Diseases That Are

Preventable by
Vaccination
Diseases That Are
Preventable by
Vaccination
Polio, Tetanus, Measles,
and Mumps

Mary E. Miller
Diseases That Are Preventable by Vaccination: Polio, Tetanus,
Measles, and Mumps
Copyright © Momentum Press®, LLC, 2020.

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 Abstract
Vaccinations provide an effective way to prevent fatal diseases or reduce
their symptoms. This book highlights four infectious diseases: polio,
­tetanus, measles, and mumps. These four diseases are very harmful to
human health and are difficult to treat after the infection because they are
caused by a toxin or pathogenic virus. In all four cases, the disease exhib-
its different modes of transmission and progression of symptoms, which
require unique treatment regimens. However, all cases can be prevented
by vaccinations administered prior to infection. This book summarizes
the symptoms and disease progression of all the four diseases and provides
information about the toxin or virus that causes each disease. The ability
to harness our immune system through vaccination is discussed in the
context of disease prevention. Minor and infrequent risks associated with
vaccination are also described, but the very dangerous misconception that
vaccines cause autism or other major illnesses is strongly refuted.

Keywords
polio; poliomyelitis; tetanus; lockjaw; virus; bacteria; mumps; measles;
Clostridium tetani; vaccine; vaccination
 Contents
Introduction.........................................................................................xiii

Chapter 1: Symptoms and Diagnosis......................................................1

Chapter 2: Causes and Contributing Factors..........................................9
Chapter 3: Treatment and Therapy.......................................................19
Chapter 4: Future Prospects.................................................................27

Bibliography..........................................................................................29
Glossary................................................................................................33
About the Author...................................................................................35
Index....................................................................................................37
 List of Figures
Figure 1.1 The bacterium Clostridium tetani........................................5
Figure 2.1 The poliovirus..................................................................10
Figure 2.2 The synapse......................................................................14
 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 has been sup-
portive 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 work-
ing to better understand or manage these devastating diseases.
 Introduction
The ability of diseases to be caused by microorganisms, or microbial
pathogens, has been well established through history and continues to
dramatically shape the health of individuals worldwide. Many of these
infectious diseases can be treated and even cured. For example, those
infections caused by the replication of bacteria in the human body fre-
quently can be treated using antibiotics—drugs that target the growing
bacteria and either prevent their growth or kill them. Once the bacteria
are incapacitated, the body’s natural immune system will remove the in-
fectious organisms from the body. However, some infectious diseases have
no cure. Either treatments are unable to reduce infections or the pathogen
can cause harm to the body in the absence of infection. For example,
Clostridium that cause tetanus do so by releasing a toxin into the host’s
body that causes damage and can lead to death. This toxin release does
not require an active infection. A full-sized adult can die from very small
amounts of the toxin. Therefore, once the toxin is released, killing the
bacteria does not help the patient and might lead to the release of more
toxins. For this reason, tetanus caused by Clostridium bacteria should not
be treated by antibiotics. To avoid the serious harm caused by secreted
bacterial toxins, an individual must either avoid exposure to the toxin or
neutralize the toxin with vaccines before the toxins can harm the patient.
Like bacterial toxins, treatments for viral infections are more difficult
to manage. For viral infections, antibiotics are not effective because the
targets of many antibiotics are unique to bacteria, so the target of the
antibiotic is not present in the virus. The bacterial structures normally tar-
geted by antibiotics are not needed by the virus because the virus uses host
cells and enzymes to live and replicate. Viral reliance of host cells causes
another problem with treatments since most drugs that would kill the
virus are likely to kill the host as well. A virus must replicate inside host
cells to cause clinical harm, but it is difficult to design drugs that can in-
hibit viral replication without harming healthy host cells. For this reason,
medical interventions that cure viral infections are uncommon compared
xiv INTRODUCTION

with cures for bacterial infections. For viral infections, effective treatments
depend more heavily on vaccines to help the host’s immune system to
recognize and remove the pathogenic virus from the body. Just as ridding
the body of particular bacterial toxins is more effective with vaccines, rid-
ding the body of pathogenic viruses reduces disease symptoms and dra-
matically improves survivability from serious viral infections. This book
highlights four infectious diseases: polio, tetanus, measles, and mumps.
These four diseases significantly affect human health but are difficult to
treat after the infection because they are caused by a toxin or pathogenic
virus. In each case, the pathogen exhibits different modes of transmission
and progression of symptoms, which require unique treatment regimens.
However, all cases can be controlled through preventative vaccinations
administered prior to infection.

