![[title]](https://draxe.com/wp-content/uploads/2015/12/ScabiesGraphic.jpg "[title]")
>> good afternoon. i think we'll begin. i want to remind you that there is no course next week. there will be no session next week. this is part of the austerity budget we were put on to drop one week.
but i hope the following week everybody will return. all right. i see a lot of new faces here. let me just briefly explain what this is. is there anybody who doesn't know what it is? it's the brooklyn bridge.
why do we put up the brooklyn bridge for the simple reason it's sort of the almost logo for this course. it's intended to bridge two different worlds and life is never thesome when you built a bridge. that's the whole purpose of it
and that's the purpose of all these sessions we've hadow. this is the 11th year. okay. so today's topic is ticks, lyme and others. i sort of got intrigued by origin of words. so i looked up what's the origin
of a tick. according to what i found it's from old dutch standing for tick which means sort of a light touch. just for the hell of it you might like to know it's the basis for the word ticket. so when you get a ticket, it's
like a light touch. i guess the idea that is the tick makes a light touch but the consequences of it can be extremely serious, varied and occasionally even lethal. so ticks transmit diseases like lyme which we're going to focus on today.
we'll talk about others two fever rocky mountain spotted fever -- and others. and these can be very serious diseases. so this is actually a complicated process. it's not so simple. one thinks about how does
transmission occur. like in the case of lyme disease, what really accounts for the extremely varied clinical manifestations of the disease. acute, chronic, intermittent. a lot going on there exposed to an agent.
where do we stand regarding diagnosis, understanding what is, what isn't lyme disease. what's the status of treatment. prognosis, prevention. every time i walk across the campus late at night, i see deer wandering around. they are not necessarily our
friends, so to discuss items and many others of importance. we're very fortunate to have two investigators year at nih to discuss this bridging between between the tick on one hand and the disease or diseases on the other.
so our first speaker is tom schwan, who got his ph.d. at berkley in medical entomology. and then went through kenya for several years. he did graduate work at yale. in kenya, he was interested in the ecology of fleas and plague in kenya.
he came to the nih in 1986 when he jned the rocky mountain lab which is part of the nih in montana in god's country. and there he has conducted really extremely exciting and continuing very productive work. he's a tenured investigator. and his interest is in the tick,
the biology and how it does what it does. now regarding what it does, our second speaker is adriana marques who is a physician scientist. and came to nih in 1993 as a post doctoral fellow in infectious diseases having
graduated from medical school and had training including medicine and pulmonology in brazil where she's originally from. adriana as taken part in this course before actually discussing, you may help herpes zoster and we were exposed to
some of her extraordinary research and texting of the vaccine and so forth. and another area of her interest and productivity has been in lyme disease, which she has been involved in with almost since its discovery, at leasin this part of the world, emanating
from many epidemic in the town of lyme, new jersey. and was studied here by alan steewho wrote extensively about it and adriana was part of this group. so we welcome both of you. am i wrong? did
do you want to begin? >> thank you. i think i'm wired. can you hear me in the back? okay, great. it's a pleasure to be here. thanks for the introduction, and those helping me be here. and hopefully what i have will
be of interest and i'm going to brief you on this talk. my first assignment is to convince you how ticks stand out among all other blood being arthropods with the potential to transmit very many dangerous and infe if you look at this table of
blood-feeding insects, mosquitoes, i'm sure you've all been fed on mosquitoes, black flies, all of these have an incomplete or a complete metamorphosis where the image stages is very different from the adult stages. they do not feed on blood.
on the adult stage it's only the female that feed on blood. ticks and fleas have images that are not blood faders but both adults females and males take blood. then the metamorphosis why the youngsters look like adults and feed on blood.
they are ultimately short lived when we think about how long tick can give especially the -- soft tick. so the second point, they're not insects, they're arachnids. you were already told that. so they have a different biology and morphology.
if you look at these they have not an insect plan. on the left is the typical hard tick and is the -- and on the right are my tick of voice vector [indiscernible] the main differences besides what you can see is the hard tick the single larvae disaij
and then the adults. they feed as larvae and when they feed once as adults, they mate and die. life's done. the soft ticks have a larvae stage and multiple stages and once they feed enough times to reach adulthood, then the adults
can feed repeatedly. they do not die after a single blood meal. and each time they feed, they have the potential to lay a new batch of eggs. blood means advancing the live cycle, blood means eggs, it mean a new generation of ticks.
so the soft tick on the right, when you add up all the life stages and once the adult is reached they can feed repeatedly and they can look for -- can live a long time without a blood meal. these can live from egg to adult or 20 years.
they far outlive the adult, the vertebra host that feed on them. because of that, they're not just vectors of many agents, they're also the reservoir and keep them maintained in nature. ticks are adapted to getting into the host's skin. here's an electromike graph of
the -- below with these directed teeth and on the top they have two -- digits. once they find the right place to put their mouth parts in, they start cutting with the digits and they're splitting and the saliva has all sorts of pharmacoagents in it to keep it
going -- of all blood feeding arthropods that shows -- he's done by far the best work. but the saliva is extremely complex. so the ticks are pushing, cutting spitting until they create a hemorrhage of leaky blood, and then they begin to
suck it up. so they're pool feeders, they're not like mosquitoes and they keep that blood flowing because of the components in the saliva. the hard ticks take days to feed. here's a anymore foe scalp layer es.
it takes five days for that tick to look like on the right. they are slow feeders. this is small. this is the primary vector stage for a lot of these pathogens of humans. the soft ticks feed in minutes to an hour.
this is the same tick on the left and right taken before it fed and 45 minutes later. so they are rapid feeders and have a very different biology and life-style than the hard ticks do. the work that describes ticks and all blooding arthropods have
a biological vector for pathogen agent was done by -- and frederick -- published in 1893. and in 1935, craig published and wrote the demonstration that the cattle tick emlates is the vector of texas fever, furnished the first incontrovertible evidence of the transmission of
a disease by an arthropod. this predated the scabies and malaria, fleas and plague and mosquitoes. there's something wrong with that quote and i finished a couple months with students and i pounded this into them time and time again.
arthropods who feed on blood do not transmit a disease. they transmit an agent that may lead to a disease process and the host becomes infected. so that's the second point. ticks are great and ticks don't transmit diseases, they transmit eights -- agents that can cause
how wonderful ticks are, they are blood feeders. they feed on nothing else. they have to feed on blood at all stages. they are long lived and because of those two biological facts they are very important as reservoirs and vectors of many
pathogenic agents. this is a develop fully engorged -- from west africa. and my wife took that picture. the lit is fairly long for why in the united states you do not want ticks to feed on you. there are 12 diseases that we know of and i've listed them who
are. i'm not going to talk about most of these. they're all fascinating. they are all public health problems in the u.s. and parts of canada. what i do want to talk about a little bit is a spot of fear
because the history of our laboratory in the institute and my passion, which is tick [indiscernible] fever and i'll do a brief historical introduction for lyme disease. most of these diseases are listed up here. you can only get by tick bite.
