4 Part 3: Sexual Transmission Of Lyme Disease - Is There Evidence?

This article is the continuation of "Part 2: Sexual Transmission of Lyme Disease - Is There Evidence?", our series on sexual transmission and contact studies involving Borrelia burgdorferi.

To review the content of the first article briefly: We discussed the fact that no human sexual transmission studies of Borrelia burgdorferi have been conducted to date and reviewed the outcomes of animal studies on contact transmission and sexual (venereal) transmission. Based on all studies which could be found, there was evidence that Borrelia burgdorferi may be transmitted between at least some animals either via exposure to infected urine or by consumption of raw milk. The possibility that animals could transmit Borrelia burgdorferi to each other via sexual intercourse has only been examined in a few controlled studies, no cases have been confirmed so far, and it remains an issue of speculation in studies where uninfected animals came in contact with infected ones and developed a positive of antibody response (and in some cases, even signs of infection).

What follows below is some notes on studies which are listed in Table 1 in "Part 2: Sexual Transmission of Lyme Disease - Is There Evidence?" as well as notes on additional papers on Borrelia burgdorferi transmission studies which were not included in that table as they were speculative and not based on controlled studies.

Additional Notes On Studies Included In Part Two's Table

The 1994 paper, "Distribution of Borrelia burgdorferi in host mice in Pennsylvania", is a study where samples are taken from ear tissue from mice from different counties around the state of Pennsylvania. When a sample was positive by darkfield microscopy and fluorescent-antibody testing, it was sent to the CDC for further evaluation.

In the discussion section of this paper, the authors state that a group tagged mice in one county which repeatedly tested negative before began to turn up positive during the winter in areas where no vector ticks had been found - and because of this, the authors speculate this group of mice may not have been infected by ticks. However, there is no evidence in their paper which confirms an alternative method of infection. Because of this, I wouldn't cite this paper to support a method of contact or sexual transmission of Lyme disease between mice. It is a mystery how one specific group of mice in Indiana County were infected during the winter.

I run into the same problem with the 1997 publication, "Tick-raccoon associations and the potential for Lyme disease spirochete transmission in the coastal plain of North Carolina". In it, the authors discover that while raccoons in the South are highly infected with Borrelia burgdorferi, none of the vector ticks which they find on them appear to have high spirochetal loads, and a low percentage of them are infected with Borrelia burgdorferi. The ticks which latch onto the raccoons the most are Amblyomma americanum - Lone Star ticks - and studies in the past showed they are incompetent vectors of Borrelia burgdorferi but are great at transmitting Ehrlichia and other pathogens.

The authors go on to speculate that maybe the raccoons are infected via urine, but also actually refer to the 1994 paper on host mice above, wondering if sexual or oral contact may be the cause for raccoons' high rate of Borrelia burgdorferi infection. There is no evidence here which confirms this method of transmission occurred in this study - it is just something the scientists are wondering about. More recent research supports the idea that Amblyomma americanum ticks are infected with other strains of Borrelia, and today raccoons in North Carolina may be infected with those - but at the time of this study, the raccoons' infections were considered unusual because the ticks collected did not appear to be full of spirochetes in general.

Relevant Reviews, Summaries, and Editorials Outside The Scope of Part Two's Table

One of the most cited papers on Borrelia, "Biology of Borrelia Species"(1986) by Dr. Alan Barbour and Dr. Stanley Hayes, quotes research on the presence of Borrelia spirochetes in urine dating back to 1938: Chung and Wei's "Studies on the transmission of relapsing fever in North China I. Observations on the mechanism of transmission of relapsing fever in man." In a short passage, they mention that "Spirochetes in the urine could enter the host through the mucous membranes of the conjunctiva, mouth, or nose". It is this early research which perhaps set the stage for stringent laboratory rules about how to handle Borrelia burgdorferi spirochetes - that and the knowledge that other spirochetes, Leptospira, could infect people through contact with urine.

In another paper not included in the table in Part 2, "Epidemiologic Studies of Lyme disease in horses and their public  health significance" there was passing mention of horse bite transmitting Lyme disease to a man in 1987 in Belgium. I am fortunate to have located the case study online describing the transmission of Lyme disease via a horse bite, "Horse Reservoir for Borrelia burgdorferi?" (Lancet, Apr. 25, 1987), and read the full text. It is an interesting case, in that it describes a man who was bitten on the neck by a horse with Lyme disease who went on to develop a erythema migrans (EM) rash and additional symptoms of Lyme disease shortly thereafter. No mention of the location of the rash was made in the case study, but had it stated it was directly at the bite site it would have strengthened the case for the infection being caused by the horse bite. As it stands, the history, timing of exposure, and clinical evidence do point to the possibility that a horse bite could have given this man Lyme disease - but this appears to be a rare case as I have not found other similar case studies.

A paper from 1991, "Borrelia burgdorferi: another cause of foodborne illness?" is an editorial letter which refers to studies mentioned in the table, and was written by researchers who questioned whether or not Borrelia burgdorferi was a risk to the food supply. They mention another study from 1990, "Thermal inactivation of Borrelia burgdorferi, the cause of Lyme disease," where it was discussed that refrigerated milk at 5° C contained viable Borrelia burgdorferi after 46 days and that high-temperature short-time (HTST) pasteurization may not kill all Borrelia burgdorferi in milk, thus raising questions as to whether the temperature should be raised and how much. The authors do not have an answer for their own questions - they only raise them for consideration.

The 1992 paper, "Lyme Borreliosis in dairy cattle" and 1994 paper, "Lyme Borreliosis in domestic animals" were not included in the table because both are overviews on Lyme disease studies on animals which refer to existing studies otherwise mentioned in the table and do not contain new experiments;  references used in one paper are also used in the other. In the first paper, references to finding spirochetes in cattle milk, urine, and colostrum are cited which are mentioned in the second. In the second paper, it is mentioned that cats have been infected via experimental inoculation of B. burgdorferi by intravenous, oral, and conjunctival routes. Both papers cite other papers already listed in the table, and as such, I have not included these two papers in the table order to avoid duplication of data.

While not directly addressed in the studies above,  pasteurization seems likely to reduce odds of Borrelia burgdorferi survival.

Studies listed in Table 1 indicate that spirochetes can turn up in urine, milk, and colostrum samples, but positive samples in these studies came from animals which have not been treated with antibiotics (which affect Lyme disease) and/or fluids such as raw milk which has not been pasteurized - which suggests that the possibility of human infection from consuming animal products is going to be extremely low because most meat is cooked and milk is pasteurized.

"Thermal inactivation of Borrelia burgdorferi, the cause of Lyme disease" is the only paper I've reviewed which suggests that milk should be pasteurized at a higher temperature to ensure all spirochetes are dead.

What happens to milk during pasteurization all depends on how it's pasteurized: High-temperature short-time (HTST) pasteurization is when milk is subjected to a temperature of 71.5 °C (160 °F) to 74°C (165 °F), for about 15 to 30 seconds. Low-temperature long-time treatment is when milk is pasteurized at 63 °C (145 °F) for 30 minutes. And ultra-pasteurization is when one heats milk or cream to 138 °C (280 °F) for 2 seconds to extend the refrigerated shelf life of milk from 60 to 90 days.

This of course raises the question: At what temperature does Borrelia burgdorferi die?

Porcella and Schwan wrote in 2001 that:

"In vitro cultivation of B. burgdorferi at various temperatures demonstrates that the spirochete replicates most quickly at 37 °C. An increase in temperature to 39 °C retards growth significantly, while a 24 hour exposure at 41 °C kills all spirochetes in the culture." 

According to a 2008 research study by Juliet Kim, "Differential Temperature Susceptibility and Survival of Borrelia burgdorferi and Borrelia hermsii":

"... on average, the Lyme disease bacterium had a higher survival at the higher temperatures than the relapsing fever agent, with a mean survival (95% confidence interval) of 1.62 (0.06– 43.6) X10-4 vs. 3.16 (1.02- 9.77) X10-4 at 50 °C and 38.3 (1.18- 1250) X10-6 vs. 1.96 (23.5- 16.3) X10-6 at 51 °C."