Distinguishing between Virus and Bacteria

Virus and bacteria are very different types of microorganisms, and each
has its own mechanism of spreading, symptoms, approaches to limit dis-
ease progression, availability of treatment, and preventative measures.
Bacteria are single cells that grow, reproduce, metabolize, and respond
to their environment using their own cellular components. Usually, mi-
croorganisms grow outside the human body and are a natural part of
the world around us. Some bacterial make up the healthy collection of
bacteria in the human gut, called the microbiota, which assist in the di-
gestion of food and healthy immune functions. In some cases, a bacterial
cell can grow inside the human body and produce toxins, or replicate and
produce pathological infections. Once pathogenic bacteria replicate in
the body, they might become so numerous that they interfere with bodily
functions and cause disease. To be clear, not all bacteria cause disease, and
the role of natural bacteria in our bodies, the microbiota, is a positive and
important one.
The bacterial cell is a very complicated machine. Bacteria contain
their own genetic material in the form of DNA, reproduce, extract nutri-
ents from the environment, convert these nutrients into vital molecules,
and respond to environmental changes that increase survival. Most bacte-
rial cells are surrounded by a lipid membrane, called a cell membrane.
 INTRODUCTION
xv

The membrane is encased in a complex of sugars and proteins, called a

cell wall, which provides structure and protection to the bacteria. Many
antibiotics target the cell wall and cripple this outer structure, causing
the bacteria to stop growing or break open and die. Embedded in the cell
membrane and cell wall are proteins (receptors) with regions that extend
outward beyond the surface of the cell to communicate with other cells
and detect changes in the environment. These external structures can be
recognized by the human immune system or serve as a target for some
vaccines. Some bacteria form spores, which are specialized cells encased
in especially tough cell walls that shield spores from harsh conditions—
such as dehydration. Bacterial spores do not grow or reproduce, but can
survive for extended periods of time. When growth conditions return to
optimal, the spores germinate and the resulting cells reproduce to form a
population of bacteria. Toxins that cause tetanus are released during this
germination process.
Bacterial cells are autonomous and can grow independent of the host
cell machinery because bacteria independently carry out the basic func-
tions of life, such as genome replication and cell division. In contrast, vi-
ruses are not cells. Viruses are obligate intracellular parasitic organisms,
meaning that a virus is not able to replicate until after it has infected a living
cell. There are many different types of viruses, but most have a very simple
structure—essentially a genome protected by a shell of proteins called the
viral capsid. Some types of viruses are enveloped viruses, because their
capsids are surrounded by a lipid membrane. Most viral membranes are
derived from host cell membranes co-opted by the viruses as they exit
host cells. The viral genome can be composed of DNA, or the genome
can be composed of a slightly different type of nucleic acid called RNA.
Viral genomes can be single-stranded or double-stranded molecules. All
viral genomes serve as genetic instructions for gene expression. For some
RNA viruses, the RNA might be converted to DNA first, which is used to
produce RNA again later in the viral life cycle. This diversity in genome
structure means that some viruses contain auxiliary enzymes; so when they
infect host cells, the viral genome can be acted upon by host cell enzymes.
Regardless of the type of genome, all viruses replicate only with help from
a host cell. Once inside a host cell, the virus depends on the machinery
within infected cells to make more genomes, more capsids, and assemble
xvi INTRODUCTION

these components into new virus particles. Once new viruses are assem-
bled, they must exit the infected cell so they can infect new host cells. An
important distinction between viruses and bacteria is that bacteria make
their own proteins, lipids, and DNA, whereas a virus depends on the in-
fected host cell’s enzymes to make these molecular components used to
produce the next generation of viruses. Since the virus depends on the
host cell to replicate, many scientists do not considered them to be living
organisms, though they do exhibit many traits of living organisms.
Many species of viruses face a biological dilemma. They require a live
host cell to survive, but as viruses replicate inside their host cells, viruses
frequently kill infected host cells that were responsible for producing
the next generation of viruses. For this reason, a virally infected host cell
often loses its ability to function and therefore has the potential to disrupt
bodily functions and cause a disease. Different types of viruses infect dif-
ferent types of host cells. Host cell specificity of infection is an import-
ant part of understanding how two different viruses cause two different
diseases. For some diseases, symptoms due to viral infection reflect loss of
cellular function because infected cells are impaired or killed. For other
viral pathogens, the host’s immune response to the virus produces the
disease symptoms. The ability of a virus to infect particular types of cells
is determined by the chemical and structural complementarity between
receptor proteins on the surface of the host cell and viral capsid proteins.
Viral infection requires close physical contact between host cell proteins
and viral proteins. In the case of many viruses that infect humans, phys-
ical interaction allows the virus to be endocytosed or brought inside the
host cell. Viruses can also spread from one human cell to another through
naturally occurring trafficking pathways. If scientists can determine how
the viral receptor interacts with the host cell proteins, they might be able
to predict which cell types are infected by the virus. Once the infected
cells are identified, we might be able to understand the molecular causes
of symptoms associated with viral disease.

