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vii
 FOCUS ON UNDERSTANDING . . . Confirming Pages

Student-Friendly Illustrations Focus Figure

Introduce the “big picture” Dendritic cell

Innate immunity

Focus figures provide an overview or highlight a key

concept. Activation
Activates T cells that
bind antigens
representing “danger”

Naive B cell Naive helper T cell Naive cytotoxic T cell

Keep the big picture in focus

A highlighted mini-version of the overview figure is Proliferation
and differentiation
often incorporated into the upper left corner of subse- Plasma cells
TH cells TC cells

quent figures, helping students see how those figures Produce

antibodies
Deliver
cytokines
Deliver “death
packages”

fit into the big picture.

Effector action
and consequence

Macrophage that Macrophage with Infected Infected “self”

Antibodies Antibodies bind has engulfed increased killing power “self” cell cell undergoes
antigen invaders apoptosis
Adaptive immunity Adaptive immunity
(humoral) (cell-mediated)

FIGURE 15.1 Overview of the Adaptive Immune Response Humoral immunity protects against antigens in blood and tissue fluid (extracellular
antigens); cell-mediated immunity protects against antigens within host cells (intracellular antigens). In this diagram, solid arrows represent the path
of a cell or molecule; dashed arrows represent a cell’s interactions and effector functions; antigen receptors and memory cells are not shown.
Development
Hematopoietic stem cell
Immature B cells: As
these develop, a
? How does cell-mediated immunity eliminate intracellular antigens?
functionally limitless
assortment of B-cell
receptors is randomly Antigen X
generated.

Naive B cells: Each

cell is programmed to Other descendants become memory lymphocytes, long- The structure of an antibody molecule accounts for its
recognize a specific
epitope on an antigen;
B-cell receptors guide B cell W B cell X B cell Y B cell Z lived cells that can be activated more quickly if the antigen ability to protect against an invader. An antibody has two
recognizing antigen X
that recognition.
is encountered again. Memory cells are responsible for the functional regions: the two identical arms and the single stem
Development effectiveness of the secondary response. of the Y-shaped molecule (see figure 15.1). The ends of the
Activation Selected B cell receives confirmation from a specific
TH cell that a response is warranted (not shown
Activated B cells: here; process is illustrated in figure 15.11)

Hematopoietic stemarms are the parts that attach to antigens. By binding to anti-
cell
These cells can
proliferate because
their B-cell receptors
are bound to antigen X
Humoral Immunity gens, the antibodies can neutralize their effects. For example,
Immature B cells: As When a naive B cell detects an extracellular antigen, that B cell antibody-coated viral particles cannot attach to receptors on
and the cells have
received required
signals from TH cells.
may become activated, allowing it to proliferate (see figure 15.1). cells and, therefore, cannot enter the cells. Antibodies are very
Proliferation and
these develop, a Some of the descendants of activated B cells differentiate to specific with respect to their binding, so the immune system
B-cell receptor
functionally limitless
1 2 3
differentiation
become plasma cells, which are effector B cells. Plasma cells must produce many different varieties, each with a slightly
Antigen
assortment of B-cell
Endosome make Y-shaped proteins called antibodies. These proteins bind different set of “arms.” Although the set of arms of different
to the surfaces of cells, toxins, viruses, and other antigens, antibody molecules varies, the stem portion is functionally
Plasma cells
(effector B cells):
These descendants of
receptors is randomly and in doing so, protect the body against the Antigeneffects of thatX similar—it serves as a “red flag” that sticks out from the sur-
activated B cells
secrete large quantities
of antibody molecules
generated. antigen. For example, antibodies that bind diphtheria toxin face of an antibody-bound antigen. This tags the antigen for
that bind to antigen X.
B-cell receptor binds B cell internalizes antigen. protect
B cell degrades antigen intopatients from the effects of the toxin (see A Glimpse rapid elimination by macrophages or other components of the
Memory B cells: to antigen. of History).
peptide fragments. immune system. attachment of viruses
Naive B cells: Each
These long-lived
descendants of
activated B cells
recognize antigen X 388
when it is encountered
again.
Antigen
cellMHCisclassprogrammed
II
to 5a T-cell receptor

fragment recognize a specific

Effector action 4 TH cell recognizes
molecule
Antibodies:
antigen fragment
These neutralize the
invader and tag it for epitope onMicrobial an antigen; and activates B cell.
destruction.

B-cell receptors
antigen
presented.
guide B cell W
Cytokine delivery B cell X
and0999x_ch15_386-414.indd 388 B cell Y 11/01/17 10:27 AM B cell Z
that recognition. Harmless 5b recognizing antigen X
antigen Dendritic cells in the tissue collect
presented. No TH cell recognizes particulate and soluble antigen and then
Peptide fragments are
FIGURE 15.10
antigen fragment; travel to the secondary lymphoid tissues.
presented on MHC class II B cell becomes
molecules.
Activation
anergic.
Selected B cell receives confirmation from a specific
Lymphoid organ
TH cell that a response is warranted (not shown
Activated B cells: here; process is illustrated in figure 15.11)
FIGURE 15.11
These cells can
MHC class I molecule
Co-stimulatory molecule
Dendritic cells presenting
microbial peptides produce
Dendritic cells presenting “self”
peptides or other harmless
co-stimulatory molecules. material do not produce
proliferate because MHC class II molecule co-stimulatory molecules.

their B-cell receptors T-cell receptor T-cell receptor T-cell receptor T-cell receptor
are bound to antigen X CD4 CD8 CD4
Normal
CD8 CD8 T-cell receptor
cytoplasmic MHC class I
and the cells have proteins molecule

received required
signals from TH cells.
Naive T cells that recognize antigen presented Naive T cells that recognizeAll
antigen presented
nucleated cellsbypresent
dendriticpeptides
cells from TC cells do not recognize peptides
by dendritic cells expressing co-stimulatory molecules not expressing co-stimulatory molecules become anergic or, in
can become activated.
cytoplasmic proteins on MHC class I molecules.
the case of CD4+ cells, may become regulatory T cells.
presented by healthy “self” cell.

(a)
Anergic T cells cannot respond and eventually undergo apoptosis.
Activated T cells proliferate and differentiate.
Regulatory T cells prevent certain immune responses.
Virus
Proliferation and Viral Cytokines

FIGURE 15.20 proteins

differentiation
Targeted delivery
of a “death package”

Virally infected “self” cells TC cell recognizes viral peptide Target cell undergoes apoptosis.
present viral peptides on presented by an infected “self” cell
MHC class I molecules. and initiates apoptosis in that target.
It also releases cytokines that alert
neighboring cells.
1 2 3 CD4
(b) Cytokine delivery T-cell receptor

Plasma cells FIGURE 15.21

(effector B cells): Secretion
of cytokines

These descendants of
“Provides a logical unfolding
activated Bconceptual
cells framework that Macrophage Macrophage degrades Peptide fragments TH cell recognizes a presented

fosters better understanding.”

engulfs materials. proteins in phagosome are presented on MHC peptide and responds by activating
secrete large quantities into peptide fragments. class II molecules. the macrophage. It also releases
cytokines that stimulate TC cells.
of antibody molecules
—Jamal
that Bittar, X.
bind to antigen University of Toldeo
FIGURE 15.22
Memory B cells:
viii These long-lived
descendants of
activated B cells
recognize antigen X
 Rev.Confirming Pages

420 Chapter 16 Host-Microbe Interactions

Distribution of the Pathogen

Infections are often described according to the distribution of
the causative agent in the body. In a localized infection, the
microbe is limited to a small area; an example is a boil caused
by Staphylococcus aureus. In a systemic infection, the infec-
tious agent is disseminated (spread) throughout the body; an
example is Lyme disease. Systemic infections often include

Walk through the processes Confirming Pages

a characteristic set of signs and symptoms—such as fever,
fatigue, and headache—that result from the systemic immune
1 The microorganism must be present in every case of the disease, but
response to the infecting agent. not in healthy hosts.

Step-by-step figures direct the student using numbered icons,
often with corresponding icons in the text.
FIGURE 7.3 Three Functional Types of
RNA Molecules The different functional
types of RNA—messenger RNA (mRNA),
ribosomal RNA (rRNA), and transfer RNA DNA
(tRNA)—are transcribed from different
genes. The mRNA is translated, and the
tRNA and rRNA fold into characteristic three-
dimensional structures that each play a role
in protein synthesis.
Protein-encoding gene
Transcription
Messenger RNA (mRNA)
Translation
The suffix -emia means “in the blood.” Thus, bacteremia
indicates that bacteria are circulating in the bloodstream. Note
that this term does not necessarily imply a disease state. A per-
Part I Life and Death of Microorganisms 181
son can become bacteremic for a short period of time after
forceful tooth brushing. On the other hand, infection-induced
bacteremia can lead to a life-threatening systemic inflammatory
rRNA gene tRNA gene response, a condition called sepsis. Toxemia indicates that tox-
ins are circulating in the bloodstream. The organism that causes 2 The microorganism must be grown in pure culture from diseased hosts.
tetanus, for instance, produces a localized infection yet its tox-
ins circulate in the bloodstream. The term viremia indicates
that viral particles are circulating in the bloodstream. sepsis
Ribosomal RNA (rRNA) Transfer RNA (tRNA)
MicroAssessment 16.3
A primary pathogen can cause disease in an otherwise

? “The text and illustrations are ’tight’ and give each other
Ribosomal RNA is a component of ribosomes.
What are ribosomes?
healthy individual; an opportunist causes disease in an
immunocompromised host. The course of infectious disease
includes an incubation period, illness, and a period of
good support.”
Protein 3 The same disease must be produced when a pure culture of the
convalescence. Infections can be acute, chronic, or latent; they microorganism is introduced into susceptible hosts.
can be localized or systemic.

—Richard Regulating
RNA is synthesized using a region of one of the two
Shipee, Vincennes
Gene Expression
strands of DNA as a template. In making the RNA molecule,
or transcript, the base-pairing rules apply except that uracil,
rather than thymine, pairs with adenine. The interaction of
DNA and RNA is only temporary, however, and the transcript
quickly separates from the template.
Three different functional types of RNA are required for gene
expression, and these are transcribed from different sets of genes
(figure 7.3). Most genes encode proteins and are transcribed
into messenger RNA (mRNA). The information encrypted in
mRNA is decoded according to the genetic code, which corre-
lates each set of three nucleotides to a particular amino acid.
Some genes are never translated into proteins; instead the RNAs
themselves are the final products. These genes encode either
ribosomal RNA (rRNA) or transfer RNA (tRNA), each of
which plays a different but critical role in protein synthesis.
Gene A
University
Although a cell’s DNA can encode thousands of different pro-
teins, not all of them are needed at the same time or in equal
quantities. Because of this, cells require mechanisms to regu-
late the expression of certain genes.
A fundamental aspect of gene regulation is the cell’s
ability to quickly destroy mRNA. Within minutes of being
produced, transcripts are degraded by cellular enzymes.
Although this might seem wasteful, it actually provides cells
with an important regulatory mechanism. If transcription of a
gene is turned “on,” transcripts will continue to be available
for translation. If it is then turned “off,” the number of tran-
scripts will rapidly decline. By simply regulating the synthe-
sis of mRNA molecules, a cell can quickly change the levels
of protein production (figure 7.4).
Gene B Gene C
5. Why are diseases caused by opportunists becoming more
frequent?
6. Give an example of a microbe that causes a latent infection.
7. What factors might contribute to a long incubation period?
16.4 ■ Determining the Cause
of an Infectious Disease 4 The same microorganism must be recovered from the experimentally
infected hosts.
Learning Outcome
FIGURE 16.3 Koch’s Postulates These criteria provide a foundation
6. List Koch’s postulates, and compare them to the molecular
for establishing that a given microbe causes a specific disease.
Koch’s postulates.
?
Why is it not possible to use Koch’s postulates to show that Treponema pallidum
causes syphilis?
Criteria are needed to guide scientists as they try to determine
the cause of an infectious disease. They can also be helpful
1 The microorganism must be present in every case of the
when studying the disease process. disease.
2 The microorganism must be grown in pure culture from
Koch’s Postulates diseased hosts.
Koch’s postulates—the criteria that Robert Koch used to 3 The same disease must be produced when a pure culture
show that Bacillus anthracis causes anthrax (see A Glimpse of of the microorganism is introduced into susceptible hosts.
History)—provide a foundation for establishing that a given 4 The microorganism must be recovered from the experi-
microbe causes a specific infectious disease (figure 16.3): mentally infected hosts.

