"Mrs. Huckleby told me that the hospital sent Ernestine home for Christmas. She was discharged on December 19. She got steadily worse during her stay at home, and she was readmitted on December 27. It was a pretty dreary Christmas for the Hucklebys. Amos Charles took sick while Ernestine was home—on Christmas
• Eve. He went to bed with an earache, and when he woke up Christmas morning, he said he couldn't see very well. The next day, Dorothy took sick. It began as a generalized malaise. Then
she began to feel 'woobly.' Then she couldn't walk at all, and her speech began to slur. Meanwhile much the same thing was happening to Amos Charles—trouble walking, trouble talking, trouble seeing. Then he went into what Mrs. Huckleby called a 'rage.'
t was a good descriptive word. He was wild, uncoordinated, thrashing around on the bed. He and Dorothy both got steadily worse. They sank into coma. And, finally, on Sunday, they had to go into the hospital. I spent the rest of Monday talking to the Alamogordo doctors, and then to Huckleby. He wasn't easy to talk to. He was shy, and he didn't say much. He raised his hogs in a couple of pens he rented at a hog farm on the outskirts of town. He collected garbage from his neighbors, and he fed his hogs a mixture of that and grain and water. He cooked it because the law required that garbage be treated that way for feed. He stored his grain in a shed at home, and he kept the shed locked. I saw the grain—what was left of it. It was a mixture of grain and chaff. Anyone would have wondered about it. Most of the grain was coated with a pink warning dye. Huckleby said he had stopped feeding the grain as soon as he heard it was dangerous. I said I certainly hoped so. I questioned him particularly about the sickness that had afflicted his hogs in October. He told me this. When he saw his hogs one morning, they were well. When he saw them next, around four o'clock that afternoon, they were blind and staggering, sick and dying. That was strange. I hadn't ruled out encephalitis in the children, but this was different. There almost had to be a connection between the sick hogs and that chemically treated grain. And I couldn't connect a sudden illness and sudden death with any chronic poisoning.
"Everybody was still thinking in terms of encephalitis. That was the admitting diagnosis on Amos Charles and Dorothy at Providence Memorial Hospital. I spent Tuesday and Wednesday in El Paso. I read the records and I talked to the doctors involved. The relevant test results were either normal or not very helpful. The children's kind of blindness was identified as tunnel, or gun-barrel, vision—a constriction of the visual fields. Urinalysis was positive for protein in all three patients, and the presence of protein in the urine always indicates some impairment of function, which is unusual in most encephalitides. And I saw the patients. It was terrible. I'll never forget them. It was shattering. Amos Charles was a big, husky, good-looking boy, and he lay there just a vegetable. His brain was gone. Ernestine was much the same. Dorothy was a little more alive. Her arms kept waving back and forth. Pendular ataxia, it's called. The charts on the children spelled everything out.
"I talked to Ed on Tuesday afternoon, and he drove down to El Paso that night. He had his rubella campaign well started, and he was eager to get back into the Huckleby investigation. He brought some confusing news along. One of Jon Thompson's people had run down the source of Huckleby's grain and identified at least one formulation of the material it was treated with. It was a fungicide called Panogen. Panogen is cyano-methyl mercury guanidine. And mercury is a classic poison. It's one of the most dangerous of the heavy metals. Well, that should have clarified things a bit, but it didn't. It only added to the confusion. Because the clinical picture the Huckleby children presented looked nothing like classic mercury poisoning. The textbook symptoms of acute mercury poisoning are essentially gastrointestinal—nausea, vomiting, abdominal pain, bloody stools. That and severe kidney damage. Chronic mercury poisoning is entirely different. The kidneys are not seriously involved. Apparently, they can safely handle small amounts of mercury. The features in chronic mercurial- ism are an inflammation of the mouth, muscular tremors—the famous hatter's shakes—and a characteristic personality change. Shyness, embarrassment, irritability. Like the Mad Hatter in Alice in Wonderland. We didn't know what to think.
