[ music ] >> welcome. thank you so much for joiningus for the second lecture in the we were there series. this one is to acknowledge40 years
since the discoveryof legionella. this series was started toenable individuals who learned and experienced sentinelcdc outbreaks to share those insightsand stories so that those
of us can continue their work. and now for a few words fromthe current cdc director, dr. frieden. >> i'm looking forwardto this session so i'm going to be very brief. you'll hear about crackingthe case in legionella. it's a story of persistence andhard work, and it's a number of firsts -- the firsttime anyone took a computer into the field, i understand.
in fact, it was the firsttime i heard about cdc, and i could remember sittingat the breakfast room table with my family and myfather reading about cdc, identifying legionella. and he said, "you know, cdc, that's a pretty goodorganization." technology that we use evolves, and we have now reallyfancy tools. but getting to the root cause
of a public health problemis still a challenge that requires sophisticatedlook at the data, understanding what's reallyhappening in the field, dedication and hard work,following intuition, boots on the ground, andit shows the importance of our laboratories whichare essential to all of cdc's progress and success. when a job is done and crisesare resolved, people return to their work oftenwithout much public acclaim,
but even if they don't makeheadlines, they're the heroes and nonetheless definitelypeople to whom we owe tremendousthanks. so we thank everyone involvedin identification of legionella for all that they've doneand think of all the people who have been diagnosedand treated with this disease since 1976. thank you very much. [ applause ]
>> thank you, dr. frieden. and now a short video to takeus back to 1976, and thank you to the cdc museum forlending us the video. >> good evening. in the past few days, a virus-like mysteryillness has killed 15 persons and hospitalizedat least 42 others. all of the victims had gathered at the same conventionin philadelphia.
>> a lot of people had diedin a short amount of time, and people didn't know why. >> i got a call frommy cdc supervisor. >> we have a littleproblem with some pneumonias in pennsylvania state. i would like you todrive up in the morning. and as an eis officerand as an epidemiologist, i had to learn whatwas going on. >> the two latestvictims stayed here
at the bellevue stratford hotelwhile they were in philadelphia. >> two more people arenow known to have died. one more death. another death was reportedand 110 persons are still ill, several of them critically. >> specimens werebrought back to cdc. all the cultures were negative. quickly, we knew this was nota typical infectious disease. what emerged was aseries of hypotheses.
was it related to the food? where they ate? where they slept? where they partied? >> we asked about exposureto water and drinks and liquor and cigarettes. then all these sorts of information are broughttogether in the line list. >> you make a big chart, whichwould have every patient's name
and any sort of thing wecan think of that might lead to some exposure to someunknown infectious agent. >> all these varioushypotheses were testing and coming to dead ends. >> we collected all thespecimens we knew to collect. we asked all thequestions we knew to ask. >> we just didn'tknow what it was. >> the death toll now 27. the latest victims, twomen, pennsylvania residents,
american legion members, and they had attendedthe convention. >> it was very frustratingfor us at cdc not to be able to give an answer. so after three weeks,we went home, and we wrote up ourinvestigation. one of the people who read thisthick memorandum was joe mcdade. >> i had been at the cdc lessthan a year just basically one of the foot soldiersdown in the trenches.
>> he also went to a partyover christmas he's told me. and he got an earful fromsome guest at the party. some of the comments wereless than complimentary about why they hadn't found it. he was insulted by that,and went back to the lab over christmas and re-examinedhis guinea pig slides. >> all of a sudden what i sawwas one microscopic field was teaming with bacteria. so i knew i had something.
>> he found it and namedit legionella pneumophila. >> we had a disease. we had a cause of this epidemic. federal health officialsbelieve they've found the cause of legionnaire's disease. >> and so it's really thecombination of the people in the field and the peopleback in the laboratory, which has been the waythat the cdc has done it from the beginning.
maybe they'll find abetter way some time in the future, buti don't think so. >> and now to share someadditional insights, i am inviting david fraserand joe mcdade to come and tell us their stories. thank you. >> at 9:15 mondaymorning august 2, 1976, a veterans administrationphysician in philadelphia calledcdc to report four deaths
from pneumonia in people whohad attended the american legion convention there july 21 to 24. his call was routed to thenewly created swine flu unit, which had commandeeredthe old auditorium a close by clifton road. first year eis officers,phil graitcer and bob craven, just out of the eiscourse received that call. they alerted the pennsylvaniastate health department
and sought an invitationfor a cdc team. by that time, the knowndeath toll had risen to 11. they set about gatheringmaterials for the investigation includingmaterials for bacterial culture from jim feely, specialpathogens laboratory section. feely alerted me because iheaded the epidemiology branch that partnered withhis laboratory. i called graitcer and cravenoffering ted tsai
also afirst year eis officer for the investigation team. i cited the occasionaloccurrence of pneumococcal pneumoniaoutbreaks as an argument for having somebodyin my branch included. early that afternoon, the pennsylvania healthdepartment invitation was received, and a three personteam left for pennsylvania. tsai to harrisburg,graitcer to philadelphia
and craven to pittsburgh. early that evening,david sensor called a meeting of all cdc personnel who knewsomething about the outbreak, and he asked phil brachman to designate a seniorepidemiologist to head the field team. and phil asked me to do that. so i left early tuesdaymorning to harrisburg. what i'd like to focus on in mycomments today are on a series
of strategic decisionsthat we had to make to focus the investigation. the first is the coordination ofthe state, local and cdc teams. pennsylvania's secretaryof health, leonard bachman, had made harrisburgthe headquarters for the investigation. that's the state capitol. but who was to leadthe investigation? after some discussion,we decided that bachman
and william parkin, thestate epidemiologist, would be the public face,would lead press conferences, would direct publichealth nurses and work with the american legion. i asked only to be thesupervisor of the eis officers, which i assumed would give mecontrol over the investigation. the state laboratory director, vern picoewould organize the collection, splitting and shippingof specimens both
to his laboratories and tocdc where he would coordinate with walt dowdle. lew polk, the actingcommissioner of public health in philadelphia andbob sharrar, the infectious diseasesdirector, would oversee philadelphiahealth department staff. there were a numberof challenges in this investigation. first, we needed a workingdefinition of a case,
a case of whatever this was. we needed to set upa surveillance system for a disease which was nowspread all over pennsylvania because people had dispersed from the conventionin philadelphia. and to that end, we used whatwas then a very impressive cadre of public healthnurses to visit every hospital in pennsylvania everyday for the first seven or ten days of theinvestigation.
we needed to collect specimensof various sorts from autopsies. we needed serum, urine,sputum from ill people. we needed paired serum frompeople with cases as well as from household contactsof both cases and controls in case there was --turned out to be evidence of person-to-person spread. and then we needed environmentalsampling for which dusty rhodes and george mallison from cdcwere very helpful in organizing. one of the very important thingswe needed was a denominator.
many -- several thousand peoplehad attended the convention in philadelphia, but theamerican legion did not have a master list of who attended. they didn't know the delegates. they didn't know theother legionnaires. they didn't know thewomen's auxiliary members or other family memberswho had attended. so we were first facedwith getting a denominator. and then we didn't knowwhat the agent was.
the outbreak investigationstarted on the second of august. by the fourth of august, weknew it was not swine flu, and within the week, we werepretty certain it wasn't anything we knew about. so that was a challenge. because we didn't know an agent, there was great pressinterest in the problem. there was much public anxiety,and conspiracy theories around the bicentennialof our country cropped up.