Low levels of gene A No transcription of gene B Continuous transcription of Confirming Pages

transcription generates leads to no synthesis of gene C generates many
some transcripts of protein B. transcripts of the gene.
the gene.
and0999x_ch16_415-438.indd 420 11/01/17 05:05 PM

624 Chapter 24 Digestive System Infections

Translation of each of
the gene A transcripts Encourage deeper understanding
24.1 Anatomy, Physiology,
■ first physically breaking down food into small particles, then
chemically breaking down those particles even further, and
generates some protein A. and Ecology of the finally absorbing the available nutrients. The waste material
FiguresDigestive
haveSystem
accompanyingquestions that encourage that remains is eliminated as feces.
The digestive system includes two general components:
Translation of each of the gene C transcripts
students to think more carefully about the concept illus-
Learning Outcomes
generates many molecules of protein C. the digestive tract and the accessory organs (figure 24.1). The
1. Describe the functions of the main components of the upper digestive tract is a hollow tube that starts at the mouth and ends
and lower digestive tract.
trated in a figure.
2. Identify the functions of the liver and other accessory organs.
at the anus. When referring only to the stomach and the intes-
tines, the term gastrointestinal tract is often used. The acces-
3. Describe the significance of the normal intestinal microbiota. sory organs, which include the salivary glands, liver, and
pancreas, support the process of digestion by producing vital
The main purpose of the digestive system is to convert the enzymes and other substances that help break down food.
food we eat into a form that the body’s cells can use as a Like the respiratory system and the skin, the digestive tract
source of energy and raw materials for growth. It does this by is one of the body’s major boundaries with the environment.
FIGURE 7.4 The Level of Gene Expression Can Be Controlled
? How does the fact that mRNA is quickly degraded help a cell control gene
expression? Organ Function

Oral cavity Obtains and

processes food

Salivary Secrete saliva

Parotid salivary gland glands
Oral cavity containing Mumps
and0999x_ch07_178-205.indd 181 10/30/17 02:09 PM tongue and teeth Esophagus Transports food to
Dental caries stomach
Periodontal disease Salivary glands

Esophagus Stomach Stores food; mechanical

Esophagitis digestion; breaks down
some proteins

Introduce the body systems

Pancreas Secretes digestive
Stomach enzymes
Liver Gastritis
Hepatitis Gastric ulcer
Liver Produces bile to assist

Each disease chapter includes a stunning figure that intro-

Gallbladder Pancreas in fat digestion
Pancreatitis
Small intestine Gallbladder Stores bile until

duces the students to the anatomy of the body system. Enteritis

Duodenal ulcer Large intestine
Dysentery
needed

Appendix Colitis Small Site of most digestion

Appendicitis intestine and absorption
Rectum
Anus of nutrients

Food
molecules Large Absorbs some water
intestine and minerals;
Epithelial cells prepares waste
with microvilli Villus

Upper digestive tract

Lower digestive tract
Smooth
muscle
Capillaries
Nerve fibers
Lymphatic vessel

FIGURE 24.1 The Digestive System Some of the disease conditions that can affect the system are shown in red.
? What is the role of villi and microvilli in the small intestine?

ix
and0999x_ch24_623-663.indd 624 10/24/17 01:34 PM
 FOCUS ON UNDERSTANDING . . . First Pages

Student-Friendly Chapter Features

Confirming Pages

ell Structure

Provide the tools for understanding

Key Terms for each chapter are defined on the
26 Nervous System Infections
KEY TERMS
Arbovirus Arthropod-borne RNA
virus, carried by vectors such as
mosquitoes.
Blood-Brain Barrier Cells that work
Meninges Membranes covering the
brain and spinal cord.
Meningitis Inflammation of the
meninges.

opening page. together to restrict exchange between

the bloodstream and the brain.
Central Nervous System (CNS)
Brain and spinal cord.
Cerebrospinal Fluid (CSF) Fluid
produced in the brain that flows
within and around the CNS.
Encephalitis Inflammation
of the brain.
Peripheral Nervous System (PNS)
Division of the nervous system that
carries information to and from
the CNS.
Transmissible Spongiform
Encephalopathy (TSE) Chronic
degenerative brain disease caused
by prions; characterized by spongy
appearance of brain tissue.

to escape were captured and brought back in handcuffs. The Carville

10 µm (b) 10 µm leprosarium was finally closed and converted to a military-style acad-
Structure of West Nile virus particles. ©Science Picture Co/Getty Images
emy for high school dropouts in 1999.
aining agent sticks to and coats the flagella. This increases their diameter so they can be seen with the light Because the word leprosy carries centuries of dark overtones,
icum (peritrichous flagella); (b) Vibrio cholerae (polar flagellum). Source: Dr. William A. Clark/CDC A Glimpse of History many people prefer to use the term Hansen’s disease, a name that

ntifying bacteria? Share the history Today it is hard to appreciate the fear and loathing once attached to
leprosy (lepros, meaning “scaly”). The Bible refers to several disfig-
honors the discoverer of the causative bacterium.

N
uring skin diseases, including leprosy, and people suffering from the ervous system infections are frightening. They threaten
A Glimpse of History opens each chapter, featur- diseases are portrayed as filthy, outcast, or condemned by God for sin.
Moses called lepers “unclean” and proclaimed they must live away
a person’s ability to move, feel, or even think. Con-
sider poliomyelitis, which can result in a paralyzed
ing engaging stories about the men and women who from others. In the Middle Ages, lepers attended their own symbolic
burial before being sent away.
limb or the inability to breathe without mechanical assistance.
aracterize an organism. For dye that binds to structures in all cells; it can be used for Hansen’s disease (leprosy) can result in loss of fingers or toes
pioneered
gella distributed around thethe field of microbiology.
determining the total number of microbial cells in a sample.
Gerhard Henrik Armauer Hansen (1841–1912) was a Norwegian
physician with many interests, ranging from science to religion to
or deformity of the face. Infections of the brain or its covering
polar exploration. When he was 32 years old, Hansen went into medi- membranes can render a child deaf or intellectually disabled.
nt called peritrichous (peri Another fluorescent dye binds to all cells but is changed by cal research, and was named assistant to Dr. Daniel C. Danielson, a Before the discovery of antibiotics, bacterial infections of the
rs have a single flagellum cellular processes, so it can be used to distinguish between leading authority on leprosy. Danielson believed that leprosy was a nervous system were often fatal. Fortunately, these infections
hereditary disease of the blood and considered the idea that the dis- are uncommon.
ed polar (see figure 3.19). live and dead cells (see figure 3.8). Some fluorescent dyes ease was contagious as a “peasant superstition.” Hansen, however,

Define the expectations

ncluding a tuft of flagella at bind to the mycolic acids in the cell walls of Mycobacterium
species, making the dyes useful in a staining procedure simi-
disproved Danielson’s hypothesis in careful studies conducted over
a number of years. He found a unique bacterium associated with the 26.1 ■ Anatomy, Physiology,
disease in every leprosy patient he studied. His 1873 report of the
and Ecology of the Nervous
Learning outcomes are found
lar to the acid-fast stain. at the
mycolic acids beginning findings marked the first time that a specific bacterium was linked
to a disease—almost a decade before Koch’s proof of the cause of System
A special technique called immunofluorescence is
gs of each numbered used tosection,
tag specificallowing
cell componentsorganization,
with a fluorescent dye
tuberculosis.
In the United States, even during the first half of the twentieth Learning Outcomes

evaluation,
erve total cells, a subset of andattached
s on their surface, depending
One example is a fluorescent
assessment of instruction.
to an antibody (see figure 18.6). By tagging a protein
unique to a given microbe, immunofluorescence can be used
to detect and identify that organism. Antibodies, and how
they are obtained, will be described in chapters 15 and 18.
century, people diagnosed with leprosy risked having their houses
burned to destroy the source of infection. Their names were changed
to avoid embarrassing their family, and they were sent to a leprosarium
such as the one at Carville, Louisiana, surrounded by a 12-foot fence
topped with barbed wire. Sufferers were separated from spouses and
children and denied the right to marry or vote. Those who attempted
1. Describe how information flows through and between neurons.
2. Differentiate between the central nervous system and the
peripheral nervous system.
3. Explain how bone, cerebrospinal fluid, meninges, and the
blood-brain barrier protect the central nervous system.

antibody 694

and0999x_ch26_694-727.indd 694 11/02/17 11:32 AM

the community). Microbes that typically inhabit body sites for the commun
MicroAssessment 3.2
extended periods are resident microbiota, whereas temporary alter the m
Dyes are used to stain cells so they can be seen against an
unstained background. The Gram stain is the most commonly occupants are transient microbiota. Changes oc
used differential stain. The acid-fast stain is used to detect Assess understanding
Considering how important the microbiome is to human the host (su
Mycobacterium species. Specific dyes and techniques are
used to observe cell structures such as capsules, endospores, Ahealth,
MicroAssessment at is
relatively little theknown
end ofabout
each its
numbered
members.section
As the activitie
and flagella. Fluorescent dyes and tags can be used to observe
(b) 10 µm
total cells, a subset of cells, or cells that have certain proteins on
summarizes
described inthe concepts
chapter and isincludes
1, that quicklyreview questions,
changing, usu-
as several An intriguin
d Tags (a) To detect a
mple, a dye that binds mycolic
their surface. large-scale
ally featuringresearch
one thatefforts are studying
stimulates criticalthis diverse(indicated
thinking popula- ome was th
a modification of the acid-fast
nge was used to stain all other
4. What are the functions of a primary stain and a counterstain?
bytion. Thebulb
a light studies typically use metagenomics, the sequence
icon). microbiota
5. Describe one error in the staining procedure that would
ag specific molecules—in result in a Gram-positive bacterium appearing pink.
analysis of the DNA extracted directly from a given environ- Obese peop
cule unique to Streptococcus
s
6. What color would a Gram-negative bacterium be in an acid- ment, which allows scientists to investigate all microbes in thin individ
d to identify bacteria?
fast stain? a sample, including those that have not yet been grown in roidetes. As
culture. metagenomics biome chang
Researc
Engage the reader MicroByte microbiome
There are more bacteria in just one person’s mouth than there are example, the
MicroBytes found throughout the chapter provide small 10/31/17 11:19 AM
people in the world! (an imbalan
“bytes” of information, capturing the reader’s attention. disease. Alt
is too early
x
Composition of the Microbiome than showin
Babies begin acquiring their microbiota at birth, when they
 Confirming Pages

Part III Microorganisms and Humans 381

Highlight the relevance FOCUS ON A CASE

A 9-year-old boy with cystic fibrosis—
14.1
The patient was treated with antibiot- aeruginosa cells to form biofilms.

Focus on a Case boxes describe realistic clinical, veterinary,

a genetic disease that causes a number of ics, with only limited success. Like most The biofilm protects the bacterial
problems, including the buildup of thick cystic fibrosis patients, he developed a cells from various components of the
sticky mucus in the lungs—complained of chronic lung infection that continued to immune system, including antimicro-

or environmental situations, along with questions and discus- increasing fatigue, shortness of breath, and
worsening cough. When his mother took him
to the doctor, she mentioned that his cough
require repeated treatment.
1. What role did cystic fibrosis play in
bial peptides and phagocytes. Bacte-
ria growing within a biofilm are much
more difficult for the immune system
the disease process?
sions designed to highlight the relevance of the information. was productive, meaning that it contained
sputum (pronounced spew-tum). She was 2. What is the significance of the mucoid
phenotype of the colonies?
to destroy. EPS
3. Siderophores help the bacterium obtain
particularly concerned that the sputum was iron from the host. Recall that the
a blue-green color. His doctor immediately 3. How would the siderophore (the body produces iron-binding proteins,
suspected a lung infection by Pseudomonas iron-binding compound) benefit the including lactoferrin and transferrin;
aeruginosa—a common complication of bacterium? this prevents microbes from using the
cystic fibrosis. A sputum sample was col- 4. Why would the boy’s lung infection host’s iron and thereby limits their
lected and sent to the clinical laboratory. make his pre-existing respiratory growth. Microorganisms that make
In the clinical laboratory, the sample problems even worse? Confirming
siderophores Pagesessentially engage in a
was plated onto MacConkey agar and blood “tug-of-war” with the body over iron.
agar and incubated. Mucoid colonies sur- This tug-of-war is especially important
rounded by a bluish-green color grew on Discussion for P. aeruginosa because iron levels
both types of agar media. The colonies 1. Cystic fibrosis patients often have an influence biofilm formation. When
on MacConkey had no pink coloration, accumulation of thick mucus in their iron is limiting, P. aeruginosa cells
382 Chapter 14 The Innate Immune Response
so the medical technologist concluded lungs, which interferes with the muco- are motile and do not initiate biofilm
that the cells did not ferment lactose. She ciliary escalator and other first-line formation.

