Shame: the elephant in the room
BMJ 2002; 324 doi: https://doi.org/10.1136/bmj.324.7338.623 (Published 16 March 2002) Cite this as: BMJ 2002;324:623All rapid responses
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It is important to make the distinction between these as they are
often used interchangeably and frequently incorrectly.
Shame is and external issue whereas guilt is personal internal and is
therefore not visible but it may have the same effect on the 'shamed'.
There are cultural differences. In certain parts of the world shame or
face are the most serious of 'deficiencies' and often linked to honour.
Guilt may appear a non issue and with seemingly no noticeable effect on
the individual There may even be a sense of achievement in managing to
avoid detection.
Competing interests:
None declared
Competing interests: No competing interests
The entire Endocrinological world should hang their heads in total
shame at the way they treat Thyroid patients and ignore with contempt
their ongoing suffering
The obstinate insistance that Thyroxine / Synthyroid and Thyroid
Blood tests especially TSH are PERFECT and must be defended at all costs
is doing a huge diservice to countless millions of suffering patients
Those very few enlightened Doctors who have dared to speak out on the
subject and use lateral thinking or unconventional treatments/ medications
on their patients and have suceeded in restoring to health those patients
whom the Establishment Endocrinologists have thrown on the scrapheap have
been witchunted into oblivion by sheer jealousy of success and an arrogant
refusal by the Establishment to admit that they are WRONG
Far far too many thyroid patients are "Sick and tired of feeling Sick
and Tired " on useless Thyroxine
Start giving them T3 or Armour Thyroid and just see those patients
regaine their lives
Then reinstate pioneering doctors who showed the way back into a
profession they loved and a disease they actually understood
Competing interests: No competing interests
It's been ten years since
I worked with
syphilis, so I may be a bit rusty, but I seem to recall that with
or without treatment,
blood titers of antibodies to Treponema pallidum slowly fall over
time.
With proper treatment of 2.4 mu benzethine penicillin, one shot in
each buttock, the
syphilis bacterium dies and there is no need for the body to
continue to produce
antibodies, because there is no antigen present to trigger the
immune response.
Without treatment, the immune system does successfully suppress
the syphilis bacterium,
though not totally. Due to this partially-successful defense,
again there are lower
levels of antigen and antibody titers decline, though more slowly
than with successful
treatment.
I do not think syphilis co-infection is a necessary co-factor for
HIV infection to
progress to AIDS. There are far too many cases in which syphilis
was not present, yet
which have progressed to AIDS.
I think HIV is quite sufficient by itself to cause AIDS, and needs
no cofactors
whatsoever. All people are resistant to HIV infection,
to varying degrees,except those rare people born with no functioning
immune system.
The human immune systems does successfully suppress HIV
infection after a couple of
months following initial infection, as do monkeys infected with their
species' SIV, or other mammals infected with various other lentiviruses.
This is why rates of HIV transmission through sex are extremely
high (one out of three
exposures) during early HIV infection, when the virus is still
replicating unchecked,
and extremely low during the period after primary infection, when
the immune response
has partially controlled the HIV infection. This phenomenon was
clearly shown by the
work of Christopher Pilcher's team at UNC-Chapel Hill last year,
and by others.
Interestingly, the same is true of syphilis. Rates of transmission
of syphilis are
extremely high during the sympomatic primary and secondary stages,
the first couple of
months after initial infection. Once the immune system has begun
its defense against
Treponema pallidum, syphilis is basically non-contagious, as is
HIV, except that HIV is
still highly contagious through blood transfusions, sharing
contaminated needles, etc.
I suspect the same is true of many other diseases as well. That is
why I've been such
an early and vigorous advocate of immune-based therapy for HIV,
because the immune
system is capable of suppressing the infection quite well in many
people.
But the immune therapy must be systematic, comprehensive, and
strain-specific, and must
be continually altered to account for the escape mutant viral
quasispecies of HIV which
will inevitably arise in the infected host.
I attempted to account for this problem in my 1992 model for
treatment of HIV and other
viral diseases, which is on the following website:
I suggest this approach to treatment for viral infections, including
HIV.
Sincerely,
Gary James Minter
founder and volunteer, TEST
Truth and Ethics in Science and Technology,
Research Triangle Park, NC, USA
garyjminter@alumni.duke.edu
www.minter-g.com
disclaimer: the opinions expressed in this letter reflect those of
the author and not of his employers.
Competing interests: No competing interests
Mitch Abrahams - 25 March 2002 - writes about his middle-ground
position where HIV is neither 'sole-cause' nor 'non-existent' in relation
to AIDS, he however makes an awkward comment in relation to AIDS in
Africa.
He seems to promote the idea that some action should be taken against
this 'unknown' disease in Africa, though it is uncertain exactly what
action he would suggest should be done. It appears as though he's
advocating that this action should take place in precedence over
determining the actual cause of the death and sickness. This I find
totally irresponsible. He only needs to put himself in the following
position to see how he would feel...