so much talk about phosgene, and chlamydia, nickel carbonyl and other possibilities, some ofwhich i'd never heard of before. the second set ofstrategic decisions that had to be made was around theorganization of eis officers and other cdc field staff. at it's peak, we had 33cdc staff in the field in pennsylvania notcounting scores and scores of people workinghere in atlanta
and in other cdc laboratories. one of the earlydecisions i made was that every eis officer shouldsee cases of this disease. do a physical examination. read the charts. gather the information we neededto frame a case definition. and that definition ended uphaving a clinical part in it and an epidemiologic part. clinically, to be a case, onehad to have chest x-ray evidence
of pneumonia andfever or a temperature of 102 fahrenheitor higher and cough. to meet the epidemiologicalcriteria, one had to either have attendedthe american legion convention july 21st through24th or have been in the bellevue stratford hotelsome time after july 1 prior to the onset of illness. in organizing eisofficers, we arranged morning and evening staff meetings, andyou can see here is a picture
of one of those staff meetings in the philadelphia healthdepartment office building. those reports would involve inthe morning planning the work of the day and in the eveningsummarizing what advances we made. we divided the investigationinto modular studies, which i think was animportant part of dealing with such a large group ofvery bright energetic people so that each eis officerhad primary responsibility
for one of these modules. phil rettig was in charge ofwhat we call the 10,000 survey. this was our attemptto get a denominator. and so what we did was work out an extensive questionnaireregarding whether or not people were ill, theirage, sex, medical history, what hotel they stayed in,what their activities were at the convention,and we had packets of this questionnaire deliveredby the american legion to each
of the 1000 american legionposts around pennsylvania. there, the commanderof the post knew who had attended the convention, and handed out thequestionnaires to each person who had attended or to nextof kin, had them filled out and returned them to usin harrisburg for analysis which let us knowwho had been there. then, let's see. jim shelton here.
he was in charge of the hotelcohort study where we tried to figure out whether thiswas a problem just of the bellevue stratfordhotel or of other hotels in philadelphia so wehad police detectives from philadelphia callingrandom samples of hotel guests and asking them whether they -- who had been registeredin the weeks before, the week of the convention orthe weeks after the convention to see whether therewere any other clusters
of clinical illness similar tothat of legionnaire's disease and were able to show that theonly cluster was in the week of the bellevue stratford,of the convention. then walt orenstein withcarlos lopez was in charge of a serumsurvey of hotel employees. we thought if we ever foundan agent it would be very nice to have some serumfrom the employees. bob gun over here anddick keenlyside here were in charge of a casecontrol study --
phone survey of malelegionnaire's survivors where we were asking additionalquestions largely chasing down the possibilityof airborn spread later in the august investigation. and then earlier in thevideo you saw steve thacker. he was in chargeof the line list. that was his centralresponsibility, and it -- that turned out to -- nothingcould get onto the line list without steve thacker'sapproval.
when we moved the headquartersof the investigation from harrisburg tophiladelphia after about a week, i made the decision that weshould house the harrisburg team in the bellevue stratford hotel. there were rooms available. the price was good. and i was thinking maybethere's a residual chance that there's -- the agentis still being disseminated, and we could catcha break with that.
now there were someglitches along the way. we had an episode in whichthree eis officers let's say had unauthorized removal of the data from the health departmentbuilding. they took it home with them, deciding they could dobetter analysis, the three of them overnight, than the restof us could do during the day. this was a dicey situationand has never been talked about in public before.
i conferred withphil brachman about what i should do about this, and wedecided not to penalize anyone. their motives were goodeven though the action was arguably mutinous. the -- privately, i cangive you their names later. the -- at the end of the fieldinvestigation after three weeks, we knew of 221 casesof pneumonia or severe respiratorydisease and 34 deaths. of those, 182 were legionnaire'sdisease meeting the criteria i
told you about. the other 29 -- pardon me, the other 34 were what wecalled broad street pneumonia. they had the clinicalevidence of this disease, but they hadn't been at the bellevue stratfordhotel or at the convention. they had been within a blockof the bellevue stratford hotel after july 1 andbefore their illness. broad street pneumonia.
broad street is the street on which the bellevue stratfordis located and of course a tip of the hat to john snow. the incubation periodwas two to ten days. the risk factors werebeing a formal delegate, having advanced age,being a cigarette smoker, having underlying disease. all known tests for infectiousagents or toxins were negative. there was no personto person spread.
of the household contactsof people who had been at the convention, none of 193developed clinical symptoms of legionnaire's disease, andthe attack rate among roommates of cases was approximatelythe same as the attack rate amongroommates of controls. there was no associationwith specific rooms or activities at the convention. no food -- evidence of foodborne or arthropod borne spread. there was a weak associationwith drinking water
at the bellevue stratford hotel. but 38 percent of the caseshad drunk no water there, and none of the broad streetpneumonia cases had drunk water at the hotel. it appeared to be -- andthere was an association in non-legionnaires withthat week of the convention and no association in otherweeks before or after. it apparently was anairborne problem because risk of disease was associatedwith time spent in the lobby
of the hotel or on thesidewalk just outside the hotel. that led to the third set ofstrategic decisions that we had to make, and that is howto manage the transition from a sprint to a marathon. the team had been working 12 to16 hour days for three weeks. each night i reported tophil brachman in a telephone call that would begin atmidnight or one or two and last about an hour. as the field workended, a new extended
but less fevered phasebegan in the investigation. to manage that transition, firstit was important to capture all of the informationthat had been generated in the field investigation. to that end, each eisofficer wrote up his or her investigation modulebefore leaving pennsylvania. my understanding is that thesewrite-ups are in the collection of the smithsonian institution. then there was the needto find ways periodically
to inject fresh insightand new energy into the ongoing investigation. i had very much in mind thechallenge of pontiac fever, which had occurred in1968, a respiratory disease of unknown cause in the healthdepartment building in pontiac, michigan that had veryintense cdc investigation, extremely frustrating thatwent on for two years. and there were manycdc investigators both epidemiologists andlaboratorians
who bore the emotionalscars of all that work that hadn't led to an agent. i was worried that that --that some people who had had that experience or hadheard about it would want -- would shy away from workingon legionnaire's disease and repeating that experience. to try to inject new ideas,we brought together a group of outside pathologists onseptember 8 and 9 to talk -- to go through the slidesfrom the fatal cases
of legionnaire's diseaseand tell us what they saw and what implications that mighthave for further laboratory and epidemiologic investigation. they concluded that themain pathological lesion in these cases of lungdisease was acute diffuse alveolar damage. not pneumonia. not a more typicalpneumonia, which seemed to point perhaps more toward atoxin, maybe a viral illness,
than certainly abacterial illness. in october -- on october 7,we brought together a group of senior cliniciansand epidemiologists from universitiesaround the country to go through the epidemiologicaland clinical data to advise what wemight have missed. john bennett, the head ofbacterial diseases division, took me aside at one pointduring that fall and said, "when and if you find theagent of legionnaire's disease,
you will solve the outbreakthat i could not solve in 1965 that i investigatedas an eis officer at the st. elizabeth'shospital in washington, d.c." he said, "that isthe same disease." and of course heturned out to be right. we had some positiveinterchanges during the fall trying to generatethis additional energy and new insights, presentations to the american publichealth association,
infectious disease societyof america, idsa. we had some negativeexperiences. representative john murphy of long island decided we shouldhave a hearing to point out all of the errors that centersfor disease control had made in mishandling thelegionnaire's disease outbreak. so lew polk anddavid sensor and i -- i can't rememberwhether walter dowdle had that experience or not.
