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Topic 3

Bacterial disease
Bacterial blight of rice

What it does

Bacterial blight is caused by Xanthomonas oryzae pv. oryzae. 

It causes wilting of seedlings and yellowing and drying of leaves.

Why and where it occurs

The disease is most likely to develop in areas that have weeds and stubbles of infected plants. It can occur
in both tropical and temperate environments, particularly in irrigated and rainfed lowland areas. In
general, the disease favors temperatures at 25−34°C, with relative humidity above 70%.

It is commonly observed when strong winds and continuous heavy rains occur, allowing the disease-
causing bacteria to easily spread through ooze droplets on lesions of infected plants.

Bacterial blight can be severe in susceptible rice varieties under high nitrogen fertilization.

Management

Planting resistant varieties has been proven to be the most efficient, most reliable, and cheapest way to
control bacterial blight.

Other disease control options include:

 Use balanced amounts of plant nutrients, especially nitrogen.


 Ensure good drainage of fields (in conventionally flooded crops) and nurseries.
 Keep fields clean. Remove weed hosts and plow under rice stubble, straw, rice ratoons and
volunteer seedlings, which can serve as hosts of bacteria.
 Allow fallow fields to dry in order to suppress disease agents in the soil and plant residues.

Symptoms
 Symptoms appear on the leaves of young plants as pale-green to grey-green, water-soaked streaks
near the leaf tip and margins.

 These lesions coalesce and become yellowish-white with wavy edges.

 The whole leaf may eventually be affected, becoming whitish or greyish and then dying.

 Leaf sheaths and culms of more susceptible cultivars may be attacked.


 Systemic infection results in wilting, desiccation of leaves and death, particularly of young
transplanted plants.[6]
 In older plants, the leaves become yellow and then die.

Diseased cycle

Rice plants become infected with Xanthomonas oryzae through rice seed, stem and roots that are left
behind at harvest, as well as alternative weed hosts. X. oryzae lives on dead plants and seeds and probably
moves plant-to-plant best through pattywater from irrigation or storms. Upon introduction to the host
plant, the bacterium infiltrates the plant through natural openings (water pores and growth cracks on
roots) and/or leaf and root wounds. X. oryzae grows in the plant and infects the plant's leaf veins as well
as the xylem causing blockage and plant wilting. Bacteria oozes from leaf lesions and is spread by wind
or rain, especially when strong storms occur and cause wounds to plants. X. oryzae has a wide host range
that includes Leersia sayanuka which acts as alternative host for the bacterium and are considered the
most important source of primary inoculums, as well as a great mechanism for bacterium survival.
Citrus canker

Scientific name
 
[Bacterium] Xanthomonas axonopodis 

Disease cycle
 
Citrus canker is not vectored by any organism but is spread by wind-driven rain. However, wounds
caused by feeding of the Asian citrus leaf miner (Phyllocnistis citrella Stainton) may serve as an entry
point for the bacterium if citrus canker inoculum is present. Xanthomonas axonopodis pv. citri overseason
in an infected area which appears as a canker lesion on leaf or stem. The bacteria ooze out of the lesions
when there is free moisture. During rainy weather, wind-blown rain carries the inoculum to new
susceptible hosts. The bacteria infect new plants through stomata and wounds. Pruning or hedging can cut
open mesophyll tissues, creating wounds through which the plant may be directly infected. The rain can
also cause water congestion on the leaf surface, form columns of water through the stomata and promote
infection through natural openings. Infections can form on fruit, foliage and young stem. Leaves and
stems are most susceptible to infection within the first six weeks of initial growth. Infection of fruit is
most likely to occur during the 90 day period after petal fall during fruit formation.[4] The varied size of
lesions on citrus fruit is because of the multiple cycle of infections and can reflect different-aged lesions
on the same fruit
Symptoms
 
