1.

Evolutionary Processes
1. Evolution and the Origin of Species
1. Introduction
2. 18.1Understanding Evolution
3. 18.2Formation of New Species
4. 18.3Reconnection and Speciation Rates
5. Key Terms
6. Chapter Summary
7. Visual Connection Questions
8. Review Questions
9. Critical Thinking Questions
2. The Evolution of Populations
3. Phylogenies and the History of Life
2. Biological Diversity
1. Viruses
1. Introduction
2. 21.1Viral Evolution, Morphology, and Classification
3. 21.2Virus Infections and Hosts
4. 21.3Prevention and Treatment of Viral Infections
5. 21.4Other Acellular Entities: Prions and Viroids
6. Key Terms
7. Chapter Summary
8. Visual Connection Questions
9. Review Questions
10.Critical Thinking Questions
2. Prokaryotes: Bacteria and Archaea
3. Protists
4. Fungi
All organisms are products of evolution adapted to their environment. (a) Saguaro
(Carnegiea gigantea) can soak up 750 liters of water in a single rain storm,
enabling these cacti to survive the dry conditions of the Sonora desert in Mexico
and the Southwestern United States. (b) The Andean semiaquatic lizard
(Potamites montanicola) discovered in Peru in 2010 lives between 1,570 to 2,100
meters in elevation, and, unlike most lizards, is nocturnal and swims. Scientists
still do not know how these cold-blood animals are able to move in the cold (10
to 15°C) temperatures of the Andean night. (credit a: modification of work by
Gentry George, U.S. Fish and Wildlife Service; credit b: modification of work by
Germán Chávez and Diego Vásquez, ZooKeys)

Chapter Outline

18.1 Understanding Evolution

18.2 Formation of New Species
18.3 Reconnection and Speciation Rates

All living organisms, from bacteria to baboons to blueberries, evolved at some

point from a different species. Although it may seem that living things today stay
much the same, that is not the case—evolution is an ongoing process.

The theory of evolution is the unifying theory of biology, meaning it is the

framework within which biologists ask questions about the living world. Its
power is that it provides direction for predictions about living things that are
borne out in ongoing experiments. The Ukrainian-born American geneticist
Theodosius Dobzhansky famously wrote that “nothing makes sense in biology
except in the light of evolution.”1 He meant that the tenet that all life has evolved
and diversified from a common ancestor is the foundation from which we
approach all questions in biology.

Learning Objectives

By the end of this section, you will be able to do the following:

 Describe how scientists developed the present-day theory of evolution

 Define adaptation
 Explain convergent and divergent evolution
 Describe homologous and vestigial structures
 Discuss misconceptions about the theory of evolution

Evolution by natural selection describes a mechanism for how species change

over time. Scientists, philosophers, researchers, and others had made suggestions
and debated this topic well before Darwin began to explore this idea. Classical
Greek philosopher Plato emphasized in his writings that species were static and
unchanging, yet there were also ancient Greeks who expressed evolutionary
ideas. In the eighteenth century, naturalist Georges-Louis Leclerc Comte de
Buffon reintroduced ideas about the evolution of animals and observed that
various geographic regions have different plant and animal populations, even
when the environments are similar. Some at this time also accepted that there
were extinct species.
Also during the eighteenth century, James Hutton, a Scottish geologist and
naturalist, proposed that geological change occurred gradually by accumulating
small changes from processes operating like they are today over long periods of
time. This contrasted with the predominant view that the planet's geology was a
consequence of catastrophic events occurring during a relatively brief past.
Nineteenth century geologist Charles Lyell popularized Hutton's view. A friend
to Darwin. Lyell’s ideas were influential on Darwin’s thinking: Lyell’s notion of
the greater age of Earth gave more time for gradual change in species, and the
process of change provided an analogy for this change. In the early nineteenth
century, Jean-Baptiste Lamarck published a book that detailed a mechanism for
evolutionary change. We now refer to this mechanism as an inheritance of
acquired characteristics by which the environment causes modifications in an
individual, or offspring could use or disuse of a structure during its lifetime, and
thus bring about change in a species. While many discredited this mechanism for
evolutionary change, Lamarck’s ideas were an important influence on
evolutionary thought.

Charles Darwin and Natural Selection

In the mid-nineteenth century, two naturalists, Charles Darwin and Alfred Russel
Wallace, independently conceived and described the actual mechanism for
evolution. Importantly, each naturalist spent time exploring the natural world on
expeditions to the tropics. From 1831 to 1836, Darwin traveled around the world
on H.M.S. Beagle, including stops in South America, Australia, and the southern
tip of Africa. Wallace traveled to Brazil to collect insects in the Amazon rainforest
from 1848 to 1852 and to the Malay Archipelago from 1854 to 1862. Darwin’s
journey, like Wallace’s later journeys to the Malay Archipelago, included stops
at several island chains, the last being the Galápagos Islands west of Ecuador. On
these islands, Darwin observed species of organisms on different islands that
were clearly similar, yet had distinct differences. For example, the ground finches
inhabiting the Galápagos Islands comprised several species with a unique beak
shape (Figure 18.2). The species on the islands had a graded series of beak sizes
and shapes with very small differences between the most similar. He observed
that these finches closely resembled another finch species on the South American
mainland. Darwin imagined that the island species might be species modified
from one of the original mainland species. Upon further study, he realized that
each finch's varied beaks helped the birds acquire a specific type of food. For
example, seed-eating finches had stronger, thicker beaks for breaking seeds, and
insect-eating finches had spear-like beaks for stabbing their prey.

Figure 18.2 Darwin observed that beak shape varies among finch species. He
postulated that ancestral species' beaks had adapted over time to equip the finches
to acquire different food sources.

Wallace and Darwin both observed similar patterns in other organisms and they
independently developed the same explanation for how and why such changes
could take place. Darwin called this mechanism natural selection. Natural
selection, or “survival of the fittest,” is the more prolific reproduction of
individuals with favorable traits that survive environmental change because of
those traits. This leads to evolutionary change.
For example, Darwin observed a population of giant tortoises in the Galápagos
Archipelago to have longer necks than those that lived on other islands with dry
lowlands. These tortoises were “selected” because they could reach more leaves
and access more food than those with short necks. In times of drought when fewer
leaves would be available, those that could reach more leaves had a better chance
to eat and survive than those that couldn’t reach the food source. Consequently,
long-necked tortoises would be more likely to be reproductively successful and
pass the long-necked trait to their offspring. Over time, only long-necked tortoises
would be present in the population.

Natural selection, Darwin argued, was an inevitable outcome of three principles

that operated in nature. First, most characteristics of organisms are inherited, or
passed from parent to offspring. Although no one, including Darwin and Wallace,
knew how this happened at the time, it was a common understanding. Second,
more offspring are produced than are able to survive, so resources for survival
and reproduction are limited. The capacity for reproduction in all organisms
outstrips the availability of resources to support their numbers. Thus, there is
competition for those resources in each generation. Both Darwin and Wallace’s
understanding of this principle came from reading economist Thomas Malthus'
essay that explained this principle in relation to human populations. Third,
offspring vary among each other in regard to their characteristics and those
variations are inherited. Darwin and Wallace reasoned that offspring with
inherited characteristics which allow them to best compete for limited resources
will survive and have more offspring than those individuals with variations that
are less able to compete. Because characteristics are inherited, these traits will be
better represented in the next generation. This will lead to change in populations
over generations in a process that Darwin called descent with modification.
Ultimately, natural selection leads to greater adaptation of the population to its
local environment. It is the only mechanism known for adaptive evolution.
In 1858, Darwin and Wallace (Figure 18.3) presented papers at the Linnean
Society in London that discussed the idea of natural selection. The following year
Darwin’s book, On the Origin of Species, was published. His book outlined in
considerable detail his arguments for evolution by natural selection.

Figure 18.3 Both (a) Charles Darwin and (b) Alfred Wallace wrote scientific
papers on natural selection that they presented together at the Linnean Society in
1858.

It is difficult and time-consuming to document and present examples of evolution

by natural selection. The Galápagos finches are an excellent example. Peter and
Rosemary Grant and their colleagues have studied Galápagos finch populations
every year since 1976 and have provided important evidence of natural selection.
The Grants found changes from one generation to the next in beak shape
distribution with the medium ground finch on the Galápagos island of Daphne
Major. The birds have inherited a variation in their bill shape with some having
wide deep bills and others having thinner bills. During a period in which rainfall
was higher than normal because of an El Niño, there was a lack of large hard
seeds of which the large-billed birds ate; however, there was an abundance of the
small soft seeds which the small-billed birds ate. Therefore, the small-billed birds
were able to survive and reproduce. In the years following this El Niño, the Grants
measured beak sizes in the population and found that the average bill size was
smaller. Since bill size is an inherited trait, parents with smaller bills had more
offspring and the bill evolved into a much smaller size. As conditions improved
in 1987 and larger seeds became more available, the trend toward smaller average
bill size ceased.

CAREER CONNECTION

Field Biologist

Many people hike, explore caves, scuba dive, or climb mountains for recreation.
People often participate in these activities hoping to see wildlife. Experiencing
the outdoors can be incredibly enjoyable and invigorating. What if your job
entailed working in the wilderness? Field biologists by definition work outdoors
in the “field.” The term field in this case refers to any location outdoors, even
under water. A field biologist typically focuses research on a certain species,
group of organisms, or a single habitat (Figure 18.4).

Figure 18.4 A field biologist tranquilizes a polar bear for study. (credit: Karen
Rhode)
One objective of many field biologists includes discovering new, unrecorded
species. Not only do such findings expand our understanding of the natural world,
but they also lead to important innovations in fields such as medicine and
agriculture. Plant and microbial species, in particular, can reveal new medicinal
and nutritive knowledge. Other organisms can play key roles in ecosystems or if
rare require protection. When discovered, researchers can use these important
species as evidence for environmental regulations and laws.

Processes and Patterns of Evolution

Natural selection can only take place if there is variation, or differences, among
individuals in a population. Importantly, these differences must have some
genetic basis; otherwise, the selection will not lead to change in the next
generation. This is critical because nongenetic reasons can cause variation among
individuals such as an individual's height because of better nutrition rather than
different genes.

Genetic diversity in a population comes from two main mechanisms: mutation

and sexual reproduction. Mutation, a change in DNA, is the ultimate source of
new alleles, or new genetic variation in any population. The genetic changes that
mutation causes can have one of three outcomes on the phenotype. A mutation
affects the organism's phenotype in a way that gives it reduced fitness—lower
likelihood of survival or fewer offspring. A mutation may produce a phenotype
with a beneficial effect on fitness. Many mutations will also have no effect on the
phenotype's fitness. We call these neutral mutations. Mutations may also have a
whole range of effect sizes on the organism's fitness that expresses them in their
phenotype, from a small effect to a great effect. Sexual reproduction also leads to
genetic diversity: when two parents reproduce, unique combinations of alleles
assemble to produce the unique genotypes and thus phenotypes in each offspring.
We call a heritable trait that helps an organism's survival and reproduction in its
present environment an adaptation. Scientists describe groups of organisms
adapting to their environment when a genetic variation occurs over time that
increases or maintains the population's “fit” to its environment. A platypus's
webbed feet are an adaptation for swimming. A snow leopard's thick fur is an
adaptation for living in the cold. A cheetah's fast speed is an adaptation for
catching prey.

Whether or not a trait is favorable depends on the current environmental

conditions. The same traits are not always selected because environmental
conditions can change. For example, consider a plant species that grew in a moist
climate and did not need to conserve water. Large leaves were selected because
they allowed the plant to obtain more energy from the sun. Large leaves require
more water to maintain than small leaves, and the moist environment provided
favorable conditions to support large leaves. After thousands of years, the climate
changed, and the area no longer had excess water. The direction of natural
selection shifted so that plants with small leaves were selected because those
populations were able to conserve water to survive the new environmental
conditions.

The evolution of species has resulted in enormous variation in form and function.
Sometimes, evolution gives rise to groups of organisms that become
tremendously different from each other. We call two species that evolve in
diverse directions from a common point divergent evolution. We can see such
divergent evolution in the forms of the reproductive organs of flowering plants
which share the same basic anatomies; however, they can look very different as
a result of selection in different physical environments and adaptation to different
kinds of pollinators (Figure 18.5).
Figure 18.5 Flowering plants evolved from a common ancestor. Notice that the
(a) dense blazing star (Liatrus spicata) and the (b) purple coneflower (Echinacea
purpurea) vary in appearance, yet both share a similar basic morphology. (credit
a: modification of work by Drew Avery; credit b: modification of work by Cory
Zanker)

In other cases, similar phenotypes evolve independently in distantly related

species. For example, flight has evolved in both bats and insects, and they both
have structures we refer to as wings, which are adaptations to flight. However,
bat and insect wings have evolved from very different original structures. We call
this phenomenon convergent evolution, where similar traits evolve
independently in species that do not share a common ancestry. The two species
came to the same function, flying, but did so separately from each other.

These physical changes occur over enormous time spans and help explain how
evolution occurs. Natural selection acts on individual organisms, which can then
shape an entire species. Although natural selection may work in a single
generation on an individual, it can take thousands or even millions of years for an
entire species' genotype to evolve. It is over these large time spans that life on
earth has changed and continues to change.

Evidence of Evolution
The evidence for evolution is compelling and extensive. Looking at every level
of organization in living systems, biologists see the signature of past and present
evolution. Darwin dedicated a large portion of his book, On the Origin of Species,
to identifying patterns in nature that were consistent with evolution, and since
Darwin, our understanding has become clearer and broader.

