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H AND EDUCATION CENTER
ity of Florida
BRADENTON AREC Research Report GC1973-1 February, 1973
CONTROLLING FUSARIUM WILT OF TOMATO ITH HOS REy /
Pat Crill, J. P. Jones, and S. o1' is5
Many plant breeding programs which historical supported by the
farmer, consumer, taxpayer and various granting age are't aj verely
criticized by some of these same individuals and organization the
criticism is unjustified and emanates from highly conscientious, but poorly in-
formed consumer groups. Critics of plant breeding programs have signed out plant
breeders as villans working to create agriculture disaster (1, 2, 7, 9).
In 1968, van der Plank issued a severe reprimand to all plant breeders, admon-
ishing them for using monogenic resistance and recommending that polygenically
controlled tolerance mechanism be utilized for disease control (9). He further
recommended that federal controls be placed on plant breeders and the use of
certain genes restricted. In 1972, the National Academy of Science published its
view in a report entitled Genetic Vulnerability of Major Crops (7). Much of this
report is based on the unproven axioms developed by van der Plank (9) and
Robinson (10, 11). The committee responsible for the report of the National
Academy of Sciences also advocated establishing a national committee to regulate
the activities of plant breeders (7 p. 299). The committee suggested "the
establishment of a national monitoring committee to keep a watchful eye on the
development and production of major crops... and issue warnings wherever and
whenever it feels them justified." Clearly this is a recommendation for the
regulation and control of plant breeders'and seed companies' activities.
The "van der Plankian theory" of controlling plant diseases with host resistance
as illustrated with Fusarium wilt of tomato embodies four separate concepts (9):
A. The I gene which controls resistance to race 1 F. oxysporum lycopersici is a
a strong gene (9 p. 114).
B. Race 2 of F. oxysporum lycopersici has arisen many times by mutation or other
means but never became established because stabilizing selection curbed it
(9 p. 114-115).
C. Those tomato varieties developed with monogenic vertical resistance to race 1
F. oxysporum lycopersici should be "intensely susceptible" to race 2 F.
oxysporum lycopersici because of the vertifolia effect (9 p. 153-159).
D. Horizontal resistance polygenicc tolerance) is preferred to vertical resis-
tance (monogenic resistance) as a genetic mechanism for controlling
Fusarium wilt of tomato (9 p. 129-143).
Even if these four concepts are shown to be scientifically valid, intervention
into plant breeding programs by any agency would not be warranted. If any one of
the above four concepts are shown to be invalid, even in part, then any recommen-
dations for intervention into, or control of, plant breeding programs are
scientifically unjustified. Likewise, control over seed companies, to dictate
what variety or varieties may be sold to farmers to be planted in a given area,
is also scientifically unjustified.
This paper reports data which were obtained from experiments designed specifically
to test the validity of the four concepts described above. In addition, alterna-
tive explanations are offered for each concept.
CONCEPT A: THE I GENE IS A STRONG GENE. van der Plank stated the I gene is
strong, but not quite strong enough (9 p. 114). He concluded that race 2 would
never become the menace race 1 was before the gene I was used. In this statement
it was implied that all Fusarium wilt prior to the introduction of varieties with
the I gene was incited only by race 1 (9 p. 114). On the next page the state-
ment was contradicted as follows:
"Alexander and Tucker's discovery of race 2, in a variety without the I gene,
....is evidence enough that race 2 had occurred tens of thousands, possibly
millions, of times. To dispute this is to assume that providence staged a
special and unique show for Alexander and Tucker." (9 p. 115)
Prior to the release, and utilization by farmers, of varieties with the I gene it
was not possible to determine whether wilt was caused by race 1, race 2 or any
other race. This is because it is not possible to identify races unless there are
at least two tomato genotypes which will differentiate one Fusarium isolate from
another as being genetically unique for pathogenicity. Therefore, the statement
that race 2 would not be the menace race 1 was before the gene I was used was
invalid when written since it was based upon contradictory and improperly inter-
preted data. The further statement that because the gene I is a strong gene it
is unlikely to become useless to tomato growers (p. 114) is also incorrect. Crill
et al (3, 4, 5) have shown on several occasions that the I gene is not effective
against race 2 and without the 12 gene Fusarium wilt is the limiting factor in
tomato production on Florida sand land (Table 4).