Leaf - typical citrus canker lesions on leaves will range from 2-10 mm in size and will have raised
concentric circles on the underside of the leaf. Frequently lesions will be surrounded by a water-soaked
margin and a yellow halo. As a canker lesion ages, it may lose it palpable roughness, but the concentric
circles will still be visible with a hand lens (on the underside of the leaf). The yellow halo eventually
changes to dark brown or black and the water-soaked margin surrounding the lesion may diminish. The
middle of the lesion (on underside of leaf) will be corky in texture with a volcano or pimple-like point.
With the exception of very young lesions, lesions always penetrate through both sides of the leaf. In the
presence of damage, the lesion may follow the contours of the damage and therefore may not be circular.
In older lesions, a saprophytic white fungus may grow over the center of the lesion. The center of
a lesion may fall out producing a shot hole appearance.
Fruit - typical citrus canker lesions on fruit will range from 1-10 mm in size. Larger lesions usually
penetrate a few millimeters into the rind. Fruit lesions may vary in size and may coalesce.
Fruit lesions consist of concentric circles. On some varieties these circles are raised with a rough texture
on other varieties the concentric circles are relatively flat like the surface of a record. The middle of
the lesion will be corky in texture with a volcano or pimple like point. The center of a lesion may crack
and has a crusty material inside that resembles brown sugar. Frequently on green fruit a yellow halo will
be visible; however it will not be visible on ripened fruit. Lesions may have a water-soaked margin and
the water-soaked margin is especially evident on smaller lesions. In the presence of damage
the lesion may follow the contours of the damage therefore not being circular. In older lesions a
saprophytic white fungus may grow over the center of the lesion.

Management
Quarantine measures are implemented in areas where citrus canker is not endemic or has been obliterated
to prevent the introduction of X. axonopodis. On the other hand, in regions where citrus canker
occurs, Integrated Pest Management (IPM) is utilized. The most notable feature of this management
program is the transposition of susceptible citrus plants to field resistant citrus cultivars. Apart from using
resistant cultivars in fields, there are several measures that are taken to control citrus canker from causing
failed crop. The measures can be divided into three major categories: exclusion, eradication and
sanitation.

Exclusion
Citrus trees or fruits from outside of the country are inspected to ensure they are bacteria-free trees. Under
the management program, the production of Xac (X. axonopodis pv. citri)-free nursery trees for exclusion
of canker from orchard is also mandatory. Because the bacteria can be introduced from countries with
endemic canker or canker outbreaks, strict restrictions on citrus importation are implemented in citrus-
growing countries. Citrus trees will only be grown on canker-free fields at least one year after effective
eradication. Planting sites are also chosen to minimize favorable environmental conditions for the spread
of X. axonopodis. For example, areas with strong wind are avoided to decrease the dispersal of bacterial
inoculum to the susceptible citrus trees
Eradication
Once citrus canker is introduced into a field, removal of the infected trees is enacted to halt further spread
of the bacteria. For instance, in Florida between 2000 and 2006, all citrus trees within 1,900 feet (580 m)
of infected trees were required to be eradicated. In the process, the infected trees are uprooted and burned.
In urban areas, the trees are cut down and chipped, then disposed of in landfills
Sanitation
X. axonopodis pv. citri can be transmitted by mechanical means such as humans and machinery. As a
sanitation measure, the workers in citrus orchards are required to do thorough decontamination of
personnel and equipment to prevent the spread of bacteria from the infected areas. Aerosol inoculum is
able to cause infection in wetted foliage in the zone of bacterial dispersal. Vehicles can also become
contaminated by contacting the wet foliage. Contaminated equipment and machines can be disinfected by
spraying bactericide.

Scab of potato

Common scab of potatoes is a soil-borne disease caused by the bacteria-like organism Streptomyces


scabies.
This organism attacks:

 potato stems
 potato stolons
 potato roots
 young, rapidly growing tubers, which stimulates the growth of unsightly corky tissue.

Treatment

The following control measures have all been proven effective against scab in potatoes. However, in most
cases a combination of these techniques will be required.

 Plant certified, disease-free seed potatoes and resistant varieties whenever possible. We


suggest using the russet-skinned varieties since they have more resistance to the disease.

 Rotate root crops by planting in alternate locations to limit the disease.

