A STUDY OF STEWART'S DISEASE OF SWEET CORN CAUSED
BY PHYTOMONAS STEWARTI

BY
C. W. FRUTCHEY

A THESIS
Presented to the Graduate School of Michigan State College
of Agriculture and Applied Science in Partial Fulfillment
of Requirements for the Degree of Doctor of Philosophy

Botany Department
East Lansing, Michigan
1935

ProQuest Number: 10008307

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Ac knowle dgement s
The writer is very grateful to Dr* J* H. Muncie
and Dr. E. A. Bessey for criticism and correction of
the manuscript.

And to Dr. Muncie for help in organiz­

ing the various experiments.
The writer is also grateful to Dr. P. W. Fabian
for criticism and correction of the manuscript.
Acknowledgements are made to Dr. C. H. Mahoney
who kindly furnished seed of a large number of varieties
when they were most needed, and to Professor Ray Hutson
for identification of species of insects.

98853

Table of contents
Introduction -------------------------------------

1

Literature review --------------------------------

2

Economic importance --------------------------

9

Symptoms of the d i s e a s e ------------------.---------10
Methods of inoculation andvarietalresistance ----- 13
Table I
— — 14-16
Infested soil as a source ofinoculum-------------- 13
Infected seed as a source ofinoculum-------------- 19
Table I I --------------- ------------ -----20-22
Table I I I
---- ----------------- -------- 23
Table I V ------------- ---------------------- 24
The role of infected seed in the transmission of the
d i s e a s e ------------------------- ----------------- 26
Table V ----------.....-.....— ------ 29
Figure I ------31
Figure I I ------------------------------------ 32
Figure I I I ----------------------------------- 33
Insects in relation to diseasetransmission ------- 34
Wilt produced by organismsassociated with Phytomonas
stewarti ---------------------Table V I
-----------Table V I I
-----------

38
40
43

Anatomy of corn in relation to w i l t ------------44
Table V I I I ------------ --- -------------- - 46-47
Control --— *-------------------------49
Table I X --------------- ---------------------- 51
Discussion---------------------------------

52

Summary and- conclusions -----------------------

58

Bibliography-------------------- ------------------60

1

Introduction
In the summer of 1932 there was a serious outbreak
in Michigan of bacterial wilt commonly known as Stewartfs
disease of sweet corn*

This disease is caused by the

bacterial organism Phytomonas stewarti (Smith) com* S* A. B.
According to The Plant Disease Survey (31) it also was
prevalent In high percentages throughout the middle western
and eastern Atlantic states as well as being reported in
Ontario, Canada that year*

In the central and southern

counties of Michigan sweet corn fields with 100 percent
infection were not uncommon.

Although the severity of the

disease is influenced by climatic conditions, it has been
present each year since 1932 in smaller quantities with
regional and individual field outbreaks from time to time*
Prior to 1932 Stewart's disease had not caused any serious
trouble in Michigan although it had been found as early as
1898 by Erwin F* Smith in Berrien county in the southwestern
portion of the state.

Since that date a few plants affected

with bacterial wilt have been found from year to year within
the state.
The general epiphytotic occurring in 1932 raised the
question how it was possible for such large amounts of
natural inoculum to have accumulated either within the soil,
plant debris, seed, or insects and to have caused such high
percentages of infection that year without having caused
greater losses prior to this.

2

Studies of Stewart»s disease of sweet corn were there­
fore begun in the summer of 1932.

The various phases of the

disease and its control studied were seed treatment practices,
transmission of the disease by insect vectors, methods of
artificial inoculation and varietal resistance, the soil as
a source of inoculum, the role of infected seed in the
transmission of the disease, and wilt caused by P^ stewarti
and associated organisms.

Literature Review
Bacterial wilt of sweet corn was first discovered in
New York by Stewart (28) in 1894.

Stewart described the

disease symptoms and was able to isolate and culture the
bacterial organism but was unsuccessful in attempts at
artificial inoculation.

The organism was briefly described

and its presence in great abundance demonstrated in the
vascular tissue although its pathogenicity was not established.
In 1897 Stewart sent a culture to Erwin F. Smith
requesting him to name the organism.

After a series of

cultural tests he described the bacterium as a medium sized
rod, rounded at the ends, with one polar flagellum, and gave
it the name Pseudomonas stewarti in honor of the discoverer.
In the same publication Smith reported seeing the disease in
the southwestern portion of Michigan in 1898.

3

Halsted (2) mentions finding the bacterial wilt in
New Jersey in 1899 but states that only one variety, Firstof-all showed symptoms of the disease.
In 1901 Smith (21) published a more complete account
of the cultural characteristics of the organism and in 1903
(22) was able to complete proof that Pseudomonas stewarti
was the causal agent of bacterial wilt.

Inoculating five

hundered sweet corn plants by spraying a bacterial suspension
on the leaves and by placing drops of bacteria in the fluid
oozing from the water pores at the tips of the leaves, typical
infections were obtained.

By both methods of inoculation a

total of more than three hundred plants showed wilt symptoms.
In a publication six years later he (23) concluded that infected
seed was the main source of dissemination of the disease and
that treatment of the seed with mercuric chloride 1 : 1000 for
15 minutes would control it.
Between 1909 and 1914 Smith (24) in a section in Bacteria
in Relation to Plant Diseases and in his book (25) Bacterial
Diseases of Plants, gave a comprehensive report of five years
data, describing all phases of the disease in great detail*
The organism was described and demonstrated in all of the
vascular tissue of the plant including the bas^ of the kernel*
The symptoms were described and infected s«ea as a means of
dissemination was stressed witn a statement that treatment
with mercuric chloride 1 : 1000 for 20 minutes was not an

4

adequate control*
McCulloch (11) in 1918 after making fourteen isolations
of the bacterial wilt organism on corn from several snates
was unable to find motile forms and could not demonstrate
flagella by the use of special stains*

Two types of agar

colonies were obtained, alike in every respect except the
surface view on agar, one having a smooth flat surface, the
other a central depression.

The organism was renamed

Aplanobacter stewarti (Smith) because of the absence of
motility,
Rand and Cash (14) reported in 1921 that the early
varieties of sweet corn were more susceptible than the
later ones with only a trace of wilt in field corn.

They

were able to produce no infection from infested soil nor
old infected corn stalks but isolated the wilt bacterium
from the base of the kernel and from parts of the endosperm,
finding no trace of it in the embryo*

They concluded that

abundant soil moisture and high temperature were principal
factors influencing the development of Stewart’s disease
although they believed that injury caused by insect larvae
was closely correlated with its appearance.

Later (15)

they discovered that the adults of the brassy flea beetle
Chaetocnema pulicaria Horn., the toothed flea beetle
Chaetocnema denticulata Horn., and the twelve-spotted cucumber

5

beetle Diabrotica duodecimpunctata Oliv. were direct agents
of transmission of bacterial wilt and found larval injury
of an unknown origin associated with, the disease plants found
in the controls.

Their previous findings were verified (16)

in 1933 and they suggest that much of the late season
infection is due to insect transmission.

They stated that

infected seed probably plays its major role in the trans­
portation of the disease from one region to another.

Very

low percentages of wilt were found in plants grown in the
greenhouse where insects were controlled.
Reddy (17), experimenting with resistance and sus­
ceptibility of dent, flint, and sweet corn found that none
of them showed any marked resistance.

There was no evidence

of infection from soil previously exposed to bacterial
infestation and it was concluded that seed disinfection was
Ineffective in control.
Reddy and Holbert (18) tested bacterial wilt resistance
of various inbred and hybrid lines of dent corn.

The wilt

organism was isolated from wilted plants of the Golden Bantam
variety, and inoculations were made by means of hypodermic
injection into the stalk of the partially grown seedings.
Wo apparent correlation between resistance and vegetative
vigor was found.
Thomas (29) reported Stewart’s disease prevalent in

6

Ohio in 1924,

The disease was briefly described and the

suggestion was made that the main source of the inoculum
is in the infected seed.

Some of his results indicated

that the organism might cause infection from infested soil.
Later (30) Thomas gave a report on a study of bacteriophage
associated with Pj»_ stewarti.

The bacteriophage could be

isolated from roots and lower nodes of diseased plants
and. from infected seed.

Soaking naturally infected seed

in bacteriophage cultures of relatively high titer, the
percentage of wilted plants were greatly decreased in com­
parison to the controls.

All plants were subjected to the

presence of the twelve-spotted cucumber beetles, flea
beetles, and chinch bugs.
As a result of the epiphytotic of bacterial wilt of
corn occurring in 1932, investigations were initiated at
various institutions and several publications concerning
Stewart’s disease have been released since that time.
Noteworthy among these is the work of Ivanoff of Wisconsin,
and that of Elliott and co-workers of the United States
Department of Agriculture.
Ivanoff (4) reports that the western corn root worm,
the larval stage of Diabrotica longicornis Say., transmits
bacterial wilt from diseased to healthy plants.

Several

bacterial organisms were found in wilted plants which on

7

inoculation into corn plants caused symptoms such as strip­
ing, yellowing, and wilting*

These organisms differed from

Phytomonas stewarti both in the symptoms they caused and in
their physiology.

In a later publication (5) on pathogenesis

a selective medium was developed for culturing P*_ stewarti.
It was demonstrated that the organism would not infect corn
plants without the presence of a wound; the organism was
found to be present in the kernel but did not produce in­
fection to any great extent when insects were absence.

Still

later (6) he learned that Phytomonas vascularum an organism
causing a vascular disease in sugar cane, when inoculated
into sweet corn produced symptoms similar to those caused
by P^ stewarti. When inoculated into sorghum Eolcus sorghum,
Sudan grass

sundanensis,and yellow fox-tail Setaria

glauca, P_;_ stewarti produced symptoms similar to those which
it causes on sweet corn.
Ivanoff and Riker (8) tested resistance against
P. stewarti by means of natural and artificial inoculations
into a large number of corn plants.

