Catastrophe: An Investigation Into the Origins of the Modern World
spark an outbreak.
    When there is excessive rainfall, vegetation growth increases. Thus there is more food available for herbivorous animals and insects, and rodents—including those that are carriers of the plague bacterium but are themselves immune to it—therefore breed more. Their larger numbers enable a greater survival rate vis-à-vis the slower-breeding predators who feed off the rodents, and a rodent breeding explosion occurs. In order to find their own foraging territory, the cumulative range of the rodents has to increase, and a virtual bow wave of these plague-carrying wild animals spreads inexorably outward over a period of months. Soon the creatures come into contact with other normally plague-free rodents, which then spread the disease to humans.
    In the slightly less likely, though theoretically feasible, drought scenario, lack of rainfall and food kills huge numbers of plague-carrying wild rodents and the larger predators that normally eat them. However, the minute the drought is over, the fast-breeding rodents recover their numbers quickly compared to the slower-breeding predators. There is then, for a few years, a great imbalance between hunter and hunted in favor of the hunted. A breeding explosion takes place and the plague-infested rodents spread like wildfire.
    However, the most dramatic scenario of all is one in which a severe drought is followed by significantly increased rainfall. That, or something very much like it, is almost certainly what took place in East Africa during the worldwide climatic chaos of the 530s.
    While weather was without doubt the motor that drove the spread of plague in East Africa, the key vector was the humble flea. Although the rodents were immune to plague, the fleas that lived on them were not. Fleas die of plague—but it’s actually the process of dying itself that helps them spread the disease.
    As a flea becomes ill, and under specific climatic conditions, part of its gut becomes blocked by a mixture of multiplying plague bacteria and clotted blood. 12 The flea then begins to starve, and becomes so ravenous that it will jump onto virtually anything that moves, irrespective of whether it is its normal host species or not. Of course, the flea’s hunger will not be satisfied, because its gut is blocked. So it will move rapidly from host to host, biting each one—and consequently spreading plague—in an impossible mission to quell its hunger. 13 The disease itself thus produces the very mechanism for its own spread.
    The species in East Africa that were probably the reservoirs for the disease were gerbils and multimammate mice. The sandy-colored gerbil normally has two litters (totaling ten offspring) per year. Gerbils are very territorial, and an individual will travel two to three miles per season in search of an area it can control as its own exclusive territory. Thus in optimal food conditions, when gerbil numbers increased, the need of each gerbil to find its own territory would have resulted in a wave of plague-carrying individuals spreading outward at substantial speed.
    The multimammate mouse—a dark brown rodent about the size of a golden hamster—lives in colonies consisting of up to fifty individuals. Their gestation time is twenty-three days, and they have two litters per year. Normally they have only five offspring per litter, but when there is optimal food availability, the number can treble to fifteen. A pair can produce over a thousand descendants in a year. Today they are still a principal wild host of plague in Africa.
    It is likely that the gerbils and multimammate mice then passed the disease to a ratlike creature in the genus
Arvicanthus.
The latter would not have been immune to plague, but in appropriate climatic conditions would have outbred even the multimammate mouse: In wet weather it can achieve densities of up to a hundred per acre, and it and its offspring can produce thousands of new individuals per year. Neither the multimammate mouse
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