"You go to see your doctor, but unfortunately there is no-one you can
speak to. Fortunately though, you're in luck, because there's a very
qualified team of doctors and statisticians from the first world who are
sitting at a desk with a fancy computer behind a large glass window. All
you need to do - along with everyong else from your village - is stand in
line and walk past the window. Then, come back tomorrow once they've
analysed the results of the (visual) test and developed the latest and
greatest cure for your illness - One pill to cure all ills! Don't worry if
it doesn't work, or makes you feel even more sick, they'll come up with a
new 'better' pill soon enough."
Africa's problems are great:
* They've got bigger things to deal with than AIDS - how about
poverty first? Then development that creates jobs, health and education?
Of course, in the meantime you still need to make sure they have the
medication for REAL, TREATABLE, IDENTIFIABLE diseases like TB, maleria,
syphalis, etc.
The only pill that will cure Africa is the triple-cocktail-therapy
of:
* CANCEL THIRD-WORLD DEBT,
* PROVIDE RELEVANT INVESTMENT FOR DEVELOPMENT,
* ENSURE CONTINUED EQUAL FAIR TRADE.
After all, it's the pill that first-world countries offer to their
citizens and neighbours all the time.
ALSO;
Munir E. Nassar M.D. - 26 March 2002 - writes that "blame" is a
better word than "shame" if applied to who he sees as the problem -
researchers and pharmaceutical big-business (not physicians).
I can't see how physicians get to avoid blame. A lawyer who advises
a client on old or not-quite-up-to-date law cannot claim ignorance when
the client blames him for shoddy work. Similarly, it is physicians'
responsibility to keep informed of ALL areas of research pertaining to
their skills as well as the GOOD AND BAD of drugs available (not only
those that big-business markets). It is surely the physicians'
responsibility to know what others are saying about the efficacy of drugs
- not only what the pharmaceutical firm tells them.
Further, I don't think that society (NOTE - and therefore also the
individuals in society) should take blame in those places where society
has set up organisations to provide assistance to physicians in keeping up
to date with medical developments (in both formal research and practical
consensus remedies). Provided that there are also organisations that
provide assistance to patients in recognising where and when they might be
getting bad advice from physicians, drug companies and the general media.
Phew... what a lot to say!!
Competing interests: No competing interests
The "rapid response" by John Scythes to this article has 87
references. This is more than the average review article in a specialist
journal. Whilst it is undoubtably of interest to a specialist, as a letter
to a general medical and lay audience, surely this is somewhat over the
top.
No competing interests.
Competing interests: No competing interests
Professor Davidoff is quite right to point out that great harm is
often done by inappropriate treatments whose safety and efficacy were
established as often by anecdotal evidence than by rigorous review. We are
now learning, for instance, that the coxibs that selectively inhibit
inducible prostaglandins also inhibit a physiologically important pathway.
Parts of the COX-2 pathway are physiologic - especially for kidney and
heart function - and therefore not only pathologic. This has led to
ongoing changes in the guidelines for selective COX inhibitors.
With respect to harm, some of the earlier hypoglycemic drugs may be
similar to the triple-drug anti-HIV therapies now used in the developed
world to treat AIDS. In fact, the harm from HIV treatment may turn out to
be a much bigger tragedy than that from older hypoglycemic drugs,
selective COX inhibitors, or for that matter, treatments like out-patient
anti-arrhythmics and all the teratogens. AIDS physicians spend far too
much of their time managing the often horrific side effects of the current
anti-retroviral regimens, such as dislipidaemia, hypertension,
lipodistrophy, heart attack, stroke, kidney failure, cytochrome P-450
interference/liver failure, fatigue, anaemia, depression, etc.
In addition, these regimens, while seemingly reducing the number of
deaths in the short-term, have resulted in unusual and unexpected changes
in AIDS-defining events. (1, 2) This has cast confusion as to when - or
even if - to initiate these triple-drug treatments. (3) We may be
witnessing a repeat of the situation with zidovudine ten years ago when,
despite early hopes, the largest and longest study in asymptomatic
individuals with HIV demonstrated little - if any - survival benefit, (4)
with the earlier higher dosages causing substantial morbidity.
The lack of progress in achieving sustainable benefits with the HIV-
based lifelong regimens, and in developing an efficacious HIV vaccine, has
led AIDS "dissidents" such as David Rasnick and Peter Duesberg to posit
that the aetiology of AIDS needs to be re-assessed. They point out that in
some contexts HIV/AIDS appears to be quite difficult to transmit. They
cite the lack of evidence for heterosexual transmission of T-cell subset
abnormalities from hemophiliacs to their spouses, (5) as well as the
recognized absence of HIV seroconversion or AIDS among health care workers
with documented percutaneous HIV injuries. (6, 7) Later studies suggest
this phenomenon may in fact represent natural immunity to HIV, as
evidenced by high levels of HIV-specific CD8-bearing cytotoxic T-
lymphocytes. (8-10)
However, in the well-studied male homosexual cohorts in the
industrialised West, AIDS does seem to be overwhelmingly associated with
sexual transmission. This is why most HIV treaters, and even some AIDS
dissidents, (11) while acknowledging gaps in our understanding of
pathogenesis, cannot reconcile the Duesberg/Rasnick non-infectious
aetiology (based on drugs and malnutrition) with the many multi-partner
homosexual men who apparently share only sexual exposure as an AIDS risk.
