Diseases of Chickpea, Lentil, Pigeon Pea, and Tepary Bean in Continental United States and

Puerto Rico
Author(s): Walter J. Kaiser
Source: Economic Botany, Vol. 35, No. 3 (Jul. - Sep., 1981), pp. 300-320
Published by: Springer on behalf of New York Botanical Garden Press
Stable URL: http://www.jstor.org/stable/4254300
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 Diseases of Chickpea, Lentil, Pigeon Pea,
and Tepary Bean in Continental United
States and Puerto Rico1
WALTER J. KAISER2

The Leguminosae (pea or bean family) are composed of some 690 genera and
18,000 species (Purseglove, 1968). It is the second largest family of seed plants
(following the Gramineae)(Aykroyd and Doughty, 1964). Within the Legumino-
sae, there are 18-20 species that are cultivatedwidely for their edible seeds which
are high in protein (17-25+%) (Aykroyd and Doughty, 1964). The seeds of le-
gumes are second only to cereals as the most importantsource of food for humans
and animals (National Academy of Sciences, 1979).
The term food legume generallyis given to species of Leguminosae,the seeds,
pods, and/or leaves of which are eaten by humans. The word pulse is used in
some countries colonized by Great Britain,like India and Pakistan,to denote the
dry, mature seeds which are consumed by humans.
A chronic protein deficiency exists in most developing countries of the world
(Mayer, 1976). In these countries food legumes usually provide the main, and at
times the only, source of protein and essential amino acids in the diets of poorer
inhabitantsfor social, economic, or religious reasons. Legumes are an important
complement to diets heavily dependent on high carbohydratefoods (cereals and
root and tuber crops) (National Academy of Sciences, 1979).
In the United States and its territories, several food legumes are grown on a
commercial scale. After soybean [Glycinemax (L.) Merr.] and peanut (Arachis
hypogaea L.) (which are also classified as oil crops), bean (Phaseolus vulgaris
L.) is the most importantfood legume cultivated in the United States (USDA,
1979a). The seeds of some food legumes, like bean, pea (Pisum sativum L.),
soybean, and lentil (Lens culinaris Medik.) are exported in large quantitiesand
aid in correctingthe nation's sizeable balance of trade deficits (USDA, 1979a).
In most developed countries of the world, with the exception of Japan, food
legumes are consumed in small amounts, and, therefore, contributeminimallyto
satisfying daily protein requirements.Protein from animal sources satisfies most
of that need, but this is a very inefficient method of producingprotein (Mayer,
1976). With the recent dramaticrise in the cost of energy and nitrogenousfertil-
izers, a search will be made to find cheaper, energy-savingmethods of increasing
food production. Food legumes will undoubtedlyassume a more importantrole
in providinga largershare of the proteinrequirementsof the inhabitantsof many
developed countries, including the United States, particularlyas the price of

1 Received 25 August 1980;accepted 28 December 1980.Presentedat the Symposiumon Legumes

at the Twenty-firstAnnualMeetingof the Society for Economic Botany, Bloomington,Indiana,June
16-17, 1980; symposiumorganizedby Dr. A. Douglas Kinghorn.Mentionof a trade name or pro-
prietaryproductdoes not constitutea guaranteeor warrantyof the productby the U.S.D.A. anddoes
not imply its approvalto the exclusion of other productsthat may also be suitable.
2 ResearchPlantPathologist,RegionalPlantIntroductionStation, U.S.D.A., SEA, AR, 59 Johnson

Hall, WashingtonState University, Pullman,WA 99164.

Economic Botany, 35(3), 1981, pp. 300-320

(O 1981, by the New York Botanical Garden, Bronx. NY 10458
1981] KAISER: LEGUME DISEASES 301

TABLE 1. LIST OF PATHOGENS AND THE DISEASES THEY CAUSE IN CHICKPEA, LENTIL,
PIGEON PEA, AND TEPARY BEAN IN CONTINENTAL U.S. AND PUERTO RICO.

Type of disease
Foliage
Seed
or Mosaic Stem Pod
seed- Yel- and/or and/or spot
ling Root low- defor- Spot- petiole or
Crop Pathogen rota rot Wilt ing mation ting blight rot

Chickpea Fungi:
(Cicer Fusarium lateritium
arietinum) f. sp. ciceri + +
F. oxysporum f. sp.
ciceri + +
F. solani f. sp. pisi + +
Macrophomina phaseolina + +
Pythium ultimum + + ?
Rhizoctonia solani + + ?
Verticillium albo-atrum + +
Virus or virus-like:
Alfalfa mosaic + + ?
Bean yellow mosaic + + ?
Pea enation mosaic ? + +
Lentil Fungi:
(Lens Alternaria alternata +
culinaris) Ascochyta pinodella + +
Botrytis cinerea + + + ?
Cladosporium herbarum +
Fusarium oxysporum f.
sp. lentis ? +
F. roseum 'Avenaceum' +
F. solani f. sp. pisi + +
Pythium'ultimum + +
Rhizoctonia solani + +
Sclerotinia sclerotiorum ? ? + + +
Verticillium albo-atrum + +

Virusor virus-like:
Alfalfamosaic +
Bean yellow mosaic +
Pea enation mosaic +
Pea streak + ? +
Pigeon pea Fungi:
(Cajanus Alternaria tenuissima + +
cajan) Botyrosphaeria
xanthocephala ?
Cercospora cajani +
C. instabilis +
Colletotrichum cajani + + + +
Creonectria
grammicospora ?
Fusarium semitectum +
Megalonectria
pseudotrichia ?
302 ECONOMICBOTANY [VOL. 35

TABLE 1. CONTINUED.

Type of disease

Foliage
Seed
or Mosaic Stem Pod
seed- Yel- and/or and/or spot
ling Root low defor- Spot- petiole or
Crop Pathogen rota rot Wilt ing mation ting blight rot

Phoma sp. + + +
Phomopsis sp. + +
Physalospora sp. +
Phytophthora parasitica +
Pleonectria megalospora ?
Rhizoctonia ferrugena +
Sclerotium rolfsii + + +
Uredo cajani + ?
Uromyces dolicholi + ?
Virus or virus-like:
Rhynchosia mosaic + +
Witches'-broom + +
Nematodes:
Criconemoides sp. +
Helicotylenchus dihystera +
Hoplolaimus galeatus +
Meloidogyne arenaria +
M. javanica +
Pratylenchus brachyurus +
P. schribneri +
Rotylenchulus reniformis +
Trichodorus christiei +
Tylenchorhynchus
claytoni +
Tepary bean Fungi:
(Phaseolus Fusarium solani f. sp.
acutifolius phaseoli +
var. Sclerotinia sclerotiorum + + + +
latifolius) Uromyces phaseoli
var. typica + ?

Bacteria:
Pseudomonas phaseolicola + + ? +
Xanthomonas phaseolicola + + ? +
Virus or virus-like:
Alfalfa mosaic ? +
Bean common mosaic +
Bean golden mosaic + +
Curly top +
Pod mottle +
Whitefly-transmitted
agents + +
a+, pathogen capable of producing disease in host; +, pathogen may or may not produce disease in host; ?, pathogenicity of
microorganism in doubt.
19811 KAISER: LEGUME DISEASES 303

animal protein increases and people become more concerned about conserving
their nation's scarce naturalresources and dwindlingenergy supplies.
To anticipate some of the problems that may be encounteredin expandingthe
area undercultivationof differentfood legumes, it will be necessary to investigate
the differentfactors which may adversely affect production.Diseases frequently
limit yields and reduce quality of edible legumes in the United States and else-
where. The diseases of some of these crops, like bean (Silbernageland Zaumeyer,
1973; Zaumeyer and Meiners, 1975), pea (Hagedorn, 1974, 1976) and soybean
(Sinclairand Shurtleff, 1975)have been reviewed elsewhere. It is the purpose of
this paper to discuss the diseases of 4 less common food legumes that are culti-
vated in the continentalUnited States and Puerto Rico. These crops are chickpea
(Cicer arietinum L.), lentil, pigeon pea [Cajanus cajan (L.) Huth], and tepary
bean (Phaseolus acutifolius A. Gray). For easy reference, the pathogensaffecting
these 4 crops in the continental United States and Puerto Rico have been listed
according to the type of disease(s) produced in each crop (Table 1).

CHICKPEA (CICER ARIETINUM L.)

Chickpea, also called garbanzo, gram, or Bengal gram, is an annual, self-pol-

linated food legume that is cultivated in many countries of the world, frequently
under semiaridconditions (van der Maesen, 1972). In 1978, chickpeas were cul-
tivated worldwide on 10,481,000ha (26,202,500 acres) with over 90% grown in
India (FAO, 1979).Chickpeasare grown commerciallyin the United States, pri-
marily in the central coastal areas of California.In 1978, 5,200 ha (13,000 acres)
were harvested in California(California,1980). However, in the same year, im-
ports of chickpea seeds into the United States exceeded $7,500,000 (USDA,
1979b). Currently,there is an interest in testing chickpea as an alternativecrop
in the drylandareas of other states, e.g., northernIdaho and eastern Washington
(Anonymous, 1980;W. J. Kaiser, unpublished).