we spent two hoursbeing excoriated by representative murphy. and then in earlynovember, ted tsai and i and others finished the draftof an epitude, the memorandum that was mentioned in the video. and i took copies of thataround to many laboratories both in the bureau ofepidemiology and bureau of labs, wanting to thank laboratoriansfor their work up to that point and then to encourage them tocontinue their investigation,
at which point i would turnthe podium over to joe mcdade. >> thank you very much. at the time that ifirst came to cdc, there were two mainorganization groups, the bureau of epidemiology andthe bureau of laboratories. i was assigned to theleprosy and rickettsia branch in the bureau of laboratoriesand worked under the supervision of the late charles shepherd,which is shown here on the right with me in a photograph thatwas taken about that time.
shep had expertise in bothareas, although he spent most of his time working on leprosy. my activities were mainlyinvolved with rickettsial work, although we both worked togetheron legionnaire's disease. now at that time,for the period, cdc then again had excellentanalytical capabilities and diagnostic capabilities, andit wasn't very long until just about everybody in the bureauof labs seemed to be involved. after influenza and a few
of the other usual suspects wereeliminated from consideration, everybody was asked to rule outvarious possible etiologies. my task was to ruleout the possibility that the disease was q fever,the letter q meaning query, which didn't seem quiteplausible to me at the time. first of all, q fever wasassociated with contact with domestic animalsor their environs, although you couldalso become infected by a consuming unpasteurizeddairy product.
but more importantly, qfever was rarely fatal, but nonetheless decidedwhat i would do is to go through the diagnosticalgorithm. well, rickettsia as a grouppresented a bit of a problem in terms of diagnosisbecause as many of you know, their obligateintracellular bacteria, which can only begrown in living tissue. and there was a well-establishedalgorithm for diagnosing qfever at the time.
you used experimentalanimals, guinea pigs, took a clinical specimenfrom the patient and inoculated guinea pig aftera suitable incubation period if they developed signs ofinfection, usually fever. you would collecttissues from that animal, passage intoembryonated eggs to get an established culturein the yolk sacs of the egg for further characterizationand identification. and so that's exactly theprocedure that i started
to -- that i followed. so i got a bit of lung tissuefrom one of the patients and using some buffermade it into a suspension and inoculated guinea pigs. and i expected to wait quite atime until they would see fever because usually with q fever, anincubation period of maybe seven to 12 days, but fortwo or three days, all of a sudden theydeveloped very high fever. and i recall coming backto the lab that morning
after checking the animalssaying out loud to nobody in particular that theanimals really seemed unusual, have such high feversat that time. about 45 minutes later, igot a call from a reporter from the atlanta journalconstitution wanting to know about the results of myexperiments with guinea pigs, which of course turned out tobe a very brief conversation. but any rate, it didn'tseem like q fever, but i went throughthe process anyway,
and so sort of likethis i collected tissue from the guinea pigs. and the first thing that idid was make impression smears on glass slides that iwould stain and examine under microscope to see ifthey contained any rickettsia. second thing i did was makethat into a suspension -- tissues into a suspensionand put several drops of that on different bacteriologicmedia to see if any bacteria were present,
and then i inoculatedthe remainder, some of the suspension intoembryonated eggs to try to cultivate rickettsia. but before i did, iadded a solution -- a bit of a solutionof antibiotics which were commonly usedat that time in rickettsia. they were designedto inhibit the growth of most common bacterialcontaminants but allowing therickettsia to grow.
well, the results did notseem particularly unusual. nothing grew in theembryonated eggs, which suggested norickettsia were present. no q fever or rickettsiawhich was not unexpected. i found nothing growing on anyof the bacteriologic media. and when i looked at thestains and the smears of the guinea pig tissues, i would see an occasionalrare rod-shaped bacterium. at the time, i was trying tothink what it might be due to.
my conclusion was that it wasprobably normal bacterial flora from human lung tissuebecause basically that was all that the people in thebacteriology labs were finding in their cultures of tissues that they were studyingfrom the epidemic. and the other way of looking atthis course was to see whether or not there were any elevatedlevels to q fever, rickettsia and convalescentserum specimens, and all those specimen --
all those tests werejust stone cold negative. so at that point in time, i thought well whatcaused all this fever? and i said well thepossibility could be some sort of a toxic compoundwhich was very consistent with the thinking at the time. so having ruled out q fever, ifelt my job was done back to my day job and didn't reallygive it much consideration other then occasional discussionswith people in the labs.
and it was sometimeas david said -- i think it was in november whenhe brought back his epitude which was very thoroughbut very concise. if there's anything youcan think of, let me know. and i thought, wellyou know, i didn't know that there was necessarilyanything that i could do at that point. then came the turningpoint in december as mentioned in the video clip.
my wife and i attended achristmas party and engaged in a conversation with aman, never told me his name, and i didn't know him. and chatting a bit aboutlegionnaire's disease and all of a sudden he got alittle bit more aggressive, and i don't rememberwhat he said exactly, but i do remember him saying, "everybody knowsall you scientists at cdc are kind of weird."
and he said, "but youknow, we count on you to figure these things out." he said, "there's something outthere that's killing people, and it could do it again, and wedon't know what's causing it." he said, "that's really scary." well, it was a hit personally and professionallyto think about that. and i thought about itin the next few days but still didn't quiteknow what i could do.
but then my compulsive naturetook over the following week. it was the week betweenchristmas and new years and something i've done foras long as i could remember. i always cherish the quietin the lab at that time, long before cell phonesand email or anything else. hardly anybody was there. time to clean up yourdesk, clean up the lab and get ready for the new year. i remember going into the backlab where the microscope was
and there was a woodenslide box and had the slides from the guinea pig tissues,and i thought, "well, you know, i should probablytake one more look at these before ifile them away." so i started lookingand same thing. i would see a few occasionalrod-shaped bacteria, and then i came acrossthis exact -- this is the exactslide that i saw. now the upper hand corner whatyou see is what may to you look
like sort of justa blob of stain. if you look carefullyon the periphery, you can see somerod-shaped bacteria. if you focus up and downwith the microscope, which i obviously can'tdo here, it was clear that there was a cluster of organisms was there, whichsaid to me, this is something which is actually growing there. i don't think that this issomething that i can overlook.
so i'm hooked -- i haveto do something about it. i said, well before you find outwhat it is, you're going to have to be able to grow it out. i thought i don't knowhow i'm going to do that. it didn't grow before. i thought well i'll trysomething a little different. i get the leftover guinea pigsuspension, and i'll put it back in the embryonated eggs, and this time i won'tadd any antibiotics.