"We couldn't dismiss the possibility of mercury. But we couldn't quite accept it, either. The only thing we were finally certain about was that we weren't up against an acute viral encephalitis. The clinical picture—particularly the gradual development of symptoms—and the epidemiology made it quite unlikely. It made it incredible. We decided that we were left with two general possibilities. One was a more insidious kind of encephalitis —a slow-moving viral infection of the brain. The other was an encephalopathy. Encephalitis is a disease of the gray matter—or gray nervous tissue—of the brain. Encephalopathy involves the white matter—the conducting nerve fibers. A toxic encephalopathy was the kind we chiefly had in mind. The cause could be one of a variety of substances. The heavy metals, of course. Arsenic. Or numerous drugs on the order of sedatives and tranquilizers. The slow-moving-viral possibilities were more exotic. Rabies is in that class. And kuru, a fatal neurological infection in New Guinea that is perpetuated by cannibalism. And scrapie, a disease of sheep, but a human possibility. And others. The trouble was that Ed and I weren't neurologists. But I had a friend who was—Dr. James Schwartz, at Emory University, in Atlanta. So, just on a chance, I called him up and gave him the clinical picture and asked him what he thought it sounded like. He gave us quite a shock. He said it sounded a lot like one of the multiple scleroses —a rapidly progressive demyelinating process called Schilder's disease. Except, he said, three cases would constitute an epidemic, and an epidemic of Schilder's disease had never been reported before. He was inclined to doubt that one ever would be. Another, and more reasonable, possibility, he said, was heavy-metal poisoning. Except that our picture wasn't quite right for lead. Or mercury. Or anything else that readily came to mind. I thanked him just the same. Ed and I decided we had better go back to Alamo-gordo.
"We went back on Thursday. Jon Thompson joined us there, and we spent most of the day at the Huckleby house, taking it apart. It would have been very exciting to turn up the first epidemic of Schilder's disease in history, but we decided that my talk with Dr. Schwartz had just about narrowed the possibilities down to a toxic encephalopathy, and we were looking for a possible source of poisoning. Ed and Jon had already searched the house, of course, but this time we really left no stone unturned. We went through every room and everything in every room. We went through the medicine cabinet. We checked the cooking utensils. Some pottery clay, for example, is mixed with lead, and there is sometimes lead in old pots and pans. We looked for spoiled food. We examined everything in the family freezer, including what was left of the hog they slaughtered back in September. We didn't find anything new or suspicious, though. We had another useless talk with Huckleby, and ate dinner and went back to the motel, and we were sitting there around eleven o'clock trying to think of what to do next—when the telephone rang. It was a call for me from Dr. Alan Hinman, in Atlanta. Alan was one of my bosses. He's the assistant chief to Mike Gregg in the Viral Diseases Branch at CDC, and he was calling from his office—at one o'clock in the morning! It was fantastic. And then it got more fantastic.
"Here's what Alan had to tell me. That afternoon, he said, just before quitting time, Mike Gregg had gone in to see Alexander Langmuir—Dr. Langmuir was then director of the Epidemiology Program at CDC—about something, and as he was leaving, he mentioned the Huckleby outbreak. Mike said there was this damn disease out in New Mexico with gun-barrel vision and ataxia and coma, and we didn't know what to make of it. Dr. Langmuir said oh? Then he stopped and blinked, and said it sounded to him as if it might be Minamata disease. Mike looked blank. Dr. Langmuir laughed, and picked up a reprint on his desk. He said his secretary had dumped a pile of accumulated reprints on his desk to either discard or keep on file, and this was one he had just finished looking at. It was a paper from World Neurology for November, 1960, and it was entit
led 'Minamata Disease: The Outbreak of a Neurologic Disorder in Minamata, Japan, and Its Relationship to the Ingestion of Seafood Contaminated by Mercuric Compounds." Well, Mike took it home and read it, and it struck him just as hard. So he called up Alan, and Alan came over and got the reprint and read it, and he reacted in the same way, only more so. He drove down to the office and got into the library and checked the references, and there wasn't any question in his mind. Our problem was Minamata disease. He read me the original paper. It began like this: 'In 1958, a severe neurologic disorder was first recognized among persons living in the vicinity of Minamata Bay, Japan. Now 83 cases have been recorded, most ending fatally or with permanent severe disability. Epidemiologic investigations . . . helped to