Al TERNATIVE EXPLANATION FOR CONCEPT A: Plant breeders have been aware that some
genes for resistance were more effective than others ever since the first disease
resistant crop varieties were specifically developed by Orton, The terminology
used by plant breeders and pathologists to explain the effectiveness of-control"
has involved words and phrases such as: immune, highly resistant, moderately -
reoistant, field.resistant, etc, The usefulness of disease resistance geneo has
been measured by how long they remain effective when placed into varieties and
released for commercial use. The "strong gene weak gene" concept does not
provide any better means of predicting the useful time span of a resistance gene
than other procedures plant breeders were previously using. When the I gene was
first incorporated into commercial tomato varieties, it was not possible to
predict how long it would be effective against Fusarium wilt. The same situation
was true for the gene controlling resistance to race 2 Fusarium wilt, gray leaf-
spot, and nailhead rust. These resistance genes have all been most effective
and most long-lived. They would all have to be classified as strong genes based
upon our present knowledge but at the time they were first utilized by the breeder
no one knew whether or not they would be effective. The primary reason these
genes were effective is suitable mechanisms of variation did not exist in the
pathogen whereby it could adapt to the host population with the resistance gene.
The formation of new races is most likely an interaction among both host and
pathogen genes and not just a function of the host as implied by the "strong gene -
weak gene" concept.
CONCEPT B: STABILIZING SELECTION CURBED RACE 2. The concept of stabilizing
selection as presented by van dcr Plank is a proposal to explain the selection and
survival of pathogen races in nature. Stabilizing selection states that simple
races are more fit to survive than complex races or race I Fusarium gxyspAor
lycopersici is more fit to survive than race 2 F. oxysporum lycopersici. The
presumed reason for race 1 surviving better than race 2 is that race 1 is a more
simple race, i.e. it has fewer genes for pathogenicity than race 2. We are of the
opinion the only difference between race 1 and race 2 is a single gene which
controls the ability of the fungus to cause disease in varieties with the I
genes. Since no perfect stage exists for F. oxysporum vlcopersici it has not
been possible to determine the genetic differences between race 1 and race 2 but
no evidence is available to suggest more than one gene. Grill et al (6) have
assumed that virulence (measured by degree of disease development among isolates
within a single race on a wide range of host genotypes) is polygenically controlled
but that pathogenicity (difference between race 1 and 2 in ability to cause disease
on differential varieties with genotypes ilii2i IlI2 i i2, 1 1 9I ) is mono-
genically controlled. We do not think that just because a fungus has one more gene
for pathogenicity than another it is better adapted to survive, either as a
saprophyte or a parasite. In all probability this allele exists in both races
In 1968 van der Plank stated "race 2 has occurred often enough and has had time
enough to be common, had stabilizing selection not curbed it" (9 p. 115). Crill
et al (5) have offered evidence to refute this statement. They studied Fusari'jm
developing in a commercial tomato farming operation of 120 acres over a three year
period (Table 4) and concluded there was no evidence of stabilizing selection. It
was not possible to duplicate the field conditions exactly as specified by van der
Plank as being necessary. To adequately test this hypothesis it would be necessary
to grow varieties which are susceptible to both race 1 and race 2 on a commercial
scale for several years in soil uniformly infested with equal amounts of race .1 .
and race 2. At the termination of the experiment the amount of race 1 would be
compared with the amount of race 2 and if race 1 was predominant in significant
amounts then stabilizing selection could be assumed operative. Such an experiment
is not feasible because (1) no tomato farmer is going to grow a suitably large
acreage of a wilt susceptible variety, (2) a method of uniformly infesting coil
with race 1 and race 2 in equal amounts has not been developed, and (3) no assay
technique is available to differentiate race 1 from race 2 on the large scale that
would be necessary. The concept of stabilizing selection is so defined and
worded it is nearly impossible to disprove. Any data which are against the
stabilizing selection hypothesis can be dismissed by invoking the "weak gene'
philosophy. Since a great deal of the van der Plank theory was based on the
Fusarium wilt of tomato interaction and on the stated fact that the I gene is a
strong gene, it is much more difficult for the defenders of stabilizing selection
to invoke the "weak-gene" philosophy in this instance.