Vaccinations Are Safe and Save Lives

A small but vocal number of people promote a misconception about the
side effects of vaccinations. The misconception is based on a publication
 INTRODUCTION
xvii

that incorrectly linked vaccination to autism. This publication has been

retracted, but the retraction did not generate as much attention as the
original erroneous publication. It is important to emphasize this point—
several teams of scientists repeatedly have disproven that vaccines cause
autism! Many reputable and independent organizations have all con-
firmed that vaccines are not associated with autism: the Autism Science
Foundation, the American Academy of Pediatrics, the Autistic Self-­
Advocacy Network, the Autism Society of America, the National Autistic
Society, Autistica, the Thinking Person’s Guide to Autism, the Ameri-
can Medical Association, the Center for Disease Control and Prevention
(CDC), the March of Dimes, the National Association of Pediatric Nurse
Practitioners, the American Academy of Child and Adolescent Psychia-
try, the World Health Organization (WHO), and the Child Neurology
Foundation.
All vaccines described in this book either prevent infection or reduce
symptoms from infections. Substantial side effects can be associated with
some vaccines, but autism is not one of them. The harm caused by patho-
genic infection that leads to disease are almost always much greater than
the side effects of vaccination. Individuals who do not get vaccinated
place vulnerable individuals, such as newborn infants, at risk of disease
progression that can result in death due to infection. Other vulnerable
people include children under the age of 5, the elderly, diabetics, the se-
verely allergic, and those with compromised immune systems for any of
several reasons. In many cases, herd immunity, sometimes referred to as
community immunity, is critical in protecting the most vulnerable in-
dividuals. Herd immunity is when enough individuals in a community
are resistant to a disease so that spread of the disease is reduced. With
widespread immunization, the disease is unlikely reach more vulnerable
members of the community. Vaccinations are the easiest way to produce
herd immunity. To be clear, these vaccinations are protective and do not
cause autism, and the original paper that claimed otherwise has been re-
tracted due to faulty science.
Many who incorrectly believe that vaccines cause autism focus their
attention on thimersol that had been used as a preservative in multidose
vials of vaccines. Once inside a person, thimersol breaks down into eth-
ylmercury and thiosalicylate that are removed from the body by natural
xviii INTRODUCTION

physiological processes. Ethylmercury is different from methylmercury,

the neurotoxic form of mercury that can accumulate in large fish such as
tuna. The only harmful effects of ethylmercury are those caused by aller-
gies. Scientists have never found any connections between thimersol and
autism. In an effort to be overly cautious, thimersol has been eliminated
or greatly reduced in vaccines produced in the United States since 1999.
All childhood vaccines, including all of the ones discussed in this book,
lack thimersol.
Each pathogen discussed in this book is targeted in a distinct way as a
result of successful immunization. Common to each vaccine is the inocu-
lation of an attenuated virus or bacteria. Attenuated strains of pathogens
stimulate an immune response but fail to produce the disease because the
pathogen is weakened. Some attenuated strains cannot infect any cells,
whereas other attenuated strains can infect, but their symptoms are mild
and not harmful. In order to gain the immunological protection from a
virus due to vaccination, an individual must be exposed to an attenuated
strain of the pathogen. The exact dosage and form of attenuation is deter-
mined by careful research and clinical studies that have been thoroughly
vetted as safe and effective.
To understand how a human immune system detects, targets, and
removes pathogens from the host, we must consider the molecular inter-
actions that facilitate normal immunity. Immune systems are successful
because each immune protein has a very specific molecular shape and
function. Two proteins that physically interact in a stable and function-
ally relevant way co-evolved because their intermolecular contact was
beneficial. Additionally, proteins with similar but slightly different shapes
are composed of similar substructures, or domains, that exhibit similar
functions. For this reason, proteins are frequently grouped into structur-
ally similar categories on the basis of shared domains. For example, there
are many types of antibodies, also called immunoglobulins (Ig), with
similar structures and resulting functions. Antibodies can be divided into
distinctive subtypes with distinctive immune functions. Even antibodies
of the same subtype will vary in subtle ways that cause them to bind to
one and only one molecule called an antigen. Antibodies bind to their re-
spective antigens and are very important components of the immune sys-
tem. If two antibodies have exactly the same structure, then they would
 INTRODUCTION
xix

bind to two copies of the exact same antigen. Antigen specificity means
that the immune system can distinguish between self (nonharmful mol-
ecules produced by the individual’s body) and nonself (foreign and often
harmful molecules, such as those produced by pathogens). Molecules
bound by antibodies are removed from the body by white blood cells of
the immune system. Antibody-mediated immune responses begin with
the antibody binding to its antigen, followed by white blood cell binding
to the antibody–antigen complex. Antibodies bind to white blood cells
via a portion of the antibody protein that does not bind to the antigen.
Antibodies bound to their antigens adhere to white blood cells via recep-
tor proteins on the surface of the white blood cells. When antibodies
physically interact with their receptors on the surface of immune cells,
those immune cells engulf and degrade the foreign material bound to the
antibody. In this way, antibodies mediate the clearing from the foreign-
body material and pathogens.
There are five different antibody subtypes, or classes: IgM (pronounced
eye-gee-em), IgD (pronounced eye-gee-dee), IgG (pronounced eye-gee-gee),
IgE (pronounced eye-gee-ee), and IgA (pronounced eye-gee-ay). Each sub-
type of antibody exists with nearly infinite subtle shape variations that
allow each antibody variant to bind to a distinct antigen. When a white
blood cell interacts with foreign material, a type of white blood cell called
a B cell will produce and secrete many identical antibodies that are spe-
cific to its unique antigen. The first subtype of antibody produced by all
B cells is IgM. The presence of IgM in the bloodstream indicates a new
antigen exposure has occurred. IgD is usually co-expressed with IgM, but
IgD is usually bound to the surface of the B cell, causing IgD to function
as an antigen receptor that allows a specific interaction between the B cell
and the antigen. IgE, IgA, and IgG are produced when an individual is
exposed to the same antigen a second time after an initial IgM response.
IgE function evolved to provide protection against larger parasites, such
as worms, but in many cases, its most noticeable effect is the production
of allergy symptoms. IgA antibodies provide protection in mucosal mem-
branes of the body, such as tear ducts and intestines. IgG is the most com-
mon antibody subtype found circulating in blood. IgG plays a vital role
in protecting the body from foreign material, such as toxins, bacteria, and
viruses located in the blood, lymph, or tissues of the body. IgG represents
xx INTRODUCTION