Diseases
Different diseases affect chickpea when they are grown under drylandas com-
pared to irrigatedconditions. In some countries, like India or Iran, diseases of
this crop are an importantfactor contributingto low and erraticyields and quality
(Kaiser and Danesh, 1971b;Nene et al., 1978; Sen Gupta, 1974). Much of our
knowledge of chickpea diseases in the United States is from research carriedout
in Californiaduringthe last 25-30 yr.
Cultivation of chickpeas in the southern coastal counties of Californiadates
back to the foundingof the Spanish missions over 175yr ago (Smith et al., 1950).
By the mid-1930s,chickpeas had become a commercialcrop in this region with
an annual productionof some 2,500,000 lb (1,136,364 kg) (Smith et al., 1950).Of
the several diseases reportedto affect chickpeas in this region, Erwin and Snyder
(1958) considered virus yellows and Fusarium wilt to be the most serious and
widespread. Symptoms of both diseases in chickpea consisted of yellowing and
wilting of the foliage and death of infected plants. Symptomsof differentwilt-like
disorders of chickpea are illustrated and described in a recent publication by
Nene et al. (1978). At least 3 viruses were isolated from yellows-affected plants
in California(Snyder et al., 1956). These were identifiedas bean yellow mosaic,
304 ECONOMIC BOTANY [VOL. 35

1S~~~~~~~~~~~~~~

Fig. 1-4. Fig. 1. Fusarium root rot (right)is a serious soilbornedisease of chickpea worldwide.
Roots of infected plants(right)are darkin color and rotted;healthyplants(left). Fig. 2. Lentil plants
(lightcolored)in a fieldplantingare dying due to root rot caused by a complexof soilbornepathogens,
includingPythium ultimum and Rhizoctonia solani. Fig. 3. Infectionof pigeon pea foliage by the rust
pathogenmay result in prematuredefoliationand reduced yields. Fig. 4. Stuntedtepary bean plant
(left) is infected with the NY 15 strainof bean common mosaic virus; healthyplant (right).
1981] KAISER: LEGUME DISEASES 305

alfalfa mosaic, and pea enation mosaic viruses. Bean yellow mosaic virus was
isolated most frequently from plants exhibiting symptoms of virus yellows. In-
cidence of virus yellows varied from year to year but in some plantingsas many
as 50%of the plants were infected (Snyder et al., 1956). Yields of virus-infected
chickpea are usually reduced by more than 50%(Kaiser and Danesh, 1971a)and
mortality may be high, particularlywhen plants are infected early (Kaiser and
Danesh, 1971a;Snyder et al., 1956).
The pathogen causing Fusarium wilt of chickpea in the south coastal areas of
Californiawas identifiedas FusariumlateritiumNees emend. Snyder & Hans. f.
sp. ciceri (Padwick) Erwin (Erwin, 1958a). The fungus produced typical wilt
symptoms of the shoot and discolorationof the vascular elements. Erwin (1957,
1958b) also identified another soil-borne pathogen, Verticillium albo-atrum
Reinke & Berth., as causing a chickpea wilt disease of minor importance in
California. The isolates of V. albo-atrum from chickpea were microsclerotial
types.
In recent years, the commercial chickpea-producingareas in Californiahave
shifted northwardto the central coastal region of the state (Phillips, 1979;Wes-
terlund et al., 1974). In a survey of 7 chickpea plantings in California'scentral
coastal area between 1971 and 1972, Westerlundet al. (1974) identifiedthe fol-
lowing fungi as causing root rot and wilt diseases of chickpea: Fusarium oxy-
sporum Schlecht. f. sp. ciceri (Padwick)Matuoand Sato, F. solani (Mart.)Appel
& Wr. f. sp. pisi (E. R. Jones) Snyder & Hans., Macrophominaphaseolina
(Tassi) Goid., Pythium ultimum Trow., and Rhizoctonia solani Kuhn. Virus dis-
eases are less a problemthan in the south coastal areas (Westerlundet al., 1974).
Fusariumsolani f. sp. pisi (Fig. 1) is an importantroot rot pathogenof chickpea
in California,as it was shown earlierto be in Washington(Kraft, 1969). Wester-
lund et al. (1974)isolated F. solani f. sp. pisi from 47%of wilted chickpeaplants,
but F. oxysporum f. sp. ciceri from only 6%. Also, they failed to isolate F.
lateritium f. sp. ciceri from diseased chickpeas and they were unable to prove
the pathogenicityof several of Erwin's originalisolates of this fungusto chickpea.
However, Erwin's originalisolates that were tested by Westerlundet al. (1974)
may have lost their pathogenicityto chickpea after being kept in culture for over
15 yr. Both Fusarium wilt and root rot were severe in fields previously cropped
to chickpea, but they were not found in fields planted to chickpea for the first
time (Westerlundet al., 1974).
Pythium ultimum and Rhizoctonia solani caused pre- and post-emergence
damping-offand necrosis and death of small chickpea roots in California(Smith
et al., 1950; Westerlundet al., 1974). Both pathogens were isolated most fre-
quently from diseased plants on land with no previous history of chickpea pro-
duction. Pythiumultimumis also the cause of a serious pre-emergencedamping-
off disease of white-seededchickpeas in the Palouse regionof eastern Washington
(Kaiser and Hannan, 1981).Emergenceof nontreatedchickpea seeds was reduced
by 60-80% or more by P. ultimum in Palouse soils with no previous history of
chickpea cultivation.
Macrophominaphaseolina may induce a wilting disease of chickpea plants
grown underdrylandconditions, but only where plants receive less than adequate
water (Westerlundet al., 1974). This pathogen generally is not a problem in the
field when adequate soil moisture is maintained.
306 ECONOMIC BOTANY [VOL. 35

Erwin (1958a) found 4 chickpea lines that had high levels of resistance to F.
lateritium f. sp. ciceri. These lines need to be tested for their resistance to Fu-
sarium wilt caused by F. oxysporumf. sp. ciceri. In 1978,Phillips(1979)screened
279 lines from the InternationalCrops Research Institutefor the Semi-AridTrop-
ics (ICRISAT), Hyderabad, India. Thirty-fouraccessions remainedfree of wilt
symptoms.
The prevalenceof Fusariumdiseases only in fields previouslycroppedto chick-
pea suggests the importanceof crop rotation (Westerlundet al., 1974). Both F.
solani f. sp. pisi (Westerlundet al., 1974)and F. oxysporumf. sp. ciceri (Haware
et al., 1978)are carriedon the seed which is one methodby which Fusarium wilt
and root rot can be introducedinto new areas. Haware et al. (1978) showed that
the wilt Fusarium was eradicated from seed by treatment with a mixture of
Benomyl (methyl-1-[butylcarbamoyl]-2-benzimidazolecarbamate) and Thiram
(bis-[dimethylthiocarbamoyl]disulfide).
Ascochyta blight [Ascochyta rabiei (Pass.) Lab.] is a potentially devastating
seedborne disease of chickpea which until recently was not reported from the
Western Hemisphere. In 1974, Ascochyta blight caused extensive damage to
experimentalchickpea plantings at Saskatoon, Canada (Morralland McKenzie,
1974). Wet, cool weather favors disease development. Apparently,the pathogen
was introducedinto Canadaon importedchickpea seed. Since A. rabiei is readily
seedborne, care should be exercised when chickpea seeds are importedinto the
United States for research or commercial purposes. Additional research is re-
quired to determinewhether A. rabiei can be eradicatedfrom chickpea seed by
thermotherapyand/or chemical means. Preliminaryresults indicated that treat-
ment of Ascochyta-infected chickpea seed with certain chemical compounds,
especially the benzimidazoles, greatly increased emergence and reduced disease
incidence and severity in seedlings (Kaiser et al., 1973).

LENTIL (LENS CULINARIS MEDIK.)

The cultivatedlentil is a self-pollinated,cool-season annualthat is of Old World

origin and one of the first food crops to be cultivated by man (Zohary, 1976).In
the United States, lentils are grown commerciallyin the Palouse regionof eastern
Washington and northernIdaho in rotation with wheat (Triticumaestivum L.)
and dry-ediblepeas. Lentils were first plantedin the Palouse in 1916(Youngman,
1968), and have since become an importantcash crop. In 1978, lentils were har-
vested from 52,400 ha (131,000acres) (Idaho, 1979;Washington,1978). Much of
the lentil crop produced in the Palouse is exported. The value of lentil exports
in 1978exceeded $15,000,000(USDA, 1979b).