ALTERNATIVE EXPLANATION OF CONCEPT B: There is little doubt that the phenomenon
termed "stabilizing selection' does exist. Many plant breeders and pathologists
have observed that some races are more predominant than others. They have also
noted that race formation varies from species to species of pathogens. Van der
Plank termed this phenomenon stabilizing selection and noted that those races most
fit to survive are those with the fewest genes for pathogenicity. Nelson (8) has
recently questioned the validity of the stabilizing selection hypothesis and con-
cluded the concept itself may not really exist. Hare(1) has indicated that the
sole difference among races 1, 2 and 3 of Fusarium wilt of pea, excluding their
different genes for pathogenicity, is their rate of growth. Each race presumably
has the same number of genes for pathogenicity yet in mixed cultures race 1 always
predominates over race 2 and race 2 always over race 3. Growth rate then rather
than the number of genes for pathogenicity determines which races predominate.
Several other examples could be cited and other explanations given but the comments
of Hare(1), Nelson (8) and Crill et al (3, 4) are adequate for this discussion.
CONCEPT C: THE VERTIFOLIA EFFECT OCCURS IN THE LYCOPERSICON FUSARIUM SYSTEM.
The vertifolia effect with respect to breeding tomatoes for resistance to rFua?3iiim
wilt has been discussed by Crill et al (5), Robinson defined the vertifolia effect
as the loss of horizontal resistance during the process of breeding for vertical
(1)Hare, W.W. Comments at the discussion session entitled "Stabilizing Selection:A
Controversy" presented at the annual meetings of the American Phytopathological
Society in Mexico City, Mexico on August 9, 1972.
resistance (10). In tomato breeding jargon this translates as the general loss of
tolerance to a given pathogen by a host plant variety which has been developed with
specific monogenic resistance by the plant breeder (3). The-term 'vertifolia
effect' was coined to explain the loss of tolerance in the potato variety 'Verti-
folia' to Phytophthera infestans. 'Vertifolia' was developed with monogenic
resistance to P. infestans. A race of P. infestans evolved which could success-
fully attack the monogenic resistant 'Vertifolia' and the result was severe
blight symptoms, From this incident it was concluded the genes for tolerance to
late blight had been lost by the plant breeders in the development of 'Vertifolia.'
Van der Plank stated "a vertifolia effect seems to be almost inevitable wherever
resistance is needed and vertical resistance is great'' (9 p. 159) and "great
selection pressure and great vertical resistance are needed for a great vertifolia
effect" (9 p, 155). The data in tables 1, 2 and 3 indicated there was no
vertifolia effect" operating in the Lycopersicon:Fusarium system. When the
monogenically resistant (vertically resistant) variety 'Floradel' which has the
gene I is compared to the tolerant (horizontally resistant) varieties 'Marglobe'
and 'Rutgers' in all instances 'Floradel' had less disease from race 2 than did
'Marglobe' and 'Rutgers' (Tables 1, 2, 3).
In a series of experiments designed specifically to test for the vertifolia
effect, Grill et al (5) concluded the vertifolia effect did not necessarily operate
in the Lvcopersicon:Fusarium system. They evaluated 36 tomato varieties which were
developed by 15 different breedini, programs including commercial seedcompanies,
food processors, state and federal experiment stations, A definite loss of
tolerance was noted in one variety and a possible loss in nine others (Table 5).
They concluded the vertifolia effect concept was invalid since most of the
varieties with the I gone were no more susceptible to race 2 than those without
the I -cnc, but known to be tolerant to race 1 (Table 5),
LTinTiTT'E EXPLANATIONOF CONCEPT C: Most plant breeders working with disease
resistance have experienced the loss of resistance or tolerance in certain breeding
lines. It is, in fact, a rather common occurrence, especially if screening
techniques are not fully adequate. The most common explanation is the plant
selected from the screened population was not a resistant plant but rather an
escape. In those breeding programs where progeny testing is routinely conducted,
it is possible to determine how often susceptible escapes were selected as being
resistant. In those programs where screening programs are inadequate, or where
progeny testing is not done routinely, it would be quite easy to lose resistance
genes, particularly those associated with polygenic tolerance or horizontal re"
sistance. It is not a foregone conclusion that tolerance genes will be lost when
the plant breeder is concentrating on monogenic resistance as stated by van der
Plank. Rather, the possibility exists that tolerance genes will be lost when
the breeder is concentrating on monogenic resistance unless he makes an effort
not to lose such tolerance genes.
