Infectious Human

Diseases
Infectious Human
Diseases
Bacteria and Viruses

Mary E. Miller
Infectious Human Diseases: Bacteria and Viruses
Copyright Momentum Press, LLC, 2017.

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First published in 2017 by

Momentum Press, LLC
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www.momentumpress.net

ISBN-13: 978-1-94474-983-5 (print)

ISBN-13: 978-1-94474-984-2 (e-book)

Momentum Press Human Diseases and Conditions Collection

DOI: 10.5643/9781944749842

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 Abstract
Infectious diseases caused by bacteria and viruses exist in many forms
and significantly affect human health. The sources of infectious diseases
are vast, but in most cases arise from infectious microorganism such
as bacteria or viruses that are able to establish growth or replication in
humans, harming specific systems of the human body. This book intro-
duces the reader to the basic differences between bacteria and viruses,
particularly focusing on structures that contribute to the infectious prop-
erties of the microorganism. Chapters describe the cause, mode of trans-
mission, symptoms, and treatments of five important diseases, taking into
consideration the molecular interactions between host cells and infectious
agents. Specifically, examples of viral infection (Influenza caused by the
Influenza virus and hemorrhagic fever caused by the Ebola virus) and spe-
cific examples of bacterial infections (salmonellosis caused by Salmonella,
gastrointestinal disease caused by Shiga-like toxin E. coli, and tuberculosis
caused by Mycobacterium tuberculosis) are discussed in each chapter. The
book ends with some future work related to treatment of these critical
infectious diseases, noting the importance of drug resistance of infectious
agents in treatment regimens.

Keywords
bacteria, Ebola, Ebola virus disease, EVD, Escherichia coli. flu, Influenza,
MDR, Salmonella, Salmonellosis, Shiga-like toxin, STEC, TB, Tubercu-
losis, virus
 Contents
List of Figures and Tables........................................................................ix
Acknowledgments....................................................................................xi
Introduction.........................................................................................xiii
Chapter 1 Symptoms and Diagnosis................................................. 1
Chapter 2 Causes and Contributing Factors...................................... 7
Chapter 3 Treatment and Therapy.................................................. 19
Chapter 4 Future Prospects............................................................. 25
Bibliography..........................................................................................29
Glossary.............................................................................................. 33
About the Author................................................................................ 37
Index....................................................................................................39
 List of Figures and Tables

Figure A The lipid bilayer of the cellular membrane

andpeptidoglycan of the cell wall.................................... xvi
Figure 2.1 Influenza virus8
Figure 2.2 The Ebola virus12
Figure 2.3 S. typhimurium14
Figure 2.4 E. coli16
Figure 2.5 M. tuberculosis18

TABLE
Table 4.1 Examples of drugs that target various steps of
influenza infection...........................................................26
 Acknowledgments

I would like to thank Malcolm Campbell for the opportunity to make

contributions to this book series. His forward approach to science and
scientific pedagogy is inspiring. I thank my husband David and daughter
Mallory for their patience and support of these efforts. I am fortunate to
work at Rhodes College, which has supported my professional and intel-
lectual development. I take pride that I have worked with outstanding
students, and thank them for inspiring my passion for science education.
My outstanding mentors, colleagues, and collaborators have made it pos-
sible to carry out rigorous research and forward high-impact educational
practices. Specifically, I thank Mitch Smith, Dan Engel, Jeff Becker, Fred
Cross, and Pam Hanson, whose advice and influence have shaped my
professional success. The editorial staff at Momentum Press have been
supportive and kind, and I appreciate their work in the production of
this book. I hope that some aspect of this work is helpful for individuals
working to better understand or manage these devastating diseases.
 Introduction

Infectious diseases have shaped human evolution, society, and culture

for centuries. Our understanding of diseases and the microorganisms
that cause them is a critical aspect to human social interactions and
survival. Highly pathogenic microorganisms clearly impact society since
they can cause deadly diseases in humans, and even less pathogenic
infections impact our ability to work, play, and care for our families. In
some parts of the world, treatments are taken for granted. In other parts
of the world, treatable diseases are lethal because of ethno-cultural and
economic inaccessibility of medicine. Some infectious diseases are incur-
able, and this can generate fear and confusion in times of disease out-
break. In 2013, the Centers for Disease Control and Prevention (CDC)
identified three critical public health practices for treating and control-
ling infectious diseases: strong public health foundations; interventions;
and health policies. No matter the type of infectious disease or causative
agent, these basic practices can reduce disease occurrence and increase
survivability. The causative agents of infectious diseases are almost always
microorganismsorganisms too small to be seen without magnification.
Each causative agent has its own mechanism of spreading, symptoms,
approaches to control disease progression, and availability of treatment.
Sometimes standard treatments exist, but availability is uncertain. Unfor-
tunately, standard treatments can lose their efficacy in the face of evolving
microorganisms. For some infections, there are no treatments or cures.
This book highlights five infectious diseases that significantly impact
human health and exhibit different modes of transmission, progression of
symptoms, and treatment regimes.
Infectious diseases can be spread by direct transmission from one
person to another, or by human contact with animals. Transmission can
occur through the air via pathogen-containing small droplets after coughs
or sneezes, through touching a surface that has been contaminated with
microorganisms, or through bodily fluids such as blood, mucous, or
xiv INTRODUCTION