Laboratory techniques for semisolid plating of Borrelia burgdorferi require that samples do not exceed 52 °C, which is in the ballpark of the highest temperature on average that Borrelia burgdorferi die off in vitro in Kim's study.

It would seem either a lower temperature exposure of 41 °C over a longer duration is needed to kill all spirochetes or a higher temperature at shorter duration. Pasteurization is a minimum over 10 °C higher than these temperatures where spirochetes died off - so the question becomes how long can spirochetes survive at temperatures this high? Perhaps this is an issue requiring further research.

Summary of Findings From This Three Part Series

There is not one study to date which has been conducted which provides evidence sexual transmission of Borrelia burgdorferi, the spirochete which causes Lyme disease, occurs between humans. (I am reserving discussion on the Middelveen et al study for later - and so far the abstract does not indicate it is a transmission study.)

Far as is known, there is no study to date which has been conducted which provides evidence sexual transmission of Borrelia burgdorferi occurs between animals, either - and very few controlled studies on venereal transmission in animals have been completed (Are there more than three?).

There is some evidence that at least some animals under certain circumstances may contract infection with Borrelia burgdorferi through contact in some way. The two most plausible routes appear to be through exposure to urine and ingestion of raw milk.

Studies on pasteurization of raw milk and the temperature at which Borrelia burgdorferi lead one to believe that most if not all of Borrelia burgdorferi will die when raw milk is pasteurized - but I would like an expert spirochetologist to weigh in on this, though, and cover what is posted about laboratory plating requirements.

Researchers have at times speculated that sexual transmission of Borrelia burgdorferi may occur between animals, but there has been more speculation than there have been actual controlled studies to support this hypothesis.

Some of this speculation came about after finding out uninfected contact animals exposed to infected animals developed a positive antibody response for Borrelia burgdorferi as well as signs of infection. If sexual contact between these animals occurred, it was not recorded as having been observed in the holding pen/cage.

So, to answer the question about sexual transmission of Lyme disease between humans and also between animals: So far there is no evidence that it occurs. There are also few studies which test this possibility.

Thus ends another chapter in this ongoing notebook, Camp Other blog... I'm tired, I go crash now.

[Placeholder for references of all papers listed in this three part series to be added soon.]

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0 Part 2: Sexual Transmission Of Lyme Disease - Is There Evidence?

Syrian hamsters mating. From How to Breed
Syrian Hamsters on wikiHow.

This article is the continuation of "Part 1: Sexual Transmission Of Lyme Disease - Is There Evidence?", our series on sexual transmission and contact studies involving Borrelia burgdorferi.

To review the content of the first article briefly: We discussed three studies which are often used online to support the idea that Lyme disease could be a sexually transmitted disease between human patients. While two of those studies provided some evidence patients had spirochetal DNA in their bodily fluids, none of the studies provided evidence that Lyme disease is sexually transmitted by people. Setting aside the yet-to-be available Middelveen et al study, there are no studies to date which provide evidence that Lyme disease can be sexually transmitted in humans and there are very few studies which investigate this method of transmission in animals. We also had an introduction to Dr. Elizabeth Burgess' Lyme disease transmission studies, the criticism from Dr. Burgdorfer which they received, and took a glance at her study findings.

In Part 2 of this series, we'll be looking more closely at the results of  Dr. Burgess' studies and that of other researchers on contact transmission and the potential for sexual transmission of Lyme disease in animals.

The Tally So Far: Studies On Lyme Disease Sexual Transmission And Contact Transmission

So far, I have not located any studies on Lyme disease and sexual transmission in humans, and found only a few studies about human sexual secretions containing Borrelia burgdorferi DNA.

Is this lack of research on this method of transmission in people an oversight by researchers who are more focused on observing tickborne transmission? Or has the dominant view of researchers been that based on Lyme disease's pathogenesis, human sexual transmission of Borrelia burgdorferi is highly unlikely if not impossible - so why conduct more studies on it? Either way one answers, there is very little research on different transmission methods of Lyme disease in people.

What we do have are early animal studies which were designed to investigate the nature of Lyme disease transmission through various methods - methods such as: how much more effective needle inoculation was compared to tick bites in transmitting infection; injecting mice with the urine of infected cattle to see if they would get infected; a few studies where it was hoped animals would copulate and that one could determine if sexual transmission could occur.

To date, there are more animal studies which are about the potential for contact transmission of Borrelia burgdorferi -which means any kind of contact between animals either directly or indirectly via exposure to their blood, saliva, feces, urine, milk, or colostrum - than there are studies specifically about sexual or venereal transmission. It is the results of these early animal studies which were hoped would give one a better idea of whether or not other non-tickborne methods of transmission might also be possible in people, too.

Given the wide range of data available from different animal model transmission studies over a period of nearly fifteen years, I've decided to place them into a table to view them all in one place.

In general, the study data in the table below fall under the following five categories:

1. Evidence of the presence or absence of Borrelia burgdorferi in different bodily fluids of animals. These are not transmission studies. These are studies which demonstrate spirochetes or spirochetal DNA can be found in various secretions, but they do not show that such spirochetes or infection can be passed on to another host animal.
   
   
2. Evidence that the use of needle inoculation/subcutaneous injection of infected bodily fluids from animals can transmit Borrelia burgdorferi to uninfected animals and a tick was not required.
   
   
3. Evidence pointing to oral inoculation as a potential route of transmission. These are studies where the researcher deliberately tried to infect an animal with Borrelia burgdorferi (or a substance assumed to contain it) either orally or oronasally, then looked at the results.
   
   
4. Evidence supporting or rejecting sexual (venereal) transmission of Borrelia burgdorferi between studied animals.
   
   
5. Evidence suggesting that an uninfected animal became infected somehow by being housed in the same space as an animal already infected with Borrelia burgdorferi. These studies suggest that contact transmission may have occurred because no direct action was taken by the researcher to infect the control/uninfected animal, and no ticks were deliberately introduced to the control/uninfected animal.

For the purpose of focusing discussion, the table below mostly displays information related to the possibility of oral, contact, and sexual (venereal) transmission and not much transmission data via needle inoculation (though some of the studies also focus on that method of transmission and may be mentioned in passing).

Table 1: Evidence For The Presence of Borrelia Burgdorferi Infection Via Different Forms of Inoculation and Potential Contact Transmission