CONCEPT D: HORIZONTAL RESISTANCE IS PREFERRED TO VERTICAL RESISTANCE FOR DISEASE
CONTROL. This concept is the entire theme of van der Plank's book (9) and although
implied in almost every paragraph it is never stated clearly. It is stated "in
certain circumstances vertical resistance ought to be as stable and enduring as
horizontal resistance" (9 p. 88-90) and these circumstances occur when
stabilizing selection is operating. Stabilizing selection is the basis of success
when vertical resistance is used by the breeder"(9 p. 117). "To overcome vertical
resistance the pathogen must become less aggressive on the susceptible varieties "
(9 p. 123) but this is not true for horizontal resistance. "Horizontal resis-
tance is more stable than vertical resistance and this stability is attributed to
the stability of the races of the pathogen"(9 p. 122). "This stability does not
exclude new races from appearing or old races from disappearing but a stable
balance is maintained among all the various races"(9 p. 122). The facts ob-
tained from the Lycopersicon:Fusarium system thus far do not support the theory
that horizontal resistance is superior to vertical resistance (3, 4, 5, 6).
Grill et al (4) have shown in field studies of commercial acreages of tomatoes
when highly tolerant varieties (possess good horizontal resistance) are compared
with varieties that are monogenically resistant (vertically resistant) the
monogenic resistance is superior. Yields from monogenic resistant varieties
were much greater than those from tolerant varieties. Yield data from the crop
rotations tolerant variety-tolerant variety and resistant variety-tolerant variety
were compared. Yields of the tolerant variety-tolerant variety rotation were
reduced by one-half in the second crop season (5).
ALTERNATIVE EXPLANATION OF CONCEPT D: Crill et al (3) have discussed the advan-
tages and disadvantages of monogenic resistance versus polygenic tolerance. They
cited the following reasons for plant breeders to use monogenic resistance in
preference to tolerance. These included the following: (a) the host reaction to
the pathogen is quite obvious which makes it possible to develop workable
screening techniques in the shortest time period, (b) varieties are not suscep-
tible to the pathogen when released to the farmer which results in higher yields
than would be obtained with only tolerant varieties, (c) the spread of the
pathogen is curtailed with a resistant variety; whereas, susceptible but tolerant
varieties encourage dissemination of the pathogen. They did not mention the very
serious problem which a plant breeder would confront if he utilized only hori-
zontal resistance polygenicc tolerance) and was working with multiple disease
resistance. From the plant breeders viewpoint the most serious objection to the
preference of horizontal resistance polygenicc tolerance) to vertical (mono-
genic) resistance is that it is unmanageable. If it is assumed the breeder has 5
unlinked monogenes which control resistance to 5 diseases it is obvious he must
screen very large populations of recombinant progeny if he is ever to find a
plant which is resistant to all 5 pathogens. Not only must the breeder find
the one plant, he must find numerous others, some of which hopefully possess
desirable horticultural characters. In most breeding programs this objective
would not be rapidly accomplished because of the sheer numbers of progeny which
must be evaluated. If the progeny which are resistant to the five diseases are
evaluated, they will be found to segregate, and in the simplest of cases would
have to be grown for at least three generations to establish a fixed line. In
all probability these homozygous resistant inbred lines which are resistant to all
5 diseases will be deficient in horticultural characters. To improve the plant
type, a series of backcrosses must be initiated which unfixes the homozygous
state of the 5 disease resistance genes and the same involved screening and
selection process for all 5 diseases must be gone through again by the breeder.
In the above discussion it was assumed that the 5 monogenes were dominant,
dominance was complete and resistance was not associated with any undesirable
characters. Such conditions are unlikely to exist in nature and even with
monogenes the procedure is going to be long and tedious. If, however, the
plant breeder is told he must use only horizontal resistance polygenicc tolerance),
the problem truly becomes unmanageable. If it is now assumed the same 5
diseases will be controlled by horizontal resistance and a minimum of three genes
controls each character the breeder must keep track of at least 15 genes. Most
polygenic tolerance mechanisms behave like Fusarium wilt tolerance in tomato.