Resistance was found

in some oi their inbred and hybrid strains and they conclude
that it is due to inherent vigor, time of maturation, and
true resistance.

Resistance seemed to show as a dominant

inherited factor.
Ivanoff, Riker, and Dickson (9) state that Diabrotica

8

longicornis Say. transmitted the disease from wiloea to
healthy plants.

They also found isolates of Stewarts

organism which differed somewhat in pathogenicity and
physiology.
Holbert, Elliott, and Koehler (3) working in Illinois
found bacterial wilt to be prevalent with abundant local
lesions on the leaves.

The bacteria were not present in

the leaf veins below the lesions on the leaf blade nor were
they present in the sheath nor in the bundles of the stalk
below the infected leaf.

They noted different strains of the

pathogen and a marked resistance to bacterial wilt in certain
inbred strains of corn and their crosses.
Poss and Elliott (12) isolated Phytomonas stewarti from
overwintered adults of the flea beetle, Chaetocnema puliearla
Horn.

Of 40 species of insects from which isolations were

made only

pullcaria yielded the wilt organism. P_^ stewarti

was found in about 75 percent of the cases of this insect col­
lected before any Gorn plants were present.

In their work

there was no evidence that infection might occur from soil
infested with the bacterial organism.
Clinton and Singleton (1) made a large number of crosses
producing inbred and hybrid strains of Whipple some of which
they report to be quite resistant to bacterial wilt.
Smith (26) reports a hybrid variety of sweet corn

9

Golden Cross Bantam which stood up very well in resistance to
bacterial wilt in his field trials.
Mahoney, Muncie, and Marston (10) found the early varieties
to be the most susceptible to bacterial wilt.

Golden Cross

and Top Cross Bantam showed some infection in the field but
slight loss in marketable ears.
Economic Importance.
Bacterial wilt on the more susceptible sweet corn
varieties and depending on the intensity of Infection may cause
100 percent loss in the field.

In the Summer of 1932 in

Michigan sweet corn fields were in many instances a total loss.
One field of 55 acres of sweet corn near Morcenci was completely
ruined by general infection of bacterial wilt.

Another crop

near Lansing was so severely attacked that the grower was un­
able to sell more than |>1Q5 worth from a forty acre field.
Infection followed by necrosis was exceedingly high in all of
the College plots and small garden plots as well as commercial
fields suffered greatly from this disease.

Since 1932 Stewart’s

disease in Michigan has been present but not nearly so Intense
as it was that year.
Similar conditions have been reported from the middle
western and eastern Atlantic states.

The Plant Disease Survey

(31) reports the losses caused by Stewart’s disease for 1931,
1932, and 1933.

In 1931 only three states showed as much as

three percent reduction in yield due to wilt.

Losses in West

10

Virginia were estimated to be ten percent, Ohio and New
Jersey each three percent*

In 1932 seven states reported

losses of five or more percent due to bacterial wilt.
Pennsylvania had 45 percent, Indiana 20 percent, Michigan 15
percent, West Virginia, Ohio, and New York each 10 percent,
Iowa five percent, and Connecticut four and one-half percent.
In 1933 the intensity of the disease decreased somewhat in
comparison to that in 1932.
five or more percent.

Nine states showed a loss of

Maine, Connecticut, and Iowa each re­

cord a loss of five percent,

Massachusetts and Indiana each

ten percent, New York 11 percent, Michigan and Ohio six and
seven percent respectively, and Pennsylvania 25 percent.
Illinois reports heavy losses for 1932 and 1933 (32) but there
is no recorded estimate of percentage loss.

The disease

decreased with nearly the same sharp break in 1934 as it arose
in 1932.
Symptoms of the Disease
In the light of recent knowledge it has been found that
the same or very similar symptoms heretofore attributed
exclusively to infection by Phytomonas stewarti may be caused
by certain other organisms as well.

Ivanoff (4), (6) mentions

other organisms which are able to infect corn and which cause
symptoms similar to those produced by
some distinction between these symptoms.

stewarti and made
Nevertheless the gen­

eral symptoms attributable to infection by P. stewarti are

11

widely known, and the wilt disease can he identified by these

^

for all particable purposes.

If the plant is in the seedling

stage when general infection sets in, the leaves wilt, show­
ing a water-soaked bluish cast at first.

The plants become

a lighter or yellowish color later turning brown witn a
shrivelled dried out appearance.
finally dying results.

Dwarfing shrinking and

This type of wilting is always ac­

companied oy a discoloration of the interior of the nodes
three or more above the adventitious roots and a general basal
rotting, usually if not always, associated with other bacterial
and fungus organisms.

The plant may not be completely infect­

ed, but the disease is often manifested by local leaf lesions
which occur on the veins, at the tips, or at the margins.
These local lesions are quite similax* in color to those result­
ing from severe infection.

When infected, the leaf margin

becomes water soaked and darkened, gradually shrinking and
rolling upward so that the edges turn in toward the midrib •
The water-soaked, discolored streaks may appear along the veins
from a few millimeters in length to that of the entire leaf,
and from one or two millimeters in width to one-half inch or
more.

These areas shrink and sink below the level of the

uninfected epidermis.

The infected portion may dry and shrink

until it pulls away irom the live tissue in whrch case it falls
out leaving a hole through the leaf.

The tips of the leaves

may show lesions which often becoming discolored and dried,

12

roll up and break off leaving the green lower portion of the
lear with a blunt, end*

If the plane is in tne tassel stage

when infection sets in, the tassels become dwarfed and bleach­
ed in appearance, and the leaves may partly or entirely wilt.
The leaves may stick together above the enclosed tassel due
to exuding organisms when they are in a water soaked condition.
This prevents emergence of the tassels and causes the stalk to
bend in the form of a loop due to later elongation.

It is not

the intention to give the impression that all of these condit­
ions appear on any one plant nor even in one field where wilt
is prevalent, but to present a composite of symptoms which may
be found.

Pathogenic strains of the bacterial wilt organism

have been isolated from plants showing the various individual
symptoms described.
Symptoms that may closely resemble those of Stewart’s
disease occur both in sweet and field corn.

The writer has

found a species of Fusarium causing a foot rot and wilting
which is similar in appearance to the seedling stage of
Stewart’s disease.

A bacterial organism producing white

colonies on potato dextrose agar has also been recovered which
if not identical is closely related physiologically to
Phytomonas dlssolvens Rosen.

This organism causes basal

rotting and leaf wilting very similar to the symptoms of
bacterial wilt caused by P. stewarti and which may be readily

13

mistaken unless proved otherwise by isolations.

Drought

alone, if severe, may produce a type of wilting and yellowing
of corn plants somewhat similar to those of the systemic type
of Stewarts disease.

Late spring frosts and mechanical in­

jury at the base of the plant can likewise give similar
results.
Methods of Inoculation and Varietal Resistance
After a number of isolations were made and cultures of
P . stewarti obtained, various methods of inoculation were
tried in order to cause wilt artificially.

A suspension of

the bacteria was sprayed on the leaves and stems, the seeds
were soaked in a broth culture of the organism, and hypodermic
injections were made into the stems of plants a foot or more
In height.
results.

All of these methods gave more or less negative
The hypodermic injections into the stems gave local

lesions but not the typical wilting occurring in the field at
that time.

From these preliminary trials it was found that a

heavy hypodermic injection of a broth culture of the bacterial
wilt organism at the crown of the plant was the most effective
way of producing bacterial wilt artificially.

Ivanoff (7)

recently reported a modification of this method.
In order to determine if there was any difference in
resistance inoculations were made using a large number of
hybrid and inbred strains of corn.

The included lots of seed

14

received by Dr. C. H. Mahoney of the Department of Horti­
culture from Dr. E. S. Haber of Iowa State College and from
Mr. Glen M. Smith of The United States Department of Agriculture
as well as some commercial varieties of corn.

Two plots of

seed of these varieties were planted in the greenhouse at differ­
ent times.

In each plot 10 lots of 20 seed or a total of 400

seeds of each variety were planteu in rhe two plots.

The corn

was planted in rows and inoculated when about three Inches tall.
The first ten plants in each lot were inoculated and the second
ten left as controls, there being ten replications of inoculated
and control plants of each variety in each ploto

All of these

Inoculations were made with a hypodermic needle at the crown
of the plant and observations were made to determine the length
of time necessary for symptoms to develop.

The incubation

period not only in these tests but in others was found to vary
from two to ten days with symptoms becoming noticeable usually
in about four or five days, and the most severely Infected
plants being completely dead in about three weeks.

The results

of these inoculation tests are recorded in Table I*
Table I
The number or plants, the percentages of wilt developing
in the inoculated and control plants, and The average percent
of wilt for both of these groups.