Year	Publication	Oral Inoculation		Contact	Spirochetal DNA	Whole Cell Spirochetes	Antibody Test	Culture/ PCR Status
1986	Experimental inoculation of dogs with Borrelia burgdorferi	N		Y	n/a	N	IFA+ n=1/1 contact  exposed dog	no PCR completed
1986	Experimental inoculation of Peromyscus spp. with Borrelia burgdorferi: evidence of contact transmission	N		Y	n/a	+ n=1/1 blood, contact mouse	Exp 1: IFA+ n=2/2 contact mice; 4 log2, 6 log2 Exp 2: +n=10/10 contact mice 4 log2-6 log2 Burgess speculates local IgA reaction possible instead of systemic IgG	no PCR completed
1986	The prevalence and significance of Borrelia burgdorferi in the urine of feral reservoir hosts	n/a		n/a	n/a	+ n=2 urine, via darkfield +n=21/22 kidneys, positive correlation w/ Babesia presence	n/a	no PCR completed
1986	Suspected borreliosis in cattle	Y cat fed infected milk		n/a	n/a	+ n=2/6 urine, via darkfield	IFA+ +n=1/1 cat fed infected milk had 1:164 titer +n=5/5 mice 1:8-1:32 titers with sc inoculation of milk +n=5/5 mice 1:32-1:64 titers with sc inoculation of urine	- cultures negative in blood, urine, and milk no PCR completed
1987	Oral infection of Peromyscus maniculatus with Borrelia burgdorferi and subsequent transmission by Ixodes dammini	Y		N	n/a	+ n=1/10 blood, + n=1/10 organs +n=1/10 blood (tick-fed) +n=1/10 organs (tick-fed)	IFA+ +n=10/10 orally infected mice +n=10/10 mice from ticks that fed on orally infected mice; 6 orally infected mice developed symptoms	no PCR completed
1988	The urinary bladder, a consistent source of Borrelia burgdorferi in experimentally infected white-footed mice (Peromyscus leucopus)	n/a		N	n/a	- 0/15 urine samples + 2/15 blood samples + tissue samples: bladder, kidney, spleen	n/a	+ tissue culture, no PCR
1988	Clinical and serologic evaluations of induced Borrelia burgdorferi infection in dogs.	n/a		Y	n/a	n/a	IFA antibody + ELISA + n=1 control dog elevated + IgG	no PCR completed
1988	Borrelia burgdorferi infection in Wisconsin horses and cows	Y n=3 mice inoculated with cow urine		n/a	n/a	+ n=2/10 cow urine + n=2/3 colostrum - all milk samples	IFA+ IgG n=2/3 colostrum titer, n=1/3 cows ~1:512 n=2/3 mice 1:64; 1:28	samples cultured, no PCR completed
1989	Experimental inoculation of mallard ducks (Anas platyrhynchos) with Borrelia burgdorferi	Y n=4 ducks		n/a	n/a	+ n=1/4 cloaca secretion, + n=1/4 kidney	IFA+ n=3/4 kidneys of orally inoculated ducks; +n=1/4 mesentery	positive cultures, no PCR completed
1990	Experimental infection of the white-footed mouse with Borrelia burgdorferi	Y		n/a	n/a	+ n=1 blood	IFA+ all asymptomatic mice	tissue culture, no PCR completed
1991	Experimental infection of dogs with Borrelia burgdorferi	N		Y	n/a	+ n=1 urine, blood of contact dog	IFA+ +n=1 uninoculated dog near 1 infected dog both asymptomatic	no PCR completed
1991	Relative infectivity of Borrelia burgdorferi in Lewis rats by various routes of inoculation	Y oronasally		N	n/a	- n=0/13 oronsally infected - n=0/6 males venereally - n=0/7 females venereally	only needle inoculated rats +	n/a
1992	Experimentally induced infection of cats with Borrelia burgdorferi	Y n=2		n/a	n/a	+ n=2 blood smear; n=1 lung	n=2 orally inoculated IFA+ n=2 ocularly inoculated IFA+	no PCR completed
1993	Detection of Borrelia burgdorferi in Urine of Peromyscus leucopus by Inhibition Enzyme-Linked Immunosorbent Assay	N		n/a	+n=57/87 whole cells or subunits in urine	+ n=57/87 whole cells or subunits in urine	+IFA +ELISA +n=47/75 serum +n=57/87 antigens in urine	+n=50/87 tissue culture; +n=36/50 infected bladders no PCR completed
1994	Experimental infection of dogs with Borrelia burgdorferi	N		Y	n/a	+ n=1/4 infected dog blood, urine	IFA+ +n=1/1 control dog, 1:128 (max titer) +n=2/2 guinea pigs inoculated with urine, 1:128	no PCR completed
1994	Distribution of Borrelia burgdorferi in host mice in Pennsylvania	n/a		Y see notes part 3	n/a	+ n=112 isolations/1619 mice (from ear tissue)	IFA+ in tick-bitten mice see notes part 3	no PCR completed
1996	Lyme Borreliosis in the laboratory mouse	-		-	-	-	- see below	-
1996	Dissemination of Borrelia burgdorferi after experimental infection in dogs	N		n/a		- n=0/6 urine culture		- culture bladder PCR completed - urine
1997	Tick-raccoon associations and the potential for Lyme disease spirochete transmission in the coastal plain of North Carolina	n/a		Y see notes part 3	n/a	n/a	IFA+ see notes part 3	no PCR was completed
1998	Viable Borrelia burgdorferi in the urine of two clinically normal horses	n/a		n/a	n/a	+n=2/5 horses, urine	+	+PCR FA on urine samples
1999	Investigation of venereal, transplacental, and contact transmission of the Lyme disease spirochete, Borrelia burgdorferi, in Syrian hamsters	N		N	n/a	-n=0/6 female hamsters, -n=0/6 male hamsters infected venereally no mice contact infected	- IFA in 6/6 venereal test hamsters and all contact mice	- tissue samples, no PCR was completed

Table Key:

+ positive - negative

n= #/# number of samples or study animals infected or not infected out of the total studied

n/a not applicable to study or no data available in given paper


Notes On The Above Table

While every effort was made for this table to be comprehensive, it may not be complete. (If you know of any additional publications and data which apply, please comment below so that I may add the paper to this table.)

Note that certain papers which have been cited online pointing to different methods of contact transmission or evidence of Borrelia burgdorferi spirochetes or spirochetal DNA in bodily fluids were not included in the above table. This is because these specific papers were either review or editorial papers which cited more than one study already included in the above table, and I did not want to give the impression that additional studies were completed where the studies and findings were reproduced by another researcher. (I do, however, mention these papers in part 3 of this series on sexual transmission.)

Note also that in certain columns data is lacking or relies on older methods:

In some studies, antibody testing was not completed on animals because the research goal was to focus on finding evidence of Borrelia DNA and/or spirochetes in a given sample and not to measure antibodies in the host animal.

In the 1980's and early 1990's, PCR studies were not performed on many samples. This is because at the time PCR was a relatively recent invention, was at first a slow and labor intensive process, and not many researchers had access to it. Also, there was some discussion over what the best method was to use on specific samples, and it hadn't been completely determined yet.

Immunofluorescent antibody (IFA) assay testing was the primary method of testing samples for the presence of antibodies, rather than ELISA or Western blot. This method has been considered less sensitive than others, but given studies listed use one or more monoclonal antibodies specific to Borrelia burgdorferi (such as H5332, specific to North American OspA) the positive results obtained are noteworthy.

So What Do These Studies Indicate or Suggest?

1.  Contact transmission of Borrelia burgdorferi could occur between specific animals under specific conditions.

While there is some evidence that some animals can be experimentally infected with Lyme disease through an oral or ocular route, it is unclear if animals end up infected through these routes in the natural world. It's important to note that dosages and the method used in a laboratory experiment may not have their parallel in real life conditions. Optimally, observing how infections occur in the wild would be best - but it is difficult to study animals in the wild to determine exactly when and how they get infected.

What the data in this table reflects is that there is some evidence to suggest that contact transmission via urine may be a concern with some animals - particularly cattle and mice. One study on ducks points to the possibility of oral transmission, though no one has duplicated it thus far or extended additional transmission research to other kinds of birds.

Based on the studies reviewed, if a form of contact transmission can occur in animals, it appears to happen inconsistently and in low numbers of animals - and so far appears to happen more frequently in specific species. Perhaps repeat studies with larger groups of animal subjects would be helpful - or perhaps they would demonstrate that contact transmission still only occurs in relatively few subjects under narrowly defined conditions. We just don't know.

There is also some evidence that certain animals are highly unlikely to contract Lyme disease via contact transmission via urine, such as Lewis rats and Syrian hamsters.

Additional autopsy studies in such cases that demonstrate where spirochetes are found in infected animals can be useful as they can indicate why spirochetes were not likely to be found in urine based on which tissues spirochetes colonized.

2.  In some cases, it is not exactly clear how contact animals were infected in individual studies. All we know is they had positive antibody tests and some showed signs of infection.

Based on the studies within the above table, the following studies resulted in at least a positive IFA result in a contact animal, and in some cases evidence of spirochetal infection:

1. Experimental inoculation of dogs with Borrelia burgdorferi.
2. Experimental inoculation of Peromyscus spp. with Borrelia burgdorferi: evidence of contact transmission.
3. Clinical and serologic evaluations of induced Borrelia burgdorferi infection in dogs.
4. Experimental infection of dogs with Borrelia burgdorferi.
5. Distribution of Borrelia burgdorferi in host mice in Pennsylvania.
6. Tick-raccoon associations and the potential for Lyme disease spirochete transmission in the coastal plain of North Carolina.

Of these studies, the last two listed above contained speculation by the researchers about whether or not mice and raccoons could contract Lyme disease through other methods outside of a tick bite - and neither of those two studies were completed under lab conditions and had control animals.

As for the remaining four studies, there is no indication exactly how uninfected control animals ended up with positive antibody tests and signs of infection when in the presence of infected animals. Apparently it has happened - but how and why it happened in a number of these studies even when animals are in captivity is unclear.