and so several days laterthe embryo showed signs of infection. i dissected out some yolk sactissues, and i stained them and looked at themmicroscopically. and this is what i saw. you can see in the manyrod-shaped bacteria there in that long serpentine chainis actually a whole long chain of bacteria, which had notseparated whenever they divided. well, at this point, idiscussed it with dr. shepherd,
and we both agreedthat the first thing that we really needed todo was to find out whether or not it had anythingto do with the outbreak. and so shep went upstairsand talked to gary noble who was head of the influenzalaboratory at the time and had some legionnaires'sdisease specimens on hand. and he brought us down a handfulof convalescent specimens. and so the logichere, of course, is to look for antibodiesin those serum specimens
to the bacterium, which wouldbe evidence of causality. those tests were set up by thelate martha redus who was a wonderful person, an outstanding technician andvern newhouse who was our staff epidemiologistwas in the lab at the time. i'll spare you the detailsof the laboratory testing, but the bottom line is ifany antibodies were present to the bacterium in those serumspecimens, whenever we looked at that slide underneaththe fluorescent microscope,
it would stain bright green. and this is what we saw. so by that time, we thoughtwe might be on to something, and it was early evening, butnobody was going anywhere. gary noble gave usanother set of specimens. this time they were all coded. they were acccuteconvalescent specimens from the outbreak. there were specimens frompatients with other pneumonias,
and as well as normalcontrol serum specimens from the serum bank. and martha set up the testagain, and we both read them. at the end, we broke the code,and it was very, very clear. all the controlledspecimens were negative, and all the legionnaire'sdisease specimens either showed arising titers to this bacteriumor standing high titers. so coming days obviously thepace of serologic testing picked up many more specimens from thelegionnaire's outbreak as well
as many other specimenscontrolled tight that we added in. and finally, i think itwas somewhere maybe -- i think it was either thursdayor friday, june 13 and 14, the week before jimmy carter'spresidential inauguration, we went to visit dr. sensorat his office to tell him what we had. and there were someother people present. i don't know who they are.
i don't know who theywere so i can't tell you who was there at that time. shepherd being a very cautiousinvestigator wanted an extended period of time to rule allpossible outlying factors even repeating the experimentsin a different lab to make sure it wasn't somethingthat was in our environment that was causing usto pick these up. and discussion wentback and forth. and the last thing iremember dr. sensor saying is,
"let's see where weare next tuesday." well, next tuesday therewas a special edition of the mmwr thatwas impressed -- shepherd evidently had worked inpreparing that over the weekend. it contained the results ofour serologic testing as well as some of the salientepidemiologic features. i remember, i'm pretty certainit was that exact same day that shep and i went back andtalked to david sensor again. this time we had someadditional results to report.
14 specimens from the st.elizabeth outbreak of 1965, we also had tested those. 13 of the 14 were alsopositive to the same bacterium. i understand, buti can't confirm that they actuallyheld the presses of that special mmwr articlewhile they inserted a three or four line statementputting those results that were in there. well, any rate, within a day
or two specimens arecoming in from everywhere. martha and i are right up abouthere with requests for testing. but it became very clear, veryclear that the tedious process of trying to grow thisorganism and embryonated eggs and using experimentalanimals was going to be very rate limiting,and we needed to learn how to culture the organismon bacteriologic media. well, try it again, but if youweren't successful the first time, why would yoube successful now?
well, first of all,we thought at least that we had a pure cultureof the organism so that if it was very slow growingit would not be overgrown by any other contaminatingorganisms that might be there. secondly, the yolk sacswere very highly infected, and they had large numbers and sometimes that's veryimportant whenever you're trying to establish -- whenever you'retrying to establish growth of an organism on a new medium.
and sometimes too, whichyou can have as a carryover of new trends that mightcome from the yolk sacs, which might be beneficialin getting it started. and so i gave thisyolk sac to bob weaver in the bacteriology division. i think he inoculated 18different bacteriologic media multiple times, incubated them at various differentconcentrations of co2 and temperature and whatever.
and finally after about a weekor so, he started to see growth on one particular plate. and it turned out thatit was mueller hinton agar. but it was the supplementthat was important. it was isovitalexthat contained iron and most importantlythe amino acid sistine. well, that was not stilla very sensitive kind of a culture medium, andit needed to be improved and so i would be very remiss
if i did not mention the effortsabsolutely herculean efforts of these two people and theirstaff at improving the media. george gorman on the left and the late james feeleyon the right. and their group one byone added ingredients, subtracted ingredients,incubated this way and that way and finally came up with whatwas feeley gorman agar and served us well forboth clinical testing and environmentalsampling at that time.
still needed someimprovements, and it was. additional improvements madeby others over the years to provide the standard medium. the other thing thatit enabled us to do, you could finallygrow the organism free of any extraneous hosttissues, which allowed you to characterize theorganism in great detail. and some of thatwork which proved to be most importantwas done by don brenner
and arnold steigerwalt in the bacteriology divisionwhen they analyzed the dna of the organism, which turnedout to be a new species and a new genusand a new family, and it was calledlegionella pneumophila. well, something that wasnot well known at the time but over the yearsat walter reed, they had also donediagnostic work for various infectious diseases,and they also used guinea pigs
as part of their work. and over the years, they hadisolated four rickettsia-like agents from guinea pigswhich they considered to be commensal organismswhich they could not associate with the patient's illnessesthat were being investigated. i was aware of that and shepand i ran into marilyn bozeman who worked at walter reed atasm conference in new orleans, and we talked about that. she sent us cultures of thosefour isolates and brenner
and steigerwalt analyzed thoseagain, their dna composition. one of them an isolatemade in 1947 was identical to legionella pneumophila. two others were thesame species. one isolated in 1943, whichwas identical to each other but another species and thefourth was yet another species. and at about the same timeworking with bill cherry and roger mckinney andann hã©bert and others in the bacteriologydivision, we were able to show
that legionella had more thanone serotype so that we knew that we were coming intosomething that was going to be much more complex. we had no idea what thecomplexity would be. so the question is alwaysask how do we miss it? how do we -- how dideverybody miss it? the people at walter reedhad it in their hands. that was a very,very solid group of investigatorsthere over the years.
i followed a lot of theirwork, and i can only -- i can only conclude that therelative lack of sensitivity of serologic tests thatwere available during that period all the way back to the 1940's probablyhindered them in any effort that they may have made to tryto associate those organisms with the patientsby antibody testing. well, how did the people here and the other investigations-- how did we miss it?
well, as you seenit wouldn't grow. and the other thing isyou couldn't see it. you couldn't see it. this is formalin fixedtissue that was stained by the tissue gram staincalled brown-brenn stain and what you can see are thelung cells that are there, but you cannot seeany organisms. and so afterwards,after we found out that they likely werecaused by a bacterial infection,
the pathologist went back and used a very intensive silverimpregnation technique called the dieterle silverimpregnation technique to see if organisms were there. and this is what they foundwith the very same tissue. and it confirmed they werein fact absolutely there. how was i able to see it, andthey weren't if it's fortuitous? it was fortuitous. the stain that you use
for rickettsial testingis active ingredients carbolfuchsin. it stains things red. and remember that i stainedfresh guinea pig tissue and could see it. later, francis chandlerwho worked in the pathology lab tried tostain formalin fixed tissue with carbolfuchsin, and itdid not work in his hand. so all of that was afortuitous circumstance.
well, finally at the end,there were the skeptics. and as they should be...as they should be-- healthy skepticism then ranged from theconspiracy theorists to people who had vested interest in otherpossible etiologies and to some who absolutely scoffedat the idea that you could ever find a newinfectious agent considered ranging anywhere fromoutrageous to anachronistic to just virtually impossible.
but eventually wewon them all over, and it happened relativelyquickly and had not so much to do -- had not so much to do with the serologic results wepresented but more importantly, those results contrasted againsta mountain, virtual mountain of negative test results thataccumulated by the labs at cdc and elsewhere every possibletoxic chemical, toxic medical, biological toxin,infectious agents, all of which proved negative.
and one of my recurringmemories of that period is of all the people into thelabs who slogged away at this, coming up with individualresults that were negative, all of which seemedinsignificant but when viewed in the aggregate, gainedincreased purchase. and as i think of itin another respect, it was very muchlike a jigsaw puzzle. the picture is neverreally entirely clear until the last pieceis put in place.