Diseases
Consideringthe importance of lentil as an alternate cash crop in the Pacific
Northwest, little informationhas been published on its diseases in the United
States. The first publishedreportof fungus diseases affectinglentils in the Pacific
Northwest was by Wilson and Brandsbergin 1965. They made numerousisola-
tions from diseased, field-grownlentil seedlings over a 2-yr period and found
several soilborne fungi to be incitants of root (Fig. 2) and stem diseases of lentil
in the Palouse region. Fungi pathogenicin their greenhouse and field inoculation
19811 KAISER: LEGUME DISEASES 307

studies included Ascochyta pinodella L. K. Jones, Botrytis cinerea Pers. ex Fr.,

Fusarium oxysporum (possibly F. oxysporum f. sp. lentis Vasudeva & Sriniva-
san), Fusarium roseum (Lk.) Snyd. & Hans. 'Gibbosum,' Rhizoctonia sp., Scle-
rotinia sclerotiorum (Lib.) d By., and Verticillium albo-atrum. In the Palouse
region, Rhizoctonia solani has been isolated from discolored roots of diseased
lentils and isolates of the fungus were pathogenic to germinatingseeds and roots
of inoculated lentils (W. J. Kaiser, unpublisheddata). With high moisture con-
ditions, S. sclerotiorumcan cause severe damageto the lentil crop in this region
(Amer. Dry Pea & Lentil Assoc., 1980).
Fusarium wilt caused by F. oxysporumf. sp. lentis is one of the most important
diseases of lentil in some lentil-producingcountries, such as India (Sen Gupta,
1974). Wilson and Brandsberg(1965) isolated cultures of F. oxysporum from
diseased Palouse lentils that were similar in cultural and morphologicalcharac-
teristics and in pathogenicity to a known isolate of F. oxysporum f. sp. lentis.
Their pathogenic isolates of F. oxysporumcaused a root rot and vascular wilt of
inoculated lentils.
Although Botrytis cinerea was isolated infrequentlyfrom diseased lentil seed-
lings, Wilson and Brandsberg(1965) considered it to be a potentially important
pathogen of lentil in the Pacific Northwest. Recent studies have demonstrated
that B. cinerea is transmittedin a low percentage of seed of field-grownPalouse
lentils (W. J. Kaiser, unpublisheddata).
Foliar diseases of lentil are usually of minor importancein the Palouse. Fungi
associated with foliar diseases include Alternaria tenuis Nees. [=A. alternata
(Fries) Keisslers], Cladosporium herbarum Pers. ex Fr., and Stemphylium bot-
ryosum Wallr. (Wilson and Brandsberg, 1965). In Canada, Alternaria sp. and
Cladosporium sp. also were associated with leaf blight diseases of lentil (Mc-
Kenzie and Morrall, 1975).
Lentils are a cool season crop with an indeterminategrowth habit. High tem-
peratures adversely affect growth and flowering of lentils and may predispose
plants to disease. For instance, in greenhouse studies, Lin and Cook (1977)dem-
onstrated that F. solani f. sp. pisi, normallya root rot pathogen of pea (Pisum
sativum), caused a black root rot of lentil at high (25-30 C), but not at low (<20
C) soil temperatures. In nature, F. solani f. sp. pisi would normally not be a
pathogen of lentil because average soil temperaturesfound in the Palouse during
the lentil growing season are below 25 C.
Pythium ultimum is an important seed-rotting, damping-off, and/or root rot
pathogen of several food crops in the Pacific Northwest, including peas and
wheat, that are grown in rotation with lentil (Kraftand Burke, 1971;Cook et al.,
1980). This pathogen has been isolated from discolored roots of lentil seedlings
and flowering plants exhibiting symptoms of stunting and chlorosis in Iran and
Washington state (Kaiser and Homer, 1980; W. J. Kaiser, unpublisheddata).
Several isolates of P. ultimum from different food crops grown in the Palouse
region were pathogenic to lentils in greenhouse inoculationtests (W. J. Kaiser,
unpublisheddata). In the absence of obvious root rot symptoms, Lin and Cook
(1977) found lentil inoculated with P. ultimumto be smaller in size and to have
fewer branches than noninoculatedplants.
New or modifiedculturalpractices, like minimumtillage cultivationto control
erosion, may affect the importanceand severity of previously minor or uniden-
308 ECONOMIC BOTANY [VOL. 35

tified diseases of a crop. An example of this phenomenonwith lentils was dem-

onstrated recently by Lin and Cook (1977). They showed how a previously un-
diagnosed root rot disease of lentil caused by Fusarium roseum 'Avenaceum'
increased in importance when nontilled lentils were direct-seeded into undis-
turbed (zero tillage), dead bluegrass sod in eastern Washington.
The lentil crop in the Pacific Northwest is free from the ravages of a few
important and destructive diseases. Notable among these is Ascochyta blight
(Ascochyta sp., possibly A. lentis Bond. & Vassil.), a seedborne disease that
attacksthe leaves, stems, pods, and seeds of lentil. Ascochyta blightwas reported
recently in Canada (Slinkard and Drew, 1980), where it is considered to be a
potentially importantdisease of lentil (R. A. A. Morrall, personal communica-
tion). Every effort should be made to exclude this and other potentially devas-
tating diseases from lentil-growingareas of the United States.
In Iran, lentils are naturally infected by alfalfa mosaic (AMV), bean yellow
mosaic (BYMV), cucumbermosaic, and pea leaf roll viruses (Kaiser, 1973),while
in Italy, they are a naturalhost of pea enation mosaic virus (PEMV)(Vovlas and
Rana, 1972).Informationis meageron the distribution,incidence, and importance
of virus diseases of lentil in the United States. In the Palouse area, several viruses
have been isolated from diseased lentils, includingAMV, BYMV-type isolates,
PEMV, and pea streak virus (R. 0. Hampton, personal communication).Inci-
dence of virus infection appears to vary greatly from year to year and may be
relatedto migrationsof aphidvectors and the proximityof virus-infectedalternate
hosts to lentil plantings. Virus diseases of lentil is an area that merits additional
research.
Pea seedborne mosaic virus (PSbMV) may be a potential threat to the lentil
crop in the Pacific Northwest (Hampton and Muehlbauer, 1977). However, pri-
mary or secondary infection of lentil by PSbMV has not yet been observed in the
field. PSbMV is easily transmittedfrom peas, a naturalhost of the virus, to lentils
by artificialmeans and is then seed-transmittedin lentil at frequenciesof 32-44%
(Hamptonand Muehlbauer,1977). Four lentil lines in the USDA plant introduc-
tion (PI) collection were found to be immuneto PSbMV (Haddadet al., 1978).

PIGEON PEA [CAJANUS CAJAN (L.) HUTH.]

The pigeon pea is a woody, short-livedperennialshrubthat is cultivatedwidely

in the tropics and subtropics, often as an annual. It is a drought-tolerantcrop
frequently grown in semiaridregions on poor soils (De, 1974;Purseglove, 1968;
Royes, 1976). Pigeon peas, also called arhar,red gram, Congo pea, and gandul,
are cultivated on some 3,000,000 ha (7,500,000 acres) worldwide, with over 90%
of the productionin India (Rachie and Roberts, 1974). In the Americantropics,
the pigeon pea is an importantfood crop where the seeds are consumed as green
(immature)or dry (mature)peas. In some countries, it is also used as forage for
animals or as a green manureor cover crop (Purseglove, 1968;Morton, 1976).
The Commonwealthof Puerto Rico is the only location in the United States
where pigeon peas are presently grown as a commercialcrop. Pigeon pea is the
most importantfood legume cultivated in Puerto Rico, where an importantcan-
ning industry has developed around this crop. During 1975-1976, pigeon peas
were harvested from approximately6,000 ha (15,000 acres) (ConjuntoTechno-
l6gico, 1977).However, due to an increaseddemandfor fresh, canned, and frozen
1981] KAISER: LEGUME DISEASES 309

pigeon peas, over 870,000kg were importedinto Puerto Rico and the continental
United States during 1978-1979 (USDA, 1979c).

Diseases
A number of diseases of varying severity affect the roots, stems, petioles,
leaves, pods, and seeds of the pigeon pea in tropical and subtropicalareas of the
United States, includingFlorida, Hawaii, Puerto Rico, and Texas (Barnes, 1973;
Nene, 1978; Spence, 1975; USDA, 1960). The diseases are caused primarilyby
fungi, althougha few disordersof unknownetiology with virus- or mycoplasma-
like symptoms have been observed in Puerto Rico (Maramoroschet al., 1974a,b;
Bird et al., 1975;Vakili and Maramorosch,1974).
Much of the pioneeringresearch on pigeon pea diseases in the Western Hemi-
sphere was done by researcherslocated at the Mayagiiezand Rlo Piedrasexper-
iment stations in Puerto Rico, beginning in the early 1900s. A majority of the
early studies dealt with diseases caused by fungi, particularlythose inciting dis-
eases of the foliage, stems, and pods.
Over 60 yr ago, Stevenson (1917) reported on the etiology and occurrence of
several diseases of pigeon pea in Puerto Rico. These were leaf spots caused by
Cercospora cajani P. Henn. [=Mycovellosiella cajani (P. Henn.) Rangel &
Trotter], Uromyces dolicholi Arth. and an unknown stem canker disease, pos-
sibly of fungal etiology.
Two rust diseases have been reportedto infect pigeon pea in the United States
(CommonwealthMycological Institute, 1968;Nene, 1978;Spence, 1975;Tucker,
1927a;USDA, 1960).These rusts were identifiedas Uredo cajani Syd. and Uro-
myces dolicholi. Some confusion exists concerning the proper identificationof
these 2 fungi on pigeon pea foliage. Differentiationis possible only when the telial
spore stage is found and this has yet to be observed in U. cajani (Commonwealth
Mycological Institute, 1968).Rust is a potentiallyimportantdisease of pigeon pea
in the Caribbean(Fig. 3). In Jamaicaand Trinidad,Spence (1975)observed that
severe rust infection resulted in the shedding of infected leaves and may be
responsible for significantyield reductions. Many of the dwarf pigeon pea vari-
eties developed by the University of the West Indies are highly susceptible to
rust infection. Pigeon pea varieties recommendedfor cultivation in Puerto Rico
are tolerant to rust (ConjuntoTechnologico, 1977). Differentstrainsof U. cajani
may exist in the Caribbeanarea (Spence, 1975).
Two Cercospora species, C. cajani and C. instabilis Rangel, cause leaf spot
diseases of pigeon pea in Puerto Rico (Nene, 1978;Stevenson, 1917, 1918;Tuck-
er, 1927a; USDA, 1960). Infection may result in prematureshedding of leaves.
The Cercospora lesions on pigeon pea leaves are similar to those caused by
Colletotrichum cajani. Cercospora leaf spots are common diseases of pigeon pea
in Puerto Rico and are generally of minor importance(Tucker, 1927a).
Anthracnosecaused by Colletotrichumcajani is an importantfoliar disease of
pigeon pea that was first described in Brazil in 1916 (Rangel, 1916). In 1925, C.
cajani caused a destructive disease of the leaves, pods, and seeds of pigeon pea
in Puerto Rico (Tucker, 1927a,b).The disease was most severe duringperiods of
heavy rainfall. Infection by C. cajani frequently resulted in spotting, necrosis,
deformation,and/or sheddingof pigeon pea pods and leaves, and shrivelingand
reductionin size of infected seeds (Tucker, 1927a,b). Symptoms of C. cajani on
310 ECONOMICBOTANY [VOL. 35

