Banana (19 page)

It turned out that Malaysia was a terrible place—maybe the worst place on earth—to grow the Cavendish. Evolution was what had
attacked
the Cavendish. Malaysia's wild banana population is hugely varied for a reason: The fruit has been developing there longer than just about anywhere else in the world. Since the diseases and the organisms they strike tend to evolve with each other—creating an alternating equilibrium of virulence and resistance—Ploetz quickly guessed that the types of Panama disease found in Malaysia, having had tens of thousands of years to develop, would likely be “as diverse as the bananas.”

Malaysia's native bananas developed resistance to the diseases that grew along with them. Newcomer fruit had no such inherited advantage.

The answer was suddenly obvious. This wasn't a recently emerged mutation of the blight that destroyed the Gros Michel. This “new” race of Panama disease had been in the Asian soil all the time, living in balance amidst mostly immune plants. The earlier incarnation of Panama disease had probably been brought to the Americas, where it did the most damage, from Asia. The same process was now happening in reverse: Bananas were being brought to the disease.

History is filled with examples of how destructive a disease one population has already been proven to withstand can be when introduced to nonresistant groups. In the United States, chestnut trees were nearly wiped out by an imported blight in the early 1900s. Today, a malady called Sudden Oak Death, which initially appeared in the Pacific Northwest, is arriving along the eastern seaboard, possibly through shrubs and soil sold by commercial nurseries. In human history, such incursions are often tragic and calamitous: Smallpox killed up to 90 percent of the Native American population within a few decades of initial European contact.

This wasn't a new kind of Panama disease at all. What was destroying bananas in Asia was a long-lost progenitor of the strain that appeared in the Americas a century earlier. It had never crossed Wallace's line. This version of Panama disease, which Ploetz dubbed Race 4, had long since reached a biological truce with the other organisms it shared the forest with. Our Cavendish had no such evolutionary defenses. It returned to a home it no longer knew—and that no longer knew it.

The Asian banana rush was over. Panama disease was back. Randy Ploetz knew what that meant. Race 4 would spread. Maybe it would take twenty years. Maybe more. Maybe less. One thing was certain: “The moment it hits a new continent,” Ploetz said, “it will be game over.”

E
VER SINCE CLAUDE WARDLAW,
the pioneering banana breeder who worked in Trinidad in the 1920s, became the first to suspect that Panama disease was being spread by plantation building, those researching the fruit have maintained that humans could stop the malady by adopting some relatively simple practices: learning to farm better, enforcing quarantines, and making sure contaminated water and soil aren't transported between plantations.

The idea is a good one. But in practice it has almost never worked. Hadi Bux Leghari, a technical manager at a Pakistani plantation called Asim Agriculture Farm, learned this frustrating lesson when he attempted to fight another banana malady.

Bunchy Top is almost as scary as Panama disease. The virus is transmitted by aphids, tiny insects that feed on plant sap. Aphids carry disease-causing microbes to many plants, causing diseases with exotic names—cucumber mosaic virus, plum pox—much in the way mosquitoes cause malaria and yellow fever in humans. The aphid's fecundity is legendary. Millions of the insects can be born in a matter of hours.

Bunchy Top appeared in Pakistan in 1989, hitting plantations along the country's southern coast, near a village called Thatta. (It arrived in that country after having followed a century-long path from its first recorded outbreak, on Fiji, in 1889, through Australia then Sri Lanka, India, Bangladesh, and Burma. It is now present in Hawaii, where it has caused a 30 percent decline in local banana production over the past decade.) Growers and the agricultural technicians called in to investigate couldn't initially identify the malady that would soon spread through Pakistan's Cavendish crop. Plants afflicted with the unknown blight were easy to recognize, though, with leaves bunching together then descending in ever-more-compact spirals until the plant's shape resembled the multilayered petals of a rose. Infected plants rarely produced fruit or grew beyond three feet high.

As the plague spread across Pakistan, losses averaged between 25 percent and 75 percent per plantation. Many experienced total destruction: Not a single plant survived. Without knowing what they were attempting to fight, growers doused their crops with every chemical they had available. Nothing worked. Samples of diseased banana tissue were sent to scientists across the world. Finally, in 1991, the diagnosis was made.