establish the relationship of this illness to the consumption of seafood from Minamata Bay. The effluent from a large chemical manufacturing plant which emptied into the bay had been suspected as the source of a toxic material contaminating fish and shellfish. Subsequent work has provided evidence that the responsible toxin is associated with the discharge of organic-mercury-containing effluent from the chemical factory.' The clinical features had a familiar sound. Ataxic gait. Clumsiness of the hands. Dysarthria, or slurred speech. Dysphagia, or difficulty in swallowing. Constriction of the visual fields. Deafness. Spasticity. Agitation. Stupor and coma. And this: 'Intellectual impairment occurs in severely affected patients; children seem particularly liable to serious residual defects.' And, finally, there was this: 'When the first cases were recognized, Japanese B encephalitis was considered as a diagnostic possibility; however, evidence against encephalitis (aside from the cardinal clinical features) includes the following: the onset of symptoms was usually subacute and not accompanied by fever, cases were limited geographically, and they occurred throughout the year.' The Minamata paper would have been enough for me, but Alan had found another that was even more convincing. It had the title 'Epidemiological Study of an Illness in the Guatemala Highlands Believed to Be Encephalitis,' and it had been published in the Boletin de la Oficina Sanitaria Panamericana in 1966. The passage that really clinched it was this: 'Possible toxic elements in food, such as edible mushrooms, were investigated. In the course of this investigation it was noted that during the period of the year in which the illness occurred, many families, and especially the poorest, ate part of the wheat given them for seed, which had been treated with a fungicide known commercially as Panogen—an organic-mercury compound.'
"That was the key—that word 'organic.' It instantly clarified everything. Panogen is cyano methyl mercury guanidine, and cyano methyl mercury guanidine is an organic mercury compound. Ed and I were perfectly well aware of that, but the significance just hadn't penetrated. When we thought of mercury, we naturally thought of inorganic mercury. That's the usual source of mercurialism. But the pathology of the two afflictions is very different. Organic-mercury poisoning has always been something of a rarity. Until recently, anyway. At the time of the Minamata report, the total number of cases of organic mercurialism on record was only thirty-nine. And only five of them were American. Well, I finally finished talking to Alan and gave the news to Ed and Jon, and we all immediately agreed. It was a fantastic kind of coincidence—Dr. Langmuir, Minamata, Guatemala. But it fitted to the letter. Or practically. Talking it over, we did see one objection. The behavior of the Huckleby hogs. Chronic poisoning doesn't produce a sudden, fatal illness. It doesn't, and—the way it turned out—it didn't. On Monday, January 19, I went out and had another talk with Huckleby, and I don't know why, but this time we got along much better than we had before, and he finally said that he could have been mistaken—that it probably wasn't all that sudden, that his hogs probably did get sicker and sicker over a period of several weeks.
"The only thing we needed now was proof. It arrived that night—Monday night—in another call from Alan. He had had a call from Mr. Barthel at the Toxicology Laboratory. Mr. Barthel had analyzed Ed's samples of grain and pork and urine, and he had found mercury in everything but two of the urine samples. The two negative samples were those of the two youngest Huckleby children. One of them was two years old and the other was just ten months, and neither of them had eaten any of the pork. The highest mercury levels were found in the patients' urine. That, of course, was as expected. One of the lowest was Mrs. Huckleby's. Which was fortunate. After all, she was pregnant. But the fact that she and the other asymptomatic members of the family showed any mercury at all was unexpected. It raised a question, and it was a question that would have bothered us if we hadn't been doing a little reading in the literature on our own. The question was: Why didn't all the pork-eating Hucklebys get sick? They all consumed about the same amount of meat. We found an acceptable answer in a 1940 paper in the British Quarterly Journal of Medicine. The paper was entitled 'Poisoning by Methyl Mercury Compounds,' and the relevant passage read, 'The fact that eight men, exposed in a similar way to the four patients, excreted mercury in the urine, yet showed no symptoms or signs of disease, suggests that most of- the workers absorbed mercury compounds, but that only four . . . were susceptible to them.' That was the best explanation—Ernestine and Amos' Charles and Dorothy were simply more susceptible to mercury than the others. It satisfied me, anyway. And the next day I flew home to Atlanta."
