STUDIES ON MUSKMELON WILT,
CAUSED BY FUSA_B_1_U:b4_ @ULBIGENUM
CKE. AND MASS. VAR.

NIVEUM WR. F. 2.

 

Thesis for the Degree of M. S.
MICHIGAN STATE COLLEGE

Howard Nile Miller
1941

......)

. , .3... .....h.» .. ..
WWW???» ....

 

         

 

s. _ 2.. .. .d
.. \v..2 7... 13”.”... ...m.
. 4&4 . m....\\

     

                             
              

 

o . ,

2 I \.F

. ”Vivi I
. . ...

us A .. . «(J .
a 2..

.. ..I 1.... _. 7.
\yL . 4V» .2,.‘

  

.....S .. kph; ...-.Iu.....
a. K ‘ ..- ..2 \ 4.0.
., ("flariaL a

i O 2 ‘1’. .’\\ .%

2 fi‘ . . —'. n.u
0‘. .5. 34.24. ._

 

 

. .2 .
w n . ‘ I .
I 2m? ; .24 .,
. . .2 L .1 . ..xr. u x 2 .2? 22 2 .‘\__ n
...?»2..L:.2....-§; ...... .-.. . .. .. .
.v PL. .dd-.\2. .72» . a. 2 .-. . »\. .\ . 2 l . . . . .
2‘th. . ..11: ..\l I It .4 o . . ., 2 7A ‘ IV.- :34 . ..ntx: . an 2 v ....- .\ I. ... x .2 f : . 2 ~ .7. 1
- 2v .. . A- . . .. . . I 2. . II . . . , . . 2 \ ...! 2 . . 2 I . 5|? 2. Jr
,6. . n.‘ W .L4 .2 Ar}. , .hhml «#2212. .- . .I. . .\ .M. _. . . . 2. / . .14....1. ..2 .. “2. _ «r. _. «13/ /. ... ’r. . n.3, 322.1 ....\4.2 x 4.. nkvv. a . . rIH 0’4 1. ..cflm . r
f. 3 I . a ... . A .v .. . . 1...? .f. ... . .. X154... 5 . . . I . o . . K ..I. . x A. 2. D 3“ ... .I .2»! . . ..\.. I wtnik . Y. 21 - I . N .. 7 0 .IV... ...I M - 2. . I Y. . .. v. .
pf. ....... .. .m!‘ a... . , [I v . ..I f.o ..lr‘. a- 2 2 3 ....I. ...z {4‘ N2 2... .\ ..2. . . \v H/. 1.. . . i . .541 . . -. .t. . . .4- ... . . .nin... .
,CI a. .l ..‘ 04.» .2 . .\...‘ .. . . ... . .. I . v . .. HUI». .t‘ (Kc. ”.0...)... . a. V2. . . 0 I . .. 2‘ IIJ . .J V .. .a r o lo 1 u .241! 4‘ I u. «5.1. \‘O s . u n ‘ (1., I 2‘ n C \
<mV«vn.ll_ O. . ...-rt ‘7 ~o u . , 2 . .tN.. .4 . .. \. . . . \ .t .I (2! 2t ..hw cf 2 . r a: \J u . . .. .. .. . ,u\a/\'N . a . . .PwV Wduh .. \ T’l.\ . 4” v I
2 . . .2 . . . .. . . ...11. . , y... N- V .. . .
2 . 2 2‘ ~ .2 . . . .. .. 1
. 2 , ..Jr.’ .. . J. . , 2..
In ‘. I. u‘ w
. ..v r . p 90'
'2'. 7.6.. . r
u 2.2 (1 «in
. v ...- .

.u . . _
..2 iv. .
H. .IA12! .- fl 2’.
. .. . s.r\. .
.20; . .2 . .. . -
an- - ..o 1.24 \. J. -. .
1 . I .2I \ u
5,4. ... «to ...f.fi. . .
a . . . ..
.. - ... .2 4.5.2:. .
U? I .4II. .h .‘
)Ar.r. s '.u . ./CN~\ In.“ .I l .2!
54.2.12. . (4.1 O
3 J22: ...,wr .
2.. . .. 3. .49. .r
If .«mfl...» - .
1 c . .

.7» o
. l], ‘3‘.) .. . v
.\ .2. .... :3... ...2.
v I. . .2 a .D
_ aux v. «1. pl
, . -2-.; .3..- .22..
MIA. IE)! 1‘...qu : . . ..
n. fix M v . .‘7 r 2 .
.' x. .1 r. a.
.Nt(nz .. 0
f . a. ,

  

’11.: . ,2......2

. .» «lo... ‘14::
...mww‘. H.795!....W..3~.
e 2%. . ._ A_ . ._ ._ ._ .1 .... » _ _ - _ ... ...

2 . . . . #2..
Jr . 2. . 2 .. . _ . . . . . . . ... 2 .. . .. . . . . . \ .. . .. 2 . . . . . . . .. ....fl 3! 811v
$22231. - ,2. 2 .. .. ,.. u 2 ... . ... .. x . . _ . . 2. . ._ , . . 2 . . 2. . . . . .3. ’30.

"MC. A21. . .. . . . .. . .. , . . .. . ’2.er

.
. a
. 4 . u 2 2 . A 4 ,
. .. . . . . 1 . LT
. . . , ... .. . . . . . . . 2 . . . 4 .. 2 . \2 I .
a . . 2 . . . . . _ . . u . . . . . 2 . . . . .. ,
. . . . . . .. . . 2 . ... 2 . A ... ..

 

I
. .
a

3; c :95 VLj’i';
A‘ ' ‘

‘ ‘s

v

w ”I “L
:6 23:15“

. ' ‘J

-~.~; 2:, ~‘r:-s .

4.3V ‘5 'e'...- ‘*-‘1\..§\k'1' "

'.._ \f-n-‘f 393:,“
3". "\V'fih.

r
¢
t
~

:-
n

. t

.3}: .‘ j -
$.19 f: A“ )1.
.l‘nf‘f' T“: . y’. \. "ii“. ‘.
‘5: '.' ' "' I'A.‘.It;-

:_ . ' .

A a Fir
.~ ..gi

.§l

.."'v";

_. . V .
.‘z";':::3'- ’f-' ~.
. .4“ _l-."“

'I

5’ .' x‘f‘

I 5' ;\ I‘
I- ‘.. ‘ . ‘ ..
s .00 .
fig". ‘13:. \ ~ .
‘ P‘s
. 4. p" -
K . x

. ‘v-

k

3“:
\'».P " h.
h r "1"

jfi- ;

I 0
..,.~-. 4

are“

p

’4‘ L‘Qod‘él

‘. "i"

. :‘d

 

 

. 3 '11) . . ‘ .l f}! "-7 '_ :Lyky . ' b" ' i I ‘rwi‘fi: ~13"; 2““! ELY. 0. '. L. . .‘ é ' ‘ '. - t .. i ‘ . ~. . ‘ 'r' ' ‘ ' _. t.‘ --q 1"“‘
' .:. ' 1' Iva-“V" _ ~»-' .. PJsa~_x.\‘+¢r-.';rn run- my; 9.3.: .. 16.3%" .fléer-{nmfi ,' - “iv Him-f ._ a» .-- ”s I

 

STUDIES ON MUSKMELON WILT, CAUSED BY FUSARIUM

EULBIGEEUH CKE. AND mass. VAR.

 

NIVEUM VL.F.2.

by
HOWARD NILE ElllER

A THESIS
Submitted to the Graduate School of Michigan
State College of Agriculture and Applied
Science in partial fulfillment of the
requirements for the degree of

MASTER OF SCIENCE

Department of Botany

1941

ACKNOWLEDGEMENTS

The writer is grateful to Dr. J. H. Muncie for
advice and suggestions given throughout this study.