Aetiologic hypotheses may therefore need to be expanded to include
other immune regulating infectious diseases that could be a co-factor for
the nearly irreversible loss of CD-4 helper cell-driven anamnestic
responses in AIDS. (12-15) The resulting down-regulating cytokines from
such a disease, transmitted through blood products - cytokines which would
escape viral inactivation techniques - could then contribute to the immune
suppression in transfusion cases, in coagulopathies and globinopathies,
(16-19) and in mother-to-child AIDS, given the intimate relationship
between the course of disease in children and the severity of the disease
in their mothers. (20) Chronic exposure to these immuno-regulatory
molecules from infected individuals - whether transmitted during ongoing
haemophilia treatments, breast-feeding, or immune system ontogeny in utero
- may well play as important a role as HIV in the induction of AIDS.
In the industrialised West, the most likely infection that could best
set the stage for the immunology seen in HIV/AIDS, (21-29) often
undetected and untreated (30-33) among homosexual male blood donors
preceding the modern AIDS epidemic, is Osler's Great Masquerader -
syphilis. Both the Olso (34) and Tuskegee (35) natural history studies of
untreated syphilis, as well as many other authors, (36-49) have raised the
likelihood of excess mortality from long-standing untreated syphilis, i.e.
deaths not associated with late lesions but due instead to pneumonia,
consumption and cancer. This idea faded into the background, however,
amidst the euphoria surrounding the efficacy of penicillin in early acute
syphilis.
It is generally accepted today that current syphilis screening
techniques are sufficiently sensitive to diagnose the disease in HIV-
infected persons. It should be noted, however, that the current concept
for detecting syphilis in most of the world is still based on the
Wassermann reaction. This was first developed in 1906 to detect non-
specific auto-antibodies to cardiolipin extracted from liver emulsions of
still-born syphilitic babies. Despite a strong correlation between
reactivity in this non-specific screening assay and symptomatic or acute
early syphilis, this indirect method is not sensitive for assessing
prevalence of the disease as a whole, nor always reliable in detecting the
incidence of the acute infectious stages. (50-52)
To make matters worse, these anti-lipoidal tests (including the
modern reagents used today) have never worked well for re-infection. This
was demonstrated by several experimental investigators in the 1940s and
1950s, using both animal and human subjects. (38, 53-58) In some of these
models, infection and/or re-infection with T. pallidum was symptomless and
often produced no reaction in the Venereal Disease Research Laboratory
(VDRL) test, i.e. the sensitivity could approach zero, despite proven
dissemination of T. pallidum. Patients who no longer react to re-exposure
in the VDRL these days are perhaps "syphilised", to quote a term first
coined by Joseph Auzias-Turenne (1813-1870). He observed that after
catching syphilis a few times, the classical symptoms were never seen
again. (59, 60)
An elegant summary of this ongoing phenomenon was made a century
later by Evan W. Thomas, one of America's greatest authorities on
syphilis: "Within 2 years after infection, untreated syphilis produces
immune changes in the host which, with rare exceptions, are permanent and
make it impossible for tissues to react to subsequent infection with
development of early syphilitic lesions." (50) Thomas made this assertion
after following over two thousand treated patients in New York City, where
he saw only one exception to this rule. The introduction of penicillin did
not alter this finding. This failure to develop early lesions again upon
re-exposure has important implications for the reliability of the non-
treponemal tests, which have been widely trusted for decades, including in
populations at risk for multiple exposures.
Investigators have repeatedly issued warnings about the very high
rates of syphilis among multi-partner homosexual men. (61-63) Classical
understanding teaches that the specific treponemal antibodies (as measured
by the TPHA, FTA-Abs, and TPI assays) remain for life in virtually all
individuals with secondary or later stage syphilis - treated or not. Given
the overwhelming epidemiologic correlation between syphilis and HIV, (64-
66) it follows that there should be a high rate of treponemal antibody in
this population.
To test this assumption, back in the late 1980s investigators at the
Toronto Hospital began screening HIV-infected men - presumably at great
risk for syphilis - using quantified treponemal tests. They found, much to
their surprise, precipitously falling titres of these specific antibodies
to T. pallidum among many of these men, often in the absence of any
evidence of syphilis diagnosis or treatment. (67, 68) Of the 500 HIV-
positive men ultimately screened, not one reacted in the VDRL test. (69)
The sero-reversion of treponemal antibody, which has been reported by
others, (70-72) is found often among men who never knew they had been
infected with syphilis. This loss of antibody also appears to be selective
within the polyclonal activation associated with progressive HIV
infection, (68, 73) i.e. antibodies to other infections remain at the same
levels. This could be due to chronic persistence of the disease in spite
of treatment, (74) or symptomless reinfection. Whatever the mechanism, it
remains unclear why syphilis never behaves as an opportunistic infection
among HIV-coinfected patients. (75) Or is HIV, as some have suggested, (76
-78) the actual opportunistic infection here?