a circulating molecular memory of at least two previous antigen exposures

and subsequent immune responses. Immunological memory in the form
of IgG, IgE, and IgA produces a rapid and vigorous response to antigens
after the first exposure, because the antibodies are already present in the
body. Health care providers can determine whether an individual needs
to be vaccinated, or has been vaccinated, by identifying one of these three
different classes of antibodies that also binds to the antigen of interest.
For example, tuberculosis (TB) testing is performed by injecting a small
amount of harmless TB protein under the skin. If swelling and increased
blood supply follow (a rash), the person has either been exposed to TB
or been vaccinated. Immunological memory is why vaccinations are
effective—­the vaccine provides the first exposure to a pathogenic antigen
so that a healthy immune system can respond to subsequent exposures
more effectively, reducing the chance of disease progression. Booster shots
are needed for some diseases, such as tetanus, to ensure that the number
of antibodies is sufficiently high to provide adequate protection.
 CHAPTER 1

Symptoms and Diagnosis

Symptoms and Diagnosis of Polio

Polio, or poliomyelitis, is paralysis resulting from an infection by the
poliovirus. Infection by the poliovirus could occur anywhere in the
world, though aggressive vaccination efforts have eliminated the virus
(as of 2019) from every country except three: Afghanistan, Pakistan, and
Nigeria. Poliovirus infection is very serious, with approximately 72 percent
of infected individuals showing symptoms of the infection. Early flulike
symptoms include sore throat, fever, fatigue, nausea, headache, and stom-
ach pain, which usually last for 2 to 5 days at which point they go away. A
smaller percentage of infected individuals will develop more severe symp-
toms, such as paresthesia (pins and needles feeling in the legs). Approxi-
mately 25 percent of infected individuals will develop meningitis, which
means that the infection of the virus will spread to the spinal cord and/or
the brain. Only about 0.5 percent of infected individuals will get polio,
paralysis of arms or legs or both, that can lead to permanent disability.
The long-term effects of poliovirus infection vary, with some individuals
showing symptoms 15 to 40 years after a full recovery from an infec-
tion. These long-lasting symptoms are called post-polio syndrome and
usually include muscle pain, weakness, or paralysis. Of those individuals
who experience polio (paralysis), between 2 and 10 percent will die from
the infection, usually due to paralysis of the diaphragm, a muscle needed
for breathing. Taken together, the overall risk of death is significant, with
about 0.01 to 0.05 percent mortality of individuals who become infected
with poliovirus. This mortality rate is high, since for every 10,000 indi-
viduals infected with the poliovirus, 1 to 5 will die. What makes poliovi-
rus particularly concerning is its ability to spread very quickly with high
rates of disability and death among infected individuals.
2 DISEASES THAT ARE PREVENTABLE BY VACCINATION

Diagnosis of poliovirus infection involves the identification of the

virus in patient samples. Poliovirus can be isolated from cerebrospinal
fluid, though this is rarely used for diagnosis. The most common source
of specimen is from patient feces or throat swabs. The most sensitive way
to determine whether or not poliovirus is present is to detect the presence
of the viral genome in patient samples or by culturing virus (allowing the
virus to replicate). Both of these sensitive tests are conducted only in con-
trolled laboratory settings, due, in part, to the potential hazard of working
with live and infectious poliovirus. The poliovirus genome is composed of
RNA; so in order to detect viral RNA in patient samples, the poliovirus
RNA genome is copied into a DNA version first so that it can be ampli-
fied through a molecular technique called polymerase chain reaction
(PCR). PCR can detect the DNA copy of the viral RNA genome because
it is specific to unique segments of the viral genome. PCR amplifies only
a particular segment until this segment is abundant enough to detect. The
presence of poliovirus can also be determined by quantifying IgG or IgM
poliovirus antibodies circulating in the blood. However, antibody detec-
tion cannot be used for patients who have been vaccinated since they too
would produce poliovirus antibodies regardless of their infection status.
Currently, infection with the poliovirus and pathological development
of poliomyelitis are both part of the National Notifiable Disease Surveil-
lance System (NNDSS), meaning that they are among the 120 diseases
that must be reported to the CDC that tracks especially harmful diseases
within populations and develops appropriate responses to protect local
communities.