15

Table I (continued)
____________________ Plot I___________ Plot II__________________
Variety
number percent number percent average percent
used_____________ plants wilt
plants wilt
wilt
Iowa hybrids
85.5
97
76.2
B — 23 inoculated
96
66*6
0.5
0
96
1
” uninoculated
92
74.3
67.3
82,3
98
B — 64 Inoculated
85
16.6
89
97
11. 3
H uninoculated
22.5
87
81.6
84.8
87.6
B — 122 inoculated 91
0
86
0
0
" uninoculated
83
80.1
89
75.3
97
84.5
B — 34 inoculated
99
16.8
10.1
11 uninoculated
84
25
88.6
100
83
78.5
B — 69 inoculated
93
0
0
94
0
91
M uninoculated
100
100
87
100
83
B— 10 inoculated
0
0
73
0
86
M uninoculated
81.5
96
80.2
83.3
B— 50 inoculated
72
24.5
19.8
86
69
30
w uninoculated
72.6
75
88
87
70.1
B— 30 inoculated
15.9
87
16.1
83
15.7
w uninoculatdd
79.6
87
81.6
77
65
B — 38 inoculated
0
89
0
0
67
uninoculated
100
*
—
—
100
73
B— 19 inoculated
-—
28 *
28
uninoculated
75
-—
54.2*
94
54.2
B— 21 inoculated
0 *
—
—
0
11 uninoculated
81
—
—
100 *
100
C— 108 inoculated 84
—
-0 *
0
n uninoculated
88
31
94
50
11.1
C— 118 inoculated 90
26.3
19.4
33.7
98
11 uninoculated
92
31.7
26.8
79
23
C--20 inoculated 100
11.6
87
11.5
11.7
94
" uninoculated
—
—
79.2*
77
79.2
C— 34 inoculated
0 *
—
—
0
71
" uninoculated
45.7
53.5
86
37.9
0— 117 inoculated 87
23.4
89
10.1
37.8
82
” uninoculated
39.5
39
100
40
C— 125 inoculated 100
1.5
100
1
0
91
” uninoculated
24.1
38.8
85
10.7
93
C— 23 inoculated
0
0
84
0
99
" uninoculated
68.5
91
75.8
60.9
87
C--31 inoculated
15.2
14.1
85
17.4
86
11 uninoculated
42.6
51.1
90
34.4
93
C— 113 inoculated
1.1
2.1
93
0
84
rt uninoculated
96.7
93.5
92
100
C— 115 inoculatad 91
26.9
91
12.1
87
57.5
n uninoculated

n
n

16

Table

I

(continued)

______________________ Plot I________ Plot II __________________
Variety
number percent number percent average percent
used
plants wilt
wilt
plants wilt
Iowa hybrids
100
50
51.6
C— 22 inoculated
93
50.8
33.9
n uninoculated
44.5
88
22.8
92
40
47
126
inoculated
100
100
54
0
2.1
100
1
n uninoculated
93
Iowa selfed
66.6
78.9
100
90
90
1857 inoculated
1.3
" uninoculated
91
11
6.5
78
100
85.1
92.4
1876 inoculated
90
94
0
99
5.8
90
" uninoculated
11.1
92.8
88.3
89
97.8
1804 inoculated
94
2.2
4.3
0
93
89
n uninoculated
Golden Cross Bantam
88.2
91
85.3
100
95
inoculated
0
0
0
90
98
uninoculated
Purdue Bantam
90
94 .4
87.8
99
81.8
inoculated
16.4
21.4
91
11
98
uninoculated
Yellow Bantam Maine
83.9
72.4
57.1
70
93
inoculated
29.5
19.8
96
70
42.8
uninoculated
* Note In plot II these records were lost and there
not enough seed left to repeat the trials*
These results indicate that immunity to the disease in
a corn plant would be relatively difficult to obtain, but that
there may be a difference in resistance between varieties*
Clinton and Singleton (1) found that several of their Whipple
strains of sweet corn were quite resistant under field conditions,depending upon natural inoculation for infection*

Golden

Cross Bantam has been grown very successfully in Indiana, Ohio,
Pennsylvania, and New York with little loss from wilt.

However,

both of these varieties are susceptible when inoculated artifici­
ally in the above manner, and in 1934 Golden Cross Bantam

17

showed 100 percent in the field in three different plots at
the Michigan Station and was the most susceptible of any
variety grown*

Ivanoff and Riker (8) report hybrids and

inbreds which stood up well in the field when subjected to
this method of inoculation#

This method of inoculation is

very severe and puts a variety to the most vigorous test of
resistance.

Immunity may not be needed for practical purposes,

and there may be varieties that will stand up well in the field
where conditions for wilt development are very favorable.
Such varieties, however, might not be resistant enough to with­
stand this method of inoculation, using a virulent culture of
P . stewarti.
It will be noted in Table I that high percentages of
wilted plants were found in some of the uninoculated varieties.
Early workers carrying on investigations of Stewart’s disease
believed infected seed to be the main source of inoculum and
the chief agent of dissemination.

The results of later tests,

however, cast some doubt upon this hypothesis due to the fact
that bacterial wilt did not always develop from seed obtained
from plants showing high percentages of infection.

Rand and

Cash (16) found only aDout two percent wilt resulting from
infected seed where other sources of inoculum were negligible,
and Ivanoff (5) reports similar results.
The percentages of wilt as shown in the uninoculated

18

controls in Table I do not harmonize with these later dis­
coveries.

As the plants were grown in the greenhouse, there

were only three sources of inoculum which presented themselves,
namely, infected seed, infested soil, and insects.

Experiments

were conducted, therefore, to determine from which source or
sources the inoculum could have arisen that caused the infection
in the controls of Table I.
Infested Soil a Source of Inoculum
Smith (20) believed the organism causing bacterial wilt
of corn was disseminated from plan-c to plant through the soil
by cultivation.

The results of Thomas1 (29; experiments

indicated that infection might occur from infested soil.
Reddy (17) states that there was no evidence thau infection
occurred from soil previously exposed to bacterial infestation#
Rand and Cash (16) were not able to obtain any infection from
infested soil nor from old infected corn stalks,

roos and

Elliott (12) found no evidence to show that infection of plants
ever- occurred by means of soil infested with the bacterial
wilt organism.

Ivanoff (5) found no evidence of soil infesta­

tion by ;p^ stewarti causing the disease without other agencies
present but was able with his selective medium to isolate the
organism from the soil and from infected plant debris.
The writer has never been able to isolate the organism
from the soil.

It can be isolated from diseased corn stalks

19

for a limited length, of time, but the results obtained in
t;hese experiments show no indications that the bacterial
organism is able to winter over in soil or plant debris*
During the winters of 1932 anu 1933 ana 193^ both of which
were extremely cold for this section, flasks of sterilized
and unsterilized soil heavily inoculated with a culture of
P * stewarti were left out of doors*

In the spring after they

had thawed plantings were made from the s^il Doth of Ivanoff1s
selective medium and on potato dextrose agar*
wilt organism was not recovered*
the field.

The bacterial

The same is true of soil in

However, there is a possibility that this condition

may vary in different sections of the country and there may be
some soils which would harbor the organism for longer periods
of time*
Prom the above results it can be concluded that soil
infestation did not cause the wilt that occurred in the
uninoculated controls as shown in Table I.

With this factor

eliminated it was necessary therefore to determine what role
infected seed and insect transmission played in the production
of Stewartfs disease*
Infected Seed as a Source of Inoculum
As the control plants shown in Table I were not umformily free from the disease, and as there was some question re­
garding the ability of the seed to carry the bacterial organism

20

from generation to generation, it became necessary to
determine the actual percentage of wilt that would De due
only to infection from the seed.
the greenhouse and the field.

Plants were grown both in

The inbred and hybrid strains

shown in Table I in addition to some others were grown as one
group.

These were grown

in the greenhouse only, due to a

limited amount of seed; the

soil was sterilized and the green­

house fumigated with nicotine sulfate as often as was necessary
to keep down the insect population.

Another group or lot of

plants from seed of diseased Golden Bantam corn was grown both
in the greenhouse and the field.

The only source of inoculum

that was eliminated in this instance in the greenhouse was
insects because the soil was not sterilized but fumigation was
carried out regularly thus eliminating to a great extent insect
agents of transmission.
The fact that the same varieties of plants grown in the
field had a higher percentage of wilt than did those which
grew in the greenhouse indicated a correlation between insect
injury and the amount ofwilt produced.
experiment are tabulated

The results

of this

in Table II.
Table II

Greenhouse plants grown in pots of sterilized soil with
the number healthy, the number wilted, and the average percent
wilted.

21

Table II (continued)
____________
Lot I________ Lot II________ Lot III
Average
V a r i e t y n u m b e r number number number number number percent
used
wilted clean wilted clean wilted clean wilt
Iowa hybrids
B — 23
1
14
1
34
2
44
4*2
B— 64
1
33
2
13
26
7.7
3
B— 122
5
21
0
15
46
1
6.8
B— 34
51
1
1
11
5.6
4
40
—
B— 69
1
39
1
41
2.4
B — 10
1
29
31
0
2.7
11
1
—
B--50
1
49
1
29
2.5
B— 30
0
41
24
3.4
1
21
2
...
60
0
1.9
B— 38
43
2
B--19
0
49
19
1.2
1
11
0
B— 21
0
41
0
0
0
42
14
29
C — 108
0
41
0
16
1.1
1
3.9
13
21
63
2
C— 118
1
1
4.6
0
51
41
4
12
1
C— 20
0
43
1.1
0
31
15
C— 34
1
2.5
39
0
24
14
0
2
C— 117
2.2
27
0
12
51
1
1
C— 125
2.8
10
34
60
1
1
1
C— 23
-1.0
47
C— 31
0
1
51
20
1.1
10
0
61
1
0
C — 113
2.9
25
47
.
26
0
2
1
C— 115
4.2
25
31
2
36
1
1
C — 22
0.0
37
0
16
0
35
0
126
16
1.2
36
0
31
1
0
69
Iowa selfed
2.8
70
3
34
0
1857
3.6
32
49
1
2
1876
3.7
0
24
36
44
2
2
1804
3.3
29
2
42
1
16
0
917
2.1
0
15
33
43
1
1
13
1.2
0
16
36
1
31
0
69
1.9
19
41
1
1
41
0
42
2.4
0
22
22
35
2
0
9
Purdue hybrids
Golden Cross
—
2.2
48
1
41
1
Bantam
3.2
64
26
3
0
Purdue 51
14
4.7
1
41
3
27
0
1403
39
3.5
19
3
0
24
0
1310
1.3
31
1
41
0
1303
31
8.6
3
41
6
23
0
1413

22

Table II (continued)
Lot; III
Lot I
Lot II
Variety
number number number number number number percent
used
wilted clean wilted clean wilted clean wilt
Hybrid
Golden Cross
2.4
19
0
2
43
0
17
Bantam
Commercials
3.0
17
40
0
41
2
1
Pur. Bantam
—
0
29
0
35
Pur. Bantam(b) 0
Yellow Bantam
1.1
26
0
37
0
29
1
Maine
Quaker Hill
Golden Cross
6.4
21
2
3
35
32
2
Bantam
Associated
Seed Growers
Golden Cross
35
1.1
1
13
0
44
Bantam
She eley
Golden Cross
4.3
23
1
42
24
2
1
Bantam
Barron
1.1
31
1
0
32
31
0
Sunshine
Average of all
3.0
25
1.9
1.6
32.5
36.5
1 .3
Varieties

0

Total for all varieties, clean ^ 4075; wilted — 95; percent wilt-3,£»
The seed of the above strains of sweet corn came from
plants showing a nigh percentage of wilt in 1932.

