The deaths of six people nationwide this summer from a “brain-eating ameba” are tragic, but the fatal infection is not a new threat lurking in warm lake waters.
Nearly 40 years ago, in the late 1960s, the same kind of single-cell organisms made a sudden appearance in Virginia, killing two people with an inflammation of the brain.
One of the cases was evaluated by a young pathology resident at Medical College of Virginia in Richmond, Dr. Joseph H. Callicott Jr., who later practiced general pathology in Lynchburg for more than 30 years.
The patient had died very rapidly and with a diagnosis of meningitis.
“We had examined the tissues and had not really pinpointed the cause of the infection,” Callicott said. “I had seen these structures in the brain, but did not know what they were.”
As luck would have it, a pathology journal article shortly thereafter described a Texas man’s death from Primary Amebic Meningoencephalitis (PAM). The cause was Naegleria fowleri, an ameba known to live in warm waters.
Looking at the accompanying photo of tissues, Callicott knew instantly, “That’s exactly what we’re dealing with here.” The senior attending pathologists at MCV agreed.
Again, with luck, when Callicott and his colleagues presented the case at a clinical pathology conference, a senior faculty pathologist told him “this is strikingly similar to the peculiar epidemic we had in the summer of 1951-52 in Richmond.” Five young people had died in 1951 and four more died in 1952.
“I think you ought to take a look at those cases,” he told Callicott, who then began to research the materials from those cases.
“He was right,” Callicott said.
An ameba is a one-celled life form much larger than a bacterium. A free-living ameba is not dependent on a host as part of its life cycle. Naegleria is similar to another free-living ameba, Acanthamoeba, whose presence in contact lens solution led to a nationwide recall to forestall potentially blinding eye damage from the ameba.
It was only in 1959, Callicott said, that a researcher demonstrated that a free-living ameba caused a form of meningitis in animals.
Then about four year later, four cases of human brain disease were reported in Australia and the cause was confirmed as being amebic. One of the researchers was Dr. M. Fowler - the “fowleria” of Naegleria fowleri.
Callicott published on PAM cases, first in January 1968 in the American Journal of Clinical Pathology and the second in October in The Journal of the American Medical Association (JAMA). A third, in 1971, appeared in the Archives of Environmental Health. The last two were co-authored.
Callicott’s first article on PAM looked at seven cases (six diagnosed retrospectively from the 1950s) at MCV from 1951 through 1966, in patients ranging from 8- to 25-years-old.
They’d had headaches for several days, a history of swimming in warm waters, and spinal fluid findings that showed no bacteria. Their deaths occurred in an average of 22 hours after hospitalization, following a grim cascade of symptoms such as stiff neck and high temperatures, loss of awareness and death.
In the first 1968 article, Callicott noted that the lack of bacteria in the patient’s spinal fluid at autopsy was usually attributed to the use of antibiotics in earlier treatment. By using lab culture tests that detect ameba early in evaluation of the patient, he noted, treatment might be possible.
He also concluded that the infection is probably more common than was previously thought.
In 1968, Callicott and a group of researchers studied the spinal fluid specimens from 357 MCV patients, including one who had died from Naegleria infection and one who had lived after having had meningitis from Acanthamoeba.
In 1971, Callicott co-authored an article based on autopsy material from 22 patients who had died in Virginia from undiagnosed meningitis, encephalitis or meningoencephalitis. That article, a survey of the problem in Virginia, included compiled data from July 1937 to July 1969. They found 16 cases, most associated with swimming in three lakes near Richmond in the Chesterfield County area.
In the late 1960s, Virginia had a population of about 4.7 million, and Callicott and the co-authors looked at records from the largest general and military hospitals in the state for patients who may have died of PAM. Only records and tissue sections of autopsied patients were selected. In that article, 54 cases of PAM had been reported worldwide. Of those, 30 percent (16 cases) came from Virginia.
In almost every case, the person had been swimming in warm lake waters. Today, Naegleria is tracked as a waterborne disease by the federal Centers for Disease Control and Prevention. CDC data shows 23 Naegleria infections documented in the United States between 1995 and 2004.
PAM remains a rare disease, said the now-retired Callicott, who had a continued interest in Naegleria fowleri and was always on the lookout for it in his Lynchburg practice.
In the 30 years he’s practiced in Lynchburg, “We’ve never had a case - which is good,” he said.
Callicott says unanswered questions still remain about the ameba. In recent research involving cultures of nasal microorganisms, Naegleria’s been detected, even though the person is not ill.
And some of the people diagnosed with PAM have not been swimming in warm waters, like the Texas man whose published case study first drew Callicott’s interest. He’d been hospitalized with liver disease.
“The other thing is the totally unanswered question - why do so few people get this disease? That’s the good news. It’s a hard disease to catch.
“I don’t think anyone understands why out of thousands of people in a body of water, one or two will come down with the disease.”
One theory is the force of lake water going into the nose - say if a swimmer is diving, or boisterously cavorting underwater. The ameba gets moved upward through the nasal passages, where it gains access to membranes near the oxygen-rich brain.
“They get in there and start proliferating,” Callicott said, adding it’s not an environment that this kind of ameba seeks, because it is fatal to the patient and then to the ameba.
Callicott said he wouldn’t worry about swimming in a big lake, as there is a “good flow of water and the turnover is good. These organisms live naturally on bacteria and algae and things that are in water and at the bottom of lakes.”
“Would I get into a farm pond, in the middle of summer, with no water exchange to it?” he asked. “I don’t believe I would.”
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