EPWS 310 - Plant Pathology
Lectures - Fall 1997
Lecture 1
1. Call role
2. Introduce Karen Braun and Sue Fender
3. Go over syllabus - outline of course
4. Textbook- Agrios - corrections to textbook handout
I. Definition "Plant Pathology" - the study of plant diseases.
A. The study of Plant Pathology includes several aspects:
1)
2)
3)
4)
the living entities and the environmental conditions that cause disease in
plants
the mechanisms by which these factors produce disease in plants
the interactions between the disease-causing agents and the diseased
plant
the methods of preventing or controlling disease and alleviating the damage
it causes.
B. Plant pathology involves many disciplines:
Biology, meteorology, plant physiology, soil science, microbiology (mycology,
bacteriology, virology), nematology, horticulture, physics, plant anatomy,
epidemiology, biochemistry, genetic engineering, computer science, mathematics
and the list goes on.
C. Plant pathologists' investigate plant disorders caused by:
Fungi, bacteria, viruses, viroids, nematodes, mycoplasmas, parasitic higher plants,
and protozoa.
Plant pathologists' also investigate nutritional disorders of
imbalances in plants that reduce yield and may increase susceptibility to
pathogens.
D. What is a plant disease?
Any disruption (biotic or abiotic) of the plants normal metabolism. This is often
expressed in dollar amounts.
Agrios-"The malfunctioning of host cells and tissues that results from their
coninuous irritation by a pathogenic agent or environmental factor and leads to the
development of symptoms. Disease in a condition involving abnormal changes in
the form, physiology, integrity, or behavior of the plant.
E. What is a pathogen?
An agent that causes, incites, or induces disease?
1. Incite to riot -
once triggered it takes off.
tumefaciens, incites crown gall.
Example- Agrobacterium
2. Cause -
the host, pathogen, and environment all interact to result in a
disease. A pathogen all by itself cannot cause disease.
3. Induce -
Probably the best. Pathogens induce disease.
F. How do pathogens cause disease?
1)
2)
3)
4)
Weakening the host by continually absorbing food from the host cells for
their own use. Pythium, mistletoe,
Killing or disturbing the metablolism of host cells through toxins, enzymes,
or growth-regulating substances they secrete. Foolish disease of rice,
Gibberella fujikuroi; Bacterial soft rots, Erwinia carotovora
blocking the transportation of food, mineral nutrients, and water through the
conductive tissues. Verticillium wilt, Fusarium wilt.
consuming the contents of the host cells upon contact. nematodes.
LECTURE 2
G. Why study plant pathology?
Note: excess eating in US, yet 35,000 people die daily due to chronic starvation. In
addition, even with surpluses, more efficient and less environmentally damaging
production techniques are always needed.
1. Food, fiber, chemicals, and atmosphere is sustained and dependent on plants.
2. Plants and products are damaged which results in loss of life or lifestyle.
3. Plant pathogens are competing for our food source.
*8000 fungi in North America cause 80,000 different diseases.
*180 species of bacteria
*500 different viruses cause plant diseases
*150 different nematodes
4. Example - Tomato is attacked by 80 fungi, 11 bacteria, 16 viruses, and a
number of nematodes.
H. The beginning of Plant Pathology
In 1845, a tragedy struck Ireland. The days were warm and sunny that summer
and the potato crop was growing well. THe weather turned overcast and rainy for weeks,
the potato plants rotted as the Irish peasants watched. This event more than any other
gave rise to the science of Plant Pathology. In the 19th century the peasant farmer
became dependent on the potato. The potato originated in the highlands of South
America. The Spanish conquistadors discovered this tuber and the first potato arrived in
Spain around 1570. It was a well established food crop in Ireland by the 1800's. The
potato provided high nutrition and caused a burst in population from 4.5 million in 1800 to
8 million in 1845. The grain crops grown by the peasants were used to pay the rent to
landowners in England. Only a small number of potatoes were brought to Europe and so
the genetic diversity wsa very limited. That is, the Irish potato was genetically uniform.
What contributed to this epidemic? 1) A large population was dependent on a single
crop. 2) Weather conditions turned cool and wet, which was favorable to the pathogen 3)
the pathogen was present. In 1846 the weather was the same. One million people died
of starvation and 1.5 million migrated because of the famine.
Dr. C. Montagne, a French physician in Napoleon's army, first described the fungus
found on the potatoes. He shared his observations with Rev. M. J. Berkeley, who
recognized that this new fungus was connected with the blight. His rival was Dr. John
Lindley, a botany professor at University College in London, who did not believe that the
fungus was the cause of the blight. Their arguments were published in The Gardener's
Chronicles . These were intense. Read The Advance of the Fungi, by E. C. Large for
more juicy details. Anton De Bary, the father of Plant Pathology, a German botanist,
performed the experiments that proved the role of the fungus in the blight. The notion of
causality established the science of plant pathology.
In 1860, Louis Pasteur disproved the dogma of Spontaneous Generation (Flies
come from rotten meat (Redi, Italian), rats come from old rags and moldy cheese). This
theory was replaced by the germ theory in which it was finally recognized that microbes
were inducers of disease.
Read: THE MICROBE HUNTERS, The Advance of the Fungi, Famine on the Wind
LECTURE 3
II. Current crop losses due to plant diseases
A. Estimated production of world's major food crops.
1. Note that the crops that are high on the list have many diseases that have been
investigated.
2. Estimated 1982 world crop production and preharvest losses (in millions of tons
and percent of world production lost to diseases, insects and weeds.
3. Note that of the 13 crops listed diseases are the major problem on 8.
4. Estimated 1982 crop production and preharvest losses (in Millions of tons) and
percent lost to diseases and other pests(insects, weeds) in developed and
developing countries.
5. Note that in every crop, developing countries have a higher loss to disease,
insects and weeds.
6. Percentage of all produce lost to deseases, insects and weeds by continent or
region. Note percent loss in developing countries.
7. Postharvest losses in developing countries are estimated at between 10-25%.
In developing countries between
F. The total loss to pests in the U. S. is estimated at 40% and for the entire world
to about 48% of all food crops.
III. History of Plant Pathology
A. Genetic uniformity
1. History - Anthropologists tell us that humans began as foragers (nut and fruit
gatherers) and nomadic hunters. In time, humans learned how to grow crops and
development of societies began. As humankind has developed agriculture, the need for
breeders, agriculturalists, plant scientist, and plant pathologist came around. We have
moved from a society where everyone was at one time involved in growing crops or
domestic animals, to a society in which only 2-3% of the United States population is
involved in Agriculture. With our intense agricultural system, we have been able to
produce enough food to feed the world. However, we have also left ourselves open to
severe epidemics because of our limited gene source. That is, many of our major crops
are genetically uniform within their particular species. (Page 143 Agrios).
-Example: Dry beans are grown on 1.4 million acres. Total varieties are 25. 2 major
varieties are grown on 60% of the acreage. (overhead)
a. Pesticide use. Note that the use of pesticides to control plant diseases and other
pests has been increasing steadily at an annual rate of about 14% since the mid-1950's.
So far, about 35% of all pesticides are applied in the U.S. and Canada, 45% in Europe,
and the remaining 20% in the rest of the world.
b. Agricultural land lost. In the United States, two million acres of land each year
are converted from agricultural to nonagricultural uses, including 420,000 acres for urban
development, an equal amount for reservoirs and flood control, and nearly one million
acres for parks, wilderness, and wildlife areas. The amount of cropland is decreasing at
an annual rate of 3 %. How long can it continue? With this decrease in farmland the use
of pesticides will become greater, and the tendency to rotate crops or use long term
cultural practices will decrease.
2. Genetic make-up of crops in the past.
They were not the seed of careful genetic crosses and many generations of
inbreeding and back-crossing to obtain maximum yields but
the a result of many years of survivor selection by farmers. These were seeds that would
grow into plants that could produce some yield despite competition from weeds, insects,
pathogens, and poor soil fertility.
General resistance to a multitude of pests in plants selected under such
circumstances ensured at least some harvest, even if the maximum was not possible.
Heterozygous populations.
-characteristics, Genetic diversity, many kinds of crops interspersed, slash and
burn (nomadic ag.), Incas of Peru developed crop rotation laws (Ex. potatoes planted in
the same soil every seven years).
3. Examples of epidemics as a result of genetic uniformity
a. Late blight of potato in Northern Europe (1845-6). Talk about it later.
b. Southern corn leaf blight(1970)-the result of the widespread use of corn
hybrids containing the Texas male-sterile cytoplasm. Caused over $1 billion loss in the
corn crop. The pathogen is Bipolaris maydis. The pathogen had been observed for
several years, but it was never a serious problem. In 1970, nearly 80% of all hybrid field
corn produced in the U. S. contained TMS cytoplasm. A genetic change or a population
shift occurred in the B. maydis population. A new race of B. maydis was found to be
particularly virulent on corn with TMS cytoplasm. The new race was called Race T to
differentiate it from Race O that caused a minor leaf spot disease. Race T was much
more aggressive and could reproduce a new generation of infective spores within 51 hrs.
In many southern states, entire fields were destroyed and 80-100% were common.
Components of an epidemic
1. Susceptible host- change in susceptibility
2. Genetic change in the pathogen population.
3. Environmental factors- B. maydis likes hot, humid conditions.
4. TimeGo over the disease triangle and disease pyramid.
b. Helminthosporium blight of Victoria oats- Many varieties were replaced by the
rust-resistant Victoria oat variety. Unfortunately, this variety was very susceptible to
Helmithosporium victoriae, previously a minor pathogen.
c. Coffee rust in Ceylon (COFFEE or TEA)- The whole island was planted to
coffee for England to drink. Coffee (Coffea arabica) was grown in the Dutch-English
colonies of Ceylon(Sri lanka), Java, and Sumatra. The English loved their coffee. A rust
fungus called Hemileia vastatrix, reached Ceylon in 1875. nearly 400,000 acres (160,000
hectares) were covered with coffee trees. The trees were very susceptible to the fungus.
The fungus can liberate about 150,000 spores per leaf pustule. One leaf can have 100's
of pustules. No effective chemical fungicides were available. In 1870 Ceylon exported
100 million pounds of coffee. In 1889, production was down to 5 million pounds.
Production of coffee ceased and the crop was switched to TEA.
Marshall K. Ward was hired by the British government to find a way to stop the
rust epidemic.
He didn't stop the epidemic, but he was able to warn us about
monculture. He also observed that it is very important to anticipate the disease and not to
wait for symptoms to appear before spraying .
LECTURE 4:
B. Great names in Plant Pathology
Earliest recorded history is found in Genesis. The blight, blast, and mildew were induced
by fungi. We still use these terms to describe disease symptoms.
The greek philosopher Theophrastus (370-286 B. C.) was the first to write about
diseases of trees, cereals, and legumes. He made the interesting observation that
plant disease was more severe in low lying areas.
For the next 2000 years little progress was made in the area of plant pathology. In 1660,
Anton Van Leeuwenhoek (1632-1723)(a janitor), first saw bacteria. He had a
hobby of grinding lenses. He made 247 different microscopes that could enlarge
objects 40 to 270 times. He saw stagnant water teeming with life.
In 1729, Micheli described the spores of Rhizopus (a common bread mold). When
these 'dust particles' were placed on freshly cut slices of melon, the same fungus
was reproduced. He concluded that the spores were the fungal seeds and that
these seeds were carried through the air.
In 1755 Tillet added black dusts from wheat to seeds and kept some seed clean. He
observed that the seed that had the bunt or stinking smut dust had more disease.
He showed from his experiments that stinking smut, bunt, of wheat is a contagious
disease. However, Tillet believed it was a poisonous substance contained in the
dust, rather than living organisms.
In 1807, Prevost proved that bunt is the cause of bunt of wheat. He was able to control
the disease by dipping the seed in copper sulfate. We still use copper sulfate
today. Unfortunately, most scientist of the day still believed in spontaneous
generation and thought microbes were the result rather than the agent of disease.
Dr. C. Montagne, a French physician in Napoleon's army, first described the fungus
found on the potatoes. He shared his observations with Rev. M. J. Berkeley, who
recognized that this new fungus was connected with the blight. His rival was Dr.