semen from an infected person. Although some infections are caused by

eukaryotes, most infectious diseases are caused by bacteria and viruses.
Bacteria are cellular in nature. Cells can vary widely in size and shape.
Human cells work together to comprise the tissues and organs of our
bodies. A bacterial cell alone conducts all of the essential functions of
lifegrowth, metabolism, reproduction, and interactions with its envi-
ronment. Most bacteria are not harmful to humans, and many are benefi-
cial, such as the microbiota bacteria that normally live in the human gut
and assist in our digestive processes. When a bacterium gains access to a
part of the human body where it isnt usually found, it can reproduce and
interfere with bodily functions to the point of causing a human disease. A
virus is not a cell, and typically is not considered alive because it cannot
grow, reproduce, or metabolize on its own. Viruses survive by using a host
cell to perform these functions that often harm or kill the host cell.
When a virus enters a host cell that is part of the human body, it has the
potential to disrupt bodily functions and cause a particular disease. A virus
is able to infect only a subset of cell types, which explains why a given
virus will cause a particular type of disease. Similarly, not all bacterial
species can grow in all parts of the human body, so only certain species of
bacteria will cause a corresponding disease. This specificity of infection,
the ability of bacteria or viruses to infect specific human cells or tissues,
relates to the structure of the microorganism, its host cell, and bacterial or
viral mechanisms of reproduction.

Bacteria and Viruses

Bacteria are single-celled organisms that are able to carry out all of the
critical functions of life. Most bacteria are smaller in size than human
cells and simpler in cellular structure. For example, human cells house
their genome in a structure called the nucleus, while many bacteria lack
this structure and maintain their genome more loosely inside the cell.
Despite these organizational differences, both bacteria and human cells
use their genome to drive the synthesis of gene products critical for cellular
survival. In bacteria, the genome is composed of DNA and encodes genes
that are used to direct the synthesis of gene products, including proteins.
 INTRODUCTION
xv

The process by which a gene is used to encode a protein involves an

intermediary step where the DNA is used to produce a similar but distinct
molecule called RNA. The RNA code is used to produce proteins that
carry out critical functions in the cell. Proteins are composed of amino
acid chains, and each amino acid has chemical and structural proper-
ties that determine the proteins overall shape and thus its function. The
structure of a protein dictates how it interacts with other proteins, and
what it can do. For example, a protein with one shape might work deep
within a cell and be involved in turning on and off genes. Other proteins,
encoded by different genes, will take up residence at the surface of a cell
and bind (physically interact) with surface components of host tissues or
cells during an infection. Other genes encode protein enzymes that work
to produce carbohydrate (sugar) or lipid (fat) polymers used by the cell
for a variety of functions. The basic mechanism of gene expression, where
DNA encodes RNA that drives protein synthesis, is highly conserved and
is present in the cells of all species. Viruses are usually composed of the
viral genome and a protein covering the genome. Viruses are noncellular
since they are unable to express gene products on their own and must use
their host cellular machinery to produce proteins needed for metabolism
and viral replication.
Bacteria lack most or all membrane-bound organelles that compart-
mentalize cellular processes in the way that is observed inside human
cells. Cellular membranes are composed of lipids, embedded or a ssociated
proteins, and carbohydrates. In a bacterial cell, the membrane that e ncases
the cell is composed of two lipid layers (one lipid bilayer, FigureA)
and is called the cellular plasma membrane. Bacteria have a cellular
plasma membrane that provides a protective barrier between the inside
and outside of the cell, but most bacterial species lack internal membrane
systems that compartmentalize processes. Given the harsh environmental
changes that bacteria must survive, it is not surprising that covering the
cellular plasma membrane is an additional protective layer called the cell
wall or cell envelope that is essential for bacterial survival. The cell wall/
cell envelope provides further mechanical protection for the bacteria and
gives the bacteria a characteristic shape, such as a sphere or a rod. The
composition and layering of materials outside of the plasma membrane
xvi INTRODUCTION

can vary among different species of bacteria. Many species have a pepti-
doglycan layer composed of a polymer of two alternating sugars called
N-acetylglucosamine (NAG) and N-acetylmuramic acid (NAM). Short
chains of three to five amino acids are attached to the N-acetylmuramic
acid. These short amino acid chains can be connected together or cross-
linked (FigureA). Crosslinks between peptidoglycans are the targets for
a type of antibacterial medicine called beta-lactam antibiotics, such as
penicillin. The strength of the crosslinks between peptidoglycans can be
distinguished using staining techniques, and this allows bacteria to be
classified as either Gram-positive (more crosslinks, for example bacteria
of the genus Staphylococcus) or Gram-negative (fewer crosslinks, for
example bacteria of the genus Salmonella). Some types of bacteria do
not have peptidoglycan cell wall/envelope and thus are not susceptible to
beta-lactam antibiotics.

