Infectious Human

Diseases of the Intestine

Infectious Human
Diseases of the Intestine

Mary E. Miller
Infectious Human Diseases of the Intestine

Copyright © Momentum Press®, LLC, 2019.

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 Abstract
Intestinal diseases are a significant health issue worldwide, with varying
causative infections resulting in symptoms that range from mild or as-
ymptomatic to death within hours. Understanding the cause of the dif-
ferent forms of intestinal disease is a critical aspect of proper management
of these diseases that can save lives.
This book describes the current understanding of symptoms, diag-
nosis, mode of transmission, and treatments of four important intestinal
diseases, taking into consideration the molecular interactions between
host cells and infectious agents. Specifically, dysentery caused by infection
with Entamoeba histolytica, giardiasis caused by infection with Giardia,
shigellosis caused by infection with Shigella, and cholera caused by infec-
tion with Vibrio cholera, are discussed in each chapter.
The author also discusses future work related to prevention and treat-
ment of these critical infectious diseases, given that the eradication of these
diseases is unlikely. Awareness of how these diseases are spread and how they
can be contained is a growing public health concern, particularly after nat-
ural and human-made disasters where public hygiene may be compromised.

Keywords
cholera; diarrhea; dysentery; Entamoeba histolytica; Giardia; giardiasis;
­intestinal; Shigella; Vibrio cholerae
 Contents

Introduction...........................................................................................ix
Chapter 1 Symptoms and Diagnosis...................................................1
Chapter 2 Causes and Contributing Factors.......................................7
Chapter 3 Treatment and Therapy....................................................19
Chapter 4 Future Prospects...............................................................23
Conclusion............................................................................................25
Bibliography..........................................................................................27
Glossary................................................................................................31
About the Author����������������������������������������������������������������������������������33
Index���������������������������������������������������������������������������������������������������35
 Introduction
Different forms of infectious diarrhea, or gastroenteritis, have shaped
world populations, altered economic welfare, and influenced the out-
comes of wars. Gastroenteritis can be caused by a number of infectious
agents ranging from viruses to bacteria to multicellular protozoa. Three
serious forms of intestinal diseases include dysentery, cholera, and giar-
diasis. Each of these diseases is caused by different infectious microbes,
but in all cases, the function of the intestine is impaired. Symptoms can
vary dramatically, with some individuals unaware that they are carrying
and transmitting the infection whereas other individuals die from an in-
fection within days of the onset of symptoms. Intestinal diseases that re-
sult from infection by a microorganism are not restricted to any particular
geographical area, though populations at the greatest risk are where the
potential of ingesting contaminated material is highest. Locations at the
highest risk are areas with insufficient infrastructure to ensure food and
water hygiene, particularly after natural or manmade disasters. Awareness
of potential transmission of these diseases is a key aspect to controlling
outbreaks of infection.
Infectious diseases can be spread by many routes. In the case of dysen-
tery, cholera, and giardiasis, the route is fecal-oral transmission, mean-
ing that infectious organisms are shed in feces of an infected person and
spread when another person consumes food or water contaminated with
the infected feces. Fecal-oral transmission occurs through handling of
contaminated materials or through insect vectors, such as a house fly, that
might touch a contaminated item and then someone’s food. Avoiding
these diseases requires rigorous hygiene practices to ensure that there is no
fecal contamination of any materials that might be consumed by a per-
son. When an infection occurs, disease symptoms will vary in intensity.
­Epidemics or outbreaks of disease can be tracked when reporting systems
and community response systems are effective. An outbreak would mean
that there are more cases than expected in a given area. These diseases can
x INTRODUCTION

be endemic, meaning that the infectious organism occurs naturally in

the environment and sustains a consistent frequency of infection within
a given population. Usually, endemic means one documented case in the
previous three years with evidence that spread has occurred locally. Out-
breaks can be seasonal, and therefore somewhat predictable, or they can
be sporadic and difficult to anticipate. In endemic areas, an epidemic
leads to an increase in disease occurrence in a defined period of time.
When epidemics spread to a large geographical region, such as an entire
country or many continents worldwide, the outbreaks is considered a
pandemic.