These strains

were all more or less susceptible to the attack of P • stewarti
as can be concluded from the results or inoculations presented
in Table I, yet none of them produced any large amount of wilt
when grown in the greenhouse in sterilized soil in the absence
of insects.

Golden Cross Bantam had 8.6 percent wilted plants

which was the highest reading of any strain, and in many there
was not a single plant which showed the disease*

it is also

23

true that in many cases the uninoculated controls in Table I
showed a much higher wilt reading than occurred in any of the
same strains in Table II#

It is therefore quite evident that

either insect agencies or soil Infested with the bacterial
wilt organism had some Influencing effect upon the production
of wilt in the controls of Table I#

It would also indicate

that infected seed has a small role in the production of the
disease even when plants are grown in the greenhouse with
other sources of infection eliminated.
It was therefore decided to eliminate only one of the
above mentioned infection possibilities when a duplication of
plants were grown in the field.

In the summer of 1934 seed

from diseased Golden Bantam plants was planted both in a
greenhouse which was kept fumigated frequently and In the
field.

The soil was not sterilized in either case but the

greenhouse plants were kept free from insects.

The results

are shown in Table III and IV•
Table III
Plants grown in a fumigated greenhouse in unsterilized
soil, showing the relation of insect injury to the number of
wilt, and the percentage of wilt.
number number number number wilted with percent
wilt
plantings plants healthy wilted insect injury
3.0
6
4
324
334
1.
6.0
3
8
173
184
2.
1.7
0
286
5
291
3.
4.2
4
5
203
212
4.
1.5
0
534
526
8
5.
5
8.2
10
167
182
6.
3.7
0
107
103
4
7.

24

Table IV
Two plots of plants grown in -che field not excluding
insects.

J

Plot
Readings
number number number number wilted with percent
taken
plants healthy wilteu insect injury______wilt
wilt
July 1, 1934 2331
23l2
~TU
0.8
Aug. 6, 1934
41
36
1.7
Sept. 1,1934 2322
1509
813
Vll
35.0

2327 2286

Plot II
July 1,
Aug. 6,
Sept.1,

1934 1101
1934 1096
1934 1090

1090
1081
733

11
15
357

8
15
297

1.0
1.5
32.8

The most striking feature of table XV is that very little
wilt snowed up until August.

It will likewise be noticed that

insect injury of diseased plants increased proportionally with
the increase In wilo.

The insect injury was largely the work

of larvae feeding around the base of the plants.

At no time

could definite bacterial wilt leaf lesions be attributed to
inoculation by leaf feeding insects.

It is doubtful in this

case that the late infection was due to diseased seed as the
kernels were rotted away and no longer in evidence berore the
wilt became noticeable to any great extent.

The only means

by which infected seed could have played a part would have
been for the organism to have gained entrance into the young
seedling from the seed and x-here remained dormant until
August when the planes were practically mature.

Delayed

appearance oi the symptoms after Infection was thought by
early worker^ to occur.

However, in the light of present

25

day knowledge of the appearance of the symptoms after
artificially inoculation, it is very doubtful if such a dormant
period exists*

Due to the fact that the same lots of seed

produced very little wilt in the greenhouse where conditions,
other than insect infectation, were very favorable for the
appearance of the disease, it is reasonable to conclude in
this experiment that larvae of insects played a major role
in infection in the field rather than infested soil or
infected seed*
The results in Table II show clearly that not all of the
wilt in the control plants in Table I could be due to infected
seed.

Varieties C — 22, C--115, C— 118, and Maine Yellow

Bantam for examples had 33.9, 26.9, 26.3, and 29.5 percent wilt
respectively.

These varieties when grown in sterilized soil

in the greenhouse where other sources of inoculum were
eliminated showed only 4.2, 2.9, 3.9, and 1.1 percent wilted
plants respectively.

Soil infested with the bacterial wilt

organism and insect transmission of the disease were the only
sources of infection eliminated in these experiments.

It was

found that isolations from suspected infected seed yielded
P. stewartl in approximately 12 percent of the trials.

This

as can be seen is a higher percentage than there were infected
plants when factors other than infected seed were eliminated.
As this fact indicates that not all of the infected seed will
give rise to wilted plants, studies of this nature were made

26

and are given in the next phase of the work.
Tk® role of infected seed In the transmission of the disease
Results of previous experiments had shown that the
organism was carried in the seed, and that it was possible to
isolate an organism from the interior of the seed and to pro­
duce bacterial wilt with the organism obtained.

It was also

found by isolations that the percentages of seed infected with
the organism were greater in all cases than were the percent­
ages of wilted plants occuring when this seed was planted and
the insects agents were controlled.

Various workers have shown

by isolations from and sectioning of the diseased kernel that
the organism was present in the old vascular tissue of the
chalazal region of the endosperm.

Rand and Cash (16) isolated

P . stewarti from the endosperm, but there is no record of the
organism being recovered from the embryo region.

The question

at once was raised as to why greenhouse plants grown in steril­
ized soil from seed known to be infected did not show a greater
percentage of bacterial wilt*

In addition isolations of the

pathogen could be readily made from kernels one year old.
This condition showed that the bacterium was still alive and
did not die out before the next year's planting.

Also seed

one year old would produce just as much wilt as seed only a
month or two old.

Experiments were therefore inaugurated to

determine what connection there might be between inoculum
within the seed and the occurence of the disease.

27

In order to be certain that infection came from the
interior of the seed, surface sterilized kernels were
germinated and grown on sterile agar slats in large test
tubes until the young seedlings were about four inches in
length.

Altogether 500 young seedlings were grown in this

manner from seed collected from Golden Bantam plants
definitely affected with bacterial wilt.

Only 53 or 10.6

percent of these plants showed symptoms of the disease.
Plantings of bits of the infected leaf and stem tissue were
made on potato dextrose agar plates and P_. stewarti and a
white bacterial organism were isolated from each of the
diseased plants.
Experiments also were carried on to verify the results
of Ivanoff's (5) work showing that infection with P. stewarti
takes place only through wounds.

In these tests 500 kernels

of clean seed were germinated and grown on agar in petri
dishes.

After the kernels had germinated 0.1 c.c of a

virulent broth culture of P^ stewarti was dropped upon the
kernel at the point of emergence of the epicotyl.

No wilt

was produced even when the organism was growing on the agar
around the tip of the shoot and root and over the kernel.
This experiment as well as those of Ivanoff show that a
wound is necessary for
the plant tissue.

stewarti to gain entrance into

From these facts it seemed reasonable to

28

assume that the organism within the vascular tissue at the
base of the kernel was fixed and not able to invade the embryo
at the time of germination, unless some injury occurred which
would afford an avenue of entrance*

Experiments were there­

fore carried on to determine if possible the soundness of the
above hypothesis.
Several hundred sweet corn seeds were surface sterilized
by repeated rinsing in alcohol, mercuric chloride 1:1000,
and sterile water.

By this method any organisms within the

seed were not affected.

These seeds were then germinated by

the f,rag doll11 method and after the epicotyl and hypocotyl had
emerged the kernels were punctured with a fine needle through
the chalazal region into the embryo to a point where the young
root and shoot separate.

Two punctures were made in each seed,

each time passing the needle through some of the vascular tissue
that had connected the kernel to the cob.

Controls were treated

in a like manner in every way except puncturing.

These plants

were grown in the greenhouse in sterilized soil and for the most
part under a large muslin covered insect proof cage.

The green­

house was fumigated each time a new lot of seedlings was planted.
The results of the experiments expressed as percentages of wilted
plants in the punctured seedlings and the controls are shown in
Table V.

The percentages of infected seed as determined by

isolations are given in the text.

These isolations were made

2.9

from corresponding lots of seed as those used for the puncture
experiments in order to know approximately the percentages of
inoculum present.
Table V
Number of wilted plants and the percentages of wilt as
found in the punctured seedlings and controls.
Punctured seedlings

Plantings Variety used
1.
Golden Bantam
n
ti
2.
it
it
3.
Golden Nugget
4.
5.
Golden Bantam
6.

7.
8.

TI

IT

Extra Early
Golden Bantam
tt

it

number number number
plants healthy wilted
43
68
25
53
34
19
50
75
25
186
153
33
191
26
165
40
214
174
374
232

295
191

percent
wilt
37
36
33.3
18
13.6
18.7

79
41

21.1
17.1

Controls
1.
2.

3.
4.
5.
6•
7.
8.

Golden Bantam
n
ii

ti
it

Golden Nugget
Golden Bantam
ii
it
Extra Early
Golden Bantam
ii 11

11

94
48
207
161
263
211

67
44
196
145
261
194

7
4
11
16
2
17

9.5
8.3
5.3
10
0.7<
8.1

241
197

226
179

15
18

6.2
9.1

The results of this experiment show very clearly that
injury through ohe chalazal region of the corn kernel, after
germination, into the base of the young shoot caused the
disease to be expressed in much greater percentages than when
injury had not taken place.

The percentages of wilted plants

were much higher in the injured plants than in the controls.

30

It is also clearly shown in Table V that in the controls
there were more kernels with bacterial infection than there
were wilt infected seedlings when the seed was planted.

It

may then be concluded that the greater part of the bacterial
wilt inoculum is unable to gain entrance into the young seed­
ling at the time of germination unless a path of entrance was
made by some agent other than P.stewarti.
agent to create the avenue of entrance and

If there were no
stewarti was

not able to gain entrance in the absence of wounds as proved,
the controls in Table V should have been completely free of
wilt.