John Lindley, a botany professor at University College in London, who did not
believe that the fungus was the cause of the blight. Their arguments were
published in The Gardener's Chronicles . These were intense. Read The
Advance of the Fungi, by E. C. Large for more juicy details. Anton De Bary, the
father of Plant Pathology, a German botanist, performed the experiments that
proved the role of the fungus in the blight.
In 1860, Louis Pasteur disproved the dogma of Spontaneous Generation (Flies come
from rotten meat (Redi, Italian), rats come from old rags and moldy cheese). This
theory was replaced by the germ theory in which it was finally recognized that
microbes were inducers of disease.
Read: THE MICROBE HUNTERS, for a good time.
In 1880, an epidemic on grapes in France hit. Downy mildew (Plasmopara viticola) hit.
The grape vines were going down and so was the wine industry (50 billion dollars).
Alexis Millardet was a botany professor. One day he observed that some of the
grapes were not suffering from Downy mildew. He also observed that these
grapes were covered with a substance that looked like bird excrement. He talked
to the farmer and the farmer said he put a mixture of Copper and lime on the
plants to stop kids from eating the grapes. From this came the first fungicide,
Bordeaux mixture. Bordeaux mixture is effective against many fungi and
bacteria, is inexpensive, and even today, over 100 years later, is the most widely
used fungicide in the world.
How to prove pathogenicity: Koch's postulates
Robert Koch, a German microbiologist, who worked on anthrax of sheep developed a
method to prove pathogenicity.
Koch's postulates:
1. The symptoms and any evidence of the pathogen in the diseased host are
carefullly described.
2. The suspected pathogen is isolated from the diseased host and from all
other contaminating microorganisms, usually on a nutrient medium
that will keep the organism alive. A description is made of the
suspected pathogen.
3. A healthy host is inoculated with the suspected pathgen. It is later
observed for symptoms, which must be identical to those described in
Step 1.
4. The pathogen is reisolated from the inoculated host and must be identical
to the organism described in Step 2.
R. J. Petri, a student of Koch first developed dishes to cut down on contaimination. They
were called Petri dishes.
In 1878, Thomas Burrill, an American Plant Pathologist, implicated a bacterium as the
disease agent of the fire blight disease in Northe America that was causing the
death of apple and, especially, pear trees. Another American plant bacteriologist,
Erwin F. Smith, contributed greatly to our understanding of bacteria. He was the
first president of the American Cancer Society in the early 1900's. He had done
some extensive work on Agrobacterium tumefaciens, causal agent of Crown gall.
Causes tumorous growth (Hypertrophy- a plant overgrowth due to abnormal cell
enlargement).
In 1892, a Russian scientist named D. Ivanoski, first showed that viruses could cause
disease. He worked with TMV (Tobacco mosaic virus).
Controversy with A. Mayer. a german scientist who thought it was a bacteria.
Norman Borlaug, a plant pathologist, received the Nobel Peace Prize in 1970 for his
contributions to the development of high yielding wheat, which led to the media
phrase Green revolution.
Roger Beachy, Steve Tankesly, Brian Stackawicz
IV. Diagnosis of Plant Disease
Diagnosis of plant disease is both an art and a science. In lab today we will discuss the
differences between biotic or abiotic symptoms. That is the first step in diagnosis, to
determine between environmental and organismal effects. We will also look at different
reference sources that are used for diagnosis and ID. Today, I want to go over the basic
symptoms of pathogens and parasites.
A. Diseases caused by parasitic higher plants- Ex. dodder, mistletoe, witchweed) look
for the presence of the parasitic higher plant.
B. Diseases caused by nematodes- Look for nematode in the root zone and root tissue
of the plant. Look also for knots (Root knot nematode). ID nematode on the basis
of the stylet and morphlogy of the nematode.
8
C. Diseases caused by fungi and bacteria- When fungi or bacteria are found in the plant
tissue, it must be determined whether the organism is a pathogen or secondary
saprophyte.
Fungi- The morphology of the fungal hyphae, spores and fruiting structures needs to be
determined. After iD, an appropriate text can be consulted to see whether that
organism has been found as a pathogen on your plant. Special media, special
environments.
Bacteria- Based on symptoms, the appearance of a large number of bacteria in the area,
and the absence of any other pathogens. Bacteria are very small (1-2 um) and are
difficult to ID based on morphology. Use selective media and reinoculation.
Immunodiagonstic techniques have also been developed for many plant
pathogenic bacteria.
C. Diseases caused by mycoplasmas- Diseases caused by mycoplasms appear as
stunting of plants, yellowing or reddening of leaves, proliferation of shoots and roots,
abnormal flowers, and eventual decline and death of the plant. Mycoplasmas are small,
wall-less bacteria that live in the phloem of the hosts, invisible. Therefore, diagnosis is
based on symptoms, graft transmission, insect vectors, electron microscopy, sensitivity to
certain antibiotics (Tetracycline but not penicillin), sensitivity to high temperatures, and
serodiagnostic tests.
D. Diseases caused by viruses and viroidsepinasty, curling, stunting, discoloration.
ID also by
ID by symptoms-mosaics, streaking,
1. virus transmission test to specific host- use vectors such as insect, nematode, fungus,
or mite. Vector- an animal able to transmit a pathogen.
2. seradiagnostic tests.
3. electron microscopy.
4. Microscopic examination of infected cells for specific crystalline or amorphous
inclusions.
5. electrophoresis
6. Hybridization of commercially available radioactive DNA complementary to a certain
viroid RNA, with the viroid RNA present in plant sap and attached to a membrane
filter.
Lecture 5:
V. Parasitism and disease development
A. Terminology1. Parasite- an organism that lives on or in some other organism and obtains its food
from the latter. Shakespeare- beside the table.
2. Symbiosis- both host and non-host benefit. Mycorrhizal fungi, Rhizobium bacteria
(nitrogen fixers).
3. Pathogenicity- The ability of the parasite to interfere with one or more of the essential
functions of the plant, with parasitism frequently playing an important, but not
always the most important role.
4. Biotrophs, obligate parasites- They can grow and reproduce in nature only in living
hosts. e.g. rusts, powdery mildew, downy mildew, viruses, viroids, mycoplasmas,
nematodes, fastidious bacteria, protozoa.
5. Nonobligate parasites- Parasites that can live on either living or dead hosts and on
various nutrient media. Most fungi and bacteria.
6. Facultive saprophytes- Parasites that can live on dead organic matter, but live most of
their life cycle on a living host.
7. Facultative parasites- Parasites that live most of their lives on dead organic matter but
under certain environmental conditions, can attack living tissue and become
parasitic.
8. Saprophyte- organisms that lives on dead organic tissue.
9. Virulence-the degree of pathogenicity of a given pathogen. Often a quantitative scale
when comparing isolates in a population. Avirulence.
(Draw scale) Virulence (10)-------------------------Avirulence (1)
Pathogenicity is a qualitative scale- either a pathogen or not.
10. Aggressiveness- a quantitative measure of the severity of disease over time in a
pathogen population. The one that develops faster is the most aggressive. May
be the same amount of disease at the end of the season.
B. Obligate vs. non-obligate parasite- Obligate parasite doesn't kill the host directly, but
redirects the nutrients to itself. The non-obligate parasite usually kills the plant
cells with enzymes or a toxin and then digest the host cells. The non-obligate lives
like a saprophyte in a living host.
C. Stages in the development of disease
The disease cycle- involves the changes in the plant and the plant's symptoms as well
as those in the pathogen and spans periods withina growing season and from one
growing season to the next. It refers primarlily to the appearance, development,
and perpetuation of the disease as the pathogen relates to it rather than to the
pathogen itself.
1. Inoculation
2. Penetration
3. Establishment of infection
4. Colonization (invasion)
5. growth and reproduction of the pathogen
6. dissemination of the pathogen
7. survival of the pathogen in the absence of the hos (overwintering or
oversummering of the pathogen).
EDIT FINISHES HERE AUGUST 29, 1995
1. Inoculation- when the pathogen comes in contact with the host. Inoculum- the
pathogen (s) that come into contact with the host.
Examples of inoculum- in fungi, spores, sclerotia, mycelium. Individuals of
bacteria, viruses, viroids, mycoplasmas. In nematodes- adult, larvae, eggs.
Propagule=one unit of inoculum. Colony forming units.
A. Types of inoculum- Primary inoculum - inoculum that survives the overwintering
or oversummering. The infections it causes are called primary infections. Secondary
inoculum- inoculum produced from primary infections. The secondary inoculum in turn
induces primary infections.
B. Sources of inoculum-plant debri, or soil
-seedborne, transplants, tubers, propagative material
-perennial weeds or alternate hosts
*Fungi, bacteria, parasitic higher palnts, and nematodes either produce their inoculum on
the surface of infected plants or their inoculum reaches the plant surface when the
infected tissue breaks down. Viruses, viroids, mycoplasmas, and fastidious bacteria
produce their inoculum within the plants; such inoculum asmost mever reaches the palnt
surface in nature and, therefore, cannot by itself escape from one plant and spread to
another.
C. Landing or Arrival of Inoculum-wind-most does not reach susceptible hosts.
-water
-insects-most efficient.
2. PenetrationA. Germination of Spores and seeds-requires certain environmental conditions
-resting spores or germinates immediately????
*spore germination is often stimulated by exudates of the plant roots, leaves, or
fruit. Nutrients(sugars and amino acids).
*Fungistasis- Due to toxic metabolites in the soil or competition, the spore is not
able to germinate or the hyphae lyses soon after germination. Explain hypae and germ
tube. Fungistasis is often counteracted by the root exudates. Soil that is fungistatic is
called suppressive soil.
-What affects direction to penetration sites?? moisture, temp., soil texture, plant
exudates, thigmotropic (contact) responses to the topography of the leaf surface resulting
in germ tubes growing at right angle to cuticular ridges that gererally surround stomata.
Zoospores- chemical stimuli, sone of elongation of roots, physical simuli, nutrient
gradient.
-Seeds penetrate by producing a radicle that penetrates or produces a haustoria.
-Nematodessame conditions, Carbon dioxide and some amino acids.
Nematodes are generally attacted more to the roots of host plants but also go to nonhost.
B. Attachment of Pathogen to host
How do they stick? Viruses, mycoplasmas, protozoa, and fastidious bacteria are placed
directly into cells of plants by their vectors. Fungi, bacteria, and parasitic higher plants
must first become attached. They have on their surface polysaccharides, glycoproteins,
polymers of hexosamines, and fibrillar materials, when moistened becomes sticky and
helps the plant to adhere. LECTINS. Germ tubes also have this characteristic. The
muscilaginous material contains degradative enzymes that chew away the outer cell wall.
C. Recognition between host and pathogen
Not known for sure how recognition works. If the plant responds quickly to the pathogen
the end result is often resistance.
D. Penetration-the act.
1. Natural openings-stomata, lenticels, hydathodes, nectarthodes. Bacteria, fungi,
nematodes.
2. Wounds- fruits and vegetables. Fungi, Bacteria, viruses (Vectored)
3. Direct penetration- enzymatic or pressure. Fungi, parasitic higher plants,
nematodes.
Direct penetration- Explain about appressorium, penetration peg, intercellular hyphae,
intracellular hyphae, haustoria. Penetration in parasitic higher plants is similar to fungi.
Penetration by nematodes is accomplished by repeated back and forth thrusts of their
stylets.
3. Infection- the process by which pathogens establish contact with the susceptible cells
or tissues of the host and procure nutrients form them. During infection pathogens grow
or multiply, or both, within the plant tissues and invade and colonize the plant to a lesser
or greater extent.
-one result of infections is symptoms. An infection that does not appear right away
is called a latent infection. The latency is due to environmental conditions or maturity
level of the host. Symptoms can occur at 2 days or 2 years (mycoplasmas) depending on
the pathogens, environment and host.
IN most cases, symptoms occur within two
weeks of intial invasion.
-Incubation period- the time between inoculation and the appearance of diseae
symptoms.
-Invasion- Subcuticular (black spot on rose, apple scab), surface of the plant but
send haustoria into the epidermis (powdery mildew, downy mildew), intracellular or
intercellular (rusts), xylem tissue (Fusarium, Verticillium). Bacteria invade intercellularly
until the cell wall breaksdown and then the bacteria grows intracellularly. Viruses, viroids,
and mycoplasmas invade intracellularly, nematodes invade intercellularly in most cases.