young pigeon pea leaves and pods were similarto those frequentlyobserved on
beans (Phaseolus vulgaris) infected with anthracnose caused by C. lindemuthian-
um (Sacc. & Magn.) Briosi & Cav. However, the bean anthracnose pathogen
does not infect pigeon pea nor vice versa.
Periodically, stem and crown canker diseases of pigeon peas have occurredin
epidemic proportions in Puerto Rico. A Phoma sp. was reported by Alvarez
Garcia (1960) and Lopez Rosa (1969) to cause a serious stem canker disease of
pigeon pea in commercialplantingson the island. The pathogen, which is trans-
mitted in a low percentageof seeds (Lopez Rosa, 1969)affects both seedlings and
older plants, sometimes resulting in death of infected plants (Aponte Aponte,
1963). Pycnidia of the pathogen developed in lesions on stems, branches, and
pods (Alvarez Garcia, 1960). Phoma isolates appeared to vary greatly in their
pathogenicityto pigeon pea. A few were highly virulent to Kaki pigeon pea, but
the majoritywere avirulent(Lopez Rosa, 1969). Lopez Rosa (1969)observed the
perfect stage of Phoma on agar media, and found it to be a heterothallicasco-
mycete. Ascospore cultures formed pycnidia in 4-5 days. No mention was made
regardingthe identityof the perfect stage nor whether it was pathogenicto pigeon
pea. Earlier, Leach and Wright (1930) had reported that a collar rot and stem
canker disease of pigeon pea in Trinidadwas caused by Physalospora sp., an
ascomycete, which had 2 pycnidialstages belongingto Phoma and Macrophoma.
Phytophthoraparasitica Dastur is a potentially importantpathogen of pigeon
pea in Puerto Rico (Kaiser and Melendez, 1978;Abrams et al., 1978). Necrotic,
depressed cankers developed on stems, branches, and petioles of naturallyin-
fected and artificiallyinoculated plants. Cankersup to 6 cm in length frequently
girdledstems, causingbranchesabove infection sites to wilt and die. Several food
crops grown in rotation with pigeon pea in Puerto Rico were also hosts of P.
parasitica, notably eggplantand tomato (Kaiser and Melendez, 1978).Pigeon pea
isolates of the pathogenwere more virulentto pigeon pea thanthose fromeggplant
and tomato. Woundingof pigeon pea tissues favored infection. In India, other
Phytophthora spp. have been identifiedas the cause of a stem blight disease of
pigeon pea (Amin et al., 1978;Kannaiyanet al., 1980;Pal et al., 1970;Williams
et al., 1975).
Stevenson (1917, 1918)isolated several fungi from the dead wood and bark of
pigeon pea plants in Puerto Rico. He believed that some of these fungi were
involved in the death and rotting of stems of mature plants, particularlyMega-
lonectria pseudotrichia (Schw.) Speg., Creonectria grammicospora (Ferd. &
Winge) Seaver (=Nectria grammicospora Ferd. & Winge), and Pleonectria meg-
alospora Speg. [=Thyronectria megalospora (Speg.) Seaver & Chardon] (Ste-
venson, 1917, 1918). However, pathogenicity of these fungi to pigeon pea was
not tested. Tucker (1927a) reported that perithecia of Botryosphaeriaxantho-
cephala (Syd. & Butl.) Th. & Syd. were found in the barkof diseased pigeon pea
plants in Puerto Rico. Although B. xanthocephala was associated with a serious
canker disease, Tucker (1927a) did not demonstrateits pathogenicityto pigeon
pea.
Tucker (1927a)reportedRhizoctoniaferrugena Matz. to cause a pre- and post-
emergence damping-offdisease of pigeon pea seedlings in Puerto Rico and that
the disease was most destructive duringwet weather. He found the host range
of R. ferrugena was extensive and includes several vegetable crops that were
1981] KAISER: LEGUME DISEASES 311

grown in rotation with pigeon pea. Parmeterand Whitney (1970) observed that
an isolate of R. ferrugena obtained from the Centraalbureauvoor Schimmelcul-
tures, The Netherlands, had clamp connections and formed sclerotia similar to
those of Sclerotiumrolfsii Sacc. It is possible that Tuckermay have been dealing
with a fungus resemblingS. rolfsii. Sclerotiumrolfsii was isolated from dead and
dying pigeon pea seedlings from Isabela, Puerto Rico, and the fungus proved to
be pathogenic to seedlings of this crop in greenhouse inoculation studies (W. J.
Kaiser and P. L. Melendez, unpublisheddata).
Recently in Puerto Rico, the role of internallyseedborne fungi on germination
and emergence of seeds in the field was revealed (Ellis and Paschal, 1977, 1979;
Ellis et al., 1977, 1978). During 1976, emergence of seed in several commercial
plantingswas low (28-45%)and it appearedthat the high incidence of internally
seedborne fungi was a primaryfactor contributingto poor seed germination,thus
limitingcommercialproductionof pigeon pea in Puerto Rico (Ellis and Paschal,
1979). Fungi frequentlyisolated from poor quality pigeon pea seed (as measured
by seed germinationand seedling emergence) were Alternaria tenuissima (Fr.)
Wilts., Fusarium semitectum Berk. & Rav., Lasiodiplodia theobromae Pat.,
Phomopsis sp., Aspergillus sp., Cladosporium sp., and Penicillium sp. There
was a negative correlationbetween the occurrence of A. tenuissima, F. semitec-
tum, L. theobromae and Phomopsis sp. and in vitro germinationand field emer-
gence of pigeon pea seed (Ellis et al., 1977). Pigeon pea seed quality also was
correlatedwith the site of productionin PuertoRico. The qualityof seed produced
at Isabela, Puerto Rico, a high-rainfallarea, was poor in comparisonwith seed
produced at Fortuna, Puerto Rico, an arid, low-rainfallarea (Ellis et al., 1978).
Delaying the harvest of seed past maturity frequently resulted in a significant
increase in the incidence of Phomopsis sp., A. tenuissima, F. semitectum, and
L. theobromae. Treatmentof pigeon pea seed from Isabela, Puerto Rico, with
Captan (N-trichloromethylthio-4-cyclohexene-1,2-dicarboximide) and Thiram
(protectant fungicides) or Benomyl (systemic fungicide) significantlyincreased
germinationand field emergence over nontreated seeds. Likewise, foliar appli-
cations of Benomyl several times duringthe growingseason significantlyreduced
subsequent infection of seed by several internallyseedborne fungi that played a
majorrole in reducingseed quality.
Recent investigationswith internallyseedborne fungi have emphasizedthe im-
portantrole that these microorganismsplay in reducingqualityof seed of pigeon
pea and other food legumes produced in Puerto Rico (Ellis et al., 1977). Addi-
tionally, they point out the need of selecting suitable sites in Puerto Rico, like
the south coastal area, for the productionof high quality seed for use in estab-
lishing new plantings(Ellis et al., 1978;ConjuntoTechnologico, 1977).
A few virus- and mycoplasma-likediseases of uncertainetiology affect pigeon
pea in Puerto Rico and other islands in the Caribbean(Bird and Sanchez, 1971;
Bird et al., 1975;Maramoroschet al., 1974a,b).Since the late 1950s, Bird and his
colleagues (1971, 1975)in Puerto Rico have studied various 'rugaceous' diseases
that affect differentfood crops and weed species in the Caribbean.These ruga-
ceous diseases are transmittedby whiteflies(Bemisia tabaci Genn.). One of these
diseases, Rhynchosia mosaic, infects pigeon pea naturallyin Puerto Rico, pro-
ducing a yellow mosaic symptom (Bird et al., 1975).The primaryreservoirof the
yellow mosaic pathogenis Rhynchosiaminima DC., a wild legume. Several high-
312 ECONOMIC BOTANY [VOL. 35