but if you look at fever, most people get that by an aerosol inhalation to affected tissues. you can get this by tick fly bites. this is called lawnmower -- where you run over dead rabbits and they get mnemonic tularemia. they call it lawnmower
tularemia. the first tick-borne disease that was recognized and got a lot of attention is now called rocky mountain spotted fever. this is a terminal case. this is sort of a picture. everyone knows of rocky mountain labs.
the bacterium is an intracellular bacteria and they get into the endothelial cells of the vascular tissue and they can cause a toxic lific system so you have this lash in the lay 1800s was called black measles. in the late 1800's, people were dying of this in parts of idaho.
people didn't know what was causing it or how people got the infection. a long history of this and many books. i wanted to focus on one individual howard rickets because he discovered the wood tick in western montana as a
vector for transmitting the agent which he also discovered. that's why the agent now is called -- named in his honor because of his discoveries. in 1906 the surgeon general sent out another person, walter king and these two guys actually worked together and sort of
competed. they went back to the labs in chicago and washington. within ten days of each other they both published until papers on the role of wood tick and transmitting the agent. and that created some conflict. you have to be careful i guess
what words i use here. so, four years later rickets was dead. he went to mexico to work on endemic or epidemic typhus and he contracted the infection and died in mexico in late 1910. this is the wood tick. we saw it last week and got 80
of these for some of our studies. tick season was begun in one day and these ticks are sexually dimorphic. that's the male on the team and female on the bottom. rick has described this as the vector of fever.
there's all sorts of work that went on to describe what animals are primarily important in maintaining these ticks and in third from the left or second from the right that's clearance birdseye and he was born in bringing lynn. after he worked on the u.s.
biological survey he went to labrador and noticed how the traditional populations used cold winds chills and low temperatures to freeze food and he went back to new york and founded the birdseye food industry. they wanted to learn how to
control it. again the government research rosco worked with ralph parker to develop the first vascular teen. this is a great two-page article describing how bad the ticks are out there. they got several things wrong
here but of course it's pretty cool but here's spencer in the insert and then that big big tick coming out of the valley which is not even a wood tick. that's the name of the -- so he didn't get the right genus tick. the call was to develop the vaccine.
the way they did it was occupied this old school house and had none infected wood ticks on guinea pigs. these ticks were then ground up, the bacteria were chemically activated, they sucked up the -- and that was the tick vaccine for quite a few years.
it was effective and reduced mortality rate. in 1927 a big building was constructed in 1928 and this is our rocky mountain labs. there's over 30 something buildings on the 33 acres and we have our director of intramural research here who comes out
along with the whole crew. a lot of them come out here, dr. baron. mark, have you ever been out there? no. all right, well, this became a vaccine factory. now just a few comments about
the [indiscernible] fever today. it was discovered in the valley over a hundred years ago. it's found throughout the united states. here's a cdc distribution map for 18 years and in those 18 years it's been recorded for just about all the lower 48.
rocky mountains are not the hot spots so there's a name change for spotted fever but still it's an important and in my opinion very important tick borne here's the number of cases over the last 1993 to 2010. there are more cases of spotted fever now than ever.
it hasn't gone away. in 2008, there were 2500 cases. like most tick-borne and occupied-borne diseases, there's a seasonal pattern for onset because ticks are cold blooded therefore it has to be warm are for ticks to be active and take a blood meal.
this from cdc shows in most cases spotted fever peaks in late spring and the summer. this is typical for most other diseases in north temperate latitudes. and then this is an interesting graph showing, but the incidence and case fatality rate.
and the red is incidence back since the 20's. and you can see the incidence is high now as it ever was inspite of it being on everyone's radar screen. the fatality rate dropped tremendously in the late 40's and early 50's because of the
advent of antibiotics. not very many people die of spotted fever. but they die because it's know spotted in time. there were probably 2000 cases with 5% mortality rate which means 10 people die of spotted fever.
last year a young lady died at st. pat's hospital two miles from where rickets made his discoveries and was diagnose the post mortem. shouldn't happen, sorry. sorry, that's my shouldn't be happening. let's move on to the brilla.
hard ticks on the left soft ticks on the right. both feeders on the left, fast on the right. i'm not going to talk much about our research but to us, this is really interesting and fascinating disease. it's a spirochete soonosis.
you make a single blood smear look at it under a microscope and look for it. i'll show you a picture of this in a minute. that's how he diagnosed it. in parts of africa there are significant mortality rates associated with the infection of
related species. the only folks that die of it in north america are usuallien fants who are infected. the last case of that was 2000. this is one of the first fever curse for fever. i like this because it was published in 1905.
so if you can look at one of these, the dark line across here is normal body temperature and this is a fever curve for dutto this. they discovered what was causing it, how it was transmitted. it was tick transmitted. and both of them got infected
during autopsies of infected patients. they both published their fever curves in there 1905 papers. this is dutton's fever curve. fever back to normal, fever back to normal. fever back to normal. fever spire keats cause an
illness and then the spire keats are cleared by an antibody response and there's a rare variance that has a differ outer surface. they can repopulate the blood and the person gets sick again. there's another antibody response to that new population
and the body is cleared. there's another variance that can repopulate. so the infection is cyclic and causes of disease that's called a relapse in fever. now these bugs didn't evolve to give fever a relapse in illness. they resolved to repeated to
increase the lengths of time an infected host could provide spire keats to a fast feeding tick. it's a very interesting evolution of bacteria and a tick that feeds quickly on peripheral the first case in north america identified in 1915 them those
five cases came those infections were as a result of vermin coming from abandoned gypsies camping near the cabin where the people got insected. they didn't even mention ticks this map shows distribution of three stages of ticks that each has their own species of
spirochetes throughout the u.s. our efforts trying to make that a more complete map which is one here. this is a map of the primary cause of fever in north america. it's maintained in cycles of small mammals, squirrels, chip monks.
the spirochetes are maintained in nature. people can get bit and come down with a fever. there are two different genetic types we worked on in the laboratory. each dot represents an isolate we have established and whether
it's a genotype this or genotype that. and so this is about the only diagram i'll show. every gene you look at in that spirochetes can type it in one type or another. why that's of interest i'll try to get that across in a couple
minute. this is one genetic type or another. here's a spirochete. this is how you diagnose the infection in humans if the spirochetes are abundant enough to be the detectable by microscopy.
you need 10,000 spirochetes per mill otherwise you miss it. the standard way of approaching it is still not very sensitive. now i will zoom in on one focus to understand how people get fever in north america. it all points to -- about two hours north of on you
here it is. it's the largest natural fresh water lake west of the mississippi. and this island right here is where it all starts. i'm going to tell you a story. this is a wild horse island, about 2300 aconsider.
it's the largest island on the lake. it used -- they are grant fathered in properties around the perimeter and many of those have cabins. and the outbreak was about right here on the south shore of this island.
