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Transcript of Artigo (Fito) Traduzindo
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University of WyomingCooperative Extension ServiceCollege of Agriculture
Trade or brand names used in this publication are used only for the purpose of educational information. The information given
herein is supplied with the understanding that no discrimination is intended, and no endorsement information of products by the
Agricultural Research Service, Federal Extension Service, or State Cooperative Extension Service is implied. Nor does it imply
approval of products to the exclusion of others which may also be suitable.
Issued in furtherance of Cooperative Extension work, acts of May 8 and June 30,1914, in cooperation with the U.S. Department
of Agriculture, Glen Whipple, Director, Cooperative Extension Service, University of Wyoming Laramie, WY. 82071.
Persons seeking admission, employment or access to programs of the University of Wyoming shall be considered without regard
to race, color, national origin, sex, age, religion, political belief, handicap, or veteran status.
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AN INTRODUCTION TO PLANT PATHOLOGY AND PLANT DISEASE
MANAGEMENT
Gary D. Franc, Associate Professor
Department of Plant Sciences
INTRODUCTION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
THE DISEASE TRIANGLE . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
The Pathogen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
Fungi . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
Bacteria . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
Nematodes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2
Viruses and Viroids . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2
The Host . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2
The Environment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2
Temperature . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2
Moisture . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
Wind . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
Other Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
DISEASE DIAGNOS IS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
DISEASE DEVELOPMENT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
PLANT DISEASE CONTROL . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4
Exclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4
Evasion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4
Eradication . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
Resistance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
Environmental Modification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
Protection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
Chemical Controls . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
Fumigants a nd Sterilants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5Nematicides . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
Seed T reatments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
Protectan ts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
Systemics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
Integrated Methods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
ADDITIONAL INFORMATION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6
PLANT PATHOLOGY TERMINOLOGY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6
REFERENCES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7
ADDITIONAL READING . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7
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INTRODUCTION
Anyone working as a p lant professio nal will need to
determine why plants appear abnormal and what
control measures, if any, are appropriate. This manual
introduces the reader to the subject of plant pathology
and the information it contains w ill aid in
understanding how plant diseases develop as well as
the various methods used for control. Terminology
importan t to the study of plant dise ases is ident ified
for the reader by printing in bold/italicsand isdefined either in t he text or in the section on 'Plan t
Pathology Terminology.'
THE DISEASE TRIANGLE
Plant disease results when a specific agent, such as
pe rs is tent un favo rabl e envi ronm ental cond itio ns or
the acti vity of a pat hogen, disrupts physiolo gical
function s causing p lants to deviate from normal
development. The word 'persisten t' is used to
distinguish between a disease which develops over
time and an injury which occurs, more or less,
instantaneously.
Noninfec tious diseases , perhaps m ore app ropria tely
called disorders , do not spread from plant to plant.
These disorders result from the pla nt's exposure to
such factors as unfavorable weather, mechanical
damage, nutrient deficiencies, excess salts or toxic
chemicals. Although disorders canpredispose plants
to infection by pathogens, d isorders are not directly
treated using pesticides. The remainder of this manual
emphasizes the discussion of infectious plant diseases
caused by pathogens.
An infectious disease results when apathogen lives
in close association with the host plant. The pathogenis functioning as a parasite since this relationship
usually benefits the pathogen at the host's expe nse.
Although r elationships resulting in disease are often
complex, three critical factors must be p resent in
order for a particular disease to result. The three
factors necessary for disease development are (1) the
pathogen must be p resen t, (2) a susceptible host must
be presen t and (3 ) the proper en vironm ent must be
present, permit ting infecti on of the host . These factors
give us the concept of the disease triangle (Figure 1).
Production practices followed by large growers andhome ga rdene rs serve to modif y the int eract ion of
these thr ee factors t o reduce (o r unwittingly increase)
the overall impact and severity of plant diseases.
Plant professionals use the disease triang le concept to
simplify remembering and understanding how a
part ic ular di seas e deve lops an d why vari ous cont ro l
strategies are used. The pathogen, host and
environment are discussed in more detail below.