To Dr. J. H. Iuncie and to Dr. I. A. Bessey the
writer is indebted for the criticism and correction
of the manuscript.

Acknowledgement is made to Dr. C. Guinn Barr for
suggestions in the chemical work. and to Ir. Ralph
Lewis for help with the photographic work.

.13 2.123 1

TABLE OF CONTENTS

Introduction.
History.
Distribution.
Spread in Michigan.
Economic Importance.
Symptoms.
Pathogenicity.
Variations in Pathogenicity of Different Isolates.
Cultural Characteristics of Isolates.
Relationship of Parasite to Host.
Pathological Histology.
Mode of Infection.
Growth of Parasite in the Host.
Deans by Which Fusarium.bulbigenum.giveum.Induces Wilting
Varietal Resistance.
Summary.
Bibliography.
Description of rlates.

LIST OF PLATES

PlateSI and 11. Ten day old petri dish cultures
of different strains of Fusarium bulbigenum

niveum.

Plate 111. Cross section of muskmelon'stem from

a Fusarium.infected plant.

Plate IV. Cross section of a muskmelon seed coat

internally infected with the wilt fungus.
Plate v. Hybrid melon (Pollock x afg. 126067).

Plates VI. Hybrid melon (Honey Dew x afg. 126063).

Studies on Huskmelon Wilt, Caused by Eusazium
bglbigenum Cke. and mess. var.

m Wr.f.2.

INTRODUCTION

Muskmelons have been produced for several years
as a profitable crop in California, Arizona, Colorado;_
Texas, Michigan. Maryland, and.many other states.'
Within recent years. the muskmelon acreage has in-
creased somewhat rapidly and the season of consumption
has become longer. The shipping season in commercial
regions begins about the first of May with shipments
from.the Imperial Valley of California and some sections
of Texas and Florida. The peak of carlot shipments is
reached in June and July with late shipments from.Mich-
igan, Indiana, parts of Colorado and California. Accord-
ing to statistics compiled by the Bureau of Agricultural
Economics the total acreage of commercial muskmelon pro-l
duction for the United States in 1938 was 123,250, with
an approximate yield of 15,103,000 crates.

lflchigan ranks sixth.in production of muskmelons
representing a crop income of approximately $717,000
annually. In the past the growing of muskmelons as a

part of a systematic crap rotation tended to minhmize

the injurious effects of diseases. More recently, due
to increased intensive cultivation, and a lack of avail-
able land for rotation, diseases have become limiting
factors in.muskmelon production. In the intensive musk-
nwlon growing areas in southwestern Michigan losses of
25 to 65 per cent of the crap have been reported from
leaf spot or blight. Anthracnose and mildews have been
limiting factors in other production areas. Among these
serious diseases is a comparatively new one known as
Fusarium.wilt. Because of its apparent rapid and wide
dissemination, and a lack of effective control measures,
other than by growing resistant varieties, its further
investigation is desirable.

fiistogy 91 the Disease

Fusarium.wilt of muskmelons is a relatively new
disease. It was first described in detail by Leach
and Currence (l) in 1938.

In 1898 Sturgis (2) observed a Fusarium.fruiting
on the stems of a wilted.muskmelon in a field where
bacterial wilt was prevalent. He made no inoculations,
but suggested that it might be in part responsible for
the very prevalent wilt diseases of muskmelons. He
states that the organism was a species of Fusarium

possibly the same as the one associated with wilt of

watermelons.

In the same year Selby (3) reported a wilt of cucump
hers and muskmelons and stated that it appeared “to be
due to the same or to a similar fungus to that causing
the southern watermelon wilt described by E. F. Smith."
He made no inoculations and did not study it further.

Stone (4) in 1911 described a Fusarium.stam rot of
cucumbers and muskmelons in the greenhouse but did not
identify the pathogen.

In 1920 Taubenhaus (5) “published a report on Wilts
of the Watermelon and Related CrOps,' but no reference
is made to a Fuserium.wilt of muskmelons.

A.serious disease of muskmelons in France was de-
scribed by DufrEnoy (6) in 1921. According to the author
the disease appears to be due to a Fusarium.which.he iden-
tifies as Fusarium solani var. gyagum sub. var. (7). His
description of the symptoms and studies of the organism
indicate that this disease was probably the same as the
disease in question.

Cook (7) in 1923 called attention to a disease of
muskmelons in the greenhouse. Symptoms appeared as brown
streaks on the stems from which he isolated a pure cul-
ture of a Fusarium, 'very similar to Fusarium.v§§infectum.'
no inoculations were made to determine its pathogenicity.

WOllenweber (8) isolated a Fusarium.from muskmelon

fruits in Canada, but no wilting of plants was observed.

Fusarium.wilt of muskmelons was reported fromiNew
Yerk in 1930 and 1931 by Chupp (9), from.lunnesota by
Leach.(10) in 1931 and was first found in Berrien County
lflchigan in 1936.

Distzibution

The Fusarium.wilt of muskmelons is reported as
spreading and becoming increasingly destructive in
several states. In 1937 the disease was reported
from Connecticut and Washington (11). Chupp reported
a gradual spread of the disease in Mbnroe and Niagara
counties in New Ybrk, and Leach reported a 2 per cent
loss in.NUnnesota (11). The same year zgsariwm‘pgly
bigenum.piveum.wilt was reported from.New Ybrk by O.
A. Reinking, Who stated that specimens had been sent
in from.Schenectady and Lockport (12).

In 1939 Fusarig sp. causing muskmelon wilt in .
New York was reported by Chupp as follows; “Gradually
spreading in Ontario Lake District. Observed it in
Schenectady county for the first time.” (13)

zygarium.bulbigenum niveum f.2 in lflnnesota was
reported more destructive than for several previous
years and was spreading and becoming more destructive
each year, according to Carl J. Fidel (13).

The disease has also been reported from.haryland
(14), and from.nflssouri (15).

Fusarium.wilt is becoming particularly hmportant in
Michigan. It was found in Berrien County first in 1936
where approximately one to two per cent infected plants
were found in one large field. Since that time isola-
tions have been made by Muncie and KenKnight from.Van
Buren, Bay, and wayne Counties. Reports from growers
indicate that the disease has occurred in one or two other

locations in the state.

Dc ongmig Impoztance
Fusarium.wilt is capable of destroying_75 to 90 per

cent of a crop during favorable seasons where the soil is
heavily infested. Ninety per cent losses have been re-
ported from.linnesota by Leach (1). KenKnight andeewis,
in a survey of the muskmelon areas of Berrien County lich-
igan in 1939 report the following observations: 'In a
small field, perhaps two or three acres, where Seaton's
‘melons were, the vines were nearly all dead except for

the Seaton selections. The five rows of selections were
on the edge of the field. None of the vines were dead
although some of them were badly spotted with lacrospor-
ium. We found, upon carefully surveying the rest of the
field, only five living plants. These were not especially
badly blighted by lacrosporium. It was concluded that
Fusarium wilt was the cause of the death of the other
plants.”

In the summer of 1940 the writer found five to ten

per cent Fusarium.wilt in several fields in Berrien County.
In some of the fields bacterial wilt was prevalent and an
exact estimate of Fusarium wilt could not be made.

An estimate of the actual annual 1083, due to Fusar-
ium wilt, in muskmelon production cannot be determined

until a.more extensive survey is made.