yielding pigeon pea lines developed in Puerto Rico have resistance to yellow
mosaic (Bird et al., 1975).
A witches'-broomdisease of pigeon pea has been reportedfrom several coun-
tries, includingPuerto Rico, DominicanRepublic, and Haiti (Hirumiet al., 1973;
Maramoroschet al., 1974a,b;Nene, 1978;Vakiliand Maramorosch,1974).Symp-
toms of witches'-broomfrequently consisted of a dwarfingof leaves and a pro-
liferationof shoots at the nodes. Electron micrographsof pigeon pea tissues from
witches'-broom-infectedplants revealed the presence of mycoplasma-likeorgan-
isms and rhabdovirus-likeparticles (bullet-shaped)in phloem cells (Hirumiet al.,
1973;Maramoroschet al., 1974a,b).The vector of the disease is unknown.There
was a high incidence of witches'-broomin Haiti. This disease is a potentialthreat
to pigeon pea cultivationin Puerto Rico (Vakili and Maramorosch,1974).
In the Caribbean,surveys of agriculturalsoils have shown that various plant
parasiticnematodes are associated with the roots of pigeon pea (Ayala, 1962a,b;
Singh, 1975). High populationdensities of differentecto- and endoparasiticnem-
atode species aroundpigeon pea roots result in damage to the roots which con-
tributeto poor growth and reduced seed yields from diseased plants. As early as
1911, pigeon peas were reported to be a natural host of rootknot nematodes
[Heterodera radicicola (Greef) Muller (=Meloidogyne spp.)] in the United States
(Bessey, 1911). In Puerto Rico, pigeon pea roots are attacked by Meloidogyne
javanica (Treub.) Chitwood, Rotylenchulus spp. (including R. reniformis Linford
& Oliveira), Criconemoides sp., Helicotylenchus sp., and Hoplolaimus sp. (Ay-
ala, 1962a,b). Rotylenchulusreniformis appears to be the most importantnem-
atode pathogen of the roots of pigeon pea and several other food crops in Puerto
Rico (Ayala, 1962a;Ayala and Ramirez, 1964; Steiner, 1960). In Hawaii during
the 1930s, several legumes, includingpigeon pea, were tested as potentialrotation
and trap crops for pineapple on land that was heavily infested with rootknot
nematodes. Pigeon peas proved to be one of the most rootknot-resistantlegumes
tested (Godfrey, 1928).
In greenhouse studies, pigeon peas were shown to be a good host for several
ecto- and endoparasiticnematode species when planted in soils from cotton,
peanut, and soybean fields in Alabama (Ingram and Rodriquez-Kabana,1977;
Rodriquez-Kabanaand Ingram, 1978).These included Helicotylenchusdihystera
(Cobb) Sher, Hoplolaimus galeatus (Cobb) Thorne, Meloidogyne arenaria Chit.,
Pratylenchus brachyurus (Godfrey) Filipjev and Schuurmans Steckhoven, P.
schribneri Steiner, Trichodorus christiei Allen, and Tylenchorhynchus claytoni
Steiner.

TEPARY BEAN (PHASEOLUS ACUTIFOLIUS A. GRAY)

The tepary bean is a drought-tolerantannualthat originatedin the New World,

probably in the southwestern United States and northwesternMexico (Evans,
1976;Nabhan and Felger, 1978;NationalAcademy of Sciences, 1979;Purseglove,
1968). From archeologicalremains, it appearsthat the tepary bean was a domes-
ticated crop in Mexico over 5,000 yr ago. Teparies are still found growing in the
wild at elevations up to 1,650 m as far south as Guatemalaand as far north as
central Arizona (Nabhanand Felger, 1978).Cultivatedlines of P. acutifolius are
classified as var. latifolius Freeman. Tepary beans are adapted to hot, arid en-
vironments and will usually produce a crop in 60-90 days under these harsh
1981] KAISER: LEGUME DISEASES 313

conditions where other Phaseolus species, like bean (P. vulgaris) would fail.
They will not tolerate frost or waterlogged soils. Hendry (1918) reported that
tepary seeds germinatedrapidly in soils with low moisture content, but rotted
quickly in cold, moist soils. Teparies had become an importantfield crop in the
arid Southwest by 1918where in Californiaalone they were cultivated on some
6,800 ha (17,000 acres) (Hendry, 1919), but their importance declined rapidly
thereafter, due to a combinationof factors, includingsmall seed size, flavor and
odor when cooked, changingland-use trends, and culturalpreferences (Hendry,
1918; Nabhan and Felger, 1978; National Academy of Sciences, 1979). Today
tepary beans are cultivated for their edible dry seeds on a limited scale by com-
mercial and subsistence farmersin southwesternNorth America (Nabhan, 1979;
Nabhan and Felger, 1978).
Teparies are a potentially importanthigh-proteinfood legume suited to culti-
vation in the aridand semiaridregions of the world. It may be possible to transfer
some of the tepary bean's desirable characteristics,such as tolerance to drought
and heat, to other Phaseolus species by interspecific hybridization(National
Academy of Sciences, 1979;Waines, 1978).

Diseases
Very little informationis available on the diseases affecting wild or domesti-
cated tepary beans under naturalconditions in the arid regions of southwestern
North America. In one of the earliest reports on cultivation of this crop in the
United States, Freeman (1912, 1913) mentions that tepary beans differed from
beans in being more resistant to heat, drought, and insect pests. However, no
mention was made of diseases. Subsequently, several reports have appearedin
the literature on the susceptibility or resistance of tepary bean accessions to
different diseases. A majorityof these reports are based on infection of teparies
by variouspathogensin field or greenhousetrials, but not undernaturalconditions
in farmers' fields. A recent report by the National Academy of Sciences (1979)
on tropical legumes states that while some tepary bean accessions are highly
resistant to the bean common blight bacterium [Xanthomonasphaseoli (E. F.
Sm.) Dows.], they are only mildly resistantto most other diseases and pests. Our
knowledge of the diseases affecting tepary beans in nature is fragmentaryand
incomplete.
Tepary beans are reportedto be infected either experimentallyor naturallyby
several viruses. In 1922, Nelson (1932) observed naturalspread of a seedborne
bean virus, presumablybean common mosaic virus (BCMV)from virus-infected
beans to differentPhaseolus species, includingtepary bean, in field trials at East
Lansing, Michigan.Several tepary bean accessions were shown to be susceptible
to naturaland artificialinfection in Puerto Rico and Iran, respectively, by 2 or
more strains of BCMV (Kaiser and Mossahebi, 1974;W. J. Kaiser, unpublished
data). The virus was also transmittedin 20-25% of the seed harvested from the
Puerto Rican BCMV-infected tepary bean plants (W. J. Kaiser, unpublished
data).
Provvidentiand Cobb (1975)reportedseed transmissionof BCMVrangingfrom
7-22% in 4 P. acutifolius PI (USDA plant inventory)accesssions. All inoculated
plants of 15 P. acutifolius accessions were susceptible in greenhouse inoculation
studies to 3 isolates of BCMV from P. vulgaris (Provvidentiand Cobb, 1975).
314 ECONOMIC BOTANY [VOL. 35

