Oral History Program Wayne Jensen Interviewed by Carmen Anderson 14 July 1972 Oral History Program Weber State University Stewart Library Ogden, Utah Wayne Jensen Interviewed by Carmen Anderson 14 July 1972 Copyright © 2014 by Weber State University, Stewart Library Mission Statement The Oral History Program of the Stewart Library was created to preserve the institutional history of Weber State University and the Davis, Ogden and Weber County communities. By conducting carefully researched, recorded, and transcribed interviews, the Oral History Program creates archival oral histories intended for the widest possible use. Interviews are conducted with the goal of eliciting from each participant a full and accurate account of events. The interviews are transcribed, edited for accuracy and clarity, and reviewed by the interviewees (as available), who are encouraged to augment or correct their spoken words. 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It is recommended that this oral history be cited as follows: Wayne Jensen, an oral history by Carmen Anderson, 14 July 2012, WSU Stewart Library Oral History Program, Archives, Stewart Library, Weber State University, Ogden, UT. iii Dr. Wayne Jensen and Dr. Malcolm McDonald Abstract: This is an oral history interview with Dr. Wayne Jensen, conducted by Carmen Anderson on July 14, 1972, at the Bear River Research Station near Brigham City, Utah. The Bear River Research Station is a field station of the Northern Prairie Wildlife Research Center, which is one of three major wildlife research centers in the United States. It was established to investigate wildlife diseases with particular emphasis on the diseases of waterfowl and determine how to control them. In this interview, Dr. Jensen discusses his work studying the effects of botulism on humans, animals, and birds and the methods being taken to control botulism, particularly in waterfowl. CA: Dr. Jensen would you tell us a little bit about yourself and how you became interested in your present work? WJ: Before the Second World War, I was a graduate student in microbiology. It was my intention to be an industrial microbiologist. During the war, I was assigned to Fort Detrick in Maryland, which was a biological warfare station. At that time, I got interested in medical bacteriology. After the war was over, I decided that if I was going to be a medical bacteriologist (microbiologist), I should have a bit of medical background. So I went to Cornell University and got a degree in veterinary medicine. I had no interest in practicing veterinary medicine. Directly after that, I went to Johns Hopkins University and did two years of post-doctoral work in microbiology. I finished there in 1952 and worked as a staff member of the Microbiology Department for the next three year. During that period, I worked on a study for the United States Army. This was related to work being done at Fort 1 Detrick in biological warfare. The study was related to clostridium botulinum, which is the cause of a disease of almost all warm blooded animals, including humans. After this contract was finished, I started looking for other work and I was still interested in botulism so I attempted to find a position in that field. Botulism in humans is not a very wide-spread disease. We have something like fifteen or twenty cases a year. At that time, there wasn't a great deal of research done in the human disease, but botulism in aquatic birds was still a serious problem. About the only place work was being done was here at the Bear River Research Station at Brigham City. So I applied for a job and got it. I came here in 1955, and I've been here for more than seventeen years. It's just become a part of my life, and I'll probably spend the rest of it right here. CA: Tell us about the Bear River Research Station, its history, and why it was established. WJ: The Bear River Research Station was established here for about the same reason I came here. Starting in the early part of this century there were records of tremendous die-offs of aquatic birds from a disease that was called Western Duck Sickness, for want of a better name. The cause of it was not known. It was attributed to various things such as a high salt content of the water, salinum poisoning, and parasites. Almost every conceivable cause of the disease was considered during that period of time. It was not until 1930 that several groups of workers, putting the results of their studies together, found that the western duck sickness that had plagued this area for years was actually botulism a food poisoning. It was not uncommon in those days for hundreds of thousands of birds 2 to die each year from this disease. This was quite disturbing to conservationists and hunters, of course. It was considered to be necessary to try to control the disease. That is one of the reasons the Bear River Research Station was established here. It was actually the primary reason it was established here, because botulism was the most serious disease of water fowl that was known at that time. The station here, the first building, was completed in about 1936. At least a limited amount of work on avian botulism and other disease has been carried on here since that time. The Bear River Research Station, currently, is a field station of the Northern Prairie Wildlife Research Center, which is one of three major wildlife research centers in the United States. Our assignment is to investigate wildlife diseases in general, with particular emphasis on the diseases of waterfowl. At the present time, we are concentrating almost entirely on avian botulism although we do have a parasitologist who is concerned primarily with studying the parasites—the internal parasites of waterfowl and the effect of these parasites on their hosts. CA: Is botulism the only disease or do you work with lead poisoning? WJ: Botulism is by no means the only disease that we are concerned about. It's the disease that we are professionally and primarily concerned with. One reason for this, of course, is that it's a spectacular disease. When we have an outbreak of botulism on the refuge or in any of the areas in the western part of the United States, sometimes thousands or even hundreds of thousands of birds will die. This 3 will arouse the interest and concern of the public. Our bureau has instructed us to emphasize avian botulism over the others. You asked specifically about lead poisoning. There is a disease problem on this refuge and in every area where hunting is permitted. It's one that we're not professionally concerned with, simply because we don't have enough time to do it. Our staff is small and even to do adequate studies of avian botulism is more than we can handle in the way it should be handled. CA: Do you know what particular foods or conditions cause the botulism? WJ: That's been one of the major aims of the research programs that have been carried on here. I mentioned before, I think, that the disease is a food poisoning. It's caused by toxins produced by a bacterium known as clostridium botulinum. There are six types of this organism. It's the same genus and the same species but it is divided up into six types designated A through F, because of small chemical differences in the make-up of the toxins. To illustrate what I mean about small differences, each toxin produces about the same kind of disease experimentally in the host. If one is immunized against type A, for example, he is not immune to type D. There is enough chemical difference among the six types of toxins so that immunizing us—or animals—against one type doesn't protect us against other types. Of the six types, A, B, and E are the most serious causes of sickness and death in people. F is a relatively new type and there have been only two or three outbreaks attributed to type F toxin. In birds in the western part of the United States, the cause, as far as we know, is always the C type. The C type again, as far as we know, is not a serious disease in humans. 4 Let me tell you a little bit more about the disease in wild birds. The sources of toxins can be almost any decomposing organic material. The bacterium, clostridium botulinum, is not very fastidious in its food requirements or preferences. It grows in a wide variety of materials. The carcasses of invertebrate animals, invertebrate insects, for example, are media in which toxin can be produced. The body the carcass of any kind of a vertebrate animal a duck, or muskrat or anything of that kind can also serve as the medium in which the botulinum toxins are formed. After the animal dies, the tissues are consumed by the bacterium. In the course of its normal metabolism, it produces the toxin as an end product. The toxin is a very ordinary protein. It's a protein very similar to many that we consume every day. It differs from other proteins in that it's very highly toxic. The birds pick it up in the marsh much in the same way as humans do. Food that they consume has been contaminated with the organism that produces the toxin, and they unsuspectingly consume it. Within a very short time, if the dose of toxin is large enough, they become paralyzed and, in many cases, die. In the case of human botulism, home processed foods are most commonly at fault. The bacterium is a rugged, hardy organism. It forms a spore that is highly resistant to heat and chemical action. If the home canning process is not done properly—if the heat is not intense enough—spores that might be in the food survive the heat treatment. Then, after the canned food is stored away, the organism starts to grow and produces the toxin. Sometimes this is very obvious to the people who are expecting to consume it. It will not smell right or not taste right, and they may not eat it at all, or they may just taste it and discard it. In other cases, 5 there is very little change in the odor or in the taste—at least not enough to be disagreeable, and the people go ahead and eat it. Then they are very likely to come down with botulism. The disease in both mammals and birds is a neural intoxication: in other words, the toxin affects primarily the peripheral nerves of the body and paralysis results. Death, then, is caused ordinarily by inability to breathe. The nerves that supply the muscles that are essential to breathing are paralyzed and the victim simply suffocates. An interesting point about these botulinim toxins is their very great toxicity compared to other poisonous materials. The botulinum toxins are undoubtedly the most poisonous substances that are known to man. It was estimated by a research worker several years ago that seven ounces of pure type A toxin would be enough to kill the entire human population of the earth. So you can see it takes a very few molecules to do its damage. CA: Are there any other diseases that you are working with that might be of interest to us as we deal with the waterfowl? WJ: The diseases, other than avian botulism and parasitic diseases, that I mentioned before are rather incidental as far as we're concerned. They come to our attention by way of our diagnostic laboratory. We do offer, as a service, diagnosis of diseases of wild species, particularly wild birds. These specimens are sent to us from all over the western half of the United States. We accept materials from all states west of the Mississippi and occasionally from states on the other side. In the course of these diagnostic procedures, we encounter diseases that are not a part of our research program. They are simply uncovered in the course of our work. 6 CA: How does water pollution affect your work other than through botulism or is that the only one? WJ: Water pollution, particularly pollution with pesticides, of course, has effects