It is the unknown method of contact transmission in such studies which has led to speculation by others that sexual transmission may have occurred between animals. However, without a definite confirmation that sexual contact was the route of transmission, what happened remains a mystery.

We do not have documentation in a number of cases of whether or not infected and contact animals were housed together indoors or outdoors, or if they were isolated from birds or other environmental factors which may have introduced infected ticks or Borrelia burgdorferi. Without more data, it is difficult to determine whether or not animals may have been infected via a different route.

All the same, there is research above which indicates point #1 - that animals can be infected by other animals' secretions, although how often it happens and how is a good question. So far, urine and raw milk ingestion appears to be a plausible mode of transmission between some animals.

3.  There haven't been many animal studies specifically focused on sexual or venereal transmission.

Based on the studies within the above table, the following studies were specifically focused on sexual or venereal transmission and their results:

Title	Sexual or Venereal Transmission?
Investigation of venereal, transplacental, and contact transmission of the Lyme disease spirochete, Borrelia burgdorferi, in Syrian hamsters	- negative
Relative infectivity of Borrelia burgdorferi in Lewis rats by various routes of inoculation	- negative
Lyme Borreliosis in the laboratory mouse	- negative

Of three papers where experiments were specifically designed to see if venereal transmission occurred between animals, the results of all three were negative.

Three seems like a very small number of studies, and they were only completed on rats, Syrian hamsters, and mice. If you, the reader, knows of any additional studies on sexual or venereal transmission of Lyme disease in animals which were not included here - please comment below with the title(s) and link(s) to the paper(s).

Some Researchers Weigh In On Non-Tick Methods Of Transmission

More has been said about the methods of transmission in mice than any other animal because mice are used more extensively in a lab environment for the study of Lyme disease than any other species.

In 1996, Dr. Stephen Barthold wrote "Lyme Borreliosis in the laboratory mouse"in the Journal of Spirochetal and Tick-Borne Disease. On pages 23-24, he states:

"There has been no evidence of contact transmission or detection of viable spirochetes in urine of laboratory mice. Lung, bladder, and kidney are frequently infected, but spirochetes in these tissues are present in the connective tissue of the serosa, subserosa, submucosa (bladder), and periarterial connective tissue (lung, kidney), rather than lumina of tubules, ureters, bladder, or airways."

Based on his research up to that point in time, mice were not transmitting spirochetes through their urine to uninfected mice, and spirochetes which were found in autopsies were deeply embedded in connective tissue and not lining the vessels or surface of ureters, bladders, or bronchial tubes. In other words, if live spirochetes were present, they would be highly unlikely to be found in urine.

His findings differ from those of Dr. Burgess, and those of Dr. Magnarelli.

Magnarelli et al in the paper, "Detection of Borrelia burgdorferi in Urine of Peromyscus leucopus by Inhibition Enzyme-Linked Immunosorbent Assay" determined that 57 out of 87 mice had either subunits or whole cell Borrelia burgdorferi in their urine.

Despite this high number, Magnarelli et al cited their own difficulties in detecting evidence of Lyme disease infection in mice consistently:

"For more than half of the field-collected mice tested, there was concordance in the results of the serum antibody, culture, and urine analyses. Similar results were records for four of five laboratory-bred mice inoculated with B. burgdorferi. However, there were discrepancies. B. burgdorferi antigens sometimes were detected in urine from field-collected mice without supportive data from antibody assays or culture work. This was particularly noticeable in animals captured during October and November, a period after peak nymphal I. scapularis population levels had been reached."

The authors also pointed out that antibody-positive serum and titers can be low especially during early infection, successful culturing of B. burgdorferi depended partially on the number of spirochetes present in host tissues, and that occasionally, serum antibody analyses and culturing results were positive, while urine antigen test results were negative - antigens may not always be released into urine.

In 2001, we have what may have been the last published words from Dr. Burgess on contact transmission in the book, "Infectious Diseases of Wild Mammals" published by Iowa State University Press, chapter 26. Authored by Dr. Richard Brown and Dr. Elizabeth Burgess, the chapter contains this quote:

"Although direct transmission may occur in some situations, it has not been easily substantiated (Mather et al 1991) and has yet to be shown as epidemiologically important." 

The authors supported the idea that direct transmission of spirochetes may occur between animals under certain circumstances - but it's not easy to provide evidence of what exactly happened and it occurs in only a very small number of cases.

More recently, in 2010, in the book, Borrelia: Molecular Biology, Host Interaction and Pathogenesis by Horizon Press, on p. 381, the most recent note on transmission stated:

"Mice are also susceptible to infection following intragastric inoculation of very high doses of B. burgdorferi N40, but there is no evidence for contact transmission (Barthold, 1991) or in utero (placental) transmission, although maternal infection may cause fetal death (Silver et al, 1995; Weis et al, 1997)."

Since our focus here is on contact, venereal, and oral transmission and not maternal/in utero (a topic worthy of a post in itself), it's notable that mice can be infected intragastrically based on Barthold's studies - though it takes high doses to do so, and it is a question how likely it is such doses would be found in nature. According to Burgess, Peromyscus are apparently susceptible to oral inoculation with B. burgdorferi, since oral infection with ~400 spirochetes resulted in sufficient spirochetemia to infect Ixodes (previously dammini) scapularis larvae.

That there has been a variety of study outcomes regarding mice, transmission, and inoculation routes leads to questions about whether or not it is not just species that matters when it comes to how Lyme disease affects the host - but also the individual genetic background of the host animal.

One should take note that anyone studying Borrelia burgdorferi in wild type mice should make sure they do not use mice which are naturally resistant to infection with Lyme disease due to a particular genetic variant of the antigen receptor TLR2, because such mice can greatly affect study outcome.

Could it be that the discrepancies Magnarelli et al found in their research was due in part to the presence of mice in their study group which had this genetic variant?

Future Directions

One question this raises for some reading along is how likely is it that Borrelia burgdorferi spirochetes can be found in human urine, and is there evidence of non-sexual transmission of Lyme disease between people? This is a question that will be discussed in an upcoming blog post, as there have been a number of studies on testing human urine samples for the presence of Lyme disease.

But the main question which kicked off this post is this one: Will we have any evidence in the near future that Borrelia burgdorferi can be sexually transmitted between partners?

So far, we do not, though a recent paper by Middelveen et al, "Isolation and Detection of Borrelia burgdorferi from human vaginal and seminal secretions" is the first publication to make the claim in its abstract that live motile spirochetes have been found in vaginal and seminal secretions, and that because two partners in the study share the same strain of Borrelia burgdorferi in their secretions, odds are greater than random chance that one partner passed Borrelia burgdorferi to the other.

For these claims, I currently have no evidence. And unfortunately, my ability to give the paper a thorough review is limited without access to the full text of the paper. Once the Middelveen et al paper is out of embargo and I have read the entire paper, it deserves its own future blog entry given how important this topic has become for many patients.

To sum up: Sexual transmission of tickborne diseases - is there evidence? Answer: Not so far. But existing studies to date provide evidence that oral inoculation and urine transmission may occur in a few cases in animals.

Questions For Further Discussion:

• Why did different researchers have different results when it comes to the issue of contact transmission?
  
  
• How much did animal species play a role in the outcome?
  
  
• Why is it in a number of cases, uninfected animals exposed to infected animals had positive antibodies for Borrelia burgdorferi but were culture negative and no spirochetes could found in tissues post-mortem?
  
  
• How did duration of untreated infection in the host relate to the odds of finding spirochetal DNA or a spirochete in a given sample?
  
  
• How did the timing of testing of the host animal relate to the odds of finding spirochetal DNA or a spirochete in a given sample?
  
  
• How do methods and materials and test conditions affect outcomes (e.g. urine acids can lyse cells) ?
  
  
• How did the researchers demonstrate they had ruled out or eliminated other potential methods of transmission via experimental design?
  
  
• What - if any - connection is there between nonsexual modes of Lyme disease transmission and a sexual one?

Coming up next:

Part 3: Sexual Transmission Of Lyme Disease - Is There Evidence?

The next post will include notes on some of the above studies mentioned in the table and
additional studies which have been cited when mentioning transmission methods of
Borrelia burgdorferi. The temperature at which Borrelia burgdorferi dies
off will also be discussed in relationship to pasteurization.

