WASHINGTON – Once anthrax spores germinate in the lungs, they can quickly kill their host. But, contrary to popular belief, the spores can remain dormant for months.
So, are anthrax spores like a ticking time bomb in the chests of the at least 43 Americans who have tested positive for exposure? Not likely.
Just because nasal swab cultures turn up spores, doesn’t mean they’re also in their lungs, or they’re in large enough numbers to create an infection. And the antibiotics those exposed are taking should kill any bacteria that might form there, as long as they take the drug for the full 60-day course.
More troubling, however, are those who have been exposed and don’t know it – and aren’t taking antibiotics. Spores could be hibernating in their lungs without revealing their presence through any telltale symptoms, such as painful swelling under the sternum and sudden high fever. By then, it’s too late.
Of those exposed, at least eight have been infected with the inhaled form of anthrax, and three have died. Many are just now showing up at hospitals with flu-like symptoms after being exposed weeks earlier.
But the incubation time between exposure and symptoms can run much longer than a few weeks.
“Germination may occur up to 60 days later,” says a May 1999 JAMA report, “Anthrax as a Biological Weapon: Medical and Public Health Management.”
“The process responsible for the delayed transformation of spores to vegetative cells is poorly understood but well-documented,” states the report, written by several doctors.
It cites the Sverdlovsk anthrax case, for example.
On April 2, 1979, a biowarfare facility in Sverdlovsk, Russia, accidentally released a plume of anthrax spores into the air that killed 68 of the 77 reported cases of pulmonary anthrax downwind from the release point.
Victims showed fatal symptoms as late as 43 days after exposure, the JAMA study says.
In experimental monkeys, “fatal disease occurred up to 58 days and 98 days after exposure,” it said.
“Viable spores have been demonstrated in the mediastinal lymph nodes of monkeys 100 days after exposure,” the report said.
(The far-less-lethal skin form of anthrax, in contrast, does not have a prolonged latency period. In Sverdlovsk, cutaneous cases developed no later than 12 days after the release of spores.)
Once germination occurs, disease follows rapidly – from within hours to a few days – because replicating bacteria release toxins leading to hemorrhage, edema and necrosis of the lymph nodes between the lungs.
Inhalational anthrax occurs when spore-bearing particles of 1 to 5 microns in diameter are breathed in and deposited into alveolar spaces in the lungs.
“A lethal dose sufficient to kill 50 percent of persons exposed to it is 2,500 to 55,000 inhaled anthrax spores,” says the JAMA study on anthrax.
There, they are transported by lymphatic vessels to lymph nodes in the mediastinum, the membranous space between the lungs.
Toxins form rapidly thereafter, swelling the lymph nodes – something easily diagnosed with chest X-rays.
“That’s what you expect to see in an anthrax X-ray – a large lymph node in [the] chest,” said Dr. George Miceli, director of emergency medicine at Boca Raton Community Hospital, where many of the Florida anthrax patients have been treated.
Robert Stevens, a 63-year-old tabloid photographer, died of inhalation anthrax after opening an anthrax-laced letter at his American Media Inc. office in Boca Raton. He went into a coma not long after being admitted to the hospital.
Sen. Bill Frist, R-Tenn., last week predicted that Stevens would be the first and last to die from the anthrax outbreak.
“I predict we’ll see no more deaths from anthrax,” said Frist, a medical doctor.
But within days, two Washington postal workers, Joseph P. Curseen, 47, and Thomas L. Morris Jr., 55, died from pulmonary anthrax.
Once in the nodes, anthrax toxins cause “hemorrhagic thoracic lymphadenitis and hemorrhagic mediastinitis.” Simply put, the nodes swell, crushing down on the lungs, and eventually explode. Death follows soon after.
All 68 Russians who died from inhalation anthrax died this way.
“Massive lymphadenopathy and expansion of the mediastinum led to stridor in some cases,” the JAMA study says. Stridor is a harsh, high-pitched whistling sound produced in breathing by an obstruction in the bronchi.
The spore-protected anthrax bacterium is particularly hardy, resistant to heat and dryness and even antiseptics. In the body, it feeds off amino acids, nucleosides and glucose found in the blood and tissues.
But in the open air, it is more vulnerable.
Water, humidity, thermal stress, the presence of oxygen and ultraviolet light can all decay anthrax agents, according to Dean Wilkening, a physicist and bioterror expert at Stanford University.
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