Fossils

Fossils provide solid evidence that organisms from the past are not the same as
those today, and fossils show a progression of evolution. Scientists determine the
age of fossils and categorize them from all over the world to determine when the
organisms lived relative to each other. The resulting fossil record tells the story
of the past and shows the evolution of form over millions of years (Figure 18.6).
For example, scientists have recovered highly detailed records showing the
evolution of humans and horses (Figure 18.6). The whale flipper shares a similar
morphology to bird and mammal appendages (Figure 18.7) indicating that these
species share a common ancestor.

Figure 18.6 In this (a) display, fossil hominids are arranged from oldest (bottom)
to newest (top). As hominids evolved, the skull's shape changed. An artist’s
rendition of (b) extinct species of the genus Equus reveals that these ancient
species resembled the modern horse (Equus ferus) but varied in size.
Anatomy and Embryology

Another type of evidence for evolution is the presence of structures in organisms

that share the same basic form. For example, the bones in human, dog, bird, and
whale appendages all share the same overall construction (Figure 18.7) resulting
from their origin in a common ancestor's appendages. Over time, evolution led to
changes in the bones' shapes and sizes different species, but they have maintained
the same overall layout. Scientists call these synonymous parts homologous
structures.

Figure 18.7 The similar construction of these appendages indicates that these
organisms share a common ancestor.

Some structures exist in organisms that have no apparent function at all, and
appear to be residual parts from a past common ancestor. We call these unused
structures without function vestigial structures. Other examples of vestigial
structures are wings on flightless birds, leaves on some cacti, and hind leg bones
in whales. Not all similarities represent homologous structures. As explained
in Determining Evolutionary Relationships, when similar characteristics occur
because of environmental constraints and not due to a close evolutionary
relationship, it is an analogy or homoplasy. For example, insects use wings to fly
like bats and birds, but the wing structure and embryonic origin are completely
different. These are analogous structures (Figure 20.8).

LINK TO LEARNING

Watch this video exploring the bones in the human body.

Another evidence of evolution is the convergence of form in organisms that share

similar environments. For example, species of unrelated animals, such as the
arctic fox and ptarmigan, living in the arctic region have been selected for
seasonal white phenotypes during winter to blend with the snow and ice (Figure
18.8). These similarities occur not because of common ancestry, but because of
similar selection pressures—the benefits of predators not seeing them.

Figure 18.8 The white winter coat of the (a) arctic fox and the (b) ptarmigan’s
plumage are adaptations to their environments. (credit a: modification of work by
Keith Morehouse)

Embryology, the study of the anatomy of an organism's development to its adult

form, also provides evidence of relatedness between now widely divergent groups
of organisms. Mutational tweaking in the embryo can have such magnified
consequences in the adult that tends to conserve embryo formation. As a result,
structures that are absent in some groups often appear in their embryonic forms
and disappear when they reach the adult or juvenile form. For example, all
vertebrate embryos, including humans, exhibit gill slits and tails at some point in
their early development. These disappear in the adults of terrestrial groups but
adult forms of aquatic groups such as fish and some amphibians maintain them.
Great ape embryos, including humans, have a tail structure during their
development that they lose when they are born.

Biogeography

The geographic distribution of organisms on the planet follows patterns that we

can explain best by evolution in conjunction with tectonic plate movement over
geological time. Broad groups that evolved before the supercontinent Pangaea
broke up (about 200 million years ago) are distributed worldwide. Groups that
evolved since the breakup appear uniquely in regions of the planet, such as the
unique flora and fauna of northern continents that formed from the supercontinent
Laurasia and of the southern continents that formed from the supercontinent
Gondwana. The presence of members of the plant family Proteaceae in Australia,
southern Africa, and South America was most predominant prior to the southern
supercontinent Gondwana breaking up.

Marsupial diversification in Australia and the absence of other mammals reflect

Australia’s long isolation. Australia has an abundance of endemic species—
species found nowhere else—which is typical of islands whose isolation by
expanses of water prevents species to migrate. Over time, these species diverge
evolutionarily into new species that look very different from their ancestors that
may exist on the mainland. Australia's marsupials, the Galápagos' finches, and
many species on the Hawaiian Islands are all unique to their one point of origin,
yet they display distant relationships to ancestral species on mainlands.
Molecular Biology

Like anatomical structures, the molecular structures of life reflect descent with
modification. DNA's universality reflects evidence of a common ancestor for all
of life. Fundamental divisions in life between the genetic code, DNA replication,
and expression are reflected in major structural differences in otherwise
conservative structures such as ribosome components and membrane structures.
In general, the relatedness of groups of organisms is reflected in the similarity of
their DNA sequences—exactly the pattern that we would expect from descent
and diversification from a common ancestor.

DNA sequences have also shed light on some of the mechanisms of evolution.
For example, it is clear that the evolution of new functions for proteins commonly
occurs after gene duplication events that allow freely modifying one copy by
mutation, selection, or drift (changes in a population’s gene pool resulting from
chance), while the second copy continues to produce a functional protein.

Misconceptions of Evolution

Although the theory of evolution generated some controversy when Darwin first
proposed it, biologists almost universally accepted it, particularly younger
biologists, within 20 years after publication of On the Origin of Species.
Nevertheless, the theory of evolution is a difficult concept and misconceptions
about how it works abound.

LINK TO LEARNING

This site addresses some of the main misconceptions associated with the theory
of evolution.
Evolution Is Just a Theory

Critics of the theory of evolution dismiss its importance by purposefully

confounding the everyday usage of the word “theory” with the way scientists use
the word. In science, we understand a “theory” to be a body of thoroughly tested
and verified explanations for a set of observations of the natural world. Scientists
have a theory of the atom, a theory of gravity, and the theory of relativity, each
which describes understood facts about the world. In the same way, the theory of
evolution describes facts about the living world. As such, a theory in science has
survived significant efforts to discredit it by scientists. In contrast, a “theory” in
common vernacular is a word meaning a guess or suggested explanation. This
meaning is more akin to the scientific concept of “hypothesis.” When critics of
evolution say it is “just a theory,” they are implying that there is little evidence
supporting it and that it is still in the process of rigorous testing. This is a
mischaracterization.

Individuals Evolve

Evolution is the change in a population's genetic composition over time,

specifically over generations, resulting from differential reproduction of
individuals with certain alleles. Individuals do change over their lifetime,
obviously, but this is development and involves changes programmed by the set
of genes the individual acquired at birth in coordination with the individual’s
environment. When thinking about the evolution of a characteristic, it is probably
best to think about the change of the average value of the characteristic in the
population over time. For example, when natural selection leads to bill-size
change in medium ground finches in the Galápagos, this does not mean that
individual bills on the finches are changing. If one measures the average bill size
among all individuals in the population at one time and then measures them in
the population several years later, this average value will be different as a result
of evolution. Although some individuals may survive from the first time to the
second, they will still have the same bill size; however, there will be many new
individuals who contribute to the shift in average bill size.

Evolution Explains the Origin of Life

It is a common misunderstanding that evolution includes an explanation of life’s

origins. Conversely, some of the theory’s critics believe that it cannot explain the
origin of life. The theory does not try to explain the origin of life. The theory of
evolution explains how populations change over time and how life diversifies the
origin of species. It does not shed light on the beginnings of life including the
origins of the first cells, which define life. Importantly, biologists believe that the
presence of life on Earth precludes the possibility that the events that led to life
on Earth can repeat themselves because the intermediate stages would
immediately become food for existing living things.

However, once a mechanism of inheritance was in place in the form of a molecule

like DNA either within a cell or pre-cell, these entities would be subject to the
principle of natural selection. More effective reproducers would increase in
frequency at the expense of inefficient reproducers. While evolution does not
explain the origin of life, it may have something to say about some of the
processes operating once pre-living entities acquired certain properties.

Organisms Evolve on Purpose

Statements such as “organisms evolve in response to a change in an environment”

are quite common, but such statements can lead to two types of
misunderstandings. First, do not interpret the statement to mean that individual
organisms evolve. The statement is shorthand for “a population evolves in
response to a changing environment.” However, a second misunderstanding may
arise by interpreting the statement to mean that the evolution is somehow
intentional. A changed environment results in some individuals in the population,
those with particular phenotypes, benefiting and therefore producing
proportionately more offspring than other phenotypes. This results in change in
the population if the characteristics are genetically determined.

It is also important to understand that the variation that natural selection works
on is already in a population and does not arise in response to an environmental
change. For example, applying antibiotics to a population of bacteria will, over
time, select a population of bacteria that are resistant to antibiotics. The
resistance, which a gene causes, did not arise by mutation because of applying
the antibiotic. The gene for resistance was already present in the bacteria's gene
pool, likely at a low frequency. The antibiotic, which kills the bacterial cells
without the resistance gene, strongly selects individuals that are resistant, since
these would be the only ones that survived and divided. Experiments have
demonstrated that mutations for antibiotic resistance do not arise as a result of
antibiotic.

In a larger sense, evolution is not goal directed. Species do not become “better”
over time. They simply track their changing environment with adaptations that
maximize their reproduction in a particular environment at a particular time.
Evolution has no goal of making faster, bigger, more complex, or even smarter
species, despite the commonness of this kind of language in popular discourse.
What characteristics evolve in a species are a function of the variation present
and the environment, both of which are constantly changing in a nondirectional
way. A trait that fits in one environment at one time may well be fatal at some
point in the future. This holds equally well for insect and human species.

Chapter Outline

21.1 Viral Evolution, Morphology, and Classification

21.2 Virus Infections and Hosts

21.3 Prevention and Treatment of Viral Infections

21.4 Other Acellular Entities: Prions and Viroids

Viruses are noncellular parasitic entities that cannot be classified within any
kingdom. They can infect organisms as diverse as bacteria, plants, and animals.
In fact, viruses exist in a sort of netherworld between a living organism and a
nonliving entity. Living things grow, metabolize, and reproduce. In contrast,
viruses are not cellular, do not have a metabolism or grow, and cannot divide by
cell division. Viruses can copy, or replicate themselves; however, they are
entirely dependent on resources derived from their host cells to produce progeny
viruses—which are assembled in their mature form. No one knows exactly when
or how viruses evolved or from what ancestral source because viruses have not
left a fossil record. Some virologists contend that modern viruses are a mosaic of
bits and pieces of nucleic acids picked up from various sources along their
respective evolutionary paths.

Learning Objectives

By the end of this section, you will be able to do the following:

 Describe how viruses were first discovered and how they are detected
 Discuss three hypotheses about how viruses evolved
 Describe the general structure of a virus
 Recognize the basic shapes of viruses
 Understand past and emerging classification systems for viruses
 Describe the basis for the Baltimore classification system

Viruses are diverse entities: They vary in structure, methods of replication, and
the hosts they infect. Nearly all forms of life—from prokaryotic bacteria and
archaeans, to eukaryotes such as plants, animals, and fungi—have viruses that
infect them. While most biological diversity can be understood through
evolutionary history (such as how species have adapted to changing
environmental conditions and how different species are related to one another
through common descent), much about virus origins and evolution remains
unknown.

Discovery and Detection

Viruses were first discovered after the development of a porcelain filter—the

Chamberland-Pasteur filter—that could remove all bacteria visible in the
microscope from any liquid sample. In 1886, Adolph Meyer demonstrated that a
disease of tobacco plants—tobacco mosaic disease—could be transferred from
a diseased plant to a healthy one via liquid plant extracts. In 1892, Dmitri
Ivanowski showed that this disease could be transmitted in this way even after
the Chamberland-Pasteur filter had removed all viable bacteria from the extract.
Still, it was many years before it was proved that these “filterable” infectious
agents were not simply very small bacteria but were a new type of very small,
disease-causing particle.

Most virions, or single virus particles, are very small, about 20 to 250 nanometers
in diameter. However, some recently discovered viruses from amoebae range up
to 1000 nm in diameter. With the exception of large virions, like the poxvirus and
other large DNA viruses, viruses cannot be seen with a light microscope. It was
not until the development of the electron microscope in the late 1930s that
scientists got their first good view of the structure of the tobacco mosaic virus
(TMV) (Figure 21.1), discussed above, and other viruses (Figure 21.2). The
surface structure of virions can be observed by both scanning and transmission
electron microscopy, whereas the internal structures of the virus can only be
observed in images from a transmission electron microscope. The use of electron
microscopy and other technologies has allowed for the discovery of many viruses
of all types of living organisms.

Figure 21.2 Most virus particles are visible only by electron microscopy. In these
transmission electron micrographs, (a) a virus is as dwarfed by the bacterial cell
it infects, as (b) these E. coli cells are dwarfed by cultured colon cells. (credit a:
modification of work by U.S. Dept. of Energy, Office of Science, LBL, PBD;
credit b: modification of work by J.P. Nataro and S. Sears, unpub. data, CDC;
scale-bar data from Matt Russell)

Evolution of Viruses

Although biologists have a significant amount of knowledge about how present-

day viruses mutate and adapt, much less is known about how viruses originated
in the first place. When exploring the evolutionary history of most organisms,
scientists can look at fossil records and similar historic evidence. However,
viruses do not fossilize, as far as we know, so researchers must extrapolate from
investigations of how today’s viruses evolve and by using biochemical and
genetic information to create speculative virus histories.
Most scholars agree that viruses don’t have a single common ancestor, nor is there
a single reasonable hypothesis about virus origins. There are current evolutionary
scenarios that may explain the origin of viruses. One such hypothesis, the
“devolution” or the regressive hypothesis, suggests that viruses evolved from
free-living cells, or from intracellular prokaryotic parasites. However, many
components of how this process might have occurred remain a mystery. A second
hypothesis, the escapist or the progressive hypothesis, suggests that viruses
originated from RNA and DNA molecules, or self-replicating entities similar to
transposons or other mobile genetic elements, that escaped from a host cell with
the ability to enter another. A third hypothesis, the virus first hypothesis, suggests
that viruses may have been the first self-replicating entities before the first cells.
In all cases, viruses are probably continuing to evolve along with the cells on
which they rely on as hosts.