Figure A The lipid bilayer of the cellular membrane and

peptidoglycan of the cell wall.
A schematic of the cellular membrane and cell wall of a Gram-positive bacteria showing
the lipid bilayer and the peptidoglycan crosslinks between amino acid chains (small circles)
attached to NAM/NAG carbohydrates (large circles). By Bradleyhintze (own work) [CC0],
viaWikimedia Commons; https://upload.wikimedia.org/wikipedia/commons/2/2f/Peptidoglycan-
membrane.png.
 INTRODUCTION
xvii

When peptidoglycans are present, the amount and composition

creates a thicker peptidoglycan structure in Gram-positive bacteria and
a thinner structure in Gram-negative bacteria. In Gram-positive bacteria,
the thick peptidoglycan layer is usually exposed to the environment.
Molecules that are attached to the peptidoglycans are displayed outside the
surface of the bacteria, such as lipoteichoic acids that can trigger a strong
immune response in humans, resulting in toxicity in an infected person.
Because Gram-negative bacteria generally lack exposed lipoteichoic acid,
they are targeted less by the human immune system and therefore are
more prone to survive in the human body. While both Gram-positive and
Gram-negative bacteria have a peptidoglycan layer outside of the plasma
membrane, Gram-negative bacteria have a second lipid bilayer membrane
outside of the thinner peptidoglycan layer called the outer membrane.
This creates the periplasmic space in Gram-negative bacteria, which
contains the peptidoglycan layer and spans that region between the
plasma membrane and the outer membrane. In the case of Gram-negative
bacteria, molecules including proteins and carbohydrates embedded in
this outer membrane will be presented at the surface of the bacteria. For
example, lipopolysaccharides (LPS) are found almost exclusively on
the surface of Gram-negative bacteria. LPS play a critical role in human
disease, because they are endotoxins.
Other critical surface structures for bacteria include flagella, pili, and
capsules. Flagella are highly organized structures composed of a basal body
and a filament. The basal body is embedded in the cellular plasma membrane,
firmly anchoring the flagella to the surface of the bacteria. The filament is a
cylindrical structure, made of flagellin proteins, that extends from the surface
of the bacteria. The composition, number, and arrangement of filaments in
the flagella are used to identify different types of bacteria. Bacterial flagella
spin rapidly to generate cell motility from a propeller-like propulsion force.
Pili are also made of protein but are less complex in their structure and
are more likely used by the bacteria to physically attach to other bacteria
or to surfaces in the environment. Capsules are secreted by some bacteria
to create a protective layer, composed primarily of carbohydrates, around
the outside of the bacteria, though they are not thought to be essential
for viability of the bacteria. Capsules usually allow Gram-positive and
Gram-negative bacteria to evade some aspects of the human immune system.
xviii INTRODUCTION

Compared to bacteria, most viruses are simpler in structure, though the

diversity of virus is impressively large. Viruses are obligate intracellular
parasitic organisms, and infection often results in the death of the host
cell. Viruses always contain a genome made of DNA or RNA and a
protein capsid that surrounds and packages the genome. Some viruses
also have a cell membrane surrounding them, usually a modified version
of the host cell membrane obtained as the virus exits the host cell. Viruses
infect and redirect the metabolism of their specific hosts such as bacterial
or human cells. Viruses are classified based on their shape, their chemi-
cal composition, and their mode of replication. There are approximately
21 virus families that can infect humans, and these viruses represent a
small percentage of the many viruses that exist in nature to infect cells
from a very diverse catalog of host species. Among the many human
viruses, some are helicalwhere capsid proteins coat the genome of the
virus, and as a unit this creates a spiral shapeand some are icosahedral,
where capsid consists of a protein polyhedron of 20 equilateral sides.
Viral genomes can exist as either RNA or DNA and be single stranded
(ss), so that there is a single chain of nucleotides, or double stranded (ds),
where two chains of nucleotides pair together. Viral genomes can be of
one continuous piece or several linear or circular molecules. When the
virus has an RNA genome that can be used directly to make a protein, it is
called a positive-sense or plus-sense RNA virus. If the RNA must be used
to make a complementary strand of RNA before it can be used as a tem-
plate for protein synthesis, it is called an antisense, or negative-sense, or
minus-sense RNA virus. Viruses that carry DNA as the genetic material
are referred to as DNA viruses. DNA viruses can also be ss or ds and will
be converted to RNA using host proteins. In the case where the RNA
genome must be converted to DNA as a part of viral replication, the
virus is classified as a retrovirus. In all cases, the viral genome is used as
a template for the synthesis of additional viral genomes and viral pro-
teins using the same protein enzymes that the host cell uses to make host
genomes and proteins. Once made, the viral genome associates with
the viral protein capsid creating a new virus, which can leave the host
cell to infect another cell. The mode of viral infection may result in an
enveloped virus, where the virus modifies and carries with it a segment of
the host cell membrane when it leaves. The mode of disease transmission
 INTRODUCTION
xix