Knowing his opponent's name did little to help Leghari. He'd surveyed dozens of plantations across the country, and the results were discouraging. “There are so many areas affected by BBTVD [Banana Bunchy Top Virus Disease],” Leghari noted in a 2006 report for the United Nations Food and Agriculture Organization. The situation in some regions was apocalyptic: “The whole area is devastated,” the investigator wrote of a growing region called Khairpur. “The district is supposed to have more than 20,000 acres of banana. It is ruined.” The area of land turned fallow by Bunchy Top represents more than one-third of Pakistan's predisease plantation holdings. That's a loss of about 140 million pounds of bananas annually, or about 10 percent of total production for a major banana-exporting country like Costa Rica. (Pakistan's bananas are mostly consumed domestically.)

With no conventional treatments available to completely inoculate the fruit against the virus or prevent the aphids from arriving in the first place, Leghari attempted to institute complex control measures as a way of containing the malady. He developed an eleven-step plan that, if implemented, could at least contain the spread of Bunchy Top. The program included ensuring that initial planting materials were free of disease; that a cocktail of pesticides and biological control agents be applied to the plants; that manual thinning—the aphids live on weeds interspersed beneath the banana plants—be done regularly; that planting areas be kept free of debris like the fallen leaves and stems that form a plantation's underlying mat; and that individual plants be isolated by growing them at greater distances from one another. Each plantation also needed to have a natural barrier—rows of high trees—on its perimeter.

When Leghari tested the plan at his own plantation, it succeeded. The variety of measures, none of which would have been terribly effective if used alone, combined to slow the disease to a near stop. Yields increased, and infection dropped to less than 1 percent.

Rigorous discipline can be effective. Australia has managed to keep Panama disease in check by erecting physical barriers between plantations and enforcing strict quarantine procedures. But Australia is a rich country with plenty of technical resources, and as Houbin Chen—the Chinese scientist who removes his shoes when he travels between plantations in Guangdong, only to watch as dozens of people on foot, animal, and bicycle track infected dirt alongside him—learned, the problem with this seeming panacea is that it requires a kind of discipline that appears to be impossible in the patchwork plantations where most bananas are grown.

Parts of Leghari's report bristle with anger and dismay. Sixty students were trained in his technique at the Asim plantation, with the hope that they'd spread out to the countryside and transfer their knowledge to local growers. It didn't work. In 2003 Leghari made a two-day presentation to farmers in the hard-hit Khairpur district: “I explained to them how [their bananas are] getting infected with BBTVD,” he recalled. “This is the time you should start to manage your bananas by controlling the vector [the aphids] and removing diseased plants.” But the measures seemed too complex, too time-consuming, too expensive: Not only would additional labor have to be hired and new materials have to be bought, but the number of plants actually produced would be severely decreased. (These same issues have become a problem at large-scale banana operations around the world, where growers play chemical leapfrog with a growing array of banana maladies. In a tight-margin business, such activity can quickly lead to unprofitability.) In Khairpur, Leghari left the plantations knowing he'd failed in his mission: “They refused to accept my open offer [for assistance in fighting Bunchy Top],” he recalled. “They have now lost 100 percent of their crop.”

BUNCHY TOP HAS SPREAD IN ASIA AND THE PACIFIC
,
but like Panama disease, it has yet to reach the Americas. Black Sigatoka, which was first noted in the early 1970s, has. As I walked through the Honduran plantation with Juan Fernando Aguilar, viewing row after row of numbered plants—each representing a different generation of hybrid—I asked the scientist which plants were being bred for resistance to Panama disease.

“A few,” he laughed, “but we've got a bigger problem right now.”

We stepped toward a smallish banana plant. It looked skeletal, nearly bare. The few remaining leaves were yellow and mottled with expanding spots of black. If Panama disease is the uncontrollable natural disaster, then Sigatoka is today's most dangerous, immediate attacker and, like Pakistan's Bunchy Top, a worrying portent. “In spite of other diseases and pests, none has jeopardized the production of bananas as severely as Sigatoka,” wrote Del Monte researcher Douglas Marín in a 2003 issue of
Plant Disease
.