Infectious Intestinal Disease

In the cases of intestinal diseases such as dysentery, cholera, and giar-
diasis, some symptoms of the diseases are common (such as loose stool).
However, each disease is distinct and results from infection by different
microorganisms. The infectious microorganism can be a prokaryotic bac-
terium, as in the case of dysentery and cholera, or a eukaryotic proto-
zoan, as in the case of amoebic dysentery and giardiasis. Regardless of the
cause, before a microbe can reach the small and large intestines, it must
survive the natural defense mechanisms of the human body, including
the highly acidic environment of the stomach. For this reason, infectious
microbes must have evolved mechanisms for survival in these harsh con-
ditions—either in the form of distinct cellular structures or physiological
states. For protozoans, the infectious organism is ingested in the form of a
cyst that can withstand extreme condition, such as a very acidic stomach.
The cyst is also able to withstand harsh environmental conditions outside
of the human body, which is why a cyst is the most likely form spread
during a disease outbreak. For bacteria, many physiological or structural
mechanisms enable survival in the acidic environment of the stomach.
The causative agents of dysentery and cholera are not ingested as inactive
and resistant spores or cysts. Rather, they gain physiological tolerance to
the acidic environment or must be ingested in numbers great enough to
ensure survival of some percentage of the ingested microorganisms.
Like all living organisms, the microorganisms that cause intestinal
diseases are able to grow and respond to their environments by changing
 INTRODUCTION
xi

the production proteins or other macromolecules that are encoded by the

pathogen’s genome. In prokaryotes, the genome structure can vary and
is usually one or more circular pieces of DNA. Some species carry addi-
tional small circular DNAs called plasmids that encode additional genes,
such as antibiotic resistance genes, that allow the bacteria to survive under
harsh environmental conditions. In the case of protozoans, the genome is
composed of a collection of linear pieces of DNA (e.g., the protozoan that
causes giardiasis has 5 linear chromosomes). The genome will include/
encode all of the genes of the organism. A gene is a segment of DNA that
can be used as template to make a complementary RNA molecule. The
RNA molecule either performs a function directly or is used as a template
for the cells to produce a particular protein. Proteins perform many func-
tions, ultimately providing the machinery and structures that make up
a living cell. Cells are the most basic unit of life in nature and are com-
mon to all living things. Different types of cells have different shapes and
sizes—each uniquely formed because of the genes that are active within
any given cell; only a subset of genes are active at any given time. For ex-
ample, proteins can work inside cells as an enzyme to metabolize critical
nutrients, or may function as a structural unit of a cell, giving the cell its
shape that contributes to the cell’s function. Changes in DNA sequence
will give rise to changes in RNA and can produce changes in proteins.
Therefore, changes in DNA sequence, or mutations, have the potential
to cause functional and structural changes in a cell. DNA mutations that
cause functional changes can result in two distinct but similar strains or
species of a microorganism, each able to give rise to different severities of
disease, or no disease at all. Further complicating clinical outcomes from
infection is that the genome of an infectious organism can be changed
if it is infected by a virus. A virus is acellular and is not considered an
independent form of life because it must infect another cell to metabolize
and reproduce. Different types of viruses can infect different types of cells,
with preferences for either prokaryotic or eukaryotic cells. Sometimes, a
virus carries genes that make the microbe more dangerous, so the infect-
ing microorganisms can be characterized further by any viruses or virus
genomes within the pathogen. Human cells contain their own individu-
alized genomes that encode variant proteins that might make a person
more or less susceptible to infection by a microorganism. Therefore, two
xii INTRODUCTION