There is a lack of dominance and resistance is additive. Also, to detect such
resistance it is of utmost necessity to control the environment for pathogenesis
(6) and utilize the proper inoculum potential (3, 6). This requires rather
elaborate plant pathogenic techniques for just one disease and is impossible
far five separate diseases, each of which has its own special climatic conditions
for proper development including temperature, pH, daylength, etc. In addition
it is also extremely important to have the isolate of the pathogen which possesses
the proper genes for pathogenicity. When dealing with monogenic resistance, the
.uly important criteria are to have adequate inoculum and that it be pathogenic.
assistance is either present or absent with monogene. With horizontal resistance
(polygenic tolerance) the host:pathogen interaction varies from slightly suscep-
tible to severely diseased or dead. The facilities necessary to synthesize a
horticulturally desirable plant which possesses the maximum in horizontal
resistance to 5 diseases are incomprehensible.
SULMARY AND CONCLUSIONS
Four concepts developed by van der Plank (9) and illustrated with Fusarium wilt
of tomato are discussed. The observations made by van der Plank are not disputed;
rather, alternative explanations of these same observations are presented, based
upon a background of the genetics and breeding of multiple disease resistant
tomato varieties. Hopefully, those who are advocating the placement of controls
on plant breeders and seed companies and the monitoring of variety development
activities will realize there exists more than one explanation for many of the
phenomena associated with disease control via host resistance. The scientific
information is not yet available whereby any agency or organization can dictate
to plant breeders and seed companies how they should develop varieties as
advocated by van der Plank (9) and Horsfall et al (7).
The ultimate conclusion we have drawn is the information is not yet available
whereby any agency can dictate to the plant breeder how he should develop
varieties. The government-dictated policy of plant breeding in the U.S.S.R.
served to economically cripple the Russian nation because the farmers could not
provide an adequate food supply. The dictates based upon the wrong theories of
one man (Lysenko) brought economic disaster to Russia. If the National Academy
of Sciences committee on the Genetic Vulnerability of Major Crops has their way
in establishing a national board of control over plant breeders and seed
companies the same could happen to food production in the United States.
1. Adams, M. W., A. H. Ellingboe, E. C. Rossman. 1971. Biological uniformity and
disease epidemics. BioScience 21:1067-1070.
2. Apple, J. L. 1972. Intensified pest management needs of developing nations.
3. Crill, P., J. P. Jones, D. S. Burgis, S. S. Woltz. 1972. Controlling Fusarium
wilt of tomato with resistant varieties. Plant Dis. Reptr. 56:695-699.
4. Crill, P., J. P. Jones, D. S. Burgis. 1973. Failure of horizontal resistance
to control Fusarium wilt of tomato. Plant Dis. Reptr. 56: (in press).
5. Crill, P., J. P. Jones, D. S. Burgis. 1973. Absence of a vertifolia effect in
the Lvcopersicon:Fusarium host-parasite interaction. Plant Dis. Reptr. 57
6. Crill, P., J. P. Jones, S. S. Woltz. 1971. Breeding tomatoes for resistance
to race 2 Fusarium wilt. Univ. of Fla. AREC Bradenton Mimeo Report BR71-4.
7. Horsfall, J. G. (Editor). 1972. Genetic vulnerability of major crops. Nat'l
Academy of Sciences, 2102 Constitution Avenue, N.W., Washington, D.C. 20418.
8. Nelson, R. R. 1972. Stabilizing racial populations of plant pathogens by use
of resistance genes. Journal Environmental Quality 1:220-227.
9. van der Plank, J.E. 1968. Disease Resistance in Plants. Academic Press, Inc.,
New York, N.Y. 206 pages.
10. Robinson, R. A. 1969. Disease resistance terminology. Rev. Applied Mycology
11. Robinson, R. A. 1971. Vertical resistance. Rev. Pl. Path. 50:233-239.
Table 1. Host response of tomato varieties to races 1 and 2 and number of diseased
plants per 75 inoculated with F. oxysporum f. lycopersici race 2.
: Number of days after inoculation
VARIETY :Host Responsea: 5 : 10 : 20
:Inoculum level : Inoculum level: Inoculum level
:race l:race 2 :High Med Low : High Med Low : High Med Low Mean
Walter R R 0 0 0 0 0 0 0 0 0 0
Bonny Best S S 55 43 10 68 72 28 69 73 32 58
Indian River R T 15 26 6 33 46 14 40 46 18 35
Floradel R T 18 20 1 36 30 7 40 46 28 38
Manapal R T 22 30 3 46 52 14 52 61 19 44
Homestead 24 R T 21 12 1 41 35 7 51 40 7 33
Tropic R T 14 16 6 33 38 11 42 50 14 35
Marglobe T T 38 24 4 53 35 13 63 60 13 45
Rutgers T T 30 25 3 46 42 16 55 51 26 44
LSD .05 3.6 3.6 3.6 2.7 2.7 2.7 2.7 2.7 2.7 1.5
R = resistant, S = susceptible, T = tolerant
hLow, Med and High = 0.25 x 106, 4.25 x 106 and 10.5 x 106 spores/ml, respectively
Table 2. Disease indexa for 75 tomato plants inoculated with F. oxvsporum f.
lycopersici, race 2.