The rapid spread of, and difficulty in treating, Sigatoka is a worrying sign in the upcoming fight against Panama disease. As with Panama disease, Sigatoka infects many different banana types, ranging from subsistence bananas in Africa to our Cavendish. Also, like the malady that wiped out the Gros Michel as a commercial crop, it is a fungus that appears in multiple strains, each with different distribution and virulence. Compared to the yellow Sigatoka, which began to become widespread in the 1920s and was easier to control (with the help of Bordeaux mixture), Black Sigatoka is speedier and more calamitous. The disease arrives in wind and water and on dirt. Different regions suffer from different manifestations of the bug, each of which requires unique treatment procedures. Sigatoka kills quickly. Symptoms appear as soon as two weeks after infection, and the plant is destroyed not long after. The disease can be worse when symptoms don't readily appear, taking hold only after the fruit is harvested, so your local grocer might open a banana box and, instead of a dozen nicely green bunches, find a rotted mess.

Sigatoka can be treated, but the development of a “cure” isn't necessarily a good tiding for the future. The pesticides and fungicides in the banana grower's arsenal have widely varying levels of effectiveness on the disease. (Bordeaux mixture is no longer among them; it was banned in the 1960s.) And besides being costly, the spraying of heavy, oil-based products can damage plants. Waste materials leach into watersheds. Most of all, the health of banana workers is severely compromised. A 1999 study of women in banana-packing facilities, conducted by the National University of Costa Rica, found that their rate of leukemia and birth defects was twice the national average. Twenty percent of male Costa Rican banana workers have been left sterile, according to Jeremy Smith, writing in the April 2002 issue of the
Ecologist
. (In 2005 Chiquita, the largest banana company operating in Costa Rica, began adhering to SA8000, a comprehensive series of workplace standards developed by Social Accountability International. Local workers hailed the move—it ended a strike—but banana companies, even after they began expressing an environmental awareness in the 1990s, in general get a mixed grade in worker and environmental protection. Over the past five years, Chiquita has become the banana company with the highest levels of compliance, up and down its supply chain. Other banana growers have good programs in some countries and nonexistent ones in others, usually claiming that they're simply middlemen, buying from contract growers who bear true responsibility for obeying local, and usually poorly enforced, regulations.)

Conventional hybrid breeding has not fared well against Sigatoka. Scientists have created plants that are resistant, but often not by much. The standard Cavendish develops symptoms of Sigatoka in about 222 days. A typical lab-bred variety might last just ninety-six hours more. Even worse, nearly every treatment for the disease is ultimately foiled by the fungi's rapid mutation cycle. Within as little as two or three years, immunity is developed—and the malady returns, ferociously. Quarantine and clean-farming measures can help large-scale plantations but are difficult to maintain in the tiny, randomly distributed plots of African villages or even in places like Ecuador, where hundreds of smaller farmers form the first link in a chain that leads to the global banana packers and our supermarkets. The current approach, a chemical blitzkrieg, means that Sigatoka so far hasn't affected the supply of Cavendish bananas to the United States and Europe, but the sickness has had far-reaching effects in Africa, where even the loss of a few plants per village can have disastrous nutritional consequences.

The real lesson of Sigatoka isn't necessarily in how bananas react to the disease: it is in how the disease reacts to the banana. The cost of the fight against Sigatoka is rapidly pushing against the borderline of benefits, says Adolfo Martinez, the agricultural economist who directs FHIA. “Ten years ago,” he told me, as we walked to the Honduran research facility's library, which is situated where there used to be a bowling alley for banana company executives, “we sprayed once or twice a month. Now, we're up to weekly treatments or even more.” Those extra applications of Sigatoka-fighting chemicals aren't just bad for the environment and workers. They're also expensive, costing up to an extra $500 per acre every time they're needed. Bananas have to be cheap, and treating them continuously isn't. Something, Martinez says, has to give.

No solution developed in over a century of studying and treating the blight has resulted in anything more than a fruit that is just mildly stronger. Sigatoka's rate of “improvement” is far greater than anything anyone has come up with to fight it. Every remedy results in a more powerful malady. That's a common problem in nearly every aspect of fighting disease, whether in people or plants, and the only reason it hasn't appeared in Panama disease is that there's nothing yet forcing that malady to evolve into stronger and more virulent forms.

If there is an answer—to
all
of these maladies—it lies in the natural pace of evolution and resistance. In order to save the banana, the fruit has to jump a few steps ahead—and there's only one way to do that.