The Pathogen
Fungi, bacteria, viruses, viroids, nemato des, parasitic
plants (dodder and mistle toe) , phytoplasmas, and
protozoa are examples of var ious pathogens tha t
cause plant diseases. General descriptions of the most
common and economically important classes of
pathogen s are lis ted belo w. I t is importan t to
remember that man y beneficial microorganisms exist
in nature, and that only a small frac tion infects plants.
Fungi. Bread molds and mushrooms are examples offungi familiar to all of us. Most of the 100,000 fungus
species identified by scientists are only saproph ytes
and not capable of infecting plants. However, more
than 8,000 plant pathogenic species have been
identified making f ungi the most numerous and
economically impor tant class of plant pat hogens. The
great diversity o f fungi and the co mplex and intricate
life cycles of some pla nt pathogenic species make
generalizations difficult.
Plant infection by fun gi occu rs via a g reat variety of
mechanisms. Some species directly penetrate plant
surfaces or enter through n atural openings, whileothers require wounds or i njury for infection. During
disease development, many species of fungi produce
spores which are dispersed by wind, water or by other
means. Each spore may cause a new infection
resulting in a rapid increase in disease incidence and
severity. Some fungi form special re sting spore s
whic h perm it surv ival for lon g peri ods of time
(several months or years) in soil or plant d ebris.
Fungi are identified primarily from their mo rphology,
with emphasis placed on their reproductive structures.
Laboratory techniques can be used to induce
sporulat ion in many fung i if reproduc tive structuresare not vi sible on pla nt tissue.
Bacteria. Bacteria are perhap s the second most
economically important class of plant pathogens.
Bacteria are considered more primitive than fungi and
general ly have simpl er life cycles. With few
exceptions, bacteria exist as single cells and increase
in numbers by dividing in to two cells during a
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process c alled binary fissio n. Their ab ili ty to rap idly
reproduce when environmental conditions are
favorabl e give bacteria their potential for causing an
explosive increase in disease.
Some species are ab le to survive o n healthy-
appearing plant surfaces as epiphytes, and only cause
disease when environmental conditions are favorable
or when injuries, such as those c aused by hail, occur.
Overwintering weed hosts, infected seedstocks orcontami nated cr op debris may serve as the initial
source of bacterial inoculum. The p resence of certain
bacterial species on p lant surfaces increa ses frost
sensitivity while other species are able to move lon g
distances in aerosols or i rrigation water.
Bacterial ooze on plant surfaces or bacterial
streamin g can aid in the identification of bacterial
diseases when working in the field. However,
laboratory methods are usually required for
identification.
Nematodes. Nemat odes ar e microscopic round wo rmsthat reside in the soil. Disease induced by nematodes
usual ly resu lts in po or plant growth a nd may be
overlooked when there are no healthy plants av ailable
for comparison. Roots of poorly growing plants
should be examined carefully for evidence of
nematode feeding. Sym ptoms ma y be deform ed roots
or galls.
Feeding by plant-pathogenic species can cause
disease by direct interference with normal plant
developmen t, by interacting with other disease
causi ng organisms or by acting as a vector for
pathogens. Al though most plant pa thogen ic spec iesaffect only roots, some species infect stem, foliar and
bud tissues.
Viruses and Viroids. Viruses and viroids are
extremely tiny particles consisting of protein and
genetic materia l (viruses) or genetic materi al with no
associated protein (viroids). Biologists disagree on
whether viruses and viroids should be classified as
'living' since they are true obligate para sites incapable
of carrying out any physiol ogical processes in the
absence of a host.
In order for disease to spread, these particles must bephys ical ly inserted into a l iv ing h ost c el l by vectors
includi ng insects or ma n, or they ma y be transmitted
through s eeds, tubers, grafts or merel y by physica l
contact between healthy and infected plants. The
metho d(s) of transmission for a specific virus or
viroid is a charact eristic of that pathogen a nd the
disease it causes. Once in serted into a host, the
physiologic al processe s of the cel l are re directed into
the manufacture of more particles. Chemical controls
usually target insec t vectors and some disinfe ctants
inactivate viruse s, rendering the m noninfectious.