people infected by the exact same microbial strain can respond differently
because key genes differ due to mutations in their genomes.
Intestinal functions can be disrupted through the growth of the in-
fecting microorganism or through toxins produced by the pathogen.
Gastrointestinal disease results from the disruption of one or more basic
functions of intestine. When considering how mutations change the vir-
ulence, or the ability of a microorganism to cause disease, attention is
paid to mutations in genes that encode virulence factors. A virulence
factor can be any molecule or structure of an organism that allows it to
cause disease, but the term is usually reserved for factors that play a large
role in the more serious forms of diseases. Most virulence factors facilitate
a direct, physical interaction between host and pathogen, induce an im-
mune response from the host, or produce a type of toxin that can harm
host cells. In each of these three categories, the virulence factor is encoded
by the microbe’s genome and is one or more proteins produced by the mi-
crobe during infection. Once produced, some toxins are released outside
of the microorganism and are called exotoxins, whereas others are called
endotoxins because they remain inside the pathogen. When a pathogen is
killed and cleared from the body, exotoxins may remain and cause dam-
age to host cells, which is why they are particularly dangerous.
Exotoxins are particularly concerning because very little exotoxin can
impair the function of intestinal cells. Bacterial exotoxins fall into one of
three categories: Type I, II, and III. Type I exotoxins stimulate host cells
to produce PAMPS, or pathogen-associated molecular patterns, which
permit the bacteria to bind to host cells as a consequence of the host’s im-
mune response. Specifically, the host responds to the presence of the bac-
teria by releasing chemical messengers called cytokines and chemokines.
These molecules are part of a healthy host immune response, but one
consequence is the initiation of inflammation that can harm host tissues.
Type I exotoxins are also referred to as superantigens because of their
ability to stimulate a vigorous host immune response that causes damage
to the host. In contrast to type I exotoxins that harm the host indirectly,
type II exotoxins directly damage the host cell membranes or associated
cellular structures. Each cell is surrounded by a cellular membrane that is
composed of lipids and proteins. A cell membrane surrounds and protects
the cell and the embedded proteins allow the cell to communicate and
 INTRODUCTION
xiii

interact with the environment outside of the cell. Some membrane pro-
teins anchor the cell to the extracellular matrix. The extracellular matrix
helps support and position the cells correctly. Some type II exotoxins are
proteases that digest other proteins. The targets of type II include extra-
cellular matrix proteins, whereas others target proteins that produce pores
used to regulate the movement of materials in and out of the cell. Type
II exotoxins can also be phospholipases that destroy the lipids that form
a cell’s membrane. Exotoxins that disrupt cell membrane function impair
intestinal cells and often kill cells of the intestine.
Type III toxins are two-component protein complexes that directly
harm cells. Type III toxins can be referred to as A-B toxins, because of
the two protein components that make up the toxin. The B component
physically interacts with proteins, called receptors, embedded in the host
membrane and allows component A to get inside of the host cell. Com-
ponent A disrupts a function inside of the host cell and causes direct
harm. Once the B component has interacted with its receptor protein,
either both A and B enter the cell, or only the A component enters the
cell. Once the A component is inside of the host cell, it alters specific host
cell proteins by carrying out an enzymatic reaction. This component A
reaction is called ribosylation because it removes an ADP–ribosyl group
from a molecule called NAD and then adds ADP–ribose group to an-
other protein in the cell. Once the host protein has been ribosylated, its
function is impaired. The identity of the target protein varies depending
on the specific shape and function of the component A exotoxin, which is
encoded in the pathogen’s genome. Different bacteria will produce differ-
ent A-B toxins, which target and impair different host cell proteins that
harm or kill host cells. In many cases, pathogens can carry many virulence
factors and will produce combinations of type I, II, and/or III exotoxins.
Serious diseases are caused by exotoxins against which hosts have evolved
immune defenses. Infected hosts try to recognize and clear exotoxins pro-
teins from the body, even if the pathogen has been killed.

The Human Intestine and Diarrhea

Intestinal infections frequently give rise to diarrhea, or loose stool, in
response to the presence of infecting microorganisms. The production of
xiv INTRODUCTION