between potential host organisms is determined by viral morphology and

replication mechanism. For example, an enveloped virus will not survive
for extended periods of time outside bodily fluids and the ability of a virus
to physically attach and enter a host cell will limit the repertoire of host
cell types.
Transmission of infectious disease can occur through many routes, but
infection requires introduction and reproduction of the microorganism
in the human body. In this book, we will describe five types of infections
that impact human health. The influenza virus causes the flu, and the
Ebola virus causes hemorrhagic fever. Shiga-like toxin Escherichia coli
causes gastrointestinal infections, Salmonella causes food poisoning, and
Mycobacterium tuberculosis causes tuberculosis infections. For each
example, the symptoms, diagnosis, and mode of transmission of infection
will be described in the context of disease prevention and progression.
Available treatments that target the bacteria or virus will be described,
including complications of drug resistance in certain treatment regimens.
 CHAPTER 1

Symptoms and Diagnosis

Symptoms and Diagnosis of the Flu

Influenza, or the flu, is a contagious respiratory illness caused by an
influenza virus infection. In patients, infection causes symptoms that range
from mild to severe illness, and at times it can result in hospitalization
or death. Flu can onset rapidly, between 1 and 4 days after exposure to
another person with the flu. Symptoms include fever, aches, chills, and
fatigue with most cases also showing sneezing, stuffy nose, sore throat,
chest discomfort, and headache. At times, young children also experience
vomiting and diarrhea. Flu symptoms can have some common features
to a cold that shows a more gradual onset of symptoms, and colds less
frequently show the symptoms of fever and headache.
The Centers for Disease Control and Prevention (CDC) track influ-
enza that usually peaks in the United States during the fall and winter,
most often during February. The CDC monitors where, when, subtype of
virus, hospitalizations, and death causes by influenza. The CDC coordi-
nates with the World Health Organization (WHO) to determine changes
in influenza virus subtype that might influence vaccine components. This
effort currently involves 112 countries and 6 WHO Collaborating Cen-
ters. In 2016, the CDC collected data from 350 sites in 60 countries
and found that approximately 10 percent of all hospitalizations due to
respiratory issues in children younger than 18 years were due to influenza
infections, half of which occurred in Africa and Southeast Asia. Influenza
is a serious healthcare concern for children all over the world.
2 INFECTIOUS HUMAN DISEASES

Symptoms and Diagnosis of Ebola Virus Disease

Ebola virus disease (EVD) is a hemorrhagic fever in humans caused
by an Ebola virus infection. Initial symptoms include fever, severe
headache, muscle pain, weakness, fatigue, diarrhea, vomiting, stomach
pain, unexplained bleeding or bruising, and sore throat. As the disease
progresses, symptoms can include vomiting, diarrhea, rash, impaired kid-
ney and liver function, internal and external bleeding, low blood cell and
platelet counts, and elevated liver enzymes. It takes between 1 and 21days
for symptoms to appear after a patient is exposed to Ebola virus, though
the average is 8 to 10 days. Ebola virus is considered one of the most viru-
lent and pathogenic viruses in the world, thought to be anywhere from
40to 90 percent lethal during outbreaks.
Symptoms of Ebola can be confused with symptoms of malaria,
typhoid fever, and meningitis. Confirmation of Ebola includes detecting
the presence of Ebola proteins, host antibodies against Ebola virus, Ebola
virus RNA, Ebola virus particles in the patients body, or Ebola virus
grown in a laboratory from patient body samples. Ebola detection is com-
plicated by the fact that patient samples could spread disease, so sample
collection, transportation, and handling require extreme caution. No test
currently exists that can detect the presence of Ebola prior to the onset of
symptoms. Recently, the United States Food and Drug Administration
(FDA) has granted emergency use to the Ebola Virus Triage Test (Idylla
EBOV Test), which is capable of detecting in about 100 minutes Ebola
Zaire RNA with minimal sample handling after collection and does not
require cold storage.
When diagnosed in the United States, physicians are required to
report the incident to the National Notifiable Disease Surveillance
System (NNDSS). Patients can also be reported as a person under inves-
tigation (PUI) when the symptoms of EVD are present and the patient
has potentially come in contact with another person with EVD within
the past 21 days. Individuals at higher risk include those with direct
exposure to bodily fluids or mucus membranes from EVD patients, for
example when caring for a patient. Intermediate risk might include close
contact, defined as within three feet, of an infected EVD patient for long
periods of time. Lower risk contact might include shaking a patients hand.
 Symptoms and Diagnosis 3

When caring for an Ebola patient, physical contact is safe with the aid of
personal protective equipment such as gloves, goggles, and masks.