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1 Part 1: Sexual Transmission Of Lyme Disease - Is There Evidence?

Male and female Ixodes ricinus ticks mating. 

A number of patients with Lyme disease have wondered if there is any other way to contract Lyme disease other than a tick bite. It's not an uncommon question to ask, given that not everyone remembers getting a tick bite, and nymphs are so small they can bite and infect someone without anyone ever knowing they were there.

Of all the questions which lead one to pause for a moment regarding the possible methods of transmission of Lyme disease, it has to be this one: Can Lyme disease be sexually transmitted between partners?

This is an interesting question, and the overwhelming majority of researchers and medical professionals out there have stated that no, Lyme disease cannot be sexually transmitted between people.

They will state other forms of transmission can occur outside of a tick bite: Borrelia burgdorferi, the bacteria which causes Lyme disease, could be transmitted between ticks while they are mating (sexual transmission of relapsing fever spirochetes also occurs between ticks). It could be transmitted between ticks during co-feeding on the same mammal. It could be passed from a mother to her child's placenta in utero during pregnancy, and in some cases, to the fetus itself. But they will state that thus far, there is no evidence that Lyme disease can be sexually transmitted between mammals including humans.

My Initial Thoughts On The Issue Of Sexual Transmission

I didn't care much about answering the sexual transmission question when I first contracted Lyme disease. Partly because I was so sick, sex was the last thing on my mind, and I wasn't up to having any. Yeah, sad but true. For the most part, I concerned myself with treatment, rest, and getting better.

Time and again, it's clear the question about whether or not Lyme disease can be sexually transmitted is important to others as it has been raised in support groups, on online patient fora, in chat rooms, and at conferences. So it's a question that keeps coming back, and now that a new abstract by Middelveen et al has been making the rounds concerning sexual transmission of Lyme disease, the topic has become the focus of discussion by the media and among patients yet again.

So I started investigating the issue of sexual transmission of Lyme disease, and while I came across a number of stories online where patients are convinced either they were infected by their spouse or had infected their spouse - actual studies regarding this phenomenon have been lacking. In reading of all the documentation on Lyme disease transmission I could get a hold of prior to writing this entry, I found one patient blog which offered a good layperson's summary of the literature regarding Lyme disease and sexual transmission: "Sexual Transmission of Lyme disease" on A Lyme Disease Journal by J. Mankoff.

Ms. Mankoff writes about the difficulty in finding scientific papers on Lyme disease sexual transmission studies using both animal and human models - and unfortunately, my own experience mirrored hers.

In doing the research for this post, I initially learned the following things about publications to date:

• Setting aside Middelveen et al's recent abstract for now, there has not been one published study which provides any evidence that live spirochetes can be passed on from one human to another through sexual intercourse or sexual contact.
• There is scant evidence that spirochetal DNA can be found in human seminal and vaginal secretions.
• There is limited evidence that spirochetal DNA can be found in human breast milk.
• There are animal studies which demonstrate uninfected animals placed in the same cages with infected animals can develop antibody responses to Borrelia burgdorferi.
• There are animal studies which demonstrate that animals infected with spirochetes do not pass them on to uninfected animals in the same cage.
• There are animal studies which indicate that the bladder and kidneys can be very good locations from which to culture spirochetes.
• There are animal studies which indicate spirochetal DNA can be high in urine samples.
• There are animal studies which indicate spirochetal DNA can be absent in urine samples.

When you look at this list, you'll notice that I went from discussing sexual transmission of Lyme disease to looking for spirochetes in sexual fluids and breast milk to looking for spirochetes in urine - probably not the direction anyone imagined I'd go. But that's because to date, more studies have been completed which indicate spirochetes are present in urine than studies which indicate spirochetes appear in sexual fluids - so I'm going to end up talking about those studies, too.

Evidence of Borrelia burgdorferi - Lyme disease DNA - in human semen and vaginal secretions

So far, while there is research which indicates Borrelia burgdorferi DNA has been found in samples of vaginal and seminal secretions, there is no research to date which has conclusively shown that live motile Borrelia burgdorferi spirochetes have been passed from one partner to another.

The distinction between having evidence of Borrelia burgdorferi DNA and having live motile Borrelia burgdorferi spirochetes is an important one: Having Borrelia burgdorferi DNA is like holding a strand of my hair in your hand - whereas having a live, motile Borrelia burgdorferi spirochete is like having me sitting in your living room drinking a beer. Hair DNA is a part of me, but it isn't all of me.

This distinction is important to remember when reviewing one of the most frequently cited papers online on the presence of Borrelia burgdorferi DNA in human vaginal and seminal secretions, "Recovery of Lyme Spirochetes by PCR in Semen Samples of Previously Diagnosed Lyme Disease Patients" presented by Dr. Gregory Bach at the 14th International Scientific Conference on Lyme Disease in April, 2001.

Unfortunately, when I reviewed all the major online repositories (Google Scholar, PubMed, Oxford Journals, etc.), this paper and its abstract was not listed anywhere and a general search outside of repositories did not point to any peer-reviewed sources. I eventually tracked down a copy of the abstract on Jenna's Lyme Blog, and am reproducing it here (with minor typo corrections) to make a few comments on it:

Recovery of Lyme Spirochetes By PCR In Semen Samples of Previously Diagnosed Lyme Disease Patients (2001)

Lyme disease, being a spirochete with pathology similar to syphilis, is often found difficult to treat due to the spirochete invading sanctuary sites and displaying pleomorphic characteristics such as a cyst (L-form). Because a significant portion of sexually active couples present to my office with Lyme disease, with only one partner having a history of tick exposure, the question of possible secondary (sexual) vector of transmission for the spirochete warrants inquiry.

Additionally, sexually active couples seem to have a marked propensity for antibiotic failure raising the question of sexually active couples re-infecting themselves through intimate contact.

METHODS:

Lyme spirochetes/DNA have been recovered from stored animal semen. Recovery of spirochete DNA from nursing mother’s breast milk and umbilical cord blood by PCR (confirmed by culture/microscopy), have been found in samples provided to my office.

RESULTS:

Surprisingly, initial laboratory testing of semen samples provided by male Lyme patients (positive by western blot/PCR in blood) and the male sexual partner of a Lyme infected female patient were positive approximately 40% of the time.

PCR recovery of Lyme DNA nucleotide sequences with microscopic confirmation of semen samples yielded positive results in 14/32 Lyme patients (13 male semen samples and 1 vaginal pap).

ALL positive semen/vaginal samples in patients with known sexual partners resulted in positive Lyme titers/PCR in their sexual partners. 3/4 positive semen patients had no or unknown sexual partners to be tested. These preliminary findings warrant further study. Currently a statistical design study to evaluate the possibility of sexual transmission of the spirochete is being undertaken.

Our laboratory studies confirm the existence of Lyme spirochetes in semen/vaginal secretions. Whether or not further clinical studies with a larger statistical group will support the hypothesis of sexual transmission remains to be seen. A retrospective clinical study is also underway.

We are reviewing the medical records, collecting semen samples of patients who were previously diagnosed with current and previously treated Lyme disease are being asked to provide semen, pap, and blood samples for extensive laboratory testing.

CONCLUSION:

With the initially impressive data, we feel the subsequent statistical study on the sexual transmission of the Lyme spirochete will illuminate a much broader spectrum of public health concerns associated with the disease than the originally accepted tick borne vector.

At first glance, someone reading this study may get excited: Hey, they found evidence of Lyme disease bacteria in semen and vaginal fluid. But on further reading, it becomes clear that the paper focuses on PCR recovery of Lyme DNA nucleotide sequences and the results of western blots - not whole spirochetes.

There are unanswered questions about this study based on the abstract: We don't know what kind of microscopic confirmation was conducted and why it was mostly conducted on semen. We don't know if patients had other possible routes of exposure to spirochetes. We don't know if the DNA sequences recovered matched between sexual partners. We don't know whether any of the patients who were sampled had recently taken antibiotics and if the spirochetal DNA that was detected was the result of their bodies trying to purge a massive die-off of spirochetes. What kind of treatment patients in the study had received so far is an unknown.

I would agree with one message in the conclusion - that additional studies on spirochetal DNA or spirochetes in sexual fluids could be informative and help confirm or deny these findings.

