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April 2015

60

Ear rots of maize:

A continuous threat to food safety and security

D

iplodia ear rot caused by

Stenocarpella maydis

, Fusarium

ear rot caused by

Fusarium verticillioides

and Gibber-

ella ear rot caused by the

Fusarium graminearum

species

complex are the major ear rot diseases occurring in

South Africa.

These diseases have been identified as recurring problems through-

out maize producing areas. The fungi causing these diseases also

cause maize stalk rots which result in plant lodging. Maize ear rots

result in yield losses and grain quality reduction through discoloured

kernels, observed during the grain grading process and production

of mycotoxins.

Stenocarpella maydis

,

F. verticillioides

and the

Fusarium gramine-

arum

species complex produce mycotoxins that are toxic to hu-

mans and livestock. It is important to remember that environmental

conditions favourable for ear rots do not correspond to conditions

causing stalk rots, even though the same fungi are involved.

Each ear rot disease must be seen as an individual disease as cli-

matic and/or environmental conditions for the development of each

disease varies. These diseases will be discussed separately.

Diplodia ear rot

Symptoms in maize

Diplodia ear rot symptoms (

Photo 1

and

Photo 2

) associated with

infections during early ear development are the yellowing and dry-

ing of husk leaves while stalks and leaves remain green. Infection

generally begins at the ear base and ramifies upwards (

Photo 3

). The

entire ear becomes overgrown with a white mycelial growth.

A cross section of an infected ear shows black spore-producing bod-

ies at the kernel bases. Late season infections may occur when ker-

nel moisture is low and symptoms are less obvious. Embryos only

become infected and slightly discoloured, but no ramification of

the rest of the kernel occurs. Such symptomless infections are lo-

cally referred to as “skelm Diplodia”.

Life cycle and epidemiology

Stenocarpella maydis

spores are transmitted by air, seed and soil.

Airborne spores result in heavy infections of up to 10 m from the

inoculum source and the number of successful infections is re-

duced with distance. Single spores travelling long distances may

lead to trace infections which may then develop into an epidemic

focal point. Infected maize seed is an important inoculum source

which may result in seedling and crown rot diseases. However, the

majority of

S. maydis

infected kernels do not germinate.

Spores land behind leaf or ear sheaths where they germinate and

infect stalks or ears. Spore germination is inhibited by exposure to

sunlight and desiccation. Free water is necessary for germination.

Germination may take up to seven days and germinated spores

may enter tissue and lie dormant until conditions are favourable for

fungal growth through the tissues.

Mycelial colonisation

is accompanied by cell wall degradation ahead

of the growing pathogen. This is due to enzymes that are secreted.

Fungal ramification of maize ears begins at the shank. Cob tissue

colonisation begins at the attachment with embryonic tissues and

proceeds into the endosperm. Similarly stalk ramification may also

occur. These infected tissues develop fruiting bodies (pycnidia),

which produce spores during the subsequent season.

Economic importance

Yield losses caused by diplodia ear rot have not yet been quanti-

fied because the harvest method, the make of the harvester, speed,

and settings among other factors, all affect the percentage of

rotten kernels that remain in the grain bin or trailer. Rotten kernels

that are light are blown out during the harvesting process, the per-

centage depending on abovementioned factors.

This implies that where diplodia ear rot infections are serious,

damage is twofold. Firstly, if a low percentage of rotten kernels are

discarded during the harvesting process, serious grain quality re-

ductions occur. Secondly, where a high percentage of rotten kernels

are discarded in the harvest process, it will improve grain quality,

but manifest itself as yield loss.

A number of mycotoxins have been isolated and identified from

S. maydis

infected grain. Diplodiatoxin, dipmatol and three chae-

toglobosins have been found in

S. maydis

infected material. Re-

cently diplonine, a neurotoxin produced by

Stenocarpella maydis

,

was isolated and identified by researchers at the ARC-Grain Crops

Institute (ARC-GCI) in collaboration with toxicologists at the ARC-

Onderstepoort Veterinary Institute.

Planned research includes the development of techniques to identify

and quantify these toxins in maize samples to determine the levels

of each mycotoxin in various tissues produced by different isolates.

Not all

S. maydis

isolates are toxic. For example, two isolates from

the same field may be fed to ducklings with one being toxic and the

other not. This makes decisions difficult on whether or not to use

Diplodia-infected grain for feed.

Milling infected grain is thought to reduce the heat-sensitive toxin

and ensure that total Diplodia-infected grain content of feed rations

is lower than 10%. Techniques enabling researchers to quantify

the presence of these toxins will assist in determining which grain/

isolates are toxic and which are not.

Animals, particularly cattle, being fed Diplodia-infected rations

must be monitored. As soon as symptoms of reluctance to move,

standing with wide-based stance, poor coordination, walking stiff-

legged with a high stepping gait, falling, paralysis, constipation,

salivation and tremors are observed, animals must be removed im-

mediately and fed on healthy rations. Recovery rates are high, but

animals will die if kept on the infected ration.

Diplodia ear rot / Fusarium ear rot / Gibberella ear rot

ON FARM LEVEL

Integrated pest control

BRADLEY FLETT

and

EDSON NCUBE,

ARC-Grain Crops Institute