Fungal Plant Diseases- Red rot of sugarcane, Early blight of potato

 Red rot:

Organism: Glomerella tucumanensis/ Colletotrichum falcatum

Red rot disease is caused by the fungus Glomerella tucumanensis, previously called Colletotrichum falcatum. This is one of the most severe of the known diseases of sugarcane. It is widely distributed throughout the sugar­cane-growing countries of the world.

 

Symptoms

• Infection in the stem is internal and the presence of the disease is not visible externally.
• Upon splitting a diseased cane during the early stages of the disease, it will be found that the fibro-vascular bundles near the base are reddish in colour. A gummy dark-red material oozes out of the cells filling the in­tercellular spaces. The soluble pigment present in this ooze, is absorbed by the cell wall producing the characteristic red rot appearance.

·       As the disease advances the red colour spreads to the surrounding tissues and irregular discoloured blotches are formed, which may be reddish or yellowish or white with red margins.

• When the infection becomes old, the blood-red colour changes to straw colour. The stem shrinks and split cane gives sour smell and shows red tissue with white cross-bands.
• Sometimes, the pith inside the cane is filled with blackish brown liquid and exhibits alcohol odour.
• About this time the upper leaves of the stem turn pale and gradually droop down. Ultimately the entire plant withers and droops down. The first external evidences of disease are the drooping, withering, and finally yellowing of the upper leaves, followed by wilting of the entire leaves, and finally the entire plant.
• The external symptoms appear only after16 - 21 days after infection and entire cane dries off in  10 days time.

 

In areas where the disease appears in a severe epidemic form, the en­tire crop withers and droops resulting in a complete loss of crop. Though the fungus attacks all parts of the host above ground, stems and midribs of leaves are more susceptible to fungal attack.

Reddish lesion on leaf midrib  Orange to yellow leaf         Inner reddish region

Management Removal of the affected plants at an early stage and soil drenching with Carbendazim The cut ends and entire plant should be dipped in a fungicide solution (Bordeaux mixture) If the disease is noticed in the field, the leaves and canes should be collected and destroyed by burning. Treatment with Carbendazim before planting should be done Use fungitoxic chemicals like Bavistan, Benomyl, Topsin and Aretan for complete elimination of rot infection. Plant healthy crops in a disease- free area. The red rot affected field must be rotated with rice for one season and other crops for two seasons. Growing of recommended resistant and moderately resistant varieties

Red rot of sugarcane is hard to control because the stalk from which seeds are prepared has been largely affected from the time of planting, and fungicides cannot reach the infected tissues inside a diseased seed sett. Therefore careful selec­tion of red rot-free seed setts is recommended for planting. Seed should always be taken from disease-free nurseries and examined regularly. Before planting, it should be carefully examined and those which show reddening should be discarded.

 

The spread of the red rot can be prevented during the growing season by timely inspection and burning of the affected clumps followed by sanitation. Hot water treatment of seeds and treating seed with fungicides is often effective. The use of sugarcane varieties resistant to red rot is also recommended. The possibilities of an epidemic is very much minimized with the practice of long crop rotations (2 to 3 years) where planting is done in plots. One of the best ways to reduce the incidence of the disease is to raise healthy stock for planting in plots especially fertilized, cultivated, and kept disease-free by constant care.

 

Early blight of potato

Organism–Alternaria solani,

 

Early blight is a common foliage disease of potato and tomato. It is of common occurrence both in cold as well as in warm regions in India and abroad where, potatoes and tomatoes are grown. The pathogen causes injury to the leaves as a leaf spot disease and lead to premature defoliation. Finally it causes tuber rot of potato and fruit rot of tomato.

 Symptoms: 

• The disease appears on the leaflets, 3-4 weeks after the crop is sown as small, isolated, scattered pale brown to dark spots, oval or angular in shape mostly up to 3 or 4 mm in diameter.
• The chlorotic zone increases with the increase in size of the spot. As a rule the oldest (lowest) leaves are affected first and the disease progresses upwards.
• The necrotic tissue of the spot often shows a series of concentric ridges, a symptom characteristic of this disease
• The number of spots on the leaflets may be a few but if the conditions are favourable the spots increase in number and size involving the entire leaf surface.
• In the advanced stage when the number of spots is numerous, the leaf shows signs of old age and droops.
• The spots become hard in dry weather and the leaflets curl. Under humid conditions, the diseased areas coalesce and big rotting patches appear on the leaf surface.
• In severe cases of infection the leaves dry up, shrivel and drop off.
• Falling of leaves starts with the older (lower) ones until a few remain at the top. 
• Stems and petioles may also develop brown to dark lesions which may finally lead to collapse of the entire over-ground portion of the plant.
• Further, there isinfection and rotting of potato tubers. The surface lesions on the potato tubers are a little darker than the healthy skin and slightly sunken. They are irregular or circular in shape. The older lesions develop fissures.
• The injury to the foliage may lead to premature defoliation reduces photosynthetic activity of the plant. Consequently the tubers formed remain small and a few in number. This reduces crop yield. The disease alos result in rotting of tubers.