Most virus diseases are identified by characteristic
symptoms coupled with electron microscopy and/or
serological tests. Viroid identification requires even
more specialized detection methods.
The HostLevels of resistanceor susceptibility of the host plant
will affect disease development. Plants with high
level s of res istanc e are essentially immun e or not
susceptible and do not allow the pathogen to become
established, e ven if present. Plants with lower levels
of resistance may become i nfected but only al low the
pathogen to develop slowly, limiting the ec onomic
impact of the disease to accep table levels. Stress,
such as that bro ught on by an unfavorable
environment, poor fe rtility or irrigation will affect a
host pla nt's ability to resi st infec tion and , therefore,
also effects dise ase development.
In some cases, resistan ce in th e host i s overc ome by
the pathogen, resulting in rapid and devastating
disease development . This risk is increased if large
produc ti on are as are plan ted to a monocu ltur e of
identical hosts. Therefore, genetic diversity of host
plants will decre ase the r isk of catastroph ic losses.
The Environment
Environmental conditions play a large role in disease
development and disease severity. However, broad
generalizations about environmental effects have
many exceptions. The disease triangle shows that the
environment influences disease development byinteracting with b oth the host and pathogen.
Furthermore, environmental stress can predispose
plants to infect ious disease. Several important
environmental factors are given below.
Temperature. Temperature greatly influences disease
development. Temperatures that are not ideal for the
host plant induce stress and predispose plants to
disease by lowering host r esistance. This may occur
for hosts de termined t o be resistant under normal
growing conditions.
Temperature also affects the amount of inoculumavail able. Cold winters interr upt the disease c ycle by
killing pathogens or vectors that otherwise may
persist unti l the next growing s eason. During the
growing se ason, temperature will directly influence
the pathogens abi lity to reproduce and infe ct the
host. This will directly affect the rate of disease
development, disease severity or even if diseased
plan ts wi ll ap pear in the firs t place.
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Moisture. Abundant, prolonged or repeated moisture
is the predominant factor in the development of most
epidemics caused by fungi, bacteria and nematodes.
Although relationships can be complex, rain, greater
relative humidity or prolonged dew periods will
increase the likelihood of many, but not all, diseases.
Moisture affects the host by inducing new growth that
may be more susceptible, or re sistant, to infection.
Moisture also induces sporulation of fungi,replication of bacteria and m obility of nematodes,
thus, increasing th e amount and disper sal of available
inoculum. For other p athogens, rain may suppress
movement of insects acting as vectors of pathogens,
thus reducing disease spread.
Wind. Fungal spores, vectors, and, to a lessor e xtent,
bacter ia and n ematodes , can be dispersed b y the
action of wind. This will en able pathogens to move
from infected plants to healthy plants. Wind can also
injur e hosts, thus providing an a venue f or infect ion
and/or increasing susceptibility to some p athogens.
Other Factors. There are many factors including light
inten sity, light quality, soil pH, fertility an d soil type
that influence disease development. Relationships can
be complex with environmental influences being
exerted on the host and the pathogen. Each disease
must be studied carefully to determine what
interactions ar e important for its development.
DISEA SE DIA GNOSIS
Diagn osis requires knowledge of what i s normal for
the host p lant as well as knowledge of p roblems that
occur red in the past. Accurate diagn osis is critical for
deci ding if a disease is present and if effective cont rolmeasures are available or justified. An accurate
diagnosis is based upon rec ognition of specific signs
of the pathogen on the host as well as the presence of
symptoms on the host.
Signsare defined as the vi sible presence of the
pathogen or pro ducts of the pathogen on the host
plan t. Fungal sp ores , f ruiting st ructures that bear
spores and bacterial ooze are all examples of signs. In
contrast, symp tom sare the e xternal and internal
react ions or a lterat ions of a plant as a result of
disease. For example, dead spots in leaves or bark,
rotte n spots i n fruits or tube rs, swel lings on roots orbranch es , clus tere d b ranc hes, unnatu ra l colo r or
shape and vascular discoloration in stems are all
symptoms that may aid in diagnosis of a plant
disease.