As this was not found to be the case and as isolations

from corresponding lots of seed showed on uhe average 18.7
percent of the kernels to be infected with £•_ stewarti and 7.2
percent of the kernels to contain a bacteria.1 organism which
produced white colonies on potato dextrose agar, studies were
made of insect transmission of the disease, and the role played
by organisms associated with

stewarti.

The fact that wilted plants were more prevalent when the
tissues of the seed were punctured through the chalazal region
into the young seedling correlates very well with other phases
of our knowledge of Stewart's disease.
number of insect larvae

There are known to be a

that feed within the kernel shortly

after germination and if they penetrate farther, as some of
them do, they could infect the young plant from its own seed

31

merely as a contact agent of dissemination.

Examples of some

of these insects are the seed-corn maggot and several small
maggots of this group, as the cabbage and the onion maggots*
Figures 1, 2, and 3 show the relation between the chalazal
region and the embryo.

u m itnm rrr n liir

Figure I

32

Figure II

Figure m

34

Insects in relation to disease transmission
During the severe epiphytotic of Stewart’s disease in
1932 many specimens were sent in to the plant pathological
laboratory by growers.

These specimens varied in height from

six to eighteen inches and nearly all of them were infected
systemically with Pj_ stewarti.

Most of the plants showed the

wilting and necrotic conditions typical of the disease,
accompanied by a soft rot at the base of the stalk.

In many

of these plants small larvae were found feeding in the base of
the stem and often two or three inches above the crown.

It

was assumed at first that these larvae were those which commonly
follow the soft rot condition in plant tissue.

Later they were

identified by the Entomology Department as larvae of the seedcorn maggot, Hylemyia cillcrura Meigen.

Isolations were made

both from the exterior surface by placing the maggot in a tube
of broth and plating from this medium, and from the alimentary
tract after disinfecting the surface of the maggot and dis­
secting.

Cultures of P. stewarti were readily recovered from

both regions but especially from the latter.

In 1933 only a

few of these maggots were found and again isolations made from
the alimentary tract yielded

stewarti. In 1934 some of the

adults of Hylemyia cilicrura were collected and placed upon
plants growing under muslin cages in the field.

A close watch

was kept but none of the plants showed any symptoms until three
weeks after introduction of the insects, when symptoms began to

35

appear.

A short time later when about three-fourths of the

plants had become diseased, they were pulled and examined*
Every wilted plant showed larval injury, some still having
the larvae within the plant tissue, although most of them
had gone into the ground to pupate before they could be re­
covered.

Of the 93 plants exposed to these insects 67 plants

or 72 percent showed typical wilt while the controls showed
only an occasional wilted plant.

These maggots were not re­

covered from the soil and as they were rather scarce during
1934 probably due to the preceding cold winter, the experiment
had to be discontinued for the time being.

It is hoped that

more larvae of the seed-corn maggot can be secured in 1935 and
more data obtained regarding their activity as an agent in
dissemination.

The fact that the maggot does attack corn

plants and also carries P*_ stewarti in a virulent condition
internally is conclusive evidence of its role in wilt dis­
semination.

The length of time

stewarti is carried within

the insect and how long the organism remains pathogenic there,
is however, still a question.
Another type of insect found to carry

stewarti

from diseased to healthy plants was the common wheat wireworm,
Agriotes mancus Cand .
infected field corn.

These insects were found in wilt

The field from which the specimens were

taken had been in sod for a number of years and consequently
was well infested with wireworms.

On cutting across the stem

36

of corn plants injured by wireworms bacteria oozed out in a
slimy yellow mass from the vascular bundles, while only a few
uninjured plants showed bacterial wilt.

Some of these worms

were collected, brought into the laboratory and placed on agar
plates of Ivanoff’s (5) selective medium where they were
allowed to crawl about for a few minutes.
colonies of

In a few days

stewarti were in evidence and proved to be

pathogenic when inoculated into corn plants.

Of the inoculated

plants 78 percent showed wilting while the controls showed only
one or two percent of wilt.

Isolations were made from the

alimentary tract of a few of the wireworms but in no case
could

stewarti be recovered.

After allowing the wireworms

to crawl about on the agar plates, they were removed and allowed
to feed upon corn plants in pots of sterilized soil.

Wilting

of the plants followed soon after injury by feeding of the wire­
worms.

Isolations made from the wilted plants showed the

presence of the bacterial wilt organism.

Every plant that was

injured by the wireworms wilted and wilting always followed
injury as long as they were present.

When the wireworms were

left in pots for two weeks in the absence of corn plants, the
wilt organism could no longer be isolated from them.

In this

case they probably acted merely as mechanical carriers of
inoculum.

Wireworms are of minor importance in the field

because they are never prevalent in large enough numbers to
cause severe loss unless the soil is soddy.

Because they do not

37

harbor the causal bacterium for any length of time, the
inoculum would, have to be present in an infected plant before
wireworms could act as agents of dissemination*
Hand and Cash (15) were the first workers to definitely
prove that insects were associated with the transmission of
bacterial wilt.

They were able to transmit the disease from

diseased to healthy plants by transferring two species of flea
beetle, Chaetocnema pulicaria Horn, and C_. denticulata Horn.,
and the twelve-spotted cucumber beetle, Diabrotica
duodecimpunctata Oliv. to leaves of the corn plant.

Poos and

Elliott (12) isolated cultures of Pj^ stewarti from the flea
beetle Chaetocnema pulicaria Horn, early in the spring before
there were any corn plants that could have furnished the
inoculum.

This is the only proven case of an insect carrying

the organism over winter, although there may be other similar
insects which harbor P^ stewarti.

The infected flea beetles

produced the disease when allowed to feed on leaves of healthy
plants.

There is little evidence that any great amount of

inoculum can live over winter in the soil, and it is almost
certain that the organism would not live in the soil for as
long as two or more years.
Prom evidence at hand and from that of the above workers
it can be concluded that insects play an important role in
the dissemination of the disease.

However, there is also

evidence that the wilt producing organism is carried in the

38

seed and in the absence of both insects and soil infestation
will cause a small amount of wilt.

Smith (24), Rand and Cash

(16), and Ivanoff (5) were able to isolate the organism from
the seed, and it also has been repeatedly done by the writer
at this station.
Wilt produced by organisms associated with P . stewarti
During the progress of the various experiments there
were found two parasitic organisms that are sometimes as­
sociated with P._ stewarti.

One of them is a species of

Pusarium and the other is a white bacterial organism produc­
ing glistening white colonies on potato agar and believed
to be closely related physiologically to Phytomonas
dissolvens Rosen.

Both of these organisms were found to be

parasitic and to play a part in the appearance of Stewart*s
disease under some conditions.
The species of Fusarium causing a foot rot of corn may
be but is not necessarily associated with P_* stewarti.

This

Pusarium in the wilt disease is probably not an important
factor for the reason that it is so virulently parasitic, that
the effects of the wilt bacterium are overshadowed by those of
the fungus.

Many of the plants attacked by this Fusarium were

killed before they reached the soil surface.

Those that were

attacked after they were several inches tall wilted with some­
what different symptoms than those of Stewart*s disease.

The

plants became pale yellow in color with the absence of a water

39

soaked appearance.

The fungus could be Isolated from wilted

plants along with Stewart's organism, and the two together in
bujture would often be closely associated, the bacterium
growing along the fungus hyphae. However, but very little
loss from bacterial wilt was caused by this combination as
the Pusarium is a more virulent pathogen than P^ stewarti.
In none of the specimens could the wilting which somewhat
resembled Stewart's disease be attributed to the bacterial
wilt organism.

In this case P_* stewarti seemed to follow

rather than to be the direct causal agent in wilting.
It was found in a previous phase of the work that both
P . stewarti and this white bacterium could be isolated from
infected kernels.
plants.

They could also be isolated from diseased

This was particularly true in the controls of Table V

all of which yielded both organisms upon isolation.

It Is

especially to be noted that none of the wilted plants in the
controls contain

stewarti alone, and that many of the

wilted plants in the punctured seedlings contained P^_ stewarti
alone.

In Table VI is recorded the results of isolations from

corresonding lots of seed as used in Table V.

40

Table VI
Organisms present as determined by isolation in lots of
seed corresponding to those of Table V*
number number with
of
P. stewarti
Isolations kernels
X#
220
57
2.
180
41
3.
272
63
4.
260
31
5.
204
24
6.
215
33
7.
271
62
8.
231
37

number with
white
organism
24
13
15
23
4
19
20
17

percent percent
P.
white
stewarti organii
25.9
10.9
22.9
7.2
23.2
5.5
11.9
8.8
2.0
11.8
15.3
8.8
22.9
7.4
16.0
7.3

The white bacterial organism plays a very important role in
the production of the disease from infected seed when other
factors are absent.

It is capable of causing a routing of the

seed and the basal portions of the plant and producing wilt
symptoms in the leaves,

ihis organism alv^ne Is not highly

pathogenic but causes a basal rotting with some leaf symptoms
as shown in plate H I .

After the adventitious roots are formed

the infected plants seem to take on new vigor and resume growth,
although the organism is in the plant tissue as determined by
isolations.

This organism is often found associated with P.

stewarti in the seed and ,-la.nt tissue although this is not
necessarily the case.

When making isolations the two organisms

may be recoveredm a mixed culture and are sometimes difficult
to separate on plating.

Stanley and Orton (27J reported the

presence of a white organism when isolations were made ror
stewarti. It is possible that the organism reported by them

41

and identified as P . dis solvens Rosen may be the same
bacterium as the one found in these investigations*
inoculations were made with pure cultures of the white
organism by hypodermic injections into the base of seedlings
grown in sterilized soil in the greenhouse, and it was reisolated both from the leaves and sterns of the infected plants.
The organism travels up the vascular bundles as is the case
with P^ stewarti and the symptoms are manifested within a few
days*

This pathogen seems to be more destructive in cloudy

weather at relatively high temperatures*

This is probably due

to the slower growth of the plant in cloudy weather and the
rapid growth of the organism at relatively high temperatures,
25 to 30 degree Centigrade*

The peculiar leaf rolling and

water soaking of the central leaves as shown in Plate III are
characteristic symptoms produced by this organism* although
f . stewarti may also be present in plants showing these
symptoms.