that we really don't understand yet. I think everyone has heard about the effects that DDT, for example, has on egg shell thinning in some species of birds. The DDT disrupts the normal metabolism of the birds to the point that they produce eggs with very thin shells, which are very easily broken. For that reason many of young fail to develop. They die in the egg or the parents destroy the young by simply sitting on the nest. The eggs don't have the strength to resist their weight. CA: Are all birds affected by the same botulism? WJ: As far as we know, most of the birds that are lost to botulism in the western part of the United States are affected by the type C toxin. This is one I think I mentioned before. It is not apparently, a serious hazard to man. There have been only five or six reported cases of type C botulism in man. These are not very well documented. There is some doubt that man is susceptible to the type C toxin. This is getting a little bit away from your original question but it's one that is commonly asked and it might be a good place to work it in. The hunting season on the Bear River Refuge commonly comes toward the end of an outbreak of botulism. There are still sick birds that have consumed this very potent toxin. We are commonly asked, is this a hazard to the hunters? Probably thousands of these birds have been shot through the hunting season because, particularly for the hunters who are not so good, the sick ones are easier to hit. Many of them have been taken home and eaten. To our knowledge, there never has been a case of 7 botulism in man from the consumption of a bird with botulism. This may be because people are just not very susceptible to the type C toxin. It also probably is explained at least in part by the fact that all the botulinum toxins are heat susceptible. They are destroyed very readily by heat. So, in the normal cooking process, the toxin ordinarily would be destroyed. To go back to the question of whether birds are all susceptible to the same type of botulism: birds are probably susceptible to all types but as a naturally occurring disease type C in the western part of the United States and type E in the Great Lakes area are the only two types that have been described in epizootic proportions. There might be occasionally cases of other types, but as far as these big outbreaks are concerned, C and E are the ones that we worry about. Would you want me at this time, to tell you about type E botulism? This is quite a different thing from the type C botulism that we have in this area. CA: Yes, go ahead. WJ: Type E botulism in birds was unknown until the winter of 1963 and 1964, when an outbreak involving several thousand aquatic birds occurred on the eastern shore of Lake Michigan. The cause of the losses was considerably in doubt. A clue to the possible cause came because of a small outbreak in people occurred at the same time. There were only seven or eight people involved. It turned out that all these people had consumed smoked fish from the Great Lakes area. After this fact was known—that people about the same time had had type E botulism—wildlife research workers checked that possibility as an explanation for the losses in birds. It turned out that the birds indeed had died from type E botulism. This is a kind of 8 unusual thing, because the only outbreaks of type E botulism in birds that we know of have occurred in the Great Lake area. So as far as your question is concerned, I think we are safe to say that probably ninety percent of botulism in birds is of either C or E type. CA: What kind of conditions lead up to an outbreak of botulism? WJ: There are several factors that contribute to the beginning of an outbreak. These are not always clear. There are probably others that we don't even know about yet. For one thing, the organism the bacterium requires a reasonably warm temperature, although it will grow over a fairly wide temperature range, say from roughly 208 to 40 degrees Celsius. These temperatures are easily attained during the summer months. The organism also requires a food source, of course. We suspect that one of the most commonly utilized food sources would be the carcasses of invertebrate animals that have just died a natural death. The bacterium is so widespread in the marsh that almost every living creature, including the personnel of this station, has some of these bacterial spores within their bodies. Whether they die of botulism or some other cause, after death, their body tissues serve as a medium in which the toxin can be produced. So we have to have a proper temperature, we have to have suitable nutrients, and, as far as we can learn experimentally, almost any vertebrate or invertebrate body tissue is very satisfactory for the organism to produce its toxin in. Clostridium botulinum is a very strict anaerobe. In other words, it will not grow in the presence of atmospheric oxygen. CA: Would you tell us about how your research projects are financed? 9 WJ: Ordinarily with great difficulty. Our funds are appropriated to us through the Bureau of Sport Fisheries and Wildlife. The funds at the Washington level are allotted to the research laboratories and the other field stations. In our case, the funds are given first to the Northern Prairie Wildlife Research Center, which is our mother station. At this center, the money is divided up among the different projects that require it. I don't think I'm out of line in mentioning that it is difficult to get funds for wildlife disease research, primarily because there isn't a general public interest in wildlife disease. This is something we would like to change, but it's very difficult to do. When we have disastrous botulism outbreaks, for example, at least a small number of the public get aroused and want something done about it. In years of that kind, we have a little more luck in getting