Powdery mildew is one of the most common and serious diseases of pea which is prevalent throughout the world. In India this disease was first time reported by Butler (1918) from Dehradun.
  • Initial symptoms appear as minute discoloured patches with thin fine meshwork of white mycelium arising at many places on the upper surface of lower leaves (Plate-1) and these white patches soon join together to form larger whitish floury areas.
  • In severe cases of disease development, both upper and lower surfaces of the leaf are infected.
  • The conidia and condidiophores are produced in such profusion that the foliage looks as if dusted with flour and the whole crop in the field appeared white from a distance.
  • With the progress of the disease, similar symptoms are also noticed on tendrils, petioles and stems.
  • Pods are infected in all the developmental stages, but immature pods are more prone to rapid infection.
  • The affected pods show white floury patches consisting of white powdery mass and these patches then turn light brown and finally dark brown in colour and later become necrotic.
  • Such infected pods are either unmarketable or fetch minimum price in the open market.


  • The disease is caused by Erysiphe pisi DC.
  • The fungus is ectoparasitic, spreading on the surface of the host and sending haustoria into the epidermal cells to draw out nourishment.
  • The fungus hyphae are hyaline and septate and conidiophores arise from it vertically bearing conidia either singly or in short chains (Plate-2).
  • Conidia are ellipsoid to ovoid, mature conidia fall off and get dispersed by wind.
  • Later in the season, cleistothecia (sexual stage) appear as dark coloured, round, minute bodies scattered in the mycelial web.
  • The peridium is composed of distinct polygonal cells and is provided with a number of myceloid appendages.
  • Each cleistothecium contains usually 2-8 asci and these asci originate from a single point in the fruiting body, appearing in a fanlike manner.
  • They are ovate, nearly sessile and 46-72 x 30-45 µ in size.
  • The asci contain 2-8 ascospores, which are elliptical, hyaline and unicellular.


Disease cycle and epidemiology:
  • In areas, where, cleistothecia are formed, ascospores play an important role as a source of primary inoculums (Fig.1).
  • However, in other areas, the pathogen overwinters in conidial stage on different collateral hosts of the pathogen like Pisum arvense, Lupinus, Medicago, Lathyrus aphaca, L. culinaris, Medicago hispida, Melilotus inica, Vicia sativa, V. hirsute and Aeschynomene indica.
  • There are reports that the pathogen survives in seed as dormant mycelium but the concept of seed borne nature of the disease could never be confirmed.
  • Ascospores or conidia germinate by producing a germ tube which produces an appresorium on its tip and continues growing ectophytically.
  • Each conidia of the fungus have 52 per cent moisture and germinate easily under dry conditions, so they are called as “dry weather fungus”.
  • Conidiophores bearing conidia are produced by the growing mycelium.
  • Conidia are passively dispersed and cause secondary spread of the disease.
  • The disease is more prevalent in dry weather and moderate temperatures.
  • A temperature range of 10-30oC is favourable for conidial germination with optimum being at 20oC.
  • A fairly dry soil and heavy application of nitrogenous fertilizers increase the disease incidence.


  • Collect and destroy the plant debris.
  • Remove all the collateral hosts from in and around the field.
  • Early sown (Late September to early October) crops escape the disease.
  • A large number of cvs. /lines possessing resistance against this disease have been reported which can be used for sowing or in breeding programme for developing resistant varieties (Solan nirog, Rachna etc.).
  • Use of biocontrol agent like Ampelomyces quisqualis serve as a best alternative to combat with this pathogen.
  • With the initiation of flowering, spray the crop with wettable sulphur (0.20 %) dinocap (0.05 %) or carbendazim (0.05%) or hexaconazole (0.05%) or triadimefon (0.1%) or fenarimol (0.04%) or difenoconazole (0.03%) and repeat at 10-14 days interval.


This is an important disease prevalent in those areas where pea is cultivated in autumn. In northern plains of India, wilt is a serious problem in the early sown (September planted) pea crop.

Symptoms of the diseases appear as true wilt and near wilt which are described below:

True wilt:
  • Initially, the lower leaves look pale yellow and droop downwards (Plate-3).
  • With the progress of the disease, similar symptoms appear on the upper leaves also and the affected plants give a stunted look.
  • Slowly the upper plant parts loose their turgidity and the whole plants topple down.
  • Stems are shriveled and some of the root lets are also injured.
  • In diseased plants, yellow to orange brown discolouration of vascular system of upper tap root extending up to the stem is evident.