 

Symptoms on Leaves: The disease can be seen as small, scattered, pale brown spots on the leaflets. These spots are covered with growth of the fungus.

Necrotic Area: In the necrotic area of the spots concentric ridges develop to produce a characteristics board effect.

Target Board: ‘Target Board’ is the most characteristics symptom of early blight of potato.

Vein Chlorosis: Later, vein chlorosis may also occur.

Curling of Leaves: In dry weather the spots turn hard and the leaves curling can be seen.

Rotting of Leaves: In humid weather big totting patches appear on leaf surface.

Severe Attack: Leaves shrivel and fall off. Stems show brown to black necrotic lesions on the skin. Rotten plant may collapse.

 

Transmission

 

Early Blight of Potato is very common disease of potato in India. The occurrence of the disease can be seen few weeks after sowing the tubers. But, the damage to the crop is more during the tuber formation. The disease can be seen both in the cool and warm areas. Farmers of hills and plains, both face this serious disease.

·       The fungus remains viable in infected leaves for many years.

·       Conidia and mycelium survive in the soil on plant debris to cause primary infection to next crop.

·       Contaminated tubers also act as a source of primary infection. 

• Climatic or soil conditions which are unfavourable to the host and reduce its physiological vigour tend to promote the disease.
• The disease spreads and becomes serious when the season begins with abundant moisture followed by high temperatures because these conditions are unfavourable to the host.
• Weaker plants are more susceptible to disease than the healthier ones.
• High soil fertility tends to reduce the severity of disease.
• Periods of continued drought also check its spread.

 Management

 

·       As in the case of other soil borne diseases, crop rotation and field sanitation are the two rational measures which provide effective check against primary infection from spores in the infected plant debris.

·       Infected dry leaves and dead plants should be burned immediately after harvest.

·       Application of regular sprays (with Bordeaux mixture or other suitable fungicides) throughout the period of plant growth effectively control the early blight.

 

 

Bordeaux mixture is a fungicide made of copper sulphate and calcium hydroxide (lime). Bordeaux mixture—a combination of copper sulfate, lime, and water—is an effective fungicide and bactericide used for decades to control diseases of fruit and nut trees, vine fruits, and ornamental plants.

It is widely used to control potato blight, peach leaf curl and apple scab.

Bordeaux mixture has copper ions (Cu²⁺) which inhibit fungal enzymes and prevent germination. It is used preventively, before the fungal disease occurs. It is sprayed on the plants usually once a year.

Because the copper ions build up in the soil, continuous use will cause heavy metal pollution. Copper also bioaccumulates in organisms. So its use is restricted in some countries

 

Fungal Diseases - Fusarium Wilt, Wilt of cotton

 

Diseases are a major limiting factor for crop production. Diseases can be caused by infectious microorganisms that include fungi, bacteria, viruses and nematodes. These diseases are contagious and can spread from plant to plant in a field, often very rapidly when environmental conditions are favorable.  

1) Fusarium Wilt

Organism - Fusarium oxysporum f.sp. lycopersici 

Wilt diseases are caused by pathogens that invade the vascular system (xylem tissue) and disrupt water flow through the plant. Fusarium wilt is the major wilt disease of tomato.  This is a warm-weather disease caused by the fungus Fusarium oxysporum.

Symptom

• The first symptom of the disease is drooping and wilting of lower leaves with a loss of green colour (chlorosis)
• Affected leaflets wilt and die. The younger leaves may die in succession and symptoms continue in subsequent leaves.
• Often leaves on only one side of the stem turn golden yellow at first.
• The disease progresses up the stem. At later stage, browning of vascular system occurs.
•  The stem of wilted plants shows no soft decay, but when cut lengthwise, the lower stem will have a dark brown discoloration of the water-conducting vessels.
• Soon the petiole and the leaves droop and wilt until all of the foliage is killed and the plant becomes stunted and dies.

Transmission

• The fungus is soil-borne and passes upward from the roots into the water-conducting system of the stem. Blocking of the water-conducting vessels is the main reason for wilting.
• The fungus survives and persists indefinitely in field soil.
• Invasion occurs through wounds in roots growing through infested soil.
• Long-distance spread is through seed and transplants.
• Soils become infested by planting infected transplants and from movement of infested soil by wind and water erosion or on farm implements.