>> and now a few words for -- to describe a morerecent investigation from dr. isaac benowitz. >> good morning. as i was walking up here,i heard someone murmur that those are tough acts tofollow, and i certainly agree. so last summer in 2015, thenew york city health department investigated a large outbreakof legionnaire's disease so it's the second largestoutbreak in the u.s.
after the 1976 outbreak thatyou've just heard about. now that i've given away thepunch line, what i want to focus on is really some of themethods and tools that we used in that investigation, how weused some of the information that we've accumulatedover the last 40 years, learning about legionnaire'sdisease to take this investigationin a very different way. so even now, we know thatlegionnaire's disease exists, but these patients really look-- most of them look like a lot
of other patients withcommunity-acquired pneumonia and so if you don't testfor legionnaire's disease, if you don't find it in the lab, you won't know that'swhat the patient has. and while it does grow inculture as dr. mcdade described, it doesn't grow innormal sputum culture that most patients would get in an outpatient orhospital setting. it only grows onspecial media and most
of the time thosecultures aren't run. and so most casesare only picked up by urine antigen test kitthat's getting much wider use in recent years. in new york city, we getat least 2 or 300 cases of legionnaire's diseaseevery single year. all of them generatedby that urine test. and we investigateall those cases, but most of them have nothingin common with each other.
we define an outbreak or cluster when we find often there'sa handful of cases linked to each other in space and time, and that's what triggersour investigations. on july 17, we picked up acluster and we had a sense that we were ontosomething much bigger than our typical investigation. there were eight cases thathad all had onset of symptoms within the last two weeks.
they were reported to thehealth department just within the last four daysbefore the signal was generated. but even then, we still had noidea what we were looking at, where these cases had come from. in the last 40 years, so manyinvestigations of outbreaks of legionnaire's disease,many of them led or joined by cdc investigators haveidentified many sources of these bacteriain the environment. shower heads inside buildingsand other plumbing systems,
water fountains and displays,market misting systems and cooling towers whichare heat dispersal systems that are on top of buildings. these systems captureheat from air conditioning and other industrial processes,and they capture that water into a tank, capture thatheat into a tank of water and then large fansblow off the heat. but when that wateris contaminated with legionella bacteria, itleads to aerosol dispersion
that can go for milesaround a single source. and that type of informationis incredibly helpful in modern investigationsbecause it tells us that we can use the distributionof cases to help understand where we might lookfor the source. so if we see several casesclustered in space and time and they all livein the same building or they've all visited the samebuilding, it makes us think about an indoor source,something like shower heads
or maybe some sort ofdecorative fountain. but when we find severalcases that are linked in space and time, but they haven'tbeen in the same building, they've just been in the samearea, that makes us think about outdoor exposureslike cooling towers. our investigation in new yorkcity ultimately found 138 cases. there were 16 deaths, 12 percentmortality rate, and we think that it's the -- the attributes of the neighborhoodreally helped us
to understand why there was suchsevere morbidity and mortality. this outbreak happened inthe south bronx, a very poor and immigrant heavy area ofnew york city, very high levels of poverty, numberof people going without needed medical care. many people who smokeand many people with chronic diseases includingdiabetes, hiv and others. we spent a lot of time going around doing a traditionalepi investigation.
we talked to all those people. we asked them wherethey had been, where they had spent time duringthe two weeks before their illness onset. and what we found was that manyof them lived in this one area about six square milesover seven zip codes in the south bronx, and thatwas all that linked them. they hadn't been inthe same buildings. they certainly didn'tlive in the same building.
there were some people who likethe broad street pneumonias in philadelphia had spenttime -- had visited this area, had gone there to work. but didn't live there, andso again we knew we were onto some sort ofoutdoor exposure, and we didn't know what. we stood on the shoulders ofall those prior investigations. we knew we were looking mostlikely for a cooling tower. and so at this point we wantedto find all the cooling towers
that were in this area, butthis is six square miles. it's a densely populated area. there are a lot of buildings,a lot of commercial activity. and there was no listof cooling towers. nobody requires you topermit your cooling tower. no one requires you to registerit with the city or with anyone. and so that was ourreal challenge. where are the cooling towers? we found some of them throughsome city administrative data.
sometimes when peopleput up buildings, they list in theirbuilding permits that there's a cooling tower butoften these are installed later. we spent a lot of time searchingarial imagery, actually sitting at our desks lookingat cool earth. you can look at a neighborhood. you can zoom in onevery single building, and like this pictureshown here, you can find the coolingtowers from above.
we actually talked to a rapidresponse team from google and asked them whetherthere was a way to computationally searchthese neighborhoods? and they said, "well,really having people look at the pictures is probablygoing to be your best bet." we found a total of 55cooling towers in this area, a huge number to visitand sample and so we plan to sample all of themprioritized based on the clustering ofpatient's home as shown here,
which are these green dots. this shows the cooling towers,and it doesn't show all them. so what i'm showing here arethe triangles are the cooling towers, and the onesin red are the ones where we did a rapid testusing pcr for legionella dna. this is a quick test. doesn't tell us ifthere's viable bacteria in the cooling tower, but tellsus basically whether legionella have been there anytimerecently.
and that was enoughto let us act quickly. at this point, there werestill dozens and dozens of case reports pouring in. lot of people gettingsick in the community. we knew that waiting until wecould culture environmental samples would putus back a week, maybe two weeks beforewe could start closing down cooling towers andforcing them to clean up. so these red towers within 24hours when we collected samples,
we had pcr results fromour state laboratory. that was enough action -- thatwas enough information for us to issue commissioner's orders to all these coolingtower owners to shut down and start remediation while wedid additional testing to figure out which one actuallymatched all these patients. and we found one. so this is the pfge, pulsedfield gel electrophoresis block from our early investigation.
that first row at the topshows a single pfge pattern that matches all26 of the patients for whom we're ableto obtain isolates. we didn't get isolatesfrom all of them. this is actually a very goodshine that requires a lot of additional lab work fromall of the hospitals involved. that second row showsthe pfge pattern from what i'll call coolingtower a. one cooling tower near the center of the outbreakwith a pfge pattern
that is indistinguishablefrom all those patients. these other rowsshow pfge patterns from other cooling towerisolates in this area, and none of themmatched our patients. we're excited wefound the source. we had -- we put togethera big press conference. this is mary bassett, thecommissioner of health for new york city announcingthat the outbreak is over. we have found the source.