Symptoms and Diagnosis of Tetanus

The disease tetanus is the contraction, or tightening, of muscles in the
body resulting from toxins released during an infection with the bacteria
Clostridium tetani. These muscle contractions can persist from minutes
to weeks. Most cases of tetanus occur in adults, with very serious disease
progression in those over 65, and in mothers/newborns if the mothers are
not protected in advance by the tetanus vaccine. In the United States, 197
reported cases occurred from 2009 to 2015, and approximately 30 cases
 Symptoms and Diagnosis 3

a year are reported. Tetanus symptoms usually occur 3 to 21 days after

infection, with most cases showing symptoms on day 14. Occasionally, a
delay in symptom onset can vary widely from 1 day to several months de-
pending on the type and location of the site of infection that introduced
the Clostridium into the body.
Muscle contractions caused by tetanus can cause jaw muscles to
tighten and close (lockjaw), making speaking and swallowing difficult.
Muscle contractions caused by tetanus may occur throughout the body
and can take the form of reflex spasms, which are brief muscle contrac-
tions, sometimes triggered by muscle stretching or stimulation of the five
senses. Painful contractions often begin with jaw and neck muscles, fol-
lowed by muscles in the chest and abdomen. Occasionally, muscle rigidity
is confined to the site of Clostridium infection. The involuntary tighten-
ing of muscles can be intense, causing broken bones and breathing dif-
ficulty. Other tetanus symptoms include staring, laryngospasm (spasms
of the vocal cords), pulmonary embolism (blood clot that moves into the
lungs and causes a blockage), aspiration pneumonia (pneumonia from
breathing in foreign material into the lung), stomach pain, headache, and
fever. If the secreted Clostridium toxin reaches the brainstem of the cen-
tral nervous system, then symptoms can include autonomic dysfunction.
Symptoms associated with autonomic dysfunction usually occur later in
infections and can include changes in blood pressure, heart rate, sweating,
bradyarrhythmia (irregular heartbeats), and cardiac arrest.
More than 80 percent of tetanus cases are described as generalized
tetanus, with initial symptoms of muscle contractions of the jaw fol-
lowed by painful contractions in the neck, trunk, or extremities of the
body. These muscle responses can cause patients to bend backward with
an arched back. Some patients might drool or lose control over urina-
tion and defecation. In severe cases, uncontrolled muscle contractions can
progress to convulsions or seizures. Other neuronal dysfunction can vary
greatly depending on prior immunity to Clostridium infection, amount
of toxin present in the patient, and age of the patient. The closer the site
of infection is to the nervous system, the faster disease progression oc-
curs. Generalized tetanus is a serious complication and can cause death
10 to 20 percent of the time. Localized tetanus describes cases where
4 DISEASES THAT ARE PREVENTABLE BY VACCINATION

symptoms are more confined to the area of infection. Localized tetanus

cases are milder and usually occur in individuals with previous immunity
to Clostridium infection, though localized tetanus can progress to gener-
alized tetanus. Cephalic tetanus is very rare and is confined to muscles
or nerves of the head and neck. This type of tetanus is more common
when infections result from head laceration, skull fracture, eye injury,
or dental injury so that Clostridium spores enter the body in these areas.
Symptoms include neck stiffness, problems swallowing, lockjaw, retracted
eyelids, abnormal eye movement (deviated gaze), and risus sardonicus,
which translates from Latin as spasms of the facial muscles that cause the
appearance of abnormal smiling. Cephalic tetanus can also progress to
generalized tetanus. Neonatal tetanus can occur in newborns if tetanus
arises within the first month of life and usually results from umbilical
cord stump contamination. Neonatal tetanus can be lethal, and according
to the WHO, 49,000 newborn children died worldwide for this reason in
2013. Although astonishing, these numbers are greatly reduced compared
with 1988 when 787,000 newborns died from tetanus worldwide. Infants
whose mothers were vaccinated usually do not get tetanus because of the
babies exhibit immunity gained passively from their mothers. When teta-
nus occurs in the mother during pregnancy or after birth (up to 6 weeks),
the infection is called maternal tetanus.
The diagnosis of tetanus is usually preceded by rapid onset of muscle
contractions with no other observable cause. There is no specific labora-
tory test used for diagnosis. The identification of Clostridium bacteria is
not necessary for diagnosis, since very few toxin-secreting cells are suffi-
cient to cause disease. When the bacterium is present, it is detected as a
spore-forming, motile, and swarming rod-shaped cell with distinct nutri-
tional requirements and structural features (spores at one end creating a
“tennis-racket” appearance, as shown in Figure 1.1). Some additional dis-
eases have similar symptoms to tetanus and should be considered during
diagnosis. Strychnine (rat poison) ingestion can show symptoms similar
to tetanus. Lockjaw can also be caused by encephalitis, side effects from
phenothiazine (antipsychotics used to treat schizophrenia and other psy-
chotic disorders), as well as other diseases involving the jaw. Tetanus is
part of the NNDSS, meaning that all diagnosed cases must be reported
to the CDC.
 Symptoms and Diagnosis 5

Figure 1.1 The bacterium Clostridium tetani. Diagram on the left

shows the overall structure of the bacteria and the position of the
spore as it is formed within the bacteria. The image to the right is
a micrograph of a group of C. tetani bacteria, the causative agent of
tetanus. The diagram is by Kholmes16—Own work, CC BY-SA 4.0
(https://creativecommons.org/licenses/by-sa/4.0)], from Wikimedia:
https://commons.wikimedia.org/w/index.php?curid=40504343. The
micrograph is by the Center for Disease Control and Prevention’s
Public Health Image Library, identification number #6372; PD-
USGov-HHS-CDC; from Wikimedia: https://upload.wikimedia.org/
wikipedia/commons/1/18/Clostridium_tetani.jpg.