Symptoms

Six general symptoms of Fusarium wilt are known.
These are: damping off, seedling wilt, seedling_rot,
wilt of more mature plants in the field, stunting, and
root canker. In heavily infested soil seedlings may
die before they emerge. (These symptoms may be confused
with.damping off caused by other fungi. Seedling wilt
is first observed as a wilting of the cotyledons, char-
acterized by a loss of turgidity and.a limp feeling
when taken between the fingers. These cotyledonary
leaves may wither and dry up before further wilting of
the plant occurs. Later the entire seedling droops
over, and if pulled the root appears brown with necrotic
or rotted tip. On older seedlings especially in cool
soils, the disease acts as a root rot, the parts below
ground being completely necrotic. Small local lesions
may he found on the hypocotyl, or the plant may wilt
without any evidence of local necrosis. The seedling
symptoms are found to be closely correlated with temper-

ature and moisture factors.

The first symptom.on older plants is nearly always
a wilting of one or more runners. The wilt generally
starts at the tip of the runner. In the early stages of
wilting, plants wilt during the day and regain turgidity
at night. Before the plant is completely wilted necrotic
lesions may appear on the stem near the ground line.
These lesions usually involve only one side of the stem
extending for some distance as a long narrow brown streak,
but sooner or later the whole plant wilts and dies. The
necrotic lesions on old stems first appear as dark green,
collapsed tissue that later turn brown. Droplets of red
gumplike material are secreted from.these stem lesions
and harden on the surface. If.moisture conditions are
favorable necrotic lesions on plants become severed with
salmon pink masses of fungus spores. The roots_of infected
plants appear browned or necrotic often cankered of split.
The necrotic areas may involve only the hypocotyl but more
generally the entire root system. If cross sections are
cut through.the stems of wilted plants the vascular bundles
show brown streaks. This is a characteristic symptom that
can be used to distinguish Fusariwm wilt frmm bacterial
wilt. {

If the plants remain alive until the fruits are set,
infection of the latter may occur. This infection appears
as a rotted area at the stem end of the fruit which later

becomes covered with pinkish-white myoelial growth.

Two additional symptoms have been observed on plants

growing in the greenhouse and to a lesser extent in the
field. The first is a chlorotic spotting of the leaves
and stunting of the plants. Later these chlorotic

leaves or spots appear as scorched areas. The second
symptom.is characterized by short internodes and an ex-
cessive number of male flowers near the ends of the run-
ners. The flowers are smaller and usually paler in color
than normal ones. These last symptoms have been observed
repeatedly, and where they did occur, the plants were

dead from.Fusarium wilt later in the season.

Pathogenicity

Variations in Pathogenicity of Different Isolates_

Cultures of the muskmelon wilt pathogen were obtained
from.diseased field.material by surface sterilizing pieces
of stems or roots with.mercuric chloride and plating on
potato dextrose agar. When the fungus grew out of the
material transfers were made to tubes of potato agar.
These were kept in stock culture. Three of the isolations
used in this work were obtained from Leach in Minnesota.
Transfers from these were made for the stock cultures.

All cultures thus obtained were used in subsequent infec-
tion experiments.

A typical infection experiment consisted in growing
the Fusariwm isolate to be used in sterile oats contained
in a wide mouth flask. After four or six weeks, when
growth had spread throughout the cats, some of the material

was mixed with sterile soil in which muskmelon seedlings

were then grown either by planting seed directly in the
inoculated soil or by transplanting seedlings that had

been growing in sterile soil, to the inoculated soil.
Infection and typical wilting of the seedlings resulted
from many such experiments. Some of the isolates did

not produce wilting, however. These were discarded as
being of very low pathogenicity or else a saprophytic
form.of Fusarium that closely resembled the Fusarigm.bglpie
g§_r_i_up_i Niveum causing muskmelon wilt.

In the infection experiments a wide variation was
observed in the pathogenicity; namely, length of time for
wilting and severity of infection, of the different iso-
lates. Investigations were then conducted to describe
variations of Fusarium.bulbigenum niveum as to pathogen-
icity and cultural characteristics.

A limited number of isolates were used in these ex-
periments. Selections were made on the basis of cultural
characteristics and location from which the original iso-
lation was made. Some of the isolates have been in culture
for two or three years, but the greater number were iso-
lated by the writer from diseased plant material. The
sources of the isolates used in this investigation are
shown in Table 1. .Each isolate is designated by an Arabic

numeral.

10

Table 1- Sources of isolates used in investigation

 

 

 

Trace or Form or Date Of

Isolate collection materia1_r Contributor igplation
1 Minnesota culture Leach 1937
11 Minnesota culture Leach 1937
12 Ingham Co.Mich. melon vines Miller 1940
14 Runnesota culture Leach 1937
15 Bay Co.Mich. culture KenKnight 1939
16 Ingham.Co.Mich. melon vines Miller 1940
21 Berrien Co.Mich melon vines Miller 1940
23 Wayne Co.Mich. culture Kenknight 1939
25 VanBuren Co. Mich culture Muncie 1938
26 Berrien Co.Mich melon vines Miller 1940
27 Berrien Co.Mich.melon vines Miller 1940
30 Berrien Co.Mich melon vines Miller 1940
31 Berrien Co.Mich melon vines Miller 1940
50 Berrien Co.Mich melon vines Miller 1940

 

w

In order to obtain a pure strain for each of the iso-
lates used, monoconidial cultures were made by using the
micro-manipulator method. A spore suspension was made
from each tube culture of the isolate. Single spores were
picked from a drop of each suspension with the micro-needle
and placed on agar drOps suspended on cover glasses over Van.
Tieghem cells in sterile petri dishes. After the Spores had
germinated bits of the mycelial growth were transferred to
sterile potato dextrose agar plates. Test tube slants were
made from the agar plates by brushing spores from the plate
with a fine needle and transferring to the tube slant.

The different isolates were tested in the greenhouse
on muskmelon seedlings over a period of twelve months.

The plants were grown in six inch pots filled to Within

11

one inch of the top with a mixture of well rotted compost
and sand that had been steamed for twelve hours.

The inoculum used to infect the soil was obtained by
growing the fungus in oat cultures as previously described.
The contents of one flask containing a given isolate were
thoroughly:mixed with.the soil in two pots using equal
amounts in each pot. Fourteen sets of pots were thus pre-
pared with the various strains. Two pots which received no
inoculum were used as checks.

Several series of tests were made using Pride of Wis-
consin variety of muskmelon for the host. This variety was
used because of its comparatively high susceptibility.
Oeually six to eight seeds were planted in each pot. In
some of the tests the seeds were germinated in sterile soil
and four to six uniform seedlings were then transplanted to
the inoculated pots. This latter method assured a.more uni-
form stand and more unifrom wilting of the plants within
each set of pots.

The observed symptoms of seedling infection in these
tests were similar to those previously described. A num-
ber of seedlings grown in the infested soil was found to
be stunted but otherwise normal. In most cases these
plants later wilted from Fusarium infection.

The various isolates were found to differ in virulence.
This condition is clearly shown in Table 2. In this set of
experiments the seeds were planted directly in inoculated

80110

12

Table 2- Results of pathogenicity tests with various
isolates of Fusarium bulbigenum niveum f.2.

 

 

 

Number of Number of Percentage of
Isolgte plants plants wilted plants wilted
l 11 6 54.5
11 10 1 10.0
12 10 8 80.0
14 9 5 55.5
15 11 4 36.2
16 10 2 20.0
21 11 2 18.0
23 8 2 25.0
25 10 6 60.0
26 9 1 11.0
27 11 1 9.9
30 9 0 0
31 11 3 27.2
50 9 4 44.4
check 12 0 0

 

i

 

Plantshwere approximately 18 days old.

The length of time required to produce the first
symptoms of infection varied also with the different strains

as shown in Table 3.