Narrowing, mottling, deformation,and twisting of the leaflets and stuntingwere

symptomsfrequentlyobserved in teparybean plants infected with BCMV (Kaiser
and Mossahebi, 1974;Provvidentiand Cobb, 1975)(Fig. 4).
In addition to BCMV, teparies were experimentallyinfected by other viruses,
notably alfalfa mosaic (Zaumeyerand Thomas, 1957), bean yellow mosaic (Zau-
meyer and Thomas, 1957), curly top (USDA, 1960), pod mottle virus (Zaumeyer
and Thomas, 1957), and at least 4 whitefly-transmitted(Bemisia tabaci) mosaic
diseases of Phaseolus lunatus L., Jacquemontia tamnifolia Griseb., Merremia
quinquefolia Hall., and Rhynchosia minima (Bird et al., 1975; G'amez, 1971). The
mosaic disease of P. lunatus, also called bean golden mosaic or bean golden
yellow mosaic, is an importantdisease of bean and lima bean in several countries
of the Caribbeanand Centraland South America (Bird et al., 1975;Costa, 1975;
Gamez, 1971). Granillo et al. (1975) reported the high incidence of a whitefly-
borne disease of P. acutifolius in variety trials in the coastal area of El Salvador.
The disease was believed to be due to bean golden yellow mosaic.
The roots of tepary bean are susceptible to Fusarium solani f. sp. phaseoli
(Burkh.) Snyd. & Hans., a soilbornefungus that causes a serious root rot disease
of bean worldwide (USDA, 1960;Zaumeyerand Thomas, 1957). Fusarium root
rot could become an importantdisease of P. acutifolius if they are planted on
land with a history of bean root rot. This Fusarium disease is frequently more
serious on beans that are growingunderwater stress (Silbernageland Zaumeyer,
1973)as may occur when beans and tepary beans are grown under drylandcon-
ditions in arid and semiaridregions of the world. Tepary beans are susceptible
to white mold (Sclerotinia sclerotiorum) in California(J. G. Waines, personal
communication).Teparies will likely prove to be hosts to other soilborne fungi
and nematodes that are pathogens of bean, notably Pythium spp., Rhizoctonia
solani, Thielaviopsis basicola (Berk. & Br.) Ferr., Sclerotium rolfsii, and Me-
loidogyne spp. (USDA, 1960; Silbernagel and Zaumeyer, 1973; Zaumeyer and
Thomas, 1957).
Three of the diseases reported to affect the foliage of teparies are bean rust
[Uromycesphaseoli (Pers.) Wint. var. typica Arth.] (USDA, 1960;Zaumeyerand
Thomas, 1957),bean common blight(X. phaseoli) (Zaumeyerand Thomas, 1957),
and bean halo blight [Pseudomonasphaseolicola (Burkh.)Dows.] (M. L. Schus-
ter, personal communication).The latter 2 bacterial pathogens are seedborne in
bean and probablywould be transmittedin seed of susceptibletepary bean lines.
Spread and disease development of both bacterial diseases are favored by rain
and humid weather conditions.
The leaves and pods of many P. acutifolius accessions are highly tolerant to
most isolates of X. phaseoli (Schuster, 1955;Schuster et al., 1973).Honma(1956)
succeeded in makingan interspecificcross between P. vulgaris and P. acutifolius
by employingembryoculturetechniques. He obtained4 F1plantswhich appeared
similar to the P. vulgaris parent. Progeny from these 4 F1 plants varied greatly
in their reaction to X. phaseoli (Honma, 1956). Field and greenhouse screening
of the progeny from this interspecificcross eventually resulted in the release of
the variety Great Northern (GN) Nebraska #1, Sel. 27, which exhibited a high
level of tolerance to X. phaseoli isolates from the United States (Coyne and
Schuster, 1974; M. L. Schuster, personal communication).Recently, GN Ne-
1981] KAISER: LEGUME DISEASES 315

braska #1, Sel. 27 was shown to be slightly susceptible to isolates of X. phaseoli

from Uganda and Colombia (Schuster et al., 1973). This variety is also tolerant
to P. phaseolicola races 1 and 2 (Coyne and Schuster, 1974).Since it was released
in the mid-1960s,GN Nebraska #1, Sel. 27 has been used as a source of resistance
to common bacterial blight and halo blight by bean breeders in many countries
(M. L. Schuster, personal communication).
In Puerto Rico, Vakili (1976) screened 151 P. acutifolius lines (many of which
were PI accessions) for resistance to several diseases, includingbacterialblight,
bean common mosaic virus, root rot, and rust. He selected several lines that had
moderateto highresistanceto one or more of these diseases. Seed of the multiple-
disease resistant selections were being increased for release to interested re-
searchers.
STRATEGIES FOR CONTROLLING DISEASES OF FOOD LEGUMES

Various methods are used to control diseases affecting edible legumes in the
United States and its territories. These include the use of chemicals, resistant
varieties, and culturalpractices.
Economic and environmentalconsiderationsprobablywill lead to a significant
reduction in the applicationof pesticides to control foliar and soilborne diseases
of many crops like the food legumes. However, applicationof fungicides to seed
should continue to be an importantmethod of controllingdamping-offand other
seedling diseases.
Culturalpractices continue to be used extensively to control soilbornediseases
caused by fungi and nematodes that attack the roots of edible legumes. Crop
rotation is one method commonly used to control soilborne diseases that have a
narrowhost range, e.g., the Fusarium wilt or root rot diseases of chickpea. Other
cultural methods, like eradication of overwinteringand/or alternative hosts of
certain pathogens or removal of crop residues may be required to achieve a
satisfactorylevel of control of certain diseases.
Host plant resistanceoffers the most promisingand potentiallyimportantmeth-
od of controlling diseases of many food crops. Disease resistance has proved
useful in controllingmany diseases of edible legumes (National Academy of Sci-
ences, 1972, 1979),but much more remainsto be done in developmentof multiple
disease- and pest-resistantcultivars of these food crops. It is possible that more
emphasis will be given to host plant resistance as costs of other control measures
that depend heavily on the use of fossil fuel energy and other scarce resources
rise. This method of control requires that researchers have access to a large,
variable source of germ plasm of differentfood legumes to use in their breeding
programs.Plant germ plasm collections of numerousfood crops have been main-
tained at variouslocations in the United States for many years. These germplasm
collections are an integralpart of the National Plant GermplasmSystem (NPGS).
The NPGS is a coordinatedeffort amongfederal, state, and private organizations
in the United States to collect, introduce, maintain, evaluate, catalog, and dis-
tribute all types of plant germ plasm (USDA, 1977).
Most or all plant germ plasm availableto researchersfrom germ plasm centers
in the United States have PI (USDA plantinventory)accession numbersassigned
to them. The germplasmcollections for the 4 legume crops reviewed in this paper
316 ECONOMIC BOTANY [VOL. 35

are located at 2 of the 4 state-federalregional plant introductionstations in the

United States:
Pullman, Washington:chickpea, lentil, tepary bean
Experiment, Georgia:pigeon pea
Significantstrides have been made in the last 30 yr in controllinga numberof
importantdiseases of food legumes and other crops. However, much remainsto
be done in preventingcrop losses due to diseases and pests, particularlyin the
developing countrieswhere chronicfood shortagesare a commonoccurrenceand
could worsen as the populationsof these countries increase. New approachesof
disease control must conserve resources and energy and promote a clean envi-
ronment. The researchchallenges are great and the opportunitiesfor success are
promising.
LITERATURE CITED

Abrams, R., A. Morales, and F. J. Julia. 1978. Status of researchon pigeon peas in Puerto Rico.
Trop. GrainLegumeBull. 11 & 12: 17-21.
Alvarez Garcia, L. A. 1960. Phoma canker of pigeonpeas in Puerto Rico. J. Agric. Univ. Puerto
Rico 44: 28-30.
Amer. Dry Pea & Lentil Assoc. 1980. Bull. 51 (July 18, 1980).
Amin, K. S., B. Baldev, and F. J. Williams. 1978. Phytophthoracajani, a new species causingstem
blight on Cajanuscajan. Mycologia70: 171-176.
Anonymous. 1980. WashingtonFarmer-Stockman105(20):12A.
Aponte Aponte, F. 1963. El cultivo de gandulesen PuertoRico. CaribbeanAgric. 1: 191-197.
Ayala, A. 1962a. Pathogenicityof the reniformnematodeon various hosts. J. Agric. Univ. Puerto
Rico 46: 73-82.
. 1962b. Occurrenceof the nematode Meloidogynejavanica on pigeon pea roots in Puerto
Rico. J. Agric. Univ. Puerto Rico 46: 154-156.
, and C. T. Ramirez. 1964. Host-range,distribution,and bibliographyof the reniformnema-
tode, Rotylenchulusreniformis,with special referenceto PuertoRico. J. Agric. Univ. Puerto
Rico 48: 140-161.
Aykroyd, W. R., and J. Doughty. 1964. Legumesin HumanNutrition.FAO NutritionalStudiesNo.
19. Food and AgricultureOrganizationof the United Nations, Rome.
Barnes, R. F. 1973. A preliminarylist of literatureon pigeon pea [Cajanus cajan (L.) Millsp.]plant
pathology. Univ. West Indies, Dept. Biol. Sci. Bull. No. 1.
Bessey, E. A. 1911. Root-knotand its control. U.S. Dept. Agric. BureauPlantIndustry,Bull. No.
217.
Bird, J., and J. Sinchez. 1971. Whitefly-transmitted viruses in PuertoRico. J. Agric. Univ. Puerto
Rico 55: 461-467.
1 , R. L. Rodriquez,and F. J. Julia. 1975. Rugaceous(whitefly-transmitted) viruses in
Puerto Rico. In J. Bird and K. Maramorosch,eds., TropicalDiseases of Legumes, pp. 3-25.
Academic Press, New York.
CaliforniaCrop and Livestock ReportingService. 1980. Field crop review. Vol. 1, Jan. 28, 1980.
CommonwealthMycologicalInstitute. 1968. Distributionmaps of plant diseases. Map No. 236, 3rd
edit.
ConjuntoTechnol6gicoparala Producci6nde Gandules.Su Situaci6nEcon6micay sus Perspectivas.
1977. Estaci6n Exp. Agric., Univ. PuertoRico. Publ. 116.
Cook, R. J., J. W. Sitton, and J. T. Waldher. 1980. Evidence for Pythiumas a pathogenof direct-
drilledwheat in the PacificNorthwest. P1. Dis. Reporter64: 102-103.
Costa, A. S. 1975. Increasein the populationdensity of Bemisia tabaci, a threatof widespreadvirus
infection of legume crops in Brazil. In J. Bird and K. Maramorosch,eds., TropicalDiseases
of Legumes, pp. 27-49. Academic Press, New York.
Coyne, D. P., and M. L. Schuster. 1974. Breedingand genetic studies of toleranceto several bean
(Phaseolus vulgaris L.) bacterialpathogens.Euphytica23: 651-656.
1981] KAISER: LEGUME DISEASES 317