Symptoms and Diagnosis of Salmonellosis

Salmonellosis is an acute gastroenteritis caused by bacteria of the genus
Salmonella and is estimated to account for $365 million in direct medical
costs each year in the United States. Salmonellosis causes approximately
1.2 million foodborne illnesses in the United States per year, 19,000 hos-
pital stays, and 380 deaths. Symptoms include fever, abdominal pain,
diarrhea, nausea, and vomiting. Some individuals develop pain in joints
called reactive arthritis. If reactive arthritis develops, then additional
symptoms such as eye irritation and painful urination may occur. Most
symptoms can occur between 6 and 72 hours after exposure, usually
developing between 12 and 36 hours. Symptoms can last between 4
and 7days. In about 8 percent of laboratory confirmed cases of Salmo-
nella infections, the infection can become invasive, meaning the bacte-
ria spread throughout the body from the gastrointestinal tract. Invasive
infections can become life threatening, though usually only for the very
young, very old, or individuals with compromised immune systems.
Invasive infections can spread to the blood (bacteremia), membranes lin-
ing the brain and spinal cord (meningitis), bone (osteomyelitis), or joint
(septic arthritis). On rare occasions, a type of Salmonella infection can
cause typhoid fever, where the patient experiences symptoms approxi-
mately 1to 2 weeks after eating contaminated food, and symptoms can
last from 3days to 2 months. Symptoms in this more serious case include
fever of 104C, weakness, abdominal pain, coughing, nosebleeds, delirium,
and enlarged organs, which can progress to very serious stages and at
times result in death.
Salmonella diagnosis is confirmed by Salmonella bacteria being
grown from patient samples in a diagnostic laboratory. Once confirmed,
Salmonella isolated from patient samples are sent to public health labo-
ratories for serotyping and DNA sequence analysis. The public health
laboratory would report their findings to the CDC Enteric Disease
Surveillance System. If the serotype or DNA sequence analysis reveals
an atypical type of Salmonella, then samples would be sent to a CDC
4 INFECTIOUS HUMAN DISEASES

National Salmonella Reference Laboratory for further study. This system

functions as part of the NNDSS, which allows tracking of Salmonella
outbreaks and helps to inform national food safety policies in the United
States. Other examples of surveillance networks include the Laboratory-
based Enteric Disease Surveillance (LEDS), which collects information
to assess geographic differences and long-term trends of serotypes of
Salmonella and other enteric microbes. Detection of short-term outbreaks
is facilitated through PulseNet, a network of laboratories in the United
States that conduct DNA analysis of microbes to determine if common
causes can be identified for outbreaks throughout the nation. Antimicro-
bial resistant forms of microbes that cause foodborne illnesses, including
Salmonella, are tracked through the National Antimicrobial Resistance
Monitoring SystemEnteric Bacteria (NARMS).

Symptoms and Diagnosis of Shiga Toxin-Producing

Escherichia coli (STEC) Infection
Escherichia coli bacteria are part of the normal microbiota that supports
our digestive system. However, certain subtypes of E. coli can cause
diseases such as urinary tract infections, respiratory illnesses, pneumonia,
and gastrointestinal disease. Pathogenic E. coli bacteria are described as
pathotypes depending on the type of diseases they cause, the mecha-
nism by which the disease is caused, and the level of virulence, or dam-
age, caused by the infection. Recently, E. coli has been associated with
outbreaks of virulent diarrheagenic disease in humans, specifically caused
by a type of E. coli that produces a specific toxin called Shiga-like toxin
(Shiga-like toxin E. coli, or STEC). STEC is a leading cause of pathogenic
bacterial enteric infections and produces severe stomach cramping, diar-
rhea, vomiting, fever, and fatigue. Infections can vary in intensity, with
progress ranging from mild to severe. Symptoms usually present about
3 to 4 days after exposure but can range from 1 to 10 days. In most
cases, symptoms resolve naturally in 3 to 8 days. In approximately 5 to
10 percent of STEC infections, the patient experiences complications
and develop hemolytic uremic syndrome (HUS). HUS usually occurs
about 7 days after symptoms initially present, usually as diarrhea symp-
toms decrease. Of those patients who develop HUS, 3 to 5 percent die
 Symptoms and Diagnosis 5