13

Table 3- Virulence of 14 isolates expressed in percentage
of plants wilted based on time required for

 

 

 

 

 

 

 

 

 

wilting.
“Parcentage of plants wiltingi
‘Number of Days after_pl§pp;pg;

Isolgte plgnts 6 8 10 ;1_____
1 8 0 12.5 25.0 100.0
11 8 O O 12.5 25.0
12 8 25 62.5 100.0 100.0
14 8 0 50.0 50.0 100.0
15 8 0 37.0 75.0 100.0
16 8 50 87.5 87.5 100.0
21 8 0 0 25.0 75.0
23 8 0 O 62.5 75.0
25 8 O 12.5 25.0 25.0
26 8 0 0 25.0 78.5
27 8 0 0 0 0
30 8 0 12.5 25.0 37.5
31 8 0 12.5 12.0 25.0
50 8 0 25.0 62.5 100.0

check 8 O 0 0 O

 

Strain 12 produced the greatest amount of wilt in a

given period of time; strain 16 ranked second, and strain

‘15, third.

more virulent in the early part of the experiments.

However, in some instances other strains were

These

three strains were consistently pathogenic and highly

virulent.

Throughout the experiments several other strains

produced an equal percentage of wilting but over a longer

period of time.

The results of these experiments indicate the presence

of strains of the muskmelon wilt organisms.

However, some

of the variations noted may be due to uncontrollable fac-

14

tors such as distribution and growth.of the organism
throughout the soil, root injury of the host, natural
variations in susceptibility of individual plants and
slight natural variations that might occur even within
a single strain of the pathogen. Discrepancies also
occur between recent isolations and those that have
been kept in culture for some time. .It was noted that
a single passage of a Fusarium.strain of the latter
through the host markedly increased its virulence.

The stability of any isolate or strain cannot be
considered permanently dependable. In several cases
the reisolations from.infected plants in the greenhouse
were not macroscopically like the parent isolate. Never-
theless, all of this does not lessen the fact that in the
field one may pick up strains with varying degrees of viru-

lence, and a resistant or susceptible plant is conditioned

by the virulence of the particular strain of the organism.

Cultural Chgracteristics of Isolates

 

Studies were made on the cultural characteristics of
the fourteen isolates when grown on potato dextrose agar.
Each of the isolates was reisolated from.wilted seedlings
from.the pathogenicity tests and plated on agar. When
growth had spread over the plate uniform disks were cut
from each of these and transplanted to fresh agar plates.
Cultures were classified according to macroscopic appear-

ance of the colonies using criteria similar to those used

15

by Wellman in describing cultural characteristics of
strains of w W (16). Briefly described
the cultural classes are:

Com letel a ressed, A; flat slimy, appressed to
the agar, no fluffy aerial mycelium; mat forming a tough
film over the agar; color, vinaceous purple (17) but
ranging to pink or buff.

angzmggiapp_pppppgggd, 1A5 Most of mat slimy, tough
appressed, but small tufts or bunches of white cottony
aerial mycelium; color, pale purple or salmon.

Intermediate paised, IR; Underneath.mat appressed,
slimy, vinaceous purple to pink, mostly covered with thin
water-soaked, white aerial mycelium.

Fully raised, R; Mat raised, velvety, compact, white,

 

with two or three purple or buff colored rings seen from
the bottom of the plate.

The greatest difference in growth characteristics of
Fusarium bulbigenum niveum.strains were observed on ten
day old growth on potato dextrose agar. Table 4. The
cultures were held at room temperature and in diffused

light.

 

 

 

 

 

. .
{.5

h v

. A. I.lpr.. i?h..rl|

16

Nberoscopic growth characters of 14 Fusarium
bulbigenum piveum isolates grouped according to
culture classes.

W

Type of

Table 4-

 

 

Culture Isolate mat Aerial Growth
Wowtm micelisa CM
11 appressed none buff with 5.5
slimy small red
A center
14 do. do. purple and 5.0
white
streaked
21 appressed cottony purple with 5.0
dry white white
tuft in margin
center
IA
23 appressed white, white
slimy scattered, transparent 5.0
water-soaked
26 appressed scanty white to 5.5
dry very small buff, light
scattered and darker
white tufts rings
IR 16 Slightly scanty purple and 4.5
raised growth white
dry over all streaked
white
woolly
l slightly scanty white with 5.5
raised growth pink
dry over all streaks
white
cottony
IR 15 slimy white pale pink 5.0
appressed water-soaked to buff
margin thick at
center
50 raised white yellow 5.0
' " hair-like center,
growth white
over all margin

17

 

Table 4- pontinued:

 

 

Type of ‘ A
Culture Isolate met Aerial iGrowth
grpup pumbe; gpowth pypglipgp Cplpr p_;p:Cm.
31 do. white very faintly 8.0
tall hair- pink
like threads
27 do. thick white white, 4.0
cottony small pink
tuft blotches
R
12 do. very thick white to 3.5
white felt- slightly
like yellow
30 do. white thick faint pink 5.5
velvet-like to yellow
25 do. thick white 6.0

woolly

In spite of the marked difference in appearance of the
strains of Fusarium bulbigenum.niveum.(Plates I and II) the
writer found no close correlation between cultural character-
istics and pathogenicity. Strain 12, the most highly viru-
1ent,occurred in cultural class R, with abundant, white, felt-
1ike aerial mycelium. Strains 15 and 16, next in rank of vir-
ulence, occurred in chase IR, with.underneath.mat appressed,
vinaceous purple to pink and covered with thin white aerial
.mycelium. Strain 14, slightly less virulent, occurred in
class A, with a tough appressed mat, vinaceous purplein
color, slimy, and without aerial mycelium. On account of
the relatively small number of cultures grown and with the

fine distinctions between the rather numerous - 14 - patho-

18

genicity classes, irregularities in the general trends
are unavoidable. A closer relationship might be shown
between cultural types and pathogenicity with more ex-
tensive experiments. It was noted in this work that a
greater percentage of highly virulent strains did appear
in the groups with light colored abundant aeria1.mycelia1

growth.

Relationship of the Paragite to Host

Pathological Histology

Mode of Infection
Histological studies were made by killing and fixing

diseased material with chrompacetic acid, washing and em»
bedding in paraffin in the usual manner, and cutting with
a microtome. Different stains and staining technic were
employed depending upon the type of material and the sec-
tions. Sections were mounted in balsam. In some of the
studies free hand sections were employed. In every case
where sections were made for histological studies some of
the same material was surface sterilized and plated on
agar. From these plates reisolations of Epsarium bulbigenum
niveum F2. were made and the pathogenicity of the organism
determined by infection experiments. This procedure elimin-
ated the possibility of dealing with a saprophytic fungus
that might have been present in the sectioned material.
Observations and histological studies indicate that

19

infection may occur through the root tip or hypocotyl.
In wilted seedlings the hypocotyl often appears browned
and cross sections show mycelial strands and necrotic
areas in the tissue, the root showing no indication of
infection. In some seedlings a necrosis of the tips of
the roots is the first histological symptoms of the dis-
ease. In older plants infection may occur through the
root tip or through small cracks or injuries at the base
of the stem Just at the top of the ground. The writer
has observed that stems of rapidly growing succulent
plants in the greenhouse often crack at the ground level.
Infection may occur through these cracks.