Some HIV patients who have no history of treated syphilis, nor recent
VDRL reactivity, have been found with T-cell-independent IgM responses to
T. pallidum, suggesting an active infection. (79) This finding was
recently documented again in Toronto. (80) Using recombinant T. pallidum
antigens and SDS-PAGE, investigators here screened 557 random, non-nominal
specimens from clinics serving high-risk homosexual populations. They
found 27 cases of syphilis, i.e., a prevalence of nearly 5%, in stark
contrast to the Ontario annual incident rate of under 0.001%. Furthermore,
56% (15/27) had detectable anti-treponemal IgM. Only 33% (9/27) were
detected by the MHA-Tp (equivalent to the European TPHA) at the standard
cut-off, and none were VDRL-positive. This may suggest defective antigen
processing. Sexual contacts had never been traced for 74% (20/27) of these
newly-identified latent cases, nor likely ever will be.
These diagnostic concerns may well extend beyond the HIV/AIDS
context. The Ontario Public Health Laboratory, as a syphilis serology
reference lab in North America (along with those of James N. Miller at
UCLA and Sandra A. Larsen at the CDC), banked many biologic false-positive
specimens collected during routine screening. In other words, the
specimens reacted in the VDRL, but were non-reactive in the standard MHA-
Tp confirmatory test. However, applying the newer standard described above
to 119 specimens, the Ontario lab flagged 11 as possibly syphilitic. Six
results were equivocal, and five were indubitable positives by Western
Blot. (80) The families, contacts, and individual patients have not had
the benefit of this knowledge. At least one other center has documented
this problem with false-negative treponemal testing in HIV injection drug-
users. (81)
It is therefore urgent that clinicians worldwide re-screen all their
patients - including those without HIV - for treponemal antibody using
better tests until revised guidelines are issued. A better understanding
of the treponematoses, such as syphilis, will then likely become an
integral part of AIDS care. An improved detection system should ideally be
based on batched recombinant treponemal antigens. (82) Confirmation of an
inappropriate immune response to syphilis can then be provided by IgM-SDS
PAGE, direct detection by PCR of treponemal DNA, (83) or a strip assay
(84) where individual recombinant antigens bind the antibodies. These
kinds of assays are available, some licensed commercially, and costs are
often comparable to existing VDRL/TPHA technology. The quality and safety
of health care may materially benefit when blood donor lots are
additionally screened with better treponemal tests, and the syphilitic
cases further evaluated. As well, earlier findings of low T-cell levels in
populations with high syphilis rates (85) should be re-assessed.
There is now ample evidence to have another look at the Great
Masquerader. We may learn that syphilis plays a role in AIDS beyond merely
facilitating HIV transmission - and may have done so for centuries, as a
result of the "syphilisation" effect on the Gell and Coombs Type IV
immunologic recall. (86) Is syphilis the "elephant in the room" of AIDS -
to quote Professor Davidoff, "something so big and disturbing that we
don't even see it, despite the fact that we keep bumping into it"? (87)
Our continued reliance on a nearly century-old diagnostic concept for such
a deadly infectious disease may well be seen as a shameful act in years to
come.
John Scythes
Colman Jones
Toronto, Canada
More of these concerns can be found online at
http://cbc.ca/ideas/Aids
References
1. DeSimone JA, Pomerantz RJ, Babinchak TJ. Inflammatory Reactions in
HIV-1-Infected Persons after Initiation of Highly Active Antiretroviral
Therapy. Ann Intern Med 2000; 133(6):447-54.
2. Langford TD, Letendre SL, Marcotte TD, Ellis RJ, McCutchan JA,
Grant I, et al. Severe, demyelinating leukoencephalopathy in AIDS patients
on antiretroviral therapy. AIDS 2002 (16):1019-1029.
3. Pomerantz RJ. Initiating antiretroviral therapy during HIV
infection: confusion and clarity. JAMA 2001; 286(20):2597-9.
4. Concorde: MRC/ANRS randomised double-blind controlled trial of
immediate and deferred zidovudine in symptom-free HIV infection. Concorde
Coordinating Committee. Lancet 1994; 343(8902):871-81.
5. Kreiss JK, Kasper CK, Fahey JL, Weaver M, Visscher BR, Stewart JA,
et al. Nontransmission of T-cell subset abnormalities from hemophiliacs to
their spouses. JAMA 1984; 251(11):1450-4.
6. National surveillance program on occupational exposure to the
human immunodeficiency virus among health care workers in Canada. CMAJ
1988; 138(1):31-3.
7. Duesberg PH. Human Immunodeficiency virus and acquired
immunodeficiency syndrome: Correlation but not causation. Proc Natl Acad
Sci USA 1989; 86:755-64.
8. Shearer GM, Clerici M. Protective immunity against HIV infection:
has nature done the experiment for us? Immunol Today 1996; 17(1):21-4.
9. Bernard NF, Yannakis CM, Lee JS, Tsoukas CM. Human
immunodeficiency virus (HIV)-specific cytotoxic T lymphocyte activity in
HIV-exposed seronegative persons. J Infect Dis 1999; 179(3):538-47.
10. Goh WC, Markee J, Akridge RE, Meldorf M, Musey L, Karchmer T, et
al. Protection against human immunodeficiency virus type 1 infection in
persons with repeated exposure: evidence for T cell immunity in the
absence of inherited CCR5 coreceptor defects. J Infect Dis 1999;
179(3):548-57.
11. Stewart GT. Duesberg & Rasnick Reviewed: Can Drugs Alone
Explain American Aids? Reappraising AIDS 1999; 7(11):1.
