Amerithrax (3 page)

twice from the waterfall.

Stevens was feeling better on Saturday, having under-

gone a brief recovery. This was the “honeymoon,” “eclipse,” or “false recovery” period of the disease. It meant that Ste- vens’s immune system was fighting back. The same day, back in Boca Raton, Blanco was suffering from a nonpro- ductive cough. He had intermittent fever and a stuffy nose. The backs of his upper eyelids were inflamed.

On Sunday the Stevenses drove to Duke University in Durham to visit their daughter’s boyfriend, and Stevens saw the onset of a mild flu with fever—a cough, then chills and vomiting. Like Blanco, he had felt fatigue and muscle aches at first. But if it was flu, why wasn’t he experiencing nasal congestion or a runny nose? He had breathing problems and vague chest pains. His medical history included cardiovas- cular disease, hypertension, and gout, but none of the symp- toms he was now experiencing—headache, muscle aches, and shortness of breath. Stevens wondered if he had picked up some infection in the woods or fishing. He had drunk some water from a stream.

The Stevenses strolled the blue-gray stone walkways of Duke University’s West Campus. The 210-foot Duke Chapel tower dominated the fifty-five wooded acres there. The seventy-seven stained-glass windows of the Gothic ca- thedral shone in the morning light and the air was crisp. They heard the strains of an organ with more than five thou- sand pipes. A nondenominational hymn wafted over the landscaped acres. Beyond was the stadium, the Medical Chapel Center, and the VA Hospital.

By afternoon, Stevens’s cough had worsened. His breathing had become more labored and his head was throb- bing. Inside his body, the sticks and tangled threads had multiplied into billions. They teemed venomously, like little snakes, in what had been robust tissues. They choked veins and arteries and with their poison turned healthy red blood a sinister black. Stevens was feeling so poor that he and his wife were forced to return early from North Carolina on Sunday evening. During the ten-hour drive back, Bob’s con- dition worsened. When they got home, he gave Maureen a kiss good night as he always did. “He said, ‘I love you,’” she recalled. “And those were his last coherent words to me.”

On Monday, October 1, Ernie Blanco experienced inter- mittent periods of confusion at home and work. He seemed not to know who he was. Blanco was admitted to a local Miami hospital for examination that day. Tests for Legion- naires’ disease and hantavirus proved negative and the ER staff could find no blisters or skin lesions. Blanco’s white blood count was normal, but his throat was sore. Listening with his stethoscope, the doctor heard the characteristic wheezing sounds of pneumonia. Blanco’s inflamed lungs certainly suggested that. The elderly man’s chest X ray, taken back to front, revealed diffuse consolidation through- out his left lung and bloody secretions scattered through the lower lobe of his right lung.

Remarkably, Blanco’s X ray findings were dominated by large and progressive pulmonary infiltrations, not by medi- astinal widening. Mediastinal widening, an enlarged space under the breastbone and between the lungs, would have suggested another respiratory disease altogether, but one that common sense said had to be out of the question. Doctors decided to use computed tomography, a technique more sen- sitive and detailed than plain X rays. A series of X rays analyzed by a computer provided several cross-sectional views and a dye injected into the bloodstream clarified ab- normalities in Blanco’s chest. His CT showed left upper and lower infiltrates consistent with pneumonia. A recurrent left pleural effusion (a fluid buildup in the pleural space) called for placement of a chest tube. Blanco was prescribed an intravenous antibiotic, azithromycin, and hospitalized for pneumonia. His chart read:

Temperature 38.5
°
C, heart rate 109/min, respiratory rate 20/min, and blood pressure 108/61 mm Hg. The patient has bilateral conjunctival injection and bilateral pulmo- nary rhonchi. Examination, including assessment of neu- rologic function, was otherwise unremarkable. Admission laboratory results included normal WBC [white blood cell] count and serum chemistries, except for hypoalbu- minemia, elevated hepatic transaminases, borderline hy- ponatremia, and increased creatinine. Arterial blood gas values showed hypoxia.

