Sei sulla pagina 1di 25

Infectious Human Diseases of the Intestine

Infectious Human Diseases of the Intestine

Mary E. Miller

Infectious Human Diseases of the Intestine Mary E. Miller

Infectious Human Diseases of the Intestine

Copyright © Momentum Press ® , LLC, 2019.

All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means— electronic, mechanical, photocopy, recording, or any other except for brief quotations, not to exceed 250 words, without the prior permission of the publisher.

First published in 2019 by Momentum Press ® , LLC 222 East 46th Street, New York, NY 10017

ISBN-13: 978-1-94474-987-3 (paperback) ISBN-13: 978-1-94474-988-0 (e-book)

Momentum Press Human Diseases and Conditions Collection

Cover and interior design by S4Carlisle Publishing Services Private Ltd., Chennai, India

First edition: 2019

10 9 8 7 6 5 4 3 2 1

Printed in the United States of America.


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.


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




Chapter 1

Symptoms and Diagnosis


Chapter 2

Causes and Contributing Factors


Chapter 3

Treatment and Therapy


Chapter 4

Future Prospects








About the Author





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



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



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



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



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



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.



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



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.


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 dysentery, 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



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



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



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 B 12 . 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



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.


ACE, 14 Amebiasis, 2 Ampicillin, 20 Anaerobic parasite, 9 Antimicrobial peptides, 18 Azithromycin, 19

Bacterial flora, xv Blood-borne shigellosis, 1

Cathepsin B-like proteases, 17 Cellular membrane, xii CFTR. See Cystic fibrosis transmembrane conductance regulator Chemokines, xii Chime, xiv Chloramphenicol, 20 Cholera causes and contributing factors of,


conclusion, 25 future prospects, 23–24 symptoms and diagnosis of, 3–4 treatments and therapies for, 20–21 Ciprofloxacin, 19 Cotrimoxazole, 20 Crystal VC dipstick, 4 CTXφ bacteriophage, 13 Cystic fibrosis transmembrane conductance regulator (CFTR), 13 Cytokines, xii

Diphenoxylate, 19 DNA, xi Doxycycline, 21 Dysentery causes and contributing factors of,


future prospects, 23–24 symptoms and diagnosis of, 1–3 treatments and therapies for, 19–20

E. dispar, 11 Encystation, 16 Endemic, definition of, x Entamoeba histolytica, 2, 11 Epidemics of disease, ix Epithelial cells, xv Exotoxins, xii Extracellular matrix, xiii

Fecal-oral transmission, ix 58-kDa protein, 18 5-nitroimidazole, 22 Free oxygen radicals, 19

Gastroenteritis, ix Genome, xi Giardia, 4 Giardia intestinalis, 15 Giardia lamblia–specific antigen 65 (GSA 65) protein, 5 Giardiasis causes and contributing factors of,


conclusion, 25 future prospects, 23–24 symptoms and diagnosis of, 4–5 treatments and therapies for, 22 Giardins, 17 Global Task Force on Cholera Control, 3 Globotriasylceramide (Gb3), 8

Hemolysins function, 14 Human intestine and diarrhea, xiii–xvi



Lopreamide, 19

Ribosylation, xiii

Malnutrition, 13

RNA, xi

Metronidazole, 22, 19


boydii, 7

Microbiota, xv–xvi


dysenteriae, 7

Musca domestica, 8

S. flexneri, 7

Mutations, xi


sonnei, 7

Naladixic acid, 20 National Antibiotic Resistance Monitoring System (NARMS), 20, 24 Nitazoxanide, 22

O antigen, 3–4 Oral rehydration solution (ORS), 20 ORS. See Oral rehydration solution Osmolarity, xiv Outbreaks of disease, ix

Pandemic, definition of, x Pathogen, xi Pepto-Bismol, 19 PFDR. See Puryvate::Ferredoxin oxidoreductase Pilus toxins, 14 Proteins, xi Protozoa, ix Puryvate::Ferredoxin oxidoreductase (PFDR), 22

Receptors, xiii Ribosomal RNA (rRNA), 9

Shiga toxin (Stx), 8 Shigella, 1 Shigellosis, 1 Stool antigen detection assays, 5 Superantigens, xii

TcpP toxin, 14 Tetracycline resistance, 20 Tinidazole, 22 Treatment Center of the International Center for Diarrheal Disease Research, 20 Trimethoprim-sulfamethoxazole (Sxt), 20 Trophozoites, 9, 16

V. cholerae O139, 11

Variant surface proteins (VSP), 17 Vibrio cholera, 3 Virulence factors, xii VSP. See Variant surface proteins

WC/rBS vaccine, 21

Zona occludens toxin (ZOT), 14


A. Malcolm Campbell, Editor

Hereditary Blindness and Deafness: The Race for Sight and Sound by Todd T. Eckdahl

Genetic Diseases or Conditions: Cystic Fibrosis, The Salty Kiss by Todd T. Eckdahl

Gradual Loss of Mental Capacity from Alzheimer’s by Mary E. Miller

Hemophilia: The Royal Disease by Todd T. Eckdahl

Sickle Cell Disease: The Evil Spirit of Misshapen Hemoglobin by Todd T. Eckdahl

Auto-Immunity Attacks the Body by Mary E. Miller

Huntington’s Disease: The Singer Must Dance by Todd T. Eckahl

Nerve Disease ALS and Gradual Loss of Muscle Function: Amytrophic Lateral Sclerosis by Mary E. Miller

Infectious Human Diseases by Mary E. Miller

Breast Cancer: Medical Treatment, Side Effects, and Complementary Therapies by K.V. Ramani, Hemalatha Ramani, B.S. Ajaikumar, and Riri G. Trivedi

Acquired Immunodeficiency Syndrome (AIDS) Caused by HIV by Mary E. Miller

Down Syndrome: One Smart Cookie by Todd T. Eckahl

Diseases Spread by Insects or Ticks by Mary E. Miller

Autism Spectrum Disorder: He Prefers to Play Alone by Todd T. Eckahl

Cancer by Mary E. Miller

Muscular Dystrophy: I’m Grateful I’ve Proved Them Wrong by Todd T. Eckahl

Diseases Caused by Dietary Problems by Mary E. Miller

Momentum Press offers over 30 collections including Aerospace, Biomedical, Civil, Environmental, Nanomaterials, Geotechnical, and many others. We are a leading book publisher in the field of engineering, mathematics, health, and applied sciences.

Announcing Digital Content Crafted by Librarians

Concise e-books business students need for classroom and research

Momentum Press offers digital content as authoritative treatments of advanced engineering topics by leaders in their field. Hosted on ebrary, MP provides practitioners, researchers, faculty, and students in engineering, science, and industry with innovative electronic content in sensors and controls engineering, advanced energy engineering, manufacturing, and materials science.

Momentum Press offers library-friendly terms:

perpetual access for a one-time fee

no subscriptions or access fees required

unlimited concurrent usage permitted

downloadable PDFs provided

free MARC records included

free trials

The Momentum Press digital library is very affordable, with no obligation to buy in future years.

For more information, please visit or to set up a trial in the US, please contact