Prevention & Treatment:

• The affected plants should be removed and destroyed.
• For control, grow plants in pathogen-free soil
• Use disease-free transplants
• Grow only cultivars with resistance to Fusarium wilt. Growing tomato varieties resistant to Fusarium wilt is the most effective means of control.
• Crop rotation with a non-host crop such as cereals is also an effective control method
• Spot drench with Carbendazim (0.1%)

 

2) Wilt of cotton

Organism - Fusarium oxysporum f.sp. vasinfectum & Verticillium dahlia

 

Vascular wilts, such as Fusarium wilt and Verticillium wilt, are capable of significantly reducing cotton yields, and negatively impacting fiber quality. Properly diagnosing these diseases is critical in developing a management system. While subtle differences can be observed in the field, laboratory examinations are often required to differentiate the two diseases. Variety selection is the most effective factor in reducing wilt associated losses.

Fusarium wilt

Causal agent: Fusarium oxysporum f. sp. vasinfectum (Fov)

Disease development depends on host susceptibility and pathogen - infection by Fov is more if root-knot nematode (Meloidogyne incognita)  infection is present.  Disease occurs in warmer temperatures and sandy soils.

Fusarium can cause severe symptoms in susceptible cotton varieties. These include a general wilt and yellowing and necrosis of lower leaf margins. The vascular system of infected plants is discolored brown in affected portions of the tissue. This is most apparent in the lower stem and upper taproot. The discoloration starts in the taproot, spreads into the stem, and is generally continuous in contrast to the speckling nature of the discoloration in plants affected by Verticillium wilt.

Symptoms

occur throughout the growing season

• Initial symptoms consist of chlorosis and wilting on the margin of the leaf

• Infected seedlings often die, and may be confused with seedling disease. In seedlings and young plants, cotyledons and leaves wilt, may turn necrotic, and even fall off the plant, resulting in bare stems.

• Diseased plants exhibit a continuous discoloration of the vascular tissue

· Seedlings of susceptible varieties often die and in mildly affected plants, lower leaves develop symptoms but plants survive, but with reduced vigor and noticeable stunting.

• Fusarium wilt occur more if root-knot nematode infection is present. Certain strains of the causal fungus only cause symptoms when plants are also infected with the root knot nematode. In those cases, galls are usually prevalent on lateral roots.

 

 

Transmission

·       The fungus sustains itself on the outer surface of roots of many crops and weeds and survives indefinitely in soil.

·       The pathogen is seed-borne in cotton, causing long-distance spread,

·      Is also spread whenever infested soil is transported on boots, farm equipment, in flood irrigation, etc.

 

Verticillium wilt

Organism: Verticillium dahliae

Disease development depends on host: variety, developmental stage, and plant density, pathogen: defoliating vs. non- defoliating type, aggressiveness, and inoculum density. Occurs in  cool, wet environments

Symptoms

• Initial root infections occur early; symptoms are more evident post-bloom

• Infected plants may be wilted or stunted

• Chlorosis or necrosis of leaf margins and interveinal areas may be

• Light to dark brown discoloration (speckled) is prominent in the vascular system

• Severe defoliation can result, leading to reductions in yield and fiber quality

        

Management of cotton wilt

• Proper identification of pathogen is required. Sample infected plants for presence of  Fov / Verticillium

• Use pathogen-free seed produced in disease-free fields at all times

• Assay soil for root-knot nematodes- Nematode risk level will influence management options-  Use of nematicides will indirectly lead to less Fusarium wilt damage. Control of the root knot nematode is important to managing Fusarium wilt caused by most genotypes of the causal fungus. Nematicides, root knot nematode-resistant varieties or both are often necessary in fields infested with the nematode

• Rotation to any crop other than cotton prevents an increase in the soil population of Fusarium but may not significantly reduce the number of spores in the soil. The fungus will sustain itself on the roots of most plants, including weeds (without causing any symptoms), and cannot be eliminated by crop rotation alone.

• Remove infected plants. Use disease resistant varieties/cultivars for several seasons to reduce wilt severity in subsequent years

• Any field operation that moves soil from one location to another can spread spores of the fungus and introduce it to other fields. Washing soil from equipment with pressurized water will help limit the spread of Fusarium

• Other containment options include restricting traffic in affected patches, destroying affected plants and surrounding non-symptomatic plants, and stopping irrigation of affected patches in order to prevent movement of infested soil.