-Colonization- by fungi- can grow throughout the plant and then produce spores by
the millions.
Bacteria- divide every 20 to 30 minutes. Number becomes very large. Fastidious
bacteria and mycoplasmas reproduce much slower than bacteria and are usually in lower
numbers in the plant.
Viruses and Viroids-reporduce in the individual cells. 10 million virus particles per cell.
Nematodes- female lays about 300-600 eggs, about 1/2 are females. Two to 12
generations produces per year. Each generation increases the number of nematodes in
the soil by 100 fold.
4. Dissemination - spread of pathogen inoculum.
Almost all dissemination of pathogens that is responsible for plant disease outbreaks, and
even for disease occurrences of minor economic importace, is carried out passively by
such agents as air, water, insects, certain other animals, and humans.
Air-most of these spores do not contact a susceptible hosts. They have a better
chance in monculture. What would they have hit in a polyculture? Rusts occur at several
thousand meters abouve infected fields and can be carried for miles.
Water- Important in disseminating pathogens in three ways:
1. Bacteria, nematodes, and spores, sclerotia and mycelial fragments of fungi present in
the soil are disseminated by rain or irrigation water that moves on the surface re through
the soil.
2. All bacteria and the spores of many fungi are exuded in a sticky liquid and depend for
their dissemination on rain or irrigation water, which
either washes them downward or splashes them in all directions.
3. Raindrops or drops from overhead irrigation pick up the fungal spores and any
bacteria present in the air and wash them downward where some of them may land on
susceptible plants.
*Water dissemination is more efficient in that the pathogens land on an already wet
surface and can move or germinate immediately.
-Insects, mites, nematodes, and other vectorsAphids and leafhoppers are primary vectors for viruses. Leafhoppers are the main
vectors for mycoplasmas and fastidious bacteria. The Dutch elm disease also depends
on the a bug. In these vectored diseases, the pathogen is completely dependent on the
vector.
*Very efficient method of transmission.
Humans-within a field, machinery, tools, airplane.
Examples-Dutch elm disease, white pine blister rust, downy mildew of grape.
5. Survival- When the host tissue dies, whether an annual or perennial plant, the
pathogen survives until the new season.
a. Methods of survival
-fungi- perennial plants, mycelium in infected tissues (Cankers, spores on bud
scales, fallen , infected leaves or fruits. Annual plants- mycelium in infected plant debris,
as resting spores, sclerotia, on seeds, tubers. Some are soil inhabitants- able to survive
indefinitely as saprophytes (Pythium, Fusarium, Rhizoctonia). They usually have several
hosts. Soil transients- are specialized parasites that generally live in close association
with their host buyt may survive in the soil for relatively short periods of time. Rusts
overwintering on plants grown at warmer temperatures and move from them to crops
grown in jcolder climates as temperature allows. Rust go form annual to perennial and
overwinters in the perennial.
2. bacteria-same as fungi. Many overwinter in insect vector.
3. viruses-in living plant tissue such as the tops and roots of perennial plants, the
vegetative propagating organs, and in the seeds of some hosts. Some viruses overwinter
in their vectors. TMV (cigarettes).
4. Nematodes-as eggs in the soil and in plant roots .
5. Parasitic plants- survive either as seeds or as their vegetative form on their
host.
LECTURE 7
How pathogens attack plants - in more detail...
A. It is a war out there!!!
PATHOGEN
HOST PLANT
1. Penetration with pressure
Intricate cell wall and cuticle
2. Penetration with enzymes
Suberization, antifungal enzymes
(Chitinases, B-glucanases). Deactivation
of pathogen enzymes
3. Toxins
Detoxification by enzymes
4. Growth regulators and general
virulence factors
Biochemical defense (Phytoalexins,
hypersensitive response, phenols)
B. Mechanical forces exerted by pathogens on host tissues
For a pathogen to exist it must enter the plant, obtain nutrients from the plant and
neutralize the plant defenses.
1. What plant parasites enter by mechanical pressure?? some fungi, parasitic higher
(flowering plants) plants, and nematodes.
2. Show overhead of cell wall diagram3. The parasite first adheres to the plant surface. The fungus forms an appressorium-a
flattened bulblike structure. This increases the area of adherence between the two
organisms. From the appressorium a penetration peg forms.
C. Chemical weapons of pathogens
The effects caused by pathogens in plants are largely chemical in nature.
Main groups:
Enzymes (most common)
Toxins (2nd most common)
Growth regulators (3rd most common)
Polysaccharides (least common)
All plant pathogens can produce these compounds except for the viruses and viroids. but
Viruses and viroids can stimulate the plant to produce these compounds.
1. Enzymes-large protein molecules that catalyze all the interrelated chemical
reactions in a living cell.
(Show cell wall overhead)
Enzymatic degradation of cell wall substances
a. cuticular wax- no pathogens are known that produce enzymes that can degrade
waxes. Fungi and parasitic higher plants apparently penetrate wax layers by means of
mechanical force alone. Example-wax layer on apples and other fruit.
b. Cutin- an insoluble polyester of mostly branched derivatives of C16 and C18 hydroxy fatty
acids.
Cutinases - esterases - they break the ester linkages between cutin molecules and
release monomers as well as oligomers. Draw reactionMany fungi and at least one bacterium (Streptomyces scabies) have been shown to
produce cutinases. Fungi produce small amts. of cutinase all the time. When this small
amt. acts on the cutin, the cutin monmers cause a 1000x increase in the amt. of cutinase.
c. Pectic substances - constitute the main component of the middle lamella. They are
polysaccharides consisting mostly of galacturonan molecules interspersed with rhamnose
molecules and side chans of galacturonan and other sugars. Draw structure of
galacturonan and glucose molecule.
Pectinases-pectolytic enzymes
*Pectin methyl esterases-removes branches of pectin chain that does not effect the pectin
chain length, but this does affect the solubility and open it up to attack by other enzymes.
*Polygalacturonase-chain splitting pectinase. Adds a water molecule hydrolyzing the
linkage between 2 galacturonan molecules.
*Pectic lyases or transeliminases- Split the chain by removing a molecule of water.
* Endo-pectinases vs. exo-pectinases.
Show overhead on page 70 and re-explain the activity of the enzymes.
Drawing below.
Autocatalytic induction-the galacturonan monomers serve as inducters for inhanced
synthese and relaese of pectolytic enzymes which further increasse the amount of
galacturonan monomers.
When the monomer concentrations become too high, catabolite repression occurs
and the production of enzymes is stopped.
*damage done by pectic enzymes-tissue maceration-separation of cell walls. Occlusion
of vessels. Weaken the primary cell wall and upset the osmotic balance of the cell
causing the cell to burst.
d. Cellulose-consist of chains of glucose molecules. The cellulose content of tissues
varies from about 12% in non-woody tissues of grasses to about 50 % in mature wood
tissues to more than 90% in the cotton fibers. The spaces between microfibrils and
between micelles or cellulose chains within the microfibrils may be filled with pectins and
hemicellulose and probably some lignin at maturation.
Several Cellulases- C1-attacks native cellulose by cleaving cross linkages between
chains.
C2-breaks the chains down farther.
CX-breaks the chains down into disaccharide cellobiose.
B-glucosidase- breaks disaccharide into glucose.
Draw structure-
E. Hemicelluloses-complex mistures of polysaccharide polymers, the composition and
frequency of which seem to vary among plant tissues, plant species, and with the
developmental stage of the plant. They are a primary component of the cell wall and may
also be in the middle lamella and the secondary wall.
*many different kinds of hemicellulases-xylanase, galactanase, glucanase,
arabinase, mannase...................................
F. Lignin - Found in the middle lamella, in the cell wall of xylem vessels, and in the fibers
that strengthen plants. The lignin content of mature wood plants wries from 15 to 38
percetn and is second only to cellulose.
Structure of lignin-phenylpropanoid.
*Only about 500 species of fungi can degrade lignin.
These are almost all
basidiomycetes. The largest group is clled the white rot fungi and they produce
ligninases.
F. Enzymatic degradation of substances contained in plant cells
ProteinasesAmylases- starch
Lipases, phospholipases-oils and fats, membranes.
LECTURE 8
Microbial toxins in Plant Disease.
A. DefinitionToxin-a non-enzymic metabolite of one organism which is injurious to another.
Mycotoxin- a toxin produced by a fungus.
Toxins are produced by mircroorganisms and cause damage to the host cell. The usually
act directly on the cell protoplast.
B. Mode of action *Permeability of the cell membrane increased
*Inactivate or inhibit enzyme activity
*Act as a antimetabolite inducing a deficiency for an essental growth factor.
C. Non-host specific toxins- Toxins that affect a wide range of host plants. These toxins
affect many differetn plants and increase the exztent of disease but are not essential for
the pathogen to cause disease.
Example- Phaseolotoxin
*Phaseolotoxin-Caused by Pseudomonas syringae pv. phaseolicola, causes halo
blight of bean.
It is a ornithine-alanine-arginine tripeptide carrying a phosphosulfamyl group. Plant
enzymes cleave the peptide bonds and release alanine, arginine and
phosphosulfamylornithine.
Phosphosulfamylornithine is the acive moiety of
phaseolotoxin. PSO binds to the active site and inactivates the enzyme ornithine
carbamoyltransferase which normally converts ornithine to citrulline, a precurser of
aginine (an essential amino acids- what do a string of AA make????) Ornithine
accumulates and depletes arginine.
ASSIGNMENT--Read about Tabtoxin, tentoxin, and Fusicoccin. Know how one of these
works, what is the organisms responsible etc.
D. Host-specific toxins- a substance produced by a pathogenic microorganism that, at
physiological concentrations, is toxic only to the hosts of that plant pathogen and shows
little or no toxicity against nonsusceptible plants. Most host-specific toxins must be
present for disease to occur.
Examples- 1) Victorin or HV toxin- caused by Helminthosporium victoriae.
2) T-toxin- Helminthosporium maydis race T
3) AK-toxin- Alternaria alternata
4) AM-toxin- Alternaria alternata (A. mali)
Example- T-toxin-Southern corn leaf blight
Resistance and susceptibility to H. maydis T and its toxin are inherited maternally (in
cytoplasmic genes). Virulence and T-toxin are controlled by the same gene in H. maydis.
T-toxin acts on the mitochondria of susceptible cells. It causes early loss of matrix
density, renders them nonfunctional, and inhibits ATP synthesis. T-toxin also causes
selective uptake of certain ions, inhibition of root growth in seedlings and closure of
stomata.
ASSIGNMENT-- Know about one other host specific toxin, inside and out.
Growth Regulators in Plant Disease
Growth regulators= hormones
1. Auxins
2. gibberellins
3. cytokinins
4. ethylene
5. ABA-Abscisic acid
Characteristics1. Work in small concentrations
2. Usually synthesized a distance from the site of action.
3. Promotes synthese of messenger-RNA molecules.
*The effects of pathogen-produced growth regulators on plants is stunting, overgrowths,
rosetting, excessive root branching, stem malformation, leaf epinasty, defoliation,
suppression of bud growth.
1. AUXINS - Indole -3-acetic acid (IAA) is the auxin that occurs naturally in plants. The
effects of IAA:
- cell elongation and differentiation
- cell membrane permeability
- general increase in respiration, promotes protein synthesis
A) Cause of auxin increase:
- plant
- pathogen stressing plant
- pathogen produced
- degradation of IAA oxidase - breaks down excess amount of
in normal plant metabolism
IAA
EXAMPLES
1) Pseudamonas solanacearum causes bacterial wilt of solanaceous plants
(tomato, pepper, tobacco, potato). It causes a 100-fold increase in IAA.
- Increased plasticity of the cell wall because of IAA leaves the cell wall more open
to pectinases and cellulases
- Increased IAA also inhibits lignificatiojn
2) Crown gall Agrobacterium tomefaciens produces galls on over 100 plant
species. Galls or tumors develop on the roots, stems, and petioles.
- Tumor cells contain higher than normal amounts of IAA and cytokinen. The plant
cell is conditioned to over-produce these hormones.
3) Pseudomonas savastoni - knot disease of olive, oleander, and privet, produces
IAA and induces gall formation.