As technology advances, scientists may develop and refine additional hypotheses

to explain the origins of viruses. The emerging field called virus molecular
systematics attempts to do just that through comparisons of sequenced genetic
material. These researchers hope one day to better understand the origin of
viruses—a discovery that could lead to advances in the treatments for the ailments
they produce.

Viral Morphology

Viruses are noncellular, meaning they are biological entities that do not have a
cellular structure. They therefore lack most of the components of cells, such as
organelles, ribosomes, and the plasma membrane. A virion consists of a nucleic
acid core, an outer protein coating or capsid, and sometimes an
outer envelope made of protein and phospholipid membranes derived from the
host cell. Viruses may also contain additional proteins, such as enzymes, within
the capsid or attached to the viral genome. The most obvious difference between
members of different viral families is the variation in their morphology, which is
quite diverse. An interesting feature of viral complexity is that the complexity of
the host does not necessarily correlate with the complexity of the virion. In fact,
some of the most complex virion structures are found in the bacteriophages—
viruses that infect the simplest living organisms, bacteria.

Morphology

Viruses come in many shapes and sizes, but these features are consistent for each
viral family. As we have seen, all virions have a nucleic acid genome covered by
a protective capsid. The proteins of the capsid are encoded in the viral genome,
and are called capsomeres. Some viral capsids are simple helices or polyhedral
“spheres,” whereas others are quite complex in structure (Figure 21.3).
Figure 21.3 Viral capsids can be (a) helical, (b) polyhedral, or (c) have a complex
shape. (credit a “micrograph”: modification of work by USDA ARS; credit b
“micrograph”: modification of work by U.S. Department of Energy)

In general, the capsids of viruses are classified into four groups: helical,
icosahedral, enveloped, and head-and-tail. Helical capsids are long and
cylindrical. Many plant viruses are helical, including TMV. Icosahedral
viruses have shapes that are roughly spherical, such as those of poliovirus or
herpesviruses. Enveloped viruses have membranes derived from the host cell that
surrounds the capsids. Animal viruses, such as HIV, are frequently
enveloped. Head-and-tail viruses infect bacteria and have a head that is similar
to icosahedral viruses and a tail shaped like helical viruses.

Many viruses use some sort of glycoprotein to attach to their host cells via
molecules on the cell called viral receptors. For these viruses, attachment is
required for later penetration of the cell membrane; only after penetration takes
place can the virus complete its replication inside the cell. The receptors that
viruses use are molecules that are normally found on cell surfaces and have their
own physiological functions. It appears that viruses have simply evolved to make
use of these molecules for their own replication. For example, HIV uses the CD4
molecule on T lymphocytes as one of its receptors (Figure 21.4). CD4 is a type
of molecule called a cell adhesion molecule, which functions to keep different
types of immune cells in close proximity to each other during the generation of a
T lymphocyte immune response.
Figure 21.4 A virus and its host receptor protein. The HIV virus binds the CD4
receptor on the surface of human cells. CD4 receptors help white blood cells to
communicate with other cells of the immune system when producing an immune
response. (credit: modification of work by NIAID, NIH)

One of the most complex virions known, the T4 bacteriophage (which infects
the Escherichia coli) bacterium, has a tail structure that the virus uses to attach to
host cells and a head structure that houses its DNA.

Adenovirus, a non-enveloped animal virus that causes respiratory illnesses in

humans, uses glycoprotein spikes protruding from its capsomeres to attach to host
cells. Non-enveloped viruses also include those that cause polio (poliovirus),
plantar warts (papillomavirus), and hepatitis A (hepatitis A virus).

Enveloped virions, such as the influenza virus, consist of nucleic acid (RNA in
the case of influenza) and capsid proteins surrounded by a phospholipid bilayer
envelope that contains virus-encoded proteins. Glycoproteins embedded in the
viral envelope are used to attach to host cells. Other envelope proteins are
the matrix proteins that stabilize the envelope and often play a role in the
assembly of progeny virions. Chicken pox, HIV, and mumps are other examples
of diseases caused by viruses with envelopes. Because of the fragility of the
envelope, non-enveloped viruses are more resistant to changes in temperature,
pH, and some disinfectants than enveloped viruses.

Overall, the shape of the virion and the presence or absence of an envelope tell
us little about what disease the virus may cause or what species it might infect,
but they are still useful means to begin viral classification (Figure 21.5).

VISUAL CONNECTION

Figure 21.5 Complex Viruses. Viruses can be either complex or relatively simple
in shape. This figure shows three relatively complex virions: the bacteriophage
T4, with its DNA-containing head group and tail fibers that attach to host cells;
adenovirus, which uses spikes from its capsid to bind to host cells; and the
influenza virus, which uses glycoproteins embedded in its envelope to bind to
host cells. The influenza virus also has matrix proteins, internal to the envelope,
which help stabilize the virion’s shape. (credit “bacteriophage, adenovirus”:
modification of work by NCBI, NIH; credit "influenza virus": modification of
work by Dan Higgins, Centers for Disease Control and Prevention)

Which of the following statements about virus structure is true?

a. All viruses are encased in a viral membrane.

b. The capsomere is made up of small protein subunits called capsids.
c. DNA is the genetic material in all viruses.
d. Glycoproteins help the virus attach to the host cell.

Types of Nucleic Acid

Unlike nearly all living organisms that use DNA as their genetic material, viruses
may use either DNA or RNA. The virus core contains the genome—the total
genetic content of the virus. Viral genomes tend to be small, containing only those
genes that encode proteins which the virus cannot get from the host cell. This
genetic material may be single- or double-stranded. It may also be linear or
circular. While most viruses contain a single nucleic acid, others have genomes
divided into several segments. The RNA genome of the influenza virus is
segmented, which contributes to its variability and continuous evolution, and
explains why it is difficult to develop a vaccine against it.

In DNA viruses, the viral DNA directs the host cell’s replication proteins to
synthesize new copies of the viral genome and to transcribe and translate that
genome into viral proteins. Human diseases caused by DNA viruses include
chickenpox, hepatitis B, and adenoviruses. Sexually transmitted DNA viruses
include the herpes virus and the human papilloma virus (HPV), which has been
associated with cervical cancer and genital warts.
RNA viruses contain only RNA as their genetic material. To replicate their
genomes in the host cell, the RNA viruses must encode their own enzymes that
can replicate RNA into RNA or, in the retroviruses, into DNA. These RNA
polymerase enzymes are more likely to make copying errors than DNA
polymerases, and therefore often make mistakes during transcription. For this
reason, mutations in RNA viruses occur more frequently than in DNA viruses.
This causes them to change and adapt more rapidly to their host. Human diseases
caused by RNA viruses include influenza, hepatitis C, measles, and rabies. The
HIV virus, which is sexually transmitted, is an RNA retrovirus.

The Challenge of Virus Classification

Because most viruses probably evolved from different ancestors, the systematic
methods that scientists have used to classify prokaryotic and eukaryotic cells are
not very useful. If viruses represent “remnants” of different organisms, then even
genomic or protein analysis is not useful. Why?, Because viruses have no
common genomic sequence that they all share. For example, the 16S rRNA
sequence so useful for constructing prokaryote phylogenies is of no use for a
creature with no ribosomes! Biologists have used several classification systems
in the past. Viruses were initially grouped by shared morphology. Later, groups
of viruses were classified by the type of nucleic acid they contained, DNA or
RNA, and whether their nucleic acid was single- or double-stranded. However,
these earlier classification methods grouped viruses differently, because they
were based on different sets of characters of the virus. The most commonly used
classification method today is called the Baltimore classification scheme, and is
based on how messenger RNA (mRNA) is generated in each particular type of
virus.
 Past Systems of Classification

Viruses contain only a few elements by which they can be classified: the viral
genome, the type of capsid, and the envelope structure for the enveloped viruses.
All of these elements have been used in the past for viral classification (Table
21.1 and Figure 21.6). Viral genomes may vary in the type of genetic material
(DNA or RNA) and its organization (single- or double-stranded, linear or circular,
and segmented or non-segmented). In some viruses, additional proteins needed
for replication are associated directly with the genome or contained within the
viral capsid.

Virus Classification by Genome Structure

Genome Structure Examples

 RNA  Rabies virus, retroviruses

 DNA  Herpesviruses, smallpox virus

 Single-stranded  Rabies virus, retroviruses

 Double-stranded  Herpesviruses, smallpox virus

 Rabies virus, retroviruses,

 Linear herpesviruses, smallpox virus
 Circular  Papillomaviruses, many
bacteriophages

 Parainfluenza viruses
 Non-segmented: genome consists of a
 Influenza viruses
single segment of genetic material
 Genome Structure Examples

 Segmented: genome is divided into

multiple segments

Table21.1

Figure 21.6 Viruses can be classified according to their core genetic material and
capsid design. (a) Rabies virus has a single-stranded RNA (ssRNA) core and an
enveloped helical capsid, whereas (b) variola virus, the causative agent of
smallpox, has a double-stranded DNA (dsDNA) core and a complex capsid.
Rabies transmission occurs when saliva from an infected mammal enters a
wound. The virus travels through neurons in the peripheral nervous system to the
central nervous system, where it impairs brain function, and then travels to other
tissues. The virus can infect any mammal, and most die within weeks of infection.
Smallpox is a human virus transmitted by inhalation of the variola virus, localized
in the skin, mouth, and throat, which causes a characteristic rash. Before its
eradication in 1979, infection resulted in a 30 to 35 percent mortality rate. (credit
“rabies diagram”: modification of work by CDC; “rabies micrograph”:
modification of work by Dr. Fred Murphy, CDC; credit “small pox micrograph”:
modification of work by Dr. Fred Murphy, Sylvia Whitfield, CDC; credit
“smallpox photo”: modification of work by CDC; scale-bar data from Matt
Russell)

Viruses can also be classified by the design of their capsids (Table

21.2 and Figure 21.7). Capsids are classified as naked icosahedral, enveloped
icosahedral, enveloped helical, naked helical, and complex. The type of genetic
material (DNA or RNA) and its structure (single- or double-stranded, linear or
circular, and segmented or non-segmented) are used to classify the virus core
structures (Table 21.2).

Virus Classification by Capsid Structure

Capsid Classification Examples

Naked icosahedral Hepatitis A virus, polioviruses

Epstein-Barr virus, herpes simplex

Enveloped icosahedral virus, rubella virus, yellow fever
virus, HIV-1

Influenza viruses, mumps virus,

Enveloped helical
measles virus, rabies virus

Naked helical Tobacco mosaic virus

 Capsid Classification Examples

Complex with many proteins; some have

Herpesviruses, smallpox virus,
combinations of icosahedral and helical
hepatitis B virus, T4 bacteriophage
capsid structures

Table21.2

Figure 21.7 Transmission electron micrographs of various viruses show their

capsid structures. The capsid of the (a) polio virus is naked icosahedral; (b) the
Epstein-Barr virus capsid is enveloped icosahedral; (c) the mumps virus capsid is
an enveloped helix; (d) the tobacco mosaic virus capsid is naked helical; and (e)
the herpesvirus capsid is complex. (credit a: modification of work by Dr. Fred
Murphy, Sylvia Whitfield; credit b: modification of work by Liza Gross; credit c:
modification of work by Dr. F. A. Murphy, CDC; credit d: modification of work
by USDA ARS; credit e: modification of work by Linda Stannard, Department
of Medical Microbiology, University of Cape Town, South Africa, NASA; scale-
bar data from Matt Russell)
Baltimore Classification

The most commonly and currently used system of virus classification was first
developed by Nobel Prize-winning biologist David Baltimore in the early 1970s.
In addition to the differences in morphology and genetics mentioned above, the
Baltimore classification scheme groups viruses according to how the mRNA is
produced during the replicative cycle of the virus.

Group I viruses contain double-stranded DNA (dsDNA) as their genome. Their

mRNA is produced by transcription in much the same way as with cellular DNA,
using the enzymes of the host cell.

Group II viruses have single-stranded DNA (ssDNA) as their genome. They

convert their single-stranded genomes into a dsDNA intermediate before
transcription to mRNA can occur.

Group III viruses use dsRNA as their genome. The strands separate, and one of
them is used as a template for the generation of mRNA using the RNA-dependent
RNA polymerase encoded by the virus.

Group IV viruses have ssRNA as their genome with a positive polarity, which
means that the genomic RNA can serve directly as mRNA. Intermediates of
dsRNA, called replicative intermediates, are made in the process of copying the
genomic RNA. Multiple, full-length RNA strands of negative
polarity (complementary to the positive-stranded genomic RNA) are formed
from these intermediates, which may then serve as templates for the production
of RNA with positive polarity, including both full-length genomic RNA and
shorter viral mRNAs.

Group V viruses contain ssRNA genomes with a negative polarity, meaning

that their sequence is complementary to the mRNA. As with Group IV viruses,
dsRNA intermediates are used to make copies of the genome and produce mRNA.
In this case, the negative-stranded genome can be converted directly to mRNA.
Additionally, full-length positive RNA strands are made to serve as templates for
the production of the negative-stranded genome.

Group VI viruses have diploid (two copies) ssRNA genomes that must be
converted, using the enzyme reverse transcriptase, to dsDNA; the dsDNA is
then transported to the nucleus of the host cell and inserted into the host genome.
Then, mRNA can be produced by transcription of the viral DNA that was
integrated into the host genome.

Group VII viruses have partial dsDNA genomes and make ssRNA intermediates
that act as mRNA, but are also converted back into dsDNA genomes by reverse
transcriptase, necessary for genome replication.

