Amerithrax (4 page)
After the honeymoon phase, the next phase strikes like lightning. The patient suffers respiratory distress, cyanosis, and diaphoresis as microbes multiply in lymph nodes, spreading tissue-destroying toxins to other organs via the bloodstream. A patient infected through the lungs typically suffers distinctive damage to the area between the lungs just below the sternum. That was the case with Stevens.
Phillip Lee called the Centers for Disease Control and Prevention in Atlanta. He spoke with Tanja Popovic, head of the Epidemiologic Investigations Laboratory, and told her of his findings. Stevens’s specimens were driven to Atlanta, where CDC lab chief Richard Meyer processed them for anthrax DNA. The specimens tested positive in two quick preliminary tests, but the final confirmation would not be ready until the next morning.
Stevens’s condition progressively deteriorated. He had low blood pressure and worsening renal insufficiency. His lips became blue-tinged and his body even more bluish. An- thrax victims often erupted with massive, excruciating blis- ters, turning the skin black and leathery. Frantic lab work
of all isolates at the state lab and at the CDC corroborated inhalational anthrax. One report read:
Presumptive isolation of
B. anthracis
. . . was confirmed by gamma phage lysis, presence of a capsule, detection of capsule and cell-wall antigens by direct fluorescent antibody, and
B. anthracis
–specific polymerase chain re- action. [PCR is a technique for copying DNA. The DNA from a single cell is sufficient to start a polymerase chain reaction in which a specific segment of DNA can be copied more than two hundred thousand times in a lab.]
On Thursday morning, physicians called an emergency press conference—the first public announcement that a man in Florida had anthrax. “Perhaps he contracted it in the woods,” they said. The possibility of an outbreak was dis- missed by U.S. Health and Human Services Secretary Tommy G. Thompson, who said, “[It’s] an isolated case and it’s not contagious... We do know that [Stevens] drank wa- ter out of a stream when he was traveling to North Carolina last week. But as far as [contamination from] wool or other things, it’s entirely possible. We haven’t got all of the in- vestigations done and we’re doing a tremendous, extensive job of investigating everything. There is no terrorism.”
The element of bioterrorism had been the first thought in many peoples’ minds since it had only been twenty-three days since the collapse of the Twin Towers. Despite denials, the scare had officially begun.
That afternoon, Florida Lt. Gov. Frank Brogan reported to the media that “a sixty-three-year-old man [had] been hospitalized for pulmonary [inhalational] anthrax.” Florida Secretary of Health John Agwunobi elaborated: “The dis- ease is not contagious. While rare, it can be caught natu- rally.” The Palm Beach Health Department said the case was isolated, but was “very likely” to be fatal.
Later the same day, Florida Department of Health and CDC epidemiologists and lab workers arrived in Palm Beach County to assist. That night, Dr. Brad Perkins, chief of men- ingitis and special pathogens at the Atlanta-based CDC, re- ceived an urgent call at his daughter’s piano recital. Over
low, bubbly mess marbled with red.
Around 3:30 p.m., Dr. Perkins took his team to AMI and met with the editors who knew Stevens. He hoped he could get a clue from them since Stevens had been unable to speak. “That was a fairly dramatic meeting,” Perkins re- ported later, “because we were sitting in a room with people who had known him. This was a universally loved guy.” Just then Dr. Perkins’s cell phone beeped—Bob Stevens had died at 4:00 p.m., dead from inhaling thousands of dangerous spores, the first known anthrax fatality in the United States since 1976.
“Everyone was just in utter disbelief,” said Perkins. Death usually follows severe respiratory symptoms within thirty-six hours and that timing indicated he might have been infected earlier than thought, before his trip to North Car- olina.
And what of Ernie Blanco, the man who may have de- livered a contaminated letter? He may have gotten the pow- der in his lungs too. In his case nothing yet had been confirmed. Though clinical anthrax was suspected once they learned of Stevens’s death, Blanco showed no signs of clin- ical infection. Why? Doctors took a nasal swab from him and began to incubate it in a petri dish to see if it grew anthrax spores. They believed they would. In the meanwhile,
the hospital informed Blanco’s family he too might have been exposed to anthrax.
Late that afternoon, the world media, state and federal agencies, even the White House began speculating and won- dering if the anthrax was connected in some way with the recent terrorist attacks. The White House had expected a biological attack would be next. Dr. Perkins remained fo- cused on “leading a solid, scientific investigation.”
Early the following day, Saturday, October 6, medical examiner Dr. Sherif Zaki and his CDC team arrived by char- tered jet and went immediately to the West Palm Beach medical examiner’s office to perform the autopsy. Whenever there is the slightest reason to suspect the possibility of a homicide, an autopsy is always done. The Palm Beach County coroner, Dr. Lisa Flannagan, would make the initial incisions. Under the burning lights, the examiner, dressed like the others in biohazard mask, plastic face shield, and three layers of gloves (one pair Kevlar-reinforced), ap- proached a sloped metal table where the bagged body lay. The table’s upper half had a grated surface. At the other end was a shallow tub that ran beneath a grating flowing with water. After the bag was unzipped, a careful examination of the victim’s skin, scalp, and entire surface of his body would be made. Then the interior of the body would be examined over the next three hours.