feces, or stool, in humans is regulated by specialized tissues in a healthy

human digestive system that functions to absorb nutrients from the food
we eat and water we drink. The digestive system includes many organs,
from mouth to stomach to intestine, that function collectively to take
in nutrients and remove waste (in the form of feces) from the body. The
small intestine specializes in absorbing nourishment, and the large intes-
tine specializes in water absorption. Both the small and large intestines
are muscular tubes, where food is broken down while nutrients and water
are absorbed into the bloodstream. Material that enters the small intestine
from the stomach is usually a semisolid and enters the small intestine as a
liquid called chyme. Approximately 80 percent of the water in chyme is
absorbed in the intestine due to an osmolarity gradient. Specialized pro-
tein channels that are embedded in the cellular membrane allow chloride,
sodium, and potassium ions out of cells and into the space between the
cells. Water moves through channels too into this space to balance its con-
centration gradient. Water moves across the epithelial cells and eventually
reaches the blood. Most nutrients are absorbed in the small intestine,
and once passed to the large intestine the remaining water is removed be-
fore reaching the rectum where the feces will exit the body. As feces exits
the body, normal stool is a solid material made up of indigestible food
(roughage) and bacteria. The production of feces involves the function of
both the large and small intestine and leads to the production of 150 mL
of feces for every 500 mL of food that enters the large intestine.
The intestine is composed of several layers of tissues or groups of
specialized cells that work together to carry out a function for the body.
Some organisms, such as bacterial prokaryotes, consist of a single cell.
Eukaryotic multicellular organisms, such as humans, are comprised
­
of trillions of cells working together to make up tissues, which work
­together as organs allowing the whole organism to live. In tissues, differ-
ent types of cells work together to give the tissue specialized structure and
function. Each type of cell within a tissue will have a defined position and
shape that contributes to the cell’s function within a tissue. Many differ-
ent types of cells exist within the intestinal layers. In the case of the large
intestine, the layers of tissue include the mucosa, which is the innermost
layer and lines the inside of the tube-like intestine. Absorptive cells called
enterocytes and goblet cells, for example, are located in the mucosa layer.
 INTRODUCTION
xv

Absorptive cells absorb water and nutrients, whereas goblet cells produce
mucus to lubricate the feces as it moves through the intestine. These and
other specialized cells are scattered among epithelial cells that contribute
to the lining of the mucosa. Epithelial cells are bound together through
extracellular structures that prevent water from flowing freely between the
cells. The integrity of this mucosal lining is critical to the function of the
intestine, which primarily regulates water and nutrient absorption. In the
case of intestinal diseases, the water absorption process is disrupted, giv-
ing rise to diarrhea and the possible consequence of dehydration. Some
intestinal diseases cause dramatic water loss and loss in nutrient absorp-
tion that can lead to shock and possibly death. Since the small intestine
mostly absorbs nutrients and the large intestine absorbs water, it is pos-
sible to remove large parts of the large intestine without disrupting nutri-
ent uptake. This surgical intervention is used for some conditions of the
large intestine such as severe inflammatory bowel diseases, but is rarely
used to treat diseases caused by infectious microorganisms.
The primary symptom of intestinal diseases is diarrhea, which is de-
fined as an increase in the volume of feces or in the frequency of produc-
ing feces. Diarrhea can also occur due to other physiological problems,
some not associated directly with the intestine. As part of the normal
digestive process, a lot of water is secreted into the lumen of the small
intestine and then reabsorbed before it reaches the large intestine. If for
any reason water secretion outpaces absorption diarrhea will occur. For
example, diarrhea associated with cholera can occur due to defects in
water secretion. Another cause of diarrhea caused by intestinal disease
is the loss of intestinal epithelium integrity, which damages the intesti-
nal tube, as exampled by diarrhea caused by giardiasis. Leakage of blood
into the intestine makes water reabsorption less efficient, too. Intestinal
damage triggers a host immune response that causes inflammation that
exacerbates the diarrhea. As the immune response is triggered, cytokines
and chemokines are produced that stimulate more water secretion. As
the immune response continues, epithelial cells also die, and as they are
replaced, the immature cells are less able to absorb water leading to more
water loss and through diarrhea.
Bacteria naturally present in a healthy person is called the bacte-
rial flora or microbiota and can be comprised of hundreds of different
xvi INTRODUCTION

bacterial species all living together in a productive way to support bacte-

rial growth and some functions of the intestine. These bacteria can be
helpful in the processing of the food waste products, synthesizing vita-
mins (e.g., biotin, pantothenic acid, and vitamin K), and protecting the
colon from harmful bacteria. The intestinal flora are not able to move to
other parts of the body where they might cause harm because they cannot
cross the mucosal layer of the intestine. These types of bacteria remain in
the lumen, or interior space of the intestine, continue to grow and help
the normal function of the intestine.
 CHAPTER 1

