1. Panama Wilt (Fusarium Wilt)
Symptoms
Panama wilt, also known as Fusarium wilt, is one of the most devastating diseases of banana. The disease manifests initially as yellowing of the lower leaf margins, progressing upward to younger leaves. Affected leaves wilt, collapse, and hang down along the pseudostem, creating a characteristic "skirt" appearance. Internal symptoms include reddish-brown to black discoloration of the vascular tissues in the rhizome and pseudostem. The disease eventually causes complete plant death, and infected plants rarely produce harvestable fruit. Young suckers from diseased plants show stunted growth and rapid wilting.
Etiology
The causal organism is Fusarium oxysporum f. sp. cubense (Foc), a soil-borne fungus. There are four physiological races: Race 1 affects Gros Michel and other cultivars; Race 2 affects cooking bananas; Race 3 affects Heliconia species; and Race 4, particularly Tropical Race 4 (TR4), affects Cavendish varieties and poses the greatest current threat to global banana production. The fungus produces chlamydospores that can survive in soil for decades, making eradication nearly impossible.
Disease Cycle
The fungus survives in soil and infected plant debris as chlamydospores for over 30 years. Infection occurs through root wounds or natural openings. The pathogen colonizes the root cortex and enters the vascular system through the xylem vessels. Once inside, it spreads systemically throughout the plant, producing microconidia that are carried in the sap stream, blocking water and nutrient transport. The fungus multiplies within the plant and returns to the soil when the plant dies, where it produces survival structures. Spread occurs through contaminated soil, water, infected planting material, farm equipment, and footwear.
Management
Cultural practices: Use disease-free planting material from tissue culture. Practice strict quarantine measures to prevent introduction into new areas. Avoid movement of soil, tools, and equipment from infected to healthy fields. Remove and destroy infected plants including rhizomes. Implement crop rotation is ineffective due to long survival of spores, but fallowing for extended periods may reduce inoculum. Practice good drainage and avoid waterlogging.
Biological control: Use non-pathogenic strains of Fusarium oxysporum and beneficial microorganisms like Trichoderma spp. and Pseudomonas fluorescens as soil amendments.
Chemical control: Soil fumigation with chemicals has limited effectiveness and is environmentally problematic. No effective fungicides are currently available for field control.
Resistance: Plant resistant varieties where available. Research focuses on developing TR4-resistant Cavendish cultivars through conventional breeding and genetic modification.
2. Sigatoka Disease (Black and Yellow Sigatoka)
Symptoms
Sigatoka diseases primarily affect banana leaves, reducing photosynthetic capacity and causing premature ripening of fruits. Yellow Sigatoka (caused by Mycosphaerella musicola) begins as small yellowish-brown spots that enlarge into streaks with light centers and dark brown margins. Black Sigatoka (caused by Mycosphaerella fijiensis), the more severe form, starts as small brown streaks that develop into elongated spots with gray centers surrounded by yellow halos. As the disease progresses, spots coalesce, causing extensive leaf necrosis and premature leaf death. Severe infection leads to reduced bunch size, premature fruit ripening, and poor fruit quality. The disease follows distinct stages: initial spots (Stage 1), streak formation (Stage 2), spot enlargement (Stage 3), spot maturation with distinct coloration (Stage 4), depression of spot centers (Stage 5), and leaf drying and death (Stage 6).
Etiology
Yellow Sigatoka is caused by Mycosphaerella musicola (anamorph: Pseudocercospora musae), while Black Sigatoka is caused by Mycosphaerella fijiensis (anamorph: Paracercospora fijiensis). Both are Ascomycete fungi that produce both sexual (ascospores) and asexual (conidia) spores. Black Sigatoka is more aggressive, has a shorter life cycle, and is more resistant to fungicides than Yellow Sigatoka. The fungi thrive in warm, humid conditions with temperatures between 25-28°C and high relative humidity (>90%).
Disease Cycle
The fungi overwinter as mycelium in infected leaves and produce conidia during favorable conditions. Conidia are disseminated by wind, rain splash, and water to healthy leaves where they germinate and penetrate through stomata. After an incubation period of 2-4 weeks for Yellow Sigatoka and 2-3 weeks for Black Sigatoka, symptoms appear. The fungus develops stromata in leaf tissue that produce perithecia containing ascospores. Ascospores are forcibly discharged during wet periods and serve as primary inoculum for new infections. The disease spreads rapidly during rainy seasons with continuous leaf wetness. Secondary spread occurs through repeated cycles of conidial production throughout the growing season.