it matches. it's coming froma cooling tower. we shut down thecooling tower weeks ago. it's cleaned up. there have been no more cases. hurray. unfortunatelyin the real world, public health is sometimesa bit more complex. we went back a few dayslater after we issued orders for mediation at all of thecooling towers in this area,
and we collectedadditional samples to make sure thecleaning was going well, that we hadn't missedanything, and we found something that didn't turn up onour initial sampling. a second cooling tower thati'll call cooling tower b had legionella bacteria. we hadn't found anybacteria when we had sampled that tower originally. and furthermore, the pfgepattern exactly matched cooling
tower a and all the patients. and so this is a problem. we've already madea big media splash. we've announced thatwe found the source. we've cleaned it up. did we name the right source? so this is a problem. and so we had to move beyondour very good laboratory results from pfge and figure out what --
which of these sourceswas actually the cause of the outbreak. we're able to throwsome statistics to it. we looked at the clusteringof the patient's homes and even just lookingat this photo, this map, you can see thatthe cases are -- do seem to be morestrongly clustered around cooling tower a.but that wasn't enough to really convince us.
we went back to the laboratory, and we used wholegenome sequencing. so this is reallyadvanced technology. this is something thatour state laboratory up in albany had just developed in the previous months usingsome seed money from cdc. there had been the smallerlegionnaire's outbreak about a year earlier, and theysaid, "you know, we really want to start developing a wholegenome sequencing pipeline."
and they had just built this. they ran through all of ourisolates from this outbreak, a number of earlier ones and so this diagram hereshows the relationships of all of the legionella isolatesby whole genome sequencing from new york city overa several year period. it's a little complex, butit's actually pretty simple. the large -- the largerdots represent more isolates that match each other, andthe shorter lines represent
closer relationships. and so this large greendot, large green circle, represents cooling towera and all of the patients for whom we obtained isolates. they all matched. not a single sequencewas different. and that little round circle off to the right is coolingtower b. it differed by one single nucleotidepolymorphism, also called a snp
and didn't matchany of the cases. and we had a big sigh of relief because we had namedthe right source. but when we take a stepback, we also realized that this is 40 yearsafter a team of cdc and pennsylvaniainvestigators discovered that legionnaire'sdisease existed and that it could bespread by cooling towers. over the past 40 years,there have been a number
of guidelines written to helpcooling tower owners manage the possibility of contaminationin their systems, and a lot of these outbreaksi think helped to demonstrate that those guidelines on theirown are not having the impact that we need them to have. we need to do better to ensure that cooling towers aremaintained properly, that we don't havethese bacteria floating out into the air formiles and miles leading
to the severe pneumonia. and so in new york city,we took the next step. we worked with the healthdepartment and the city council. we passed comprehensiverules for cleaning tower -- for cooling tower registration,maintenance and cleaning. and so this law we call thecooling tower law is the first of its kind in theunited states. it represents what we seeas a shift in the focus of cooling tower maintenancefrom engineering upkeep
to public health risk reduction. it's intended to decreasethe legionella contamination at cooling towers acrossthe city and to reduce or eliminate the outbreaksthat result from that. and so looking backover 40 years, a lot of the tools are similar. we've used some verynew laboratory methods. we really think thatthis is hopefully new era where the addition ofregulations in addition
to the guidelines and knowledgewill move us even farther to reduce the possibilityof legionnaire's cases and outbreaks inthe u.s. thank you. >> thank you so much,dr. fraser and dr. mcdade and dr. benowitz. i appreciate your insights. and now i would ask thatthey return to the stage and that dr. lucas and dr. kunzand laura come up and share some of the insights thatthey have from the work
that they've doneon legionnaire's. and while they're taking theirseats, i'm going to remind you of who was involved in theinitial investigations. so i would just liketo make a quick start to give a littleperspective from then and now. and i hope it's beenvery apparent that from the verybeginning legionella and legionnaire'sdisease has required on the microbiological sidethe forefront of technology.
back in 1976, thatentailed the creation of entirely new artificialmedia, new diagnostic techniques, newserologic techniques and 2016, we're looking at wholegenome sequencing and a lot of new dna involved techniques. so we've gone from having aproblem identifying the organism to having a problemfiguring out which one of the organisms we foundwas actually resulting in the outbreak.
and i think movingforward as we try to increase the preventionefforts we'll use the microbiology to kind of direct those -- target those so we can identifythe strains of legionella that are most likelyto cause a problem. >> hi, jasen kunz herefrom national center for environmental health. we closely partner on thelegionnaire's disease effort. so environmentalhealth expertise is key
to understanding and addressingthe environmental factors that allow legionella to surviveand reach a susceptible host. for example, water temperature,water flow in buildings, building pipes and disinfectantlevels can all effect legionella growth. so due to the sensitivityof legionella to environmental factors, environmental practitionersare ideally situated to provide expertiseessential to both responding
to legionnaire'sdisease outbreaks and preventing future ones. so environmental health response in legionnaire's diseaseoutbreaks helps improve prevention practices by translating theselessons learned into evidence based preventionguidance for building managers and owners, really getting tothe root cause of the outbreak. at cdc, the structure
of legionella activitieshas involved over time. representatives from thethree core disciplines -- we call it the three-leggedstool of environmental health, lab and epidemiology participate in all major discussionsregarding legionnaire's disease prevention and response. so a current priority is to build environmentalhealth capacity and public healthdepartments so that measures
to prevent the growthof legionella in building water systems areboth promoted and adopted. >> hi. i'm laura cooley. i'm a medical epidemiologist with the respiratorydiseases branch. the rate of reported legionellascases has increased 286 percent over the past 15 years. the reason for this increaseis likely multifactorial. the higher rates could representa true increase in the frequency
of disease related to factorssuch as a greater number of people at risk eitherdue to underlying illness or immunocompromisingmedications, aging u.s. populationand maybe an aging plumbing infrastructure. increased testing for legionnaire's diseasecould also be playing a role. but even with this increase, we think legionnaire's diseaseis likely under diagnosed.
early diagnosis with appropriateclinical testing for populations at risk is a vital stepto reducing the number and size of outbreaks. prevention, though,is really the key to reversing the increase inincidence as the vast majority of reported cases are neverlinked to a particular outbreak. a new industry standardfor prevention of legionella amplicationand transmission in building water systemswas published in 2015.
describes the use of watermanagement programs in buildings with large and complexwater systems. this year cdc and itspartners developed a tool kit to facilitate implementationof this new standard, which we were able to sharevia an mmwr vital signs release in june. the goals of these activitieswas to raise awareness of the increasing problemof legionnaire's disease so that clinicians will morefrequently order the appropriate
diagnostic tests andthat building owners and managers will take the stepsneeded to improve prevention. >> is it all rightto ask a question? >> it is. it is now. we are now opening thefloor to questions including from a panelist toanother panelist. >> opening it up. just first thank you so muchfor coming back and coming down from new york and sharingwith us this sort of history
on the future oflegionnaire's disease. there's so much to comment on. it was just tremendous, butthere were a couple things that dr. fraser anddr. mcdade talked about that i think are reallyimportant for us to here today. one is how helpful itwas to have criticism. i hadn't really realizedthat it was that -- hearing this attackedat the christmas party, it really motivated you.