due to renal (kidney) failure. Symptoms of HUS include blood platelet

deficiency causing bleeding and slow clot formation (thrombocytopenia),
loss of red blood cells (hemolytic anemia), kidney failure, frequent urina-
tion, fatigue, and paleness, especially in the lower eyelids. Very young
children and the elderly are most at risk for the more severe symptoms,
and HUS is the most common cause of acute renal failure in children.
Diagnosis of STEC involves laboratory testing of stool (feces) sam-
ples from patients to detect the presence of STEC of specific subtypes.
Laboratory tests to identify STEC in patient samples can include growing
STEC in the diagnostic laboratory from patient samples. This requires
specific growth conditions and might not identify all pathotypes of STEC.
More recently, laboratory tests that can identify proteins present on the
surface of the STEC, DNA sequences of the STEC, or the Shiga-like
toxin produce a more rapid identification of STEC. Recommendations
for diagnosis of STEC were developed by the CDC in 2006 and were
recently updated to recommend tests that include more pathotypes of
STEC. Early diagnosis of STEC usually leads to better patient outcomes.
Antibiotic treatment of STEC can cause serious complications, so under-
standing that symptoms are due to STEC, rather than another infectious
agent, is important before treating the disease.

Symptoms and Diagnosis of Tuberculosis

Tuberculosis (TB) is a serious infectious disease of the lungs. TB typically
leads to nodule or tubercle formation in the infected tissue. Symptoms
of TB include a cough lasting at least 3 weekscough that produces
sputum with blood, chest pain, weakness, weight loss, fever, and night
sweats. TB can infect other parts of the body, too. TB infection of the
kidney can cause bloody urine, whereas infection of the spine can cause
back pain. Symptoms can be mild initially, and if left undiagnosed
for months, the bacteria might spread to other people. TB can also be
latent, so that individuals carry the bacteria but do not show symptoms;
however, asymptomatic individuals cannot spread the disease.
Diagnosis of TB incorporates an understanding of the medical history
of the patient and physical examination to determine if TB symptoms are
present. Laboratory tests, such as the TB skin test or TB blood tests, are
6 INFECTIOUS HUMAN DISEASES

used to determine if a person is infected. Pulmonary TB can be detected by

chest X-rays. To confirm these results, the TB bacteria would be identified
in patient samples. Historically, identification was made by observation
through microscopic inspection of a patients sputum with a 50 percent
success rate in detecting TB infections in patients. More recent diagnostic
tests of patient sputum include GeneXpert MTB/RIF, which detects in
less than 2 hours bacterial DNA that causes TB and that codes for rifam-
picin antibiotic resistance. Patients can also be tested for the presence of
interferon-gamma, a molecule by immune cells secreted in response to
bacterial or viral infections. Blood tests called interferon-gamma release
assays can detect elevated levels of interferon-gamma, which would sup-
port a TB diagnosis in conjunction with additional supporting evidence.
 Index
Abstinence, 13 Candidate medications, 25
Acute gastroenteritis, 14 Capsid, xvi, 12
Airborne virus particles, 10 Capsules, xv
Amantadine, 20 Cattle, 15
Amino acid, xiii, 17 Cefotaxime, 21
Amoxicillin, 21 Ceftriaxone, 21
Ampicillin, 21 Cells
Animal carriers, identifying, 27 envelope, xiii
Animal-to-person transmission, of infected, 10
Ebola virus, 13 of liver, 12, 13
Antibacterial treatments, 27 membrane, 17
Antibiotic resistant, rise of, 22 wall synthesis, 21, 23
Antibiotics, 21 Cellular death, 17
treatments of, 22 Cellular membranes, xiii
use of, 22 and peptidoglycans, lipid bilayer
Antigenic shift, 7 of, xiv
Antigens, 7 Cellular plasma membrane, xiii, xv
Antimicrobial drugs, 22 Centers for Disease Control and
Antimicrobial resistant, 4 Prevention (CDC), xi,
Antisense RNA virus, xvi 1, 20, 22, 26
Antiviral drugs, 19 Chronic health issues, 11
Antiviral treatments, 27 Ciprofloxacin, 21
Arbidol, 25 Containment, 21
Arthritis Contaminated food, consumption of,
reactive, 3 14, 1516
septic, 3 Cough, 5
Avian flu viruses, 910 Criproflaxacin, 21
Avigen (favipiravir), 25 Cuevavirus, 11
Cytokines, 2627
Back pain, 5
Bacteremia, 3 DAS181 (Fludase), 25
Bacteria, xiixvii Dendritic cells, 13
released, 18 Diarrhea, 15
Bacterial transcription, 22 Diffusely adherent E. coli (DAEC), 15
Basal body, xv DNA, xiixiii, xvi
Beta-lactam antibiotics, xiv replication, 10
Bird flu, 8 sequence analysis, 34
Blood platelet deficiency, 5 Drugs
Blood vessels, leaking of, symptoms, 13 for influenza infection, 26
Bloody urine, 5 resistant, 27
Budding virus, 10 Dysentery disease, causative agent
Bundibugyo ebolavirus, 11 of, 16
40 INDEX