Pj_ stewarti alone may produce symptoms somewhat

similar to these.
There was no attempt made to identify or classify this
organism other than to note the symptoms it produced on corn
and to determine some of its physiological properties on
culture media.

It grows as a white, glistening, round colony

on potato dextrose agar.

In this medium the colonies are

raised, smooth, convex, and opaque*

Under oil immersion in a

42

hanging drop there appeared to be both motile and non-motile
forms.

The organism is a short rod often occurring in chains;

it forms acid and gas in dextrose, galactose, mannit, sucrose,
maltose, lactose, and raffinose; the bacterium made only a
fair growth in gelatin and caused only slight liquefaction.
Growth is cloudy in potato dextrose broth producing a scummy
pellicle around the top of the tube.

It precipitates slowly

and stains readily with carbol fuchsin.
It will be noted that the percentage of kernels showing
the white bacterial organism in Table VI corresponds closely
to the percentages of wilted plants which appeared in the
control plants as shown in Table V.

The question arose as to

the part played by this organism in the wilted plants of the
controls.

The answers that presented themselves were two,

11) that this organism could induce a type of wilt similar
to that caused by P^ stewarti, and (2) that this organism
was held within the seed with P_;_ stewarti and at the time of
germination was able to cause a rotting of the embryo tissue
allowing P_. stewarti to gain entrance into the young plant.
Results of inoculation tests as indicated above proved the
organism to be parasitic, producing on the corn plant symptoms
similar to those induced by P_^ stewarti.
To determine the effect of this whitw bacterium when
associated with P^ stewarti, pauhogenicxty tests were made of
the organism alone and in combination.

Apparently clean corn

43

seed that had been soaked in water was divided into two lots
and treated as follows! (1) the seed coats were broken in
several places by scratching with a needle on -che opposi-ce
side from the embryo, and (2) the seed coats were lert un­
broken.

Each lot of seed was separated into three groups of

200 kernels each.

One group was soaked in a broth culture of

the white organism, another group was soaked in a broth
culture of f . stewarti, and the third group was soaked in a
mixture of broth cultures of the two organisms.
received the same treatment.

Both lots

The results are striking.

In

only two groups were there any wilted plants, both of which
occurred in groups where the seed coat had been broken.

One

had been soaked, in a broth culiury of the white organism alone,
and the other had been soaked in a mixture of brotn cultures of
the white organism and P^ stewarti.

No wilted plants resulted

in those groups in whicn the seed coat was left unbroken and
P. stewarti was not able to infect after the seed coat had been
broken.

The results are given in Table VII.
Table VII

Results of inoculations with P_j_ stewarti, the white
bacterium associated with It, and a mixture of the two
organisms into which corn kernels with broken and unbroken
seed coats were soaked.
Kernels with broken
Kernels with unbroken
seed coats
seeds coats
Inoculum
plants wilted
pianus wilted
___________ number_____percent_____ number_______ percent
White organism
121
60.5
0
- 0
P. stewarti
0
0
0
u
Both organisms
167
83.5
0
0

44

Neither of the organisms were able to penetrate through
the seed coat either alone or together•

The white bacterium

was able to penetrate the tissues of the young seedling at
germination and produce wilt after uhe seed cuat was broken,
but

stewarti alone was net auls to penetrate even after the

seed coat was broken.

Both organisms could be isolated from

the wilted planus which resulted after the seed with oroken
coats had been soaked in a nuxture of broth cultures of the
two organisms.

This is evidence that P^_ stewarti does not

disintegrate living tissue to any extent, and is not aole to
migrate from the chalazal region in^o vhe embryo and vascular
tissue of the seedings.
to play a double role.

The white organism apparently is able
It can infect the plant alone if present

in the seed causing wilting ana in some cases ueath, and it can
attack and rot away the tissue allowing ]?_•_ stewarti to gain
entrance into the vascular tissue where the wilt organism
causes more necrotic and systemic conditions than does the white
bacterium,

rlates I, II, and III show different types uf

wilting ae caused by these two organisms.
Anatomy of corn in relation to wilt.
Prom observation in tne field and. from published results
of other workers some varieties are more resistant directly
or indirectly thun otners, and the suggestion was made that
the number of vascular bundles might be an influenceing factor
in resistance.

Experiments were therefore conducted to determine

45

if possible the relation between the number of vascular bundles
of corn plants and the amount of wilt found in these varieties#
Both healthy mature plants and those showing symptoms of
Stewart*s disease of five different varieties were collected
and the bundles counted at the second internode above the
crown.
section*

Free hand sections were made of the entire cross
To more clearly differentiate the vascular bundle?,

the sections were treated with phloroglucinol and a drop of
25 percent hydrochloric acid which gave them a pink color that
showed very well under the binocular microscope.

The cross

sections were suspended from a slide which was mounted on an­
other with small strips of wood separating the two.

This

allowed enough space between the slides for the sections which
were about one-half millimeter in thickness.

The moisture on

the sections caused them to adhere to the top slide which was
charted in squares about two millimeters square with a diamond
point pencil.

The five varieties of corn selected were extreme

in that some showed great susceptibility and others showed high
resistance.

The number of bundles, area in square millimeters,

and average number of bundles per square millimeter of cross
section are given in Table VIII.

46

Table V i n
The number of bundles, the area in square millimeters,
the average number of bundles per square millimeter for both
healthy and wilted corn plants of five different varieties#

Variety
used
1593
it
tt
ri
It

t!
It
ii
tt

tt

Average
all
1588
n
tt
tt
11
tt
ri
tt
It
tt

Average
all
51xG.B.
n
tt

tt
n
tt

it
tt
it

tt

Average
all

Healthy__________
Wilted
ave• number
ave. number
number area in bundles
number area in bundles
bundles sq • mm. per sq. mm bundles sq • mm. per sq. mm.
472
346.37
1.37
365
78.54
4.65
462
298.64
1.55
416
148.25
2.8
566
330.05
1.71
414
113.09
3.66
507
346.36
1.46
506
275.8
1.83
408
247.18
1.65
458
290.72
1.58
376
220.07
1.71
405
201.06
2.01
396
201.06
1.97
430
1.66
258.43
of
277.99
448
1.61
425.25 153.92
2.76
410
' 264.47
1.61
523
620.73
1.63
454
247.14
1.84
508
261.28
1.94
435
240.52
1.81
489
268.79
1.82
434
479
247.14
1.75
247.14
1.94
406
207.13
1.96
493
2.05
240.52
521
1.99
261.28
2.86
441
153.93
441
220.1
2.0
496
298.64
1.66
1.41
476
336.53
469
240.52
1.95
1.75
405
233.42
1.59
296.78
472
of
1.77
251.79
1.86
477.5
447.12 256.18
233.42
254.47
491
2.1
536
2.1
254.47
1.92
1.54
510
330.05
490
1.86
298.64
554
598
283.53
2.11
2.06
503
213.82
2.35
564
272.88
1.79
1.90
570
317.3
559
293.77
1.79
254.47
457
499
251.64
1.98
309.13
1.94
287.71
1.77
600
509
265.91
1.48
286.51
1.93
394
553
4.02
151.74
478
306.02
1.56
610
2.43
494
208.66
324.93
1.52
507
of
475.5
2.06
252.86
287.04
1.65
522.1

47

Table VIII (continuedj
Healthy____________________ Wilted
ave. number
area, number
Varity number area in bundles
number area in bundles
used
bundles sq. mm. per sq. mm bundles sq. mm. per sq. mm.
1594
519
337.81 1.53
489
1.87
261.28
n
631
388.46 1.62
504
268.79
1.88
H
540
306.02 1.76
454
298.64
1.52
11
566
268.79 2.11
460
1.91
240.52
11
476
314.15 1.52
1.69
408
240.52
51
531
298.64 1.78
512
330.05
1.55
u
410
275.8
1.48
421
3.27
128.68
II
437
314.16 1.39
it
514
420.53 1.22
ii
618
419.09 1.47
Average of
524.2
all
334.34 1.57
464
252.64
1.84
2x1339 540
406.11 1.33
5 73 " ~ 170.62
3.35
ii
555
2.38
566
233.42
380.13 1.49
ii
637
2.80
314.16 1.68
528
226.98
n
1.91
565
388.45 1.45
541
283.53
ii
2.24
226.98
587
380.13 1.54
508
ii
560
367.78 1.52
11
466
311.01 1.49
II
433.73 1.28
555
11
448.62 1.10
494
11
573
347.68 1.64
Average of
2.46
228.31
562.8
377.78 1. 44
543.4
all
Too little research has been done on the anatomy of
the corn plant to substantiate any hypothesis relating the
number of vascular bundles to resistance.

It is known that

the number of vascular bundles in a corn plant besides being
dependent on hereditary factors are also dependent on the
number of leaves that develop.

The number of leaves in turn

are likewise dependent on inherent factors, two facts which

48

mean that the total number of bundles within a corn stem at
any one place is quite variable.

It will be noted in Table

VIII that the number of bundles per square millimeter in the
wilted stems is greater than that in the healthy stems, but it
will also be noted that the total cross section area is smaller
in the wilted plant stems than in the healthy stems.

This

probably means that the total size of the stem was stunted due
to the disease, and the number of vascular bundles being more
or less fixed developed the same as in the healthy stem, thus
crowding the same number of bundles together in a smaller stem*
There is one possibility that the number of vascular
bundles might influence the resistance which a variety might
exert*

The number of bundles in a corn stem is dependent

upon the number of leaves and the number of leaves is dependent
upon the time of tassel formation.