and here's the cabin where it happened. this is typical for how most people in north america get they stay in a higher elevation in the forest. the rabin's infested with ticks. they are living with the rodents also the birds living in that
cabin. these ticks are nocturnal. most people get this infection when they're sleeping. the ticks cometh and orient to the carbon dioxide that the patient is respiring. they climb on, suck and get off. when people wake up they never
know they were bitten or if they do feel an issue they think it was a mosquito. there's a family reunion in 2002 and five of the 21 got sick. i got calls from doctors saying could this be -- it's a long story it's a lot of fun. i think one of the papers
discussed here i am going up into the attic to get material so we can look for ticks. my wife went up with me. peace a good scout and i went -- she's a good scout. and i went up with the state epidemiologist. and i hear bringing out
material. brought it back to the lab. these are the -- processed all this organic degree. there's a light on the top lighting its light and heat. ticks don't like that and they go away and they fall into a funnel at the bottom.
we process the teller and we found -- which i said this many times it was for me a lot of fun because with all the work on ticks in montana, this tick had never been found there in the then on the left is a panel of emoh fluorescent -- two of the we were able to establish there
was a focus of fever on that what happened is a good samaritan showed up first decided to clean up the place. he went up to the attic and tried to clean up the rodent and bird mess. the people who got infected slept in the two bedrooms where
he pulled out the material. ticks must have fallen through from the attic down into those two bedrooms. all the other 16 people that slept elsewhere didn't get it. already. so the next year we went back up there to tell the association
what to look for, what happened. and there i am talking. i was with the state epidemiologist, the county health officer. well, on your left, there's a lady that you can't see but she was listening. and the next year both her kids
got relapse in fever. i show this because you can find it on the web. it's different on the internet, this article. i got a call late at night saying i'm so and so's sister, i just got back from wild horse i'm in a albuquerque and i am
sick and my nephew is sick do -- linda the mother was already on the way to the hospital with her two kids. and she walked in the er and said my kids are sick, they have an ever lasting fever look at the blood. and of course they didn't
believe her, but they took blood samples, ran off to the lab and came back about 20 minutes later and said you're absolutely right. both your kids have spirochetes in your blood. maybe you can't read it but it says linda not only rushed the
children to the hospital she helped the doctor diagnose the illness, all right. so within 12 hours of onset, those kids were diagnosed and treated whereas the outbreak the year before, many, three of those five people who got sick wound up in intensive care
hundreds of thousands of dollars of medical bills because they didn't get diagnosed in time. these kids got diagnosed in 12 hours and treated. what was fun though is we got diagnostic sample from those kids. they excellent in the same bed
on the porch. and from one kid isolated one genetic type and from the other kid we isolated the other. so right in that very same bed, there were ticks or a tick single or duly infected with both genetic types. so that's, we've been working on
that the last few years. that's actually quite fascinating. it was a support of three year study looking at the ecology of lasting fever at the lake. i'm fine on time at the moment. now we move into the southern range of this bug.
that arrow points to an historic observatory, mount wilson observatory built and started in 1904. and as you can see vertical towers which are and a horizontal tower which are telescopes. they have helio stats.
the sun reflects in another and down to a large refracking lens. there are stellar telescopes. the 6 on inch reflector was there and then the hundred inch reflector. the hundred inch -- the history of that place is just amazing. an astronomer got sick there.
he called me and said i'm not getting the help i'm supposed to get, all right. so from that 150 foot tower i took this picture looking at the horizontal snow telescope built in 1904. so one mentioned scientific america so you can go on-line
and read about this or especially. it says of telescope and ticks. how the observatory became an infectious disease site. it was an golden opportunity for a medical entomologist. that was me, all right. [laughter]
and the situation was this. he got relapsing fever not by sleeping in that horizontal steal scope building but by cleaning rodent degree which is another way you can get infected. the worse case -- when he was cleaning out these materials and
the tick walks out and feeds. they can transmit in seconds after attachment. as soon as they start spitting the salivary glands are this astronomer was cleaning out degree and a few days later he noticed welts. he got sick he got so sick he
had his wife drive him down to la and they told him he had mono new closes. they sent him up to the mountain. he got better and got sick. he got so sick he had his wife drive him down to another clinic.
they told him he had some other viral infection and didn't treat him and sent him back up to his house. he got better, he got worse. he got so sick his wife took him to a third place. by this time, the guy was smart enough, he went on-line and
decided he had -- fever. he was taken to the clinic the third time he told the doctor i think i've got -- fever i live at 5700 feet, i have welts, and they said that only occurs in third world countries. he never got diagnosed and that's when he contacted me.
he was treated specifically a got better. the diagnose was never made. he contacted me again with lab support. i went down there and with the astronomer's ingenious new tick trap that he developed, here's our famous tick that we named
wilson, all right. and wilson came back to rocky mountain labs and fed on a mouse. i was really thrilled because i went down there and brought back one tick on one trip. they are hard to catch. it's a most virulent strain that
i've seen on my 27 years and we're trying to figure out what, why that is. so with rtb's help we got the genome sequence, we're comparing it to other isolates. i'm going to jump to africa real quick. with the relapsing nature of the
disease, in africa one could think it could be easily misdiagnosed as malaria. in mali where we have an excellence of research with their support they're all right here all four of them they're able to do a study in mali for looking to see if there was the
risk for human infections where it could be misdiagnosed as malaria. because the symptoms as on this are similar. so onset, fever, they're listed up there. so here's mali almost a year with the coup.
the african country with this international center and with dr. soom -- they all supported this project and many others over there. we visited 20 villages over a several year period and some multiple villages. and we found multiple sites
where there are spirochetes circulating right in these people's houses, all right. so just a few shots. here's the elders in soromba. we had to negotiate with our maliian cohorts who work in the villages. they've all been great.
we have ambassadors over there so i'm showing folks there how these live traps are working. in my hand is an aluminum trap. we put them in there shut the door and process them. this is a typical morning stretch which in itself is a dilemma because these are not
all the same species of rodent. we had to spend a lot of time and effort making sure we knew what we were catching. this is not catching and the folks don't want us releasing these things back into their houses, all right. so over the several years we
trapped over 800 animals. i had a great high school student who had great eyes and maria feldman could look a all these slides and this is what we're looking for. these are spirochetes in the same blood smear. and through all of our lookings,
we were able to five file in mali who had animals actively infected with spirochetes at the time we trapped them. we also do serology and using western blot analysis this shows all the proteins separated for the spirochete and a recombinant protein that helped with our
diagnosis. the four panels on the left are good nice positive serum samples and the ones on the right are negative. by doing our serology we found 14 of the 20 villages actually had -- gave us a better coverage for the activity.
and then we have to find the ticks and this is a reverse, this is series and robuck leaf blower and we modified it so it sucks rather than blows. we found 750 ticks through a variety of permits we brought them back to montana. about 18% of those ticks are
so right in the houses people living with the shrews and rodents, the ticks are right there. about 18% of them are infected. totally different process situation are in the united states where people usually go to a fancy recreational
property, temporarily get bit, maybe infected. go back maybe hundreds or a thousand miles and get diagnosed somewhere else if they get diagnosed. so ecology is very different. but clearly relapsing fever looks like it could be a problem
in mali. just a couple comments and i'll close. just a lead-in on lyme disease, you all obviously have heard about lyme disease when it emerged in the mid 70's here. it's continuing in the news. most papers start with it's the
most prevalent air born disease in the united states which it is. this is the cover of news week back in 1989. just a couple comments on the epidemiological investigation because i think it's really cool.