 Potato scab is most prevalent in dry, alkaline soils. Decrease soil pH by adding elemental
sulfur. The disease is controlled or greatly suppressed at soil pH levels of 5.2 or lower.
Simple and affordable soil test kits are available to check pH often.

 Tilling in a cover crop — mustard, canola, alfalfa — prior to planting potatoes will help
reduce infection.
 Some growers report success spreading agricultural gypsum prior to planting at a rate of 25
lbs per 2,000 sq ft. This will raise the calcium content of your soil and help build strong cell
walls in plants. (Note: S. scabies disrupts the development of cell walls resulting in lesions.)

 Adequate irrigation during early tuber development may have a dramatic effect on common


scab infection, but you will need to keep the soil damp for 2-6 weeks. This technique is
effective because high soil moisture promotes growth of a bacteria that can crowd out S.
scabies on the potato surface.

 Do NOT overwater.

Symptoms

The symptoms of potato common scab are quite variable and occur on the surface of the potato tuber. The
disease forms several types of corklike lesions – surface (Fig. 1), raised (Fig. 2), and pitted lesions (Fig.
3). Sometimes surface lesions are also referred to as russeting, particularly on round whites, because the
general appearance resembles the skin of a russet-type tuber. Pitted lesions vary in depth, although on
average they extend 1/8 inch deep. The type of lesion formed on a tuber is thought to be determined by a
combination of host resistance, aggressiveness of the pathogen strain, time of infection and environmental
conditions. Scab symptoms are usually first noticed late in the growing season or at harvest. Tubers are
susceptible to infection as soon as they are formed. Lesions start out as small brownish spots, which
enlarge into water-soaked circular lesions within a few weeks of infection. These circular lesions may
coalesce, forming large scabby areas (Fig. 3). Scab is most severe when tubers develop under warm, dry
soil conditions with a soil pH above 5.2 (Fig. 4). Common scab is greatly suppressed in soils with a pH of
5.2 or lower. However tubers grown in acidic soil may develop scab-like lesions. These may be due to
acid scab, a similar disease to common scab caused by the related pathogen S. acidiscabies. The acid scab
pathogen can grow in soils with a pH as low as 4.0. Acid scab and common scab are hard to differentiate
– lesions caused by S. acidiscabies are similar to those caused by S. scabies.

Disease Cycle

Common scab of potato is an efficient saprophyte that can overwinter either in soil or on the surface of
tubers and crop residues. The pathogen is spread from one location to another by splashing water
(irrigation or rain) and wind, and on seed tubers and farm equipment with leftover soil residue. Most soils
where potatoes are grown in Michigan have a resident population of S. scabies. The population may be
reduced by rotation with grain crops or other non-hosts but cannot be eliminated entirely because it
reproduces to some extent on organic matter in the soil.

Streptomyces scabies has branced mycelium. Its spore-producing hyphae develop into corkscrew-like
spiral chains with cross walls that eventually constrict and break off into individual spores. As spores
mature, they develop a gray or melanized pigmentation. When a spore comes into contact with a suitable
host, it will germinate and the infection process begins.
The optimum temperature for infection of potato tubers by S. scabies is 68 to 72 degrees F, but the
pathogen can attack tubers in the soil with a wide range of temperatures, form 50 to 88 degrees F.
Infection usually begins at the onset of tuberization. The pathogen primarily invades lenticels but will
take advantage of any open wound on the surface of the potato tuber. After penetration, the pathogen can
grow through up to three peridermal cell layers, causing the cells to die. The bacterium then feeds on
these cells saprophytically. The pathogen also secretes a compound that promotes raped cell division in
the living cells surrounding the lesion. This causes the tuber to produce several layers of cork (suberized)
cells that isolate the bacterium and the surrounding tuber cells. As the tuber cells above this suberized
layer die, the pathogen feeds on them. As the suberized layers are pushed out and sloughed off, the
pathogen grows and multiplies in the additional dead cells. This growth cycle may occur several times
throughout the growing season, enlarging the lesion. Lesion size will also vary depending on when
infection occurs. Generally, the earlier a tuber becomes infected, the larger the lesion.

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