Provide perspective F O C U S Y O U Rnoted P E the R Sblue-green

PECTIV
plates and in the sputum, knowing that
For Schistosoma, the Inflammatory Response Delivers
P. aeruginosa makes several pigmented
E on1the
color 4.1 agar defenses. With a compromised (weak-
ened) mucociliary escalator, microbes
that are inhaled are not easily removed.
4. In response to a bacterial infection in
the lungs, an inflammatory response
develops. The capillaries in the area
Schistosoma species, compounds that flat-
give riselongitudinal
to colors ranging groove in which In headdition,
clasps his the accumulated
multiplies asexuallymucus in a specific become fresh- leaky, allowing fluids to enter
Focus Your Perspective boxes show how micro-
the parasitic
worms that cause thefrom yellow
disease to blue. One
schistoso- of thepartner
female pigments serves as
to live in life-long a nutrient water
embrace sourcesnail
for bacteria.
host. The infected the snail
tissues.thenThose fluids cover the
miasis (also called snail functions
fever oras a siderophore,
bilharzia), which is a mol-
(schistosoma 2. The mucoid
means “split-body,” refer- colonies suggest
releases large that the of cercariae,
numbers respiratory whichsurfaces, thereby interfer-

organisms and their products influence our lives in

use the immune response eculeto that
assistbinds
them iron. ring to the
in Another long slit). To bacterium
is impor- reproduce, the produces can infect a human host to ing
an extracellu- complete
with gas the exchange. In addition,
completing one portion tantoffortheir complex
biofilm formation. worms migrate
Further testing to the tiny lar veins of either
material parasite’s
that forms life cycle.
a capsule or a inflammation recruits neutrophils to
life cycle. the
showed that the bacterium was an oxidase-
schistosomiasis intestines or the bladder (depending on The
slime layer. This material, also referred symptoms of schistomiasis are
the area. Some of the neutrophils will

many different ways. A person can become

schistosomes by wading
positive, infected
withortheswimming
with
Gram-negative
physician’sininitial
water that contains a larval form of the par-
therod,
lays
schistosome
consistent species), where
hundreds of ova per day.
suspicions.
to the adult worms—which effectively
to astheextracellular
stances
female
In contrast
(EPS), allows
duepolymeric
to the manysub-
If these
ova that aredie,
ova are swept to thein liver
Pseudomonas
bloodstream, the resulting inflammatory
not releasing
expelled. the destructive enzymes
their by the as a result.
granules

asite called cercariae, which are released hide from the immune system—the eggs process and granuloma formation gradually
from infected snails. Cercariae penetrate provoke a strong inflammatory response. destroy liver cells. The cells are replaced
skin by burrowing through with the aid of This pushes the eggs to the closest body with scar tissue, causing the liver to mal- Confirming Pages
digestive enzymes. They then move into surface, in a manner similar to what is function. In turn, this results in a fluid
the bloodstream, where they mature into experienced as a sliver in the skin works its buildup in the abdominal cavity, as well
adult worms that canamountlive for overof pus in a confined
25 years. way out.region In the case constitutes
of speciesanthat abscess
deposit asmacrophages
malnutrition. and Chronic giant cells accumulate, and granulomas
schistosomiasis
Adult worms mask(see themselves
figure 22.2). from theabscess ova in veins near the intestine, the eggs are can also damage
form. the lungs
giant cells, and bladder, and
granulomas
immune system by coating The themselves
extent 21with pushed out into
of inflammation varies the intestinal
depending tract,onwherethe occasionally, the central nervous system.
various blood proteins, 546an Chapter
ability that pro-Respiratorythey are System Infections
eliminated in feces. Ova of spe- Despite their complex life cycle, Schis-
nature of the injury, but the response is localized, begins
vides them with a primitive stealth “cloak- cies that deposit the eggs near the bladder Damaging
tosoma species areEffectshighly successful para-
of Inflammation
immediately upon injury, and increases rapidly. A short-term
Introduce the concepts ing device.”
Schistosoma species
sexes, and the male
F O C have
inflammatory
characterized
U S separate
and female by
N P Nare
Oresponse
wormsan abundance
are
pushed
isE called
Ueliminated
M Oacute into the

of neutrophils.
age that contains
bladder,
N IinAinflammation
urine. If untreated
schistosome As eggs
where they
andsew-
the reaches
infec-
is
sites. Not only are they adept at avoiding
The inflammatory
certain immune responses
tem that lead
otherwise prevents
processthat
firedestruction,
to their
can be
from spreading
compared to a sprinkler sys-
would
they in a building. Although
manage to locate each Pneumonia
tion other in theisblood-
is brought a under
diseasefresh of thewater,
control, lower respiratory
resolution
the ova of tract
caninflammation
hatch, in which
releas- antibodies
the learned
have process are produced
tousually
exploit limitsduring
the a B-cell and
damage
inflammatory response, however,
restores phago-the
function,

Focus on a Disease boxes introduce a general cate- stream. The male’s the
body alveoli
has (aira deepsacs) ofing thea lungs fill withstage fluids such as pus cytes can
response remove
for itself
their own the microbes. mucociliary escalator, capsules,
begins. Neutrophils stop entering ciliated thelarvalarea, and that infects
macrophages and response canspread.
cause significant harm. One undesirable
and blood. It typically results from an inflammatory response to opsonization by antibodies
clean up the
microbial damage
infection of by
the ingesting
lungs, and dead is the cells
leading and debris.
cause of death As consequence
The damaging is that
effectssome enzymes are
of pneumonia andlargely
toxic aproducts con-
result of the
theduearea heals, new capillaries grow, destroyed tissues are tained withinresponse phagocytic cells are inevitably
agent. Asreleased, damag-
gory of disease (pneumonia, diarrheal disease, menin- as the membranes that replaced,
Signs
to infectious
surround
If the
and scar
and Symptoms
body’s
disease
tissueand
the brain
defenses
in the United
forms. spinal cord,
States.

cannot limit the infection,

sacrifices infected macrophages
chronic
inflammatory
ing tissues.
become
If
and interfere
leaky during
so that
inflammation
with
they
O2 and
to the
inflammation,
is limited,
causative
cannot playfluids
CO2 exchange. such asIn in
the capillaries
host collect in the alveoli
a response
addition, to a cut
phagocytes
the consequences canThe be severe, and even life-threatening.
of pneumoniaAs to include
an invader, and it also recruits various components of the
gitis, sexually transmitted infections), giving students
signs symptoms generally cough,
occurs. youThis is anda long-term inflammatory and other theleukocytes are recruitedby thetoprocess
the site isof normally
infection mini-
and
you learn more about inflammation
infectious
chills, shortness diseases,of breath, will
fever,notice that pain.immune
chest In severesystemcases, to thefinger,
region. damage caused
process that of can last forresult years. In(bluish
chronic mucus
mal. Ifproduction increases.
occurs Accumulating leukocytes and mucus
many of the most severe the effects
patient may infection
develop cyanosis from the skin inflammation,
color) due to the process in a delicate system, however, such
create a thick substance that may clog the alveoli, a condition
a framework for understanding specific diseases. inflammatory response.

Cell Death and the

poor blood oxygenation. Pneumonia ranges from mild to life-
threatening, depending largely on the causative agent but also on
any Inflammatory
underlying health problems Response of the patient. Some
MicroAssessment 14.8
The inflammatory
called consolidation. Consolidation is most common in severe
bacterial pneumonia.
pathogens response is initiated when microbes invade
The Confirming
inflammatory Pages response seen in severe
cause what is referred to as atypical pneumonia oror tissues are
“walking pneu- damaged.pneumonia
The outcome often affects nerve
is dilation of small endings
bloodin the pleura, causing pain.
In addition to traumatic cell death (necrosis) that results from
monia,” a term that reflects the mild symptoms. vessels, Pneumonias leakage are of fluids from those vessels, and migration
Epidemiology
tissue damage, host cells can self-destruct. This capability
often accompanied by a productive cough, meaning that a pus- and of leukocytes out of thePneumonias
bloodstreamare andoften
into categorized
the tissue. as either community-acquired,
allows the host to eliminate any
mucus-containing 381cells
and0999x_ch14_362-385.indd
no longer needed,
fluid called sputum comes up from and Inflammation
the lungs.helps contain meaningan infection,
that theybut the response
develop in members of the general 11/01/17 public,05:01
or PM
it
16also serves
Chapteras1a mechanism
Humans To forMicrobial
anddiagnose
the sacrificing World “self”
pneumonia, cells that
a physician itself can be
uses a stethoscope to damaging.
lis- Apoptosis destroys “self”
healthcare-associated, cells without
meaning that they develop in hospital-
might otherwise spreadten anforinfection. One type
a characteristic of programmed
crackling or bubbling sound initiating
that occurs inflammation;
in pyroptosis
ized patientstriggers
or otheranpeopleinflammatory
within the healthcare system. Some
response.

Inspire the learner

cell death avoids an inflammatory
the lungs as air response,
passes bywhereas fluid in another
the alveoli. A chest X ray will types of community-acquired pneumonia (CAP) are contagious.
FOCUS ON THE FUTURE 1.1 Most, however, originate from the patient’s own upper respira-
type promotes one. likely be done to determine which parts of the lung 22.are infected;
Describe two general events that can initiate inflammation.
Meet the Microbiomes!
Apoptosis areas of “off”;
(apo means infection usually
ptosis meansappear as white shadows.
“falling”) 23. TheDescribe patient two changestory inmicrobiota.
cells undergoing These apoptosis.
organisms may gain access to the lungs
is As
a programmed cell may
death alsothatbe does
askednot to give
triggera sputum
an sample, which can be exam-
inflam- when a person inadvertently inhales his or her own throat secre-
24. Infection of the fallopian
discussed, tubes can lead to infertility. Why
you study this textbook, you will prob- andthat could be onto grown in the laboratory, and tions. As the HumanCAPs,Microbiome Project
Focus on the Future boxes describe pending chal-
ined apoptosis,
microscopically inoculated appropriate laboratory with healthcare-associated pneumonias (HAPs)
matory response.
amazed During the dying we cells
now undergo
know would repre-this be so?led to greater insight into the role of micro-
ably be by how
media much
as part weofknowthe process to identify athat those or
bacterial examples
fungal cause often occur when the patient inadvertently inhales his or her own
certain
about changes. For example,
the microbial the
Youshape have of the sentcell less changes,
than 1% of all microbes. Compli- organisms in health and disease. It also
ofworld.
pneumonia. upper respiratory microbiota. Patients at particular risk are those

lenges facing current and future microbiologists.

enzymes
already cut
read,the
forDNA,
example, andthatpieces of the cellcating
the human bud theoff,matter
effec-even more is the fact that opened on
up many new areas for research. For
mechanical ventilators used to help breathing, because the ven-
Pathogenesis a microorganism’s example, how many disease states are due
microbiome
tively shrinking affects our
the cell. well-being,
Some changes andappear to serve as a behavior 14.9 in the■labora-Fever tilator tube allows a portal for microorganisms to enter the lower
that life
signal on this planet Microbes
to macrophages could
that notthe that
exist cause
remainswith-of pneumonia
torycell
the canareare
be often
quite
to be opportunists
different from that cause
that in a to imbalances in our normal microbiota?
airways.
out microbes. But thedisease more you only when
learn, thethe mucociliary
natural situation. escalator
So, yes, or other
we know defenses
a great Can we treat any of those by packaging
engulfed without the events associated with inflammation. Learning Outcome Treatment and Prevention
more you will realizeofhow the little
respiratory
we actu-tractdeal, are but not itfunctioning
really represents optimally.
only the Condi-
tip of certain microbes as an oral pill? Can we
If the pattern recognition
ally know! Although tions
receptors in a macrophage’s 13. Describe the induction
track andmicrobial
the outcomes of fever.
profiles of an individual
that have
scientists stud-withthe
interfere theiceberg.
function of the mucociliary esca- Bacterial and fungal pneumonias are treated with antimicrobial
cytoplasm are triggered,
ied microorganisms for that
hundreds
lator includecellofalcohol
might
years, and initiate Thepyroptosis
narcotic depth
use as of well
our understanding
as viral respiratory about tomedications,
predict changes chosenin health?
according ThetoNational
the susceptibility of the causative
(pyro
mostmeans
of the“fire”).
advances Unlike apoptosis,
occurred
infections this programmed
afteras the
such influenza.microbialThat is self-patients
communities
why isFever
rapidly
who have isincreasing
aninflu-
important host defense
Microbiome
agent. Unfortunately,mechanism
Initiative now andthat
promises
bacteria ato strong
pro-
cause healthcare-associated
destruction
start of thetriggers
GoldenanAge inflammatory
enzaoforMicrobiology. response.that
other illnesses Thus,
due pyroptosis
to what
damage could indication
be considered
the respiratory tractthe of
orGolden infectious
inter- vide disease,
additionalparticularly
pneumonias areinsights, buta will
bacterial
also lead
often multi-drug-resistant. one.In general, there are no
Most studies focusedfere on with
microorganisms
the patient’s ability Age ofto Microbiomes.
cough are moreAssusceptible was already to toeffective
many new questions.for viral pneumonias.
treatments
developing pneumonia. Organisms that cause pneumonia fre- Vaccines are available to prevent pneumococcal disease but
quently make a capsule. Because of the capsule, alveolar mac- not the other types of pneumonia. Prevention therefore involves
rophages that normally destroy invading microbes in the lungs staying out of crowded situations and avoiding other respiratory
cannot effectively eliminate the pathogen initially. Once opsonizing illnesses.
Summary
and0999x_ch14_362-385.indd 382 11/01/17 05:01 PM