The characteristics of each group in the Baltimore classification are summarized

in Table 21.3 with examples of each group.

Baltimore Classification

Mode of
mRNA
Group Characteristics Production Example

mRNA is
transcribed
Double-stranded Herpes simplex
I directly from
DNA (herpesvirus)
the DNA
template
 Mode of
mRNA
Group Characteristics Production Example

DNA is
converted to
Single-stranded double- Canine parvovirus
II
DNA stranded form (parvovirus)
before RNA is
transcribed

mRNA is
Childhood
Double-stranded transcribed
III gastroenteritis
RNA from the RNA
(rotavirus)
genome

Genome
Single stranded Common cold
IV functions as
RNA (+) (picornavirus)
mRNA

mRNA is
Single stranded transcribed Rabies
V
RNA (-) from the RNA (rhabdovirus)
genome
 Mode of
mRNA
Group Characteristics Production Example

Reverse
transcriptase
makes DNA
from the RNA
genome; DNA
Single stranded is then
Human
RNA viruses incorporated in
VI immunodeficiency
with reverse the host
virus (HIV)
transcriptase genome;
mRNA is
transcribed
from the
incorporated
DNA

The viral
genome is
double-
Double stranded
stranded DNA,
DNA viruses Hepatitis B virus
VII but viral DNA
with reverse (hepadnavirus)
is replicated
transcriptase
through an
RNA
intermediate;
 Mode of
mRNA
Group Characteristics Production Example

the RNA may

serve directly
as mRNA or as
a template to
make mRNA

Table21.3

Learning Objectives

By the end of this section, you will be able to do the following:

 List the steps of replication and explain what occurs at each step
 Describe the lytic and lysogenic cycles of virus replication
 Explain the transmission of plant and animal viruses
 Discuss some of the diseases caused by plant and animal viruses
 Discuss the economic impact of plant and animal viruses

Viruses are obligate, intracellular parasites. A virus must first recognize and
attach to a specific living cell prior to entering it. After penetration, the invading
virus must copy its genome and manufacture its own proteins. Finally, the
progeny virions must escape the host cell so that they can infect other cells.
Viruses can infect only certain species of hosts and only certain cells within that
host. Specific host cells that a virus must occupy and use to replicate are
called permissive. In most cases, the molecular basis for this specificity is due to
a particular surface molecule known as the viral receptor on the host cell surface.
A specific viral receptor is required for the virus to attach. In addition, differences
in metabolism and host-cell immune responses (based on differential gene
expression) are a likely factor in determining which cells a virus may target for
replication.

Steps of Virus Infections

A virus must use its host-cell processes to replicate. The viral replication cycle
can produce dramatic biochemical and structural changes in the host cell, which
may cause cell damage. These changes, called cytopathic effects, can change cell
functions or even destroy the cell. Some infected cells, such as those infected by
the common cold virus known as rhinovirus, die through lysis (bursting)
or apoptosis (programmed cell death or “cell suicide”), releasing all progeny
virions at once. The symptoms of viral diseases result both from such cell damage
caused by the virus and from the immune response to the virus, which attempts
to control and eliminate the virus from the body.

Many animal viruses, such as HIV (human immunodeficiency virus), leave the
infected cells of the immune system by a process known as budding, where
virions leave the cell individually. During the budding process, the cell does not
undergo lysis and is not immediately killed. However, the damage to the cells
that the virus infects may make it impossible for the cells to function normally,
even though the cells remain alive for a period of time. Most productive viral
infections follow similar steps in the virus replication cycle: attachment,
penetration, uncoating, replication, assembly, and release (Figure 21.8).

Attachment

A virus attaches to a specific receptor site on the host cell membrane through
attachment proteins in the capsid or via glycoproteins embedded in the viral
envelope. The specificity of this interaction determines the host—and the cells
within the host—that can be infected by a particular virus. This can be illustrated
by thinking of several keys and several locks, where each key will fit only one
specific lock.

LINK TO LEARNING

This video explains how influenza attacks the body.

Entry

Viruses may enter a host cell either with or without the viral capsid. The nucleic
acid of bacteriophages enters the host cell “naked,” leaving the capsid outside the
cell. Plant and animal viruses can enter through endocytosis (as you may recall,
the cell membrane surrounds and engulfs the entire virus). Some enveloped
viruses enter the cell when the viral envelope fuses directly with the cell
membrane. Once inside the cell, the viral capsid degrades, and then the viral
nucleic acid is released and becomes available for replication and transcription.

Replication and Assembly

The replication mechanism depends on the viral genome. DNA viruses usually
use host-cell proteins and enzymes to replicate the viral DNA and to transcribe
viral mRNA, which is then used to direct viral protein synthesis. RNA viruses
usually use the RNA core as a template for synthesis of viral genomic RNA and
mRNA. The viral mRNA directs the host cell to synthesize viral enzymes and
capsid proteins, and assemble new virions.

Of course, there are exceptions to this pattern. If a host cell does not provide the
enzymes necessary for viral replication, viral genes supply the information to
direct synthesis of the missing proteins. Retroviruses, such as HIV (group VI of
the Baltimore classification scheme), have an RNA genome that must be reverse
transcribed into DNA, which then is incorporated into the host cell genome. To
convert RNA into DNA, retroviruses must contain genes that encode the virus-
specific enzyme reverse transcriptase that transcribes an RNA template to DNA.
Reverse transcription never occurs in uninfected host cells—the enzyme reverse
transcriptase is only derived from the expression of viral genes within the infected
host cells. The fact that HIV produces some of its own enzymes not found in the
host has allowed researchers to develop drugs that inhibit these enzymes without
affecting the host’s metabolism.

This approach has led to the development of a variety of drugs used to treat HIV
and has been effective at reducing the number of infectious virions (copies of
viral RNA) in the blood to non-detectable levels in many HIV-infected
individuals.

Egress

The last stage of viral replication is the release of the new virions produced in the
host organism, where they are able to infect adjacent cells and repeat the
replication cycle. As you’ve learned, some viruses are released when the host cell
dies, and other viruses can leave infected cells by budding through the membrane
without directly killing the cell.

VISUAL CONNECTION
Figure 21.8 The influenza reproductive cycle. In influenza virus infection,
glycoproteins on the capsid attach to a host epithelial cell. Following this, the
virus is engulfed. RNA and proteins are then made and assembled into new
virions.

Influenza virus is packaged in a viral envelope that fuses with the plasma
membrane. This way, the virus can exit the host cell without killing it. What
advantage does the virus gain by keeping the host cell alive?

LINK TO LEARNING

Watch a video on viruses, identifying structures, modes of transmission,

replication, and more.
Different Hosts and Their Viruses

As you’ve learned, viruses often infect very specific hosts, as well as specific
cells within the host. This feature of a virus makes it specific to one or a few
species of life on Earth. On the other hand, so many different types of viruses
exist on Earth that nearly every living organism has its own set of viruses trying
to infect its cells. Even prokaryotes, the smallest and simplest of cells, may be
attacked by specific types of viruses. In the following section, we will look at
some of the features of viral infection of prokaryotic cells. As we have learned,
viruses that infect bacteria are called bacteriophages (Figure 21.9). Archaea have
their own similar viruses.

Bacteriophages

Figure 21.9 Bacteriophages attached to a host cell (transmission electron

micrograph). In bacteriophage with tails, like the one shown here, the tails serve
as a passageway for transmission of the phage genome. (credit: modification of
work by Dr. Graham Beards; scale-bar data from Matt Russell)
Most bacteriophages are dsDNA viruses, which use host enzymes for DNA
replication and RNA transcription. Phage particles must bind to specific surface
receptors and actively insert the genome into the host cell. (The complex tail
structures seen in many bacteriophages are actively involved in getting the viral
genome across the prokaryotic cell wall.) When infection of a cell by a
bacteriophage results in the production of new virions, the infection is said to
be productive. If the virions are released by bursting the cell, the virus replicates
by means of a lytic cycle (Figure 21.10). An example of a lytic bacteriophage is
T4, which infects Escherichia coli found in the human intestinal tract.
Sometimes, however, a virus can remain within the cell without being released.
For example, when a temperate bacteriophage infects a bacterial cell, it replicates
by means of a lysogenic cycle (Figure 21.10), and the viral genome is
incorporated into the genome of the host cell. When the phage DNA is
incorporated into the host-cell genome, it is called a prophage. An example of a
lysogenic bacteriophage is the λ (lambda) virus, which also infects
the E. coli bacterium. Viruses that infect plant or animal cells may sometimes
undergo infections where they are not producing virions for long periods. An
example is the animal herpesviruses, including herpes simplex viruses, the cause
of oral and genital herpes in humans. In a process called latency, these viruses
can exist in nervous tissue for long periods of time without producing new
virions, only to leave latency periodically and cause lesions in the skin where the
virus replicates. Even though there are similarities between lysogeny and latency,
the term lysogenic cycle is usually reserved to describe bacteriophages. Latency
will be described in more detail in the next section.

VISUAL CONNECTION
Figure 21.10 A temperate bacteriophage has both lytic and lysogenic cycles. In
the lytic cycle, the phage replicates and lyses the host cell. In the lysogenic cycle,
phage DNA is incorporated into the host genome, where it is passed on to
subsequent generations. Environmental stressors such as starvation or exposure
to toxic chemicals may cause the prophage to excise and enter the lytic cycle.

Which of the following statements is false?

a. In the lytic cycle, new phages are produced and released into the
environment.
b. In the lysogenic cycle, phage DNA is incorporated into the host genome.
c. An environmental stressor can cause the phage to initiate the lysogenic
cycle.
d. Cell lysis only occurs in the lytic cycle.

Plant Viruses
Most plant viruses, like the tobacco mosaic virus, have single-stranded (+) RNA
genomes. However, there are also plant viruses in most other virus categories.
Unlike bacteriophages, plant viruses do not have active mechanisms for
delivering the viral genome across the protective cell wall. For a plant virus to
enter a new host plant, some type of mechanical damage must occur. This damage
is often caused by weather, insects, animals, fire, or human activities like farming
or landscaping. Movement from cell to cell within a plant can be facilitated by
viral modification of plasmodesmata (cytoplasmic threads that pass from one
plant cell to the next). Additionally, plant offspring may inherit viral diseases
from parent plants. Plant viruses can be transmitted by a variety of vectors,
through contact with an infected plant’s sap, by living organisms such as insects
and nematodes, and through pollen. The transfer of a virus from one plant to
another is known as horizontal transmission, whereas the inheritance of a virus
from a parent is called vertical transmission.

Symptoms of viral diseases vary according to the virus and its host (Table 21.4).
One common symptom is hyperplasia, the abnormal proliferation of cells that
causes the appearance of plant tumors known as galls. Other viruses
induce hypoplasia, or decreased cell growth, in the leaves of plants, causing thin,
yellow areas to appear. Still other viruses affect the plant by directly killing plant
cells, a process known as cell necrosis. Other symptoms of plant viruses include
malformed leaves; black streaks on the stems of the plants; altered growth of
stems, leaves, or fruits; and ring spots, which are circular or linear areas of
discoloration found in a leaf.

Some Common Symptoms of Plant Viral Diseases

 Symptom Appears as

Hyperplasia Galls (tumors)

Hypoplasia Thinned, yellow splotches on leaves

Cell necrosis Dead, blackened stems, leaves, or fruit

Abnormal growth patterns Malformed stems, leaves, or fruit

Discoloration Yellow, red, or black lines, or rings in stems, leaves, or

Table21.4

Plant viruses can seriously disrupt crop growth and development, significantly
affecting our food supply. They are responsible for poor crop quality and quantity
globally, and can bring about huge economic losses annually. Others viruses may
damage plants used in landscaping. Some viruses that infect agricultural food
plants include the name of the plant they infect, such as tomato spotted wilt virus,
bean common mosaic virus, and cucumber mosaic virus. In plants used for
landscaping, two of the most common viruses are peony ring spot and rose mosaic
virus. There are far too many plant viruses to discuss each in detail, but symptoms
of bean common mosaic virus result in lowered bean production and stunted,
unproductive plants. In the ornamental rose, the rose mosaic disease causes wavy
yellow lines and colored splotches on the leaves of the plant.

Animal Viruses

Animal viruses, unlike the viruses of plants and bacteria, do not have to penetrate
a cell wall to gain access to the host cell. The virus may even induce the host cell
to cooperate in the infection process. Non-enveloped or “naked” animal viruses
may enter cells in two different ways. As a protein in the viral capsid binds to its
receptor on the host cell, the virus may be taken inside the cell via a vesicle during
the normal cell process of receptor-mediated endocytosis. An alternative method
of cell penetration used by non-enveloped viruses is for capsid proteins to
undergo shape changes after binding to the receptor, creating channels in the host
cell membrane. The viral genome is then “injected” into the host cell through
these channels in a manner analogous to that used by many bacteriophages.

Enveloped viruses also have two ways of entering cells after binding to their
receptors: receptor-mediated endocytosis, or fusion. Many enveloped viruses
enter the cell by receptor-mediated endocytosis in a fashion similar to that seen
in some non-enveloped viruses. On the other hand, fusion only occurs with
enveloped virions. These viruses, which include HIV among others, use special
fusion proteins in their envelopes to cause the envelope to fuse with the plasma
membrane of the cell, thus releasing the genome and capsid of the virus into the
cell cytoplasm.

After making their proteins and copying their genomes, animal viruses complete
the assembly of new virions and exit the cell. As we have already discussed using
the example the influenza virus, enveloped animal viruses may bud from the cell
membrane as they assemble themselves, taking a piece of the cell’s plasma
membrane in the process. On the other hand, non-enveloped viral progeny, such
as rhinoviruses, accumulate in infected cells until there is a signal for lysis or
apoptosis, and all virions are released together.