There are no more leaves

formed after the tassel begins to develop and as the total
number of vascular bundles depends upon the number of leaves,
the date of development of the tassel would influence the
total number of vascular bundles.

However, there is so little

known about this subject that definite conclusions cannot be
drawn*
There is a large field open in which to work on the
subject of resistance in corn to Stewart's disease.

It is

of course difficult to determine the factor in the host that
makes it resistant unless it is known definitely just what

49

factors, if any, other than the pathogen influence the
development of the disease.

If insects are the main dis­

seminating agents, then a variety would undoubtedly have to
be resistant to their attack as well as the action of the
parasite itself.

For practical purposes though the common

methods of plants breeding are the quickest for yielding a
remedy.
Control
There are no known methods of controlling this disease
other than the use of resistant varieties.

Smith’s (26)

Golden Cross Bantam has proven resistant in the field in
other states.

Clinton and Singleton ^1) found strains of

Whipple to be quite resistant.

And Ivanoff and Riker (8)

report several strains of sweet corn that were resistant to
both artificial and natural Inoculation in both the field
and greenhouse.

The use of these varieties has probably

saved considerable loss in some sections. .
Gontrol by seed treatment has been found to be in­
effective.

As early as 1909 Smith (23) reported results of

experiments in which mercuric chloride seed treatment seemed
to control bacterial wilt to some extent.

Later (24) he found

the bacterial organism within the kernel and expressed doubt
as to the effectiveness of this treatment for the internal
disinfection of the kernel.

At the Michigan Station, the

50

writer in cooperation with. Dr. J. H. Muncie tried out under
field conditions In 1932 and 1933 various seed treatments
none of which proved effective.

These treatments were

mercuric chloride 1:1000, Semesan jr. as a dust treatment,
several phenol compounds, Hexylresorcinol of varying con­
centrations, a chlorine dust compound, and dry heat at 60° C.
for one hour.

The results were based on percentage of wilted

plants in the treated plots in comparison to those found in
the controls.
In the winter of 1934 and 1935, a series of isolations
was made from the interior of kernels from wilted plants.
The results showed that the organism was recovered in fewer
cases and that the percentage of Infected kernels decreased
in the same lot of corn when 95 percent alcohol was used to
remove the air before the kernels were surfaced sterilized
with mercuric chloride.

Accordingly, four replications of

seed treatments were carried on (1) using 95 percent alcohol
soak for 15 minutes followed by a 15 minute soak in 1:1000
mercuric chloride, (2) mercuric chloride 1:1000 alone as a
soak for 15 minutes, and (3) untreated controls.

It is

obvious that for the controls it was impossible tv have seed
surface sterilized without using some disinfectant.

This

was accomplished by washing for long periods of time in
sterile water and by repeated rinsing for short periods of
not more than 30 seconds xn alcohol and repealed washing in

51

sterile water.

The number and percent of kernels infected

with p*_ stewarti and an associated white bacterial organism
are shown in Table IX.
Table IX
Total number of kernels treated and those from which
s^Qwarti and the associated bacterium could be isolated
aTter treatment with alcohol, mercuric chloride, and from
those untreated.
number
number
percent percent
Treatment number number with P . with white
white
P.
used
treated healthy stewarti organism
stewarti organism
Trial
treated
(a)
204
204
0
0
0
0
I
(b)
220
218
1
1
0.5
0.5
(c)
136
121
6
3
4.4
2.2
fr.9
204
5
(a)
228
2
2.2
9
4.2
II (b)
216
188
15
6.9
9.4
200
81
31
24.4
(c )
332
3.3
5.8
"327
~ “12
21
“ ' ’Taj '
360
7.0
277
39
24
11.5
III (b)
340
47
15.6
184
69
23
(c)
300
4.6
2.5
260
13
7
(a)
280
4.5
14
8
273
25
IV (b)
312
12.6
23.9
39
250
yl
^c)
380
2.3
7.5
2.52
248.7
7.5
(a) ' 268
4.05
6.72
239
20
12
V
(b)
272
9.95
18.95
188.7
61.7
30
(c)
287
V. represents an average of all.
(a) represents
■cre&tment or 95 percent alcohol
followed by mercuric chloride 1:1000.
(b) represents treatment with mercuric chloride alone.
(c) represents untreated controls.
It will be noted that the first lot of seed treated
showed but small percentages of wilt even in the controls.
This was a Golden Bantam variety which had shown very little
wilt in the field and came from relatively clean plants.

52

The evidence at hand and that by other workers, of
insect dissemination of Stewart's disease, and the evidence
that infected seed alone as an agent of dissemination does
not cause a high percentage of wilted plants, indicates that
seed disinfection although completely effective would not
control the disease under most conditions*

However, the fact

that the organism is carried within the seed' and, therefore
affords a source of inoculum to insect agents, makes desirable
some seed treatment that will sterilize the interior of the
seed without injuring the embryo.

The results of seed

disinfection in the beginning of these investigations are
probably in error due to the fact that the insect agents of
dissemination at that time were not considered nor controlled.
The results show that the treatment:s employed are not
effective in disinfecting the interior of the kernel although
the alcohol and the mercuric chloride treatment reduced the
number of infected seeds somewhat.

P_. stewarti was recovered

from a rather high percentage of the kernels in the controls
as shown in Table IX.

It is possible by isolations to determine

that the percentage of infected kernels within a variety is
higher than the percentage of wilted plants that will be
produced when the same kernels are planted.
Discussion
Stewart's disease caused by P. stewarti (Smith) com.

53

S. A. B. is a disease of corn plants and in general causes a
wilting of the entire plant at any time from the seedling
stage until the plants are nearly mature.

The bacterial

organism is a vascular parasite and in systemic cases of wilt
plugs up the xylem vessels from the base of the plant causing
a deficiency of water and subsequent wilting.

Depending on the

region of the plant inoculated either naturally or artificially,
local or systemic conditions may result.

If a young suscept­

ible plant is inoculated at the crown in such a manner that a
large number of bundles become infected with a virulent culture
of P. stewarti, complete wilting will occur in a very short
time*

However, if only a small portion of the bundles is

infected, local lesions and wilting will occur and the plant
may survive and produce more or less normal ears.

Sometimes

the ears and kernels are small and deformed with the ear poorly
filled on a plant that shows quite general systemic cymptoms
but that has survived the disease until it reached maturity.
The conditions and factors influencing outbreaks of
Stewart’s disease are undoubtedly many, some of which are quite
well known.

It is believed by most investigators that high

temperature, abundant soil moisture, and high humidity favor
the development of wilt.

The conditions that influence the

development of the disease other than weather are: (1) the
presence of the pathogen, (2) the resistance of the host to

54

the pathogen, (3) infected seed, (4) insect carriers, and (5)
other organisms associated with the pathogen*
The pathogen causing Stewart's disease is present in,
and can he isolated from, kernels produced on diseased plants*
According to Ivanoff (5) it can he isolated from old infected
corn stalks and from the soil,

Boos and Elliott (12) found it

present in the alimentary tract of the flea beetle Chaetoenema
pulicaria Horn., and the writer was able to isolate it from
the alimentary tract of the seed-corn maggot Hylemyia oilferura
Meigen.

So the sources of inoculum are numerous enough to

provide infection when conditions are favorable.
There have been a number of varieties of corn produced
which have shown resistance to oacterial wilt.

Smith (26)

produced the variety Golden Cross Bantam which has stood up
well in the field in Indiana, New York, and other states.
This variety is very susceptible to artificial inoculation
and has shown little promise of resistance in Michigan.

In

the summer of 1934 Golden Cross Bantam was the only variety
in any of the College plots that showed 100 percent wilt.
The Whipple variety developed by Clinton and Singleton (1)
seems to be quite tolerant to the disease m

Michigan but

not highly resistant to artificial inoculation.

Ivanoff (8)

has produced some inbreds and hybrids wh^ch Soood up well
under artificial inoculations both in the field and green­
house.

These strains have not been tesued in Michigan.

55

Phytomonas stewarti has been found in ohe seed of
wilted plants since the discovery of the disease, Smith (24)
and Ivanoff (5) were able to clearly demonstrate the presence
of the bacterium in the chy.lazal region.
also been corroborated by the writer.

These findings have

The pathogen is easily

isolated from Infected kernels and some lots of seed have
shown as high as 25 percent infection.

The organism is carried

over winter in this manner and affords a source of Inoculum
when the seeds are germinated.
controlled
high.

wps

In no case when insects were

the percentage of wilt caused by infected seed

It was found that puncturing through the chalazal region

into the base of the epicotyl at germination would greatly
increase wilt if the organism was present in the seea.

The

percent of wilt in these punctured seedlings was much greater
than in the controls.

This indicates that the organism is

fixed within the endosperm of the seed and is freed upon injury
as might occur by the larvae of insects feeding within the
kernel•
As there is no evidence -chat the pathogen is harbored
in the soil for any length of time, it must be present from
some other source to cause infection.

The two known sources

of the organism are the seed and insects.

Poos and h'lliott(12)

isolaced th« organism from the adults of the flea beetle.
C h a e toenema pulicaria Horn, early in the spring before these

56

insects could have obtained the parasite by feeding in
infected host plants#

This is definite proof that the wilt

bacterium may be carried over winter by insects#

There is

some doubt as to the amount of wilt infection produced by
leaf and stem feeding insects.

U&ing a pathogen that reacted

very virulently when Inoculated into the crown of corn plants,
the leaves were inoculated by spraying on a broth culture
followed by pin pricks and by direct injection into the mid­
rib with a fine pointed hypodermic needle.

In none of the

plants was there a single case of systemic wilt.

Local

lesions varying in size would form but always toward the tip
of the leaf from the point of inoculation.

It was Impossible

to isolate the organism from a part of the leaf below the
point of inoculation and it was quite easy to isolate from
the region above or toward the tip from this point.

This

would indicate that the pathogen will travel up the vascular
tissue but is not able to pass downward.
further study.