alan steer i mentioned working at yale and the state health dent people were approached by two mothers in the lyme, old lyme area of connecticut. so here's the connecticut river and long island sound. and what we're looking like was an outbreak or too many people
with juvenile rheumatoid arthritis just didn't fit. so dr. steer began an investigation and i just want to show the map on two pages. the folks at yale for this particular study, they looked at both sides of the connecticut river and over a year period
1977 and on the east side there were 35 cases in that year. and on the west side there were eight. and the study done by bob wallace and his crew in the art bow virus unit collected ticks in that area and found that on the east side of the connecticut
river they collected 578 scab laser and on the west just 54. so this suggested and alan steer, they were all linked in to this was a tick infection. -- reference center for arbor viruses. they knew how to look for viruses but didn't know how to
look for bacteria. a post doc there not too long after this, i got to know the characters. they just didn't look in the right place. this just lists some of the attempts to isolate virus. tick pools, fighting flies, mass
tissues. but of course when you try to isolate a virus in a tissue culture system, what do you do? you add antibiotics. to control the bacterial contamination of the inoculum. it wasn't until late 1981 when dr. burg dorf -- looking at
ticks to figure out what were all of the -- in these ticks and they couldn't find them. one day willie was doing stain preps that came from long eyeland and he saw the spirochetes. he had done his ph.d. in spirochetes switzerland back in
the late 40's. he knew what spirochetes looked like. what he would do is open these up carefully take out the mid guts put them on a slide fix them stain them and he sought the spirochetes. they had a culture medium
infected tick tissues went into a culture medium. the brugz grew and they published their important paper and science in 1982. so these ticks are three hosts. some are one host two homes some are hosts. these scapularis feeds the
larvae on one host and drops off. feeds on another host drops off -- deer -- not maintaining a propagating spirochetes. this is a cdc map showing the distribution by county for the two primary vectors. just a final point on
protection. again here's the unfed on the left. you can see the mid gut here. this takes three to five days. what's interesting is that in these ticks in an unfed tick the spirochetes are restricted to the mid gut.
they're not in the salary bland. so when these ticks attach and begin to feed, they begin to bring in blood and fluid in the skin. they warm up and the spirochetes begin to replicate. get into the salivary -- so joe heisman has done some great work
on that. all right, last slide. the only good way right now to protect yourself from tick bites is to not let the ticks bite you. it's been that way since they've been discovered. nothing has changed in myion.
reduce tick bites, the way you dress i had four people go out last week and came back with 80 ticks and they did what they were supposed to do, pants and the socks, shirt into the pants, belt tight. they didn't use repellants because they didn't think this
were going to get anything last they hit a good spot. some people arthrotheir active. i've had people showing up saying i am moving from new jersey because i'm tired of the lyme disease. i met people that actually moved from an endemic area to
non-endemic area. for anying tick-borne disease the point is to get the ticks off as fast as you can, don't let them feed on you. okay, that's it. [applause] >> thank you, are thank you very much.
we have time for a few questions. i would only ask if you show your hand. >> is the story of the lasting fever different because the altitude in mali is pretty low? on mount wilson you have [indiscernible]
>> right. well, what i didn't say and i'll say now, there are other species in north america that are found at sea level. there are more ticks that have [indiscernible] sea level california, there's a -- in texas.
those don't cause very many human infections. i focused on the one where the spirochetes infects most people. there's different species that have found different locations. >> do rodents and deer show the symptoms? >> well, in nature, deer are
pretty much refractory. if we're talking about -- spirochetes i think deer pretty much refractory. they may kill the spirochetes. they are not good hosts for the i think once infected you can be infected for life. there are mice in the lab that
people use for different disease models for arthritis and neurological studies. but i think primarily the white-footed mouse i don't think shows any clinical symptoms when they're infected. once they're infected they probably are infected for life.
>> [indiscernible] >> dogs get lyme disease. i didn't talk, i didn't want to talk about vaccine which is a hole interesting study. but dogs get lyme disease, they can develop a lameness, lethargy, loss of appetite. there's a vaccine still
available, it's the whole -- vaccine for dogs. the dogs certainly get infected and sick. there may be a lot of dogs who get infected and convert that don't show clinical disease. but dogs certainly are susceptible and can become sick.
same with rats and fever. we've been working on that. >> are there any morphological differences between the spirochetes that you observe in the lyme disease compared to the relapsing fever. how can you distinguish between the two?
>> between the blood -- i'm not sure ... >> do spirochetes all look the same? >> just tell them yes, all so these things are in part define by their morphology. it can vary in length and can vary with the growth phrase when
these spirochetes longate and divide so depending where they are in their growth they can have different lengths. they have a cylinder surrounded by a membrane. thspace between the membranes they have to gel. this have filaments and motors
that drive the spirochetes to become mobile. and since spirochetes are defined by the number of flagella they have. so people will cross-section them or look at them in different places and say they have 10 flagella or 15.
the fact that syphilis has relatively few flagella but causing fever has many flagella. they vary like we vary in height in this room spirochetes have. we have to look at averages and ranges. i've been fooled. we had a -- in st. louis.
i looked at one scope, i would have sworn they were >> yes. there's a variety of specific stages that will help. we have antibodies that will recognize one species of spirochete and nothing else. there are specifics to --
spirochetes and they are very helpful. >> i have heard that the severity of the damage a tick can cause is somehow related to the last blood bath the tick has had. is that true? >> what i heard for example was
a north american deer versus an australian field mouse. the field mouse would be worse. global health people said that at a lecture several months ago. >> you got me stumped on that. >> okay. very quickly you mentioned as a treatment antibiotics.
is there other treatment. there are a variety of symptoms. >> are we talking about relapsing feveryes. so there is one potential outcome that one has to monitor and it's called the -- reaction. so when people typically have spirochete infection especially
relapsing fever there can be so many spirochetes in the blood system and they are killed by antibiotics in those cell's live. a person will go into shock. they can have a toxic shock to so actually, in africa, people sometimes in east africa people
have died when they go antibiotic treatment because they develop such a severe shock from the treatment that they die, you know. well thank you very much. and there will be time for more questions after the next talk. >> hi, everybody.
i work here at the clinical -- it's a pleasure to be here today and talk about our research and about the disease. i'm not going to touch base too much about the other infections by ticks. it was mentioned there are other important diseases but we do not
have enough time today. i have here today mr. gordon who is one of the patients who have -- continued to participate. and he was kind enough to come and talk about his disease. i thought we would start, maybe you can tell how it starts.