1.1 ■ The Dispute over Spontaneous Generation

Microorganisms in the Environment
The belief in spontaneous generation was challenged by Francesco
∙ 
Summary briefly reviews the key points. Pneumococcal
Redi in the seventeenth century. Pneumonia Microorganisms replenish blood
the O2oxygenation
require to breathe and theyple
Pneumococci are an important cause of community-acquired
who the
convert survive
leads
that humans and
without
nitrogen
to cyanosis
other animals (bluish skin color). Peo-
gas in treatment
the air into sweat heavily as tempera-
Early Experiments a form that other organismsture
canfalls
use. to normal after 7 to 10 days.
∙ 
Short Answer questions review major chapter concepts. pneumonia
The experiments of John
pneumonia
ous generation while those
(CAP), accounting
Needham supported
patients
of Lazzaro requiring
Spallazani
for about 60% of the adult
the idea of spontane-
Commercial Benefits of Microorganisms
hospitalization.
did not.
∙ 
Multiple Choice questions allow self-testing; answers are pro- Review the information
Microorganisms are used Causative
in the production
Agent of bread, wine, beer,
Experiments of Pasteur and cheeses. Bacteria are used to degrade toxic pollutants as well as
Signs and Symptoms
The experiments of Louis Pasteur disproved spontaneous genera- Pneumococcal pneumonia is caused by Streptococcus pneu-
to synthesize a variety of different useful products. Biotechnology
vided in Appendix IV. Typical
tion and supported what
(figure 1.2).
is now signs
known and
as thesymptoms of pneumococcal
theory of biogenesis dependspneumonia
on members of themoniae,
start after an incubation of 1 to 3 days. They are usually pre-
microbiala world.
Gram-positive diplococcus known as pneumococ-
cus. The cells, which are often elongated with a tapered end,
∙ 
Application questions provide an opportunity to use knowledge End-of-chapter review encourages students to revisit the
Experiments of Tyndallceded
John Tyndall showed gestion,
by 1 to 2 days of runny nose and upper
that someafter which the are
person experiences
respiratory con-
Microorganisms
sudden
are wonderful
Microbes as Research Tools
are referred to as lancet-shaped
model organisms (figure 21.11). (A lancet is
to study because
microbial forms not killed by they havefever
the same a surgical
and fundamental instrument
metabolic withproperties
and genetic a pointed end.) The most striking
of microbiology to solve real-world problems. information.
boiling. He and Ferdinand
resistant forms of some
Cohnchills.
shaking
bacteria.
breath
discovered
The endospores,
severe chestthepain
heat-is aggravated
or cough, causing shallow, rapid breathing. becauseBlood
byforms.
as higher life
from
bacteria
characteristic
each Experimental
capsule,
grow rapidly
of S.
results can
which
on simple,
pneumoniae
be obtained
is responsible
inexpensive
is its thick polysaccharide
quickly
for the organism’s virulence.
growth media.

∙ 
Critical Thinking questions encourage practice in analysis and the lungs
The Golden Age of Microbiology makes the sputum pinkish or rust-colored;
The field of microbiology blossomed after Pasteur and others
poor
Microbes and Disease There are over 90 different serotypes of S. pneumoniae, each
Pathogens cause disease, but the death rate from infectious dis- Confirming Pages
disproved spontaneous generation, leading to the Golden Age of
problem solving that can be used by the student in any subject. Microbiology. Discoveries during this time led to the acceptance
of the Germ Theory of Disease.
eases has declined over the past 100 years or so as a result of
disease-prevention efforts including vaccination (figure 1.4). More
needs to be done to prevent emerging infectious diseases, some
The Scientific Method of which are new or newly recognized (figure 1.5). Some chronic dis-
The scientific methodand0999x_ch21_531-573.indd
includes (1) observing an occurrence and eases are caused by microorganisms.
546 11/01/17 04:53 PM
asking a question about that situation; (2) developing a hypothesis
that explains the occurrence and devising an experiment that tests 1.3 ■ Members of the Microbial World
the hypothesis; (3) doing the experiment, collecting the data, and Considering that small size is the only shared Partfeature of all
III Microorganisms and Humans 457
drawing conclusions; and (4) communicating the results, methods, microbes, the group is tremendously diverse (figure 1.6). All living
and conclusions. A scientific theory is an explanation supported organisms are classified into three domains: Bacteria, Archaea,
by a vast body of experimental evidence. and Eukarya (table 1.1). The small size of microbes requires mea-
The Immune Wars The surements
Pathogens not commonly used in everyday life
Fight Back The(figure 1.7).
Return of the Humans

Build the story Innate1.2 ■ Microbiology: A Human Perspective

Immunity (chapter 14) Pathogenesis Scientific
(part of Names
chapter 16) (Knowledge Is Power)
Adaptive Immunity
The Human (chapter 15)
Microbiome The first part of a scientific name indicates Immunization
the genus, and (part
the of chapter 18)
The normal microbiota is essential to human health. The second part the species; these are written inEpidemiology
italics or underlined
(chapter 19)
microbiome is an interacting community of microorganisms as (table 1.2). Members of the same species can vary, so strain designa-
Logical chapter order helps students understand
Antimicrobial Medications (chapter 20)
well as their genetic information. tions are sometimes used.

and connect the concepts. FIGURE 18.1 The Host-Pathogen Trilogy

? How does immunization prevent disease?

and0999x_ch01_001-018.indd 16 10/30/17 12:16 PM

IMMUNIZATION xi

18.1 ■ Principles of Immunization certain diseases, and (3) block the action of microbial toxins.
 FOCUS ON UNDERSTANDING . . .
Student-Friendly Descriptions
Include analogies Confirming Pages

WHY? Analogies provide students a comfortable framework for making sense

Confirming Pages
of difficult topics. Here’s an example from chapter 14.
Focus Figure
Security walls Security cameras Security teams

Innate Immunity The innate immune system has three Part I Life and Death of Microorganisms 145
Prevent entry Detect invaders Eliminate threat

general
TABLE 6.1 components:
Electron Carriers first-line defenses, sensor systems,
and innate effector actions. As a useful analogy, think of the
Carrier
Oxidized Form
(Accepts Electrons)
Reduced Form
(Donates Electrons)
Typical Fate of
Electrons Carried
(a)

defense systems of a high-security building or compound: First-line defenses Sensor systems Innate effector actions
–

The first-line defenses are the security walls surrounding e Prevent microbial entry Detect damage and microbial Eliminate invader
invasion
Electron Electron
carrier Interferon response

the property; the sensor systems are the security cameras

Nicotinamide adenine dinucleotide (carries 2 NAD+ + 2 e– + 2 H+ ⇌ NADH + H+ Used to generate a proton motive
Skin and mucous
membranes
Pattern recognition
receptors (PRRs)
Phagocytosis
electrons and 1 proton) force that can drive ATP synthesis
scattered throughout the property, monitoring the environ-
Flavin adenine dinucleotide (carries 2 electrons
and 2 protons; i.e., 2 hydrogen atoms)
FAD + 2 e– + 2 H+ ⇌ FADH2 Used to generate a proton motive
force that can drive ATP synthesis
Antimicrobial Complement system Complement activation
substances

ment for signs of invasion; and the effector actions are the
Nicotinamide adenine dinucleotide phosphate
(carries 2 electrons and 1 proton)
NADP+ + 2 e– + 2 H+ ⇌ NADPH + H+ Biosynthesis Inflammatory response

security teams sent to remove any invaders that have been

Fever

carried by NADPH have an entirely different fate; they are When E. coli cells degrade glucose molecules, they use
used to detected,
reduce compoundsthereby eliminating steps that not (figure
theof threat 14.1a). (b)
during biosynthetic reactions. a series only release energy but also form a FIGURE 14.1 Defense Systems (a) Systems that protect a high-security compound. (b) Components of innate immunity that protect the body
Note, however, that many microbial cells can convert reduc- dozen or so precursor metabolites. Other organisms use the against infection. a (left): ©Steve Cole/E+/Getty Images; a (middle): ©James Lauritz/Photodisc/Getty Images; a (right): ©Moodboard/Brand X Pictures/Getty Images

ing power in the form of NADH to NADPH. same steps but sometimes lack the ability to convert a certain ? What is the role of the sensor systems in innate immunity?

precursor metabolite into a compound needed for biosynthe-

Precursor Metabolites
Certain intermediates of catabolic pathways can be used in ana-
bolic pathways. These intermediates—precursor metabolites—
Emphasize the logic
serve as carbon skeletons from which subunits of macromolecules
can be made (table 6.2). For example, the precursor metabolite
pyruvate can be converted to any one of three amino acids: ala-
WHY? Descriptions that emphasize the logic of processes make it easier for
nine, leucine, or valine.
sis. Any essential compounds that a cell cannot synthesize
must be provided from an external source. glucose-salts medium
A cell’s metabolic pathways make it easy for that cell
to use glucose for multiple purposes. Think of the cells as
extensive biological recycling centers that routinely process
millions of glucose molecules (figure 6.9). Molecules that
remain on the central deconstruction line are oxidized com-
pletely to CO2, releasing the maximum amount of energy.
destroying pathogens while maintaining relatively stable con-
ditions within the human body—a state called homeostasis
(homeo means “similar” and stasis means “standing still”).
Failure to do that can be deadly.
Like other multicellular organisms, the human body
has several mechanisms of defense. Innate immunity is the
routine protection present at birth; it is germ-line encoded,
meaning that it is passed from one generation to the next, and
includes anatomical barriers as well as certain cell types and
To simplify the description of the immune system, it is
helpful to consider it as a series of individual parts. This chap-
ter will focus almost exclusively on innate immunity. Remem-
ber, however, that although the various parts are discussed
separately, their actions are connected and coordinated. In fact,
as you will see in chapter 15, certain components of the innate
defenses educate the adaptive defenses, helping them recog-
nize that a particular antigen represents a microbial invader.

Recall from chapter 4 that E. coli can grow in glucose-
students to understand and retain the information. Here’s an example from
salts medium, which contains only glucose and a few inor-
ganic salts. This means that the glucose is serving two
chapter 6.
purposes in the cell: (1) the energy source, and (2) the
starting point from which all cell components are made—
Some breakdown intermediates, however, can exit that line
chemicals. In addition to innate immunity, vertebrates have
to be used in biosynthesis. The exit points are located at the evolved a more specialized defense system, providing protec- 14.1 ■ Overview of the Innate
steps immediately after a precursor metabolite is made. So tion called adaptive immunity. This develops throughout life Immune Defenses
once a precursor metabolite is made in catabolism, it can
be further oxidized to release energy, or it can be used in
as a result of exposure to microbes or certain other types of for-
eign material, and substantially increases the host’s ability to Learning Outcome
GLUCOSE

2 Pentose phosphate Yields

1 Glycolysis

including proteins, lipids, carbohydrates, and nucleic acids. biosynthesis. defend itself. The substance that causes an immune response is ~ ~
pathway + Reducing

1. Outline the fundamental components of the innate defenses.

Starts the oxidation of glucose
Oxidizes glucose to pyruvate
ATP
power

by substrate-level
called an antigen. Each time the body is exposed to an antigen, phosphorylation

the adaptive defense system first “learns” and then “remem-

Glucose molecules The innate immune system has three general components: first-
bers” the most effective response to that specific antigen; it line defenses, sensor systems, and innate effector actions. As a
TABLE 6.2 Precursor Metabolites then reacts accordingly if the antigen is encountered again. An useful analogy, think of the defense systems of a high-security
Precursor Metabolite Pathway Generated Biosynthetic Role important action of the adaptive immune response is the pro- building or compound: The first-line defenses are the secu-
Yields Reducing
power

duction of proteins called antibodies. These bind specifically rity walls surrounding the property; the sensor systems are the
Biosynthesis 5 Fermentation
Glucose-6-phosphate Glycolysis Lipopolysaccharide to antigens, thereby targeting them for destruction or removal security cameras scattered throughout the property, monitoring Reduces pyruvate
or a derivative

Fructose-6-phosphate Glycolysis Peptidoglycan by other host defenses. The adaptive immune response can the environment for signs of invasion; and the effector actions
Pyruvate Pyruvate Acids, alcohols, and gases

Dihydroxyacetone phosphate Glycolysis Lipids (glycerol component) alsoTo:

Lipid
To:
destroy the body’s own cells—referred
Amino acid to as host cells are the security teams sent to remove any invaders that have
3a Transition step
CO2 CO2

3-Phosphoglycerate Glycolysis Proteins (the amino acids cysteine, glycine, and serine)
or “self” cells—that are infected with
synthesis
a virus or other invader.
synthesis
been detected, thereby eliminating the threat (figure 14.1a).
Yields
Reducing
power

Acetyl- Acetyl-
CoA CoA

Phosphoenolpyruvate Glycolysis Proteins (the amino acids phenylalanine, tryptophan, and tyrosine) 363
Pyruvate Glycolysis Proteins (the amino acids alanine, leucine, and valine)
x2 CO2