12. Sher A, Gazzinelli RT, Oswald IP, Clerici M, Kullberg M, Pearce
EJ, et al. Role of T-cell derived cytokines in the downregulation of
immune responses in parasitic and retroviral infection. Immunol Rev 1992;
127:183-204.
13. Rook GA, Onyebujoh P, Stanford JL. TH1/TH2 switching and loss of
CD4+ T cells in chronic infections: an immunoendocrinological hypothesis
not exclusive to HIV. Immunol Today 1993; 14(11):568-9.
14. Bentwich Z, Maartens G, Torten D, Lal AA, Lal RB. Concurrent
infections and HIV pathogenesis. AIDS 2000; 14:2071-81.
15. Clerici M, Declich S, Rizzardini G. African Enigma: Key Player in
Human Immunodeficiency Virus Pathogenesis in Developing Countries? Clin
Diagn Lab Immunol 2001; 8(5): 864-6.
16. Seremetis SV, Aledort LM, Bergman GE, Bona R, Bray G, Brettler D,
et al. Three-year randomised study of high-purity or intermediate-purity
factor VIII concentrates in symptom-free HIV-seropositive haemophiliacs:
effects on immune status. Lancet 1993; 342(8873):700-3.
17. de Biasi R, Rocino A, Miraglia E, Mastrullo L, Quirino AA. The
impact of a very high purity factor VIII concentrate on the immune system
of human immunodeficiency virus-infected hemophiliacs: a randomized,
prospective, two-year comparison with an intermediate purity concentrate.
Blood 1991; 78(8):1919-22.
18. Lee CA. High purity factor VIII concentrates and HIV infection.
BMJ 1992; 304(6827):641.
19. Pasi KJ, Hill FG. In vitro and in vivo inhibition of monocyte
phagocytic function by factor VIII concentrates: correlation with
concentrate purity. Br J Haematol 1990; 76(1):88-93.
20. Blanche S, Mayaux MJ, Rouzioux C, Teglas JP, Firtion G, Monpoux
F, et al. Relation of the course of HIV infection in children to the
severity of the disease in their mothers at delivery. N Engl J Med 1994;
330(5):308-12.
21. Hrncir Z, Kraus Z, Tichy M. Non-specific humoural immunity
response in latent and tertiary syphilis. Br J Vener Dis 1972; 48(2):108-
12.
22. Wright DJ, Grimble AS. Why is the infectious stage of syphilis
prolonged? Br J Vener Dis 1974; 50(1):45-9.
23. Shannon R, Booth SD. The pattern of immunological responses at
various stages of syphilis. Br J Vener Dis 1977; 53(5):281-6.
24. Jensen JR, Jorgensen AS, Thestrup-Pedersen K. Depression of
natural killer cell activity by syphilitic serum and immune complexes. Br
J Vener Dis 1982; 58(5):298-301.
25. Jensen JR, From E. Alterations in T lymphocytes and T-lymphocyte
subpopulations in patients with syphilis. Br J Vener Dis 1982; 58(1):18-
22.
26. Gschnait F, Schoenwald E, Schmidt BL, Luger A. Laboratory
evidence for impaired cellular immunity in different stages of syphilis. J
Invest Dermatol 1982; 79(1):40-1.
27. Fitzgerald TJ. The Th1/Th2-like switch in syphilitic infection:
is it detrimental? Infect Immun 1992; 60(9):3475-9.
28. Podwinska J, Zaba R, Chomik M, Bowszyc J. The ability of
peripheral blood mononuclear cells of rabbits infected with Treponema
pallidum to produce IL-2. FEMS Immunol Med Microbiol 1993; 7(3):257-64.
29. Podwinska J, Lusiak M, Zaba R, Bowszyc J. The pattern and level
of cytokines secreted by Th1 and Th2 lymphocytes of syphilitic patients
correlate to the progression of the disease. FEMS Immunol Med Microbiol
2000; 28(1):1-14.
30. Pereyra AJ, Voller RL. A graphic guide for clinical management of
latent syphilis. Calif Med 1970; 112(5):13-8.
31. Holmes KK, in Wintrobe MM, editor. Harrison's Principles of
Internal Medicine. 7th ed. New York: McGraw Hill, 1974.
32. Fichtner RR, Aral SO, Blount JH, Zaidi AA, Reynolds GH, Darrow
WW. Syphilis in the United States: 1967-1979. Sex Transm Dis 1983;
10(2):77-80.
33. Centers for Disease Control. Sexually Transmitted Diseases Fact
Sheet. 35th ed. U.S. Dept. of Health and Human Services, Center for
Prevention Services, Atlanta, GA. 1981; 81-8195.
34. Gjestland T. The Olso study of untreated syphilis: an
epidemiologic investigation of the natural course of the syphilitic
infection based upon a re-study of the Boeck-Bruusgaard material. Acta
Derm Venereol 1955; 35 Suppl 34: 343-366.
35. Kampmeier RH. Final Report on the "Tuskegee Syphilis Study".
South Med J 1974; 67(11):1349-53.
36. Hobbs AB. Syphilis; A Study. Ass Life Ins Dir Am 1925; 13:14-31.
37. Blakely DN. Syphilis from the Life Insurance Standpoint. Med Ins
& Health Conserv 1927; 42:446.
