December 5, 2001	Wednesday	Ramazan 19, 1422

NEW YORK: On Oct 2, 1980, a 47-year-old woman from south Lake Tahoe, California, lost her 9-month-old pet cat to an acute infection. Three days later, the woman’s own temperature shot up, but she still went to her job at a day-care centre. The fever worsened; she developed chest pains and shortness of breath. Two days later she drove herself to the hospital. The diagnosis was pneumonia, and she was treated with tetracycline. Shortly afterward the woman died. Not until four days later did anyone realize that the woman had died of plague. Fearing that treatment might arrive too late, doctors rushed prophylactic antibiotics to the children and staff at the day-care centre. Luckily, no one exposed to the woman fell ill.

People tend to think that the horrors of plague are confined safely to the past. Plague, the black death, burned through the mediaeval world of Europe, killing about one of every four people. But by the mid-18th century, epidemic plague had died down. The terrible days of deserted cities and heaps of the dead fell into the dim past on the Continent, although plague never disappeared - more than 10 million died of it in India less than a century ago.

Plague’s current sluggishness poses a number of questions: How could a disease that does not seem to be highly contagious, as evidenced by the story of the woman who worked at the day-care centre, slaughter millions in a short period of time? Why is it possible that epidemic plague could return? To understand the threat of plague, it is important to know not only how plague survives and spreads within its hosts but also how it spreads among them. Yersinia pestis, the bacterium that causes plague, probably descended from Yersinia pseudotuberculosis, one of a group of relatively benign intestinal diseases. Sometime in the past 1,500 to 20,000 years, Y. pestis lost a set of genes for proteins called adhesins, which bind the bacteria to intestinal walls.

Robert Brubaker, a microbiologist and plague expert at Michigan State University, suggests that the loss of those genes may have enabled Y. pestis to move with deadly speed throughout the host. Overriding the body’s defences by suppressing the signalling between key immune cells, plague races through the lymphatic system, invading organs such as the spleen, the lungs and especially the liver. The bacterium normally thrives in rodent populations, passing from one animal to another via the bites of plague-infected fleas. How the germ is transmitted to humans determines how the disease takes hold. If a person is bitten by a plague-infected flea, agonizingly painful egg-sized swellings of the lymph nodes called buboes develop in the neck, the armpit or the groin. Buboes give one type of plague its name - bubonic. Without prompt and massive antibiotic treatment, 50 to 60 per cent of those infected with this form of plague will die.

An even deadlier form, pneumonic plague, develops when a person inhales Y. pestis. In the United States, plague cases tend to crop up in the bubonic form, usually among people in the American Southwest who have been exposed to prairie dogs or ground squirrels and their fleas. The handful of American cases in humans have occurred by zoonosis - transmission from animals. Specifically, the cause is always flea bites or direct exposure to a sick animal.

Is it possible that at times during the three pandemics plague actually became a human disease, one that did not depend on transmission from infected rats? It could happen in two ways. Kenneth Gage, plague section chief of the CDC, notes that historically plague may have been transmitted among humans by the so-called human flea, Pulex irritans, or via airborne transmission. Could the black death have begun as a flea-spread disease and adapted during an epidemic to become a highly transmissible airborne disease? Perhaps. Mediaeval Italy swarmed with fleas. The sinister costume of mediaeval plague doctors - the long, beaky nosepiece filled with spices, and a cloak of fine waxed cloth - apparently protected them from flea bites.

Pulex irritans, the human flea, is a much less efficient vector of plague than the rat flea Xenopsylla cheopis. In order to transmit plague, Pulex irritans must bite a host with lots of bacteria in the blood and pass the bacteria on to the next host quickly. Thus the virulence of a disease transmitted by the human flea should markedly increase, producing a more rapid course of illness and a higher death toll.

We would also expect human-adapted strains, at least during a pneumonic epidemic, to display greater transmissibility. “To get a toehold in the human population, a newly introduced pathogen must be at least slightly transmissible,” says Paul Ewald, a professor of evolutionary biology. “Using this toehold as a starting point, natural selection would act to increase transmissibility.” —Dawn/NYT News Service (c) New York Times.