Because most diseases encountered have previously
been described, it is usually p ossible to di agnose a
specimen by comparison with the symptoms and signs
of pathoge ns already described for diseases of that
part icular host . Books, manuals and p ictures a re very
useful aids in diagnosis of many plant diseases.
Experienced diagnosticians recognize many diseases
on sight or are able to quickly narrow down
poss ib il ities t o s everal choices. Although experience
is the best teacher, the general guidelines listed below
will help focus attention on information needed for
accurate diagnosis.
1. Carefully describe the
characteristics that make the plant
appear abnormal (symptoms).
2. Determine the distribution of
symptoms in the host by looking at
the entireplant.
3. Determine if evidence of the
pathogen (signs) exist.
4. Determine the distribution of
affected plants in the field.
If dia gnosis is still not p ossible , contac t fieldm en or
your local Cooperative Extension Educator for
assistance. Specimens can be mailed by your
Extension Educator to the University of Wyoming,
when additional assistance is required.
DISEASE DEVELOPMENT
Every i nfecti ous disea se requi res a series of
sequential ev ents in order for disease to develop. This
series of e vents is ca lled the disease cycle. Although
the specific characteristics are unique for each
disease, the general events in the disease cycl e are;
(1) dispersal of the pathogen to the host, (2)
penetrat ion a nd infect ion of the host, (3) i nvasion a nd
colonization o f the host, (4) reproduction o f the
pa thogen , (5) pathogen di spersa l (6) pa thogen
survival between growing seasons and/or in the
absence of a host.
Completion of events #1-5 is onegenerationof the
pa th ogen and, depe nd ing on th e pa thogen , can be
repeated before the growing season ends at event #6.
The generation time and the number of generations a
pathogen completes dur ing one season determines the
dynamics of disease development and the potential
for plant or crop loss. Graphic representations of
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disea se severity over time are called disease progress
curvesand are discussed below for Fi gures 2, 3 and
4.
Mon ocyclic pathogens have a maximum of one
generation per growing season and possess a
characteristic disease progress curve (Figure 2).
Pathogens are monocyclic because environmental
conditions or other physical factors prevent repeating
events #1-5 until the next growing season; examples
are Verticilliumwilt and some other soil-borne
diseases. Other pathogens are monocyclic because
their life cycle requ ires at least one season to
complete; examples are cedar-apple rust and corn
smut.
Polycyc lic pathogens complete more than one
generation per growing season and, therefore, areable to reproduce and infect additional healthy plants
during the current gr owing season (Figure 3). As the
potent ial for the number o f generat ions in creases (i.e .,
the generation time decreases), so does the potential
for devastating losses. Some fung i have such short
gener ation times that steps i n the cy cle of
pathogenesis completely over lap r esulting in a
continuous series of new i nfections giving the
appearance of explosive disease development.
Examples of polycyclic pathogens can be found in
virtually all classes of p athogens including fungi,
bacter ia , nematodes and viruses. Several examples
are early and late bl ight of potatoes, and wheat a ndbean rust .
The time over which disease develops in a production
area or region for both monocyclic and polycyclic
diseases can vary from days to yea rs and is a
characteristic of the specific disease involved. Severe
losses ca n occur regardless of the speed at wh ich
disease develops and can result from both monocyclicand polycyclic pathogens.
PLANT DISEASE CONTROL
Control measures are used to interrupt or weaken at
least one of the six sequential events in the disease
cycle (see above). In ge neral, monocyclic dise ases are
most efficiently suppressed by reducing the amount of
the initial inoculum at events #1 and/or 6. P olycyclic
diseases are most effici ently suppressed by reducing
the in itial inoculum a nd/or by re ducing the rate of
disease increase that occurs when events #1-5 are
repeated. Various control methods commonly used to
reduce or eliminate disease are categorized below;much overlap exists between categories.
Exclusion. The disease tri angle illustrates that if the
pathogen and hos t rem ain separate d, no disea se wil l
develop. Disease co ntrol metho ds that maintain
separation can be very effective. However, this
approach to disease control is largely regulatory in
natu re and includes quara ntines, inspections, use of
pa thogen-f ree plan t mate rials, ce rtif icat ion o f s eed
stocks, and b y other means.
