriaeis the most clinically significant as it is responsible for epidemics
with high mortality. The major virulence factor of S. dysenteriae type 1 is the Shiga
toxin, which is a verotoxin as in E. coli. Low inoculum is needed to produce infection.

Mode of Transmission
Shigellosis is transmitted by the four F's, namely "food, fingers, flies, and fomites."lt may also
be transmitted through sexual contact.

Clinical Findings

Shigellosis is characterized by a short incubation period of 1—3 days. It is

characterized by lower abdominal pain, fever, and bloody, mucoid diarrhea. Bowel
movement is accompanied by tenesmus or strained defecation. In adults, more than 50%
of cases resolve spontaneously In children and the elderly, severe dehydration may lead
to
death. Complications include (1) perforation of the colon, (2) hemolytic-uremic syndrome
similar to E. coli, and (3) Ekiri syndrome, a fulminant type ofencephalopathy. Like
Salmonella, a carrier state may occur•

Laboratory Diagnosis
1. Stool examination revealing leukocytes (wbc) and/or red blood cells in fresh stool
specimen
2. culture offeces or rectal swab specimen (EMB or MacConkey's agar)
 Infections of Gastrointestinal Tract

reatment and Prevention

The mainstay of management is fluid and electrolyte replacement. Antimicrobial agents
ch as ciprofloxacin, ampicillin, doxycycline, and trimethoprim-sulfamethoxazole are
effective •nst the organism.
pßventive measures include (1) sanitary control of water, food, and milk; (2) proper sewage
j.sposal, and fly control; (3) patient isolation and disinfection of excreta; (4) detection of
carriers, especially food handlers; and (5) prompt antibiotic treatment of infected
individuals.

Yersinia enteroco/itica
Y. enterocolitica is also a member of the family Enterobacteriaceae and are gram-
negative, urease-positive rods. Urease produced by the organism neutralizes the gastric acid
allowing the organism to survive and colonize the intestines.

Mode of Transmission
Ingestion of food (meat and dairy products) or water contaminated by feces of domestic
animals is the primary mode of transmission. The organism may also be transmitted through
fomites.

Clinical Findings
The organism causes inflammation and ulceration in the tissues affected. Early symptoms
include fever, abdominal pain, and diarrhea that is watery to bloody. The terminal ileum may
be involved and if the mesenteric lymph nodes are involved, it may present itself as right
lower quadrant pain and may be misdiagnosed as acute appendicitis. One to two weeks after
onset, some patients develop arthralgia, arthritis, and erythema nodosum. The organism, in
rare instances, may cause pneumonia, meningitis, or sepsis. It is however a self-limiting
infection.

Laboratory Diagnosis
Y enterocolitica can grow in most culture media and can grow best with "cold enrichment"
or at low temperature of 4 oc.
Treatment and Prevention
Most cases of diarrhea are self-limited and do not require antimicrobial therapy. There are
no specific preventive measures, however, preventing contamination of food and water may
be helpful in preventing infection.
 o
c33f_) Microbiology and Parasitology: A Textbook and Laboratory Manual for the Health sciences

Vibnb cho/erae
The Vibrios are among the most common bacteria in surface waters worldwide. r
a comma-shaped, curved, motile rod with a polar flagellum. V. cholerae serogroups
01 cause cholera epidemics. Occasionally, serogroups non-Ol/non-0139
V.cholerae serogroups 01 is divided into serotypes (Inaba, Hikojima, and Ogawa) and b
ioIllness. (classical and El tor). V. cho/erae 01 biotype El tor is the most common cause of
cholera epidemics while serogroup 0139 or the Bengal strain was identified as the strain th
the most recent (8th) epidemic ofcholera and has been identified n c 0 eragen as the or
firstcholera toxin) strainth stimulates prolonged hypersecretion
ofwater and electrolytes. It is pathogeniconly for humans

Mode of Transmission
The disease is spread by ingestion of contaminated food and water. Person-to_ person
transmission is rare because the infectious dose is very high.