Ribose-5-phosphate Pentose phosphate cycle Nucleic acids and proteins (the amino acid histidine) To: To:
Carbohydrate Nucleic acid CO2

Erythrose-4-phosphate Pentose phosphate cycle Proteins (the amino acids phenylalanine, tryptophan, and tyrosine) synthesis synthesis 3b TCA cycle
Incorporates an acetyl
and0999x_ch14_362-385.indd 363 group and releases CO2 11/01/17 05:01 PM
Acetyl-CoA Transition step Lipids (fatty acids) (TCA cycles twice)

α-Ketoglutarate TCA cycle Proteins (the amino acids arginine, glutamate, glutamine, and proline) Yields
~ ~ + Reducing
power
ATP
Oxaloacetate TCA cycle Proteins (the amino acids aspartate, asparagine, isoleucine, lysine, methionine, by substrate-level
phosphorylation
4 Cellular respiration
Uses the electron transport
chain to convert reducing
and threonine) power to proton motive force

CO2 molecules + energy

Yields
~ ~
ATP
by oxidative
phosphorylation

and0999x_ch06_139-177.indd 145 10/30/17 01:59 PM

Introduce the players Certain intermediates Reinforce the concept A cell’s Put the pieces
of catabolic pathways can be used in anabolic path- metabolic pathways make it easy for together Three key
ways. These intermediates—precursor metabolites— that cell to use glucose for multiple metabolic pathways—
serve as carbon skeletons from which subunits of purposes. Think of the cells as exten- the central metabolic
macromolecules can be made (table 6.2). sive biological recycling centers that pathways—gradually
routinely process millions of glucose oxidize glucose to CO2
molecules (­figure 6.9). Molecules (figure 6.10). The path-
that remain on the central decon- ways are catabolic, but
struction line are oxidized completely the precursor metabo-
to CO2, releasing the maximum lites and reducing
amount of energy. Some breakdown power they generate
intermediates, however, can exit that can also be diverted for
line to be used in biosynthesis. use in biosynthesis.
xii
 Confirming Pages

Contents xxix

Student-Friendly Disease Presentations

24 Digestive System Infections 623 25 Blood and Lymphatic Infections 664

Help students think like experts A Glimpse of History 623

Key Terms 623
A Glimpse of History 664
Key Terms 664

Within each body system chapter, diseases are24.1separated

and Ecology of theby
Anatomy, Physiology, 25.1 Anatomy, Physiology, and
Ecology of the Blood and

major taxonomic category (bacteria, viruses, fungi,Thep­ Upper

rotozoa).
Digestive System 624
Digestive ©Garry Watson/Science Source
Lymphatic Systems 665
The Heart 665 ©Susumu Nishinaga/Science Source

This organization reflects a major consideration with respect

System 625
The Lower Digestive System 626
to treatment options, an important consideration
UPPERfor students
DIGESTIVE SYSTEM INFECTIONS
going into healthcare-related fields. 24.2 Bacterial Diseases of the Upper Digestive
System 627
684 Chapter 25 Blood and Lymphatic Infections
TABLE 25.12 Dengue Fever, Chikungunya, and Zika Virus Disease Compared
Dengue Fever
Signs and symptoms Often asymptomatic; fever, headache,
rash, and severe joint pain; in
dengue hemorrhagic fever (DHF),
bleeding and shock can occur, as
well as disseminated intravascular
coagulation (DIC).
Incubation period Usually 4 to 7 days
Causative agents Dengue virus serotypes DENV1,
DENV2, DENV3, and DENV4; RNA
virus of Flaviviridae
Pathogenesis Pro-inflammatory cytokines cause
leaky blood vessels, dehydration, and
hemorrhaging. In DHF, DIC and shock
may be fatal.
Epidemiology Mosquito-borne; found predominantly
in tropical and subtropical regions
but range is increasing; DHF usually
occurs in children under 15 years old.
Treatment and prevention Treatment: analgesics for pain; oral
rehydration therapy and blood or
platelet transfusions if bleeding
occurs. Prevention: vector control;
vaccine in limited areas.
Chikungunya
Chikungunya (pronounced chik-en-gun-ye), commonly
Chikungunya
Similar to dengue fever, but followed
by severe joint pain that may become
chronic
Usually 3 to 7 days
Chikungunya virus; RNA virus of
Togaviridae
Release of cytokines that affect
immune cells; bone destruction.
Mosquito-borne; mainly in Africa
and Asia, but now in Europe and the
Americas.
Treatment: analgesics for pain and
oral rehydration. Prevention: vector
control.
by affecting the immune system. Infection stimulates sig-
nificant release of cytokines and eventual decrease of helper B 651
Blood Vessels 665
Lymphatics (Lymphatic Vessels) 665
Spleen 666
25.2 Bacterial Diseases of the Blood and Lymphatic
Systems 666
Infective Endocarditis 666
Dental Caries (Tooth Decay) 627
Sepsis and Septic Shock 667
Periodontal
Rev.Confirming Pages Disease 629
Plague (“Black Death”) 669
Acute Necrotizing Ulcerative Gingivitis 630
Lyme Disease 671
Helicobacter pylori Gastritis 631
Vibrio vulnificus Infection 674
24.3 Viral Diseases of the Upper Digestive System 634 Tularemia (“Rabbit Fever” or “Deer Fly Fever”) 675
Oral Herpes Simplex (Cold Sores) 634 Brucellosis (“Undulant Fever” or “Bang’s Disease”) 676
Mumps 635
25.3 Viral Diseases of the Blood and Lymphatic
Zika Virus Disease
LOWER DIGESTIVE SYSTEM INFECTIONS Systems 678
Usually asymptomatic; mild disease
with fever, rash, joint pain, red eyes; Infectious Mononucleosis (“Mono” or “Kissing
FOCUS
rare nervous system ON DIARRHEAL
involvement; DISEASES 637 Disease”) 678
congenital Zika syndrome
24.4 Bacterial Diseases of the Lower Digestive System 637 Ebola Virus Disease (EVD) and Marburg Virus
Cholera 638 Disease (MVD) 680
2 to 14 days
Shigellosis 639 Yellow Fever 681
Zika virus; RNA virus of Flaviviridae
Escherichia coli Gastroenteritis 641 Dengue Fever 681
Salmonella Gastroenteritis 643 Chikungunya 684
Virus binds to receptors on a variety
of cells; enters fluid aroundTyphoid
fetus and and Paratyphoid Fevers 645 Zika Virus Disease 685
Campylobacteriosis 645
brain; affects neural stem cells.
25.4 Protozoan Diseases of the Blood and Lymphatic
Clostridium difficile Infection (CDI) 646
Mosquito-borne and sexually Systems 686
transmitted; females should avoid
24.5 Viral Diseases of the Lower Digestive System—
pregnancy for 8 weeks after Malaria 686
exposure; males should use condoms
for 6 months. Intestinal Tract 648
FOCUS ON A CASE 25.1 683
Rotavirus Gastroenteritis 648
Treatment: no specific treatment.
Prevention: vector control.
Norovirus Gastroenteritis 649 SUMMARY 691
REVIEW QUESTIONS 692
24.6 Viral Diseases of the Lower Digestive System—
Liver 650
Hepatitis A 650 26 Nervous System Infections 694
Hepatitis
A Glimpse of History 694

Provide a consistent conceptual framework

T cells. Severe joint disease may be related to loss of bone C 654
Hepatitis
known as CHIK, got its name from an African word meaning
cells as a result of viral infection. Key Terms 694
“that which bends up” because people with the disease show
bent posture due to severe joint pain. Although CHIK is not a 24.7 Protozoan Diseases of the Lower Digestive
Epidemiology
System 655 26.1 Anatomy, Physiology,
new disease, there have been several recent outbreaks, mak-
ing it an emerging disease.
CHIK occurs mainly in Africa, Asia, and Southeast Asia,
where the mosquito vectors are common. Recent Giardiasis
epidem- 655 Disease discussions are separated into consistent subsec-
and Ecology of the
Nervous System 694
ics have occurred in several other areas, however,Cryptosporidiosis
associated (“Crypto”) 656
tions, providing a conceptual framework and breaking the
Signs and Symptoms ©Science Picture Co/Getty Images
The signs and symptoms of CHIK are similar to those of den- with the inadvertent introduction and spread of theCyclosporiasis
mosquito 657
A. albopictus. This vector is now present in Brazil, Central CENTRAL NERVOUS SYSTEM INFECTIONS
gue and include fever that typically lasts 2 to 5 days, followed
America, the United States, and many EuropeanAmebiasis
countries, 658
by severe joint pain (especially in the extremities—fingers,
toes, wrists, and ankles) that can persist for weeks or months. where it has adapted to favorable environmental conditions. material into “bite-sized” pieces.
FOCUS ON MENINGITIS 697 Confirming Pages
In 2013, Chikungunya virus was reportedFOCUS ONtime
for the first A CASE
in 24.1 633
Sometimes patients develop chronic joint pain that differenti- 26.2 Bacterial Diseases of the Central Nervous
ates CHIK from dengue fever. Patients often develop a rash. Caribbean nations. Since then, it has spread throughout the
Americas. SUMMARY 661 System 697
Nonspecific symptoms include headache, conjunctivitis and
photophobia, back pain, nausea, and general malaise. The dis- REVIEW QUESTIONS 662 570 Pneumococcal Meningitis 698
Chapter 21 Respiratory System Infections
Treatment and Prevention
ease is seldom fatal.
There is no specific treatment for CHIK. Analgesics and non-
Causative Agent steroidal anti-inflammatory drugs such as ibuprofen are used Diseases in Review 21.1
CHIK is caused by chikungunya virus, an enveloped, single- to reduce the joint pain. Fluids are given to reduce dehydration
stranded RNA virus of the Togaviridae family. It is transmitted from fever. As with most mosquito-borne diseases, CHIK can Respiratory System Diseases
by Aedes mosquito species, mostly A. aegypti and A. albopictus. be prevented by effective vector control—destroying the vec-
tor and protecting the population by use of insect repellents
Pathogenesis and0999x_fm_i-xxxii.indd
and insecticide-impregnated mosquito netting. A vaccine for xxix Disease Causative Agent Comment 11/02/17 01:59 PM Summary Table
The disease mechanism of chikungunya is largely unknown, CHIK is currently in clinical trials. The main characteristics BACTERIAL INFECTIONS OF THE UPPER RESPIRATORY TRACT

but it appears, like dengue fever, to cause its damaging effects of chikungunya are presented in table 25.12. Conjunctivitis (pink eye), otitis
media (earache), sinus infection
Streptococcal pharyngitis
(“strep throat”)
Diphtheria
and0999x_ch25_664-693.indd 684 11/02/17 11:26 AM
VIRAL INFECTIONS OF THE UPPER RESPIRATORY TRACT
Common cold
Adenovirus pharyngitis
Usually Haemophilus
influenzae or Streptococcus
pneumoniae
Streptococcus pyogenes
(group A streptococcus)
Corynebacterium
diphtheriae
Rhinoviruses and other
viruses
Adenoviruses
Often occur together; factors involved in the transmission are
unknown.
Treated with antibiotics, partly to avoid sequelae; must be Table 21.3
distinguished from viral pharyngitis, which cannot be treated with
antibiotics.
Toxin-mediated disease characterized by pseudomembrane in Table 21.4
the upper respiratory tract. Preventable by vaccination.
Runny nose, sore throat, and cough are due to the inflammatory Table 21.5
response and cell destruction.
Similar to the common cold but with fever; spread to the lower Table 21.6
respiratory tract can result in severe disease.

Summarize each disease’s characteristics BACTERIAL INFECTIONS OF THE LOWER RESPIRATORY TRACT
Pneumococcal pneumonia Streptococcus pneumoniae Organism common in the throat of healthy people; causes
disease when mucociliary escalator is impaired or with
underlying conditions. Vaccine that protects against multiple
Table 21.7

Summary tables serve as brief reminders of the important features of each

strains is available.
Klebsiella pneumonia Klebsiella species, Common hospital-acquired bacterium; characterized by thick, Table 21.7
commonly K. pneumoniae bloody, jelly-like sputum. Drug resistance is a major problem.

disease. Major diseases are represented with an enhanced summary table

Mycoplasmal pneumonia Mycoplasma pneumoniae Relatively mild pneumonia; common among college students Table 21.7
(“walking pneumonia”) and military recruits. Cannot be treated with medications that
inhibit cell wall synthesis.
Pertussis (“whooping cough”) Bordetella pertussis Characterized by frequent violent coughing. Preventable by Table 21.8

that includes an outline of the disease process keyed to a human figure, Tuberculosis (“TB”) Mycobacterium tuberculosis
vaccination.
Most infections result in latent tuberculosis infection (LTBI), but
these can reactivate to cause tuberculosis disease (TB disease).
Table 21.9

showing the entry and exit of the pathogen.