As you will learn in the next module, animal viruses are associated with a variety
of human diseases. Some of them follow the classic pattern of acute disease,
where symptoms get increasingly worse for a short period followed by the
elimination of the virus from the body by the immune system and eventual
recovery from the infection. Examples of acute viral diseases are the common
cold and influenza. Other viruses cause long-term chronic infections, such as the
virus causing hepatitis C, whereas others, like herpes simplex virus, only
cause intermittent symptoms. Still other viruses, such as human herpesviruses 6
and 7, which in some cases can cause the minor childhood disease roseola, often
successfully cause productive infections without causing any symptoms at all in
the host, and thus we say these patients have an asymptomatic infection.

In hepatitis C infections, the virus grows and reproduces in liver cells, causing
low levels of liver damage. The damage is so low that infected individuals are
often unaware that they are infected, and many infections are detected only by
routine blood work on patients with risk factors such as intravenous drug use. On
the other hand, since many of the symptoms of viral diseases are caused by
immune responses, a lack of symptoms is an indication of a weak immune
response to the virus. This allows the virus to escape elimination by the immune
system and persist in individuals for years, all the while producing low levels of
progeny virions in what is known as a chronic viral disease. Chronic infection of
the liver by this virus leads to a much greater chance of developing liver cancer,
sometimes as much as 30 years after the initial infection.

As already discussed, herpes simplex virus can remain in a state of latency in

nervous tissue for months, even years. As the virus “hides” in the tissue and
makes few if any viral proteins, there is nothing for the immune response to act
against, and immunity to the virus slowly declines. Under certain conditions,
including various types of physical and psychological stress, the latent herpes
simplex virus may be reactivated and undergo a lytic replication cycle in the skin,
causing the lesions associated with the disease. Once virions are produced in the
skin and viral proteins are synthesized, the immune response is again stimulated
and resolves the skin lesions in a few days or weeks by destroying viruses in the
skin. As a result of this type of replicative cycle, appearances of cold sores and
genital herpes outbreaks only occur intermittently, even though the viruses
remain in the nervous tissue for life. Latent infections are common with other
herpesviruses as well, including the varicella-zoster virus that causes chickenpox.
After having a chickenpox infection in childhood, the varicella-zoster virus can
remain latent for many years and reactivate in adults to cause the painful
condition known as “shingles” (Figure 21.11).

Figure 21.11 A latent virus infection. (a) Varicella-zoster, the virus that causes
chickenpox, has an enveloped icosahedral capsid visible in this transmission
electron micrograph. Its double-stranded DNA genome becomes incorporated in
the host DNA and can reactivate after latency in the form of (b) shingles, often
exhibiting a rash. (credit a: modification of work by Dr. Erskine Palmer, B. G.
Martin, CDC; credit b: modification of work by “rosmary”/Flickr; scale-bar data
from Matt Russell)

Some animal-infecting viruses, including the hepatitis C virus discussed above,

are known as oncogenic viruses: They have the ability to cause cancer. These
viruses interfere with the normal regulation of the host cell cycle either by
introducing genes that stimulate unregulated cell growth (oncogenes) or by
interfering with the expression of genes that inhibit cell growth. Oncogenic
viruses can be either DNA or RNA viruses. Cancers known to be associated with
viral infections include cervical cancer, caused by human papillomavirus (HPV)
(Figure 21.12), liver cancer caused by hepatitis B virus, T-cell leukemia, and
several types of lymphoma.

Figure 21.12 HPV, or human papillomavirus, has a naked icosahedral capsid

visible in this transmission electron micrograph and a double-stranded DNA
genome that is incorporated into the host DNA. The virus, which is sexually
transmitted, is oncogenic and can lead to cervical cancer. (credit: modification of
work by NCI, NIH; scale-bar data from Matt Russell)

22.

The first electron micrograph of a virus (tobacco mosaic virus) was produced in
1939. Before that time, how did scientists know that viruses existed if they could
not see them? (Hint: Early scientists called viruses “filterable agents.”)

23.

Varicella-zoster virus is a double-stranded DNA virus that causes chickenpox.

How does its genome structure provide an evolutionary advantage over a single-
stranded DNA virus?
24.

Classify the Rabies virus (a rhabdovirus family member) and HIV-1 with both
the Baltimore and genomic structure systems. Compare your results. What
conclusions can be made about these two different methods?

25.

Why can’t dogs catch the measles?

26.

One of the first and most important targets for drugs to fight infection with HIV
(a retrovirus) is the reverse transcriptase enzyme. Why?

27.

In this section, you were introduced to different types of viruses and viral
diseases. Briefly discuss the most interesting or surprising thing you learned
about viruses.

28.

Although plant viruses cannot infect humans, what are some of the ways in which
they affect humans?

29.

A bacteriophage with a lytic life cycle develops a mutation that allows it to now
also go through the lysogenic cycle. How would this provide an evolutionary
advantage over the other bacteriophages that can only spread through lytic
cycles?

30.
Why is immunization after being bitten by a rabid animal so effective and why
aren’t people vaccinated for rabies like dogs and cats are?

31.

The vaccine Gardasil that targets human papilloma virus (HPV), the etiological
agent of genital warts, was developed after the anti-HPV medication podofilox.
Why would doctors still want a vaccine created after anti-viral medications were
available?

32.

Prions are responsible for variant Creutzfeldt-Jakob Disease, which has resulted
in over 100 human deaths in Great Britain during the last 10 years. How do
humans contract this disease?

33.

How are viroids like viruses?

34.

A botanist notices that a tomato plant looks diseased. How could the botanist
confirm that the agent causing disease is a viroid, and not a virus?

Chapter Outline

22.1 Prokaryotic Diversity

22.2 Structure of Prokaryotes: Bacteria and Archaea

22.3 Prokaryotic Metabolism

22.4 Bacterial Diseases in Humans

22.5 Beneficial Prokaryotes

In the recent past, scientists grouped living things into five kingdoms—animals,
plants, fungi, protists, and prokaryotes—based on several criteria, such as the
absence or presence of a nucleus and other membrane-bound organelles, the
absence or presence of cell walls, multicellularity, and so on. In the late
20th century, the pioneering work of Carl Woese and others compared sequences
of small-subunit ribosomal RNA (SSU rRNA), which resulted in a more
fundamental way to group organisms on Earth. Based on differences in the
structure of cell membranes and in rRNA, Woese and his colleagues proposed
that all life on Earth evolved along three lineages, called domains. The domain
Bacteria comprises all organisms in the kingdom Bacteria, the domain Archaea
comprises the rest of the prokaryotes, and the domain Eukarya comprises all
eukaryotes—including organisms in the kingdoms Animalia, Plantae, Fungi, and
Protista.

Two of the three domains—Bacteria and Archaea—are prokaryotic. Prokaryotes

were the first inhabitants on Earth, appearing 3.5 to 3.8 billion years ago. These
organisms are abundant and ubiquitous; that is, they are present everywhere. In
addition to inhabiting moderate environments, they are found in extreme
conditions: from boiling springs to permanently frozen environments in
Antarctica; from salty environments like the Dead Sea to environments under
tremendous pressure, such as the depths of the ocean; and from areas without
oxygen, such as a waste management plant, to radioactively contaminated
regions, such as Chernobyl. Prokaryotes reside in the human digestive system and
on the skin, are responsible for certain illnesses, and serve an important role in
the preparation of many foods.

Learning Objectives

By the end of this section, you will be able to do the following:

  Describe the evolutionary history of prokaryotes
 Discuss the distinguishing features of extremophiles
 Explain why it is difficult to culture prokaryotes

Prokaryotes are ubiquitous. They cover every imaginable surface where there is
sufficient moisture, and they also live on and inside virtually all other living
things. In the typical human body, prokaryotic cells outnumber human body cells
by about ten to one. They comprise the majority of living things in all ecosystems.
Some prokaryotes thrive in environments that are inhospitable for most living
things. Prokaryotes recycle nutrients—essential substances (such as carbon and
nitrogen)—and they drive the evolution of new ecosystems, some of which are
natural and others man-made. Prokaryotes have been on Earth since long before
multicellular life appeared. Indeed, eukaryotic cells are thought to be the
descendants of ancient prokaryotic communities.

Prokaryotes, the First Inhabitants of Earth

When and where did cellular life begin? What were the conditions on Earth when
life began? We now know that prokaryotes were likely the first forms of cellular
life on Earth, and they existed for billions of years before plants and animals
appeared. The Earth and its moon are dated at about 4.54 billion years in age.
This estimate is based on evidence from radiometric dating of meteorite material
together with other substrate material from Earth and the moon. Early Earth had
a very different atmosphere (contained less molecular oxygen) than it does today
and was subjected to strong solar radiation; thus, the first organisms probably
would have flourished where they were more protected, such as in the deep ocean
or far beneath the surface of the Earth. Strong volcanic activity was common on
Earth at this time, so it is likely that these first organisms—the first prokaryotes—
were adapted to very high temperatures. Because early Earth was prone to
geological upheaval and volcanic eruption, and was subject to bombardment by
mutagenic radiation from the sun, the first organisms were prokaryotes that must
have withstood these harsh conditions.

Microbial Mats

Microbial mats or large biofilms may represent the earliest forms of prokaryotic
life on Earth; there is fossil evidence of their presence starting about 3.5 billion
years ago. It is remarkable that cellular life appeared on Earth only a billion years
after the Earth itself formed, suggesting that pre-cellular “life” that could replicate
itself had evolved much earlier. A microbial mat is a multi-layered sheet of
prokaryotes (Figure 22.2) that includes mostly bacteria, but also archaeans.
Microbial mats are only a few centimeters thick, and they typically grow where
different types of materials interface, mostly on moist surfaces. The various types
of prokaryotes that comprise them carry out different metabolic pathways, and
that is the reason for their various colors. Prokaryotes in a microbial mat are held
together by a glue-like sticky substance that they secrete called extracellular
matrix.

The first microbial mats likely obtained their energy from chemicals found near
hydrothermal vents. A hydrothermal vent is a breakage or fissure in the Earth’s
surface that releases geothermally heated water. With the evolution of
photosynthesis about three billion years ago, some prokaryotes in microbial mats
came to use a more widely available energy source—sunlight—whereas others
were still dependent on chemicals from hydrothermal vents for energy and food.
Figure 22.2 A microbial mat. (a) This microbial mat, about one meter in
diameter, is growing over a hydrothermal vent in the Pacific Ocean in a region
known as the “Pacific Ring of Fire.” The mat’s colony of bacteria helps retain
microbial nutrients. Chimneys such as the one indicated by the arrow allow gases
to escape. (b) In this micrograph, bacteria are visualized using fluorescence
microscopy. (credit a: modification of work by Dr. Bob Embley, NOAA PMEL,
Chief Scientist; credit b: modification of work by Ricardo Murga, Rodney
Donlan, CDC; scale-bar data from Matt Russell)

Stromatolites

Fossilized microbial mats represent the earliest record of life on Earth.

A stromatolite is a sedimentary structure formed when minerals are precipitated
out of water by prokaryotes in a microbial mat (Figure 22.3). Stromatolites form
layered rocks made of carbonate or silicate. Although most stromatolites are
artifacts from the past, there are places on Earth where stromatolites are still
forming. For example, growing stromatolites have been found in the Anza-
Borrego Desert State Park in San Diego County, California.

Figure 22.3 Stromatolites. (a) These living stromatolites are located in Shark
Bay, Australia. (b) These fossilized stromatolites, found in Glacier National Park,
Montana, are nearly 1.5 billion years old. (credit a: Robert Young; credit b: P.
Carrara, NPS)
The Ancient Atmosphere

Evidence indicates that during the first two billion years of Earth’s existence, the
atmosphere was anoxic, meaning that there was no molecular oxygen. Therefore,
only those organisms that can grow without oxygen—anaerobic organisms—
were able to live. Autotrophic organisms that convert solar energy into chemical
energy are called phototrophs, and they appeared within one billion years of the
formation of Earth. Then, cyanobacteria, also known as “blue-green algae,”
evolved from these simple phototrophs at least one billion years later. It was the
ancestral cyanobacteria (Figure 22.4) that began the “oxygenation” of the
atmosphere: Increased atmospheric oxygen allowed the evolution of more
efficient O2-utilizing catabolic pathways. It also opened up the land to increased
colonization, because some O2 is converted into O3 (ozone) and ozone effectively
absorbs the ultraviolet light that could have otherwise caused lethal mutations in
DNA. The current evidence suggests that the increase in O2 concentrations
allowed the evolution of other life forms.

Figure 22.4 Cyanobacteria. This hot spring in Yellowstone National Park flows
toward the foreground. Cyanobacteria in the spring are green, and as water flows
down the gradient, the intensity of the color increases as cell density increases.
The water is cooler at the edges of the stream than in the center, causing the edges
to appear greener. (credit: Graciela Brelles-Mariño)
Microbes Are Adaptable: Life in Moderate and Extreme Environments

Some organisms have developed strategies that allow them to survive harsh
conditions. Almost all prokaryotes have a cell wall, a protective structure that
allows them to survive in both hypertonic and hypotonic aqueous conditions.
Some soil bacteria are able to form endospores that resist heat and drought,
thereby allowing the organism to survive until favorable conditions recur. These
adaptations, along with others, allow bacteria to remain the most abundant life
form in all terrestrial and aquatic ecosystems.