Clinical Findings
The disease is called cholera and majority of cases are asymptomatic. There is onset
ofnausea and vomiting, and profuse watery diarrhea (as much as 20-30 L/day)
abdominal cramps. The stools may resemble "rice water." There is severe dehydration
which can lead to circulatory collapse and hypovolemic shock may result in death ifthe
patient is

Laboratory Diagnosis
Diagnosis rests on the typical clinical presentation. Microscopic examination using
darkfield or phase contrast microscopy may be done to show the rapidly motile organism.
 Treatment and Prevention
Crucial to the management ofcholera is rapid fluid and electrolyte replacement.
The drug ofchoice is tetracycline. Preventive measures include health education and
improvement Of sanitation. Isolation ofpatients with disinfection of their excreta
should be done. A vaccine is available, however, it provides limited protection to
heavily exposed persons and is not effecfre
 Infections of Gastrointestinal Tract 9370

clostridium perfringens
c. perfringens is a toxin-producing organism that can produce invasive infection. It produces
toxins and enzymes that result in a spreading infection. These toxins have lethal,
necrotizing, and hemolytic properties. some strains produce a powerful enterotoxin, especially

Mode of Transmission
Infection in humans occur after ingesting food (usually meat and gravies) contaminated by dirt or

feces.

Clinical Findings
C. perfringens can produce a disease process called enteritis necroticans, an acute
necrotizing process in the small intestines that manifests with abdominal pain and bloody
diarrhea. Severe infection can lead to peritonitis and shock.

Laboratory Diagnosis
Diagnosis is done through culture under anaerobic conditions.

Treatment and Prevention

The antimicrobial agent of choice is penicillin. Antitoxins in the form of concentrated
immune globulins can be administered. There are no specific preventive measures. Food
must be adequately cooked before consumption to kill the organism.

C/ostridium diffici/e
C. difficile is also an anaerobic, gram-positive, spore-forming rod. Approximately 3% of
the general population are asymptomatic carriers of the organism in the gastrointestinal tract.
It is the most common nosocomial cause of diarrhea. The organism produces exotoxins that
cause death of enterocytes.

Mode of Transmission

C. difficile is transmitted by the fecal-oral route and hospital personnel are important
intermediaries.
 o
c33Y Microbiology and Parasitology: A Textbook and Laboratory Manual for the Health Sciences

Clinical Findings
The organism causes antibiotic-associated pseudomembranous colitis. .

The second- and third-generation cephalosporins are now considered as the now most
implicated.co causes. The diarrhea may be watery or bloody and frequently accompanied
by abdommon cramps, fever, and leukocytosis. minal

Laboratory Diagnosis
Detection oftoxins in stool specimens using ELISA or cytotoxicity test is the basis for

Treatment and Prevention

Discontinuance of administration of the offending antibiotic is the treatment of choice
followed by oral administration of either metronidazole or vancomycin. Fluid replacement
is also essential. Indiscriminate use of antibiotics should be avoided. There are no
preventive vaccines or

Baci//us anthracis
Gastrointesdnal anthrax is very rare and is acquired by entry of spores through the
mucous membranes or by ingestion of improperly cooked meat from infected animals.
Symptoms include vomiting, abdominal pain, and bloody diarrhea. The diagnosis can be
made through microscopic examination of specimen and culture.
The drug of choice for the treatment of anthrax is ciprofloxacin. Doxycycline is an
alternative drug. Control measures include: (1) proper disposal of animal carcasses, (2)
decontamination of animal products, and (3) active immunization of domestic animals with
live attenuated vaccine. Persons with high risk should be immunized.

Mycobacterium tuberculosis
Tuberculosis of the gastrointestinal tract can be caused by either M. tuberculosis
when it is swallowed after being coughed up from a lung lesion, or by M. bovis when it
is ingested in unpasteurized milk products. It is characterized by abdominal pain and
chronic diarrhea' accompanied by fever and weight loss. Intestinal obstruction or
hemorrhage may also occur• The most common site involved is the ileocecal region.
Oropharyngeal tuberculosis typically presents with painless ulcer accompanied by
lymphadenopathy.
 Infections of Gastrointestinal Tract
o

ves multidrug therapy against the organism. The BCG vaccine can be
used Treatment invol
artial resistance to tuberculosis. Pasteurization of milk and elimination of infected to
important preventive measures for intestinal tuberculosis.
Dental caries is most commonly caused by S. mutans and is associated with sucrose
lactic acid. and Periodontal diseases are mixed infections caused by different
groups of infections involve inflammation of the gums and the progressive
destruction ofthe deeper