Evasion. The use of healthy seed, planting and
growing plants under environmental conditionsunfavorable for disease development, selecting early
(or late) planting and harvest dates and maintaining
the proper distance be tween rows and fields are all
examples of methods for evading disease. The se
practices inc rease the cha nce that the ho st wil l remain
healthy or go through it s susceptible stage be fore the
pathogen reaches the h ost .
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Eradication. Eradication is the elimination or
destruction of the pathogen. Methods of eradication
include temporary removal and destruction of host
plants, chemical treatment of soil or seeds to k il l the
pathogen, and sanitation of eq uipment and s torages.
Growers routinely practice crop rotation to reduce the
amount of inoculum present to acceptable levels, by
growing a no n-host plant.
Resistance. Resistance is the growing of plants n otsusceptible to the di sease. Resistant cultivars are
usually developed through special breeding and
selection programs. Immunity or total resistance is
often unobtainable and many varieties have partial
resistance th at allo ws the pla nt to grow in spite of
contact with a pathogen.
Environmental Modification. Creating conditions
unfavorable for the pathogen is a practical disease
control method used by some growers. Proper
spacing of the plants in the field o r greenhouse will
aid in reducing humidity that favors development of
some diseases. Good soil drainage and properirrigation pr actic es are al so impor tant. Flooding fields
during the fallow period may also reduce the
incidence of some disease caused by soil borne
organisms. Environmental modification by drying
and/or refrigeration of harvested products is one of
the most common methods used to slow growth of
pa thogens a nd reduce disease.
Protection. Infection of plants may be reduced
throughprophy laxisor protection. Although
biolog ical control agen ts are used in some instances
to pro tect plants from infecti on, the mos t common
metho d to directly or indirectly protect p lants frompathogens is through the careful use o f chemicals.
Chemical Controls
Chemicals orpes ticidesare often used to help control
plant di seases . T he correc t timing of chemical
applications as well as choosing the proper chemical
is essential for good control. Labels provide
application information and the directions must be
followed.
Fumigants and Sterilants.These chemicals generally
have a broad range o f activity but are not applied to
growing plants. Soil fumigation is commo nly used toreduce nematode populations as well as other soil-
bo rne pa thogen s a nd pests. To ta l erad ic atio n o f
pa thogens and pest s is genera lly not poss ible.
Fumigants are typically expensive, difficult to apply,
highly toxic and nonselective in their activity.
Therefore, beneficial microorganisms and insects are
affected, as well.
Proper soil prepa ration, soil mo isture (appr oximately
70% field capacity) and soil temperature (55-85 F) is
critical for achieving uniform chemical distribution
and effective disease control. Methyl bromide and
chloropicrin are highly vo latile fumigants, and plastic
sheeting is require d to seal the soil surface during
their application. In contrast, metham sod ium is less
volatile and water can be used to seal the soil surface.
Label directions will give precise directions on the
soil conditions required and suitable applicationmethods.
Nemat icides. Fumigants are considered nematicides.
However, other liquid and granular chemical
formulations are available for nematode control, in
addition to fumigants. These products have low
volatility and can be applied before and after planting
many, particu larly non-food , crops. N ematicides k ill
nematodes that come in contact with the chemical and
may kill some insects, as well. Nematicides are
generally highly toxic and may contaminate ground
water when not used properly.
Seed Treatments.Seed treatments are typically
fungicides that protect the seed and germinating
seedling from infection and/or decay. Pathogens can
be seed-borne or soil-borne. S ome advantages of seed
treatments are that smal l amounts of chemical are
requi red and that seedlings are able to get o ff to a
strong start. Because treated seed is not to be used for
feed, food or processing, dyes are used to color
treated seed and treated seed should be properly
labeled. An excepti on is the treatment of high
moisture grains with acetic or propionic acid. Acid-
treated grain is commo nly used for livesto ck feed.