But finding Lyme disease Borrelia burgdorferi DNA alone in secretions is not evidence that spirochetes can be transmitted - it can be much like finding dead viral particles leaving the body of someone who recently had the flu.

And in the case of figuring out who gave a flu to who, if Jane gets the flu - she may or may not have passed on the flu to John in her office. John could have picked it up from someone else or from fomites on a doorknob. Without more data, there's no compelling evidence to suggest that his active infection traces back to Jane in particular.

The difference with a study on the sexual transmission of Lyme disease compared to transmission of the flu is that one has to demonstrate not only that the person contracted Lyme disease from a specific partner through sexual contact but one also has to provide evidence that the person did not somehow contract Lyme disease from a tick bite or by a different nonsexual mode of transmission.

To my knowledge, further clinical studies with a larger statistical group have not been conducted by Dr. Bach to support his hypothesis about Lyme disease and sexual transmission, and his 2001 study abstract leaves the reader with unanswered questions.

Here is another paper which examines Borrelia burgdorferi in human samples - but not semen or vaginal secretions:

Detection of Borrelia burgdorferi DNA by polymerase chain reaction in the urine and breast milk of patients with Lyme Borreliosis (1995)

Abstract

Current laboratory diagnosis of Lyme borreliosis relies on tests for the detection of antibodies to Borrelia burgdorferi with known limitations. By using a simple extraction procedure for urine samples, B. burgdorferi DNA was amplified by a nested PCR with primers that target the specific part of the flagellin gene. To control possible inhibition of the enzyme (polymerase), a special assay using the same primers was developed. We examined 403 urine samples from 185 patients with skin manifestations of Lyme borreliosis. Before treatment, B. burgdorferi DNA was detected in 88 of 97 patients with Lyme borreliosis. After treatment, all but seven patients became nonreactive. Six of these seven persons suffered from intermittent migratory arthralgias or myalgias, and one from acrodermatitis chronica atrophicans. Two of 49 control patients with various dermatologic disorders and none out of 22 presumably healthy persons were reactive in the PCR. In addition to urine, breast milk from two lactating women with erythema migrans was tested and also found reactive. Borrelia burgdorferi DNA can be detected with high sensitivity (91%) by a nested PCR in urine of patients with Lyme borreliosis. In addition, this test can be a reliable marker for the efficacy of treatment.

This study indicates that spirochetal DNA could be easily detected in urine using nested PCR, though today this is not a testing method for Lyme disease which is regularly used (and indeed there have been mixed reviews on how effective the use of urine is in testing for Lyme disease). While human breast milk was found to be reactive in PCR, it's important to note that no motile, whole spirochetes were recorded as being found.

While interesting, this paper does not provide evidence that Lyme disease is sexually transmitted. It only has the potential to raise - but not answer - questions about the viability of spirochetes in urine and breast milk. Additional studies would have to be completed to determine that live, whole spirochetes are present in urine and breast milk, and that transmission of spirochetes can occur via human breast milk and urine.

Others have cited a 1995 paper online as evidence pointing to Borrelia burgdorferi surviving in semen: "Viability of Borrelia burgdorferi in stored semen". That line of thinking is erroneous,  however, and to clear up the matter here:

This paper is not about Borrelia burgdorferi being found surviving in semen - it's about seeing if Borrelia burgdorferi which is manually added to semen from different animals (bull, ram, and dog) is a useful storage method. Storing Borrelia burgdorferi in semen samples is then compared to storing them in Barbour-Stoenner-Kelly (BSK) medium. Nothing in this study is relevant to providing evidence about Borrelia burgdorferi from an actual infection showing up in the host animal's semen. (And yes, I agree this is a weird experiment, and wonder what the authors were thinking when designing it - perhaps that semen's components may be nutritious for spirochetes and easier to use than BSK.)

These studies are the top three studies often cited by some to support the position that Lyme disease can be sexually transmitted between humans - however, the first two only provide some evidence that Borrelia burgdorferi DNA can be found in semen, vaginal fluid, and breast milk - while the third is only about using animal semen to store spirochetes for research purposes.

The EC Burgess Studies

One oft-cited researcher who investigated various routes of transmission of Borrelia burgdorferi in animal models was Dr. Elizabeth Burgess. Notes taken from a lecture by Tom Grier, microbiologist, at Lac Court Oreilles Convention Center said in reference to Dr. Burgess:

"Dr Elizabeth Burgess, DMV at Madison: her work has been overlooked for decades.

Her preliminary work showed that the Borrelia species of spirochete possessed some mechanism and ability to penetrate mucous membranes suggesting transmission in cattle could be through urine–to- mouth contact putting cattle at a risk, besides just ticks.

Dr Burgess’ work was harshly and unjustly criticized without investigation or inspection. A decade later we see that Borrelia is a champion at penetrating mammalian blood vessels and endothelial cells that line the blood vessels. How hard is it to imagine mucosa capillaries in cattle are exposed targets for Borrelia to penetrate on contact? Since the introduction of the veterinary Lyme vaccines, we hear little about entire herds of cattle and horses being infected."

And it's true - Dr. Burgess' work was criticized.  Some of this criticism was mentioned in an article on Lyme disease from 1989 which was published in the New York Times:

Dr. Elizabeth Burgess of the University of Wisconsin's School of Veterinary Medicine has suggested the possibility of direct spread through contaminated urine.

But other experts expressed deep skepticism about her proposal, saying further studies are needed. They also say the disease probably would not follow a seasonal pattern if the spirochete were transmitted in this way. 

''If this were true, then virtually every veterinarian and every farmer would have Lyme disease,'' said Dr. Willy Burgdorfer, scientist emeritus at the Public Health Service laboratory in Montana. Dr. Burgdorfer led the team that in 1981 isolated the spirochete, which was named for him.

That same article later goes on to discuss the possibility of ticks spreading Lyme disease via migratory birds, with Dr. Burgdorfer then saying that ''just because they can be carried on birds does not mean that ticks will spread to every corner of the country.''

Since this article's publication in 1989, numerous scientific studies have provided evidence that migratory birds spread infected ticks to various corners of the country as well as to neighboring Canada. Dr. Burgdorfer has presumably revised his view on the role of migratory birds in spreading Lyme disease given these studies.

But as of this writing, it is unknown if his criticism of Dr. Burgess remains the same. And to some degree, Dr. Burgdorfer's statement on record at the New York Times is interesting from a historical perspective because in 1989, he had co-authored a paper with Dr. Tom Schwan about the utility of culturing Lyme disease from mouse bladders and how spirochetes were not found in the urine of the mice they studied - but by 1998, he co-authored a paper about tickborne relapsing fever, citing a Linnemann et al paper from 1978 mentioning that Borrelia spirochetes could be found in the urine of human patients with acute relapsing fever.

One interesting note about Dr. Burgdorfer's paper co-authored with Dr. Schwan: He cited an earlier 1986 study by Bosler and Schultze, "The prevalence and significance of Borrelia burgdorferi in the urine of feral reservoir hosts" (mentioned in table in part two of this blog post) where 50% of the mice studied from Shelter Island had evidence of Borrelia burgdorferi in urine, but it was thought the reason that they were that highly spirochetemic was because 95% of the mice were also infected with Babesia.

With this knowledge, I wonder if at some point years after his interview with the NYT, if Dr. Burgdorfer sat down with Dr. Burgess and discussed her work over a cup of coffee while they were both working on the Journal of Spirochetal and Tick-borne Diseases for the now retired Lyme Disease Foundation, and what conclusions they shared regarding the presence of spirochetes in urine samples. Did they discuss the role of Babesia in the presence of greater spirochetemia and spirocheturia in mice?

But I digress...

What did Burgess study? Burgess was known for her work on two infections - primarily duck plague virus, caused by anatid herpesvirus 1 - and Borrelia burgdorferi infections in a wide range of animals from cats and dogs to livestock; from black bears to coyotes. She was first author on 20 papers and co-author on 16 additional papers that I could find. This was her career, her lifeblood, and a record of her work can be viewed on Google Scholar.