2. CIBBERELLINS - 1rst isolated from the fungus Gibberella fujikuroi, the cause of
"foolish seedling disease" of rice.
Effects:
- speed elongation of dwarf varieties
- promotes flowering
- stem and root elongation
- growth of fruit
- induces IAA formation
20
3) CYTOKININ - necessary for cell growth and differentiation
- inhibits senescence
- examples: kinetin (herring sperm DNA)
zeatin - from plants
Cytokinin activity increases in clubroot galls, in crown galls, in smut and rust galls, and
root infected bean and broad bean leaves
-Witches'-broom caused by fungi and bacteria
4) ETHYLENE - CH2=CH2
Effects:
- chlorosis
- leaf abscission
- epinasty
- stimulation of adventitious roots
- fruit ripening
- increased permeability of cell membranes
- stimulates phytoalexins and enzymes that may play a role in
increasing plant resistance to infection
- leaf epinasty, premature defoliation
5. ABSCISIC ACID - induces dormancy
- inhibition of seed germination
- inhibition of growth
- stomatal closure
- stimulation of fungal spore germination
It is thought that ABA is one of the factors responsible for the observed stunting of
infected plants.
LECTURE 9
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HOW PLANTS DEFEND THEMSELVES AGAINST PATHOGENS
Two basic ways plants defend that plants defend themselves against pathogens.
I. Structual defenseA. Pre-existing defense structures
-wax, cuticle, was not only imped penetration but also repel water and therefore a
moist surface in shich the pathogen can germinate.
B. Defense structures formed in response to pathogen invasion
1. Histological defense structures*Cork layers-stop the physical advance of the fungus, stops nutrients from
going to the pathogen and stops toxins that may come from the pathogen.
*Abscission layers- often occurs in Prunus sp.
Shothole of cherry.
*Tyloses-overgrowths of the protoplasts of adjacent living parenchymatous
cells which protrude into xylem vessels through pits.
*GumsC. Cellular defense structures-morphological changes in the cell wall or changes
derived from the cell wall.
Example- Callose papillae-produced by cells within minutes after
wounding and within 2-3 hrs after inoculation with microbes.
Diagram-
The man function of papillae seems to be to repair cellular damage, sometimes they
also seem to prevent the pathogen from subsequently penetrating the cell.
D. Cytoplasmic defense*Example- Necrotic defense raction: defense through hypersensitivity- The faster
the host cell dies after invasion, the more resistant to infection the plant seems to be.
II. Metabolic (Biochemical defense)
A. Pre-existing biochemical defenses*Example-ONion smudge disease caused by Colletotrichum circinans. Resistant
onion varieties have red scales and contain the phenolic compound protocatechuic acid
and catechol. These substances cause inhibition of C. circinans germination. White
scale onions are susceptible.
22
B. Defense through lack of essential factors
1. Lack of recogniton between host and pathogen.
Host cell surface may lack recognition factors.
2. Locak of host receptors and sensitive sites for toxins.
3. Lack of essental nutrients for the pathogen.
*Example-Erwinia caratovora var. atroceptica is less severe on potatoes
with low reducing sugar content than in potatoes high in reducing sugars.
III. Metabolic difense induced by the attacking pathogenA. Defense through the hypersensitive reaction.
*It occurs only in incompatible combinations.
*Changes in HR-loss of cell permeability, increased respiration,
accumulation and oxidation of phenolic compounds, production of phytoalexins.
*Results in death and collapse of the few infected cells and a few
surrounding cells.
B. Defense through increased levels of phenolic compounds.
Diagram- Phenol
Quinone
1. Phytoalexins- toxic substances produced in response to infection and
mechanical injury. Pytoalexins are produced by cells adjacent to those infected.
Resistance occurs when the phytoalexin concentration reaches a high enough
concentration to restrict pathogen growth. Phytoalexins do not occur in response to
biotrophs.
Phytoalexins are stimulated by pathogen substances called Elicitors. Elicitors are
usually part of the fungal cell wall (glucans, chitosan, glycoproteins, and
polysaccharides). In a susceptible response the pathogen is thought to have
suppressors.
*The amount of phytoalexin produced often correlates with the resistance
of the host.
*What about the virulent pathogen? How do they respond?
2. Fungitoxic phenolics released from nontoxic phenolic complexesnontoxic glycosidase that cleaves phenol and then renders it toxic.
3. The role of phenol-oxidizing enzymes in disease resistancePolyphenoloxidase (PPO)-; usually higher in resistant plants than in susceptible plants.
PPO oxidizes phenolics to quinones (more toxic to microbes). Peroxidases
23
4. The role of induced synthesis of enzymes.
Chitinase, b-glucanases, PG-inhibitors.
5. Defense through inactivation of pathogen enzymes- caused by phenols
and proteins.
6. Defense through release of fungitoxic cyanides from non-toxic
complexes. Cyanides-released by decompartmentalized hydrolytic enzymes.
7. Defense through detoxification of the pathogen toxins.
Disease Control
The best means of disease control is resistant varieties. Varieties that already have
resistance to the pathogen(s) is least expensive, most effective, and environmentally
safest.
A. Genes and Disease
Genes are located on the chromosomes of the nucleus of the cell. The
chromosomes are made of DNA. The mRNA makes a copy of the DNA code and
carries it to the cytoplasm where it locates a ribosomes. tRNA's find the amino acids
that match the code of the mRNA. In this building block affair proteins are formed and
enzymes are created. On these chromosomes are located genes that code for the
resistant mechanisms we have discussed.
Conversdely, the pathogen has genes that code for virulence mechanism. It is,
therefore, the concurrent occurence and interaction of specific genes for virulence in
the pathogne and of specific genes for susceptibility in the host that determine the
initiation and development of disease.
The gene or genes for virulence in the pathogen are usually specific for one or a
few related kinds of host plants. Also, the genes that make a host plant susceptible to a
particular pathogne are present only in that one host and possibly a few related kinds of
host plants.
2. Compatible (disease resulting) interaction
Why are some pathogens virulent to several host? Virulence genes are broad
spectrum or V-genes are very numerous.
Examples- Phymatotrichum omnivorum-- attacks 2000 different species
Puccinia graminis var. tritici --attacks wheat only
Fusarium oxysporum f. sp. lycopersici--attacks tomato only
3. Resistance is the rule, susceptibility the exception
Plants of a particular sspecies also have resistance genes. These resistance genes
may have been bred out of a particular variety or may not exist to certain pathogens. In
many casis resistance genes are found in wild accessions.
24
4. Introducing a new resistance gene
A resistance gene confers resistance to the different races of a pathogen. However, it
has been observed that once a new resistancee gene is in a plant population, new
virulent races often occur.
*How did this new population of pathogens acquire the new gene for
virulence?
-genes already present in a very small number. Race T.
H. maydis
-mutation - nuclear aand cytoplasmic
- recombination of genetic material - P. capsici. Sexual
reproduction
B. Stages of Variations in Pathogens
Species - the entire population of an organism on earth, for example a fungal
pathogen, has certain morphological characteristics in common and makes up the
species of the pathogen.
Example: Puccinia graminis - cause of stem rust of cereals.
Some of the individuals within this species attack only wheat or barley or oats.
These groups are called varieties or special forms (formae specialis).
Within these varieties or f. sp. there are races that attack only certain host plant
varieties.
Another Example: Fusarium oxysporum - wilt disease
Fusarium oxysporum f. sp. niveum
Wilt disease of watermelon
F. o. f. sp. niveum race 0, race 1, race 2
For the cereal rust pathogen, Puccinia graminis tritici there are more than 200 races.
Variants of these races sometimes only. For instance, one of the offspring of a race
can suddenly attack a new variety or can cause severe symptoms on a variety that it
could barely infect before - called a variant or Biotype. Each race may consist of
several biotypes (15A, 15B, and so on.)
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C. Types of Plant Resistance to Pathogens
Each kind of plant is a non-host to the vast majority of known plant pathogens.
Non-host are immune (non-host resistance).
Example: Elm tree resistant to Fusarium oxysporum f. sp. niveum
(Show M. Heath diagram)
1. True resistance - Disease resistance that is genetically controlled by the presence of
one, a few, or many genes. The host and pathogen are incompatible with one another
due to chemical recognition or other defense mechanisms.
2 kinds of true resistance:
1. Horizontal resistance- alos called nonspecific, general, quantitative, adult-plant,
field, or durable resistance.
Horizontal resistance is controlled by many genes (multigene resistance). *These
genes appear to exert their influence by controlling the numerous steps of the
physiological processes in; the plant that provide the materials and structures that make
up the defense mechanisms of the plant. e.g. cutin depth, plant architecture
* Afected by environment.
*Does not protect against infection but slows down disease development. There is
usually some degree of horizontal resistance.
2. Vertical resistance- very resistant to some races and very susceptible to others.
called specific, qualitative, differential.
Characteristics*usually controlled by one or a few genes. (monogenic or oligogenic)
These genes apparently control a major step in the interaction of the pathogen
with the host plant and therefore play a major role in the expression of vertical
resistance.
*Responds like an incompatible, HR, complete resistance
*limits initial inoculum.
Both horizontal and vertical resistance is generally controllde by genes in the nucleus.
Diagram of susceptible, horizontal and vertical resistance.
26
2. Apparent resistance- susceptible plants that do not become infected.
a. Disease escape-the 3 factors of disease (susceptible host, virulent pathogen,
environment) do not coincide. disease escape can be managed by using disease free
seed, vigorous seed, proper soil, planting date, depth of sowing, distance between
plants in the fields, proper crop rotation, sanitation (roguing, pruning, etc.) interplantings
and multilines, insect and vector control.
B. Tolerance to disease is the ability o fplants to produce a good crop even when
they are infected with a pathogen.
*specific inheritable traits
*vigorous
*produce a better crop when not infected.
The Gene- for-gene concept - for each gene that confers resistance in the host there
is a corresponding gene in the pathogen that confers virulence to the pathogen, and
vica versa.
*Operates in many diseases.
*Plant resistance is dominate
*Virulence in the pathogen is recessive.
Diagrams and tables about gene-for-gene
LECTURE 10
Control using cultural, biological, chemical methods
Resistant varieties are not always available so different cultural and chemical practices
have been developed to control diseae spread, incidence and severity.
I. Various Control MethodsA. Regulation- aims at excluding a pathogen form a ahost or from a certain
geographic area.
1. Quarantine and inspection.- Plant Quarantine Act of 1912
Pests introduced from abroad*Downy mildew of grape- U.S. to Europe
*Bacterial canker of citrus-S.E.Asia to U.S.
*Dutch Elm Disease- Europe to U. S.
*Chestnut Blight- Europe to U. S.
*White pine blister rust- Europe to U.S.
*Soybean cyst nematode-N.E. Asia to U.S.
B. Cultural control methods- aims at helping plants avoid contact with a pathogen
and at eradication or reducing the amount of a pathogen in a field.
1. Pathogen free plant material-seed and propagative material
2. Host eradication- wheat rust- alternate host barberry
Cedar-apple rust.
3. crop rotation
4. sanitation
5. Creating conditions unfavoralbe to the pathogen- storage, bark chips
6. soil solarization
C. Biological control- the total or partial destruction of pathogen populations by other
organisms.
1. suppressive soils
2. cross protection
3. hypervirulence
4. mycoparasitism
*The mechanisms by which antagonistic microorganisms affect pathogen populations:
1. Direct parasitism- Nematode trapped by fungus
2. Competition with the pathogen for food.
3. DIrect toxic effects ont he pathogen by antibiotic substances relaesed by
antagonist.
4. Indirect toxic effects on the pathogen by volatile substances, such as ethylene,
released by meatbolic activities of the antagonists.
28
D. Trap plants- e.g. plant rye and corn around beans. The taller rye and corn plants
trap the aphids.
E. Antagonistic plants- Asparagus and marigolds are antagonistic to nematodes.
F. Chemical methods that eradicate or reduce the inoculum.
1. Soil treatment- metalaxyl, metam-sodium, captan
2. Fumigation- nematicides, usually preplant fumigants.
e.g. Chloropicrin, vapam, methyl bromide. OFten volatile and covered with
polyethylene sheet.