>> okay, thank you very much. john gordon's my name. in the spring of 2007 i was on vacation in arizona with my wife and went on a couple of tough hikes. we came back and my left knee started to swell upand i assumed that i had injured
myself. after a couple weeks i went to see around orthopedist. i had a l of doctors around. he put me on physical therapy and i stayed on and off physical therapist throughout the summer. started about may. by august, the knee was much
bigger. a couple of times he took fluid out of the knee, dark yellow fluid, a big cup full of it but he kept coming back. eventually he gave me a cortisone shot which temporarily reduced it. by august, are september i was
having to walk around on a cane. i am fairly athletic guy so that was not a lot of fun. and this went on, continued with the different types of physical therapy. they ere putting weights on my knee trying me to get it straightened out.
i was doing all kinds of exercises. finally in december, he operated on the knee. sorry. he operated on the knee and took out a lot of tissue, synovial tissue out of the knee and also told me that basically i had a
slightly torn meniscus and it would now get better. i had physical therapy for two or threemonths aer that. the knee was getting worse again, much bigger and i finally at that point went, had my second mri, i already had one. they, from that second mri, and
i switched orthopedic surgeons at that point. they diagnosed me with pigmented nodular sign vie tice which is a disease of the tissue in the knee. i had a second surgery where they were supposed to remove all of this knee tissue and hope
that it doesn't come back. the doctor after he opened up my knee could see that the tissue was not pigmented, so he knew that i did not have that thought i might have some type of sarcoma, and sent me to see a orthed oncologist. and then an infectious disease
doctor. and i went and saw them and they decided i did not have a sarcoma from the biopsy that they had taken. and, okay, sorry about that. and ey, infectious disease doctor, very nice guy, decided that i had a rare infection
called valley fever, which you get from, it's a fungal infection in the southwest since i had been in the southwest when i got this. he put me on a massive amount of flu consaul and called me up and said your new blood tests show you don't have that.
i don't know what you have. luckily a week or two later there was a meeting with a staff and a nurse said has anyone tested this man for lyme he called me pop and said anybody -- they've tested you for lyme disease haven't they. he said no, nobody's ever
suggested that. and he says well go get a blood test. i went downstairs to the lab, he called me back two days later, said you have lyme disease definitely. he gave me a prescription for docky cycle and he said i can
treat you through abouts a clinical study at nih. if you want to participate in that my office is down the street. i arrive to see dr. marques. >> so this is -- and do you remember a tick bite. >> i do not remember a specific
tick bite. iada dog that i used to walk in a park and i would continually get poison ivy. so i would imagine that i did see some type of rash. i assumed it was poison ivy. >> so, your history is not, it' a little bit longer than the
usual patient who have -- it's not unusual, if you don't think about the diagnosis then you don't do the test. it's not going to,ist kind of a assical presentation of [indiscernible] as we're going to see in a little bit when we talk about the clinical disease.
most of the patients who acquire lyme disease do not remember a tick bite because the ticks, they're very very tiny. i will show some pictures and it's very easy to miss. so most patients will not and the rash sometimes we might miss it.
there's of course there are patients who don't acquire the rash either because they had a place they didn't see or thought it was something else or maybe they didn't have the rash. so we'll talk more about the clinical manifestations of lyme and this is kind of good time
because this is where we'll be starting soon and i will talk also about the [indiscernible] and a little bit about prevention as well. any questions? >> [indiscernible] symptoms apart from [indiscernible] >> no, i didn't.
sorry the question was did i have any other symptoms besides the swollen knee, and the answer is no. >> what was your first [iiscernible] >> the course of treatment once i arrived, once they diagnosed it was dioxen cycline, an
antibiotic. it was probably six weeks or something. >> two months. >> two months. the knee is relatively weaker i think as a result of the two surgeries and just being swollen for a year.
i also admitted the fact i went and saw a physiatrist at one point if he could figure t and he treated me with acupuncture. that doesn't work either. >> [inerble] >> dr. marques, he had localized [indiscernible] and we'll talk about diagnosis as well.
but there's also another test that can be con[indiscernible] which is the pcr in the joint fluid. i'll also mention a little bit about detection of the organism anything else you want to tell the audience? >> most patient will recover
completely. we'll talk about one of the manifestations of lymetritis that's also thought to be mixture between -- possibly left over antigens [indiscernible] >> well, i don't know when i got but when i first noticed it, it was, it was a little over a
year. >> [indiscernible] do not remember when they got infected. they will present as lymetritis and not have the manifestations of the disease. so it's hard to know exactly when it happened. when the older studies that from
the first studies -- it seems to take months for -- the arthritis is a later presentation of the >> depend on the type of arthritis. so it will depend on the type of arthritis [indiscernible] in the large joints and also depend of your history, exposed to area
have been exposed. we live in a -- here in maryland and there are lots of lyme disease. >> [indiscernible] >> he asked if i was treated with any other antibiotics through the course of seeing these other doctors.
and diagnose any reef. i was only given flu consaul near the end which i think is something quite different. and so no, i don't know of other once worked or not. >> there are other effects as well and dock cyclin is the dg of choice&for acute disease will
treat one of the -- so patients will tolerate dock cyclin and they don't have any [indiscernible] easiest one to take. >> the knee was tremendously hot in addition to being swollen. i could feel the heat thugh my pants.
one release i did feel is when they would drain the fluid out of the knee that would temporarily make it feel better and then i had two cortisone shots as i mentioned. that temporarily reduced the swelling and then it would come back within a week or two.
>> this is inflammation. >> i never saw them. >> that is extremely interesting question and there's a lot of research going on that. why would someone present a [indiscernible] and it's probably, the answer i that is not known.
it's a combination of factors between the host. ere's alys bacteria. as well as time of treatment so if you treated earlier of course you don't get the manifestations. and but why would someone disseminate [indiscernible]
versus someone who presents with arthritis later. that's a very very interesting question. >> i'm going to speak a little bit about lyme disease. so lyme disease is started by [indiscernible] which is an extracellular bacteria and
similar to the spirochetes that cause disease is invaded and disseminates and persists and this is interesting for the it causes an infection despite -- patients shoe have a strong cellular immune respondent even then you do not completely resolve the infection
in most of the cases. it's a [indiscernible] immune response and the inflammation that's produced by the immune response is what you see that causes the disease the spirochete it sell doesn't have any toxins but it has a lot of lipo proteins and they
constitute the majority of the surface exposed proteins and they are the immune gens of the bacteria. it's an interesting how it adapts to the host environment and tom has done a lot of beautiful work about that in terms of how it passes from
the -- to the tick and back. and it's very important to think about lyme disease is the infection does not provide a protective -- so you can get lyme disease more than one time and patients have got them quite a few times. it's the most common
vector-borne disease in the u.s. and most of the human cases are caused by the [indiscernible] in north america. that's the only ones we have as far as we know that causes human and got lien yeah in europe and -- and asia has -- there are a few others that cause human
disease but there are much less. it's transmuted by the [indiscernible] we talked about the 12 states account for 95% of the cases and here is maryland and virginia so we are in an endemic area here. most of the diseases are presented in june, july and
august and from december to march. this combination of people being active out in the woods as well as being active for the host. the ticks are more active [indiscernible] about a third of the cases occur in children. this is where you find the
ticks. they love this. it's like a bush. you can think about your backyard and imagine how it looks like. so in the spring they attach the larvae. there's no trans mission -- the
larvae when it hatches is not infected but at this point the first stage it feeds on a host that is chronically infected or acquired infection. for the next spring it will then feed in others in which they find they will feed the most as well but also in larger mammals.