Symptoms and Diagnosis of Measles

Measles is a highly contagious respiratory illness resulting from infection
by the measles virus. Before the measles vaccine was developed in 1963,
approximately 549,000 reported measles cases and about 500 deaths oc-
curred annually in the United States. Furthermore, about 48,000 patients
required hospitalization and roughly 1,000 patients develop chronic dis-
ability from encephalitis associated with measles infection. Development
of the measles vaccine greatly reduced measles cases. Unfortunately, due
to parents refusing to vaccinate their children, 1,109 cases were reported
6 DISEASES THAT ARE PREVENTABLE BY VACCINATION

in the United States as of July 2019. The large number of measles cases in
2019 is part of an avoidable trend: 372 total cases were reported in 2018,
120 in 2017, and 86 in 2016. People with measles in 2019, mostly chil-
dren, reflects measles cases occurring in 23 states and is the largest since
1994 and after measles was declared eliminated in the United States in
2004. The increasing trend in measles occurrence is a concern because any
measles case increases the risk of infection of those individuals more sus-
ceptible to infection. Of those individuals who develop measles, compli-
cations can occur where 1 in 1,000 measles cases will result in encephalitis
and permanent brain damage, and 2 in 1,000 will experience respiratory
and neurological complications. Very rarely, patients can develop a fatal
degenerative disease of the central nervous system called subacute scleros-
ing panencephalitis (SSPE). Seven to ten years after infection, SSPE can
cause symptoms including seizures, behavioral changes, and intellectual
impairment. SSPE symptoms can occur in healthy adults or children who
had been infected by measles, but SSPE is more common in children
under 5 years of age, pregnant women, and individuals with compromised
immune systems such as HIV patients and some types of cancer patients.
Most individuals who get measles in the United States are not vaccinated.
Although outbreaks of measles are relatively uncommon in the United
States thanks to wide use of vaccination, large measles outbreaks have
been documented recently in England, France, Germany, India, and the
Philippines among populations who have not been vaccinated.
Symptoms of the measles include fever (up to 105ºF), coughing,
malaise, inflammation of the mucous membranes in the nose (coryza),
and inflammation of the thin clear layer of tissue that covers the white
part of the eyes (conjunctivitis). Symptoms usually appear between 7 and
14 days after exposure. The most common symptom is a skin rash on the
body that appears 3 to 5 days after symptoms begin. This rash can begin
as flat inflamed spots around the hairline of the patient, spreading to the
neck, trunk, arms, legs, and feet. Additional small raised inflamed bumps
may form on top of the flat spots. As these spots spread, they can fuse
and the fever associated with measles can spike. For most patients, the
rash and fever subside after a few days. Patients are considered contagious
4 days before and 4 days after the formation of the rash. Small white spots
 Symptoms and Diagnosis 7

(pathognomonic enanthema, or Koplik spots) also might appear in the

mucous membranes of the mouth 3 days after the onset of symptoms.
Diagnosis of measles requires laboratory confirmation using measles
virus detection in patient samples. Patient samples are obtained as swabs
from the nose or throat, in addition to a blood sample. Urine can also
contain virus, so a urine sample might contribute to a measles diagnosis.
Patient samples are tested using an antibody method in which the anti-
body specifically binds to protein components of the virus. PCR can be
used to detect the RNA viral genome after it is enzymatically converted
to DNA. If measles virus is detected, additional molecular tests identify
the specific subtype of measles virus within a given patient. Knowing the
molecular details of an infection allows public health officials track the
spread of viral outbreaks so they can determine the origin of the infection.
In the United States, measles is part of the NNDSS, which means health
care professionals are required by law to report cases of the measles within
24 hours so that the source of infections can be identified and the scale of
the outbreak can be minimized.

Symptoms and Diagnosis of Mumps

Mumps is a viral infection of the salivary glands that can be prevented by
vaccination. Mumps causes very painful tenderness and swelling of one or
both parotid salivary glands, which are located in the neck and jaw. Swell-
ing begins between 1 and 3 days after infection, starting in front of the
lower part of the ear and extending downward through the soft tissue of
the face and neck. Swelling peaks around day 3 of the infection and then
subsides over the following week. Salivary glands on one side of the face
might swell before the other, and in 25 percent of the cases, only one side
swells. As swelling worsens, the jawline will not be visible. Frequently,
ears are pushed upward or at an angle by swollen parotid glands. Mumps
looks different from swollen lymph nodes, since the lymph nodes are lo-
cated behind the ear instead in front of it. In about 10 percent of mumps
cases, salivary glands located below the floor of the mouth (submandibu-
lar and sublingual salivary glands) swell too. Fever can precede the swell-
ing by several days and prior to any swelling, patients might experience
8 DISEASES THAT ARE PREVENTABLE BY VACCINATION