3. Aerial spray4. PostharvestHandout covering different chemicals.
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Bacterial Diseases
Prokaryotes- singal celled microorganisms that have a c3ell membrane and a cell wall
surrounding the cytoplasm. Thje later containing small 70s ribosomes and genetic
material (DNA) not bound by a membrane, that is, not organized into a nucleus.
I. Kinds of Prokaryotes
A. Bacteria
B. Mollicutes or mycoplasmsalike organisms (MLO). Lack a cell wall and have only a
typical single unit membrane.
A. Bacterial diseases
1. General characteristics*1600 spcies known. Most are saprophytic decomposers.
* 80 species cause diseaes in plants. Most are facultative saprophytes and can be
grown on artificial media. The fastidious vascular bacteria are difficult to grow in
culture.
2. Morphologya. Almost all phytopathogenic bacteria are rod-shaped.
b. Most have a slime layer or capsule surrounding them.
c. Most have delicate flagella.
*polar flagella
*peritrichous- over the entire surface.
3. ReproductionAsexual- binary fission.
Occurs by the inward growth of the cytoplasmic membrane toward the center forming a
transverse membranous partition dividing the cytoplasm into two approximately equal
parts.
Bacteria may divide every 20 minutes under favorable conditions. 1 million in 10 hours.
4. Ecology and SpreadPlant pathogenic bacteria can develop in the host as a parasite, in plant debri or in the
soil as saprophytes.
a. In host-e.g. Erwinia amylovora-fire blight of pome fruits. Plant-to-plant infection
cycle.
b.Soil inhabitants- Agrobacterium tumefaciens-crown gall
Psuedomonas solanacearum-bacterial wilt of solanaceous crops.
Streptomyces scabies- common scab of potato.
c. Soil invaders- survive as long as the debri in the soil.
30
Dissemination- water, insects, animals, humans.
II. Major Genera
A. Agrobacterium-crown gall
B. Clavibacter (Corynebacterium)- Gram positive.
C. Erwinia- facultative anaerobes.
*Amylovora-necrotic or wilt diseases.
*Carotovara-soft rots, pectolytic activity.
D.Pseudomonas*Fluorescent
*non-fluorescent
E. Xanthomonas- Usually yellow on media
*all species are plant pathogens and are found only in association with plants or
plant material.
F. Streptomyces- Slender branched hyphae without cross walls. At maturity the aerial
mycelium forms chains of three to many spores. Gram positive.
G. Xylella*Single straight rods
*non-motile
*aerobic
*nutritionally fastidious
*habitat is xylem of plant tissue.
III. Examples of diseases in each of these generaA. Agrobacterium tumefaciens- Crown gall. Note lab notes.
Note disease cycle on page 562.
B. Clavibacter- Ring rot of potato Clavibacter michiganense subsp. michiganense
*Dissemination- contaminated seed, Knives
*Entry- wounds, colonize xylem vessels
*Symptoms- wilting late in the season
-yellowing of leaves-ionterveinal area
in tuberslight yellow vascular discoloration
bacterial ooze
cheezy rot develops
continuous ring of cavities.
*overwinters- infected tubers
-dried slime on machines, crates, sacks
-do not overwinter in soil
*Control-healthy seed, sanitation, disinfect knives.
31
C. ErwiniaExamples to know1. Fire Blight of Pome fruits- Erwinia amylovora, Figure 12-17
2. Soft rot of numerous fleshy fruits- E. carotovora pv. carotovora Figure 12-24.
D. Pseudomonas- 1. Southern bacterial wilt of solanaceous plants (Moko disease of
Banana) caused by Pseudomonas solanacearum. Non-flourescent.
*Location-present in tropics and warmer climates.
*Host-Banana, tobacco, tomato, potato, eggplant. Can also attack peasnuts, soybeans,
plantains. Known as Granville wilt of tobacco or a brown rot of potato.
*Symptoms-Sudden wilt. Plants die rapidly
-development of adventitious roots
-cross sections of stem are black and ooze a whitish bacterial exudate
-bacterial pockets are present around vascular bundles in the pith and cortex.
*Overwinters-diseased plants, plant debri
-vegetative progagative organs
-infected knives
*Entry-wounds
*Control-resistant varieties
-rotation
-santitation
-diseased plants should be cut up and burned.
2. Pseudomonas canker disease- P. syringae pv. syringae- causes the bacterial
canker of stone fruit and pome fruit trees.
*Fungal cankers are often sunken and soft. Bacterial cankers often appear as
splits in the stem, necrotic areas within the woody cylinder, or as scabby excrescences
on the surface of the tissue.
Common name- Bacterial canker and gummosis of stone fruit trees.
*occurs all over the world. It also afects pear, citrus, lilac, rose, ornamentals,
some vegetables and some small grains.
*Disease is known as bud blast, blossom blast, dieback, spur blight, and twig
blight.
*Losses can be from 10-75% in a young orchard.
32
*Symptoms-forms cankers accompanied by gum exudation. Infection develops at
the base of an infected spur and spreads upward and to a lesser extent down and to
the sides. Cortical tissues are brown to bright orange. First noticed in late winter or
early spring. As the tree brads dormancy gum is produced by the tee and breaks
through the bark.
*The pathogen action- Produces a phytotoxin-syringomycin. The bacteria of
many P. syringae strains are ice-nucleation-active, that is, they serve as nuclei for ice
formation, and therefore cause frost injury to plants, at relatively high freezing
temperatures. These same strains produce bacteriocins toxic against
non-ice-nucleation active strains, thus assuring a competive advantage for themselves.
*Development of disease- note overhead-overwinters in active cankers, infected buds, and leaves, epiphytically
(existing on the surface of a plant or plant organ without causing infection) on buds and
limbs, and even on weeds and non-susceptible hosts.
-infection takes plance in fall or winter entering through pruning cuts.
Bacteria move intercellularly and advance into the bark and into the medullary rays of
the phloem and xylem. Cankers develop in the fall after dormancy sets in . At the end
of cold weather the cankers develop quickly.
-Host response- Callus tissue. The ability to wall infection seems to be
correlated with varietal resistance but is also affected by the age and succulence of the
palnt, the temperature and rainfall during a season, and the type of rootsock on which
the tree is growing.
-Control- use healthy budwood
-graft to resistant root stock and graft high
-chemical control copper and streptomycin.
E. Xanthomonas- Examples to know: X. campestris pv. citri- Citrus Canker
*It came to the U.S. from Japan. It hit Florida in 1910 and spread to the gulf
states and beyond. It was eradicated from Florida in 10 yrs. after the destruction of 1/4
million bearing trees, 3 million nursery trees. It was totally eliminated from the U.S. in
1949. It showed up again in Florida in 1984. Destruction of 17 million nursery and
young orchanr trees by 1985 occurred before it was eradicated.
2. X. campestris pv. malvacearum- Angualr leaf spot of cotton.
Symptoms- causes angular to irregular black spots on leaves and cotton bolls.
- during hot humid weather the bacteria may invade and rot the bolls and
cause them to rot, drop or to become distorted.
33
F. Streptomyces - S. scabies- causes common potato scab. Note disease cycle on
page 576 of Agrios.
G. Xylella- Fastidious vascular bacteria previously known as rickettsialike organisms or
RLO. Phloem limited and xylem limited. These are parasitic bacteria that cannot easily
be grown on simple culture media. Nearly all are gram negative. (NOTE OVERHEAD).
Mycoplasmas
Class-Mollicutes
Order-Mycoplasmatales
Family-Mycoplasmataceae, genus Mycoplasma
Family-Acholeplasmataceae, genus Acholeplasma
Family-Spiroplasmataceae, genus Spiroplasma
Note overhead-diseases caused by this group.
THE FUNGI- Lectures by Dr. Craig Liddell
TerminologyHypha- filamentous structure
Eukaryote
Cell wall
Mycelium- 0.5 to 100 um width
Some basidiomycetes may cover 2-3 kilometers
100,000 species of fungi. 8000 to 10000 species cause disease.
Eukaryotes- Fungal characteristics.
*Reproduce by spores (sexual or asexual)
*Heterotrophic some autotrophic species fix CO2 by osciizing amino acids.
*not chlorophyll containing
*cell wall composition in chitin an/or cellulose.
*Think in terms of nuclei, fungi often have more than one nucleus.
* Coenocytic vs. septate
*Two types of asexual spores1. conidia (um)- forms on the blown out end or cut off end of a mycelial thallus.
2. sporangiospores-are produced internally inside a sac-like structure.
34
Sexual spores- Oospores, Ascospores, Basidiospores- product of nuclear fusion and
genetic recombination.
Deuteromycotina- the imperfect fungi. Never observed to reproduce sexually.
Diagram of generalized life cycle of Fungi-
25 different orders of fungi cause disease.
Kingdom Myceteae
Pathogens occur in a number of different orders.
Slides of different diseases (mainly Phycomycetes).
Order Chytridioles
-class Chytridiomycetes
All pathogens in this order only
Olpidium
Physoderma
Synchytrium
Urophlyctis
-No mycelia
-simple Thallus
-Rhizoids
Most cause root rots or disease below soil line.
Main diseases are hypertrophy(cell enlargement) and hyperplosia(increase in cell
division).
-All of these are obligate pathogens. They do not live on sapophytes.
-Resting spores survive for several years. There are sexual reproductive
spores.
-2 degrees spread by zoospores. They swim in the soil. Most will
germinate w/o root exudate.
Olpidium-Not a pathogen
-Root parasiteThis is important because it is a virus vector.
Main ones: Tobacco necrosis virus.
Lettuce Big vein.
Lettuce, field crops, grain
The only time it is a factor is when if
Big vein = Olpidium
Physoderma
viruses.
-Brown spot of maize occurs above the soil level.
-Minor disease first found in India.
-Locally
in SE USA. (Florida and Georgia)
-Cover lesion around leaf and sheath.
-Cover abscission and flagging.
Urophlyctis
-cover crown wort of alfalfa.
-Cell proliferation.
-Hyperplosia and hypertrophy.
-Widespread in U.S.
-First in Ecuador.
Synchytrium
S. endobioticum Black wort of potato wort disease - cell
proliferation.
Thallus of fungus inside potato tube.
NOTE HANDOUT
Note generalized sexual outline.
-zoospores acting as sametes. (isosametes: gametes or 2
degree zoospores are identical).
-Plamusamy: fusion of protoplast
-Kaosamy: fusion of nuclei.
-Reproduction occurs inside host.
-Produce single zoospore. 1 whiplash flagella.
-They can proliferate asexually.
-Certain temperatures cause them to fuse. as temp. cools they
fuse.
-Black swellings on tubes.
-Does not spread in potatoes.
-Very dependent of free water.
-Isiotrophic: chemical control is very difficult.
-Good resistance
-Quarantine and seed certification are the primary means of
control.
-resting spores can last 12 years. Crucifers can reduce these.
Rotation not a good option.
Plasmodiophoales
NOTE LIFE CYCLE OF P. brassicae
-Classified as myxomycetes in Agrior. Not accepted now.
-They have been moved to Amastigomycota.
Single order Plasmodiophorales
-They
were classified in myxomycetes because of amoeboid stage.
-Diseases: Plasmodiophora brassicae - club root of crucifers
Polymyxa graminis - root rot of cereals
Spungospora subterranea - Powdery scab of potato. Virus
vector.
-All biotrophs and obligate pathogens.
-Can survive in the soil for many years.
NOTE DISEASE CYCLE OF P. brassicae
-Resting spore germ to zoospore which is myxoamoeboid. No flagella.
-Infect root hair to form Plasmodium.
-Coenocytic become multinucleate. Spread into epidermal cells.
-Form zoosporangium. Zoospores are released from the host.
-Form 2 degree zoospores. These zoospores can fuse or can cycle
asexually.
-Clubroot resting spores. These can stay alive in the soil.
Powdery scab: much smaller. many root diseases can cause
damping off to no symptoms at all. Triggered by specific
temperature.
Polymyxa grominis - root rot of cereals.
Virus vector: Soilborne wheat mosaic V.
Barly yellow mosaic V.
Oat mosaic
Wheat spindle streak
Peanut clump V.
-Zoosporic pathogen. Zoospores are the primary vectors.
Spungospora subterranea
-Initial symptons: wilting and chlorosis.