It is not definitely known by what means the tip of
the germ tube or mycelium penetrates the outer cell wall
of the epidermal cells, where infection occurs through
the root tip, but it is probably accomplished by the ex-
cretion of some dissolving enzyme. These cell walls in
the young root tip are not especially thick and do not
seem to be cutinized. In the staining they do not stain
more deeply than do the other cell walls of the cortical

tissue.

lggpwth of the parasite in the host

Immediately upon penetration of the epidermal cells,
a food relationship is established with the host and the
germ tube becomes rapidly growing mycelium. Growth is

intracellular and the cell walls seem to offer little

20

resistance to the passage of the hyphae. The fungus
spreads rapidly in the vascular tissue, and growth.may
spread into the cortical cells. (Plate III). While

the greatest amount of vegetative growth occurs in the
vascular tissue near the point of infection it is not
limited and may grow for great lengths through the vas-
cular bundles. Cross sections of a fruit peduncle five
feet from.the point of infection showed hyphal strands in
the vascular tissue. At this point the mycelium.seems
to be confined to the vessels. The fungus is probably
not able to penetrate the walls of these old lignified
vessels. It has been noted that the mycelium here is
very scant. The explanation is probably to be found in
the meager supply of organic food in the vessels.

Some disintegration of cortical and vascular cells
along with a distinct browning occurs at the place of
infection and where the vegetative growth of the fungus
is abundant. Cross sections of stems at the point of in-
fection when stained lightly retained this brown color,
and often showed crystal-like darker stained inclusions
in the disintegrated tissue.

Leach and Currence (1) report that long distance
dissemination of.muskmelon wiltis accomplished by means
of infected seed. They observed the mycelial strands of
wilt fungus under the seed coat in sectioned seed from

rotted fruits.

21

Further investigations were.made by the writer on
this problem. Seeds were taken from infected portions
of fruit, washed free of the placenta and killed in
picric acid. The seeds were thoroughly washed and em»
bedded in paraffin. Sections 14 microns thick were cut
with a rotary microtome, stained several hours with saf-
rinin, counterstained with light green and mounted in bal-
sam. Upon examination, mycelium was found to be present
in the thin walled tissue of the seed coat and in the re-
.mains of the nucellus. (Plate IV). This mycelium.may
possibly have entered through the funiculus or micropyle.

Further evidence of seed infection was obtained by
surface sterilizing some of the seed from infected fruits
with.mercuric chloride and plating on sterile agar. When
germination of the seed occurred the fungus mycelium grew
out from.the inside of the seed along with the developing
embryo. It was also noted that the surface of seed from

infected fruits carried the wilt pathogen.

means by Which Fusariumpbulbigenum niveum.Induces Wilting

Two theories have been proposed to account for wilting

 

in plants induced by different species of bacteria and fungi.
The mechanical plugging theory was cited by Stewart (18) in
1897 and by Smith (19) in 1899. This theory suggests that
the growth of the organism within the vessels and the forma-
tion of gums and tylosses cut off the water supply and con-

sequently the plant wilts. More recently it has been shown

22

that certain fungi and bacteria when grown on broth.media
produce substances that are toxic to plants and cause
wilting in this way. This latter theory is more generally
accepted now, and it is with this theory that the writer
is concerned here.

One of the first to experiment on the factors involved
in the wilting of a plant attacked by a microorganism was
Hutchinson (20) of India. In 1913 working on a disease .
of tobacco which he considered to be caused by Bacillus
solanacearum, he fed plants a substance which had been
precipitated by alcohol from pure bOuillon cultures of the
pathogen. The plants which obtained this substance de-
veloped wilt while those fed a boiled solution of the same
substance did not wilt. He considered the wilting as,

a consequence of protoplasmic intoxication.

Coons (21) reporting on the work of Goss in 1916 calls
attention to the wilting of potato plants when placed in a
filtrate representing a synthetic solution upon which a
species of Fusarium had been grown. .Control plants placed
in an uninoculated.medium.remained healthy. It was con-
cluded that wilting was due to poisons generated by the
fungus.

In 1919 Brandes (22) published a report on Banana
Wilt in which he included results from.experiments con-

ducted to show the relation between excretions of toxic

substances by the parasite and the symptoms exhibited

23

by the attacked host. He noted that the fungus was not
present in quantities sufficient to cause serious ob-
struction to the passage of water, and concluded from
his work that certain toxins were produced by the fungus
that would produce typical symptoms of the disease.

White (23) working with W W demon-
strated the presence of toxic substances in the filtrate
from broth cultures of the organism. He concluded that
organic acids are present in the filtrate which are toxic
to tomato plants. He also showed that the toxins are
non-specific.

in 1923 Fahmy (24) studied the toxic substances pro-
duced by Fusarium solan;_when the organism.was grown on
Richard's solution. he found that the toxic effect of
the filtrate was not due to the change in pn and showed
that the unknown toxic substance was thermo-stable and
non-volatile.

Picado (25) 1925 attempted to determine the nature
of the substance secreted by palasitic fungi in which
the host tissues are either injured or killed at some
distance frmm the point of attack. he worked with Eggpig
gillium albo-atrum, 1,duboys- both parasites of the potato,
Fusarium.solani from the potato;‘!, cubense, the pathogen
of banana wilt; and with a saprophytic Penicillium. The
results indicated that the withering of the plants, the

browning of the vessles, and the destruction of the tissue

24

were not all produced by the same causes, although in
each instance evidence was seen of the action of sub-
stances having toxic properties, such action resulting

in the symptoms produced by the different diseases.

After extracting the albuminoids, enzymes, and toxins
from the mycelium.with alcohol and concentrating the
liquid he obtained a waxy brownish residue. This proved
to be thermo-stable and very toxic to plants. Picado's
conclusions are that 'the poisons produced by the fungi
are not true toxins in the sense of toxins against which
immunization is possible. They may be compared in action
to poisons found in some mushrooms, such as Amanita
toxins.” He suggests that the action at a distance from
certain parasitic fungi may be due to a chronic poisoning
of the plant.

Rosen (26) in 1926 working with filtrates from broth
cultures of Fusarium.vasinfectum.concludes that there are
at least two toxic substances present in the filtrates.
One is a volatile compound slightly alkaline, and the
other is an organic salt in the form of a nitrite.

Ludthe and Ahmet (27) in 1953 attempted to isolate
the toxin from.culture fluid of,§usarium.vasinfectum by
drying in vaccum and extracting with methyl alcohol.

This residue showed high wilting power. It was further
purified until an 0.5 per cent solution killed plants in
a short time. According to the writers the substance is

a viscous hygrOSCOpic brown amine.

25

The common method used in proving the presence of
toxic substances is to grow the pathogen on some nutrient
medium, filter the organism.from the medium, and place
the plants, usually with their roots cut off, into the
filtrate. This method has been used by the writer. In
Table 5 are given in brief outline form the experiments
conducted and the results. In all the experiments vigor-
ously growing seedlings were used. They were pulled,
their roots cut off under water, and the plants trans-
ferred to test flasks or tubes containing the filtrate.

The filtrates used were obtained by growing the
organism.on CoonS' synthetic medium.for six weeks and
then filtering the medium through a Berkefeld, type N
filter to remove all the spores and bits of mycelium.

The filtrations were made under aseptic conditions. The
filtrate was then tested for sterility by plating on agar.
No growth occurred, which indicated that results obtained
from the ensuing experiments could not be due to infec-

tion of the plant with the fungus or other organisms.

26

Table 5- Action of various filtrates obtained from broth
cultures of Fusarium bulbigenum niveum.