On Tuesday at 2:30 a.m., Bob Stevens awoke suddenly in his Lantana home. The previous day, he had gone to work but had been forced home with a temperature. Like Ernie Blanco he seemed not to know where he was. He was feverish, confused, and overcome with nausea, vomit- ing, and chills. Stevens had a 102-degree fever and became so disoriented that he tried to get up and go to work. This alarmed his wife, who took him to the emergency room at JFK Medical Center in nearby Atlantis. Though alert and interactive, he spoke nonsensically. He didn’t know who he was, where he was, or what day it was. Stevens was admit- ted for evaluation at 2:20 p.m. The ER staff scrambled to diagnose and treat whatever it was Bob Stevens had. Initial pulmonary, heart, and abdominal examinations were re- ported as normal:

Temperature was 39.2
°
C, heart rate 109/min; blood pres- sure and respiratory rate were normal. No nuchal rigidity was observed. Admission laboratory values included a normal total white blood cell (WBC) count, but the plate- let count was low. Serum chemistries were normal, ex- cept for borderline hyponatremia and elevated total bilirubin. He had mild metabolic acidosis.

Almost five hours after admission into isolation, Stevens had generalized seizures. He lost consciousness and was in- tubated for airway protection because of rapid respiratory deterioration. Maureen, who had been sent home at 5:30 p.m., returned at 7:45. At that time a radiologist was studying Stevens’s initial chest X ray and comparing it to one he had had taken at JFK a year earlier. The ghostly gray film, also showing the three chest monitors attached to Stevens’s chest, revealed an enlarged space under his breastbone. It cast a wide, unsettling shadow. “Prominent superior medi- astinum and possible small left pleural effusion” was entered on his chart. The widened area between his lungs signified diseased and enlarged lymph nodes. All of the structures between his lungs—the esophagus, trachea, main bronchi, great vessels, and lymph nodes—were inflamed and bloody. As a whole this was called “hemorrhagic mediastinitis.”

There was fluid around the patient’s lungs, cloudy yellow and tinged with blood.

Stevens was tested for meningitis, an inflammation of the covering of the brain and the spinal cord, which is caused by a bacterial or viral infection. The brain and spinal cord are usually very resistant to infection, so when they do be- come infected, it is very serious business indeed. Stevens’s early symptoms were classic—fever, sore throat, and vom- iting following a respiratory illness. Although meningitis is more common in infants than adults, the staff at JFK were very concerned because the disease can lead to death within hours.

After a single dose of cefotaxime, Stevens was started on an alphabet of multiple antibiotics—ceftazidime, genta- micin, metronidazole, doxycycline (a tetracycline), ampicil- lin, and trimethoprim-sulfamethoxazole. The antibiotic cocktail only made Stevens worse, in fact nearly killed him. When some of the bacteria that had triggered meningitis inside Stevens’s spinal cord and brain were slain, they split open, discharging three different poisons into his brain. The sudden toxic influx initiated a grand mal epileptic seizure.

That evening a specialist in infectious diseases at JFK, Dr. Larry M. Bush, continued to fret over a cloudy sample of Stevens’s cerebrospinal fluid. Something did not fit. He had incubated the sample for seven hours. While studying the specimen under the microscope, Dr. Bush astutely re- alized the odd rod-shaped bacteria were not the kind that usually cause meningitis. Three species of bacteria account for more than 80 percent of all cases of meningitis:
Neisseria meningitidis
,
Hemophilus influenzae
, and
Streptococcus pneumoniae
. What was the bacteria that had infected Ste- vens’s brain and its meninges? A gram stain of Stevens’s fluid most resembled the topography of a broken country road, but a purple road twisting among blue-violet trees on a red-violet landscape. Bush consulted the notes:

Cerebrospinal fluid (CSF) analysis showed WBC [white blood cell] count 4,750/

L (81% neutrophils), red blood cell count 1,375/

L, glucose 57 mg/dL (serum glucose

174 mg/dL), and protein 666 mg/dL. Microscopy ex-

amination of the CSF showed many gram-positive ba- cilli.