they will transmute the infection if they are infected. so in the late spring and early summers. these are the main culprits in transmissions to humans because they're so tiny and it's hard to see them. and after they become an adult
and will feed again and will show in larger animals. if they are infected they can transmute again and the cycle starts again. as we talked about the [indiscernible] in the environment. it's important in maintaining
the ticks -- correlation of the number of the ticks. you see this is the size of a poppy seed and this is the size of a sesame seavmentd when it engorges it's not much bigger so it's very very easy to miss. now we have a confirmed probable lyme disease is a disease that
has to be reported to the health departments and then the health departments would move off to the cdc. i will go over the case definition a little bit later. in the united states lyme disease is very regional but it is spreading.
so these are 1998 and this is -- and becomes hyper endemic. this is a paper showing that they kind of the infected was correlated with the human incidence. so of course the more humans infected the more likely you're going to have human cases.
research they also found there's a variation of the genotype for -- that seems to be more likely to be transmitted and to cause disease so that's a very interesting of research going on so how -- personal protection. right now we don't have a vaccine for humans so what you
can do is to avoid the habitats and [indiscernible] promptly after exposure showing the chances because you wash off the ticks and remove the clothing. they take a while, they don't just go and bite you. they will walk around for a while so there's some time
before that and that could be how it works. how to remove the tick, try to remove the tick from the skin as soon as possible. the best way to have a fine tweezer and firmly grasp the tick very close to the skin and then pull it out and clean the
skin with soap and water. if you leave a little piece, it's okay. there won't be anymore transmission. it's just going to come out as a foreign body. avoid crushing the tick's body as possible and just clean with
alcohol. do not use petroleum jelly or nail polish and other products just like that makes things more difficult. for tick bites has been study and one dose of dock cycline has been shown to decrease the rate of lyme disease.
and right now the recommendations are that if you know that a tick is an adult [indiscernible] which mean that you know, and that being attach for at least 36 hours. you can start the prophylaxis within 7-2 hours of the time that the tick was removed.
and -- where the ticks have at least a good percentage of being there's no indication to dock cycline treatment which is an issue being used in children or pregnant women. there's no to test for airborne agents because even if you find doesn't mean it will be
transmitted and what are you going to do with that information. it's an expense. and there's no need for serological testing for a tick bite just think about it. there's no time there, there's no point in doing the antibody
test at that point. [indiscernible] should be monitored closely for signs and symptoms of a tick-borne disease which is usually fever and rash sometimes with or without a rash. up to 30 days. and if you develop a skin lesion
or bile like infection like fever, something like that, fatigue. within this month you should seek attention and possibly treatment for tick-borne the recommendations are the same, if it was a long time ago and received [indiscernible] was
in the market in 2002 is not, the vaccine is not effective anymore if you actually received it a while ago. or if you have lyme disease. as we said having lyme disease is not protected. other thing that can be done and the cbc has a very nice stage
about lyme disease which [indiscernible] reducing the that's great because you see like the balance it's very easy when the kids walk through the brush here and that's why you would get lyme disease. try to avoid having deer around and the other thing that
possibility is the tick control and springtime application could resist the tick populations between 68 to 100%. and it should be showed that reductions in the population indicates lyme disease and that has to be easier reduction. and i just saw today in the
paper about virginia and disease -- production of the disease in the discussion. so let's talk a little bit about the disease itself. we divided the disease in three stages. stage one is the look alike infection -- what people's know
as the bull's eye rash. i'm going to show to you the bull's eye rash is most often than not not a bull's eye. if it occurs that the site of the tick by the 28 days after the tick bite what happens is [indiscernible] start growing outwards and it's like slowly
expanding. it has a rash which means it is red. depending on where in the body it is, they can look not round and oval, they can look like different shapes. most of the time in the u.s. is rash is homogeneous which means
it's all red. the clearing in the center is less common. sometimes you can see where the bite is and occasionally people can have some vesicles at the site. and most of the time the rash is not that symptomatic, that might
be a little tender or a little itchy but not severe. people see that and they have this huge rash on their back and they didn't do anything. so these are some of the pictures of rashes. these are pretty kind of classical but you can see that
this is completely red. maybe a little darker. this one has a which is just homogeneously red. this is all culture conformed -- so these are the gold standard. there are no -- they all proven to be lyme disease. so most you can see that most
[indiscernible] home jean quite a few patients will have signs, general signs and symptoms, mostly myalgia, fevers [indiscernible] you're going to see another stage and we'll talk about that. there could be -- with the rash. so this is one time of your
question about why people might -- differently. we don't know but some people seem to take a while and something to do -- some people seem to disseminate quickly. patients can have a [indiscernible] but different from the relapsing fever, it's
very very very hard to, you would be extremely rare to actually see the -- in the it's actually very there are much fewer numbers. patients can have [indiscernible] they can have systemic symptoms as we just mentioned, about 10 to 20% of
the patients present just with the systemic, especially headaches, myalgias and fever. the differentiation is you don't have much of the symptoms so it's kind of we should think of flu-like description the systemic disease, this can happen in about 10 to 20% of the
patient that present with just about 15% of the untreated patients will present with acute [indiscernible] and that is, presents present with meningitis. this meningitis is a lethal -- it's more like a viral type meningitis more than a bacterial
type of meningitis. patients are not as sick as patients who have bacterial meningitis emergency. they will have this headache, they will have other problems, other symptoms but they are not like in coma. a coma manifestation is facial
palsy. that's the muscles on the face and the patient will present with a paralysis of the face. people call bell's palsy but pel's palsy is when you don't know the cause. in this case it's a facial palsy and it can be other
neuropathies -- which can present one side one time and then a few days after the other side. this could be, this should be the highest point on the differential because there are various things that could cause and patients can also have this
port sense neuropathy. the meningitis is associated with death and what you have, you have the severe pain. what happened is the measures have the severe back pain and they can't find, they end up in physical therapy until something happens.
maybe the fascial palsy shows up or someone sees they have a rash and they realize that could be but that is -- and that's a manifestation that is not for, it's something in you're they have certain parts of europe have much more -- infection and that seems to be more
neurotropic -- and they have more. the first description we do see a few patients here but i will say they don't seem this occurs in about 5% of one treated patients and the main manifestation is age of ventricular block which means
the heart is not passing from one chamber to the other and people will have, well they have -- people will present with these blocks can be different grade. and can be type one to type three where it's completely blocked.
and this, it's important to think about for the er physicians and the cardiologists. i've had a few patients present with that and they had a pacemaker as a result of the treatment. rarely patients might present to
a myocarditis [indiscernible] but we see this in europe. about 5% of the patients, this came out of this vaccine studies when patients were followed yearly. about 5% seem to have a single they acquire the infection they didn't have a manifestation or
they can't remember anything. so they. most patients will go into what we call [indiscernible] and that's what most patients with arthritis present. you have alter right -- arthritis as an acute or subacute.
patients will go to develop [indiscernible] in the u.s. and this came from the studies, the early core of patients. patients who have intermittent attacks in one or a few joints especially the knee and then sometimes it becomes chronic. but some patients will just
present with the this was the classical part. in europe there was a skin condition called [indiscernible] there are the pictures. and it just left and can find the -- neuro they presented with the neuropathy is heart to diagnose.