malaise, headache, and anorexia. Rarely, the flu can cause swelling of the
parotid salivary glands and can be confused for the mumps. Individuals
who have not been vaccinated for mumps can develop complications of
the infection caused by an aggressive inflammation response to the viral
infection. Complications of infection can include hearing loss (in about
4 percent of cases), encephalitis (less than 1 percent of cases), pancreatitis
(less than 1 percent of cases), and meningitis (up to 15 percent of cases).
Mumps complications are more likely to occur in adults than children.
Men who contract the mumps are at risk (3–10 percent of infected men)
of inflammation of the testes (orchitis), with 60 to 83 percent of orchitis
cases being restricted to only one testis. Additional rare complications of
mumps infection can include inflammation of the ovaries (oophoritis)
or breast tissue (mastitis). Some people who are infected by the mumps
virus may exhibit only respiratory symptoms or no symptoms at all. In
approximately half of all mumps patients, the virus is found in the central
nervous system, though symptoms associated with this aspect of infection
are rare.
In 2012, the CDC published guidelines for diagnosing mumps. A
probable mumps infection is defined as a person who has experienced sal-
ivary gland swelling for 2 days or more and tested positive for an immune
response to the mumps, or has been in contact with someone already di-
agnosed with mumps. Initial tests for probable cases involve the detection
of IgM antibodies to the mumps virus in patient samples. If a person has
had a mumps vaccine, levels of IgM may be too low to measure but IgG
that bind to measles are easier to detect. A case of mumps is confirmed by
finding viruses in patient samples. Viruses can be detected in laboratories
by a PCR test to amplify part of the viral genome, or by growing in the
lab mumps virus isolated from patient samples. The presence of the virus
in a patient does not mean that the patient has the mumps, so a rigor-
ous diagnosis should include the presence of mumps symptoms described
earlier. In the United States, mumps is part of the NNDSS, a national
notifiable condition, so health care professionals are required by law to
report cases of the mumps.
 Index
A C
Adults
causes of death, xiii
long-term immunity, 24
mumps complications, 8
tetanus vaccine, 2
vaccination booster, 19
Adverse reactions, to measles
vaccines, 24
Advisory Committee on
Immunization Practices
(ACIP), 25
Antibiotic carryover, 20
Antibiotics, xiii
Antibodies, xviii, 11
Antibody-antigen complex, xix
Antibody-binding sites, 11
Antigen, xix, xviii
Antitoxin, in tetanus, 22
Attenuated polioviruses, 20
Attenuated viruses, 23
Autism, xvii, xviii, 24, 27
Autism, 24
B xiv, xv, xvi
B cells, xix, 16
Bacteria, xiii
cell membrane, xiv
cell wall, xv
receptors, xv
structure of, xiv
virus, distinguished with,
xiv–xvi
Bacterial spores, xv
Bacterial toxins, xiii
Blood circulation, IgG role in, xix
Booster, 22–23
Breast tissue (mastitis), mumps
infection, 8
Brunhilde and Mahoney strain
serotype, 11, 19
Capsid proteins, 11
Carryover antibiotics, 20
CD150, 16
CD155, 11
Cell membrane, xiv
Cell wall, xv
Center for Disease Control and
Prevention (CDC), 4
guidelines for measles diagnosis, 8
polio vaccine, 19
Cephalic tetanus, 4
Childhood mortality, 16
Children, MMR vaccine
combination, 25
Clostridium, xiii, 3
localized tetanus, 4
Clostridium tetani, 2, 5, 12, 21
tetanus toxins, 13
Community immunity, xvii
D
Dendritic cells, 16
Deoxyribonucleic acid (DNA),
E
Edmonston virus, 23
Encephalitis, 4
in measles patients, 16
Enveloped viruses, xv
Ethylmercury, xvii, xviii
F
Fecal-to-oral contamination,
poliovirus, 9
Flaccid paralysis, 14
Flagella, 12
Flu, 8
Foreign material, IgG role against, xix
38 INDEX
G Infectious diseases, xiii, 1
Generalized tetanus, 3
Guillain-Barré syndrome, 24
H vaccine (IPV)
Health care professionals, 8
Health care providers, xx
Healthy immune system, xx
Hemagglutinin-neuraminidase (HN)
proteins, 17
Hematopoietic stem cells, 16
Herd immunity, xvii
Host cells, xv, xvi
Human protein receptor, 11
Human tetanus immune globulin
(HTIg), 21
Human-to-human contact, restriction
to poliovirus, 9
I Measles, xiv
IgA antibody, xix, xx
IgD antibody, xix
IgE antibody, xix, xx
IgG antibody, xix, xx, 2, 18
IgM antibody, xix, 2
detection in mump infected patient
sample, 8
Immune system, xiii
antibody-mediated immune
response, xix
long-term immunity, 27
Immunization, xvii, xviii, 23
Immunoglobulin intravenous
(IGIV), 21
Immunoglobulins (Ig), xviii
Immunological memory, xx
Inactivated polio vaccine (IPV),
19–20
Infected individuals
measles
causes and contributing
factors, 16
symptoms and diagnosis, 6
polio
causes and contributing factors, 9
palliative treatments, 19
symptoms and diagnosis, 1
Inflammatory bowel disease, 24
Inoculation, attenuated virus or
bacteria, xviii
IPV. See Inactivated polio
L
Lansing and MEF-I serotype, 11–12,
19
Leon and Saukett serotype, 12, 19
Localized tetanus, 3–4
Lockjaw, 4, 22
Lymphocytes, 16
M
Macrophages, 16
Mahoney type 1 virus, 20
Maternal tetanus, 4
causes, 15–17
contributing factors, 15–17
diagnosis, 5–7
serious anaphylactic reactions, 24
symptoms, 5–7
therapies, 23–25
treatments, 23–25
vaccination (age of 12 and 15
months), 23–24
vitamin A deficiency, 24–25
Measles, mumps, and rubella (MMR)
vaccines, 25
Measles, mumps, rubella, and
varicella-zoster (MMRV)
vaccines, 25
MEF-1 type 2 virus, 20
Membrane vesicles, 13
Meningitis, 1
Metalloproteinase, 13
Metronidazole, 22
Microbial pathogens, xiii
Microbiota, xiv
Microorganisms, xiii
Middle East Force serotype, 12–13, 19
Monovalent OPV (mOPV), 20
Morbillivirus, 15
Mortality rates, 1, 17, 25
 INDEX
39