De, D. N. 1974. Pigeon pea. In J. Hutchinson,ed., EvolutionaryStudies in WorldCrops, pp. 79-

87. CambridgeUniv. Press.
Ellis, M. A., S. R. Foor, and P. L. M6lendez. 1976. Effect of internallyseed-bornefungi on ger-
minationof pigeon pea in Puerto Rico. (Abstr.) Mem. Soc. PuertorriquenaCienciasAgric. 2:
8-9.
, and E. H. PaschalII. 1977. Methodsof controllinginternallyseedbornefungiof pigeon pea
(Cajanus cajan). Proc. Amer. Phytopathol.Soc. 4: 176.
, and . 1979. Effect of fungicideseed treatmenton internallyseedbornefungi, germi-
nation and field emergenceof pigeon pea (Cajanuscajan). Seed Sci. & Technol. 7: 75-81.
andE. Rosario. 1977. Similaritiesin the internallyseedbornefungiof fourleguminous
crops. Proc. Amer. Phytopathol.Soc. 4: 176.
1 , E. J. Ravalo, and E. Rosario. 1978. Effect of growinglocation on internally-seed-
borne fungi, seed germination,and field emergence of pigeon pea in Puerto Rico. J. Agric.
Univ. PuertoRico 62: 355-362.
Erwin, D. C. 1957. Fusariumand Verticilliumwilt diseases of Cicerarietinum.(Abstr.)Phytopath-
ology 47: 10.
. 1958a. Fusarium lateritium f. ciceri, incitant of Fusarium wilt of Cicer arietinum. Phyto-
pathology48: 498-501.
1958b. Verticilliumwilt of Cicerarietinumin southernCalifornia.P1.Dis. Reporter42: 1111.
and W. C. Snyder. 1958. Yellowingof garbanzobeans. Calif. Agric. 12: 6, 16.
Evans, A. M. 1976. Beans. In N. W. Simmonds, ed., Evolution of Crop Plants, pp. 168-172.
Longman,London.
Food and AgricultureOrganization(FAO) of the United Nations. 1979. ProductionYearbook.Vol.
32. Rome.
Freeman, G. F. 1912. Southwesternbeans and teparies. Univ. ArizonaAgric. Exp. Sta. Bull. No.
68: 573-619.
1913. The tepary, a new cultivatedlegume from the Southwest. Bot. Gaz. 56: 395-417.
Gamez, R. 1971. Los virus del frijolin Centroamerica.I. Transmisi6npor moscas blancas(Bemisia
tabaci Gen.) y plantashospedantesdel virus del mosaico dorado.Turrialba21: 22-27.
Godfrey, G. H. 1928. Legumes as rotationand trap crops for pineapplefields. Hawaii Assoc. Pine-
apple CannersExp. Sta. Bull. No. 10.
Granillo,C., A. Diaz, M. Anaya, and L. A. Bermudezde Paz. 1975. Diseases transmittedby Bemisia
tabaci in El Salvador.In J. Bird and K. Maramorosch,eds., TropicalDiseases of Legumes,
pp. 51-53. AcademicPress, New York.
Haddad,N. I., F. J. Muehlbauer,and R. 0. Hampton. 1978. Inheritanceof resistanceto pea seed-
borne mosaic virus in lentils. Crop Sci. 18: 613-615.
Hagedorn, D. J. 1974. Virus diseases of pea, Pisum sativum. Amer. Phytopathol.Soc. Monogr.
No. 9.
1976. Handbookof pea diseases. Univ. WisconsinExtension Publ. Al 167. Madison,WI.
Hampton,R. O., and F. J. Muehlbauer. 1977. Field transmissionof the pea seedbornemosaic virus
in lentils. PI. Dis. Reporter61: 235-238.
Haware, M. P., Y. L. Nene, and R. Rajeshwari. 1978. Eradicationof Fusariumoxysporumf. sp.
ciceri transmittedin chickpea seed. Phytopathology68: 1364-1367.
Hendry, G. W. 1918. Bean culture in California.Univ. Calif. Agric. Exp. Sta. Bull. No. 294: 285-
348.
. 1919. Climaticadaptationsof the white teparybean. J. Amer. Soc. Agron. 11: 247-252.
Hirumi, H., K. Maramorosch,and E. Hichez. 1973. Rhabdovirusand mycoplasmalikeorganism:
naturaldual infectionof Cajanuscajan. (Abstr.)Phytopathology63: 202.
Honma, S. 1956. A bean interspecifichybrid.J. Heredity47: 217-220.
Idaho Crop and Livestock ReportingService. 1979. Idaho AgriculturalStatistics.
Ingram, E. G., and R. Rodriquez-Kabana. 1977. Subceptibilityof pigeon pea to plant parasitic
nematodes. Proc. Amer. Phytopathol.Soc. 4: 177.
Kaiser, W. J. 1973. Etiologyand biology of viruses affectinglentil (Lens esculenta Moench.)in Iran.
Phytopathol.Medit. 12: 7-14.
, and D. Danesh. 1971a. Biology of four viruses affecting Cicerarietinumin Iran. Phytopath-
ology 61: 372-375.
318 ECONOMIC BOTANY [VOL. 35

, and . 1971b. Etiology of virus-inducedwilt of Cicer arietinum.Phytopathology61:

453-457.
, and R. M. Hannan. 1981. Preemergencedamping-offof chickpea in the Palouse region of
eastern Washingtoncaused by Pythiumultimum.(Abstr.) Phytopathology70: 230.
, and G. M. Horner. 1980. Root rot of irrigatedlentils. Canad.J. Bot. 58: 2549-2556.
, and P. L. Melendez. 1978. A Phytophthorastem canker disease of pigeon pea in Puerto
Rico. P1. Dis. Reporter62: 240-242.
, and G. H. Mossahebi. 1974. Naturalinfectionof mungbeanby bean commonmosaic virus.
Phytopathology64: 1209-1214.
, M. Okhovat,and G. H. Mossahebi. 1973. Effect of seed-treatmentfungicideson controlof
Ascochyta rabiei in chickpeaseed infected with the pathogen.P1.Dis. Reporter57: 742-746.
Kannaiyan,J., 0. K. Ribeiro, D. C. Erwin, and Y. L. Nene. 1980. Phytophthorablight of pigeon
pea in India. Mycologia72: 169-181.
Kraft, J. M. 1969. Chickpea,a new host of Fusariumsolani f. sp. pisi. PI. Dis. Reporter53: 110-
111.
, and D. W. Burke. 1971. Pythiumultimumas a root pathogenof beans and peas in Wash-
ington. PI. Dis. Reporter55: 1056-1060.
Krauss, F. G. 1932. The pigeon pea (Cajanusindicus)-its improvement,culture,and utilizationin
Hawaii. HawaiiAgric. Exp. Sta. Bull. 64.
Leach, R., and J. Wright. 1930. Collarand stem cankerof (Cajanusindicus) pigeon pea caused by
a species of Physalospora. Mem. Imp. Coll. Trop. Agric. (Mycol. Ser.) i.
Lin, Yi-Sheng, and R. J. Cook. 1977. Root rot of lentils caused by Fusariumroseum 'Avenaceum.'
P1. Dis. Reporter61: 752-755.
L6pez Rosa, J. H. 1969. Phoma sp., the causal agentof pigeon pea canker.(Abstr.)Phytopathology
59: 1348.
Maramorosch,K., H. Hirumi, M. Kimura,J. Bird, and N. G. Vakili. 1974a. Pigeon pea witches'
broom disease. (Abstr.)Phytopathology64: 582-583.
1 , , , and . 1974b. Diseases of pigeon pea in the Caribbeanarea:
an electron microscopestudy. FAO P1.Protect. Bull. 22: 32-36.
Mayer, J. 1976. The dimensionsof humanhunger.Sci. Amer. 235: 40-49.
McKenzie, D. L., and R. A. A. Morrall. 1975. Diseases of specialty crops in Saskatchewan:II.
Notes on field pea in 1973-74 and on lentil in 1973. Canad.P1.Dis. Surv. 55: 97-100.
Morrall,R. A. A., and D. L. McKenzie. 1974. A note on the inadvertentintroductionto North
America of Ascochyta rabiei, a destructivepathogenof chickpea. PI. Dis. Reporter58: 342-
345.
Morton, J. F. 1976. The pigeon pea (Cajanuscajan Millsp.), a high-protein,tropicalbush legume.
Hortscience 11: 11-19.
Muehlbauer,F. J., and J. M. Kraft. 1978. Effect of pea seed genotype on preemergencedamping-off
and resistanceto Fusariumand Pythiumroot rot. Crop Sci. 18: 321-323.
Nabhan,G. P. 1979. Teparybeans-the effects of domesticationon adaptationsto aridenvironments.
Arid Lands Newslett. 10: 11-16.
, and F. S. Felger. 1978. Tepariesin southwesternNorth America.Econ. Bot. 32: 2-19.
National Academy of Sciences. 1972. Genetic vulnerabilityof majorcrops. Washington,DC.
. 1979. Tropicallegumes:resourcesfor the future. Washington,DC.
Nelson, R. 1932. Investigationsin the mosaic diseases of bean (Phaseolus vulgarisL.). Mich. State
Coll. Agric. Exp. Sta. Tech. Bull. No. 118.
Nene, Y. L. 1978. A world list of pigeonpea [Cajanuscajan (L.) Millsp.] and chickpea (Cicer
arietinumL.) pathogens.ICRISATPulse PathologyProgressReport3. Hyderabad,India.
, M. P. Haware, and M. V. Reddy. 1978. Diagnosis of some wilt-like disordersof chickpea
(Cicer arietinumL.). Info. Bull. No. 3, InternationalCrops ResearchInstitutefor the Semi-
Arid Tropics, Hyderabad,India.
Pal, M., J. S. Grewal,and A. K. Sarbhoy. 1970. A new stem rot of arharcaused by Phytophthora.
IndianPhytopathol.23: 583-587.
Parmeter,J. R., Jr., and H. S. Whitney. 1970. Taxonomyand nomenclatureof the imperfectstate.
In J. R. Parmeter,Jr., ed., Rhizoctoniasolani, Biology and Pathology,pp. 7-19. Univ. Calif.
Press, Berkeley.
1981] KAISER: LEGUME DISEASES 319

Phillips,J. C. 1979. Descriptionand evaluationof chickpeagermplasmin coastal California.Amer.