it's like a mild -- and there's also polar neuropathy. indeaf low myelitis is extremely rare. mostly even in europe it's rare and it's very very rare in the u.s. i think most of the time there's one or two cases that we've
seen. but it's very rare. so said lyme disease is disease that has to be reportable it's important to think about that as i talk about the if you have a patient who has [indiscernible] rash or the physician made the diagnosis
of -- rash with non-exposure. that's all that you need for confirmed case. and this is going to i'll touch base again on this about when we talk about treatment. you can have -- that's okay but if you have these two things that's all that you need.
if you have a later manifestation, then laboratory becomes more important point. probable case -- and then suspected cases, a case of [indiscernible] where there's no known exposure and no evidence of infection. and a case that is like for
laboratories that report to the health department. throughs no clinical information to go. we just a laboratory report with searologist. so the method for the diagnosis of lyme disease, there's two main things.
direct about the detection of the cause of the organism or indirect, you're detecting immune response to the causative organism. so the direct methods culturing or detection of dna from clinical -- indirect in the case of lung disease will be
defection of antibodies against the problem with direct methods is that -- very hard to find. it's not as many -- where you have lots of them and easily find them. you can find it in about, depending whose hands it is, i would say around 50% of the best
labs you can find for a kind biopsy or the blood samples of a patient who has not received antibiotics and in an acute stages of the disease. it's a very important tool for research and for learning about the disease but in clinical practice is not that much
easier. and it's actually the culture needs a special culture media and not all the laboratories will have and it's kind of [indiscernible] with lyme arthritis for reasons that are unclear. that body fluid has a very good
sensitivity of pcr on patients who have lymetritis and are untreated. for presentations like lyme meningitis, it's very very hard to find brellia by culture. it's probably less than 10%. so keep this in mind. most of the testing that is done
is done by indirect methods which you are looking for the immune response to the brellia. right now the recommendations are that we use -- the first system is a very sensitive -- and it's negative you don't need any testing but if positive you do the next stage which is the
western blot. the interpretation of the western bullet is the interpretation of the illness -- and there are criterias what are positive ieg block. the problems with this is that the sensitivity of the test increase.
so [indiscernible] who are very early in their infection most of these patients will be negative. they will be serologically negative and that's what we expect on infection because it takes sometimes for you to make the antibodies. so at this page if the patient
has -- that you think -- that's all you need to treat them. you can do testing but you don't need to not treat them because the answers of being negative at this change are quite high. and the test is not going to be that helpful. tests are not yes.
where the tests are most helpful is patients who have later in their disease stage two and three. and this with patients with [indiscernible] and this illustrates what you've been saying. it depends how long you've been
sick. you have -- and then the serology mains that a positive -- western block in this case ign western block. you can see it's very early in the disease. only about 40% and very few will be presented with your test.
these are patients who present in the first week second week thursday week and fourth week of so you can see as you go longer you're much more locker to be positive. if you're very early which is -- they will not be positive at this point and that's what we
expect of this type of test because you just haven't had time enough to make antibodies for that. one of the issues we've discussed a lot in the field is about a different algorithm for the serology just because of this big problem or should we
even have that at this early stage. this is 509 study which was just published not too long ago showing similar just a much more complete view. this is the [indiscernible] is a peptide vasoizer and this is just to mash it up.
and as you can see single em means patients were very early in their disease. patients were a little bit if you are, they have hard time they disseminated. this is these are patients with convalescence and this is belated disease [indiscernible]
as you can see the tests work much better on this portion. this is a clinical diagnose. an important point is the false positive rates of these tests. and that is very important just keep in mind this. so the -- has the most of the false positive rates and this
is -- this is another study similar to before showing that acute em is the same progression of the antibody response. so when you're talking about serology of lyme disease, it's very important to think about who are you testing. and what stage of the disease
that patients have. so patients with lyme [indiscernible] will hardly likely to be negative and that is what we expect of the test. important points that we have is that the current serological phase we have do not distinguish ten active and inactive
so patients can have positive responses for [indiscernible] therapy for a long long long time. and that be including antibodies. a positive igm response will not distinguished clearly between lyme disease and other
conditions. so viral infections 50% will have a positive response. it's important to think of other disease, autoimmune disease which will increase the chance of false positive test. in a patient with low probability of lyme disease rule
out the disease but it's more likely a false positive because you have to think about the predict different value of that so no test is 100% specific. just talking about specifics most are 100% specific and these tests do have a false positive rate.
so if you're using people who somewhere very low chance of having lyme disease, then your chance of getting a false positive test is much higher than if you are using someone that you suspect has lyme a big challenge for this test is that the properties of the test
there's about 3.4 million lyme serologies done in the u.s. annually and compared with about 38,000 of cases. so you're doing, we're doing a lot of testing in patients they were not suspecting lyme treatment for lyme disease is oral antibiotic as we talked
about dock cycline is a drug of choice for certain it's easier to take twice a day. it's important because dock cycline also treats plasma which is a co-infection that can be transmade and can be extremely dangerous. so [indiscernible] effects of
dock cycline and thought respond to other antibiotics. so that's another reason. so for patients who have [indiscernible] and this is the treatment between ten days to three weeks the recommendation is two weeks just make it but these studies have varied
between 10 to 30. and the second other choices are moxy -- for the carjack disease patients have improved sufficiently you could move then. if europe there have been trials of oral doxycycline for acute neurological disease and didn't
work as well as -- we don't have -- in the u.s. [indiscernible] you can repeat the oral for another two to four weeks so up to two months. the iv is four weeks. so i mentioned about [indiscernible] and its condition where the persistent
is -- to therapy. you can find the -- either by pcr of the fluid or pcr of the synovial tissue remove it during surgery. it takes many years like four years. and it is caused by infection [indiscernible] and there's very
interesting data came out that showed retained -- antigens which may play a role in the maintaining itself the alkalinity or at outer right tice much these patients have a greater response to this outer surface protein a rotein a and they are associated with [indiscernible]
so there's this basis for alkalinity. so there's this also association with this tlr1 poly morphens and reducing tlr1 correlated for great inflammation with more and also with certain strains of -- that falls into this ist one of the ways that these are
divided which shows a longer th1 inflammatory response. and just showing the -- antigens adjacent to the [indiscernible] and associating mice very long after antibiotic therapy. there might be certain -- which is very hard to clab up and that's why the contributing.
i will talk about chronic lyme disease which is a contentious issue and i will talk mostly about post lyme disease syndrome. in this paper in the new england journal in 2007 this chronic lyme disease is very confusing entity.
and i'm not talking about patients that have late lyme disease is different from this. these are symptoms -- the first cat gree would be patients who have symptoms of cause with no [indiscernible] or the second way is patients have another [indiscernible] and is
formulated to be [indiscernible] who have symptoms -- they have evidence of [indiscernible] but the history doesn't have any objective clinical findings that are kind with lyme disease. these are, this one is the patient we'll talk, there have been studied the best because
it's the easiest to define and to study. so post lyme disease symptoms patients who have had lyme disease have been treated and have intermittent or persistent symptoms after being sectioned and they don't have any other explanation for their symptoms.