Prokaryotes thrive in a vast array of environments: Some grow in conditions that

would seem very normal to us, whereas others are able to thrive and grow under
conditions that would kill a plant or an animal. Bacteria and archaea that are
adapted to grow under extreme conditions are called extremophiles, meaning
“lovers of extremes.” Extremophiles have been found in all kinds of
environments: the depths of the oceans, hot springs, the Arctic and the Antarctic,
in very dry places, deep inside Earth, in harsh chemical environments, and in high
radiation environments (Figure 22.5), just to mention a few. Because they have
specialized adaptations that allow them to live in extreme conditions, many
extremophiles cannot survive in moderate environments. There are many
different groups of extremophiles: They are identified based on the conditions in
which they grow best, and several habitats are extreme in multiple ways. For
example, a soda lake is both salty and alkaline, so organisms that live in a soda
lake must be both alkaliphiles and halophiles (Table 22.1). Other extremophiles,
like radioresistant organisms, do not prefer an extreme environment (in this
case, one with high levels of radiation), but have adapted to survive in it (Figure
22.5). Organisms like these give us a better understanding of prokaryotic diversity
and open up the possibility of finding new prokaryotic species that may lead to
the discovery of new therapeutic drugs or have industrial applications.
Extremophiles and Their Preferred Conditions

Extremophile Conditions for Optimal Growth

Acidophiles pH 3 or below

Alkaliphiles pH 9 or above

Thermophiles Temperature 60–80 °C (140–176 °F)

Hyperthermophiles Temperature 80–122 °C (176–250 °F)

Psychrophiles Temperature of -15-10 °C (5-50 °F) or lower

Halophiles Salt concentration of at least 0.2 M

Osmophiles High sugar concentration

Table22.1

Figure 22.5 Radiation-tolerant prokaryotes. Deinococcus radiodurans,

visualized in this false color transmission electron micrograph, is a prokaryote
that can tolerate very high doses of ionizing radiation. It has developed DNA
repair mechanisms that allow it to reconstruct its chromosome even if it has been
broken into hundreds of pieces by radiation or heat. (credit: modification of work
by Michael Daly; scale-bar data from Matt Russell)

Prokaryotes in the Dead Sea

One example of a very harsh environment is the Dead Sea, a hypersaline basin
that is located between Jordan and Israel. Hypersaline environments are
essentially concentrated seawater. In the Dead Sea, the sodium concentration is
10 times higher than that of seawater, and the water contains high levels of
magnesium (about 40 times higher than in seawater) that would be toxic to most
living things. Iron, calcium, and magnesium, elements that form divalent ions
(Fe2+, Ca2+, and Mg2+), produce what is commonly referred to as “hard” water.
Taken together, the high concentration of divalent cations, the acidic pH (6.0),
and the intense solar radiation flux make the Dead Sea a unique, and uniquely
hostile, ecosystem1 (Figure 22.6).

What sort of prokaryotes do we find in the Dead Sea? The extremely salt-tolerant
bacterial mats include Halobacterium, Haloferax volcanii (which is found in
other locations, not only the Dead Sea), Halorubrum sodomense,
and Halobaculum gomorrense, and the archaean Haloarcula marismortui,
among others.
Figure 22.6 Halophilic prokaryotes. (a) The Dead Sea is hypersaline.
Nevertheless, salt-tolerant bacteria thrive in this sea. (b) These halobacteria cells
can form salt-tolerant bacterial mats. (credit a: Julien Menichini; credit b: NASA;
scale-bar data from Matt Russell)

Unculturable Prokaryotes and the Viable-but-Non-Culturable State

The process of culturing bacteria is complex and is one of the greatest discoveries
of modern science. German physician Robert Koch is credited with discovering
the techniques for pure culture, including staining and using growth media.
Microbiologists typically grow prokaryotes in the laboratory using an appropriate
culture medium containing all the nutrients needed by the target organism. The
medium can be liquid, broth, or solid. After an incubation time at the right
temperature, there should be evidence of microbial growth (Figure 22.7). Koch's
assistant Julius Petri invented the Petri dish, whose use persists in today’s
laboratories. Koch worked primarily with the Mycobacterium
tuberculosis bacterium that causes tuberculosis and developed guidelines,
called Koch's postulates, to identify the organisms responsible for specific
diseases. Koch's postulates continue to be widely used in the medical community.
Koch’s postulates include that an organism can be identified as the cause of
disease when it is present in all infected samples and absent in all healthy samples,
and it is able to reproduce the infection after being cultured multiple times. Today,
cultures remain a primary diagnostic tool in medicine and other areas of
molecular biology.
Figure 22.7 Bacteria growing on blood agar plates. In these agar plates, the
growth medium is supplemented with red blood cells. Blood agar becomes
transparent in the presence of hemolytic Streptococcus, which destroys red blood
cells and is used to diagnose Streptococcus infections. The plate on the left is
inoculated with non-hemolytic Staphylococcus (large white colonies), and the
plate on the right is inoculated with hemolytic Streptococcus (tiny clear colonies).
If you look closely at the right plate, you can see that the agar surrounding the
bacteria has turned clear. (credit: Bill Branson, NCI)

Koch's postulates can be fully applied only to organisms that can be isolated and
cultured. Some prokaryotes, however, cannot grow in a laboratory setting. In fact,
over 99 percent of bacteria and archaea are unculturable. For the most part, this
is due to a lack of knowledge as to what to feed these organisms and how to grow
them; they may have special requirements for growth that remain unknown to
scientists, such as needing specific micronutrients, pH, temperature, pressure, co-
factors, or co-metabolites. Some bacteria cannot be cultured because they are
obligate intracellular parasites and cannot be grown outside a host cell.

In other cases, culturable organisms become unculturable under stressful

conditions, even though the same organism could be cultured previously. Those
organisms that cannot be cultured but are not dead are in a viable-but-non-
culturable (VBNC) state. The VBNC state occurs when prokaryotes respond to
environmental stressors by entering a dormant state that allows their survival. The
criteria for entering into the VBNC state are not completely understood. In a
process called resuscitation, the prokaryote can go back to “normal” life when
environmental conditions improve.

Is the VBNC state an unusual way of living for prokaryotes? In fact, most of the
prokaryotes living in the soil or in oceanic waters are non-culturable. It has been
said that only a small fraction, perhaps one percent, of prokaryotes can be cultured
under laboratory conditions. If these organisms are non-culturable, then how is it
known whether they are present and alive? Microbiologists use molecular
techniques, such as the polymerase chain reaction (PCR), to amplify selected
portions of DNA of prokaryotes, e.g., 16S rRNA genes, demonstrating their
existence. (Recall that PCR can make billions of copies of a DNA segment in a
process called amplification.)

The Ecology of Biofilms

Some prokaryotes may be unculturable because they require the presence of other
prokaryotic species. Until a couple of decades ago, microbiologists used to think
of prokaryotes as isolated entities living apart. This model, however, does not
reflect the true ecology of prokaryotes, most of which prefer to live in
communities where they can interact. As we have seen, a biofilm is a microbial
community (Figure 22.8) held together in a gummy-textured matrix that consists
primarily of polysaccharides secreted by the organisms, together with some
proteins and nucleic acids. Biofilms typically grow attached to surfaces. Some of
the best-studied biofilms are composed of prokaryotes, although fungal biofilms
have also been described, as well as some composed of a mixture of fungi and
bacteria.

Biofilms are present almost everywhere: they can cause the clogging of pipes and
readily colonize surfaces in industrial settings. In recent, large-scale outbreaks of
bacterial contamination of food, biofilms have played a major role. They also
colonize household surfaces, such as kitchen counters, cutting boards, sinks, and
toilets, as well as places on the human body, such as the surfaces of our teeth.

Interactions among the organisms that populate a biofilm, together with their
protective exopolysaccharidic (EPS) environment, make these communities
more robust than free-living, or planktonic, prokaryotes. The sticky substance that
holds bacteria together also excludes most antibiotics and disinfectants, making
biofilm bacteria hardier than their planktonic counterparts. Overall, biofilms are
very difficult to destroy because they are resistant to many common forms of
sterilization.

VISUAL CONNECTION

Figure 22.8 Development of a biofilm. Five stages of biofilm development are

shown. During stage 1, initial attachment, bacteria adhere to a solid surface via
weak van der Waals interactions (forces produced by induced electrical
interactions between atoms). During stage 2, irreversible attachment, hairlike
appendages called pili permanently anchor the bacteria to the surface. During
stage 3, maturation I, the biofilm grows through cell division and recruitment of
other bacteria. An extracellular matrix composed primarily of polysaccharides
holds the biofilm together. During stage 4, maturation II, the biofilm continues to
grow and takes on a more complex shape. During stage 5, dispersal, the biofilm
matrix is partly broken down, allowing some bacteria to escape and colonize
another surface. Micrographs of a Pseudomonas aeruginosa biofilm in each of
the stages of development are shown. (credit: D. Davis, Don Monroe, PLoS)

Compared to free-floating bacteria, bacteria in biofilms often show increased

resistance to antibiotics and detergents. Why do you think this might be the case?

Learning Objectives

By the end of this section, you will be able to do the following:

 Describe the basic structure of a typical prokaryote

 Describe important differences in structure between Archaea and Bacteria

There are many differences between prokaryotic and eukaryotic cells. The name
"prokaryote" suggests that prokaryotes are defined by exclusion—they are not
eukaryotes, or organisms whose cells contain a nucleus and other internal
membrane-bound organelles. However, all cells have four common structures:
the plasma membrane, which functions as a barrier for the cell and separates the
cell from its environment; the cytoplasm, a complex solution of organic
molecules and salts inside the cell; a double-stranded DNA genome, the
informational archive of the cell; and ribosomes, where protein synthesis takes
place. Prokaryotes come in various shapes, but many fall into three
categories: cocci (spherical), bacilli (rod-shaped), and spirilli (spiral-shaped)
(Figure 22.9).
Figure 22.9 Common prokaryotic cell types. Prokaryotes fall into three basic
categories based on their shape, visualized here using scanning electron
microscopy: (a) cocci, or spherical (a pair is shown); (b) bacilli, or rod-shaped;
and (c) spirilli, or spiral-shaped. (credit a: modification of work by Janice Haney
Carr, Dr. Richard Facklam, CDC; credit c: modification of work by Dr. David
Cox; scale-bar data from Matt Russell)

The Prokaryotic Cell

Recall that prokaryotes are unicellular organisms that lack membrane-bound

organelles or other internal membrane-bound structures (Figure 22.10). Their
chromosome—usually single—consists of a piece of circular, double-stranded
DNA located in an area of the cell called the nucleoid. Most prokaryotes have a
cell wall outside the plasma membrane. The cell wall functions as a protective
layer, and it is responsible for the organism’s shape. Some bacterial species have
a capsule outside the cell wall. The capsule enables the organism to attach to
surfaces, protects it from dehydration and attack by phagocytic cells, and makes
pathogens more resistant to our immune responses. Some species also have
flagella (singular, flagellum) used for locomotion, and pili (singular, pilus) used
for attachment to surfaces including the surfaces of other cells. Plasmids, which
consist of extra-chromosomal DNA, are also present in many species of bacteria
and archaea.
Figure 22.10 The features of a typical prokaryotic cell. Flagella, capsules, and
pili are not found in all prokaryotes.

Recall that prokaryotes are divided into two different domains, Bacteria and
Archaea, which together with Eukarya, comprise the three domains of life (Figure
22.11).

Figure 22.11 The three domains of living organisms. Bacteria and Archaea are
both prokaryotes but differ enough to be placed in separate domains. An ancestor
of modern Archaea is believed to have given rise to Eukarya, the third domain of
life. Major groups of Archaea and Bacteria are shown.

Characteristics of bacterial phyla are described in Figure 22.12 and Figure 22.13.
Major bacterial phyla include the Proteobacteria, the Chlamydias, the
Spirochaetes, the photosynthetic Cyanobacteria, and the Gram-positive bacteria.
The Proteobacteria are in turn subdivided into several classes, from the Alpha- to
the Epsilon proteobacteria. Eukaryotic mitochondria are thought to be the
descendants of alphaproteobacteria, while eukaryotic chloroplasts are derived
from cyanobacteria. Archaeal phyla are described in Figure 22.14.
Figure 22.12 The Proteobacteria. Phylum Proteobacteria is one of up to 52
bacteria phyla. Proteobacteria is further subdivided into five classes, Alpha
through Epsilon. (credit “Rickettsia rickettsia”: modification of work by CDC;
credit “Spirillum minus”: modification of work by Wolframm Adlassnig; credit
“Vibrio cholera”: modification of work by Janice Haney Carr, CDC; credit
“Desulfovibrio vulgaris”: modification of work by Graham Bradley; credit
“Campylobacter”: modification of work by De Wood, Pooley, USDA, ARS,
EMU; scale-bar data from Matt Russell)

Figure 22.13 Other bacterial phyla. Chlamydia, Spirochetes, Cyanobacteria, and

Gram-positive bacteria are described in this table. Note that bacterial shape is not
phylum-dependent; bacteria within a phylum may be cocci, rod-shaped, or spiral.
(credit “Chlamydia trachomatis”: modification of work by Dr. Lance Liotta
Laboratory, NCI; credit “Treponema pallidum”: modification of work by Dr.
David Cox, CDC; credit “Phormidium”: modification of work by USGS;
credit “Clostridium difficile”: modification of work by Lois S. Wiggs, CDC;
scale-bar data from Matt Russell)
Figure 22.14 Archaeal phyla. Archaea are separated into four phyla: the
Korarchaeota, Euryarchaeota, Crenarchaeota, and Nanoarchaeota.
(credit “Halobacterium”: modification of work by NASA;
credit “Nanoarchaeotum equitans”: modification of work by Karl O. Stetter;
credit “Korarchaeota”: modification of work by Office of Science of the U.S.
Dept. of Energy; scale-bar data from Matt Russell)
The Plasma Membrane of Prokaryotes

The prokaryotic plasma membrane is a thin lipid bilayer (6 to 8 nanometers) that

completely surrounds the cell and separates the inside from the outside. Its
selectively permeable nature keeps ions, proteins, and other molecules within the
cell and prevents them from diffusing into the extracellular environment, while
other molecules may move through the membrane. Recall that the general
structure of a cell membrane is a phospholipid bilayer composed of two layers of
lipid molecules. In archaeal cell membranes, isoprene (phytanyl) chains linked to
glycerol replace the fatty acids linked to glycerol in bacterial membranes. Some
archaeal membranes are lipid monolayers instead of bilayers (Figure 22.15).