Legionellosis (“legionnaires’
disease”)
Inhalation anthrax
Legionella pneumophila
Bacillus anthracis
Treated using combination drug therapy, but drug resistance is
an increasing problem.
Transmitted via aerosolized water drops; smokers and those with Table 21.10
impaired defenses are most at risk of developing disease.
Rare zoonotic disease; may be associated with bioterrorism; Table 21.11
high case-fatality rate.

Review the diseases as a group VIRAL INFECTIONS OF THE LOWER RESPIRATORY TRACT
Influenza (“flu”) Influenza viruses New vaccine developed yearly; viruses change seasonally due
to antigenic drift; antigenic shifts cause pandemics.
Table 21.12

Respiratory syncytial virus RSV Serious disease in infants, young children, and the elderly. Table 21.13

Each disease chapter ends with a table that summarizes the key features of
infections
Hantavirus pulmonary syndrome Hantaviruses Acquired via inhaled dust contaminated with rodent saliva, urine, Table 21.14
or feces. Frequently fatal.

the diseases discussed in that chapter. SARS and MERS Coronaviruses

FUNGAL INFECTIONS OF THE RESPIRATORY TRACT
Coccidioidomycosis Coccidioides immitis
Emerging zoonotic diseases.

Environmental reservoir (soil in semi-arid desert areas); most

Table 21.15

(“valley fever”)
Histoplasmosis (“spelunker’s
disease”)
Pneumocystis pneumonia (PCP)
Histoplasma capsulatum
Pneumocystis jirovecii
(formerly carinii)
Table 21.16
infections are asymptomatic.
Environmental reservoir (soil enriched with bird or bat Table 21.17
droppings); most infections are asymptomatic.
Organism is an opportunistic fungus that causes serious lung Table 21.18
disease in immunocompromised people, such as those with
HIV/AIDS.

and0999x_ch21_531-573.indd 570 xiii

11/01/17 04:53 PM
 UPDATES—Maintaining
the Cutting Edge
Global Changes
■ Continued “wordsmithing” to improve the clarity and
readability of the descriptions
■ Updated disease statistics, vaccine recommendations,
treatments, and terminology
■ Replaced former “Future Opportunities” boxes with
“Focus on the Future” boxes
■ Deleted some boxes to make room for updates and other
changes
New! “Focus on . . . ” Disease Boxes
These boxes cover a general category of disease, giving
students a framework and the terminology for understand-
ing the more focused coverage of individual diseases. In
essence, they help students see the “forest” before learning
about the “trees.”
■ Chapter 21—Focus on Pneumonia
■ Chapter 24—Focus on Diarrheal Diseases
■ Chapter 26—Focus on Meningitis
■ Chapter 27—Focus on Sexually Transmitted Infections
Key Changes in Individual Chapters
Chapter 1 – Humans and the Microbial World
■ Retitled and expanded the section on the normal micro-
biota (now The Human Microbiome)
■ Added information about the National Microbiome Ini-
tiative (NMI)
■ Added congenital Zika syndrome to the list of emerging
diseases
■ Substituted MERS for SARS in the discussion of evolu-
tion of pathogens to infect new hosts
Chapter 2 – The Molecules of Life
■ Simplified the discussion of polysaccharide structures
■ Updated the discussion of D-amino acids
■ Added a table showing relative electronegativities of
common atoms in biology (table 2.3)
xiv
Chapter 3 – Microscopy and Cell Structure
■ New section on super-resolution microscopes, including
an accompanying figure (figure 3.9)
■ Retitled the section on atomic force microscopes (now
Scanning Probe Microscopes)
■ Modified the headings in the cell structure sections to
provide clearer distinction between sections on prokary-
otic and eukaryotic cells
Chapter 4 – Dynamics of Microbial Growth
■ Created a new figure to illustrate the principles of selec-
tive and differential media (figure 4.10)
■ Added a new MicroByte on the global agar shortage
Chapter 5 – Control of Microbial Growth
■ Updated the information about the EPA’s efforts to
encourage the use of less toxic options for germicidal
chemicals, and added a figure (figure 5.9) showing the
new “Safer Choice” label
■ Enhanced the coverage of high pressure processing
(HPP)
■ Updated the coverage of triclosan to include restrictions
on its use in personal care products
■ Updated coverage of the use of chlorine and iodine as
disinfectants
Chapter 6 – Microbial Metabolism: Fueling
Cell Growth
■ Revised the description of vitamins
Chapter 7 – The Blueprint of Life, from DNA
to Protein
■ New chapter opening photo
■ Modified figure 7.13 so that reading frame #1 starts with
AUG
■ Revised the description of capping of eukaryotic
pre-mRNA
Chapter 8 – Bacterial Genetics
■ Added an overview figure showing the three mechanisms
of horizontal gene transfer (figure 8.18), in place of the
previous summary table (was table 8.3)
■ Created a new section, “Bacterial Defenses Against
Invading DNA” (section 8.10), by moving and revising
what was section 13.4. This change introduces restric-
tion enzymes and CRISPR systems before they are
discussed in section 9.1 (Fundamental Tools Used in
Biotechnology)
■ Simplified the table on DNA repair (table 8.2)
■ Simplified the summary table on mobile genetic elements
(now table 8.3)
Chapter 9 – Biotechnology
■ Added a subsection that describes the use of CRISPR in
biotechnology, including a supporting figure (figure 9.3)
■ Combined what was sections 9.1–9.3 (Applications of
Genetic Engineering, Techniques Used in Genetic Engi-
neering, and Concerns Regarding Genetic Engineering)
■ Retitled the subsection on next-generation sequencing
methods (now High-Throughput Sequencing Methods)
and expanded to include nanopore sequencing and its use
in the International Space Station
■ Expanded the section on PCR by adding information
about RT-PCR and q-PCR
■ Added a “Focus on the Future” box about Precision
Medicine
Chapter 10 – Identifying and Classifying
Microorganisms
■ Updated figure 10.1 to include a part that illustrates the
new Tree of Life based on ribosomal protein sequences
■ Expanded the information about whole genome sequenc-
ing to characterize strain differences, and added informa-
tion about the Genome Trakr Network
Chapter 11 – The Diversity of Bacteria and
Archaea
■ Added Methanopyrus kandleri, the current record-holder
for high-temperature growth, to the section on methane-
generating hyperthermophiles
■ Updated the information on Chlamydia species to no
longer state that they lack detectable peptidoglycan; also
changed the question that accompanies the figure show-
ing Chlamydia (now figure 11.26)
Chapter 12 – The Eukaryotic Members of the
Microbial World
■ Updated the description of lichens to indicate that
genetic and molecular evidence suggests that they may
include more than two partners
■ Revised figure 12.12 to accompany an updated presen-
tation of eukaryotic phylogeny
■ Reduced the coverage of arthropod groups (some
information was moved to chapters that describe
arthropod-borne diseases)
Chapter 13 – Viruses, Viroids, and Prions
■ Added icons that correlate steps in figure 13.5 (steps in
the replication of lytic phage T4 in E. coli) with descrip-
tions in the accompanying narrative
■ Moved the previous section on bacterial defenses against
phages to chapter 8, so that restriction enzymes and
CRISPR systems are covered earlier (before ­chapter 9,
which describes their use in biotechnology)
■ Added a new rendition of the figure that illustrates ani-
mal virus replication strategies (figure 13.12) for easier
understanding
Chapter 14 – The Innate Immune Response
■ Moved the Focus Figure (figure 14.1) into section 14.1
■ Simplified figure 14.5
Chapter 15 – The Adaptive Immune Response
■ Changed the critical thinking question in MicroAssess-
ment 15.5
■ Expanded the legend for figure 15.25
Chapter 16 – Host-Microbe Interactions
■ Added the definition of microbiome to the key terms
■ Changed the title of section 16.2 to The Human Micro-
biome (was The Normal Microbiota)
■ Introduced the term dysbiosis
■ Added a subsection on damage to the host in section
16.9 (Mechanisms of Viral Pathogenesis)
Chapter 17 – Immunological Disorders
■ Updated coverage of hypersensitivity reactions, particu-
larly asthma, systemic anaphylaxis, and immune com-
plex diseases
xv
 ■ Updated and increased coverage of immunotherapy to
treat allergic reactions
■ Added MicroByte on sublingual immunotherapy (SLIT)
as an alternative to allergy shots
■ Moved coverage of tuberculin skin test to the presenta-
tion of tuberculosis in section 21.4
Chapter 18 – Applications of Immune
Responses
■ Updated the information about polio eradication efforts
by including the switch from trivalent to bivalent OPV
■ Reorganized and refined the section on vaccines (sec-
tion 18.2) by incorporating a new subsection titled “The
Importance of Vaccines,” rearranging the order of the
tables, and separating the list of non-routine vaccines
into a new table (table 18.5); also updated the table
entries
■ Added information about the monoclonal antibody
recently approved for use as part of the protocol for
treating inhalation anthrax
■ Created a new “Focus on the Future” box that describes
cancer immunotherapies, including CAR T cells
Chapter 19 – Epidemiology
■ Updated the table of notifiable infectious diseases
(table 19.1)
■ Added a new table that lists the most common nosoco-
mial infections (table 19.3)
■ Added a subsection on visitors to the section that
describes potential reservoirs for nosocomial infections
■ Added new coverage of National Healthcare Safety
­Network (NHSN)
Chapter 20 – Antimicrobial Medications
■ Expanded the section on development of antibiotics by
adding information about Generating Antibiotic Incen-
tives Now (GAIN)
■ Added information about the newest glycopeptide anti-
biotics (dalbavancin and oritavancin) and the newest
oxazolidinone (tedizolid)
■ Updated the list of antiviral medications by adding
NS5A inhibitors (used to treat HCV)
■ Changed the “Focus on the Future” box to cover the
National Action Plan for Combating Antibiotic Resis-
tant Bacteria
xvi
Chapter 21 – Respiratory System Infections
■ Added new box, “Focus on Pneumonia,” presenting gen-
eral characteristics of this important category of respira-
tory diseases
■ Added a new section on inhalation anthrax
■ Added a new section on SARS and MERS
■ Rearranged section 21.2 to begin with milder diseases
(pink eye, earache, sinus infections)
■ Updated and focused the coverage of pneumococcal
pneumonia and Klebsiella pneumonia
■ Pertussis: revised the information about the epidemiol-
ogy and the treatment and prevention; added a new photo
(figure 21.16)
■ Tuberculosis: increased the coverage of tuberculin skin
test and added an accompanying figure (figure 21.21)
Chapter 22 – Skin Infections
■ Added new section on cutaneous anthrax
■ Added mention of ceftaroline as a new β-lactam antibi-
otic that can be used for treating MRSA
■ Moved section on Lyme disease to chapter 25 (Blood and
Lymphatic Infections)
■ Rocky Mountain spotted fever: revised the information on
the signs and symptoms and the pathogenesis
■ Rubeola: revised the introduction and the information
about the epidemiology and the prevention
Chapter 23 – Wound Infections
■ Deleted coverage of actinomycosis (lumpy jaw)
■ Removed photo showing an individual with sporotricho-
sis (was figure 23.14)
Chapter 24 – Digestive System Infections
■ Added new box, “Focus on Diarrheal Diseases,” present-
ing general characteristics of this important category of
intestinal disease
■ Periodontal disease and ANUG: revised the descriptions
of causative agents
■ Mumps: revised the description of epidemiology
■ Cholera: added information about the new FDA-approved
vaccine
■ Shigellosis: updated the description of treatment
■ Clostridium difficile infection (CDI): added information
about fidaxomicin for treatment
 ■ Norovirus: added update about the recent cultivation of
the virus in the laboratory
■ Hepatitis C: revised the introduction and added informa-
tion about the new treatments
Chapter 25 – Blood and Lymphatic Infections
■ Reorganized coverage throughout
■ Revised coverage of anatomy, especially the lymphatics
■ Added new section on Zika virus disease
■ Dengue fever: added information about the new vaccine
■ Chikungunya: standardized the organization of the section
■ Added a new table that compares Dengue fever, Chikun-
gunya, and Zika Virus disease (table 25.12)
■ Added a section on Lyme disease (moved from chapter 22)
■ Revised the coverage of infective endocarditis (previ-
ously SBE)
Chapter 26 – Nervous System Infections
■ Added new box, “Focus on Meningitis,” presenting gen-
eral characteristics of this important category of nervous
system diseases
■ Reorganized to separate central nervous system (CNS)
diseases from peripheral nervous system (PNS) diseases;
superheadings added
■ Pneumococcal and meningococcal meningitis: updated
and focused the coverage
■ Polio: updated the coverage
■ Changed African sleeping sickness to African trypanoso-
miasis; revised the descriptions of the epidemiology and
the treatment
Chapter 27 – Genitourinary Tract Infections
■ Added new box, “Focus on Sexually Transmitted Infec-
tions,” presenting general characteristics of this impor-
tant category of genitourinary infections
■ Added coverage on Mycoplasma genitalium infections
■ Updated figure 27.21 (The Global HIV/AIDS Epidemic)
to reflect changes in numbers
■ Updated figure 27.25 (HIV Replication)
■ Updated and modified figure 27.26 (was Deaths Due to
AIDS) to include global number of people receiving ART
Chapter 28 – Microbial Ecology
■ Revised the section on terrestrial habitats to emphasize
the microbiome
■ Changed the order of the questions in MicroAssessment
28.4
Chapter 29 – Environmental Microbiology:
Treatment of Water, Wastes, and Polluted
Habitats
■ Deleted the “Focus on the Future” box (“Better Identifi-
cation of Pathogens in Water and Wastes”)
Chapter 30 – Food Microbiology
■ Moved the description of starter culture
■ Updated the names of the organisms used to make fer-
mented foods
■ Revised the section on making beer
■ Deleted the “Focus on the Future” box (“Using Micro-
organisms to Nourish the World”)
xvii
Acknowledgments
First and foremost, special thanks goes to Gene Nester, the
leader of the team that wrote the first version of what became
Microbiology, A Human Perspective. His efforts helped pio-
neer a new type of introductory microbiology textbook,
designed specifically for students entering healthcare-related
fields. This edition proudly builds on that original vision.
We would also like to thank the reviewers and other
instructors who guided us as we developed this edition, as well
as those whose input has helped the text evolve over the years.
Deciding what to eliminate, what to add, and what to rear-
range is always difficult, so we appreciate your suggestions.
Past students have been incredibly helpful as well. Every
question helps us decide which parts of the textbook need
more clarification, and every compliment lets us know when
we’re on the right track.
Special thanks also go to our friends, families, and col-
leagues for picking up the many hairs we tore out while work-
ing on the textbook. Revising a textbook is an all-consuming
task—from the initial development stage to proofing the pages
during production—and numerous people have acted as advi-
sors and cheerleaders throughout. This text would not exist
without the contributions of our strong group of supporters.
A list of acknowledgments is not complete without thank-
ing our fearless leaders and friends from McGraw-Hill. Our
product developer Michelle Gaseor and portfolio manager
Marija Magner not only gave inspiration and sound advice,
but they also laughed at our jokes and barely rolled their eyes
at our idiosyncrasies. Marija Magner and Valerie Kramer
helped ensure that word got out about this new edition, allow-
ing it to find the way into your hands. It was wonderful to
have Vicki Krug as our content project manager to guide us
through some rocky waters on the way to publication. Addi-
tionally, we would like to thank Jonathan Miller and digital
content project manager Brent dela Cruz for helping produce
our digital resources that support the text and Lisa Burgess,
who provided many wonderful photographs.
We hope that this text will be interesting and educational
for students and helpful to instructors. Our goal is excellence,
so with that in mind we would appreciate any comments and
suggestions from our readers.
Reviewers for the Ninth Edition
Jason Adams, College of Dupage
Carollyn Boykins-Winrow, Tidewater Community College
Carron Bryant, East Mississippi Community College
Christine Clouser, University of Minnesota
Joyce Doan, Bethel University
Jose Fernandez Romero, Borough of Manhattan Community
College, CUNY
Eric Ford, East Mississippi Community College
Julie Gibbs, College of Dupage
Dale Horeth, Tidewater Community College
Sara Reed Houser, Jefferson College of Health Sciences
Ilko Iliev, Southern University at Shreveport
Andrew Iverson, William Rainey Harper College
Kristen Joachimides, North Seattle College
Amine Kidane, Columbus State
Terrence Miller, Central Carolina Community College
Kari Naylor, University of Central Arkansas
Krista Peppers, University of Central Arkansas
Cynthia Ripoll, Delgado Community College
Rachael Romain, Columbus State Community College
Ben Rowley, University of Central Arkansas
Syed Shahabuddin, College of Lake County
Roger Wainwright, University of Central Arkansas
Kate Wilwohl, Bethel University
Jessica Wohlgamuth-Benedum, Columbus State Community
College