E. coli O104:H4, 17 managing, 20

E. coli O157:H7, 17 symptoms of, 1, 19
Ebola hemorrhagic fever. See Ebola therapy for, 1920
virus disease (EVD) treatments, 1920, 2526
Ebola virus, xvii, 2, 1114, 2627 vaccine, 20, 26
nonhuman reservoir of, 13 Fluoroquinolone, 23
patients, 25 Folate metabolism, 21
Ebola virus disease (EVD), 27 Food and Drug Administration
causes and contributing factors, 1114 (FDA), 2, 19, 22, 25
detection of, 2 Food poisoning, xvii
symptoms and diagnosis of, 23 Food preparation, 21, 22
treatment and therapy for, 2021 Foodborne diseases, 15
Ebola Virus Triage Test (Idylla Foodborne pathogen, 14
EBOV Test), 2
Electrolyte balance, 22 Gastrointestinal disease, 4
Endocytosis, 10, 12, 16 Gastrointestinal infections, xvii
Endothelial cells, 13 Gb3. See Globotriaosylceramide
Endotoxins, xv Genes, xiixiii
Energy production, 23 GeneXpert MTB/RIF, 6
Enteric Disease Surveillance System, diagnostic test, 23
CDC, 3 Genome-wide sequencing approach, 26
Enteric infections, 4 Genome, xii
Enteroaggregative E. coli (EAEC), 15 protein-coated, 10
Enterobacteriaceae, 14 viral, xvi, 10, 7, 12
Enterohemorrhagic E. coli (EHEC). Globotriaosylceramide, 16
See Shiga-like toxin- Glycolipids, 16, 17
producing E Coli (STEC) Glycoproteins (GP), 12, 13, 16
Enteroinvasive E. coli (EIEC), 15 Gram-negative bacteria, xiv, xv, 14
Enteropathogenic E. coli (EPEC), 15 Gram-positive bacteria, xiv, xv
Enterotoxigenic E. coli (ETEC), 15 Granuloma, 18
Enveloped virus, xvixvii
Epithelial cells, 10 H antigen protein, 15, 17
of blood vessels, 12 H1N1 virus, 9, 20
Escherichia Coli, xvii, 1517, 27, 22, 45 H3N2 virus, 9, 20
Ethambutol, 22, 23 H5N1 virus, 9
Extensively drug resistant TB H5N2 virus, 9
(XDR-TB), 23 H5N8 virus, 9
Health issues, chronic, 11
Fatty acids, 17 Healthcare workers, 14
Favipiravir (Avigen), 25 Helical virus, xvi
Feces, 5 Hemagglutinin (HA), 78, 10
Filament, xv Hemolytic anemia, 5
Filoviridae virus, 11 Hemolytic uremic syndrome (HUS),
Flagella, xv, 15 4, 5, 22
Flu, xvii Hemorrhage, 13
causes and contributing factors Hemorrhagic fever, xvii
of, 711 Highly pathogenic avian influenza
complications of, 11 (HPAI), 9
diagnosis of, 1 HIV/AIDS, 17
 INDEX
41