 

 

 

W A
Treatment of No. of No. Time for
Exp. no. filtrate Plants lants w lted wiltin
I(a) filtered musk- , 5 5 15 hours
Berkefeld N. melon
1(b) medium.un— do. 5 O
inoculated
2 filtered do. 5 5 15 hours
BerkefEId No '
3(a) do. tomatoes 5 3 25 hours
5(b) do. beans 5 5 24 hours
4 autoclaved musk- 5 5 15 hours
15 pds. (melon
5(a) Dil'n. l-l do. 3 s 24 hours
5(b) Dil'n. 1-2 do. 3 5 33 hours
5(c) Dil'n. 1-5 do. 3 2 33 hours
6 filtered . 5 4 55 hours
Berkefeld N. do. with
roots
W M

 

Experimentsl(a) and 1(b). The results of these exper-
iments demonstrate the presence of toxic substances in the
filtrate from broth cultures of Fusarium.bulbigenum niveum.
Wilting of all the plants which were placed in the inocu-
lated medium.occurred in fifteen hours with no recovery‘
when transferred to water. The plants which were placed in
the uninoculated medium showed no wilting after twenty-four

hours.

27

Experiment 2 was designed to show the effect of the
pH change in the medium.on the plant. A portion of the
inoculated.medium.was adjusted to the original pH of the
broth and again tested on plants. Wilting of the plants
occurred after fifteen hours which indicates that the
toxic effects of the filtrate are not due to the pH of
the'solution.

Experiments 3(a) and 5(b) show the non-specific
properties of Fusarium bglplggpgm,p;1§pm,toxin. When
bean and tomato seedlings were cut off under water and
placed in portions of the toxic filtrate typical wilting
occurred. ‘

Experiment 4 was designed to see if the toxic proper-
ties of the filtrate were inactivated by heating. A
portion of the filtrate was autoclaved at fifteen pounds
pressure for twenty minutes. It was then checked on cut
stems of muskmelon seedlings for wilting. After fifteen
hours all the plants showed typical wilting. The results
indicate that the toxin produced is thermo-stable.

Experiment 5 shows the effect of diluting the filtrate.
Dilutions 1-1, 1-2 and 1-5 were made using distilled water.
Each dilution produced wilting of the plant but the higher
the dilution the longer time required for wilting.

Experiment 6 shows that the toxic substance can be
absorbed by the unbroken roots. Wilting occurred ten

to twelve hours later in this case than when the roots were

28

cut from.the plants before placing them in the toxic
filtrate.

In brief, the results of the foregoing experi-
ments demonstrate the production of a toxic substance
by Egggglpm bulbigenum gizgum_Which is capable of pro-
ducing wilt in plants. The toxic substance is thermo-
stable and non-specific. It is effective in compara-
tively weak concentrations, and can be absorbed by the
roots of the plant.

To determine the chemical nature of the toxic
materials produced by Fusarium bulbigenum niveum the
following chemical studies were undertaken. The meth-
ods used were, in the main, standard procedure for the
isolation and identification of organic compounds from
fungus material or from solutions which contain the
substances. The materials used were fungus mats which
had been growing on Richard's solution for six to eight
weeks, and the filtrates obtained from the solution.

The fungus mats were dried to constant weight in
a 65 degree oven and ground to a fine powder with a mor-
tar and pestle. The powder was shaken up with water,
warmed over a low flame and filtered. The filtrate was
tested for toxic properties on cut muskmelon stems.
all plants placed in the filtrate showed distinct wilting
at the end of two hours, and after twelve hours they were

completely wilted and drying. No recovery occurred when

29

they were transferred to water.

Some of the filtrate from.the fungus mats containing
the water soluble material was shaken up with 80% alcohol
and filtered. The residue, a slight, brownish, gum-like
mass on the filter paper, was but slightly soluble in
ether, insoluble in 80% alcohol and soluble to slightly
soluble in water. Minute traces in aqueous solution were
highly toxic to muskmelon plants.

The flaky brown substance which contained the toxins
was analyzed chemically according to the procedure given
by Mann and Saunders (28). Nitrogen determinations were
made using the Lassaigne Sodium Test. Some of the sub-
stance was heated with.molten sodium, extracted with
water, boiled with ferrous sulphate, and treated with
ferric chloride. HCl was then added and a Prussian Blue
precipitate settled out, thus giving a positive test for
an organic nitrogen compound. The Lassaigne Sodium Test
for sulphur was negative.

Ammonia was evolved on heating when the substance
was treated with concentrated NaOH solution. Treatment
with dilute sodium.carbonatesolution liberated carbon
dioxide. In addition to these reactions the substance
reacted with nitrous acid evolving nitrogen. The fore-
going reactions indicate the presence of an acid amide,
acid nitrile or imide of dibasic acids. Further attempts

to isolate a definite compound were unsuccessful.

30

Attempts were made to isolate the toxins from the
culture medium on which W W 2.211299; had
been growing. The solution was filtered free of all the
fungus material and shaken up with 80% alcohol. A heavy
buff colored precipitate settled out, which when filtered,
dried, and redissolved in water, produced typical wilting
of plants in 12-24 hours. This.material precipitated
from.the culture medium gave similar reactions to those
given by the toxic.material extracted from.the mycelial
mats. Some further tests were conducted. A benzoyl
derivative was made from.the toxic substance using the
Schotten-Baumann reaction. A small amount of the pre-
cipitate was treated with.Na0H. Two to three cubiccen-
timeters benzoyl chloride were added and the mixture
was shaken vigorously for five minutes. A thick suspen-
sion resulted. The solution was then filtered and the
residue washed with water, transferred to about 15
cubic centimeters absolute alcohol in a small evaporating
dish,.mixed thoroughly, heated to boiling and again fil-
tered. The alcoholic filtrate was cooled and a very fine
white precipitate settled out.) This benzoyl derivative
was thoroughly dried on a slide in air and the melting
point determined. This ranged from 79-86 degrees centi-
grade. Further attempts to purify and identify this com-
pound have so far been unsuccessful. The melting point

and other reactions of the derivative indicate the presence

51

of an amine in the original substance.

All chemical tests were necessarily made with minute
quantities of the material, and certain tests were not
always clear cut. Purification and identification of
the toxins produced by Fusarium bulbigenum niveum respon-
sible for the wilting of muskmelon plants awaits further

investigation.

Egggggglqresistance

Some progress has been made in developing muskmelon
strains resistant to Eusarium bulbigenum glzggm, Hybrid
melons more or less resistant to the wilt disease have
been developed at the Minnesota Experiment Station (29).
Some work has also been done at the Michigan Experiment
Station and similar work is in progress at the Maryland
Station (14).

Since resistant varieties are necessary for control,
and no entirely satisfactory ones have been develOped that
meet the requirements of the Michigan grower, further breed-
ing and selection work was begun by the writer at the Mich-
igan Experiment station in 1940. The data and observations
that follow form.a progress report of that work.

For parent stock use was made of two Minnesota hybrids,
wilt resistant 10-58, and 11-58, several commercial varieties,
and several varieties of Afghanistan muskmelons. The seed

of the latter varieties were obtained through H. L. Seaton,

32

Horticulture Department from W. E. Whitehouse, Senior
Horticulturist of the United States Department of Agri-
culture. The Afghanistan varieties were used because
they represented possibly more closely the wild strains
of muskmelons in the hope that they would show more re-
sistance to the wilt pathogen than the highly developed
American commercial varieties.

The first plantings were made in the greenhouse in
heavily infested soil. Crosses and self pollinations
were made throughout the flowering season. A high per-
centage of the pollinations set under greenhouse condi-
tions. From the resistance vines a great many selections
of both the crosses and self-pollinations were obtained
for further study.

‘In Table 6- a comparative index of resistance under
greenhouse conditions for the commercial varieties used
in the breeding work is given.

Table 6- Index of wilt resistance of seedlings of certain

varieties of.muskmelons planted in the greenhouse
infil940.