Near wilt:
  • Symptoms are also similar to those described above except for their slow development.
  • In this case, the vascular discolouration of the roots is typically brick red and usually extends up to the growing tip.
  • Cortical decay is also observed in lower parts of the stem and upper tap root.
  • The disease is caused by Fusarium oxysporum Schlech. ex. Fr. f.sp. pisi (Hall) Snyd. & Hansen (race 1= wilt; race 2= near wilt).
  • The hypha of the fungus is septate, delicate white to peach coloured, usually with a purple tinge.
  • Micro-conidia are borne on simple phialides arising laterally on hyphae or from short less branched conidiophores and these are oval ellipsoid to cylindrical or curved.
  • Macroconidia are borne on branched conidiophores or on the surface of sporodochia and these are thin walled, 3-5 septate, fusoid-subulate and pointed at both ends.
  • Chlamydospores are both terminal and intercalary.
Disease cycle and epidemiology:
  • The pathogen is soil borne and can survive in the soil for several years.
  • The fungus causes infection of the fibrous roots or epicotyl region, grows both inter and intracellularly in the cortex and ultimately concentrates in the xylem vessels.
  • After death of the plant, the fungus continues to grow and sporulate on the stem cortex, resulting in the production of soil borne inoculum.
  • The disease progresses fast at 21o C while near wilt requires 24-28o C.
  • True wilt is not serious in very wet soils while wet soils favour near wilt.
  • Neutral to alkaline soils favour true wilt while the acidic soils retard it.
  • Collect and destroy the infected plant debris.
  • Follow long crop rotation in the infested fields.
  • Use healthy seed and treat the seed with carbendazim (0.2%).
  • Use resistant sources, if available. Trichoderma spp. were found to be antagonistic to this pathogen but their utility in disease management has not yet been ascertained.

Pea rust is an important disease, which occurs quite frequently in pea growing areas in North and North western parts of India. Two rusts have been reported on peas caused by Uromyces pisi (Pers.) de Bary and Uromyces viciae-fabae (Schroet) of which the latter is of worldwide occurrence.


  • The symptoms appear on all above ground parts of the plant.
  • Infection is evident first as minute, raised pustules, which later become distinct, yellowish, circular sori (plate-4a).
  • The yellow spots have aecia and persist for longer time.
  • The uredo pustules develop on both surfaces of the leaves as well as on other parts and give light brown powdery appearance to the plants in case of severe infections.
  • Late in the season, teleuto pustules also develop on the leaves but most commonly on stems and petioles (Plate-4b). They are dark brown or almost black in colour.


  • The disease is caused by Uromyces viciae fabae (Grev.) Fuckel.
  • On peas, the pycnia occur in small groups associated with the aecia.
  • The aecia are cupulate and 0.3 to 0.4 mm in diameter.
  • The peridium is short and whitish.
  • The aeciospores are round to angular or elliptical with hyaline wall and the wall of these spores is verucose.
  • The urediniospoes are round to ovate, light brown, echinulate, with 3-4 equatorial germ pores.
  • The telia occur in the same sorus as the uredia are dark brown to black.
  • The teliospores are subglobose, ovate or elliptic with rounded or flattened apex, which is considerably thickened and appears papillate, smooth and are brown in colour.
Disease cycle and epidemiology:
  • It is an autoecious rust with all its spore stages on the same host.
  • The rust is seed borne in broad beans but in peas and lentil, it is mainly survive as teliospores in crop debris.
  • In India, the rust appears to survive on weed hosts belonging to Lathyrus, Vicia etc. and the spores are wind blown to the main crop.
  • The teliospores on germination produce a promycelium on which sporidia are borne.
  • The sporidia germinate and germ tube infects the host, produce pycnia and finally aecial cups are produced.
  • Uredia occur late in the season and are not of much importance in secondary spread.
  • Later in the season, teliospores are produced which help in overwintering of the pathogen.
  • Prevalence of low temperature (17-22o C) coupled with high humidity, dew or frequent light rain showers are favourable for initiation of the disease by aeciospores.
  • Rust severity and pustules/plant increase progressively with an increase in the duration of leaf wetness up to 24 h, at optimum temperature of 20oC.
  • Collect and destroy infected plant debris.
  • Follow long crop rotations avoiding broad beans, Vicia and Lathyrus in rotation.
  • In disease prone, areas sow the crop early.
  • With the initiation of the disease, spray the crop with mancozeb (0.25%) or hexaconazole (0.1%) or triadimefon (0.1%) or difenoconazole (0.05%) and repeat at 10 to 14 days interval depending on the severity of the disease.
Last modified: Monday, 12 March 2012, 6:07 AM