Management
Cultural practices: Remove and destroy severely infected leaves (deleafing) to reduce inoculum. Practice wider plant spacing to improve air circulation and reduce humidity. Ensure proper drainage to minimize leaf wetness duration. Use clean, disease-free planting material. Apply adequate fertilization to maintain plant vigor, as healthy plants show better tolerance.
Chemical control: Apply protectant fungicides (e.g., chlorothalonil, mancozeb) and systemic fungicides (e.g., propiconazole, azoxystrobin, trifloxystrobin) in rotation to prevent resistance development. Implement early warning systems based on weather conditions to optimize spray timing. Aerial spraying may be necessary in large commercial plantations. Apply mineral oils to reduce spore germination and spread.
Biological control: Use antagonistic fungi such as Trichoderma spp. and bacteria like Bacillus subtilis as foliar sprays.
Resistance: Plant resistant or tolerant varieties such as FHIA hybrids (FHIA-01, FHIA-02, FHIA-23) where acceptable. Breeding programs continue to develop resistant Cavendish-type bananas.
3. Bunchy Top Disease
Symptoms
Bunchy top is a viral disease characterized by progressive dwarfing and distinctive leaf symptoms. Infected plants show stunted growth with leaves emerging in a rosette or "bunchy" appearance at the top of the pseudostem. Leaves are narrow, stiff, brittle, and upright with shortened petioles. The most diagnostic symptom is the presence of dark green streaks or dots along the veins on the underside of leaves and leaf petioles, creating a morse code-like pattern. Leaf margins may show chlorosis and necrosis. As the disease progresses, the entire plant becomes severely stunted, and the pseudostem appears abnormally thin. Infected plants rarely produce fruit, and if fruit forms, bunches are small and malformed. Suckers from infected plants also show symptoms and perpetuate the disease.
Etiology
The causal agent is Banana bunchy top virus (BBTV), a single-stranded DNA virus belonging to the genus Babuvirus in the family Nanoviridae. The virus has six circular DNA components (designated as DNA-R, DNA-U3, DNA-S, DNA-M, DNA-C, and DNA-N) and is one of the smallest plant viruses. BBTV is transmitted exclusively by the banana aphid, Pentalonia nigronervosa, in a persistent, circulative manner. The virus is not transmitted mechanically, through soil, or true seed, making the aphid vector critical to disease spread.
Disease Cycle
The primary source of inoculum is infected planting material (suckers and tissue culture plants contaminated with viruliferous aphids). The banana aphid acquires the virus by feeding on infected plants for a minimum acquisition period of 4-24 hours. After acquisition, the virus circulates through the aphid's hemolymph and reaches the salivary glands. Following a latent period of 10-20 hours, the aphid becomes viruliferous and can transmit the virus for its entire life (7-10 days). Transmission occurs when the infective aphid feeds on healthy plants, with a minimum inoculation feeding period of 15 minutes. Within the plant, the virus replicates and spreads systemically through the phloem. Symptoms typically appear 3-5 months after infection in mature plants and 2-3 months in suckers. The aphid is attracted to young, actively growing plants and virus-infected plants, facilitating disease spread. Secondary spread occurs through movement of viruliferous aphids from infected to healthy plants, and through planting of infected suckers.
Management
Use of disease-free planting material: This is the most critical control measure. Use certified tissue culture plants or suckers from disease-free areas. Inspect all planting material carefully for aphids and disease symptoms before planting.
Eradication: Immediately remove and destroy infected plants including the entire mat (mother plant and all suckers) along with roots to eliminate virus reservoirs. In areas with high disease incidence, area-wide eradication programs involving complete removal of all banana plants (infected and healthy) followed by a banana-free fallow period of 3-6 months can break the disease cycle.
Vector control: Apply systemic insecticides (e.g., imidacloprid, thiamethoxam) as soil drenches or foliar sprays to control aphid populations. Install yellow sticky traps to monitor and reduce aphid numbers. Mulching with reflective materials may repel aphids.
Cultural practices: Remove wild banana species and ornamental Heliconia plants near plantations as they serve as alternate hosts. Establish buffer zones around new plantations. Practice roguing by regularly inspecting fields and removing symptomatic plants before aphid populations build up. Avoid ratooning in heavily infected areas; instead, establish new plantings with clean material in disease-free locations.
Quarantine: Implement strict quarantine regulations to prevent movement of planting material from infected to disease-free areas. BBTV is a notifiable disease in many countries.
Resistance: No immune varieties exist, but some cultivars show tolerance. Research is ongoing to develop resistant varieties through conventional breeding and genetic engineering approaches.