 

Initial Percentage of plants
Variety # Name of variety stand wiltin
Days after planting
__ 15 24 30 _gl

 

#45 Mildew Resistant 42 19 54 64 85
Honey Rock 36 33 55 61 86

10-38 lfinn. Wilt Resist. 36 8 12 16 22
26647M‘ T. Whittaker 36 ll 33 5O 75
10-25 Pollock 42 5.5 26 26 30
11.38 Minn. Wilt Resist. 34 2.7 8.3 8.3 8.3
‘*3-8(l) Hearts of Gold 42 10 25 60 65
*2-18(4) Hearts of Gold 42 12 52 54 70

 

 

 

 

 

‘*I&eld selected Hearts of Gold

33

The Afghanistan varieties are not included in this
(table, for most of the ones used Slowed a much higher
degree of resistance under the conditions of the test.
They did, however, show symptoms of infection, but the
greater part of them survived until their fruits were
smature. It was thought that a more accurate check on
the resistance could be obtained by growing them under
field conditions. Growth of the Afghanistan varieties
in the greenhouse was much.more vigorous than that of
the commercial varieties. Fewer fruits were set and
they were large and of very poor quality and flavor.
The breeding and selection work was continued in
the field during the summer of 1940. Plantings consisted
of previous greenhouse selections of both crosses and
selfs based on degree of indicated resistance and commer-
cial possibilities, and were made in heavily infested soil.
The method of hand pollinating in the field consisted
in covering both staminate and pistillate flowers before
they opened. At the time of covering, the pistillate flowers,
that were to be used in the crosses, were opened and the
anthers removed. (This was necessary since some of the
flowers on muskmelons are perfect. When the flowers opened
the pollen was applied and the pistillate flower again
covered until it closed. Considerable difficulty has been
encountered in making hand-pollinations in the field. The

pollination records slow that only four per cent of the

34

attempts were successful.

Minnesota varieties showed almost total resistance up
until the melons begin ripening. However, before the fruits
were gone some of the vines had succumbed to wilt. The
ribbed Minnesota hybrid #10-38 showed greater possibilities
than #11-38 under Michigan conditions. The Afghanistan
varieties were much less resistant under field conditions
than they had been in the greenhouse. However, several of
the hybrid selections did show promise. Below is a short
description of three selections from selfs made on these
hybrids.

Selection 9-40 (hybrid-Pollock x wigglgeoev)
This strain is highly resistant to Fusarium.
The fruit is elongate to oval, slightly netted,
large and somewhat variable in shape. The size

of the seed cavity is rather large, quality of
flesh poor. Plate V.

§§lection 21-40 ihybrid-Honerlnew x Afg.126063)

The fruit of this strain is slightly oval to
round, yellow when ripe. It is ribbed and
distinctly netted. Flesh is yellow, seed
cavity small, quality fair. The vine is
coarse and vigorous, with moderate to high
resistance. Plate VI.

Selection 17-40 (hybrid-Hales BestlZEAfg.126041)

This selection is approximately 50 per cent
resistant. The fruits are oval, smooth, ribbed,
yellow when ripe. Seed cavity is small and the
quality of flesh good.

 

Some of the commercial hybrids showed varying degrees
of resistance. Selections were also made during the sum-
mer of 1940 from commercial fields in different muskmelon
areas of the state. On Kenneth Johnson's farm in Berrien
County a single hill of Hearts of Gold was found growing
at the end of the season in a four acre field when all
the other plants had either died from.Fusarium wilt or
EmcIOSporium leaf spot. Two fruits were obtained from
this plant for further work in the breeding and select-
ing program.

A further planting of hybrids and field selections
was made in the greenhouse during the winter of 1940-1941.
Additional crosses, selfs and close-pollinations have been
made from which selections will be obtained for further
field plantings. Table 7 gives the relative resistance
of the 1941 greenhouse plantings.

Table 7- Index of wilt resistance of certain selections of

muskmelons grown in the greenhouse during the win-
ter of 1949-1941.

 

 

 

 

 

 

 

 

 

 

W - i.—
Percentage of plants infected

Variety or Date of at different dates
selection planting Date observed

. _;g-7-4o l2-20-40__;;l§;gl 2-17-41 412;;2;
*Hearts of Gold 10 15 31 45
Nfinn. 10-38 0 5 20 25
Selection 21-40 0 5 5 10
Mildew Resist. #45 15 2O 35 6O
Selection 9-40 1 10 10 20
Selection 27-40 10 15 30 5O

 

*Field selected from Berrien County - 1940

36

Selection 21-40 was about 90% resistant under the
conditions of the test. Selection 9-40 ranked second
with 80% resistance and the Minnesota hybrid showed 75%
resistance. The field selected Hearts of Gold, while
not as resistant showed a great deal of promise with a

few very resistant individual plants.

Summary

Fusarium wilt is a comparatively new disease of
muskmelons. It is caused by a specific fungus, Egggg-
gpm bulbigenum.niveum F.2, which was first described
in detail by Leach and Currence in 1938. The disease ap-
pears as a distinct wilting of the plants which may take
place during the seedling stage or when the plants are
more mature.

During hot, dry seasons, in soils that have become
infested with the organism, the disease may become of
great economic importance. Leases up to 90% of the
crop have been reported.

The fungus enters its host through small root tips
or through injuries on the roots or the hypocotyl by
means of conidial germ tubes or through direct penetra-
tion by the mycelium. It grows intracellularly setting
up a food relationship with the host. The most abundant
growth occurs in the vascular tissue and may appear at

great distance from the point of infection. Fruits may

37

become infected with the organism in which case wide
spread dissemination is enhanced by transmission of
the fungus on or in the seed.

Physiologic Specialization exists within the
species Fusarium bulbigenum gigggm F.2. Both path-
ogenic and cultural tests have shown distinct differ-
ences in the 14 isolates studied.

Wilting of muskmelon plants infected with Fusarium
bulbgggnum.nivegg‘has been shown to be due to toxic sub-
stances produced by the organism, Chemical analysis of
these substances indicate that the toxins are amines,
amino acids, or other closely related compounds.

The most satisfactory control neasure for Fusarium
wilt has been in the production and use of wilt-resistant
varieties. The relative resistance of certain varieties
is shown in Table 6. It will be noted also that certain
hybrids bred and selected by the writer during the course
of these studies show promise of giving biotypes that will
be much.more highly resistant than the original parent
commercial stock, and by a continued program of breeding
and selection may be developed into pure strains with de-

sirable commercial qualities.

l.

2.

3.

4.

5.

7.

8.

9.

10.

ll.

12.

13.

Literature Cited

Leach, J. G. and Currence, T. M. Fusarium wilt of

Nmskmelons in Minnesota. Minn. Agr. Exp.
Sta. TeChc BUI. 129. 19380

Sturgis, William C. Some common diseases of melons.
Conn. Agr. Exp. Sta. Ann. Rept. 22 (1898):
225-235. 1898.

'Selby, A. D. Further studies of cucumber, melon, and

tomato diseases, with experiments. Ohio
Agr. Exp. Sta. Bul. 105. 1899.

Stone, G. E. Fusarium disease of cucumbers, and other
plants. Mass. Agr. Exp. Sta. Ann. Rept.
23 (Part II): 62-65. 1911.

Taubenhaus, J. J. Wilts of watermelon and related crops.
Texas Agr. Exp. Sta. Bul. 260. 1920.

Dufrenoy, J. Les maladies du melon. Ann. des. Epiphyties.
13 405-420. 1921.

Cook, M. T. A greenhouse disease of melons. Phytopath.
Lg: 462-463. 1925.

Wollenweber, H. W. and Reinking, O. A. Die Fusarien.
Paul Parley, Berlin. 1935.