 

Mueller Hinton Agar (MHA)

Mueller Hinton Media contains Beef Extract, Acid Hydrolysate of Casein, Starch and Agar. Beef Extract and Acid Hydrolysate of Casein provide nitrogen, vitamins, carbon, amino acids, sulphur and other essential nutrients. Starch is added to absorb any toxic metabolites produced. Starch hydrolysis yields dextrose, which serves as a source of energy. Agar is the solidifying agent. Final pH 7.3 ± 0.1 at 25ºC

Composition of Mueller Hinton Agar (MHA)

Ingredients	Gms/Litre
Beef extract	2.0
Acid hydrolysate of casein	17.5
Starch	1.5
Agar	17.0

 Uses of MHA

1. The major use of Mueller Hinton Agar is for antimicrobial susceptibility testing. It has become the standard medium for the  Kirby-Bauer method

2. It can be used to cultivate Neisseria

3. It is specified in FDA Bacteriological Analytical Manual for food testing, and procedures commonly performed on aerobic and facultative anaerobic bacteria.

Why MHA is used for antibiotic susceptibility testing?

1. It is a non-selective, non-differential medium. This means that almost all organisms plated on here will grow.

2. It contains starch. Starch is known to absorb toxins released from bacteria, so that they cannot interfere with the antibiotics. It also mediates the rate of diffusion of the antibiotics through the agar.

3. It is a loose agar. This allows for better diffusion of the antibiotics than most other plates. A better diffusion leads to a truer zone of inhibition.

4. MHA shows acceptable batch-to-batch reproducibility for susceptibility testing.

5. MHA is low in sulfonamide, trimethoprim, and tetracycline inhibitors (i.e. concentration of inhibitors thymidine and thymine is low in MHA).

6. It supports the growth of most non-fastidious bacterial pathogens.

Limitations of MHA

1. Numerous factors can affect results: inoculum size, rate of growth, medium formulation and pH. Strict adherence to protocol is required to ensure reliable results.

2. Drug inactivation may result from the prolonged incubation times required by slow growers.

3. This medium is recommended for susceptibility testing of pure cultures only. Inoculum density may affect the zone size.

4. Heavy inoculum may result in smaller zones or too less inoculum may result in bigger zones. 

5. Fastidious organisms may not grow on this medium and may require supplementation of blood. 

6. As antimicrobial susceptibility is carried with antibiotic disc, proper storage of the disc is desired which may affect the potency of the disc. 

Bombay blood group

 The rare, Bombay blood group was first discovered in Mumbai ( Bombay) in 1952 by Dr Y M Bhende. Each red blood cell has antigen over its surface, which helps determine which group it belongs to. In addition to the common A, B, D antigens in the positive blood group people, H antigen is also seen in all blood groups. Thus, in the AB positive blood group,  antigens A, B, D and H are found. A positive will have A, D and H antigens; B positive will have B, D and H antigens. O positive lack A, B but have D antigen. In the Bombay blood group, also called hh, is deficient in expressing antigen H, meaning the RBC has no antigen H. Thus, in hh, there are no A or B antigens, so they are similar to O group. But they alos lack H antigen, hence called Bombay blood group. Could be D positive or negative.

Blood type A is the most ancient, and it existed before the human species evolved from its hominid ancestors

Rarest blood type?

• AB-negative (. 6 percent)
• B-negative (1.5 percent)
• AB-positive (3.4 percent)

O+ is the most frequently occurring blood type and is found in 37 percent of the population. O- is found in six percent of the population

O positive donors who are CMV negative are known as Heroes for Babies at the Red Cross because it is the safest blood for transfusions for immune deficient newborns

Of the eight main blood types, people with type O have the lowest risk for heart disease. People with types AB and B are at the greatest risk

• People with A and AB blood have the highest rates of stomach cancer.

Type O individuals may be more likely to develop peptic ulcers caused by Helicobacter pylori bacterium than other blood types, and that type O women may have more risk of fertility problems

The golden blood type or Rh null blood group contains no Rh antigens (proteins) on the red blood cell (RBC). This is the rarest blood group in the world, with less than 50 individuals having this blood group

Rh incompatibility - If a woman who is Rh negative and a man who is Rh positive have a baby, the fetus may have Rh-positive blood, inherited from the father. Rh incompatibility usually isn't a problem if it's the mother's first pregnancy because the baby's blood does not normally enter the mother's circulatory system. During the birth, the mother's and baby's blood can mix. The mother's body recognizes the Rh protein as a foreign substance and begin making antibodies  against the Rh protein.Rh antibodies are harmless until the mother's second or later pregnancies. If she is next carrying another Rh-positive child, her Rh antibodies will recognize the Rh proteins on the surface of the baby's blood cells as foreign. Her antibodies will pass into the baby's bloodstream and attack those cells. This can make the baby's red blood cells swell and rupture. This is known as hemolytic or Rh disease of the newborn.