Figure 22.15 Bacterial and archaeal phospholipids. Archaeal phospholipids

differ from those found in Bacteria and Eukarya in two ways. First, they have
branched phytanyl sidechains instead of linear ones. Second, an ether bond
instead of an ester bond connects the lipid to the glycerol.
The Cell Wall of Prokaryotes

The cytoplasm of prokaryotic cells has a high concentration of dissolved solutes.

Therefore, the osmotic pressure within the cell is relatively high. The cell wall is
a protective layer that surrounds some cells and gives them shape and rigidity. It
is located outside the cell membrane and prevents osmotic lysis (bursting due to
increasing volume). The chemical composition of the cell wall varies between
Archaea and Bacteria, and also varies between bacterial species.

Bacterial cell walls contain peptidoglycan, composed of polysaccharide chains

that are cross-linked by unusual peptides containing both L- and D-amino acids
including D-glutamic acid and D-alanine. (Proteins normally have only L-amino
acids; as a consequence, many of our antibiotics work by mimicking D-amino
acids and therefore have specific effects on bacterial cell-wall development.)
There are more than 100 different forms of peptidoglycan. S-layer (surface layer)
proteins are also present on the outside of cell walls of both Archaea and Bacteria.

Bacteria are divided into two major groups: Gram positive and Gram negative,
based on their reaction to Gram staining. Note that all Gram-positive bacteria
belong to one phylum; bacteria in the other phyla (Proteobacteria, Chlamydias,
Spirochetes, Cyanobacteria, and others) are Gram-negative. The Gram staining
method is named after its inventor, Danish scientist Hans Christian Gram (1853–
1938). The different bacterial responses to the staining procedure are ultimately
due to cell wall structure. Gram-positive organisms typically lack the outer
membrane found in Gram-negative organisms (Figure 22.16). Up to 90 percent
of the cell-wall in Gram-positive bacteria is composed of peptidoglycan, and most
of the rest is composed of acidic substances called teichoic acids. Teichoic acids
may be covalently linked to lipids in the plasma membrane to form lipoteichoic
acids. Lipoteichoic acids anchor the cell wall to the cell membrane. Gram-
negative bacteria have a relatively thin cell wall composed of a few layers of
peptidoglycan (only 10 percent of the total cell wall), surrounded by an outer
envelope containing lipopolysaccharides (LPS) and lipoproteins. This outer
envelope is sometimes referred to as a second lipid bilayer. The chemistry of this
outer envelope is very different, however, from that of the typical lipid bilayer
that forms plasma membranes.

VISUAL CONNECTION

Figure 22.16 Cell walls in Gram-positive and Gram-negative bacteria. Bacteria

are divided into two major groups: Gram positive and Gram negative. Both
groups have a cell wall composed of peptidoglycan: in Gram-positive bacteria,
the wall is thick, whereas in Gram-negative bacteria, the wall is thin. In Gram-
negative bacteria, the cell wall is surrounded by an outer membrane that contains
lipopolysaccharides and lipoproteins. Porins are proteins in this cell membrane
that allow substances to pass through the outer membrane of Gram-negative
bacteria. In Gram-positive bacteria, lipoteichoic acid anchors the cell wall to the
cell membrane. (credit: modification of work by "Franciscosp2"/Wikimedia
Commons)

Which of the following statements is true?

 a. Gram-positive bacteria have a single cell wall anchored to the cell
membrane by lipoteichoic acid.
b. Porins allow entry of substances into both Gram-positive and Gram-
negative bacteria.
c. The cell wall of Gram-negative bacteria is thick, and the cell wall of Gram-
positive bacteria is thin.
d. Gram-negative bacteria have a cell wall made of peptidoglycan, whereas
Gram-positive bacteria have a cell wall made of lipoteichoic acid.

Archaean cell walls do not have peptidoglycan. There are four different types of
archaean cell walls. One type is composed of pseudopeptidoglycan, which is
similar to peptidoglycan in morphology but contains different sugars in the
polysaccharide chain. The other three types of cell walls are composed of
polysaccharides, glycoproteins, or pure protein. Other differences between
Bacteria and Archaea are seen in Table 22.2. Note that features related to DNA
replication, transcription and translation in Archaea are similar to those seen in
eukaryotes.

Differences and Similarities between Bacteria and Archaea

Structural Characteristic Bacteria Archaea

Cell type Prokaryotic Prokaryotic

Cell morphology Variable Variable

Cell wall Contains peptidoglycan Does not contain pepti

Cell membrane type Lipid bilayer Lipid bilayer or lipid m

 Structural Characteristic Bacteria Archaea

Plasma membrane lipids Fatty acids-glycerol ester Phytanyl-glycerol ethe

Chromosome Typically circular Typically circular

Replication origins Single Multiple

RNA polymerase Single Multiple

Initiator tRNA Formyl-methionine Methionine

Streptomycin inhibition Sensitive Resistant

Calvin cycle Yes No

Table22.2

Reproduction

Reproduction in prokaryotes is asexual and usually takes place by binary fission.

(Recall that the DNA of a prokaryote is a single, circular chromosome.)
Prokaryotes do not undergo mitosis; instead, the chromosome is replicated and
the two resulting copies separate from one another, due to the growth of the cell.
The prokaryote, now enlarged, is pinched inward at its equator and the two
resulting cells, which are clones, separate. Binary fission does not provide an
opportunity for genetic recombination or genetic diversity, but prokaryotes can
share genes by three other mechanisms.

In transformation, the prokaryote takes in DNA shed by other prokaryotes into

its environment. If a nonpathogenic bacterium takes up DNA for a toxin gene
from a pathogen and incorporates the new DNA into its own chromosome, it too
may become pathogenic. In transduction, bacteriophages, the viruses that infect
bacteria, may move short pieces of chromosomal DNA from one bacterium to
another. Transduction results in a recombinant organism. Archaea also have
viruses that may translocate genetic material from one individual to another.
In conjugation, DNA is transferred from one prokaryote to another by means of
a pilus, which brings the organisms into contact with one another, and provides a
channel for transfer of DNA. The DNA transferred can be in the form of a plasmid
or as a composite molecule, containing both plasmid and chromosomal DNA.
These three processes of DNA exchange are shown in Figure 22.17.

Reproduction can be very rapid: a few minutes for some species. This short
generation time coupled with mechanisms of genetic recombination and high
rates of mutation result in the rapid evolution of prokaryotes, allowing them to
respond to environmental changes (such as the introduction of an antibiotic) very
quickly.
Figure 22.17 Gene transfer mechanisms in prokaryotes. There are three
mechanisms by which prokaryotes can exchange DNA. In (a) transformation, the
cell takes up prokaryotic DNA directly from the environment. The DNA may
remain separate as plasmid DNA or be incorporated into the host genome. In (b)
transduction, a bacteriophage injects DNA into the cell that contains a small
fragment of DNA from a different prokaryote. In (c) conjugation, DNA is
transferred from one cell to another via a mating bridge, or pilus, that connects
the two cells after the sex pilus draws the two bacteria close enough to form the
bridge.

EVOLUTION CONNECTION

The Evolution of Prokaryotes

How do scientists answer questions about the evolution of prokaryotes? Unlike

with animals, artifacts in the fossil record of prokaryotes offer very little
information. Fossils of ancient prokaryotes look like tiny bubbles in rock. Some
scientists turn to genetics and to the principle of the molecular clock, which holds
that the more recently two species have diverged, the more similar their genes
(and thus proteins) will be. Conversely, species that diverged long ago will have
more genes that are dissimilar.

Scientists at the NASA Astrobiology Institute and at the European Molecular

Biology Laboratory collaborated to analyze the molecular evolution of 32
specific proteins common to 72 species of prokaryotes.2 The model they derived
from their data indicates that three important groups of bacteria—
Actinobacteria, Deinococcus, and Cyanobacteria (collectively
called Terrabacteria by the authors)—were the first to colonize land.
Actinobacteria are a group of very common Gram-positive bacteria that produce
branched structures like fungal mycelia, and include species important in
decomposition of organic wastes. You will recall that Deinococcus is a genus of
bacterium that is highly resistant to ionizing radiation. It has a thick peptidoglycan
layer in addition to a second external membrane, so it has features of both Gram-
positive and Gram-negative bacteria.

Cyanobacteria are photosynthesizers, and were probably responsible for the

production of oxygen on the ancient earth. The timelines of divergence suggest
that bacteria (members of the domain Bacteria) diverged from common ancestral
species between 2.5 and 3.2 billion years ago, whereas the Archaea diverged
earlier: between 3.1 and 4.1 billion years ago. Eukarya later diverged from the
archaean line. The work further suggests that stromatolites that formed prior to
the advent of cyanobacteria (about 2.6 billion years ago) photosynthesized in an
anoxic environment and that because of the modifications of the Terrabacteria for
land (resistance to drying and the possession of compounds that protect the
organism from excess light), photosynthesis using oxygen may be closely linked
to adaptations to survive on land.

Learning Objectives

By the end of this section, you will be able to do the following:

 Identify bacterial diseases that caused historically important plagues and

epidemics
 Describe the link between biofilms and foodborne diseases
 Explain how overuse of antibiotics may be creating “super bugs”
 Explain the importance of MRSA with respect to the problems of antibiotic
resistance
To a prokaryote, humans may be just another housing opportunity. Unfortunately,
the tenancy of some species can have harmful effects and cause disease. Bacteria
or other infectious agents that cause harm to their human hosts are
called pathogens. Devastating pathogen-borne diseases and plagues, both viral
and bacterial in nature, have affected humans and their ancestors for millions of
years. The true cause of these diseases was not understood until modern scientific
thought developed, and many people thought that diseases were a “spiritual
punishment.” Only within the past several centuries have people understood that
staying away from afflicted persons, disposing of the corpses and personal
belongings of victims of illness, and sanitation practices reduced their own
chances of getting sick.

Epidemiologists study how diseases are transmitted and how they affect a
population. Often, they must following the course of an epidemic—a disease that
occurs in an unusually high number of individuals in a population at the same
time. In contrast, a pandemic is a widespread, and usually worldwide, epidemic.
An endemic disease is a disease that is always present, usually at low incidence,
in a population.

Long History of Bacterial Disease

There are records about infectious diseases as far back as 3000 B.C. A number of
significant pandemics caused by bacteria have been documented over several
hundred years. Some of the most memorable pandemics led to the decline of cities
and entire nations.

In the 21st century, infectious diseases remain among the leading causes of death
worldwide, despite advances made in medical research and treatments in recent
decades. A disease spreads when the pathogen that causes it is passed from one
person to another. For a pathogen to cause disease, it must be able to reproduce
in the host’s body and damage the host in some way.

The Plague of Athens

In 430 B.C., the Plague of Athens killed one-quarter of the Athenian troops who
were fighting in the great Peloponnesian War and weakened Athens’s dominance
and power. The plague impacted people living in overcrowded Athens as well as
troops aboard ships that had to return to Athens. The source of the plague may
have been identified recently when researchers from the University of Athens
were able to use DNA from teeth recovered from a mass grave. The scientists
identified nucleotide sequences from a pathogenic bacterium, Salmonella
enterica serovar Typhi (Figure 22.20), which causes typhoid fever.3 This disease
is commonly seen in overcrowded areas and has caused epidemics throughout
recorded history.
Figure 22.20 Salmonella enterica. Salmonella enterica serovar Typhi, the
causative agent of Typhoid fever, is a Gram-negative, rod-shaped gamma
proteobacterium. Typhoid fever, which is spread through feces, causes intestinal
hemorrhage, high fever, delirium, and dehydration. Today, between 16 and 33
million cases of this re-emerging disease occur annually, resulting in over
200,000 deaths. Carriers of the disease can be asymptomatic. In a famous case in
the early 1900s, a cook named Mary Mallon (“Typhoid Mary”) unknowingly
spread the disease to over fifty people, three of whom died. Other serotypes
of Salmonella cause food poisoning. (credit: modification of work by NCI, CDC)
Bubonic Plagues

From 541 to 750, the Plague of Justinian, an outbreak of what was likely bubonic
plague, eliminated one-quarter to one-half of the human population in the eastern
Mediterranean region. The population in Europe dropped by 50 percent during
this outbreak. Astoundingly, bubonic plague would strike Europe more than
once!