Motor neurons, 11 Penicillin, 22

Mucosal membranes of body, IgA role Permanent neurological sequelae. See
in, xix Guillain-Barré syndrome
Mumps, xiv Peyer’s patches, 11
causes, 17–18 Picornaviridae, 9
contributing factors, 17–18 Polio, xiv
symptoms and diagnosis, 7–8 causes, 9–12
therapies, 25–26 contributing factors, 9–12
treatments, 25–26 diagnosis, 1–2
vaccination of, 25 symptoms, 1–2
Mumps vaccine, 23 therapies, 19–21
Muscle contractions treatments, 19–21
characteristics in tetanus, 13 Poliomyelitis, 2. See also Polio
diagnosis of tetanus, 4 Poliovirus, 1, 2
by tetanus, 3 Polymerase chain reaction (PCR), 7
Muscle rigidity, 3 Post exposure prophylaxis (PEP), 24
Post-polio syndrome, 1
N
National Notifiable Disease R
Surveillance System Receptors, xv
(NNDSS), 2, 4, 7, 8 Ribonucleic acid (RNA), xv, 9
Nectin-4, 16 measles virus, 15
Neonatal tetanus, 4, 23 poliovirus, 2, 11
Neuromuscular junction, 13 Rubella vaccine, 23
Neuron membrane fusion, 13
Neurotransmitters, 15 S
Newborn infants, xvii Sabin 1 to 3 serotypes, 20
Non-Edmonston virus-based Saukett type 3 virus, 20
strains, 23 Serotypes, 11
Signaling lymphocyte activation
O molecule (SLAM), 16
Obligate intracellular parasitic Subacute sclerosing panencephalitis
organisms, xv (SSPE), 6, 17
Oral poliovirus vaccine (OPV), 20 Sympathetic nervous system, 13
Ovaries (oophoritis), mumps Synaptobrevin, 13
infection, 8
T
P T cells, 16
Paralysis, 1, 9 Tetanolysin, 13
lysed neurons, 11 Tetanospasmin, 13, 14, 15, 22
Parasites, IgE role against, xix Tetanus
Parotid salivary glands, viral causes, 12–15
infection in, 7 Clostridium infection, 3
Pathogenic virus, xiv contributing factors, 12–15
Pathological infections, xiv, xvii diagnosis, 2–5
Patient samples, in measles immunity, 22
diagnosis, 7 symptoms, 2–5
40 INDEX

Tetanus (continue ) Vaccine

therapies, 21–23 cost of, 23
treatments, 21–23 measles vaccine, 23
Tetanus-toxoid-containing vaccine Vaccine-associated paralytic polio
(TTCV), 22 (VAPP), 20–21
Thimersol, xvii, xviii Varicella vaccine, 23
Thiosalicylate, xvii Vesicular synaptic membrane protein
Thrombocytopenic purpura, 24 (VAMP), 13–15
Thymocytes, 16 Viral capsid, xv
Toxin virus, xiv Viral genomes, xv
Trafficking pathways, xvi Viral infection
Transmission electron microscopy, 10 effective treatments, xiv
Trivalent OPV (tOPV), 20 medical interventions, xiii
TTCV. See Tetanus-toxoid-containing mumps, 7
vaccine (TTCV) risk management, xiii
Tuberculosis (TB) testing, xx Virus, xiii, xvi
attack rate, 26
V bacteria, distinguished with, xiv–xvi
Vaccination intracellular parasitic organisms, xv
allergic reaction to, 19, 24, 25 PCR test, 8
to health care workers, 24 structure of, xv
herd immunity, xvii
to international travelers, 24 W
measles, 15–16 Wound cleaning, in tetanus, 21–22
mothers/newborns, tetanus
vaccine, 2
mumps, 7 Z
side effects, xvi, xvii, 19 Zinc-dependent metalloproteinase, 13
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