Her most notable works related to Borrelia burgdorferi transmission in animals are:

• 1986 Experimental inoculation of dogs with Borrelia burgdorferi 
• 1986 Experimental inoculation of Peromyscus spp. with Borrelia burgdorferi: evidence of contact transmission 
• 1987 Oral infection of Peromyscus maniculatus with Borrelia burgdorferi and subsequent transmission by Ixodes dammini
• 1988 Borrelia burgdorferi infection in Wisconsin horses and cows
• 1989 Experimental inoculation of mallard ducks (Anas platyrhynchos) with Borrelia burgdorferi
• 1992 Experimentally induced infection of cats with Borrelia burgdorferi

I tried to track down Dr. Burgess to ask her about her work, but this task was not successful; she appears to have retired and does not have an active online presence. However, I was able to acquire copies of the full text of her papers for my own review.

Dr. Burgess' studies suggest that contact transmission from infected animals to uninfected animals can and does occur, though not consistently - and that even if there is no evidence of spirochetes being transferred from infected animals to uninfected animals, that uninfected animals housed with infected animals develop a positive antibody response to Borrelia burgdorferi. Her research also indicates that spirochetes can be found in animal urine and it is suggested that oral contact with that urine could lead to infection.

Her findings - now as they were then - have been considered by some to be controversial. Other researchers have conducted similar experiments and their results conflicted with those of Burgess. Or  they had negative results after running similar experiments using different animal models - which indicates that perhaps the ability for an animal to either transmit Borrelia burgdorferi via oral/urine contact or contract it that way is entirely species dependent.

Coming up next:

We'll take a closer look at suspected cases of contact transmission between animals infected with Borrelia burgdorferi and uninfected animals, and how these cases may have led to the question of whether or not sexual transmission of Lyme disease between animals occurred in Part 2 of "Sexual Transmission Of Lyme Disease - Is There Evidence?"

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0 Admin Note: Pardon The Mess...But I'm Changing The Blog

You might have noticed that this blog has had its format changed a lot in the past 24 hours. Apologies to anyone who found it disorienting, but it was something that had to be done.

Initially my intent was to do one thing and one thing only:  make room for an upcoming post which contains a wide table that wouldn't fit in my 3 column format. So I began pushing the links and widgets from two separate columns into one column so I could have a wider area for posts. Then I realized that it took much longer for the page to load, and there was a big white space below the posts next to the giant list of links I was forced to make when moving them all into one column.

Suffice it to say, one thing lead to another and before I knew it, I was more than halfway through an overhaul of the site's layout.

So here we are... I'm not sure I'm done with it (though hopefully close to it) and if you're a regular reader of this blog, it might be useful for me to point out what these changes have been, how they might affect you, and my thoughts on any near-future changes:

The logo has taken a vacation.

It's nothing personal, it just needed a break (as I have as well) and was tired of holding up the top of the page. So I took it offline, where it has decided to go off to a spa in Bayern, lose some weight, and promised to introduce me to some new friends. (I'm not sure what to make of this, but at any rate, hopefully our new logo will come back, refreshed and resized.)

"Posts people are reading this week" list was removed.

The posts which were on that list were there mainly because people found them through a search engine or were already familiar with the blog and came back for a second look. Few people used them to read an older post, and more than half of my readers are regulars looking for new posts. Given this, I decided to retire this list.

The long list of blog post links which bordered the left side of the page have been moved.

They have not been deleted, they now live on their own page which is linked to on the toolbar at the top of this page: Popular Posts.

Interesting as they were, they began slowing down the loading of this page and their presence prompted me to install a third column to the layout in the first place - which I now realize was a dumb decision if I ever intend to put tables of data on my blog or perhaps might want to post a diagram, scientific illustration, web comics, or a video with large dimensions. (The table on this page about tickborne disease transmission times already looks better.)

Sometimes less is more. So right. Gone.

<<  The "view all posts" link is gone, along with its cool retro graphic. 

Sorry, it just had to go. I hadn't clicked on it in a while, but a few days ago I tried it and found out it didn't work. It didn't work on my laptop, it didn't work on phones... it didn't work on anything. I don't know if Blogger decided to no longer support this feature or if it just stopped working with my blog once it reached a certain number of posts. Either way, it isn't working so it's gone.

If you used it a lot (or even at all), I recommend that instead you either search for a blog on a given topic by using the handy search tool on the sidebar or scroll down and browse the archives to find a specific blog post.

The blog rolls for science blogs and Lyme disease patient blogs (relocated to the footer below) now display the 5 most recently updated blogs. 

I have had a hard time deciding what to do with displaying blog rolls - particularly patient blogs. Two of the blogs on my patient roll as of this writing are no longer writing about Lyme disease. They have moved on, which is great news - but I'm not sure whether to retain their blogs since they are either unlikely to be updated or will be off topic. My compromise for the time being was to set the blog roll widget to only display the top 5 most recently updated blogs and the rest remain behind a link, where if you want to see them, just click it and the rest of the blogs - outdated as they are - will display.

It may be that I end up removing some of the blogs from my rolls and replace them with others. I haven't decided yet, but I could use recommendations for good blogs by patients about science and chronic illness management in general to add to the rolls. I've been thinking broadening the category from "Lyme disease patient blogs" to something more general about chronic illness (but which is still focused more on Lyme disease and other tickborne infections). Nothing solid yet. Update: I added "chronic illness" to the blog roll title, and PhDisabled blog.

Future changes?

I don't plan on making major future changes after this any time soon, unless one counts refreshing the logo (or header and logo area, to be precise) as a major change. My basic aim lately is to simplify everything, though, so you can at least make some predictions what direction near-future changes in the design and layout of this blog will be.

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5 On Stephen Hawking, Disability, and Capability: What Are Limitations?

A few months ago, I read an article in The Telegraph about a doctor in the UK who made a statement about how people who receive disability benefits should not because if Stephen Hawking could work, then pretty much everyone could work.

The Telegraph quotes Dr. Peverley, who practices in Sunderland, England:

“We are, as a profession, dedicated to making our patients as healthy as possible, and yet a proportion of punters are hell bent on trying to prove they’re really ill, and need us to confirm it." 

“The fact is, nearly everyone is capable of some kind of work. I had considered, at one point, putting up a portrait of Professor Stephen Hawking in my consulting room with a caption that said, ‘This bloke is not on the sick’.”

Dr. Peverley is one of a number of doctors and politicians who have been engaged in a strange war on the disabled in the UK. This war began during Prime Minister David Cameron's term in office, and has been reflected in the hiring of private firm, Atos, to complete disability assessments on new patients and reassess those already disabled for the purpose of getting them off a disability pension and put them back to work.

In theory, getting people with disabilities back to work who are capable of work sounds good. One problem is, though, that Atos doesn't appear to be doing a good job of determining just who is eligible to work again and who should remain on a disability pension.

Since 2008, Atos has conducted more than 1.5 million disability assessments. However, during this time there have been more than 600,000 appeals at a cost of £60 million. A number of these appeals were based on reevaluations of disabled people who were in fact still quite disabled, but their new evaluation forms were filled with erroneous or incomplete information which did not characterize patients' degree of disability properly.

One doctor, Dr. Greg Wood, who used to work as an evaluator for Atos became a whistleblower. When interviewed by the newspaper he revealed that he had been not only encouraged - but ordered - to downplay the severity of patients' disabilities or misstate their limitations so as to get them off the disability pension rolls.

Which brings me back to Dr. Peverley. Dr. Peverley sounds like the kind of doctor who would comply with whatever Atos asked him to do in order to get patients off disability and return them to work, no matter how sick or how poorly suited to work they would be.

The Telegraph article later states, regarding Dr. Peverley:

He said that being declared “fit to work” did not mean patients had to do a laborious job.

“Being found fit for some kind of employment by Atos does not mean you’re necessarily capable of being an FBI agent or a lumberjack”, Dr Peverley said.

“However, you might be able to work at a desk on a telephone, or hold a lollipop on a zebra crossing."

On one hand, he makes a good point: Many people with disabilities and chronic illness can do something and many are not completely incapacitated. They may be disabled in some way, but they are capable of completing a task.