The chain of laboratory evidence that linked the Huckleby children's affliction to the diet of the Huckleby hogs brought the epidemiological investigation of the outbreak to an end. As it happened, however, that was not the end of the case. On Monday, January 19—the day on which Dr. Likosky and Dr. Pierce and Mr. Thompson wound up their joint investigation—the case took a new and ominous turn.
The turn occurred in Clovis, New Mexico, a livestock center some two hundred miles northeast of Alamogordo, and it was set in motion by a state sanitarian on duty there named Cadi- Lancaster. Mr. Lancaster was the investigator who had identified Panogen as a chemical contaminant in the Huckleby grain. His second contribution to the case stemmed from a monitoring impulse that prompted him to leaf through the recent records of a Clovis hog broker. He didn't have far to look—only back to Friday, January 16. On that day, he was interested to read, the broker had bought a consignment of twenty-four hogs from a grower in Alamogordo. What particularly interested Mr. Lancaster was the grower's name. He knew it: the man was one of the Huckleby group who had included treated grain in their hog feed. He also knew that all the growers in that group had been instructed to withhold their hogs from market until otherwise notified. The feeding of treated grain had been stopped by horrified common consent at the very start of the investigation, but that was not enough to render the hogs safe for immediate use. Organic mercury is eliminated slowly from living tissue. It has a half-life there of two or three months. Mr. Lancaster sought out the broker. The broker stood appalled. He hadn't known. He had had no way of knowing. What was worse, he added, he had already disposed of the hogs. They were part of a shipment of two hundred forty-eight hogs that had gone out on Friday afternoon to a packing plant in Roswell. Mr. Lancaster turned to the telephone.
The recipient of Mr. Lancaster's call was Carl Henderson, chief of the Consumer Protection Section of the New Mexico Health and Social Services Department, and he received it in his office at Santa Fe. He thanked Mr. Lancaster for his enterprise, and sat in thought for a moment. Then he himself put in a call—to the packing plant in Roswell. The manager there heard the news with a groan. Yes, he said, he had the Alamogordo hogs, but that was the most he could say. He didn't know which they were. They were no longer hogs. The big Clovis shipment had been slaughtered on Saturday, and it was simply so many carcasses now. In that case, Mr. Henderson said, he had no choice but to immobilize the lot. The plant was therewith informed that all those two hundred forty-eight carcasses were under state embargo. Mr. Henderson hung up and moved to reinforce his pronouncement. His move was at once effective. The following day, January 20, the United States Department of Agriculture, through the Slaughter Inspection Division of its Consumer and Marketi
ng Service, placed the state-embargoed carcasses under the further and stronger restraint of a federal embargo, and arranged for a sample of each carcass to be tested for mercury at the Agricultural Research Center, in Beltsville, Maryland. That same day, the state extended its embargo to the grain-fed hogs still in the possession of Huckleby and his five companion growers in Alamogordo. The next day, the hogs were tallied and found to total two hundred and fifteen head. One hog was selected from each grower's herd and killed and autopsied, and specimens were sent to the Toxicology Laboratory of the Food and Drug Administration, in Atlanta, for definitive examination.
Two days later, still shaken by Mr. Lancaster's discovery, the New Mexico Health and Social Services Department took another protective step. A cautionary letter, signed by Dr. Bruce D. Storrs, director of the Medical Services Division, was distributed to every physician and veterinarian in the state. The letter read:
A recent outbreak of central-nervous-system disease among three children of an Alamogordo family has been traced to the ingestion of pork contaminated with a methyl-mercury compound. The animal involved had been fed over a period of several weeks with grain treated with this material. At the time it was butchered, the hog appeared to be in good health, and visual inspection of the carcass during processing failed to reveal any significant abnormalities. Laboratory analysis of the meat eaten by the family, however, revealed a high concentration of methyl mercury.
The grain had been obtained by the children's father, free of charge, in the form of castoff "sweepings" from a seed company located in eastern New Mexico. This was mixed with garbage and fed to the hogs despite the knowledge that it had been treated with the fungicide. Several weeks after slaughter of the boar, 14 of the family's remaining 17 hogs became ill with symptoms of blindness and staggering gait. Over a three-week period, 12 died and the remaining two were permanently blind.
The Medical Detectives Volume I Page 27
