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The watermelon mystery.



The mystery began on June 4, 1954:An Upton, Massachusetts, family, the Edisons, came down with severe stomach cramps, vomiting, and diarrhea. At first, Dr. Bernard F. McKernan, a general practitioner, diagnosed gastroenteritis. But as more, similar cases were reported--the Smiths, the Browns, the Millers--he began to suspect something else, an outbreak of food poisoning; to be specific, salmonella. Dr. McKernan learned that patients had eaten only one food in common--watermelon from a supermarket at nearby Milford. However, salmonella poisoning had never been known to come from watermelon. Dr. Gilbert E. Gayler, the state district health officer, came in to survey the outbreak--17 cases in all. That's when Dr. Joseph P. Reardon and I came up from the State Department of Public Health. We inspected the supermarket, obtained stool samples from clerks, and took samples from the watermelons (now pulled from the shelves), from the knife used to cut them, and even from a shelf where the knife was kept. I had misgivings about the watermelon theory. It went against my grain, but if melon wasn't responsible, what was?


"Our laboratory is on a skeletonbasis over the weekend. We don't have the funds to function at full strength seven days a week. As a rule, however, there's always somebody there--the bacteriologists take turns--and this weekend it was Mrs. Holmes. She kept me in touch with developments. As expected, there were several, and as hoped, they told the story--the only possible story. Dr. McKernan was right. By Sunday night, the laboratory had confirmed him on every point. It confirmed his clinical diagnosis of salmonellosis. All of the patient stools were teeming with salmonellae. So were the Smith and the Miller watermelon samples. That confirmed the melon as the vehicle of infection. It also pretty definitely linked the outbreak to the Milford supermarket. Then, thanks to Dr. Reardon, the shelf swab completed the chain. It produced a magnificent culture. I still find that hard to believe. The odds against it were literally astronomical. It was an extraordinary stroke of luck--and a very fortunate one, as well, because the swab I'd taken of the knife itself was negative. What happened, I suppose, was that the knife had been washed after Dr. McKernan embargoed the melons. The knife was our only disappointment. We got one other negative culture--from the melon slice that Dr. Gayler had picked up at the store--but that was hardly a blow. Just the reverse, as a matter of fact. It provided an acceptable answer to one of the two big questions that the positive cultures raised. It explained why the outbreak was confined to just those 17 customers of the Milford supermarket. Dr. Gayler's melon was clean because the bulk of the melons were clean. If all, or most, or even many of the melons had been contaminated, the outbreak pattern would have been quite different. There would have been cases scattered all over the Milford area. But none of the doctors polled by Dr. Gayler had seen a sign of gastroenteritis. The conclusion was practically unavoidable. There must have been only two or three contaminated melons, and by some freak of circumstance they ended up in Upton. "The other question was, of course, the essence of the problem. It was also the essence of my discontent--the root of all my misgivings. How did the contaminated melons get that way? How could something with so thick a hide have ever got contaminated? To answer that--to even attempt an answer--we needed to know a little more about the organism involved. We knew it was salmonella, but we didn't know the serotype--the species. When we did, we might have a lead. However, sero-typing calls for antigenic analyses that most laboratories--including ours at that time--are not equipped to perform. We relied for such work on the New York Salmonella Center, at Beth Israel Hospital, in Manhattan. Accordingly, on Monday morning we prepared a sample culture and sent it off to the center for specific identification. If all went well, we would have a report in a couple of days or so.

"The salmonella is a curious groupof pathogens. It differs in many important respects from the other bacteria commonly associated with food poisoning--such as the staphylococci and Clostridium botulinum, the botulism organism. For one thing, salmonella is inherently infectious to man. The ingestion of food containing a quantity of living salmonellae commonly results in illness. Moreover, because salmonella is perfectly adapted for growth and reproduction within the human body, the quantity need not be an enormous one. With the others, the mechanism is quite different. Botulism and staphylococcus food poisoning are intoxications rather than infections. Their cause is not the living organism but a toxin excreted in the food by the organism in the course of its proliferation there. In other words, the food itself is poisonous. That largely explains why staphylococcus food poisoning comes on so much faster than salmonellosis. Botulism takes longer--sometimes three or four days--but it isn't a gastroenteritis. It's primarily a disease of the central nervous system--and an extremely serious one. Fortunately, it is easily controlled. C. botulinum lives in the soil and can grow and elaborate its toxin only in a total absence of oxygen. Most outbreaks of botulism in this country are traced to home-canned vegetables inexpertly washed and processed and eaten without further cooking. Although heat has little or no effect on the botulism organism itself, proper cooking will safely destroy the toxin. The staphylococci enterotoxin, on the other hand, is highly heat resistant. In addition, the staphylococcus organism is ubiquitous in nature. It's even been isolated from the air of rooms. And it is perhaps the commonest cause of boils and other skin and wound infections. Nevertheless, the control of staphylococcus food poisoning is not--at least potentially--too difficult. Refrigeration will prevent the development of the toxin, and good common-sense hygiene on the part of food handlers will do the rest. Salmonellosis would seem to be as easily controlled. Cooking, refrigeration, and cleanliness are all helpful precautions. The first will destroy the organism, and the others will retard its growth. But the problem is more complicated than that. Infected human beings are not alone responsible for the spread of salmonellosis. Salmonella can live in the intestinal tract of almost any animal, including those that are closest to man--dogs, rats, mice, cows, chickens. And, to make matters worse, it appears to be a perfect parasite. It can live and propagate in most such animals without any visible signs of harm to the animal.