Denise Anderson
Sarah Salm
Deborah Allen

xviii
Contents
About the Authors iv

PART I Covalent Bonds 22

Life and Death of Microorganisms Hydrogen Bonds 23
Molarity 24
1 Humans and the Microbial World 1 Chemical Reactions 24

2.3 Water, pH, and Buffers 25

A Glimpse of History 1
Water 25
Key Terms 1
pH of Aqueous Solutions 25
1.1 The Dispute over Buffers 26
Spontaneous Generation 2
Early Experiments 2 2.4 Organic Molecules 27
Experiments of Pasteur 2 ©INTERFOTO/Alamy Stock Photo Carbohydrates 28
Experiments of Tyndall 2 Lipids 30
The Golden Age of Microbiology 3 Proteins 32
The Scientific Method 3 Nucleic Acids 37
1.2 Microbiology: A Human Perspective 5 FOCUS ON A CASE 2.1 30
The Human Microbiome 5 FOCUS YOUR PERSPECTIVE 2.1: Right-Handed and Left-Handed
Microorganisms in the Environment 6 Molecules 35
Commercial Benefits of Microorganisms 6 SUMMARY 40
Microbes as Research Tools 7 REVIEW QUESTIONS 41
Microbes and Disease 7
1.3 Members of the Microbial World 10 3 Microscopy and Cell Structure 44
Scientific Names 11
Bacteria 13 A Glimpse of History 44
Archaea 13 Key Terms 44
Eukarya 13
MICROSCOPY AND CELL
Acellular Infectious Agents 14 MORPHOLOGY
FOCUS ON A CASE 1.1 9 3.1 Microscopes 45 Source: Janice Haney Carr/CDC
FOCUS YOUR PERSPECTIVE 1.1: Every Rule Has an Exception 12 Principles of Light Microscopy: Bright-Field Microscopes 45
FOCUS ON THE FUTURE 1.1: Meet the Microbiomes! 16 Light Microscopes That Increase Contrast 48
SUMMARY 16 Light Microscopes That Detect Fluorescence 49
REVIEW QUESTIONS 17 Electron Microscopes 50
Scanning Probe Microscopes 51
2 The Molecules of Life 19 3.2 Preparing Specimens for Light
Microscopy 52
A Glimpse of History 19 Simple Staining 52
Key Terms 19 Differential Staining 52
2.1 Elements and Atoms 20 Special Stains to Observe Cell Structures 55
Atomic Structure 20 Fluorescent Dyes and Tags 56
Isotopes 20 3.3 Morphology of Prokaryotic Cells 57
©McGraw-Hill Education/Lisa Burgess
The Role of Electrons 21 Shapes 57
2.2 Chemical Bonds and Reactions 22 Arrangements 57
Ions and Ionic Bonds 22 Multicellular Associations 58

xix
xx Contents

PROKARYOTIC CELLS
4 Dynamics of Microbial Growth 92
3.4 The Cytoplasmic Membrane of Prokaryotic
Cells 59 A Glimpse of History 92
Structure of the Cytoplasmic Membrane 60 Key Terms 92
Permeability of the Cytoplasmic Membrane 61 4.1 Principles of Microbial
The Role of the Cytoplasmic Membrane in Energy Growth 92
Transformation 61
Transport of Small Molecules Across the Cytoplasmic 4.2 Microbial Growth in ©McGraw-Hill Education/Lisa Burgess
Membrane 62 Nature 93
Protein Secretion 64 Biofilms 94
Interactions of Mixed Microbial
3.5 The Cell Wall of Prokaryotic Cells 65
Communities 95
Peptidoglycan 65
The Gram-Positive Cell Wall 65 4.3 Microbial Growth in Laboratory
The Gram-Negative Cell Wall 67 Conditions 95
Antibacterial Substances That Target Peptidoglycan 69 Obtaining a Pure Culture 96
Cell Wall Type and the Gram Stain 69 The Growth Curve 97
Bacteria That Lack a Cell Wall 69 Colony Growth 98
Cell Walls of Archaea 69 Continuous Culture 98
3.6 Structures Outside the Cell Wall of Prokaryotic 4.4 Environmental Factors That Influence
Cells 70 Microbial Growth 99
Capsules and Slime Layers 72 Temperature Requirements 99
Flagella 72 Oxygen (O2) Requirements 100
Pili 74 pH 101
3.7 Internal Components of Prokaryotic Cells 75 Water Availability 102
Chromosome and Plasmids 75 4.5 Nutritional Factors That Influence Microbial
Ribosomes 75 Growth 102
Cytoskeleton 75 Required Elements 102
Storage Granules 76 Growth Factors 103
Gas Vesicles 76 Energy Sources 103
Endospores 76 Nutritional Diversity 103
EUKARYOTIC CELLS 4.6 Cultivating Microorganisms in the
Laboratory 105
3.8 Cytoplasmic Membrane of Eukaryotic Cells 79
General Categories of Culture Media 105
Structure and Function of the Cytoplasmic Membrane 79
Special Types of Culture Media 106
Transfer of Molecules Across the Cytoplasmic Membrane 81
Providing Appropriate Atmospheric
3.9 Protein Structures Within Eukaryotic Cells 82 Conditions 107
Ribosomes 82 Enrichment Cultures 108
Cytoskeleton 82
Flagella and Cilia 83 4.7 Methods to Detect and Measure
Microbial Growth 109
3.10 Membrane-Bound Organelles of Eukaryotic Cells 84 Direct Cell Counts 109
Nucleus 84 Viable Cell Counts 110
Mitochondria 84 Measuring Biomass 113
Chloroplasts 86 Detecting Cell Products 114
Endoplasmic Reticulum (ER) 86
Golgi Apparatus 87 FOCUS ON A CASE 4.1 104
Lysosomes and Peroxisomes 88 FOCUS YOUR PERSPECTIVE 4.1: Can Microorganisms Live on
Only Rocks and Water? 105
FOCUS ON A CASE 3.1 70 FOCUS ON THE FUTURE 4.1: Seeing How the Other
FOCUS YOUR PERSPECTIVE 3.1: Pathogens Hijacking Actin 83 99% Lives 115

SUMMARY 88 SUMMARY 116

REVIEW QUESTIONS 90 REVIEW QUESTIONS 117
 Contents xxi

5 Control of Microbial Growth 119 6.2 Enzymes 148

A Glimpse of History 119
Key Terms 119
5.1 Approaches to
Control 119
Principles of Control 120
Situational Considerations 120
5.2 Selecting an Antimicrobial Procedure 123
Type of Microbes 123
Number of Microorganisms 123
Environmental Conditions 124
Risk for Infection 124
Composition of the Item 124
5.3 Using Heat to Destroy Microorganisms and
Viruses 124
Moist Heat 124
Dry Heat 127
Mechanisms and Consequences of Enzyme Action 148
Cofactors 149
Environmental Factors That Influence Enzyme Activity 150
Allosteric Regulation 150
Enzyme Inhibition 151
6.3 The Central Metabolic Pathways 153
©Arthur Tilley/Getty Images Glycolysis 153
Pentose Phosphate Pathway 155
Transition Step 155
Tricarboxylic Acid (TCA) Cycle 155
6.4 Cellular Respiration 157
The Electron Transport Chain (ETC)—Generating a
Proton Motive Force 157
ATP Synthase—Using the Proton Motive Force to
Synthesize ATP 159
ATP Yield of Aerobic Respiration in Prokaryotes 160
6.5 Fermentation 162

5.4 Using Other Physical Methods 6.6 Catabolism of Organic Compounds Other Than
to Remove or Destroy Microbes 127 Glucose 164
Filtration 127 Polysaccharides and Disaccharides 164
Irradiation 128 Lipids 166
High Pressure 129 Proteins 166

5.5 Using Chemicals to Destroy Microorganisms 6.7 Chemolithotrophs 166

and Viruses 129 6.8 Photosynthesis 167
Effectiveness of Germicidal Chemicals 129 Capturing Radiant Energy 167
Selecting the Appropriate Germicidal Chemical 130 Converting Radiant Energy into Chemical Energy 169
Classes of Germicidal Chemicals 131
6.9 Carbon Fixation 170
5.6 Preservation of Perishable Products 134
Calvin Cycle 170
Chemical Preservatives 134
Low-Temperature Storage 135 6.10 Anabolic Pathways—Synthesizing Subunits from
Reducing the Available Water 135 Precursor Molecules 171
Lipid Synthesis 171
FOCUS ON A CASE 5.1 122 Amino Acid Synthesis 172
FOCUS ON THE FUTURE 5.1: Too Much of a Good Thing? 136 Nucleotide Synthesis 173
SUMMARY 136
FOCUS ON A CASE 6.1 164
REVIEW QUESTIONS 137
FOCUS YOUR PERSPECTIVE 6.1: Mining with Microbes 167