38. Neisser & Landsteiner, cited in Chesney, A. Immunity in
Syphilis. Baltimore: Williams and Wilkins Co., 1927, p. 26.
39. Strickler A. Diseases of the Skin and Syphilis. Philadelphia:
F.A. Davis Co., 1927. p. 369.
40. Hall AF. Under-Treatment Versus Over-Treatment of Syphilis. J
Indiana Med Ass 1935; 28:587
41. Morgan HJ. The Prognosis of Syphilis. JAMA 1939; 112:311-7.
42. Moore JE. Unresolved Clinical Problems of Syphilology. Am J Syph
Gonor and Ven Dis 1939; 23(1):701-11.
43. Reynolds F. Syphilis. In: Christian HA, editor. Oxford Medicine
1948; 5(3):665-668.
44. Rosahn PD. The adverse influence of syphilitic infection on the
longevity of mice and men. Am Med Ass Arch Derm Syph 1952; 66(5):547-568.
45. Smith JL. Spirochetes in Late Seronegative Syphilis. Springfield,
Ill.: Charles C. Thomas, 1969. p. 181-221.
46. Chandler FW, McClure HM, Campbell WG, Watts JC. Pulmonary
pneumocystosis in nonhuman primates. Arch Pathol Lab Med 1976; 100(3):163-
7.
47. Horvath I. Experimental Mouse Syphilis for the Syphilis
Eradication Program. WHO Biology and Pathogenicity of Treponemes
conference, University of Birmingham, 11-13 April 1989.
48. Larsen SA. Syphilis Diagnosis Dynamics. 9th International Meeting
of the ISSTDR 1991 Banff, Alberta, abstract no. C-12 273.
49. Scythes JB. Animal Model for Aids Immunology, Secondary to
Symptomless Infection with Treponema Pallidum. Int Conf AIDS 1992; 8(3):36
(abstract no. PuA 6154)
50. Thomas EW. Syphilis: Its Course and Management. New York:
Macmillan, 1949. p. 10.
51. Luger A. In: Young H, McMillan A, editors. The Immunological
Diagnosis of Sexually Transmitted Diseases. New York: Marcel Dekker, 1988.
p. 250-1.
52. Masawe AEJ, Lumholt G, Aho K, Lassus A. Unusual behaviour of
serological tests for syphilis in Ugandan Africans. Br J Vener Dis 1972;
48:345-9.
53. Moore JE. The Modern Treatment of Syphilis. 2nd ed. Springfield,
Ill.: Charles C. Thomas, 1941. p. 26.
54. Beerman H. The Problem of Reinoculation of Human Beings with
Spirochaeta Pallida. Am J Syph Gonor Ven Dis 1946; 30(2):173-92.
55. Arnold RC, Mahoney JF, Cutler JC. Reinfection in experimental
syphilis in rabbits following penicillin therapy. Am J Syph Gonor Ven Dis
1947; 31(3):264-7.
56. Arnold RC, Mahoney JF, Cutler JC. Reinfection in experimental
syphilis in rabbits following penicillin therapy. Am J Syph Gonor Ven Dis
1947; 31(5):489-92.
57. Magnuson HJ, Rosenau BJ, Clark JW. The Duration of Acquired
Immunity in Experimental Syphilis. Am J Syph Gonor & Ven Dis 1949;
33:297-302.
58. Magnuson HJ, Thomas EW, Olansky S, Kaplan BI, De Mello L, Cutler
JC. Inoculation Syphilis in Human Volunteers. Medicine 1956; 35:33-82.
59. Quetel C. History of Syphilis. Baltimore: The Johns Hopkins
University Press, 1990. p. 112-114.
60. Sherwood J. Syphilization: human experimentation in the search
for a syphilis vaccine in the nineteenth century. J Hist Med Allied Sci
1999; 54(3): 364-86.
61. Morton RS, Harris JRW, editors. Recent Advances in Sexually
Transmitted Diseases. London: Churchill Livingstone, 1975. p. 92-4.
62. Lukehart SA, Holmes KK. In: Fauci AS, Braunwald E, Isselbacher
KJ, editors. Harrison's Principles of Internal Medicine. New York: McGraw-
Hill, 1998. p. 1023-33.
63. Centers for Disease Control and Prevention. Resurgent bacterial
sexually transmitted disease among men who have sex with men King
County, Washington, 1997-1999. MMWR 1999; 48:773-777.
64. Renzullo PO, McNeil JG, Gardner LI, Brundage JF. Inpatient
morbidity among HIV-infected male soldiers prior to their diagnosis of HIV
infection. Am J Public Health 1991; 81(10):1280-4.
65. Veuqelers PJ, van Zessen G, Sandfort TG, Coutinho RA, van
Griensven GJ. HIV prevalence and magnitude of the male homosexual
population in Amsterdam. Int Conf AIDS. 1992; 8(2):C326 (abstract no. PoC
4486)
66. Blocker ME, Levine WC. HIV prevalence in patients with syphilis,
United States. Sex Transm Dis 2000; 27(1):53-9.