Protectants.These chemicals are usually applied to
the seed or foliage of the gro wing crop so that a
protec tive chemical barr ie r o ver the host surface
prev en ts the in itia l infect ion. These products must no t
be toxic to the hos t.
Systemics.These are applied to the seed or growing
crop and are often absorbed and transmitted
systemica lly within the plant. These substance s may
kill or suppress the pathogen growing within host
tissue and, therefore , may hav e a curative or
therapeutic effe ct. Some systemics have very
selective activity and, through repeated use, becomeineffec tive due to selection for insensitive funga l
isolates.
Integrated Methods
Frequently, a number of control methods are
integratedor used simultaneously to reduce the
economic loss of plant d iseases. Relying on a single
method for disease co ntrol frequently results in
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failure. Integrated methods c an reduce costs
associated with more expensive control methods and
decrease the risk associated with dependence on a
single method of control. Added benefits of
integrated methods are that disease co ntrol is
generally greater than for each method used
individually (Figure 4).
ADDITIONAL INFORMATION
Numerous reference books and publ icat ions are
available that p rovide summaries of specific plant
diseases, their c ontrol, and photogra phs to aid
diagnosis. The professional society of plant
patholog ist s, The American Phytopathological
Society , offers many of these publications for sale at
reasonable prices (approximately $35.00). ContactAP Sat (800) 328-7560, or
write; 3340 Pilot Knob Road, St. Paul, MN 551 21-
2097. Some of the publications listed in the section
ADDITION AL READING are readily available
through AP S.
PLANT PATHOLOGY TERMINOLOGY
Atrophy- A lack of development of certain plant
parts or t issues .
Bactericide - A compound toxic to bacteria.
Canker - A diseased or dead area in the bark and
wood of trees or shrubs characterized by a drying out
of the tissues.Cell- The smallest unit that makes up a plant and
cons ists of the cellular contents (proto plasm)
surrounded by a cell wall.
Damping-off - A type of seedling di sease in which the
stem deca ys in the vicinity of or bel ow the soil line.
Disease Cycle - The chain of events involved in
disease development, including the stages of
developmen t of the pathogen and the effect of disease
on the host.
Ecology - The study which deals with the effect of
environmental fac tors, such as soil, climate, and
culture on the occurrence, severity, and distribution
of plant diseases.
Environment- The external conditions and influences
that surround living organisms.
Epidermis- The superficial layer o f cells occurring
on all plant parts.
Exudate - Material that has been fo rced out.Fungal - Relating to fung i.
Fungi cide - A compound tox ic to fungi.
Gall - An unusual en largement o n some portion of a
plant.
Host - The plant upon which a parasite lives.
Hyperplasia- A symptom due to an abnormal
increase in the number of individual cells.
Hypertrophy- An symptom due to an abnormal
increase in the size of individual cells.
Hyphae - Fungal filaments which collectively form
the mycelium of a fungus.
Immune- Cannot be infected by a given pathogen.
Incubation period - The period between the time theinoc ulum is introd uced o nto the host and the time
when the diseased condition becomes evident.
Infection - The process of the pathogen gaining
entrance to the host and becoming established as a
pa rasi te .
Infection court - Speci fic area on a plant whe re a
pathogen gains entranc e to the hos t.
Infest - To overrun or contaminate.
Inoculum - The pathogen, or its parts, that can cause
infection.
Inoculation- The process of transferr ing inoculum to
host.
Lesion - A diseased region of the host.Local invasion - That involving only a portion of the
plant.
Mummy- A dried, dise ased fruit.
Mycelium - The group of hyphae that form the fungal
body.
Necros is - A symptom marked by r apid death o f the
host or parts of the host.
Nemati ci de - A compound toxic to nematode s.
Obligate - Necessar y or essential.
Obligate parasite- Organisms that live on ly as
parasit es.
Pathogen- A disease-p roducing agent.
Pathogenicity- Ability of an organism to producedisease.
Pathology - The study of disease.
Pesticide - A compound toxic to a specific pest(s).
Physiology - The study of metabolic processes,
activities and phenomena related to life.
Predispose - Make favorable for.
Primar y infection - The first infection of a host by the
overwintering or over summering inoculum.
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