On the other hand, he entirely misses the point that being able to work at a regular, part time or full time job is not just about being capable of doing a task once or even here and there - it's about being able to consistently perform certain tasks repeatedly on a regular basis, typically daily, often at long stretches of time without a break. And to do so in a workplace which may only allow you a minimum of flexibility in your work hours and may or may not permit you to work from home at all.

Stephen Hawking, in a short BBC interview about his autobiographical film, Hawking (by Vertigo Films - not to be confused with the film, Hawking, starring Benedict Cumberbatch), discusses his own disability and his view of it includes acknowledgments which Dr. Peverley does not make:



Stephen Hawking acknowledges that in his situation, he was very fortunate that his disability in some ways has been an asset which allows him to avoid teaching or attending more boring committee meetings so he can spend more time doing his own research on theoretical physics. He admits that because he cannot talk to people quickly, he tends drift off on a mental tangent about some aspect of physics while around other people. He also acknowledges that with his kind of disability, it has not been a drawback to working in his field because he can do theoretical physics in his head. His physical capabilities aren't necessary to do his work.

Stephen Hawking recognizes his good fortune despite his misfortune - of this it's quite clear. And it's this message he wants everyone watching to hold on to. But he also states that some of his good fortune has been due to the support and love of his family and friends, his upbringing, the opportunity he had to get a solid education until his physical condition began to deteriorate, the care he received for many years from the National Health Service, and the fact that his condition has been a form of motor neuron disease which has given him a chance to go deep into his mind to explore new concepts while outliving doctors' expectations about his lifespan.

It might have been more traumatic for Stephen Hawking to have lost his cognitive capabilities than it was to have lost his physical capabilities because his life up until the point his condition began to worsen was already about academia, about learning and innovative thinking.

Only Stephen Hawking can really say what his choice would have been if it were given to him - I'm just guessing. But it's very clear that his complex internal mental world is where he lives, works, and plays - and if that were to be cut off from him, depression and losing the will to live might follow. This world is a big part of who he is.

Stephen Hawking is visibly physically disabled. And yet he has certain abilities others with different disabilities do not have: He can see, hear, communicate with others on and off the internet, and think clearly and rationally. He can create whole models of the Universe inside his head. He can sleep 8 hours a night, wake up refreshed, and get around with the assistance of a wheelchair and a personal assistant. While he is physically impaired, others act as his physical extensions to care for him - whether it be eating, bathing, dressing, or using the toilet. With such support, he can focus on his work.

But just because Stephen Hawking can do what he does does not mean all people with disabilities and chronic illnesses can do what he does. No one would expect someone with short term memory problems and difficulty learning and retaining new information to be able to explore problems of theoretical physics in their head any more than one would expect Stephen Hawking to start washing windows and painting the trim.

I can think of any of a number of disabilities and chronic illnesses which could impair people to the degree that a regular part time or full time job would be impossible for them. Those with severe anxiety, severe depression, bipolar disorder, or PTSD can be so overwhelmed by managing their condition that at times it is enough work just to get through the next hour - let alone day or week. Those who have cancer and have many side effects from chemotherapy and fatigue may not be able to work. Those who have frequent flareups of autoimmune diseases or have conditions which require multiple surgeries over time and recoveries and/or multiple regular tests and scans every week or two may not be able work. Those who have more than one medical condition to manage may end up spending so much time and energy in their management that it would interfere with working.

Some disabilities and illnesses get in the way of accomplishing things in a number of spheres in life more than others. Some disabilities and illnesses are more disruptive or have the potential to be more disruptive than others for holding down a regular job with regular hours and regular deadlines.

It is this last bit around which I think Dr. Peverley - and those like him - has a blind spot: The issue of employment being contingent upon consistency and reliability.

When it comes to someone being disabled or chronically ill, their capability and consistent ability to do work is different from their disability or illness. In the UK, the 2010 Equality Act defines disability as “a physical or mental impairment that has a ‘substantial’ and ‘long-term’ negative effect on your ability to do normal daily activities.” This definition covers a wide range of conditions, from mental illness and learning disabilities to chronic physical illness and long term physical impairments.

Sure, someone with moderate myalgic encephalomyelitis, fibromyalgia, or chronic Lyme disease might be able to hold up up a sign as a crossing guard for a few minutes one day. But can they do it for the next fifteen minutes? Can they do it for three hours a day? Can they do it for three hours a day, five days a week, for ten months of the year? If they can't - and an employer witnesses that their crossing guard begins to fail to carry out this supposedly easy task (easy for whom?) by leaving their station early or calling in sick too many days in a row, then they will not be a crossing guard for long.

Even if this crossing guard job were a job one could do, how on earth could it provide the disabled or chronically ill individual with enough financial support to keep a roof over their head? In all reality it can't, and so even if one could work 15-20 hours a week, within one's maximum capacity for work under the best of conditions, the wages earned from being a crossing guard are small. Anyone doing such work would need additional forms of support. And even if the disabled and chronically ill individual were to be capable of this type of job, one has to consider as an employer, if your employee will be capable of doing such job for at least an intermediate length of time if not the long run - and if one is a disabled or ill employee with such job, whether doing such a job with such frequency will have a negative impact on one's health.

The same applies to Dr. Peverley's assumption about anyone with a disability or chronic illness being able to hold down a desk job. Maybe some people with disabilities or chronic illness can. Maybe some people can't. In this Telegraph article, Dr. Peverley makes it sound as if everyone can and this, again, brings up the same issues that the crossing guard job has: Someone could have trouble sitting for long periods of time due to pain and fatigue, someone could have trouble consistently performing other duties required of the job due to their individual disability or illness.

In all of these situations, Dr. Peverley overlooks two realities:

One is that the way most work is organized is that there is a daily routine and expectation where - no matter what the job is - employers want employees who will be able to show up to work on time, work at a consistent level, leave work at a certain time (often later than originally intended), work day in and out, and meet deadlines at regular intervals.

Two is that in many ways, being disabled or chronically ill can interfere with this very structure of expectations and routine around which work is organized, and because of this, employers who fear the disabled or chronically ill will not meet expectations can either discriminate against hiring those who are visibly disabled or chronically ill, and/or more easily let go of employees with disabilities and chronic illnesses if simple accommodations aren't enough to help the employees accomplish their jobs under existing terms.

The missing piece that would help empower more disabled and chronically ill people enter the workforce that is currently not part of our modern workplace culture is to adapt jobs and adapt workplace infrastructures to accommodate the person who is disabled and/or chronically ill - not the other way around.

The situation for many disabled and chronically ill people is that they may not work at their best under circumstances which are normal and typical for the average able-bodied, healthy worker. In order to empower those who can work to some degree, the best accommodation comes from acknowledging the person with disability or chronic illness' circumstances and work with them to create a suitable position and environment.

In this respect, Stephen Hawking has the kind of support that many people with disabilities and chronic illnesses do not: Throughout the film of his life, people value Hawking's opinion and ideas and bend over backward to accommodate him, with graduate students often also serving as personal assistants early in Hawking's career. As time goes on, hired nurses and assistants take their place. Personal care, assistive technology, and Hawking's research position are all created specifically to support him in doing his work as much as it is possible - rather than having Hawking be given only a few accommodations which might make the simple act of living possible.

People with disabilities and chronic illnesses who could work and contribute something to society are better able to contribute if society as a whole begins to integrate a concept of working with disabilities and chronic illness into existing economies and workplaces. Workplaces and technology can evolve to create jobs which empower those with disabilities and chronic illnesses to work as much as it is possible.

Rather than have the standard job with typical requirements and routines, jobs would have to be created which disabled and chronically ill people can do which do not rely on consistency or on meeting deadlines at regular - often short - intervals.

Jobs and workplace infrastructures would have to be created which can flex around the circumstances of a person's reality, strengths, and weaknesses - rather than to try to shoehorn the disabled or chronically ill person into a job and workplace which permits a few small changes that help accommodate the person to try to work at the job in the same way able-bodied and healthy people do.

The support should be there to accommodate people in reaching goals whether or not they conform to standard workplace expectations. And not to do so in order to make the Dr. Peverleys of the world shut up and feel righteous about their idea that those with disabilities and chronic illnesses should be able to get off disability pensions and work - but to empower anyone to pursue goals, to follow dreams, to have some hand in supporting themselves and having a sense of a future despite the cards they've been dealt.

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