and so we are in an era whereattack and criticism is common, but i think the idea that itcan be a motivator is helpful. and the other comment isyour remarks, dr. fraser, about consciously trying tofigure out how to transition so i think the pastseveral years at the agency we've really beensprinting through marathons, and the idea thatyou were thinking through how were we going to keep engagementmotivation especially
after negative experiencesin the past? i guess maybe just the thirdthing is -- since both of you -- both of the investigationstalked a little bit about the politics, i wonderif people want to expand on that more becausei remember hearing that it was quitepolitical in 1976 and understand it may havebeen recently as well. so opening it up for youto explore those things. >> as long as ten or 15years after this outbreak,
seemingly on anniversary, i canalmost count on a telephone call from a journalisttalking about many things and almost always the topiccame up about how the stories in the newspaper must haveinfluenced what i was doing. seems self-congratulatory to me,but truth be told, that had -- for me personally had absolutelynothing to do with it. just prior to coming to cdc,i had been out of the country for five years, rarely sawan english language paper, had a little t.v. this big whichi seldom looked at or whatever.
the man at the christmasparty -- i'll never know -- certainly got me thinking aboutit again, but i think ultimately for me was a matterof a certain amount of only this audience canappreciate the true value of being compulsive. and i wouldn't put thoseslides away without looking at them one more time. it was my week, and if i foundsomething that was there, i knew it would drive me nutsuntil i figured out what it was.
at that point, i thoughtit was something inocuous. i just needed to identify it. so i don't know how peoplerespond to various things and various stimulusfrom the outside. certainly, you cannotignore yourself to that. i think for everybody inthis room it's the fire in the belly thatkeeps you going. i mean, certainly thepeople who slog away in the trenches anonymouslyduring all these outbreaks
dotting i's and crossing t's because they knowultimately it contributes to the final picture. so i don't know howto judge that. just my off the cuffreaction to it. >> i might add observationsabout the role of the press in this in 1976. there were three reporters with whom i had quite closecontact during that time
from the new york timesfrom the washington post and from the philadelphiaenquirer. and two of those reporters dida great job, very impressive. and i found my discussionswith them to be quite helpful. the third was trainedas an eis officer. and he got a theory -- or hearda theory from some scientists and decided to shape hisreporting to support that theory and ran a series of articlesin the new york times about nickel carbonyl being thecause of legionnaire's disease.
and the washington post reportercame up to me after the second or third of the story andsaid, "my editor asked me when i'm going to file astory about nickel carbonyl, and i've told him idon't see a story there. tell me, am i missingsomething?" and i said, "you'renot missing anything. it's -- this is anidea that's taken on its own life quiteunrelated to the science either in the laboratoryor the epidemiology.
and so we need to notbe swept up by it. >> and could add that david knows this probably justslipped his mind for the moment that the source of nickelcarbonyl was eventually traced back to the scalpelblades that were used for proferring thetissues during autopsy. >> first thanks to all ofyou for spectacular talks. i'd like to ask dr. fraser and dr. benowitz why theirepidemics respectively ended?
>> ask the question again. my -- presbycusisis getting to me. >> well, i have the same. why did the epidemics end inpennsylvania and in new york? >> i don't know. >> i also don't know. there was an interesting moment. as dr. fraser describeda few days into his team's investigation,
they knew that they weren'tsure what they were looking for. in ours, we knew what we werelooking at, and it's probably about 1.5 week inwe were tracking down all the casesas fast as we could. we were building our epi curve,and one day don weiss who is one of the medical epidemiologists at the new york city healthdepartment was the lead on the investigation sendsan email around to the team and said, "you know,look at that epi curve."
and what he had pointed out was that we had very quicklynarrowed down the source. we had forced the coolingtower to shut down. and epi curve had tailedoff a little too fast. we -- our actions in closingdown that cooling tower and forcing remediation ornot what stops the outbreak. they are what preventedit from recurring from that coolingtower or another one. but legionella hasits own life cycle.
there was a corian treatmentsystem at that cooling tower. somewhere in the daysbefore we got there, the level of legionellahad gone down low enough that it wasn't still posinga threat to the neighborhood. we don't know if that'sbecause the weather was cooler and the cooling systemwasn't running as hard and wasn't dispersing as much, whether legionella wasdoing something on its own. there's still so much science tobe defined with this organism.
it has like seven differentlife stages and i know claressa, >> yeah, so this is where ithink the modern era can maybe help inform some of thisbecause as isaac said, yes there is thelegionella life cycle. it grows. it's a parasiteof the proteus that lives in the environmentto begin with. we haven't even begun todefine its host range. it's very, very broad, which iswhy it causes problems for us. but we're also lookingto metagenomics to kind
of get an idea of whatother organisms are there in the milieu thatthe legionella are and as isaac mentioned,they found another strain that was almost identicalto the one that caused the outbreakjust down the road, but it didn't seem tobe making anybody sick. i doubt that it was due to thatone single base pair change. it was probably somethingelse in the environment. that's what we needto figure out now.
>> let me ask a questionon that. maybe i'm over simplifyingthis, but it sounds like a lot of the effort isplaced on legionella in the water once it comesout of the pipe as opposed to water sheds, water use, waterreuse and all those other kinds of things which getsdown to the basic ecology and how the organism thrivesand grows and whatever and so makes me wonderif you go upstream. hate to use that analogy,but certainly true
that you can get even a betteridea about prevention as opposed to worrying aboutdecontaminating cooling towers and other things, and i don'tknow whether there's anyone in the research communitynot necessarily at cdc that's looking at it ina more ecologic broader sense. >> so yes, actually there aremany people who are looking at the ecology of legionella. we have lots of colleagues inthe u.s. and around the world. some of the thingswe've discovered is
that the distribution ofstrains is not really even. the northeast fortunatelyor unfortunately seems to have a preponderanceof the strains that we know are associated withlarge outbreaks whereas perhaps in the southwest of the unitedstates those strains are not as prevalent. other countries may havedifferent species all together. australia tends to getlegionella longbeachae as opposed to pneumophila.
so there's a lot we don't know about the distributionof the organism. there's a lot we don'tknow about its persistence and colonization and onething i think we need to really remember isthis is a manmade disease. it's the distribution systems. it's the aerosolization. it's the warm water and coolingtowers that allow this organism that evolved intothe environment
to become a problem for humans. so we need to figure out what about our modern society wecan change to fix that problem. >> hi, i'm david bell thedivision of viral diseases. i really love these talks, and i couldn't resista personal comment. i was in philadelphiain august 1976. i was home visiting myparents in between third and fourth year medical school.
and all this was going on. it was in the papersevery day as you know. i was already interested in cdc, but this was the first time myparents understood what cdc did. i previously never quite beenable to explain it to them. so i thank both of you for that,and it was certainly wonderful to come here in 1979as eis and meet you. but the other thing thatdidn't quite come out is that this was philadelphia'spremiere hotel.
we didn't have a ritz carlton. we had the bellevue stratford. and it was a magnificentbuilding in the center of downtown withdoorman and all that. and for this to happen inthis hotel was just amazing. i mean -- and the hotellater went bankrupt. after it was over, the governor and the mayor stayedovernight there to try and convince people it was okay.
it didn't work,still uncomfortable. but it was just -- great talk. thank you for doing this. >> yes. i have acouple of comments because i was an employee atthe time myself and not too long after played on the samesoftball team called the rocky mountain spottedfielders with joe mcdade. dave frazier, you mentionedthe organizational names, the bureau of epidemiologyand bureau of laboratories.
back then, that was itother then the cafeteria and maybe the snack bar. so cdc was a lotsimpler organization, but a sign of the politicalpressure at the time was that there was anunprecedented step taken. we were ordered in everylaboratory no matter what part of the bureau oflaboratories we were in to shut down our normal operationsand to take specimens from a central locationthat was on the first floor
of building seven in garynoble's area of operations that i had to go up to andliterally work as a ferry boy to all of the laboratoriescoming into a room that looked like grand central autopsy suite where there werepulmonary tissues, spleen and every othertype of postmortem sample that had been taken fromthe deceased patients in philadelphia. and being sliced,diced and distributed
to all the laboratories at cdc. that's all we didfor that entire week. and of course as you said, allthe results came back negative because we were ordered to look for what we werespecialized in working on. and it call came back negative. and i don't think that's everbeen even approximated in -- steve monroe turning around. you would have had apoplexy
because in this lab peoplewere still mouth pipetting. something we were trying toget some of the old timers to stop doing even then. it was a very difficultsituation. but i just wanted torelate that story. cdc shut down. the whole laboratory operationshut down just for this effort. and i don't think thatwas done either before or since in that manner.