67. MacFadden DK, Notenboom RH, Scythes JB. Syphilis - A Role In
Sexually Acquired AIDS? WHO Biology and Pathogenicity of Treponemes
conference, University of Birmingham, 11-13 April 1989
68. Notenboom RH, MacFadden DK. Reliability of Syphilis Tests in
Patients with HIV. Int Conf AIDS 1992; 8(2):B94 (abstract no. PoB 3044)
69. Fralick RA, Scythes JB, Notenboom RH, MacFadden DK. Syphilis and
HIV: Seroprevalence and Clinical Observations in HIV Clinic, Toronto. Sex
Trans Dis 1994; 21: Suppl 183, abstract 271.
70. Evans BA, McLean KA, Dawson SG, Teece SA, Bond RA, MacRae KD, et
al. Trends in sexual behaviour and risk factors for HIV infection among
homosexual men, 1984-7. BMJ 1989; 298(6668):215-8.
71. Haas JS, Bolan G, Larsen SA, Clement MJ, Bacchetti P, Moss AR.
Sensitivity of treponemal tests for detecting prior treated syphilis
during human immunodeficiency virus infection. J Infect Dis 1990;
162(4):862-6.
72. Johnson PD, Graves SR, Stewart L, Warren R, Dwyer B, Lucas CR.
Specific syphilis serological tests may become negative in HIV infection.
AIDS 1991; 5(4):419-23.
73. Sjovall P, Flamholc L, Kroon BM, Bredberg A. HIV infection and
loss of treponemal test reactivity. Acta Derm Venereol 1991; 71(5):458.
74. Wicher K, Wicher V. Immunopathology of syphilis. In: Schell RF,
Musher DM, editors. Pathogenesis and Immunology of Treponemal Infection.
New York: Marcel Dekker, 1983. p. 144.
75. Rompalo AM, Joesoef MR, O'Donnell JA, Augenbraun M, Brady W,
Radolf JD, et al. Clinical manifestations of early syphilis by HIV status
and gender: results of the syphilis and HIV study. Sex Transm Dis 2001;
28(3):158-65.
76. Levy JA, Ziegler JL. Acquired immunodeficiency syndrome is an
opportunistic infection and Kaposi's sarcoma results from secondary immune
stimulation. Lancet 1983; 2(8341):78-81.
77. Marion SA, Schechter MT, Weaver MS, McLeod WA, Boyko WJ,
Willoughby B, et al. Evidence that prior immune dysfunction predisposes to
human immunodeficiency virus infection in homosexual men. J Acquir Immune
Defic Syndr. 1989; 2(2):178-86.
78. Clerici M, Shearer GM. A TH1-->TH2 switch is a critical step
in the etiology of HIV infection. Immunol Today 1993; 14(3):107-11.
79. Musher DM, Hamill RJ, Baughn RE. Effect of human immunodeficiency
virus (HIV) infection on the course of syphilis and on the response to
treatment. Ann Intern Med 1990; 113(11):872-81.
80. denHollander N, Berry R, Fearon M. Treponemal Based Screening for
Syphilis - Detecting Latent Cases. General Meeting of the American Society
for Microbiology. 2000; C-367.
81. Erbelding EJ, Vlahov D, Nelson KE, Rompalo AM, Cohn S, Sanchez P,
et al. Syphilis serology in human immunodeficiency virus infection:
evidence for false-negative fluorescent treponemal testing. J Infect Dis
1997; 176(5):1397-400.
82. Schmidt BL, Edjlalipour M, Luger A. Comparative evaluation of
nine different enzyme-linked immunosorbent assays for determination of
antibodies against Treponema pallidum in patients with primary syphilis. J
Clin Microbiol 2000; 38(3):1279-82.
83. Liu H, Rodes B, Chen CY, Steiner B. New Tests for Syphilis:
Rational Design of a PCR Method for Detection of Treponema pallidum in
Clinical Specimens Using Unique Regions of the DNA Polymerase I Gene. J
Clin Microbiol 2001; 39:1941-46.
84. Hagedorn H, Kraminer-Hagedorn A, De Bosschere K, Hulstaert F,
Pottel H, Zrein M. Evaluation of INNO-LIA Syphilis Assay as a Confirmatory
Test for Syphilis. J Clin Microbiol 2002; 40(3):973-8.
85. Bartholomew C, Saxinger WC, Clark JW, Gail M, Dudgeon A, Mahabir
B, et al. Transmission of HTLV-I and HIV among homosexual men in Trinidad.
JAMA 1987; 257(19):2604-8.
86. Dattner B. The Management of Neurosyphilis. New York: Grune &
Stratton, 1944. p. 333.
87. Davidoff F. Shame: the elephant in the room. BMJ 2002; 324:623-4.
Competing interests: No competing interests
As a cancer patient whose bad experiences were a direct result of
closed, defensive attitudes (BMJ 1998;316:1890-3) I was left damaged,
incredulous and needing answers. Despite later pleas for change in the
name of humanity, the total refusal to stop practices which caused
unnecessary suffering and pain seemed due only to the shame which would
follow if past and current practices were acknolwedged to be unacceptable.
Surely this, more than any other factor, is what has prevented
clinicians from learning from one another, contributed to low cancer
survival rates, and continues to hold back healthcare improvements.
Consultants have long been accused of arrogance. Universal recognition of
their dilemmas, of having to admit some degree of failure before they can
change and improve, might allow them to take that first step -
acknowledgement of reality.