VARIETY : 5 : 10 : 20
: Inoculum level : Inoculum level : Inoculum level
: High Med Low : High Med Low: High Med Low Mean
Walter 0 0 0 0 0 0 0 0 0
Bonny Best 2.0 1.5 0.3 3.5 3.4 0.8 4.2 4.3 1.4
Indian River 0.5 0.7 0.2 1.0 1.4 0.4 1.4 1.9 0.76
Floradel 0.5 0.6 0.01 1.2 1.0 0.1 1.5 1.7 0.9
Manapal 0.6 1.0 0.1 1.5 1.9 0.4 1.7 2.5 0.7
Homestead 24 0.6 0.3 0.04 1.4 1.0 0.2 1.9 1.6 0.25
Tropic 0.5 0.4 0.2 1.0 1.0 0.3 1.5 1.7 0.5
Marglobe 1.2 0.8 0.08 2.0 1.3 0.3 2.5 2.5 0.5
RutRers 0.9 0.7 0.07 1.7 1.5 0.4 2.3 1.9 0.9
LSD .05 0.1 0.1 0.1 0.12 0.12 0.12 0.13 0.13 0.13 0.07
a0 = no disease; 5 = dead
bow, Med and High = 0.25 x 10 4.25 10 and 10.5 x 106 spores/ml, respectively
L~ow, Md and High = 0.25 10 4.25 x 10 and 10.5 x 10 spores/il, respectively.
Table 3. Host response of tomato varieties to races 1 and 2 and number of dead
plants per 75 inoculated with F. oxvsporum f. vlcopersici, race 2.
: Number of days after inoculation
VARIETY : :5 :10 20
:_:Inoculum levelb-: Inoculum level : Inoculum level
: race l:race 2 : High Med Low : High Med Low : High Med Low Mean
Walter R R 0 0 0 0 0 0 0 0 0
Bonny Best S S 0 1 0 19 21 2 49 45 6
Indian River R T 0 0 0 2 2 1 2 14 6
Floradel R T 0 0 0 6 4 0 8 6 0
Manapal R T 0 1 5 4 6 0 4 14 2
Homestead 24 R T 1 0 0 5 1 0 11 10 1
Tropic R T 0 0 0 0 0 0 3 2 3
Marglobe T T 0 1 0 6 5 0 13 16 2
Rutgers T T 1 0 0 5 6 0 14 11 1
LSD .05 1.4 1.4 1.4 2.7 2.7 2.7 1.5
R = resistant, S susceptible, T = tolerant
bLow, Med and High = 0.25 x 106, 4.25 x 106 and 10.5 x 106 spores/ml, respectively
Table 4. Percentage of race 2 Fusarium-infected plants in five tomato fields
with three different host rotations initiating with uncleared virgin
land in 1970.
Field Host Rotation % Infected No. No.
No. 1971 1972 1972 Samples Acres
I Homestead 24 Homestead 24 74 10 10
II Homestead 24 Walter 0 20 20
III Homestead 24 Homestead 24 43 20 25
IV Walter Homestead 24 3 50 50
V Homestead 24 Homestead 24 62 12 15
Table 5. Host response as measured by disease index for 36 tomato varieties
inoculated with races 1 and 2 of Fusarium oxysporum lycopersici.
*Mean index is the average rating of five replications, each consisting of 20
observations. Individual plants were rated using a 0-5 scale where 0=no disease
and 5=dead. The average plant disease rating can be obtained by dividing the
mean indices in the table by 20.
USDA & Colo. AES
S. Carolina AES
Johnson & Stokes
Campbell Soup Co.
Campbell Soup Co.
Campbell Soup Co.
W. A. Burpee Co.
V. A. Burpee Co.
W. A. Burpee Co.
Peto Seed Co.
Asgrow Seed Co.
Asgrow Seed Co.
Race 1 Race 2