Symptoms and Diagnosis

Symptoms and Diagnosis of the Dysentery

Dysentery is a disease of the intestines that results in severe diarrhea
with blood or mucus in the stool. Symptoms can include pain in the
abdomen, fever, and a feeling of incomplete defecation. Symptoms are
coupled to an inflammatory response in the colon that occurs because
of infection by a microorganism. Several different types of microorgan-
isms can cause d ­ ysentery, including the bacteria Shigella, the eukaryotic
amoeba Entamoeba histolytica, and some strains of the bacteria Escherichia
coli. Depending on the type of infecting microorganism, progression can
cause severe disease of other organs in the body, such as the liver, lungs,
or brain.
When a patient suffers from gastrointestinal disease caused by ­Shigella,
it is called shigellosis. There are an estimated 164.7 million Shigella
­infections worldwide each year that include both endemic occurrences
and epidemic outbreaks. Symptoms may include diarrhea, fever, stomach
cramps, and the feeling that they need to pass stool when their bowels are
empty. Shigella are able to infect the epithelial cells of the mucosa in the
colon. As the infection spreads, it can cause ulcer, bleeding, and inflam-
mation. In more serious forms of the disease, visibly bloody diarrhea can
occur. Symptoms typically begin about 2 days after the infection occurs
and subside within 5 days. While infected, people can spread Shigella
to others which is particularly concerning when patients have very mild
or undetectable symptoms, so they unknowingly spread the disease. In
severe cases, Shigella can be spread to the blood system resulting in a
blood-borne disease. Blood-borne shigellosis is life-threatening with a fa-
tality rate of 46 percent. Complications associated with shigellosis include
hemolytic-uremic syndrome that can lead to kidney failure and is one of
2 INFECTIOUS HUMAN DISEASES OF THE INTESTINE

the most common causes of kidney failure in children (though not neces-
sarily because of Shigella infections). In rare cases associated with Shigella
dysenteriae infections, the colon can become paralyzed so that it is unable
to pass feces or gas, which causes swelling, fever, pain, weakness, and
­disorientation. Other complications of shigellosis can include hypoxia
(low oxygen levels), reactive arthritis, and some neurological problems.
Hyponatremia (abnormal electrolyte balance) and pneumonia can also
occur, but these two diseases are uncommon consequences of Shigella
infections.
Dysentery can also be caused from an infection by Entamoeba histo-
lytica, and when this occurs the disease is called amebiasis. E. histolytica
is distributed worldwide though it is more common in tropical regions.
Approximately 50 million infected individuals experience gastrointesti-
nal symptoms, and approximately 100,000 deaths occur per year. Most
individuals who are infected with E. histolytica do not show symptoms,
with only 10 to 20 percent getting sick. Long-term travelers (more than
6 months) are at higher risk of contracting amebiasis than short-term
travelers (less than 1 month). Risk also increases for pregnant, immu-
nocompromised, diabetic, and alcoholic individuals and patients taking
corticosteroids. If symptoms occur, they usually develop 2 to 4 weeks
after infection, though some cases take longer to become symptomatic.
Symptoms include loose feces, stomach pain, and stomach cramping.
More severe cases, such as amebic dysentery, cause stomach pain, bloody
feces, and fever. In rare cases, infection spreads to the liver, and in even
more rare cases it can spread to other parts of the body such as the lung
or brain.
Diagnosis of both shigellosis and amebiasis involves identifying the
infecting microorganism in the patient’s feces. Detection of Shigella infec-
tion involves sampling patient feces and allowing bacteria in the sample
to grow in the laboratory for identification. These tests can be designed
to distinguish Shigella species and antibiotic resistant forms of the bacte-
ria, which can aid in treatment. Molecular tests designed to detect spe-
cific regions of the bacterial genome can also be used to diagnose specific
species and drug resistance. For amebiasis, identification may involve
­concentrating microorganisms present in a stool sample and looking for
the presence of E. histolytica cysts. Visual detection can be aided with
 Symptoms and Diagnosis 3

the use of stains, such as trichome, which can help visualize the parasites
when using a microscope. Since amoebas have a complex life cycle, it
can be difficult to diagnose the disease based on histological approaches,
and these approaches may not distinguish between pathogenic and non-
pathogenic parasites. Improved methods include antibody-based and
DNA tests to ensure that protozoan cysts identified in patient samples are
capable of triggering dysentery.