Chupp, Charles. Fusarium wilt of muskmelons. Plant
Disease Reporter, supplement,§;: 116. 1931.

Leach, J. G..A destructive Fusarium wilt of muskmelons.
Phytopath., 23: 554-556. 1933.

Report on Fusarium.wilt of muskmelons.
Plant Disease Reporter, supplement 110: 289.
1938. '

Reinking, O. A. Cantaloupe wilt is spreading in the state.
N. Y. State Sta. Farm. Res. Bul. 3 (1937)
NO. 40

Eidol, Carl J. and Chupp, Charles. Reports on Fusarium
wilt of muskmelon. Plant Disease Reporter,
supplement 119: 211. 1939.

l4. Mahoney, C. H. Breeding of Fusarium wilt-resistant
cantaloupes. Maryland Exp. Sta. Ann.
Rept. 59; 49. 1938.

15. Chupp, Charles. Plant Disease Reporter, supplement
8;: 116. 1931.

16. Wellman, F. L. .A technique for studying host resis-
tance and pathogenicity in tomato
Fusarium wilt. Phytopath. 22: 945-956.
1939.

17. Ridgway, R. Color Standards and Color Nomenclature.
Hoen and Co. Baltimore, Md. 1912.

18. Stewart, F. C. A bacterial disease of sweet corn. N. Y.
sane Agr. Exp. Sta. Bul. 130. 1897.

19. Smith, E. F. Wilt disease of cotton, watermelon and
cOWpea. U.S. Dept. Agr. Div. Veg. Physiol,
and Path. Bul. 17. 1899. .

20. Hutchinson, C. M. Rangpur tobacco wilt. India Dept.
Agr. Mam. Bact.Ser. 1: 67-83. 1913.

21. Coons, G. H. Report of the Botanist. Mich. Bd. Agr.
Ann. Rept. 55: 256-271. 1916.

22. Brandes, E. w. Banana wilt. Phytopath. 3:339-389. 1919.

23. White, W. P. Studies on tomato wilt. Jour. Agr. Res.
35: 197-239. 1927.

24. Famhy, T. The production by Fusarium solani of a
toxic excretory substance capable of caus-
ing wilting in plants. Phytopath. ,;§:
543-5500 1923.

25. Picado, C. Sur l'action a distance des champignons
phytopathogens. Con. Path. Veg. Stras-
bourg 1923. 28-34. 1923.

26. Rosen, H. R. Factors to determine the means by which
the cotton wilt fungus, Fusarium vasin-
fectum induces wilting. Jour. Agr. Res.
33} 1143-1162. 1926.

27.

29.

Ludthe, M. and Ahmet, H. Uber einen pflanzlichem
Welkstoff. Biochem. Zeitschrift.
257:256-266. 1933.

Mann, F. G. and Saunders, B. C. Practical Organic
Chemistry. Longmans, Green and Co.,
1936.

Currence, T. M. and Leach, J. G. Progress in de-
veloping muskmelon strains resistant
to Fusarium. Proc. Amer. Soc. Hort.
Sci. pg: 481-482. 1934.

Description of Plates

Plates I and II. Ten day old petri dish cultures of dif-
ferent strains of Fusapgum bulbigenum
giveum. Growth on potato dextrose agar.
Isolates l, l2, l5 and 50, intermediate
raised, aerial mycelium. Isolates 11
and 14, mycelium.completely appressed.
Isolate 16, section of raised mycelium.
Isolates 21 and 26 intermediate appressed.
Isolates 25, 30 and 27 raised, thick
aeria1.mycelium.

Plate III. Cross section of a muskmelon stem from
a Fusarium infected plant. From a paraf-
fin section stained with Safranin and
light green. (Note mycelium in the vessels.)

Plate IV. Cross sectioncnf a muskmelon seed coat
internally infected with the wilt fungus.
(a) Thickened cells of the outer seed
coat,(b) Parenchyma cells of inner seed
coat. (c) Densely compressed cells of
the remains of the nucellus. (d) mycelium
of the wilt pathogen..

Plate V. Hybrid melon. Cross between Honey Dew
and Afghanistan variety 126063. Picture -
a selection from the 2nd generation.

Plate VI. Hybrid melon. Cross between Pollock and
Afghanistan variety 126067. Picture -
a selection from the 2nd generation.
(Note netting and size of seed cavity.)

 

PLATE I

 

 

PLATE II

 

PLATE III

 

PLATE IV

 

 

VI

A.

(7“,?

PLA

7

fig...
(I

L‘V’i- T‘fii

 

 

 

n

. . v. . .. n.
. _. t .x . s n . 4... n .
a . .. . vav . . . .. l .. ., . .-
... . ... . . ,. t . . .v . . . .
.. w ., ... u. . . . , . .
.4 ., .
r. . . . , . . .. . .
. ... . . . . . . .. . v 1 .. t . . .
. . . . .. .. . . . . . c A . ,
v. .. a . . . . . n u . . .. . .
. . . . p . . , l. . . . . ... l
o . .. l . .... . u. .. .
. ... . .. . . I , i. . ..., . nu . . , . v
. ~ .. 4 . .. .. .. .., . v . v . . .. .
. . . . a. . . .. u. a . .. .. . . . s 1
. - , -. . a A . .. ... , u. , I»: s. . . , . A
. ... l . . . . . . ‘i
. . l . . . . .
. . . . . . a . . . u r . ._1 \n‘h)
. . ‘ u v. 0 . .I. U. r h I Al .I -t
. .- . . .. .. , , ; . . .. .. . . . . . .
. . . .: .... . . . l. . a . ., . a .. . .. o .
. . . . . l i . .. i .n l . . . I
a . . . . - ,a . . . s . .. I u t . . .
. . . . . .. . , . . .. . e . . . , .,
. . - t . . . . . . . ...
. . . v i . . .
. .. . t . . i. . . . . _ t. o . . 4.. . ... .. ... .. ... v v
v . . . t . , . . . . . . . z t. . . . . .
4 . .\ . I .. l . . n. . . .
.. u, . .. . . . ax .. . . a .
. . . : , I . .. . a. . t .
. . ... . r . . . w ..- . . . i. .- .
. I . . . . .. .
.. .. ..
n . _ .. -
. u y. a
i

. n . \’ . \- I“..V
us‘WN . I

...1... .. ..... ...n .3271: -.....a. .n. 3,... ...: .
. . . I...‘ . Pt I i? \...A. _ .v
.125.” r:- thvéflft Jcflfiw.

a. «‘7,

J .
. J‘s.y
.u

  

 

. I
k

. .u. . , ....
'.l~ 1. .Q. . .0
.~ ”A. ..f‘ ... . $

4‘

. m,

,4. \...\ . . . .
.... 1M. . ..

. .\..7. , 3... o

. . .. . is “sari-.1. is... ......I a...

. x. , . . ..n I . .... . . _ x T‘\.\. ...

\VLJ..... . . Q. . x . .1 . ...J r. . . .. .. . ...; , .. Kul\ 39:41. w.“

_ . . . . . . . ., .... . .. «1...... 9.....4.

s
b...

.. C... .

_ .... .IJII ..
1. . wt.
1.1%.. . 1 ‘r\

a . 4 . . a
...nnakfifltwlrlvvuw» log. .

 

.\
.lo
p

a ..r

a ..
.
... . . , . o . -
. . ...i
. . a t

..

I l‘.
... .

. 5 . _
. J
y

M"

,.-r.
A!

51.
J

r
.‘

¢

+7.

-' INF!" ."

 

.M- I.

‘~ fl

s." '
\
n

‘ V
_‘*'.‘._.

..A ”- :-
n

’-
Ill
'

l
l