Abstract
Coconut palms (Cocos nucifera L.) can be affected by several types of Lethal Yellowing (LY) diseases worldwide. Some of the syndromes are caused by phytoplasmas, small bacteria that are impossible to detect by light microscopy. Amplification of a given gene of the phytoplasmas by polymerase chain reaction (PCR) is the most convenient diagnosis method. The problem is that there are at least 28 “groups” of phytoplasmas and only one pair of primers -P1/P7- commonly used for PCR. As these primers belong to a very conserved gene, false positives are frequent. Consequently, alternative primers specific to one “strain” (or subgroup) have to be used, such as LY-F/LY-R for the Caribbean LY, Rohde primers for LD Tanzania. Such specific primers are sometimes restrictive. Indeed, there is variability within each strain and the sequence of the primers has to be adapted to that variability. There are at least five LY subgroups. The subgroups can only be identified by restriction fragment length polymorphism or sequencing. In Africa, two subgroups of LY phytoplasmas have been identified so far.
Highlights
In the 1830s, a disease resembling what is known today in the Caribbean as Coconut Lethal Yellowing (LY) was rife in the Cayman Islands [1, 2]
We found variability in the 16S/23S sequence of isolates collected in Ghana and those collected in Mozambique [45]
In Ghana, after several trials were set up to test how coconut varieties reacted to CSPW between 1981 and 2007, it turned out that, on the contrary, the VTT is fairly resistant to CSPW and the Malayan Yellow Dwarf (MYD) is highly susceptible [47]
Summary
It is in the Caribbean – the West Indies – that LYTS were reported for the first time at the end of the 20th century [1, 2]. The west coast of Florida has remained relatively unscathed, mainly due to serious epidemiological monitoring, combined with rapid containment measures (felling, insecticide treatments and antibiotic treatments) It was not until the very beginning of the 1980s, that LY took a real leap to the tip of the Yucatan peninsula in Mexico. Not until the very beginning of the 1980s, that LY took a real leap to the tip of the Yucatan peninsula in Mexico In this case, the hypothesis most often put forward is human introduction of infectious vectors from Florida. From the Yucatan tip, the disease gradually decimated the coconut plantings as far as Vera Cruz. Phytoplasmas have been reported to be the etiological agents of those wilts, they do not belong to the 16S rDNA group containing the phytoplasmas of coconut LYTS in Africa and the Caribbean (Group 16S rDNA IV)
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