Symptoms and Diagnosis of Cholera

Cholera is a serious gastrointestinal disease caused by infection of the bac-
teria Vibrio cholerae. A major health concern worldwide, cholera can cause
death within hours of the onset of symptoms. Worldwide, approximately
21,000 to 143,000 deaths occur from cholera each year, and between 1.3
and 4 million individuals contract the disease. Cholera cases are not well
documented sometimes, and reporting of cholera cases is not mandatory
in many areas. In many areas, cholera is considered endemic and thus
is a constant health concern. Outbreaks of cholera can be seasonal, or
sporadic, frequently associated with heavy rainfalls. Outbreaks can vary
in scale. If a region has not had a case in at least 3 years and one new case
occurs, it would be considered an outbreak. In 2018 outbreaks have been
recorded in Somalia (March 29, 2018); Kinshasa, Democratic Republic
of the Congo (March 2, 2018); Mozambique (February 19, 2018); and
United Republic of Tanzania (January 12, 2018). In 2017, 35 partners in
the Global Task Force on Cholera Control developed a strategy to reduce
deaths by 90 percent before the year 2030.
Most infected individuals show mild-to-moderate cholera symptoms
that include acute watery diarrhea with dehydration. Severe dehydration
causes lethargy, dry mouth, weak or absent pulse, low blood pressure, and
low amounts of urine. Symptoms usually occur between 12 hours and
5 days after infection. Since many diseases cause diarrhea, diagnosis of
cholera requires identification of V. cholerae in the patient’s feces. Iden-
tification of V. cholerae in feces can be performed using rapid diagnostic
tests, but should be confirmed in a laboratory setting where bacteria are
isolated and grown from patient samples. Subtyping, or serotyping, iso-
lates is done using molecular tests that identify the O antigen or specific
4 INFECTIOUS HUMAN DISEASES OF THE INTESTINE

regions of the bacteria’s genome. The O antigen is a sugar expressed on

the surface of the bacterium that can vary between different strains and
be used to distinguish between pathogenic and nonpathogenic bacteria.
Rapid tests can identify V. cholerae but are less able to identify serotypes
or drug susceptibility; hence, slower molecular diagnosis methods are
required for optimal treatments. In some areas, molecular tools are not
available, so rapid tests such as Crystal VC dipstick can give an early
warning to public health professionals of a potential outbreak. Positive
rapid test results should be followed up by culturing the bacteria from
patient fecal samples. The WHO recommends that instances involving
children younger than 2 years of age experiencing acute diarrhea with
dehydration, or instances of death from diarrhea, should be considered
a suspected case of cholera. In areas where a cholera outbreak has been
confirmed, any aged person with similar symptoms should be suspected
of having cholera. Confirmed cases of cholera would include those cases
where V. cholerae O1 or O139 antigens are confirmed by molecular tests.

Symptoms and Diagnosis of Giardiasis

Giardia is the one of the most common global causes of intestinal disease
in people. Giardia infects approximately 2 percent of adults and 6 to 8
percent of children in developed nations, and 33 percent of individuals in
developing countries. Infection by Giardia results in an intestinal disease
called giardiasis. Though some people show no symptoms, most people
with giardiasis experience a combination of symptoms that include diar-
rhea, gas that smells like rotten eggs, greasy stools that might float, stom-
ach cramps, abdominal cramps, nausea, and dehydration. In rare cases,
itchy skin, hives, and swollen eyes/joints might occur. Symptoms nor-
mally appear one to three weeks after infection. Sometimes symptoms go
away and then reappear after days or weeks. Infection impedes nutrient
absorption in the patient, particularly fats, lactose, and vitamin A and
vitamin B12. In severe cases, developmental delays in children might be
caused by Giardia infections.
To diagnose giardiasis, the patient is tested for the presence of
pear-shaped Giardia cysts with flagella, which are long extensions from
the cyst used for movement. Staining for the cyst-form Giardia can
 Symptoms and Diagnosis 5