This point requires

In all probability the larva of these insects

play a more important role as an agent of inoculum inoculation
than do the adults as they feed near the base of the plant
and would account for more plugging of the vascular tissue by
the bacterial wilt organism in this manner.

There is evidence

that several other species of insects transmit the disease from
plant to plant in the field.

Rand and Cash (16) found the adult

of the two flea beetles, Chaetoenema pulicaria and C •_

57

dentioulat a, and the larval stage of the twelve-spotted cu­
cumber beetle, Diabrotica duodecimpunotata Oliv. to dissem­
inate wilt in the field.

Ivanoff (4) transmitted the disease

from wilted to healthy plants with the western corn root worm,
larval stage of Diabrotioa longioornis Say., and states that
the wilt bacterium may gain entrance into the roots of corn
plants through wounds made by the white grub, Phyllphaga sp.
In this work the larval stage of the seed-corn maggot,
Hylemyia cilicrura Meign. was found associated with wilted
plants and cultures of
alimentary tract.

stewarti could be isolated from the

The wheat wireworm, larval stage of Agriotes

mane us Cand. was also found to harbor the wilt organism on
its surface for a short period of time.

Both of these insects

were capable of transmitting wilt, the wireworm mechanically,
and the seed-corn maggot by carrying the organism internally.
Two other organisms found associated with P_»_ stewarti
were parasitic on corn plants.

A species of Fusarium causing

a foot rot of corn was accompanied by P^ stewarti and the two
grew together in culture.

A white bacterial organism was

found associated with P^ stewarti in the seed and in wilted
plants.

Its presence was essential for Stewart*s organism

to gain entrance into the plant from infected seed, and it
was able, in pure culture to cause wilt symptoms similar to
those caused by ]?•_ stewarti. This bacterium is not highly
parasitic and. does not as a rule cause necrotic conditions.

58

Ivanoff (4) also mentions organisms other than P*_ stewarti
that would produce symptoms in corn plants similar to those
of bacterial wilt.
Summary and Conclusions
1.

Inoculation tests were made on a large number of

inbred, hybrid, and commercial varieties of sweet corn.
None of these strains showed marked resistance.

Hypodermic

injections of a broth culture of the pathogen at the base of
the plant was found to be the best method of producing wilt
artificially.

Strains of corn immune to Stewart’s disease

will be relatively difficult to obtain.
2.

Leaf inoculation by hypodermic injections and the

needle prick methods failed to develop systemic infection of
bacterial wilt.
3.

stewarti was found not to be carried in the

soil

for any great length of time.
4.

Infected seed grown in sterilized soil in the absence

of insects produced very little wilt.

Alone in infected seed

P. stewarti will not cause the disease to develop unless
agencies are present which will carry the inoculum into

other
the

young plant.
L l stewarti

was found to be fixed within the

endosperm of the kernel and could not penetrate into the seed­
ling at germination unless aided by injury.

Insects and asso­

ciated organisms will produce an avenue of entrance through

59

the embryo and into the vascular tissue of the young seed­
ling.
6.

The larvae of the seed-corn maggot

ciliorura Meigen. carries P . stewarti in its alimentary
tract.

The wheat wireworm, larval stage of Agrintew man mis

Cand. transmitted the disease from one plant to another.
Insects were the chief agents of dissemination of the disease
in the field.
7.

Organisms associated with

stewarti were studied.

One, a species of Pusarium was the leading parasite with P.
stewarti secondary.

The other a white bacterium was secondary

in parasitic activity but its presence was essential before
P. stewarti could gain entrance into the seedling from infected
seed.
8.

Alcohol as a pre-soak for mercuric chloride helped

reduce the percentage on internally infected seed.

Seed treat­

ment practices at present are ineffective as control measures.
9.

Certain varieties of sweet corn showing field resist­

ance in many localities showed a high percentage of bacterial
wilt under Michigan conditions.
not been tested at this Station.

Some of these varieties have
However, the main methods of

control at the present time are through the use of resistant
varieties•

60

Literature Cited

(1 )*

Clinton, Gr.P• and W.R. Singleton. Stewart’s disease or
bacterial wilt of sweet corn.
Conn. Agr. Exp. Sta. Cir. Bui. 96: 25-36.
Pig. 7-10. 1934.

(2 ).

Halsted, B.D. Sweet corn smut and bacterial disease.
Bui. Torr. Bot. Club 26: 77. 1899.

(3).

Holbert, J.R., C. Elliott, and B* Koehler. Bacterial
leaf blight of dent corn.
Abstract Phytopath. 23: 15-16. 1933.

(4).

Ivanoff, S.S. Bacterial wilt of corn.
Abstract Phytopath: 23: 18. 1933,

(5).

________ Stewarts wilt disease of corn, with emphasis
on the life history of Phytomonas stewarti in
relation to pathogenesis.
Jour. Agr. Res. 47: 749-770. PI. 1-3. Pig. 1-2.
1933.

(6 ).

(7).

______ Inoculation tests with Phytomonas stewarti and
P. vascularum.
Abstract Phytopath. 25: 21. 1935.
_______ A plant inoculator.
Phytopath. 24: 74-76. Fig. 1. 1934.
and A.J. Riker. Resistance of sweet corn to
bacterial wilt.
Abstract Phytopath. 25: 21. 1935.

(8 ).

(9) .
-

and J.G. Dickson. Bacterial wilt of corn
caused by more than one strain of bacteria.
Wise. Agr. Exp. Sta. Bui. 425 (Ann. Rp t . 49):
107-108. Fig. 27. 1933.

( 10) .

Mahoney, C.H., J.H. Muncie, and A.R. Marston. Sweet
corn variety and strain test for 1933.
Mich. Agr. Exp. Sta* Quart. Bui. 16: 162-166.
1934.

(11 ).

McCulloch, L.A* Morphological and cultural note on
the organism causing Stewart’s disease of
sweet corn.
Phytopath. 8: 440-442 PI. 1. 1918.

61

(12).

Poos, F.W., and C. Elliott. Bacterial wilt of corn
and its insect vectors.
Abstract Phytopath. 25: 32. 1935.

(13).

Rand, F.V. Bacterial wilt or Stewart!s disease of corn.
Canner 56: 164-165. 1923.

(14).

________ and L.C. Cash. Stewarts disease of corn.
Jour. Agr. Res. 21: 263-264. 1921.

(15)

________ Further evidence of insect dissemination of
bacterial wilt of corn.
Science (n.S.) 59: 67-69. 1929.

•

(16).

_________ Bacterial wilt of corn.
U.S. Dept, Agr. Tech. Bui. 362*. 1-30. PI. 1-3.
1933.

(17).

Reddy, C.S. Experiments with Stewart’s disease on dent,
flint, and sweet corn.
Abstract Phytopath. 11: 31. 1921.

(18).

________ and J.R. Holbert. Difference in resistance to
bacterial wilt in inbred strains and crosses of
dent corn.
Jour. Agr. Res. 36: 905-910. Fig. 1-2. 1928.

(19).

Rosen, H.R. Bacterial stalk rot of corn.
Phytopath. 16: 241-267. Fig. 1-5. 1926.

(20 ).

Smith, E.F. Notes on Stewart’s sweet corn germ
Pseudomonas stewarti N. sp.
Amer. Assoc. Adv. Sci. Proc. 47: 422-426. 1898.
The cultural characters of Pseudomonas hyacinthi,
Ps. campestris, Ps phaseoli, and Ps. stewarti--four one-flagellate yellow bacteria parasitic on
plants.
U. S. Dept. Agr. Div. Veg. Physiol, and Path. Bui.
28: 1-153. Fig. 1. 1901.

(21 ).

(22 ).

(23) .

.

Completed proof that Pseudomonas stewarti is the
cause of the sweet corn disease of Long Island.
Science (n.s.) 17: 457-458. 1903.
Seed corn as a means of disseminating Bacterium
stewarti.
Science (n.s.) 30: 223-224. 1909*

62

(24)*

_______ Bacteria in relation to plant diseases.
Carnegie Institute of Washington Pub. 27 (3):
89-147. PI. 1-11. Pig. 1-2 and 39-64. 1914.

(25).

_______ Bacterial diseases of plants.
160-176. Fig. 100-118. W.B. Saunders Co.,
Philadelphia. 1920.

(26).

Smith, Glen M. Golden Cross Bantam sweet corn.
U. S. Dept. Agr. Cir. Bui. 268: 1-12. Pig. 1-6.
1933.

(27). Stanley, A.R., and C.R. Orton. Bacterial stalk rot of
sweet corn.
Abstract Phytopath. 22: 26. 1932.
(28).

Stewart, P.C. Abacterial disease of sweet corn.
N. Y. (Geneva) Agr. Exp. Sta. Bui. 130: 422439. 1897.

(29).

Thomas, R.C. Stewart's disease or bacterial wilt of
sugar corn.
Ohio Agr. Exp. Sta. Monthly Bui* 9: 81-84. 1924.

(30).

A bacteriophage in relation to Stewart's disease
of corn.
Phytopath. 25: 371-372. 1935.

(31).

Preliminary estimates of crop losses 1931, 1932, 1933.
The Plant Disease Survey. Division of Mycology
and Disease Survey.
Untied States Department of Agriculture.
Tables 16, 17, and 18. February 1, 1935.

(32).

U. S. Dept. Agr.

Plant Disease Reporter 19; 38. 1 9 3 ^

Explanation of plates

Plate I -- Plants showing systemic infection after
inoculation with a pure culture of P. stewarti.
Plate II -- Plant showing the leaves sticking together
clue to bacteria oozing from the leaf surface. P. stewarti
end the white bacterium are often found together in
plants showing symptoms of this type.
Plate III --- Healthy plants inoculated with a pure
culture of the'white bacterium. Note the center leaf
rolled' up tightly. This is a very characteristic
symptom produced by this organism.
Plate IV -- Plants grown in sterilized soil and in the
absence of insects. Wilt produced by puncturing through
the chalazal region at the base of the kernel with a
fine needle.

plate I

Plate II

Plate III