Host cell, xii, 10, 1920 Metabolism, 10

immune system, 20 Microbiota bacteria, xii, 4
membrane, 10, 16 Microbiota genomes, 26
surface, 8 Milk, unpasteurized, 16
HPAI H5N1, 9 Minus-sense RNA virus. See Antisense
Human body, 21 RNA virus
Human cells, xii Monocytes, 13
Human genome, genetic variation Mucous membranes, 13
in, 26 Mycobacterium tuberculosis, xvii,
Human immune system, 7, 11, 17, 1718, 23, 27
2627 airborne transmission, spreads by, 17
Hydration, 20, 22 cell wall structure of, 17
Mycolic acid, 17, 23
Immune response, 20
Immune system, cells of, 12, 13 N-acetylneuraminic acid, 8
Inavir (laninamivir), 25 National Antimicrobial Resistance
Infection, 4 Monitoring System
avoiding, 20 (NARMS), 21
viral, 7, 13 National Notifiable Disease
Infectious diseases, causative agents Surveillance System
of, xi (NNDSS), 2, 4
Influenza A, 7, 20 National Salmonella Reference
subtypes of, 910 Laboratory, 4
Influenza B virus, 9, 20 Natural immunity, 20
Influenza C virus, 8, 20 Negative-sense RNA virus. See
Influenza D virus, 89 Antisense RNA virus
Influenza virus, xvii, 7, 8, 9, 10. See Neuraminidase (NA), 7, 9, 10
also Flu inhibitors, 19
Interferon-gamma, 6 Niemann-Pick C1 (NPC1) protein, 12
treatment, 26 Nodules, 18, 23
Interferons, 26, 27 Nonimmune cells, 13
Invasive infections, 3 Nontyphoidal Salmonella, 15
Isoniazid, 22, 23 Novel therapies and drugs, 27
Nucleus, xii
Laboratory-based Enteric Disease
Surveillance (LEDS), 4 O antigen protein, 15, 17
Laninamivir (Inavir), 25 Obligate intracellular parasitic
Lipopolysaccharides (LPS), xv, 15 organisms, xvi
Lipoteichoic acids, xv Oseltamivir (Tamaflu), 25
Livestock management, 22 Oseltamivir, 19
Low pathogenic avian influenza Oseltamivir-resistant influenza A
(LPAI), 9 virus, 27
Osteomyelitis, 3
M2 protein, 10, 20
Macrophage cells, 13, 17, 27 Pandemic, 9
Marburg Virus Disease (MVD), 12 Pathogens
Marburgvirus, 1112 novel, retooling current treatments
MDR-TB, 23 for, 25
Meningitis, 3 resistant, 27
42 INDEX

Pathotypes, 4 Salmonella typhimurium, 14, 15

Patient tracking, 13 Salmonellosis
Penicillin, xiv causes and contributing factors,
Peptidoglycan, 17 1415
layer, xivxv food preparation, 21
Peramivir (Rapivab), 19, 25 symptoms and diagnosis of, 34
Periplasmic space, xv treatment and therapy for, 21
Person-to-person transmission, of Septic arthritis, 3
Ebola virus, 13 Serotypes, 15, 17
Person under investigation (PUI), 2 Serotyping, 34
Phase II clinical trials, 25 Serovars, 15
Phase III clinical trials, 25 Shiga-like toxin, 4, 5, 1617, 22
Pili, xv Shiga-like toxin-producing E Coli
Plus-sense RNA virus, xvi (STEC)
Pneumonia, 4 causes and contributing factors,
Positive-sense RNA virus. See Plus- 1517
sense RNA virus food preparation, 22
Protein synthesis, 10, 16, 23, 25 swallowing, 15
Protein, xiii symptoms and diagnosis of, 45
viral, xvi, 10 treatment and therapy for, 22
Public health laboratories, 3 Shigella dysenteriae, 16
Pulmonary tuberculosis, 6, 18 Sialic acid, 10, 1920. See also
PulseNet, 4 N-acetylneuraminic acid
Pyrazinamide, 22, 23 Sputum, 6
Staphylococcus, xiv
Quarantine, 13 Stool, laboratory testing of, 5
Sudan ebolavirus, 11
Rapivab (peramivir), 19, 25 Sugar-modified lipids, 16
Relenza (zanamivir), 19, 25 Sugar polymer, 17
Renal failure, in children, 5 Super bug, 22
Replication mechanism, xvi
Resistance, 23 Tai Forest ebolavirus, 11
Resistant pathogens, 27 Tamaflu (v), 25
Respiratory illnesses, 4 Tamiflu, 19
Reston ebolavirus, 11 Thrombocytopenia, 5
Rifampicin-resistant tuberculosis (RR- Thymine, 21
TB), 23 Tissues, infected, 10
Rifampin, 22 Trachea, 8
RNA, xiii, xvi, 23, 25 Trimethoprim, 21
polymerase enzyme, 25 Tuberculosis (TB), 26
segment, 7 blood test, 56
rpoB gene, muatations in, 23 causes and contributing factors,
1718
S. bongori, 15 pulmonary, 6, 18
S. enterica, 15 pulmonary, 6
S. enteritidis, 14 skin test, 56
S. javiana, 14 symptoms and diagnosis of, 56
S. newport, 14 treatment and therapy for, 2223
Salmonella, 3, 14, 15, 21, 27 Typhoidal Salmonella, 15
 INDEX
43

Urinary tract infections, 4 engulfed, 10

Vacuole, 12
Vegetables, consumption of, 14
Verocytotoxin-producing E. coli
(VTEC). See Shiga-like toxin-
producing E Coli (STEC)
Verotoxins, 16
Vesicle formation, 16
Viralhost interactions, 26
Virulence, 4
Virus, 20
budding, 10
classification of, xvi
enveloped, xvixvii
helical, xvi
identification tools, 27
White blood cells, 13, 1718
World Health Organization (WHO),
1, 13, 20, 26
X-rays, chest, 6
Zaire ebolavirus, 11
Zanamivir (Relenza), 19, 25
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