funds. In general, people just don't know about wildlife diseases. They're not aware of them except in the spectacular botulism outbreaks. There are, of course, many, many diseases of wildlife that I haven't mentioned. They are not being studied, because there just aren't people and funds to do it. Avian botulism gets more attention than most, because you see the dead birds in large masses. There are other diseases of wildlife that work more slowly and over wider areas. They probably kill as many individual birds in a year as botulism. You see, botulism is a seasonal disease. We lose lots of birds during the summer, but the numbers that die in the winter and spring months are relatively small. So we have all these dead birds concentrated at one time and within relatively small areas too. These are the ones that catch the public eye, but there are many diseases that are going on all the time that we're not doing anything about because we just don't have the people and the money to do it. Even in the 10 course of the limited amount of diagnostic work that we can do here in our laboratory, we find many diseases that no one is investigating for the reasons I have pointed out. We think that the wildlife diseases deserve more attention than they are getting, but we've got to have more public support in order to get the funds we need to do it. Studies involving pesticides are usually better funded, because the general public is aware of pesticides now. Everyone knows about the possible effects of DDT, and mercury, and other things we read about in the newspaper all the time. We're willing to contribute to studies of these and their effects, because we know that we and our children and our grandchildren will probably be affected by them. The same thing is true of the study of the control of nuisance animals, nuisance birds for example. This is something else that concerns the general public. In these cases, it's easier to get funds, but until we can arouse more public interest in wildlife diseases, we're just not going to be well funded. CA: What are the hopes of being able to control botulism? WJ: If we could apply the technology that we already have available, the hopes would be high. By that, I mean we have the information we need to prevent botulism in human populations or populations of domestic animals. Both humans and farm animals can be immunized against botulism, if the risk is high enough to justify it. This is commonly done in laboratory workers who are at high risk because we are working with highly potent toxins. Most of us have had a series of immunizing doses of toxoid to protect us against the disease in case we should accidently swallow the toxins that we are transferring by means of pipettes and so forth. 11 Surprisingly though, even before these toxoids were generally available for us in humans, a laboratory accident has never been reported—a laboratory case of botulism in people. I think this is because the people who work with the toxins are aware of the danger and are extremely careful. It's the only explanation I can think of for that. At any rate, there have been no known cases of botulism in people acquired from a mishap in the laboratory. In some parts of the southern United States and in South Africa there have been problems with types C and D botulism in domestic animals, particularly cattle. Cattle, apparently, acquire the disease from gnawing on bones, perhaps those of little rodents that have died from some reason or other. They are usually deficient in some minerals such as phosphorus and they chew on the bones as a means of supplementing their diet. In the course of this, they consume the remains of the flesh of the animal in which the toxin has been formed. So in cases of this kind, it is practical to immunize the animals with toxoids. This produces an active immunity, which is fairly sound for perhaps a year, after which a booster shot is necessary. In the case of humans, the obvious way to prevent the disease is simply to be sure that all foods that might harbor the toxin are well cooked, because even though the toxin is there, boiling the food for twenty minutes makes it nontoxic as far as the botulinum toxins are concerned. There really is no excuse for botulism in people, because those that are in constant contact with the toxins can be immunized and those who run only the very slight risk of eating food from a contaminated home canned food of some kind can eliminate the possibility of botulism simply by cooking the food properly. 12 These methods, of course, are not appropriate for a wild bird population. We can't get the birds to line up at the front door and come in and get their immunizing shots. We really can get to them only after they are sick, and this sometimes is too late. What we are aiming at is possibly to limit the amount of nutrient material that is available for the bacterium to grow in and produce its toxin. If we assume that this is largely invertebrate material, there might be ways that we can control these invertebrate populations and keep them at a low level. In the early years of my stay here, our thought was a chemical method of limiting the invertebrate populations: preventing them from rising to peaks and then dying off and providing that mass medium in which the toxin can be produced. In recent years, of course, it just isn't the thing to do to go spreading pesticides around a waterfowl marsh. If this approach is to be used, it's going to have to be a biological control of some kind. These are ordinarily very difficult to do. You see, on this refuge alone, which is roughly 65,000 acres, we have anywhere from 25,000 to 35,000 acres of water area at the time botulism outbreaks usually occur, which incidentally is ordinarily about now on to the end of September. This is the usual beginning of a botulism outbreak. With an area like