-As roots develop, tubes swell. Large
form.
-Natural opening or wound needed.
-70% of hyperplasia and hypertrophy is non-plasmodial.
Control is: Crop hygiene, sanitation.
Certified seeds.
Maintain pH avove 7. (Plasmodiophora 6) Spores don't
germinate.
Resistance.
Maintain good drainage.
Don't overirrigate.
Class: Oomycetes
Lower fungi - coenocytic, aseptate thallus,sporangua not ceniden, and
often have zoospores.
Gymnomycata = naked (no cell wall) Amoeboid?
Mastigomycata = flagellated fungus
Amastigomycata = non-flagellated fungus
subdivision zysomycotone (not a very clean division)
Higher fungi - subdivision Ascomycotino (no motile spores)
subdivision Deuteromycotino
subdivision Basidoomycotino
-Includes major pathogens: Pythium, Phytophthora, Downy mildews
(also known as "water molds").
-"water molds" better used w/ Saprolegnia
-Primary difference between Gymnomycata and Chytridiomycetes is
Anisogamous gametes.
Characteristics - Mostly zoosporic; biflagellate.
Coencytic mycelia.
Well developed mycelia.
Sexual spore is called an oospore.
Sexual reproduction - occurs by gametangiol centact.
Male gamete: antheridium (ia)
Female gamete: oogonium (ia)
Plant diseases caused by VIRUSES
Lecture 1.
Viruses-defined, a nucleoprotein that is too small to be seen with a light microscope,
multiplies only in living cells, and has the ability to cause to disease.
A. Characteristics of viruses
1. Morphology- various shapes and sizes.
a) Rigid rod shaped- e. g. tobacco mosaic virus, 15x300 nm.
a) Flexous thread - e. g. maize dwarf mosaic. Appear as long flexible
threads
b) rabdoviruses- short, bacillulike rods approximately 3 to 5 times as long
as they are wide. e. g. lettuce necrotic yellows virus (52 x 300 nm).
c) Spherical-polyhedral- e. g. Tomato spotted wilt virus (70-80 nm in
diameter).
2. Composition- nucleic acid (RNA or DNA) and a protein coat.
The proportion of nucleic acid to protein varies from 5-40% with the protein
making up the remainder of the virus (95-60%). The nucleic acid of most viruses is
made up of RNA (Ribose nucleic acid), but at least 25 viruses have been shown to
contain DNA (Deoxyribose nucleic acid).
3. What viruses are not-they do not divide
-they do not consist of cells
-they cannot produced enzymes, toxins, proteins, or RNA, DNA.
-they cannot penetrate plant cells.
4. Viruses are:
-dependent on vector transmission; insects, fungi, nematodes, plants
(rootstocks, grafts,seed, pollen), animals, man.
-dependent on the metabolic processes of the plant to replicate
-the malfunctioning of the plant due to the virus results in disease
symptoms.
5. Virus Symptoms: Note fig. 14-11
6. show slides
a) reduced growth, dwarfing and stunting. Systemic symptoms.
b) local lesions,
c) latent viruses-no disease causes in the host. Symptomless carriers
d) masked- plants that remain temporarily symptomless under certain
environmentaly conditions.
e) common systemic plant symptoms-mosaics and ring spots.
7. Physiology of virus-infected plants- How do they affect a plant?
-decrease in photosynthesis
-decrease the amount of growth regulating substances (hormones) in the
plant, by inducing an increase in growth-inhibiting substances (Ethylene and ABA).
-initially increases respiration
8. Virus transmission-Viruses are not disseminated by wind and water unless their
vector is disseminated by that method. e. g. Olpidium-big vein.
-Vegetative propagation, buds, grafts, cuttings, tubers, corms, bulbs,
rhizomes. Transmission may also occur through natural root grafts.
-Mechanical transmission through sap- closely spaced plants. e. g. potato
virus X.
-Seed transmission- 100 viruses have been reported to be transmitted by
seed. e. g. Tobacco ring-spot virus in soybean, squash mosaic virus in muskmelon,
barley stripe mosaic virus in barley.
-Pollen transmission- e.g. stone fruit ring spot virus in sour cherry.
-Insect transmission- the most common and economically most important
means of transmission of viruses in the field is by insect vectors.
Orders that transmit viruses1. Homoptera- aphids and leafhoppers, these are the largest group that
transmit viruses. also includes white flies, mealy bugs, scale insects and treehoppers.
2. Hemiptera- true bugs, thrips, beetles, and grasshoppers.
Virus transmission is much more prevalent with insects that have piercing and sucking
mouthparts compared to the chewing mouthparts.
a) The most important transmitter is the aphid. Several aphid species can
transmit the same stylet-borne virus and the same aphid species can transmit several
viruses, but in many cases the vector-virus relationship is quite specific.
b) Leafhopper-transmitted viruses cause disturbances in plants that arise
primarily in the region of th phloem. All leafhopper-transmitted viruses are circulatory,
several are known to multiply in the vector and some persist through the molt and are
trasmitted to a greater or lesser degree through the egg stage of the vector.
Aspects of insect transmission1. Style-borne or non-persistent- carry plant viruses on their stylets.
2. Circulative or persistent- they accumulate the virus internally and then
introduce the virus into plant tissues again.
3. Propagative viruses- circulative viruses that multiply in their respective
vectors.
c) Mite transmission- Family Eriophyidae, shown to transmit nine viruses.
e. g. wheat streak mosaic, peach mosaic, and fig mosaic viruses. Peircing and sucking
mouth parts.
d) Nematode transmission- they transmit 27 known viruses. The virus
nematode relationship seems to be somewhat specific. e. g. Longidorus and
Xiphinema vector poylhedral-shaped viruses such as tomato ring spot virus.
Trichodorus and Paratrichodorus transmit two rod-shaped viruses, tobacco rattle, and
pea early browing viruses. The virus is not carried through the molts or through the
eggs.
e) fungus transmission- e. g. Olpidium - lettuce big vein ; Polymyxawheat mosaic virus and beet necrotic yellow vein virus; Spongospora- potato mop top
virus. Some of these viruses are borne internally and some externally.
f) dodder- Cuscuta sp. The dodder spreads from one plant to the next and
transmits the virus through its vascular system.
B. How Viruses infect plants.
1. Review of transcription and translationMitosis- A) Interphase, Chromosomes have duplicated and the duplicated
chromosomes are attached to one another at the centromere (Kinetochore).
A group of enzymes called DNA polymerase copies the DNA code. The DNA
molecule is made up of nucleotide bases (guanine, adenine, thiamine, and cytosine)
Pyrimidines and Purines. Pyrimidines fit with purines and purines only fit with
pyrimidines in the DNA molecule. A-T, C-G. In RNA molecules T is replaced with
uracil=U. On the chromosome which contains genes that code for particular enzymes
and proteins, 3 of these bases code for a particular amino acid which are the building
blocks for proteins.
Diagram of how the bases match up and what happens after replication.
Diagram of Chromosome, centromere and sister chromosome.
Diagram of cell components- DNA, nucleus, nucleoli, endoplasmic reticulum,
ribosomes.
B) Prophase-nucleoli begin to disappear, chromosomes begin to appear,
nuclear membrane begins to disappear.
C) Metaphase-spindle fibers, made form microtubules, appear at the poles
of the cell. The centromere of each doublet becomes attached to spindle fibers and
migrate to a point on the equitorial plane of the cell.
D) Anaphase- begins when the sister chromatids separate from one
another.
E) Telophase- the chromosome reaching the opposite pole begin to uncoil,
the nucleoli reappear, the nuclear membrane comes back, the cell plate begins to form,
a cell wall is secreted on each side of the cell plate and cell division (cytokinesis) is
complete.
2) Transcription-Translation- the process that takes the message (code) from the
nucleus to the cytoplasm and to the platform of protein synthesis is called transcription.
The DNA molecule codes for specific proteins and enzymes. RNA polymerase copies
the particular area of the DNA molecule that has the desired code and this code is
called mRNA. The messenger RNA is taken out of the nucleus and attaches to a
ribosomal RNA. The rRNA acts as a platform for protein synthesis. This process is
called translation. On the rRNA the mRNA is translated to make the specified protein.
The transfer RNA codes for specific amino acids. Amino acids are the building blocks
of proteins. The tRNA attack to themselves the amino acid coded for on the MRNA.
The amino acids are lined up on the rRNA and they form proteins upon binding
together.
3) Infection of plant cells by viruses- Viruses enter cells passively through wounds,
insects, etc. The viruses may also be engulfed by the cell in a process called
pinocytosis- a process in which particles are engulfed in small vesicles formed by deep
invagination of plasma membranes. It is in this membrane that the protein coat of the
virus is removed. The protein coat is also referred to as a capsid. The protein subunits
are called capsomeres. Demonstrate what a protein subunit looks like and how it
attaches to the RNA virion.
Summary of replication events: e. g. TMV
i) the infectious virus RNA acts as mRNA for the viral replicase enzyme or the cell
RNA polymerase, which is synthesized on the cytoplasmic ribosomes.
ii) Complementary ("mirror image") strands of RNA act as templates for
replicase-catalyzed synthesis of viral ("plus") RNA.
iii) the new viral ("plus") RNA contains the genetic information for synthesis of coat
protein on cytoplasmic rRNA with the help of tRNA.
iv) coat protein polymerizes around viral ("plus") RNA , to form new virions.
NOTE HANDOUTS
B. Important viruses of New Mexico
1. Alfalfa mosaic of pepper- vector aphids, mechanical
2. Cucumber mosaic of cucurbits-aphids, cucumber beetle, seed
3. Curly top of pepper-beet leafhopper
4. Big vein of lettuce-Olpidium, fungus
5. Lettuce infectious yellows-white fly
6. Pepper mottle virus-Aphids
7. Tomato spotted wilt virus- thrips
1. Alfalfa mosaic of pepper-Calico virus. Worldwide distribution.
Host- legumes, potato, tomato and tobacco and herbaceous and woody plants in
several families. Found in alfalfa fields.
Dissemination- It is spread by 14 aphid sp. (non-persistent) and 10-50% of the
seed contains this virus.
Symptoms- Causes mild stunting and whitish, blotchy leaves. It is also called
calico virus.
It only a problem when chile is planted in a field where alfalfa grew the previous
year, where volunteer alfalfa plants grow in the field, or when chile is planted next to an
alfalfa field.
Control-don't plant close to chile.
2. Cucumber mosaic of cucurbits- Worldwide in distribution and has perhaps the
broadest host range of all viruses.
Host- cucumbers, melons, squash, peppers, spinach, tomatoes, celery, beets,
bean, banana, crucifers, many ornamentals, and many weeds.
Symptoms- usually attacks about 6 week old plants. The young developing
leaves become mottled, distorted and wrinkled, and their edges begin to curl downward.
Fruit becomes distorted, pale green or white areas, raised green areas. The fruit taste
bitter.
Overwinters- in perrenial weeds, flowers, and crop plants. e.g. many perrennial
weeds harbor the virus in the roots and then in the spring the
virus is transported up the plant to the growth tip where viruses can transmit the
disease. Causes a systemic infection.
Control- use of resistant varieties, elimination of weed hosts, and control of the
insect vectors.
3. Curly top of pepperHost- also attacks cucurbits, tomato, beans, and other vegetables. Other hostsmustards, tumbleweeds, in which they build up in high numbers. The disease is more
severe when heavier than normal rains occur during fall and winter, shich support the
growth of winter annual plants.
Dissemination- the beet leafhopper
Symptoms-stiff, erect, yellowing, stunting, reduced yield. Leaves curl upward.
Control- Sanitation-remove diseased plants.
-Home-owners- shade plants. Leafhoppers do not feed in shaded areas.
- plant a thick stand and thin.
-spraying for the leafhopper has not been effective.
4. Big Vein of lettucesymptoms- leaf veins and adjacent tissue is clear, leaves pucker, stand more
upright and edges appear frilled. Maturity of the heads is delayed.
Transmission- soil borne fungus- Olpidium , makes it possible to build up in soils.
Control- crop rotation
-avoid fields with Big vein history
-clean farm equipment and do not let tail water from an infested field rum into
non-infested field.
5. Lettuce infectious yellows- Serious in Southern California.
Symptoms- yellowing of bottom leaves at 4-5 leaf stage. Yellowing occurs on
wrapper leaves.