Gram-
positive
bacilli? In the bacterial universe, gram- positive bacteria are a minority. A gram stain is a method of staining microorganisms using crystal violet, iodine, and a contrasting dye called gram stain. One of the major char- acteristics of bacteria is whether they take Dr. Hans Gram’s concoction. Microorganisms that retain the violet color are said to be “gram-positive.” Those that don’t are said to be “gram-negative.” Practically the only infections caused by gram-positive bacilli are erysipelothricosis, listeriosis... and anthrax.

The specialist believed he was looking at
Bacillus an- thracis
in the patient’s spinal fluid. But this was an aston- ishingly rare disease, especially in nature. The bacteria had not been seen clinically in the United States in almost a quarter century.

ON
Wednesday, October 3, Stevens began his second day in the hospital. Doctors were still deeply concerned. The photo editor remained feverish and unresponsive to deep stimuli. His fever continued to rise and his lungs were filling with fluid. Dr. Bush called the county Health Department director, Jean Marie Malecki, to tell her of his findings. She in turn notified the Florida Department of Health in Jack- sonville of a possible anthrax case in Palm Beach County. It would take twenty-four hours for technician Phillip Lee to know for sure because Stevens’s spinal fluid and blood

cultures had to incubate. As early as two to three days after onset of symptoms gram-positive bacilli can grow on a blood culture.

As yet, no one had connected the cases of Stevens and Ernie Blanco, one of apparent meningitis and the other pneumonia. The only similarity was that both their X rays had been abnormal. Blood cultures obtained from Ernie Blanco the day before showed no growth of infection after initiation of antibiotics. Cefotaxime and ciprofloxacin had been prescribed.

At the end of the day-long incubation period,
B. anthra- cis
was isolated from Stevens’s spinal fluid and blood cul- tures. The result provided more confirmation that the rarest form of anthrax had infected someone. Health workers now thought Stevens was an isolated case. Apparently he had contracted some natural form of anthrax. Initially, they had been puzzled to see infection building in Stevens’s lungs and enlarged lymph nodes. Immune cells dispatched by Ste- vens’s system to consume microbes in the lungs must have transported microbes back to lymph nodes and infected them. The bacteria had multiplied there, spreading tissue- destroying toxins to other organs via the bloodstream.

Antibiotics can kill or halt bacterial growth. But the un- known bacteria had produced a toxin that rapidly blocked the blood and lymph systems, sending Stevens into shock. Doctors now treated him with the antibiotics levofloxacin, clindamycin, and penicillin G. Penicillin is used to treat most gram-positive bacterial infections, but the doctors were not hopeful. If the infection was systemic, its treatment was problematic.

When the Bacillus of Anthrax went visiting with gold cane and top hat, it carried no calling card. Inhalational an- thrax, once it announced its presence, was already a death sentence. By that point it was too late to save victims who had already begun to suffer the distinctive blue or dark swellings along their chest and neck that mark the late onset of inhalation anthrax, also known as pulmonary anthrax.

If high doses of penicillin are injected into the blood- stream at short intervals seven to ten days
before
the first toxins are released, there is a 100 percent rate of survival.

Even if detected within the first few days of exposure it is highly treatable. According to David Straus, a Texas Tech University microbiologist, “If you inhaled the spores now and someone gave you antibiotics you would survive be- cause the organisms would not multiply to the density needed to kill you. But the pulmonary form of the disease is almost invariably lethal because it isn’t recognized in time.” Vaccines exist for anthrax, as they do for smallpox, but are in short supply. Anthrax vaccines are best given eighteen months before exposure, but there is some protec- tion after three doses of the four-dose regimen.

The inhalational variety of anthrax (very rare in nature) is invariably fatal if antibiotic treatment is not given before symptoms begin to show, usually after one to two days. Survival rate at that point is only about 10 to 20 percent. Once symptoms begin: a one- to four-day phase of malaise, frequent fatigue, mild fever and chills, nausea, vomiting, headache, myalgia, grogginess, and nonproductive cough followed by a brief period of improvement; no remedy may be possible.