6 Microbial Metabolism: Fueling Cell

FOCUS ON THE FUTURE 6.1: Fueling the Future 174

Growth 139 SUMMARY 175

REVIEW QUESTIONS 176
A Glimpse of History 139
Key Terms 139 7 The Blueprint of Life, from DNA to Protein 178
6.1 Principles of Microbial
A Glimpse of History 178
Metabolism 140
Key Terms 178
Energy 140
©Comstock/Getty Images
Components of Metabolic 7.1 Overview 179
Pathways 142 Characteristics of DNA 179
Precursor Metabolites 145 Characteristics of RNA 180
©MOLEKUUL/SPL/age fotostock
Overview of Catabolism 146 Regulating Gene Expression 181
xxii Contents

7.2 DNA Replication 182 8.5 Mutant Selection 215

Initiation of DNA Replication 182 Direct Selection 215
The Process of DNA Replication 183 Indirect Selection 215
Screening for Possible Carcinogens 217
7.3 Gene Expression in Bacteria 185
Transcription 185 HORIZONTAL GENE TRANSFER AS A MECHANISM
Translation 187 OF GENETIC CHANGE

7.4 Differences Between Eukaryotic and Prokaryotic 8.6 DNA-Mediated Transformation 219
Gene Expression 192 Competence 219
The Process of Transformation 220
7.5 Sensing and Responding to Environmental
Fluctuations 194 8.7 Transduction 222
Signal Transduction 194 8.8 Conjugation 223
Natural Selection 195 Plasmid Transfer 224
Chromosome Transfer 225
7.6 Bacterial Gene Regulation 197
F′ Donors 226
Mechanisms to Control Transcription 197
The lac Operon as a Model 199 8.9 The Mobile Gene Pool 227
Plasmids 227
7.7 Eukaryotic Gene Regulation 200 Transposons 229
7.8 Genomics 202 Genomic Islands 229
Analyzing a Prokaryotic DNA Sequence 203 Phage DNA 230
Metagenomics 203 8.10 Bacterial Defenses Against Invading DNA 231
Restriction-Modification Systems 231
FOCUS ON A CASE 7.1 196
CRISPR Systems 231
FOCUS YOUR PERSPECTIVE 7.1: RNA: The First
Macromolecule? 194 FOCUS ON A CASE 8.1 230
FOCUS ON THE FUTURE 7.1: Gems in the Genomes? 203 FOCUS YOUR PERSPECTIVE 8.1: The Biological Function of DNA: A
Discovery Ahead of Its Time 223
SUMMARY 203
REVIEW QUESTIONS 204 FOCUS YOUR PERSPECTIVE 8.2: Bacteria Can Conjugate with
Plants: A Natural Case of Genetic Engineering 228

8 Bacterial Genetics 206 SUMMARY 233

REVIEW QUESTIONS 234
A Glimpse of History 206
Key Terms 206 9 Biotechnology 236
8.1 Genetic Change in
A Glimpse of History 236
Bacteria 207
Key Terms 236
MUTATION AS A MECHANISM ©Dr. Gopal Murti/Science Source
9.1 Fundamental Tools Used
OF GENETIC CHANGE in Biotechnology 237
8.2 Spontaneous Mutations 208 Restriction Enzymes 237
©Anthony Bradshaw/Photographer’s
Base Substitution 208 DNA Gel Electrophoresis 237 Choice/Getty Images
Deletion or Addition of Nucleotides 209 CRISPR/Cas9 238
Transposons (Jumping Genes) 210 9.2 Genetic Engineering 240
8.3 Induced Mutations 210 Genetically Engineered Bacteria 240
Chemical Mutagens 210 Genetically Engineered Eukaryotes 242
Transposition 212 Techniques Used to Clone DNA 243
Radiation 212 Concerns Regarding Genetic Engineering 245
9.3 DNA Sequencing 246
8.4 Repair of Damaged DNA 212
DNA Sequencing Methods 246
Repair of Errors in Nucleotide Incorporation 213
Repair of Modified Nucleobases in DNA 214 9.4 Polymerase Chain Reaction (PCR) 249
Repair of Thymine Dimers 214 Variations of Conventional PCR 249
SOS Repair 214 PCR Methods 250
 Contents xxiii

9.5 Probe Technologies 254

Colony Blotting 254
11 The Diversity of Bacteria and Archaea 279
Fluorescence In Situ Hybridization (FISH) 254
A Glimpse of History 279
DNA Microarrays 255 Key Terms 279

FOCUS ON A CASE 9.1 253 METABOLIC DIVERSITY

FOCUS ON THE FUTURE 9.1: Precision Medicine 256
11.1 Anaerobic
SUMMARY 257 Chemotrophs 280 ©Science Photo Library RF/Getty Images
REVIEW QUESTIONS 257 Anaerobic Chemolithotrophs 280
Anaerobic Chemoorganotrophs—Anaerobic
Respiration 282
PART I I Anaerobic Chemoorganotrophs—Fermentation 282
The Microbial World 11.2 Anoxygenic Phototrophs 284
Purple Bacteria 284
10 Identifying and Classifying Green Bacteria 284
Microorganisms 259 Other Anoxygenic Phototrophs 285
11.3 Oxygenic Phototrophs 285
A Glimpse of History 259
Key Terms 259
Cyanobacteria 285

10.1 Principles of 11.4 Aerobic Chemolithotrophs 287

Taxonomy 260 Sulfur-Oxidizing Bacteria 287
Strategies Used to Identify Nitrifiers 287
Microorganisms 260 ©AJ Photo/HOP American/SPL/Science Hydrogen-Oxidizing Bacteria 288
Source
Strategies Used to Classify Microorganisms 260 11.5 Aerobic Chemoorganotrophs 288
Nomenclature 263 Obligate Aerobes 289
10.2 Identification Methods Based on Phenotype 263 Facultative Anaerobes 290
Microscopic Morphology 263 ECOPHYSIOLOGICAL DIVERSITY
Culture Characteristics 264
Metabolic Capabilities 264 11.6 Thriving in Terrestrial Environments 291
Serological Testing 267 Bacteria That Form a Resting Stage 292
Protein Profile 267 Bacteria That Associate with Plants 293
11.7 Thriving in Aquatic Environments 294
10.3 Identification Methods Based on Genotype 268
Sheathed Bacteria 295
Detecting Specific Nucleotide Sequences 268
Prosthecate Bacteria 295
Sequencing Ribosomal RNA Genes 269
Bacteria That Derive Nutrients from Other
10.4 Characterizing Strain Differences 270 Organisms 296
Biochemical Typing 270 Bacteria That Move by Unusual Mechanisms 297
Serological Typing 270 Bacteria That Form Storage Granules 298
Molecular Typing 270 11.8 Animals as Habitats 299
Phage Typing 271 Bacteria That Inhabit the Skin 299
Antibiograms 272 Bacteria That Inhabit Mucous Membranes 302
10.5 Classifying Microorganisms 273 Obligate Intracellular Parasites 303
Sequence Analysis of Ribosomal Components 273 11.9 Archaea That Thrive in Extreme Conditions 304
DNA Hybridization 275 Extreme Halophiles 304
G + C Content 275 Extreme Thermophiles 305
Phenotypic Methods 275
FOCUS ON A CASE 11.1 299
FOCUS ON A CASE 10.1 273 FOCUS ON THE FUTURE 11.1: Astrobiology: Searching for Life
FOCUS ON THE FUTURE 10.1: Pushing the Limits of MALDI-TOF MS 276 Beyond Earth 306

SUMMARY 276 SUMMARY 306

REVIEW QUESTIONS 277 REVIEW QUESTIONS 308
xxiv Contents

12 The Eukaryotic Members of the Microbial 13.2 Bacteriophages 338

Lytic Phage Infections: T4 Phage as a Model 338
World 310
Temperate Phage Infections: Lambda Phage as a
Model 340
A Glimpse of History 310
Filamentous Phage Infections: M13 Phage
Key Terms 310
as a Model 341
12.1 Fungi 311
13.3 The Roles of Bacteriophages in Horizontal Gene
Types of Fungi 312
Transfer 342
Structure of Fungi 312
©Biophoto Associates/Science Source Generalized Transduction 342
Fungal Habitats 314
Specialized Transduction 342
Symbiotic Relationships of Fungi 314
Reproduction in Fungi 315 13.4 Methods Used to Study Bacteriophages 343
Economic Importance of Fungi 316
13.5 Animal Virus Replication 344
Medical Importance of Fungi 317
Attachment 344
12.2 Algae 317 Penetration and Uncoating 344
Types of Algae 318 Synthesis of Viral Proteins and Replication of the
Structure of Algae 318 Genome 344
Algal Habitats 318 Assembly and Maturation 348
Algal Reproduction 319 Release 348
Medical Importance of Algae 319 13.6 Categories of Animal Virus Infections 349
Acute Infections 349
12.3 Protozoa 320
Persistent Infections 349
Types of Protozoa 320
Structure of Protozoa 320 13.7 Viruses and Human Tumors 351
Protozoan Habitats 321 13.8 Cultivating and Quantitating Animal Viruses 352
Protozoan Reproduction 321 Cultivating Animal Viruses 352
Medical Importance of Protozoa 323 Quantitating Animal Viruses 354
12.4 Slime Molds and Water Molds 323 13.9 Plant Viruses 355
Slime Molds 323
13.10 Other Infectious Agents: Viroids and Prions 356
Water Molds 324
Viroids 356
12.5 Multicellular Parasites: Helminths 324 Prions 357
Life Cycles and Transmission of Helminths 325
FOCUS ON A CASE 13.1 354
Roundworms (Nematodes) 326
FOCUS YOUR PERSPECTIVE 13.1: Microbe Mimicker 333
Tapeworms (Cestodes) 327
Flukes (Trematodes) 328 SUMMARY 358
REVIEW QUESTIONS 360
12.6 Arthropods 328

FOCUS ON A CASE 12.1 322

FOCUS YOUR PERSPECTIVE 12.1: What Causes River PA RT III
Blindness? 326 Microorganisms and Humans
SUMMARY 329
REVIEW QUESTIONS 331 14 The Innate Immune Response 362

13 Viruses, Viroids, and Prions 332

A Glimpse of History 362
Key Terms 362

A Glimpse of History 332 14.1 Overview of the Innate

Key Terms 332 ­Immune Defenses 363
13.1 General Characteristics 14.2 First-Line Defenses 364 ©Science Photo Library RF/Getty Images
of Viruses 333 Physical Barriers 364
Viral Architecture 334 Antimicrobial Substances 365
©AMI Images/Science Source
Viral Taxonomy 336 Normal Microbiota (Flora) 366
Another random document with
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 THE TABLET
OF CONFUCIUS
A PORCELAIN-FRONTED
TEMPLE ON
THE YANGTZE.

The manufacture of porcelain has for centuries made China

celebrated. It may be of interest to refer to the fact that we owe the
existence of our Worcester porcelain works to the attempt made by a
chemist to produce porcelain in England similar to the Chinese. A
great many temples in the Empire province of Sze Chuan have their
fronts and roofs of this porcelain. They are most gorgeous in colour,
and have the appearance of being jewelled.
A PORCELAIN-FRONTED
TEMPLE ON
THE YANGTZE
CHILD EATING RICE
WITH CHOPSTICKS.

The Chinese eat an enormous number of things which the Western

turns from, or which he doesn’t know of. As a rule the Chinese are
good cooks, and the food is wholesome, steaming being the
favourite method. Rice is the staff of life to the masses, who eat it
mixed with fried cabbage or some other flavouring ingredient. It is
seldom eaten alone. So common and universal is rice eating that,
while in French the equivalent of “How do you do?” is “How do you
carry yourself?” and in Italian “How do you stay?” in Chinese the
equivalent is “Have you eaten rice?”
CHILD EATING RICE
WITH CHOPSTICKS
FORT ON
THE PEKING WALL.

City walls are a great feature of the country. The illustration is of a

fort on one of the angles of the wall of Peking, the interest of it lying
in the fact that the guns showing in the embrasures are dummies,
being simply painted wood. Probably the cost of real guns went into
the pockets of some official entrusted with providing the armament of
the fort.
 FORT ON
THE PEKING WALL
ANOTHER FORT ON
THE WALL OF PEKING.

This fort is filled with carronades, old guns still kept there, though
absolutely useless, being honeycombed with disuse and rust.
 ANOTHER FORT ON
THE WALL OF PEKING
COLOSSAL ASTRONOMICAL
INSTRUMENTS
ON THE PEKING WALL.

Many hundred years old, but as bronze castings they are reckoned
to be amongst the finest in the world. And as astronomical
instruments their results differ very little from those obtained by
astronomers from appliances of the most modern construction.
COLOSSAL ASTRONOMICAL
INSTRUMENTS
ON THE PEKING WALL
CHIEN MUN GATE.

Perhaps the most interesting and picturesque feature of the country

is its city gates. There is a great family likeness between them, the
usual fort-like building surmounting the wall where it is pierced by the
gate. It is not a fort, however. In it are kept the gongs and other
musical instruments by means of which are announced the rising
and the setting of the sun. This is the gate which was blown up by
the Japanese in their recent attack on and entry into the city. It is the
largest and most important gate in Peking.
CHIEN MUN GATE