Soc. Agron. Abstr. 1979:72.
Provvidenti,R., and E. D. Cobb. 1975. Seed transmissionof bean common mosaic virus in tepary
bean. PI. Dis. Reporter59: 966-969.
Purseglove, J. W. 1968. TropicalCrops:Dicotyledons. Wiley, New York.
Rachie, K. O., and L. M. Roberts. 1974. Grainlegumes of the lowlandtropics. Advances Agron.
26: 1-132.
Rangel, E. 1916. Fungos parasitasdo guando Cajanusindicus Spreng.Lavoura 18: 5-12.
Raychaudhuri,S. P. 1977. A Manualof VirusDiseases of TropicalPlants.MacmillanCo. IndiaLtd.,
Delhi.
Rodriquez-Kabana,R., and E. G. Ingram. 1978. Susceptibilityof pigeon peas to plant parasitic
nematodesin Alabama.Nematropica8: 32-34.
Royes, W. V. 1976. Pigeon pea. In N. W. Simmonds,ed., Evolutionof Crop Plants, pp. 154-156.
Longman,London.
Schuster, M. L. 1955. A methodfor testing resistanceof beans to bacterialblights. Phytopathology
45: 519-520.
, D. P. Coyne, and B. Hoff. 1973. Comparativevirulence of Xanthomonasphaseoli strains
from Uganda, Colombia,and Nebraska. P1.Dis. Reporter57: 74-75.
Sen Gupta, P. K. 1974. Diseases of majorpulse crops in India. PANS (Pest. Artic. News Summ.)
20: 409-415.
Silbernagel,M. J., and W. J. Zaumeyer. 1973. Beans. In R. R. Nelson, ed., BreedingPlants for
Disease Resistance, pp. 253-269. Penn. State Univ. Press, Univ. Park, PA.
Sinclair, J. B., and M. C. Shurtleff,eds. 1975. Compendiumof Soybean Diseases. Amer. Phyto-
pathol. Soc., St. Paul, MN.
Singh,N. D. 1975. Evaluationof nematodepopulationin pigeonpea. In J. Birdand K. Maramorosch,
eds., TropicalDiseases of Legumes, pp. 147-149. Academic Press, New York.
Slinkard,A. E., and B. N. Drew. 1980. Lentil productionin western Canada.Univ. Saskatchewan
Ext. Div. Publ. 413.
Smith, F. L., B. J. Hall, and H. W. Schwalm. 1950. Garbanzos.Univ. Calif. Agric. Exp. Sta. &
Exten. Service Leaflet.
Snyder, W. C., A. 0. Paulus, and A. H. Gold. 1956. Virus yellows of garbanzo. (Abstr.) Phyto-
pathology46: 27.
Spence, J. A. 1975. The importanceof diseases in relationto the grainlegume researchprogramin
the eastern Caribbean.In J. Bird and K. Maramorosch,eds., TropicalDiseases of Legumes,
pp. 151-155. AcademicPress, New York.
Steiner, G. 1960. Tres conferenciassobre nematologia.Agric. Exp. Sta., Univ. Puerto Rico Misc.
Publ. 32.
Stevenson, J. A. 1917. Diseases of vegetable and gardencrops. J. Dept. Agric. Porto Rico 1: 93-
117.
. 1918. A check list of Porto Rican fungi and a host index. J. Dept. Agric. Porto Rico 2: 125-
264.
Tucker, C. M. 1927a. Reportof the plantpathologist.Porto Rico (Mayagiiez)Agric. Exp. Sta. Rep.
1925:24-40.
. 1927b. Pigeon pea anthracnose.J. Agric. Res. 34: 589-596.
United States Departmentof Agriculture. 1960. Index of plant diseases in the United States. Agric.
HandbookNo. 165.
1977. The nationalplant germplasmsystem. Agr. Res. Serv. Prog. Aid No. 1188.
1979a. AgriculturalStatistics. 1979. U.S. Gov. PrintingOffice, Washington,DC.
1979b. U.S. Foreign agriculturaltrade statistical report, calendar year 1978. Economics,
Statistics, and CooperativesService, USDA. Washington,DC.
. 1979c. Foreignagriculturaltradeof the United States (FATUS). Economics, Statistics, and
CooperativesService, USDA. Washington,DC.
Vakili, N. G. 1976. Annualreport. MayagiiezInstituteof TropicalAgriculture,Mayagiiez,Puerto
Rico.
, and K. Maramorosch. 1974. "Witches'-broom"disease caused by mycoplasmalikeorgan-
isms on pigeonpeas(Cajanuscajan) in PuertoRico. P1. Dis. Reporter58: 96.
320 ECONOMIC BOTANY [VOL. 35

van der Maesen, L. J. G. 1972. Cicer L., a monographof the genus, with special referenceto the
chickpea (Cicer arietinum L.), its ecology and cultivation. Meded. Landbouwhogeschool,
Wageningen72-10.
Vovlas, C., and G. L. Rana. 1972. Le virosi delle plante ortensi in Puglia. VII. Lens esculenta
Moench. ospite naturaledel virus del mosaico con enazioni de Pisello. Phytopathol.Medit.
11: 97-102.
Waines, J. G. 1978. Proteincontents, grainweights, and breedingpotentialof wild and domesticated
tepary beans. Crop Sci. 18: 587-589.
WashingtonCrop and Livestock ReportingService. 1978. WashingtonAgriculturalStatistics.
Westerlund, F. V., Jr., R. N. Campbell, and K. A. Kimble. 1974. Fungal root rots and wilt of
chickpea in California.Phytopathology64: 432-436.
Williams, F. J., K. S. Amin, and B. Baldev. 1975. Phytophthorastem blight of Cajanus cajan.
Phytopathology65: 1029-1030.
Wilson, V. E., and J. Brandsberg. 1965. Fungiisolatedfrom diseased lentil seedlingsin 1963-64.P1.
Dis. Reporter49: 660-662.
Youngman,V. E. 1968. Lentils-a pulse of the Palouse. Econ. Bot. 22: 135-139.
Zaumeyer,W. J., and J. P. Meiners. 1975. Disease resistance in beans. AnnualRev. Phytopathol.
13: 313-334.
, and H. R. Thomas. 1957. A monographicstudy of bean diseases and methods for their
control. U.S. Dept. Agric. Tech. Bull. No. 868.
Zohary,D. 1976. Lentil. In N. W. Simmonds,ed., Evolutionof CropPlants,pp. 163-164. Longman,
London.

Plant Classification.Lyman Benson. 2nd ed. 901 pp. illus. D. C. Heath and Company,
Lexington, Massachusetts, 1979. $22.95.
The first edition of Plant Classificationis outstanding.Benson has now come out with
an updatedand completelyrevised book thatbears little resemblanceto the originaledition
except for the splendidand profuse black-and-whiteline drawingsmost of which are new.
Depending upon the previous training of the student, this volume could be used as a
comprehensive text for a one-semester course or for a less concentrated two-semester
course in plant taxonomy and classification.
As an authority on Ranunlculus and Cactaceae in particular,Benson has numerous
examples of the formerin the section on keying in which he uses examples of keys from
13 different books covering practically all areas of the United States. He compares the
various ways by which the differentauthorskey a plant to a species of Ranunculusin all
except one, Long and Lakela's Flora of Tropical Florida. Ranunculus does not occur in
the area, and a species of Citrus is the example used in this instance.
I particularlylike Benson's discussion of the majorsystems of classificationfrom Theo-
phrastusto Cronquist.Coverageof familiesand ordersof dicotyledonsand of morphology
and economic plants of the groups is especially good. There is a minimumof factualerror
in this magnificentvolume. My main regret is that the publisher's proof readers let so
many printer'serrorsthrough.
This attractiveand splendidlybound and printedbook should be owned by all botanists
regardlessof their specialization.
EDWARD T. BROWNE, JR., MEMPHIS STATE UNIVERSITY, MEMPHIS, TN 38152