Fusarium wilt of oil palm caused by Fusarium oxysporum f. sp elaeidis (Foe) has in the past rendered oil palm production uneconomic in some regions of Central and West Africa, where it is endemic. It is an anomaly that the disease has not appeared in South-east Asia, where the palm lines used are susceptible to African Foe isolates and the climate should be conducive. Various evidence and speculation are offered here to explain the absence of the disease so far. Foe is a soil-borne fungus that infects intact roots, traverses the cortex to the stele to invade the xylem and systemically colonise entire palms. Yield loss and even death result from induced water stress and hormonal imbalance. Disease spread is localised and typical of a soil-borne pathogen. Breeding for resistance over several decades has markedly reduced losses and disease incidence, even though expression of resistance appears to be partial. Resistance is proving durable, probably because Foe is monophyletic and resistance is based on multiple genes. Contamination of seed and pollen by Foe, has implications for importation of oil palm breeding material from the African centre of diversity. Isolated outbreaks in South America were linked to inter-continental seed movement. Quarantine has long been enforced for imported seed and pollen imported to Malaysia. This laboratory devised a method of fungicide infiltration for eradication of Foe from seed and the method is used by some seed companies to their market advantage, and in intermediate quarantine on exported seed batches. Specific DNA, PCR-based probes for rapid detection of the oil palm pathotype has long been required to distinguish Foe from the commonly present species F. oxysporum; advanced progress based on a unique Foe virulence gene is described. This article will consider the biology, spread, impact, detection and control of this aggressive pathogen in order to enhance or maintain awareness of the disease in this region and maintain the status quo of plantations remaining free from Fusarium wilt.