Oral thrush is most commonly caused by C. albicans and is associated with a variety
of predisposing factors like immunosuppression and intake of broad-spectrum
antibiotics among others.
Mumps is a highly communicable infection characterized by inflammation of the
saliv glands. ary

H. pylori produces urease which enables it to survive the acidity of the stomach. It is
a common cause of gastritis, peptic ulcer, gastric carcinoma, and MALT lymphomas.
The most common causes of hepatitis are viruses. Hepatitis A and E are acquired
through the fecal-oral route while Hepatitis B, C, and D are acquired by sexual,
parenteral, and transplacental transmission.
Food poisoning can be caused by S. aureus, C. perfringens, B. cereus, and C.
botulinum.
S. aareus causes food poisoning with the shortest incubation period.
The virulent strains of V.parahemolyticus produce Kanagawa hemolysin and it is the
most common cause of bacterial gastroenteritis associated with seafood.
There are 5 pathogenic groups of E. coli namely: (I) enterotoxigenic E. coli (ETEC), (2)
enteropathogenic E. coli (EPEC), (3) enteroaggregative E. coli (EAEC), (4)
enterohemorrhagicE. coli (EHEC), and (5) enteroinvasive E. coli (EIEC).
Typhoid fever is caused by both S. typhi (most common) and S. paratyphi. It is
acquired through ingestion of contaminated dairy products, poultry, and eggs.
Shigellosis is characterized by lower abdominal pain, fever, and bloody, mucoid
diarrhea with tenesmus.
V. cholerae serogroups 01 and 0139 cause cholera epidemics. Cholera is characterize d
by profuse diarrhea (rice water stools) accompanied by vomiting resulting to se vere
dehydration, and can even result in the death of the patient.
Mycobacterium tuberculosis and M. bovis can cause intestinal tuberculosis from
ingestion Of contaminated milk and its products.
 QUESTIONS
Infections of Gastrointestinal Tract
G0410
o
SELf.AssEssMENT

Sgnte: Score:
Secoon Date:

. A 50-year woman was brought to the emergency room because of profuse diarrhea and
I Case. The stool is described as "rice water"-like in appearance. The patient is a resident of omiting.
pavans, Quezon City and works as a scavenger. P.E. reveals a severely dehydrated patient with
åready pulse and hypotension.

1. This is most probably a case of:

a. Salmonellosis c. Cholera

b. Shigellosis d. Amoebiasis

2. The severe diarrhea is due to which of the following virulence factors of the

causative agent?
a. Capsule c.
Toxin

b. Teichoic acid d. Flagellum

3. The infection is most probably acquired through:

a. Ingestion of contaminated food and water
b. Ingestion of contaminated poultry products
c. Indirect contact via inanimate objects
d. Contact with asymptomatic carrier

4. If this is a case of cholera, which group of Vibrio cholera is a common cause of

epidemics of cholera?

a. V. cholerae 01 c. Bengal strain

b. V. cholerae non-Ol d. All of the above
 5. This infection is best managed by:
a. Fluid and electrolyte replacement
b. Giving Tetracycline
c. Isolation of the patient
d. All of the above
o
c34& Microbiology and Parasitology: A Textbook and Laboratory Manual for the Health Sciences

Multiple Choice.

1. The Shigellla species that produces Shiga toxin.

a. S.flexneri c. S. sonnei d. S. dysenteriae
b. S. boydii

2. Infection with which hepatitis virus almost always leads to fulminant

hepatitis?
a. Hepatitis A c. Hepatitis C
b. Hepatitis B d. Hepatitis D

3. Gastroenteritis caused by this is most frequently associated with ingestion

contaminated seafood.
a. S. aureus c. V.parahemolyticus
b. S. typhi d. S.flexneri

4. Food poisoning with the shortest incubation period:

a. B. cereus c. C. Perfringens
b. S. aureus d. C. botulinum

5. Antibiotic-associated pseudomembranous enterocolitis is caused by:

a. C. botulinum c. C. perfringens

b. C. difficile d. B. cereus

6. It is the most common cause of traveler's diarrhea.

a. ETEC c. EAEC
b. EPEC d. EIEC
7. It is associated with hemolytic uremic syndrome.

a. EHEC c. V. cholerae
b. S. dysenteriaed. A and B

8. It occurs as co-infection or super-infection with Hepatitis D virus.

a. HAV c. HCV
b. HBV d. HEV