Transmission-white fly (Sweet potato white fly, and Poinsetta white fly).
Control- control white fly.
6. Pepper mottle virus- Comon in New Mexico.
Symptoms- misshapen leaves that become quite puckered. The leaves also have
light and dark pathches that give them a mottled appearance. The fruit is misshapened
and smaller than normal. Stunts palnts and reduces yield. Occurs in late summer or
early fall and usually affects red chile yield.
Transmission-aphid
Overwinters- in Datura sp. weeds each winter. The virus in the chile dies when
the plant freezes.
Control- get rid of weeds.
7. Tomato Spotted Wilt virusoccurs in all temperate and subtropical regions of the world and has an extremely wide
host range
Host- tomato, tobacco, dahlia, and pineapple
Symptoms- bronzing and one-sided growth, chlorosis, necrosis, stunting, and
enation. On chile peppers the pods have patches of yellow that never turn red. Ring
spots occur on leaves, stem ends wither and die.
Overwinters-in perrenial plants and weed hosts near chile fields.
Transmission- At least 4 species of Thrips.
Control- Plant away from onion fields, spray onions for thrips.
Summary of Control-no viruscides available
-resistant varieties
-control vector
-destroy weed host
-remove diseased plants
NEMATODES
Kingdom Animal
Phylum Nematoda
Introductory comments- Nematodes, also called eelworms, are free living soilborne
organism. They survive in the soil and feed on microscopic plants and animals.
Numerous species attack and parasiize humans and animals.
-Well known human pathogens- 'pinworms', Elephantiasis, and trichinosis.
-They live in water in soil pores and the narrow layer of water on soil particles.
They are the biggest problems in sandy soils.
Morphology - 300-1000 um, with some up to 4 mm. Easily observed under a
microscope. Round in cross section with smooth, unsegemented bodies, without legs
or other appendages. The females of some species, become swollen at amturity and
have pear-shaped or sheroid bodies. (Note figure and handout).
Anatomy- Transparent, Covered by a colorless cuticle. The cuticle molts when a
nematode goes through its successive larval stages.
-The digestive system is a hollow tube extending from the mouth
through the esophagus, intestine, rectum, and anus. Lips, usually six in number,
surround the mouth.
-All plant-parasitic nematodes have a hollow stylet or spear, which is used
to puncture plant cells.
Reproduction- The female has one or two ovaries, followed by and oviduct and uterus
terminating in a vulva. The male has a testis, semianl vesicle, and a terminus in a
common opening with the intestine. A pair of protrusible, copulatory spicules are also
present in the male. Reproduction in nematodes is through eggs and may be sexual,
hermaphroditic, or parthenogenetic. Many species lack males.
*Hermaphrodites- processing both male and female sex organs.
*Parthenogenetic- capable of reproducing without males.
Life-cycle- They begin with as an egg and mature into an adult after four molts. In
between, the nematodes exist as "juveniles" of increasing size. In most cases these
juveniles look the same as the adults but smaller. Adults are sexually mature. The
nematode is an obligate parasite. Second stage juveniles hatch from eggs and move
to host plants to feed.
-Two feeding habits: Ectoparasites - feeding from the surface of plants.
Endoparasites - penetrate the plant tissue.
-The hollow stylet allows the nematode to pierce plant cells and ingest their contents.
Some economically important nematodes1. Seed gall nematodes- Anguina sp. These were the first nematodes disacovered to
destroy plants. These nematodes swim from the soil to the developing grain head in a
layer of water on the plant surface and burrow into the developing flowers. They form
galls in the fruit. These galls were often replanted the next year.
2. Pinewood nematode- Bursaphelenchus sp. This nematodeinfects and kills pine
trees. Pines in the U. S. are somewhat resistant- e.g. Norway or blue spruce.
However, Scotch pine is highly susceptible. Japanese forest of red and black pines
have been totally wiped out by this nematode. Restrictions on U.S. lumber to Europe
and Asia have resulted because of the pine wood nematode.
3. Lesion nematode- Pratylenchus sp. also called the pin nematode of many plants.
This nematode penetrates and feeds on root cells, leaving behind dead and dying cells
that become brown. The lesions are often invaded by other microorganisms.
Endoparasite.
4. Cyst nematode- Heterodera sp. Big problem on Soybean. It is often called the
Soybean cyst nematode-H. glycines. This nematode overwinters as a brown cyst that
formed on the roots.
5. **Root knot nematode- Meloidogyne incognita. More than a dozen species known.
The root rot nematode is distributed throughout the world and occurs in a wide variety
of crop plants. It is most severe in areas of warm climate, and causes extensive
economic loss in nursery plants as well as in row crops.
Symptoms- Primary symptom is tumefaction- irregularly shaped galls. Apical
growth ceases. Lesions sometimes are present. Feeding by both the males and
females stimulates hyperplasia and hypertrophy in the roots.
Overwinters- eggs between crop seasons in the soil. In a warm, moist enviroment
the eggs hatch, liberating the second larval stage.
Colonization- Male nematodes live parasitically in the roots for several weeks and
then undergo three molts in rapid succession before emerging from the root. Adult
males are thought to live free in the soil.
Females that have entered the roots remain there after molting and increase in
size. The become pear shaped about 3 weeks after penetration, and they protrude into
what would have been vascular tissue. Cell walls in the vicinity of the head of
sedentary females are digested and the several adjoining cells coalesce to form 'giant
cells'. Food materials essential to the continued nourishment of the nematode collect in
these cavities.
At maturity, the posterior end of the female either protrudes through the surface of
the gall tissue or lies very near the surface. Eggs are laid in a gelatinous matrix
extruded from the vulva.
Control- Nematicides
-Biological control- Bacillus sp.
- mycorrhizal fungi-Glomus sp.
-Resistance
-santitation
Plant Diseases caused by parasitic higher plants
Introduction- 2500 species of higher plants are known to live parasitically on other
plants.
-They vary greatly in there taxonomic botanical classification.
-some have chlorophyll, some do not
-some attack roots, others attack shoots.
-Only a few of the known parasitic higher plants cause important diseases on
agricultural crops or forest trees.
Botanical famileis and genera of important parasitic higher plants
I. Those that attack above ground portions of plant.
Family: Cuscutaceae
Genus: Cuscuta, the dodders
Family: Viscaceae
Genus: Arceuthobium, dwarf mistletoe of conifers
Genus: Phoradendron, the American true mistletoe of
broadleaved trees.
Genus: Viscum, the European true mistletoes
II. Those that attack below ground portions of plant.
Family: Orobanchaceae
Genus: Orobanche, the broom rapes of tobacco
Family: Scrophulariaceae
Genus: Striga, the witchweeds of many monocotyledonous
Examples1. Dodder-Cuscuta sp.
Occurs in Europe and North America.
plants.
Host: Problem on alfalfa and clover. Other crops, onions, sugar beets, ornamentals,
and potatoes.
Symptoms: Orange or yelow vine strands grow and entwine around the stems and the
other above grownd parts of the plant. Produce whit, pink or yellow flowers. The
infected plant becomes weakened by the parasite, vigor decreases and yield declines.
NOTE DISEASE CYCLE
Control: Prevent introduction-exclusion
-dodder free seed
-limit the movement of domestic animals
-spray with contact herbicides. 2,4-D
- Spot spray at low concentrations with Glyphosate (Round-up). Has been
shown in some studies to be effective even when it was applied after dodder was
attached to alfalfa and controlled the pathogen without causing apparent injury to
alfalfa.
2. Dwarf mistletoe of conifersOccurs in all parts of the world where conifers occur. Big problem in Southwest and
Pacific coast. Trees can be retarded, deformed or killed.
Growth height reduced by 50 to 80%. TImber quality reduced.
Note disease cycle-plants either male or female -diecious
- produce flower after 4-6 years. Male dies after flowering. Female dies after fruit
dispersal.
-Intermal pressure expels the seed upward or obliquely (out) for distances up to
15 meters.
-Birds can also transmit seeds.
Control: remove diseased part of tree.
-resistance is being sought.
3. Witchweed- Striga sp.
Serious parasitic weed in Africa, Asia, and Australia before 1900. Discovered for
the first time in America, in North and South Carolina. Good quarantines have limited
spread.
Host: corn, sugarcane, rice, tovacco, and some small grains.
Symptoms: stunting and chlorosis. Looks like acute drought.
Losses from slight to 100%.
Note disease cylce-life cylce of weed takes 90 to 120 days. Germination to seed
release.
-depends on the plant for water, minerals and organic substrate
as
well.
-overwinters as seeds. usually dormant for 15-18 months.
-the haustorium disolves the host root cells through enzymic
secretions and penetrates the host roots within 8-24 hours.
Control: Sanitation, control movement from infested areas into uninfested areas on
treansplants, agricultural products and machinery.
-Catch crops, force germination of the witchweed. then plow uner or use weed
killers.
-trap crops, nonhost legumes, the witchweed germinates but cannot infect plants
so the witchweed starves.
-Ethylene injection into fallow soil. Stimulates germination and the witchweed dies
since no host is present.
-herbicides-trifluralin, paraquat, oxyfluorfen.
Biotechnology and Plant Pathology
Biotechnology- the manipulation, genetic modification, and multiplication of living
organisms through novel technologies, such as tissue culture and genetic engineering,
resulting in the production of improved or new organisms and products that can be
used in a variety of ways.
Advantages of Biotechnology1. rapid clonal propagationn of plants
2. accelerates and expands the limits of plant breeding
3. makes possible the production of plant products under tissue culture
conditions.
Why Plant Pathology is important to Biotechnology1. Increased production of clones will mean a greater need to obtain
pathogen-free mother plants. THe increased crowding, genetic uniformity, and the
prolonged exposure of the plants to marginal nutritional and environmental conditions
before and after they are set out in the field are likely to amke them susceptible to
catastrophic sudden outbreads of pathogen infections.
2. New plant varieties added through biotechniques will probably exhibit greater
instability toward the environment and pathogenic microflora.
3. The best vectors for moving genes are plant pathogens. e.g. A. tumefaciens
and the Cauliflower mosiac virus.
4. The genes to be inserted in plants will be resistance genes that plant
pathologist will need to identify.
5. Control of many plant diseases is likely to come about either by inserting
resistance genes inot plants by genetic engineering techniques, or by genetically
engineering microorganisms that can effectively antagonize or compete with particular
pathogens.
A. Tissue culture and BiotechnologyEach Somatic cell (non-reproductive) of the plant contains the complete
complement of DNA in it's nucleus. Only some of the DNA information is used for the
function of any particular cell. Example- leaf epidermis cells contain the same genes
that root cells contain. Growth hormones, proteins, and very complex control
mechanisms control what genes are used. Unlike animal cells, plant cells retain the
ability to change their function and take on new roles at different times.
e.g. cutting from plants- stem cells can produce roots. F. C. Steward grew mature
carrot phloem cells in coconut milk (necessary cytokinins) and they produced new
plants. Theory - fact, If a specific gene could be transferred to the nuclear DNA of a
single plant cell, that cell could then
be regenerated into an entire plant in which each cell would contain the new gene in its
nucleus.
Protoplasts-removal of the cell wall of plants with degredative enzymes allows the cells
to grow and multiply in culture. After obtaining 100's of cells some have added plant
toxins, salts, etc. and the surviving cells were grown to check for resistance. Limited
success.
B. Recombinant DNA and genetic engineering: Traditional breeding of plants often
takes several generations which means several years. e. g. new wheat variety that is
resistant to a new rust race- approxiamely 7 - 10 yrs. Genetic engineering has the
potential to transfer any genetic sequence to the nucleus of any palnt cell.
Steps in genetic engineering:
1. identification of a specific gene sequence that controls the desired trait
2. removal of a functional gene sequence from the donor organism
3. transfer of the gene sequence to the nucleus of the receptor organism, followed
by expression of the trait
Identification of these sequences are simplest in prokaryotes. Restriction enzymes are
used to cut the DNA. Ligases are enzymes that seal the cut ends of DNA so that the
transferred sequence can be inserted into another piece of DNA.
Note handout and overhead- the new DNA containing the introduced sequence is known as recombinant DNA
(rDNA).