>> thanks, jim. yeah. follow up on thatcomment mainly for dr. mcdade. as you pointed out and jimjust mentioned, i mean, there was a lot of importantwork by laboratory staff looking for what we knew to look forand the negative results. but it strikes me this isa case where, you know the quote that most advances in scienceare not accompanied by eureka but rather -- well that's weird. and so for me thelesson here is to not
so quickly discountthings to say, "oh, i've looked for my bug, and it'snot my bug so i'm going to try to go back to mynormal day job." but this notion of finding thatone weird result and taking it to ground to figure outwhat's really going on and so i guess the questionis how can we make sure that the current generationthat's staffed in the lab have that same fire in the bellyas you described it so that when they get something weirdthey don't just discount it,
but they try to runit to ground to figure out what's really going on. >> now that theme isrepeated so many times. one of the books iread many years ago -- i'm trying to rememberthe exact title. thomas kuntz book, the structureof scientific revolutions. have you ever heard that? any rate, it's on amuch broader scale, but basically what his thesis is
that we all get lockedcup in paradigms. and earth was thecenter of the universe. and if something didn't workwith that, it was some sort of anomalous observationthat you throw away or you get thrown in jail. and over time his theorywas it's the anomaly that really pushesthings along either in a greater or longer scale. and you think about iteven in molecular terms
when people were studyingribosomal dna and transfer dna and messenger rna and throwingaway all the rest that's being useless and now you findthe small interfering rnas that direct so much oftranscription and translation and effect everythingthat's done. so looking at thosethat way i can tell you that was not my mind set atthe particular time to do that because i was very -- to me it just didn't seemlike a credible thing.
go ahead and do what you'relooking for and then move on. and it was only whenyou saw something that just drove younuts that you had to do something about it. i think it'd be useful ifyou ever have some time. it's not exactly beachreading, but it's -- i felt it was a veryinteresting thing which kind of changes the wayyou look at things. >> cindy whitney with therespiratory diseases branch.
now obviously the way weinvestigate these outbreaks is we would look at the epi curve. we would recognize thisexplosive onset of cases, and we would do thekind of investigation that isaac describedwhere we would go look at the cooling towers andtry to quickly sample them. in your case in philadelpia,you obviously wouldn't have had that associationwith cooling towers. so did you -- once youidentified the bacteria,
did you try to goback and figure out how the hotel mighthave given this -- spread this to thepeople and are we sure -- do we really understand which cooling tower thismight have came from? >> by the time, we wereable to grow this bacterium from environmental specimens. the specimens were alreadymore than a year old. and we wouldn't have recoveredlegionella from those specimens.
i can recall talkingwith george mallison about the cooling towers onthe top of the bellevue -- the cooling tower on topof the bellevue stratford. and him describing howcooling tower effluent moves around in urban environments. and what we observed as an outbreak i think wasquite consistent with that. that is the drift is exhausted out the top of thecooling tower.
it tends to layer acrossthe roof of the building and then is drawn downthe sides of the building in these canyons --in urban canyons. the air intakes forthe lobby, for example, where it came off theside of the building, and it would have been quitepossible for that drift to come down the side of the buildingand be drawn into the lobby as well of course asonto the sidewalk. but we never nailed thatdown in philadelphia.
that was inferenced that largelywas advanced by joe showing that pontiac fever was causedalso by legionella pneumophila, and the role of the evaporativecondenser in the health departmentbuilding at pontiac had beenvery well worked out by the investigatorsat the time in 1968. we just didn't recognize therelevance of that work in 1976 until joe could tieit to pontiac fever. >> hi. my name isjeff mercante,
i'm in the legionellalab here at the cdc. i want to say thank you verymuch for all of your insight. it was a wonderful presentation. something that we don'toften get a chance to do is name things here. those days seem longgone for finding lots of new things thatwe get to name. and so i had the opportunity toread a lot of documents related to the original legionnaire'sdisease investigation.
and one of the things ididn't come across much of was a discussion ofhow to name the bacterium. i was wondering if there was anydiscussion amongst yourselves as far as how wego about naming it? do we name it for ourselves? do we name it for thepeople that infected? i wonder if you had any notes onhow that was actually decided? >> i can comment on that. i don't know what theprocedures are now
and maybe steve monroe cantell me about the virologist. the virologist, of course,viruses get their names. a lot of the arboviruses at least via the locationwhere they're found. you know, like zikavirus found somewhere in south africa, i think. uganda, yeah, in uganda. in the bacteriology worldat the time, it seemed to me that there were usualways of doing --
some of them werehonorific where the person who isolated the organism, the organism will benamed after that person. and so that was an optionthat was presented to me, and i did not thinkthat was appropriate because actually legionella wentall the way back to the 1940's. there were so many otherpeople who had worked on it. and i actually didn'tget the name down. i was hopeful that theorganism would turn
out to be primarily onethat infected lung tissue, which is why i came up withthe name pneumophila having an affinity for the lungs,and legionella was intended to be honorific and remindingthe people from that convention, and i think we also had somerepresentatives from cdc talk to the american legionfolks to find out whether or not they wouldconsider it that way. the other factor innaming it that way -- we lose a lot sometimesin our scientific history
when we don't connect itwith something or some place, and i think by namingit legionella, it would always bring peopleback to that initial outbreak which then conjures up exactlyits explosive potential, its epidemiology and so on. and so after getting all thespelling whether to put an a or an e or whatever,and i discussed it with a very knowledgeableperson in the cdc at the library at the time to make suremy latin was correct.
we decided to name itlegionella pneumophila and another species later wasnamed after marilyn bozeman who provided the "c"isolates and so on. and so that's sort ofhow that came about. >> thank you. >> and thank you. susan, do you have a question? >> no question. just want to remind everyonethat's watching we have a new
website for this lecture series. please take a moment togo there and if you worked on legionnaire's, share yourstory with us on the website. there's a place youcan email us and share that information,and we welcome that. so do take a minuteand go to the site. this particular recording willbe posted within the next couple of weeks on that site andour first in the series which was may 25 isalready live on the site.
so in case you missed it,you can go see that now. and i'd like to take a momentto ask anybody who has worked on a legionnaire'soutbreak to stand
Idsa Diabetic Foot,and be acknowledged, please. thank you again to ourpresenters and to the museum for lending us the video. we appreciate all the supportand the work that you've done.
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