How might patients, patients' organisations and consumer groups
extend a helping hand? By discussion, liaison, demonstrating understanding
and acceptance of the past without blame; by involvement in medical
education at all levels we could open minds and open doors to brighter
futures for clinicians and patients.
Competing interests: No competing interests
Editor,
The BMJ editorial titled “Shame: the elephant in the room” (1) examines
the issue of shame mainly from a service provider’s perspective. It
highlights the improvements necessary in order to improve the safety and
quality of medical care. It states “countering shame can motivate health
care providers to learn and improve, bolstering their competence and their
sense of self worth leading to better quality service provision”.
It is also important in our view, to examine the issue of shame from
a patient’s perspective. A topical example is the national strategy for
sexual health and HIV (2).This is a welcome step towards addressing a
worrying increase in both the incidence and prevalence of sexually
transmitted infections (STIs), particularly among young adults and
teenagers. Many still consider STIs a moral issue with the resultant
negative attitudes towards cases persisting even among health care
providers.
This increases the stigma and shame that patients with STIs feel when
having to talk about their problem. Patients have great difficulty talking
about their sexual health and initiatives targeted towards primary care
such as update courses on taking a sexual history are to be applauded.
It is embarrassment and shame that prevents patients from seeking help
from available services, and also leads in many cases to reluctance to
inform their sexual contacts due to the shame of admitting the source of
infection may have been outside of an established relationship.
The message that all services for STIs are confidential needs to be
put across, particularly for school children, teenagers and young adults.
Victims of sexual assault with or without alcohol intoxication are in a
special category. These individuals have been both physically and
emotionally traumatised, and suffer feelings of fear and shame. Emergency
services and law enforcement agencies have mechanisms built into their
systems to deal with these issues, but cases do not always present to them
first. Concerns about STIs need to be dealt with sensitively.
Improvements in communication between parents and their children,
sexual partners, school nurses and students and general practitioners as a
first point of contact between the patients and available services is key
to scaring off this elephant that patients inevitably carry around with
them.
Bolanle Akinosi, Specialist Registrar in Public health Medicine
R. Nicholas Pugh, Consultant in Communicable Disease Control
Walsall Heath Authority, Lichfield House, 27-31 Lichfield Street,
Walsall WS1 1TE
Correspondence to akinosib@ha.walsall-ha.wmids.nhs.uk
References
1. Davidoff, F. Shame: the elephant in the room. Managing shame is
important for improving health care. BMJ 2002; 324: 623-4
2. Department of Health. The national strategy for sexual health and HIV.
London: Department of Health, 2001. www.doh.gov.uk/nshs/index.htm
Competing interests: No competing interests
Dear Sir:
I would like to disagree with Dr Davidoff's paper(1) and suggest a
better alternative than "shame".
If for the sake of argument, the
information about the deleterious effect of tobutamide on the myocardiun
became retroactively known to physicians prescribing it, the duty of those
physicians would be to immediately inform their patients taking
tolbutamide to discontinue the drug. The patients I think would be
grateful for the physicians vigilance concerning their care. There is no
shame because of a specific ignorance or lack of information that was not
available initially about the effect of tolbutamide on the heart.
Such a problem has no malice or preconceived harm toward the patient.
Such a problem is fortunately not very common in clinical practice.
Recently it has surfaced with the class drug Cox 2-inhibitor in patients
with Rheumatoid arthritis and its untoward effect on first occurrence of
heart failure and on promoting relapse of heart failure(2).
If the word "shame" is to be used, which I think it is out of context,
blame maybe a better word directed to the researches and the business
promoting machine of the drug firms, for lack of accuracy in the work they
are supposed to do on a particular drug prior to its introduction on the
market.
References
1- Davidoff F; Editorial, BMJ March 17 2002
2- Feenstra J et al: Association of NSAIDS and
First Occurrence of Heart failure and
Relapsing Heart Failure.Arch Int Med Vol 162
#3; Feb. 11,2002.
Competing interests: No competing interests
SARS and “decompression sickness” – the “butterfly effect”?
There have been over 8500 cases of SARS worldwide with over 800
deaths from this condition. With these numbers there has been a large
morbidity and a huge amount of fear generated worldwide. It, however, has
not been recognised as a contributory cause of decompression sickness (the
bends) in scallop divers in the West Coast of Scotland.
We should be reminded of the chaos theory as originally described in
the early 1960’s by Edward Lorenz, a mathematician and meteorologist. He
described the string of seemingly unrelated links creating a completely
unpredictable result as the “butterfly effect”. i.e a butterfly flaps its
wings in South America causing a tornado in Texas.
A man sneezes in a crowd in China
SARS becomes a health problem
The people of Japan stop going out socially
Japanese restaurants have a downturn in their trade with a reduction in
the demand for the delicacy razor-shell fish
Razor-shell fish divers in the West Coast of Scotland no longer have a
market so start diving for scallops
Scallop diving is much deeper
Divers get decompression sickness (DCS)
We at the Dunstaffnage Hyperbaric Unit, have seen and treated 6 cases
of DCS in the first 6 months of this year in scallop divers when the usual
incidence is 1 to 2 per year. I rest my case
Competing interests:
None declared
Competing interests: No competing interests