produce misleading results since the number of infecting organisms can

vary greatly during an infection. For this reason, antibody-based tests are
better at diagnosing Giardia. Stool antigen detection assays use antibod-
ies to test feces for the presence of Giardia proteins, such as the Giardia
lamblia–specific antigen 65 (GSA 65) protein. To determine Giardia sub-
type, molecular DNA tests are required to distinguish variable regions of
the parasite’s genome.
 Index
ACE, 14 future prospects, 23–24
Amebiasis, 2 symptoms and diagnosis of, 1–3
Ampicillin, 20 treatments and therapies for, 19–20
Anaerobic parasite, 9
Antimicrobial peptides, 18 E. dispar, 11
Azithromycin, 19 Encystation, 16
Endemic, definition of, x
Bacterial flora, xv Entamoeba histolytica, 2, 11
Blood-borne shigellosis, 1 Epidemics of disease, ix
Epithelial cells, xv
Cathepsin B-like proteases, 17 Exotoxins, xii
Cellular membrane, xii Extracellular matrix, xiii
CFTR. See Cystic fibrosis
transmembrane conductance Fecal-oral transmission, ix
regulator 58-kDa protein, 18
Chemokines, xii 5-nitroimidazole, 22
Chime, xiv Free oxygen radicals, 19
Chloramphenicol, 20
Cholera Gastroenteritis, ix
causes and contributing factors of, Genome, xi
11–15 Giardia, 4
conclusion, 25 Giardia intestinalis, 15
future prospects, 23–24 Giardia lamblia–specific antigen 65
symptoms and diagnosis of, 3–4 (GSA 65) protein, 5
treatments and therapies for, 20–21 Giardiasis
Ciprofloxacin, 19 causes and contributing factors of,
Cotrimoxazole, 20 15–18
Crystal VC dipstick, 4 conclusion, 25
CTXφ bacteriophage, 13 future prospects, 23–24
Cystic fibrosis transmembrane symptoms and diagnosis of, 4–5
conductance regulator treatments and therapies for, 22
(CFTR), 13 Giardins, 17
Cytokines, xii Global Task Force on Cholera
Control, 3
Diphenoxylate, 19 Globotriasylceramide (Gb3), 8
DNA, xi
Doxycycline, 21 Hemolysins function, 14
Dysentery Human intestine and diarrhea,
causes and contributing factors of, xiii–xvi
7–11
conclusion, 25 Infectious intestinal disease, x–xiii
36 INDEX

Lopreamide, 19 Ribosylation, xiii

RNA, xi
Malnutrition, 13
Metronidazole, 22, 19 S. boydii, 7
Microbiota, xv–xvi S. dysenteriae, 7
Musca domestica, 8 S. flexneri, 7
Mutations, xi S. sonnei, 7
Shiga toxin (Stx), 8
Naladixic acid, 20 Shigella, 1
National Antibiotic Resistance Shigellosis, 1
Monitoring System Stool antigen detection assays, 5
(NARMS), 20, 24 Superantigens, xii
Nitazoxanide, 22
TcpP toxin, 14
O antigen, 3–4 Tetracycline resistance, 20
Oral rehydration solution (ORS), 20 Tinidazole, 22
ORS. See Oral rehydration solution Treatment Center of the International
Osmolarity, xiv Center for Diarrheal Disease
Outbreaks of disease, ix Research, 20
Trimethoprim-sulfamethoxazole
Pandemic, definition of, x (Sxt), 20
Pathogen, xi Trophozoites, 9, 16
Pepto-Bismol, 19
PFDR. See Puryvate::Ferredoxin V. cholerae O139, 11
oxidoreductase Variant surface proteins (VSP), 17
Pilus toxins, 14 Vibrio cholera, 3
Proteins, xi Virulence factors, xii
Protozoa, ix VSP. See Variant surface proteins
Puryvate::Ferredoxin oxidoreductase
(PFDR), 22 WC/rBS vaccine, 21

Receptors, xiii Zona occludens toxin (ZOT), 14

Ribosomal RNA (rRNA), 9
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