-the normal bacteria are exposed to the plasmid or bacteriophage (virus)
-when the recipient cell absorbs the recombinant DNA and begins to express the
gene by producing the protein it coded for, the cell is said to be 'transformed'.
Examples-1. genetic information for the production of human insulin has been
transferred to a bacteria. The bacteria produces the same kind of insulin a human
would produce. Saves diabetic patient money and no allergic response.
2. Ice-nucleating bacteria- some bacteria (Pseudomonas syringae) have a cell
wall protein that acts as a nucleus for ice formation. These bacteria are found on the
leaf surface. In fact, ice-nucleating bacteria, marketed under the name Snowmax, are
mixed with water to increase artificial snow production for ski slopes.
When the ice-nucleating bacteria are present on the leaf surface, frost damage is
greater due to ice crystal formation. When ice-nucleating bacteria are removed from
the leaf surface, plants can survive to -5 C (23 F) without suffering frost damage.
Lindow, a plant pathologist at Berkeley, removed the gene that controlled the
ice-nucleating protein. The ice+ were well adapted to the leaf surface. The ice- were
also well adapted to the surface. By spraying the ice minus, the plants are able to
withstand colder temperatures.
Crown Gall Bacteria-The natural genetic engineer
A. T. has a plasmid (small piece of DNA independent of normal chromosomal DNA)
that induces tumor formation in its host by transfering a segment of the Ti plasmid
(tumor-inducing) in the plant nucleus. Only a small section of the Ti plasmid (T-DNA) is
transferred into the host DNA. The foreign gene is put into a E. coli plasmid.
Recombination between E. C. and A. T. results in an A.t. plasmid with an incorporated
foreign gene. The plant is inoculated with the A.t. bacteria and the foreign gene is
incorporated into the plant genome.
NOTE HANDOUT AND OVERHEAD
Other successes of genetic engineering:
-Tomato plants resistant to tobacco mosaic virus-Roger Beachy
- Herbicide resistant plants
- Plants that produce the Bt toxin.
-tobacco plants that glow in the dark. They contain the fire-fly gene, luciferase.
Environmental effects on infectious plant disease development Chap. 7 in Agrios
Environmental factors that effect plant diseaseTemperature
Moisture
Wind
Light
Soil pH
Plant Nutrition
Herbicides
Temperature
Both plants and pathogens require certain temperatures to grow and reproduce.
The low temperatures of fall, winter and early spring are below the required temp. for
most pathogens.
A. Variation within pathogens1. Cool temperatures-Typhula and Fusarium- Snow mold of cereals and turf
grasses, thrive only in cool seasons or cold regions.
Phytophthora infestans- most serious in northern latitudes and only a problem in
the subtropics in the winter. P. capsici- needs warmer conditions in order to be
infective.
2. High temperatures- Phymatotrichum root rot (Cotton root rot), Fusarium wilt,
brown rot of stone fruits (Monilia).
B. Principles- the closer you get to greenhouse conditions the easier it is to control
environmental conditions.
-always try to favor the host and discourage the pathogen. The most rapid
disease development (i.e. the shortest time required for the completion of a disease
cycle), usually occurs when the temperature is optimum for the development of the
pathogen but is above or below the optimum for the development of the host.
-Example, Puccinia graminis tritici , uredospore cycle (asexual)
Time required for disease cycle
temp.
22 days
5C
15 days
10 C
5-6 days
23 C
- In some diseases, the optimum temperature for disease develpment seems to
be different from those of both pathogen and host.
e.g. #1. Thielaviopsis basicola , black root rot of tobacco.
-opt. temp. for disease=17 to 23 C
-opt temp. for plant growth= 28 to 29 C
-opt temp. for pathogen growth= 22 to 28 C
*the pathogen grows poorly at these temperatures but not as poorly as the plant which
is also weakened. If tobacco is grown in warm temperatures the disease is rarely seen.
e.g. #2. Fusarium roseum graminiarum, pathogenic on both wheat and corn. Wheat
grows at cooler temperatures while corn grows at warmer temp.
Diagram of growth rates of wheat, pathogen, corn. The pathogen is in-between the opt.
of the host.
Diagram Disease incidence of corn and wheat. Wheat grown in warm=disease
increases. Corn grown in cold=disease increases.
-Viruses, variable depending on the virus. Virus producing yellows or leaf-roll ringspot
symptoms are most pronounced n the spring. New growth produced during the
summer on mosaic- or ringspot-infected plant usually shows only mild symptoms or is
completely free from symptoms.
Moisture in the form of rain, irrigation, humidity, dew. Moisture has the greatest effect
on germination of fungal spores and penetration of the host by the germ tube.
-role in dissemination, splashing rain or wind blown rain, irriagtion water.
-increases the succulence of plants often increasing their susceptibility.
Overwatering, waterlogging.
-occurence of disease in a particular geographical location can usually be
correlated with the amount of moisture.
-the number of disease cycles per season of many of these diseases is closely
correlated with the number of rainfalls per season.
e. g. apple scab, needs continuous wetting of the leaves, fruit, for at least 9 hrs. for
infection to take place at the opt range (18-23 C) of temp. for the pathogen.
Parameters for apple scab infection:
Time of tissue wetness
9 hr
14 hr
10 C
28 hr
6C
temperature
18-23 C
If the length of the weeing period is less than the mnimum required for the particular
temperature, the pathogen fails to establish itself in the host and to produce disease.
Note diagrams of different pathogens dependence on free moisture.
Diagram #1 Anthracnose
Diagram #2 Downy mildew
Diagram #3 Rusts
Diagram #4 powdery mildew, viruses.
Soilborne pathogens- variation
1. High moisture- Pythium-increases zoospores for infection purpose. High moisture
also weakens the plant-reduced O2 availability, lowering the temp. of soils. Others
pathogens that cause problems in high moisture-Phytophthora, Rhizoctonia,
Sclerotinia, and Sclerotium, bacteria (Erwinia, Pseudomonas) and most nematodes.
2. Low moisture- Fusarium solani, dry root rot of beans, Streptomyces scabies,
common scab of potatoes.
Wind- influences spread of pathogen, drying of wet plant surface. e. g. Puccinia
pathway. Wind also damages plants. The plants can rub against each other and
transmit viruses.
Light- Less important than moisture or temperature. Limited light does cause etiolation
to occur in plants and therefore, cause a higher degree of susceptibility to nonobligate
pathogens such as Botrytis and Fusarium . This low light often decreases susceptibility
to obligate pathogens such as Puccinia.
-low light increases susc. to viruses.
pH- Acid pH controls scab of potato, Texas root rot (P. omnivorum) and Black shank of
tobacco (Phytophthora parasitica).
Alkaline soils- decrease clubroot of cabbage- Plasmodiophora brassicae. Germination
of spores is often decreased due to alkaline soils in some pathogens.
The effect of soil acidity seems to be principally on the pathogen, although in some, a
weakening of the host through altered nutrition that is induced by the soil acidity may
affect the incidence and severity of the disease.
Nutritional
-Obligate parasites are more active on vigorous growing plants.
-Non-obligate usually invade through wounds or weakened tissue.
Specific examplesNitrogen- high, increases fire blight on pear, wheat to stem rust and powdery mildew.
low- Fusarium wilt, Alternaia solani, Pythium.
Phosphorus reduces the severity of take-all disease of barley (Gaeumannomyces
graminis) and potato scab (caused by Streptomyces scabies).
-increases the severity of CMV on spinach and glume blotch (Septoria) on wheat.
Phosphorus seems to increase resistnce either by improving the balance of nutrients in
the plant or by accelerating the maturity of the crop and allowing it to escape infection
by pathogens that prefer younger tissues.
Potassium- reduces severity of stem rust of wheat, early blight of potato,
-increases severity of nematodes and rice blast (Pyricularia oryzae).
K+ directly affects the various stages of pathogen establishment and development in
the host. K+ promotes wound healing, delays maturity and senescence.
Calcium- reduces diseases caused by stem pathogen (Fusarium, Rhizoctonia,
Sclerotium and Botrytis and some nematodes.
-increases black shank of tobacco.
The effect of calcium on disease resistance seems to result from its effect on the
composition of cell walls and their resistane to penetration by pathogens.
In general, make sure plants have a balanced nutrition
Herbicides- Increase- Rhizoctonia solani on sugar beets and cotton, Fusarium wilt of
tomatoes and cotton, and Sclerotium stem rots of various crops.
-Decrease disease of Phytophthora collar rot of various crops.
Pollution
Read from 'Plant stress from Air Pollution'
Pollution is a problem in many urban areas of the U.S. Show overhead.
Kinds of pollutants that harm plants:
I. Primary pollutants- relaeased into the atmosphere and harm plants directly.
A. Hydrogen fluoride- Source- Pottery, cement, ceramics, and brick inducstries,
ore smelters; phosphate fertilizer factories.
Symptoms- Marginal necrosis and tip dieback of leaves; "tipburn" of
grasses and conifers.
B. Sulfur dioxide (SO2) - Source - combustion of high sulfur coal; factory stacks;
engine exhaust.
Symptoms- Interveinal necrosis of leaves; general yellowing; growth
suppression.
C. Nitrogen oxides (NOx)- source - Similar to SO2; SO2 and NOx combine with
atmospheric water to form "acid rain". Mention the devastation of forest in the
Northeast.
II. Secondary pollutants- pollutants that originate from engine exhaust but must be
chemically converted in the presence of sunlight before they are chemicals toxic to
plants.
A. Ozone (03)- most destructive air pollutant. Reduces yield in cotton , soybean,
cirtus. Enters stomates and causes necrotic specks.
Source-Exhaust of internal combustion engines; stratosphere; lightning
formed in sunlight; major component of "smog".
Symptoms- Upper surface stippling, mottling, bleaching; tissue collapse;
stunting; flowering and bud formation depressed.
Show overhead.
B. Peroxacetyl nitrate (PAN)- "silver leaf"
Source- Exhaust of internal combustion engines; formed in sunlight;
important component of "smog".
Symptoms- "Silver leaf"; necrotic spots, especially on lower leaf surfaces;
stunting; young leaves most susceptible to damage.
Review of Control Methods
Control using cultural, biological, chemical methods
Resistant varieties are not always available so different cultural and chemical practices
have been developed to control diseae spread, incidence and severity.
I. Various Control MethodsA. Regulation- aims at excluding a pathogen form a ahost or from a certain
geographic area.
1. Quarantine and inspection.- Plant Quarantine Act of 1912
Pests introduced from abroad*Downy mildew of grape- U.S. to Europe
*Bacterial canker of citrus-S.E.Asia to U.S.
*Dutch Elm Disease- Europe to U. S.
*Chestnut Blight- Europe to U. S.
*White pine blister rust- Europe to U.S.
*Soybean cyst nematode-N.E. Asia to U.S.
B. Cultural control methods- aims at helping plants avoid contact with a pathogen
and at eradication or reducing the amount of a pathogen in a field.
1. Pathogen free plant material-seed and propagative material
2. Host eradication- wheat rust- alternate host barberry
Cedar-apple rust.
3. crop rotation
4. sanitation
5. Creating conditions unfavoralbe to the pathogen- storage, bark chips
6. soil solarization
C. Biological control- the total or partial destruction of pathogen populations by other
organisms.
1. suppressive soils
2. cross protection
3. hypervirulence
4. mycoparasitism
*The mechanisms by which antagonistic microorganisms affect pathogen populations:
1. Direct parasitism- Nematode trapped by fungus
2. Competition with the pathogen for food.
3. DIrect toxic effects ont he pathogen by antibiotic substances relaesed by
antagonist.
4. Indirect toxic effects on the pathogen by volatile substances, such as ethylene,
released by meatbolic activities of the antagonists.
D. Trap plants- e.g. plant rye and corn around beans. The taller rye and corn plants
trap the aphids.
E. Antagonistic plants- Asparagus and marigolds are antagonistic to nematodes.
F. Chemical methods that eradicate or reduce the inoculum.
1. Soil treatment- metalaxyl, metam-sodium, captan
2. Fumigation- nematicides, usually preplant fumigants.
e.g. Chloropicrin, vapam, methyl bromide. OFten volatile and covered with
polyethylene sheet.
3. Aerial spray4. PostharvestHandout covering different chemicals.