Bubonic plague is caused by the bacterium Yersinia pestis. One of the most
devastating pandemics attributed to bubonic plague was the Black Death (1346
to 1361). It is thought to have originated in China and spread along the Silk Road,
a network of land and sea trade routes, to the Mediterranean region and Europe,
carried by fleas living on black rats that were always present on ships. The Black
Death was probably named for the tissue necrosis (Figure 22.21c) that can be one
of the symptoms. The "buboes" of bubonic plague were painfully swollen areas
of lymphatic tissue. A pneumonic form of the plague, spread by the coughing and
sneezing of infected individuals, spreads directly from human to human and can
cause death within a week. The pneumonic form was responsible for the rapid
spread of the Black Death in Europe. The Black Death reduced the world’s
population from an estimated 450 million to about 350 to 375 million. Bubonic
plague struck London yet again in the mid-1600s (Figure 22.21). In modern times,
approximately 1,000 to 3,000 cases of plague arise globally each year, and a
“sylvatic” form of plague, carried by fleas living on rodents such as prairie dogs
and black footed ferrets, infects 10 to 20 people annually in the American
Southwest. Although contracting bubonic plague before antibiotics meant almost
certain death, the bacterium responds to several types of modern antibiotics, and
mortality rates from plague are now very low.
Figure 22.21 The Black Death. The (a) Great Plague of London killed an
estimated 200,000 people, or about 20 percent of the city’s population. The
causative agent, the (b) bacterium Yersinia pestis, is a Gram-negative, rod-shaped
bacterium from the class Gammaproteobacteria. The disease is transmitted
through the bite of an infected flea, which is carried on a rodent. Symptoms
include swollen lymph nodes, fever, seizure, vomiting of blood, and (c) gangrene.
(credit b: Rocky Mountain Laboratories, NIAID, NIH; scale-bar data from Matt
Russell; credit c: Textbook of Military Medicine, Washington, D.C., U.S. Dept.
of the Army, Office of the Surgeon General, Borden Institute)

LINK TO LEARNING

Watch a video on the modern understanding of the Black Death—bubonic plague

in Europe during the 14th century.

Migration of Diseases to New Populations

One of the negative consequences of human exploration was the accidental

“biological warfare” that resulted from the transport of a pathogen into a
population that had not previously been exposed to it. Over the centuries,
Europeans tended to develop genetic immunity to endemic infectious diseases,
but when European conquerors reached the western hemisphere, they brought
with them disease-causing bacteria and viruses, which triggered epidemics that
completely devastated many diverse populations of Native Americans, who had
no natural resistance to many European diseases. It has been estimated that up to
90 percent of Native Americans died from infectious diseases after the arrival of
Europeans, making conquest of the New World a foregone conclusion.

Emerging and Re-emerging Diseases

The distribution of a particular disease is dynamic. Changes in the environment,

the pathogen, or the host population can dramatically impact the spread of a
disease. According to the World Health Organization (WHO), an emerging
disease (Figure 22.22) is one that has appeared in a population for the first time,
or that may have existed previously but is rapidly increasing in incidence or
geographic range. This definition also includes re-emerging diseases that were
previously under control. Approximately 75 percent of recently emerging
infectious diseases affecting humans are zoonotic diseases. Zoonoses are
diseases that primarily infect animals but can be transmitted to humans; some are
of viral origin and some are of bacterial origin. Brucellosis is an example of a
prokaryotic zoonosis that is re-emerging in some regions, and necrotizing
fasciitis (commonly known as flesh-eating bacteria) has been increasing in
virulence for the last 80 years for unknown reasons.
Figure 22.22 Emerging diseases. The map shows regions where bacterial
diseases are emerging or re-emerging. (credit: modification of work by NIH)

Some of the present emerging diseases are not actually new, but are diseases that
were catastrophic in the past (Figure 22.23). They devastated populations and
became dormant for a while, just to come back, sometimes more virulent than
before, as was the case with bubonic plague. Other diseases, like tuberculosis,
were never eradicated but were under control in some regions of the world until
coming back, mostly in urban centers with high concentrations of
immunocompromised people. WHO has identified certain diseases whose
worldwide re-emergence should be monitored. Among these are three viral
diseases (dengue fever, yellow fever, and zika), and three bacterial diseases
(diphtheria, cholera, and bubonic plague). The war against infectious diseases has
no foreseeable end.

Figure 22.23 Lyme Disease. Lyme disease often, but not always, results in (a) a
characteristic bullseye rash. The disease is caused by a (b) Gram-negative
spirochete bacterium of the genus Borrelia. The bacteria (c) infect ticks, which in
turn infect mice. Deer are the preferred secondary host, but the ticks also may
feed on humans. Untreated, the disease causes chronic disorders in the nervous
system, eyes, joints, and heart. The disease is named after Lyme, Connecticut,
where an outbreak occurred in 1995 and has subsequently spread. The disease is
not new, however. Genetic evidence suggests that Ötzi the Iceman, a 5,300-year-
old mummy found in the Alps, was infected with Borrelia. (credit a: James
Gathany, CDC; credit b: CDC; scale-bar data from Matt Russell)

Foodborne Diseases

Prokaryotes are everywhere: They readily colonize the surface of any type of
material, and food is not an exception. Most of the time, prokaryotes colonize
food and food-processing equipment in the form of a biofilm, as we have
discussed earlier. Outbreaks of bacterial infection related to food consumption
are common. A foodborne disease (commonly called “food poisoning”) is an
illness resulting from the consumption the pathogenic bacteria, viruses, or other
parasites that contaminate food. Although the United States has one of the safest
food supplies in the world, the U.S. Centers for Disease Control and Prevention
(CDC) has reported that “76 million people get sick, more than 300,000 are
hospitalized, and 5,000 Americans die each year from foodborne illness.”

The characteristics of foodborne illnesses have changed over time. In the past, it
was relatively common to hear about sporadic cases of botulism, the potentially
fatal disease produced by a toxin from the anaerobic bacterium Clostridium
botulinum. Some of the most common sources for this bacterium were non-acidic
canned foods, homemade pickles, and processed meat and sausages. The can, jar,
or package created a suitable anaerobic environment where Clostridium could
grow. Proper sterilization and canning procedures have reduced the incidence of
this disease.
While people may tend to think of foodborne illnesses as associated with animal-
based foods, most cases are now linked to produce. There have been serious,
produce-related outbreaks associated with raw spinach in the United States and
with vegetable sprouts in Germany, and these types of outbreaks have become
more common. The raw spinach outbreak in 2006 was produced by the
bacterium E. coli serotype O157:H7. A serotype is a strain of bacteria that carries
a set of similar antigens on its cell surface, and there are often many different
serotypes of a bacterial species. Most E. coli are not particularly dangerous to
humans, but serotype O157:H7 can cause bloody diarrhea and is potentially fatal.

All types of food can potentially be contaminated with bacteria. Recent outbreaks
of Salmonella reported by the CDC occurred in foods as diverse as peanut butter,
alfalfa sprouts, and eggs. A deadly outbreak in Germany in 2010 was caused by E.
coli contamination of vegetable sprouts (Figure 22.24). The strain that caused the
outbreak was found to be a new serotype not previously involved in other
outbreaks, which indicates that E. coli is continuously evolving. Outbreaks of
listeriosis, due to contamination of meats, raw cheeses, and frozen or fresh
vegetables with Listeria monocytogenes, are becoming more frequent.

Figure 22.24 Foodborne pathogens. (a) Vegetable sprouts grown at an organic

farm were the cause of an (b) E. coli outbreak that killed 32 people and sickened
3,800 in Germany in 2011. The strain responsible, E. coli O104:H4, produces
Shiga toxin, a substance that inhibits protein synthesis in the host cell. The toxin
(c) destroys red blood cells resulting in bloody diarrhea. Deformed red blood cells
clog the capillaries of the kidney, which can lead to kidney failure, as happened
to 845 patients in the 2011 outbreak. Kidney failure is usually reversible, but
some patients experience kidney problems years later. (credit c: NIDDK, NIH)

Biofilms and Disease

Recall that biofilms are microbial communities that are very difficult to destroy.
They are responsible for diseases such as Legionnaires’ disease, otitis media (ear
infections), and various infections in patients with cystic fibrosis. They produce
dental plaque and colonize catheters, prostheses, transcutaneous and orthopedic
devices, contact lenses, and internal devices such as pacemakers. They also form
in open wounds and burned tissue. In healthcare environments, biofilms grow on
hemodialysis machines, mechanical ventilators, shunts, and other medical
equipment. In fact, 65 percent of all infections acquired in the hospital
(nosocomial infections) are attributed to biofilms. Biofilms are also related to
diseases contracted from food because they colonize the surfaces of vegetable
leaves and meat, as well as food-processing equipment that isn’t adequately
cleaned.

Biofilm infections develop gradually and may not cause immediate symptoms.
They are rarely resolved by host defense mechanisms. Once an infection by a
biofilm is established, it is very difficult to eradicate, because biofilms tend to be
resistant to most methods used to control microbial growth, including antibiotics.
The matrix that attaches the cells to a substrate and to other another protects the
cells from antibiotics or drugs. In addition, since biofilms grow slowly, they are
less responsive to agents that interfere with cell growth. It has been reported that
biofilms can resist up to 1,000 times the antibiotic concentrations used to kill the
same bacteria when they are free-living or planktonic. An antibiotic dose that
large would harm the patient; therefore, scientists are working on new ways to
get rid of biofilms.
Antibiotics: Are We Facing a Crisis?

The word antibiotic comes from the Greek anti meaning “against”
and bios meaning “life.” An antibiotic is a chemical, produced either by
microbes or synthetically, that is hostile to or prevents the growth of other
organisms. Today’s media often address concerns about an antibiotic crisis. Are
the antibiotics that easily treated bacterial infections in the past becoming
obsolete? Are there new “superbugs”—bacteria that have evolved to become
more resistant to our arsenal of antibiotics? Is this the beginning of the end of
antibiotics? All these questions challenge the healthcare community.

One of the main causes of antibiotic resistance in bacteria is overexposure to

antibiotics. The imprudent and excessive use of antibiotics has resulted in the
natural selection of resistant forms of bacteria. The antibiotic kills most of the
infecting bacteria, and therefore only the resistant forms remain. These resistant
forms reproduce, resulting in an increase in the proportion of resistant forms over
non-resistant ones. In addition to transmission of resistance genes to progeny,
lateral transfer of resistance genes on plasmids can rapidly spread these genes
through a bacterial population. A major misuse of antibiotics is in patients with
viral infections like colds or the flu, against which antibiotics are useless. Another
problem is the excessive use of antibiotics in livestock. The routine use of
antibiotics in animal feed promotes bacterial resistance as well. In the United
States, 70 percent of the antibiotics produced are fed to animals. These antibiotics
are given to livestock in low doses, which maximize the probability of resistance
developing, and these resistant bacteria are readily transferred to humans.

LINK TO LEARNING

Watch a recent news report on the problem of routine antibiotic administration to

livestock and antibiotic-resistant bacteria.
One of the Superbugs: MRSA

The imprudent use of antibiotics has paved the way for the expansion of resistant
bacterial populations. For example, Staphylococcus aureus, often called “staph,”
is a common bacterium that can live in the human body and is usually easily
treated with antibiotics. However, a very dangerous strain, methicillin-
resistant Staphylococcus aureus (MRSA) has made the news over the past few
years (Figure 22.25). This strain is resistant to many commonly used antibiotics,
including methicillin, amoxicillin, penicillin, and oxacillin. MRSA can cause
infections of the skin, but it can also infect the bloodstream, lungs, urinary tract,
or sites of injury. While MRSA infections are common among people in
healthcare facilities, they have also appeared in healthy people who haven’t been
hospitalized, but who live or work in tight populations (like military personnel
and prisoners). Researchers have expressed concern about the way this latter
source of MRSA targets a much younger population than those residing in care
facilities. The Journal of the American Medical Association reported that, among
MRSA-afflicted persons in healthcare facilities, the average age is 68, whereas
people with “community-associated MRSA” (CA-MRSA) have an average age
of 23.4
Figure 22.25 MRSA. This scanning electron micrograph shows methicillin-
resistant Staphylococcus aureus bacteria, commonly known as MRSA. S.
aureus is not always pathogenic, but can cause diseases such as food poisoning
and skin and respiratory infections. (credit: modification of work by Janice Haney
Carr; scale-bar data from Matt Russell)

In summary, the medical community is facing an antibiotic crisis. Some scientists

believe that after years of being protected from bacterial infections by antibiotics,
we may be returning to a time in which a simple bacterial infection could again
devastate the human population. Researchers are developing new antibiotics, but
it takes many years of research and clinical trials, plus financial investments in
the millions of dollars, to generate an effective and approved drug.

30.

Describe briefly how you would detect the presence of a non-culturable

prokaryote in an environmental sample.
31.

Why do scientists believe that the first organisms on Earth were extremophiles?

32.

A new bacterial species is discovered and classified as an endolith, an

extremophile that lives inside rock. If the bacteria were discovered in the
permafrost of Antarctica, describe two extremophile features the bacteria must
possess.

33.

Mention three differences between bacteria and archaea.

34.

Explain the statement that both types, bacteria and archaea, have the same basic
structures, but built from different chemical components.

35.

A scientist isolates a new species of prokaryote. He notes that the specimen is a

bacillus with a lipid bilayer and cell wall that stains positive for peptidoglycan.
Its circular chromosome replicates from a single origin of replication. Is the
specimen most likely an Archaea, a Gram-positive bacterium, or a Gram-negative
bacterium? How do you know?

36.

Think about the conditions (temperature, light, pressure, and organic and
inorganic materials) that you may find in a deep-sea hydrothermal vent. What
type of prokaryotes, in terms of their metabolic needs (autotrophs, phototrophs,
chemotrophs, etc.), would you expect to find there?

37.

Farmers continually rotate the crops grown in different fields to maintain

nutrients in the soil. How would planting soybeans in a field the year after the
field was used to grow carrots help maintain nitrogen in the soil?

38.

Imagine a region of soil became contaminated, killing bacteria that decompose

dead plants and animals. How would this effect the carbon cycle in the area? Be
specific in stating where carbon would accumulate in the cycle.

39.

Explain the reason why the imprudent and excessive use of antibiotics has
resulted in a major global problem.

40.

Researchers have discovered that washing spinach with water several times does
not prevent foodborne diseases due to E. coli. How can you explain this fact?

41.

Your friend believes that prokaryotes are always detrimental and pathogenic.
How would you explain to them that they are wrong?

42.

Many people use antimicrobial soap to kill bacteria on their hands. However,
overuse may actually increase the risk of infection. How could this occur?