the symptom is they seriously have shown it is between -- depending how you define post lyme disease symptoms versus syndrome is between 10-40% of the patients. most common symptoms are -- headache, neck stiffness [indiscernible] finding and
concentration. [indiscernible] presentation and delay it with therapy and does not correlate with the duration of the initial therapy and children are less likely to develop [indiscernible] and why these symptoms happen is very controlled [indiscernible]
some of the facts patients reporting symptoms increase over time so there is decrease of the number. when you finish about a third who has symptoms acquired at three months 20% at 12 months and 13%. so the symptoms improve with no
other [indiscernible] occur in modern infections and it's actually relatively common. this is a core of patients in australia who had acute fever and raw virus infection. and the fatigue was predicted by the severity of the illness as well as the this -- incidence was
similar. so 35% have fatigue, 27% -- at 12 months and this is after following the patient. so infectious fatigue is actually [indiscernible] symptoms specific symptoms are quite common in the population. and the population of the
cross-section survey. 15% had -- and 8% had clinic fatigue [indiscernible] and it's something there are two studies. they are from the slovenia group, there is a lot of lyme disease in -- they followed patients and controls with antibody therapies.
there's no difference in severity -- or severity of patients who are treated for [indiscernible] controls. and of course patients had other contributions. now the biggest question contention with that could just be due to infection.
could be a persistence of things that have been shown is that symptomatic patients are not more likely to be sero positive than patients who don't have symptoms. they don't seem to develop the objective manifestations of light lyme disease and they
don't go on and develop by current methods we don't find it directly. there is a control -- double blinded studies of and they show that -- had no stained benefits but did have adverse events. there's some interesting data from the animals and this has
been in the research that's going on right now. it shows [indiscernible] in the dogs, mice and monkeys. the spirochetes are not -- so you can't culture them after but in some of the studies, that use the diagnosis [indiscernible] to diagnose the
these are laboratory here that placed with the mice. they then check in the monkeys check it for evidence beret law. they found evident of beret law and they were able to transmute to the skid mice and it is to be nauticallurable and is very very low.
what it does mean for -- it is this big piece of evolution. we showed the microbial dna can persist in the mammalian tissues for extended periods so just to have a positive doesn't mean it is alive. and then there are questions of the antibiotic treatments some
of these studies were adequate. so this is interesting and is evolving as we speak. so future directions i think the most important will think that i think are very important is improvement of the direct methods for the [indiscernible] in samples of patients i think
that will be extremely important. improve the current serological diagnostic much more for the early patients and develop help follow response to therapy, for example bio markers of acute infection is extremely important in the field.
under the underlying mechanism of lyme disease and how to distinguish the symptoms from other illnesses, how to best manage these patients. work of the things right now in the field and of course prevention which would be wonderful if we have more
evidence of -- borne illness. i don't have enough time -- unknown chick-borne disease [indiscernible] is the person who have done mostly in this is a disease that was caused by the tick and the rash looks very much like a -- rash but it is not caused by
[indiscernible] so what causes this disease is unknown. so this is when the -- style occurred so we have both of them. and it can cause a lot, we don't know what causes it how to manage these patients everything how to best treat these patients
and how to diagnose these and it can cause a lot of -- show the difference between the rash from mo from a the rash of new york [indiscernible] and these are pictures from papers about the rashes. you can see that this is a big issue.
and we don't know what causes it this is in fact diagnosing treatment of these patients for lyme disease, characterization of the laboratory tests because we have both here. so if you have a negative test it's because they have real lyme disease or they have something
else. and evaluation of the future lyme disease vaccines. so we present with -- with the increase in the lone star tick and this increase even more this is going to be much more of an issue and this is a disease we have not being able to find a
pathogen yet. going back to this one here, that's why i think new techniques to discover but other possible tick-borne in essence these are our current protocols we do have clinical research and clinical protocols here to see patients with lyme disease and
evaluate other manifestations of the disease. and thank you. [applause] >> if you have a question please speak loudly. >> you mentioned that one of the types of prevention against ticks was to use insect
propellants [indiscernible] works per se. >> that's a question for you. they do work but also the [indiscernible] you can tell much more about that than i can. >> you're right. they are not insects but the repellants [indiscernible]
yes, so they work. >> what was there before it was absorbed that there was this many epidemics in mind. >> there's a very interesting discussion about that. so cases that's what lyme disease has been in europe since the beginning of the centuries
because people have been put together so the -- syndrome was described as the [indiscernible] and how it started -- there's actually a case in the u.s. even before they describe it [indiscernible] but as someone has mentioned, the -- logical evaluation that was done by
[indiscernible] at that time was at the same time the connection was the -- vns the disease because then you could have a past. you could actually look over and see what is. but you talk about how it spreads.
>> it came from europe is that what you're saying? >> some people think that birds fly across the atlantic help to disseminate the spirochetes. there's been a lot of work looking at the very genetic structure of these populations. >> these are big birds
>> no. that could happen but i mean it's hard, no one knows the answer. >> at the same time increase of dear. >> you mentioned maryland and virginia were two of the states where there was a big problem.
oop just wondering, if you get pitten by a tick in this area, what's the chance that you'll get lyme disease? i mean, is it 10%, is it 80% from a single tick by bite. >> i don't know if i can answer that, it's small, less than 10%. it's all luck.
so in the prophylaxis studies they did some analysis dated on that and it is -- your chances are small it all depends on what happens, how long they stay. i'm not sure if it's less than 10% even though highly indicated but i'm not sure exactly of the numbers.
>> you suggested the immune response for lyme is pretty against. i was wondering what the mechanisms are by which the -- is able to resist very intense immune response. that's like the most interesting question.
how does it occur, how and it -- and where does it survive. in the beginning there's a big burst and they get killed some of them but then some of them will survive. so the immune response is not completely -- it just doesn't get rid of everything.
how and where do the spirochetes hide. most later they will present. it's interesting how does it happen. >> there is the genetic >> maybe other pieces together too. like dna response, complement.
and does it then become -- don't express and becomes [indiscernible] to start replicating again. >> i just wonder if lyme disease models [indiscernible] disease or how about. >> there are deferring times when you can donate.
but i'm not aware with of any cases of lyme disease being transmute by blood transfusion that i know. i might be wrong. [indiscernible] i don't talk about co-infections. so plasma in -- can be carried would it same tick and other
ones that can be carried by the same tick. these are the main ones. it can be carried in the blood supply there's a whole testing and how to best test for that. i'm not aware of a case -- but i know the blood bank does defer for most after the treatment and
so people can donate again. you showed the graph of increasing cases of lyme is that reported cases or -- >> reported. >> report. a number of under reporting is a big question and how many cases go under reported is actually a
very interesting question. but how many are under reported. >> i'm not finished. and also the last two bars had something unusual in the top it had probability. the bars -- is that the -- >> that's the year that cdc changes to both confirmed,
probably and suspected. >> so the top layer is probable. >> that's what i thought, okay. are all people in the field required to report. in the case of your patient here the doctors he saw didn't even know it. so it didn't get reported.
>> when you make the diagnosis you're supposed to report. >> when you make the diagnosis. >> i think we have to stop now because the fire marshall -- thank you very much.
0 comments:
Post a Comment