Panama Disease of Banana: Panama disease (also known as Fusarium wilt/ Panama wilt) is a fungal infection that affects banana trees (Musa spp.). The fungus Fusarium oxysporum f. sp. cubense (Foc) causes wilting disease in plants. Since the pathogen is immune to fungicides, phytosanitary steps are the only way to contain it.
A Panama disease epidemic pretty much wiped out commercial Gros Michel banana development in the 1950s. The Gros Michel banana has been the most popular cultivar, and Fusarium wilt causes huge losses and forces farmers to turn to disease-resistant varieties. The Cavendish banana, today's most common cultivar, is currently threatened by a current epidemic of Panama disease spread by the strain Tropical Race 4 (TR4).
The epidemic of Panama disease hasn't really impacted all banana-producing countries. TR4 (Tropical Race 4) had first been discovered in Taiwan and easily expanded across Australia, Indonesia, Malaysia, China, and the Philippines. In 2013, the disease was discovered in Jordan. TR4 subsequently evolved to Vietnam and Laos, and also to Pakistan and Lebanon in the Middle East.
The disease subsequently dispersed to Africa in 2015, with outbreaks in Mozambique and Oman. TR4 appeared in Colombia in August 2019, a country in Latin America that is home to the world's largest banana exporters.
Banana Disease in Panama is Distinguished by Two External Symptoms:
Yellow leaf syndrome is characterized by the yellowing of the leaf's border, which gradually contributes to the petiole's bending.
Green leaf syndrome is characterized by the retention of the leaves' green colour accompanied by the twisting of the petiole, similar to yellow leaf syndrome. A vascular discoloration characterizes the disease on the inside. As the pathogen restricts the plant's water and nutrients transport, yellowing starts in the rhizomes and roots and progresses to a reddish-brown colour in the pseudostem.
The banana pseudostem will break as the infection progresses, and the entire plant will ultimately collapse.
External symptoms are frequently confused with those of bacterial wilt of banana,
But There are Several Ways to Tell the Two Diseases Apart:
Although fusarium wilt affects older leaves first, bacterial wilt affects younger leaves first.
There are no signs of Fusarium wilt on developing buds or suckers, no noticeable exudates inside the vine, and no effects in the fruit. Symptoms of bacterial wilt include twisted or necrotic buds, bacterial ooze inside the fruit rot, plant, and necrosis.
Recovery is unlikely after a banana plant has been infected, but if it does happen, rapidly evolving suckers will be damaged and will spread disease if planted.
Fusarium oxysporum f. sp. cubense (Foc) belongs to the Fusarium oxysporum species complex, a morphologically related group of ascomycete fungi. The plant pathogenic fungi of such species complexes are categorized into about 150 different groups depending on their distinct host species (formae speciales, f.sp.). Fusarium oxysporum f.sp. cubense is a fungal infection that often affects banana (Musa) species. The cubense specific type has also been categorized into four races, each of which targets a different category of banana genotypes.
In the 1960s, Race 1 was implicated in the Panama disease epidemic, which wiped out most of Central America's Gros Michel banana plantations. Race 1 targets several banana AAB genomic group members, such as the Silk subgroup, Abacá, Ducasse, Pisang Awak, Maqueo, the Pome subgroup, and Lady Finger, in contrast to Gros Michel. Race 1 is immune to Cavendish cultivars.
With the ABB genome and the Bluggoe subgroup, Race 2 causes impacts on the cooking bananas.
Race 3 of Fusarium oxysporum f.sp. heliconiae, which infects Heliconia spp., was not considered a banana pathogen and this has been called Fusarium oxysporum f.sp. heliconiae.
Race 4 is the cause of the latest Panama disease epidemic because it is pathogenic to the Cavendish cultivars presently being used (AAA genome). Tropical Race 4 (TR4) and Subtropical Race 4 (SR4) are two subtypes of Race 4. (STR4). During abiotic tension, the latter only destroys Cavendish and Race 1 and 2 susceptibles.
Replanting the plant's basal shoot which develops just after the existing plant has been cut down is how modern commercially harvested banana plants reproduce asexually. Since the fruit is triploid, there are no seeds, and the male flower may not carry pollen appropriate for pollination, sexual reproduction is unlikely. As a result, all bananas of a particular breed have almost identical genetics.
Spores or contaminated material spread the disease through surface water or farming practices. The process through which new banana plants are planted is among the most significant matters in the disease's distribution. Suckers are collected from a single plant and clonally propagated to produce new plants.
Since around 30 to 40% of suckers from a diseased plant were infected, but not many of them display symptoms, therefore the chances of growing a new, already diseased plant were relatively more. Eventually, the infection is defined to infect some weeds despite causing symptoms, implying that it can thrive in the disappearance of banana plants and go undetected in a later planting location. Since no sexual process (teleomorph) has indeed been observed, FOC is assumed to exist mostly asexually. Somatic hybridization and the parasexual cycle can also lead to recombination events.
The above means that perhaps the disease's existence and dissemination are entirely dependent on asexual structures and spores. The disease is carried by chlamydospores, which are produced when a tree dies and therefore can live for up to 30 years throughout the soil. Such chlamydospores may germinate and hyphae can reach the roots, triggering infection, if the weather is perfect and host roots are available. As inflorescences arise, the number of symptomatic plants increases, as well as the maximum disease occurrence happens just before harvest. Microconidia are formed and continue to spread inside the plant's vascular system after it has been infected. Macroconidia is yet another asexual spore that can be characterized by the presence of Panama disease-killed plants.
Fungicides and some other chemical and biological control factors so far have proven ineffective in combating Panama disease in bananas, or that have proven effective in vitro or in greenhouses. To avoid the spread of Panama disease from polluted areas, the much more widely used methods are sanitation and quarantine. The growth of banana plants resistant to Fusarium oxysporum f. sp. cubense is, nevertheless, the much more successful weapon against Panama disease. Banana clonal reproduction has resulted in a scarcity of several other types. While efforts have been made to develop resistant varieties, bananas are triploids that do not produce seeds, making this a difficult task.
Creating clones via tissue cultures instead of suckers has been found to be highly effective in breeding resistant varieties, which seem to have a lower success rate in disease resistance, yield, and other important commercial traits. Nonetheless, these measures have culminated in the most successful prevention method for the Panama banana disease.
Q1. Does Panama Disease Affect Humans?
Ans. The tropical race 4 of the Panama disease isn't really harmful to humans and has no effect on the fruit. The fungus has no effect on the plant's health or ability to grow fruit.
Q2. When did the Panama Virus First Appear?
Ans. Our grandparents and parents consumed a delightful banana named Gros Michel, or Big Mike in colloquial words, during the first half of the twentieth century. However, a destructive strain of the fungus that causes Fusarium Wilt (Panama disease) washed over almost most banana plantations in Central and South America in the 1950s.