"Nor is that all. New species ofsalmonella turn up every year. Since 1885, when the first member of the group was described--by an American pathologist named Daniel E. Salmon--literally hundreds of species have been identified. The total now known is well in excess of 400. So far, I'm glad to say, most of them don't exhibit any unusual pathogenic powers. They produce a disagreeable but not usually fatal illness. But that doesn't mean they never will. A more virulent species might emerge tomorrow. The multitude of species is not in itself particularly disturbing. It actually has a certain epidemiological value. Many apparently unrelated outbreaks of salmonellosis have been linked through identification of the species involved. It also sometimes happens that the identity of the species will indicate the ultimate source of the trouble. It has been the custom for many years to name a newly discovered species for the place where it first was found. The names of some no longer have any geographical significance. In the intervening years, the species they denote have been found in many different places. Salmonella montevideo is one of that increasingly widespread group. So, among others, are S. oranienburg, S. newport, S. derby, S. bareilly, and S. panama. A good many more, however, are still essentially regional species--such as, to mention just a few, S. dar-es-salaam, S. moscow, S. bronx, S. israel, S. marylebone, S. ndola, S. oslo, and S. fresno. Another is S. miami. And that was the one we got. That was the Upton organism.

"I had a telegram from Dr. IvanSaphra, the chief bacteriologist at the New York Salmonella Center, around four o'clock on Tuesday. The late Dr. Saphra, I should say--he died in 1957. A great pity. He was a fine man, and an outstanding one in his field, as his work in this case plainly testifies. Our culture didn't reach him until sometime Tuesday morning, but he had it typed that afternoon. It often takes longer than that to identify a relatively common species. To even think of S. miami in this part of the country was remarkable. The implications of his report were even more so. S. miami, as its name suggests, is a Florida organism. It has been recovered in several human outbreaks in that area, and from many different animals. We could hardly have hoped for a more provocative lead--or one that so comfortably simplified the problem. It was only necessary to find a link between Florida and Massachusetts. What might have transported S. miami from way down there to here? An animal host? Not likely. Our examination of the supermarket had produced no evidence of rodent infestation. A human carrier? The answer to that was on my desk in a laboratory report on the specimen stools from the fruit-and-vegetable clerks. They were negative of salmonella. What else? Well, unless I was very much mistaken, Florida was a major source of produce for the Northeastern market in the spring and early summer. I put in a call to the supermarket at Milford and had a word with the manager. He was most cooperative. Their melons were Florida melons.

"That seemed to tell the story--theonly reasonable story. We could scratch the store off the list. The trouble didn't originate there. It came up with the melons from Florida. To be sure, that was largely an inference, but it had the ring of truth. No other explanation was warranted by the facts. It wasn't, of course, the whole story. It didn't tell us how the contaminated melons got contaminated. That basic question still loomed. But it helped. We had sufficient data now to at least make a stab at an answer. We began with a train of assumptions. Suppose a melon had come in contact with infected animal droppings down there in some Florida field--or for that matter, after it was harvested and stacked in the local jobber's warehouse. Suppose some of that material adhered to the skin of the melon. Suppose it was still there when the melon arrived at the store. And suppose it was still there when the clerk took his knife and sliced up the melon for sale. What then? It was easy enough to find out. All we needed was a watermelon.

"I picked one up on theway to the office on Thursday. We lugged it into the laboratory, and Mrs. Holmes prepared a dilute suspension of S. miami from one of the positive cultures. She swabbed some of the material on the skin of the melon. Then, using a clean knife, she cut a slice out of the melon at that point. The next step was to demonstrate the result. We made two sets of cultures from the meat where it had come in contact with the knife. The first was made immediately after the melon was cut, and the second a few hours later--when the organism would have had time to establish itself better. We then tried a different approach. We deliberately contaminated the knife with our S. miami suspension and cut off another slice of melon and made a culture from that. The idea, of course, was to see if a knife could spread the infection from one melon to another. At that point, we called it a day. For good measure, however, we left the original slice of melon overnight on the laboratory table. Fifteen hours or so at room temperature would give the remaining S. miami a really good chance to grow. The following day, we made a culture from that exposed slice.

"We got the first results on Saturday. Theyweren't exactly discouraging. I went down to the laboratory and read them myself. On the other hand, they fell a bit short of convincing. The first set, made right after the first slice was cut, was practically nothing--just a hint of S. miami. There was a little more life in the two other Thursday cultures. They each produced a colony or two. That left the overnight culture. I won't pretend that we waited for Sunday with bated breath. The results of the other cultures were an indication that we might expect something fairly conclusive. So I was fully prepared for the best. But I wasn't prepared for what we actually got. It wasn't just a good solid cluster of colonies. It was any number of colonies--innumerable colonies. It was an S. miami metropolis."
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Title Annotation:cause of outbreak of salmonella
Author:Roueche, Berton
Publication:Saturday Evening Post
Date:Jan 1, 1986
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