Veterinarians can often tell an animal has died from anthrax by its sudden death and by the blood and bloody fluid that have oozed from its orifices. Anthrax bacteria in the decaying carcass are likely to be killed off by the bacteria of putrefaction; anaerobes (bacteria that can multiply without free oxygen) from the intestines do the clean-up work. The greater danger of anthrax lies in the blood that spills from the animal and drains into the soil, where the bacteria can then assume a protective spore form. (In a real sense, then, anthrax needs its host to die so that the disease may continue.) Relative temperature, along with varying blood and soil conditions, determines whether spores actually will form. Once formed, though, they can be devilishly hard to eliminate.
Burying dead animals in pits, as Virgil suggested, never really disposed of anthrax. In spore form, its bacteria have been known to persist in soil for as long as seventy years, well after the memory of the site is lost. When an old site is disturbed — as new fields are plowed, new gravel pits dug, or new roads laid — or when a spring flood brings spores to the surface, animal outbreaks can flare as if from nowhere. Animal and human anthrax ravaged Europe and Asia throughout history, with major outbreaks in Germany in the fourteenth century and in central Europe and Russia in the seventeenth century, and these epidemics most likely originated from old reservoirs where diseased animals had been buried.
Attacking anthrax contamination has its problems, especially when attempted on a large scale. It takes three hours at 140 degrees centigrade to sterilize a five-ton load of bones in an industrial digester. Four decades after the World War II testing of anthrax weapons at Gruinard Island off the coast of Scotland, the British used formaldehyde to the depth of six inches to ensure the soil was rid of spores.
In humans, an anthrax infection can begin in one of three ways. Infection through the skin (cutaneous anthrax) is what Virgil described and is the most common and obvious form. It begins with a tiny pimple. In a few hours this eruption becomes a reddish-brown irritation and swelling that turns into an ulcer, the "feverish blister" that splits the skin. The black scablike crust that the lesion develops gives the disease its name, anthracis, the Latin transliteration of the Greek word for coal. In Russian, anthrax is also called "Siberian ulcer" (Siberskaya yazva), because of the prevalence of the disease in that region. Indeed, czarist Russia and the former Soviet Union, with their huge rural area, had among the world's highest levels of recorded anthrax outbreaks. Without treatment, the fatality rate for cutaneous anthrax can be 20 percent. In this century, sulfamides, penicillin, tetracycline, and other relatively accessible drugs have reduced fatality to 5 percent and less.
As noted, there are two other ways of contracting anthrax in humans: Over the years, a distinction has been drawn between gastrointestinal anthrax, acquired by eating tainted meat, and inhalation anthrax, acquired by breathing in the deadly spores. This distinction immediately raises the issue of "portal of entry," of whether the spores enter the body through the mouth and digestive system or through the respiratory system, an issue central to the Sverdlovsk outbreak.