that, it's very difficult to try to control the organism. It's too vast an area to try to chemically treat for any purpose like killing the organism or inactivating the toxin. Even controlling the invertebrate life would be a tremendous task. At the present time, the things that are done sometimes are to use frightening devices to move the birds out of the hazardous area. If the birds aren't there, they're not going to pick up the toxin. But, of course, this is not a solution to the problem. We've spent millions of dollars developing this 13 habitat for the use of waterfowl, and it's defeating our purpose to drive them out at the time of the year when they can make the most use of it. That is sort of a stop gap measure—something that can be done to prevent catastrophic losses. It has recently been discovered by a group of Japanese worker—and this work has been extended by people in this country—that the capacity of Clostridium botulinum, at least in some types and some strains of the organism, the capacity of this organism to produce toxin is dependent upon its infection by a bacterial virus, it's called a bacteriophage. It's a virus similar to the ones that infect people or other animals. Strangely, in some types and some strains of the organism, if the bacterium is cured of this viral infection, it no longer produces toxins. It's been our experience in the laboratory that simply in the course of transferring our stock cultures—our stock cultures are the ones that we maintain just to keep the bacterium alive for experimental use—we inoculate them into our liquid nutrient medium and periodically transfer bits of this to a fresh culture. After it's used up the original nutrients, we transfer the organism to a new culture. In the course of doing this, the type C organisms, in particular, lose their ability to produce toxin. Just how we're going to go about making use of this, we don't know, but we think this a characteristic that should be investigated. If we can determine the factors that influence the rate of toxin production, then we might be able to use this in a water management plan that would help to control botulism. For example, right now we don't know what influence things like salt concentration of the marsh water or the alkalinity have on the rate of decline in toxin producing capacity. We are just 14 beginning to see if we can utilize this characteristic of the organism to our own disadvantage, we hope. CA: What are some of the facilities you have outside the lab for holding experimental animals? WJ: Our particular domain, the research station, is rather small. It's limited to this area immediately around the research station. Our only facilities out there are holding pens for normal animals we purchase for experimental use—housing for them until the time that we need them—and holding pens for birds that are being used experimentally to determine their susceptibility to botulinum toxins or some other agents. You noticed behind the laboratory, we have a rather large fly-proof pen—sixty feet by twenty feet, I think—which was constructed for the reason which I mentioned earlier. In order to keep our birds from getting botulism before the time we're ready to use them for botulism research, we have to keep the flies away. For two years before we found out why this was happening, we lost birds from consumption of toxin-carrying flies. It’s is a rather elaborate holding pen. It seemed to be the only solution to that particular problem. You noticed, also, that we have a smaller white building next to this pen, which is divided up into four compartments. This is simply housing for birds which are being used experimentally to determine the susceptibility of a particular species of birds to toxin. They vary considerably among the species in their susceptibility to the toxin. We must give them various doses by month, measured doses, very carefully measured. We call this a toxin titration. We start out with a highly toxic material and make serial dilutions of it. From each dilution, we give doses to experimental birds. There will be a point 15 where there is a kind of a break. The birds on one side will die and those in the next higher dilution will live. By doing this, we can determine the amount of toxin that it takes to kill a particular species of bird. It is important to us to know the susceptibility of the different species, because if we see a fairly large number of any particular species sick or dead from botulism, it gives us an idea as to what the sources of toxins are. If we know what the food habits are of the particular species of birds, we know how high a toxin level it takes to kill this particular species. The difference is quite large. For example, when we give oral doses of toxin to ducks, we find that it takes somewhere between 20,000 to 40,000 times as much as it takes to kill a mouse by injection in our routine diagnostic procedure. So ducks are not highly susceptible, based on the susceptibility of the mouse by the intraperitoneal route. That sounds like a fairly large dose, but then we find in the case of the California gull, for example, that it takes 10 to 20 times as much as it does to kill a duck. If we see large numbers of California gulls with botulism out there, it gives us an indication that the levels of toxin in the marsh are fairly high. By knowing this about a number of different species of birds, it gives us something on which to base an estimate as to where the toxin is coming from and what the levels of toxin are. When these titrations are done, the birds are kept in this pen I was just telling about. After they are given their dose of toxin, they are watched very carefully and the severity of signs of intoxication and the time of death are recorded. By doing this, we can measure what we call the median lethal dose for any particular species of birds. 16