Dr. Flannagan made the familiar Y-shaped incision, folded the skin back, then snipped away each of the ribs with a pair of gardening shears. The chest cavity was a lake of blood. They had never seen so much. With a ladle they bailed it out so they could see what they were doing. Be- cause of potential contamination of the morgue, they stop- pered the huge quantity of tainted blood inside containers. All of the victim’s internal organs were glistening—shot through with signature gram-positive rods of
Bacillus an- thracis
from three to eight micrometers in length.
Dr. Zaki and his team examined them to absolutely con- firm the type of anthrax that had caused Stevens’s death. The surgeon cleared his mind and, like any good detective, began his postmortem examination with no preconceived ideas. They had found no hint of cutaneous anthrax on the
The mechanics of the victim’s death were laid out on the tilted table to be read as clearly as a road map or book. Airborne anthrax spores had settled into tiny sacs in Ste- vens’s lungs. Spores are always more deadly when inhaled because they are disseminated more widely within the body. Bacteria from spores germinating in his lungs had produced several toxins that attacked his cells. Beset by a killer like anthrax, the lymph had accelerated its already speedy flow, moving bacteria to lymph nodes to be destroyed. But when the lymph nodes failed to overcome the infection, the mul- tiplying bacteria inflamed the lymph nodes. They became enlarged, bloody, black, and necrotic. The surgeon could see that. It was a horrible way to die. Stuck to the inside of his lungs was more of the thick, gobby paste. Foamy, golden- yellow glue, anthrax sputum exudate, was everywhere.
Rapidly, the rods and threads must have swept through Stevens’s body, causing toxic shock, internal ulceration, and bleeding. Once blood poisoning had developed, death had followed the onset of the fulminant phase in one to two days. A secondary pneumonia infection had developed, fol- lowed by shock, coma, and instant respiratory collapse. By counting backward the doctor might be able to determine when Stevens had been infected, but not how, nor where the source of that infection was now. His autopsy findings indicated:
Gangrenous lesions in different parts of the lungs, massive thoracic and gastrointestinal bleeding and inflammatory infiltrates. Hemorrhagic mediastinal lymphadenitis, and immunohistochemical staining showed disseminated
B. anthracis
in multiple organs.
The surgeons examined the patient’s cerebrospinal fluid and noted the documented meningitis findings. Meningitis often accompanies inhalational anthrax. Anthrax meningitis, a complication of that form, is characteristically hemor- rhagic. Decades earlier, in the world’s worst accidental in-
In complete medicolegal autopsies the brain is removed and inspected for evidence of disease. A rubber block under the victim’s shoulder blades pushes the chest upward and causes the head to fall back so the skull can be sawed open. The surgeon, after carefully avoiding penetration of the brain beneath, gives a twist to a T-shaped bone chisel forced into the cut line. This lifts the skullcap, which is pried off, cranial material still clinging, and allows the victim’s brain to be removed for inspection. In this instance, though, after much debate, it was agreed that it was far too dangerous to open the skull with an electric saw. A saw’s blade, moving back and forth at high speed, might spread anthrax spores in a cloud of bone dust. Thus, this important step was never accomplished. However, if it had, even the most hardened doctor would have been startled by what lay beneath. After all, who would expect to encounter that rarity of all rarities— the so-called cardinal’s cap?
The top of the victim’s brain had turned to blood.
INHALATIONAL
anthrax places a bloody cap upon its vic- tim’s head like the cap a British judge wore when pronounc- ing a death sentence. As parts of Stevens’s body had turned blue from lack of oxygen, the brain tissue had swollen. It had bled horribly, hemorrhaging in the small blood vessels of the brain membrane as badly as the blood had filled Ste- vens’s chest. Though ghastly, the “cardinal’s cap” serves a
In the meantime, where had the spores come from? So far the investigation had revealed no obvious exposure to
B. anthracis.
At first Florida and federal health officials be- lieved that Stevens’s infection was a fluke, the result of nat- ural or accidental exposure. Federal officials speculated that he had been contaminated by the deadly spores while drink- ing out of a tainted stream in North Carolina. But tests at specialized labs all confirmed his inhalational anthrax re- sulted from exposure to dust containing airborne spores. It was possible to distinguish anthrax contracted from airborne spores from the intestinal variety.
Perhaps Stevens, while fishing, breathed in death from some animal that had lain moldering in the soil for a half- century. Just what were the occurrences of natural anthrax in that region? They would have to check. And what about Duke University where Stevens had visited on Sunday? Spores might have strayed accidentally from bioresearch labs at Duke, though that was unlikely. Frantic tests and lab work spanning the weekend would determine if he had con- tracted the disease on vacation. “No one has any idea where this came from,” said Martin Hugh-Jones of Louisiana State University and head of the World Health Organization’s group on anthrax.
While flu kills twenty thousand Americans every year, anthrax had never been reported in the soil or in animals in the U.S. east of the Mississippi River. In fact, there was only one fatal case of inhalational anthrax between 1933 and 1955 in a study of 117 cases. The nation had recorded only 18 cases of inhalation anthrax in the twentieth century and none since 1978. The last Florida case occurred back in 1956. How could Bob Stevens have developed such a re- markable form of a rare disease?
Anthrax cannot be transferred from one person to an- other, although the bacterium is communicable from animals to humans. Butchers, tanners, farmers—those processing goat hair or goat skins or shearing wool were most at risk. Historically, those who have come into contact with the con-